DiseaseName	Regulator	Target	RegulationDiretion	Experimental.method.for.lncRNA.target	ExpressionPattern	Experimental.method.for.lncRNA.expression	Data.accession	Data.accession2	influencedFunction	regulatoryMechanism	regulatoryType	levelOfRegulation	Drugs	cancerStemCell	hallmark	diseaseCategory	DiseaseName2	RegulatorType	TargetType	RegulatorEnsembleID	lncRegulatorPosition	TargetEnsembleID	lncTargetPosition	RegulatorEntrezID	TargetEntrezID	RegulatorAliases	TargetAliases	Evidence	PubMedID	RID	SearchregulatoryMechanism	clincal.application	RegulatorCTC	TargetCTC
Papillary thyroid carcinoma	LINC00313	miR-4429	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000185186	GRCh38_21:43461960-43479534	NA	NA	114038	NA	C21orf84|CH507-42P11.5|NCRNA00313	NA	Long noncoding RNA LINC00313 modulates papillary thyroid cancer tumorigenesis via sponging miR-4429	29940766	RID00001	ceRNA or sponge	NA	NA	NA
Malignant glioma	FAM83H-AS1	CDKN1A	negatively-E	RIP;RNA pull-down assay;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734140-143746337	ENSG00000124762	NA	100128338	1026	onco-lncRNA-3	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21).FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A;thereby influencing the cell cycle and proliferation	29870057	RID00002	epigenetic regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	NEAT1	TGFB1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-139-5p)	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105329	NA	283131	7040	LINC00084|NCRNA00084|TncRNA|VINC	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NEAT1 upregulates TGF-beta1 to induce hepatocellular carcinoma progression by sponging hsa-mir-139-5p.	29797561	RID00003	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	NEAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-448)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000148516	NA	283131	6935	LINC00084|NCRNA00084|TncRNA|VINC	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1.Overexpression of NEAT1 can induce breast cancer cell growth, migration, and invasion by inhibiting miR-448 and upregulating ZEB1	29323713	RID00004	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	ZFPM2-AS1	MIF	positively-F	mass spectrometry;western blot;RNA pull-down assay;RIP	upregulation	qPCR;microarray;sequencing	GSE1279;TCGA	GSE1279.zip;STAD.zip	cancer progression(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000240972	NA	102723356	4282	SCAT3	GIF|GLIF|MMIF	ZFPM2-AS1, a novel lncRNA, attenuates the p53 pathway and promotes gastric carcinogenesis by stabilizing MIF;tumor-activated ZFPM2-AS1 could bind to and protect the degradation of macrophage migration inhibitory factor (MIF);Knockdown of MIF expression diminished ZFPM2-AS1's impact on p53 expression in gastric cancer cells.	29985481	RID00005	interact with protein	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	SNHG1	miR-448	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+);immune evasion(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Evading Immune Detection	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.SNHG1 directly contacted with miR-448, which could negatively regulate IDO;Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.	29886172	RID00006	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	NA
Breast cancer	SNHG1	IDO1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+);immune evasion(+)	ceRNA(miR-448)	regulation	NA	NA	NA	Evading Immune Detection	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000131203	NA	23642	3620	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	IDO|IDO-1|INDO	LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.SNHG1 directly contacted with miR-448, which could negatively regulate IDO;Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.	29886172	RID00007	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00222	GSK3B	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+);WNT signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203801	GRCh38_6:108751654-108769942	ENSG00000082701	NA	387111	2932	C6orf181|NCRNA00222|dJ354J5.2	NA	Long non-coding RNA LINC00222 regulates GSK3beta activity and promotes cell apoptosis in lung adenocarcinoma;overexpression of LINC00222 enhanced the activity of glycogen synthase kinase-3beta(GSK3beta), which is a key element of the Wnt signaling pathway;Enforced expression of LINC00222 significantly inhibited the proliferation, migration and invasive ability of lung adenocarcinoma cells	29990868	RID00008	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	TP73-AS1	CASP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000164305	NA	57212	836	KIAA0495|PDAM	CPP32|CPP32B|SCA-1	Enhanced expression of lncRNA TP73-AS1 predicts adverse phenotypes for cholangiocarcinoma and exerts oncogenic properties in vitro and in vivo.silencing of TP73-AS1 facilitates apoptosis via activating caspase-3 and caspase-9;TP73-AS1 could also facilitate migration and invasion potential of CCA cells;TP73-AS1 transcription is enhanced in both CCA tissue samples and cell lines, and this upregulation is closely associated with larger tumor size (p=0.008) and advanced TNM stage	29966969	RID00009	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Cholangiocarcinoma	TP73-AS1	CASP9	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000132906	NA	57212	842	KIAA0495|PDAM	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Enhanced expression of lncRNA TP73-AS1 predicts adverse phenotypes for cholangiocarcinoma and exerts oncogenic properties in vitro and in vivo.silencing of TP73-AS1 facilitates apoptosis via activating caspase-3 and caspase-9;TP73-AS1 could also facilitate migration and invasion potential of CCA cells;TP73-AS1 transcription is enhanced in both CCA tissue samples and cell lines, and this upregulation is closely associated with larger tumor size (p=0.008) and advanced TNM stage	29966969	RID00010	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Ovarian cancer	PVT1	miR-133a	negatively-F	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long non-coding RNA PVT1 promotes cell proliferation and invasion through regulating miR-133a in ovarian cancer;qRT-PCR and luciferase reporter assays demonstrated PVT1 regulated miR-133a expression;Knockdown of PVT1 inhibited cell proliferation, migration and invasion through negative regulating miR-133a in OC cells	29957467	RID00011	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Colorectal cancer	FEZF1-AS1	PKM	positively-F	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	qRT-PCR;microarray	NA	NA	STAT3 signaling pathway(+);cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000067225	NA	154860	5315	NA	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	LncRNA-FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling.FEZF1-AS1 could bind and increase the stability of the pyruvate kinase 2 (PKM2) protein;these data provide mechanistic insights into the regulation of FEZF1-AS1 on both STAT3 signaling and glycolysis by binding PKM2 and increasing its stability;LncRNA-FEZF1-AS1 Promotes Tumor proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling	29914894	RID00012	interact with protein	metastasis	NA	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Retinoblastoma	DANCR	MMP9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-34c;miR-613)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000100985	NA	57291	4318	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA DANCR aggravates retinoblastoma through miR-34c and miR-613 by targeting MMP-9.our results reveal that DANCR function as competing endogenous RNA (ceRNA) for miR-34c and miR-613 to modulate progression and metastasis in RB oncogenesis via targeting MMP-9	29744877	RID00013	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	HOTTIP	miR-216a-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Long non-coding RNA HOTTIP promotes prostate cancer cells proliferation and migration by sponging miR-216a-5p;Bioinformatics online programs predicted that HOTTIP sponge miR-216a-5p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOTTIP could negatively regulate the expression of miR-216a-5p in PCa cells	29884766	RID00014	ceRNA or sponge	NA	NA	NA
Gastric cancer	PEG10	miR-3200	negatively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	NA	NA	EDR|HB-1|MEF3L|Mar2|Mart2|RGAG3|RTL2|SIRH1	NA	Knockdown of long non-coding RNA PEG10 inhibits growth, migration and invasion of gastric carcinoma cells via up-regulating miR-3200;	29940767	RID00015	expression association	NA	NA	NA
Gastric cancer	CCAT1	BMI1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000168283	NA	100507056	648	CARLO5|CARLo-5|onco-lncRNA-40	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Knockdown of long noncoding RNA CCAT1 inhibits cell growth, invasion and peritoneal metastasis via downregulation of Bmi-1 in gastric cancer;The results showed that CCAT1 knockdown markedly inhibited cell proliferation, migration and invasion, arrested the cell cycle at G0/G1 phase in vitro, and inhibited peritoneal metastasis in nude mice, along with the downregulation of Bmi-1	29940756	RID00016	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Esophageal cancer	GAS5	miR-301a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Promotes proliferation, Migration, and Invasion by Regulation of miR-301a in Esophageal Cancer;miR-301a appeared to be directly sponged by GAS5	29386089	RID00017	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Malignant glioma	CCDC26	miR-203	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR;northern blot	NA	NA	cell growth(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229140	GRCh38_8:128634199-129683770	NA	NA	137196	NA	RAM	NA	Silencing of lncRNA CCDC26 Restrains the Growth and Migration of Glioma Cells In Vitro and In Vivo via Targeting miR-203; miR-203 is a direct target of CCDC26	28600863	RID00018	ceRNA or sponge	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Lung adenocarcinoma	CRNDE	CDKN1A	negatively-E	RNAi;ChIP	upregulation	qRT-PCR	NA	NA	radioresistance(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000124762	NA	NA	1026	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression;the mechanistic investigations showed that CRNDE could interact with PRC2 and recruit its core component EZH2 to p21 (CDKN1A) promoter regions and repress its transcription;	28550688	RID00019	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	LINC00858	CDK14	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-139)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000058091	NA	170425	5218	CRCAL-2	PFTAIRE1|PFTK1	Long noncoding RNA LINC00858 promotes osteosarcoma through regulating miR-139-CDK14 axis;LINC00858 was identified to sponge miR-139 to form RNA-induced silencing complex (RISC) using luciferase reporter assay and RNA immunoprecipitation;these data prove that LINC00858/miR-139/CDK14 axis promotes the tumorigenesis of osteosarcoma	29944887	RID00020	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	HOTAIR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell migration(+)	ceRNA(miR-23b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148516	NA	100124700	6935	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA HOTAIR contributes to the malignancy of hepatocellular carcinoma by enhancing epithelial-mesenchymal transition via sponging miR-23b-3p from ZEB1;Our in vitro experiments suggested that HOTAIR promoted invasion and migration of HCC cells through enhancing EMT via sponging miR-23b-3p from ZEB1. Finally, the in vivo experiments indicated that HOTAIR could promote metastasis of HCC by enhancing EMT in vivo.	29778425	RID00021	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HAGLR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-130a-3p)	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000148516	NA	401022	6935	HOXD-AS1|MIR7704HG|Mdgt	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	HOXD-AS1 Exerts Oncogenic Functions and Promotes Chemoresistance in Cisplatin-Resistant Cervical Cancer Cells;These results collectively show that HOXD-AS1 can act as a competing endogenous RNA to upregulate ZEB1 expression via miR-130a-3p	29896986	RID00022	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial cancer	TDRG1	VEGFA	positively-F	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000112715	NA	732253	7422	LINC00532|lincRNA-NR_024015	MVCD1|VEGF|VPF	LncRNA TDRG1 enhances tumorigenicity in endometrial carcinoma by binding and targeting VEGF-A protein;RNA binding protein immunoprecipitation (RIP) assays confirmed that lncRNA TDRG1 directly binds to VEGF-A protein;knockdown of VEGFA in lncRNA TDRG1-overexpressing endometrial carcinoma cells reversed the effects of lncRNA TDRG1 on cell proliferation, invasion, migration and apoptosis	29920344	RID00023	interact with protein	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Colorectal cancer	LIFR-AS1	TNFAIP3	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	microarray;qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-29a)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000118503	NA	100506495	7128	NA	A20|AISBL|OTUD7C|TNFA1P2	Functional role of a long non-coding RNA LIFR-AS1/miR-29a/TNFAIP3 axis incolorectal cancer resistance to pohotodynamic therapy;LIFR-AS1 serves as a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of CRC to PDT	29807108	RID00024	ceRNA or sponge	chemoresistance	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	THORLNC	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell stemness(+)	transcriptional regulation	binding/interaction	RNA-RNA	cisplatin	CSC	Limitless Replicative Potential	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000137693	NA	100506797	10413	NA	COB1|YAP|YAP2|YAP65|YKI	LncRNA THOR attenuates cisplatin sensitivity of nasopharyngeal carcinoma cells via enhancing cells stemness;THOR could enhance YAP transcriptional activity via directly binding to YAP and suppressing its translocation from nuclear to cytoplasm	29959065	RID00025	transcriptional regulation	chemoresistance	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	LINC00339	FOXM1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000111206	NA	29092	2305	HSPC157|NCRNA00339	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long non-coding RNA LINC00339 facilitates the tumorigenesis of non-small cell lung cancer by sponging miR-145 through targeting FOXM1;Luciferase reporter assay and RNA immunoprecipitation (RIP) revealed that LINC00339 promoted the NSCLC progression via FOXM1 via targeting miR-145	29906749	RID00026	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung adenocarcinoma	NNT-AS1	miR-129-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR;sequencing	TCGA	LUAD.zip	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	NA	NA	100652772	NA	NA	NA	LncRNA NNT-AS1 promotes the proliferation, and invasion of lung cancer cells via regulating miR-129-5p expression;we identified that NNT-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-129-5p in lung cancer	29857296	RID00027	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	NA
Breast cancer	CBR3-AS1	TGFB1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000105329	NA	100506428	7040	PlncRNA-1|PlncRNA1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-beta1 and downregulating PHGDH;Upregulation of PlncRNA-1 promoted the expression of TGF-beta1, but inhibited the expression of PHGDH;LncRNA PlncRNA-1 overexpression reduced the proliferation rate, but increased the apoptosis rate of breast cancer cells, while treatment with TGF-beta inhibitor reduced those effects of PlncRNA-1 overexpression	29626321	RID00028	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	CBR3-AS1	PHGDH	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell growth(-);cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000092621	NA	100506428	26227	PlncRNA-1|PlncRNA1	3-PGDH|3PGDH|HEL-S-113|NLS|NLS1|PDG|PGAD|PGD|PGDH|PHGDHD|SERA	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-beta1 and downregulating PHGDH;Upregulation of PlncRNA-1 promoted the expression of TGF-beta1, but inhibited the expression of PHGDH;LncRNA PlncRNA-1 overexpression reduced the proliferation rate, but increased the apoptosis rate of breast cancer cells, while treatment with TGF-beta inhibitor reduced those effects of PlncRNA-1 overexpression	29626321	RID00029	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE111065)
Colorectal cancer	HOTAIR	CDKN1A	negatively-E	RT-qPCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Down-Regulated LncRNA-HOTAIR Suppressed Colorectal Cancer Cell proliferation,Invasion, and Migration by Mediating p21	29808247	RID00030	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	HOTAIR	RUNX3	negatively-F	RPI-Seq;RIP;RNA pull-down assay	NA	NA	NA	NA	cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000020633	NA	100124700	864	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AML2|CBFA3|PEBP2aC	HOTAIR induces the ubiquitination of Runx3 by interacting with Mex3b and enhances the invasion of gastric cancer cells;We found that HOTAIR was bound to Runx3 protein and identified the fragment of HOTAIR spanning 1951-2100 bp as the specific binding site;Inhibition of HOTAIR significantly suppressed gastric cancer cell migration and invasion through upregulating claudin1, which could be reversed by co-deficiency of Runx3.	29417297	RID00031	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	ZEB2-AS1	HMGB1	positively-E	RIP;luciferase reporter assay	upregulation	microarray	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000189403	NA	100303491	3146	ZEB2-AS|ZEB2AS|ZEB2NAT	HMG-1|HMG1|HMG3|SBP-1	LncRNA ZEB2-AS1 promotes pancreatic cancer cell growth and invasion through regulating the miR-204/HMGB1 axis; ZEB2-AS1 exerted as a ceRNA and negatively regulated miR-204 expression;HMGB1 was identified as a down-stream target of miR-204	29753015	RID00032	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Hepatocellular carcinoma	FUNDC2P4	CDH1	positively-E	western blot	downregulation	microarray;qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227009	GRCh38_22:39155525-39155945	ENSG00000039068	NA	100127979	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA FUNDC2P4 down-regulation promotes epithelial-mesenchymal transition by reducing E-cadherin expression in residual hepatocellular carcinoma after insufficient radiofrequency ablation;overexpression of FUNDC2P4 inhibited proliferation, invasion and migration potential and up-regulated E-cadherin expression in SMMC-7721 cells, whereas silencing FUNDC2P4 promoted these potentials	29295626	RID00033	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Malignant glioma	SNHG12	ELAVL1	interact	RIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000066044	NA	85028	1994	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	ELAV1|HUR|Hua|MelG	Long non-coding RNA SNHG12 promotes the proliferation and migration of glioma cells by binding to HuR;RIP and RNA pull-down assays demonstrated that SNHG12 was associated with and was stabilized by HuR	30015836	RID00034	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Melanoma	LNCRNA-ATB	YAP1	positively-E	RNA pull-down assay;RT-qPCR;western blot	upregulation	microarray;qRT-PCR	GSE3189	GSE3189.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-590-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000137693	NA	114004396	10413	NA	COB1|YAP|YAP2|YAP65|YKI	lncRNA-ATB functions as a competing endogenous RNA to promote YAP1 by sponging miR-590-5p in malignant melanoma;lncRNA-ATB functions as a competing endogenous RNA (ceRNA) to enhance Yes associated protein 1 expression by competitively sponging microRNA miR-590-5p;lncRNA-ATB functions as a ceRNA to promote MM proliferation and invasion	29956757	RID00035	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Colorectal cancer	CYTOR	NRP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+);cell growth(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000099250	NA	112597	8829	C2orf59|LINC00152|NCRNA00152	BDCA4|CD304|NP1|NRP|VEGF165R	Long non-coding RNA 00152 functions as a competing endogenous RNA to regulate NRP1 expression by sponging with miRNA-206 in colorectal cancer;lnc00152 overexpression promoted epithelial-mesenchymal transition (EMT) and increased neuropilin-1 (NRP1) expression in the CRC cells;the critical role of lnc00152 in tumor growth and progression in CRC	29956750	RID00036	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761)
Colon cancer	MALAT1	HMGB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	LncRNA MALAT1 induces colon cancer development by regulating miR-129-5p/HMGB1 axis;miR-129-5p was identified and confirmed as a direct regulator of MALAT1;MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer;miR-129-5p mimics were able to restrain the progression of colon cancer cells;Inhibition of MALAT1 can inhibit the proliferation of colon cancer	29226325	RID00037	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Hepatocellular carcinoma	NEAT1	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-485)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|NCRNA00084|TncRNA|VINC	ADMIO|ADMIO1|APRF|HIES	The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR-485 and enhancing the expression of the STAT3;sh-STAT3 was able to restrain HCC cell migration and invasion process;NEAT1 inhibiton can repress HCC growth, migration, and invasion. NEAT1 paraspeckle promotes human hepatocellular carcinoma progression by strengthening IL-6/STAT3 signaling.Destruction of paraspeckle formation by silencing the paraspeckle essential components NEAT1_2 or NONO could suppress IL-6-induced STAT3 phosphorylation in HCC cells.Our results demonstrate that paraspeckle can nuclear entrap the inhibitors of IL-6/STAT3 signaling as well as DNA damage, and then strengthen the promoting effect on HCC progression by IL-6. Mechanistically, paraspeckle promotes IL-6-induced STAT3 phosphorylation by binding and trapping peroxiredoxin-5 (PRDX5) mRNA in nucleus, decreasing protein level of PRDX5 which can directly interact with STAT3 and inhibit STAT3 phosphorylation.	29219178;30377567	RID00038	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	MALAT1	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-124)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168610	NA	378938	6774	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ADMIO|ADMIO1|APRF|HIES	The lncRNA MALAT1 contributes to non-small cell lung cancer development via modulating miR-124/STAT3 axis;Downregulation of MALAT1 can inhibit NSCLC development by enhancing miR-124 and decreasing STAT3 expression;shMALAT1 can inhibit NSCLC cell proliferation, colony formation and apoptosis	29215698	RID00039	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Lung adenocarcinoma	SNHG5	CASP1	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	ceRNA(miR-377)	regulation	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000137752	NA	387066	834	C6orf160|LINC00044|NCRNA00044|U50HG	ICE|IL1BC|P45	The long non-coding RNA SNHG5 regulates gefitinib resistance in lung adenocarcinoma cells by targetting miR-377/CASP1 axis;SNHG5 overexpression sensitized gefitinib resistant; Overexpression of SNHG5 suppressed the expression of miR-377, while the knockdown of SNHG5 increased the miR-377 expression;CASP1 was predicted as a downstream target of miR-377	29592872	RID00040	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	FOXP4-AS1	LATS1	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000131023	NA	101060264	9113	NA	WARTS|wts	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID00041	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	TUG1	miR-29c	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Upregulation of Long Noncoding RNA TUG1 Promotes Bladder Cancer Cell proliferation, Migration, and Invasion by Inhibiting miR-29c;There were direct interactions between miR-29c and the binding sites of TUG1	29321088	RID00042	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Urinary bladder cancer	LNCRNA-ATB	miR-126	negatively-F	qRT-PCR;luciferase reporter assay	NA	NA	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	NA	GRCh38_14:19126530-19128974	NA	NA	114004396	NA	NA	NA	Long Noncoding RNA ATB Promotes proliferation, Migration, and Invasion in Bladder Cancer by Suppressing MicroRNA-126;lncRNA-ATB overexpression significantly promoted cell viability, migration, and invasion in T24 cells;lncRNA-ATB was a molecular sponge of miR-126 and exerted tumor-promoting effects by downregulation of miR-126	29321082	RID00043	ceRNA or sponge	NA	NA	NA
Retinoblastoma	SP1	PANDAR	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	Sustained Angiogenesis	Cancer	Retinoblastoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000281450	GRCh38_6:36673621-36675126	6667	101154753	NA	PANDA	SP1-induced upregulation of lncRNA PANDAR predicts adverse phenotypes in retinoblastoma and regulates cell growth and apoptosis in vitro and in vivo;SP1 could bind directly to the PANDAR promoter region and activate its transcription;PANDAR was increased in RB tissues and cells, and this upregulation was associated with advanced IIRC stage, positive optic nerve invasion, and lower differentiation grade in RB patients	29778422	RID00044	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	STAT1	LINC00174	positively-E	luciferase reporter assay;RNA pull-down assay;RNAi;JARSPAR	upregulation	sequencing	TCGA	COAD.zip	cancer progression(+);prognosis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000115415	NA	ENSG00000179406	GRCh38_7:66376044-66493566	6772	285908	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	NCRNA00174	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ;the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients;transcription factor STAT1 mediated LINC00174 expression in CRC	29729381	RID00045	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE86978)
Colorectal cancer	LINC00174	TAZ	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis(+)	ceRNA(miR-1910-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000179406	GRCh38_7:66376044-66493566	ENSG00000102125	NA	285908	6901	NCRNA00174	BTHS|CMD3A|EFE|EFE2|G4.5|LVNCX|Taz1	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ;the aberrant overexpression of LINC00175 indicated the poor prognosis of CRC patients;LINC00174 contributed to CRC progression by regulating miR-1910-3p/TAZ signal pathway	29729381	RID00046	ceRNA or sponge	prognosis	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TP73-AS1	EZH2	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation;ceRNA(miR-449a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000106462	NA	57212	2146	KIAA0495|PDAM	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA TP73-AS1 promotes non-small cell lung cancer progression by competitively sponging miR-449a/EZH2;miR-449a both targeted the 3'-UTR of TP73-AS1 and EZH2;the knockdown of TP73-AS1 inhibited NSCLC cell proliferation, tumor growth and cycle progression in vivo and in vitro	29803931	RID00047	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Triple-receptor negative breast cancer	GAS5	miR-196a-5p	negatively-F	qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA GAS5 suppresses triple negative breast cancer progression through inhibition of proliferation and invasion by competitively binding miR-196a-5p;GAS5 can bind to miR-196a-5p and there is a negative relationship between GAS5 and miR-196a-5p expression;GAS5 functioned as a competing endogenous RNA (ceRNA) antagonizing tumor promotion of miR-196a-5p-expressing TNBC cells	29793177	RID00048	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Endometrial cancer	MIR22HG	DAPK1	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000196730	NA	84981	1612	C17orf91	DAPK|ROCO3	LncRNA MIR22HG negatively regulates miR-141-3p to enhance DAPK1 expression and inhibits endometrial carcinoma cells proliferation;miR-141-3p was identified and confirmed to be the target of MIR22HG;DAPK1 was confirmed to be regulated by MIR22HG and miR-141-3p	29775889	RID00049	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Chronic myeloid leukemia	MEG3	miR-21	negatively-E	RNA pull-down assay;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	epigenetic regulation;sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long noncoding RNA MEG3 inhibits proliferation of chronic myeloid leukemia cells by sponging microRNA21;Overexpression of MEG3 and silencing the expression of miR-21 inhibited proliferation and induced apoptosis.lncRNA MEG3 and its target miR21 may serve as novel therapeutic targets for CML blast crisis; and demethylation drugs might also have potential clinical application in treating CML blast crisis.	29772439	RID00050	ceRNA or sponge	NA	NA	NA
Pancreatic cancer	MIAT	miR-133a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	The interaction of long non-coding RNA MIAT and miR-133 play a role in the proliferation and metastasis of pancreatic carcinoma;Bioinformatics analysis and luciferase reporter assay validated that miR-133 may target MIAT 3'-UTR;	29772434	RID00051	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	NA
Hepatocellular carcinoma	SOX21-AS1	CDKN1A	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000124762	NA	100507533	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA SOX21-AS1 is associated with progression of hepatocellular carcinoma and predicts prognosis through epigenetically silencing p21;SOX21-AS1 epigenetically silenced p21 via recruiting EZH2 to the promoter of p21;SOX21-AS1 can interact with p21 to affect hepatocellular carcinoma progression	29772433	RID00052	epigenetic regulation	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	DICER1-AS1	ATG5	positively-E	luciferase reporter assay;RIP;western blot	upregulation	microarray;RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell autophagy(+)	ceRNA(miR-30b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000235706	GRCh38_14:95157645-95181475	ENSG00000057663	NA	400242	9474	DICER1-AS	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	LncRNA DICER1-AS1 promotes the proliferation, invasion and autophagy of osteosarcoma cells via miR-30b/ATG5;miR-30b was verified to target 3'-UTR of DICER1-AS1 and ATG5	29772430	RID00053	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Tongue squamous cell carcinoma	CASC15	miR-33a-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664185-22654455	NA	NA	401237	NA	CANT|LINC00340|lnc-SOX4-1	NA	Long non-coding RNA CASC15 promotes tongue squamous carcinoma progression through targeting miR-33a-5p; Moreover, we showed that the expression of CASC15 was negatively related with miR-33a-5p expression in TSCC tissues.Ectopic expression of CASC15 promoted TSCC cell proliferation, cycle, and migration through targeting miR-33a-5p	29804249	RID00054	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	NA
Non-small cell lung cancer	FOXO1	RP11-838N2.4	negatively-E	ChIP	upregulation	microarray;RT-PCR	NA	NA	chemoresistance(+)	histone modification	binding/interaction	RNA-RNA	erlotinib	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000150907	NA	ENSG00000266835	GRCh38_18:3466250-3478978	2308	NA	FKH1|FKHR|FOXO1A	NA	Exosome-mediated transfer of lncRNA RP11-838N2.4 promotes erlotinib resistance in non-small cell lung cancer.forkhead box protein O1 (FOXO1) could bind to the promoter region of lncRNA RP11-838N2.4, resulting in its silencing through the recruitment of histone deacetylase.	29845246	RID00055	epigenetic regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	NA
Hepatocellular carcinoma	FTX	PPARG	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cancer progression(+)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	TF	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000132170	NA	100302692	5468	LINC00182|MIR374AHG|NCRNA00182	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARgamma	lncRNA Ftx promotes aerobic glycolysis and tumor progression through the PPARgamma pathway in hepatocellular carcinoma;peroxisome proliferator-activated receptor gamma (PPARgamma) expression in human HCC tissues and cell lines was positively correlated with lncRNA Ftx	29845188	RID00056	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Laryngeal squamous cell carcinoma	MIR31HG	miR-31	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);cell cycle(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long non-coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR-31;LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR-31 expression.Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues.	29737563	RID00057	expression association	NA	NA	NA
Osteosarcoma	BTG3-AS1	miR-21	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000280594	GRCh38_21:17611744-17633199	NA	NA	110806272	NA	NA	NA	Long non-coding RNA ASBEL promotes osteosarcoma cell proliferation, migration,and invasion by regulating microRNA-21;Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR-21;PP2A was a direct target of miR-21;we verified that ASBEL-miR-21-PP2A pathway might play critical regulatory effects on the pathogenesis of osteosarcoma	29323740	RID00058	expression association	NA	NA	NA
Hepatocellular carcinoma	CASC2	miR-24-3p	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR-24-3p;the expression of CASC2 was negatively related to miR-24-3p expression in the HCC tissues;CASC2 could negatively regulate the expression of miR-24-3p in vitro	29091305	RID00059	expression association	NA	UP(LIHC);DATA(GSE117623)	NA
Gastric cancer	TFAP4	TRERNA1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000090447	NA	ENSG00000231265	GRCh38_20:50040716-50041504	7023	100887755	AP-4|bHLHc41	LINC00651|treRNA	Elevated TFAP4 regulates lncRNA TRERNA1 to promote cell migration and invasion in gastric cancer;TFAP4 specifically regulated the transcriptional activity of TRERNA1 by binding to the E box motifs in the TRERNA1 promoter;TRERNA1 was upregulation in gastric carcinogenesis and promoted cell migration and invasion in GC	29845218	RID00060	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Pancreatic cancer	PVT1	TGFB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000105329	NA	5820	7040	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00061	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	PVT1	SMAD2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000175387	NA	5820	4087	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00062	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	PVT1	SMAD3	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000166949	NA	5820	4088	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HSPC193|HsT17436|JV15-2|LDS1C|LDS3|MADH3	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00063	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	PVT1	SMAD4	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000141646	NA	5820	4089	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	DPC4|JIP|MADH4|MYHRS	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00064	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Lung cancer	OIP5-AS1	miR-378a-3p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Long non-coding RNA OIP5-AS1 promotes proliferation of lung cancer cells and leads to poor prognosis by targeting miR-378a-3p;OIP5-AS1 functions as a competing endogenous RNA of miR-378a-3p;the speed of tumor growth was increased and decreased when OIP5-AS1 was upregulation and downregulated	29897167	RID00065	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	NA
Colon cancer	XIST	WNT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000125084	NA	7503	7471	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	BMND16|INT1|OI15	Long non-coding RNA XIST sponges miR-34a to promotes colon cancer progression via WNT/beta-catenin signaling pathway;the growth rate of cells transfected with si-XIST was significantly decreased compared to that with si-NC, which was reversed by miR-34a targeted with 3'-UTR;Moreover, miR-34a suppressed the expression of WNT1 by binding with the 3'-UTR	29679755	RID00066	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Urinary bladder cancer	LSINCT5	MYCNOS-01	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENST00000641263	GRCh38_2:15936265-15941582	101234261	NA	NA	NA	LSINCT5 activates Wnt/beta-catenin signaling by interacting with NCYM to promote bladder cancer progression;LSINCT5 could physically interact with NCYM, a de novo gene product from the MYCN cis-antisense RNA and inhibit GSK3beta activity leading to enhanced Wnt/beta-catenin signaling activation and epithelial mesenchymal transition.	29772237	RID00067	interact with protein	NA	UP(PRAD);DATA(GSE104209)	NA
Prostate cancer	PCSEAT	EZH2	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	PRAD.zip	cell proliferation(+)	ceRNA(miR-143-3p;miR-24-2-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	NA	GRCh38.p13:41576148-41581634	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA PCSEAT exhibits an oncogenic property in prostate cancer and functions as a competing endogenous RNA that associates with EZH2;PCSEAT promotes cell proliferation, at least in part by affecting miR-143-3p- and miR-24-2-5p-mediated regulation of EZH2, suggesting that PCSEAT and EZH2 competitively sponge miR-143-3p and miR-24-2-5p	29803673	RID00068	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic ductal adenocarcinoma	PVT1	ULK1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR;ISH	GSE15471;GSE16515	GSE15471.zip;GSE16515.zip	cell autophagy(+);cancer progression(+)	ceRNA(miR-20a-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000177169	NA	5820	8408	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG1|ATG1A|UNC51|Unc51.1|hATG1	LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis;PVT1 promoted cyto-protective autophagy and cell growth by targeting ULK1;PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression	30001707	RID00069	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MALAT1	miR-142-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	metformin	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Metformin, a first-line drug for type 2 diabetes mellitus, disrupts the MALAT1/miR-142-3p sponge to decrease invasion and migration in cervical cancer cells;the direct interaction between miR-142-3p and MALAT1 were located in the 3'untranslated region (3'UTR) of lncRNA MATAL1	29704494	RID00070	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Cholangiocarcinoma	NEAT1	CDH1	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000039068	NA	283131	999	LINC00084|NCRNA00084|TncRNA|VINC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells;NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression	29970216	RID00071	epigenetic regulation	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Tongue cancer	KCNQ1OT1	EZR	positively-E	luciferase reporter assay	upregulation	microarray;RT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);Ezrin/Fak/Src signaling pathway(-)	ceRNA(miR-211-5p)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000092820	NA	10984	7430	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CVIL|CVL|HEL-S-105|VIL2	LncRNA KCNQ1OT1 regulates proliferation and cisplatin resistance in tongue cancer via miR-211-5p mediated Ezrin/Fak/Src signaling;miR-211-5p harbor binding sites for the 3'-UTRof Ezrin Mrna;KCNQ1OT1 facilitates tumor growth and chemo-resistance by acting as a competing endogenous RNA (ceRNA) to modulate the expression of miR-211-5p	29970910	RID00072	ceRNA or sponge	chemoresistance	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Cholangiocarcinoma	SNHG1	CDKN1A	negatively-E	RIP;RNA pull-down assay	upregulation	microarray;RT-PCR	TCGA;GSE76297	CHOL.zip;GSE76297.zip	cell proliferation(+);cell migration(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000124762	NA	23642	1026	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma;SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A;SNHG1 knockdown extensively inhibited CCA cell migration as well as proliferation in vitro and in vivo	29970899	RID00073	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	linc-UFC1	LIN28B	negatively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-498)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:161152776-161158856	ENSG00000187772	NA	NA	389421	NA	NA	Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b; UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression	29970131	RID00074	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	SNHG7	GALNT7	positively-E	RNAi;luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+);cancer progression(+);cell proliferation(+);cell metastasis(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000109586	NA	84973	51809	NCRNA00061	GALNAC-T7|GalNAcT7	Long non-coding RNA-SNHG7 acts as a target of miR-34a to increase GALNT7 level and regulate PI3K/Akt/mTOR pathway in colorectal cancer progression;Further results indicated that SNHG7 facilitated the proliferation and metastasis as a competing endogenous RNA to regulate GALNT7 expression by sponging miR-34a in CRC cell lines.SNHG7 also played the oncogenic role in regulating PI3K/Akt/mTOR pathway by competing endogenous miR-34a and GALNT7.	29970122	RID00075	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Ovarian cancer	UCA1	ABCB1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-129)	regulation	NA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000085563	NA	652995	5243	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	UCA1 confers paclitaxel resistance to ovarian cancer through miR-129/ABCB1 axis;UCA1 silencing induced PTX sensitivity of SKOV3/PTX and HeyA-8/PTX cells by de-repressing ABCB1 through sponging miR-129	29777711	RID00076	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Prostate cancer	FENDRR	RUNX1	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);cell invasion(-);cell migration(-)	ceRNA(miR-18a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000159216	NA	400550	861	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	Long non-coding RNA FENDRR reduces prostate cancer malignancy by competitively binding miR-18a-5p with RUNX1;FENDRR and RUNX1 contain potential target sites for miR-18a-5p;The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1	29465000	RID00077	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Multiple myeloma	FEZF1-AS1	AKT3	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-610)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000117020	NA	154860	10000	NA	MPPH|MPPH2|PKB-GAMMA|PKBG|PRKBG|RAC-PK-gamma|RAC-gamma|STK-2	Long non-coding RNA FEZF1-AS1 promotes cell growth in multiple myeloma via miR-610/Akt3 axis;our data indicated that FEZF1-AS1 functioned as a competing endogenous RNA in MM cells that regulated miR-610 expression, which suppressed Akt3;FEZF1-AS1 promoted MM cells proliferation through regulating miR-610/Akt3 axis.Akt3 acted a target of miR-610 and positively related to FEZF1-AS1	29864963	RID00078	ceRNA or sponge	NA	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Non-small cell lung cancer	NEAT1	IGF2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell metastasis(+)	ceRNA(let-7a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000167244	NA	283131	3481	LINC00084|NCRNA00084|TncRNA|VINC	C11orf43|GRDF|IGF-II|PP9974	lncRNA NEAT1 competes against let-7a to contribute to non-small cell lung cancer proliferation and metastasis;Luciferase reporter assay validated direct binding of NEAT1/let-7a and let-7a/IGF-2;NEAT1 regulates lung cancer cell progression by competing endogenous RNA network of NEAT1/let-7a/IGF2	29864936	RID00079	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Cervical cancer	BCYRN1	miR-138	negatively-F	luciferase reporter assay	upregulation	qRT-PCR;northern blot	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000236824	GRCh38_2:47335315-47335514	NA	NA	618	NA	BC200|BC200a|LINC00004|NCRNA00004	NA	Long non-coding RNA BCYRN1 promotes the proliferation and metastasis of cervical cancer via targeting microRNA-138 in vitro and in vivo.	29552212	RID00080	ceRNA or sponge	metastasis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	NA
Chondrosarcoma	BCAR4	MTOR	positively-E	western blot;RNAi;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);mTOR signaling pathway(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000198793	NA	400500	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long non-coding RNA BCAR4 promotes chondrosarcoma cell proliferation and migration through activation of mTOR signaling pathway.Impact statement LncRNA BCAR4 promoted chondrosarcoma cell proliferation and migration through activation of mTOR signaling pathway, and thus contributed to chondrosarcoma progression.mTOR signaling pathway was epigenetically activated by BCAR4-induced hyperacetylation of histone H3.	28399646	RID00081	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Non-small cell lung cancer	BCAR4	VIM	negatively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000026025	NA	400500	7431	NA	NA	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00082	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	BCAR4	CDH2	positively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000170558	NA	400500	1000	NA	CD325|CDHN|CDw325|NCAD	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00083	expression association	metastasis	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Non-small cell lung cancer	BCAR4	CDH1	positively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000039068	NA	400500	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00084	expression association	metastasis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	BLACAT1	ABCB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	ceRNA(miR-361)	regulation	NA	oxaliplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000085563	NA	101669762	5243	LINC00912|linc-UBC1|onco-lncRNA-30	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long noncoding RNA BLACAT1 modulates ABCB1 to promote oxaliplatin resistance of gastric cancer via sponging miR-361.	29710482	RID00085	ceRNA or sponge	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	TUG1	MKI67	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148773	NA	55000	4288	LINC00080|NCRNA00080|TI-227H	KIA|MIB-|MIB-1|PPP1R105	Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC. Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	29277771	RID00086	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Non-small cell lung cancer	TUG1	HOXB7	negatively-E	RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000260027	NA	55000	3217	LINC00080|NCRNA00080|TI-227H	HHO.C1|HOX2|HOX2C|Hox-2.3	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421;29277771	RID00087	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE111065,GSE55807)
Non-small cell lung cancer	TUG1	EZH2	interact	RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421;27485439	RID00088	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	TP53	TUG1	positively-E	ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000253352	GRCh38_22:30969245-30979395	7157	55000	BCC7|BMFS5|LFS1|P53|TRP53	LINC00080|NCRNA00080|TI-227H	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421	RID00089	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Acute myeloid leukemia	CASC15	SOX4	positively-E	luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE75461;GSE17459	GSE75461.zip;GSE17459.zip	cell survival(+);cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000124766	NA	401237	6659	CANT|LINC00340|lnc-SOX4-1	EVI16	The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia; At the cellular level, CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4. we found that CASC15 enhances YY1-mediated regulation of the SOX4 promoter;CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4.	28724437	RID00090	transcriptional regulation	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Melanoma	CASC2	PLXNC1	positively-E	luciferase reporter assay	downregulation	microarray	GSE86373	GSE86373.zip	tumorigenesis(-)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000136040	NA	255082	10154	C10orf5	CD232|PLXN-C1|VESPR	Long non-coding RNA CASC2 inhibits tumorigenesis via the miR-181a/PLXNC1 axis in melanoma.Our results demonstrated that lncRNA CASC2 can promote PLXNC1 expression by sponging miR-181a, thereby inhibiting the proliferation and invasion of melanoma cells, indicating that lncRNA CASC2 functions via the miR-181a/PLXNC1 axis in melanoma.	29514220	RID00091	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	miR-21	CASC2	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	255082	NA	C10orf5	Downregulation of lncRNA CASC2 by microRNA-21 increases the proliferation and migration of renal cell carcinoma cells.The present study provides evidence indicating that CASC2 targeted by miR-21 acts as a tumor suppressor in RCC. Therefore, CASC2 may be considered a novel target for the diagnosis and treatment of RCC.	27222255	RID00092	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Osteosarcoma	CASC2	miR-181a	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a;ectopic expression of CASC2 suppressed miR-181a expression and enhanced the expression of Ras association domain family member 6 (RASSF6), PTEN and ATM in osteosarcoma cell, which were the direct target gene of miR-181a	29194827	RID00093	expression association	NA	UP(LIHC);DATA(GSE117623)	NA
Osteosarcoma	CASC2	RASSF6	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000169435	NA	255082	166824	C10orf5	NA	Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a.Ectopic expression of CASC2 suppressed the osteosarcoma cell proliferation,colony formation and invasion through regulating RASSF6 expression;the expression of RASSF6 was positively correlated with the expression of CASC2 in osteosarcoma tissues	29194827	RID00094	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	CASC2	PIAS3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-18a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000131788	NA	255082	10401	C10orf5	ZMIZ5	Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a.This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth	27198161	RID00095	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE86978)
Colorectal cancer	CASC2	STAT3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000168610	NA	255082	6774	C10orf5	ADMIO|ADMIO1|APRF|HIES	The long noncoding RNA CASC2 functions as a competing endogenous RNA by sponging miR-18a in colorectal cancer. In this study, CASC2 expression was significantly decreased in CRC tissues and CRC cell lines.Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a. This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth in vitro and in vivo by extending the G0/G1-S phase transition.	27198161	RID00096	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	CASC2	FBXW7	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-)	ceRNA(miR-367)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000109670	NA	255082	55294	C10orf5	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	Long non-coding RNA CASC2 suppresses epithelial-mesenchymal transition of hepatocellular carcinoma cells through CASC2/miR-367/FBXW7 axis;Further studies demonstrated that CASC2 could function as a competing endogenous RNA (ceRNA) by sponging miR-367 in HCC cells;further investigations disclosed that FBXW7 was a downstream target of miR-367 and CASC2 prohibited EMT progression and subsequently exerted its anti-metastatic effects via CASC2/miR-367/FBXW7 axis in HCC cells	28716020	RID00097	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	CASC2	miR-362-5p	negatively-F	luciferase reporter assay;qRT-PCR	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR-362-5p/Nf-kB axis.we determined that CASC2 regulates HCC cell activity by targeting miR-362-5p and thus inhibiting the NF-kB pathway.we identified the microRNA miR-362-5p as an endogenous target of CASC2	29319182	RID00098	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Epithelial ovarian cancer	CASC2	EIF4A3	negatively-F	RIP	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);cancer progression(-)	interact with protein	binding/interaction	RNA-protein	sanguinarine	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000141543	NA	255082	9775	C10orf5	DDX48|Fal1|MUK34|NMP265|NUK34|RCPS|eIF-4A-III|eIF4A-III|eIF4AIII	Sanguinarine inhibits epithelial ovarian cancer development via regulating long non-coding RNA CASC2-EIF4A3 axis and/or inhibiting NF-kB signaling or PI3K/AKT/mTOR pathway. Our findings reveal that sanguinarine exhibits antitumor effects in epithelial ovarian cancer cells possible via regulating CASC2-EIF4A3 axis and/or inhibiting NF-kB signaling or PI3K/AKT/mTOR pathway.EIF4A3 was identified as a CASC2 binding protein.	29571014	RID00099	interact with protein	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761)
Colorectal cancer	CASC7	ING3	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259758	GRCh38_8:140520156-140529501	ENSG00000071243	NA	NA	54556	NA	Eaf4|ING2|MEAF4|p47ING3	Long non-coding RNA CASC7 inhibits the proliferation and migration of colon cancer cells via inhibiting microRNA-21;CASC7 and ING3 were both a target of miR-21 in CRC cells, and CASC7 could control ING3 expression by regulating miR-21. Moreover, we have found that CASC7 inhibited colon cancer cell proliferation and migration via miR-21/ING3 axis. These observations suggested that CASC7 played an important role in CRC pathogenesis and may be considered as a novel diagnostic marker of CRC.	28954383	RID00100	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	CASC8	FGFR1	interact	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);glucose metabolic process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000246228	GRCh38_8:127289817-127482139	ENSG00000077782	NA	727677	2260	CARLO1|CARLo-1|LINC00860	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Long Noncoding RNA Cancer Susceptibility Candidate 8 Suppresses the Proliferation of Bladder Cancer Cells via Regulating Glycolysis.Overexpression of CASC8 remarkably suppressed the bladder cancer cell proliferation. Mechanistically, we illustrated that CASC8 reduced the glycolysis of bladder cancer cells via interacting with the fibroblast growth factor receptor 1 (FGFR1).	28759252	RID00101	interact with protein	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Esophagus squamous cell carcinoma	CASC9	PDCD4	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000150593	NA	101805492	27250	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	H731	Up-regulation of lncRNA CASC9 promotes esophageal squamous cell carcinoma growth by negatively regulating PDCD4 expression through EZH2.Our study firstly demonstrates that lncRNA CASC9 functions as an oncogene by negatively regulating PDCD4 expression through recruiting EZH2 and subsequently altering H3K27me3 level.Furthermore interfering CASC9 decreased cell proliferation and blocked cell cycle G1/S transition.	28854977	RID00102	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Esophagus squamous cell carcinoma	CASC9	EZH2	interact	RIP;RNA pull-down assay;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000106462	NA	101805492	2146	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Up-regulation of lncRNA CASC9 promotes esophageal squamous cell carcinoma growth by negatively regulating PDCD4 expression through EZH2;enhancer of zeste homolog2 (EZH2) could bind to both CASC9 and PDCD4 promoter region. Interfering CASC9 reduced the enrichment of EZH2 and H3K27me3 in the PDCD4 promoter region	28854977	RID00103	interact with protein	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	CASC9	ABCB1	positively-E	RNAi;western blot	upregulation	microarray;qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	paclitaxel;adriamycin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000085563	NA	101805492	5243	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Silence of cancer susceptibility candidate 9 inhibits gastric cancer and reverses chemoresistance.In addition, CASC9 knockdown in BGC823/DR and SGC7901/DR cells restored chemosensitivity to paclitaxel and adriamycin. This was associated with decreased expression of multidrug resistance 1 (MDR1) protein	28146436	RID00104	expression association	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Gastric cancer	CAT104	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	ceRNA(miR-381)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:148879196-148879701	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Noncoding RNA CAT104 Promotes Cell Viability, Migration, and Invasion in Gastric Carcinoma Cells Through Activation of MicroRNA-381-Inhibiting Zinc Finger E-box-Binding Homeobox 1 (ZEB1) Expression.Bioinformatics analysis found that CAT104 was negatively bound to miR-381. Zinc finger E-box-binding homeobox 1 (ZEB1) was identified as a direct target of miR-381.	29295724	RID00105	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	CCAT1	miR-33a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	The lncRNA CCAT1 Upregulates proliferation and Invasion in Melanoma Cells via Suppressing miR-33a.Bioinformatics analysis predicted that miR-33a acted as a target of CCAT1, which was confirmed by dual-luciferase reporter assay.CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma	28409554	RID00106	ceRNA or sponge	NA	NA	NA
Renal cell carcinoma	CCAT1	BIRC7	positively-F	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000101197	NA	100507056	79444	CARLO5|CARLo-5|onco-lncRNA-40	KIAP|LIVIN|ML-IAP|MLIAP|RNF50	LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein.RNA pulldown and RIP assays showed that CCAT1 was physically associated with Livin protein. Livin was significantly inhibited by CCAT1 silencing;CCAT1 silencing could inhibit the growth of RCC in vivo that was accompanied by the reduction of Livin in RCC tissues. CCAT1 inhibits RCC cell apoptosis and increases cell viability through up-regulation of Livin	28470345	RID00107	interact with protein	NA	NA	NA
Nasopharynx carcinoma	CCAT1	CPEB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(-)	ceRNA(miR-181a)	regulation	NA	paclitaxel	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000137449	NA	100507056	132864	CARLO5|CARLo-5|onco-lncRNA-40	CPE-BP2|CPEB-2|hCPEB-2	LncRNA CCAT1 modulates the sensitivity of paclitaxel in nasopharynx cancers cells via miR-181a/CPEB2 axis.Bioinformatics analysis and luciferase reporter assay indicated that the upregulation CCAT1 sponges miR-181a in NPC cells. Furthermore, RNA immuno-precipitation assays showed that miR-181a could directly bind to CCAT1 mRNA in NPC cells. We restored miR-181a in NPC cells, and found restoration of miR-181a re-sensitized the NPC cells to paclitaxel in vitro. In addition, our results also showed that miR-181a was a modulator of paclitaxel sensitivity due to its regulative effect on cell apoptosis via targeting CPEB2 in NPC cells.	28358263	RID00108	ceRNA or sponge	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Lung adenocarcinoma	CCAT1	BCL2L1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(let-7c)	regulation	NA	docetaxel	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000171552	NA	100507056	598	CARLO5|CARLo-5|onco-lncRNA-40	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells.the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells.	27566568	RID00109	ceRNA or sponge	chemoresistance	NA	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Laryngeal squamous cell carcinoma	CCAT1	ZFX	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000005889	NA	100507056	7543	CARLO5|CARLo-5|onco-lncRNA-40	ZNF926	Long non-coding RNA CCAT1/miR-218/ZFX axis modulates the progression of laryngeal squamous cell cancer.colon cancer-associated transcript-1 knockdown inhibits proliferation and invasion of laryngeal squamous cell cancer cells through enhancing zinc finger protein, X-linked by sponging microRNA-218	28631575	RID00110	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE67939,GSE41245)
Epithelial ovarian cancer	CCAT1	ADAM17	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-152)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000151694	NA	100507056	6868	CARLO5|CARLo-5|onco-lncRNA-40	ADAM18|CD156B|CSVP|NISBD|NISBD1|TACE	Long non-coding RNA CCAT1 promotes metastasis and poor prognosis in epithelial ovarian cancer.We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion. our study first revealed a critical role of CCAT1-miR-152/miR-130b-ADAM17/WNT1/STAT3/ZEB1 regulatory network in EOC cell metastasis.	28754469	RID00111	ceRNA or sponge	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Epithelial ovarian cancer	CCAT1	WNT1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-152)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000125084	NA	100507056	7471	CARLO5|CARLo-5|onco-lncRNA-40	BMND16|INT1|OI15	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00112	ceRNA or sponge	metastasis,prognosis	NA	NA
Epithelial ovarian cancer	CCAT1	STAT3	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-130b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000168610	NA	100507056	6774	CARLO5|CARLo-5|onco-lncRNA-40	ADMIO|ADMIO1|APRF|HIES	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00113	ceRNA or sponge	metastasis,prognosis	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Epithelial ovarian cancer	CCAT1	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-130b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000148516	NA	100507056	6935	CARLO5|CARLo-5|onco-lncRNA-40	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00114	ceRNA or sponge	metastasis,prognosis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CCAT1	CDK1	positively-E	luciferase reporter assay;RNA pull-down assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000170312	NA	100507056	983	CARLO5|CARLo-5|onco-lncRNA-40	CDC2|CDC28A|P34CDC2	Long non-coding RNA colon cancer-associated transcript 1 functions as a competing endogenous RNA to regulate cyclin-dependent kinase 1 expression by sponging miR-490-3p in hepatocellular carcinoma progression.	28381168	RID00115	ceRNA or sponge	NA	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Colon cancer	CCAT2	miR-145	negatively-E	CRISPR/Cas9	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	maturation process	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	A novel mechanism of lncRNA and miRNA interaction: CCAT2 regulates miR-145 expression by suppressing its maturation process in colon cancer cells; We have observed that modulated expression of CCAT2 regulates the expression of miR-145 in colon cancer HCT-116 and HT-29 cells. In contrast, stable up-regulation of CCAT2 decreases mature miR-145 and increases the expression of several CSC markers in colon cancer cells. These results indicate CCAT2 selectively blocks miR-145 maturation by inhibiting pre-miR-145 export to cytoplasm;Knockout of CCAT2 increases miR-145 and negatively regulates miR-21 in HCT-116 cells, impairs proliferation and differentiation	28964256	RID00116	expression association	NA	NA	NA
Epithelial ovarian cancer	CCAT2	miR-424	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	Long Noncoding RNA CCAT2 Knockdown Suppresses Tumorous Progression by Sponging miR-424 in Epithelial Ovarian Cancer.	28550684	RID00117	ceRNA or sponge	NA	NA	NA
Lung adenocarcinoma	LINC00460	FOXA1	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	LUAD.zip	cell growth(+)	ceRNA(miR-302c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000129514	NA	728192	3169	NA	HNF3A|TCF3A	LncRNA LINC00460 promotes tumor growth of human lung adenocarcinoma by targeting miR-302c-5p/FOXA1 axis. LINC00460 promotes LC progression by competitively binding miR-302c-5p and regulating FOXA1 signal pathway.	30359741	RID00118	ceRNA or sponge	NA	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Hepatocellular carcinoma	THORLNC	CTNNB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000168036	NA	100506797	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA THOR promotes liver cancer stem cells expansion via beta-catenin pathway.THOR was upregulation in liver CSCs and could promote HCC cells dedifferentiation and liver CSCs expansion by targeting beta-catenin signaling.the self-renewal capacity between THOR knockdown HCC cells and control cells, which further confirmed that beta-catenin was required in THOR promoted liver CSCs expansion.	30359743	RID00119	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	LINC00319	KLF12	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	sequencing;qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-1207-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000118922	NA	284836	11278	C21orf125|NCRNA00319|PRED49	AP-2rep|AP2REP|HSPC122	Long non-coding RNA 319 facilitates nasopharyngeal carcinoma carcinogenesis through regulation of miR-1207-5p/KLF12 axis. Rescue assay was performed to further confirm that LINC00319 contributed to NPC progression by regulating miR-1207-5p/KLF12 signal pathway. LINC00319 acts as a ceRNA for miR-1207-5p in NPC	30243935	RID00120	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Retinoblastoma	H19	miR-143	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Knockdown of lncRNA-H19 inhibits cell viability, migration and invasion while promotes apoptosis via microRNA-143/RUNX2 axis in retinoblastoma.Knockdown of lncRNA-H19 acted a tumor suppressive role in Y79 cells through up-regulating miR-143. Moreover, miR-143 exerted tumor suppressive effects on Y79 cells by targeting RUNX2, along with inhibition of the PI3K/AKT/mTOR pathways.	30551533	RID00121	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Retinoblastoma	H19	RUNX2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000124813	NA	283120	860	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	Knockdown of lncRNA-H19 inhibits cell viability, migration and invasion while promotes apoptosis via microRNA-143/RUNX2 axis in retinoblastoma.Knockdown of lncRNA-H19 acted a tumor suppressive role in Y79 cells through up-regulating miR-143. Moreover, miR-143 exerted tumor suppressive effects on Y79 cells by targeting RUNX2, along with inhibition of the PI3K/AKT/mTOR pathways.	30551533	RID00122	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	HULC	RTKN	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000114993	NA	728655	6242	HCCAT1|LINC00078|NCRNA00078	NA	Long non-coding RNA HULC interacts with miR-613 to regulate colon cancer growth and metastasis through targeting RTKN.	30551459	RID00123	ceRNA or sponge	metastasis	NA	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Acute lymphocytic leukemia	HOXA-AS2	HOXA3	positively-E	RNAi;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);EGFR/Ras/Raf/MEK/ERK signaling pathway(+)	transcriptional regulation	regulation	NA	glucocorticoid	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000105997	NA	285943	3200	HOXA3as	HOX1|HOX1E	TCF7L2 activated HOXA-AS2 decreased the glucocorticoid sensitivity in acute lymphoblastic leukemia through regulating HOXA3/EGFR/Ras/Raf/MEK/ERK pathway. we found that lncRNA HOXA-AS2 was highly expressed both in prednisone insensitive ALL cell lines and patient samples. Gain or loss-of-function assays revealed that HOXA-AS2 enhanced GC resistance via promoting cell proliferation and inhibiting cell apoptosis. Furthermore, we validated that HOXA-AS2 upregulation HOXA3, thereby activating EGFR/Ras/Raf/MEK/ERK signaling pathway. HOXA3 is a target of HOXA-AS2	30551418	RID00124	transcriptional regulation	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	MIAT	EPHA2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-520d-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000142627	NA	440823	1969	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	ARCC2|CTPA|CTPP1|CTRCT6|ECK	Deregulation of miR-520d-3p promotes hepatocellular carcinoma development via lncRNA MIAT regulation and EPHA2 signaling activation.We also demonstrated that MIAT may function as a sponge competitive endogenous RNA for miR-520d-3p, and thus regulate the molecular expression of EPHA2.Decreased level of miR-520d-3p was relevant to poor overall survival,whereas miR-520d-3p up-regulation resulted in a marked inhibition of cell growth,migration and invasion.	30551417	RID00125	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)
Non-small cell lung cancer	LINC01510	CDK14	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	prognosis(-);cancer progression(+)	ceRNA(miR-339-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000058091	NA	100996266	5218	NA	PFTAIRE1|PFTK1	Increased expression of LINC01510 predicts poor prognosis and promotes malignant progression in human non-small cell lung cancer.mechanistic studies revealed that LINC01510 exerted its oncogenic functions in NSCLC through miR-339-5p-mediated regulation of CDK14.LINC01510 positively regulates CDK14 expression through sponging miR-339-5p in NSCLC cells	30399588	RID00126	ceRNA or sponge	prognosis	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	SNHG16	MUC5AC	positively-E	luciferase reporter assay;qRT-PCR;ELISA	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	ceRNA(miR-146a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000215182	NA	100507246	4586	Nbla10727|Nbla12061|ncRAN	MUC5|TBM|leB|mucin	Increased expression of long non-coding RNA SNHG16 correlates with tumor progression and poor prognosis in non-small cell lung cancer.miR-146a is further identified and confirmed to be the target of SNHG16, and SNHG16 functions by targeting miR-146a. Subsequently, MUC5AC, a major mucin in the human respiratory tract correlated with post-operative metastasis and recurrence of NSCLC, is confirmed to be regulated by SNHG16 and miR-146a, and plays a positive role in promoting cell proliferation, migration and invasion	30287374	RID00127	ceRNA or sponge	metastasis,recurrence,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	EGFR-AS1	miR-223	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.Bioinformatics analysis and a luciferase reporter assay confirmed that EGFR-AS1 mediated cell proliferation and chemoresistance through directly binding to microRNA-223. Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.	30431074	RID00128	ceRNA or sponge	chemoresistance,prognosis	NA	NA
Acute lymphocytic leukemia	SNHG16	miR-124-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor-suppressive function(+)	epigenetic regulation;sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557764-76565348	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long non-coding RNA SNHG16 has Tumor suppressing effect in acute lymphoblastic leukemia by inverse interaction on hsa-miR-124-3p.SNHG16 is upregulation in ALL, and its inhibition has tumor suppressive effect in ALL, likely through epigenetic interaction on hsa-miR-124-3p.	30380185	RID00129	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	NA
Hepatocellular carcinoma	DGCR5	CTNNB1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000168036	NA	26220	1499	LINC00037|NCRNA00037	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00130	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	DGCR5	CCND1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000110092	NA	26220	595	LINC00037|NCRNA00037	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00131	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	DGCR5	GSK3B	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000082701	NA	26220	2932	LINC00037|NCRNA00037	NA	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00132	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	HIF1A-AS2	TP53	negatively-E	luciferase reporter assay;immunoprecipitation	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	transcriptional regulation	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000141510	NA	100750247	7157	3'aHIF-1A|aHIF	BCC7|BMFS5|LFS1|P53|TRP53	The long noncoding RNA HIF1A-AS2 facilitates cisplatin resistance in bladder cancer.Mechanically, we found that HIF1A-AS2 suppressed the transcription activity of p53 family proteins by promoting the expression of high-mobility group A1 (HMGA1).This study suggests that upregulation HIF1A-AS2 hampers the p53 family proteins dependent apoptotic pathway to promote Cis resistance in bladder cancer.	30216500	RID00133	transcriptional regulation	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	SNHG6	SNAI1	interact	western blot;immunofluorescence assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124216	NA	641638	6615	HBII-276HG|NCRNA00058|U87HG	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer. SNHG6 is involved in regulation of EMT in BC, whichmay be mediated by Snail1/2	30168179	RID00134	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	SNHG6	SNAI2	interact	western blot;immunofluorescence assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000019549	NA	641638	6591	HBII-276HG|NCRNA00058|U87HG	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer.SNHG6 is involved in regulation of EMT in BC, whichmay be mediated by Snail1/2	30168179	RID00135	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	NA
Urinary bladder cancer	SNHG6	NUAK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000074590	NA	641638	9891	HBII-276HG|NCRNA00058|U87HG	ARK5	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer. SNHG6 may partly regulate themigration and invasion of BC cells through the hsa-miR-125b-NUAK1 pathway	30168179	RID00136	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	LOC728196	TCF7	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	GSE83511	GSE83511.zip	tumorigenesis(+)	ceRNA(miR-513c)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENST00000651138	GRCh38.p13:111510602-111513888	ENSG00000081059	NA	728196	6932	NA	TCF-1	LncRNA LOC728196/miR-513c axis facilitates glioma carcinogenesis by targeting TCF7.Mechanistic studies further demonstrated that LOC728196 acts as the sponge for miR-513c to upregulate TCF7 expression.	30179681	RID00137	ceRNA or sponge	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00052	SOX9	negatively-E	luciferase reporter assay	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000125398	NA	145978	6662	NCRNA00052|TMEM83	CMD1|CMPD1|SRA1|SRXX2|SRXY10	LINC00052/miR-101-3p axis inhibits cell proliferation and metastasis by targeting SOX9 in hepatocellular carcinoma.LINC00052 downgulated SOX9 to inhibit HCC cells proliferation and metastasis by interacting with miR-101-3p.	30098428	RID00138	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Breast cancer	MEG3	NFKB1	positively-E	immunofluorescence staining	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000109320	NA	55384	4790	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-kB and p53.these results suggest that MEG3 inhibits breast cancer growth and induces breast cancer apoptosis, partially via the activation of the ER stress, NF-kB and p53 pathways, and that NF-kB signaling is required for MEG3-induced p53 activation in breast cancer cells.	30556250	RID00139	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	MEG3	TP53	positively-E	RNAi;western blot	downregulation	qRT-PCR;ISH	NA	NA	cell growth(-);apoptosis process(+);cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-kB and p53.these results suggest that MEG3 inhibits breast cancer growth and induces breast cancer apoptosis, partially via the activation of the ER stress, NF-kB and p53 pathways, and that NF-kB signaling is required for MEG3-induced p53 activation in breast cancer cells.Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation,migration and invasion by depending on p53's transcriptional activity.Surprisingly,overexpression of MEG3 activates p53's transcriptional activity by decreasing MDM2's transcription level, and thus stabilizes and accumulates P53.	30556250;27166155	RID00140	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	BABAM2-AS1	NR4A3	positively-E	RIP;RNA pull-down assay;western blot;ChIP	downregulation	microarray;qRT-PCR	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(-);cell survival(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_2:27889456-27891114	ENSG00000119508	NA	100302650	8013	NA	CHN|CSMF|MINOR|NOR1|TEC	BRE-AS1 reduces NSCLC cell viability, represses NSCLC cell proliferation, and induces NSCLC cell apoptosis in vitro, and represses NSCLC tumor growth in vivo. our data demonstrate that BRE-AS1 represses NSCLC cell growth and survival via up-regulating NR4A3.Mechanistic investigation revealed that BRE-AS1 physically binds STAT3, reduces the binding of STAT3 to the promoter of NR4A3, relieves the repression of NR4A3 caused by STAT3, and up-regulates NR4A3 expression.	30227111	RID00141	transcriptional regulation	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	ZFHX4-AS1	FAT4	negatively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	GSE33447;GSE26910	GSE33447.zip;GSE26910.zip	cell migration(+);cell invasion(+);Hippo signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253661	GRCh38_8:76491200-76683308	ENSG00000196159	NA	100192378	79633	NA	CDHF14|CDHR11|FAT-J|FATJ|HKLLS2|NBLA00548|VMLDS2	Down-regulated long non-coding RNA RNAZFHX4-AS1 suppresses invasion and migration of breast cancer cells via FAT4-dependent Hippo signaling pathway. FAT4 was the target gene of lncRNA ZFHX4-AS1, and lncRNA ZFHX4-AS1 silencing increased FAT4 expressions	30546116	RID00142	transcriptional regulation	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hemangioma	MEG3	miR-494	negatively-F	luciferase reporter assay;RIP;western blot	downregulation	qRT-PCR	NA	NA	PTEN/PI3K/AKT signaling pathway(-);tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Hemangioma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	lncRNA MEG3 Suppresses the tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway.	30562741	RID00143	ceRNA or sponge	NA	NA	NA
Liver fibrosis	HOTTIP	TGFBR1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106799	NA	100316868	7046	HOXA-AS6|HOXA13-AS1|NCRNA00213	AAT5|ACVRLK4|ALK-5|ALK5|ESS1|LDS1|LDS1A|LDS2A|MSSE|SKR4|TBR-i|TBRI|TGFR-1|tbetaR-I	Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a.Dual-Luciferase Reporter Assay was performed to validate the interaction between miR-148a and HOTTIP, TGFBR1, or TGFBR2.	30562760	RID00144	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Liver fibrosis	HOTTIP	TGFBR2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000163513	NA	100316868	7048	HOXA-AS6|HOXA13-AS1|NCRNA00213	AAT3|FAA3|LDS1B|LDS2|LDS2B|MFS2|RIIC|TAAD2|TBR-ii|TBRII|TGFR-2|TGFbeta-RII	Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a.Dual-Luciferase Reporter Assay was performed to validate the interaction between miR-148a and HOTTIP, TGFBR1, or TGFBR2.	30562760	RID00145	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Laryngeal carcinoma	DGCR5	miR-195	negatively-F	RIP	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000237517	GRCh38_22:18970514-18994628	NA	NA	26220	NA	LINC00037|NCRNA00037	NA	Knockdown of DGCR5 enhances the radiosensitivity of human laryngeal carcinoma cells via inducing miR-195.microRNA (miR)-195 was predicted as a direct downstream target of DGCR5.	30549038	RID00146	ceRNA or sponge	NA	NA	NA
Pre-eclampsia	WDR86-AS1	LITAF	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cell proliferation(+);cell migration(+)	ceRNA(miR-10b-3p)	regulation	NA	NA	NA	Tumor Promoting Inflammation;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000243836	GRCh38_7:151409161-151413354	ENSG00000189067	NA	100131176	9516	NA	PIG7|SIMPLE|TP53I7	A potential regulatory network among WDR86-AS1, miR-10b-3p, and LITAF is possibly involved in preeclampsia pathogenesis.WDR86-AS1 and LITAF mRNA were confirmed as targets of miR-10b-3p. WDR86-AS1 downregulated miR-10b-3p but promoted LITAF expression. Microarray analyses revealed that LITAF controlled the inflammatory responses and migration and proliferation of HTR-8/SVneo cells under hypoxia.	30552989	RID00147	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE111842,GSE51827,GSE75367,GSE86978)
Retinoblastoma	CDKN2B-AS1	ATM	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149311	NA	100048912	472	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AT1|ATA|ATC|ATD|ATDC|ATE|TEL1|TELO1	The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway.The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB.	30355646	RID00148	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Retinoblastoma	CDKN2B-AS1	E2F1	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000101412	NA	100048912	1869	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	E2F-1|RBAP1|RBBP3|RBP3	The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway.The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB.	30355646	RID00149	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Retinoblastoma	OIP5-AS1	AGPAT2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-340-5p)	regulation	NA	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000169692	NA	729082	10555	cyrano|linc-OIP5	1-AGPAT2|BSCL|BSCL1|LPAAB|LPAAT-beta	Long noncoding RNA OIP5-AS1 causes cisplatin resistance in osteosarcoma through inducing the LPAATbeta/PI3K/AKT/mTOR signaling pathway by sponging the miR-340-5p.	30548308	RID00150	ceRNA or sponge	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Hepatocellular carcinoma	NORAD	miR-202-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);TGF-beta signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	The long noncoding RNA NORAD enhances the TGF-beta pathway to promote hepatocellular carcinoma progression by targeting miR-202-5p.NORAD overexpression was demonstrated to promote HCC cell migration and invasion.	30537113	RID00151	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Malignant glioma	GACAT3	NAMPT	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-135a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000105835	NA	104797537	10135	LINC01458|lncRNA-AC130710	1110035O14Rik|PBEF|PBEF1|VF|VISFATIN	Long noncoding RNA GACAT3 promotes glioma progression by sponging miR-135a.the present study was the first to show that GACAT3 regulates the expression of NAMPT to promote glioma progression by sponging miR-135a.	30536379	RID00152	ceRNA or sponge	NA	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	GClnc1	CDKN1A	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);p53 signaling pathway(-)	NA	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_6:159679116-159681261	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA GClnc1 promotes tumorigenesis in osteosarcoma by inhibiting p53 signaling. Mechanistically, GClnc1 directly binds to p53 and blocks the binding of p53 to acetyltransferase p300, and thereby suppresses acetylation of p53, leading to the reduced expression of p21 and BAX.	30454890	RID00153	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Retinoblastoma	GClnc1	TP53	interact	RNA pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);p54 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Retinoblastoma	lncRNA	TF	NA	GRCh38_6:159679116-159681261	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA GClnc1 promotes tumorigenesis in osteosarcoma by inhibiting p53 signaling. Mechanistically, GClnc1 directly binds to p53 and blocks the binding of p53 to acetyltransferase p300, and thereby suppresses acetylation of p53, leading to the reduced expression of p21 and BAX.	30454890	RID00154	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	ZEB1-AS1	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);apoptosis process(-)	ceRNA(miR-409-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA ZEB1-AS1/miR-409-3p/ZEB1 feedback loop is involved in the progression of non-small cell lung cancer. Our study found that ZEB1-AS1 was upregulation in NSCLC cells and knockdown of ZEB1-AS1 significantly inhibited cell growth and induced cell apoptosis. Mechanically, miR-409-3p was confirmed as a direct target of ZEB1-AS1 and negatively regulated by ZEB1-AS1 via competing endogenous RNA (ceRNA) mechanism; miR-409-3p inhibited ZEB1 expression by directly binding to the 3'UTR.	30448056	RID00155	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	PVT1	ANGPTL4	negatively-E	RIP	upregulation	sequencing;qRT-PCR	GSE61850	GSE61850.zip	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000167772	NA	5820	51129	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ARP4|FIAF|HARP|HFARP|NL2|PGAR|TGQTL|UNQ171|pp1158	Long Non-coding RNA PVT1 Promotes Cell proliferation and Migration by Silencing ANGPTL4 Expression in Cholangiocarcinoma. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth,migration, and apoptosis progression.	30388624	RID00156	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Asthma	WSPAR	TIMMDC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000113845	NA	105664404	51300	LncTCF7|TCONS_00009511	C3orf1|MC1DN31	lncTCF7 regulated TIMMDC1 expression indeed and PDGF-BB treated ASMCs exhibited elevated levels of lncTCF7 and TIMMDC1.Our study uncovered that lncTCF7 facilitated human ASMCs growth and migration via targeting TIMMDC1 thus activating AKT signaling, providing a novel possible target for asthma therapy.	30528236	RID00157	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Cervical cancer	AL589986.2	MDM2	interact	RNA pull-down assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell invasion(-);angiogenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000236427	GRCh38_1:152205858-152207057	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer. DHX9 bound to E3 ubiquitin ligase MDM2, and this interaction is enhanced by lnc-CCDST. Thus, lnc-CCDST promotes DHX9 degradation by serving as a scaffold to facilitate the formation of MDM2 and DHX9 complexes. A long noncoding RNA, named lnc-CCDST, is significantly downregulated in CC tissues, and binds to pro-oncogenic DHX9. DHX9 is upregulation in CC tissue, and promotes CC cell motility and angiogenesis.	30518908	RID00158	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	AL589986.2	DHX9	interact	RNA pull-down assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell invasion(-);angiogenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000236427	GRCh38_1:152205858-152207057	ENSG00000135829	NA	NA	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer. DHX9 bound to E3 ubiquitin ligase MDM2, and this interaction is enhanced by lnc-CCDST. Thus, lnc-CCDST promotes DHX9 degradation by serving as a scaffold to facilitate the formation of MDM2 and DHX9 complexes. A long noncoding RNA, named lnc-CCDST, is significantly downregulated in CC tissues, and binds to pro-oncogenic DHX9. DHX9 is upregulation in CC tissue, and promotes CC cell motility and angiogenesis.	30518908	RID00159	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	C5orf66-AS1	RING1	positively-E	RIP;luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	CESC.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249082	GRCh38_5:135038831-135040047	ENSG00000204227	NA	101927953	6015	Epist	RING1A|RNF1	Long non-coding RNA C5orf66-AS1 promotes cell proliferation in cervical cancer by targeting miR-637/RING1 axis. LncRNA C5orf66-AS1, as a competitive endogenous RNA (ceRNA), regulated the effect of RING1 on the proliferation, apoptosis and cell cycle of cervical cancer cells through adsorbing miR-637.	30518760	RID00160	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Pancreatic cancer	SNHG1	NOTCH1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148400	NA	23642	4851	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AOS5|AOVD1|TAN1|hN1	Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch-1 signaling pathway in pancreatic cancer.SNHG1 was significantly upregulation in PC cells. Knockdown of SNHG1 could obviously suppress cell proliferation, invasion, and migration. Furthermore, SNHG1 knockdown inhibited the activation of the Notch-1 signaling pathway and inhibited the expression of N-cadherin, Hes1, Vimentin, Notch-1.The inhabitation was reversed when Notch-1 was overexpressed in si-SNHG1 cells.	30520072	RID00161	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Salivary gland adenoid cystic carcinoma	ADAMTS9-AS2	ITGA6	positively-E	luciferase reporter assay;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);PI3K/AKT signaling pathway(+);MEK/ERK signaling pathway(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Salivary gland carcinoma	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000091409	NA	100507098	3655	NA	CD49f|ITGA6B|VLA-6	Upregulation of lncRNA ADAMTS9-AS2 Promotes Salivary Adenoid Cystic Carcinoma Metastasis via PI3K/Akt and MEK/Erk Signaling.Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, and thus it activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis.	30217729	RID00162	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Breast cancer	SNHG6	MAPK6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000069956	NA	641638	5597	HBII-276HG|NCRNA00058|U87HG	ERK3|HsT17250|PRKM6|p97MAPK	Long non-coding RNA SNHG6 enhances cell proliferation, migration and invasion by regulating miR-26a-5p/MAPK6 in breast cancer.In the present study, we found that SNHG6 was highly expressed in BC tissues and cell lines, which was associated with poorer clinicopathologic features.SNHG6 serves as an endogenous sponge by directly binding to miR-26a-5p and down-regulating miR-26a-5p expression. Knockdown of SNHG6 inhibited BC cell proliferation, migration and invasion in vitro and in vivo. Furthermore, bioinformatics analysis and luciferase reporter indicated that MAPK6 was validated as a target of miR-26a-5p. Therefore, our study may reveal a novel SNHG6/miR-26a-5p/MAPK6 pathway regulatory axis in BC pathogenesis.	30522015	RID00163	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	LINC00472	PDCD4	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-93-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000150593	NA	79940	27250	C6orf155|P53RRA	H731	Long non-coding RNA LINC00472 suppresses hepatocellular carcinoma cell proliferation, migration and invasion through miR-93-5p/PDCD4 pathway.In the present study, we have demonstrated that long non-coding RNA (lncRNA) LINC00472 was low expressed in human HCC tissues and cell lines compared with adjacent non-tumor liver tissues and normal liver cell lines respectively. LINC00472 was also low expressed in HCC tissues from patients with metastasis compared with tissues from patients without metastasis. Forced expression of LINC00472 suppressed cell proliferation, migration, invasion and promoted cell apoptosis in HCC cells Huh-7 and SMMC-7721. MiR-93-5p was a direct target of LINC00472, and miR-93-5p directly targeted PDCD4. The miR-93-5p/PDCD4 pathway mediated the suppressing role of LINC00472 in HCC cells.	30522853	RID00164	ceRNA or sponge	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Laryngeal squamous cell carcinoma	snaR	TGFB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	NA	association	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	NA	GRCh38_19:47918429-47918550	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Overexpression of lncRNA snaR is correlated with progression and predicts poor survival of laryngeal squamous cell carcinoma.In the present study, we found that plasma levels of snaR were upregulated in patients with laryngeal squamous cell carcinoma (LSCC) than in healthy controls. Overexpression of snaR resulted in upregulation of TGF-beta1 in cells of human LSCC cell lines, while exogenous TGF-beta1 treatment showed no significant effect on snaR expression. snaR overexpression and exogenous TGF-beta1 treatment promoted LSCC cell proliferation, migration, and invasion.Therefore, overexpression of lncRNA snaR is correlated with progression and predicts poor survival of LSCC and the mechanism of its actions is likely related to TGF-beta1.	30506952	RID00165	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AFAP1-AS1	AFAP1	positively-E	western blot;luciferase reporter assay	upregulation	sequencing;qRT-PCR	NA	NA	cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	Long non-coding RNA AFAP1-AS1 plays an oncogenic role in promoting cell migration in non-small cell lung cancer.In this study, we conducted global lncRNA profiling and identified that AFAP1-AS1 is significantly upregulated in NSCLC, suggesting that AFAP1-AS1 may be important for lung cancer development. AFAP1-AS1 functions through positively regulating the expression of AFAP1 protein.this study demonstrates that AFAP1-AS1 acts as an oncogene in NSCLC to promote cell migration partly by upregulating AFAP1 expression	30293090	RID00166	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Osteosarcoma	SNHG4	miR-224-3p	negatively-F	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	NA	NA	prognosis;cell growth(+);cancer recurrence(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000281398	GRCh38_5:139274102-139284899	NA	NA	724102	NA	NCRNA00059|U19H	NA	LncRNA SNHG4 promotes tumour growth by sponging miR-224-3p and predicts poor survival and recurrence in human osteosarcoma.The expression level of lncRNA SNHG4 was significantly elevated in osteosarcoma samples and cell lines as compared with the adjacent normal tissues. Our findings demonstrated that LncRNA SNHG4 promoted tumour growth by sponging miR-224-3p and represented a poor prognostic factor in patients with osteosarcoma.we found that lncRNA SNHG4 acted as a sponge of miR-224-3p, and miR-224-3p mimic reversed SNHG4 induced tumour-promoting effects in osteosarcoma cells.	30152090	RID00167	ceRNA or sponge	recurrence,prognosis	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	NA
Renal cell carcinoma	HOTAIR	ST8SIA4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113532	NA	100124700	7903	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PST|PST1|SIAT8D|ST8SIA-IV	Long noncoding RNA HOTAIR promotes renal cell carcinoma malignancy through alpha-2, 8-sialyltransferase 4 by sponging microRNA-124.In this study, HOTAIR level was confirmed to be significantly upregulated in RCC samples and RCC cell lines compared with those in the paired adjacent tissues and normal renal cell line. HOTAIR directly bound to miR-124, while miR-124 mediated the expression of ST8SIA4 in RCC cell lines. ST8SIA4 was upregulated in RCC tissues and RCC cell lines.Further results indicated that HOTAIR promoted the proliferation and metastasis as a competing endogenous RNA to regulate ST8SIA4 expression by sponging miR-124 in RCC.	30105850	RID00168	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	UCA1	MAPK1	positively-E	immunoblot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000100030	NA	652995	5594	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.Suppression of long non-coding RNA UCA1 inhibits proliferation and invasion and induces apoptosis in human lung cancer cells.the lncRNA UCA1 suppression (p < 0.05) significantly inhibited the migration and invasion of the NCI-H23 lung cancer at least in part via inhibition of mitogen-activated protein kinase 1 (MAPK1).	30556875;30468471	RID00169	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	UCA1	miR-143	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.It was found that the lncRNA UCA was significantly upregulated in the lung cancer cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.	30556875	RID00170	expression association	NA	UP(PAAD);DATA(GSE40174)	NA
Non-small cell lung cancer	FENDRR	miR-761	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000268388	GRCh38_16:86474529-86509099	NA	NA	400550	NA	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	NA	Long non-coding RNA FENDRR inhibits NSCLC cell growth and aggressiveness by sponging miR-761.We found a marked down-regulation of FENDRR in NSCLC tissues compared to tumor-adjacent tissues. Moreover, the over-expression of FENDRR restrained the growth of NSCLC cell in vivo. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. We found that there were potential binding sites between FENDRR and miR-761 and the level of miR-761 was inversely associated with the expression of ENDRR in NSCLC tissues. Finally, the rescue experiments suggested that the anti-oncogenic role of FENDRR was at least partially mediated by miR-761 in NSCLC.	30556873	RID00171	ceRNA or sponge	NA	NA	NA
Colorectal cancer	LINC01503	FOXK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-4492)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000164916	NA	100506119	221937	NA	FOXK1L	Long non-coding RNA LINC01503 promotes colorectal cancer cell proliferation and invasion by regulating miR-4492/FOXK1 signaling.The present study indicated that LINC01503 was significantly upregulated in CRC tissues compared with that in adjacent normal tissues. it was revealed that LINC01503 serves as a sponge for microRNA (miR)-4492, which targets forkhead box K1 (FOXK1) in CRC cells. it was demonstrated that restoration of FOXK1 abolished the inhibitory effect of LINC01503 knockdown on CRC cell proliferation and invasion.	30542444	RID00172	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	LINC00662	LIN28A	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell stemness(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	CSC	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Lung cancer	lncRNA	TF	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000131914	NA	148189	79727	NA	NA	Long non-coding RNA Linc00662 promotes cell invasion and contributes to cancer stem cell-like phenotypes in lung cancer cells. Linc00662 had direct interaction with Lin28, and the Linc00662 function was dependent on Lin28. We demonstrate that overexpression of Linc00662 enhances lung cancer cell metastasis and CSC stemness by interacting with Lin28 in human lung cancer, which could be utilized as a potential diagnostic and therapeutic target for lung cancer patients.The interaction between Linc00662 and Lin28 was confirmed by RNA immunoprecipitation and RNA pulldown assay.	30256974	RID00173	interact with mRNA	metastasis	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Renal cell carcinoma	TUG1	YAP1	positively-E	western blot;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-9)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000137693	NA	55000	10413	LINC00080|NCRNA00080|TI-227H	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA TUG1 promotes cell proliferation and migration of renal cell carcinoma via regulation of YAP. In the current study, we observed a positive correlation between TUG1 expression and YAP expression in RCC. In addition, we found that TUG1 could bind to miR-9; therefore, TUG1 could positively control YAP expression via downregulation of miR-9 level. Furthermore, we observed that inhibition of cell proliferation and cell migration induced by TUG1 silencing could be reversed by overexpression of YAP in RCC cell lines.Using microRNA database (miRDB), the sequencealignment of TUG1, YAP 3'UTR, and miR-9 showed complementary binding sites of TUG1 and YAP 3'UTR for miR-9.	30132963	RID00174	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Colon cancer	PVT1	miR-26b	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA Plasmacytoma Variant Translocation 1 (PVT1) Promotes Colon Cancer Progression via Endogenous Sponging miR-26b. We demonstrate that the expression of PVT1 was significantly higher in tumor tissue compared with the adjacent normal tissue with a lower expression of miR-26b. Our results suggest that PVT1 could promote metastasis and proliferation of colon cancer via endogenous sponging and inhibiting the expression of miR-26b, which may highlight the significance of lncRNA PVT1 in colon cancer tumorigenesis.	30504754	RID00175	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Prostate cancer	LINC00844	NDRG1	positively-E	ChIP;western blot	downregulation	sequencing;qRT-PCR	ERP000550	ERP000550	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000237949	GRCh38_10:58999482-59066396	ENSG00000104419	NA	100507008	10397	NA	CAP43|CMT4D|DRG-1|DRG1|GC4|HMSNL|NDR1|NMSL|PROXY1|RIT42|RTP|TARG1|TDD5	Novel lncRNA LINC00844 Regulates Prostate Cancer Cell Migration and Invasion through AR Signaling. The expression of LINC00844 is higher in normal prostate compared with malignant and metastatic prostate cancer clinical specimens. Mechanistic evidence reveals that LINC00844 is important in facilitating AR binding to the chromatin. Finally, LINC00844 mediates its phenotypic effects in part by activating the expression of NDRG1, a crucial cancer metastasis suppressor. This study highlights the function of the lncRNA, LINC00844, in regulating global AR-regulated genes in prostate cancer by modulating AR binding to chromatin.	30115758	RID00176	transcriptional regulation	metastasis	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Multiple myeloma	CYTOR	miR-497	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	NA	Long intergenic non-protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA-497.It was identified that the expression of LINC00152 was significantly upregulated in plasma cells from patients with MM vs. healthy subjects. A luciferase reporter assay indicated that microRNA (miR)-497 is a direct target of LINC00152, and its expression levels were inversely correlated with those of LINC00152 in MM tissues.knockdown of LINC00152 promoted caspase-3/9 activity and apoptosis in MM cells.knockdown of LINC00152 by transfecting MM cells with LINC00152-specific short hairpin RNA expression plasmids significantly inhibited cell proliferation.	30272368	RID00177	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	NA
Pituitary adenoma	IFNG-AS1	ESRP2	interact	RNA pull-down assay	upregulation	qRT-PCR;FISH	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000255733	GRCh38_12:67989445-68234686	ENSG00000103067	NA	100885789	80004	GS1-410F4.2|NEST|Tmevpg1	RBM35B	Long-noncoding RNA IFNG-AS1 exerts oncogenic properties by interacting with epithelial splicing regulatory protein 2 (ESRP2) in pituitary adenomas. shRNA-mediated IFNG-AS1 knockdown in HP75 cells significantly inhibited tumor progression. Epithelial splicing regulatory protein 2 (ESRP2) was demonstrated to be a target protein of IFNG-AS1 in PA; knocking down ESRP2 reversed the tumor-inhibitory effects of IFNG-AS1 knockdown, and overexpressing ESRP2 abolished the tumor-promoting effects of IFNG-AS1 overexpression in HP75 cells.	30322807	RID00178	interact with protein	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Gastric cancer	TP73-AS1	SDAD1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000198301	NA	57212	55153	KIAA0495|PDAM	NA	LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis.TP73-AS1 was upregulated in GC tissues and cell lines. Furthermore, TP73-AS1 exerted oncogenic role in GC through promoting cell growth and metastasis. In addition, TP73-AS1 was certified as a ceRNA by regulating miR-194-5p/SDAD1 axis.	30279010	RID00179	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)
Prostate cancer	AR	TMPO-AS1	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	prognosis;cancer progression(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000257167	GRCh38_12:98512973-98516422	367	100128191	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	Overexpression of AR-regulated lncRNA TMPO-AS1 correlates with tumor progression and poor prognosis in prostate cancer. we found that TMPO-AS1 could be a useful diagnostic and prognostic marker for PCa, whose expression was upregulated in PCa samples and associated with poorer prognosis. In PCa cells, TMPO-AS1 was predominantly localized in the cytoplasm and directly down-regulated by AR. Based on primary screening, we found that TMPO-AS1 could be a useful diagnostic and prognostic marker for PCa, whose expression was upregulated in PCa samples and associated with poorer prognosis.	30105831	RID00180	transcriptional regulation	prognosis	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Pre-eclampsia	MEG3	SMAD7	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000101665	NA	55384	4092	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CRCS3|MADH7|MADH8	The Role and Molecular Mechanism of Long Nocoding RNA-MEG3 in the Pathogenesis of Preeclampsia.The expression of MEG3 was lower in tissues from patients with preeclampsia having an EMT decline, as well as a messenger RNA expression of smad7. In HTR-8/SVneo cells with overexpressed MEG3, the invasion and migration functions were enhanced and accompanied by higher EMT and a significantly increased expression of smad7.	29361889	RID00181	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	CEBPB	UCA1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell viability(+);cell growth(+);colony formation(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	TF	lncRNA	ENSG00000172216	NA	ENSG00000214049	GRCh38_19:15828206-15836328	1051	652995	C/EBP-beta|IL6DBP|NF-IL6|TCF5	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	C/EBPbeta promotes the viability of human bladder cancer cell by contributing to the transcription of bladder cancer specific lncRNA UCA1.Here we report that the expression of UCA1 was dramatically inhibited in 5637 cells with C/EBPbeta down-regulation. Additionally, the function tests indicated that C/EBPbeta could promote 5637 cells growth and colony formation by inducing the expression level of UCA1.	30376994	RID00182	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	CDKN2B-AS1	ARHGAP18	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);cell migration(+)	ceRNA(miR-153-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000146376	NA	100048912	93663	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	MacGAP|SENEX|bA307O14.2	LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis. CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. CDKN2BAS upregulated the expression of Rho GTPase activating protein 18 (ARHGAP18) by sponging microRNA-153-5p (miR-153-5p), and thus promoted HCC cell migration.Luciferase reporter assay showed that miR-153-5p inhibited the luciferase activity of ARHGAP18 wt-3'UTR but had no effect on the ARHGAP18 mut-3'UTR. Besides, CDKN2BAS downregulated the expression of Kruppel-like factor 13 (KLF13) and activated MEK-ERK1/2 signaling, thus reducing apoptosis in HCC cells.	30510148	RID00183	ceRNA or sponge	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)
Hepatocellular carcinoma	CDKN2B-AS1	KLF13	negatively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	MEK/ERK signaling pathway(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000169926	NA	100048912	51621	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	BTEB3|FKLF2|NSLP1|RFLAT-1|RFLAT1	LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis. CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. CDKN2BAS upregulated the expression of Rho GTPase activating protein 18 (ARHGAP18) by sponging microRNA-153-5p (miR-153-5p), and thus promoted HCC cell migration.Luciferase reporter assay showed that miR-153-5p inhibited the luciferase activity of ARHGAP18 wt-3'UTR but had no effect on the ARHGAP18 mut-3'UTR. Besides, CDKN2BAS downregulated the expression of Kruppel-like factor 13 (KLF13) and activated MEK-ERK1/2 signaling, thus reducing apoptosis in HCC cells. knockdown of CDKN2BAS up-regulated KLF13 protein level	30510148	RID00184	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00707	ELAVL1	interact	RNA pull-down assay;RIP	upregulation	microarray;qRT-PCR	GSE58828	GSE58828.zip	cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000066044	NA	100507127	1994	NA	ELAV1|HUR|Hua|MelG	The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR.In this study, we identified that LINC00707 was excessively expressed in GC tissues and correlated with advanced stage, larger tumor size, lymph node metastasis and poorer prognosis in GC patients.	30502359	RID00185	interact with protein	metastasis,prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Triple-receptor negative breast cancer	PDCD4-AS1	PDCD4	positively-F	RIP;RNA stability assay;RNA pull-down assay	downregulation	sequencing;qRT-PCR	NA	NA	cancer progression(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000203497	GRCh38_10:110869868-110872233	ENSG00000150593	NA	282997	27250	NA	H731	A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability.Both PDCD4-AS1 and PDCD4 show reduced expression in TNBC cell lines and in patients, and depletion of PDCD4-AS1 compromised the cellular levels and activity of PDCD4. Mechanistically, PDCD4-AS1 stabilizes PDCD4 RNA by forming RNA duplex and controls the interaction between PDCD4 RNA and RNA decay promoting factors such as HuR. Our studies demonstrate crucial roles played by NAT lncRNAs in regulating post-transcriptional gene expression of key oncogenic or tumor suppressor genes, thereby contributing to TNBC progression.	30496290	RID00186	interact with mRNA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Endometriosis	CCDC144NL-AS1	MMP9	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000233098	GRCh38_17:20868433-21002276	ENSG00000100985	NA	440416	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Knockdown of long non-coding RNA CCDC144NL-AS1 attenuates migration and invasion phenotypes in endometrial stromal cells from endometriosis. CCDC144NL-AS1 expression was up-regulated in EC tissues compared to EU and normal endometrial (NE) tissues.Western blot analysis revealed that knockdown of CCDC144NL-AS1 attenuated the protein levels of vimentin filaments and MMP-9, but not N-cadherin or beta-catenin. CCDC144NL-AS1 depletion suppressed the migration and invasion of hEM15A cells, but exerted no effects on cell adhesion, proliferation, apoptosis or cell cycle.	30496345	RID00187	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Endometriosis	CCDC144NL-AS1	VIM	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000233098	GRCh38_17:20868433-21002276	ENSG00000026025	NA	440416	7431	NA	NA	Knockdown of long non-coding RNA CCDC144NL-AS1 attenuates migration and invasion phenotypes in endometrial stromal cells from endometriosis.Western blot analysis revealed that knockdown of CCDC144NL-AS1 attenuated the protein levels of vimentin filaments and MMP-9, but not N-cadherin or beta-catenin. CCDC144NL-AS1 depletion suppressed the migration and invasion of hEM15A cells, but exerted no effects on cell adhesion, proliferation, apoptosis or cell cycle.	30496345	RID00188	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Triple-receptor negative breast cancer	MIR4435-2HG	FZD7	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111036776-111523376	ENSG00000155760	NA	541471	8324	NA	FzE3	LncRNA AWPPH promotes the growth of triple-negative breast cancer by up-regulating frizzled homolog 7 (FZD7).We observed that AWPPH was significantly up-regulated in tumor tissues than in paired adjacent healthy tissues of patients. AWPPH overexpression promoted cancer cell proliferation and up-regulated FZD7 expression. We conclude that LncRNA AWPPH may promote the growth of triple-negative breast cancer by up-regulating FZD7.	30333256	RID00189	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	CDKN2B-AS1	NAP1L1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	microarray;qRT-PCR	GSE65485;TCGA	GSE65485.zip;LIHC.zip	cell growth(+);cell metastasis(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(let-7c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000187109	NA	100048912	4673	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NAP1|NAP1L|NRP	LncRNA CDKN2B-AS1 promotes tumor growth and metastasis of human hepatocellular carcinoma by targeting let-7c-5p/NAP1L1 axis. Here, we identified a novel oncogenic lncRNA CDKN2B-AS1, which was highly expressed in HCC and positively associated with large tumor size, microvascular invasion, high tumor grade, advanced tumor stage and reduced survival of HCC patients. Mechanistically, CDKN2B-AS1 promoted nucleosome assembly protein 1 like 1 (NAP1L1) expression by sponging let-7c-5p, thereby activated PI3K/AKT/mTOR signaling in HCC cells.	30165194	RID00190	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Urinary bladder cancer	OIP5-AS1	OIP5	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000104147	NA	729082	11339	cyrano|linc-OIP5	5730547N13Rik|CT86|LINT-25|MIS18B|MIS18beta|hMIS18beta	LncRNA OIP5-AS1 predicts poor prognosis and regulates cell proliferation and apoptosis in bladder cancer.There was a positive association between OIP5-AS1 expression and OIP5 expression in bladder cancer tissues.OIP5-AS1 is a useful biomarker for predicting clinical progression and poor prognosis and promotes cell proliferation through modulating OIP5 expression.	30485498	RID00191	expression association	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Colorectal cancer	MAP3K20-AS1	CDKN1A	negatively-E	RT-qPCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238133	GRCh38_2:173166446-173282036	ENSG00000124762	NA	339751	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA MLK7-AS1 promotes proliferation in human colorectal cancer via downregulation of p21 expression.this is the first study to report that MLK7-AS1 has potential as a biomarker and may promote proliferation in CRC partially through downregulating p21 expression.Furthermore, RT-qPCR and western blot assays revealed that p21 may be a potential downstream target of MLK7-AS1.	30535460	RID00192	transcriptional regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	ZEB1	HCCL5	positively-E	ChIP-qPCR	upregulation	qRT-PCR	NA	NA	cell migration(+);cell viability(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000148516	NA	ENSG00000263080	GRCh38_16:11341809-11345299	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	NA	Super-enhancer-associated long non-coding RNA HCCL5 is activated by ZEB1 and promotes the malignancy of hepatocellular carcinoma.HCCL5 was transcriptionally driven by ZEB1 via a super-enhancer and was significantly and frequently overexpressed in human HCC tissues, correlating with worse overall survival of HCC patients. this study characterizes HCCL5 as a super-enhancer-driven lncRNA promoting HCC cell viability, migration, and EMT.	30482773	RID00193	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Hepatoblastoma	STAT3	LUCAT1	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	LIHC.zip	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000248323	GRCh38_5:91054834-91314547	6774	100505994	ADMIO|ADMIO1|APRF|HIES	SCAL1|SCAT5	STAT3-activated lncRNA LUCAT1 drives cell proliferation, migration and invasion in hepatoblastoma through regulating miR-301b/STAT3 axis. Further mechanism investigation revealed that LUCAT1 increased STAT3 expression through competitively binding to miR-301b.In conclusion, LUCAT1 was activated by STAT3 and promoted cell proliferation, migration and invasion in hepatoblastoma through modulating miR-301b/STAT3 axis.	30479162	RID00194	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)
Hepatoblastoma	LUCAT1	STAT3	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	LIHC.zip	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-301b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000168610	NA	100505994	6774	SCAL1|SCAT5	ADMIO|ADMIO1|APRF|HIES	STAT3-activated lncRNA LUCAT1 drives cell proliferation, migration and invasion in hepatoblastoma through regulating miR-301b/STAT3 axis. Further mechanism investigation revealed that LUCAT1 increased STAT3 expression through competitively binding to miR-301b.In conclusion, LUCAT1 was activated by STAT3 and promoted cell proliferation, migration and invasion in hepatoblastoma through modulating miR-301b/STAT3 axis.	30479162	RID00195	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	NEAT1	CDK14	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-107)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000058091	NA	283131	5218	LINC00084|NCRNA00084|TncRNA|VINC	PFTAIRE1|PFTK1	Knockdown of NEAT1 repressed the malignant progression of glioma through sponging miR-107 and inhibiting CDK14.it was revealed that NEAT1 could modulate miR-107 via serving as an endogenous sponge of miR-107. The direct binding correlation between NEAT1 and miR-107 was validated in our study. In addition, cyclin dependent kinase 14 (CDK14) was predicted as an messenger RNA target of miR-107 and the association between them was confirmed in our research.	30480816	RID00196	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Retinoblastoma	NEAT1	CXCR4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000121966	NA	283131	7852	LINC00084|NCRNA00084|TncRNA|VINC	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR-204/CXCR4 axis.We found NEAT1 and CXCR4 expression levels were elevated, whereas miR-204 expression was decreased in RB tissues and cells. NEAT1 functioned as a competing endogenous RNA for miR-204 to regulate CXCR4 expression.	30479013	RID00197	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	LINC00460	SPHK2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-613)	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000063176	NA	728192	56848	NA	SK 2|SK-2|SPK 2|SPK-2	Long noncoding RNA LINC00460 promotes carcinogenesis via sponging miR-613 in papillary thyroid carcinoma.knockdown of LINC00460 suppressed cell proliferation, migration, and invasion, and inhibited expression of sphingosine kinase 2 (SphK2, a target of miR-613) in PTC cells, at least in part, by regulating miR-613. These findings suggested that LINC00460 could function as a competing endogenous RNA to regulate SphK2 expression by sponging miR-613 in PTC.	30478856	RID00198	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE67939,GSE75367,GSE86978)
T-cell leukemia	CDKN2B-AS1	CDKN1A	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);NF-kB signaling pathway(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000124762	NA	100048912	1026	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA ANRIL Supports Proliferation of Adult T-Cell Leukemia Cells through Cooperation with EZH2. In the present study, we show that the expression level of the lncRNA ANRIL was elevated in HTLV-1-infected cell lines and clinical ATL samples. In addition, we observed that the ANRIL/EZH2 complex repressed p21/CDKN1A transcription through H3K27 trimethylation of the p21/CDKN1A promoter. Taken together, our results implicate that the lncRNA ANRIL, by cooperating with EZH2, supports the proliferation of HTLV-1-infected cells, which is thought to be critical for oncogenesis. In this study, we demonstrated that the lncRNA ANRIL was important for maintaining the proliferation of ATL cells in vitro and in vivo ANRIL was shown to activate NF-kB signaling through forming a ternary complex with EZH2 and p65. Furthermore, epigenetic inactivation of p21/CDKN1A was involved in the oncogenic function of ANRIL.	30258009	RID00199	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Triple-receptor negative breast cancer	CERNA2	CDK6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(let-7b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000105810	NA	642934	1021	HOST2|lncRNA-HOST2	MCPH12|PLSTIRE	Knockdown of long non-coding RNA HOST2 inhibits the proliferation of triple negative breast cancer via regulation of the let-7b/CDK6 axis.A positive correlation was identified between the expression of HOST2 and cyclin-dependent kinase 6 (CDK6) in tumor tissues.It was hypothesized and confirmed that let-7b, a previously reported target miRNA of HOST2, was able to directly bind to the 3'UTR of CDK6 and repress its expression.	30483747	RID00200	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Prostate cancer	PANTR1	ROCK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000067900	NA	100506421	6093	LINC01158|linc-Brn1a|linc-POU3F3	P160ROCK|ROCK-I	Long noncoding RNA POU3F3 promotes cancer cell proliferation in prostate carcinoma by upregulating rho-associated protein kinase 1. In this study we found that POU3F3 and rho-associated protein kinase 1 (ROCK1) were both increased in tumor tissues than in adjacent healthy tissues of patients with prostate carcinoma. lncRNA POU3F3 may promote cancer cell proliferation in prostate carcinoma by upregulating ROCK1.	30474879	RID00201	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LSINCT5	HMGA2	interact	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000149948	NA	101234261	8091	NA	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516.RIP in combination with mass spectrometry identified HMGA2 as the LSINCT5 binding partner. LSINCT5 could bind to HMGA2 and decrease proteasome-mediated HMGA2 degradation leading to EMT activation.	30472720	RID00202	interact with protein	NA	UP(PRAD);DATA(GSE104209)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	LSINCT5	STAT3	positively-E	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-)	ceRNA(miR-4516)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000168610	NA	101234261	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516. LSINCT5 also served as a competing endogenous RNA (ceRNA) for miR-4516, resulting in increased STAT3/BclxL expression and attenuated apoptosis.Previous results showed that miR-4516 targets STAT3 transcript and downregulates STAT3, pSTAT3, and BclxL expression.	30472720	RID00203	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	LSINCT5	BCL2L1	positively-E	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-)	ceRNA(miR-4516)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000171552	NA	101234261	598	NA	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516. LSINCT5 also served as a competing endogenous RNA (ceRNA) for miR-4516, resulting in increased STAT3/BclxL expression and attenuated apoptosis.Previous results showed that miR-4516 targets STAT3 transcript and downregulates STAT3, pSTAT3, and BclxL expression.	30472720	RID00204	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Ulcerative colitis	CDKN2B-AS1	miR-323b-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00205	expression association	NA	UP(SKCM);DATA(GSE38495)	NA
Ulcerative colitis	CDKN2B-AS1	TLR4	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000136869	NA	100048912	7099	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARMD10|CD284|TLR-4|TOLL	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00206	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Ulcerative colitis	CDKN2B-AS1	MYD88	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000172936	NA	100048912	4615	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	MYD88D	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00207	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ulcerative colitis	CDKN2B-AS1	RELA	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000173039	NA	100048912	5970	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CMCU|NFKB3|p65	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00208	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colon cancer	AC123023.1	JAG2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236452	GRCh38_3:34203244-34268811	ENSG00000184916	NA	NA	3714	NA	HJ2|SER2	Long noncoding RNA ENST00000455974 plays an oncogenic role through up-regulating JAG2 in human DNA mismatch repair-proficient colon cancer.Here, firstly, we observed that ENST00000455974 was gradual increased across colon normal-adenoma-carcinoma-metastasis sequence by quantitative real-time PCR. ENST00000455974 was mainly located in the nucleus of colon cancer cells and it promoted the growth and metastasis of pMMR CC cells through up-regulating JAG2.	30473216	RID00209	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	CARMN	AXIN2	positively-E	luciferase reporter assay	downregulation	sequencing;qRT-PCR	TCGA	BLCA.zip	WNT/beta-catenin signaling pathway(-);cancer progression(-)	ceRNA(miR-1275)	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000249669	GRCh38_5:149406689-149432835	ENSG00000168646	NA	728264	8313	NA	AXIL|ODCRCS	LncRNA miR143HG suppresses bladder cancer development through inactivating Wnt/beta-catenin pathway by modulating miR-1275/AXIN2 axis.miR143HG was identified to inhibit the level of miR-1275, whereas miR-1275 directly targeted AXIN2, a negative regulator of the Wnt/beta-catenin pathway. Restoration of miR-1275 or knockdown of AXIN2 significantly rescued the proliferation, migration, and invasion abilities of BCa cells. We found that miR143HG might be acompeting endogenous RNA (ceRNA) for miR-1275. There were two potential binding sites for miR-1275 in miR143HG. miR143HG directly interacted with miR-1275.	30471109	RID00210	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Oral squamous cell carcinoma	CASC2	miR-21	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cancer recurrence(-)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Downregulation of lncRNA CASC2 promotes the postoperative local recurrence of early oral squamous cell carcinoma.Transfection of CASC2 expression vectors led to significantly inhibited tumor cell proliferation and reduced miRNA-21 expression levels.	30467776	RID00211	expression association	recurrence	UP(LIHC);DATA(GSE117623)	NA
Retinoblastoma	XIST	ZEB1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA XIST promotes the epithelial to mesenchymal transition of retinoblastoma via sponging miR-101. Moreover,we found that XIST functioned as a competing endogenous RNA (ceRNA) for miR-101 to regulate the de-repression of its endogenous targets ZEB1 and ZEB2.	30472203	RID00212	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	XIST	ZEB2	positively-E	RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169554	NA	7503	9839	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA XIST promotes the epithelial to mesenchymal transition of retinoblastoma via sponging miR-101. Moreover,we found that XIST functioned as a competing endogenous RNA (ceRNA) for miR-101 to regulate the de-repression of its endogenous targets ZEB1 and ZEB2.	30472203	RID00213	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Bladder urothelial carcinoma	MEG3	miR-96	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.MEG3 overexpression resulted in miR-96 downregulation along with TPM1 upregulation, which inhibited cell proliferation and cell cycle but promoted cell apoptosis of bladder urothelial carcinoma cells in vitro, and at the same time inhibited tumor growth in vivo.	30461333	RID00214	expression association	NA	NA	NA
Bladder urothelial carcinoma	MEG3	TPM1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000140416	NA	55384	7168	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	C15orf13|CMD1Y|CMH3|HEL-S-265|HTM-alpha|LVNC9|TMSA	Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.MEG3 overexpression resulted in miR-96 downregulation along with TPM1 upregulation, which inhibited cell proliferation and cell cycle but promoted cell apoptosis of bladder urothelial carcinoma cells in vitro, and at the same time inhibited tumor growth in vivo.	30461333	RID00215	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Gastric cancer	UCA1	ZEB2	positively-E	luciferase reporter assay;RIP	upregulation	microarray;sequencing	GSE53137;GSE93512;TCGA	GSE53137.zip;GSE93512.zip;STAD.zip	cell metastasis(+)	ceRNA(miR-203)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000169554	NA	652995	9839	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer.Our findings indicated that UCA1 plays a critical role in metastatic GC by mediating sponge regulatory axis miR-203/ZEB2.we detected that expression level of ZEB2, a transcription factor related to tumor metastasis, was regulated by UCA1 in GC cells. we found that UCA1 could directly interact with miR-203 and lead to the release of miR-203-targeted transcripts ZEB2.	30464170	RID00216	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	GAS5	miR-26a	negatively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell autophagy(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Knockdown of growth-arrest specific transcript 5 restores oxidized low-density lipoprotein-induced impaired autophagy flux via upregulating miR-26a in human endothelial cells.We further demonstrated that GAS5 directly bound to miR-26a in HAECs. GAS5 knockdown inhibited cell apoptosis and activated autophagy flux, whereas inhibition of miR-26a reversed the effect of GAS5 in HAECs.	30468731	RID00217	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Head and neck squamous cell carcinoma	MIR31HG	HIF1A	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);tumorigenesis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000100644	NA	554202	3091	LncHIFCAR|hsa-lnc-31	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA MIR31HG targets HIF1A and P21 to facilitate head and neck cancer cell proliferation and tumorigenesis by promoting cell-cycle progression.MIR31HG overexpression or co-expression of HIF1A-positive and p21-negative could serve as a poor prognostic factor for LSCC patients.MIR31HG KD decreased the expression of HIF1A and CCND1 but increased expression of p21. The ingenuity pathway analysis and Western blot indicated that MIR31HG regulated cell cycle progression via HIF1A and p21 in HNSCC.	30458787	RID00218	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Head and neck squamous cell carcinoma	MIR31HG	CDKN1A	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);tumorigenesis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000124762	NA	554202	1026	LncHIFCAR|hsa-lnc-31	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MIR31HG targets HIF1A and P21 to facilitate head and neck cancer cell proliferation and tumorigenesis by promoting cell-cycle progression.MIR31HG overexpression or co-expression of HIF1A-positive and p21-negative could serve as a poor prognostic factor for LSCC patients.MIR31HG KD decreased the expression of HIF1A and CCND1 but increased expression of p21. The ingenuity pathway analysis and Western blot indicated that MIR31HG regulated cell cycle progression via HIF1A and p21 in HNSCC.	30458787	RID00219	expression association	prognosis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Endometrial cancer	NEAT1	LEF1	positively-E	western blot;luciferase reporter assay	downregulation	microarray	GSE29435	GSE29435.zip	cell cycle(+);cell viability(+)	ceRNA(miR-146b-5p)	regulation	NA	progesterone	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000138795	NA	283131	51176	LINC00084|NCRNA00084|TncRNA|VINC	LEF-1|TCF10|TCF1ALPHA|TCF7L3	Investigations on the mechanism of progesterone in inhibiting endometrial cancer cell cycle and viability via regulation of long noncoding RNA NEAT1/microRNA-146b-5p mediated Wnt/beta-catenin signaling.Lymphoid enhancing factor 1 (LEF1) was positively associated with NEAT1, and eventually hsa_miR-146b-5p was validated to target both LEF1 and NEAT1.Downstream gene c-myc or MMP9 regulated by upstream gene LEF1 in Wnt/beta-catenin signaling pathway was remarkably increased in Ishikawa cells and positively related with NEAT1. Progesterone inhibited cell cycle and viability through regulating NEAT1/miR-146b-5p axis via Wnt/beta-catenin signaling pathway.	30452118	RID00220	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	NORAD	FOXO6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-608)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	100132074	LINC00657	NA	The long noncoding RNA NORAD promotes the growth of gastric cancer cells by sponging miR-608.NORAD acted as a competitive endogenous RNA (ceRNA), which sponged miR-608 and suppressed the expression of miR-608 in gastric cancer cells. Further experiments demonstrated that miR-608 targeted the forkhead box O6 (FOXO6) and negatively regulated the expression of FOXO6.Overexpression of FOXO6 attenuated the inhibitory effect of miR-608 on the gastric cancer cell growth.	30453063	RID00221	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Osteosarcoma	BDNF-AS	CASP3	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000164305	NA	497258	836	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CPP32|CPP32B|SCA-1	LncRNA BDNF-AS is associated with the malignant status and regulates cell proliferation and apoptosis in osteosarcoma.The in vitro studies indicated that BDNF-AS overexpression inhibits OS cell proliferation and promotes cell apoptosis through regulating cleaved caspase-3.	30352834	RID00222	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Gastric cancer	NBAT1	SOX9	negatively-F	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000125398	NA	729177	6662	CASC14|NBAT-1	CMD1|CMPD1|SRA1|SRXX2|SRXY10	A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.NBAT1 interacted with Sox9, and reduced its protein stability by promoting it from polyubiquitination and proteasome-dependent degradation. Moreover, we revealed that Sox9 could occupy the NBAT1 promoter to inactivate its transcription.	30287498	RID00223	interact with protein	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Gastric cancer	SOX9	NBAT1	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000125398	NA	ENSG00000260455	GRCh38_6:22133205-22147193	6662	729177	CMD1|CMPD1|SRA1|SRXX2|SRXY10	CASC14|NBAT-1	A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.NBAT1 interacted with Sox9, and reduced its protein stability by promoting it from polyubiquitination and proteasome-dependent degradation. Moreover, we revealed that Sox9 could occupy the NBAT1 promoter to inactivate its transcription.	30287498	RID00224	transcriptional regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)	NA
Melanoma	UCA1	miR-185-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell motility(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/beta-catenin signaling pathway.We found that miR-185-5p could directly bind to UCA1 at the miRNA recognition site, and there existed a negative relationship between UCA1 and miR-185-5p. Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/beta-catenin signaling pathway.	30144501	RID00225	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	NA
Malignant glioma	SNHG12	FOXP1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000114861	NA	85028	27086	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	12CC4|HSPC215|MFH|QRF1|hFKH1B	Long noncoding RNA SNHG12 facilitates the tumorigenesis of glioma through miR-101-3p/FOXP1 axis.it was found that SNHG12 harbored the complementary binding sites with miR-101-3p at 3'-UTR, acting as a miRNA 'sponge'. Furthermore, miR-101-3p also targeted the 3'-UTR of FOXP1 mRNA.	30098431	RID00226	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)
Melanoma	FOXD2-AS1	AKT1	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	TCGA	SKCM.zip	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000142208	NA	84793	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	FOXD2-AS1 correlates with the malignant status and regulates cell proliferation, migration, and invasion in cutaneous melanoma.The results of loss-of-function study showed that inhibition of FOXD2-AS1 suppresses cutaneous melanoma cell proliferation, migration and invasion through regulating phospho-Akt expression.	30426532	RID00227	expression association	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	IGF2-AS	IGF2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000167244	NA	51214	3481	IGF2-AS1|IGF2AS|PEG8	C11orf43|GRDF|IGF-II|PP9974	Long Noncoding RNA IGF2AS is Acting as an Epigenetic Tumor Suppressor in Human Prostate Cancer.IGF2AS was downregulated in both PCa cell lines and human PCa tumors. IGF2 was downregulated by IGF2AS overexpression. Conversely, IGF2 upregulation revered the suppressing function of IGF2AS on PCa proliferation and invasion.	30423304	RID00228	expression association	NA	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Systemic lupus erythematosus	THRIL	CCL2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000108691	NA	102659353	6347	BRI3BP-AS1|BRI3BPAS1|Linc1992|TCONS_00020260	NA	Long noncoding RNA THRIL contributes in lipopolysaccharide-induced HK-2 cells injury by sponging miR-34a.THRIL worked as a sponge of microRNA-34a (miR-34a) and it could directly target MCP-1.LncRNA THRIL was highly expressed in the LPS stimulated cells, and THRIL overexpression aggravated LPS-induced cell damage as cell viability was decreased, and apoptosis and the release of proinflammatory cytokines were increased.THRIL overexpression aggravated LPS-induced injury possibly via sponging miR-34a, and thus preventing MCP-1 from degradation by miR-34a. The THRIL/miR-34a/MCP-1 axis might play critical roles in SLE.	30414207	RID00229	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(PAAD);DATA(GSE40174)
Oral squamous cell carcinoma	STAT3	HNF1A-AS1	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000241388	GRCh38_12:120941728-120980965	6774	283460	ADMIO|ADMIO1|APRF|HIES	C12orf27|HAS1|NCRNA00262	STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.HNF1A-AS1 was positively regulated by the transcription factor STAT3. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00230	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)
Oral squamous cell carcinoma	HNF1A-AS1	NOTCH1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000148400	NA	283460	4851	C12orf27|HAS1|NCRNA00262	AOS5|AOVD1|TAN1|hN1	It was uncovered that the expression of Notch1 and Hes1 (the core factors of Notch signaling pathway) was negatively regulated by HNF1A-AS1 knockdown. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00231	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	HNF1A-AS1	HES1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000114315	NA	283460	3280	C12orf27|HAS1|NCRNA00262	HES-1|HHL|HRY|bHLHb39	It was uncovered that the expression of Notch1 and Hes1 (the core factors of Notch signaling pathway) was negatively regulated by HNF1A-AS1 knockdown. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00232	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Ovarian cancer	HOTTIP	CTNNB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HOTTIP is a significant indicator of ovarian cancer prognosis and enhances cell proliferation and invasion.we demonstrated that inhibition of lncRNA HOTTIP suppressed Wnt/beta-catenin signaling by downregulating beta-catenin expression.	30452402	RID00233	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	FER1L4	PTEN	positively-E	immunohistochemical staining;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA Fer-1-like family member 4 suppresses hepatocellular carcinoma cell proliferation by regulating PTEN in vitro and in vivo. PTEN was highly expressed in HCC tissues compared with normal adjacent tissues and was positively associated with FER1L4.	30431133	RID00234	expression association	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	FLVCR1-DT	E2F3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-573)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000198468	GRCh38_1:212852105-212858126	ENSG00000112242	NA	642946	1871	NA	E2F-3	Long non-coding RNA FLVCR1-AS1 contributes to the proliferation and invasion of lung cancer by sponging miR-573 to upregulate the expression of E2F transcription factor 3.Results revealed that FLVCR1-AS1 was markedly upregulated in NSCLC tissues and cell lines. FLVCR1-AS1 functioned as a competing endogenous RNA (ceRNA) by directly binding to miRNA-573, and E2F transcription factor 3 (E2F3) was identified as a down-stream target of miR-573.	30309647	RID00235	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Lung adenocarcinoma	SNHG6	E2F7	positively-E	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	TCGA	LUAD.zip	cell motility(+);epithelial to mesenchymal transition(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000165891	NA	641638	144455	HBII-276HG|NCRNA00058|U87HG	NA	SNHG6 functions as a competing endogenous RNA to regulate E2F7 expression by sponging miR-26a-5p in lung adenocarcinoma.mechanistic experiments identified that SNHG6 functions as a competing endogenous RNA (ceRNA) through competitively sponging miR-26a-5p to regulate E2F7 expression, cell motility and EMT in LUAD cells.	30257360	RID00236	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	DBH-AS1	miR-138	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000225756	GRCh38_9:133654586-133657313	NA	NA	138948	NA	NCRNA00118	NA	LncRNA DBH-AS1 facilitates the tumorigenesis of hepatocellular carcinoma by targeting miR-138 via FAK/Src/ERK pathway.DBH-AS1 acted as a molecular sponge of miR-138 to downregulate miR-138 expression. DBH-AS1 silencing and miR-138 overexpression reduced cell viability, inhibited colony formation, and induced apoptosis. Also, DBH-AS1 overexpression attenuated miR-138-mediated anti-proliferation and pro-apoptosis effects. Additionally, miR-138 overexpression gave rise to a blockage on FAK/Src/ERK pathway, while this effect was undermined by increased DBH-AS1.	30142544	RID00237	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	NA
Colorectal cancer	kcna3	YAP1	negatively-E	Immunofluorescence assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177272	GRCh38_1:110653560-110674940	ENSG00000137693	NA	NA	10413	NA	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA kcna3 inhibits the progression of colorectal carcinoma through down-regulating YAP1 expression.up-regulation of lncRNA kcna3 decreased YAP1 protein expression and accelerated its degradation. The effects of lncRNA kcna3 overexpression on cell growth and tumorigenesis inhibition and apoptosis promotion were weakened when the expression of YAP1 was up-regulated.	30099342	RID00238	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Gastric cancer	LINC00473	MMP2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000087245	NA	90632	4313	C6orf176|LNC473|bA142J11.1	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LINC00473 predicts poor prognosis and regulates cell migration and invasion in gastric cancer.The study in vitro indicated that silencing of LINC00473 had no effect on GC cell viability, but inhibited GC cell migration and invasion through modulating MMP2 and MMP9 expression.	30071345	RID00239	expression association	prognosis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DATA(GSE40174)
Gastric cancer	LINC00473	MMP9	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000100985	NA	90632	4318	C6orf176|LNC473|bA142J11.1	CLG4B|GELB|MANDP2|MMP-9	LINC00473 predicts poor prognosis and regulates cell migration and invasion in gastric cancer.The study in vitro indicated that silencing of LINC00473 had no effect on GC cell viability, but inhibited GC cell migration and invasion through modulating MMP2 and MMP9 expression.	30071345	RID00240	expression association	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	GAS5	HOXA5	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-196a-5p)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106004	NA	60674	3202	NCRNA00030|SNHG2	HOX1|HOX1.3|HOX1C	Lowly-expressed lncRNA GAS5 facilitates progression of ovarian cancer through targeting miR-196-5p and thereby regulating HOXA5.LncRNA GAS5 depressed OA development by targeting miR-196a-5p and thereby down-regulating HOXA5 expression, providing substance for developing lncRNA-based strategies to treat OA.The HOXA5 was found to reverse the effects imposed by miR-196a-5p on viability, proliferation and apoptosis of OA cells	30201235	RID00241	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Endometrial cancer	NIFK-AS1	miR-146a	negatively-F	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000236859	GRCh38_2:121649320-121728563	NA	NA	254128	NA	NA	NA	Long non-coding RNA NIFK-AS1 inhibits M2 polarization of macrophages in endometrial cancer through targeting miR-146a. The expression of NIFK-AS1 and miR-146a were decreased and increased in tumor-associated macrophages of endometrial cancer patients, respectively. NIFK-AS1 could interact with miR-146a and increased the expression of Notch1 through downregulating miR-146a. Further experiments revealed that miR-146a overexpression attenuated the effect of NIFK-AS1 on suppressing the M2 polarization of macrophages and the estrogen-induced proliferation, migration and invasion of endometrial cancer cells.	30176290	RID00242	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	NA
Colon cancer	FALEC	STAT3	interact	RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	phosphorylation	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000168610	NA	100874054	6774	FAL1|LINC00568|ncRNA-a1	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA FAL1 promotes proliferation and inhibits apoptosis of human colon cancer cells.FAL1 was found to interact with STAT3 at 200 to 400 bp and promote phosphorylation of STAT3. In addition, we found that knockdown of STAT3 in HT29 cells abolished the effects of FAL1 on cell proliferation as well as the expression of TGF-beta1 and Bcl-2.our results indicate that FAL1 expression was remarkably up-regulated in colon tumor tissues as compared to corresponding tumor-adjacent normal tissues.	30290064	RID00243	interact with protein	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Glioblastoma	LINC00599	KLF16	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	TF	ENSG00000253230	GRCh38_8:9899871-9906678	ENSG00000129911	NA	157627	83855	NA	BTEB4|DRRF|NSLP2	Long noncoding RNA-RNCR3 overexpression deleteriously affects the growth of glioblastoma cells through miR-185-5p/Kruppel-like factor 16 axis.we found that RNCR3 overexpression promotes Kruppel-like factor 16 (KLF16) expression through inhibiting the level of miR-185-5p. We demonstrated that KLF16 is a direct target of miR-185-5p. An increased miR-185-5p level by a miR-185-5p mimic or decreased KLF16 by KLF16 small interfering RNA both reversed the function of RNCR3 overexpression on GBM cell growth and apoptosis.	29953649	RID00244	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	XIST	miR-214-3p	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Upregulation of lncRNA XIST may suppress EOC development, possibly through sponging effect to induce hsa-miR-214-3p downregulation. Lentivirus-mediated XIST upregulation had significant anticancer effects in CAOV3 and OVCAR3 cells by suppressing cancer cell proliferation, invasion, increasing cisplatin chemosensitivity and inhibiting in vivo tumor growth.	30207107	RID00245	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Oral squamous cell carcinoma	HOTAIR	MAP1LC3B	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000140941	NA	100124700	81631	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ATG8F|LC3B|MAP1A/1BLC3|MAP1LC3B-a	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00246	expression association	chemoresistance	NA	UP(LIHC,PAAD,PRAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Oral squamous cell carcinoma	HOTAIR	ATG3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000144848	NA	100124700	64422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APG3|APG3-LIKE|APG3L|PC3-96	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00247	expression association	chemoresistance	NA	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939,GSE86978)
Oral squamous cell carcinoma	HOTAIR	ATG7	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000197548	NA	100124700	10533	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APG7-LIKE|APG7L|GSA7	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00248	expression association	chemoresistance	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	HOTAIR	MTOR	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000198793	NA	100124700	2475	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00249	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Clear cell renal cell carcinoma	miR-182-5p	MALAT1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Elevated miR-182-5p Associates with Renal Cancer Cell Mitotic Arrest through Diminished MALAT-1 Expression.Overexpression of miR-182-5p-inhibited cell proliferation, colony formation, apoptosis, and led to G2-M-phase cell-cycle arrest by directly targeting MALAT-1 .Transient knockdown of MALAT-1 mimicked the effects of miR-182-5p overexpression.	30037856	RID00250	expression association	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Non-small cell lung cancer	MIR4435-2HG	miR-6754-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000172965	GRCh38_2:111036776-111523376	NA	NA	541471	NA	NA	NA	Long noncoding RNA LINC00978 promotes cell proliferation and invasion in non-small cell lung cancer by inhibiting miR-6754-5p.it was demonstrated that LINC00978 served as a competing endogenous RNA sponge for microRNA (miR)-6754-5p, which was downregulated in NSCLC tissues.it was demonstrated that inhibition of miR-6754-5p reversed the effects of LINC00978 knockdown on NSCLC cell proliferation, migration, invasion and apoptosis.	30221669	RID00251	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	NA
Atherosclerosis	MALAT1	SOCS1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(-)	ceRNA(miR-155)	regulation	NA	NA	NA	Tumor Promoting Inflammation;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185338	NA	378938	8651	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CIS1|CISH1|JAB|SOCS-1|SSI-1|SSI1|TIP-3|TIP3	The suppression of ox-LDL-induced inflammatory cytokine release and apoptosis of HCAECs by long non-coding RNA-MALAT1 via regulating microRNA-155/SOCS1 pathway.we found that MALAT1 could suppress the inflammatory cytokine release and cell apoptosis via sponging miR-155 to increase SOCS1 level, which in turn restrained JAK-STAT pathway. miR-155 regulatedthe production of pro-inflammatory cytokines and theapoptosis of HCAECs via directly targeting SOCS1.	30314869	RID00252	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	SOX2-OT	miR-194-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000242808	GRCh38_3:180989762-181836880	NA	NA	347689	NA	NCRNA00043|SOX2OT	NA	The SOX2OT/miR-194-5p axis regulates cell proliferation and mobility of gastric cancer through suppressing epithelial-mesenchymal transition.the in vitro experiments revealed that knockdown of SOX2OT inhibited cell proliferation and mobility through suppressing EMT via targeting miR-194-5p in GC.miR-194-5p expression was negatively regulated by SOX2OT expression in GC cells	30405772	RID00253	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	NA
Breast cancer	MALAT1	miR-145	negatively-E	RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 promotes angiogenesis of breast cancer.knockdown of endogenous MALAT1 significantly increased miR-145 levels in MCF-7 cells.This outcome revealed that MALAT1 promoted angiogenesis in BC, which may be related to the expression of miR-145.	30226550	RID00254	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Prostate cancer	VPS9D1-AS1	MYC	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	PRAD.zip	cell proliferation(+)	ceRNA(miR-184)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000261373	GRCh38_16:89711856-89718165	ENSG00000136997	NA	100128881	4609	MYU	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA MYU promotes prostate cancer proliferation by mediating the miR-184/c-Myc axis.lncRNA MYU upregulated c-Myc by competitively binding miR-184 and then induced the proliferation of prostate cancer. RNAhybrid (34) was used to predict the binding sites of miR-184 /MYU and miR-184/3'UTR of c-Myc.	30132573	RID00255	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Malignant glioma	HOXA10-AS	HOXA10	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell survival(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	TF	ENSG00000253187	GRCh38_7:27168619-27171915	ENSG00000253293	NA	100874323	3206	HOXA-AS4	HOX1|HOX1.8|HOX1H|PL	HOXA10-AS: A novel oncogenic long non-coding RNA in glioma.HOXA10-AS markedly regulated the expression of the homeobox A10 (HOXA10) gene.The results of the present study demonstrated that HOXA10-AS promoted cell growth and survival through activation of HOXA10 gene expression in glioma.Further statistical analysis demonstrated a significant and positive correlation between HOXA10 and HOXA10-AS gene expression	30132568	RID00256	expression association	NA	NA	NA
Renal ischemia-reperfusion injury	MALAT1	HIF1A	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100644	NA	378938	3091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The long non-coding RNA MALAT1 is increased in renal ischemia-reperfusion injury and inhibits hypoxia-induced inflammation.Knockdown of MALAT1 by siRNA significantly up-regulated the expression of HIF-1a and NF-kB proteins in CoCl2-treated HK2 cells. The expression of MALAT1 is increased in renal ischemia-reperfusion injury. It is likely that MALAT1 inhibits the hypoxia-induced inflammatory response through the NF-kB pathway.	30277425	RID00257	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Renal ischemia-reperfusion injury	MALAT1	NFKB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	The long non-coding RNA MALAT1 is increased in renal ischemia-reperfusion injury and inhibits hypoxia-induced inflammation.Knockdown of MALAT1 by siRNA significantly up-regulated the expression of HIF-1a and NF-kB proteins in CoCl2-treated HK3 cells. The expression of MALAT1 is increased in renal ischemia-reperfusion injury. It is likely that MALAT1 inhibits the hypoxia-induced inflammatory response through the NF-kB pathway	30277425	RID00258	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	IATPR	ROCK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000067900	NA	101929447	6093	NA	P160ROCK|ROCK-I	Long non-coding RNA linc-ITGB1 promotes cell proliferation, migration, and invasion in human hepatoma carcinoma by up-regulating ROCK1.We conclude that lncRNA LINC-ITGB1 can promote the proliferation, migration, and invasion of HCC cells by up-regulating ROCK1.	30279202	RID00259	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	RMRP	MYC	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	TF	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000136997	NA	6023	4609	CHH|NME1|RMRPR|RRP2	MRTL|MYCC|bHLHe39|c-Myc	c-Myc, RMRP, and miR-34a-5p form a positive-feedback loop to regulate cell proliferation and apoptosis in multiple myeloma.RMRP functions as a miR-34a-5p sponge to promote cell proliferation and repress cell apoptosis through upregulation of c-Myc in MM.c-Myc isa direct target of miR-34a-5p.	30389523	RID00260	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	TMEM75	SIM2	positively-E	RNAi	upregulation	qRT-PCR	GSE70880	GSE70880.zip	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280055	GRCh38_8:127946559-127948723	ENSG00000159263	NA	641384	6493	NA	HMC13F06|HMC29C01|SIM|bHLHe15	Long noncoding RNA TMEM75 promotes colorectal cancer progression by activation of SIM2.We also found that the expression of SIM2 was upregulated and positively correlated that of TMEM75 in colorectal cancer tissues. Furthermore, ectopic expression of SIM2 rescued TMEM75 depletion-induced inhibition on cell proliferation, migration and invasion in colorectal cancer.	29964097	RID00261	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Papillary thyroid carcinoma	HOXA-AS2	HOXA3	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-15a-5p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000105997	NA	285943	3200	HOXA3as	HOX1|HOX1E	LncRNA HOXA-AS2 facilitates tumorigenesis and progression of papillary thyroid cancer through modulating miR-15a-5p/HOXA3 axis.Further mechanism investigation revealed that HOXA-AS2 upregulated the expression of HOXA3 by sponging miR-15a-5p.Additionally, FOXD2-AS1 was found to upregulate HOXA3 expression by binding to miR-15a-5p. the putative binding sequence between miR-15a-5p and HOXA3 was obtained from TargetScan.	30375256	RID00262	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Pre-eclampsia	PSG10P	IL1RAP	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000248257	GRCh38_19:42839368-42855718	ENSG00000196083	NA	653492	3556	PSG10|PSG12	C3orf13|IL-1RAcP|IL1R3	Potential regulatory network in the PSG10P/miR-19a-3p/IL1RAP pathway is possibly involved in preeclampsia pathogenesis.Lower levels of miR-19a-3p, but higher levels of PSG10P and IL1RAP were observed in PE placentas and the trophoblast cells in hypoxia. Luciferase reporter assays confirmed that PSG10P and IL1RAP were both direct targets of miR-19a-3p. Exposure to hypoxia inhibited cell viability, migration, and invasion of HET8/SVneo and TEV-1 cells.	30370628	RID00263	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Endometriosis	MALAT1	CDKN1A	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	ERK/MAPK signaling pathway(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Down-regulation of long non-coding RNA MALAT1 inhibits granulosa cell proliferation in endometriosis by up-regulating P21 via activation of the ERK/MAPK pathway.We first found that MALAT1 lncRNA was significantly down-regulated in endometriosis GCs.	30371869	RID00264	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Pancreatic cancer	DUXAP8	CDKN1A	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000124762	NA	503637	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID00265	epigenetic regulation	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Pancreatic cancer	DUXAP8	KLF2	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000127528	NA	503637	10365	NA	LKLF	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID00266	epigenetic regulation	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	LINC00961	SNAI2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cancer progression(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000235387	GRCh38_9:35909483-35937153	ENSG00000019549	NA	NA	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.the messenger RNA and protein expression levels of epithelial-mesenchymal transition (EMT)-associated markers Slug and N-cadherin in RCC cell lines were dramatically inhibited by overexpressing LINC00961.LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.	30367453	RID00267	expression association	NA	NA	NA
Renal cell carcinoma	LINC00961	CDH2	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cancer progression(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000235387	GRCh38_9:35909483-35937153	ENSG00000170558	NA	NA	1000	NA	CD325|CDHN|CDw325|NCAD	LINC00962 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.the messenger RNA and protein expression levels of epithelial-mesenchymal transition (EMT)-associated markers Slug and N-cadherin in RCC cell lines were dramatically inhibited by overexpressing LINC00961.LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma	30367453	RID00268	expression association	NA	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Cervical cancer	DANCR	ROCK1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-335-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000067900	NA	57291	6093	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	P160ROCK|ROCK-I	LncRNA DANCR promotes cervical cancer progression by upregulating ROCK1 via sponging miR-335-5p.Further cellular behavioral this study demonstrated that DANCR promoted cervical cancer progression by functioning as a competing endogenous RNA (ceRNA) to regulate ROCK1 expression via sponging miR-335-5p.experiments revealed that miR-335-5p mimics and ROCK1 knockdown reversed the effects of upregulated DANCR on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of cervical cancer cells by rescue assays. DANCR andROCK1 share the similar binding sites for miR-335-5p.	30362591	RID00269	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	H19	TWIST1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Involvement of H19/miR-326 axis in hepatocellular carcinoma development through modulating TWIST1.The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR-326 and modulate TWIST1 levels in HCC pathogenesis. we observed that inhibition of H19 can repress HCC cell growth, migration, and invasion in vitro. miR-326 mimics can also inhibit HCC progression.the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression.TWIST1 was a direct target of miR-326.	303625122270:275	RID00270	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Cervical cancer	HOTAIR	HIF1A	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100644	NA	100124700	3091	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Overexpression of HOTAIR leads to radioresistance of human cervical cancer via promoting HIF-1alpha expression. HOTAIR also upregulated the expression of HIF-1alpha in HeLa and C33A cell exposed to radiation. HIF-1alpha knockdown reversed increasing cell viability and reducing apoptosis of HeLa and C33A cell induced by HOTAIR overexpression.	30355300	RID00271	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	DLX6-AS1	E2F1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-197-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000101412	NA	285987	1869	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	E2F-1|RBAP1|RBBP3|RBP3	Long noncoding RNA DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.our finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.In the cellular functional assays, silenced DLX6-AS1 expression by siRNAs inhibited the proliferation, invasion and tumor growth in vitro and in vivo.we found that E2F1acted as the target protein of miR-197-5p with the 3'UTR combination.	30366080	RID00272	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cervical cancer	GAS5	STAT3	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000168610	NA	60674	6774	NCRNA00030|SNHG2	ADMIO|ADMIO1|APRF|HIES	Growth arrest-specific 5 attenuates cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21. the decrease of miR-21 associated proteins phosphorylated STAT3 and E2F3 was seen in GAS5 overexpressed cells.The GAS5 deficiency also reduced miR-21 target proteins TIMP3 and PDCD4 expressions.We proved GAS5 could suppress miR-21 expression. The overexpressions of GAS5 expression reduced the basal levels of E2F3 and phosphorylated STAT3, which could be elevated byintroducing siGAS5 (Figure 4c). Levels of two miR-21 target proteins,TIMP3, and PDCD4, were reduced by siGAS5.	30352127	RID00273	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	GAS5	miR-21	negatively-F	RNAi;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt.Growth arrest-specific 5 attenuates cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21. the decrease of miR-21 associated proteins phosphorylated STAT3 and E2F3 was seen in GAS5 overexpressed cells.The GAS5 deficiency also reduced miR-21 target proteins TIMP3 and PDCD4 expressions.We proved GAS5 could suppress miR-21 expression. The overexpressions of GAS5 expression reduced the basal levels of E2F3 and phosphorylated STAT3, which could be elevated byintroducing siGAS5 (Figure 4c). Levels of two miR-21 target proteins,TIMP3, and PDCD4, were reduced by siGAS5.	28472815;30352127	RID00274	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Cervical cancer	GAS5	PTEN	positively-E	western blot;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt.In this study, we found a negative correlation between GAS5 and miR-21 in CC tissue and cell lines and identified a repression feedback between GAS5 and miR-21. GAS5 can function as a tumor suppressor by regulating growth, apoptosis, invasion, and migration in CC cells by regulating PTEN and PDCD4 that are also miR-21 targets.	28472815	RID00275	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Cervical cancer	GAS5	AKT1	negatively-E	western blot;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000142208	NA	60674	207	NCRNA00030|SNHG2	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt. GAS5 overexpression and SiHa/cDDP cells with miR-21 knockdown  had a down-regulated level of pAkt.	28472815	RID00276	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	HOTAIR	IGF2BP2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000073792	NA	100124700	10644	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IMP-2|IMP2|VICKZ2	Long noncoding RNA HOTAIR silencing inhibits invasion and proliferation of human colon cancer LoVo cells via regulating IGF2BP2.the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial-mesenchymal transition.The dual luciferase reporter gene assay was initially used for testify the regulating relationship between lncRNA HOTAIR and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)	30335892	RID00277	transcriptional regulation	NA	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Clear cell renal cell carcinoma	MALAT1	ACVR2B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000114739	NA	378938	93	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ACTRIIB|ActR-IIB|HTX4	LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR-194-5p/ACVR2B signaling.MALAT1 could directly target miR-194-5p to suppress its expression, and ACVR2B was the targeted molecule of miR-194-5p. Finally, ACVR2B could reverse the effects exerted by miR-194-5p on viability, proliferation, and apoptosis of KIRC cells.	30334578	RID00278	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE86978)
Cervical cancer	ZEB1-AS1	ZEB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA ZEB1-AS1 promotes cell invasion and epithelial to mesenchymal transition through inducing ZEB1 expression in cervical cancer.we found that knockdown of ZEB1-AS1 significantly inhibited ZEB1 expression.	30425516	RID00279	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HNF1A-AS1	CDC34	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell cycle(+)	ceRNA(miR-661)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000099804	NA	283460	997	C12orf27|HAS1|NCRNA00262	E2-CDC34|UBC3|UBCH3|UBE2R1	EGR1-Mediated Transcription of lncRNA-HNF1A-AS1 Promotes Cell-Cycle Progression in Gastric Cancer.HNF1A-AS1 functioned as competing endogenous RNA (ceRNA) by binding to miR-661, upregulating the expression of cell division cycle 34 (CDC34), which is a direct target of miR-661.Overexpression of HNF1A-AS1 enhanced cell proliferation and promoted cell-cycle progression, whereas knockdown of HNF1A-AS1 elicited the opposite effects.	30185552	RID00280	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(NSCLC,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939,GSE41245)
Gastric cancer	EGR1	HNF1A-AS1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000120738	NA	ENSG00000241388	GRCh38_12:120941728-120980965	1958	283460	AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268|ZNF225	C12orf27|HAS1|NCRNA00262	Early growth response protein 1 (EGR1) directly bound the HNF1A-AS1 promoter region and activated its transcription. Overexpression of EGR1 enhanced cell proliferation and promoted cell-cycle promotion, similar to the function of HNF1A-AS1.	30185552	RID00281	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)
Osteosarcoma	APTR	YAP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000137693	NA	100505854	10413	RSBN1L-AS1	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA APTR contributes to osteosarcoma progression through repression of miR-132-3p and upregulation of yes-associated protein 1.We confirmed miR-132-3p to be a target for APTR, and its expression was demonstrated to be inhibited by APTR.knockdown of APTR and overexpression of miR-132-3p both,remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis.Yes-associated protein 1 (YAP1) was determined as an inhibitory target of miR-132-3p. knockdown of APTR and overexpression of miR-132-3p both,remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis.our findings demonstrated that the repression of YAP1 protein expression and the suppression of Ki-67, MMP9, and Bcl2 expression induced by APTR knockdown required increased miR-132-3p. Thus, APTR contributed to OS progression through repression of miR-132-3p and upregulation of YAP1 expression	30317613	RID00282	ceRNA or sponge	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Cholangiocarcinoma	Lnc-EPIC1	MYC	interact	RIP;CRISPR/Cas9	upregulation	qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA EPIC1 promotes cholangiocarcinoma cell growth.our results show that Lnc-EPIC1 promotes CCA cancer progression by targeting Myc.Loss-and-gain of Lnc-EPIC1 contributes to the CCA cell growth, colony formation, cell apoptosis and also cell cycle. Myc has been reported to directly interact with Lnc-EPIC1 in several cancer cells.	30205958	RID00283	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Laryngeal squamous cell carcinoma	PVT1	miR-519d-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR-519d-3p.LncRNA PVT1 is consistently overexpressed in human LSCC, and overexpression of lncRNA PVT1 contributes to the proliferation and migration of LSCC through inhibiting miR-519d-3p expression.Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR-519d-3p.	30304557	RID00284	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Parkinson's disease	SNHG1	GSK3B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cytotoxicity(+)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Tumor Promoting Inflammation	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000082701	NA	23642	2932	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Upregulated lncRNA small nucleolar RNA host gene 1 promotes 1-methyl-4-phenylpyridinium ion-induced cytotoxicity and reactive oxygen species production through miR-15b-5p/GSK3beta axis in human dopaminergic SH-SY5Y cells.SNHG1 was demonstrated to interact with miR-15b-5p. Moreover, SNHG1 could attenuate the inhibitory effects of miR-15b-5p on MPP+ -induced cytotoxicity and production of ROS.The inhibitory effects of SNHG1 knockdown or miR-15b-5p overexpression on MPP+ -induced cytotoxicity and reactive oxygen species (ROS) production were abrogated by upregulation of GSK3beta.GSK3betais a target gene of miR-15b-5p.	30302821	RID00285	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MNX1-AS1	MAPK3	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000102882	NA	645249	5595	CCAT5	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00286	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MNX1-AS1	MAPK1	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000100030	NA	645249	5594	CCAT5	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00287	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MNX1-AS1	MAPK8	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000107643	NA	645249	5599	CCAT5	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00288	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	UCA1	miR-26a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA UCA1 sponges miR-26a to regulate the migration and proliferation of vascular smooth muscle cells.This study reveals that lncRNA UCA1 act as an endogenous sponge of miR-26a and downregulates miR-26a expression levels, and thereby relieving the inhibition of its target gene PTEN and alleviates VSMCs proliferation against atherosclerosis.LncRNA UCA1 sponges miR-26a to regulate the migration and proliferation of vascular smooth muscle cells.	29908280	RID00289	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	NA
Gastric cancer	HOXC-AS3	YBX1	interact	RNA pull-down assay;mass spectrometry	upregulation	sequencing	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251151	GRCh38_12:53981509-53985519	ENSG00000065978	NA	100874365	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	A novel long noncoding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1.our data demonstrate that abnormal histone modification-activated HOXC-AS3 may play important roles in gastric cancer oncogenesis.A novel long noncoding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1.	30286788	RID00290	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Liver fibrosis	miR-212	MEG3	negatively-F	RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Gastrointestinal system disease	Fibrosis	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	LncRNA-MEG3 inhibits activation of hepatic stellate cells through SMO protein and miR-212.MEG3 was confirmed as a target of microRNA-212 (miR-212). miR-212 was partly responsible for the effects of MEG3 on EMT process.we demonstrate that MEG3 inhibits Hh-mediated EMT process in liver fibrosis via SMO protein and miR-212.LncRNA-maternally expressed gene 3 (MEG3) functions as a tumor suppressor in cancers and has been shown to play a vital role in EMT process.Accordingly,MEG3-inhibited EMT process could be partly suppressed by miR-212.	30282972	RID00291	ceRNA or sponge	NA	NA	NA
Liver fibrosis	MEG3	SMO	interact	RIP;deletion-mapping analysis	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000128602	NA	55384	6608	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CRJS|FZD11|Gx|SMOH	LncRNA-MEG3 inhibits activation of hepatic stellate cells through SMO protein and miR-212.an interaction between MEG3 and SMO protein was predicted.we demonstrate that MEG3 inhibits Hh-mediated EMT process in liver fibrosis via SMO protein and miR-212.LncRNA-maternally expressed gene 3 (MEG3) functions as a tumor suppressor in cancers and has been shown to play a vital role in EMT process.	30282972	RID00292	interact with protein	NA	NA	UP(PAAD);DATA(GSE40174)
Gastric cancer	LINC00460	KDM2A	positively-E	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	TCGA 	STAD.zip	cell proliferation(+);cell migration(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000173120	NA	728192	22992	NA	CXXC8|FBL11|FBL7|FBXL11|JHDM1A|LILINA	LINC00460 modulates KDM2A to promote cell proliferation and migration by targeting miR-342-3p in gastric cancer.we confirmed that LINC00460 could up-regulate KDM2A expression by competitively binding to miR-342-3p in GC cells. Furthermore, the suppressive effects of LINC00460 down-regulation on GC cell proliferation, migration and invasion were partially reversed by a miR-342-3p inhibitor.	30323616	RID00293	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	UBE2CP3-001	MMP9	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_4:57072549-57073311	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas. The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U87 glioma cells.Downregulation of UBE2CP3-001 could inhibit cell migration (p< 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01).	30393485	RID00294	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	UBE2CP3-001	TRAF3IP2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_4:57072549-57073311	ENSG00000056972	NA	NA	10758	NA	ACT1|C6orf2|C6orf4|C6orf5|C6orf6|CANDF8|CIKS|PSORS13	The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas. The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U88 glioma cells.Downregulation of UBE2CP3-001 could inhibit cell migration (p< 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01).	30393485	RID00295	expression association	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827)
Epithelial ovarian cancer	MIAT	miR-330-5p	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	LncRNA myocardial infarction-associated transcript promotes cell proliferation and inhibits cell apoptosis by targeting miR-330-5p in epithelial ovarian cancer cells.LncRNA MIAT promoted cell proliferation and inhibited cell apoptosis by negative regulation of miR-330-5p in epithelial ovarian cancer cells.we revealed that MIAT might function as an endogenous miR-330-5p sponge to regulate the target gene of miR-330-5p in epithelial ovarian cancer progression.	30393480	RID00296	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	NA
Osteosarcoma	HAGLR	CDKN1C	negatively-E	RIP;western blot;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000129757	NA	401022	1028	HOXD-AS1|MIR7704HG|Mdgt	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2.our study confirmed that HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis.	30119259	RID00297	epigenetic regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	SNHG12	MCL1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-320a)	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000143384	NA	85028	4170	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Long noncoding RNA SNHG12 mediates doxorubicin resistance of osteosarcoma via miR-320a/MCL1 axis.knockdown of SNHG12 contributed to the upregulation of miR-320a and improved the sensitivity of doxorubicin. Additionally, miR-320a inhibited the expression of Myeloid cell leukemia 1 (MCL1).miR-320a targeted to MCL1.	30119255	RID00298	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	MEG3	PDCD4	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	ceRNA(miR-141)	regulation	NA	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150593	NA	55384	27250	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	H731	Overexpression of MEG3 sensitizes colorectal cancer cells to oxaliplatin through regulation of miR-141/PDCD4 axis.MEG3 suppressed miR-141 expression in HCT116/OXA cells. Moreover, MEG3 elevated PDCD4 expression through targeting miR-141, acting as a competing endogenous RNA (ceRNA). Low MEG3 expression was correlated with poor prognosis of CRC patients. Overexpression of MEG3 improved oxaliplatin sensitivity of HT29/OXA and HCT116/OXA cells.	30119236	RID00299	ceRNA or sponge	prognosis,chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Esophagus squamous cell carcinoma	FTH1P3	SP1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000185591	NA	2498	6667	FTHL3|FTHL3P	NA	Long non-coding RNA FTH1P3 regulated metastasis and invasion of esophageal squamous cell carcinoma through SP1/NF-kB pathway.Knockdown of FTH1P3 notably decreased the proliferation, migration, and invasion capacity of ESCC cells. Silencing of FTH1P3 decreased the expression of specificity protein 1 (Sp1) and NF-kB (p65) in EC9706 and EC1.	30119232	RID00300	expression association	metastasis	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	FTH1P3	RELA	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000173039	NA	2498	5970	FTHL3|FTHL3P	CMCU|NFKB3|p65	Long non-coding RNA FTH1P3 regulated metastasis and invasion of esophageal squamous cell carcinoma through SP1/NF-kB pathway.Knockdown of FTH1P3 notably decreased the proliferation, migration, and invasion capacity of ESCC cells. Silencing of FTH1P3 decreased the expression of specificity protein 1 (Sp1) and NF-kB (p65) in EC9706 and EC1.	30119232	RID00301	expression association	metastasis	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	NORAD	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000169554	NA	647979	9839	LINC00657	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA NORAD upregulate SIP1 expression to promote cell proliferation and invasion in cervical cancer.the underlying mechanism studies showed that lncRNA NORAD could sponge miR-590-3p to promote the proliferation and invasion of CC cells via upregulating SIP1 expression.Previous study showed that SIP1 could act as a target of miR-590-3pin intrahepatic cholangiocarcinoma.	30119219	RID00302	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Osteosarcoma	OIP5-AS1	CDK14	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-223)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000058091	NA	729082	5218	cyrano|linc-OIP5	PFTAIRE1|PFTK1	Long noncoding RNA OIP5-AS1 accelerates CDK14 expression to promote osteosarcoma tumorigenesis via targeting miR-223.miR-223 was predicted to target the 3'-UTR of OIP5-AS1 and constituted RNA induced silencing complex, which was confirmed by RNA immunoprecipitation and luciferase reporter assay. Besides, miR-223 targeted the CDK14 mRNA 3'-UTR.	30119217	RID00303	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Retinoblastoma	THORLNC	MYC	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000136997	NA	100506797	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	LncRNA THOR acts as a retinoblastoma promoter through enhancing the combination of c-myc mRNA and IGF2BP1 protein. Down-regulation of lncRNA THOR with siRNA significantly repressed cell growth, migration and S phase accumulation, while induced cell apoptosis and G1 phase reduction and reduced the expression of c-myc.this study makes clear that lncRNA THOR is up-regulated in retinoblastoma, and its over-expression significantly enhances the malignant phenotype transformation of retinoblastoma cells through up-regulating c-myc expression via enhancing its combination with TGF2BP1 protein.	30119193	RID00304	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Osteoarthritis	FOXD2-AS1	CCND1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000110092	NA	84793	595	NA	BCL1|D11S287E|PRAD1|U21B31	LncRNA FOXD2-AS1 regulates chondrocyte proliferation in osteoarthritis by acting as a sponge of miR-206 to modulate CCND1 expression.qRT-PCR showed that expression of FOXD2-AS1 and Cyclin D1 (CCND1) was upregulated in OA cartilage tissues, while miR-206 expression was significantly decreased.TargetScan showed a potential miR-206 binding sequence in the 3'UTR of CCND1 (Fig. 4A). Luciferase reporter assay revealed that miR-206 mi-mics reduced the luciferase activity of CCND1-Wt group but not CCND1-Mut group in HEK293 T cells.	30119190	RID00305	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	HAGLR	MMP9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000100985	NA	401022	4318	HOXD-AS1|MIR7704HG|Mdgt	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA HOXD-AS1 promotes non-small cell lung cancer migration and invasion through regulating miR-133b/MMP9 axis.we found that miR-133b was a direct downstream target of HOXD-AS1 in NSCLC. miR-133b inhibition reverse the inhibitory effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of MMP-9 (a target of miR-133b) in NSCLC cells.Increased HAGLR expression promotes non-small cell lung cancer proliferation and invasion via enhanced de novo lipogenesis.Furthermore, the expression levels of p21 and matrix metallopeptidase-9 (MMP-9) were dysregulated when HAGLR expression was suppressed.	29958139;28443464	RID00306	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	LOC441178	ROCK1	negatively-E	RNAi;immunohistochemistry	downregulation	microarray	GSE30784;GSE9844	GSE30784.zip;GSE9844.zip	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENST00000400831	GRCh38_6:167679626-167683787	ENSG00000067900	NA	NA	6093	NA	P160ROCK|ROCK-I	Long Noncoding RNA LOC441178 Reduces the Invasion and Migration of Squamous Carcinoma Cells by Targeting ROCK1.we found that rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) is one of the functionally relevant targets of LOC441178 in squamous cells, which is negatively correlated with LOC441178 in tumor tissues from OSCC patients.	30364063	RID00307	transcriptional regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	TUG1	miR-219a-5p	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Targeting the FOXM1-regulated long noncoding RNA TUG1 in osteosarcoma. we found that TUG1 was upregulated by FOXM1 (Forkhead Box M1) in osteosarcoma cells. TUG1 accelerated osteosarcoma proliferation, migration, and invasion by competitively sponging miR-219a-5p, leading to upregulation of Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase Catalytic Subunit Alpha and activation of the protein kinase B (AKT) signaling pathway. In addition, the AKT pathway activation promoted TUG1 expression by upregulating the expression of FOXM1, forming a positive feedback loop in osteosarcoma.	30099814	RID00308	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Osteosarcoma	FOXM1	TUG1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000111206	NA	ENSG00000253352	GRCh38_22:30969245-30979395	2305	55000	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LINC00080|NCRNA00080|TI-227H	Targeting the FOXM1-regulated long noncoding RNA TUG1 in osteosarcoma. we found that TUG1 was upregulated by FOXM1 (Forkhead Box M1) in osteosarcoma cells. TUG1 accelerated osteosarcoma proliferation, migration, and invasion by competitively sponging miR-219a-5p, leading to upregulation of Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase Catalytic Subunit Alpha and activation of the protein kinase B (AKT) signaling pathway. In addition, the AKT pathway activation promoted TUG1 expression by upregulating the expression of FOXM1, forming a positive feedback loop in osteosarcoma.	30099814	RID00309	transcriptional regulation	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Hirschsprung's disease	FALEC	AKT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000142208	NA	100874054	207	FAL1|LINC00568|ncRNA-a1	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA FAL1 functions as a ceRNA to antagonize the effect of miR-637 on the down-regulation of AKT1 in Hirschsprung's disease. FAL1 could positively regulate AKT1 expression by competitively binding to miR-637. FAL1 regulates the miR-637 target gene, AKT1. Cell functional analyses indicated that FAL1 overexpressing notably promoted cell proliferation and migration.	30062828	RID00310	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC01606	miR-423-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000253301	GRCh38_8:57142659-57244793	NA	NA	100507651	NA	NA	NA	The long non-coding RNA LINC01606 contributes to the metastasis and invasion of human gastric cancer and is associated with Wnt/beta-catenin signaling.We also revealed that LINC01606 might be associated with miR-423-5p to regulate the level to which the Wnt/beta-catenin signaling pathway is activated.	30142387	RID00311	expression association	metastasis	NA	NA
Breast cancer	SNHG14	PABPC1	positively-E	ChIP;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);tumorigenesis(+)	histone modification	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000070756	NA	104472715	26986	115HG|IC-SNURF-SNRPN|LNCAT|NCRNA00214|U-UBE3A-ATS|UBE3A-AS|UBE3A-AS1|UBE3A-ATS|UBE3AATS	PAB1|PABP|PABP1|PABPC2|PABPL1	Long non-coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation.ChIP assays demonstrated that lncRNA SNHG14 may induce PABPC1 expression through modulating H3K27 acetylation in the promoter of PABPC1 gene, thus resulting in the activation of Nrf2 signalling pathway. These data suggest that lncRNA SNHG14 promotes breast cancer tumorigenesis and trastuzumab resistance through regulating PABPC1 expression through H3K27 acetylation.	30063126	RID00312	epigenetic regulation	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	HOTAIR	MET	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105976	NA	100124700	4233	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AUTS9|DFNB97|HGFR|RCCP2|c-Met	LncRNA HOTAIR/miR-613/c-met axis modulated epithelial-mesenchymal transition of retinoblastoma cells.HOTAIR was verified to directly target miR-613, and c-met was the direct target gene of miR-613 (P < 0.05).up-regulated HOTAIR and down-regulated miR-613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). c-met prohibited the functioning of miR-613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05).	30030888	RID00313	ceRNA or sponge	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Malignant glioma	PVT1	GREM1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+);BMP signaling pathway(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000166923	NA	5820	26585	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	C15DUPq|CKTSF1B1|CRAC1|CRCS4|DAND2|DRM|DUP15q|GREMLIN|HMPS|HMPS1|IHG-2|MPSH|PIG2	LncRNA PVT1 Facilitates tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway.lncRNA PVT1 acted as a sponge of miR-128-3p and, thus, influenced the BMP signaling pathway downstream proteins BMP2 and BMP4 through regulating GREM1. MiR-128-3p Targeted and Regulated GREM1.	30120709	RID00314	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE55807)
Colorectal cancer	GAS5	FOXO3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000118689	NA	60674	2309	NCRNA00030|SNHG2	AF6q21|FKHRL1|FKHRL1P2|FOXO2|FOXO3A	lncRNA GAS5 inhibits colorectal cancer cell proliferation via the miR-182-5p/FOXO3a axis.A dual-luciferase reporter assay showed that GAS5 could negatively regulate the expression of microRNA (miR)-182-5p. Upregulated miR-182-5p abrogated the effect of GAS5 overexpression on CRC cell proliferation and apoptosis.Furthermore, GAS5 positively regulated the expression of FOXO3a in CRC cells. It has been reported that FOXO3a, a pro-apoptotic transcription factor and direct target of the PI3K-AKT signaling pathway, may be the direct target of miR-182-5p. Binding sites between GAS5 and miR-182-5p were predicted using DIANA tools.	30066886	RID00315	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(BRCA);DATA(GSE51827,GSE86978)
Pre-eclampsia	uc003fir	CCL5	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000271503	NA	NA	6352	NA	D17S136E|RANTES|SCYA5|SIS-delta|SISd|TCP228|eoCP	LncRNA uc003fir promotes CCL5 expression and negatively affects proliferation and migration of trophoblast cells in preeclampsia.The chemokine CCL5 was directly regulated by lncRNA uc003fir. LncRNA uc003fir regulated CCL5 directly, which may mediate the recruitment of pro-inflammatory cytokines released from monocytes and other leukocytes.	30527126	RID00316	transcriptional regulation	chemoresistance	NA	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Non-small cell lung cancer	TBILA	GCSAM	positively-E	RIP;RNA pull-down assay	upregulation	sequencing;qRT-PCR	TCGA	LUSC_LUAD.zip	S100A7/JAB1 signaling pathway(+);cancer progression(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000261488	GRCh38_3:112133423-112135359	ENSG00000174500	NA	112806053	257144	NA	NA	The TGFbeta-induced lncRNA TBILA promotes non-small cell lung cancer progression in vitro and in vivo via cis-regulating HGAL and activating S100A7/JAB1 signaling.Upregulated TBILA promotes human germinal center-associated lymphoma (HGAL) expression by binding to the Smad transcription factor complex, thereby enhancing RhoA activation.The TGFbeta-induced lncRNA TBILA promotes non-small cell lung cancer progression in vitro and in vivo via cis-regulating HGAL and activating S100A7/JAB1 signaling.	29908210	RID00317	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	SNHG1	CDKN2B	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000147883	NA	23642	1030	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00318	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	SNHG1	KLF2	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000127528	NA	23642	10365	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	LKLF	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00319	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SNHG1	CCND2	negatively-E	luciferase reporter assay;western blot	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	ceRNA(miR-154-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000118971	NA	23642	894	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	KIAK0002|MPPH3	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.SNHG1 acted as a sponge for miR-154-5p, reducing its ability to repress Cyclin D2 (CCND2) expression.SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00320	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	NEAT1	miR-342-3p	negatively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Blockade of NEAT1 represses inflammation response and lipid uptake via modulating miR-342-3p in human macrophages THP-1 cells.miR-342-3p was predicted as a downstream target of NEAT1 and the correlation between them was confirmed in our study. Moreover, overexpression of miR-342-3p could also greatly suppress inflammation response and lipid uptake in THP-1 cells. we observed that NEAT1 was significantly increased in THP-1 cells	30259979	RID00321	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Atherosclerosis	GSC-DT	BMI1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-134)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_14:94770642-94773607	ENSG00000168283	NA	108868751	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134.DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways.	30158376	RID00322	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Lung cancer	NKX2-1-AS1	CD274	negatively-E	RNAi;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell migration(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253563	GRCh38_14:36519278-36523016	ENSG00000120217	NA	100506237	29126	NA	B7-H|B7H1|PD-L1|PDCD1L1|PDCD1LG1|PDL1|hPD-L1	NKX2-1-AS1 negatively regulates CD274/PD-L1, cell-cell interaction genes, and limits human lung carcinoma cell migration.Furthermore, NKX2-1-AS1 interferes with NKX2-1 protein binding to the CD274-promoter, likely by NKX2-1 protein-NKX2-1-AS1 interactions.	30258080	RID00323	transcriptional regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Cervical cancer	ZEB1-AS1	VIM	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000026025	NA	220930	7431	NA	NA	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00324	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Cervical cancer	ZEB1-AS1	CDH2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000170558	NA	220930	1000	NA	CD325|CDHN|CDw325|NCAD	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00325	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Cervical cancer	ZEB1-AS1	CDH1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000039068	NA	220930	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00326	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Cervical cancer	ZEB1-AS1	MAPK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000100030	NA	220930	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00327	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CDKN2B-AS1	miR-191	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Knockdown long non-coding RNA ANRIL inhibits proliferation, migration and invasion of HepG2 cells by down-regulation of miR-191.These data demonstrated that ANRIL knockdown suppressed proliferation, migration, invasion, and promoted apoptosis in HepG2 cells by down-regulating miR-191 and inactivating NF-kB and Wnt/beta-catenin signaling pathways.	30249208	RID00328	expression association	NA	UP(SKCM);DATA(GSE38495)	NA
Ovarian cancer	MAP3K20-AS1	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000238133	GRCh38_2:173166446-173282036	ENSG00000137693	NA	339751	10413	NA	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA MLK7-AS1 promotes ovarian cancer cells progression by modulating miR-375/YAP1 axis.Taken together, our study showed for the first time that MLK7-AS1 interacted with miR-375 to promote proliferation, metastasis, and EMT process in ovarian cancer cells through upregulating YAP1.	30249278	RID00329	ceRNA or sponge	metastasis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	TWIST1	DUXAP9	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000122691	NA	ENSG00000225210	GRCh38_14:19062316-19131167	7291	503638	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	NA	Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.Mechanical studies showed that INC01296 harbored miR-598, acting as a microRNA sponge. Besides, miR-598 targeted the 3'-UTR of Twist1. Interestingly, transcription factor Twist1 could bind with the promoter of INC01296 and activate its transcriptional level.Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.	30240003	RID00330	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)
Non-small cell lung cancer	DUXAP9	TWIST1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-598)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000122691	NA	503638	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.Mechanical studies showed that INC01296 harbored miR-598, acting as a microRNA sponge. Besides, miR-598 targeted the 3'-UTR of Twist1. Interestingly, transcription factor Twist1 could bind with the promoter of INC01296 and activate its transcriptional level.Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.	30240003	RID00331	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(SKCM);DATA(GSE38495)
Urinary bladder cancer	DGCR5	CDKN1A	positively-E	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	prognosis;cancer progression(-)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000124762	NA	26220	1026	LINC00037|NCRNA00037	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulation of lncRNA DGCR5 correlates with better prognosis and inhibits bladder cancer progression via transcriptionally facilitating P21 expression.Knockdown of P21 could significantly rescue the suppressed proliferation, migration, and invasion of BCa cells by DGCR5 overexpression. we found that DGCR5 interacted with AT-rich interaction domain 1A (ARID1A), a chromatin remodeling protein, to promote P21 transcription.	30238982	RID00332	epigenetic regulation	prognosis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Papillary thyroid carcinoma	SNHG15	YAP1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	Hippo signaling pathway(+)	ceRNA(miR-200a-3p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000137693	NA	285958	10413	C7orf40|Linc-Myo1g|MYO1GUT	COB1|YAP|YAP2|YAP65|YKI	LncRNA SNHG15 acts as a ceRNA to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma.The mechanical investigation indicated that SNHG15 upregulated YAP1 by sponging miR-200a-3p. LncRNA SNHG15 acts as a ceRNA to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma.The binding sites between 3<U+00C3><U+0192>a?U+0161><U+00C3><U+201A><U+00C2><U+00A1><U+00C3><U+0192><U+00C6>?U+00C3><U+201A><U+00C2>¤UTR of YAP1and miR-200a-3p were predicted (Fig.6c). Similarly,luciferase reporter vectors were constructed to demon-strate the combination between miR-200a-3p and YAP1.	30237435	RID00333	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	SNHG8	CCND1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell cycle(+)	ceRNA(miR-542-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000110092	NA	100093630	595	LINC00060|NCRNA00060	BCL1|D11S287E|PRAD1|U21B31	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00334	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	SNHG8	CASP3	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000164305	NA	100093630	836	LINC00060|NCRNA00060	CPP32|CPP32B|SCA-1	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00335	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	SNHG8	CDK6	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell cycle(+)	ceRNA(miR-542-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000105810	NA	100093630	1021	LINC00060|NCRNA00060	MCPH12|PLSTIRE	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00336	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Cardiac hypertrophy	CASC15	TLR4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cardiac hypertrophy(+)	ceRNA(miR-432-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000136869	NA	401237	7099	CANT|LINC00340|lnc-SOX4-1	ARMD10|CD284|TLR-4|TOLL	Upregulation of lncRNA VDR/CASC15 induced by facilitates cardiac hypertrophy through modulating miR-432-5p/TLR4 axis.CASC15 can upregulate TLR4 by competitively binding miR-432-5p. CASC15 was highly expressed in cardiac hypertrophic model. Results of immunofluorence staining revealed that cell surface area enlarged by Ang-II was decreased when CASC15 was silenced.	29966657	RID00337	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	WSPAR	TCF7	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000081059	NA	105664404	6932	LncTCF7|TCONS_00009511	TCF-1	Down-regulation of lncTCF7 inhibits cell migration and invasion in colorectal cancer via inhibiting TCF7 expression. RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays showed that LncTCF7 recruits BAF170 to activate the TCF7 promoter and regulate TCF7 expression.	30225781	RID00338	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Pre-eclampsia	DLX6-AS1	GADD45A	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-376c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000116717	NA	285987	1647	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	DDIT1|GADD45	Long non-coding RNA DLX6-AS1 is upregulated in preeclampsia and modulates migration and invasion of trophoblasts through the miR-376c/GADD45A axis.DLX6-AS1 interacted with miR-376c, and that overexpression of DLX6-AS1 significantly reduced expression of miR-376c in HTR-8/SVneo cells. Also, miR-376c targeted and downregulated GADD45A in HTR-8/SVneo cells. Overexpression of GADD45A effectively attenuated a miR-376c-induced increase in the proliferation, migration and invasion of HTR-8/SVneo cells. lncRNA DLX6-AS1 was confirmed to be significantly upregulated in the placentas of patients with preeclampsia, compared with normal controls.	30055134	RID00339	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Colon cancer	LINC-ROR	miR-145	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Non-Coding RNA lincRNA-ROR Promotes the Progression of Colon Cancer and Holds Prognostic Value by Associating with miR-145.Knockdown of lincRNA-ROR restored the expression of miR-145, and had a significant influence on colon cancer cell proliferation, migration and invasion.	27071407	RID00340	expression association	prognosis	UP(LIHC);DATA(GSE117623)	NA
Lung cancer	CCAT1	miR-218	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Epigenetic silencing of miR-218 by the lncRNA CCAT1, acting via BMI1, promotes an altered cell cycle transition in the malignant transformation of HBE cells induced by cigarette smoke extract.Depletion of CCAT1 attenuated the CSE-induced decreases of miR-218 levels, suggesting that miR-218 is negatively regulated by CCAT1 in HBE cells exposed to CSE.This epigenetic silencing of miR-218 by CCAT1 induces an altered cell cycle transition through BMI1 and provides a new mechanism for CSE-induced lung carcinogenesis.	27212446	RID00341	epigenetic regulation	NA	NA	NA
Neuroblastoma	LncND	miR-143-3p	negatively-F	Ago2-IP;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Neuroblastoma	lncRNA	miRNA	NA	GRCh38_2:663814-666523	NA	NA	NA	NA	NA	NA	A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.Binding and release of miR-143-3p by LncND control the expression of Notch receptors.	27263970	RID00342	ceRNA or sponge	NA	NA	NA
Immune thrombocytopenia	MEG3	miR-125a-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	immune response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Immune Detection	Immune system disease	Thrombocytopenia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 inhibits microRNA-125a-5p expression and induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura.MEG3 interacted with miR-125a-5p and inhibited its expression, and MEG3/miR-125a-5p contributed to induce immune imbalance of Treg/Th17 in ITP.	27522004	RID00343	ceRNA or sponge	NA	NA	NA
Osteoarthritis	linc-UFC1	miR-34a	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	GRCh38_1:161152776-161158856	NA	NA	NA	NA	NA	NA	Long Noncoding RNA UFC1 Promotes proliferation of Chondrocyte in Osteoarthritis by Acting as a Sponge for miR-34a.	27529373	RID00344	ceRNA or sponge	NA	NA	NA
Liver fibrosis	TP53COR1	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	fibrotic(-)	ceRNA(miR-181b)	association	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000171862	NA	102800311	5728	TRP53COR1|linc-p21|lincRNA-p21	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Identification of a Novel lincRNA-p21-miR-181b-PTEN Signaling Cascade in Liver Fibrosis.We demonstrated that lincRNA-p21 enhanced PTEN expression by competitively binding miR-181b.	27610008	RID00345	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Cardiac hypertrophy	MIAT	miR-150	negatively-F	RNAi;bioinformatics	upregulation	qPCR	NA	NA	cell growth(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression. MIAT inhibition also partly restored the miR-150 levels under Ang II treatment. MIAT can suppress miR-150 expression in cardiomyocytes and miR-150 is a downstream effector of MIAT in the development of cardiac hypertrophy.	27649667	RID00346	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	NA
Leukemia	HOTAIRM1	miR-20a	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00347	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	NA
Leukemia	HOTAIRM1	miR-125b	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00348	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	NA
Leukemia	HOTAIRM1	miR-106b	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00349	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	NA
Pancreatic carcinoma	LINC-ROR	miR-124	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	gemcitabine	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Linc-ROR confers gemcitabine resistance to pancreatic cancer cells via inducing autophagy and modulating the miR-124/PTBP1/PKM2 axis.Linc-ROR siRNA significantly sensitized PANC-1 and MIAPaCa-2 cells to gemcitabine, while linc-ROR overexpression significantly reduced the sensitivity. In both pancreatic cell lines and PADC tissues, linc-ROR is negatively correlated with miR-124 expression. In addition, dual luciferase assay verified two 8mer binding sites between miR-124 and linc-ROR.	27785603	RID00350	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Pancreatic carcinoma	LINC-ROR	PKM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	NA	association	NA	gemcitabine	NA	Sustained Angiogenesis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000067225	NA	100885779	5315	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	Linc-ROR confers gemcitabine resistance to pancreatic cancer cells via inducing autophagy and modulating the miR-124/PTBP1/PKM2 axis.Linc-ROR siRNA showed similar effect as 3-MA on enhancing gemcitabine-induced cell apoptosis and also reduced PKM2 expression. In addition, miR-124 mimics also alleviated autophagy in pancreatic cancer cells. Both miR-124 mimics and PKM2 siRNA enhanced gemcitabine-induced cell apoptosis.	27785603	RID00351	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Osteosarcoma	PVT1	BCL2	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00352	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	PVT1	CCND1	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000110092	NA	5820	595	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00353	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Osteosarcoma	PVT1	FASN	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000169710	NA	5820	2194	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FAS|OA-519|SDR27X1	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00354	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Kidney disease	MALAT1	ELAVL1	negatively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-23c)	regulation	NA	NA	NA	Evading Apoptosis	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy. luciferase assays showed that miR-23c, as a target of MALAT1, directly repressed ELAVL1 expression and then decreased the expression of its downstream protein NLRP3. The expression of MALAT1 antagonized the effect of miR-23c on the downregulation of its target ELAVL1 and inhibited hyperglycemia-induced cell pyroptosis.	27964927	RID00355	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Breast cancer	TUG1	miR-9	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA Taurine-Upregulated Gene 1 Promotes Cell proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells.The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. Using the starBase v2.0 database, miR-9 was found to potentially bind to TUG1.To verify the relationship between TUG1 and miR-9, a dual luciferase reporter assay was performed by constructing a reporter containing the binding site in TUG1-WT or the mutant. The luciferase activity of the reporter containing TUG1-WT was reduced in cells transfected with the miR-9 mimic.	28053623	RID00356	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Liver fibrosis	HOTAIR	PTEN	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	fibrotic(+)	DNA methylation;ceRNA(miR-29b)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis.HOTAIR was confirmed a target of miR-29b and lack of the miR-29b binding site in HOTAIR prevented the suppression of miR-29b, suggesting HOTAIR contributes to PTEN expression downregulation via sponging miR-29b. Collectively, we demonstrate that HOTAIR downregulates miR-29b expression and attenuates its control on epigenetic regulation, leading to enhanced PTEN methylation, which contributes to the progression of liver fibrosis.	28129115	RID00357	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Diabetic retinopathy	MIAT	miR-29b	negatively-F	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	Long non-coding RNA MIAT acts as a biomarker in diabetic retinopathy by absorbing miR-29b and regulating cell apoptosis.miR-29b controled MIAT to regulate its expression and MIAT overexpression suppressed miR-29b.luciferase activity assay was used to detect the target-specific selectivity between miR-29b and MIAT.	28246353	RID00358	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	NA
Myocardial infarction	ZFAS1	CRP	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000132693	NA	441951	1401	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	PTX1	Knockdown of Long Non-Coding RNA-ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti-Apoptosis by Regulating miR-150/CRP.The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150.C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150.The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP.	28295592	RID00359	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	NA
Lung adenocarcinoma	LINC-ROR	FSCN1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-145)	regulation	NA	docetaxel	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000075618	NA	100885779	6624	ROR|lincRNA-RoR|lincRNA-ST8SIA3	FAN1|HSN|SNL|p55	Long noncoding RNA ROR regulates chemoresistance in docetaxel-resistant lung adenocarcinoma cells via epithelial mesenchymal transition pathway.The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145.The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145, therefore, releasing the miR-145 target FSCN1, and thus contributing to the acquisition of chemoresistance and EMT phenotypes of docetaxel-resistant LAD cells.	28388536	RID00360	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Cardiac fibrosis	GAS5	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell growth(-);fibrotic(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Fibrosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA GAS5 controls cardiac fibroblast activation and fibrosis by targeting miR-21 via PTEN/MMP-2 signaling pathway. In this study, we confirmed that GAS5 was lowly expressed in cardiac fibrosis tissues as well as activated cardiac fibroblast. We found that up-regulated GAS5 decreased the expression of miR-21 significantly. GAS5 has a complementary region with miR-21, and it can repress the expression of miR-21 in RISC complex. Furthermore, GAS5 that upregulated or downregulated the expression of PTEN through miR-21 in cardiac fibroblasts.	28526319;23933812	RID00361	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic ductal adenocarcinoma	LINC-ROR	let-7family	negatively-F	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.We observed that linc-ROR expression was increased in CSLCs. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.We conclude that, as a crucial oncogene, linc-ROR promotes cell proliferation, invasiveness and contributes to stem cell properties of CSLCs in PDAC via acting as a ceRNA to regulate function of microRNAs.	28580169	RID00362	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Colon cancer	PART1	DNMT3A	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	DNA methylation;ceRNA(miR-143)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000119772	NA	25859	1788	NCRNA00206	DNMT3A2|M.HsaIIIA|TBRS	PART-1 functions as a competitive endogenous RNA for promoting tumor progression by sponging miR-143 in colorectal cancer.PART-1 functioned as a ceRNA of DNMT3A,by sponging miR-143. Finally, PART-1 induced tumor progression by regulating DNMT3A.	28619512	RID00363	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Lung injury	FOXD3-AS1	miR-150	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Respiratory system disease	Injury	lncRNA	miRNA	ENSG00000230798	GRCh38_1:63320884-63324441	NA	NA	100996301	NA	pasFOXD3	NA	Long noncoding RNA FOXD3-AS1 regulates oxidative stress-induced apoptosis via sponging microRNA-150.	28655711	RID00364	ceRNA or sponge	NA	NA	NA
Osteosarcoma	cir-GLI2	miR-125b-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	circRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Circular RNA GLI2 promotes osteosarcoma cell proliferation, migration, and invasion by targeting miR-125b-5p. functional experiments validated that cir-GLI2 exerted the tumor-promoting effects on osteosarcoma cells via negatively targeting miR-125b-5p	28695772	RID00365	ceRNA or sponge	NA	NA	NA
Breast cancer	PTENP1	PTEN	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell growth(-);tumorigenesis(-)	ceRNA(miR-19b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	PTENP1 acts as a ceRNA to regulate PTEN by sponging miR-19b and explores the biological role of PTENP1 in breast cancer.Moreover, PTENP1 could upregulate PTEN via its ceRNA interaction on miR-19b, as well as induced the upregulation of p53 and downregulation of p-AKT. Enhanced PTENP1 could inhibit BC cell growth, metastasis and tumourigenicity by inhibiting miR-19b and facilitating PTEN in BC, thereby may represent a novel target for diagnosis and treatment of BC.	28731027	RID00366	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Epithelial ovarian carcinoma	PCA3	miR-106b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225937	GRCh38_9:76691980-76863307	NA	NA	50652	NA	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	NA	Research results show that lncRNA PCA3 may coordinate EOC tumorigenesis through disrupting miR-106b regulated gene expression.Bioinformatic predictions and dual-luciferase reporter assays indicate that the 3'UTR of PCA3 has potential binding sites for miR-106b-5p	28864116	RID00367	ceRNA or sponge	NA	NA	NA
Non-small cell lung cancer	SNHG12	miR-138	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long Noncoding RNA Small Nucleolar RNA Host Gene 12 Inhibits Cell Growth and Induces Apoptosis by Upregulating miR-138 in Nonsmall Cell Lung Cancer.	28872894	RID00368	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Triple-receptor negative breast cancer	circGFRA1	GFRA1	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-34a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	circRNA	PCG	NA	NA	ENSG00000151892	NA	NA	2674	NA	GDNFR|GDNFRA|GFR-ALPHA-1|RET1L|RETL1|TRNR1	circGFRA1 and GFRA1 act as ceRNAs in triple negative breast cancer by regulating miR-34a.Knockdown of circGFRA1 inhibited proliferation and promoted apoptosis in TNBC. we conclude that circGFRA1 may function as a competing endogenous RNA (ceRNA) to regulate GFRA1 expression through sponging miR-34a to exert regulatory functions in TNBC.	29037220	RID00369	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Pulmonary fibrosis	LNCRNA-ATB	ZEB1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Respiratory system disease	Fibrosis	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000148516	NA	114004396	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA-ATB promotes EMT during silica-induced pulmonary fibrosis by competitively binding miR-200c.Collectively, silica-stimulated macrophages secreted TGF-beta1 to induce lncRNA-ATB in epithelia cells, promoting EMT by binding with miR-200c and releasing ZEB1.	29113749	RID00370	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ischemic stroke	MEG3	PDCD4	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell death(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150593	NA	55384	27250	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	H731	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate ischemic neuronal death by targeting miR-21/PDCD4 signaling pathway.MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with programmed cell death 4 (PDCD4) mRNA for directly binding to miR-21, which mediates ischemic neuronal death	29238035	RID00371	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Kidney disease	LINC01619	FOXO1	positively-E	luciferase reporter assay;RIP;western blot	downregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-27a)	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000257242	GRCh38_12:91984976-92142914	ENSG00000150907	NA	256021	2308	C12orf79	FKH1|FKHR|FOXO1A	Long Noncoding RNA LINC01619 Regulates MicroRNA-27a/Forkhead Box Protein O1 and Endoplasmic Reticulum Stress-Mediated Podocyte Injury in Diabetic Nephropathy.LINC01619 exerted biological function by serving as a sponge for miR-27a, which negatively targeted forkhead box protein O1 (FOXO1) and activated ER stress	29334763	RID00372	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Glioblastoma	TUSC7	miR-10a	negatively-F	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Long non-coding RNA TUSC7 inhibits temozolomide resistance by targeting miR-10a in glioblastoma.TUSC7 acted by directly targeting and silencing expression of miR-10a gene, and miR-10a mediated TUSC7-induced inhibition on TMZ resistance in U87TR cells.	29397407	RID00373	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Brain injury	GAS5	miR-23a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell injury(+);hippocampal neuron function(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury. Mechanistically, GAS5 regulated hippocampal neuron function by sponging miR-23a.	29428721	RID00374	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Glioblastoma	MALAT1	miR-101	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA-101 in glioblastoma. Importantly, we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR-101 signaling pathway via directly binding it in GBM cells.	29479863	RID00375	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Hepatocellular carcinoma	LINC-ROR	RAD18	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	radioresistance(+);DNA repair(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Liver cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000070950	NA	100885779	56852	ROR|lincRNA-RoR|lincRNA-ST8SIA3	RNF73	Long non-coding RNA ROR promotes radioresistance in hepatocelluar carcinoma cells by acting as a ceRNA for microRNA-145 to regulate RAD18 expression.Further mechanistic investigations revealed that lincRNA-ROR exerted its biological effects by acting as a competing endogenous RNA (ceRNA) for miR-145 to regulate RAD18 expression, thereby promoting DNA repair	29559320	RID00376	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	FLVCR1-DT	MET	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-513c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000198468	GRCh38_1:212852105-212858126	ENSG00000105976	NA	642946	4233	NA	AUTS9|DFNB97|HGFR|RCCP2|c-Met	LncRNA FLVCR1-AS1 acts as miR-513c sponge to modulate cancer cell proliferation, migration, and invasion in hepatocellular carcinoma.In mechanism, FLVCR1-AS1 acted as a competitive endogenous RNAs to sponge miR-513c which targeted the mRNA of MET for degradation. By directly sponging miR-513c, FLVCR1-AS1 increased MET expression in HCC, and then promoted HCC progression.	29574975	RID00377	ceRNA or sponge	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Osteosarcoma	NEAT1	BCL2	positively-E	RNAi;starBase	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34c)	regulation	NA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171791	NA	283131	596	LINC00084|NCRNA00084|TncRNA|VINC	Bcl-2|PPP1R50	Knockdown of the oncogene lncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma.overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c The results in vivo also confirmed that knockdown of NEAT1 sensitized the OS cells to DPP-induced tumor regression, delayed the tumor growth with reduced levels of Ki-67, BCL-2, and cyclin D1 signals, suggesting that NEAT1 is an oncogene and chemotherapy resistant factor in OS.	29654165	RID00378	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	NEAT1	CCND1	positively-E	RNAi;starBase	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34c)	regulation	NA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000110092	NA	283131	595	LINC00084|NCRNA00084|TncRNA|VINC	BCL1|D11S287E|PRAD1|U21B31	Knockdown of the oncogene lncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma.overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c The results in vivo also confirmed that knockdown of NEAT1 sensitized the OS cells to DPP-induced tumor regression, delayed the tumor growth with reduced levels of Ki-67, BCL-2, and cyclin D1 signals, suggesting that NEAT1 is an oncogene and chemotherapy resistant factor in OS.	29654165	RID00379	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Acute myeloid leukemia	UCA1	HK2	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glucose metabolic process(+)	ceRNA(miR-125a)	regulation	NA	adriamycin	NA	Reprogramming Energy Metabolism	Cancer	Leukemia	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000159399	NA	652995	3099	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HKII|HXK2	Knockdown of LncRNA-UCA1 suppresses chemoresistance of pediatric AML by inhibiting glycolysis through the microRNA-125a/hexokinase 2 pathway.Additionally, UCA1 functioned as a ceRNA of miR-125a by directly binding to miR-125a. HK2, a target of miR-125a, was positively regulated by UCA1 in HL60 and HL60/ADR cells	29663500	RID00380	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Kidney injury	NEAT1	miR-204	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis	Other	Injury	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 plays an important role in sepsis-induced acute kidney injury by targeting miR-204 and modulating the NF-kB pathway.	29669307	RID00381	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Invasive bladder transitional cell carcinoma	MALAT1	FOXQ1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164379	NA	378938	94234	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HFH1	LncRNA MALAT1 promotes tumor growth and metastasis by targeting miR-124/foxq1 in bladder transitional cell carcinoma (BTCC).MALAT1 may function as a ceRNA to sponge miR-124, thus modulating the derepression of foxq1, miR-124 target gene, in post-transcriptional levels	29736319	RID00382	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Gastric cancer	LINC00483	SPAG9	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);MAPK signaling pathway(+)	ceRNA(miR-30a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000008294	NA	NA	9043	NA	CT89|HLC-6|HLC4|HLC6|JIP-4|JIP4|JLP|PHET|PIG6	Linc00483 as ceRNA regulates proliferation and apoptosis through activating MAPKs in gastric cancer. Linc00483 regulates SPAG9 by acting as a ceRNA and interacting with miR-30a-3p	29761936	RID00383	ceRNA or sponge	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE60407)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Temporal lobe epilepsy	H19	let-7b	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Nervous system disease	Epilepsy	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 contributes to apoptosis of hippocampal neurons by inhibiting let-7b in a rat model of temporal lobe epilepsy.Finally, we show that H19 might function as a competing endogenous RNA to sponge microRNA let-7b in the regulation of cellular apoptosis	29795132	RID00384	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Esophagus squamous cell carcinoma	DUXAP10	CDKN1A	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000244306	GRCh38_14:19268853-19337730	ENSG00000124762	NA	503639	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA DUXAP10 modulates cell proliferation in esophageal squamous cell carcinoma through epigenetically silencing p21. Results of mechanism experiments suggested that DUXAP10 motivated ESCC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21.	30215547	RID00385	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Ovarian cancer	LINC01139	TGFB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000105329	NA	339535	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LINK-A lncRNA promotes migration and invasion of ovarian carcinoma cells by activating TGF-beta pathway.LINK-A overexpression led to up-regulated TGF-beta1 in ovarian carcinoma cells and promoted cell migration and invasion.	30061183	RID00386	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	snaR	GAB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_19:47918429-47918550	ENSG00000033327	NA	NA	9846	NA	NA	LncRNA snaR upregulates GRB2-associated binding protein 2 and promotes proliferation of ovarian carcinoma cells.	30093110	RID00387	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Osteosarcoma	SNHG20	RUNX2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);apoptosis process(-)	ceRNA(miR-139)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124813	NA	654434	860	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	LncRNA SNHG20 knockdown suppresses the osteosarcoma tumorigenesis through the mitochondrial apoptosis pathway by miR-139/RUNX2 axis.Bioinformatics analysis revealed that miR-139 both targeted with the 3'-UTR of runt-related transcription factor 2 (RUNX2) and SNHG20, which was verified by luciferase reporter assay and RNA immunoprecipitation (RIP).	30072099	RID00388	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	WDFY3-AS2	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180769	GRCh38_4:84965534-85011277	ENSG00000170558	NA	NA	1000	NA	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00389	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Hepatocellular carcinoma	MIAT	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000170558	NA	440823	1000	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00390	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Hepatocellular carcinoma	MEG3	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000170558	NA	55384	1000	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00391	expression association	NA	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Glioblastoma	LINC01446	TPT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-489-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000205628	GRCh38_7:53655508-53811952	ENSG00000133112	NA	401337	7178	GS1-179L18.1	HRF|TCTP|p02|p23	LncRNA LINC01446 promotes glioblastoma progression by modulating miR-489-3p/TPT1 axis.Mechanistically, bioinformatics analysis showed that LINC01446 acted as a sponge for miR-489-3p which targeted TPT1	30029885	RID00392	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Lung cancer	Lnc-EPIC1	MYC	interact	RIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA EPIC1 promotes human lung cancer cell growth. Together, our results show that Lnc-EPIC1 promotes human lung cancer cell growth possibly by targeting MYC. Long non-coding RNA (LncRNA) EPIC1 (Lnc-EPIC1) is a MYC-interacting LncRNA. Lnc-EPIC1 directly associated with MYC protein in the nuclei of A549 cells.	30029875	RID00393	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	RAD51-AS1	RAD51	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	chemosensitivity(+);radiosensitivity(+);DNA repair(-)	interact with mRNA	binding/interaction	RNA-RNA	melatonin;corylin;chemotherapeutic agent etoposide (VP16)	NA	Genome Instability and Mutation	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245849	GRCh38_15:40686183-40695107	ENSG00000051180	NA	100505648	5888	TODRA	BRCC5|FANCR|HRAD51|HsRad51|HsT16930|MRMV2|RAD51A|RECA	Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair.Whole-transcriptome and gain- and loss-of-function analyses revealed that melatonin induces expression of the long noncoding RNA RAD51-AS1, which binds to RAD51 mRNA to inhibit its translation, effectively decreasing the DNA repair capacity of HCC cells and increasing their sensitivity to chemotherapy and radiotherapy.Animal models further demonstrated that a combination of melatonin and the chemotherapeutic agent etoposide (VP16) can significantly enhance tumor growth inhibition compared with monotherapy. Our results show that melatonin is a potential adjuvant treatment for chemotherapy and radiotherapy in HCC.RAD51-AS1, which bound to RAD51 mRNA, thereby inhibiting RAD51 protein expression, thus inhibiting the DNA damage repair ability of HCC cells.	30201872;29749376	RID00394	interact with mRNA	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	SLCO4A1-AS1	CTNNB1	positively-F	RNA pull-down assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell growth(+);cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000168036	NA	100127888	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA SLCO4A1-AS1 facilitates growth and metastasis of colorectal cancer through beta-catenin-dependent Wnt pathway.SLCO4A1-AS1 interacts with beta-catenin. Mechanistically, SLCO4A1-AS1 activates Wnt/beta-catenin signaling. SLCO4A1-AS1 enhanced the stability of beta-catenin by impairing the interaction of beta-catenin with GSKbeta and inhibiting its phosphorylation.	30201010	RID00395	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	SMAD4	LINP1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000141646	NA	ENSG00000223784	GRCh38_10:6709530-6740532	7040	108570035	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	TGF-beta/SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer.Here, we demonstrated that the transcription of lncRNA in nonhomologous end joining (NHEJ) pathway 1 (LINP1) was inhibited by TGF-beta1 in a SMAD4-dependent manner	30416386	RID00396	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	NA
Gastric cancer	lncR-D63785	MEF2D	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-422a)	regulation	NA	doxorubicin	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_17:34610748-34611354	ENSG00000116604	NA	NA	4209	NA	NA	The Long Noncoding RNA D63785 Regulates Chemotherapy Sensitivity in Human Gastric Cancer by Targeting miR-422a.This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.These results indicate that lnRNA-D63785 could be related to doxorubicin (DOX) resistance in human gastric cancer.	30195778	RID00397	ceRNA or sponge	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Pre-eclampsia	HOXA11-AS	RND3	negatively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000115963	NA	221883	390	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ARHE|Rho8|RhoE|memB	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID00398	epigenetic regulation	NA	NA	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065,GSE55807)
Pre-eclampsia	HOXA11-AS	HOXA7	positively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000122592	NA	221883	3204	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ANTP|HOX1|HOX1.1|HOX1A	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.In the cytoplasm, HOXA11-AS modulates HOXA7 expression by sponged miR-15b-5p,affecting trophoblast cell proliferation.	30195759	RID00399	ceRNA or sponge	NA	NA	NA
Atherosclerosis	HOTAIR	miR-330-5p	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Silence of long intergenic noncoding RNA HOTAIR ameliorates oxidative stress and inflammation response in ox-LDL-treated human macrophages by upregulating miR-330-5p.By carrying out bioinformatics analysis, miR-330-5p was predicted as a target of HOTAIR and the correlation between them was validated in our current study	30187491	RID00400	ceRNA or sponge	NA	NA	NA
Atherosclerosis	XIST	NOD2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-320)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000167207	NA	7503	64127	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ACUG|BLAU|BLAUS|CARD15|CD|CLR16.3|IBD1|NLRC2|NOD2B|PSORAS1|YAOS	Further experiments identified XIST regulated the expression of Nucleotide-Binding Oligomerization Domain 2 (NOD2) by sponging miR-320.	29902461	RID00401	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Urinary bladder cancer	LINC01605	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000253414	GRCh38_8:37421341-37554183	ENSG00000100985	NA	100507420	4318	LincDUSP	CLG4B|GELB|MANDP2|MMP-9	High LINC01605 expression predicts poor prognosis and promotes tumor progression via up-regulation of MMP9 in bladder cancer. our results shed light on that LINC01605, as a new prognostic biomarker, could promote the proliferation, migration, and invasion of BC cells via activating EMT signaling pathway and up-regulating MMP9 expression	30054424	RID00402	expression association	prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	NEAT1	DDX5	interact	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000108654	NA	283131	1655	LINC00084|NCRNA00084|TncRNA|VINC	G17P1|HLR1|HUMP68|p68	The lncRNA NEAT1 activates Wnt/beta-catenin signaling and promotes colorectal cancer progression via interacting with DDX5. Mechanistically, we found that NEAT1 directly bound to the DDX5 protein, regulated its stability, and sequentially activated Wnt signaling.	30185232	RID00403	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MIR31HG	ST7L	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	ceRNA(miR-575)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000007341	NA	554202	54879	LncHIFCAR|hsa-lnc-31	FAM4B|ST7R|STLR	Long noncoding RNA MIR31HG inhibits hepatocellular carcinoma proliferation and metastasis by sponging microRNA-575 to modulate ST7L expression.	30176933	RID00404	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Laryngeal squamous cell carcinoma	SNHG1	YAP1	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000137693	NA	23642	10413	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	COB1|YAP|YAP2|YAP65|YKI	A positive feedback regulation between long noncoding RNA SNHG1 and YAP1 modulates growth and metastasis in laryngeal squamous cell carcinoma.Mechanistically, SNHG1 promotes YAP1 expression and Hippo signaling activity by competitively sponging miR-375	30323965	RID00405	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Thyroid carcinoma	MEG3	miR-182	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	131I	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 enhances 131I sensitivity in thyroid carcinoma via sponging miR-182	30021359	RID00406	ceRNA or sponge	NA	NA	NA
Renal cell carcinoma	HOTTIP	LATS2	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000150457	NA	100316868	26524	HOXA-AS6|HOXA13-AS1|NCRNA00213	KPM	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID00407	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Meningioma	LINC00460	MMP9	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-539)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Meningioma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000100985	NA	728192	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA LINC00460 targets miR-539/MMP-9 to promote meningioma progression and metastasis.Bioinformatics tools predicted that miR-539 both targeted with the 3'-UTR of LINC00460 and MMP-9 mRNA,which was confirmed by luciferase reporter assay and western blot analysis. In summary, our study reveals that LINC00460 promotes MMP-9 expression through targeting miR-539	29906745	RID00408	ceRNA or sponge	metastasis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	HOXB13-AS1	HOXB13	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000229637	GRCh38_17:48720802-48724758	ENSG00000159184	NA	NA	10481	NA	HPC9|PSGD	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma. Mechanistically, we showed that HOXB13-AS1 overexpression increased DNMT3B-mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP),epigenetically suppressing HOXB13 expression.	30105866	RID00409	epigenetic regulation	NA	NA	UP(PAAD);DATA(GSE40174)
Alzheimer's disease	RP11-543N12.1	miR-324-3p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	miRNA	ENSG00000261410	GRCh38_16:83383016-83398170	NA	NA	NA	NA	NA	NA	Regulatory effects of the long non-coding RNA RP11-543N12.1 and microRNA-324-3p axis on the neuronal apoptosis induced by the inflammatory reactions of microglia. RP11-543N12.1 targeted miR-324-3p to suppress proliferation and promote apoptosis in the AD cell model.The interaction between RP11-543N12.1 and miR-324-3p was confirmed with a dual-luciferase reporter gene assay	29956723	RID00410	ceRNA or sponge	NA	NA	NA
Myocardial infarction	CRRL	HOPX	positively-E	luciferase reporter assay;RT-qPCR	upregulation	qPCR;sequencing	ERR315356;ERR315430;SRR643778;SRR643779	ERR315356;ERR315430;SRR643778;SRR643779	cardiomyocyte regeneration(-);cardiac repair(-)	ceRNA(miR-199a-3p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000050165	GRCh38_11:11965873-11979916	ENSG00000171476	NA	NA	84525	NA	NA	Loss of long non-coding RNA CRRL promotes cardiomyocyte regeneration and improves cardiac repair by functioning as a competing endogenous RNA.Furthermore, we demonstrated that CRRL acts as a competing endogenous RNA (ceRNA) by directly binding to miR-199a-3p and thereby increasing the expression of Hopx,a target gene of miR-199a-3p and a critical negative regulatory factor of CM proliferation	30125571	RID00411	ceRNA or sponge	NA	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Multiple myeloma	MALAT1	NFE2L1	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000082641	NA	378938	4779	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.	29487387	RID00412	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Multiple myeloma	MALAT1	KEAP1	positively-E	RIP;ChIP;IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116044	NA	378938	9817	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.	29487387	RID00413	epigenetic regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Gastric cancer	SNHG6	CDKN1A	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells.Knockdown of SNHG6 stimulated p21 expression and the tumor-suppressive effect of SNHG6 in GC cells was dependent on p21.Our findings show that SNHG6 knockdown inhibits GC development by upregulating p21; this effect is dependent on the activation of the JNK pathway and suppression of EZH2 expression.	30031062	RID00414	epigenetic regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Ischemic stroke	TUG1	AURKA	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000087586	NA	55000	6790	LINC00080|NCRNA00080|TI-227H	AIK|ARK1|AURA|BTAK|PPP1R47|STK15|STK6|STK7	LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells.	30200102	RID00415	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Papillary thyroid carcinoma	UCA1	BRD4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000141867	NA	652995	23476	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP|HUNK1|HUNKI|MCAP	Furthermore, UCA1 competed with BRD4 for miR-204 binding. miR-204 knockdown enhanced BRD4 expression	30015945	RID00416	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Anaplastic thyroid carcinoma	UCA1	MYC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-135a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000136997	NA	652995	4609	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA UCA1 promotes anaplastic thyroid cancer cell proliferation via miR-135a-mediated c-myc activation.In addition, using luciferase assays, it was confirmed that miR-135a directly bound to UCA1 and the 3' untranslated region of c-myc, and UCA1 competed with c-myc for miR-135a binding. miR-135a inhibition may upregulate c-myc expression	30015867	RID00417	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Parkinson's disease	SNHG1	SIAH1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cytotoxicity(+)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000196470	NA	23642	6477	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	SIAH1A	LncRNA SNHG1 promotes alpha-synuclein aggregation and toxicity by targeting miR-15b-5p to activate SIAH1 in human neuroblastoma SH-SY5Y cells	29217406	RID00418	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE55807)
Esophagus squamous cell carcinoma	lncRNA-ECM	ICAM1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENST00000589379	GRCh38_19:10285801-10289019	ENSG00000090339	NA	NA	3383	NA	BB2|CD54|P3.58	LncRNA-ECM is overexpressed in esophageal squamous cell carcinoma and promotes tumor metastasis.The expression level of ICAMI was directly correlated with the expression of lncRNA-ECM, suggesting that ICAM1 may be the downstream target gene of lncRNA-ECM.	30128011	RID00419	expression association	metastasis	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367)
Malignant glioma	UCA1	ZEB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000148516	NA	652995	6935	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA UCA1 sponges miR-204-5p to promote migration, invasion and epithelial-mesenchymal transition of glioma cells via upregulation of ZEB1.	30107990	RID00420	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	XIST	miR-155-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p	30091314	RID00421	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Hepatocellular carcinoma	JPX	XIST	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);tumorigenesis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	lncRNA	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000229807	GRCh38_X:73820649-73852723	554203	7503	DCBALD06|ENOX|LINC00183|NCRNA00183	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p. JPX knock-in significantly increased XIST expression and inhibited HepG2 cell growth in vitro or tumor formation in vivo in a XIST dependent manner.	30091314	RID00422	expression association	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Hepatocellular carcinoma	SNHG5	GSK3B	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000082701	NA	387066	2932	C6orf160|LINC00044|NCRNA00044|U50HG	NA	Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-26a-5p/GSK3beta signal pathway.Taken together, SNHG5 promotes HCC progression by competitively binding miR-26a-5p and regulating GSK3beta and Wnt/beta-catenin signal pathway.	30166525	RID00423	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	AGAP2-AS1	MYD88	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000172936	NA	100130776	4615	PUNISHER	MYD88D	SP1-induced lncRNA AGAP2-AS1 expression promotes chemoresistance of breast cancer by epigenetic regulation of MyD88.ChIP assays showed that AGAP2-AS1-bound CBP increased the enrichment of H3K27ac at the promoter region of MyD88, thus resulting in the upregulation of MyD88.	30157918	RID00424	epigenetic regulation	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	ANCR	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000105329	NA	282	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	lncRA ANCR Inhibits Non-Small Cell Lung Cancer Cell Migration and Invasion by Inactivating TGF-beta Pathway.ANCR can inhibit NSCLC cell migration and invasion by downregulating TGF-beta1 expression.	30154397	RID00425	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	NEAT1	miR-506	negatively-F	RIP;western blot;RNA pull-down assay	upregulation	qPCR;microarray	GSE45158	GSE45158.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long noncoding RNA NEAT1, regulated by LIN28B, promotes cell proliferation and migration through sponging miR-506 in high-grade serous ovarian cancer	30154460	RID00426	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Urinary bladder cancer	RP11-79H23.3	PTEN	positively-E	RIP;western blot	downregulation	qPCR;microarray	GSE89006	GSE89006.zip	angiogenesis(-);tumorigenesis(-);cell metastasis(-)	ceRNA(miR-107)	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_8:78837529-78840522	ENSG00000171862	NA	NA	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer.upregulation of RP11-79H23.3 inhibited the angiogenesis, tumorigenesis, and lung metastasis in vivo, whereas RP11-79H23.3 knockdown exerted a contrary role.	30149689	RID00427	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Malignant glioma	CDKN2B-AS1	miR-203a	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell cycle(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Effect of lncRNA ANRIL silencing on anoikis and cell cycle in human glioma via microRNA-203a	30197521	RID00428	expression association	NA	UP(SKCM);DATA(GSE38495)	NA
Prostate cancer	TINCR	TRIP13	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000071539	NA	257000	9319	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	16E1BP|MVA3	LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer.TINCR plays a tumor suppressive role in regulating prostate cancer cell proliferation, migration and invasion through modulating TRIP13 expression	30154672	RID00429	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Gastric cancer	CDKN2B-AS1	BMI1	positively-E	RNAi;Targetscan	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-99a)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000168283	NA	100048912	648	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Knockdown of long non-coding RNA ANRIL inhibits tumorigenesis in human gastric cancer cells via microRNA-99a-mediated down-regulation of BMI1.	30156609	RID00430	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Osteosarcoma	CDKN2B-AS1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164305	NA	100048912	836	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CPP32|CPP32B|SCA-1	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Moreover, our mechanistic research findings verified that ANRIL-influenced growth and apoptosis may be partly through regulation of caspase-3 and Bcl-2.	30147340	RID00431	expression association	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Osteosarcoma	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Moreover, our mechanistic research findings verified that ANRIL-influenced growth and apoptosis may be partly through regulation of caspase-3 and Bcl-2.	30147340	RID00432	expression association	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	CDKN2B-AS1	MTA1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000182979	NA	100048912	9112	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin	30147340	RID00433	expression association	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	CDKN2B-AS1	TIMP2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000035862	NA	100048912	7077	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CSC-21K|DDC8	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin.	30147340	RID00434	expression association	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	CDKN2B-AS1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000039068	NA	100048912	999	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin	30147340	RID00435	expression association	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	DLEU1	KPNA3	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000102753	NA	10301	3839	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	IPOA4|SRP1|SRP1gamma|SRP4|hSRP1	LncRNA DLEU1 contributes to colorectal cancer progression via activation of KPNA3.Here we revealed that DLEU1 was crucial for activation of KPNA3 by recruiting SMARCA1, an essential subunit of the NURF chromatin remodeling complex, in CRC. DLEU1 was indispensible for the deposition of SMARCA1 at the promoter of KPNA3 gene.	30098595	RID00436	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	E2F1	LSINCT5	positively-E	ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000281560	GRCh38_5:2712591-2715237	1869	101234261	E2F-1|RBAP1|RBBP3|RBP3	NA	E2F1 induces LSINCT5 transcriptional activity and promotes gastric cancer progression by affecting the epithelial-mesenchymal transition.Mechanistic investigations showed that LSINCT5 is a direct transcriptional target of E2F1.	30127643	RID00437	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(PRAD);DATA(GSE104209)
Renal fibrosis	DNMT1	MEG3	negatively-E	RNAi;5-ethynyl-2'- deoxyuridine assay;bisulfite DNA sequencing assay	downregulation	qPCR	NA	NA	cell viability(-);cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Fibrosis	PCG	lncRNA	ENSG00000130816	NA	ENSG00000214548	GRCh38_14:100779410-100861031	1786	55384	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	miR-185 affected the EMT, cell viability and proliferation via DNMT1/MEG3 pathway in TGF-beta1-induced renal fibrosis.Furthermore, we demonstrated that DNMT1 regulated the MEG3 expression via altering the CpGs methylation level of MEG3 promoter in TGF-beta1-induced renal fibrosis	30095214	RID00438	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	NA
Hepatocellular carcinoma	NEAT1	IL6	positively-E	RNAi	upregulation	sequencing	TCGA	LIHC.zip	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000136244	NA	283131	3569	LINC00084|NCRNA00084|TncRNA|VINC	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	NEAT1 paraspeckle promotes human hepatocellular carcinoma progression by strengthening IL-6/STAT3 signaling.Destruction of paraspeckle formation by silencing the paraspeckle essential components NEAT1_2 or NONO could suppress IL-6-induced STAT3 phosphorylation in HCC cells.Our results demonstrate that paraspeckle can nuclear entrap the inhibitors of IL-6/STAT3 signaling as well as DNA damage, and then strengthen the promoting effect on HCC progression by IL-6. Mechanistically, paraspeckle promotes IL-6-induced STAT3 phosphorylation by binding and trapping peroxiredoxin-5 (PRDX5) mRNA in nucleus, decreasing protein level of PRDX5 which can directly interact with STAT3 and inhibit STAT3 phosphorylation.	30377567	RID00439	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Colorectal cancer	PVT1-214	LIN28A	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR;microarray	GSE109454	GSE109454.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-128)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENST00000522875	GRCh38_8:129001506-129108902	ENSG00000131914	NA	NA	79727	NA	NA	Long noncoding RNA PVT1-214 promotes proliferation and invasion of colorectal cancer by stabilizing Lin28 and interacting with miR-128.we found that PVT1-214 not only upregulation Lin28 protein expression in CRC cells by stabilizing Lin28, but also participated in crosstalk with Lin28 mRNA through competition for miR-128 binding, imposing an additional level of post-transcriptional regulation	30076414	RID00440	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Papillary thyroid carcinoma	PVT1	IGF1R	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	ceRNA(miR-30a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000140443	NA	5820	3480	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CD221|IGFIR|IGFR|JTK13	Long noncoding RNA PVT1 enhances the viability and invasion of papillary thyroid carcinoma cells by functioning as ceRNA of microRNA-30a through mediating expression of insulin like growth factor 1 receptor.	29803929	RID00441	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Lung cancer	TINCR	FBXW7	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-544a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000109670	NA	257000	55294	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer;TINCR acted as a competing endogenous RNA (ceRNA) to sequester miR-544a from its target gene FBXW7	29324317	RID00442	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367)
Neuroblastoma	ETS1-AS1	HNRNPK	interact	RIP;EMSA;RNA pull-down assay	upregulation	qPCR;microarray;sequencing	GSE16476	GSE16476.zip	cancer progression(+);beta-catenin signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000254588	GRCh38_11:128526142-128530389	ENSG00000165119	NA	101929517	3190	pancEts-1	AUKS|CSBP|HNRPK|TUNP	Long Noncoding RNA pancEts-1 Promotes Neuroblastoma Progression through hnRNPK-Mediated beta-Catenin Stabilization;pancEts-1(ETS1-AS1) bound to hnRNPK to facilitate its physical interaction with beta-catenin	29311158	RID00443	interact with protein	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	GAS8-AS1	ATG5	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell autophagy(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000057663	NA	750	9474	C16orf3	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	LncRNA GAS8-AS1 inhibits cell proliferation through ATG5-mediated autophagy in papillary thyroid cancer;GAS8-AS1 inhibited proliferation, activated autophagy, and increased ATG5 expression. Downregulation of ATG5 reversed GAS8-AS1-mediated activation of autophagy leading to cell death.	29327301	RID00444	expression association	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Nasopharynx carcinoma	FOXD2-AS1	S100A1	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	HNSC.zip	tumorigenesis(+);cell growth(+)	ceRNA(miR-363-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000160678	NA	84793	6271	NA	S100|S100-alpha|S100A	Long non-coding RNA FOXD2-AS1 aggravates nasopharyngeal carcinoma carcinogenesis by modulating miR-363-5p/S100A1 pathway;FOXD2-AS1 contributed to NPC progression by regulating miR-363-5p/S100A1 signal pathway. Partially through sponging miR-363-5p,and then up-regulating S100A1, FOXD2-AS1 facilitates NPC cell growth.	29248577	RID00445	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(SKCM);DATA(GSE38495)
Melanoma	PVT1	miR-200c	negatively-E	RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma. the lncRNA PVT1 may contribute to the tumorigenesis and metastasis of melanoma through binding to EZH2 and regulating the expression of miR-200c	29286144	RID00446	epigenetic regulation	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Oral squamous cell carcinoma	H19	EZH2	positively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE3524	GSE3524.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA H19 promotes cell proliferation and invasion by acting as a ceRNA of miR-138 and releasing EZH2 in oral squamous cell carcinoma;H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138.our findings suggest that H19 functions as an oncogene by inhibiting miR-138 and facilitating EZH2 expression in OSCC. Thus, lncRNA H1 may represent a potential therapeutic target for OSCC.	29344674	RID00447	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Melanoma	H19	E2F3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+);cell growth(+)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000112242	NA	283120	1871	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-3	Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis;H19 may function as the sponge of miR-106a-5p to up-regulate E2F3 expression, and consequently promote the glucose metabolism and growth of melanoma	29350287	RID00448	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Malignant glioma	CDKN2B-AS1	SIRT1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-34a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000096717	NA	100048912	23411	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	SIR2|SIR2L1|SIR2alpha	Knockdown of long non-coding RNA ANRIL inhibits proliferation, migration, and invasion but promotes apoptosis of human glioma cells by upregulation of miR-34a;ANRIL was upregulation in glioma, and its inhibition could repress cell proliferation, migration and invasion but inhibit cell apoptosis through miR-34a-mediated downregulation of Sirt1, involving the inactivation of the PI3K/AKT and mTOR pathways	29057547	RID00449	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	XIST	TGFB1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-185)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000105329	NA	7503	7040	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	XIST promotes gastric cancer (GC) progression through TGF-beta1 via targeting miR-185;XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-beta1 by sponging miR-185 in GC	29053187	RID00450	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	HIF1A	UCA1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+);PTEN/AKT signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000100644	NA	ENSG00000214049	GRCh38_19:15828206-15836328	3091	652995	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HIF-1alpha-induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway;lncRNA UCA1 was induced by HIF-1alpha and HIF-1alpha interacts with the HIF-1alpha response element in the promoter region of UCA1. Finally, we observed that HIF-1alpha induced cell growth through the UCA1/PTEN/AKT signaling pathway	29328452	RID00451	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	TUG1	SOX4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124766	NA	55000	6659	LINC00080|NCRNA00080|TI-227H	EVI16	Long Non-Coding RNA TUG1 Promotes Proliferation and Inhibits Apoptosis of Osteosarcoma Cells by Sponging miR-132-3p and Upregulating SOX4 Expression;TUG1 knockdown suppressed proliferation and promoted apoptosis by upregulating miR-132-3p and downregulating SOX4 in primary OS cells	29436190	RID00452	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Malignant glioma	HOXA9	HOTAIR	positively-E	ChIP	upregulation	microarray	TCGA	GBM.zip	prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000078399	NA	ENSG00000228630	GRCh38_12:53962308-53974956	3205	100124700	ABD-B|HOX1|HOX1.7|HOX1G	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The long non-coding RNA HOTAIR is transcriptionally activated by HOXA9 and is an independent prognostic marker in patients with malignant glioma;HOXA9 binds directly to the promoter of HOTAIR;GBM patients with high HOTAIR expression had a significantly reduced overall survival, independently of other prognostic variables	29644006	RID00453	transcriptional regulation	prognosis	NA	NA
Pancreatic cancer	SPRY4-IT1	CDC20	positively-E	western blot;RNAi	NA	NA	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000117399	NA	100642175	991	SPRIGHTLY	CDC20A|bA276H19.3|p55CDC	Long non-coding RNA SPRY4-IT1 promotes cell proliferation and invasion by regulation of Cdc20 in pancreatic cancer cells;suppression of SPRY4-IT1 inhibited the expression of Cdc20 in pancreatic cancer cells	29489909	RID00454	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	LNC00312	CCNB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	ENSG00000134057	NA	NA	891	NA	CCNB	Long non-coding RNA 00312 downregulates cyclin B1 and inhibits hepatocellular carcinoma cell proliferation in vitro and in vivo; Lnc00312 downregulated cyclin B1 and induced G2-M cell cycle arrest in HCC cells	29432732	RID00455	expression association	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Rhabdomyosarcoma	MYCNOS-01	MYCN	negatively-E	RNAi;western blot;immunofluorescence	upregulation	qPCR;microarray	NA	NA	cell growth(-)	post-transcriptional level	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skeletal muscle cancer	lncRNA	TF	ENST00000641263	GRCh38_2:15936265-15941582	ENSG00000134323	NA	NA	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	The long non-coding RNA MYCNOS-02 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells;MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels;MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein level;Reduction of MYCNOS-01 or MYCN expression decreased cell growth. An alternative transcript of MYCNOS, MYCNOS-01, post-transcriptionally regulates MYCN levels and affects growth in MYCN-amplified rhabdomyosarcoma and neuroblastoma cells.	29466962	RID00456	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Neuroblastoma	MYCNOS-01	MYCN	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENST00000641263	GRCh38_2:15936265-15941582	ENSG00000134323	NA	NA	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	The long non-coding RNA MYCNOS-02 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells;MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels;MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein level;Reduction of MYCNOS-01 or MYCN expression decreased cell growth	29466962	RID00457	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	HNF1A	HNF1A-AS1	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000135100	NA	ENSG00000241388	GRCh38_12:120941728-120980965	6927	283460	HNF-1A|HNF1|HNF4A|IDDM20|LFB1|MODY3|TCF-1|TCF1	C12orf27|HAS1|NCRNA00262	The HNF1alpha-regulated lncRNA HNF1A-AS1 reverses the malignancy of hepatocellular carcinoma by enhancing the phosphatase activity of SHP-1;HNF1alpha activated the transcription of HNF1A-AS1 by directly binding to its promoter region;knockdown of HNF1A-AS1 reversed the suppressive effects of HNF1alpha on the migration and invasion of HCC cells	29466992	RID00458	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)
Hepatocellular carcinoma	HNF1A-AS1	PTPN6	interact	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000111679	NA	283460	5777	C12orf27|HAS1|NCRNA00262	NA	The HNF1alpha-regulated lncRNA HNF1A-AS1 reverses the malignancy of hepatocellular carcinoma by enhancing the phosphatase activity of SHP-1.HNF1A-AS1 directly bound to the C-terminal of SHP-1 with a high binding affinity and increased the phosphatase activity of SHP-1;Inhibition of SHP-1 enzymatic activity substantially reversed the HNF1alpha- or HNF1A-AS1-induced reduction on the metastatic property of HCC cells	29466992	RID00459	interact with protein	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Breast cancer	UCA1	YAP1	positively-E	luciferase reporter assay;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-18a)	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000137693	NA	652995	10413	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	COB1|YAP|YAP2|YAP65|YKI	Long non-coding RNA UCA1 desensitizes breast cancer cells to trastuzumab by impeding miR-18a repression of Yes-associated protein 1;A luciferase reporter assay confirmed the association of miR-18a with wild-type UCA1 but not with UCA1 mutated at the predicted miR-18a-binding site. The direct targeting of YAP1 by miR-18a was verified by the observation that miR-18a mimic suppressed luciferase expression from a construct containing the YAP1 3' untranslated region.	29408336	RID00460	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	LINC00261	HES1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000114315	NA	140828	3280	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	HES-1|HHL|HRY|bHLHb39	LINC00261 suppresses cell proliferation, invasion and Notch signaling pathway in hepatocellular carcinoma.upregulation of LINC00261 significantly inhibited Notch signaling by downregulating Notch1 and Hes-1 expression in HCC cells.	29278875	RID00461	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	LINC00261	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000148400	NA	140828	4851	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	AOS5|AOVD1|TAN1|hN1	LINC00261 suppresses cell proliferation, invasion and Notch signaling pathway in hepatocellular carcinoma.upregulation of LINC00261 significantly inhibited Notch signaling by downregulating Notch1 and Hes-1 expression in HCC cells.	29278875	RID00462	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	CDKN2B-AS1	TGFB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105329	NA	100048912	7040	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;Knockdown of ANRIL significantly decreased the levels of TGF-beta1 and p-Smad2	29278879	RID00463	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	CDKN2B-AS1	SMAD2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000175387	NA	100048912	4087	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway	29278879	RID00464	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Prostate cancer	CDKN2B-AS1	SMAD7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000101665	NA	100048912	4092	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CRCS3|MADH7|MADH8	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;Knockdown of ANRIL significantly decreased the levels of TGF-beta1 and p-Smad2,and increased the level of p-Smad7 in prostate cancer LNCap cells	29278879	RID00465	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	CDKN2B-AS1	let-7a	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells	29278879	RID00466	expression association	NA	UP(SKCM);DATA(GSE38495)	NA
Glioblastoma	H19	NKD1	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000140807	NA	283120	85407	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Naked1	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter;by showing that its expression is inversely linked to that of NKD1, a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter	29643989	RID00467	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	NA
Osteosarcoma	CDKN2B-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL is associated with a poor prognosis of osteosarcoma and promotes tumorigenesis via PI3K/Akt pathway;knockdown of ANRIL could significantly decrease the expression level of phosphorylated PI3K and AKT in OS cells	29520337	RID00468	expression association	prognosis	UP(SKCM);DATA(GSE38495)	NA
Osteosarcoma	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA ANRIL is associated with a poor prognosis of osteosarcoma and promotes tumorigenesis via PI3K/Akt pathway;knockdown of ANRIL could significantly decrease the expression level of phosphorylated PI3K and AKT in OS cells	29520337	RID00469	expression association	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HOTAIR	MAPK1	positively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-23b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targetting miR-23b/MAPK1 axis;HOTAIR may competitively bind miR-23b and modulate the expression of MAPK1 indirectly in cervical cancer cells	29335299	RID00470	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	H19	miR-152	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 promotes proliferation and invasion in human glioma cells by downregulating miR-152;H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression;H19 and miR-152 directly regulated each other. Taken together, H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression, providing evidence for the potential application of H19 as a biomarker and therapy target for glioma.	29422115	RID00471	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Cervical cancer	NCK1-DT	CDK1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-6857)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000170312	NA	101927597	983	NA	CDC2|CDC28A|P34CDC2	LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway;NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation	29416014	RID00472	ceRNA or sponge	NA	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Testicular germ cell cancer	SPRY4-IT1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Testicular cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000142208	NA	100642175	207	SPRIGHTLY	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours;Knockdown of SPRY4 and SPRY4-IT1 also led to a significant reduction in the phosphorylation of Akt;SPRY4 and SPRY4-IT1 may act as oncogenes in TGCTs via activation of the PI3K/Akt signalling pathway.	29410498	RID00473	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	CCND2-AS1	CDH2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000255920	GRCh38_12:4247981-4276252	ENSG00000170558	NA	103752584	1000	CCND2-AS2	CD325|CDHN|CDw325|NCAD	LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma;CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration	29366479	RID00474	expression association	NA	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Papillary thyroid carcinoma	CCND2-AS1	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000255920	GRCh38_12:4247981-4276252	ENSG00000026025	NA	103752584	7431	CCND2-AS2	NA	LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma;CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration	29366479	RID00475	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Glioblastoma	SNHG7	miR-5059	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	NCRNA00061	NA	Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095;we found that SNHG7 directly inhibited miR-5095, which targeted the 3' UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/beta-catenin signaling pathway in GBM;SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095. miR-5095 was a potential miRNA target for SNHG7. There are two putative binding sites for miR-5095 in SNHG7.	29360452	RID00476	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	NA
Lung cancer	UCA1	HMGB1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000189403	NA	652995	3146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HMG-1|HMG1|HMG3|SBP-1	Long non-coding RNA UCA1 promotes lung cancer cell proliferation and migration via microRNA-193a/HMGB1 axis;UCA1 promoted the miR-193a expression and miR-193a could bind to the predicted binding site of UCA1. In summary, our study demonstrated that UCA1 exerts oncogenes activity in lung cancer, acting mechanistically by upregulating HMGB1 expression through 'sponging' miR-193a.	29355524	RID00477	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Gastric cancer	BG981369	SOX4	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:172885475-172885888	ENSG00000124766	NA	NA	6659	NA	EVI16	lncRNA BG981369 Inhibits Cell Proliferation, Migration, and Invasion, and Promotes Cell Apoptosis by SRY-Related High-Mobility Group Box 4 (SOX4) Signaling Pathway in Human Gastric Cancer;we found that SOX4 may act as a downstream mediator of BG981369, suggesting that BG981369 inhibits proliferation, migration, and invasion, and promotes apoptosis by targeting SOX4 in the GC cell lines	29398692	RID00478	expression association	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Acute lymphocytic leukemia	LINC-PINT	HMOX1	positively-E	RNAi	downregulation	qPCR	NA	NA	chemoresistance(+);cell viability(-);cell proliferation(-)	NA	regulation	NA	panobinostat;curcumin	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000100292	NA	378805	3162	LincRNA-Pint|MKLN1-AS1|PINT	HMOX1D|HO-1|HSP32|bK286B10	Deregulation of linc-PINT in acute lymphoblastic leukemia is implicated in abnormal proliferation of leukemic cells;linc-PINT induced the transcription of HMOX1 which reduced the viability of ALL cells. Intriguingly, we observed that treatment with anti-tumoral epigenetic drugs like LBH-589 (Panobinostat) and Curcumin induced the expression of linc-PINT and HMOX1 in ALL. These results indicate that the downregulation of linc-PINT plays a relevant role in the pathogenesis of ALL, and linc-PINT re-expression may be one of the mechanisms exerted by epigenetic drugs to reduce cell proliferation in ALL.	29560114	RID00479	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Malignant glioma	DANCR	RAB1A	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-634)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000138069	NA	57291	5861	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	RAB1|YPT1	LncRNA DANCR functions as a competing endogenous RNA to regulate RAB1A expression by sponging miR-634 in glioma;DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression;DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma	29301870	RID00480	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Non-small cell lung cancer	HNF1A-AS1	miR-17-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000241388	GRCh38_12:120941728-120980965	NA	NA	283460	NA	C12orf27|HAS1|NCRNA00262	NA	Long non-coding RNA HNF1A-AS1 promotes cell proliferation and invasion via regulating miR-17-5p in non-small cell lung cancer;Bioinformatics analysis and luciferase reporter assay revealed that HNF1A-AS1 interacted with miR-17-5p by directly targeting it.lncRNA HNF1A-AS1 promoted lung cancer cells proliferation and invasion via regulating miR-17-5p	29289833	RID00481	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	NA
Colorectal cancer	HOTTIP	SGK1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000118515	NA	100316868	6446	HOXA-AS6|HOXA13-AS1|NCRNA00213	SGK	Knockdown of the long non-coding RNA HOTTIP inhibits colorectal cancer cell proliferation and migration and induces apoptosis by targeting SGK1;luciferase reporter assay suggested that knockdown of HOTTIP could target decreasing the expression of Serum- and glucocorticoid-inducible kinase 1 (SGK1) gene, and we subsequently verified that up-regulation of the SGK1 gene promoted cell proliferation and migration and inhibited cell apoptosis in HCT-116 and SW620 cell lines.up-regulation of the SGK1 emerged the opposite effect with knockdown of HOTTIP.	29274585	RID00482	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	XLOC_008466	miR-216b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	NA	GRCh38_10:43323011-43327969	NA	NA	NA	NA	NA	NA	Bioinformatics analysis revealed that XLOC_008466 sponged miR-216b with the complementary binding sites at 3'-UTR;our study reveals the tumor promoting role of XLOC_008466 in cervical cancer carcinogenesis	29247951	RID00483	ceRNA or sponge	NA	NA	NA
Lung adenocarcinoma	OIP5-AS1	BCL2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-448)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000171791	NA	729082	596	cyrano|linc-OIP5	Bcl-2|PPP1R50	Long non-coding RNA OIP5-AS1 functions as an oncogene in lung adenocarcinoma through targeting miR-448/Bcl-2. We also certified that OIP5-AS1 could sponge and regulate miR-448 to affect cell function in lung adenocarcinoma. MiR-448 could target Bcl-2 and affect the expression of Bcl-2.	29247949	RID00484	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Thyroid cancer	SPRY4-IT1	TGFB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000105329	NA	100642175	7040	SPRIGHTLY	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA SPRY4-IT was concerned with the poor prognosis and contributed to the progression of thyroid cancer. silenced SPRY4-IT1 could increase the levels of transforming growth factor-beta1 (TGF-beta1) and p-Smad2/3 and function mediated by si-SPRY4-IT1 could be rescued by the interference of TGF-beta1;SPRY4-IT1 might become a novel prognostic factor in the clinical behaviors of TC patients and participated in the progression of TC through targeting TGF-beta/Smad signaling pathway	29234152	RID00485	expression association	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	CCAT1	miR-148b	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Down-regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR-148b in breast cancer;CCAT1 could negatively regulate miR-148b expression;overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. Luciferase reporter assay was performed to confirm the interaction between CCAT1 and miR-148b in breast cancer cells	29024383	RID00486	ceRNA or sponge	NA	NA	NA
Cervical cancer	HOTAIR	miR-206	negatively-E	RNAi;RNA-FISH	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells;These elucidates that the phenotypic effects of migration and invasion observed after HOTAIR inhibition, at least in part, through the regulation of MKL1 via inhibition of miR206 expression in HeLa cells. These data indicate the existence of a positive feedback loop between HOTAIR and MKL1.Luciferase reporter assays and CHIP were used to determine how MKL1 regulates HOTAIR. High level of MKL1 significantly correlate with HOTAIR expression in Cervical cancer patient.In this study, we further confirmed that knockdown HOTAIR could enhance miR206 RNA expression level in HeLa cells.	29391067	RID00487	expression association	NA	NA	NA
Cervical cancer	HOTAIR	MRTFA	positively-E	western blot	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196588	NA	100124700	57591	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSAC|MAL|MKL|MKL1|MRTF-A	LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells;These elucidates that the phenotypic effects of migration and invasion observed after HOTAIR inhibition, at least in part, through the regulation of MKL1 via inhibition of miR206 expression in HeLa cells. These data indicate the existence of a positive feedback loop between HOTAIR and MKL1.Luciferase reporter assays and CHIP were used to determine how MKL1 regulates HOTAIR. High level of MKL1 significantly correlate with HOTAIR expression in Cervical cancer patient.In this study, we further confirmed that knockdown HOTAIR could enhance miR206 RNA expression level in HeLa cells.	29391067	RID00488	expression association	NA	NA	NA
Nephroblastoma	LINC00473	CHUK	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000213341	NA	90632	1147	C6orf176|LNC473|bA142J11.1	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	LINC00473 antagonizes the tumour suppressor miR-195 to mediate the pathogenesis of Wilms tumour via IKKalpha;LINC00473 harboured binding sites for miR-195 and limited miR-195 availability in a dose-dependent manner;IKKalpha was the downstream of LINC00473/miR-195 signals and could be directly targeted by miR-195 to participate LINC00473-induced tumour progression;Loss-of-function of LINC00473 in vivo effectively promoted the regression of Wilms tumour via miR-195/IKKalpha-mediated growth inhibition	29159834	RID00489	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG7	FAIM2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-193b)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000135472	NA	84973	23017	NCRNA00061	LFG|LFG2|NGP35|NMP35|TMBIM2	miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer;oncogene SNHG7 predicted a poor clinical outcome and functioned as competitive endogenous RNA (ceRNA) antagonized microRNA-193b (miR-193b) to up-regulate the FAIM2 level in NSCLC;forced expression of SNHG7 could down-regulate miR-193b to elevate the FAIM2 level of tumour cells, leading to impaired miR-193b/FAIM2-induced tumour progression	29131440	RID00490	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD);DATA(GSE40174)
Malignant glioma	TP73-AS1	PPP1R13L	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000104881	NA	57212	10848	KIAA0495|PDAM	IASPP|NKIP1|RAI|RAI4	The Long Noncoding RNA TP73-AS1 Interacted with miR-124 to Modulate Glioma Growth by Targeting Inhibitor of Apoptosis-Stimulating Protein of p53;TP73-AS1 inhibited the brain glioma growth and metastasis as a competing endogenous RNA (ceRNA) through miR-124-dependent iASPP regulation	29412778	RID00491	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Osteosarcoma	CERNA2	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000171791	NA	642934	596	HOST2|lncRNA-HOST2	Bcl-2|PPP1R50	Prognostic value of long non-coding RNA HOST2 expression and its tumor-promotive function in human osteosarcoma. we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells;the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000)	29509239	RID00492	expression association	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	CERNA2	BAX	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000087088	NA	642934	581	HOST2|lncRNA-HOST2	BCL2L4	Prognostic value of long non-coding RNA HOST2 expression and its tumor-promotive function in human osteosarcoma. we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells;the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000)	29509239	RID00493	expression association	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	AF119895	NXF3	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-6508-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:186618535-186621317	ENSG00000147206	NA	NA	56000	NA	NA	AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p;AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3'UTR;	29274323	RID00494	ceRNA or sponge	NA	NA	NA
Osteosarcoma	CRNDE	NOTCH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000148400	NA	NA	4851	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	AOS5|AOVD1|TAN1|hN1	LncRNA, CRNDE promotes osteosarcoma cell proliferation, invasion and migration by regulating Notch1 signaling and epithelial-mesenchymal transition;Overexpression of CRNDE was found to enhance the activity of Notch1 signaling and promote epithelial-mesenchymal transition (EMT)	29246789	RID00495	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	HOTAIR	miR-34a	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	sponge;histone modification	binding/interaction	RNA-RNA	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/beta-catenin signaling pathways by up-regulating miR-34a;HOTAIR directly bound to miR-34a. LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer.	29080815;26136075	RID00496	ceRNA or sponge	chemoresistance	NA	NA
Hepatocellular carcinoma	CDKN2B-AS1	miR-122-5p	negatively-F	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Knockdown of LncRNA ANRIL suppresses cell proliferation, metastasis, and invasion via regulating miR-122-5p expression in hepatocellular carcinoma;ANRIL was demonstrated to directly bind to miR-122-5p and inhibit its expression	29127494	RID00497	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	NA
Breast cancer	TP73-AS1	ZEB1	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-200a)	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000148516	NA	57212	6935	KIAA0495|PDAM	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;TP73-AS1 promoted ZEB1 expression via competing with ZEB1 3'UTR for miR-200a binding;ZEB1 could bind to the promoter region of TP73-AS1 to activate its expression	28857253	RID00498	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	TP73-AS1	TWIST1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000122691	NA	57212	7291	KIAA0495|PDAM	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;Suppressing TP73-AS1 expression to rescue miR-200a expression, thus to inhibit ZEB1 and Twist expression and up-regulate E-cadherin might improve breast cancer cell invasion and migration	28857253	RID00499	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Breast cancer	TP73-AS1	CDH1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000039068	NA	57212	999	KIAA0495|PDAM	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;Suppressing TP73-AS1 expression to rescue miR-200a expression, thus to inhibit ZEB1 and Twist expression and up-regulate E-cadherin might improve breast cancer cell invasion and migration	28857253	RID00500	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung adenocarcinoma	SPRY4-IT1	EZH2	negatively-F	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma;The interaction between SPRY4-IT1 and EZH2 was determined using a RNA pull-down assay and a RNA immunoprecipitation (RIP) assay. EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression	28796375	RID00501	interact with protein	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MALAT1	EGFR	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell motility(+);cell growth(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000146648	NA	378938	1956	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195;Malat1 acted as a circular endogenous RNA (ceRNA) for miR-195;Malat1 silence could not suppress HCC cell growth and motility when miR-195 was knocked down. EGFR was a direct target of miR-195. miR-195 overexpression could not suppress HCC cell growth and motility when the 3'UTR site of EGFR was overexpressed.	28722813	RID00502	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Ovarian cancer	TDRG1	miR-196	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000204091	GRCh38_6:40334775-40387590	NA	NA	732253	NA	LINC00532|lincRNA-NR_024015	NA	The role of the long non-coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR-93/RhoC pathway; LncRNA TDRG1 downregulation upregulation miR-93 expression, while its overexpression reduced miR-93 expression; LncRNA TDRG1 has microRNA-93 (miR-93) binding sites	28984384	RID00503	ceRNA or sponge	NA	NA	NA
Ovarian cancer	TDRG1	RHOC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000155366	NA	732253	389	LINC00532|lincRNA-NR_024015	ARH9|ARHC|H9|RHOH9	The role of the long non-coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR-93/RhoC pathway;TDRG1 downregulation reduced the expression of Ras homolog gene family member C (RhoC)	28984384	RID00504	expression association	NA	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Cervical cancer	NEAT1	miR-101	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA-101;the expression of mircoRNA-101 (miR-101) target gene Fos was positively associated with NEAT1 expression due to NE1 competitive molecular sequestering of miR-101 via base pairing	29207151	RID00505	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Gastric cancer	H19	ERBB2	positively-E	luciferase reporter assay;Immunoprecipitation;western blot;RT-qPCR;RNAi	upregulation	qPCR	NA	NA	prognosis(-)	ceRNA(let-7c)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141736	NA	283120	2064	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	H19 functions as a competing endogenous RNA to regulate human epidermal growth factor receptor expression by sequestering let-7c in gastric cancer;The results of the present study suggest that H19 may function as a competing endogenous RNA to regulate HER2 expression by sequestering let-7c in GC cells. Assessment of tumor diameter and pathological tumor stage suggested that increased H19 expression was associated with a poorer prognosis in patients with GC.	29207111;24055342;27660891	RID00506	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Gastric cancer	SNHG12	miR-320	negatively-F	western blot;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	LncRNA SNHG12 regulates gastric cancer progression by acting as a molecular sponge of miR-320;miR-320 was directly regulated by SNHG12 and suppression of miR-320 expression reversed the inhibitory effects of SNHG12 siRNA on GC cell proliferation and invasion	29207106	RID00507	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Pancreatic cancer	XLOC_000647	NLRP3	negatively-E	western blot;IHC;luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cancer progression(-);epithelial to mesenchymal transition(+);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_1:247332910-247393369	ENSG00000162711	NA	NA	114548	NA	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCAS1|FCU|KEFH|MWS|NALP3|PYPAF1	Long non-coding RNA XLOC_000647 suppresses progression of pancreatic cancer and decreases epithelial-mesenchymal transition-induced cell invasion by down-regulating LRP3;XLOC_000647 functions as a novel tumor suppressor of lncRNA and acts as an important regulator of NLRP3, inhibiting cell proliferation, invasion, and EMT in PC;a significantly negative correlation was observed between XLOC_000647 levels and its genomic nearby gene NLRP3, XLOC_000647 decreased NLRP3 by inhibiting its promoter activity.	29386037	RID00508	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Lung cancer	CAV1	HOTAIR	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000105974	NA	ENSG00000228630	GRCh38_12:53962308-53974956	857	100124700	BSCL3|CGL3|LCCNS|MSTP085|PPH3|VIP21	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Cav-1 promote lung cancer cell proliferation and invasion through lncRNA HOTAIR;CAV-1 could regulate the expression of HOTAIR;knockdown of the expression of HOAIR partially reverses the promotion of cell viability and invasion induced by CAV-1	29080835	RID00509	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	NA
Endometrial cancer	HAND2-AS1	HAND2	positively-E	RNAi;western blot	downregulation	qPCR;microarray;sequencing	TCGA;GSE17025	UCEC.zip;GSE17025.zip	cell invasion(-);cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000164107	NA	79804	9464	DEIN|NBLA00301|UPH	DHAND2|Hed|Thing2|bHLHa26|dHand	Long non-coding RNA HAND2-AS1 inhibits invasion and metastasis in endometrioid endometrial carcinoma through inactivating neuromedin U;Down-regulation of HAND2-AS1 and HAND2 was correlated with tumor grade, lymph node metastasis and recurrence of EEC patients;Similarly, overexpression of HAND2 also inhibited migration and invasion EEC cells indicating that HAND2-AS1 and HAND2 had a concordant role in the progression of EEC. HAND2 was not regulated by HAND2-AS1 in EEC	29107108	RID00510	expression association	metastasis,recurrence	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,BRCA);DATA(GSE117623,GSE41245)
Endometrial cancer	HAND2-AS1	NMU	negatively-E	RNAi;western blot	downregulation	qPCR;microarray;sequencing	NA	NA	cell invasion(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000109255	NA	79804	10874	DEIN|NBLA00301|UPH	NA	Long non-coding RNA HAND2-AS1 inhibits invasion and metastasis in endometrioid endometrial carcinoma through inactivating neuromedin U;the anti-tumorigenic effect of HAND2-AS1 was mediated by down-regulating NMU	29107108	RID00511	expression association	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	NA
Gastric cancer	NEAT1	STAT3	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-506)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|NCRNA00084|TncRNA|VINC	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA NEAT1-modualted miR-506 regulates gastric cancer development through targeting STAT3;it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer	29363783	RID00512	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	UCA1	miR-122	negatively-F	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells;UCA1 acted as an miR-122 sponge to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122	28548636	RID00513	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	NA
Pancreatic ductal adenocarcinoma	FEZF1-AS1	FEZF1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE61166	GSE61166.zip	cancer progression(+)	ceRNA(miR-506)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000128610	NA	154860	389549	NA	FEZ|HH22|ZNF312B	FEZF1-AS1/miR-107/ZNF312B axis facilitates progression and Warburg effect in pancreatic ductal adenocarcinoma;FEZF1-AS1 may act as an endogenous sponge by competing for miR-107, thereby modulating the derepression of ZNF312B;Downregulation of FEZF1-AS1 or ZNF312B significantly inhibited proliferation, colony formation, migration, and invasion of PDAC cells in vitro, whereas the miR-107 inhibitor abrogated the effect of dow-regulation of FEZF1-AS1 or ZNF312B in reducing oncogenic capacities of PDAC cells	29348628	RID00514	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Esophagus squamous cell carcinoma	NKILA	NFKBIA	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);cell metastasis(-)	phosphorylation	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	NKILA inhibits NF-kB signaling and suppresses tumor metastasis;NKILA could inhibit phosphorylation of IkBalpha, suppress p65 nuclear translocation and downregulate the expression of NF-kB target genes in ESCC cells. The long non-coding RNA (lncRNA) NKILA (nuclear transcription factor NF-kB interacting lncRNA) functions as a suppressor in human breast cancer and tongue cancer.	29348395	RID00515	interact with protein	metastasis	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Esophagus squamous cell carcinoma	NKILA	RELA	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000173039	NA	105416157	5970	NA	CMCU|NFKB3|p65	NKILA inhibits NF-kB signaling and suppresses tumor metastasis;NKILA could inhibit phosphorylation of IkBalpha, suppress p65 nuclear translocation and downregulate the expression of NF-kB target genes in ESCC cells	29348395	RID00516	expression association	metastasis	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastrointestinal stromal tumor	CCDC26	KIT	interact	RNA pull-down assay;RNAi	downregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	imatinib	NA	NA	Cancer	Gastrointestinal stromal tumor	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000157404	NA	137196	3815	RAM	C-Kit|CD117|MASTC|PBT|SCFR	CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT;CCDC26 can interact with c-KIT and that CCDC26 knockdown can upregulate c-KIT expression	29423012	RID00517	interact with protein	chemoresistance	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Lung cancer	PVT1-5	SLC7A5	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-126)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_8:127794533-128101252	ENSG00000103257	NA	NA	8140	NA	4F2LC|CD98|D16S469E|E16|LAT1|MPE16	Long non-coding RNA PVT1-5 promotes cell proliferation by regulating miR-126/SLC7A5 axis in lung cancer;knockdown of lncRNA-PVT1-5 in cells could down-regulate the expression of SLC7A5;lncRNA-PVT1-5 may function as a competing endogenous RNA (ceRNA) for miR-126 to promote cell proliferation by regulating the miR-126/SLC7A5 pathway, suggesting that lncRNA-PVT1-5 plays a crucial role in lung cancer progression and lncRNA-PVT1-5/miR-126/SLC7A5 regulatory network may shed light on tumorigenesis in lung cancer	29277611	RID00518	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827)
Gastric cancer	LOC101927497	miR-574-5p	negatively-F	RNA antisense purification	downregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000237819	GRCh38_7:92836483-92917187	NA	NA	101927497	NA	NA	NA	Functional role of lncRNA LOC101927497 in N-methyl-N'-nitro-N-nitrosoguanidine-induced malignantly transformed human gastric epithelial cells;LncRNA LOC101927497 functions as a suppressor by interacting with miR-574-5p, thus inhibiting the malignant phenotype of GES-1-T cells	29223541	RID00519	ceRNA or sponge	NA	NA	NA
Gastric cancer	STAT3	HAGLROS	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor malignant transformation(+);cell autophagy(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000226363	GRCh38_2:176177717-176179008	6774	102800310	ADMIO|ADMIO1|APRF|HIES	NA	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy;Mechanistic investigations showed that HAGLROS was a direct target of transcriptional factor STAT3	29329543	RID00520	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Gastric cancer	HAGLROS	MTOR	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(+);cell autophagy(-)	ceRNA(miR-100-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179008	ENSG00000198793	NA	102800310	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition	29329543	RID00521	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Gastric cancer	HAGLROS	RHEB	positively-F	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(+);cell autophagy(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179008	ENSG00000106615	NA	102800310	6009	NA	NA	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. HAGLROS interacted with mTORC1 components to activate mTORC1 signaling pathway which was known to be an important negative signal of autophagy. Here activation of mTORC1 signaling pathway by HAGLROS inhibited autophagy, thereby promoted excessive proliferation and maintained the malignant phenotype of GC cells.	29329543	RID00522	interact with protein	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Malignant glioma	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00523	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Malignant glioma	H19	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00524	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	H19	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00525	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Nasopharynx carcinoma	LINC00460	IL6	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-149-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000136244	NA	728192	3569	NA	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	LncRNA-LINC00460 facilitates nasopharyngeal carcinoma tumorigenesis through sponging miR-149-5p to up-regulate IL6;LINC00460 contributed to the progression of NPC through regulating miR-149-5p/IL6 signal pathway	28987345	RID00526	ceRNA or sponge	NA	NA	DOWN(BRCA);DATA(GSE75367,GSE86978)
Osteosarcoma	SNHG12	NOTCH2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000134250	NA	85028	4853	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	AGS2|HJCYS|hN2	LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p;	29229388	RID00527	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	SNHG15	miR-211-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983023-44986961	NA	NA	285958	NA	C7orf40|Linc-Myo1g|MYO1GUT	NA	Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p;SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration	29217194	RID00528	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	NA
Ovarian cancer	SNHG20	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000168036	NA	654434	1499	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Up-regulation of long non-coding RNA SNHG20 promotes ovarian cancer progression via Wnt/beta-catenin signaling;lncRNA SNHG20 knockdown inhibited Wnt/beta-catenin signaling activity by suppressing beta-catenin expression and reversing the downstream target gene expression	29101241	RID00529	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	LINC00176	miR-9	negatively-F	RNAi;MS2-tagged RNA purification	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000196421	GRCh38_20:64034344-64039962	NA	NA	NA	NA	NA	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00530	ceRNA or sponge	NA	NA	NA
Hepatocellular carcinoma	LINC00176	miR-185	negatively-F	RNAi;MS2-tagged RNA purification	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000196421	GRCh38_20:64034344-64039962	NA	NA	NA	NA	NA	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00531	ceRNA or sponge	NA	NA	NA
Hepatocellular carcinoma	MYC	LINC00176	positively-E	RNAi;ChIP	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000196421	GRCh38_20:64034344-64039962	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00532	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	NA
Pancreatic ductal adenocarcinoma	KRAS	CCAT2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	MEK/ERK signaling pathway(+);oncogenic role(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000133703	NA	ENSG00000280997	GRCh38_8:127400399-127402150	3845	101805488	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	LINC00873|NCCP1	CCAT2 is an oncogenic long non-coding RNA in pancreatic ductal adenocarcinoma.CCAT2 was regulated by KRAS through MEK/ERK signaling pathway.Additionally, KRAS inhibition markedly decreased CCAT2 promoter activity by more than 60%, indicating that KRAS might regulate CCAT2 expression at transcriptional level.	29298720	RID00533	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	NA
Ovarian cancer	HAGLR	FZD4	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	OV.zip	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-608)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000174804	NA	401022	8322	HOXD-AS1|MIR7704HG|Mdgt	CD344|EVR1|FEVR|FZD4S|Fz-4|Fz4|FzE4|GPCR|hFz4	HOXD-AS1 promotes cell proliferation, migration and invasion through miR-608/FZD4 axis in ovarian cancer;HOXD-AS1 was detected to positively regulate the expression of frizzled family receptor 4 (FZD4) by competitively binding to miR-608	29416930	RID00534	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE55807)
Esophagus squamous cell carcinoma	miR-196a	GAS5	negatively-F	luciferase reporter assay;ChIRP-RT-qPCR	upregulation	qPCR	NA	NA	cell growth(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Negative regulation of lncRNA GAS5 by miR-196a inhibits esophageal squamous cell carcinoma growth;miR-196a could bind to the seventh exon of GAS5.Additionally, both GAS5 and miR-196a could bind to Ago2 which is a key component of the RNA-induced silencing complex (RISC). Together, these results suggest that GAS5 functions as a tumor suppressor gene in ESCC and is regulated by miR-196a involved in RISC.	29170131	RID00535	ceRNA or sponge	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Osteosarcoma	LUCAT1	ABCB1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-200c)	regulation	NA	methotrexate	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000085563	NA	100505994	5243	SCAL1|SCAT5	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis;miR-200c both targeted the 3'-UTR of LUCAT1 and ABCB1 mRNA, suggesting the modulation of LUCAT1 on ABCB1 through sponging miR-200c;Rescue experiments confirmed the combined role of LUCAT1, miR-200c and ABCB1 on osteosarcoma proliferation, invasion and methotrexate resistance	29170124	RID00536	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Colorectal cancer	CPS1-IT1	HIF1A	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-);cell autophagy(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000100644	NA	29034	3091	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA CPS1-IT1 suppresses EMT and metastasis of colorectal cancer by inhibiting hypoxia-induced autophagy through inactivation of HIF-1alpha;CPS1-IT1 suppresses EMT and autophagy by inhibiting the activation of HIF-1alpha in CRC	29017924	RID00537	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteosarcoma	TUG1	FOXA1	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-212-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000129514	NA	55000	3169	LINC00080|NCRNA00080|TI-227H	HNF3A|TCF3A	LncRNA TUG1 promotes cell proliferation and suppresses apoptosis in osteosarcoma by regulating miR-212-3p/FOXA1 axis;FOXA1 was identified as a target of miR-212-3p and TUG1 functioned as a ceRNA to upregulate FOXA1 by sponging miR-212-3p in OS cells	29793327	RID00538	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Triple-receptor negative breast cancer	CYTOR	BRCA1	negatively-E	RNAi;immunohistochemical staining	upregulation	qPCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000012048	NA	112597	672	C2orf59|LINC00152|NCRNA00152	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer;linc00152 partially enhanced breast cancer tumorigenesis by inactivation of the BRCA1/PTEN through DNA methyltransferases	29156515	RID00539	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Triple-receptor negative breast cancer	CYTOR	PTEN	negatively-E	RNAi;immunohistochemical staining	upregulation	qPCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171862	NA	112597	5728	C2orf59|LINC00152|NCRNA00152	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer;linc00152 partially enhanced breast cancer tumorigenesis by inactivation of the BRCA1/PTEN through DNA methyltransferases	29156515	RID00540	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	TP53COR1	miR-130b	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);PTEN/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	NA	GRCh38_6:36663392-36667296	NA	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	LncRNA-p21 inhibited the proliferation of osteosarcoma cells via the miR-130b/PTEN/AKT signaling pathway;lncRNA-p21 overexpression up-regulated the protein level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a well-known inhibitor of AKT signaling.Moreover, our gain and loss function assay showed that the promotion of PTEN by lncRNA-p21 was mediated by miR-130b, an oncogene overexpressed in OS tissue.PTEN expression was positively correlated with lncRNA-p21 expression in OS tissue (r = 0.630,p<0.0001), and PTEN expression was negatively correlated with miR-130b expression (r = 0.378,p= 0.0161)	29136769	RID00541	expression association	NA	NA	NA
Osteosarcoma	TP53COR1	PTEN	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);PTEN/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000171862	NA	102800311	5728	TRP53COR1|linc-p21|lincRNA-p21	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-p21 inhibited the proliferation of osteosarcoma cells via the miR-130b/PTEN/AKT signaling pathway;lncRNA-p22 overexpression up-regulated the protein level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a well-known inhibitor of AKT signaling.Moreover, our gain and loss function assay showed that the promotion of PTEN by lncRNA-p21 was mediated by miR-130b, an oncogene overexpressed in OS tissue.PTEN expression was positively correlated with lncRNA-p21 expression in OS tissue (r = 0.630,p<0.0001), and PTEN expression was negatively correlated with miR-130b expression (r = 0.378,p= 0.0161)	29136769	RID00542	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Malignant glioma	CASC2	MTOR	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+);cytotoxicity(+);cell autophagy(-)	ceRNA(miR-193a-5p)	regulation	NA	temozolomide	NA	Tumor Promoting Inflammation;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000198793	NA	255082	2475	C10orf5	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR-193a-5p and regulating mTOR expression;CASC2 is downregulated in gliomas, resulting in increased miR-193a-5p level and a decrease in mTOR expression, which further induces protective autophagy, leading to TMZ resistance	29136760	RID00543	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Choriocarcinoma	MALAT1	FBXW8	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000174989	NA	378938	26259	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FBW6|FBW8|FBX29|FBXO29|FBXW6	The long non-coding RNA MALAT1 interacted with miR-218 modulates choriocarcinoma growth by targeting Fbxw8;miR-218-mediated Fbxw8 regulation was required for MALAT1-induced choriocarcinoma cell proliferation	29096355	RID00544	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	DUXAP9	MMP9	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000100985	NA	503638	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long intergenic noncoding RNA 01296 aggravates gastric cancer cells progress through miR-122/MMP-9;LINC01296 sponged miR-122, which was proved to target MMP-9;LINC01296 was positively correlated with MMP-9 expression, while miR-122 was negatively correlated to it	29091895	RID00545	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	WSPAR	EPCAM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);self-renewal(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000119888	NA	105664404	4072	LncTCF7|TCONS_00009511	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	LncRNATCF7 promotes the growth and self-renewal of glioma cells via suppressing the miR-200c-EpCAM axis;lncTCF7 enhanced the self-renewal of glioma cells via up-regulating the expression of epithelial cell adhesion molecule (EpCAM);ncTCF7 bound to miR-200c and decreased the abundance of miR-200c	29091867	RID00546	ceRNA or sponge	NA	NA	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Gastric cancer	GACAT3	miR-497	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	LncRNA GACAT3 promotes gastric cancer progression by negatively regulating miR-497 expression;GACAT3 directly binds to microRNA-497 (miR-497), and GACAT3 expression was inversely correlated with miR-497 expression	29091858	RID00547	ceRNA or sponge	NA	NA	NA
Thyroid cancer	CCAT1	miR-143	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line;CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143;CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143	29791590	RID00548	ceRNA or sponge	metastasis	NA	NA
Prostate cancer	HULC	BECN1	interact	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	radioresistance(-);cell autophagy(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000126581	NA	728655	8678	HCCAT1|LINC00078|NCRNA00078	ATG6|VPS30|beclin1	LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells;HULC knockdown promoted autophagy through interaction with Beclin-2 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.	29694502	RID00549	interact with protein	NA	NA	DOWN(NSCLC,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Prostate cancer	HULC	MTOR	positively-E	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	radioresistance(-);cell autophagy(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000198793	NA	728655	2475	HCCAT1|LINC00078|NCRNA00078	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells;HULC knockdown promoted autophagy through interaction with Beclin-2 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.	29694502	RID00550	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Breast cancer	GACAT3	CCND2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000118971	NA	104797537	894	LINC01458|lncRNA-AC130710	KIAK0002|MPPH3	LncRNA GACAT3 predicts poor prognosis and promotes cell proliferation in breast cancer through regulation of miR-497/CCND2;GACAT3 and cyclin D2 (CCND2) contained a binding site of miR-497;GACAT3 may act as a ceRNA for miR-497, enhancing the expression of CCND2	29945347	RID00551	ceRNA or sponge	prognosis	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	H19	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression. Here we found that H19 levels are remarkably increased in bladder cancer tissues, and upregulated H19 promotes bladder cancer cell migration in vitro and in vivo. H19 is associated with enhancer of zeste homolog 2 (EZH2), and that this association results in Wnt/beta-catenin activation and subsequent downregulation of E-cadherin. A significant negative correlation is also observed between H19 levels and E-cad levels in vivo. These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression. Inhibition of E-cadherin expression by lnc-RNA H19 to facilitate bladder cancer metastasis;RNA interference is applied to knockdown H19 expression in bladder cancer cell, and found potentiated E-cadherin expression (p< 0.05), accompanied with weakened metastatic potency (p< 0.05)	23354591;29614625	RID00552	transcriptional regulation	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	AB073614	JAK2	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);JAK/STAT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000096968	NA	NA	3717	NA	JTK10|THCYT3	LncRNA AB073614 induces epithelial-mesenchymal transition of colorectal cancer cells via regulating the JAK/STAT3 pathway;LncRNA AB073614 knockdown in SW480 and HCT116 cells significantly promoted the protein expression levels of E-cadherin and Occludin, and decreased the expressions of N-cadherin and Vimentin, then further decreased the cell migration and invasion ability. Interestingly, the expression of phosphorylated STAT3 was also down-regulated. Also, the Western blotting result326 showed that JAK inhibitor (AT9283) was able to block the STAT3 phosphorylation induced by lncRNA AB073614 overexpression. All these results indicate that lncRNA AB073614 can induce the expression of EMT cell markers and regulate the process of EMT of CRC cells through regulating the JAK/STAT3 pathway activation.	29439310	RID00553	expression association	NA	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	AB073614	STAT3	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);JAK/STAT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_3:149173591-149175492	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	LncRNA AB073614 induces epithelial- mesenchymal transition of colorectal cancer cells via regulating the JAK/STAT3 pathway;LncRNA AB073614 knockdown in SW480 and HCT116 cells significantly promoted the protein expression levels of E-cadherin and Occludin, and decreased the expressions of N-cadherin and Vimentin, then further decreased the cell migration and invasion ability. Interestingly, the expression of phosphorylated STAT3 was also down-regulated	29439310	RID00554	expression association	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Lung cancer	DANCR	miR-216a	negatively-E	RIP;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712404-52720351	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	LncRNA DANCR Promotes Lung Cancer by Sequestering miR-216a;The miR-216a level in cancer cells was negatively correlated with DANCR expression;DANCR upregulation is a potential indicator of aggressive lung cancer	29651883	RID00555	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	NA
Gastric cancer	TMEM238L	VIM	interact	RIP	downregulation	microarray	NA	NA	cancer progression(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000026025	NA	100289255	7431	NA	NA	Long noncoding RNA LINC00675 enhances phosphorylation of vimentin on Ser83 to suppress gastric cancer progression;Mechanistic investigations revealed that LINC00675 interacted with vimentin, a protein involved in cell metastasis, and enhanced its phosphorylation level on Ser83 to result in the collapse of vimentin filament in GC cells	29107103	RID00556	interact with protein	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Multiple myeloma	CCAT1	HOXA1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000105991	NA	100507056	3198	CARLO5|CARLo-5|onco-lncRNA-40	BSAS|HOX1|HOX1F	Long non-coding RNA CCAT1 promotes multiple myeloma progression by acting as a molecular sponge of miR-181a-5p to modulate HOXA1 expression;CCAT1 positively regulated HOXA1 expression through sponging miR-181a-5p in MM cells	29228867	RID00557	ceRNA or sponge	NA	NA	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Breast cancer	GAS5	ATG3	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-23a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000144848	NA	60674	64422	NCRNA00030|SNHG2	APG3|APG3-LIKE|APG3L|PC3-96	Effect of the LncRNA GAS5-MiR-23a-ATG3 Axis in Regulating Autophagy in Patients with Breast Cancer;GAS5 was found to act as a microRNA sponge in a pathway that included miR-23a and its target gene ATG3	30007957	RID00558	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939,GSE86978)
Breast cancer	LINC00518	ABCC1	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-199a)	regulation	NA	adriamycin;vincristine;paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000183674	GRCh38_6:10429255-10435015	ENSG00000103222	NA	221718	4363	C6orf218	ABC29|ABCC|GS-X|MRP|MRP1	Linc00518 Contributes to Multidrug Resistance Through Regulating the MiR-199a/MRP1 Axis in Breast Cancer;linc00518 could act as a molecular sponge of miR-199a to repress MRP1 expression;MRP1 depletion increased the sensitivity of MCF-7/ADR cells to ADR, VCR and PTX, and this effect was attenuated following miR-199a inhibition or linc00518 overexpression	30001527	RID00559	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	RP11-789C1.1	CDH1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-5003)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000250266	GRCh38_4:170273919-170283079	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-Coding RNA RP11-789C1.1 Suppresses Epithelial to Mesenchymal Transition in Gastric Cancer Through the RP11-789C1.1/MiR-5003/E-Cadherin Axis;miR-5003 was the target of both RP11-789C1.1 and E-cadherin;at both the mRNA and protein level, silencing RP11-789C1.1 remarkably reduced the expression of E-cadherin and promoted EMT, which were reversed by knocking down miR-5003. LncRNA RP11-789C1.1 directly targets miR-5003-3p in gastric cancer;miR-5003-3p promotes migration, invasion, and EMT by directly targeting E-cadherin in gastric cancer	29991048	RID00560	ceRNA or sponge	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	PVT1	INCENP	positively-E	RNAi;Tarbase;starBase;lncACTdb;TANRIC	upregulation	qPCR;microarray;sequencing	TCGA;GSE54236;GSE49515;GSE60502;GSE58208;GSE98269;GSE57957;GSE49713	LIHC.zip;GSE54236.zip;GSE49515.zip;GSE60502.zip;GSE58208.zip;GSE98269.zip;GSE57957.zip;GSE49713.zip	cell proliferation(+)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000149503	NA	5820	3619	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	A Preliminary Investigation of PVT1 on the Effect and Mechanisms of Hepatocellular Carcinoma: Evidence from Clinical Data, a Meta-Analysis of 840 Cases, and In Vivo Validation. The in silico prediction revealed that there were complementary sequences between PVT1 and miR-424-5p as well as between miR-424-5p and INCENP;whereas a positive correlation trend was found between PVT1 and INCENP based on data from TCGA; the upregulation of PVT1 could promote HCC cell proliferation in vitro and vivo	29975928	RID00561	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	PCGEM1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000067560	NA	64002	387	LINC00071|NCRNA00071|PCAT9	ARH12|ARHA|RHO12|RHOH12	LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00562	expression association	NA	UP(PAAD);DATA(GSE60407)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Epithelial ovarian cancer	PCGEM1	YAP1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000137693	NA	64002	10413	LINC00071|NCRNA00071|PCAT9	COB1|YAP|YAP2|YAP65|YKI	LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00563	expression association	NA	UP(PAAD);DATA(GSE60407)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Epithelial ovarian cancer	PCGEM1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000087245	NA	64002	4313	LINC00071|NCRNA00071|PCAT9	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00564	expression association	NA	UP(PAAD);DATA(GSE60407)	UP(PAAD);DATA(GSE40174)
Epithelial ovarian cancer	PCGEM1	BCL2L1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000171552	NA	64002	598	LINC00071|NCRNA00071|PCAT9	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00565	expression association	NA	UP(PAAD);DATA(GSE60407)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Epithelial ovarian cancer	PCGEM1	RPS6KB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000108443	NA	64002	6198	LINC00071|NCRNA00071|PCAT9	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00566	expression association	NA	UP(PAAD);DATA(GSE60407)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Lung cancer	RCC2-AS1	RCC2	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell autophagy(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227751	GRCh38_1:17406760-17407382	ENSG00000179051	NA	114515514	55920	NA	TD-60	LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2;LCPAT1 was shown to bind to RCC2, and RCC2 mediated the effect of LCPAT1 on cell autophagy, migration, invasion and EMT in lung cancer	29913439	RID00567	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	LINC01121	GLP1R	negatively-E	luciferase reporter assay	upregulation	microarray	GSE14245;GSE27890;GSE16515	GSE14245.zip;GSE27890.zip;GSE16515.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cAMP/PKA signaling pathway(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000205054	GRCh38_2:45164816-45323397	ENSG00000112164	NA	400952	2740	UNQ6975	GLP-1|GLP-1-R|GLP-1R	LINC01121 Inhibits Cell Apoptosis While Facilitating proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R; GLP1R was indeed a target of LINC01121;the LINC01121 vector group exhibited increased expressions of LINC01121; decreased mRNA and protein levels of GLP1R, Bad, cAMP, and PKA; increased protein levels of CREB, Bcl-2, PCNA, p-PKA and p-CREB; increased cell proliferation, migration and invasion; and decreased cell apoptosis;LINC01121 functions as a tumor promoter by means of its involvement in the process of translational repression of the GLP1R and inhibition of the cAMP/PKA signaling pathway	29843149	RID00568	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Gastric cancer	MT1JP	RUNX3	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000020633	NA	4498	864	MT1|MT1J|MT1NP|MTB	AML2|CBFA3|PEBP2aC	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00569	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Gastric cancer	MT1JP	CDKN1A	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000124762	NA	4498	1026	MT1|MT1J|MT1NP|MTB	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00570	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	MT1JP	BCL2L11	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000153094	NA	4498	10018	MT1|MT1J|MT1NP|MTB	NA	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00571	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SH3PXD2A-AS1	CDKN1C	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000129757	NA	100505839	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID00572	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	SH3PXD2A-AS1	KLF2	negatively-E	RNAi;RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000127528	NA	100505839	10365	NA	LKLF	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID00573	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	HOTAIR	miR-203a-3p	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	RNA-RNA	cisplatin;paclitaxel	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR is a Prognostic Biomarker for the proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/beta-Catenin Signaling Pathway;HOTAIR interacts with miR-203a-3p.To analyze whether HOTAIR and miR-203a-3p could regulate drug-resistance of CRC cells, we treated CRC cells with CDDP after HOTAIR knockdown or miR-203a-3p overexpression. As expected, CDDP inhibited cell proliferation in a dose-dependent manner. HOTAIR knockdown or miR-203a-3p overexpression increased the sensitivity of CRC cells to CDDP. We confirmed these results with another chemotherapy drug, PTX. HOTAIR knockdown and miR-203a-3p overexpression increased the sensitivity of CRC cells to PTX.Therefore, these data suggested that HOTAIR could enhance the drug resistance of CRC cells.HOTAIR suppressed the expression of miR-203a-3p, thus inducing Wnt/beta-catenin signaling activation and CRC cell proliferation and chemoresistance enhancements.HOTAIR promotes the proliferation and chemoresistance of CRC cells through targeting miR-203a-3p-Wnt/beta-catenin signaling pathway.	29680837	RID00574	ceRNA or sponge	chemoresistance,prognosis	NA	NA
Hepatocellular carcinoma	LNCDQ	CDH1	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_1:155234457-155239960	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulation of LncDQ is Associated with Poor Prognosis and Promotes Tumor Progression via Epigenetic Regulation of the EMT Pathway in HCC;LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells	29669339	RID00575	epigenetic regulation	prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Malignant glioma	CYTOR	BMI1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-16)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000168283	NA	112597	648	C2orf59|LINC00152|NCRNA00152	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell proliferation and Invasion by Interacting with MiR-16;LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression.LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion	29669323	RID00576	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Cervical cancer	SNHG12	miR-424-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p;Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion	29533945	RID00577	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Malignant glioma	SNHG16	PRMT5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-4518)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000100462	NA	100507246	10419	Nbla10727|Nbla12061|ncRAN	HRMT1L5|HSL7|IBP72|JBP1|SKB1|SKB1Hs	LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma;SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518;Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells	29529599	RID00578	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Lung adenocarcinoma	LINC00707	CDC42	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000070831	NA	100507127	998	NA	CDC42Hs|G25K|TKS	The Long Intergenic Noncoding RNA 00707 Promotes Lung Adenocarcinoma Cell proliferation and Migration by Regulating Cdc42;Microarray analysis and rescue assays suggested that Cdc42 is an important target gene involved in the carcinogenesis of LINC00707	29482190	RID00579	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	EPEL	CCNB1	positively-E	RNAi	upregulation	microarray	GSE31210;GSE50081	GSE31210.zip;GSE50081.zip	cell proliferation(+);prognosis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_4:182138658-182144515	ENSG00000134057	NA	NA	891	NA	CCNB	The LncRNA EPEL Promotes Lung Cancer Cell proliferation Through E2F Target Activation;EPEL knockdown specifically down-regulated the expression of cell cycle-related E2F target genes, including Cyclin B1 (CCNB1), in lung cancer cells but not that of apoptosis- or metabolism-related E2F target genes. EPEL interacted with E2F1 and regulated the expression of the E2F target genes by changing the binding efficiency of E2F1 to the E2F target promoters.Moreover, the expression levels of EPEL and CCNB1 both alone and in combination were robust prognostic markers for lung cancer.	29448242	RID00580	expression association	prognosis	NA	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Osteosarcoma	GAS5	TIMP2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-203a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000035862	NA	60674	7077	NCRNA00030|SNHG2	CSC-21K|DDC8	LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a;miR-203a was negatively regulated by lncRNA GAS5;TIMP2 was a target of miR-203a and the anti-growth and anti-metastasis actions of miR-203a suppression were reversed by TIMP2 silencel;lncRNA GAS5 silence, miR-203a overexpression, and TIMP2 silence could activate PI3K/AKT/GSK3beta signaling while block NF-kB signaling	29414815	RID00581	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Clear cell renal cell carcinoma	DGCR5	EGFR	positively-F	RIP;mass spectrometry	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000146648	NA	26220	1956	LINC00037|NCRNA00037	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way.LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR	29393141	RID00582	interact with protein	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Malignant glioma	HOXA-AS2	EGFR	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-373)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000146648	NA	285943	1956	HOXA3as	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis;HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways.	29310118	RID00583	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Gastric cancer	ZEB1-AS1	miR-335-5p	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000237036	GRCh38_10:31206278-31320447	NA	NA	220930	NA	NA	NA	Downregulation of miR-335-5p by Long Noncoding RNA ZEB1-AS1 in Gastric Cancer Promotes Tumor proliferation and Invasion;miR-335-5p expression was downregulated and negatively correlated with ZEB1-AS1 expression in GC tissues;miR-335-5p expression was directly regulated by ZEB1-AS1	29215918	RID00584	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	NA
Non-small cell lung cancer	PVT1	miR-497	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of LncRNA PVT1 inhibits tumorigenesis in non-small-cell lung cancer by regulating miR-497 expression;PVT1 could directly interact with miR-497;knockdown of PVT1 inhibited cell viability, invasion and induced apoptosis in NSCLC by regulating miR-497 expression	29133127	RID00585	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Esophagus squamous cell carcinoma	miR-548k	NPTN-IT1	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000281183	GRCh38_15:73567012-73569294	NA	101241892	NA	lncRNA-LET	Up-regulated miR-548k promotes esophageal squamous cell carcinoma progression via targeting long noncoding RNA-LET;Mechanistically, we found that miR-548k directly targets and represses the expression of long noncoding RNA-LET (lncRNA-LET), and further down-regulates p53 and up-regulates NF90.	29126868	RID00586	ceRNA or sponge	NA	NA	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Papillary thyroid carcinoma	BISPR	miR-21-5p	negatively-E	luciferase reporter assay;RNA pull-down assay	upregulation	microarray	NA	NA	cancer progression(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000282851	GRCh38_19:17405686-17419324	NA	NA	105221694	NA	lncBST2	NA	LncRNA BISPR promotes the progression of thyroid papillary carcinoma by regulating miR-21-5p;BISPR promoted the development of TPC cells by inhibiting miR-21-5p expression; BISPR stimulated propagation and invasiveness of TPC cells by depressing miR-21-5p	29856242	RID00587	expression association	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Osteosarcoma	SNHG1	NOB1	positively-E	luciferase reporter assay	upregulation	microarray	GSE85537	GSE85537.zip	tumorigenesis(+);cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000141101	NA	23642	28987	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ART-4|MST158|MSTP158|NOB1P|PSMD8BP1	Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma;SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS	29115574	RID00588	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Multiple myeloma	NEAT1	MCL1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-193a)	regulation	NA	dexamethasone	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000143384	NA	283131	4170	LINC00084|NCRNA00084|TncRNA|VINC	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway;NEAT1 acts as a molecular sponge for miR-193a. The in-depth study revealed that during the development of DEX resistance in these cells, the miR-193a levels were decreased, which resulted in the increased expression of the target gene myeloid cell leukemia-1 (MCL1).MCL1,which acts as key determinants in cell proliferation,differentiation, and tumorigenesis, was identified as a downstream target of miR-193a.	29205703	RID00589	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	H19	E2F1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	The long noncoding RNA H19 promotes cell proliferation via E2F-1 in pancreatic ductal adenocarcinoma.In conclusion, H19 is overexpressed and plays oncogenic role in PDAC through promoting cancer cell proliferation via the upregulation of E2F-1.E2F-1 was overexpressed in PDAC tissues with possible correlation with H19 expression level. In conclusion, H19 is overexpressed and plays oncogenic role in PDAC through promoting cancer cell proliferation via the upregulation of E2F-1.Long noncoding RNA H19 derived miR-675 regulates cell proliferation by down-regulating E2F-1 in human pancreatic ductal adenocarcinoma;the suppressed cell proliferation caused by H19 knockdown could be rescued by inhibiting miR-675 expression	27573434;29344285	RID00590	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteosarcoma	HULC	miR-122	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma;HULC functioned as an endogenous sponge for miR-122, and its silence functioned through upregulating miR-122	28688193	RID00591	ceRNA or sponge	NA	NA	NA
Breast cancer	TP73-AS1	TFAM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000108064	NA	57212	7019	KIAA0495|PDAM	MTDPS15|MTTF1|MTTFA|TCF6|TCF6L1|TCF6L2|TCF6L3	TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition;TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a	28639399	RID00592	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Tongue cancer	Lnc-EGFR	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000258451	GRCh38_14:20693480-20707120	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long noncoding RNA Lnc-EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer;the oncogenic potential of Lnc-EGFR, which was achieved by positive regulation of EGFR in human tongue cancer	29138845	RID00593	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	AC078922.1	miR-31	negatively-F	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	RNA-RNA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000257241	GRCh38_12:69946543-69947081	NA	NA	NA	NA	NA	NA	The long non-coding RNA ENST00000547547 reduces 5-fluorouracil resistance of colorectal cancer cells via competitive binding to microRNA-31;ENST00000547547 reduced the chemoresistance of 5-FU via competitive binding to miR-31 in 5-FU-resistant CRC cell lines	29115526	RID00594	ceRNA or sponge	chemoresistance	NA	NA
Colorectal cancer	RP11-317J10.2	CCND1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_8:85442047-85464915	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Downregulation of LncRNA-RP11-317J10.2 promotes cell proliferation and invasion and predicts poor prognosis in colorectal cancer.This study reveals a crucial role for lncRNA-RP11-317J10.2 in CRC growth and invasion via upregulation of cyclin D1 expression. Cyclin D1 was upregulated by lncRNA-RP11-317J10.2 knockdown, and co-expression of cyclin D1-targeting siRNA abrogates the pro-tumorigenic effects of lncRNA-RP11-317J10.2 knockdown.	29073791	RID00595	expression association	prognosis	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	PCAT7	miR-134-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	prognosis(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000231806	GRCh38_9:94555054-94603990	NA	NA	101928099	NA	PCAN-R2	NA	Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC);Rescue assays were carried out to confirm the contribution of PCAT7 to the progression of NSCLC cells by targeting miR-134-5p.	29275424;28728844	RID00596	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE55807)	NA
Non-small cell lung cancer	NPTN-IT1	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000148400	NA	101241892	4851	lncRNA-LET	AOS5|AOVD1|TAN1|hN1	Downregulation of long non-coding RNA LET predicts poor prognosis and increases Notch signaling in non-small cell lung cancer;highlight a novel lncRNA-LET/Notch axis in regulating NSCLC cell fate and tumor progression;we demonstrated that lncRNA-LET overexpression significantly reduced the expression of Notch1 intracellular Domain (NICD1) in H292 cells while knockdown of lncRNA-LET increased NICD1 expression in H1975 cells	29416684	RID00597	expression association	prognosis	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	SUMO1P3	miR-320a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000235082	GRCh38_1:160317403-160317706	NA	NA	474338	NA	NA	NA	The long non-coding RNA SUMO1P3 facilitates breast cancer progression by negatively regulating miR-320a;SUMO1P3 binds to miR-320a,which has been identified as a tumor suppressor in various cancers, including breast cancer	29312511	RID00598	ceRNA or sponge	NA	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	NA
Malignant glioma	PVT1	EZH2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2;exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion	29046366	RID00599	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	SNHG1	CDH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000039068	NA	23642	999	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00600	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	SNHG1	VIM	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000026025	NA	23642	7431	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00601	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SNHG1	CDH2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000170558	NA	23642	1000	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CD325|CDHN|CDw325|NCAD	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00602	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Esophagus squamous cell carcinoma	SNHG1	NOTCH1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148400	NA	23642	4851	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AOS5|AOVD1|TAN1|hN1	knockdown of SNHG1 suppressed the Notch signaling pathway by reducing the Notch1 and Hes-1 expression levels in ESCC cells	29081407	RID00603	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SNHG1	HES2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000069812	NA	23642	54626	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	bHLHb40	knockdown of SNHG1 suppressed the Notch signaling pathway by reducing the Notch1 and Hes-2 expression levels in ESCC cells	29081407	RID00604	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Endometrial cancer	CCAT2	miR-216b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	Knockdown of lncRNA CCAT2 inhibits endometrial cancer cells growth and metastasis via sponging miR-216b;CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways	29036788	RID00605	ceRNA or sponge	metastasis	NA	NA
Gastric cancer	CCAT1	miR-219-1	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	LncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miR-219-1.the roles of CCAT1 on cell proliferation, apoptosis and invasion were inhibited by miR-219-1;CAT1 promotes the tumorigenesis and progression of GC by negative-regulating miR-219-1.In addition, miR-219-1 was predicted and convinced a direct target of CCAT1.	29231252	RID00606	ceRNA or sponge	NA	NA	NA
Urinary bladder cancer	HULC	ZIC2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000043355	NA	728655	7546	HCCAT1|LINC00078|NCRNA00078	HPE5	Long non-coding RNA HULC promotes bladder cancer cells proliferation but inhibits apoptosis via regulation of ZIC2 and PI3K/AKT signaling pathway; moreover, overexpression of HULC significantly up-regulated ZIC2 expression level	28946549	RID00607	expression association	NA	NA	NA
Hepatocellular carcinoma	PVT1	miR-214	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes hepatocellular carcinoma progression through regulating miR-214.RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2).	28800314	RID00608	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Gastric cancer	SALL4	DANCR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101115	NA	ENSG00000226950	GRCh38_4:52712404-52720351	57167	57291	DRRS|HSAL4|ZNF797	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	Long noncoding RNA DANCR is activated by SALL4 and promotes the proliferation and invasion of gastric cancer cells;DANCR is activated by SALL4 in gastric cancer cells and exerted its oncogenic activities through the activation of beta-catenin pathway.	29416741	RID00609	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)
Pancreatic cancer	GAS5	PTEN	positively-E	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell metastasis(-)	ceRNA(miR-32-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA GAS5 suppresses pancreatic cancer metastasis through modulating miR-32-5p/PTEN axis;GAS5 positively regulated the expression of PTEN through miR-32-5p;GAS5 suppressed the proliferation, migration and invasion of PC cells through regulating miR-32-5p/PTEN axis.The interaction between GAS5 and miR-32-5p in PC cells	29225772	RID00610	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	CCAT1	SOX4	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-130a-3p)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000124766	NA	100507056	6659	CARLO5|CARLo-5|onco-lncRNA-40	EVI16	LncRNA CCAT1/miR-130a-3p axis increases cisplatin resistance in non-small-cell lung cancer cell line by targeting SOX4;CCAT1 directly interacted with miR-130a-3p and negatively regulated miR-130a-3p expression. CCAT1 contributed to DDP resistance of A549/DDP cells by down-regulating miR-130a-3p.miR-130a-3p was found to directly target SOX4 to suppress its expression.CCAT1/miR-130a-3p axis enhanced DDP resistance of NSCLC cells by targeting SOX4, providing potential targets to overcome DDP resistance and improve efficacy of chemotherapy for patients with NSCLC.	29020498	RID00611	ceRNA or sponge	chemoresistance	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Breast cancer	uc.38	PBX1	negatively-E	RIP;western blot	downregulation	qPCR	NA	NA	apoptosis process(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_1:161127332-161127555	ENSG00000185630	NA	NA	5087	NA	CAKUHED	uc.38 induces breast cancer cell apoptosis via PBX1;uc.38 negatively regulated the expression of the pre-B-cell leukaemia homeobox 1 (PBX1) protein and subsequently affected the expression of Bcl-2 family members, ultimately inducing breast cancer cell apoptosis	29312798	RID00612	interact with protein	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE75367)
Endometrial carcinoma	MEG3	PI3K	interact	RIP	downregulation	qPCR	NA	NA	tumorigenesis(-);cancer progression(-);PI3K signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 inhibit endometrial carcinoma tumorigenesis and progression through PI3K pathway; RNA immunoprecipitation assay (RIP) showed that MEG3 can combine directly with PI3K.	29094270	RID00613	interact with protein	NA	NA	NA
Epithelial ovarian cancer	HAGLR	miR-133a-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	LncRNA HOXD-AS1 promotes epithelial ovarian cancer cells proliferation and invasion by targeting miR-133a-3p and activating Wnt/beta-catenin signaling pathway;HOXD-AS1 promoted cell proliferation, invasion, and EMT process through sponging miR-133a-3p in EOC cells	29239819	RID00614	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	NA
Colorectal cancer	SOX21-AS1	MYO6	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000196586	NA	100507533	4646	NA	DFNA22|DFNB37	Long non-coding RNA SOX21-AS1 sponges miR-145 to promote the tumorigenesis of colorectal cancer by targeting MYO6;miR-145 was proved to be the target of SOX21-AS1;myosin VI (MYO6) was found to be one of the targets of miR-145	29217166	RID00615	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807,GSE75367)
Melanoma	FALEC	CDKN1A	negatively-E	RIP;western blot;ChIP;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000124762	NA	100874054	1026	FAL1|LINC00568|ncRNA-a1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21;we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21	29196104	RID00616	epigenetic regulation	prognosis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	DLX6-AS1	MMP2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-203a)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000087245	NA	285987	4313	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA DLX6-AS1 aggravates hepatocellular carcinoma carcinogenesis by modulating miR-203a/MMP-2 pathway;miR-203a potentially targeted DLX6-AS1 3'-UTR, suggesting the interaction between miR-203a and DLX6-AS1. Furthermore, miR-203a also targeted MMP-2 mRNA 3'-UTR, which was validated by luciferase reporter assay;This results and findings provide a novel insight for HCC tumorigenesis	29145165	RID00617	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Colorectal cancer	HNF1A-AS1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000168036	NA	283460	1499	C12orf27|HAS1|NCRNA00262	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00618	expression association	prognosis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	HNF1A-AS1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000110092	NA	283460	595	C12orf27|HAS1|NCRNA00262	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00619	expression association	prognosis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	HNF1A-AS1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000136997	NA	283460	4609	C12orf27|HAS1|NCRNA00262	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00620	expression association	prognosis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Urinary bladder cancer	ZEB2-AS1	miR-27b	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000238057	GRCh38_2:144517978-144521477	NA	NA	100303491	NA	ZEB2-AS|ZEB2AS|ZEB2NAT	NA	LncRNA ZEB2-AS1 promotes bladder cancer cell proliferation and inhibits apoptosis by regulating miR-27b;ZEB2-AS1 promoted tumorigenesis and development of BC through down-regulating tumor-suppressive miR-27b.According to the sequences of predicted binding sites be-tween ZEB2-AS1 and miR-27b, mutant (mut) and wild type (wt) frag-ment of ZEB2-AS1 were designed. relative luciferase activity of ZEB2-AS1-wt was significantly reduced by miR-27b mimic; while the relative luciferase activity of ZEB2-AS1-mut wasnot affected by the changes in miR-27b expression	28992472	RID00621	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	NA
Triple-receptor negative breast cancer	CDKN2B-AS1	miR-199a	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL promotes carcinogenesis via sponging miR-199a in triple-negative breast cancer;miR-199a targeted ANRIL at 3'-UTR;Rescue experiments showed that miR-199a inhibitor could reverse the tumor-suppressing role of ANRIL knockdown on TNBC proliferation and apoptosis;ANRIL overexpression modulated TNBC tumorigenesis through acting as molecular 'sponge' for miR-199a	28961506	RID00622	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	NA
B-cell acute lymphocytic leukemia	ZEB1-AS1	STAT3	positively-E	western blot	upregulation	qPCR	NA	NA	prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000168610	NA	220930	6774	NA	ADMIO|ADMIO1|APRF|HIES	LncRNA ZEB1-AS1 contributes to STAT3 activation by associating with IL-11 in B-lymphoblastic leukemia;ZEB1-AS1 could bind to IL-11 and promote IL-11 stability;ZEB1-AS1 promotes the activation of IL-11/STAT3 signaling pathway by associating with IL-11 in B-ALL;a high level of ZEB1-AS1 predicted poor prognosis of B-ALL patients	28861713	RID00623	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Pancreatic cancer	HOTTIP	HOXA9	positively-E	RNAi	upregulation	qPCR;microarray	GSE61166	GSE61166.zip	cell stemness(+)	NA	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000078399	NA	100316868	3205	HOXA-AS6|HOXA13-AS1|NCRNA00213	ABD-B|HOX1|HOX1.7|HOX1G	LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9; HOTTIP mediated HOXA9 to enhance the Wnt/beta-catenin pathway by binding to WDR5 in PCSCs;the HOTTIP/WDR5/HOXA9/Wnt axis contributes to PCSC stemness and is a potential therapeutic target for PDAC.	28947139	RID00624	expression association	NA	NA	NA
Colon cancer	HNF1A-AS1	SIRT1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000096717	NA	283460	23411	C12orf27|HAS1|NCRNA00262	SIR2|SIR2L1|SIR2alpha	Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA;HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway. These results suggested that HNF1A-AS1 regulate coloncancer cell apoptosis in part by modulating p53 expression.	28943452	RID00625	ceRNA or sponge	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	HNF1A-AS1	TP53	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000141510	NA	283460	7157	C12orf27|HAS1|NCRNA00262	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA;HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway. These results suggested that HNF1A-AS1 regulate coloncancer cell apoptosis in part by modulating p53 expression.	28943452	RID00626	expression association	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	UCA1	SF1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-184)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168066	NA	652995	7536	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BBP|D11S636|MBBP|ZCCHC25|ZFM1|ZNF162	LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression;Mechanisms investigation indicated that UCA1 could interact with miR-184 to repress its expression.The OSCC nude mice model experiments demonstrated that depletion of UCA1 further boosted CDDP-mediated repression effect on tumor growth. UCA1 accelerated proliferation, increased CDDP chemoresistance and restrained apoptosis partly through modulating SF1 via sponging miR-184 in OSCC cells, suggesting that targeting UCA1 may be a potential therapeutic strategy for OSCC patients.	29125238	RID00627	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	H19	E2F1	negatively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	Long non-coding RNA H19 regulates E2F1 expression by competitively sponging endogenous miR-29a-3p in clear cell renal cell carcinoma;down-regulated lncRNA-H19 could affect the expression of miR-29a-3p targeting E2F1 with competitively binding miR-29a-3p;Over expression of E2F1 could rescue lncRNA-H19 siRNA induced suppression on cell migration and invasion in ccRCC cells	29214011	RID00628	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	TP53COR1	PKM	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-);cell proliferation(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Prostate cancer	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000067225	NA	102800311	5315	TRP53COR1|linc-p21|lincRNA-p21	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	LincRNA-p21 suppresses development of human prostate cancer through inhibition of PKM2;We also found that the proliferation and tumorigenesis of lincRNA-p21-silenced prostate cancer cells were significantly inhibited after knocking down PKM2;We demonstrated that lincRNA-p21 blunted the prostate cancer cell proliferation and tumorigenic capacity through down-regulation of PKM2	28994148	RID00629	expression association	NA	NA	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Chordoma	MIR31HG	miR-31	negatively-E	RIP;luciferase reporter assay;RNA pull-down assay;RNAi;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID00630	epigenetic regulation	NA	NA	NA
Chordoma	MIR31HG	RNF144B	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-31)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000137393	NA	554202	255488	LncHIFCAR|hsa-lnc-31	IBRDC2|PIR2|bA528A10.3|p53RFP	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID00631	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Pancreatic cancer	CRNDE	IRS1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000169047	NA	NA	3667	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HIRS-1	Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1;We identified miR-384 as a direct target for CRNDE; CRNDE positively regulated IRS1 expression through sponging miR-384	28940804	RID00632	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Gastric cancer	GAS5	miR-222	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	The GAS5/miR-222 Axis Regulates proliferation of Gastric Cancer Cells Through the PTEN/Akt/mTOR Pathway; GAS5 directly targeted and suppressed miR-222 expression.GAS5 regulated GC cell proliferation through the PTEN/Akt/mTOR pathway by negatively regulating miR-222.	29098549	RID00633	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Osteosarcoma	MIR210HG	miR-503	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000247095	GRCh38_11:565660-568457	NA	NA	100506211	NA	NA	NA	Long Noncoding RNA miR210HG Sponges miR-503 to Facilitate Osteosarcoma Cell Invasion and Metastasis;miR-503 was verified to be the target miRNA of miR210HG using bioinformatics online program and luciferase assayl;miR-503 could reverse the role of miR210HG on osteosarcoma cells	28972855	RID00634	ceRNA or sponge	metastasis	NA	NA
Breast cancer	NEAT1	HMGA2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);cell growth(+);cell invasion(+)	ceRNA(miR-211)	regulation	NA	5-fluorouracil	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000149948	NA	283131	8091	LINC00084|NCRNA00084|TncRNA|VINC	BABL|HMGI-C|HMGIC|LIPO|STQTL9	The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer;LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis;the EMT-inducer HMGA2 was identified as a downstream target of miR-211. The interaction between NEAT1 and miR-211.	28720546	RID00635	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Melanoma	BANCR	NOTCH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000134250	NA	100885775	4853	LINC00586	AGS2|HJCYS|hN2	BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR-204; We identified that miR 204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR 204;BANCR may promote melanoma cell growth through inhibition of miR 204, leading to the activation of Notch2 pathway;Our results suggest the BANCR/miR 204/Notch2 axis mediates melanoma cell proliferation and tumor progression	29075789	RID00636	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MALAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Non-Coding RNA MALAT1 Regulates ZEB1 Expression by Sponging miR-143-3p and Promotes Hepatocellular Carcinoma Progression;ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1;MALAT1 may regulate ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression;The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p	28543721	RID00637	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thyroid cancer	MALAT1	FGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138685	NA	378938	2247	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BFGF|FGF-2|FGFB|HBGF-2	LncRNA-MALAT1 Promotes Angiogenesis of Thyroid Cancer by Modulating Tumor-Associated Macrophage FGF2 Protein Secretion;overexpression of FGF2 blocked the effects of MALAT1 siRNAs on cell migration, invasion, and angiogenesis;MALAT1-mediated FGF2 protein secretion from TAMs inhibits inflammatory cytokines release, promotes proliferation, migration, and invasion of FTC133 cells and induces vasculature formation	28543663	RID00638	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteosarcoma	GAS5	DIRAS3	positively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);epithelial to mesenchymal transition(-)	ceRNA(miR-221)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000162595	NA	60674	9077	NCRNA00030|SNHG2	ARHI|NOEY2	Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway.GAS5 could directly bind to miR-221 to decrease miR-221 expression and enhance ARHI expression;lncRNA GAS5 functions as a competing endogenous RNA for miR-221 to suppress cell growth and EMT in osteosarcoma by regulating the miR-221/ARHI pathway;Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway	28519068	RID00639	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Medulloblastoma	CDKN2B-AS1	BRI3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-323)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164713	NA	100048912	25798	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	I3	Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on proliferation and Migration by Targeting miR-323;ANRIL acted as a sponge of miR-323 and its silence functioned through up-regulating miR-323;BRI3 and CDK6 were target genes of miR-323 and the effect of BRI3 on DAOY cells was the same as ANRIL;ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3;ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR-323-mediated regulation of BRI3, which could activate p38 MAPK, ERK, and AKT as well as Wnt signaling pathway	28513871	RID00640	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Papillary thyroid carcinoma	PTCSC3	SCAI	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-574-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000173611	NA	100886964	286205	NA	C9orf126|NET40	LncRNA PTCSC3/miR-574-5p Governs Cell proliferation and Migration of Papillary Thyroid Carcinoma via Wnt/beta-Catenin Signaling; RNA Pull-down assay verified the bound of PTCSC3 and miR-574-5p; PTCSC3/miR-574-5p regulated the activity of Wnt/beta-catenin via SCAI and mediated cell proliferation and migration of PTC-1.	28513866	RID00641	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Malignant glioma	CCAT1	FGFR3	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-181b)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000068078	NA	100507056	2261	CARLO5|CARLo-5|onco-lncRNA-40	ACH|CD333|CEK2|HSFGFR3EX|JTK4	lncRNA CCAT1 Promotes Glioma tumorigenesis by Sponging miR-181b;Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process,and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b;CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRalpha.In conclusion,CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRalpha, which provides a potential therapeutic target for glioma treatment	28475287	RID00642	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Malignant glioma	CCAT1	PDGFRA	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-181b)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000134853	NA	100507056	5156	CARLO5|CARLo-5|onco-lncRNA-40	CD140A|PDGFR-2|PDGFR2	lncRNA CCAT1 Promotes Glioma tumorigenesis by Sponging miR-181b;Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process,and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b;CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRalpha.In conclusion,CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRalpha, which provides a potential therapeutic target for glioma treatment	28475287	RID00643	ceRNA or sponge	NA	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Hepatocellular carcinoma	LNCARSR	PTEN	negatively-F	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+)	interact with mRNA	binding/interaction	RNA-RNA	doxorubicin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000171862	NA	112577459	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA lncARSR Promotes Doxorubicin Resistance in Hepatocellular Carcinoma via Modulating PTEN-PI3K/Akt Pathway. lncARSR physically associates with PTEN mRNA, promotes PTEN mRNA degradation, decreases PTEN expression, and activates PI3K/Akt pathway;the effects of lncARSR overexpression on doxorubicin resistance could be reversed by PI3K/Akt pathway inhibitor, and lncARSR knockdown-induced doxorubicin sensitivity could be reversed by PTEN depletion	28464252	RID00644	interact with mRNA	chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	Lnc-BM	JAK2	positively-E	RIP;RNAi	upregulation	qPCR;microarray	GSE79540	GSE79540.zip	cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_14:62110875-62112546	ENSG00000096968	NA	NA	3717	NA	JTK10|THCYT3	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis;Lnc-BM increased JAK2 kinase activity to mediate oncostatin M- and IL-6-triggered STAT3 phosphorylation. In breast cancer cells, Lnc-BM promoted STAT3-dependent expression of ICAM1 and CCL2, which mediated vascular co-option and recruitment of macrophages in the brain, respectively. Recruited macrophages in turn produced oncostatin M and IL-6, thereby further activating the Lnc-BM/JAK2/STAT3 pathway and enhancing breast cancer brain metastases (BCBM).	29130936	RID00645	interact with protein	metastasis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Breast cancer	Lnc-BM	STAT3	positively-E	RIP;RNAi	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:62110875-62112546	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis;Lnc-BM increased JAK2 kinase activity to mediate oncostatin M- and IL-6-triggered STAT3 phosphorylation. In breast cancer cells, Lnc-BM promoted STAT3-dependent expression of ICAM1 and CCL2, which mediated vascular co-option and recruitment of macrophages in the brain, respectively. Recruited macrophages in turn produced oncostatin M and IL-6, thereby further activating the Lnc-BM/JAK2/STAT3 pathway and enhancing breast cancer brain metastases (BCBM).	29130936	RID00646	expression association	metastasis	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Acute lymphocytic leukemia	WT1	MEG3	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000184937	NA	ENSG00000214548	GRCh38_14:100779410-100861031	7490	55384	AWT1|GUD|NPHS4|WAGR|WIT-2|WT33	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MEG3 is proven to be transcriptionally activated by Wilms' tumor 1 (WT1), dysregulation of which by epigenetic silencing or mutations is causally involved in AML;MEG3 is identified as a novel target of the WT1 molecule;Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways	28400619	RID00647	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Renal cell carcinoma	LINC-ROR	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000141510	NA	100885779	7157	ROR|lincRNA-RoR|lincRNA-ST8SIA3	BCC7|BMFS5|LFS1|P53|TRP53	lncRNA ROR promotes the proliferation of renal cancer and is negatively associated with favorable prognosis.The suppression of lncRNA ROR also induced an increase in the expression of p53 and a decrease in the expression of c-Myc in vitro;lncRNA ROR was expressed at high levels in RCC tissue and cell lines, and was associated with the proliferation ability of RCC cells	29039528	RID00648	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	LINC-ROR	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136997	NA	100885779	4609	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MRTL|MYCC|bHLHe39|c-Myc	lncRNA ROR promotes the proliferation of renal cancer and is negatively associated with favorable prognosis.The suppression of lncRNA ROR also induced an increase in the expression of p53 and a decrease in the expression of c-Myc in vitro;lncRNA ROR was expressed at high levels in RCC tissue and cell lines, and was associated with the proliferation ability of RCC cells	29039528	RID00649	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	XIST	ATG7	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);cell autophagy(-)	ceRNA(miR-17)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000197548	NA	7503	10533	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	APG7-LIKE|APG7L|GSA7	Knockdown of lncRNA-XIST enhances the chemosensitivity of NSCLC cells via suppression of autophagy;knockdown of lncRNA-XIST significantly decreased autophagy by regulation of ATG7 as determined by qPCR and by western blotting;Knockdown of lncRNA-XIST restored the chemosensitivity of cisplatin-resistant A549 cells to cisplatin, which was reversed by miR-17 inhibitor and overexpression of ATG7 as determined by CCK8 assays.Dual-Luciferase reporter assays indicated that miRNA-17 can directly target ATG7; This study provides evidence that lncRNA-XIST may be a potential marker of poor response to cisplatin chemotherapy in NSCLC patients and the pathway 'lncRNA-XIST/miR-17/autophagy' may be a promising target for patients with chemoresistant NSCLC.	29130102	RID00650	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Gastric cancer	MIAT	HDAC4	positively-E	RNAi;Targetscan;qRT-PCR;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000068024	NA	440823	9759	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	AHO3|BDMR|HA6116|HD4|HDAC-4|HDAC-A|HDACA	lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis.our results demonstrated that MIAT competitively binds to miR-29a-3p and consequently upregulates the expression of HDAC4, which is a downstream target of miR-29a-3p;lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis;the present study highlighted the involvement of the MIAT/miR-29a-3p/HDAC4 axis in the development of GC	29039602	RID00651	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Gastric cancer	MALAT1	ATG12	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	chemosensitivity(+);cell autophagy(+)	ceRNA(miR-23b-3p)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000145782	NA	378938	9140	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG12|APG12L|FBR93|HAPG12	Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer;MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells.In the functional aspect, we found that knockdown of MALAT1 sensitized SGC7901/VCR cells to cisplatin as illustrated by decreased IC50 concentration	29162158	RID00652	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	XIST	PPP1R13L	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-140;miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000104881	NA	7503	10848	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	IASPP|NKIP1|RAI|RAI4	The lncRNA XIST interacts with miR-140/miR-124/iASPP axis to promote pancreatic carcinoma growth; Further, the interaction between XIST and miR-140/miR-124, between miR-140/miR-124 and iASPP was validated using RNA immunoprecipitation assays with the AGO2 antibody. XIST positively correlated with iASPP and CDK1, inversely correlated with miR-140 and miR-124,respectively; XIST might be an oncogenic lncRNA that promoted proliferation of PC cell line through inhibiting miR-140/miR-124 expression and promoting cell cycle-related factor expression, and could be regarded as a therapeutic target in human pancreatic carcinoma	29371940	RID00653	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Glioblastoma	lncHERG	miR-940	negatively-F	luciferase reporter assay	upregulation	microarray	GSE90598	GSE90598.zip	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	NA	GRCh38_7:66904120-66906297	NA	NA	NA	NA	NA	NA	Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma;Mechanistically, we found that lncHERG can serve as a sponge for miR-940 which is a tumor suppressor in cervical cancer;LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend	29296221	RID00654	ceRNA or sponge	NA	NA	NA
Pancreatic cancer	NORAD	RHOA	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;microarray	GSE15471;GSE16515	GSE15471.zip;GSE16515.zip	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-125a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000067560	NA	647979	387	LINC00657	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer; NORAD may function as a ceRNA to regulate the expression of the small GTP binding protein RhoA through competition for hsa-miR-125a-3p, thereby promoting EMT	29121972	RID00655	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Gastric cancer	DANCR	NPTN-IT1	negatively-E	RIP;RNAi;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	lncRNA	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000281183	GRCh38_15:73567012-73569294	57291	101241892	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	lncRNA-LET	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID00656	epigenetic regulation	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Melanoma	ILF3-DT	miR-200b	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00657	epigenetic regulation	NA	NA	NA
Melanoma	ILF3-DT	miR-200a	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00658	epigenetic regulation	NA	NA	NA
Melanoma	ILF3-DT	miR-429	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00659	epigenetic regulation	NA	NA	NA
Breast cancer	SOX2	PVT1	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000181449	NA	ENSG00000249859	GRCh38_8:127794526-128187101	6657	5820	ANOP3|MCOPS3	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion;a transcriptional factor binding site was found between SOX2 and PVT1 promoter and the interaction between each other was further verified by chromatin immunoprecipitation (ChIP) analysis;These data suggest that elevated expression of SOX2 can activate lncRNA PVT1 expression promoted breast cancer tumorigenesis and progression.	28882595	RID00660	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Non-small cell lung cancer	NEAT1	MAPK6	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-98-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000069956	NA	283131	5597	LINC00084|NCRNA00084|TncRNA|VINC	ERK3|HsT17250|PRKM6|p97MAPK	NEAT1/hsa-mir-98-5p/MAPK6 axis is involved in non-small-cell lung cancer development;We speculated that NEAT1 may act as a competing endogenous lncRNA to upregulate MAPK6 by attaching hsa-mir-98-5p in lung cancers;NEAT1/hsa-mir-98-5p/MAPK6 is involved in the development and progress in NSCLC;Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa-mir-98-5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa-mir-98-5p	29095526	RID00661	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	UCA1	miR-135a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer by Sponging miR-135a;miR-135a reversed the effect of UCA1 on cell apoptosis rate and cell viability in SW1990 cells	28315290	RID00662	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	NA
Uveal melanoma	FTH1P3	miR-224-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	miRNA	ENSG00000213453	GRCh38_2:27392784-27393367	NA	NA	2498	NA	FTHL3|FTHL3P	NA	Long non-coding RNA FTH1P3 facilitates uveal melanoma cell growth and invasion through miR-224-5p;Elevated expression of FTH1P3 enhanced uveal melanoma cell proliferation and migration by inhibiting miR-224-5p expression. Moreover, we found that FTH1P3 was a direct target gene of miR-224-5p in uveal melanoma cell.	29095823	RID00663	ceRNA or sponge	NA	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	NA
Cervical cancer	LINC00473	ILF2	positively-F	RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000143621	NA	90632	3608	C6orf176|LNC473|bA142J11.1	NF45|PRO3063	The long noncoding RNA LINC00473, a target of microRNA 34a, promotes tumorigenesis by inhibiting ILF2 degradation in cervical cancer;LINC00473 directly interacted with ILF2 and suppressed its degradation	29218240	RID00664	interact with mRNA	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Malignant glioma	HOXA11-AS	EZH2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Regulation of HOXA11-AS/miR-214-3p/EZH2 axis on the growth, migration and invasion of glioma cells;HOXA11-AS functioned as a competing endogenous RNA (ceRNA) for miR-214-3p, which in turn positively regulated the expression of its direct target EZH2	28946213	RID00665	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	PCAT1	HMGB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000189403	NA	100750225	3146	PCA1|PCAT-1	HMG-1|HMG1|HMG3|SBP-1	Long noncoding RNA PCAT-1 promotes invasion and metastasis via the miR-129-5p-HMGB1 signaling pathway in hepatocellular carcinoma;PCAT-1 could act as an endogenous RNA by directly binding to miR-129-5p;PCAT-1 repressed inhibitory effect of miR-129-5p and reverse high mobility group box 1 (HMGB1) expression, a target gene of miR-129-5p	28931210	RID00666	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Prostate cancer	PCAT1	FSCN1	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000075618	NA	100750225	6624	PCA1|PCAT-1	FAN1|HSN|SNL|p55	Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer;PCAT-1 could act as a miR-145-5p sponge to modulate FSCN1 expression;PCAT-1 accelerated PC cell proliferation, migration, invasion and suppressed apoptosis by up-regulating FSCN1 mediated via miR-145-5p;Rescue experiments demonstrated that miR-145-5p restoration attenuated the promotive effects of PCAT1 on PC progression, while Fascin-1 (FSCN1) upregulation relieved the anti-cancer role of miR-145-5p in PC	28922730	RID00667	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Triple-receptor negative breast cancer	MALAT1	miR-129-5p	negatively-F	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer;we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p.MALAT1 regulated miR-129-5p expression by directly binding to it.	28915533	RID00668	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Malignant glioma	HOTTIP	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000148516	NA	100316868	6935	HOXA-AS6|HOXA13-AS1|NCRNA00213	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA HOTTIP promotes hypoxia-induced epithelial-mesenchymal transition of malignant glioma by regulating the miR-101/ZEB1 axis;HOTTIP sponged endogenous miR-101 and inhibited its activity, which resulted in increased ZEB1 expression and promoted process of EMT	28886531	RID00669	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	FEZF1-AS1	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000039068	NA	154860	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID00670	epigenetic regulation	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	UCA1	GRK2	negatively-F	RNA pull-down assay;RIP;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000173020	NA	652995	156	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADRBK1|BARK1|BETA-ARK1	Long noncoding RNA UCA1 promotes tumour metastasis by inducing GRK2 degradation in gastric cancer;we report that the lncRNA UCA1 increases the metastatic ability of gastric cancer (GC) cells by regulating GRK2 protein stability by promoting Cbl-c-mediated GRK2 ubiquitination and degradation;This process then activates the ERK-MMP9 signalling pathway. LncRNA UCA1 interacts with GRK2 and promotes GRK2 degradation via ubiquitination.	28843497	RID00671	interact with protein	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00963	PGK1	positively-F	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+);AKT/mTOR signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000102144	NA	100506190	5230	MetaLnc9	HEL-S-68p|MIG10|PGKA	MetaLnc9 Facilitates Lung Cancer Metastasis via a PGK1-Activated AKT/mTOR Pathway;Mechanistic investigations showed that LINC00963 (MetaLnc9) interacted with the glycolytic kinase PGK1 and prevented its ubiquitination in NSCLC cells, leading to activation of the oncogenic AKT/mTOR signaling pathway.	28923857	RID00672	interact with protein	metastasis	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Intrahepatic cholangiocarcinoma	CCAT1	miR-152	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	LncRNA-CCAT1 Promotes Migration, Invasion, and EMT in Intrahepatic Cholangiocarcinoma Through Suppressing miR-152.bioinformatics analysis and luciferase reporter assay revealed that CCAT1 directly bound to the miR-152, which has been reported to serve as a tumor suppressor in variety cancers.	28921383	RID00673	ceRNA or sponge	NA	NA	NA
Lung cancer	YY1	PVT1	positively-E	ChIP;luciferase reporter assay;DNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000249859	GRCh38_8:127794526-128187101	7528	5820	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Transcription Factor YY1 Modulates Lung Cancer Progression by Activating lncRNA-PVT1;we showed that YY1 could directly bind to the promoter region of (long noncoding RNA-plasmacytoma variant translocation 1 [lncRNA-PVT1]) and activated its transcription through the consensus YY1 motif	28972861	RID00674	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Nasopharynx carcinoma	HOTAIR	FASN	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000169710	NA	100124700	2194	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FAS|OA-519|SDR27X1	LncRNA HOTAIR contributes to the tumorigenesis of nasopharyngeal carcinoma via up-regulating FASN;Knockdown of HOTAIR led to downregulation of FASN in NPC cells, thus suppressing cell proliferation and invasion;We suggest that HOTAIR is important in the progression and recurrence of NPC, perhaps through upregulating FASN	29228426	RID00675	expression association	recurrence	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	NORAD	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000171862	NA	647979	5728	LINC00657	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression;we identified that both LINC00657 and PTEN mRNA were targets of miR-106a-5p by using dual-luciferase reporter assay	28919047	RID00676	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	XIST	PDCD4	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-21-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000150593	NA	7503	27250	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	H731	Long non-coding RNA XIST regulates PDCD4 expression by interacting with miR-21-5p and inhibits osteosarcoma cell growth and metastasis;we affirmed that XIST regulated PDCD4 expression by competitively binding to miR-21-5p. XIST inhibited cell proliferation and cell mobility by competitively binding to miR-21-5p and upregulating PDCD4 in OS	29048648	RID00677	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Osteosarcoma	SOX2-OT	SOX2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell motility(+)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	NCRNA00043|SOX2OT	ANOP3|MCOPS3	LncRNA SOX2-OT is a novel prognostic biomarker for osteosarcoma patients and regulates osteosarcoma cells proliferation and motility through modulating SOX2;LncRNA SOX2-OT positively regulated SOX2 expression in osteosarcoma cells and positively associated with SOX2 expression in osteosarcoma tissues. The rescued-function studies suggested that SOX2 is necessary for lncRNA SOX2-OT induced osteosarcoma cells migration, invasion, and expression of cancer stem cell biomarkers	28960757	RID00678	expression association	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	MEG3	ADH4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-664)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000198099	NA	55384	127	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ADH-2|HEL-S-4	Overexpression of Long Non-Coding RNA MEG3 Inhibits proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA-664;MEG3 over-expression imposes another level of post-transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR-664 target gene, ADH4, through competitive sponging miR-664;MEG3 overexpression inhibited the proliferation of HCC cells, at least in part by affecting miR-664 mediated regulation of ADH4.	28374914	RID00679	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Ovarian cancer	DLEU1	CDK1	positively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000170312	NA	10301	983	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	CDC2|CDC28A|P34CDC2	DLEU1 contributes to ovarian carcinoma tumourigenesis and development by interacting with miR-490-3p and altering CDK1 expression;Short interfering RNA silencing of DLEU1 produced opposite results, where qRT-PCR showed increased miR-490-3p expression;The dual-luciferase reporter assay revealed a direct interaction between DLEU1 and miR-490-3p;we suggest that through interaction with miR-490-3p, DLEU1 may influence the expression of CDK1, CCND1 and SMARCD1 protein, subsequently promoting the development and progression of EOC. MiR-490-3p plays a tumour suppressor role in epithelial ovarian cancer by targeting CDK1 regulation and influencing SMARCD1 and cyclin D1 (CCND1) expressions.	28598010	RID00680	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Colorectal cancer	PCAT1	MYC	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000136997	NA	100750225	4609	PCA1|PCAT-1	MRTL|MYCC|bHLHe39|c-Myc	Down regulation of the long non-coding RNA PCAT-1 induced growth arrest and apoptosis of colorectal cancer cells;Our study revealed a tumorigenic effect of lncRNA PCAT-1 in CRC cells, and this effect is partly dependent on the inhibition of c-myc	28855110	RID00681	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Malignant glioma	PWAR5	EZH2	interact	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-);cancer progression(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000279192	GRCh38_15:24985053-24988232	ENSG00000106462	NA	8123	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA PAR5 inhibits the proliferation and progression of glioma through interaction with EZH2;in vitro restoration of PAR5 expression inhibited human glioma cell proliferation, invasion and migration by binding to EZH2 and regulating oncogene expression	29048683	RID00682	interact with protein	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	SNHG15	VEGFA	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-153)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000112715	NA	285958	7422	C7orf40|Linc-Myo1g|MYO1GUT	MVCD1|VEGF|VPF	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis.According to the bioinformatic database (RNAhybrid), we predicted that SNHG15 may be associated with the miR-153 binding sites. Furthermore, dual-luciferase gene reporter assay proved that SNHG15 could bind to miR-153 at the predicted binding sites.miR-153 binds to the 3'-UTR of VEGFA and Cdc42.	29048682	RID00683	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Malignant glioma	SNHG15	CDC42	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-153)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000070831	NA	285958	998	C7orf40|Linc-Myo1g|MYO1GUT	CDC42Hs|G25K|TKS	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis	29048682	RID00684	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	AP000439.3	CCND1	positively-E	western blot;RNAi	downregulation	sequencing	GSE64590;TCGA	GSE64590.zip;BRCA.zip	cell cycle(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000261347	GRCh38_11:69467598-69469705	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Silencing one of most prominent lncRNA, AP000439.3, resulted in inhibition of cell cycle progression and proliferation. Further study revealed AP000439.3 can regulate expression of CCND1 through enhancing estrogen receptor induction of CCND1;Genome-wide study of ER-regulated lncRNAs shows AP000439.3 may function as a key regulator of cell cycle in breast cancer	29048636	RID00685	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	MIAT	ZEB1	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000148516	NA	440823	6935	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer;the knockdown of MIAT significantly downregulated the expression of the zinc finger E-box binding homeobox 1 (ZEB1), that was upregulation in NSCLC and that promoted cell invasion;we found that MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner;MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ZEB1 pathway	28843520	RID00686	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MT1DP	MT1F	positively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000205361	GRCh38_16:56643705-56644786	ENSG00000198417	NA	326343	4494	MTM	MT1	Decreased long non-coding RNA MTM contributes to gastric cancer cell migration and invasion via modulating MT1F;we found a positive correlation between the expression level of MTM and MT1F both in cell and tissue samples;MT1F overexpression decreased GC cell migration and invasion, while knockdown of MT1F restored cell migration and invasion in MTM-overexpressing GC cells, suggesting MT1F as a key target of MTM	29228617	RID00687	expression association	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)
Renal cell carcinoma	RP11-436H11.5	BCL2L2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-335-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000105618	GRCh38_5:124734618-124735175	ENSG00000129473	NA	NA	599	NA	BCL-W|BCL2-L-2|BCLW|PPP1R51	LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma;Luciferase reporter assay results demonstrated that lncRNA RP11-436H11.5 enhanced BCL-W expression by regulating miR-335-5p expression. LncRNA RP11-436H11.5 could function as a miR-335-5p decoy to derepress expression of BCL-W	29070041	RID00688	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Colorectal cancer	SNHG17	CDKN1C	negatively-E	RIP;ChIP;RNAi	upregulation	microarray	GSE21510	GSE21510.zip	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000129757	NA	388796	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long non-coding RNA SNHG17 is an unfavourable prognostic factor and promotes cell proliferation by epigenetically silencing P57 in colorectal cancer;Mechanistic studies revealed the capability of lncRNA SNHG17 to epigenetically suppress P57 by binding to enhancer of zeste homolog 2 (a key component of polycomb repressive complex 2) in CRC cells, and quantitative real-time polymerase chain reaction assays demonstrated that SNHG17 expression levels were inversely correlated with those of P57 in CRC tissues	28933484	RID00689	epigenetic regulation	prognosis	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	MALAT1	BCL2	positively-E	CRISPR;qRT-PCR;RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells;the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes (Bcl-2 and MMP-13).MALAT1 may suppress miR-125b by acting as a molecular sponge in bladder cancer. All together, these data suggest that the MALAT1-miR-125b-Bcl-2/MMP-13 axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	29151968	RID00690	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	MALAT1	MMP13	positively-E	CRISPR;qRT-PCR;RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137745	NA	378938	4322	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG3|MANDP1|MDST|MMP-13	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells;the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes (Bcl-2 and MMP-13).MALAT1 may suppress miR-125b by acting as a molecular sponge in bladder cancer. All together, these data suggest that the MALAT1-miR-125b-Bcl-2/MMP-13 axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	29151968	RID00691	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	UICLM	ZEB2	positively-E	IHC;RIP;luciferase reporter assay	upregulation	microarray	NA	NA	cell metastasis(+)	ceRNA(miR-215)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233392	GRCh38_2:240954617-240967451	ENSG00000169554	NA	NA	9839	NA	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA UICLM promotes colorectal cancer liver metastasis by acting as a ceRNA for microRNA-215 to regulate ZEB2 expression;Mechanistic investigations revealed that UICLM induced its biological effects by regulating ZEB2, as the oncogenesis facilitated by UICLM was inhibited by ZEB2 depletion	29187907	RID00692	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	Lnc-Myd88	MYD88	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:38103490-38122445	ENSG00000172936	NA	NA	4615	NA	MYD88D	Long non-coding RNA Myd88 promotes growth and metastasis in hepatocellular carcinoma via regulating Myd88 expression through H3K27 modification;we confirmed a new long non-coding RNA Myd88 aberrant upregulation in HCC located upstream of Myd88 and verified a positive regulation relationship between them indicating that Lnc-Myd88 might participate in the enhanced expression of Myd88 in HCC;ChIP assays demonstrated that Lnc-Myd88 might increase Myd88 expression through enhancing H3K27Ac in the promoter of Myd88 gene, thus resulting in the activation of both NF-kB and PI3K/AKT signal pathways	29022910	RID00693	epigenetic regulation	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	HULC	ATG7	negatively-F	RIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000197548	NA	728655	10533	HCCAT1|LINC00078|NCRNA00078	APG7-LIKE|APG7L|GSA7	The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma;our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1;RIP indicated that ATG7 interacted with HULC	29022892	RID00694	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	HULC	ITGB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000150093	NA	728655	3688	HCCAT1|LINC00078|NCRNA00078	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma;our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1;We found that ITGB1 siRNA co-transfection with HULC reversed the function of HULC in inducing ovarian cancer cell migration and invasive ability	29022892	RID00695	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Renal cell carcinoma	PVT1	MCL1	positively-E	western blot;RNAi	upregulation	qPCR;sequencing	TCGA	KIRC.zip	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000143384	NA	5820	4170	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Long noncoding RNA PVT1 inhibits renal cancer cell apoptosis by up-regulating Mcl-1. PVT1 knockdown promoted apoptosis, inhibited renal cancer cell proliferation, decreased Mcl-1, and increased cleaved caspase-3 and cleaved PARP. PVT1 increased Mcl-1 mRNA levels in renal cancer cells by promoting mRNA stability without influencing its transcription.	29254209	RID00696	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	CCAT1	ITPKB	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(-)	ceRNA(miR-410)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000143772	NA	100507056	3707	CARLO5|CARLo-5|onco-lncRNA-40	IP3-3KB|IP3K|IP3K-B|IP3KB|PIG37	Long noncoding RNA CCAT1 functions as a ceRNA to antagonize the effect of miR-410 on the down-regulation of ITPKB in human HCT-116 and HCT-8 cells;In summary, these data demonstrated that miR-410 could promote cell proliferation and reduce apoptosis by inhibiting ITPKB expression and the expression of lnc CCAT1 antagonized the effect of miR-410.	29190961	RID00697	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367,GSE41245)
Nasopharynx carcinoma	XIST	miR-29c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	radioresistance(-);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Downregulation of lncRNA X Inactive Specific Transcript (XIST) Suppresses Cell proliferation and Enhances Radiosensitivity by Upregulating mir-29c in Nasopharyngeal Carcinoma Cells;Knockdown of XIST and miR-29c overexpression both resulted in a dramatic suppression of cell proliferation, a marked enhancement of radiosensitivity, and an obvious increase of gamma-H2AX foci formation in NPC cells;Luciferase reporter assay and qRT-PCR analysis demonstrated that XIST interacts with miR-29c and negatively regulates its expression	28985197	RID00698	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Non-small cell lung cancer	SNHG20	CDKN1A	negatively-E	RIP;RNAi;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124762	NA	654434	1026	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA SNHG20 promotes non-small cell lung cancer cell proliferation and migration by epigenetically silencing of P21 expression;SNHG20 could interact with EZH2 (enhancer of zeste homolog 2), thereby repressing P21 expression	28981099	RID00699	epigenetic regulation	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	FOXC2-AS1	MMP2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-3182)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000087245	NA	103752587	4313	ODRUL	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA ODRUL Contributes to Osteosarcoma Progression through the miR-3182/MMP2 Axis;ODRUL knockdown significantly inhibits OS cell proliferation, migration, invasion, and tumor growth in vitro and in vivo by decreasing matrix metalloproteinase (MMP) expression;ODRUL could directly interact with miR-3182 and upregulate MMP2 expression via its competing endogenous RNA activity on miR-3182 at the posttranscriptional level.	28750740	RID00700	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Nasopharynx carcinoma	MALAT1	CAPNS1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000126247	NA	378938	826	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1/miR-124/Capn4 axis regulates proliferation, invasion and EMT in nasopharyngeal carcinoma cells; MALAT1 promoted proliferation, invasion and EMT of NPC cells through de-repressing Capn4 by sponging miR-124	28857668	RID00701	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Urinary bladder cancer	H19	DNMT3B	positively-E	luciferase reporter assay;IHC;IF;RNA pull-down assay;RIP	upregulation	qPCR;microarray	GSE89006	GSE89006.zip	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-29b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000088305	NA	283120	1789	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ICF|ICF1|M.HsaIIIB	lncRNA H19 regulates epithelial-mesenchymal transition and metastasis of bladder cancer by miR-29b-3p as competing endogenous RNA;Mechanistically, we proved that H19 could directly bind to miR-29b-3p (miR-29b) and derepress the expression of target DNMT3B;we demonstrated for the first time that H19 might function as ceRNA (competing endogenous RNA) for miR-29b-3p and relieve the suppression for DNMT3B, which led to EMT and metastasis of BC	28779971	RID00702	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	GAS5	FOXO1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell stemness(-);tumor malignant transformation(-)	ceRNA(miR-196a-5p)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Brain glioma	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150907	NA	60674	2308	NCRNA00030|SNHG2	FKH1|FKHR|FOXO1A	GAS5 suppresses malignancy of human glioma stem cells via a miR-196a-5p/FOXO1 feedback loop;We demonstrate that GAS5 suppresses GSC malignancy by binding to miR-196a-5p. miR-196a-5p, an onco-miRNA, stimulates GSC proliferation, migration, and invasion, in addition to reducing levels of apoptosis;miR-196a-5p specifically downregulates the expression of forkhead box protein O1 (FOXO1) by targeting its 3' untranslated region (3'-UTR);we also show that FOXO1 promotes GAS5 transcription, thus forminga positive feedback loop	28666797	RID00703	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	NEAT1	miR-613	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1 promotes cell proliferation and invasion in hepatocellular carcinoma by negative regulating miR-613 expression;we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression;lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1.miR-613 isa target of NEAT1 in HCC cells.	28783584	RID00704	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Hepatocellular carcinoma	GHET1	ATF1	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000123268	NA	102723099	466	lncRNA-GHET1	EWS-ATF1|FUS/ATF-1|TREB36	LncRNA GHET1 activated by H3K27 acetylation promotes cell tumorigenesis through regulating ATF1 in hepatocellular carcinoma;RNA pull-down assays supported that GHET1 could bind to ATF1 protein; overexpression of ATF1 almost completely reversed the GHET1 knockdown mediated inhibition on the proliferation, migration, invasion and EMT of HCC cells	28772210	RID00705	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Cholangiocarcinoma	PCAT1	WNT1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000125084	NA	100750225	7471	PCA1|PCAT-1	BMND16|INT1|OI15	Long noncoding RNA PCAT1 regulates extrahepatic cholangiocarcinoma progression via the Wnt/beta-catenin-signaling pathway;PCAT1 is a competing endogenous for microRNA (miR)-122, with bioinformatics analysis and luciferase-reporter assay results demonstrating that PCAT1 regulated WNT1 expression via miR-122;PCAT1 silencing inhibited ECC progression by reducing Wnt/beta-catenin signaling through miR-122 repression and WNT1 expression	28753454	RID00706	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Endometrial cancer	HOTAIR	BECN1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000126581	NA	100124700	8678	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ATG6|VPS30|beclin1	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00707	expression association	chemoresistance	NA	DOWN(NSCLC,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Endometrial cancer	HOTAIR	ABCB1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000085563	NA	100124700	5243	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00708	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Endometrial cancer	HOTAIR	ABCB4	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000005471	NA	100124700	5244	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00709	expression association	chemoresistance	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	DANCR	AXL	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell stemness(+)	ceRNA(miR-33a-5p)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000167601	NA	57291	558	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	ARK|JTK11|Tyro7|UFO	lncRNA DANCR promotes tumor progression and cancer stemness features in osteosarcoma by upregulating AXL via miR-33a-5p inhibition;pull-down assays and luciferase reporter assays indicated that DANCR upregulation expression of the receptor tyrosine kinase AXL by competitively binding to miR-33a-5p;DANCR increases CSCs function by upregulating AXL via competitively binding to miR-33a-5p, and this function is sequentially performed through the PI3K-Akt signaling pathway	28642170	RID00710	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE67939)
Non-small cell lung cancer	BLACAT1	miR-144	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	LINC00912|linc-UBC1|onco-lncRNA-30	NA	Long Noncoding RNA Bladder Cancer Associated Transcript 1 Promotes the proliferation, Migration, and Invasion of Nonsmall Cell Lung Cancer Through Sponging miR-144; Bioinformatics methods and luciferase reporter assay revealed the close link within miR-144 and BLACAT1 3'-untranslated region (UTR)	28885863	RID00711	ceRNA or sponge	NA	NA	NA
Malignant glioma	HOXA11-AS	miR-140-5p	negatively-F	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Long Noncoding RNA HOXA11-AS Functions as miRNA Sponge to Promote the Glioma tumorigenesis Through Targeting miR-140-5p;Bioinformatics prediction forecast that miR-140-5p directly targeted HOXA11-AS at 3'-UTR, which was confirmed by luciferase reporter assay;In vitro rescue experiment assays, miR-140-5p inhibitor transfection, could reverse the function of HOXA11-AS knockdown on the proliferation, cell cycle arrest, and apoptosis	28832185	RID00712	ceRNA or sponge	NA	NA	NA
Uveal melanoma	HOXA11-AS	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124762	NA	221883	1026	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID00713	epigenetic regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Uveal melanoma	HOXA11-AS	miR-124	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID00714	ceRNA or sponge	NA	NA	NA
Lung adenocarcinoma	CASC2	SOX4	negatively-E	RNAi	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000124766	NA	255082	6659	C10orf5	EVI16	Long noncoding RNA CASC2 inhibits metastasis and epithelial to mesenchymal transition of lung adenocarcinoma via suppressing SOX4;epithelial to mesenchymal transition (EMT) process of LAC cells and SOX4 expression was suppressed by upregulating CASC2	29131257	RID00715	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Gastric cancer	SNHG7	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000147883	NA	84973	1030	NCRNA00061	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of gastric cancer cells by repressing the P15 and P16 expression;Relative expression of SNHG7 is upregulation in gastric cancer tissues and cells, and partially contributes to the development and progression of gastric cancer through regulation of p15 and p16 expressions	29131253	RID00716	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Gastric cancer	SNHG7	CDKN2A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000147889	NA	84973	1029	NCRNA00061	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of gastric cancer cells by repressing the P15 and P16 expression;Relative expression of SNHG7 is upregulation in gastric cancer tissues and cells, and partially contributes to the development and progression of gastric cancer through regulation of p15 and p16 expressions	29131253	RID00717	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Gastric cancer	MEG3	TP53	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	lncRNA MEG3 inhibit proliferation and metastasis of gastric cancer via p53 signaling pathway;overexpression of lncRNA MEG3 could also increase the expression of p53	28975980	RID00718	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Multiple myeloma	MALAT1	HMGB1	positively-E	RIP	upregulation	qPCR	NA	NA	cell autophagy(+);apoptosis process(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	LncRNA MALAT-1 Elevates HMGB1 to Promote Autophagy Resulting in Inhibition of Tumor Cell Apoptosis in Multiple Myeloma; MALAT-1 knockdown facilitated the degradation of HMGB1 at the post-translational level via increase of the ubiquitination of HMGB1 in MM cells. MALAT-1 was shown to promote autophagy in MM through upregulation of HMGB1; LncRNA MALAT-1 increases the expression level of HMGB1 in MM thereby promotes autophagy resulting in the inhibition of apoptosis.	28295550	RID00719	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Pancreatic cancer	XIST	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-133a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000146648	NA	7503	1956	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LncRNA XIST Promotes Pancreatic Cancer proliferation Through miR-133a/EGFR;as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting;XIST was positively correlated with EGFR	28295543	RID00720	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	HAS2-AS1	HAS2	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;microarray	GSE84807	GSE84807.zip	epithelial to mesenchymal transition(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000248690	GRCh38_8:121639293-121994185	ENSG00000170961	NA	594842	3037	HAS2-AS|HAS2AS|HASNT|NCRNA00077	NA	Long noncoding RNA HAS2-AS1 mediates hypoxia-induced invasiveness of oral squamous cell carcinoma; the hypoxia-induced HAS2-AS1 expression is dependent on HIF-1alpha which directly binds to and activates the transcription of HAS2-AS1;HAS2-AS1 mediates hypoxia-induced epithelial mesenchymal transition of OSCC cells via stabilizing HAS2.	28485478	RID00721	expression association	NA	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Malignant glioma	MEG3	miR-93	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);PI3K/AKT signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 inhibits cell growth of gliomas by targeting miR-93 and inactivating PI3K/AKT pathway; miR-93 was predicted a direct target of lncRNA-MEG3 by bioinformatics analysis;Overexpressed MEG3 counteracted the role of miR-93 in facilitating proliferation and inhibiting apoptosis in U-251 cells	28791407	RID00722	ceRNA or sponge	NA	NA	NA
Non-small cell lung cancer	HOXA11-AS	SP1	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000185591	NA	221883	6667	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non-small cell lung cancer cells;HOXA11-AS functions as a competing endogenous RNA to regulate transcriptional factor Sp1 expression via sponging miR-124	29034803	RID00723	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG1	DNMT1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000130816	NA	23642	1786	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	LncRNA-SNHG1 contributes to gastric cancer cell proliferation by regulating DNMT1;LncRNA-SNHG1 accelerated the proliferation of gastric cancer cells obviously and increased the expression of DNMT1	28754593	RID00724	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	HAGLR	miR-147a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	HOXD-AS1 functions as an oncogenic ceRNA to promote NSCLC cell progression by sequestering miR-147a;We found that lncRNA HOXD-AS1 was specifically upregulation (P<0.001) in NSCLC tissues and promoted cancer cell growth by targeting miR-147a;The dual-luciferase reporter assay showed that HOXD-AS1 could negatively regulate the expression of miR-147a	29033588	RID00725	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	NA
Hepatocellular carcinoma	NNT-AS1	CDK6	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-363)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000105810	NA	100652772	1021	NA	MCPH12|PLSTIRE	Long noncoding RNA NNT-AS1 promotes hepatocellular carcinoma progression and metastasis through miR-363/CDK6 axis;Bioinformatics analysis and luciferase reporter assay validated that miR-363 targeted NNT-AS1 and CDK6 3'-UTR;NNT-AS1 competed with CDK6 for miR-363 binding and could increase CDK6 expression	29179477	RID00726	ceRNA or sponge	metastasis	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Lung cancer	IGFBP4-1	IGFBP4	negatively-E	RNAi	upregulation	qPCR	NA	NA	energy metabolic process(+);cancer progression(+)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_17:40439467-40439917	ENSG00000141753	NA	NA	3487	NA	BP-4|HT29-IGFBP|IBP4|IGFBP-4	Overexpression of lncRNA IGFBP4-1 reprograms energy metabolism to promote lung cancer progression;lnc-IGFBP4-1 was observed to negatively correlate with gene IGFBP4, and lower expression level of IGFPB4 was found after lnc-IGFBP4-1-overexpression was transfected into PC9 cells, higher expression level of IGFPB4 was also found after lnc-IGFBP4-1-downregulation was transfected into GLC-82 cells, which indicates that IGFBP4 may exert its targeting function regulated by lnc-IGFBP4-1	28946875	RID00727	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE55807)
Esophagus squamous cell carcinoma	HOTTIP	HOXA13	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-30b);histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells;harboring a miR-30b-binding site, HOTTIP as a molecular sponge mainly regulated miR-30b level in the nucleus and modulated the repression of HOXA13 mediated by miR-30b in the cytoplasm, resulting in the positive HOTTIP/HOXA13 correlation;HOTTIP upregulation snail1 by competitively binding miR-30b, subsequently promoting epithelial-mesenchymal transition (EMT) and invasion.HOTTIP recruits WDR5 to the HOXA13 promoter and activatesHOXA13 transcription.HOTTIP directly bound the adaptor protein WDR5 and drove histone H3 lysine 4 trimethylation and HOXA13 gene transcription in ESCC cells.	28534516	RID00728	ceRNA or sponge	metastasis	NA	UP(LIHC);DATA(GSE117623)
Cervical cancer	PVT1	miR-424	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA PVT1 Facilitates Cervical Cancer Progression via Negative Regulating of miR-424;lowered expression of miR-424 could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines. Our results reveal a tumor-promoting role for PVT1, acting as a competing endogenous RNA (ceRNA) or a molecular sponge in negatively modulating miR-424	28276314	RID00729	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Non-small cell lung cancer	GAS5	miR-135b	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Inhibits tumorigenesis and Enhances Radiosensitivity by Suppressing miR-135b Expression in Non-Small Cell Lung Cancer; Luciferase reporter assay confirmed that GAS5 could directly target miR-135b and negatively regulate its expression;GAS5 inhibits tumorigenesis and enhances radiosensitivity by suppressing miR-135b expression in NSCLC cells	28117028	RID00730	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Breast cancer	H19	CUL4A	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139842	NA	283120	8451	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway;we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down;we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression. CUL4A was greatly decreased by knockdown of H19 lncRNA in MCF-7/Dox1600/shH19 cells	29190892	RID00731	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	H19	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	doxorubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway;we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down;we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression	29190892	RID00732	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Osteosarcoma	PARTICL	WWOX	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000286532	GRCh38_2:85537462-85538666	ENSG00000186153	NA	100630918	51741	PARTICLE	D16S432E|EIEE28|FOR|FRA16D|HHCMA56|PRO0128|SCAR12|SDR41C1|WOX1	The long non-coding RNA PARTICLE is associated with WWOX and the absence of FRA16D breakage in osteosarcoma patients;PARTICLE over-expression ameliorated WWOX promoter activity in U2OS harboring FRA16D non-breakage;It can be concluded that the lncRNA PARTICLE influences the WWOX tumor suppressor and in the absence of WWOX FRA16D breakage, it is associated with OS metastasis-free survival	29152092	RID00733	expression association	metastasis,prognosis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842)
Nasopharynx carcinoma	PCAT7	ELF2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-134-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000231806	GRCh38_9:94555054-94603990	ENSG00000109381	NA	101928099	1998	PCAN-R2	EU32|NERF|NERF-1A|NERF-1B|NERF-1a,b|NERF-2	Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma;These results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p.CAT7 accelerates NPC cell growth partially by spongeing miR-134-5p, and then up-regulating ELF2.	28728844	RID00734	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	TUG1	CPEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-186)	regulation	NA	methotrexate	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000137449	NA	55000	132864	LINC00080|NCRNA00080|TI-227H	CPE-BP2|CPEB-2|hCPEB-2	TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis;bioinformatics analysis showed that miR-186 could directly bind to TUG1, suggesting TUG1 might worked as a ceRNA to sponge miR-186;our study also showed that CPEB2 was the direct target of miR-186 in colorectal cancer cells.	28302487	RID00735	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Liver cancer	HULC	HMGA2	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000149948	NA	728655	8091	HCCAT1|LINC00078|NCRNA00078	BABL|HMGI-C|HMGIC|LIPO|STQTL9	The long noncoding RNA HULC promotes liver cancer by increasing the expression of the HMGA2 oncogene via sequestration of the microRNA-186;microRNA-186 inhibited HMGA2 expression by targeting the 3'-untranslated region (3'-UTR) of HMGA2 mRNA;HULC acted as a competing noncoding RNA to sequester miR-186 and thereby relieved miR-186-mediated HMGA2 repression;We conclude that the long noncoding RNA HULC increases HMGA2 expression by sequestering miR-186 post-transcriptionally and thereby promotes liver cancer growth	28765279	RID00736	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	DPP10-AS1	TIMP3	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	microarray	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000235026	GRCh38_2:115126622-115161384	ENSG00000100234	NA	NA	7078	NA	HSMRK222|K222|K222TA2|SFD	Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3;BC032913 enhanced the mRNA and protein expression of TIMP3 and inhibited Wnt/beta-catenin pathway activity, thus suppressing CRC metastasis in vitro and in vivo;the obtained data show that BC032913 plays an inhibitory role in CRC aggression by upregulating TIMP3, followed by inactivation of the Wnt/beta-catenin pathway	28918047	RID00737	expression association	metastasis	NA	UP(SKCM);DATA(GSE38495)
Gastric cancer	TRERNA1	SNAI1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	as enhancer	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000124216	NA	100887755	6615	LINC00651|treRNA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition;we demonstrate that lncRNA TRERNA1 acts like an enhancer of SNAI1 to promote cell invasion and migration and to contribute to metastasis of gastric cancer (GC)	28918030	RID00738	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Gastric cancer	TRERNA1	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000039068	NA	100887755	999	LINC00651|treRNA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition. TRERNA1 functions as a scaffold to recruit EZH2 to epigenetically silence epithelial-mesenchymal transition marker CDH1 by H3K27me3 of its promoter region;our findings indicated that TRERNA1 serves as a critical effector in GC progression by regulating CDH1 at the transcription level	28918030	RID00739	epigenetic regulation	metastasis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Ovarian cancer	MALAT1	miR-200c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Noncoding RNA MALAT1 Functions as a Sponge of MiR-200c in Ovarian Cancer;bioinformatics analysis suggested that3'-UTR of lncRNA MALAT1 and miR-200c have a complementarity region;luciferase assays verified the existence of direct binding between miR-200c and lncRNA MALAT1;lncRNA MALAT1 is a oncogene in ovarian cancer, involved in the regulation of cell viability, migration and invasion abilities of ovarian cancer cells, which achieved its biological function by regulating miR-200c expression; miR-200c expression was significantly decreased in ovarian cancer, which is negatively correlated with MALAT1 expression	28899458	RID00740	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Hepatocellular carcinoma	MVIH	ARID1A	interact	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_10:78038556-78040701	ENSG00000117713	NA	NA	8289	NA	B120|BAF250|BAF250a|BM029|C1orf4|CSS2|ELD|MRD14|OSA1|P270|SMARCF1|hELD|hOSA1	ARID1A represses hepatocellular carcinoma cell proliferation and migration through lncRNA MVIH;we reveal that ARID1A interacts with lncRNA MVIH through some region(s) or domain(s) including ARID domain and C-terminal ARID1A protein binding domain;ARID1A upregulates its downstream target CDKN1A and suppresses HCC cell proliferation and migration through inhibiting MVIH	28716731	RID00741	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Osteosarcoma	XIST	CDKN1A	negatively-E	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000124762	NA	7503	1026	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21;mechanistic analysis revealed that Xist can repress P21 expression to regulate OS cell cycle and proliferation by binding to EZH2	29254174	RID00742	epigenetic regulation	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Malignant glioma	XIST	miR-29c	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	Genome Instability and Mutation	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with PS1, positively related with MGMT	28831025	RID00743	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Malignant glioma	XIST	SP1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	NA	association	NA	temozolomide	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000185591	NA	7503	6667	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with PS1, positively related with MGMT	28831025	RID00744	expression association	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	XIST	MGMT	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	NA	association	NA	temozolomide	NA	Genome Instability and Mutation	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000170430	NA	7503	4255	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with SP1, positively related with MGMT	28831025	RID00745	expression association	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	NEAT1	miR-128	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1 negatively regulates miR-218 expression and promotes breast cancer progression;NEAT1 promoted cell invasion and proliferation by negatively regulating miR-218 in breast cancer.miR-218 was shown to be a direct target of NEAT1 in breast cancer cells	28946559	RID00746	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Non-small cell lung cancer	GAS5	PTEN	positively-E	RIP;western blot;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-21)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	GAS5 knockdown reduces the chemo-sensitivity of non-small cell lung cancer (NSCLC) cell to cisplatin (DDP) through regulating miR-21/PTEN axis;GAS5 could compete with PTEN for miR-21 binding;We further verified that the interaction between GAS5 and miR-21 was required in the regulation of NSCLC chemo-sensitivity to DDP through PTEN pathway	28686971	RID00747	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Renal cell carcinoma	LncRNA-SARCC	miR-143-3p	negatively-E	RIP;ChIP;RNAi	downregulation	qPCR	NA	NA	cancer progression(-);chemoresistance(-)	transcriptional regulation	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENST00000460407	GRCh38_3:152834693-152841439	NA	NA	NA	NA	NA	NA	LncRNA-SARCC suppresses renal cell carcinoma (RCC) progression via altering the androgen receptor(AR)/miRNA-143-3p signals;LncRNA-SARCC bound and destabilized AR protein with an inhibition of AR function, which led to transcriptionally de-repress miR-143-3p expression, thus inhibition of its downstream signals including AKT, MMP-13, K-RAS and P-ERK.Notably, treating with Sunitinib, the multi-targeted receptor tyrosine kinase inhibitor, increased the expression of LncRNA-SARCC, which decreased RCC cells resistance to Sunitinib. AR could directly decrease miR-143-3p expression by binding to the potential androgen response elements (AREs) in its promoter.	28644440	RID00748	transcriptional regulation	chemoresistance	NA	NA
Non-small cell lung cancer	PVT1	MMP9	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-200a);ceRNA(miR-200b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000100985	NA	5820	4318	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CLG4B|GELB|MANDP2|MMP-9	lncRNA-PVT1 Facilitates Invasion Through Upregulation of MMP9 in Nonsmall Cell Lung Cancer Cell;Specifically, lncRNA-PVT1 directly interacted with miR-200a and miR-200b, which suppressed MMP9 expression;lncRNA-PVT1 functions as a competitive endogenous RNA to regulate MMP9 expression through competitively binding the common microRNAs, miR-200a and miR-200b	28731781	RID00749	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HCG11	IGF2BP1	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000159217	NA	493812	10642	CTA-14H9.3|bK14H9.3	CRD-BP|CRDBP|IMP-1|IMP1|VICKZ1|ZBP1	Modulation of IGF2BP1 by long non-coding RNA HCG11 suppresses apoptosis of hepatocellular carcinoma cells via MAPK signaling transduction;Knockdown of both indicators led to decreased cell viability, proliferation, and migration ability in HepG2 cells while the cell apoptosis and G1 cell cycle arrest were induced after knockdown of HCG11 and IGF2BP1; HCG11 exerted its effect on HCC via interaction with IGF2BP1, leading to activation of MAPK signaling, which eventually promoted the progression of HCC	28677801	RID00750	interact with protein	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Breast cancer	H19	DNMT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-152)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000130816	NA	283120	1786	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152;A negative correlation between H19 and miR-152 and positive correlation between H19 and DNMT1 mRNA were observed	28544374	RID00751	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	HOXA5	LINC00312	positively-E	ChIP;IHC	downregulation	qPCR;microarray	GSE10072;GSE19804;GSE66654	GSE10072.zip;GSE19804.zip;GSE66654.zip	cell proliferation(-);apoptosis process(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	TF	lncRNA	ENSG00000106004	NA	NA	GRCh38_3:8571782-8574668	3202	29931	HOX1|HOX1.3|HOX1C	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	Long non-coding RNA 00312 regulated by HOXA5 inhibits tumour proliferation and promotes apoptosis in Non-small cell lung cancer;we found that HOXA5 could bind in the promoter of linc00312 and up-regulated the expression of it.	28338293	RID00752	transcriptional regulation	NA	NA	NA
Esophagus squamous cell carcinoma	MALAT1	CKS1B	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	radioresistance(+)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000173207	NA	378938	1163	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 affects the efficacy of radiotherapy for esophageal squamous cell carcinoma by regulating Cks1 expression;MALAT1 acted as one positive regulator of the radioresistance of ESCC, at least partly due to its promotion on Cks1 expression;Cks1 expression was also downregulated by MALAT1 siRNA, while Cks1 siRNA strongly recovered MALAT1-induced radioresistance in vitro	27935117	RID00753	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Acute myeloid leukemia	H19	ID2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-19a);ceRNA(miR-19b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000115738	NA	283120	3398	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GIG8|ID2A|ID2H|bHLHb26	LncRNA H19 regulates ID2 expression through competitive binding to hsa-miR-19a/b in acute myelocytic leukemia;the results of the bioinformatic analysis revealed potential hsa-miR-19a/b-3p binding sites in lncRNA H19 and ID2;it was demonstrated that the knockdown of lncRNA H19 resulted in increased expression of hsa-microRNA (miR)-19a/b and decreased expression of inhibitor of DNA binding 2 (ID2) in AML cells;the results of the present study suggest that lncRNA H19 regulates the expression of ID2 through competitive binding to hsa-miR-19a and hsa-miR-19b, which may serve a role in AML cell proliferation	28765931	RID00754	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE55807)
Non-small cell lung cancer	RP11-713B9.1	CADM1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_11:115174977-115175324	ENSG00000182985	NA	NA	23705	NA	NA	Down-regulation of long noncoding RNA RP11-713B9.1 contributes to the cell viability in non-small cell lung cancer (NSCLC);the overexpression of RP11-713B9.1 resulted in significant upregulation of TSLC1 and inhibition of H460 cell viability, while the opposite effects were observed following the knockdown of RP11-713B9.1 in A549 cells	28765887	RID00755	expression association	NA	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Gastric cancer	TUG1	SOX4	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124766	NA	55000	6659	LINC00080|NCRNA00080|TI-227H	EVI16	MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4;the results of the current study indicate that the downregulation of miR-381 by lncRNA-TUG1 promoted the metastasis of GC cells by inhibiting SOX4	28927144	RID00756	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	HOTAIR	SLC2A1	positively-E	RIP;western blot;RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+);mTOR signaling pathway(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Evading Apoptosis;Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000117394	NA	100124700	6513	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling;HOTAIR promoted glycolysis by upregulating glucose transporter isoform 1 (GLUT1) and activating mammalian target of rapamycin (mTOR) signaling	28731193	RID00757	interact with protein	NA	NA	UP(PAAD,PRAD);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE67939)
Colorectal cancer	SNHG3	MYC	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	COAD.zip	cancer progression(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000136997	NA	8420	4609	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	MRTL|MYCC|bHLHe39|c-Myc	The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer;Mechanistic investigations demonstrated that SNHG3 functioned as a competing endogenous RNA (ceRNA) to 'sponge' miR-182-5p, thus leading to the release of c-Myc from miR-182-5p and modulating the expression of c-Myc;SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes	28731158	RID00758	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	PCAT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000124762	NA	100750225	1026	PCA1|PCAT-1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA PCAT-1 over-expression promotes proliferation and metastasis in gastric cancer cells through regulating CDKN1A;PCAT-1 knockdown through shRNA in AGS and MGC-803 cells inhibited cell proliferation, migration and invasion by regulating CDKN1A	28571676	RID00759	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	LOC90784	BAX	positively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000087088	NA	NA	581	NA	BCL2L4	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00760	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LOC90784	CDK4	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00761	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	LOC90784	CCND1	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00762	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	LOC90784	MMP2	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00763	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	LOC90784	MMP9	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00764	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HULC	COX2	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	cell growth(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	4513	HCCAT1|LINC00078|NCRNA00078	COII|MTCO2	lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein;HULC promoted the growth of HCC cells through elevating COX-2 protein;knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells	28634076	RID00765	interact with protein	NA	NA	NA
Colorectal cancer	XIST	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long noncoding RNA XIST expedites metastasis and modulates epithelial-mesenchymal transition in colorectal cancer.luciferase activity assay indicated that lncRNA XIST could bind directly with miR-200b-3p;knockdown of lncRNA XIST significantly reduced the expression of ZEB1, which was the direct target of miR-200b-3p, and the tumor suppressive effects caused by knockdown of lncRNA XIST could be rescued by re-expression of ZEB1 in CRC cells;our study demonstrated how lncRNA XIST regulates CRC progression and metastasis by competing for miR-200b-3p to modulate the expression of ZEB1	28837144	RID00766	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	ZEB1-AS1	ZEB1	positively-E	RIP;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long noncoding RNA ZEB1-AS1 epigenetically regulates the expressions of ZEB1 and downstream molecules in prostate cancer;we found that RNAi-mediated downregulation of ZEB1-AS1 induced significant ZEB1 inhibition while artificial overexpression of ZEB1-AS1 rescued ZEB1 expression, which means that ZEB1-AS1 promotes ZEB1 expression;ZEB1-AS1 bound and recruited histone methyltransferase MLL1 to the promoter region of ZEB1, induced H3K4me3 modification therein, and activated ZEB1 transcription;Biologically, ZEB1-AS1 promoted proliferation and migration of prostate cancer cells	28830551	RID00767	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	PVT1	HK2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+);cancer progression(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000159399	NA	5820	3099	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HKII|HXK2	Long non-coding RNA PVT1 promotes glycolysis and tumor progression by regulating miR-497/HK2 axis in osteosarcoma;PVT1 acted as molecular sponge to repress miR-497; HK2 was a direct target of miR-497 and overexpression of HK2 attenuated the suppressive effect of miR-497 on glycolysis;these findings suggested that PVT1 contributes to OS cell glucose metabolism, cell proliferation, and motility through the miR-497/HK2 pathway	28602700	RID00768	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	ABHD11-AS1	RHOC	positively-F	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000155366	NA	171022	389	LINC00035|NCRNA00035|WBSCR26	ARH9|ARHC|H9|RHOH9	Role of the lncRNA ABHD11-AS1 in the tumorigenesis and progression of epithelial ovarian cancer through targeted regulation of RhoC; Overexpression of ABHD11-AS1 upregulation the expression of RhoC and its downstream molecules P70s6k, MMP2 and BCL-xL; lncRNA ABHD11-AS1 could directly combine with RhoC; RhoC is a direct target of the lncRNA ABHD11-AS1.	28818073	RID00769	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Liver cancer	HAGLR	SOX4	positively-E	RIP;RNA pull-down assay;ChIP	upregulation	qPCR;microarray	GSE84402	GSE84402.zip	cell metastasis(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000124766	NA	401022	6659	HOXD-AS1|MIR7704HG|Mdgt	EVI16	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4;STAT3 could specifically interact with the promoter of HOXD-AS1 and activate HOXD-AS1 transcription;Overexpression of HOXD-AS1 competitively bound to miR-130a-3p that prevented SOX4 from miRNA-mediated degradation, thus activated the expression of EZH2 and MMP2 and facilitated HCC metastasis	28810927	RID00770	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Liver cancer	STAT3	HAGLR	positively-E	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE84402	GSE84402.zip	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000224189	GRCh38_2:176164051-176188958	6774	401022	ADMIO|ADMIO1|APRF|HIES	HOXD-AS1|MIR7704HG|Mdgt	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4;STAT3 could specifically interact with the promoter of HOXD-AS1 and activate HOXD-AS1 transcription.HOXD-AS1 is regulated by the transcriptional factor STAT3, it significantly upregulation in HCC and can be used as a prognosis biomarker for HCC patients. HOXD-AS1 functions as a ceRNA that competitively binds to miR-130a-3p, then upregulates SOX4 and promotes HCC cell metastasis.	28810927	RID00771	transcriptional regulation	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Colorectal cancer	CRNDE	DUSP5	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE21510	GSE21510.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000138166	NA	NA	1847	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	DUSP|HVH3	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID00772	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	CRNDE	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE21511	GSE21511.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000124762	NA	NA	1026	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID00773	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Malignant glioma	LINC00461	TOP2A	positively-E	starBase;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-411-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000131747	NA	645323	7153	NA	TOP2|TP2A	Oncogenic effects of evolutionarily conserved noncoding RNA ECONEXIN on gliomagenesis. Functional analysis of ECONEXIN in glioma cell lines, U87 and U251, showed it was dominantly located in the cytoplasm and interacted with miR-411-5p via two binding sites within ECONEXIN;Inhibition of ECONEXIN upregulation miR-411-5p together with the downregulation of its target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, resulting in decreased cell proliferation;Our data demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in glioma	28368417	RID00774	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Gastric cancer	XIAP-AS1	XIAP	positively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000237331	GRCh38_X:123872626-123873932	ENSG00000101966	NA	106480735	331	NA	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	The long noncoding RNA XIAP-AS1 promotes XIAP transcription by XIAP-AS1 interacting with Sp1 in gastric cancer cells;XIAP-AS1 knockdown promoted tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in gastric tumor cells, as cleaved caspase-3 and caspase-9 was detected;tumor cell proliferation was inhibited by XIAP-AS1 knockdown in response to TRAIL administration; XIAP-AS1 is a potential target for TRAIL-induced apoptosis in gastric cancer cells	28792527	RID00775	transcriptional regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	LINC0086	miR-214	negatively-F	luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000178947	GRCh38_X:135421943-135428074	NA	NA	NA	NA	NA	NA	Long Noncoding RNA LINC0086 Functions as a Tumor Suppressor in Nasopharyngeal Carcinoma by Targeting miR-214;upregulation of LINC0086 dramatically decreased the expression of miR-214, an oncogene in several cancers, in C666-1 and HK-1 cells;An miR-214 binding site was found in the 3'-UTR of LINC0086;the suppressive effects of LINC0086 on NPC cell growth were reversed by overexpression of miR-214 in vitro and in vivo	28245169	RID00776	ceRNA or sponge	NA	NA	NA
Oral squamous cell carcinoma	LINC00668	VEGFA	positively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-297)	regulation	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000112715	NA	400643	7422	NA	MVCD1|VEGF|VPF	Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma;Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression	28564590	RID00777	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Non-small cell lung cancer	H19	miR-21	negatively-F	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Association of long non-coding RNA H19 and microRNA-21 expression with the biological features and prognosis of non-small cell lung cancer;Increased expression of H19 and miR-21 was positively correlated with advanced tumor-node-metastasis stage and tumor size;H19 and miR-21 interact in the regulation of NSCLC, and with greater expression of both H19 and miR-21, overall survival decreased	(<ce><de><U+02B5><d1><e9><U+05A4><U+02B5>)28799568	RID00778	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	NA
Peripheral primitive neuroectodermal tumor	MYC	MALAT1	positively-E	ChIP	upregulation	qPCR;microarray	GSE93677	GSE93677.zip	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Sarcoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000251562	GRCh38_11:65497688-65506516	4609	378938	MRTL|MYCC|bHLHe39|c-Myc	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Identification of a Novel SYK/c-MYC/MALAT1 Signaling Pathway and Its Potential Therapeutic Value in Ewing Sarcoma. Ectopic expression of SYK rescued the cytotoxicity triggered by SYK-depletion associated with the reactivation of both AKT and MYC; MALAT1, was identified to be dependent on SYK-mediated signaling;c-MYC, a SYK-promoted gene, bound to the promoter of MALAT1 and transcriptionally activated MALAT1, which further promoted the proliferation of EWS cells	28336564	RID00779	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	HOXA11-AS	LATS1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000131023	NA	221883	9113	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	WARTS|wts	Promotion of LncRNA HOXA11-AS on the proliferation of hepatocellular carcinoma by regulating the expression of LATS1;RIP and CHIP experiments showed that HOXA11-AS inhibited the expression of LATS1 genes by binding enhancer of zeste homolog 2 (EZH2) proteins	28829501	RID00780	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thyroid cancer	H19	let-7a	negatively-E	bioinformatics	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Effects of long non-coding RNA H19 and microRNA let7a expression on thyroid cancer prognosis;This study demonstrated that increased lncRNA H19 and decreased miRNA let7a expression levels are associated with poor prognosis in TC patients. An inverse relationship between lncRNA H19 and miRNA let7a expression levels was exhibited	28655518	RID00781	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	NA
Epithelial ovarian cancer	ERLNC1	CDK4	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000135446	NA	101929441	1019	ElncRNA1|TC0101441	CMM3|PSK-J3	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00782	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Epithelial ovarian cancer	ERLNC1	CDK6	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000105810	NA	101929441	1021	ElncRNA1|TC0101441	MCPH12|PLSTIRE	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00783	expression association	NA	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Epithelial ovarian cancer	ERLNC1	CCND1	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000110092	NA	101929441	595	ElncRNA1|TC0101441	BCL1|D11S287E|PRAD1|U21B31	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00784	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	HNF1A-AS1	SOX4	positively-E	bioinformatics;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-214)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000124766	NA	283460	6659	C12orf27|HAS1|NCRNA00262	EVI16	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4;The result of luciferase activity assay showed that luciferase activity was strongly weakened by the combination of LncR-HAS1 WT and miR-214 mimic;the expression of SOX-4, a predicted target gene of miR-214, was suppressed by HAS1-siRNA and was increased by miR-214 inhibitor	28656277	RID00785	ceRNA or sponge	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Osteosarcoma	ZEB1-AS1	miR-200s	negatively-F	western blot;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000237036	GRCh38_10:31206278-31320447	NA	NA	220930	NA	NA	NA	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell proliferation and Migration;Our results showed that ZEB1-AS1 functions as a molecular sponge for miR-200s and relieves the inhibition of ZEB1 caused by miR-200s;Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration	28075045	RID00786	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	NA
Cervical cancer	PVT1	miR-195	negatively-E	western blot;RNA pull-down assay;RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(-)	histone modification;sponge	regulation	NA	paclitaxel	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells;PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195;PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region;PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells;Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX;Based on these findings, we infer that PVT1 could decrease miR-195 expression via enhancing histone H3K27me3 in the miR-195 promoter region and also via direct sponging of miR-195	28296507	RID00787	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Malignant glioma	MALAT1	RAP1B	positively-E	Targetscan;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-101)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127314	NA	378938	5908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	K-REV|RAL1B	Long non-coding RNA MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101;MALAT1 and Rap1B knockdown could inhibit proliferation and induce apoptosis of glioma cells;MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. Rap1B is a target of miR-101.	28551849	RID00788	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE38495,GSE55807)
Colorectal cancer	LL22NC03-N64E9.1	KLF2	negatively-E	RIP;western blot;ChIP	upregulation	qPCR;microarray;sequencing	TCGA;GSE9348;GSE41328	COAD.zip;GSE9348.zip;GSE41328.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_22:15796959-15798346	ENSG00000127528	NA	NA	10365	NA	LKLF	A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer; Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2;We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2.	28938648	RID00789	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	FER1L4	miR-106a-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	prognosis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	C20orf124	NA	Long non-coding RNA Fer-1-like protein 4 acts as a tumor suppressor via miR-106a-5p and predicts good prognosis in hepatocellular carcinoma;We found that down-regulated FER1L4 increased the expression of miR-106a-5p significantly and there was a reciprocal repression between FER1L4 and miR-106a-5p;we identified FER1L4 as a target of miR-106a-5p by using dual-luciferase reporter assay; FER1L4, as well as miR-106a-5p, can predict the clinical prognosis of HCC alone or combined.	28759956	RID00790	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	NA
Hepatocellular carcinoma	HAGLR	ARHGAP11A	positively-E	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	ceRNA(miR-19a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000198826	NA	401022	9824	HOXD-AS1|MIR7704HG|Mdgt	GAP (1-12)	The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma. we identified that HOXD-AS1 upregulation the Rho GTPase activating protein 11A (ARHGAP11A) by competitively binding to microRNA-19a (miR19a), resulting in induced metastasis	28724429	RID00791	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE67939)
Hepatocellular carcinoma	HAGLR	RGS3	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000138835	NA	401022	5998	HOXD-AS1|MIR7704HG|Mdgt	C2PA|RGP3	The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma.the regulator of G-protein signaling 3 (RGS3), a potential inhibitor of the MEK-ERK1/2 signaling axis, was also found to be downregulated by ectopic HOXD-AS1 overexpression, leading to a remarkably reduced apoptotic effect.	28724429	RID00792	expression association	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Osteosarcoma	SNHG15	miR-141	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell autophagy(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983023-44986961	NA	NA	285958	NA	C7orf40|Linc-Myo1g|MYO1GUT	NA	LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141;SNHG15 knockdown and miR-141 overexpression significantly suppressed cell proliferation, invasion, migration and autophagy while SNHG15 overexpression and miR-141 repression exhibited the opposite effects on OS cells;SNHG15 could directly interact with miR-141 and regulate its expression;Our data showed that SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141	28720111	RID00793	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	NA
Hepatocellular carcinoma	CPS1-IT1	HIF1A	negatively-E	RNAi	downregulation	qPCR;sequencing	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000100644	NA	29034	3091	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Melatonin suppresses hepatocellular carcinoma progression via lncRNA-CPS1-IT-mediated HIF-1alpha inactivation;We observed that melatonin significantly inhibited the proliferation, migration, and invasion of HCC cells and significantly induced the expression of the transcription factor FOXA2 in HCC cells. This increase in FOXA2 expression resulted in upregulation of lncRNA-CPS1 intronic transcript 1 (CPS1-IT1), which reduced HIF-1alpha activity and consequently resulted in the suppression of epithelial-mesenchymal transition (EMT) progression and HCC metastasis.	29137263	RID00794	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gallbladder cancer	UCA1	CDKN1A	negatively-E	western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID00795	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gallbladder cancer	UCA1	CDH1	negatively-E	western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000039068	NA	652995	999	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID00796	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	MALAT1	EZH2	interact	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID00797	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	AB073614	SOX7	negatively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	NA	GRCh38_3:149173591-149175492	ENSG00000171056	NA	NA	83595	NA	NA	Long noncoding RNA AB073614 promotes the malignance of glioma by activating Wnt/beta-catenin signaling through downregulating SOX7;The level of AB073614 was found to correlate inversely with sex-determining region Y-box 7 (SOX7) expression but correlate positively with Wnt/beta-catenin signaling activity;the results indicated that AB073614 induced Wnt/beta-catenin signaling activity by repressing SOX7 expression;the findings demonstrated that AB073614 promoted the progression of glioma by targeting SOX7 to activate the Wnt/beta-catenin signaling pathway	29029454	RID00798	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	LINC00673	miR-150-5p	negatively-F	miRanda;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72403322-72592804	NA	NA	100499467	NA	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p;Overexpression of miR-150-5p suppressed lin00673's expression while inhibition of miR-150-5p led to significant upregulation of lin00673, suggesting that linc00673 could be negatively regulated by miR-150-5p, which was further confirmed by the inverse correlation between linc00673 and miR-150-5p in NSCLC patients' specimen;miR-150-5p could directly target linc00673 through luciferase assay, so linc00673 could sponge miR-150-5p and modulate the expression of a key EMT regulator ZEB1 indirectly;miR-150-5p inhibition abrogated linc00673 silence mediated proliferation, migration, invasion and EMT suppressing effect	28697764	RID00799	ceRNA or sponge	NA	NA	NA
Breast cancer	HOXA-AS2	miR-520c-3p	negatively-F	starBase;OncomiRDB;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000253552	GRCh38_7:27107777-27134302	NA	NA	285943	NA	HOXA3as	NA	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge;microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells.	28545023	RID00800	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Gastric cancer	TINCR	PDK1	negatively-E	RNAi;luciferase reporter assay;RNAhybrid	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-375)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000152256	NA	257000	5163	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	NA	The long noncoding RNA, TINCR, functions as a competing endogenous RNA to regulate PDK1 expression by sponging miR-375 in gastric cancer;the low expression of TINCR increased cell apoptosis and inhibited the proliferation of GC cells, while the downregulation of miR-375 reversed the function;TINCR could negatively regulate the miR-375 expression and increased the PDK1 expression in GC cells. The ceRNA regulatory network of TINCR/miR-375/PDK1 allows us to better understand the pathogenesis of GC and facilitate the development of long noncoding RNA (lncRNA)-directed diagnostics in GC.	28744139	RID00801	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Osteosarcoma	ANCR	CDKN1A	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000124762	NA	282	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID00802	epigenetic regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	ANCR	CDKN1B	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000111276	NA	282	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID00803	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	GAS5	miR-23a	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Suppresses tumorigenesis by Inhibiting miR-23a Expression in Non-Small Cell Lung Cancer;Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a and reversely regulated its expression;miR-23a overexpression significantly abolished GAS5 overexpression-induced inhibition of proliferation and invasion, as well as promotion of apoptosis in NSCLC cells	28059053	RID00804	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Bladder urothelial carcinoma	CCEPR	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_10:59173963-59176464	ENSG00000132646	NA	105682749	5111	CCHE1|lncRNA-CCHE1	ATLD2	Increased expression of long non-coding RNA CCEPR is associated with poor prognosis and promotes tumorigenesis in urothelial bladder carcinoma. we found CCEPR upregulates the expression of PCNA in mRNA and protein level to promote cancer growth.	28574830	RID00805	expression association	prognosis	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Cervical cancer	RSU1P2	MYC	positively-E	RegRNA;Targetscan;PicTar;RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(let-7a)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000232554	GRCh38_10:45099487-45154606	ENSG00000136997	NA	100133308	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells;We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a;The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity	27487126	RID00806	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	lnc-Sox5	IDO1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cytotoxicity(-)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000115934	GRCh38_12:23181334-23251499	ENSG00000131203	NA	NA	3620	NA	IDO|IDO-1|INDO	Long noncoding RNA lnc-sox5 modulates CRC tumorigenesis by unbalancing tumor microenvironment. Our results also showed that the expression of indoleamine 2,3-dioxygenase 1 (IDO1) was significantly reduced by lnc-sox5 knock-down and therefore modulated the infiltration and cytotoxicity of CD3+CD8+T cells	28632999	RID00807	expression association	NA	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	TUG1	miR-145	negatively-F	western blot;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA TUG1 influences papillary thyroid cancer cell proliferation, migration and EMT formation through targeting miR-145;These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145, and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells	28645161	RID00808	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	MIR4435-2HG	YBX1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111036776-111523376	ENSG00000065978	NA	541471	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker;Mechanistically, lncRNA-AWPPH interacts with YBX1, promotes YBX1-mediated activation of SNAIL1 translation, and upregulates SNAIL1 expression;Furthermore, lncRNA-AWPPH promotes YBX1-mediated activation of PIK3CA transcription, upregulates PIK3CA expression, and activates PI3K/AKT pathway.this study identifies a novel lncRNA termed lncRNA-AWPPH which is highly expressed in HCC, indicates poor prognosis of HCC patients, and promotes HCC cell proliferation, migration, and in vivo tumor growth and metastasis via a novel regulatory mechanism of interacting with YBX1	28428004	RID00809	interact with protein	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	CCAT2	CDKN2B	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000147883	NA	101805488	1030	LINC00873|NCCP1	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer;we confirmed that CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells	28531944	RID00810	epigenetic regulation	NA	NA	UP(LIHC);DATA(GSE117623)
Breast cancer	MEG3	CDH1	positively-E	western blot;RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-421)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer;We further revealed that endogenous miR-421 expression was negatively regulated by MEG3 in breast cancer cells and MEG3 regulated E-cadherin expression by sponging to miR-421 in breast cancer cells	28463794	RID00811	ceRNA or sponge	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Nasopharynx carcinoma	HULC	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000141510	NA	728655	7157	HCCAT1|LINC00078|NCRNA00078	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA Highly upregulation in Liver Cancer Activates p53-p21 Pathway and Promotes Nasopharyngeal Carcinoma Cell Growth. Downregulation of HULC activated p53 and induced the increased expression of p21, which finally caused cell cycle arrest and cell apoptosis	28445086	RID00812	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	HULC	CDKN1A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124762	NA	728655	1026	HCCAT1|LINC00078|NCRNA00078	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA Highly upregulation in Liver Cancer Activates p53-p21 Pathway and Promotes Nasopharyngeal Carcinoma Cell Growth. Downregulation of HULC activated p53 and induced the increased expression of p21, which finally caused cell cycle arrest and cell apoptosis	28445086	RID00813	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Epithelial ovarian cancer	MALAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA MALAT1 promotes proliferation and metastasis in epithelial ovarian cancer via the PI3K-AKT pathway. silencing of MALAT1 hindered the expression of epithelial-to-mesenchymal transition (EMT)-related genes and MMPS. The evidence showed that MALAT1 induce EMT via PI3K/AKT pathway; Moreover, matrix metalloproteases (MMPs) such as MMP2 and MMP9, which are involved in migration/invasion, were also reduced.	28770968	RID00814	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Epithelial ovarian cancer	MALAT1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	LncRNA MALAT1 promotes proliferation and metastasis in epithelial ovarian cancer via the PI3K-AKT pathway. silencing of MALAT1 hindered the expression of epithelial-to-mesenchymal transition (EMT)-related genes and MMPS. The evidence showed that MALAT1 induce EMT via PI3K/AKT pathway; Moreover, matrix metalloproteases (MMPs) such as MMP2 and MMP9, which are involved in migration/invasion, were also reduced.	28770968	RID00815	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
T-cell lymphoblastic lymphoma	MEG3	AIFM2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-214)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Lymphoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000042286	NA	55384	84883	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AMID|PRG3	The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma;Luciferase activity assay further confirmed the targeting relationship between MEG3 and miR-214;AIFM2 protein was predicted as a target of miR-214;The expression of AIFM2 was increased by MEG3 and was downregulated by miR-214 mimic	28534937	RID00816	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Nasopharynx carcinoma	CDKN2B-AS1	let-7a	negatively-F	starBase;RNAhybrid;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);tumorigenesis(+);cytotoxicity(-)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Tumor Promoting Inflammation	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL represses tumorigenicity and enhances cisplatin-induced cytotoxicity via regulating microRNA let-7a in nasopharyngeal carcinoma;Luciferase assay revealed that ANRIL could negatively regulate miR-let-7a expression;ANRIL directly interacts with let-7a and regulates its expression. these data indicated that knockdown of ANRIL represses tumorigenicity and enhances DDP-induced cytotoxicity via regulating microRNA let-7a in NPC cells.In this study,the main purpose of this study was to investigate the role of ANRIL in NPC tumorigenesis,the association between ANRIL and cisplatin sensitivity and their underlying mechanism in NPC.	28117929	RID00817	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	NA
Malignant glioma	CASC2	miR-181a	negatively-F	RNAi;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	chemoresistance(-);cell growth(-)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway;CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ;CASC2 could inhibit the miR-181a expression by direct targeting in TMZ-resistant glioma cells. Results showed that CASC2 was inversely correlated with miR-181a, positively correlated with PTEN; miR-181a was inversely related with PTEN	28121023	RID00818	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Malignant glioma	CASC2	PTEN	positively-E	RNAi;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	chemoresistance(-);cell growth(-)	ceRNA(miR-181a)	regulation	NA	temozolomide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway;CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ;CASC2 could inhibit the miR-181a expression by direct targeting in TMZ-resistant glioma cells. Results showed that CASC2 was inversely correlated with miR-181a, positively correlated with PTEN; miR-181a was inversely related with PTEN	28121023	RID00819	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Esophagus squamous cell carcinoma	MEG3	CDH1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay;	downregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer. MEG3 acts as a ceRNA to regulate expression of E-cadherin and FOXO1 by competitively binding miR-9 and may be used as a potential biomarker in predicting ESCC patients' progression and prognosis	28539329	RID00820	ceRNA or sponge	prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	MEG3	FOXO1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay;	downregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150907	NA	55384	2308	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	FKH1|FKHR|FOXO1A	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer. MEG3 acts as a ceRNA to regulate expression of E-cadherin and FOXO1 by competitively binding miR-9 and may be used as a potential biomarker in predicting ESCC patients' progression and prognosis	28539329	RID00821	ceRNA or sponge	prognosis	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Prostate cancer	GAS5	CDKN1B	positively-E	RIP;western blot;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000111276	NA	60674	1027	NCRNA00030|SNHG2	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA GAS5 Inhibits Cellular proliferation by Targeting P27Kip1;Subsequent analysis demonstrated that P27Kip1, a known regulator of cell cycle, was positively regulated by GAS5 and upregulation of GAS5 increased its promoter activity	28396462	RID00822	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	XLOC_006390	KMT5A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27187247-27192686	ENSG00000183955	NA	NA	387893	NA	NA	Long non-coding RNA XLOC_006390 promotes cervical cancer proliferation and metastasis through the regulation of SET domain containing 8;SET8 was also increased in cervical cancer tissues and its expression was positively associated with XLOC_006390, and XLOC_006390 regulated SET8 expression;lncRNA XLOC_006390 promotes cervical cancer cell growth and metastasis through the regulation of SET8.	28534991	RID00823	expression association	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	RP11-169D4.1	CDH1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	PCG	NA	GRCh38_11:72570660-72573229	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Functional significance of the long non-coding RNA RP11-169D4.1 as a metastasis suppressor in laryngeal squamous cell carcinoma by regulating CDH1;We further verified that miR-205-5p had binding sites with RP11 169D4.1 and that RP11-169D4.1 could regulate the expression of CDH1.a positive correlation between the expression of RP11-169D4.1 and CDH1.	28534968	RID00824	expression association	metastasis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	SPRY4-IT1	miR-101-3p	negatively-F	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	NA	GRCh38_5:142317636-142318322	NA	NA	100642175	NA	SPRIGHTLY	NA	Long non-coding RNA SPRY4-IT1 promotes proliferation and invasion by acting as a ceRNA of miR-101-3p in colorectal cancer cells;SPRY4-IT1 could negatively regulate the expression of miR-101-3p in colorectal carcinoma cells. The bioinformatics prediction revealed putative miR-101-3p binding sites within SPRY4-IT1 transcripts	28720069	RID00825	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	NA
Thyroid cancer	LINC00312	PI3K	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);PI3K/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	Long Noncoding RNA LINC003121 Inhibits proliferation and Invasion of Thyroid Cancer Cells by Suppression of the Phosphatidylinositol-3-Kinase (PI3K)/Akt Signaling Pathway;LINC00312-mediated tumor suppression in TC cells may occur via suppression of activation of the PI3K/Akt signaling pathway and expression of MMP-9, and the role of MMP-9 expression induced by overexpressed LINC00312 or si-LINC00312 could be weakened by LY294002 (PI3K inhibitor). Results revealed that overexpression of LINC00312 significantly decreased the expressions of PI3K and p-Akt (both P<0.05), low expression of LINC00312 significantly increased the expressions of PI3K and p-Akt (both P<0.05)	29969438	RID00826	expression association	NA	NA	NA
Thyroid cancer	LINC00312	AKT1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);PI4K/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	ENSG00000142208	NA	29931	207	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Noncoding RNA LINC003121 Inhibits proliferation and Invasion of Thyroid Cancer Cells by Suppression of the Phosphatidylinositol-3-Kinase (PI3K)/Akt Signaling Pathway;LINC00312-mediated tumor suppression in TC cells may occur via suppression of activation of the PI3K/Akt signaling pathway and expression of MMP-9, and the role of MMP-9 expression induced by overexpressed LINC00312 or si-LINC00312 could be weakened by LY294002 (PI3K inhibitor). Results revealed that overexpression of LINC00312 significantly decreased the expressions of PI3K and p-Akt (both P<0.05), low expression of LINC00312 significantly increased the expressions of PI3K and p-Akt (both P<0.05)	29969438	RID00827	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	JMJD6	HOTAIR	positively-E	luciferase reporter assay;ChIP;electromobility shift assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000070495	NA	ENSG00000228630	GRCh38_12:53962308-53974956	23210	100124700	PSR|PTDSR|PTDSR1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	JMJD6 induces HOTAIR, an oncogenic lincRNA, by physically interacting with its proximal promoter;In ChIP assays, JMJD6 bound this region suggesting that JMJD6 may be directly recruited to the HOTAIR promoter;concurrent high expression of both genes correlated with poor survival when individual expression of either gene showed no significant association in TCGA datasets. We propose that high JMJD6 expression may achieve higher levels of HOTAIR in breast tumors. Further, since high levels of HOTAIR promote metastasis and death, blocking JMJD6 may be useful in preventing such events.	29229759	RID00828	transcriptional regulation	metastasis	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)	NA
Colon cancer	LINC00261	CTNNB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000168036	NA	140828	1499	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy. LINC00261 might down-regulate nuclear beta-catenin through restraining beta-catenin from cytoplasm into nuclei or it could also promote beta-catenin degradation and inhibit activation of Wnt pathway;LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight	29267503	RID00829	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	TUG1	CCND1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000110092	NA	55000	595	LINC00080|NCRNA00080|TI-227H	BCL1|D11S287E|PRAD1|U21B31	Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer;In vitro experiments revealed that TUG1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells, while TUG1 knockdown caused increased cell growth via promoting cell cycle progression and regulating the expression of CCND1 and CDK4	28950664	RID00830	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	TUG1	CDK4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000135446	NA	55000	1019	LINC00080|NCRNA00080|TI-227H	CMM3|PSK-J3	Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer;In vitro experiments revealed that TUG1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells, while TUG1 knockdown caused increased cell growth via promoting cell cycle progression and regulating the expression of CCND1 and CDK4	28950664	RID00831	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	MIR100HG	miR-100	positively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	host	regulation	NA	cetuximab	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00832	expression association	chemoresistance	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	NA
Colorectal cancer	MIR100HG	miR-125b	positively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	host	regulation	NA	cetuximab	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00833	expression association	chemoresistance	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	NA
Colorectal cancer	GATA6	MIR100HG	negatively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	transcriptional regulation	regulation	protein-DNA	cetuximab	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000141448	NA	ENSG00000255248	GRCh38_11:122028325-122556721	2627	399959	NA	AGD1|linc-NeD125|lncRNA-N2	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00834	transcriptional regulation	chemoresistance	UP(BRCA);DATA(GSE109761,GSE111065)	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)
Hepatocellular carcinoma	miR-215	PCAT1	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	100750225	NA	PCA1|PCAT-1	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma;We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays;We also found that post-transcriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 up-regulated PCAT-1 expression and promoted cell viability.Of note, gene profiling assays suggested that the kinase CRK-like proto-oncogene, adaptor protein (CRKL), is a potential downstream target of the miR-215-PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation.	28887306	RID00835	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	PCAT1	CRKL	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000099942	NA	100750225	1399	PCA1|PCAT-1	NA	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma;We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays;We also found that post-transcriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 up-regulated PCAT-1 expression and promoted cell viability.Of note, gene profiling assays suggested that the kinase CRK-like proto-oncogene, adaptor protein (CRKL), is a potential downstream target of the miR-215-PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation.	28887306	RID00836	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	LINC-ROR	DUSP7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000164086	NA	100885779	1849	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MKPX|PYST2	Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer;linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation;Taken together, these results suggest that linc-RoR promotes estrogen-independent growth and activation of MAPK/ERK pathway of breast cancer cells by regulating the ERK-specific phosphatase DUSP7	29041978	RID00837	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	FILNC1	MYC	positively-E	western blot;RNA pull-down assay	upregulation	qPCR;sequencing	TCGA	KIRC.zip	energy metabolic process(-)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Kidney cancer	lncRNA	TF	ENSG00000231426	GRCh38_6:139677639-139860476	ENSG00000136997	NA	100132735	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Energy stress-induced lncRNA FILNC1 represses c-Myc-mediated energy metabolism and inhibits renal tumor development;We show that FILNC1 deficiency leads to enhanced glucose uptake and lactate production through upregulation of c-Myc;Upon energy stress, FILNC1 interacts with AUF1, a c-Myc mRNA-binding protein, and sequesters AUF1 from binding c-Myc mRNA, leading to downregulation of c-Myc protein; the authors show that upon energy stress FoxOs induce the expression of the long non-coding RNA FILNC1, which inhibits survival of RCC by downregulating c-Myc and c-Myc-dependent metabolic rewiring	28978906	RID00838	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Osteosarcoma	FENDRR	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000087245	NA	400550	4313	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Antisense lncRNA FOXF1-AS1 Promotes Migration and Invasion of Osteosarcoma Cells Through the FOXF1/MMP-2/-9 Pathway;FOXF1-AS1 as well as FOXF1 silencing significantly inhibited cell proliferation, migration, invasion of OS cells and tumor growth both in vitro and vivo through decreasing the expression of MMP2 and MMP9, whereas enhanced expression of FOXF1-AS1 had the opposite effects;we concluded that FOXF1-AS1 may promote migration and invasion of OS cells through the FOXF1/MMP-2/-9 pathway	29104509	RID00839	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Osteosarcoma	FENDRR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000100985	NA	400550	4318	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4B|GELB|MANDP2|MMP-9	Antisense lncRNA FOXF1-AS1 Promotes Migration and Invasion of Osteosarcoma Cells Through the FOXF1/MMP-2/-9 Pathway;FOXF1-AS1 as well as FOXF1 silencing significantly inhibited cell proliferation, migration, invasion of OS cells and tumor growth both in vitro and vivo through decreasing the expression of MMP2 and MMP9, whereas enhanced expression of FOXF1-AS1 had the opposite effects;we concluded that FOXF1-AS1 may promote migration and invasion of OS cells through the FOXF1/MMP-2/-9 pathway	29104509	RID00840	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gallbladder cancer	NMRAL2P	TWIST1	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000122691	NA	344887	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00841	expression association	NA	NA	UP(SKCM);DATA(GSE38495)
Gallbladder cancer	NMRAL2P	VIM	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000026025	NA	344887	7431	NA	NA	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00842	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gallbladder cancer	NMRAL2P	CDH2	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000170558	NA	344887	1000	NA	CD325|CDHN|CDw325|NCAD	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00843	expression association	NA	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Gallbladder cancer	NMRAL2P	CDH1	negatively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000039068	NA	344887	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00844	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophageal cancer	TPM1-AS	TPM1	negatively-E	western blot;immunoprecipitation	downregulation	qRT-PCR	NA	NA	cell migration(-)	alternative splicing	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259498	GRCh38_15:63046034-63049387	ENSG00000140416	NA	111064646	7168	TPM1-AS1	C15orf13|CMD1Y|CMH3|HEL-S-265|HTM-alpha|LVNC9|TMSA	Natural antisense transcript TPM1-AS regulates the alternative splicing of tropomyosin I through an interaction with RNA-binding motif protein 4; Mechanismly, the interaction of TPM1-AS with RBM4 hindered binding of RBM4 to TPM1 pre-mRNA and inhibited RBM4 to promote endogenous exon 2a inclusion of TPM1; Taken together, the results suggest that a natural antisense TPM1-AS regulates the alternative splicing of TPM1 through an interaction with RBM4 and involves in TPM1-mediated filopodium formation and migration of cancer cells	28754317	RID00845	interact with mRNA	NA	NA	UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Gastric cancer	AFAP1-AS1	AKT1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000142208	NA	84740	207	AFAP1-AS|AFAP1AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells;AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.	28451917	RID00846	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	AFAP1-AS1	PTEN	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000171862	NA	84740	5728	AFAP1-AS|AFAP1AS	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells;AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.	28451917	RID00847	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Atherosclerosis	RP11-714G18.1	LRP2BP	positively-E	western blot;luciferase reporter assay;FISH	downregulation	qPCR;microarray	GSE97210	GSE97210.zip	cell migration(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000250410	GRCh38_4:185370725-185390928	ENSG00000109771	NA	NA	55805	NA	NA	LncRNA-RP11-714G18.1 suppresses vascular cell migration via directly targeting LRP2BP. Mechanistically, RP11-714G18.1 could directly bind to its nearby gene LRP2BP and increased the expression of LRP2BP.	29363163	RID00848	transcriptional regulation	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Pre-eclampsia	MVIH	JUNB	positively-E	mass spectrometry	upregulation	qRT-PCR	NA	NA	cell growth(+);angiogenesis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cardiovascular system disease	Eclampsia	lncRNA	TF	NA	GRCh38_10:78038556-78040701	ENSG00000171223	NA	NA	3726	NA	AP-1	Promotion of trophoblast invasion by lncRNA MVIH through inducing Jun-B. Mass spectrometry analysis revealed that MVIH could modulate Jun-B protein expression, which has been reported to potentially regulate cell growth and angiogenesis	29083110	RID00849	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	LINC00958	VEGFC	positively-E	RIP;ChIP;RNAi;IHC	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000150630	NA	100506305	7424	BLACAT2	Flt4-L|LMPH1D|LMPHM4|VRP	Long noncoding RNA BLACAT2 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. we demonstrate that BLACAT2 epigenetically upregulation VEGF-C expression by directly associating with WDR5, a core subunit of human H3K4 methyltransferase complexes.	29355840	RID00850	epigenetic regulation	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Intervertebral disc degeneration	FAF1	MAPK1	positively-E	RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000185104	GRCh38_1:50437028-50960267	ENSG00000100030	NA	NA	5594	CGI-03|HFAF1s|UBXD12|UBXN3A|hFAF1	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA FAF1 promotes intervertebral disc degeneration by targeting the Erk signaling pathway. The results of the present study demonstrated that the expression of FAF1 was upregulated in patients with disc bulging, herniation and IDD, and the expression of FAF1 was positively correlated with the grade of disc degeneration according to the patients' Pfirrmann score. The expression of phosphorylated extracellular signal-regulated kinase (Erk), a possible target of FAF1, was consistent with the expression of FAF1. In addition, it was elucidated that inactivation of the Erk signaling pathway by PD98059 reversed the effect of FAF1 on NP cell proliferation. Taken together, these results demonstrated that FAF1 was vital in the proliferation of NP cells by modulating the Erk signaling pathway, which suggests that FAF1 may be a novel marker in the early diagnosis of IDD and a therapeutic target for patients.	29257270	RID00851	expression association	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Myocardial ischemia	TUG1	BNIP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000176171	NA	55000	664	LINC00080|NCRNA00080|TI-227H	NIP3	LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR-145-5p-Binp3 axis.	29207102	RID00852	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Myocardial ischemia	TUG1	miR-145-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR-145-5p-Binp3 axis.In addition, miR-145-5p was negatively regulated by TUG1, and TUG1 overexpression aggravated hypoxia-induced injury via the downregulation of miR-145-5p.	29207102	RID00853	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Osteosarcoma	MEG3	MDM2	positively-E	RNAi	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000135679	NA	55384	4193	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ACTFS|HDMX|hdm2	MEG3 inhibits proliferation and invasion and promotes apoptosis of human osteosarcoma cells. Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis.It was demonstrated that the upregulation of MEG3 significantly increased the transactivation of p53 and induced downstream changes in protein expression	29434890	RID00854	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	MEG3	TP53	positively-E	RNAi	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	MEG3 inhibits proliferation and invasion and promotes apoptosis of human osteosarcoma cells. Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis.It was demonstrated that the upregulation of MEG3 significantly increased the transactivation of p53 and induced downstream changes in protein expression	29434890	RID00855	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	SCHLAP1	MAPK1	positively-E	western blot;northern blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-198)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000281131	GRCh38_2:180692104-180916939	ENSG00000100030	NA	101669767	5594	LINC00913|PCAT11|PCAT114	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Noncoding RNA SChLAP1 Accelerates the proliferation and Metastasis of Prostate Cancer via Targeting miR-198 and Promoting the MAPK1 Pathway. Furthermore, our results showed that SChLAP1 interacted with miR-198 and subsequently modulated the MAPK1 signaling pathway in prostate cancer. miR-198 and MAPK1 had a targeted correlation	28492138	RID00856	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pulmonary hypertension	MEG3	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Down-regulation of lncRNA MEG3 promotes hypoxia-induced human pulmonary artery smooth muscle cell proliferation and migration via repressing PTEN by sponging miR-21. dual-luciferase reporter assay was applied to dissect the binding between PTEN and miR-21 and the results showed a decrease of luciferase activity in PASMCs co-transfected with wild-type PTEN and miR-21 mimics while restoration of luciferase activity was observed in cells co-transfected with mutant PTEN and miR-21 mimics.	29198701	RID00857	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	RAB11B-AS1	RAB11B	negatively-F	luciferase reporter assay;western blot;IHC	downregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000269386	GRCh38_19:8374373-8390685	ENSG00000185236	NA	100507567	9230	MIR4999HG	H-YPT3|NDAGSCW	Long non-coding RNA RAB11B-AS1 prevents osteosarcoma development and progression via its natural antisense transcript RAB11B. RAB11B-AS1 expression correlates negatively with RAB11B expression in OS tissues. Luciferase reporter assay illuminated that RAB11B-AS1 regulates RAB11B expression through antisense pairing. Thus our findings revealed that lnc-RAB11B-AS1 prevents osteosarcoma development and progression via inhibiting RAB11B expression, indicating lnc-RAB11B-AS1 as a potential therapeutic target for osteosarcoma.	29928484	RID00858	interact with mRNA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Hypertrophic scar	COL1A2-AS1	SMAD7	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	TF	NA	GRCh38_7:94367212-94392192	ENSG00000101665	NA	101927525	4092	TCONS_00013888|lncRNA8975-1	CRCS3|MADH7|MADH8	LncRNA COL1A2-AS1 inhibits the scar fibroblasts proliferation via regulating miR-21/Smad7 pathway. we found that miR-21 was involved in lncRNA COL1A2-AS1-induced expression of Smad7, by which COL1A2-AS1 acted as endogenous sponge to adsorb miR-21 and in turn regulated Smad7 and a cascade of molecular to play a protective role in hypertrophic scar	29117538	RID00859	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hypertrophic scar	COL1A2-AS1	miR-21	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	miRNA	NA	GRCh38_7:94367212-94392192	NA	NA	101927525	NA	TCONS_00013888|lncRNA8975-1	NA	LncRNA COL1A2-AS1 inhibits the scar fibroblasts proliferation via regulating miR-21/Smad7 pathway. we found that miR-21 was involved in lncRNA COL1A2-AS1-induced expression of Smad7, by which COL1A2-AS1 acted as endogenous sponge to adsorb miR-21 and in turn regulated Smad7 and a cascade of molecular to play a protective role in hypertrophic scar	29117538	RID00860	ceRNA or sponge	NA	NA	NA
Heart failure	FTX	BCL2L2	negatively-E	Targetscan;RNAhybrid;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-29b-1-5p)	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000129473	NA	100302692	599	LINC00182|MIR374AHG|NCRNA00182	BCL-W|BCL2-L-2|BCLW|PPP1R51	Long noncoding RNA FTX regulates cardiomyocyte apoptosis by targeting miR-29b-1-5p and Bcl2l2. We then found that FTX functions as endogenous sponge for miR-29b-1-5p and regulates the activity of miR-29b-1-5p.Bcl2l2 was found to harboring a potential target site for miR-29b-1-5p.	29117536	RID00861	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Osteosarcoma	SNHG1	WNT2B	positively-E	starBase;RegRNA;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-577)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000134245	NA	23642	7482	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	WNT13	Up-regulated lnc-SNHG1 contributes to osteosarcoma progression through sequestration of miR-577 and activation of WNT2B/Wnt/beta-catenin pathway. we also found that miR-577 could act as a ceRNA of SNHG1 in OS cells and the promotion of OS progression induced by lnc-SNHG1 overexpression required the inactivity of miR-577	29108989	RID00862	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	CYTOR	PRKAA1	positively-E	Targetscan;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000132356	NA	112597	5562	C2orf59|LINC00152|NCRNA00152	AMPK|AMPKa1	LINC00152/miR-139-5p regulates gastric cancer cell aerobic glycolysis by targeting PRKAA1. We also found that miR-139-5p was down-regulated by long intergenic non-coding RNA 152 (LINC00152) in gastric cancer cells.It is reported that miR-139-5p is a target miRNA of long non-codingRNA LINC00152. PRKAA1 was a target gene of miR-139-5p in gastric cancer cells	29156518	RID00863	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Atherosclerosis	MIAT	STAT3	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-181b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000168610	NA	440823	6774	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	ADMIO|ADMIO1|APRF|HIES	MIAT promotes proliferation and hinders apoptosis by modulating miR-181b/STAT3 axis in ox-LDL-induced atherosclerosis cell models. Moreover, MIAT enhanced STAT3 expression through sequestering miR-181b as a molecular sponge. Furthermore, MiR-181b hindered cell growth, induced cell cycle arrest and promoted apoptosis by directly targeting STAT3.	29136944	RID00864	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	TP73-AS1	TGFA	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-194)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000163235	NA	57212	7039	KIAA0495|PDAM	TFGA	Long non-coding RNA TP73-AS1 sponges miR-194 to promote colorectal cancer cell proliferation, migration and invasion via up-regulating TGFalpha. Bioinformatics analysis and luciferase reporter assay indicated that TP73-AS1 could bind directly with miR-194, and TP73-AS1 negatively regulated the expression of miR-194 in CRC cells. TGFalpha is a direct target of miR-194	30010111	RID00865	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Ovarian cancer	SNHG3	GSK3B	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	oncogenic role(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000082701	NA	8420	2932	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	NA	Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer. SNHG3 functioned as an oncogene by regulating GSK3beta/beta-catenin signaling activity in ovarian cancer	29758922	RID00866	expression association	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	SNHG3	CTNNB1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	oncogenic role(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000168036	NA	8420	1499	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer. SNHG3 functioned as an oncogene by regulating GSK3beta/beta-catenin signaling activity in ovarian cancer	29758922	RID00867	expression association	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	MYC	DANCR	positively-E	RNAi;ChIP	upregulation	qRT-PCR;sequencing	GSE51010;TCGA	GSE51010.zip;OV.zip	cell proliferation(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000226950	GRCh38_4:52712404-52720351	4609	57291	MRTL|MYCC|bHLHe39|c-Myc	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	MYC Targeted Long Noncoding RNA DANCR Promotes Cancer in Part by Reducing p21 Levels. Here, we report that MYC stimulates the transcription of DANCR, a long noncoding RNA (lncRNA) that is widely overexpressed in human cancer. Our observations expand knowledge of how MYC drives cancer cell proliferation by identifying DANCR as a critical lncRNA widely overexpressed in human cancers.	29180471	RID00868	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)
Ovarian cancer	DANCR	CDKN1A	negatively-E	RNAi	upregulation	qRT-PCR;sequencing	TCGA	OV.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000124762	NA	57291	1026	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	MYC Targeted Long Noncoding RNA DANCR Promotes Cancer in Part by Reducing p21 Levels. Mechanistic investigations indicated that DANCR limited the expression of cell-cycle inhibitor p21 (CDKN1A) and that the inhibitory effects of DANCR loss on cell proliferation could be partially rescued by p21 silencing.	29180471	RID00869	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Aortic valve disease	TUG1	RUNX2	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124813	NA	55000	860	LINC00080|NCRNA00080|TI-227H	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 in aortic valve calcification.human Runx2 3'-UTRfragments containing putative binding sites for the miR-204-5p reportervector and the Runx2 promoter reporter vector were used in Dual-luciferase Reporter Assays.	29016735	RID00870	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	KLF3-AS1	GIT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000231160	GRCh38_4:38602438-38664914	ENSG00000108262	NA	79667	28964	NA	NA	MSC-derived exosomes promote proliferation and inhibit apoptosis of chondrocytes via lncRNA-KLF3-AS1/miR-206/GIT1 axis in osteoarthritis. Results also demonstrated that KLF3-AS1 acted as a competitive endogenous RNA (ceRNA) by sponging miR-206 to facilitate GIT1 expression	30324848	RID00871	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hirschsprung's disease	LOC100507600	BMI1	negatively-E	western blot;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-128-1-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000226806	GRCh38_2:135820191-135823087	ENSG00000168283	NA	100507600	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long non-coding RNA LOC100507600 functions as a competitive endogenous RNA to regulate BMI1 expression by sponging miR128-1-3p in Hirschsprung's disease. Downregulation of LOC100507600 repressed cell migration and proliferation and didn't affect cell apoptosis or cycle. In sum, our study researches the potential diagnostic value of LOC100507600 in HSCR and deduces that LOC100507600 can contributes to HSCR as a competitive endogenous RNA to regulate BMI1 expression by sponging miR128-1-3p.	29429387	RID00872	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	GAPLINC	EEF2K	positively-E	western blot;luciferase reporter assay;FISH	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-661)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000103319	NA	100505592	29904	LINC01540	CaMKIII|HSU93850|eEF-2K	Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway. Bioinformatic analysis and luciferase reporter confirmed that miR-661 targeted GAPLINC and eEF2K 3'-UTR and was negatively correlated with the expression of GAPLINC and eEF2K. Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.	30522114	RID00873	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	HOXA-AS2	S100A4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-520c-3p)	regulation	NA	adriamycin	NA	Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000196154	NA	285943	6275	HOXA3as	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	Knockdown of Long Noncoding RNA HOXA-AS2 Suppresses Chemoresistance of Acute Myeloid Leukemia via the miR-520c-3p/S100A4 Axis. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay and anti-Ago2 RIP assay.HOXA-AS2 could negatively regulate the expression of miR-520c-3p in ADR cells. S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay.	30466095	RID00874	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SNHG16	ZEB1	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+)	ceRNA(miR-205)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000148516	NA	100507246	6935	Nbla10727|Nbla12061|ncRAN	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Noncoding RNA SNHG16 Promotes Cell proliferation by Sponging MicroRNA-205 and Upregulating ZEB1 Expression in Osteosarcoma. ZEB1 was the target gene of miR-205	30453308	RID00875	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CERNA2	JAK2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000096968	NA	642934	3717	HOST2|lncRNA-HOST2	JTK10|THCYT3	Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway.The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.	30453302	RID00876	expression association	metastasis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Hepatocellular carcinoma	CERNA2	STAT3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000168610	NA	642934	6774	HOST2|lncRNA-HOST2	ADMIO|ADMIO1|APRF|HIES	Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway.The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.	30453302	RID00877	expression association	metastasis	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	XIST	SGK1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-124)	regulation	NA	doxorubicin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000118515	NA	7503	6446	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	SGK	Knockdown of Long Non-Coding RNA XIST Inhibited Doxorubicin Resistance in Colorectal Cancer by Upregulation of miR-124 and Downregulation of SGK1.XIST positively regulated SGK1 expression by interacting with miR-124 in DOX-resistant CRC cells. binding sites of miR-124 were identified in the 3'UTR of SGK1 mRNA.XIST exerted regulatory function in resistance of DOX possibly through miR-124/SGK1 axis, shedding new light on developing promising therapeutic strategy to overcome chemoresistance in CRC patients.	30439718	RID00878	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	CRNDE	IRX5	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	oncogenic role(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000176842	NA	NA	10265	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HMMS|IRX-2a|IRXB2	Long-Noncoding RNA Colorectal Neoplasia Differentially Expressed Gene as a Potential Target to Upregulate the Expression of IRX5 by miR-136-5P to Promote Oncogenic Properties in Hepatocellular Carcinoma. CRNDE acted as a tumor oncogene by exhibiting oncogenic properties of human HCC and revealed a novel CRNDE-miR-136-5P-IRX5 regulatory network in HCC .Using a bioinformatics databases (Starbase, RNAhybrid), miR-136-5P is a putative target of CRNDE in several miRNAs. MiR-136-5P inhibited the expression of IRX5 by targeting its 3'UTR and miR-136-5P was involved in the CRNDE-regulated expression of IRX5.	30423553	RID00879	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Ischemic stroke	MALAT1	MDM2	positively-E	western blot;FISH	upregulation	qRT-PCR	NA	NA	p53 signaling pathway(+)	NA	regulation	NA	NA	NA	Genome Instability and Mutation	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135679	NA	378938	4193	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ACTFS|HDMX|hdm2	MALAT1 Activates the P53 Signaling Pathway by Regulating MDM2 to Promote Ischemic Stroke. Both MALAT1 and MDM2 were localized in the nuclei. Down regulation of MALAT1 and MDM2 enhanced cell proliferation ability and reduced apoptosis, resulting in decreased infarct size in MCAO/R brains. These results indicate that MALAT1/MDM2/p53 signaling pathway axis may provide more effective clinical therapeutic strategy for patients with ischemic stroke.	30419554	RID00880	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	HOXA-AS2	GPC3	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-520c-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000147257	NA	285943	2719	HOXA3as	DGSX|GTR2-2|MXR7|OCI-5|SDYS|SGB|SGBS|SGBS1	HOXA-AS2 Promotes Proliferation and Induces Epithelial-Mesenchymal Transition via the miR-520c-3p/GPC3 Axis in Hepatocellular Carcinoma. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. By bioinformatic analysis and dual-luciferase reporter assay, we found that miR-223-3p directly targeted the 3'-untranslated region (UTR) of Glypican-3 (GPC3), one of the key players in HCC.	30415263	RID00881	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DATA(GSE117623)
Papillary thyroid carcinoma	HOXA-AS2	S100A4	positively-E	western blot;luciferase reporter assay;RIP;IHC	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-520c-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000196154	NA	285943	6275	HOXA3as	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	Long Noncoding RNA HOXA-AS2 Promotes Papillary Thyroid Cancer Progression by Regulating miR-520c-3p/S100A4 Pathway. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOXA-AS2 and miR-520c-3p in PTC.MiR-520c-3p was down-regulated in PTC tissues, and S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay.	30384358	RID00882	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiomyopathy	KCNQ1OT1	miR-214-3p	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell death(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	miRNA	ENSG00000269821	GRCh38_11:2608328-2699994	NA	NA	10984	NA	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1.	30355944	RID00883	expression association	NA	UP(BRCA);DATA(GSE111842)	NA
Cardiomyopathy	KCNQ1OT1	CASP1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell death(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000137752	NA	10984	834	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	ICE|IL1BC|P45	LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1.	30355944	RID00884	expression association	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	H19	SOX4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR;sequencing	TCGA;GSE16011;GSE4290	GBM.zip;GSE16011.zip;GSE4290.zip	epithelial to mesenchymal transition(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000124766	NA	283120	6659	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	EVI16	H19 Functions as a Competing Endogenous RNA to Regulate EMT by Sponging miR-130a-3p in Glioma. H19 and SOX4 are both direct target of miR-130a-3p. H19 could compete with SOX4 via sponging miR-130a-3p.	30282068	RID00885	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Colorectal adenocarcinoma	H19	miR-194-5p	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma. H19 modified miR-194-5p expression through directly targeting at it. LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.	30278464	RID00886	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Colorectal adenocarcinoma	H19	FOXM1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111206	NA	283120	2305	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma. H19 modified miR-194-5p expression through directly targeting at it. LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.	30278464	RID00887	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	MALAT1	VIM	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-30a-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma. Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion.	30278452	RID00888	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	AFAP1-AS1	IRF7	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000185507	NA	84740	3665	AFAP1-AS|AFAP1AS	IMD39|IRF-7|IRF-7H|IRF7A|IRF7B|IRF7C|IRF7H	lncRNA AFAP1-AS1 promotes migration and invasion of non-small cell lung cancer via up-regulating IRF7 and the RIG-I-like receptor signaling pathway.	30278439	RID00889	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Cervical cancer	DLG1-AS1	ZHX1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-107)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000227375	GRCh38_3:197298252-197303755	ENSG00000165156	NA	100507086	11244	NA	NA	lncRNA DLG1-AS1 Promotes Cell proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer.	30231238	RID00890	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Lung cancer	HOTAIR	EZH2	interact	RIP;RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	interact with protein	binding/interaction	RNA-protein	ATL-1;erlotinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Repression of PDK1- and LncRNA HOTAIR-Mediated EZH2 Gene Expression Contributes to the Enhancement of Atractylenolide 1 and Erlotinib in the Inhibition of Human Lung Cancer Cells. While silencing HOTAIR inhibited the expressions of PDK1 and EZH2, overexpression of HOTAIR reduced the ATL-1-reduced PDK1 and EZH2 protein expressions and EZH2 promoter activity. In addition, ATL-1 reduced the HOTAIR binding to the EZH2 protein. Thus, targeting the PDK1- and HOTAIR-mediated downstream molecule EZH2 by the combination of ATL-1 and erlotinib potentially facilitates the development of an additional novel strategy to combat lung cancer. major bioactive compound of Atractylodes macrocephula Koidz atractylenolide 1 (ATL-1)	30223276	RID00891	interact with protein	chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	PVT1	HILPDA	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000135245	NA	5820	29923	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Non-Coding RNA PVT1/miR-150/ HIG2 Axis Regulates the Proliferation, Invasion and the Balance of Iron Metabolism of Hepatocellular Carcinoma. PVT1 could directly bind to microRNA (miR)-150 and down-regulate miR-150 expression. miR-150 directly targets 3-UTR of HIG2 to regulate its expression	30205391	RID00892	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE111842,GSE109761,GSE55807)
Ovarian cancer	HOTAIR	CCND1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer.HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.	30205383	RID00893	ceRNA or sponge	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Ovarian cancer	HOTAIR	CCND2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000118971	NA	100124700	894	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	KIAK0002|MPPH3	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer.	30205383	RID00894	ceRNA or sponge	NA	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	GAS5	PDCD4	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150593	NA	60674	27250	NCRNA00030|SNHG2	H731	Association Between the Deletion Allele of Ins/Del Polymorphism (Rs145204276) in the Promoter Region of GAS5 with the Risk of Atherosclerosis. GAS5 directly targets miR-21 and functions as a competing endogenous RNA to suppress miR-21 expression.GAS5 positively regulated PDCD4 expression via inhibiting miR-21 expression. In summary, rs145204276 was associated with the risk of atherosclerosis by affecting the proliferation and apoptosis of endothelial cells via regulating the GAS5/miR-21/PDCD4 signaling pathway.	30205366	RID00895	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Breast cancer	KCNQ1OT1	CCNE2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000175305	NA	10984	9134	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CYCE2	The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells. KKCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2.	30157476	RID00896	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	SNHG6	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE14333;GSE37892;GSE20916;GSE18105;TCGA	GSE14333.zip;GSE37892.zip;GSE20916.zip;GSE18105.zip;COAD.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells.	30157475	RID00897	epigenetic regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	EGFR-AS1	EGFR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000146648	NA	100507500	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer. And the expression of EGFR-AS1 positively correlated with EGFR in tissues	30138934	RID00898	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Multiple myeloma	MEG3	HOXA11	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE5900;GSE2658	GSE5900.zip;GSE2658.zip	cancer progression(-)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000005073	NA	55384	3207	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HOX1|HOX1I|RUSAT1	Long Non-Coding RNA MEG3 Functions as a Competing Endogenous RNA to Regulate HOXA11 Expression by Sponging miR-181a in Multiple Myeloma. Importantly, several mechanism experiments revealed that MEG3, acting as an endogenous competitive RNA, could contend with miR-181a to inhibit tumor progression. Our present work supplies the first discovery of a MEG3/miR-181a/HOXA11 regulatory network in MM and highlights that MEG3 may serve as a promising target for MM therapy in the future.	30134227	RID00899	ceRNA or sponge	NA	NA	NA
Multiple myeloma	LINC00515	ATG14	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	ceRNA(miR-140-5p)	regulation	NA	melphalan	NA	Evading Apoptosis	Cancer	Myeloma	lncRNA	PCG	ENSG00000260583	GRCh38_21:25582775-25583224	ENSG00000126775	NA	282566	22863	NA	ATG14L|BARKOR|KIAA0831	Linc00515 enhanced autophagy and chemoresistance of melphalan-resistant myeloma by directly inhibiting miR-140-5p, which elevated ATG14 level. Results were shown by the dual-luciferase reporter gene assay that linc00515 directly targeted miR-140-5p, which directly bound to ATG14	30121664	RID00900	ceRNA or sponge	chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	BCYRN1	NPR3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000113389	NA	618	4883	BC200|BC200a|LINC00004|NCRNA00004	ANP-C|ANPR-C|ANPRC|C5orf23|GUCY2B|NPR-C|NPRC	Long Noncoding RNA BCYRN1 Promotes the proliferation of Colorectal Cancer Cells via Up-Regulating NPR3 Expression	30114690	RID00901	expression association	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	NA
Hepatocellular carcinoma	TUG1	ZEB1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-142-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148516	NA	55000	6935	LINC00080|NCRNA00080|TI-227H	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1. miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulation ZEB1 was via direct binding to miR-142-3p. ZEB1 was identified as a target of miR-142-3p.	30092578	RID00902	ceRNA or sponge	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Spinal cord glioma	LINC01260	CARD11	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);NF-kB signaling pathway(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000283440	GRCh38_20:44656451-44663498	ENSG00000198286	NA	79015	84433	NA	BENTA|BIMP3|CARMA1|IMD11|IMD11A|PPBL	Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-kB Signaling Pathway.CARD11 was confirmed to be a target gene of LINC01260 and was found to be involved in regulating the NF-kB pathway. A dual-luciferase reporter assay was conducted to verify the target relationship between LINC01260 and CARD11. Our findings demonstrate that overexpression of LINC01260 inhibits spinal cord glioma cell proliferation, migration and invasion by targeting CARD11 via NF-kB signaling suppression	30071522	RID00903	transcriptional regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pituitary cancer	SNHG1	TGFBR2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-302;miR-372;miR-373;miR-520)	regulation	NA	NA	NA	NA	Cancer	Pituitary cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000163513	NA	23642	7048	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AAT3|FAA3|LDS1B|LDS2|LDS2B|MFS2|RIIC|TAAD2|TBR-ii|TBRII|TGFR-2|TGFbeta-RII	Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/beta-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.	30048990	RID00904	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pituitary cancer	SNHG1	RAB11A	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-302;miR-372;miR-373;miR-520)	regulation	NA	NA	NA	NA	Cancer	Pituitary cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000103769	NA	23642	8766	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	YL8	Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/beta-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.	30048990	RID00905	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Breast cancer	LOC101930370	SHH	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	ceRNA(miR-1471)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245213	GRCh38_4:173131933-173169652	ENSG00000164690	NA	101930370	6469	NA	HHG1|HLP3|HPE3|MCOPCB5|SMMCI|ShhNC|TPT|TPTPS	LOC101930370/MiR-1471 Axis Modulates the Hedgehog Signaling Pathway in Breast Cancer. LOC101930370 positively regulates the expression of SHH by sponging miR-1471	30041193	RID00906	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Clear cell renal cell carcinoma	MIAT	LOXL2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-29c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000134013	NA	440823	4017	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	LOR|LOR2|WS9-14	Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma.Our data indicated that MIAT might be an oncogenic lncRNA that promoted proliferation and metastasis of ccRCC, and could be a potential therapeutic target in human ccRCC.	30041179	RID00907	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE55807)
Lung adenocarcinoma	NEAT1	USF1	positively-E	luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE7670;GSE10072;GSE19188;GSE31210;GSE27262;GSE4376;TCGA	GSE7670.zip;GSE10072.zip;GSE19188.zip;GSE31210.zip;GSE27262.zip;GSE4376.zip;COAD.zip	tumorigenesis(+);cancer progression(+)	ceRNA(miR-193a-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000158773	NA	283131	7391	LINC00084|NCRNA00084|TncRNA|VINC	FCHL|FCHL1|HYPLIP1|MLTF|MLTFI|UEF|bHLHb11	The LncRNA NEAT1 Accelerates Lung Adenocarcinoma Deterioration and Binds to Mir-193a-3p as a Competitive Endogenous RNA. The dual-luciferase reporter assay demonstrated that miR-193a-3p directly targeted NEAT1 at its 3'-UTR. NEAT1 may function as a ceRNA to sponge miR-193a-3p and abrogate the inhibitory effect of miR-193a-3p on USF1. Our findings indicate that NEAT1 plays important roles in the occurrence and progression of LUAD. It may exert its role by acting as a ceRNA to regulate miR-193a-3p.	30036873	RID00908	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	LUCAT1	AKT1	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	KIRC.zip	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000142208	NA	100505994	207	SCAL1|SCAT5	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Non-Coding RNA LUCAT1 Promotes Proliferation and Invasion in Clear Cell Renal Cell Carcinoma Through AKT/GSK-3beta Signaling Pathway. Mechanistic investigations showed that LUCAT1 induced cell cycle G1 arrest by regulating the expression of cyclin D1, cyclin-dependent kinase 4, and phosphorylated retinoblastoma transcriptional corepressor 1. Moreover, LUCAT1 promoted proliferation and invasion in ccRCC cells partly through inducing the phosphorylation of AKT and suppressing the phosphorylation of GSK-3beta	30032137	RID00909	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	LUCAT1	GSK3B	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	KIRC.zip	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000082701	NA	100505994	2932	SCAL1|SCAT5	NA	Long Non-Coding RNA LUCAT1 Promotes Proliferation and Invasion in Clear Cell Renal Cell Carcinoma Through AKT/GSK-3beta Signaling Pathway.Moreover, LUCAT1 promoted proliferation and invasion in ccRCC cells partly through inducing the phosphorylation of AKT and suppressing the phosphorylation of GSK-3beta	30032137	RID00910	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MALAT1	ATG7	positively-E	luciferase reporter assay;western blot	Upregulation	qPCR	NA	NA	cell autophagy(+);cell invasion(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000197548	NA	378938	10533	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG7-LIKE|APG7L|GSA7	Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer.MARCH7 interacted with MALAT1 by miR-200a (microRNA-200a). MARCH7 may function as a competing endogenous RNA (ceRNA) to regulate the expression of ATG7 by competing with miR-200a.	29794480	RID00911	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	CDR1-AS	miR-135a	negatively-F	RIP;RNA pull-down assay;RNA-FISH	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	circRNA	miRNA	NA	NA	NA	NA	103611090	NA	CDR1NAT|CDR1as|ciRS-7	NA	CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a.	29694981	RID00912	ceRNA or sponge	NA	NA	NA
Lupus nephritis	TUG1	miR-223	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell injury(-)	NA	regulation	NA	NA	NA	NA	Urinary system disease	Nephritis	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 protects renal tubular epithelial cells against injury induced by lipopolysaccharide via regulating microRNA-223. LPS administration inhibited HK-2 cell viability and proliferation, increased expression of pro-inflammatory factors, and promoted cell apoptosis. TUG1 overexpression protected HK-2 cells against LPS-induced injury via negatively regulating miR-223 expression.	29800915	RID00913	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Osteoarthritis	ZFAS1	WNT3A	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000154342	NA	441951	89780	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Role of long noncoding RNA ZFAS1 in proliferation, apoptosis and migration of chondrocytes in osteoarthritis. overexpressed ZFAS1 significantly decreased Wnt3a factors.Our study demonstrates that ZFAS1 may promote chondrocyte proliferation, and migration, and decrease apoptosis and matrix synthesis in OA possible via targeting Wnt3a signaling.	29703568	RID00914	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DATA(GSE40174)
Breast cancer	HOTAIR	PTEN	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Downregulation of Long Noncoding RNA HOTAIR and EZH2 Induces Apoptosis and Inhibits Proliferation, Invasion, and Migration of Human Breast Cancer Cells. HOTAIR could bind specifically to EZH2 and PTEN, highlighting the capability of HOTAIR to inhibit the expression of PTEN by recruiting EZH2 in breast cancer.the downregulation of HOTAIR or silencing of EZH2 was revealed to repress the proliferation, invasion, and migration, while acting to promote the apoptosis of the breast cancer cells.	30048163	RID00915	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Endometrial cancer	LINC00261	FOXO1	positively-E	RIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000150907	NA	140828	2308	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	FKH1|FKHR|FOXO1A	Long noncoding RNA LINC00261 regulates endometrial carcinoma progression by modulating miRNA/FOXO1 expression. Overexpressed LINC00261 lowered these dissociative miRNAs, resulting in increase of FOXO1 protein levels.LINC00261 promotes FOXO1 expression through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion.	30019459	RID00916	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Chronic myeloid leukemia	STAT3	MEG3	negatively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	JAK/STAT signaling pathway(+);cell proliferation(+);apoptosis process(-)	phosphorylated	binding/interaction	protein-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	TF	lncRNA	ENSG00000168610	NA	ENSG00000214548	GRCh38_14:100779410-100861031	6774	55384	ADMIO|ADMIO1|APRF|HIES	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00917	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Chronic myeloid leukemia	MEG3	JAK2	negatively-E	RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	JAK/STAT signaling pathway(-);cell proliferation(-);apoptosis process(+)	mediate protein interactions	binding/interaction	protein-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000096968	NA	55384	3717	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	JTK10|THCYT3	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00918	interact with protein	NA	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Chronic myeloid leukemia	MEG3	miR-147	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	JAK/STAT signaling pathway(-);cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00919	ceRNA or sponge	NA	NA	NA
Esophageal cancer	FALEC	PDK1	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);AKT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000152256	NA	100874054	5163	FAL1|LINC00568|ncRNA-a1	NA	Long non-coding RNA FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in esophageal cancer cells. Overexpressed FAL1 activated Akt pathway via interacting with PDK1 in EC cell lines.FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in EC cells. These findings revealed that FAL1 exhibited oncogenic activity in EC, and inhibiting FAL1 might be useful for preventing the progression of EC.The interaction effect between FAL1 and 3-phosphoinositide-dependent protein kinase 1 (PDK1) was evaluated by chromatin immunoprecipitation (ChIP) assay.	30178844	RID00920	interact with protein	NA	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Malignant choroid melanoma	FOXCUT	MMP9	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Choroid cancer	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000100985	NA	101927703	4318	LINC01379|TCONS_00011636	CLG4B|GELB|MANDP2|MMP-9	Coordinated targeting of MMP-2/MMP-9 by miR-296-3p/FOXCUT exerts tumor-suppressing effects in choroidal malignant melanoma. Bioinformatics prediction and our experiments validated that MMP-2 and MMP-9 were simultaneously targeted by miR-296-3p and FOXC1 promoter upstream transcript (FOXCUT). Our data indicated that MMP-2/MMP-9 was coordinately targeted by two non-coding RNAs, miR-296-3p and FOXCUT, which were decreased, and tumor-suppressing factors in CMM.	29260433	RID00921	transcriptional regulation	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant choroid melanoma	FOXCUT	MMP2	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Choroid cancer	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000087245	NA	101927703	4313	LINC01379|TCONS_00011636	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Coordinated targeting of MMP-2/MMP-9 by miR-296-3p/FOXCUT exerts tumor-suppressing effects in choroidal malignant melanoma. Bioinformatics prediction and our experiments validated that MMP-2 and MMP-9 were simultaneously targeted by miR-296-3p and FOXC1 promoter upstream transcript (FOXCUT). Our data indicated that MMP-2/MMP-9 was coordinately targeted by two non-coding RNAs, miR-296-3p and FOXCUT, which were decreased, and tumor-suppressing factors in CMM.	29260433	RID00922	transcriptional regulation	NA	NA	UP(PAAD);DATA(GSE40174)
Colon cancer	CASC15	LGR5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+)	ceRNA(miR-4310)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000139292	NA	401237	8549	CANT|LINC00340|lnc-SOX4-1	FEX|GPR49|GPR67|GRP49|HG38	LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR-4310/LGR5/Wnt/beta-catenin signaling pathway. CASC15 was observed to act as a sponge to suppress microRNA (miR)-4310 that targeted LGR5. Through the inhibition of miR-4310, CASC15 promoted leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/beta-catenin signaling pathway. The results revealed that the inhibition of the Wnt/beta-catenin signaling pathway in CASC15-overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion.	29956772	RID00923	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	AFAP1-AS1	TCF4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(-);cell invasion(-)	ceRNA(miR-4695-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196628	NA	84740	6925	AFAP1-AS|AFAP1AS	E2-2|FECD3|ITF-2|ITF2|PTHS|SEF-2|SEF2|SEF2-1|SEF2-1A|SEF2-1B|SEF2-1D|TCF-4|bHLHb19	Long noncoding RNA AFAP1-AS1 enhances cell proliferation and invasion in osteosarcoma through regulating miR-4695-5p/TCF4-beta-catenin signaling. AFAP1-AS1 served as a sponge to repress the level of microRNA (miR)-4695-5p, which targeted transcription factor (TCF)4, a pivot effector of Wnt/beta-catenin signaling pathway. It was demonstrated that overexpression of AFAP1-AS1 inhibited the expression of miR-4695-5p, while miR-4695-5p overexpression decreased TCF4 expression and reduced activation of Wnt/beta-catenin pathway.AFAP1-AS1 knockdown significantly inhibited the proliferation and invasion of OS cells in vitro.	29901121	RID00924	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)
Colorectal cancer	PCBP2-OT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124762	NA	102157401	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	uc.338 targets p21 and cyclin D1 via PI3K/AKT pathway activation to promote cell proliferation in colorectal cancer. Further investigations in vivo and in vitro revealed that uc.338 could promote proliferation and cell cycle G1/S transition, and might target p21 downregulation and cyclin D1 upregulation via the PI3K/AKT pathway in CRC cells.	29901203	RID00925	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	PCBP2-OT1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000110092	NA	102157401	595	NA	BCL1|D11S287E|PRAD1|U21B31	uc.338 targets p21 and cyclin D1 via PI3K/AKT pathway activation to promote cell proliferation in colorectal cancer. Further investigations in vivo and in vitro revealed that uc.338 could promote proliferation and cell cycle G1/S transition, and might target p21 downregulation and cyclin D1 upregulation via the PI3K/AKT pathway in CRC cells.	29901203	RID00926	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Thyroid cancer	BANCR	MAP1LC3A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000101460	NA	100885775	84557	LINC00586	ATG8E|LC3|LC3A|MAP1ALC3|MAP1BLC3	Effects of serine/threonine-protein kinase B-Raf-activated long-chain non-coding RNA on apoptosis and autophagy in thyroid carcinoma cells. Inhibition of lncRNA-BANCR expression attenuated the proliferation and invasion ability of thyroid cancer cells; but the apoptosis was enhanced; the expression levels of autophagy protein LC3-I and LC3-II were also increased.Western blot was used to detect the changes of autophagy proteins LC3-I and LC3-II after the lncRNA-BANCR expression was suppressed.	30124210	RID00927	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Thyroid cancer	BANCR	MAP1LC3B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000140941	NA	100885775	81631	LINC00586	ATG8F|LC3B|MAP1A/1BLC3|MAP1LC3B-a	Effects of serine/threonine-protein kinase B-Raf-activated long-chain non-coding RNA on apoptosis and autophagy in thyroid carcinoma cells. Inhibition of lncRNA-BANCR expression attenuated the proliferation and invasion ability of thyroid cancer cells; but the apoptosis was enhanced; the expression levels of autophagy protein LC3-I and LC3-II were also increased.Western blot was used to detect the changes of autophagy proteins LC3-I and LC3-II after the lncRNA-BANCR expression was suppressed.	30124210	RID00928	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Esophagus squamous cell carcinoma	PART1	BCL2	positively-E	RIP;miRcode;Targetscan;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-129)	regulation	NA	gefitinib	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000171791	NA	25859	596	NCRNA00206	Bcl-2|PPP1R50	Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA. Knockdown of lncRNA PART1 potently promoted the gefitinib-induced cell death, while elevated PART1 promoted gefitinib resistance by competitively binding to miR-129 to facilitate Bcl-2 expression in ESCC cells.	30049286	RID00929	ceRNA or sponge	chemoresistance	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	Upregulation of lncRNA-ATB by Transforming Growth Factor beta1 (TGF-beta1) Promotes Migration and Invasion of Papillary Thyroid Carcinoma Cells. lncRNA-ATB overexpression promoted tumor cell migration and invasion, lncRNA-ATB overexpression showed no significant effects on TGF-beta1 expression, and TGF-beta1 treatment increased the expression level of lncRNA-ATB. Upregulation of lncRNA-ATB by TGF-b1 promotes migration and invasion of PTC cells.	30042377	RID00930	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Endometrial cancer	PVT1	FGFR1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000077782	NA	5820	2260	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Long non-coding RNA PVT1 promotes malignancy in human endometrial carcinoma cells through negative regulation of miR-195-5p. We observed that PVT1 promotes malignant cell behavior by decreasing miR-195-5p expression. Binding of PVT1 and miR-195-5p was confirmed using luciferase assays.At the molecular level, either PVT1 knockdown or miR-195-5p overexpression resulted in a decrease of acidic fibroblast growth factor receptor (FGFR1)4 and basic fibroblast growth factor (FGF2).5 FGFR1 and FGF2 are targets of miR-195-5p that play a critical role in endometrial carcinoma by activating PI3K/AKT and MAPK/Erk pathways.	30031900	RID00931	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Endometrial cancer	PVT1	FGF2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000138685	NA	5820	2247	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BFGF|FGF-2|FGFB|HBGF-2	Long non-coding RNA PVT1 promotes malignancy in human endometrial carcinoma cells through negative regulation of miR-195-5p. We observed that PVT1 promotes malignant cell behavior by decreasing miR-195-5p expression. Binding of PVT1 and miR-195-5p was confirmed using luciferase assays.At the molecular level, either PVT1 knockdown or miR-195-5p overexpression resulted in a decrease of acidic fibroblast growth factor receptor (FGFR1)4 and basic fibroblast growth factor (FGF2).5 FGFR1 and FGF2 are targets of miR-195-5p that play a critical role in endometrial carcinoma by activating PI3K/AKT and MAPK/Erk pathways.	30031900	RID00932	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Alzheimer's disease	NEAT1	CDK5R1	negatively-E	RNAi	downregulation	qPCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000176749	NA	283131	8851	LINC00084|NCRNA00084|TncRNA|VINC	CDK5P35|CDK5R|NCK5A|p23|p25|p35|p35nck5a	Multiple Layers of CDK5R1 Regulation in Alzheimer's Disease Implicate Long Non-Coding RNAs. We demonstrated that NEAT1 and HOTAIR negatively regulate CDK5R1 mRNA levels, while MALAT1 has a positive effect. we observed a strong positive correlation between CDK5R1 and NEAT1 expression levels in brain tissues, suggesting a possible neuroprotective role of NEAT1 in AD to compensate for increased CDK5R1 levels. Overall, our work provides evidence of another level of CDK5R1 expression regulation mediated by lncRNAs and points to NEAT1 as a biomarker, as well as a potential pharmacological target for AD therapy.	29997370	RID00933	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colorectal cancer	SPINT1-AS1	SPINT1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000261183	GRCh38_15:40835808-40844387	ENSG00000166145	NA	102724362	6692	NA	HAI|HAI1|MANSC2	Increased expression of antisense lncRNA SPINT1-AS1 predicts a poor prognosis in colorectal cancer and is negatively correlated with its sense transcript. Compared with AN tissues, the expression of SPINT1-AS1 was increased in CRC tissues, while SPINT1 mRNA expression was decreased in CRC, and there was an obviously negative correlation between SPINT1-AS1 expression and its sense transcript.SPINT1-AS1 is upregulation in CRC tissues and plays an essential role in CRC progression and prognosis.	30022840	RID00934	expression association	prognosis	DOWN(BRCA);UP(BRCA);DATA(GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Glioblastoma	CASC2c	F10	positively-E	RNAi	downregulation	qPCR	NA	NA	macrophage polarization(-)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046821-118210153	ENSG00000126218	NA	NA	2159	NA	NA	Coagulation Factor X Regulated by CASC2c Recruited Macrophages and Induced M2 Polarization in Glioblastoma Multiforme. although the lncRNA CASC2c has been verified to function as a miR-101 competing endogenous RNA (ceRNA) to promote miR-101 target genes in GBM cells, we first confirmed that CASC2c did not function as a miR-338-3p ceRNA to promote FX expression, and that FX was a target gene of miR-338-3p.CASC2c interacted with and reciprocally repressed miR-338-3p.we first found that FX was highly expressed and positively correlated with TAM density in human GBM. CASC2c repressed M2 subtype macrophage polarization. Our findings revealed a novel mechanism highlighting CASC2c and FX as potential therapeutic targets to improve GBM patients by altering the GBM microenvironment.	30034397	RID00935	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Astrocytoma	CASC2c	CPEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Astrocytoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046821-118210153	ENSG00000214575	NA	NA	64506	NA	CPE-BP1|CPEB|CPEB-1|h-CPEB|hCPEB-1	Coagulation Factor X Regulated by CASC2c Recruited Macrophages and Induced M2 Polarization in Glioblastoma Multiforme. lncRNA CASC2c directly bound miR-101 and influenced miR-101 to mature, and CASC2c acted as a competing endogenous RNA (ceRNA) of miR-101 to competitively regulate CPEB1 and promote the malignant growth of astrocytoma	29458374;28252647	RID00936	ceRNA or sponge	NA	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Atherosclerosis	miR-103	lncWDR59	negatively-F	RNAi;RNAhybrid	upregulation	qPCR	NA	NA	cell proliferation(+);DNA damage(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Genome Instability and Mutation	Cardiovascular system disease	Atherosclerosis	miRNA	lncRNA	NA	NA	NA	GRCh38_8:111444252:111449827	NA	NA	NA	NA	miR-103 promotes endothelial maladaptation by targeting lncWDR59. Here we show that hyperlipidemia- and oxLDL-induced upregulation of miR-103 inhibits EC proliferation and promotes endothelial DNA damage through targeting of novel lncWDR59. these data indicate that miR-103 programs ECs toward a maladapted phenotype through targeting of lncWDR59, which may promote atherosclerosis.	29980665	RID00937	ceRNA or sponge	NA	NA	NA
Spinal cord injury	MALAT1	miR-199b	negatively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Other	Injury	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKbeta/NF-kB signaling pathway. we confirmed that LPS-induced MALAT1 activated IKKbeta/NF-kB signaling pathway and promoted the production of proinflammatory cytokines TNF-alpha and IL-1beta through downregulating miR-199b.	29631367	RID00938	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Pneumonia	CRNDE	FOXM1	positively-E	RNAi	upregulation	qPCR	NA	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Lung disease	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000111206	NA	NA	2305	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Knockdown CRNDE alleviates LPS-induced inflammation injury via FOXM1 in WI-38 cells. FOXM1 was up-regulated by CRNDE and FOXM1 silence blocked the effect of CRNDE overexpression in cell apoptosis, inflammation and activation of NF-kB and JAK/STAT signaling pathways.	29864958	RID00939	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung adenocarcinoma	NORAD	TGFB1	positively-E	luciferase reporter assay	upregulation	qPCR;sequencing	GSE109296	GSE109296.zip	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000105329	NA	647979	7040	LINC00657	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long noncoding RNA NORAD regulates transforming growth factor-beta signaling and epithelial-to-mesenchymal transition-like phenotype. Here, we show that NORAD upregulates transforming growth factor-beta (TGF-beta) signaling and regulates TGF-beta-induced epithelial-to-mesenchymal transition (EMT)-like phenotype, which is a critical step in the progression of lung adenocarcinoma, A549 cells.	29722104	RID00940	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cataract	KCNQ1OT1	SMAD4	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Nervous system disease	Cataract	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000141646	NA	10984	4089	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	DPC4|JIP|MADH4|MYHRS	Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial-mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells. In the present study, KCNQ1OT1 and mothers against decapentaplegic homolog (SMAD)4 expression levels were upregulation in human cataract lens posterior capsular samples	29749509	RID00941	expression association	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Prostate cancer	PCGEM1	miR-148a	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	MEF2-activated long non-coding RNA PCGEM1 promotes cell proliferation in hormone-refractory prostate cancer through downregulation of miR-148a. Expression levels of PCGEM1 in PC3 cancer cells were demonstrated to be regulated by MEF2, as PCGME1 mRNA was increased by MEF2 overexpression but decreased by MEF2 silencing.the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR-148a that controls cell apoptosis. downregulation of PCGEM1 expression in PC3 cells increased expression of miR-148a. By contrast, overexpression of PCGEM1 decreased miR-148a expression. Finally, PCGME1 silencing by small interfering RNA significantly induced early cell apoptosis but this effect was reduced by a miR-148a inhibitor.	29749452	RID00942	expression association	NA	UP(PAAD);DATA(GSE60407)	NA
Pre-eclampsia	PGK1P2	PGK1	positively-E	RNAi;Targetscan	downregulation	qPCR	NA	NA	angiogenesis(+);glucose metabolic process(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Sustained Angiogenesis;Reprogramming Energy Metabolism	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000213290	GRCh38_19:12559571-12561105	ENSG00000102144	NA	5233	5230	PGK2	HEL-S-68p|MIG10|PGKA	Dysfunction of pseudogene PGK1P2 is involved in preeclampsia by acting as a competing endogenous RNA of PGK1. We also found PGK1P2 acted as a competing endogenous RNA (ceRNA) to regulate PGK1 expression through miR-330-5p.The levels of PGK1 and PGK1P2 mRNA and PGK1 protein in severe preeclamptic decidua were lower than those in normal pregnant controls.We proved that PGK1 and PGK1P2 are a pair of ceRNAs against miR-330-5p and they play a vital role in human decidualization by regulating angiogenesis and glycolysis metabolism.	30177069	RID00943	ceRNA or sponge	NA	UP(SKCM,BRCA);DATA(GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Major depressive disorder	NONHSAG045500	SLC6A4	negatively-E	RNAi	downregulation	qPCR	NA	NA	antidepressant(+);serotonin transporter(+)	NA	association	NA	NA	NA	NA	Disease of mental health	Major depressive disorder	lncRNA	PCG	NA	GRCh38_6:143503458-143506147	ENSG00000108576	NA	NA	6532	NA	NA	Therapeutic Antidepressant Potential of NONHSAG045500 in Regulating Serotonin Transporter in Major Depressive Disorder. Only the overexpression of NONHSAG045500 could significantly inhibit the expression of SERT;	29955033	RID00944	expression association	NA	NA	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Medulloblastoma	LOXL1-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	NA	NA	100287616	NA	NA	NA	LncRNA LOXL1-AS1 Promotes the proliferation and Metastasis of Medulloblastoma by Activating the PI3K/AKT Pathway. Western blot analysis further revealed that knockdown of LOXL1-AS1 decreased the phosphorylated levels of PI3K and AKT without affecting their total protein levels.	30050750	RID00945	expression association	metastasis	DOWN(BRCA);DATA(GSE111842)	NA
Medulloblastoma	LOXL1-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000142208	NA	100287616	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	LncRNA LOXL1-AS1 Promotes the proliferation and Metastasis of Medulloblastoma by Activating the PI3K/AKT Pathway. Western blot analysis further revealed that knockdown of LOXL1-AS1 decreased the phosphorylated levels of PI3K and AKT without affecting their total protein levels.	30050750	RID00946	expression association	metastasis	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	MALAT1	CHUK	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000213341	NA	378938	1147	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation. we found that MALAT1-knockdown HepG2 and Huh7 cells expressed lower p-NF-kB,p-IKKaandp-IkBain comparison to the MALAT1 scramble-transfected liver cancer cells.	29702091	RID00947	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	MALAT1	PARP1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143799	NA	378938	142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation.	29702091	RID00948	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Liver cancer	MALAT1	NFKB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation.	29702091	RID00949	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MIR22HG	HMGB1	negatively-E	luciferase reporter assay;RIP	downregulation	microarray	GSE14520;TCGA	GSE14520.zip;LIHC.zip	cell proliferation(-);cell invasion(-);cell metastasis(-)	ceRNA(miR-22-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000189403	NA	84981	3146	C17orf91	HMG-1|HMG1|HMG3|SBP-1	Identification and Functional Characterization of Long Non-coding RNA MIR22HG as a Tumor Suppressor for Hepatocellular Carcinoma. MIR22HG derived miR-22-3p to target high mobility group box 1 (HMGB1), thereby inactivating HMGB1 downstream pathways. miR-22-3p suppression, HuR or HMGB1 overexpression rescued the inhibitory effects caused by MIR22HG overexpression. Forced expression of MIR22HG in HCC cells significantly suppressed proliferation, invasion, and metastasis in vitro and in vivo.	30083257	RID00950	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Osteoarthritis	DANCR	SPHK2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-577)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000063176	NA	57291	56848	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	SK 2|SK-2|SPK 2|SPK-2	Long non-protein coding RNA DANCR functions as a competing endogenous RNA to regulate osteoarthritis progression via miR-577/SphK2 axis. The study also showed that DANCR acted as a competitive endogenous RNA to sponge miR-577, which targeted the mRNA of SphK2 to regulate the survival of OA chondrocytes. the study revealed that lncRNA DANCR might promote the proliferation of OA chondrocytes and reduce apoptosis through the miR-577/SphK2 axis.	29678573	RID00951	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE67939,GSE75367,GSE86978)
Pneumonia	HAGLROS	miR-100	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(-);PI3K/AKT/NF-kB signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000226363	GRCh38_2:176177717-176179008	NA	NA	102800310	NA	NA	NA	Long noncoding RNA HAGLROS regulates cell apoptosis and autophagy in lipopolysaccharides-induced WI-38 cells via modulating miR-100/NF-kB axis. there was a negative correlation between HAGLROS and miR-100, and the effects of HAGLROS downregulation on LPS-induced apoptosis and autophagy in WI-38 cells were by regulation of miR-100.Knockdown of HAGLROS inhibited the activation of PI3K/AKT/NF-kB pathway. Furthermore, NFkB3 was verified as a functional target of miR-100 and effects of miR-100 inhibition on LPS-induced WI-38 cell injury were alleviated by knockdown of NFkB3.	29673591	RID00952	expression association	NA	NA	NA
Renal cell carcinoma	SNHG1	miR-137	positively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Long Noncoding RNA Small Nucleolar RNA Host Gene 1 (SNHG1) Promotes Renal Cell Carcinoma Progression and Metastasis by Negatively Regulating miR-137.High levels of SNHG1 were correlated with poor prognosis of RCC patients. Knockdown of SNHG1 suppressed the proliferation, invasion, and EMT capacity in RCC. Overexpression of SNHG1 participates in RCC tumorigenesis by regulating miR-137.	29874202	RID00953	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	NA
Retinoblastoma	CYTOR	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171791	NA	112597	596	C2orf59|LINC00152|NCRNA00152	Bcl-2|PPP1R50	Knockdown of LINC00152 significantly inhibited cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and caspase-3 and caspase-8 activities in vitro, as well as suppressing tumorigenesis in vivo. We identified several genes related to proliferation, apoptosis, and invasion including Ki-67, Bcl-2, and MMP-9 that were transcriptionally inactivated by LINC00152.	29922070	RID00954	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	CYTOR	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000100985	NA	112597	4318	C2orf59|LINC00152|NCRNA00152	CLG4B|GELB|MANDP2|MMP-9	Knockdown of LINC00152 significantly inhibited cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and caspase-3 and caspase-8 activities in vitro, as well as suppressing tumorigenesis in vivo. We identified several genes related to proliferation, apoptosis, and invasion including Ki-67, Bcl-2, and MMP-9 that were transcriptionally inactivated by LINC00152.	29922070	RID00955	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Idiopathic pulmonary fibrosis	H19	COL1A1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	fibrotic(+)	ceRNA(miR-196a)	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000108821	NA	283120	1277	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	EDSARTH1|EDSC|OI1|OI2|OI3|OI4	The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis.We further demonstrated that H19 was a direct target of miR-196a and was associated with COL1A1 expression by sponging miR-196a. downregulation of H19 alleviated fibroblast activation and lung fibrosis, and this effect was blocked by a miR-196a inhibitor. Knockdown of H19 Inhibited COL1A1, a Target of miR-196a	29411215	RID00956	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Cholangiocarcinoma	DUXAP9	MYCN	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+);cancer progression(+)	ceRNA(miR-5095)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000134323	NA	503638	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	Long noncoding RNA LINC01296 promotes tumor growth and progression by sponging miR-5095 in human cholangiocarcinoma. LINC01296 was demonstrated to sponge microRNA-5095 (miR-5095), which targets MYCN proto-oncogene bHLH transcription factor (MYCN) mRNA in human CCA. By inhibition of miR-5095, LINC01296 overexpression upregulation the expression of MYCN and promoted cell viability, migration and invasion in CCA cells.	29620172	RID00957	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	PVT1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000198793	NA	5820	2475	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00958	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	PVT1	ABCC1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000103222	NA	5820	4363	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC29|ABCC|GS-X|MRP|MRP1	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00959	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	PVT1	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000085563	NA	5820	5243	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00960	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Colorectal cancer	PVT1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00961	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pulmonary fibrosis	PCAT29	RASAL1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000111344	NA	104472713	8437	NA	RASAL	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00962	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065)
Pulmonary fibrosis	PCAT29	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000102882	NA	104472713	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00963	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pulmonary fibrosis	PCAT29	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000100030	NA	104472713	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00964	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pulmonary fibrosis	PCAT29	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000105329	NA	104472713	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00965	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pulmonary fibrosis	PCAT29	miR-221	positively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	miRNA	ENST00000560655	GRCh38_15:69592200-69695750	NA	NA	104472713	NA	NA	NA	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00966	expression association	NA	UP(LIHC);DATA(GSE117623)	NA
Urinary bladder cancer	NORAD	PUM2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cancer progression(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000055917	NA	647979	23369	LINC00657	PUMH2|PUML2	High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer. MTT and colony formation assay demonstrated that knockdown of NORAD results in lower proliferation in TSSCUP cells, whereas PUM2 expression was upregulation and E2F3 downregulated.High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer.	29605462	RID00967	expression association	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	NORAD	E2F3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cancer progression(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000112242	NA	647979	1871	LINC00657	E2F-3	High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer. MTT and colony formation assay demonstrated that knockdown of NORAD results in lower proliferation in TSSCUP cells, whereas PUM2 expression was upregulation and E2F3 downregulated.High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer.	29605462	RID00968	expression association	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Cervical cancer	BDNF-AS	BDNF	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000176697	NA	497258	627	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	ANON2|BULN2	Long noncoding RNA BDNF-AS is downregulated in cervical cancer and has anti-cancer functions by negatively associating with BDNF.BDNF-AS overexpression is anti-cancer by inhibiting proliferation and migration in vitro, and transplantation in vivo.BDNF-AS is downregulated in CC. Overexpressing BDNF-AS may inhibit CC, possibly through inverse regulation on BDNF.	29572178	RID00969	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Neuroblastoma	PAUPAR	PAX6	positively-F	RNA pull-down assay;ChIP	upregulation	microarray	GSE110033	GSE110033.zip	neurogenesis(+)	epigenetic regulation	association	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000281880	GRCh38_11:31812307-32002405	ENSG00000007372	NA	103157000	5080	NA	AN|AN2|ASGD5|D11S812E|FVH1|MGDA|WAGR	The long non-coding RNA Paupar promotes KAP1-dependent chromatin changes and regulates olfactory bulb neurogenesis. We show here that the Paupar lncRNA directly binds KAP1, an essential epigenetic regulatory protein, and thereby regulates the expression of shared target genes important for proliferation and neuronal differentiation.Paupar-KAP1 genome-wide co-occupancy reveals a fourfold enrichment of overlap between Paupar and KAP1 bound sequences, the majority of which also appear to associate with PAX6.	29661885	RID00970	epigenetic regulation	NA	NA	UP(LIHC);DATA(GSE117623)
Pre-eclampsia	H19	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00971	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Pre-eclampsia	H19	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000142208	NA	283120	207	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00972	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	H19	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00973	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Myocarditis	TUG1	miR-29b	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation	Cardiovascular system disease	Myocarditis	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR-29b. TUG1 negatively modulated the expression of miR-29b and miR-29b mimic blocked the effect of TUG1 overexpression on cell viability, apoptosis, inflammation and inactivation of NF-kB and JAK/STAT signaling pathways in LPS-stimulated H9c2 cells.	29518613	RID00974	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Fatty liver disease	H19	SREBF1	positively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	steatosis(+);hepatic lipid homeostasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000072310	NA	283120	6720	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	SREBP1|bHLHd1	Long noncoding RNA H19 interacts with polypyrimidine tract-binding protein 1 to reprogram hepatic lipid homeostasis. H19 RNA interacts with PTBP1 to facilitate its association with sterol regulatory element-binding protein 1c mRNA and protein, leading to increased stability and nuclear transcriptional activity. Ectopic expression of H19 induces steatosis and pushes the liver into a pseudo-fed state in response to fasting by promoting sterol regulatory element-binding protein 1c protein cleavage and nuclear translocation.Our study unveils an H19/PTBP1/sterol regulatory element-binding protein 1 feedforward amplifying signaling pathway to exacerbate the development of fatty liver.	29140550	RID00975	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Fatty liver disease	H19	PTBP1	interact	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	steatosis(+);hepatic lipid homeostasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000011304	NA	283120	5725	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HNRNP-I|HNRNPI|HNRPI|PTB|PTB-1|PTB-T|PTB2|PTB3|PTB4|pPTB	Long noncoding RNA H19 interacts with polypyrimidine tract-binding protein 1 to reprogram hepatic lipid homeostasis. H19 RNA interacts with PTBP1 to facilitate its association with sterol regulatory element-binding protein 1c mRNA and protein, leading to increased stability and nuclear transcriptional activity. Ectopic expression of H19 induces steatosis and pushes the liver into a pseudo-fed state in response to fasting by promoting sterol regulatory element-binding protein 1c protein cleavage and nuclear translocation.Our study unveils an H19/PTBP1/sterol regulatory element-binding protein 1 feedforward amplifying signaling pathway to exacerbate the development of fatty liver.	29140550	RID00976	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	HOTAIR	SNAI1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);tumorigenesis(+);cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Effects of Targeting lncRNA HOTAIR on the Invasion and Nude Mouse Tumorigenicity of Epithelial Ovarian Cancer Cells The lncRNA HOTAIR low expression resulted in increasing E-cadherin and decreasing snail expression detected by qRT-PCR in the shHOTAIR transfected SKOV3 cells of xenograft tumor,compared with the scramble control (P<0.05).Targeting lncRNA HOTAIR expression in SKOV3 cells with RNA interference can decrease snail,increase E-cadherin and significantly reduce the invasion and tumorigenicity of epithelial ovarian cancer SKOV3 cells.	30014633;24662839	RID00977	expression association	metastasis,prognosis	NA	UP(PAAD);DATA(GSE40174)
Epithelial ovarian cancer	HOTAIR	CDH1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);tumorigenesis(+);cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Effects of Targeting lncRNA HOTAIR on the Invasion and Nude Mouse Tumorigenicity of Epithelial Ovarian Cancer Cells The lncRNA HOTAIR low expression resulted in increasing E-cadherin and decreasing snail expression detected by qRT-PCR in the shHOTAIR transfected SKOV3 cells of xenograft tumor,compared with the scramble control (P<0.05).Targeting lncRNA HOTAIR expression in SKOV3 cells with RNA interference can decrease snail,increase E-cadherin and significantly reduce the invasion and tumorigenicity of epithelial ovarian cancer SKOV3 cells.	30014633;24662839	RID00978	expression association	metastasis,prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Alzheimer's disease	MALAT1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L4	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00979	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Alzheimer's disease	MALAT1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164305	NA	378938	836	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CPP32|CPP32B|SCA-1	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00980	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Alzheimer's disease	MALAT1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00981	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Alzheimer's disease	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00982	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Alzheimer's disease	MALAT1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198793	NA	378938	2475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00983	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Alzheimer's disease	MALAT1	GSK3B	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000082701	NA	378938	2932	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00984	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Fatty liver disease	LNCARSR	SREBF1	positively-E	RNAi	upregulation	qPCR	NA	NA	adipogenesis(+);steatosis(+)	NA	regulation	NA	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	TF	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000072310	NA	112577459	6720	NA	SREBP1|bHLHd1	we identified that lncARSR regulated hepatic lipogenesis via upregulating SREBP-1c, the key regulatory molecule involved in lipogenesis.our data indicated that lncARSR potentially contributes to the hepatic steatosis in NAFLD, which may be a new therapeutic target against NAFLD.	29555473	RID00985	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Skin squamous cell carcinoma	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00986	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Skin squamous cell carcinoma	MALAT1	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00987	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Skin squamous cell carcinoma	MALAT1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00988	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC01138	PRMT5	interact	RNAi;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000274020	GRCh38_1:148290889-148519604	ENSG00000100462	NA	388685	10419	LINC00875	HRMT1L5|HSL7|IBP72|JBP1|SKB1|SKB1Hs	The LINC01138 drives malignancies via activating arginine methyltransferase 5 in hepatocellular carcinoma. LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumorigenicity, tumour invasion and metastasis by physically interacting with arginine methyltransferase 5 (PRMT5) and enhancing its protein stability by blocking ubiquitin/proteasome-dependent degradation in HCC.	29679004	RID00989	interact with protein	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Rheumatoid arthritis	GAPLINC	miR-382-5p	negatively-F	miRanda;PITA;RNAhybrid;RNAi;CLIP-seq	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540	NA	Long Non-Coding RNA GAPLINC Promotes Tumor-Like Biologic Behaviors of Fibroblast-Like Synoviocytes as MicroRNA Sponging in Rheumatoid Arthritis Patients. Further verification of this model demonstrated that silencing of GAPLINC increased miR-382-5p and miR-575 expression.The results of this study suggest that GAPLINC may function as a novel microRNAs sponging agent affecting the biological characteristics of RA-FLSs.GAPLINC may also promote RA-FLS tumor-like behaviors in a miR-382-5p-dependent and miR-575-dependent manner. GAPLINC suppression in RA-FLS cells revealed significant alterations in cell proliferation, invasion, migration, and proinflammatory cytokines production.	29692777	RID00990	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	NA
Rheumatoid arthritis	GAPLINC	miR-575	negatively-F	miRanda;PITA;RNAhybrid;RNAi;CLIP-seq	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540	NA	Further verification of this model demonstrated that silencing of GAPLINC increased miR-382-5p and miR-575 expression.The results of this study suggest that GAPLINC may function as a novel microRNAs sponging agent affecting the biological characteristics of RA-FLSs.GAPLINC may also promote RA-FLS tumor-like behaviors in a miR-382-5p-dependent and miR-575-dependent manner. GAPLINC suppression in RA-FLS cells revealed significant alterations in cell proliferation, invasion, migration, and proinflammatory cytokines production.	29692777	RID00991	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	NA
Cervical cancer	HOTAIR	miR-17-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer Interacting With MicroRNA-17-5p. Pearson's correlation analysis indicated that miR-17-5p expression was negatively correlated to that of HOTAIR. Luciferase reporter assay revealed that miR-17-5p directly targeted HOTAIR 3'-UTR.our results reveal the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p.Loss-of-function experiments showed that HOTAIR knockdown inhibited the proliferation, migration, and invasion of cervical cells.In summary, our results reveal the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer.	28745272	RID00992	ceRNA or sponge	NA	NA	NA
Polycystic ovary syndrome	NPTN-IT1	TIMP2	positively-E	western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);apoptosis process(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000035862	NA	101241892	7077	lncRNA-LET	CSC-21K|DDC8	LncRNA-LET inhibits cell viability, migration and EMT while induces apoptosis by up-regulation of TIMP2 in human granulosa-like tumor cell line KGN. Overexpression of lncRNA-LET inhibits cell viability, migration and EMT process, and increases apoptosis in KGN cells by up-regulating the expression of TIMP2 and activating the Wnt/beta-catenin and notch signaling pathways.	29432996	RID00993	expression association	NA	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	E2F1	RGMB-AS1	positively-E	qRT-PCR;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000246763	GRCh38_5:98769618-98773469	1869	503569	E2F-1|RBAP1|RBBP3|RBP3	NA	LncRNA RGMB-AS1 is activated by E2F1 and promotes cell proliferation and invasion in papillary thyroid carcinoma.Results of CHIP assay showed that E2F1 bound to lncRNA RGMB-AS1 promoter region.	29687852	RID00994	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Pre-eclampsia	HK2P1	HK2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	ceRNA(miR-6887-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228612	GRCh38_X:80571871-80574607	ENSG00000159399	NA	642546	3099	HK2P	HKII|HXK2	Dysregulated Pseudogene HK2P1 May Contribute to Preeclampsia as a Competing Endogenous RNA for Hexokinase 2 by Impairing Decidualization. there was a significant positive correlation between the expression of HK2P1 and HK2, and HK2P1 regulated the HK2 expression via competition for the shared miR-6887-3p. Downregulated HK2P1 or HK2 inhibited human endometrial stromal cells proliferation and differentiation. By sequence alignment, we found miR-6887-3p had 4 potential binding sites in HK2P1 as well as in the 3'-UTR of HK2	29440331	RID00995	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Atherosclerosis	ENST00113	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	NA	NA	NA	NA	NA	NA	LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis. we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID00996	expression association	NA	NA	NA
Atherosclerosis	ENST00113	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID00997	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	ENST00113	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID00998	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Cerebral ischemia-reperfusion injury	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Mechanism of MALAT1 preventing apoptosis of vascular endothelial cells induced by oxygen-glucose deficiency and reoxidation. After OGD-R, over-expression of MALAT1 lentivirus increased phosphatidylinositol 3-kinase (PI3K) activity.This study first proposed that lncRNA MALAT1 can protect human cerebrovascular endothelial cells from OGD-R-induced apoptosis through a PI3K-dependent mechanism.Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells. lentiviral knockdown of MALAT1 decreased PI3K activities and the activation of Akt phosphorylation.In conclusion, to the best of our knowledge, the present study was the first to suggest that lncRNA MALAT1 may protect human brain vascular endothelial cells from OGD-R-induced apoptosis via a PI3K-dependent mechanism.	29575939;28413461	RID00999	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Lung adenocarcinoma	MALAT1	CDKN1A	negatively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells. Flow cytometry analysis revealed that MALAT1-depleted cells exhibited G1 cell cycle arrest. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.p21 and FAS, well-known p53 targets, were upregulation by MALAT1 knockdown in A549 human lung adenocarcinoma cells. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.	29632545	RID01000	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	FAS	negatively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026103	NA	378938	355	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells. Flow cytometry analysis revealed that MALAT1-depleted cells exhibited G1 cell cycle arrest. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.p21 and FAS, well-known p53 targets, were upregulation by MALAT1 knockdown in A549 human lung adenocarcinoma cells. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.	29632545	RID01001	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Multiple myeloma	PDIA3P1	G6PD	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	regulation	RNA-DNA	bortezomib	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000180867	GRCh38_1:147172744-147179622	ENSG00000160211	NA	171423	2539	NA	G6PD1	LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma. we revealed that PDIA3P interacts with c-Myc to enhance its transactivation activity and binding to G6PD promoter, stimulating G6PD expression and PPP flux. PDIA3P promotes cell proliferation and bortezomib resistance through G6PD and the pentose phosphate pathway LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma.we found lncRNA Protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P) is highly expressed in MM.	29501744	RID01002	transcriptional regulation	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	FENDRR	FOXF1	positively-E	luciferase reporter assay;RNAi;ChIP	downregulation	sequencing	TCGA	LUSC_LUAD.zip	tumorigenesis(-)	ceRNA(miR-424)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000103241	NA	400550	2294	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ACDMPV|FKHL5|FREAC1	FENDRR can upregulate FOXF1 by competitively binding to miR-424. FENDRR, a long intergenic non-coding RNA (lincRNA) that functions to inhibit lung cancer by affecting expressions of an abundant number of genes, including the tumor suppressor FOXF1.	29293945	RID01003	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Chronic myeloid leukemia	MEG3	miR-184	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long Noncoding RNA MEG3 Inhibits Cell Proliferation and Metastasis in Chronic Myeloid Leukemia via Targeting miR-184. overexpression of MEG3 significantly decreased the expression of miR-184, and MEG3 knockdown markedly increased it. Furthermore, our results showed that MEG3 interacted with miR-184 and subsequently mitigated the proliferation and invasion of leukemia cells by downregulating related proteins.	28653609	RID01004	ceRNA or sponge	metastasis	NA	NA
Gastric cancer	NEAT1	miR-335-5p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 regulates the proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis. In addition, lncRNA NEAT1 inhibited the expression of miR-335-5p, and miR-335-5p targeted ROCK1 in BGC-823 cells. miR-335-5p overexpression significantly inhibited cell proliferation, migration and invasion, which was counteracted by ROCK1 overexpression concurrently. Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.	29544562	RID01005	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Gastric cancer	NEAT1	ROCK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|NCRNA00084|TncRNA|VINC	P160ROCK|ROCK-I	Long non-coding RNA NEAT1 regulates the proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis. In addition, lncRNA NEAT1 inhibited the expression of miR-335-5p, and miR-335-5p targeted ROCK1 in BGC-823 cells. miR-335-5p overexpression significantly inhibited cell proliferation, migration and invasion, which was counteracted by ROCK1 overexpression concurrently. Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.	29544562	RID01006	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	miR-122	HOTTIP	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	Hepatitis C virus core impacts expression of miR122 and miR204 involved in carcinogenic progression via regulation of TGFBRAP1 and HOTTIP expression. Our data suggests that the pathways of miR204-HPCAL1-lncRNAHOTTIP and miR122-TGFBRAP1 were likely involved in the carcinogenic progress due to the presence of HCV core, and that overexpression of miR122 and miR204 might inhibit the HCC progress by down-regulation of TGFBRAP1 and HOTTIP expression.	29535540	RID01007	expression association	NA	NA	NA
Hepatocellular carcinoma	miR-204	HOTTIP	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. These results elucidate that the miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis.Hepatitis C virus core impacts expression of miR122 and miR204 involved in carcinogenic progression via regulation of TGFBRAP1 and HOTTIP expression. Our data suggests that the pathways of miR204-HPCAL1-lncRNAHOTTIP and miR122-TGFBRAP1 were likely involved in the carcinogenic progress due to the presence of HCV core, and that overexpression of miR122 and miR204 might inhibit the HCC progress by down-regulation of TGFBRAP1 and HOTTIP expression.	26710269;29535540	RID01008	ceRNA or sponge	NA	NA	NA
Nasopharynx carcinoma	TGFB1	MALAT1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(-);cell migration(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TGF-beta regulates the ERK/MAPK pathway independent of the SMAD pathway by repressing miRNA-124 to increase MALAT1 expression in nasopharyngeal carcinoma.constant TGF-beta stimulation repressed miR-124 expression, whereas miR-124 overexpression antagonized TGF-beta-promoted NPC cell growth and migration.	29710466	RID01009	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Osteocarcinoma	LIN28A	MALAT1	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	RNA stability	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Osteocarcinoma	TF	lncRNA	ENSG00000131914	NA	ENSG00000251562	GRCh38_11:65497688-65506516	79727	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RNA binding protein Lin28A promotes osteocarcinoma cells progression by associating with the long noncoding RNA MALAT1. Lin28A was found to harbor binding sites on MALAT1 sequences and associated with MALAT1, and increased MALAT1 stability and expression.Lin28A knockdown inhibited OS cells proliferation, migration, invasion and promoted cell apoptosis;Expressions of Lin28A and long noncoding RNA MALAT1 were positively correlated.	29204769	RID01010	interact with mRNA	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Alzheimer's disease	EBF3-AS	EBF3	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	TF	NA	GRCh38_10:129837700-129842171	ENSG00000108001	NA	NA	253738	NA	COE3|EBF-3|HADDS|O/E-2|OE-2	Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease. These results revealed that lncRNA EBF3-AS promoted neuron apoptosis in AD, and involved in regulating EBF3 expression.The expression of EBF3 was downregulated in Abeta25-35- and OA-treated SH-SY5Y, which was reversed by EBF3-AS knockdown.	29298096	RID01011	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Gorham's disease	MALAT1	VEGFA	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-22-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Gorham's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MVCD1|VEGF|VPF	MALAT1 enhanced the proliferation of human osteoblasts treated with ultra-high molecular weight polyethylene by targeting VEGF via miR-22-5p. Knockdown of MALAT1 inhibited the growth of UHMWPE-treated hFOB 1.19 cells, and this effect was associated with the upregulation of OPG, and downregulation of RANKL and VEGF.	29328414	RID01012	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Malignant glioma	SNHG16	E2F1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-20a-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000101412	NA	100507246	1869	Nbla10727|Nbla12061|ncRAN	E2F-1|RBAP1|RBBP3|RBP3	Long non-coding RNA SNHG16 contributes to glioma malignancy by competitively binding miR-20a-5p with E2F1. We also found that SNHG16 may act as a ceRNA for miR-20a-5p, enhancing the expression of E2F1.miR-20a-5p mimic enhanced the inhibition of cell proliferation, invasion, migration, and EMT, and increase of apoptosis induced by SNHG16 knockdown. In conclusion, SNHG16 promotes glioma tumorigenesis by sponging miR-20a-5p, leading to the enhancement of its endogenous targets E2F1. The data provides a new clue for the role of SNHG16/miR-20a-5p/E2F1 in the development of glioma.	29685003	RID01013	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Atherosclerosis	HOTTIP	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000110092	NA	100316868	595	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01014	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Atherosclerosis	HOTTIP	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000132646	NA	100316868	5111	HOXA-AS6|HOXA13-AS1|NCRNA00213	ATLD2	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01015	expression association	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Atherosclerosis	HOTTIP	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01016	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Atherosclerosis	HOTTIP	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000136997	NA	100316868	4609	HOXA-AS6|HOXA13-AS1|NCRNA00213	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01017	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Chronic myeloid leukemia	H19	BCR-ABL	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Hypomethylation-mediated H19 overexpression increases the risk of disease evolution through the association with BCR-ABL transcript in chronic myeloid leukemia. H19 overexpression, a frequent event in CML, was associated with higher BCR-ABL transcript involving in disease progression.Moreover, H19 DMR/ICR hypomethylation in CML may be one of the mechanisms mediating H19 overexpression.	28776669	RID01018	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Atherosclerosis	MEG3	miR-223	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Melatonin prevents endothelial cell pyroptosis via regulation of long noncoding RNA MEG3/miR-223/NLRP3 axis. We found that lncRNA MEG3 enhanced pyroptosis in HAECs. Moreover, MEG3 acted as an endogenous sponge by sequence complementarity to suppress the function of miR-223 and to increase NLRP3 expression and enhance endothelial cell pyroptosis.	29024030	RID01019	ceRNA or sponge	NA	NA	NA
Atherosclerosis	MEG3	NLRP3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000162711	NA	55384	114548	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCAS1|FCU|KEFH|MWS|NALP3|PYPAF1	Melatonin prevents endothelial cell pyroptosis via regulation of long noncoding RNA MEG3/miR-223/NLRP3 axis. We found that lncRNA MEG3 enhanced pyroptosis in HAECs. Moreover, MEG3 acted as an endogenous sponge by sequence complementarity to suppress the function of miR-223 and to increase NLRP3 expression and enhance endothelial cell pyroptosis.	29024030	RID01020	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Psoriasis	MSX2P1	S100A7	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-6731-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000229590	GRCh38_17:58157028-58157800	ENSG00000143556	NA	55545	6278	HPX5|HSHPX5|MSX2P	PSOR1|S100A7c	Up-regulated lncRNA-MSX2P1 promotes the growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7. Competitive endogenous RNAs (ceRNAs) regulate RNA transcripts by competing for shared miRNAs and play critical roles in disease development. Immunohistochemistry demonstrated significantly increased expression levels of S100A7 in psoriatic lesions, compared with normal skin tissue. We observed a positive correlation between lncRNA-MSX2P1 expression and S100A7 expression. In addition, miR-6731-5p suppressed proliferation, accelerated apoptosis in IL-22-stimulated keratinocytes, and decreased the expressions of S100A7, IL-12beta, IL-23, HLA-C,CCHCR1, TNF-alpha, and NF-kB proteins. Our data demonstrated that MSX2P1 facilitate the progression and growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7.	29339075	RID01021	ceRNA or sponge	NA	NA	UP(BRCA);DATA(GSE55807)
Non-small cell lung cancer	GHET1	LATS1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000131023	NA	102723099	9113	lncRNA-GHET1	WARTS|wts	Knockdown of lncRNA GHET1 suppresses cell proliferation, invasion and LATS1/YAP pathway in non small cell lung cancer. Knockdown of lncRNA GHET1 suppressed cell proliferation and invasion capacity and Epithelial-Mesenchymal Transition (EMT) phenomenon of NSCLC cells. Moreover, we demonstrated that knockdown of lncRNA GHET1 suppresses LATS1/YAP pathway signaling pathway by downregulating YAP1 expression in NSCLC cells.	29286919	RID01022	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	GHET1	YAP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000137693	NA	102723099	10413	lncRNA-GHET1	COB1|YAP|YAP2|YAP65|YKI	Knockdown of lncRNA GHET1 suppresses cell proliferation, invasion and LATS1/YAP pathway in non small cell lung cancer. Knockdown of lncRNA GHET1 suppressed cell proliferation and invasion capacity and Epithelial-Mesenchymal Transition (EMT) phenomenon of NSCLC cells. Moreover, we demonstrated that knockdown of lncRNA GHET1 suppresses LATS1/YAP pathway signaling pathway by downregulating YAP1 expression in NSCLC cells.	29286919	RID01023	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	GAS5	EZH2	negatively-E	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	apoptosis process(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106462	NA	60674	2146	NCRNA00030|SNHG2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA GAS5 promotes bladder cancer cells apoptosis through inhibiting EZH2 transcription. GAS5 effectively repressed EZH2 transcription by directly interacting with E2F4 and recruiting E2F4 to EZH2 promoter. We previously reported that miR-101 induced the apoptosis of BC cells by inhibiting the expression of EZH2. Interestingly, the present study showed that downregulation of EZH2 by GAS5 resulted in overexpression of miR-101 in T24 and EJ cells.	29445179	RID01024	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Atherosclerosis	H19	WNT1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-148b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000125084	NA	283120	7471	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BMND16|INT1|OI15	H19 knockdown suppresses proliferation and induces apoptosis by regulating miR-148b/WNT/beta-catenin in ox-LDL-stimulated vascular smooth muscle cells. H19 inhibited miR-148b expression by direct interaction. Further mechanical explorations showed that WNT1 was a target of miR-148b and H19 acted as a competing endogenous RNA (ceRNA) of miR-148b to enhance WNT1 expression.H19 facilitated proliferation and inhibited apoptosis through modulating WNT/beta-catenin signaling pathway via miR-148b in ox-LDL-stimulated HA-VSMCs, implicating the potential values of H19 in AS therapy.	29415742	RID01025	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Osteoarthritis	SNHG5	SOX2	positively-E	luciferase reporter assay;RIP;RNAi	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000181449	NA	387066	6657	C6orf160|LINC00044|NCRNA00044|U50HG	ANOP3|MCOPS3	LncRNA SNHG5/miR-26a/SOX2 signal axis enhances proliferation of chondrocyte in osteoarthritis. The relationship between SNHG5 and miR-26a was confirmed by RIP and the luciferase reporter assays. SOX2 was identified as a target gene of miR-26a by the luciferase reporter assay. Rescue assay was applied to verify the relationship among SNHG5, miR-26a, and SOX2. Our current study demonstrated that SNHG5 is involved in the mechanism of OA through functioning as a ceRNA to competitively sponge miR-26a, therefore, regulating the expression of SOX2.	29409014	RID01026	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(LIHC);DATA(GSE117623)
Spinal cord ischemia-reperfusion injury	CASC7	miR-30c	positively-E	RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000259758	GRCh38_8:140520156-140529501	NA	NA	NA	NA	NA	NA	Hydrogen sulfide upregulation lncRNA CasC7 to reduce neuronal cell apoptosis in spinal cord ischemia-reperfusion injury rat.knockdown of CasC7 could upregulate miR-30c expression, promote cell apoptosis and downregulate miR-30c's target gene expression.	29571256	RID01027	ceRNA or sponge	NA	NA	NA
Gastric cancer	ZEB1	HOTAIR	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000148516	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6935	100124700	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Knock-down of ZEB1 inhibits the proliferation, invasion and migration of gastric cancer cells. Conclusion Knock-down of ZEB1 expression by RNA interference can decease lncRNA HOTAIR expression and restrain cell proliferation, invasion and migration in gastric cancer BGC823 cells	28871949	RID01028	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Urinary bladder cancer	HOTAIR	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Tetracycline-controllable artificial microRNA-HOTAIR + EZH2 suppressed the progression of bladder cancer cells. we also found that HOTAIR expression was positively correlated with EZH2 expression	28671703	RID01029	expression association	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Thyroid cancer	LINC00312	miR-197-3p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p	28539331	RID01030	expression association	NA	NA	NA
Pancreatic cancer	linc-DYNC2H1-4	MMP3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell stemness(+)	ceRNA(miR-145)	regulation	NA	NA	CSC	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_11:102831703-102832102	ENSG00000149968	NA	NA	4314	NA	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Linc-DYNC2H1-4 promotes EMT and CSC phenotypes by acting as a sponge of miR-145 in pancreatic cancer cells. We proved that MMP3, the nearby gene of linc-DYNC2H1-4 in the sense strand, was also a target of miR-145. Downregulation of MMP3 by miR-145 was reverted by linc-DYNC2H1-4, indicating that competing with miR-145 is one of the mechanisms for linc-DYNC2H1-4 to regulate MMP3.	28703793	RID01031	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Atherosclerosis	TSLP	HOTAIR	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	PCG	lncRNA	ENSG00000145777	NA	ENSG00000228630	GRCh38_12:53962308-53974956	85480	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis. TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis.	28615347	RID01032	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	NA
Hirschsprung's disease	MEG3	miR-770-5p	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung's disease. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay.To determine whether MEG3 functions via the miR-770-5p/SRGAP1 pathway, we firstly transfected 293T and SH-SY5Y cells with MEG3 siRNA, miR-770-5p expression was downregulated, whereas SRGAP1 was upregulation at the mRNA and protein levels. Secondly, infection of the two cell lines with MEG3-overexpression lentivirus resulted in increased MEG3 expression levels, whereas SRGAP1 expression was downregulated at the mRNA and protein levels	29050236	RID01033	expression association	NA	NA	NA
Hirschsprung's disease	MEG3	SRGAP1	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000196935	NA	55384	57522	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ARHGAP13|NMTC2	Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung's disease. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay.To determine whether MEG3 functions via the miR-770-5p/SRGAP1 pathway, we firstly transfected 293T and SH-SY5Y cells with MEG3 siRNA, miR-770-5p expression was downregulated, whereas SRGAP1 was upregulation at the mRNA and protein levels. Secondly, infection of the two cell lines with MEG3-overexpression lentivirus resulted in increased MEG3 expression levels, whereas SRGAP1 expression was downregulated at the mRNA and protein levels	29050236	RID01034	expression association	NA	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065)
Epithelial ovarian cancer	SLC7A11-AS1	SLC7A11	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-);cell migration(-)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000250033	GRCh38_4:138057464-138178177	ENSG00000151012	NA	641364	23657	NA	CCBR1|xCT	Antisense lncRNA As-SLC7A11 suppresses epithelial ovarian cancer progression mainly by targeting SLC7A11. We also demonstrated that overexpression of As-SLC7A11 could significantly suppress the expression of SLC7A11, indicating a negative correlation between As-SLC7A11 and SLC7A11 in ovarian cancer cells.	29441937	RID01035	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE60407)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	SNHG1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000136997	NA	23642	4609	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA SNHG1 promotes cell proliferation and tumorigenesis in colorectal cancer via Wnt/beta-catenin signaling. Moreover, SNHG1 can promote the expression of target genes, and SNHG1 expression is positively correlated with WNT expression. SNHG1 regulates colorectal cancer by the Wnt signaling pathway. Next, Pearson's correlation was conducted to compare the expression of SNHG1 and Myc. The results show that there was a positive correlation between SNHG1 and c-Myc expression (Fig. 5B), also with the correlation between SNHG1 and TCF7 expression as shown in Fig. 5C. siSNHG1 downregulates the gene expression of c-Myc/MMP-7/CyclinD1/TCF7/LEF in both mRNA and protein levels, while the oeSNHG1 has shown an opposite tendency.	29441936	RID01036	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	SNHG1	TCF7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000081059	NA	23642	6932	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	TCF-1	Long non-coding RNA SNHG1 promotes cell proliferation and tumorigenesis in colorectal cancer via Wnt/beta-catenin signaling. Moreover, SNHG1 can promote the expression of target genes, and SNHG1 expression is positively correlated with WNT expression. SNHG1 regulates colorectal cancer by the Wnt signaling pathway. Next, Pearson's correlation was conducted to compare the expression of SNHG1 and Myc. The results show that there was a positive correlation between SNHG1 and c-Myc expression (Fig. 5B), also with the correlation between SNHG1 and TCF7 expression as shown in Fig. 5C. siSNHG1 downregulates the gene expression of c-Myc/MMP-7/CyclinD1/TCF7/LEF in both mRNA and protein levels, while the oeSNHG1 has shown an opposite tendency.	29441936	RID01037	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Osteoarthritis	PVT1	miR-488-3p	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 Regulates Chondrocyte Apoptosis in Osteoarthritis by Acting as a Sponge for miR-488-3p	28520497	RID01038	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Esophageal cancer	MALAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA MALAT1 functions as a competing endogenous RNA to regulate the expressions of ZEB1 and ZEB2 by sponging miR-200a and promotes invasion and migration of esophageal cancer cells through inducing epithelial-mesenchymal transition	28635228	RID01039	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	MALAT1	ZEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA MALAT1 functions as a competing endogenous RNA to regulate the expressions of ZEB1 and ZEB2 by sponging miR-200a and promotes invasion and migration of esophageal cancer cells through inducing epithelial-mesenchymal transition	28635228	RID01040	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	LINC00630	HDAC1	positively-F	mass spectrometry;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223546	GRCh38_X:102769158-102885406	ENSG00000116478	NA	100287765	3065	NA	GON-10|HD1|KDAC1|RPD3|RPD3L1	DDX23-Linc00630-HDAC1 axis activates the Notch pathway to promote metastasis. By RNA pull-down and mass spectrometry we identified Histone deacetylases 1 (HDAC1) and DEAD-box helicase 23 (DDX23) as the linc00630-binding protein that associated with mechanism of linc00630.DDX23 can specific bind with the promoter of Linc00630 to up-regulate the RNA level and high level of linc00630 strength the protein stability of HDAC1 to regulate the downstream pathway.	28473661	RID01041	interact with protein	metastasis	UP(LIHC);DOWN(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE60407,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Non-small cell lung cancer	LINC00630	DDX23	positively-F	mass spectrometry;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223546	GRCh38_X:102769158-102885406	ENSG00000174243	NA	100287765	9416	NA	PRPF28|SNRNP100|U5-100K|U5-100KD|prp28	DDX23-Linc00630-HDAC1 axis activates the Notch pathway to promote metastasis. By RNA pull-down and mass spectrometry we identified Histone deacetylases 1 (HDAC1) and DEAD-box helicase 23 (DDX23) as the linc00630-binding protein that associated with mechanism of linc00630.DDX23 can specific bind with the promoter of Linc00630 to up-regulate the RNA level and high level of linc00630 strength the protein stability of HDAC1 to regulate the downstream pathway.	28473661	RID01042	interact with protein	metastasis	UP(LIHC);DOWN(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE60407,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Endometrial carcinoma	NEAT1	HMGA1	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000137309	NA	283131	3159	LINC00084|NCRNA00084|TncRNA|VINC	HMG-R|HMGA1A|HMGIY	NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/beta-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells	28447190	RID01043	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Clear cell renal cell carcinoma	DLEU2	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-30a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000169554	NA	8847	9839	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The putative tumor suppressor microRNA-30a-5p modulates clear cell renal cell carcinoma aggressiveness through repression of ZEB2. In addition, miR-30a-5p may be downregulated by the long non-coding RNA DLEU2.Increasing evidence has shown that lncRNAs contain motifs with sequences complementary to miRNAs and can inhibit miRNAs expression and activity. To examine whether miR-30a-5p is regulated in such a manner in ccRCC cells, interactions between miR-30a-5p and lncRNAs were predicted using starBASE v2.0. The lncRNA DLEU2 was identified as containing a conserved target site in the miR-30a-5p seed region	28569782	RID01044	ceRNA or sponge	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	UCA1	CCND1	positively-E	RIP;luciferase reporter assay;ChIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000110092	NA	652995	595	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA UCA1 induced by SP1 promotes cell proliferation via recruiting EZH2 and activating AKT pathway in gastric cancer.This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.	28569779	RID01045	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Prostate cancer	lncRNA625	miR-432	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	NA	GRCh38_17:81709333-81712153	NA	NA	NA	NA	NA	NA	lncRNA625 could functionally inhibit PC3 cells proliferation and promote cells apoptosis through regulating the Wnt/beta-catenin pathway by targeting miR-432. miR-432 is a direct target of lncRNA625. Most importantly, we further found that miR-432 could deactivate Wnt/beta-catenin pathway via suppressing TRIM29 and PYGO2 directly.	28678327	RID01046	ceRNA or sponge	NA	NA	NA
Hepatocellular carcinoma	miR-26a	MEG3	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MicroRNA-26a inhibits proliferation and metastasis of human hepatocellular carcinoma by regulating DNMT3B-MEG3 axis. we demonstrated that DNA methyltransferase 3b (DNMT3B) was a direct target gene of miR-26a.It verified again that DNMT3B could imitate the effect of 5-aza-CdR to down-regulate the expression of MEG3 in HCC cells.Together, the present study added miR-26a/DNMT3B/MEG3 axis to the complex mechanisms of HCC development.	28440439	RID01047	epigenetic regulation	metastasis	NA	NA
Nasopharynx carcinoma	FOXCUT	FOXC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000054598	NA	101927703	2296	LINC01379|TCONS_00011636	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	The long noncoding RNA FOXCUT promotes proliferation and migration by targeting FOXC1 in nasopharyngeal carcinoma.FOXCUT expression was positively correlated with FOXC1 expression	28635400	RID01048	expression association	metastasis	NA	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	AL163636.1	EGFR	positively-F	luciferase reporter assay;RNA pull-down assay;mass spectrometry;RIP	upregulation	qPCR	NA	NA	immune evasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Immune Detection	Cancer	Liver cancer	lncRNA	PCG	ENSG00000258451	GRCh38_14:20693480-20707120	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long noncoding RNA lnc-EGFR stimulates T-regulatory cells differentiation thus promoting hepatocellular carcinoma immune evasion. lnc-EGFR specifically binds to EGFR and blocks its interaction with and ubiquitination by c-CBL, stabilizing it and augmenting activation of itself and its downstream AP-1/NF-AT1 axis, which in turn elicits EGFR expression.	28541302	RID01049	interact with protein	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	LINC00673	HOXA5	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106004	NA	100499467	3202	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	HOX1|HOX1.3|HOX1C	Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5	28423732	RID01050	epigenetic regulation	metastasis	NA	NA
T-cell acute lymphocytic leukemia	TLX3	MIR99AHG	positively-F	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000164438	NA	ENSG00000215386	GRCh38_21:15928296-16645467	30012	388815	HOX11L2|RNX	NA	Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia.Finally, we established that TLX3 directly regulates miR-125b production through binding and transactivation of LINC00478, a long noncoding RNA gene, which is the host of miR-99a/Let-7c/miR-125b. Altogether, our results reveal an original functional link between TLX3 and oncogenic miR-125b in T-ALL development.	29296717	RID01051	interact with protein	NA	NA	UP(LIHC);DATA(GSE117623)
T-cell acute lymphocytic leukemia	MIR99AHG	miR-125b	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	host	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000215386	GRCh38_21:15928296-16645467	NA	NA	388815	NA	NA	NA	Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia.Finally, we established that TLX3 directly regulates miR-125b production through binding and transactivation of LINC00478, a long noncoding RNA gene, which is the host of miR-99a/Let-7c/miR-125b. Altogether, our results reveal an original functional link between TLX3 and oncogenic miR-125b in T-ALL development.	29296717	RID01052	expression association	NA	UP(LIHC);DATA(GSE117623)	NA
Breast cancer	UCA1	miR-18a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Urothelial carcinoma-associated 1 enhances tamoxifen resistance in breast cancer cells through competitively inhibiting miR-18a. UCA1 directly interacted with miR-18a and reduced its expression in ER positive breast cancer cells. UCA1 was significantly upregulation in tamoxifen resistant LCC2, LCC9, and BT474 cells than in tamoxifen sensitive MCF-7 cells.	28416841	RID01053	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	NA
Parkinson's disease	HOTAIR	LRRK2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000188906	NA	100124700	120892	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AURA17|DARDARIN|PARK8|RIPK7|ROCO2	The long noncoding RNA HOTAIR promotes Parkinson's disease by upregulating LRRK2 expression. With the presence of HOTAIR overexpression in SH-SY5Y cells, the expression of LRRK2 was increased compared with that in the control.	28445933	RID01054	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cerebral ischemia-reperfusion injury	MALAT1	AKT1	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells. lentiviral knockdown of MALAT1 decreased PI3K activities and the activation of Akt phosphorylation.In conclusion, to the best of our knowledge, the present study was the first to suggest that lncRNA MALAT1 may protect human brain vascular endothelial cells from OGD-R-induced apoptosis via a PI3K-dependent mechanism	28413461	RID01055	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	HOTAIR	ADAMTS5	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154736	NA	100124700	11096	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADAM-TS 11|ADAM-TS 5|ADAM-TS5|ADAMTS-11|ADAMTS-5|ADAMTS11|ADMP-2	Long non-coding RNA HOTAIR promotes expression of ADAMTS-5 in human osteoarthritic articular chondrocytes. Lentiviral overexpression and knockdown of HOTAIR markedly increased and decreased the expression of ADAMTS-5, respectively.In conclusion, this study provides the first evidence supporting that HOTAIR strongly promotes the expression of ADAMTS-5 by increasing its mRNA stability in human OA articular chondrocytes; this effect is enhanced by TNF-alpha. It adds new insights into the pathogenesis of OA and suggests that HOTAIR could be a new therapeutic target for ADAMTS-5 inhibition in human OA cartilage.	29441864	RID01056	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Osteosarcoma	MEG3	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148400	NA	55384	4851	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AOS5|AOVD1|TAN1|hN1	MEG3 long non-coding RNA prevents cell growth and metastasis of osteosarcoma. In addition, MEG3 over-expression markedly inhibited Notch1, Hes1,TGF-beta and N-cadheren expression, and the expression level of E-cadheren was improved. These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-beta signaling pathway, thus providing a potential therapeutic target for OS treatment	29198132	RID01057	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	MEG3	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105329	NA	55384	7040	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-beta signaling pathway, thus providing a potential therapeutic target for OS treatment	29198132	RID01058	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myocardial infarction	H19	SOX8	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell injury(-);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-139)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000005513	NA	283120	30812	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139.H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139.These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.	29179202	RID01059	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Type 2 diabetes mellitus	lncRNA-p3134	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01060	expression association	circulating	NA	NA
Type 2 diabetes mellitus	lncRNA-p3134	AKT2	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	ENSG00000105221	NA	NA	208	NA	NA	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01061	expression association	circulating	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Type 2 diabetes mellitus	lncRNA-p3134	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01062	expression association	circulating	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Osteoarthritis	GAS5	KLF2	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(-);inflammatory response(-);NF-kB signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation;Sustained Angiogenesis	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000127528	NA	60674	10365	NCRNA00030|SNHG2	LKLF	LncRNA GAS5 Overexpression Reverses LPS-Induced Inflammatory Injury and Apoptosis Through Up-Regulating KLF2 Expression in ATDC5 Chondrocytes. KLF2 was predicted and verified as a target of GAS5, and GAS5 functioned through regulating expression of KLF2. Besides, aberrant expression of KLF2 regulated expressions of key kinases involved in the NF-kB and Notch pathways.	29448248	RID01063	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	RP11-445H22.4	CXCR4	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-301a)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	GRCh38_20:44694892-44746021	ENSG00000121966	NA	NA	7852	NA	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis. miR-301a directly bound to RP11-445H22.4, and suppression of miR-301a inversed the effects of RP11-445H22.4 inhibition. Furthermore, CXCR4 was a direct target of miR-301a, and CXCR4 silencing increased cell viability, decreased apoptosis and inflammatory cytokines secretions in LPS-treated ATDC5 cells. Besides, we found that CXCR4 silencing blocked LPS-activated NF-kB and MAPK/ERK pathways. The study indicated that lncRNA RP11-445H22.4-miR-301a-CXCR4 axis played an important role in cartilage ATDC5 cells and provided a theoretical basis of lncRNA RP11-445H22.4 in OA.	29414810	RID01064	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CCAT1	let-7c	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT signaling pathway(+);cell proliferation(+)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	CCAT1 stimulation of the symmetric division of NSCLC stem cells through activation of the Wnt signalling cascade. CCAT1 inhibition decreased the ratio of symmetric division of stem cells, and both Let-7c and Axitinib significantly abolished CCAT1 induction of symmetric division by inhibiting Wnt signalling. Restoration of Let-7c blocked the CCAT1 effects, forming the CCAT1/Let-7c/Wnt regulatory axis to control the division of lung cancer stem cells.CCAT1 stimulation of the symmetric division of NSCLC stem cells through activation of the Wnt signalling cascade.	29350683	RID01065	expression association	NA	NA	NA
Hepatocellular carcinoma	TUG1	miR-455-3p	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(+);glucose metabolic process(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Taurine up-regulated gene 1 functions as a master regulator to coordinate glycolysis and metastasis in hepatocellular carcinoma. we showed that knockdown of taurine up-regulated gene 1 (TUG1) induces marked inhibition of cell migration, invasion, and glycolysis through suppression of microRNA (miR)-455-3p. knockdown of TUG1 enhanced binding of the co-repressor p21 to E2F1 when these transcriptional factors are occupying the miR-455 promoter. MiR-455-3p, which is transcriptionally repressed by p21, directly targets the 3' untranslated region of adenosine monophosphate-activated protein kinase subunit beta 2 (AMPKbeta2). The TUG1/miR-455-3p/AMPKbeta2 axis regulates cell growth, metastasis, and glycolysis through regulation of hexokinase 2 (HK2).TUG1 is clearly associated with HK2 overexpression and unfavorable prognosis in HCC patients.Our data collectively highlight that novel regulatory associations among TUG1, miR-455-3p, AMPKbeta2, and HK2 are an important determinant of glycolytic metabolism and metastasis in HCC cells and support the potential utility of targeting TUG1/HK2 as a therapeutic strategy for HCC.	28802060	RID01066	expression association	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	TUG1	HK2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(+);glucose metabolic process(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000159399	NA	55000	3099	LINC00080|NCRNA00080|TI-227H	HKII|HXK2	Taurine up-regulated gene 1 functions as a master regulator to coordinate glycolysis and metastasis in hepatocellular carcinoma. we showed that knockdown of taurine up-regulated gene 1 (TUG1) induces marked inhibition of cell migration, invasion, and glycolysis through suppression of microRNA (miR)-455-3p. knockdown of TUG1 enhanced binding of the co-repressor p21 to E2F1 when these transcriptional factors are occupying the miR-455 promoter. MiR-455-3p, which is transcriptionally repressed by p21, directly targets the 3' untranslated region of adenosine monophosphate-activated protein kinase subunit beta 2 (AMPKbeta2). The TUG1/miR-455-3p/AMPKbeta2 axis regulates cell growth, metastasis, and glycolysis through regulation of hexokinase 2 (HK2).TUG1 is clearly associated with HK2 overexpression and unfavorable prognosis in HCC patients.Our data collectively highlight that novel regulatory associations among TUG1, miR-455-3p, AMPKbeta2, and HK2 are an important determinant of glycolytic metabolism and metastasis in HCC cells and support the potential utility of targeting TUG1/HK2 as a therapeutic strategy for HCC.	28802060	RID01067	expression association	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00589	STAT3	positively-F	RIP;RNAi;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+);IL6/STAT3 signaling pathway(-)	phosphorylation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000168610	NA	619351	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA TSLNC8 is a tumor suppressor that inactivates the interleukin-6/STAT3 signaling pathway. TSLNC8 significantly suppresses the proliferation and metastasis of HCC cells in vitro and in vivo. TSLNC8 exerts its tumor suppressive activity by competitively interacting with transketolase and signal transducer and activator of transcription 3 (STAT3) and modulating the STAT3-Tyr705 and STAT3-Ser727 phosphorylation levels and STAT3 transcriptional activity, thus resulting in inactivation of the interleukin-6-STAT3 signaling pathway in HCC cells.	28746790	RID01068	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Rheumatoid arthritis	ZFAS1	miR-27a	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	LncRNA ZFAS1 promotes cell migration and invasion of fibroblast-like synoviocytes by suppression of miR-27a in rheumatoid arthritis. Further investigation demonstrated that ZFAS1 directly interacted with miR-27a and decreased miR-27a expression. ZFAS1 promotes RA-FLS migration and invasion in an miR-27a-dependent manner.	28721682	RID01069	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	NA
Kidney injury	MALAT1	miR-146a	negatively-E	RIP;western blot	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Other	Injury	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Mechanism of long non-coding RNA MALAT1 in lipopolysaccharide-induced acute kidney injury is mediated by the miR-146a/NF-kB signaling pathway. The results revealed that the upregulation of MALAT1 reduced the expression of miR-146a, and there was a negative linear correlation between MALAT1 and miR-146a in a RNA-induced silencing complex-dependent manner.miR-146a was found to be transcriptionally induced by NF-kB, and miR-146a repressed the pro-inflammatory NF-kB pathway and downstream transcription factors. The expression levels of miR-146a were lower in the kidney injury specimens and NRK-52E cells, compared with those in the controls.	29115409	RID01070	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Hepatic ischemia-reperfusion injury	MEG3	NFE2L2	negatively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	hepatic function(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000116044	NA	55384	4780	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HEBP1|IMDDHH|NRF2	The mechanism of long non-coding RNA MEG3 for hepatic ischemia-reperfusion: Mediated by miR-34a/Nrf2 signaling pathway.we demonstrated that MEG3 functioned as a competing endogenous RNA (ceRNA) for miR-34a, and there was reciprocal repression between MEG3 and miR-34a.MEG3 protected hepatocytes from HIR injury through down-regulating miR-34a expression, which could add our understanding of the molecular mechanisms in HIR injury.	28708282	RID01071	ceRNA or sponge	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	MEG3	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);apoptosis process(-);JNK/WNT signaling pathway(+)	ceRNA(miR-127)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148516	NA	55384	6935	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Knockdown of lncRNA MEG3 inhibits viability, migration, and invasion and promotes apoptosis by sponging miR-127 in osteosarcoma cell. MEG3 acted as an endogenous sponge by binding to miR-127. More interestingly, MEG3 silence could not suppress OS-732 cells growth and metastasis when miR-127 was knocked down. ZEB1 was a target gene of miR-127, and miR-127 overexpression-induced impairments in cell growth and metastasis were attenuated when ZEB1 was overexpressed. Moreover,miR-127 suppression activated JNK and Wnt signaling pathways, while these activations were recovered by ZEB1 silence.	28636101	RID01072	ceRNA or sponge	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	MALAT1	miR-127-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1/miR-127-5p Regulates Osteopontin (OPN)-Mediated Proliferation of Human Chondrocytes Through PI3K/Akt Pathway. MALAT1 could directly bind to miR-127-5p to inhibit its expression, so as to rescue OPN expression and promote chondrocyte proliferation through PI3K/Akt pathway.miR-127-5p inhibition could promote chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt;	28590075	RID01073	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Acute liver failure	miR-19a	NBR2	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(-);AMPK/PPARalpha signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Other	Liver failure	miRNA	lncRNA	NA	NA	ENSG00000198496	GRCh38_17:43125551-43153671	NA	10230	NA	NCRNA00192	MiR-19a Affects Hepatocyte Autophagy via Regulating lncRNA NBR2 and AMPK/PPARalpha in D-GalN/Lipopolysaccharide-Stimulated Hepatocytes. Moreover, both NBR2 and PPARalpha were targeted regulated by miR-19a according to luciferase reporter assay. our data suggested that miR-19a negatively controlled the autophagy of hepatocytes attenuated in D-GalN/LPS-stimulated hepatocytes via regulating NBR2 and AMPK/PPARalpha signaling. In hepatic tissue of 20 ALF patients and D-GalN/LPS-stimulated hepatocytes, miR-19a was upregulation and NBR2 was downregulated.	28586153	RID01074	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)
Hepatocellular carcinoma	DGCR5	KLF14	positively-E	RIP;RNA pull-down assay;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	ceRNA(miR-346)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000266265	NA	26220	136259	LINC00037|NCRNA00037	BTEB5	LncRNA DGCR5 represses the development of hepatocellular carcinoma by targeting the miR-346/KLF14 axis. MiR-346 was found to be increased in HCC cells and DGCR5 can act as a sponge of miR-346 to modulate the progression of HCC.Kruppel-like factor 14 (KLF14) was predicted as a downstream target of miR-346 and miR-346 can induce the development of HCC by inhibiting KLF14.DGCR5 overexpression could repress HCC cell growth, migration, and invasion considerably. Taken together, it was indicated in our study that DGCR5 can restrain the progression of HCC through sponging miR-346 and modulating KLF14 in vitro.	30216442	RID01075	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Malignant glioma	GAS5	miR-18a-5p	negatively-F	starBase;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA GAS5 regulates the proliferation, migration, and invasion of glioma cells by negatively regulating miR-18a-5p. we identified one miR-18a-5p-binding site within exon 2 of GAS5 that is partially responsible for the tumor-suppressor functions of GAS5. Taken together, our findings suggest that GAS5 is a tumor suppressor in human gliomas that acts in part by repressing miR-18a-5p.	30078184	RID01076	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Osteosarcoma	MALAT1	CDK9	positively-E	RIP;RNA pull-down assay;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136807	NA	378938	1025	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C-2k|CDC2L4|CTK1|PITALRE|TAK	MALAT1 induces osteosarcoma progression by targeting miR-206/CDK9 axis. MALAT1 can function as a competing endogenous RNA by sponging miR-206.CDK9 was predicted as a downstream gene of miR-206, and we observed that MALAT1 can regulate osteosarcoma progress by modulating CDK9 expression via sponging miR-206.It was found that miR-206 was decreased and CDK9 was elevated in human osteosarcoma cells.It was exhibited that knockdown of MALAT1 was able to inhibit osteosarcoma cell proliferation, which suggested that MALAT1 played an oncogenic role in osteosarcoma development.	30076726	RID01077	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Acute-on-chronic liver failure	TNF	HIF1A-AS1	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Other	Liver failure	PCG	lncRNA	ENSG00000232810	NA	ENSG00000258777	GRCh38_14:61681041-61695823	7124	100750246	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	5'aHIF-1A|5'aHIF1alpha	Long noncoding RNA hypoxia-inducible factor 1 alpha-antisense RNA 1 promotes tumor necrosis factor-alpha-induced apoptosis through caspase 3 in Kupffer cells. we found that HIF1A-AS1 could be upregulation by TNF-alpha by lncRNA array analysis and knockdown of HIF1A-AS1 significantly rescued cell apoptosis induced by TNF-alpha.Moreover, inhibition of HIF1A-AS1 markedly reduced mRNA level of caspase 3 which can be significantly enhanced by TNF-alpha.	29369172	RID01078	expression association	NA	DOWN(LIHC);DATA(GSE117623)	NA
Acute-on-chronic liver failure	HIF1A-AS1	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Other	Liver failure	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	we found that HIF1A-AS1 could be upregulation by TNF-alpha by lncRNA array analysis and knockdown of HIF1A-AS1 significantly rescued cell apoptosis induced by TNF-alpha.inhibition of HIF1A-AS1 markedly reduced mRNA level of caspase 3 which can be significantly enhanced by TNF-alpha.	29369172	RID01079	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Hepatocellular carcinoma	HOTAIR	OGFR	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000060491	NA	100124700	11054	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Integrated Proteomic and Transcriptomic Analysis Reveals Long Noncoding RNA HOX Transcript Antisense Intergenic RNA (HOTAIR) Promotes Hepatocellular Carcinoma Cell Proliferation by Regulating Opioid Growth Factor Receptor (OGFr). Further functional studies of the opioid growth factor receptor (OGFr), a negative biological regulator of cell proliferation in HCC, revealed that HOTAIR exerts its effects on cell proliferation, at least in part, through the regulation of OGFr expression.	29079719	RID01080	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	H19	miR-130b	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	inflammatory response(+);adipogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Silencing of H19 inhibits the adipogenesis and inflammation response in ox-LDL-treated Raw264.7 cells by up-regulating miR-130b. the adding of LncRNA H19 abolished the facilitating effect of miR-130b inhibitor on adipogenesis and inflammation response by up-regulating the expression of miR-130b. The bioinformatic analysisshowed that there existed complementary site of miR-130b in H19 RNA.	29172088	RID01081	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Lung adenocarcinoma	LINC00472	DEDD	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-24-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000158796	NA	79940	9191	C6orf155|P53RRA	CASP8IP1|DEDD1|DEFT|FLDED1|KE05	Long Noncoding RNA LINC00472 Inhibits Proliferation and Promotes Apoptosis of Lung Adenocarcinoma Cells via Regulating miR-24-3p/ DEDD. Both LINC00472 and death effector domain-containing DNA-binding protein can bind to miR-24-3p. Long Noncoding RNA LINC00472 Inhibits Proliferation and Promotes Apoptosis of Lung Adenocarcinoma Cells via Regulating miR-24-3p/ DEDD.	30175664	RID01082	ceRNA or sponge	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Coronary artery disease	GAS5	MTOR	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000198793	NA	60674	2475	NCRNA00030|SNHG2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Plasma Long Non-Coding RNA (lncRNA) GAS5 is a New Biomarker for Coronary Artery Disease. GAS5 knockdown significantly increased the level of phospho-mTOR (p-mTOR), and GAS5 overexpression significantly decreased the level of p-mTOR.GAS5 plays a role as upstream regulator of the mTOR pathway to participate in the development of CAD.	29267258	RID01083	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Head and neck squamous cell carcinoma	circPVT1	miR-497-5p	NA	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Head and neck cancer	circRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	The oncogenic role of circPVT1 in head and neck squamous cell carcinoma is mediated through the mutant p53/YAP/TEAD transcription-competent complex. circPVT1 acts as an oncogene modulating the expression of miR-497-5p and genes involved in the control of cell proliferation.	29262850	RID01084	ceRNA or sponge	NA	NA	NA
Bronchopulmonary dysplasia	MALAT1	CDC6	positively-E	RNAi	upregulation	qPCR;microarray	GSE25286;GSE43830	GSE25286.zip;GSE43830.zip	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Other	Bronchopulmonary dysplasia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000094804	NA	378938	990	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDC18L|HsCDC18|HsCDC6|MGORS5	Long non-coding RNA MALAT1 protects preterm infants with bronchopulmonary dysplasia by inhibiting cell apoptosis. Bioinformative data analysis of MALAT1 knockdown in WI-38 cells showed various differentially expressed genes were found enriched in apoptosis related pathway. Down-regulation of antiapoptopic gene, CDC6 expression was further verified by q-PCR result.we found that up-regulation of lncRNA MALAT1 could protect preterm infants with BPD by inhibiting cell apoptosis.	29237426	RID01085	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Esophagus squamous cell carcinoma	LINC-ROR	SOX9	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell motility(+);chemoresistance(+);self-renewal(+)	ceRNA(miR-15b;miR-33a;miR-129;miR-145;miR-206)	regulation	NA	cisplatin	CSC	Limitless Replicative Potential	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000125398	NA	100885779	6662	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CMD1|CMPD1|SRA1|SRXX2|SRXY10	Linc-ROR promotes esophageal squamous cell carcinoma progression through the derepression of SOX9. A positive correlation between linc-ROR and SOX9 expression was found in clinical ESCC specimens (r=0.562, P=0.036), cell lines, and tumorspheres.Silencing of linc-ROR significantly inhibited cell proliferation, motility, chemoresistance, and self-renewal capacity. Mechanistically, linc-ROR modulating the derepression of SOX9 by directly sponging multiple miRNAs including miR-15b, miR-33a, miR-129, miR-145, and miR-206. We foundthat linc-ROR repression resulted in the sensitization of EC9706 cells to cisplatin, which is one of the most fre-quently used chemotherapeutic drug for esophageal cancer. The observation that linc-ROR and SOX9 are coordinatelyexpressed in ESCC tissues led to the hypothesis that linc-ROR might promote stem cell-like properties and cancerprogression through the regulation of pluripotency tran-scription factor SOX9.	29237490	RID01086	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Myocardial infarction	XIST	PDE4D	positively-E	luciferase reporter assay	upregulation	qPCR;microarray	GSE66360	GSE66360.zip	apoptosis process(+);cell proliferation(-)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000113448	NA	7503	5144	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ACRDYS2|DPDE3|HSPDE4D|PDE43|PDE4DN2|STRK1	LncRNA XIST regulates myocardial infarction by targeting miR-130a-3p. XIST and PDE4D were overexpressed in post-MI myocardial cells, while miR-130a-3p was underexpressed in post-MI myocardial cells. High-expressed XIST and PDE4D both promoted myocardial cell apoptosis. High-expressed XIST also inhibited myocardial cell proliferation. XIST down-regulated miR-130a-3p and PDE4D was a direct target of miR-130a-3p. LncRNA XIST promotes MI by targeting miR-130a-3p. MI induced by PDE4D can be reversed by miR-130a-3p.	29226319	RID01087	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE86978)
Ischemic stroke	HIF1A-AS2	HIF1A	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-153-3p)	regulation	NA	NA	NA	Sustained Angiogenesis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000100644	NA	100750247	3091	3'aHIF-1A|aHIF	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	lncRNAs HIF1A-AS2 facilitates the up-regulation of HIF-1alpha by sponging to miR-153-3p, whereby promoting angiogenesis in HUVECs in hypoxia.HIF1A-AS2 serves as a 'sponge' to miR-153-3p, which decreased the post-transcriptional silencing of HIF-1alpha by miR-153-3p. This function of HIF1A-AS2 facilitated the activation of HIF-1alpha/VEGFA/Notch1 cascades, by which HUVECs viability, migration ability and tube formation were promoted.	28985553	RID01088	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	LINC00941	SNAI1	positively-E	RNA pull-down assay;RIP	upregulation	microarray	GSE70880;TCGA	GSE70880.zip;LIHC.zip	epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-34a)	regulation	NA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000235884	GRCh38_12:30755167-30802602	ENSG00000124216	NA	100287314	6615	lncRNA-MUF	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Mesenchymal Stem Cells Promote Hepatocarcinogenesis via lncRNA-MUF Interaction with ANXA2 and miR-34a. We identified a novel lncRNA that we termed lncRNA-MUF (MSC-upregulation factor) that is highly expressed in HCC tissues and correlated with poor prognosis. Depleting lncRNA-MUF in HCC cells repressed EMT and inhibited their tumorigenic potential. Conversely, lncRNA-MUF overexpression accelerated EMT and malignant capacity. Mechanistic investigations showed that lncRNA-MUF bound Annexin A2 (ANXA2) and activated Wnt/beta-catenin signaling and EMT. Furthermore, lncRNA-MUF acted as a competing endogenous RNA for miR-34a, leading to Snail1 upregulation and EMT activation.	28947421	RID01089	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE60407,GSE38495)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	LINC00941	ANXA2	interact	RNA pull-down assay;RIP	upregulation	microarray	GSE70880;TCGA	GSE70880.zip;LIHC.zip	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000235884	GRCh38_12:30755167-30802602	ENSG00000182718	NA	100287314	302	lncRNA-MUF	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Mesenchymal Stem Cells Promote Hepatocarcinogenesis via lncRNA-MUF Interaction with ANXA2 and miR-34a. We identified a novel lncRNA that we termed lncRNA-MUF (MSC-upregulation factor) that is highly expressed in HCC tissues and correlated with poor prognosis. Depleting lncRNA-MUF in HCC cells repressed EMT and inhibited their tumorigenic potential. Conversely, lncRNA-MUF overexpression accelerated EMT and malignant capacity. Mechanistic investigations showed that lncRNA-MUF bound Annexin A2 (ANXA2) and activated Wnt/beta-catenin signaling and EMT. Furthermore, lncRNA-MUF acted as a competing endogenous RNA for miR-34a, leading to Snail1 upregulation and EMT activation.	28947421	RID01090	interact with protein	prognosis	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE60407,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Intervertebral disc degeneration	RP11-296A18.3	HIF1A	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENST00000366181.2	GRCh38_1:51195095-51235096	ENSG00000100644	NA	NA	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA-RP11-296A18.3/miR-138/HIF1A Pathway Regulates the Proliferation ECM Synthesis of Human Nucleus Pulposus Cells (HNPCs). RP11-296A18.3 regulates HNPC proliferation and ECM synthesis through miR-138. As the target gene of miR-138, hypoxia-inducible factor 1-alpha (HIF1A) was closely associated with cell proliferation which was also regulated by RP11-296A18.3 via miR-138. RP11-296A18.3 was positively correlated to HIF1A.We revealed that RP11-296A18.3 promote HIF1A expression through sponging miR-138, thus to promote HNPC proliferation and ECM synthesis.	28543639	RID01091	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Atherosclerosis	TP53COR1	OLR1	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000173391	NA	102800311	4973	TRP53COR1|linc-p21|lincRNA-p21	CLEC8A|LOX1|LOXIN|SCARE1|SLOX1	Long intergenic noncoding RNA p21 mediates oxidized LDL-induced apoptosis and expression of LOX-1 in human coronary artery endothelial cells. Lentiviral overexpression of lincRNA-p21 markedly increased oxLDL-induced apoptosis and the expression of LOX-1 in HCAECs.	28983628	RID01092	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	XIST	LARP1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-374a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000155506	NA	7503	23367	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	LARP	LARP1 is regulated by the XIST/miR-374a axis and functions as an oncogene in non-small cell lung carcinoma. we found that XIST functioned as a competing endogenous RNA to suppress miR-374a, which regulated its downstream target LARP1. The expression of miR-374a was negatively correlated with the expression of LARP1 in NSCLC tissues. Knockdown of LARP1 inhibited cell proliferation, migration and invasion in NSCLC cells and tumourigenicity in H520 cells.	29039571	RID01093	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thyroid cancer	H19	IRS1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169047	NA	283120	3667	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HIRS-1	Long Noncoding RNA H19 Inhibits Cell Viability, Migration, and Invasion Via Downregulation of IRS-1 in Thyroid Cancer Cells. Furthermore, long noncoding RNA H19 negatively regulated the expression of insulin receptor substrate 1 and thus effect on cell proliferation and apoptosis. Insulin receptor substrate 1 regulated the activation of phosphatidyl inositide 3-kinases/AKT and nuclear factor kB signal pathways. In conclusion, long noncoding RNA H19 could suppress cell viability, migration, and invasion via downregulation of insulin receptor substrate 1 in SW579 and TPC-1 cells.	29332545	RID01094	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Hepatitis	MALAT1	CXCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	inflammatory response(+);fibrotic(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Gastrointestinal system disease	Liver disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163735	NA	378938	6374	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENA-78|SCYB5	Altered expression of MALAT1 lncRNA in nonalcoholic steatohepatitis fibrosis regulates CXCL5 in hepatic stellate cells. Two potential target mRNAs, syndecan 4 (SDC4), and C-X-C motif chemokine ligand 5 (CXCL5) were identified for hepatocellular carcinoma upregulation lncRNA and MALAT1, respectively, but only CXCL5 showed differential expression among the different histologic classes. Knockdown of MALAT1 expression reduced CXCL5 transcript and protein levels by 50% and 30%, respectively, in HepG2 cells. The expression of MALAT1 and CXCL5 was upregulation in activated hepatic stellate (LX-2) cells compared to cells in the quiescent state, and MALAT1 expression was regulated by hyperglycemia and insulin in HepG2 cells, but only by insulin in LX-2 cells. Dysregulated lncRNA expression is associated with inflammation and fibrosis in NASH.	28993096	RID01095	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Skin disease	H19	DSG1	negatively-E	western blot;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-130b-3p)	regulation	NA	NA	NA	NA	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000134760	NA	283120	1828	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CDHF4|DG1|DSG|EPKHE|EPKHIA|PPKS1|SPPK1	H19 lncRNA regulates keratinocyte differentiation by targeting miR-130b-3p. we demonstrated that lncRNA-H19 act as an endogenous 'sponge', which binds directly to miR-130b-3p and therefore inhibits its activity on Dsg1. MiR-130b-3p was illustrated to inhibit keratinocyte differentiation by targeting Dsg1. H19 regulates Dsg1 expression and the consequent keratinocyte differentiation through miR-130b-3p.Aberrant differentiation of keratinocytes has been demonstrated to be associated with a number of skin diseases.	29192645	RID01096	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	uc.339	CCNE2	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cell growth(+);cell migration(+);tumorigenesis(+)	ceRNA(miR-339-3p;miR-663b-3p;miR-95-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_12:53677039-53677887	ENSG00000175305	NA	NA	9134	NA	CYCE2	Transcribed ultraconserved region 339 promotes carcinogenesis by modulating tumor suppressor microRNAs. To investigate the mechanism of action of uc.339, we hypothesized that the T-UCR might work as a decoy for complementary mature miRNAs. A structural analysis of the uc.339 transcript with the RNAhybrid algorithm14 revealed the presence of sequences complementary to three mature miRNAs (namely, miR-339-3p, -663b-3p, and -95-5p from now on referred to as miR-339, -663b, and -95, respectively) in the uc.339 RNA transcript. We find that transcribed uc.339 is upregulation in archival NSCLC samples, functioning as a decoy RNA for miR-339-3p,-663b-3p, and -95-5p. As a result, Cyclin E2, a direct target of all these microRNAs is upregulation, promoting cancer growth and migration.	29180617	RID01097	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	YAP1	BCAR4	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+);glucose metabolic process(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Reprogramming Energy Metabolism	Cancer	Breast cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000262117	GRCh38_16:11819829-11828845	10413	400500	COB1|YAP|YAP2|YAP65|YKI	NA	LncRNA wires up Hippo and Hedgehog signaling to reprogramme glucose metabolism. The expression levels of BCAR4 and YAP are positively correlated in tissue samples from breast cancer patients, where high expression of both BCAR4 and YAP is associated with poor patient survival outcome.YAP promotes the expression of BCAR4, which subsequently coordinates the Hedgehog signaling to enhance the transcription of glycolysis activators HK2 and PFKFB3.	28963395	RID01098	transcriptional regulation	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	NA
Prostate cancer	HOTAIR	miR-193a	negatively-E	ChIP;luciferase reporter assay;western blot	NA	NA	NA	NA	cancer progression(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691	RID01099	epigenetic regulation	NA	NA	NA
Prostate cancer	miR-193a	HOTAIR	negatively-F	ChIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691	RID01100	ceRNA or sponge	NA	NA	NA
Endometriosis	MALAT1	miR-200c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo. We demonstrated that expression of MALAT1 in ectopic endometrial specimens was negatively correlated with that of miR-200c and that MALAT1 knockdown increased the level of miR-200c in HESCs. Exogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). The MALAT1/miR-200c sponge may be a potential therapeutic target for endometriosis.	29116025	RID01101	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Colon cancer	LINC01567	miR-93	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000224310	GRCh38_16:24661422-24671062	NA	NA	400511	NA	LOCCS	NA	Long intergenic non-protein-coding RNA 1567 (LINC01567) acts as a sponge against microRNA-93 in regulating the proliferation and tumorigenesis of human colon cancer stem cells.We also found an lncRNA, LOCCS, with obviously upregulation expression in colon CSCs. Knockdown of LOCCS reduced cell proliferation, invasion, migration, and generation of tumor xenografts. Furthermore, microRNA-93 (miR-93) and Musashi-1 mediated the tumor suppression of LOCCS knockdown. There was reciprocal repression between LOCCS and miR-93. Research on mechanisms suggested direct binding, as a predicted miR-93 binding site was identified in LOCCS.	29110645	RID01102	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Breast cancer	HOTAIR	miR-34a	NA	NA	NA	NA	NA	NA	cell autophagy(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	The Long Noncoding RNA HOTAIR in Breast Cancer: Does Autophagy Play a Role. HOTAIR can regulate autophagy, important for breast cancer cells survival, through the interaction with miRNAs specific for autophagy genes and directly with these genes.Many studies point at miR-34a as a major component of HOTAIR-miRNAs-cancer cross-talk. The most important role of HOTAIR can be attributed to cancer progression as its overexpression stimulates invasion and metastasis. These studies point at miR-34a as an important element of HOTAIR regulation, which was suggested earlier. Similarly, HOTAIR was reported to indirectly regulate miR-34a expression.	29469819	RID01103	expression association	metastasis	NA	NA
Estrogen-receptor negative breast cancer	WDR7-7	GPER1	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(-)	NA	regulation	NA	calycosin	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSP00000409300.1,ENST00000449340.1	GRCh38_1:111439890-111449308	ENSG00000164850	NA	NA	2852	NA	NA	Calycosin inhibits the in vitro and in vivo growth of breast cancer cells through WDR7-7-GPR30 Signaling. Here, we show that calycosin inhibited the proliferation of both ER- (MDA-MB-468 and SKBR3) and ER+ breast cancer cells (MCF-7 and T47D) and that these inhibitory effects were associated with the up-regulation of the long non-coding RNA (lncRNA) WDR7-7.  The target of WDR7-7, G-protein coupled estrogen receptor 30 (GPR30, formerly known as GPER), was present in both ER+ and ER- breast cancer cells, as confirmed by a luciferase reporter assay. we demonstrate that the expression of WDR7-7 is reduced in breast cancer cell lines and that the overexpression of WDR7-7 inhibits growth through a mechanism that involves G-protein coupled estrogen receptor 30 (GPR30).in all four GPR30-positive breast cancer lines, calycosin decreased the phosphorylation levels of SRC, EGFR, ERK1/2 and Akt, but the inhibition of WDR7-7 blocked these changes and increased proliferation. These results suggest the possibility that calycosin inhibited the proliferation of breast cancer cells, at least partially, through WDR7-7-GPR30 signaling, which may explain why calycosin can exert inhibitory effects on ER- breast cancer.	29096683	RID01104	expression association	chemoresistance	NA	NA
Osteosarcoma	XIST	RSF1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);oncogenic role(+)	ceRNA(miR-193a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000048649	NA	7503	51773	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	HBXAP|RSF-1|XAP8|p325	RSF1 functions as an oncogene in osteosarcoma and is regulated by XIST/miR-193a-3p axis. RSF1 was identified as a direct target of miR-193a-3p.we found that miR-193a-3p was negatively correlated with RSF1 expression in OS tissues.our data showed that XIST could function as competing endogenous RNA to repress miR-193a-3p, which regulated its downstream target RSF1. RSF1 inhibition suppressed OS cell proliferation and invasion. In conclusion, our findings demonstrated that the XIST/miR-193a-3p/RSF1 axis might contribute to the progression and act as a therapeutic target of OS patients.	28843909	RID01105	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Pancreatic ductal adenocarcinoma	YY1	SOX2-OT	negatively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000242808	GRCh38_3:180989762-181836880	7528	347689	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	NCRNA00043|SOX2OT	Yin Yang-1 suppresses pancreatic ductal adenocarcinoma cell proliferation and tumor growth by regulating SOX2OT-SOX2 axis. Luciferase reporter, electrophoretic mobility shift (EMSA), and chromatin immunoprecipitation (ChIP) assays revealed binding of YY1 to the SOX2OT promoter. Moreover, YY1 suppressed PDAC cell proliferation through SOX2OT transcriptional inhibition and subsequent decreased SOX2 expression.	28867247	RID01106	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Non-small cell lung cancer	LINC00346	JAK2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255874	GRCh38_13:110863987-110870251	ENSG00000096968	NA	283487	3717	C13orf29|NCRNA00346	JTK10|THCYT3	The expressions of LINC00346 were relatively high in NSCLC tissues and cells. LINC00346 promotes the proliferation and inhibits the apoptosis of NSCLC cells through regulating the JAK-STAT3 signaling pathway.Western blotting showed that LINC00346 could exert its function through partially regulating the Janus kinase/signal transducer and activator of transcription 3 (JAK-STAT3) signaling pathway.	29228425	RID01107	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Non-small cell lung cancer	LINC00346	STAT3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000255874	GRCh38_13:110863987-110870251	ENSG00000168610	NA	283487	6774	C13orf29|NCRNA00346	ADMIO|ADMIO1|APRF|HIES	The expressions of LINC00346 were relatively high in NSCLC tissues and cells. LINC00346 promotes the proliferation and inhibits the apoptosis of NSCLC cells through regulating the JAK-STAT3 signaling pathway.Western blotting showed that LINC00346 could exert its function through partially regulating the Janus kinase/signal transducer and activator of transcription 3 (JAK-STAT3) signaling pathway.	29228425	RID01108	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	IATPR	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000148516	NA	101929447	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Knockdown of long noncoding RNA linc-ITGB1 suppresses migration, invasion of hepatocellular carcinoma via regulating ZEB1.Further study revealed that silenced linc-ITGB1 inhibited the expression of ZEB1 and then suppressed epithelial to mesenchymal transition (EMT), which was important during the metastasis of hepatocellular carcinoma.The results indicate that linc-ITGB1, a novel oncogene in tumorigenesis, could promote the metastasis and EMT via ZEB1, which may offer a possible therapeutic target in hepatocellular carcinoma.	29228420	RID01109	expression association	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	TP73-AS1	miR-142	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	NA	57212	NA	KIAA0495|PDAM	NA	Knockdown of long non-coding RNA TP73-AS1 inhibits osteosarcoma cell proliferation and invasion through sponging miR-142.	29864904	RID01110	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Urinary bladder cancer	FOXD2-AS1	ABCC3	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-143)	binding/interaction	RNA-RNA	gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000108846	NA	84793	8714	NA	ABC31|EST90757|MLP2|MOAT-D|MRP3|cMOAT2	Long noncoding RNA FOXD2-AS1 accelerates the gemcitabine-resistance of bladdercancer by sponging miR-143.Bioinformatics program and validation experiments confirmed that FOXD2-AS1 positively regulated ABCC3 protein through targeting miR-143, acting as a competing endogenous RNA (ceRNA)	29674277	RID01111	ceRNA or sponge	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	ZFAS1	miR-329	negatively-F	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 facilitates bladder cancer tumorigenesis by sponging miR-329	29653362	RID01112	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	NA
Non-small cell lung cancer	DANCR	miR-758-3p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712404-52720351	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	The long non-coding RNA-DANCR exerts oncogenic functions in non-small cell lung cancer via miR-758-3p.we concluded that DANCR promotes NSCLC cell proliferation, migration and invasion by regulating the tumor suppressor miR-758-3p.	29635134	RID01113	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	NA
Oral cavity cancer	CDKN2B-AS1	miR-125a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	The role of long non-coding RNA ANRIL in the carcinogenesis of oral cancer by targeting miR-125a.Furthermore, we found a negative correlation between ARNIL and miR-125a, and ARNIL acts as a miRNA-sponge by directly interacting with miR-125a.	29635126	RID01114	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	NA
Colorectal cancer	HEIH	BCL2L1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000171552	NA	100859930	598	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long Noncoding RNA HEIH Promotes Colorectal Cancer tumorigenesis via Counteracting miR-939 Mediated Transcriptional Repression of Bcl-xL. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor kB (NF-kB), increases the binding of NF-kB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL.	29081216	RID01115	expression association	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Colorectal cancer	HEIH	miR-939	negatively-F	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long Noncoding RNA HEIH Promotes Colorectal Cancer tumorigenesis via Counteracting miR-939 Mediated Transcriptional Repression of Bcl-xL. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor kB (NF-kB), increases the binding of NF-kB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL.	29081216	RID01116	ceRNA or sponge	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	NA
Ovarian cancer	NEAT1	ROCK1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-382-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|NCRNA00084|TncRNA|VINC	P160ROCK|ROCK-I	Long non-coding RNA NEAT1 promoted ovarian cancer cells' metastasis through regulation of miR-382-3p/ROCK1 axial	29790629	RID01117	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	GAS5	SPRY2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000136158	NA	60674	10253	NCRNA00030|SNHG2	IGAN3|hSPRY2	Long non-coding RNA GAS5 inhibits ovarian cancer cell proliferation via the control of microRNA-21 and SPRY2 expression.Luciferase assay data indicated that miR-21 was a direct target of GAS5 and that SPRY2 was a target gene of miR-21 in ovarian cancer-derived A2780 cells	29896229	RID01118	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Non-small cell lung cancer	SNHG1	MTDH	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000147649	NA	23642	92140	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	3D3|AEG-1|AEG1|LYRIC|LYRIC/3D3	Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p	29466052	RID01119	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Breast cancer	MAGI2-AS3	FAS	positively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000026103	NA	100505881	355	NA	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL).	29679339	RID01120	expression association	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	MAGI2-AS3	FASLG	positively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000117560	NA	100505881	356	NA	ALPS1B|APT1LG1|APTL|CD178|CD95-L|CD95L|FASL|TNFSF6|TNLG1A	Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL).	29679339	RID01121	expression association	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	HAGLR	miR-217	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	HOXD-AS1 functionedas a competing endogenous RNA for miR-217	29749477	RID01122	ceRNA or sponge	prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	NA
Gastric cancer	MEG3	miR-21	negatively-E	western blot	downregulation	qPCR	NA	NA	cell motility(+);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer.The expression of miR-21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT. Co-transfection of lncRNA-MEG3 and miR-21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3, suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer.	29749532	RID01123	expression association	NA	NA	NA
Breast cancer	ITGB2-AS1	ITGB2	positively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227039	GRCh38_21:44921051-44929678	ENSG00000160255	NA	100505746	3689	NA	CD18|LAD|LCAMB|LFA-1|MAC-1|MF17|MFI7	LncRNA ITGB2-AS1 Could Promote the Migration and invasion of Breast Cancer Cells through Up regulating ITGB2	29941860	RID01124	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	MIR22HG	YBX1	negatively-E	RNAi	downregulation	microarray;sequencing	GSE31210;GSE68465;TCGA	GSE31210.zip;GSE68465.zip;LUSC_LUAD.zip	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000065978	NA	84981	4904	C17orf91	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01125	expression association	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	MIR22HG	MET	negatively-E	RNAi	downregulation	microarray;sequencing	NA	NA	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000105976	NA	84981	4233	C17orf91	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01126	expression association	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Lung cancer	MIR22HG	CDKN1A	negatively-E	RNAi	downregulation	microarray;sequencing	NA	NA	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000124762	NA	84981	1026	C17orf91	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01127	expression association	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Head and neck cancer	HOTAIRM1	DLGAP1	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000170579	NA	100506311	9229	HOXA-AS1|HOXA1-AS1|NCRNA00179	DAP-1|DAP-1-ALPHA|DAP-1-BETA|DAP1|DLGAP1A|DLGAP1B|GKAP|SAPAP1	HOTAIRM1 competed endogenously with miR-148a to regulate DLGAP1 in head and neck tumor cells.HOTAIRM1 was confirmed as a tumor suppressor via sponging miR-148a and promote the expression of DLGAP1, which could be regarded as an important target for the prevention and treatment of HNT.	29905017	RID01128	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	PVT1	STAT1	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-);immunotherapies(-)	histone modification	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000115415	NA	5820	6772	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	Long noncoding RNA PVT1 inhibits interferon-alpha mediated therapy for hepatocellular carcinoma cells by interacting with signal transducer and activator of transcription 1.Taken together, these results for the first time indicate that IFN-alpha treatment promotes oncogenic PVT1 expression in HCC cells, which interacts with STAT1 to inhibit IFN-alpha signaling, ultimately blocking IFN-alpha-induced cells apoptosis, suggesting that lncRNA PVT1 may be a potential target to improve IFN-alpha-mediated HCC immunotherapies.	29715456	RID01129	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	HULC	PTEN	negatively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-15a)	regulation	NA	NA	CSC	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000171862	NA	728655	5728	HCCAT1|LINC00078|NCRNA00078	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA HULC accelerates liver cancer by inhibiting PTEN via autophagy cooperation to miR15a.Of significance, our observations also revealed that HULC inhibited PTEN through ubiquitin-proteasome system mediated by autophagy-P62	29895332	RID01130	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Liver cancer	HULC	SQSTM1	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-15a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000161011	NA	728655	8878	HCCAT1|LINC00078|NCRNA00078	A170|DMRV|FTDALS3|NADGP|OSIL|PDB3|ZIP3|p60|p62|p62B	Long noncoding RNA HULC accelerates liver cancer by inhibiting PTEN via autophagy cooperation to miR15a.Mechanistically, HULC increasesthe expression of P62 via decreasing mature miR15a.	29895332	RID01131	ceRNA or sponge	NA	NA	UP(PAAD,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE41245)
Colorectal cancer	UCA1	CDKN1B	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Up-regulation of UCA1/mTOR axis suppressed p27 and miR-143 while the expression of CCND1 and KRAS were significantly increased compared with control.CAF-CM induces the upregulation of UCA1 in sw480 cells and leading to upregulation of mTOR. UCA1 in cooperation with mTOR regulates downstream key effectors and induces CCND1 and suppresses p27 and miR-143, subsequently, directs the cell proliferation, EMT and metastasis of CRC cell	29948578	RID01132	expression association	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	UCA1	MTOR	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000198793	NA	652995	2475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Taken together, these results highlight the vital role of cooperation between lncRNA UCA1 and mTOR in proliferation and metastasis.	29948578	RID01133	expression association	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	UCA1	KRAS	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000133703	NA	652995	3845	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Up-regulation of UCA1/mTOR axis suppressed p27 and miR-143 while the expression of CCND1 and KRAS were significantly increased compared with control.CAF-CM induces the upregulation of UCA1 in sw480 cells and leading to upregulation of mTOR. UCA1 in cooperation with mTOR regulates downstream key effectors and induces CCND1 and suppresses p27 and miR-143, subsequently, directs the cell proliferation, EMT and metastasis of CRC cell	29948578	RID01134	expression association	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Non-small cell lung cancer	HOTAIR	miR-613	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long Noncoding RNA (lncRNA) HOTAIR Affects tumorigenesis and Metastasis of Non-Small Cell Lung Cancer by Upregulating miR-613.The targeting relationship between HOTAIR and miR-613 was further confirmed through the luciferase report assay.	29187267	RID01135	ceRNA or sponge	metastasis	NA	NA
Osteosarcoma	TUG1	miR-153	negatively-F	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Knockdown of Long Noncoding RNA TUG1 Inhibits the Proliferation and Cellular Invasion of Osteosarcoma Cells by Sponging miR-153	28411362	RID01136	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Melanoma	PVT1	miR-26b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Melanoma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA PVT1 Promotes Melanoma Progression via Endogenous Sponging miR-26b	28409552	RID01137	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Triple-receptor negative breast cancer	LINC-ROR	MUC1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000185499	NA	100885779	4582	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ADMCKD|ADMCKD1|CA 15-3|CD227|EMA|H23AG|KL-6|MAM6|MCD|MCKD|MCKD1|MUC-1|MUC-1/SEC|MUC-1/X|MUC1/ZD|PEM|PEMT|PUM	LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1.Furthermore, lincRNA-ROR functions as a competing endogenous RNAs (ceRNA) which sponges miR-145 and therefore upregulate the expression of Mucin1 (MUC1).	29673594	RID01138	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC);UP(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Endometrial carcinoma	HOTAIR	NPM1	negatively-E	RIP;western blot;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-646)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181163	NA	100124700	4869	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	B23|NPM	Long noncoding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via the miR-646/NPM1 axis.Taken together, our findings presented that HOTAIR could regulate NPM1 via interacting with miR-646, thereby governing the viability, migration, and invasion of EC cells.	29466670	RID01139	ceRNA or sponge	metastasis	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Cervical cancer	SNHG20	ADAM10	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);MEK/ERK signaling pathway(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000137845	NA	654434	102	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	AD10|AD18|CD156c|CDw156|HsT18717|MADM|RAK|kuz	LncRNA SNHG20 promotes cell proliferation and invasion via miR-140-5p-ADAM10 axis in cervical cancer.Our study demonstrated that SNHG20 could function as an oncogenic lncRNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.	29604594	RID01140	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Malignant glioma	SNHG6	CDKN1A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA SNHG6 acts as a prognostic factor to regulate cell proliferation in glioma through targeting p21	29579705	RID01141	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Prostate cancer	SNHG7	CCND1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-503)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000110092	NA	84973	595	NCRNA00061	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503	29571017	RID01142	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	lncRNA-CTD-2108O9.1	LIFR	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENST00000508986	GRCh38_5:38425036-38427376	ENSG00000113594	NA	NA	3977	NA	CD118|LIF-R|SJS2|STWS|SWS	Long non-coding RNA-CTD-2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor	29603493	RID01143	expression association	metastasis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Glioblastoma	CYTOR	miR-107	negatively-F	starBase;RNAi	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	NA	LncRNA LINC00152 promoted glioblastoma progression through targeting the miR-107 expression	29671226	RID01144	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	NA
Colorectal cancer	OIP5-AS1	DYRK1A	positively-E	western blot;luciferase reporter assay	downregulation	qPCR;microarray	GSE95606	GSE95606.zip	radioresistance(-)	ceRNA(miR-369-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000157540	NA	729082	1859	cyrano|linc-OIP5	DYRK|DYRK1|HP86|MNB|MNBH|MRD7	LncRNA OIP5-AS1 regulates radioresistance by targeting DYRK1A through miR-369-3p in colorectal cancer cells	29773344	RID01145	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	TP63	LINC01503	positively-E	ChIP;RIP;luciferase reporter assay;RNA pull-down assay;mass spectrometry	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation;super-enhancer	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000073282	NA	ENSG00000233901	GRCh38_9:129332300-129359541	8626	100506119	AIS|B(p51A)|B(p51B)|EEC3|KET|LMS|NBP|OFC8|RHS|SHFM4|TP53CP|TP53L|TP73L|p40|p51|p53CP|p63|p73H|p73L	NA	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients.	29454790	RID01146	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	XIST	NOTCH1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-137)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148400	NA	7503	4851	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AOS5|AOVD1|TAN1|hN1	Furthermore,XIST could act as an endogenous sponge by directly binding to miR-137,negatively regulating its expression. Notch-1 was identified as a direct target gene of miR-137, with the XIST-miR-137 axis regulating activation of the Notch-1 pathway. We identified a branch of the XIST/miR-137/Notch-1 pathway that regulates proliferation and TGF-beta1-induced EMT in NSCLC,which could be involved in NSCLC progression. Knockdown of XIST suppressed cell proliferation and TGF-b1-induced EMT in A549 and H1299 cells	29812958	RID01147	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	HAGLR	E2F8	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-130a)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000129173	NA	401022	79733	HOXD-AS1|MIR7704HG|Mdgt	E2F-8	HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8	29341117	RID01148	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	AWPPH	SMAD4	negatively-E	RIP;ChIP	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell autophagy(+);cell migration(+);apoptosis process(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111195866-111495161	ENSG00000141646	NA	NA	4089	NA	DPC4|JIP|MADH4|MYHRS	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression.LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.Then, RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2.	29231261	RID01149	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	XIST	MAPK1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-194-5p)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000100030	NA	7503	5594	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	LncRNA XIST functions as a molecular sponge of miR-194-5p to regulate MAPK1 expression.In brief, the above results elucidate the important role of XIST in HCC tumorigenesis, suggesting that XIST might be a candidate prognostic biomarker and a novel therapeutic target for treating HCC.	29227532	RID01150	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	H19	miR-484	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 promotes epithelial-mesenchymal transition (EMT) by targeting miR-484 in human lung cancer cells.	29219208	RID01151	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	NA
Prostate cancer	MALAT1	AKAP12	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-145-5p)	regulation	NA	docetaxel	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131016	NA	378938	9590	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP250|SSeCKS	Long noncoding RNA MALAT1 enhances the docetaxel resistance of prostate cancer cells via miR-145-5p-mediated regulation of AKAP12	29633510	RID01152	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Colorectal cancer	H19	GRN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	ceRNA(miR-29b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000030582	NA	283120	2896	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling	29754471	RID01153	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00554	MARCKSL1	positively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260738	GRCh38_13:99994899-99997909	ENSG00000175130	NA	100861542	65108	NA	F52|MACMARCKS|MLP|MLP1|MRP	The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating cells via the protein kinase C substrates MARCKS and MARCKSL1. In conclusion,lncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1.Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes.	29588366	RID01154	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Hepatocellular carcinoma	LINC00554	MARCKS	positively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260738	GRCh38_13:99994899-99997909	ENSG00000277443	NA	100861542	4082	NA	80K-L|MACS|PKCSL|PRKCSL	The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating cells via the protein kinase C substrates MARCKS and MARCKSL1. In conclusion,lncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1.Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes.	29588366	RID01155	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939,GSE86978)
Endometrial carcinoma	ABHD11-AS1	CCND1	positively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000110092	NA	171022	595	LINC00035|NCRNA00035|WBSCR26	BCL1|D11S287E|PRAD1|U21B31	LncRNA ABHD11-AS1 promotes the development of endometrial carcinoma by targeting cyclin D1.LncRNA ABHD11-AS1 functions as an oncogene to promote cell proliferation and invasion in endometrial carcinoma by positively targeting cyclin D1. RNA pull down demonstrated that lncRNA ABHD11-AS1 binds directly to cyclin D1.	29799152	RID01156	interact with protein	NA	UP(BRCA);DATA(GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	AFAP1-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000124762	NA	84740	1026	AFAP1-AS|AFAP1AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA AFAP1-AS1 predicts a poor prognosis and regulates non-small cell lung cancer cell proliferation by epigenetically repressing p21 expression	29793547	RID01157	epigenetic regulation	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Papillary thyroid carcinoma	RP5-1024C24.1	MPPED2	positively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000254489	GRCh38_11:30584130-30630508	ENSG00000066382	NA	NA	744	NA	239FB|C11orf8	The Long Non-Coding RNA RP5-1024C24.1 and Its Associated-Gene MPPED2 Are Down-Regulated in Human Thyroid Neoplasias and Act as Tumour Suppressors	29783666	RID01158	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	LINC00599	miR-185-5p	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000253230	GRCh38_8:9899871-9906678	NA	NA	157627	NA	NA	NA	Long non-coding RNA RNCR3 promotes prostate cancer progression through targeting miR-185-5p	29887969	RID01159	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Hepatocellular carcinoma	LINC00473	USP9X	positively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000124486	NA	90632	8239	C6orf176|LNC473|bA142J11.1	DFFRX|FAF|FAM|MRX99|MRXS99F	Long noncoding RNA LNC473 inhibits the ubiquitination of survivin via association with USP9X and enhances cell proliferation and invasion in hepatocellular carcinoma cells	29605299	RID01160	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE55807)
Urinary bladder cancer	ZFAS1	KLF2	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	BLCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000127528	NA	441951	10365	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	LKLF	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01161	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	ZFAS1	NKD2	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	BLCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000145506	NA	441951	85409	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	Naked2	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01162	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	NA
Urinary bladder cancer	ZFAS1	ZEB2	negatively-E	RNAi	downregulation	qPCR;microarray	TCGA	BLCA.zip	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000169554	NA	441951	9839	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01163	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	ZFAS1	ZEB1	negatively-E	RNAi	downregulation	qPCR;microarray	TCGA	BLCA.zip	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000148516	NA	441951	6935	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01164	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	PVT1	TWIST1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	PRAD.zip	epithelial to mesenchymal transition(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000122691	NA	5820	7291	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Long noncoding RNA PVT1 promotes EMT via mediating microRNA-186 targeting of Twist1 in prostate cancer.We then confirmed that PVT1 acts as a sponge for miRNA-186-5p and positively regulates Twist1 by a sponge effect.	29452232	RID01165	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	NEAT1	PNPLA2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000177666	NA	283131	57104	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1-modulated abnormal lipolysis via ATGL drives hepatocellular carcinoma proliferation.NEAT1 regulated ATGL expression by binding miR-124-3p. Additionally, NEAT1 knockdown attenuated HCC cell growth through miR-124-3p/ATGL/DAG+FFA/PPARalpha signaling.	29764424	RID01166	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	GAPLINC	MAPK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-378)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000100030	NA	100505592	5594	LINC01540	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long noncoding RNA GAPLINC promotes gastric cancer cell proliferation by acting as a molecular sponge of miR-378 to modulate MAPK1 expression	29785127	RID01167	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical squamous cell carcinoma	PVT1	TGFB1	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000105329	NA	5820	7040	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA PVT1 promotes the growth of HPV positive and negative cervical squamous cell carcinoma by inhibiting TGF-beta1	29760583	RID01168	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	UCA1	miR-144	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Noncoding RNA Urothelial Carcinoma-Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144	28762326	RID01169	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	NA
Breast cancer	CAMTA1-DT	miR-20b	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell motility(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000237436	GRCh38_1:6783892-6784843	NA	NA	110841581	NA	lncCAMTA1	NA	Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of the Human Breast Cancer Cell Line MDA-MB-231 via Targeting miR-20b. The results showed that lncCAMTA1 expression promoted cell viability and migration/invasion, while knockdown of lncCAMTA1 promoted cell apoptosis via binding with miR-20b. lncCAMTA1 negatively regulated miR-20b expression. VEGF was a target of miR-20b, leading to the modification of the phosphorylation levels of MAPK, ERK, JAK, STAT1, and STAT3. Our findings suggested that lncCAMTA1 might promote proliferation and mobility of human breast cancer cells via binding with miR-20b. VEGF was a direct target of miR-20b and regulated activation of the MAPK/ERK and JAK/STAT3 signaling pathways. Therefore lncCAMTA1 has potential as a novel cancer diagnostic marker and as a putative novel therapeutic target for breast cancer treatment.	28550685	RID01170	ceRNA or sponge	NA	NA	NA
Acute promyelocytic leukemia	CEBPB	NEAT1	positively-E	ChIP;luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	cell differentiation(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000172216	NA	ENSG00000245532	GRCh38_11:65422774-65445540	1051	283131	C/EBP-beta|IL6DBP|NF-IL6|TCF5	LINC00084|NCRNA00084|TncRNA|VINC	C/EBPbeta contributes to transcriptional activation of long non-coding RNA NEAT1 during APL cell differentiation.we performed chromatin immunoprecipitation and luciferase reporter assays to demonstrate that C/EBP family transcription factor C/EBPbeta bind to and transactivate the promoter of lncRNA NEAT1 through the C/EBPbeta binding sites both around -54 bp and -1453 bp upstream of the transcription start site.	29111326	RID01171	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Hepatocellular carcinoma	MIAT	miR-214	negatively-F	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214	29097358	RID01172	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	NA
Malignant glioma	PVT1	miR-190a-5p	negatively-F	ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p. In conclusion, PVT1-miR-190a-5p/miR-488-3p-MEF2C-JAGGED1 axis is involved in proliferation and progression of glioma. Thus, PVT1 may become a novel target in glioma therapy.	29501773	RID01173	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Malignant glioma	PVT1	miR-488-3p	negatively-F	ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p	29501773	RID01174	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Colorectal cancer	TMEM238L	miR-942	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000263429	GRCh38_17:10794913-10804099	NA	NA	100289255	NA	NA	NA	Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/beta-catenin signaling	29524886	RID01175	expression association	metastasis	NA	NA
Hepatoblastoma	OIP5-AS1	ZEB1	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-186a-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000148516	NA	729082	6935	cyrano|linc-OIP5	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Kockdown of OIP5-AS1 expression inhibits proliferation, metastasis and EMT progress in hepatoblastoma cells through up-regulating miR-186a-5p and down-regulating ZEB1. OIP5-AS1 is a ceRNA in Hepatoblastoma cells through modulating miR-186a-5p/ZEB1	29475118	RID01176	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	SP1	positively-F	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185591	NA	378938	6667	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 promotes lung adenocarcinoma by directly interacting with specificity protein 1	29575609	RID01177	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	RP11-552M11.4	BRCA2	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243960	GRCh38_1:111438638-111441364	ENSG00000139618	NA	NA	675	NA	BRCC2|BROVCA2|FACD|FAD|FAD1|FANCD|FANCD1|GLM3|PNCA2|XRCC11	Long non-coding RNA RP11-552M11.4 promotes cells proliferation, migration and invasion by targeting BRCA2 in ovarian cancer.Rescue experiment and luciferase reporter assay showed that lncRNA RP11-552M11.4 regulated SKOV3 cells functions through binding BRCA2. Further experiments in A-2780 cells also validated that lncRNA RP11-552M11.4 induced A-2780 cell proliferation while repressing apoptosis by targeting BRCA2. LncRNA RP11-552M11.4 inhibits BRCA2 expression by interacting at binding site in SKOV3 cells.	29478268	RID01178	interact with mRNA	NA	NA	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE51827,GSE86978)
Breast cancer	lncRNA-PRLB	SIRT1	positively-E	luciferase reporter assay;RIP	downregulation	qPCR;microarray	TCGA	BRCA.zip	cell proliferation(+);cell metastasis(+);chemoresistance(+)	ceRNA(miR-4766-5p)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253802	GRCh38_8:40333173-40343363	ENSG00000096717	NA	NA	23411	NA	SIR2|SIR2L1|SIR2alpha	A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer.our findings indicated that lncRNA could regulate the progression and chemoresistance of breast cancer via modulating the expression levels of miR-4766-5p and SIRT1. LncRNA-PRLB promotes proliferation, metastasis, and chemoresistance partly by regulating SIRT1 expression through protecting it from miR-4766-5p-mediated degradation.LncRNA-PRLB abundantly sponges miR-4766-5p and miR-4766-5p promotes cell proliferation, metastasis, and chemoresistance in breast cancer. miR-4766-5p targets SIRT1 and regulates its expression.	29752439	RID01179	ceRNA or sponge	metastasis,chemoresistance	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MRUL	ABCB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	adriamycin;vincristine	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENST00000432937	GRCh38_7:87152361-87196337	ENSG00000085563	NA	NA	5243	NA	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long noncoding RNA MRUL promotes ABCB1 expression in multidrug-resistant gastric cancer cell sublines;Heterologous luciferase reporter assays demonstrated that MRUL might positively affect ABCB1 expression in an orientation- and position-independent manner.Furthermore, the relative expression levels of MRUL in GC tissues were negatively correlated with in vitro growth inhibition rates of GC specimens treated with chemotherapeutic drugs and indicated a poor prognosis for GC patients. MRUL knockdown in SGC7901/ADR and SGC7901/VCR cells led to increased rates of apoptosis, increased accumulation, and reduced doxorubicin (Adriamycin [ADR]) release in the presence of ADR or vincristine.	24958102	RID01180	expression association	chemoresistance,prognosis	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	UCA1	SMARCA4	negatively-F	RNA pull-down assay;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000127616	NA	652995	6597	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA urothelial carcinoma associated 1 induces cell replication by inhibiting BRG1 in 5637 cells; we identified BRG1 as a UCA1 binding partner using an in vitro RNA pull-down assay, and RNA-binding protein immunoprecipitation assay confirmed UCA1-BRG binding in bladder cancer cells in vivo. UCA1 impairs both binding of BRG1 to the p21 promoter and chromatin remodeling activity of BRG1.Collectively, these results demonstrate that UCA1 promotes bladder cancer cell proliferation by inhibiting BRG1.	24993775	RID01181	interact with protein	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Urinary bladder cancer	UCA1	CDKN1A	negatively-E	RNA pull-down assay;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA urothelial carcinoma associated 1 induces cell replication by inhibiting BRG1 in 5637 cells; we identified BRG1 as a UCA1 binding partner using an in vitro RNA pull-down assay, and RNA-binding protein immunoprecipitation assay confirmed UCA1-BRG binding in bladder cancer cells in vivo. UCA1 impairs both binding of BRG1 to the p21 promoter and chromatin remodeling activity of BRG1.Collectively, these results demonstrate that UCA1 promotes bladder cancer cell proliferation by inhibiting BRG1.	24993775	RID01182	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Pancreatic cancer	H19	HMGA2	negatively-E	luciferase reporter assay;RNAi;qRT-PCR	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(let-7)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	H19 promotes pancreatic cancer metastasis by derepressing let-7's suppression on its target HMGA2-mediated EMT;We further demonstrated that H19 promoted PDAC cell invasion and migration at least partially by increasing HMGA2-mediated epithelial-mesenchymal transition (EMT) through antagonizing let-7.H19 was reported as a sponge to antagonizing let-7.	24055342;17437991;24920070	RID01183	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	MALAT1	PTBP2	positively-F	RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117569	NA	378938	58155	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	PTBLP|brPTB|nPTB	Long non-coding RNA MALAT1 promotes tumour growth and metastasis in colorectal cancer through binding to SFPQ and releasing oncogene PTBP2 from SFPQ/PTBP2 complex; MALAT1 could bind to SFPQ, thus releasing PTBP2 from the SFPQ/PTBP2 complex. In turn, the increased SFPQ-detached PTBP2 promoted cell proliferation and migration;MALAT1 and PTBP2 were overexpressed, both of which were associated closely with the invasion and metastasis of CRC	25025966	RID01184	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807,GSE86978)
Prostate cancer	H19	miR-675	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI;we found that the expression level of either H19 or miR-675 in P69 cells was negatively associated with the expression of transforming growth factor beta induced protein (TGFBI);Dual luciferase reporter assays showed that miR-675 directly bound with 3'UTR of TGFBI mRNA to repress its translation	24988946	RID01185	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Prostate cancer	H19	TGFBI	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000120708	NA	283120	7045	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BIGH3|CDB1|CDG2|CDGG1|CSD|CSD1|CSD2|CSD3|EBMD|LCD1	lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI;we found that the expression level of either H19 or miR-675 in P69 cells was negatively associated with the expression of transforming growth factor beta induced protein (TGFBI);Dual luciferase reporter assays showed that miR-675 directly bound with 3'UTR of TGFBI mRNA to repress its translation	24988946	RID01186	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE51827,GSE75367,GSE86978)
Lung cancer	SOX2-OT	EZH2	positively-E	RIP;RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000106462	NA	347689	2146	NCRNA00043|SOX2OT	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival;knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions	24927902	RID01187	interact with protein	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung cancer	SOX2-OT	CCNB1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000134057	NA	347689	891	NCRNA00043|SOX2OT	CCNB	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival.Sox2 overlapping transcript (Sox2ot) is a long noncoding RNA (lncRNA), localized on human chromosome 3q26.33, which is frequently amplified in lung squamous cell carcinomas (SCCs). In this study, we found that Sox2ot was up-regulated over two folds in 53.01% of human primary lung cancers (44/83). Importantly, knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions. Altogether, our data suggested that Sox2ot plays an important role in regulating lung cancer cell proliferation, and may represent a novel prognostic indicator for the disease.	24927902	RID01188	expression association	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Lung cancer	SOX2-OT	CDK1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000170312	NA	347689	983	NCRNA00043|SOX2OT	CDC2|CDC28A|P34CDC2	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival.Sox2 overlapping transcript (Sox2ot) is a long noncoding RNA (lncRNA), localized on human chromosome 3q26.33, which is frequently amplified in lung squamous cell carcinomas (SCCs). In this study, we found that Sox2ot was up-regulated over two folds in 53.01% of human primary lung cancers (44/83). Importantly, knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions. Altogether, our data suggested that Sox2ot plays an important role in regulating lung cancer cell proliferation, and may represent a novel prognostic indicator for the disease.	24927902	RID01189	expression association	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Colon cancer	HOTAIR	CDH1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01190	expression association	metastasis,prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colon cancer	HOTAIR	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000026025	NA	100124700	7431	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01191	expression association	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colon cancer	HOTAIR	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01192	expression association	metastasis,prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	LINC-ROR	ZEB2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-205)	regulation	NA	tamoxifen	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000169554	NA	100885779	9839	ROR|lincRNA-RoR|lincRNA-ST8SIA3	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.our data revealed that linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205;linc-ROR prevented the degradation of mir-205 target genes, including the EMT inducer ZEB2; Thus our results indicate that linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs. Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205.down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	24922071;28063065	RID01193	ceRNA or sponge	metastasis,chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	H19	RUNX1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	host(miR-675)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000159216	NA	283120	861	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells.Subsequently, the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in AGS cells, and knockdown of H19 or miR-675 enhanced RUNX1 expression.To our knowledge, this is the time to demonstrate that RUNX1 serves as a link between H19/miR-675 axis and Akt/mTOR signaling and is a pivotal mediator in gastric cancer progression induced by H19/miR-675. The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1;we found that miR-675 was positively expressed with H19 and was a pivotal mediator in H19-induced gastric cancer cell growth promotion;the tumor suppressor Runt Domain Transcription Factor1 (RUNX1) was confirmed to be a direct target of miR-675 using a luciferase reporter assay and Western blotting analyses;our study demonstrated that the novel pathway H19/miR-675/RUNX1 regulates gastric cancer development	26931432;24388988	RID01194	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Oesophageal adenocarcinoma	HNF1A-AS1	H19	positively-E	RNAi;western blot	upregulation	qPCR;sequencing	GSE48240	GSE48240.zip	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	lncRNA	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000130600	GRCh38_11:1995176-2001470	283460	283120	C12orf27|HAS1|NCRNA00262	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Long non-coding RNA HNF1A-AS1 regulates proliferation and migration in oesophageal adenocarcinoma cells.The well known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs;Our findings suggest that dysregulation of HNF1A-AS1 participates in oesophageal tumorigenesis, and that this participation may be mediated, at least in part, by modulation of chromatin and nucleosome assembly as well as by H19 induction	24000294	RID01195	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(NSCLC);DATA(GSE74639)
Cervical cancer	TUSC8	MYC	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	prognosis(+);cell proliferation(-)	interact with protein	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000237361	GRCh38_13:44400250-44405984	ENSG00000136997	NA	400128	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Low expression of long noncoding XLOC_010588 indicates a poor prognosis and promotes proliferation through upregulation of c-Myc in cervical cancer;Western blot assays confirmed that XLOC_010588 physically associates with c-Myc, consequently decreasing the expression of c-Myc	24667250	RID01196	interact with mRNA	prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	H19	ISM1	positively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101230	NA	283120	140862	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	C20orf82|ISM|Isthmin|bA149I18.1|dJ1077I2.1	Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer;An H19 co-expression network identified ISM1 as a binding protein of H19, and its expression was positively correlated with that of H19; Our results suggest that the effect of H19 in GC is mediated by the direct upregulation of ISM1 and the indirect suppression of CALN1 expression via miR-675.	24810858	RID01197	interact with protein	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Gastric cancer	H19	CALN1	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000183166	NA	283120	83698	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CABP8	Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer;CALN1 was identified as a target gene of miR-675 and its expression was negatively correlated with that of miR-675;H19 RNA actively binds to ISM1 and miR-675 targets CALN1;Our results suggest that the effect of H19 in GC is mediated by the direct upregulation of ISM1 and the indirect suppression of CALN1 expression via miR-675	24810858	RID01198	interact with protein	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	HOTAIR	ERBB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cancer progression(+)	ceRNA(miR-331-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141736	NA	100124700	2064	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer;HOTAIR may act as a ceRNA, effectively becoming a sink for miR-331-3p, thereby modulating the derepression of HER2 and imposing an additional level of post-transcriptional regulation;HOTAIR overexpression represents a biomarker of poor prognosis in gastric cancer, and may confer malignant phenotype to tumor cells.Finally, the positive HOTAIR/HER2 correlation was significantly associated with advanced gastric cancers.	24775712	RID01199	ceRNA or sponge	prognosis	NA	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Urinary bladder cancer	UCA1	WNT6	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);WNT signaling pathway(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000115596	NA	652995	7475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 increases chemoresistance of bladder cancer cells by regulating Wnt signaling.we showed that UCA1 positively regulates expression of wingless-type MMTV integration site family member 6 (Wnt6) in human bladder cancer cell lines. UCA1 and Wnt6 expression is also positively correlated in vivo. Up-regulation of UCA1 activates Wnt signaling in a Wnt6-dependent manner;We finally demonstrate that UCA1 increases the cisplatin resistance of bladder cancer cells by enhancing the expression of Wnt6	24495014	RID01200	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	BANCR	CDH1	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000039068	NA	100885775	999	LINC00586	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01201	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Non-small cell lung cancer	BANCR	CDH2	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000170558	NA	100885775	1000	LINC00586	CD325|CDHN|CDw325|NCAD	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01202	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Non-small cell lung cancer	BANCR	VIM	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000026025	NA	100885775	7431	LINC00586	NA	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01203	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Urinary bladder cancer	MALAT1	SUZ12	positively-F	RIP;RNA pull-down assay;ChIP;western blot;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178691	NA	378938	23512	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CHET9|JJAZ1	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;malat1 is associated with suppressor of zeste 12 (suz12), and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression. We performed RIP with antibodies against ezh2 or suz12 from nuclear extracts of T24 and RT4 cells. We observed a significant enrichment of malat1 with the suz12 antibody compared with the nonspecific immunoglobulin G (IgG) antibody control.	24449823	RID01204	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	TGFB1	MALAT1	positively-E	RNA pull-down assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;TGF-beta induces malat1 expression and EMT in bladder cancer cells;malat1 knockdown inhibits TGF-beta-induced EMT;targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGF-beta;These data suggest that malat1 is an important mediator of TGF-beta-induced EMT	24449823	RID01205	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	HOTAIR	RBM38	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132819	NA	100124700	55544	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HSRNASEB|RNPC1|SEB4B|SEB4D|dJ800J21.2	Long non-coding RNA HOTAIR promotes cell migration and invasion via down-regulation of RNA binding motif protein 38 in hepatocellular carcinoma cells;HOTAIR could promote migration and invasion of HCC cells by inhibiting RBM38, which indicated critical roles of HOTAIR and RBM38 in HCC progression	24663081	RID01206	expression association	NA	NA	DOWN(PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE41245)
Gastric cancer	miR-148a	MEG3	positively-E	MS-PCR;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MiR-148a regulates MEG3 in gastric cancer by targeting DNA methyltransferase 1;The positive correlation of MEG3 and miR-148a was further confirmed in SGC-7901 and BGC-823 gastric cancer cell lines; transfection of MEG3 siRNA into gastric cancer cells diminished the suppression of proliferation induced by overexpression of miR-148a;Our results suggest that the suppression of miR-148a may contribute to the down-regulation of MEG3 in gastric cancer by modulation of DNMT-1	24515776	RID01207	epigenetic regulation	NA	NA	NA
Breast cancer	UCA1	CDKN1B	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes breast tumor growth by suppression of p27(Kip1);although hnRNP I enhances the translation of p27 (Kip1) through interaction with the 5'-untranslated region (5'-UTR) of p27 mRNAs, the interaction of UCA1 with hnRNP I suppresses the p27 protein level by competitive inhibition;we show a negative correlation between p27 and UCA in the breast tumor cancer tissue microarray	24457952	RID01208	interact with protein	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	H19	miR-675	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	host	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675;we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression;introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells	24466011	RID01209	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Esophagus squamous cell carcinoma	HOTAIR	WIF1	negatively-E	RNAi;ChIP;western blot	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156076	NA	100124700	11197	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	WIF-1	HOTAIR, a prognostic factor in esophageal squamous cell carcinoma, inhibits WIF-1 expression and activates Wnt pathway;inverse correlation between HOTAIR and WIF-1 expression was demonstrated both in ESCC cells and tissues;HOTAIR directly decreased WIF-1 expression by promoting its histone H3K27 methylation in the promoter region and then activated the Wnt/beta-catenin signaling pathway;This newly identified HOTAIR/WIF-1 axis clarified the molecular mechanism of ESCC cell metastasis	24118380	RID01210	epigenetic regulation	metastasis,prognosis	NA	NA
Urinary bladder cancer	miR-125b	MALAT1	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Hsa-miR-125b suppresses bladder cancer development by down-regulating oncogene SIRT7 and oncogenic long non-coding RNA MALAT1;we report that hsa-miR-125b and oncogene SIRT7/oncogenic long non-coding RNA MALAT1 were inversely expressed in bladder cancer;Binding sites were confirmed between hsa-miR-125b and SIRT7/MALAT1;Up-regulation of hsa-miR-125b or down-regulation of SIRT7 inhibited proliferation, motility and increased apoptosis. The effects of up-regulation of hsa-miR-125b were similar to that of silencing MALAT1 in bladder cancer as we had previously described	24396870	RID01211	ceRNA or sponge	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Lung adenocarcinoma	HOTAIR	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	The long noncoding RNA HOTAIR contributes to cisplatin resistance of human lung adenocarcinoma cells via downregualtion of p21(WAF1/CIP1) expression;HOTAIR was observed to be significantly downregulated in cisplatin-responding LAD tissues, and its expression was inversely correlated with p21 mRNA expression;siRNA/p21 or pcDNA/p21 could partially rescue the effects of siRNA/HOTAIR1 or pcDNA/HOTAIR on both p21 expression and cisplatin sensitivity in LAD cells;our findings suggest that upregulation of HOTAIR contributes to the cisplatin resistance of LAD cells, at least in part, through the regulation of p21 expression	24155936	RID01212	expression association	chemoresistance	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	HOTAIR	HOXA5	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106004	NA	100124700	3202	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX1|HOX1.3|HOX1C	The long non-coding RNA HOTAIR indicates a poor prognosis and promotes metastasis in non-small cell lung cancer. Our findings indicate that HOTAIR is significantly up-regulated in NSCLC tissues, and regulates NSCLC cell invasion and metastasis, partially via the down-regulation of HOXA5	24103700	RID01213	expression association	metastasis,prognosis	NA	NA
Non-small cell lung cancer	MEG3	TP53	positively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA MEG3 inhibits NSCLC cells proliferation and induces apoptosis by affecting p53 expression;Our findings indicate that MEG3 is significantly down-regulated in NSCLC tissues that could be affected by DNA methylation, and regulates NSCLC cell proliferation and apoptosis, partially via the activition of p53	24098911	RID01214	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	BLACAT1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);cell survival(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000178691	NA	101669762	23512	LINC00912|linc-UBC1|onco-lncRNA-30	CHET9|JJAZ1	linc-UBC1 physically associates with polycomb repressive complex 2 (PRC2) and acts as a negative prognostic factor for lymph node metastasis and survival in bladder cancer;RIP and ChIP assay confirmed that linc-UBC1 physically associates with PRC2 complex and regulates histone modification status of target genes.RNA immunoprecipitation (RIP) was performed to confirm that linc-UBC1 physically associates with EZH2 and SUZ12, core components of polycomb repressive complex 2 (PRC2).	23688781	RID01215	interact with protein	metastasis,prognosis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	BLACAT1	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);cell survival(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000106462	NA	101669762	2146	LINC00912|linc-UBC1|onco-lncRNA-30	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	linc-UBC1 physically associates with polycomb repressive complex 2 (PRC2) and acts as a negative prognostic factor for lymph node metastasis and survival in bladder cancer;RIP and ChIP assay confirmed that linc-UBC1 physically associates with PRC2 complex and regulates histone modification status of target genes.RNA immunoprecipitation (RIP) was performed to confirm that linc-UBC1 physically associates with EZH2 and SUZ12, core components of polycomb repressive complex 2 (PRC2).	23688781	RID01216	interact with protein	metastasis,prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Acute promyelocytic leukemia	HOXA-AS2	TNFSF10	negatively-E	western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000121858	NA	285943	8743	HOXA3as	APO2L|Apo-2L|CD253|TL2|TNLG6A|TRAIL	HOX antisense lincRNA HOXA-AS2 is an apoptosis repressor in all trans retinoic acid treated NB4 promyelocytic leukemia cells; The increase in death of HOXA-AS2 knockdown cells was accompanied by an elevated TNF-related apoptosis-inducing ligand (TRAIL) levels, but ATRA-induced NB4 cells treated with TRAIL did show an increase in HOXA-AS2 expression;These results demonstrate that all trans retinoic acid (ATRA) induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway	23649634	RID01217	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Prostate cancer	CBR3-AS1	AR	positively-E	RIP;western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);apoptosis process(-);cell proliferation(+)	ceRNA(miR-34c;miR-297)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000169083	NA	100506428	367	PlncRNA-1|PlncRNA1	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa.The prostate cancer-up-regulated long noncoding RNA PlncRNA-1 modulates apoptosis and proliferation through reciprocal regulation of androgen receptor;PlncRNA-1 suppression by siRNA resulted in a decrease of androgen receptor (AR) mRNA, protein and AR downstream target	26808578;22264502	RID01218	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Hepatocellular carcinoma	H19	miR-200	positively-E	RNA pull-down assay;ChIP;RIP;western blot	downregulation	qPCR	NA	NA	cell metastasis(-);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma;H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation. The results demonstrate that H19 can alter the miR-200 pathway, thus contributing to mesenchymal-to-epithelial transition and to the suppression of tumor metastasis	23222811	RID01219	epigenetic regulation	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Urinary bladder cancer	UCA1	CREB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118260	NA	652995	1385	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CREB|CREB-1	Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells;UCA1 alteration paralleled to the expression and phosphorylation of CREB, and UCA1 obviously influenced AKT expression and activity;cell cycle progression was greatly reduced after PI3-K pathway was blocked by LY294002, indicating that UCA1 affected cell cycle progression through CREB	22285928	RID01220	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. In vitro assays in the HCC cell line Bel7402 demonstrated that knockdown of HOTAIR lincRNA reduced cell proliferation and was associated with reductions in levels of matrix metalloproteinase-9 and vascular endothelial growth factor protein, which are important for cell motility and metastasis	22289527	RID01221	expression association	metastasis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. In vitro assays in the HCC cell line Bel7402 demonstrated that knockdown of HOTAIR lincRNA reduced cell proliferation and was associated with reductions in levels of matrix metalloproteinase-9 and vascular endothelial growth factor protein, which are important for cell motility and metastasis	22289527	RID01222	expression association	metastasis	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Osteosarcoma	HOTAIR	CDKN2A	negatively-E	ChIP	upregulation	qPCR	NA	NA	chemosensitivity(+);cell viability(+);apoptosis process(-)	DNA methylation	regulation	NA	DNMT1 inhibitor	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000147889	NA	100124700	1029	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	A novel interplay between HOTAIR and DNA methylation in osteosarcoma cells indicates a new therapeutic strategy.A series of experiments show that HOTAIR represses the expression of CDKN2A through inhibiting the promoter activity of CDKN2A by DNA hypermethylation. Functionally, HOTAIR depletion increases the sensibility of OS cells to DNMT1 inhibitor through regulating the viability and apoptosis of OS cells via HOTAIR-miR126-DNMT1-CDKN2A axis.	28730284	RID01223	epigenetic regulation	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Osteosarcoma	HOTAIR	DNMT1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(+);cell viability(+);apoptosis process(-)	NA	regulation	NA	DNMT1 inhibitor	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	A novel interplay between HOTAIR and DNA methylation in osteosarcoma cells indicates a new therapeutic strategy. Further evidence shows that HOTAIR activates the expression of DNMT1 through repressing miR-126, which is the negative regulator of DNMT1; Functionally, HOTAIR depletion increases the sensibility of OS cells to DNMT1 inhibitor through regulating the viability and apoptosis of OS cells via HOTAIR-miR126-DNMT1-CDKN2A axis.	28730284	RID01224	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteoarthritis	NEAT1	SPP1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-181c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000118785	NA	283131	6696	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1/miR-181c Regulates Osteopontin (OPN)-Mediated Synoviocyte Proliferation in Osteoarthritis;among which NEAT1 showed to inversely regulate miR-181c;By performing Luciferase assays, we revealed that NEAT1 competed with OPN for miR-181c binding;OPN mRNA, and NEAT1 expression was upregulation, whereas miR-181c expression was downregulated, indicating that targeting NEAT1 to rescue miR-181c expression so as to inhibit OPN expression and synoviocyte proliferation might be an efficient strategy for OA treatment	28379604	RID01225	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE86978)
Liver fibrosis	NEAT1	KLF6	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	fibrotic(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067082	NA	283131	1316	LINC00084|NCRNA00084|TncRNA|VINC	BCD1|CBA1|COPEB|CPBP|GBF|PAC1|ST12|ZF9	NEAT1 accelerates the progression of liver fibrosis via regulation of microRNA-122 and Kruppel-like factor 6;both NEAT1 and KLF6 are targets of miR-122;Pull-down assay confirmed a direct interaction between miR-122 and NEAT1; KLF6 and miR-122 were required for the effects of NEAT1 on HSC activation. NEAT1 contributes to HSC activation via competitively binding miR-122	28864835	RID01226	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE67939)
Osteosarcoma	ZBTB7A	LINC00473	negatively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	binding/interaction	protein-DNA	cisplatin	NA	NA	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000178951	NA	ENSG00000112541	GRCh38_6:165924048-165988039	51341	90632	FBI-1|FBI1|LRF|TIP21|ZBTB7|ZNF857A|pokemon	C6orf176|LNC473|bA142J11.1	ZBTB7A Enhances Osteosarcoma Chemoresistance by Transcriptionally Repressing lncRNA LINC00473-IL24 Activity;we found that ZBTB7A is increased in cisplatin-resistant osteosarcoma cells and that elevated ZBTB7A inhibits cisplatin-induced apoptosis by repressing LINC00473 expression;ZBTB7A directly binds to the promoter and suppresses the transcription of LINC00473	28942243	RID01227	transcriptional regulation	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Osteosarcoma	LINC00473	IL24	negatively-E	western blot;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	binding/interaction	RNA-DNA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000162892	NA	90632	11009	C6orf176|LNC473|bA142J11.1	C49A|FISP|IL10B|MDA7|MOB5|ST16	ZBTB7A Enhances Osteosarcoma Chemoresistance by Transcriptionally Repressing lncRNA LINC00473-IL24 Activity;Additionally, our data indicate that LINC00473 interacts with the transcript factor C/EBPbeta, facilitating its binding to the promoter of IL24, leading to decrease chemoresistance.	28942243	RID01228	transcriptional regulation	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	NEAT1	miR-194	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression;Luciferase reporter assay validated that NEAT1 could interact with miR-194 and negatively modulated its expression;inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells	29047232	RID01229	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Esophagus squamous cell carcinoma	GHET1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000039068	NA	102723099	999	lncRNA-GHET1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01230	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	GHET1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000170558	NA	102723099	1000	lncRNA-GHET1	CD325|CDHN|CDw325|NCAD	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01231	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Esophagus squamous cell carcinoma	GHET1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000026025	NA	102723099	7431	lncRNA-GHET1	NA	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01232	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	AC132217.4	IGF2	positively-F	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);epithelial to mesenchymal transition(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_11:2129121-2129964	ENSG00000167244	NA	NA	3481	NA	C11orf43|GRDF|IGF-II|PP9974	LncRNAAC132217.4, a KLF8-regulated long non-coding RNA, facilitates oral squamous cell carcinoma metastasis by upregulating IGF2 expression;One of the lncRNAs, termed AC132217.4, was remarkably upregulation and promoted cell migration and epithelial-mesenchymal transition (EMT) by upregulating IGF2 expression; AC132217.4 interacted with the 3'UTR of IGF2 mRNA and increased its stability, leading to increased IGF2 levels	28823965	RID01233	interact with mRNA	metastasis	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Esophagus squamous cell carcinoma	KLF8	AC132217.4	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000102349	NA	NA	GRCh38_11:2129121-2129964	11279	NA	BKLF3|ZNF741	NA	LncRNAAC132217.4, a KLF8-regulated long non-coding RNA, facilitates oral squamous cell carcinoma metastasis by upregulating IGF2 expression. we found that KLF8 binds to the upstream sequence of AC132217.4, activating its expression at the transcriptional level, which accelerated OSCC metastasis via the AC132217.4-IGF2 axis both in vitro and in vivo	28823965	RID01234	transcriptional regulation	metastasis	NA	NA
Malignant glioma	MALAT1	STMN1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117632	NA	378938	3925	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C1orf215|LAP18|Lag|OP18|PP17|PP19|PR22|SMN	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01235	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Malignant glioma	MALAT1	RAB5A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000144566	NA	378938	5868	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RAB5	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01236	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD);DATA(GSE40174,GSE67980,GSE104209,GSE60407)
Malignant glioma	MALAT1	ATG4D	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000130734	NA	378938	84971	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG4-D|APG4D|AUTL4	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01237	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Recurrent miscarriage	YY1	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Other	Recurrent miscarriage	TF	lncRNA	ENSG00000100811	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7528	100124700	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The YY1-HOTAIR-MMP2 Signaling Axis Controls Trophoblast Invasion at the Maternal-Fetal Interface.Bioinformatics analysis identified two YY1-binding sites in the HOTAIR promoter region, and chromatin immunoprecipitation (ChIP) analysis verified that YY1 binds directly to its promoter region.HOTAIR overexpression effectively elevated matrix metalloproteinase 2 (MMP2) expression via the PI3K-AKT signaling pathway, enhancing trophoblast migration and invasion.	28750739	RID01238	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	NA
Recurrent miscarriage	HOTAIR	MMP2	positively-E	western blot	upregulation	qPCR	NA	NA	cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Other	Recurrent miscarriage	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087245	NA	100124700	4313	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	The YY1-HOTAIR-MMP2 Signaling Axis Controls Trophoblast Invasion at the Maternal-Fetal Interface.Bioinformatics analysis identified two YY1-binding sites in the HOTAIR promoter region, and chromatin immunoprecipitation (ChIP) analysis verified that YY1 binds directly to its promoter region.HOTAIR overexpression effectively elevated matrix metalloproteinase 2 (MMP2) expression via the PI3K-AKT signaling pathway, enhancing trophoblast migration and invasion.	28750739	RID01239	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Myasthenia gravis	IFNG-AS1	HLA-DRB1	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	immune response(-)	NA	regulation	NA	NA	NA	Evading Immune Detection	Immune system disease	Autoimmune disease of the nervous system	lncRNA	PCG	ENSG00000255733	GRCh38_12:67989445-68234686	ENSG00000196126	NA	NA	3123	NA	DRB1|HLA-DR1B|HLA-DRB|SS1	IFNA-AS1 regulates CD4+ T cell activation in myasthenia gravis though HLA-DRB1;IFNG-AS1 could reduce the expression of HLA-DRB and HLA-DOB and they had a negative correlation in MG;Furthermore IFNG-AS1 influenced the expression levels of CD40L and CD4+ T cells activation in MG patient partly depend on effecting the HLA-DRB1 expression. It suggests that IFNG-AS1 may be involved in CD4+T cell-mediated immune responses in MG	28822831	RID01240	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE111842,GSE51827,GSE75367,GSE86978)
Liver fibrosis	H19	EPCAM	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	fibrotic(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000119888	NA	283120	4072	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	H19 promotes cholestatic liver fibrosis by preventing ZEB1-mediated inhibition of epithelial cell adhesion molecule; H19RNA impeded ZEB1's inhibitory action by interacting with ZEB1 protein to prevent its binding to the EpCAM promoter;Hepatic overexpression of ZEB1 or knockdown of EpCAM diminished H19-induced fibrosis;The up-regulation of H19RNA and EpCAM correlated positively with the down-regulation of ZEB1 in primary sclerosing cholangitis and primary biliary cirrhosis liver specimens	28407375	RID01241	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Osteosarcoma	TUG1	EZH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-144-3p)	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	TUG1 promotes osteosarcoma tumorigenesis by upregulating EZH2 expression via miR-144-3p;TUG1 regulated miR-144-3p expression through direct binding;EZH2, a verified target of miR-144-3p was upregulation in osteosarcoma tissues and negatively correlated with miR-144-3p;EZH2 was negatively regulated by miR-144-3p and positively regulated by TUG1;EZH2, a verified target of miR-144-3p was upregulation in osteosarcoma tissues and negatively correlated with miR-144-3p. EZH2 was negatively regulated by miR-144-3p and positively regulated by TUG1	28902349	RID01242	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Aortic valve disease	MALAT1	SMAD4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141646	NA	378938	4089	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DPC4|JIP|MADH4|MYHRS	LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4;MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers;we identified Smad4 as a direct target of miR-204;MALAT1 positively regulated the expression of Smad4 through sponging miR-204, and promoted osteogenic differentiation of VICs	28522163	RID01243	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Pulmonary fibrosis	MALAT1	PIK3R1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);fibrotic(+)	ceRNA(miR-503)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000145675	NA	378938	5295	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MiR-503 modulates epithelial-mesenchymal transition in silica-induced pulmonary fibrosis by targeting PI3K p85 and is sponged by lncRNA MALAT1; overexpressed miR-503 inhibited silica-induced pulmonary fibrosis by attenuating the severity and the distribution of lesions in vivo and limiting the process of epithelial-mesenchymal transition (EMT) in vitro;the up-regulated lncRNA Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), acted as a competing endogenous RNA (ceRNA), can directly bound to miR-503, which indicated that lncRNA MALAT1 may modulate the expression of miR-503 thus triggering the activation of downstream fibrotic signaling pathways;Taken together, our data suggested that MALAT1-miR-503-PI3K/Akt/mTOR/Snail pathway plays critical roles in silica-induced pulmonary fibrosis. PI3K p85, also named PIK3R1, is a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), and it also consists of a catalytic subunit, p110	28900284	RID01244	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE51827,GSE55807,GSE86978)
Colorectal cancer	PURPL	TP53	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000250337	GRCh38_5:27217714-27496994	ENSG00000141510	NA	643401	7157	LINC01021	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer;Targeted depletion of PURPL in colorectal cancer cells results in elevated basal p53 levels and induces growth defects in cell culture and in mouse xenografts	28877474	RID01245	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hirschsprung's disease	AFAP1-AS1	RAP1B	positively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000127314	NA	84740	5908	AFAP1-AS|AFAP1AS	K-REV|RAL1B	LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR; Knockdown of AFAP1-AS in 293T and SH-SY5Y cells suppressed cell proliferation, migration, and induced the loss of cell stress filament integrity, possibly due to AFAP1-AS sequestering miR-181a in HSCR cells;Furthermore, AFAP1-AS could down-regulate RAP1B via its competing endogenous RNA (ceRNA) activity on miR-181a.These findings suggest that aberrant expression of lncRNA AFAP1-AS, a ceRNA of miR-181a, may involve in the onset and progression of HSCR by augmenting the miR-181a target gene, RAP1B.	28924375	RID01246	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE38495,GSE55807)
Non-small cell lung cancer	miR-101-3p	MALAT1	negatively-F	western blot;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MiR-101-3p inhibits the growth and metastasis of non-small cell lung cancer through blocking PI3K/AKT signal pathway by targeting MALAT-1;overexpression of miR-101-3p could significantly inhibit the proliferation, migration and invasion of NSCLC cells in vitro, as well as MALAT-1 expression;miR-101-3p could specifically repress MALAT-1 expression through direct binding;MALAT-1 overexpression completely reversed the miR-101-3p-induced suppression on the viability, migration and invasion of NSCLC cellsand MALAT-1 expression;we confirmed that miR-101-3p could block the MALAT-1-induced activation of PI3K/AKT signal pathway and resulted in the inhibition on the growth and metastasis of NSCLC cells in vivo	28738500	RID01247	ceRNA or sponge	metastasis	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	NEAT1	SIN3A	interact	RIP;ChIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell migration(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000169375	NA	283131	25942	LINC00084|NCRNA00084|TncRNA|VINC	WITKOS	The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer;the FOXN3-NEAT1-SIN3A complex represses genes including GATA3 that are critically involved in epithelial-to-mesenchymal transition (EMT);We demonstrated that the FOXN3-NEAT1-SIN3A complex promotes EMT and invasion of breast cancer cells in vitro as well as dissemination and metastasis of breast cancer in vivo;Elevation of both FOXN3 and NEAT1 expression during breast cancer progression corresponded to diminished GATA3 expression, and high levels of FOXN3 and NEAT1 strongly correlated with higher histological grades and poor prognosis;Our experiments uncovered that NEAT1 is a facultative component of the SIN3A complex, shedding light on the mechanistic actions of NEAT1 and the SIN3A complex	28805661	RID01248	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)
Breast cancer	NEAT1	GATA3	negatively-E	RIP;ChIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000107485	NA	283131	2625	LINC00084|NCRNA00084|TncRNA|VINC	HDR|HDRS	The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer;the FOXN3-NEAT1-SIN3A complex represses genes including GATA3 that are critically involved in epithelial-to-mesenchymal transition (EMT);We demonstrated that the FOXN3-NEAT1-SIN3A complex promotes EMT and invasion of breast cancer cells in vitro as well as dissemination and metastasis of breast cancer in vivo;Elevation of both FOXN3 and NEAT1 expression during breast cancer progression corresponded to diminished GATA3 expression, and high levels of FOXN3 and NEAT1 strongly correlated with higher histological grades and poor prognosis;Our experiments uncovered that NEAT1 is a facultative component of the SIN3A complex, shedding light on the mechanistic actions of NEAT1 and the SIN3A complex	28805661	RID01249	transcriptional regulation	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(BRCA);DATA(GSE55807)
Malignant glioma	MIR155HG	miR-155	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	epithelial to mesenchymal transition(+)	host	regulation	NA	NSC141562	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234883	GRCh38_21:25561909-25575168	NA	NA	114614	NA	BIC|MIRHG2|NCRNA00172	NA	Blocking MIR155HG/miR-155 axis inhibits mesenchymal transition in glioma;MIR155HG reduction by small interfering RNA inhibited cell proliferation, migration, invasion, and orthotopic glioma growth by repressing the generation of its derivatives miR-155-5p and miR-155-3p;High-throughput screening indicated that the MIR155HG/miR-155 axis inhibitor NSC141562 may be a useful candidate anti-glioma drug	28371892	RID01250	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	NA
Malignant glioma	LINC01139	LDHA	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000134333	NA	339535	3939	NA	GSD11|HEL-S-133P|LDHM|PIG19	Long non-coding RNA LINK-A promotes glioma cell growth and invasion via lactate dehydrogenase A; we found that lactate dehydrogenase A (LDH-A) was regulated by LINK-A, and enforced expression of LDH-A promoted glycolysis and proliferation in glioma cells	28714007	RID01251	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Multiple myeloma	OIP5-AS1	KLF10	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PTEN/PI3K/AKT signaling pathway(-);cell proliferation(-);apoptosis process(+)	ceRNA(miR-410)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Myeloma	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000155090	NA	729082	7071	cyrano|linc-OIP5	EGR-alpha|EGRA|TIEG|TIEG1	LncRNA OIP5-AS1 loss-induced microRNA-410 accumulation regulates cell proliferation and apoptosis by targeting KLF10 via activating PTEN/PI3K/AKT pathway in multiple myeloma;downregulated expression of lncRNA OIP5-AS1 was inversely correlated with miR-410 expression in MM tissues;LncRNA OIP5-AS1 could modulate the miR-410 expression and regulate its target KLF10/PTEN/AKT-mediated cellular behaviors.we predicted a target by Starbase 2.0 and found lncRNA OIP5-AS1 is a molecular sponge that modulates miR-410.	28796257	RID01252	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE86978)
Osteoarthritis	UCA1	miR-204-5p	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell survival(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA-UCA1 enhances MMP-13 expression by inhibiting miR-204-5p in human chondrocytes;These results suggested that UCA1 played as an important regulator of survival and matrix synthesis of chondrocytes partly through suppressing the miR-204-5p expression	29207643	RID01253	expression association	NA	UP(PAAD);DATA(GSE40174)	NA
Hepatocellular carcinoma	lncSHRG	HES6	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_2:91636683-91659949	ENSG00000144485	NA	NA	55502	NA	C-HAIRY1|HES-6|bHLHb41|bHLHc23	LncSHRG promotes hepatocellular carcinoma progression by activating HES6;Here we identified that a long noncoding RNA, lncSHRG, was greatly upregulation in human hepatocellular carcinoma samples. lncSHRG recruits SATB1 to bind to HES6 promoter and initiates HES6 expression	29050307	RID01254	transcriptional regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Type 2 diabetes mellitus	IGF2-AS	IGF2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	angiogenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000167244	NA	51214	3481	IGF2-AS1|IGF2AS|PEG8	C11orf43|GRDF|IGF-II|PP9974	Inhibition of long noncoding RNA IGF2AS promotes angiogenesis in type 2 diabetes. IGF2AS inhibition has angiogenic effect in diabetic GK mMVE cells. The functions of IGF2AS in type 2 diabetes are very likely through the inverse regulation of IGF2, but independent of IGF1.	28570978	RID01255	expression association	NA	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Lung cancer	XIST	PPP1R13L	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-140)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000104881	NA	7503	10848	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	IASPP|NKIP1|RAI|RAI4	lncRNA XIST interacts with miR-140 to modulate lung cancer growth by targeting iASPP.lncRNA-XIST was specifically upregulation in lung cancer cell lines and promoted lung cancer cell growth through targeting miR-140	28656261	RID01256	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	LINC00313	SOX2	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	RNA-DNA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000185186	GRCh38_21:43461960-43479534	ENSG00000181449	NA	114038	6657	C21orf84|CH507-42P11.5|NCRNA00313	ANOP3|MCOPS3	Long noncoding RNA linc00617 exhibits oncogenic activity in breast cancer. We demonstrated that linc00617 upregulation the expression of stemness factor Sox2 in breast cancer cells, which was shown to promote the oncogenic activity of breast cancer cells by stimulating epithelial-to-mesenchymal transition and enhancing the tumor-initiating capacity. Thus, our data indicate that linc00617 functions as an important regulator of EMT and promotes breast cancer progression and metastasis via activating the transcription of Sox2	26207516	RID01257	transcriptional regulation	metastasis	NA	UP(LIHC);DATA(GSE117623)
Pancreatic ductal adenocarcinoma	MIR31HG	miR-193b	negatively-F	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE28735	GSE28735.zip	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b. Inhibition of miR-193b expression significantly upregulation the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	26549028	RID01258	ceRNA or sponge	NA	NA	NA
Hepatocellular carcinoma	lnc-DILC	IL6	negatively-E	RIP	downregulation	qPCR;microarray	NA	NA	cell growth(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641470	ENSG00000136244	NA	NA	3569	NA	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis. Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. The putative binding locus of lnc-DILC within IL-6 promoter was confirmed by pull down assay. Consistently, the oligoribonucleotide mimics and an oligodeoxynucleotide decoy of lnc-DILC abrogated the effects on IL-6 transcription, STAT3 activation and LCSC expansion triggered by lnc-DILC depletion and lnc-DILC overexpression.	26812074	RID01259	transcriptional regulation	NA	NA	DOWN(BRCA);DATA(GSE75367,GSE86978)
Hepatocellular carcinoma	lnc-DILC	STAT3	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000198176	GRCh38_13:113584721-113641470	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis. Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. The putative binding locus of lnc-DILC within IL-6 promoter was confirmed by pull down assay. Consistently, the oligoribonucleotide mimics and an oligodeoxynucleotide decoy of lnc-DILC abrogated the effects on IL-6 transcription, STAT3 activation and LCSC expansion triggered by lnc-DILC depletion and lnc-DILC overexpression.	26812074	RID01260	expression association	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Melanoma	SPRY4-IT1	DPP4	negatively-E	RNAi	upregulation	qPCR;microarray;sequencing	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000197635	NA	100642175	1803	SPRIGHTLY	NA	The Long Noncoding RNA SPRIGHTLY Regulates Cell Proliferation in Primary Human Melanocytes.Because down-regulation of DPPIV is known to be associated with malignant transformation in melanocytes, SPRIGHTLY-mediated DPPIV down-regulation may play an important role in melanoma pathobiology.	26829028	RID01261	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Cervical cancer	OIP5-AS1	ELAVL1	negatively-E	RIP;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-424)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000066044	NA	729082	1994	cyrano|linc-OIP5	ELAV1|HUR|Hua|MelG	LncRNA OIP5-AS1/cyrano sponges RNA-binding protein HuR.Tagging OIP5-AS1 with MS2 hairpins to identify associated microRNAs revealed that miR-424 interacted with OIP5-AS1 and competed with HuR for binding to OIP5-AS1.We propose that OIP5-AS1 serves as a sponge or a competing endogenous (ce)RNA for HuR, restricting its availability to HuR target mRNAs and thereby repressing HuR-elicited proliferative phenotypes.	26819413	RID01262	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Laryngeal squamous cell carcinoma	H19	DNMT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-148a-3p)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000130816	NA	283120	1786	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis.In this study, we reported that the lncRNA H19 was upregulated in LSCC. We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown. In summary, our study demonstrated that the lncRNA H19 promoted LSCC progression via miR-148a-3p and DNMT1.	26872375	RID01263	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	MALAT1	CDH1	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. RIP and ChIP assays suggest that EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression.	26848980	RID01264	epigenetic regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Metabolic syndrome	MEG3	HDAC7	positively-E	RNAi;luciferase reporter assay	downregulation	qPCR	NA	NA	cell protection(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	NA	Syndrome	Metabolic syndrome	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000061273	NA	55384	51564	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HD7|HD7A|HDAC7A	Pioglitazone up-regulates long non-coding RNA MEG3 to protect endothelial progenitor cells via increasing HDAC7 expression in metabolic syndrome.Overexpression of MEG3 resulted in the down-regulation of miR-140-5p. The luciferase reporter assay and RIP assay showed that MEG3 targeted miR-140-5p. In addition, the HDAC7 expression levels were regulated by miR-140-5p and MEG3. HDAC7 is a target gene of miR-140-5p.	26898430	RID01265	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	MALAT1	SNAI2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	radioresistance(+)	ceRNA(miR-1)	regulation	NA	NA	CSC	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000019549	NA	378938	6591	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma. Interestingly, we found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients.	26482776	RID01266	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Non-small cell lung cancer	MEG3	SKP2	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-3163)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000145604	NA	55384	6502	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	FBL1|FBXL1|FLB1|p45	Skp2 regulates non-small cell lung cancer cell growth by Meg3 and miR-3163. These data suggest that the Skp2 may be regulated by Meg3 at post-transcriptional level. Bioinformatics analyses showed that miR-3163 bound to 3'-UTR of Skp2 mRNA in NSCLC cells to inhibit its translation, which was supported by luciferase reporter assay. Meg3 augmented the effects of miR-3163 on Skp2 mRNA, possibly through binding-induced function enhancement, which was supported by the double fluorescent in situ hybridization showing co-localized intracellular Meg3 and miR-3163 signals in NSCLC cells. Thus, our data suggest that Meg3 and miR-3163 may coordinate suppression of translation of Skp2 mRNA in NSCLC cells to inhibit NSCLC cell growth.	26482610	RID01267	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Cancer	FOXD3	OLA1P2	positively-E	ChIP	upregulation	qPCR;microarray	GSE76583	GSE76583.zip	tumor-suppressive function(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Cancer	TF	lncRNA	ENSG00000187140	NA	ENSG00000213671	GRCh38_17:20775642-20776905	27022	106479059	AIS1|Genesis|HFH2|VAMAS2	NA	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene. Subsequently, upregulation FOXD3 protein transcriptionally activates lncRNA OLA1P2 expression. OLA1P2 upregulation markedly affects STAT3 signaling pathway activity by inhibiting the nuclear import of phosphorylated STAT3.	26898989	RID01268	transcriptional regulation	NA	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Cancer	OLA1P2	STAT3	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE76583	GSE76583.zip	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000213671	GRCh38_17:20775642-20776905	ENSG00000168610	NA	106479059	6774	NA	ADMIO|ADMIO1|APRF|HIES	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene. Subsequently, upregulation FOXD3 protein transcriptionally activates lncRNA OLA1P2 expression. OLA1P2 upregulation markedly affects STAT3 signaling pathway activity by inhibiting the nuclear import of phosphorylated STAT3. OLA1P2 interacts directly with STAT3 due to OLA1P2 sharing the same conservative STAT3 transcription response element as STAT3 targets.	26898989	RID01269	interact with protein	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	MALAT1	miR-140	negatively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	blood-tumor barrier(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140.	26619802	RID01270	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Hepatocellular carcinoma	UHRF1	MEG3	negatively-E	RNAi;Bisulfite Sequencing	downregulation	qPCR	NA	NA	cell proliferation(-);prognosis(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000276043	NA	ENSG00000214548	GRCh38_14:100779410-100861031	29128	55384	ICBP90|Np95|RNF106|TDRD22|hNP95|hUHRF1|huNp95	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.	25641194	RID01271	epigenetic regulation	prognosis	UP(PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE86978)	NA
Hepatocellular carcinoma	MEG3	TP53	interact	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);cell proliferation(-);apoptosis process(+);cell growth(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals;Evading Apoptosis;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA MEG3 Interacts with p53 Protein and Regulates Partial p53 Target Genes in Hepatoma Cells.In conclusion, our data demonstrates that MEG3 functions as a tumor suppressor in hepatoma cells through interacting with p53 protein to activate p53-mediated transcriptional activity and influence the expression of partial p53 target genes.Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26444285;27432655;25641194;26992211	RID01272	interact with protein	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Cervical cancer	MALAT1	miR-145	negatively-F	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 modulates radiosensitivity of HR-HPV+ cervical cancer via sponging miR-145. By performing RNA-binding protein immunoprecipitation (RIP) assay and RNA pull-down assay, we confirmed that miR-145 and MALAT1 were in the same Ago2 complex and there was a reciprocal repression between them.	26311052	RID01273	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Pancreatic cancer	LINC-ROR	NANOG	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000111704	NA	100885779	79923	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer. In conclusions, we demonstrated that decreased ROR expression could inhibit cell proliferation, invasion, and tumourigenicity by modulating Nanog.	26636540	RID01274	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Colorectal cancer	ZFAS1	CDK1	positively-E	RIP;RNA pull-down assay	upregulation	qPCR;sequencing	NA	NA	cell cycle(+);apoptosis process(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000170312	NA	441951	983	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	CDC2|CDC28A|P34CDC2	Long non-coding RNA ZFAS1 interacts with CDK1 and is involved in p53-dependent cell cycle control and apoptosis in colorectal cancer. We identified Cyclin-dependent kinase 1 (CDK1) as interacting partner of ZFAS1 by pull-down experiment and RNA immunoprecipitation. Further, we have predicted by bioinformatics approach ZFAS1 to sponge miR-590-3p, which was proved to target CDK1.	26506418	RID01275	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Hepatocellular carcinoma	miR-203	HULC	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC. Furthermore, we identified that miR-203 modulated ADAM9 and HULC in a novel post-transcriptional regulatory mechanism. Over-expression of HULC partly rescued the miR-203-mediated antitumor effects.	26179263	RID01276	ceRNA or sponge	metastasis	NA	NA
Cervical cancer	MEG3	miR-21-5p	negatively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long noncoding RNA MEG3 is downregulated in cervical cancer and affects cell proliferation and apoptosis by regulating miR-21.Furthermore, we focused on the function and molecular mechanism of MEG3, finding that overexpression of MEG3 reduced the level of miR-21-5p expression, causing inhibition of proliferation and increased apoptosis in cervical cancer cells.	26574780	RID01277	expression association	NA	NA	NA
Urinary bladder cancer	UCA1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000148516	NA	652995	6935	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01278	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	UCA1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000169554	NA	652995	9839	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01279	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	UCA1	FSCN1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000075618	NA	652995	6624	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FAN1|HSN|SNL|p55	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01280	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Coronary artery disease	CDKN2B-AS1	YY1	interact	RIP	upregulation	qPCR	NA	NA	inflammatory response(+)	interact with protein	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Coronary artery disease	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000100811	NA	100048912	7528	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	Long non-coding RNA ANRIL regulates inflammatory responses as a novel component of NF-kB pathway.For the first time, we establish the connection between ANRIL and NF-kB pathway and show that ANRIL regulates inflammatory responses through binding with YY1. The newly identified TNF-alpha-NF-kB-ANRIL/YY1-IL6/8 pathway enhances understanding of the etiology of CAD and provides potential therapeutic target for treatment of CAD.	26618242	RID01281	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Cervical cancer	MALAT1	GRB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000177885	NA	378938	2885	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASH|EGFRBP-GRB2|Grb3-3|MST084|MSTP084|NCKAP2	MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells.MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis.	26242259	RID01282	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	miR-192	HOTTIP	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. These results elucidate that the miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis.	26710269	RID01283	ceRNA or sponge	NA	NA	NA
Prostate cancer	MALAT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 enhances oncogenic activities of EZH2 in castration-resistant prostate cancer.Using EZH2 antibody-based RNA immunoprecipitation-coupled high throughput sequencing (RIP-seq), we demonstrated that EZH2 binds to MALAT1, a long non-coding RNA (lncRNA) that is overexpressed during PCa progression. GST pull-down and RIP assays demonstrated that the 3' end of MALAT1 interacts with the N-terminal of EZH2. Together, these data indicate that MALAT1 may be a crucial RNA cofactor of EZH2 and that the EZH2-MALAT1 association may provide a new avenue for development new strategies for treatment of CRPC.	26516927	RID01284	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Liver cancer	UCA1	TERT	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000164362	NA	652995	7015	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	CUDR promotes liver cancer stem cell growth through upregulating TERT and C-Myc.Therefore, CUDR-CCND1 complex loads onto the long noncoding RNA H19 promoter region that may lead to reduce the DNA methylation on H19 promoter region and then to enhance the H19 expression. Strikingly, the overexpression of H19 increases the binding of TERT to TERC and reduces the interplay between TERT with TERRA, thus enhancing the cell telomerase activity and extending the telomere length. On the other hand, insulator CTCF recruits the CUDR-CCND1 complx to form the composite CUDR-CCND1-insulator CTCF complex which occupancied on the C-myc gene promoter region, increasing the outcome of oncogene C-myc. Ultimately, excessive TERT and C-myc lead to liver cancer stem cell and hepatocyte-like stem cell malignant proliferation.	26513297	RID01285	expression association	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Liver cancer	UCA1	MYC	positively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000136997	NA	652995	4609	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MRTL|MYCC|bHLHe39|c-Myc	CUDR promotes liver cancer stem cell growth through upregulating TERT and C-Myc.Therefore, CUDR-CCND1 complex loads onto the long noncoding RNA H19 promoter region that may lead to reduce the DNA methylation on H19 promoter region and then to enhance the H19 expression. Strikingly, the overexpression of H19 increases the binding of TERT to TERC and reduces the interplay between TERT with TERRA, thus enhancing the cell telomerase activity and extending the telomere length. On the other hand, insulator CTCF recruits the CUDR-CCND1 complx to form the composite CUDR-CCND1-insulator CTCF complex which occupancied on the C-myc gene promoter region, increasing the outcome of oncogene C-myc. Ultimately, excessive TERT and C-myc lead to liver cancer stem cell and hepatocyte-like stem cell malignant proliferation.	26513297	RID01286	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Liver fibrosis	GAS5	CDKN1B	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-222)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000111276	NA	60674	1027	NCRNA00030|SNHG2	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA.We identified GAS5 as a target of microRNA-222 (miR-222) and showed that miR-222 could inhibit the expression of GAS5. Interestingly, GAS5 could also repress miR-222 expression. A pulldown assay further validated that GAS5 could directly bind to miR-222. As a competing endogenous RNAs, GAS5 had no effect on primary miR-222 expression. In addition, GAS5 was mainly localized in the cytoplasm. Quantitative RT-PCR further demonstrated that the copy numbers of GAS5 per cell are higher than those of miR-222. GAS5 increased the level of p27 protein by functioning as a competing endogenous RNA for miR-222, thereby inhibiting the activation and proliferation of HSCs.	26446789	RID01287	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	TINCR	KLF2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000127528	NA	257000	10365	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	LKLF	SP1-induced upregulation of the long noncoding RNA TINCR regulates cell proliferation and apoptosis by affecting KLF2 mRNA stability in gastric cancer.Mechanistic analyses indicated that TINCR could bind to STAU1 (staufen1) protein, and influence KLF2 mRNA stability and expression, then KLF2 regulated cyclin-dependent kinase genes CDKN1A/P21 and CDKN2B/P15 transcription and expression, thereby affecting the proliferation and apoptosis of GC cells.	25728677	RID01288	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MEG3	E2F3	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-141)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000112242	NA	55384	1871	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	E2F-3	MiR-141 Inhibits Gastric Cancer Proliferation by Interacting with Long Noncoding RNA MEG3 and Down-Regulating E2F3 Expression.These findings together suggested that miR-141 could be interacting with MEG3 and targeting E2F3, and these factors may play important anti-tumor effects in GC pathogenesis and provide therapeutic targets in the clinics.	26233544	RID01289	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	miR-1	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1.MiR-1 functioned as a tumor suppressor by targeting K-RAS and MALAT1.	26275461	RID01290	ceRNA or sponge	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Chronic heart failure	LSINCT5	CASP1	positively-E	RNAi;qRT-PCR;western blot	upregulation	qPCR;microarray	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000137752	NA	101234261	834	NA	ICE|IL1BC|P45	Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1beta signaling pathway.The results of the present study indicated that LSINCT5 silencing by small interfering RNA inhibits caspase-1/IL-1beta signaling, and suppresses apoptosis in BNP-treated HCM cells. Therefore, high expression levels of BNP promote the apoptosis of myocardial cells through the lncRNA LSINCT5 mediator, which activates the caspase-1/IL-1beta signaling pathway.	26323562	RID01291	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Chronic heart failure	LSINCT5	IL1B	positively-E	RNAi;qRT-PCR;western blot	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000125538	NA	101234261	3553	NA	IL-1|IL1-BETA|IL1F2	Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1beta signaling pathway.The results of the present study indicated that LSINCT5 silencing by small interfering RNA inhibits caspase-1/IL-1beta signaling, and suppresses apoptosis in BNP-treated HCM cells. Therefore, high expression levels of BNP promote the apoptosis of myocardial cells through the lncRNA LSINCT5 mediator, which activates the caspase-1/IL-1beta signaling pathway.	26323562	RID01292	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	SIRT1-AS	SIRT1	interact	RNA stability assay;ribonuclease protection assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with mRNA;mutation(622U>C)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_10:67916698-67918946	ENSG00000096717	NA	106633813	23411	NA	SIR2|SIR2L1|SIR2alpha	A novel mutation in SIRT1-AS leading to a decreased risk of HCC. SIRT1-AS overexpression promoted the proliferation of the human HCC cell lines by upregulating the SIRT1 protein level. The mechanism was that SIRT1-AS bound to SIRT1 mRNA at 3'UTR, masked the miR-29c binding site and stabilized SIRT1 mRNA. A single-nucleotide mutation (622U>C) in the SIRT1-AS sequence was found when we used gene sequencing as an assistant approach for HCC diagnosis. Bioinformatics and the RNase protection assay revealed that the mutation led to a marked alteration in the secondary structure of SIRT1-AS and caused its inability to bind with SIRT1 mRNA. The results of the present study suggest that the 622C mutant of SIRT1 antisense transcript suppresses HCC cell line proliferation, decreases the risk of HCC and is a potential target for gene therapy.	26324025	RID01293	interact with mRNA	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	HOTAIR	CCNJ	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);mitosis progression(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000107443	NA	100124700	54619	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	bA690P14.1	Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer.Moreover, we have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter.	26469956	RID01294	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	HOTAIR	miR-205	negatively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer.Moreover, we have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter.This study elucidates an important role that miR-205 had in the regulation of proliferation, migration and invasion of bladder cancer cells, suggesting a potential therapeutic target for combating bladder cancer.	26469956	RID01295	epigenetic regulation	NA	NA	NA
Urinary bladder cancer	TUG1	ZEB2	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qPCR;microarray	NA	NA	radioresistance(+);epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000169554	NA	55000	9839	LINC00080|NCRNA00080|TI-227H	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Double-negative feedback loop between long non-coding RNA TUG1 and miR-145 promotes epithelial to mesenchymal transition and radioresistance in human bladder cancer cells.Interestingly, TUG1 decreased the expression of miR-145 and there was a reciprocal repression between TUG1 and miR-145 in an Argonaute2-dependent manner. ZEB2 was identified as a down-stream target of miR-145 and TUG1 exerted its function through the miR-145/ZEB2 axis.	26318860	RID01296	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Colon cancer	FER1L4	miR-106a-5p	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-);tumor-suppressive function(+);prognosis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	C20orf124	NA	Long non-coding RNA Fer-1-like protein 4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer.In addition, significant negative correlation between FER1L4 and miR-106a-5p expression levels was observed. Among the colon cancer cell lines, FER1L4 levels were relatively lower, with concurrent high levels of miR-106a-5p. Our findings indicated that FER1L4 could exert a tumor suppressive impact on colon cancer, which at least, in part, through suppressing miR-106a-5p expression, and depletion of FER1L4, alone or combined with overexpression of miR-106a-5p, is predictive of poor prognosis in colon cancer and may play a crucial role in cancer prevention and treatment.	26224446	RID01297	expression association	prognosis	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	NA
Liver cancer	HOTAIR	SETD2	negatively-E	RIP;ChIP;RT-PCR;western plot;luciferase reporter assay	upregulation	RT-PCR	NA	NA	DNA repair(-);cell growth(+);cell proliferation(+)	transcriptional regulation	regulation	NA	NA	CSC	Genome Instability and Mutation;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181555	NA	100124700	29072	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HBP231|HIF-1|HIP-1|HSPC069|HYPB|KMT3A|LLS|SET2|p231HBP	LncRNA HOTAIR promotes human liver cancer stem cell malignant growth through downregulation of SETD2.Long non-coding RNA HOTAIR predicts negative tumor prognosis and exhibits oncogenic activity. Herein, we demonstrate HOTAIR promotes human liver cancer stem cell malignant growth through downregulation of SETD2. Mechanistically, HOTAIR reduces the recuritment of the CREB, P300, RNA polII onto the SETD2 promoter region that inhibits SETD2 expression and its phosphorylation.	26172293	RID01298	transcriptional regulation	prognosis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	TUG1	KLF2	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000127528	NA	55000	10365	LINC00080|NCRNA00080|TI-227H	LKLF	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.	26336870	RID01299	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	UCA1	miR-143	negatively-F	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143.There are direct interactions between miR-143 and the miRNA recognition sites of UCA1. UCA1 is present in Ago2-containing RNA-induced silencing complex (RISC), through association with miR-143. Through downregulating miR-143, UCA1 can modulate breast cancer cell growth and apoptosis.	26439035	RID01300	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	NA
Gastric cancer	MEG3	BCL2	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-181)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Bcl-2|PPP1R50	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate gastric cancer progression.MEG3 is decreased in GC patients and cell lines, and its expression was associated with metastatic GC. Furthermore, MEG3 could up-regulated Bcl-2 via its competing endogenous RNA (ceRNA) activity on miR-181a.	26253106	RID01301	ceRNA or sponge	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	PCA3	PRUNE2	interact	RNase-resistant assay;RNA-FISH	NA	NA	NA	NA	tumor-suppressive function(+);RNA editing(+)	RNA editing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000106772	NA	50652	158471	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	BMCC1|BNIPXL|C9orf65|KIAA0367	PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing.	26080435	RID01302	interact with mRNA	NA	NA	UP(LIHC);DOWN(NSCLC);DATA(GSE117623,GSE74639)
Cervical cancer	HOTAIR	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	radioresistance(+);cell proliferation(+);apoptosis process(-);cell migration(+);cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HOTAIR enhanced aggressive biological behaviors and induced radioresistance via inhibiting p21 in cervical cancer.Moreover, a high level of HOTAIR was notably associated with radioresistance and downregulation of p21 in the primary cultured cervical cancer cells. Further, we demonstrated that elevated HOTAIR could induce radio-resistance via inhibiting p21 in HeLa cells, while knockdown of HOTAIR upregulated p21 and consequentially increased the radiosensitivity of C33A cells.	25547435	RID01303	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	WSPAR	TCF7	positively-E	RNA pull-down assay;mass spectrometry;ChIP	upregulation	qPCR;microarray;northern blot	GSE66515;GSE66529	GSE66515.zip;GSE66529.zip	self-renewal(+);WNT signaling pathway(+)	epigenetic regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000081059	NA	105664404	6932	LncTCF7|TCONS_00009511	TCF-1	The long noncoding RNA lncTCF7 promotes self-renewal of human liver cancer stem cells through activation of Wnt signaling. Mechanistically, lncTCF7 recruits the SWI/SNF complex to the promoter of TCF7 to regulate its expression, leading to activation of Wnt signaling. Our data suggest that lncTCF7-mediated Wnt signaling primes liver CSC self-renewal and tumor propagation.	25842979	RID01304	epigenetic regulation	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Chronic myeloid leukemia	BGLT3	PTEN	positively-E	luciferase reporter assay	NA	NA	NA	NA	tumor-suppressive function(+)	ceRNA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000260629	GRCh38_11:5244554-5245546	ENSG00000171862	NA	103344929	5728	BGL3|LINC01083|lncRNA-BGL3	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	A long noncoding RNA critically regulates Bcr-Abl-mediated cellular transformation by acting as a competitive endogenous RNA.Further experiments demonstrated that lncRNA-BGL3 functioned as a competitive endogenous RNA for binding these microRNAs to cross-regulate PTEN expression. Taken together, these results reveal that Bcr-Abl-mediated cellular transformation critically requires silence of tumor-suppressor lncRNA-BGL3 and suggest a potential strategy for the treatment of Bcr-Abl-positive leukemia.	24837367	RID01305	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Glioblastoma	XIST	miR-152	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152.Further, there was reciprocal repression between XIST and miR-152. Mechanistic investigations defined the direct binding ability of the predicted miR-152 binding site on the XIST. In addition, XIST and miR-152 are probably in the same RNA induced silencing complex (RISC). Finally, miR-152 mediated the tumor-suppressive effects that knockdown of XIST exerted.	25578780	RID01306	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Renal cell carcinoma	MALAT1	EZH2	interact	RIP;western blot;qPCR	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2 and Interacts with miR-205.We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas beta-catenin expression was decreased through Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	25600645	RID01307	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Renal cell carcinoma	MALAT1	miR-205	negatively-F	luciferase reporter assay;RIP;ChIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2 and Interacts with miR-205.We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas beta-catenin expression was decreased through Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	25600645	RID01308	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Non-small cell lung cancer	PANDAR	BCL2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-);prognosis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000171791	NA	101154753	596	PANDA	Bcl-2|PPP1R50	Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2.We also showed that PANDAR-mediated growth regulation is in part due to the transcriptional modulation of Bcl-2 by interacting with NF-YA, thus affecting NSCLC cell apoptosis. The p53/PANDAR/NF-YA/Bcl-2 interaction might serve as targets for NSCLC diagnosis and therapy.	25719249	RID01309	expression association	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Atherosclerosis	RP5-833A20.1	miR-382-5p	positively-E	RNAi	upregulation	microarray	NA	NA	cholesterol homeostasis(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000237853	GRCh38_1:61248945-61253510	NA	NA	NA	NA	NA	NA	RP5-833A20.1/miR-382-5p/NFIA-dependent signal transduction pathway contributes to the regulation of cholesterol homeostasis and inflammatory reaction. Moreover, we showed that long noncoding RNA RP5-833A20.1 may decreases NFIA expression by inducing hsa-miR-382-5p expression in vitro.	25265644	RID01310	expression association	NA	NA	NA
Atherosclerosis	RP5-833A20.1	NFIA	negatively-E	RNAi	upregulation	microarray	NA	NA	cholesterol homeostasis(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000237853	GRCh38_1:61248945-61253510	ENSG00000162599	NA	NA	4774	NA	BRMUTD|CTF|NF-I/A|NF1-A|NFI-A|NFI-L	RP5-833A20.1/miR-382-5p/NFIA-dependent signal transduction pathway contributes to the regulation of cholesterol homeostasis and inflammatory reaction. Moreover, we showed that long noncoding RNA RP5-833A20.1 may decreases NFIA expression by inducing hsa-miR-382-5p expression in vitro.	25265644	RID01311	expression association	NA	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Osteoarthritis	MEG3	VEGFA	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	angiogenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000112715	NA	55384	7422	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MVCD1|VEGF|VPF	The Long Noncoding RNA MEG3 Is Downregulated and Inversely Associated with VEGF Levels in Osteoarthritis.The results show that human MEG3 is significantly downregulated in OA patients compared to normal cartilage samples. However, higher levels of VEGF mRNA and protein are found in OA compared to the control. Moreover, MEG3 levels are inversely associated with VEGF levels, suggesting that MEG3 may be involved in OA development through the regulation of angiogenesis.	26090403	RID01312	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Tongue squamous cell carcinoma	miR-26a	MEG3	negatively-E	RNAi;Methylation-specific PCR	downregulation	microarray	GSE51829;GSE51700	GSE51829.zip;GSE51700.zip	cell proliferation(-);cell cycle(-);apoptosis process(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma.Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR-26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue.Considering the poor prognostic outcomes associated with reduced miR-26a and MEG3, our findings imply that these factors likely play important antitumor effects in TSCC pathogenesis.Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma. We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR-26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue. Furthermore, the overexpression of miR-26a or MEG3 in SCC-15 and CAL27 cells inhibited cell proliferation and cell cycle progression, and promoted cell apoptosis.It could therefore be of interest to investigate a possible link between miR-148a and MEG3 expression in ovarian cancer. In addition, miR-26a and MEG3 expression were correlated in TSCC (Tongue Squamous Cell Carcinoma) cells and it has been postulated that this relationship depends on the ability of miR-26a to target DNMT3B in this model and thus prevent meg3 promoter methylation	25537514;24343426	RID01313	epigenetic regulation	prognosis	NA	NA
Liver fibrosis	MEG3	TP53	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell growth(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Gastrointestinal system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Inhibitory effects of long noncoding RNA MEG3 on hepatic stellate cells activation and liver fibrogenesis. Enforced expression of MEG3 in LX-2 cells inhibited TGF-beta1-induced cell proliferation, while promoting cell apoptosis. More importantly, overexpression of MEG3 could activate p53 and mediate cytochrome c release, subsequently leading to caspase-3-dependent apoptosis in TGF-beta1-treated LX-2 cells.	25201080	RID01314	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	VLDLR-AS1	ABCG2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell viability(+);cell cycle(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236404	GRCh38_9:2421597-2643359	ENSG00000118777	NA	401491	9429	linc-VLDLR|lincRNA-VLDLR	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	Involvement of extracellular vesicle long noncoding RNA (linc-VLDLR) in tumor cell responses to chemotherapy.RNAi-mediated knockdown of linc-VLDLR decreased cell viability and abrogated cell-cycle progression. Moreover, knockdown of linc-VLDLR reduced expression of ABCG2 (ATP-binding cassette, subfamily G member 2), whereas overexpression of this protein reduced the effects of VLDLR knockdown on sorafenib-induced cell death.	24874432	RID01315	expression association	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(PAAD);DATA(GSE40174)
Prostate cancer	PCGEM1	miR-145	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells.To test this hypothesis, the interaction between PCGEM1 and miR-145 was examined using a luciferase reporter assay.We demonstrate a reciprocal negative control relationship between PCGEM1 and miR-145 that regulates both LNCaP cell proliferation and nu/nu PCa tumor growth.	25200485	RID01316	ceRNA or sponge	NA	UP(PAAD);DATA(GSE60407)	NA
Non-small cell lung cancer	MALAT1	BCL2	positively-E	RNAi	downregulation	microarray	NA	NA	prognosis(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	Prognostic impact of Bcl-2 depends on tumor histology and expression of MALAT-1 lncRNA in non-small-cell lung cancer.Among the tested apoptotic markers only Bcl-2 demonstrated prognostic impact (hazard ratio = 0.64, p = 0.012). Besides tumor histology, prognostic impact of Bcl-2 was also found to depend on MALAT-1 lncRNA expression. Gene expression analysis of A549 adenocarcinoma cells with differential MALAT-1 lncRNA expression demonstrated an influence on the expression of Bcl-2 and its interacting proteins. We found Bcl-2 expression to depend on MALAT-1 expression status in a positively related manner. i.e., strong MALAT-1 expression results in elevated Bcl-2 expression values (log-fold change = 0.46), confirming the hypothesis of Guo et al.Best transfection rates and strongest downregulation of MALAT-1 lncRNA was achieved in A549 lung cancer cell line.	25036876	RID01317	expression association	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	OIP5-AS1	YAP1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000137693	NA	729082	10413	cyrano|linc-OIP5	COB1|YAP|YAP2|YAP65|YKI	Knockdown of linc-OIP5 inhibits proliferation and migration of glioma cells through down-regulation of YAP-NOTCH signaling pathway.Further mechanistic studies revealed the effect of linc-OIP5 knockdown on glioma cell phenotype at least partially through down-regulation of YAP and inhibition of Notch signaling pathway activity.	28189759	RID01318	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Gastric cancer	HOXA11-AS	CTNNB1	positively-E	ChIP;RIP	upregulation	microarray;sequencing	TCGA;GSE50710;GSE58828;GSE65801;GSE51575;GSE29431;GSE54002;GSE20842;GSE21510;GSE56140;GSE57957;GSE53624;GSE18842;GSE19188;GSE19804;GSE21933;GSE30219;GSE31210;GSE32863;GSE43458	STAD.zip;GSE50710.zip;GSE58828.zip;GSE65801.zip;GSE51575.zip;GSE29431.zip;GSE54002.zip;GSE20842.zip;GSE21510.zip;GSE56140.zip;GSE57957.zip;GSE53624.zip;GSE18842.zip;GSE19188.zip;GSE19804.zip;GSE21933.zip;GSE30219.zip;GSE31210.zip;GSE32863.zip;GSE43458.zip	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000168036	NA	221883	1499	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID01319	epigenetic regulation	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	HOXA11-AS	KLF2	negatively-E	ChIP;RIP	upregulation	microarray;sequencing	TCGA;GSE50710;GSE58828;GSE65801;GSE51575;GSE29431;GSE54002;GSE20842;GSE21510;GSE56140;GSE57957;GSE53624;GSE18842;GSE19188;GSE19804;GSE21933;GSE30219;GSE31210;GSE32863;GSE43458	STAD.zip;GSE50710.zip;GSE58828.zip;GSE65801.zip;GSE51575.zip;GSE29431.zip;GSE54002.zip;GSE20842.zip;GSE21510.zip;GSE56140.zip;GSE57957.zip;GSE53624.zip;GSE18842.zip;GSE19188.zip;GSE19804.zip;GSE21933.zip;GSE30219.zip;GSE31210.zip;GSE32863.zip;GSE43458.zip	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000127528	NA	221883	10365	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	LKLF	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID01320	epigenetic regulation	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	RP11-708H21.4	AKT1	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01321	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	RP11-708H21.4	MTOR	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01322	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	RP11-708H21.4	RPS6KB1	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000108443	NA	NA	6198	NA	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01323	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	LUCAT1	CDKN1A	negatively-E	ChIP;RIP	upregulation	sequencing	TCGA	LUSC_LUAD.zip	cell proliferation(+);cell growth(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000124762	NA	100505994	1026	SCAL1|SCAT5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.	28423699	RID01324	epigenetic regulation	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	LUCAT1	CDKN1C	negatively-E	ChIP;RIP	upregulation	sequencing	TCGA	LUSC_LUAD.zip	cell proliferation(+);cell growth(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000129757	NA	100505994	1028	SCAL1|SCAT5	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.	28423699	RID01325	epigenetic regulation	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Esophagus squamous cell carcinoma	PHBP1	PHB	positively-F	RNase protection assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell growth(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000213091	GRCh38_6:150042546-150043353	ENSG00000167085	NA	5246	5245	NA	HEL-215|HEL-S-54e|PHB1	Pseudogene PHBP1 promotes esophageal squamous cell carcinoma proliferation by increasing its cognate gene PHB expression.we reported that human prohibitin gene pseudogene 1 (PHBP1) was upregulation in ESCC. Mechanisms analysis revealed that PHBP1 transcript as an antisense transcript of PHB is partially complementary to PHB mRNA and formed an RNA-RNA hybrid with PHB, consequently inducing an increase of PHB expression at both the mRNA and protein levels.	28404970	RID01326	interact with mRNA	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	MALAT1	TRAF6	positively-E	RNAi;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-146b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000175104	NA	378938	7189	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MGC:3310|RNF85	Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis.we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b 5p to down-regulate its expression in HCC.TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6.	28404923	RID01327	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	UC.134	LATS1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;microarray	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:158526708-158528574	ENSG00000131023	NA	110599565	9113	NA	WARTS|wts	A novel lncRNA uc.134 represses hepatocellular carcinoma progression by inhibiting CUL4A-mediated ubiquitination of LATS1.The overexpression of uc.134 inhibited HCC cell proliferation, invasion, and metastasis in vitro and in vivo, whereas the knockdown of uc.134 produced the opposite results.we demonstrated that uc.134 inhibits the CUL4A-mediated ubiquitination of LATS1 and increases YAPS127 phosphorylation to silence the target genes of YAP.	28420424	RID01328	expression association	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	UC.134	YAP1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;microarray	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:158526708-158528574	ENSG00000137693	NA	110599565	10413	NA	COB1|YAP|YAP2|YAP65|YKI	A novel lncRNA uc.134 represses hepatocellular carcinoma progression by inhibiting CUL4A-mediated ubiquitination of LATS1.The overexpression of uc.134 inhibited HCC cell proliferation, invasion, and metastasis in vitro and in vivo, whereas the knockdown of uc.134 produced the opposite results.we demonstrated that uc.134 inhibits the CUL4A-mediated ubiquitination of LATS1 and increases YAPS127 phosphorylation to silence the target genes of YAP. The use of this lncRNA may offer a promising treatment approach by inhibiting YAP and activating Hippo kinase signaling.	28420424	RID01329	expression association	metastasis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Prostate cancer	CBR3-AS1	TGFB1	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000105329	NA	100506428	7040	PlncRNA-1|PlncRNA1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01330	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	CBR3-AS1	CDH2	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000170558	NA	100506428	1000	PlncRNA-1|PlncRNA1	CD325|CDHN|CDw325|NCAD	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01331	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Prostate cancer	CBR3-AS1	CCND1	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000110092	NA	100506428	595	PlncRNA-1|PlncRNA1	BCL1|D11S287E|PRAD1|U21B31	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01332	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Prostate cancer	CBR3-AS1	CDH1	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000039068	NA	100506428	999	PlncRNA-1|PlncRNA1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01333	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	tumor-suppressive function(+);cell growth(-);apoptosis process(+)	ceRNA(miR-106b;miR-93)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay. Thus, we revealed a tumor suppressive role of PTENP1 as ceRNA in GC and pinpointed the specific miRNAs decoyed by PTENP1, highlighting the emerging roles of ceRNAs in the biological regulation of GC cells and their possible clinical significance.	28212532	RID01334	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	NKILA	SNAI1	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000124216	NA	105416157	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01335	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	NKILA	NFKB1	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01336	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	NKILA	NFKBIA	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01337	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Breast cancer	CRNDE	CTNNB1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000168036	NA	NA	1499	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01338	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	CRNDE	MYC	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000136997	NA	NA	4609	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01339	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	CRNDE	CCND1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000110092	NA	NA	595	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01340	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	CRNDE	miR-136	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01341	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	NA
Malignant glioma	XIST	RAC1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-137)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136238	NA	7503	5879	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA XIST exerts oncogenic functions in human glioma by targeting miR-137.our data further showed that XIST could up-regulate the expression of miR-137 targeted gene Rac1 through acting as an endogenous sponge of miR-137. In addition, we found that Rac1 inhibition or miR-137 overexpression could suppress glioma cells proliferation induced by XIST overexpression.	28469789	RID01342	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Gastric cancer	HNRNPKP2	CXCR4	negatively-E	RNAi;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227347	GRCh38_2:136199114-136200503	ENSG00000121966	NA	389053	7852	NA	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	DC-SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis.DC-SIGNR promoted gastric cancer liver metastasis mediated with HNRNPKP2 which expression was regulated by STAT5A. And HNRNPKP2 decreased the expression of downstream target gene CXCR4.	28403883	RID01343	expression association	metastasis	UP(SKCM,BRCA);DATA(GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	STAT5A	HNRNPKP2	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000126561	NA	ENSG00000227347	GRCh38_2:136199114-136200503	6776	389053	MGF|STAT5	NA	DC-SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis.DC-SIGNR promoted gastric cancer liver metastasis mediated with HNRNPKP2 which expression was regulated by STAT5A. And HNRNPKP2 decreased the expression of downstream target gene CXCR4.STAT5A promoted HNRNPKP2 expression after knockdown DC-SIGNR.	28403883	RID01344	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(SKCM,BRCA);DATA(GSE38495,GSE109761,GSE111065)
Hepatocellular carcinoma	TP73-AS1	HMGB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000189403	NA	57212	3146	KIAA0495|PDAM	HMG-1|HMG1|HMG3|SBP-1	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation. Knockdown of TP73-AS1 inhibited the HCC proliferation and the expression levels of HMGB1, RAGE and NF-kB in HCC cells.we confirmed that miR-200a could directly bind to TP73-AS1 and the 3'UTR of HMGB1; TP73-AS1 competed with HMGB1 for miR-200a binding.	28403886	RID01345	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Hepatocellular carcinoma	TP73-AS1	AGER	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000204305	NA	57212	177	KIAA0495|PDAM	NA	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation. Knockdown of TP73-AS1 inhibited the HCC proliferation and the expression levels of HMGB1, RAGE and NF-kB in HCC cells.we confirmed that miR-200a could directly bind to TP73-AS1 and the 3'UTR of HMGB1; TP73-AS1 competed with HMGB1 for miR-200a binding.	28403886	RID01346	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Lung cancer	PRAL	TP53	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000279296	GRCh38_17:6772831-6776116	ENSG00000141510	NA	109245082	7157	lncRNA-PRAL	BCC7|BMFS5|LFS1|P53|TRP53	P53 Regulation-Association Long Non-Coding RNA (LncRNA PRAL) Inhibits Cell Proliferation by Regulation of P53 in Human Lung Cancer.Overexpression of PRAL inhibited cell proliferation by upregulating the expression of P53.	28396580	RID01347	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	XIST	PTEN	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-181a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171862	NA	7503	5728	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression.The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects.MiR-181a can promote HCC metastasis by targeting PTEN, which is regulated by lncRNA XIST.	28388883	RID01348	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Endometrial cancer	LINC00672	LASP1	negatively-E	RNAi;western blot;immunofluorescence assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000263874	GRCh38_17:38925168-38929384	ENSG00000002834	NA	100505576	3927	NA	Lasp-1|MLN50	Long non-coding RNA LINC00672 contributes to p53 protein-mediated gene suppression and promotes endometrial cancer chemosensitivity. Here, we report that a lincRNA, LINC00672, which possesses an ultra-conserved region, is aberrantly down-regulated during the development of EC. LINC00672 overexpression could lower the levels of LASP1 and slow the development of malignant phenotypes of EC both in vitro and in vivo Moreover, LINC00672 significantly increased the 50% inhibitory concentration of paclitaxel in EC cells and increased the sensitivity of xenograft mice to paclitaxel. These findings indicate that LINC00672 can influence LASP1 expression as a locus-restricted cofactor for p53-mediated gene suppression, thus impacting EC malignancies and chemosensitivity to paclitaxel.	28232485	RID01349	expression association	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	CCAT1	SPRY4	negatively-E	ChIP;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000187678	NA	100507056	81848	CARLO5|CARLo-5|onco-lncRNA-40	HH17	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.	27956498	RID01350	epigenetic regulation	NA	NA	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065)
Esophagus squamous cell carcinoma	CCAT1	HOXB13	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000159184	NA	100507056	10481	CARLO5|CARLo-5|onco-lncRNA-40	HPC9|PSGD	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.CCAT1 regulates HOXB13 as a molecular decoy for miR-7, a microRNA that targets both CCAT1 and HOXB13, thus facilitating cell growth and migration. Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.	27956498	RID01351	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	LNCSRLR	IL6	positively-E	ChIP	upregulation	microarray	GSE87121	GSE87121.zip	sorafenib tolerance(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000240032	GRCh38_3:146066344-146069185	ENSG00000136244	NA	109729161	3569	lncRNA-SRLR	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long noncoding RNA-SRLR elicits intrinsic sorafenib resistance via evoking IL-6/STAT3 axis in renal cell carcinoma.Herein, we identified a long non-coding RNA referred to as lncRNA-SRLR (sorafenib resistance-associated lncRNA in RCC) that is upregulation in intrinsically sorafenib-resistant RCCs. lncRNA-SRLR directly binds to NF-kB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance.	27841868	RID01352	expression association	NA	NA	DOWN(BRCA);DATA(GSE75367,GSE86978)
Renal cell carcinoma	LNCSRLR	STAT3	positively-E	RNAi;western blot	upregulation	microarray	GSE87121	GSE87121.zip	sorafenib tolerance(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Kidney cancer	lncRNA	TF	ENSG00000240032	GRCh38_3:146066344-146069185	ENSG00000168610	NA	109729161	6774	lncRNA-SRLR	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA-SRLR elicits intrinsic sorafenib resistance via evoking IL-6/STAT3 axis in renal cell carcinoma.Herein, we identified a long non-coding RNA referred to as lncRNA-SRLR (sorafenib resistance-associated lncRNA in RCC) that is upregulation in intrinsically sorafenib-resistant RCCs. lncRNA-SRLR directly binds to NF-kB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance.	27841868	RID01353	expression association	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Liver cancer	GASAL1	E2F1	negatively-E	RNAi	downregulation	NA	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000101412	NA	401472	1869	NA	E2F-1|RBAP1|RBBP3|RBP3	A novel lncRNA, GASL1, inhibits cell proliferation and restricts E2F1 activity. GASL1 silencing enhanced cell proliferation, while, conversely, its ectopic expression inhibited proliferation. Knockdown of GASL1 also enhanced E2F1-induced apoptosis, suggesting the existence of an E2F/GASL1 negative feedback loop.low levels of GASL1 are associated with decreased survival of liver cancer patients.	28423601	RID01354	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	lncRNA-BCAT1	CCND1	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_12:24810022-24949459	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01355	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	lncRNA-BCAT1	MYC	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_12:24810022-24949459	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01356	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	lncRNA-BCAT1	MMP2	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_12:24810022-24949459	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01357	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Colorectal cancer	lncRNA-BCAT1	CTNNB1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE18560;GSE44097	GSE18560.zip;GSE44097.zip	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_12:24810022-24949459	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.We focused on AK091631, a novel lncRNA, which we named lncRNA-beta-catenin associated transcript 1 (LncRNA-BCAT1). lncRNA-BCAT1 expression was decreased in CRC tissues, and was negatively associated with beta-catenin in both CRC tissues and cell lines.These results suggest that lncRNA-BCAT1 overexpression inhibits CRC cell growth and invasion via Wnt/beta-catenin pathway blockade, and that lncRNA-BCAT1 is repressed by Wnt/beta-catenin signaling.	28416735	RID01358	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Glioblastoma	MALAT1	TYMS	positively-E	RNAi;luciferase reporter assay	downregulation	sequencing;qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-203)	regulation	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000176890	NA	378938	7298	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HST422|TMS|TS	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. MALAT1 is down-regulated in GBM patients showing response to TMZ treatment by RT-qPCR. The gain and loss-function experiments revealed that miR-203 was down-regulated by MALAT1 and this interaction has reciprocal effects. Besides, thymidylate synthase (TS) mRNA was identified as a direct target of miR-203. LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression.	28187000	RID01359	ceRNA or sponge	chemoresistance,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(SKCM);DATA(GSE38495)
Urinary bladder cancer	TUG1	HMGB1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);radiosensitivity(-)	NA	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000189403	NA	55000	3146	LINC00080|NCRNA00080|TI-227H	HMG-1|HMG1|HMG3|SBP-1	Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression. The expression level of TUG1 and HMGB1 mRNA and protein was about twice higher in bladder cancer tissues than that in adjacent normal tissues. LncRNA TUG1 knockdown enhances radiosensitivity of bladder cancer by suppressing HMGB1 expression. TUG1 acts as a potential regulator of radioresistance of bladder cancer, and it may represent a promising therapeutic target for bladder cancer patients.	28376901	RID01360	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Osteosarcoma	AK093407	STAT3	positively-F	RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	NA	GRCh38_8:125613468-125614465	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long non-coding RNA AK093407 promotes proliferation and inhibits apoptosis of human osteosarcoma cells via STAT3 activation.we showed that AK093407 interacted with STAT3, and promoted its phosphorylation. Lastly, we showed that STAT3 activation was essential for the effects of AK093407 on cell proliferation and apoptosis as the overexpression of AK093407 in the presence of STAT3 inhibitor did not promote cell proliferation and inhibit cell apoptosis.	28469961	RID01361	interact with protein	NA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Breast cancer	SNHG16	E2F5	positively-E	qRT-PCR;RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+)	ceRNA(miR-98)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000133740	NA	100507246	1875	Nbla10727|Nbla12061|ncRAN	E2F-5	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.We predicted SNHG16 as a competitive endogenous RNA (ceRNA) of E2F transcription factor 5 protein (E2F5) via competition for the shared miR-98 through bioinformatics analysis, and proved this regulation using relative quantitative real-time PCR (qRT-PCR).we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues.	28232182	RID01362	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Malignant glioma	PSMD6-AS1	MDM2	interact	RNAi;luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243410	GRCh38_3:64011964-64016246	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	Long non-coding RNA ENST00462717 suppresses the proliferation, survival, and migration by inhibiting MDM2/MAPK pathway in glioma.we identified MDM2 as a direct target of lnc00462717 and lnc00462717 played a role by partially regulating the MDM2/MAPK pathway. Bioinformatics analysis revealed that ENST00462717 is located on chromosome 12 upstream of the MDM2 promoter region and the lnc00462717 and MDM2 are transcribed from the same DNA strand in UCSC genome database.	28189682	RID01363	transcriptional regulation	NA	UP(SKCM);DOWN(BRCA);DATA(GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Tongue cancer	lnc-Sox5	ELAVL1	positively-F	RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);tumor growth(+);apoptosis process(-);cell cycle(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000115934	GRCh38_12:23181334-23251499	ENSG00000066044	NA	NA	1994	NA	ELAV1|HUR|Hua|MelG	HuR Stabilizes lnc-Sox5 mRNA to Promote Tongue Carcinogenesis. RNA immunoprecipitation suggested that HuR directly bound to and stabilized lnc-Sox5 RNA. Consistently, HuR knockdown reduced the level of lnc-Sox5 in Tca8113 cells.Both lnc-Sox5 knockdown and HuR knockdown suppressed Tca8113 cell tumorigenesis in xenograft models.	28371600	RID01364	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	PVT1	HIF1A	positively-E	luciferase reporter assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-186)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000100644	NA	5820	3091	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer.Further functional experiments indicated up-regulation of PVT1 promoted the GC cell proliferation and invasion, while down-regulation of PVT1 inhibited cell proliferation and invasion. In addition, PVT1 could directly interact with miR-186 in GC cells and this interaction lead to the inhibition of downstream of HIF-1alpha expression.Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	28122299	RID01365	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	UCA1	CASP3	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-);cell proliferation(+)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000164305	NA	652995	836	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CPP32|CPP32B|SCA-1	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01366	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Cervical cancer	UCA1	CDK2	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000123374	NA	652995	1017	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN2|p33(CDK2)	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01367	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	UCA1	CDKN1A	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01368	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	LINC-ROR	TP53	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000141510	NA	100885779	7157	ROR|lincRNA-RoR|lincRNA-ST8SIA3	BCC7|BMFS5|LFS1|P53|TRP53	The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway. We discovered that lincRNA-ROR was upregulation in CRC cell lines and tissue samples. LincRNA-ROR decreases sensitivity to radiotherapy via the negative regulation of p53/miR-145 and may represent a potential target for the treatment of CRC.Long Non-Coding RNA Reprogramming (ROR) Promotes Cell Proliferation in Colorectal Cancer via Affecting P53. The expression level of lncRNA-ROR was elevated in CRC tissues when compared to adjacent tissues (n=78). Protein levels of p53 and p53 target genes were affected by lncRNA-ROR in vitro, and downregulation of lncRNA-ROR impeded tumorigenesis in vivo. Our study demonstrates that lncRNA-ROR participates in controlling CRC proliferation, viability, and apoptosis, partially by modulating p53, which provides potential and prospective therapeutic targets for CRC.	27696511;28216611	RID01369	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Colorectal cancer	LINC-ROR	miR-145	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	radioresistance(+);cell proliferation(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway.LincRNA-ROR decreases sensitivity to radiotherapy via the negative regulation of p53/miR-145 and may represent a potential target for the treatment of CRC.	27696511	RID01370	expression association	NA	UP(LIHC);DATA(GSE117623)	NA
Prostate cancer	LINC01116	GAPDH	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000111640	NA	375295	2597	TALNEC2	G3PD|GAPD|HEL-S-162eP	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01371	expression association	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Prostate cancer	LINC01116	MAP1LC3B2	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000258102	NA	375295	643246	TALNEC2	ATG8G	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01372	expression association	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,BRCA);UP(PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE55807,GSE86978)
Prostate cancer	LINC01116	H2AFY	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000113648	NA	375295	9555	TALNEC2	H2A.y|H2A/y|H2AF12M|MACROH2A1.1|mH2A1|macroH2A1.2	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01373	expression association	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	FTX	MTDH	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000147649	NA	100302692	92140	LINC00182|MIR374AHG|NCRNA00182	3D3|AEG-1|AEG1|LYRIC|LYRIC/3D3	Long noncoding RNA FTX is upregulation in gliomas and promotes proliferation and invasion of glioma cells by negatively regulating miR-342-3p.FTX directly inhibited the expression of miR-342-3p, which subsequently regulates the expression of AEG-1. miR-342-3p Directly Targeted AEG-1. Collectively, FTX is critical for proliferation and invasion of glioma cells by regulating miR-342-3p and AEG-1.	28112756	RID01374	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Colorectal cancer	MALAT1	CDH1	negatively-E	qRT-PCR;RNAi;western blot;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2.MALAT1 is overexpressed in colorectal cancer patients and correlated with tumor metastasis. LncRNA MALAT1 knockdown enhances E-cadherin expression and inhibits oxaliplatin-induced EMT in colorectal cancer cells. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin.	28069878	RID01375	epigenetic regulation	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Non-small cell lung cancer	HAGLR	CDKN1A	positively-E	RNAi;western blot	upregulation	qRT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000124762	NA	401022	1026	HOXD-AS1|MIR7704HG|Mdgt	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Increased HAGLR expression promotes non-small cell lung cancer proliferation and invasion via enhanced de novo lipogenesis. Furthermore, the expression levels of p21 and matrix metallopeptidase-9 (MMP-9) were dysregulated when HAGLR expression was suppressed.	28443464	RID01376	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	PVT1	MYC	positively-E	RNAi;qRT-PCR	upregulation	qRT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	The expression pattern of long non-coding RNA PVT1 in tumor tissues and in extracellular vesicles of colorectal cancer correlates with cancer progression.The results also showed that by down-regulating the PVT1 expression, the c-Myc expression was suppressed, the cell proliferation was inhibited, and cell apoptosis was increased. Taken together, these findings implicated that PVT1 may be a new oncogene co-amplified with c-Myc in colorectal cancer tissues and extracellular vesicles and functionally correlated with the proliferation and apoptosis of colorectal cancer cells.Taken together, these findings implicated that PVT1 may be a new oncogene co-amplified with c-Myc in colorectal cancer tissues and extracellular vesicles and functionally correlated with the proliferation and apoptosis of colorectal cancer cells.	28381186	RID01377	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Malignant glioma	KCNQ1OT1	CCNE2	positively-E	RNAi;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor-suppressive function(-)	ceRNA(miR-370)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000175305	NA	10984	9134	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CYCE2	Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells' Malignancy by Activating miR-370/CCNE2 Axis.Knockdown of KCNQ1OT1 decreased the expression level of Cyclin E2 (CCNE2) by binding to miR-370. Further, miR-370 bound to CCNE2 3'UTR region and decreased the expression of CCNE2. These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.	28381990	RID01378	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Anaplastic large cell lymphoma	LINC01013	SNAI1	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lymphoma	lncRNA	TF	ENSG00000228495	GRCh38_6:132131888-132169374	ENSG00000124216	NA	100507254	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma. LINC01013 induced snail, resulting in activation of fibronectin and enhanced ALCL cell invasion.	28331184	RID01379	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Nasopharynx carcinoma	LOC100129148	KLF12	positively-E	RNAi;qRT-PCR;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	ceRNA(miR-539-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	NA	GRCh38_7:139417462-139427526	ENSG00000118922	NA	100129148	11278	NA	AP-2rep|AP2REP|HSPC122	Long non-coding RNA LOC100129148 functions as an oncogene in human nasopharyngeal carcinoma by targeting miR-539-5p.Over-expressed LOC100129148 favored, but silenced LOC100129148 hampered cell proliferation in NPC cells. Additionally, LOC100129148 enhanced the KLF12 expression through functioning as a competitive 'sponge' for miR-539-5p.	28328537	RID01380	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Osteosarcoma	MALAT1	HMGB1	positively-E	RNAi;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-142-3p;miR-129-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.By using online tools, we screen out 2 candidate miRNAs, miR-142-3p and miR-129-5p which may be associated with both MALAT1 and HMGB1. Luciferase reporter assay revealed a direct interaction between the 2 miRNAs and MALAT1, respectively, via a putative binding site within MALAT1. Meanwhile,both the 2 miRNAs could bind to HMGB1 3'-untranslated region (3'-UTR) and regulate HMGB1 expression. Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis.	28346809	RID01381	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Hepatocellular carcinoma	RB1-DT	RB1	negatively-E	RIP;RNA pull-down assay;5-aza-2'-deoxycytidine treatment;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);tumor growth(+)	DNA methylation	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231473	GRCh38_13:48296162-48303661	ENSG00000139687	NA	100862704	5925	LINC00441|ncRNA-RB1	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.Here we focused on the bidirectional transcripted long noncoding RNA (Linc00441) with neighbor gene RB1 to investigate whether Linc00441 is involved in the suppression of RB1 in HCC. We found that aberrant upregulation intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement.	28300839	RID01382	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	LINC00092	PFKFB2	interact	RNAi;RNA pull-down assay;western blot	upregulation	microarray	GSE82059	GSE82059.zip	cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225194	GRCh38_9:96019724-96027993	ENSG00000123836	NA	100188953	5208	NCRNA00092	PFK-2/FBPase-2	Long Noncoding RNA LINC00092 Acts in Cancer-Associated Fibroblasts to Drive Glycolysis and Progression of Ovarian Cancer. CXCL14 is over-expressed in CAFs of metastatic lesion of ovarian cancer and predicts clinical outcome. Mechanistic studies showed that LINC00092 bound a glycolytic enzyme, the fructose-2,6-biphosphatase PFKFB2, thereby promoting metastasis by altering glycolysis and sustaining the local supportive function of CAFs.	28087599	RID01383	interact with protein	metastasis	DOWN(PRAD);DATA(GSE67980)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	UCA1	BCL2	positively-E	RNAi;qRT-PCR	NA	NA	NA	NA	cell viability(+);cell motility(+)	ceRNA(miR-184)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000171791	NA	652995	596	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Bcl-2|PPP1R50	Artesunate suppresses the viability and mobility of prostate cancer cells through UCA1, the sponge of miR-184.Then we determined that the miR-184/Bcl-2 axis might be the downstream signaling pathway of UCA1 upon ART treatment. UCA1 binds to miR-184 through its seed sequences and may function as a sponge for miR-184. Bcl-2, a key anti-apoptotic factor and one of the verified direct targets of miR-184.	28209917	RID01384	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	CASC2	CTNNB1	negatively-E	RNAi;western blot;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);WNT/beta-catenin signaling pathway(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000168036	NA	255082	1499	C10orf5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Down-regulation of lncRNA CASC2 promotes cell proliferation and metastasis of bladder cancer by activation of the Wnt/beta-catenin signaling pathway.	28199978	RID01385	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	SNHG1	SOX9	positively-E	luciferase reporter assay;RNAi	upregulation	sequencing;qRT-PCR	TCGA	LUSC_LUAD.zip	WNT/beta-catenin signaling pathway(+);cancer progression(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000125398	NA	23642	6662	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CMD1|CMPD1|SRA1|SRXX2|SRXY10	upregulation lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/beta-catenin signaling pathway.We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p. In addition, we identified that SOX9 acted as a target of miR-101-3p, and SOX9 played the oncogenic role in NSCLC by activating Wnt/beta-catenin signaling pathway.	28147312	RID01386	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Astrocytoma	CASC2c	miR-101	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Astrocytoma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046821-118210153	NA	NA	NA	NA	NA	NA	CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis. We investigated the role of a new long non-coding RNA CASC2c binding with miR-101. CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1.	28252647	RID01387	ceRNA or sponge	prognosis	NA	NA
Ovarian cancer	MEG3	miR-214	negatively-F	RNAi;luciferase reporter assay	NA	NA	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer.There were at least two binding sites between MEG3 and miR-214. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance.Curcumin can restore MEG3 levels via demethylation. MEG3 upregulation can decrease EVs mediated transfer of miR-214 in ovarian cancer cells, thereby reducing drug resistance.	28175963	RID01388	ceRNA or sponge	chemoresistance	NA	NA
Urinary bladder cancer	SPRY4-IT1	EZH2	positively-E	RNAi;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2. human EZH2 3'UTR fragment containing putative binding sites for miR-101-3p reporter vector and the EZH2 promoter reporter vector were adopted forDual-luciferase Reporter Assays.	27998761	RID01389	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MALAT1	SRSF1	positively-E	RNAi;western blot;qRT-PCR	upregulation	sequencing	NA	NA	cancer progression(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136450	NA	378938	6426	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASF|SF2|SF2p33|SFRS1|SRp30a	Long Noncoding RNA MALAT1 Promotes Hepatocellular Carcinoma Development by SRSF1 Upregulation and mTOR Activation. Here we report that the lncRNA MALAT1 is upregulation in hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induction of the oncogenic splicing factor SRSF1. Our results reveal a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulation.	27993818	RID01390	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	NEAT1	CTNNB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168036	NA	283131	1499	LINC00084|NCRNA00084|TncRNA|VINC	CTNNB|EVR7|MRD19|NEDSDV|armadillo	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed.lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01391	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	NEAT1	CDH2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000170558	NA	283131	1000	LINC00084|NCRNA00084|TncRNA|VINC	CD325|CDHN|CDw325|NCAD	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed.lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01392	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Breast cancer	NEAT1	CDH1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000039068	NA	283131	999	LINC00084|NCRNA00084|TncRNA|VINC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed. lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01393	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	SNHG5	KLF4	positively-E	RNAi;qRT-PCR;luciferase reporter assay;immunohistochemical assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-32)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000136826	NA	387066	9314	C6orf160|LINC00044|NCRNA00044|U50HG	EZF|GKLF	The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.it was reported that Kruppel-like factor 4 (KLF4) is a target gene of miR-32. In agreement with SNHG5 being a decoy for miR-32, we showed that KLF4 suppression by miR-32 could be partially rescued by SNHG5 overexpression, whereas miR-32 mimic rescued SNHG5 overexpression-mediated suppression of GC cell migration.	27871067	RID01394	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Colon cancer	H19	VDR	positively-E	RNAi;luciferase reporter assay;western blot	NA	NA	NA	NA	chemoresistance(+)	ceRNA(miR-675-5p)	regulation	NA	1,25(OH)2D3	CSC	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111424	NA	283120	7421	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NR1I1|PPP1R163	H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells. H19, on the other hand, was able to inhibit the expression of VDR through microRNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo.A potential binding site of miR-675-5p was identified in the 3'UTR of VDR mRNA utilizing the online prediction system Targetscan.	28189050	RID01395	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE75367)
Malignant glioma	PVT1	ATG7	positively-E	RNAi;western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration;angiogenesis(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000197548	NA	5820	10533	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	APG7-LIKE|APG7L|GSA7	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186.The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.MiR-186 binds to the 3' untranslated regions of Atg7 and Beclin1.	28351322	RID01396	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Malignant glioma	PVT1	BECN1	positively-E	RNAi;western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration;angiogenesis(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000126581	NA	5820	8678	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG6|VPS30|beclin1	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186.The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.MiR-186 binds to the 3' untranslated regions of Atg7 and Beclin1.	28351322	RID01397	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Epithelial ovarian cancer	RP11-190D6.2	WWOX	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_16:78237362-78241218	ENSG00000186153	NA	NA	51741	NA	D16S432E|EIEE28|FOR|FRA16D|HHCMA56|PRO0128|SCAR12|SDR41C1|WOX1	A new tumor suppressor lncRNA RP11-190D6.2 inhibits the proliferation, migration, and invasion of epithelial ovarian cancer cells.We found that RP11-190D6.2 expression was positively correlated with WWOX expression. The WWOX antisense transcript RP11-190D6.2 expression was markedly downregulated in tumor tissues compared with normal tissues.The analyses in EOC implicate that RP11-190D6.2 may play a pivotal role in the regulation of tumor metastasis, suggesting that RP11-190D6.2 may serve as a potential biomarker and therapeutic target for EOC.	28280357	RID01398	expression association	metastasis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842)
Cervical cancer	MALAT1	VIM	positively-E	RNAi;qRT-PCR	upregulation	RT-PCR;qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells.miRNA-143 decreased cell invasion and migration potency, downregulated vimentin and upregulation E-cadherin expression, while MALAT1 had the opposite effects. In conclusion, the low expression of miRNA-143 and high expression of MALAT1 in cervical cancer cells could possibly potentiate cell invasion/migration and alter the levels of vimentin and E-cadherin. Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	28252165;26798987	RID01399	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Cervical cancer	MALAT1	CDH1	negatively-E	RNAi;qRT-PCR	upregulation	RT-PCR;qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells.miRNA-143 decreased cell invasion and migration potency, downregulated vimentin and upregulation E-cadherin expression, while MALAT1 had the opposite effects. In conclusion, the low expression of miRNA-143 and high expression of MALAT1 in cervical cancer cells could possibly potentiate cell invasion/migration and alter the levels of vimentin and E-cadherin. Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	28252165;26798987;27658300	RID01400	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	SNHG6-003	MAP3K7	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-26a;miR-26b)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921690-66925541	ENSG00000135341	NA	NA	6885	NA	NA	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-beta-activated kinase 1 (TAK1). TAK1 was a directtarget of miR-26a/b. Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulation in human cancers, exhibiting a co-expression pattern. Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis. In contrast, SNHG6-003-overexpressing cells were protected from5-fluorouracil toxicity as shown by lower levels of apoptosis,cleaved PARP and cleaved caspase-3 (Figures 2e and f). Thissuggested that SNHG6-003 may boost the resistance of HCC cellsto chemotherapy with 5-fluorouracil	27530352	RID01401	ceRNA or sponge	chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Liposarcoma	PILRLS	TCL1A	interact	RNA pull-down assay;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lipomatous cancer	lncRNA	PCG	NA	GRCh38_5:66563850-66566010	ENSG00000100721	NA	NA	8115	NA	TCL1	A novel long noncoding RNA PILRLS promote proliferation through TCL1A by activing MDM2 in Retroperitoneal liposarcoma.RNA pull-down assay found PILRLS can specific binding with TCL1A which also regulate the expression level of TCL1A. Our work for the first time demonstrated PILRLS can activating the MDM2 by binding with TCL1A which suppress the P53 pathway to promote the unlimited growth of retroperitoneal Liposarcoma cells.	28129655	RID01402	interact with protein	NA	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Liposarcoma	PILRLS	MDM2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lipomatous cancer	lncRNA	PCG	NA	GRCh38_5:66563850-66566010	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	A novel long noncoding RNA PILRLS promote proliferation through TCL1A by activing MDM2 in Retroperitoneal liposarcoma.RNA pull-down assay found PILRLS can specific binding with TCL1A which also regulate the expression level of TCL1A. Our work for the first time demonstrated PILRLS can activating the MDM2 by binding with TCL1A which suppress the P53 pathway to promote the unlimited growth of retroperitoneal Liposarcoma cells.	28129655	RID01403	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	AK058003	SNCG	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	host(miR-15a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_10:86948677-87023220	ENSG00000173267	NA	NA	6623	NA	BCSG1|SR	Long non-coding RNA AK058003, as a precursor of miR-15a, interacts with HuR to inhibit the expression of gamma-synuclein in hepatocellular carcinoma cells.lncRNA-AK058003 can reduce the expression of mRNA stabilizing protein HuR and act as a precursor of miR-15a to suppress gamma-synuclein-mediated cell proliferation and the metastasis of hepatocellular carcinoma.	28035067	RID01404	expression association	metastasis	NA	UP(BRCA);DATA(GSE55807)
Pancreatic cancer	miR-216a	MALAT1	negatively-F	luciferase reporter assay	NA	NA	NA	NA	apoptosis process(-);cell cycle(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression.Based on these findings, we infer that miR-216a induces apoptosis both in the presence and absence of gemcitabine in pancreatic cancer cells by silencing MALAT1 expression.	28034748	RID01405	ceRNA or sponge	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	LINC-ROR	miR-205	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell invasion(+)	NA	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205. In MDA-MB-231 cells, down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	28063065	RID01406	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Breast cancer	LINC-ROR	ZEB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell invasion(+)	NA	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205.down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	28063065	RID01407	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	CCAT2	TGFB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000105329	NA	101805488	7040	LINC00873|NCCP1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01408	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	CCAT2	SMAD2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000175387	NA	101805488	4087	LINC00873|NCCP1	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01409	expression association	metastasis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	CCAT2	SMN1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000172062	NA	101805488	6606	LINC00873|NCCP1	BCD541|GEMIN1|SMA|SMA1|SMA2|SMA3|SMA4|SMA@|SMN|SMNT|T-BCD541|TDRD16A	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01410	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Thyroid carcinoma	NEAT1	miR-214	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214.NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced beta-catenin (a direct target of miRNA-214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA-214, presenting a reciprocal repression correlation.	28000845	RID01411	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Gallbladder cancer	AFAP1-AS1	TWIST1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000122691	NA	84740	7291	AFAP1-AS|AFAP1AS	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01412	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(SKCM);DATA(GSE38495)
Gallbladder cancer	AFAP1-AS1	VIM	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000026025	NA	84740	7431	AFAP1-AS|AFAP1AS	NA	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01413	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gallbladder cancer	AFAP1-AS1	CDH1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000039068	NA	84740	999	AFAP1-AS|AFAP1AS	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01414	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Prostate cancer	PVT1	miR-146a	negatively-E	RNAi;qRT-PCR;5-azacytidine	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter. Our study suggested a regulatory relationship between lncRNA PVT1 and miR-146a during the process of the prostate cancer tumorigenesis. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a.	27794184	RID01415	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Non-small cell lung cancer	LncRNA-HIT	ZEB1	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_7:27195637-27197624	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulation of LncRNA-HIT promotes migration and invasion of non-small cell lung cancer cells by association with ZEB1. LncRNA-HIT (HOXA transcript induced by TGFbeta) was recently identified. LncRNA-HIT functions as a prometastasis oncogene by directly associating with ZEB1 to regulate NSCLC.	27790864	RID01416	interact with protein	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HOTAIR	miR-22	negatively-F	luciferase reporter assay	upregulation	amplicon sequencing	NA	NA	cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Identification of genetic variation in the lncRNA HOTAIR associated with HPV16-related cervical cancer pathogenesis.This genetic variant showed the propensity of a secondary structure alteration and gain of a miR-22 binding site in HOTAIR, which was found to be concordant with miR-22 over-expression in low HOTAIR CaCx cases compared to controls. We found that miR-22 expression negatively correlated with HOTAIR and E7 expression. Reduced luciferase activity of a HOTAIR rs2366152C expression plasmid in C33A cells through miR-22 co-transfection confirmed the ability of miR-22 to specifically target rs2366152C-harbouring HOTAIR lncRNA in CaCx cells, ultimately leading to its down-regulation.Here, we aimed at identifying functionally relevant genetic variants that may be employed to differentiate between clinically distinct CaCx subtypes, i.e., those exhibiting high HOTAIR levels and molecular signatures of metastasis and those lacking such signatures in the presence of low HOTAIR expression levels.	27683269	RID01417	ceRNA or sponge	metastasis	NA	NA
Gallbladder cancer	MALAT1	MCL1	positively-E	luciferase reporter assay;RNA pull-down assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143384	NA	378938	4170	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells. Furthermore, MALAT1 silencing decreased GBC cell proliferation and the S phase cell population and induced apoptosis in vitro. These data demonstrated that the MALAT1/miR-363-3p/MCL-1 regulatory pathway controls the progression of GBC.	27420766	RID01418	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	RP5-833A20.1	NFIA	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);cell cycle(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000237853	GRCh38_1:61248945-61253510	ENSG00000162599	NA	NA	4774	NA	BRMUTD|CTF|NF-I/A|NF1-A|NFI-A|NFI-L	Long non-coding RNA RP5-833A20.1 inhibits proliferation, metastasis and cell cycle progression by suppressing the expression of NFIA in U251 cells.The mRNA and protein levels of NFIA were markedly inhibited by overexpression of RP5-833A20.1 in the U251 cells.	27779670	RID01419	expression association	metastasis	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Lung adenocarcinoma	RMRP	miR-206	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	NA	NA	6023	NA	CHH|NME1|RMRPR|RRP2	NA	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01420	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	NA
Lung adenocarcinoma	RMRP	FMNL2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000157827	NA	6023	114793	CHH|NME1|RMRPR|RRP2	FHOD2	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01421	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	RMRP	KRAS	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000133703	NA	6023	3845	CHH|NME1|RMRPR|RRP2	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01422	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Lung adenocarcinoma	RMRP	SOX9	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000125398	NA	6023	6662	CHH|NME1|RMRPR|RRP2	CMD1|CMPD1|SRA1|SRXX2|SRXY10	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01423	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Osteosarcoma	LINC00161	IFIT2	positively-E	luciferase reporter assay;RIP	NA	NA	NA	NA	chemosensitivity(+);apoptosis process(+)	ceRNA(miR-645)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226935	GRCh38_21:28539318-28540355	ENSG00000119922	NA	118421	3433	C21orf100|Linc-USP16|NCRNA00161	G10P2|GARG-39|IFI-54|IFI-54K|IFI54|IFIT-2|ISG-54 K|ISG-54K|ISG54|P54|cig42	Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. the same sequence-specific binding of miR-645 to LINC00161 or IFIT2 3'UTR	27609068	RID01424	ceRNA or sponge	chemoresistance	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	lncRNA-Unigene56159	SNAI2	negatively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	sequencing;qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-645)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_3:78597238-79767998	ENSG00000019549	NA	NA	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells. We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues.Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug.	27597739	RID01425	ceRNA or sponge	NA	NA	NA
Malignant glioma	CCAT1	miR-410	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1 promotes glioma cell proliferation via inhibiting microRNA-410. Luciferase reporter assay confirmed that CCAT1 targeted miR-410. Correlation analysis showed that CCAT1 expression was negatively related to miR-410 expression in glioma cancer tissues. In addition, down-regulation of miR-410 reversed the inhibitory effect of si-CCAT1 on glioma proliferation. These data demonstrated that lncRNA-CCAT1 promoted glioma cell proliferation via inhibiting miR-410, providing a new insight about the pathogenesis of glioma proliferation.	27765628	RID01426	ceRNA or sponge	NA	NA	NA
Renal cell carcinoma	LNCARSR	YAP1	interact	RNA pull-down assay;RIP;RNA-FISH	upregulation	qRT-PCR	NA	NA	self-renewal(+);tumorigenesis(+);cell metastasis(+)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000137693	NA	112577459	10413	NA	COB1|YAP|YAP2|YAP65|YKI	A feed-forward loop between lncARSR and YAP activity promotes expansion of renal tumour-initiating cells.Knockdown of lncARSR attenuates the self-renewal, tumorigenicity and metastasis of renal T-ICs. Mechanistically,the binding of lncARSR to YAP impedes LATS1-induced YAP phosphorylation and facilitates YAP nuclear translocation.	27886176	RID01427	interact with protein	metastasis	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	linc-cdh4-2	CDH4	positively-F	RNAi;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_20:61252261-61940617	ENSG00000179242	NA	NA	1002	NA	CAD4|R-CAD|RCAD	Long non-coding RNA linc-cdh4-2 inhibits the migration and invasion of HCC cells by targeting R-cadherin pathway.Mechanistically, the linc cdh4-2 could up-regulate the protein level of R-cadherin through direct binding that might improve the protein stability. Over expression of linc-cdh4-2 could significantly increase the protein levels of R-cadherin and decrease the protein levels of small GTPase RAC1. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway.	27765630	RID01428	interact with protein	NA	NA	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	linc-cdh4-2	RAC1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_20:61252261-61940617	ENSG00000136238	NA	NA	5879	NA	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA linc-cdh4-2 inhibits the migration and invasion of HCC cells by targeting R-cadherin pathway.Mechanistically, the linc cdh4-2 could up-regulate the protein level of R-cadherin through direct binding that might improve the protein stability. Over expression of linc-cdh4-2 could significantly increase the protein levels of R-cadherin and decrease the protein levels of small GTPase RAC1. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway.	27765630	RID01429	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Malignant glioma	SNHG18	SEMA5A	negatively-E	RNAi;western blot;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546200-9550609	ENSG00000112902	NA	100505806	9037	NA	SEMAF|semF	Upregulation of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 Promotes Radioresistance of Glioma by Repressing Semaphorin 5A.	27788958	RID01430	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cholangiocarcinoma	H19	IL6	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	sequencing;qRT-PCR	GSE76743;GSE57539;GSE67106;GSE55146	GSE76743.zip;GSE57539.zip;GSE67106.zip;GSE55146.zip	cell migration(+);cell invasion(+)	ceRNA(let-7a;let-7b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136244	NA	283120	3569	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	27809873	RID01431	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Cholangiocarcinoma	HULC	CXCR4	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	sequencing;qRT-PCR	GSE76743;GSE57539;GSE67106;GSE55146	GSE76743.zip;GSE57539.zip;GSE67106.zip;GSE55146.zip	cell migration(+);cell invasion(+)	ceRNA(miR-372;miR-373)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000121966	NA	728655	7852	HCCAT1|LINC00078|NCRNA00078	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	27809873	RID01432	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG5	MTA2	interact	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	epigenetic regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000149480	NA	387066	9219	C6orf160|LINC00044|NCRNA00044|U50HG	MTA1L1|PID	Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex.	27065326	RID01433	epigenetic regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	H19	RB1	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139687	NA	283120	5925	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01434	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	H19	E2F1	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01435	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	H19	CDK8	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000132964	NA	283120	1024	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	K35	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01436	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Colorectal cancer	H19	CTNNB1	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth;cell migration(+)	ceRNA(miR-200a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168036	NA	283120	1499	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing beta-Catenin Expression in Colorectal Cancer. H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues.beta-Catenin was identified as a target gene of miR-200a. H19 regulated beta-catenin expression and activity by competitively binding to miR-200a. H19 promotes cell proliferation by competitively binding to miR-200a and derepressing beta-catenin in CRC. H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	28164117;27789274	RID01437	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	GIHCG	miR-200b	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01438	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	GIHCG	miR-200a	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01439	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	GIHCG	miR-429	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01440	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	HOTAIR	miR-1	negatively-F	luciferase reporter assay;RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues; The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1.	27895772	RID01441	ceRNA or sponge	NA	NA	NA
Esophageal cancer	UCA1	SOX4	positively-E	RNAi;qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124766	NA	652995	6659	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	EVI16	lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer.Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA).	27667646	RID01442	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Breast cancer	UCA1	HIF1A	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-18a)	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000100644	NA	652995	3091	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1alpha feedback regulatory loop.The upregulation UCA1 sponges miR-18a, which is a negative regulator of HIF1alpha. One recent study found that miR-18a can directly targetthree prime untranslated region (3'UTR)of HIF1alpha and suppresses its expression.	27629141	RID01443	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colon cancer	HULC	NKD2	negatively-E	RIP;RNA pull-down assay;RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000145506	NA	728655	85409	HCCAT1|LINC00078|NCRNA00078	Naked2	Long noncoding RNA HULC promotes colorectal carcinoma progression through epigenetically repressing NKD2 expression. Mechanistically, RNA immunoprecipitation (RIP) and RNA pull-down experiment demonstrated that HULC could simultaneously interact with EZH2 to repress underlying targets NKD2 transcription. In addition, rescue experiments determined that HULC oncogenic function is partly dependent on repressing NKD2.	27496341	RID01444	epigenetic regulation	NA	NA	NA
Malignant glioma	H19	VASH2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-29a)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000143494	NA	283120	79805	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a.Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a. In addition, miR-29a targeted 3'-UTR region of vasohibin 2 (VASH2) and decreased its expression. VASH2 has been identified as an angiogenic factor. Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a. In conclusion, the results indicated that knockdown of H19 suppressed glioma induced angiogenesis by inhibiting microRNA-29a, which may modulate the onset of glioma by regulating biological behaviors of glioma vascular endothelial cells.	27543358	RID01445	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Liver cancer	HULC	TERF2	positively-E	ChIP;western blot;qRT-PCR;luciferase reporter assay;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000132604	NA	728655	7014	HCCAT1|LINC00078|NCRNA00078	NA	HULC cooperates with MALAT1 to aggravate liver cancer stem cells growth through telomere repeat-binding factor 2. Mechanistically, both HULC and MALAT1 overexpression enhanced RNA polII, P300,CREPT to load on the promoter region of telomere repeat-binding factor 2(TRF2), triggering the overexpression, phosphorylation and SUMOylation of TRF2.	27782152	RID01446	transcriptional regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Liver cancer	MALAT1	TERF2	positively-E	ChIP;western blot;qRT-PCR;luciferase reporter assay;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132604	NA	378938	7014	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	HULC cooperates with MALAT1 to aggravate liver cancer stem cells growth through telomere repeat-binding factor 2.Mechanistically, both HULC and MALAT1 overexpression enhanced RNA polII, P300,CREPT to load on the promoter region of telomere repeat-binding factor 2(TRF2), triggering the overexpression, phosphorylation and SUMOylation of TRF2.	27782152	RID01447	transcriptional regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	FENDRR	EZH2	interact	RIP	downregulation	qRT-PCR;microarray	NA	NA	cell metastasis(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Limitless Replicative Potential;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000106462	NA	400550	2146	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Loss of long noncoding RNA FOXF1-AS1 regulates epithelial-mesenchymal transition, stemness and metastasis of non-small cell lung cancer cells.Interestingly, we found that FOXF1-AS1 physically associates with PRC2 components EZH2 and loss of FOXF1-AS1 mediates cell migration and stem-like properties require EZH2. These results suggested that FOXF1-AS1 might regulate EMT, stemness and metastasis of NSCLC cells via EZH2, indicating it as a therapeutic target for future treatment of NSCLC.	27577075	RID01448	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	FTX	miR-374a	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000230590	GRCh38_X:73940435-74293574	NA	NA	100302692	NA	LINC00182|MIR374AHG|NCRNA00182	NA	Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/beta-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells. In conclusion, these findings suggest that lnc-FTX may act as a tumor suppressor in HCC through physically binding miR-374a and MCM2. It may also be one of the reasons for HCC gender disparity and may potentially contribute to HCC treatment.	27065331	RID01449	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	NA
Hepatocellular carcinoma	FTX	MCM2	interact	RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000073111	NA	100302692	4171	LINC00182|MIR374AHG|NCRNA00182	BM28|CCNL1|CDCL1|D3S3194|DFNA70|MITOTIN|cdc19	Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/beta-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells. In conclusion, these findings suggest that lnc-FTX may act as a tumor suppressor in HCC through physically binding miR-374a and MCM2. It may also be one of the reasons for HCC gender disparity and may potentially contribute to HCC treatment.	27065331	RID01450	interact with protein	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE111842,GSE51827,GSE86978)
Liver cancer	UCA1	TP53	interact	RIP	upregulation	RT-PCR	NA	NA	cell growth(+)	interact with protein;mutation(N340Q/L344R)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000141510	NA	652995	7157	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCC7|BMFS5|LFS1|P53|TRP53	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR. P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1-(TERT-HOTAIR-TERRA).	27167190	RID01451	interact with protein	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Liver cancer	UCA1	PIM1	positively-E	ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell growth(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000137193	NA	652995	5292	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	PIM	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR.P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1- (TERT-HOTAIR-TERRA).	27167190	RID01452	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Liver cancer	UCA1	PKM	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000067225	NA	652995	5315	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR.P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1- (TERT-HOTAIR-TERRA).	27167190	RID01453	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Breast cancer	BRCA1	NEAT1	negatively-E	RNAi;western blot;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000012048	NA	ENSG00000245532	GRCh38_11:65422774-65445540	672	283131	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	LINC00084|NCRNA00084|TncRNA|VINC	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis.In this study, we delineate the role of the novel BRCA1/lncRNA NEAT1 signaling axis in breast tumorigenesis. BRCA1 inhibits NEAT1 expression potentially through binding to its genomic binding site upstream of the NEAT1 gene. BRCA1 deficiency in human normal/cancerous breast cells and mouse mammary glands leads to NEAT1 overexpression. Our studies show that NEAT1 upregulation resulting from BRCA1 deficiency stimulates in vitro and in vivo breast tumorigenicity.	27556296	RID01454	transcriptional regulation	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Breast cancer	NEAT1	miR-129-5p	negatively-E	luciferase reporter assay;RNAi;qRT-PCR;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency	27556296	RID01455	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Breast cancer	NEAT1	WNT4	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000162552	NA	283131	54361	LINC00084|NCRNA00084|TncRNA|VINC	SERKAL|WNT-4	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency	27556296	RID01456	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Colorectal cancer	LINC01133	SRSF6	interact	RIP;western blot;RNA pull-down assay	downregulation	microarray	NA	NA	cell metastasis(-);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124193	NA	100505633	6431	NA	B52|HEL-S-91|SFRS6|SRP55	Long non-coding RNA LINC01133 inhibits epithelial-mesenchymal transition and metastasis in colorectal cancer by interacting with SRSF6. we confirmed that the EMT process was regulated by LINC01133 in CRC cells dependent on the presence of SRSF6. These data suggest that LINC01133 inhibits the EMT and metastasis by directly binding to SRSF6 as a target mimic, and may serve as a prognostic biomarker and an effective target for anti-metastasis therapies for CRC.	27443606	RID01457	interact with protein	metastasis,prognosis	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC-ROR	POU5F1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000204531	NA	100885779	5460	ROR|lincRNA-RoR|lincRNA-ST8SIA3	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01458	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	LINC-ROR	SOX2	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000181449	NA	100885779	6657	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ANOP3|MCOPS3	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01459	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Gastric cancer	LINC-ROR	NANOG	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000111704	NA	100885779	79923	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01460	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Gastric cancer	LINC-ROR	PROM1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000007062	NA	100885779	8842	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01461	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE109761)
Hepatocellular carcinoma	GPC3-AS1	GPC3	positively-E	RNA pull-down assay;ChIP;RIP;ChIRP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000286096	GRCh38_X:133897443-133897934	ENSG00000147257	NA	110806308	2719	NA	DGSX|GTR2-2|MXR7|OCI-5|SDYS|SGB|SGBS|SGBS1	Long noncoding RNA glypican 3 (GPC3) antisense transcript 1 promotes hepatocellular carcinoma progression via epigenetically activating GPC3. Furthermore, we found that GPC3-AS1 physically associated with P300/CBP-associated factor and recruited it to the GPC3 gene body region, consequently inducing an increase in euchromatic histone marks and activating GPC3 transcription. Moreover, the effects of GPC3-AS1 on HCC cell proliferation and migration were dependent on the upregulation of GPC3.	27573079	RID01462	epigenetic regulation	NA	NA	UP(LIHC);DATA(GSE117623)
Osteosarcoma	MFI2	FOXP4	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	NA	GRCh38_3:196987559-197029816	ENSG00000137166	NA	NA	116113	NA	hFKHLA	Overexpression of long non-coding RNA MFI2 promotes cell proliferation and suppresses apoptosis in human osteosarcoma.Furthermore, the expression of forkhead box P4 (FOXP4) was significantly increased and it was positively associated with lncRNA MFI2 expression in tumor tissues. All the results indicated lncRNA MFI2 could promote proliferation and migration of osteosarcoma cells by regulating FOXP4 expression, which suggested critical roles of lncRNA MFI2 and FOXP4 in occurrence and development of human osteosarcoma.	27513470	RID01463	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Osteosarcoma	BCAR4	GLI2	positively-E	ChIRP;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000074047	NA	400500	2736	NA	CJS|HPE9|PHS2|THP1|THP2	Long noncoding RNA BCAR4 promotes osteosarcoma progression through activating GLI2-dependent gene transcription. Chromatin isolation by RNA purification assay showed that BCAR4 physically associates with the promoters of GLI2 target genes.	27460090	RID01464	transcriptional regulation	NA	NA	UP(PAAD);DATA(GSE40174)
Lung adenocarcinoma	HOTAIR	miR-326	negatively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1. Decreased miR-326 expression was also detected in tumor tissues sampled from LAD patients treated with cisplatin-based chemotherapy and was proved to be correlated with high expression of SP1 and decreased sensitivity to cisplatin. Furthermore, we show that the long noncoding RNA HOTAIR repression reverses chemoresistance of LAD cells partially through modulation of miR-326/SP1 pathway. In summary, we unveil a branch of the HOTAIR/miR-326/SP1 pathway that regulates chemoresistance of LAD cells. Results showed that si-HOTAIR increased miR-326 expression (Fig.6b) and synergistically reduced SP1 expression (Fig.6c),ultimately enhanced sensitivity to cisplatin in A549/CDDPcells. HOTAIR regulates cisplatin resistance via miR-326/SP1 pathway.	27460077	RID01465	expression association	chemoresistance	NA	NA
Lung adenocarcinoma	HOTAIR	SP1	negatively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000185591	NA	100124700	6667	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1. Decreased miR-326 expression was also detected in tumor tissues sampled from LAD patients treated with cisplatin-based chemotherapy and was proved to be correlated with high expression of SP1 and decreased sensitivity to cisplatin. Furthermore, we show that the long noncoding RNA HOTAIR repression reverses chemoresistance of LAD cells partially through modulation of miR-326/SP1 pathway. In summary, we unveil a branch of the HOTAIR/miR-326/SP1 pathway that regulates chemoresistance of LAD cells. Results showed that si-HOTAIR increased miR-326 expression (Fig.6b) and synergistically reduced SP1 expression (Fig.6c),ultimately enhanced sensitivity to cisplatin in A549/CDDPcells. HOTAIR regulates cisplatin resistance via miR-326/SP1 pathway.	27460077	RID01466	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	MALAT1	MMP14	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000157227	NA	378938	4323	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.	27564100	RID01467	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Melanoma	MALAT1	SNAI1	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124216	NA	378938	6615	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.	27564100	RID01468	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	CAMTA1-DT	CAMTA1	negatively-E	RNAi;qRT-PCR;western blot;ChIRP	upregulation	microarray;qRT-PCR	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+)	epigenetic regulation	binding/interaction	RNA-DNA	NA	CSC	Insensitivity to Antigrowth Signals;Limitless Replicative Potential	Cancer	Liver cancer	lncRNA	TF	ENSG00000237436	GRCh38_1:6783892-6784843	ENSG00000171735	NA	110841581	23261	lncCAMTA1	CANPMR	Long Noncoding RNA lncCAMTA1 Promotes Proliferation and Cancer Stem Cell-Like Properties of Liver Cancer by Inhibiting CAMTA1. Mechanistically, we demonstrated that lncCAMTA1 physically associates with the calmodulin binding transcription activator 1 (CAMTA1) promoter, induces a repressive chromatin structure, and inhibits CAMTA1 transcription.	27669232	RID01469	epigenetic regulation	NA	NA	UP(LIHC,PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE75367)
Malignant glioma	NEAT1	NRAS	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(let-7e)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000213281	NA	283131	4893	LINC00084|NCRNA00084|TncRNA|VINC	ALPS4|CMNS|N-ras|NCMS|NRAS1|NS6	Knockdown of NEAT1 restrained the malignant progression of glioma stem cells by activating microRNA let-7e.A potential binding region between NEAT1 and microRNA let-7e was confirmed by dual-luciferase assays. Upregulation of NEAT1 reduced the expression of let-7e. NEAT1 knockdown and let-7e overexpression both reduced NRAS protein expression. NRAS was identified as a direct target of let-7e and promoted oncogenesis in GSCs.	27556696;26306906	RID01470	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Non-small cell lung cancer	XIST	KLF2	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000127528	NA	7503	10365	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	LKLF	Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression.Mechanistically, RNA immune-precipitation (RIP) and RNA pull-down experiment demonstrated that XIST could simultaneously interact with EZH2 to suppress transcription of its potential target KLF2.	27501756	RID01471	epigenetic regulation	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial carcinoma	FER1L4	PTEN	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA FER1L4 suppresses cancer cell proliferation and cycle by regulating PTEN expression in endometrial carcinoma. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition. We conclude that one mechanism by which lncRNAs function in in tumorigenesis is as ceRNAs for tumor suppressor mRNAs.	27381864	RID01472	ceRNA or sponge	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Gallbladder cancer	miR-17-3p	GCASPC	negatively-F	luciferase reporter assay;RNAi;RNA pull-down assay	downregulation	microarray;qRT-PCR	GSE62335	GSE62335.zip	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	miRNA	lncRNA	NA	NA	ENSG00000224073	GRCh38_6:159639307-159640101	NA	112441427	NA	lnc-SOD2-1	Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase-Dependent Cell Proliferation in Gallbladder Cancer.	27450454	RID01473	ceRNA or sponge	NA	NA	NA
Gastric cancer	KRT7-AS	KRT7	positively-F	RNAi;qRT-PCR;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000257671	GRCh38_12:52245048-52247448	ENSG00000135480	NA	109729127	3855	NA	CK7|K2C7|K7|SCL	Long non-coding antisense RNA KRT7-AS is activated in gastric cancers and supports cancer cell progression by increasing KRT7 expression.KRT7-AS formed an RNA-RNA hybrid with KRT7 and controlled KRT7 expression at both the mRNA and the post-transcriptional levels.We conclude that lncRNA KRT7-AS promotes GC, at least in part, by increasing KRT7 expression.	26876208	RID01474	interact with mRNA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE51827,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807,GSE75367)
Gastric cancer	XIST	EZH2	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-101)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression. Furthermore, an inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted.	27620004	RID01475	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Acute myeloid leukemia	linc-223	IRF4	positively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell differentiation(-);tumorigenesis(-)	ceRNA(miR-125-5p)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000274536	GRCh38_X:66015461-66020422	ENSG00000137265	NA	NA	3662	NA	LSIRF|MUM1|NF-EM5|SHEP8	The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA. Here, we identify the host transcript of miR-223, linc-223, as a novel functional long non-coding RNA (lncRNA) in AML. We also demonstrate that endogenous linc-223 localizes in the cytoplasm and acts as a competing endogenous RNA for miR-125-5p, an oncogenic microRNA in leukemia. Among the validated miR-125-5p target mRNAs, we focused on the transcription factor IRF4 (interferon regulatory factor 4).In particular, we show that linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo.Therein, these findings indicate that the newly identified lncRNA linc-223 may have an important role in myeloid differentiation and leukemogenesis, at least in part, by cross-talking with IRF4 mRNA.	27517498	RID01476	ceRNA or sponge	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	CLMAT3	CDKN1B	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249035	GRCh38_5:151676945-151725473	ENSG00000111276	NA	101927096	1027	CTB-113P19.1|SPARC-AS1	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Downregulated long non-coding RNA CLMAT3 promotes the proliferation of colorectal cancer cells by targeting regulators of the cell cycle pathway. In this study, we demonstrate that lncRNA-CLMAT3 expression was significantly increased in colorectal cancer cells compared with a normal intestinal mucous cell line and that inhibition of lncRNA-CLMAT3 suppressed colorectal cancer cell proliferation in vitro. We also found that this reduced colorectal cancer cell proliferation due to lncRNA-CLMAT3 knockdown is associated with G0/G1 cell-cycle arrest induction and apoptosis enhancement. Furthermore, lncRNA-CLMAT3 knockdown enhanced Cdh1 expression and resulted in p27Kip accumulation via increased Skp2 protein ubiquitination.	27391344	RID01477	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CLMAT3	CDH1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249035	GRCh38_5:151676945-151725473	ENSG00000039068	NA	101927096	999	CTB-113P19.1|SPARC-AS1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulated long non-coding RNA CLMAT3 promotes the proliferation of colorectal cancer cells by targeting regulators of the cell cycle pathway. In this study, we demonstrate that lncRNA-CLMAT3 expression was significantly increased in colorectal cancer cells compared with a normal intestinal mucous cell line and that inhibition of lncRNA-CLMAT3 suppressed colorectal cancer cell proliferation in vitro. We also found that this reduced colorectal cancer cell proliferation due to lncRNA-CLMAT3 knockdown is associated with G0/G1 cell-cycle arrest induction and apoptosis enhancement. Furthermore, lncRNA-CLMAT3 knockdown enhanced Cdh1 expression and resulted in p27Kip accumulation via increased Skp2 protein ubiquitination.	27391344	RID01478	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung cancer	CAR10	EGFR	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000148848	GRCh38_10:126012381-126388455	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. The lncRNA CAR intergenic 10 (CAR10) was up-regulated. CAR10 bound and stabilized transcription factor Y-box-binding protein 1 (YB-1), leading to up-regulation of the epidermal growth factor receptor (EGFR) and proliferation of lung cancer cells. Knockdown of CAR10 inhibited cell growth in vitro and tumor growth in vivo. These results demonstrate the role of lncRNAs in environmental lung carcinogenesis, and CAR10-YB-1 represents a potential therapeutic target.	27322209	RID01479	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Lung cancer	CAR10	YBX1	interact	RNAi;RNA pull-down assay;RIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000148848	GRCh38_10:126012381-126388455	ENSG00000065978	NA	NA	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. The lncRNA CAR intergenic 10 (CAR10) was up-regulated. CAR10 bound and stabilized transcription factor Y-box-binding protein 1 (YB-1), leading to up-regulation of the epidermal growth factor receptor (EGFR) and proliferation of lung cancer cells. Knockdown of CAR10 inhibited cell growth in vitro and tumor growth in vivo. These results demonstrate the role of lncRNAs in environmental lung carcinogenesis, and CAR10-YB-1 represents a potential therapeutic target.	27322209	RID01480	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	XIST	PDK1	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000152256	NA	7503	5163	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma. In this study, we found that XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p. We proposed that XIST was responsible for hepatocellular carcinoma cell proliferation, and XIST exerted its function through the miR-139-5p/PDK1 axis.	28231734	RID01481	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	TRPM2-AS	SHC1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	sequencing	TCGA	LUSC_LUAD.zip	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000160691	NA	101928607	6464	TRPM2-AS1	SHC|SHCA	Downregulation of a novel long noncoding RNA TRPM2-AS promotes apoptosis in non-small cell lung cancer. Here, we identified a novel long noncoding RNA TRPM2-AS from published dataset and found TRPM2-AS is widely upregulated in non-small cell lung cancer tissues compared with adjacent non-tumor tissues. Further experiments showed that silence of TRPM2-AS upregulated SHC1 and silence of SHC1 partially reversed cell apoptosis after TRPM2-AS knockdown. In summary, the novel long noncoding RNA TRPM2-AS upregulated in non-small cell lung cancer, and downregulation of TRPM2-AS promotes apoptosis in vitro.	28231726	RID01482	expression association	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)
Colorectal adenocarcinoma	miR-491-5p	PRINS	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	NA	GRCh38_10:24247125-24256046	NA	100169750	NA	NCRNA00074	TFF3-dependent resistance of human colorectal adenocarcinoma cells HT-29/B6 to apoptosis is mediated by miR-491-5p regulation of lncRNA PRINS. In silico-based expression analysis revealed TFF3-mediated regulation of selected microRNAs as well as long non-coding RNAs (lncRNAs), whereas miR-491-5p was identified to target the lncRNA 'psoriasis susceptibility-related RNA gene induced by stress' (PRINS).Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS. Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS.	28149533	RID01483	ceRNA or sponge	NA	NA	NA
Breast cancer	HOTAIR	TP53	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	self-renewal(+);cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141510	NA	100124700	7157	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCC7|BMFS5|LFS1|P53|TRP53	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024;28407576	RID01484	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	HOTAIR	CDKN1A	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024	RID01485	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Breast cancer	HOTAIR	SOX2	positively-E	RNAi;qRT-PCR;western blot;ChIP	upregulation	qRT-PCR	NA	NA	self-renewal(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-34a)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181449	NA	100124700	6657	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ANOP3|MCOPS3	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024;25512558	RID01486	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Neuroblastoma	GAS5	BRCA1	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000012048	NA	60674	672	NCRNA00030|SNHG2	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma.Global sequencing and ELISA arrays revealed that the loss of GAS5 induced p53, BRCA1, and GADD45A, which appeared to modulate cell cycle arrest in concert. Complementation with only the FL GAS5 clone could rescue cell cycle arrest, stabilizing HDM2, and leading to the loss of p53.	28035057	RID01487	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Neuroblastoma	GAS5	TP53	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	BCC7|BMFS5|LFS1|P53|TRP53	The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma.Global sequencing and ELISA arrays revealed that the loss of GAS5 induced p53, BRCA1, and GADD45A, which appeared to modulate cell cycle arrest in concert. Complementation with only the FL GAS5 clone could rescue cell cycle arrest, stabilizing HDM2, and leading to the loss of p53.	28035057	RID01488	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	CYTOR	IL24	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000162892	NA	112597	11009	C2orf59|LINC00152|NCRNA00152	C49A|FISP|IL10B|MDA7|MOB5|ST16	Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression.LINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. EZH2 was shown to bind the promoter region of IL24, while LINC00152 knockdown reduced the histone H3 lysine 27 trimethylation (H3K27me3) occupancy of the IL24 promoter locus (Fig. 5h). However, LSD1 did not bind the IL24 promoter locus (Additional file 5: Figure S3d). These results indicated that LINC00152 repression of target IL24 expression occured, at least partially, through interaction with EZH2.	28109288	RID01489	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	H19	LIN28A	positively-E	luciferase reporter assay;RNAi	downregulation	qPCR	NA	NA	cell stemness(+)	ceRNA(let-7)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Breast cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000131914	NA	283120	79727	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.Here we show that breast cancer stem cells (BCSCs) express high levels of H19. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples.	28102845	RID01490	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DATA(GSE117623)
Glioblastoma	TUG1	VEGFA	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-299)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	LINC00080|NCRNA00080|TI-227H	MVCD1|VEGF|VPF	Long non-coding RNA taurine upregulated 1 enhances tumor-induced angiogenesis through inhibiting microRNA-299 in human glioblastoma.Bioinformatics analysis and luciferase reporter assay revealed that TUG1 influenced tumor angiogenesis via directly binding to the miR-299 and there was a reciprocal repression between TUG1 and miR-299 in the same RNA-induced silencing complex. Moreover, knockdown of TUG1 reduced the expression of vascular endothelial growth factor A (VEGFA), which was defined as a functional downstream target of miR-299.Overall, the results demonstrated that TUG1 enhances tumor-induced angiogenesis and VEGF expression through inhibiting miR-299. Also, the inhibition of TUG1 could provide a novel therapeutic target for glioblastoma treatment.	27345398	RID01491	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Papillary thyroid carcinoma	HIT000218960	HMGA2	negatively-E	western blot;RNAi	downregulation	qPCR;microarray	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	TF	NA	GRCh38_12:66352406-66352634	ENSG00000149948	NA	NA	8091	NA	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long noncoding RNA HIT000218960 promotes papillary thyroid cancer oncogenesis and tumor progression by upregulating the expression of high mobility group AT-hook 2 (HMGA2) gene.In the microarray data, we observed that a newly identified lncRNA, HIT000218960, was significantly upregulated in PTC tissues and associated with a well-known oncogene, high mobility group AT-hook 2 (HMGA2) gene. Both in normal thyroid tissues and PTC tissues, the expression of HIT000218960 was significantly positively correlated with that of HMGA2 mRNA. Those findings suggest that HIT000218960 might acts as a tumor promoter through regulating the expression of HMGA2.	27929737	RID01492	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	XIST	MACC1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000183742	NA	7503	346389	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	7A5|SH3BP4L	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.In the present study, we found that XIST expression was significantly increased in GC tissues and cell lines. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis.	27911852	RID01493	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807)
Papillary thyroid carcinoma	PTCSC2	FOXE1	negatively-F	luciferase reporter assay;RIP;ChIP	downregulation	qPCR;sequencing	TCGA	THCA.zip	p53 signaling pathway(-);predisposition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000236130	GRCh38_9:97699625-97853080	ENSG00000178919	NA	101928337	2304	NA	FKHL15|FOXE2|HFKH4|HFKL5|NMTC4|TITF2|TTF-2|TTF2	MYH9 binds to lncRNA gene PTCSC2 and regulates FOXE1 in the 9q22 thyroid cancer risk locus. We propose that the interaction between the lncRNA, its binding protein MYH9, and the coding gene FOXE1 underlies the predisposition to PTC triggered by rs965513.	28049826	RID01494	interact with protein	NA	NA	UP(PAAD);DATA(GSE40174)
Colorectal cancer	CRNDE	TCF4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	5-fluorouracil;oxaliplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000196628	NA	NA	6925	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	E2-2|FECD3|ITF-2|ITF2|PTHS|SEF-2|SEF2|SEF2-1|SEF2-1A|SEF2-1B|SEF2-1D|TCF-4|bHLHb19	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/beta-catenin signaling.In this study, we found that the expression levels of the CRNDE were upregulated in CRC clinical tissue samples.We identified microRNA miR-181a-5p as an inhibitory target of CRNDE.CRNDE binds to miR-181a-5p and represses its expression. We also determined that beta-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/beta-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression.We found that CRNDE knockdown (Fig. 4a) and miR-181a-5p overexpression (Fig. 4b) appeared to increase the sensitivity of CRC cells to 5-Fu treatment and therefore further inhibited cell growth. Consistently, CRNDE knockdown (Fig. 4c) and miR-181a-5p overexpression (Fig. 4d) led to increased sensitivity of CRC cells to Oxa treatment, and CRNDE overexpression (Additional file 4c) and miR-181a-5p knockdown (Additional file 4d) led to decreased Oxa sensitivity of CRC cells.	28086904	RID01495	ceRNA or sponge	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)
Colorectal cancer	CRNDE	CTNNB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	5-fluorouracil;oxaliplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000168036	NA	NA	1499	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/beta-catenin signaling.In this study, we found that the expression levels of the CRNDE were upregulated in CRC clinical tissue samples.We identified microRNA miR-181a-5p as an inhibitory target of CRNDE.CRNDE binds to miR-181a-5p and represses its expression. We also determined that beta-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/beta-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression.We found that CRNDE knockdown (Fig. 4a) and miR-181a-5p overexpression (Fig. 4b) appeared to increase the sensitivity of CRC cells to 5-Fu treatment and therefore further inhibited cell growth. Consistently, CRNDE knockdown (Fig. 4c) and miR-181a-5p overexpression (Fig. 4d) led to increased sensitivity of CRC cells to Oxa treatment, and CRNDE overexpression (Additional file 4c) and miR-181a-5p knockdown (Additional file 4d) led to decreased Oxa sensitivity of CRC cells.	28086904	RID01496	ceRNA or sponge	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	SNHG12	MAP3K11	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);tumorigenesis(+);cell metastasis(+)	ceRNA(miR-199a-5p;miR-199b-5p)	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000173327	NA	85028	4296	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma.SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues. There were direct interactions between miR-199a/b-5p and the binding site of SNHG12. SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-kB pathway. Eventually, SNHG12 was able to modulate the expression of the miR-199a/b-5p target gene, MLK3, and thus affected the NF-kB pathway.	28073380	RID01497	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	MALAT1	ITGB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-183)	regulation	NA	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150093	NA	378938	3688	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation.Previous studies have demonstrated that MALAT1 (metastasis associated with lung adenocarcinoma transcript-1, also named NEAT2) is over-expressed in multiple carcinomas, consistent with our findings as it was increased in melanoma cancer tissues and cells (Figure 3A and 3B). We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin beta1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1. Collectively, we found a new signaling pathway promoting melanoma development by MALAT1-miR-183-ITGB1 axis, which may be clinically valuable as new targets for malignant melanoma therapy.	27966454	RID01498	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Small cell lung cancer	TUG1	LIMK2	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+)	histone modification	regulation	NA	cisplatin;adriamycin;etoposide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000182541	NA	55000	3985	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 is involved in cell growth and chemoresistance of small cell lung cancer by regulating LIMK2b via EZH2.We found that TUG1 was overexpressed in SCLC tissues.We further demonstrated that TUG1 can regulate the expression of LIMK2b (a splice variant of LIM-kinase 2) via binding with enhancer of zeste homolog 2 (EZH2), and then promoted cell growth and chemoresistance of SCLC.After knockdown of TUG1, the IC50 values of H446DDP and H69AR cells significantly decreased with treatment of chemotherapeutic drugs including DDP, ADM or VP-16 (Fig. 4a). Three chemotherapy drugs [Cisplatin (DDP; Shandong, China), Adriamycin (ADM; Jiangsu, China) Etoposide (VP-16; Jiangsu, China),] were used. Furthermore, we conducted ChIP assays and found that knockdown of TUG1 decreased the binding of EZH2 and H3K27me3 levels across the LIMK2b promoter compared to cells transfected with siNC (Fig. 6f). Taken together, these data suggest that TUG1 is required to target EZH2 occupancy and activity to epigenetically modulate the expression of LIMK2b.	28069000	RID01499	epigenetic regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Lung cancer	MEG3	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression.	27852821	RID01500	epigenetic regulation	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung cancer	MEG3	miR-200b	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01501	epigenetic regulation	NA	NA	NA
Lung cancer	MEG3	miR-200a	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01502	epigenetic regulation	NA	NA	NA
Lung cancer	MEG3	miR-429	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01503	epigenetic regulation	NA	NA	NA
Lung cancer	MEG3	miR-200c	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01504	epigenetic regulation	NA	NA	NA
Lung cancer	MEG3	miR-141	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01505	epigenetic regulation	NA	NA	NA
Laryngeal squamous cell carcinoma	HOTAIR	EZH2	interact	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The role of long non-coding RNA HOTAIR in the progression and development of laryngeal squamous cell carcinoma interacting with EZH2.HOTAIR and EZH2 were over-expressed in LSCC tissue. The higher expression was significantly related to T phase, pathological grades, and risk of lymphatic metastasis of LSCC. Suppressing HOTAIR expression stimulated EZH2 expressing, promoted the proliferation of AMC-HN8 cells, and increased the sensitivity to cis-platinum of the LSCC cells.	27542077	RID01506	interact with protein	metastasis,chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	MALAT1	GLI2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-202)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000074047	NA	378938	2736	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CJS|HPE9|PHS2|THP1|THP2	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression.We found that MALAT1 was upregulated in GC tissues and higher MALAT1 expression was correlated with larger tumor size, lymph node metastasis, and TNM stage. Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202.	27887846	RID01507	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Lung adenocarcinoma	XIST	BAG1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(let-7i)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000107262	NA	7503	573	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	BAG-1|HAP|RAP46	LncRNA XIST promotes human lung adenocarcinoma cells to cisplatin resistance via let-7i/BAG-1 axis.LncRNA XIST expression was markedly increased in cisplatin-resistant A549/DDP cells compared with parental A549 cells as shown by qRT-PCR.LncRNA XIST overexpression in A549 cells increased their chemosensitivity to cisplatin both in vitro and in vivo by protecting cells from apoptosis and promoting cell proliferation. By contrast, LncRNA XIST knockdown in A549/DDP cells decreased the chemoresistance. We revealed that XIST functioned as competing endogenous RNA to repress let-7i, which controlled its down-stream target BAG-1. We proposed that XIST was responsible for cisplatin resistance of LAD cells and XIST exerted its function through the let-7i/BAG-1 axis.	28961027	RID01508	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD,BRCA);DOWN(SKCM,BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE41245)
Renal cell carcinoma	DLX6-AS1	PTEN	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000171862	NA	285987	5728	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis. In this study, we identified an upregulated lncRNA, DLX6-AS1, in RCC tumor tissues compared with normal kidney tissues. Our data suggested that DLX6-AS1 promoted RCC cell growth and tumorigenesis via targeting miR-26a. PTEN is the direct target of miR-26a in RCC cells. In addition, we observed that PTEN overexpression restored the renal cancer cell growth and also rescued the RCC tumorigenesis. In summary, we conclude that DLX6-AS1 promotes renal cell carcinoma development via regulation of miR-26a/PTEN axis.	28881158	RID01509	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	ANCR	EZH2	negatively-E	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell metastasis(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	282	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The degradation of EZH2 mediated by lncRNA ANCR attenuated the invasion and metastasis of breast cancer.Here we report the discovery of ANCR modulating the stability of EZH2, and hence in the invasion and metastasis of breast cancer cells. We determined that ANCR potentiated the CDK1-EZH2 interaction, which then increased the intensity of phosphorylation at Thr-345 and Thr-487 sites of EZH2, facilitating EZH2 ubiquitination and hence its degradation.	27716745	RID01510	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	LINC00161	PTEN	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-21;miR-590-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226935	GRCh38_21:28539318-28540355	ENSG00000171862	NA	118421	5728	C21orf100|Linc-USP16|NCRNA00161	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression.Here, we found that Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p. These interactions led to repression of AKT pathway and inhibition of HCC cell proliferation and migration.	29179215	RID01511	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	H19	CBL	negatively-E	western blot;RNAi	upregulation	qPCR;microarray	NA	NA	chemosensitivity(-);cell viability(+);apoptosis process(-);tumorigenesis(+);cell metastasis(+)	host(miR-675-5p)	regulation	NA	Huaier	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000110395	NA	283120	867	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	C-CBL|CBL2|FRA11B|NSLL|RNF55	Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway.MiR-675-5p was identified as a mature product of H19. Upregulating miR-675-5p reversed the inhibitory effects of Huaier extract, whereas downregulating miR-675-5p sensitized breast cancer cells to the effect of Huaier extract. In addition, Huaier extract increased the expression of CBL protein, a direct target of miR-675-5p. Collectively, the data demonstrate that Huaier extract reduces viability and induces apoptosis in breast cancer cells via H19-miR-675-5p-CBL axis regulation.H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b. We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested. In addition, H19 is also a precursor for microRNA-675 (miR-675) and generates two mature miRNAs, miR-675-5p (miR-675) and miR-675-3p (miR-675*)	29145193	RID01512	expression association	metastasis,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Pancreatic neuroendocrine tumor	MEG3	BRI3	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-183)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000164713	NA	55384	25798	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	I3	MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183.MEG3 was low expressed in BON1 and QGP-1 cells. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/beta-Catenin signaling in BON1 cells.	29132136	RID01513	ceRNA or sponge	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Urinary bladder cancer	UCA1	ARL2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell growth(+);mitochondrial function(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000213465	NA	652995	402	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ARFL2	LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway. UCA1, as a competing endogenous RNA (ceRNA), regulates mitochondrial function through upregulating ARL2. ARL2 is a direct target of miR-195 and can be repressed by either miR-195 overexpression or UCA1 inhibition. Animal experiments further indicated that UCA1 promoted bladder tumor growth by regulating miR-195 /ARL2. These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo.	29130995	RID01514	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE51827)
Hepatocellular carcinoma	HANR	GSK3B	interact	RNA pull-down assay;western blot	upregulation	qPCR;microarray	NA	NA	chemoresistance(+);tumorigenesis(+)	phosphorylation	binding/interaction	RNA-protein	doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_12:12875477-12876136	ENSG00000082701	NA	NA	2932	NA	NA	LncRNA HANR Promotes tumorigenesis and Increase of Chemoresistance in Hepatocellular Carcinoma.HANR was demonstrated to be up-regulated in HCC patients and HCC cell lines.Increased HANR expression in HCC predicted short survival of patients. Knock-down of HANR markedly retarded cell proliferation, suppressed HCC xenograft/orthotopic tumor growth, induced apoptosis and enhanced chemosensitivity to doxorubicin, while over-expression of HANR showed the opposite effects. It was found that HANR bind to GSKIP for regulating the phosphorylation of GSK3beta in HCC.	29055955	RID01515	interact with protein	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	UPF1	MALAT1	negatively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	RNA stability	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000005007	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5976	378938	HUPF1|NORF1|RENT1|pNORF1|smg-2	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1.The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1.	28942451	RID01516	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Urinary bladder cancer	XIST	AR	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169083	NA	7503	367	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR).XIST and AR were upregulated in bladder cancer tissues and positively correlated. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3'UTR of AR to regulate its expression. These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.	28869948	RID01517	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Non-small cell lung cancer	PVT1	miR-195	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195. PVT1 directly interacted with miR-195 and regulated its expression. Moreover, PVT1 knockdown improved radiosensitivity of NSCLC cells in vitro and in vivo by sponging miR-195.	28848163	RID01518	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Pancreatic carcinoma	TUG1	EZH2	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-382)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation,Migration and EMT Phenotype Formation Through Sponging Mir-382. In this study, we reported that TUG1 was overexpressed in PC tissues and cell lines, and high expression of TUG1 predicted poor prognosis. Collectively, these findings revealed that TUG1 functions as an oncogenic lncRNA that promotes tumor progression, at least partially, by functioning as an endogenous 'sponge' and competing for miR-382 binding to the miRNA target EZH2.	28813705	RID01519	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	SNHG6	ZEB1	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000148516	NA	641638	6935	HBII-276HG|NCRNA00058|U87HG	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.In this study, we revealed that SNHG6 was overexpressed in gastric cancer tissues and cell lines. Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446	RID01520	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG6	CDKN1B	negatively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000111276	NA	641638	1027	HBII-276HG|NCRNA00058|U87HG	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446	RID01521	epigenetic regulation	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	AFAP1-AS1	MMP2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000087245	NA	84740	4313	AFAP1-AS|AFAP1AS	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma.In this study, we found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. AFAP1-AS1 silencing inhibited cell migration partly due to decrease the expression of MMP-2 and MMP-9.	28535506	RID01522	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(PAAD);DATA(GSE40174)
Cholangiocarcinoma	AFAP1-AS1	MMP9	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000100985	NA	84740	4318	AFAP1-AS|AFAP1AS	CLG4B|GELB|MANDP2|MMP-9	Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma.In this study, we found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. AFAP1-AS1 silencing inhibited cell migration partly due to decrease the expression of MMP-2 and MMP-9.	28535506	RID01523	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	XLOC_008466	MMP2	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-874)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:43323011-43327969	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.XLOC_008466 is up-regulated in NSCLC patients. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression. A bioinformatics analysis using TargetScan, microRNA.org, and miRanda indicated that MMP2 and XIAP were potential targets of miR-874.	28501870	RID01524	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	XLOC_008466	XIAP	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-874)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:43323011-43327969	ENSG00000101966	NA	NA	331	NA	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.XLOC_008466 is up-regulated in NSCLC patients. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression. A bioinformatics analysis using TargetScan, microRNA.org, and miRanda indicated that MMP2 and XIAP were potential targets of miR-874.	28501870	RID01525	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	CRNDE	E2F3	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-45)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000112242	NA	NA	1871	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	E2F-3	Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145.CRNDE was highly expressed in GC cell lines and tissues;Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145.	28490034	RID01526	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	CRNDE	TCF7L2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-217)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000148737	NA	NA	6934	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	TCF-4|TCF4	The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/beta-Catenin Signaling Pathway.In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells.The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/beta-catenin signaling through binding miR-217 competitively.	28472810	RID01527	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)
Urinary bladder cancer	LINC-ROR	ZEB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition.ZEB1 was a target gene of ROR and was positive correlation with the level of ROR in cancer tissues.ZEB1 is target of ROR.Rescue assays were performed to further confirm that ROR contributes to the progression of BC cells through targeting ZEB1.	28463831	RID01528	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	XIST	miR-186-5p	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p.We confirmed that XIST was upregulated in NSCLC cell lines and tissues.Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p. Furthermore, we showed that miR-186-5p has a binding site for XIST.	28448993	RID01529	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	NA
Colorectal cancer	TUSC7	CDK6	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-211-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000105810	NA	285194	1021	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	MCPH12|PLSTIRE	The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer.In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p.	28214867	RID01530	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Esophagus squamous cell carcinoma	H19	CDH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01531	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	H19	VIM	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01532	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	H19	MMP9	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000100985	NA	283120	4318	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01533	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	NEAT1	CTBP2	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	ceRNA(miR-129)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000175029	NA	283131	1488	LINC00084|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis.NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells. Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129. CTBP2 restoration overturned cell viability and invasion suppression mediated by NEAT1 knockdown or miR-129 overexpression.	29147064	RID01534	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE67939)
Chronic myeloid leukemia	UCA1	ABCB1	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-16)	regulation	NA	imatinib	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000085563	NA	652995	5243	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	lncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.The function of drug efflux mediated by multidrug resistance protein-1 (MDR1) is considered as a main reason for IM drug resistance in CML cells.UCA1 was significantly upregulated in K562/IM and K562/IM-R cells compared with K562 cells, and UCA1 in K562/IM cells was higher than that in K562/IM-R cells. In the present study, long noncoding RNA (lncRNA) UCA1 was identified as an important modulator of MDR1 by a model system of leukemia cell lines with a gradual increase of MDR1 expression and IM resistance. Overexpression of UCA1 increased MDR1 expression to promote IM resistance of CML cells.we demonstrated that UCA1 functions as a competitive endogenous (ceRNA) of MDR1 through completely binding the common miR-16.	27854515	RID01535	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Pancreatic ductal adenocarcinoma	HOTAIR	miR-34a	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma.Loss of miR-34a contributed to EZH2-mediated cell growth in PDAC cells. As HOTAIR was shown to be overexpressed in PDAC.	27594424	RID01536	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	PCBP2-OT1	RASAL1	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with mRNA	binding/interaction	RNA-RNA	sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000111344	NA	102157401	8437	NA	RASAL	Long non-coding RNA TUC338 is functionally involved in sorafenib-sensitized hepatocarcinoma cells by targeting RASAL1.Higher levels of TUC338 were found both in HCC tissues and cell lines. Higher levels of TUC338 were found both in HCC tissues and cell lines, knockdown of TUC338 was accompanied with increased expression of RASAL1 in HCC cell line with increased proliferation and invasion ability, knockdown of TUC338 could activate the RASAL1 pathway and inhibit tumor growth genes by directly targeting RASAL1 3'-UTR. These findings provide direct evidence that the TUC338/RASAL1 axis might play an essential role in sorafenib-resistance of liver cancer cells, suggesting the signaling cohort could serve as a novel therapeutic target for the treatment of chemotherapy resistant liver cancer.	27878301	RID01537	interact with mRNA	chemoresistance	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065)
Gallbladder cancer	CYTOR	HIF1A	positively-E	RIP;western blot;luciferase reporter assay;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000100644	NA	112597	3091	C2orf59|LINC00152|NCRNA00152	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1alpha via miR-138. LINC00152 is significantly upregulated in gallbladder cancer and associated with clinicopathologic characteristics. Mechanistic analyses indicated that LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of hypoxia inducible factor-1alpha (HIF-1alpha). LINC00152 positively regulates HIF-1alpha, a target of miR-138.	28077595	RID01538	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Pancreatic cancer	PVT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124762	NA	5820	1026	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA PVT1 Promotes EMT and Cell Proliferation and Migration Through Downregulating p21 in Pancreatic Cancer Cells. It showed that plasmacytoma variant translocation 1 expression was significantly upregulated in pancreatic cancer tissues or cell line compared to normal groups. Plasmacytoma variant translocation 1 downregulation significantly inhibited zinc finger E-box-binding protein 1/Snail expression but promoted p21 expression, and it also inhibited the cell proliferation and migration.	28355965	RID01539	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Pancreatic cancer	HOTAIR	miR-663b	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter.Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.	27895308	RID01540	epigenetic regulation	NA	NA	NA
Pancreatic cancer	HOTAIR	IGF2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000167244	NA	100124700	3481	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C11orf43|GRDF|IGF-II|PP9974	Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter.Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.	27895308	RID01541	expression association	NA	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Colorectal cancer	SNHG5	STAU1	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell survival(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000124214	NA	387066	6780	C6orf160|LINC00044|NCRNA00044|U50HG	PPP1R150|STAU	SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization. Here, we identify and characterize SNHG5 as a stable cytoplasmic lncRNA with up-regulated expression in colorectal cancer. Importantly, knockdown of key SNHG5 target transcripts, including SPATS2, induces apoptosis and thus mimics the effect seen following SNHG5 depletion. Mechanistically, we suggest that SNHG5 stabilizes the target transcripts by blocking their degradation by STAU1.	28004750	RID01542	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Ovarian cancer	MALAT1	PPP1R13L	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-506)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104881	NA	378938	10848	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	IASPP|NKIP1|RAI|RAI4	Long noncoding RNA MALAT1-regulated microRNA 506 modulates ovarian cancer growth by targeting iASPP.lncRNA-MALAT1 was specifically upregulated in ovarian cancer cell lines and promoted ovarian cancer-cell growth through targeting microRNA (miR)-506. In addition, miR-506-dependent iASPP regulation was required in MALAT1-induced ovarian cancer-cell growth. MalaT1 regulated mir-506 by direct targeting. mir-506 regulated iASPP expression by direct targeting.	28031721	RID01543	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	miR-376c-3p	CYTOR	negatively-F	RNAi;bioinformatics	downregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.we found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Interestingly, microRNA (miR)-376c-3p down-regulated the expression of LINC00152 in CSC cells.	28078002	RID01544	ceRNA or sponge	NA	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)
Gastric cancer	AC009084.3	MUC2	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-34c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000280416	GRCh38_16:66944660-66945096	NA	NA	NA	4583	NA	MLP|MUC-2|SMUC	Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c. LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression.we searched from miRanda database and found that miR-34c might be one regulatory gene of MUC2.	27835575	RID01545	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	SNHG1	miR-195	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1(SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195. The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration in vitro through the inhibition of miR-195. This suggests that miR-195 is a direct downstream target of lncRNA SNHG1. lncRNA SNHG1 may contribute to the aggravation of HCC through the inhibition of miR-195.	27932778	RID01546	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	NA
Colorectal cancer	lnc-GNAT1-1	PEBP1	positively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000204282	GRCh38_3:50191612-50196516	ENSG00000089220	NA	NA	5037	NA	NA	A novel long non-coding RNA lnc-GNAT1-1 is low expressed in colorectal cancer and acts as a tumor suppressor through regulating RKIP-NF-kB-Snail circuit.In vivo study showed that overexpression of lnc-GNAT1-1 could suppress the liver metastasis of CRC cells. Finally, we explored the underlying mechanism of the role lnc-GNAT1-1 plays in CRC, and found a positive correlation between lnc-GNAT1-1 and Raf kinase inhibitor protein (RKIP) expression both in cells and in patients' tissues. We further found that lnc-GNAT1-1 could regulate the RKIP-NF-kB-Snail circuit in CRC.	27912775	RID01547	expression association	metastasis	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Hepatocellular carcinoma	MALAT1	SIRT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000096717	NA	378938	23411	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SIR2|SIR2L1|SIR2alpha	The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1.	28720061	RID01548	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	GAS5	FOXO1	negatively-E	luciferase reporter assay;RIP;RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-205;miR-196a)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150907	NA	60674	2308	NCRNA00030|SNHG2	FKH1|FKHR|FOXO1A	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression. Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively.	28671039	RID01549	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Osteosarcoma	FOXC2-AS1	FOXC2	positively-F	luciferase reporter assay;RIP;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with mRNA	binding/interaction	RNA-RNA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000176692	NA	103752587	2303	ODRUL	FKHL14|LD|MFH-1|MFH1	Antisense lncRNA FOXC2-AS1 promotes doxorubicin resistance in osteosarcoma by increasing the expression of FOXC2.FOXC2-AS1 and FOXC2 are mainly located in the cytoplasm and form an RNA-RNA double-stranded structure in the overlapping region, which is necessary for FOXC2-AS1 to regulate the expression of FOXC2 at both the transcription and post-transcription levels. In addition, transcription factor FOXC2 also contributes to doxorubicin resistance through inducing the expression of the classical multi-drug resistance-related ABCB1 gene similar to FOXC2-AS1. Thus, we concluded that the lncRNA FOXC2-AS1 may promote doxorubicin resistance in OS by increasing the expression of transcription factor FOXC2, further facilitating ABCB1 expression.	28323030	RID01550	interact with mRNA	chemoresistance	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Clear cell renal cell carcinoma	MRCCAT1	NPR3	negatively-E	luciferase reporter assay;RIP;RNAi	upregulation	qPCR;microarray	GSE88948	GSE88948.zip	cell metastasis(+);P38/MAPK signaling pathway(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	ENST00000237853	GRCh38_5:95885098-95962071	ENSG00000113389	NA	NA	4883	NA	ANP-C|ANPR-C|ANPRC|C5orf23|GUCY2B|NPR-C|NPRC	Long noncoding RNA MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 and activating p38-MAPK signaling. The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway.	28659173	RID01551	epigenetic regulation	metastasis	NA	NA
Malignant glioma	CYTOR	FEZF1	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-103a-3p)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000128610	NA	112597	389549	C2orf59|LINC00152|NCRNA00152	FEZ|HH22|ZNF312B	Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway.Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs by binding to miR-103a-3p, which functions as a tumor suppressor.In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1), a direct target of miR-103a-3p which played an oncogenic role in GSCs. FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A). CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.	28651608	RID01552	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Pancreatic cancer	HOTAIR	TNFRSF10B	negatively-E	ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	conatumumab;tigatuzumab	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000120889	NA	100124700	8795	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CD262|DR5|KILLER|KILLER/DR5|TRAIL-R2|TRAILR2|TRICK2|TRICK2A|TRICK2B|TRICKB|ZTNFR9	The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer.These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression.Some TRAIL and DR4/DR5 agonist antibodies, including conatumumab (AMG655, antibody for DR5) and tigatuzumab (CS-1008/TRA-8, antibody for DR5), have also been used for treating several types of cancers	28476883	RID01553	epigenetic regulation	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LNCRNA-ATB	FERMT2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-200b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000073712	NA	114004396	10979	NA	KIND2|MIG2|PLEKHC1|UNC112|UNC112B|mig-2	Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis.Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts.Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC.	28640252	RID01554	ceRNA or sponge	NA	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE111065)
Melanoma	HEIH	miR-200a	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes' promoters and modulate the expression of EZH2 target genes in HCC. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC.	28487474	RID01555	epigenetic regulation	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	NA
Melanoma	HEIH	miR-200b	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes'promoters and modulate the expression of EZH2 target genes in HCC [27]. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC [28,29].	28487474	RID01556	epigenetic regulation	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	NA
Melanoma	HEIH	miR-429	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes'promoters and modulate the expression of EZH2 target genes in HCC [27]. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC [28,29].	28487474	RID01557	epigenetic regulation	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	NA
Colorectal cancer	FBXL19-AS1	miR-203	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000260852	GRCh38_16:30919319-30923269	NA	NA	283932	NA	NCRNA00095	NA	Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203. Among these dysregulated lncRNAs, FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors.Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development.	28479250	RID01558	ceRNA or sponge	metastasis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	NA
Lung cancer	POU5F1	NEAT1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000204531	NA	ENSG00000245532	GRCh38_11:65422774-65445540	5460	283131	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	LINC00084|NCRNA00084|TncRNA|VINC	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression.Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.	28615056	RID01559	transcriptional regulation	prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Lung cancer	POU5F1	MALAT1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000204531	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5460	378938	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression.Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.	28615056	RID01560	transcriptional regulation	prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Lung adenocarcinoma	CDKN2B-AS1	PARP1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);mitochondrial signaling pathway(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000143799	NA	100048912	142	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells.Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2.ANRIL decreases Bcl-2 expression and increases PARP expression.	28402932	RID01561	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Lung adenocarcinoma	CDKN2B-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);mitochondrial signaling pathway(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells.Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2.ANRIL decreases Bcl-2 expression and increases PARP expression.	28402932	RID01562	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	H19	CYTH3	positively-E	RNAi;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-200b;miR-200c)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000008256	NA	283120	9265	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ARNO3|GRP1|PSCD3|cytohesin-3	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b. We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (lncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b. We found that this ability enabled H19 to modulate the expression of the microRNA targets Git2 and Cyth3, respectively, which encode regulators of the RAS superfamily member adenosine 5'-diphosphate (ADP) ribosylation factor (ARF), a guanosine triphosphatase (GTPase) that promotes cell migration associated with EMT and disseminating tumor cells.	28611183	RID01563	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	H19	GIT2	positively-E	RNAi;RIP	upregulation	qPCR	NA	NA	mesenchymal to epithelial transition(+)	ceRNA(let-7b)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139436	NA	283120	9815	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CAT-2|CAT2|PKL	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b. We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (lncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b. We found that this ability enabled H19 to modulate the expression of the microRNA targets Git2 and Cyth3, respectively, which encode regulators of the RAS superfamily member adenosine 6'-diphosphate (ADP) ribosylation factor (ARF), a guanosine triphosphatase (GTPase) that promotes cell migration associated with EMT and disseminating tumor cells.	28611183	RID01564	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	HOXA11-AS	miR-200b	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	epigenetic regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID01565	epigenetic regulation	prognosis	NA	NA
Colon cancer	CRNDE	HNRNPUL2	interact	RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);RAS/MAPK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000214753	NA	NA	221092	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HNRPUL2|SAF-A2	Long noncoding RNA CRNDE stabilized by hnRNPUL2 accelerates cell proliferation and migration in colorectal carcinoma via activating Ras/MAPK signaling pathways.The promoting effects of CRNDE on the cell proliferation, cell cycling and metastasis of CRC cells were confirmed both in vitro and in vivo by gain-of-function and loss-of-function experiments. Mechanistically, it was demonstrated that CRNDE could form a functional complex with heterogeneous nuclear ribonucleoprotein U-like 2 protein (hnRNPUL2) and direct the transport of hnRNPUL2 between the nucleus and cytoplasm. hnRNPUL2 that was accumulated in the cytoplasm could interact with CRNDE both physically and functionally, increasing the stability of CRNDE RNA.	28594403	RID01566	interact with protein	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	CASC2	PTEN	positively-E	luciferase reporter assay;RNAi;western blot	downregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-21)	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Modulation of CASC2/miR-21/PTEN pathway sensitizes cervical cancer to cisplatin. CASC2 expression was down-regulated in cervical cancer tissues.CACS2 overexpression could sensitize DDP-resistant cervical cancer cell (HeLa/DDP and CaSki/DDP) to DDP. Further functional experiments indicate that CASC2 upregulated PTEN expression by direct inhibiting miR-21 in the DDP-resistant cancer cells, leading to the down-regulation of p-AKT protein.	28495512	RID01567	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Esophageal cancer	HOTAIR	SNAI2	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000019549	NA	100124700	6591	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.Mechanistic investigations revealed lncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.LncRNA-HOTAIR acts as a miR-148a sponge to positively regulate Snail2 expression, enhance cell invasion and metastasis, and promote the EMT in EC.	28441714;30223861	RID01568	ceRNA or sponge	metastasis	NA	NA
Lung squamous cell carcinoma	SNHG1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148516	NA	23642	6935	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA SNHG1 regulates zinc finger E-box binding homeobox 1 expression by interacting with TAp63 and promotes cell metastasis and invasion in Lung squamous cell carcinoma. SNHG1 was one of over-expressed lncRNAs in SCC tissues. Rather than direct interaction, SNHG1 regulated ZEB1 expression by suppressing the activity of p63 TA isoform (TAp63), which is a repressor of ZEB1 and physically associates with SNHG1. Furthermore, SNHG1 promoted ZEB1 expression and promoted cell proliferation, metastasis, invasive but inhibited apoptosis of SCC cells via the TAp63/ZEB1 pathway.	28415044	RID01569	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	TCONS_00026907	ELK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-203)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	NA	GRCh38_19:14792302-14792753	ENSG00000126767	NA	NA	2002	NA	NA	LncRNA-TCONS_00026907 is involved in the progression and prognosis of cervical cancer through inhibiting miR-143-5p.To confirm TCONS_00026907 regulates expression of ELK1 through inhibiting miR-143-5p, overexpression of miR-143-5p and silencing of ELK1 were, respectively, performed in HeLa and SiHa cells. Results showed that TCONS_00026907 level was significantly higher in cervical cancer tissues compared to noncancerous tissues and the survival rate was lower in the high expression group. Our study identifies TCONS_00026907 as a potent proto-oncogene and indicates that TCONS_00026907/miR143-5p/ELK1 regulatory pathway plays an important role in cervical cancer.TCONS_00026907 serving as a ceRNA accelerates ELK1 expression through inhibition of miR-143-5p and regulates C-fos, Cyclin D1, and Bcl-2 expression.	28544557	RID01570	ceRNA or sponge	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	PVT1	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-186-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000137693	NA	5820	10413	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	COB1|YAP|YAP2|YAP65|YKI	Long non-coding RNA PVT1 serves as a competing endogenous RNA for miR-186-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma.It was found that there was direct interaction between miR-186-5p and the binding site of plasmacytoma variant translocation 1 by performing dual-luciferase assay and RNA immunoprecipitation assay. Furthermore, it was identified that plasmacytoma variant translocation 1 regulated the expression of the miR-186-5p target gene, yes-associated protein 1. Taken together, plasmacytoma variant translocation 1 served as an endogenous sponge for miR-186-5p to reduce its inhibiting effect on yes-associated protein 1 and thus promoted the tumorigenesis of hepatocellular carcinoma.	28656879	RID01571	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Endometrial carcinoma	TUSC7	miR-23b	negatively-F	RNA pull-down assay	downregulation	qPCR	NA	NA	chemosensitivity(+)	sponge	binding/interaction	RNA-RNA	cisplatin;paclitaxel	NA	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Long non-coding RNA tumor suppressor candidate 7 advances chemotherapy sensitivity of endometrial carcinoma through targeted silencing of miR-23b.the low expression of TUSC7 was confirmed in endometrial carcinoma tissues. TUSC7 upregulation inhibited proliferation, blocked cells at G1 phase, and advanced apoptosis and chemotherapy sensitivity to cisplatin (CDDP) and paclitaxel (Taxol) in HEC1A/CR cell line. Furthermore, miR-23b was upregulated in endometrial carcinoma and negatively correlated with the expression of TUSC7. RNA pull-down assay indicated that TUSC7 could specifically silence the expression of miR-23b in HEC1A/CR cell line; miR-23b was a target gene of TUSC7. In summary, long non-coding RNA TUSC7 was underexpressed in endometrial carcinoma, especially in endometrial carcinoma chemotherapy-resistant tissues and cell lines and acted as a potential tumor suppressor gene to inhibit cell growth as well as advance the chemotherapy sensitivity through targeted silencing of miR-23b, which might provide a new therapeutic target to endometrial carcinoma.	28653877	RID01572	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Gastric cancer	MSTO2P	miR-335	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);colony formation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000203761	GRCh38_1:155745829-155750137	NA	NA	100129405	NA	MSTO2	NA	Long non-coding RNA MSTO2P promotes the proliferation and colony formation in gastric cancer by indirectly regulating miR-335 expression. LncRNA MSTO2P showed the highest expression level and was upregulated in gastric cancer and metastatic tissues. Long non-coding RNA misato family member 2, pseudogene influenced biologic functions in gastric cancer cells via indirectly regulating the activation of miR-335.	28618927	RID01573	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	NA
Esophageal cancer	SNHG1	CST3	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-338)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000101439	NA	23642	1471	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ARMD11|HEL-S-2	LncRNA Snhg1, a non-degradable sponge for miR-338, promotes expression of proto-oncogene CST3 in primary esophageal cancer cells.lncRNA-Snhg1 was significantly upregulated in esophageal carcinoma tissues and promoted esophageal carcinoma cell growth. Furthermore, our results from bioinformatics, luciferase reporter gene and RNA pull-down assays indicated that Snhg1 could be directly bound by miR-338. Snhg1 acted as a non-degradable sponge to relieve the suppression on CST3 caused by miR-338. In conclusion, lncRNA-Snhg1 promoted cell proliferation by acting as a non-degradable sponge for the tumor suppressor miR-338 in esophageal cancer cells.	28423738	RID01574	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Gastric cancer	TUG1	miR-145-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p.TUG1 could directly bind to miR-145-5p and repress miR-145-5p expression. TUG1 overexpression significantly relieved the inhibition on GC cell proliferation and invasion in vitro and tumor growth in vivo, mediated by miR-145-5p overexpression.	27983921	RID01575	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	PCAT14	miR-372	negatively-E	RNAi;methylation-specific PCR	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000280623	GRCh38_22:23536881-23547797	NA	NA	NA	NA	NA	NA	Long noncoding RNA PCAT-14 induces proliferation and invasion by hepatocellular carcinoma cells by inducing methylation of miR-372. lncRNA PCAT-14 is overexpressed in patients with hepatocellular carcinoma (HCC). In addition, PCAT-14 inhibits miR-372 expression by inducing methylation of the miR-372 promoter. Simultaneously, miR-372 eliminates the effects of PCAT-14 on proliferation, invasion, and cell cycle in HCC cells.	28415780	RID01576	epigenetic regulation	NA	NA	NA
Esophagus squamous cell carcinoma	PVT1	LASP1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-203)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000002834	NA	5820	3927	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Lasp-1|MLN50	Upregulation of the long non-coding RNA PVT1 promotes esophageal squamous cell carcinoma progression by acting as a molecular sponge of miR-203 and LASP1. Here, we showed that PVT1 expression is significantly up-regulated in ESCC tumor samples compared with their normal counterparts.miR-203, which has been reported to be down-regulated in ESCC, could bind to PVT1. a significant inverse correlation between PVT1 and miR-203.we firstly confirmed direct binding of miR-203 to the 3'-UTR of LASP1.Our results suggest that PVT1 promote ESCC progression via functioning as a molecular sponge for miR-203 and LASP1 and provide the first evidence of dysregulated PVT1/miR-203/LASP1 axis in ESCC.	28404954	RID01577	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	SNHG1	CDK7	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-199a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000134058	NA	23642	1022	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CAK|CAK1|CDKN7|HCAK|MO15|STK1|p39MO15	SNHG1 lncRNA negatively regulates miR-199a-3p to enhance CDK7 expression and promote cell proliferation in prostate cancer.We found that SNHG1 was aberrantly up-regulated in prostate carcinoma tissues; while, miR-199a-3p was abnormally down-regulated. The level of SNHG1 in prostate cancer was significantly negatively correlated with that of miR-199a-3p. Our data indicated that SNHG1 could interact with miR-199a-3p and inhibit the activity of miR-199a-3p in prostate cancer cells. In addition, miR-199a-3p could target the 3' UTR of CDK7 and suppress CDK7 expression. More importantly, SNHG1 increased CDK7 expression by competitively binding miR-199a-3p, and then promoted cell proliferation and cell cycle progression in prostate cancer. 	28400279	RID01578	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Hepatocellular carcinoma	AF113014	EGR2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-20a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_10:63527874-63529035	ENSG00000122877	NA	NA	1959	NA	AT591|CHN1|CMT1D|CMT4E|KROX20	LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells.In this study, AF113014 is a new lncRNA identified from Microarray. Expression of AF113014 was down-regulated in HCC cell lines. Functionally, AF113014 inhibited proliferation of HCC cells both in vitro and in vivo, whereas the opposite effect was observed when AF113014 knockdown. Moreover, we identified that Egr2, a tumor suppressor gene, was a downstream target gene of AF113014.Interestingly, we found that there was base complementary relationship between AF113014, miRNA-20a and Egr2-3 'UTR.	28542387	RID01579	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE86978)
Osteosarcoma	FENDRR	ABCB1	negatively-E	western blot	upregulation	qPCR;microarray	NA	NA	chemosensitivity(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000085563	NA	400550	5243	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1.Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells.	29069754	RID01580	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Osteosarcoma	FENDRR	ABCC1	negatively-E	western blot	upregulation	qPCR;microarray	NA	NA	chemosensitivity(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000103222	NA	400550	4363	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ABC29|ABCC|GS-X|MRP|MRP1	LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1.Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells.	29069754	RID01581	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	HOTAIR	NOTCH3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000074181	NA	100124700	4854	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CADASIL|CADASIL1|CASIL|IMF2|LMNS	LncRNA HOTAIR acts a competing endogenous RNA to control the expression of notch3 via sponging miR-613 in pancreatic cancer.Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.	28415631	RID01582	ceRNA or sponge	NA	NA	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807,GSE75367)
Thyroid cancer	n340790	miR-1254	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_8:94427712-94436952	NA	NA	NA	NA	NA	NA	The lncRNA n340790 accelerates carcinogenesis of thyroid cancer by regulating miR-1254. Here, we found that the lncRNA n340790 was highly expressed in human thyroid cancer tissues and was strongly correlated with the clinical characteristics of patients.Furthermore, we discovered that n340790 could act as an endogenous sponge by directly binding to miR-1254 and downregulating miR-1254 expression. In addition, miR-1254 could inhibit the stimulatory effect of n340790 on the growth and invasion of thyroid cancer cells.	28559970	RID01583	ceRNA or sponge	NA	NA	NA
Colorectal cancer	UCC	miR-143	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	GSE75970	GSE75970.zip	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	NA	GRCh38_2:9579498-9581745	NA	NA	NA	NA	NA	NA	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. Our results suggest that UCC and miR-143 may be promising molecular targets for CRC therapy.	28492554	RID01584	ceRNA or sponge	NA	NA	NA
Renal cell carcinoma	HOTAIR	HIF1A	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-217)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100644	NA	100124700	3091	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA HOTAIR regulates HIF-1alpha/AXL signaling through inhibition of miR-217 in renal cell carcinoma.In this study, we first demonstrated that HOTAIR expression was upregulated, which was correlated with tumor progression, and miR-217 downregulated in Rcc tissues and cells. Importantly, HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1alpha expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. a direct interaction between miR-217 and the 3'UTR of HIF-1alpha.	28492542	RID01585	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Epithelial ovarian carcinoma	MEG3	ATG3	positively-F	RIP	downregulation	qPCR	NA	NA	cell autophagy(-);tumorigenesis(-);cancer progression(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000144848	NA	55384	64422	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	APG3|APG3-LIKE|APG3L|PC3-96	Upregulation of the lncRNA Meg3 induces autophagy to inhibit tumorigenesis and progression of epithelial ovarian carcinoma by regulating activity of ATG3. we found that the expression of Meg3 was lower in epithelial ovarian carcinoma.Upregulated expression of Meg3 also suppressed tumorigenesis in vivo in a xenograft mouse model through upregulating ATG3 expression. RIP (ribonucleoprotein immunoprecipitation) and RNA pull-down assays showed that Meg3 was co-immunoprecipitated with ATG3. In addition, Meg3 protected ATG3 mRNA from degradation following treatment with actinomycin D. Overall, our results suggest that the lncRNA Meg3 acts as a tumor suppressor in EOC by regulating ATG3 activity and inducing autophagy.	28423647	RID01586	interact with mRNA	NA	NA	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939,GSE86978)
Medulloblastoma	MIR100HG	CDK6	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000105810	NA	399959	1021	AGD1|linc-NeD125|lncRNA-N2	MCPH12|PLSTIRE	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01587	ceRNA or sponge	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Medulloblastoma	MIR100HG	MYCN	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	TF	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000134323	NA	399959	4613	AGD1|linc-NeD125|lncRNA-N2	MODED|N-myc|NMYC|ODED|bHLHe37	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01588	ceRNA or sponge	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	UP(PAAD);DATA(GSE40174)
Medulloblastoma	MIR100HG	SNCAIP	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000064692	NA	399959	9627	AGD1|linc-NeD125|lncRNA-N2	SYPH1|Sph1	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01589	ceRNA or sponge	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Medulloblastoma	MIR100HG	KDM6A	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000147050	NA	399959	7403	AGD1|linc-NeD125|lncRNA-N2	KABUK2|UTX|bA386N14.2	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01590	ceRNA or sponge	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	CDKN2B-AS1	miR-125a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	radiosensitivity(-);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL inhibits proliferation, induces apoptosis, and enhances radiosensitivity in nasopharyngeal carcinoma cells through regulating miR-125a.Luciferase reporter assay was performed to verity the direct target of miR-125a. LncRNA ANRIL was evidently elevated in NPC tissues and cell lines. Moreover, knockdown of ANRIL repressed proliferation, promoted apoptosis, and improved radiosensitivity in NPC via functioning as a miR-125a sponge.	28402230	RID01591	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	NA
Uveal melanoma	CANT1	JPX	positively-E	ChIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000225470	GRCh38_X:73944182-74070408	NA	554203	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	DCBALD06|ENOX|LINC00183|NCRNA00183	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01592	epigenetic regulation	metastasis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)
Uveal melanoma	CANT1	FTX	positively-E	ChIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000230590	GRCh38_X:73940435-74293574	NA	100302692	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	LINC00182|MIR374AHG|NCRNA00182	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01593	epigenetic regulation	metastasis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Uveal melanoma	CANT1	XIST	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000229807	GRCh38_X:73820649-73852723	NA	7503	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01594	expression association	metastasis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Pancreatic cancer	MEG3	PI3K	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	lncRNA MEG3 had anti-cancer effects to suppress pancreatic cancer activity. MEG3 gene expression was negatively correlated with PI3K expression. The MEG3 was negatively correlated with tumor size, Metastasis and Vascular invasion in pancreatic cancer (P<0.05, respectively). MEG3 over-expressing had anti-cancer effects to suppress pancreatic cancer activity by regulation PI3K/AKT/Bcl-2/Bax/Cyclin D1/P53 and PI3K/AKT/MMP-2/MMP-9 signaling pathways.	28320094	RID01595	expression association	metastasis	NA	NA
Hepatocellular carcinoma	HNF1A-AS1	NKD1	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000140807	NA	283460	85407	C12orf27|HAS1|NCRNA00262	Naked1	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID01596	epigenetic regulation	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	NA
Hepatocellular carcinoma	HNF1A-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000124762	NA	283460	1026	C12orf27|HAS1|NCRNA00262	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID01597	epigenetic regulation	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG20	CDH1	negatively-E	RIP;RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000039068	NA	654434	999	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA SNHG20 predicts a poor prognosis for HCC and promotes cell invasion by regulating the epithelial-to-mesenchymal transition.In vitro, loss-function assays revealed that knockdown of SNHG20 inhibited cell proliferation and invasion, whereas, gain-of-function promoted cell proliferation and invasion.Mechanistic investigation revealed that SNHG20 could bind to enhancer of zeste homolog 2 (EZH2) and regulated E-cadherin expression.Our results showed that the SNHG20/EZH2/E-cadhein regulator pathway might contribute to the development of novel therapeutic strategies for HCC patients.	28282787	RID01598	epigenetic regulation	prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	TUG1	ROCK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-335-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000067900	NA	55000	6093	LINC00080|NCRNA00080|TI-227H	P160ROCK|ROCK-I	Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells.In our research, we found that TUG1 was elevated and correlated with a poor prognosis in osteosarcoma patients. Moreover, we revealed that TUG1 and Rho-associated coiled-coil-containing protein kinase 1 (ROCK1), a metastasis-related gene targeted by microRNA-335-5p (miR-335-5p), had the same miR-335-5p combining site. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p.	28205334	RID01599	ceRNA or sponge	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	CASC9	HIF1A	interact	RNAi	upregulation	qPCR	NA	NA	cell growth(+);glucose metabolic process(+);tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000100644	NA	101805492	3091	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The Long Noncoding RNA Cancer Susceptibility Candidate 9 Promotes Nasopharyngeal Carcinogenesis via Stabilizing HIF1alpha.In this study, we identified that lncRNA cancer susceptibility candidate 9 (CASC9) is highly expressed in NPC tissues, which facilitates cell growth and is correlated with a poor prognosis of cancer patients. The underlying molecular mechanism revealed that CASC9 interacts with HIF1alpha and enhances the stabilization of HIF1alpha. Activation of HIF1alpha by overexpressed CASC9 promotes the glycolysis and tumorigenesis of NPC cells.Downregulation of CASC9 significantly inhibits NPC cancer cell growth.	28398871	RID01600	interact with protein	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	HULC	YBX1	positively-F	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+);tumorigenesis(+)	phosphorylation	regulation	NA	cisplatin	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000065978	NA	728655	4904	HCCAT1|LINC00078|NCRNA00078	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA HULC modulates the phosphorylation of YB-1 through serving as a scaffold of extracellular signal-regulated kinase and YB-1 to enhance hepatocarcinogenesis. Meanwhile, HULC could promote cell proliferation, migration, and invasion in vitro and inhibit cisplatin-induced apoptosis. YB-1 is a major component of translationally inactive messenger ribonucleoprotein particles which keeps mRNA in a silent state. Our study further demonstrated that HULC could promote the phosphorylation of YB-1 protein, which leads to the release of YB-1 from its bound mRNA.	28027578	RID01601	interact with protein	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colon cancer	H19	HMGA1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000137309	NA	283120	3159	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HMG-R|HMGA1A|HMGIY	H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1.We found that H19 was overexpressed in colon cancer tissues and cell lines. Moreover, the high-mobility group A (HMGA1) protein was predicted as a target of miR-138. HMGA1 was suppressed by H19 shRNA and could be up-regulated by miR-138 inhibitor. The migration and invasion ability of colon cancer was restrained by H19 shRNA and promoted by miR-138 inhibitor.	28358427	RID01602	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Colorectal cancer	XIST	MAPK1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000100030	NA	7503	5594	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA XIST functions as an oncogene in human colorectal cancer by targeting miR-132-3p. The expression level of XIST was significantly increased in both CRC tissues sample and CRC cells. XIST promoted CRC cell proliferation by affecting the cell cycle. In addition, XIST and miR-132-3p were inhibited by each other reciprocally. MAPK1 was proved to be a direct target spot of miR-132-3p. We claim that XIST was responsible for CRC cell proliferation working by the miR-132-3p/MAPK1 axis.	28730777	RID01603	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	lncRNA-PE	miR-200a	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	NA	GRCh38_5:132190148-132191509	NA	NA	NA	NA	NA	NA	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01604	transcriptional regulation	NA	NA	NA
Hepatocellular carcinoma	lncRNA-PE	miR-200b	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	NA	GRCh38_5:132190148-132191509	NA	NA	NA	NA	NA	NA	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01605	transcriptional regulation	NA	NA	NA
Hepatocellular carcinoma	lncRNA-PE	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_5:132190148-132191509	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01606	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Neuroblastoma	MALAT1	AXL	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000167601	NA	378938	558	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ARK|JTK11|Tyro7|UFO	LncRNA-MALAT1-mediated Axl promotes cell invasion and migration in human neuroblastoma.We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1.Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.	28468579	RID01607	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE67939)
Renal cell carcinoma	UCA1	CDKN1A	negatively-E	RIP;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495. In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. n addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR-495. These findings illuminated that urothelial carcinoma-associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495.	28466784	RID01608	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Renal cell carcinoma	UCA1	miR-495	negatively-F	RIP;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495. In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. n addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR-495. These findings illuminated that urothelial carcinoma-associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495.	28466784	RID01609	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	NA
Neuroblastoma	MYCN	SNHG1	positively-E	bioinformatics	upregulation	qPCR;sequencing	GSE62564	GSE62564.zip	prognosis(-)	amplification	regulation	NA	NA	NA	NA	Cancer	Neuroblastoma	TF	lncRNA	ENSG00000134323	NA	ENSG00000255717	GRCh38_11:62851984-62855953	4613	23642	MODED|N-myc|NMYC|ODED|bHLHe37	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	Co-expression analysis identifies long noncoding RNA SNHG1 as a novel predictor for event-free survival in neuroblastoma. In conclusion, our study unveils that SNHG1 is up-regulated by MYCN amplification and could be a potential prognostic biomarker for high-risk NB intervention.	27517149	RID01610	expression association	prognosis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Thyroid cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);TGF-beta/SMAD signaling pathway(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA ANRIL promotes the invasion and metastasis of thyroid cancer cells through TGF-beta/Smad signaling pathway.ANRIL expression was significantly up-regulated in TC tissues and cells (P < 0.001). ANRIL may reduce p15INK4B expression through inhibiting TGF-beta/Smad signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 cells.	27507052	RID01611	expression association	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Malignant glioma	TUG1	PTEN	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171862	NA	55000	5728	LINC00080|NCRNA00080|TI-227H	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells.TUG1 expression was confirmed to be upregulated in glioma tissues, and showed an inverse correlation with downregulated miR-26a.The bioinformatics prediction revealed putative miR-26a binding sites within TUG1 transcripts. Further experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3'UTR.TUG1 could serve as a miR-26a sponge in human glioma cells, contributing to the upregulation of PTEN. This study revealed a new TUG1/miR-26a/PTEN regulatory mechanism and provided a further understanding of the tumor-suppressive role of TUG1 in glioma development.	27363339	RID01612	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Nasopharynx carcinoma	RBM24	MALAT1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000112183	NA	ENSG00000251562	GRCh38_11:65497688-65506516	221662	378938	RNPC6|dJ259A10.1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma. In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Overall, these findings suggest a novel role of RBM24 as a tumor suppressor. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.	27584791	RID01613	expression association	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	EGF	LINC01089	negatively-E	ChIP	downregulation	qPCR;microarray	E-MTAB-4821	E-MTAB-4821.zip	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000138798	NA	ENSG00000212694	GRCh38_12:121795267-121803906	1950	338799	HOMG4|URG	LIMT	LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis. Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter.We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo. In conclusion, lncRNAs dynamically regulated by growth factors might act as novel drivers of cancer progression and serve as prognostic biomarkers.	27485121	RID01614	epigenetic regulation	metastasis,prognosis	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Non-small cell lung cancer	H19	MACC1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000183742	NA	283120	346389	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	7A5|SH3BP4L	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01615	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807)
Non-small cell lung cancer	H19	EGFR	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000146648	NA	283120	1956	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01616	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	H19	CTNNB1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168036	NA	283120	1499	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01617	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	H19	MAPK3	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000102882	NA	283120	5595	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01618	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	H19	MAPK1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000100030	NA	283120	5594	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01619	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HOTAIR	HLA-G	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204632	NA	100124700	3135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MHC-G	Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer.HOTAIR expression was obviously increased in cervical cancer tissue.Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a. HOTAIR negatively regulated miR-148a expression via direct interaction. These results indicate that HOTAIR-induced downregulation of miR-148a attenuated the post-transcriptional regulation of miR-148a on HLA-G, contributing to HLA-G upregulation.Our data suggest that HOTAIR plays an important oncogenic role in cervical cancer and might serve as a marker for cervical cancer prognosis and a potential target for therapeutic intervention.	27574106	RID01620	ceRNA or sponge	prognosis	NA	UP(PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE111842,GSE111065,GSE51827,GSE86978)
Ovarian cancer	HOTAIR	RAB22A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-124)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124209	NA	100124700	57403	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR controls the expression of Rab22a by sponging miR-373 in ovarian cancer. In patients with ovarian cancer, HOTAIR was significantly upregulated. HOTAIR functioned as a ceRNA, and acted as a sink for microRNA (miR)-373, thereby regulating the expression of Rab22a. The upregulation of HOTAIR contributed to the malignant progression of ovarian cancer cells. Therefore, the positive regulation between HOTAIR and Rab22a can be partially attributed to the ceRNA regulatory network through miR-373.	27484896	RID01621	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Hepatocellular carcinoma	MEG3	HSPA5	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000044574	NA	55384	3309	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.	27432655	RID01622	expression association	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	MEG3	NFKB1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000109320	NA	55384	4790	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.	27432655	RID01623	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	ZEB1-AS1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000087088	NA	220930	581	NA	BCL2L4	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01624	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	ZEB1-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000171791	NA	220930	596	NA	Bcl-2|PPP1R50	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01625	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	ZEB1-AS1	CCND1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000110092	NA	220930	595	NA	BCL1|D11S287E|PRAD1|U21B31	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01626	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Malignant glioma	ZEB1-AS1	CDK2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000123374	NA	220930	1017	NA	CDKN2|p33(CDK2)	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01627	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	ZEB1-AS1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01628	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	ZEB1-AS1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000087245	NA	220930	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01629	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(PAAD);DATA(GSE40174)
Malignant glioma	ZEB1-AS1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000100985	NA	220930	4318	NA	CLG4B|GELB|MANDP2|MMP-9	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01630	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	ZEB1-AS1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000170558	NA	220930	1000	NA	CD325|CDHN|CDw325|NCAD	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01631	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Malignant glioma	ZEB1-AS1	ITGB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000150093	NA	220930	3688	NA	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01632	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	ZEB1-AS1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000039068	NA	220930	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	A Long Noncoding RNA ZEB1-AS1 Promotes tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01633	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	MALAT1	TGFA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	ceRNA(miR-376a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163235	NA	378938	7039	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TFGA	MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A.Here, we showed that MALAT1 was increased in human OS cell lines and tissues and promoted OS cell growth, while MALAT1 knockdown suppressed OS cell growth. There was a direct interaction between MIR376A and MALAT1 via a putative MIR376A binding site within the MALAT1 3'-untranslated region (3'-UTR). There was also a direct interaction between MIR376A and the TGFA 3'-UTR. Thus, MALAT1 may promote OS cell growth through inhibition of MIR376A, leading to increased expression of TGFA. Our results suggest a MALAT1/MIR376A/TGFA axis mediates OS cell proliferation and tumor progression.	27458156	RID01634	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Prostate cancer	SOCS2-AS1	TNFSF10	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+);apoptosis process(-)	epigenetic regulation	association	NA	docetaxel	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000246985	GRCh38_12:93542022-93571768	ENSG00000121858	NA	144481	8743	NA	APO2L|Apo-2L|CD253|TL2|TNLG6A|TRAIL	Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.suppressor of cytokine signaling 2-antisense transcript 1 (SOCS2-AS1), the expression of which was higher in castration-resistant prostate cancer model cells.SOCS2-AS1 promoted castration-resistant and androgen-dependent cell growth. We found that SOCS2-AS1 knockdown up-regulated genes related to the apoptosis pathway, including tumor necrosis factor superfamily 10 (TNFSF10), and sensitized prostate cancer cells to docetaxel treatment. Moreover, we also demonstrated that SOCS2-AS1 promotes androgen signaling by modulating the epigenetic control for AR target genes including TNFSF10 These findings suggest that SOCS2-AS1 plays an important role in the development of castration-resistant prostate cancer by repressing apoptosis.	27342777	RID01635	epigenetic regulation	chemoresistance	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	NEAT1	E2F3	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-377-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112242	NA	283131	1871	LINC00084|NCRNA00084|TncRNA|VINC	E2F-3	Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.In our studies, we identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression.we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression.	27351135	RID01636	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	TUG1	CELF1	negatively-E	RIP;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000149187	NA	55000	10658	LINC00080|NCRNA00080|TI-227H	BRUNOL2|CUG-BP|CUGBP|CUGBP1|EDEN-BP|NAB50|NAPOR|hNab50	Long noncoding RNA TUG1 is downregulated in non-small cell lung cancer and can regulate CELF1 on binding to PRC2. Knockdown of TUG1 significantly promoted the proliferation of NSCLC cells. The results demonstrated that TUG1 RNA was bound to enhancer of zeste protein 2/embryonic ectoderm development (EZH2/EED), which is essential for PRC2. Finally, our designed ChIP assay revealed that the EZH2/EED was bound to the promotor region of CELF1 within 992 bp upstream of the transcript start site.	27485439	RID01637	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	PVT1	miR-200b	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b.Our results revealed that PVT1 is upregulated in cervical cancer tissues.Mechanistically, we verified that PVT1 binds to EZH2, recruits EZH2 to the miR-200b promoter, increases histone H3K27 trimethylation level on the miR-200b promoter, and inhibits miR-200b expression. Furthermore, the effects of PVT1 on cervical cell proliferation and migration depend upon silencing of miR-200b.	27272214	RID01638	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Endometrial carcinoma	MEG3	NOTCH1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148400	NA	55384	4851	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AOS5|AOVD1|TAN1|hN1	LncRNA-MEG3 inhibits cell proliferation of endometrial carcinoma by repressing Notch signaling.Significant downregulation of MEG3 was observed in EC samples compared to control, while the protein levels of Notch1 and Hes1 were both upregulated. Cell proliferation was obviously inhibited by MEG3 overexpression, while opposite improved result was obtained in MEG3 knockout cells. Interestingly, MEG3-induced changes could be reversed by Notch1 regulators.Downregulated MEG3 exhibited an anti-proliferative role in EC by repressing Notch signaling pathway.	27470401	RID01639	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Endometrial carcinoma	MEG3	HES1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000114315	NA	55384	3280	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HES-1|HHL|HRY|bHLHb39	LncRNA-MEG3 inhibits cell proliferation of endometrial carcinoma by repressing Notch signaling.Significant downregulation of MEG3 was observed in EC samples compared to control, while the protein levels of Notch1 and Hes1 were both upregulated. Cell proliferation was obviously inhibited by MEG3 overexpression, while opposite improved result was obtained in MEG3 knockout cells. Interestingly, MEG3-induced changes could be reversed by Notch1 regulators.Downregulated MEG3 exhibited an anti-proliferative role in EC by repressing Notch signaling pathway.	27470401	RID01640	expression association	NA	NA	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Her2-receptor positive breast cancer	HOTAIR	FOXM1	positively-E	RNAi;luciferase reporter assay	upregulation	sequencing	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000111206	NA	100124700	2305	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.HOTAIR is a long non-coding RNA that is overexpressed, promotes metastasis and is predictive of decreased survival.HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. Analysis of breast cancer gene expression data indicates that HOTAIR is co-expressed with FOXA1 and FOXM1 in HER2-enriched tumours, and these factors enhance the prognostic power of HOTAIR in aggressive HER2+ breast tumours.	27378691	RID01641	expression association	metastasis,prognosis	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Her2-receptor positive breast cancer	HOTAIR	FOXA1	positively-E	RNAi;luciferase reporter assay	upregulation	sequencing	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129514	NA	100124700	3169	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3A|TCF3A	Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.HOTAIR is a long non-coding RNA that is overexpressed, promotes metastasis and is predictive of decreased survival.HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. Analysis of breast cancer gene expression data indicates that HOTAIR is co-expressed with FOXA1 and FOXM1 in HER2-enriched tumours, and these factors enhance the prognostic power of HOTAIR in aggressive HER2+ breast tumours.	27378691	RID01642	expression association	metastasis,prognosis	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Glioblastoma	HOTAIR	PDCD4	negatively-E	ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000150593	NA	100124700	27250	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	H731	Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	27277755	RID01643	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Skin squamous cell carcinoma	PICSAR	DUSP6	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000139318	NA	378825	1848	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	HH19|MKP3|PYST1	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01644	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE51827,GSE75367,GSE86978)
Skin squamous cell carcinoma	PICSAR	MAPK3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000102882	NA	378825	5595	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01645	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Skin squamous cell carcinoma	PICSAR	MAPK1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000100030	NA	378825	5594	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01646	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	UCA1	FOXM1	positively-E	western blot;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-507)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111206	NA	652995	2305	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma.UCA1 expression was discovered to be upregulated in melanoma tissues and cells.We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507.	27389544	RID01647	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Malignant glioma	CRNDE	PIWIL4	positively-E	western blot;IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-384)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000134627	NA	NA	143689	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HIWI2|MIWI2	CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis.Colorectal neoplasia differentially expressed (CRNDE) is the most upregulated long noncoding RNA (lncRNA) in glioma.In addition, the expression of miR-384 was negatively correlated with CRNDE expression. A binding region between CRNDE and miR-384 was confirmed using luciferase assays.Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression.PIWIL4 was identified as a target of miR-384 and plays an oncogenic role in glioma.	27058823	RID01648	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	miR-148b-3p	HOTAIR	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.RT-qPCR revealed that the expression level of miR-148b-3p was significantly lower in A172 cells compared with HA1800 cells. Bioinformatics and luciferase reporter assays showed that miR-148b-3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence. In summary, the results indicated that miR-148b-3p inhibits malignant biological behaviors of glioma cells by directly targeting HOTAIR.	27446363	RID01649	ceRNA or sponge	NA	NA	NA
Hepatocellular carcinoma	TUSC7	EPHA4	negatively-E	luciferase reporter assay;IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-10a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000116106	NA	285194	2043	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	EK8|HEK8|SEK|TYRO1	Long non-coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma.In this study, we observed that the expression of TUSC7 was immensely decreased in HCC. Moreover, TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis.	27002617	RID01650	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE111065,GSE75367)
Epithelial ovarian cancer	UCA1	MMP14	positively-E	luciferase reporter assay;RIP;IHC	upregulation	qPCR	NA	NA	cell metastasis(-)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000157227	NA	652995	4323	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	UCA1 functions as a competing endogenous RNA to suppress epithelial ovarian cancer metastasis.UCA1 was aberrantly upregulated in EOC tissues and cells.The results showed that UCA1 could function as an endogenous sponge by directly binding to miR-485-5p. Depletion of UCA1 was involved in the downregulation of matrix metallopeptidase 14 (MMP14) expression, a target gene of miR-485-5p.	26867765	RID01651	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Osteosarcoma	TUSC7	BCL2	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000171791	NA	285194	596	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Bcl-2|PPP1R50	Long non-coding RNA tumor suppressor candidate 7 functions as a tumor suppressor and inhibits proliferation in osteosarcoma.Here, we reported a novel lncRNA, tumor suppressor candidate 7 (TUSC7), was significantly downregulated in osteosarcoma tissues compared with paired non-tumor tissues and low expression of TUSC7 indicated poor survival.Western blot showed that after silence of TUSC7, the proapoptotic Bcl2 expression was downregulated.	26781978	RID01652	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatoblastoma	TUG1	VEGFA	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(-);angiogenesis(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	LINC00080|NCRNA00080|TI-227H	MVCD1|VEGF|VPF	Targeting long non-coding RNA-TUG1 inhibits tumor growth and angiogenesis in hepatoblastoma. We previously reveal that lnRNA-TUG1 is upregulated in hepatoblastoma specimens by microarray analysis. TUG1, miR-34a-5p, and VEGFA constitutes to a regulatory network, and participates in regulating hepatoblastoma cell function, tumor progression, and tumor angiogenesis.LncRNA-TUG1 functions as miR-34a-5p sponge in hepatoblastoma cell.LncRNA-TUG1 regulates the expression of miR-34a-5p target gene, VEGFA, in hepatoblastoma cell.	27362796	RID01653	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Colorectal cancer	CASC11	HNRNPK	interact	RNA pull-down assay;RIP;IHC	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000165119	NA	100270680	3190	CARLO7|CARLo-7|LINC00990|TCONS_00014535	AUKS|CSBP|HNRPK|TUNP	Long non-coding RNA CASC11 interacts with hnRNP-K and activates the WNT/beta-catenin pathway to promote growth and metastasis in colorectal cancer.Here, we report that cancer susceptibility candidate 11 (CASC11) was upregulated in CRC tissues;Furthermore, CASC11 can target heterogeneous ribonucleoprotein K (hnRNP-K) to activate WNT/beta-catenin signaling in CRC cells. In addition, we found that c-Myc directly bound to the promoter regions of CASC11 and increased promoter histone acetylation to enhance CASC11 expression.	27012187	RID01654	transcriptional regulation	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	MYC	CASC11	positively-E	RNA pull-down assay;RIP;IHC	NA	NA	NA	NA	cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000249375	GRCh38_8:127686343-127738987	4609	100270680	MRTL|MYCC|bHLHe39|c-Myc	CARLO7|CARLo-7|LINC00990|TCONS_00014535	Long non-coding RNA CASC11 interacts with hnRNP-K and activates the WNT/beta-catenin pathway to promote growth and metastasis in colorectal cancer.Here, we report that cancer susceptibility candidate 11 (CASC11) was upregulated in CRC tissues;Furthermore, CASC11 can target heterogeneous ribonucleoprotein K (hnRNP-K) to activate WNT/beta-catenin signaling in CRC cells. In addition, we found that c-Myc directly bound to the promoter regions of CASC11 and increased promoter histone acetylation to enhance CASC11 expression.	27012187	RID01655	epigenetic regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(LIHC);DATA(GSE117623)
Gastric cancer	RMRP	CCND2	positively-E	RNAi;miRcode	downregulation	qPCR;microarray	GSE47850	GSE47850.zip	cell growth(+);biomarker	ceRNA(miR-206)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000118971	NA	6023	894	CHH|NME1|RMRPR|RRP2	KIAK0002|MPPH3	LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.RMRP is downregulated during gastric carcinogenesis. Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression.miR-206 is a potential tumor suppressor with G0/G1 cell cycle arrest by targeting the Cyclin D2.	27192121	RID01656	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Prostate cancer	DANCR	TIMP2	negatively-E	western blot;RNA pull-down assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000035862	NA	57291	7077	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CSC-21K|DDC8	Long noncoding RNA DANCR promotes invasion of prostate cancer through epigenetically silencing expression of TIMP2/3.In the present study, we found the expression of DANCR increases in prostate cancer tissues and cells compared to normal prostate tissues and cells.Mechanistically, we found that TIMP2/3, which are critical metastasis inhibitor of prostate cancer, were down-regulated by DANCR synergistically with EZH2 through epigenetically silencing their promoter by chromatin immunoprecipitation assay.	27191265	RID01657	epigenetic regulation	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	DANCR	TIMP3	negatively-E	western blot;RNA pull-down assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000100234	NA	57291	7078	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	HSMRK222|K222|K222TA2|SFD	Long noncoding RNA DANCR promotes invasion of prostate cancer through epigenetically silencing expression of TIMP2/3.In the present study, we found the expression of DANCR increases in prostate cancer tissues and cells compared to normal prostate tissues and cells.Mechanistically, we found that TIMP2/3, which are critical metastasis inhibitor of prostate cancer, were down-regulated by DANCR synergistically with EZH2 through epigenetically silencing their promoter by chromatin immunoprecipitation assay.	27191265	RID01658	epigenetic regulation	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(SKCM);DATA(GSE38495)
Glioblastoma	HIF1A-AS2	HMGA1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell stemness(+)	NA	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Brain glioma	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000137309	NA	100750247	3159	3'aHIF-1A|aHIF	HMG-R|HMGA1A|HMGIY	The Long Non-coding RNA HIF1A-AS2 Facilitates the Maintenance of Mesenchymal Glioblastoma Stem-like Cells in Hypoxic Niches.We identified hypoxia-inducible factor 1 alpha-antisense RNA 2 (HIF1A-AS2) as a subtype-specific hypoxia-inducible lncRNA, upregulated in mesenchymal GSCs.Among the HIF1A-AS2 interactome, IGF2BP2 and DHX9 were identified as direct partners. This association was needed for maintenance of expression of their target gene, HMGA1. Downregulation of HIF1A-AS2 led to delayed growth of mesenchymal GSC tumors, survival benefits, and impaired expression of HMGA1 in vivo.	27264189	RID01659	expression association	NA	NA	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Gastric cancer	HOXA13	HOTTIP	positively-E	luciferase reporter assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000106031	NA	ENSG00000243766	GRCh38_7:27198575-27207259	3209	100316868	HOX1|HOX1J	HOXA-AS6|HOXA13-AS1|NCRNA00213	Oncogenic function of the homeobox A13-long noncoding RNA HOTTIP-insulin growth factor-binding protein 3 axis in human gastric cancer. Knockdown of HoxA13 caused the downregulation of long non-coding RNA HOTTIP and insulin growth factor-binding protein 3 (IGFBP-3) genes, indicating that both were targets of HoxA13. Concurrent regulation of HoxA13-HOTTIP was mediated by the mixed lineage leukemia-WD repeat domain 5 complex, which caused the trimethylation of H3K4 and then stimulated cell proliferation. HoxA13 transactivated the IGFBP-3 promoter through the HOX-binding site.	27144338	RID01660	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Malignant glioma	H19	ABCB1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01661	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Malignant glioma	H19	ABCC1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000103222	NA	283120	4363	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC29|ABCC|GS-X|MRP|MRP1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01662	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	H19	ABCG2	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000118777	NA	283120	9429	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01663	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Breast cancer	BCYRN1	BCL2L1	negatively-F	RIP;ChIP;IHC	upregulation	qPCR	NA	NA	oncogenic role(+)	alternative splicing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000171552	NA	618	598	BC200|BC200a|LINC00004|NCRNA00004	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Regulation of alternative splicing of Bcl-x by BC200 contributes to breast cancer pathogenesis.In this study, we show that BC200 is upregulated in breast cancer. Mechanistically, BC200 contains a 17-nucleotide sequence complementary to Bcl-x pre-mRNA, which may facilitate its binding to Bcl-x pre-mRNA and recruitment of heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1, a known splicing factor. Together, these results suggest that BC200 plays an oncogenic role in breast cancer. Thus, BC200 may serve as a prognostic marker and possible target for attenuating deregulated cell proliferation in estrogen-dependent breast cancer.	27277684	RID01664	interact with mRNA	prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Malignant glioma	LNCRNA-ATB	TGFB2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000092969	NA	114004396	7042	NA	G-TSF|LDS4|TGF-beta2	Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time.ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-beta2.Recent study has reported that miR-200a suppresses renal cell carcinoma development by directly targeting TGF-beta2.	27267902	RID01665	ceRNA or sponge	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Medulloblastoma	CRNDE	CASP3	negatively-E	IHC	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000164305	NA	NA	836	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CPP32|CPP32B|SCA-1	Long non-coding RNA CRNDE promotes tumor growth in medulloblastoma.Our data suggest that transcript levels of CRNDE are elevated in clinical medulloblastoma tissues instead of in adjacent non-cancerous tissues.In vivo data further showed that proliferating cell nuclei antigen (PCNA) was decreased, whereas the apoptosis initiator cleaved-caspase-3 was increased upon CRNDE knockdown in cancerous tissues from the mouse model.	27383309	RID01666	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Medulloblastoma	CRNDE	PCNA	negatively-E	IHC	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000132646	NA	NA	5111	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ATLD2	Long non-coding RNA CRNDE promotes tumor growth in medulloblastoma.Our data suggest that transcript levels of CRNDE are elevated in clinical medulloblastoma tissues instead of in adjacent non-cancerous tissues.In vivo data further showed that proliferating cell nuclei antigen (PCNA) was decreased, whereas the apoptosis initiator cleaved-caspase-3 was increased upon CRNDE knockdown in cancerous tissues from the mouse model.	27383309	RID01667	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Thyroid cancer	H19	YES1	positively-E	luciferase reporter assay;IHC 	upregulation	qPCR	NA	NA	cell cycle(+)	ceRNA(miR-17-5p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000176105	NA	283120	7525	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HsT441|P61-YES|Yes|c-yes	Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer.H19 expression was higher in tumor samples and in thyroid cancer cell lines than nontumor tissues and normal thyroid cells.H19 was identified as a target of miR-17-5p, by Dual-Luciferase Reporter assays and RNA-binding protein immunoprecipitation assays. H19 antagonized the function of miR-17-5p on upregulation of its target YES1 and inhibited miR-17-5p-induced cell cycle progression.	27093644	RID01668	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE109761,GSE55807,GSE75367)
Uveal melanoma	PAUPAR	HES1	negatively-E	ChIP;western blot	downregulation	qPCR	NA	NA	tumorigenesis(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Uveal cancer	lncRNA	TF	ENSG00000281880	GRCh38_11:31812307-32002405	ENSG00000114315	NA	103157000	3280	NA	HES-1|HHL|HRY|bHLHb39	PAUPAR lncRNA suppresses tumourigenesis by H3K4 demethylation in uveal melanoma.We show that lncRNA PAUPAR is present at low levels in UM tissues and cell lines and modulates the tumourigenesis of UM in vitro and in vivo. The ectopic expression of PAUPAR in UM cells revealed that PAUPAR acts as a necessary UM suppressor and induces the silencing of HES1 expression, which significantly reduces tumour metastasis. Mechanistically, PAUPAR modulates HES1 expression by inhibiting histone H3K4 methylation.	27214741	RID01669	epigenetic regulation	metastasis	NA	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Colorectal cancer	DUXAP9	TWIST1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000122691	NA	503638	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01670	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	DUXAP9	SNAI1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000124216	NA	503638	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01671	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	DUXAP9	VIM	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000026025	NA	503638	7431	NA	NA	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01672	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	DUXAP9	TJP1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000104067	NA	503638	7082	NA	ZO-1	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01673	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Gastric cancer	HOTTIP	HOXA13	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	HOTTIP and HOXA13 are oncogenes associated with gastric cancer progression.We found that HOTTIP was upregulated in gastric cancer cell lines. Moreover, downregulation of HOTTIP led to decreased expression of homeobox protein Hox-A13 (HOXA13) in gastric cancer cell lines. HOXA13 was involved in HOTTIP-induced malignant phenotypes of gastric cancer cells.	27108607	RID01674	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Epithelial ovarian cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC). Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation.	27095571	RID01675	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Epithelial ovarian cancer	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC). Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation.	27095571	RID01676	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	MALAT1	MMP13	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137745	NA	378938	4322	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG3|MANDP1|MDST|MMP-13	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01677	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Ovarian cancer	MALAT1	MMP19	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000123342	NA	378938	4327	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CODA|MMP18|RASI-1	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01678	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE38495,GSE111842,GSE55807,GSE67939,GSE75367)
Ovarian cancer	MALAT1	ADAMTS1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000154734	NA	378938	9510	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C3-C5|METH1	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01679	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	linc-UFC1	CTNNB1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01680	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	linc-UFC1	MAPK1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01681	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	linc-UFC1	CDK4	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01682	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	linc-UFC1	CCND1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01683	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	linc-UFC1	RB1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000139687	NA	NA	5925	NA	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01684	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AGAP2-AS1	LATS2	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000150457	NA	100130776	26524	PUNISHER	KPM	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID01685	epigenetic regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AGAP2-AS1	KLF2	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000127528	NA	100130776	10365	PUNISHER	LKLF	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID01686	epigenetic regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	HNF1A-AS1	BCL2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(+)	ceRNA(miR-30b-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000171791	NA	283460	596	C12orf27|HAS1|NCRNA00262	Bcl-2|PPP1R50	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p. HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines. HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. ATG5 is a direct target of miR-30b and thereby a ceRNA for HNF1A-AS1.	27084450	RID01687	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HNF1A-AS1	ATG5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(+)	ceRNA(miR-30b-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000057663	NA	283460	9474	C12orf27|HAS1|NCRNA00262	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p. HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines. HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. ATG5 is a direct target of miR-30b and thereby a ceRNA for HNF1A-AS1.	27084450	RID01688	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Nasopharynx carcinoma	H19	EZH2	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-630)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma.Herein, we found that H19 was overexpressed in NPC tissues and poorly differentiated cell lines.Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner.	27040767	RID01689	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Her2-receptor positive breast cancer	GAS5	PTEN	positively-E	IHC;RNAi	downregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-21)	regulation	NA	trastuzumab	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer.Expression of the lncRNA GAS5 was decreased in trastuzumab-resistant SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. This work identifies GAS5 as a novel prognostic marker and candidate drug target for HER2-positive breast cancer.	27034004	RID01690	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Renal cell carcinoma	LNCARSR	AXL	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34;miR-449)	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000167601	NA	112577459	558	NA	ARK|JTK11|Tyro7|UFO	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA. Here we identified an lncRNA, named lncARSR (lncRNA Activated in RCC with Sunitinib Resistance), which correlated with clinically poor sunitinib response. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	27117758	RID01691	ceRNA or sponge	chemoresistance	NA	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE67939)
Renal cell carcinoma	LNCARSR	MET	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34;miR-449)	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000105976	NA	112577459	4233	NA	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA. Here we identified an lncRNA, named lncARSR (lncRNA Activated in RCC with Sunitinib Resistance), which correlated with clinically poor sunitinib response. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	27117758	RID01692	ceRNA or sponge	chemoresistance	NA	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Non-small cell lung cancer	LINC00673	NCALD	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	microarray	GSE18842	GSE18842.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000104490	NA	100499467	83988	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer.We identified an oncogene, linc00673, whose expression level was upregulated by bioinformatics analyses and qRT-PCR analyses in NSCLC. Further mechanistic analyses indicated that the oncogenic activity of linc00673 is partially attributable to its repression of NCALD through association with the epigenetic repressor LSD1, Histone demethylase lysine specific demethylase 1.	27027352	RID01693	epigenetic regulation	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	MALAT1	CTNNB1	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01694	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	MALAT1	EZH2	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01695	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	MALAT1	LIN28A	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131914	NA	378938	79727	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01696	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	FTX	DDX58	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	host(miR-545)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000107201	NA	100302692	23586	LINC00182|MIR374AHG|NCRNA00182	RIG-I|RIG1|RIGI|RLR-1|SGMRT2	Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.We demonstrated that the lncRNA Ftx and Ftx-derived miR-545 were up-regulated in both HCC tissues and cells. MiR-545 was positively correlated with lncRNA Ftx expression.We found that miR-545 was a pivotal mediator in Ftx-induced promotion of HCC cell growth. Subsequently, we identified RIG-I as a direct target of miR-545. The expression of RIG-I was downregulated in HCC tissues and was inversely correlated with miR-545 expression. In conclusion, our study demonstrates that the novel pathway lncRNA Ftx/miR-545/RIG-I promotes HCC development by activating PI3K/Akt signaling, and it may serve as a novel prognostic biomarker and therapeutic target for HCC.	26992218	RID01697	expression association	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE41245)
Hepatocellular carcinoma	SNHG1	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000141510	NA	23642	7157	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA SNHG1 predicts a poor prognosis and promotes hepatocellular carcinoma tumorigenesis.In this study, we found SNHG1 was upregulated in HCC tissues in comparison with adjacent liver tissues in both publicly available microarray data and our own cohort. Further experiments revealed that SNHG1 promotes HCC cells proliferation through inhibiting p53 and p53-target genes expression.	27133041	RID01698	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	UCA1	PARP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	association	NA	adriamycin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000143799	NA	652995	142	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Silence of long noncoding RNA UCA1 inhibits malignant proliferation and chemotherapy resistance to adriamycin in gastric cancer.UCA1 was highly expressed in gastric cancer tissues and cells, and its high expression level had a positive correlation with some malignant pathological characteristics of gastric cancer, such as higher grade and poor differentiation. The chemotherapy resistance to adriamycin of SGC7901/ADR cells was depressed by UCA1 silence, and IC50 for adriamycin presented a conspicuous depression.UCA1 silence advanced apoptosis induced by adriamycin in SGC7901/ADR cells, up-regulated cleaved PARP protein expression and depressed the expression of anti-apoptosis protein Bcl-2. These results demonstrated that chemotherapy resistance changes induced by UCA1 silence might be mediated by the cell apoptosis pathway.	27056384	RID01699	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Gastric cancer	UCA1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	association	NA	adriamycin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000171791	NA	652995	596	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Bcl-2|PPP1R50	Silence of long noncoding RNA UCA1 inhibits malignant proliferation and chemotherapy resistance to adriamycin in gastric cancer.UCA1 was highly expressed in gastric cancer tissues and cells, and its high expression level had a positive correlation with some malignant pathological characteristics of gastric cancer, such as higher grade and poor differentiation. The chemotherapy resistance to adriamycin of SGC7901/ADR cells was depressed by UCA1 silence, and IC50 for adriamycin presented a conspicuous depression.UCA1 silence advanced apoptosis induced by adriamycin in SGC7901/ADR cells, up-regulated cleaved PARP protein expression and depressed the expression of anti-apoptosis protein Bcl-2. These results demonstrated that chemotherapy resistance changes induced by UCA1 silence might be mediated by the cell apoptosis pathway.	27056384	RID01700	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pancreatic cancer	LINC-ROR	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway. In the present study, we found that linc-ROR was upregulated in PC tissues. Mechanistically, we confirmed that linc-ROR up-regulates ZEB1 and then induces epithelial-mesenchymal transition (EMT), which promotes the aggressive biological behaviors of PC.	26898939	RID01701	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	MALAT1	PROM1	negatively-E	IHC;ChIP	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000007062	NA	378938	8842	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	The Ribonucleic Complex HuR-MALAT1 Represses CD133 Expression and Suppresses Epithelial-Mesenchymal Transition in Breast Cancer. In this study, we show that a ribonucleoprotein complex including the long noncoding RNA MALAT1 and the RNA-binding protein HuR (ELAVL1) binds the CD133 promoter region to regulate its expression. In conclusion, our findings suggest that the failure of a repressive complex to form or stabilize in breast cancer promotes CD133 upregulation and an EMT-like program, providing new mechanistic insights underlying the control of prometastatic processes.	27197265	RID01702	transcriptional regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(BRCA);DATA(GSE109761)
Osteosarcoma	H19	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200s)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.	27008415	RID01703	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	H19	ZEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200s)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169554	NA	283120	9839	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.	27008415	RID01704	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Osteosarcoma	FGFR3-AS1	FGFR3	positively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_4:1807353-1808406	ENSG00000068078	NA	NA	2261	NA	ACH|CD333|CEK2|HSFGFR3EX|JTK4	Long noncoding RNA FGFR3-AS1 promotes osteosarcoma growth through regulating its natural antisense transcript FGFR3.FGFR3-AS1 was upregulated in osteosarcoma.Through antisense pairing with FGFR3 3'UTR, FGFR3-AS1 increases FGFR3 mRNA stability and upregulates FGFR3 expression. The expression of FGFR3-AS1 and FGFR3 is positively correlated in osteosarcoma tissues.	27022737	RID01705	interact with mRNA	NA	NA	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	PVT1	LATS2	negatively-E	IHC;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000150457	NA	5820	26524	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	KPM	Long Noncoding RNA PVT1 Promotes Non-Small Cell Lung Cancer Cell Proliferation through Epigenetically Regulating LATS2 Expression.Here, we found that PVT1 was upregulated in 105 human NSCLC tissues compared with normal samples.RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription.	26908628	RID01706	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	CCAT1	MYC	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell differentiation(+);cell growth(+)	ceRNA(miR-155)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia.In this study, the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients.By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155.Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155.	26923190	RID01707	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LINC00668	CDKN2B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000147883	NA	400643	1030	NA	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01708	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC);DATA(GSE117623)
Gastric cancer	E2F1	LINC00668	positively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000265933	GRCh38_18:6919496-6929966	1869	400643	E2F-1|RBAP1|RBBP3|RBP3	NA	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01709	transcriptional regulation	prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Gastric cancer	LINC00668	CDKN2A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000147889	NA	400643	1029	NA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01710	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Gastric cancer	LINC00668	CDKN1A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000124762	NA	400643	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01711	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	LINC00668	CDKN1B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000111276	NA	400643	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01712	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00668	CDKN1C	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000129757	NA	400643	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01713	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	MEG3	GDF15	positively-E	western blot;IHC	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26992211	RID01714	expression association	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Hepatocellular carcinoma	MEG3	MDM2	negatively-E	western blot;IHC	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000135679	NA	55384	4193	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ACTFS|HDMX|hdm2	Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26992211	RID01715	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	XIST	SMAD7	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-92b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000101665	NA	7503	4092	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CRCS3|MADH7|MADH8	MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XIST.Mechanistic investigations suggested that Smad7, which exhibited an inverse relationship with miR-92b expression in HCC, was a direct target of miR-92b and could reverse its effects on HCC tumorigenesis. Furthermore, long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and miR-92b could directly interact with and repress each other, and XIST could inhibit HCC cell proliferation and metastasis by targeting miR-92b.	27100897	RID01716	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	MYC	TINCR	negatively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000223573	GRCh38_19:5558167-5578349	4609	257000	MRTL|MYCC|bHLHe39|c-Myc	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/beta-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression.It reported that c-Myc binding to the Sp1 transcription factor via the c-Myc central region and inhibition of Sp1 transcriptional activity on the cell cycle/growth arrest mechanism [19]. TINCR, transcribed by Sp1, was repressed by c-Myc.	27009809	RID01717	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Colorectal cancer	TINCR	EPCAM	negatively-F	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000119888	NA	257000	4072	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/beta-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression.TINCR specifically binds to EpCAM and regulates its proteolysis.	27009809	RID01718	interact with protein	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Osteosarcoma	miR-141	H19	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.The overexpressed miR-141 suppressed H19 and miR-675 expression in hFOB1.19 cells. Taken together, our study revealed that tumor-suppressor miR-141 overexpression suppressed osteoblasts proliferation but induced apoptosis through down-regulating H19 or miR-675 in osteosarcoma.	27186302	RID01719	expression association	NA	NA	UP(NSCLC);DATA(GSE74639)
Colon cancer	Lnc34a	miR-34a	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	epigenetic regulation	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	A long non-coding RNA targets microRNA miR-34a to regulate colon cancer stem cell asymmetric division.Here we report a novel LncRNA, Lnc34a, that is enriched in colon cancer stem cells (CCSCs) and initiates asymmetric division by directly targeting the microRNA miR-34a to cause its spatial imbalance.Lnc34a recruits Dnmt3a via PHB2 and HDAC1 to methylate and deacetylate the miR-34a promoter simultaneously, hence epigenetically silencing miR-34a expression independent of its upstream regulator, p53. Lnc34a levels affect CCSC self-renewal and colorectal cancer (CRC) growth in xenograft models. Lnc34a is upregulated in late-stage CRCs, contributing to epigenetic miR-34a silencing and CRC proliferation.	27077950	RID01720	epigenetic regulation	NA	NA	NA
Esophagus squamous cell carcinoma	TP73-AS1	BDH2	positively-E	RNAi;western blot	upregulation	qPCR;microarray	NA	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	5-fluorouracil;cisplatin	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000164039	NA	57212	56898	KIAA0495|PDAM	DHRS6|EFA6R|PRO20933|SDR15C1|UCPA-OR|UNQ6308	Knockdown of long non-coding RNA TP73-AS1 inhibits cell proliferation and induces apoptosis in esophageal squamous cell carcinoma. Our results show that lncRNA TP73-AS1 and BDH2 levels are generally upregulated in esophageal cancer tissues and are strongly correlated with tumor location or TNM stage in clinical samples. LncRNA TP73-AS1 knockdown inhibited BDH2 expression in EC9706 and KYSE30 cells, whereas BDH2 knockdown repressed esophageal cancer cell proliferation and induced apoptosis via the caspase-3 dependent apoptotic pathway. In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin.	26799587	RID01721	expression association	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE55807)
Non-small cell lung cancer	TATDN1	CDH1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000147687	GRCh38_8:124488485-124539458	ENSG00000039068	NA	NA	999	CDA11	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01722	expression association	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Non-small cell lung cancer	TATDN2	ERBB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000157014	GRCh38_3:10248023-10281218	ENSG00000141736	NA	NA	2064	NA	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01723	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Non-small cell lung cancer	TATDN3	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203705	GRCh38_1:212791828-212816830	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01724	expression association	metastasis	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE67939)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	TATDN1	EZR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000147687	GRCh38_8:124488485-124539458	ENSG00000092820	NA	NA	7430	CDA11	CVIL|CVL|HEL-S-105|VIL2	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01725	expression association	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Colorectal cancer	UCA1	CREB1	positively-E	RIP;luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-204-5p)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118260	NA	652995	1385	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CREB|CREB-1	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.We found that UCA1 was up-regulated in CRCs and negatively correlated with survival time in two CRC cohorts. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression. The present work provides the first evidence of a UCA1-miR-204-5p-CREB1/BCL2/RAB22A regulatory network in CRC and reveals that UCA1 and CREB1 are potential new oncogenes and prognostic factors for CRC.	27046651	RID01726	ceRNA or sponge	prognosis,chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	AFAP1-AS1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000067560	NA	84740	387	AFAP1-AS|AFAP1AS	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling.Expression of AFAP1-AS1 is increased in human HCC tissues and correlates with poor prognosis.the decreased expression levels of AFAP1-AS1, RhoA and Rac2 in si-AFAP1-AS1 group compared with the si-NC group (P<0.01).	26892468	RID01727	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Hepatocellular carcinoma	AFAP1-AS1	RAC2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000128340	NA	84740	5880	AFAP1-AS|AFAP1AS	EN-7|Gx|HSPC022|p21-Rac2	Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling.Expression of AFAP1-AS1 is increased in human HCC tissues and correlates with poor prognosis.the decreased expression levels of AFAP1-AS1, RhoA and Rac2 in si-AFAP1-AS1 group compared with the si-NC group (P<0.01).	26892468	RID01728	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	GAS5	MMP2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000087245	NA	60674	4313	NCRNA00030|SNHG2	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Lentiviral-mediated overexpression of long non-coding RNA GAS5 reduces invasion by mediating MMP2 expression and activity in human melanoma cells.Overexpressing lncRNA GAS5 inhibited the migration and invasion ability of melanoma SK-Mel-110 cells, partially by decreasing the MMP2 expression and its activity.	26846479	RID01729	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Ovarian cancer	BACE1-AS	BACE1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell proliferation(-);cell invasion(-)	NA	association	NA	anisomycin	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000278768	GRCh38_11:117288453-117293571	ENSG00000186318	NA	100379571	23621	BACE1-AS1|BACE1AS|NCRNA00177	ASP2|BACE|HSPC104	Long non-coding RNA BACE1-AS is a novel target for anisomycin-mediated suppression of ovarian cancer stem cell proliferation and invasion.The mRNA expression levels of long non-coding RNA (lncRNA) beta-site APP cleaving enzyme 1 antisense strand (BACE1-AS) were significantly increased in anisomycin-treated OCSCs compared to controls. Finally, when expression of lncRNA BACE1-AS was silenced using siRNA, BACE1 expression was downregulated and the antiproliferative and anti-invasive effects of anisomycin were reduced.	26783004	RID01730	expression association	chemoresistance	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE51827)
Breast cancer	MALAT1	CDK4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135446	NA	378938	1019	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CMM3|PSK-J3	miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells.Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. MALAT1 increased the expression of CDK4, a target of miR-124	26918449	RID01731	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	MT1JP	TP53	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell cycle(-);apoptosis process(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000141510	NA	4498	7157	MT1|MT1J|MT1NP|MTB	BCC7|BMFS5|LFS1|P53|TRP53	LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway.By associating with the RNA-binding protein TIAR, MT1JP enhanced the translation of the master transcription factor p53, thereby regulating a series of pathways involving p53, such as the cell cycle, apoptosis and proliferation.Taken together, we identified MT1JP as a critical factor in restraining cell transformation by modulating p53 translation through interactions with TIAR, and this finding is likely to shed new light on future investigations about posttranscriptional or translational effects of lncRNAs during cell transformation.	26909858	RID01732	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Melanoma	SAMMSON	C1QBP	interact	RIP;IHC	upregulation	qPCR	NA	NA	mitochondrial function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000108561	NA	101927152	708	LINC01212	NA	Melanoma addiction to the long non-coding RNA SAMMSON. Mechanistically, SAMMSON interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function.Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted anti-melanoma therapeutic responses.	27008969	RID01733	interact with protein	NA	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE67939,GSE86978)
Hepatocellular carcinoma	UCA1	CDK2	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell cycle phase transition (G1/S)(+)	epigenetic regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000123374	NA	652995	1017	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN2|p33(CDK2)	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID01734	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	UCA1	CDKN1B	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID01735	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	HULC	ESM1	positively-E	IHC	upregulation	qPCR	NA	NA	angiogenesis(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000164283	NA	728655	11082	HCCAT1|LINC00078|NCRNA00078	endocan	HULC long noncoding RNA silencing suppresses angiogenesis by regulating ESM-1 via the PI3K/Akt/mTOR signaling pathway in human gliomas. This process induced anoikis and blocked the cell cycle at G1/S phase via the PI3K/Akt/mTOR signaling pathway, thus regulating the tumor-related genes involved in the above biological behavior in human glioma U87MG and U251 cells. However, these effects were reversed by ESM-1 overexpression, suggesting a mediating role of ESM-1 in the pro-angiogenesis effect of HULC.	26894862	RID01736	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	MALAT1	PCDH10	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138650	NA	378938	57575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OL-PCDH|PCDH19	MALAT1 long ncRNA promotes gastric cancer metastasis by suppressing PCDH10.In particular, we found that long noncoding RNA (lncRNA) MALAT1 binds EZH2, suppresses the tumor suppressor PCDH10, and promotes gastric cellular migration and invasion.	26871474	RID01737	epigenetic regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Colon cancer	HOTAIR	CASP2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106144	NA	100124700	835	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CASP-2|ICH1|NEDD-2|NEDD2|PPP1R57	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.Luciferase assays identified caspase 2, an initiator caspase, to be a new target of miR-125a-5p.In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. These findings indicate that miR-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	26962687	RID01738	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Colon cancer	HOTAIR	miR-125a-5p	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.Luciferase assays identified caspase 2, an initiator caspase, to be a new target of miR-125a-5p.In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. These findings indicate that miR-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	26962687	RID01739	expression association	NA	NA	NA
Colorectal cancer	MALAT1	AKAP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127914	NA	378938	10142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP-9|AKAP350|AKAP450|CG-NAP|HYPERION|LQT11|MU-RMS-40.16A|PPP1R45|PRKA9|YOTIAO	Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation.These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells.Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro.MALAT1 promotes colorectal cancer cell proliferation/migration/invasion via PRKA kinase anchor protein 9. overexpression of MALAT1 via RNA activation promoted CRC cell proliferation, invasion and migration in vitro, and stimulated tumor growth and metastasis in mice in vivo. Among these genes, PRKA kinase anchor protein 9 (AKAP-9) was significantly up-regulated at both mRNA and protein levels. Importantly, knockdown of AKAP-9 blocked MALAT1-mediated CRC cell proliferation, migration and invasion. These data indicate that MALAT1 may promote CRC tumor development via its target protein AKAP-9.	26887056;25446987	RID01740	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Colorectal cancer	MALAT1	SRSF1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136450	NA	378938	6426	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASF|SF2|SF2p33|SFRS1|SRp30a	Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation.These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells.Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro.	26887056	RID01741	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	FEZF1-AS1	FEZF1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000128610	NA	154860	389549	NA	FEZ|HH22|ZNF312B	Long non-coding RNA FEZF1-AS1 facilitates cell proliferation and migration in colorectal carcinoma.Here, we discovered a novel long noncoding RNA (lncRNA) FEZF1 antisense RNA1 (FEZF1-AS1) is markedly upregulated in human primary colorectal carcinoma (CRC) and associated with CRC metastasis and poor prognosis.We further discovered that the downregulation of FEZF1-AS1 reduced its sense-cognate gene FEZF1 mRNA and protein expression in CRC cells. There was a positive correlation between FEZF1-AS1 and FEZF1 expression in CRC. Moreover, FEZF1 knockdown also significantly suppressed CRC cell proliferation, migration, and invasion. Our findings indicate that the dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction.	26848625	RID01742	expression association	metastasis,prognosis	NA	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	LINC01133	KLF2	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000127528	NA	100505633	10365	NA	LKLF	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01743	epigenetic regulation	NA	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC01133	CDKN1A	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124762	NA	100505633	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01744	epigenetic regulation	NA	UP(BRCA);DATA(GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	LINC01133	CDH1	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000039068	NA	100505633	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01745	epigenetic regulation	NA	UP(BRCA);DATA(GSE111065)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung adenocarcinoma	RGMB-AS1	RGMB	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000174136	NA	503569	285704	NA	DRAGON	Long Noncoding RNA RGMB-AS1 Indicates a Poor Prognosis and Modulates Cell Proliferation, Migration and Invasion in Lung Adenocarcinoma.The expression of lncRNA RGMB-AS1 was inversely correlated with that of repulsive guidance molecule b (RGMB) in lung adenocarcinoma tissues, and UCSC analysis and fluorescence detection assay indicated that lncRNA RGMB-AS1 may be involved in the development of human lung adenocarcinoma by regulating RGMB expression though exon2 of RGMB.	26950071	RID01746	expression association	prognosis	NA	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE51827)
Pancreatic cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	fenofibrate	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of LncRNA MEG3.Fenofibrate significantly inhibited proliferation of pancreatic cancer cells, increased MEG3 expression and p53 levels. Moreover, knockdown of MEG3 attenuated cytotoxicity induced by fenofibrate. Furthermore, overexpression of MEG3 induced cells death and increased p53 expression. Our results indicated fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of MEG3.	26850851	RID01747	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Malignant glioma	MALAT1	MMP2	negatively-E	IHC	downregulation	qPCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.	26938295	RID01748	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Gastric cancer	CCAT1	HNRNPA1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+)	ceRNA(miR-490)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000135486	NA	100507056	3178	CARLO5|CARLo-5|onco-lncRNA-40	ALS19|ALS20|HNRPA1|HNRPA1L3|IBMPFD3|UP 1|hnRNP A1|hnRNP-A1	The long noncoding RNA colon cancer-associated transcript-1/miR-490 axis regulates gastric cancer cell migration by targeting hnRNPA1.In this study, we provide the first evidence that CCAT1 regulates miR-490 in gastric cancer (GC) cells. Interestingly, miR-490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR-490 expression was downregulated in GC. The negative correlation between miR-490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR-490-binding site, and deletion of this binding site abolishes their miR-490 responsiveness. Post-transcriptional CCAT1 silencing by miR-490 significantly suppressed GC cell migration. Furthermore, miR-490 directly bound to the hnRNPA1 mRNA 3'-UTR to repress its translation.	26825578	RID01749	ceRNA or sponge	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	MALAT1	TJP1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104067	NA	378938	7082	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ZO-1	Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	26798987	RID01750	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	MALAT1	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	26798987	RID01751	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	CYTOR	CDKN2B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000147883	NA	112597	1030	C2orf59|LINC00152|NCRNA00152	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID01752	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Gastric cancer	CYTOR	CDKN2A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000147889	NA	112597	1029	C2orf59|LINC00152|NCRNA00152	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID01753	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Breast cancer	PANDAR	CDKN2A	negatively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle phase transition (G1/S)(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000147889	NA	101154753	1029	PANDA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression.In this study, we investigated the role of lncRNA PANDAR in the progression of breast cancer and found that PANDAR was up-regulated in breast cancer tissues and cell lines. The knockdown of PANDAR suppresses G1/S transition of breast cancer cells. We demonstrated mechanistically that the regulation of G1/S transition by PANDAR was partly due to the transcriptional modulation of p16(INK4A).	26927017	RID01754	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	PVT1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000147883	NA	5820	1030	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer.Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines.In conclusion, our study demonstrated that PVT1 might serve as a promising biomarker for diagnosis and prognosis of NSCLC, and it could promote the proliferation of NSCLC cells by downregulating p15 and p21 expression.	26490983	RID01755	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	PVT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124762	NA	5820	1026	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer.Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines.In conclusion, our study demonstrated that PVT1 might serve as a promising biomarker for diagnosis and prognosis of NSCLC, and it could promote the proliferation of NSCLC cells by downregulating p15 and p21 expression.	26490983	RID01756	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	SNHG12	AMOT	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000126016	NA	85028	154796	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes cell proliferation and migration by upregulating angiomotin gene expression in human osteosarcoma cells.SNHG12 and AMOT messenger RNA (mRNA) expression was upregulated in osteosarcoma tissues and cell lines when compared with normal tissues and cells. Upregulation of AMOT mRNA was associated with upregulation of SNHG12.This preliminary study has shown that the lncRNA SNHG12 promotes cell proliferation and migration by upregulating AMOT gene expression in osteosarcoma cells in vivo and in vitro.	26486328	RID01757	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Pancreatic ductal adenocarcinoma	HOTAIR	WIF1	negatively-E	RNAi	upregulation	qPCR	NA	NA	radiosensitivity(-)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156076	NA	100124700	11197	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	WIF-1	The long non-coding RNA HOTAIR affects the radiosensitivity of pancreatic ductal adenocarcinoma by regulating the expression of Wnt inhibitory factor 1. HOX transcript antisense intergenic RNA (HOTAIR) is overexpressed in PDAC.And HOTAIR silencing increased the expression of WIF-1. Furthermore, the overexpression of WIF-1 revealed that HOTAIR modulated the radiosensitivity of PDAC cells by regulating the expression of WIF-1.	26482614	RID01758	expression association	NA	NA	NA
Breast cancer	MALAT1	KDM5B	positively-E	IHC	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117139	NA	378938	10765	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CT31|JARID1B|MRT65|PLU-1|PLU1|PPP1R98|PUT1|RBBP2H1A|RBP2-H1	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.Compared with other breast cancer types, the highly metastatic MDA-MB-231 cells concurrently exhibited increased expression levels of Lysine-specific demethylase 5B protein (KDM5B) and long non-coding RNA (lncRNA), MALAT1, suggesting their functional association.KDM5B-silencing in the TNBC cells correlated with the upregulation of hsa-miR-448 and led to suppression of MALAT1 expression with decreased migration, invasion and clonogenic capacity in vitro.	26917489	RID01759	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Breast cancer	MALAT1	miR-448	negatively-E	IHC	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.Compared with other breast cancer types, the highly metastatic MDA-MB-231 cells concurrently exhibited increased expression levels of Lysine-specific demethylase 5B protein (KDM5B) and long non-coding RNA (lncRNA), MALAT1, suggesting their functional association.KDM5B-silencing in the TNBC cells correlated with the upregulation of hsa-miR-448 and led to suppression of MALAT1 expression with decreased migration, invasion and clonogenic capacity in vitro.	26917489	RID01760	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Gastric cancer	TUG1	CDKN1C	negatively-E	RIP;ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000129757	NA	55000	1028	LINC00080|NCRNA00080|TI-227H	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation.	26913601	RID01761	epigenetic regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Neuroblastoma	MALAT1	FGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138685	NA	378938	2247	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BFGF|FGF-2|FGFB|HBGF-2	The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.	26848616	RID01762	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Colorectal cancer	CTNNB1	KCNQ1OT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000269821	GRCh38_11:2608328-2699994	1499	10984	CTNNB|EVR7|MRD19|NEDSDV|armadillo	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	Regulation of functional KCNQ1OT1 lncRNA by beta-catenin.Here, we show that the KCNQ1OT1 transcriptional level was significantly increased in human colorectal cancer cells in which beta-catenin was excessively accumulated in the nucleus. Additionally, overexpression of beta-catenin resulted in an increase in KCNQ1OT1 lncRNA-coated territory. On the other hand, knockdown of beta-catenin resulted in significant decrease of KCNQ1OT1 lncRNA-coated territory and an increase in the mRNA expression of the SLC22A18 and PHLDA2 genes that are regulated by KCNQ1OT1. We showed that beta-catenin can promote KCNQ1OT1 transcription through direct binding to the KCNQ1OT1 promoter. Our evidence indicates that beta-catenin signaling may contribute to development of colorectal cancer by functioning as a novel lncRNA regulatory factor via direct targeting of KCNQ1OT1.	26868975	RID01763	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	UP(BRCA);DATA(GSE111842)
Pancreatic cancer	lncRNA-NUTF2P3-001	KRAS	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-3923)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENST00000448540	GRCh38_9:77580245-77580628	ENSG00000133703	NA	NA	3845	NA	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Hypoxia-induced lncRNA-NUTF2P3-001 contributes to tumorigenesis of pancreatic cancer by derepressing the miR-3923/KRAS pathway.Microarray co-assay for lncRNAs and mRNAs demonstrates that lncRNA-NUTF2P3-001 is remarkably overexpressed in pancreatic cancer and chronic pancreatitis tissues, which positively correlates with KRAS mRNA expression. The dual-luciferase reporter assay further validates that lncRNA-NUTF2P3-001 and 3'UTR of KRAS mRNA competitively bind with miR-3923.	26755660	RID01764	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Hepatocellular carcinoma	MALAT1	EPAS1	positively-E	RNAi;IHC;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	transcriptional regulation	association	protein-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116016	NA	378938	2034	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ECYT4|HIF2A|HLF|MOP2|PASD2|bHLHe73	A MALAT1/HIF-2alpha feedback loop contributes to arsenite carcinogenesis.We have found that MALAT1, a non-coding RNA, is over-expressed in the sera of people exposed to arsenite and in hepatocellular carcinomas (HCCs). In addition, hypoxia-inducible factor (HIF)-2alpha is up-regulated in HCCs, and MALAT1 and HIF-2alpha have a positive correlation in HCC tissues. In turn, HIF-2alpha transcriptionally regulates MALAT1, thus forming a positive feedback loop to ensure expression of arsenite-induced MALAT1 and HIF-2alpha, which are involved in malignant transformation.	26735578	RID01765	transcriptional regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Colon cancer	AOC4P	UHRF1	positively-F	RIP;RNA pull-down assay;ChIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000276043	NA	90586	29128	NA	ICBP90|Np95|RNF106|TDRD22|hNP95|hUHRF1|huNp95	Long noncoding RNA UPAT promotes colon tumorigenesis by inhibiting degradation of UHRF1.UPAT interacts with and stabilizes the epigenetic factor UHRF1 by interfering with its beta-transducin repeat-containing protein (TrCP)-mediated ubiquitination.	26768845	RID01766	interact with protein	NA	NA	UP(PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE86978)
Malignant glioma	DNMT1	MEG3	negatively-E	Methylation-specific polymerase chain reaction;5-aza-2'-deoxycytidine treatment	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis proces(-)s;p53 signaling pathway(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Genome Instability and Mutation	Cancer	Brain glioma	PCG	lncRNA	ENSG00000130816	NA	ENSG00000214548	GRCh38_14:100779410-100861031	1786	55384	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Epigenetic repression of long non-coding RNA MEG3 mediated by DNMT1 represses the p53 pathway in gliomas.In this investigation we showed that the downregulation of MEG3 expression due to hypermethylation of MEG3 was observed in gliomas tissues. In addition, DNMT1 was involved in MEG3 promoter methylation, and was inversely correlated with MEG3 expression in gliomas. The inhibition of DNMT1 repressed the proliferation, clone formation, and induced apoptosis in glioma cells.These results suggest that DNMT1-mediated MEG3 hypermethylation caused the loss of MEG3 expression, followed by the inhibition of the p53 pathways in gliomas.	26676363	RID01767	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	NA
Ovarian cancer	HOTAIR	PIK3R3	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000117461	NA	100124700	8503	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	p55|p55-GAMMA|p55PIK	HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3.The expression of HOTAIR and PIK3R3 in ovarian SKOV3 and OVCAR3 was increased compared with A2780 cells (P<0.05). The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced (p<0.05).	26826873	RID01768	expression association	NA	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Laryngeal squamous cell carcinoma	NEAT1	CDK6	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-107)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105810	NA	283131	1021	LINC00084|NCRNA00084|TncRNA|VINC	MCPH12|PLSTIRE	Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway.NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression.Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107.Based on two databases targetscan (www.targetscan.org) and starbase (starbase.sysu.edu.cn), we found that CDK6 is a potential target of miR-107 while NEAT1 may acts as a regulator of miR-107.	26822763	RID01769	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Nasopharynx carcinoma	HOTAIR	VEGFA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Long noncoding RNA Hotair mediated angiogenesis in nasopharyngeal carcinoma by direct and indirect signaling pathways. In this study, we discovered that lncRNA Hotair was extremely abundant in NPC cells and clinical NPC samples.Our study also demonstrated that Hotair promoted angiogenesis through directly activating the transcription of angiogenic factor VEGFA as well as through GRP78-mediated upregulation of VEGFA and Ang2 expression.	26717040	RID01770	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Nasopharynx carcinoma	HOTAIR	ANGPT2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000091879	NA	100124700	285	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AGPT2|ANG2	Long noncoding RNA Hotair mediated angiogenesis in nasopharyngeal carcinoma by direct and indirect signaling pathways. In this study, we discovered that lncRNA Hotair was extremely abundant in NPC cells and clinical NPC samples.Our study also demonstrated that Hotair promoted angiogenesis through directly activating the transcription of angiogenic factor VEGFA as well as through GRP78-mediated upregulation of VEGFA and Ang2 expression.	26717040	RID01771	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	PANTR1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000110092	NA	100506421	595	LINC01158|linc-Brn1a|linc-POU3F3	BCL1|D11S287E|PRAD1|U21B31	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01772	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	PANTR1	CDK4	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000135446	NA	100506421	1019	LINC01158|linc-Brn1a|linc-POU3F3	CMM3|PSK-J3	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01773	expression association	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	PANTR1	CDKN2C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000123080	NA	100506421	1031	LINC01158|linc-Brn1a|linc-POU3F3	INK4C|p18|p18-INK4C	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01774	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	PANTR1	RB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000139687	NA	100506421	5925	LINC01158|linc-Brn1a|linc-POU3F3	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01775	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	HOTAIR	ELAVL1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000066044	NA	100124700	1994	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ELAV1|HUR|Hua|MelG	A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and Neck Squamous Cell Carcinoma Progression and Metastasis. Moreover, HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. Finally, HuR and HOTAIR levels were positively correlated and significantly up-regulated in tumours samples.We demonstrated the existence of a regulatory loop in which the expression of HOTAIR and HuR is reciprocally and temporally regulated during the metastasis and progression of HNSCC.	27941336;25112469	RID01776	ceRNA or sponge	metastasis	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	MEG3	ILF3	interact	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000129351	NA	55384	3609	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CBTF|DRBF|DRBP76|MMP4|MPHOSPH4|MPP4|MPP4110|NF-AT-90|NF110|NF110b|NF90|NF90a|NF90b|NF90c|NF90ctv|NFAR|NFAR-1|NFAR-2|NFAR110|NFAR2|NFAR90|TCP110|TCP80	The mechanism of adenosine-mediated activation of lncRNA MEG3 and its antitumor effects in human hepatoma cells.The co-expression network of MEG3 was generated by GO analysis and ILF3 was identified as MEG3 binding protein by RNA pulldown and western blot analysis. Ectopic expression of MEG3 increased p53, caspase-3 mRNA and protein levels, decreased MDM2 and cyclin D1 mRNA and protein levels, as well as ILF3 protein expression in HepG2 cells. These findings are the first to identify that adenosine increases MEG3 expression by inhibition of DNA methylation and its antitumor effects is involved in MEG3 activation. ILF3 may participate in the anticancer regulation of MEG3 by interacting with MEG3.	26647875	RID01777	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Small cell lung cancer	HOTAIR	HOXA1	negatively-E	RIP;Bisulfite Sequencing PCR	downregulation	qPCR	NA	NA	chemoresistance(-)	DNA methylation	regulation	NA	cisplatin;adriamycin;etoposide	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105991	NA	100124700	3198	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSAS|HOX1|HOX1F	Long noncoding RNA-HOTAIR affects chemoresistance by regulating HOXA1 methylation in small cell lung cancer cells.Moreover, HOXA1 methylation increased in the resistant cells using bisulfite sequencing PCR. Depletion of HOTAIR reduced HOXA1 methylation by decreasing DNMT1 and DNMT3b expression. The interaction between HOTAIR and HOXA1 was validated by RNA immunoprecipitation. Taken together, our study suggested that HOTAIR mediates chemoresistance of SCLC by regulating HOXA1 methylation and could be utilized as a potential target for new adjuvant therapies against chemoresistance.A total of three anticancer drugs (Cisplatin (CDDP; Shandong, China), Adriamycin (ADM; Jiangsu, China), and Etoposide (VP-16; Jiangsu, China)) were obtained from commercial sources and were dissolved according to the manufacturer's instructions and tested in eight concentrations.	26707824	RID01778	epigenetic regulation	chemoresistance	NA	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Ovarian cancer	TGFB1	MALAT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01779	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Ovarian cancer	MALAT1	MAP2K1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169032	NA	378938	5604	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01780	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MALAT1	MAPK3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102882	NA	378938	5595	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01781	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MALAT1	MAPK14	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112062	NA	378938	1432	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01782	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Ovarian cancer	MALAT1	MAPK8	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000107643	NA	378938	5599	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01783	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	H19 serves as a diagnostic biomarker and up-regulation of H19 expression contributes to poor prognosis in patients with gastric cancer.H19 expression was remarkably increased in GC tissues and cell lines compared with that in the normal control.Furthermore, knockdown of H19 expression by siRNA could inhibit cell migration and invasion in GC cells partly via regulating E-cadherin protein expression. H19 might serve as a promising biomarker for early detection and prognosis prediction of GC.	26774144	RID01784	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung cancer	PCAT6	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228288	GRCh38_1:202810954-202812156	ENSG00000141510	NA	100506696	7157	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	BCC7|BMFS5|LFS1|P53|TRP53	Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells.n this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation.	27458097	RID01785	expression association	metastasis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Lung cancer	PCAT6	MYC	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228288	GRCh38_1:202810954-202812156	ENSG00000136997	NA	100506696	4609	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	MRTL|MYCC|bHLHe39|c-Myc	Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells.n this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation.	27458097	RID01786	expression association	metastasis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	miR-190a	TRERNA1	negatively-F	luciferase reporter assay	downregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000231265	GRCh38_20:50040716-50041504	NA	100887755	NA	LINC00651|treRNA	miR-190a inhibits epithelial-mesenchymal transition of hepatoma cells via targeting the long non-coding RNA treRNA. In this study, we show that miR-190a can silence treRNA post-transcriptionally. Suppression of treRNA by miR-190a led to significant changes of mesenchymal-epithelial transition markers and impaired migration and invasion capability of hepatoma cells. TCGA data indicated that miR-190a exhibited lower expression in hepatoma tissues, especially from patients with vascular tumor invasion, compared to normal tissues.	26608035	RID01787	ceRNA or sponge	NA	NA	NA
Gallbladder cancer	H19	TWIST1	positively-E	IHC	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition.The overexpression of H19 in GBC cells enhanced tumor invasion and promoted EMT by upregulated transcription factor Twist1.	27073719	RID01788	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Acute promyelocytic leukemia	PVT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia.Moreover, PVT1 knockdown by RNA interference led to suppression of the MYC protein level, and cell proliferation was inhibited.	26545364	RID01789	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Embryonic carcinoma	H19	POU5F1	positively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000204531	NA	283120	5460	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01790	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Embryonic carcinoma	H19	NANOG	positively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111704	NA	283120	79923	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01791	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Embryonic carcinoma	H19	CDH1	negatively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01792	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Embryonic carcinoma	H19	FUT4	negatively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000196371	NA	283120	2526	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01793	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)
Liver cancer	miR-675	H19	positively-E	RIP;ChIP;IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer.Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1alpha expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3) , histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac).Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. Strikingly, H19 may induce and activate tumor-specific pyruvate kinase M2 (PKM2) which is essential for the Warburg effect in its dimer and for gene expression in its teramer during tumorigenesis.	26376677	RID01794	epigenetic regulation	NA	NA	UP(NSCLC);DATA(GSE74639)
Liver cancer	H19	PKM	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000067225	NA	283120	5315	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer.Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1alpha expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3) , histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac).Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. Strikingly, H19 may induce and activate tumor-specific pyruvate kinase M2 (PKM2) which is essential for the Warburg effect in its dimer and for gene expression in its teramer during tumorigenesis.	26376677	RID01795	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	MYC	H19	positively-E	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-);cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000130600	GRCh38_11:1995176-2001470	4609	283120	MRTL|MYCC|bHLHe39|c-Myc	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	c-Myc-regulated long non-coding RNA H19 indicates a poor prognosis and affects cell proliferation in non-small-cell lung cancer.Multivariate analyses found that H19 expression could serve as an independent prognostic factor for overall survival of NSCLC. Moreover, chromatin immunoprecipitation (ChIP) assays revealed that H19 was a direct transcriptional target of c-Myc. And, knockdown of H19 significantly inhibited NSCLC cell proliferation both in vitro and in vivo. In conclusion, our study demonstrated that H19 is involved in the oncogenesis of NSCLC, and H19 may be a potential diagnostic and target for new therapies in patients with NSCLC.c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively.	26482621;26722426	RID01796	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(NSCLC);DATA(GSE74639)
Non-small cell lung cancer	H19	miR-107	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively.	26722426	RID01797	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Colorectal cancer	ETS1	BANCR	negatively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(+);cell invasion(+);cell metastasis(+)	histone modification	regulation	NA	fentanyl	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000134954	NA	ENSG00000278910	GRCh38_9:69296682-69311111	2113	100885775	ETS-1|EWSR2|c-ets-1|p54	LINC00586	Fentanyl inhibits the invasion and migration of colorectal cancer cells via inhibiting the negative regulation of Ets-1 on BANCR.Fentanyl induced BANCR upregulation and Ets-1 downregulation in CRC cells. Further studies showed that Ets-1 negatively regulated BANCR expression via the deacetylation of histones H3 within BANCR promoter.	26296467	RID01798	epigenetic regulation	metastasis,chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Malignant glioma	CRNDE	XIAP	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);tumor malignant transformation(+)	ceRNA(miR-186)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000101966	NA	NA	331	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2. In conclusion, CRNDE played an oncogenic role of GSCs through the negative regulation of miR-186. Both CRNDE and miR-186 could be regarded as potential targets in the glioma therapy.	26231038	RID01799	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	CRNDE	PAK5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);tumor malignant transformation(+)	ceRNA(miR-186)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000101349	NA	NA	57144	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2. In conclusion, CRNDE played an oncogenic role of GSCs through the negative regulation of miR-186. Both CRNDE and miR-186 could be regarded as potential targets in the glioma therapy.	26231038	RID01800	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	NA
Malignant glioma	HOTAIR	FGF1	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113578	NA	100124700	2246	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AFGF|ECGF|ECGF-beta|ECGFA|ECGFB|FGF-1|FGF-alpha|FGFA|GLIO703|HBGF-1|HBGF1	Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326.Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.These results suggested that FGF1 was a direct target of miR-326.	26183397	RID01801	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Lung cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/beta-catenin signaling pathway.The present study detected that the expression levels of Meg3 were significantly lower in cisplatin-resistant A549/DDP lung cancer cells, compared with those in parental A549 cells. The results of the present study also demonstrated that the Meg3-mediated chemosensitivity enhancement was associated with the induction of cell-cycle arrest and increased apoptosis, through regulation of p53, beta-catenin and survivin, which is a target gene of the WNT/beta-catenin signaling pathway.	26059239	RID01802	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Lung cancer	MEG3	CTNNB1	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168036	NA	55384	1499	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/beta-catenin signaling pathway.The present study detected that the expression levels of Meg3 were significantly lower in cisplatin-resistant A549/DDP lung cancer cells, compared with those in parental A549 cells. The results of the present study also demonstrated that the Meg3-mediated chemosensitivity enhancement was associated with the induction of cell-cycle arrest and increased apoptosis, through regulation of p53, beta-catenin and survivin, which is a target gene of the WNT/beta-catenin signaling pathway.	26059239	RID01803	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Brain cancer	TUG1	HSF2	positively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	blood-tumor barrier(-)	ceRNA(miR-144)	regulation	NA	NA	NA	NA	Cancer	Brain cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000025156	NA	55000	3298	LINC00080|NCRNA00080|TI-227H	HSF 2|HSTF 2	The long noncoding RNA TUG1 regulates blood-tumor barrier permeability by targeting miR-144.Both bioinformatics and luciferase reporter assays demonstrated that TUG1 influenced BTB permeability via binding to miR-144. Furthermore, Knockdown of TUG1 also down-regulated Heat shock transcription factor 2 (HSF2), a transcription factor of the heat shock transcription factor family, which was defined as a direct and functional downstream target of miR-144. HSF2 up-regulated the promoter activities and interacted with the promoters of ZO-1, occludin, and claudin-5 in GECs. In conclusion, our results indicate that knockdown of TUG1 increased BTB permeability via binding to miR-144 and then reducing EC tight junction protein expression by targeting HSF2. Thus, TUG1 may represent a useful future therapeutic target for enhancing BTB permeability.	26078353	RID01804	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE67939)
Hepatocellular carcinoma	CDKN2B-AS1	KLF2	negatively-E	RIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000127528	NA	100048912	10365	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	LKLF	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID01805	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Her2-receptor positive breast cancer	LNCRNA-ATB	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	trastuzumab	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000148516	NA	114004396	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.We identified long noncoding RNA activated by TGF-beta (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients.SKBR-3 which is HER-2 overexpressed breast cancer cell line. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. lnc-ATB shares regulatory miR-200c with ZEB1 and ZNF 217 which has been proven to be the direct targets of miR-200c in TR SKBR-3 cells.	25871474	RID01806	ceRNA or sponge	metastasis,chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Her2-receptor positive breast cancer	LNCRNA-ATB	ZNF217	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	trastuzumab	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000171940	NA	114004396	7764	NA	ZABC1	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.We identified long noncoding RNA activated by TGF-beta (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients.SKBR-3 which is HER-2 overexpressed breast cancer cell line. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. lnc-ATB shares regulatory miR-200c with ZEB1 and ZNF 217 which has been proven to be the direct targets of miR-200c in TR SKBR-3 cells.	25871474	RID01807	ceRNA or sponge	metastasis,chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Her2-receptor positive breast cancer	LNCRNA-ATB	PTEN	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	ceRNA(miR-21)	regulation	NA	trastuzumab	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000171862	NA	114004396	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.Lapatinib upregulates GAS5 in trastuzumab-resistant breast cancer through mTOR pathway. Additionally, inhibition of mTOR by rapamycin increases the expression of GAS5.In summary, GAS5, regulated by mTOR pathway, serves as a ceRNA of miR-21 to regulate PTEN in the development of breast cancer trastuzumab resistance (Figure 5c).	25871474	RID01808	ceRNA or sponge	metastasis,chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Prostate cancer	MTOR	GAS5	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000198793	NA	ENSG00000234741	GRCh38_1:173858559-173868882	2475	60674	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	NCRNA00030|SNHG2	Reciprocal regulation of GAS5 lncRNA levels and mTOR inhibitor action in prostate cancer cells.mTOR inhibition enhances GAS5 transcript levels in certain prostate cancer cell lines. This selectivity is likely to be related to endogenous GAS5 expression levels, since GAS5 lncRNA is itself required for mTOR inhibitor action in prostate cancer cells. This lncRNA promotes the apoptosis of prostate cancer cells and its levels decline as prostate cancer cells acquire castrate-resistance, so that enhancing GAS5 expression may improve the effectiveness of chemotherapies.	25650269	RID01809	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Triple-receptor negative breast cancer	miR-148a	HOTAIR	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer. In this study, we found that HOTAIR was increased in the peripheral blood mononuclear cells and cancer tissues from breast cancer patients, and was especially higher in patients with metastatic breast cancer. In addition, we found that estrogen promoted HOTAIR through its receptor GPER and estrogen-induced breast cancer cell migration was reversed by deleting HOTAIR in TN breast cancer cells MDA-MB-231 and BT549. Furthermore, we identified that E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients.	25928008	RID01810	expression association	metastasis	NA	NA
Pancreatic ductal adenocarcinoma	HOTTIP	HOXA13	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+)	NA	regulation	NA	gemcitabine	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	The long non-coding RNA HOTTIP promotes progression and gemcitabine resistance by regulating HOXA13 in pancreatic cancer.Microarray analyses revealed that HOTTIP was one of the most significantly upregulated lncRNAs in PDAC tissues compared with pancreatic tissues.Furthermore, knockdown of HOXA13 by RNA interference (siHOXA13) revealed that HOTTIP promoted PDAC cell proliferation, invasion, and chemoresistance, at least partly through regulating HOXA13. As a crucial tumor promoter, HOTTIP promotes cell proliferation, invasion, and chemoresistance by modulating HOXA13. Therefore, the HOTTIP/HOXA13 axis is a potential therapeutic target and molecular biomarker for PDAC.	25889214	RID01811	expression association	chemoresistance	NA	UP(LIHC);DATA(GSE117623)
Prostate cancer	AR	PCGEM1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000227418	GRCh38_2:192749845-192776899	367	64002	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LINC00071|NCRNA00071|PCAT9	The long non-coding RNA PCGEM1 is regulated by androgen receptor activity in vivo.PCGEM1 was sharply down-regulated following castration and up-regulated upon AR activation in vivo. PCGEM1 and PRNCR1 were implicated in progression of prostate cancer (PCa) as transcriptional co-regulators of the androgen receptor (AR).	25744782	RID01812	expression association	NA	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)	UP(PAAD);DATA(GSE60407)
Osteosarcoma	miR-9	MALAT1	negatively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	17beta-estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner. Here we found that the high dose of E2 treatment upregulated miR-9 thus posttranscriptionally regulated MALAT-1 RNA level in OS cells, and then the downregulation of MALAT-1 inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) processes in the E2-dose dependent and ER-independent ways.	25592968	RID01813	expression association	metastasis	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	CCAT1	HMGA2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(let-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000149948	NA	100507056	8091	CARLO5|CARLo-5|onco-lncRNA-40	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.CCAT1 levels are markedly increased in HCC tissues compared with pair-matched noncancerous hepatic tissues. CCAT1 promotes the proliferation and migration of HCC cells. CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7.	25884472	RID01814	ceRNA or sponge	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	CCAT1	MYC	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(let-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.CCAT1 levels are markedly increased in HCC tissues compared with pair-matched noncancerous hepatic tissues. CCAT1 promotes the proliferation and migration of HCC cells. CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7.	25884472	RID01815	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Neuroblastoma	NBAT1	REST	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000084093	NA	729177	5978	CASC14|NBAT-1	DFNA27|GINGF5|HGF5|NRSF|WT6|XBR	The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation. CpG methylation and a high-risk neuroblastoma associated SNP on chromosome 6p22 functionally contribute to NBAT-1 differential expression. Loss of NBAT-1 increases cellular proliferation and invasion. It controls these processes via epigenetic silencing of target genes. NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST.	25517750	RID01816	expression association	NA	NA	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Breast cancer	HOTAIR	miR-7	negatively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway.In addition, the downregulation of miR-7 in BCSCs may be indirectly attributed to lincRNA HOTAIR by modulating the expression of HoxD10 that promotes the expression of miR-7.	25070049	RID01817	expression association	NA	NA	NA
Hepatocellular carcinoma	SPP1	HOTAIR	positively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	PCG	lncRNA	ENSG00000118785	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6696	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Osteopontin enhances the expression of HOTAIR in cancer cells via IRF1.Interestingly, our data demonstrated that OPN could regulate PI3K/AKT and IRF1 expression and signaling, thereby influencing the expression of HOTAIR. We therefore conclude that OPN, as an extracellular matrix protein, can stimulate the expression of HOTAIR by attenuating the inhibitory effect of IRF1, and this results in promotion of the invasion and metastasis of cancer cells.	24999034	RID01818	expression association	metastasis	UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE86978)	NA
Non-small cell lung cancer	EZH2	SPRY4-IT1	negatively-E	IHC;RNAi;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000106462	NA	NA	GRCh38_5:142317636-142318322	2146	100642175	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	SPRIGHTLY	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01819	epigenetic regulation	metastasis	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Non-small cell lung cancer	SPRY4-IT1	CDH1	positively-E	IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000039068	NA	100642175	999	SPRIGHTLY	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01820	expression association	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Non-small cell lung cancer	SPRY4-IT1	VIM	positively-E	IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000026025	NA	100642175	7431	SPRIGHTLY	NA	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01821	expression association	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Endometrial cancer	LINC-ROR	miR-145	negatively-F	RNAi;site-directed mutagenesis kit	upregulation	qPCR;FISH	NA	NA	cell differentiation(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	24589415	RID01822	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Cancer	TGFB1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	regulation	NA	NA	CSC	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7040	100124700	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines. We found that treatment with TGF-beta1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-beta1, and also the colony-forming capacity of colon and breast cancer cells.	24022994	RID01823	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Cancer	miR-21	GAS5	negatively-F	RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cancer	miRNA	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Negative regulation of lncRNA GAS5 by miR-21.This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Importantly, there is a putative miR-21-binding site in exon 4 of GAS5; deletion of the miR-21-binding site abolishes this activity.We further show that the biotin-labeled GAS5-RNA probe is able to pull down the key component (AGO2) of the RNA-induced silencing complex (RISC) and we subsequently identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs. Together, these results suggest that miR-21 targets not only tumor-suppressive protein-coding genes but also lncRNA GAS5.	23933812	RID01824	ceRNA or sponge	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Osteosarcoma	E2F3	ERICD	positively-E	ChIP	downregulation	qPCR	NA	NA	apoptosis process(-);DNA damage(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Evading Apoptosis;Genome Instability and Mutation	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000112242	NA	ENSG00000280303	GRCh38_8:140636281-140638283	1871	104355217	E2F-3	ERIC|LINC01130|TCONS_00014875	The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage.Here, we report that lncRNA XLOC 006942, which we named ERIC, is regulated by E2F1 and, most probably, also E2F3. We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Our data identify ERIC as a novel lncRNA that is transcriptionally regulated by E2Fs, and restricts apoptosis induced by E2F1, as well as by DNA damage.	24168400	RID01825	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)	NA
Osteosarcoma	E2F1	ERICD	positively-E	ChIP	downregulation	qPCR	NA	NA	apoptosis process(-);DNA damage(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Evading Apoptosis;Genome Instability and Mutation	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000101412	NA	ENSG00000280303	GRCh38_8:140636281-140638283	1869	104355217	E2F-1|RBAP1|RBBP3|RBP3	ERIC|LINC01130|TCONS_00014875	The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage.Here, we report that lncRNA XLOC 006942, which we named ERIC, is regulated by E2F1 and, most probably, also E2F3. We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Our data identify ERIC as a novel lncRNA that is transcriptionally regulated by E2Fs, and restricts apoptosis induced by E2F1, as well as by DNA damage.	24168400	RID01826	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Osteosarcoma	loc285194	miR-211	negatively-F	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709788-116717040	NA	NA	NA	NA	NA	NA	LncRNA loc285194 is a p53-regulated tumor suppressor.In this study, we show that loc285194 is a p53 transcription target; ectopic expression of loc285194 inhibits tumor cell growth both in vitro and in vivo. Through deletion analysis, we identify an active region responsible for tumor cell growth inhibition within exon 4, which harbors two miR-211 binding sites. Importantly, this loc285194-mediated growth inhibition is in part due to specific suppression of miR-211. Together, these results suggest that loc285194 is a p53-regulated tumor suppressor, which acts in part through repression of miR-211.	23558749	RID01827	ceRNA or sponge	NA	NA	NA
Cancer	RASSF1-AS1	RASSF1	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE5823;GSE11118;GSE10879;GSE12056;GSE13471	GSE5823.zip;GSE11118.zip;GSE10879.zip;GSE12056.zip;GSE13471.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000281358	GRCh38_3:50337511-50338300	ENSG00000068028	NA	102060282	11186	ANRASSF1	NA	The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation.ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region.	23990798	RID01828	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	RAB4B-EGLN2	EGLN2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000171570	GRCh38_19:40778242-40808418	ENSG00000269858	NA	100529264	112398	EGLN2|EIT-6|EIT6|HIF-PH1|HPH-1|HPH-3|PHD1|RERT-lncRNA	EIT-6|EIT6|HIF-PH1|HIFPH1|HPH-1|HPH-3|PHD1	An insertion/deletion polymorphism within RERT-lncRNA modulates hepatocellular carcinoma risk.Genotype-phenotype correlation studies showed that the deletion allele was significantly correlated with higher expression of both EGLN2 and RERT-lncRNA [a long noncoding RNA whose sequence overlaps with Ras-related GTP-binding protein 4b (RAB4B) and EGLN2)] in vivo and in vitro. Furthermore, RERT-lncRNA expression was also significantly correlated with EGLN2 expression in vivo, consistent with in vitro gain-of-function study that showed overexpressing RERT-lncRNA upregulated EGLN2.Taken together, rs10680577 contributes to hepatocarcinogenesis, possibly by affecting RERT-lncRNA structure and subsequently EGLN2 expression, making it a promising biomarker for early diagnosis of HCC.	23026137	RID01829	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Cancer	MEG3	GDF15	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Activation of p53 by MEG3 non-coding RNA.We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter.Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways.	17569660	RID01830	transcriptional regulation	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Cancer	MEG3	TP53	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Activation of p53 by MEG3 non-coding RNA.We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter.Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways.	17569660	RID01831	transcriptional regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	H19	ABCB1	negatively-E	western blot;RNAi;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	chemoresistance(+)	DNA methylation	regulation	NA	doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells.In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells.H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Antisense H19 oligonucleotides transfection induced a marked increase in the percentage of MDR1 promoter methylation and decrease in MDR1 expression in R-HepG2 cells. Thus, the H19 gene is believed to induce P-glycoprotein expression and MDR1-associated drug resistance at least in liver cancer cells through regulation of MDR1 promoter methylation.	17297456	RID01832	epigenetic regulation	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Breast cancer	E2F1	H19	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000130600	GRCh38_11:1995176-2001470	1869	283120	E2F-1|RBAP1|RBBP3|RBP3	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	H19 mRNA-like noncoding RNA promotes breast cancer cell proliferation through positive control by E2F1. We show here that H19 transcription is up-regulated during the S-phase of growth-stimulated cells and that the H19 promoter is activated by E2F1 in breast cancer cells. Consistently, we demonstrate by chromatin immunoprecipitation assays that endogenous E2F1 is recruited to the H19 promoter in vivo. we conclude that the H19 RNA is actively linked to E2F1 to promote cell cycle progression of breast cancer cells.	15985428	RID01833	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(NSCLC);DATA(GSE74639)
Triple-receptor negative breast cancer	MYC	SNHG12	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000197989	GRCh38_1:28578538-28583132	4609	85028	MRTL|MYCC|bHLHe39|c-Myc	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer.SNHG12 is upregulated in TNBC. Mechanistic investigations show that SNHG12 is a direct transcriptional target of c-MYC. Silencing SNHG12 expression inhibits TNBC cells proliferation and apoptosis promotion, whereas SNHG12 overexpression has the opposite effect. In addition, we reveal that SNHG12 may promote cells migration by regulating MMP13 expression.	28337281	RID01834	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Triple-receptor negative breast cancer	SNHG12	MMP13	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000137745	NA	85028	4322	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	CLG3|MANDP1|MDST|MMP-13	C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer.SNHG12 is upregulated in TNBC. Mechanistic investigations show that SNHG12 is a direct transcriptional target of c-MYC. Silencing SNHG12 expression inhibits TNBC cells proliferation and apoptosis promotion, whereas SNHG12 overexpression has the opposite effect. In addition, we reveal that SNHG12 may promote cells migration by regulating MMP13 expression.	28337281	RID01835	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Cervical cancer	HOTAIR	MTOR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(+);apoptosis process(-)	NA	regulation	NA	propofol	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000198793	NA	100124700	2475	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer	26523512	RID01836	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Oral squamous cell carcinoma	MALAT1	CTNNB1	positively-E	IHC	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of beta-catenin and NF-kB were attenuated, while elevated MALAT1 level triggered the expression of beta-catenin and NF-kB. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo.	26522444	RID01837	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Oral squamous cell carcinoma	MALAT1	NFKB1	positively-E	IHC	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of beta-catenin and NF-kB were attenuated, while elevated MALAT1 level triggered the expression of beta-catenin and NF-kB. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo.	26522444	RID01838	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LNCRNA-ATB	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000039068	NA	114004396	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA-ATB mediated E-cadherin repression promotes the progression of colon cancer and predicts poor prognosis.Long non-coding RNA-activated by TGF-beta (lncRNA-ATB) promotes the invasion-metastasis cascade in hepatocellular carcinoma via downregulating E-cadherin (E-cad) and inducing epithelial-to- mesenchymal transition (EMT) and is clinically significant in human colon cancer.	26487301	RID01839	expression association	metastasis,prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colon cancer	LNCRNA-ATB	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000039068	NA	114004396	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA-ATB mediated E-cadherin repression promotes the progression of colon cancer and predicts poor prognosis.Reduction of lncRNA-ATB increased expression of epithelial markers E-cad, ZO-1, and decreased expression of mesenchymal markers ZEB1 and N-cadherin (N-cad), and significantly influenced colon cancer cell progression. Long non-coding RNA-activated by TGF-beta may act on colon tumorigenesis by suppressing E-cad expression and promoting EMT process, and lncRNA-ATB inhibition may provide a promising therapeutic option for suppressing colon cancer progression.	26487301	RID01840	expression association	prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Neuroblastoma	MIR100HG	miR-125b-1	positively-E	ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	host	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. We also demonstrate that linc-NeD125 functions independently of the hosted microRNA, by reducing cell proliferation and activating the antiapoptotic factor BCL-2.	26480000	RID01841	expression association	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	NA
Neuroblastoma	MIR100HG	BCL2	positively-E	RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000171791	NA	399959	596	AGD1|linc-NeD125|lncRNA-N2	Bcl-2|PPP1R50	Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. We also demonstrate that linc-NeD125 functions independently of the hosted microRNA, by reducing cell proliferation and activating the antiapoptotic factor BCL-2.	26480000	RID01842	expression association	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	PACERR	PTGS2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000273129	GRCh38_1:186680622-186681446	ENSG00000073756	NA	103752588	5743	PACER|PTGS2-AS1|PTGS2AS1	COX-2|COX2|GRIPGHS|PGG/HS|PGHS-2|PHS-2|hCox-2	P50-associated COX-2 extragenic RNA (PACER) overexpression promotes proliferation and metastasis of osteosarcoma cells by activating COX-2 gene.Downregulation of PACER significantly suppressed the expression of COX-2, and the effects of PACER on cell proliferation and invasion were rescued by COX-2 overexpression.Taken together, these findings suggest that PACER promotes proliferation and metastasis of osteosarcoma cells by activating the COX-2 gene and its own expression was influenced by DNA methylation.	26476537	RID01843	expression association	metastasis	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Diffuse large B-cell lymphoma	TP53COR1	CCND1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000110092	NA	102800311	595	TRP53COR1|linc-p21|lincRNA-p21	BCL1|D11S287E|PRAD1|U21B31	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01844	expression association	chemoresistance	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Diffuse large B-cell lymphoma	TP53COR1	CDK4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000135446	NA	102800311	1019	TRP53COR1|linc-p21|lincRNA-p21	CMM3|PSK-J3	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01845	expression association	chemoresistance	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Diffuse large B-cell lymphoma	TP53COR1	CDKN1A	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000124762	NA	102800311	1026	TRP53COR1|linc-p21|lincRNA-p21	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01846	expression association	chemoresistance	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	WT1-AS	WT1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);apoptosis process(+);JAK/STAT signaling pathway(-)	transcriptional regulation	binding/interaction	RNA-DNA	doxorubicin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000183242	GRCh38_11:32435518-32458769	ENSG00000184937	NA	51352	7490	WIT-1|WIT1|WT1-AS1|WT1AS	AWT1|GUD|NPHS4|WAGR|WIT-2|WT33	WT1-AS promotes cell apoptosis in hepatocellular carcinoma through down-regulating of WT1.WT1-AS expression correlated negatively with WT1 expression in HCC tumor tissue. Kaplan-Meier curve analysis revealed that WT1-AS expression is a reliable indicator of HCC prognosis. The downregulation of WT1 expression by WT1-AS promoted cell apoptosis by suppressing the JAK/STAT3 signaling pathway. Bioinformatics analysis showed that WT1-AS downregulates WT1 by binding to the TATA region of the WT1 promotor. WT1-AS was also able to reverse WT1-mediated resistance to Dox based chemotherapy in HCC cells.	26462627	RID01847	transcriptional regulation	chemoresistance,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Clear cell renal cell carcinoma	MALAT1	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma.Together these data indicated that by binding miR-200s family, especially miR-200c, MALAT1 acts as a ceRNA for the target ZEB2 mRNA thereby modulating the derepression of ZEB2 and imposing an additional level of post-transcriptional regulation. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC.	26461224	RID01848	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	EZH2	HOTAIR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2146	100124700	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Analysis of the Polycomb-related lncRNAs HOTAIR and ANRIL in bladder cancer.We also observed a significant correlation between EZH2 and HOTAIR expression levels. Using overexpression, knockdown, and pharmacological approaches in bladder cancer cell lines, we also observed that EZH2 regulates HOTAIR expression.The observed HOTAIR regulation by EZH2 and the possibility of modulating EZH2 activity with specific inhibitors open new possible paths to be explored in bladder cancer therapy.	26457124	RID01849	expression association	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	NA
Hepatocellular carcinoma	STAT3	WSPAR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000249073	GRCh38_5:133913677-133917269	6774	105664404	ADMIO|ADMIO1|APRF|HIES	LncTCF7|TCONS_00009511	Long noncoding RNA lncTCF7, induced by IL-6/STAT3 transactivation, promotes hepatocellular carcinoma aggressiveness through epithelial-mesenchymal transition. we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HCC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HCC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies.	26452542	RID01850	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Gastric cancer	WT1-AS	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000183242	GRCh38_11:32435518-32458769	ENSG00000100030	NA	51352	5594	WIT-1|WIT1|WT1-AS1|WT1AS	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Decreased expression of long non-coding RNA WT1-AS promotes cell proliferation and invasion in gastric cancer.Finally, we found that WT1-AS overexpression could decrease ERK protein phosphorylation. Our study indicates that WT1-AS is significantly down-regulated in gastric cancers and may be correlated with tumor progression.	26449525	RID01851	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gallbladder cancer	FAM30A	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000226777	GRCh38_14:105917979-105932642	ENSG00000168036	NA	9834	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Noncoding RNA KIAA0125 Potentiates Cell Migration and Invasion in Gallbladder Cancer. Moreover, the expression of beta-Catenin was increased and the expression of Vimentin was decreased in GBC-SD/M cells after KIAA0125 knockdown.	26448925	RID01852	expression association	NA	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gallbladder cancer	FAM30A	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000226777	GRCh38_14:105917979-105932642	ENSG00000026025	NA	9834	7431	NA	NA	Long Noncoding RNA KIAA0125 Potentiates Cell Migration and Invasion in Gallbladder Cancer. Moreover, the expression of beta-Catenin was increased and the expression of Vimentin was decreased in GBC-SD/M cells after KIAA0125 knockdown.	26448925	RID01853	expression association	NA	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Liver fibrosis	TP53COR1	CDKN1A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000124762	NA	102800311	1026	TRP53COR1|linc-p21|lincRNA-p21	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	lincRNA-p21 inhibits hepatic stellate cell activation and liver fibrogenesis via p21.Our results show that over-expression of lincRNA-p21 promotes up-regulation of p21 at both the mRNA and protein levels. Furthermore, lincRNA-p21 inhibited cell-cycle progression and proliferation of primary HSCs through enhancement of p21 expression.	26433205	RID01854	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Thyroid cancer	PVT1	TSHR	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000165409	NA	5820	7253	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CHNG1|LGR3|hTSHR-I	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID01855	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Thyroid cancer	PVT1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000110092	NA	5820	595	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID01856	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	GAS1RR	GAS1	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000180447	NA	100506834	2619	LncRNA-Hh	NA	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01857	transcriptional regulation	NA	NA	NA
Breast cancer	TWIST1	GAS1RR	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000122691	NA	ENSG00000226237	GRCh38_9:86948666-87002033	7291	100506834	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	LncRNA-Hh	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01858	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	NA
Breast cancer	GAS1RR	SOX2	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000181449	NA	100506834	6657	LncRNA-Hh	ANOP3|MCOPS3	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01859	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Breast cancer	GAS1RR	POU5F1	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000204531	NA	100506834	5460	LncRNA-Hh	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01860	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colon cancer	YAP1	RMRP	positively-E	ChIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);Hippo/YAP signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000269900	GRCh38_9:35657751-35658018	10413	6023	COB1|YAP|YAP2|YAP65|YKI	CHH|NME1|RMRPR|RRP2	Wnt activated beta-catenin and YAP proteins enhance the expression of non-coding RNA component of RNase MRP in colon cancer cells.As expected, Wnt signal activation significantly induced the RMRP transcription thru beta-catenin and YAP transcription factors. More importantly, YAP protein was critical for RMRP transcription by association to the proximal site near the transcription start site of the RMRP gene, a Pol III promoter, along with beta-catenin and TBX5 proteins. We propose that the interplay of Wnt and Hippo signaling pathways could regulate target genes, coding or non-coding, by the beta-catenin/YAP/TBX5 transcription complex in cancer cells.Association of beta-catenin and YAP to the RMRP promoter in conjunction with DNA binding proteins, TCF and TBX5, lead to the enhanced expression of RMRP.	26415221	RID01861	transcriptional regulation	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)
Colon cancer	CTNNB1	RMRP	positively-E	ChIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);Hippo/YAP signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000269900	GRCh38_9:35657751-35658018	1499	6023	CTNNB|EVR7|MRD19|NEDSDV|armadillo	CHH|NME1|RMRPR|RRP2	Wnt activated beta-catenin and YAP proteins enhance the expression of non-coding RNA component of RNase MRP in colon cancer cells	26415221	RID01862	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)
Osteosarcoma	FOXC2-AS1	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000085563	NA	103752587	5243	ODRUL	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	A long non-coding RNA contributes to doxorubicin resistance of osteosarcoma.LncRNA microarray revealed that lncRNA ODRUL was the most up-regulated expressed in the doxorubicin-resistant OS cell line.In addition, we found that the expression of classical drug resistance-related ATP-binding cassette, subfamily B, member 1 (ABCB1) gene was decreased after the lncRNA ODRUL knockdown. Thus, we concluded that lncRNA ODRUL may act as a pro-doxorubicin-resistant molecule through inducing the expression of the classical multidrug resistance-related ABCB1 gene in osteosarcoma cells.	26408180	RID01863	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Gastric cancer	HOXA-AS2	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124762	NA	285943	1026	HOXA3as	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01864	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	HOXA-AS2	PLK3	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000173846	NA	285943	1263	HOXA3as	CNK|FNK|PLK-3|PRK	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01865	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE75367)
Gastric cancer	HOXA-AS2	DDIT3	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000175197	NA	285943	1649	HOXA3as	AltDDIT3|C/EBPzeta|CEBPZ|CHOP|CHOP-10|CHOP10|GADD153	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01866	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	SP1	MALAT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6667	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1 cooperates with Sp3 to upregulate MALAT1 expression in human hepatocellular carcinoma. The results showed a high expression of Sp1, Sp3 and MALAT1 in HCC vs. paired non-tumor liver tissues, which was associated with the AFP level (Sp1, r=7.44, P=0.0064; MALAT1, r=12.37, P=0.0004). Co-silencing of Sp1 and Sp3 synergistically repressed MALAT1 expression. Sp1 binding inhibitor, mithramycin A (MIT), also inhibited MALAT1 expression in HCC cells. In conclusion, the upstream of MALAT1 contains five Sp1/3 binding sites, which may be responsible for MALAT1 transcription. Inhibitors, such as MIT, provide a potential therapeutic strategy for HCC patients with MALAT1 overexpression.	26352013	RID01867	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	SP3	MALAT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000172845	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6670	378938	SPR2	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1 cooperates with Sp3 to upregulate MALAT1 expression in human hepatocellular carcinoma. The results showed a high expression of Sp1, Sp3 and MALAT1 in HCC vs. paired non-tumor liver tissues, which was associated with the AFP level (Sp1, r=7.44, P=0.0064; MALAT1, r=12.37, P=0.0004). Co-silencing of Sp1 and Sp3 synergistically repressed MALAT1 expression. Sp1 binding inhibitor, mithramycin A (MIT), also inhibited MALAT1 expression in HCC cells. In conclusion, the upstream of MALAT1 contains five Sp1/3 binding sites, which may be responsible for MALAT1 transcription. Inhibitors, such as MIT, provide a potential therapeutic strategy for HCC patients with MALAT1 overexpression.	26352013	RID01868	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Burkitt lymphoma	MYC	MINCR	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lymphoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000253716	GRCh38_8:143280161-143281690	4609	100507316	MRTL|MYCC|bHLHe39|c-Myc	LINC01604	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01869	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)
Burkitt lymphoma	MINCR	AURKA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000087586	NA	100507316	6790	LINC01604	AIK|ARK1|AURA|BTAK|PPP1R47|STK15|STK6|STK7	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01870	expression association	NA	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Burkitt lymphoma	MINCR	AURKB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000178999	NA	100507316	9212	LINC01604	AIK2|AIM-1|AIM1|ARK-2|ARK2|AurB|IPL1|PPP1R48|STK-1|STK12|STK5|aurkb-sv1|aurkb-sv2	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01871	expression association	NA	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)	DOWN(PAAD,BRCA);UP(SKCM);DATA(GSE60407,GSE38495,GSE111842)
Burkitt lymphoma	MINCR	CDT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000167513	NA	100507316	81620	LINC01604	DUP|RIS2	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01872	expression association	NA	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)	UP(PAAD);DATA(GSE40174)
Liver cancer	UCA1	HULC	positively-E	ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	DNA methylation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	lncRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000285219	GRCh38_6:8435568-9294133	652995	728655	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HCCAT1|LINC00078|NCRNA00078	Long Noncoding RNA CUDR Regulates HULC and beta-Catenin to Govern Human Liver Stem Cell Malignant Differentiation. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like cells by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On the other hand, excessive CUDR triggers hepatocyte-like cells malignant transformation. Mechanistically, we identify CUDR causes highly upregulated in liver cancer (HULC) and beta-catenin abnormal expression by inhibiting HULC promoter methylation and promoting beta-catenin promoter-enhancer chromatin looping formation mediated by CUDR-ccctc-binding factor (CTCF) complex, which recruits more RNA polII and P300. Strikingly, HULC and beta-catenin activity are crucial for CUDR oncogenic function.	26347501	RID01873	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	NA
Liver cancer	UCA1	CTNNB1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	chromatin looping;enhancer	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168036	NA	652995	1499	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Noncoding RNA CUDR Regulates HULC and beta-Catenin to Govern Human Liver Stem Cell Malignant Differentiation. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like cells by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On the other hand, excessive CUDR triggers hepatocyte-like cells malignant transformation. Mechanistically, we identify CUDR causes highly upregulated in liver cancer (HULC) and beta-catenin abnormal expression by inhibiting HULC promoter methylation and promoting beta-catenin promoter-enhancer chromatin looping formation mediated by CUDR-ccctc-binding factor (CTCF) complex, which recruits more RNA polII and P300. Strikingly, HULC and beta-catenin activity are crucial for CUDR oncogenic function.	26347501	RID01874	chromatin looping	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Osteoarthritis	PCGEM1	miR-770-5p	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	PCGEM1 stimulates proliferation of osteoarthritic synoviocytes by acting as a sponge for miR-770.the results revealed that prostate cancer gene expression marker 1 (PCGEM1) was significantly overexpressed in osteoarthritic synoviocytes. We demonstrate that PCGEM1 act as sponge lncRNA for miR-770 that regulates proliferation/apoptosis and autophagy, and suggest PCGEM1 as possible target for OA therapy.	26340084	RID01875	ceRNA or sponge	NA	UP(PAAD);DATA(GSE60407)	NA
Cancer	MALINC1	PURA	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(+);cell cycle(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000245146	GRCh38_5:140071312-140109274	ENSG00000185129	NA	100505636	5813	LINC01024|MA-linc1	MRD31|PUR-ALPHA|PUR1|PURALPHA	A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel.We further demonstrate that MA-linc1 predominantly functions in cis to repress expression of its neighboring gene, Puralpha, which is often deleted in human cancers and whose ectopic expression inhibits cell cycle progression.In agreement with its suggested role in M phase, inhibition of MA-linc1 enhances apoptotic cell death induced by the antimitotic drug, Paclitaxel and this enhancement of apoptosis is rescued by Puralpha knockdown.	26337085	RID01876	expression association	chemoresistance	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	PRDM16-DT	CDKN2B	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177133	GRCh38_1:3059615-3068437	ENSG00000147883	NA	440556	1030	NA	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Upregulated expression of long non-coding RNA LINC00982 regulates cell proliferation and its clinical relevance in patients with gastric cancer.n this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Kaplan-Meier analysis demonstrated that decreased LINC00982 expression contributed to poor overall survival and disease-free survival of patients. A multivariate survival analysis also indicated that LINC00982 could be an independent prognostic marker. Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions.	26334618	RID01877	expression association	prognosis	NA	UP(LIHC);DATA(GSE117623)
Gastric cancer	PRDM16-DT	CDKN2A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177133	GRCh38_1:3059615-3068437	ENSG00000147889	NA	440556	1029	NA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Upregulated expression of long non-coding RNA LINC00982 regulates cell proliferation and its clinical relevance in patients with gastric cancer.n this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Kaplan-Meier analysis demonstrated that decreased LINC00982 expression contributed to poor overall survival and disease-free survival of patients. A multivariate survival analysis also indicated that LINC00982 could be an independent prognostic marker. Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions.	26334618	RID01878	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
T-cell acute lymphocytic leukemia	NALT1	NOTCH1	positively-F	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000237886	GRCh38_9:136546212-136549893	ENSG00000148400	NA	101928483	4851	LINC01573|MIR4674HG|NALT|TCONS_l2_00029132	AOS5|AOVD1|TAN1|hN1	LncRNA NALT interaction with NOTCH1 promoted cell proliferation in pediatric T cell acute lymphoblastic leukemia. In this study, we reported that lncRNA named NALT which was located near NOTCH1 within 100 bp away. We confirmed that up-regulation of NALT associating with NOTCH1 in human samples. Taken together, we found a neighbor of NOTCH1, Lnc-RP11-611D20.2 (named NALT) which could regulate the NOTCH1 signal pathway through cis-regulation. the NALT might interact with NOTCH1 or influence the function of NICD induced cell proliferation.	26330272	RID01879	interact with protein	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatitis C	STAT3	IGF2-AS	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	TF	lncRNA	ENSG00000168610	NA	ENSG00000099869	GRCh38_11:2140501-2148666	6774	51214	ADMIO|ADMIO1|APRF|HIES	IGF2-AS1|IGF2AS|PEG8	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01880	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Hepatitis C	STAT3	RN7SK	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	TF	lncRNA	ENSG00000168610	NA	ENSG00000283293	GRCh38_6:52995621-52995948	6774	125050	ADMIO|ADMIO1|APRF|HIES	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01881	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(PAAD,BRCA);UP(BRCA);DATA(GSE60407,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatitis C	RN7SK	PI4P	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000283293	GRCh38_6:52995621-52995948	NA	NA	125050	NA	NA	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01882	expression association	NA	DOWN(PAAD,BRCA);UP(BRCA);DATA(GSE60407,GSE109761,GSE111065,GSE51827,GSE86978)	NA
Hepatitis C	IGF2-AS	PI4P	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	NA	NA	51214	NA	IGF2-AS1|IGF2AS|PEG8	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01883	expression association	NA	NA	NA
Breast cancer	BCAR4	ERBB2	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	lapatinib	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000141736	NA	400500	2064	NA	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. A similar effect was observed upon knockdown of ERBB2/3 and exposure to lapatinib, implying that BCAR4 acts in an ERBB2/3-dependent manner.BCAR4 encodes a functional protein, which drives proliferation of endocrine-resistant breast cancer cells. Lapatinib, a clinically approved EGFR/ERBB2 inhibitor, counteracts BCAR4-driven tumor cell growth, a clinical relevant observation.	26317614	RID01884	expression association	chemoresistance	NA	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Breast cancer	BCAR4	ERBB3	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	lapatinib	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000065361	NA	400500	2065	NA	ErbB-3|FERLK|HER3|LCCS2|MDA-BF-1|c-erbB-3|c-erbB3|erbB3-S|p180-ErbB3|p45-sErbB3|p85-sErbB3	Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. A similar effect was observed upon knockdown of ERBB2/3 and exposure to lapatinib, implying that BCAR4 acts in an ERBB2/3-dependent manner.BCAR4 encodes a functional protein, which drives proliferation of endocrine-resistant breast cancer cells. Lapatinib, a clinically approved EGFR/ERBB2 inhibitor, counteracts BCAR4-driven tumor cell growth, a clinical relevant observation.	26317614	RID01885	expression association	chemoresistance	NA	UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Lung cancer	SPRY4-IT1	MMP2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000087245	NA	100642175	4313	SPRIGHTLY	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Effect of Long Non-coding RNA SPRY4-IT1 on Invasion and Migration of A549 Cells.Transwell assays showed that the numbers of transmembrane A549 cells were significantly higher in SPRY4-IT1 over expression group than that in control group (P<0.05). Meanwhile, over expression of SPRY4-IT1 reduced the expression of MMP-2 and MMP-9. Over expression of SPRY4-IT1 enhanced the invasion and migration of A549 cells. MMP-2 and MMP-9 might play an important role in this regulation.	26302345	RID01886	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD);DATA(GSE40174)
Lung cancer	SPRY4-IT1	MMP9	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000100985	NA	100642175	4318	SPRIGHTLY	CLG4B|GELB|MANDP2|MMP-9	Effect of Long Non-coding RNA SPRY4-IT1 on Invasion and Migration of A549 Cells.Transwell assays showed that the numbers of transmembrane A549 cells were significantly higher in SPRY4-IT1 over expression group than that in control group (P<0.05). Meanwhile, over expression of SPRY4-IT1 reduced the expression of MMP-2 and MMP-9. Over expression of SPRY4-IT1 enhanced the invasion and migration of A549 cells. MMP-2 and MMP-9 might play an important role in this regulation.	26302345	RID01887	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pituitary adenoma	MEG3	TP53	positively-E	RNAi;northern blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Tumor suppression by MEG3 lncRNA in a human pituitary tumor derived cell line.Human clinically non-functioning pituitary adenomas (NFAs) account for approximately 40% of diagnosed pituitary tumors. When induced in culture, MEG3 caused cell cycle arrest at the G1 phase. In addition, inactivation of p53 completely abolished tumor suppression by MEG3, indicating that MEG3 tumor suppression is mediated by p53.	26284494	RID01888	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	GAS5	CDK6	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	GAS5 Inhibits Gastric Cancer Cell Proliferation Partly by Modulating CDK6. GAS5 expression was significantly lower in GC tissues relative to normal tissues, and its lower expression was correlated with larger tumor size and a more advanced clinical stage of GC. GAS5 induced growth arrest of GC cells through inhibition of G1-S phase translation. The action of GAS5 may be mediated by upregulation of P21 and suppression of CDK6.	26278580	RID01889	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Gastric cancer	GAS5	CDKN1A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000124762	NA	60674	1026	NCRNA00030|SNHG2	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	GAS5 Inhibits Gastric Cancer Cell Proliferation Partly by Modulating CDK6. GAS5 expression was significantly lower in GC tissues relative to normal tissues, and its lower expression was correlated with larger tumor size and a more advanced clinical stage of GC. GAS5 induced growth arrest of GC cells through inhibition of G1-S phase translation. The action of GAS5 may be mediated by upregulation of P21 and suppression of CDK6.Decreased expression of long noncoding RNA GAS5 indicates a poor prognosis and promotes cell proliferation in gastric cancer. we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression. lncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer. In this study, we found that lncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. lncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and lncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. lncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of lncRNA GAS5 in suppressing stomach carcinogenesis, and the lncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing lncRNA-based therapies for stomach cancer.	26278580;25959498;24884417	RID01890	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Lung cancer	HOTTIP	CDC25C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000158402	NA	100316868	995	HOXA-AS6|HOXA13-AS1|NCRNA00213	CDC25|PPP1R60	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01891	expression association	NA	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung cancer	HOTTIP	CCNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000134057	NA	100316868	891	HOXA-AS6|HOXA13-AS1|NCRNA00213	CCNB	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01892	expression association	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Lung cancer	HOTTIP	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000110092	NA	100316868	595	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01893	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Lung cancer	HOTTIP	BAD	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000002330	NA	100316868	572	HOXA-AS6|HOXA13-AS1|NCRNA00213	BBC2|BCL2L8	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01894	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Lung cancer	HOTTIP	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000171791	NA	100316868	596	HOXA-AS6|HOXA13-AS1|NCRNA00213	Bcl-2|PPP1R50	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01895	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	HOTTIP	BCL2L1	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000171552	NA	100316868	598	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01896	expression association	NA	NA	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Non-small cell lung cancer	TARDBP	MALAT1	positively-F	RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell growth(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000120948	NA	ENSG00000251562	GRCh38_11:65497688-65506516	23435	378938	ALS10|TDP-43	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Regulation of MALAT1 expression by TDP43 controls the migration and invasion of non-small cell lung cancer cells in vitro.We also confirm that TDP-43 directly bound to MALAT1 RNA by a RNA immunoprecipitation (RIP) assay and by luciferase reporter activity assay. In a RT-PCR assay, silencing TDP-43 expression effectively decreased MALAT1 RNA transcript level. In contrast, TDP-43 overexpression markedly increased MALAT1 transcript level. In summary, these findings demonstrated that MALAT1 expression by regulation of TDP-43 controls cellular growth, migration, and invasion of NSCLCs.	26265046	RID01897	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Nasopharynx carcinoma	EZH2	NPTN-IT1	negatively-E	western blot;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000106462	NA	ENSG00000281183	GRCh38_15:73567012-73569294	2146	101241892	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	lncRNA-LET	Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell.lncRNA-LET was significantly downregulated in nasopharyngeal carcinoma (NPC) tissues compared with corresponding normal tissues. Importantly, we found lncRNA-LET is transcriptional repressed by EZH2-mediated H3K27 histone methylation on the LET promoter. The expressions of EZH2 and lncRNA-LET are significantly inversely correlated in NPC tissues. Collectively, these findings indicate a pivotal role for lncRNA-LET in NPC cell proliferation and apoptosis, and reveal an epigenetic mechanism for lncRNA-LET dysregulation.	26243049	RID01898	epigenetic regulation	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Colorectal cancer	ETS2	UCA1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000157557	NA	ENSG00000214049	GRCh38_19:15828206-15836328	2114	652995	ETS2IT1	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Increased urothelial cancer associated 1 is associated with tumor proliferation and metastasis and predicts poor prognosis in colorectal cancer. qPCR analysis confirmed that UCA1 was upregulated in CRC (p<0.001) and the expression of UCA1 was statistically correlated with lymph node metastasis (P=0.040), distant metastasis (P=0.043) and tumor stage (P=0.010). To further investigate the regulatory mechanisms of UCA1, we identified that Ets-2 bound to the UCA1 core promoter using luciferase assays.	26238511	RID01899	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	MEG3	BCL2	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+);mitochondrial signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Bcl-2|PPP1R50	Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway. The results showed that MEG3 was evidently downregulated in RCC tissues (P<0.05) and RCC cell lines (P<0.05). The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h (P<0.05). Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h (P<0.05). Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm (P<0.05). Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression (P<0.05).	26223924	RID01900	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	MEG3	CASP9	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+);mitochondrial signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000132906	NA	55384	842	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway. The results showed that MEG3 was evidently downregulated in RCC tissues (P<0.05) and RCC cell lines (P<0.05). The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h (P<0.05). Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h (P<0.05). Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm (P<0.05). Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression (P<0.05).	26223924	RID01901	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Cancer	LINC-ROR	TESC	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell growth(+);cell metastasis(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000088992	NA	100885779	54997	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CHP3|TSC	Long non-coding RNA ROR decoys gene-specific histone methylation to promote tumorigenesis. Here, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis.	26169368	RID01902	epigenetic regulation	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842,GSE109761)
Urinary bladder cancer	TGFB1	ZEB2-AS1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000238057	GRCh38_2:144517978-144521477	7040	100303491	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	ZEB2-AS|ZEB2AS|ZEB2NAT	TGFbeta1 secreted by cancer-associated fibroblasts induces epithelial-mesenchymal transition of bladder cancer cells through lncRNA-ZEB2NAT.Interestingly, a long non-coding RNA, ZEB2NAT, was demonstrated to be essential for this TGFbeta1-dependent process. ZEB2NAT depletion reversed CAF-CM-induced EMT and invasion of cancer cells, as well as reduced the ZEB2 protein level. Consistently, TGFbeta1 mRNA expression is positively correlated with ZEB2NAT transcript and ZEB2 protein levels in human bladder cancer specimens. Our data revealed a novel mechanism that CAFs induces EMT and invasion of human UBC cells through the TGFbeta1-ZEB2NAT-ZEB2 axis.	26152796	RID01903	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Urinary bladder cancer	ZEB2-AS1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000169554	NA	100303491	9839	ZEB2-AS|ZEB2AS|ZEB2NAT	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	TGFbeta1 secreted by cancer-associated fibroblasts induces epithelial-mesenchymal transition of bladder cancer cells through lncRNA-ZEB2NAT.Interestingly, a long non-coding RNA, ZEB2NAT, was demonstrated to be essential for this TGFbeta1-dependent process. ZEB2NAT depletion reversed CAF-CM-induced EMT and invasion of cancer cells, as well as reduced the ZEB2 protein level. Consistently, TGFbeta1 mRNA expression is positively correlated with ZEB2NAT transcript and ZEB2 protein levels in human bladder cancer specimens. Our data revealed a novel mechanism that CAFs induces EMT and invasion of human UBC cells through the TGFbeta1-ZEB2NAT-ZEB2 axis.	26152796	RID01904	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	AK058003	SNCG	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_10:86948677-87023220	ENSG00000173267	NA	NA	6623	NA	BCSG1|SR	Unregulated long non-coding RNA-AK058003 promotes the proliferation, invasion and metastasis of breast cancer by regulating the expression levels of the gamma-synuclein gene. The expression levels of lncRNA-AK058003 were increased significantly in the breast cancer tissues and were found to strongly correlate with the severity of the breast cancer clinical stage. Bioinformatics analysis revealed that the gamma-synuclein gene (SNCG) may be a target gene regulated by lncRNA-AK058003. Furthermore, the proliferation, invasion and migration rates of the MCF-7 breast cancer cells were significantly reduced. Therefore, the results demonstrated that unregulated lncRNA-AK058003 in breast cancer cells promotes cancer cell proliferation, invasion and metastasis via the regulation of SNCG expression.	26136884	RID01905	expression association	metastasis	NA	UP(BRCA);DATA(GSE55807)
Ovarian cancer	HOTAIR	MAPK1	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion. The expression of HOTAIR and MAPK1 in ovarian SKOV3, ES-2, and OVCAR3 increased compared with A2780 and COC1 cells (P<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05). The proliferation, migration, and invasion was inhibited in ovarian SKOV3 after silencing HOTAIR or MAPK1 (p<0.05).	26117268	RID01906	interact with protein	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	BRD4	HOTAIR	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	I-BET151	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000141867	NA	ENSG00000228630	GRCh38_12:53962308-53974956	23476	100124700	CAP|HUNK1|HUNKI|MCAP	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The Bromodomain protein BRD4 controls HOTAIR, a long noncoding RNA essential for glioblastoma proliferation. Treatment of GBM cells with the BET bromdomain inhibitor I-BET151 reduced levels of the tumor-promoting lncRNA HOX transcript antisense RNA (HOTAIR) and restored the expression of several other GBM down-regulated lncRNAs. Conversely, overexpression of HOTAIR in conjunction with I-BET151 treatment abrogates the antiproliferative activity of the BET bromodomain inhibitor. Moreover, chromatin immunoprecipitation analysis demonstrated binding of Bromodomain Containing 4 (BRD4) to the HOTAIR promoter, suggesting that BET proteins can directly regulate lncRNA expression. Our data unravel a previously unappreciated mechanism through which BET proteins control tumor growth of glioblastoma cells and suggest that modulation of lncRNA networks may, in part, mediate the antiproliferative effects of many epigenetic inhibitors currently in clinical trials for cancer and other diseases.	26111795	RID01907	transcriptional regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Hepatocellular carcinoma	ZEB1-AS1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulation of long noncoding RNA ZEB1-AS1 promotes tumor metastasis and predicts poor prognosis in hepatocellular carcinoma. We found that ZEB1-AS1 is frequently upregulated in HCC samples, especially in metastatic tumor tissues. DNA methylation analysis shows a tumor-specific ZEB1-AS1 promoter hypomethylation. Aberrant methylation is tightly correlated with overexpression of ZEB1-AS1 in HCC. Patients with ZEB1-AS1 hypomethylation or with high ZEB1-AS1 expression have poor recurrence-free survival. Functionally, ZEB1-AS1 promotes tumor growth and metastasis, acts as an oncogene in HCC. The ZEB1-AS1 gene is located in physical contiguity with ZEB1 and positively regulates the ZEB1 expression. ZEB1 inhibition partially abrogates ZEB1-AS1-induced epithelial to mesenchymal transition (EMT) and cancer metastasis. Our results provide novel insights into the function of lncRNA-driven hepatocarcinogenesis, highlight the important role of ZEB1-AS1 and ZEB1 in HCC progression, and indicate that ZEB1-AS1 may be served as a valuable prognostic biomarker for HCC.	26073087	RID01908	expression association	metastasis,recurrence,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	ZFAS1	ZEB1	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000148516	NA	441951	6935	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01909	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	ZFAS1	MMP14	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000157227	NA	441951	4323	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01910	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	ZFAS1	MMP16	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000156103	NA	441951	4325	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	C8orf57|MMP-X2|MT-MMP2|MT-MMP3|MT3-MMP	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01911	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Aortic aneurysm	HIF1A-AS1	CASP3	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01912	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Aortic aneurysm	HIF1A-AS1	CASP8	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000064012	NA	100750246	841	5'aHIF-1A|5'aHIF1alpha	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01913	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Aortic aneurysm	HIF1A-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000171791	NA	100750246	596	5'aHIF-1A|5'aHIF1alpha	Bcl-2|PPP1R50	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01914	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	RGMB-AS1	RGMB	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell differentiation(-);cell metastasis(-);TNM stage(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000174136	NA	503569	285704	NA	DRAGON	Study on expression of lncRNA RGMB-AS1 and repulsive guidance molecule b in non-small cell lung cancer.The results of qRT-PCR showed that lncRNA RGMB-AS1 expression was significantly higher in NSCLC tissues than in adjacent normal tissues, while RGMB mRNA showed an opposite trend. Correlation analysis indicated that the expression of lncRNA RGMB-AS1and RGMB mRNA were inversely correlated. We identified lncRNA RGMB-AS1 was upregulated and RGMB was downregulated in NSCLC patients. Both were related to differentiation status, lymph node metastases and TNM stage. Studies also indicated that lncRNA RGMB-AS1 and RGMB were inversely correlated.	26055877	RID01915	expression association	metastasis	NA	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE51827)
Myocardial infarction	H19	FADD	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	myocardial necrosis(-)	ceRNA(miR-103a-3p;miR-107)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168040	NA	283120	8772	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GIG3|MORT1	MicroRNA-103/107 Regulate Programmed Necrosis and Myocardial Ischemia/Reperfusion Injury Through Targeting FADD.Our results show that FADD participates in H2O2-induced necrosis by influencing the formation of RIPK1 and RIPK3 complexes in H9c2 cells. We further demonstrate that miR-103/107 target FADD directly. Knockdown of miR-103/107 antagonizes necrosis in the cellular model and also myocardial infarction in a mouse ischemia/reperfusion model. The miR-103/107-FADD pathway does not participate in tumor necrosis factor-alpha-induced necrosis. In exploring the molecular mechanism by which miR-103/107 are regulated, we show that long noncoding RNA H19 directly binds to miR-103/107 and regulates FADD expression and necrosis.Our results reveal a novel myocardial necrosis regulation model, which is composed of H19, miR-103/107, and FADD. Modulation of their levels may provide a new approach for preventing myocardial necrosis.	26038570	RID01916	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Hepatocellular carcinoma	HOTAIR	miR-218-5p	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01917	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	HOTAIR	BMI1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168283	NA	100124700	648	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01918	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	HOTAIR	CDKN2A	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000147889	NA	100124700	1029	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01919	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Gastric cancer	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);prognosis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	A Long Non-coding RNA Activated by Transforming Growth Factor-beta is an Independent Prognostic Marker of Gastric Cancer.The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor (hazard ratio 3.50; 95 % CI 1.73-7.44; p = 0.0004). miR-200c levels were lower and ZEB1 levels were higher in the high lncRNA-ATB group than in the low lncRNA-ATB group. Treatment with TGF-beta in GC cell lines resulted in morphological EMT changes, upregulation of lncRNA-ATB and ZEB1, and downregulation of miR-200c and CDH1. SB431542 reduced lncRNA-ATB expression.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGF-beta/miR-200s/ZEB axis, resulting in a poor prognosis in GC. LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients.	25986864	RID01920	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Acute myeloid leukemia	HOTAIR	KIT	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000157404	NA	100124700	3815	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C-Kit|CD117|MASTC|PBT|SCFR	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID01921	ceRNA or sponge	prognosis	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Gastric cancer	GAS5	YBX1	positively-F	western blot;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell cycle(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000065978	NA	60674	4904	NCRNA00030|SNHG2	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	lncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer. In this study, we found that lncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. lncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and lncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. lncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of lncRNA GAS5 in suppressing stomach carcinogenesis, and the lncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing lncRNA-based therapies for stomach cancer.	25959498	RID01922	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	PVT1	ABCB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000085563	NA	5820	5243	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01923	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Gastric cancer	PVT1	ABCC1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000103222	NA	5820	4363	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC29|ABCC|GS-X|MRP|MRP1	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01924	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	PVT1	MTOR	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000198793	NA	5820	2475	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01925	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Oral squamous cell carcinoma	HOTAIR	CDH1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA HOTAIR promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in oral squamous cell carcinoma. Furthermore, significant negative correlation between HOTAIR levels and E-cadherin levels was found in OSCC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 and H3K27me3 with the E-cadherin promoter.	25901533	RID01926	epigenetic regulation	metastasis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung adenocarcinoma	ZXF2	MYC	negatively-F	western blot;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_8:134211865-134320447	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of Long Non-Coding RNA ZXF2 Promotes Lung Adenocarcinoma Progression Through c-Myc Pathway. The expression of ZXF2 was 2 fold or higher in 27 out of 40 (67.5%) cases of lung adenocarcinoma specimens than that in non-cancerous tissues (P<0.05). ZXF2 was overexpressed in lung adenocarcinoma tissues and the high expression of ZXF was closely related to tumor progression through c-Myc related pathway. Given the fact that both ZXF2 and c-Myc are located in the same chromosome 8q24.2 loci, the potential interaction between ZXF2 and c-Myc might be a novel target for treatment of lung adenocarcinoma.	25896422	RID01927	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gallbladder cancer	IATPR	CTNNB1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000168036	NA	101929447	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines. Moreover, cell migration and invasion were reduced by over twofold in linc-ITGB1 knockdown cells probably due to upregulation of beta-catenin and downregulation of vimentin, slug, and TCF8.	25893892	RID01928	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gallbladder cancer	IATPR	VIM	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000026025	NA	101929447	7431	NA	NA	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01929	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gallbladder cancer	IATPR	SNAI2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000019549	NA	101929447	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01930	expression association	NA	NA	NA
Gallbladder cancer	IATPR	ZEB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000148516	NA	101929447	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01931	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	PVT1	MRPL28	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000086504	NA	5820	10573	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MAAT1|p15	Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16. Moreover, we further confirmed that PVT1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of p15 and p16.	25890171	RID01932	epigenetic regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE67939)
Gastric cancer	PVT1	CDKN2A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000147889	NA	5820	1029	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16	25890171	RID01933	epigenetic regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Triple-receptor negative breast cancer	EGFR	HOTAIR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(+)	NA	association	NA	lapatinib	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000146648	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1956	100124700	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01934	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)	NA
Triple-receptor negative breast cancer	ABL1	HOTAIR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(+)	NA	association	NA	imatinib	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000097007	NA	ENSG00000228630	GRCh38_12:53962308-53974956	25	100124700	ABL|CHDSKM|JTK7|bcr/abl|c-ABL|c-ABL1|p150|v-abl	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01935	expression association	metastasis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	NA
Triple-receptor negative breast cancer	CTNNB1	HOTAIR	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1499	100124700	CTNNB|EVR7|MRD19|NEDSDV|armadillo	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01936	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	NA
Lung cancer	lnc-bc060912	PARP1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_22:46330875-46333698	ENSG00000143799	NA	NA	142	NA	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Functional Characterization of Long Noncoding RNA Lnc_bc060912 in Human Lung Carcinoma Cells.Here we have identified a lncRNA termed Lnc_bc060912 whose expression is increased in human lung and other tumors. we found that Lnc_bc060912 interacted with the two DNA damage repair proteins PARP1 and NPM1. Together, these results suggest that Lnc_bc060912, via PARP1 and NPM1, affects cell apoptosis and may play important roles in tumorigenesis and cancer progression.	25848691	RID01937	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Lung cancer	lnc-bc060912	NPM1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_22:46330875-46333698	ENSG00000181163	NA	NA	4869	NA	B23|NPM	Functional Characterization of Long Noncoding RNA Lnc_bc060912 in Human Lung Carcinoma Cells.Here we have identified a lncRNA termed Lnc_bc060912 whose expression is increased in human lung and other tumors. we found that Lnc_bc060912 interacted with the two DNA damage repair proteins PARP1 and NPM1. Together, these results suggest that Lnc_bc060912, via PARP1 and NPM1, affects cell apoptosis and may play important roles in tumorigenesis and cancer progression.	25848691	RID01938	interact with protein	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	MALAT1	SOX2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(-);self-renewal(+);cell stemness(+)	NA	regulation	NA	gemcitabine	CSC	Self Sufficiency in Growth Signals;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000181449	NA	378938	6657	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ANOP3|MCOPS3	Long noncoding RNA MALAT-1 enhances stem cell-like phenotypes in pancreatic cancer cells.In this study, our data showed that MALAT-1 was Upregulated in CSCs and could increase the proportion of pancreatic CSCs, maintain self-renewing capacity, decrease the chemosensitivity to anticancer drugs, and accelerate tumor angiogenesis in vitro. The underlying mechanisms may involve in increased expression of self-renewal related factors Sox2. Collectively, we for the first time found the potential effects of MALAT-1 on the stem cell-like phenotypes in pancreatic cancer cells, suggesting a novel role of MALAT-1 in tumor stemness, which remains to be fully elucidated.	25811929	RID01939	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Pre-eclampsia	HOTAIR	CASP3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	Long noncoding RNA HOTAIR modulates the function of trophoblast cells in pre-eclampsia. The level of HOTAIR in severe pre-eclampsia groups was significantly increased compared to normal pregnant placentas (P<0.05). Western blot assay showed that the apoptotic proteins Caspase-3 showed an obvious increase in HOTAIR overexpression group while decreased in si-HOTAIR group. And BCL-2 presented an opposite trend.	25807808	RID01940	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Pre-eclampsia	HOTAIR	BCL2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	Long noncoding RNA HOTAIR modulates the function of trophoblast cells in pre-eclampsia. The level of HOTAIR in severe pre-eclampsia groups was significantly increased compared to normal pregnant placentas (P<0.05). Western blot assay showed that the apoptotic proteins Caspase-3 showed an obvious increase in HOTAIR overexpression group while decreased in si-HOTAIR group. And BCL-2 presented an opposite trend.	25807808	RID01941	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Varicosity	GAS5	ANXA2	interact	RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Varicosity	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000182718	NA	60674	302	NCRNA00030|SNHG2	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Low expression of lncRNA-GAS5 is implicated in human primary varicose great saphenous veins. we selected the lower expressed lncRNA-GAS5 (growth arrest specific transcript 5) for functional assessments. RNA pull-down experiment revealed a direct bind of lncRNA-GAS5 to a Ca2+-dependent RNA-binding protein, Annexin A2. Further experiments showed that silencing of Annexin A2 reduced the HSVSMCs proliferation and vice versa. In the context of lncRNA-GAS5 knockdown, silencing of Annexin A2 reduced the proliferation of HSVSMCs while overexpression of Annexin A2 increased the proliferation. Thus, the low expression of lncRNA-GAS5 may facilitate HSVSMCs proliferation and migration through Annexin A2 and thereby the pathogenesis of GSV varicosities.	25806802	RID01942	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Lung cancer	SP1	MALAT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6667	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1-mediated transcriptional regulation of MALAT1 plays a critical role in tumor. Sp1 knockdown also decreased the MALAT1 and inhibited A549 lung cancer cells' growth and invasion in vitro. Furthermore, knockdown of Sp1 also mimicked the inhibition of MALAT1 in A549 lung cancer cells' growth and metastasis in vivo.	25773124	RID01943	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Glioblastoma	WIF1	MALAT1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);WNT signaling pathway(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	PCG	lncRNA	ENSG00000156076	NA	ENSG00000251562	GRCh38_11:65497688-65506516	11197	378938	WIF-1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WIF1 re-expression in glioblastoma inhibits migration through attenuation of non-canonical WNT signaling by downregulating the lncRNA MALAT1.The aim of this study was the dissection of WIF1-associated tumor-suppressing effects mediated by canonical and non-canonical WNT signaling. Hence, loss of WIF1 enhances the migratory potential of glioblastoma through WNT5A that activates the WNT/Ca(2+) pathway and MALAT1.	25772239	RID01944	expression association	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	UCA1	FGFR1	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-216b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000077782	NA	652995	2260	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway.UCA1 could act as an endogenous sponge by directly binding to miR-216b and downregulation miR-216b expression. In addition, UCA1 could reverse the inhibitory effect of miR-216b on the growth and metastasis of HCC cells, which might be involved in the derepression of fibroblast growth factor receptor 1 (FGFR1) expression, a target gene of miR-216b, and the activation of ERK signaling pathway.	25760077	RID01945	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Breast cancer	NKILA	NFKB1	interact	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01946	interact with protein	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	NKILA	NFKBIA	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01947	interact with protein	metastasis,prognosis	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Breast cancer	NKILA	NFKBIB	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000104825	NA	105416157	4793	NA	IKBB|TRIP9	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01948	interact with protein	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	MEG3	BMP4	negatively-E	western blot;RIP	downregulation	qPCR	NA	NA	cell differentiation(+)	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000125378	NA	55384	652	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BMP2B|BMP2B1|MCOPS6|OFC11|ZYME	Upregulation of lncRNA MEG3 Promotes Osteogenic Differentiation of Mesenchymal Stem Cells From Multiple Myeloma Patients By Targeting BMP4 Transcription.Here we showed that MEG3 was critical for SOX2 transcriptional repression of the BMP4. MEG3, which is located near the BMP4 gene, could dissociate the transcription factor SOX2 from the BMP4 promoter.	25753650	RID01949	transcriptional regulation	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Breast cancer	SPRY4-IT1	ZNF703	positively-E	qPCR;RNAi	upregulation	qPCR;microarray	GSE62507	GSE62507.zip	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000183779	NA	100642175	80139	SPRIGHTLY	NLZ1|ZEPPO1|ZNF503L|ZPO1	The long noncoding RNA SPRY4-IT1 increases the proliferation of human breast cancer cells by upregulating ZNF703 expression.The knockdown of SPRY4-IT1 significantly suppressed proliferation and caused apoptosis of breast cancer cells in vitro. Furthermore, we discovered that ZNF703 was a target of SPRY4-IT1 and was downregulated by SPRY4-IT1 knockdown.	25742952	RID01950	transcriptional regulation	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC);DATA(GSE117623)
Osteosarcoma	HOTAIR	MMP2	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087245	NA	100124700	4313	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Overexpression of Long Non-Coding RNA HOTAIR Promotes Tumor Growth and Metastasis in Human Osteosarcoma.experiments demonstrated that knockdown of HOTAIR could notably suppress cellular proliferation, inhibit invasion and decrease the secretion of MMP2 and MMP9 in osteosarcoma.	25728753	RID01951	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Osteosarcoma	HOTAIR	MMP9	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Overexpression of Long Non-Coding RNA HOTAIR Promotes Tumor Growth and Metastasis in Human Osteosarcoma.experiments demonstrated that knockdown of HOTAIR could notably suppress cellular proliferation, inhibit invasion and decrease the secretion of MMP2 and MMP9 in osteosarcoma.	25728753	RID01952	expression association	metastasis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteoporosis	DANCR	IL6	positively-E	RNAi	upregulation	qPCR	NA	NA	biomarker(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000136244	NA	57291	3569	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long non-coding RNA-DANCR in human circulating monocytes: a potential biomarker associated with postmenopausal osteoporosis. we found significant upregulation of DANCR in the blood mononuclear cells (MNCs) from low-BMD patients with the qRT-PCR analyses. We further found that DANCR promoted the expression of IL6 and TNF-alpha at both mRNA level and protein level in MNCs. Furthermore, we found that DANCR-induced IL6 and TNF-alpha in MNCs had bone-resorbing activity. These results indicate that DANCR is involved in the pathology of osteoporosis and may be as a biomarker for postmenopausal osteoporosis.	25660720	RID01953	expression association	circulating	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Osteoporosis	DANCR	TNF	positively-E	RNAi	upregulation	qPCR	NA	NA	biomarker(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000232810	NA	57291	7124	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA-DANCR in human circulating monocytes: a potential biomarker associated with postmenopausal osteoporosis. we found significant upregulation of DANCR in the blood mononuclear cells (MNCs) from low-BMD patients with the qRT-PCR analyses. We further found that DANCR promoted the expression of IL6 and TNF-alpha at both mRNA level and protein level in MNCs.	25660720	RID01954	expression association	circulating	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC);DATA(GSE117623)
Malignant glioma	LINC-ROR	PROM1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);self-renewal(-)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000007062	NA	100885779	8842	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Expression and Functional Role of Reprogramming-Related Long Noncoding RNA (lincRNA-ROR) in Glioma. To explore its functional role, gain- and loss-of-function studies were performed to assess the effect of lincRNA-ROR on cell proliferation, expression rate of GSCs marker CD133, and glioma stem sphere-forming ability in vitro. We found that the lincRNA-ROR expression was significantly lower in glioma tissues than in adjacent normal tissues. Knockdown of lincRNA-ROR expression by small hairpin RNA (shRNA) significantly elevated the cell proliferation and enhanced the CD133 expression rate and glioma stem sphere-forming ability in U87 cells, while overexpression of lincRNA-ROR in U87 cells showed the opposite effect.	25651893	RID01955	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE109761)
Malignant glioma	LINC-ROR	KLF4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);self-renewal(-)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136826	NA	100885779	9314	ROR|lincRNA-RoR|lincRNA-ST8SIA3	EZF|GKLF	Expression and Functional Role of Reprogramming-Related Long Noncoding RNA (lincRNA-ROR) in Glioma. Moreover, we found that the expression of lincRNA-ROR was negatively correlated with stem cell factor KLF4 and the up- and down-regulation of lincRNA-ROR resulted in inverse modulation of KLF4 messenger RNA (mRNA) expression. Our results suggest that the reprogramming-related lincRNA-ROR may serve as a novel tumor suppressor gene in glioma, which can inhibit the proliferation of cancer cell and self-renewal of GSCs, partly by inhibiting the KLF4 expression.	25651893	RID01956	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	CDKN2B-AS1	TERT	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	beta-Elemene	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164362	NA	100048912	7015	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	beta-Elemene inhibits the proliferation of esophageal squamous cell carcinoma by regulating long noncoding RNA-mediated inhibition of hTERT expression. It was also shown by flow cytometry that, compared with the scramble-treated group (negative control), the proliferation index value of ECA-109 cells in the si-CDKN2B-AS1 treatment group was notably increased (25.7 vs. 51.7%) and the TERT protein level was increased by 67.25% after the cells were treated with si-CDKN2B-AS1. The chemotherapeutic drug beta-elemene suppressed the proliferation of esophageal carcinoma ECA-109 cells by regulating the inhibition of hTERT expression by lncRNA CDKN2B-AS1.	25646744;30223861	RID01957	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	UP(PAAD);DATA(GSE40174)
Liver cancer	HULC	CLOCK	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000134852	NA	728655	9575	HCCAT1|LINC00078|NCRNA00078	KAT13D|bHLHe8	A long noncoding RNA perturbs the circadian rhythm of hepatoma cells to facilitate hepatocarcinogenesis. our data show that an lncRNA, HULC, is responsible for the perturbations in circadian rhythm through upregulating circadian oscillator CLOCK in hepatoma cells, resulting in the promotion of hepatocarcinogenesis. our data exhibited that CLOCK was implicated in the HULC-accelerated proliferation of hepatoma cells in vitro and in vivo.	25622901	RID01958	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE86978)
Hepatocellular carcinoma	HULC	PPARA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000186951	NA	728655	5465	HCCAT1|LINC00078|NCRNA00078	NR1C1|PPAR|PPARalpha|hPPAR	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01959	expression association	NA	NA	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	HULC	ACSL1	positively-E	RNAi	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000151726	NA	728655	2180	HCCAT1|LINC00078|NCRNA00078	ACS1|FACL1|FACL2|LACS|LACS1|LACS2	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01960	transcriptional regulation	NA	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HULC	miR-9	negatively-E	luciferase reporter assay;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01961	epigenetic regulation	NA	NA	NA
Hepatocellular carcinoma	RXRA	HULC	positively-E	western blot;luciferase reporter assay;mutant in binding site	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000186350	NA	ENSG00000285219	GRCh38_6:8435568-9294133	6256	728655	NR2B1	HCCAT1|LINC00078|NCRNA00078	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. cholesterol addition was sufficient to upregulate HULC expression through a positive feedback loop involving the retinoid receptor RXRA, which activated the HULC promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01962	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	NA
Diabetes mellitus	MIAT	VEGFA	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Sustained Angiogenesis	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000112715	NA	440823	7422	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	MVCD1|VEGF|VPF	lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA. RNA immunoprecipitation, and in vitro studies revealed that MIAT functioned as a competing endogenous RNA, and formed a feedback loop with vascular endothelial growth factor and miR-150-5p to regulate endothelial cell function.studies revealed that MIAT knockdown obviously ameliorated diabetes mellitus-induced retinal microvascular dysfunction in vivo, and inhibited endothelial cell proliferation, migration, and tube formation in vitro. MIAT Regulates the Expression of miR-150-5p Target Gene, VEGF.This study highlights the involvement of lncRNA-MIAT in pathological angiogenesis and facilitates the development of lncRNA-directed diagnostics and therapeutics against neovascular diseases.	25587098	RID01963	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Pancreatic neuroendocrine tumor	MEG3	MET	negatively-E	western blot;ChIP	downregulation	qPCR;microarray	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105976	NA	55384	4233	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors. Therefore, a tumor-suppressor long noncoding RNA (MEG3) and suppressed protooncogene (c-MET) combination could elicit menin's tumor-suppressor activity. Interestingly, MEG3 and c-MET expression was also altered in human sporadic insulinomas (insulin secreting PNETs) with hypermethylation at the MEG3 promoter CRE-site coinciding with reduced MEG3 expression.Furthermore, in MIN6 mouse insulinoma cells, DNA-demethylating drugs blocked cell proliferation and activated Meg3 expression. Our data suggest that the epigenetic activation of lncRNA MEG3 and/or inactivation of c-MET could be therapeutic for treating PNETs and insulinomas.	25565142	RID01964	transcriptional regulation	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Liver fibrosis	TET3	HIF1A-AS1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Gastrointestinal system disease	Fibrosis	PCG	lncRNA	ENSG00000187605	NA	ENSG00000258777	GRCh38_14:61681041-61695823	200424	100750246	hCG_40738	5'aHIF-1A|5'aHIF1alpha	TET3 mediates the activation of human hepatic stellate cells via modulating the expression of long non-coding RNA HIF1A-AS1. The result hinted that TET3 activate HSCs through modulating the expression of HIF1A-AS1. To confirm this hypothesis, RNA interference was performed to silence the HIF1A-AS1. Results showed that HIF1A-AS1 silencing lead to enhancing in cell proliferation and declining apoptosis. Taken together, TET3 can mediate the activation of HSCs via modulating the expression of the long non-coding RNA HIF1A-AS1.	25550811	RID01965	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Thoracoabdominal aorta aneurysm	HIF1A-AS1	CASP3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01966	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Thoracoabdominal aorta aneurysm	HIF1A-AS1	CASP8	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000064012	NA	100750246	841	5'aHIF-1A|5'aHIF1alpha	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01967	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Thoracoabdominal aorta aneurysm	HIF1A-AS1	BCL2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000171791	NA	100750246	596	5'aHIF-1A|5'aHIF1alpha	Bcl-2|PPP1R50	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01968	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	miR-101-3p	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01969	ceRNA or sponge	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Esophagus squamous cell carcinoma	miR-217	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01970	ceRNA or sponge	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Esophagus squamous cell carcinoma	MALAT1	CDKN1A	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01971	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	MALAT1	DCTN6	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104671	NA	378938	10671	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WS-3|WS3|p27	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01972	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	MALAT1	MYBL2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101057	NA	378938	4605	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	B-MYB|BMYB	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01973	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	MDC1-AS1	MDC1	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	tumor-suppressive function(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000224328	GRCh38_6:30703067-30713184	ENSG00000137337	NA	106478956	9656	MDC1-AS	NFBD1	A novel antisense long noncoding RNA regulates the expression of MDC1 in bladder cancer. we found that the expression levels of MDC1-AS and MDC1 was down-regulated in bladder cancer. After over-expression of MDC1-AS, increased levels of MDC1 were observed in bladder cancer cells. We also found a remarkably inhibitory role of antisense lncRNA MDC1-AS on malignant cell behaviors in bladder cancer cells EJ and T24. Subsequently, knockdown of MDC1 revealed that suppressing role of MDC1-AS was attributed to up-regulation of MDC1. In summary, we have identified a novel antisense lncRNA MDC1-AS, which may participate in bladder cancer through up-regulation of its antisense tumor-suppressing gene MDC1.	25514464	RID01974	expression association	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807,GSE75367)
Prostate cancer	PCGEM1	AR	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);metabolic process(+)	NA	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000169083	NA	64002	367	LINC00071|NCRNA00071|PCAT9	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	A long noncoding RNA connects c-Myc to tumor metabolism. In prostate cancer, prostate cancer gene expression marker 1 (PCGEM1) is an androgen-induced prostate-specific lncRNA whose overexpression is highly associated with prostate tumors. PCGEM1's tumorigenic potential has been recently shown to be in part due to its ability to activate androgen receptor (AR).Together, our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells. By being a coactivator for both c-Myc and AR, PCGEM1 reprograms the androgen network and the central metabolism in a tumor-specific way, making it a promising target for therapeutic intervention.	25512540	RID01975	expression association	NA	UP(PAAD);DATA(GSE60407)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Prostate cancer	PCGEM1	MYC	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);metabolic process(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000136997	NA	64002	4609	LINC00071|NCRNA00071|PCAT9	MRTL|MYCC|bHLHe39|c-Myc	A long noncoding RNA connects c-Myc to tumor metabolism. we report a novel function of PCGEM1 that provides growth advantages for cancer cells by regulating tumor metabolism via c-Myc activation. PCGEM1 binds directly to target promoters, physically interacts with c-Myc, promotes chromatin recruitment of c-Myc, and enhances its transactivation activity.our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells.Together, our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells. By being a coactivator for both c-Myc and AR, PCGEM1 reprograms the androgen network and the central metabolism in a tumor-specific way, making it a promising target for therapeutic intervention.	25512540	RID01976	transcriptional regulation	NA	UP(PAAD);DATA(GSE60407)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	LINC00974	KRT19	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-642a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	ENSG00000171345	NA	147093	3880	NA	CK19|K19|K1CS	A novel biomarker Linc00974 interacting with KRT19 promotes proliferation and metastasis in hepatocellular carcinoma.We further investigated the interaction pattern of Linc00974 and KRT19. MiR-642 was identified, by acting as the competing endogenous RNA in regulating Linc00974 and KRT19. Linc00974 was increased owing to an abnormal hypomethylation promoter, which induced the upregulation of KRT19 via ceRNA interaction, resulting in the activation of the Notch and TGF-beta pathways as detected by cDNA microarray.	25476897	RID01977	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	MALAT1	PCNA	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132646	NA	378938	5111	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ATLD2	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01978	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Osteosarcoma	MALAT1	MMP9	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01979	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	MALAT1	PI3K	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01980	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Osteosarcoma	MALAT1	AKT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01981	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	HOTAIR	EZH2	interact	RIP	downregulation	sequencing	TCGA	GBM.zip	cell cycle(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTAIR promotes glioblastoma cell cycle progression in an EZH2 dependent manner. In this study, we found that EZH2 (predominant PRC2 complex component) inhibition blocked cell cycle progression in glioma cells, consistent with the effects elicited by HOTAIR siRNA. However, the inhibition of LSD1 did not affect cell cycle progression in glioma cells. These results suggest that HOTAIR might regulate cell cycle progression through EZH2.In conclusion, HOTAIR promotes cell cycle progression in glioma as a result of the binding of its 5' domain to the PRC2 complex.Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	25428914;27277755	RID01982	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Prostate cancer	PCAT1	miR-3667-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1	NA	The long non-coding RNA PCAT-1 promotes prostate cancer cell proliferation through cMyc. The PCAT-1-cMyc relationship is mediated through the post-transcriptional activity of the MYC 3' untranslated region, and we characterize a role for PCAT-1 in the disruption of MYC-targeting microRNAs. To further elucidate a role for post-transcriptional regulation, we demonstrate that targeting PCAT-1 with miR-3667-3p, which does not target MYC, is able to reverse the stabilization of cMyc by PCAT-1. This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer.	25425964	RID01983	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Prostate cancer	PCAT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	post-transcriptional level	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000136997	NA	100750225	4609	PCA1|PCAT-1	MRTL|MYCC|bHLHe39|c-Myc	The long non-coding RNA PCAT-1 promotes prostate cancer cell proliferation through cMyc. The PCAT-1-cMyc relationship is mediated through the post-transcriptional activity of the MYC 3' untranslated region, and we characterize a role for PCAT-1 in the disruption of MYC-targeting microRNAs. To further elucidate a role for post-transcriptional regulation, we demonstrate that targeting PCAT-1 with miR-3667-3p, which does not target MYC, is able to reverse the stabilization of cMyc by PCAT-1. This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer.	25425964	RID01984	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	miR-125b-5p	HOTTIP	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	Long non-coding RNA HOTTIP is frequently up-regulated in hepatocellular carcinoma and is targeted by tumour suppressive miR-125b. In our profiling study, HOTTIP was identified as the most significantly up-regulated lncRNA in human HCCs, even in early stage of HCC formation. Functionally, knock-down of HOTTIP attenuated HCC cell proliferation in vitro and markedly abrogated tumourigenicity in vivo. HOTTIP is an antisense lncRNA mapped to the distal end of the HOXA gene cluster. Knock-down of HOTTIP significantly suppressed the expression of a number of HOXA genes.Furthermore, we identified miR-125b as a post-transcriptional regulator of HOTTIP. Ectopic expression of miR-125b reduced HOTTIP-coupled luciferase activity and suppressed the endogenous level of HOTTIP. Moreover, in human HCCs, HOTTIP expression negatively correlated with that of miR-125b.HOTTIP is a novel oncogenic lncRNA, which negatively regulated by miR-125b. Overexpression of HOTTIP contributes to hepatocarcinogenesis by regulating the expression of its neighbouring protein-coding genes.	25424744	RID01985	ceRNA or sponge	metastasis	NA	NA
Nasopharynx carcinoma	TP53	LOC401317	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	GSE60379	GSE60379.zip	cell cycle(-);apoptosis process(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	TF	lncRNA	ENSG00000141510	NA	NA	GRCh38_7:28449124-28451460	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	NA	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Further studies indicated that LOC401317 is directly regulated by p53 and that ectopic expression of LOC401317 inhibits HNE2 cell proliferation in vitro and in vivo by inducing cell cycle arrest and apoptosis.	25422887	RID01986	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	NA
Nasopharynx carcinoma	LOC401317	CDKN1A	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID01987	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Nasopharynx carcinoma	LOC401317	CCND1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60381	GSE60381.zip	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID01988	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Nasopharynx carcinoma	LOC401317	CCNE1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60382	GSE60382.zip	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000105173	NA	NA	898	NA	CCNE|pCCNE1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID01989	expression association	NA	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Nasopharynx carcinoma	LOC401317	CASP3	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60383	GSE60383.zip	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000164305	NA	NA	836	NA	CPP32|CPP32B|SCA-1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID01990	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Nasopharynx carcinoma	LOC401317	PARP1	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000143799	NA	NA	142	NA	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID01991	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Prostate cancer	ESR1	NEAT1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000245532	GRCh38_11:65422774-65445540	2099	283131	ER|ESR|ESRA|ESTRR|Era|NR3A1	LINC00084|NCRNA00084|TncRNA|VINC	The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer. Among putatively ERalpha-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists.	25415230	RID01992	transcriptional regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Neuroblastoma	POU3F3	DALIR	positively-E	ChIP	downregulation	qPCR	NA	NA	cell differentiation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Neuroblastoma	TF	lncRNA	ENSG00000198914	NA	NA	GRCh38_2:104860077-104861124	5455	104940698	BRN1|OTF8|brain-1|oct-8	DALI	The long non-coding RNA Dali is an epigenetic regulator of neural differentiation. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans.	25415054	RID01993	transcriptional regulation	NA	NA	NA
Neuroblastoma	DALIR	DNMT1	interact	ChIP	downregulation	qPCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	NA	GRCh38_2:104860077-104861124	ENSG00000130816	NA	104940698	1786	DALI	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The long non-coding RNA Dali is an epigenetic regulator of neural differentiation. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans.	25415054	RID01994	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Long non-coding RNA HOTAIR is associated with human cervical cancer progression. The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues.Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. Therefore, HOTAIR may promote tumor aggressiveness through the upregulation of VEGF and MMP-9 and EMT-related genes.	25405331	RID01995	expression association	metastasis	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cervical cancer	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA HOTAIR is associated with human cervical cancer progression. The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues.Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. Therefore, HOTAIR may promote tumor aggressiveness through the upregulation of VEGF and MMP-9 and EMT-related genes.	25405331	RID01996	expression association	metastasis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Triple-receptor negative breast cancer	LINC-ROR	ARF6	positively-E	Targetscan;RNAi;MS2 binding assay	upregulation	qPCR;sequencing	TCGA	BRCA.zip	cell invasion(-)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000165527	NA	100885779	382	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	lincRNA-RoR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6. Interestingly, lincRNA-RoR is dramatically upregulated in TNBC and in metastatic disease and knockdown restores miR-145 expression.Investigation of miR-145-regulated pathways involved in tumor invasion revealed a novel target, the small GTPase ADP-ribosylation factor 6 (Arf6).lincRNA-RoR is overexpressed in TNBC where it serves as competitive endogenous RNA for miR-145. miR-145 directly targets the 3'UTR of ARF6 mRNA. Subsequent analysis demonstrated that ARF6, a known regulator of breast tumor cell invasion, is dramatically upregulated in TNBC and in breast tumor metastasis. Mechanistically, ARF6 regulates E-cadherin localization and affects cell-cell adhesion. These results reveal a lincRNA-RoR/miR-145/ARF6 pathway that regulates invasion in TNBCs.	25253741	RID01997	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Acute promyelocytic leukemia	PRAM1	NEAT1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	PCG	lncRNA	ENSG00000133246	NA	ENSG00000245532	GRCh38_11:65422774-65445540	84106	283131	PML-RAR|PRAM-1	LINC00084|NCRNA00084|TncRNA|VINC	Inhibition of long non-coding RNA NEAT1 impairs myeloid differentiation in acute promyelocytic leukemia cells. we found that nuclear enriched abundant transcript 1 (NEAT1), a lncRNA essential for the formation of nuclear body paraspeckles, is significantly repressed in de novo APL samples compared with those of healthy donors. We further provide evidence that NEAT1 expression was repressed by PML-RARalpha.	25245097	RID01998	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Ovarian cancer	FALEC	BMI1	interact	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000168283	NA	100874054	648	FAL1|LINC00568|ncRNA-a1	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer. we identified an oncogene, focally amplified lncRNA on chromosome 1 (FAL1), whose copy number and expression are correlated with outcomes in ovarian cancer. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.The high degree of similarity between FAL1- and BMI1-mediated transcriptional repression strongly indicates a functional interaction between FAL1 and BMI1.	25203321	RID01999	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Ovarian cancer	FALEC	CDKN1A	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000124762	NA	100874054	1026	FAL1|LINC00568|ncRNA-a1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.	25203321;25367941	RID02000	epigenetic regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Multiple myeloma	MALAT1	LTBP3	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	biomarker(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168056	NA	378938	4054	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DASS|GPHYSD3|LTBP-3|LTBP2|STHAG6|pp6425	Activation of LTBP3 gene by a long noncoding RNA (lncRNA) MALAT1 transcript in mesenchymal stem cells from multiple myeloma. Our data suggested that lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1, and recruitment of Sp1 to the promoter.Our knowledge of the role of MALAT1 in cellular transformation is pointing toward its potential use as a biomarker and a target for novel therapeutic approaches in multiple myeloma	25187517	RID02001	transcriptional regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Endometrial fibrosis	miR-29b-3p	MEG3	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Reproductive system disease	Fibrosis	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MicroRNA-29b inhibits TGF-beta1-induced fibrosis via regulation of the TGF-beta1/Smad pathway in primary human endometrial stromal cells. ectopic overexpression of miR-29b increased the expression levels of MEG3, inhibited myofibroblast-like cell proliferation and induced apoptosis.	27035110	RID02002	expression association	NA	NA	NA
Malignant glioma	GAS5	miR-222	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Gas5 Exerts Tumor-suppressive Functions in Human Glioma Cells by Targeting miR-222. We showed that the introduction of Gas5 by plasmid transfection increased the expression of tumor suppressor Bcl-2-modifying factor (bmf) and Plexin C1 via directly targeting and reducing the expression of miR-222.knockdown of miR-222 attenuated U87 and U251 cell migration and invasion by upregulating Plexin C1, and cofilin was a crucial regulator targeted by Plexin C1.In summary, we show that Gas5 suppresses tumor malignancy by downregulating miR-222, which may serve as a promising therapy for glioma.	26370254	RID02003	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Nasopharynx carcinoma	EWSAT1	CCND1	positively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-326-5p;miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000110092	NA	283673	595	LINC00277|NCRNA00277|TMEM84	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p. mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters.Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	27816050	RID02004	ceRNA or sponge	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Malignant glioma	MEG3	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-19a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion by Acting as a Competing Endogenous RNA of miR-19a. miR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration, and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis.Bioinformatics analyses (TargetScan, miRanda, and starBase V2.0) showed that phosphatase and tensin homolog (PTEN) is a target of miR-19a with complementary binding sites in the 3'-UTR.	28276316	RID02005	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	XIST	BCL2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-449a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171791	NA	7503	596	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	Bcl-2|PPP1R50	The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer.the expression levels of XIST were significantly elevated. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2.knockdown of XIST by siRNA significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis.Hence, by competing with Bcl-2 to bind miR-449a, XIST influences the regulation of tumor progression in NSCLC.	28248928	RID02006	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteonecrosis	HOTAIR	SMAD7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell differentiation(-);cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000101665	NA	100124700	4092	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CRCS3|MADH7|MADH8	Long non-coding RNA HOTAIR inhibits miR-17-5p to regulate osteogenic differentiation and proliferation in non-traumatic osteonecrosis of femoral head.HOTAIR downregulation induced by si-HOTAIR led to the increase of miR-17-5p expression and the decrease of miR-17-5p target gene SMAD7 expression.The following experiments showed that downregulation of HOTAIR contributed to the reduced DNA methylation level of miR-17-5p promotor.	28207735	RID02007	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteonecrosis	HOTAIR	miR-17-5p	negatively-E	5-Aza-CdR	upregulation	qPCR	NA	NA	cell differentiation(-);cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR inhibits miR-17-5p to regulate osteogenic differentiation and proliferation in non-traumatic osteonecrosis of femoral head.HOTAIR downregulation induced by si-HOTAIR led to the increase of miR-17-5p expression and the decrease of miR-17-5p target gene SMAD7 expression.The following experiments showed that downregulation of HOTAIR contributed to the reduced DNA methylation level of miR-17-5p promotor	28207735	RID02008	epigenetic regulation	NA	NA	NA
Chronic myeloid leukemia	MEG3	miR-21-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02009	ceRNA or sponge	chemoresistance	NA	NA
Chronic myeloid leukemia	MEG3	ABCC1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000103222	NA	55384	4363	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC29|ABCC|GS-X|MRP|MRP1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02010	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Chronic myeloid leukemia	MEG3	ABCB1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000085563	NA	55384	5243	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02011	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Chronic myeloid leukemia	MEG3	ABCG2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000118777	NA	55384	9429	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02012	expression association	chemoresistance	NA	UP(PAAD);DATA(GSE40174)
Gallbladder cancer	TUG1	miR-300	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 promotes cell proliferation and metastasis by negatively regulating miR-300 in gallbladder carcinoma.TUG1 expression was significantly overexpressed in GBC tissues. Mechanically, we found that TUG1 is upregulated by TGF-beta1, and knockdown of TUG1 inhibited GBC cell EMT. Furthermore, we identified that miR-300, which has been reported as a suppressor in other types of cancer, is negatively regulated by TUG1.	28178615	RID02013	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	HULC	SIRT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell autophagy(+)	NA	regulation	NA	oxaliplatin;5-fluorouracil;pirarubicin	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000096717	NA	728655	23411	HCCAT1|LINC00078|NCRNA00078	SIR2|SIR2L1|SIR2alpha	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells. In this study, we for the first time demonstrated that treatment with antitumor reagents such as oxaliplatin, 5-fluorouracil and pirarubicin (THP) dramatically induced HULC expression and protective autophagy. Silencing of HULC sensitized HCC cells to the three antitumor reagents via inhibiting protective autophagy.Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1.	28166203	RID02014	expression association	chemoresistance	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	HULC	USP22	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell autophagy(+)	NA	regulation	NA	oxaliplatin;5-fluorouracil;pirarubicin	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124422	NA	728655	23326	HCCAT1|LINC00078|NCRNA00078	USP3L	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells. we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.HULC does not act as a miRNA sponge to suppress the expression and activity of the threemiRNAs. Furthermore, we found that HULC didn't affect thestability of the three miRNAs using actinomycin D (Supplementary Figure 4D), suggesting that HULC may downregulate the thre emiRNAs through transcription inhibition or epigenetic regulation.	28166203	RID02015	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Colorectal cancer	miR-200a-3p	H19	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing beta-Catenin Expression in Colorectal Cancer. H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues. H19 overexpression facilitated colon cancer cell proliferation, whereas H19 knockdown inhibited cell proliferation. miR-200a bound to H19 and inhibited its expression, thereby decreasing CRC cell proliferation.	28164117	RID02016	ceRNA or sponge	NA	NA	UP(NSCLC);DATA(GSE74639)
Non-small cell lung cancer	DUXAP8	EGR1	negatively-E	RIP;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000120738	NA	503637	1958	NA	AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268|ZNF225	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB. We identified a transcribed pseudogene named DUXAP8 that is upregulated in tumor tissues. DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02017	epigenetic regulation	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)
Non-small cell lung cancer	DUXAP8	RHOB	negatively-E	RIP;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000143878	NA	503637	388	NA	ARH6|ARHB|MST081|MSTP081|RHOH6	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02018	epigenetic regulation	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Liver fibrosis	HOTAIR	MEG3	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	histone modification	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	lncRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000214548	GRCh38_14:100779410-100861031	100124700	55384	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.	27979710	RID02019	epigenetic regulation	NA	NA	NA
Liver fibrosis	HOTAIR	miR-148b	negatively-F	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.	27979710	RID02020	ceRNA or sponge	NA	NA	NA
Colorectal cancer	BLACAT1	MRPL28	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000086504	NA	101669762	10573	LINC00912|linc-UBC1|onco-lncRNA-30	MAAT1|p15	Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation.	28277544	RID02021	epigenetic regulation	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE67939)
Multiple myeloma	CRNDE	miR-451a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	Long Noncoding RNA CRNDE Promotes Multiple Myeloma Cell Growth by Suppressing miR-451. In this study, we found that the CRNDE expression level, in MM samples and cell lines, is higher than that in the control detected by real-time qPCR, which is also closely related to tumor progression and poor survival in MM patients. Bioinformatics analysis and luciferase assay reveal the interaction by complementary bonding between CRNDE and miR-451. Pearson's correlation shows that CRNDE is negatively correlated to miR-451 expression in human MM samples. Our study illustrates that lncRNA CRNDE induces the proliferation and antiapoptosis capability of MM by acting as a ceRNA or molecular sponge via negatively targeting miR-451, which could act as a novel diagnostic marker and therapeutic target for MM.	28276319	RID02022	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	NA
Gastric cancer	MALAT1	CDH5	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000179776	NA	378938	1003	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	7B4|CD144	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02023	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	MALAT1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02024	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	MALAT1	MMP14	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000157227	NA	378938	4323	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02025	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Gastric cancer	MALAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02026	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Gastric cancer	MALAT1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02027	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	MALAT1	MAPK1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100030	NA	378938	5594	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02028	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MALAT1	PTK2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169398	NA	378938	5747	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FADK|FAK|FAK1|FRNK|PPP1R71|p125FAK|pp125FAK	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02029	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE75367)
Gastric cancer	MALAT1	PXN	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000089159	NA	378938	5829	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02030	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Tongue cancer	MALAT1	JAG1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101384	NA	378938	182	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AGS|AGS1|AHD|AWS|CD339|DCHE|HJ1|JAGL1	Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1.lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo.In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.	28260102	RID02031	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE111842,GSE51827,GSE86978)
Gastric adenocarcinoma	SRF	HOTAIR	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000112658	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6722	100124700	MCM1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells. miR-101-3p could directly target and suppress the expression of the serum response factor (SRF) gene, which is a transcription factor of HOTAIR, a well-characterized tumor promoter lncRNA. silencing of either SRF or HOTAIR could counteract the promotion of gastric adenocarcinoma cell proliferation and invasion by miR-101-3p inhibition. Our findings indicate that miR-101-3p suppresses HOTAIR-induced proliferation and invasion through directly targeting SRF in gastric carcinoma cells.	28251884	RID02032	transcriptional regulation	NA	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	NA
Gastric cancer	SP1	LINC00673	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000227036	GRCh38_17:72403322-72592804	6667	100499467	NA	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02033	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Gastric cancer	LINC00673	KLF2	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000127528	NA	100499467	10365	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	LKLF	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02034	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00673	LATS2	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000150457	NA	100499467	26524	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	KPM	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02035	epigenetic regulation	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	SP1	AGAP2-AS1	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000255737	GRCh38_12:57726271-57728356	6667	100130776	NA	PUNISHER	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02036	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Gastric cancer	AGAP2-AS1	CDKN1A	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000124762	NA	100130776	1026	PUNISHER	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02037	epigenetic regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	AGAP2-AS1	CDH1	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000039068	NA	100130776	999	PUNISHER	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02038	epigenetic regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	FEZF1-AS1	CDKN1A	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000124762	NA	154860	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. ChIP assays demonstrated that LSD1 could directly bind to the promoter of P21, inducing H3K4me2 demethylation. knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis.	28209170	RID02039	epigenetic regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Malignant glioma	PTCSC3	LRP6	negatively-E	RNAi	downregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cell proliferation(-);cell migration(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000070018	NA	100886964	4040	NA	ADCAD2|STHAG7	Long noncoding RNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) inhibits proliferation and invasion of glioma cells by suppressing the Wnt/beta-catenin signaling pathway. LncRNA PTCSC3 was significantly downregulated in glioma cell lines. The study also demonstrated that LRP6, as a receptor of the Wnt/beta-catenin pathway, was a target of lncRNA PTCSC3. By evaluating the expression levels of Axin1, active beta-catenin, c-myc, and cyclin D1, the study indicated that lncRNA PTCSC3 inhibited the activation of the Wnt/beta-cateninpathway through targeting LRP6.In western blot analysis, lncRNA PTCSC3 overexpression downregulated LRP6 expression, subsequently suppressing the expression of active beta-catenin, C-myc and cyclin D1, while increasing Axin1 expression, and vice versa. LncRNA PTCSC3 inhibits the proliferation and migration of glioma cells and suppresses Wnt/beta-catenin signaling pathway by targeting LRP6. LncRNA PTCSC3 is a potential therapeutic target for treatment of glioma.	28187755	RID02040	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065)
Chondrosarcoma	HOTAIR	miR-454-3p	negatively-E	Bisulfite sequencing analysis;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02041	epigenetic regulation	prognosis	NA	NA
Renal cell carcinoma	HOTAIR	KDM6B	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132510	NA	100124700	23135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	JMJD3	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.In the present study, HOTAIR expression was elevated in tissues of renal cell carcinoma compared to adjacent normal tissues, and positively correlated with metastasis (P<0.05). Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05).	28177890	RID02042	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	HOTAIR	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05). Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.	28177890	RID02043	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	HOTAIR	PCDHB5	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113209	NA	100124700	26167	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-BETA5	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3. Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05). Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.	28177890	RID02044	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Breast cancer	PTCSC1	DHX9	interact	RIP;Co-immunoprecipitation	upregulation	qPCR	NA	NA	AKT signaling pathway(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENST00000664551.1	GRCh38.p13:133054959-133057767	ENSG00000135829	NA	100302522	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	LncRNA AK023948 is a positive regulator of AKT. Among lncRNAs identified from this screen, we demonstrate that AK023948 is a positive regulator for AKT. Knockout of AK023948 suppresses, whereas rescue with AK023948 restores the AKT activity. Mechanistically, AK023948 functionally interacts with DHX9 and p85. Importantly, AK023948 is required for the interaction between DHX9 and p85 to hence the p85 stability and promote AKT activity. AK023948 is upregulated in breast cancer; interrogation of TCGA data set indicates that upregulation of DHX9 in breast cancer is associated with poor survival. Together, this study demonstrates two previously uncharacterized factors AK023948 and DHX9 as important players in the AKT pathway, and that their upregulation may contribute to breast tumour progression.	28176758	RID02045	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Inflammatory bowel disease	CBR3-AS1	TJP1	positively-E	RNAi	downregulation	qPCR	NA	NA	intestinal epithelial barrier(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000104067	NA	100506428	7082	PlncRNA-1|PlncRNA1	ZO-1	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease. DSS induced injury of intestinal epithelial barrier, while overexpression of PlncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.	28153728	RID02046	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Inflammatory bowel disease	miR-34c-5p	CBR3-AS1	negatively-F	RNA pull-down assay;luciferase reporter assay	downregulation	qPCR	NA	NA	intestinal epithelial barrier(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	miRNA	lncRNA	NA	NA	ENSG00000236830	GRCh38_21:36131767-36175815	NA	100506428	NA	PlncRNA-1|PlncRNA1	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease. DSS induced injury of intestinal epithelial barrier, while overexpression of PlncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.	28153728	RID02047	ceRNA or sponge	NA	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)
Oral squamous cell carcinoma	TLR3	lnc-IL7R	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Oral cavity cancer	PCG	lncRNA	ENSG00000164342	NA	ENSG00000168685	GRCh38_5:35852695-35879603	7098	NA	CD283|IIAE2	NA	The TLR3 Agonist Inhibit Drug Efflux and Sequentially Consolidates Low-Dose Cisplatin-Based Chemoimmunotherapy while Reducing Side Effects. TLR3 negatively manipulated the inflammation-related long noncoding RNA lnc-IL7R, which was upregulated during this chemotherapy. Knockdown of lnc-IL7R improved the chemotherapy sensitivity. Knockdown of lnc-IL7R improved the chemotherapy sensitivity. Overall, this study provided preclinically new instructions for the PIC/cisplatin utilization to target tumor microenvironment and strengthen the low-dose cisplatin-based chemotherapy with reduced side effects.	28138030	RID02048	expression association	chemoresistance	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Malignant glioma	UCA1	PPP1R13L	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000104881	NA	652995	10848	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	IASPP|NKIP1|RAI|RAI4	The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP. In this study, we firstly found that UCA1 was upregulated in glioma tumor samples and negatively correlated with survival time. Our results showed that upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation. MiR-182 directly binds to the iASPP 3'UTR and inhibits iASPP expression	28137422	RID02049	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Retinoblastoma	BDNF-AS	CDC42	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000070831	NA	497258	998	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CDC42Hs|G25K|TKS	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02050	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	BDNF-AS	CCNE1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000105173	NA	497258	898	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CCNE|pCCNE1	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02051	expression association	prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Retinoblastoma	BDNF-AS	BDNF	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000176697	NA	497258	627	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	ANON2|BULN2	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02052	expression association	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	LINC00511	CDKN1C	negatively-E	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000129757	NA	400619	1028	LCAL5|onco-lncRNA-12	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long Intergenic Noncoding RNA 00511 Acts as an Oncogene in Non-small-cell Lung Cancer by Binding to EZH2 and Suppressing p57. We found LINC00511 was upregulated and associated with oncogenesis, tumor size, metastasis, and poor prognosis in NSCLC. LINC00511 affected cell proliferation, invasiveness, metastasis, and apoptosis in multiple NSCLC cell lines. Mechanistically, LINC00511 bound histone methyltransferase enhancer of zeste homolog 2 ((EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), a highly conserved protein complex that regulates gene expression by methylating lysine 27 on histone H3), and acted as a modular scaffold of EZH2/PRC2 complexes, coordinated their localization, and specified the histone modification pattern on the target genes, including p57, and consequently altered NSCLC cell biology.	27845772	RID02053	epigenetic regulation	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Melanoma	NKILA	NFKB1	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	The long non-coding RNA NKILA inhibits the invasion-metastasis cascade of malignant melanoma via the regulation of NF-kB. Real-time PCR (qRT-PCR) showed that NKILA was expressed at low levels in human melanoma tissues. Furthermore, qRT-PCR showed that NF-kB, which was negatively correlated with NKILA, was highly expressed in human melanoma tissues. Moreover, our results indicated that NKILA inhibited the carcinogenesis of melanoma cells through the inhibition of NF-kB in vitro. More importantly, we found that NKILA suppressed the growth of melanoma tumors via NF-kB in vivo. In conclusion, NKILA suppressed the development of malignant melanoma via the regulation of NF-kB and may be a potential therapeutic target in patients with melanoma.	28123845	RID02054	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	POU5F1	AK055347	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000204531	NA	NA	GRCh38_1:166057426-166166969	5460	NA	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	NA	Transcription factor Oct4 promotes osteosarcoma by regulating lncRNA AK055347. The present study observed Oct4 was markedly increased in osteosarcoma cell lines and in human osteosarcoma tissue samples. Notably, downregulation of Oct4 decreased the expression of AK055347, a newly identified long noncoding RNA (lncRNA) in human tissues. The downregulation of AK055347 by siRNA resulted in a significant suppressive effect on proliferative and invasive ability, and promotion of cell apoptosis in osteosarcoma cells.	28123573	RID02055	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Oral squamous cell carcinoma	TUG1	CTNNB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000168036	NA	55000	1499	LINC00080|NCRNA00080|TI-227H	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02056	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Oral squamous cell carcinoma	TUG1	CCND1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000110092	NA	55000	595	LINC00080|NCRNA00080|TI-227H	BCL1|D11S287E|PRAD1|U21B31	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02057	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	TUG1	MYC	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000136997	NA	55000	4609	LINC00080|NCRNA00080|TI-227H	MRTL|MYCC|bHLHe39|c-Myc	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02058	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LNCRNA-ATB	miR-141-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	NA	GRCh38_14:19126530-19128974	NA	NA	114004396	NA	NA	NA	Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFbeta2 feedback loop. We found that lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-beta actives lnc-ATB and TGF-beta2 directly binds mir-141-3p. Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner.	28115163	RID02059	ceRNA or sponge	NA	NA	NA
Gastric cancer	TGFB2	LNCRNA-ATB	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000092969	NA	NA	GRCh38_14:19126530-19128974	7042	114004396	G-TSF|LDS4|TGF-beta2	NA	Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFbeta2 feedback loop. We found that lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-beta actives lnc-ATB and TGF-beta2 directly binds mir-141-3p. Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner.	28115163	RID02060	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	NA
Colorectal cancer	HOXA-AS2	CDKN1A	negatively-E	RIP;western blot;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124762	NA	285943	1026	HOXA3as	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02061	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	HOXA-AS2	KLF2	negatively-E	RIP;western blot;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000127528	NA	285943	10365	HOXA3as	LKLF	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02062	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	UCA1	CCND1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000110092	NA	652995	595	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCL1|D11S287E|PRAD1|U21B31	A long noncoding RNA UCA1 promotes proliferation and predicts poor prognosis in glioma.LncRNA UCA1 expression in the glioma samples was obviously higher as compared with the normal brain samples (P < 0.001), and the expression was correlated significantly with grading of the tumors (P < 0.05). LncRNA UCA1 can promote the proliferation and cell cycle progression of glioma cells by upregulating cyclin D1 transcription.	28105536	RID02063	expression association	prognosis	UP(PAAD);DATA(GSE40174)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	GAS5	IL10	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);ERK1/1 signaling pathway(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000136634	NA	60674	3586	NCRNA00030|SNHG2	CSIF|GVHDS|IL-10|IL10A|TGIF	Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression. In this study, we found that GAS5 was commonly downregulated in CRC tissues, serum of CRC patients and CRC cell lines. We further demonstrated that knockdown of GAS5 increased the expression and secretion of interleukin-10 (IL-10) and vascular endothelial growth factor (VEGF-A) via NF-kB and Erk1/2 pathways. The cytokines IL-10 and VEGF-A inhibited by GAS5 may provide targets for lncRNA-based therapies for CRC.	28099146	RID02064	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	GAS5	VEGFA	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);ERK1/2 signaling pathway(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000112715	NA	60674	7422	NCRNA00030|SNHG2	MVCD1|VEGF|VPF	Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression.We further demonstrated that knockdown of GAS5 increased the expression and secretion of interleukin-10 (IL-10) and vascular endothelial growth factor (VEGF-A) via NF-kB and Erk1/2 pathways.	28099146	RID02065	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cervical cancer	TUG1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171791	NA	55000	596	LINC00080|NCRNA00080|TI-227H	Bcl-2|PPP1R50	Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl-2 and caspase-3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial-mesenchymal transition (EMT).	28088836	RID02066	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	TUG1	CASP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000164305	NA	55000	836	LINC00080|NCRNA00080|TI-227H	CPP32|CPP32B|SCA-1	Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl-2 and caspase-3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial-mesenchymal transition (EMT).	28088836	RID02067	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	CCAT2	ZBTB7A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000178951	NA	101805488	51341	LINC00873|NCCP1	FBI-1|FBI1|LRF|TIP21|ZBTB7|ZNF857A|pokemon	LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer. CCAT2 and Pokemon were over-expressed in NSCLC tissue and cells. CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21; The results indicated that CCAT2 promotes tumorigenesis by over-expression of Pokemon, and the potential mechanism might relate to the Pokemon related gene p21.	28088736	RID02068	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CCAT2	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000124762	NA	101805488	1026	LINC00873|NCCP1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer.CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21;	28088736	RID02069	expression association	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Retinoblastoma	CCAT1	miR-218-5p	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1 promotes human retinoblastoma SO-RB50 and Y79 cells through negative regulation of miR-218-5p. LncRNA CCAT1 promotes the proliferation migration and invasion, and reduces cell apoptosis of SO-RB50 and Y79 cells, probably through negative modulation of miR-218-5p.	28088735	RID02070	expression association	NA	NA	NA
Hepatocellular carcinoma	ACTA2-AS1	ACTA2	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000107796	NA	100132116	59	UC001kfo|ZXF1|uc001kfo.1	ACTSA	Long non-coding RNA UC001kfo promotes hepatocellular carcinoma proliferation and metastasis by targeting alpha-SMA. The present study found that the expression of UC001kfo was upregulated in HCC tissues and cell lines in comparison with tumour-adjacent tissues and normal hepatocytes, respectively. UC001kfo was verified to promote the proliferation, metastasis and epithelial-mesenchymal transition (EMT) in HCC cells in both in vitro and in vivo assays. Mechanistically, alpha-SMA was indicated as a potential target gene of UC001kfo in mediating HCC metastasis.	28088733	RID02071	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE55807)
Gastric cancer	TGFB1	UCA1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000214049	GRCh38_19:15828206-15836328	7040	652995	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02072	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Gastric cancer	UCA1	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124216	NA	652995	6615	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02073	expression association	metastasis	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Gastric cancer	UCA1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000026025	NA	652995	7431	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02074	expression association	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	UCA1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000039068	NA	652995	999	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02075	expression association	metastasis	UP(PAAD);DATA(GSE40174)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	UCA1	TJP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000104067	NA	652995	7082	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ZO-1	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02076	expression association	metastasis	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Chronic myeloid leukemia	HULC	MYC	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	imatinib	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000136997	NA	728655	4609	HCCAT1|LINC00078|NCRNA00078	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548	RID02077	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Chronic myeloid leukemia	HULC	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000171791	NA	728655	596	HCCAT1|LINC00078|NCRNA00078	Bcl-2|PPP1R50	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548	RID02078	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Klatskin's tumor	MALAT1	CXCR4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000121966	NA	378938	7852	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Long Non-Coding RNA MALAT1 Interacts With miR-204 to Modulate Human Hilar Cholangiocarcinoma Proliferation, Migration, and Invasion by Targeting CXCR4. In our research, lncRNA-MALAT1 was specifically upregulated in HCCA tissues and cell lines, and was associated with pathological T stage, a larger tumor size, and perineural invasion.In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration, and invasion. By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion. Taken together, our data indicated that MALAT1 might play an oncogenic role in HCCA through miR-204-dependent CXCR4 regulation, and could be regarded as a therapeutic target in HCCA.	28059437	RID02079	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	LINC00052	ERBB3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000065361	NA	145978	2065	NCRNA00052|TMEM83	ErbB-3|FERLK|HER3|LCCS2|MDA-BF-1|c-erbB-3|c-erbB3|erbB3-S|p180-ErbB3|p45-sErbB3|p85-sErbB3	HER3 and LINC00052 interplay promotes tumor growth in breast cancer.Here we report that the lncRNA LINC00052 expression correlates positively with HER3/ErbB3 levels in breast cancer cells. Gene silencing of LINC00052 diminished both LINC00052 and HER3 expression and reduced cancer cell growth in vitro and in vivo. LINC00052 overexpression promoted cancer cell growth in vitro and in vivo and increased HER3-mediated downstream signaling.Taken together, our results indicate that high LINC00052 levels predict activation of HER3-mediated signaling, and LINC00052 expression level may serve as a potential biomarker for HER3 targeted antibody cancer therapies.	28036286	RID02080	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Osteosarcoma	PANDAR	CDKN2C	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000123080	NA	101154753	1031	PANDA	INK4C|p18|p18-INK4C	Long Noncoding RNA PANDA Positively Regulates Proliferation of Osteosarcoma Cells. PANDA was highly expressed in U2OS cells, and its expression was induced by DNA damage. Silencing PANDA caused arrest at the G1 phase of the cell cycle, leading to inhibition of cell proliferation. Quantitative RT-PCR showed that silencing PANDA increased mRNA levels of the cyclin-dependent kinase inhibitor p18, which caused G1 phase arrest.	28011477	RID02081	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Malignant glioma	H19	miR-675-5p	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	host	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 is overexpressed in glioma tissue, is negatively associated with patient survival, and promotes tumor growth through its derivative miR-675. These effects of lncRNA H19 appeared to be intermediated by miR-675. The latter was overexpressed in glioma tissue and was negatively associated with patient survival. Supporting the involvement of miR-675, its antagomir decreased proliferation of glioma cell lines, whereas its mimic increased proliferation of NHA cells.	27981546	RID02082	expression association	NA	UP(NSCLC);DATA(GSE74639)	NA
Retinoblastoma	HOTAIR	RB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000139687	NA	100124700	5925	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Long non-coding RNA regulates proliferation and invasion via activating Notch signalling pathway in retinoblastoma. HOTAIR expression was found to be significantly upregulated in human retinoblastomas tissues as compared with that in paracancerous tissues. Knockdown of HOTAIR restricted the proliferation and invasion of the more invasive retinoblastoma Y79 cells, and led to G0/G1 arrest, possibly through inhibiting phospho-RB1, RB1 and CCNE.	27966488	RID02083	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	HOTAIR	CCNE1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105173	NA	100124700	898	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCNE|pCCNE1	Long non-coding RNA regulates proliferation and invasion via activating Notch signalling pathway in retinoblastoma.Knockdown of HOTAIR restricted the proliferation and invasion of the more invasive retinoblastoma Y79 cells, and led to G0/G1 arrest, possibly through inhibiting phospho-RB1, RB1 and CCNE.	27966488	RID02084	expression association	NA	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Choriocarcinoma	LINC00261	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000164305	NA	140828	836	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	CPP32|CPP32B|SCA-1	Long Noncoding RNA LINC00261 Suppresses Cell Proliferation and Invasion and Promotes Cell Apoptosis in Human Choriocarcinoma. The transcription level of LINC00261 was significantly lower in choriocarcinoma tissues and in choriocarcinoma cell lines. Meanwhile, it promoted cell apoptosis and the relative activities of caspase 3 and caspase 9 in choriocarcinoma JEG-3 and JAR cells.	27983929	RID02085	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Choriocarcinoma	LINC00261	CASP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000132906	NA	140828	842	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long Noncoding RNA LINC00261 Suppresses Cell Proliferation and Invasion and Promotes Cell Apoptosis in Human Choriocarcinoma. The transcription level of LINC00261 was significantly lower in choriocarcinoma tissues and in choriocarcinoma cell lines. Meanwhile, it promoted cell apoptosis and the relative activities of caspase 3 and caspase 9 in choriocarcinoma JEG-3 and JAR cells.	27983929	RID02086	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Malignant glioma	TUG1	miR-145-5p	negatively-F	western blot;ChIP	upregulation	qPCR	NA	NA	self-renewal(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment. In this study, we find that Notch1 activation in GSCs specifically induces expression of the lncRNA, TUG1. TUG1 coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by locus-specific methylation of histone H3K27 via YY1-binding activity in the nucleus. Our results highlight the importance of the Notch-lncRNA axis in regulating self-renewal of glioma cells and provide a strong rationale for targeting TUG1 as a specific and potent therapeutic approach to eliminate the GSC population.	27922002	RID02087	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Malignant glioma	NOTCH1	TUG1	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	protein-DNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000148400	NA	ENSG00000253352	GRCh38_22:30969245-30979395	4851	55000	AOS5|AOVD1|TAN1|hN1	LINC00080|NCRNA00080|TI-227H	Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment. In this study, we find that Notch1 activation in GSCs specifically induces expression of the lncRNA, TUG1. TUG1 coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by locus-specific methylation of histone H3K27 via YY1-binding activity in the nucleus. Our results highlight the importance of the Notch-lncRNA axis in regulating self-renewal of glioma cells and provide a strong rationale for targeting TUG1 as a specific and potent therapeutic approach to eliminate the GSC population.	27922002	RID02088	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Malignant glioma	MALAT1	miR-155	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. Our results showed that the expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues.The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.	27904771	RID02089	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Malignant glioma	MALAT1	FBXW7	positively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109670	NA	378938	55294	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. Our results showed that the expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues.The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.	27904771	RID02090	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367)
Gastric cancer	HOTAIR	miR-126-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP1 signaling pathway(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02091	ceRNA or sponge	chemoresistance	NA	NA
Gastric cancer	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP0 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02092	expression association	chemoresistance	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Gastric cancer	HOTAIR	PIK3R2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP1 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105647	NA	100124700	5296	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MPPH|MPPH1|P85B|p85|p85-BETA	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02093	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	SPRY4-IT1	TWIST1	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_5:142317636-142318322	ENSG00000122691	NA	100642175	7291	SPRIGHTLY	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02094	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	SPRY4-IT1	VIM	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000026025	NA	100642175	7431	SPRIGHTLY	NA	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02095	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	SPRY4-IT1	CDH1	negatively-E	ChIP;western blot;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	histone modification	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000039068	NA	100642175	999	SPRIGHTLY	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02096	epigenetic regulation	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Endometrial cancer	BANCR	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000087245	NA	100885775	4313	LINC00586	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway. qRT-PCR revealed that the expression of lncRNA BANCR was higher in type 1 EC (P<0.01). knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression. BANCR is highly expressed in type 1 EC tissue and promotes EC-cell proliferation, migration, and invasion by activating ERK/MAPK signaling pathway that regulates MMP2/MMP1 expression. BANCR is expected to become a prognostic marker and therapeutic target in type 1 EC.	27898420	RID02097	expression association	prognosis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DATA(GSE40174)
Endometrial cancer	BANCR	MMP1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000196611	NA	100885775	4312	LINC00586	CLG|CLGN	Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway.knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression.	27898420	RID02098	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteosarcoma	EWSAT1	MEG3	positively-E	RNAi	NA	NA	NA	NA	cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	lncRNA	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000214548	GRCh38_14:100779410-100861031	283673	55384	LINC00277|NCRNA00277|TMEM84	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Long Noncoding RNA EWSAT1 Promotes Osteosarcoma Cell Growth and Metastasis Through Suppression of MEG3 Expression. In the present study, gain- and loss-of-function assays demonstrated that EWSAT1 enhanced OS cell proliferation, migration, and invasion. Further mechanistic studies found that EWSAT1 positively regulated lncRNA MEG3 expression in the transcriptional level. Finally, we observed that EWSAT1 facilitates OS cell growth and metastasis through regulation of MEG3, suggesting that EWSAT1-MEG3 axis might be a promising target for OS treatment.	27860482	RID02099	expression association	metastasis	NA	NA
Pre-eclampsia	SPRY4-IT1	ELAVL1	interact	RIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000066044	NA	100642175	1994	SPRIGHTLY	ELAV1|HUR|Hua|MelG	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02100	interact with protein	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Pre-eclampsia	SPRY4-IT1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000168036	NA	100642175	1499	SPRIGHTLY	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02101	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pre-eclampsia	SPRY4-IT1	WNT3	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000108379	NA	100642175	7473	SPRIGHTLY	INT4|TETAMS	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02102	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC);DATA(GSE117623)
Pre-eclampsia	SPRY4-IT1	WNT5B	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000111186	NA	100642175	81029	SPRIGHTLY	NA	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02103	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Estrogen-receptor positive breast cancer	H19	PMAIP1	negatively-E	ChIP;western blot;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141682	NA	283120	5366	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	APR|NOXA	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02104	epigenetic regulation	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE111842,GSE51827)
Estrogen-receptor positive breast cancer	ESR1	H19	positively-E	western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000130600	GRCh38_11:1995176-2001470	2099	283120	ER|ESR|ESRA|ESTRR|Era|NR3A1	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02105	expression association	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(NSCLC);DATA(GSE74639)
Gastric cancer	YAP1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000228630	GRCh38_12:53962308-53974956	10413	100124700	COB1|YAP|YAP2|YAP65|YKI	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02106	expression association	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	NA
Gastric cancer	YAP1	H19	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000130600	GRCh38_11:1995176-2001470	10413	283120	COB1|YAP|YAP2|YAP65|YKI	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02107	expression association	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	UP(NSCLC);DATA(GSE74639)
Gastric cancer	YAP1	MALAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10413	378938	COB1|YAP|YAP2|YAP65|YKI	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02108	expression association	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Gastric cancer	YAP1	LATS2-AS1-001	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	NA	GRCh38_13:21005157-21018122	10413	NA	COB1|YAP|YAP2|YAP65|YKI	NA	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02109	expression association	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	NA
Lung cancer	RB1	MEG3	negatively-E	5-azadC;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);RB signaling pathway(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000139687	NA	ENSG00000214548	GRCh38_14:100779410-100861031	5925	55384	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Expression of the lncRNA Maternally Expressed Gene 3 (MEG3) Contributes to the Control of Lung Cancer Cell Proliferation by the Rb Pathway. Treatment of these cells with palbociclib also decreased the expression of pRb-regulated DNA methyltransferase 1 (DNMT1), while conversely, knockdown of DNMT1 resulted in increased expression of MEG3. As gene methylation has been suggested for MEG3 regulation, we found that palbociclib resulted in decreased methylation of the MEG3 locus similar to that observed with 5-aza-deoxycytidine.while analysis of the TCGA database revealed decreased MEG3 expression in human lung tumors harboring a disrupted RB pathway. Together, these data suggest that disruption of the pRb-DNMT1 pathway leads to a decrease in MEG3 expression, thereby contributing to the pro-proliferative state of certain cancer cells.	27832204	RID02110	epigenetic regulation	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Hepatocellular carcinoma	CRNDE	miR-384	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	LncRNA CRNDE promotes hepatic carcinoma cell proliferation, migration and invasion by suppressing miR-384. Herein, we found that the expression of CRNDE was increased in human hepatic carcinoma (HCC) tissues and cell lines. Moreover, we indicated CRNDE negatively regulated miR-384 expression in HCC. In addition, we found that CRNDE accelerated the expression levels of NF-kB and p-AKT though inhibition of miR-384.	27822419	RID02111	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	NA
Cancer	TP53TG1	YBX1	interact	ChIP;western blot	downregulation	qPCR	NA	NA	chemoresistance(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	compounds that damage DNA	NA	Genome Instability and Mutation	Cancer	Cancer	lncRNA	TF	ENSG00000182165	GRCh38_7:87322943-87345528	ENSG00000065978	NA	11257	4904	LINC00096|NCRNA00096|P53TG1|P53TG1-D|TP53AP1	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Epigenetic inactivation of the p53-induced long noncoding RNA TP53 target 1 in human cancer. we show that TP53TG1 binds to the multifaceted DNA/RNA binding protein YBX1 to prevent its nuclear localization and thus the YBX1-mediated activation of oncogenes. TP53TG1 epigenetic inactivation in cancer cells releases the transcriptional repression of YBX1-targeted growth-promoting genes and creates a chemoresistant tumor.The epigenetic loss of TP53TG1 therefore represents an altered event in an lncRNA that is linked to classical tumoral pathways, such as p53 signaling, but is also connected to regulatory networks of the cancer cell.	27821766	RID02112	interact with protein	chemoresistance	DOWN(PAAD,BRCA);UP(BRCA);DATA(GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	BX357664	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02113	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	BX357664	MAPK14	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000112062	NA	NA	1432	NA	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02114	expression association	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Renal cell carcinoma	BX357664	HSPB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000106211	NA	NA	3315	NA	CMT2F|HEL-S-102|HMN2B|HS.76067|HSP27|HSP28|Hsp25|SRP27	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02115	expression association	metastasis	NA	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Colon cancer	GSEC	DHX36	negatively-F	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE20916	GSE20916.zip	cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280832	GRCh38_11:126340889-126355587	ENSG00000174953	NA	399972	170506	DCPS-AS1|ST3GAL4-AS1	DDX36|G4R1|MLEL1|RHAU	The novel G-quadruplex-containing long non-coding RNA GSEC antagonizes DHX36 and modulates colon cancer cell migration. In this study, we analyze the gene expression profiles of colon cancer tissues and identify a previously unannotated lncRNA, FLJ39051, that we term GSEC (G-quadruplex-forming sequence containing lncRNA), as a lncRNA that is upregulated in colorectal cancer.We also show that GSEC binds to the DEAH box polypeptide 36 (DHX36) RNA helicase via its G-quadruplex-forming sequence and inhibits DHX36 G-quadruplex unwinding activity.	27797375	RID02116	interact with protein	NA	DOWN(BRCA);DATA(GSE111842,GSE51827)	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	PVT1	FOXM1	positively-F	western blot;RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000111206	NA	5820	2305	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion. The lncRNA PVT1 was significantly upregulated in gastric cancer tissues compared with ANTs. PVT1 enhanced gastric cancer cell proliferation and invasion in vitro and in vivo. PVT1 directly bound FOXM1 protein and increased FOXM1 posttranslationally. Moreover, PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription.	27756785	RID02117	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Gastric cancer	FOXM1	PVT1	positively-E	western blot;RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000111206	NA	ENSG00000249859	GRCh38_8:127794526-128187101	2305	5820	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion.PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription.	27756785	RID02118	transcriptional regulation	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Aortic valve stenosis	H19	NOTCH1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	biomineral tissue development(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148400	NA	283120	4851	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AOS5|AOVD1|TAN1|hN1	Altered DNA Methylation of Long Noncoding RNA H19 in Calcific Aortic Valve Disease Promotes Mineralization by Silencing NOTCH1.We documented that lncRNA H19 (H19) was increased in calcific aortic valve disease.Gene promoter analyses showed that H19 silenced NOTCH1 by preventing the recruitment of p53 to its promoter. A knockdown of H19 in valve interstitial cells (VICs) increased the expression of NOTCH1 and decreased the level of RUNX2 and BMP2, 2 downstream targets repressed by NOTCH1.In rescue experiments, the transfection of a vector encoding for the active Notch intracellular domain prevented H19-induced mineralization of valve interstitial cells.	27789555	RID02119	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	91H	H19	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	lncRNA	NA	GRCh38_11:1995176-1995988	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications. We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development.	27780718	RID02120	epigenetic regulation	NA	NA	UP(NSCLC);DATA(GSE74639)
Breast cancer	91H	IGF2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_11:1995176-1995988	ENSG00000167244	NA	NA	3481	NA	C11orf43|GRDF|IGF-II|PP9974	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications. We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development.	27780718	RID02121	epigenetic regulation	NA	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Breast cancer	SATB1	UCA1	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(-);cell survival(-)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	TF	lncRNA	ENSG00000182568	NA	ENSG00000214049	GRCh38_19:15828206-15836328	6304	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer. SATB1 is highly expressed in aggressive breast cancer cells and promotes growth and metastasis by reprograming gene expression. long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was upregulated by SATB1 depletion. Upregulation of UCA1 coincided with increased H3K4 trimethylation (H3K4me3) levels and decreased H3K27 trimethylation (H3K27me3) levels. Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells.	27697109	RID02122	epigenetic regulation	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Uveal melanoma	HIC1	lncRNA-numb	positively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Uveal cancer	TF	lncRNA	ENSG00000177374	NA	ENSG00000284930	GRCh38_14:73460935-73463642	3090	NA	ZBTB29|ZNF901|hic-1	NA	HIC1 modulates uveal melanoma progression by activating lncRNA-numb. In this study, we found that HIC1 acted as a tumor suppressor and that its expression was downregulated in UM. Moreover, through long non-coding RNA (lncRNA) microarray and real-time PCR, we found that expression of lncRNA-numb was activated by HIC1 in UM. The results provide evidence that lncRNA-numb is a newly proposed tumor suppressor that is involved in HIC1-induced phenotypes. Taken together, our studies of UM reveal a critical role of HIC1 in the regulation of tumorigenesis, at least partly through its downstream target, lncRNA-numb, and provide a potential therapeutic target for UM.	27449031	RID02123	expression association	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE51827,GSE75367,GSE86978)	NA
Nasopharynx carcinoma	NEAT1	ZEB1	positively-E	western blot;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);radioresistance(-)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000148516	NA	283131	6935	LINC00084|NCRNA00084|TncRNA|VINC	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma.We found that lncRNA NEAT1 was significantly upregulated in NPC cell lines and tissues. we found that there was reciprocal repression between NEAT1 and miR-204. ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.	27020592	RID02124	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	SNHG7	FAIM2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000135472	NA	84973	23017	NCRNA00061	LFG|LFG2|NGP35|NMP35|TMBIM2	lncRNA-SNHG7 promotes the proliferation, migration and invasion and inhibits apoptosis of lung cancer cells by enhancing the FAIM2 expression. In the present study, we found that the expression levels of lncRNA-SNHG7 mRNA and protein obviously increased in lung cancer tissues compared to adjacent non-cancerous tissues.In addition, lncRNA-SNHG7 was of positive relevance with FAIM2 in human lung cancer tissues.	27666964	RID02125	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD);DATA(GSE40174)
Malignant glioma	H19	PPP1R13L	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000104881	NA	283120	10848	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	IASPP|NKIP1|RAI|RAI4	The lncRNA H19 interacts with miR-140 to modulate glioma growth by targeting iASPP. lncRNA-H19 was specifically upregulated in glioma cell lines and promoted glioma cell growth through targeting miR-140. Knockdown of H19 inhibited the proliferation and invasion of human glioma cell and suppressed its metastasis in vitro and in vivo. In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth. IASPP mRNA is a direct target of miR-140.	27693036	RID02126	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Stroke	MEG3	TP53	positively-F	western blot;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	neuronal death(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA MEG3 activation of p53 mediates ischemic neuronal death in stroke.MEG3 directly binds with the p53 DNA binding domain (DBD) consisting of amino acids 271-282 (p53-DBD), which stimulates p53-mediated transactivation and mediates ischemic neuronal death.	27651151	RID02127	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	UCA1	CDKN1B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes the tumorigenesis in pancreatic cancer. In this study, we detected the mRNA expression of UCA1 in 128 PC patients by qRT-PCR, and found that UCA1 expression was significantly, up-regulated in tumor tissues than that in matched adjacent non-tumor tissues (p<0.05). Meanwhile, UCA1 expression negative-correlated with p27 in PC tissues (r2=0.46, p<0.01), and knockdown of p27 partly abrogated the cell proliferative activities caused by UCA1 (p<0.05).	27562722	RID02128	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	CCDC26	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000132646	NA	137196	5111	RAM	ATLD2	Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. We found that the CCDC26 expression was significantly higher in PC tissues than in normal tissues. Moreover, we found that the expression of CCDC26 was positively correlated with PCNA and Bcl2. Our data suggest that CCDC26 may be identified as a novel oncogene in PC, and responsible for growth and apoptosis of cancer cell, partly by regulating the PCNA and Bcl2 expression. This work provides a novel biomarker and therapeutic target of PC for cancer clinic in future.	27470572	RID02129	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Pancreatic cancer	CCDC26	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000171791	NA	137196	596	RAM	Bcl-2|PPP1R50	Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. We found that the CCDC26 expression was significantly higher in PC tissues than in normal tissues. Moreover, we found that the expression of CCDC26 was positively correlated with PCNA and Bcl2. Our data suggest that CCDC26 may be identified as a novel oncogene in PC, and responsible for growth and apoptosis of cancer cell, partly by regulating the PCNA and Bcl2 expression. This work provides a novel biomarker and therapeutic target of PC for cancer clinic in future.	27470572	RID02130	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Thyroid cancer	MALAT1	IQGAP1	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000140575	NA	378938	8826	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HUMORFA01|SAR1|p195	MALAT1 promotes the proliferation and invasion of thyroid cancer cells via regulating the expression of IQGAP1. we discovered the higher level of MALAT-1 and expression of IQGAP1 in thyroid cancer tissues and in thyroid cancer cells compared to that in the control. MALAT-1 could upregulate the expression of IQGAP1 in thyroid cancer cells. In addition, IQGAP1 knockdown reversed the decreasing cell proliferation and invasion of thyroid cancer induced by MALAT-1 overexpression.	27470543	RID02131	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gallbladder cancer	MALAT1	ANXA2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000182718	NA	378938	302	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206. In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect.	27191262	RID02132	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Gallbladder cancer	MALAT1	KRAS	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000133703	NA	378938	3845	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206. In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect.	27191262	RID02133	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Non-small cell lung cancer	WSPAR	EPCAM	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	self-renewal(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000119888	NA	105664404	4072	LncTCF7|TCONS_00009511	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	Long noncoding RNA TCF7 promotes invasiveness and self-renewal of human non-small cell lung cancer cells. We showed that lncTCF7 increased slug expression to promote the invasive capability of NSCLC cells and upregulated EpCAM expression to promote the self-renewal.	27766570	RID02134	ceRNA or sponge	NA	NA	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	WSPAR	SNAI2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000019549	NA	105664404	6591	LncTCF7|TCONS_00009511	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long noncoding RNA TCF7 promotes invasiveness and self-renewal of human non-small cell lung cancer cells. We showed that lncTCF7 increased slug expression to promote the invasive capability of NSCLC cells and upregulated EpCAM expression to promote the self-renewal.	27766570	RID02135	transcriptional regulation	NA	NA	NA
Malignant glioma	miR-23b-3p	TUSC7	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	miRNA	lncRNA	NA	NA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Long Non-coding RNA TUSC7, a Target of miR-23b, Plays Tumor-Suppressing Roles in Human Gliomas. TUSC7 was poorly expressed in tissues and cell lines of glioma, and the lower expression was correlated with glioma of the worse histological grade. Bioinformatics analysis showed that TUSC7 specifically binds to miR-23b. MiR-23b was up-regulated in glioma and negatively correlated with the expression of TUSC7. The miR-23b expression was inhibited remarkably by the upregulation of TUSC7 and the reciprocal inhibition was determined between TUSC7 and miR-23b.We conclude that the lncRNA TUSC7 acted as a tumor suppressor gene negatively regulated by miR-23b, suggesting a novel therapeutic strategy against gliomas.	27766072	RID02136	ceRNA or sponge	NA	NA	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	UCA1	miR-196a-5p	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin;gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells. Urothelial Cancer Associated 1 (UCA1), an lncRNA, is reportedly upregulated in human bladder carcinoma and promotes cancer cell proliferation, migration, invasion, and drug resistance. UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	27591936	RID02137	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	NA
Urinary bladder cancer	UCA1	CDKN1B	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin;gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells. Urothelial Cancer Associated 1 (UCA1), an lncRNA, is reportedly upregulated in human bladder carcinoma and promotes cancer cell proliferation, migration, invasion, and drug resistance. UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	27591936	RID02138	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	CYTOR	ERBB4	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);AKT signaling pathway(-)	ceRNA(miR-193a-3p)	regulation	NA	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000178568	NA	112597	2066	C2orf59|LINC00152|NCRNA00152	ALS19|HER4|p180erbB4	Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer.This study showed that a novel lncRNA, long intergenic noncoding RNA 152 (Linc00152 ), promoted tumor progression and conferred resistance to oxaliplatin (L-OHP)-induced apoptosis in vitro and in vivo. It antagonized chemosensitivity through acting as a competing endogenous RNA to modulate the expression of miR-193a-3p, and then erb-b2 receptor tyrosine kinase 4 (ERBB4). Consistent with above findings, the specific AKT signaling inhibitor and activator were used, respectively, which demonstrated that Linc00152 contributed to L-OHP resistance at least partly through activating AKT pathway. Collectively, our findings established Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance.Previous reports suggest that miR-193a-3p suppresses tumor proliferation, invasion, and metastasis by directly targeting and downregulating the expression of ERBB4.	27633443	RID02139	ceRNA or sponge	metastasis,chemoresistance,prognosis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE111842)
Malignant glioma	HOTTIP	BABAM2	negatively-F	RIP	downregulation	qPCR	NA	NA	cell growth(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000158019	NA	100316868	9577	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo.Furthermore, HOTTIP could directly bind to the brain and reproductive expression (BRE) gene and down-regulate BRE gene expression. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02140	interact with mRNA	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807)
Malignant glioma	HOTTIP	CDK2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000123374	NA	100316868	1017	HOXA-AS6|HOXA13-AS1|NCRNA00213	CDKN2|p33(CDK2)	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02141	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	HOTTIP	CCNA2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000145386	NA	100316868	890	HOXA-AS6|HOXA13-AS1|NCRNA00213	CCN1|CCNA	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02142	expression association	NA	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807,GSE67939)
Malignant glioma	HOTTIP	TP53	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000141510	NA	100316868	7157	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCC7|BMFS5|LFS1|P53|TRP53	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02143	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	BC032469	TERT	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249201	GRCh38_5:1173141-1178605	ENSG00000164362	NA	NA	7015	NA	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	Upregulated long non-coding RNA BC032469 enhances carcinogenesis and metastasis of esophageal squamous cell carcinoma through regulating hTERT expression. Western blot analysis revealed that BC032469 regulated the expression of human telomerase reverse transcriptase (hTERT), which is important for cell proliferation and metastasis.	27726103;30223861	RID02144	expression association	metastasis	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Gallbladder cancer	H19	FOXM1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111206	NA	283120	2305	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer. We demonstrated H19 was overexpressed and negatively correlated with miR-342-3p in GBC. Furthermore, transwell invasion assays and cell cycle assays indicated that H19 knockdown inhibited both cells invasion and proliferation, but this effects was attenuated by co-transfection of siRNA-H19 and miR-342-3p inhibitor in GBC cells. Our results suggest a potential ceRNA regulatory network involving H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in GBC. This mechanism may contribute to a better understanding of GBC pathogenesis and provides potential therapeutic strategy for GBC.	27716361	RID02145	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung cancer	PCBP2-OT1	CCNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000134057	NA	102157401	891	NA	CCNB	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis. These results suggested the pro-oncogenic potential of uc.338 in lung cancer, which might provide novel clues for the diagnosis and treatment of lung cancer in the clinic.	27712590	RID02146	expression association	NA	NA	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Lung cancer	PCBP2-OT1	CDC25C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000158402	NA	102157401	995	NA	CDC25|PPP1R60	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02147	expression association	NA	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung cancer	PCBP2-OT1	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124216	NA	102157401	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02148	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Lung cancer	PCBP2-OT1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000170558	NA	102157401	1000	NA	CD325|CDHN|CDw325|NCAD	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02149	expression association	NA	NA	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Lung cancer	PCBP2-OT1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000026025	NA	102157401	7431	NA	NA	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02150	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Lung cancer	PCBP2-OT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000039068	NA	102157401	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02151	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Keloid	H19	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Keloid	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long non-coding RNA H19 promotes the proliferation of fibroblasts in keloid scarring. The results confirmed that knockdown of H19 inhibited mTOR and VEGF expression.In summary, the results indicate that H19 may be associated with increased proliferative activity of keloid fibroblasts, which may be mediated by mTOR and VEGF.	27698867	RID02152	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Keloid	H19	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Keloid	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000112715	NA	283120	7422	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MVCD1|VEGF|VPF	Long non-coding RNA H19 promotes the proliferation of fibroblasts in keloid scarring. The results confirmed that knockdown of H19 inhibited mTOR and VEGF expression.In summary, the results indicate that H19 may be associated with increased proliferative activity of keloid fibroblasts, which may be mediated by mTOR and VEGF.	27698867	RID02153	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Gastric cancer	UCA1	miR-27b-3p	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	adriamycin;cisplatin;5-fluorouracil	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Non-Coding RNA (LncRNA) Urothelial Carcinoma Associated 1 (UCA1) Increases Multi-Drug Resistance of Gastric Cancer via Downregulating miR-27b. UCA1 was significantly upregulated in the cancerous tissues and its expression was negatively correlated with miR-27b expression level. UCA1 knockdown and miR-27b overexpression reduced IC50 of ADR, DDP, and 5-FU in SGC-7901/ADR cells and increased ADR induced cell apoptosis.UCA1 is negatively correlated with miR-27b expression in gastric cancer tissue. Knockdown of UCA1 restored miR-27b expression in gastric cancer cells. The UCA1-miR-27b axis was involved in regulation of chemosensitivity of gastric cancer cells.	27694794	RID02154	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	NA
Endometrial adenocarcinoma	NEAT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000136997	NA	283131	4609	LINC00084|NCRNA00084|TncRNA|VINC	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma. The expression levels of NEAT1 were elevated in EEC tissues and cell lines, and higher expression levels of NEAT1 were positively correlated with FIGO stage and lymph node metastasis. Tumor metastasis real-time PRC array showed that six metastasis-related genes (c-myc, insulin like growth factor 1(IGF1), matrix metallopeptidase 2 (MMP-2) and matrix metallopeptidase 7(MMP-7) were up-regulated, and Cadherin 1 and TIMP metallopeptidase inhibitor 2 were down-regulated) in NEAT1-overexpressing HEC-59 cells. Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02155	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Endometrial adenocarcinoma	NEAT1	EIF4G1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000114867	NA	283131	1981	LINC00084|NCRNA00084|TncRNA|VINC	EIF-4G1|EIF4F|EIF4G|EIF4GI|P220|PARK18	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02156	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial adenocarcinoma	NEAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000087245	NA	283131	4313	LINC00084|NCRNA00084|TncRNA|VINC	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02157	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Endometrial adenocarcinoma	NEAT1	MMP7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000137673	NA	283131	4316	LINC00084|NCRNA00084|TncRNA|VINC	MMP-7|MPSL1|PUMP-1	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02158	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Lung cancer	CPS1-IT1	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000164305	NA	29034	836	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	CPP32|CPP32B|SCA-1	Long Noncoding RNA CPS1-IT1 Suppresses Cell Proliferation and Metastasis in Human Lung Cancer. It was found that lncRNA CPS1-IT1 was significantly lower in cancerous tissues than in noncancerous tissues. While cell apoptosis was induced, CPS1-IT1 overexpression promoted the activities of caspase 3 and caspase 9 without affecting that of caspase 8. These observations were suggestive of the tumor-suppressive role of lncRNA CPS1-IT1 in lung cancer.	27662619	RID02159	expression association	metastasis	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Lung cancer	CPS1-IT1	CASP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000132906	NA	29034	842	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long Noncoding RNA CPS1-IT1 Suppresses Cell Proliferation and Metastasis in Human Lung Cancer.While cell apoptosis was induced, CPS1-IT1 overexpression promoted the activities of caspase 3 and caspase 9 without affecting that of caspase 8. These observations were suggestive of the tumor-suppressive effect role of lncRNA CPS1-IT1 in lung cancer.	27662619	RID02160	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Osteosarcoma	TUG1	POU2F1	negatively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000143190	NA	55000	5451	LINC00080|NCRNA00080|TI-227H	OCT1|OTF1|oct-1B	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells, which involved the derepression of POU class 2 homeobox 1 (POU2F1) expression. In conclusion, our study elucidated a novel TUG1/miR-9-5p/POU2F1 pathway, in which TUG1 acted as a ceRNA by sponging miR-9-5p, leading to downregulation of POU2F1 and facilitating the tumorigenesis of osteosarcoma.	27658774	RID02161	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807)
Osteosarcoma	TUG1	miR-9-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells, which involved the derepression of POU class 2 homeobox 1 (POU2F1) expression. In conclusion, our study elucidated a novel TUG1/miR-9-5p/POU2F1 pathway, in which TUG1 acted as a ceRNA by sponging miR-9-5p, leading to downregulation of POU2F1 and facilitating the tumorigenesis of osteosarcoma.	27658774	RID02162	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	NA
Renal cell carcinoma	MALAT1	BIRC7	positively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101197	NA	378938	79444	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	KIAP|LIVIN|ML-IAP|MLIAP|RNF50	Biological function and mechanism of MALAT-1 in renal cell carcinoma proliferation and apoptosis: role of the MALAT-1-Livin protein interaction.LncRNA MALAT-1 and the Livin protein were highly expressed in RCC tissues, as well as in RCC 786-O and Caki-1 cell lines. The RIP results showed that MALAT-1 promoted the expression of the Livin protein in 786-O and Caki-1 cells by enhancing the stability of the protein.	27655020	RID02163	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Gastric cancer	CASC2	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000102882	NA	255082	5595	C10orf5	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway. Our results showed that CASC2 was significantly downregulated in human GC tissues and cell lines by quantitative RT-PCR. Overexpression of CASC2 in GC cells significantly inhibited the cell growth in vitro and in vivo. We further found that MAPK pathway especially the ERK1/2 and JNK component were involved in the CASC2 mediated GC cell proliferation. Moreover, combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro.	27648142	RID02164	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	CASC2	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000100030	NA	255082	5594	C10orf5	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway.combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro. Thus, these results indicated that CASC2 might serve as a tumor suppressor lncRNA that suppressed cell proliferation by inactivation of MAPK pathway.	27648142	RID02165	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	CASC2	MAPK8	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000107643	NA	255082	5599	C10orf5	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway.combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro. Thus, these results indicated that CASC2 might serve as a tumor suppressor lncRNA that suppressed cell proliferation by inactivation of MAPK pathway.	27648142	RID02166	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	IRAIN	KLF2	negatively-E	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000127528	NA	104472848	10365	IGF1R-AS	LKLF	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02167	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	IRAIN	CDKN2B	negatively-E	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000147883	NA	104472848	1030	IGF1R-AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02168	epigenetic regulation	NA	NA	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	LINC00312	miR-197-3p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p. LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion.	27631965	RID02169	ceRNA or sponge	NA	NA	NA
Breast cancer	NEAT1	EZH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|NCRNA00084|TncRNA|VINC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2. lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation. Taken together, our data indicated that NEAT1 might be an oncogenic lncRNA that promoted proliferation of BC and could be regarded as a therapeutic target in human BC.	28034643	RID02170	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Chronic myeloid leukemia	HOTAIR	ABCC1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+)	NA	association	NA	imatinib	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000103222	NA	100124700	4363	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC29|ABCC|GS-X|MRP|MRP1	The role of long noncoding RNA HOTAIR in the acquired multidrug resistance to imatinib in chronic myeloid leukemia cells.Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control. Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment. In addition, the activation of PI3K/Akt was greatly attenuated when HOTAIR was knocked down in K562-imatinib cells.These data suggest that the knockdown of HOTAIR may play a crucial role in improving acquired resistance to imatinib in CML K562-R cells via PI3K/Akt pathway.	27875938	RID02171	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SPRY4-IT1	ZNF703	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000183779	NA	100642175	80139	SPRIGHTLY	NLZ1|ZEPPO1|ZNF503L|ZPO1	Upregulated long noncoding RNA SPRY4-IT1 contributes to increased cell viability by activating zinc finger 703 expression in esophageal squamous cell carcinoma.We validated that SPRY4-IT1 was upregulated in ESCC tissues of advanced clinical stages.In vitro function assays demonstrated that SPRY4-IT1 cause promotion of cell viability in ESCC cells. We further verified that SPRY4-IT1 could also activate the expression of ZNF703 in ESCC cells, which might contribute to the role of SPRY4-IT1 in ESCC cells.	27453415	RID02172	expression association	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC);DATA(GSE117623)
Gastric cancer	MALAT1	EGFL7	positively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000172889	NA	378938	51162	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NEU1|VE-STATIN|ZNEU1	Overexpressed MALAT1 promotes invasion and metastasis of gastric cancer cells via increasing EGFL7 expression. The expression of MALAT1 was up-regulated in GC tissues and three cell lines. ChIP assay showed that MALAT1 regulated EGFL7 expression by altering the level of H3 histone acetylation in EGFL7 promoter.Up-regulated MALAT1 promoted the invasion and metastasis of GC, and the increase of EGFL7 expression was a potential mechanism via altering its H3 histone acetylation level.	27259812	RID02173	epigenetic regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	LINC01225	EGFR	positively-F	RIP	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260386	GRCh38_1:31500085-31508566	ENSG00000146648	NA	149086	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LINC01225 promotes occurrence and metastasis of hepatocellular carcinoma in an epidermal growth factor receptor-dependent pathway. Here, we verified that LINC01225 was upregulated in HCC. LINC01225 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR, and subsequently fine tune the EGFR/Ras/Raf-1/MEK/MAPK signaling pathway. Knockdown of LINC01225 resulted in inhibited cell proliferation and invasion with activated apoptosis and cell cycle arrest in vitro.	26938303	RID02174	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	NPTN-IT1	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	cell invasion(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000141510	NA	101241892	7157	lncRNA-LET	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA-Low Expression in Tumor inhibits the invasion and metastasis of esophageal squamous cell carcinoma by regulating p53 expression. lncRNA-LET expression was decreased in primary ESCC tissues when compared with paired healthy tissues, and was identified to be associated with the clinical features. Overexpression of lncRNA-LET was observed to inhibit the migration and invasion of ESCC cells, and modulate p53 expression levels in human ESCC cell lines in vitro.	26935396	RID02175	expression association	metastasis	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hypertrophic cardiomyopathy	CHAST	PLEKHM1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);cardiac hypertrophy(+)	NA	regulation	NA	NA	CSC	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	NA	GRCh38_11:103363213-103364651	ENSG00000225190	NA	NA	9842	NA	AP162|B2|OPTA3|OPTB6	Long noncoding RNA Chast promotes cardiac remodeling. Chast negatively regulated Pleckstrin homology domain-containing protein family M member 1 (opposite strand of Chast), impeding cardiomyocyte autophagy and driving hypertrophy. In accordance, CHAST homolog in humans was significantly up-regulated in hypertrophic heart tissue from aortic stenosis patients and in human embryonic stem cell-derived cardiomyocytes upon hypertrophic stimuli.	26888430	RID02176	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Ovarian cancer	NRCP	STAT1	positively-F	RIP	upregulation	microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENST00000481169	GRCh38_3:149162410-149221827	ENSG00000115415	NA	NA	6772	NA	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	Long Noncoding RNA Ceruloplasmin Promotes Cancer Growth by Altering Glycolysis. NRCP was highly upregulated in ovarian tumors, and knockdown of NRCP resulted in significantly increased apoptosis, decreased cell proliferation, and decreased glycolysis compared with control cancer cells. We identified NRCP as an intermediate binding partner between STAT1 and RNA polymerase II, leading to increased expression of downstream target genes such as glucose-6-phosphate isomerase.	26686630	RID02177	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	NRCP	GPI	positively-E	RNAi	upregulation	microarray	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENST00000481169	GRCh38_3:149162410-149221827	ENSG00000105220	NA	NA	2821	NA	AMF|GNPI|NLK|PGI|PHI|SA-36|SA36	Long Noncoding RNA Ceruloplasmin Promotes Cancer Growth by Altering Glycolysis. NRCP was highly upregulated in ovarian tumors, and knockdown of NRCP resulted in significantly increased apoptosis, decreased cell proliferation, and decreased glycolysis compared with control cancer cells. We identified NRCP as an intermediate binding partner between STAT1 and RNA polymerase II, leading to increased expression of downstream target genes such as glucose-6-phosphate isomerase.	26686630	RID02178	expression association	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE86978)
Cancer	LINC-ROR	HNRNPD	interact	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000138668	NA	100885779	3184	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AUF1|AUF1A|HNRPD|P37|hnRNPD0	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02179	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Cancer	LINC-ROR	PTBP1	interact	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000011304	NA	100885779	5725	ROR|lincRNA-RoR|lincRNA-ST8SIA3	HNRNP-I|HNRNPI|HNRPI|PTB|PTB-1|PTB-T|PTB2|PTB3|PTB4|pPTB	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02180	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cancer	LINC-ROR	MYC	negatively-E	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	RNA stability	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136997	NA	100885779	4609	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MRTL|MYCC|bHLHe39|c-Myc	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02181	interact with mRNA	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Loeys-Dietz syndrome	TGFB1	AK056155	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Genetic disease	Autosomal dominant disease	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_1:181059435-181061937	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	Long noncoding RNA AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway.Then we further verified that AK056155 was also overexpressed in aortic aneurysm patients by RT-PCR. Moreover, we demonstrated that the expression of AK056155 can be enhanced by TGF-beta1 in a concentration or time depended manner in HUVECs by RT-PCR. Furthermore, the expression of AK056155 was reduced with treatment of PI3K inhibitor (LY294002) or AKT inhibitor (GDC-0068) in combination with TGF-beta1. These results indicate that AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway, it may provide a promising target gene to prevent LDS develop in to aortic aneurysm.	26617788	RID02182	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Lung cancer	miR-217	MALAT1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Posttranscriptional silencing of the lncRNA MALAT1 by miR-217 inhibits the epithelial-mesenchymal transition via enhancer of zeste homolog 2 in the malignant transformation of HBE cells induced by cigarette smoke extract.the CSE-induced increase of MALAT1 expression was blocked by an miR-217 mimic, indicating that miR-217 negatively regulates MALAT1 expression.	26415832	RID02183	expression association	NA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	NBAT1	DKK1	negatively-E	ChIP;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000107984	NA	729177	22943	CASC14|NBAT-1	DKK-1|SK	NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2. ectopic NBAT1 inhibits migration and invasion of breast cancer cells. Mechanistic study shows that NBAT1 is associated with PRC2 member EZH2 and regulates global gene expression profile. Among them, DKK1 (dickkopf WNT signaling pathway inhibitor 1) is found to be regulated by NBAT1 in a PRC2 dependent manner, and is responsible for NBAT1's effects in inhibiting migration and invasion of breast cancer cells.	26378045	RID02184	epigenetic regulation	metastasis	NA	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	LUADT1	CDKN1B	negatively-E	ChIP	upregulation	qPCR;microarray	GSE66654	GSE66654.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000111276	NA	106182249	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27.Further analysis indicated that LUADT1 may regulate cell cycle progression by epigenetically inhibiting the expression of p27.RNA immunoprecipitation and chromatin immunoprecipitation assays confirmed that LUADT1 binds to SUZ12, a core component of polycomb repressive complex 2, and mediates the trimethylation of H3K27 at the promoter region of p27.	26291312	RID02185	epigenetic regulation	NA	UP(NSCLC,PRAD,SKCM);DATA(GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	NEAT1	MET	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-449b-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105976	NA	283131	4233	LINC00084|NCRNA00084|TncRNA|VINC	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis. By real-time PCR, we suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met. This regulation menchaism promotes glioma pathogenesis and may provide a potential target for the prognosis and treatment of glioma.	26242266	RID02186	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Lung cancer	GPLD1	CDKN2B-AS1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000112293	NA	ENSG00000240498	GRCh38_9:21994139-22128103	2822	100048912	GPIPLD|GPIPLDM|PIGPLD|PIGPLD1|PLD	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Down-regulation of Phospholipase D Stimulates Death of Lung Cancer Cells Involving Up-regulation of the Long ncRNA ANRIL. the expression level of antisense noncoding RNA in the INK4 locus (ANRIL) was increased up to 13.6-fold by PLD inhibition in H460 human lung cancer cells. Moreover, knockdown of ANRIL using its specific small-interfering RNA significantly suppressed PLD inhibition-induced apoptosis.	25964559	RID02187	expression association	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE55807)	UP(SKCM);DATA(GSE38495)
Esophagus squamous cell carcinoma	LINC01426	RUNX1	interact	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	alternative splicing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000234380	GRCh38_21:34745757-34784886	ENSG00000159216	NA	100506385	861	lincRNA-uc002yug.2	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	LincRNA-uc002yug.2 involves in alternative splicing of RUNX1 and serves as a predictor for esophageal cancer and prognosis. lincRNA-uc002yug.2 promoted a combination of RUNX1 and alternative splicing (AS) factors in the nucleus to produce more RUNX1a, the short isoform and inhibitor of RUNX1, and reduce CEBPalpha (CCAAT/enhancer-binding protein-alpha) gene expression, thereby promoting ESCC progression.These results indicated that lincRNA-uc002yug.2 might involve in AS of RUNX1/AML1 and serve as a predictor for esophageal cancer and prognosis.	25486427	RID02188	interact with mRNA	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Liver cancer	RUNX1	MT1DP	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000159216	NA	ENSG00000205361	GRCh38_16:56643705-56644786	861	326343	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	MTM	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02189	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)	NA
Liver cancer	YAP1	MT1DP	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000205361	GRCh38_16:56643705-56644786	10413	326343	COB1|YAP|YAP2|YAP65|YKI	MTM	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02190	transcriptional regulation	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	NA
Liver cancer	MT1DP	FOXA1	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000205361	GRCh38_16:56643705-56644786	ENSG00000129514	NA	326343	3169	MTM	HNF3A|TCF3A	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02191	expression association	NA	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Osteoarthritis	GAS5	miR-21-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(+);autophagic response(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	A long non-coding RNA, GAS5, plays a critical role in the regulation of miR-21 during osteoarthritis. The expression level of miR-21 was significantly reduced in OA patients, and the ectopic expression of GAS5 is capable of suppressing miR-21 induction. Consistent with GAS5 experiments, the introduction of miR-21 stimulated the apoptosis of chondrocytes and inhibited the expression levels of autophagic complexes, including LC-3B. Together, these results show that GAS5 contributes to the pathogenesis of OA by acting as a negative regulator of miR-21 and thereby regulating cell survival.	25196583	RID02192	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
B-cell lymphoma	FAS-AS1	FAS	negatively-F	RIP;ChIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);autophagic response(-)	alternative splicing	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_10:88991422-88992975	ENSG00000026103	NA	100302740	355	FAS-AS|FASAS|SAF	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	FAS-antisense 1 lncRNA and production of soluble versus membrane Fas in B-cell lymphoma. We found that the alternative splicing of Fas in lymphomas is tightly regulated by a long-noncoding RNA corresponding to an antisense transcript of Fas (FAS-AS1).EZH2-mediated repression of FAS-AS1 promoter can be released by DZNeP (3-Deazaneplanocin A) or overcome by ectopic expression of FAS-AS1, both of which increase levels of FAS-AS1 and correspondingly decrease expression of sFas. Treatment with Bruton's tyrosine kinase inhibitor or EZH2 knockdown decreases the levels of EZH2, RBM5 and sFas, thereby enhancing Fas-mediated apoptosis. This is the first report showing functional regulation of Fas repression by its antisense RNA.Treatment with Bruton's tyrosine kinase inhibitor or EZH2 knockdown decreases the levels of EZH2, RBM5 and sFas, thereby enhancing Fas-mediated apoptosis. This is the first report showing functional regulation of Fas repression by its antisense RNA.FAS-AS1 binds RBM5 and interferes with RBM5-mediated exon 6 skipping of Fas pre-mRNA.	24811343	RID02193	interact with mRNA	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	MYC	H19	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000130600	GRCh38_11:1995176-2001470	4609	283120	MRTL|MYCC|bHLHe39|c-Myc	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	c-Myc-induced, long, noncoding H19 affects cell proliferation and predicts a poor prognosis in patients with gastric cancer.The results show that lncRNA H19 is overexpressed in tumor tissues compared with adjacent normal tissues. exogenous c-Myc significantly induces H19 expression, and the expression of H19 was positively correlated with the c-Myc levels in the 80 samples used in our study. In conclusion, our study demonstrates that the altered expression of lncRNA H19, which is induced by c-Myc, is involved in the development and progression of GC by regulating cell proliferation and shows that H19 may be a potential diagnostic and prognostic target in patients with GC.	24671855	RID02194	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(NSCLC);DATA(GSE74639)
Esophagus squamous cell carcinoma	PANTR1	POU3F3	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000198914	NA	100506421	5455	LINC01158|linc-Brn1a|linc-POU3F3	BRN1|OTF8|brain-1|oct-8	Increased levels of the long intergenic non-protein coding RNA POU3F3 promote DNA methylation in esophageal squamous cell carcinoma cells. Levels of a lincRNA encoded by a gene located next to POU3F3 (linc-POU3F3) were significantly higher in ESCC than neighboring nontumor tissues. In RNA immunoprecipitation assays, linc-POU3F3 was associated with the EZH2 messenger RNA (mRNA). Overexpression of linc-POU3F3 in cell lines increased their proliferation and ability to form colonies, and reduced the expression of POU3F3 mRNA, whereas knockdown of linc-POU3F3 increased the levels of POU3F3 mRNA. CpG islands in POU3F3 were densely hypermethylated in cell lines that overexpressed linc-POU3F3; methylation at these sites was reduced by knockdown of linc-POU3F3. Pharmacologic inhibition of EZH2 increased the levels of POU3F3 mRNA and significantly reduced binding of DNA methyltransferase (DNMT)1, DNMT3A, and DNMT3B to POU3F3. Levels of linc-POU3F3 are increased in ESCC samples from patients compared with nontumor tissues. This noncoding RNA contributes to the development of ESCC by interacting with EZH2 to promote methylation of POU3F3, which encodes a transcription factor.	24631494	RID02195	epigenetic regulation	NA	NA	NA
Small cell lung cancer	HOTAIR	ASTN1	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000152092	NA	100124700	460	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ASTN	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02196	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Small cell lung cancer	HOTAIR	PCDHA1	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204970	NA	100124700	56147	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-ALPHA1	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02197	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Small cell lung cancer	HOTAIR	MUC5AC	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000215182	NA	100124700	4586	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MUC5|TBM|leB|mucin	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02198	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Small cell lung cancer	HOTAIR	NTM	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000182667	NA	100124700	50863	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CEPU-1|HNT|IGLON2|NTRI	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02199	expression association	NA	NA	UP(LIHC);DATA(GSE117623)
Small cell lung cancer	HOTAIR	PTK2B	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000120899	NA	100124700	2185	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CADTK|CAKB|FADK2|FAK2|PKB|PTK|PYK2|RAFTK	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02200	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	AR	PCAT18	positively-E	RNAi	upregulation	qPCR;sequencing	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000265369	GRCh38_18:26687621-26703638	367	728606	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LINC01092	Identification of a long non-coding RNA as a novel biomarker and potential therapeutic target for metastatic prostate cancer. AR activation dramatically up-regulated PCAT18 expression in vitro and in vivo. PCAT18 silencing significantly (p<0.001) inhibited PCa cell proliferation and triggered caspase 3/7 activation, with no effect on non-neoplastic cells. PCAT18 silencing also inhibited PCa cell migration (p<0.01) and invasion (p<0.01).	24519926	RID02201	expression association	metastasis	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)	UP(LIHC);DATA(GSE117623)
Ischemic stroke	CDKN2B-AS1	CARD8	positively-E	RNAi	NA	NA	NA	NA	predisposition(+)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105483	NA	100048912	22900	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CARDINAL|DACAR|DAKAR|NDPP|NDPP1|TUCAN	Regulation of CARD8 expression by ANRIL and association of CARD8 single nucleotide polymorphism rs2043211 (p.C10X) with ischemic stroke. Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.	24385277	RID02202	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Urinary bladder cancer	H19	EZH2	interact	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression. Here we found that H19 levels are remarkably increased in bladder cancer tissues, and upregulated H19 promotes bladder cancer cell migration in vitro and in vivo. H19 is associated with enhancer of zeste homolog 2 (EZH2), and that this association results in Wnt/beta-catenin activation and subsequent downregulation of E-cadherin. A significant negative correlation is also observed between H19 levels and E-cad levels in vivo. These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression. Inhibition of E-cadherin expression by lnc-RNA H19 to facilitate bladder cancer metastasis;RNA interference is applied to knockdown H19 expression in bladder cancer cell, and found potentiated E-cadherin expression (p< 0.05), accompanied with weakened metastatic potency (p< 0.05)	23354591;29614625	RID02203	interact with protein	metastasis	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	HGF	H19	positively-E	northern blot;ISH	upregulation	qRT-PCR	NA	NA	cell migration(+);morphogenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000019991	NA	ENSG00000130600	GRCh38_11:1995176-2001470	3082	283120	DFNB39|F-TCF|HGFB|HPTA|SF	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Cross-talk between mesenchyme and epithelium increases H19 gene expression during scattering and morphogenesis of epithelial cells. Using a blocking antibody, HGF/SF was identified as the fibroblast-derived growth factor capable of inducing H19 expression and cell morphogenesis. We further demonstrated that H19 promoter activity was stimulated by various growth factors using transient transfection in MDCK epithelial cells. HGF/SF was more efficient than EGF or FGF-2 in transactivating the H19 promoter, whereas IGF-2, TGFbeta-1, and TNF-alpha were ineffective. This activation by HGF/SF was prevented by pharmacological inhibition of MAP kinase or of phospholipase C. We conclude that H19 is a target gene for HGF/SF, a known regulator of epithelial/mesenchymal interactions, and suggest that the up-regulation of H19 may be implicated in morphogenesis and/or migration of epithelial cells.	11969291	RID02204	transcriptional regulation	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(NSCLC);DATA(GSE74639)
Mantle cell lymphoma	MALAT1	EZH2	positively-F	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02205	interact with protein	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Mantle cell lymphoma	MALAT1	CDKN1A	negatively-E	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02206	epigenetic regulation	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Mantle cell lymphoma	MALAT1	CDKN1B	negatively-E	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111276	NA	378938	1027	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02207	epigenetic regulation	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	NEAT1	miR-506-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p. Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers. Additionally, our results confirmed that the tumor-promoting effects of NEAT1 in PC cells is at least partly through negative modulation of miR-506-3p.	27888106	RID02208	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	NA
Endometrial adenocarcinoma	MALAT1	miR-200c	negatively-F	luciferase reporter assay;IHC	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma. In the present study, we first showed that miR-200c levels were higher in most EEC specimens than in non-tumor tissues, while MALAT1 levels were lower. Moreover, we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-beta increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro. In summary, miR-200c/MALAT1 axis is a target with therapeutic potential in EEC.	27693631	RID02209	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Prostate cancer	PCA3	PRKD3	positively-E	IHC;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-1261)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000115825	NA	50652	23683	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	EPK2|PKC-NU|PKD3|PRKCN|nPKC-NU	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells. Prostate cancer antigen 3 (PCA3), also known as differential display code 3 (DD3), is one such lncRNA that maps to chromosome 9q21-22. PCA3 expression is highly specific to PCa. Here, we demonstrated that binding of Snail to the promoter region of PCA3 could activate the expression of PCA3. Down-regulation of PCA3 by silencing could increase the expression of the miRNA-1261, which then targeted at the PRKD3 gene (protein kinase D3) through competitive sponging. In summary, these results suggest that the transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	27743381	RID02210	ceRNA or sponge	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	SNAI1	PCA3	positively-E	IHC;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000124216	NA	ENSG00000225937	GRCh38_9:76691980-76863307	6615	50652	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells. Prostate cancer antigen 3 (PCA3), also known as differential display code 3 (DD3), is one such lncRNA that maps to chromosome 9q21-22. PCA3 expression is highly specific to PCa. Here, we demonstrated that binding of Snail to the promoter region of PCA3 could activate the expression of PCA3. Down-regulation of PCA3 by silencing could increase the expression of the miRNA-1261, which then targeted at the PRKD3 gene (protein kinase D3) through competitive sponging. In summary, these results suggest that the transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	27743381	RID02211	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	NA
Hepatocellular carcinoma	PCBP2-OT1	BMI1	interact	ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000168283	NA	102157401	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long noncoding RNA uc.338 promotes cell proliferation through association with BMI1 in hepatocellular carcinoma. lncRNA ultraconserved element 338 (uc.338) was first found to be upregulated in HCC and promote cell growth. RNA-immunoprecipitation and RNA pull-down assays showed that uc.338 associated with BMI1. We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1.We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1. uc.338 also modulated the transcription of CDKN1A. The oncogenic activity of uc.338 is partially due to its repression of p21. uc.338 may be a potential target for HCC therapy.	27154519	RID02212	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	PCBP2-OT1	CDKN1A	negatively-E	ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124762	NA	102157401	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA uc.338 promotes cell proliferation through association with BMI1 in hepatocellular carcinoma. lncRNA ultraconserved element 338 (uc.338) was first found to be upregulated in HCC and promote cell growth. RNA-immunoprecipitation and RNA pull-down assays showed that uc.338 associated with BMI1. We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1.We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1. uc.338 also modulated the transcription of CDKN1A. The oncogenic activity of uc.338 is partially due to its repression of p21. uc.338 may be a potential target for HCC therapy.	27154519	RID02213	transcriptional regulation	NA	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Atherosclerosis	SMILR	HAS2	positively-E	RNAi	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000255364	GRCh38_8:122414332-122428551	ENSG00000170961	NA	105375734	3037	NA	NA	Smooth Muscle Enriched Long Noncoding RNA (SMILR) Regulates Cell Proliferation.knockdown of SMILR markedly reduced cell proliferation. We focused on a novel lncRNA (Ensembl: RP11-94A24.1), which we termed smooth muscle-induced lncRNA enhances replication (SMILR). Following stimulation, SMILR expression was increased in both the nucleus and cytoplasm, and was detected in conditioned media. Furthermore, knockdown of SMILR markedly reduced cell proliferation. Mechanistically, we noted that expression of genes proximal to SMILR was also altered by interleukin-1alpha/platelet-derived growth factor treatment, and HAS2 expression was reduced by SMILR knockdown.	27052414	RID02214	expression association	NA	UP(PRAD);DATA(GSE104209)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Renal cell carcinoma	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	High expression of long non-coding RNA lncRNA-ATB is correlated with metastases and promotes cell migration and invasion in renal cell carcinoma. we found that long non-coding ribonucleic acid activated by transforming growth factor beta knockdown could (i) inhibit cell proliferation; (ii) trigger apoptosis; (iii) reduce epithelial-to-mesenchymal transition program; (iv) suppress cell migration and invasion.Our data have shown that long non-coding ribonucleic acid activated by transforming growth factor beta actively functions as a regulator of epithelial-to-mesenchymal transition during renal cell carcinoma metastasis, which suggests that long non-coding ribonucleic acid activated by transforming growth factor beta may be a potential prognostic biomarker and therapeutic target for renal cell carcinoma.	26848077	RID02215	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Hepatocellular carcinoma	PRAL	TP53	positively-F	Immunocoprecipitation	downregulation	qPCR;microarray	NA	NA	cell growth(-);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000279296	GRCh38_17:6772831-6776116	ENSG00000141510	NA	109245082	7157	lncRNA-PRAL	BCC7|BMFS5|LFS1|P53|TRP53	Systemic genome screening identifies the outcome associated focal loss of long noncoding RNA PRAL in hepatocellular carcinoma. The integrative analysis of long noncoding RNA (lncRNA) expression profiles with SCNVs in hepatocellular carcinoma (HCC) led us to identify the recurrent deletion of lncRNA-PRAL (p53 regulation-associated lncRNA) on chromosome 17p13.1, whose genomic alterations were significantly associated with reduced survival of HCC patients. We found that lncRNA-PRAL could inhibit HCC growth and induce apoptosis in vivo and in vitro through p53. Subsequent investigations indicated that the three stem-loop motifs at the 5' end of lncRNA-PRAL facilitated the combination of HSP90 and p53 and thus competitively inhibited MDM2-dependent p53 ubiquitination, resulting in enhanced p53 stability.	26663434	RID02216	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG15	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000087245	NA	285958	4313	C7orf40|Linc-Myo1g|MYO1GUT	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Upregulated expression of long noncoding RNA SNHG15 promotes cell proliferation and invasion through regulates MMP2/MMP9 in patients with GC. In this study, we identified a novel lncRNA SNHG15, whose expression was upregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. knockdown of SNHG15 expression by siRNA could inhibit cell proliferation and invasion and induce apoptosis, while ectopic expression of SNHG15 promoted cell proliferation and invasion in GC cells partly via regulating MMP2 and MMP9 protein expression.	26662309	RID02217	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(PAAD);DATA(GSE40174)
Gastric cancer	SNHG15	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000100985	NA	285958	4318	C7orf40|Linc-Myo1g|MYO1GUT	CLG4B|GELB|MANDP2|MMP-9	Upregulated expression of long noncoding RNA SNHG15 promotes cell proliferation and invasion through regulates MMP2/MMP9 in patients with GC. In this study, we identified a novel lncRNA SNHG15, whose expression was upregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. knockdown of SNHG15 expression by siRNA could inhibit cell proliferation and invasion and induce apoptosis, while ectopic expression of SNHG15 promoted cell proliferation and invasion in GC cells partly via regulating MMP2 and MMP9 protein expression.	26662309	RID02218	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Liver cancer	HULC	SPHK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000176170	NA	728655	8877	HCCAT1|LINC00078|NCRNA00078	SPHK	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).	26540633	RID02219	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	UCA1	GLS2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glutamine metabolic process(+)	ceRNA(miR-16)	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000135423	NA	652995	27165	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	GA|GLS|LGA|hLGA	Long non-coding RNA UCA1 promotes glutamine metabolism by targeting miR-16 in human bladder cancer.Real-time reverse transcriptase-polymerase chain reaction demonstrated that the RNA level of urothelial carcinoma-associated 1 and GLS2 was positively correlated in bladder cancer tissues and cell lines.Furthermore, luciferase reporter assays indicated that there was a miR-16 binding site in urothelial carcinoma-associated 1, and it showed appreciable levels of sponge effects on miR-16 as readouts in a dose-dependent manner. Moreover, the seed region of miR-16 directly bound to the 3'UTR of GLS2 mRNA and regulated GLS2 expression level.Together, our results revealed that urothelial carcinoma-associated 1 regulated the expression of GLS2 through interfering with miR-16, and repressed ROS formation in bladder cancer cells.	26373319	RID02220	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE60407,GSE38495,GSE111842)
Papillary thyroid carcinoma	PTCSC3	S100A4	negatively-E	RNAi	downregulation	qRT-PCR;microarray	NA	NA	cell motility(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000196154	NA	100886964	6275	NA	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	PTCSC3 Is Involved in Papillary Thyroid Carcinoma Development by Modulating S100A4 Gene Expression.Expression data from PTC cell lines pinpointed S100A4 as the most significantly downregulated gene in the presence of PTCSC3. S100A4 was upregulated in tumor tissue while PTCSC3 was strongly downregulated. PTCSC3 downregulates S100A4, leading to a reduction in cell motility and invasiveness. We propose that PTCSC3 impacts PTC predisposition and carcinogenesis through the S100A4 pathway.	26274343	RID02221	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	miR-1-3p	UCA1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);apoptosis process(+);cell motility(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	miRNA	lncRNA	NA	NA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Hsa-miR-1 downregulates long non-coding RNA urothelial cancer associated 1 in bladder cancer. Here, we report that downregulated hsa-miR-1 and upregulated lncRNA urothelial cancer associated 1 (UCA1) were inversely expressed in bladder cancer. The binding site between UCA1 and hsa-miR-1 was confirmed. Overexpression of hsa-miR-1 inhibited bladder cancer cell growth, induced apoptosis, and decreased cell motility. Knockdown of UCA1 expression phenocopied the effects of upregulation of hsa-miR-1. This study provides evidence for hsa-miR-1 to play tumor suppressive roles via downregulating lncRNA UCA1 in bladder cancer, which may have potential therapeutic significance.	25015192	RID02222	ceRNA or sponge	NA	NA	UP(PAAD);DATA(GSE40174)
Cancer	ABALON	BCL2L1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	ENSG00000281376	GRCh38_20:31721507-31723409	ENSG00000171552	NA	103021294	598	INXS	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis. We identified and characterized a long non-coding RNA (lncRNA) named INXS, transcribed from the opposite genomic strand of BCL-X, that was 5- to 9-fold less abundant in tumor cell lines from kidney, liver, breast and prostate and in kidney tumor tissues compared with non-tumors. Three apoptosis-inducing agents increased INXS lncRNA endogenous expression in the 786-O kidney tumor cell line, increased BCL-XS/BCL-XL mRNA ratio and activated caspases 3, 7 and 9. These effects were abrogated in the presence of INXS knockdown. Similarly, ectopic INXS overexpression caused a shift in splicing toward BCL-XS and activation of caspases, thus leading to apoptosis. BCL-XS protein accumulation was detected upon INXS overexpression.	24992962	RID02223	expression association	NA	UP(PRAD,BRCA);DOWN(SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Liver cancer	YAP1	MALAT1	positively-E	luciferase reporter assay;IHC;RIP;ChIP	upregulation	qPCR	NA	NA	cell motility(-);cell growth(-)	transcriptional regulation;post-transcriptional level	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10413	378938	COB1|YAP|YAP2|YAP65|YKI	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. Here, we characterised the oncoprotein Yes-associated protein (YAP), which up-regulated metastasis-associated lung adenocarcinoma transcript 1 (Malat1) expression at both transcriptional and post-transcriptional levels, whereas serine/arginine-rich splicing factor 1 (SRSF1) played an opposing role. SRSF1 inhibited YAP activity by preventing its co-occupation with TCF/beta-catenin on the Malat1 promoter. We also revealed that overexpression of YAP combined with a knockdown of SRSF1 resulted in conspicuously enhanced transwell cell mobility, accelerated tumour growth rate, and loss of body weight in a tail vein-injected mouse models. Thus, disrupting the interaction between YAP and SRSF1 may serve as a crucial therapeutic method in liver cancer.	24468535	RID02224	transcriptional regulation	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Liver cancer	SRSF1	MALAT1	negatively-E	luciferase reporter assay;IHC;RIP;ChIP	upregulation	qPCR	NA	NA	cell motility(-);cell growth(-)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000136450	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6426	378938	ASF|SF2|SF2p33|SFRS1|SRp30a	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. Here, we characterised the oncoprotein Yes-associated protein (YAP), which up-regulated metastasis-associated lung adenocarcinoma transcript 1 (Malat1) expression at both transcriptional and post-transcriptional levels, whereas serine/arginine-rich splicing factor 1 (SRSF1) played an opposing role. SRSF1 inhibited YAP activity by preventing its co-occupation with TCF/beta-catenin on the Malat1 promoter. We also revealed that overexpression of YAP combined with a knockdown of SRSF1 resulted in conspicuously enhanced transwell cell mobility, accelerated tumour growth rate, and loss of body weight in a tail vein-injected mouse models. Thus, disrupting the interaction between YAP and SRSF1 may serve as a crucial therapeutic method in liver cancer.	24468535	RID02225	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Kawasaki disease	THRIL	TNF	interact	RNA pull-down assay	upregulation	NA	NA	NA	immune response(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Evading Immune Detection	Immune system disease	Lymph node disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000232810	NA	102659353	7124	BRI3BP-AS1|BRI3BPAS1|Linc1992|TCONS_00020260	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	The long noncoding RNA THRIL regulates TNFalpha expression through its interaction with hnRNPL.Finally, THRIL expression was correlated with the severity of symptoms in patients with Kawasaki disease, an acute inflammatory disease of childhood. Collectively, our data provide evidence that lincRNAs and their binding proteins can regulate TNFalpha expression and may play important roles in the innate immune response and inflammatory diseases in humans.	24371310	RID02226	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Colorectal cancer	IGF1	CRNDE	negatively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000017427	NA	ENSG00000245694	GRCh38_16:54845189-54929189	3479	NA	IGF|IGF-I|IGFI|MGF	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CRNDE, a long non-coding RNA responsive to insulin/IGF signaling, regulates genes involved in central metabolism.In colorectal cancer cells, we demonstrate that treatment with insulin and insulin-like growth factors (IGF) repressed CRNDE nuclear transcripts, including those encompassing gVC-In4. The results suggest that CRNDE expression promotes the metabolic changes by which cancer cells switch to aerobic glycolysis (Warburg effect). This is the first report of a lncRNA regulated by insulin/IGFs, and our findings indicate a role for CRNDE nuclear transcripts in regulating cellular metabolism which may correlate with their upregulation in colorectal cancer.	24184209	RID02227	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)
B-cell acute lymphocytic leukemia	BALR-6	SP1	positively-E	luciferase reporter assay;northern blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Leukemia	lncRNA	TF	NA	GRCh38_3:17962572-18268922	ENSG00000185591	NA	NA	6667	NA	NA	BALR-6 regulates cell growth and cell survival in B-lymphoblastic leukemia.overexpression of BALR-6 isoforms in both human and mouse cell lines caused increased proliferation and decreased apoptosis. Luciferase reporter assays demonstrated an enhancement of SP1-mediated transcription in the presence of BALR-6. Specifically, our findings suggest that BALR-6 expression regulates the transcriptome downstream of SP1, and that this may underlie the function of BALR-6 in B-ALL.	26694754	RID02228	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	NDC80	BX647187	positively-E	RNAi;northern blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000080986	NA	NA	GRCh38_3:111096428-111098928	10403	NA	HEC|HEC1|HsHec1|KNTC2|TID3|hsNDC80	NA	The mitotic regulator Hec1 is a critical modulator of prostate cancer through the long non-coding RNA BX647187 in vitro. Our results showed that Hec1 mRNA and protein were significantly overexpressed in Human PCa tissues and several PCa cell lines.Through bioinformatics analysis and knockdown Hec1 in PCa cells, we found LncRNA BX647187 was positively regulated by Hec1. We further demonstrated that suppression of BX647187 in PCa cells significantly reduced cell proliferation and promoted apoptosis. Thus, we conclude that Hec1 is consistently overexpressed in human PCa and Hec1 is closely linked with human PCa progression through the meditator LncRNA BX647187.	26612002	RID02229	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE55807)	NA
Gastric cancer	BC032469	TERT	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-1207-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249201	GRCh38_5:1173141-1178605	ENSG00000164362	NA	NA	7015	NA	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	Long noncoding RNA BC032469, a novel competing endogenous RNA, upregulates hTERT expression by sponging miR-1207-5p and promotes proliferation in gastric cancer. Here, we report that BC032469, a novel lncRNA, expressed highly in gastric cancer tissues. Mechanistically, BC032469 could directly bind to miR-1207-5p and effectively functioned as a sponge for miR-1207-5p to modulate the derepression of hTERT. Thus, BC032469 may function as a ceRNA to impair miR-1207-5p-dependent hTERT downregulation, suggesting that it may be clinically valuable as a poor prognostic biomarker of gastric cancer.	26549025	RID02230	ceRNA or sponge	prognosis	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02231	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	CDKN2B-AS1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000087088	NA	100048912	581	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	BCL2L4	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02232	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	CDKN2B-AS1	CYCS	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000172115	NA	100048912	54205	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CYC|HCS|THC4	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02233	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(NSCLC,PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	CDKN2B-AS1	DIABLO	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000284934	NA	100048912	56616	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	DFNA64|SMAC	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02234	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	CDKN2B-AS1	CASP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000132906	NA	100048912	842	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02235	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Urinary bladder cancer	CDKN2B-AS1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164305	NA	100048912	836	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CPP32|CPP32B|SCA-1	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02236	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Urinary bladder cancer	CDKN2B-AS1	PARP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000143799	NA	100048912	142	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02237	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Non-small cell lung cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR;RT-PCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long Noncoding RNA ANRIL Regulates Proliferation of Non-small Cell Lung Cancer and Cervical Cancer Cells.qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.	26408699	RID02238	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Cervical cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR;RT-PCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long Noncoding RNA ANRIL Regulates Proliferation of Non-small Cell Lung Cancer and Cervical Cancer Cells.qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.	26408699	RID02239	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Papillary thyroid carcinoma	BANCR	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000110092	NA	100885775	595	LINC00586	BCL1|D11S287E|PRAD1|U21B31	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02240	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Papillary thyroid carcinoma	BANCR	TSHR	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000165409	NA	100885775	7253	LINC00586	CHNG1|LGR3|hTSHR-I	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02241	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Ovarian cancer	AB073614	MAPK3	positively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	GSE18521;GSE38666	GSE18521.zip;GSE38666.zip	cell proliferation(+);cell invasion(+);cell cycle(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000102882	NA	NA	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02242	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	AB073614	MAPK1	positively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	GSE18521;GSE38667	GSE18521.zip;GSE38667.zip	cell proliferation(+);cell invasion(+);cell cycle(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02243	expression association	prognosis	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	FOXM1	FRGCA	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000111206	NA	ENSG00000236663	GRCh38_21:43140523-43141092	2305	NA	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	NA	LncRNA-AP001631.9 promotes cell migration in gastric cancer. In the present study, through microarray analysis, we screened out a new LncRNA (LncRNA-AP001631.9), which was regulated by FOXM1, a well-known carcinogenetic factor and aimed to reveal the functional roles of this novel LncRNA in gastric cancer development. The data from qRT-PCR confirmed that the expression level of LncRNA-AP001631.9 was positively correlated with that of FOXM1.	26261500	RID02244	expression association	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)	NA
Gastric cancer	BANCR	NFKB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000109320	NA	100885775	4790	LINC00586	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-kB1.BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-kB1 (P50/105) expression and 3'UTR of NF-kB1 activity. Overexpression of NF-kB1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-kB1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis.BANCR was highly expressed both in gastric tumor tissues and in cancer cells. NF-kB1 and miR-9 were involved in the role of BANCR in gastric cancer cell growth and apoptosis.	26248136	RID02245	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	AFAP1-AS1	AFAP1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	Upregulated long non-coding RNA AFAP1-AS1 expression is associated with progression and poor prognosis of nasopharyngeal carcinoma. AFAP1-AS1 expression was upregulated in NPC and associated with NPC metastasis and poor prognosis. In vitro experiments demonstrated that AFAP1-AS1 knockdown significantly inhibited the NPC cell migration and invasive capability. AFAP1-AS1 knockdown also increased AFAP1 protein expression. AFAP1-AS1 promoted cancer cell metastasis via regulation of actin filament integrity.	26246469	RID02246	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Lung cancer	AFAP1-AS1	AFAP1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	AFAP1-AS1, a long noncoding RNA upregulated in lung cancer and promotes invasion and metastasis. One lncRNA, actin filament associated protein 1 antisense RNA1 (AFAP1-AS1), was the most significantly upregulated in lung cancer and associated with poor prognosis. AFAP1-AS1 knockdown also increased the expression of its antisense protein coding gene, actin filament associated protein 1 (AFAP1), and affected the expression levels of several small GTPase family members and molecules in the actin cytokeratin signaling pathway, which suggested that AFAP1-AS1 promoted cancer cell metastasis via regulation of actin filament integrity.	26245991	RID02247	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Pancreatic cancer	NUF2	AF339813	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000143228	NA	NA	GRCh38_13:93293507-93295109	83540	NA	CDCA1|CT106|NUF2R	NA	Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. Our results showed that NUF2 mRNA and protein were significantly overexpressed in Human PC tissues and several PC cell lines. Through bioinformatics analysis and knockdown NUF2 in PC cells, we found LncRNA AF339813 was positively regulated by NUF2.	26045769	RID02248	expression association	NA	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)	NA
Hepatocellular carcinoma	SP1	CDKN2B-AS1	negatively-E	IHC;western blot;ChIP;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000240498	GRCh38_9:21994139-22128103	6667	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	25966845	RID02249	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	BANCR	CDKN1A	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	post-transcriptional level	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000124762	NA	100885775	1026	LINC00586	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Downregulated Long Noncoding RNA BANCR Promotes the Proliferation of Colorectal Cancer Cells via Downregualtion of p21 Expression. we show that BANCR expression was significantly down-regulated in colorectal cancer tissues compared with normal tissues. We also determined that pCDNA-BANCR-mediated colorectal cancer cell proliferation was associated with induction of G0/G1 cell-cycle arrest and apoptosis enhancement through regulation of p21, and its effects were most likely posttranscriptional.	25928067	RID02250	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	TUSC7	miR-23b-3p	negatively-F	luciferase reporter assay;ChIP;RIP	downregulation	microarray	NA	NA	cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Reciprocal repression between TUSC7 and miR-23b in gastric cancer. The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients. Furthermore, we showed that TUSC7 was a direct transcriptional target of p53 via interaction of p53 with the putative p53-response element in the upstream region of TUSC7. Finally, we demonstrated reciprocal repression between TUSC7 and miR-23b; in contrast to TUSC7, miR-23b promoted cell growth. The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. Because there was one miR-23b binding site and two miR-320d binding sites (Fig. 5a) in TUSC7, we deleted these site (TUSC7-del) and determined that the corresponding construct no longer suppressed miR-23b or miR-320d	25765901	RID02251	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	NA
Gastric cancer	TP53	TUSC7	positively-E	luciferase reporter assay;ChIP;RIP	upregulation	microarray	NA	NA	cell growth(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000243197	GRCh38_3:116709235-116723581	7157	285194	BCC7|BMFS5|LFS1|P53|TRP53	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Reciprocal repression between TUSC7 and miR-23b in gastric cancer. The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients. Furthermore, we showed that TUSC7 was a direct transcriptional target of p53 via interaction of p53 with the putative p53-response element in the upstream region of TUSC7. Finally, we demonstrated reciprocal repression between TUSC7 and miR-23b; in contrast to TUSC7, miR-23b promoted cell growth. The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	25765901	RID02252	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Gastric cancer	NOTCH1	AK022798	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000148400	NA	ENSG00000162757	GRCh38_1:209779208-209784559	4851	NA	AOS5|AOVD1|TAN1|hN1	NA	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02253	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	NA
Gastric cancer	AK022798	ABCC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000103222	NA	NA	4363	NA	ABC29|ABCC|GS-X|MRP|MRP1	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02254	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	AK022798	CASP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000164305	NA	NA	836	NA	CPP32|CPP32B|SCA-1	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02255	expression association	chemoresistance	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Gastric cancer	AK022798	CASP8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000064012	NA	NA	841	NA	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02256	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Esophagus squamous cell carcinoma	BOK-AS1	CCN4	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234235	GRCh38_2:241544403-241558977	ENSG00000270132	NA	100379249	8840	BOK-AS|BOKAS|NAToB|NCRNA00151	NA	Targeting WISP1 to sensitize esophageal squamous cell carcinoma to irradiation. We found that WISP1, a downstream target gene of Wnt/beta-catenin pathway, was re-expressed in 67.3% of ESCC patients as an oncofetal gene. Further studies revealed that WISP1 contributed to radioresistance primarily by repressing irradiation-induced DNA damage and activating PI3K kinase. LncRNA BOKAS was up-regulated following radiation and promoted WISP1 expression and resultant radioresistance.	25749038	RID02257	expression association	NA	NA	NA
Lung cancer	BANCR	MAPK14	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000112062	NA	100885775	1432	LINC00586	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways. The results showed that BANCR levels were downregulated in LC cells. We further found that MAPK pathways were involved in the BANCR-mediated cell proliferation and migration of LC. Moreover, BANCR was found to regulate LC proliferation and migration via not ERK MAPK, but p38 MAPK and JNK inactivations.	25661343	RID02258	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Lung cancer	BANCR	MAPK8	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000107643	NA	100885775	5599	LINC00586	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways. The results showed that BANCR levels were downregulated in LC cells. We further found that MAPK pathways were involved in the BANCR-mediated cell proliferation and migration of LC. Moreover, BANCR was found to regulate LC proliferation and migration via not ERK MAPK, but p38 MAPK and JNK inactivations.	25661343	RID02259	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CDKN2B-AS1	KLF2	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000127528	NA	100048912	10365	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	LKLF	Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. In this study, we reported that ANRIL expression was increased in NSCLC tissues, and its expression level was significantly correlated with tumor-node-metastasis stages and tumor size. Furthermore, we uncover that ANRIL could not repress p15 expression in PC9 cells, but through silencing of KLF2 and P21 transcription.	25504755	RID02260	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CDKN2B-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000124762	NA	100048912	1026	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. In this study, we reported that ANRIL expression was increased in NSCLC tissues, and its expression level was significantly correlated with tumor-node-metastasis stages and tumor size. Furthermore, we uncover that ANRIL could not repress p15 expression in PC9 cells, but through silencing of KLF2 and P21 transcription.	25504755	RID02261	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	CDKN2B-AS1	miR-99a-5p	negatively-E	RIP;ChIP;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.	24810364;25504755	RID02262	epigenetic regulation	prognosis	UP(SKCM);DATA(GSE38495)	NA
Gastric cancer	CDKN2B-AS1	miR-449a	negatively-E	RIP;ChIP;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.	24810364;25504755	RID02263	epigenetic regulation	prognosis	UP(SKCM);DATA(GSE38495)	NA
Urinary bladder cancer	AATBC	CCND1	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000110092	NA	284837	595	NA	BCL1|D11S287E|PRAD1|U21B31	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02264	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	AATBC	CDK4	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000135446	NA	284837	1019	NA	CMM3|PSK-J3	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02265	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	AATBC	RB1	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000139687	NA	284837	5925	NA	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02266	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	AATBC	CDKN2C	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000123080	NA	284837	1031	NA	INK4C|p18|p18-INK4C	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02267	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Urinary bladder cancer	AATBC	CASP9	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000132906	NA	284837	842	NA	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. inhibition of AATBC induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3.	25473900	RID02268	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Urinary bladder cancer	AATBC	CASP3	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000164305	NA	284837	836	NA	CPP32|CPP32B|SCA-1	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. inhibition of AATBC induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3.	25473900	RID02269	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Urinary bladder cancer	AATBC	MAPK8	negatively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000107643	NA	284837	5599	NA	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. The investigation for the signaling pathway revealed that the apoptosis following AATBC knockdown was mediated by activation of phosphorylated JNK and suppression of NRF2. Furthermore, JNK inhibitor SP600125 could attenuate the apoptotic effect achieved by AATBC knockdown, confirming the involvement of JNK signaling in the induced apoptosis.	25473900	RID02270	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	AATBC	NFE2L2	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000116044	NA	284837	4780	NA	HEBP1|IMDDHH|NRF2	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. The investigation for the signaling pathway revealed that the apoptosis following AATBC knockdown was mediated by activation of phosphorylated JNK and suppression of NRF2. Furthermore, JNK inhibitor SP600125 could attenuate the apoptotic effect achieved by AATBC knockdown, confirming the involvement of JNK signaling in the induced apoptosis.	25473900	RID02271	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	AB074278	EMP1	interact	RNAi	upregulation	qRT-PCR;microarray	GSE55433	GSE55433.zip	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_17:63039470-63041178	ENSG00000134531	NA	NA	2012	NA	CL-20|EMP-1|TMP	Identification of differentially expressed long noncoding RNAs in bladder cancer. Focusing upon a promising candidate, we implicate upregulation of AB074278 in apoptosis avoidance and the maintenance of a proproliferative state in cancer through a potential interaction with EMP1, a tumor suppressor and a negative regulator of cell proliferation.	25165097	RID02272	interact with protein	NA	NA	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761)
Cervical cancer	TMPOP2	CDH1	negatively-E	RNAi;RIP	upregulation	microarray;qRT-PCR	GSE55940	GSE55940.zip	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	ENSG00000039068	NA	100533619	999	lncRNA-EBIC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding RNA-EBIC promotes tumor cell invasion by binding to EZH2 and repressing E-cadherin in cervical cancer.Then, we found a specific differentially expressed lncRNA can physically bind to enhancer of zeste homolog2 (EZH2) by using RNA immunoprecipitation. We termed it as EZH2-binding lncRNA in cervical cancer [lncRNA-EBIC]. We also found that the association between lncRNA-EBIC and EZH2 was required for the repression of E-cadherin, which was a key molecular in the metastasis of cervical cancer. Conclusion: These results demonstrated that lncRNA-EBIC was an oncogenic lncRNA, which could promote tumor cell invasion in CC by binding to EZH2 and inhibiting E-cadherin expression.	25007342	RID02273	epigenetic regulation	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	miR-129-5p	GACAT3	negatively-F	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	104797537	NA	LINC01458|lncRNA-AC130710	lncRNA-AC130710 targeting by miR-129-5p is upregulated in gastric cancer and associates with poor prognosis. Moreover, miR-129-5p may play an important role in the downregulation of AC130710 in gastric cancer cells.	24969565	RID02274	ceRNA or sponge	prognosis	NA	NA
Melanoma	BANCR	MAPK3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000102882	NA	100885775	5595	LINC00586	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02275	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	BANCR	MAPK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000100030	NA	100885775	5594	LINC00586	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02276	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	BANCR	MAPK8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000107643	NA	100885775	5599	LINC00586	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02277	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	DNMT1	ADAMTS9-AS2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	PCG	lncRNA	ENSG00000130816	NA	ENSG00000241684	GRCh38_3:64684909-65053439	1786	100507098	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	NA	A new tumor suppressor LncRNA ADAMTS9-AS2 is regulated by DNMT1 and inhibits migration of glioma cells. The results showed that the ADAMTS9-AS2 expression was significantly downregulated in tumor tissues compared with normal tissues and reversely associated with tumor grade and prognosis. We also found that ADAMTS9-AS2 expression was negatively correlated with DNA methyltransferase-1 (DNMT1). In addition, DNMT1 knockdown led to remarkable enhancement of ADAMTS9-AS2 expression. By 5-aza-dC treatment, the ADAMTS9-AS2 expression was also reactivated. The results suggested that ADAMTS9-AS2 is a novel tumor suppressor modulated by DNMT1 in glioma. LncRNA ADAMTS9-AS2 may serve as a potential biomarker and therapeutic target for glioma.	24833086	RID02278	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Glioblastoma	APTR	CDKN1A	negatively-E	RIP;northern blot;ChIP;RNA pull-down assay;Immunoprecipitation;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000124762	NA	100505854	1026	RSBN1L-AS1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. we performed an siRNA screen of human lncRNAs required for cell proliferation, and identified a novel lncRNA, APTR, that acts in trans to repress the CDKN1A/p21 promoter independent of p53 to promote cell proliferation. A different module of APTR associates with and recruits the Polycomb repressive complex 2 (PRC2) to epigenetically repress the p21 promoter. A decrease in APTR is necessary for the induction of p21 after heat stress and DNA damage by doxorubicin, and the levels of APTR and p21 are anti-correlated in human glioblastomas. Our data identify a new regulator of the cell-cycle inhibitor CDKN1A/p21 that acts as a proliferative factor in cancer cell lines and in glioblastomas and demonstrate that Alu elements present in lncRNAs can contribute to targeting regulatory lncRNAs to promoters.	24748121	RID02279	epigenetic regulation	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	ANRIL inhibits p15(INK4b) through the TGFbeta1 signaling pathway in human esophageal squamous cell carcinoma. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor beta1 (TGFbeta1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFbeta1 signaling pathways.	24747824	RID02280	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Esophagus squamous cell carcinoma	CDKN2B-AS1	TGFB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105329	NA	100048912	7040	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	ANRIL inhibits p15(INK4b) through the TGFbeta1 signaling pathway in human esophageal squamous cell carcinoma. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor beta1 (TGFbeta1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFbeta1 signaling pathways.	24747824	RID02281	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AK126698	CTNNB1	negatively-E	RNAi	upregulation	microarray;qRT-PCR	GSE43494	GSE43494.zip	chemoresistance(-);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_3:195715440-195719235	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.Knockdown lncRNA AK126698 not only greatly decreased NKD2 which can negatively regulate Wnt/beta-catenin signaling but also increased the accumulation and nuclear translocation of beta-catenin, and significantly depressed apoptosis rate induced by cisplatin in A549 cells.Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	RID02282	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	AK126698	NKD2	positively-E	RNAi	upregulation	microarray;qRT-PCR	GSE43494	GSE43494.zip	chemoresistance(-);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_3:195715440-195719235	ENSG00000145506	NA	NA	85409	NA	Naked2	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.Knockdown lncRNA AK126698 not only greatly decreased NKD2 which can negatively regulate Wnt/beta-catenin signaling but also increased the accumulation and nuclear translocation of beta-catenin, and significantly depressed apoptosis rate induced by cisplatin in A549 cells.Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	RID02283	expression association	chemoresistance	NA	NA
Hepatocellular carcinoma	HEIH	EZH2	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	microarray	GSE27462	GSE27462.zip	cell growth(+)	histone modification	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000106462	NA	100859930	2146	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans.We also found that lncRNA-HEIH plays a key role in G(0) /G(1) arrest, and further demonstrated that lncRNA-HEIH was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes.	21769904	RID02284	interact with protein	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Acute lymphocytic leukemia	CDKN2B-AS1	CDKN2A	positively-E	RNAi	NA	NA	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147889	NA	100048912	1029	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	A polymorphism in the chromosome 9p21 ANRIL locus is associated to Philadelphia positive acute lymphoblastic leukemia.rs564398, mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype. We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.	21414664	RID02285	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Acute lymphocytic leukemia	CDKN2B-AS1	CDKN2B	positively-E	RNAi	NA	NA	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	A polymorphism in the chromosome 9p21 ANRIL locus is associated to Philadelphia positive acute lymphoblastic leukemia.rs564398, mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype. We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.	21414664	RID02286	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Osteosarcoma	LOC285194	FLT1	negatively-E	RNAi	downregulation	microarray;qRT-PCR;RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709788-116717040	ENSG00000102755	NA	NA	2321	NA	FLT|FLT-1|VEGFR-1|VEGFR1	Recurrent focal copy-number changes and loss of heterozygosity implicate two noncoding RNAs and one tumor suppressor gene at chromosome 3q13.31 in osteosarcoma. Notably, these CNAs often involve the noncoding RNAs LOC285194 and BC040587 and, in some cases, a tumor suppressor gene that encodes the limbic system-associated membrane protein (LSAMP). depleting either LSAMP or LOC285194 promoted proliferation of normal osteoblasts by regulation of apoptotic and cell-cycle transcripts and also VEGF receptor 1.	20048075	RID02287	expression association	NA	NA	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Cervical cancer	BOK-AS1	BOK	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234235	GRCh38_2:241544403-241558977	ENSG00000176720	NA	100379249	666	BOK-AS|BOKAS|NAToB|NCRNA00151	BCL2L9|BOKL	A natural antisense transcript, BOKAS, regulates the pro-apoptotic activity of human Bok. Overexpression of BOKAS alone exhibited no significant anti- or pro-apoptotic activity but it was able to inhibit Bok-induced apoptosis in HeLa cells. Our results suggest that BOKAS may function specifically in the human testis, where it serves as an antisense molecule to regulate Bok-induced apoptosis.	19287972	RID02288	expression association	NA	NA	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Cancer	CDKN2B-AS1	CDKN2B	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell growth(-);tumorigenesis(-)	epigenetic regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA. Here we show that many TSGs have nearby antisense RNAs, and we focus on the role of one RNA in silencing p15, a cyclin-dependent kinase inhibitor implicated in leukaemia. We found an inverse relation between p15 antisense (p15AS) and p15 sense expression in leukaemia. A p15AS expression construct induced p15 silencing in cis and in trans through heterochromatin formation but not DNA methylation; the silencing persisted after p15AS was turned off, although methylation and heterochromatin inhibitors reversed this process. The p15AS-induced silencing was Dicer-independent. Expression of exogenous p15AS in mouse embryonic stem cells caused p15 silencing and increased growth, through heterochromatin formation, as well as DNA methylation after differentiation of the embryonic stem cells.	18185590	RID02289	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Gastric cancer	lncRNA-LOWEG	LIFR	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENST00000508986	GRCh38_5:38425036-38427376	ENSG00000113594	NA	NA	3977	NA	CD118|LIF-R|SJS2|STWS|SWS	A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion.western blot and real-time PCR analysis suggested that lncRNA-LOWEG is positively correlated with the expression of leukemia inhibitory factor receptor (LIFR) gene at the translational level. LncRNA-LOWEG is a tumor suppressor that inhibits GC cell invasion. And LIFR gene is up-regulated by lncRNA-LOWEG.	26537802	RID02290	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Endometrial cancer	GAS5	PTEN	positively-E	luciferase reporter assay;RNAi;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-103a-3p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells. The prediction of bioinformatics online revealed that GAS5 could bind to miR-103, which was further found to be regulated by GAS5. To further investigate the mechanism of the regulation of PTEN and miR-103 by GAS5, HHUA and JEC cells were transfected with luciferase reporter vector containing PTEN 3<U+00C3>￠a<U+201A><U+00AC><U+00CB><U+0153>UTR and miR-103 mimic, or miR-103 mimic + GAS5 plasmid. Through measuring the luciferase activity and the mRNA level of PTEN, we found that they were both reduced in cells transfected with miR-103 mimic (Fig. 4a). we identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells.	26511107	RID02291	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Epithelial ovarian cancer	GAS5	BAX	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000087088	NA	60674	581	NCRNA00030|SNHG2	BCL2L4	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02292	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	GAS5	BAK1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000030110	NA	60674	578	NCRNA00030|SNHG2	BAK|BAK-LIKE|BCL2L7|CDN1	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02293	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Epithelial ovarian cancer	GAS5	CASP3	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000164305	NA	60674	836	NCRNA00030|SNHG2	CPP32|CPP32B|SCA-1	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02294	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Epithelial ovarian cancer	GAS5	CASP9	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000132906	NA	60674	842	NCRNA00030|SNHG2	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02295	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Intrahepatic cholangiocarcinoma	CPS1-IT1	CPS1	positively-E	IHC;RNAi;western blot	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000021826	NA	29034	1373	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	CPSASE1|PHN	Co-expression of the carbamoyl-phosphate synthase 1 gene and its long non-coding RNA correlates with poor prognosis of patients with intrahepatic cholangiocarcinoma. Knockdown of CPS1 andor CPS1-IT1 reduced the proliferation and increased the apoptosis of ICC-9810 cells.Carbamoyl-phosphate synthase 1 (CPS1) and its lncRNA CPS1 intronic transcript 1 (CPS1-IT1) were observed to be upregulated in ICC.In conclusion, CPS1 and CPS1-IT1 may serve an important role in ICC development by promoting the proliferation of ICC cells. Furthermore, CPS1 and CPS1-IT1 were associated with poor liver function and reduced survival rates.	26499888	RID02296	expression association	prognosis	NA	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Hepatocellular carcinoma	GAS5	PDCD4	positively-E	western blot;RNAi;luciferase reporter assay	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150593	NA	60674	27250	NCRNA00030|SNHG2	H731	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21.The present report demonstrates that there are lower levels of GAS5, PDCD4, and PTEN and higher levels of microRNA-21 (miR-21) in HCC tissues than in adjacent normal tissues.Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive); in contrast, there are opposite changes in HCCLM3 cells (highly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Thus, GAS5 acts as a tumor suppressor in HCCs through negative regulation of miR-21 and its targets and proteins about migration and invasion in cancer cells, which may be a target for treating HCC.	26404135	RID02297	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Hepatocellular carcinoma	GAS5	PTEN	positively-E	western blot;RNAi;luciferase reporter assay	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21.The present report demonstrates that there are lower levels of GAS5, PDCD4, and PTEN and higher levels of microRNA-21 (miR-21) in HCC tissues than in adjacent normal tissues.Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive); in contrast, there are opposite changes in HCCLM3 cells (highly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Thus, GAS5 acts as a tumor suppressor in HCCs through negative regulation of miR-21 and its targets and proteins about migration and invasion in cancer cells, which may be a target for treating HCC.	26404135	RID02298	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	DBH-AS1	CDK6	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000105810	NA	138948	1021	NCRNA00118	MCPH12|PLSTIRE	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02299	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	DBH-AS1	CCND1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000110092	NA	138948	595	NCRNA00118	BCL1|D11S287E|PRAD1|U21B31	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02300	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	DBH-AS1	CCNE1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000105173	NA	138948	898	NCRNA00118	CCNE|pCCNE1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02301	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Hepatocellular carcinoma	DBH-AS1	CDKN2A	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000147889	NA	138948	1029	NCRNA00118	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02302	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	DBH-AS1	CDKN1A	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000124762	NA	138948	1026	NCRNA00118	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02303	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	DBH-AS1	CDKN1B	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000111276	NA	138948	1027	NCRNA00118	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02304	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	HBX	DBH-AS1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell survival(+);MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	PCG	lncRNA	NA	NA	ENSG00000225756	GRCh38_9:133654586-133657313	NA	138948	NA	NCRNA00118	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC.	26393879	RID02305	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)
Hepatocellular carcinoma	TP53	DBH-AS1	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell survival(+);MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000225756	GRCh38_9:133654586-133657313	7157	138948	BCC7|BMFS5|LFS1|P53|TRP53	NCRNA00118	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC.	26393879	RID02306	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)
Colon cancer	DACOR1	CBS	negatively-E	RIP;western blot	downregulation	qRT-PCR;sequencing	TCGA	COAD.zip	cell growth(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_15:67000001-67200000	ENSG00000160200	NA	100131796	875	LP2570|TCONS_00023265	CBSL|HIP4	DNMT1-associated long non-coding RNAs regulate global gene expression and DNA methylation in colon cancer. One lncRNA, TCONS_00023265, which we named DACOR1 (DNMT1-associated Colon Cancer Repressed lncRNA 1), shows high, tissue-specific expression in the normal colon (including colon crypts) but was repressed in a panel of colon tumors and patient-derived colon cancer cell lines. DACOR1 induction resulted in down-regulation of Cystathionine beta-synthase, which is known to lead to increased levels of S-adenosyl methionine-the key methyl donor for DNA methylation. Induction of DACOR1 in colon cancer cell lines significantly reduced their ability to form colonies in vitro, suggesting a growth suppressor function.	26307088	RID02307	epigenetic regulation	NA	NA	DOWN(BRCA);DATA(GSE41245)
Gastric cancer	FER1L4	PTEN	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition.	26306906	RID02308	ceRNA or sponge	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	EGFR-AS1	EGFR	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000146648	NA	100507500	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long noncoding RNA, EGFR-AS1, a target of GHR, increases the expression of EGFR in hepatocellular carcinoma. EGFR-AS1 has been found to inhibit the expression of EGFR. We found that impeded expression of GHR decreased the expression of EGFR and EGFR-AS1 in vivo and in vitro. Then, it was verified that EGFR and EGFR-AS1 were relatively upregulated in HCC tissue, and they were significantly related to some clinical characteristics and patient prognosis. Furthermore, EGFR-AS1 was determined to promote HCC development by improving the ability of invasion and proliferation of HCC cells in vitro, and it was also found to affect the cell cycle. Our study identified that EGFR-AS1 may promote HCC genesis and development. EGFR-AS1 may act as a prognostic factor in HCC.	26271667	RID02309	expression association	prognosis	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	GHR	EGFR-AS1	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000112964	NA	ENSG00000224057	GRCh38_7:55179750-55188934	2690	100507500	GHBP|GHIP	NA	The long noncoding RNA, EGFR-AS1, a target of GHR, increases the expression of EGFR in hepatocellular carcinoma. EGFR-AS1 has been found to inhibit the expression of EGFR. We found that impeded expression of GHR decreased the expression of EGFR and EGFR-AS1 in vivo and in vitro. Then, it was verified that EGFR and EGFR-AS1 were relatively upregulated in HCC tissue, and they were significantly related to some clinical characteristics and patient prognosis. Furthermore, EGFR-AS1 was determined to promote HCC development by improving the ability of invasion and proliferation of HCC cells in vitro, and it was also found to affect the cell cycle. Our study identified that EGFR-AS1 may promote HCC genesis and development. EGFR-AS1 may act as a prognostic factor in HCC.	26271667	RID02310	expression association	prognosis	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE51827)	NA
Lung adenocarcinoma	DLX6-AS1	DLX6	negatively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell differentiation(+);TNM stage(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000006377	NA	285987	1750	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	NA	Expression of long non-coding RNA DLX6-AS1 in lung adenocarcinoma. The expression level of lncRNA DLX6-AS1 in LAC tissues was significantly higher compared to paired adjacent normal lung tissues (P<0.05). High DLX6-AS1 expression levels were significantly associated with both histological differentiation and TNM stage. Down-regulation of lncRNA DLX6-AS1 expression decreased the DLX6 mRNA and protein levels.	26052251	RID02311	expression association	NA	NA	DOWN(BRCA);DATA(GSE67939)
Hepatocellular carcinoma	DANCR	CTNNB1	negatively-E	RNAi;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell stemness(+)	RNA stability	binding/interaction	RNA-RNA	NA	CSC	Limitless Replicative Potential	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000168036	NA	57291	1499	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1. We found that lncRNA-DANCR is overexpressed in stem-like HCC cells, and this can serve as a prognostic biomarker for HCC patients. Experiments showed that DANCR markedly increased stemness features of HCC cells to promote tumorigenesis and intra-/extrahepatic tumor colonization. Experiments showed that DANCR markedly increased stemness features of HCC cells to promote tumorigenesis and intra-/extrahepatic tumor colonization. Additionally, we found that the role of DANCR relied largely on an association with, and regulation of, CTNNB1. Association of DANCR with CTNNB1 blocked the repressing effect of microRNA (miR)-214, miR-320a, and miR-199a on CTNNB1.	25964079	RID02312	interact with mRNA	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Myeloid leukemia	CCDC26	KIT	positively-E	IHC;western blot	downregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000157404	NA	137196	3815	RAM	C-Kit|CD117|MASTC|PBT|SCFR	Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression. We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. DNA microarray and quantitative polymerase chain reaction screening for differentially expressed genes between KD clones and non-KD control cells revealed significant up-regulation of the tyrosine kinase receptor, KIT, hyperactive mutations of which are often found in AML. We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression. A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered.	25928165	RID02313	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Lung adenocarcinoma	GAS5	EGFR	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000146648	NA	60674	1956	NCRNA00030|SNHG2	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib, which could be reversed by overexpressing GAS5.	25925741	RID02314	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Lung adenocarcinoma	GAS5	IGF1R	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000140443	NA	60674	3480	NCRNA00030|SNHG2	CD221|IGFIR|IGFR|JTK13	The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib, which could be reversed by overexpressing GAS5.	25925741	RID02315	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Cervical cancer	CCEPR	PCNA	positively-F	western blot;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	NA	GRCh38_10:59173963-59176464	ENSG00000132646	NA	105682749	5111	CCHE1|lncRNA-CCHE1	ATLD2	Long noncoding RNA CCHE1 promotes cervical cancer cell proliferation via upregulating PCNA. In this study, we found that cervical carcinoma high-expressed lncRNA 1 (lncRNA-CCHE1) was significantly upregulated in cervical cancer tissues.By contrast, the depletion of CCHE1 inhibits the proliferation of cervical cancer cells. RNA pull-down assays confirmed that CCHE1 physically associates with proliferating cell nuclear antigen (PCNA) messenger RNA, consequently enhances the expression of PCNA.The expression of CCHE1 and PCNA is significantly correlated in cervical cancer tissues. The depletion of PCNA abolishes the effects of CCHE1 on the proliferation of cervical cancer cells. Taken together, these findings indicate that CCHE1 plays a pivotal role in cervical cancer cell proliferation via increasing PCNA expression and serves as a potential prognostic biomarker and therapeutic target in human cervical cancer.	25921283	RID02316	interact with mRNA	prognosis	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Prostate cancer	AR	DRAIC	negatively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000245750	GRCh38_15:69462921-69843120	367	145837	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02317	transcriptional regulation	metastasis,prognosis	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)	UP(BRCA);DATA(GSE55807)
Prostate cancer	AR	PCAT29	negatively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENST00000560655	GRCh38_15:69592200-69695750	367	104472713	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02318	transcriptional regulation	metastasis,prognosis	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)	UP(LIHC);DATA(GSE117623)
Prostate cancer	FOXA1	DRAIC	positively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000129514	NA	ENSG00000245750	GRCh38_15:69462921-69843120	3169	145837	HNF3A|TCF3A	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02319	transcriptional regulation	metastasis,prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)	UP(BRCA);DATA(GSE55807)
Prostate cancer	FOXA1	PCAT29	positively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000129514	NA	ENST00000560655	GRCh38_15:69592200-69695750	3169	104472713	HNF3A|TCF3A	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02320	transcriptional regulation	metastasis,prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Gallbladder cancer	CCAT1	BMI1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-218-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000168283	NA	100507056	648	CARLO5|CARLo-5|onco-lncRNA-40	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long non-coding RNA CCAT1 promotes gallbladder cancer development via negative modulation of miRNA-218-5p. In this study, we demonstrated that CCAT1 was upregulated in gallbladder cancer (GBC) tissues. CCAT1 silencing downregulated, whereas CCAT1 overexpression enhanced the expression of miRNA-218-5p target gene Bmi1 through competitively 'spongeing' miRNA-218-5p. Our data revealed that CCAT1 knockdown impaired the proliferation and invasiveness of GBC cells, at least in part through affecting miRNA-218-5p-mediated regulation of Bmi1. Moreover, CCAT1 transcript level was correlated with Bmi1 mRNA level in GBC tissues. Together, these results suggest that CCAT1 is a driver of malignancy, which acts in part through 'spongeing' miRNA-218-5p.	25569100	RID02321	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Malignant glioma	CASC2	miR-21-5p	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	tumor-suppressive function(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21.In this study, we confirmed that CASC2 was lowly expressed in glioma tissues as well as in U251 and U87 glioma cell lines. We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner. Furthermore, bioinformatics, luciferase reporter assays and pull-down assay confirmed that miR-21 binds to CASC2 in a sequence-specific manner. Introduction of miR-21 largely abrogated CASC2-mediated inhibition of glioma cell proliferation, migration, and invasion, and promotion of cell apoptosis. This study demonstrated that CASC2 plays a tumor suppressive role in glioma via negative regulation of miR-21, which may be a novel therapeutic target for treating gliomas.	25446261	RID02322	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	NA
Peripheral primitive neuroectodermal tumor	EWSR1	EWSAT1	positively-E	RNAi;western blot	upregulation	microarray;sequencing	GSE60949	GSE60949.zip	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Sarcoma	PCG	lncRNA	ENSG00000182944	NA	ENSG00000212766	GRCh38_15:69072926-69095820	2130	283673	EWS|EWS-FLI1|bK984G1.4	LINC00277|NCRNA00277|TMEM84	Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis. We determined that long noncoding RNA-277 (Ewing sarcoma-associated transcript 1 [EWSAT1]) is upregulated by EWS-FLI1 in pMPCs. Inhibition of EWSAT1 expression diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in soft agar, whereas EWSAT1 inhibition had no effect on other cell types tested. Together, our data reveal that EWSAT1 is a downstream target of EWS-FLI1 that facilitates the development of Ewing sarcoma via the repression of target genes.	25401475	RID02323	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978,GSE41245)	NA
Pancreatic ductal adenocarcinoma	RPL13AP23	OS9	positively-E	RNAi;IHC;luciferase reporter assay;ChIP	downregulation	qRT-PCR	NA	NA	cell invasion(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000242990	GRCh38_12:57674665-57675250	ENSG00000135506	NA	441641	10956	RPL13A_10_1240	ERLEC2|OS-9	A novel long non-coding RNA ENST00000480739 suppresses tumour cell invasion by regulating OS-9 and HIF-1alpha in pancreatic ductal adenocarcinoma. We determined that the ENST00000480739 expression level was remarkably decreased in tumorous tissues compared with their corresponding non-tumorous tissues. Besides, enforced expression of ENST00000480739 suppressed PDAC cells' invasion in vitro. Overexpression of ENST00000480739 significantly increased both mRNA and protein levels of OS-9, and the luciferase assays confirmed that ENST00000480739 positively regulates OS-9 by activating the transcription level of the OS-9 promoter. We further found that ENST00000480739 may target hypoxia-inducible factor-1alpha (HIF-1alpha) expression by upregulating OS-9.	25314054	RID02324	transcriptional regulation	NA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	RPL13AP23	HIF1A	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000242990	GRCh38_12:57674665-57675250	ENSG00000100644	NA	441641	3091	RPL13A_10_1240	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	A novel long non-coding RNA ENST00000480739 suppresses tumour cell invasion by regulating OS-9 and HIF-1alpha in pancreatic ductal adenocarcinoma.	25314054	RID02325	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	GAPLINC	CD44	positively-E	RNAi;luciferase reporter assay	upregulation	microarray	GSE50710	GSE50710.zip	cell invasion(-);cell proliferation(-);prognosis	ceRNA(miR-211-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000026508	NA	100505592	960	LINC01540	CDW44|CSPG8|ECMR-III|HCELL|HUTCH-I|IN|LHR|MC56|MDU2|MDU3|MIC4|Pgp1	Long noncoding RNA GAPLINC regulates CD44-dependent cell invasiveness and associates with poor prognosis of gastric cancer.GAPLINC is a 924-bp-long lncRNA that is highly expressed in gastric cancer tissues. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effects of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression. Mechanistic investigations revealed that GAPLINC regulates CD44 as a molecular decoy for miR211-3p, a microRNA that targets both CD44 and GAPLINC.	25277524	RID02326	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Colon cancer	MYC	CCAT1	positively-E	RNAi;IHC;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	NA	GRCh38_8:127207382-127219268	4609	100507056	MRTL|MYCC|bHLHe39|c-Myc	CARLO5|CARLo-5|onco-lncRNA-40	C-Myc-activated long noncoding RNA CCAT1 promotes colon cancer cell proliferation and invasion. Our results revealed that CCAT1 was significantly overexpressed in colon cancer tissues when compared with normal tissues, and its increased expression was correlated with patients' clinical stage, lymph nodes metastasis, and survival time after surgery. Moreover, c-Myc could promote CCAT1 transcription by directly binding to its promoter region, and upregulation of CCAT1 expression in colon cancer cells promoted cell proliferation and invasion.	25185650	RID02327	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	NA
Gastric cancer	FENDRR	FN1	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000115414	NA	400550	2335	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CIG|ED-B|FINC|FN|FNZ|GFND|GFND2|LETS|MSF|SMDCF	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02328	expression association	metastasis,prognosis	NA	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Gastric cancer	FENDRR	MMP2	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000087245	NA	400550	4313	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02329	expression association	metastasis,prognosis	NA	UP(PAAD);DATA(GSE40174)
Gastric cancer	FENDRR	MMP9	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000100985	NA	400550	4318	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4B|GELB|MANDP2|MMP-9	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02330	expression association	metastasis,prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	FOXCUT	FOXC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000054598	NA	101927703	2296	LINC01379|TCONS_00011636	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	A novel long non-coding RNA FOXCUT and mRNA FOXC1 pair promote progression and predict poor prognosis in esophageal squamous cell carcinoma. Here, we showed that a novel long non-coding RNA FOXCUT (FOXC1 promoter upstream transcript) and its neighboring gene FOXC1 played a similar important role in the oncogenesis and progression of esophageal squamous cell carcinoma (ESCC). Notably elevated FOXCUT and FOXC1 expression levels were observed in cancerous tissues compared to adjacent noncancerous tissues the expression of FOXCUT was positively correlated with expression of FOXC1 in ESCC specimens.Assays in vitro demonstrated that knockdown of either FOXCUT or FOXC1 remarkably inhibited cell proliferation, colony formation, migration, invasion in ESCC cells. In conclusion, FOXCUT may be functionally involved in the tumor progression and survival of ESCC patients, at least in part, by modulating FOXC1. FOXCUT and FOXC1 may function as a lncRNA-mRNA gene pair, which may represent a potential prognostic biomarker and therapeutic target for ESCC patients.	25031703	RID02331	expression association	prognosis	NA	UP(SKCM);DATA(GSE38495)
Gastric cancer	GAS5	E2F1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000101412	NA	60674	1869	NCRNA00030|SNHG2	E2F-1|RBAP1|RBBP3|RBP3	Decreased expression of long noncoding RNA GAS5 indicates a poor prognosis and promotes cell proliferation in gastric cancer. We found that GAS5 expression was markedly downregulated in gastric cancer tissues, and associated with larger tumor size and advanced pathologic stage. Finally, we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression.The results showed that the expression of E2F1 was significantly decreased and the expression of cyclin D1 was also downregulated in gastric cancer cells transfected with pCDNA3.1-GAS5.	24884417	RID02332	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	MTOR	GAS5	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(-);apoptosis process(+)	NA	regulation	NA	docetaxel;5-fluorouracil	NA	Evading Apoptosis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000198793	NA	ENSG00000234741	GRCh38_1:173858559-173868882	2475	60674	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	NCRNA00030|SNHG2	Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy. GAS5 silencing attenuated cell responses to apoptotic stimuli, including classical chemotherapeutic agents; the extent of cell death was directly proportional to cellular GAS5 levels. Imatinib action in contrast, was independent of GAS5. GAS5 lncRNA promoted the apoptosis of triple-negative and oestrogen receptor-positive cells but only dual PI3K/mTOR inhibition was able to enhance GAS5 levels in all cell types. Reduced GAS5 expression attenuates apoptosis induction by classical chemotherapeutic agents in breast cancer cells, providing an explanation for the relationship between GAS5 expression and breast cancer patient prognosis. Clinically, this relationship may be circumvented by the use of GAS5-independent drugs such as imatinib, or by restoration of GAS5 expression. The latter may be achieved by the use of a dual PI3K/mTOR inhibitor, to improve apoptotic responses to conventional chemotherapies.GAS5 silencing diminished docetaxel-induced apoptosis and the associated loss of culture viability in both MCF7 (Fig. 3c) and T-47D cells (Fig. 3d). Similar effects were observed regarding 5-FU action in MCF7 (Fig. 3e) and T-47D (Fig. 3f) cells, whereas, imatinib action was unaffected by GAS5 silencing.	24789445	RID02333	expression association	chemoresistance,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Breast cancer	PI3K	GAS5	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(-);apoptosis process(+)	NA	regulation	NA	docetaxel;5-fluorouracil	NA	Evading Apoptosis	Cancer	Breast cancer	PCG	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy. GAS5 silencing attenuated cell responses to apoptotic stimuli, including classical chemotherapeutic agents; the extent of cell death was directly proportional to cellular GAS5 levels. Imatinib action in contrast, was independent of GAS5. GAS5 lncRNA promoted the apoptosis of triple-negative and oestrogen receptor-positive cells but only dual PI3K/mTOR inhibition was able to enhance GAS5 levels in all cell types. Reduced GAS5 expression attenuates apoptosis induction by classical chemotherapeutic agents in breast cancer cells, providing an explanation for the relationship between GAS5 expression and breast cancer patient prognosis. Clinically, this relationship may be circumvented by the use of GAS5-independent drugs such as imatinib, or by restoration of GAS5 expression. The latter may be achieved by the use of a dual PI3K/mTOR inhibitor, to improve apoptotic responses to conventional chemotherapies.GAS5 silencing diminished docetaxel-induced apoptosis and the associated loss of culture viability in both MCF7 (Fig. 3c) and T-47D cells (Fig. 3d). Similar effects were observed regarding 5-FU action in MCF7 (Fig. 3e) and T-47D (Fig. 3f) cells, whereas, imatinib action was unaffected by GAS5 silencing.	24789445	RID02334	expression association	chemoresistance,prognosis	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Colorectal cancer	CCAT1	MYC	positively-E	northern blot;ISH;ChIP;RNA pull-down assay	upregulation	qPCR;RT-PCR	NA	NA	tumorigenesis(+)	chromatin looping;super-enhancer	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Human colorectal cancer-specific CCAT1-L lncRNA regulates long-range chromatin interactions at the MYC locus. Here we demonstrate that a long noncoding RNA (lncRNA), CCAT1-L, is transcribed specifically in human colorectal cancers from a locus 515 kb upstream of MYC. This lncRNA plays a role in MYC transcriptional regulation and promotes long-range chromatin looping. Importantly, the CCAT1-L locus is located within a strong super-enhancer and is spatially close to MYC. Knockdown of CCAT1-L reduced long-range interactions between the MYC promoter and its enhancers. In cis overexpression of CCAT1-L enhances MYC expression and promotes tumorigenesis.	24662484	RID02335	chromatin looping	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	GHET1	MYC	positively-E	RIP;RNAi;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	RNA stability	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000136997	NA	102723099	4609	lncRNA-GHET1	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA GHET1 promotes gastric carcinoma cell proliferation by increasing c-Myc mRNA stability. In this study, we found that lncRNA gastric carcinoma high expressed transcript 1 (lncRNA-GHET1) was up-regulated in gastric carcinoma. RNA pull-down and immunoprecipitation assays confirmed that GHET1 physically associates with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) and enhances the physical interaction between c-Myc mRNA and IGF2BP1, consequently increasing the stability of c-Myc mRNA and expression. The expression of GHET1 and c-Myc is strongly correlated in gastric carcinoma tissues. these findings indicate that GHET1 plays a pivotal role in gastric carcinoma cell proliferation via increasing c-Myc mRNA stability and expression, which suggests potential use of GHET1 for the prognosis and treatment of gastric carcinoma.	24397586	RID02336	interact with mRNA	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	GAS5	TP53	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	BCC7|BMFS5|LFS1|P53|TRP53	A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer.The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues (P<0.05) and was highly related to tumor size and TNM stage (P<0.05). Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up-regulated p53 expression and down-regulated transcription factor E2F1 expression.	24357161	RID02337	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	GAS5	E2F1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000101412	NA	60674	1869	NCRNA00030|SNHG2	E2F-1|RBAP1|RBBP3|RBP3	A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer.The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues (P<0.05) and was highly related to tumor size and TNM stage (P<0.05). Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up-regulated p53 expression and down-regulated transcription factor E2F1 expression.	24357161	RID02338	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	GAS5	CDK6	negatively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	RNA stability	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	Downregulation of GAS5 promotes bladder cancer cell proliferation, partly by regulating CDK6. In the present study, we found that the GAS5 expression is commonly downregulated in bladder cancer cell lines and human specimens. Knockdown of GAS5 promotes bladder cancer cell proliferation, whereas forced expression of GAS5 suppresses cell proliferation. We further demonstrated that knockdown of GAS5 increases CDK6 mRNA and protein levels in bladder cancer cells.	24069260	RID02339	interact with mRNA	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Pancreatic cancer	GAS5	CDK6	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	Downregulation of gas5 increases pancreatic cancer cell proliferation by regulating CDK6. We verify that the expression level of gas5 is significantly decreased in pancreatic cancer tissues compared with normal control. We further demonstrate that gas5 negatively regulates CDK6 (cyclin-dependent kinase 6) expression in vitro and in vivo. knockdown of CDK6 partially abrogates gas5-siRNA-induced cell proliferation. More importantly, knockdown of CDK6 partially abrogates gas5-siRNA-induced cell proliferation.	24026436	RID02340	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Colon cancer	CCAT2	MYC	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000136997	NA	101805488	4609	LINC00873|NCCP1	MRTL|MYCC|bHLHe39|c-Myc	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02341	expression association	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colon cancer	CCAT2	miR-17-5p	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02342	expression association	metastasis	NA	NA
Colon cancer	CCAT2	miR-20a-5p	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02343	expression association	metastasis	NA	NA
Prostate cancer	CTBP1-AS	CTBP1	negatively-E	immunoprecipitation;northern blot;RNAi;IHC	upregulation	sequencing	NA	NA	cell cycle(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000280927	GRCh38_4:1210120-1218591	ENSG00000159692	NA	285463	1487	PCAT10	BARS|HADDTS	Androgen-responsive long noncoding RNA CTBP1-AS promotes prostate cancer. CTBP1-AS directly represses CTBP1 expression by recruiting the RNA-binding transcriptional repressor PSF together with histone deacetylases. CTBP1-AS also exhibits global androgen-dependent functions by inhibiting tumour-suppressor genes via the PSF-dependent mechanism thus promoting cell cycle progression.	23644382	RID02344	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MYC	CCAT1	positively-E	ChIP;RNAi;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000136997	NA	NA	GRCh38_8:127207382-127219268	4609	100507056	MRTL|MYCC|bHLHe39|c-Myc	CARLO5|CARLo-5|onco-lncRNA-40	Long noncoding RNA CCAT1, which could be activated by c-Myc, promotes the progression of gastric carcinoma.c-Myc directly binds to the E-box element in the promoter region of CCAT1, and when ectopically expressed increased promoter activity and expression of CCAT1. abnormally expressed CCAT1 promotes cell proliferation and migration.	23143645	RID02345	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	NA
Chronic lymphocytic leukemia	DLEU2	miR-15a-5p	positively-E	ChIP;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-)	host	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000231607	GRCh38_13:49956670-50125720	NA	NA	8847	NA	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	NA	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1. Here we demonstrate that the putative tumor suppressor DLEU2 acts as a host gene of these microRNAs. Mature miR-15a/miR-16-1 are produced in a Drosha-dependent process from DLEU2 and binding of the Myc oncoprotein to two alterative DLEU2 promoters represses both the host gene transcript and levels of mature miR-15a/miR-16-1. We additionally show that DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	19591824	RID02346	expression association	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	NA
Chronic lymphocytic leukemia	DLEU2	miR-16-1-3p	positively-E	ChIP;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-)	host	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000231607	GRCh38_13:49956670-50125720	NA	NA	8847	NA	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	NA	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1. Here we demonstrate that the putative tumor suppressor DLEU2 acts as a host gene of these microRNAs. Mature miR-15a/miR-16-1 are produced in a Drosha-dependent process from DLEU2 and binding of the Myc oncoprotein to two alterative DLEU2 promoters represses both the host gene transcript and levels of mature miR-15a/miR-16-1. We additionally show that DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	19591824	RID02347	expression association	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	NA
Breast cancer	GAS5	SNORD50A	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	host(snoRNA)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	snoRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	26799	NCRNA00030|SNHG2	RNU50|U50	GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer.GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. The GAS5 gene has no significant protein-coding potential but expression encodes small nucleolar RNAs (snoRNAs) in its introns. Taken together with the recent demonstration of tumor suppressor characteristics in the related snoRNA U50, our observations suggest that such snoRNAs form a novel family of genes controlling oncogenesis and sensitivity to therapy in cancer.	18836484	RID02348	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	NA
Hepatocellular carcinoma	HULC	SNAI1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124216	NA	728655	6615	HCCAT1|LINC00078|NCRNA00078	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Molecular mechanism of HEIH and HULC in the proliferation and invasion of hepatoma cells. The expression of HEIH and HULC in hepatocellular carcinoma cell line was significantly increased compared with human normal hepatocyte line (P<0.05). Over-expression of HULC up-regulated the expression of Snail in HepG2.	26550214	RID02349	expression association	NA	NA	UP(PAAD);DATA(GSE40174)
Gastric cancer	HNF1A-AS1	RRM1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000167325	NA	283460	6240	C12orf27|HAS1|NCRNA00262	R1|RIR1|RR1	Expression and clinical significance of long non-coding RNA HNF1A-AS1 in human gastric cancer. LncRNAs microarray analysis results exhibited that HNF1A-AS1 was downregulated in GCs tissues (mean fold change 2.06, p<0.05), which was further confirmed by qRT-PCR.Furthermore, low HNF1A-AS1 expression was associated with tumor size/diameter (p=0.005, multivariate analysis), levels of serum carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9), and RRM1 expression in tissue samples (p=0.028, p=0.009, and p=0.006, respectively).Taken together, our data indicate that lncRNA HNF1A-AS1 may be a regulator of GC, and thus, it may have potential as a novel biomarker and treatment target for this type of cancer.	26472090	RID02350	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Gastric cancer	HNF1A-AS1	CEACAM5	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000105388	NA	283460	1048	C12orf27|HAS1|NCRNA00262	CD66e|CEA	Expression and clinical significance of long non-coding RNA HNF1A-AS1 in human gastric cancer. LncRNAs microarray analysis results exhibited that HNF1A-AS1 was downregulated in GCs tissues (mean fold change 2.06, p<0.05), which was further confirmed by qRT-PCR.Furthermore, low HNF1A-AS1 expression was associated with tumor size/diameter (p=0.005, multivariate analysis), levels of serum carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9), and RRM1 expression in tissue samples (p=0.028, p=0.009, and p=0.006, respectively).Taken together, our data indicate that lncRNA HNF1A-AS1 may be a regulator of GC, and thus, it may have potential as a novel biomarker and treatment target for this type of cancer.	26472090	RID02351	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(NSCLC,PAAD);DATA(GSE74639,GSE40174)
Prostate cancer	HOTAIR	AR	interact	ISH;ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell growth(-);cell invasion(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000169083	NA	100124700	367	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LncRNA HOTAIR Enhances the Androgen-Receptor-Mediated Transcriptional Program and Drives Castration-Resistant Prostate Cancer. Here, we report HOTAIR as an androgen-repressed lncRNA, and, as such, it is markedly upregulated following androgen deprivation therapies and in CRPC. We further demonstrate a distinct mode of lncRNA-mediated gene regulation, wherein HOTAIR binds to the AR protein to block its interaction with the E3 ubiquitin ligase MDM2, thereby preventing AR ubiquitination and protein degradation. Consequently, HOTAIR expression is sufficient to induce androgen-independent AR activation and drive the AR-mediated transcriptional program in the absence of androgen. Functionally, HOTAIR overexpression increases, whereas HOTAIR knockdown decreases, prostate cancer cell growth and invasion.	26411689;25895025;28082728	RID02352	interact with protein	NA	NA	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Breast cancer	ESR1	HOTAIR	negatively-E	Chromosome conformation capture (3C) assay;RIP;RNA pull-down assay;ChIP	upregulation	microarray;sequencing	GSE61270	GSE61270.zip	chemoresistance(+);cancer progression(+)	chromatin looping;enhancer;interact with protein	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2099	100124700	ER|ESR|ESRA|ESTRR|Era|NR3A1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer. In this study, we report that HOTAIR (HOX antisense intergenic RNA) is upregulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or by tamoxifen treatment. In conclusion, the long non-coding RNA HOTAIR is directly repressed by ER and its upregulation promotes ligand-independent ER activities and contributes to tamoxifen resistance. Further, chromosome conformation capture (3C) experiment demonstrated estrogen-induced DNA looping between the transcription start site (TSS) of the HOTAIR gene (anchor primer- AP) and the ER-bound enhancer (P4). HOTAIR directly interacts with ER and enhances ER transcriptional activities.	26364613;23375982	RID02353	interact with protein	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	NA
Urinary bladder cancer	H19	TP53	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	host(miR-675)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BCC7|BMFS5|LFS1|P53|TRP53	H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation. Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro.Western blotting analysis further identified that miR-675 inhibited p53 activation, decreased the ratio of Bax/Bcl-2 and cyclin D1 expression in bladder cancer cells;	26198047	RID02354	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	HOTAIR	HLA-G	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	immune evasion(+)	ceRNA(miR-152)	regulation	NA	NA	NA	Evading Immune Detection	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204632	NA	100124700	3135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MHC-G	Long non-coding RNA HOTAIR promotes HLA-G expression via inhibiting miR-152 in gastric cancer cells. Significant HOTAIR overexpression was observed in GC tissues, as well as strong positive correlations with HLA-G levels in both tissue and peripheral blood samples, detected by real-time PCR and ELISA assays respectively.bioinformatics analysis indicated the interaction between HOTAIR and miR-152, which shows potential regulation on HLA-G.Moreover, the negative regulation of miR-152 on HLA-G was verified in GC cells, while miR-152 induced decrease of HLA-G 3'UTR activity could be attenuated by HOTAIR co-overexpression with the assistant of mutation studies. Therefore, it was concluded that HOTAIR overexpression might also get involved in tumor escape mechanisms, involving HLA-G upregulation via inhibiting miR-152. Furthermore, this study recommended the potential application of HOTAIR in GC immunotherapy for better prognosis and improved survival.	26187665	RID02355	ceRNA or sponge	prognosis	NA	UP(PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE111842,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	YAP1	H19	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000130600	GRCh38_11:1995176-2001470	10413	283120	COB1|YAP|YAP2|YAP65|YKI	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The YAP1 oncogene contributes to bladder cancer cell proliferation and migration by regulating the H19 long noncoding RNA. YAP1 and H19 expression levels were markedly elevated in bladder cancer tissues and cells, and H19 expression was found to be significantly associated with YAP1 expression. YAP1 was found to enhance H19 expression, whereas H19 had no significant effect on YAP1 expression in bladder cancer cells. Our results emphasize the importance of YAP1 and H19 in bladder cancer progression and indicate that H19, at least in part, is induced by YAP1 overexpression.	26163939	RID02356	expression association	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	UP(NSCLC);DATA(GSE74639)
Gastric cancer	H19	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-141)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer. H19 expression was found to be inversely correlated to miR-141 expression in gastric cancer cells and tissues. MiR-141 binds to H19 in a sequence specific manner, and suppresses H19 expression and functions including proliferation and invasion. MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1. These results were the first to demonstrate that H19 and miR-141 could compete with each other and affect their target genes in gastric cancer, which provide important clues for understanding the key roles of lncRNA-miRNA functional network in cancer.	26160158	RID02357	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	H19	VIM	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02358	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	H19	ZEB1	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02359	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	H19	ZEB2	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169554	NA	283120	9839	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02360	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Papillary thyroid carcinoma	MEG3	RAC1	negatively-F	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136238	NA	55384	5879	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA MEG3 suppresses migration and invasion of thyroid carcinoma by targeting of Rac1. the present study demonstrates that MEG3 was significantly down-regulated in papillary thyroid carcinoma (PTC) tissues with lymph-node metastasis than in primary thyroid cancer. In addition, we also showed that Rac1 was negatively regulated by lncRNA-MEG3 at the posttranscriptional level, via a specific target site within the 3'UTR by dual luciferase reporter assay. The expression of Rac1 was inversely correlated with lncRNA-MEG3 expression in PTC tissues.	25997963	RID02361	interact with mRNA	metastasis	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Breast cancer	BCAR4	SNIP1	interact	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000163877	NA	400500	79753	NA	PML1|PMRED	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02362	interact with protein	metastasis,chemoresistance	NA	UP(LIHC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	BCAR4	PPP1R10	interact	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000204569	NA	400500	5514	NA	CAT53|FB19|PNUTS|PP1R10|R111|p99	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02363	interact with protein	metastasis,chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Breast cancer	BCAR4	GLI2	positively-E	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000074047	NA	400500	2736	NA	CJS|HPE9|PHS2|THP1|THP2	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02364	epigenetic regulation	metastasis,chemoresistance	NA	UP(PAAD);DATA(GSE40174)
B-cell lymphoma	DLEU2	MYB	negatively-E	western blot;northern blot;luciferase reporter assay	downregulation	RT-PCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lymphoma	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000118513	NA	8847	4602	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	Cmyb|c-myb|c-myb_CDS|efg	c-Myb oncoprotein is an essential target of the dleu2 tumor suppressor microRNA cluster. Here we demonstrate that the Pax5 oncoprotein downregulates the dleu2 gene and at the same time boosts expression of its own heterodimeric partner c-Myb.Moreover, forced overexpression of miR-15a/16 reduces endogenous c-Myb levels and compromises Pax5 function. Conversely, restoration of c-Myb levels partly alleviates tumors suppressive effects of miR-15a/16, suggesting that c-Myb is a key downstream target of this microRNA cluster.	18708755	RID02365	expression association	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	NA
B-cell lymphoma	PAX5	DLEU2	negatively-E	western blot;northern blot;luciferase reporter assay	downregulation	RT-PCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lymphoma	TF	lncRNA	ENSG00000196092	NA	ENSG00000231607	GRCh38_13:49956670-50125720	5079	8847	ALL3|BSAP	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	c-Myb oncoprotein is an essential target of the dleu2 tumor suppressor microRNA cluster. Here we demonstrate that the Pax5 oncoprotein downregulates the dleu2 gene and at the same time boosts expression of its own heterodimeric partner c-Myb.Moreover, forced overexpression of miR-15a/16 reduces endogenous c-Myb levels and compromises Pax5 function. Conversely, restoration of c-Myb levels partly alleviates tumors suppressive effects of miR-15a/16, suggesting that c-Myb is a key downstream target of this microRNA cluster.	18708755	RID02366	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)
Breast cancer	HOTAIR	EZH2	interact	ISH;RNAi;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell metastasis(-);chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	platinum	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	20393566;28420874;30048163	RID02367	interact with protein	metastasis,chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	HOTAIR	SUZ12	interact	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.	20393566	RID02368	interact with protein	metastasis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	HOTAIR	EED	interact	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000074266	NA	100124700	8726	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	COGIS|HEED|WAIT1	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.	20393566	RID02369	interact with protein	metastasis	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	HOTAIR	JAM2	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154721	NA	100124700	58494	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C21orf43|CD322|JAM-B|JAMB|PRO245|VE-JAM|VEJAM	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02370	epigenetic regulation	metastasis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	HOTAIR	ABL2	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000143322	NA	100124700	27	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABLL|ARG	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02371	epigenetic regulation	metastasis	NA	UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	HOTAIR	SNAI1	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02372	epigenetic regulation	metastasis	NA	UP(PAAD);DATA(GSE40174)
Breast cancer	HOTAIR	LAMB3	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196878	NA	100124700	3914	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AI1A|BM600-125KDA|LAM5|LAMNB1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02373	epigenetic regulation	metastasis	NA	NA
Breast cancer	HOTAIR	LAMC2	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000058085	NA	100124700	3918	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	B2T|BM600|CSF|EBR2|EBR2A|LAMB2T|LAMNB2	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02374	epigenetic regulation	metastasis	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE40174)
Breast cancer	HOTAIR	HOXD10	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000128710	NA	100124700	3236	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX4|HOX4D|HOX4E|Hox-4.4	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02375	epigenetic regulation	metastasis,prognosis	NA	NA
Breast cancer	HOTAIR	PRG1	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	23574	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02376	epigenetic regulation	metastasis,prognosis	NA	NA
Breast cancer	HOTAIR	PCDH10	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000138650	NA	100124700	57575	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	OL-PCDH|PCDH19	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion.	20393566	RID02377	epigenetic regulation	metastasis,prognosis	NA	UP(LIHC);DATA(GSE117623)
Breast cancer	HOTAIR	PCDHB5	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113209	NA	100124700	26167	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-BETA5	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion.	20393566	RID02378	epigenetic regulation	metastasis,prognosis	NA	UP(PAAD);DATA(GSE40174)
Breast cancer	HOTAIR	PGR	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000082175	NA	100124700	5241	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NR3C3|PR	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02379	epigenetic regulation	metastasis,prognosis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	HOTAIR	EPHA1	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	angiogenesis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000146904	NA	100124700	2041	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	EPH|EPHT|EPHT1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02380	epigenetic regulation	metastasis,prognosis	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE75367)
Prostate cancer	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);PI3K/AKT signaling pathway(-);cell growth(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	ectopic expression of PTENP1 resulted in the upregulation of PTEN, accompanied by the blockage of PI3K/AKT pathway and growth inhibition in prostate (DU145) and renal (ACHN and SN12PM6) cancer cells [3, 6]. Specifically, PTENP1 can modulate PTEN levels by sponging miR21 in ACHN and SN12PM6 renal cancer cells, while exerting its decoy effect by trapping miR17, miR19b and miR20a, which would otherwise target PTEN and several autophagy gene transcripts in Mahlavu HCC cells.	20577206;24172333	RID02381	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Clear cell renal cell carcinoma	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);PI3K/AKT signaling pathway(-);cell growth(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	ectopic expression of PTENP1 resulted in the upregulation of PTEN, accompanied by the blockage of PI3K/AKT pathway and growth inhibition in prostate (DU145) and renal (ACHN and SN12PM6) cancer cells [3, 6]. Specifically, PTENP1 can modulate PTEN levels by sponging miR21 in ACHN and SN12PM6 renal cancer cells, while exerting its decoy effect by trapping miR17, miR19b and miR20a, which would otherwise target PTEN and several autophagy gene transcripts in Mahlavu HCC cells.We found that PTENP1 is downregulated in ccRCC tissues and cells due to methylation.	25249556;24172333	RID02382	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(-);cell proliferation(-);cell migration(-);cell invasion(-);cell autophagy(+);apoptosis process(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02383	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	PTENP1	ULK1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000177169	NA	11191	8408	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	ATG1|ATG1A|UNC51|Unc51.1|hATG1	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02384	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	PTENP1	ATG7	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000197548	NA	11191	10533	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	APG7-LIKE|APG7L|GSA7	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02385	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	PTENP1	SQSTM1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000161011	NA	11191	8878	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	A170|DMRV|FTDALS3|NADGP|OSIL|PDB3|ZIP3|p60|p62|p62B	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02386	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	UP(PAAD,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE41245)
Hepatocellular carcinoma	PTENP1	PHLPP1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(-)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000081913	NA	11191	23239	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	PHLPP|PLEKHE1|PPM3A|SCOP	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02387	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE51827,GSE55807)
Breast cancer	HOTAIR	LAMTOR5	interact	RIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000134248	NA	100124700	10542	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HBXIP|XIP	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02388	interact with protein	NA	NA	UP(NSCLC,PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	HOTAIR	KDM1A	interact	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02389	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	HOTAIR	CCNA2	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000145386	NA	100124700	890	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCN1|CCNA	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02390	epigenetic regulation	NA	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807,GSE67939)
Breast cancer	HOTAIR	EIF4E	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000151247	NA	100124700	1977	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AUTS19|CBP|EIF4E1|EIF4EL1|EIF4F|eIF-4E	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02391	epigenetic regulation	NA	NA	UP(LIHC,SKCM,BRCA);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	HOTAIR	LDHA	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000134333	NA	100124700	3939	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	GSD11|HEL-S-133P|LDHM|PIG19	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02392	epigenetic regulation	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Breast cancer	HOTAIR	CCNA1	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000133101	NA	100124700	8900	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CT146	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02393	epigenetic regulation	NA	NA	UP(PAAD);DATA(GSE40174)
Lung cancer	HOTAIR	MMP9	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Role of HOTAIR long noncoding RNA in metastatic progression of lung cancer. Among the tested lncRNAs, HOTAIR and NEAT1 were most highly expressed in lymph node metastasis. However, only HOTAIR was subsequently found to be involved in lung cancer cell motility and invasion, as assessed by in vitro migration and invasion assay. Finally, our experiments suggest that HOTAIR promoted gelatinase activity in these cells.Our data indicates that HOTAIR is overexpressed in metastatic lung cancer tissue, which is prospectively associated with the ability of HOTAIR to promote lung cancer cell motility and invasion.	25010625	RID02394	expression association	metastasis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	MIA2	negatively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150527	NA	378938	4253	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTAGE5|MEA6|MGEA|MGEA11|MGEA6|TALI	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02395	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Lung adenocarcinoma	MALAT1	ROBO1	negatively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169855	NA	378938	6091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DUTT1|SAX3	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02396	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Lung adenocarcinoma	MALAT1	GPC6	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000183098	NA	378938	10082	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OMIMD1	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02397	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	MALAT1	ADGRL2	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117114	NA	378938	23266	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CIRL2|CL2|LEC1|LPHH1|LPHN2	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02398	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Lung adenocarcinoma	MALAT1	CDCP1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163814	NA	378938	64866	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD318|SIMA135|TRASK	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02399	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Lung adenocarcinoma	MALAT1	ABCA1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000165029	NA	378938	19	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ABC-1|ABC1|CERP|HDLDT1|TGD	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02400	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	DRD1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000184845	NA	378938	1812	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DADR|DRD1A	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02401	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Lung adenocarcinoma	MALAT1	COL6A1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142156	NA	378938	1291	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BTHLM1|OPLL|UCHMD1	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02402	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE86978)
Lung adenocarcinoma	MALAT1	STC1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000159167	NA	378938	6781	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	STC	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02403	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE55807)
Lung adenocarcinoma	MALAT1	MCAM	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000076706	NA	378938	4162	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD146|HEMCAM|METCAM|MUC18|MelCAM	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02404	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Lung adenocarcinoma	MALAT1	PRKCE	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171132	NA	378938	5581	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	PKCE|nPKC-epsilon	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02405	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	MVIH	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:78038556-78040701	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion.  In this study, we found that lncRNA MVIH levels were increased in NSCLC tissues compared with adjacent normal tissues. Furthermore, knockdown of MVIH expression by siRNA could inhibit cell proliferation and invasion, while ectopic expression of MVIH promoted cell proliferation and invasion in NSCLC cells partly via regulating MMP2 and MMP9 protein expression. Our findings present that increased lncRNA MVIH could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and invasion.	24793017;25491133	RID02406	expression association	prognosis	NA	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	MVIH	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:78038556-78040701	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion.  In this study, we found that lncRNA MVIH levels were increased in NSCLC tissues compared with adjacent normal tissues. Furthermore, knockdown of MVIH expression by siRNA could inhibit cell proliferation and invasion, while ectopic expression of MVIH promoted cell proliferation and invasion in NSCLC cells partly via regulating MMP2 and MMP9 protein expression. Our findings present that increased lncRNA MVIH could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and invasion.	24793017;25491133	RID02407	expression association	prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	NFE2L2	LUCAT1	interact	ChIP;western blot;RNAi	upregulation	qPCR;microarray	GSE29006	GSE29006.zip	cytotoxicity(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tumor Promoting Inflammation	Cancer	Lung cancer	TF	lncRNA	ENSG00000116044	NA	ENSG00000248323	GRCh38_5:91054834-91314547	4780	100505994	HEBP1|IMDDHH|NRF2	SCAL1|SCAT5	The expression of SCAL1 is regulated transcriptionally by nuclear factor erythroid 2-related factor (NRF2), as determined by the small, interfering RNA (siRNA) knockdown of NRF2 and kelch-like ECH-associated protein 1 (KEAP1). A nuclear factor erythroid-derived 2 (NF-E2) motif was identified in the promoter region that shows binding to NRF2 after its activation. Functionally, the siRNA knockdown of SCAL1 in human bronchial epithelial cells shows a significant potentiation of cytotoxicity induced by CSE in vitro.	23672216;25491133	RID02408	transcriptional regulation	NA	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	GAS6-AS1	GAS6	negatively-E	RNAi	downregulation	qPCR	NA	NA	prognosis(+);cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233695	GRCh38_13:113815630-113845744	ENSG00000183087	NA	650669	2621	NA	AXLLG|AXSF	Low expression of long noncoding RNA GAS6-AS1 predicts a poor prognosis in patients with NSCLC.In this study, we reported a new lncRNA GAS6-AS1 (GAS6 antisense RNA 1), whose expression was downregulated in tumor tissues in 50 patients with non-small cell lung cancer (NSCLC) compared with those in the adjacent normal tissues (P<0.001).GAS6-AS1 level was inversely correlated with GAS6 (growth-arrest-specific gene6) mRNA level (Pearson's correlation -0.620). In conclusion, our study demonstrated that altered lncRNA GAS6-AS1 expression might be involved in the development and progression of NSCLC by influencing its host gene and promised to be a potential diagnostic target in patients with NSCLC.	23979857;25491133	RID02409	expression association	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	TARID	TCF21	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;25491133	RID02410	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Lung cancer	TARID	GADD45A	interact	ChIP;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;25491133	RID02411	interact with protein	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Gallbladder cancer	HOTAIR	miR-130a	negatively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer.We demonstrate that HOTAIR is a direct target of c-Myc through interaction with putative c-Myc target response element (RE) in the upstream region of HOTAIR in gallbladder cancer cells. A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. We predicted that HOTAIR harbors a miRNA-130a binding site. Our data showed that this binding site is vital for the regulation of miRNA-130a by HOTAIR. Moreover, a negative correlation between HOTAIR and miRNA-130a was observed in gallbladder cancer tissues. Finally, we demonstrate that the oncogenic activity of HOTAIR is in part through its negative regulation of miRNA-130a.	24953832;25491133	RID02412	ceRNA or sponge	NA	NA	NA
Gallbladder cancer	MYC	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Gallbladder cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000228630	GRCh38_12:53962308-53974956	4609	100124700	MRTL|MYCC|bHLHe39|c-Myc	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer.We demonstrate that HOTAIR is a direct target of c-Myc through interaction with putative c-Myc target response element (RE) in the upstream region of HOTAIR in gallbladder cancer cells. A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. We predicted that HOTAIR harbors a miRNA-130a binding site. Our data showed that this binding site is vital for the regulation of miRNA-130a by HOTAIR. Moreover, a negative correlation between HOTAIR and miRNA-130a was observed in gallbladder cancer tissues. Finally, we demonstrate that the oncogenic activity of HOTAIR is in part through its negative regulation of miRNA-130a.	24953832;25491133	RID02413	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	NA
Laryngeal squamous cell carcinoma	HOTAIR	PTEN	negatively-E	RNAi;Methylation-Specific and Bisulfite Sequencing PCR	upregulation	qPCR	NA	NA	oncogenic role(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long intergenic noncoding RNA HOTAIR is overexpressed and regulates PTEN methylation in laryngeal squamous cell carcinoma. HOTAIR levels were significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues. Moreover, PTEN methylation was significantly reduced in Hep-2 cells depleted of HOTAIR. Taken together, these results suggest that the oncogenic role of HOTAIR in LSCC is related to promotion of PTEN methylation. HOTAIR could serve as a marker for LSCC prognosis and a potential target for therapeutic intervention.	23141928;25491133	RID02414	epigenetic regulation	prognosis	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Colorectal cancer	HOTAIR	SUZ12	positively-E	RNAi	upregulation	qPCR;microarray	GSE21815	GSE21815.zip	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	Long noncoding RNA HOTAIR regulates polycomb-dependent chromatin modification and is associated with poor prognosis in colorectal cancers.In this study, we examined the status and function of HOTAIR in patients with stage IV colorectal cancer (CRC) who have liver metastases and a poor prognosis. HOTAIR expression levels were higher in cancerous tissues than in corresponding noncancerous tissues and high HOTAIR expression correlated tightly with the presence of liver metastasis.gene set enrichment analysis using cDNA array data revealed a close correlation between expression of HOTAIR and members of the PRC2 complex (SUZ12, EZH2, and H3K27me3). Our findings suggest that HOTAIR expression is associated with a genome-wide reprogramming of PRC2 function not only in breast cancer but also in CRC, where upregulation of this long ncRNA may be a critical element in metastatic progression.	21862635	RID02415	expression association	metastasis,prognosis	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	HOTAIR	EZH2	interact	RIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	5-fluorouracil	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer. To investigate whether HOTAIR is associated with EZH2 in CRC, an RNA immunoprecipitation (RIP) assay was performed, and the results showed a significant enrichment of HOTAIR with EZH2 antibody compared with the non-specific IgG (immunoglobulin G) antibody in both HT29 and SW480 cells	28918035;21862635	RID02416	interact with protein	metastasis,chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Renal cell carcinoma	miR-141	HOTAIR	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Long non-coding RNA HOTAIR is targeted and regulated by miR-141 in human cancer cells. We found that HOTAIR expression is inversely correlated to miR-141 expression in renal carcinoma cells. HOTAIR promotes malignancy, including proliferation and invasion, whereas miR-141 suppresses malignancy in human cancer cells. miR-141 binds to HOTAIR in a sequence-specific manner and suppresses HOTAIR expression and functions, including proliferation and invasion.	20333681	RID02417	ceRNA or sponge	NA	NA	NA
Gastric cancer	HOTAIR	MMP1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196611	NA	100124700	4312	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG|CLGN	Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer.The expression level of HOTAIR in cancer tissues was higher than that in adjacent noncancerous tissues. In vitro, inhibition of HOTAIR in GC cells could reduce invasiveness, as well as the expression of MMP1 and MMP3. In addition, suppression of HOTAIR could reverse EMT process.	23847441	RID02418	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	HOTAIR	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000149968	NA	100124700	4314	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer.The expression level of HOTAIR in cancer tissues was higher than that in adjacent noncancerous tissues. In vitro, inhibition of HOTAIR in GC cells could reduce invasiveness, as well as the expression of MMP1 and MMP3. In addition, suppression of HOTAIR could reverse EMT process.	23847441	RID02419	expression association	NA	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	COL1A1	HOTAIR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000108821	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1277	100124700	EDSARTH1|EDSC|OI1|OI2|OI3|OI4	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Induction of long intergenic non-coding RNA HOTAIR in lung cancer cells by type I collagen. Our findings indicate that tumor-promoting Col-1 up-regulates the expression of HOTAIR in NSCLC cells. These initial results warrant further investigation of HOTAIR and other lincRNA genes in lung tumorigenesis. Moreover the expression of HOTAIR and Col-1 was concurrently up-regulated in human non-small cell lung cancer.	23668363	RID02420	expression association	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)	NA
Breast cancer	KMT2A	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000118058	NA	ENSG00000228630	GRCh38_12:53962308-53974956	4297	100124700	ALL-1|CXXC7|HRX|HTRX1|MLL|MLL1|MLL1A|TRX1|WDSTS	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02421	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	NA
Breast cancer	KMT2C	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000055609	NA	ENSG00000228630	GRCh38_12:53962308-53974956	58508	100124700	HALR|KLEFS2|MLL3	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02422	transcriptional regulation	NA	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	NA
Breast cancer	CREBBP	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000005339	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1387	100124700	CBP|KAT3A|MKHK1|RSTS|RSTS1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02423	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Breast cancer	EP300	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000100393	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2033	100124700	KAT3B|MKHK2|RSTS2|p300	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02424	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	NA
Cancer	NBR2	PRKAG1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000181929	NA	10230	5571	NCRNA00192	AMPKG	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02425	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Cancer	NBR2	PRKAA1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000132356	NA	10230	5562	NCRNA00192	AMPK|AMPKa1	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02426	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Cancer	NBR2	PRKAA2	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000162409	NA	10230	5563	NCRNA00192	AMPK|AMPK2|AMPKa2|PRKAA	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02427	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807)
Cancer	NBR2	PRKAB1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000111725	NA	10230	5564	NCRNA00192	AMPK|HAMPKb	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02428	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Urinary bladder cancer	UCA1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000198793	NA	652995	2475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02429	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Urinary bladder cancer	UCA1	STAT3	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168610	NA	652995	6774	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADMIO|ADMIO1|APRF|HIES	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02430	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Urinary bladder cancer	UCA1	miR-143	negatively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02431	expression association	NA	UP(PAAD);DATA(GSE40174)	NA
Urinary bladder cancer	UCA1	HK2	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000159399	NA	652995	3099	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HKII|HXK2	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02432	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00462	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233610	GRCh38_13:48576974-48578088	NA	NA	100129597	NA	NA	NA	Long noncoding RNA linc00462 promotes hepatocellular carcinoma progression. Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway.	28622593;30134946	RID02433	expression association	NA	NA	NA
Hepatocellular carcinoma	LINC00462	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233610	GRCh38_13:48576974-48578088	ENSG00000142208	NA	100129597	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA linc00462 promotes hepatocellular carcinoma progression. Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway.	28622593;30134946	RID02434	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells.The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway.	28592124;30134946	RID02435	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Cholangiocarcinoma	MALAT1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);PI4K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells.The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway.	28592124;30134946	RID02436	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Chronic myeloid leukemia	HULC	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548;30134946	RID02437	expression association	NA	NA	NA
Chronic myeloid leukemia	HULC	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	PI4K/AKT signaling pathway(+);cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000142208	NA	728655	207	HCCAT1|LINC00078|NCRNA00078	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548;30134946	RID02438	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	CDKN2B-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL indicates a poor prognosis of cervical cancer and promotes carcinogenesis via PI3K/Akt pathways.Our results showed that the expression of lncRNA ANRIL was significantly increased both in cervical cancer tissues and cell lines.Finally, western blot indicated that the PI3K/Akt pathway was found to be inactivated in cervical cancer cells after ANRIL inhibition.	27899255;30134946	RID02439	expression association	prognosis	UP(SKCM);DATA(GSE38495)	NA
Cervical cancer	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	PI4K/AKT signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA ANRIL indicates a poor prognosis of cervical cancer and promotes carcinogenesis via PI3K/Akt pathways.Our results showed that the expression of lncRNA ANRIL was significantly increased both in cervical cancer tissues and cell lines.Finally, western blot indicated that the PI3K/Akt pathway was found to be inactivated in cervical cancer cells after ANRIL inhibition.	27899255;30134946	RID02440	expression association	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC00473	STK11	negatively-E	luciferase reporter assay	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cell growth(+);metabolic process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000118046	NA	90632	6794	C6orf176|LNC473|bA142J11.1	LKB1|PJS|hLKB1	cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth.Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription.	27140397;30134946	RID02441	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	LINC00473	NONO	interact	RIP;western blot	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cAMP signaling pathway(+);metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223414	GRCh38_6:165924048-165988039	ENSG00000147140	NA	90632	4841	C6orf176|LNC473|bA142J11.1	MRXS34|NMT55|NRB54|P54|P54NRB|PPP1R114	cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth.Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription.	27140397;30134946	RID02442	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Nasopharynx carcinoma	CDKN2B-AS1	SLC2A1	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	CSC	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000117394	NA	100048912	6513	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CSE|DYT17|DYT18|DYT9|EIG12|GLUT|GLUT-1|GLUT1|GLUT1DS|HTLVR|PED|SDCHCN	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02443	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD,PRAD);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE67939)
Nasopharynx carcinoma	CDKN2B-AS1	LDHA	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	CSC	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000134333	NA	100048912	3939	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	GSD11|HEL-S-133P|LDHM|PIG19	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02444	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Nasopharynx carcinoma	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	mTOR signaling pathway(+);glucose metabolic process(+)	NA	regulation	NA	NA	CSC	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02445	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	CRNDE	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000198793	NA	NA	2475	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	CRNDE, a long-noncoding RNA, promotes glioma cell growth and invasion through mTOR signaling. In this study, the upregulation of CRNDE was confirmed in both primary specimens from glioma patients and in vitro with cell lines. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma.	25813405;30134946	RID02446	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Cervical cancer	LNMICC	NPM1	interact	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	lipid metabolic process(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENST00000518880	GRCh38_8:81279871-81281446	ENSG00000181163	NA	NA	4869	NA	B23|NPM	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02447	interact with protein	metastasis	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Cervical cancer	LNMICC	FABP5	interact	RNAi	upregulation	qPCR	NA	NA	lipid metabolic process(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENST00000518880	GRCh38_8:81279871-81281446	ENSG00000164687	NA	NA	2171	NA	E-FABP|EFABP|KFABP|PA-FABP|PAFABP	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02448	expression association	metastasis	NA	DOWN(LIHC,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495,GSE111842)
Cervical cancer	miR-190	LNMICC	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	lipid metabolic process(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	miRNA	lncRNA	NA	NA	ENST00000518880	GRCh38_8:81279871-81281446	NA	NA	NA	NA	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02449	ceRNA or sponge	metastasis	NA	NA
Cholangiocarcinoma	TUG1	SIRT3	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	glutamine metabolic process(+);prognosis(-)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000142082	NA	55000	23410	LINC00080|NCRNA00080|TI-227H	SIR2L3	LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis. We found that TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that sponges miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. In view of the above results, we used the TargetScan algorithm to find out whether glutaminase (GLS), glutamate dehydrogenase (GDH), and/or their regulators are targets of miR-145. Results revealed Sirt3, a positive regulator of GDH [21], and glutaminase 1 (GLS1) as potential targets of miR-145 (Figure 7A). Transfection experiments showed that ectopic expression of miR-145 significantly reduced Sirt3 and GDH, but not GLS1 protein levels (Figure 7B). To confirm that Sirt3 is a direct target of miR-145, the full length 3-UTR fragments of Sirt3 and corresponding mutant counterparts were cloned directly downstream of the firefly luciferase gene.	29371936	RID02450	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE55807)
Cholangiocarcinoma	TUG1	GLUD1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	glutamine metabolic process(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148672	NA	55000	2746	LINC00080|NCRNA00080|TI-227H	GDH|GDH1|GLUD	LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis. We found that TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that sponges miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. In view of the above results, we used the TargetScan algorithm to find out whether glutaminase (GLS), glutamate dehydrogenase (GDH), and/or their regulators are targets of miR-145. Results revealed Sirt3, a positive regulator of GDH [21], and glutaminase 1 (GLS1) as potential targets of miR-145 (Figure 7A). Transfection experiments showed that ectopic expression of miR-145 significantly reduced Sirt3 and GDH, but not GLS1 protein levels (Figure 7B). To confirm that Sirt3 is a direct target of miR-145, the full length 3-UTR fragments of Sirt3 and corresponding mutant counterparts were cloned directly downstream of the firefly luciferase gene.	29371936	RID02451	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	SBF2-AS1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000124762	NA	283104	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulated long non-coding RNA SBF2-AS1 promotes proliferation in esophageal squamous cell carcinoma. Patients with advanced ESCC exhibited increased upregulation of SBF2-AS1.Gene Set Enrichment Analysis revealed that genes associated with cell cycle biological processes, including the cancer suppressor gene cyclin-dependent kinase 1A (CDKN1A), were significantly associated with SBF2-AS1 in ESCC tissues. Further validation confirmed that CDKN1A expression levels were increased in ECA-109 cells following SBF2-AS1 silencing. The results of the present study demonstrate that SBF2-AS1 is significantly upregulated in ESCC, and that silencing of SBF2-AS1 inhibits the proliferative and invasive ability of ESCC cells. SBF2-AS1 may be a novel biomarker and therefore a potential therapeutic target for ESCC.	29552140	RID02452	expression association	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	SBF2-AS1	CDKN1A	negatively-E	RNAi;RIP;ChIP	upregulation	microarray	GSE19804	GSE19804.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000124762	NA	283104	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer. High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer.We speculated that SBF2-AS1 might negatively regulate P21. RNA immunoprecipitation discovered that SBF2-AS2 could bind with a core component of polycomb repressive complex2, SUZ12. Additionally chromatin immunoprecipitation assay demonstrated that, after silencing SBF2-AS1, the enrichment of SUZ12 and trimethylation of histone 3 lysine 27 decreased at the promoter region of P21.We demonstrated that SBF2-AS1 is upregulated in NSCLC and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients.	27154193	RID02453	epigenetic regulation	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	SBF2-AS1	SUZ12	interact	RIP	upregulation	microarray	GSE19804	GSE19804.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000178691	NA	283104	23512	NA	CHET9|JJAZ1	High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer. High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer.We speculated that SBF2-AS1 might negatively regulate P21. RNA immunoprecipitation discovered that SBF2-AS2 could bind with a core component of polycomb repressive complex2, SUZ12. Additionally chromatin immunoprecipitation assay demonstrated that, after silencing SBF2-AS1, the enrichment of SUZ12 and trimethylation of histone 3 lysine 27 decreased at the promoter region of P21.We demonstrated that SBF2-AS1 is upregulated in NSCLC and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients.	27154193	RID02454	interact with protein	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	CASC9	LAMC2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);PI3K/AKT signaling pathway(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000058085	NA	101805492	3918	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	B2T|BM600|CSF|EBR2|EBR2A|LAMB2T|LAMNB2	LncRNA CASC9 promotes esophageal squamous cell carcinoma metastasis through upregulating LAMC2 expression by interacting with the CREB-binding protein. In this study, we found that CASC9 was significantly upregulated in ESCC tissues, with further analysis revealing that elevated CASC9 expression was associated with ESCC prognosis and metastasis. Mechanistically, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assay indicated that CASC9 could bind with the transcriptional coactivator CREB-binding protein (CBP) in the nucleus. Chromatin immunoprecipitation (ChIP) assay additionally illustrated that CASC9 increased the enrichment of CBP and H3K27 acetylation in the LAMC2 promoter, thereby upregulating LAMC2 expression. In conclusion, we demonstrate that CASC9 upregulates LAMC2 expression by binding with CBP and modifying histone acetylation. Activates the FAK-PI3K/Akt signaling pathways through upregulating LAMC2 expression by interacting with the CREB-binding protein	29511340;30223861	RID02455	epigenetic regulation	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE40174)
Esophagus squamous cell carcinoma	CASC9	CREBBP	interact	RIP	upregulation	qPCR	NA	NA	cell metastasis(+);PI4K/AKT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000005339	NA	101805492	1387	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	CBP|KAT3A|MKHK1|RSTS|RSTS1	LncRNA CASC9 promotes esophageal squamous cell carcinoma metastasis through upregulating LAMC2 expression by interacting with the CREB-binding protein. In this study, we found that CASC9 was significantly upregulated in ESCC tissues, with further analysis revealing that elevated CASC9 expression was associated with ESCC prognosis and metastasis. Mechanistically, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assay indicated that CASC9 could bind with the transcriptional coactivator CREB-binding protein (CBP) in the nucleus. Chromatin immunoprecipitation (ChIP) assay additionally illustrated that CASC9 increased the enrichment of CBP and H3K27 acetylation in the LAMC2 promoter, thereby upregulating LAMC2 expression. In conclusion, we demonstrate that CASC9 upregulates LAMC2 expression by binding with CBP and modifying histone acetylation. Activates the FAK-PI3K/Akt signaling pathways through upregulating LAMC2 expression by interacting with the CREB-binding protein	29511340;30223861	RID02456	interact with protein	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LUCAT1	DNMT1	interact	RIP	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000130816	NA	100505994	1786	SCAL1|SCAT5	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The long noncoding RNA LUCAT1 promotes tumorigenesis by controlling ubiquitination and stability of DNA methyltransferase 1 in esophageal squamous cell carcinoma. LUCAT1 was significantly upregulated in ESCC cell lines and cancer tissue compared with normal cells and adjacent normal tissues.Moreover, LUCAT1 siRNA reduced DNA methyltransferase 1 (DNMT1) protein levels without affecting transcription. Patients with high LUCAT1 expression had significantly lower survival rates than patients with low LUCAT1 expression. Our results thus suggest that LUCAT1 regulates the stability of DNMT1 and inhibits the expression of tumor suppressors through DNA methylation, leading to the formation and metastasis of ESCC. We identified LUCAT1 as a potential target for drug development and as a biomarker for ESCC. Binds to DNMT1 and regulates its stability, inhibits the expression of tumor suppressors through DNA methylation.	29247823;30223861	RID02457	interact with protein	metastasis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	LINC01672	BPTF	interact	RIP	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/2 signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000171634	NA	100505887	2186	NMR	FAC1|FALZ|NEDDFL|NURF301	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02458	interact with protein	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Esophagus squamous cell carcinoma	LINC01672	MMP3	positively-E	RNAi	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/3 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000149968	NA	100505887	4314	NMR	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02459	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	LINC01672	MMP10	positively-E	RNAi	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/4 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000166670	NA	100505887	4319	NMR	SL-2|STMY2	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02460	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	NA
Esophagus squamous cell carcinoma	NSUN2	LINC01672	negatively-E	RIP;RNA pull-down assay;mass spectrometry;RNA methylation assay	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(-);cell invasion(-);chemoresistance(-);ERK1/5 signaling pathway(-)	DNA methylation	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	PCG	lncRNA	ENSG00000037474	NA	ENSG00000228750	GRCh38_1:6724637-6730012	54888	100505887	MISU|MRT5|SAKI|TRM4	NMR	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02461	epigenetic regulation	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	UP(SKCM);DATA(GSE38495)
Esophagus squamous cell carcinoma	SNHG16	ZEB1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-140-5p)	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000148516	NA	100507246	6935	Nbla10727|Nbla12061|ncRAN	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	SNHG16/miR-140-5p axis promotes esophagus cancer cell proliferation, migration and EMT formation through regulating ZEB1. RIP, RNA pulldown system and dual luciferase reporter assay further provided evidence that SNHG16 directly targets miR-140-5p by binding with microRNA binding site harboring in the SNHG16 sequence. Furthermore, bioinformatics analysis revealed that ZEB1 is a target of miR-140-5p in ESCC. Collectively, our findings suggested that SNHG16 could act as an oncogenic lncRNA that promotes tumor progression through acting as an endogenous 'sponge' by competing with miR-140-5p, thereby regulating target ZEB1.	29416674;30223861	RID02462	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	HOTAIR	CCND1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell cycle(-)	ceRNA(miR-1)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma.The lncRNA HOX transcript antisense RNA (HOTAIR) was reported to be dysregulated and correlated with the progression of ESCC.Besides, we found that HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. Taken together, our study elucidated a novel HOTAIR /miR-1/CCND1 regulatory axis in which HOTAIR acted as a competing endogenous RNA by sponging miR-1 and upregulated CCND1 expression, thereby facilitating the tumorigenesis of ESCC.	27816685	RID02463	ceRNA or sponge	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	HOTAIR	HK2	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+)	ceRNA(miR-125;miR-143)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000159399	NA	100124700	3099	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HKII|HXK2	HOTAIR regulates HK2 expression by binding endogenous miR-125 and miR-143 in oesophageal squamous cell carcinoma progression.We highlight the molecular mechanisms by which HOTAIR could influence the expression of Hexokinase 2 (HK2) in ESCC through binding miR-125 and miR-143 directly. Taken together, this study identified a functional lncRNA HOTAIR involved with regulation of glycolysis via miRNA-125/miRNA-143-HK2 in ESCC cells. The competitive endogenous RNA(ceRNA) model of HOTAIR/miR-125 and miR143/HK2 interaction might serve as important targets for ESCC diagnosis and therapy.	29156804	RID02464	ceRNA or sponge	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	XIST	EZH2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2.Our data indicated that XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines.Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression. Moreover, enforced expression of EZH2 significantly attenuated the anti-proliferation activity upon XIST knockdown. Conclusively, XIST plays an important role in malignant progression of ESCC via modulation of miR-101/EZH2 axis.Luciferase assays further confirmed that miR-101 could bind to the 3-UTR of EZH2. Based on the online database (http://starbase.sysu.edu.cn/), we searched for miRNAs containing complementary bases with XIST and focused on miR-101.XIST promotes tumor growth of ESCC via regulation of miR-101/EZH2 axis in vivo	29100288	RID02465	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	TUSC7	TMPRSS11E	positively-E	RIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	chemoresistance(-);cell proliferation(-)	ceRNA(miR-224)	regulation	NA	cisplatin;5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000087128	NA	285194	28983	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	DESC1|TMPRSS11E2	LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1.TUSC7 was downregulated in ESCC tissues and cells, and low TUSC7 indicated worse overall survival. TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224. We also confirmed DESC1 inhibited chemotherapy resistance of ESCC cells via EGFR/AKT.miR-224 could bind to the two sites of TUSC7.DESC1 was a direct target of miR-224.TUSC7 inhibited cell proliferation and chemotherapy resistance via miR-224-regulated DESC1	29530057	RID02466	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE55807)
Esophagus squamous cell carcinoma	LINC01503	DUSP6	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000139318	NA	100506119	1848	NA	HH19|MKP3|PYST1	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02467	interact with protein	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LINC01503	MAPK1	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000100030	NA	100506119	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02468	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LINC01503	MAPK3	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000102882	NA	100506119	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation.phospho-p44/42 MAPK (Erk1/2)	29454790	RID02469	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LINC01503	PI3K	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	NA	NA	100506119	NA	NA	NA	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02470	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	NA
Esophagus squamous cell carcinoma	LINC01503	PA2G4	interact	RNA pull-down assay;western blot	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000170515	NA	100506119	5036	NA	EBP1|HG4-1|p38-2G4	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02471	interact with protein	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Esophagus squamous cell carcinoma	EZR-AS1	SMYD3	interact	ChIP;RIP	upregulation	sequencing	SRP064894	SRP064894	cell motility(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000185420	NA	101409257	64754	NA	KMT3E|ZMYND1|ZNFN3A1|bA74P14.1	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.	29253179	RID02472	interact with protein	NA	NA	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE55807)
Esophagus squamous cell carcinoma	EZR-AS1	EZR	positively-E	RNAi;Immunofluorescence;RNA pull-down assay;luciferase reporter assay	upregulation	sequencing	SRP064895	SRP064895	cell motility(+);cell invasion(+)	transcriptional regulation;histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000092820	NA	101409257	7430	NA	CVIL|CVL|HEL-S-105|VIL2	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.	29253179	RID02473	epigenetic regulation	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Esophagus squamous cell carcinoma	AK001796	MDM2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111196350-111344098	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma. we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples.The results showed that MDM2 was downregulated and the expression of p53 and its target gene p21 were significantly upregulated in both Eca-109 and TE-1 cell lines after transfection with siRNA-AK001796 (Fig. 3a-c).	29568233;30223861	RID02474	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	AK001796	TP53	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111196350-111344098	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma. we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples.The results showed that MDM2 was downregulated and the expression of p53 and its target gene p21 were significantly upregulated in both Eca-109 and TE-1 cell lines after transfection with siRNA-AK001796 (Fig. 3a-c).	29568233;30223861	RID02475	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	CYTOR	EGFR	positively-E	starBase	upregulation	microarray	GSE53624	GSE53624.zip	cell growth(+)	ceRNA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000146648	NA	112597	1956	C2orf59|LINC00152|NCRNA00152	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Construction of differential mRNA-lncRNA crosstalk networks based on ceRNA hypothesis uncover key roles of lncRNAs implicated in esophageal squamous cell carcinoma.crosstalks between LINC00152 and EGFR, LINC00240 and LOX gene family were identified, which were associated with the function of response to wounding and extracellular matrix-receptor interaction.	27966444;30223861	RID02476	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	CASC2	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);cell proliferation(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-18a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	The long noncoding RNA CASC2 inhibits tumorigenesis through modulating the expression of PTEN by targeting miR-18a-5p in esophageal carcinoma.We found the expression of CASC2 to be significantly downregulated in EC tissues and EC cell lines; moreover, low expression of CACS2 was associated with advanced TNM stage and lymph node metastases.Furthermore, upregulation of CASC2 significantly inhibited the proliferation of EC cells both in vitro and in vivo as well as their invasion in vitro; it also induced the apoptosis of EC9706 and EC1 cells. Our experiments suggest that CASC2, acting as a competing endogenous RNAs (ceRNAs) of miR-18a-5p, exerts its biological effects by modulating the expression of PTEN. These findings indicate that the CASC2-miR-18a-5p-PTEN axis may be a novel target for further studies aimed at the prevention and treatment of EC.	28964779;30223861	RID02477	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Esophageal cancer	MALAT1	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway.Meanwhile, expression of Ezh2, Notch1, Hes1, MMP-9, and Vimentin was significantly decreased and expression of E-cadherin was significantly increased when cells were transfected with sh-MALAT1 compared with the nontransfected cells (P<0.05). However, when cells were cotransfected with both sh-MALAT1 and pcDNA3.1-Ezh2, the protein expression changes induced by sh-MALAT1 were recovered. MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	29916899;30223861	RID02478	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophageal cancer	MALAT1	NOTCH1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148400	NA	378938	4851	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AOS5|AOVD1|TAN1|hN1	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway.Meanwhile, expression of Ezh2, Notch1, Hes1, MMP-9, and Vimentin was significantly decreased and expression of E-cadherin was significantly increased when cells were transfected with sh-MALAT1 compared with the nontransfected cells (P<0.05). However, when cells were cotransfected with both sh-MALAT1 and pcDNA3.1-Ezh2, the protein expression changes induced by sh-MALAT1 were recovered. MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	29916899;30223861	RID02479	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	TTN-AS1	SNAI1	positively-E	luciferase reporter assay	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000124216	NA	100506866	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02480	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Esophagus squamous cell carcinoma	TTN-AS1	FSCN1	positively-E	luciferase reporter assay	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000075618	NA	100506866	6624	NA	FAN1|HSN|SNL|p55	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02481	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	TTN-AS1	ELAVL1	positively-E	RIP	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000066044	NA	100506866	1994	NA	ELAV1|HUR|Hua|MelG	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02482	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	HOTTIP	WDR5	positively-F	RIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196363	NA	100316868	11091	HOXA-AS6|HOXA13-AS1|NCRNA00213	BIG-3|CFAP89|SWD3	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells;harboring a miR-30b-binding site, HOTTIP as a molecular sponge mainly regulated miR-30b level in the nucleus and modulated the repression of HOXA13 mediated by miR-30b in the cytoplasm, resulting in the positive HOTTIP/HOXA13 correlation;HOTTIP upregulation snail1 by competitively binding miR-30b, subsequently promoting epithelial-mesenchymal transition (EMT) and invasion. HOTTIP recruits WDR5 to the HOXA13 promoter and activates HOXA13 transcription. HOTTIP directly bound the adaptor protein WDR5 and drove histone H3 lysine 4 trimethylation and HOXA13 gene transcription in ESCC cells.	28534516	RID02483	interact with protein	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	HNF1A-AS1	VEGFA	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000112715	NA	283460	7422	C12orf27|HAS1|NCRNA00262	MVCD1|VEGF|VPF	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4; HAS1-siRNA also restrained the expression of migration marker proteins matrix metalloproteinase-9 (MMP-9) and vascular endothelial cell growth factor (VEGF).	28656277;30223861	RID02484	expression association	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	HNF1A-AS1	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000100985	NA	283460	4318	C12orf27|HAS1|NCRNA00262	CLG4B|GELB|MANDP2|MMP-9	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4; HAS1-siRNA also restrained the expression of migration marker proteins matrix metalloproteinase-9 (MMP-9) and vascular endothelial cell growth factor (VEGF).	28656277;30223861	RID02485	expression association	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	POU6F2-AS2	YBX1	interact	RIP	upregulation	qPCR	NA	NA	DNA repair(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000233854	GRCh38_7:38980370-39013551	ENSG00000065978	NA	100689074	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA POU6F2-AS2 is associated with oesophageal squamous cell carcinoma. Here, we describe a novel lncRNA POU6F2-AS2 specifically expressed in OSCC. POU6F2-AS2 is involved in the DNA damage response and regulates cells survival after ionizing radiation. POU6F2-AS2 interacts with Ybx1 protein and regulates its chromatin localization. Our current study represents the first description of an OSCC associated lncRNA that modulates DNA repair.	27033944;30223861	RID02486	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	MALAT1	POU5F1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204531	NA	378938	5460	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	In vitro studies revealed that knock-down of MALAT1 reduced cell proliferation, migration and number of tumor spheres representing putative stem cell-like cells, along with increasing cell apoptosis. Moreover, MALAT1 downregulation induced a decrease of Beta-catenin, Lin28, EZH2 and EMT stem genes as OCT4, while promoted E-cadherin expression. Of note, EZH2 overexpression completely reverted repression of Beta-catenin and Lin28 induced by MALAT1-targeting siRNAs, thus supporting EZH2-dependent activity of MALAT1 in ESCC.	29739426;27015363	RID02487	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	MALAT1	NANOG	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	CSC	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111704	NA	378938	79923	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues.  In our report, we found that down-regulation of MALAT1 notably declined the expression of beta-catenin, Lin28, Ezh2 and EMT stem genes, such as OCT4 and Nanog, while increased the E-cadherin expression level	27015363	RID02488	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Gastric cancer	HOTAIR	EZH2	interact	RIP	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/beta-catenin signaling pathways by up-regulating miR-34a;HOTAIR directly bound to miR-34a. LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer.RIP experiments were performed using the EZH2 antibodies for immunoprecipitation. The results of chromatin immunoprecipitation (ChIP) assays showed that EZH2 could directly bind to the promoter region of miR34a and mediate H3K27me3 modification, while knockdown of HOTAIR and EZH2 led to reduced EZH2 and H3K27 binding ability.	29080815;26136075;28970725	RID02489	interact with protein	chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	HOTAIR	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	HOX transcript antisense intergenic RNA represses E-cadherin expression by binding to EZH2 in gastric cancer. The expression of HOTAIR was up-regulated in GC tumorous tissues compared with the para-tumorous tissues. Significantly negative correlation between HOTAIR and E-cadherin was found in GC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 with the E-cadherin promoter. Knockdown of HOTAIR by siRNA in GC cells suppressed the migration and invasion of GC cells.	28970725	RID02490	epigenetic regulation	NA	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	MALAT1	EZH2	interact	RIP	upregulation	sequencing	TCGA	STAD.zip	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 long ncRNA promotes gastric cancer metastasis by suppressing PCDH10.In particular, we found that long noncoding RNA (lncRNA) MALAT1 binds EZH2, suppresses the tumor suppressor PCDH10, and promotes gastric cellular migration and invasion.	26871474	RID02491	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Anaplastic large cell lymphoma	MALAT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02492	interact with protein	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Anaplastic large cell lymphoma	MALAT1	SUZ12	interact	RIP	upregulation	qPCR	NA	NA	prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178691	NA	378938	23512	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CHET9|JJAZ1	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02493	interact with protein	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Anaplastic large cell lymphoma	MALAT1	BMI1	positively-E	RIP	upregulation	qPCR	NA	NA	prognosis(-)	histone modification	association	NA	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168283	NA	378938	648	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02494	epigenetic regulation	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Breast cancer	MALAT1	TEAD1	interact	ChIRP-MS	upregulation	qPCR	NA	NA	cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000187079	NA	378938	7003	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AA|NTEF-1|REF1|TCF-13|TCF13|TEAD-1|TEF-1	Long noncoding RNA MALAT1 suppresses breast cancer metastasis.Mechanistically, the MALAT1 lncRNA binds and inactivates the prometastatic transcription factor TEAD, preventing TEAD from associating with its co-activator YAP and target gene promoters.Malat1 interacts with TEAD1's transactivation domain, the same domain that mediates the YAP-TEAD1 interaction. MALAT1 inhibits the transcriptional activity of TEAD. ITGB4 and VEGFA are TEAD target genes regulated by MALAT1.  Taken together, these data demonstrate that ITGB4 and VEGFA are TEAD target genes and are negatively regulated by MALAT1.	30349115	RID02495	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065)
Breast cancer	MALAT1	VEGFA	interact	RIP;ChIP;ChIRP	upregulation	qPCR	NA	NA	angiogenesis(-);cell metastasis(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MVCD1|VEGF|VPF	The mutant p53-ID4 complex controls VEGFA isoforms by recruiting lncRNA MALAT1.In this study, we demonstrate that oncogenic splicing factor SRSF1 bridges MALAT1 to mutant p53 and ID4 proteins in breast cancer cells. Mutant p53 and ID4 delocalize MALAT1 from nuclear speckles and favor its association with chromatin. This enables aberrant recruitment of MALAT1 on VEGFA pre-mRNA and modulation of VEGFA isoforms expression. Interestingly, VEGFA-dependent expression signatures associate with ID4 expression specifically in basal-like breast cancers carrying TP53 mutations. Our results highlight a key role for MALAT1 in control of VEGFA isoforms expression in breast cancer cells expressing gain-of-function mutant p53 and ID4 proteins.In BC cells, oncogenic splicing factor SRSF1 bridges MALAT1 to mutant p53 and ID4 proteins, favoring its chromatin association and thus inducing the expression of various VEGF-A isoforms, indicating a role of MALAT1 in the promotion of angiogenesis	28652379;30349115	RID02496	interact with mRNA	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Urinary bladder cancer	MALAT1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02497	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MALAT1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02498	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	MALAT1	SNAI2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000019549	NA	378938	6591	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02499	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Urinary bladder cancer	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02500	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	MALAT1	MTOR	positively-E	RNAi	upregulation	sequencing	NA	NA	cancer progression(+);mTOR signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198793	NA	378938	2475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long Noncoding RNA MALAT1 Promotes Hepatocellular Carcinoma Development by SRSF1 Upregulation and mTOR Activation. Here we report that the lncRNA MALAT1 is upregulation in hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induction of the oncogenic splicing factor SRSF1. Our results reveal a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulation.	27993818	RID02501	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Osteosarcoma	MALAT1	RET	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell stemness(+)	ceRNA(miR-129-5p)	regulation	NA	NA	CSC	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000165731	NA	378938	5979	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDHF12|CDHR16|HSCR1|MEN2A|MEN2B|MTC1|PTC|RET-ELE1	MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. Moreover, rescue experiment and luciferase reporter assay results indicated that MALAT1 modulates RET expression by sponging miR-129-5p in osteosarcomas. Furthermore, MALAT1 augmented the expression of downstream proteins of the RET-Akt pathway. Our data revealed for the first time that MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway and provides potential therapeutic targets for osteosarcoma treatment.	30481748	RID02502	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Malignant glioma	MALAT1	MMP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02503	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	MALAT1	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102882	NA	378938	5595	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02504	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	MALAT1	MAPK1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100030	NA	378938	5594	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02505	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	LINC01118	miR-134	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000222005	GRCh38_2:46698940-46822804	NA	NA	388948	NA	NA	NA	LINC01118 Modulates Paclitaxel Resistance of Epithelial Ovarian Cancer by Regulating miR-134/ABCC1. LINC01118 was highly expressed in EOC tissues and chemoresistant cells. Biological function experiments showed LINC01118 could facilitate paclitaxel resistance and promote migration and invasion while inhibiting apoptosis of EOC cells. Moreover, LINC01118 targets miR-134 and then affects ABCC1 expression. CONCLUSIONS LINC01118 acted as an oncogene and modulated EOC paclitaxel sensitivity by regulating miR-134/ABCC1.	30521500	RID02506	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	NA
Epithelial ovarian cancer	LINC01118	ABCC1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000222005	GRCh38_2:46698940-46822804	ENSG00000103222	NA	388948	4363	NA	ABC29|ABCC|GS-X|MRP|MRP1	LINC01118 Modulates Paclitaxel Resistance of Epithelial Ovarian Cancer by Regulating miR-134/ABCC1. LINC01118 was highly expressed in EOC tissues and chemoresistant cells. Biological function experiments showed LINC01118 could facilitate paclitaxel resistance and promote migration and invasion while inhibiting apoptosis of EOC cells. Moreover, LINC01118 targets miR-134 and then affects ABCC1 expression. CONCLUSIONS LINC01118 acted as an oncogene and modulated EOC paclitaxel sensitivity by regulating miR-134/ABCC1.	30521500	RID02507	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	PVT1	SOX2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000181449	NA	5820	6657	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ANOP3|MCOPS3	Long non-coding RNA PVT1 functions as an oncogene in ovarian cancer via upregulating SOX2.Compared with normal tissues, the expression of lnc-PVT1 T1 was remarkably upregulated in tumor tissues.Moreover, both the mRNA and protein levels of SOX2 were suppressed after knockdown of lnc-PVT1 in vitro. Besides, the expression of SOX2 in tumor tissues was positively correlated to lnc-PVT1. Lnc-PVT1 could enhance the invasion and proliferation of ovarian cancer cells through upregulating SOX2, which might serve as a new therapeutic target for the treatment of ovarian cancer.	30468460	RID02508	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Colon cancer	PVT1	RUNX2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);cell proliferation(+)	ceRNA(miR-30d-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124813	NA	5820	860	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	Long non-coding RNA PVT1 functions as an oncogene in human colon cancer through miR-30d-5p/RUNX2 axis. PVT1 expression was significantly higher in tumor tissues than in peritumoral tissues, and was associated with lymph node metastasis, tumor stage and survival time of these patients.PVT1 expression was significantly higher in tumor tissues than in peritumoral tissues, and was associated with lymph node metastasis, tumor stage and survival time of these patients.These results indicate that PVT1 could promote metastasis and proliferation of colon cancer via suppressing miR-30d-5p/RUNX2 axis, which may offer a new way for interpreting the mechanism of colon cancer development.	29552759	RID02509	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	PVT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA PVT1 promotes ovarian cancer progression by silencing miR-214.The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines.The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.	30197791	RID02510	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	PVT1	miR-214	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 promotes ovarian cancer progression by silencing miR-214.The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines.The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.	30197791	RID02511	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	NA
Ovarian cancer	DANCR	IGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000167244	NA	57291	3481	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	C11orf43|GRDF|IGF-II|PP9974	Long non-coding RNA DANCR upregulates IGF2 expression and promotes ovarian cancer progression.The expression of DANCR in ovarian cancer samples was significantly higher than that of the corresponding normal tissues.In addition, both the mRNA and protein expression levels of insulin-like growth factor 2 (IGF2) were remarkably upregulated after DANCR overexpression. Furthermore, the results found that the expression level of IGF2 was positively correlated with DANCR expression in ovarian cancer tissues. In this study, we revealed that DANCR could enhance the proliferation, migration and invasion capacities of ovarian cancer cells by upregulating IGF2. Our findings might offer a potential therapeutic choice for patients with ovarian cancer.	31114986	RID02512	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Gastric cancer	HOXA11-AS	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(-);cell metastasis(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948;27651312	RID02513	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	HOXA11-AS	KDM1A	interact	RIP	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000004487	NA	221883	23028	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	AOF2|BHC110|CPRF|KDM1|LSD1	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02514	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HOXA11-AS	DNMT1	interact	RIP	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000130816	NA	221883	1786	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02515	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	HOXA11-AS	miR-1297	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02516	ceRNA or sponge	NA	NA	NA
Cancer	H19	miR-675	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02517	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Cancer	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02518	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Cancer	H19	SNAI2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000019549	NA	283120	6591	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02519	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Endometrial cancer	H19	let-7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02520	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Endometrial cancer	H19	HMGA2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02521	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Endometrial cancer	H19	IGF2BP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136231	NA	283120	10643	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CT98|IMP-3|IMP3|KOC|KOC1|VICKZ3	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02522	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495)
Endometrial cancer	H19	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136997	NA	283120	4609	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MRTL|MYCC|bHLHe39|c-Myc	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02523	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Ovarian cancer	H19	let-7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02524	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	NA
Ovarian cancer	H19	HMGA2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02525	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Ovarian cancer	H19	IGF2BP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136231	NA	283120	10643	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CT98|IMP-3|IMP3|KOC|KOC1|VICKZ3	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02526	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495)
Ovarian cancer	H19	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136997	NA	283120	4609	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MRTL|MYCC|bHLHe39|c-Myc	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02527	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Ovarian cancer	CDKN2B-AS1	MET	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105976	NA	100048912	4233	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Long non-coding RNA ANRIL predicts poor prognosis and promotes invasion/metastasis in serous ovarian cancer. We found that ANRIL levels were elevated in SOC tissues compared with normal controls and were highly correlated with advanced FIGO stage, high histological grade, lymph node metastasis, and poor prognosis. SiRNA-mediated ANRIL silencing in these cells impaired cell migration and invasion. Based on the metastasis-related mRNA microarray analysis and subsequent western blotting confirmation, we found that MET and MMP3 are key downstream genes of ANRIL involved in SOC cell migration/invasion.	25845387	RID02528	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Ovarian cancer	CDKN2B-AS1	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149968	NA	100048912	4314	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Long non-coding RNA ANRIL predicts poor prognosis and promotes invasion/metastasis in serous ovarian cancer. We found that ANRIL levels were elevated in SOC tissues compared with normal controls and were highly correlated with advanced FIGO stage, high histological grade, lymph node metastasis, and poor prognosis. SiRNA-mediated ANRIL silencing in these cells impaired cell migration and invasion. Based on the metastasis-related mRNA microarray analysis and subsequent western blotting confirmation, we found that MET and MMP3 are key downstream genes of ANRIL involved in SOC cell migration/invasion.	25845387	RID02529	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	CDKN2B-AS1	CBX7	interact	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000100307	NA	100048912	23492	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02530	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	histone modification	regulation	NA	NA	CSC	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02531	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Prostate cancer	CDKN2B-AS1	CDKN2A	negatively-E	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	histone modification	regulation	NA	NA	CSC	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147889	NA	100048912	1029	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02532	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Ovarian cancer	HOXA11-AS	VEGFA	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000112715	NA	221883	7422	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	MVCD1|VEGF|VPF	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02533	expression association	prognosis	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Ovarian cancer	HOXA11-AS	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000100985	NA	221883	4318	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CLG4B|GELB|MANDP2|MMP-9	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02534	expression association	prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	HOXA11-AS	CTNNB1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000168036	NA	221883	1499	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02535	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	HOXA11-AS	CDH1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000039068	NA	221883	999	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02536	expression association	prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Ovarian cancer	HOXA11-AS	SNAI1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124216	NA	221883	6615	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02537	expression association	prognosis	NA	UP(PAAD);DATA(GSE40174)
Ovarian cancer	HOXA11-AS	TWIST1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000122691	NA	221883	7291	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02538	expression association	prognosis	NA	UP(SKCM);DATA(GSE38495)
Ovarian cancer	HOXA11-AS	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000026025	NA	221883	7431	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02539	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Epithelial ovarian cancer	HOTAIR	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02540	expression association	metastasis,prognosis	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	HOTAIR	MMP3	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000149968	NA	100124700	4314	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02541	expression association	metastasis,prognosis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Epithelial ovarian cancer	HOTAIR	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000026025	NA	100124700	7431	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02542	expression association	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Lung cancer	MEG3	PHLPP1	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000081913	NA	55384	23239	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	PHLPP|PLEKHE1|PPM3A|SCOP	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02543	expression association	NA	NA	UP(LIHC);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE51827,GSE55807)
Lung cancer	MEG3	JUN	interact	RIP;RNAi	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000177606	NA	55384	3725	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AP-1|AP1|c-Jun|p39	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02544	interact with protein	NA	NA	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)
Lung cancer	MEG3	HIF1A	positively-E	RNAi	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000100644	NA	55384	3091	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02545	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Epithelial ovarian cancer	CERNA2	HMGA2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000149948	NA	642934	8091	HOST2|lncRNA-HOST2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02546	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Epithelial ovarian cancer	CERNA2	DICER1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000100697	NA	642934	23405	HOST2|lncRNA-HOST2	DCR1|Dicer|Dicer1e|GLOW|HERNA|K12H4.8-LIKE|MNG1|RMSE2	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02547	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	CERNA2	MYC	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000136997	NA	642934	4609	HOST2|lncRNA-HOST2	MRTL|MYCC|bHLHe39|c-Myc	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02548	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Epithelial ovarian cancer	CERNA2	IMP3	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000177971	NA	642934	55272	HOST2|lncRNA-HOST2	BRMS2|C15orf12|MRPS4	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02549	expression association	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842)
Epithelial ovarian cancer	CERNA2	let-7b	negatively-F	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000285972	GRCh38_10:84167228-84172093	NA	NA	642934	NA	HOST2|lncRNA-HOST2	NA	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Here we report, for the first time, that HOST2 promotes tumor cell migration, invasion and proliferation in epithelial ovarian cancer by working in key aspects of biological behaviors. In the present study, bioinformatics analysis indicated that HOST2 binds with microRNA let-7b, a potent tumor suppressor, which was then verified to target HOST2. Our results showed that HOST2 harbors a let-7b binding site and modulates let-7b availability by acting as a molecular sponge. HOST2 inhibits let-7b functions, which post-transcriptionally suppress the expression of targets, including some oncogenes that regulate cell growth and motility. Additionally, understanding HOST2/let-7b-dependent regulation may lead to alternative approaches for the diagnosis and cure of this deadly disease.	25292198	RID02550	ceRNA or sponge	NA	NA	NA
Ovarian cancer	LSINCT5	NEAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000245532	GRCh38_11:65422774-65445540	101234261	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02551	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Ovarian cancer	LSINCT5	PSPC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000121390	NA	101234261	55269	NA	PSP1	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02552	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	LSINCT5	NEAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000245532	GRCh38_11:65422774-65445540	101234261	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02553	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Breast cancer	LSINCT5	PSPC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000121390	NA	101234261	55269	NA	PSP1	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02554	expression association	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Ovarian cancer	LNCOC1	miR-34a	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE36668;GSE18520;GSE9891;GSE26193;GSE63885	GSE36668.zip;GSE18520.zip;GSE9891.zip;GSE26193.zip;GSE63885.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000253741	GRCh38_8:142701857-142727016	NA	NA	100288181	NA	Lnc-OC1	NA	A novel lncRNA, Lnc-OC1, promotes ovarian cancer cell proliferation and migration by sponging miR-34a and miR-34c.In the present study, we identified a novel lncRNA, LOC100288181 (named as Lnc-OC1), which acted as a key regulator in the development and progression of OC.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34a and miR-34c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34a and miR-34c. In conclusion, our results suggest that the Lnc-OC1-miR-34a/34c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.	29576507	RID02555	ceRNA or sponge	NA	NA	NA
Ovarian cancer	LNCOC1	miR-34c	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE36668;GSE18520;GSE9891;GSE26193;GSE63885	GSE36668.zip;GSE18520.zip;GSE9891.zip;GSE26193.zip;GSE63885.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000253741	GRCh38_8:142701857-142727016	NA	NA	100288181	NA	Lnc-OC1	NA	A novel lncRNA, Lnc-OC1, promotes ovarian cancer cell proliferation and migration by sponging miR-34a and miR-34c.In the present study, we identified a novel lncRNA, LOC100288181 (named as Lnc-OC1), which acted as a key regulator in the development and progression of OC.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34a and miR-34c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34a and miR-34c. In conclusion, our results suggest that the Lnc-OC1-miR-34a/34c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.	29576507	RID02556	ceRNA or sponge	NA	NA	NA
Ovarian cancer	H19	NFE2L2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000116044	NA	283120	4780	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HEBP1|IMDDHH|NRF2	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02557	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Ovarian cancer	H19	NQO1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000181019	NA	283120	1728	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DHQU|DIA4|DTD|NMOR1|NMORI|QR1	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02558	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(NSCLC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE74639,GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Ovarian cancer	H19	GSR	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000104687	NA	283120	2936	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GR|HEL-75|HEL-S-122m	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02559	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	H19	G6PD	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000160211	NA	283120	2539	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	G6PD1	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02560	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	H19	GCLC	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000001084	NA	283120	2729	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GCL|GCS|GLCL|GLCLC	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02561	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827)
Ovarian cancer	H19	GCLM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000023909	NA	283120	2730	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GLCLR	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02562	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Ovarian cancer	H19	GSTP1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000084207	NA	283120	2950	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DFN7|FAEES3|GST3|GSTP|HEL-S-22|PI	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02563	expression association	recurrence,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE86978)
Ovarian cancer	ERLNC1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000087245	NA	101929441	4313	ElncRNA1|TC0101441	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Effects of oestrogen on long noncoding RNA expression in oestrogen receptor alpha-positive ovarian cancer cells. Particularly, elevated TC0101441 expression was correlated with lymph node metastasis, showing a metastatic potential. Results of in vitro assays further confirmed the pro-metastatic effect of TC0101441 and revealed that knockdown of TC0101441 also impaired E2-induced EOC cell migration/invasion by at least partly, regulating MMP2 and MMP3.	24380700	RID02564	expression association	metastasis	NA	UP(PAAD);DATA(GSE40174)
Ovarian cancer	ERLNC1	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000149968	NA	101929441	4314	ElncRNA1|TC0101441	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Effects of oestrogen on long noncoding RNA expression in oestrogen receptor alpha-positive ovarian cancer cells. Particularly, elevated TC0101441 expression was correlated with lymph node metastasis, showing a metastatic potential. Results of in vitro assays further confirmed the pro-metastatic effect of TC0101441 and revealed that knockdown of TC0101441 also impaired E2-induced EOC cell migration/invasion by at least partly, regulating MMP2 and MMP3.	24380700	RID02565	expression association	metastasis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Ovarian cancer	HOTAIR	CCNE1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105173	NA	100124700	898	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCNE|pCCNE1	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02566	expression association	NA	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Ovarian cancer	HOTAIR	BRCA1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000012048	NA	100124700	672	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02567	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Ovarian cancer	HOTAIR	BCL2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02568	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	HOTAIR	CASP3	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02569	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Ovarian cancer	HOTAIR	CASP9	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132906	NA	100124700	842	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02570	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Ovarian cancer	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+)	NA	regulation	NA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28420874	RID02571	expression association	chemoresistance	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	PVT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 was suggested as a MYC activator. Investigation of the mechanism of silencing of PVT1 or MYC in ovarian and breast cancer cell lines demonstrated reduced levels of PVT1 or MYC inhibited cell proliferation, reduced levels of PVT1 but not MYC increased cell apoptosis, indicating that increased expression of both MYC and PVT1 contributed to the pathophysiology of ovarian cancer and breast cancer pathophysiology; however, PVT1 acted independently of MYC in generation of the apoptotic phenotype	17908964	RID02572	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	PVT1	MYC	positively-E	RNAi;western blot	upregulation	qPCR;sequencing	TCGA	BRCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 was suggested as a MYC activator. Investigation of the mechanism of silencing of PVT1 or MYC in ovarian and breast cancer cell lines demonstrated reduced levels of PVT1 or MYC inhibited cell proliferation, reduced levels of PVT1 but not MYC increased cell apoptosis, indicating that increased expression of both MYC and PVT1 contributed to the pathophysiology of ovarian cancer and breast cancer pathophysiology; however, PVT1 acted independently of MYC in generation of the apoptotic phenotype	17908964;25043044	RID02573	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Epithelial ovarian cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02574	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	MEG3	GDF15	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02575	expression association	NA	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Epithelial ovarian cancer	MEG3	RB1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000139687	NA	55384	5925	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02576	expression association	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	AB073614	AKT1	positively-E	RNAi	upregulation	qPCR;microarray	GSE18521;GSE38666	GSE18521.zip;GSE38666.zip	cell proliferation(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02577	expression association	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	XIST	XIAP	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	apoptosis process(+);chemoresistance(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000101966	NA	7503	331	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	The charm of the results by Silver's and Xiao's researches raise the interesting that communication between BRCA1 and Xist-coated Xi may be a reflection of a larger role for BRCA1 in maintaining heterochromatin structure or function. Of note, Mechanistic investigations found that down-regulation of Xist might increase the expression level of X-linked inhibitor of apoptosis (XIAP) and block Taxol-induced apoptosis to cause resistance phenotype, suggesting that Xist may be a potential marker for chemotherapeutic responses in ovarian cancer.Down-regulated expression of XIAP has been shown to induce apoptosis in chemoresistant human ovarian cancer cells (24). Down-regulation of XIST might increase the expression level of XIAP and block drug-induced apoptosis to cause resistance phenotype.	12492109	RID02578	expression association	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	MALAT1	AURKB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178999	NA	378938	9212	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AIK2|AIM-1|AIM1|ARK-2|ARK2|AurB|IPL1|PPP1R48|STK-1|STK12|STK5|aurkb-sv1|aurkb-sv2	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02579	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PAAD,BRCA);UP(SKCM);DATA(GSE60407,GSE38495,GSE111842)
Lung adenocarcinoma	MALAT1	LAYN	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204381	NA	378938	143903	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02580	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	MALAT1	HMMR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000072571	NA	378938	3161	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD168|IHABP|RHAMM	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02581	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung adenocarcinoma	MALAT1	SLC26A2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000155850	NA	378938	1836	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	D5S1708|DTD|DTDST|EDM4|MST153|MSTP157	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02582	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	CCT4	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115484	NA	378938	10575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CCT-DELTA|Cctd|SRB	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02583	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939)
Lung adenocarcinoma	MALAT1	PTBP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119314	NA	378938	9991	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ROD1	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02584	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	CTHRC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164932	NA	378938	115908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02585	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(SKCM,BRCA);DATA(GSE38495,GSE55807)
Lung adenocarcinoma	MALAT1	FHL1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000022267	NA	378938	2273	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FCMSU|FHL-1|FHL1A|FHL1B|FLH1A|KYOT|RBMX1A|RBMX1B|SLIM|SLIM-1|SLIM1|SLIMMER|XMPMA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02586	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	MALAT1	CXCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163735	NA	378938	6374	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENA-78|SCYB5	MALAT1 is an oncogenic long non-coding RNA associated with tumor invasion in non-small cell lung cancer regulated by DNA methylation. Here we showed that the expression of MALAT1 was upregulated in non-small cell lung cancer cells (NSCLCs) or tissues as compared with the normal lung cell or tissues. Thus, the knockdown of MALAT1 led to decreased cell migration and invasion. Next we also found that CXCL5 as a downstream gene of MALAT1 regulated cell migration and invasion.	26884862	RID02587	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Breast cancer	MALAT1	ELAVL1	interact	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	The Ribonucleic Complex HuR-MALAT1 Represses CD133 Expression and Suppresses Epithelial-Mesenchymal Transition in Breast Cancer. In this study, we show that a ribonucleoprotein complex including the long noncoding RNA MALAT1 and the RNA-binding protein HuR (ELAVL1) binds the CD133 promoter region to regulate its expression. In conclusion, our findings suggest that the failure of a repressive complex to form or stabilize in breast cancer promotes CD133 upregulation and an EMT-like program, providing new mechanistic insights underlying the control of prometastatic processes.	27197265	RID02588	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Colon cancer	PTEN	MALAT1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000171862	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5728	378938	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02589	expression association	metastasis	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Colon cancer	MALAT1	EPCAM	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119888	NA	378938	4072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02590	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Colon cancer	MALAT1	ITGB4	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132470	NA	378938	3691	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD104|GP150	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02591	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	PTEN	MALAT1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000171862	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5728	378938	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02592	expression association	metastasis	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	MALAT1	EPCAM	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119888	NA	378938	4072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02593	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Breast cancer	MALAT1	ITGB4	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132470	NA	378938	3691	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD104|GP150	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;30349115;29739426	RID02594	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Cervical cancer	MALAT1	miR-375	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.	27658300	RID02595	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Cervical cancer	MALAT1	CDH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170558	NA	378938	1000	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD325|CDHN|CDw325|NCAD	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.	27658300	RID02596	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Endometrial carcinoma	PCDH10	MALAT1	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	Wnt/beta-catenin signaling pathway(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	PCG	lncRNA	ENSG00000138650	NA	ENSG00000251562	GRCh38_11:65497688-65506516	57575	378938	OL-PCDH|PCDH19	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A novel wnt regulatory axis in endometrioid endometrial cancer.MALAT1 as a downstream target of the protocad herin10 (PCDH10) gene, a Wnt pathway negative regulatory element, shedding light on a novel targetable PCDH10-Wnt/beta-catenin-MALAT1 axis. Gene expression profiling revealed as part of the transcriptomic changes induced by PCDH10 a reduction in levels of MALAT1, a long noncoding RNA, that mediated tumor suppression functions of PCDH10 in EEC cells. We found that MALAT1 transcription was regulated by Wnt/beta-catenin signaling via TCF promoter binding and PCDH10 decreased MALAT1 by modulating this pathway.	25085246	RID02597	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	MALAT1	CCAR2	interact	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000158941	NA	378938	57805	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DBC-1|DBC1|KIAA1967|NET35|p30 DBC|p30DBC	Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation. The interaction between MALAT1 and depleted in breast cancer 1 (DBC1) was validated using RNA pull-down and RNA immunoprecipitation. Further mechanistic studies reveal that MALAT1 binding competes with the interaction between sirtuin1 (SIRT1) and DBC1, which then releases SIRT1 and enhances its deacetylation activity. Consequently, the deacetylation of p53 reduces the transcription of a spectrum of its downstream target genes, promotes cell proliferation and inhibits cell apoptosis. Our results uncover a novel mechanism by which MALAT1 regulates the activity of p53 through the lncRNA-protein interaction.	28973437	RID02598	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MALAT1	TP53	negatively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141510	NA	378938	7157	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCC7|BMFS5|LFS1|P53|TRP53	Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation. The interaction between MALAT1 and depleted in breast cancer 1 (DBC1) was validated using RNA pull-down and RNA immunoprecipitation. Further mechanistic studies reveal that MALAT1 binding competes with the interaction between sirtuin1 (SIRT1) and DBC1, which then releases SIRT1 and enhances its deacetylation activity. Consequently, the deacetylation of p53 reduces the transcription of a spectrum of its downstream target genes, promotes cell proliferation and inhibits cell apoptosis. Our results uncover a novel mechanism by which MALAT1 regulates the activity of p53 through the lncRNA-protein interaction.	28973437	RID02599	epigenetic regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	In vitro studies revealed that knock-down of MALAT1 reduced cell proliferation, migration and number of tumor spheres representing putative stem cell-like cells, along with increasing cell apoptosis. Moreover, MALAT1 downregulation induced a decrease of beta-catenin, Lin28, EZH2 and EMT stem genes as OCT4, while promoted E-cadherin expression. Of note, EZH2 overexpression completely reverted repression of Beta-catenin and Lin28 induced by MALAT1-targeting siRNAs, thus supporting EZH2-dependent activity of MALAT1 in ESCC.	29739426	RID02600	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	MALAT1	MIA2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150527	NA	378938	4253	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTAGE5|MEA6|MGEA|MGEA11|MGEA6|TALI	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02601	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Esophagus squamous cell carcinoma	MALAT1	HNF4G	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164749	NA	378938	3174	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NR2A2|NR2A3	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02602	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Esophagus squamous cell carcinoma	MALAT1	ROBO1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169855	NA	378938	6091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DUTT1|SAX3	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02603	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Esophagus squamous cell carcinoma	MALAT1	CCT4	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115484	NA	378938	10575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CCT-DELTA|Cctd|SRB	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02604	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939)
Esophagus squamous cell carcinoma	MALAT1	CTHRC1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164932	NA	378938	115908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02605	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(SKCM,BRCA);DATA(GSE38495,GSE55807)
Gastric cancer	MALAT1	IGF1R	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000140443	NA	378938	3480	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD221|IGFIR|IGFR|JTK13	Moreover, knock-down of MALAT1 in GC cells inhibited cell proliferation, cell cycle progression, migration and invasion, and promoted apoptosis. Mechanistically, miR-122-IGF-1R signaling was found involved in dysregulated MALAT1 expression. Indeed, enforced miR-122 expression inhibited, whereas miR-122 inhibitor increased MALAT1 in GC cell lines. miR-122-mediated regulation of MALAT1 involved IGF-1R, a target of miR-122, whose expression positively correlated with MALAT1 in GC cell lines	27486823;29739426	RID02606	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Gastric cancer	MALAT1	miR-122	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Moreover, knock-down of MALAT1 in GC cells inhibited cell proliferation, cell cycle progression, migration and invasion, and promoted apoptosis. Mechanistically, miR-122-IGF-1R signaling was found involved in dysregulated MALAT1 expression. Indeed, enforced miR-122 expression inhibited, whereas miR-122 inhibitor increased MALAT1 in GC cell lines. miR-122-mediated regulation of MALAT1 involved IGF-1R, a target of miR-122, whose expression positively correlated with MALAT1 in GC cell lines	27486823;29739426	RID02607	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Pancreatic ductal adenocarcinoma	MALAT1	ELAVL1	interact	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell autophagy(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	Long Noncoding RNA MALAT1 Promotes Aggressive Pancreatic Cancer Proliferation and Metastasis via the Stimulation of Autophagy.Mechanistically, we found that MALAT1 interacted with RNA binding protein HuR, and silencing of MALAT1 greatly enhanced the posttranscriptional regulation of TIA-1 and had further effects on inhibiting autophagy. MALAT1 was speculated to regulate tumorigenesis via HuR-TIA-1-mediated autophagic activation.	27371730	RID02608	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Pancreatic ductal adenocarcinoma	MALAT1	TIA1	negatively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell autophagy(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116001	NA	378938	7072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TIA-1|WDM	Long Noncoding RNA MALAT1 Promotes Aggressive Pancreatic Cancer Proliferation and Metastasis via the Stimulation of Autophagy.Mechanistically, we found that MALAT1 interacted with RNA binding protein HuR, and silencing of MALAT1 greatly enhanced the posttranscriptional regulation of TIA-1 and had further effects on inhibiting autophagy. MALAT1 was speculated to regulate tumorigenesis via HuR-TIA-1-mediated autophagic activation.	27371730	RID02609	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Pancreatic cancer	MALAT1	LATS1	positively-E	western blot;IHC	upregulation	qPCR	NA	NA	Hippo/YAP signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131023	NA	378938	9113	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WARTS|wts	Study on mechanism about long noncoding RNA MALAT1 affecting pancreatic cancer by regulating Hippo-YAP signaling. The microarray analysis determined that lncRNA MALAT1 in pancreatic cancer was highly expressed. LncRNA MALAT1 presented an extremely high expression level in pancreatic cancer tissues and cells. After transfected with si-MALAT1, the proliferation of AsPC-1 cells decreased, induce apoptosis of AsPC-1 cells, and migration and invasion ability were reduced. The tendency of LATS1 expression level was down-regulated and YAP1 show the opposite trend in the Hippo-YAP signaling. The in vivo assay was found that the tumor to be small in size and volume, and the expression of Ki-67 was decreased. High expression of lncRNA MALAT1 in PC disorder the proliferation, apoptosis, and migration and invasion ability via influence Hippo-YAP signaling pathway.	29215734	RID02610	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	MALAT1	YAP1	negatively-E	western blot;IHC	upregulation	qPCR	NA	NA	Hippo/YAP signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137693	NA	378938	10413	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	COB1|YAP|YAP2|YAP65|YKI	Study on mechanism about long noncoding RNA MALAT1 affecting pancreatic cancer by regulating Hippo-YAP signaling. The microarray analysis determined that lncRNA MALAT1 in pancreatic cancer was highly expressed. LncRNA MALAT1 presented an extremely high expression level in pancreatic cancer tissues and cells. After transfected with si-MALAT1, the proliferation of AsPC-1 cells decreased, induce apoptosis of AsPC-1 cells, and migration and invasion ability were reduced. The tendency of LATS1 expression level was down-regulated and YAP1 show the opposite trend in the Hippo-YAP signaling. The in vivo assay was found that the tumor to be small in size and volume, and the expression of Ki-67 was decreased. High expression of lncRNA MALAT1 in PC disorder the proliferation, apoptosis, and migration and invasion ability via influence Hippo-YAP signaling pathway.	29215734	RID02611	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Osteosarcoma	MALAT1	CDH1	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID02612	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	TGFB1	MALAT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID02613	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Osteosarcoma	MALAT1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067560	NA	378938	387	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA MALAT1 as a potential therapeutic target in osteosarcoma.Furthermore, MALAT1 knockdown delayed tumor growth in an osteosarcoma xenograft model. Specifically, we found that administration of MALAT1 siRNA decreased the protein levels of RhoA and its downstream effectors Rho-associated coiled-coil containing protein kinases (ROCKs). We observed that MALAT1 expression was up-regulated in human osteosarcoma cell lines and tissues.	26575981	RID02614	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Osteosarcoma	MALAT1	ROCK1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067900	NA	378938	6093	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	P160ROCK|ROCK-I	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.Furthermore, we confirmed that MALAT1 and ROCK1/ROCK2 which were targeted by microRNA-144-3p (miR-144-3p) shared the same miR-144-3p combining site. Furthermore, the constructed luciferase assay verified that MALAT1 was a target of miR-144-3p.Finally, we affirmed that an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overly expressed in osteosarcoma.	28938647;26575981	RID02615	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	MALAT1	ROCK2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000134318	NA	378938	9475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ROCK-II	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.Furthermore, we confirmed that MALAT1 and ROCK1/ROCK2 which were targeted by microRNA-144-3p (miR-144-3p) shared the same miR-144-3p combining site. Furthermore, the constructed luciferase assay verified that MALAT1 was a target of miR-144-3p.Finally, we affirmed that an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overly expressed in osteosarcoma.	28938647;26575981	RID02616	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Peripheral primitive neuroectodermal tumor	SYK	MALAT1	positively-E	RIP;luciferase reporter assay;ChIP;IHC	upregulation	qPCR;microarray	GSE93677	GSE93677.zip	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Sarcoma	PCG	lncRNA	ENSG00000165025	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6850	378938	p72-Syk	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Identification of a Novel SYK/c-MYC/MALAT1 Signaling Pathway and Its Potential Therapeutic Value in Ewing Sarcoma. Ectopic expression of SYK rescued the cytotoxicity triggered by SYK-depletion associated with the reactivation of both AKT and MYC; MALAT1, was identified to be dependent on SYK-mediated signaling;c-MYC, a SYK-promoted gene, bound to the promoter of MALAT1 and transcriptionally activated MALAT1, which further promoted the proliferation of EWS cells	28336564	RID02617	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Colorectal cancer	MALAT1	EZH2	interact	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2.MALAT1 is overexpressed in colorectal cancer patients and correlated with tumor metastasis. LncRNA MALAT1 knockdown enhances E-cadherin expression and inhibits oxaliplatin-induced EMT in colorectal cancer cells. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin.	28069878	RID02618	interact with protein	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colon cancer	MALAT1	AKAP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127914	NA	378938	10142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP-9|AKAP350|AKAP450|CG-NAP|HYPERION|LQT11|MU-RMS-40.16A|PPP1R45|PRKA9|YOTIAO	Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1. By genome-wide profiling, Yang et al. showed that among 243 genes regulated by MALAT1 in CRC cells, PRKA kinase anchor protein 9 (AKAP-9) was significantly upregulated at both mRNA and protein level. Of note, knockdown of AKAP-9 rescued MALAT1-induced CRC cell proliferation, migration and invasion. MALAT1 was also associated with colon cancer progression by stimulating tumor associated dendritic cells (TADC)-derived production of CCL5; consistently, MALAT1 blockade by siRNAs significantly dampened CCL5-induced migration and invasion of CRC cells	25546229;29739426	RID02619	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Colon cancer	MALAT1	CCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000271503	NA	378938	6352	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	D17S136E|RANTES|SCYA5|SIS-delta|SISd|TCP228|eoCP	Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1. By genome-wide profiling, Yang et al. showed that among 243 genes regulated by MALAT1 in CRC cells, PRKA kinase anchor protein 9 (AKAP-9) was significantly upregulated at both mRNA and protein level. Of note, knockdown of AKAP-9 rescued MALAT1-induced CRC cell proliferation, migration and invasion. MALAT1 was also associated with colon cancer progression by stimulating tumor associated dendritic cells (TADC)-derived production of CCL5; consistently, MALAT1 blockade by siRNAs significantly dampened CCL5-induced migration and invasion of CRC cells	25546229;29739426	RID02620	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Multiple myeloma	MALAT1	SP1	interact	RIP;ChIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	biomarker;tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Sustained Angiogenesis	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185591	NA	378938	6667	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Activation of LTBP3 gene by a long noncoding RNA (lncRNA) MALAT1 transcript in mesenchymal stem cells from multiple myeloma. Our data suggested that lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1, and recruitment of Sp1 to the promoter.Our knowledge of the role of MALAT1 in cellular transformation is pointing toward its potential use as a biomarker and a target for novel therapeutic approaches in multiple myeloma.Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	25187517;29290968	RID02621	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	MALAT1	EZH2	interact	ChIP;western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02622	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Multiple myeloma	MALAT1	MCL1	negatively-E	western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143384	NA	378938	4170	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02623	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	MALAT1	CDK6	negatively-E	western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000105810	NA	378938	1021	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MCPH12|PLSTIRE	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02624	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Multiple myeloma	MALAT1	miR-29a	positively-E	RNAi;ChIP	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02625	epigenetic regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Multiple myeloma	MALAT1	miR-29b	positively-E	RNAi;ChIP	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02626	epigenetic regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	NA
Lung adenocarcinoma	HOTAIR	HELLS	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000119969	NA	100124700	3070	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ICF4|LSH|Nbla10143|PASG|SMARCA6	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.LSH (lymphoid-specific helicase), also called HELLS (helicase, lymphoid specific)	26658322	RID02627	interact with protein	NA	NA	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842)
Lung adenocarcinoma	HOTAIR	FOXA1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129514	NA	100124700	3169	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3A|TCF3A	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.	26658322	RID02628	expression association	NA	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Lung adenocarcinoma	HOTAIR	FOXA2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000125798	NA	100124700	3170	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3B|TCF3B	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.	26658322	RID02629	expression association	NA	NA	NA
Lung cancer	STAT3	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Lung cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6774	100124700	ADMIO|ADMIO1|APRF|HIES	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract.The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression.	25447409	RID02630	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	NA
Lung cancer	HOTAIR	miR-326	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR.	27186394	RID02631	expression association	NA	NA	NA
Lung cancer	HOTAIR	PHOX2A	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000165462	NA	100124700	401	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARIX|CFEOM2|FEOM2|NCAM2|PMX2A	MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR.	27186394	RID02632	expression association	NA	NA	NA
Non-small cell lung cancer	HOTAIR	TP53	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141510	NA	100124700	7157	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCC7|BMFS5|LFS1|P53|TRP53	A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer.Our results showed that HOTAIR expression was significantly higher in the cancer tissues than that in the adjacent normal tissue, and was negatively correlated with p53 functionality rather than expression. We identified two binding sites of p53 on the promoter region of HOTAIR, where the p53 protein would bind to and suppress the HOTAIR mRNA transcription. Inversely, overexpression of lncRNA HOTAIR inhibited the expression of p53 in A549 cells. Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). Modulation of p53 expression alternated the lncRNA HOTAIR expression and cell invasion in NSCLC cells	27695348	RID02633	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TP53	HOTAIR	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7157	100124700	BCC7|BMFS5|LFS1|P53|TRP53	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer.Our results showed that HOTAIR expression was significantly higher in the cancer tissues than that in the adjacent normal tissue, and was negatively correlated with p53 functionality rather than expression. We identified two binding sites of p53 on the promoter region of HOTAIR, where the p53 protein would bind to and suppress the HOTAIR mRNA transcription. Inversely, overexpression of lncRNA HOTAIR inhibited the expression of p53 in A549 cells. Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). Modulation of p53 expression alternated the lncRNA HOTAIR expression and cell invasion in NSCLC cells	27695348	RID02634	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	NA
Lung cancer	HOTAIR	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168036	NA	100124700	1499	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Radiotherapy induced Lewis lung cancer cell apoptosis via inactivating beta-catenin mediated by upregulated HOTAIR.	26339352	RID02635	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Liver cancer	HOTAIR	CHUK	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000213341	NA	100124700	1147	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02636	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	HOTAIR	IKBKB	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000104365	NA	100124700	3551	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IKK-beta|IKK2|IKKB|IMD15|IMD15A|IMD15B|NFKBIKB	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02637	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Liver cancer	HOTAIR	IKBKG	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000269335	NA	100124700	8517	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AMCBX1|EDAID1|FIP-3|FIP3|Fip3p|IKK-gamma|IKKAP1|IKKG|IMD33|IP|IP1|IP2|IPD2|NEMO|ZC2HC9	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02638	epigenetic regulation	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	HOTAIR	CCND1	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression.	28791413	RID02639	expression association	NA	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	HOTAIR	STAT3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);chemoresistance(+)	NA	association	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168610	NA	100124700	6774	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADMIO|ADMIO1|APRF|HIES	Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression. Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway.	28791413;29250186	RID02640	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	FOXC1	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000054598	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2296	100124700	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues; The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1. FOXC1 binding to the promoter region of HOTAIR was confirmed using a chromatin immunoprecipitation assay	27895772	RID02641	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	NA
Liver fibrosis	HOTAIR	EZH2	interact	luciferase reporter assay;RIP;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.To confirm the association of Hotair and epigenetic repressor, we performed RIP with an antibody against enhancer of zeste homologue 2 (EZH2, an important subunit of the PRC2 complex) from nuclear extracts of LX-2 cells. We observed significant enrichment of Hotair with the EZH2 antibody, but no enrichment of GAPDH compared with the nonspecific IgG control antibody (Fig. 7A). Using a specific antibody against SUZ12, another member of the PRC2 complex, we found Hotair enrichment, but not GAPDH mRNA enrichment (Fig. 7B).	27979710	RID02642	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Liver fibrosis	HOTAIR	SUZ12	interact	luciferase reporter assay;RIP;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.To confirm the association of Hotair and epigenetic repressor, we performed RIP with an antibody against enhancer of zeste homologue 2 (EZH2, an important subunit of the PRC2 complex) from nuclear extracts of LX-2 cells. We observed significant enrichment of Hotair with the EZH2 antibody, but no enrichment of GAPDH compared with the nonspecific IgG control antibody (Fig. 7A). Using a specific antibody against SUZ12, another member of the PRC2 complex, we found Hotair enrichment, but not GAPDH mRNA enrichment (Fig. 7B).	27979710	RID02643	interact with protein	NA	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	HOTAIR	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000085563	NA	100124700	5243	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway.Together, these findings indicated that knockdown of HOTAIR in Huh7 cells decreased STAT3 activity and ABCB1 expression, and increased chemosensitivity to cisplatin. Thus HOTAIR could serve as a novel potential therapeutic target to reverse multidrug resistance in HCC.	29250186	RID02644	expression association	chemoresistance	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Prostate cancer	HOTAIR	PRC2	interact	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Infiltrating mast cells enhance prostate cancer invasion via altering LncRNA-HOTAIR/PRC2-androgen receptor (AR)-MMP9 signals and increased stem/progenitor cell population. Mechanism dissection revealed infiltrating mast cells could decrease AR transcription via modulation of the PRC2 complex with LncRNA-HOTAIR at the AR 5' promoter region in PCa cells. The consequences of suppressing AR may then increase PCa cell invasion via increased MMP9 expression and/or increased stem/progenitor cell population.	25895025;28082728	RID02645	interact with protein	NA	NA	NA
Prostate cancer	HOTAIR	MMP9	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Infiltrating mast cells enhance prostate cancer invasion via altering LncRNA-HOTAIR/PRC2-androgen receptor (AR)-MMP9 signals and increased stem/progenitor cell population. Mechanism dissection revealed infiltrating mast cells could decrease AR transcription via modulation of the PRC2 complex with LncRNA-HOTAIR at the AR 5' promoter region in PCa cells. The consequences of suppressing AR may then increase PCa cell invasion via increased MMP9 expression and/or increased stem/progenitor cell population.	25895025;28082728	RID02646	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	miR-34a	HOTAIR	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	GSE47657	GSE47657.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+) 	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.miR-34a directly targeted HOTAIR in PCa cells, which showed that genistein inhibited the growth of PCa cells by downregulating oncogenic HOTAIR that was also targeted by the tumor suppressor miR-34a.	23936419	RID02647	ceRNA or sponge	NA	NA	NA
Prostate cancer	HOTAIR	EZH2	interact	luciferase reporter assay;ChIP	upregulation	qPCR;sequencing	TCGA	PRAD.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691;29221985	RID02648	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Prostate cancer	HOTAIR	DNMT1	interact	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	HOTAIR-mediated reciprocal regulation of EZH2 and DNMT1 contribute to polyphyllin I-inhibited growth of castration-resistant prostate cancer cells in vitro and in vivo.Our results show that PPI inhibits growth of CRPC cells through inhibition of HOTAIR expression, subsequently; this results in the repression of DNMT1 and EZH2 expressions. The interactions among HOTAIR, DNMT1 and EZH2, and reciprocal regulation of DNMT1 and EZH2 contribute to the overall responses of PPI. This study reveals a novel mechanism for HOTAIR-mediated regulating DNMT1 and EZH2 in response to PPI in inhibition of the growth of CRPC cells.	29221985	RID02649	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	RHOC	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000155366	NA	ENSG00000228630	GRCh38_12:53962308-53974956	389	100124700	ARH9|ARHC|H9|RHOH9	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02650	transcriptional regulation	prognosis	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	NA
Breast cancer	MRTFA	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000196588	NA	ENSG00000228630	GRCh38_12:53962308-53974956	57591	100124700	BSAC|MAL|MKL|MKL1|MRTF-A	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02651	transcriptional regulation	prognosis	NA	NA
Breast cancer	SRF	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000112658	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6722	100124700	MCM1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02652	transcriptional regulation	prognosis	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	NA
Breast cancer	TGFB1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell stemness(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	CSC	Limitless Replicative Potential;Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7040	100124700	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines EMT. contributes to tumor invasion and metastasis in many types of cancer and highly correlates with the acquisition of CSC characteristics. One study found that treatment with transforming growth factor beta 1 (TGF-betea1) increased HOTAIR expression and triggered EMT formation. Conversely, blockade of HOTAIR reversed the TGF-beta1-induced EMT and reduced the colony-forming capacity of breast cancer cells. This result indicated that HOTAIR was involved in multiple signaling pathways in EMT in breast cancer cells	24022994	RID02653	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	NA
Breast cancer	HOTAIR	BCL2L2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129473	NA	100124700	599	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL-W|BCL2-L-2|BCLW|PPP1R51	Long Noncoding RNA HOTAIR Modulates MiR-206-mediated Bcl-w Signaling to Facilitate Cell Proliferation in Breast Cancer.Moreover, the levels of HOTAIR were positively associated with those of Bcl-w in clinical breast cancer samples. As expected, we observed that HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. Mechanistically, we found that miR-206 was capable of inhibiting the expression of Bcl-w by directly binding to the 3'UTR of Bcl-w mRNA. Interestingly, HOTAIR could increase the expression of Bcl-w through sequestering miR-206 at post-transcriptional level.	29222472	RID02654	ceRNA or sponge	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Colorectal cancer	HOTAIR	miR-545	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent. High HOTAIR expression levels inhibited miR-545, thereby increasing CRC cell proliferation.Differential expressions of HOTAIR, miR-545, and EGFR were observed in cancerous tissues in comparison to non-cancerous tissues. By expressional management of miR-545, we observed that miR-545 negatively regulated cell proliferation. Also luciferase reporter assay revealed that miR-545 inhibited regulated EGFR expression by affecting its 3'-UTR activity. In addition, miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. Monitoring of tumor growth in mice showed that miR-545 overexpression suppressed LOVO tumor growth. Our data suggested that HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.	28364379	RID02655	expression association	NA	NA	NA
Colorectal cancer	HOTAIR	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000146648	NA	100124700	1956	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent. High HOTAIR expression levels inhibited miR-545, thereby increasing CRC cell proliferation.Differential expressions of HOTAIR, miR-545, and EGFR were observed in cancerous tissues in comparison to non-cancerous tissues. By expressional management of miR-545, we observed that miR-545 negatively regulated cell proliferation. Also luciferase reporter assay revealed that miR-545 inhibited regulated EGFR expression by affecting its 3'-UTR activity. In addition, miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. Monitoring of tumor growth in mice showed that miR-545 overexpression suppressed LOVO tumor growth. Our data suggested that HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.	28364379	RID02656	expression association	NA	NA	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	HOTAIR	miR-218	negatively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	epigenetic regulation	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02657	epigenetic regulation	chemoresistance	NA	NA
Colorectal cancer	HOTAIR	VOPP1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	NA	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154978	NA	100124700	81552	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ECOP|GASP|WBP1L2	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02658	expression association	chemoresistance	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	HOTAIR	NFKB1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	NA	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02659	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HOTAIR	RPS6KB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	propofol	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000108443	NA	100124700	6198	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer	26523512	RID02660	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Ovarian cancer	HOTAIR	NFKB1	positively-E	ChIP;luciferase reporter assay;RNAi;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+);prognosis(-)	transcriptional regulation	regulation	protein-DNA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28118613;29843138;28420874	RID02661	transcriptional regulation	chemoresistance,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	HOTAIR	IL6	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+);prognosis(-)	NA	regulation	NA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000136244	NA	100124700	3569	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28118613;29843138;28420874	RID02662	expression association	chemoresistance,prognosis	NA	DOWN(BRCA);DATA(GSE75367,GSE86978)
Ovarian cancer	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	platinum	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02663	interact with protein	chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	HOTAIR	NFKB1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02664	expression association	chemoresistance	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	HOTAIR	IL6	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000136244	NA	100124700	3569	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02665	expression association	chemoresistance	NA	DOWN(BRCA);DATA(GSE75367,GSE86978)
Breast cancer	HOTAIR	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02666	expression association	chemoresistance	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	HOTAIR	BCL2	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02667	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	HOTAIR	BAX	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087088	NA	100124700	581	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL2L4	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02668	expression association	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	HOTAIR	CASP3	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02669	expression association	NA	NA	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Head and neck squamous cell carcinoma	HOTAIR	CYCS	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000172115	NA	100124700	54205	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CYC|HCS|THC4	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02670	expression association	NA	NA	UP(NSCLC,PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTAIR promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in oral squamous cell carcinoma. Furthermore, significant negative correlation between HOTAIR levels and E-cadherin levels was found in OSCC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 and H3K27me3 with the E-cadherin promoter.	25901533	RID02671	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Laryngeal squamous cell carcinoma	HOTAIR	miR-21	negatively-E	RNAi	upregulation	qPCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Combined detection of serum exosomal miR-21 and HOTAIR as diagnostic and prognostic biomarkers for laryngeal squamous cell carcinoma.Serum exosomal miR-21 and HOTAIR were significantly correlated with the clinical parameters of laryngeal squamous cell carcinoma (LSCC) and combined evaluation of their serum expressions may be considered a valuable biomarker and promising predicting tool for LSCC.	25099764	RID02672	expression association	prognosis	NA	NA
Esophagus squamous cell carcinoma	HOTAIR	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02673	expression association	metastasis,prognosis	NA	UP(PAAD);DATA(GSE40174)
Esophagus squamous cell carcinoma	HOTAIR	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168036	NA	100124700	1499	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02674	expression association	metastasis,prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	HOTAIR	CDH1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02675	expression association	metastasis,prognosis	NA	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Acute myeloid leukemia	HOTAIR	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02676	expression association	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Acute myeloid leukemia	HOTAIR	KDM1A	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02677	expression association	prognosis	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	HOTAIR	DNMT3A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);prognosis(-)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000119772	NA	100124700	1788	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	DNMT3A2|M.HsaIIIA|TBRS	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172;27748863	RID02678	ceRNA or sponge	prognosis	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Acute myeloid leukemia	HOTAIR	DNMT3B	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000088305	NA	100124700	1789	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ICF|ICF1|M.HsaIIIB	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02679	expression association	prognosis	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Acute promyelocytic leukemia	HOTAIRM1	ITGA4	positively-E	RNAi	upregulation	qPCR;microarray	GSE49516	GSE49516.zip	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000115232	NA	100506311	3676	HOXA-AS1|HOXA1-AS1|NCRNA00179	CD49D|IA4	Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.Blockade of HOTAIR myeloid 1 (HOTAIRM1), a human HOXA gene cluster and a novel myeloid-specific lncRNA, resulted in the retained expression of many otherwise all-trans retinoic acid (ATRA)-induced cell cycle and DNA replication genes, abated ATRA induction of cell surface leukocyte activation, defense response, and other maturation-related molecules, all of which were accompanied by the retained expression of the alpha-4-integrin gene (ITGA4) (CD49d) and decreased induction of integrin alpha X (ITGAX) (CD11c) in NB4 acute promyelocytic leukemia cells.	24824789	RID02680	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute promyelocytic leukemia	HOTAIRM1	ITGAX	negatively-E	RNAi	upregulation	qPCR;microarray	GSE49516	GSE49516.zip	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000140678	NA	100506311	3687	HOXA-AS1|HOXA1-AS1|NCRNA00179	CD11C|SLEB6	Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.Blockade of HOTAIR myeloid 1 (HOTAIRM1), a human HOXA gene cluster and a novel myeloid-specific lncRNA, resulted in the retained expression of many otherwise all-trans retinoic acid (ATRA)-induced cell cycle and DNA replication genes, abated ATRA induction of cell surface leukocyte activation, defense response, and other maturation-related molecules, all of which were accompanied by the retained expression of the alpha-4-integrin gene (ITGA4) (CD49d) and decreased induction of integrin alpha X (ITGAX) (CD11c) in NB4 acute promyelocytic leukemia cells.	24824789	RID02681	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Melanoma	LINC00673	MMP9	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000100985	NA	100499467	4318	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	CLG4B|GELB|MANDP2|MMP-9	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02682	expression association	NA	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Melanoma	LINC00673	POU4F1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000152192	NA	100499467	5457	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	BRN3A|Oct-T1|RDC-1|brn-3A	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02683	interact with protein	NA	NA	NA
Melanoma	LINC00673	AR	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000169083	NA	100499467	367	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02684	interact with protein	NA	NA	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Non-small cell lung cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02685	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Non-small cell lung cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02686	interact with protein	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Non-small cell lung cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02687	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Head and neck cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02688	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Head and neck cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02689	interact with protein	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Head and neck cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02690	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02691	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	NA
Ovarian cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02692	interact with protein	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Ovarian cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02693	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
T-cell acute lymphocytic leukemia	LUNAR1	IGF1R	negatively-E	ChIP	upregulation	sequencing	GSE57982	GSE57982.zip	Notch signaling pathway(+);cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Sustained Angiogenesis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000278090	GRCh38_15:99014526-99031054	ENSG00000140443	NA	104564224	3480	NA	CD221|IGFIR|IGFR|JTK13	Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Finally we have shown that one specific Notch-regulated lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to enhance IGF1R mRNA expression and sustain IGF1 signaling. These results confirm that lncRNAs are important downstream targets of the Notch signaling pathway, and additionally they are key regulators of the oncogenic state in T-ALL.	25083870	RID02694	transcriptional regulation	NA	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
T-cell acute lymphocytic leukemia	NOTCH1	LUNAR1	negatively-E	ChIP	upregulation	sequencing	GSE57982	GSE57982.zip	Notch signaling pathway(+);cell growth(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	PCG	lncRNA	ENSG00000148400	NA	ENSG00000278090	GRCh38_15:99014526-99031054	4851	104564224	AOS5|AOVD1|TAN1|hN1	NA	Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Finally we have shown that one specific Notch-regulated lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to enhance IGF1R mRNA expression and sustain IGF1 signaling. These results confirm that lncRNAs are important downstream targets of the Notch signaling pathway, and additionally they are key regulators of the oncogenic state in T-ALL.	25083870	RID02695	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	NA
Cancer	TP53COR1	HNRNPK	interact	RNA pull-down assay;RNAi;RIP;ChIP	upregulation	microarray	GSE21761	GSE21761.zip	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000165119	NA	102800311	3190	TRP53COR1|linc-p21|lincRNA-p21	AUKS|CSBP|HNRPK|TUNP	A large intergenic noncoding RNA induced by p53 mediates global gene repression in the p53 response. licRNA-p21 in the p53 transcriptional response. Induction of p53 activates the transcription of lincRNA-p21 by binding to its promoter (top left). LincRNA-p21 binds to hnRNP-K, and this interaction imparts specificity to genes repressed by p53 induction. The observed transcriptional repression by lincRNA-p21 is mediated through the physical association with hnRNP-K. This interaction is required for proper genomic localization of hnRNP-K at repressed genes and regulation of p53 mediates apoptosis.	20673990	RID02696	interact with protein	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	HOTAIR	EZH2	interact	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition.More recently, it has been proposed that HOTAIR may act as an intermediate factor in the interaction of Snail and EZH2, facilitating Snail recruitment of EZH2 to specific genomic targets repressed by Snail. Thus, HOTAIR appears to be the linking factor of this putative Snail-HOTAIR-EZH2 tripartite epithelial-esenchymal transition (EMT)-promoting repressor switch in HCC.	27452518;29685978	RID02697	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	HOTAIR	SNAI1	interact	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition.More recently, it has been proposed that HOTAIR may act as an intermediate factor in the interaction of Snail and EZH2, facilitating Snail recruitment of EZH2 to specific genomic targets repressed by Snail. Thus, HOTAIR appears to be the linking factor of this putative Snail-HOTAIR-EZH2 tripartite epithelial-esenchymal transition (EMT)-promoting repressor switch in HCC.	27452518;29685978	RID02698	interact with protein	NA	NA	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	MALAT1	CDH2	negatively-E	RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170558	NA	378938	1000	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD325|CDHN|CDw325|NCAD	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;malat1 is associated with suppressor of zeste 12 (suz12), and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression.	24449823	RID02699	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Urinary bladder cancer	MALAT1	CDH1	negatively-E	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	epigenetic regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;TGF-beta induces malat1 expression and EMT in bladder cancer cells;malat1 knockdown inhibits TGF-beta-induced EMT;targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGF-beta;These data suggest that malat1 is an important mediator of TGF-beta-induced EMT	24449823	RID02700	epigenetic regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Chronic lymphocytic leukemia	MIAT	POU5F1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell survival(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000204531	NA	440823	5460	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias.Sattari et al. found that MIAT is upregulated in aggressive forms of chronic lymphocytic leukaemia (CLL). The study also revealed that MIAT is involved in a positive regulatory feedback loop with Oct4, as suppression of one led to reduced expression of the other Furthermore, we show that MIAT constitutes a regulatory loop with OCT4 in malignant mature B cell, as was previously reported in mouse pulripotent stem cell, and that both molecules are essential for cell survival.	27527866;29685978	RID02701	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Lung adenocarcinoma	CRNDE	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	radioresistance(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000106462	NA	NA	2146	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression;the mechanistic investigations showed that CRNDE could interact with PRC2 and recruit its core component EZH2 to p21 (CDKN1A) promoter regions and repress its transcription;	28550688	RID02702	interact with protein	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cholangiocarcinoma	SNHG1	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE76297	GSE76297.zip	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000106462	NA	23642	2146	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma;SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A;SNHG1 knockdown extensively inhibited CCA cell migration as well as proliferation in vitro and in vivo	29970899	RID02703	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cholangiocarcinoma	PVT1	EZH2	interact	RIP	upregulation	qPCR;microarray	GSE26566	GSE26566.zip	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Non-coding RNA PVT1 Promotes Cell proliferation and Migration by Silencing ANGPTL4 Expression in Cholangiocarcinoma. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth,migration, and apoptosis progression.PVT1 Binds with EZH2 to Coregulate Target Genes, Especially ANGPTL4.	30388624	RID02704	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	SNHG1	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE9348;GSE8671;GSE29621	GSE9348.zip;GSE8671.zip;GSE29621.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000106462	NA	23642	2146	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID02705	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	CRNDE	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000106462	NA	NA	2146	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID02706	interact with protein	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	TUG1	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.RIP with rabbit monoclonal anti-EZH2, anti-SUZ12, anti-SNRNP70 and preimmune IgG from HepG2 and Hep3B cell extracts. RNA levels in immunoprecipitates were determined by qPCR. Expression levels of TUG1 RNA were presented as fold enrichment in EZH2 and SUZ12 relative to IgG immunoprecipitates.	26336870	RID02707	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	TUG1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000178691	NA	55000	23512	LINC00080|NCRNA00080|TI-227H	CHET9|JJAZ1	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.RIP with rabbit monoclonal anti-EZH2, anti-SUZ12, anti-SNRNP70 and preimmune IgG from HepG2 and Hep3B cell extracts. RNA levels in immunoprecipitates were determined by qPCR. Expression levels of TUG1 RNA were presented as fold enrichment in EZH2 and SUZ12 relative to IgG immunoprecipitates.	26336870	RID02708	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	LUCAT1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000106462	NA	100505994	2146	SCAL1|SCAT5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.LUCAT1 functions as a tumor activator by epigenetically regulating p21 and p57 expression which are required to target EZH2 occupancy.	28423699	RID02709	interact with protein	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	CCAT1	EZH2	interact	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000106462	NA	100507056	2146	CARLO5|CARLo-5|onco-lncRNA-40	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.The existence of independent binding sites for EZH2 and SUV39H1 on CCAT1 suggests that CCAT1 may bridge EZH2 and SUV39H1. EZH2 IP retrieved SUV39H1, and SUV39H1 IP retrieved EZH2 in turn from Eca-109. Knockdown CCAT1 (ASO) of the IP abrogated the interaction between EZH2 and SUV39H1, suggesting that CCAT1 is required to bridge this interaction.	27956498	RID02710	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	CCAT1	SUV39H1	interact	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000101945	NA	100507056	6839	CARLO5|CARLo-5|onco-lncRNA-40	H3-K9-HMTase 1|KMT1A|MG44|SUV39H	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.The existence of independent binding sites for EZH2 and SUV39H1 on CCAT1 suggests that CCAT1 may bridge EZH2 and SUV39H1. EZH2 IP retrieved SUV39H1, and SUV39H1 IP retrieved EZH2 in turn from Eca-109. Knockdown CCAT1 (ASO) of the IP abrogated the interaction between EZH2 and SUV39H1, suggesting that CCAT1 is required to bridge this interaction.	27956498	RID02711	interact with protein	NA	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)
Lung cancer	MEG3	JARID2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000008083	NA	55384	3720	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	JMJ	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID02712	interact with protein	NA	NA	UP(LIHC,PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807)
Lung cancer	MEG3	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000106462	NA	55384	2146	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID02713	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Clear cell renal cell carcinoma	MRCCAT1	EZH2	interact	RIP;ChIP;RNA pull-down assay;western blot	upregulation	microarray	GSE88948	GSE88948.zip	cell metastasis(+);P38/MAPK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	ENST00000237853	GRCh38_5:95885098-95962071	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 and activating p38-MAPK signaling. The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway.To test this, we performed RIP assay with an antibody against EZH2 (an important subunit of the PRC2 complex), and found a significant enrichment of MRCCAT1 with EZH2, compared with IgG control.	28659173	RID02714	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	TUG1	EED	interact	ChIP;RIP	downregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000074266	NA	55000	8726	LINC00080|NCRNA00080|TI-227H	COGIS|HEED|WAIT1	Long noncoding RNA TUG1 is downregulated in non-small cell lung cancer and can regulate CELF1 on binding to PRC2. Knockdown of TUG1 significantly promoted the proliferation of NSCLC cells. The results demonstrated that TUG1 RNA was bound to enhancer of zeste protein 2/embryonic ectoderm development (EZH2/EED), which is essential for PRC2. Finally, our designed ChIP assay revealed that the EZH2/EED was bound to the promotor region of CELF1 within 992 bp upstream of the transcript start site.	27485439	RID02715	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	LINC00668	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000106462	NA	400643	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.Moreover, we also found that LINC00668 plays a key role in the gastric cancer cell cycle by epigenetically silencing CDK inhibitors by binding to PRC2, which could in part account for LINC00668-mediated cell growth regulation.RNA immunoprecipitation (RIP) assays showed that the endogenous LINC00668 was enriched in the anti-EZH2 RIP fraction relative to the input compared to the IgG fraction. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that LINC00668 was enriched in the anti-SUZ12 RNA-IP fraction.	27036039	RID02716	interact with protein	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	LINC00668	SUZ12	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000178691	NA	400643	23512	NA	CHET9|JJAZ1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.Moreover, we also found that LINC00668 plays a key role in the gastric cancer cell cycle by epigenetically silencing CDK inhibitors by binding to PRC2, which could in part account for LINC00668-mediated cell growth regulation.RNA immunoprecipitation (RIP) assays showed that the endogenous LINC00668 was enriched in the anti-EZH2 RIP fraction relative to the input compared to the IgG fraction. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that LINC00668 was enriched in the anti-SUZ12 RNA-IP fraction.	27036039	RID02717	interact with protein	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	TUG1	EZH2	interact	ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. endogenous TUG1 was enriched in the anti-EZH2 RIP fraction relative to the input compared with the IgG fraction both in AGS and BGC-823 cell lines. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous TUG1 was obviously enriched in the anti-SUZ12 RNA-IP fraction.	26913601	RID02718	interact with protein	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	TUG1	SUZ12	interact	ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000178691	NA	55000	23512	LINC00080|NCRNA00080|TI-227H	CHET9|JJAZ1	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. endogenous TUG1 was enriched in the anti-EZH2 RIP fraction relative to the input compared with the IgG fraction both in AGS and BGC-823 cell lines. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous TUG1 was obviously enriched in the anti-SUZ12 RNA-IP fraction.	26913601	RID02719	interact with protein	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	CDKN2B-AS1	EZH2	interact	RNAi;RIP	upregulation	qPCR;microarray	GSE45435;GSE56140	GSE45435.zip;GSE56140.zip	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000106462	NA	100048912	2146	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID02720	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	CDKN2B-AS1	SUZ12	interact	RNAi;RIP	upregulation	qPCR;microarray	GSE45435;GSE56140	GSE45435.zip;GSE56140.zip	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000178691	NA	100048912	23512	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHET9|JJAZ1	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID02721	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Cancer	RASSF1-AS1	SUZ12	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE5823;GSE11118;GSE10879;GSE12056;GSE13471	GSE5823.zip;GSE11118.zip;GSE10879.zip;GSE12056.zip;GSE13471.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000281358	GRCh38_3:50337511-50338300	ENSG00000178691	NA	102060282	23512	ANRASSF1	CHET9|JJAZ1	The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation.ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region.We demonstrated that ANRASSF1 formed an lncRNA/DNA hybrid, which mediated the recruitment of SUZ12, a member of PRC2, to the RASSF1A promoter.	23990798	RID02722	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	HOXA-AS2	EZH2	interact	RIP;RNAi	upregulation	qPCR;microarray	GSE15459	GSE15459.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000106462	NA	285943	2146	HOXA3as	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated.	26384350	RID02723	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	LINC00511	EZH2	interact	RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000106462	NA	400619	2146	LCAL5|onco-lncRNA-12	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Intergenic Noncoding RNA 00511 Acts as an Oncogene in Non-small-cell Lung Cancer by Binding to EZH2 and Suppressing p57. We found LINC00511 was upregulated and associated with oncogenesis, tumor size, metastasis, and poor prognosis in NSCLC. LINC00511 affected cell proliferation, invasiveness, metastasis, and apoptosis in multiple NSCLC cell lines. Mechanistically, LINC00511 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), a highly conserved protein complex that regulates gene expression by methylating lysine 27 on histone H3), and acted as a modular scaffold of EZH2/PRC2 complexes, coordinated their localization, and specified the histone modification pattern on the target genes, including p57, and consequently altered NSCLC cell biology.	27845772	RID02724	interact with protein	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	NBAT1	EZH2	interact	RIP;RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000106462	NA	729177	2146	CASC14|NBAT-1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2. ectopic NBAT1 inhibits migration and invasion of breast cancer cells. Mechanistic study shows that NBAT1 is associated with PRC2 member EZH2 and regulates global gene expression profile. Among them, DKK1 (dickkopf WNT signaling pathway inhibitor 1) is found to be regulated by NBAT1 in a PRC2 dependent manner, and is responsible for NBAT1's effects in inhibiting migration and invasion of breast cancer cells.	26378045	RID02725	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	CDKN2B-AS1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000178691	NA	100048912	23512	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHET9|JJAZ1	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous ANRIL was obviously enriched in the anti-SUZ12 RNA-IP fraction.	24810364;25504755	RID02726	interact with protein	prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Glioblastoma	APTR	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000106462	NA	100505854	2146	RSBN1L-AS1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. APTR is present in immunoprecipitates of EZH2 or SUZ12, but not of ORC2 (negative control protein). An unrelated RNA, GAPDH mRNA was also not precipitated with EZH2 or SUZ12.	24748121	RID02727	interact with protein	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Glioblastoma	APTR	SUZ12	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000178691	NA	100505854	23512	RSBN1L-AS1	CHET9|JJAZ1	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. APTR is present in immunoprecipitates of EZH2 or SUZ12, but not of ORC2 (negative control protein). An unrelated RNA, GAPDH mRNA was also not precipitated with EZH2 or SUZ12.	24748121	RID02728	interact with protein	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Pancreatic cancer	HOTTIP	WDR5	interact	RIP	upregulation	qPCR	NA	NA	cell stemness(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196363	NA	100316868	11091	HOXA-AS6|HOXA13-AS1|NCRNA00213	BIG-3|CFAP89|SWD3	LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9; HOTTIP mediated HOXA9 to enhance the Wnt/beta-catenin pathway by binding to WDR5 in PCSCs;the HOTTIP/WDR5/HOXA9/Wnt axis contributes to PCSC stemness and is a potential therapeutic target for PDAC.	28947139	RID02729	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	LINC00958	WDR5	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000196363	NA	100506305	11091	BLACAT2	BIG-3|CFAP89|SWD3	Long noncoding RNA BLACAT2 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. we demonstrate that BLACAT2 epigenetically upregulation VEGF-C expression by directly associating with WDR5, a core subunit of human H3K4 methyltransferase complexes.	29355840	RID02730	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HOXA11-AS	WDR5	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000196363	NA	221883	11091	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	BIG-3|CFAP89|SWD3	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID02731	interact with protein	metastasis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HOXA11-AS	STAU1	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124214	NA	221883	6780	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	PPP1R150|STAU	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID02732	interact with protein	metastasis	NA	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Osteosarcoma	FOXP4-AS1	KDM1A	interact	ChIP;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000004487	NA	101060264	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID02733	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	FOXP4-AS1	EZH2	interact	ChIP;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000106462	NA	101060264	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID02734	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic cancer	DUXAP8	KDM1A	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE16515;GSE15932;GSE15471	GSE16515.zip;GSE15932.zip;GSE15471.zip	cell proliferation(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000004487	NA	503637	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID02735	interact with protein	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	DUXAP8	EZH2	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE16515;GSE15932;GSE15471	GSE16515.zip;GSE15932.zip;GSE15471.zip	cell proliferation(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000106462	NA	503637	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID02736	interact with protein	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pre-eclampsia	HOXA11-AS	KDM1A	interact	RIP;ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000004487	NA	221883	23028	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	AOF2|BHC110|CPRF|KDM1|LSD1	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID02737	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	HOXA11-AS	EZH2	interact	RIP;ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID02738	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Renal cell carcinoma	HOTTIP	KDM1A	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000004487	NA	100316868	23028	HOXA-AS6|HOXA13-AS1|NCRNA00213	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID02739	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	HOTTIP	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106462	NA	100316868	2146	HOXA-AS6|HOXA13-AS1|NCRNA00213	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID02740	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	FEZF1-AS1	KDM1A	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000004487	NA	154860	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID02741	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	FEZF1-AS1	EZH2	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000106462	NA	154860	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID02742	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung adenocarcinoma	CYTOR	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000106462	NA	112597	2146	C2orf59|LINC00152|NCRNA00152	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression.LINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. EZH2 was shown to bind the promoter region of IL24, while LINC00152 knockdown reduced the histone H3 lysine 27 trimethylation (H3K27me3) occupancy of the IL24 promoter locus (Fig. 5h). However, LSD1 did not bind the IL24 promoter locus (Additional file 5: Figure S3d). These results indicated that LINC00152 repression of target IL24 expression occured, at least partially, through interaction with EZH2.	28109288	RID02743	interact with protein	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Glioblastoma	HOTAIR	KDM1A	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	27277755	RID02744	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AGAP2-AS1	KDM1A	interact	RIP;ChIP	upregulation	qPCR;microarray	GSE18842;GSE19188	GSE18842.zip;GSE19188.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000004487	NA	100130776	23028	PUNISHER	AOF2|BHC110|CPRF|KDM1|LSD1	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID02745	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AGAP2-AS1	EZH2	interact	RIP;ChIP	upregulation	qPCR;microarray	GSE18842;GSE19188	GSE18842.zip;GSE19188.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000106462	NA	100130776	2146	PUNISHER	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID02746	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	LINC00673	KDM1A	interact	RIP;RNA pull-down assay;ChIP	upregulation	qPCR;microarray	GSE18842	GSE18842.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000004487	NA	100499467	23028	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AOF2|BHC110|CPRF|KDM1|LSD1	Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer.We identified an oncogene, linc00673, whose expression level was upregulated by bioinformatics analyses and qRT-PCR analyses in NSCLC. Further mechanistic analyses indicated that the oncogenic activity of linc00673 is partially attributable to its repression of NCALD through association with the epigenetic repressor LSD1, Histone demethylase lysine specific demethylase 1.	27027352	RID02747	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC01133	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000106462	NA	100505633	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID02748	interact with protein	NA	UP(BRCA);DATA(GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	LINC01133	KDM1A	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000004487	NA	100505633	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID02749	interact with protein	NA	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	DUXAP8	EZH2	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000106462	NA	503637	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02750	interact with protein	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	DUXAP8	KDM1A	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000004487	NA	503637	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02751	interact with protein	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00673	EZH2	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106462	NA	100499467	2146	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02752	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	LINC00673	KDM1A	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000004487	NA	100499467	23028	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AOF2|BHC110|CPRF|KDM1|LSD1	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02753	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	AGAP2-AS1	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE51575;GSE65801	GSE51575.zip;GSE65801.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000106462	NA	100130776	2146	PUNISHER	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02754	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	AGAP2-AS1	KDM1A	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE51575;GSE65801	GSE51575.zip;GSE65801.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000004487	NA	100130776	23028	PUNISHER	AOF2|BHC110|CPRF|KDM1|LSD1	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02755	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	FEZF1-AS1	KDM1A	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000004487	NA	154860	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. ChIP assays demonstrated that LSD1 could directly bind to the promoter of P21, inducing H3K4me2 demethylation. knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis.	28209170	RID02756	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	HOXA-AS2	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000106462	NA	285943	2146	HOXA3as	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02757	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	HOXA-AS2	KDM1A	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000004487	NA	285943	23028	HOXA3as	AOF2|BHC110|CPRF|KDM1|LSD1	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02758	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	IRAIN	EZH2	interact	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000106462	NA	104472848	2146	IGF1R-AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02759	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic cancer	IRAIN	KDM1A	interact	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000004487	NA	104472848	23028	IGF1R-AS	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02760	interact with protein	NA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MEG3	DNMT1	interact	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);prognosis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130816	NA	55384	1786	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.	25641194	RID02761	interact with protein	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	GIHCG	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257698	GRCh38_12:57930115-57936345	ENSG00000106462	NA	100506844	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID02762	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	GIHCG	DNMT1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257698	GRCh38_12:57930115-57936345	ENSG00000130816	NA	100506844	1786	NA	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID02763	interact with protein	NA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	HOXA11-AS	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID02764	interact with protein	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	HOXA11-AS	DNMT1	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000130816	NA	221883	1786	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID02765	interact with protein	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Chondrosarcoma	HOTAIR	EZH2	interact	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02766	interact with protein	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Chondrosarcoma	HOTAIR	DNMT1	interact	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02767	interact with protein	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	RB1-DT	DNMT3A	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231473	GRCh38_13:48296162-48303661	ENSG00000119772	NA	100862704	1788	LINC00441|ncRNA-RB1	DNMT3A2|M.HsaIIIA|TBRS	Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.Here we focused on the bidirectional transcripted long noncoding RNA (Linc00441) with neighbor gene RB1 to investigate whether Linc00441 is involved in the suppression of RB1 in HCC. We found that aberrant upregulation intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement.	28300839	RID02768	interact with protein	NA	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Acute myeloid leukemia	HOTAIR	CCND1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID02769	ceRNA or sponge	prognosis	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Acute myeloid leukemia	HOTAIR	MDM2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000135679	NA	100124700	4193	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ACTFS|HDMX|hdm2	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID02770	ceRNA or sponge	prognosis	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	PANTR1	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000106462	NA	100506421	2146	LINC01158|linc-Brn1a|linc-POU3F3	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Increased levels of the long intergenic non-protein coding RNA POU3F3 promote DNA methylation in esophageal squamous cell carcinoma cells. Levels of a lincRNA encoded by a gene located next to POU3F3 (linc-POU3F3) were significantly higher in ESCC than neighboring nontumor tissues. In RNA immunoprecipitation assays, linc-POU3F3 was associated with the EZH2 messenger RNA (mRNA). Overexpression of linc-POU3F3 in cell lines increased their proliferation and ability to form colonies, and reduced the expression of POU3F3 mRNA, whereas knockdown of linc-POU3F3 increased the levels of POU3F3 mRNA. CpG islands in POU3F3 were densely hypermethylated in cell lines that overexpressed linc-POU3F3; methylation at these sites was reduced by knockdown of linc-POU3F3. Pharmacologic inhibition of EZH2 increased the levels of POU3F3 mRNA and significantly reduced binding of DNA methyltransferase (DNMT)1, DNMT3A, and DNMT3B to POU3F3. Levels of linc-POU3F3 are increased in ESCC samples from patients compared with nontumor tissues. This noncoding RNA contributes to the development of ESCC by interacting with EZH2 to promote methylation of POU3F3, which encodes a transcription factor.	24631494	RID02771	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	HOXB13-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229637	GRCh38_17:48720802-48724758	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma. Mechanistically, we showed that HOXB13-AS1 overexpression increased DNMT3B-mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP),epigenetically suppressing HOXB13 expression.	30105866	RID02772	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	FAM83H-AS1	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734140-143746337	ENSG00000106462	NA	100128338	2146	onco-lncRNA-3	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21).FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A;thereby influencing the cell cycle and proliferation	29870057	RID02773	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	SOX21-AS1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000106462	NA	100507533	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SOX21-AS1 is associated with progression of hepatocellular carcinoma and predicts prognosis through epigenetically silencing p21;SOX21-AS1 epigenetically silenced p21 via recruiting EZH2 to the promoter of p21;SOX21-AS1 can interact with p21 to affect hepatocellular carcinoma progression	29772433	RID02774	interact with protein	prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	SNHG6	EZH2	interact	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.In this study, we revealed that SNHG6 was overexpressed in gastric cancer tissues and cell lines. Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446;30031062	RID02775	interact with protein	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cholangiocarcinoma	NEAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|NCRNA00084|TncRNA|VINC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells;NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression	29970216	RID02776	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
T-cell leukemia	CDKN2B-AS1	EZH2	interact	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);NF-kB signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000106462	NA	100048912	2146	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA ANRIL Supports Proliferation of Adult T-Cell Leukemia Cells through Cooperation with EZH2. In the present study, we show that the expression level of the lncRNA ANRIL was elevated in HTLV-1-infected cell lines and clinical ATL samples. In addition, we observed that the ANRIL/EZH2 complex repressed p21/CDKN1A transcription through H3K27 trimethylation of the p21/CDKN1A promoter. Taken together, our results implicate that the lncRNA ANRIL, by cooperating with EZH2, supports the proliferation of HTLV-1-infected cells, which is thought to be critical for oncogenesis. In this study, we demonstrated that the lncRNA ANRIL was important for maintaining the proliferation of ATL cells in vitro and in vivo ANRIL was shown to activate NF-kB signaling through forming a ternary complex with EZH2 and p65. Furthermore, epigenetic inactivation of p21/CDKN1A was involved in the oncogenic function of ANRIL.	30258009	RID02777	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteosarcoma	HAGLR	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000106462	NA	401022	2146	HOXD-AS1|MIR7704HG|Mdgt	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2.our study confirmed that HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis.	30119259	RID02778	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	DUXAP10	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000244306	GRCh38_14:19268853-19337730	ENSG00000106462	NA	503639	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA DUXAP10 modulates cell proliferation in esophageal squamous cell carcinoma through epigenetically silencing p21. Results of mechanism experiments suggested that DUXAP10 motivated ESCC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21.	30215547	RID02779	interact with protein	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Melanoma	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma. the lncRNA PVT1 may contribute to the tumorigenesis and metastasis of melanoma through binding to EZH2 and regulating the expression of miR-200c	29286144	RID02780	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Glioblastoma	H19	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter;by showing that its expression is inversely linked to that of NKD1, a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter	29643989	RID02781	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	SH3PXD2A-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000106462	NA	100505839	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID02782	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	LNCDQ	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_1:155234457-155239960	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of LncDQ is Associated with Poor Prognosis and Promotes Tumor Progression via Epigenetic Regulation of the EMT Pathway in HCC;LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells	29669339	RID02783	interact with protein	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA PVT1 promotes hepatocellular carcinoma progression through regulating miR-214.RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2).	28800314	RID02784	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Melanoma	FALEC	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000106462	NA	100874054	2146	FAL1|LINC00568|ncRNA-a1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21;we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21	29196104	RID02785	interact with protein	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Chordoma	MIR31HG	EZH2	interact	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000106462	NA	554202	2146	LncHIFCAR|hsa-lnc-31	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID02786	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	DANCR	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	57291	2146	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID02787	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	DANCR	HDAC3	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000171720	NA	57291	8841	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	HD3|KDAC3|RPD3|RPD3-2	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID02788	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Melanoma	ILF3-DT	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000106462	NA	147727	2146	ILF3-AS1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID02789	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	SNHG20	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000106462	NA	654434	2146	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA SNHG20 promotes non-small cell lung cancer cell proliferation and migration by epigenetically silencing of P21 expression;SNHG20 could interact with EZH2 (enhancer of zeste homolog 2), thereby repressing P21 expression	28981099	RID02790	interact with protein	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Uveal melanoma	HOXA11-AS	EZH2	interact	RIP;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID02791	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	TRERNA1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000106462	NA	100887755	2146	LINC00651|treRNA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition. TRERNA1 functions as a scaffold to recruit EZH2 to epigenetically silence epithelial-mesenchymal transition marker CDH1 by H3K27me3 of its promoter region;our findings indicated that TRERNA1 serves as a critical effector in GC progression by regulating CDH1 at the transcription level	28918030	RID02792	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteosarcoma	XIST	EZH2	interact	ChIP;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21;mechanistic analysis revealed that Xist can repress P21 expression to regulate OS cell cycle and proliferation by binding to EZH2	29254174	RID02793	interact with protein	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	HOXA11-AS	EZH2	interact	ChIP;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Promotion of LncRNA HOXA11-AS on the proliferation of hepatocellular carcinoma by regulating the expression of LATS1;RIP and CHIP experiments showed that HOXA11-AS inhibited the expression of LATS1 genes by binding enhancer of zeste homolog 2 (EZH2) proteins	28829501	RID02794	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cervical cancer	PVT1	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-);epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	paclitaxel	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells;PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195;PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region;PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells;Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX;Based on these findings, we infer that PVT1 could decrease miR-195 expression via enhancing histone H3K27me3 in the miR-195 promoter region and also via direct sponging of miR-195	28296507;27272214	RID02795	interact with protein	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	LL22NC03-N64E9.1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_22:15796959-15798346	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer; Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2;We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2.	28938648	RID02796	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gallbladder cancer	UCA1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID02797	interact with protein	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteosarcoma	ANCR	EZH2	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	282	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID02798	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	CCAT2	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000106462	NA	101805488	2146	LINC00873|NCCP1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer;we confirmed that CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells	28531944	RID02799	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	SNHG6	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells.	30157475	RID02800	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	UCA1	EZH2	interact	ChIP;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA UCA1 induced by SP1 promotes cell proliferation via recruiting EZH2 and activating AKT pathway in gastric cancer.This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.	28569779	RID02801	interact with protein	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	LINC00673	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106462	NA	100499467	2146	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5	28423732	RID02802	interact with protein	metastasis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Urinary bladder cancer	AWPPH	EZH2	interact	RIP	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell autophagy(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111195866-111495161	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression.LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.Then, RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2.	29231261	RID02803	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic cancer	MALAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. RIP and ChIP assays suggest that EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression.	26848980	RID02804	interact with protein	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colon cancer	HULC	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000106462	NA	728655	2146	HCCAT1|LINC00078|NCRNA00078	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HULC promotes colorectal carcinoma progression through epigenetically repressing NKD2 expression. Mechanistically, RNA immunoprecipitation (RIP) and RNA pull-down experiment demonstrated that HULC could simultaneously interact with EZH2 to repress underlying targets NKD2 transcription. In addition, rescue experiments determined that HULC oncogenic function is partly dependent on repressing NKD2.	27496341	RID02805	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	XIST	EZH2	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression.Mechanistically, RNA immune-precipitation (RIP) and RNA pull-down experiment demonstrated that XIST could simultaneously interact with EZH2 to suppress transcription of its potential target KLF2.	27501756	RID02806	interact with protein	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Small cell lung cancer	TUG1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	cisplatin;adriamycin;etoposide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA TUG1 is involved in cell growth and chemoresistance of small cell lung cancer by regulating LIMK2b via EZH2.We found that TUG1 was overexpressed in SCLC tissues.We further demonstrated that TUG1 can regulate the expression of LIMK2b (a splice variant of LIM-kinase 2) via binding with enhancer of zeste homolog 2 (EZH2), and then promoted cell growth and chemoresistance of SCLC.After knockdown of TUG1, the IC50 values of H446DDP and H69AR cells significantly decreased with treatment of chemotherapeutic drugs including DDP, ADM or VP-16 (Fig. 4a). Three chemotherapy drugs [Cisplatin (DDP; Shandong, China), Adriamycin (ADM; Jiangsu, China) Etoposide (VP-16; Jiangsu, China),] were used. Furthermore, we conducted ChIP assays and found that knockdown of TUG1 decreased the binding of EZH2 and H3K27me3 levels across the LIMK2b promoter compared to cells transfected with siNC (Fig. 6f). Taken together, these data suggest that TUG1 is required to target EZH2 occupancy and activity to epigenetically modulate the expression of LIMK2b.	28069000	RID02807	interact with protein	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic ductal adenocarcinoma	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma.Loss of miR-34a contributed to EZH2-mediated cell growth in PDAC cells. As HOTAIR was shown to be overexpressed in PDAC.	27594424	RID02808	interact with protein	NA	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic cancer	HOTAIR	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	conatumumab;tigatuzumab	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer.These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression.Some TRAIL and DR4/DR5 agonist antibodies, including conatumumab (AMG655, antibody for DR5) and tigatuzumab (CS-1008/TRA-8, antibody for DR5), have also been used for treating several types of cancers	28476883	RID02809	interact with protein	chemoresistance	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Melanoma	HEIH	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000106462	NA	100859930	2146	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes' promoters and modulate the expression of EZH2 target genes in HCC. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC.	28487474	RID02810	interact with protein	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	HNF1A-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000106462	NA	283460	2146	C12orf27|HAS1|NCRNA00262	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID02811	interact with protein	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	SNHG20	EZH2	interact	RIP	upregulation	qPCR	NA	NA	cell invasion(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000106462	NA	654434	2146	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA SNHG20 predicts a poor prognosis for HCC and promotes cell invasion by regulating the epithelial-to-mesenchymal transition.In vitro, loss-function assays revealed that knockdown of SNHG20 inhibited cell proliferation and invasion, whereas, gain-of-function promoted cell proliferation and invasion.Mechanistic investigation revealed that SNHG20 could bind to enhancer of zeste homolog 2 (EZH2) and regulated E-cadherin expression.Our results showed that the SNHG20/EZH2/E-cadhein regulator pathway might contribute to the development of novel therapeutic strategies for HCC patients.	28282787	RID02812	interact with protein	prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	PVT1	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA PVT1 Promotes Non-Small Cell Lung Cancer Cell Proliferation through Epigenetically Regulating LATS2 Expression.Here, we found that PVT1 was upregulated in 105 human NSCLC tissues compared with normal samples.RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription.	26908628	RID02813	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	UCA1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell cycle phase transition (G1/S)(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID02814	interact with protein	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	CYTOR	EZH2	interact	RIP	upregulation	qPCR;microarray	GSE15459	GSE15459.zip	cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000106462	NA	112597	2146	C2orf59|LINC00152|NCRNA00152	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID02815	interact with protein	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Thyroid cancer	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID02816	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	BLACAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000106462	NA	101669762	2146	LINC00912|linc-UBC1|onco-lncRNA-30	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation.	28277544	RID02817	interact with protein	prognosis	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	SPRY4-IT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02818	interact with protein	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Estrogen-receptor positive breast cancer	H19	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02819	interact with protein	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Papillary thyroid carcinoma	BANCR	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000106462	NA	100885775	2146	LINC00586	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02820	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cervical cancer	TMPOP2	EZH2	interact	RIP	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	ENSG00000106462	NA	100533619	2146	lncRNA-EBIC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA-EBIC promotes tumor cell invasion by binding to EZH2 and repressing E-cadherin in cervical cancer.Then, we found a specific differentially expressed lncRNA can physically bind to enhancer of zeste homolog2 (EZH2) by using RNA immunoprecipitation. We termed it as EZH2-binding lncRNA in cervical cancer [lncRNA-EBIC]. We also found that the association between lncRNA-EBIC and EZH2 was required for the repression of E-cadherin, which was a key molecular in the metastasis of cervical cancer. Conclusion: These results demonstrated that lncRNA-EBIC was an oncogenic lncRNA, which could promote tumor cell invasion in CC by binding to EZH2 and inhibiting E-cadherin expression.	25007342	RID02821	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung adenocarcinoma	LUADT1	SUZ12	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000178691	NA	106182249	23512	NA	CHET9|JJAZ1	A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27.Further analysis indicated that LUADT1 may regulate cell cycle progression by epigenetically inhibiting the expression of p27.RNA immunoprecipitation and chromatin immunoprecipitation assays confirmed that LUADT1 binds to SUZ12, a core component of polycomb repressive complex 2, and mediates the trimethylation of H3K27 at the promoter region of p27.	26291312	RID02822	interact with protein	NA	UP(NSCLC,PRAD,SKCM);DATA(GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Glioblastoma	HOTAIRM1	SP1	positively-E	luciferase reporter assay;RIP;siRNA;starBase;TargetScanHuman;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-137)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000185591	NA	100506311	6667	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	Over-expression of long noncoding RNA HOTAIRM1 promotes cell proliferation and invasion in human glioblastoma by up-regulating SP1 via sponging miR-137.The relative expression levels of HOTAIRM1, miR-137 and specificity protein 1 were detected by qRT-PCR or western blot.The interactions among HOTAIRM1, miR-137 and specificity protein 1 were predicted by starBase and TargetScanHuman and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The levels of HOTAIRM1 and specificity protein 1 were significantly increased while miR-137 was significantly decreased in glioblastoma tissues and cells. Knockdown of HOTAIRM1 suppressed proliferation and invasion in glioblastoma cells. Moreover, miR-137 was bound to HOTAIRM1, and specificity protein 1 was identified as a target of miR-137. The protein level of specificity protein 1 was repressed by silencing the expression of HOTAIRM1, whereas the effect was restored by inhibiting the expression of miR-137.Downregulation of HOTAIRM1 expression suppressed the proliferation and invasion of glioblastoma cells by down-regulating specificity protein 1 expression via sponging miR-137, indicating a promising strategy for glioblastoma treatment.	31876683	RID02823	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	PVT1	TRAF3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;siRNA;starBase;western blot	upregulation	qRT-PCR	NA	NA	cell autophagy(-);cell viability(-);apoptosis process(+);inflammatory response(+)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000131323	NA	5820	7187	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP-1|CD40bp|CRAF1|LAP1|RNF118	Knockdown of PVT1 inhibits IL-1beta-induced injury in chondrocytes by regulating miR-27b-3p/TRAF3 axis.The levels of PVT1, microRNA (miR)-27b-3p, and tumor necrosis factor receptor-associated factor 3 (TRAF3) were detected by quantitative real-time polymerase chain reaction or western blot.The starBase 2.0 predicted there were putative complementary sequences of PVT1 and miR-27b-3p.Moreover, the potential binding sites of miR-27b-3p and TRAF3 were predicted by StarBase 2.0. To validate the association between them, luciferase reporter assay using TRAF3-wt and TRAF3-mut and RIP assays were performed in C28/I2 cells. We found that PVT1 expression was enhanced in OA patients and IL-1beta-treated C28/I2 cells. Silence of PVT1 promoted cell viability and autophagy but suppressed apoptosis and inflammatory response in IL-1beta-treated C28/I2 cells. To explore the role of PVT1 in IL-1beta-induced injury, its abundance was knocked down using si-PVT1 in IL-1beta-treated C28/I2 cells.miR-27b-3p was confirmed as a target of PVT1 and its deficiency reversed the suppressive effect of PVT1 knockdown on IL-1beta-induced injury.  Collectively, knockdown of PVT1 increased cell viability and autophagy but inhibited apoptosis and inflammatory response in chondrocytes treated by IL-1beta via up-regulating miR-27b-3p and down-regulating TRAF3.	31863917	RID02824	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Atherosclerosis	MEG3	miR-147	negatively-F	overexpression;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+);JAK/STAT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 inhibits HMEC-1 cells growth, migration and tube formation via sponging miR-147.The expression levels of MEG3 during tube formation were tested by qRT-PCRMEG3 was down-regulated during tube formation of HMEC-1 cells. Overexpressed MEG3 inhibited HMEC-1 cells growth, migration and tube formation capacity.The relative luciferase activity was significantly reduced by co-transfection with miR-147 and MEG3-wt, rather than co-transfection with miR-147 and MEG3-mt. RNA-IP assay revealed that miR-147 could be pulled down by MEG3, and MEG3 could also be pulled down by miR-147, indicating the binding relationship between MEG3 and miR-147. MEG3 could bind with miR-147 and repress miR-147 expression.MiR-147 induced ICAM-1 expression, and contained ICAM-1 target sequences.The anti-atherogenic actions of MEG3 were inhibited by miR-147, and the anti-atherogenic actions of miR-147 suppression were also inhibited when ICAM-1 was overexpressed. Further, ICAM-1 overexpression showed activated roles in Wnt/beta-catenin and Jak/Stat signaling pathways.MEG3 inhibited HMEC-1 cell growth, migration and tube formation. The anti-atherogenic actions of MEG3 might be mediated via sponging miR-147, and thereby repressing the expression of ICAM-1.	31863691	RID02825	ceRNA or sponge	NA		
Atherosclerosis	MEG3	ICAM1	negatively-E	overexpression;shRNA	downregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+);JAK/STAT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000090339	NA	55384	3383	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BB2|CD54	LncRNA MEG3 inhibits HMEC-1 cells growth, migration and tube formation via sponging miR-147.MEG3 was down-regulated during tube formation of HMEC-1 cells. MEG3 expression suppressed cells viability, migration and tube formation, while induced apoptosis. MEG3 could bind with miR-147 and repress miR-147 expression.Here we found that ICAM-1 was highly expressed in overexpressed-miR-147 cells and was low expressed in low-expressed-miR-147 cells, indicating ICAM-1 was positively regulated by miR-147.Short hairpin RNA-intracellular cell adhesion molecule-1 (sh-ICAM-1) repressed cell growth, migration and invasion.Further, ICAM-1 overexpression showed activated roles in Wnt/beta-catenin and Jak/Stat signaling pathways.MEG3 inhibited HMEC-1 cell growth, migration and tube formation. The anti-atherogenic actions of MEG3 might be mediated via sponging miR-147, and thereby repressing the expression of ICAM-1.	31863691	RID02826	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367)
Allergic rhinitis	GAS5	EZH2	negatively-E	shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106462	NA	60674	2146	NCRNA00030|SNHG2	ENX-1|EZH1|KMT6|KMT6A	Exosomal long non-coding RNA GAS5 suppresses Th1 differentiation and promotes Th2 differentiation via downregulating EZH2 and T-bet in allergic rhinitis.The interference of LncGAS5 was conducted in OVA-EXO using shRNA against LncGAS5, and qRT-PCRconfirmed the downregulation of LncGAS5 in OVAEXOshRNA- LncGAS5.The result showed that LncGAS5 was upregulated in AR epithelial samples, AR-EXO, and OVA-EXO. The coincubation of AR-EXO and CD4+ T cells suppressed Th1 differentiation and promoted Th2 differentiation, which is mediated by LncGAS5 in AR-EXO. The LncGAS5 in AR-EXO inhibited transcription and expression of EZH2,OVA-EXO coincubation reduced the transcriptional activity of EZH2, which was negated by OVA-EXOshRNA-LncGAS5 coincubation, as shown by the modifications in the luciferase activity .And it also inhibited T-bet expression at mRNA and protein levels.In summary, our findings demonstrated that LncGAS5 in AR epithelium-derived exosomes is the key mediator in Th1/Th2 differentiation, providing a possible therapeutic target of AR.	31841965	RID02827	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Allergic rhinitis	GAS5	TBX21	negatively-E	shRNA	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000073861	NA	60674	30009	NCRNA00030|SNHG2	T-bet|TBLYM	Exosomal long non-coding RNA GAS5 suppresses Th1 differentiation and promotes Th2 differentiation via downregulating EZH2 and T-bet in allergic rhinitis.The interference of LncGAS5 was conducted in OVA-EXO using shRNA against LncGAS5, and qRT-PCRconfirmed the downregulation of LncGAS5 in OVAEXOshRNA- LncGAS5.The result showed that LncGAS5 was upregulated in AR epithelial samples, AR-EXO, and OVA-EXO. The coincubation of AR-EXO and CD4+ T cells suppressed Th1 differentiation and promoted Th2 differentiation, which is mediated by LncGAS5 in AR-EXO. The LncGAS5 in AR-EXO inhibited transcription and expression of EZH2,OVA-EXO coincubation reduced the transcriptional activity of EZH2, which was negated by OVA-EXOshRNA-LncGAS5 coincubation, as shown by the modifications in the luciferase activity .And it also inhibited T-bet expression at mRNA and protein levels.In summary, our findings demonstrated that LncGAS5 in AR epithelium-derived exosomes is the key mediator in Th1/Th2 differentiation, providing a possible therapeutic target of AR.	31841965	RID02828	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Myocardial infarction	LINC00528	COX2	positively-E	LncBase;lncRNASNP2;luciferase reporter assay;western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000269220	GRCh38_22:17777322-17779481	ENSG00000198712	NA	200298	4513	C22orf37|FLJ40542	COII|MTCO2	LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis. In the present study, qRT-PCR;ISHowed that LINC00528 was significantly increased in post-MI cells compared with normal cells.Subsequently, we analyzed the potential targets of LINC00528 via bioinformatics method (LncBase and lncRNASNP2), and miR-143-3p ranked top among those candidates. Afterwards, qRT-PCR;ISHowed that miR-143-3p expression was significantly decreased in post-MI cells compared with normal cells.Luciferase reporter assay showed that miR-143-3p mimics significantly reduced the luciferase activities of LINC00528-WT group.Luciferase reporter assay showed that miR-143-3p mimics attenuated the luciferase activity of COX-2-Wt rather than COX-2-Mut.western blot showed that miR-143-3p mimics decreased COX-2 protein expression in post-MI cells.We firstly explored the expression of COX-2 in post-MI cells transfected with si-LINC00528 and miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI patients treatment.	31833800	RID02829	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	
Malignant glioma	UPF1	CYTOR	negatively-F	RIP;starBase;Targetscan;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+);cell invasion(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000005007	NA	ENSG00000222041	GRCh38_2:87454781-87636740	5976	112597	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	C2orf59|LINC00152|MGC4677|NCRNA00152	UPF1 alleviates the progression of glioma via targeting lncRNA CYTOR. Relative levels of UPF1 and CYTOR in collected tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.Furthermore, RIP assay verified the interaction between UPF1 and CYTOR in glioma cells.UPF1 was downregulated in glioma tissues and cells.CYTOR was found to be up-regulated in glioma tissues.Here, the presence of binding sites in the promoter regions of Overexpression of UPF1 Suppressed the Proliferation and Invasion Abilities in Glioma.UPF1 and CYTOR was predicted through star-Base v2.0 and Targetscan. The overexpression of CYTOR abolished the inhibitory effect of UPF1 on glioma invasiveness, indicating that UPF1 suppresses the growth and invasiveness in glioma via targeting CYTOR. UPF1 is down-regulated in glioma and alleviates the progression of glioma via targeting CYTOR.	31799670	RID02830	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)
Colorectal cancer	SNHG14	KRAS	positively-E	siRNA;DianaTools;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	ceRNA(miR-944)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000133703	NA	104472715	3845	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	K-Ras4B|KRAS1|KRAS2	Long noncoding RNA SNHG14 accelerates cell proliferation, migration, invasion and suppresses apoptosis in colorectal cancer cells by targeting miR-944/KRAS axis through PI3K/AKT pathway.The expression of SNHG14 and miR-944 was analyzed by qRT-PCRto investigate the potential role of SNHG14 and miR-944 in CRC.Up-Regulation of SNHG14 While Down-Regulation of miR-944 in CRC. A significant decline of SNHG14 expression was noticed in SW620 and HCT116 cells transfected with si-SNHG14#1, si-SNHG14#2 and si-SNHG14#3, indicating high transfection efficiency. Depletion of SNHG14 Repressed Cell Proliferation, Migration, Invasion and Induced Apoptosis in CRC Cells by Blockage of PI3K/AKT Pathway.By searching from online database Diana- Tools, we observed that there were potential binding sites between SNHG14 and miR-944 (Figure 4A). Decreased luciferase activity in SW620 and HCT116 cells co-transfected with SNHG14 WT and miR-944 validated the interaction between SNHG14 and miR-944.SNHG14 was a Sponger of miR-944. Bioinformatics analysis by DianaTools predicted that miR-944 was capable of binding to 3'-untranslated regions (3'UTR) of KRAS. Luciferase activity reduced remarkably in SW620 and HCT116 cells co-transfected with KRAS 3'UTR WT and miR-944, manifesting the interaction between KRAS and miR-944.KRAS was a Target of miR-944 SNHG14 contributed to cell proliferation, migration and invasion, while suppressed apoptosis in CRC cells by targeting miR-944/KRAS axis through PI3K/AKT pathway, representing novel biomarkers for CRC therapy.	31799655	RID02831	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Hepatocellular carcinoma	ZFAS1	miR-193a-3p	negatively-F	shRNA;LncBase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 promotes hepatocellular carcinoma proliferation by epigenetically repressing miR-193a-3p.The ZFAS1 expression in 60 HCC patients tissues and 2 HCC cell lines was detected via RT-qPCR.Results showed that ZFAS1 was significantly up-regulated in HCC tissue samples compared to that of adjacent normal tissues.The results of the CCK8 assay showed that overexpression of ZFAS1 significantly enhanced the growth ability of HepG2 cells.Overexpression of ZFAS1 Promoted Proliferation of HepG2 HCC Cells.DIANA LncBASE Predicted v.2 was used to search for miRNAs that contained complementary base with ZFAS1.However, the expression of miR-193a-3p was markedly higher in sh-ZFAS1 cells than in control cells. Luciferase reporter gene assay revealed that co-transfection of ZFAS1-WT and miR-193a-3p largely decreased the luciferase activity.ZFAS1 could enhance the proliferation of HCC cells by suppressing miR- 193a-3p, which might be a potential therapeutic target in HCC.	31799651	RID02832	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Rheumatoid arthritis	PICSAR	miR-4701-5p	negatively-F	siRNA;starBase;LncBase;luciferase reporter assay	upregulation	qRT-PCR	GSE128813	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000275874	GRCh38_21:44999208-45004727	NA	NA	378825	NA	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	NA	LncRNA PICSAR promotes cell proliferation, migration and invasion of fibroblast-like synoviocytes by sponging miRNA-4701-5p in rheumatoid arthritis.The accession number is GSE128813.The microarray data (IncRNAs and mRNAs) were acquired from the two groups between RA-FLS and non-RA control FLSs. We analyzed the expression of these 5 IncRNAs by qRT-PCRand found that LINC001 62 (IncRNA PICSRA) was the one that was most significantly over-expressed compared to con- trol. We further performed PICSAR- siRNA silencing to determine whether the elevated IncRNA PICSAR expression on RA-FLSs was functional. The results suggested that PICSAR knockdown significantly decreased IL-6,IL-8 and MMP-3 production of RA-FLSs compared to the NC-siRNA control group.Suppression of PICSAR decreases the migration and invasion of RA- FLSs in vitro.To verify whether PICSAR could act as a ceRNA for a certain miRNA, the bioinformatics programs starBase v3.0 and LncBase v2, the most used high throughput AGO CLIP-Seq libraries, were used to seek miRNAs which may have interacted with PICSAR.To confirm the targeting relationship between PICSAR and miR -4701-5p, a luciferase reporter assay was conducted according to the predicted binding site.We further conducted the western blot to test whether the target protein of miR-4701-5p such as ST3Gal I expression could be affected by the differential expression of IncRNA PICSAR.Our results reveal PICSAR may exert an essential role in promoting synovial invasion and joint destruction by sponging miR-4701-5p in RA and that IncRNA PICSAR may act as a biomarker of RA.	31791845	RID02833	ceRNA or sponge	NA		
Multiple myeloma	UCA1	IL6R	positively-E	luciferase reporter assay;western blot;shRNA;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(+);JAK2/STAT3 signaling pathway(+)	ceRNA(miR-331-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000160712	NA	652995	3570	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CD126|gp80|IL-1Ra|IL-6R|IL6RA	Long noncoding RNA UCA1 regulates proliferation and apoptosis in multiple myeloma by targeting miR-331-3p/IL6R axis for the activation of JAK2/STAT3 pathway.The expression of UCA1 and miR-331-3p in MM tumors and the corresponding normal tissues were evaluated using qRT-PCRAs illustrated in Figure 1A-B, the expression of UCA1 was up-regulated, whereas miR-331-3p was down-regulated in MM tumors compared with normal tissues.Extremely high transfection efficiency was detected in NCI-H929, and RPMI- 8226 cells were stably transfected with sh- UCA1-1, sh-UCA1-2, and sh-NC.These findings implicated that deficiency of UCA1 inhibits cell proliferation and induces apoptosis in MM.Bioinformatics tool Star- Base2.0 displayed that miR-331-3p includes the binding sites of UCA1.Luciferase activity decreased in both NCI-H929 and RPMI-8226 cells transfected with WT-UCA1 and miR-331-3p compared with that of MUT-UCA1 group.All the data indicated that restoration of UCA1 promotes cell proliferation and inhibits apoptosis in MM.Based on bioinformatics analysis searched by StarBase2.0, miR-331-3p has the potential to bind to 3'UTR of UCA1.An evident reduction of luciferase activity was noticed in NCI-H929 and RPMI- 8226 cells co-transfected with IL6R 3'UTR WT and miR-331-3p.UCA1 accelerates proliferation and suppresses apoptosis in MM by targeting miR-331-3p/IL6R axis to activate JAK2/ STAT3 pathway, providing potential targets for the diagnosis and therapy of MM.	31773675	RID02834	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thoracoabdominal aorta aneurysm	LUCAT1	MYRF	positively-E	FISH;LncLocator;DIANA;starBase;luciferase reporter assay;RIP;overexpression;shRNA;microT;miRanda;miRmap;PITA;RNA22	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Aortic aneurysm	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000124920	NA	100505994	745	SCAL1|SCAT5	C11orf9|MRF|Ndt80|pqn-47	LUCAT1 contributes to MYRF-dependent smooth muscle cell apoptosis and may facilitate aneurysm formation via the sequestration of miR-199a-5p.LUCAT1 as an elevated lncRNA in AAA. However, the specific role of LUCAT1 in SMCs functions was a secret.At first, short hairpin RNAs (shRNAs) were transfected into SMCs against LUCAT1 and the inhibiting efficiency was validated by qRT-PCRassay.Next, LUCAT1 overexpressing vector (pcDNA3.1/LUCAT1) and control vector (pcDNA3.1) were transfected into SMCs.Altogether, LUCAT1 was proved anti-proliferative in SMCs.Compared with the non-targeting group, SMCs transfected with sh-LUCAT1#1/2 plasmids underwent caspase-3 activity and TUNEL assays.As presented in the TUNEL assay, increased LUCAT1 expression also propelled SMCs apoptosis. Collectively, LUCAT1 was proapoptotic in SMCs.Taking advantage of LncLocator prediction, the primary sublocalization of LUCAT1 was probed to be cytoplasmic.Experiment result from FISH assay was consistent to 3A, which indicated that abundance of LUCAT1 was in cytoplasmic of SMCs.Six potential miRNAs for LUCAT1 were predicted by DIANA and starbase.MiR-199a-5p was the most significant altered miRNA following LUCAT1 overexpression or inhibition.As detected in luciferase reporter assay, the co-transfection of miR-199a-5p mimics and LUCAT1-WT decreased the luciferase activity in SMCs (Figure 3E). RIP assay data described the abundant binding of LUCAT1 and miR-199a-5p in the anti-Ago2 group rather than in anti-IgG.Subsequently, seven bioinformatics tools (microT, miRanda, miRmap, PITA, and RNA22) unveiled two shared target genes (MYRF and TXLNB) of miR-199a-5p.Overexpressing LUCAT1 enhanced both mRNA and protein levels of MYRF and subsequent miR-199a-5p upregulation reversed the stimulating trend.All findings indicated that MYRF was a target of LUCAT1/miR-199a-5p.These findings unmasked that the pro-apoptosis impact of LUCAT1 in SMCs via directly targeting miR-199a-5p to elevate MYRF expression, which may provide valuable information on AAA prevention.	31769911	RID02835	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	NEAT1	CD276	negatively-F	shRNA;ELISA;luciferase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	JAK2/STAT3 signaling pathway(+);macrophage polarization(+)	ceRNA(miR-214)	regulation	RNA-protein	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000103855	NA	283131	80381	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	B7-H3|B7H3|B7RP-2	LncRNA NEAT1 sponges miR-214 to regulate M2 macrophage polarization by regulation of B7-H3 in multiple myeloma. The expression of NEAT1 and miR-214 was modified by transfection with the shNEAT1 or miR-214 inhibitor. The expression of NEAT1, miR-214 and B7-H3 in MM patient tissues and cells was analyzed by RTqPCR. ELISA assay was used to determine the release of B7-H3 in the supernatant of cell culture.The macrophage polarization markers were examined by RT-qPCR and western blot. The interaction between NEAT1, miR-214 and B7-H3 was analyzed by Dual- Luciferase reporter and RIP assays. AG490 was used to block the JAK2/STAT3 signaling. Co-culture of THP-1 and RPMI 8226 cells was used for macrophage polarization.NEAT1 and B7-H3 were up-regulated, but miR-214 was obviously down-regulated in MM patients. B7- H3, NEAT1 and miR-214 were associated with overall survival time of MM patients. NEAT1 silencing induced miR-214 and inhibited the expression and release of B7-H3 and then suppressed M2 macrophage polarization via inhibiting the JAK2/STAT3 signaling.NEAT1 promoted M2 macrophage polarization by sponging miR-214 and then regulating B7-H3, thus accelerating MM progression via the JAK2/STAT3 signaling pathway. Our study revealed novel mechanisms of M2 macrophage polarization and provided new potential clinical therapeutic targets for MM.	31731055	RID02836	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Osteosarcoma	DANCR	CDH2	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);p38/MAPK signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000170558	NA	57291	1000	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CD325|CDHN|NCAD	Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway.ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection.The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells.ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCRinduced inhibition of cell migration and invasion.Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.	31727012	RID02837	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Osteosarcoma	DANCR	CDH1	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);p38/MAPK signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000039068	NA	57291	999	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CD324|UVO|uvomorulin	Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway.ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection.The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells.ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCRinduced inhibition of cell migration and invasion.Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.	31727012	RID02838	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	DANCR	p-p38MAPK	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);p38/MAPK signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway.ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection.The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells.ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCRinduced inhibition of cell migration and invasion.Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.	31727012	RID02839	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Esophagus squamous cell carcinoma	SNHG8	KPNA2	negatively-F	siRNA;luciferase reporter assay;RIP;Targetscan;starBase;miRDB;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-411)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000262472	NA	100093630	3838	LINC00060|NCRNA00060	IPOA1|QIP2|RCH1|SRP1alpha	SNHG8 is upregulated in esophageal squamous cell carcinoma and directly sponges microRNA-411 to increase oncogenicity by upregulating KPNA2. SNHG8 expression in ESCC tissues and cell lines was determined via RT-qPCR.The data indicated that SNHG8 expression was much higher in ESCC tissues relative to the adjacent normal tissues.To assess the influence of SNHG8 on the malignant char- acteristics of ESCC, Eca109 and TE-1 cells were trans- fected with si-SNHG8 or si-scramble.These findings suggested that SNHG8 may exert an oncogenic action on the aggressiveness of ESCC cells in vitro.To test our hypothesis, the potential miRNAs sponged by SNHG8 were predicted by bioinformatics analysis.The luciferase reporter assay was carried out to gain more insights into the potential interaction between SNHG8 and miR-411.In addition, the RIP assay revealed that miR-411 and SNHG8 were notably enriched in Ago2 pellets but not in the IgG , indicating that miR-411 is an SNHG8-targeted miRNA.MiR-411 may have a tumor-suppressive function in the regula- tion of biological activities of ESCC.To elucidate the mechanisms underlying the activity of miR-411 in ESCC cells, online target exploratory software tools TargetScan, StarBase 3.0, and miRDB were employed to search for the putative target of miR-411.KPNA2 was noted (Figure 5A), and this prediction was verified by the luciferase reporter assay.In addition, we determined the expression of KPNA2 mRNA and protein in miR-411 overexpressing Eca109 and TE-1 cells.These results validated KPNA2 as a direct target of miR-411 in ESCC cells.SNHG8 may play oncogenic roles in the malignancy of ESCC by sponging miR-411 to increase KPNA2 expression. The SNHG8-miR-411-KPNA2 pathway may be a novel target for the treatment of patients with ESCC and offer potential biomarkers for the diagnosis and prognosis of ESCC.	31695414	RID02840	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	MYC	PVT1	positively-E	siRNA;ChIP	upregulation	qRT-PCR	TCGA;GSE45267	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000249859	GRCh38_8:127794526-128187101	4609	5820	bHLHe39|c-Myc|MYCC	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Silencing of lncRNA PVT1 by miR-214 inhibits the oncogenic GDF15 signaling and suppresses hepatocarcinogenesis. Silencing endogenous c-Myc could significantly inhibited PVT1 expression in both SMMC-7721 and HepG2 cells with c-Myc siRNAs.Consistently, there is an obvious c-Myc binding peak at the PVT1 promoter in HepG2 cells based on the ENCODE ChIP-seq data.Interestingly, we noticed that there was a potential, conserve P53 binding site (P53-RE) at 516bp upstream of the PVT1 transcription start site (TSS) predicted by Match 1.0 software based on the TRANSFAC matrix.Over-expressed P53 leads to significantly decreased PVT1 expression in both SMMC-7721 and HepG2 cells.EMSA assays demonstrated that P53-containing HepG2 nuclear extracts bound only to the biotin-labeled oligonucleotide probe with the PVT1 P53-RE or the P53 consensus sequence (P53-cons).In line with results, we did observe significantly negative expression correlation between P53 and PVT1 in HCC tissues (Fig. 1G), elucidating the transcriptional repressor role of P53 in PVT1 expression regulation.LncRNA PVT1 was significantly overexpressed in various cancerous tissues including liver hepatocellular carcinoma (LIHC) compared to the normal tissues.There are 4 line with the TCGA data, we also observed evidently upregulated PVT1 in HCC tissues compared to normal specimens in our cohort (P < 0.05) and a cohort of Taiwanese HCC individuals (GSE45267) (P < 0.01).To identify miRNAs suppressing PVT1 in HCC, we predicted potential candidate miRNAs by both the miRCode software and the RegRNA software.Dual luciferase reporter gene assays were then conducted to examine the potential miR-214-lncRNA interaction.Tumor growth rate of xenografts with elevated miR-214 (miR-214) or silenced PVT1 (shPVT1) was significantly suppressed compared to control xenografts.So the miR-214 inhibits HCC proliferation and invasion via suppressing lncRNA PVT1.To identify the downstream signaling pathway of the miR-214- PVT1 axis effect on HCC, we performed gene expression profiling of HepG2 cells transfected with NC RNA, miR-214 mimics, siPVT1-1 or siPVT1-2.We selectively validated twenty-one genes identified by microarray profiling using qRT-PCR(Fig. 4B), considering their potential involvement in HCC and other malignancies. Among these candidate downstream genes, GDF15, a crucial HCC driver gene, was choose to be investigated.silencing GDF15 expression with siRNAs (siGDF15-1 and siGDF15-2) was able to significantly inhibit proliferation of SMMC-7721 and HepG2 cells (all P < 0.01). Colony formation assays elucidated that knock-down GDF15 expression significantly suppressed clone formation of HCC cells.Consistently, there were significantly elevated GDF15 expression in HCC tissues compared to normal tissues in either TCGA LIHC samples or in an Italian prospective cohort (GSE54236). Interestingly, we also observed a significantly positive expression correlation between lncRNA PVT1 and GDF15 in the GSE54236 dataset.Collectively, our results show that the c-Myc/P53/miR-214-PVT1-GDF15 axis is implicated in HCC development, shedding light on the mechanistic actions of PVT1 and representing potential targets for HCC clinical intervention.	31677796	RID02841	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Hepatocellular carcinoma	TP53	PVT1	negatively-E	Match;EMSA	upregulation	qRT-PCR	TCGA;GSE45267	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000249859	GRCh38_8:127794526-128187101	7157	5820	LFS1|p53	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Silencing of lncRNA PVT1 by miR-214 inhibits the oncogenic GDF15 signaling and suppresses hepatocarcinogenesis. Silencing endogenous c-Myc could significantly inhibited PVT1 expression in both SMMC-7721 and HepG2 cells with c-Myc siRNAs.Consistently, there is an obvious c-Myc binding peak at the PVT1 promoter in HepG2 cells based on the ENCODE ChIP-seq data.Interestingly, we noticed that there was a potential, conserve P53 binding site (P53-RE) at 516bp upstream of the PVT1 transcription start site (TSS) predicted by Match 1.0 software based on the TRANSFAC matrix.Over-expressed P53 leads to significantly decreased PVT1 expression in both SMMC-7721 and HepG2 cells.EMSA assays demonstrated that P53-containing HepG2 nuclear extracts bound only to the biotin-labeled oligonucleotide probe with the PVT1 P53-RE or the P53 consensus sequence (P53-cons).In line with results, we did observe significantly negative expression correlation between P53 and PVT1 in HCC tissues (Fig. 1G), elucidating the transcriptional repressor role of P53 in PVT1 expression regulation.LncRNA PVT1 was significantly overexpressed in various cancerous tissues including liver hepatocellular carcinoma (LIHC) compared to the normal tissues.There are 4 line with the TCGA data, we also observed evidently upregulated PVT1 in HCC tissues compared to normal specimens in our cohort (P < 0.05) and a cohort of Taiwanese HCC individuals (GSE45267) (P < 0.01).To identify miRNAs suppressing PVT1 in HCC, we predicted potential candidate miRNAs by both the miRCode software and the RegRNA software.Dual luciferase reporter gene assays were then conducted to examine the potential miR-214-lncRNA interaction.Tumor growth rate of xenografts with elevated miR-214 (miR-214) or silenced PVT1 (shPVT1) was significantly suppressed compared to control xenografts.So the miR-214 inhibits HCC proliferation and invasion via suppressing lncRNA PVT1.To identify the downstream signaling pathway of the miR-214- PVT1 axis effect on HCC, we performed gene expression profiling of HepG2 cells transfected with NC RNA, miR-214 mimics, siPVT1-1 or siPVT1-2.We selectively validated twenty-one genes identified by microarray profiling using qRT-PCR(Fig. 4B), considering their potential involvement in HCC and other malignancies. Among these candidate downstream genes, GDF15, a crucial HCC driver gene, was choose to be investigated.silencing GDF15 expression with siRNAs (siGDF15-1 and siGDF15-2) was able to significantly inhibit proliferation of SMMC-7721 and HepG2 cells (all P < 0.01). Colony formation assays elucidated that knock-down GDF15 expression significantly suppressed clone formation of HCC cells.Consistently, there were significantly elevated GDF15 expression in HCC tissues compared to normal tissues in either TCGA LIHC samples or in an Italian prospective cohort (GSE54236). Interestingly, we also observed a significantly positive expression correlation between lncRNA PVT1 and GDF15 in the GSE54236 dataset.Collectively, our results show that the c-Myc/P53/miR-214-PVT1-GDF15 axis is implicated in HCC development, shedding light on the mechanistic actions of PVT1 and representing potential targets for HCC clinical intervention.	31677796	RID02842	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Hepatocellular carcinoma	miR-214	PVT1	negatively-F	miRcode;RegRNA;siRNA;luciferase reporter assay;shRNA;overexpression	upregulation	qRT-PCR	TCGA;GSE45267	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Silencing of lncRNA PVT1 by miR-214 inhibits the oncogenic GDF15 signaling and suppresses hepatocarcinogenesis. Silencing endogenous c-Myc could significantly inhibited PVT1 expression in both SMMC-7721 and HepG2 cells with c-Myc siRNAs.Consistently, there is an obvious c-Myc binding peak at the PVT1 promoter in HepG2 cells based on the ENCODE ChIP-seq data.Interestingly, we noticed that there was a potential, conserve P53 binding site (P53-RE) at 516bp upstream of the PVT1 transcription start site (TSS) predicted by Match 1.0 software based on the TRANSFAC matrix.Over-expressed P53 leads to significantly decreased PVT1 expression in both SMMC-7721 and HepG2 cells.EMSA assays demonstrated that P53-containing HepG2 nuclear extracts bound only to the biotin-labeled oligonucleotide probe with the PVT1 P53-RE or the P53 consensus sequence (P53-cons).In line with results, we did observe significantly negative expression correlation between P53 and PVT1 in HCC tissues (Fig. 1G), elucidating the transcriptional repressor role of P53 in PVT1 expression regulation.LncRNA PVT1 was significantly overexpressed in various cancerous tissues including liver hepatocellular carcinoma (LIHC) compared to the normal tissues.There are 4 line with the TCGA data, we also observed evidently upregulated PVT1 in HCC tissues compared to normal specimens in our cohort (P < 0.05) and a cohort of Taiwanese HCC individuals (GSE45267) (P < 0.01).To identify miRNAs suppressing PVT1 in HCC, we predicted potential candidate miRNAs by both the miRCode software and the RegRNA software.Dual luciferase reporter gene assays were then conducted to examine the potential miR-214-lncRNA interaction.Tumor growth rate of xenografts with elevated miR-214 (miR-214) or silenced PVT1 (shPVT1) was significantly suppressed compared to control xenografts.So the miR-214 inhibits HCC proliferation and invasion via suppressing lncRNA PVT1.To identify the downstream signaling pathway of the miR-214- PVT1 axis effect on HCC, we performed gene expression profiling of HepG2 cells transfected with NC RNA, miR-214 mimics, siPVT1-1 or siPVT1-2.We selectively validated twenty-one genes identified by microarray profiling using qRT-PCR(Fig. 4B), considering their potential involvement in HCC and other malignancies. Among these candidate downstream genes, GDF15, a crucial HCC driver gene, was choose to be investigated.silencing GDF15 expression with siRNAs (siGDF15-1 and siGDF15-2) was able to significantly inhibit proliferation of SMMC-7721 and HepG2 cells (all P < 0.01). Colony formation assays elucidated that knock-down GDF15 expression significantly suppressed clone formation of HCC cells.Consistently, there were significantly elevated GDF15 expression in HCC tissues compared to normal tissues in either TCGA LIHC samples or in an Italian prospective cohort (GSE54236). Interestingly, we also observed a significantly positive expression correlation between lncRNA PVT1 and GDF15 in the GSE54236 dataset.Collectively, our results show that the c-Myc/P53/miR-214-PVT1-GDF15 axis is implicated in HCC development, shedding light on the mechanistic actions of PVT1 and representing potential targets for HCC clinical intervention.	31677796	RID02843	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Ovarian cancer	PCAT1	NEK2	positively-E	siRNA;overexpression;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);WNT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000117650	NA	100750225	4751	PCA1|PCAT-1|PiHL	NEK2A|NLK1|PPP1R111|RP67	PCAT1 promotes the proliferative and migratory potentials of ovarian cancer via targeting NEK2PCAT1 promotes the proliferative and migratory potentials of ovarian cancer via targeting NEK2.Expression levels of PCAT1 and NEK2 in OC tissues and cell lines were detected by quantitative Real-time polymerase chain reaction (qRT-PCR.Knockdown or over-expression of PCAT1 and NEK2 were achieved by siRNA or lentivirus transfection, respectively. Subsequently, cell viability, apoptosis, cell cycle progression and migration were determined by cell counting kit-8 (CCK-8), flow cytometry and transwell assay, respectively.Furthermore, the protein levels of relative genes in Wnt pathway were detected by western blot.PCAT1 was highly expressed in OC tissues and cell lines, especially in tumor tissues with stage III-IV compared with stage I-II.In vitro experiments confirmed that PCAT1 knockdown obviously inhibited proliferative and migratory potentials, whereas induced apoptosis of OC cells.Meanwhile, overexpression of PCAT1 remarkably upregulated the expression level of NEK2, which was the target gene of PCAT1. Interestingly, NEK2 knockdown could obviously suppress cell migration. Furthermore, western blot results elucidated that PCAT1 knockdown could inhibit the protein levels of relative genes in Wnt pathway in OC cells.Meanwhile, overexpression of PCAT1 remarkably upregulated the expression level of NEK2, which was the target gene of PCAT1. Interestingly, NEK2 knockdown could obviously suppress cell migration. Furthermore, western blot results elucidated that PCAT1 knockdown could inhibit the protein levels of relative genes in Wnt pathway in OC cells.	31646554	RID02844	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807,GSE67939)
Osteoarthritis	HOTAIR	miR-130a-3p	negatively-F	luciferase reporter assay;siRNA;overexpression;starBase;RIP	upregulation	RT-PCR	NA	NA	apoptosis process(+);cell viability(-);cell growth(-);cell autophagy(-);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR-induced apoptosis is mediated by sponging miR-130a-3p to repress chondrocyte autophagy in knee osteoarthritis.The levels of HOTAIR mRNA were significantly elevated in the OA resection regions compared to unaffected cartilage samples.By using chondrocytes as an in vitro model, we silenced and overexpressed the HOTAIR gene, respectively, by siRNA interference and pcDNA3.0-HOTAIR transfection, and then assessed the role of HOTAIR on the cell apoptosis.Results of EdU assays showed that chondrocyte proliferation was enhanced by siHOTAIR transfection and inhibited by HOTAIR overexpression.Upregulation of HOTAIR expression could induce cartilage degradation.We selected the top four potential HOTAIR target miRNAs as predicted by the Starbase platform.We preformed RT-PCRto analyze the levels of miR-130a- 3p expression that accompanied the silencing or overexpression of HOTAIR in chondrocytes, and also conducted dual-luciferase reporter assays to detect HOTAIR-targeted miR-130a-3p.We have performed the RNA immunoprecipitation and the enrichment of miR-130a-3p and HOTAIR in AGO2- containing miRNPs on chondrocytes compared with its expression in control IgG immunoprecipitates was found.Our results showed a reciprocal regulatory effect of HOTAIR on miR-130a-3p, suggesting that HOTAIRadsorbed miR-130a-3p to isolate its binding site and inhibit its expression.Overall, our data revealed that aberrantly high expression of HOTAIR resulted in massive apoptosis events caused by the sponging of miR-130a-3p to suppress autophagy in chondrocytes, which, in turn, might trigger KOA. Therefore, inhibition of HOTAIR-mediated apoptosis might be a potential mechanism that can be targeted by gene therapy of KOA.	31642563	RID02845	ceRNA or sponge	NA		
Cervical cancer	LINC00467	KIF23	positively-E	siRNA;starBase;RAID;western blot;luciferase reporter assay;Targetscan;LncTBD;RIP;RNA pull-down assay;overexpression	upregulation	microarray;RT-qPCR	GSE7803;GSE9750;GSE63514	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);tumorigenesis(+)	ceRNA(miR-107)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000137807	NA	84791	9493	C1orf97|MGC14801	KNSL5|MKLP-1|MKLP1	Long Intervening Noncoding 00467 RNA Contributes to tumorigenesis by Acting as a Competing Endogenous RNA against miR-107 in Cervical Cancer Cells.microarray-based analyses on cervical cancererelated microarrays GSE7803 and GSE9750 revealed that KIF23 was highly expressed in cervical cancer. The Starbase website speculated that miR- 107, miR-15a-5p, and miR-103a-3p might be the target miRNAs for KIF23. In addition, RAID version 2.0 website further verified the existence of a binding site between miR-107 and LINC00467. Furthermore, the GSE63514 microarray revealed that the expression of LINC00467 in cervical cancer was significantly higher compared with adjacent normal tissues. The results of RT-qPCR and western blotshowed that the expression of LINC00467 and KIF23 was increased, whereas that of miR-107 was decreased, in cervical cancer in comparison with the adjacent normal tissues.These results suggested that LINC00467 might play a crucial role in the progression of cervical cancer by regulating the KIF23 expression.Compared with the blank group, there were no significant differences in the expression of EMT-related proteins (N-cadherin and E-cadherin) in the si-LINC00467 NC and LINC00467 NC groups.Compared with the blank group, there were no significant differences in the expression of EMT-related proteins (N-cadherin and E-cadherin) in the si-LINC00467 NC and LINC00467 NC groups.The online prediction webites TargetScan and LncTBD revealed that there were binding sites between LINC00467 and miR-107, and between the 30 untranslated region in KIF23 and miR-107, suggesting that miR-107 could bind to LINC00467 and KIF23 independently. Moreover, results from dualluciferase reporter gene assay showed that luciferase activity was significantly diminished in the miR-107 mimic group versus the NC group in LINC00467-WT plasmids.Furthermore, the results of RIP and RNA pull-down assays showed that WT-miR-107 enriched more LINC00467 compared with MUT-miR-107 and bio-NC, which further validated that LINC00467 binds to miR-107.Thus, the above results indicated that LINC00467 competitively binds to miR-107 to regulateKIF23.Cell proliferation, migration, invasion, and EMT in vitro were inhibited as a result of lentiviral-mediated LINC00467 knockdown and miR-107 overexpression in cervical cancer. In addition, LINC00467 silencing or miR-107 up-regulation repressed tumorigenic ability in xenograft tumor-bearing nude mice in cervical cancer in vivo. LINC00467 silencing or miR-107 up-regulation may serve as novel potential strategies for the treatment of cervical cancer.	31640853	RID02846	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Prostate cancer	SOX2-OT	CFL2	positively-E	FISH;starBase;DIANA;luciferase reporter assay;RIP;microT;miRmap;PicTar;Targetscan;shRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);cell migration(+)	ceRNA(miR-369-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000165410	NA	347689	1073	DKFZp761J1324|NCRNA00043|SOX2OT	NEM7	Long noncoding RNA SOX2-OT facilitates prostate cancer cell proliferation and migration via miR-369-3p/CFL2 axis. Herein, we applied RT-qPCR to measure the expression of SOX2-OT in PC tissue samples and PC cells. In comparison with neighboring normal tissues, SOX2-OT expression was significantly increased in PC tissues.With the intention of deciphering the potential mechanism of SOX2-OT in PC, we first adopted subcellular fractionation and FISH analyses to detect the localization of SOX2-OT in cytoplasm and nucleus of PC cells. The result suggested that SOX2-OT was majorly distributed in cytoplasm of PC3 and DU145 cells.Subsequently, through the prediction of starBase and DIANA databases, miR-143-3p and miR-369-3p was discovered to have the binding ability with SOX2- OT.Then luciferase reporter assay delineated a dramatically decreased luciferase activity of pmirGLO-SOX2-OTWT induced by upregulation of miR-369-3p in PC3 and DU145 cells.Moreover, a significant enrichment of SOX2-OT and miR-369-3p in anti-Ago2 group was observed through RIP analysis, further verifying that SOX2-OT could bind with miR-369-3p in PC3 and DU145 cells.According to the data from five databases (microT, miRmap, PITA, PicTar, TagetScan), venn diagramwas drawn and showed the candidate mRNA that could bind with miR-369-3p in Fig. 3A. Then RIP assay displayed that SOX2-OT, miR-369-3p and CFL2 were aggregated in Ago2 antibody, hinting that they all existed in RNA-induced silencing complex (RISC) in PC3 and DU145 cells.Moreover, a binding site between miR-369-3p and CFL2 was predicted by starBase.Due to the better knockdown efficiency of CFL2 by transfection with sh-CFL2#1, sh-CFL2#1 was utilized in the following tests.To sum up, SOX2-OT accelerates cell proliferation and migration by targeting miR-369-3p/CFL2 axis in PC.	31623830	RID02847	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Breast cancer	LINC00673	MARK4	positively-E	LncBook;Targetscan;luciferase reporter assay;siRNA;overexpression	upregulation	qRT-PCR;sequencing	GSE133331;TCGA;MiTranscriptome	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);cell migration(+);Hippo signaling pathway(+);cell growth(+)	ceRNA(miR-515-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000007047	NA	100499467	57787	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	FLJ90097|KIAA1860|MARKL1|Nbla00650|PAR-1D	LINC00673 is activated by YY1 and promotes the proliferation of breast cancer cells via the miR-515-5p/MARK4/Hippo signaling pathway. To investigate the expression of LINC00673 in breast cancer, the MiTranscriptome database was applied, and LINC00673 was expressed at higher levels in breast cancer samples than in normal breast tissues . This finding was further validated by TCGA breast cancer data showing that LINC00673 was upregulated in breast cancer tissues compared to normal tissues.These results showed that LINC00673 expression was markedly increased in tumor tissues compared with normal tissues.Moreover, the knockdown of LINC00673 enhanced bax expression and reduced bcl-2 and cyclin D1 levels in breast cancer cells, confirming that LINC00673 is involved in apoptosis and cell cycle progression.We used both the LncBook and TargetScan databases to search for miRNAs that could be closely associated with LINC00673 and MARK4, and together these databases identified 258 miRNAs that may act as targets of LINC00673 and MARK4.Among these miRNAs, we verified that the expression of 18 miRNAs were significantly increased by the knockdown of LINC00673.We verified that the knockdown of LINC00673 negatively regulated miR- 515-5p in both MDA-MB-231 and MDA-MB-453 cells.Dual-luciferase assays indicated that there was a significant reduction in luciferase activities after the cotransfection of miR-515-5p mimics and a wild-type LINC00673 or MARK4 reporter vector, but this reduction was not observed with the transfection of mutant LINC00673 and MARK4 reporter vectors.Finally, the treatment of MDA-MB-231 and MDA-MB-453 cells with si-LINC00673 and miR- 515-5p inhibitors attenuated the reduction in MARK4, YAP and TAZ mRNA transcript levels caused by LINC00673 knockdown.Similarly, the cotransfection of cells with Lv-LINC00673 and the miR-515-5p mimic attenuated the LINC00673-mediated increasein cell proliferation.In summary, these results showed that LINC00673 promoted tumor cell growth at least in part by acting as a ceRNA for miR-515-5p and thus regulating the MARK4/Hippo signaling pathways.To further examine the transcriptional regulation model of LINC00673 in breast cancer, we searched the TRAN SFAC and JASPAR databases to identify transcription factors that may regulate LINC00673.To explore whether LINC00673 is a downstream target of YY1, we knocked down YY1 by siRNA in MDAMB- 231 cells, which led to a significant decrease in LINC00673 expression.Moreover, ChIP assays showed that the LINC00673 promoter was specifically pulled down by a YY1-specific antibody but not the control antibody. Taken together, these findings suggest that YY1 is a bona fide transcriptional activator of LINC00673.YY1-activated LINC00673 may exert an oncogenic function by acting as a sponge for miR-515-5p to upregulate the MARK4 and then inhibit Hippo signaling pathway, and may serve as a potential therapeutic target.	31623640	RID02848	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978,GSE41245)
Breast cancer	YY1	LINC00673	positively-E	TRANSFAC;JASPAR;siRNA;ChIP	upregulation	qRT-PCR;sequencing	GSE133331;TCGA;MiTranscriptome	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);cell migration(+);Hippo signaling pathway(+);cell growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000227036	GRCh38_17:72290091-72640472	7528	100499467	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	LINC00673 is activated by YY1 and promotes the proliferation of breast cancer cells via the miR-515-5p/MARK4/Hippo signaling pathway. To investigate the expression of LINC00673 in breast cancer, the MiTranscriptome database was applied, and LINC00673 was expressed at higher levels in breast cancer samples than in normal breast tissues . This finding was further validated by TCGA breast cancer data showing that LINC00673 was upregulated in breast cancer tissues compared to normal tissues.These results showed that LINC00673 expression was markedly increased in tumor tissues compared with normal tissues.Moreover, the knockdown of LINC00673 enhanced bax expression and reduced bcl-2 and cyclin D1 levels in breast cancer cells, confirming that LINC00673 is involved in apoptosis and cell cycle progression.We used both the LncBook and TargetScan databases to search for miRNAs that could be closely associated with LINC00673 and MARK4, and together these databases identified 258 miRNAs that may act as targets of LINC00673 and MARK4.Among these miRNAs, we verified that the expression of 18 miRNAs were significantly increased by the knockdown of LINC00673.We verified that the knockdown of LINC00673 negatively regulated miR- 515-5p in both MDA-MB-231 and MDA-MB-453 cells.Dual-luciferase assays indicated that there was a significant reduction in luciferase activities after the cotransfection of miR-515-5p mimics and a wild-type LINC00673 or MARK4 reporter vector, but this reduction was not observed with the transfection of mutant LINC00673 and MARK4 reporter vectors.Finally, the treatment of MDA-MB-231 and MDA-MB-453 cells with si-LINC00673 and miR- 515-5p inhibitors attenuated the reduction in MARK4, YAP and TAZ mRNA transcript levels caused by LINC00673 knockdown.Similarly, the cotransfection of cells with Lv-LINC00673 and the miR-515-5p mimic attenuated the LINC00673-mediated increasein cell proliferation.In summary, these results showed that LINC00673 promoted tumor cell growth at least in part by acting as a ceRNA for miR-515-5p and thus regulating the MARK4/Hippo signaling pathways.To further examine the transcriptional regulation model of LINC00673 in breast cancer, we searched the TRAN SFAC and JASPAR databases to identify transcription factors that may regulate LINC00673.To explore whether LINC00673 is a downstream target of YY1, we knocked down YY1 by siRNA in MDAMB- 231 cells, which led to a significant decrease in LINC00673 expression.Moreover, ChIP assays showed that the LINC00673 promoter was specifically pulled down by a YY1-specific antibody but not the control antibody. Taken together, these findings suggest that YY1 is a bona fide transcriptional activator of LINC00673.YY1-activated LINC00673 may exert an oncogenic function by acting as a sponge for miR-515-5p to upregulate the MARK4 and then inhibit Hippo signaling pathway, and may serve as a potential therapeutic target.	31623640	RID02849	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	
Esophageal cancer	ADAMTS9-AS2	CDH3	negatively-E	immunohistochemical staining;western blot;overexpression;shRNA;lncATLAS;FISH;MethPrimer;RPIseq;RIP;RNA pull-down assay;ChIP	downregulation	RT-qPCR	GSE45670	NA	cell proliferation(+);cell invasion(+);cell migration(+)	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000062038	NA	100507098	1001	NA	CDHP|PCAD	Long noncoding RNA ADAMTS9-AS2 suppresses the progression of esophageal cancer by mediating CDH3 promoter methylation.Analysis of the gene expression data set GSE45670 revealed that the lncRNA ADAMTS9-AS2 was significantly downregulated in esophageal cancer.The results of RT-qPCR showed that esophageal cancer tissues exhibited relatively lower expressions of ADAMTS9-AS2 compared to adjacent normal tissues.To investigate the impact of ADAMTS9-AS2 on cancer cells, we established the ADAMTS9-AS2 overexpressed (oe-ADAMTS9-AS2) OE21 cell line. Compared with sh-NC treatment, sh-ADAMTS9-AS2-1 treatment, and sh-ADAMTS9-AS2-2 treatment led to decreased expressions of ADAMTS9-AS2, while sh-ADAMTS9-AS2-1 reached about 80% interference efficiency; therefore, sh-ADAMTS9-AS2-1 was selected for further experiments.Overexpression of ADAMTS9-AS2 inhibits proliferation, invasion and migration of esophageal cancer cells.We found that the expression of CDH3 was negatively associated with that of ADAMTS9-AS2.Following the correlation analysis, the expression of CDH3 in esophageal cancer tissues was determined by immunohistochemical staining and western blot Our results revealed that esophageal cancer tissues presented with higher expressions of CDH3 compared to adjacent normal tissues.To further investigate how ADAMTS9-AS2 regulates CDH3 expression, we applied the lncATLAS website  to predict the subcellular localization of ADAMTS9-AS2.Consistent with the prediction from the lncATLAS website, the FISH assay findings demonstrated that ADAMTS9-AS2 was mainly located in the nucleus of the esophageal cancer cell line OE21.Subsequently, CpG islands in CDH3 promoter region were predicted using the MethPrimer website, the results of which revealed that CPG islands existed in the CDH3 promoter region.We then investigated whether ADAMTS9-AS2 affected the expression of CDH3 by mediating the methylation levels of the CDH3 promoter.Additionally, by analyzing the RPIseq database , we found the binding relationship between ADAMTS9-AS2 and the sequences of DNA methyltransferases DNMT1, DNM3A and DNM3B. Next, the RIP assay was applied to confirm the interaction between ADAMTS9-AS2 and DNMT1/DNMT3.Meanwhile, RNA pull-down results revealed that ADAMTS9-AS2 directly bound to DNMT1, DNMT3A, and DNMT3B, further verifying the binding relationship between DNMT1/ DNMT3 (A/B) and ADAMTS9-AS2.In addition, ChIP results showed that the expression of CDH3 promoter region was increased in the experiment groups in comparison to IgG treatment, suggesting that DNMT1/DNMT3 (A/B) was enriched in the promoter region of CDH3.The above-mentioned results indicated that ADAMTS9-AS2 recruited DNMT1/DNMT3 (A/B) to the CDH3 promoter, which led to hypomethylation of CpG sites and inhibited CDH3 transcription.Overexpressed ADAMTS9-AS2 aids in the suppression of esophageal cancer development, which is achieved via inducing CDH3 promoter methylation.	31621118	RID02850	epigenetic regulation	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065)
Gastric cancer	NEAT1	EZH2	positively-E	miRcode;luciferase reporter assay;Targetscan;shRNA;overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell viability(+);apoptosis process(-)	ceRNA(miR-26a;miR-26b)	regulation	RNA-protein	Oxaliplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ENX-1|EZH1|KMT6|KMT6A	Upregulation of nuclear-enriched abundant transcript 1 confers oxaliplatin resistance to gastric cancer.NEAT1 was upregulated in oxaliplatin-resistant GC cells.The cell viabilities of NEAT1 knockdown cells were significantly decreased in comparison with cells transfected with control shRNA.Interestingly, we also observed that NEAT1 silencing in oxaliplatin-resistant GC cells resulted in a higher percentage of apoptotic cells with oxaliplatin treatment in comparison with normal GC cells transfected with NEAT1 shRNA.These results supported that knockdown of NEAT1 resulted in oxaliplatin resistance in GC cells.In addition, colony formation assays also demonstrated that cells including HGC-27 and BGC-823 with NEAT1 overexpression formed higher numbers of colonies in comparison with cells transfected with the control plasmid.We then predicted the possible targets of NEAT1 using MiRcode.MiR-26-5p including miR-26a-5p and miR-26b-5p were identified as targets of NEAT1.Mutated NEAT1 (NEAT1-MUT) were incorporated into luciferase reporter vector and then the cells were co-transfected with miR-26a, miR-26b, or miR-control.We next explored the possible targets of miR-26 using Targetscan. EZH2 was identified as a target of both miR-26a and miR-26b.Interestingly, we found that the expressions of EZH2 were increased in the cells transfected with the plasmid containing NEAT1 sequence and the expressions of EZH2 were decreased in the cells transfected with the plasmid containing shNEAT1 sequence (Figures 5E and 5F), indicating that theoverexpression of NEAT1 attenuated the inhibitory effects of miR-26 on EZH2.The roles of NEAT1 in the regulation of oxaliplatin resistance to GC are in part by ameliorating the inhibitory effect of miR-26 on EZH2.	31617275	RID02851	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	LINC01342	HIF3A	positively-E	RIP;DIANA;miRDB;luciferase reporter assay	upregulation	microarray;qRT-PCR	GSE38666	NA	cell proliferation(+);cell metastasis(+);colony formation(+);cell migration(+)	ceRNA(miR-30c-2-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000223823	GRCh38_1:1137017-1144056	ENSG00000124440	NA	254099	64344	NA	bHLHe17|IPAS|MOP7|PASD7	LINC01342 promotes the progression of ovarian cancer by absorbing microRNA-30c-2-3p to upregulate HIF3A.By analyzing the expression profile in GSE38666, LINC01342 was remarkably upregulated in OC tissue compared with its level in the normal tissue.A subcellular distribution analysis showed that LINC01342 was mainly enriched in the cytoplasm of OC cells. Prediction of target genes of LINC01342 via the Diana and miRDB algorithms revealed 17 potential target miRNAs. The qRT-PCRdata showed that microRNA-30c-2-3p and miR-30c-1-3p were markedly downregulated in A2780 and H08910 cells.The silencing of LINC01342 suppressed the proliferative and metastatic capacities of A2780 and H08910 cells.The silencing of microRNA-30c-2-3p enhanced the clonality and migratory capacity of OC cells.An RNA binding protein immunoprecipitation assay showed that microRNA-30c-2-3p, LINC01342, and HIF3A could bind to argonaute RISC catalytic component 2.The overexpression of HIF3A reversed the inhibited migration and clonality in QC cells with LINC01342 knockdown.In short, the upregulated LINC01342 in OC absorbs microRNA-30c-2-3p to release HIF3A. Thus, upregulated HIF3A expression accelerates the progression of OC.	31595977	RID02852	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	LINC00205	EPHX1	positively-E	shRNA;overexpression;Targetscan;starBase;luciferase reporter assay;RegRNA;siRNA	downregulation	qRT-PCR	NA	NA	cell migration(+);apoptosis process(-);cell growth(+)	ceRNA(miR-184)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223768	GRCh38_21:45288035-45297806	ENSG00000143819	NA	642852	2052	NCRNA00205	EPHX	LINC00205 modulates the expression of EPHX1 through the inhibition of miR-184 in hepatocellular carcinoma as a ceRNA.Several studies have shown that low expression of epoxide hydrolase 1 (EPHX1) is closely associated with varying human cancers, including hepatocellular carcinoma (HCC).Bioinformatics databases (TargetScan and starBase) were used to predict putative miRNAs that may regulate the expression of EPHX1. As shown in Figure 1a, miR-184 was predicted as a potential regulatory factor for EPHX1. The luciferase activity assay showed that the miR-184 mimics significantly reduced WT EPHX1 3'-UTR reporter activity in comparison with the NC mimics but did not block MUT EPHX1 3'-UTR reporter activity.Putative interacting lncRNAs were searched in the online database starBase and RegRNA It was predicted that LINC00205 was a potential interacting lncRNA of miR-184. In addition, miR-184 impeded the luciferase activity of WT LINC00205 rather than that of the MUT, denoting that LINC00205 directly binds to miR-184.The expression of LINC00205 in both tumor and normal tissues via qRTPCR, which revealed that in comparison with that in normal tissues, the LINC00205 expression was remarkably decreased in tumor tissues and displayed a negative association with the miR-184 expression level in tumors.HepG2 cells were cotransfected with si-LINC00205 (or si-NC) and the miR-184 inhibitor (or inhibitor control) for evaluating the regulatory role of LINC00205/miR-184 in biological processes.The LINC00205/miR-184 axis regulated cell growth, apoptosis, and migration.Taken together, the results of this study suggest that as a competing endogenous RNA, LINC00205 may regulate EPHX1 by inhibiting miR-184 in the progression of HCC and that targeting the LINC00205/miR-184/ EPHX1 axis may provide a treatment protocol for patients.	31566711	RID02853	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Cholangiocarcinoma	ZFAS1	USF1	positively-E	luciferase reporter assay;western blot;Targetscan;siRNA;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-296-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000158773	NA	441951	7391	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	bHLHb11|MLTFI|UEF	Up-regulation of ZFAS1 indicates dismal prognosis for cholangiocarcinoma and promotes proliferation and metastasis by modulating USF1 via miR-296-5p. To investigate the transcription level of ZFAS1 in paired CCA and adjacent normal tissues, quantitative real-time PCR was carried out to quantify ZFAS1 expression. The results showed that ZFAS1 was significantly overexpressed in CCA tissues.ZFAS1 is overexpressed in CCA cell lines and knockdown of ZFAS1 inhibits cell proliferation migration and invasion in vitro and in vivo.Wild and mutant ZFAS1 sequences were inserted into pmirGLO reporter, and the luciferase activity in CCLP-1 and RBE cells were cotransfected with miR-296-5p mimics or miR-NC and pmirGLO-ZFAS1-WT or pmirGLO-ZFAS1-Mut.And the binding motif of miR-296-5p and USF1 3'UTR was predicted by TargetScan database.Next step, shZFAS1, si-ZFAS1-1, miR-296-5p inhibitor (inh-miR-296-5p) and related negative controls were conducted in vivo which reflected the tumour-promoting role in both growing speed and tumour weight. And western blot with CCLP-1 cell demonstrated the evidence of ZFAS1/miR-296-5p/ USF1 axis. So that, knockdown of ZFAS1 decreased miR-296-5p but increased USF1, and either of ZFAS1 and miR-296-5p or miR-296-5p and USF1 3'UTR could bind directly.In the present study, we predicted that the potential transcription factor USF1 could bind to ZFAS1 promoter region at two binding sites E1 (-1878 to -1872) and E2 (-1530 to -1524) with relative high scores by using JASPAR database. After that, we assessed the binding motifs of several recently discovered CCA-related lncRNAs-promoters by JASPAR and found USF1 might bind some lncRNAs-promoters with relative high scores to activate oncogenic lncRNAs.In conclusion, ZFAS1 might promote cholangiocarcinoma proliferation and metastasis by modulating USF1 via miR-296-5p.	31565837	RID02854	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	USF1	ZFAS1	positively-E	JASPAR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	TF	lncRNA	ENSG00000158773	NA	ENSG00000177410	GRCh38_20:49278178-49299600	7391	441951	bHLHb11|MLTFI|UEF	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	Up-regulation of ZFAS1 indicates dismal prognosis for cholangiocarcinoma and promotes proliferation and metastasis by modulating USF1 via miR-296-5p. To investigate the transcription level of ZFAS1 in paired CCA and adjacent normal tissues, quantitative real-time PCR was carried out to quantify ZFAS1 expression. The results showed that ZFAS1 was significantly overexpressed in CCA tissues.ZFAS1 is overexpressed in CCA cell lines and knockdown of ZFAS1 inhibits cell proliferation migration and invasion in vitro and in vivo.Wild and mutant ZFAS1 sequences were inserted into pmirGLO reporter, and the luciferase activity in CCLP-1 and RBE cells were cotransfected with miR-296-5p mimics or miR-NC and pmirGLO-ZFAS1-WT or pmirGLO-ZFAS1-Mut.And the binding motif of miR-296-5p and USF1 3'UTR was predicted by TargetScan database.Next step, shZFAS1, si-ZFAS1-1, miR-296-5p inhibitor (inh-miR-296-5p) and related negative controls were conducted in vivo which reflected the tumour-promoting role in both growing speed and tumour weight. And western blot with CCLP-1 cell demonstrated the evidence of ZFAS1/miR-296-5p/ USF1 axis. So that, knockdown of ZFAS1 decreased miR-296-5p but increased USF1, and either of ZFAS1 and miR-296-5p or miR-296-5p and USF1 3'UTR could bind directly.In the present study, we predicted that the potential transcription factor USF1 could bind to ZFAS1 promoter region at two binding sites E1 (-1878 to -1872) and E2 (-1530 to -1524) with relative high scores by using JASPAR database. After that, we assessed the binding motifs of several recently discovered CCA-related lncRNAs-promoters by JASPAR and found USF1 might bind some lncRNAs-promoters with relative high scores to activate oncogenic lncRNAs.In conclusion, ZFAS1 might promote cholangiocarcinoma proliferation and metastasis by modulating USF1 via miR-296-5p.	31565837	RID02855	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Pituitary neuroendocrine tumor	XIST	FGF2	positively-E	siRNA;DIANA;RAID;FISH;luciferase reporter assay;RIP;RNA pull-down assay;immunohistochemistry	upregulation	microarray;RT-qPCR	GSE51618	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-424-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000138685	NA	7503	2247	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	FGFB	LncRNA XIST depletion prevents cancer progression in invasive pituitary neuroendocrine tumor by inhibiting bFGF via upregulation of microRNA-424-5p.At first, microarray analysis was used to screen the invasive PitNET-related lncRNAs. From the invasive PitNET-related lncRNA expression dataset GSE51618, lncRNA XIST with high expression at a large FC in invasive PitNET was exhibited as the candidate lncRNAs. In addition, a prior study revealed that siRNA-mediated bFGF gene silencing has the potential to inhibit the proliferation, migration and invasion of human PitNET cells.Besides, the DIANA TOOLS with score <<-.95 and RAID v2.0 with score <<-.5 databases were employed to explore whether XIST could act as a ceRNA of miRNA to regulate bFGF, finding that both XIST and bFGF had hsa- miR-424-5p binding sites. MiR-424 was found to inhibit the progression of cervical cancer.Therefore, we speculate that XIST may act as a ceRNA of miR-424-5p to regulate the expression of bFGF, thus influencing cell prolif- eration and invasion in invasive PitNET.For the purpose of exploring whether XIST was dysregulated in invasive PitNET, RT-qPCR was performed to determine the expression of XIST in normal pituitary tissues, non- invasive PitNET tissues, and invasive PitNET tissues.There existed binding sites between miR-424-5p and bFGF, miR-424-5p and XIST predicted by RAID v2.0, which was then verified by dual-luciferase reporter gene assay.Moreover, the RNA-pull down test reflected that the relative enrichment of miR-424-5p was relatively high in the cells transfected with Bio-Wt-XIST, while no changes were found in the cells transfected with Bio-Mut-XIST, proving that Bio-Wt-XIST may potentially promote the enrichment of miR-424-5p. RIP results depicted that the expression of XIST binding to AGO2 increased, indicating that XIST could bind AGO2 protein.Immunohistochemistry imaging further indicated that bFGF was mainly located in the nucleus and the positive rate of bFGF was increased in invasive PitNET tissues.All in all, XIST could serve as a ceRNA of miR-424-5p to elevate the expression of bFGF.Up-regulated miR-424-5p inhibits proliferation, migration and invasion, and promotes cell cycle arrest and apoptosis of invasive PitNET cells by decreasing bFGF expression.	31564894	RID02856	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	LINC00473	HMGA2	positively-E	luciferase reporter assay;RIP;overexpression;western blot	upregulation	qPCR	NA	NA	cell viability(+)cell proliferation(+);colony formation(+);apoptosis process(-);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000223414	NA	ENSG00000149948	NA	90632	8091	C6orf176|LNC473|bA142J11.1	BABL|HMGIC|LIPO	LINC00473 promotes hepatocellular carcinoma progression via acting as a ceRNA for microRNA-195 and increasing HMGA2 expression.qPCR assays exhibited the LINC00473 was highly expressed in HCC cell lines.HCC cell viability was significantly slowed down by loss of LINC00473 as suggested by CCK-8 assays. Foe another, the data of EdU experiments demonstrated that Huh-7 and HepG2 cell proliferation was restrained by the knockdown of LINC00473.Loss of LINC00473 prevented HCC cell colony formation and induced cell apoptosis.Inhibition of LINC00473 repressed HCC cell migration and invasion.Luciferase reporter plasmids of WT-LINC00473 and MUT-LINC00473 were constructed.Subsequently, to validate whether LINC00473 can sponge miR-195, RIP experiment was conducted.We found that overexpression of miR-195 inhibited HMGA2 mRNA expression in HCC cells.western blot assays indicated that HMGA2 protein level was inhibited by LV-shLINC00473 and miR-195 inhibitors demonstrated an opposite process.Silence of LINC00473 repressed HCC progression in vivo.Taken all these together, our study revealed the significance of LINC00473/miR-195/HMGA2 signaling axis for the first time in HCC progression. It was suggested the potential possibility of LINC00473 as an indicator for HCC.	31562977	RID02857	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Chronic obstructive pulmonary disease	TUG1	DUSP6	positively-E	knockdown;luciferase reporter assay;overexpression	upregulation	qRT-PCR	NA	NA	inflammatory response(+);fibrotic(+)	ceRNA(miR-145-5p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000139318	NA	55000	1848	FLJ20618|LINC00080|NCRNA00080	MKP-3|PYST1	Long non-coding RNA TUG1 promotes airway remodelling by suppressing the miR-145-5p/DUSP6 axis in cigarette smoke-induced COPD.To determine whether TUG1 expression was associated with COPD and identify its possible correlation with airway remodelling, we performed qRT-PCRTUG1 levels increased significantly as COPD progressed.Knockdown of TUG1 reduced CSE-triggered inflammation and airway remodelling in HBE cells and lung fibroblasts in vitro.To examine the mechanisms by which TUG1 exerted its effects on the pathogenesis of airway remodelling, we predicted miRNA target sites using an online bioinformatic database and identified miR-145-5p as an lncRNA with relevant binding sites in the TUG1 mRNA.We constructed luciferase reporter vectors that contained the wild-type (wt) or mutated (mut) binding sequences for miR-145-5p in TUG1, and luciferase reporter assay results showed that luciferase activity was suppressed in TUG1-wt cells but was not affected in TUG1-mut cells, suggesting that miR-145-5p is a TUG1-targeting miRNA.These results indicated that TUG1 positively regulated DUSP6 expression by sponging miR-145-5p in HBE cells and lung fibroblasts.Finally, we performed gain-of-function assays by introducing a DUSP6 overexpression vector into HBE cells and lung fibroblasts with TUG1 knockdown.TUG1 knockdown might have a protective effect on airway remodelling in a DUSP6-dependent manner.Thus, TUG1 may be a promising therapeutic target in CS-induced airway inflammation and fibroblast activation.	31557398	RID02858	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE51827,GSE75367,GSE86978)
Colorectal cancer	LINC00460	WWC2	negatively-E	LncMAP;western blot;ChIP;luciferase reporter assay;RIP;overexpression;shRNA	upregulation	microarray;RT-qPCR	GSE41328;GSE89076;GSE75970	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000151718	NA	728192	80014	NA	BOMB|FLJ22029	Down-Regulation of LINC00460 Represses Metastasis of Colorectal Cancer via WWC2. Initial analysis of GSE41328 and GSE89076 microarray data revealed a high expression of LINC00460 in CRC. Subsequent RT-qPCR results showed that the expression of LINC00460 in CRC tissues was significantly higher than that in adjacent normal colorectal tissues.The aforementioned findings demonstrated that LINC00460 is expressed highly in CRC tissues and cells.Silencing of LINC00460 Represses Proliferation, Migration, Invasion, and EMT of CRC Cells.In order to identify the relationship among LINC00460, ERG, and WWC2, we employed the LncMAP Web site and found the regulatory effect of LINC00460 on the expression of WWC2 through the transcription factor ERG.Through analysis of the GSE75970 dataset, WWC2 expression was found to be significantly decreased in CRC compared with the normal control. Subsequently, western blotwas conducted to detect the protein expression patterns of WWC2 in RKO cells, and the results showed no significant differences in the protein expression of WWC2 among the GapmeR-NC, pLV-EGFP-N, and blank groups.Next, ChIP assay was performed to verify whether ERG could bind to WWC2.ERG bound to the promoter region of WWC2, and not the upstream region outside of the putative ERG.Then, a dual luciferase reporter gene assay was performed to further validate the interaction among LINC00460, ERG, and WWC2.Additionally, RIP assay data (Fig. 3f) indicated that there was no statistical significance in LINC00460 expression in each group with IgG antibody.Furthermore, the results of RT-qPCR displayed that mRNA expression of WWC2 was increased in the anti-LINC00460GapmeR group, but was markedly decreased in the pLV-EGFP-N-LINC00460 group, which was reversed in the pcDNA3-LINC00460 + si-ERG group. These results revealed that LINC00460 exerts its effects by inhibiting the expression of WWC2 via ERG.Relative to the pLV-EGFP-N-LINC00460 group, cell proliferation in the pLV-EGFP-N-LINC00460 + pLV-EGFP-N-WWC2 group and the pLV-EGFP-N-LINC00460 + pSIH1-HI-copGFP-sh- ERG group was found to be significantly reduced.So LINC00460 was robustly induced while WWC2 was poorly expressed in CRC. In addition, LINC00460 could downregulate WWC2 through interaction with ERG, which led to promoted invasion, migration, and EMT of CRC cells in addition to tumor growth in vivo.Taken together, the key findings of the current study provided evidence suggesting that silencing of LINC00460 could potentially suppress EMT of CRC cells by increasing WWC2 via ERG, and highlighting that knockdown of LINC00460 could serve as a therapeutic target for CRC treatment.	31541369	RID02859	transcriptional regulation	metastasis		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE86978)
Colorectal cancer	LINC00460	ERG	negatively-F	LncMAP;western blot;ChIP;luciferase reporter assay;RIP;overexpression;shRNA	upregulation	microarray;RT-qPCR	GSE41328;GSE89076;GSE75970	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000157554	NA	728192	2078	NA	erg-3|p55	Down-Regulation of LINC00460 Represses Metastasis of Colorectal Cancer via WWC2. Initial analysis of GSE41328 and GSE89076 microarray data revealed a high expression of LINC00460 in CRC. Subsequent RT-qPCR results showed that the expression of LINC00460 in CRC tissues was significantly higher than that in adjacent normal colorectal tissues.The aforementioned findings demonstrated that LINC00460 is expressed highly in CRC tissues and cells.Silencing of LINC00460 Represses Proliferation, Migration, Invasion, and EMT of CRC Cells.In order to identify the relationship among LINC00460, ERG, and WWC2, we employed the LncMAP Web site and found the regulatory effect of LINC00460 on the expression of WWC2 through the transcription factor ERG.Through analysis of the GSE75970 dataset, WWC2 expression was found to be significantly decreased in CRC compared with the normal control. Subsequently, western blotwas conducted to detect the protein expression patterns of WWC2 in RKO cells, and the results showed no significant differences in the protein expression of WWC2 among the GapmeR-NC, pLV-EGFP-N, and blank groups.Next, ChIP assay was performed to verify whether ERG could bind to WWC2.ERG bound to the promoter region of WWC2, and not the upstream region outside of the putative ERG.Then, a dual luciferase reporter gene assay was performed to further validate the interaction among LINC00460, ERG, and WWC2.Additionally, RIP assay data (Fig. 3f) indicated that there was no statistical significance in LINC00460 expression in each group with IgG antibody.Furthermore, the results of RT-qPCR displayed that mRNA expression of WWC2 was increased in the anti-LINC00460GapmeR group, but was markedly decreased in the pLV-EGFP-N-LINC00460 group, which was reversed in the pcDNA3-LINC00460 + si-ERG group. These results revealed that LINC00460 exerts its effects by inhibiting the expression of WWC2 via ERG.Relative to the pLV-EGFP-N-LINC00460 group, cell proliferation in the pLV-EGFP-N-LINC00460 + pLV-EGFP-N-WWC2 group and the pLV-EGFP-N-LINC00460 + pSIH1-HI-copGFP-sh- ERG group was found to be significantly reduced.So LINC00460 was robustly induced while WWC2 was poorly expressed in CRC. In addition, LINC00460 could downregulate WWC2 through interaction with ERG, which led to promoted invasion, migration, and EMT of CRC cells in addition to tumor growth in vivo.Taken together, the key findings of the current study provided evidence suggesting that silencing of LINC00460 could potentially suppress EMT of CRC cells by increasing WWC2 via ERG, and highlighting that knockdown of LINC00460 could serve as a therapeutic target for CRC treatment.	31541369	RID02860	interact with protein	metastasis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cholangiocarcinoma	MEG3	TRAF3	negatively-F	luciferase reporter assay;starBase;Targetscan;western blot;shRNA	downregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000131323	NA	55384	7187	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CAP-1|CD40bp|CRAF1|LAP1|RNF118	Long non-coding RNA MEG3 represses cholangiocarcinoma by regulating miR-361-5p/TRAF3 axis.Firstly, the expression level of MEG3 in 20 CCA tissues and 20 normal tissues was detected by qRT-PCR Our results showed that MEG3 expression was remarkably downregulated in CCA tissues compared with the normal tissues.Putative MEG3 targets were predicted by bioinformatics analysis Starbase.Moreover, we conducted a Luciferase Reporter Assay to prove the predicted binding sites between MEG3 and miR-361-5p, and the results confirmed the direct targeting relationship between miR-361-5p and MEG3.MEG3 Influenced Cell Viability and Apoptosis in CCA Cells Through Down-Regulating MiR-361-5p Expression.TRAF3 is found effective in various cancers, but few reports clarified how it works in cholangiocarcinoma. TargetScan Release 7.1 was used to predict the targets of miR-361-5p, and the complementary sites of TRAF3 in miR-361-5p were firstly predicted.Then, the Luciferase Reporter Assay was used to confirm this prediction.All the results above illustrated the fact that TRAF3 was a direct target of miR-361-5p.qRT-PCRand western blot assay indicated that TRAF3 significantly decreased in CCA tumor tissues compared with the normal tissues.We confirmed that TRAF3-shRNA might reverse the tumor-repressive effects of miR-361-5p inhibitor on CCA cell lines.And we find MEG3 repressed CCA by inhibiting the NF-kB signaling pathway by downregulating miR-361-5p expression in CCA cells.Our results suggested that MEG3 repressed cholangiocarcinoma by downregulating miR-361-5p expression. Meanwhile, the suppression of miR-361-5p might improve CCA survival by targeting TRAF3 and inhibiting the NF-kB pathway, which might help to develop new strategies for CCA therapy.	31539122	RID02861	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Osteoarthritis	DNM3OS	IGF1	negatively-F	starBase;luciferase reporter assay;overexpression;siRNA;Targetscan;western blot	downregulation	qRT-PCR	NA	NA	cell viability(+);cell proliferation(+);apoptosis process(-);cell invasion(+);cell migration(+)	ceRNA(miR-126)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000230630	GRCh38_1:172138397-172144840	ENSG00000017427	NA	100628315	3479	DNM3-AS1|MIR199A2HG	IGF|IGF-I|IGF1A|IGFI	LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells.To explore whether DNM3OS and miR-126 changed in OA chondrocytes, the expression levels of DNM3OS and miR-126 were detected by qRT-PCRassay in 45 OA patients and 20 normal patients.DNM3OS was low-expressed in OA tissues, had negative correlation with miR-126 and promoted CHON-001 cells viability.To investigate the underlying mechanism of DNM3OS in OA, online software starBase v2.0 was used to observe the miRNAs interacting with DNM3OS.The luciferase reporters results further confirmed that the overexpression of miR-126 was suppressed by the binding RNA DNM3OS-Wild-type (WT) construct, while RNA DNM3OS-Mutated-type (MUT) did not change significantly.Moreover, miR-126 expression was greatly suppressed by overexpressed DNM3OS but enhanced by DNM3OS silencing compared with their corresponding controls.The cell viability was decreased or increased by mimic or inhibitor, moreover, co-transfecting the cells with si- DNM3OS and miR-126 inhibitor promoted cell viability.To determine the miR-126 target genes involved in OA progression, targetscan 7.2 was used to predict the target gene of miR-126.Furthermore, the luciferase reporter results showed that the binding RNA IGF1-WT construct suppressed overexpressed miR-126, while RNA IGF1- MUT did not change significantly. Additionally, RT-qPCR and western blotrevealed that the restoration of miR-126 expression suppressed the IGF1 mRNA and protein, which were enhanced by the upregulation of IGF1.Restoring IGF1 expression improved the suppressive effects of miR-126 overexpression in cell proliferation and attenuated the promoting effects of miR-126 overexpression on cell apoptosis.The up-regulation of miR-126 suppressed the migration and invasion by regulating IGF1.Our results showed that DNM3OS could affect the CHON-001 cell proliferation and apoptosis by regulating IGF1 by sponging miR-126.	31526393	RID02862	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Gastric cancer	LINC-PINT	HIF1A	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(+);tumor growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000100644	NA	378805	3091	FLJ43663|LincRNA-Pint|MKLN1-AS1|PINT	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	Linc-pint overexpression inhibits the growth of gastric tumors by downregulating HIF-1. The expression of Linc-pint and HIF-1alpha mRNA in gastric biopsies from patients with gastric cancer and healthy controls was determined via RT-qPCR .Linc-pint is downregulated and HIF-1 is upregulated in patients with gastric cancer.Expression of Linc-pint and HIF-1 mRNA is negatively correlated in patients with gastric cancer.Linc-pint expression in gastric biopsies is associated with the size of primary tumors.SNU- 1 and AGS cells were transfected with a Linc-pint expression vector, and the expression of HIF-1 was determined via western blot,Linc-pint is a potential upstream inhibitor of HIF-1 in gastric cancer cells.Linc-pint overexpression inhibits the proliferation of gastric cancer cells. The significant association between Linc-pint expression and tumor size suggested that Linc-pint is involved in tumor growth.In conclusion, overexpression of Linc-pint may inhibit the growth of gastric tumors via downregulation of HIF-1.	31524232	RID02863	expression association	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Pancreatic cancer	DANCR	MMP16	positively-E	starBase;shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-33b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000156103	NA	57291	4325	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	C8orf57|DKFZp761D112|MT3-MMP	LncRNA DANCR promotes proliferation and metastasis in pancreatic cancer by regulating miRNA-33b.DANCR expression is increased in PC tissues and cell lines.To explore potential molecular mechanisms, a target prediction program was used with the starBase v2.0 database to predict the possible targets of DANCR.To explore the effect of DANCR on miR-33b expression, the level of miR-33b was measured through qRT-PCRin PANC-1 and SW1990 cells following DANCR knockdown, and the results showed that miR-33b levels were increased in PC cells transfected with shDANCR compared with control cells.Moreover, luciferase reporter vectors were constructed containing the DANCR-Wt or DANCR-Mt, and luciferase reporter assays were carried out to confirm whether miR-33b is a direct target of DANCR.Downregulation of DANCR levels inhibited the proliferation and invasion of PC cells and EMT phenotypes by negatively modulating miR-33b expression.To further explore whether DANCR functioned as a miRNA sponge to positively regulate mRNA expression in a ceRNA-dependent manner, we predicted miR-33b target sites in an online bioinformatics database and predicted that DANCR and MMP16 mRNAs contain the same binding site for miR-33b.Results indicated that DANCR functioned as a miR- 33b sponge to positively regulate MMP16 expression in PC cells.Collectively, the data reveal that DANCR exerts its function by regulating miR-33b/MMP16 expression, implying an important role for a lncRNA-siRNA-sRNA functional network and suggesting a novel potential therapeutic target for PC.	31515968	RID02864	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Esophageal cancer	LINC-PINT	MIR543	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000212040	NA	378805	100126335	LincRNA-Pint|MKLN1-AS1|PINT	MIRN543|hsa-mir-543|mir-543	Linc-PINT acted as a tumor suppressor by sponging miR-543 and miR-576-5p in esophageal cancer. We found that linc-PINT expressed lower in esophageal cancer cell lines (KY-SE, TE-1, and Eca-109) than it did in the normal esophagus cell line, HEEC. Furthermore, we used qRT-PCRto investigate the potential targets of linc-PINT and the results showed that the expression of miR-543 and miR-576-5p were consistent in the three esophageal cancer cell lines: they expressed higher in cancer cell lines than those in HEEC.The dual-luciferase reporter gene assay indicated that linc-PINT could directly regulate miR-543 and miR-576-5p.As for the proliferation tests, CCK-8 tests indicated that the downregulation of linc-PINT would lead to an increased proliferation rate in Eca-109 cell line.The upregulation of miR-543 and miR-576-5p could promote migration. The downregulation of miR-543 and miR-576-5p could inhibit migration.In conclusion, linc-PINT-siR-543/miR- 576-5p pathway could predict the prognosis and provide novel therapeutic targets for esophageal cancer.	31464068	RID02865	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Esophageal cancer	LINC-PINT	miR-576-5p	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000231721	GRCh38_7:130938963-131110176	NA	NA	378805	NA	FLJ43663|LincRNA-Pint|MKLN1-AS1|PINT	NA	Linc-PINT acted as a tumor suppressor by sponging miR-543 and miR-576-5p in esophageal cancer. We found that linc-PINT expressed lower in esophageal cancer cell lines (KY-SE, TE-1, and Eca-109) than it did in the normal esophagus cell line, HEEC. Furthermore, we used qRT-PCRto investigate the potential targets of linc-PINT and the results showed that the expression of miR-543 and miR-576-5p were consistent in the three esophageal cancer cell lines: they expressed higher in cancer cell lines than those in HEEC.The dual-luciferase reporter gene assay indicated that linc-PINT could directly regulate miR-543 and miR-576-5p.As for the proliferation tests, CCK-8 tests indicated that the downregulation of linc-PINT would lead to an increased proliferation rate in Eca-109 cell line.The upregulation of miR-543 and miR-576-5p could promote migration. The downregulation of miR-543 and miR-576-5p could inhibit migration.In conclusion, linc-PINT-siR-543/miR- 576-5p pathway could predict the prognosis and provide novel therapeutic targets for esophageal cancer.	31464068	RID02866	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Gastric cancer	SNHG16	NRP1	positively-E	siRNA;luciferase reporter assay;miRDB;Targetscan;LncBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-628)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000099250	NA	100507246	8829	Nbla10727|Nbla12061|ncRAN	CD304|NRP|VEGF165R	Long noncoding RNA SNHG16 silencing inhibits the aggressiveness of gastric cancer via upregulation of microRNA-628-3p and consequent decrease of NRP1. The results showed that expres- sion levels of miR-628 were lower in gastric cancer tissue samples relative to adjacent normal tissues.Bioinformatics analysis was carried out and iden- tified two potential miR-628-binding sites in an lncRNA called SNHG16.The luciferase reporter assay was then conducted to confirm the prediction, and the results showed that restoration of miR-628 expression greatly decreased the luciferase activities of wt-SNHG16 but not mut-SNHG16 in BGC-823 and SGC-7901 cells.To explore the roles of SNHG16 in the biological char- acteristics of gastric cancer, si-SNHG16 was used to silence endogenous SNHG16 expression in BGC-823 and SGC-7901 cells.Furthermore, cotransfection with antagomir-628 abrogated si-SNHG16-mediated effects on the proliferation (Figure 7D, P<0.05), apoptosis, migration, and invasive- ness of BGC-823 and SGC-7901 cells. To gain an in-depth understanding of the mechanisms behind the activity of miR-628 in gastric cancer, the putative targets of miR-628 were predicted via bioinfor- matics analysis.NRP1 is a direct target of miR-628 in gastric cancer.Downregulation of SNHG16 inhibits the proliferation, migration, and invasiveness and induces apoptosis of gastric cancer cells.Our findings elucidate how the SNHG16-miR-628-NRP1 pathway serves as a regulatory network playing crucial roles in gastric cancer progression, suggesting that this pathway may be a novel target of anticancer therapy.	31447585	RID02867	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761)
Non-small cell lung cancer	PART1	JAK1	positively-E	starBase;luciferase reporter assay;RNA pull-down assay;overexpression;shRNA;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);JAK/STAT signaling pathway(+);tumor growth(+)	ceRNA(miR-635)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000162434	NA	25859	3716	DKFZP586D0823|NCRNA00206	JAK1A|JAK1B|JTK3	Long noncoding RNA PART1 promotes progression of non-small cell lung cancer cells via JAK-STAT signaling pathway. PART1 was significantly upregulated in NSCLC cell lines, A549, H1650, SK-MES-1, and H1975, in comparison with the control cells.According to starbase analysis, we proposed that PART1 may harbor potential binding site for miR-635 (Figure 6C). Moreover, luciferase reporter assay showed that miR-635 mimics dramatically decreased luciferase activity of reporter gene with wild-type PART1 compared with that of negative control.RNA pull down also revealed enrichment of miR-635 via overexpression of PART1, confirming the binding ability between PART1 and miR-635. Moreover, miR-635 was downregulated by overexpression of PART1, upregulated by knockdown of PART1. In general, PART1 directly bound to and inhibited miR-635 expression in NSCLC cells.The downstream target mRNA for miR-635 was predicted as 3'UTR of JAK1 and 3 via Targetscan.Results showed that addition of pcDNA-JAK1 or pcDNA-JAK3 increased the expression of p-STAT3, TIMP-1 and Pim-1 decreased by miR-635, activating JAK-STAT signaling pathway.PART1 enhanced proliferation, migration, and invasion of NSCLC cells via JAK-STAT signaling pathway.PART1 knocking down suppressed xenograft tumor growth via inactivating of JAK-STAT signaling pathway.In conclusion, our findings clarified the biologic significance of PART1/miR-635/JAK-STAT axis in NSCLC progression and provided novel evidence that PART1 may be a new potential therapeutic target for the treatment of NSCLC.	31436388	RID02868	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	PART1	JAK3	positively-E	starBase;luciferase reporter assay;RNA pull-down assay;overexpression;shRNA;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);JAK/STAT signaling pathway(+);tumor growth(+)	ceRNA(miR-635)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000105639	NA	25859	3718	DKFZP586D0823|NCRNA00206	JAK-3|JAK3_HUMAN|JAKL|L-JAK|LJAK	Long noncoding RNA PART1 promotes progression of non-small cell lung cancer cells via JAK-STAT signaling pathway. PART1 was significantly upregulated in NSCLC cell lines, A549, H1650, SK-MES-1, and H1975, in comparison with the control cells.According to starbase analysis, we proposed that PART1 may harbor potential binding site for miR-635 (Figure 6C). Moreover, luciferase reporter assay showed that miR-635 mimics dramatically decreased luciferase activity of reporter gene with wild-type PART1 compared with that of negative control.RNA pull down also revealed enrichment of miR-635 via overexpression of PART1, confirming the binding ability between PART1 and miR-635. Moreover, miR-635 was downregulated by overexpression of PART1, upregulated by knockdown of PART1. In general, PART1 directly bound to and inhibited miR-635 expression in NSCLC cells.The downstream target mRNA for miR-635 was predicted as 3'UTR of JAK1 and 3 via Targetscan.Results showed that addition of pcDNA-JAK1 or pcDNA-JAK3 increased the expression of p-STAT3, TIMP-1 and Pim-1 decreased by miR-635, activating JAK-STAT signaling pathway.PART1 enhanced proliferation, migration, and invasion of NSCLC cells via JAK-STAT signaling pathway.PART1 knocking down suppressed xenograft tumor growth via inactivating of JAK-STAT signaling pathway.In conclusion, our findings clarified the biologic significance of PART1/miR-635/JAK-STAT axis in NSCLC progression and provided novel evidence that PART1 may be a new potential therapeutic target for the treatment of NSCLC.	31436388	RID02869	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Neuroblastoma	KCNQ1OT1	BAX	positively-E	LncBase;RIP;shRNA;RNA pull-down assay		qRT-PCR;sequencing	NA	NA	apoptosis process(-)	ceRNA(miR-296-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000087088	NA	10984	581	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	BCL2L4	Long noncoding RNA KCNQ1OT1 promotes apoptosis in neuroblastoma cells by regulating miR-296-5p/Bax axis.By performing quantitative real-time PCR (qRT-PCR, western blot and flow cytometry assays we analysed the expression of apoptotic markers in NB cells transfected with miR-296-5p mimics or inhibitor. Pathway-specific PCR array allowed us to identify the target genes of miR-296-5p. Using LncBase online tool, we predicted lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) as an upstream regulator of miR-296-5p. The binding of KCNQ1OT1 and miR-296-5p was validated via RNA immunoprecipitation and Biotin pull-down assays. We also demonstrate that miR-296-5p suppresses apoptosis of NB cells in vitro and in vivo. Mechanistically, miR-296-5p directly bound the 30UTR of Bax mRNA, thus repressing Bax at the mRNA and protein level. Moreover, through bioinformatic analysis and molecular experiments, we showed that KCNQ1OT1 sponged miR-296-5p and impaired its effect on NB cell apoptosis. In summary, KCNQ1OT1 is a potent promoting factor of cell apoptosis, which acts by sponging miR- 296-5p and upregulating Bax. Our findings identify a regulatory axis of cell fate in NB cells.	31433907	RID02870	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00665	MAP4K3	positively-E	starBase;luciferase reporter assay;RIP;RNA pull-down assay;siRNA;western blot;Targetscan	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);cell autophagy(-)	ceRNA(miR-186-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000011566	NA	100506930	8491	CIP2A-BP	GLK|MAPKKKK3|RAB8IPL1	Long Intergenic Non-Protein Coding RNA 665 Regulates Viability, Apoptosis, and Autophagy via the MiR-186-5p/MAP4K3 Axis in Hepatocellular Carcinoma. The expressions of LINC00665, miR-186-5p, and MAP4K3 were determined by qRT-PCRStarBase analysis, luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down were performed to identify associations among LINC00665, miR-186-5p, and MAP4K3. western blot was utilized to examine the expressions of MAP4K3, Beclin-1, and LC3. Tumor growth was evaluated in a xenograft model.Elevations in LINC00665 were observed in HCC tissues and cells. The overall survival of HCC patients with high levels of LINC00665 was shorter than those with low levels. In vitro, LINC00665 depletion inhibited viability and induced apoptosis and autophagy. miR-186-5p interacted with LINC00665 and was downregulated in HCC tissues and cells. Upregulation of miR-186- 5p inhibited viability and induced apoptosis and autophagy, which were attenuated by upregulation of LINC00665. MAP4K3 was found to possess binding sites with miR-186-5p and was upregulated in HCC tissues and cells. MAP4K3 depletion inhibited viability and induced apoptosis and autophagy, which were attenuated by miR-186-5p inhibitor. In vivo, miR-186-5p expression was negatively correlated with LINC00665 or MAP4K3 in HCC tissues, while LINC00665 was positively correlated with MAP4K3. LINC00665 knockdown suppressed tumor growth.LINC00665 was involved in cell viability, apoptosis, and autophagy in HCC via miR-186-5p/MAP4K3 axis, which may provide a new approach for HCC treatment.	31433582	RID02871	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842)
Cervical cancer	ZNF667-AS1	PEG3	positively-E	luciferase reporter assay;RNA pull-down assay;overexpression;siRNA	downregulation	microarray;RT-qPCR	GSE26787;GSE63514;GSE63678;GSE9750;GSE27678	NA	cell cycle(+);cell invasion(+)	ceRNA(miR-93-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000166770	GRCh38_19:56477250-56504362	ENSG00000198300	NA	100128252	5178	MORT	KIAA0287|ZKSCAN22|ZNF904|ZSCAN24	Long noncoding RNA ZNF667-AS1 reduces tumor invasion and metastasis in cervical cancer by counteracting microRNA-93-3p-dependent PEG3 downregulation. The sequencing results of AffymetrixTM U133A Plus 2.0 platform were selected from the GSE26787 expression dataset. In addition, the remaining three gene expression datasets (GSE63514, GSE63678, and GSE9750) including the CC and normal samples were obtained from the GEO database.In order to identify lncRNAs that are differentially expressed in CC, we performed a comprehensive lncRNA profiling analysis using the GEO datasets (GSE27678, GSE63514, GSE63678, and GSE9750). Through analysis of microarray data (GSE27678 and GSE63514), expression of ZNF667-AS1 and PEG3 was found to be downregulated in CC.The expression of ZNF667-AS1, miR-93-3p, and PEG3 was subsequently determined in resected CC versus adjacent normal tissues, using RT-qPCR.As shown in Fig. 4B, compared with the cells without transfection, luciferase activity was significantly decreased upon cotransfection with miR-93-3p mimic and ZNF667-AS1-Wt.Competitive binding between ZNF667-AS1 and miR-93-3p was confirmed with the RNA pull-down experiment.miR-93-3p could specifically bind to PEG3. After overexpressing or silencing ZNF667-AS1, ZNF667-AS1 was found to downregulate miR-93-3p and upregulate PEG3.ZNF667-AS1 negatively regulates miR-93-3p and inhibits cell invasion and cycle via PEG3.These key findings demonstrated that upregulation of ZNF667-AS1 could suppress the progression of CC via the modulation of miR-93-3p-dependent PEG3, suggesting a potential therapeutic target for the treatment of CC.	31420931	RID02872	ceRNA or sponge	metastasis	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE51827,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Kidney disease	PVT1	FOXA1	negatively-E	luciferase reporter assay;RIP;shRNA	upregulation	RT-qPCR	NA	NA	cell injury(+);apoptosis process(+)	DNA methylation	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000129514	NA	5820	3169	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HNF3A	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.Initially, RT-qPCR was performed to determine the expression of lncRNA PVT1, and the results showed that the expression of lncRNA PVT1 in the DN patients (n = 32) was significantly higher than that in the normal control (n = 26).It was predicted that there was a target binding site between PVT1 and FOXA1, which was further verified by the dual-luciferase reporter gene assay.Additionally, the RIP assay was employed to determine the binding proteins of PVT1, and the results showed.Through determination of the expression of H3K27me3 and EZH2 in the enriched products, it was found that the expression of H3K27me3 and EZH2 in the sh-PVT1 group was significantly lower than that in the sh-NC group and that the recruitment level in the HG medium was higher than that in the NG medium.Silencing of PVT1 or overexpression of FOXA1 inhibits the apoptosis and damage of podocytes in DN.The key findings of this study collectively indicate that the suppression of lncRNA PVT1 exerts inhibitory effects on podocyte damage and apoptosis via FOXA1 in DN, which is of clinical significance.	31371698	RID02873	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Osteosarcoma	MNX1-AS1	KISS1	negatively-E	shRNA;western blot;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000170498	NA	645249	3814	CCAT5|LOC645249|MAYA	NA	Long non-coding RNA MNX1-AS1 promoted osteosarcoma proliferation and invasion via inhibiting KISS1. RT-qPCR was conducted for detecting MNX1-AS1 expression in 44 osteosarcoma patients'-tissues and 3 osteosarcoma cell lines.The MNX1-AS1 expression level of osteosarcoma cells was markedly higher than that of hFOB 1.19.MNX1-AS1 Promoted Cell Proliferation in Osteosarcoma Cells.MNX1-AS1 Promoted Cell Invasion in Osteosarcoma Cells.RT-qPCR results showed that the expression level of KISS1 in osteosarcoma cells was higher in MNX1-AS1/shRNA group compared with the KISS1 level in the control group.western blot assay also showed that after MNX1-AS1 was overexpressed, KISS1 could be downregulated.Besides, the KISS1 expression level was negatively correlated to MNX1-AS1 expression in osteosarcoma tissues.Our study demonstrated that MNX1-AS1 could enhance osteosarcoma cell proliferation and invasion by inhibiting KISS1, which might contribute to the therapy for osteosarcoma.	31364121	RID02874	expression association	NA	UP(BRCA);DATA(GSE55807)	
Laryngeal squamous cell carcinoma	SNHG12	WWP1	positively-E	miRDB;mirDIP;miRcode;siRNA;luciferase reporter assay	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);cell viability(+)	ceRNA(miR-129-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000123124	NA	85028	11059	ASLNC04080|C1orf79|LINC00100|PNAS-123	AIP5|DKFZP434D2111	Small Nucleolar RNA Host Gene 12 (SNHG12) Promotes Proliferation and Invasion of Laryngeal Cancer Cells via Sponging miR-129-5p and Potentiating WW Domain-Containing E3 Ubiquitin Protein Ligase 1 (WWP1) Expression.LSCC shares similar mechanisms of carcinogenesis with HNSCC. We preliminarily explored the role of SNHG12 in HNSCC using the TCGA database.Then, RT-qPCR was applied to validated this result in 22 LSCC tissues and 22 paired adjacent normal tissues.SNHG12 was overexpressed and predicted worse survival in LSCC.As interaction with mRNA via miRNA is the most common functional mechanism for lncRNA in the cytoplasm, we used the ceRNA theory to reveal its biological mechanism. Bioinformatic analysis using miRDB, mirDIP ,miRcode predicted that miR-129-5p is a mutual target of SNHG12.According to the predicted binding sites, we constructed SNHG12-MUT and SNHG12-WT vectors to perform dual luciferase reporter testing.All these results indicate that SNHG12 interacts with miR-129-5p and modulates its expression in LSCC cells.SNHG12 was successfully silenced by siRNA transfection as evaluated by RT-qPCR.miR-129-5p inhibition promoted cell viability.Further phenotypic experiments were conducted to determine whether SNHG12 regulates proliferation and invasion through WWP1.Our study demonstrated that SNHG12 promoted LSCC cells progression via sponging miR-129-5p and potentiating WWP1 expression.	31348766	RID02875	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE86978)
Laryngeal carcinoma	MEG3	APAF1	positively-E	luciferase reporter assay;western blot;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(+)	ceRNA(miR-23a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000120868	NA	55384	317	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	APAF-1|CED4	LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR-23a/APAF-1 axis. MEG3 expression in 50 laryngeal cancer tissue samples was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR).MEG3 was down-regulated in laryngeal cancer tissues, and the low MEG3 expression was associated with advanced clinical stage.Our results suggest that MEG3 inhibits the proliferation and induces the apoptosis of laryngeal cancer cells in vitro.MEG3 inhibits the growth and proliferation and induces the apoptosis of laryngeal cancer cells in vivo.To confirm whether miR-23a binds to MEG3 specifically, a luciferase reporter assay was employed.Moreover, we found that overexpression of MEG3 reduced miR-23a expression in Hep-2 and AMC-HN-8 cells.As APAF-1 is a target of miR-23a16 and miR-23a has be demonstrated to bind to MEG3 specifically through luciferase reporter assay.These data suggest that the regulation of APAF-1 by MEG3 is mediated by miR-23a.Furthermore, MEG3 may act as a ceRNA to regulate APAF-1 expression by competitive binding to miR-23a, thereby regulating the progression of laryngeal cancer.	31328388	RID02876	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Spinal cord injury	Mirt2	miR-429	negatively-F	overexpression;shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(-);inflammatory response(-);apoptosis process(-);p38/MAPK signaling pathway(-);NF-kB signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA Mirt2 relieves lipopolysaccharide-induced injury in PC12 cells by suppressing miR-429. The expression of lncRNA Mirt2 in PC12 cells following LPS stimulation was detected by using qRT-PCR.lncRNA Mirt2 was up-regulated during SCI.Overexpression of lncRNA Mirt2 alleviated LPS-induced injury.Overexpression of lncRNA Mirt2 alleviated LPS-induced injury through decreasing pro-inflammatory cytokine release and suppressing cell apoptosis.Luciferase reporter assay results indicated that miR-429 could directly bind with lncRNA Mirt2, as the luciferase activity was significantly reduced by transfection with miR-429 mimic and Mirt2-wt.Apart from miR-429, miR-34a-5p was also found to be downregulated by lncRNA Mirt2.Relative luciferase activity was significantly declined by transfection with miR-34a-5p mimic and Mirt2-wt.lncRNA Mirt2 inactivated the NF-kB and p38MAPK signal pathways through down-regulating miR-429.lncRNA Mirt2 exerts protective effects in an in vitro model of SCI by down-regulating miR-429. This study shed light on the treatment of SCI by using the lncRNA-miRNA regulation network.	31309444	RID02877	ceRNA or sponge	NA		
Spinal cord injury	Mirt2	miR-34a-5p	negatively-F	overexpression;shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(-);inflammatory response(-);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA Mirt2 relieves lipopolysaccharide-induced injury in PC12 cells by suppressing miR-429. The expression of lncRNA Mirt2 in PC12 cells following LPS stimulation was detected by using qRT-PCR,lncRNA Mirt2 was up-regulated during SCI.Overexpression of lncRNA Mirt2 alleviated LPS-induced injury.Overexpression of lncRNA Mirt2 alleviated LPS-induced injury through decreasing pro-inflammatory cytokine release and suppressing cell apoptosis.Luciferase reporter assay results indicated that miR-429 could directly bind with lncRNA Mirt2, as the luciferase activity was significantly reduced by transfection with miR-429 mimic and Mirt2-wt.Apart from miR-429, miR-34a-5p was also found to be downregulated by lncRNA Mirt2.Relative luciferase activity was significantly declined by transfection with miR-34a-5p mimic and Mirt2-wt.lncRNA Mirt2 inactivated the NF-kB and p38MAPK signal pathways through down-regulating miR-429.lncRNA Mirt2 exerts protective effects in an in vitro model of SCI by down-regulating miR-429. This study shed light on the treatment of SCI by using the lncRNA-miRNA regulation network.	31309444	RID02878	ceRNA or sponge	NA		
Papillary thyroid carcinoma	MIR22HG	CDKN1B	positively-E	luciferase reporter assay;overexpression;siRNA;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-24-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000111276	NA	84981	1027	C17orf91|DKFZp686O06159|MGC14376	KIP1|P27KIP1	MIR22HG inhibits cell growth, migration and invasion through regulating the miR-24-3p/ p27kip1 axis in thyroid papillary carcinomas. The results of qRT-PCR;ISHowed that lncRNA MIR22HG significantly expressed low in TPC-1, KAT-5, BCPAP, K1 and BHP5-16 cells compared with normal cell line.To further explore the underlying regulatory mechanism of MIR22HG, the bioinformatics analysis was used to predict its target miRNA; the results showed that mir-24-3p was a potential target of MIR22HG.By luciferase reporter assays, we found that the luciferase activity of MIR22HG-WT was significantly decreased by binding to the sites of miR- 24-3p.Otherwise, overexpression of MIR22HG inhibited miR-24-3p expression in TCP-1 and BCPAP cell lines. Meanwhile, we also transfected si-NC, si-MIR22HG#1and si- MIR22HG#2 into TCP-1 and BCPAP cell lines and qRT-PCRanalysis showed that MIR22HG expressed lower.To further elucidate the regulatory network of miR-24-3p, we found that p27kip1 has complement sites to bind to miR-24-3p in 3'UTR through using bioinformatics software targetScan, which could be a potential target gene of miR-24-3p.MiR-24-3p Regulated Cell Proliferation, Apoptosis, Migration and Invasion Through Targeting p27kip1 in Thyroid Papillary Carcinomas.MIR22HG inhibited cell growth through modulating p27kip1 by decreasing miR-24-3p expression in thyroid papillary carcinomas, providing a new modulate mechanism and therapeutic targets in thyroid papillary carcinomas.	31298336	RID02879	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	TUSC7	NUMB	positively-E	luciferase reporter assay;fluorescent immunohistochemistry	downregulation	qRT-PCR	cBioPortal;CANCER GENOMICS	NA	cell stemness(+);Notch signaling pathway(-)	ceRNA(miR-146)	regulation	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000133961	NA	285194	8650	LINC00902|LOC285194|LSAMP-AS3|NCRNA00295	C14orf41	TUSC7 suppression of Notch activation through sponging MiR-146 recapitulated the asymmetric cell division in lung adenocarcinoma stem cells.Suppressed TUSC7 expression in non-small cell lung cancer (NSCLC) was confirmed with an established public data base cBioPortal, and in specimens of NSCLCs.Clinical identification of lower expressed TUSC7 in NSCLC.Based on further analysis using CANCER GENOMICS online data(http://www.cbioportal.org/), a total of six databases consisted of more expansive sources of data on squamous lung cancer and adenocarcinoma tissues.TUSC7 suppressed the stem cells expansion through Notch signaling inhibition.TUSC7 induced the stem cells' asymmetric division.Bioinformatics established a possible connection between TUSC-7 and miR-146. TUSC7 was predicated to correlate with miR-146 at the possible binding site.The co-transfection of luciferase reporters containing 3'UTR sequence and miR-146a mimics reduced nearly 60% of the luciferase intensity.The alignment of miR-146a and 3'UTR of NUMB was constructed by using enhanced green fluorescent protein (EGFP) reporter assay.MiR-146 decreased NUMB expression post-transcriptionally.The decreasing of tumor suppressive miR-146 was necessary in TUSC- 7 conducted renewal repression, despite it alone could also reduce the renewal efficiency, indicating that more complicated non-coding genes may be involved in its regulation.	31279783	RID02880	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Colorectal cancer	FEZF1-AS1	OTX1	positively-E	western blot;siRNA;immunohistochemical assay	upregulation	sequencing;qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000115507	NA	154860	5013	NA	NA	The lncRNA FEZF1-AS1 Promotes the Progression of Colorectal Cancer Through Regulating OTX1 and Targeting miR-30a-5p. Our previous research identified differentially expressed lncRNAs in 10 CRC tissues and 10 matched nontumor tissues by next-generation sequencing (NGS).qRT-PCRwas performed to detect the relative expression of FEZF1-AS1 in the SW480, HCT116, HT29, DLD-1, and RKO cell lines.A high level of FEZF1-AS1 expression might play an important role in colorectal cancer.western blot showed that silencing FEZF1-AS1 suppressed the expression of OTX1.OTX1 regulated epithelial-mesenchymal transition (EMT) to promote CRC progression.FEZF1-AS1 knockdown downregulated the EMT markers vimentin and N-cadherin, whereas it upregulated the expression of the epithelial marker E-cadherin.An immunohistochemical assay was used to detect the expression of OTX1 in 40 clinical CRC tissues and their normal counterparts.These results indicated that FEZF1-AS1 exerts its function in CRC cells through the FEZF1-AS1/OTX1/ EMT signaling pathway.We predicted numerous miRNAs that could be bound to FEZF1-AS1 by using the bioinformatics tool StarBase.We examined the expression of these four miRNAs by qRT-PCRafter FEZF1-AS1 knockdown in HCT116 cells.The overexpression of miR-30a-5p suppressed the expression of FEZF1-AS1, and an miR-30a-5p inhibitor increased the expression of FEZF1-AS1.A dual-luciferase reporter assay showed that an miR-30a-5p mimics inhibited luciferase activity when it was cotransfected with pGL3-FEZF1-AS1-fragment-2, but not with the other two fragments.The Reciprocal Repression of FEZF1-AS1 and miR-30a-5p and miR-30a-5p Repression Promoted CRC Cell Proliferation and Migration.We used three algorithms, TargetScan, TargetMiner, and miRDB, to identify putative cotarget genes of miR-30- a-5p. We predicted that NT5E was a target of miR-30a-5p.A dualluciferase reporter assay was used to verify our predictions, and miR-30a-5p mimics inhibited luciferase activity when cotransfected with NT5E-3'-UTR-WT.The FEZF1-AS1/miR-30a-5p Axis Regulates CRC Cell Migration and Proliferation by Targeting NT5E.Our results indicated that the mechanism by which FEZF1-AS1 positively regulates the expression of NT5E is through sponging miR-30a-5p. Our study demonstrated that lncRNA FEZF1-AS1 is involved in the development of CRC and may serve as a diagnostic and therapeutic target for CRC patients.	31270006	RID02881	expression association	NA		
Colorectal cancer	FEZF1-AS1	NT5E	positively-E	starBase;overexpression;siRNA;luciferase reporter assay;Targetscan;TargetMiner;miRDB	upregulation	sequencing;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-[0-9]0a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000135318	NA	154860	4907	NA	CALJA|CD73|eN|eNT|NT5	The lncRNA FEZF1-AS1 Promotes the Progression of Colorectal Cancer Through Regulating OTX1 and Targeting miR-30a-5p. Our previous research identified differentially expressed lncRNAs in 10 CRC tissues and 10 matched nontumor tissues by next-generation sequencing (NGS).qRT-PCRwas performed to detect the relative expression of FEZF1-AS1 in the SW480, HCT116, HT29, DLD-1, and RKO cell lines.A high level of FEZF1-AS1 expression might play an important role in colorectal cancer.western blot showed that silencing FEZF1-AS1 suppressed the expression of OTX1.OTX1 regulated epithelial-mesenchymal transition (EMT) to promote CRC progression.FEZF1-AS1 knockdown downregulated the EMT markers vimentin and N-cadherin, whereas it upregulated the expression of the epithelial marker E-cadherin.An immunohistochemical assay was used to detect the expression of OTX1 in 40 clinical CRC tissues and their normal counterparts.These results indicated that FEZF1-AS1 exerts its function in CRC cells through the FEZF1-AS1/OTX1/ EMT signaling pathway.We predicted numerous miRNAs that could be bound to FEZF1-AS1 by using the bioinformatics tool StarBase.We examined the expression of these four miRNAs by qRT-PCRafter FEZF1-AS1 knockdown in HCT116 cells.The overexpression of miR-30a-5p suppressed the expression of FEZF1-AS1, and an miR-30a-5p inhibitor increased the expression of FEZF1-AS1.A dual-luciferase reporter assay showed that an miR-30a-5p mimics inhibited luciferase activity when it was cotransfected with pGL3-FEZF1-AS1-fragment-2, but not with the other two fragments.The Reciprocal Repression of FEZF1-AS1 and miR-30a-5p and miR-30a-5p Repression Promoted CRC Cell Proliferation and Migration.We used three algorithms, TargetScan, TargetMiner, and miRDB, to identify putative cotarget genes of miR-30- a-5p. We predicted that NT5E was a target of miR-30a-5p.A dualluciferase reporter assay was used to verify our predictions, and miR-30a-5p mimics inhibited luciferase activity when cotransfected with NT5E-3'-UTR-WT.The FEZF1-AS1/miR-30a-5p Axis Regulates CRC Cell Migration and Proliferation by Targeting NT5E.Our results indicated that the mechanism by which FEZF1-AS1 positively regulates the expression of NT5E is through sponging miR-30a-5p. Our study demonstrated that lncRNA FEZF1-AS1 is involved in the development of CRC and may serve as a diagnostic and therapeutic target for CRC patients.	31270006	RID02882	ceRNA or sponge	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Pulmonary hypertension	MALAT1	KLF5	positively-E	LncBase;luciferase reporter assay;RIP;Targetscan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-124-3p.1)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102554	NA	378938	688	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BTEB2|CKLF|IKLF	Long non-coding RNA MALAT1 sponges miR-124-3p.1/KLF5 to promote pulmonary vascular remodeling and cell cycle progression of pulmonary artery hypertension. To determine whether MALAT1 may be involved in the pathologic process of PAH, a total of eight paired PAH and normal PA tissue samples from patients with PAH were used to determine the expression of MALAT1 by RT-qPCR analysis.MALAT1 is highly expressed in PA tissues and HPASMCs derived from patients with PAH.The presence of a putative binding site for hsa-miR-124-3p.1 in the MALAT1 transcript was identified using LncBase Predicted v.2 .These results indicate a negative correlation between MALAT1 and hsa-miR-124-3p.1. Luciferase reporter plasmids harboring wild-type MALAT1 and mutant MALAT1 3'-UTR sequences containing the predicted hsa-miR-124-3p.1 binding sites were generated.The RIP assay results demonstrated that MALAT1 and hsa-miR-124-3p.1 were significantly enriched in AGO2 immunoprecipitates when compared with the IgG-pellet,indicating that MALAT1 and hsa-miR-124-3p.1 were located in the same RISC.To investigate the mechanism of action of hsa-miR-124-3p.1 in HPASMCs, bioinformatics analysis (http://www.targetscan.org/) was used to identify a complementary binding site between hsa-miR-124-3p.1 and the 3'-UTR of KLF5.The effect of MALAT1 on the proliferation and migration of HPASMCs was largely offset by the miR-124-3p.1 mimic in MALAT1-silenced cells.the growth and migration of HPASMCs by sponging hsa-miR-124-3p.1. Ultimately, these results demonstrate that MALAT1 may regulate KLF5 expression by binding competitively to hsa-miR-124-3p, thus promoting the growth of HASMCs.In addition, the results contribute to what is known regarding the role of MALAT1 in PAH development and provide a novel theoretical basis for the development of new therapeutic interventions for patients with PAH.	31257528	RID02883	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Colorectal cancer	LINC00668	USP47	positively-E	FISH;luciferase reporter assay;starBase;RIP;RNA pull-down assay;shRNA;Targetscan;microT;miRmap;PicTar;RNA22	upregulation	qRT-PCR	GEPIA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);tumor malignant transformation(+)	ceRNA(miR-188-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000170242	NA	400643	55031	NA	NA	LINC00668 promotes tumorigenesis and progression through sponging miR- 188-p and regulating USP47 in colorectal cancer. To assess the expression of LINC00668 in colorectal cancer (CRC) tissues, we obtained RNA sequencing expression data for 275 colorectal carcinoma tissue samples and 349 normal tissue samples from GEPIA database.For further verification, quantitative real-time polymerase chain reaction (qRT-PCR was performed to further determine expression profile of LINC00668 in both CRC tissues and cell lines.LINC00668 is significantly upregulated in colorectal cancer tissues and cells.FISH assay showed that LINC00668-specific staining was identified in the cytoplasm of LoVo and RKO cells.Subsequently, a prediction algorithm of lncRNA-miRNA interaction, Starbase 3.0 was employed to evaluate targeted miRNA of LINC00668.Then we experimentally tested these four microRNAs in a CRC cell line by the biotin-lncRNA pull-down method.RNA immunoprecipitation (RIP) assay with qRTPCR analysis was performed to investigate whether LINC00668 is regulated by miR-188-p in this manner.Moreover, a dual-luciferase gene reporter assay was performed for further confirmation upon examining overexpressive and inhibitory efficiency of miR-188-p.miR-188-p inhibition reverses LINC00668-knockdown-mediated effect on proliferation, migration and apoptosis in CRC cells.we utilized miRNA-mRNA interaction module of Starbase 3.0 to predict targets of miRNA and refined the results by selecting 5 target-predicting programs (Targetscan, microT, PicTar, miRmap, and RNA22). Only USP47 was co-predicted by five programs to be the downstream gene of miR-188-p.The malignant behavior of colorectal cancer cells was regulated by LINC00668/miR-188-p/USP47 axis.Conclusively, our findings demonstrated that lncRNA LINC00668 acted as an oncogenic role in CRC cells by sponging miR-188-p and upregulating USP47 and may represent a potential marker for CRC patients.	31233752	RID02884	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE55807)
Colorectal cancer	SNHG15	SIRT1	positively-E	shRNA;Targetscan;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	tumor growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000096717	NA	285958	23411	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	SIR2L1	RETRACTED ARTICLE: Long noncoding RNA SNHG15 enhances the development of colorectal carcinoma via functioning as a ceRNA through miR-141/SIRT1/Wnt/--catenin axis. SNHG15 is highly expressed in CRC tissues and cells.We thus investigated whether SNHG15 regulated CRC development via sponging miR-141. As displayed in Figure 3(A), miR-141 was markedly increased in both CaCO-2 and HCT-1-16 cells after transfection with sh-SNHG15 (p < .01), deducting a possible negative regulation pattern between SNHG15 and miR-141 in CRC cells.SNHG15 regulates tumor growth and metastasis by targeting miR-141TargetScan prediction software confirmed that there exists a binding sequence between miR-141 and SIRT1. Luciferase reporter assay was subsequently performed, which confirmed that miR-141 could directly interact with SIRT1.SIRT1 is a downstream target of miR-141.SIRT1 is a downstream target of miR-141.Thus we propose that Wnt/b-catenin signals may be a down- river regulator in mediating the impacts of SNHG15 in CRC and SNHG15-miR-141-SIRT1 axis may pave a new sight in explaining the biological processes of CRC.	31213086	RID02885	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SCAMP1	LMX1A	positively-E	starBase;shRNA;luciferase reporter assay;RIP;Targetscan;overexpression	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-499a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000085365	GRCh38_5:78360611-78480739	ENSG00000162761	NA	9522	4009	SCAMP37	LMX1|LMX1.1	Knockdown of LncRNA SCAMP1 suppressed malignant biological behaviours of glioma cells via modulating miR-499a-5p/LMX1A/NLRC5 pathway. The expression levels of SCAMP1 in NBTs, glioma tissues, NHA and glioma cell lines were detected by qRT-PCR Results showed that SCAMP1 was significantly up-regulated in glioma tissues and cell lines.Using bioinformatics database (Starbase), SCAMP1 was identified as a potential target of miR-499a-5p. To clarify whether SCAMP1 could bind to miR-499a-5p through the putative binding site, the expression of miR-499a-5p in U87 and U251 cells transfected with sh-SCAMP1 was firstly detected.Dual-luciferase assay was further quantified the interaction between SCAMP1 and miR-499a-5p.In addition, RIP assay showed that the expressions of SCAMP1 and miR-499a-5p were both increased in the anti-Ago2 group compared with that in anti-normal group.Results above indicated that there was a reciprocal repression feedback loop between SCAMP1 and miR-499a-5p.Bioinformatics database (TargetScan) was used to identify that LMX1A was a potential downstream target of miR-499a-5p.Bioinformatics database (Targetscan) speculated that miR-499a-5p may target LMX1A-3-UTR. Hence the LMX1A expression of glioma cells altered SCAMP1 and miR-499a-5p expression was firstly detected. Results showed that SCAMP1 knockdown or miR-499a-5p overexpression obviously inhibited LMX1A mRNA and protein expression.The results showed that overexpressed LMX1A significantly rescued the inhibitory effect of overexpressed miR-499a-5p on cell proliferation, migration and invasion, moreover diminished cell apoptotic percentage.In conclusion, our study clarifies that SCAMP1/miR-499a-5p/LMX1A/ NLRC5 axis plays a critical role in modulating malignant progression of glioma cells, which provide a novel therapeutic strategy for glioma treatment.	31207033	RID02886	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE86978)	UP(PAAD);DATA(GSE40174)
Esophageal cancer	LINC00184	PTEN	negativley-E	overexpression;shRNA;immunofluorescence assay;MethPrimer;ChIP;RIP	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);mitochondrial function(-);AKT signaling pathway(+)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000224939	GRCh38_1:234629311-234634780	ENSG00000171862	NA	100302691	5728	HANC|NCRNA00184	BZS|MHAM|MMAC1|PTEN1|TEP1	LINC00184 silencing inhibits glycolysis and restores mitochondrial oxidative phosphorylation in esophageal cancer through demethylation of PTEN.By analyzing the expression profile of EC in the TCGA database, LINC00184 expression was shown to be noticeably higher in either esophageal adenocarcinoma samples or ESCC samples than that in normal controls.The results of RT-qPCR showed that LINC00184 expression was dramatically elevated in EC tissues relative to adjacent normal tissues.Pearson's correlation analysis showed that the expression of LINC00184 was negatively correlated with PTEN expression in EC.We over-expressed or silenced LINC00184 in EC cells.Additionally, online comparison through BLAST found that LINC00184 may bind to PTEN promoter in RNA-DNA manner.CpG islands were observed in the PTEN promoter by bioinformatic analysis using MethPrimer website.In contrast, the PTEN methylation level in EC cells transfected with sh-LINC00184 was lower than that in cells transfected with sh-NC.The CHIP assay was conducted after over-expression and silencing of LINC00184 in EC cells.RIP assay revealed that there is an elevation in the enrichment of LINC00184 by DNMT1 after over-expression of LINC00184.Inhibition of PTENmethylation suppresses proliferation,migration, glycolysis and recovers mitochondrial OXPHOS in EC cells.The extent of Akt phosphorylation in EC cells enhanced noticeably after over-expression of LINC00184.Taken together, the LINC00184/PTEN/Akt axis mediates glycolysis and mitochondrial OXPHOS in EC cells. This study highlighted a potential intervention target for treating EC.	31201145	RID02887	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	PTENP1	PTEN	positively-E	siRNA;luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);chemoresistance(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-20a)	regulation	RNA-protein	Adriamycin	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	BZS|MHAM|MMAC1|PTEN1|TEP1	PTENP1/miR-20a/PTEN axis contributes to breast cancer progression by regulating PTEN via PI3K/AKT pathway. The levels of PTENP1, PTEN and miR-20a were measured by qRT-PCR PTENP1 and PTEN are concomitantly downregulated in BC tissues and cell lines.To better understand the role of PTENP1 in BC progression, we manipulated the expression of PTENP1 by transfecting PTENP1 or siPTENP1 in BC cell lines.In addition, the length of PTENP1 and the non-coding potential also identified through online bioinformatic tools.These data indicated that low levels of PTENP1 and PTEN might promote the BC progression and associate with the poor clinical prognosis.According to the bioinformatic analysis, we determined the predicted binding sites. Dual-luciferase reporter gene assay confirmed that PTENP1 was a direct target of miR-20a.RIP assay was performed on BC cell line extracts using anti-Ago2 antibody.PTENP1 is a direct target of miR-20a and a positive regulator of PTEN.In addition, PTENP1 functioned as an endogenous sponge of miR-20a to regulate PTEN expression, which mediated BC cells proliferation, invasion and drug resistance via activation the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.Overexpressed miR-20a promoted PI3K/Akt signal activity in MDA-MB-231 cells.Collectively, these data indicated that PTENP1/miR-20a/PTEN axis involved in the malignant behaviors of BC cells, illuminating the possible mechanism mediated by PTEN via PI3K/Akt pathway. Targeting PTENP1/ miR-20a/PTEN may provide a potential diagnosis and treatment strategy for BC.	31196157	RID02888	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	LINC00261	SFRP2	negatively-F	RNAhybrid;luciferase reporter assay;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);WNT signaling pathway(+)	ceRNA(miR-522-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000145423	NA	140828	6423	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	FRP-2|SARP1|SDF-5	Overexpression of LINC00261 inhibits non-small cell lung cancer cells progression by interacting withmiR-522-3p and suppressing Wnt signaling.We applied qRT-PCRto explore expression levels of LINC00261 in collected adjacent normal lung tissues and NSCLC tissues.LINC00261 was decreased in NSCLC tissue and predicted favorable prognosis.Bioinformatic analysis through web predictive tool (RNAhybrid) showed that a miRNA named miR-522-3p had potential targeted sites of LINC00261.Luciferase activity when miR-522-3p mimic and LINC00261-WT were cotransfected into A549 cells was significantly lower than the group containing miRNC and LINC00261-WT.To further explore whether LINC00261 could regulate protein expression and related signaling pathway, we performed bioinformatic analysis and found SFRP2 was a potential target protein for miR-522-3p . Then luciferase reporting assay was conducted and results confirmed that miR-522-3p could combine with SFRP2 . Overexpression of miR-522-3p significantly decreased expression of SFRP2 and pcDNA-LINC00261 transfection remarkably increased SFRP2 mRNA expression  and protein expression .Overexpression of miR-522-3p significantly ameliorated suppressive effects of LINC00261 on proliferation and invasion of NSCLC cells.Furthermore, in NSCLC tissues a positive correlation between RNA expression of LINC00261 and SFRP2 was found,SFRP2 is a suppressive regulator in Wnt signaling.Overexpression of LINC00261 modulated the expression level of SFRP2 and inhibited wnt signaling pathway.Taken together, our study demonstrated that LINC00261 suppressed NSCLC cells progression via sponging miR-522-3p and inhibiting Wnt signaling.	31190356	RID02889	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	PSTAR	HNRNPK	positively-F	RNA pull-down assay;RIP;shRNA	downregulation		NA	NA	cell proliferation(-);cell cycle(-);p53 signaling pathway(-)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000165119	NA	NA	3190	NA	CSBP|HNRPK|TUNP	Long Noncoding RNA p53-Stabilizing and Activating RNA Promotes p53 Signaling by Inhibiting Heterogeneous Nuclear Ribonucleoprotein K deSUMOylation and Suppresses Hepatocellular Carcinoma.The expression levels of PSTAR are more down-regulated in HCC cell lines compared with PHHs.We therefore performed RNA pull-down assays to identify the PSTAR-protein complex.RNA immunoprecipitation assays showed enrichment of PSTAR in complexes precipitated by antibodies against hnRNP K as compared with control immunoglobulin G.We observed that knockdown of PSTAR leads to a decrease of p53 protein levels.PSTAR inhibits HCC cell proliferation and tumorigenicity through inducing p53-mediated cell cycle arrest.This study sheds light on the tumor suppressor role of lncRNA PSTAR, a modulator of the p53 pathway, in HCC.	31148184	RID02890	expression association	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	CPS1-IT1	CCN1	negativley-E	RPIseq;Co-immunoprecipitation;overexpression	downregulation	RT-qPCR	NA	NA	cell metastasis(+)	ceRNA(BRG1)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000145386	NA	29034	3491	CPS1-IT|CPS1IT|PRO0132	CYR61|GIG1|IGFBP10	Long noncoding RNA CPS1-IT1 suppresses melanoma cell metastasis through inhibiting Cyr61 via competitively binding to BRG1.To study the role of CPS1-IT1 in melanoma, the expression status of CPS1-IT1 in a total of 84 pairs of human melanoma tissues and adjacent nontumor tissues are first tested by RT-qPCR in our study.CPS1-IT1 is downregulated in human melanoma tissues and cell lines.Forced expression of Cyr61 attenuates repressive impact of CPS1-IT1 overexpression on metastasis in melanoma.A potential binding of CPS1-IT1 with BRG1, a core subunit of SWI/SNF complex, is predicted by using online RPISeq.We find that CPS1-IT1 is extremely harvested in BRG1-immunoprecipitated complex in both A375 and MEL-RM cells, just as the enrichment of U1 in SNRNP70- induced immunoprecipitations.Collectively, CPS1-IT1 impairs Cyr61 expression in melanoma through competitively interacting with BRG1 and thus obstructing the SWI/SNF complex-induced transcription activation of Cyr61.Jointly, CPS1-IT1 controls melanoma metastasis through impairing Cyr61 expression via competitively binding with BRG1, uncovering a novel potential therapeutic and prognostic biomarker for patients with melanoma.	31111478	RID02891	ceRNA or sponge	metastasis,prognosis		
Colorectal cancer	LINC00052	CALCOCO1	positively-E	LncBase;luciferase reporter assay;Targetscan;miRDB;immunohistochemical staining;overexpression;siRNA	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-574-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000012822	NA	145978	57658	FLJ31461|NCRNA00052|TMEM83	calphoglin|Cocoa|KIAA1536	Long noncodingRNALINC00052 inhibits colorectal cancer metastasis by sponging microRNA-574-5p to modulate CALCOCO1 expression. LINC00052 expression was detected in 24 pairs of CRC tissues and we found that it was obviously decreased than adjacent tissues.A bioinformatics database (DIANA-LncBase; June 2016 release) was used to predict some miRNAs associated with LINC00052 online.we found that the expression levels of many miRNAs,such as miR-608, miR-5004-5p and especially miR-574-5p, were reduced in mRNA levels when LINC00052 was overexpressed in HT-29 cells. When LINC00052 was knocked down, miR-574-5p was upregulated the mostly.Small miRNA recognition sequence's bioinformatics analysis showed that there was a miR-574-5p-binding site in the sequences of LINC00052.A dualluciferase reporter assay was performed to demonstrate the specific binding site of miR-574-5p in the sequences of LINC00052.Bioinformatics methods (TargetScan; miRDB) was applied to predict some possible target genes of miR-574-5p, such as forkhead box I2 (FOXI2), zinc finger protein 337 (ZNF337), and CALCOCO1.Among the screened targets, we focused on CALCOCO1 because of its lowest expression level in CRC cells when we overexpressed miR-574-5p and it was upregulated when suppressed miR-574-5p.To verify whether CALCOCO1 was a target of miR-574-5p, a dual-luciferase gene reporter analysis was carried out to demonstrated the specific binding sites for CALCOCO1 3-UTR and miR-574-5p.Immunohistochemical (IHC) staining also showed lower CALCOCOL expression in CRC tissues than that in normal ones.In addition, transwell analysis showed that LINC00052 inhibited migration and invasion in CRC cell, while miR-574-5p stimulated them, furthermore, miR-574-5p recovered LINC000 52's effect on restraining CRC cell metastasis.LINC00052 could downregulate miR-574-5p expression and upregulate CALCOCO1 expression in vivo, thereby inhibiting the metastasis of CRC cells.	31104316	RID02892	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807)
Endometriosis	H19	ITGB3	positively-E	shRNA;Targetscan;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000259207	NA	283120	3690	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CD61|GP3A|GPIIIa	LncRNA-H19 regulates cell proliferation and invasion of ectopic endometrium by targeting ITGB3 via modulating miR-124-3p. The expression of H19, miR-124-3p, and ITGB3 in normal, eutopic, and ectopic endometrial stromal cells was detected by real-time PCR.H19 levels were increased in the ectopic endometrium of women with endometriosis as compared to healthy subjects and eutopic endometrium subjects with endometriosis.Knockdown of H19 increased the expression of miR-148a-3p, miR-124-3p, and let-7a- 5p in ectopic endometrium, while decreasing the expression of miR-98-5p.Application of TargetScan software suggested that the 3'UTR region of ITGB3 may be a binding site for miR-124-3p.Knockdown of H19 decreased ITGB3 protein expression in ectopic endometrium.A luciferase reporter assay showed that upregulation of miR-124-3p suppressed luciferase activity and ITGB3 expressionl.miR-124-3p regulates cell proliferation and invasion by targeting ITGB3 expression.From these results, we can infer that in endometriosis both miR-124-3p and ITGB3 operate as downstream effector proteins in the H19-signaling pathway. Down-regulation of lncRNA-H19 could inhibit ectopic endometrial cell proliferation and invasion by modulating miR-124-3p and ITGB3, offering a novel target for treatment.	31085188	RID02893	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE75367)
Breast cancer	LINC00473	miR-497	negatively-F	starBase;luciferase reporter assay;RIP;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000223414	NA	NA	NA	90632	NA	C6orf176|LNC473|bA142J11.1	NA	Long noncoding RNA LINC00473 indicates a poor prognosis of breast cancer and accelerates tumor carcinogenesis by competing endogenous sponging miR-497.The mRNA levels of LINC00473 were evaluated using 122-paired human BC samples and adjacent normal breast specimens using RT-qPCR.LINC00473 expression was significantly upregulated in BC tissues.We searched an online bioinformatics tool: starBase, to predict the target miRNA of LINC00473.Dual luciferase reporter analyses were performed, and the data revealed that co-transfection of the LINC00473 wild-type (LINC00473 wt) plasmids and miR-497 mimics resulted in remarkable decrease of luciferase activity in BC cells.The results of RIP assays indicated that LINC00473 and miR-497 were markedly enriched in Ago2-containing beads when compared with the input groups.We overexpressed LINC00473 or reduced LINC00473 expression in BC cells and subsequently applied qRT-PCRanalysis to measure the expression of miR-497.High expression of LINC00473 was correlated with lymph node metastasis, clinical stage, and poorer outcome in BC patients.Knockdown of LINC00473 resulted in the suppression of tumor cell proliferation, promotion of cells apoptosis, inhibition of cells metastasis.Our data revealed that LINC00473 acted as a tumor promoter in BC and LINC00473/miR-497 axis may be a novel therapeutic strategy for this tumor.	31081095	RID02894	ceRNA or sponge	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	
Acute myeloid leukemia	SBF2-AS1	ZFP91	positively-E	luciferase reporter assay;RIP;Targetscan;miRBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-188-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000186660	NA	283104	80829	NA	PZF|ZNF757	Long noncoding RNA SBF2-AS1 act as a ceRNA to modulate cell proliferation via binding with miR-188-5p in acute myeloid leukemia. SBF2-AS1 mRNA expression was significantly increased in AML samples.In addition, we determined SBF2-AS1 expression in AML cells, qRT-PCRresults showed that SBF2-AS1 expression was significantly increased in AML cell lines.Dual-luciferase assay showed that the luciferase activity was significantly decreased by co-transfection with miR-188-5p mimics and SBF2-AS1-Wt vector.RIP assay revealed that both SBF2-AS1 and miR-188-5p expression was highly enriched in Ago2 immunoprecipitates relative to control IgG immunoprecipitates.Next, we determined the mechanisms underlying the activity of miR-188-5p in AML, TargetScan and miRBase showed that ZFP91 was predicted as a putative target of miR-188-5p.SBF2-AS1 inhibition decreased AML cells proliferation ability in vitro. Flow cytometry assays showed that SBF2-AS1 inhibition induced AML cells apoptosis and arrested AML cells in G0/G1 phase.And the effects of SBF2- AS1 suppression on AML cells progression could be abolished by miR-188-5p inhibitors. Moreover, we found that SBF2-AS1 inhibition reduced tumor growth in vivo. Taken together, our findings elucidated that SBF2-AS1 could act as a miRNA sponge in AML progression, and provided a potential therapeutic strategy for AML treatment.	31062614	RID02895	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	SNHG16	TIMP3	positively-E	starBase;luciferase reporter assay;overexpression;siRNA	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-175p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000100234	NA	100507246	7078	Nbla10727|Nbla12061|ncRAN	SFD	The encouraging role of long noncoding RNA small nuclear RNA host gene 16 in epithelial-mesenchymal transition of bladder cancer via directly acting on miR-17-5p/ metalloproteinases 3 axis.The real-time PCR was launched on the amplification instrument.SNHG16 expression was positively correlated with the expression of miR-17-5p among the bladder cancer crowds , which was consistent with the results derived from starBase software.The dual luciferase reporter gene assay was performed to figure out whether targeted regulations were present among SNHG16, miR-17-5p, and TIMP3.Furthermore, overexpression of SNHG16 and miR-17-5p both enhanced the viability, proliferation, migration, and invasion.Transfections of pcDNA3.1- SNHG16 and si-SNHG16, respectively, resulted in overexpression and underexpression of miR-17-5p, and the dual luciferase reporter gene assay demonstrated a targeted relationship between SNHG16 and miR-17-5p.The expression of TIMP3 was subjected to targeted regulation of miR-17-5p (P < 0.05), and its overexpression could reverse the effects of miR-17-5p on proliferation and metastasis.Conclusively, purposeful modification of SNHG16/miR-17-5p/ TIMP3 signaling might be conducive to postpone the aggravation of bladder cancer.	31026378	RID02896	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(SKCM);DATA(GSE38495)
Ovarian cancer	CDKN2B-AS1	miR-411-3p	negatively-F	shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-);cell migration(+);cell invasion(+);HIF1A/VEGF/P38 signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Long noncoding RNA CDKN2B-AS1 interacts with miR-411e3p to regulate ovarian cancer in vitro and in vivo through HIF-1a/VEGF/P38 pathway.We found that the expression level of CDKN2B-AS1 was significantly higher than that in normal HOSE cells.The expression levels of miR-411e3p were measured in CDKN2B-AS1shRNA (Sh-CDKN2BAS1) transfected SKOV-3 cells by qRT-PCRTo confirm this possibility, the wild type sequence of CDKN2B-AS1 (CDK-wt) or its mutant sequence (CDK-mut) was subcloned into the pMIR luciferase reporter and then cotransfected with miR-411e3p mimics or controls into SKOV- 3 cells.These results indicated that there are direct interactions between miR-411e3p and the miRNA recognition sites of CDKN2B-AS1.The enhanced apoptosis and confined cell growth induced by Sh-CDKN2B-AS1 in SKOV-3 cells were executed by sponging miR-411e3p.Sh-CDKN2B-AS1 suppresses migration and invasion of SKOV- 3 cells.Sh-CDKN2B-AS1 significantly downregulated the expression of HIF1a, VEGF and p-P38, while miR- 411e3p inhibitor obviously upregulated the expression of HIF1a, VEGF and p-P38.Sh-CDKN2B-AS1 inhibits tumor growth in vivo.Collectively, CDKN2BAS1 modulated these activities possibly though miR-411e3p/HIF1a/VEGF/P38 pathway.	31014670	RID02897	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Non-small cell lung cancer	LINC-PINT	PDCD4	positively-E	luciferase reporter assay;RIP;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);tumorigenesis(+)	ceRNA(miR-208a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000150593	NA	378805	27250	FLJ43663|LincRNA-Pint|MKLN1-AS1|PINT	H731	Long noncoding RNA LINC-PINT inhibits non-small cell lung cancer progression through sponging miR-218-5p/PDCD4. The levels of LINC-PINT were assessed in NSCLC tissue (n-36) and adjacent non-tumour tissues using qRT-PCROur data showed that LINC-PINT expression reduced in NSCLC tissues compared to adjacent non-tumour tissues.LINC-PINT inhibits NSCLC cell proliferation and cell cycle in vitro.LINC-PINT inhibits NSCLC cell migration and invasion.To explore whether miR-208a-3p was a potential target of LINC-PINT in A549 cell, the luciferase reporter assay was used.Next, RNA immunoprecipitation (RIP) assay showed that LINC-PINT and miR-208a-3p were enriched in A549 cell.Moreover, overexpression of LINC-PINT reduced miR-208a- 3p expression in A549 cell.LINC-PINT overexpression A549 cell was transfected with miR-208a-3p mimics.These results suggested that miR-208a-3p/PDCD4 might be the target of LINC-PINT in NSCLC cell.The results presented that transfection with PDCD4 inhibitor partially rescued the effect of LINC-PINT on cell proliferation, cycle progression, migration and invasion, suggesting that PDCD4 mediates the effects of LINC-PINT on NSCLC cells.LINC-PINT inhibits the tumourigenesis of NSCLC in vivo.These findings indicated that LINC-PINT functions as a tumour-suppressor that exerts important regulatory roles in NSCLC progression by sponging miR-208a-3p/PDCD4.	31010333	RID02898	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Acute myeloid leukemia	MALAT1	miR-96	negatively-F	luciferase reporter assay;knockdown;starBase;miRanda;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);chemosensitivity(-);cell viability(+)	sponge	binding/interaction	RNA-RNA	Cytarabine	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000199158	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 knockdown inhibits proliferation and enhances cytarabine chemosensitivity by upregulating miR-96 in acute myeloid leukemia cells. We firstly identified the expression profiles of MALAT1 and miR-96 in serum samples from 29 AML patients and 17 healthy volunteers by qRT-PCR Results showed that MALAT1 expression level was significantly increased and miR-96 expression level was significantly decreased in AML patients.Bioinformatics online predictive databases (Starbase, http:// starbase.sysu.edu.cn/; miRanda, http://www.microrna.org/) predicted the potential miRNAs that contained putative binding sites with MALAT1 and found that miR-96 formed the complementary bases pairing with MALAT1.To validate the crosstalk between MALAT1 and miR-96 was through direct binding, luciferase reporter assay was performed.qRT-PCRanalysis showed that MALAT1 knockdown elevated miR-96 expression in HL60 and THP-1 cells, suggesting that MALAT1 served as a competing endogenous RNA that regulated miR-96 expression.miR-96 overexpression induced apoptosis of HL60 and THP-1 cells. Additionally, MALAT1 knockdowninduced viability inhibition of HL60 and THP-1.These findings demonstrated that inhibition of miR-96 abolished the effects of MALAT1 on the viability and apoptosis of AML cells.miR-96 downregulation attenuated the effects of MALAT1 knockdown on Ara-C sensitivity in AML cells.Knockdown of MALAT1 inhibited the proliferation, induced apoptosis, and enhanced Ara-C sensitivity of AML cells. Additionally, MALAT1 suppressed miR-96 expression by acting as a molecular sponge of miR-96 in AML cells. miR-96 downregulation abolished the effects of MALAT1 knockdown on the proliferation, apoptosis, Ara-C sensitivity in AML cells.In conclusion, MALAT1 knockdown inhibited proliferation, promoted apoptosis and enhanced Ara-C sensitivity in AML cells by upregulating miR-96, providing novel insights into the critical role of MALAT1 as a miRNA sponge in AML.	30970520	RID02899	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Non-small cell lung cancer	miR-142-3p	MALAT1	negatively-E	overexpression;luciferase reporter assay;shRNA	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MicroRNA-142-3p/MALAT1 inhibits lung cancer progression through repressing beta-catenin expression. The level of miR- 142-3p was decreased in NSCLC tissues while MALAT1 mRNA level was up-regulated.To confirm the association between miR-142-3p and MALAT1, mimic-miR-142-3p or mimic-NC was transfected into H1299 cells. Results showed that miR-142-3p up-regulation decreased the expression of MATAL1. Then, we carried out luciferase reporter assay to further explore the interaction between miR-142-3p and MALAT1. And results showed that up-regulation of miR-142-3p significantly decreased the luciferase activity, whereas mutated binding sites between miR-142-3p and MALAT1 abolished miR-142-3p effect in H1299 cells.Overall, these results clarified that miR-142-3p down-regulated beta-catenin expression through down-regulating MALAT1 in NSCLC.Compared with the control group, stable transfection of mimic-miR-142-3p increased miR-142-3p expression while sh-MALAT1 and sh-beta-catenin decreased MALAT1 and beta-catenin expression, respectively.Moreover, down-regulation of either MALAT1 or beta-catenin inhibited H1299 cell proliferation and migration , as well as increased cell apoptosis.Taken together, these results suggested that miR-142-3p inhibited the progression of NSCLC through inactivating MALAT1/beta-catenin signaling.Taken together, our study makes clear that miR-142-3p functions as a tumor suppressor in NSCLC progression through inhibiting MALAT1/beta-catenin signaling.	30970294	RID02900	ceRNA or sponge	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Atherosclerosis	CDKN2B-AS1	ADAM10	negatively-E	western blot;overexpression;shRNA;FISH;ChIP;RIP;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cholesterol homeostasis(-);inflammatory response(+)	DNA methylation	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000137845	NA	100048912	102	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	CD156C|HsT18717|kuz|MADM	Long non-coding RNA CDKN2B-AS1 reduces inflammatory response and promotes cholesterol efflux in atherosclerosis by inhibiting ADAM10 expression.RT-qPCR results demonstrated that the relative expression of CDKN2B-AS1 in atherosclerotic plaque tissues was significantly lower than that in non-atherosclerotic internal mammary artery (IMA) tissues.The mRNA and protein expression of CDKN2B-AS1 and ADAM10 in each group was detected by RT-qPCR and western blotthe transcription as well as the protein levels of CDKN2B-AS1 were significantly higher while that of ADAM10 in the oe-CDKN2B-AS1 group was significantly lower (p < 0.05); compared with the sh-NC group, the transcription level and protein expression of CDKN2B-AS1 were significantly reduced while those of ADAM10 in the sh-CDKN2B-AS1 group were significantly increased (p < 0.05). The obtained results revealed that CDKN2B-AS1 negatively regulated the expression of ADAM10.The cellular localization of CDKN2B-AS1 as detected by fluorescence in situ hybridization (FISH).The CHIP assay was applied in order to detect the enrichment of DNMT1 (methyltransferase) in the ADAM10 promoter region of each group.The RNA-binding protein immunoprecipitation (RIP) assay further verified the binding of DNMT1 (methyltransferase) to CDKN2B-AS1 in each group.The RNA-pull down assay was then performed to detect the level of DNMT1 (methyltransferase) pulled down by CDKN2B-AS1 in each group.Taken together, CDKN2B-AS1 can interact with DNMT1 and recruit DNMT1 binding to ADAM10 promoter region, in turn promoting methylation and inhibition of ADAM10 expression.Overexpression of CDKN2B-AS1 methylates ADAM10, inhibits atherosclerotic inflammatory response, and promotes cholesterol efflux.Altogether, lncRNA CDKN2B-AS1 can inhibit the transcription of ADAM10 via DNMT1-mediated ADAM10 DNA methylation, consequently preventing inflammatory response of atherosclerosis and promoting cholesterol efflux.	30926762	RID02901	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	MAGI2-AS3	SMG1	positively-E	luciferase reporter assay;RNA pull-down assay;overexpression;Targetscan;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-374b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000157106	NA	100505881	23049	ENST00000414797	ATX|KIAA0421|LIP	LncRNA MAGI2-AS3 inhibits hepatocellular carcinoma cell proliferation and migration by targeting the miR-374b-5p/SMG1 signaling pathway. In our study, qRT-PCRis used to determine the expression of MAGI2-AS3 in 88 paired HCC tissues and adjacent nontumor tissues. The data show that MAGI2- AS3 expression in HCC tissues is significantly downregulated compared with paired nontumor tissues.TargetScan analysis (TargetScan Human 6.0) suggests that the 3'-UTR of SMG1, a protein that involved in nonsense-mediated mRNA decay (NMD) has been already identified as a tumor suppressor in several cancers.Then the luciferase reporter assay reveals that only the miR-374b-5p mimics could markedly reduce the luciferase activity of wild type SMG1.The next pull down assay further demonstrates the specific interaction between miR-374b-5p and SMG1.These data exhibit that SMG1 is the target of miR-374b-5p and it can be regulated by MAGI2-AS3.The MTT assay indicates that knockdown of SMG1 reverses the inhibited cell proliferation ability induced by the overexpression of MAGI2-AS3. And the apoptosis rate shows a large reduction when co-transfecting with si-SMG1 and pcDNA3.1/ MSGI2-AS3. Moreover, silenced SMG1 restores the suppressed cell migration capacity in pcDNA3.1/MSGI2-AS3 transfected HepG2 cells.	30924168	RID02902	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807)
Gastric cancer	LINC01138	miR-1273e	negatively-F	miRDB;luciferase reporter assay;RNA pull-down assay;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);MAPK signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000215863	NA	NA	NA	388685	NA	FLJ39739|LINC00875	NA	Long Intergenic Non-Protein-Coding RNA 01138 Accelerates Tumor Growth and Invasion in Gastric Cancer by Regulating miR-1273e.Expressions of LINC01138 and miR-1273e in GC tissues and cell lines were measured by qRT-PCRassay. The interaction between LINC01138 and miR-1273e was predicted by the online tool miRDB, verified by dual-luciferase reporter and RNA pull-down assays. Effects of LINC01138 knockdown or miR-1273e overexpression on cell viability, proliferation, apoptosis, invasion, and migration were evaluated by MTT, colony formation assay, flow cytometry, and Transwell assays. Target genes of miR-1273e were predicted by KEGG analysis, and involvement of the mitogen-activated protein kinase (MAPK) pathway was confirmed by qRT-PCRassay.LINC01138 was increased but miR-1273e was decreased in GC tissues and cell lines. Knockdown of LINC01138 suppressed GC cell viability, proliferation, invasion, and migration, and promoted GC cell apoptosis. We demonstrated that LINC01138 contributed to GC progression by directly sponging and inhibiting miR-1273e. Moreover, the MAPK pathway was verified to participate in the promotive effects of LINC01138 on GC progression.LINC01138 activated the MAPK signaling pathway by inhibiting miR-1273e to promote GC cell proliferation, invasion, and migration, and inhibit GC cell apoptosis, suggesting that the LINC01138/miR-1273e/MAPK axis is a promising therapeutic target for GC.	30902962	RID02903	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	
Glioblastoma	MIR155HG	ANXA2	positively-E	RNAhybrid;luciferase reporter assay;RIP;Targetscan;miRNAWalk;siRNA	upregulation	qRT-PCR	TCGA;CGGA;Rembrandt	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-185)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234883	GRCh38_21:25561810-25575168	ENSG00000182718	NA	114614	302	BIC|miPEP155|MIRHG2|NCRNA00172	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	The miR155HG/miR-185/ANXA2 loop contributes to glioblastoma growth and progression. To explore miR155HG expression in human astrocytoma tissues, we examined three public human astrocytoma databases (TCGA, CGGA and Rembrandt) and found overexpression of miR155HG in GBM.RNA hybrid bioinformatics tools showed that miR155HG contains a putative binding site for miR-185-5p as tumor suppressor in a wide range of tumors.To explore the possible interactions between miR155HG and miR-185-5p, RIP was performed in U87 cells.Then we constructed a luciferase reporter plasmid containing the putative miR-185-5p binding site from miR155HG, as well as a mutant construct in which the binding site was mutated.Bioinformatics analytical tools TargetScan and miRNAWalk 2.0 showed that the 3'-UTR of ANXA2 mRNA contained a seed sequence of miR-185-5p.Furthermore, inhibiting miR155HG by siRNA downregulated ANXA2 levels in U87 and GP1 cells, which could be reversed by treatment with miR-185-5p inhibitor.MiR155HG and miR-185-5p participate in GBM growth by regulating the proliferation and apoptosis of GBM cells.p-STAT3 might directly promote miR155HG expression in GBM.Bioinformatics tools identified three putative binding regions for p-STAT3 in the miR155HG promoter. ChIP assays confirmed that p-STAT3 could bind putative binding region 2 (- 1548 bp to - 1411 bp) but not binding region 1 (- 275 bp to - 161 bp) and binding region 3 (- 1982 bp to - 1972 bp) in the miR155HG promoter. Two luciferase reporter plasmids containing either the entire miR155HG promoter region 2000 bp to 1000 bp upstream of the transcription start site (wt-pGL3) or the promoter deleted for binding region 2 (mut-pGL3) were transfected into GBM cells along with or without STAT3 phosphorylation inhibitor.Together these results indicated that the activated transcription factor p-STAT3 plays a key role in ANXA2-driven miR155HG expression and promotes GBM cell growth, through the DNA binding activity of the p-STAT3 transcription factor.Our results demonstrated that overexpressed miR155HG in GBM can sponge miR-185 to promote ANXA2 expression, and ANXA2 stimulates miR155HG level through phosphorylated STAT3 binding to the miR155HG promoter. We establish the miR155HG/miR185/ANXA2 loop as a mechanism that underlies the biological functions of miR155HG and ANXA2 in GBM and further suggest this loop may serve as a therapeutic target and/or prognostic biomarker for GBM.	30898167	RID02904	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Glioblastoma	STAT3	MIR155HG	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	TCGA;CGGA;Rembrandt	NA	cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000168610	NA	ENSG00000234883	GRCh38_21:25561810-25575168	6774	114614	APRF	BIC|miPEP155|MIRHG2|NCRNA00172	The miR155HG/miR-185/ANXA2 loop contributes to glioblastoma growth and progression. To explore miR155HG expression in human astrocytoma tissues, we examined three public human astrocytoma databases (TCGA, CGGA and Rembrandt) and found overexpression of miR155HG in GBM.RNA hybrid bioinformatics tools showed that miR155HG contains a putative binding site for miR-185-5p as tumor suppressor in a wide range of tumors.To explore the possible interactions between miR155HG and miR-185-5p, RIP was performed in U87 cells.Then we constructed a luciferase reporter plasmid containing the putative miR-185-5p binding site from miR155HG, as well as a mutant construct in which the binding site was mutated.Bioinformatics analytical tools TargetScan and miRNAWalk 2.0 showed that the 3'-UTR of ANXA2 mRNA contained a seed sequence of miR-185-5p.Furthermore, inhibiting miR155HG by siRNA downregulated ANXA2 levels in U87 and GP1 cells, which could be reversed by treatment with miR-185-5p inhibitor.MiR155HG and miR-185-5p participate in GBM growth by regulating the proliferation and apoptosis of GBM cells.p-STAT3 might directly promote miR155HG expression in GBM.Bioinformatics tools identified three putative binding regions for p-STAT3 in the miR155HG promoter. ChIP assays confirmed that p-STAT3 could bind putative binding region 2 (- 1548 bp to - 1411 bp) but not binding region 1 (- 275 bp to - 161 bp) and binding region 3 (- 1982 bp to - 1972 bp) in the miR155HG promoter. Two luciferase reporter plasmids containing either the entire miR155HG promoter region 2000 bp to 1000 bp upstream of the transcription start site (wt-pGL3) or the promoter deleted for binding region 2 (mut-pGL3) were transfected into GBM cells along with or without STAT3 phosphorylation inhibitor.Together these results indicated that the activated transcription factor p-STAT3 plays a key role in ANXA2-driven miR155HG expression and promotes GBM cell growth, through the DNA binding activity of the p-STAT3 transcription factor.Our results demonstrated that overexpressed miR155HG in GBM can sponge miR-185 to promote ANXA2 expression, and ANXA2 stimulates miR155HG level through phosphorylated STAT3 binding to the miR155HG promoter. We establish the miR155HG/miR185/ANXA2 loop as a mechanism that underlies the biological functions of miR155HG and ANXA2 in GBM and further suggest this loop may serve as a therapeutic target and/or prognostic biomarker for GBM.	30898167	RID02905	transcriptional regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)
Ovarian cancer	TUG1	LRG1	positively-E	overexpression;western blot;shRNA;ELISA	upregulation	qPCR	NA	NA	cell migration(+);angiogenesis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171236	NA	55000	116844	FLJ20618|LINC00080|NCRNA00080	LRG	Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich alpha-2-glycoprotein-1.We first employed qPCR to measure lncRNA TUG1 expression level in ovarian cancer cells.. Results showed that compared with normal cells (IOSE80), SKOV3 or CAOV3 cells presented significantly higher TUG1 expression.qPCR found that knockdown of TUG1 significantly decreased LRG1 mRNA levels in both SKOV3 and CAOV3 cells.western blot further confirmed lower levels of LRG1 after TUG1 down-regulation.In addition, the secretion level of LRG1 was further quantified by ELISA, and we found that TUG1 knockdown efficiently suppressed LRG1 in cultured supernatants.In a rescue assay, we found that the replenishment of 0.5 ug/ml recombinant LRG1 protein into sh-TUG1- transfected cells enhanced angiogenesis compared with sh-TUG1.Therefore, LRG1 might be one of TUG1-mediated secretory factors mediating endothelial cell migration and tumor angiogenesis.qPCR showed that transcript levels of angiogenesis-related genes, including VEGF, TGF-beta, and Ang-1, were significantly down-regulated in HUVECs cells cultured in condition medium from SKOV3 or CAOV3 cells with TUG1 knockdown.In western blot, consistent results were obtained as TUG1 knockdown efficiently suppressed VEGF, TGF-beta, and Ang-1 protein expression, and replenishment of LRG1 protein rescued these effects.In summary, our results suggested that TUG1 mediated LRG1 secretion from ovarian cancer cells, and LRG1 further potentiated proliferation, migration, and angiogenesis of endothelial cells.Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis. Anti-Cancer Drugs 30:562-70 Copyright - 2019 Wolters Kluwer Health, Inc. All rights reserved.	30896502	RID02906	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Ovarian cancer	TUG1	VEGFA	positively-F	western blot;shRNA	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich alpha-2-glycoprotein-1.We first employed qPCR to measure lncRNA TUG1 expression level in ovarian cancer cells.. Results showed that compared with normal cells (IOSE80), SKOV3 or CAOV3 cells presented significantly higher TUG1 expression.qPCR found that knockdown of TUG1 significantly decreased LRG1 mRNA levels in both SKOV3 and CAOV3 cells.western blot further confirmed lower levels of LRG1 after TUG1 down-regulation.In addition, the secretion level of LRG1 was further quantified by ELISA, and we found that TUG1 knockdown efficiently suppressed LRG1 in cultured supernatants.In a rescue assay, we found that the replenishment of 0.5 ug/ml recombinant LRG1 protein into sh-TUG1- transfected cells enhanced angiogenesis compared with sh-TUG1.Therefore, LRG1 might be one of TUG1-mediated secretory factors mediating endothelial cell migration and tumor angiogenesis.qPCR showed that transcript levels of angiogenesis-related genes, including VEGF, TGF-beta, and Ang-1, were significantly down-regulated in HUVECs cells cultured in condition medium from SKOV3 or CAOV3 cells with TUG1 knockdown.In western blot, consistent results were obtained as TUG1 knockdown efficiently suppressed VEGF, TGF-beta, and Ang-1 protein expression, and replenishment of LRG1 protein rescued these effects.In summary, our results suggested that TUG1 mediated LRG1 secretion from ovarian cancer cells, and LRG1 further potentiated proliferation, migration, and angiogenesis of endothelial cells.Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis. Anti-Cancer Drugs 30:562-70 Copyright - 2020 Wolters Kluwer Health, Inc. All rights reserved.	30896502	RID02907	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Ovarian cancer	TUG1	TGFB1	positively-E	western blot;shRNA	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000105329	NA	55000	7040	FLJ20618|LINC00080|NCRNA00080	CED|DPD1|TGFB|TGFbeta	Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich alpha-2-glycoprotein-1.We first employed qPCR to measure lncRNA TUG1 expression level in ovarian cancer cells.. Results showed that compared with normal cells (IOSE80), SKOV3 or CAOV3 cells presented significantly higher TUG1 expression.qPCR found that knockdown of TUG1 significantly decreased LRG1 mRNA levels in both SKOV3 and CAOV3 cells.western blot further confirmed lower levels of LRG1 after TUG1 down-regulation.In addition, the secretion level of LRG1 was further quantified by ELISA, and we found that TUG1 knockdown efficiently suppressed LRG1 in cultured supernatants.In a rescue assay, we found that the replenishment of 0.5 ug/ml recombinant LRG1 protein into sh-TUG1- transfected cells enhanced angiogenesis compared with sh-TUG1.Therefore, LRG1 might be one of TUG1-mediated secretory factors mediating endothelial cell migration and tumor angiogenesis.qPCR showed that transcript levels of angiogenesis-related genes, including VEGF, TGF-beta, and Ang-1, were significantly down-regulated in HUVECs cells cultured in condition medium from SKOV3 or CAOV3 cells with TUG1 knockdown.In western blot, consistent results were obtained as TUG1 knockdown efficiently suppressed VEGF, TGF-beta, and Ang-1 protein expression, and replenishment of LRG1 protein rescued these effects.In summary, our results suggested that TUG1 mediated LRG1 secretion from ovarian cancer cells, and LRG1 further potentiated proliferation, migration, and angiogenesis of endothelial cells.Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis. Anti-Cancer Drugs 30:562-70 Copyright - 2021 Wolters Kluwer Health, Inc. All rights reserved.	30896502	RID02908	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	TUG1	ANGPT1	positively-E	western blot;shRNA	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000154188	NA	55000	284	FLJ20618|LINC00080|NCRNA00080	Ang1|KIAA0003	Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich alpha-2-glycoprotein-1.We first employed qPCR to measure lncRNA TUG1 expression level in ovarian cancer cells.. Results showed that compared with normal cells (IOSE80), SKOV3 or CAOV3 cells presented significantly higher TUG1 expression.qPCR found that knockdown of TUG1 significantly decreased LRG1 mRNA levels in both SKOV3 and CAOV3 cells.western blot further confirmed lower levels of LRG1 after TUG1 down-regulation.In addition, the secretion level of LRG1 was further quantified by ELISA, and we found that TUG1 knockdown efficiently suppressed LRG1 in cultured supernatants.In a rescue assay, we found that the replenishment of 0.5 ug/ml recombinant LRG1 protein into sh-TUG1- transfected cells enhanced angiogenesis compared with sh-TUG1.Therefore, LRG1 might be one of TUG1-mediated secretory factors mediating endothelial cell migration and tumor angiogenesis.qPCR showed that transcript levels of angiogenesis-related genes, including VEGF, TGF-beta, and Ang-1, were significantly down-regulated in HUVECs cells cultured in condition medium from SKOV3 or CAOV3 cells with TUG1 knockdown.In western blot, consistent results were obtained as TUG1 knockdown efficiently suppressed VEGF, TGF-beta, and Ang-1 protein expression, and replenishment of LRG1 protein rescued these effects.In summary, our results suggested that TUG1 mediated LRG1 secretion from ovarian cancer cells, and LRG1 further potentiated proliferation, migration, and angiogenesis of endothelial cells.Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis. Anti-Cancer Drugs 30:562-70 Copyright - 2022 Wolters Kluwer Health, Inc. All rights reserved.	30896502	RID02909	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111065)
Chronic nonbacterial prostatitis	GAS5	COX2	negatively-E	RIP;RNA pull-down assay;siRNA;overexpression;western blot	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell injury(+)	histone modification	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Reproductive system disease	Prostatitis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000198712	NA	60674	4513	NCRNA00030|SNHG2	COII|MTCO2	Overexpression of lncRNA GAS5 suppresses prostatic epithelial cell proliferation by regulating COX-2 in chronic non-bacterial prostatitis.The expression of GAS5 was significantly decreased in prostatitis tissues, while the mRNAand protein levels of COX-2 were dramatically increased in prostatitis tissues.The expression of GAS5 and COX-2 was determined by RT-PCRand western blotGAS5 was considered to regulate the expression of COX-2 by RNA pull-down and RIP assay. GAS5 knockdown was performed in RWPE-1 cells and HPECs by si-GAS5 transfection, and the downregulation of GAS5 was confirmed by RT-PCRThe COX-2 level was markedly decreased after the overexpression of GAS5 in LPS-induced RWPE-1 cells and HPECs.Up-regulation of GAS5 could reduce the COX-2 protein level by promoting ubiquitination.Overexpression of GAS5 suppressed COX-2 and inhibited proliferation of prostatitis cells.Overexpressed GAS5 alleviated the injury of CNP in vivo.Our findings revealed that overexpression of GAS5 inhibited cell proliferation via negatively regulating the expression of COX-2, thus alleviating the progression of CNP.	30892130	RID02910	epigenetic regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Pre-eclampsia	LINC00261	TIMP4	positively-E	overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-558)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000157150	NA	140828	7079	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	NA	Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway.The expression levels of Linc00261 in the placental tissues of 30 control pregnant women and 30 women with severe PE were compared by using quantitative realtime polymerase chain reaction (qRT-PCR, and the expression level of Linc00261 in the PE group was significantly higher than the control group.To further decipher the role of Linc00261 in the trophoblast invasion and migration, we performed the bioinformatics analysis to predict the potential miRNAs that could interact with Linc00261, and we found that miR-558 harbored the complementary sequences with Linc00261.We then constructed the luciferase vector containing the wild-type and mutant (mutated bases were shown in red letters) binding sequences of Linc00261.Overexpression of miR-558 suppressed the luciferase activity, while knockdown of miR-558 increased the luciferase activity of HTR-8/SVneo cells with the luciferase reporter vector containing the wild-type Linc00261 segments.We also performed the bioinformatics to predict the downstream targets of miR-558 and found that miR-558 could bind to the 3'UTR of TIMP4.We then constructed the luciferase vector containing the wildtype and mutant.Overexpression of miR-558 suppressed the mRNA and protein levels of TIMP4; while knockdown of miR-558 increased the mRNA and protein levels of TIMP4 in HTR-8/SVneo cells.Linc00261 suppressed cell invasion and migration via targeting miR-558/ TIMP4 axis in trophoblasts.	30891826	RID02911	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Myocardial infarction	STAT1	SPAAR	positively-E	JASPAR;ChIP;Co-immunoprecipitation	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell viability(-);PI3K/AKT/GSK3beta signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cardiovascular system disease	Myocardial infarction	TF	lncRNA	ENSG00000115415	NA	ENSG00000235387	GRCh38_9:35909490-35937153	6772	158376	ISGF-3|STAT91	LINC00961|SPAR	STAT1-avtiviated LINC00961 regulates myocardial infarction by the PI3K/AKT/GSK3beta signaling pathway.The expression level of LINC00961 was elevated after hypoxia treatment.The RT-qPCR assay was conducted to determine the transfection efficiency.Recent research have confirmed that STAT1 plays a pivotal role in cardiovascular diseases and is highly expressed and activated in ischemic heart diseases including MI.By browsing bioinformatic tools (UCSC genome browser and JASPAR database), we verified that STAT1 possessed the putative potential binding sites for the promoter region of LINC00961.The ChIP assay revealed the enriched expression of LINC00961 in anti-STAT1 immunoprecipitated lysate, which suggested the binding of STAT1 with the promoter region of LINC00961.To further elucidate the regulation of STAT1 on LINC00961, STAT1 was overexpressed in cells that underwent transfection with pcDNA3.1/STAT1 plasmids and enhanced expression of STAT1 markedly increased LINC00961 expression level.Inhibition of PI3K/AKT signaling OR GSK3beta pathway blocks the cardioprotection of LINC00961 knockdown in hypoxia injury.Namely, we concluded that STAT1-avtiviated LINC00961 accelerated MI via the PI3K/AKT/GSK3beta pathway, which may provide clues for the treatment of patients with MI.	30887575	RID02912	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Breast cancer	CDR1-AS	CCNE1	positively-E	overexpression;Targetscan;luciferase reporter assay;siRNA	upregulation	RT-PCR	NA	NA	chemosensitivity(-)	ceRNA(miR-7)	regulation	RNA-protein	5-fluorouracil	NA	NA	Cancer	Breast cancer	circRNA	PCG	NA	NA	ENSG00000105173	NA	103611090	898	CDR1NAT|CDR1as|ciRS-7	CCNE	Inhibition of circular RNA CDR1as increases chemosensitivity of 5-FU-resistant BC cells through up-regulating miR-7.The BC cells (MCF-7, SKBR-3, MDAMB- 231 and HCC-1937) had substantially increased CDR1as expression.Targetscan software indicates the bind site of CDR1as and miR-7.RT-PCRwas applied to determine the expression of CDR1as.Targetscan database was used to evaluate the target genes of miR-7 and CCNE1 was selected as a target gene for further analysis.Double luciferase reporter assay (Figure 3D) showed that in wide type, compared with CCNE1-Wt + miR-7 NC group, the luciferase activity of CCNE1-Wt + miR-7 mimics group was decreased.Inhibition of miR-7 reverses the enhancement on chemosensitivity of 5-FU-resistant BC cells caused by CDR1as silencing.The results of xenograft model also implied that silencing of CDR1as could enhance the chemosensitivity of 5-FU-resistant BC cells.	30884120	RID02913	ceRNA or sponge	chemoresistance		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Hepatocellular carcinoma	Lnc-UCID	DHX9	negatively-F	siRNA;overexpression;RNA pull-down assay;RIP;EMSA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000135829	NA	NA	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	lnc-ucid is up-reg ulate d in hcc tissues, and sile ncing lnc-ucid inhibits tumor growth in vitro and in vivo. These lncRNAs were therefore examined in our study cohort by quantitative real-time PCR. Compared with nontumor liver tissues, more than 50% increases in the RNA levels.To explore how lnc-UCID up-regulated CDK6, RNA pull-down assays were used to identify lnc-UCID-associated proteins. DHX9, an RNA helicase with RNA-binding activity, was identified in the protein complexes pulled down by lnc-UCID.RNA immunoprecipitation (RIP) assay was performed to further confirm the in vivo interaction between lnc-UCID and DHX9.Results revealed 850-1030-nt to be the core sequence for lnc-UCID binding to DHX9.We found that DHX9 knockdown significantly increased the protein and mRNA levels of CDK6, but had no impact on the level of CDK6 precursor mRNA. Furthermore, silencing DHX9 dramatically prolonged the half-life of CDK6 mRNA and increased the proportion of CDK6 mRNA present in the polyribosomal fraction, indicating that DHX9 may negatively regulate CDK6 expression through a posttranscriptional regulatory mechanism.To explore whether DHX9 could bind directly to CDK6 mRNA, RIP assays with a DHX9 antibody were performed and the amount of CDK6 mRNA was detected by quantitative real-time PCR with a series of primers covering the entire CDK6 transcript.Three fragments within the 3'-untranslated region (UTR) of CDK6 mRNA, which were respectively detected by primer sets 2, 9 and 10, were significantly enriched in the anti-DHX9 immunoprecipitates.RNA pull-down assays revealed that DHX9 was pulled down by CDK6-DBE1 and lnc-UCID-core.These results showed that DHX9 interacted with lnc-UCID and CDK6 mRNA, and that both lnc- UCID and DHX9 regulated CDK6 expression.We next investigated whether lnc-UCID bound competitively to DHX9 and sequestered it from CDK6 mRNA. RIP assays showed that CDK6- DBE1 and lnc-UCID.lnc-UCID may disrupt the association between DHX9 and the CDK6-3'UTR.further explored whether other mechanisms exist. miR-148a, a tumor-suppressive microRNA,(24,25) was predicted to bind to the 407-428-nt region of lnc- UCID by using the TargetScan database.A dual-luciferase reporter assay showed that miR-148a expression significantly attenuated the luciferase activity of the reporter with wildtype lnc-UCID.Furthermore, the expression of miR-148a was frequently downregulatedand was negatively correlated with lnc-UCID level in HCC tissues.Consistently, overexpression of miR-148a reduced DNA replication and cell growth of hepatoma cells.Taken together, amplification of the lnc-UCID gene and down-regulation of miR-148a may lead to increased expression of lnc-UCID, which binds to DHX9 and abrogates its inhibition on CDK6 expression, resulting in up-regulation of CDK6 and in turn uncontrolled cell proliferation.	30865310	RID02914	expression association	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	Lnc-UCID	CDK6	positively-E	siRNA;overexpression;RNA pull-down assay;RIP;Co-immunoprecipitation;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(DHX9)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000105810	NA	NA	1021	NA	MCPH12|PLSTIRE	lnc-ucid is up-reg ulate d in hcc tissues, and sile ncing lnc-ucid inhibits tumor growth in vitro and in vivo. These lncRNAs were therefore examined in our study cohort by quantitative real-time PCR. Compared with nontumor liver tissues, more than 50% increases in the RNA levels.To explore how lnc-UCID up-regulated CDK6, RNA pull-down assays were used to identify lnc-UCID-associated proteins. DHX9, an RNA helicase with RNA-binding activity, was identified in the protein complexes pulled down by lnc-UCID.RNA immunoprecipitation (RIP) assay was performed to further confirm the in vivo interaction between lnc-UCID and DHX9.Results revealed 850-1030-nt to be the core sequence for lnc-UCID binding to DHX9.We found that DHX9 knockdown significantly increased the protein and mRNA levels of CDK6, but had no impact on the level of CDK6 precursor mRNA. Furthermore, silencing DHX9 dramatically prolonged the half-life of CDK6 mRNA and increased the proportion of CDK6 mRNA present in the polyribosomal fraction, indicating that DHX9 may negatively regulate CDK6 expression through a posttranscriptional regulatory mechanism.To explore whether DHX9 could bind directly to CDK6 mRNA, RIP assays with a DHX9 antibody were performed and the amount of CDK6 mRNA was detected by quantitative real-time PCR with a series of primers covering the entire CDK6 transcript.Three fragments within the 3'-untranslated region (UTR) of CDK6 mRNA, which were respectively detected by primer sets 2, 9 and 10, were significantly enriched in the anti-DHX9 immunoprecipitates.RNA pull-down assays revealed that DHX9 was pulled down by CDK6-DBE1 and lnc-UCID-core.These results showed that DHX9 interacted with lnc-UCID and CDK6 mRNA, and that both lnc- UCID and DHX9 regulated CDK6 expression.We next investigated whether lnc-UCID bound competitively to DHX9 and sequestered it from CDK6 mRNA. RIP assays showed that CDK6- DBE1 and lnc-UCID.lnc-UCID may disrupt the association between DHX9 and the CDK6-3'UTR.further explored whether other mechanisms exist. miR-148a, a tumor-suppressive microRNA,(24,25) was predicted to bind to the 407-428-nt region of lnc- UCID by using the TargetScan database.A dual-luciferase reporter assay showed that miR-148a expression significantly attenuated the luciferase activity of the reporter with wildtype lnc-UCID.Furthermore, the expression of miR-148a was frequently downregulatedand was negatively correlated with lnc-UCID level in HCC tissues.Consistently, overexpression of miR-148a reduced DNA replication and cell growth of hepatoma cells.Taken together, amplification of the lnc-UCID gene and down-regulation of miR-148a may lead to increased expression of lnc-UCID, which binds to DHX9 and abrogates its inhibition on CDK6 expression, resulting in up-regulation of CDK6 and in turn uncontrolled cell proliferation.	30865310	RID02915	ceRNA or sponge	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	MIR148A	Lnc-UCID	negatively-E	Targetscan;luciferase reporter assay;overexpression	upregulation	qRT-PCR	NA	NA	cell growth(+);cell cycle(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	miRNA	lncRNA	ENSG00000199085	NA	NA	NA	406940	NA	MIRN148|MIRN148A|hsa-mir-148|mir-148a	NA	lnc-ucid is up-reg ulate d in hcc tissues, and sile ncing lnc-ucid inhibits tumor growth in vitro and in vivo. These lncRNAs were therefore examined in our study cohort by quantitative real-time PCR. Compared with nontumor liver tissues, more than 50% increases in the RNA levels.To explore how lnc-UCID up-regulated CDK6, RNA pull-down assays were used to identify lnc-UCID-associated proteins. DHX9, an RNA helicase with RNA-binding activity, was identified in the protein complexes pulled down by lnc-UCID.RNA immunoprecipitation (RIP) assay was performed to further confirm the in vivo interaction between lnc-UCID and DHX9.Results revealed 850-1030-nt to be the core sequence for lnc-UCID binding to DHX9.We found that DHX9 knockdown significantly increased the protein and mRNA levels of CDK6, but had no impact on the level of CDK6 precursor mRNA. Furthermore, silencing DHX9 dramatically prolonged the half-life of CDK6 mRNA and increased the proportion of CDK6 mRNA present in the polyribosomal fraction, indicating that DHX9 may negatively regulate CDK6 expression through a posttranscriptional regulatory mechanism.To explore whether DHX9 could bind directly to CDK6 mRNA, RIP assays with a DHX9 antibody were performed and the amount of CDK6 mRNA was detected by quantitative real-time PCR with a series of primers covering the entire CDK6 transcript.Three fragments within the 3'-untranslated region (UTR) of CDK6 mRNA, which were respectively detected by primer sets 2, 9 and 10, were significantly enriched in the anti-DHX9 immunoprecipitates.RNA pull-down assays revealed that DHX9 was pulled down by CDK6-DBE1 and lnc-UCID-core.These results showed that DHX9 interacted with lnc-UCID and CDK6 mRNA, and that both lnc- UCID and DHX9 regulated CDK6 expression.We next investigated whether lnc-UCID bound competitively to DHX9 and sequestered it from CDK6 mRNA. RIP assays showed that CDK6- DBE1 and lnc-UCID.lnc-UCID may disrupt the association between DHX9 and the CDK6-3'UTR.further explored whether other mechanisms exist. miR-148a, a tumor-suppressive microRNA,(24,25) was predicted to bind to the 407-428-nt region of lnc- UCID by using the TargetScan database.A dual-luciferase reporter assay showed that miR-148a expression significantly attenuated the luciferase activity of the reporter with wildtype lnc-UCID.Furthermore, the expression of miR-148a was frequently downregulatedand was negatively correlated with lnc-UCID level in HCC tissues.Consistently, overexpression of miR-148a reduced DNA replication and cell growth of hepatoma cells.Taken together, amplification of the lnc-UCID gene and down-regulation of miR-148a may lead to increased expression of lnc-UCID, which binds to DHX9 and abrogates its inhibition on CDK6 expression, resulting in up-regulation of CDK6 and in turn uncontrolled cell proliferation.	30865310	RID02916	expression association	NA		
Hepatocellular carcinoma	AB209371	SNAI1	positively-E	luciferase reporter assay;western blot;overexpression;Targetscan;siRNA	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000124216	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	LncRNA-AB209371 promotes the epithelial-mesenchymal transition of hepatocellular carcinoma cells. The present study demonstrated that the expression of Snail1 in HCC tissues was significantly higher compared with its expression in tissues adjacent to primary sites, as determined via western blot.The relative levels of AB209371 and hsa-miR199a-p in primary and metastatic HCC tissues were significantly increased compared with adjacent normal tissue.Bioinformatics analysis identified a seven-based hsa-miR199a-5p seed sequence in the 3miR199a-5Snail1 mRNA.The inhibitive ability of mimics was regained following AB209371 silencing.The theoretical binding sites of hsa-miR199a-5p and AB209371 were predicted using the bioinformatics software targetScan-Recombinant lentiviruses (Lv-NC, Lv-siRNA-AB209371, Lv-Snail1 and Lv-miR199a-5p) were used to infect MHCC97-H cells.AB209371 silencing inhibits EMT in TGF-beta1 induced HCC cells.Additionally, AB209371 silencing combined with hsa-miR199a-5p overexpression may be an effective means to inhibit the metastasis of HCC and the EMT of HCC cells.	30864719	RID02917	ceRNA or sponge	metastasis		UP(PAAD);DATA(GSE40174)
Acute renal injury	MEG3	TNF	positively-E	western blot;siRNA;overexpression;luciferase reporter assay;immunohistochemical staining	upregulation	RT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-199a-5p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000228978	NA	55384	7124	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DIF|TNF-alpha|TNFA|TNFSF2	Inhibition of lncRNA MEG3 protects renal tubular from hypoxia-induced kidney injury in acute renal allografts by regulating miR-181b/TNF-alpha signaling pathway. Real-time polymerase chain reaction (RT-PCR analysis found that the levels of MEG3 and miR-181b-5p were increased and decreased respectively in grafted kidney.Real-time polymerase chain reaction (RT-PCR analysis found that the levels of MEG3 and miR-181b-5p were increased and decreased respectively in grafted kidney. The western blot assay showed that TNF-alpha was upregulated in the kidney and in HK-2 cells. Administering MEG3-specific small interfering RNA (siRNA) in mice silenced MEG3 expression and protected kidney renal allograft from injury. Bioinformatical analysis and luciferase assay indicated that MEG3 is a target of miR-181b-5p. MEG3 inhibition and overexpression promoted and suppressed miR-181b-5p levels respectively. In addition, western blot and immunohistochemical staining suggested that decreased TNF-alpha expression was observed in the kidney. In contrary to MEG3, miR181b overexpression attenuated hypoxia-induced HK-2 cell apoptosis, as well as suppressed hypoxiainduced TNF-alpha upregulation. In luciferase reporter assay, we confirmed that miR-181b directly bound to the 3'untranslated region (3'UTR) of TNFalpha, thereby negatively regulating the TNF-alpha expression. Our data suggested that MEG3 functions as a competing endogenous RNA for miR-181b to regulate the TNF-alpha expression in hypoxia-induced kidney injury in acute renal allografts.	30860638	RID02918	ceRNA or sponge	NA		DOWN(LIHC);DATA(GSE117623)
Tongue squamous cell carcinoma	SPAAR	CTNNB1	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000235387	GRCh38_9:35909490-35937153	ENSG00000168036	NA	158376	1499	LINC00961|SPAR	armadillo|beta-catenin|CTNNB	Long noncoding RNA LINC00961 inhibited cell proliferation and invasion through regulating the Wnt/beta-catenin signaling pathway in tongue squamous cell carcinoma. LINC00961 was downregulated in TSCC samples.We indicated that the protein expression of beta-catenin was decreased in SCC1 cell after treated with pcDNA-LINC00961 by using western blot.In addition, we showed that overexpression of LINC00961 decreased the mRNA expression of beta-catenin in SCC1 cell by using qRT-PCRassay.Downregulated expression of LINC00961 induced cell proliferation in SCC1 cell and this effect can be inhibited by treating with the Wnt/beta-catenin inhibitor XAV-939. Moreover, knockdown of LINC00961 promoted cell invasion in SCC1 cell and this effect could be blocked with the Wnt/beta-catenin inhibitor XAV-939.We indicated that overexpression of LINC00961 decreased beta-catenin expression. Knockdown of LINC00961 promoted cell proliferation and invasion partly via promoting the Wnt/beta-catenin signaling pathway. These results suggested that LINC00961 was downregulated in TSCC tissues and acted as a tumor suppressor gene in the development of TSCC.	30854692	RID02919	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Infantile hemangioma	CYTOR	MKI67	positively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);AKT/mTOR signaling pathway(+);Notch signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000148773	NA	112597	4288	C2orf59|LINC00152|MGC4677|NCRNA00152	MIB-1|PPP1R105	Linc00152 knockdown inactivates the Akt/mTOR and Notch1 pathways to exert its anti-hemangioma effect.To confirm it, the expressions of Linc00152 in 12 IH tissues and corresponding adjacent normal tissues were determined by qRT-PCR The results showed that Linc00152 expression in the IH tissues was higher than that in the adjacent normal tissues.Knockdown of Linc00152 suppresses the Akt/mTOR pathway.Knockdown of Linc00152 suppresses the Notch1 pathway.The Ki67 expression was decreased after si-Linc00152 transfection, which confirmed the inhibitory effect of Linc00152 knockdown on cell proliferation.Further investigations showed that the inhibitory effects of si-Linc00152 on cell proliferation and Ki67 expression were mitigated by Notch1 overexpression.Knockdown of Linc00152 inhibits proliferation and induces apoptosis by the Akt/mTOR pathway in HemECs.Knockdown of Linc00152 suppressed HemECs proliferation and induced apoptosis via inhibiting Akt/mTOR and Notch1 signaling pathways.	30851338	RID02920	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Multiple myeloma	TUG1	HDAC4	positively-E	starBase;RIP;luciferase reporter assay;siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(-)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000068024	NA	55000	9759	FLJ20618|LINC00080|NCRNA00080	BDMR|HA6116|HD4|HDAC-4|HDAC-A|HDACA|KIAA0288	Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p. The relative expression of TUG1 was measured in 24 newly diagnosed MM samples and eight healthy donors-tissues by qRT-PCR Results revealed that TUG1 expression was significantly increased inMMpatients compared with the healthy donors-sample.To verify whether TUG1 could act as a ceRNA for a certain miRNA, bioinformatics software Starbase2.0 was used to hunt for TUG1 targets. Among miRNAs, miR-29b-3p was selected as the predicted target with the high score.To confirm this predication, luciferase reporter assay was conducted. As shown in Figure 3B, overexpression of miR-29b significantly decreased luciferase activity of WT-TUG1, but not of MT-TUG1. RIP experiment further confirmed that Ago2 antibody-enriched immunoprecipitation emerged more abundant TUG1 andmiR-29b-3pRNAcomparedwith the control group.In addition, we found that TUG1 knockdown increased miR-29b-3p expression in NCI-H929 cells, whereas overexpression of miR-29b-3p reduced TUG1 expression in NCI-H929 cells.These data revealed that miR-29b-3p can directly bind to TUG1 in a usual way.Knockdown of TUG1 suppresses cell progression and induced cell apoptosis.MiR-29b-3p inhibition reverses effects of TUG1 knockdown in MM cells.Based on the ceRNA competition principle, we concluded that the authentic target mRNAs of miR-29b-3p should be regulated by TUG1.These results suggested that TUG1 could serve as a ceRNA to regulate HDAC4 expression by competitively binding miR-29b-3p in MM cells.These findings suggested that TUG1 exerted an oncogenic role in MM by acting as a competing endogenous RNA of miR-29b-3p, and implied the potential application of TUG1 in treatment for MM.	30842339	RID02921	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	SPAAR	CRLS1	positively-E	LncBase;western blot;luciferase reporter assay;overexpression;Targetscan;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-5581-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000235387	GRCh38_9:35909490-35937153	ENSG00000088766	NA	158376	54675	LINC00961|SPAR	C20orf155|CLS1|dJ967N21.6|GCD10	Small regulatory polypeptide of amino acid response negatively relates to poor prognosis and controls hepatocellular carcinoma progression via regulating microRNA-5581-3p/human cardiolipin synthase 1. It was found that LINC00961 was distinctly downregulated in HCC tissues in contrast to the corresponding nontumor tissues.LINC00961 overexpression inhibits cell proliferation, invasion, and migration in HCC cells.With the assistance of LncBase v.2 in DIANA tools, we found that LINC00961 contained potential sequences that were complementary to miR-5581-3p.Then, the luciferase reporter assay showed that the increased level of miR-5581-3p resulted in dimmed luciferase activity of the LINC00961-WT instead of that of LINC00961-Mut.miR-5581-3p upregulation recovered the inhibited cell proliferation, migration, and invasion induced by LINC00961 upregulation in HCC cells.CRLS1, which has been found to play an important role in inhibiting cell growth in HCC (Bidkhori et al., 2018), was predicted to be the downstream target of miR-5581-3p through TargetScan website.LINC00961 regulates CRLS1 expression in HCC through competitively binding with miR-5581-3p.On the whole, our findings disclosed that LINC00961 played a suppressive role in HCC progression via modulating miR-5581-3p/CRLS1, thus providing a potentially effective target for the prognosis and treatment of patients with HCC.	30825207	RID02922	ceRNA or sponge	prognosis		UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Diabetes mellitus	H19	VDR	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-675)	regulation	NA	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000111424	NA	283120	7421	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NR1I1|PPP1R163	A negative feedback loop of H19/miR-675/EGR1 is involved in diabetic nephropathy by downregulating the expression of the vitamin D receptor.  The relative expression of H19, miR-675, and VDR was measured by qRT-PCRand western blotThe relative expression of miR-675 was higher in the presence of H19, whereas the expression of both VDR and EGR1 messenger RNA was decreased in the presence of H19 or miR-675.To verify the above hypothesis, luciferase activities were detected in CIHP-1 or HEK 293 cells treated with miR-675 mimics or H19 following the transfection of wild-type/mutant VDR. The relative luciferase activity of wild-type VDR was obviously reduced in CIHP-1 cells treated with miR-675 mimics,validating VDR as a target of miR-625.The luciferase activity of CIHP-1 cells treated with H19 promoters was evidently increased compared with that in the blank control group.In this negative feedback loop, H19 negatively regulates the expression of VDR by upregulating the expression of miR-675. The reduced VDR expression leads to the downregulation of EGR1 expression. As EGR1 is positively related to H19, the downregulation of EGR1 also inhibits the expression of H19.the expression of VDR by upregulating the expression of miR-675. The reduced VDR expression leads to the downregulation of EGR1 expression. As EGR1 is positively related to H19, the downregulation of EGR1 also inhibits the expression of H19.	30815865	RID02923	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE75367)
Diabetes mellitus	EGR1	H19	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Disease of metabolism	Diabetes mellitus	TF	lncRNA	ENSG00000120738	NA	ENSG00000130600	GRCh38_11:1995171-2001470	1958	283120	225|AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	A negative feedback loop of H19/miR-675/EGR1 is involved in diabetic nephropathy by downregulating the expression of the vitamin D receptor.  The relative expression of H19, miR-675, and VDR was measured by qRT-PCRand western blotThe relative expression of miR-675 was higher in the presence of H19, whereas the expression of both VDR and EGR1 messenger RNA was decreased in the presence of H19 or miR-675.To verify the above hypothesis, luciferase activities were detected in CIHP-1 or HEK 293 cells treated with miR-675 mimics or H19 following the transfection of wild-type/mutant VDR. The relative luciferase activity of wild-type VDR was obviously reduced in CIHP-1 cells treated with miR-675 mimics,validating VDR as a target of miR-625.The luciferase activity of CIHP-1 cells treated with H19 promoters was evidently increased compared with that in the blank control group.In this negative feedback loop, H19 negatively regulates the expression of VDR by upregulating the expression of miR-675. The reduced VDR expression leads to the downregulation of EGR1 expression. As EGR1 is positively related to H19, the downregulation of EGR1 also inhibits the expression of H19.the expression of VDR by upregulating the expression of miR-675. The reduced VDR expression leads to the downregulation of EGR1 expression. As EGR1 is positively related to H19, the downregulation of EGR1 also inhibits the expression of H19.	30815865	RID02924	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	UP(NSCLC);DATA(GSE74639)
Colorectal cancer	MALAT1	SLAIN2	positively-E	starBase;miRcode;immunohistochemistry;RIP;RNA pull-down assay;luciferase reporter assay;overexpression;shRNA;FISH	upregulation	qPCR	TCGA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-106b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109171	NA	378938	57606	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FLJ21611|KIAA1458	MALAT1 sponges miR-106b-5p to promote the invasion and metastasis of colorectal cancer via SLAIN2 enhanced microtubules mobility.In order to understand the role ofmiR-106b-5p in CRC, we analyzed the expression of miR-106b-5p in CRC in The Cancer Genome Altas (TCGA) dataset. The level of miR-106b was significantly decreased in tumor tissues.We selected the pairs of lncRNA-miRNA that were supported by at least three algorithms from StarBase and also filtered the pairs of lncRNA-miRNA from miRcode database.qPCR was used to analyze the level of these four lncRNAs in 20 pairs of normal and CRC tissues.An anti-GFP RNA immunoprecipitation (RIP) assay was performed, and the results showed that miR-106b-5p was only enriched in wild-type MALAT1, while the enrichment caused by mut MALAT1 was not significant as compared to the MS2 control.The RNA pull-down assay revealed that miR-106b-5p could be pulled down by biotin-labeled wild-type MALAT1.A luciferase reporter construct containing MALAT1 (wild-type or miR-106b-5p binding site mutated type) was generated and co-transfected into SW480 cells or HCT-8 cells with miR-106b-5p inhibitor ormiR-106b-5pmimics, respectively.AGO2 is essential in miRNA-induced posttranscriptional repression or degradation of RNA to form an RNA-induced silencing complex (RISC) combined with the miRNA targets, which was confirmed with an anti-AGO2 RIP assay.To further elucidate the correlation between MALAT1 and miR- 106b-5p, CRC cells were transfectedwithMALAT1 overexpression plasmids or shMALAT1.RNA fluorescence in situ hybridization (FISH) assay was performed for their cellular localization.MALAT1 regulates the expression of SLAIN2 through competitive interaction with miR-106b-5p.miR-106b-5p served as a suppressor in combination with MALAT1/miR-106b-5p/SLAIN2, which might be a group of potential prognostic biomarkers in the prognosis of CRC.	30797712	RID02925	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Retinoblastoma	PVT1	NOTCH2	positively-E	miRBase;miTarget;Targetscans;luciferase reporter assay;overexpression;siRNA	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-488-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000134250	NA	5820	4853	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of lncRNA PVT1 inhibits retinoblastoma progression by sponging miR-488-3p.Expression levels of PVT1 in RB tissues (n=78) and normal retina tissues were analyzed using RT-qPCR and the results revealed that the relative expression of PVT1 in RB tissues was strikingly higher compared to the normal tissues.Potential miRNA candidates targeting PVT1 were predicted using miRBase, miTarget, and TargetScanS.MiR-488-3p expression was downregulated in RB tissues compared with those in normal tissues based on RT-qPCR analysis.To examine the potential lncRNA-siRNA interaction,we constructed luciferase reporter vectors containing wild or mutant PVT1 putative binding sites in miR-488-3p.We investigated the role of PVT1 on miR-488-3p regulation and found that knockdown of PVT1 significantly upregulated miR-488-3p expression. Interestingly, overexpression of miR-488-3p evidently increasing the expression of PVT1 and downregulation of miR-488-3p showed the opposite effects. These results proved that PVT1 may function as miR-488-3p sponge.Consistently, notch2 protein expression showed the same alteration in RB cells.Notch2 mRNA and proteins levels were observably decreased when transfected with si-PVT1 in both two RB cell lines.Taken together, above data revealed that PVT1/miR-488-3p/notch2 regulatory pathway promotes the tumorigenesis of RB.In general, our results demonstrated that PVT1 may be a novel biomarker for prognosis and a new target for the treatment of RB.	30797143	RID02926	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	FOXA2	LINC00261	positively-E	shRNA	downregulation	sequencing	TCGA	NA	DNA damage(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000125798	NA	ENSG00000259974	GRCh38_20:22547671-22578642	3170	140828	HNF3B	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	LINC00261 Is an Epigenetically Regulated Tumor Suppressor Essential for Activation of the DNA Damage Response.To exclude lncRNAs differentially expressed due to effects of in vitro cell culture, we compared this set of lncRNAs to those differentially expressed in publicly available datasets of primary human LUAD tumors profiled by TCGA.Identification of LINC0261 as a tumor suppressor in LUAD.To determine the major pathways affected by LINC00261 function, we performed RNA sequencing (RNA-seq) on the H522-CMV-NEO and H522-CMV-LINC00261 table cell lines.LINC00261 was able to increase the amount of detectable ATM phosphorylation.The increased activation of ATM in the presence of LINC00261 was striking, as ATM is the sensor of DNA damage within the cell.shRNAmediated ablation of FOXA2 decreased endogenous expression of LINC00261. However, knockdown of LINC00261 did not affect FOXA2 levels.FOXA2 was able to induce LINC00261 expression, and the entire locus underwent hypermethylation in LUAD, leading to loss of expression. We have thus identified an epigenetically deregulated lncRNA, whose loss of expression in LUAD promotes the malignant phenotype and blocks activation of the DNA damage machinery, predisposing lung cells to cancer development.These findings identify LINC00261 as a tumor suppressor that blocks cellular proliferation by activating the DNA damage response and suggest that epigenetic therapy to inhibit DNA methylation may enhance treatment of LUAD.	30796052	RID02927	transcriptional regulation	NA		UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	LINC00261	ATM	positively-E		downregulation	sequencing	TCGA	NA	DNA damage(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000149311	NA	140828	472	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	ATA|ATC|ATD|ATDC|TEL1|TELO1	LINC00261 Is an Epigenetically Regulated Tumor Suppressor Essential for Activation of the DNA Damage Response.To exclude lncRNAs differentially expressed due to effects of in vitro cell culture, we compared this set of lncRNAs to those differentially expressed in publicly available datasets of primary human LUAD tumors profiled by TCGA.Identification of LINC0261 as a tumor suppressor in LUAD.To determine the major pathways affected by LINC00261 function, we performed RNA sequencing (RNA-seq) on the H522-CMV-NEO and H522-CMV-LINC00261 table cell lines.LINC00261 was able to increase the amount of detectable ATM phosphorylation.The increased activation of ATM in the presence of LINC00261 was striking, as ATM is the sensor of DNA damage within the cell.shRNAmediated ablation of FOXA2 decreased endogenous expression of LINC00261. However, knockdown of LINC00261 did not affect FOXA2 levels.FOXA2 was able to induce LINC00261 expression, and the entire locus underwent hypermethylation in LUAD, leading to loss of expression. We have thus identified an epigenetically deregulated lncRNA, whose loss of expression in LUAD promotes the malignant phenotype and blocks activation of the DNA damage machinery, predisposing lung cells to cancer development.These findings identify LINC00261 as a tumor suppressor that blocks cellular proliferation by activating the DNA damage response and suggest that epigenetic therapy to inhibit DNA methylation may enhance treatment of LUAD.	30796052	RID02928	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Coronary atherosclerotic heart disease	MALAT1	MAPK1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell autophagy(-);mTOR signaling pathway(+);cell viability(+);apoptosis process(-)	ceRNA(miR-15b-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100030	NA	378938	5594	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	MALAT1/miR-15b-5p/ MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway.MALAT1 was overexpressed in CAD blood samples and EPCs. Knockdown of MALAT1 and MAPK1 promoted cell viability, autophagy and further suppressed the development of CAD. AntagoMALAT1 protects mice against atherosclerosis.LncRNA MALAT1 inhibited EPCs autophagy and increased cell viability while repressed apoptosis of CAD via activating mTOR signaling pathway.	30787203	RID02929	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	HAGLR	miR-204	negatively-F	luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|Mdgt|MIR7704HG	NA	Knockdown of lncRNA HOXD-AS1 suppresses proliferation, migration and invasion and enhances cisplatin sensitivity of glioma cells by sponging miR-204.knockdown of HOXD-AS1 suppressed proliferation, migration and invasion and enhanced DDP sensitivity of glioma cells through sequestering miR-204, providing a promising therapeutic target for glioma patients.To explore the role of HOXD-AS1 in glioma, we firstly analyzed the expression level of HOXD-AS1 in glioma tissues from TCGA-GBM dataset. HOXD-AS1 was significantly up-regulated in glioma tumor tissues compared with normal tissues (Fig. 1A). To validate the result, we performed qRT-PCRanalysis to detect HOXD-AS1 expression in 40 paired glioma tumor and adjacent normal tissues. Consistently, HOXD-AS1 was remarkably increased in glioma tumor tissues compared with adjacent normal tissues (Fig. 1B).To investigate the functional role of HOXD-AS1 in glioma, U87 and U251 cells were transfected with si-con or si-HOXD-AS1. The results of qRT-PCRanalysis indicated that introduction of si-HOXD-AS1 dramatically decreased HOXD-AS1 expression in U87 and U251 cells (Fig. 2A). To explore the effect of HOXD-AS1 on the proliferation of glioma cells, MTT assay was performed in U87 and U251 cells. The results revealed that HOXD-AS1 knockdown remarkably suppressed the proliferation of U87 and U251 cells (Fig. 2B and 2C). Moreover, down-regulation of HOXD-AS1 obviously reduced the number of cell colonies in U87 and U251 cells (Fig. 2D). To further explore the effect of HOXD-AS1 on migration and invasion of glioma cells, Transwell assays was performed in U87 and U251 cells. Compared with the control groups, transfection of si-HOXD-AS1 significantly inhibited the migration and invasion in U87 and U251 cells (Fig. 2E and F). Collectively, these results suggested that knockdown of HOXD-AS1 suppressed proliferation, migration and invasion in glioma cells.To confirm this prediction, luciferase reporter assay was performed in U87 and U251 cells. Results demonstrated that miR-204 overexpression dramatically reduced the luciferase activity of the wild-type reporter vector (HOXD-AS1-WT), but not the mutant reporter vector (HOXD-AS1-MUT) in U87 and U251 cells (Fig. 4B and 4C). The effect of HOXD-AS1 on miR-204 expression in glioma cells was further explored by qRT-PCRanalysis. HOXD-AS1 knockdown remarkably elevated miR-204 expression, while HOXD-AS1 overexpression considerably reduced miR-204 expression in U87 and U251 cells (Fig. 4D and 4E). Moreover, miR-204 expression was obviously down-regulated in glioma tumor tissues (Fig. 4F). Furthermore, the expression of miR-204 was dramatically decreased in glioma cells (Fig. 4G). Correlation analysis revealed that miR-204 expression was negatively correlated with HOXD-AS1 expression in glioma tumor tissues (Fig. 4H). All these data suggested that HOXD-AS1 may act as a miR-204 sponge in glioma cells.	30784927	RID02930	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	
Corneal neovascularization	MIAT	MIR1246	negatively-E	RNA pull-down assay;RIP	upregulation		NA	NA	cell proliferation(+);cell migration(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Keratitis	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000283203	NA	440823	100302142	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	MIRN1246|hsa-mir-1246	lncRNA MIAT suppression alleviates corneal angiogenesis through regulating miR-1246/ACE.The expression of MIAT and Ang II was increased, while miR-1246 was decreased in CRNV rat model. VEGF stimulation significantly promoted cell proliferation and migration of HUVECs.MIAT directly regulated the expression of miR-1246.	30782069	RID02931	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Urinary bladder cancer	SNHG14	VAMP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000220205	NA	104472715	6844	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	SYB2|VAMP-2	LncSNHG14 promotes the development and progression of bladder cancer by targeting miRNA-150-5p.The overexpression of SNHG14 accelerated the proliferative potential and cell cycle progression of BCa cells. SNHG14 was confirmed to bind to miRNA-150-5p. MiRNA-150-5p remained a low expression in BCa tissues. VAMP2 was the target gene of miRNA-150-5p.LncSNHG14 overexpression accelerates proliferative potential and cell cycle progression of BCa cells through absorbing miRNA-150-5p to degrade VAMP2 expression.SNHG14 was highly expressed in BCa tissues and cell lines. The overexpression of SNHG14 accelerated the proliferative potential and cell cycle progression of BCa cells. SNHG14 was confirmed to bind to miRNA-150-5p. MiRNA-150-5p remained a low expression in BCa tissues. Moreover, miRNA-150-5p overexpression suppressed proliferative potential and cell cycle progression of BCa cells, which could reverse the promotive role of SNHG14 on behaviors of BCa cells. Furthermore, VAMP2 was the target gene of miRNA-150-5p. VAMP2 overexpression reversed the biological function of miRNA-150-5p in inhibiting proliferative potential and cell cycle progression of T24 and UC9 cells.	30779068	RID02932	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Atherosclerosis	H19	ACP5	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000102575	NA	283120	54	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	HPAP|TRAP	Long Noncoding RNA-H19 Contributes to Atherosclerosis and Induces Ischemic Stroke via the Upregulation of Acid Phosphatase 5.Lentivirus-mediated H19-forced expression upregulated ACP5 protein levels,promoted cell proliferation and suppressed the apoptosis. IncRNA-H19 promoting ACP5 protein expression contributed to atherosclerosis and increased the risk of ischemic stroke. H19 and ACP5 Expressions Were Elevated in Patients With Atherosclerosis Subsequently, the expressions of H19 and ACP5 in blood serum of atherosclerotic patients and healthy population were determined. The results showed that H19 and ACP5 expressions were significantly increased in atherosclerotic patients, suggesting the positive regulatory effect of H19 (Figure 4A) on ACP5 expression (Figure 4B).Simultaneously, an evaluation of cell apoptosis was detected. Our results revealed that caspase3 (apoptotic marker protein) was significantly downregulated in lncRNA-H19-overexpressed cell lines (Figure 6A). Supportably, flow cytometry also showed declined cell apoptosis (Figure 6B). These results suggest that lncRNA-H19 overexpression can inhibit cell apoptosis.lncRNA-H19 Positively Regulates ACP5 Expression at the Post-transcript Level To further understand the regulatory relationship between H19 and ACP5, dual-luciferase reporter system was constructed. The results showed that the activity of fluorescent protein was significantly enhanced after co-transformation of ACP5 mRNA/pGL3-BS and lncRNA-H19 (Figure 7), indicating that lncRNA-H19 upregulates the content of ACP5 protein.	30778327	RID02933	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Atherosclerosis	LINC00299	AURKA	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000236790	GRCh38_2:7988683-8488284	ENSG00000087586	NA	339789	6790	C2orf46|FLJ45673|NCRNA00299	AIK|ARK1|AurA|BTAK|PPP1R47|STK15|STK6|STK7	Linc00299/miR-490-3p/AURKA axis regulates cell growth and migration in atherosclerosis.Long non-coding RNA (lncRNA) plays a crucial role in regulating various cellular processes in atherosclerosis. The present study identified the regulation of Linc00299, via miR-490-3p targeting Aurora kinase A (AURKA), on migration and proliferation of endothelial cells and vascular smooth muscle cells (VSMCs) during atherosclerosis. The expression of RNAs was assessed by real-time PCR. The proliferation, apoptosis and migration were detected using MTT assay, Annexin V/PI staining and Transwell system, respectively. Bindings of Linc00299/miR-490-3p and subsequent miR-490-3p/AURKA were verified by luciferase and biotin pull-down assays. The protein expression of AURKA was detected by western blot. Expressions of Linc00299 and miR-490-3p were upregulated and downregulated in atherosclerosis patients, respectively. Both Linc00299 knockdown and miR-490-3p overexpression suppressed cell proliferation, increased apoptosis and inhibited migration of VSMCs and HUVECs. Linc00299 directly bound to miR-490-3p which targeted AURKA. The regulation of Linc00299 on expression of AURKA and proliferation and migration of VSMCs were dependent on miR-490-3p. Atherosclerosis-increased Linc00299 acts as a sponge of miR-490-3p to upregulate AURKA, and as a result increases proliferation and migration in VSMCs and HUVECs. Our study reveals an important effect of Linc00299/miR-490-3p/AURKA axis on regulating cell proliferation and migration in atherosclerosis.	30734057	RID02934	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Melanoma	TUG1	RGS1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-29c-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000090104	NA	55000	5996	FLJ20618|LINC00080|NCRNA00080	1R20|BL34|IER1|IR20	Long non-coding RNA TUG1 recruits miR-29c-3p from its target gene RGS1 to promote proliferation and metastasis of melanoma cells.To determine the expression of TUG1 in melanoma cells, TUG1 expression levels were initially investigated using RT-qPCR assays. TUG1 was found to be highly expressed in melanoma cell lines (Fig. 2A). Moreover, TUG1 was more highly expressed in SK-MEL-2 cells compared with A375 cells. A TUG1 overexpression plasmid and siRNA sequences against TUG1 were used and transfected to melanoma cell lines in order to investigate the role of this protein in melanoma.It has been reported that the upregulation of TUG1 may promote the proliferation of cancer cells (27,28), although its potential contribution to the pathogenicity of melanoma remains elusive. Therefore, the proliferation of melanoma cells was assessed using CCK-8 assays at 0, 24, 48 and 72 h following transfection. The overexpression of TUG1 significantly promoted A375 cell proliferation, while TUG1 knockdown significantly suppressed SK-MEL-2 cell proliferation (Fig. 3A). The effect of TUG1 on melanoma cell apoptosis was validated by flow cytometry. Overexpression of TUG1 suppressed the induction of apoptosis in A375 cells, whereas the depletion of TUG1 by si-TUG1 induced the apoptotic cascade in SK-MEL-2 cells (Fig. 3B). Similarly, the Transwell invasion assay indicated that TUG1 upregulation significantly induced the invasion of A375 cells, whereas knockdown of TUG1 significantly reduced the invasive capacity of SK-MEL-2 cells (Fig. 3C). As expected, the overexpression of TUG1 enhanced the proliferation and invasive ability of A375 cells, whereas the depletion of TUG1 suppressed the proliferation and invasive activity of SK-MEL-2 cells. Subsequently, dual-luciferase reporter assays were performed in order to explore the interaction between miR-29c-3p and TUG1. The data indicated that TUG1 upregulated the luciferase activity of pmirGLO-TUG1. Moreover, miR-29c-3p mimics reversed the inductive effect of pmirGLO-TUG1, and reduced the luciferase activity of pmirGLO-TUG1 (Fig. 6B).Furthermore, the pull-down assay indicated that miR-29c-3p was precipitated by the TUG1 probe (Fig. 6D). These data revealed that TUG1 acted as a ceRNA to regulate the expression of miR-29c-3p and promote the expression of RGS1 in melanoma.	30720136	RID02935	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE86978)
Pancreatic cancer	LINC00052	miR-330-3p	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+);cell migration(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000259527	GRCh38_15:87576929-87579866	NA	NA	145978	NA	NCRNA00052|TMEM83	NA	LINC00052 functions as a tumor suppressor through negatively modulating miR-330-3p in pancreatic cancer.we observed that the LINC00052 was obviously downregulated in several pancreatic cancer cell lines. Overexpression of LINC00052 greatly repressed AsPC-1 and SW1990 cell proliferation, triggered the apoptosis and prevented cell cycle in the G1 phase. For another, AsPC-1 and SW1990 cell migration and invasion capacity were also obviously repressed by LINC00052 upregulation. Moreover, miR-330-3p was elevated in pancreatic cancer cells and can function as a target of LINC00052 confirmed by luciferase reporter and RNA Immunoprecipitation (RIP) experiments.InFigure 2a, LINC00052 was greatly enhanced by LV-LINC00052 in AsPC-1 and SW1990 cells. In Figure 2b,c, EDU experiments indicated that the pancreatic cancer cell proliferation was depressed by overexpression of LINC00052. In addition, as displayed in Figure 2d,e, AsPC-1 and SW1990 cell cycle progression were blocked by LV-LINC00052. Besides, pancreatic cancer apoptosis was dramatically elevated by LV-LINC00052 (Figure 2f,g). These data indicated that the overexpression of LINC00052 repressed pancreatic canceMeanwhile, the binding sites between the LINC00052 and miR-330-3pwere manifested in Figure 4a. In Figure 4b, the mutations were made in LINC00052 which could target miR-330-3p.Cotransfection of WT-LINC00052 with miR-330-3p mimics repressed the reporter activity in AsPC-1 cells (Figure 4c). The RIP assay indicated that the LINC00052 and miR-330-3p were more abundant in Ago2 pellet (Figure 4d). These indicated that the miR-330-3p might be a target of LINC00052r proliferation, blocked cell cycle in the G1 phase and increased cell apoptosis.	30712321	RID02936	expression association	NA	UP(LIHC);DATA(GSE117623)	
Nonalcoholic fatty liver disease	MEG3	LRP6	positively-E	luciferase reporter assay	upregulation		NA	NA	mTOR signaling pathway(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fatty liver disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000070018	NA	55384	4040	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ADCAD2	LncRNA MEG3 functions as a ceRNA in regulating hepatic lipogenesis by competitively binding to miR-21 with LRP6.Our mechanistic studies demonstrated that MEG3 competitively binds to miR-21 with LRP6, followed by the inhibition of the mTOR pathway, which induces intracellular lipid accumulation. MEG3 helps to alleviate lipid over-deposition, probably by binding to miR-21 to regulate the expression of LRP6. Our results suggest the potency of MEG3 as a biomarker for NAFLD and as a therapeutic target for treatment.	30711569	RID02937	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065)
Kaposi's sarcoma	OIP5-AS1	DNMT1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Viral infectious disease	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000130816	NA	729082	1786	cyrano|linc-OIP5	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Oncogenic KSHV-encoded interferon regulatory factor upregulates HMGB2 and CMPK1 expression to promote cell invasion by disrupting a complex lncRNA-OIP5-AS1/miR-218-5p network.we report that vIRF1 promotes endothelial cell migration, invasion and proliferation by down-regulating miR-218-5p to relieve its suppression of downstream targets high mobility group box 2 (HMGB2) and cytidine/uridine monophosphate kinase 1 (CMPK1). Mechanistically, vIRF1 inhibits p53 function to increase the expression of DNA methyltransferase 1 (DNMT1) and DNA methylation of the promoter of pre-miR-218-1, a precursor of miR-218-5p, and increases the expression of a long non-coding RNA OIP5 antisense RNA 1 (lnc-OIP5-AS1), which acts as a competing endogenous RNA (ceRNA) of miR-218-5p to inhibit its function and reduce its stability.these results define a novel complex lnc-OIP5-AS1/miR-218-5p network hijacked by vIRF1 to promote invasiveness and motility of KSHV-induced tumors.	30699189	RID02938	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Focal segmental glomerulosclerosis	LOC105375913	SNAI1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	fibrotic(+)	ceRNA(miR-27b)	regulation	NA	NA	NA	NA	Urinary system disease	Nephritis	lncRNA	TF	NA	NA	ENSG00000124216	NA	105375913	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Upregulated long noncoding RNA LOC105375913 induces tubulointerstitial fibrosis in focal segmental glomerulosclerosis.The competitive binding between LOC105375913 and miR-27b increased the level of snail and promoted fibrogenesis in tubular cells.the activation of C3a/p38/XBP-1s pathway induces the expression of LOC105375913 in tubular cells, and LOC105375913 increases the level of snail and induces tubulointerstitial fibrosis through competitive binding of miR-27b in tubular cells of FSGS patients.Bioinformatic analysis with RNAHybrid software showed that, LOC105375913 contains the response element of miR-27b (Fig. 4h). RNA pull-down and PCR analysis showed that miR-27b directly bound to LOC105375913 in tubulointerstitial tissues, and this binding was significantly increased in the tissues of FSGS patients compared to normal controls (Fig. 4i). Treatment with C3a increased the binding between LOC105375913 and miR-27b, which was prevented by LOC105375913 siRNA (Fig. 4j). Silence of LOC105375913 also decreased the level of snail in C3a-treated tubular cells (Fig. 4k).	30679767	RID02939	ceRNA or sponge	NA		UP(PAAD);DATA(GSE40174)
Osteoarthritis	SYNE3	YAF2	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-141)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000176438	GRCh38_14:95407266-95516650	ENSG00000015153	NA	161176	10138	C14orf139|C14orf49|FLJ25605|LINC00341|NCRNA00341|Nesp3|Nesprin-3|NET53	NA	A LINC00341-mediated regulatory pathway supports chondrocyte survival and may prevent osteoarthritis progression.Further investigation has revealed that LINC00341 interacts with miR-141 to suppress its functional binding to the 3'-untranslated region of YY1-associated factor 2 (YAF2) messenger RNA. Aberrant downregulation of LINC00341 thus may ultimately lead to inhibition of the YAF2 protein, which has been implicated to be an antiapoptotic factor. Our study has revealed a new noncoding RNA-mediated regulatory network that highly likely protects chondrocytes by preventing apoptosis under normal conditions.The potential interaction between LINC00341 and miR-141 was further assessed in a luciferase reporter system. The cDNA of LINC00341 and a mutant version with disrupted miR-141 binding were engineered into a luciferase reporter vector. The reporter vectors were transfected into HEK 293T cells in the presence of miR-141 supplementation or miR-141 inhibitor. The results suggested that miR-141 could strongly suppress luciferase production when the LINC00341 sequence but not the mutant version was engineered downstream of the luciferase gene, supporting a direct functional binding of miR-141 to the LINC00341 sequence (Figure 2D and 2E).Because Ago2 is required for miRNAs to bind to their targets, we used an anti-Ago2 antibody to immunopreci pitate the associated RNAs. qRT-PCRassays were performed to quantitate LINC00341 and miR-141. It seemed that both noncoding RNAs were enriched with similar efficiencies by anti-Ago2, suggesting that they might be Ago2 binding targets with partial base-pair interactions (Figure 2F).The potential binding of miR-141 to the 3'-UTR of YAF2 was further assessed in a luciferase reporter system. The cDNA of the YAF2 3'-UTR and a mutant version with disrupted miR-141 binding were engineered downstream of the luciferase gene in the reporter vector. The reporter vectors were transfected into HEK 293T cells in the presence or absence of miR-141 supplementation. Increasing the level of miR-141 in cells could inhibit the production of luciferase activities from the reporter vector containing the wild-type YAF2 3'-UTR but not the mutant version (Figure 4B). The results strongly supported the fact that miR-141 directly binds to the 3'-UTR of YAF2 mRNA to inhibit the production of this protein.	30672021	RID02940	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE55807)
Parkinson's disease	TP53COR1	alpha-synuclein	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	ceRNA(miR-1277-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000145335	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson's Disease through Activating alpha-Synuclein Expression.Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of alpha-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells.To verify whether lincRNA-p21 sponged miR-1277-5p, we performed RIP and dual-luciferase assays. It has been known that miRNAs degrade mRNA and inhibit translation in an Argonaute 2 (AGO2)-dependent manner by binding to their targets [19]. We conducted anti-AGO2 RIP in SH-SY5Y cells transiently overexpressing miR-1277-5p to pull down lincRNA-p21 using control IgG or AGO2 antibodies, followed by PCR analysis for lincRNA-p21 levels. As presented in Figure 2(d), compared with the anti-IgG control, lincRNA-p21 pulled down with anti-AGO2 antibodies was enriched obviously in SH-SY5Y cells transfected with miR-1277-5p mimics. However, GAPDH was not pulled down with anti-AGO2 antibodies. This result suggested that miR-1277-5p could directly target lincRNA-p21 in AGO2 manner. Besides, the wide-type lincRNA-p21 sequence (WT) or the sequence with mutated binding sites of miR-1277-5p (Mut) was inserted into the 3'-UTR of the renilla luciferase in ps-CHECK2 vector (Figure 2(e)). As shown in Figure 2(f), after overexpressing of miR-1277-5p, the luciferase activities of WT reporter were decreased significantly compared with the Mut reporter. On the contrary, the luciferase activities of WT reporter were increased remarkably compared with the Mut control after inhibition of expression of miR-1277-5p. These results demonstrated that lincRNA-p21 suppressed the activity of miR-1277-5p via direct binding between them and lincRNA-p21 might be regarded as a competing endogenous RNA (ceRNA) for miR-1277-5p.According to the online database TargetScan (http://www.targetscan.org), alpha-synuclein is a target gene of miR-1277-5p. In order to verify whether miR-1277-5p bound to alpha-synuclein, we performed the luciferase assay. The wide-type alpha-synuclein sequence (WT) or the sequence with mutated binding sites of miR-1277-5p (Mut) was inserted into the 3'-UTR of the renilla luciferase in ps-CHECK2 vector (Figure 3(a)). As shown in Figure 3(b), after cotransfecting with alpha-synuclein WT luciferase reporter and miR-1277-5p mimics, the activity of luciferase was decreased significantly compared with the NC mimics group (P < 0.01). However, the luciferase activity was increased remarkably after cotransfecting with alpha-synuclein WT luciferase reporter and miR-1277-5p inhibitor (P < 0.001). Besides, there was no difference in alpha-synuclein Mut group. Next, we tested the effects of miR-1277-5p on the mRNA and protein expression levels of alpha-synuclein. After transfection of miR-1277-5p mimics, the alpha-synuclein mRNA expression level was decreased significantly compared with the NC mimics group (Figure 3(c), P < 0.01). However, alpha-synuclein mRNA expression level was increased remarkably after transfection of miR-1277-5p inhibitor in SH-SY5Y cells (Figure 3(c), P < 0.001). Similarly, alpha-synuclein protein expression level was suppressed obviously in miR-1277-5p mimics group compared with the NC mimics group (Figure 3(d), P < 0.05). Conversely, the alpha-synuclein was upregulated significantly after inhibition of miR-1277-5p in SH-SY5Y cells treated with MPP+ (Figure 3(e), P < 0.01). In a word, above results indicated that alpha-synuclein was the target gene of miR-1277-5p in PD model.When cells were cotransfected with pcDNA3.1-lincRNA-p21 and miR-1277-5p, the luciferase activity was decreased remarkably compared with the pcDNA3.1-lincRNA-p21 and NC mimics group (P < 0.01). When cells were cotransfected with pcDNA3.1 and miR-1277-5p mimics, the luciferase was inhibited significantly compared with pcDNA3.1+NC mimics group (P < 0.05). Conversely, as presented in Figure 4(b), the luciferase activity was suppressed obviously after inhibition of lincRNA-p21 (P < 0.05). After inhibition of lincRNA-p21 and miR-1277-5p, the luciferase activity was increased significantly compared with the corresponding negative group (P <0.01). After cotransfection of si-NC and miR-1277-5p inhibitor, the luciferase activity was upregulated evidently (P < 0.05). These results indicated that miR-1277-5p mimics could counteract the luciferase activity. Besides, we verified the effects of lincRNA-p21 and miR-1277-5p on the alpha-synuclein mRNA expression level. Data showed that overexpression of lincRNA-p21 could increase significantly the alpha-synuclein mRNA expression level (Figure 4(c), P < 0.01). However, after overexpression of lincRNA-p21 and miR-1277-5p at the same time, the alpha-synuclein mRNA expression level was decreased evidently compared with the pcDNA3.1-lincRNA-p21+NC mimics group (Figure 4(c), P < 0.01). As presented in Figure 4(d), inhibition of lincRNA-p21 restrained the expression of alpha-synuclein (P < 0.01). When SH-SY5Y cells were transfected with si-lincRNA-p21 and miR-1277-5p inhibitor concurrently, the alpha-synuclein mRNA expression level was increased significantly compared with the si-lincRNA-p21+NC inhibitor group (P < 0.01). Furthermore, overexpression of lincRNA-p21 caused the inhibition of cell viability, but this effect could be counteracted significantly by overexpression of miR-1277-5p (Figure 4(e), P < 0.001). The ELISA assay demonstrated that overexpression of lincRNA-p21 led to increased caspase-3 activity remarkably in SH-SY5Y cells (Figure 4(f), P < 0.001). However, the effect of lincRNA-p21 on the caspase-3 activity was decreased notably by overexpression of miR-1277-5p (Figure 4(f), P < 0.01). These results suggested that lincRNA-p21 could regulate the expression of alpha-synuclein via miR-1277-5p.	30671473	RID02941	ceRNA or sponge	NA		
Irritable bowel syndrome	TUG1	MIR127	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	apoptosis process(-);inflammatory response(-);NF-kB signaling pathway(-);Notch signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Intestinal disease	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000207608	NA	55000	406914	LINC00080|NCRNA00080|TI-227H	MIRN127|miRNA127|mir-127	Overexpression of long non-coding RNA TUG1 alleviates TNF-alpha-induced inflammatory injury in interstitial cells of Cajal.TUG1 overexpression protected ICC from TNF-alpha-induced apoptosis and pro-inflammatory cytokines expression. TUG1 suppression showed opposite effects. MiR-127 was negatively regulated by TUG1 and implicated in the action of TUG1 in ICC. MiR-127 up-regulation largely reversed the effects of TUG1 on TNF-alpha-treated ICC. Mechanistically, TUG1 inhibited TNF-alpha-induced activation of NF-kB and Notch pathways in ICC by down-regulating miR-127.TUG1 attenuated TNF-alpha-caused apoptosis and inflammatory response in ICC by down-regulating miR-127 and then inactivating NF-kB and Notch pathways.The expression level of miR-127 in ICC was significantly reduced after TUG1 overexpression and enhanced after TUG1 suppression (p <0.01, Figure 3A and 3B).	30657572	RID02942	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Diabetes mellitus	LINC00458	BMF	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	calcium signaling pathway(+);cell senescence(+)	ceRNA(miR-34c-5p)	regulation	RNA-protein	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000234787	GRCh38_13:54115783-54142319	ENSG00000104081	NA	100507428	90427	ES3|LncRNA-ES3	FLJ00065	lncRNA-ES3/miR-34c-5p/BMF axis is involved in regulating high-glucose-induced calcification/senescence of VSMCs .Overexpression of miR-34c-5p alleviated calcification/senescence of HA-VSMCs, whereas inhibition of miR-34c-5p received the opposite results. Bcl-2 modifying factor (BMF) was a functional target of miR-34c-5p and it was involved in the process of calcification/senescence of HA-VSMCs. lncRNA-ES3 acted as a competing endogenous RNAs (ceRNA) of miR-34c-5p to enhance BMF expression.Bioinformatics analysis showed that some complementary sites existed between miR-34c-5p and lncRNA-ES3 (Figure 3A). Moreover, qRT-PCRverified that the level of lncRNA-ES3 was markedly increased in HA-VSMCs treated with HG (Figure 3B). However, OC did not influence the expression of lncRNA-ES3. Hence, we intended to further explore whether miR-34c-5p could directly interact with lncRNA-ES3. Firstly, overexpression of miR-34c-5p by transfecting miR-34c-5p mimics to HA-VSMCs significantly reduced lncRNA-ES3 expression (Figure 3C). When introducing shlncRNA-ES3 to knockdown lncRNA-ES3 expression, we found that the shlncRNA-ES3-2 variant was the most effective to inhibit the expression of lncRNA-ES3 (Figure 3D), hence we chose it for the downstream study. In the knockdown study, the expression of lncRNA-ES3 elevated the expression of miR-34c-5p (Figure 3E). Subsequently, the luciferase reporter assay showed that the overexpression of miR-34c-5p significantly decreased the relative luciferase activity of the WT-lncRNA-ES3 reporter, but miR-34c-5p had no effect on luciferase activity of Mut-lncRNA-ES3 reporter, in which the putative binding sites between lncRNA-ES3 and miR-34c-5p were mutant (Figure 3F). Lastly, biotin-labeled miR-34c-5p pull-down assay was performed to verify that the sequence of miR-34c-5p could highly bind with lncRNA-ES3 (Figure 3G). Additionally, RIP assay was performed using Ago2 antibody to explore whether miR-34c-5p and lncRNA-ES3 were involved in RNA-induced silencing complex (RISC). The results showed that miR-34c-5p and lncRNA-ES3 were substantially enriched by Ago2 antibody compared with control IgG antibody (Figure 3H), which suggested that miR-34c-5p and lncRNA-ES3 were present in RISC. Based on these data, we could draw a conclusion that lncRNA-ES3 and miR-34c-5p could combine with each other in HA-VSMCs.The following luciferase assay demonstrated that enforced expression of miR-34c-5p markedly suppressed the luciferase activity of WT-BMF reporter, while no change was observed in the luciferase activity of Mut-BMF reporter after miR-34c-5p overexpression (Figure 4D). Collectively, these data indicated that BMF was the target of miR-34c-5p and that lncRAN-ES3 acted as a ceRNA of miR-34c-5p to regulate expression of the target gene, BMF, in HA-VSMCs.	30654331	RID02943	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Rheumatoid arthritis	MEG3	NLRC5	negatively-E		downregulation		NA	NA	inflammatory response(-)	NA	association	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000140853	NA	55384	84166	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CLR16.1|FLJ21709|NOD27	Long noncoding RNA MEG3 regulates rheumatoid arthritis by targeting NLRC5.we used complete Freund's adjuvant (CFA)-induced rats as RA animal models. The level of MEG3 significantly reduced in CFA-induced synovial tissues and FLSs, whereas the NLRC5 levels were increased. Enforced expression of MEG3 may be responsible for the decreased level of NLRC5 and inflammatory cytokine level. The results of methylation-specific PCR suggested that the MEG3 gene promoter was significantly methylated in CFA-induced synovial tissues and FLSs.	30644097	RID02944	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Prostate cancer	LEF1-AS1	LEF1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000138795	NA	641518	51176	NA	TCF10|TCF1ALPHA|TCF7L3	Long noncoding RNA LEF1-AS1 silencing suppresses the initiation and development of prostate cancer by acting as a molecular sponge of miR-330-5p via LEF1 repression. LEF1-AS1 and LEF1 were highly expressed while miR-330-5p was poorly expressed in PCa.RNA crosstalk revealed that LEF1-AS1 bound to miR-330-5p and LEF1 was the target gene of miR-330-5p. Silenced LEF1-AS1 or elevated miR-330-5p exhibited inhibited EMT processes, reduced ability of proliferation, invasion and migration, coupling with decreased tumorigenesis and LNM in nude mice. The key findings of this study collectively propose downregulation of LEF1-AS1 competing with miR-330-5p to inhibit EMT, invasion and migration of PCa by LEF1 repression.RT-qPCR was performed to measure the expression of LEF1-AS1, miR-330-5p, and LEF1 in tissues. The RT-qPCR results (Figure 1e) showed that compared with the control group, the PCa group had significantly increased LEF1-AS1 and LEF1 expression, while significantly decreased miR-330-5p expression (p < 0.05).	30613973	RID02945	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	CYTOR	CDK14	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1182)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000058091	NA	112597	5218	C2orf59|LINC00152|MGC4677|NCRNA00152	PFTAIRE1|PFTK1	TCF3-activated LINC00152 exerts oncogenic role in osteosarcoma through regulating miR-1182/CDK14 axis. LINC00152 was highly expressed in osteosarcoma tissues and cell lines. Moreover, MTT and colony formation assays revealed that knockdown of LINC00152 significantly suppressed cell proliferation. mechanism investigation revealed that LINC00152 was predominantly located in the cytoplasm of OS cells and acted as a competing endogenous RNA (ceRNA) in OS by regulating miR-1182/CDK14 axis. Collectively, LINC00152 was activated by TCF3 and promotes cell proliferation and migration in osteosarcoma via miR-1182-CDK14 axis.At first, we detected the expression of LINC0052 in OS. qRT-PCRanalysis revealed that LINC00152 was overexpressed in osteosarcoma tissues compared with adjacent normal tissues (Fig. 1A).Finally, we conducted rescue assays to confirm the function of LINC00152-miR-1182-CDK14 axis in OS cell proliferation, migration and invasion. It was found that cell proliferation induced by LINC00152 knockdown was partly reversed by miR-1182 inhibitor or pcDNA-CDK14 (Fig. 5A). Additionally, the inhibitory effects of LINC00152 knockdown on cell migration and invasion were partially rescued by miR-1182 inhibitor or pcDNA-CDK14 (Fig. 5C ). These results sug-gested that LINC00152 promoted osteosarcoma progression via mod-ulating miR-1182/CDK14 axis.	30600185	RID02946	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Keloid formation	HOXA11-AS	TGFbetaR1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);angiogenesis(+)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	NA	Other	Keloid formation	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Long non-coding RNA HOXA11-AS accelerates the progression of keloid formation via miR-124-3p/TGFbetaR1 axis.We found that HOXA11-AS and TGFbetaR1 were significantly up-regulated, while miR-124-3p was down-regulated both in keloid tissues or fibroblasts than in normal skin tissues or fibroblasts. Functionally, high expression of HOXA11-AS essentially inhibited cell apoptosis and promoted fibroblast-induced angiogenesis. Mechanistically, miR-124-3p was identified as a downstream effector to be involved in HOXA11-AS-mediated phenotypes through directly targeting TGFbetaR1, thus modulating PI3K/Akt signaling pathway. Taken together, our findings revealed that HOXA11-AS inhibits cell apoptosis and promotes angiogenesis through miR-124-3p/TGFbetaR1 axis, contributing to the progression of keloid formation, which might provide a novel target for keloid therapy.	31878829	RID02947	ceRNA or sponge	NA		
Pneumonia	SNHG16	IGF2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+);inflammatory response(+)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000167244	NA	100507246	3481	Nbla10727|Nbla12061|ncRAN	C11orf43|FLJ44734|IGF-II	Long non-coding RNA SNHG16 promotes lipopolysaccharides-induced acute pneumonia in A549 cells via targeting miR-370-3p/IGF2 axis.SNHG16 and IGF2 were upregulated while miR-370-3p was downregulated in serum of acute pneumonia patients and LPS-induced A549 cells. SNHG16 regulated proliferation, apoptosis and inflammatory cytokines by inhibiting miR-370-3p in LPS-induced A549 cells. MiR-370-3p targeted IGF2 and inhibited LPS-induced inflammatory injury via IGF2 in A549 cells. Furthermore, SNHG16 was verified to promote IGF2 expression by sponging miR-370-3p in A549 cells.CONCLUSION: SNHG16 impeded cell viability and promoted apoptosis, inflammatory injury by targeting IGF2 mediated by miR-370-3p in LPS-induced A549 cells.	31841752	RID02948	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Laryngeal squamous cell carcinoma	LINC01605	miR-493-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000253414	GRCh38_8:37516399-37521447	NA	NA	100507420	NA	LincDUSP|TCONS_00014973	NA	LINC01605 promotes the proliferation of laryngeal squamous cell carcinoma through targeting miR-493-3p.LINC01605 was upregulated and miR-493-3p was downregulated in LSCC tissues. Knockdown of LINC01605 inhibited proliferative ability, and stimulated apoptosis in HEp-2 and AMC-HN-8 cells. Moreover, LINC01605 directly bound to miR-493-3p, and the former negatively regulated the level of the latter.	31841192	RID02949	ceRNA or sponge	NA		
Osteoarthritis	MCM3AP-AS1	HMGB1	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-142-3p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000189403	NA	114044	3146	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	DKFZp686A04236|HMG1|HMG3|SBP-1	LncRNA MCM3AP-AS1 regulates miR-142-3p/HMGB1 to promote LPS-induced chondrocyte apoptosis.We found that MCM3AP-AS1 was up-regulated in OA. Bioinformatics analysis showed that MCM3AP-AS1 may interact with miR-142-3p, which can inhibit the apoptosis of chondrocytes. MCM3AP-AS1 over-expression led to up-regulated expressions of HMGB1, which is a target of miR-142-3p.MCM3AP-AS1 may regulate miR-142-3p/HMGB1 to promote LPS-induced chondrocyte apoptosis.	31836002	RID02950	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Atherosclerosis	GAS5	ABCA1	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);lipid accumulation(+);cholesterol homeostasis(-)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000165029	NA	60674	19	NCRNA00030|SNHG2	ABC1|HDLDT1|TGD	Knockdown of GAS5 Inhibits Atherosclerosis Progression via Reducing EZH2-Mediated ABCA1 Transcription in ApoE -/- Mice.GAS5 can inhibit the expression of ATP-binding cassette transporter A1 (ABCA1) by binding to enhancer of zeste homolog 2 (EZH2).knockdown of GAS5 can potentially promote reverse-transportation of cholesterol and inhibit intracellular lipid accumulation, ultimately preventing the progression of atherosclerosis via reducing EZH2-mediated transcriptional inhibition of ABCA1 by histone methylation.According to the prediction results from bioinformatics website available at http://pridb.gdcb.iastate.edu/RPISeq/, GAS5 may directly bind to EZH2. Besides, EZH2 was demonstrated to function together with lncRNA previously.20,21 Hence, an RNA pull-down experiment was conducted in order to determine whether GAS5 can bind to EZH2. western blotrevealed the presence of the EZH2 protein, indicating that EZH2 can bind to GAS5 (Figure 3A). The results of RNA binding protein immunoprecipitation (RIP) experiment revealed that, after RNA was extracted from the pull-down protein solution by the EZH2 antibody, GAS5 could be detected using qRT-PCR(Figure 3B) (p < 0.05), further verifying the mutual interaction between GAS5 and EZH2 proteins.It has been reported that GAS5 was highly expressed in the atherosclerotic plaque and downregulated GAS5 could suppress the ox-LDL-induced THP-1 cell apoptosis.19 In order to identify the expression and role of GAS5 in atherosclerosis, the expression of GAS5 on a cellular level was determined. The localization of GAS5 in THP-1 macrophage-derived foam cells was determined by fluorescence in situ hybridization (FISH). qRT-PCRresults demonstrated that the expression of GAS5 in THP-1 macrophage-derived foam cells was much higher than that in THP-1 macrophages (Figure 1A) (p < 0.05).	31830648	RID02951	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	TUG1	PTEN	negatively-E		upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171862	NA	55000	5728	FLJ20618|LINC00080|NCRNA00080	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA TUG1 was upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts.lncRNA TUG1 over-expression led to downregulated PTEN, while lncRNA TUG1 siRNA silencing played an opposite role.lncRNA TUG1 knockdown may serve as a promising therapeutic target for osteoporosis by inhibiting the proliferation and promoting the apoptosis of osteoclasts through PTEN.	31815638	RID02952	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	NR2F1-AS1	FOXA1	positively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(-);apoptosis process(-)	ceRNA(miR-483-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000129514	NA	441094	3169	FLJ42709	HNF3A	Long noncoding RNA NR2F1-AS1 enhances the malignant properties of osteosarcoma by increasing forkhead box A1 expression via sponging of microRNA-483-3p.NR2F1-AS1 knockdown inhibited OS cell proliferation, migration, and invasion and promoted cell cycle arrest and apoptosis in vitro and slowed tumor growth in vivo. NR2F1-AS1 was found to function as a competing endogenous RNA by directly sponging microRNA-483-3p (miR-483-3p) and upregulating its target oncogene forkhead box A1 (FOXA1).  NR2F1-AS1 plays an oncogenic role in OS through sponging miR-483-3p and thereby upregulating FOXA1, suggesting an additional target for osteosarcoma therapeutics.To verify this, a luciferase reporter assay was carried out in HOS and U2OS cells after cotransfection with either NR2F1-AS1-wt or NR2F1-AS1-mut and either agomir-483-3p or agomir-NC. The results showed that agomir-483-3p transection, which significantly increased miR-483-3p expression (Figure 3C, P < 0.05), reduced the luciferase activity of NR2F1-AS1-wt (P < 0.05). In contrast, the luciferase activity of NR2F1-AS1-mut was not affected by miR-483-3p overexpression in HOS and U2OS cells (Figure 3D). Additionally, results from a RIP assay of HOS and U2OS cells indicated that NR2F1-AS1 was preferentially enriched on AGO2-containing beads (Figure 3E, P < 0.05), suggesting that miR-483-3p is a target of NR2F1-AS1.Two bioinformatics tools, miRDB and TargetScan 7.1, were used to predict the potential target of miR-483-3p. As illustrated in Figure 4F, the 3'-UTR of FOXA1 mRNA contains a 7-bp complementary sequence that may directly interact with miR-483-3p. A luciferase reporter assay was performed to confirm that miR-483-3p can directly bind to the 3'-UTR of FOXA1 mRNA. The results suggested that the luciferase activity of HOS and U2OS cells transfected with FOXA1-wt was restrained by miR-483-3p overexpression (P < 0.05). In contrast, the luciferase activity of FOXA1-mut was unaffected by agomir-483-3p cotransfection (Figure 4G). RT-qPCR and western blot were then performed to measure the levels of FOXA1 mRNA and protein in the HOS and U2OS cells that were transfected with either agomir-483-3p or agomir-NC. The data showed that ectopic miR-483-3p expression significantly decreased the expression of FOXA1 in HOS and U2OS cells at both the mRNA (Figure 4H, P < 0.05) and protein levels (Figure 4I, P < 0.05). Furthermore, RT-qPCR analysis indicated that FOXA1 mRNA expression was higher in OS tissue samples than in the adjacent normal tissues (Figure 4J, P < 0.05). Furthermore, FOXA1 expression was negatively correlated with the miR-483-3p level (Figure 4K; R2 = 0.4589, P < 0.0001). As a whole, these results confirmed the role of miR-483-3p as a tumor-suppressive miRNA in OS and identified FOXA1 as a direct target gene of miR-483-3p in OS.	31801112	RID02953	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Hepatocellular carcinoma	DUXAP9	MIR760	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000211575	NA	503638	100126348	LINC01296|LNMAT1	MIRN760|hsa-mir-760|mir-760	LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma.LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. Moreover, its expression was closely related to lymph node metastasis and poor prognosis of LCa.	31799652	RID02954	ceRNA or sponge	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Esophageal cancer	CCAT2	MIR145	negatively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	radiosensitivity(-);p53 signaling pathway(-);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000269936	NA	101805488	406937	LINC00873|NCCP1	MIRN145|miR-145|miRNA145	lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR-145/p70S6K1 and p53 pathway. knockdown of CCAT2 enhanced radiosensitivity of EC cells and promoted apoptosis by increasing Bax/Bcl2 and active-caspase 3/caspase 3 following X-ray treatment.These results showed that CCAT2 promoted the radiotherapy resistance of EC cells via negative regulation of the miR-145/p70S6K1 and the p53 signaling pathways and associated elements may be potential targets for improving the sensitivity of EC radiotherapy.	31789385	RID02955	expression association	NA		
Esophageal cancer	CCAT2	p70S6K1	positively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	radiosensitivity(-);p53 signaling pathway(-);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR-145/p70S6K1 and p53 pathway. These results showed that CCAT2 promoted the radiotherapy resistance of EC cells via negative regulation of the miR-145/p70S6K1 and the p53 signaling pathways and associated elements may be potential targets for improving the sensitivity of EC radiotherapy.	31789385	RID02956	expression association	NA		
Esophageal cancer	CCAT2	TP53	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	radiosensitivity(-);p53 signaling pathway(-);apoptosis process(-)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000141510	NA	101805488	7157	LINC00873|NCCP1	LFS1|p53	lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR-145/p70S6K1 and p53 pathway. These results showed that CCAT2 promoted the radiotherapy resistance of EC cells via negative regulation of the miR-145/p70S6K1 and the p53 signaling pathways and associated elements may be potential targets for improving the sensitivity of EC radiotherapy.	31789385	RID02957	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	VIM-AS1	vimentin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000229124	GRCh38_10:17214239-17230018	NA	NA	100507347	NA	NA	NA	Long non-coding RNA VIM-AS1 promotes prostate cancer growth and invasion by regulating epithelial-mesenchymal transition.VIM-AS1 was expressed significantly higher in PCa tissues comparing with normal prostate tissues.Inhibition of VIM-AS1 reduced cell proliferation, migration and invasion of PC3 cells but overexpression of VIM-AS1 promoted cell growth, migration and invasion. We also found VIM-AS1 promoted the expression of vimentin, which further promoted epithelial-mesenchymal transition (EMT) of PCa cells.lncRNA VIM-AS1 was overexpressed in PCa tissues and cell lines and promoted PCa proliferation and metastasis via EMT through regulating vimentin, which might provide a novel target for the diagnosis and therapy for PCa.	31786880	RID02958	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	
Urinary bladder cancer	NEAT1	HMGB1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-410)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000189403	NA	283131	3146	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DKFZp686A04236|HMG1|HMG3|SBP-1	Long non-coding RNA NEAT1 promotes bladder progression through regulating miR-410 mediated HMGB1.Then it was indicated that NEAT1 silence greatly inhibited bladder cancer cell proliferation with an increased ratio of apoptotic cells and severe cell cycle arrest.we speculated that miR-410 was as a downstream target of NEAT1. Then, the targeting association between them was proved in our research and we implicated miR-410 was dramatically restrained in bladder cancer cells. Meanwhile, it was exhibited that miR-410 was negatively regulated by NEAT1. Apart from these, HMGB1 was speculated as a downstream target of miR-410.Up-regulation of miR-410 restrained HMGB1 levels and NEAT1 can regulate HMGB1 level via sponging miR-410.rrently,the correlation between NEAT1 and miR-410 was ex hibited in Fig. 5A. dual-luciferase reporter assay was conducted (Fig. 5B). The luciferase reporter plasmid containing the WT-NEAT1 with miR-410 mimics were co-transfected and a decreased reporter activity was demonstrated (Fig. 5C). NEAT1 and miR-410 were much more enriched in Ago2 pellet (Fig. 5D). RNA pull-down assay with miR 410-bio probe induced the level of NEAT1 than NC-bio or miR-410probes (Fig. 5E). These implied miR-410 might be a target of NEAT1.Moreover, WT-HMGB1 and MUT-HMGB1 binding sites were manifested in Fig. 7A and 7B. Co-transfection of the luciferase reporter plasmid containing WT-HMGB1 with miR-410 mimics caused an in hibited reporter activity (Fig. 7C). In addition, HMGB1 was remarkably inhibited by miR-410 mimics in T24 and J82 cells (Fig.7D). In Fig. 7E and 7 F, HMGB1 levels were down-regulated by NEAT1 deletion and up-regulated by NEAT1 overexpression. These findings indicated NEAT1 regulated bladder cancer development through regulating miR-410 and HMGB1.	31734579	RID02959	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Non-small cell lung cancer	SP1	LINC01638	positively-E	western blot;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000233521	GRCh38_22:27221349-27225134	6667	105372978	NA	NA	SP1-regulated LINC01638 promotes proliferation and inhibits apoptosis in non-small cell lung cancer.The expression of LINC01638 is upregulated in NSCLC tissues and cells, and the highly expressed LINC01638 is modulated by the transcription factor SP1 and promotes the proliferation but represses the apoptosis of NSCLC cells via the PTEN/AKT signaling pathway.	31696478	RID02960	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)
Cervical cancer	LncRNATCF7	DNMT1	positively-E	western blot;luciferase reporter assay;TargetScan	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-155)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	NA	NA	ENSG00000130816	NA	NA	1786	NA	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	LncRNATCF7 up-regulates DNMT1 mediated by HPV-18 E6 and regulates biological behavior of cervical cancer cells by inhibiting miR-155.inhibition of TCF-7 can inhibit invasion and migration of cervical cancer cells; enhanced miR-155 after the inhibition of TCF-7 can promote the invasion and migration of cervical cancer cells; compared with NC group, the tumor volume and weight of TCF-7-siRNA group tumor-bearing was significantly reduced.CONCLUSIONS: TCF-7 plays an important role in the development of cervical cancer. TCF-7 can target miR-155 to regulate the invasion and migration of cervical cancer cells.	31696464	RID02961	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteogenesis imperfecta	XIXT	RUNX2	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell differentiation(-)	ceRNA(miR-30a-5p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	NA	NA	ENSG00000124813	NA	NA	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	LncRNA XIXT promotes osteogenic differentiation of bone mesenchymal stem cells and alleviates osteoporosis progression by targeting miRNA-30a-5p.LncRNA XIXT was significantly downregulated, and miRNA-30a-5p was upregulated in the serum of osteoporosis patients. The osteogenic differentiation-related genes (ALP, RUNX2) and XIXT were markedly upregulated in a time-dependent manner, while miRNA-30a-5p level gradually decreased in hBMSCs with the prolongation of osteogenesis. The knockdown of XIXT inhibited the osteogenic differentiation of hBMSCs. LncRNA XIXT upregulated RUNX2 by absorbing miRNA-30a-5p, and thus induced hBMSCs osteogenesis to alleviate osteoporosis.	31696458	RID02962	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Steroid-induced avascular necrosis of the femoral head	MALAT1	ATF4	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell differentiation(-)	ceRNA(miR-214)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000128272	NA	378938	468	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CREB-2|TAXREB67|TXREB	LncRNA-MALAT1 promotes osteogenic differentiation through regulating ATF4 by sponging miR-214: Implication of steroid-induced avascular necrosis of the femoral head.MALAT1 was down-regulated and miR-214 was up-regulated in SANFH tissues. DEX inhibited osteogenic differentiation of BMSC in a dose-dependent manner, leading to decreased MALAT1, increased miR-214, as well as reduced ALP activity and decreased expression of RUNX2, ALP and OCN. Either overexpression of MALAT1 or inhibition of miR-214 improved DEX-induced inhibition of BMSC osteogenic differentiation. MALAT1 was down-regulated, while miR-214 was elevated in SANFH tissues. MALAT1 promoted osteogenesis differentiation by sponging miR-214 to upregulate ATF4.	31678133	RID02963	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)
Nasopharynx carcinoma	H19	REXO2	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-675-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000076043	NA	283120	25996	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CGI-114|REX2|RFN|SFN	H19/miR-675-5p Targeting SFN Enhances the Invasion and Metastasis of Nasalpharyngeal Cancer Cells.The expression of H19 and miR-675-5p are significantly higher in NPC cells than in NP69 cell (P<0.05). The over-expression of miR- 675-5p inhibits the expression of 14-3-3xigema protein. SFN is the target gene of miR-675-5p. MiR-675-5p targets SFN, downregulates its protein expression and promotes the invasion and metastasis of NPC.	31677258	RID02964	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(PAAD,PRAD,BRCA);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE41245)
Psoriasis	MEG3	Caspase8	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-21)	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 influences the proliferation and apoptosis of psoriasis epidermal cells by targeting miR-21/caspase-8.MEG3 inhibits proliferation and promotes apoptosis of Activated-HaCaT (Act-HaCaT) and Activated-HHEKs (Act- HHEK) by regulating miR-21, and the binding site between MEG3 and miR-21 was identified. We also found that miR-21 could inhibit the level of caspase-8 and identified the binding site between caspase-8 and miR-21.	31660855	RID02965	ceRNA or sponge	NA		
Atherosclerosis	SNHG16	miR-17-5p	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);inflammatory response(+);NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	LncRNA SNHG16 promoted proliferation and inflammatory response of macrophages through miR-17-5p/NF-kB signaling pathway in patients with atherosclerosis.We found that SNHG16 was increased in AS patients and THP-1 macrophage-derived foam cells. SNHG16 overexpression promoted proliferation, inflammatory response and increased levels of IKKbeta, p-IkBalpha, p-p65 in THP-1 macrophages, while SNHG16 downregulation led to the opposite results. Luciferase gene reporter assay confirmed that SNHG16 could directly bind with miR-17-5p. Moreover, the proliferation, inflammatory factors and NF-kB signaling factors were significantly repressed after transfecting miR-17-5p mimic into THP-1 macrophages, while it led to the opposite results after transfecting miR-17-5p inhibitor.	31646601	RID02966	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Silicosis	HOTAIR	TNFSF14	positively-E	western blot	downregulation		NA	NA	inflammatory response(-)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000125735	NA	100124700	8740	HOXC-AS4|HOXC11-AS1|NCRNA00072	CD258|HVEM-L|LIGHT|LTg	MiR-326 Inhibits Inflammation and Promotes Autophagy in Silica-Induced Pulmonary Fibrosis through Targeting TNFSF14 and PTBP1.The results showed miR-326 is down-regulated in the fibrotic lung tissues of silica-treated mice, while increased expression of miR-326 attenuates silica-induced pulmonary fibrosis in vivo. Tumor necrosis factor superfamily-14 (TNFSF14) and polypyrimidine tract-binding protein 1 (PTBP1) are identified as the targets of miR-326. MiR-326 dampens pulmonary inflammation through targeting TNFSF14 and promotes autophagy activity of fibroblasts through targeting PTBP1. LncRNA HOTAIR facilitates inflammation via sponging miR-326.we demonstrate that miR-326 inhibits inflammation and promotes autophagy activity by targeting TNFSF14 and PTBP1 separately to alleviate silica-induced pulmonary fibrosis.	31642316	RID02967	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Silicosis	HOTAIR	PTBP1	positively-E	western blot	downregulation		NA	NA	cell autophagy(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000011304	NA	100124700	5725	HOXC-AS4|HOXC11-AS1|NCRNA00072	HNRNP-I|HNRPI|pPTB|PTB|PTB-1|PTB2|PTB3|PTB4	MiR-326 Inhibits Inflammation and Promotes Autophagy in Silica-Induced Pulmonary Fibrosis through Targeting TNFSF14 and PTBP1.The results showed miR-326 is down-regulated in the fibrotic lung tissues of silica-treated mice, while increased expression of miR-326 attenuates silica-induced pulmonary fibrosis in vivo. Tumor necrosis factor superfamily-14 (TNFSF14) and polypyrimidine tract-binding protein 1 (PTBP1) are identified as the targets of miR-326. MiR-326 dampens pulmonary inflammation through targeting TNFSF14 and promotes autophagy activity of fibroblasts through targeting PTBP1. LncRNA HOTAIR facilitates inflammation via sponging miR-326.we demonstrate that miR-326 inhibits inflammation and promotes autophagy activity by targeting TNFSF14 and PTBP1 separately to alleviate silica-induced pulmonary fibrosis.	31642316	RID02968	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Silicosis	HOTAIR	miR-326	negatively-E	western blot	upregulation		NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-326 Inhibits Inflammation and Promotes Autophagy in Silica-Induced Pulmonary Fibrosis through Targeting TNFSF14 and PTBP1.The results showed miR-326 is down-regulated in the fibrotic lung tissues of silica-treated mice, while increased expression of miR-326 attenuates silica-induced pulmonary fibrosis in vivo. Tumor necrosis factor superfamily-14 (TNFSF14) and polypyrimidine tract-binding protein 1 (PTBP1) are identified as the targets of miR-326. MiR-326 dampens pulmonary inflammation through targeting TNFSF14 and promotes autophagy activity of fibroblasts through targeting PTBP1. LncRNA HOTAIR facilitates inflammation via sponging miR-326.we demonstrate that miR-326 inhibits inflammation and promotes autophagy activity by targeting TNFSF14 and PTBP1 separately to alleviate silica-induced pulmonary fibrosis.	31642316	RID02969	ceRNA or sponge	NA		
Osteoarthritis	MALAT1	ADAMTS5	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(-);cell autophagy(+)	ceRNA(miR-145)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000154736	NA	378938	11096	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ADAMTS11|ADMP-2	LncRNA MALAT1/MiR-145 Adjusts IL-1beta-Induced Chondrocytes Viability and Cartilage Matrix Degradation by Regulating ADAMTS5 in Human Osteoarthritis.long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) promotes metastasis in cancers and functions as a sponge for miR-145MALAT1 was upregulated, and miR-145 was downregulated in OA samples and IL-1beta-induced chondrocytes. Mechanically, miR-145 could directly bind to MALAT1 and ADAMTS5. Moreover, miR-145 expression was negatively correlated with MALAT1 and ADAMTS5 expression in OA patients, whereas MALAT1 and ADAMTS5 expression was positively correlated.	31637891	RID02970	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Malignant glioma	TPT1-AS1	STMN1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell autophagy(-)	ceRNA(miR--770-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000170919	GRCh38_13:45341345-45417975	ENSG00000117632	NA	100190939	3925	NA	C1orf215|FLJ32206|Lag|LAP18|OP18|PP17|PP19|PR22|SMN	Long noncoding RNA TPT1-AS1 downregulates the microRNA-770-5p expression to inhibit glioma cell autophagy and promote proliferation through STMN1 upregulation.miR-770-5p, which directly targeted STMN1, could be downregulated by TPT1-AS1.TPT1-AS1 can function to competitively bind to miR-770-5p, thus regulatEing STMN1 expression. Moreover, glioma cell proliferation and autophagy could be mediated through the TPT1-AS1/miR-770-5p/STMN1 axis. From our data we conclude an inhibitory function of TPT1-AS1 in glioma cell autophagy by downregulating miR-770-5p and upregulating STMN1, which may be instrumental for the therapeutic targeting and clinical management of glioma.	31637705	RID02971	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Endometrial cancer	LSINCT5	HMGA2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000149948	NA	101234261	8091	NA	BABL|HMGIC|LIPO	Long noncoding RNA LSINCT5 promotes endometrial carcinoma cell proliferation, cycle, and invasion by promoting the Wnt/beta-catenin signaling pathway via HMGA2.The authors observed positively correlated and aberrantly up-regulated LSINCT5 and HMGA2 in EC. LSINCT5 deficiency significantly inhibited cell proliferation, cell cycle progression, and induced apoptosis. Meanwhile, cell migration and invasion were greatly compromised by the LSINCT5 knockdown. LSINCT5 stabilized HMGA2, which subsequently stimulated activation of Wnt/beta-catenin signaling and consequently contributed to the oncogenic properties of LSINCT5 in EC.Our data uncovered the oncogenic activities and highlighted the mechanistic contributions of the LSINCT5-HMGA2-Wnt/beta-catenin signaling pathway in EC.	31632465	RID02972	expression association	NA	UP(PRAD);DATA(GSE104209)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Cervical cancer	PVT1	SMAD3	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000166949	NA	5820	4088	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HsT17436|JV15-2|MADH3	LncRNA PVT1 promotes proliferation and invasion through enhancing Smad3 expression by sponging miR-140-5p in cervical cancer.Results PVT1 and Smad3 were upregulated, and miR-140-5p was downregulated in cervical cancer cells. PVT1 could bind directly with miR-140-5p, and Smad3 was a downstream target of miR-140-5p. Inhibition of PVT1 could enhance expression of miR-140-5p, inhibit the expression of Smad3, significantly inhibited the proliferation, migration, invasion in cervical cancer cells.	31626590	RID02973	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG8	PDGFRA	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-491)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000134853	NA	100093630	5156	LINC00060|NCRNA00060	CD140a|GAS9|PDGFR2	LncRNA SNHG8 promotes proliferation and invasion of gastric cancer cells by targeting the miR-491/PDGFRA axis.we determined that miRNA-491 was not only downregulated in stomach cancer but also inhibited GC cell progression induced by SNHG8. Further investigation demonstrated that SNHG8 promoted the proliferation and invasion of GC cells by targeting the miR-491/PDGFRA axis. LncRNA SNHG8 promoted the proliferation and invasion of GC cells by targeting the miR-491/PDGFRA axis, which might provide new insight for potential therapeutic strategies for GC in the future.	31620977	RID02974	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Colorectal cancer	GAS5	YY1AP1	negatively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	tumorigenesis(-)	NA	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000163374	NA	60674	55249	NCRNA00030|SNHG2	HCCA2|YAP|YY1AP	Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m 6 A reader YTHDF3. GAS5 directly interacts with WW domain of YAP to facilitate translocation of endogenous YAP from the nucleus to the cytoplasm and promotes phosphorylation and subsequently ubiquitin-mediated degradation of YAP to inhibit CRC progression in vitro and in vivo. Notably, we demonstrate the m6A reader YTHDF3 not only a novel target of YAP but also a key player in YAP signaling by facilitating m6A-modified lncRNA GAS5 degradation, which profile a new insight into CRC progression. Clinically, lncRNA GAS5 expressions is negatively correlated with YAP and YTHDF3 protein levels in tumors from CRC patients.	31619268	RID02975	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
B lymphocytic leukaemia	GAS5	miR-222	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Hematologic cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long non-coding RNA GAS5 regulates human B lymphocytic leukaemia tumourigenesis and metastasis by sponging miR-222. The results showed that the expression of lncRNA GAS5 was decreased in B lymphocytic leukaemia patients compared with the healthy group.cell culture experiments indicated that lncRNA GAS5 overexpression decreased B lymphocytic leukaemia cell proliferation, promoted B lymphocytic leukaemia cell apoptosis, arrested B lymphocytic leukaemia cells in the G1 phase of the cell cycle, and inhibited B lymphocytic leukaemia cell invasion. Finally, the luciferase reporter assay showed a direct target interaction between lncRNA GAS5 and miR-222. The regression analysis showed a negative correlation between the levels of lncRNA GAS5 and miR-222. Thus, our data suggested that lncRNA GAS5 could effectively sponge miR-222 to modulate human B lymphocytic leukaemia cell tumourigenesis and metastasis.	31594210	RID02976	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Hepatoblastoma	PVT1	STAT3	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000168610	NA	5820	6774	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	APRF	Long noncoding RNA PVT1 promotes hepatoblastoma cell proliferation through activating STAT3.PVT1 is upregulated in human hepatoblastoma tissues as well as in hepatoblastoma cell lines. Additionally, PVT1 promotes the proliferation of hepatoblastoma cells in vitro and accelerates tumor growth in xenograft model in vivo. Mechanistically, PVT1 promotes the activation of the signal transducer and activator of transcription 3 (STAT3), which leads to the transcriptional activation of downstream targets involved in cell cycle progression, and moreover,STAT3 inhibition with the selective inhibitor stattic abolishes PVT1 pro-proliferative role in hepatoblastoma cells.PVT1 promotes hepatoblastoma cell proliferation through activating STAT3-induced cell cycle progression, which may implicate PVT1 as a potential therapeutic target for hepatoblastoma treatment	31572006	RID02977	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Skin melanoma	FOXD3-AS1	MAP3K2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-325)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000169967	NA	100996301	10746	pasFOXD3	MEKK2|MEKK2B	LncRNA FOXD3-AS1 promotes proliferation, invasion and migration of cutaneous malignant melanoma via regulating miR-325/MAP3K2. When LncRNA FOXD3-AS1 was knockdown, proliferation, invasion and migration of cutaneous malignant melanoma, and tumor weight was inhibited, and cell cycle was arrested. LncRNA FOXD3-AS1 negatively regulated the expression of miR-325, and then improved the level of MAP3K2.	31541886	RID02978	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	Chaer	PRC2	positively-E	western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long noncoding RNA Chaer mediated Polycomb Repressor Complex 2 (PRC2) activity to promote atherosclerosis through mTOR signaling.we showed that Chaer promotes cell proliferation and induces apoptosis in vitro. Mechanistically, Chaer interacts with Polycomb Repressor Complex 2 (PRC2) through inhibiting histone H3 lysine 27 methylation. Further, this interaction is induced upon mTOR signaling pathway.	31539156	RID02979	expression association	NA		
Abdominal aortic aneurysm	GAS5	YBX1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000065978	NA	60674	4904	NCRNA00030|SNHG2	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA GAS5 induces abdominal aortic aneurysm formation by promoting smooth muscle apoptosis.GAS5 expression was significantly upregulated in human AAA specimens and two murine AAA models compared to human normal aortas and murine sham-operated controls. GAS5 overexpression induced SMC apoptosis and repressed its proliferation, thereby promoting AAA formation in two murine AAA models. Y-box-binding protein 1 (YBX1) was identified as a direct target of GAS5 while it also formed a positive feedback loop with GAS5 to regulate the downstream target p21. Furthermore, GAS5 acted as a miR-21 sponge to release phosphatase and tensin homolog from repression, which blocked the activation and phosphorylation of Akt to inhibit proliferation and promote apoptosis in SMCs.	31534503	RID02980	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Abdominal aortic aneurysm	GAS5	AKT1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000142208	NA	60674	207	NCRNA00030|SNHG2	AKT|PKB|PRKBA|RAC|RAC-alpha	Long noncoding RNA GAS5 induces abdominal aortic aneurysm formation by promoting smooth muscle apoptosis.GAS5 expression was significantly upregulated in human AAA specimens and two murine AAA models compared to human normal aortas and murine sham-operated controls. GAS5 overexpression induced SMC apoptosis and repressed its proliferation, thereby promoting AAA formation in two murine AAA models. Y-box-binding protein 1 (YBX1) was identified as a direct target of GAS5 while it also formed a positive feedback loop with GAS5 to regulate the downstream target p21. Furthermore, GAS5 acted as a miR-21 sponge to release phosphatase and tensin homolog from repression, which blocked the activation and phosphorylation of Akt to inhibit proliferation and promote apoptosis in SMCs.	31534503	RID02981	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Rectal adenocarcinoma	SNHG6	miR-101-3p	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);cell proliferation(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	SNHG 6 promotes the progression of Colon and Rectal adenocarcinoma via miR-101-3p and Wnt/beta-catenin signaling pathway.SNHG6 was over-expressed in CRC, and high expression of s SNHG6 were associated with short survival times. We then identified miR-101-3p as an inhibitory target of SNHG6. Knockdown of SNHG6 significantly decreased miR-101-3p expression. Moreover, silenced SNHG6 obviously inhibited CRC cell growth, weakened cell invasion capacity and blocked the Wnt/beta-catenin signaling pathway.SNHG6 could regulate the progression of CRC via modulating the expression levels of miR-101-3p and the activity of Wnt/beta-catenin signaling.	31533634	RID02982	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Lung adenocarcinoma	FAM83A-AS1	MMP14	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000204949	GRCh38_8:123193651-123202743	ENSG00000157227	NA	100131726	4323	HCCC11	MT1-MMP	FAM83A-AS1 promotes lung adenocarcinoma cell migration and invasion by targeting miR-150-5p and modifying MMP14.we found FAM83A-AS1 to be upregulated in LUAD tissues and closely associated with tumor size, lymph node metastasis, and TNM stage. Functional investigation revealed that FAM83A-AS1 promotes LUAD cell proliferation, migration, invasion and the epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo. Mechanistically, FAM83A-AS1 functions as an endogenous sponge of miR-150-5p by directly targeting it, removing inhibition of MMP14, a target of miR-150-5p. rescue assays demonstrated that FAM83A-AS1 enhances cell migration, invasion and EMT by modulating the miR-150-5p/MMP14 pathway. Collectively, we conclude that the novel FAM83A-AS1/miR-150-5p/MMP14 axis regulates LUAD progression, suggesting an innovative therapeutic strategy for this cancer.	31522616	RID02983	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Gastric cancer	HOTAIR	CXCR4	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);RhoA signaling pathway(+)	ceRNA(miR-126)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000121966	NA	100124700	7852	HOXC-AS4|HOXC11-AS1|NCRNA00072	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	lncRNA HOTAIR promotes gastric cancer proliferation and metastasis via targeting miR-126 to active CXCR4 and RhoA signaling pathway.HOTAIR was highly expressed in gastric cancer tissues and several gastric cancer cell lines. Overexpressed HOTAIR facilitated proliferation and metastasis in vitro while HOTAIR knockdown inhibit proliferation and metastasis. A negative correlation was observed between miR-126 and HOTAIR. And, we also confirmed the decrease in miR-126 in clinic specimen. Furthermore, HOTAIR and miR-126 negatively regulated each other and then increase or decrease CXCR4 expression and downstream pathway, respectively. CXCR4 was confirmed as a direct target of miR-126. Our study demonstrated that high HOTAIR expression promote proliferation and metastasis in gastric cancer via miR-126/CXCR4 axis and downstream signaling pathways.	31517442	RID02984	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	AWPPH	TGFB1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA AWPPH participates in the metastasis of non-small cell lung cancer by upregulating TGF-beta1 expression.It was observed that AWPPH was significantly upregulated in patients with NSCLC, while AWPPH expression level did not increase with the increase of tumor size. AWPPH overexpression promoted TGF-beta1 expression in NSCLC cells, while TGF-beta1 treatment showed no significant effects on AWPPH expression. AWPPH overexpression promoted NSCLC cell migration and invasion, while TGF-beta signaling inhibition reduced this enhancing effect. Therefore, AWPPH may promote the metastasis, but not the growth of NSCLC by upregulating TGF-beta1 expression.	31516619	RID02985	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral cavity cancer	H19	CDK6	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-107)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000105810	NA	283120	1021	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PLSTIRE	Effect of long chain non-coding RNA H19 on the migration and invasion of oral cancer cells and its molecular mechanism.H19 could bind specifically to the 3'-UTR of miR-107 to modulate the expression of miR-107. Compared with that in HIOEC cells, the expression of miR-107 significantly decreased in CAL27 cells (P<0.05). The expression of miR-107 increased after transfection with siRNA H19, and anti-mir-107 co-transfection could promote the invasion and migration ability of siRNA H19 in CAL27 cells (P<0.05). Compared with that in HIOEC cells, CDK6 expression significantly increased in CAL27 cells (P<0.05), and the expression level of the gene was coregulated by H19 and miR-107 (P<0.05).CONCLUSIONS: lncRNA H19 plays an important role in the development of oral cancer. It can regulate the invasion and migration of oral cancer cells by targeting the miR-107/CDK6 signaling axis.	31512829	RID02986	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Esophagus squamous cell carcinoma	lnc-ABCA12-3	FN1	positively-E	starBase v2.0;miRcode	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-200b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000115414	NA	NA	2335	NA	CIG|ED-B|FINC|FN|FNZ|GFND|GFND2|LETS|MSF|SMDCF	Long noncoding RNA lnc-ABCA12-3 promotes cell migration, invasion, and proliferation by regulating fibronectin 1 in esophageal squamous cell carcinoma.We also found that fibronectin 1 (FN1) was upregulated in ESCC tumor tissues. The expression of FN1 messenger RNA was positively correlated with the expression of lnc-ABCA12-3 in ESCC tumor tissues. After lnc-ABCA12-3 knockdown, the expression of FN1 was downregulated.Further studies indicated that lnc-ABCA12-3 acted as a competing endogenous RNA for miR-200b-3p to regulate FN1 expression.	31512786	RID02987	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteosarcoma	LINC01116	PTEN	positively-E	RIP;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(EZH2)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000171862	NA	375295	5728	TALNEC2	BZS|MHAM|MMAC1|PTEN1|TEP1	LINC01116 promotes proliferation, invasion and migration of osteosarcoma cells by silencing p53 and EZH2.RIP assay confirmed the binding of enhancer of zeste homolog 2 (EZH2) to LINC01116. Knockdown of LINC01116 significantly up-regulated the expressions of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and p53. Moreover, EZH2 knockdown could reverse the inhibitory effect of LINC01116 on carcinogenesis of osteosarcoma.LINC01116 is highly expressed in osteosarcoma. Up-regulated LINC01116 can promote cell proliferation, invasion and cell cycle progression, while inhibiting the apoptosis of osteosarcoma cells. Furthermore, LINC01116 is involved in the development of osteosarcoma by binding to EZH2 to regulate expressions of PTEN and p53.	31486480	RID02988	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	LINC01116	TP53	positively-E	RIP;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(EZH2)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000141510	NA	375295	7157	TALNEC2	LFS1|p53	LINC01116 promotes proliferation, invasion and migration of osteosarcoma cells by silencing p53 and EZH2.RIP assay confirmed the binding of enhancer of zeste homolog 2 (EZH2) to LINC01116. Knockdown of LINC01116 significantly up-regulated the expressions of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and p53. Moreover, EZH2 knockdown could reverse the inhibitory effect of LINC01116 on carcinogenesis of osteosarcoma.LINC01116 is highly expressed in osteosarcoma. Up-regulated LINC01116 can promote cell proliferation, invasion and cell cycle progression, while inhibiting the apoptosis of osteosarcoma cells. Furthermore, LINC01116 is involved in the development of osteosarcoma by binding to EZH2 to regulate expressions of PTEN and p53.	31486480	RID02989	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Osteoporosis	UCA1	BMP-2	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell differentiation(-);BMP-2/(Smad1/5/8) signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	LncRNA UCA1 affects osteoblast proliferation and differentiation by regulating BMP-2 expression.Inhibiting lncRNA UCA1 can promote the proliferation and differentiation of osteoblasts by activating the BMP-2/(Smad1/5/8) signaling pathway in osteoblasts. Therefore, UCA1 is expected to be a new therapeutic target for OST.	31486475	RID02990	expression association	NA	UP(PAAD);DATA(GSE40174)	
Breast cancer	NEAT1	CPT1A	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell cycle(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-107)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000110090	NA	283131	1374	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CPT1|CPT1-L|L-CPT1	Long non-coding RNA nuclear paraspeckle assembly transcript 1 interacts with microRNA-107 to modulate breast cancer growth and metastasis by targeting carnitine palmitoyltransferase-1.NEAT1 expression was increased in BC cells, whereas miR-107 expression was decreased, compared with normal mammary gland cells. NEAT1 promoted the progression of BC cells through inhibiting apoptosis-associated genes and promoting cell cycle- and invasion-associated gene expression, whereas miR-107 served the opposite function. Furthermore, NEAT1 promoted the expression of CPT1A, which was mediated by miR-107. The results of the present study indicate that NEAT1 promotes the expression of CPT1A by inhibiting miR-107 to improve the progression of BC cells; therefore, NEAT1 is a potential therapeutic target of BC.	31485672	RID02991	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367)
Nonalcoholic fatty liver disease	NEAT1	ROCK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	AMPK/SREBP signaling pathway(+);lipid accumulation(+)	ceRNA(miR-146a-5p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fatty liver disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	p160ROCK	LncRNA NEAT1 promotes hepatic lipid accumulation via regulating miR-146a-5p/ROCK1 in nonalcoholic fatty liver disease.It was reported that Nuclear enriched abundant transcript 1 (NEAT1) obviously was up-regulated in NAFLD model.High levels of NEAT1 and ROCK1, and low level of miR-146a-5p were identified in NAFLD models. NEAT1 could target miR-146a-5p to promote ROCK1 expression. Knockdown of NEAT1, overexpression of miR-146a-5p and knockdown of ROCK1 inhibited lipid accumulation through activating AMPK pathway.NEAT1 may regulate NAFLD through miR-146a-5p targeting ROCK1, and further affect AMPK/SREBP pathway.	31484042	RID02992	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	LINC01198	PTEN	negatively-E	RIP;western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+)	scaffold	binding/interaction	RNA-protein	Temozolomide	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000231817	GRCh38_13:46455131-46515958	ENSG00000171862	NA	101929344	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN expression in glioma.LINC01198 was elevated in glioma, and this predicted a poorer prognosis for patients with glioma. LINC01198 knockdown inhibited, while LINC01198 overexpression promoted, glioma cell proliferation and resistance to temozolomide. Mechanistically, NEDD4-1 (neural precursor cell expressed, developmentally downregulated 4, E3 ubiquitin protein ligase) and phosphatase and tensin homolog (PTEN) were recruited by LINC01198, which functioned as a scaffold. Moreover, we showed that LINC01198 exerted its oncogenic activities by enhancing the NEDD4-1-dependent repression of PTEN.	31469661	RID02993	expression association	prognosis,chemoresistance	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Infantile hemangioma	LINC00342	HDGF	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-3619-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hemangioma	lncRNA	PCG	ENSG00000232931	GRCh38_2:95807052-95835003	ENSG00000143321	NA	150759	3068	NCRNA00342	HMG1L2	Long noncoding RNA LINC00342 promotes growth of infantile hemangioma by sponging miR-3619-5p from HDGF.LINC00342 enhanced proliferation and inhibited apoptosis in HemECs. MiR-3619-5p targeted both LINC00342 and HDGF, where LINC00342 sponged miR-3619-5p and positively regulated HDGF. HDGF knockdown rescued the effects of LINC00342 on HemECs. The LINC00342-miR-3619-5p-HDGF signaling pathway could regulate cell proliferation and apoptosis in HemECs.	31469292	RID02994	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Colorectal cancer	SNHG1	RICTOR	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-137)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000164327	NA	23642	253260	LINC00057|lncRNA16|NCRNA00057|UHG	AVO3|KIAA1999|MGC39830|PIA	Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR-137.SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis. SNHG1 increased RICTOR level in CRC via sponging miR-137. In addition, SNHG1 silencing inhibited CRC cell proliferation and migration in vitro and in vivo. SNHG1 regulated RICTOR expression by sponging miR-137 and promoted tumorgenesis in CRC.	31469189	RID02995	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Heart failure	DACH1	SERCA2a	negatively-E		upregulation		NA	NA	calcium signaling pathway(-)	NA	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000165659	NA	NA	NA	1602	NA	DACH	NA	Long Noncoding RNA-DACH1 (Dachshund Homolog 1) Regulates Cardiac Function by Inhibiting SERCA2a (Sarcoplasmic Reticulum Calcium ATPase 2a).LncDACH1 directly binds to SERCA2a. Overexpression of LncDACH1 augments the ubiquitination of SERCA2a. LncDACH1 upregulation impairs cardiac function by promoting ubiquitination-related degradation of SERCA2a.onditional knockout of LncDACH1 in cardiac myocytes resulted in increased calcium transient, cell shortening, SERCA2a protein expression, and improved cardiac function of transverse aortic constriction induced HF mice.	31446800	RID02996	expression association	NA	UP(LIHC);DATA(GSE117623)	
Myocardial infarction	GAS5	CALM2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-525-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000143933	NA	60674	805	NCRNA00030|SNHG2	CAMII|PHKD	lncRNA GAS5 regulates myocardial infarction by targeting the miR-525-5p/CALM2 axis.Our data showed that the expression of GAS5 and CALM2 in PMMC was significantly upregulated, while the expression of miR-525-5p was downregulated. Overexpression of GAS5 and CALM2 profoundly promoted the apoptosis of myocardial cell. However, the proliferation of myocardial cell was inhibited by the upregulation of GAS5 and CALM2. Moreover, GAS5 was proved to be the target of miR-525-5p and GAS5 downregulated the expression of miR-525-5p and CALM2. In addition, lncRNA GAS5 promotes MI, while CALM2 induced MI can be reversed by miR-525-5p.	31429119	RID02997	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	SNHG16	ATG4B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);chemoresistance(+);cell growth(+);cell migration(+)	ceRNA(miR-16)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000168397	NA	100507246	23192	Nbla10727|Nbla12061|ncRAN	APG4B|AUTL1|DKFZp586D1822|KIAA0943	SNHG16 promotes osteosarcoma progression and enhances cisplatin resistance by sponging miR-16 to upregulate ATG4B expression.Small nucleolar RNA host gene 16 (SNHG16) and autophagy-related 4B (ATG4B) were significantly upregulated in osteosarcoma tissues than the normal ones, and the higher expression level of SNHG16 predicted a poor prognosis in osteosarcoma patients.SNHG16 was shown to promote cell growth, migration, and invasion, while miR-16 reversed this impact. Meanwhile, overexpression of ATG4B significantly promoted the development of osteosarcoma cells attenuated by SNHG16 knockdown or miR-16 mimics. Specifically, overexpression of ATG4B promoted cisplatin-induced autophagy and inhibited cell apoptosis rate, which enhanced the cisplatin resistance in osteosarcoma cell lines.	31427084	RID02998	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Cervical cancer	TUG1	RFX7	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(+);chemoresistance(+)	NA	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000181827	NA	55000	64864	FLJ20618|LINC00080|NCRNA00080	FLJ12994|RFXDC2	Low expression of TUG1 promotes cisplatin sensitivity in cervical cancer by activating the MAPK pathway.TUG1 knockdown inhibited the proliferative rate but accelerated the apoptosis of DDP-induced CC cells. Through bioinformatics prediction, RFX7 was screened out to be the target gene of TUG1. Both mRNA and protein levels of RFX7 were downregulated by TUG1 knockdown.	31424656	RID02999	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Keloid formation	HOXA11-AS	SMAD5	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Other	Keloid formation	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000113658	NA	221883	4090	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	Dwfc|JV5-1|MADH5	Long non-coding RNA HOXA11-AS induces type I collagen synthesis to stimulate keloid formation via sponging miR-124-3p and activation of Smad5 signaling.qRT-PCRand western blot showed that HOXA11-AS and ColI were significantly upregulated, while miR-124-3p was decreased in both keloid tissues and human keloid fibroblasts (HKFs). Knockdown of HOXA11-AS inhibited cell proliferation (by CCK-8 and immunofluorescence staining of Ki67) and cell migration (by wound healing and transwell assays). Mechanistic experiments verified that HOXA11-AS acted as a sponge of micro-RNA (miR)-124-3p and Smad5 was a target of miR-124-3p. miR-124-3p sufficiently reversed the regulatory effects of HOXA11-AS, and Smad5 was involved in miR-124-3p-mediated biological functions. Furthermore, HOXA11-AS induced ColI synthesis via sponging miR-124-3p-mediated Smad5 signaling, thus promoting keloid formation.	31411918	RID03000	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Hepatocellular carcinoma	SAMD12-AS1	NPM1	positively-F	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000281641	GRCh38_8:118620498-118906155	ENSG00000181163	NA	552860	4869	C8orf26|NCRNA00252	B23|NPM	LncRNA SAMD12-AS1 promotes cell proliferation and inhibits apoptosis by interacting with NPM1.We showed that ectopic expression of SAMD12-AS1 promotes cell growth and blocks apoptosis, while knockdown of SAMD12-AS1 inhibits cell proliferation and enhances etoposide-induced apoptosis.  we determined that SAMD12-AS1 interacts with NPM1 and confirmed that SAMD12-AS1(1-350) is required for the interaction with NPM1. As it is known that NPM1 interacts with the E3 ligase HDM2 and reduces HDM2-mediated p53 degradation, we examined whether SAMD12-AS1 can affect p53 stability.	31406141	RID03001	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Colorectal cancer	CircZNF609	BAX	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	circRNA	PCG	NA	NA	ENSG00000087088	NA	NA	581	NA	BCL2L4	Expression of circZNF609 is Down-Regulated in Colorectal Cancer Tissue and Promotes Apoptosis in Colorectal Cancer Cells by Upregulating p53.There was low expression of circZNF609 in HCT116 cells, and overexpression inhibited cell proliferation but had no effect on PCNA and c-Myc protein expression. Expression of circZNF609 induced apoptosis and upregulated expression of the pro-apoptotic protein, Bax, down-regulated the expression of the anti-apoptotic protein, Bcl-2, and upregulated p53. CONCLUSIONS Expression of circZNF609 was down-regulated in colorectal cancer tissue and promoted apoptosis in colorectal cancer cells in vitro by upregulating p53.	31401644	RID03002	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CircZNF609	BCL2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	circRNA	PCG	NA	NA	ENSG00000171791	NA	NA	596	NA	Bcl-2|PPP1R50	Expression of circZNF609 is Down-Regulated in Colorectal Cancer Tissue and Promotes Apoptosis in Colorectal Cancer Cells by Upregulating p53.There was low expression of circZNF609 in HCT116 cells, and overexpression inhibited cell proliferation but had no effect on PCNA and c-Myc protein expression. Expression of circZNF609 induced apoptosis and upregulated expression of the pro-apoptotic protein, Bax, down-regulated the expression of the anti-apoptotic protein, Bcl-2, and upregulated p53. CONCLUSIONS Expression of circZNF609 was down-regulated in colorectal cancer tissue and promoted apoptosis in colorectal cancer cells in vitro by upregulating p53.	31401644	RID03003	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	CircZNF609	TP53	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	circRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	Expression of circZNF609 is Down-Regulated in Colorectal Cancer Tissue and Promotes Apoptosis in Colorectal Cancer Cells by Upregulating p53.There was low expression of circZNF609 in HCT116 cells, and overexpression inhibited cell proliferation but had no effect on PCNA and c-Myc protein expression. Expression of circZNF609 induced apoptosis and upregulated expression of the pro-apoptotic protein, Bax, down-regulated the expression of the anti-apoptotic protein, Bcl-2, and upregulated p53. CONCLUSIONS Expression of circZNF609 was down-regulated in colorectal cancer tissue and promoted apoptosis in colorectal cancer cells in vitro by upregulating p53.	31401644	RID03004	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00466	HOXA10	positively-E	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-144)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224209	GRCh38_1:63159083-63317274	ENSG00000253293	NA	199899	3206	NA	HOX1|HOX1H	Tumor-Promoting Activity of Long Noncoding RNA LINC00466 in Lung Adenocarcinoma via miR-144-Regulated HOXA10 Axis.Highly expressed LINC00466 and HOXA10 and lowly expressed miR-144 were eventually revealed in lung adenocarcinoma tissues. HOXA10 was down-regulated in response to the overexpression of miR-144, whereas inhibition of LINC00466 decreased its binding to miR-144, thereby up-regulating miR-144, which, in turn, halted the lung adenocarcinoma progression. LINC00466 silencing or miR-144 up-regulation exerted an inhibitory role in the tumorigenicity, invasion, migration, and proliferation, and it also promoted apoptosis of lung adenocarcinoma cells. LINC00466 could restrain the miR-144 expression tmicroarray-based gene expression analysis showed high expression of LINC00466 and HOXA10 in lung adenocarcinoma (Figure 3, A and B). Website prediction is available at lncATLAS (http://lncatlas.crg.eu, last accessed May 28, 2019), and fluorescence in situ hybridization assay further presented that LINC00466 was mainly located in the cytoplasm (Figure 3, C and D). Furthermore, RNA pull down, together with the RNA-binding protein immunoprecipitation assay, was performed to determine the binding ability of LINC00466 to miR-144 and LINC00466 to AGO2, respectively. The results indicated that LINC00466 enrichment was increased in wt-miR-144 when compared with mut-miR-144 (P < 0.05) (Figure 4A), revealing that miR-144 directly binds to LINC00466. When compared with IgG, the binding of LINC00466 with AGO2 was significantly increased, suggesting that LINC00466 could bind to AGO2 (P < 0.05) (Figure 4B) and suggesting that LINC00466 could competitively bind to miR-144 through binding to AGO2.o up-regulate HOXA10 and, therefore, promote lung adenocarcinoma.	31381886	RID03005	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Osteoarthritis	MEG3	TRIB2	negatively-E	RIP;RNA pull-down assay	upregulation	microarray	NA	NA	cell differentiation(-)	NA	association	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000071575	NA	55384	28951	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	GS3955|TRB2	Long non-coding RNA MEG3 inhibits chondrogenic differentiation of synovium-derived mesenchymal stem cells by epigenetically inhibiting TRIB2 via methyltransferase EZH2.Knockdown of MEG3 can induce the expression of TRIB2; conversely, overexpression of MEG3 can inhibit the expression of TRIB2. Futhermore, knockdown of the TRIB2 can rescue the MEG3 silencing-mediated promotion of chondrogenic differentiation. Moreover, RNA immunoprecipitation(RIP) and RNA pull-down assays demonstrated that MEG3 can interact with EZH2, thus recruiting it to induce H3K27me3, which promotes the methylation of TRIB2 by binding with the promoter of TRIB2 in SMSCs. Additionally, EZH2 silencing significantly rescued the MEG3 overexpression-mediated inhibition of TRIB2 expression and chondrogenic differentiation of SMSCs. Taken together, these data indicated that MEG3 regulates chondrogenic differentiation by inhibiting TRIB2 expression through EZH2-mediated H3K27me3.	31376524	RID03006	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	CDKN2B-AS1	p15	negatively-E	downexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000086504	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Long Noncoding RNA, ANRIL, Regulates the Proliferation of Head and Neck Squamous Cell Carcinoma.Depletion of ANRIL increased p15 mRNA in FaDu cells, and p15 and p16 mRNA in CAL27 cells and inhibited proliferation of these cells. Cell cycle analysis showed that depletion of ANRIL caused arrest at the G1 phase of the cell cycle.ANRIL promotes G1 phase progression by repressing p15 and p16, and thus promotes FaDu and CAL27 cell proliferation.	31366490	RID03007	expression association	NA	UP(SKCM);DATA(GSE38495)	
Head and neck squamous cell carcinoma	CDKN2B-AS1	p16	negatively-E	downexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147889	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Long Noncoding RNA, ANRIL, Regulates the Proliferation of Head and Neck Squamous Cell Carcinoma.Depletion of ANRIL increased p15 mRNA in FaDu cells, and p15 and p16 mRNA in CAL27 cells and inhibited proliferation of these cells. Cell cycle analysis showed that depletion of ANRIL caused arrest at the G1 phase of the cell cycle.ANRIL promotes G1 phase progression by repressing p15 and p16, and thus promotes FaDu and CAL27 cell proliferation.	31366490	RID03008	expression association	NA	UP(SKCM);DATA(GSE38495)	
Prostate cancer	LINC00460	Ki67	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	Downregulated LINC00460 inhibits cell proliferation and promotes cell apoptosis in prostate cancer.LINC00460 high expression was related to Tumor Size (T1-T2/T3-T4; p=0.004), and high Gleason Score. Downregulation of LINC00460 by siRNA could inhibit cancer cell proliferation and decreased Ki67 and Cyclin D1 expression. Meanwhile, downregulation of LINC00460 promoted apoptosis of cell lines and was related to PI3K/AKT pathway.CONCLUSIONS: LINC00460 could regulate cell proliferation and cell apoptosis, which might be a novel marker in prostate cancer.	31364108	RID03009	expression association	NA		
Prostate cancer	LINC00460	Cyclin D1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	Downregulated LINC00460 inhibits cell proliferation and promotes cell apoptosis in prostate cancer.LINC00460 high expression was related to Tumor Size (T1-T2/T3-T4; p=0.004), and high Gleason Score . Downregulation of LINC00460 by siRNA could inhibit cancer cell proliferation and decreased Ki67 and Cyclin D1 expression. Meanwhile, downregulation of LINC00460 promoted apoptosis of cell lines and was related to PI3K/AKT pathway.CONCLUSIONS: LINC00460 could regulate cell proliferation and cell apoptosis, which might be a novel marker in prostate cancer.	31364108	RID03010	expression association	NA		
Sepsis-induced liver injury	NEAT1	TLR4	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(Let-7a)	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial pneumonia	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000136869	NA	283131	7099	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ARMD10|CD284|hToll|TLR-4	LncRNA NEAT1 promotes inflammatory response in sepsis-induced liver injury via the Let-7a/TLR4 axis.The overexpression of lncRNA NEAT1 accompanied by Let-7a inhibition and TLR4 activation was found in sepsis-induced liver injury patients. Similarly, LPS stimulation upregulated lncRNA NEAT1 expression, and lncRNA NEAT1 inhibition decreased the levels of inflammatory cytokines in vitro.We demonstrate that lncRNA NEAT1 interacts with Let-7a, targeting TLR4 to contribute to the LPS-induced inflammatory response.	31344555	RID03011	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	PVT1	VEGFA	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000112715	NA	5820	7422	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	VEGF|VEGF-A|VPF	PVT1 Promotes Angiogenesis by Regulating miR-29c/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway in Non-Small-Cell Lung Cancer (NSCLC).Our results showed that higher PVT1 was expressed in NSCLC and the elevated PVT1 was closely related to angiogenesis and poor prognosis in NSCLC. Further functional analysis showed that higher PVT1 expression could promote angiogenesis by regulating VEGF in NSCLC. Mechanistically, the luciferase reporter assay confirmed that VEGF was the targeted gene of miR-29c. In addition, we found that miR-29c is an inhibitory target of PVT1. CONCLUSIONS We found that PVT1 promotes angiogenesis through targeting the miR-29c/VEGF signaling pathway in NSCLC.	31326971	RID03012	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Breast cancer	NEAT1	STAT3	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APRF	NEAT1/miR-124/STAT3 feedback loop promotes breast cancer progression.The results demonstrated that NEAT1 and STAT3 expression levels were increased in breast cancer tissues compared with normal breast tissues, whereas miR-124 expression was significantly decreased. Functional analyses revealed that NEAT1 promoted cell proliferation and cell cycle progression in breast cancer cells. Additionally, NEAT1 and STAT3 expression levels were negatively correlated with miR-124 levels in breast cancer tissues. the present findings revealed that NEAT1 and STAT3 formed a feedback loop via sponging miR-124 to promote breast cancer progression.	31322202	RID03013	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Pulmonary hypertension	MIR222HG	MIR221	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Pulmonary hypertension	lncRNA	miRNA	ENSG00000270069	GRCh38_X:45745210-45770274	ENSG00000207870	NA	104457406	407006	Lnc-Ang362	MIRN221|miRNA221|mir-221	LncRNA-Ang362 Promotes Pulmonary Arterial Hypertension by Regulating miR-221 and miR-222.Although overexpression of lnc-Ang362 promoted proliferation and migration of HPASMCs, inhibition of lnc-Ang362 had the opposite effect. In addition, apoptosis of HPASMCs significantly decreased after lnc-Ang362 overexpression and increased after lnc-Ang362 inhibition. Meanwhile, lnc-Ang362 upregulated miR-221 and miR-222 expression and activated the NFkB signaling pathway in HPASMCs.	31313741	RID03014	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Pulmonary arterial hypertension	MIR222HG	MIR222	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Pulmonary hypertension	lncRNA	miRNA	ENSG00000270069	GRCh38_X:45745210-45770274	ENSG00000207725	NA	104457406	407007	Lnc-Ang362	MIRN222|miRNA222|mir-222	LncRNA-Ang362 Promotes Pulmonary Arterial Hypertension by Regulating miR-221 and miR-222.Although overexpression of lnc-Ang362 promoted proliferation and migration of HPASMCs, inhibition of lnc-Ang362 had the opposite effect. In addition, apoptosis of HPASMCs significantly decreased after lnc-Ang362 overexpression and increased after lnc-Ang362 inhibition. Meanwhile, lnc-Ang362 upregulated miR-221 and miR-222 expression and activated the NFkB signaling pathway in HPASMCs.	31313741	RID03015	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Peripheral artery disease	APTR	miR-126	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Artery disease	lncRNA	miRNA	ENSG00000214293	GRCh38_7:77657659-77696277	NA	NA	100505854	NA	RSBN1L-AS1	NA	Long noncoding RNA Alu-mediated p21 transcriptional regulator promotes proliferation, migration, and pipe-formation of human microvascular endothelial cells by sponging miR-126.Knockdown of APTR inhibited cell viability and migration and reduced the number of tubular cells. Further, APTR sponged miR-126 and downregulating miR-126 to promote angiogenesis. Overexpression of APTR promoted cell activity and migration and increased the number of tubular cells via negatively regulating miR-126. APTR could elevate activating phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal-regulated kinase signal pathways via negatively regulating miR-126 to promote cell proliferation, migration, and pipe-formation. We researched the mechanism of angiogenesis that APTR elevated proliferation, migration, and pipe-formation via negatively regulating miR-126.	31310378	RID03016	ceRNA or sponge	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	
Non-small cell lung cancer	MALAT1	CXCL5	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);ERK/MAPK signaling pathway(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163735	NA	378938	6374	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ENA-78|SCYB5	High Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Expression Promotes Proliferation, Migration, and Invasion of Non-Small Cell Lung Cancer via ERK/Mitogen-Activated Protein Kinase (MAPK) Signaling Pathway.Overexpression of MALAT1 significantly strengthened the proliferation, migration, and invasion ability of H460 cells. In comparison with the NC group, expression levels of CXCL5 and p-JNK proteins were elevated, while p-MAPK and p-ERK proteins were decreased in the MALAT1-mimic group. MALAT1 targets the 3'- untranslated region (UTR) fragment of the CXCL5 gene and inhibits its translation. Disturbance of the CXCL5 gene can reduce the protein expression of MAPK, p-MEK1/2, p-ERK1/2, and p-JNK, and inhibit the proliferation, migration, and invasion of MALAT1-mimic cells. CONCLUSIONS High MALAT1 expression promotes the proliferation, migration, and invasion of non-small cell lung cancer via the ERK/MAPK signaling pathway.	31293277	RID03017	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Liver fibrosis	SCARNA10	PRC2	negatively-F	RIP	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);apoptosis process(+)	NA	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000239002	GRCh38_12:6510222-6510551	NA	NA	692148	NA	U85	NA	SCARNA10, a nuclear-retained long non-coding RNA, promotes liver fibrosis and serves as a potential biomarker.We observed that the transcript of SCARNA10 was increased in the serum and liver from patients with advanced hepatic fibrosis. Furthermore, we found that SCARNA10 promoted liver fibrosis both in vitro and in vivo through inducing hepatocytes (HCs) apoptosis and HSCs activation. Mechanistically, RNA immunoprecipitation (RIP) assays demonstrated that SCARNA10 physically associated with polycomb repressive complex 2 (PRC2). Additionally, our results demonstrated that SCARNA10 functioned as a novel positive regulator of TGF-beta signaling in hepatic fibrogenesis by inhibiting the binding of PRC2 to the promoters of the genes associated with ECM and TGFbeta pathway, thus promoting the transcription of these genes.	31281502	RID03018	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE75367,GSE86978)	
Prostate cancer	HOTAIR	FOXR2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-152)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000189299	NA	100124700	139628	HOXC-AS4|HOXC11-AS1|NCRNA00072	FOXN6|MGC21658	The mechanism of HOTAIR regulating the proliferation and apoptosis of prostate cancer cells by targeting down-regulation of miR-152 to improve the expression of FOXR2.the specific knock-down of FOXR2 inhibits the proliferation of cells and promotes cell apoptosis. According to the microRNA chip results and luciferase reporter gene assay, we found miR-152 could regulate the expression of FOXR2; and FOXR2 3 'UTR had two miR-152 binding sites, all of which could control the expression of FOXR2. The results of LNCediting and qRT-PCR suggest that HOTAIR is negatively correlated with the expression of miR-152, and is involved in the regulation of miR-152 expression in prostate cancer.FOXR2 up-regulation can promote the proliferation and inhibit the apoptosis of prostate cancer cells because that HOTAIR restrains the expression of miR-152.	31269585	RID03019	ceRNA or sponge	NA		
Urinary bladder cancer	MIR4435-2HG	MIR4288	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000265251	NA	541471	100422903	AGD2|LINC00978|MIR4435-1HG|MORRBID|lncRNA-AWPPH	NA	LINC00978 promotes bladder cancer cell proliferation, migration and invasion by sponging miR-4288.it was demonstrated that LINC00978 knockdown significantly inhibited the proliferation, migration and invasion of BCa cells. it was demonstrated that LINC00978 served as a competing endogenous RNA to sponge microRNA-4288 (miR-4288), and LINC00978 knockdown significantly increased the expression level of miR-4288 in BCa cells.	31257499	RID03020	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Kidney disease	MEG3	EGR1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	fibrotic(+);inflammatory response(+)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000120738	NA	55384	1958	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268|ZNF225	Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis.We found that MEG3 was upregulated in DN in vivo and in vitro and could enhance cell fibrosis and inflammatory response in DN. MEG3 functioned as an endogenous sponge for miR-181a in mesangial cells (MCs) via direct targeting and in an Ago2-dependent manner. MiR-181a inhibition promoted MC fibrosis and inflammatory response. In addition, Egr-1 was confirmed as a target gene of miR-181a. Further investigations verified that MEG3 promotes fibrosis and inflammatory response via the miR-181a/Egr-1/TLR4 axis in vitro and in vivo. These results provide new insights into the regulation between MEG3 and the miR-181a/Egr-1/TLR4 signaling pathway during DN progression.	31195367	RID03021	ceRNA or sponge	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)
Glioblastoma	LINC01579	EIF4G2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258754	GRCh38_15:93718542-94070898	ENSG00000110321	NA	283682	1982	NA	DAP5|NAT1|p97	LINC01579 promotes cell proliferation by acting as a ceRNA of miR-139-5p to upregulate EIF4G2 expression in glioblastoma.the expression of LINC01579 was upregulated in GBM cells and LINC01579 knockdown inhibited cell proliferation as well as promoted cell apoptosis.the results of this study verified that LINC01579 modulated cell proliferation and cell apoptosis in GBM by competitively binding with miR-139-5p to regulate EIF4G2, which provided a new clue to figure out potential therapy for patients suffered from GBM.	31187495	RID03022	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Malignant glioma	BCAR4	EGFR	positively-E		upregulation		NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000146648	NA	400500	1956	NA	ERBB|ERBB1|ERRP	Long noncoding RNA BCAR4 promotes glioma cell proliferation via EGFR/PI3K/AKT signaling pathway. we uncovered that BCAR4 activated PI3K/AKT signaling pathway in glioma through upregulating EGFR and interacting with it. Moreover, activating PI3K/AKT pathway could reverse the repressive effects caused by BCAR4 silence on the biological behaviors of glioma cells, whereas inhibition of this pathway rescued the impact of BACR4 upregulation in NHAs. These findings disclosed that BCAR4 contributes to glioma progression by enhancing cell growth via activating EGFR/PI3K/AKT pathway, providing potent evidence that BCAR4 could be an effective new target for treatment and prognosis of glioma patients.	31173355	RID03023	expression association	prognosis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Pre-eclampsia	TCL6	CDK2	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000187621	GRCh38_14:95650498-95679833	ENSG00000123374	NA	27004	1017	TCL6e1|TNG1|TNG2	NA	Overexpression of lncRNA TCL6 promotes preeclampsia progression by regulating PTEN.TCL6 was highly expressed in 42 placental tissues of PE pregnancies when compared with that of normal pregnancies. downregulation of TCL6 resulted in remarkably increased proliferation and cell cycle of trophoblast cells.western blot results indicated that TCL6 knockdown significantly upregulated CDK2 and downregulated PTEN in trophoblast cells.Overexpression of lncRNA TCL6 inhibited the proliferation of trophoblast cells and promoted PE development via targeting PTEN.	31173275	RID03024	expression association	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pre-eclampsia	TCL6	PTEN	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000187621	GRCh38_14:95650498-95679833	ENSG00000171862	NA	27004	5728	TCL6e1|TNG1|TNG2	BZS|MHAM|MMAC1|PTEN1|TEP1	Overexpression of lncRNA TCL6 promotes preeclampsia progression by regulating PTEN.TCL6 was highly expressed in 42 placental tissues of PE pregnancies when compared with that of normal pregnancies. downregulation of TCL6 resulted in remarkably increased proliferation and cell cycle of trophoblast cells.western blot results indicated that TCL6 knockdown significantly upregulated CDK2 and downregulated PTEN in trophoblast cells.Overexpression of lncRNA TCL6 inhibited the proliferation of trophoblast cells and promoted PE development via targeting PTEN.	31173275	RID03025	expression association	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Colorectal cancer	SNHG8	MIR663A	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000227195	NA	100093630	724033	LINC00060|NCRNA00060	MIR663|MIRN663|hsa-mir-663|hsa-mir-663a|mir-663a	Knockdown of SNHG8 repressed the growth, migration, and invasion of colorectal cancer cells by directly sponging with miR-663.knockdown of SNHG8 significantly inhibited the growth, migration, and invasion of colorectal cancer cells. It was predicted that miR-663 might interact with SNHG8 and the direct sponging was verified by dual-luciferase reporter assay. we revealed that SNHG8 was up-regulated in colorectal cancer and promoted the proliferation, migration, and invasion of colorectal cancer by sponging miR-663, which helps to further reveal the underlying developmental mechanism of action and provides a potential therapeutic molecule for colorectal cancer therapy in the future.	31152930	RID03026	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(BRCA);DATA(GSE109761,GSE111065)
Hepatocellular carcinoma	RPL13AP20	KCNH1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-296)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234498	GRCh38_12:12875499-12876107	ENSG00000143473	NA	387841	3756	HANR	eag|eag1|h-eag|hEAG|Kv10.1	HANR promotes lymphangiogenesis of hepatocellular carcinoma via secreting miR-296 exosome and regulating EAG1/VEGFA signaling in HDLEC cells.HANR was shown to directly bind to miR-296, and miR-296 downregulated HANR expression in HepG2 cells. Then, we observed that miR-296 inhibitor transfection in shHANR HCC cells could promote lymphatic vessel formation and invasion of HDLEC cells compared with shHANR HCC cells. EAG1 or VEGFA overexpression in HDLEC cells rescued lymphatic vessel formation and invasion in HDLEC cells coincubated with the medium of HepG2 cells expressing shHANR or miR-296 mimic.	31127654	RID03027	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE55807)
Hepatocellular carcinoma	RPL13AP20	VEGFA	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-296)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234498	GRCh38_12:12875499-12876107	ENSG00000112715	NA	387841	7422	HANR	VEGF|VEGF-A|VPF	HANR promotes lymphangiogenesis of hepatocellular carcinoma via secreting miR-296 exosome and regulating EAG1/VEGFA signaling in HDLEC cells.HANR was shown to directly bind to miR-296, and miR-296 downregulated HANR expression in HepG2 cells. Then, we observed that miR-296 inhibitor transfection in shHANR HCC cells could promote lymphatic vessel formation and invasion of HDLEC cells compared with shHANR HCC cells. EAG1 or VEGFA overexpression in HDLEC cells rescued lymphatic vessel formation and invasion in HDLEC cells coincubated with the medium of HepG2 cells expressing shHANR or miR-296 mimic.	31127654	RID03028	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Rheumatoid arthritis	NEAT1	STAT3	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APRF	Knockdown of lncRNA NEAT1 inhibits Th17/CD4 + T cell differentiation through reducing the STAT3 protein level.STAT3 protein, a critical molecule for Th17 cell differentiation, is a downstream molecule for NEAT and its cellular level can be positively targeted and regulated by NEAT via reducing the ubiquitination level. Moreover, the cotreatment of NEAT1 knockdown and STAT3 overexpression promotes Th17 cell differentiation compared with NEAT1 knockdown alone.	31119756	RID03029	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	MALAT1	RUNX2	positively-E	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	ceRNA(miR-15)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124813	NA	378938	860	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	MALAT1 regulates the transcriptional and translational levels of proto-oncogene RUNX2 in colorectal cancer metastasis.MALAT1 binds miR-15 family members, to "de-inhibit" their effect on LRP6 expression, enhances beta-catenin signaling, leading to elevated transcriptional levels of downstream target genes RUNX2.	31097689	RID03030	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney injury	NEAT1	miR-27a-3p	negatively-E	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 promotes hypoxia-induced renal tubular epithelial apoptosis through downregulating miR-27a-3p.The expression of miR-27a-3p was negatively regulated by NEAT1. Inhibition the expression of NEAT1 attenuated overexpression of miR-27a-3p enhanced CoCl2 -induced injury. In summary, an ischemia-induced injury may be enhanced by a high level of NEAT1 through targeting miR-27a-3p.	31090110	RID03031	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Ovarian cancer	SNHG14	DHX33	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-125a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000005100	NA	104472715	56919	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	DDX33|DKFZp762F2011|FLJ21972	LncSNHG14 promotes ovarian cancer by targeting microRNA-125a-5p.SNHG14 was highly expressed in ovarian cancer tissues and cell lines relative to controls.In addition, we found that SNHG14 could accelerate cell proliferation and cell cycle progression of ovarian cancer cells. Dual-Luciferase reporter gene experiments indicated that SNHG14 could bind to microRNA-125a-5p, which was lowly expressed in ovarian cancer patients.Dual-Luciferase reporter gene assay also indicated that DHX33 was a target gene of microRNA-125a-5p. The overexpression of DHX33 could attenuate the inhibitory effect of microRNA-125a-5p on cell proliferation and cell cycle in SKOV3 and OVCAR3 cells.High expression of SNHG14 can promote the ovarian cancer cell proliferation and accelerate the cell cycle by sponging microRNA-125a-5p to regulate DHX33 expression.	31081075	RID03032	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	DANCR	TGFB1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000105329	NA	57291	7040	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA ANCR is positively correlated with transforming growth factor-beta1 in patients with osteoarthritis.We observed that the plasma levels of ANCR were significantly lower, while the plasma levels of TGF-beta1 were significantly higher in osteoarthritis patients than those in healthy controls. Downregulation of ANCR effectively distinguished osteoarthritis patients from healthy controls. ANCR and TGF-beta1 expression was negatively correlated in osteoarthritis patients but not in healthy controls. ANCR overexpression promoted the proliferation of chondrocytes and inhibited TGF-beta1 expression. We concluded that ANCR might participate in osteoarthritis by downregulating TGF-beta1 and promote the proliferation of chondrocytes.	31074173	RID03033	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute pneumonia	SNHG16	CCL5	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(+)	ceRNA(miR-146a-5p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Pneumonia	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000161570	NA	100507246	6352	Nbla10727|Nbla12061|ncRAN	D17S136E|MGC17164|RANTES|SCYA5|SISd|TCP228	Long noncoding RNA SNHG16 targets miR-146a-5p/CCL5 to regulate LPS-induced WI-38 cell apoptosis and inflammation in acute pneumonia.SNHG16 was highly expressed in serum of acute stage pneumonia patients. SNHG16 was up-regulated in LPS-treated WI-38 cell model and SNHG16 knockdown obviously mitigated LPS-induced cell injury by promoting viability, restraining apoptosis and production of inflammatory cytokines. SNHG16 functioned as a competitive endogenous RNA (ceRNA) by efficaciously binding to miR-146a-5p and then restoring CC motif chemokine ligand 5 (CCL5) expression. SNHG16 regulated LPS-induced inflammation injury in WI-38 cells through competitively binding miR-146a-5p with CCL5 further mediating JNK and NF-kB pathways, which sheds novel light on diagnostics and therapeutics in pneumonia.	31071307	RID03034	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Nonalcoholic fatty liver disease	H19	PPARG	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	hepatic lipid homeostasis(+)	ceRNA(miR-130a)	regulation	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Fatty liver disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000132170	NA	283120	5468	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARG5|PPARgamma	LncRNA-H19 promotes hepatic lipogenesis by directly regulating miR-130a/PPAR-Gamma axis in non-alcoholic fatty liver disease.H19 and PPAR-Gamma were up-regulated, while miR-130a was down-regulated in NAFLD mouse and cellular model. H&E and Oil-Red O staining indicated an increased lipid accumulation. Knockdown of H19 inhibited steatosis and TG secretion in FFA-induced hepatocytes. H19 could bind to miR-130a, and miR-130a could directly inhibit PPAR-Gamma expression. Knockdown of H19 alleviated hepatic lipogenesis via directly regulating miR-130a/PPAR-Gamma axis, which is a novel mechanistic role of H19 in the regulation of NAFLD.	31064820	RID03035	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Childhood-onset asthma	LINC00882	miR-3619-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Reproductive system disease	Asthma	lncRNA	miRNA	ENSG00000242759	GRCh38_3:106449775-107240671	NA	NA	100302640	NA	NA	NA	Long non-coding RNA00882 contributes to platelet-derived growth factor-induced proliferation of human fetal airway smooth muscle cells by enhancing Wnt/beta-catenin signaling via sponging miR-3619-5p.we found that LINC00882 expression was significantly up-regulated in ASM cells stimulated with platelet-derived growth factor (PDGF).Functional experiments showed that the knockdown of LINC00882 markedly reduced the proliferation of fetal ASM cells induced by PDGF, while the overexpression of LINC00882 exhibited the opposite effect. LINC00882 negatively regulated miR-3619-5p expression in fetal ASM cells. Notably, beta-catenin was identified as a target gene of miR-3619-5p. miR-3619-5p overexpression restricted PDGF-induced cell proliferation through inhibiting Wnt/beta-catenin signaling. our results demonstrate that LINC00882 promotes PDGF-induced cell proliferation of ASM cells by enhancing Wnt/beta-catenin signaling via sponging miR-3619-5p, suggesting a potential role for LINC00882 in airway remodeling in pediatric asthma.	31014672	RID03036	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE86978)	
Colon cancer	HCP5	AP1G1	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000166747	NA	10866	164	D6S2650E|P5-1	ADTG|CLAPG1	HCP5 promotes colon cancer development by activating AP1G1 via PI3K/AKT pathway.The knockdown of HCP5 in CC cells down-regulated proliferation and migration capacities, and arrested cell cycle in the G0/G1 phase, which was reversed by the AP1G1 knockdown. In addition, HCP5 knockdown up-regulated AP1G1 expression, whereas down-regulated the expression of relative proteins in the PI3K/AKT pathway.HCP5 was significantly increased in CC and enhanced the proliferation and migration of CC cells by inhibiting the AP1G1 expression. HCP5 promoted CC development by activating the PI3K/AKT pathway.	31002129	RID03037	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Cystitis glandularis	UCA1	CCND2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell viability(+)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Cystitis	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118971	NA	652995	894	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	UCA1 promotes cell viability, proliferation and migration potential through UCA1/miR-204/CCND2 pathway in primary cystitis glandularis cells.UCA1 was up-regulated in the primary CG cells (pCGs). Then, we showed that knock out of UCA1 reduced the cell viability, inhibited the cell proliferation and restrained the migration potential and overexpression of UCA1 promoted that in pCGs. Furthermore, we demonstrated that UCA1 played its role via sponging of the miR-204 in pCGs. In addition, we illustrated that miR-204 exerted its function via targeting CYCLIN D2 (CCND2) 3'UTR at mRNA level in pCGs. Ultimately, we revealed the role and regulation of UCA1/miR-204/CCND2 regulatory axis in pCGs.	30999112	RID03038	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	LNCRNA-ATB	miR-195	negatively-E	luciferase reporter assay;biotin-avidin pull-down assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	NA	NA	NA	NA	114004396	NA	NA	NA	lncRNA-ATB promotes viability, migration, and angiogenesis in human microvascular endothelial cells by sponging microRNA-195.lncRNA-ATB overexpression increased cell viability, migration and formation of tubes, along with upregulation of matrix metalloproteinase-2 (MMP-2), MMP-9, and vascular endothelial growth factor. Then, we found lncRNA-ATB worked as a molecular sponge for miR-195, and the effects of lncRNA-ATB on HMEC-1 cells were reversed by miR-195 overexpression while were augmented by miR-195 inhibition.Phosphorylated levels of key kinases in the PI3K/AKT and MEK/ERK pathways were increased by lncRNA-ATB via miR-195. In conclusion, lncRNA-ATB enhanced cell viability, migration and angiogenesis in HMEC-1 cells through sponging miR-195. Moreover, the PI3K/AKT and MEK/ERK pathways were activated by lncRNA-ATB via miR-195.	30983015	RID03039	ceRNA or sponge	NA		
Colorectal cancer	MALAT1	EZH2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ENX-1|EZH1|KMT6|KMT6A	LncRNA MALAT1 promotes colorectal cancer development by sponging miR-363-3p to regulate EZH2 expression.We observed that MALAT1 was highly expressed in colorectal cancer tissues and cells, and MALAT1 knockdown inhibited cell proliferation as well as expression levels of EZH2 by upregulated miR-363-3p in cell models and in vivo. Moreover, miR-363-3p functions as a downstream target of MALAT1, meanwhile EZH2 was a target of miR-363-3p, suggesting MALAT1 might regulate miR-363-3p and/or EZH2 expression.	30972996	RID03040	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Oral squamous cell carcinoma	LACAT1	miR-4301	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	miRNA	NA	NA	NA	NA	105371906	NA	NA	NA	LncRNA LACAT1 promotes proliferation of oral squamous cell carcinoma cells by inhibiting microRNA-4301.the cell proliferation ability of sh-LACAT1 group was significantly decreased while cell apoptosis was oppositely increased. qRT-PCRresults showed that microRNA-4301 level was significantly elevated in cells of sh-LACAT1 group, suggesting that the expression of above two molecules was negatively correlated. Meanwhile, cell reverse experiment also demonstrated that LACAT1 and microRNA-4301 can be mutually regulated, and thereby promote the malignant progression of OSCC.	30964168	RID03041	ceRNA or sponge	NA		
Cerebral ischemic stroke	KCNQ1OT1	FOXO3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell autophagy(+);cell viability(-)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Nervous system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000118689	NA	10984	2309	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	AF6q21|FKHRL1|FOXO2|FOXO3A	KCNQ1OT1 promotes autophagy by regulating miR-200a/FOXO3/ATG7 pathway in cerebral ischemic stroke.we revealed that potassium voltage-gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) was significantly upregulated in ischemic stroke. Knockdown of KCNQ1OT1 remarkably reduced the infarct volume and neurological impairments in transient middle cerebral artery occlusion (tMCAO) mice. Mechanistically, KCNQ1OT1 acted as a competing endogenous RNA of miR-200a to regulate downstream forkhead box O3 (FOXO3) expression, which is a transcriptional regulator of ATG7. Knockdown of KCNQ1OT1 might inhibit I/R-induced autophagy and increase cell viability via the miR-200a/FOXO3/ATG7 pathway.	30945454	RID03042	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(BRCA);DATA(GSE51827,GSE86978)
Peritoneal fibrosis	AV310809	CTNNB1	positively-F	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);WNT2/beta-catenin signaling pathway	NA	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Connective tissue disease	lncRNA	PCG	NA	NA	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Novel long non-coding RNA AV310809 promotes TGF-beta1 induced epithelial-mesenchymal transition of human peritoneal mesothelial cells via activation of the Wnt2/beta-catenin signaling pathway.The expression level of AV310809 was upregulated in fibrotic peritoneum and TGF-beta1 induced EMT in HPMCs. Ectopic overexpression of AV310809 promoted EMT and activated the Wnt2/beta-catenin signaling pathway. we demonstrated that AV310809 could interact with beta-catenin and blocking beta-catenin inhibited the augmentation of EMT by AV310809. These findings indicated that AV310809 promoted TGF-beta1-induced EMT in HPMCs through the activation of the Wnt2/beta-catenin signaling pathway, possibly by targeting beta-catenin.	30935692	RID03043	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	NEAT1	SOX4	positively-E	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-133a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000124766	NA	283131	6659	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Involvement of NEAT1/miR-133a axis in promoting cervical cancer progression via targeting SOX4.NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)-133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR-133a expression. Subsequently, we validated that miR-133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR-133a and silencing of SOX4 can restrain cervical cancer progression.These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR-133a and regulate SOX4 in cervical cancer pathogenesis.	30932200	RID03044	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Prostate cancer	TUG1	RLIM	positively-E	western blot	upregulation	qRT-PCR	NA	NA	TGF-beta1/SMAD signaling pathway(+);cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000131263	NA	55000	51132	FLJ20618|LINC00080|NCRNA00080	MGC15161|NY-REN-43|RNF12	TUG1 promotes the development of prostate cancer by regulating RLIM.The overexpression of TUG1 markedly promoted the proliferative and migratory capacities of DU145 cells. However, knockdown of TUG1 obtained the opposite results. qRT-PCRconfirmed that TUG1 was positively correlated with RLIM at the mRNA level. RLIM knockdown significantly inhibited the proliferative and migratory capacities of DU145 cells. Furthermore, knockdown of TUG1 in DU145 cells markedly down-regulated TGF-beta1 and p-Smad2, whereas up-regulated p-Smad7.TUG1 is highly expressed in peripheral blood of PCa patients, which can serve as a potential diagnostic marker for PCa. The overexpression of TUG1 promotes the proliferative and migratory capacities of PCa cells. Furthermore, TUG1 promotes the development of PCa by regulating RLIM through the TGF-beta1/Smad pathway.	30915735	RID03045	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE55807)
Laryngeal carcinoma	PCAT19	PDK4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-182)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000267107	GRCh38_19:41449520-41501255	ENSG00000004799	NA	100505495	5166	LINC01190|LOC100505495	NA	lncRNA PCAT19 promotes the proliferation of laryngocarcinoma cells via modulation of the miR-182/PDK4 axis.Further studies indicated that miR-182 functioned as the bridge between PCAT19 and PDK4, which could also regulate the cellular metabolism thus affecting the cell proliferation. Furthermore, it was shown that the PCAT19/miR-182/PDK4 axis existed and regulated cell proliferation by modulating glycolysis and mitochondrial respiration. Finally, we showed that the PCAT19 knockdown decreased the tumor growth in vivo, possibly through regulating the miR-182/PDK4 axis. In conclusion, we demonstrated that lncRNA PCAT19 promoted cell proliferation and tumorigenesis by modulating the miR-182/PDK4 axis and the metabolism balance.	30868666	RID03046	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(BRCA);DATA(GSE86978)
Cervical cancer	PTTG3P	PTTG1	positively-E	western blot;shRNA;overexpression;downexpression	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000213005	GRCh38_8:66767400-66768005	ENSG00000164611	NA	26255	9232	PTTG3	EAP1|HPTTG|PTTG|securin|TUTR1	The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1.the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients' survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells.PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis.	30853662	RID03047	expression association	metastasis	UP(SKCM);DATA(GSE38495)	UP(NSCLC,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)
Cervical cancer	PTTG3P	SNAI1	positively-E	western blot;shRNA;overexpression;downexpression	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000213005	GRCh38_8:66767400-66768005	ENSG00000124216	NA	26255	6615	PTTG3	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1.the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients' survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells.PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis.	30853662	RID03048	expression association	metastasis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DATA(GSE40174)
Cervical cancer	PTTG3P	E-cadherin	negatively-E	western blot;shRNA;overexpression;downexpression	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000213005	GRCh38_8:66767400-66768005	NA	NA	26255	NA	PTTG3|rcPTTG1	NA	The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1.the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients' survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells.PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis.	30853662	RID03049	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Non-small cell lung cancer	NEAT1	SOX9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000125398	NA	283131	6662	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CMD1|CMPD1|SRA1	Overexpression of HIF-2alpha-Dependent NEAT1 Promotes the Progression of Non-Small Cell Lung Cancer through miR-101-3p/SOX9/Wnt/beta-Catenin Signal Pathway.The expressions of NEAT1 were significantly higher in both of NSCLC tissues and cells than in normal controls. High expression of NEAT1 was significantly associated with TNM stage (P=0.000) and metastasis (P=0.000). NEAT1 knockdown inhibited the proliferation, migration and invasion of NSCLC cells. Hypoxia induction mediated by HIF-2alpha promoted EMT and NEAT1 expressions. Moreover, miR-101-3p was a target of NEAT1. We also found that SOX9 was a target of miR-101-3p. Oncogenic function of NEAT1 on NSCLC progression was mediated by miR-101-3p/SOX9/Wnt/beta-catenin signaling pathway.	30845377	RID03050	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Myocardial ischemia	MALAT1	SIRT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	Notch signaling pathway(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000096717	NA	378938	23411	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	SIR2L1	Knockdown of long noncoding RNA Malat1 aggravates hypoxia-induced cardiomyocyte injury by targeting miR-217.Malat1 bound to miR-217 and Sirt1 was a direct target of miR-217. Knockdown of Malat1 aggravated hypoxia-induced H9c2 cell injury by overexpression of miR-217. Overexpression of Sirt1 alleviated H9c2 cell injury by activating phosphatidylinositol 3-kinase/protein kinase 3 (PI3K/AKT) and Notch signaling pathways.These findings suggest that Malat1 exerted important roles in hypoxia-induced cardiomyocyte injury by regulating miR-217-mediated Sirt1 and downstream PI3K/AKT and Notch signaling pathways.	30843674	RID03051	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	NORAD	EGLN2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-205)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000269858	NA	647979	112398	LINC00657	HIFPH1|PHD1	Overexpression of long non-coding RNA NORAD promotes invasion and migration in malignant melanoma via regulating the MIR-205-EGLN2 pathway.NORAD knockdown significantly inhibited migration and invasion of malignant melanoma cells and elevated the expression of miR-205, there was an interaction between miR-205 and NORAD in the RNA-induced silencing complex. Upregulation of miR-205 induced significant inhibition of migratory and invasive ability compared with the scrambled control. the regulatory effects of miR-205 on EGLN2 levels and the induction of endoplasmic reticulum stress were reversed by NORAD. In vivo, deletion of miR-205 induced tumor growth in nude mice. NORAD may play critical roles in tumorigenesis and progression of malignant melanoma by regulating of the miR-205-EGLN2 pathway, and may serve as a new therapeutic target.	30843652	RID03052	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Liver cancer	MEG3	AP1G1	positively-E	western blot;downexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell cycle(-);PI3K/AKT signaling pathway(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000166747	NA	55384	164	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ADTG|CLAPG1	MEG3 promotes liver cancer by activating PI3K/AKT pathway through regulating AP1G1. Knockdown of MEG3 significantly promoted proliferation and invasion of hepatoma cells, but accelerated cell cycle.western blotrevealed that knockdown of MEG3 reduced the level of AP1G1 and activated the PI3K/AKT pathway.  Low expression of MEG3 could promote the proliferative and invasive abilities of hepatoma cells and accelerate cell cycle. The mechanism may be related to the inhibition of AP1G1 expression and activation of PI3K/AKT pathway.	30840267	RID03053	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Ovarian cancer	Lnc00908	ANXA3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-495-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000138772	NA	NA	306	NA	ANX3	Lnc00908 promotes the development of ovarian cancer by regulating microRNA-495-5p.Overexpression of lnc00908 markedly promoted the proliferative and migratory abilities of SKOV3 and OVCAR cells. Luciferase reporter gene assay showed that lnc00908 could bind to microRNA-495-5p. However, microRNA-495-5p was significantly downregulated in OC tissues. Overexpression of microRNA-495-5p reversed the enhanced abilities of proliferation and migration in SKOV3 and OVCAR3 cells by lnc00908 overexpression. ANXA3 was a target gene of microRNA-495-5p. Moreover, overexpression of ANXA3 attenuated the inhibitory effect of miR-495-5p on the proliferative and migratory behaviors of SKOV3 and OVCAR3 cells.We found that the high expression of lnc00908 can promote the proliferation and migration abilities of OC cells through sponging microRNA-495-5p to regulate ANXA3 expression.	30840259	RID03054	ceRNA or sponge	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065)
Osteosarcoma	MALAT1	c-Met	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000105976	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Proliferation and Metastasis of Osteosarcoma Cells by Targeting c-Met and SOX4 via miR-34a/c-5p and miR-449a/b.Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. Further study showed a positive correlation between MALAT1 and c-Met or SOX4 expression. Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.	30793707	RID03055	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Osteosarcoma	MALAT1	c-Met	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-34c-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000105976	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Proliferation and Metastasis of Osteosarcoma Cells by Targeting c-Met and SOX4 via miR-34a/c-5p and miR-449a/b.Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. Further study showed a positive correlation between MALAT1 and c-Met or SOX4 expression. Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.	30793707	RID03056	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Osteosarcoma	MALAT1	SOX4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-449a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124766	NA	378938	6659	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Proliferation and Metastasis of Osteosarcoma Cells by Targeting c-Met and SOX4 via miR-34a/c-5p and miR-449a/b.Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. Further study showed a positive correlation between MALAT1 and c-Met or SOX4 expression. Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.	30793707	RID03057	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Osteosarcoma	MALAT1	SOX4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-449b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124766	NA	378938	6659	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Proliferation and Metastasis of Osteosarcoma Cells by Targeting c-Met and SOX4 via miR-34a/c-5p and miR-449a/b.Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. Further study showed a positive correlation between MALAT1 and c-Met or SOX4 expression. Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.	30793707	RID03058	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Malignant glioma	SNHG20	NSG1	negatively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000168824	NA	654434	27065	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	D4S234|D4S234E|NEEP21|P21	lncRNA small nucleolar RNA host gene 20 predicts poor prognosis in glioma and promotes cell proliferation by silencing P21.Our results suggested the high expression of lncRNA SNHG20 in human glioma tissues compared with normal brain tissues, which was related to recurrence-free survival and poor overall survival in glioma patients. knocking down the expression of lncRNA SNHG20 could inhibit the proliferation and colony formation abilities of glioma U87 cells through cell cycle arrest. Consequently, the expression of CCNA1 was inhibited, and the expression of P21 was up-regulated in U87 cells.A high lncRNA SNHG20 expression level predicts the poor prognosis for glioma patients. Moreover, lncRNA SNHG20 can promote glioma proliferation through silencing P21 and thus lncRNA SNHG20 is an independent potential prognostic biomarker for glioma patients.	30774368	RID03059	expression association	recurrence,prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	
Liver cancer	GAS5	RUNX3	positively-E	DIANA;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000020633	NA	60674	864	NCRNA00030|SNHG2	AML2|CBFA3|PEBP2A3	LncRNA GAS5 enhanced the killing effect of NK cell on liver cancer through regulating miR-544/RUNX3.We also proved the interaction of GAS5 and miR-544, and the negative regulation role of GAS5 on miR-544. GAS5 overexpression in activated NK cells increased RUNX3 expression, IFN-Gamma secretion, the NK cell cytotoxicity, the percentage of CD107a+ NK cells, and the apoptosis rate of HepG2 cells, while miR-544 mimic abolished the promotion effect of GAS5 overexpression.Finally, in vivo experiments indicated an inhibition effect of GAS5 in tumor growth. LncRNA GAS5 overexpression enhances the killing effect of NK cell on liver cancer through regulating miR-544/RUNX3.qRT-PCR was conducted to measure GAS5, miR-544, and NCR1 expression using PowerUp? SYBR? Green Master Mix (Invitrogen). The relative expressions of GAS5, miR-544 and NCR1 were calculated using the 2-Ct method;According to the bioinformatics software DIANA tools (http://diana.imis.athena-innovation.gr/DianaTools/index.php?r=site/index), there were binding sites between GAS5 and miR-544 (Figure 4a). AGO2 Ab was used for RNA immunoprecipitation. AGO2 protein was detected in Input and AGO2 groups by IP-Western (Figure 4b). GAS5 and miR-544 levels in the AGO2 group were higher than that of the Input group (Figure 4b). AGO2 was observed in the GAS5 pull-down complex, and miR-544 was enriched in the GAS5 pull-down complex, whereas miR-544 was slightly increased in the LOC pull-down complex compared with beads alone (Figure 4c). After transfection of lenti-GAS5, the miR-544 level was significantly decreased (Figure 4d), which indicated that miR-544 was negatively regulated by GAS5.	30774011	RID03060	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Liver cancer	GAS5	MIR544A	negatively-E	DIANA;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000207587	NA	60674	664613	NCRNA00030|SNHG2	MIR544|MIRN544|hsa-mir-544|hsa-mir-544a	LncRNA GAS5 enhanced the killing effect of NK cell on liver cancer through regulating miR-544/RUNX3.We also proved the interaction of GAS5 and miR-544, and the negative regulation role of GAS5 on miR-544. GAS5 overexpression in activated NK cells increased RUNX3 expression, IFN-Gamma secretion, the NK cell cytotoxicity, the percentage of CD107a+ NK cells, and the apoptosis rate of HepG2 cells, while miR-544 mimic abolished the promotion effect of GAS5 overexpression.Finally, in vivo experiments indicated an inhibition effect of GAS5 in tumor growth. LncRNA GAS5 overexpression enhances the killing effect of NK cell on liver cancer through regulating miR-544/RUNX3.qRT-PCR was conducted to measure GAS5, miR-544, and NCR1 expression using PowerUp? SYBR? Green Master Mix (Invitrogen). The relative expressions of GAS5, miR-544 and NCR1 were calculated using the 2-Ct method;According to the bioinformatics software DIANA tools (http://diana.imis.athena-innovation.gr/DianaTools/index.php?r=site/index), there were binding sites between GAS5 and miR-544 (Figure 4a). AGO2 Ab was used for RNA immunoprecipitation. AGO2 protein was detected in Input and AGO2 groups by IP-Western (Figure 4b). GAS5 and miR-544 levels in the AGO2 group were higher than that of the Input group (Figure 4b). AGO2 was observed in the GAS5 pull-down complex, and miR-544 was enriched in the GAS5 pull-down complex, whereas miR-544 was slightly increased in the LOC pull-down complex compared with beads alone (Figure 4c). After transfection of lenti-GAS5, the miR-544 level was significantly decreased (Figure 4d), which indicated that miR-544 was negatively regulated by GAS6.	30774011	RID03061	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Osteoarthritis	ATB	miR-223	negatively-E	RT-qPCR;western blot	downregulation	RT-qPCR	NA	NA	inflammatory response(-);MyD88/NF-kB signaling pathway(-);p38/MAPK signaling pathway(-)	NA	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	[Long non-coding RNA activated by transforming growth factor beta alleviates lipopolysaccharide-induced inflammatory injury via regulating microRNA-223 in ATDC5 cells].Interesting results revealed that miR-223 expression was down-regulated by lncRNA-ATB and miR-223 overexpression declined the protective effect of lncRNA-ATB on LPS-injured ATDC5 cells. Further, the signaling pathway experiments showed that lncRNA-ATB inhibited MyD88/NF-kB and p38MAPK pathways by down-regulating miR-223 in LPS-injured cells. These data demonstrated that lncRNA-ATB protected ATDC5 cells against LPS-induced inflammatory injury by repressing MyD88/NF-kB and p38MAPK pathways, which was mediated by down-regulation of miR-223.	30771739	RID03062	expression association	NA		
Atherosclerosis	MALAT1	NRF2	positively-F	RNA pull-down assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell maturation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000154727	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Loss of exosomal MALAT1 from ox-LDL-treated vascular endothelial cells induces maturation of dendritic cells in atherosclerosis development];The ox-LDL-HUVECs-Exos exhibited lower MALAT1 expression when compared with HUVECs-Exos. Furthermore, exosomes from ox-LDL-treated MALAT1-overexpressing-HUVECs (ox-LDL-HUVECs-ExosLv-MALAT1) released elevated expression of MALAT1 to iDCs, which interacted with NRF2 and activated NRF2 signaling, and thereby inhibited ROS accumulation and DCs maturation.	31305205	RID03063	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	p-EGFR	negatively-E	western blot			NA	NA	chemoresistance(+);ERBB3/PI3K/AKT signaling pathway(+);ERBB3/MAPK/ERK signaling pathway(+)	NA	regulation	RNA-protein	Osimertinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Mechanism of MALAT1 induced osimertinib resistance in HCC827 lung cancer cells].western blot showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions: MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB3/MAPK/ERK signaling pathways.	31014050	RID03064	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	p-ERBB3	negatively-E	western blot			NA	NA	chemoresistance(+);ERBB3/PI3K/AKT signaling pathway(+);ERBB3/MAPK/ERK signaling pathway(+)	NA	regulation	RNA-protein	Osimertinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Mechanism of MALAT1 induced osimertinib resistance in HCC827 lung cancer cells].western blot showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions: MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB4/MAPK/ERK signaling pathways.	31014050	RID03065	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	p-AKT	negatively-E	western blot			NA	NA	chemoresistance(+);ERBB3/PI3K/AKT signaling pathway(+);ERBB3/MAPK/ERK signaling pathway(+)	NA	regulation	RNA-protein	Osimertinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Mechanism of MALAT1 induced osimertinib resistance in HCC827 lung cancer cells].western blot showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions: MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB5/MAPK/ERK signaling pathways.	31014050	RID03066	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	p-ERK	negatively-E	western blot			NA	NA	chemoresistance(+);ERBB3/PI3K/AKT signaling pathway(+);ERBB3/MAPK/ERK signaling pathway(+)	NA	regulation	RNA-RNA	Osimertinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	[Mechanism of MALAT1 induced osimertinib resistance in HCC827 lung cancer cells].western blot showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions: MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB6/MAPK/ERK signaling pathways.	31014050	RID03067	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Pre-eclampsia	PUM1	HOTAIR	negatively-E	RIP;RNA pull-down assay;RNA stability assay	upregulation	RNAi	NA	NA	cell invasion(-)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cardiovascular system disease	Eclampsia	PCG	lncRNA	ENSG00000134644	NA	ENSG00000228630	GRCh38_12:53962308-53974956	9698	100124700	KIAA0099|PUMH1	HOXC-AS4|HOXC11-AS1|NCRNA00072	[Upregulation of PUM1 Expression in Preeclampsia Impairs Trophoblast Invasion by Negatively Regulating the Expression of the lncRNA HOTAIR.]Moreover, PUM1 regulates HOTAIR expression via a posttranscriptional mechanism. Using RNA-protein pull-down and mRNA stability assays, we identified PUM1 as a specific binding partner that decreased the half-life of HOTAIR and lowered the steady-state level of HOTAIR expression, suggesting a novel posttranscriptional regulatory mechanism. Collectively, these findings identified a novel RNA regulatory mechanism, revealing a new pathway governing the regulation of PUM1/HOTAIR in trophoblast invasion in the pathogenesis of PE.	31862314	RID03068	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)	
Congenital heart disease	NEAT1	miR-181b	positively-E	western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(+);JAK1/STAT3 signaling pathway(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	[LncRNA nuclear-enriched abundant transcript 1 regulates hypoxia-evoked apoptosis and autophagy via mediation of microRNA-181b.]Overexpressed NEAT1 vector was transfected into H9c2 cells; then, functions of NEAT1 in cell viability, apoptosis, autophagy, PI3K/AKT/mTOR and JAK1/STAT3 pathways were detected in H9c2 cells under hypoxia condition. Expression of NEAT1 and miR-181b in hypoxia and blood samples from CHD was evaluated. After miR-181b inhibitor transfection, functions of miR-181b repression in the above-mentioned cell behavior and PI3K/AKT/mTOR and JAK1/STAT3 pathways were reassessed. Overexpressed NEAT1 clearly allayed hypoxia-triggered H9c2 cells apoptosis and autophagy. The decreased NEAT1 and miR-181b were showcased in hypoxia and blood samples from CHD; meanwhile, elevated miR-181b evoked by overexpressed NEAT1 was observed in hypoxia-managed H9c2 cells. More importantly, miR-181b inhibition obviously overturned the influences of NEAT1 in hypoxia-affected H9c2 cells apoptosis and autophagy. Besides, overexpressed NEAT1 facilitated PI3K/AKT/mTOR and JAK1/STAT3 activations via enhancing miR-181b. The research exposed that NEAT1 eased hypoxia-triggered H9c2 cells apoptosis and autophagy by expediting PI3K/AKT/mTOR and JAK1/STAT3 pathways via elevating miR-181b.	31853799	RID03069	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Urinary bladder cancer	PEG10	miR-29b	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process;WNT/beta-catenin signaling pathway(+);JNK signaling pathway(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	23089	NA	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-29b-Wnt/beta-catenin-JNK axis.	30941768	RID03070	expression association	NA		
Urinary bladder cancer	PEG10	CCND1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000110092	NA	23089	595	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	BCL1|D11S287E|PRAD1|U21B31	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-30b-Wnt/beta-catenin-JNK axis.	30941768	RID03071	expression association	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	PEG10	CDK4	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000135446	NA	23089	1019	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	PSK-J3	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-31b-Wnt/beta-catenin-JNK axis.	30941768	RID03072	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	PEG10	CDK6	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000105810	NA	23089	1021	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	PLSTIRE	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-32b-Wnt/beta-catenin-JNK axis.	30941768	RID03073	expression association	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Urinary bladder cancer	PEG10	MMP2	positively-F	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000087245	NA	23089	4313	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	CLG4|CLG4A|TBE-1	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-33b-Wnt/beta-catenin-JNK axis.	30941768	RID03074	expression association	NA		UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	PEG10	MMP9	positively-F	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000100985	NA	23089	4318	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	CLG4B	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-34b-Wnt/beta-catenin-JNK axis.	30941768	RID03075	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	PEG10	VIM	positively-F	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000026025	NA	23089	7431	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	[Long noncoding RNA PEG10 facilitates bladder cancer cells proliferation, migration, and invasion via repressing microRNA-29b.]PEG10 expression in SV-HUC-1, T24, RT4, and 253J-BV cells was estimated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). After pc-PEG10 or sh-PEG10 transfection, the impacts of PEG10 on T24 and 253J-BV cell viability, migration, invasion, and the relevant proteins were disclosed via employing CCK-8, Transwell, and western blot. The relevancy between miR-29b and PEG10 was probed, and the influences of overexpressed miR-29b in above-mentioned cell biological processes were reassessed. Wnt/beta-catenin and JNK pathways were ultimately analyzed to unmake the underling mechanism. We found that overexpressed PEG10 facilitated cell viability and upregulated CyclinD1, CDK4, and CDK6 in T24 and 253J-BV cells. Cell migration and invasion were also elevated by overexpressed PEG10 through the enhancement of MMP-2, MMP-9, and Vimentin. In addition, repressed miR-29b was observed in PEG10-overexpressed T24 and 253J-BV cells. Moreover, overexpressed miR-29b overtly overturned the carcinogenic impacts of PEG10 on T24 cells. The activations of Wnt/beta-catenin and JNK pathways were enhanced by overexpressed PEG10 via mediating miR-29b. SP600125 (JNK inhibitor) disposition reversed the acceerative impacts of PEG10 on cell proliferation, migration, and invasion in T24 cells. In conclusion, the investigations testified that PEG10 gave play to the carcinogenic impacts on bladder cancer cells via mediating miR-34b-Wnt/beta-catenin-JNK axis.	30941768	RID03076	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Periodontitis	FGF13	MRLN	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	association	protein-RNA	NA	CSC	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Periodontitis	PCG	lncRNA	ENSG00000129682	NA	ENSG00000227877	GRCh38_10:59736692-59756041	2258	100507027	DEE90|FGF-13|FGF2|FHF-2|FHF2|LINC00889	LINC00948|Linc-RAM|M1|MLN|MUSER1	[Downregulation of Linc-RNA activator of myogenesis lncRNA participates in FGF2-mediated proliferation of human periodontal ligament stem cells.]We found that FGF2 mRNA was upregulated, while Linc-RAM was downregulated in PDLSCs derived from periodontitis-affected teeth than in healthy teeth. FGF2 mRNA and Linc-RAM were inversely correlated in both types of PDLSCs. FGF2 overexpression led to inhibited Linc-RAM expression in PDLSCs derived from periodontitis-affected teeth and promoted the proliferation of PDLSCs. Linc-RAM overexpression failed to significantly affect FGF2 expression but attenuated the enhancing effects of FGF2 overexpression on the proliferation of PDLSCs.</AbstractText>: We found that FGF2 mRNA was upregulated, while Linc-RAM was downregulated in PDLSCs derived from periodontitis-affected teeth than in healthy teeth. FGF2 mRNA and Linc-RAM were inversely correlated in both types of PDLSCs. FGF2 overexpression led to inhibited Linc-RAM expression in PDLSCs derived from periodontitis-affected teeth and promoted the proliferation of PDLSCs. Linc-RAM overexpression failed to significantly affect FGF2 expression but attenuated the enhancing effects of FGF2 overexpression on the proliferation of PDLSCs.Therefore, downregulation of Linc-RAM lncRNA may participate in FGF-2 mediated- proliferation of human PDLSCs.</AbstractText>: Therefore, downregulation of Linc-RAM lncRNA may participate in FGF-2 mediated- proliferation of human PDLSCs.	31378921	RID03077	expression association	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE55807)	UP(PRAD);DATA(GSE104209)
Rheumatoid arthritis	GAS5	IL18	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150782	NA	60674	3606	NCRNA00030|SNHG2	IGIF|IL-18|IL-1g|IL1F4	[LncRNA GAS5 overexpression downregulates IL-18 and induces the apoptosis of fibroblast-like synoviocytes.]In the present study, we found that plasma GAS5 was downregulated, while IL-18 was upregulated in RA patients than in healthy controls. A significant and inverse correlation between GAS5 and IL-18 was found in RA patients but not in healthy controls. IL-18 treatment did not significantly alter the expression of GAS5 in fibroblast-like synoviocytes, while GAS5 overexpression led to the inhibited expression of IL-18. GAS5 overexpression also resulted in the promoted apoptosis of fibroblast-like synoviocytes.CONCLUSIONS: Therefore, GAS5 overexpression may improve RA by downregulating IL-18 and inducing the apoptosis of fibroblast-like synoviocytes. Key points <U+2022> The present study mainly showed that overexpression of GAS5 may assist the treatment of RA. <U+2022> The mechanism of GAS5 for the treatment of RA involves the downregulating inflammatory IL-18 and mediating the apoptosis of fibroblast-like synoviocytes. <U+2022> GAS5 and IL-8 were correlated in RA patients but not in healthy controls.Linear regression was performed to analyze the correlations between plasma levels of IL-18 and GAS5 in both RA patients and healthy controls	31378921	RID03078	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE86978)
Endometriosis	H19	ACTA2	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-216a-5p)	regulation	RNA-protein	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000107796	NA	283120	59	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ACTSA	[The estrogen-regulated lncRNA H19/miR-216a-5p axis alters stromal cell invasion and migration via ACTA2 in endometriosis.]Human embryonic kidney 293 cells were used for luciferase assays to study miR-216a-5p binding sites with H19 and ACTA2. We found that H19 and ACTA2 levels were significantly higher in endometriosis euESCs than in control euESCs (P<U+2009><<U+2009>0.05) and were positively correlated in endometriosis euESCs. Luciferase assays indicated that H19 regulates ACTA2 expression via competition for inhibitory miR-216a-5p binding sites. Our results indicate that alterations in the estrogen/H19/miR-216a-5p/ACTA2 pathway regulated endometriosis euESC invasion and migration. Downregulation of H19 or ACTA2 inhibited endometriosis euESC invasion and migration	31323679	RID03079	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE55807)
Osteoarthritis	PACERR	HOTAIR	negatively-E	RT-qPCR	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	lncRNA	ENSG00000273129	GRCh38_1:186680622-186683165	ENSG00000228630	GRCh38_12:53962308-53974956	103752588	100124700	PACER|PTGS2-AS1	HOXC-AS4|HOXC11-AS1|NCRNA00072	[LncRNA PACER is down-regulated in osteoarthritis and regulates chondrocyte apoptosis and lncRNA HOTAIR expression.]PACER and HOTAIR were inversely correlated in both OA patients and healthy controls. PACER overexpression mediated the down-regulation of HOTAIR, while HOTAIR overexpression did not significantly affect PACER. PACER overexpression led to inhibited, while HOTAIR overexpression led to promoted apoptosis of chondrocyte. HOTAIR overexpression attenuated the effects of PACER overexpression. Therefore, lncRNA PACER is down-regulated in OA and regulates chondrocyte apoptosis by down-regulating lncRNA HOTAIR.	31113870	RID03080	expression association	NA		
Pre-eclampsia	TDRG1	miR-214-5p	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000204091	GRCh38_6:40334775-40387590	NA	NA	732253	NA	LINC00532|lincRNA-NR_024015	NA	[LncRNA TDRG1/miR-214-5p axis affects preeclampsia by modulating trophoblast cells.]In conclusion, TDRG1 promoted trophoblast cells viability and invasion by negatively regulating miR-214-5p expression, contributing to a better understanding of PE pathogenesis and providing new light on TDRG1-directed diagnosis and treatment. SIGNIFICANCE OF THE STUDY: In this work, we observed that TDRG1 was able to promote cell proliferation, migration, and invasion cells by suppressing the expression of miR-214-5p and regulating the Notch signalling pathway in trophoblast cells.	31885100	RID03081	interact with protein	NA		
Cervical cancer	HOTAIR	PCDH10	negatively-E	RT-qPCR;western blot;RNAi	upregulation	RT-qPCR;western blot	NA	NA	WNT/beta-catenin signaling pathway(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000138650	NA	100124700	57575	HOXC-AS4|HOXC11-AS1|NCRNA00072	KIAA1400|OL-PCDH	[HOTAIR Knockdown Decreased the Activity Wnt/beta-Catenin Signaling Pathway and Increased the mRNA Levels of Its Negative Regulators in Hela Cells.]Our study suggests a mechanism in which HOTAIR promotes the over-activation of Wnt/beta-catenin signaling pathway by downregulation of PCDH10, SOX17, AJAP1 and MAGI2 and also TET.	31820855	RID03082	epigenetic regulation	NA		UP(LIHC);DATA(GSE117623)
Cervical cancer	HOTAIR	SOX17	negatively-E	RT-qPCR;western blot;RNAi	upregulation	RT-qPCR;western blot	NA	NA	WNT/beta-catenin signaling pathway(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164736	NA	100124700	64321	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	[HOTAIR Knockdown Decreased the Activity Wnt/beta-Catenin Signaling Pathway and Increased the mRNA Levels of Its Negative Regulators in Hela Cells.]Our study suggests a mechanism in which HOTAIR promotes the over-activation of Wnt/beta-catenin signaling pathway by downregulation of PCDH10, SOX17, AJAP1 and MAGI3 and also TET.	31820855	RID03083	epigenetic regulation	NA		
Cervical cancer	HOTAIR	AJAP1	negatively-E	RT-qPCR;western blot;RNAi	upregulation	RT-qPCR;western blot	NA	NA	WNT/beta-catenin signaling pathway(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196581	NA	100124700	55966	HOXC-AS4|HOXC11-AS1|NCRNA00072	MOT8|SHREW-1|SHREW1	[HOTAIR Knockdown Decreased the Activity Wnt/beta-Catenin Signaling Pathway and Increased the mRNA Levels of Its Negative Regulators in Hela Cells.]Our study suggests a mechanism in which HOTAIR promotes the over-activation of Wnt/beta-catenin signaling pathway by downregulation of PCDH10, SOX17, AJAP1 and MAGI4 and also TET.	31820855	RID03084	epigenetic regulation	NA		UP(LIHC);DATA(GSE117623)
Cervical cancer	HOTAIR	MAGI2	negatively-E	RT-qPCR;western blot;RNAi	upregulation	RT-qPCR;western blot	NA	NA	WNT/beta-catenin signaling pathway(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000187391	NA	100124700	9863	HOXC-AS4|HOXC11-AS1|NCRNA00072	ACVRIP1|AIP1|ARIP1|KIAA0705|MAGI-2	[HOTAIR Knockdown Decreased the Activity Wnt/beta-Catenin Signaling Pathway and Increased the mRNA Levels of Its Negative Regulators in Hela Cells.]Our study suggests a mechanism in which HOTAIR promotes the over-activation of Wnt/beta-catenin signaling pathway by downregulation of PCDH10, SOX17, AJAP1 and MAGI5 and also TET.	31820855	RID03085	epigenetic regulation	NA		UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Cervical cancer	HOTAIR	TET	negatively-E	RT-qPCR;western blot;RNAi	upregulation	RT-qPCR;western blot	NA	NA	WNT/beta-catenin signaling pathway(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	[HOTAIR Knockdown Decreased the Activity Wnt/beta-Catenin Signaling Pathway and Increased the mRNA Levels of Its Negative Regulators in Hela Cells.]Our study suggests a mechanism in which HOTAIR promotes the over-activation of Wnt/beta-catenin signaling pathway by downregulation of PCDH10, SOX17, AJAP1 and MAGI6 and also TET.	31820855	RID03086	epigenetic regulation	NA		
Kidney disease	MEG3	SNAI1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell injury(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000124216	NA	55384	6615	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	[Long noncoding RNA MEG3 suppresses podocyte injury in diabetic nephropathy by inactivating Wnt/beta-catenin signaling.]In the present study, we revealed the association of lncRNA Maternally Expressed Gene 3 (MEG3) with aberrant activation of Wnt/beta-catenin signaling and the role of MEG3/Wnt axis in podocyte injury. We found that high glucose (HG) treatment suppressed MEG3 expression in cultured podocytes, activated Wnt/beta-catenin signaling and caused podocyte injury as indicated by the downregulation of podocyte-specific markers (podocin and synaptopodin) and the upregulation of snail1 and alpha-smooth muscle actin. Overexpression of MEG3 attenuated HG-induced podocyte injury by reducing Wnt/beta-catenin activity, repressing cell migration, reactive oxygen species production and increasing the viability of podocytes. Furthermore, we provided evidences that restoration of Wnt/beta-catenin signaling by specific agonist impeded the protective effect of MEG3 on podocyte injury. Current results demonstrated that MEG3/Wnt axis plays an important role in fostering podocyte injury and may serve as a potential therapeutic target for the treatment of DN	31799068	RID03087	expression association	NA		UP(PAAD);DATA(GSE40174)
Type 2 diabetes mellitus	LEGLTBC	SIRT1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell injury(+);apoptosis process(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	NA	NA	ENSG00000096717	NA	NA	23411	NA	SIR2L1	[LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis.]NONRATT003679.2 (low expression in glucolipotoxicity-treated beta cells (LEGLTBC)) was involved in glucolipotoxicity-evoked rat islet beta cell damage. LEGLTBC functioned as a molecular sponge of miR-34a in INS-1 cells. Additionally, SIRT1 was identified as a target of miR-34a and LEGLTBC promoted SIRT1 expression by sponging miR-34a. The upregulation of LEGLTBC attenuated HG/PA-induced INS-1 cell injury through the promotion of SIRT1-mediated suppression of ROS accumulation and apoptosis. This is the first study to comprehensively identify the lncRNA expression profiling of HG/PA-treated INS-1 beta cells and to demonstrate that LEGLTBC functions as a competing endogenous RNA and regulates miR-34a/SIRT1-mediated oxidative stress and apoptosis in INS-1 cells undergoing glucolipotoxicity.	31737170	RID03088	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney disease	BIRC7	LNCRNA-ATB	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	PCG	lncRNA	ENSG00000101197	NA	NA	NA	79444	114004396	KIAP|LIVIN|ML-IAP|MLIAP|RNF50	NA	[Livin is involved in TGF-beta1-induced renal tubular epithelial-mesenchymal transition through lncRNA-ATB.]Livin was upregulated in vivo and in vitro at the similar rate as the occurrence of EMT, which could be relieved when Livin was silenced. LncRNA-ATB, which is another important regulator of EMT, was also found highly expressed during this process. The silencing of lncRNA-ATB could lessen the severity of EMT, and the overexpression of lncRNA-ATB could aggravate EMT without affecting the expression of Livin.qPCR showed that the relative mRNA expression of lncRNA-ATB was significantly increased both in vivo and vitro, which indicated that lncRNA-ATB could be stimulated by TGF-beta1 and in UUO model	31700899	RID03089	expression association	NA		
Kidney disease	ATB	TGFB1	negatively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|TGFB|TGFbeta	[Livin is involved in TGF-beta1-induced renal tubular epithelial-mesenchymal transition through lncRNA-ATB.]Livin was upregulated in vivo and in vitro at the similar rate as the occurrence of EMT, which could be relieved when Livin was silenced. LncRNA-ATB, which is another important regulator of EMT, was also found highly expressed during this process. The silencing of lncRNA-ATB could lessen the severity of EMT, and the overexpression of lncRNA-ATB could aggravate EMT without affecting the expression of Livin.qPCR showed that the relative mRNA expression of lncRNA-ATB was significantly increased both in vivo and vitro, which indicated that lncRNA-ATB could be stimulated by TGF-beta1 and in UUO model;To further investigate the role of lncRNA-ATB in TGF-beta1-induced EMT, we transfected a siRNA of lncRNA-ATB to silence its expression, and transfected plasmid GV219-ATB to overexpress lncRNA-ATB. The qPCR results confirmed that lncRNA-ATB was effectively depleted or overexpressed (Figure 5C,D). The cells were divided into three groups: cells transfected with the vector marked as the control group, the group with overexpression of lncRNA-ATB marked as ATB-OE and the si-ATB treated with TGF-beta1 group. WB showed that in the ATB-OE group, E-cadherin was downregulated while alpha-SMA and vimentin were upregulated compared to the control group. Thus, we concluded that the overexpression of lncRNA-ATB could induce EMT in dependent of TGF-beta1	31700899	RID03090	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	VIM-AS1	CDH1	negatively-E	western blot;RT-PCR	upregulation	RT-PCR	NA	NA	cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000229124	GRCh38_10:17214239-17230018	ENSG00000039068	NA	100507347	999	NA	CD324|UVO|uvomorulin	[Long Noncoding RNA VIM Antisense RNA 1 (VIM-AS1) Plays an Important Role in Development of Preeclampsia by Regulation of Epithelial Mesenchymal Transition.]RT-PCRand WB assay showed that E-cadherin gene and protein expressions in Model and Blank groups were significantly upregulated compared with the NC group (P<0.001); Snail and Vimentin gene and protein expressions in the Model and Blank groups were significantly downregulated compared with the NC group (P<0.001). With VIM-AS1 supplementation, E-cadherin, Snail, and Vimentin gene and proteins expression levels in the VIM-AS1 group were significantly different compared with that in the Model group (P<0.001). CONCLUSIONS VIM-AS1 promotes preeclampsia via inducing epithelial-to-mesenchymal transition (EMT).	31685789	RID03091	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Pre-eclampsia	VIM-AS2	SNAI1	negatively-E	western blot;RT-PCR	upregulation	RT-PCR	NA	NA	cell invasion(+)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	TF	NA	NA	ENSG00000124216	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	[Long Noncoding RNA VIM Antisense RNA 1 (VIM-AS1) Plays an Important Role in Development of Preeclampsia by Regulation of Epithelial Mesenchymal Transition.]RT-PCRand WB assay showed that E-cadherin gene and protein expressions in Model and Blank groups were significantly upregulated compared with the NC group (P<0.001); Snail and Vimentin gene and protein expressions in the Model and Blank groups were significantly downregulated compared with the NC group (P<0.001). With VIM-AS1 supplementation, E-cadherin, Snail, and Vimentin gene and proteins expression levels in the VIM-AS1 group were significantly different compared with that in the Model group (P<0.001). CONCLUSIONS VIM-AS1 promotes preeclampsia via inducing epithelial-to-mesenchymal transition (EMT).	31685789	RID03092	expression association	NA		UP(PAAD);DATA(GSE40174)
Pre-eclampsia	VIM-AS3	VIM	negatively-E	western blot;RT-PCR	upregulation	RT-PCR	NA	NA	cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000026025	NA	NA	7431	NA	NA	[Long Noncoding RNA VIM Antisense RNA 1 (VIM-AS1) Plays an Important Role in Development of Preeclampsia by Regulation of Epithelial Mesenchymal Transition.]RT-PCRand WB assay showed that E-cadherin gene and protein expressions in Model and Blank groups were significantly upregulated compared with the NC group (P<0.001); Snail and Vimentin gene and protein expressions in the Model and Blank groups were significantly downregulated compared with the NC group (P<0.001). With VIM-AS1 supplementation, E-cadherin, Snail, and Vimentin gene and proteins expression levels in the VIM-AS1 group were significantly different compared with that in the Model group (P<0.001). CONCLUSIONS VIM-AS1 promotes preeclampsia via inducing epithelial-to-mesenchymal transition (EMT).	31685789	RID03093	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Thyroid cancer	LINC01410	FOXM1	positively-E	luciferase reporter assay;ChIP	upregulation	RT-qPCR;western blot	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(miR-3619-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000238113	GRCh38_9:62801461-62813486	ENSG00000111206	NA	103352539	2305	NA	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	We confirmed the elevation of LINC01410 expression in TC cells. Loss-of-function experiments indicated that LINC01410 knockdown suppressed proliferation and facilitated apoptosis in TC. Mechanism research illustrated that LINC01410 positively regulated forkhead box M1 (FOXM1) expression through targeting miR-3619-5p, and that FOXM1 in turn transcriptionally activated LINC01410. Rescue experiments validated that LINC01410 regulated TC proliferation and apoptosis through miR-3619-5p/FOXM1. Conclusions: This study demonstrated that LINC01410/miR-3619-5p/FOXM1 positive feedback loop regulated cell proliferation and apoptosis in TC, shedding a light on the molecular target identification and promising treatment improvement in TC.	31644316	RID03094	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Urinary bladder cancer	DLX6-AS1	miR-223	negatively-F	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000231764	GRCh38_7:96955141-97014088	NA	NA	285987	NA	Evf-2|FLJ34048|NCRNA00212	NA	[Long noncoding RNA DLX6-AS1 promotes cell growth and invasiveness in bladder cancer via modulating the miR-223-HSP90B1 axis]	31615303	RID03095	ceRNA or sponge	NA		
Oral squamous cell carcinoma	circPVT1	STAT3	positively-E	miRBase;Targetscan;RIP;western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	circRNA	TF	NA	NA	ENSG00000168610	NA	NA	6774	NA	APRF	[Overexpressed circPVT1 in oral squamous cell carcinoma promotes proliferation by serving as a miRNA sponge.]Mechanistically, it was demonstrated that circPVT1 possessed two targeting sites of microRNA (miRNA/miR)-125b and could effectively sponge miR-125b to release its downstream mRNA targets. Subsequently, [downstream target signal transducer and activator of transcription 3 (STAT3) was verified as a direct target of miR-125b and STAT3 expression was regulated by the circPVT1/miR-125b axis. CircPVT1 functioned as competing endogenous RNA (ceRNA) to increase the STAT3 level and cell proliferation through sponging miR-125b. In conclusion, circPVT1 regulates cell proliferation and may serve as a promising therapeutic target for OSCC patients	31485648	RID03096	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	TP73	MIR607	negatively-F	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000078900	GRCh38_1:3652516-3736201	ENSG00000207976	NA	7161	693192	CILD47|P73	MIRN607|hsa-mir-607	[Long non-coding RNA TP73 antisense RNA 1 facilitates the proliferation and migration of cervical cancer cells via regulating microRNA-607/cyclin D2]HeLa and CaSki cells transfected with siTP73-AS1 exhibited reduced proliferation, migration and invasion abilities when compared with those in the siNC group (P<0.05). Furthermore, miR-607 was found to be negatively regulated by TP73-AS1, while CCND2 was negatively regulated by miR-607. HeLa and CaSki cells transfected with siTP73-AS1 exhibited lower CCND2 mRNA and protein expression levels compared with the siNC and siTP73-AS1 + miR-inhibitor groups (P<0.05). Compared with the siNC and siTP73-AS1 +-CCND2 overexpression groups, siTP73-AS1-transfected HeLa and CaSki cells had decreased proliferation, migration and invasion abilities (P<0.05). In conclusion, the findings suggested that upregulation of TP73-AS1 promoted cervical cancer progression by promoting CCND2 via the suppression of miR-607 expression.	31432138	RID03097	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Breast cancer	MIR210HG	MUC1	positively-E	western blot;luciferase reporter assay;FISH	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-1226-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000247095	GRCh38_11:565657-568457	ENSG00000185499	NA	100506211	4582	NA	ADMCKD|ADMCKD1|CD227|MCD|MCKD|MCKD1|PEM|PUM	[The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer.]Long noncoding RNAs have been known to be involved in multiple types of malignancies, including invasive breast cancer (IBC). This study aimed to explore the role of long noncoding RNAs in IBC and elucidate the potential molecular mechanisms.Our study demonstrated that MiR210HG sponges miR-1226-3p to facilitate invasive breast cancer cell invasion and metastasis by regulating mucin-1c and EMT pathway, revealing the oncogenic role of MiR210HG in IBC cells.</AbstractText>: Our study demonstrated that MiR210HG sponges miR-1226-3p to facilitate invasive breast cancer cell invasion and metastasis by regulating mucin-1c and EMT pathway, revealing the oncogenic role of MiR210HG in IBC cells.	31399552	RID03098	ceRNA or sponge	metastasis		DOWN(LIHC);UP(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Lung cancer	CASC15	KLK12	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-766-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000186474	NA	401237	43849	LINC00340|lnc-SOX4-1	KLK-L5	[CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer.]Quantitative real-time PCR (qRT-PCR was used to assess levels of CASC15, miR-766-5p and KLK12 in lung cancer tissues or cells. western blotwas used to detect KLK12 protein expression. Ectopic expression of CASC15 was induced by a lentiviral system. CCK-8 and transwell assays were used to evaluate lung cancer cell proliferation and invasion, respectively. The interaction among CASC15, miR-766-5p and KLK12 was investigated by bioinformatical analysis and luciferase assay. In lung cancer tissue and cells, CASC15 was upregulated, while miR-766-5p was downregulated. Overexpression of CASC15 promoted lung cancer cell proliferation and invasion. A negative correlation was found between CASC15 and miR-766-5p levels. Overexpression of miR-766-6p reversed the cancer-promoting role of CASC15 in lung cancer cells, which was mediated by KLK12. The tumor-promoting role of CASC15 and tumor-suppressing role of miR-766-5p were also validated in vivo in tumor bearing mice, and KLK12 was also shown as an important mediator. CASC15 promotes lung cancer through the miR-766-5p/KLK12 axis, indicating that CASC15 is a potential therapeutic in lung cancer.	31378128	RID03099	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	Lnc34a	MIR34A	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	histone modification	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	NA	NA	ENSG00000207865	NA	NA	407040	NA	MIRN34A|miRNA34A|mir-34|mir-34a	[The molecular mechanism of LncRNA34a-mediated regulation of bone metastasis in hepatocellular carcinoma.]dual-luciferase reporter assay was conducted to find miR-34a target. The involvement of TGF-beta pathway in the BM from HCC was determined by qRT-PCR western, and elisa assays.We found that Lnc34a was significantly overexpressed in HCC tissues and associated with BM. Both in vitro and in vivo experiments indicate that the restoration or knockdown of Lnc34a expression in HCC cells had a marked effect on cellular migration, invasion, and metastasis. Mechanistic analyses suggested that Lnc34a epigenetically suppresses miR-34a expression through recruiting DNMT3a via PHB2 to methylate miR-34a promoter and HDAC1 to promote histones deacetylation. On the other hand, miR-34a targets Smad4 via the TGF-beta pathway, followed by altering the transcription of the downstream genes (i.e., CTGF and IL-11) that are associated with BM.</AbstractText>: We found that Lnc34a was significantly overexpressed in HCC tissues and associated with BM. Both in vitro and in vivo experiments indicate that the restoration or knockdown of Lnc34a expression in HCC cells had a marked effect on cellular migration, invasion, and metastasis. Mechanistic analyses suggested that Lnc34a epigenetically suppresses miR-34a expression through recruiting DNMT3a via PHB2 to methylate miR-34a promoter and HDAC1 to promote histones deacetylation	31349837	RID03100	epigenetic regulation	metastasis		
Idiopathic scoliosis	SUV39H1	BCL2	positively-E	western blot;ChIP	upregulation	RT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-15a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Spinal disease	lncRNA	PCG	ENSG00000101945	GRCh38_X:48695554-48709016	ENSG00000171791	NA	6839	596	KMT1A|SUV39H	Bcl-2|PPP1R50	[Suv39h1 promotes facet joint chondrocyte proliferation by targeting miR-15a/Bcl2 in idiopathic scoliosis patients.]Thus, our study suggests that increased chondrocyte proliferation occurs in the facet joint cartilage of IS patients compared with the control group and may be promoted by the elevated levels of H3K9me3 and SUV39H1, which regulate the miR-15a/Bcl2 pathway. This dysregulation of chondrocyte proliferation could result in abnormal spinal growth and may additionally participate in the development and progression of IS.	31337422	RID03101	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	TUG1	NFE2L2	positively-E	western blot;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	NA	Cisplatin	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000116044	NA	55000	4780	FLJ20618|LINC00080|NCRNA00080	NRF2	[LncRNA TUG1 promotes cisplatin resistance in esophageal squamous cell carcinoma cells by regulating Nrf2.]In contrast, TUG1 knockdown exerted an opposite effect. Mechanistically, RNA pull-down and RNA immunoprecipitation assays confirmed that TUG1 directly bound to nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein and elevated Nrf2 protein expression. Moreover, Nrf2-neutralizing antibody effectively reversed the TUG1 overexpression-mediated promotion of ESCC cell resistance to DDP. In conclusion, our findings demonstrated that TUG1 promoted ESCC cell resistance to DDP, at least in part, through upregulating Nrf2.	31287493	RID03102	interact with protein	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Lung adenocarcinoma	LINC00673-v4	DDX3X	positively-E	RNA pull-down assay;immunoblot	upregulation	luciferase reporter assay	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	histone modification	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000215301	NA	NA	1654	NA	CAP-Rf|DBX|DDX14|DDX3|HLP2|MRX102|MRXSSB	[Long noncoding RNA LINC00673-v4 promotes aggressiveness of lung adenocarcinoma via activating WNT/beta-catenin signaling.]. As a consequence, LINC00673-v4 promotes the aggressiveness of LAD.In vitro and in vivo experiments demonstrated that LINC00673-v4 enhanced invasiveness, migration, and metastasis of LAD cells. Mechanistically, LINC00673-v4 augmented the interaction between DDX3 and CK1epsilon and thus the phosphorylation of dishevelled, which subsequently activated WNT/beta-catenin signaling and consequently caused aggressiveness of LAD. Antagonizing LINC00673-v4 suppressed LAD metastasis in vivo. Together, our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/beta-catenin signaling in LAD and may represent a potential therapeutic target against the metastasis of LAD.In vitro and in vivo experiments demonstrated that LINC00673-v4 enhanced invasiveness, migration, and metastasis of LAD cells. Mechanistically, LINC00673-v4 augmented the interaction between DDX3 and CK1epsilon and thus the phosphorylation of dishevelled, which subsequently activated WNT/beta-catenin signaling and consequently caused aggressiveness of LAD. Antagonizing LINC00673-v4 suppressed LAD metastasis in vivo. Together, our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/beta-catenin signaling in LAD and may represent a potential therapeutic target against the metastasis of LAD.Using the Top/Fop flash luciferase assay, we assessed the effects of 10 of the most highly expressed lncRNA transcripts in LAD, as determined by integrated analysis of transcriptome sequencing data deposited at The Cancer Genome Atlas (TCGA) by Cabanski et al;To validate that LINC00673-v4 interacts with CK1epsilon, we performed RNA pull-down and immunoblotting using a CK1epsilon antibody, and the results showed that CK1epsilon was detected in the LINC00673-v4 protein complex but not in the control sample (Fig. 5B and SI Appendix, Fig. S10A). Moreover, the direct interaction was further verified by RNA immunoprecipitation (RIP) assay after UV cross-link;RNA pull-down followed by immunoblotting and RIP assay after UV cross-link were performed, and the results showed that LINC00673-v4 also directly interacted with DDX3	31235588	RID03103	epigenetic regulation	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00673-v4	CK1	positively-E	RNA pull-down assay;immunoblot;RIP	upregulation	luciferase reporter assay	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	histone modification	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	[Long noncoding RNA LINC00673-v4 promotes aggressiveness of lung adenocarcinoma via activating WNT/beta-catenin signaling.]. As a consequence, LINC00673-v4 promotes the aggressiveness of LAD.In vitro and in vivo experiments demonstrated that LINC00673-v4 enhanced invasiveness, migration, and metastasis of LAD cells. Mechanistically, LINC00673-v4 augmented the interaction between DDX3 and CK1epsilon and thus the phosphorylation of dishevelled, which subsequently activated WNT/beta-catenin signaling and consequently caused aggressiveness of LAD. Antagonizing LINC00673-v4 suppressed LAD metastasis in vivo. Together, our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/beta-catenin signaling in LAD and may represent a potential therapeutic target against the metastasis of LAD.In vitro and in vivo experiments demonstrated that LINC00673-v4 enhanced invasiveness, migration, and metastasis of LAD cells. Mechanistically, LINC00673-v4 augmented the interaction between DDX3 and CK1epsilon and thus the phosphorylation of dishevelled, which subsequently activated WNT/beta-catenin signaling and consequently caused aggressiveness of LAD. Antagonizing LINC00673-v4 suppressed LAD metastasis in vivo. Together, our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/beta-catenin signaling in LAD and may represent a potential therapeutic target against the metastasis of LAD.Using the Top/Fop flash luciferase assay, we assessed the effects of 10 of the most highly expressed lncRNA transcripts in LAD, as determined by integrated analysis of transcriptome sequencing data deposited at The Cancer Genome Atlas (TCGA) by Cabanski et al;To validate that LINC00673-v4 interacts with CK1epsilon, we performed RNA pull-down and immunoblotting using a CK1epsilon antibody, and the results showed that CK1epsilon was detected in the LINC00673-v4 protein complex but not in the control sample (Fig. 5B and SI Appendix, Fig. S10A). Moreover, the direct interaction was further verified by RNA immunoprecipitation (RIP) assay after UV cross-link;RNA pull-down followed by immunoblotting and RIP assay after UV cross-link were performed, and the results showed that LINC00673-v4 also directly interacted with DDX4	31235588	RID03104	epigenetic regulation	metastasis		
Her2-receptor positive breast cancer	ERBB2	LINC00458	positively-E		upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	protein-RNA	Lapatinib	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000141736	NA	ENSG00000234787	GRCh38_13:54115783-54142319	2064	100507428	CD340|HER-2|HER2|NEU|NGL	ES3|LncRNA-ES3	[Upregulation of pluripotent long noncoding RNA ES3 in HER2-positive breast cancer.]In addition, our data demonstrated that ES3 expression downregulated during neural differentiation. Therefore, its expression may be correlated to breast tumor differentiation status. Notably, a high expression level of ES3 in HER2-positive breast tumor tissues motivated us to investigate the effect of HER2 on ES3 expression by blocking HER2 activity with lapatinib. The results showed that ES3 expression suppressed when HER2 activity was blocked. In summary, for the first time, we found that lncRNA ES3 was significantly upregulated in HER2-positive breast tumors and may contribute to breast cancer proliferation as a downstream target of HER2.	31211468	RID03105	expression association	NA	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)	UP(LIHC);DATA(GSE117623)
Osteoarthritis	XIC	MMP13	positively-E	western blot;Targetscan;LncBase	upregulation	RT-qPCR	NA	NA	ECM degradation(+)	ceRNA(miR-1277-5p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000137745	NA	7502	4322	SXI1|XCE|XIST	CLG3|MANDP1|MDST|MMP-13	[Long non-coding RNA XIST promotes extracellular matrix degradation by functioning as a competing endogenous RNA of miR-1277-5p in osteoarthritis.]Finally, the protective effect of the downregulation of XIST on ECM degradation was verified in an OA rat model. In conclusion, the present study suggests that XIST promotes MMP-13 and ADAMTS5 expression, indicating ECM degradation, by functioning as a ceRNA of miR-1277-5p in OA. The present study proposed a novel potential target with a new working mechanism in molecular treating of OA.	31198977	RID03106	ceRNA or sponge	NA		UP(PAAD);DATA(GSE40174)
Osteoarthritis	XIST	ADAMTS5	positively-E	western blot;Targetscan;LncBase	upregulation	RT-qPCR	NA	NA	ECM degradation(+)	ceRNA(miR-1277-5p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000154736	NA	7503	11096	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ADAMTS11|ADMP-2	[Long non-coding RNA XIST promotes extracellular matrix degradation by functioning as a competing endogenous RNA of miR-1277-5p in osteoarthritis.]Finally, the protective effect of the downregulation of XIST on ECM degradation was verified in an OA rat model. In conclusion, the present study suggests that XIST promotes MMP-13 and ADAMTS5 expression, indicating ECM degradation, by functioning as a ceRNA of miR-1277-5p in OA. The present study proposed a novel potential target with a new working mechanism in molecular treating of OA.	31198977	RID03107	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC);DATA(GSE117623)
Fatty liver disease	NEAT1	AQP7	positively-F	western blot;ChIP;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	steatosis(+)	NA	association	RNA-protein	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000165269	NA	283131	364	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	AQP7L|AQP9|AQPap	[Long non-coding RNA NEAT1 promotes steatosis via enhancement of estrogen receptor alpha-mediated AQP7 expression in HepG2 cells.]In this study, we determined that the transcriptional level of AQP7 was up-regulated by estrogen receptor alpha (ERalpha) upon 17beta-estradiol (E2) and oleic acids treated HepG2 cells. Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERalpha silencing HepG2 cells by RNA-Seq. Finally, we validated that the 3' terminal nucleotides of NEAT1 were contributed for the interaction with ERalpha to facilitate AQP7 transcription to suppress liver steatosis. Overall, our study gave evidence that NEAT1 played an important role in the activation of ERalpha to regulate AQP7-mediated hepatic steatosis.	31062612	RID03108	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Fatty liver disease	NEAT1	ESR1	positively-E	western blot;ChIP;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	steatosis(-)	NA	binding/interaction	NA	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000091831	NA	283131	2099	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ER-alpha|Era|ESR|NR3A1	[Long non-coding RNA NEAT1 promotes steatosis via enhancement of estrogen receptor alpha-mediated AQP7 expression in HepG2 cells.]In this study, we determined that the transcriptional level of AQP7 was up-regulated by estrogen receptor alpha (ERalpha) upon 17beta-estradiol (E2) and oleic acids treated HepG2 cells. Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERalpha silencing HepG2 cells by RNA-Seq. Finally, we validated that the 3' terminal nucleotides of NEAT1 were contributed for the interaction with ERalpha to facilitate AQP7 transcription to suppress liver steatosis. Overall, our study gave evidence that NEAT1 played an important role in the activation of ERalpha to regulate AQP7-mediated hepatic steatosis.	31062612	RID03109	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Prostate cancer	HOTAIR	FGFR1	positively-E	TargetScan;luciferase reporter assay;western blot;RIP	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-520b)	regulation	RNA-protein	Bufalin	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000077782	NA	100124700	2260	HOXC-AS4|HOXC11-AS1|NCRNA00072	BFGFR|CD331|CEK|FLG|FLT2|H2|H3|H4|H5|KAL2|N-SAM	[Bufalin suppresses the migration and invasion of prostate cancer cells through HOTAIR, the sponge of miR-520b.]we investigated the possible network related to the antimetastatic effect of bufalin in prostate cancer (PCa) cells. We demonstrated that bufalin (0.05-10 uM) dose-dependently suppressed the proliferation of prostate cancer DU145 and PC3 cells with IC50 values of 0.89 and 1.28 uM, respectively. Furthermore, bufalin treatment significantly suppressed the cell migration and invasion. To explore the role of lncRNAs in the antimetastatic activity of bufalin, we used an lncRNA microarray and found that HOX transcript antisense RNA (HOTAIR) was the most markedly downregulated lncRNA in bufalin-treated PCa cells. Overexpression of HOTAIR counteracted the suppressing effects of bufalin on DU145 and PC3 cells. We then predicted and verified that HOTAIR upregulated FGFR1 expression by sponging miR-520b in PCa cells. In 40 patients with PCa bone metastasis, we used in situ hybridization or immunohistochemical assay to assess the HOTAIR and FGFR1 expression, which revealed that both HOTAIR and FGFR1 expression were significantly higher in bone metastasis tissues than in the primary PCa tissues.	31028291	RID03110	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Abdominal aortic aneurysm	H19	IL6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cancer progression(+)	ceRNA(let-7a)	regulation	RNA-protein	NA	NA	NA	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000136244	NA	283120	3569	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BSF2|HGF|HSF|IFNB2|IL-6	[LncRNA H19 promotes vascular inflammation and abdominal aortic aneurysm formation by functioning as a competing endogenous RNA.] Luciferase reporter assays and ex vivo experiments using VSMCs and macrophages confirmed that H19 induced aneurysm formation in part via endogenous competition with the let-7a microRNA to induce the transcription of its target gene, IL-6. This mechanism was further validated by in vivo experiments using a mutant H19 that could not effectively bind let-7a. Collectively, our study revealed a pathogenic H19/let-7a/IL-6 inflammatory pathway in AAA formation, which offers a new potential therapeutic strategy for AAA.qRT-PCRdetected the upregulation of H19 in human and mouse AAA tissue samples	30991034	RID03111	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Gastric adenocarcinoma	N-BLR	miR-200c	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	interact with protein	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	[Long Noncoding RNA N-BLR Upregulates the Migration and Invasion of Gastric Adenocarcinoma.]N-BLR expression was significantly elevated in gastric cancer cell lines and tissues compared to that in a normal gastric cell line and adjacent normal tissues (p<0.01). Two different siRNAs significantly reduced cell proliferation of gastric cancer cells compared to the siCT. siRNAs for N-BLR significantly suppressed migration and invasion in AGS and MKN28 cells. N-BLR expression was inversely correlated with miR-200c, which is known to regulate EMT.In this study, we confirmed N-BLR as a regulator of the EMT process in gastric cancer.</AbstractText>: In this study, we confirmed N-BLR as a regulator of the EMT process in gastric cancer.	30970439	RID03112	interact with protein	NA		
Atherosclerosis	lncRNA 430945	RORA	positively-E	western blot	upregulation	microarray;RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	NA	NA	ENSG00000069667	NA	NA	6095	NA	IDDECA|NR1F1|ROR1|ROR2|ROR3|RZR-ALPHA|RZRA	[lncRNA 430945 promotes the proliferation and migration of vascular smooth muscle cells via the ROR2/RhoA signaling pathway in atherosclerosis.]the study examined whether a correlation exists between lncRNA 430945 and the receptor tyrosine kinase-like orphan receptor 2 (ROR2) signaling pathway. It was found that the expression of lncRNA 430945 was high in human AS tissues, which in turn promoted angiotensin II (AngII)-induced VSMC proliferation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot showed that lncRNA 430945 mediated the AngII-induced upregulation of ROR2. In addition, the microarray and RT-qPCR results showed that the expression of lncRNA 430945 was increased considerably in AS tissues. The downregulation of lncRNA 430945 significantly suppressed AngII-induced VSMC proliferation and migration. In addition, ROR2 levels in VSMCs transfected with si-430945 were markedly lower than those cells transfected with si-NC. Additionally, western blot showed that lncRNA 430945 activated the signaling pathways associated with ROR2 and Ras homolog gene family member A (RhoA). The upregulation of lncRNA 430945 in AS promoted the proliferation and migration of VSMCs via activation of the ROR2/RhoA signaling pathway. Therefore, targeting ROR2 or RhoA may be a promising technique in developing therapeutic strategies for treating AS.	30957191	RID03113	expression association	NA		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE86978)
Atherosclerosis	lncRNA 430945	RHOA	negatively-F	western blot	upregulation	microarray;RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000067560	NA	NA	387	NA	ARH12|ARHA|EDFAOB|RHO12|RHOH12	[lncRNA 430945 promotes the proliferation and migration of vascular smooth muscle cells via the ROR2/RhoA signaling pathway in atherosclerosis.]the study examined whether a correlation exists between lncRNA 430945 and the receptor tyrosine kinase-like orphan receptor 2 (ROR2) signaling pathway. It was found that the expression of lncRNA 430945 was high in human AS tissues, which in turn promoted angiotensin II (AngII)-induced VSMC proliferation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot showed that lncRNA 430945 mediated the AngII-induced upregulation of ROR2. In addition, the microarray and RT-qPCR results showed that the expression of lncRNA 430945 was increased considerably in AS tissues. The downregulation of lncRNA 430945 significantly suppressed AngII-induced VSMC proliferation and migration. In addition, ROR2 levels in VSMCs transfected with si-430945 were markedly lower than those cells transfected with si-NC. Additionally, westernblotting showed that lncRNA 430945 activated the signaling pathways associated with ROR2 and Ras homolog gene family member A (RhoA). The upregulation of lncRNA 430945 in AS promoted the proliferation and migration of VSMCs via activation of the ROR2/RhoA signaling pathway. Therefore, targeting ROR2 or RhoA may be a promising technique in developing therapeutic strategies for treating AS.	30957191	RID03114	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Lung cancer	PCAT1	RAP1A	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000116473	NA	100750225	5906	PCA1|PCAT-1|PiHL	KREV-1|SMGP21	[LncRNA PCAT-1 upregulates RAP1A through modulating miR-324-5p and promotes survival in lung cancer.]Mechanistic investigations demonstrated that PCAT-1 can interact with miR-324-5p and repress its expression, thereby increasing the expression of its target RAP1A. Additionally, rescue experiments revealed that PCAT-1 served as an oncogene partly through sponging miR-324-5p and upregulating RAP1A in lung cancer cells.</AbstractText>: PCAT-1 overexpression remarkably promoted cell proliferation and suppressed cell apoptosis. Mechanistic investigations demonstrated that PCAT-1 can interact with miR-324-5p and repress its expression, thereby increasing the expression of its target RAP1A. Additionally, rescue experiments revealed that PCAT-1 served as an oncogene partly through sponging miR-324-5p and upregulating RAP1A in lung cancer cells.Our findings demonstrate that on account of the dual function of pro-proliferation and anti-apoptosis, PCAT-1/miR-324-5p/RAP1A may be novel candidates for application in the diagnosis, prognosis and therapy of lung cancer.</AbstractText>: Our findings demonstrate that on account of the dual function of pro-proliferation and anti-apoptosis, PCAT-1/miR-324-5p/RAP1A may be novel candidates for application in the diagnosis, prognosis and therapy of lung cancer.	32864009	RID03115	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Breast cancer	LINC01433	MYC	positively-E	western blot;ChIP;luciferase reporter assay;RIP;UCSC;starBase;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-2116-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000230176	GRCh38_20:4192932-4195953	ENSG00000136997	NA	728228	4609	LOC728228	bHLHe39|c-Myc|MYCC	[LINC01433/miR-2116-3p/MYC Feedback Loop Promotes Cell Proliferation, Migration, and the Epithelial-Mesenchymal Transition in Breast Cancer.]qRT-PCRrevealed that LINC01433 was highly expressed in BC cells. In function, LINC01433depletion suppressed BC cell proliferation, migration, and epithelial-mesenchymal transition, but induced cellapoptosis. Mechanically, chromatin immunoprecipitation and luciferase reporter assays suggested thatLINC01433 was activated by its upstream transcription factor MYC proto-oncogene (MYC). The interactionbetween LINC01433 and miR-2116-3p was verified in BC. Additionally, MYC was validated as a target gene ofmiR-2116-3p. Rescue assays demonstrated that LINC01433 promoted BC cellular process via regulating miR2116-3p/MYC axis.Conclusion: Our findings revealed a novel positive feedback loop (LINC01433/miR-2116-3p/MYC) in BCprogression and discovered the novel functional genes in BC cellular process.	30939038	RID03116	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Cancer	Olfr29-ps1	MYD88	positively-E	RNAi;miRbase;RNAHybrid;miRDB;western blot;RIP;RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000172936	NA	NA	4615	NA	NA	[The Pseudogene Olfr29-ps1 Promotes the Suppressive Function and Differentiation of Monocytic MDS]This lncRNA promoted the immunosuppressive function and differentiation of monocytic (Mo-)MDSCs invitro and in vivo. It directly sponged miR-214-3p to downregulate miR-214-3p, which may target MyD88 to modulate the differentiation and development of MDSCs. The functions of Olfr29-ps1 was dependent on IL6-mediated N6-methyladenosine (m6A) modification, which not only enhanced Olfr29-ps1, but also promoted interaction of Olfr29-ps1 with miR-214-3p. Thus, our results demonstrated that the pseudogene Olfr29-ps1 may regulate the differentiation and function of MDSCs through a m6A-modified Olfr29-ps1/miR-214-3p/MyD88 regulatory network, revealing a mechanism for the regulation of myeloid cells and also providing potentialtargets for antitumor immunotherapy.	30914411	RID03117	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atrial fibrosis	NRON	NFATC3	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Connective tissue disease	lncRNA	TF	ENSG00000253079	GRCh38_9:126408041-126408410	ENSG00000072736	NA	641373	4775	NCRNA00194	NFAT4|NFATX	[LncRNA NRON alleviates atrial fibrosis via promoting NFATc3 phosphorylation.]The aim of this study was to explore the role of NRON in the atrial fibrosis. The expression of NRON in atrial tissue was detected using qRT-PCR The protein levels of collagen I, collagen III, NFATc3 and p-NFATc3 were determined by western blot. Immunohistochemistry assay were performed to observe expression and distribution of collagen I in atrial tissues. The atrial fibroblasts were authenticated by vimentin/troponin immunofluorescence staining. Fibroblast proliferation was detected by CCK-8 assay. The morphological changes of cardiac tissue were observed by HE staining. Myocardial fibrosis was detected by masson staining. NRON expression was significantly downregulated in atrial tissues of AF. NRON suppressed fibroblast proliferation; expression of collagen I and collagen III; activation of NFATc3 and nucleu import. NRON promoted p-NFATc3 expression and alleviated atrial fibrosis in vivo. Our data indicated that NRON alleviates atrial fibrosis via promoting NFATc3 phosphorylation.	30895498	RID03118	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Triple-negative breast cancer	TROJAN	ZMYND8	negatively-E	western blot;RNA pull-down assay;RIP;ChIP	upregulation	RT-qPCR;microarray	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000101040	NA	NA	23613	NA	PRKCBP1|RACK7	[The endogenous retrovirus-derived long noncoding RNA TROJAN promotes triple-negative breast cancer progression via ZMYND8 degradation.]TROJAN promoted TNBC proliferation and invasion and indicated poor patient outcomes. We further confirmed that TROJAN could bind to ZMYND8, a metastasis-repressing factor, and increase its degradation through the ubiquitin-proteasome pathway by repelling ZNF592. TROJAN also epigenetically up-regulated metastasis-related genes in multiple cell lines. Correlations between TROJAN and ZMYND8 were subsequently confirmed in clinical samples. Furthermore, our study verified that antisense oligonucleotide therapy targeting TROJAN substantially suppressed TNBC progression in vivo. In conclusion, the long noncoding RNA TROJAN promotes TNBC progression and serves as a potential therapeutic target.	30854423	RID03119	interact with protein	metastasis		UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Hepatocellular carcinoma	LINC01093	IGF2BP1	positively-F	western blot;RNA pull-down assay	downregulation	bioinformatics	GSE84402	NA	cell proliferation(+);cell metastasis(+);cancer progression(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249173	GRCh38_4:184892858-184899553	ENSG00000159217	NA	100506229	10642	NA	IMP-1	[A novel, liver-specific long noncoding RNA LINC01093 suppresses HCC progression by interaction with IGF2BP1 to facilitate decay of GLI1 mRNA.]Mechanistic analyses indicate that LINC01093 directly binds insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), interfering with interaction between IGF2BP1 and glioma-associated oncogene homolog 1 (GLI1) mRNA. The result is degradation of GLI1 mRNA, further affecting expression of GLI1 downstream molecules involved in HCC progression. The liver-enriched lncRNA LINC01093 is a promising prognostic indicator for HCC patients, and the newly identified LINC01093-IGF2BP1-GLI1 axis shows potential for therapeutic targets in HCC. Among significantly dysregulated lncRNAs (fold change >22 or < 2-2, p < 0.05), LINC01093 was one of the most downregulated lncRNAs in HCC tissues (Figure 1A).To explore interactors with LINC01093, we conducted RNA pull-down assays in whole cell lysates from Huh7 and BEL-7402 cells with biotin-labeled sense and antisense LINC01093 RNA probes. After silver staining, a distinct band approaching 70 kDa was captured by sense LINC01093 and subjected to mass spectrometry analysis (Figure 3A, left panel). The results identified many proteins in this complex, and the overlap between two groups for the top 10 most abundant protein was with IGF2BP1 (Table SIII). western blot with anti-IGF2BP1 antibody further confirmed the existence of IGF2BP1 within LINC01093 pull-down samples (Figure 3A, right panel). In addition, RIP assays showed enrichment of LINC01093 in complex precipitated with IGF2BP1 compared with control IgG (Figure 3B). These results indicated that the IGF2BP1 protein specifically binds LINC01093;LINC01093 facilitates GLI1 mRNA decay via interacting with IGF2BP1 in HCC cells	30790682	RID03120	interact with protein	prognosis,metastasis		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	LINC01093	GLI1	negatively-E	RIP;RNA pull-down assay	downregulation	bioinformatics	NA	NA	cell proliferation(+);cell metastasis(+);cancer progression(-)	interact with protein	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000249173	GRCh38_4:184892858-184899553	ENSG00000111087	NA	100506229	2735	NA	GLI	[A novel, liver-specific long noncoding RNA LINC01093 suppresses HCC progression by interaction with IGF2BP1 to facilitate decay of GLI1 mRNA.]Mechanistic analyses indicate that LINC01093 directly binds insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), interfering with interaction between IGF2BP1 and glioma-associated oncogene homolog 1 (GLI1) mRNA. The result is degradation of GLI1 mRNA, further affecting expression of GLI1 downstream molecules involved in HCC progression. The liver-enriched lncRNA LINC01093 is a promising prognostic indicator for HCC patients, and the newly identified LINC01093-IGF2BP1-GLI1 axis shows potential for therapeutic targets in HCC. Among significantly dysregulated lncRNAs (fold change >22 or < 2-2, p < 0.05), LINC01093 was one of the most downregulated lncRNAs in HCC tissues (Figure 1A).We used RIP and RNA pull-down assays to determine the interaction between IGF2BP1 and GLI1 mRNA in HCC cells. The results demonstrated that IGF2BP1 could specifically bind to GLI1 mRNA in HCC cells (Figure S9A-B). In addition, knockdown of IGF2BP1 reduced GLI1 mRNA and protein levels in HCC cells	30790682	RID03121	interact with protein	prognosis,metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	HOTTIP	CTNNB1	positively-E	western blot;RNAi	downregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	armadillo|beta-catenin|CTNNB	[The long noncoding RNA HOTTIP promotes breast cancer cell migration, invasiveness, and epithelial-mesenchymal transition via the Wnt-beta-catenin signaling pathway.]we found that the expression of beta-catenin was significantly decreased in breast cancer cells after knock-down of HOTTIP. In a further rescue experiment using overexpression of beta-catenin, the rates of cell migration, invasiveness, and EMT of HOTTIP-silenced breast cancer cells were promoted, disclosing a potential role of the Wnt-beta-catenin signaling pathway in this process. Overall, we discovered the positive regulatory function of HOTTIP in the migration, invasiveness, and EMT of breast cancer cells, via regulating the Wnt-beta-catenin pathway.	30676763	RID03122	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Atherosclerosis	MEG8	PPARA	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(+)	ceRNA(miR-181a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000258399	GRCh38_14:100836269-100947194	ENSG00000186951	NA	79104	5465	Bsr|Irm|LINC00024|NCRNA00024|Rian|SNHG23|SNHG24|lnc-MGC	NR1C1|PPAR|PPAR-alpha|PPARalpha|hPPAR	[LncRNA MEG8 regulates vascular smooth muscle cell proliferation, migration and apoptosis by targeting PPARalpha.]Mechanically, MEG8 was found to promote the PPARalpha protein via sponging miR-181a-5p. Rescue experiments demonstrated that MEG8 and PPARalpha collectively regulate the proliferation, migration and apoptosis of VSMCs. Overall, this research illustrates that MEG8 regulates the proliferation and migration of VSMCs via the MEG8/miR-181a/PPARalpha axis.	30670309	RID03123	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807,GSE86978)
Osteoporosis	ZBTB40-IT1	WNT4	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000162552	NA	100874345	54361	NA	WNT-4	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03124	interact with protein	NA		
Osteoporosis	ZBTB40-IT1	RUNX2	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000124813	NA	100874345	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03125	interact with protein	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	ZBTB40-IT1	SP7	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000170374	NA	100874345	121340	NA	osterix|OSX	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03126	interact with protein	NA		UP(PAAD);DATA(GSE40174)
Osteoporosis	ZBTB40-IT1	SP7	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000170374	NA	100874345	121340	NA	OI11|OI12|OSX|osterix	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03127	interact with protein	NA		UP(PAAD);DATA(GSE40174)
Osteoporosis	ZBTB40-IT1	COL1A1	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000108821	NA	100874345	1277	NA	OI4	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03128	interact with protein	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Osteoporosis	ZBTB40-IT1	OPG	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000118903	NA	100874345	NA	NA	NA	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03129	interact with protein	NA		
Osteoporosis	ZBTB40-IT1	TNFSF11	positively-F	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237200	GRCh38_1:22517474-22519708	ENSG00000120659	NA	100874345	8600	NA	CD254|ODF|OPGL|RANKL|TRANCE	[LncRNA ZBTB40-IT1 modulated by osteoporosis GWAS risk SNPs suppresses osteogenesis.]In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.	30661131	RID03130	interact with protein	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteoporosis	NEAT1	SOX5	positively-F	western blot;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell differentiation(-)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000134532	NA	283131	6660	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	L-SOX5|MGC35153	[NEAT1/miR-193a-3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis.] dual-luciferase reporter assay was performed to determine the target relationship among NEAT1, miR-193a-3p, and SOX5. We found that miR-193a-3p expression was downregulated, while NEAT1 and SOX5 were upregulated in OA cartilage tissue and chondrocytes. Both upregulation of miR-193a-3p and knockdown of NEAT1 suppressed inflammation, apoptosis, and reduced the protein levels of MMP-3, MMP-13, and ADAMTS-5, while elevating ACAN and Col2a1 expression in chondrocytes. NEAT1 targeted miR-193a-3p, and SOX5 was targeted by miR-193a-3p. Silencing of miR-193a-3p reversed the NEAT1 knockdown-mediated effect on the inflammation, apoptosis, and production of the extracellular matrix. The introduction of SOX5 abolished the impact of the upregulation of miR-193a-3p on inflammation, apoptosis, and production of extracellular matrix in chondrocytes. In conclusion, NEAT1/miR-193a-3p/SOX5 axis regulates cartilage matrix degradation in human OA.	31868949	RID03131	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Cancer	XIST	SOX7	positively-E	western blot;luciferase reporter assay;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell viability(-);cell migration(-);tumorigenesis(+)	ceRNA(miR-485)	regulation	NA	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171056	NA	7503	83595	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	[Long noncoding RNA XIST participates hypoxia-induced angiogenesis in human brain microvascular endothelial cells through regulating miR-485/SOX7 axis.]Long non-coding RNAs (lncRNAs) X-inactive specific transcript (XIST) has identified to involve into the tumor cell angiogenesis. However, whether XIST contributes to Human Brain Microvascular Endothelial Cells (HBMEC) angiogenesis as well as potential mechanisms are largely unclear.METHODS: The expression of XIST, miR-485-3p and SRY-box 7 (SOX7) in HBMEC were altered by transfection. The cell viability, cell migration and tube formation of HBMEC were measured, respectively. The cross-regulations between XIST, miR-485-3p, SOX7, and vascular endothelial growth factor (VEGF) signaling pathway were investigated by RT-qPCR and western blot assay.RESULTS: In this study, we characterized the upregulation of XIST in HBMEC under hypoxia condition. Meanwhile, XIST silencing impaired hypoxia-induced cell proliferation, migration and tube formation. Besides, our integrated experiments identified that XIST may competitively bind with miR-485-3p and then modulate the derepression of downstream target SRY-box 7 (SOX7). Mechanically, knockdown of XIST impaired hypoxia-induced angiogenesis via miR-485-3p/SOX7 axis and subsequent suppression of VEGF signaling pathway.CONCLUSION: Altogether, the present study suggested that XIST is required to maintain VEGF signaling expression in HBMEC under hypoxia condition and plays a vital role in hypoxia-induced angiogenesis via miR-485-3p/SOX7 axis.	31737200	RID03132	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC);DATA(GSE117623)
Diabetic retinopathy	MALAT1	miR-203a-3p	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Long Noncoding RNA LINC01133 Confers Tumor-Suppressive Functions in Ovarian Cancer by Regulating Leucine-Rich Repeat Kinase 2 as an miR-205 Sponge.]Diabetic retinopathy (DR) is a devastating complication of diabetes. The aim of the present study is to investigate the exact role and mechanism of long noncoding RNA MALAT1 (MALAT1) in the progress of DR. An oxygen-induced retinopathy (OIR) mouse model and high glucose (HG) stimulated human retinal microvascular endothelial cells (HRMECs) were employed to mimic the pathological statues of DR. Quantitative real-time PCR (qRT-PCR and western blot results showed that MALAT1, VEGFA, and HIF-1alpha levels were increased in DR retinal tissues and HG-stimulated HRMECs, whereas the expression of miR-203a-3p was decreased. Knockdown of MALAT1 or upregulation of miR-203a-3p both suppressed HG-induced proliferation, migration, and tube formation of HRMECs. A dual-luciferase reporter assay showed that miR-203a-3p could bind to the predicted seed regions of MALAT1 as evidenced by the reduced luciferase activity. Furthermore, enforced downregulation of miR-203a-3p abolished the suppressive effect of MALAT1 silencing on HRMEC cell migration and tube formation. In conclusion, these data demonstrated that MALAT1 may affect angiogenesis by sponging miR-203a-3p in DR, suggesting that MALAT1 may act as a novel therapeutic target for the treatment of DR.	31689123	RID03133	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Pancreatic cancer	LINC01232	TM9SF2	negatively-F	western blot;luciferase reporter assay;ChIP;RIP;FISH;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000280734	GRCh38_13:99486962-99499306	ENSG00000125304	NA	102725509	9375	FLJ41590|TCONS_00021520	P76	[LINC01232 exerts oncogenic activities in pancreatic adenocarcinoma via regulation of TM9SF2.] relationship between LINC01232 and its nearby gene transmembrane 9 superfamily member 2 (TM9SF2) was investigated. The same expression pattern of TM9SF2 in TCGA PAAD samples was observed. It was found that upregulation of LINC01232 could be a crucial factor for the dysregulation of TM9SF2. Mechanistically, LINC01232 recruited EIF4A3 to boost TM9SF2 mRNA stability. Besides, our findings demonstrated that the transcriptional activation of LINC01232 and TM9SF2 was mediated by SP1. Therefore, we concluded that LINC01232 executed carcinogenic properties in PAAD progression via regulation of TM9SF2. In conclusion, this study was the first to unveil the role and molecular mechanism of LINC01232, suggesting LINC01232 as a promising molecular target for pancreatic cancer treatment.	31541081	RID03134	expression association	NA	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	SP1	LINC01232	positively-E	western blot;luciferase reporter assay;ChIP;RIP;FISH;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000280734	GRCh38_13:99486962-99499306	6667	102725509	NA	FLJ41590|TCONS_00021520	[LINC01232 exerts oncogenic activities in pancreatic adenocarcinoma via regulation of TM9SF2.] relationship between LINC01232 and its nearby gene transmembrane 9 superfamily member 2 (TM9SF2) was investigated. The same expression pattern of TM9SF2 in TCGA PAAD samples was observed. It was found that upregulation of LINC01232 could be a crucial factor for the dysregulation of TM9SF2. Mechanistically, LINC01232 recruited EIF4A3 to boost TM9SF2 mRNA stability. Besides, our findings demonstrated that the transcriptional activation of LINC01232 and TM9SF2 was mediated by SP1. Therefore, we concluded that LINC01232 executed carcinogenic properties in PAAD progression via regulation of TM9SF2. In conclusion, this study was the first to unveil the role and molecular mechanism of LINC01232, suggesting LINC01232 as a promising molecular target for pancreatic cancer treatment.	31541081	RID03135	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Thyroid cancer	MIR592	NEAT1	negatively-F	miRDB;Targetscan;LncBase;western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	miRNA	lncRNA	ENSG00000207692	NA	ENSG00000245532	GRCh38_11:65422774-65445540	693177	283131	MIRN592|hsa-mir-592|mir-592	LINC00084|NCRNA00084|TncRNA|VINC	[MicroRNA-592 suppresses the malignant phenotypes of thyroid cancer by regulating lncRNA NEAT1 and downregulating NOVA1.]The results indicated that miR<U+2011>592 was significantly downregulated in thyroid cancer samples, and its downregulation was associated with lymph node metastasis and tumor<U+2011>node<U+2011>metastasis stage. Patients with thyroid cancer and low miR<U+2011>592 expression exhibited shorter overall survival than patients with high miR<U+2011>592 expression. Overexpression of miR<U+2011>592 resulted in decreased cell proliferation, migration, and invasion in thyroid cancer. In addition, neuro<U+2011>oncological ventral antigen<U+00A0>1 (NOVA1) was identified as a novel target gene of miR<U+2011>592 in thyroid cancer cells. Furthermore, ectopic NOVA1 expression may effectively abolish the tumor<U+2011>suppressing effects of miR<U+2011>592 overexpression in thyroid cancer cells. Notably, the lncRNA NEAT1 was proposed to function as a sponge of miR<U+2011>592 in thyroid cancer cells, thereby regulating NOVA1 expression. Finally, resuming miR<U+2011>592 expression significantly impaired thyroid cancer tumor growth in<U+00A0>vivo. The results indicated that the NEAT1/miR<U+2011>592/NOVA1 pathway may play regulatory roles in thyroid cancer malignancy in<U+00A0>vitro and in<U+00A0>vivo. Our findings may provide novel insight into the pathogenesis of thyroid cancer. Therefore, this pathway may be an effective target for treating patients with this disease.	31524231	RID03136	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Renal cell carcinoma	TASR	AXL	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+);cancer progression(-)	NA	regulation	RNA-protein	Sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000215699	NA	ENSG00000167601	NA	NA	558	NA	ARK|JTK11|Tyro7|UFO	[Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression.]Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Future successful clinical trials may help in the development of a novel therapy to better suppress the RCC progression.	31501521	RID03137	expression association	chemoresistance		UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE67939)
Atherosclerosis	SNHG16	SMAD2	positively-E	RIP;western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-205)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000175387	NA	100507246	4087	Nbla10727|Nbla12061|ncRAN	JV18-1|MADH2|MADR2	[Long non-coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR-205 and modulating Smad2.]Smad2 was targeted and inversely regulated by miR-205, while being positively regulated by SNHG16 in HASMCs. Smad2 knockdown attenuated PDGF-bb-mediated actions on HASMC proliferation and migration. Both miR-205 overexpression and Smad2 knockdown partially reversed the effects of SNHG16 overexpression on HASMC proliferation and migration. Moreover, SNHG16 and Smad2 mRNA were up-regulated, while miR-205 was down-regulated in the plasma from patients with atherosclerosis. Small nucleolar RNA host gene 16 expression was inversely correlated with miR-205 expression and positively correlated with Smad2 expression in the plasma from atherosclerotic patients. In conclusion, our data showed the up-regulation of SNHG16 in pathogenic-stimulated HASMCs and clinical samples from atherosclerotic patients. Small nucleolar RNA host gene 16 regulated HASMC proliferation and migration possibly via regulating Smad2 expression by acting as a competing endogenous RNA for miR-205.	31441592	RID03138	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Laryngeal carcinoma	NEAT1	miR-29a-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	[Long noncoding RNA NEAT1 functions as an oncogene in human laryngocarcinoma by targeting miR-29a-3p.]we are committed to uncover the potential function of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the development of laryngocarcinoma.PATIENTS AND METHODS: LncRNA NEAT1 expression in laryngocarcinoma cells and 54 paired laryngocarcinoma samples was detected by Real-time quantitative polymerase chain reaction (RT-qPCR). Furthermore, the regulatory effects of NEAT1 on the proliferation and metastasis of laryngocarcinoma cells were evaluated. Biological role of NEAT1/miR-29a-3p axis was finally explored in regulating the progression of laryngocarcinoma.RESULTS: NEAT1 was upregulated in laryngocarcinoma tissues and cell lines. NEAT1 knockdown suppressed growth and invasive abilities in laryngocarcinoma cells, while overexpression of NEAT1 enhanced such abilities. Further experiments showed that miR-29a-3p was directly targeted by NEAT1, and participated in NEAT-mediated progression of laryngocarcinoma.CONCLUSIONS: NEAT1 is a novel oncogene in laryngocarcinoma and could enhance growth and invasion of laryngocarcinoma cells by targeting miR-29a-3p.	31364125	RID03139	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Pancreatic cancer	HNRNPL	PTBP1	negatively-E	TCGA;GEO;Oncomine;western blot	upregulation		NA	NA	cell migration(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000104824	GRCh38_19:38836370-38852347	ENSG00000011304	NA	3191	5725	HNRPL	HNRNP-I|HNRPI|pPTB|PTB|PTB-1|PTB2|PTB3|PTB4	[Identification of Upregulated HNRNPs Associated with Poor Prognosis in Pancreatic Cancer.] we reported that HNRNPL was commonly overexpressed in public databases and that high expression of HNRNPL in PC was positively associated with aggressive disease and poor overall survival. Downregulation of HNRNPL suppressed the abilities of migration and epithelial mesenchymal transition of PC cells in vitro, while depletion of HNRNPL did not affect the proliferation rate of PC cells. We further showed that HNRNPL might combine with RNA-binding protein, PTBP1, and function as a part of the spliceosome to regulate alternative splicing of target genes in the occurrence and development of PC. HNRNPL could be employed as an innovative prognostic biomarker and therapeutic target for PC.	31355266	RID03140	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MEG3	PTEN	positively-E	western blot;luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);cancer progression(-)	ceRNA(miR-494)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BZS|MHAM|MMAC1|PTEN1|TEP1	[MEG3 interacted with miR-494 to repress bladder cancer progression through targeting PTEN.]in bladder cancer cells, we observed htat miR-494 was increased. Then, MEG3 was overexpressed in UMUC3 and SW780 cells and it could negatively modulate miR-494 expression. Bladder cancer cell proliferation was repressed, cell apoptosis was triggered and meanwhile, the cell cycle was remarkably arrested by the overexpression of MEG3. Moreover, the increase of MEG3 suppressed bladder cancer cell migration and invasion capacity. MEG3 can sponge miR-494 and the binding sites between them were confirmed by carrying out a series of functional assays. Furthermore, PTEN was speculated as a putative target of miR-494. Meanwhile, we found that miR-494 inhibitors induced PTEN. Finally, in vivo assays were conducted to prove that MEG3 can restrain bladder tumor growth by modulating miR-494 and PTEN. In conclusion, it was suggested MEG3 can interact with miR-494 to regulate PTEN in bladder cancer development.	31294463	RID03141	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Periodontitis	FGD5-AS1	SOCS6	positively-E	western blot	upregulation	RT-qPCR	NA	NA	inflammatory response(-)	ceRNA(miR-142-3p)	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Periodontitis	lncRNA	PCG	ENSG00000225733	GRCh38_3:14920347-14948424	ENSG00000170677	NA	100505641	9306	NA	CIS4|Cish4|HSPC060|SOCS4|SSI4|STAI4|STATI4	[Abnormal expression of long noncoding RNA FGD5-AS1 affects the development of periodontitis through regulating miR-142-3p/SOCS6/NF-B pathway.]We found that the FGD5-AS1-mediated reduction in the inflammation was mediated through downside regulation of miR-142-3p, as evident from the upregulation of SOCS6, a target gene of miR-142-3p. Furthermore, the association between FGD5-AS1 and NF-B pathway was detected. FGD5-AS1 was found to protect against LPS-stimulated PDLC injury through restraining the NF-B signals. Based on these findings, we conclude that up-regulation of lncRNA FGD5-AS1 could protect against periodontitis via regulating the miR-142-3p/SOCS6/NF-B signals. Therefore, the FGD5-AS1/miR-142-3p/SOCS6 axis may act as an important indicator in explaining the pathogenesis of periodontitis.	31144533	RID03142	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Atherosclerosis	H19	POSTN	positively-E	western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	inflammatory response(-);apoptosis process(-);oxidative stress(-)	ceRNA(miR-let-7)	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000133110	NA	283120	10631	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	OSF-2|periostin|PN	[LncRNA H19/miR-let-7 axis participates in the regulation of ox-LDL-induced endothelial cell injury via targeting periostin.]periostin overexpression partly reversed the biological effects of H19 knockdown in ox-LDL-treated HUVECs, which were almost recapitulated by let-7 overexpression. In conclusion, these data suggest that H19 knockdown suppressed ox-LDL-induced inflammation, apoptosis and oxidative stress in HUVECs, which may be related to the down-regulation of periostin by interfering with let-7 bioavailability.	31054453	RID03143	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	MALAT1	POU5F1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell stemness(+)	ceRNA(miR-20b-5p)	binding/interaction	NA	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000233911	NA	378938	5460	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	[Long noncoding RNA MALAT1 mediates stem cell-like properties in human colorectal cancer cells by regulating miR-20b-5p/Oct4 axis.]We proceeded to show that both si-MALAT1 and miR-20b-5p-mimic attenuated microsphere formation and self-renewal capacity, decreased the proportion of CSCs, and downregulated the expression of proteins associated with tumor cell stemness maintenance (Oct4, Nanog, sex-determining region Y-box 2, and Notch1) and cellular metabolism (glucose transporter 1, lactate dehydrogenase B, hexokinase 2, and pyruvate kinase isozyme M2) in HCT-116 cells in vitro. In addition, a xenograft model based on Balb/c mice demonstrated that the administration of either si-MALAT1 or miR-20b-5p-mimic suppressed the tumorigenicity of HCT-116 cells in vivo. The underlying mechanisms may involve the targeting of the tumor cell stemness maintenance-related factor Oct4 by miR-20b-5p. For the first time, we present the possible underlying effects of MALAT1 in influencing the stem cell-like properties of CRC cells. We propose that microRNAs and long<U+00A0>noncoding RNAs have vital functions in mediating tumor stemness, which remain to be fully elucidated.	31012108	RID03144	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Myocardial infarction	TTTY15	miR-455-5p	negatively-F	luciferase reporter assay;RNA pull-down assay;RNAi	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);apoptosis process(-)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	miRNA	ENSG00000233864	NA	NA	NA	64595	NA	NCRNA00138	NA	[Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p.]We searched for potential target of TTTY15. Up-regulation of TTTY15 was associated with hypoxia. Silencing TTTY15 prevented hypoxia-induced cell apoptosis and rescued the cell migration and invasion. TTTY15 targeted miR-455-5p, which regulated the Jun dimerization protein 2 (JDP2) expression. Knocking down miR-455-5p abolished effects of TTTY-15 silencing on cell injury. Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p.We demonstrated that lncRNA TTTY15 was up-regulated in hypoxia. TTTY15 targeted miR-455-5p and silencing TTTY15 amelioratedhypoxia-induced cell injury in a miR-455-5p dependent manner.	30898696	RID03145	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Osteosarcoma	GAS5	ZBTB7A	negatively-E	ChIP	upregulation	RT-PCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000178951	NA	60674	51341	NCRNA00030|SNHG2	DKFZp547O146|FBI-1|LRF|pokemon|ZBTB7|ZNF857A	[ZBTB7A, a miR-663a target gene, protects osteosarcoma from endoplasmic reticulum stress-induced apoptosis by suppressing LncRNA GAS5 expression.]ZBTB7A expression levels were increased in osteosarcoma tissues and elevated ZBTB7A was associated with osteosarcoma metastasis. Further mechanistic studies revealed that miR-663a induced by ER stress directly bound to the 3'UTR of ZBTB7A and contributed to ER stress-induced ZBTB7A downregulation in osteosarcoma cells. Additionally, our data revealed that ZBTB7A bound to the promoter of LncRNA GAS5 and transcriptionally suppressed LncRNA GAS5 expression, leading to a decline in ER stress-induced cell apoptosis. Collectively, our findings reveal the prosurvival role of ZBTB7A in osteosarcoma adaptation to ER stress and suggest that the miR-663a-ZBTB7A-LncRNAGAS5 pathway is essential for the survival of human osteosarcoma cells under ER stress.	30753838	RID03146	interact with protein	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	NEAT1	GPD1L	positively-E	western blot;luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+);inflammatory response(+)	ceRNA(miR-181a)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000152642	NA	283131	23171	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	KIAA0089	[Long Noncoding RNA Nuclear Enriched Abundant Transcript 1 (NEAT1) Regulates Proliferation, Apoptosis, and Inflammation of Chondrocytes via the miR-181a/Glycerol-3-Phosphate Dehydrogenase 1-Like (GPD1L) Axis.]the correlation between NEAT1, miR-181a, and glycerol-3-phosphate dehydrogenase 1-like (GPD1L) was fully investigated. Finally, the downregulation of miR-181a was employed as a recovery experiment to explore the functional mechanism of NEAT1 in OA. RESULTS In the present study, we found that NEAT1 expression was downregulated in OA tissues, while miR-181a expression was prominently upregulated. Moreover, reduced expression of NEAT1 suppressed cell growth while elevating the apoptotic rate and increasing the abundance of inflammatory cytokines released in OA chondrocytes. Furthermore, we clarified that miR-181a was a direct sponge of NEAT1, and GPD1L was able to bind to miR-181a. Additionally, we found that downregulation of miR-181a was able to attenuate the effect of NEAT1 on apoptosis, inflammatory response, and proliferation in OA chondrocytes. CONCLUSIONS Our findings indicate that downregulation of NEAT1 aggravated progression of OA via modulating the miR-181a/GPD1L axis, providing a novel insight into the mechanism of OA pathogenesis.	31658244	RID03147	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE86978)
Osteosarcoma	miR-425-5p	TUG1	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);tumorigenesis(-)	interact with protein	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	[miR-425-5p decreases LncRNA MALAT1 and TUG1 expressions and suppresses tumorigenesis in osteosarcoma via Wnt/beta-catenin signaling pathway.]miR-425-5p decreases LncRNA MALAT1 and TUG1 expressions and suppresses tumorigenesis in osteosarcoma via Wnt/beta-catenin signaling pathway.	30986552	RID03148	interact with protein	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Osteosarcoma	miR-425-5p	MALAT1	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);tumorigenesis(-)	interact with protein	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	[miR-425-5p decreases LncRNA MALAT1 and TUG1 expressions and suppresses tumorigenesis in osteosarcoma via Wnt/beta-catenin signaling pathway.]miR-425-5p decreases LncRNA MALAT1 and TUG2 expressions and suppresses tumorigenesis in osteosarcoma via Wnt/beta-catenin signaling pathway.	30986553	RID03149	interact with protein	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Cancer	H19	miR-181a	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);MAPK signaling pathway(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	[Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function.]H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.	31267802	RID03150	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Cancer	H19	MMP2	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);MAPK signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000087245	NA	283120	4313	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	[Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function.]H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.	31267802	RID03151	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Cancer	H19	MMP9	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);MAPK signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000100985	NA	283120	4318	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CLG4B|GELB|MANDP2|MMP-9	[Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function.]H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.	31267802	RID03152	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cancer	H19	VEGFA	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);MAPK signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000112715	NA	283120	7422	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MVCD1|VEGF|VPF	[Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function.]H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.	31267802	RID03153	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cancer	H23	NOS3	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);MAPK signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000164867	NA	NA	4846	NA	ECNOS|eNOS	[Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function.]H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.	31267802	RID03154	expression association	NA		DOWN(BRCA);DATA(GSE75367)
Hepatocellular carcinoma	LINC-ROR	IL-1beta	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	inflammatory response(-)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	[LINC ROR from Hepatocarcinoma Cell-derived Exosomes Modulates Inflammation in Human Macrophages]The physiological appearance of exosomes isolated from PLC/PRF/5 cells was examined by using differential ultracentrifugation and the images were captured by transmission electron microscopy. The internalization of exosomes by THP-1 cells was examined via laser-scanning confocal microscopy. The expression of LINC ROR was analyzed through qRT-PCR The expression of interleukin (IL) -1beta was examined by ELISA.Exosomes were found spherical and the diameters mainly distribute around 100 nm. LINC ROR can be transferred by tumor derived exosomes to macrophages. Exosomes isolated from PLC/PRF/5 cells significantly expressed higher levels of LINC ROR. Suppression of LINC ROR by siRNA significantly increased the release of pro-inflammatory cytokine (IL-1beta) in THP-1 cell upon LPS stimulation.LINC ROR from hepatocarcinoma cell-derived exosomes plays an important role in regulating the inflammation of macrophages.	31106535	RID03155	expression association	NA	UP(LIHC);DATA(GSE117623)	
Parkinson's disease	Mirt2	TNF	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(-);NF-kB signaling pathway(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000228978	NA	NA	7124	NA	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	[Long non-coding RNA Mirt2 prevents TNF-alpha-triggered inflammation via the repression of microRNA-101.]Tumor necrosis factor alpha (TNF-alpha) was used to induce inflammation in SH-Sy5y cells. Mirt2 overexpressed or silenced cells were established. MicroRNA-101 (miR-101) mimic was used to up-regulate miR-101. Viable and apoptotic cells as well as reactive oxidative species (ROS) were detected after staining. Proteins associated with apoptosis, interleukin (IL) and signaling regulators were evaluated by western blot. IL secretion was assessed by ELISA. Mirt2 and miR-101 were determined by qRT-PCR We discovered that TNF-alpha weakened viability of SH-Sy5y cells and resulted in sensitivity to apoptosis with cleavage of PARP and caspase-3. Expression and secretion of IL-6 as well as generation of ROS were facilitated by TNF-alpha. However, Mirt2 overexpression moderated TNF-alpha-caused apoptosis associated with inflammation and oxidative stress. Mirt2 suppressed TNF-alpha-induced accumulation of miR-101, and based on this Mirt2 exhibited anti-inflammatory roles. Additionally, TNF-alpha-triggered phosphorylation of regulators was blocked by Mirt2 while restored by miR-101 mimic. In short Mirt2 overexpression exhibited anti-inflammatory properties through miR-101 suppression. Through down-regulating miR-101, Mirt2 blocked TNF-alpha-triggered NF-kB/p38MAPK pathway.	31513985	RID03156	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Parkinson's disease	Mirt2	miR-101	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(-)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	[Long non-coding RNA Mirt2 prevents TNF-alpha-triggered inflammation via the repression of microRNA-101.]Tumor necrosis factor alpha (TNF-alpha) was used to induce inflammation in SH-Sy5y cells. Mirt2 overexpressed or silenced cells were established. MicroRNA-101 (miR-101) mimic was used to up-regulate miR-101. Viable and apoptotic cells as well as reactive oxidative species (ROS) were detected after staining. Proteins associated with apoptosis, interleukin (IL) and signaling regulators were evaluated by western blot. IL secretion was assessed by ELISA. Mirt2 and miR-101 were determined by qRT-PCR We discovered that TNF-alpha weakened viability of SH-Sy5y cells and resulted in sensitivity to apoptosis with cleavage of PARP and caspase-3. Expression and secretion of IL-6 as well as generation of ROS were facilitated by TNF-alpha. However, Mirt2 overexpression moderated TNF-alpha-caused apoptosis associated with inflammation and oxidative stress. Mirt2 suppressed TNF-alpha-induced accumulation of miR-101, and based on this Mirt2 exhibited anti-inflammatory roles. Additionally, TNF-alpha-triggered phosphorylation of regulators was blocked by Mirt2 while restored by miR-101 mimic. In short Mirt2 overexpression exhibited anti-inflammatory properties through miR-101 suppression. Through down-regulating miR-101, Mirt2 blocked TNF-alpha-triggered NF-kB/p38MAPK pathway.	31513985	RID03157	expression association	NA		
Cholangiocarcinoma	DANCR	FBP1	negatively-E	western blot;ChIP;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000165140	NA	57291	2203	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	FBP	[Long noncoding RNA DANCR regulates proliferation and migration by epigenetically silencing FBP1 in tumorigenesis of cholangiocarcinoma.]downregulation of DANCR suppressed CCA cells proliferation in vivo. RNA-seq revealed that DANCR knockdown preferentially affected genes linked with cell proliferation and cell differentiation. Furthermore, mechanistic investigation validated that DANCR could bind EZH2 and modulate the histone methylation of promoter of FBP1, thereby regulating CCA cells growth and migration. Taken together, these results demonstrated the significant roles of DANCR in CCA and may provide a theoretical basis for clinical diagnosis and treatment of CCA.	31383847	RID03158	epigenetic regulation	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Prostate cancer	PCAT1	CENPF	negatively-E	RNAi;RT-PCR		microarray	GSE29886	NA	cell cycle(-);cell proliferation(-)	epigenetic regulation	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000117724	NA	100750225	1063	PCA1|PCAT-1|PiHL	hcp-1	In summary, PCAT1 plays an important role in the cell cycle and proliferation of prostate cancer cells by mediating the expression of CENPF, CENPE, ID1, and ID3. Thus, interfering PCAT1 may provide a novel strategy for the prevention and treatment of prostate cancer. However, more evidence in vivo is needed to evaluate the potential application.results suggest that PCAT1 may have a regulatory role in the expression of CENPF. Silencing the regulator function of PCAT1 leads to reduced CENPF expression and subsequently inhibits the carcinogenesis by disrupting its downstream functions or signaling pathways related to cell cycle through chromosomes decondensation or downregulating cell cycle proteins Cdc2 and cyclin B1 in prostate cancer cells.To obtain a gene expression matrix among samples, microarray data were preprocessed using AFFY (Gautier et al., 2004) and Limma (Smyth, 2004) package, including normexp Background Correction, Loess Normalization, and Probe Summarization	31090454	RID03159	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE55807)
Prostate cancer	PCAT1	CENPE	negatively-E	RNAi;RT-PCR		microarray	GSE29886	NA	cell cycle(-);cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000138778	NA	100750225	1062	PCA1|PCAT-1|PiHL	KIF10|PPP1R61	In summary, PCAT1 plays an important role in the cell cycle and proliferation of prostate cancer cells by mediating the expression of CENPF, CENPE, ID1, and ID3. Thus, interfering PCAT1 may provide a novel strategy for the prevention and treatment of prostate cancer. However, more evidence in vivo is needed to evaluate the potential application.results suggest that PCAT1 may have a regulatory role in the expression of CENPF. Silencing the regulator function of PCAT1 leads to reduced CENPF expression and subsequently inhibits the carcinogenesis by disrupting its downstream functions or signaling pathways related to cell cycle through chromosomes decondensation or downregulating cell cycle proteins Cdc2 and cyclin B1 in prostate cancer cells.To obtain a gene expression matrix among samples, microarray data were preprocessed using AFFY (Gautier et al., 2004) and Limma (Smyth, 2004) package, including normexp Background Correction, Loess Normalization, and Probe Summarization	31090454	RID03160	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Prostate cancer	PCAT1	ID1	negatively-E	RNAi;RT-PCR		microarray	GSE29886	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000125968	NA	100750225	3397	PCA1|PCAT-1|PiHL	bHLHb24|dJ857M17.1.2	In summary, PCAT1 plays an important role in the cell cycle and proliferation of prostate cancer cells by mediating the expression of CENPF, CENPE, ID1, and ID3. Thus, interfering PCAT1 may provide a novel strategy for the prevention and treatment of prostate cancer. However, more evidence in vivo is needed to evaluate the potential application.results suggest that PCAT1 may have a regulatory role in the expression of CENPF. Silencing the regulator function of PCAT1 leads to reduced CENPF expression and subsequently inhibits the carcinogenesis by disrupting its downstream functions or signaling pathways related to cell cycle through chromosomes decondensation or downregulating cell cycle proteins Cdc2 and cyclin B1 in prostate cancer cells.To obtain a gene expression matrix among samples, microarray data were preprocessed using AFFY (Gautier et al., 2004) and Limma (Smyth, 2004) package, including normexp Background Correction, Loess Normalization, and Probe Summarization	31090454	RID03161	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(NSCLC);DATA(GSE74639)
Prostate cancer	PCAT1	ID3	negatively-E	RNAi;RT-PCR		microarray	GSE29886	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000117318	NA	100750225	3399	PCA1|PCAT-1|PiHL	bHLHb25|HEIR-1	In summary, PCAT1 plays an important role in the cell cycle and proliferation of prostate cancer cells by mediating the expression of CENPF, CENPE, ID1, and ID3. Thus, interfering PCAT1 may provide a novel strategy for the prevention and treatment of prostate cancer. However, more evidence in vivo is needed to evaluate the potential application.results suggest that PCAT1 may have a regulatory role in the expression of CENPF. Silencing the regulator function of PCAT1 leads to reduced CENPF expression and subsequently inhibits the carcinogenesis by disrupting its downstream functions or signaling pathways related to cell cycle through chromosomes decondensation or downregulating cell cycle proteins Cdc2 and cyclin B1 in prostate cancer cells.To obtain a gene expression matrix among samples, microarray data were preprocessed using AFFY (Gautier et al., 2004) and Limma (Smyth, 2004) package, including normexp Background Correction, Loess Normalization, and Probe Summarization	31090454	RID03162	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE86978)
Cholangiocarcinoma	FENDRR	BIRC5	negatively-E	western blot;RIP;CHIP assay;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000089685	NA	400550	332	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	API4|EPR-1|survivin	[LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells.]In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blot. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blot. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K9 methylation, thereby represses CCA cell proliferation, migration and invasion.	30983519	RID03163	epigenetic regulation	NA		UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Cholangiocarcinoma	FENDRR	SETDB1	positively-F	western blot;RIP;ChIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000143379	NA	400550	9869	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	ESET|KG1T|KIAA0067|KMT1E|TDRD21	[LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells.]In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blot. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blot. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K10 methylation, thereby represses CCA cell proliferation, migration and invasion.	30983519	RID03164	epigenetic regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	FENDRR	SETDB1	NA	western blot;RIP;CHIP assay;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000143379	NA	400550	9869	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	ESET|KG1T|KIAA0067|KMT1E|TDRD21	[LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells.]In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blot. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blot. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K11 methylation, thereby represses CCA cell proliferation, migration and invasion.	30983519	RID03165	epigenetic regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	NNT-AS1	BCL9	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(-)	ceRNA(miR-485)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000116128	NA	100652772	607	RP11-159F24.1	NA	[Long non-coding RNA NNT-AS1 functions as an oncogenic gene through modulating miR-485/BCL9 in cholangiocarcinoma.]In this study, NNT-AS1 was expressed at high levels in CCA and closely associated with poor prognosis of patients with CCA. NNT-AS1 knockdown impaired cell proliferation, suppressed CCA cell migration and invasion, and restrained tumor growth in vitro. Moreover, NNT-AS1 directly bounded to miR-485 and further regulated BCL9. Finally, rescue assays verified that NNT-AS1 modulated the tumorigenesis of CCA by regulating miR-485.Taken together, NNT-AS1 played a critical biological role in the development of CCA. Our results elucidated NNT-AS1/miR-485/BCL9 axis might lead to a further understanding of the molecular mechanism of CCA.</AbstractText>: Taken together, NNT-AS1 played a critical biological role in the development of CCA. Our results elucidated NNT-AS1/miR-485/BCL9 axis might lead to a further understanding of the molecular mechanism of CCA.	31616187	RID03166	ceRNA or sponge	prognosis	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	LINC00313	MIR422A	positively-E	luciferase reporter assay;ChIP;RNAi	upregulation	RT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000185186	GRCh38_21:43461960-43479534	ENSG00000199156	NA	114038	494334	C21orf84|CH507-42P11.5|NCRNA00313	MIRN422A	[SP1-induced upregulation of long noncoding RNA LINC00313 contributes to papillary thyroid cancer progression via the miR-422a.]We observed that LINC00313 expression was significantly up-regulated in both PTC tissues and cell lines. Next, the results of bioinformatics analysis and luciferase reporter assays indicated that the transcription factor SP1 can bind to the promoter region of LINC00313 resulting in the overexpression of LINC00313 in PTC. Moreover, functional study revealed that knockdown of LINC00313 significantly suppressed cells proliferation, migration, invasion and EMT. Finally, our results indicated that LINC00313 functioned as an oncogene in PTC in part through serving as a competing endogenous RNA to modulate mi-422a expression.CONCLUSIONS: Overall, our data demonstrated that SP1-induced LINC00313 contributed to PTC progression by via competitively binding to miR-422a, which may provide a novel therapeutic strategy for PTC.	30779082	RID03167	ceRNA or sponge	NA		
Papillary thyroid carcinoma	SP1	LINC00313	positively-E	luciferase reporter assay;ChIP;RNAi	upregulation	RT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000185186	GRCh38_21:43461960-43479534	6667	114038	NA	C21orf84|NCRNA00313	[SP1-induced upregulation of long noncoding RNA LINC00313 contributes to papillary thyroid cancer progression via the miR-422a.]We observed that LINC00313 expression was significantly up-regulated in both PTC tissues and cell lines. Next, the results of bioinformatics analysis and luciferase reporter assays indicated that the transcription factor SP1 can bind to the promoter region of LINC00313 resulting in the overexpression of LINC00313 in PTC. Moreover, functional study revealed that knockdown of LINC00313 significantly suppressed cells proliferation, migration, invasion and EMT. Finally, our results indicated that LINC00313 functioned as an oncogene in PTC in part through serving as a competing endogenous RNA to modulate mi-422a expression.CONCLUSIONS: Overall, our data demonstrated that SP1-induced LINC00313 contributed to PTC progression by via competitively binding to miR-422a, which may provide a novel therapeutic strategy for PTC.	30779082	RID03168	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Pre-eclampsia	LINC00511	CCN1	positively-E	western blot;luciferase reporter assay;qRT-PCR;ChIP	downregulation	qRT-PCR	NA	NA	cell invasion(-)	ceRNA(miR-29b-p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000145386	NA	400619	3491	onco-lncRNA-12	CYR61|GIG1|IGFBP10	[AP2 mediated downregulation of lncRNA LINC00511 as a ceRNA suppresses trophoblast invasion by regulating miR-29b-3p/Cyr61 axis.]Overexpression of LINC00511 promoted trophoblast cell proliferation, migration and invasion. The transcription factor AP2 directly binds to the promoter region of LINC00511 to activate transcription. In addition, LINC00511 was enriched in cytoplasm and functioned as a molecular spong for miR-29b-3p, antagonizing its ability to repress Cyr61 protein translation.CONCLUSION: This study demonstrated that AP2 mediated downregulation of LINC00511 suppresses trophoblast invasion by regulating miR-29b-3p/ Cyr61 axis.	31542614	RID03169	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Pre-eclampsia	AP2	LINC00511	positively-E	western blot;luciferase reporter assay;qRT-PCR;ChIP	downregulation	qRT-PCR	NA	NA	cell invasion(-)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Eclampsia	PCG	lncRNA	NA	NA	ENSG00000227036	GRCh38_17:72290091-72640472	NA	400619	NA	LCAL5|onco-lncRNA-12	[AP2 mediated downregulation of lncRNA LINC00511 as a ceRNA suppresses trophoblast invasion by regulating miR-29b-3p/Cyr61 axis.]Overexpression of LINC00511 promoted trophoblast cell proliferation, migration and invasion. The transcription factor AP2 directly binds to the promoter region of LINC00511 to activate transcription. In addition, LINC00511 was enriched in cytoplasm and functioned as a molecular spong for miR-29b-3p, antagonizing its ability to repress Cyr61 protein translation.CONCLUSION: This study demonstrated that AP2 mediated downregulation of LINC00511 suppresses trophoblast invasion by regulating miR-29b-3p/ Cyr61 axis.	31542614	RID03170	transcriptional regulation	NA		UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Airway inflammation	lncRNAuc001.dgp.1	IL1R1	positively-E	FISH;western blot	upregulation	qRT-PCR;microarray	NA	NA	inflammatory response(+);NF-kB signaling pathway(+)	ceRNA(miR-3607-5p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000115594	NA	NA	3554	NA	CD121A|D2S1473|IL1R|IL1RA	[CircRNA104250 and lncRNAuc001.dgp.1 promote the PM2.5-induced inflammatory response by co-targeting miR-3607-5p in BEAS-2B cells ]lncRNAuc001.dgp.1 target miR-3607-5p and affect expression of interleukin 1 receptor 32 1 (IL1R1), which influences the nuclear factor kB (NF-kB) signaling pathway. In 33 summary, we have uncovered an underlying mechanism of airway inflammation by34 PM2.5 involving regulation of ncRNA for the first time, which provides further insights 35 into the toxicological effects of PM2.5.	31864925	RID03171	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	ST8SIA6-AS1	AKT1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000204832	GRCh38_10:17386919-17445758	ENSG00000142208	NA	100128098	207	APAL	AKT|PKB|PRKBA|RAC|RAC-alpha	[LncRNA ST8SIA6-AS1 promotes proliferation, migration and invasion in  through the p38 MAPK signalling pathway.]The high expression of ST8SIA6-AS1 was associated with estrogen receptor-negative, progesterone receptor-negative, advanced tumour-node-metastasis stage and worse survival in BC patients. In vitro functional studies revealed that high expression of ST8SIA6-AS1 promoted proliferation, invasion and migration of BC cell lines. The results of the in vivo studies indicated that upregulation of ST8SIA6-AS1 promoted xenograft tumour growth of BC. Mechanistically, ST8SIA6-AS1 regulated AKT1 and p38 mitogen-activated protein kinase (MAPK) gene expression by affecting their mRNA and protein levels, respectively, and it also affected the phosphorylation of AKT1 protein. Rescue experiments indicated that ST8SIA6-AS1 promoted BC cell proliferation, invasion and migration in a p38 MAPK signalling-mediated manner. Together, our data suggest that ST8SIA6-AS1 plays an important role in the occurrence and development of BC and may therefore serve as a promising therapeutic target.	31784750	RID03172	expression association	metastasis	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	ST8SIA6-AS1	MAPK	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000204832	GRCh38_10:17386919-17445758	NA	NA	100128098	NA	APAL	NA	[LncRNA ST8SIA6-AS1 promotes proliferation, migration and invasion in  through the p38 MAPK signalling pathway.]The high expression of ST8SIA6-AS1 was associated with estrogen receptor-negative, progesterone receptor-negative, advanced tumour-node-metastasis stage and worse survival in BC patients. In vitro functional studies revealed that high expression of ST8SIA6-AS1 promoted proliferation, invasion and migration of BC cell lines. The results of the in vivo studies indicated that upregulation of ST8SIA6-AS1 promoted xenograft tumour growth of BC. Mechanistically, ST8SIA6-AS1 regulated AKT1 and p38 mitogen-activated protein kinase (MAPK) gene expression by affecting their mRNA and protein levels, respectively, and it also affected the phosphorylation of AKT1 protein. Rescue experiments indicated that ST8SIA6-AS1 promoted BC cell proliferation, invasion and migration in a p38 MAPK signalling-mediated manner. Together, our data suggest that ST8SIA6-AS1 plays an important role in the occurrence and development of BC and may therefore serve as a promising therapeutic target.	31784750	RID03173	expression association	metastasis	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)	
Diabetic cataract	PVT1	MMP2	positively-E	western blot;FISH	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000087245	NA	5820	4313	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CLG4|CLG4A|TBE-1	[SP1-mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR-214-3p/MMP2 axis.]Emerging evidence illustrates the critical roles of long non-coding RNAs (lncRNAs) in the diabetes. However, the deepgoing regulation of lncRNA PVT1 in the diabetic cataract (DC) is still unclear. Here, present research investigates the pathologic roles and underlying mechanism by which lncRNA PVT1 regulates the DC pathogenesis. Human lens epithelial (HLE) B-3 cells were induced by the high glucose (HG) to simulate the DC microenvironment models. Results revealed that lncRNA PVT1 expression was up-regulated in the HG-induced HLE B-3 cells as compared to the normal glucose group. Transcription factor SP1 could bind with the promoter region of PVT1 and activate its transcription. Functionally, PVT1 knock-down could repress the proliferation and promote the apoptosis of HLE B-3 cells. Mechanistically, PVT1 acted as the 'miRNA sponge' to target miR-214-3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT1 for the DC pathogenesis, providing an inspiration for the DC mechanism.	31755246	RID03174	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DATA(GSE40174)
Diabetic cataract	SP1	PVT1	positively-F	western blot;FISH	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Cataract	TF	lncRNA	ENSG00000185591	NA	ENSG00000249859	GRCh38_8:127794526-128187101	6667	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	[SP1-mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR-214-3p/MMP2 axis.]Emerging evidence illustrates the critical roles of long non-coding RNAs (lncRNAs) in the diabetes. However, the deepgoing regulation of lncRNA PVT1 in the diabetic cataract (DC) is still unclear. Here, present research investigates the pathologic roles and underlying mechanism by which lncRNA PVT1 regulates the DC pathogenesis. Human lens epithelial (HLE) B-3 cells were induced by the high glucose (HG) to simulate the DC microenvironment models. Results revealed that lncRNA PVT1 expression was up-regulated in the HG-induced HLE B-3 cells as compared to the normal glucose group. Transcription factor SP1 could bind with the promoter region of PVT1 and activate its transcription. Functionally, PVT1 knock-down could repress the proliferation and promote the apoptosis of HLE B-3 cells. Mechanistically, PVT1 acted as the 'miRNA sponge' to target miR-214-3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT2 for the DC pathogenesis, providing an inspiration for the DC mechanism.	31755246	RID03175	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Melanoma	LINC00518	AP1S2	positively-E	western blot;luciferase reporter assay;FISH;RIP;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell metastasis(+)	ceRNA(miR-204-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000183674	GRCh38_6:10429255-10435015	ENSG00000182287	NA	221718	8905	C6orf218|MGC40222	MRX59|MRXS5|PGS|SIGMA1B	[Long noncoding RNA LINC00518 acts as a competing endogenous RNA to promote the metastasis of malignant melanoma via miR-204-5p/AP1S2 axis.]We found that LICN00518 was significantly upregulated in melanoma tissue, and high LICN00518 level was an independent risk factor for melanoma patients. LICN00518 promoted the invasion and migration of melanoma cells. LICN00518 exerted its role by decoying miR-204-5p to upregulate Adaptor Related Protein Complex 1 Sigma 2 Subunit (AP1S2) expression. We also demonstrated that LICN00518 promoted melanoma metastasis in vivo through pulmonary metastasis assay. This result elucidates a new mechanism for LICN00518 in the metastasis of melanoma. LICN00518 may serve as a survival indicator and potential therapeutic target in melanoma patients.	31712557	RID03176	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	FTX	HK2	positively-E	western blot	downregulation	RT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000159399	NA	100302692	3099	FLJ33139|LINC00182|MIR374AHG|NCRNA00182	NA	[Quantitative Proteomics Analysis Revealed the Potential Role of lncRNA Ftx in Promoting Gastric Cancer Progression.]HK2, which is downregulated when lncRNA Ftx is deleted and upregulated while lncRNA Ftx is overexpressed, is further validated in gastric cancer cells.The present study suggests lncRNA Ftx promotes gastric cancer progression by upregulating HK2, which provides a new perspective for the mechanism of gastric cancer progression, and thus identifies potential therapeutic targets for gastric cancer.</AbstractText>: The present study suggests lncRNA Ftx promotes gastric cancer progression by upregulating HK2, which provides a new perspective for the mechanism of gastric cancer progression, and thus identifies potential therapeutic targets for gastric cancer.	31709769	RID03177	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Colorectal cancer	KDM4C	MALAT1	positively-E	western blot;luciferase reporter assay;ChIP		RT-PCR	NA	NA	cell metastasis(+);WNT/beta-catenin signaling pathway(+)	histone modification	regulation	protein-RNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000107077	NA	ENSG00000251562	GRCh38_11:65497688-65506516	23081	378938	GASC1|JMJD2C|KIAA0780|TDRD14C	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	[JMJD2C promotes colorectal cancer metastasis via regulating histone methylation of MALAT1 promoter and enhancing beta-catenin signaling pathway.]Our present results indicated that histone demethylase JMJD2C was overexpressed in matched CRC tumor tissues of primary and metastatic foci, and CRC patients with lower JMJD2C expression in primary tumors had better prognosis with longer OS (Overall Survival). The following biological function observation suggested that JMJD2C promoted CRC metastasis in vitro and in vivo. Further molecular mechanism investigation demonstrated that JMJD2C protein translocated into the nuclear, lowered the histone methylation level of MALAT1 promoter in the sites of H3K9me3 and H3K36me3, up-regulated the expression of MALAT1, and enhanced the beta-catenin signaling pathway in CRC cells.CONCLUSION: Our data demonstrated that JMJD2C could enhance the metastatic abilities of CRC cells in vitro and in vivo by regulating the histone methylation level of MALAT1 promoter, thereby up-regulating the expression of MALAT1 and enhancing the activity of beta-catenin signaling pathway, providing that JMJD2C might be a novel therapeutic target for CRC metastasis.The protein expression and cellular localization of JMJD2C and beta-catenin were characterized by immunofluorescence staining and western blot. The histone methylation level of MALAT1 promoter region (H3K9me3 and H3K36me3) was tested by ChIP-PCR assays. The promoter activity of MALAT1 was detected by luciferase reporter assay. The expressions of MALAT1 and the downstream beta-catenin signaling pathway related genes in CRC cells were detected by real-time PCR and western blot, respectively.	31665047	RID03178	epigenetic regulation	metastasis,prognosis	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Breast cancer	NEAT1	RRM2	positively-E	Targetscan;Annolnc;starBase;OncoLnc	upregulation	RT-PCR	GSE109169	NA	prognosis	ceRNA(miR-21)	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171848	NA	283131	6241	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	C2orf48|FLJ25102	[Identification of lncRNA NEAT1/miR-21/RRM2 axis as a novel biomarker in breast cancer.]We found out that NEAT1/miR-21/RRM2 axis may play a role in BC diagnosis and prognosis. The real-time quantitative reverse transcription-polymerase chain reaction test was used to analyze the mRNA level of NEAT1, miR-21, and RRM2. western blot was used to detect the protein level of RRM2. Through the 5-ethynyl-2'-deoxyuridine assay, the proliferation of MDA-MB-231 cells was detected. Through wound healing and transwell assay, the migration of MDA-MB-231 cells was detected. Altogether, our data indicated that NEAT1, miR-21, and RRM2 were upregulated in several BC cell lines. Overexpressed of miR-21 in MDA-MB-231 cells promote proliferation and migration. Besides, our results demonstrated that overexpressed of miR-21 upregulated the level of RRM2. Accordingly, miR-21/RRM2 might be a new diagnosis and treatment target of BC.	31621912	RID03179	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteoporosis	GAS5	RUNX2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-498)	binding/interaction	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000124813	NA	60674	860	NCRNA00030|SNHG2	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	LncRNA GAS5 overexpression alleviates the development of osteoporosis through promoting osteogenic differentiation of MSCs via targeting microRNA-498 to regulate RUNX2.MicroRNA-498 was highly expressed in hMSCs derived from osteoporosis patients, whereas GAS5 and RUNX2 were lowly expressed. GAS5 overexpression significantly increased ALP activity and promoted osteogenic differentiation of hMSCs derived from osteoporosis patients. Meanwhile, GAS5 significantly promoted osteogenic differentiation by mediating microRNA-498 expression to up-regulate RUNX2. Co-overexpression of GAS5 and microRNA-498 could remarkably reverse the increase of RUNX2 expression. Besides, RUNX2 overexpression markedly elevated ALP activity.CONCLUSIONS: LncRNA GAS5 is lowly expressed in patients with osteoporosis. Overexpression of GAS5 promotes osteogenic differentiation of hMSCs through regulating microRNA-498 to up-regulate RUNX2 expression, thus alleviating the development of osteoporosis.	31599401	RID03180	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Critical limb ischaemia	GAPLINC	miR-211	negatively-E	western blot	downregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	RNA-RNA	NA	NA	NA	Other	Critical limb ischaemia	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540|lncRNA-uc002kmd.1|RP11-838N2.4|TCONS_00026238	NA	[Long non-coding RNA GAPLINC promotes angiogenesis by regulating miR-211 under hypoxia in human umbilical vein endothelial cells.] We found that hypoxia and hypoxia-inducible factor 1alpha (HIF-1alpha) increased the expression of GAPLINC in HUVEC cells. Moreover, GAPLINC overexpression down-regulated miR-211 and up-regulated Bcl2 protein expression.	31589383	RID03181	expression association	NA	UP(SKCM);DATA(GSE38495)	
Critical limb ischaemia	GAPLINC	BCL2	positively-E	western blot	downregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	RNA-protein	NA	NA	NA	Other	Critical limb ischaemia	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000171791	NA	100505592	596	LINC01540|lncRNA-uc002kmd.1|RP11-838N2.4|TCONS_00026238	Bcl-2|PPP1R50	[Long non-coding RNA GAPLINC promotes angiogenesis by regulating miR-211 under hypoxia in human umbilical vein endothelial cells.] We found that hypoxia and hypoxia-inducible factor 1alpha (HIF-1alpha) increased the expression of GAPLINC in HUVEC cells. Moreover, GAPLINC overexpression down-regulated miR-211 and up-regulated Bcl2 protein expression.	31589383	RID03182	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Critical limb ischaemia	HIF1A	GAPLINC	positively-E	western blot	downregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	NA	Other	Critical limb ischaemia	TF	lncRNA	ENSG00000100644	NA	ENSG00000266835	GRCh38_18:3466250-3478978	3091	100505592	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LINC01540	[Long non-coding RNA GAPLINC promotes angiogenesis by regulating miR-211 under hypoxia in human umbilical vein endothelial cells.] We found that hypoxia and hypoxia-inducible factor 1alpha (HIF-1alpha) increased the expression of GAPLINC in HUVEC cells. Moreover, GAPLINC overexpression down-regulated miR-211 and up-regulated Bcl2 protein expression.	31589383	RID03183	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(SKCM);DATA(GSE38495)
Liver cancer	HULC	RAB11A	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-372-3p)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000103769	NA	728655	8766	HCCAT1|LINC00078|NCRNA00078	YL8	[Long non-coding RNA highly up-regulated in liver cancer promotes exosome secretion.]HULC expression in serum exosomes of patients with HCC was higher than that in serum exosomes of healthy controls, and HULC levels were higher in liver cancer tissues than in tumor adjacent tissues. The expression of HULC in serum exosomes and liver cancer tissues correlated with the tumor-node-metastasis (TNM) classification, and HULC expression in tissues correlated with that in serum exosomes. Upregulation of HULC promoted HCC cell growth and invasion and repressed apoptosis. Notably, it also facilitated the secretion of exosomes from HCC cells. Moreover, qPCR assays showed that HULC repressed microRNA-372-3p (miR-372-3p) expression. We also identified Rab11a as a downstream target of miR-372-3p. dual-luciferase reporter assays suggested that miR-372-3p could directly bind both HULC and Rab11a.Conclusion: Our findings illustrate the importance of the HULC/miR-372-3p/Rab11a axis in HCC and provide new insights into the molecular mechanism regulating the secretion of exosomes from HCC cells.	31558873	RID03184	ceRNA or sponge	metastasis		UP(LIHC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Non-small cell lung cancer	CASC11	FOXO3	positively-E	western blot;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-498)	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000118689	NA	100270680	2309	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	AF6q21|FKHRL1|FOXO2|FOXO3A	[The positive feedback loop FOXO3/CASC11/miR-498 promotes the tumorigenesis of non-small cell lung cancer.]The positive feedback loop FOXO3/CASC11/miR-498 promotes the tumorigenesis of non-small cell lung cancer.An increasing number of studies have indicated that long noncoding RNAs (lncRNAs) are involved in the regulation of non-small-cell lung cancer (NSCLC). Nevertheless, there are still numerous undiscovered mechanisms underlying this molecular regulation. Here, the results illustrated that CASC11 is overexpressed in NSCLC tumor tissues and cell lines, which is closely related to the clinical features of NSCLC and poor survival. In functional experiments, CASC11 was shown to promote proliferation and cycle progression and enhance NSCLC tumorigenesis. In mechanical investigations, CASC11 was shown to target the miR-498/FOXO3 axis via a canonical competing endogenous RNA (ceRNA). In return, the transcription factor FOXO3 targets the CASC11 promoter region, thereby accelerating its transcription. Our findings demonstrate a crucial role for CASC11 as an oncogene in promoting NSCLC. These results reveal that CASC11 might be a potential therapeutic target for NSCLC.	31537383	RID03185	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE51827,GSE86978)
Open-angle glaucoma	RP11-820	MYOD1	positively-E	western blot;luciferase reporter assay;ChIP	upregulation	qRT-PCR;microarray	NA	NA	oxidative stress(+)	ceRNA(miR-3178)	binding/interaction	NA	NA	NA	NA	Nervous system disease	Glaucoma	lncRNA	TF	NA	NA	ENSG00000129152	NA	NA	4654	NA	MYF3|MYOD|MYODRIF|PUM|bHLHc1	[Long non-coding RNA RP11-820 promotes extracellular matrix production via regulating miR-3178/MYOD1 in human trabecular meshwork cells.]Our results revealed that lncRNA-RP11-820 was significantly upregulated under oxidative stress in HTMCs. Further investigation revealed that lncRNA-RP11-820 directly binds miR-3178, through which the expression of MYOD1 is regulated. Importantly, MYOD1 can transcriptionally activate ECM genes in HTMCs, in complex with STAT3. Taken together, our data established that oxidative stress-induced lncRNA-RP11-820 plays a key role in regulating the miR-3178/MYOD1/ECM axis in HTMCs. These findings further elucidate the pathogenic mechanism and provide a novel therapeutic target relevant to POAG.	31495061	RID03186	ceRNA or sponge	NA		
Coronary artery disease	CHROMR	miR-27b	negatively-F	ChIP;bioinformatics;western blot;RNAi	downregulation	qPCR	NA	NA	metabolic process(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000223960	GRCh38_2:178413635-178440243	NA	NA	101927027	NA	CHROME|PRKRA-AS1	NA	[The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.]we show that CHROME promotes cholesterol efflux and high-density lipoprotein (HDL) biogenesis by curbing the actions of aset of functionally related microRNAs that repress genes in those pathways. CHROME knockdown in human hepatocytes and macrophages increases the levels of miR-27b, miR-33a, miR-33b and miR-128, thereby reducing the expression of their overlapping target gene networks and associated biological functions. In particular, cells that lack CHROME show reduced expression of ABCA1, which regulates cholesterol efflux and nascent HDL particle formation. Using gain- and loss-of-function approaches, we show that CHROME promotes cholesterol efflux and HDL biogenesis by curbing the actions of a set of functionally related microRNAs that repress genes in those pathways	31410392	RID03187	expression association	NA		
Coronary artery disease	CHROMR	miR-33a	negatively-F	ChIP;bioinformatics;western blot;RNAi	downregulation	qPCR	NA	NA	metabolic process(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000223960	GRCh38_2:178413635-178440243	NA	NA	101927027	NA	CHROME|PRKRA-AS1	NA	[The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.]we show that CHROME promotes cholesterol efflux and high-density lipoprotein (HDL) biogenesis by curbing the actions of aset of functionally related microRNAs that repress genes in those pathways. CHROME knockdown in human hepatocytes and macrophages increases the levels of miR-27b, miR-33a, miR-33b and miR-128, thereby reducing the expression of their overlapping target gene networks and associated biological functions. In particular, cells that lack CHROME show reduced expression of ABCA1, which regulates cholesterol efflux and nascent HDL particle formation. Using gain- and loss-of-function approaches, we show that CHROME promotes cholesterol efflux and HDL biogenesis by curbing the actions of a set of functionally related microRNAs that repress genes in those pathways	31410392	RID03188	expression association	NA		
Coronary artery disease	CHROMR	MIR33B	negatively-F	ChIP;bioinformatics;western blot;RNAi	downregulation	qPCR	NA	NA	metabolic process(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000223960	GRCh38_2:178413635-178440243	ENSG00000207839	NA	101927027	693120	CHROME|PRKRA-AS1	MIRN33B|hsa-mir-33b|mir-33b	[The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.]we show that CHROME promotes cholesterol efflux and high-density lipoprotein (HDL) biogenesis by curbing the actions of aset of functionally related microRNAs that repress genes in those pathways. CHROME knockdown in human hepatocytes and macrophages increases the levels of miR-27b, miR-33a, miR-33b and miR-128, thereby reducing the expression of their overlapping target gene networks and associated biological functions. In particular, cells that lack CHROME show reduced expression of ABCA1, which regulates cholesterol efflux and nascent HDL particle formation. Using gain- and loss-of-function approaches, we show that CHROME promotes cholesterol efflux and HDL biogenesis by curbing the actions of a set of functionally related microRNAs that repress genes in those pathways	31410392	RID03189	expression association	NA		
Coronary artery disease	CHROMR	miR-128	negatively-F	ChIP;bioinformatics;western blot;RNAi	downregulation	qPCR	NA	NA	metabolic process(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000223960	GRCh38_2:178413635-178440243	NA	NA	101927027	NA	CHROME|PRKRA-AS1	NA	[The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.]we show that CHROME promotes cholesterol efflux and high-density lipoprotein (HDL) biogenesis by curbing the actions of aset of functionally related microRNAs that repress genes in those pathways. CHROME knockdown in human hepatocytes and macrophages increases the levels of miR-27b, miR-33a, miR-33b and miR-128, thereby reducing the expression of their overlapping target gene networks and associated biological functions. In particular, cells that lack CHROME show reduced expression of ABCA1, which regulates cholesterol efflux and nascent HDL particle formation. Using gain- and loss-of-function approaches, we show that CHROME promotes cholesterol efflux and HDL biogenesis by curbing the actions of a set of functionally related microRNAs that repress genes in those pathways	31410392	RID03190	expression association	NA		
Coronary artery disease	CHROMR	ABCA1	positively-E	ChIP;bioinformatics;western blot;RNAi	downregulation	qPCR	NA	NA	metabolic process(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000223960	GRCh38_2:178413635-178440243	ENSG00000165029	NA	101927027	19	CHROME|PRKRA-AS1	ABC1|HDLDT1|TGD	[The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.]we show that CHROME promotes cholesterol efflux and high-density lipoprotein (HDL) biogenesis by curbing the actions of aset of functionally related microRNAs that repress genes in those pathways. CHROME knockdown in human hepatocytes and macrophages increases the levels of miR-27b, miR-33a, miR-33b and miR-128, thereby reducing the expression of their overlapping target gene networks and associated biological functions. In particular, cells that lack CHROME show reduced expression of ABCA1, which regulates cholesterol efflux and nascent HDL particle formation. Using gain- and loss-of-function approaches, we show that CHROME promotes cholesterol efflux and HDL biogenesis by curbing the actions of a set of functionally related microRNAs that repress genes in those pathways	31410392	RID03191	expression association	NA		UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oxidative damage	H19	TDG	positively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell viability(-);cell proliferation(-);apoptosis process(-)	ceRNA(miR-29a)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Oxidative damage	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000139372	NA	283120	6996	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	[lncRNA H19 contributes to oxidative damage repair in the early age-related cataract by regulating miR-29a/TDG axis.]We found that lncRNA H19 and TDG were highly expressed while miR-29a was down-regulated in the three types of early ARC and HLECs exposed to ultraviolet irradiation, compared to respective controls. lncRNA H19 knockdown aggravated oxidative damage, reduced cell viability and proliferation, and promoted apoptosis in HLECs, while lncRNA H19 overexpression led to opposite effects in HLECs. Mechanistically, miR-29a bound TDG 3'UTR to repress TDG expression. lncRNA H19 up-regulated the expression of TDG by repressing miR-29a because it acted as ceRNA through sponging miR-29a. In conclusion, the interaction among lncRNA H19, miR-29a and TDG is involved in early ARC. lncRNA H19 could be a useful marker of early ARC and oxidative damage repair pathway of lncRNA H19/miR-29a/TDG may be a promising target for the treatment of ARC.	31282110	RID03192	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cancer	EMSLR	E2F1	positively-E	RNA pull-down assay;ChIP	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000232445	GRCh38_7:101308270-101314800	ENSG00000101412	NA	101927746	1869	EMS	RBBP3|RBP3	[Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.]we report the long noncoding RNA (lncRNA) E2F1 messenger RNA (mRNA) stabilizing factor (EMS) as a direct c-Myc transcriptional target. EMS functions as an oncogenic molecule by promoting G1/S cell cycle progression. Mechanistically, EMS cooperates with the RNA binding protein RALY to stabilize E2F1 mRNA, and thereby increases E2F1 expression. Furthermore, EMS is able to connect c-Myc to cell cycle control and tumorigenesis via modulating E2F1 mRNA stability.	31262817	RID03193	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cancer	MYC	EMSLR	positively-F	RNA pull-down assay;ChIP	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell cycle(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000232445	GRCh38_7:101308270-101314800	4609	101927746	bHLHe39|c-Myc|MYCC	EMS	[Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.]we report the long noncoding RNA (lncRNA) E2F1 messenger RNA (mRNA) stabilizing factor (EMS) as a direct c-Myc transcriptional target. EMS functions as an oncogenic molecule by promoting G1/S cell cycle progression. Mechanistically, EMS cooperates with the RNA binding protein RALY to stabilize E2F1 mRNA, and thereby increases E2F1 expression. Furthermore, EMS is able to connect c-Myc to cell cycle control and tumorigenesis via modulating E2F1 mRNA stability.	31262817	RID03194	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Cancer	EMSLR	RALY	positively-F	RNA pull-down assay;ChIP	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000232445	GRCh38_7:101308270-101314800	ENSG00000125970	NA	101927746	22913	EMS	HNRPCL2|P542	[Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.]we report the long noncoding RNA (lncRNA) E2F1 messenger RNA (mRNA) stabilizing factor (EMS) as a direct c-Myc transcriptional target. EMS functions as an oncogenic molecule by promoting G1/S cell cycle progression. Mechanistically, EMS cooperates with the RNA binding protein RALY to stabilize E2F1 mRNA, and thereby increases E2F1 expression. Furthermore, EMS is able to connect c-Myc to cell cycle control and tumorigenesis via modulating E2F1 mRNA stability.	31262817	RID03195	expression association	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Myocardial infarction	MALAT1	miR-144-3p	negatively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	[Long noncoding RNA MALAT1 promotes cardiomyocyte apoptosis after myocardial infarction via targeting miR-144-3p.]Our results demonstrated that the expression of MALAT1 has a higher level, while miR-144 expression significantly reduced in myocardial tissue after MI and also in left anterior descending (LAD)-ligation mice. This result was confirmed in vitro studies in HL-1 cardiomyocytes followed with hypoxia/reoxygenation. In addition, overexpression of MALAT1 by MALAT1-pcDNA injection into the mice with LAD increased myocardial apoptosis in vivo, while this effect was attenuated by miR-144 mimic. Bioinformatics analysis exhibits that 3'-UTR of MALAT1 is targeted to the miR-144-3p. Up-regulation miR-144 blunted the hypoxia- or MALAT1-induced cell apoptosis. In conclusion, the expression of MALAT1 was increased, whereas miR-144 expression was down-regulated in the myocardium after AMI. MALAT1 up-regulation plays a critical role in promoting cardiomyocytes apoptosis via targeting miR-144.	31227612	RID03196	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung adenocarcinoma	MALAT1	SMAD4	positively-E	western blot;luciferase reporter assay;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-26a)	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141646	NA	378938	4089	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DPC4|MADH4	[Te aim of the present study was to characterize whether the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/miR-26a/Smad4 axis is involved in epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs).]. In addition, upregulation of MALAT1 and downregulation of miR-26a were detected in human posterior capsule opacifcation (PCO) attached LECs and the LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR(qRT-PCR. Next, our results showed that TGF--2 induces overexpression of EMT markers in primary HLECs via a MALAT1-dependent mechanism. Te mechanism is that MALAT1 negatively regulates miR-26a and miR-26a directly targets Smad4 by luciferase reporter assays and RNA-binding protein immunoprecipitation assay. In summary, TGF--2 induces MALAT1 overexpression, which in turn MALAT1 acts as a ceRNA targeting Smad4 by binding miR-26a and promotes the progression of EMT of LECs	31143769	RID03197	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Liver cancer	HOXA11-AS	STAT3	positively-E	RNA pull-down assay;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-15a-3p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000168610	NA	221883	6774	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	APRF	[HOXA11-AS regulates JAK-STAT pathway by miR-15a-3p/STAT3 axis to promote the growth and metastasis in liver cancer.]	31099097	RID03198	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	LINC00339	ROCK1	positively-E	RNA pull-down;western blot;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-152)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000067900	NA	29092	6093	HSPC157|NCRNA00339	p160ROCK	[LINC00339 regulates ROCK1 by miR-152 to promote cell proliferation and migration in hepatocellular carcinoma.]The LINC00339 expression in HCC cancer cells (HUH7, HepG2, HUH-6, and SK-Hep-1) and tissues was assessed by quantitative real-time polymerase chain reaction (qRT-PCRThe RNA pull-down assay, luciferase reporters assay, qRT-PCR and western blot were performed to explore and confirm the interaction between LINC00339 and miR-152, between miR-152 and ROCK1	31081143	RID03199	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	DLEU1-AS1	MIR506	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	NA	NA	ENSG00000207731	NA	103689915	574511	LINC01308	MIRN506|hsa-mir-506|mir-506	[LINC01308 accelerates the malignant progression of ovarian cancer by binding to miRNA-506.]Relative level of LINC01308 in 28 pairs of OC tissues and paracancerous tissues was determined by quantitative Real-time polymerase chain reaction (qRT-PCR.Target downstream of LINC01308 was verified by dual-luciferase reporter gene assay.LINC01308 was highly expressed in OC tissues relative to controls. MiRNA-506 was found to be the target gene of LINC01308, and its level was negatively regulated by LINC01308 in OC tissues. Finally, we found that miRNA-506 knockdown reversed the regulatory effect of LINC01308 on the migratory and invasive abilities of OC cells.  OC patients with high-level LINC01308 had higher rates of lymph node metastasis and distant metastasis, and lower survival rate compared with those with low level	31081077	RID03200	expression association	metastasis		
Pulmonary disease	COPDA1	MS4A1	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Reproductive system disease	Lung disease	lncRNA	PCG	ENSG00000282430	GRCh38_CHR_HSCHR14_3_CTG1:105648695-105649828	ENSG00000156738	NA	115253418	931	NA	B1|Bp35|CD20|FMC7	[Long Noncoding RNA COPDA1 Promotes Airway Smooth Muscle Cell Proliferation in Chronic Obstructive Pulmonary Disease.]A number of variational lncRNAs were found in the comparison of nonsmokers, smokers, and smokers with COPD. GO and KEGG analyses indicated that smoking was involved in the activation of cytokines and the cell cycle, which is associated with COPD. According to the lncRNA-mRNA co-expressingnetwork and enrichment analysis, COPDA1 and one of its target gene MS4A1 were investigated, we discovered the expression of MS4A1 was closely associated with lncRNA COPDA1 expression in HBSMCs. Further study showed that lncRNA COPDA1 upregulated the expression of MS4A1 to increase store-operated calcium entry (SOCE) in the HBSMCs, resulting in the promotion of the proliferation of smooth muscle cells, as well as the airway remodeling. Discussion: COPDA1 might be involved in the regulation of certain signaling pathways in COPD and promote the proliferation of HBSMCs and might also be involved in facilitating airway remodeling.	31050548	RID03201	expression association	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	UCA1	KRAS	positively-E	luciferase reporter assay;miRanda;RNAi	upregulation	microarray	TCGA	NA	cell proliferation(+);cell growth(+)	ceRNA(miR-590-3p)	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000133703	NA	652995	3845	CUDR|LINC00178|onco-lncRNA-36|UCAT1	K-Ras4B|KRAS1|KRAS2	[The UCA1/KRAS axis promotes human pancreatic ductal adenocarcinoma stem cell properties and tumor growth.]we found that UCA1 overexpression increased the activity and expression of oncogenic KRAS. Mechanistically, upregulated UCA1 increased phospho-KRAS protein levels by interacting with hnRNPA2B1, and KRAS facilitated high cytoplasmic accumulation of hnRNPA2B1. Additionally, we identified that UCA1 functioned as a competing endogenous RNA (ceRNA) to increase the expression of KRAS via sponging miR-590-3p, and in turn, KRAS promoted UCA1 expression. Collectively, these findings suggest that the UCA1-KRAS axis plays a crucial role in PDAC progression and that UCA1 may serve as a target for new PDAC therapies.To determine the clinical relevance of UCA1 expression, we first used The Cancer Genome Atlas (TCGA) database to analyze the mRNA levels of UCA1 and found that UCA1 was highly expressed in PDAC tumor specimens compared to UCA1 expression in normal tissue (Figure 1A).To seek insight into the potential molecular mechanism connecting UCA1 with KRAS, bioinformatics analysis (miRanda; http://www.micro-RNA.org/) was applied to predict potential miRNAs targeting UCA1 and binding to the KRAS 3 UTR (Figure 7D). Next, RIP was performed to identify which candidate miRNAs were involved in the interaction with UCA1. The involvement of miR-1271, miR-143, miR-193a-3p, and miR-590-3p was confirmed, as shown in Figure S2B. Next, we found that UCA1 and KRAS have a potential miR-590-3p binding site by bioinformatics prediction (Figure 7E). In addition, miR-590-3p expression was lower in UCA1--overexpressing cells than in control cells (Figure 7F). In contrast, UCA1 knockdown resulted in the opposite effects in Mpanc96 and HPAF-II cells (Figure 7G). Moreover, miR-590-3p overexpression resulted in decreased expression of UCA1, suggesting that UCA1 negatively regulates miR-590-3p expression (Figure 7H). To clarify that the mechanism of miR-590-3p action on UCA1 is specific, we performed a luciferase activity assay to detect the potential association between UCA1 and miR-590-3p. The luciferase reporter assay revealed that the luciferase activity was significantly lower in the wild-type UCA1 group than in the vector control group, whereas the mutated UCA1 group did not show a significant response to miR-590-3p, indicating that UCA1 can directly bind to miR-590-3p.Moreover, the bioinformatics analysis and luciferase activity assay showed that miR-590-3p significantly reduced the luciferase activity of the 3'UTR-KRAS-WT reporter gene vector, but no significant change was observed for the 3'UTR- KRAS-MUT vector (Figure 8C and -and8D).8D). UCA1-WT increased the mRNA and protein levels of KRAS in PaTu8988 and PANC-1 cells compared with these levels in the control group but UCA1-MUT1 had no significant effect (Figure 8E and -and8F).8F). Taken together, these data suggested that UCA1 modulates KRAS expression by sponging miR-590-3p.	30949406	RID03202	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Pancreatic ductal adenocarcinoma	KRAS	UCA1	positively-E	luciferase reporter assay;miRanda;RNAi	upregulation	microarray	TCGA	NA	cell proliferation(+);cell growth(+)	NA	association	protein-RNA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000133703	NA	ENSG00000214049	GRCh38_19:15828206-15836328	3845	652995	K-Ras4B|KRAS1|KRAS2	CUDR|LINC00178|onco-lncRNA-36|UCAT1	[The UCA1/KRAS axis promotes human pancreatic ductal adenocarcinoma stem cell properties and tumor growth.]we found that UCA1 overexpression increased the activity and expression of oncogenic KRAS. Mechanistically, upregulated UCA1 increased phospho-KRAS protein levels by interacting with hnRNPA2B1, and KRAS facilitated high cytoplasmic accumulation of hnRNPA2B1. Additionally, we identified that UCA1 functioned as a competing endogenous RNA (ceRNA) to increase the expression of KRAS via sponging miR-590-3p, and in turn, KRAS promoted UCA1 expression. Collectively, these findings suggest that the UCA1-KRAS axis plays a crucial role in PDAC progression and that UCA1 may serve as a target for new PDAC therapies.To determine the clinical relevance of UCA1 expression, we first used The Cancer Genome Atlas (TCGA) database to analyze the mRNA levels of UCA1 and found that UCA1 was highly expressed in PDAC tumor specimens compared to UCA1 expression in normal tissue (Figure 1A).To seek insight into the potential molecular mechanism connecting UCA1 with KRAS, bioinformatics analysis (miRanda; http://www.micro-RNA.org/) was applied to predict potential miRNAs targeting UCA1 and binding to the KRAS 3 UTR (Figure 7D). Next, RIP was performed to identify which candidate miRNAs were involved in the interaction with UCA1. The involvement of miR-1271, miR-143, miR-193a-3p, and miR-590-3p was confirmed, as shown in Figure S2B. Next, we found that UCA1 and KRAS have a potential miR-590-3p binding site by bioinformatics prediction (Figure 7E). In addition, miR-590-3p expression was lower in UCA1--overexpressing cells than in control cells (Figure 7F). In contrast, UCA1 knockdown resulted in the opposite effects in Mpanc96 and HPAF-II cells (Figure 7G). Moreover, miR-590-3p overexpression resulted in decreased expression of UCA1, suggesting that UCA1 negatively regulates miR-590-3p expression (Figure 7H). To clarify that the mechanism of miR-590-3p action on UCA1 is specific, we performed a luciferase activity assay to detect the potential association between UCA1 and miR-590-3p. The luciferase reporter assay revealed that the luciferase activity was significantly lower in the wild-type UCA1 group than in the vector control group, whereas the mutated UCA1 group did not show a significant response to miR-590-3p, indicating that UCA1 can directly bind to miR-590-3p.Moreover, the bioinformatics analysis and luciferase activity assay showed that miR-590-3p significantly reduced the luciferase activity of the 3'UTR-KRAS-WT reporter gene vector, but no significant change was observed for the 3'UTR- KRAS-MUT vector (Figure 8C and -and8D).8D). UCA1-WT increased the mRNA and protein levels of KRAS in PaTu8988 and PANC-1 cells compared with these levels in the control group but UCA1-MUT1 had no significant effect (Figure 8E and -and8F).8F). Taken together, these data suggested that UCA1 modulates KRAS expression by sponging miR-590-3p.	30949406	RID03203	expression association	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD);DATA(GSE40174)
Pancreatic ductal adenocarcinoma	UCA1	HNRNPA2B1	positively-F	RIP;catRAPID	upregulation	microarray	TCGA	NA	cell proliferation(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000122566	NA	652995	3181	CUDR|LINC00178|onco-lncRNA-36|UCAT1	HNRPA2B1	[The UCA1/KRAS axis promotes human pancreatic ductal adenocarcinoma stem cell properties and tumor growth.]we found that UCA1 overexpression increased the activity and expression of oncogenic KRAS. Mechanistically, upregulated UCA1 increased phospho-KRAS protein levels by interacting with hnRNPA2B1, and KRAS facilitated high cytoplasmic accumulation of hnRNPA2B1. Additionally, we identified that UCA1 functioned as a competing endogenous RNA (ceRNA) to increase the expression of KRAS via sponging miR-590-3p, and in turn, KRAS promoted UCA1 expression. Collectively, these findings suggest that the UCA1-KRAS axis plays a crucial role in PDAC progression and that UCA1 may serve as a target for new PDAC therapies.To determine the clinical relevance of UCA1 expression, we first used The Cancer Genome Atlas (TCGA) database to analyze the mRNA levels of UCA1 and found that UCA1 was highly expressed in PDAC tumor specimens compared to UCA1 expression in normal tissue (Figure 1A).To seek insight into the potential molecular mechanism connecting UCA1 with KRAS, bioinformatics analysis (miRanda; http://www.micro-RNA.org/) was applied to predict potential miRNAs targeting UCA1 and binding to the KRAS 3 UTR (Figure 7D). Next, RIP was performed to identify which candidate miRNAs were involved in the interaction with UCA1. The involvement of miR-1271, miR-143, miR-193a-3p, and miR-590-3p was confirmed, as shown in Figure S2B. Next, we found that UCA1 and KRAS have a potential miR-590-3p binding site by bioinformatics prediction (Figure 7E). In addition, miR-590-3p expression was lower in UCA1--overexpressing cells than in control cells (Figure 7F). In contrast, UCA1 knockdown resulted in the opposite effects in Mpanc96 and HPAF-II cells (Figure 7G). Moreover, miR-590-3p overexpression resulted in decreased expression of UCA1, suggesting that UCA1 negatively regulates miR-590-3p expression (Figure 7H). To clarify that the mechanism of miR-590-3p action on UCA1 is specific, we performed a luciferase activity assay to detect the potential association between UCA1 and miR-590-3p. The luciferase reporter assay revealed that the luciferase activity was significantly lower in the wild-type UCA1 group than in the vector control group, whereas the mutated UCA1 group did not show a significant response to miR-590-3p, indicating that UCA1 can directly bind to miR-590-3p.Moreover, the bioinformatics analysis and luciferase activity assay showed that miR-590-3p significantly reduced the luciferase activity of the 3'UTR-KRAS-WT reporter gene vector, but no significant change was observed for the 3'UTR- KRAS-MUT vector (Figure 8C and -and8D).8D). UCA1-WT increased the mRNA and protein levels of KRAS in PaTu8988 and PANC-1 cells compared with these levels in the control group but UCA1-MUT1 had no significant effect (Figure 8E and -and8F).8F). Taken together, these data suggested that UCA1 modulates KRAS expression by sponging miR-590-3p.	30949406	RID03204	interact with protein	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Osteosarcoma	NORAD	NAMPT	positively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(MiR-26a-5p)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000105835	NA	647979	10135	LINC00657	PBEF|PBEF1	[Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells]Results: NAMPT and NORAD expressions were increased in OS tissue samples, while miR-26a-5p expression was decreased. Functionally, NORAD functions as a ceRNA of miR-136-5p to competitively target NAMPT. Furthermore, miR-26a-5p overexpression inhibited viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating NAMPT along with change the expressions of apoptosisrelated molecules. NORAD overexpression promoted viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating MiR-26a-5p along with changes of the expressions of apoptosis-related molecules. Conclusion: LncRNA NORAD, serving as a ceRNA of miR-26a-5p, promoted proliferation and apoptosis resistance of U2OS cells by upregulation of NAMPT.	30940661	RID03205	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	TUG1	HIF1A	positively-E	miRcode;qRT-PCR;RNAi;RIP;RNA pull-down assay;luciferase reporter assay;TargetScan	upregulation	qRT-PCR	NA	NA	cell metastasis(+);angiogenesis(+);cell proliferation(+)	ceRNA(miR-143-5p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000100644	NA	55000	3091	LINC00080|NCRNA00080|TI-227H	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	[Long non-coding RNA Taurine upregulated gene 1 promotes osteosarcoma cell metastasis by mediating HIF-1alpha via miR-143-5p.]TUG1 was significantly upregulated in OS tissues.quantitative real-time PCR was performed to evaluate TUG1 expression in OS tissues compared with normal ones. We found that TUG1 expression was significantly higher in OS tissues.Bioinformatics analysis (miRcode, http://www.mircode.org/index.php) was used to screen potential target binding miRNAs of TUG1 in OS. Among potential candidates, miR-143-5p was frequently reported as a tumour suppressor in OS16 23. The putative complementary sequences between TUG1 and miR-143-5p are illustrated in Fig. 3a. Subsequently, we performed a qRT-PCRassay to further assess the association between miR-143-5p and TUG1, which suggested that miR-143-5p was downregulated in OS tissues (Fig. 3b, P < 0.05). TUG1 was also negatively correlated with miR-143-5p in OS tissues (Fig. 3c, P < 0.05). Additionally, after assessing effects of si-TUG1 on silencing TUG1 expression (Fig. 3d, P < 0.05), we found that silencing of TUG1 via si-TUG1 transfection could lead to increased miR-143-5p accumulation compared with control groups (Fig. 3e, P < 0.05). However, upregulating or downregulating miR-143-5p had no influence on TUG1 expression (Fig. 3f, P > 0.05). To further explore whether the binding site was functional, we cloned the fragment, including the binding site as predicted by miRcode (Fig. 3a), into the pmiR-Glo vector as wild-type (pmiR-GLo-TUG1-wt) and mutated-type (pmiR-GLo-TUG1-wt). As shown in Fig. 3g, h, co-transfection of pmiR-GLo-TUG1-wt and miR-143-5p mimics greatly reduced luciferase activity compared with the pmiR-GLo-TUG1-wt + miR-NC group. Conversely, mutation of the miR-143-5p-binding site within TUG1 abrogated the inhibitory effect of miR-143-5p mimics on the reporter gene expression. Results from the RIP assay showed that TUG1 was preferentially enriched in Ago2-containing beads in OS cells (Fig. 3i), indicating that TUG1 is likely in the miR-143-5p RISC complex. Results from the miRNA pull-down demonstrated that miR-143-5p pulled down TUG1. However, miR-143-5p-mut with the mutated binding site of TUG1 failed to pull-down TUG1 (Fig. 3j), indicating that the recognition of miR-143-5p to TUG1 is in a sequence-specific manner. Together, our findings confirmed that miR-143-5p is regulated by TUG1 in OS cells through direct binding. Bioinformatic analysis (TargetScan, http://www.targetscan.org; miRDB, http://www.mirdb.org) was performed to screen potential target genes of miR-143-5p. Among the overlapped potential candidates, HIF-1alpha was chosen as a target gene for its association with OS progression as reported24 26. As indicated in Fig. 4a, the putative binding sites between HIF-1alpha and miR-143-5p were predicted by TargetScan and miRDB. dual-luciferase reporter assay was performed to determine the negative effect of miR-143-5p on the HIF-1alpha 3 UTR. The results showed that co-transfection of pmiR-Glo-HIF-1-alpha wild-type and miR-143-5p mimics greatly reduced luciferase activity compared with the HIF-1alpha-wt + miR-143-5p NC group, whereas mutation of the miR-143-5p-binding site within HIF-1alpha abrogated the inhibitory effect of miR-143-5p mimics on the reporter gene expression (Fig. 4b, P < 0.05). Inhibition of miR-143-5p significantly increased HIF-1alpha mRNA and protein expression compared with negative control siRNAs; however, silencing of TUG1 inhibited HIF-1alpha expression. Additionally, transfection with si-TUG1 could significantly reverse the effect of miR-143-5p inhibitors on HIF-1alpha mRNA and protein expression (Fig. 4c, d, P < 0.05). To better establish the direct link between the TUG-1/miR-143-5p axis and HIF-1alpha, the effect of upregulated TUG-1 and miR-143-5p on HIF-1alpha expression was investigated. Upregulation of miR-143-5p could significantly impair HIF-1alpha mRNA and protein expression compared with the negative control. In contrast, increased TUG1 promoted HIF-1alpha expression, which was reversed by the miR-143-5p mimics at the mRNA or protein levels (Fig. 4e, f, P < 0.05). Taken together, TUG1 could serve as a sponge to competitively interact with miR-143-5p and reverse miR-143-5p-induced inhibition of HIF-1alpha expression.	30911001	RID03206	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteosarcoma	TGFB1	TUG1	positively-E	RANi	upregulation	qRT-PCR	NA	NA	cell metastasis(+);angiogenesis(+);cell proliferation(+)	ceRNA(miR-143-5p)	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000253352	GRCh38_22:30969245-30979395	7040	55000	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LINC00080|NCRNA00080|TI-227H	[Long non-coding RNA Taurine upregulated gene 1 promotes osteosarcoma cell metastasis by mediating HIF-1alpha via miR-143-5p.]TUG1 was significantly upregulated in OS tissues.quantitative real-time PCR was performed to evaluate TUG1 expression in OS tissues compared with normal ones. We found that TUG1 expression was significantly higher in OS tissues.As shown in Fig. 2f, an illustration demonstrated CAF transfected si-TGF-beta co-culture with OS cells for 24 h. Following, TUG1 expression in OS cells was detected. With TGF-beta expression modification confirmed, we detected TUG1 expression in both 143B-CAFs-siTGF-beta and U2OS-CAFs-siTGF-beta as much lower than in negative groups (Fig. 2g, h, P < 0.05). Additionally, 143B and U2OS cells treated with recombinant TGF-beta protein expressed more TUG1 than 143B and U2OS cells alone (Fig. 2g, h, P < 0.05). Thus, CAFs-derived TGF-beta promotes TUG1 expression in OS cells.	30911001	RID03207	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Parkinson's disease	HOTAIR	RAB3IP	positively-E	luciferase reporter assay;RIP;bioinformatics	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-126-5p)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000127328	NA	100124700	117177	HOXC-AS4|HOXC11-AS1|NCRNA00072	FLJ22548|RABIN3|RABIN8	[LncRNA HOTAIR targets miR-126-5p to promote the progression of Parkinson's disease through RAB3IP.] the CCK-8 assay and flow cytometric analysis indicated that the knockdown of HOTAIR and RAB3IP and the overexpression of miR-126-5p significantly increased cell proliferation and reduced apoptosis in PD cells. Furthermore, the results of in vivo experiments suggested that knockdown of HOTAIR expression increased the number of TH-positive cells and the number of alpha-synuclein-positive cells decreased while reducing the apoptosis rate among DA neurons. Our study confirmed that HOTAIR promotes PD progression by regulating miR-126-5p and RAB3IP in a ceRNA-dependent manner and further clarified how HOTAIR works in PD.Bioinformatics analysis was utilized to determine the potential downstream targets of HOTAIR in PD. Luciferase assay and the RNA Binding Protein Immunoprecipitation (RIP) assay were used to validate the existence of binding sites between competing endogenous RNAs (ceRNAs). Real-time quantitative polymerase chain reaction (qRT-PCR and western blot indicated that HOTAIR and RAB3IP increased while miR-126-5p decreased in PD cells and PD mice.	30738012	RID03208	ceRNA or sponge	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761)
Atherosclerosis	AC096664.3	PPARG	positively-E	RNA pull-down assay;RNAi;qRT-PCR;siRNA	upregulation	microarray;qRT-PCR	NA	NA	cholesterol homeostasis(+)	transcriptional regulation	regulation	RNA-protein	OX-LDL	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000221085	NA	ENSG00000132170	NA	NA	5468	NA	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARG5|PPARgamma	lncRNA AC096664.3 regulated ABCG1 through PPAR-. ABCG1 expression was decreased in VSMCs treated with LV-siRNA-AC096664.3	30938872	RID03209	transcriptional regulation	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Atherosclerosis	AC096664.3	ABCG1	positively-E	RNA pull-down assay;RNAi;qRT-PCR;siRNA	upregulation	microarray;qRT-PCR	NA	NA	cholesterol homeostasis(+)	NA	regulation	RNA-protein	OX-LDL	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000221085	NA	ENSG00000160179	NA	NA	9619	NA	ABC8|WHITE1	lncRNA AC096664.3 regulated ABCG1 through PPAR-. ABCG1 expression was decreased in VSMCs treated with LV-siRNA-AC096664.3	30938872	RID03210	expression association	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE51827,GSE75367,GSE86978,GSE41245)
Cerebral infarction	CDKN2B-AS1	BCL11A	positively-E	RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000119866	NA	100048912	53335	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	BCL11A-L|BCL11A-S|BCL11A-XL|CTIP1|EVI9|HBFQTL5|SMARCM1|ZNF856	qRT-PCRwas employed in order to determine the expression of CDKN2B-AS1 in lymphocytes, and the results revealed that the expression of CDKN2B-AS1 was increased in lymphocytes obtained from peripheral blood and CSF of patients with cerebral infarction compared with those of normal individuals These findings implied that CDKN2B-AS1 can suppress the expression of MAP4K1 through recruiting BCL11A.	30870006	RID03211	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cerebral infarction	CDKN2B-AS1	MAP4K1	negatively-E	qRT-PCR;RNAi;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000104814	NA	100048912	11184	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	HPK1	qRT-PCRwas employed in order to determine the expression of CDKN2B-AS1 in lymphocytes, and the results revealed that the expression of CDKN2B-AS1 was increased in lymphocytes obtained from peripheral blood and CSF of patients with cerebral infarction compared with those of normal individuals These findings implied that CDKN2B-AS1 can suppress the expression of MAP4K1 through recruiting BCL11A.	30870006	RID03212	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cancer	EPB41L4A-AS1	TP53	positively-E	qRT-PCR;luciferase reporter assay;ChIP	upregulation	microarray	TCGA;GSE44001	NA	glycolysis(+);glutamine metabolic process(+)	transcriptional regulation	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	TF	ENSG00000224032	GRCh38_5:112160526-112164818	ENSG00000141510	NA	114915	7157	C5orf26|NCRNA00219|TIGA1	LFS1|p53	We investigated the clinical significance of EPB41L4A-AS1 in human cancers. The low expression of EPB41L4A-AS1 was associated with poor survival in several cancer types, including cervix, liver, breast, bladder and other cancers.Together, these results suggested that EPB41L4A-AS1 expression was transcriptionally regulated by p53 and PGC-1alpha.	30796006	RID03213	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Cancer	EPB41L4A-AS1	HDAC2	positively-F	RNAi;RNA pull-down assay;FISH	upregulation	microarray	TCGA;GSE44001	NA	glycolysis(+);glutamine metabolic process(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000224032	GRCh38_5:112160526-112164818	ENSG00000196591	NA	114915	3066	C5orf26|NCRNA00219|TIGA1	KDAC2|RPD3|YAF1	These results demonstrated that EPB41L4A-AS1 interacted with HDAC2, EPB41L4A-AS1 knockdown enhanced the occupation of HDAC2 on VHL and VDAC1 promoters, and finally reducing VHL and VDAC1 expression via histone modification.	30796006	RID03214	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Cancer	EPB41L4A-AS1	NPM1	negatively-F	RNAi;RNA pull-down assay;FISH	upregulation	microarray	TCGA;GSE44001	NA	glycolysis(+);glutamine metabolic process(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000224032	GRCh38_5:112160526-112164818	ENSG00000181163	NA	114915	4869	C5orf26|NCRNA00219|TIGA1	B23|NPM	Interestingly, we found that knockdown of EPB41L4A-AS1 reduced the interaction between HDAC2 and NPM1, leading to the translocation of HDAC2 from nucleolus to nucleoplasm and discretely distributed in nucleoplasm	30796006	RID03215	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Atherosclerosis	MIAT	CD47	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-149-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000196776	NA	440823	961	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	IAP|MER6|OA3	Here we show that lncRNA myocardial infarction associated transcript (MIAT) was markedly elevated in the serum of patients with symptoms of vulnerable atherosclerotic plaque and the macrophages of necrotic cores in an advanced atherosclerosis mouse model. MIAT knockdown attenuated atherosclerosis progression, reduced necrotic core size, and increased plaque stability in vivo. Furthermore, MIAT knockdown promoted clearance of apoptotic cells by macrophages in vivo and in vitro. Mechanistic studies revealed that MIAT acted as a micro RNA (miRNA) sponge to positively modulate the expression of anti-phagocytic molecule CD47 through sponging miR-149-5p. Together, these findings identified a macrophage MIAT/miR-149-5p /CD47 pathway as a key factor in the development of necrotic atherosclerotic plaques.	30755588	RID03216	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842)
Atherosclerosis	MEG3	GARS1	positively-E	qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000106105	NA	55384	2617	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CMT2D|DSMAV|GARS|GlyRS|HMN5|HMN5A|SMAD1|SMAJI	In this study, we observed that downregulated lncRNA-MEG3 expression was inversely correlated with the microRNA-26a level in coronary artery disease tissues. The overexpression of lncRNA-MEG3 could inhibit VSMCs proliferation while facilitating apoptosis. Moreover, alteration in the miR-26a/Smad1 axis could antagonize this effect. Bioinformatic analysis indicated that lncRNA-MEG3 could interact with miR-26a via complementary binding sites. The enforced expression of lncRNA-MEG3 could reduce the level of miR-26a in VSMCs, while the expression of Smad1 increases. Further, the direct binding between lncRNA-MEG3 and miR-26a was confirmed via dual-luciferase reporter assay, which indicated that lnc-MEG3 could sponge miR-26a as a competing endogenous RNA.	30745534	RID03217	ceRNA or sponge	NA		
Osteonecrosis	AWPPH	RUNX2	positively-E	RT-qPCR;RNAi	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000124813	NA	NA	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	As presented in Fig. 1A, expression of lncRNA AWPPH in MSCs was significantly decreased in patients with non-traumatic ONFH compared with in healthy people The results demonstrated that AWPPH overexpression significantly promoted (P<0.05; Fig. 4A) and shRNA silencing significantly inhibited (P<0.05; Fig. 4B) the expression of Runx2 in hMSC-BM cells.The results of the present study suggest that AWPPH may inhibit the development of non-traumatic ONFH by promoting osteoblastic differentiation through the upregulation of Runx2 expression.	31853285	RID03218	transcriptional regulation	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pituitary adenoma	RPSAP52	ELAVL1	negatively-F	qRT-PCRIP	upregulation	microarray	NA	NA	cell cycle(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000241749	GRCh38_12:65758020-65826997	ENSG00000066044	NA	204010	1994	NA	Hua|HUR|MelG	RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression could contribute to the development of pituitary adenomas. We investigated the involvement of RPSAP52 in the modulation of the expression of cell cycle-related genes, such as p21Waf1/CIP, whose deregulation plays a critical role in pituitary cell transformation. We report that RPSAP52, interacting with the RNA binding protein HuR (human antigen R), favors the delocalization of miR-15a, miR-15b, and miR-16 on the cyclin-dependent kinase inhibitor p21Waf1/CIP1 that, accordingly, results in downregulation in pituitary adenomas. A RNA immunoprecipitation sequencing (RIPseq) analysis performed on cells overexpressing RPSAP52 identified 40 messenger RNAs (mRNAs) enriched in Argonaute 2 (AGO2) immunoprecipitated samples. Among them, we focused on GAS8 (growth arrest-specific protein 8) gene. Consistently, GAS8 expression was downregulated in all the analyzed pituitary adenomas with respect to normal pituitary and in RPSAP52-overepressing cells, supporting the role of RPSAP52 in addressing genes involved in growth inhibition and cell cycle arrest to miRNA-induced degradation. This study unveils another RPSAP52-mediated molecular mechanism in pituitary tumorigenesis. 	31831098	RID03219	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Pituitary adenoma	RPSAP52	MIR15A	negatively-F	qRT-PCRIP	upregulation	microarray	NA	NA	cell cycle(-)	sponge	binding/interaction	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	miRNA	ENSG00000241749	GRCh38_12:65758020-65826997	ENSG00000283785	NA	204010	406948	RPSA_17_1251	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression could contribute to the development of pituitary adenomas. We investigated the involvement of RPSAP52 in the modulation of the expression of cell cycle-related genes, such as p21Waf1/CIP, whose deregulation plays a critical role in pituitary cell transformation. We report that RPSAP52, interacting with the RNA binding protein HuR (human antigen R), favors the delocalization of miR-15a, miR-15b, and miR-16 on the cyclin-dependent kinase inhibitor p21Waf1/CIP1 that, accordingly, results in downregulation in pituitary adenomas. A RNA immunoprecipitation sequencing (RIPseq) analysis performed on cells overexpressing RPSAP52 identified 40 messenger RNAs (mRNAs) enriched in Argonaute 2 (AGO2) immunoprecipitated samples. Among them, we focused on GAS8 (growth arrest-specific protein 8) gene. Consistently, GAS8 expression was downregulated in all the analyzed pituitary adenomas with respect to normal pituitary and in RPSAP52-overepressing cells, supporting the role of RPSAP52 in addressing genes involved in growth inhibition and cell cycle arrest to miRNA-induced degradation. This study unveils another RPSAP52-mediated molecular mechanism in pituitary tumorigenesis. 	31831098	RID03220	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pituitary adenoma	RPSAP52	MIR15B	negatively-F	qRT-PCRIP	upregulation	microarray	NA	NA	cell cycle(-)	sponge	binding/interaction	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	miRNA	ENSG00000241749	GRCh38_12:65758020-65826997	ENSG00000207779	NA	204010	406949	RPSA_17_1251	MIRN15B|hsa-mir-15b|miR-15b	RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression could contribute to the development of pituitary adenomas. We investigated the involvement of RPSAP52 in the modulation of the expression of cell cycle-related genes, such as p21Waf1/CIP, whose deregulation plays a critical role in pituitary cell transformation. We report that RPSAP52, interacting with the RNA binding protein HuR (human antigen R), favors the delocalization of miR-15a, miR-15b, and miR-16 on the cyclin-dependent kinase inhibitor p21Waf1/CIP1 that, accordingly, results in downregulation in pituitary adenomas. A RNA immunoprecipitation sequencing (RIPseq) analysis performed on cells overexpressing RPSAP52 identified 40 messenger RNAs (mRNAs) enriched in Argonaute 2 (AGO2) immunoprecipitated samples. Among them, we focused on GAS8 (growth arrest-specific protein 8) gene. Consistently, GAS8 expression was downregulated in all the analyzed pituitary adenomas with respect to normal pituitary and in RPSAP52-overepressing cells, supporting the role of RPSAP52 in addressing genes involved in growth inhibition and cell cycle arrest to miRNA-induced degradation. This study unveils another RPSAP52-mediated molecular mechanism in pituitary tumorigenesis. 	31831098	RID03221	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pituitary adenoma	RPSAP52	miR-16	negatively-F	qRT-PCRIP	upregulation	microarray	NA	NA	cell cycle(-)	sponge	binding/interaction	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	miRNA	ENSG00000241749	GRCh38_12:65758020-65826997	NA	NA	204010	NA	RPSA_17_1251	NA	RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression could contribute to the development of pituitary adenomas. We investigated the involvement of RPSAP52 in the modulation of the expression of cell cycle-related genes, such as p21Waf1/CIP, whose deregulation plays a critical role in pituitary cell transformation. We report that RPSAP52, interacting with the RNA binding protein HuR (human antigen R), favors the delocalization of miR-15a, miR-15b, and miR-16 on the cyclin-dependent kinase inhibitor p21Waf1/CIP1 that, accordingly, results in downregulation in pituitary adenomas. A RNA immunoprecipitation sequencing (RIPseq) analysis performed on cells overexpressing RPSAP52 identified 40 messenger RNAs (mRNAs) enriched in Argonaute 2 (AGO2) immunoprecipitated samples. Among them, we focused on GAS8 (growth arrest-specific protein 8) gene. Consistently, GAS8 expression was downregulated in all the analyzed pituitary adenomas with respect to normal pituitary and in RPSAP52-overepressing cells, supporting the role of RPSAP52 in addressing genes involved in growth inhibition and cell cycle arrest to miRNA-induced degradation. This study unveils another RPSAP52-mediated molecular mechanism in pituitary tumorigenesis. 	31831098	RID03222	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Nasopharynx carcinoma	CCAT1	miR7-5p	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	RNA-RNA	Solamargine	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Mechanistically, we found that solamargine decreased lncRNA colon cancer-associated transcript-1 (CCAT1) and increased miR7-5p expression. There was a reciprocal interaction of CCAT1 and miR7-5p.Of note, there was no report demonstrating a direct links of CCAT1 and miR7-5p, thus, the detailed mechanism of this interaction required to be elucidated.	31823440	RID03223	transcriptional regulation	NA		
Osteoarthritis	XIST	TIMP-3	negatively-E	RIP;RNA pull-down assay;FISH;MS-PCR	upregulation	microarray	GSE51588	NA	cell autophagy(+)	DNA methylation	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	SXI1|XCE|XIST	NA	Collectively, lncRNA XIST raises collagen degradation in OA chondrocytes after tibial plateau fracture by accelerating the methylation of TIMP-3 promoter by recruiting DNA methyltransferase.	31815654	RID03224	epigenetic regulation	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Gallbladder cancer	GATA6-AS	MIR421	negatively-E	RT-qPCR	downregulation	RT-qPCR	NA	NA	cell invasion(-);cell migration(-)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	miRNA	NA	NA	ENSG00000202566	NA	NA	693122	NA	MIRN421|hsa-mir-421	We found that GATA6-AS was downregulated in tumor tissues than in adjacent healthy tissues of GBC patients, and GATA6-AS expression levels in tumor tissues decreased with the increase of clinical stages. MiR-421 was upregulated in tumor tissues than in adjacent healthy tissues of GBC patients and was inversely correlated with the expression levels of GATA6-AS. MiR-421 overexpression failed to significantly affect GATA6-AS in GBC cells, while GATA6-AS overexpression resulted in inhibited miR-421 expression. GATA6-AS overexpression led to decreased migration and invasion rates of GBC cells. MiR-421 overexpression led to increased migration and invasion rates of GBC. Rescue experiments (co-transfection) showed that miR-421 overexpression led to attenuated effects of GATA6-AS overexpression.	31632058	RID03225	transcriptional regulation	NA		
Oral squamous cell carcinoma	LINC01234	NUPR1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+)	ceRNA(miR-637)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000176046	NA	100506465	26471	onco-lncRNA-32	COM1|p8	In our research, we showed that LINC01234 was dramatically upregulated in OSCC tissues. And interestingly, high LINC01234 expression predicted a low overall survival rate in OSCC patients. Knockdown of OSCC inhibited the proliferation of cancer cells and led to more cells restricted in G0 phase. Moreover, LINC01234 silencing decreased the migration and invasion of OSCC cells. Additionally, downregulation of LINC01234 limited OSCC tumor propagation in vivo. Mechanistic investigation elucidated that LINC01234 inhibited the activity of miR-637 to increase the expression of NUPR1. Via upregulating NUPR1 level, LINC01234 contributed to malignant behaviors of OSCC cells. Collectively, our research shows that LINC01234 exerts an important role in OSCC progression via miR-637/NUPR1 axis.	31590125	RID03226	ceRNA or sponge	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807,GSE75367)
Periodontitis	MALAT1	TLR4	positively-E	qRT-PCR;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-20a)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Periodontitis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136869	NA	378938	7099	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ARMD10|CD284|hToll|TLR-4	Primary HGFs were harvested from human gingiva. MALAT1 was detected in inflammatory and healthy gingival tissues via quantitative real-time PCR (qRT-PCR. Bioinformatics analysis, dual-luciferase reporter assay, and RNA-binding protein immunoprecipitation (RIP) were used to detect the relationship among MALAT1, toll-like receptor 4 (TLR4), and microRNA (miR) -20a. After transfection LPS-treated HGFs with MALAT1 siRNA (si-MALAT1), miR-20a mimic or overexpression MALAT1 plasmid (sno-MALAT1), the levels of MALAT1, miR-20a, TLR4, IL-6 and IL-8 were analyzed by qRT-PCR enzyme-linked immunosorbent assay, or western blot assay.MALAT1 up-regulated in inflammatory gingival tissues of chronic periodontitis. MiR-20a was bound with MALAT1 and TLR4 3'-UTR in RNA-protein complex with Ago2, respectively. Moreover, MALAT1, TLR4, IL-6, and IL-8 increased while miR-20a decreased after 1 ug/mL Porphyromonas gingivalis lipopolysaccharide (LPS) or Escherichia coli LPS stimulation. MiR-20a inhibited the expression of proinflammatory cytokines via binding to TLR4 3'-UTR. In addition, MALAT1 increased TLR4 level and the secretion of inflammatory cytokines.	31552681	RID03227	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Pulmonary hypertension	MEG3	IGF1R	positively-E	qRT-PCR;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-328-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000140443	NA	55384	3480	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CD221|IGFIR|IGFR|JTK13	To further confirm the effect of hypoxia on lncRNA-MEG3 expression, we exposed two cell lineshuman PASMCs (hPASMCs) (Figure 1C, middle panel) and mouse PASMCs (mPASMCs) (Figure 1C, right panel)-to 3% FiO2 to induce hypoxia and confirmed via real-time PCR that hypoxia augmented lncRNA-MEG3 expression in both cell lines in a time-dependent manner.These findings confirm that increased lncRNA-MEG3 leads to hypoxia-induced PASMCs proliferation and reduces apoptosis in?vivo.	31477557	RID03228	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Malignant glioma	NEAT1	miR-194-5p	negatively-F	luciferase reporter assay	upregulation		NA	NA	AKT- FGF-2/TGF-beta/VEGF signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Bioinformatic analysis and luciferase reporter assays confirmed the interaction between lncRNA NEAT1 and miR-194-5p. Importantly, lncRNA NEAT1 overexpression reversed ISL-mediated increase in miR-194-5p expression, and thereby attenuated FGF-2, TGF-beta and VEGF production. Reprogramming COX-2, mPGES-1 and CYP4A mediated-AA metabolism in glioma by flavonoid ISL inhibits the angiogenic Akt- FGF-2/TGF-beta/VEGF signaling through ceRNA effect of miR-194-5p and lncRNA NEAT1, and may serve as a novel therapeutic strategy for human glioma.	31438982	RID03229	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Rheumatoid arthritis	MEG3	MIR141	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(-)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000207708	NA	55384	406933	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MIRN141|mir-141	To identify the divergence of MEG3 expression in the synovial tissues of healthy and RA subjects, we examined MEG3 expression in these subjects and found significant upregulation of MEG3 expression in the synovial tissue of RA patients (Figure -(Figure1A).1A).	31411001	RID03230	transcriptional regulation	NA		
Kidney disease	WSPAR	miR-200c	negatively-F	RT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	endoplasmic reticulum stress(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	miRNA	ENSG00000249073	GRCh38_5:133913677-133917269	NA	NA	105664404	NA	lncTCF7|TCONS_00009511-XLOC_004555	NA	The miR-200c level was detected in lncTCF7 overexpressing cell model and the luciferase reporter gene assay was performed to verify the potential binding site of lncTCF7 with miR-200c.Results showed that the lncTCF7 expression was up-regulated, while miR-200c was significantly downregulated in patients with DN (+). In the HG model, the expression of lncTCF7 was significantly increased and some key ER stress-associated genes, such as CHOP, XBP1, and cleaved caspase3, were significantly increased, while the anti-apoptotic protein Bcl-2 was significantly decreased. However, after inhibiting the lncTCF7 expression, these gene levels were reversed. In lncTCF7 overexpressing cells, miR-200c expression was significantly down-regulated compared with the control (p<0.05) and the luciferase reporter gene assay results showed that lncTCF7 could directly bind to miR-200c. In the HG model, after inhibiting lncTCF7 expression, the miR-200c level was increased, while the ER stress-associated proteins CHOP, XBP1, and cleaved caspase3 were significantly repressed. However, these proteins were reversed after inhibiting miR-200c expression. In addition, the expressions of ER stress-associated protein and apoptotic protein in human DN patients were consistent with HG cell model.	31298342	RID03231	ceRNA or sponge	NA		
Gastric cancer	HOTAIR	NSG1	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168824	NA	100124700	27065	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	D4S234|D4S234E|NEEP21|P21	In addition, knockdown of HOTAIR can inhibit GC cell growth and affect cell cycle distribution. And knockdown of HOTAIR could enhance the protein levels of P21 and P53.Conclusion: The present study demonstrated that HOTAIR was highly expressed in GC tissues and may serve as a potential diagnostic and prognostic biomarker for GC. And HOTAIR promoted GC cell.Thus, these data demonstrated that HOTAIR promotes GC cell proliferation.	31281803	RID03232	transcriptional regulation	prognosis		
Gastric cancer	HOTAIR	TP53	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141510	NA	100124700	7157	HOXC-AS4|HOXC11-AS1|NCRNA00072	LFS1|p53	In addition, knockdown of HOTAIR can inhibit GC cell growth and affect cell cycle distribution. And knockdown of HOTAIR could enhance the protein levels of P21 and P54.Conclusion: The present study demonstrated that HOTAIR was highly expressed in GC tissues and may serve as a potential diagnostic and prognostic biomarker for GC. And HOTAIR promoted GC cell.Thus, these data demonstrated that HOTAIR promotes GC cell proliferation.	31281803	RID03233	transcriptional regulation	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	CDR1-AS	REG	positively-E	luciferase reporter assay;RT-qPCR	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-7)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	circRNA	PCG	NA	NA	NA	NA	103611090	NA	CDR1NAT|CDR1as|CIRS7|ciRS-7	NA	The CDR1as expression in breast cancer tissues and normal breast tissues before and after neoadjuvant chemotherapy was detected by RT-qPCR. The results suggested that CDR1as may play a role in the development of drug resistance in breast cancer.	31245927	RID03234	ceRNA or sponge	chemoresistance		
Chronic heart failure	GASAL1	TGFB1	negatively-E	ELISA;RT-qPCR	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000105329	NA	401472	7040	GASL1	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	We found that plasma levels of TGF-beta1 were significantly higher, while levels of GASL1 in plasma were significantly lower in chronic heart failure (CHF) patients compared to the control group. TGF-beta1 and GASL1 were inversely correlated in CHF patients. Low pretreatment plasma levels of GASL1 were closely associated with poor survival of CHF patients. GASL1 expression was not significantly affected by TGF-beta1 overexpression in cardiomyocytes, while cardiomyocytes with GASL1 overexpression showed downregulated TGF-beta1. Overexpression of GASL1 led to a decreased, while TGF-beta1 overexpression led to an increased apoptotic rate of cardiomyocytes under H2O2 treatment. In addition, TGF-beta1 overexpression attenuated the effect of GASL1 overexpression.	31223316	RID03235	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiac hypertrophy	STAT3	MEG3	positively-E	qRT-PCR;luciferase reporter assay;ChIP;northern blot	upregulation	RT-qPCR	NA	NA	cardiac hypertrophy(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	TF	lncRNA	ENSG00000168610	NA	ENSG00000214548	GRCh38_14:100779410-100861031	6774	55384	ADMIO|ADMIO1|APRF|HIES	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	All our findings revealed that STAT3-inducetd upregulation of lncRNA MEG3 controls cardiac hypertrophy by regulating miR-362-5p/HDAC9 axis. Not surprisingly, STAT3 was expressed higher in TAC group (Fig.-2E). The positive expression correlation between STAT3 and MEG3 in TAC group was analyzed by Spearman Rank correlation analysis (Fig.-2F). Furthermore, qRT-PCRand northern blot assays revealed that the expression of MEG3 in cardiomyocytes was positively regulated by STAT3 (Fig.-2G,H), indicating the positive regulatory effect of STAT3 on the expression of MEG3.	30679521	RID03236	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Cardiac hypertrophy	MEG3	HDAC9	positively-E	qRT-PCR;RNAi;RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cardiac hypertrophy(+)	ceRNA(miR-328-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000048052	NA	55384	9734	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HD7|HD7b|HD9|HDAC|HDAC7|HDAC7B|HDAC9B|HDAC9FL|HDRP|MITR	All our findings revealed that STAT3-inducetd upregulation of lncRNA MEG3 controls cardiac hypertrophy by regulating miR-362-5p/HDAC9 axis. All these experimental results indicated that MEG3 can positively regulate HDAC9 via sponging miR-361-5p.	30679521	RID03237	ceRNA or sponge	NA		DOWN(PRAD,BRCA);DATA(GSE104209,GSE51827,GSE86978)
Endometriosis	17beta-E2	LINC01541	negatively-E	western blot;RT-qPCR	downregulation		NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	regulation	protein-RNA	NA	NA	NA	Reproductive system disease	Endometriosis	PCG	lncRNA	NA	NA	ENSG00000260676	GRCh38_18:71519962-71578956	NA	100505776	NA	UTAT39	17beta-E2 promoted the migration and invasion of ESCs, and those affects were partially reversed by overexpression of LINC01541.Furthermore, cell migration and invasion assays showed that 17beta-E2 significantly promoted metastasis and invasiveness of ESCs, and these effects could also be reversed by overexpression of LINC01541 (Figure 1D,E).	30608887	RID03238	transcriptional regulation	metastasis		UP(LIHC);DATA(GSE117623)
Mantle cell lymphoma	MANCR	RUNX2	positively-E	western blot;qRT-PCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	TF	ENSG00000231298	GRCh38_10:4650158-4678185	ENSG00000124813	NA	100216001	860	CR749391|LINC00704	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	A positive correlation between serum MANCR and RUNX2 was found in MCL patients but not in controls. Upregulation of serum MANCR distinguished MCL patients from controls. MANCR overexpression promoted RUNX2 expression in MCL cells, while RUNX2 overexpression failed to significantly change the expression levels of MANCR. MANCR overexpression promoted the proliferation of MCL cells, while MANCR silencing inhibited the proliferation of MCL cells. In addition, RUNX2 overexpression attenuated the inhibitory effects of MANCR silencing on cell proliferation. However, MANCR overexpression and silencing had no significant effects on cell migration and invasion. Further bioinformatics analysis showed that MANCR may sponge miR-218 to upregulate RUNX2. Therefore, we conclude that downregulation of MANCR may inhibit cancer cell proliferation in MCL possibly by interacting with RUNX2.	31650163	RID03239	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung injury	MEG3	KLF4	positively-E	western blot;qRT-PCR	upregulation		NA	NA	PI3K/AKT signaling pathway(+);JAK/STAT signaling pathway(+)	ceRNA(miR-4262)	regulation	NA	NA	NA	NA	Respiratory system disease	Injury	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136826	NA	55384	9314	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	EZF|GKLF	LPS-induced alterations of key kinases in the PI3K/AKT and JAK/STAT pathways were reversed by KLF4 overexpression. In conclusion, MEG3 was down-regulated by LPS and its knockdown aggravated LPS-induced injury of human lung cells through miR-4262-mediated down-regulation of KLF4. The PI3K/AKT and JAK/STAT pathways were implicated.	31184231	RID03240	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Ovarian cancer	ZNF667-AS1	MIR21	negatively-E	RT-qPCR	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000166770	GRCh38_19:56477250-56504362	ENSG00000199004	NA	100128252	406991	MORT	MIRN21|hsa-mir-21|miR-21|miRNA21	Therefore, lncRNA MORT was downregulated in ovarian carcinoma and lncRNA MORT overexpression inhibited cancer cell proliferation, possibly by downregulating miRNA-21.Expression of miRNA-21 and lncRNA MORT in tumor tissues and adjacent healthy tissues of 72 patients with ovarian carcinoma were detected by RT-qPCR. As shown in Figure 1, lncRNA MORT was downregulated (Figure 1A), while miRNA-21 was upregulated (Figure 1B) in tumor tissues than in adjacent healthy tissues of ovarian carcinoma patients (P < 0.05).	31208095	RID03241	transcriptional regulation	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE51827,GSE86978)	
Lung cancer	H19	miR-6515-3p	positively-E	qRT-PCR;RNA pull-down assay	upregulation		NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Considering that miR-6515-3p is downregulated in H19-knockdown SPC-A1 and generally overexpressed in H19 upregulated patients with lung cancer, this correlation strongly suggests a hidden link between H19 and miR-6515-3p, which may actively contribute to the	31131469	RID03242	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	
Pulmonary fibrosis	ZEB1-AS1	ZEB1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	ncRNA ZEB1-AS1 promotes pulmonary fibrosis through ZEB1-mediated epithelial-mesenchymal transition by competitively binding miR-141-3p.In the present study, we found that lncRNA ZEB1 antisense RNA 1 (ZEB1-AS1) is upregulated in the lungs of BLM-induced rats and TGF-beta1-induced RLE-6TN cells, and positively correlated with the levels of ZEB1, an epithelial-mesenchymal transition (EMT) master regulator.Further experiments revealed that ZEB1-AS1 acted as competing endogenous RNA (ceRNA) of miR-141-3p: forced expression of ZEB1-AS1 reduced the expression of miR-141-3p to activate Zinc-finger Ebox Binding Homeobox 1 (ZEB1) in RLE-6TN cells.Therefore, our finding suggested lncRNA ZEB1-AS1 as a new profibrotic molecule that acts as a regulator of miR-141-3p/ZEB1 axis during lung fibrosis and demonstrated ZEB1-AS1 as a potential therapeutic target for the prevention and treatment of pulmonary fibrosis.	30755599	RID03243	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	SNHG14	miR-101	negatively-F	luciferase reporter assay	upregulation	RT-qPCR;western blot	NA	NA	cell proliferation(+);cell migration(+)cell invasion(+);chemoresistance(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	Gemcitabine	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000224078	GRCh38_15:24978583-25420336	NA	NA	104472715	NA	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	NA	RT-qPCR and western blot were used to detect the autophagy-related gene expression level.SNHG14 enhances gemcitabine resistance by sponging miR-101 to stimulate cell autophagy in pancreatic cancer.The luciferase reporter assay was used to confirm the direct interaction between SNHG14 and miR-101. The expression of SNHG14 was significantly higher in the PDAC tissues than in the normal tissues, while miR-101 was significantly downregulated in the PDAC tissues.Moreover, the correlation analysis showed that SNHG14 was negatively correlated with miR-101.Overexpression of SNHG14 and miR-101 inhibitor significantly enhanced cell proliferation, migration, and invasion rate of PDAC cell line.	30737032	RID03244	ceRNA or sponge	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	
Osteosarcoma	SNHG16	MIR340	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000198995	NA	100507246	442908	Nbla10727|Nbla12061|ncRAN	MIRN340|hsa-mir-340|mir-340	Long Noncoding RNA SNHG16 Promotes Osteosarcoma Cells Migration and Invasion via Sponging miRNA-340.We found that SNHG16 is overexpressed in OS tissues and cell lines.In addition, SNHG16 reduced miR-340 expression in OS cells.The results showed that SNHG16 involves in the migration and invasion of OS cells through sponging miRNA-340.	30726150	RID03245	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Renal fibrosis	HOTAIR	NOTCH1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell migration(+)	ceRNA(miR-124)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148400	NA	100124700	4851	HOXC-AS4|HOXC11-AS1|NCRNA00072	TAN1	Paeonol reverses promoting effect of the HOTAIR/miR-124/Notch1 axis on renal interstitial fibrosis in a rat model.HOTAIR interacted with miR-124, and miR-124 directly targeted Notch1, and HOTAIR was observed to be upregulated in RIF rats.HOTAIR activated the Notch1/Jagged1 signaling pathway by downregulating miR-124, while PAE reversed these effects of HOTAIR on the Notch1/Jagged1 signaling pathway.Overall, our study demonstrates the contributory effect of lncRNA HOTAIR on RIF by activating the Notch1/Jagged1 signaling pathway via inhibition of miR-124, whereas administration of PAE can alleviate the effects of HOTAIR on RIF.	30714138	RID03246	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Glioma	ZEB1-AS1	ZEB1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long noncoding RNA ZEB1-AS1 promotes the tumorigenesis of glioma cancer cells by modulating the miR-200c/141-ZEB1 axis.Here, we show that ZEB1-AS1 expression was higher in glioma tissues and cell lines than in corresponding noncancerous samples and primary normal human astrocytes, respectively.Dual-luciferase report assay showed that ZEB1-AS1 directly regulated microRNA-200c/141 (miR-200c/141) in glioma cells, which was confirmed by RNA immunoprecipitation assay.Additionally, ZEB1-AS1 can regulate ZEB1 through miR-200c/141.Hence, ZEB1-AS1 directly regulated miR-200c/141 in glioma cells and relieved the inhibition of ZEB1 caused by miR-200c/141.The interaction between ZEB1-AS1 and miR-200c/141-ZEB1 axis was involved in the progression of glioma cells.	30662595	RID03247	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SNHG16	NOVA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-146a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	LncSNHG16 promotes proliferation and migration of osteosarcoma cells by targeting microRNA-146a-5p.Expressions of lncSNHG16, microRNA-146a-5p and NOVA1 in OS tissues and adjacent normal tissues were determined by quantitative Real-time polymerase chain reaction (qRT-PCR.dual-luciferase reporter assay was used to verify the binding relationship of lncSNHG16 to microRNA-146a-5p, and microRNA-146a-5p to NOVA1.LncSNHG16 was highly expressed in OS tissues and cell lines.Furthermore, we verified that lncSNHG16 could bind to microRNA-146a-5p.Subsequently, NOVA1 was predicted to be the target gene of microRNA-146a-5p, and was further verified by dual-luciferase reporter gene assay.LncSNHG16 is highly expressed in OS tissues and cell lines, participating in the development of OS by downregulating microRNA-146a-5p to upregulate NOVA1 expression.	30657551	RID03248	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Sepsis-induced acute kidney injury<U+00A0>	CRNDE	miR-181a-5p	negatively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	Down-regulation of LncRNA CRNDE aggravates kidney injury via increasing MiR-181a-5p in sepsis.Interaction between CRNDE and miR-181a-5p was determined by bioinformatics analysis, RT-PCR and dual-luciferase reporter assay.We demonstrated that CRNDE was markedly down-regulated while miR-181a-5p was significantly up-regulated in sepsis models.CRNDE interacted with miR-181a-5p, and negatively regulated its expression level.Knockdown of CRNDE or transfection of miR-181a-5p significantly inhibited proliferation and promoted apoptosis of HK-2 and HEK293 cells, while overexpression of CRNDE and transfection of miR-181a-5p inhibitors had opposite effects.	31877497	RID03249	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Osteomyelitis	IQANK1	WNT3A	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-541-3p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000154342	NA	642574	89780	FAM83H-AS1|onco-lncRNA-3	NA	Long Noncoding RNA FAM83H-AS1 Modulates SpA-Inhibited Osteogenic Differentiation in Human Bone Mesenchymal Stem Cells.In this study, hBMSCs were treated with staphylococcal protein A (SpA) during osteogenic differentiation induction to mimic osteomyelitis in vitro The results of lncRNA microarray analysis revealed that FAM83H-AS1 presented the lowest expression among the significantly downregulated lncRNAs.Additionally, our findings revealed that FAM83H-AS1 negatively regulated microRNA 541-3p (miR-541-3p), and WNT3A was validated as a target gene of miR-541-3p.Mechanically, FAM83H-AS1 elevated WNT3A expression by competitively binding with miR-541-3p.	31871129	RID03250	ceRNA or sponge	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	UP(PAAD);DATA(GSE40174)
Gastric cancer	LINC00461	KDM1A	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000004487	NA	645323	23028	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	AOF2|BHC110|KDM1|KIAA0601|LSD1	Knockdown of LINC00461 inhibits cell proliferation and induces apoptosis in gastric cancer by targeting LSD1.LINC00461 level in GC tissues with different tumor node metastasis (TNM) staging and lymphatic metastasis statues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.The interaction between LINC00461 and LSD1 was explored by RNA immunoprecipitation (RIP) assay and qRT-PCRLINC00461 level was higher in GC tissues relative to matched control ones.RIP assay demonstrated the interaction between LINC00461 and LSD1.LSD1 could reverse the regulatory effect of LINC00461 on the proliferative ability of GC cells.LINC00461 mediates proliferation and apoptosis of GC cells, thereafter aggravating the progression of GC.	31858544	RID03251	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Sepsis-induced acute kidney injury<U+00A0>	CRNDE	TLR3	negatively-E	western blot	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000164342	NA	643911	7098	CRNDEP|LINC00180|LOC643911	CD283	Effect of lncRNA CRNDE on sepsis-related kidney injury through the TLR3/NF-kB pathway.After 12 h, the expression level of lncRNA CRNDE in kidney tissues of mice in each group was detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR.Finally, the expression of Toll-like receptor 3 (TLR3)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathway in kidney tissues of mice in each group was detected using western blot. Compared with the Sham group, lncRNA CRNDE level in the kidney of the LPS group was remarkably up-regulated.Furthermore, western blot displayed that CRNDE siRNA could effectively inhibit the activation of TLR3 and p65 in mouse kidney tissue induced by LPS.Inhibition of CRNDE can reduce sepsis-induced KI by blocking the activation of the TLR3/NF-kB pathway.	31841203	RID03252	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Diabetic kidney disease	GAS5	FN1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-96-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Kidney disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000115414	NA	60674	2335	NCRNA00030|SNHG2	CIG|FINC|GFND2|LETS|MSF	LncRNA GAS5 exacerbates renal tubular epithelial fibrosis by acting as a competing endogenous RNA of miR-96-5p.Renal fibrosis is at the core of various renal diseases, including diabetic kidney disease (DKD).In this study, the lncRNA GAS5 was upregulated in both TGF-beta1-treated HK-2 cells and the kidneys of HDF/STZ mice.Furthermore, miR-96-5p was downregulated in DKD mice, and this downregulation attenuated the repression of FN1(fibronectin, FN) and led to its upregulation.Our research demonstrates that knockdown of lncRNA GAS5 leads to antifibrosis by competitively binding miR-96-5p, which inhibits the expression of FN1.	31810140	RID03253	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteosarcoma	SND1-IT1	POU2F1	positively-E	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	ceRNA(miR-665)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000279078	GRCh38_7:127997597-128000077	ENSG00000143190	NA	27099	5451	C7orf54|NAG8|NSG-X	1-Oct|OTF1	LncRNA SND1-IT1 accelerates the proliferation and migration of osteosarcoma via sponging miRNA-665 to upregulate POU2F1.The relative level of SND1-IT1 in OS tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.The target gene of SND1-IT1 was predicted by bioinformatics and verified by Dual-Luciferase reporter gene assay.SND1-IT1 was upregulated in OS, knockdown of which attenuated proliferative and migratory abilities of OS cells.MiRNA-665 was the target gene of SND1-IT1, which was negatively correlated to SND1-IT1 in OS.POU2F1 was the target gene of miRNA-665.LncRNA SND1-IT1 accelerates proliferative and migratory abilities of OS via sponging miRNA-665 to upregulate POU2F1, thus stimulating the progression of OS.	31799644	RID03254	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807)
Cataract	PLCD3-OT1	PLCD3	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell viability(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-224-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Cataract	lncRNA	PCG	NA	NA	ENSG00000161714	NA	NA	113026	NA	NA	LncRNA PLCD3-OT1 Functions as a CeRNA to Prevent Age-Related Cataract by Sponging miR-224-5p and Regulating PLCD3 Expression.Real-time PCR was conducted to detect the expression pattern of lncRNA and mRNA in the clinical samples and cell model.We also performed fluorescence in situ hybridization assay to detect the location of lncRNA, and verified the endogenous competitive RNA mechanism between miRNAs, lncRNAs, and target genes via double-luciferase reporter analyses.The expression of lncRNA PLCD3-OT1 and PLCD3 were significantly decreased in ARC.PLCD3-OT1 overexpression promoted the expression of PLCD3, cell viability, proliferation, and inhibited cell apoptosis upon oxidative stress, while knockdown of PLCD3 showed the opposite results.Mechanistically, PLCD3-OT1functions through positively regulation the expression of PLCD3.In addition, PLCD3-OT1 may act as a ceRNA to regulate the expression of PLCD3 through competition for miR-224-5p.	31725166	RID03255	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(PRAD);DATA(GSE117623,GSE40174,GSE104209)
Colon cancer	PPP1R13B-DT	HIF1A	negatively-E	luciferase reporter assay;ChIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	angiogenesis(-);tumor growth(-)	translation	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000258735	GRCh38_14:103847721-103858049	ENSG00000100644	NA	145216	3091	HITT|LINC00637	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	A novel LncRNA HITT forms a regulatory loop with HIF-1alpha to modulate angiogenesis and tumor growth.Decreased HITT is associated with advanced stages of colon cancer.Restoration of the expression of HITT in cancer cells inhibits angiogenesis and tumor growth in vivo in an HIF-1alpha-dependent manner.Further study reveals that HITT inhibits HIF-1alpha expression, mainly by interfering with its translation.The reverse correlation between HITT and HIF-1alpha expression is further validated in human colon cancer tissues.	31700144	RID03256	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteosarcoma	ADPGK-AS1	miR-542-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000260898	GRCh38_15:72782835-72798199	NA	NA	100287559	NA	NA	NA	LncRNA ADPGK-AS1 regulated cell proliferation, invasion, migration and apoptosis via targeting miR-542-3p in osteosarcoma.qRT-PCRwas used to detect the expression of ADPGK-AS1 and miR-542-3p in tissues and cells.Moreover, luciferase reporter assay was used to ensure the relation between ADPGK-AS1 and miR-542-3p.LncRNA ADPGK-AS1 expression was induced while miR-542-3p expression was reduced in OS tissues and cells.Functional experiments showed that inhibition of ADPGK-AS1 could decrease cell proliferation, migration, and invasion, as well as promoted cell apoptosis in OS cells.Also, miR-542-3p has been verified to be a target miRNA of ADPGK-AS1 and miR-542-3p could reverse the effects of ADPGK-AS1 on cell proliferation, apoptosis, migration, and invasion in OS cells.	31696461	RID03257	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	
Asthma	MALAT1	EIF4E	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-150)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000151247	NA	378938	1977	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	EIF4E1|EIF4EL1|EIF4F	Upregulation of LncRNA Malat1 Induced Proliferation and Migration of Airway Smooth Muscle Cells via miR-150-eIF4E/Akt Signaling.The results showed that Malat1 was significantly upregulated in ASMCs treated with PDGF-BB, and knockdown of Malat1 effectively inhibited ASMC proliferation and migration induced by PDGF-BB.Collectively, these data indicate that Malat1, as a competing endogenous RNA (ceRNA) for miR-150, derepresses eIF4E expression and activates Akt signaling, thereby being involved in PDGF-BB-induced ASMC proliferation and migration.	31695627	RID03258	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM,BRCA);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	miR-375-3p	CCAT1	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000247844	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	The Reciprocal Interaction Between LncRNA CCAT1 and miR-375-3p Contribute to the Downregulation of IRF5 Gene Expression by Solasonine in HepG2 Human Hepatocellular Carcinoma Cells.Mechanistically, we observed that SS increased the expression of miR-375-3p, whereas reducing levels of long non-coding RNAs (lncRNAs) CCAT1 was noticed in HepG2 HCC and other cells.There was a reciprocal interaction among miR-375-3p, CCAT1, and SP1.Collectively, our results show that SS inhibits HepG2 HCC growth through the reciprocal regulation between the miR-375-3p and lncRNA CCAT1, and this results in transcription factor SP1-mediated reduction of IRF5 expression.	31681610	RID03259	expression association	NA		
Chronic obstructive pulmonary disease	MEG3	miR-218	negatively-E	luciferase reporter assay;RIP;LncBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long non-coding RNA MEG3 regulates CSE-induced apoptosis and inflammation via regulating miR-218 in 16HBE cells.The expression of MEG3 and miR-218 in COPD tissues and cigarette smoke extract (CSE)-treated 16HBE cells was detected by RT-qPCR.MEG3 and miR-218 binding interaction was predicted by LncBase Predicted v.2 and further confirmed by dual-luciferase reporter assay and RNA Immunoprecipitation (RIP) assay.MiR-218 was demonstrated as a target miRNA of MEG3.MiR-218 was downregulated in COPD tissues and (CSE)-treated or MEG3 overexpressed 16HBE cells.MEG3 regulated CSE-inhibited proliferation and CSE-induced apoptosis or inflammation by targeting miR-218, providing a possible therapeutic target for treatment of CSE-induced COPD.	31668807	RID03260	expression association	NA		
Gestational diabetes mellitus	MEG3	miR-345-3p	negatively-E	luciferase reporter assay;bioinformatics	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Genetic disease	Diabetes mellitus	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Mechanism associated with aberrant lncRNA MEG3 expression in gestational diabetes mellitus.The levels of lncRNA MEG3 in the blood and placental villous tissues of pregnant women with GDM was measured using reverse transcription-quantitative PCR.Bioinformatics analysis and dual-luciferase reporter assays were performed to investigate the association between lncRNA MEG3 and microRNA (miR)-345-3p.miR-345-3p was identified to be a direct target of lncRNA MEG3 using dual-luciferase reporter assay, which was found to be reduced in pregnant women with GDM.In conclusion, lncRNA MEG3 levels were abnormally upregulated in GDM, which participated in the development and progression of GDM by regulating human chorionic trophoblast cell physiology.	31656536	RID03261	expression association	NA		
Osteoarthritis	PART1	SOX4	positively-E	luciferase reporter assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000124766	NA	25859	6659	DKFZP586D0823|NCRNA00206	NA	LncRNA PART1 modulates chondrocyte proliferation, apoptosis, and extracellular matrix degradation in osteoarthritis via regulating miR-373-3p/SOX4 axis.steoarthritis (OA) is a common disease in articular cartilages.The expression levels of PART1 and miR-373-3p were detected in cartilage tissues and chondrocytes using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.The interactions among PART1, miR-373-3p, and SOX4 were predicted using starBase v2.0 database and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.PART1 and SOX4 were up-regulated while miR-373-3p was down-regulated in OA cartilage tissues and chondrocytes.PART1 modulated SOX4 expression by targeting miR-373-3p.PART1 and SOX4 were up-regulated while miR-373-3p was down-regulated in OA cartilage tissues and chondrocytes.PART1 promoted OA progression by regulating miR-373-3p/SOX4 axis, providing an effective therapeutic target for osteoarthritis.	31646607	RID03262	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Atherosclerosis	LINC-ROR	FGF2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-373-4p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000138685	NA	100885779	2247	lincRNA-RoR|lincRNA-ST8SIA3|ROR	FGFB	Linc-ROR targets FGF2 to regulate HASMC proliferation and migration via sponging miR-195-5p.In addition, linc-ROR acted as a competing endogenous RNA for miR-195-5p and repressed the miR-195-5p expression in HASMCs.Linc-ROR was up-regulated the miR-195-3p was down-regulated in the plasma from CAD patients when compared to normal controls.To summarize, the data of the present study identified the up-regulation of linc-ROR in Hcy-stimulated HASMCs, and further mechanistic functional studies revealed that linc-ROR promoted HASMC proliferation and migration via regulating miR-195-5p/FGF2 axis.Furthermore, fibroblast growth factor 2 (FGF2) was identified as a target of miR-195-5p and was negatively regulated by miR-195-5p in HASMCs.	31629816	RID03263	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	CASC2c	ERK1/2	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	NA	NA	NA	NA	Long noncoding RNA CASC2c inhibited cell proliferation in hepatocellular carcinoma by inactivated ERK1/2 and Wnt/beta-catenin signaling pathway.This study first investigated the expression levels of CASC2c in tumor tissues, corresponding non-tumor tissues and cells using quantitative real-time polymerase chain reaction.In the present work, we observed that CASC2c was significantly down-regulated in HCC tissues and cells.Furthermore, we demonstrated that CASC2c overexpression decreased p-ERK1/2 levels in HCC, GC, and CRC cells.The lncRNA-CASC2c has a vital role in tumorigenesis and cancer progression, and may serve as a biomarker or therapeutic target in cancer treatment via down-regulation of the ERK1/2 and Wnt/beta-catenin signaling pathways.	31625123	RID03264	expression association	NA		
Acute myeloid leukemia	SNHG1	miR-101	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	regulation	RNA-RNA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Long non-coding RNA SNHG1 indicates poor prognosis and facilitates disease progression in acute myeloid leukemia. we show that SNHG1 is highly expressed in AML specimens from non-M3 patients, as well as AML cell lines.Mechanistically, we found that an anti-tumor microRNA-101 (miR-101) is upregulated and its target genes are downregulated in AML cells after SNHG1 knockdown.Further investigations display that SNHG1 can serve as a competing endogenous RNA to inhibit miR-101.	31615767	RID03265	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Non-small cell lung cancer	UCA1	NRF2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-495)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000154727	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Deregulation of UCA1 expression may be involved in the development of chemoresistance to cisplatin in the treatment of non-small-cell lung cancer via regulating the signaling pathway of microRNA-495/NRF2.Real-time polymerase chain reaction, western blot analysis, and immunofluorescence were used to study the involvement of UCA1, miR-495, and NRF2 in chemoresistance against cisplatin.Computational analysis and luciferase assay were carried out to explore the interaction among UCA1, miR-495, and NRF2.The cisplatin-R group exhibited lower levels of UCA1 and NRF2 expression but a higher level of miR-495 expression than the cisplatin-S group.MiR-495 contained a complementary binding site of UCA1, and the luciferase activity of wild-type UCA1 was significantly reduced after the transfection of miR-495 mimics.MiR-495 directly targeted the 3'-untranslated region (3'-UTR) of NRF2, and the luciferase activity of wild-type NRF2 3'-UTR was evidently inhibited by miR-495 mimics.We suggested for the first time that high expression of UCA1 contributed to the development of chemoresistance to cisplatin through the UCA1/miR-495/NRF2 signaling pathway.	31583720	RID03266	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	
Osteoarthritis	PART1	TGFBR2	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	sponge	association	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000163513	NA	25859	7048	NCRNA00206	AAT3|FAA3|LDS1B|LDS2|LDS2B|MFS2|RIIC|TAAD2|TBR-ii|TBRII|TGFR-2|TGFbeta-RII|tbetaR-II	LncRNA PART-1 targets TGFBR2/Smad3 to regulate cell viability and apoptosis of chondrocytes via acting as miR-590-3p sponge in osteoarthritis.Osteoarthritis (OA) is a degenerative joint disease that commonly occurs in the elderly.In the present study, the PART-1 expression level was down-regulated in the OA cartilages.Silence of PART-1 decreased the cell viability and promoted chondrocytes apoptosis.MiR-590-3p was found to be the potential target, and RNA immunoprecipitation and luciferase activity assay confirmed the binding between PART-1 and miR-590-3p.Moreover, miR-590-3p was down-regulated by PART-1 and was negatively associated with PART-1.Transforming growth factor-beta receptor type 2 (TGFBR2) was positively associated with PART-1.Smad3 expression level was lower in the OA group than that in the normal group and was positively associated with the PART-1 expression level.Collectively, the study revealed that lncRNA PART-1 regulates the apoptosis of chondrocytes in OA by acting as a sponge for miR-590-3p, which subsequently regulates TGFBR2/Smad3 signalling.	31571401	RID03267	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	PART1	SMAD3	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	sponge	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000166949	NA	25859	4088	NCRNA00206	HSPC193|HsT17436|JV15-2|LDS1C|LDS3|MADH3|hMAD-3|hSMAD3|mad3	LncRNA PART-1 targets TGFBR2/Smad3 to regulate cell viability and apoptosis of chondrocytes via acting as miR-590-3p sponge in osteoarthritis.Osteoarthritis (OA) is a degenerative joint disease that commonly occurs in the elderly.In the present study, the PART-1 expression level was down-regulated in the OA cartilages.Silence of PART-1 decreased the cell viability and promoted chondrocytes apoptosis.MiR-590-3p was found to be the potential target, and RNA immunoprecipitation and luciferase activity assay confirmed the binding between PART-1 and miR-590-3p.Moreover, miR-590-3p was down-regulated by PART-1 and was negatively associated with PART-1.Transforming growth factor-beta receptor type 2 (TGFBR2) was positively associated with PART-1.Smad3 expression level was lower in the OA group than that in the normal group and was positively associated with the PART-1 expression level.Collectively, the study revealed that lncRNA PART-1 regulates the apoptosis of chondrocytes in OA by acting as a sponge for miR-590-3p, which subsequently regulates TGFBR2/Smad3 signalling.	31571401	RID03268	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LINC-ROR	MDM2	positively-E		upregulation		NA	NA	cell viability(+);cell proliferation(+);apoptosis process(-)	sponge	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000135679	NA	100885779	4193	lincRNA-RoR|lincRNA-ST8SIA3|ROR	HDM2|MGC5370	Linc-ROR regulates apoptosis in esophageal squamous cell carcinoma via modulation of p53 ubiquitination by targeting miR-204-5p/MDM2.In this study, gain-of-function assays showed that linc-ROR upregulation enhanced cell viability, promoted cell proliferation, and inhibited apoptosis.Linc-ROR positively regulates the expression of MDM2 as a molecular sponge of miR-204-5p.	31541467	RID03269	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	LINC00511	STXBP4	positively-E	luciferase reporter assay;bioinformatics	upregulation	qPCR	NA	NA	radiosensitivity(-)	ceRNA(miR-185)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000166263	NA	400619	252983	onco-lncRNA-12	MGC50337|Synip	Long noncoding RNA LINC00511 involves in breast cancer recurrence and radioresistance by regulating STXBP4 expression via miR-185.LINC00511 expression in tissues was measured by quantitative polymerase chain reaction (qPCR).MicroRNA (miRNA) targets of LINC00511 were identified by bioinformatics analysis and further validated by dual-luciferase reporter assay, qPCR, and western blotLINC00511 expression was significantly increased in breast cancer tissues and correlated with recurrence and poor survival after breast-conserving surgery followed by radiotherapy.In addition, elevated LINC00511 was found to increase syntaxin-binding protein 4 (STXBP4) expression through competitive binding to miR-185, while silencing LINC00511 decreased STXBP4 expression and increased radiosensitivity.LINC00511 inhibition impairs its competitive binding to miR-185, resulting in increased STXBP4 expression and improved radiation response in breast cancer.	31539133	RID03270	ceRNA or sponge	recurrence	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Pre-eclampsia	TUG1	miR-29b	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+);cell invasion(+);angiogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	lncRNA TUG1 modulates proliferation, apoptosis, invasion, and angiogenesis via targeting miR-29b in trophoblast cells.Placenta tissues obtained from patients with PE and healthy pregnant women were performed to measure TUG1 expression by qRT-PCRanalysis.Moreover, the luciferase reporter assay was subjected to verify the binding relationship between TUG1 and miR-29b.Here, we identified a lncRNA, TUG1, which was notably decreased in placental samples of PE patients.Furthermore, mechanistic researches revealed that TUG1 could act as a molecular sponge for miR-29b, thus regulating MCL1, VEGFA, and MMP2 to modulate PE development.</AbstractText>: Here, we identified a lncRNA, TUG1, which was notably decreased in placental samples of PE patients.	31519209	RID03271	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Sepsis	MALAT1	SMAD3	positively-E		upregulation		NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000166949	NA	378938	4088	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HsT17436|JV15-2|MADH3	Hsa-miR-346 plays a role in the development of sepsis by downregulating SMAD3 expression and is negatively regulated by lncRNA MALAT1.We showed that MALAT1 inhibited RAW264.7<U+202F>cell proliferation, while hsa-miR-346 promoted its proliferation.In this RAW264.7<U+202F>cell model, MALAT1 inhibited hsa-miR-346 expression, and upregulated SMAD3 protein expression.	31494280	RID03272	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteomyelitis	MALAT1	miR-146a	negatively-E	bioinformatics;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000253522	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1 mediates proliferation of LPS treated-articular chondrocytes by targeting the miR-146a-PI3K/Akt/mTOR axis.Results from quantitative real-time PCR (Q-PCR) showed that, in OA patients and OA cell model, the expression of MALAT1 and PI3K was clearly reduced, while the miR-146a levels were increased.Bioinformatics prediction and dual-luciferase reporter assay (DLRA) results showed that MALAT1 targets miR-146a.MALAT1 silencing also resulted in the upregulation of miR-146a.Further studies revealed that miR-146a has the opposite effect on MALAT1, and its inhibition can antagonize the function of MALAT1 silencing on cell proliferation and apoptosis.Additionally, the 3'-UTR of the Phosphoinositide 3-kinase (PI3K) gene was found to be a target of miR-146a, while PI3K protein and mRNA expression, as well as the activation of downstream Akt and mammalian target of rapamycin (mTOR) were clearly reduced upon transfection with a miR-146a mimic.	31472145	RID03273	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Osteomyelitis	MALAT1	PIK3CA	positively-E	bioinformatics;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-146a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000121879	NA	378938	5290	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PI3K	LncRNA MALAT1 mediates proliferation of LPS treated-articular chondrocytes by targeting the miR-146a-PI3K/Akt/mTOR axis.Results from quantitative real-time PCR (Q-PCR) showed that, in OA patients and OA cell model, the expression of MALAT1 and PI3K was clearly reduced, while the miR-146a levels were increased.Bioinformatics prediction and dual-luciferase reporter assay (DLRA) results showed that MALAT1 targets miR-146a.MALAT1 silencing also resulted in the upregulation of miR-146a.Further studies revealed that miR-146a has the opposite effect on MALAT1, and its inhibition can antagonize the function of MALAT1 silencing on cell proliferation and apoptosis.Additionally, the 3'-UTR of the Phosphoinositide 3-kinase (PI3K) gene was found to be a target of miR-146a, while PI3K protein and mRNA expression, as well as the activation of downstream Akt and mammalian target of rapamycin (mTOR) were clearly reduced upon transfection with a miR-146a mimic.	31472145	RID03274	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Spinal ependymoma	LINC00899	RBL2	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	GSE50161;GSE66354	NA	cancer progression(-);cell invasion(-);cell migration(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Spinal cancer	lncRNA	PCG	ENSG00000231711	GRCh38_22:46039907-46044853	ENSG00000103479	NA	100271722	5934	NA	p130|Rb2	Downregulated long non-coding RNA LINC00899 inhibits invasion and migration of spinal ependymoma cells via RBL2-dependent FoxO pathway.Spinal ependymoma related chip data (GSE50161 and GSE66354) was initially downloaded and differentially expressed lncRNAs were screened out.Our results showed that LINC00899 was up-regulated in spinal ependymoma and RBL2 was confirmed as a target gene of LINC00899 and found to be involved in regulation of FoxO pathway.LINC00899 expression increased in spinal ependymoma tissues whereas RBL2 expression decreased.Taken together, our study suggests that down-regulated LINC00899 exerts anti-oncogenic effects on spinal ependymoma via RBL2-dependent FoxO, which provides a novel therapeutic target for the treatment of spinal ependymomas.	31432742	RID03275	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple sclerosis	TUG1	NFKB1	positively-E	western blot	downregulation	RT-qPCR	NA	NA	cancer progression(-);inflammatory response(-)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	NA	Nervous system disease	Demyelinating disease	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000109320	NA	55000	4790	FLJ20618|LINC00080|NCRNA00080	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	Down-regulation of taurine-up-regulated gene 1 attenuates inflammation by sponging miR-9-5p via targeting NF-kB1/p50 in multiple sclerosis.The effect of TUG1 on inflammation in MS was evaluated by real-time PCR, western blot, ELISA and Hematoxylin-eosin staining.To further study the mechanism of TUG1 in MS, TUG1 knockdown and miR-9-5p overexpression were performed in LPS-induced BV2 cells.Notably, TUG1 expression was negatively correlated with miR-9-5p expression, while positively correlated with NF-kB1/p50.We further verified that TUG1 negatively regulated miR-9-5p expression and NF-kB1/p50 is a direct target of miR-9-5p.Down-regulation of TUG1 attenuates MS through inhibition of inflammation by sponging miR-9-5p via targeting NF-kB1/p50, suggesting that TUG1 is a potential therapeutic target for MS treatment.	31394128	RID03276	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple sclerosis	TUG1	p50	positively-E	western blot	downregulation	RT-qPCR	NA	NA	cancer progression(-);inflammatory response(-)	ceRNA(miR-9-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Demyelinating disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000101017	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Down-regulation of taurine-up-regulated gene 1 attenuates inflammation by sponging miR-9-5p via targeting NF-kB1/p50 in multiple sclerosis.The effect of TUG1 on inflammation in MS was evaluated by real-time PCR, western blot, ELISA and Hematoxylin-eosin staining.To further study the mechanism of TUG1 in MS, TUG1 knockdown and miR-9-5p overexpression were performed in LPS-induced BV2 cells.Notably, TUG1 expression was negatively correlated with miR-9-5p expression, while positively correlated with NF-kB1/p50.We further verified that TUG1 negatively regulated miR-9-5p expression and NF-kB1/p50 is a direct target of miR-9-5p.Down-regulation of TUG1 attenuates MS through inhibition of inflammation by sponging miR-9-5p via targeting NF-kB1/p50, suggesting that TUG1 is a potential therapeutic target for MS treatment.	31394128	RID03277	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Prostate cancer	DANCR	JAG1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	Docetaxel	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000270408	NA	57291	182	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	AGS|AHD|AWS|CD339|HJ1|JAGL1	Long noncoding RNA DANCR contributes to docetaxel resistance in prostate cancer through targeting the miR-34a-5p/JAG1 pathway. The abundance of DANCR, miR-34a-5p, and JAG1 mRNA was examined by quantitative reverse transcription PCR.The target relationship between DANCR and miR-34a-5p, as well as miR-34a-5p and JAG1, was demonstrated by dual-luciferase, RNA immunoprecipitation, and RNA pull-down analysis.DANCR and JAG1 were significantly upregulated, but miR-34a-5p was downregulated in DTX-resistant PC.DANCR served as a competing endogenous RNA of miR-34a-5p, leading to the derepression of miR-34a-5p target JAG1, which eventually triggered the resistance to DTX in DTX-tolerated PC.	31371987	RID03278	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE111842,GSE51827,GSE86978)
Multiple myeloma	UCA1	HGF	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);apoptosis process(-)	ceRNA(miR-1271-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000019991	NA	652995	3082	CUDR|LINC00178|onco-lncRNA-36|UCAT1	DFNB39|F-TCF|HGFB|HPTA|SF	Downregulation of lncRNA UCA1 facilitates apoptosis and reduces proliferation in multiple myeloma via regulation of the miR-1271-5p/HGF axis.The expression of RNAs in MM tissue samples and cells was evaluated through quantificational real-time polymerase chain reaction (qRT-PCR.A luciferase reporter assay was utilized to confirm the binding relationships between UCA1/HGF and miR-1271-5p.LncRNA UCA1 and HGF expression was higher in the cells and samples of patients with MM than in normal plasma cells.miR-1271-5p was confirmed to be the target of lncRNA UCA1 and HGF and to be negatively correlated with them.LncRNA UCA1 promoted proliferation and inhibited apoptosis by regulating miR-1271-5p and HGF in the human MM cell line RPMI 8226.	31356563	RID03279	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Atherosclerotic coronary heart disease	NEAT1	miR-181d-5p	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 inhibits oxidative stress-induced vascular endothelial cell injury by activating the miR-181d-5p/CDKN3 axis.The levels of NEAT1 and miR-181d-5p were measured in serum samples from ApoE-/- mice and t-BHP-treated human umbilical vein endothelial cells (HUVECs) by qRT-PCRThe potential role of NEAT1 in viability, migration and apoptosis was analyzed by CCK-8, cell metastasis, flow cytometry, dual-luciferase reporter, RNA immunoprecipitation and western blot assays using HUVECs overexpressing NEAT1.Overexpression of NEAT1 increased viability, migration and CDKN3 expression but decreased apoptotic rates, caspase-3 activity and miR-181d-5p expression in HUVECs.The expression of NEAT1 was increased, but miR-181d-5p expression was decreased in serum samples from both ApoE-/- mice and t-BHP-treated HUVECs.Altogether, these findings indicate that NEAT1 may exert a protective effect on HUVECs by regulating the miR-181d-5p/CDKN3A axis.	31352814	RID03280	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Atherosclerotic coronary heart disease	NEAT1	CDKN3A	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 inhibits oxidative stress-induced vascular endothelial cell injury by activating the miR-181d-5p/CDKN3 axis.The levels of NEAT1 and miR-181d-5p were measured in serum samples from ApoE-/- mice and t-BHP-treated human umbilical vein endothelial cells (HUVECs) by qRT-PCRThe potential role of NEAT1 in viability, migration and apoptosis was analyzed by CCK-8, cell metastasis, flow cytometry, dual-luciferase reporter, RNA immunoprecipitation and western blot assays using HUVECs overexpressing NEAT1.Overexpression of NEAT1 increased viability, migration and CDKN3 expression but decreased apoptotic rates, caspase-3 activity and miR-181d-5p expression in HUVECs.The expression of NEAT1 was increased, but miR-181d-5p expression was decreased in serum samples from both ApoE-/- mice and t-BHP-treated HUVECs.Altogether, these findings indicate that NEAT1 may exert a protective effect on HUVECs by regulating the miR-181d-5p/CDKN3A axis.	31352814	RID03281	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Ischaemic stroke	SNHG6	BCL2L11	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-181c-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000153094	NA	641638	10018	HBII-276HG|NCRNA00058|U87HG	BIM|BimEL|BimL|BimS|BOD	LncRNA SNHG6 functions as a ceRNA to regulate neuronal cell apoptosis by modulating miR-181c-5p/BIM signalling in ischaemic stroke.TTC staining, quantitative real-time PCR, cell apoptosis assay, caspase-3 activity assay, western blot, RNA immunoprecipitation and luciferase reporter assay were performed to evaluate the function and possible mechanisms of SNHG6 in the pathogenesis of ischaemic stroke.The results show that SNHG6 expression was significantly increased both OGD-induced neuronal cells and MCAO model mice.Mechanistic study further revealed that SNHG6 functioned as a competing endogenous RNA (ceRNA) for miR-181c-5p, which in turn repressed its downstream target of Bcl-2 interacting mediator of cell death (BIM) and inhibiting cell apoptosis.	31334597	RID03282	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Steatosis	SAP30-DT	PDK4	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-15b-5p)	regulation	RNA-protein	Dexamethasone	NA	Insensitivity to Antigrowth Signals	Genetic disease	Fatty liver disease	lncRNA	PCG	ENSG00000272870	GRCh38_4:173349543-173370721	ENSG00000004799	NA	105377540	5166	ENST00000608794	NA	The lncRNA ENST00000608794 acts as a competing endogenous RNA to regulate PDK4 expression by sponging miR-15b-5p in dexamethasone induced steatosis.We found that ENST00000608794 is expressed at higher levels in dexamethasone treated HepG2 cell, and ENST00000608794 can bind and be regulated by miR-15b-5p.Ectopic expression of ENST00000608794 enhanced steatosis and the protein expression of PDK4 which is a critical gene in lipid metabolism and also is a target of miR-15b-5p.Taken together, the results suggested that ENST00000608794 plays an important role in dexamethasone induced steatosis, which was partly mediated by derepressing of PDK4 through competitively binding to miR-15b-5p.	31330194	RID03283	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE86978)
Multiple uterine leiomyoma	lnc-AL445665.1-4	miR-146b-5p	positively-E	bioinformatics;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Disease of cellular proliferation	Leiomyoma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Lnc-AL445665.1-4 may be involved in the development of multiple uterine leiomyoma through interacting with miR-146b-5p.Targeted lncRNAs were selected by bioinformatics analysis, and were verified by quantitative reverse transcription-polymerase chain reaction (qRT-PCR and a dual-luciferase reporter assay.qRT-PCR;ISHowed that lnc-AL445665.1-4 expression was significantly up-regulated in MUL compared with SUL in an additional 12 and 19 paired SUL-normal and MUL-normal samples, respectively.The dual-luciferase reporter assay demonstrated the presence of binding sites on lnc-AL445665.1 for miR-146b-5p.Silencing lnc-AL445665.1-4 not only inhibited cell proliferation but also negatively regulated the expression of miR-146b-5p.Our results suggest that lnc-AL445665.1-4 may be involved in the development of MUL by interacting with miR-146b-5p	31319799	RID03284	expression association	NA		
Prostate cancer	AC024560.2	SIRT1	positively-E	bioinformatics	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236833	GRCh38_3:197660565-197665757	ENSG00000096717	NA	NA	23411	NA	SIR2|SIR2L1|SIR2alpha	[Effect of long-chain non-coding RNA-AC024560.2 on proliferation and invasion of prostate cancer cells by targeted regulation of miR-30a-5p].qRT-PCRwas used to detect the expression of AC024560.2 in 16 prostate cancer tissues and adjacent normal tissues, prostate cancer cell lines and normal prostate epithelial cells.Bioinformatics predicted possible target genes for AC024560.2.Compared with normal prostate epithelial cells, the expression of AC024560.2 in prostate cancer cell lines was significantly decreased (P<0.05), and the most significant decrease was observed in C4-2B cell lines (P<0.01).Bioinformatics predictions showed that AC024560.2 bond to miR-30a-5p, and miR-30a-5p bond to SIRT1 mRNA.The expression of AC024560.2 in the experimental group increased significantly (P<0.01), the expression of miR-30a-5p decreased significantly (P<0.01), and the expression of SIRT1 mRNA and protein increased significantly (P<0.01).AC024560.2 is lowly expressed in human prostate cancer, and may inhibit the proliferation and invasion of prostate cancer cells by regulating the expression of miR-30a-5p and SIRT1 genes.	31315374	RID03285	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	TNFSF10	FGFR1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);inflammatory response(+);apoptosis process(-)	ceRNA(miR-376-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000121858	GRCh38_3:172505508-172523475	ENSG00000077782	NA	8743	2260	Apo-2L|CD253|TL2|TRAIL	BFGFR|CD331|CEK|FLG|FLT2|H2|H3|H4|H5|KAL2|N-SAM	Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR-376-3p/FGFR1 axis.The messenger RNA levels of TNFSF10 in articular cartilage samples from patients or chondrocytes were detected by Quantitative real-time PCR assay (qRT-PCR.Then, the interaction between TNFSF10 and miR-376-3p was explored by dual-luciferase reporter test, RNA-binding protein immunoprecipitation, and RNA pull-down assay.It was found that TNFSF10 was upregulated in OA cartilages and stimulated cell proliferation, antiapoptosis, and inflammation for chondrocytes.In addition, TNFSF10 acted as a competing endogenous RNA to downregulate miR-376-3p, and the influence of TNFSF10 on chondrocytes was partly reversed by miR-376-3p.Moreover, FGFR1, as a target of miR-376-3p, had reversal functions on the outcomes mediated by miR-376-3p.The further analysis displayed that there was a negative relationship between TNFSF10 and miR-376-3p as well as miR-376-3p and FGFR1, while FGFR1 was positively related with TNFSF10.Altogether, TNFSF10 overexpression probably stimulated proliferation and inflammation, and inhibited apoptosis by regulating the miR-376-3p/FGFR1 axis, implying that its increase contributed to OA progression.	31297857	RID03286	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Idiopathic pulmonary fibrosis	PFAR	MIR15A	negatively-F	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell differentiation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Fibrosis	lncRNA	miRNA	NA	NA	ENSG00000283785	NA	NA	406948	NA	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	LncRNA PFAR contributes to fibrogenesis in lung fibroblasts through competitively binding to miR-15a.Biological information analysis and luciferase were used to identify targeted binding of lncRNA PFAR and miR-15a.western blot, quantitative reverse transcription-PCR (qRT-PCR and immunofluorescence staining were conducted to detect fibrosis-related factors.Our results showed that silencing PFAR attenuated TGF-beta1 induced fibrogenesis in primary lung fibroblasts.And miR-15a antagonized the function of PFAR and inhibited PFAR induced extracellular collagen deposition, fibroblasts proliferation, migration and differentiation.In conclusion, our results revealed that PFAR functions as a competitive endogenous RNA (ceRNA) by acting as a sponge for miR-15a, revealing a potential regulatory network involving PFAR and miR-15a with a role in the modulation of YAP1-Twist expression.	31273058	RID03287	ceRNA or sponge	NA		
Intestinal fibrosis	WWC2-AS1	FGF2	positively-E	microarray;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-16)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Intestinal disease	lncRNA	PCG	ENSG00000251128	GRCh38_4:183233628-183240634	ENSG00000138685	NA	101928734	2247	NA	FGFB	LncRNA WWC2-AS1 functions AS a novel competing endogenous RNA in the regulation of FGF2 expression by sponging miR-16 in radiation-induced intestinal fibrosis.LncRNAs were screened by microarray (Human LncRNA Array v3.0, Arraystar, Inc.) and the differentially expressed lncRNAs in RIF and non-RIF were analyzed by bioinformatics methods.WWC2-AS1 and FGF2 level was significantly higher while miR-16 was down-regulated in radiation-treated intestinal tissues.The significance of WWC2-AS1 in regulating FGF2 associated proliferation, migration, invasion and fibrosis of CCD-18Co and SEMFs by exposure to radiation was analyzed by shRNA (WWC2-AS1 shRNA) knock-down of endogenous WWC2-AS1.WWC2-AS1 more potently boosted FGF2 expression via reducing miR-16, and WWC2-AS1 shRNA remarkably inhibited FGF2 associated proliferation, migration, invasion and fibrosis of radiation treatment in vitro, further demonstrating physical interaction between miR-16 and WWC2-AS1 in radiation-induced fibrosis progress.	31262262	RID03288	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Parkinson's disease	NEAT1	miR-124	negatively-E	starBase;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 regulates MPP +-induced neuronal injury by targeting miR-124 in neuroblastoma cells.qRT-PCRwas employed to detect the expression of NEAT1, IL-1beta, IL-6 and TNF-alpha.Starbase database, RNA pull-down assay and RNA immunoprecipitation (RIP) assay were performed to verify the relationship between NEAT1 and miR-124.We found that NEAT1 expression was significantly increased in SH-SY5Y cells after MPP+ treatment in dose- and time- dependent manners.miR-124 was a target of NEAT1.Anti-miR-124 could reverse the effects caused by NEAT1 knockdown in MPP+ treated SH-SY5Y cells.Therefore, we speculated that NEAT1 may regulate MPP+ induced neuronal injury by targeting miR-124 in SH-SY5Y cells.	31228597	RID03289	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Cardiac hypertrophy	CTBP1-DT	TLR4	positively-E	luciferase reporter assay;RIP;ChIP;bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with protein	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	ENSG00000196810	GRCh38_4:1249300-1288291	ENSG00000136869	NA	92070	7099	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	ARMD10|CD284|hToll|TLR-4	Sp1-induced LncRNA CTBP1-AS2 is a novel regulator in cardiomyocyte hypertrophy by interacting with FUS to stabilize TLR4.We revealed the up-regulation of CTBP1-AS2 and TLR4 in cardiomyocyte hypertrophy models.Also, we confirmed the positive correlation between CTBP1-AS2 and TLR4 expressions in cardiomyocyte hypertrophy tissues.Mechanism research showed that CTBP1-AS2 stabilized TLR4 mRNA by recruiting FUS.In conclusion, our study uncovered CTBP1-AS2 as a novel regulator of cardiomyocyte hypertrophy through regulating TLR4, providing a new potential treatment target for cardiomyocyte hypertrophy.	31220774	RID03290	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Breast cancer	LINC00473	MAPK1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-198)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000223414	NA	ENSG00000100030	NA	90632	5594	C6orf176|LNC473|bA142J11.1	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Long noncoding RNA LINC00473 functions as a competing endogenous RNA to regulate MAPK1 expression by sponging miR-198 in breast cancer.Expression pattern of LINC00473 was analyzed using qRT-PCR(quantitative real-time polymerase chain reaction) assays in BC tissues and cells.Target prediction, luciferase assays, RNA fluorescence in situ hybridization and RNA immunoprecipitation were used to verify the role of LINC00473 as a competing endogenous RNA.In our study, we found that LINC00473 was highly expressed in BC tissues and cells, and the elevated expression was correlated with shorter overall survival in patients with BC.Furthermore, knockdown of LINC00473 significantly inhibited the capacity of proliferation, invasion and migration of BC cells.Following experiments revealed that LINC00473 may function as a competing endogenous RNA to regulate the expression of Mitogen-Activated Protein Kinase 1 (MAPK1) through competition for miR-198.	31201066	RID03291	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SRSF1	NEAT1	positively-F	RIP;microarray	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Brain glioma	PCG	lncRNA	ENSG00000136450	NA	ENSG00000245532	GRCh38_11:65422774-65445540	6426	283131	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	The RNA-binding protein SRSF1 is a key cell cycle regulator via stabilizing NEAT1 in glioma.Importantly, we identified nuclear paraspeckle assembly transcript1 (NEAT1), an upregulated long non-coding RNA (lncRNA) in glioma, as a target of SRSF1.Mechanistically, we proved that SRSF1 bound to NEAT1 and facilitated its RNA stability.The positive correlation between SRSF1 and NEAT1 levels in cancers further supported the positive regulation of NEAT1 by SRSF1.Collectively, our results provide novel insights on the splicing-independent mechanisms of SRSF1 in glioma, and confirm that NEAT1, whose stability maintained by SRSF1, implicates gliomagenesis by regulating cell cycle.	31200124	RID03292	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Breast cancer	CTBP1-AS	miR-940	negatively-F	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000280927	GRCh38_4:1210120-1218591	NA	NA	285463	NA	PCAT10	NA	Molecular mechanisms of long chain non-coding RNA CTBP1-AS in regulation of invasion and migration of breast cancer cells.qRT-PCRwas used to detect LncRNA CTBP1-AS expression levels in human normal breast epithelial cell (MCF-10A) and breast cancer cells (MCF-7, BT- 549, MDA-MB-231 and MDA-MB-435).Bioinformatics analysis was performed to predict the downstream targets of LncRNA CTBP1-AS, which were further validated by dual-luciferase reporter gene system.The results showed that LncRNA CTBP1-AS was aberrantly overexpressed in breast cancer tissues and breast cancer cells compared to the control group.Bioinformatics analysis and dual-luciferase reporter gene system results validated that microRNA-940 was the downstream target of LncRNA CTBP1-AS.Interestingly, overexpressed microRNA-940 abrogated the effects of LncRNA CTBP1-AS on cell proliferation, apoptosis, and invasion.In conclusion, overexpressed LncRNA CTBP1- AS promoted breast cancer cell proliferation, invasion as well as migration, inhibited cell apoptosis and accelerated breast cancer development by sponging microRNA-940.	31165609	RID03293	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Colorectal cancer	ADAMTS9-AS2	PHLPP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cancer progression(+)	ceRNA(miR-32)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000040199	NA	100507098	23035	NA	KIAA0931|PHLPPL|PPM3B	Identification and development of long non-coding RNA-associated regulatory network in colorectal cancer.A total of 38 differentially expressed (DE) lncRNAs, 23 DEmiRNAs and 27 DEmRNAs were identified by analysing the expression profiles of CRC obtained from The Cancer Genome Atlas (TCGA).Experimental validation was performed using clinical samples by quantitative real-time PCR (qRT-PCR, which showed that expression of the genes in the axis was associated with clinicopathological features and the correlation among them perfectly conformed to the 'ceRNA theory'.Overexpression of ADAMTS9-AS2 in colon cancer cell lines significantly inhibited the miR-32 expression and promoted PHLPP2 expression, while ADAMTS9-AS2 knockdown had the opposite effects.	31144439	RID03294	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Lupus nephritis	RP11-2B6.2	ISG	positively-E	luciferase reporter assay	upregulation	RT-qPCR;sequencing	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Urinary system disease	Nephritis	lncRNA	PCG	ENSG00000269929	GRCh38_9:94166258-94200902	NA	NA	NA	NA	NA	NA	Identification of Renal Long Non-coding RNA RP11-2B6.2 as a Positive Regulator of Type I Interferon Signaling Pathway in Lupus Nephritis.RNA sequencing was used to analyze the expression of lncRNAs in kidney biopsies from LN patients and controls.In situ hybridization, imaging flow cytometry, dual-luciferase reporter assay, and ATAC sequencing were used to study the functions of lncRNA RP11-2B6.2.RT-qPCR, ELISA, and western blot were done to detect RNA and protein levels of specific genes.Knockdown of lncRNA RP11-2B6.2 in renal cells inhibited the expression of IFN stimulated genes (ISGs), while overexpression of lncRNA RP11-2B6.2 enhanced ISG expression.	31130957	RID03295	expression association	NA		
Endometrial cancer	NR2F1-AS1	SOX4	positively-E	luciferase reporter assay	upregulation	western blot	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-363)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000124766	NA	441094	6659	FLJ42709	NA	LncRNA NR2F1-AS1 is involved in the progression of endometrial cancer by sponging miR-363 to target SOX4.Luciferase reporter assay was conducted to investigate the target gene of miR-363.The expression levels of PI3K/AKT/GSK-3beta pathway-associated factors were assayed using western blot.NR2F1-AS1 was significantly overexpressed in EC tissues and cells.miR-363 was negatively regulated by NR2F1-AS1.SOX4 was a target of miR-363.The results demonstrated that NR2F1-AS1 was highly expressed in EC, which involved in the proliferation and migration of EC cells through downregulation of miR-363 to target SOX4 and regulating PI3K/AKT/GSK-3beta pathway.	31109400	RID03296	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	UCA1	miR-185-5	negatively-E	bioinformatics;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell autophagy(-);cell growth(-)	NA	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	[Effects of Interference with UCA1 and Inhibition of miR-185-5p on Activation, Autophagy and Survival of beta-Catenin Pathway in Non-small Cell Lung Cancer].qRT-PCRwas employed to detect the mRNA levels of UCA1 and miR-185-5p.The relationship between lnRNA UCA1 and miR-185-5p was validated by bioinformatics analysis and luciferase reporter system assays. sh-UCA1 significantly decreased UCA1 expression and increased miR-185-5p expression in A549 cells, and inhibited the cell growth and autophagy, while promoted the cell apoptosis (P<0.01).Bioinformatics analysis and luciferase reporter system assays demonstrated that lncRNA UCA1 and miR-185-5 can combine effectively, indicating that they have a targating relationship. The effect of UCA1 inhibition for miR-185-5p was decreased by lncRNA UCA1 inference, and released the beta-Catenin/TCF-4, Beclin 1 and LC3  and further reduced the autophagy and growth in A549 cells.	31106532	RID03297	expression association	NA	UP(PAAD);DATA(GSE40174)	
Ischaemic stroke	H19	TP53	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cancer progression(-)	transcriptional regulation	association	NA	NA	NA	NA	Nervous system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LFS1|p53	Long noncoding RNA H19 prevents neurogenesis in ischemic stroke through p53/Notch1 pathway.Circulating H19 levels in ischemic stroke patients and the mRNA levels of p53 target genes were tested by real-time polymerase chain reaction.The expression of neurogenesis related proteins was assessed by Immunofluorescence and western blot.Circulating H19 levels were positively associated with the National Institute of Health Stroke Scale Scores of the patients in 7d, 30d and 90d after stroke attack.While inhibiting p53 on the basis of H19 knockdown reversed the pro-neurogenesis effect of H19 inhibition.Furthermore, H19 decreased the transcriptional activity of p53 and the expression of Notch1, and p53 inhibition abolished these effects of H19.ur findings demonstrate that H19 prevents the process of neurogenesis after ischemic stroke through p53/Notch1 pathway and strengthen the novel role of H19-based therapy for ischemic stroke.	31102753	RID03298	transcriptional regulation	circulating	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Ischaemic stroke	H19	NOTCH1	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000148400	NA	283120	4851	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	TAN1	Long noncoding RNA H19 prevents neurogenesis in ischemic stroke through p53/Notch1 pathway.Circulating H19 levels in ischemic stroke patients and the mRNA levels of p53 target genes were tested by real-time polymerase chain reaction.The expression of neurogenesis related proteins was assessed by Immunofluorescence and western blot.Circulating H19 levels were positively associated with the National Institute of Health Stroke Scale Scores of the patients in 7d, 30d and 90d after stroke attack.While inhibiting p53 on the basis of H19 knockdown reversed the pro-neurogenesis effect of H19 inhibition.Furthermore, H19 decreased the transcriptional activity of p53 and the expression of Notch1, and p53 inhibition abolished these effects of H19.ur findings demonstrate that H19 prevents the process of neurogenesis after ischemic stroke through p53/Notch1 pathway and strengthen the novel role of H19-based therapy for ischemic stroke.	31102753	RID03299	expression association	circulating	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Kidney injury	HOTAIR	BCL2	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	apoptosis process(-)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	Influence of lncRNA HOTAIR on acute kidney injury in sepsis rats through regulating miR-34a/Bcl-2 pathway.The messenger RNA (mRNA) expression levels of miR-34a and B-cell lymphoma-2 (Bcl-2) were detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR.The target gene of miR-34a was Bcl-2, according to the miRNA online database.MiR-34a level in kidney tissues was upregulated, while the mRNA level of Bcl-2 significantly decreased in the model group.The miR-34a level in kidney tissues decreased, while the Bcl-2 mRNA level remarkably increased in lncRNA HOTAIR mimic group.LncRNA HOTAIR overexpression can alleviate AKI in sepsis rats by inhibiting the apoptosis of kidney tissues by downregulating the miR-34a/Bcl-2 signaling pathway.	31081107	RID03300	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Kidney disease	MALAT1	ZEB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);fibrotic(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA MALAT1 facilities high glucose induced endothelial to mesenchymal transition and fibrosis via targeting miR-145/ZEB2 axis.qRT-PCRwas used to measure levels of MALAT1 and miR-145.In addition, we validated interactions of MALAT1-miR-145 and miR-145-ZEB2 by dual-luciferase reporter assays.MALAT1 was upregulated while miR-145 was downregulated in renal tissues of db/db mice.Furthermore, miR-145 binds to both MALAT1 and ZEB2.Mechanistically, MALAT1 functions as a sponge RNA for miR-145 to derepress the expression of target gene ZEB2, thereby inducing EMT and fibrosis.	31081103	RID03301	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Kidney disease	MALAT1	miR-145	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);fibrotic(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000269936	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1 facilities high glucose induced endothelial to mesenchymal transition and fibrosis via targeting miR-145/ZEB2 axis.qRT-PCRwas used to measure levels of MALAT1 and miR-145.In addition, we validated interactions of MALAT1-miR-145 and miR-145-ZEB2 by dual-luciferase reporter assays.MALAT1 was upregulated while miR-145 was downregulated in renal tissues of db/db mice.Furthermore, miR-145 binds to both MALAT1 and ZEB2.Mechanistically, MALAT1 functions as a sponge RNA for miR-145 to derepress the expression of target gene ZEB2, thereby inducing EMT and fibrosis.	31081103	RID03302	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Pneumonia	XIST	TLR4	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136869	NA	7503	7099	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ARMD10|CD284|hToll|TLR-4	Knockdown XIST alleviates LPS-induced WI-38 cell apoptosis and inflammation injury via targeting miR-370-3p/TLR4 in acute pneumonia.Luciferase reporter, RIP, and RNA pull-down assays were used to detect the combination of miR-370-3p and XIST.Besides, the tested proinflammatory factors were analysed by qRT-PCRand western blot, and their productions were quantified by ELISA.Mechanistically, XIST functioned as a competitive endogenous RNA (ceRNA) by effectively binding to miR-370-3p and then restoring TLR4 expression.Knockdown of XIST remarkably alleviated LPS-induced cell injury through increasing cell viability and inhibiting apoptosis and inflammatory cytokine levels through regulating JAK/STAT and NF-kB pathways.	31066476	RID03303	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Biliary atresia	H19	HMGA2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);fibrotic(+)	ceRNA(let-7)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Cholestasis	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BABL|HMGIC|LIPO	Long Noncoding RNA H19 Contributes to Cholangiocyte Proliferation and Cholestatic Liver Fibrosis in Biliary Atresia.Here, we show that both hepatic and serum exosomal H19 levels are positively correlated with severity of fibrotic liver injuries in BA patients.H19 deficiency protects mice from BDL-induced cholangiocyte proliferation and LF by inhibiting bile-acid-induced expression and activation of S1PR2 and sphingosine kinase 2 (SphK2).Furthermore, H19 acts as a molecular sponge for members of the microRNA let-7 family, which results in up-regulation of high-mobility group AT-hook 2 (HMGA2), a known target of let-7 and enhancement of biliary proliferation. These results indicate that H19 plays a critical role in cholangiocyte proliferation and cholestatic liver injury in BA by regulating the S1PR2/SphK2 and let-7/HMGA2 axis.	31063660	RID03304	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Biliary atresia	H19	S1PR2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);fibrotic(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Cholestasis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000267534	NA	283120	9294	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	AGR16|DFNB68|EDG5|Gpcr13|H218	Long Noncoding RNA H19 Contributes to Cholangiocyte Proliferation and Cholestatic Liver Fibrosis in Biliary Atresia.Here, we show that both hepatic and serum exosomal H19 levels are positively correlated with severity of fibrotic liver injuries in BA patients.H19 deficiency protects mice from BDL-induced cholangiocyte proliferation and LF by inhibiting bile-acid-induced expression and activation of S1PR2 and sphingosine kinase 2 (SphK2).Furthermore, H19 acts as a molecular sponge for members of the microRNA let-7 family, which results in up-regulation of high-mobility group AT-hook 2 (HMGA2), a known target of let-7 and enhancement of biliary proliferation. These results indicate that H19 plays a critical role in cholangiocyte proliferation and cholestatic liver injury in BA by regulating the S1PR2/SphK2 and let-7/HMGA2 axis.	31063660	RID03305	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Biliary atresia	H19	SPHK2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);fibrotic(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Cholestasis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000063176	NA	283120	56848	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Long Noncoding RNA H19 Contributes to Cholangiocyte Proliferation and Cholestatic Liver Fibrosis in Biliary Atresia.Here, we show that both hepatic and serum exosomal H19 levels are positively correlated with severity of fibrotic liver injuries in BA patients.H19 deficiency protects mice from BDL-induced cholangiocyte proliferation and LF by inhibiting bile-acid-induced expression and activation of S1PR2 and sphingosine kinase 2 (SphK2).Furthermore, H19 acts as a molecular sponge for members of the microRNA let-7 family, which results in up-regulation of high-mobility group AT-hook 2 (HMGA2), a known target of let-7 and enhancement of biliary proliferation. These results indicate that H19 plays a critical role in cholangiocyte proliferation and cholestatic liver injury in BA by regulating the S1PR2/SphK2 and let-7/HMGA2 axis.	31063660	RID03306	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE67939,GSE75367,GSE86978)
Diabetic retinopathy	SNHG7	SIRT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	interact with miR	association	RNA-protein	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000096717	NA	84973	23411	MGC16037|NCRNA00061	SIR2L1	Long noncoding RNA SNHG7 inhibits high glucose-induced human retinal endothelial cells angiogenesis by regulating miR-543/SIRT1 axis.Diabetic retinopathy (DR) is the serious complication of type 2 diabetes mellitus, which could lead to visual impairment.We discovered that SNHG7 was decreased in hRECs under HG stimuli.In terms of mechanism, we found that SNHG7 directly inhibited miR-543, which targeted the 3'-UTR of Silent information regulator T1 (SIRT1) mRNA and subsequently downregulated the VEGF expression in hRECs.Collectively, our results suggested that SNHG7 is a potential molecular target for attenuating HG-induced angiogenesis in the DR through regulation of the miR-543-mediated SIRT1/VEGF pathway.	31056258	RID03307	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Mycosis fungoides	CCL21	MALAT1	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell migration(+)	NA	association	protein-RNA	NA	NA	NA	Cancer	Lymphoma	PCG	lncRNA	ENSG00000137077	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6366	378938	6Ckine|CKb9|ECL|exodus-2|SCYA21|SLC|TCA4	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CCL21 Induces mTOR-dependent MALAT1 Expression, Leading to Cell Migration in Cutaneous T-Cell Lymphoma.Mycosis fungoides (MF) is indolent, but may disseminate to leukemia.nd leukemia-associated non-coding insulin-like growth factor 1 receptor activator RNA 1 (LUNAR1) in tissues from MF was studied using polymerase chain reaction and RNA interference in MF cell line MyLa were used to address this question. Expression of MALAT1 was selectively increased in MF tissues.CCL21 was found not only to mediate migration, but also to enhance MALAT1 and mammalian target of rapamycin (mTOR) activation in MyLa cells.CCL21 induced mTOR activation in MyLa cells, followed by expression of MALAT1, causing cell migration.	31028199	RID03308	expression association	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Esophagus squamous cell carcinoma	LINC00473	SPIN1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	radioresistance(+)	ceRNA(miR-374a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000223414	NA	ENSG00000106723	NA	90632	10927	C6orf176|LNC473|bA142J11.1	SPIN|TDRD24	LINC00473/miR-374a-5p regulates esophageal squamous cell carcinoma via targeting SPIN1 to weaken. We found that LINC00473 was markedly upregulated in ESCC tissues and cell lines, and its expression was remarkably related to cellular response to irradiation.Spindlin1 (SPIN1) was verified as a downstream target of miR-374a-5p, and LINC00473 upregulated SPIN1 expression through negatively modulating miR-374a-5p expression.To sum up, we demonstrated that LINC00473 facilitated radioresistance by regulating the miR-374a-5p/SPIN1 axis in ESCC.	31017716	RID03309	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Atherosclerosis	LEF1-AS1	miR-544a	negatively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000232021	GRCh38_4:108167525-108258037	NA	NA	641518	NA	NA	NA	LncRNA LEF1-AS1 regulates the migration and proliferation of vascular smooth muscle cells by targeting miR-544a/PTEN axis.The quantitative<U+00A0>real-time polymerase chain reaction was used to analyze levels of LEF1-AS1 and microRNA-544a (miR-544a).The interaction between LEF1-AS1, miR-544a, and PTEN was probed using bioinformatical analysis and dual-luciferase assay.In plasma and tissue of patients with coronary artery atherosclerosis, LEF1-AS1 was upregulated and miR-544a was downregulated.A negative correlation was found between LEF1-AS1 and miR-544a.LEF1-AS1 regulates smooth muscle cell proliferation and migration through the miR-544a/PTEN axis, indicating that LEF1-AS1 may be a potential therapeutic target in atherosclerosis.	31016789	RID03310	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Parkinson's disease	TP53COR1	CLU	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000120885	NA	102800311	1191	TRP53COR1|linc-p21|lincRNA-p21	AAG4|APO-J|APOJ|CLI|CLU1|CLU2|KUB1|NA1/NA2|SGP-2|SGP2|SP-40|TRPM-2|TRPM2	Long non-coding RNA-p21 regulates MPP +-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells.Here, the results showed that lnc-p21 was highly expressed in human neuroblastoma SH-SY5Y cells treated with MPP+.miR-625 was identified as a target of lnc-p21.Additionally, lnc-p21 positively regulated TRPM2 expression by targeting miR-625, and knockdown of TRPM2 inhibited MPP+-induced neuronal injury.	31004593	RID03311	expression association	NA		UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Parkinson's disease	TP53COR1	MIR625	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	miRNA	NA	NA	ENSG00000207781	NA	102800311	693210	TRP53COR1|linc-p21|lincRNA-p21	MIRN625|hsa-mir-625	Long non-coding RNA-p21 regulates MPP +-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells.Here, the results showed that lnc-p21 was highly expressed in human neuroblastoma SH-SY5Y cells treated with MPP+.miR-625 was identified as a target of lnc-p21.Additionally, lnc-p21 positively regulated TRPM2 expression by targeting miR-625, and knockdown of TRPM2 inhibited MPP+-induced neuronal injury.	31004593	RID03312	expression association	NA		
Parkinson's disease	TP53COR1	MIR625	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	miRNA	NA	NA	ENSG00000207781	NA	102800311	693210	TRP53COR1|linc-p21|lincRNA-p21	MIRN625|hsa-mir-625	Long non-coding RNA-p21 regulates MPP +-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells.Here, the results showed that lnc-p21 was highly expressed in human neuroblastoma SH-SY5Y cells treated with MPP+.miR-625 was identified as a target of lnc-p21.Additionally, lnc-p21 positively regulated TRPM2 expression by targeting miR-625, and knockdown of TRPM2 inhibited MPP+-induced neuronal injury.	31004593	RID03313	expression association	NA		
Pulmonary fibrosis	H19	miR-140	negatively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Knockdown of Long Noncoding RNA H19 Represses the Progress of Pulmonary Fibrosis through the Transforming Growth Factor beta/Smad3 Pathway by Regulating MicroRNA 140.Here, our observations showed that H19 expression was significantly upregulated and that of microRNA 140 (miR-140) was markedly reduced in pulmonary fibrotic tissues from idiopathic pulmonary fibrosis (IPF) patients and transforming growth factor beta1 (TGF-beta1)-induced HBE and A549 cells.Moreover, the expression of H19 was negatively correlated with the expression of miR-140 in IPF tissues.The study of molecular mechanisms showed that H19 functioned via reduction of miR-140 expression by binding to miR-140.Taken together, our findings showed that H19 knockdown attenuated pulmonary fibrosis via the regulatory network of lncRNA H19-miR-140-TGF-beta/Smad3 signaling, and H19 and miR-140 might represent therapeutic targets and early diagnostic and prognostic biomarkers for patients with pulmonary fibrosis.	30988156	RID03314	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	
Atherosclerosis	OIP5-AS1	GSK-3beta	negatively-F	ChIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Long noncoding RNA OIP5-AS1 accelerates the ox-LDL mediated vascular endothelial cells apoptosis through targeting GSK-3beta via recruiting EZH2.Results from this study found that lncRNA OIP5-AS1 was significantly over-expressed in the human umbilical vein endothelial cells (HUVECs) administered with ox-LDL.Chromatin immunoprecipitate (ChIP) revealed that lncRNA OIP5-AS1 reduced GSK-3beta expression through recruiting EZH2, a critical element of the Polycomb Repressive Complex 2 (PRC2) complex that directly bind with the GSK-3beta promoter region.Overall, these findings suggest that lncRNA OIP5-AS1 accelerates ox-LDL mediated vascular endothelial cell apoptosis through targeting GSK-3beta via recruiting EZH2, providing potential therapeutic strategies for atherosclerosis.	30972206	RID03315	interact with protein	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Osteoporosis	lnc-ob1	SP7	positively-E	ChIP;RIP	upregulation	qPCR	NA	NA	bone formation(+)	DNA methylation	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	NA	NA	ENSG00000170374	NA	NA	121340	NA	OI11|OI12|OSX|osterix	The long noncoding RNA lnc-ob1 facilitates bone formation by upregulating Osterix in osteoblasts.Here, we show that lnc-ob1 regulates osteoblast activity and bone formation in mice by upregulating the osteogenic transcription factor Osterix.Expression of lnc-ob1 is enriched in osteoblasts and upregulated during osteoblastogenesis.Mechanistically, lnc-ob1 upregulates the expression of Osterix in mouse and human osteoblasts, probably via inhibition of H3K27me3 methylation.	32694877	RID03316	epigenetic regulation	NA		UP(PAAD);DATA(GSE40174)
Atherosclerosis	AF131217.1	KLF4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(-);inflammatory response(-)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000232855	GRCh38_21:28328738-28674848	ENSG00000136826	NA	NA	9314	NA	EZF|GKLF	Shear-Sensitive lncRNA AF131217.1 Inhibits Inflammation in HUVECs via Regulation of KLF4.we identified a novel long noncoding RNA AF131217.1, which was upregulated after laminar shear stress treatment in human umbilical vein endothelial cells.Mechanistic investigations indicated that AF131217.1 acted as a competing endogenous RNA for miR-128-3p, leading to regulation of its target gene KLF4.In conclusion, our study demonstrates for the first time that laminar shear stress regulates the expression of AF131217.1 in human umbilical vein endothelial cells, and the AF131217.1/miR-128-3p/KLF4 axis plays a vital role in atherosclerosis development.	30905197	RID03317	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Atherosclerosis	CERNA1	API5	positively-E	western blot	upregulation	RT-PCR	NA	NA	cancer progression(-);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000259577	GRCh38_15:52179999-52206915	ENSG00000166181	NA	100129973	8539	LOC100129973	AAC-11|AAC11|API5L1	Long Noncoding RNA-CERNA1 Stabilized Atherosclerotic Plaques in apolipoprotein E -/- Mice.in order to investigate how a new lncRNA, CERNA1, regulates the composition of atherosclerotic plaques, we overexpressed CERNA1 in apolipoprotein E-/- (Apo E-/-) mice and analyzed the role of CERNA1 in atherosclerotic plaque stabilization.The results showed that CERNA1 inhibited the apoptosis of VSMCs and anti-inflammatory macrophages through increasing API5 level and further stabilized the atherosclerotic plaques.	30888631	RID03318	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE55807,GSE86978,GSE41245)
Osteoarthritis	lncRNA-TM1P3	MMP13	positively-E	bioinformatics;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-22)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000137745	NA	NA	4322	NA	CLG3|MANDP1|MDST|MMP-13	Long noncoding RNA TM1P3 is involved in osteoarthritis by mediating chondrocyte extracellular matrix degradation.Real-time PCR and western blotwere performed to detect expressions of miR-22, lncRNA-TM1P3, ALK1, MMP13, pSMAD1/5, SMAD1, and pSMAD5.The lncRNA-TM1P3 significantly upregulated in patients with OA, accompanied by the downregulation of miR-22 and upregulation of pSMAD1/5 and MMP13, which ultimately resulted in the degradation of the chondrocyte ECM in patients with OA.Bioinformatics analysis predicted miR-22 as a target of both lncRNA-TM1P3 and MMP13. These findings demonstrated that the lncRNA-TM1P3/miR-22/TGF-beta signaling/MMP13 axis is involved in the degradation of chondrocyte ECM in patients with OA, which could provide novel therapies for OA treatment.	30887601	RID03319	ceRNA or sponge	NA		UP(PAAD);DATA(GSE40174)
Breast cancer	MAGI2-AS	PTEN	positively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000171862	NA	NA	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA MAGI2-AS3 inhibits breast cancer cell migration and invasion via sponging microRNA-374a.In the present study, our results showed that MAGI2-AS3 can inhibit the migration and invasion of breast cancer cells.In addition, an increase in MAGI2-AS3 can inhibit microRNA-374a (miR-374a) expression in breast cancer cells.Phosphatase and tensin homolog (PTEN) was found to be an novel mRNA target of miR-374a.MAGI2-AS3 upregulation inhibited breast cancer metastatic progression by decreasing miR-374a and enhancing PTEN expression.	30883342	RID03320	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Ovarian cancer	HULC	miR-125a-3p	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	HULC functions as an oncogene in ovarian carcinoma cells by negatively modulating miR-125a-3p.The aberrant expression of highly upregulated in liver cancer (HULC) has been reported to participate in ovarian cancer development.We transfected SKOV3 cells with pEX-HULC, sh-HULC, and miR-125a-3p mimic as well as their corresponding negative controls (pEX-3, sh-NC, and NC) to alter the expression of HULC and miR-125a-3p, which were analyzed by quantitative reverse transcription PCR (qRT-PCR.In addition, HULC negatively regulated the expression of miR-125a-3p.Overexpression of HULC promoted ovarian carcinoma development by activating PI3K/AKT/mTOR signaling pathway via downregulating miR-125a-3p.	30863948	RID03321	expression association	NA		
Non-small cell lung cancer	PVT1	Beclin-1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-216b)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	The PVT1/miR-216b/Beclin-1 regulates cisplatin sensitivity of NSCLC cells via modulating autophagy and apoptosis.The expressions of PVT1, microRNA-216b (miR-216b) and apoptosis- or autophagy-related proteins were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR or western blot assay, respectively.Luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to probe the interaction between miR-216b and PVT1 or Beclin-1. PVT1 was highly expressed and associated with poor prognosis of NSCLC patients. PVT1 may function as a competing endogenous RNA for miR-216b to inhibit cisplatin sensitivity of NSCLC through regulating apoptosis and autophagy via miR-216b/Beclin-1 pathway, providing a novel target for improving chemo-therapy efficacy of NSCLC.	30859368	RID03322	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Cervical cancer	HOTAIR	MAPK1	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Long non-coding RNA HOTAIR regulates proliferation, migration and invasion of human cervical cancer cells by modulating expression of MAPK1.The expression profile of the lncRNA HOTAIR was determined by quantitative RT-PCR The results showed that the expression of lncRNA HOTAIR was significantly.HOTAIR has been reported to interact with MAPK1 in cancer cells, and in this study MAPK1 was found to be overexpressed (up to 3.7-fold) in all the cervical cancer cells and silencing of HOTAIR inhibited the expression of MAPK1 in DoTc2 cervical cancer cells.	32864005	RID03323	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lymphoma	HOTAIR	BMI1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-137)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168283	NA	100124700	648	HOXC-AS4|HOXC11-AS1|NCRNA00072	PCGF4|RNF51	Knockdown of long noncoding RNA HOTAIR inhibits cell growth of human lymphoma cells by upregulation of miR-148b.The expressions of HOTAIR, miR-148b, and BMI1 in lymphoma samples and cells (AHH-1, Raji, and U937) were quantified by quantitative reverse polymerase chain reaction (qRT-PCR.miR-148b expression was upregulated by HOTAIR inhibition.the present study demonstrated that HOTAIR knockdown inhibited the cell growth and promoted apoptosis of lymphoma cells via upregulation of miR-148b and miR-148b further regulated the expression of BMI1 via MAPK and ERK signaling pathways.	30848513	RID03324	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Aortic valve disease	OIP5-AS1	TWIST1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-149b)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000122691	NA	729082	7291	cyrano|linc-OIP5	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	LncRNA OIP5-AS1 inhibits osteoblast differentiation of valve interstitial cells via miR-137/TWIST11 axis.OIP5-AS1, miR-137 and TWIST-related protein 1 (TWIST1) expressions were detected by quantitative real-time PCR (qRT-PCR.The interaction between OIP5-AS1 and miR-137 was studied using luciferase reporter assay, RNA pull-down assay and RNA-binding protein immunoprecipitation (RIP) assay.Luciferase reporter assay was also used to identify the possible interaction between miR-137 and TWIST11.The results showed that downregulated expression of OIP5-AS1 was observed in human aortic VICs after osteogenic induction.Mechanistically, we further showed that OIP5-AS1 could relieve osteogenic differentiation of VICs via upregulating miR-137 target gene TWIST1.	30846207	RID03325	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(SKCM);DATA(GSE38495)
Cardiac carcinoma	H19	miR-130a-3p	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+);radioresistance(-)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 interacted with miR-130a-3p and miR-17-5p to modify radio-resistance and chemo-sensitivity of cardiac carcinoma cells.We also performed luciferase reporter gene assay to verify the targeted relationship between H19 and miR-130a-3p, as well as between H19 and miR-17-5p.The study results indicated that H19, miR-130a-3p, and miR-17-5p expressions within cardiac cancer tissues were significantly beyond those within adjacent nontumor tissues.H19 expression was positively correlated with both miR-130a-3p (rs = 0.43) and miR-17-5p (rs = 0.49) expressions.It was also drawn from luciferase reporter gene assay that H19 could directly target miR-130a-3p and miR-17-5p, thereby modifying the sensitivity of cardiac cancer cells to drugs and X-rays .	30843379	RID03326	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	
Cardiac carcinoma	H19	miR-17-5p	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+);radioresistance(-)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	LncRNA H19 interacted with miR-130a-3p and miR-17-5p to modify radio-resistance and chemo-sensitivity of cardiac carcinoma cells.We also performed luciferase reporter gene assay to verify the targeted relationship between H19 and miR-130a-3p, as well as between H19 and miR-17-5p.The study results indicated that H19, miR-130a-3p, and miR-17-5p expressions within cardiac cancer tissues were significantly beyond those within adjacent nontumor tissues.H19 expression was positively correlated with both miR-130a-3p (rs = 0.43) and miR-17-5p (rs = 0.49) expressions.It was also drawn from luciferase reporter gene assay that H19 could directly target miR-130a-3p and miR-17-5p, thereby modifying the sensitivity of cardiac cancer cells to drugs and X-rays .	30843379	RID03327	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	
Alzheimer's disease	BRD3OS	MEM	negatively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000235106	GRCh38_9:134025481-134034666	NA	NA	266655	NA	bA374P20.3|FLJ35348|LINC00094|NCRNA00094	NA	The role of LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis in Memantine mediated protective effects on blood-brain barrier in AD microenvironment.Furthermore, silencing LINC00094 enhance the effect of MEM on decreasing BBB permeability in AD microenvironment.The analysis of the mechanism demonstrated that reduction of LINC00094 inhibited Endophilin-1 expression by up-regulating miR-224-4p/miR-497-5p, promoted the expression of ZO-1, occludin and claudin-5, and ultimately alleviated BBB permeability in AD microenvironment.Taken together, the present study suggests that the MEM/LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment.	30801976	RID03328	expression association	NA		
Alzheimer's disease	BRD3OS	Endophilin-1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-224-4p)	regulation	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000235106	GRCh38_9:134025481-134034666	NA	NA	266655	NA	bA374P20.3|FLJ35348|LINC00094|NCRNA00094	NA	The role of LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis in Memantine mediated protective effects on blood-brain barrier in AD microenvironment.Furthermore, silencing LINC00094 enhance the effect of MEM on decreasing BBB permeability in AD microenvironment.The analysis of the mechanism demonstrated that reduction of LINC00094 inhibited Endophilin-1 expression by up-regulating miR-224-4p/miR-497-5p, promoted the expression of ZO-1, occludin and claudin-5, and ultimately alleviated BBB permeability in AD microenvironment.Taken together, the present study suggests that the MEM/LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment.	30801976	RID03329	ceRNA or sponge	NA		
Alzheimer's disease	BRD3OS	Endophilin-1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-497-5p)	regulation	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000235106	GRCh38_9:134025481-134034666	NA	NA	266655	NA	bA374P20.3|FLJ35348|LINC00094|NCRNA00094	NA	The role of LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis in Memantine mediated protective effects on blood-brain barrier in AD microenvironment.Furthermore, silencing LINC00094 enhance the effect of MEM on decreasing BBB permeability in AD microenvironment.The analysis of the mechanism demonstrated that reduction of LINC00094 inhibited Endophilin-1 expression by up-regulating miR-224-4p/miR-497-5p, promoted the expression of ZO-1, occludin and claudin-5, and ultimately alleviated BBB permeability in AD microenvironment.Taken together, the present study suggests that the MEM/LINC00094/miR-224-5p (miR-497-5p)/Endophilin-1 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment.	30801976	RID03330	ceRNA or sponge	NA		
Diabetic retinopathy	KCNQ1OT1	EGFR	positively-F	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-protein	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000146648	NA	10984	1956	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	ERBB|ERBB1|ERRP|HER1|NISBD2|PIG61|mENA	KCNQ1OT1 affects the progression of diabetic retinopathy by regulating miR-1470 and epidermal growth factor receptor.High KCNQ1OT1 expression was correlated with DR stage and low visual function.Regarding bioinformatics analysis and in vitro dual-luciferase reporter assay, there should be a negative correlation between KCNQ1OT1 and miR-1470.Additionally, mRNA of epidermal growth factor receptor (EGFR) was proved as the target of miR-1470 and EGFR targeting by miR-1470 initiated KCNQ1OT1 deficiency-induced apoptosis and promoted proliferation.The results suggested that KCNQ1OT1 could sponge miR-1470 and further regulate EGFR in DR.	30784065	RID03331	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Atherosclerosis	lncRNA-FA2H-2	MLKL	negatively-E	luciferase activity assay;ChIRP	downregulation	qRT-PCR	NA	NA	cell autophagy(+);inflammatory response(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000168404	NA	NA	197259	NA	hMLKL	The role of the LncRNA-FA2H-2-MLKL pathway in atherosclerosis by regulation of autophagy flux and inflammation through mTOR-dependent signaling.Our microarray analyses revealed that the levels of lncRNA-FA2H-2 were significantly decreased by oxidized low-density lipoprotein (OX-LDL).In vitro experiments showed that lncRNA-FA2H-2 interacted with the promoter of the MLKL gene, downregulated MLKL expression, and the binding sites between -750 and 471 were necessary for lncRNA-FA2H-2 responsiveness to MLKL.Our findings indicated that the lncRNA-FA2H-2-MLKL pathway is essential for regulation of autophagy and inflammation, and suggested that lncRNA-FA2H-2 and MLKL could act as potential therapeutic targets to ameliorate atherosclerosis-related diseases.	30683918	RID03332	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Atherosclerosis	MEG3	CDKN2A	positively-E	luciferase reporter assay	upregulation	qRT-PCR;RNA isolation	NA	NA	inflammatory response(+);apoptosis process(-)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000147889	NA	55384	1029	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ARF|CDK4I|CDKN2|CMM2|INK4|INK4a|MLM|MTS1|p14|p14ARF|p16|p16INK4a|p19|p19Arf	Silencing of MEG3 inhibited ox-LDL-induced inflammation and apoptosis in macrophages via modulation of the MEG3/miR-204/CDKN2A regulatory axis.Second, we demonstrated that ox-LDL upregulated MEG3 expression and that knockdown of MEG3 inhibited the action of ox-LDL in Raw264.7 cells.we showed that MEG3 sponged miR-204 in Raw264.7 cells treated with ox-LDL.our study identified the role of the MEG3/miR-204/CDKN2A pathway in Raw264.7 cells treated with ox-LDL, revealed a novel regulatory pathway in AS and indicated potential novel characteristic biomarkers and therapeutic targets for AS.	30672051	RID03333	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111065,GSE51827,GSE86978)
Polyp of corpus uteri	H19	miR-152	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Reproductive system disease	Uterine disease	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Progesterone ameliorates the endometrial polyp by modulating the signaling pathway of Wnt and beta-catenin via regulating the expression of H19 and miR-152.Luciferase assay was conducted to determine the effect of progesterone.Real-time polymerase chain reaction (PCR) and western blot were performed to detect the influence of progesterone on miR-152 and Wnt1.Progesterone dose-dependently increased the H19 expression level through driving the promoter efficiency of H19.H19 negatively regulated miR-152 expression by binding to miR-152.	30659641	RID03334	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Atherosclerosis	UCA1	miR-206	positively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	LncRNA UCA1 sponges miR-206 to exacerbate oxidative stress and apoptosis induced by ox-LDL in human macrophages.we observed that ox-LDL increased UCA1 expression greatly in THP-1 cells.Moreover, miR-206 was predicted as a target of UCA1 and knockdown of UCA1 was able to repress miR-206 expression.we indicated that UCA1 sponged miR-206 to exacerbate atherosclerosis events induced by ox-LDL in THP-1 cells.	30633352	RID03335	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Breast cancer	FOXD2-AS1	PFN2	positively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000070087	NA	84793	5217	NA	D3S1319E|PFL	Long non-coding RNA FOXD2-AS1/miR-150-5p/PFN2 axis regulates breast cancer malignancy and tumorigenesis.it was identified that FOXD2-AS1 expression was upregulated in BC tissue, cell lines and sphere subpopulation.Using bioinformatics analysis, a reporter gene assay and reverse transcription-polymerase chain reaction assays, it was demonstrated that microRNA (miR)-150-5p was able to bind directly with the 3'-untranslated region of FOXD2-AS1 and PFN2 mRNA.Profilin 2 (PFN2) expression was significantly upregulated in BC tissues.FOXD2-AS1 and PFN2 expression was positively correlated.Collectively, the present results demonstrated the role of the FOXD2-AS1/miR-150-5p/PFN2 axis in the development of BC, and provides novel targets for the treatment of BC, and potential biomarkers for diagnosis and prognosis of BC.	30628646	RID03336	ceRNA or sponge	prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Osteosarcoma	MEG3	miR-361-5p	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 negatively modified osteosarcoma development through regulation of miR-361-5p and FoxM1.Furthermore, real time polymerase chain reaction was utilized to determine the mRNA expressions of maternally expressed gene 3 (MEG3) and miR-361-5p, and western blotwas applied for determining the FoxM1 expression.Besides, dual luciferase reporter gene assay was adopted to verify if MEG3 can be directly targeted by miR-361-5p.MEG3 and miR-361-5p were observed to be significantly downregulated within both osteosarcoma tissues and cell lines, whereas FoxM1 was upregulated in osteosarcoma tissues and cell lines .MEG3 directly bound to miR-361-5p, and significantly upgraded its expression.The upregulated MEG3 and miR-361-5p or the downregulated FoxM1 appeared to substantially inhibit proliferation, migration, and invasion of osteosarcoma cells.The MEG3/miR-361-5p/FoxM1 axis could potentially serve as therapeutic targets or diagnostic biomarkers for osteosarcoma.	30624782	RID03337	expression association	NA		
Osteosarcoma	MEG3	FOXM1	negatively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000111206	NA	55384	2305	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	LncRNA MEG3 negatively modified osteosarcoma development through regulation of miR-361-5p and FoxM1.Furthermore, real time polymerase chain reaction was utilized to determine the mRNA expressions of maternally expressed gene 3 (MEG3) and miR-361-5p, and western blotwas applied for determining the FoxM1 expression.Besides, dual luciferase reporter gene assay was adopted to verify if MEG3 can be directly targeted by miR-361-5p.MEG3 and miR-361-5p were observed to be significantly downregulated within both osteosarcoma tissues and cell lines, whereas FoxM1 was upregulated in osteosarcoma tissues and cell lines .MEG3 directly bound to miR-361-5p, and significantly upgraded its expression.The upregulated MEG3 and miR-361-5p or the downregulated FoxM1 appeared to substantially inhibit proliferation, migration, and invasion of osteosarcoma cells.The MEG3/miR-361-5p/FoxM1 axis could potentially serve as therapeutic targets or diagnostic biomarkers for osteosarcoma.	30624782	RID03338	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Atherosclerosis	NEAT1	ARNTL	positively-E	siRNA;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000133794	NA	283131	406	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	bHLHe5|BMAL1|JAP3|MOP3|PASD3	Acrolein-induced apoptosis of smooth muscle cells through NEAT1-Bmal1/Clock pathway and a protection from asparagus extract.Expression of NEAT1, Bmal1 and Clock was decreased by acrolein, while was ameliorated by AE.We also observed that silence of NEAT1 repressed the expression of Bmal1/Clock and vice versa.	31864078	RID03339	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)
Atherosclerosis	NEAT1	CLOCK	positively-E	siRNA;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000134852	NA	283131	9575	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	bHLHe8|KAT13D|KIAA0334	Acrolein-induced apoptosis of smooth muscle cells through NEAT1-Bmal1/Clock pathway and a protection from asparagus extract.Expression of NEAT1, Bmal1 and Clock was decreased by acrolein, while was ameliorated by AE.We also observed that silence of NEAT1 repressed the expression of Bmal1/Clock and vice versa.	31864078	RID03340	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE86978)
Myocardial infarction	KLF3-AS1	SIRT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell pyroptosis(-);cancer progression(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	CSC	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000231160	GRCh38_4:38602438-38664926	ENSG00000096717	NA	79667	23411	FLJ13197	SIR2L1	LncRNA KLF3-AS1 in human mesenchymal stem cell-derived exosomes ameliorates pyroptosis of cardiomyocytes and myocardial infarction through miR-138-5p/Sirt1 axis.The relationship among miR-138-5p, KLF3-AS1, and Sirt1 was verified by dual-luciferase reporter assay.Transfection of KLF3-AS1 exosome in rats and incubation with KLF3-AS1 exosome in hypoxia cardiomyocytes both verified that overexpression of KLF3-AS1 in exosomes leads to reduced MI area, decreased cell apoptosis and pyroptosis, and attenuated MI progression.KLF3-AS1 can sponge miR-138-5p to regulate Sirt1 expression.LncRNA KLF3-AS1 in exosomes secreted from hMSCs by acting as a ceRNA to sponge miR-138-5p can regulate Sirt1 so as to inhibit cell pyroptosis and attenuate MI progression.	31847890	RID03341	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LINC01128	SFN	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+);apoptosis process(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228794	GRCh38_1:825138-859446	ENSG00000175793	NA	643837	2810	NA	YWHAS	LINC01128 expedites cervical cancer progression by regulating miR-383-5p/SFN axis.The relative expressions of RNAs were detected by real-time quantitative PCR (RT-qPCR).Luciferase reporter assay and RNA pull-down assay were to verify the molecular mechanism.LINC01128 displayed remarkable high expression in CC tissues.LINC01128 shortage could reduce the expression of SFN at mRNA and protein levels.it was proved that LINC01128 could enhance cell proliferation, migration and invasion as well as inhibit cell apoptosis by binding with miR-383-5p and upregulating SFN.	31779593	RID03342	transcriptional regulation	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Spinal tuberculosis	SNHG15	TNFRSF11A	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Tuberculosis	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000141655	NA	285958	8792	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	CD265|FEO|LOH18CR1|ODFR|PDB2|RANK|TRANCE-R	Elevated expression of lncRNA SNHG15 in spinal tuberculosis: preliminary results.Spinal tuberculosis and normal control tissues were collected, and lncRNA SNHG15 level was analyzed by real-time PCR.The lncRNA SNHG15 expression in spinal tuberculosis tissues was significantly increased compared with that in the control group .The expression of lncRNA SNHG15 was increased in RAW264.7 cells in the PPD group with increased cell proliferation, TRAP-positive cells, IL-6 and TNF-alpha secretion, as well as elevated RANK and RANKL expression which were statistically different compared with the control group.The downregulation of lncRNA SNHG15 expression could inhibit the secretion of inflammatory cytokines by regulating the RANK/RANKL pathway, thereby regulating osteoclasts.	31696491	RID03343	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Spinal tuberculosis	SNHG15	TNFSF11	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Tuberculosis	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000120659	NA	285958	8600	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	CD254|ODF|OPGL|RANKL|TRANCE	Elevated expression of lncRNA SNHG15 in spinal tuberculosis: preliminary results.Spinal tuberculosis and normal control tissues were collected, and lncRNA SNHG15 level was analyzed by real-time PCR.The lncRNA SNHG15 expression in spinal tuberculosis tissues was significantly increased compared with that in the control group .The expression of lncRNA SNHG15 was increased in RAW264.7 cells in the PPD group with increased cell proliferation, TRAP-positive cells, IL-6 and TNF-alpha secretion, as well as elevated RANK and RANKL expression which were statistically different compared with the control group.The downregulation of lncRNA SNHG15 expression could inhibit the secretion of inflammatory cytokines by regulating the RANK/RANKL pathway, thereby regulating osteoclasts.	31696491	RID03344	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteoarthritis	CAIF	MIR1246	negatively-E	transient transfections	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	ENSG00000283203	NA	NA	100302142	NA	MIRN1246|hsa-mir-1246	Long Non-Coding RNA (LncRNA) CAIF is Downregulated in Osteoarthritis and Inhibits LPS-Induced Interleukin 6 (IL-6) Upregulation by Downregulation of MiR-1246.Levels of CAIF in synovial fluid of OA patients (n=60) and healthy controls (n=60) were measuring by performing quantitative real-time polymerase chain reaction (qRT-PCR.We found that CAIF in synovial fluid was downregulated in OA patients and inversely correlated with miR-1246 and IL-6.Therefore, CAIF may downregulate miR-1246 to improve OA.	31653823	RID03345	expression association	NA		
Osteoarthritis	CAIF	IL6	negatively-E	transient transfections	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000136244	NA	NA	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	Long Non-Coding RNA (LncRNA) CAIF is Downregulated in Osteoarthritis and Inhibits LPS-Induced Interleukin 6 (IL-6) Upregulation by Downregulation of MiR-1246.Levels of CAIF in synovial fluid of OA patients (n=60) and healthy controls (n=60) were measuring by performing quantitative real-time polymerase chain reaction (qRT-PCR.We found that CAIF in synovial fluid was downregulated in OA patients and inversely correlated with miR-1246 and IL-6.Therefore, CAIF may downregulate miR-1246 to improve OA.	31653823	RID03346	expression association	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Ovarian cancer	LINC00702	KLF2	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with mRNA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000233117	GRCh38_10:4201141-4243912	ENSG00000127528	NA	100652988	10365	NA	LKLF	LINC00702 accelerates the progression of ovarian cancer through interacting with EZH2 to inhibit the transcription of KLF2.Expression level of LINC00702 in OC tissues and matched normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.Through RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assay, the interaction among LINC00702, EZH2, and KLF2 was verified.LINC00702 was upregulated in OC tissues and cell lines.The knockdown of LINC00702 or EZH2 downregulated the KLF2 level in the OC cells.It accelerates the progression of OC via interacting with EZH2 to inhibit the transcription of KLF2.	31389610	RID03347	interact with mRNA	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	UCA1	ZEB2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-498)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000169554	NA	652995	9839	CUDR|LINC00178|onco-lncRNA-36|UCAT1	KIAA0569|SIP-1|SIP1|ZFHX1B	Downregulated lncRNA UCA1 acts as ceRNA to adsorb microRNA-498 to repress proliferation, invasion and epithelial mesenchymal transition of esophageal cancer cells by decreasing ZEB2 expression.UCA1, miR-498 and ZEB2 expression in EC tissues and cells was detected by RT-qPCR or western blotThere were overly expressed UCA1 and ZEB2 and lowly expressed miR-498 in EC tissues and cells.LncRNA UCA1 acted as ceRNA to inhibit miR-498 expression and thereby increasing ZEB2 expression.This study demonstrates that inhibited UCA1 up-regulated miR-498 and down-regulated ZEB2, thereby repressing proliferation activity, invasion, migration, and EMT of EC cells.	31387451	RID03348	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Brain edema	MALAT1	AQP4	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Brain disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171885	NA	378938	361	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MIWC	Overexpression of long noncoding RNA Malat1 ameliorates traumatic brain injury induced brain edema by inhibiting AQP4 and the NF-kB/IL-6 pathway.Our results showed that Malat1 was downregulated in both the TBI rat model and the astrocyte fluid percussion injury (FPI) model, which concurred with brain edema and astrocyte swelling.overexpression of Malat1 significantly inhibited rat brain edema, meanwhile reducing interleukin-6 (IL-6), nuclear factor-kB (NF-kB), and aquaporin 4 (AQP4) expression after TBI.Quantitative real-time polymerase chain reaction and western blotalso corroborated the inhibitory effects of Malat1 on NF-kB and AQP4 expression after FPI.	31218751	RID03349	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Brain edema	MALAT1	NFKB1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Brain disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Overexpression of long noncoding RNA Malat1 ameliorates traumatic brain injury induced brain edema by inhibiting AQP4 and the NF-kB/IL-6 pathway.Our results showed that Malat1 was downregulated in both the TBI rat model and the astrocyte fluid percussion injury (FPI) model, which concurred with brain edema and astrocyte swelling.overexpression of Malat1 significantly inhibited rat brain edema, meanwhile reducing interleukin-6 (IL-6), nuclear factor-kB (NF-kB), and aquaporin 4 (AQP4) expression after TBI.Quantitative real-time polymerase chain reaction and western blotalso corroborated the inhibitory effects of Malat1 on NF-kB and AQP4 expression after FPI.	31218751	RID03350	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Brain edema	MALAT1	IL6	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Brain disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136244	NA	378938	3569	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BSF2|HGF|HSF|IFNB2|IL-6	Overexpression of long noncoding RNA Malat1 ameliorates traumatic brain injury induced brain edema by inhibiting AQP4 and the NF-kB/IL-6 pathway.Our results showed that Malat1 was downregulated in both the TBI rat model and the astrocyte fluid percussion injury (FPI) model, which concurred with brain edema and astrocyte swelling.overexpression of Malat1 significantly inhibited rat brain edema, meanwhile reducing interleukin-6 (IL-6), nuclear factor-kB (NF-kB), and aquaporin 4 (AQP4) expression after TBI.Quantitative real-time polymerase chain reaction and western blotalso corroborated the inhibitory effects of Malat1 on NF-kB and AQP4 expression after FPI.	31218751	RID03351	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Human immunodeficiency virus	CCR5AS	CCR5	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Human immunodeficiency virus infectious disease	lncRNA	PCG	ENSG00000223552	GRCh38_3:46364391-46407083	ENSG00000160791	NA	102724297	1234	NA	CC-CKR-5|CD195|CKR-5|CKR5|CMKBR5|IDDM22	CCR5AS lncRNA variation differentially regulates CCR5, influencing HIV disease outcome.Knockdown or enhancement of CCR5AS expression resulted in a corresponding change in CCR5 expression on CD4+ T cells.Reduction in CCR5 expression through inhibition of CCR5AS diminished infection of CD4+ T cells with CCR5-tropic HIV in vitro.	31209403	RID03352	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Myocardial inflammatory injury	MALAT1	TLR4	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136869	NA	378938	7099	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ARMD10|CD284|hToll|TLR-4	Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-kB axis.MALAT1 expression in PA-treated human cardiomyocytes (AC16 cells) was detected by RT-qPCR.The interaction between MALAT1 and miR-26a was evaluated by a luciferase reporter assay and RT-qPCR.The regulatory effects of MALAT1 on high mobility group box 1 (HMGB1) expression were evaluated by RT-qPCR and western blot.MALAT1 was significantly upregulated in cardiomyocytes after PA treatment.we found that MALAT1 specifically binds to miR-26a and observed a reciprocal negative regulatory relationship between these factors.We further found that the downregulation of MALAT1 represses HMGB1 expression, thereby inhibiting the activation of the Toll-like receptor 4 (TLR4)/NF-kB-mediated inflammatory response.We demonstrate that MALAT1 is induced by SFAs and its downregulation alleviates SFA-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR5/NF-kB axis. Our findings provide new insight into the mechanism underlying myocardial lipotoxic injury.	31123414	RID03353	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Myocardial inflammatory injury	MALAT1	NFKB1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-kB axis.MALAT1 expression in PA-treated human cardiomyocytes (AC16 cells) was detected by RT-qPCR.The interaction between MALAT1 and miR-26a was evaluated by a luciferase reporter assay and RT-qPCR.The regulatory effects of MALAT1 on high mobility group box 1 (HMGB1) expression were evaluated by RT-qPCR and western blot.MALAT1 was significantly upregulated in cardiomyocytes after PA treatment.we found that MALAT1 specifically binds to miR-26a and observed a reciprocal negative regulatory relationship between these factors.We further found that the downregulation of MALAT1 represses HMGB1 expression, thereby inhibiting the activation of the Toll-like receptor 4 (TLR4)/NF-kB-mediated inflammatory response.We demonstrate that MALAT1 is induced by SFAs and its downregulation alleviates SFA-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR5/NF-kB axis. Our findings provide new insight into the mechanism underlying myocardial lipotoxic injury.	31123414	RID03354	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Myocardial inflammatory injury	MALAT1	HMGB1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DKFZp686A04236|HMG1|HMG3|SBP-1	Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-kB axis.MALAT1 expression in PA-treated human cardiomyocytes (AC16 cells) was detected by RT-qPCR.The interaction between MALAT1 and miR-26a was evaluated by a luciferase reporter assay and RT-qPCR.The regulatory effects of MALAT1 on high mobility group box 1 (HMGB1) expression were evaluated by RT-qPCR and western blot.MALAT1 was significantly upregulated in cardiomyocytes after PA treatment.we found that MALAT1 specifically binds to miR-26a and observed a reciprocal negative regulatory relationship between these factors.We further found that the downregulation of MALAT1 represses HMGB1 expression, thereby inhibiting the activation of the Toll-like receptor 4 (TLR4)/NF-kB-mediated inflammatory response.We demonstrate that MALAT1 is induced by SFAs and its downregulation alleviates SFA-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR5/NF-kB axis. Our findings provide new insight into the mechanism underlying myocardial lipotoxic injury.	31123414	RID03355	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Nasopharynx carcinoma	XIST	PDCD4	negatively-E	western blot	upregulation	RT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000150593	NA	7503	27250	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	H731	[Long non-coding RNA XIST modulates cisplatin resistance by altering PDCD4 and Fas-Lexpressions in human nasopharyngeal carcinoma HNE1 cells in vitro]Realtime PCR was performed to detect the expression of XIST in cisplatin-resistant human nasopharyngeal carcinoma cell line HNE1/DDP.The expression of XIST was significantly up-regulated in HNE1/DDP cells in comparison with HNE1 cells.Down-regulation of XIST significantly increased the protein expressions of PDCD4 and Fas-L.XIST is up-regulated in HNE1/DDP cells, and down-regulation and up-regulation of XIST expression reduce and increase DDP resistance of the cells, respectively, possibly as a result of changes in the expressions of PDCD4 and Fas-L.	31068307	RID03356	expression association	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Nasopharynx carcinoma	XIC	FASLG	negatively-E	western blot	upregulation	RT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	NA	ENSG00000117560	NA	7502	356	SXI1|XCE|XIST	ALPS1B|APT1LG1|APTL|CD178|CD95-L|CD95L|FASL|TNFSF6|TNLG1A	[Long non-coding RNA XIST modulates cisplatin resistance by altering PDCD4 and Fas-Lexpressions in human nasopharyngeal carcinoma HNE1 cells in vitro]Realtime PCR was performed to detect the expression of XIST in cisplatin-resistant human nasopharyngeal carcinoma cell line HNE1/DDP.The expression of XIST was significantly up-regulated in HNE1/DDP cells in comparison with HNE1 cells.Down-regulation of XIST significantly increased the protein expressions of PDCD4 and Fas-L.XIST is up-regulated in HNE1/DDP cells, and down-regulation and up-regulation of XIST expression reduce and increase DDP resistance of the cells, respectively, possibly as a result of changes in the expressions of PDCD4 and Fas-L.	31068307	RID03357	expression association	chemoresistance		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Multiple sclerosis	OIP5-AS1	RTL1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cancer progression(-);	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Demyelinating disease	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000254656	NA	729082	388015	cyrano|linc-OIP5	HUR1|1-Mar|MART1|PEG11|SIRH2	Integrative analysis of OIP5-AS1/HUR1 to discover new potential biomarkers and therapeutic targets in multiple sclerosis.Our finding pointed out that there is a direct, moderate, and very significant correlation between the expression of OIP5-AS1 and HUR1, which seems to be at the transcriptional level (p < 0.0001). It indicates that high levels of OIP5 -AS1 cause an increase in the HUR1/OIP5-AS1 complex and further prevent HUR1 from interacting with targeted mRNAs like the proteins associated with the cell-proliferation assemblies. Conversely, the decrease in the expression level of OIP5-AS1 leads to an increase in the number of HUR1 complexes with target mRNAs. OIP5-AS1 acts as a sponge or an internal RNA for competition with HUR1, which limits its access to target mRNAs (Kim et al., 2016).In this study, peripheral blood samples were obtained from 50 relapsing-remitting MS (RR-MS) patients and 50 healthy controls. lncRNAs and their target were selected for validation using TaqMan Real-Time PCR.	30815864	RID03358	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC);DATA(GSE117623)
Malignant meningioma	LINC00702	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-4652-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloid leukemia	lncRNA	TF	ENSG00000233117	GRCh38_10:4201141-4243912	ENSG00000148516	NA	100652988	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LINC00702/miR-4652-3p/ZEB1 axis promotes the progression of malignant meningioma through activating Wnt/beta-catenin pathway.Bioinformatics analysis and mechanism experiments demonstrated that LINC00702 acted as the molecular sponge of miR-4652-3p to upregulate ZEB1 in malignant meningioma. Furthermore, high level of LINC00702 was demonstrated to be associated with the activity of Wnt/beta-catenin signaling. Moreover, miR-4652-3p and ZEB1 involved in LINC00702-mediated Wnt/beta-catenin signaling. At last, rescue assays revealed that miR-4652-3p and ZEB1 attenuated LINC00702-mediated cell proliferation and migration.	30849635	RID03359	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	MALAT1	SATB2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+)	ceRNA(miR-34c)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119042	NA	378938	23314	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FLJ21474|KIAA1034	LncRNA MALAT1 shuttled by bone marrow-derived mesenchymal stem cells-secreted exosomes alleviates osteoporosis through mediating microRNA-34c/SATB2 axis.Additionally, BMSCs-derived exosomal MALAT1 promoted osteoblast activity. Moreover, in vivo experiments indicated that miR-34c reversed the effect of MALAT1, and SATB2 reversed the effect of miR-34c in ovariectomized mice. Taken together, this study demonstrates that BMSCs-derived exosomal MALAT1 enhances osteoblast activity in osteoporotic mice by mediating the miR-34c/SATB2 axis.Based on the RT-qPCR results, we detected that MALAT1 was significantly enriched in the exosome in the BMSCs with overexpressed MALAT1 (Figure 4A).	31659145	RID03360	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Neuroblastoma	LINC02525	RPL35	positively-F	RNA pull-down assay;RIP;luciferase reporter assay;ChIP;RNAi	upregulation	qRT-PCR;sequencing	GSE114053;GSE113998;GSE132109	NA	apoptosis process(+);cell growth(+);prognosis;cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000230269	GRCh38_6:3182626-3195784	ENSG00000136942	NA	100507194	11224	lncNB1	DBA19|L35	The long noncoding RNA lncNB1 promotes tumorigenesis by interacting with ribosomal protein RPL35.The role of the lncRNA lncNB1 in cancer or normal physiology is completely unknown. RPL35 has recently been found to be over-expressed in human colorectal cancer tissues with unknown functions35. We have found that knocking down lncNB1 expression results in neuroblastoma cell growth inhibition and apoptosis, abolishes neuroblastoma cell clonogenic capacity in vitro, and leads to tumor regression in neuroblastoma-bearing mice. Consistent with these data, DEPDC1B, E2F1, and RPL35 are also required for neuroblastoma cell proliferation and/or survival. In addition, in human neuroblastoma tissues, lncNB1, E2F1, or RPL35 RNA expression positively correlates with DEPDC1B RNA expression, and high levels of lncNB1, E2F1, RPL35, or DEPDC1B expression predict poorer patient outcome. Thus, our data demonstrate that lncNB1, its binding protein RPL35 and their target protein E2F1 and target gene DEPDC1B induce neuroblastoma cell proliferation and survival. As high levels of lncNB1, RPL35, E2F1, and DEPDC1B expression in tumor tissues correlate with poor prognosis in neuroblastoma patients, our findings identify lncNB1, RPL35, and DEPDC1B as important co-factors for N-Myc-driven oncogenesis and provide therapeutic targets for neuroblastoma.The majority of patients with neuroblastoma due to MYCN oncogene amplification and consequent N-Myc oncoprotein over-expression die of the disease. The GTPase-activating protein DEPDC1B induces ERK protein phosphorylation and N-Myc protein stabilization. Importantly, lncNB1 knockdown abolishes neuroblastoma cell clonogenic capacity in vitro and leads to neuroblastoma tumor regression in mice, while high levels of lncNB1 and RPL35 in human neuroblastoma tissues predict poor patient prognosis. This study therefore identifies lncNB1 and its binding protein RPL35 as key factors for promoting E2F1 protein synthesis, N-Myc protein stability and N-Myc-driven oncogenesis, and as therapeutic targets.	31690716	RID03361	interact with protein	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Rheumatoid arthritis	HIX003209	TLR2	positively-E	RIP;Fluorescence in situ Hybridization (FISH) Assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);TLR4/NF-kB signaling pathway(+)	ceRNA(miR-6089)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000137462	NA	NA	7097	NA	CD282|TIL4	Long Non-coding RNA HIX003209 Promotes Inflammation by Sponging miR-6089 via TLR4/NF-kB Signaling Pathway in Rheumatoid Arthritis.Accumulating studies have suggested that long non-coding RNAs (lncRNAs) have drawn more and more attention in rheumatoid arthritis (RA), which can function as competitive endogenous RNAs (ceRNAs) in inflammation and immune disorders. Previously, we have found that lncRNA HIX003209 is differentially expressed in RA. However, the precise mechanism of lncRNA HIX003209 in RA is still vague. We aim to elucidate the role and its targeted microRNA of lncRNA HIX003209 in RA as ceRNA. Significantly increased expression of lncRNA HIX003209 was observed in the peripheral blood mononuclear cells (PBMCs) from RA cases. It was positively associated with TLR2 and TLR4 in RA. Besides, peptidoglycan (PGN) and lipopolysaccharide (LPS) could enhance the expression of lncRNA HIX003209, which reversely promoted the proliferation and activation of macrophages through IkBalpha/NF-kB signaling pathway. Moreover, HIX003209 was involved in TLR4-mediated inflammation via targeting miR-6089 in macrophages. LncRNA HIX003209 functions as a ceRNA and exaggerates inflammation by sponging miR-6089 through TLR4/NF-kB pathway in macrophages, which offers promising therapeutic strategies for RA.	31620132	RID03362	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Rheumatoid arthritis	HIX003209	TLR4	positively-E	RIP;Fluorescence in situ Hybridization (FISH) Assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);TLR4/NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000136869	NA	NA	7099	NA	ARMD10|CD284|hToll|TLR-4	Long Non-coding RNA HIX003209 Promotes Inflammation by Sponging miR-6089 via TLR4/NF-kB Signaling Pathway in Rheumatoid Arthritis.Accumulating studies have suggested that long non-coding RNAs (lncRNAs) have drawn more and more attention in rheumatoid arthritis (RA), which can function as competitive endogenous RNAs (ceRNAs) in inflammation and immune disorders. Previously, we have found that lncRNA HIX003209 is differentially expressed in RA. However, the precise mechanism of lncRNA HIX003209 in RA is still vague. We aim to elucidate the role and its targeted microRNA of lncRNA HIX003209 in RA as ceRNA. Significantly increased expression of lncRNA HIX003209 was observed in the peripheral blood mononuclear cells (PBMCs) from RA cases. It was positively associated with TLR2 and TLR4 in RA. Besides, peptidoglycan (PGN) and lipopolysaccharide (LPS) could enhance the expression of lncRNA HIX003209, which reversely promoted the proliferation and activation of macrophages through IkBalpha/NF-kB signaling pathway. Moreover, HIX003209 was involved in TLR4-mediated inflammation via targeting miR-6089 in macrophages. LncRNA HIX003209 functions as a ceRNA and exaggerates inflammation by sponging miR-6089 through TLR5/NF-kB pathway in macrophages, which offers promising therapeutic strategies for RA.	31620132	RID03363	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	TOB1-AS1	COG7	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000168434	NA	400604	91949	NA	NA	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03364	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827)
Non-small cell lung cancer	TOB1-AS1	COG7	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000168434	NA	400604	91949	NA	NA	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03365	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827)
Non-small cell lung cancer	TOB1-AS1	E4F1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000167967	NA	400604	1877	NA	E4F	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03366	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TOB1-AS1	E4F1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27b-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000167967	NA	400604	1877	NA	E4F	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03367	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TOB1-AS1	TSPYL4	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000187189	NA	400604	23270	NA	dJ486I3.2|KIAA0721	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03368	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Non-small cell lung cancer	TOB1-AS1	TSPYL4	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000187189	NA	400604	23270	NA	dJ486I3.2|KIAA0721	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03369	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Non-small cell lung cancer	TOB1-AS1	TSPYL4	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23c)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000187189	NA	400604	23270	NA	dJ486I3.2|KIAA0721	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03370	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Non-small cell lung cancer	TOB1-AS1	TSPYL4	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000187189	NA	400604	23270	NA	dJ486I3.2|KIAA0721	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03371	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Non-small cell lung cancer	TOB1-AS1	TSPYL4	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000187189	NA	400604	23270	NA	dJ486I3.2|KIAA0721	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03372	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Non-small cell lung cancer	TOB1-AS1	IP6K2	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000068745	NA	400604	51447	NA	IHPK2	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03373	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE55807,GSE67939)
Non-small cell lung cancer	TOB1-AS1	IP6K2	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000068745	NA	400604	51447	NA	IHPK2	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03374	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE55807,GSE67939)
Non-small cell lung cancer	TOB1-AS1	DTX3	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000178498	NA	400604	196403	NA	FLJ34766|RNF154	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03375	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	TOB1-AS1	DYNC2LI1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000138036	NA	400604	51626	NA	CGI-60|D2LIC|DKFZP564A033|LIC3	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03376	ceRNA or sponge	prognosis		UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	TOB1-AS1	DYNC2LI1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000138036	NA	400604	51626	NA	CGI-60|D2LIC|DKFZP564A033|LIC3	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03377	ceRNA or sponge	prognosis		UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	TOB1-AS1	DYNC2LI1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000138036	NA	400604	51626	NA	CGI-60|D2LIC|DKFZP564A033|LIC3	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03378	ceRNA or sponge	prognosis		UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807)
Non-small cell lung cancer	TOB1-AS1	DYNC2LI1	positively-E	StarBase;Targetscan	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000138036	NA	400604	51626	NA	CGI-60|D2LIC|DKFZP564A033|LIC3	TOB1-AS1 suppresses non-small cell lung cancer cell migration and invasion through a ceRNA network.Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer-associated mortality. Recent studies revealed that long non-coding (lnc)RNAs have crucial roles in human cancers. The present study was the first, to the best of our knowledge, to indicate that the lncRNA transducer of ERBB2, 1-antisense 1 (TOB1-AS1) acts as a tumor suppressor in NSCLC. Knockdown of TOB1-AS1 significantly induced NSCLC cell migration, invasion and proliferation. It was also demonstrated that the higher expression of TOB1-AS1 in NSCLC samples was associated with longer overall survival time. Furthermore, a TOB1-AS1-mediated competing endogenous RNA network in NSCLC was constructed, including-Homo sapiens-(hsa)-microRNA (miR)-27a-3p, hsa-miR-23a-3p, hsa-miR-23b-3p, hsa-miR-27b-3p, hsa-miR-23c, dynein cytoplasmic 2 light intermediate chain 1, E4F transcription factor 1, TSPY-like 4, component of oligomeric Golgi complex 7, inositol hexakisphosphate kinase 2 and deltex E3 ubiquitin ligase 3. Of note, dysregulation of targets of TOB1-AS1 was associated with the prognosis of NSCLC patients. The present study suggested that TOB1-AS1 may serve as a novel biomarker for NSCLC.	31772627	RID03379	ceRNA or sponge	prognosis		UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807)
Kawasaki disease	XLOC_006277	MMP-8	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;sequencing	NA	NA	cell viability(+)	NA	association	RNA-protein	NA	NA	NA	Immune system disease	Lymph node disease	lncRNA	PCG	NA	NA	ENSG00000118113	NA	NA	NA	NA	NA	Genome-wide transcriptome analysis to further understand neutrophil activation and lncRNA transcript profiles in Kawasaki disease.Kawasaki disease (KD) is the most common cause of acquired cardiac disease in children in developed countries. However, little is known regarding the role of transcriptomic targets of KD in the disease progression and development of complications, especially coronary artery aneurysms (CAA). The aim of our study was to identify transcripts affected by KD and their potential role in the disease. We enrolled 37 KD patients and collected blood samples along a comprehensive time-course. mRNA profiling demonstrated an abundance of CD177 transcript in acute KD, and in the intravenous immunoglobulin (IVIG)-resistant group compared to in the IVIG-sensitive group. lncRNA profiling identified XLOC_006277 as the most highly expressed molecule. XLOC_006277 expression in patients at acute stage was 3.3-fold higher relative to patients with convalescent KD. Moreover, XLOC_006277 abundance increased significantly in patients with CAA. XLOC_006277 knockdown suppressed MMP-8 and MMP-9 expression, both associated with heart lesions. Our result suggested that the increase of CD177pos neutrophils was associated with KD. Moreover, this study provided global long non-coding RNA transcripts in the blood of patients with KD, IVIG-resistant KD, or CAA. Notably, XLOC_006277 abundance was associated with CAA, which might contribute to further understanding of CAA pathogenesis in KD.	30674924	RID03380	expression association	NA		
Kawasaki disease	XLOC_006277	MMP9	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;sequencing	NA	NA	cell viability(+)	NA	association	RNA-protein	NA	NA	NA	Immune system disease	Lymph node disease	lncRNA	PCG	NA	NA	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Genome-wide transcriptome analysis to further understand neutrophil activation and lncRNA transcript profiles in Kawasaki disease.Kawasaki disease (KD) is the most common cause of acquired cardiac disease in children in developed countries. However, little is known regarding the role of transcriptomic targets of KD in the disease progression and development of complications, especially coronary artery aneurysms (CAA). The aim of our study was to identify transcripts affected by KD and their potential role in the disease. We enrolled 37 KD patients and collected blood samples along a comprehensive time-course. mRNA profiling demonstrated an abundance of CD177 transcript in acute KD, and in the intravenous immunoglobulin (IVIG)-resistant group compared to in the IVIG-sensitive group. lncRNA profiling identified XLOC_006277 as the most highly expressed molecule. XLOC_006277 expression in patients at acute stage was 3.3-fold higher relative to patients with convalescent KD. Moreover, XLOC_006277 abundance increased significantly in patients with CAA. XLOC_006277 knockdown suppressed MMP-8 and MMP-9 expression, both associated with heart lesions. Our result suggested that the increase of CD177pos neutrophils was associated with KD. Moreover, this study provided global long non-coding RNA transcripts in the blood of patients with KD, IVIG-resistant KD, or CAA. Notably, XLOC_006277 abundance was associated with CAA, which might contribute to further understanding of CAA pathogenesis in KD.	30674924	RID03381	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Melanoma	OIP5-AS1	GLS	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000115419	NA	729082	2744	cyrano|linc-OIP5	GLS1|KIAA0838	Long noncoding RNA OIP5-AS1 acts as a competing endogenous RNA to promote glutamine catabolism and malignant melanoma growth by sponging miR-217.The long noncoding RNA (lncRNA) OIP5-AS1 has been considered to promote the growth and metastasis of many human tumors. However, the role of OIP5-AS1 in melanoma has not been reported. In this study, we found that OIP5-AS1 levels were significantly elevated in melanoma tissue and that high OIP5-AS1 expression was an independent risk factor for the poor survival of patients with melanoma. miR-217 suppressed glutamine catabolism in melanoma cells by targeting glutaminase (GLS), the rate-limiting enzyme of glutamine catabolism. We also demonstrated that OIP5-AS1 acted as a sponge of miR-217 to upregulate GLS expression, thus promoting glutamine catabolism and melanoma growth. Overall, this result elucidates a new mechanism for OIP5-AS1 in metabolism in melanoma and provides a potential therapeutic target for patients with melanoma.	30779126	RID03382	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Myelogenous leukaemia	FENDRR	ELAVL1	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell growth(-);apoptosis process(-)	ceRNA(miR-184)	regulation	RNA-protein	Adriamycin	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000066044	NA	400550	1994	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	Hua|HUR|MelG	LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR-184 in chronic myelogenous leukaemia cells.Chemotherapy is a major anticancer therapeutic modality, however, multidrug resistance (MDR) is frequently observed and hinders treatment efficacy. Here, we investigated the role and potential mechanism of the long noncoding RNA (lncRNA) FENDRR in adriamycin resistance of chronic myeloid leukaemia (CML) cells. FENDRR overexpression attenuates adriamycin resistance, as shown by increased Rhodamine 123 accumulation, promotion of cell apoptosis in vitro and suppression of tumour growth in vivo. Mechanistically, we identified that FENDRR reduces the interaction of the RNA-binding protein HuR with MDR1 via acting as a sponge, and miR-184 competitively binds to FENDRR with HuR. Thus, the HuR/FENDRR/miR-184 interaction contributes to MDR1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.	31180580	RID03383	ceRNA or sponge	chemoresistance		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Myelogenous leukaemia	FENDRR	MDR1	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell growth(-);apoptosis process(-)	ceRNA(miR-184)	regulation	RNA-protein	Adriamycin	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000109436	NA	400550	NA	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	NA	LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR-184 in chronic myelogenous leukaemia cells.Chemotherapy is a major anticancer therapeutic modality, however, multidrug resistance (MDR) is frequently observed and hinders treatment efficacy. Here, we investigated the role and potential mechanism of the long noncoding RNA (lncRNA) FENDRR in adriamycin resistance of chronic myeloid leukaemia (CML) cells. FENDRR overexpression attenuates adriamycin resistance, as shown by increased Rhodamine 123 accumulation, promotion of cell apoptosis in vitro and suppression of tumour growth in vivo. Mechanistically, we identified that FENDRR reduces the interaction of the RNA-binding protein HuR with MDR1 via acting as a sponge, and miR-184 competitively binds to FENDRR with HuR. Thus, the HuR/FENDRR/miR-184 interaction contributes to MDR1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.	31180580	RID03384	ceRNA or sponge	chemoresistance		
Periodontitis	LncRNA-TWIST1	TWIST1	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	NA	association	NA	NA	CSC	NA	Gastrointestinal system disease	Periodontitis	lncRNA	TF	NA	NA	ENSG00000122691	NA	NA	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	LncRNA-TWIST1 Promoted Osteogenic Differentiation Both in PPDLSCs and in HPDLSCs by Inhibiting TWIST1 Expression.HPDLSCs derived from periodontal ligament tissues contribute to tooth development and tissue regeneration. Exploring the effects of long noncoding RNAs (lncRNAs) in the process of osteogenic differentiation of periodontal ligament stem cells would provide novel therapeutic strategies for tissue regeneration. The expression levels of lncRNA, which significantly changed during osteogenic differentiation, were observed by real-time quantitative PCR (q-PCR). Then, we screened for osteogenic-related lncRNA, which was initially named lncRNA-TWIST1. Moreover, we detected the mRNA expression levels of TWIST1 and osteogenesis-related genes after upregulating and downregulating lncRNA-TWIST1 in PPDLSCs (periodontal mesenchymal stem cells from periodontitis patients) and HPDLSCs (periodontal mesenchymal stem cells from healthy microenvironment), respectively. The osteogenic degree was verified by detecting ALP activity and alizarin red staining. LncRNA-TWIST1 decreased the mRNA levels of TWIST1 and promoted osteogenic differentiation in PPDLSCs, which was confirmed by the increase in osteogenesis-related gene levels (Runx2, ALP, and OCN), the increase in ALP activity, and the formation of more osteogenic nodules. In contrast, downregulating lncRNA-TWIST1 decreased the expression of osteogenesis-related genes, ALP activity, and osteogenic nodules both in PPDLSCs and in HPDLSCs. LncRNA-TWIST1 promoted osteogenic differentiation both in PPDLSCs and in HPDLSCs by inhibiting the TWIST1 expression. LncRNA-TWIST1 may be a novel therapeutic strategy to regenerate dental tissues.	31341908	RID03385	expression association	NA		UP(SKCM);DATA(GSE38495)
Cervical squamous cell carcinoma	OIS1	MTK-1	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA-OIS1 inhibits HPV-positive, but not HPV-negative cervical squamous cell carcinoma by upregulating MTK-1.Long non-coding RNA-oncogene-induced senescence 1 (lncRNA-OIS1) is a novel lncRNA that is involved in oncogene-induced senescence, while its functionality in cervical squamous cell carcinoma is unknown. In the present study, 68 human papillomavirus (HPV)-positive and 22 HPV-negative patients with cervical squamous cell carcinoma were recruited. Additionally, 40 healthy females were employed as healthy controls. Tumor tissues and adjacent healthy tissues were collected from all patients with cervical squamous cell carcinoma, and blood samples were obtained. Expression of OIS1 was detected by reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curve analysis was used to evaluate the diagnostic value of OIS1 for cervical squamous cell carcinoma. HPV-positive and HPV-negative cervical squamous cell carcinoma and normal cervical cell lines were used, and the effects of OIS1 or mitogen-activated protein kinase kinase kinase 4, (MTK-1) expression vector transfection on the proliferation of cell lines and MTK-1 expression were detected by CCK-8 assay and western blot, respectively. It was established that a reduction in OIS1 expression level in tumor tissues was apparent only in HPV-positive patients. Serum levels of OIS1 were lower in HPV-positive patients compared with that in HPV-negative patients and healthy controls, and no significant differences were observed between HPV-negative patients and healthy controls. Serum levels of OIS1 were significantly associated with tumor size, but not distant tumor metastasis. OIS1 expression level was lower in HPV-positive cancer cell lines compared with that in HPV-negative cancer cell lines, while no significant differences were observed between HPV-positive and HPV-negative normal cell lines. OIS1 overexpression inhibited and MTK-1 overexpression promoted the proliferation of HPV-positive, but not HPV-negative cancer or normal cell lines. OIS1 transfection also decreased the expression of MTK-1 in HPV-positive cancer cell lines, but not in any of the other cell lines. Therefore, it was concluded that OIS1 inhibited HPV-positive, but not HPV-negative cervical squamous cell carcinoma by upregulating MTK-1.	30854069	RID03386	expression association	metastasis		
Gastric cancer	NORAD	RHOA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);RhoA/ROCK1 signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000067560	NA	647979	387	LINC00657	ARH12|ARHA|Rho12|RHOH12	Silencing the long noncoding RNA NORAD inhibits gastric cancer cell proliferation and invasion by the RhoA/ROCK1 pathway.OBJECTIVE: The current study aimed to examine the role and mechanism of a conserved long noncoding RNA termed NORAD (noncoding RNA activated by DNA damage, also named LINC00657) in gastric cancer (GC) progression.PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to determine the expression level of relevant genes in GC cell lines. Cell proliferation was examined by cell counting kit-8 (CCK-8) assays. Cell migration and invasion were detected by transwell migration and invasion assays. Protein levels of the indicated genes were detected by western blot. Cell apoptosis was examined by <U+FB02>ow cytometry.RESULTS: Results showed that NORAD knockdown decreased cell proliferation, migration and invasion but increased cell apoptosis. NORAD knockdown affected the expression of genes related to apoptosis and Epithelial-Mesenchymal Transition (EMT). In addition, NORAD's depletion resulted in reduced Ras Homolog Family Member A (RhoA) and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) expression. Furthermore, NORAD's expression was positively correlated with RhoA and ROCK1 expressions in GC based on The Cancer Genome Atlas (TCGA) database.CONCLUSIONS: Our results demonstrate the oncogenic role of NORAD in gastric cancer progression.	31115002	RID03387	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Gastric cancer	NORAD	ROCK1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);RhoA/ROCK1 signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000067900	NA	647979	6093	LINC00657	p160ROCK	Silencing the long noncoding RNA NORAD inhibits gastric cancer cell proliferation and invasion by the RhoA/ROCK1 pathway.OBJECTIVE: The current study aimed to examine the role and mechanism of a conserved long noncoding RNA termed NORAD (noncoding RNA activated by DNA damage, also named LINC00657) in gastric cancer (GC) progression.PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to determine the expression level of relevant genes in GC cell lines. Cell proliferation was examined by cell counting kit-8 (CCK-8) assays. Cell migration and invasion were detected by transwell migration and invasion assays. Protein levels of the indicated genes were detected by western blot. Cell apoptosis was examined by <U+FB02>ow cytometry.RESULTS: Results showed that NORAD knockdown decreased cell proliferation, migration and invasion but increased cell apoptosis. NORAD knockdown affected the expression of genes related to apoptosis and Epithelial-Mesenchymal Transition (EMT). In addition, NORAD's depletion resulted in reduced Ras Homolog Family Member A (RhoA) and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) expression. Furthermore, NORAD's expression was positively correlated with RhoA and ROCK1 expressions in GC based on The Cancer Genome Atlas (TCGA) database.CONCLUSIONS: Our results demonstrate the oncogenic role of NORAD in gastric cancer progression.	31115002	RID03388	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hypertrophic scar	ASLNCS5088	GLS	positively-E	luciferase  assay	upregulation	qRT-PCR	NA	NA	cell viability(+)	ceRNA(miR-200c-3p)	regulation	RNA-protein	NA	CSC	NA	Other	Hypertrophic scar	lncRNA	PCG	NA	NA	ENSG00000115419	NA	NA	2744	NA	GLS1|KIAA0838	Blockade of lncRNA-ASLNCS5088-enriched exosome generation in M2 macrophages by GW4869 dampens the effect of M2 macrophages on orchestrating fibroblast activation.In hypertrophic scar (HS) formation, the type 2 immune response induces the alternatively activated macrophages (M2), which manipulate fibroblasts to differentiate into myofibroblasts with active biologic functions and proliferation. Myofibroblasts express alpha-smooth muscle actin (alpha-SMA) and synthesize and produce additional collagen type I and collagen type III, inducing HS formation. However, studies on the mechanism of M2 macrophage modulation are only based on the recognition of profibrotic factors such as TGF-beta1 secreted by macrophages. The influence of exosomes from M2 macrophages on scar formation is still unknown. Both M2 macrophages and myofibroblasts highly express glutaminases (GLSs). GLS is a critical enzyme in glutaminolysis and is important for M2 macrophage and fibroblast polarization. In this study, we found that in a TGF-beta1-stimulated coculture system, a long noncoding RNA (lncRNA) named lncRNA-ASLNCS5088 was enriched in M2 macrophage-derived exosomes. This lncRNA could be transferred with high efficiency to fibroblasts and acted as an endogenous sponge to adsorb microRNA-200c-3p, resulting in increased GLS and alpha-SMA expression. Pretreatment with GW4869, which impairs M2 macrophage exosome synthesis, ameliorated these pathologic changes in fibroblasts in vitro. Local injection in the late scar formation period with GW4869 reduced alpha-SMA+ fibroblasts and alleviated the fibrosis of tissue after wound healing in vivo.-Chen, J., Zhou, R., Liang, Y., Fu, X., Wang, D., Wang, C. Blockade of lncRNA-ASLNCS5088-enriched exosome generation in M2 macrophages by GW4869 dampens the effect of M2 macrophages on orchestrating fibroblast activation.	31373848	RID03389	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiovascular system disease	MEG3	TP53	negatively-F	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell viability(-);cell migration(+);apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	LFS1|p53	Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53.Angiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of cardiovascular disease. This study aimed to investigate the role of maternally expressed gene 3 (Meg3) in endothelial cell injury. A lncRNA human gene expression microarray analysis was used to identify differentially expressed lncRNAs in human umbilical vein endothelial cell (HUVECs). Cell viability, apoptosis, and migration were then assessed Ang II-treated HUVECs. qRT-PCRand western blot were performed to detect the expression level of p53 after Meg3 knockdown and overexpression. We observed that Ang II treatment decreased the Meg3 level in HUVECs. Next, both knockdown of Meg3 and Ang II decreased cell viability, increased apoptotic cell rate and impair migration function in HUVECs. Furthermore, overexpression of Meg3 inhibited cell apoptosis, and increased cell migration by enhancing p53 transcription on its target genes, including CRP, ICAM-1, VEGF, and HIF-1alpha. Our findings indicate that Meg3 might be associated with cardiovascular disease development.	30838022	RID03390	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	MALAT1	CORO1C	positively-E	luciferase reporter assay;StarBase;Targetscan	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-21-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000110880	NA	378938	23603	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	coronin-3|HCRNN4	Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells.Prostate cancer is a common malignancy with a high mortality rate. Long non-coding RNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) has been reported to serve tumor-promoting roles. However, the underlying mechanism requires further examination. In the present study, it was demonstrated that MALAT1 was increased while microRNA (miR/miRNA)-1-3p was decreased in prostate cancer cell lines. The silencing of MALAT1 inhibited migration, invasion and epithelial-mesenchymal transition, when epithelial (E)-cadherin expression level was increased, and neural (N)-cadherin, vimentin, Slug and Snail expression levels were decreased. dual-luciferase reporter assay results demonstrated that miR-1-3p bound to MALAT1 and coronin 1C (CORO1C) 3' untranslated region, and MALAT1 competed with CORO1C for the binding sites of miR-1-3p. MALAT1 inhibited the expression of miR-1-3p and vice versa. MALAT1 knockdown induced the decline of CORO1C, which was subsequently recovered by the miR-1-3p inhibitor. In addition, by inhibiting miR-1-3p or overexpressing CORO1C, the silencing of MALAT1-induced phenotypic alterations were restored. In conclusion, MALAT1 serving as a degradable miRNA sponge, may sequester miR-1-3p from CORO1C and by silencing MALAT1, migration, invasion and epithelial-mesenchymal transition may be inhibited in prostate cancer cells. MALAT1 and CORO1C may serve as novel clinical therapeutic targets for prostate cancer.	31485645	RID03391	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE51827,GSE55807)
Cardiomyopathy	GAS5	TLR4	positively-E	RNAi	downregulation	qRT-PCR	GSE123679	NA	cell invasion(+);apoptosis process(-);TLR4/NF-kB signaling pathway(+);inflammatory response(+)	ceRNA(miR-1-4p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000136869	NA	60674	7099	NCRNA00030|SNHG2	ARMD10|CD284|hToll|TLR-4	Knockdown of long noncoding RNA GAS5 protects human cardiomyocyte-like AC16 cells against high glucose-induced inflammation by inhibiting miR-21-5p-mediated TLR4/NF-kB signaling.Diabetic cardiomyopathy (DCM) is a common cause of disability and death among diabetic patients. In this study, we aimed to identify the functional role of long noncoding RNA GAS5 in human cardiomyocyte-like AC16 cells under high glucose (HG) condition. The results showed that HG treatment induced damage in AC16 cells by decreasing cell viability and increasing cell apoptosis. We also found that HG increased GAS5 expression in AC16 cells and knockdown of GAS5 protected AC16 cells from HG-induced injury. Furthermore, we confirmed that GAS5 could competitively bind with miR-21-5p and miR-21-5p inhibition alleviated the beneficial effects of GAS5 knockdown against HG stimulation. TLR4 was identified as a target of miR-21-5p in AC16 cells, and GAS5 knockdown alleviated HG-induced inflammation partly by inhibiting miR-21-5p-mediated TLR4/NF-kB signaling. Our results suggested that GAS5/miR-21-5p axis may serve as a candidate therapeutic target for DCM.	31865425	RID03392	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Multiple myeloma	H19	MCL1	positively-E	Bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	resistance(-);cell growth(+);apoptosis process(-)	ceRNA(miR-29b-3p)	regulation	RNA-protein	Bortezomib	CSC	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000143384	NA	283120	4170	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BCL2L3|Mcl-1	LncRNA H19 overexpression induces bortezomib resistance in multiple myeloma by targeting MCL-1 via miR-29b-3p.Radiotherapy, chemotherapy, autologous/allogeneic stem cell transplantation, and targeted drug therapy are currently available therapeutic options for multiple myeloma (MM), but the clinical outcome remains unsatisfactory owing to frequent occurrence of drug resistance. Anti apoptosis is one of the main mechanisms to mediate drug resistance. Studies have shown that MCL-1 plays a key role in the growth of cancer cells "escaping" drug attacks, but the underlying mechanism remains unclear. Our previous study demonstrated that lncRNA H19 was highly expressed in the serum of MM patients. Bioinformatics predicts that miR-29b-3p is the downstream target gene, and MCL-1 is the downstream target protein of miR-29b-3p. Therefore, we speculated that MCL-1 may be involved in the occurrence of drug resistance through epigenetics. On the basis of these previous findings, the present study was intended to explore the biological function of H19, interactions between the downstream target genes, and the effect of H19 on BTZ resistance of myeloma cells. In addition, in vivo experiments we have also confirmed that H19 promoted tumor growth and may develop resistance to bortezomib partly. It was found that H19 reduced cell sensitivity to the chemotherapeutic drug BTZ by working as a miRNA sponge to inhibit the expression of miR-29b-3p, enhance MCL-1 transcriptional translation and inhibit apoptosis. These findings may help gain insights into the molecular mechanism of acquired BTZ resistance and develop new drug targets for the clinical treatment of MM.	30728351	RID03393	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CASC2c	MAPK3	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);chemoresistance(-)	NA	association	RNA-protein	Cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000102882	NA	NA	5595	NA	ERK1|p44erk1|p44mapk|PRKM3	Effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells through ERK1/2 and beta-catenin signaling pathways.OBJECTIVES: This study was aimed to investigate the effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on the proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells.METHODS: The expression of CASC2c in NSCLC tissues and cell lines was detected by real-time fluorescence quantitative PCR (RT-qPCR). MTT and Transwell assay were used to determine the proliferation and migration of NSCLC cells in the experimental group and the control group respectively. The drug sensitivity test was used to confirm whether increasing the CASC2c expression level could reverse the resistance of NSCLC cells to the chemotherapy drug cisplatin. The effects of CASC2c on the expression levels of p-ERK1/2 and beta-catenin were detected by western blot.RESULTS: The results of RT-qPCR showed that CASC2c was under-expressed in NSCLC tissues and cells compared with normal adjacent lung tissues cells (p<U+2009><<U+2009>0.05). In addition, the CASC2c expression was remarkably correlated with TNM staging, tumor cell differentiation, lymph node metastasis, smoking and other pathological indicators of patients with NSCLC (p<U+2009><<U+2009>0.05). MTT and Transwell assay showed that the high-expression of CASC2c significantly reduced the proliferation and migration of NSCLC cells compared to that of the control group (p<U+2009><<U+2009>0.05). western blot assay showed that the high-expressed CASC2c can decrease the expression of phosphorylated-ERK1/2 (p-ERK1/2) and beta-catenin.CONCLUSIONS: CASC2c was low expressed in NSCLC tissues and cells. What's more, it inhibited the proliferation and migration of NSCLC cells by inhibiting the expression of p-ERK1/2 and beta-catenin and reversed NSCLC cells' resistance to the chemotherapy drug cisplatin. Therefore, CASC2c may serve as a new biomarker and therapeutic target in the diagnosis and treatment of NSCLC.	31300295	RID03394	expression association	metastasis,chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CASC2c	MAPK1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);chemoresistance(-)	NA	association	RNA-protein	Cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000100030	NA	NA	5594	NA	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells through ERK1/3 and beta-catenin signaling pathways.OBJECTIVES: This study was aimd to investigate the effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on the proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells.METHODS: The expression of CASC2c in NSCLC tissues and cell lines was detected by real-time fluorescence quantitative PCR (RT-qPCR). MTT and Transwell assay were used to determine the proliferation and migration of NSCLC cells in the experimental group and the control group respectively. The drug sensitivity test was used to confirm whether increasing the CASC2c expression level could reverse the resistance of NSCLC cells to the chemotherapy drug cisplatin. The effects of CASC2c on the expression levels of p-ERK1/2 and beta-catenin were detected by western blot.RESULTS: The results of RT-qPCR showed that CASC2c was under-expressed in NSCLC tissues and cells compared with normal adjacent lung tissues cells (p<U+2009><<U+2009>0.05). In addition, the CASC2c expression was remarkably correlated with TNM staging, tumor cell differentiation, lymph node metastasis, smoking and other pathological indicators of patients with NSCLC (p<U+2009><<U+2009>0.05). MTT and Transwell assay showed that the high-expression of CASC2c significantly reduced the proliferation and migration of NSCLC cells compared to that of the control group (p<U+2009><<U+2009>0.05). western blot assay showed that the high-expressed CASC2c can decrease the expression of phosphorylated-ERK1/2 (p-ERK1/2) and beta-catenin.CONCLUSIONS: CASC2c was low expressed in NSCLC tissues and cells. What's more, it inhibited the proliferation and migration of NSCLC cells by inhibiting the expression of p-ERK1/2 and beta-catenin and reversed NSCLC cells' resistance to the chemotherapy drug cisplatin. Therefore, CASC2c may serve as a new biomarker and therapeutic target in the diagnosis and treatment of NSCLC..	31300295	RID03395	expression association	metastasis,chemoresistance		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Human umbilical vein endothelial cell injury	MALAT1	RAC1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	ceRNA(miR-320a)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136238	NA	378938	5879	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	p21-Rac1|Rac-1|TC-25	LncRNA MALAT1 inhibits hypoxia/reoxygenation-induced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis.Angiogenesis is believed to protect against hypoxia/reoxygenation (H/R)-induced cell injury. MALAT1 and microRNA-320a (miR-320a) are involved in cancer angiogenesis. To investigate the function of the MALAT1/miR-320a axis in H/R-induced cell injury, human umbilical vein endothelial cell (HUVEC) angiogenesis was detected using the Cell Counting Kit-8 (CCK-8), Transwell migration, cell adhesion and tube formation assays. The expression of MALAT1 and miR-320a was revealed by quantitative<U+2009>reverse transcription<U+2009>polymerase chain reaction (qRT-PCR. The direct binding relationship between miR-320a and MALAT1 was detected by RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. The data indicated that H/R induces angiogenesis injury and that the expression of MALAT1 was augmented in H/R-stimulated HUVECs. Overexpression of MALAT1 alleviated H/R-stimulated HUVEC dysfunction, whereas silencing of MALAT1 exerted the opposite effects. MALAT1 also reduced miR-320a levels in HUVECs. Overexpression of miR-320a repressed the function of MALAT1 on H/R-stimulated HUVECs, whereas inhibition of miR-320a exerted the opposite effect. Additionally, miR-320a inhibition alleviated H/R-stimulated HUVEC injury via RAC1. Taken together, this investigation concluded that MALAT1 represses H/R-stimulated HUVEC injury by targeting the miR-320a/RAC1 axis.	31408432	RID03396	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Pancreatic cancer	SBF2-AS1	TWF1	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);chemoresistance(+);apoptosis process(-)	ceRNA(miR-142-3p)	regulation	RNA-protein	Gemcitabine	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000151239	NA	283104	5756	NA	A6|PTK9	Long non-coding SBF2-AS1 acting as a competing endogenous RNA to sponge microRNA-142-3p to participate in gemcitabine resistance in pancreatic cancer via upregulating TWF1.LncRNA SBF2-AS1 was highly expressed in pancreatic cancer tissues and cells.SBF2-AS1 inhibited the expression of TWF1 by competitively binding with miR-142-3p in pancreatic cancer.Our study demonstrates that knock-down of SBF2-AS1 inhibits the expression of TWF1 by competitively binding with miR-142-3p to induce gemcitabine resistance in pancreatic cancer.Knock-down of SBF2-AS1 inhibited proliferation, epithelial-mesenchymal transition, while promoting apoptosis of gemcitabine resistant pancreatic cancer cells.	31619579	RID03397	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE51827,GSE86978)
Papillary thyroid carcinoma	MYC	PAX8<U+2011>AS1:28	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	CSC	NA	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000136997	NA	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	NA	MYC promotes the development of papillary thyroid carcinoma by inhibiting the expression of lncRNA PAX8-AS1:28.As a common malignancy of the endocrine system, papillary thyroid carcinoma (PTC) seriously affects the quality of life of patients. lncRNA PAX8-AS1:28, or lnc-PSD4-1:14 has been reported to be abnormally expressed in PTC. However, the function of PAX8-AS1:28 in PTC is still unknown. Therefore, the present study aimed to investigate the functions of PAX8-AS1:28 in PTC, and to explore the possible mechanisms of action. A total of 38 patients with PTC were included and the normal thyroid follicular epithelial cell line Nthy-ori 3-1 and PTC cell line IHH-4 were also used. MYC and PAX8-AS1:28 overexpression and siRNA silencing in the cell lines were carried out. Expression of PAX8-AS1:28, PAX8 and MYC in tumor tissue, adjacent healthy tissue and different cell lines were detected by qRT-PCRand western blot Cell proliferation was measured by CCK-8 assay. Expression levels of PAX8-AS1:28 and PAX8 were lower in PTC tumor tissue and PTC cells than those in healthy tissue and normal cells. In contrast, the expression level of MYC was higher in PTC cells than that in normal cells. PAX8-AS1:28 silencing reduced the expression level of PAX8 and promoted tumor cell growth, while PAX8-AS1:28 overexpression increased the expression level of PAX8 and inhibited tumor cell growth. MYC silencing increased expression levels of PAX8-AS1:28 and PAX8 and inhibited tumor cell growth, while MYC overexpression decreased expression levels of PAX8-AS1:28 and PAX8 and promoted tumor cell growth. MYC can promote PTC by inhibiting the expression of lncRNA PAX8-AS1:28.	30720110	RID03398	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Retinoblastoma	NEAT1	miR-124	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell cycle(+);cell cycle(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 promotes retinoblastoma progression via modulating miR-124.The long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. However, the role, expression status, and the detailed mechanism of NEAT1 in retinoblastoma (RB) yet need to be unraveled. We explored the role and the mechanism of NEAT1 activity in RB. Our data show enhanced NEAT1 expression in RB-affected tissues compared with the corresponding control. Functional experiments reveal that a NEAT1 knockdown in RB cells significantly inhibits proliferation, cycle progression, and facilitates apoptosis and caspase-3 and -9 activities. Besides that, miR-124 was predicted to be a target of NEAT1 and its reduced expression, as well as the inverse correlation of NEAT1 with miR-124, was observed in RB-affected tissues. Further, luciferase and RNA immunoprecipitation (RIP) assays confirmed the interaction between NEAT1 and miR-124. Rescue experiments confirmed that the inhibition of miR-124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase-3 and -9 activities. Thus, NEAT1 promotes RB progression by sponging miR-124, providing a therapeutic target for RB.	31038819	RID03399	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Pancreatic cancer	LINC00339	IGF1R	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000140443	NA	29092	3480	HSPC157|NCRNA00339	CD221|IGFIR|IGFR|JTK13|MGC18216	LINC00339 promotes cell proliferation and metastasis in pancreatic cancer via miR-497-5p/IGF1R axis.PURPOSE: To investigate the role and mechanism of long non-coding (lnc) RNA LINC00339 in pancreatic cancer (PANC), and provided a potential target for its biological diagnosis and treatment.METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of LINC00339 in PANC tissue specimens and cell lines. The experimental cell lines differentially expressing LINC00339 were constructed by using small interfering RNA and lentivirus transfection. Cell proliferation was examined by cell counting kit-8 (CCK-8) and colony formation experiments and transwell experiments were used to assess cell invasion and migration abilities. The luciferase assay and RNA immunoprecipitation (RIP) were employed to study the target gene for LINC00339, and western blotwas utilized to measure protein expression of the downstream gene.RESULTS: The level of LINC00339 expression in PANC tissues or cells was significantly higher than that in their respective control groups. Interfering expression of LINC00339 could notably inhibit the proliferation, invasion and migration of SW1990 cells, while the over-expressing expression of LINC00339 obviously increased the growth and metastasis abilities of PANC-1 cells. LINC00339 could act as a miR-497-5p sponge, adsorbing miR-497-5p, thereby inhibiting its action by increasing the expression of its target gene IGF1R. The expression of miR-497-5p and its target gene IGF1R could be significantly altered by altering the expression of LINC00339.CONCLUSIONS: LINC00339 was markedly over-expressed in PANC tissues and cells and promoted cell proliferation, invasion, and migration via sponging miR-497-5p, thereby increasing IGF1R expression. Our study could provide a novel target for PANC diagnosis and biotherapy.	31128030	RID03400	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Alzheimer's disease	NEAT1	miR-107	negatively-F	Bioinformatics analysis;luciferase activity assay;RNAi	upregulation	western blot	NA	NA	cell injury(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000198997	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long Noncoding RNA NEAT1 Aggravates Abeta-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease.PURPOSE: Alzheimer's disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Long noncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exact role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown.RESULTS: NEAT1 expression was enhanced in Abeta-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Abeta-induced inhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundance was reduced in Abeta-treated cells, and its overexpression reversed Abeta-induced injury. Moreover, interference of miR-107 abated silencing of NEAT1-mediated inhibition of neuronal damage in Abeta-treated SH-SY5Y and SK-N-SH cells.CONCLUSION: LncRNA NEAT1 aggravated Abeta-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatment of AD.	31250578	RID03401	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Glaucoma	NR_003923	IL22RA1	positively-E	Bioinformatics analysis;luciferase activity assay;RNAi	upregulation	western blot;microarray;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);fibrotic(+);cell autophagy(+)	ceRNA(miR-760)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Glaucoma	lncRNA	PCG	NA	NA	ENSG00000142677	NA	NA	58985	NA	CRF2-9|IL22R	LncRNA NR_003923 promotes cell proliferation, migration, fibrosis, and autophagy via the miR-760/miR-215-3p/IL22RA1 axis in human Tenon's capsule fibroblasts.Noncoding RNAs (ncRNAs), including long ncRNAs (lncRNA) have manifested an important role in the pathophysiology of many diseases. Glaucoma is a primary cause of irreversible blindness worldwide. However, the involvement of lncRNAs in glaucoma remains largely unknown. Here, we performed the lncRNA expression assay based on clinical tissues and identified a specific functional lncRNA, NR_003923, and investigated its potential role in glaucoma. Knockdown of NR_003923 in human Tenon's capsule fibroblast cells (HTFs) inhibited TGF-beta-induced cell migration, proliferation, fibrosis, and autophagy. The dual-luciferase reporter assay confirmed that miR-760 and miR-215-3p interacted with NR_003923. miR-760 and miR-215-3p inhibitor reversed the effects of NR_003923 and TGF-beta-induced cell apoptosis. Moreover, the expression of miR-760 and miR-215-3p was decreased in glaucoma comparing with control. Furthermore, through microarray we found IL22RA1 was increased in glaucoma and both of miR-760 and miR-215-3p bound to the 3' UTR of IL22RA1. Overexpression of IL22RA1 enhanced HTFs migration and proliferation, while miR-760 and miR-215-3p mimics reversed these promotive biological roles induced by IL22RA1. In conclusion, NR_003923 and IL22RA1 might contribute to glaucoma progression and be a novel and potential biomarkers and therapeutic targets for glaucoma.	31391457	RID03402	ceRNA or sponge	NA		
Glaucoma	NR_003923	IL22RA1	positively-E	Bioinformatics analysis;luciferase activity assay;RNAi	upregulation	western blot;microarray;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);fibrotic(+);cell autophagy(+)	ceRNA(miR-215-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Glaucoma	lncRNA	PCG	NA	NA	ENSG00000142677	NA	NA	58985	NA	CRF2-9|IL22R	LncRNA NR_003923 promotes cell proliferation, migration, fibrosis, and autophagy via the miR-760/miR-215-3p/IL22RA1 axis in human Tenon's capsule fibroblasts.Noncoding RNAs (ncRNAs), including long ncRNAs (lncRNA) have manifested an important role in the pathophysiology of many diseases. Glaucoma is a primary cause of irreversible blindness worldwide. However, the involvement of lncRNAs in glaucoma remains largely unknown. Here, we performed the lncRNA expression assay based on clinical tissues and identified a specific functional lncRNA, NR_003923, and investigated its potential role in glaucoma. Knockdown of NR_003923 in human Tenon's capsule fibroblast cells (HTFs) inhibited TGF-beta-induced cell migration, proliferation, fibrosis, and autophagy. The dual-luciferase reporter assay confirmed that miR-760 and miR-215-3p interacted with NR_003923. miR-760 and miR-215-3p inhibitor reversed the effects of NR_003923 and TGF-beta-induced cell apoptosis. Moreover, the expression of miR-760 and miR-215-3p was decreased in glaucoma comparing with control. Furthermore, through microarray we found IL22RA1 was increased in glaucoma and both of miR-760 and miR-215-3p bound to the 3' UTR of IL22RA1. Overexpression of IL22RA1 enhanced HTFs migration and proliferation, while miR-760 and miR-215-3p mimics reversed these promotive biological roles induced by IL22RA1. In conclusion, NR_003923 and IL22RA1 might contribute to glaucoma progression and be a novel and potential biomarkers and therapeutic targets for glaucoma.	31391457	RID03403	ceRNA or sponge	NA		
Hepatocellular carcinoma	SNHG3	SMAD3	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)epithelial to mesenchymal transition(+)	ceRNA(miR-326)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000166949	NA	8420	4088	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	HsT17436|JV15-2|MADH3	miR24-2 Promotes Malignant Progression of Human Liver Cancer Stem Cells by Enhancing Tyrosine Kinase Src Epigenetically.Small nucleolar RNA host gene 3 (SNHG3), a long noncoding RNA (lncRNA), acts as an oncogene in hepatocellular carcinoma (HCC), whereas microRNA (miR)-326 plays an inhibitory role in some types of human cancers, including melanoma, osteosarcoma, and gastric cancer. In the present study, by analyzing 47 tissue specimens of human HCC, we found that the relative expression levels of SNHG3 were significantly higher in HCC tissues than those in the adjacent noncancerous tissues, whereas the relative expression levels of miR-326 were significantly lower in HCC tissues. Furthermore, the relative mRNA levels of Sma and Mad Related Family 3 (SMAD3) and zinc finger E-box binding homeobox 1 (ZEB1) were significantly higher in HCC tissues compared with the adjacent noncancerous tissues. In human HCC cell lines, SNHG3 overexpression promoted the proliferation, migration, and epithelial-mesenchymal transition and inhibited apoptosis, whereas knockdown of SNHG3 expression exerted the opposite effects. Importantly, miR-326 or miR-326 inhibitor restored the aforementioned effects of SNHG3 overexpression or SNHG3 knockdown. We thus found that the miR-326-response element is present in SNHG3 and the 3'-untranslated region of SMAD3 mRNA. In fact, SNHG3 overexpression increased the expression levels of SMAD3 and ZEB1, while miR-326 decreased the expression levels of SMAD3. These results suggest that SNHG3 may function as a competing endogenous RNA (ceRNA) for miR-326, which in turn enhances SMAD3 and ZEB1 expression. In conclusion, we propose that SNHG3 promotes HCC progression via the miR-326/SMAD3/ZEB1 signaling pathway. The findings may provide novel targets for the diagnosis and treatment of HCC.	31548493	RID03404	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG3	ZEB1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)epithelial to mesenchymal transition(+)	ceRNA(miR-326)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000148516	NA	8420	6935	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	miR24-2 Promotes Malignant Progression of Human Liver Cancer Stem Cells by Enhancing Tyrosine Kinase Src Epigenetically.Small nucleolar RNA host gene 3 (SNHG3), a long noncoding RNA (lncRNA), acts as an oncogene in hepatocellular carcinoma (HCC), whereas microRNA (miR)-326 plays an inhibitory role in some types of human cancers, including melanoma, osteosarcoma, and gastric cancer. In the present study, by analyzing 47 tissue specimens of human HCC, we found that the relative expression levels of SNHG3 were significantly higher in HCC tissues than those in the adjacent noncancerous tissues, whereas the relative expression levels of miR-326 were significantly lower in HCC tissues. Furthermore, the relative mRNA levels of Sma and Mad Related Family 3 (SMAD3) and zinc finger E-box binding homeobox 1 (ZEB1) were significantly higher in HCC tissues compared with the adjacent noncancerous tissues. In human HCC cell lines, SNHG3 overexpression promoted the proliferation, migration, and epithelial-mesenchymal transition and inhibited apoptosis, whereas knockdown of SNHG3 expression exerted the opposite effects. Importantly, miR-326 or miR-326 inhibitor restored the aforementioned effects of SNHG3 overexpression or SNHG3 knockdown. We thus found that the miR-326-response element is present in SNHG3 and the 3'-untranslated region of SMAD3 mRNA. In fact, SNHG3 overexpression increased the expression levels of SMAD3 and ZEB1, while miR-326 decreased the expression levels of SMAD3. These results suggest that SNHG3 may function as a competing endogenous RNA (ceRNA) for miR-326, which in turn enhances SMAD3 and ZEB1 expression. In conclusion, we propose that SNHG3 promotes HCC progression via the miR-326/SMAD3/ZEB1 signaling pathway. The findings may provide novel targets for the diagnosis and treatment of HCC.	31548493	RID03405	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	BCLAF1	NEAT1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000029363	NA	ENSG00000245532	GRCh38_11:65422774-65445540	9774	283131	BTF|KIAA0164	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BCLAF1 promotes cell proliferation, invasion and drug-resistance though targeting lncRNA NEAT1 in hepatocellular carcinoma.AIMS: In the present research, we aimed to investigate the effect of Bcl-2-associated transcription factor 1 (BCLAF1) on hepatocellular carcinoma and further explore the special molecular mechanism.MAIN METHODS: The expression of BCLAF1 was analyzed in tumor tissues and different hepatocellular cancer cell lines by real-time RT-PCRand western blot. Cell proliferation and invasion was explored using MTT and Transwell assay respectively. In addition, luciferase reporter assay was performed to determine the binding activity of BCLAF1 and Nuclear enrichment-rich transcription factor 1 (NEAT1) promoter. Finally, the IC50 for 5-Fluorouracil (5-Fu) was measured by MTT assay, and western blot was used to determine the expression of P-glycoprotein (P-gp) and multidrug resistance protein1 (MRP1).KEY FINDING: The result revealed that BCLAF1 was highly expressed in hepatocellular carcinoma tissues and cells. In addition, BCLAF1-siRNA inhibited the proliferation and invasion of hepatocellular carcinoma cells, and overexpression of BCLAF1 promoted proliferation and invasion. Furthermore, luciferase reporter assay demonstrated that BCLAF1 directly interact with lncNEAT1 promoter and improved NEAT1 expression, and BCLAF1 promoted proliferation and invasion through targeting lncRNA NEAT1. What's more, BCLAF1 promoted 5-Fu resistance and the expression of P-gp and MRP1 in hepatocellular carcinoma cells by targeting NEAT1.SIGNIFICANCE: The results of the present study suggested that BCLAF1 might be a new gene related to proliferation and drug-resistance of hepatocellular carcinoma. In the future, the search for a deep and reasonable mechanism for the role of BCLAF1 will help us to understand its function more comprehensively, and finally find a new method for the treatment of human cancer.	31870774	RID03406	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Osteoarthritis	SNHG1	MMPs	negatively-E	RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);p38/MAPK signaling pathway(-)	ceRNA(miR-16-5p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	LncRNA SNHG1 alleviates IL-1beta-induced osteoarthritis by inhibiting miR-16-5p-mediated p38 MAPK and NF-kB signaling pathways.Long non-coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported in the occurrence and development of several diseases, but its biological role and mechanism in osteoarthritis (OA) remain to be illuminated. In the present research, we aimed to investigate the effect of SNHG1 on IL-1beta-induced OA and its molecular mechanism. Results revealed that SNHG1 decreased the expression of MMPs, ADAMTs, collagen, and aggrecan, and ameliorates IL-1beta-induced metabolic dysfunction in normal human chondrocytes-keen. In addition, SNHG1 inhibited the expressions of pro-inflammatory cytokines in chondrocytes, including NO, PGE2, IL-6, TNF-alpha, i-NOS, and COX-2. Furthermore, luciferase reporter assay demonstrated that SNHG1 could directly interact with miR-16-5p and suppressed miR-16-5p expression and activity. What is more, miR-16-5p overexpression reversed SNHG1-inhibited aberrant catabolism and inflammation triggered by IL-1beta stimulation. Finally, SNHG1 inhibits the expression of miR-16-5p-mediated factors involved in p38MAPK and NF-kB signaling pathways, including ERK1/2, p-p38 and p-p65. Taken together, the results of our studies illuminate that SNHG1 alleviates the inflammation of IL-1beta-induced OA through the activation of miR-16-5p-mediated p38MAPK and NF-kB signaling pathway. It suggested that SNHG1 may serve as a potential target for OA diagnosis and treatment.	31383786	RID03407	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Osteoarthritis	SNHG1	ADAMTs	negatively-E	RNA pull-down assay;RNAi	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);p38/MAPK signaling pathway(-)	ceRNA(miR-16-5p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	LncRNA SNHG1 alleviates IL-1beta-induced osteoarthritis by inhibiting miR-16-5p-mediated p38 MAPK and NF-kB signaling pathways.Long non-coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported in the occurrence and development of several diseases, but its biological role and mechanism in osteoarthritis (OA) remain to be illuminated. In the present research, we aimed to investigate the effect of SNHG1 on IL-1beta-induced OA and its molecular mechanism. Results revealed that SNHG1 decreased the expression of MMPs, ADAMTs, collagen, and aggrecan, and ameliorates IL-1beta-induced metabolic dysfunction in normal human chondrocytes-keen. In addition, SNHG1 inhibited the expressions of pro-inflammatory cytokines in chondrocytes, including NO, PGE2, IL-6, TNF-alpha, i-NOS, and COX-2. Furthermore, luciferase reporter assay demonstrated that SNHG1 could directly interact with miR-16-5p and suppressed miR-16-5p expression and activity. What is more, miR-16-5p overexpression reversed SNHG1-inhibited aberrant catabolism and inflammation triggered by IL-1beta stimulation. Finally, SNHG1 inhibits the expression of miR-16-5p-mediated factors involved in p38MAPK and NF-kB signaling pathways, including ERK1/2, p-p38 and p-p65. Taken together, the results of our studies illuminate that SNHG1 alleviates the inflammation of IL-1beta-induced OA through the activation of miR-16-5p-mediated p38MAPK and NF-kB signaling pathway. It suggested that SNHG1 may serve as a potential target for OA diagnosis and treatment.	31383786	RID03408	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Asthma	AGO2	PTEN	positively-E	RNAi;luciferase activity assay	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(-);chemoresistance(+)	ceRNA(miR-21)	regulation	NA	Dexamethasone	NA	NA	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000171862	NA	27161	5728	CASC7|EIF2C2|hAGO2|LINC00980|Q10	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA-CASC7 enhances corticosteroid sensitivity via inhibiting the PI3K/AKT signaling pathway by targeting miR-21 in severe asthma.BACKGROUND: Asthma, a common chronic inflammatory disease, is treated with corticosteroid in most cases, but corticosteroid resistance in severe asthma patients seriously impairs the therapeutic effects. LncRNA-CASC7 inhibits cell proliferation and enhances drug sensitivity, but the molecular mechanisms of corticosteroid resistance in severe asthma are still unknown.METHODS: Airway smooth muscle cells (ASMCs) from healthy and severe asthmatic subjects were used in this study. The expression of CASC7 and miR-21 were modified by transfection with the pcDNA3.1-CASC7, miR-21 mimics and inhibitor. MTT assay was conducted to measure cell proliferation. ELISA assay was used to determine the secretion of CCL5, CCL11 and IL-6. The phosphorylation of glucocorticoid receptor (GR) and the PI3K/AKT signaling were assessed by western blot assays. qRT-PCRwas used to analyze the expression of CASC7, miR-21 and PTEN. dual-luciferase reporter assay was used to assess the interaction among CASC7, miR-21 and PTEN.RESULTS: Compared with AMSCs from severe asthma patients, dexamethasone inhibited cytokines (CCL5, CCL11 and IL-6) and promoted the phosphorylation of GR more significantly in normal AMSCs. CASC7 expression was suppressed while miR-21 expression and AKT activity were promoted in ASMCs from severe asthma patients. CASC7 promoted PTEN expression via directly inhibiting miR-21 expression. Overexpression of CASC7 suppressed the PI3K/AKT signaling pathway and promoted the inhibition effects of dexamethasone on cell proliferation and cytokines secretion via targeting miR-21.CONCLUSION: CASC7 increased corticosteroid sensitivity by inhibiting the PI3K/AKT signaling pathway via targeting miR-21, which provided a promising potential target for designing novel therapeutic strategy for severe asthma.	31412983	RID03409	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Atrial fibrillation	GAS5	TGFBR1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106799	NA	60674	7046	NCRNA00030|SNHG2	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	Long noncoding RNA GAS5 attenuates cardiac fibroblast proliferation in atrial fibrillation via repressing ALK5.OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have caught more attention for their role in the progression of many diseases. Among them, lncRNA GAS5 (Growth Inhibition Specificity 5) was studied in this research to identify how it affects the progression of atrial fibrillation (AF).PATIENTS AND METHODS: In 40 patients with AF and 30 patients with sinus rhythm (SR), the GAS5 expression of the right atrial appendage (RAA) tissues was detected by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Moreover, the cell proliferation assay was conducted in AC16 cells transfected with GAS5 inhibitor and mimics, respectively. Furthermore, the qRT-PCRwas performed to uncover the mechanism.RESULTS: In the research, the expression of GAS5 in RAA tissues was decreased significantly in AF patients than that in SR ones. Moreover, overexpression of GAS5 inhibited cell growth in AC16 cells, while knockdown of GAS5 promoted cell growth in AC16 cells. In addition, further experiments revealed that ALK5 was a target of GAS5 and its expression in AF tissues negatively correlated to GAS5 expression.CONCLUSIONS: These results indicate that GAS5 could inhibit cell proliferation of AF via suppressing ALK5, which may offer a new vision for interpreting the mechanism of AF development.	31539152	RID03410	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	PCAT1	miR-124-3p	negatively-F	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	Long noncoding RNA PCAT-1 knockdown prevents the development of ovarian cancer cells via microRNA-124-3p.Long noncoding RNA prostate cancer-associated transcript 1 (PCAT-1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT-1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT-1 silence in cellular activities and the molecular mechanisms. PCAT-1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real-time quantitative reverse polymerase chain reaction (qRT-PCR. Reinforced silence of PCAT-1 and microRNA (miR)-124-3p was established by transfection and identified by qRT-PCR The viability, apoptosis as well as migration and invasion were examined. western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT-1. Silencing PCAT-1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT-1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase-3, metallopeptidases, and vimentin with the restoration of miR-124-3p. However, the roles of PCAT-1 silence were weakened in the absence of miR-124-3p. PCAT-1 silence caused decrease in Wnt3a, beta-catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR-124-3p inhibitor. The tumor-suppressive role of PCAT-1 silence was mediated by miR-124-3p.	31674073	RID03411	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Osteoarthritis	MELTF-AS1	TCF4	positively-E	luciferase reporter assay;RNA immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+);inflammatory response(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000228109	GRCh38_3:196999460-197004744	ENSG00000196628	NA	100507057	6925	AC068302.3|MFI2-AS1	bHLHb19|E2-2|ITF2|SEF2-1B	Knockdown of lncRNA MFI2-AS1 inhibits lipopolysaccharide-induced osteoarthritis progression by miR-130a-3p/TCF4.AIMS: Long noncoding RNA melanotransferrin antisense RNA (MFI2-AS1) plays a vital role in the development of multiple diseases. This study aimed to investigate the effect of this lncRNA on osteoarthritis progression and explore the interaction among MFI2-AS1, microRNA (miR)-130a-3p and transcription factor 4 (TCF4).METHODS: Forty-six knee osteoarthritis tissues and 28 normal samples were collected. Human chondrocytes C28/I2 cells treated by lipopolysaccharide (LPS) were used as the model of osteoarthritis. The expression levels of MFI2-AS1, miR-130a-3p and TCF4 were detected by quantitative real-time polymerase chain reaction or western blot. LPS-induced chondrocytes injury was investigated by cell viability, apoptosis, inflammatory response and extracellular matrix degradation using MTT, flow cytometry, enzyme-linked immunosorbent assay and western blot. The target association between miR-130a-3p and MFI2-AS1 or TCF4 was confirmed by luciferase reporter assay and RNA immunoprecipitation.RESULTS: MFI2-AS1 expression was increased in osteoarthritis tissues and LPS-treated C28/I2 cells. Silence of MFI2-AS1 attenuated LPS-induced viability suppression, apoptosis production, inflammatory response and extracellular matrix degradation. MFI2-AS1 was validated as a decoy of miR-130a-3p and TCF4 was confirmed as a target of miR-130a-3p. miR-130a-3p overexpression inhibited LPS-induced cell injury in C28/I2 cells by decreasing TCF4 expression. Moreover, knockdown of MFI2-AS1 alleviated LPS-induced cell injury in C28/I2 cells by mediating miR-130a-3p and TCF4.CONCLUSION: Knockdown of MFI2-AS1 increased cell viability but suppressed apoptosis, inflammatory response and extracellular matrix degradation in LPS-treated chondrocytes by increasing miR-130a-3p and decreasing TCF4, indicating a novel target for the treatment of osteoarthritis.	31678554	RID03412	ceRNA or sponge	NA		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)
Rheumatoid arthritis	MALAT1	CTNNB1	negatively-E	Dual-luciferase reporter gene assay;CHIP;RIP	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(-);cell proliferation(-);inflammatory response(-)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	armadillo|beta-catenin|CTNNB	MALAT1-Driven Inhibition of Wnt Signal Impedes Proliferation and Inflammation in Fibroblast-Like Synoviocytes Through CTNNB1 Promoter Methylation in Rheumatoid Arthritis.Fibroblast-like synoviocytes (FLSs) participate in the pathogenesis of rheumatoid arthritis (RA). Emerging evidence has highlighted the role of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and its potential involvement in RA. In this study, we test the hypothesis that the MALAT1 might inhibit proliferation and inflammatory response of FLSs in RA. The expression of MALAT1 was examined in synovial tissues from patients with RA. The effect of MALAT1 on cultured FLSs was analyzed by introducing overexpressed MALAT1 or short hairpin RNA (shRNA) against MALAT1. To validate whether methylation of CTNNB1 promoter was affected by MALAT1 alternation, we assessed the recruitment of DNA methyltransferases to CTNNB1 promoter. In cultured FLSs with shRNA-mediated CTNNB1 knockdown or activated Wnt signaling, we found the interaction between CTNNB1 and Wnt signaling. MALAT1 expression was reduced in synovial tissues of RA. MALAT1 could bind to CTNNB1 promoter region and recruit methyltransferase to promote CTNNB1 promoter methylation, thereby inhibiting CTNNB1. Notably, MALAT1 could suppress the transcription and expression of CTNNB1, thereby modulating the Wnt signaling pathway. Silenced MALAT1 stimulated the nucleation of beta-catenin and the secretion of inflammatory cytokines including interleukin-6, interleukin-10, and tumor necrosis factor-alpha. Additionally, shRNA-mediated MALAT1 silencing elevated proliferation and suppressed apoptosis of FLSs accompanied. These findings provide evidence for the inhibitory effect of MALAT1 on proliferation and inflammation of FLSs by promoting CTNNB1 promoter methylation and inhibiting the Wnt signaling pathway. Therefore, this study provides a candidate therapeutic target for RA.	30909750	RID03413	epigenetic regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	LINC00339	DCP1A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);cancer progression(+)	ceRNA(miR-377-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000162290	NA	29092	55802	HSPC157|NCRNA00339	HSA275986|SMAD4IP1|SMIF	LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p.Up to date, the mechanism of gastric cancer (GC) development is poorly understood. This study was to demonstrate the effects of LINC00339 on GC progression. Here, we found that LINC00339 was overexpressed expressed in GC tissues and predicted poor outcome. By CCK8, colony formation and Transwell assays, we showed LINC00339 knockdown suppressed GC cell proliferation, migration, and invasion in vitro. Flow cytometry analysis (FACS) indicated that LINC00339 knockdown induced tumor cell apoptosis. Besides, we utilized the xenograft assay and found that LINC00339 depletion led to decreased tumor growth in vivo. Mechanistically, miR-377-3p was found to be inhibited by LINC00339. And LINC00339 suppressed miR-377-3p to upregulate DCP1A, which consequently promoted GC progression. In conclusion, LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p.	31188482	RID03414	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842)
Nonalcoholic fatty liver disease	NEAT1	MIR140	positively-E	western blot	upregulation	qRT-PCR	NA	NA	AMPK/SREBP-1 signaling pathway(-);cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Fatty liver disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000208017	NA	283131	406932	LINC00084|NCRNA00084|TncRNA|VINC	MIRN140|SEDN|miRNA140|mir-140	LncRNA NEAT1-MicroRNA-140 axis exacerbates nonalcoholic fatty liver through interrupting AMPK/SREBP-1 signaling.Nonalcoholic fatty liver disease (NAFLD) is a severe liver disease, which influences the health of people worldwide. However, the mechanism modulating the pathogenesis of NAFLD remains elusive. It was reported that nuclear enriched abundant transcript 1 (NEAT1) and microRNA-140 (miR-140) could regulate lipogenesis, but whether they could influence NAFLD are still unknown.</AbstractText>: Nonalcoholic fatty liver disease (NAFLD) is a severe liver disease, which influences the health of people worldwide. However, the mechanism modulating the pathogenesis of NAFLD remains elusive. It was reported that nuclear enriched abundant transcript 1 (NEAT1) and microRNA-140 (miR-140) could regulate lipogenesis, but whether they could influence NAFLD are still unknown.HepG2 cells were treated by free fatty acids (FFA) to establish the model of NAFLD in<U+00A0>vitro, and C57 mice were treated by high-fat diet to establish the model of NAFLD in<U+00A0>vivo. Cell transfection was applied to regulate the expression of NEAT1 and miR-140. western blot and qRT-PCRwere applied for measuring expression of protein and mRNA, respectively. HE staining and Oil Red O staining were used for observing liver tissues.</AbstractText>: HepG2 cells were treated by free fatty acids (FFA) to establish the model of NAFLD in<U+00A0>vitro, and C57 mice were treated by high-fat diet to establish the model of NAFLD in<U+00A0>vivo. Cell transfection was applied to regulate the expression of NEAT1 and miR-140. western blot and qRT-PCRwere applied for measuring expression of protein and mRNA, respectively. HE staining and Oil Red O staining were used for observing liver tissues.NEAT1 and miR-140 are upregulated in hepacytes under the NAFLD conditions. NEAT1 directly binds to miR-140 and acts synergistically with miR-140 to exacerbate the progression of NAFLD. Reciprocally, silence of miR-140 or NEAT1 alleviates the severity of NAFLD. The mechanistical study shows that the axis of NEAT1-miR-140 inactivates AMPK/SREBP-1 signaling during the NAFLD. .</AbstractText>: NEAT1 and miR-140 are upregulated in hepacytes under the NAFLD conditions. NEAT1 directly binds to miR-140 and acts synergistically with miR-140 to exacerbate the progression of NAFLD. Reciprocally, silence of miR-140 or NEAT1 alleviates the severity of NAFLD. The mechanistical study shows that the axis of NEAT1-miR-140 inactivates AMPK/SREBP-1 signaling during the NAFLD. .The NEAT1-miR-140 axis play a crucial role in modulation of NAFLD via inactivation of AMPK/SREBP1 signaling. This study may provide a novel insight for the treatment of NAFLD.</AbstractText>: The NEAT1-miR-140 axis play a crucial role in modulation of NAFLD via inactivation of AMPK/SREBP1 signaling. This study may provide a novel insight for the treatment of NAFLD.	31239155	RID03415	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Atherosclerosis	ENST00000602558.1	ABCG1	negatively-E	CHIP;RIP	upregulation	qRT-PCR	NA	NA	cholesterol homeostasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000160179	NA	NA	9619	NA	ABC8|WHITE1	LncRNA ENST00000602558.1 regulates ABCG1 expression and cholesterol efflux from vascular smooth muscle cells through a p65-dependent pathway.Background and aims: Long non-coding RNAs (lncRNAs) have proven to be involved in the progression of atherosclerosis and dyslipidemia. In addition, vascular smooth muscle cells (VSMCs) phenotype switching, including VSMCs-derived foam cells formation, plays a key role in the pathogenesis of atherosclerosis. LncRNA ENST00000602558.1, one of the differentially expressed lncRNAs between coronary artery disease (CAD) patients and healthy controls identified by our previous study, was located to TG and HDL susceptibility loci, but its role and underlying mechanism in the pathogenesis of atherosclerosis remain unclear. The present study aims to explore the role and underlying mechanism of ENST00000602558.1 in the regulation of cholesterol efflux from VSMCs.Methods: ABCG1 mRNA and protein expression in VSMCs was detected using qRT-PCRand western blot, respectively. ABCG1-mediated cholesterol efflux to HDL from VSMCs was measured by means of NBD-cholesterol fluorescence intensity. The binding of ENST00000602558.1 to p65 and p65 to ABCG1 promoter region was detected by RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay, respectively.Results: Overexpression of ENST00000602558.1 downregulated ABCG1 mRNA and protein expression, while knockdown of ENST00000602558.1 upregulated ABCG1 mRNA and protein expression. Consistently, ENST00000602558.1 overexpression decreased ABCG1-mediated cholesterol efflux to HDL from VSMCs by 30.38% (p < 0.001), and knockdown of ENST00000602558.1 increased ABCG1-mediated cholesterol efflux to HDL from VSMCs by 30.41% (p = 0.001). In addition to cholesterol efflux, overexpression of ENST00000602558.1 increased lipid accumulation and TC/TG levels, while knockdown of ENST00000602558.1 decreased lipid accumulation and TC/TG levels in VSMCs. Furthermore, we confirmed that ENST00000602558.1 regulated ABCG1 expression and ABCG1-mediated cholesterol efflux from VSMCs through binding to p65.	31003090	RID03416	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE51827,GSE75367,GSE86978,GSE41245)
Lung cancer	NEAT1	p-Akt	positively-E	western blot	upregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(+);chemoresistance(+)	NA	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 mediates paclitaxel-resistance of non-small cell of lung cancer through activation of Akt/mTOR signalling pathway.Development of paclitaxel-resistance is a main problem during non-small cell lung cancer (NSCLC) chemotherapy. Nuclear paraspeckle assembly transcript 1 (NEAT1) is an oncogenic long non-coding RNA (lncRNA) which has been proved to be aberrantly upregulated in many human malignancies. In this study, we investigated the mechanism by which NEAT1 contributed to paclitaxel-resistance in NSCLC. NEAT1 was upregulated significantly in paclitaxel-resistant NSCLC cell line, compared with other NSCLC cell lines and normal bronchial epithelial (BE) cell line. Knockdown of NEAT1 could reverse the paclitaxel-resistance through induction of apoptosis by increasing cleaved PARP and cleaved caspase-3 expression. Moreover, NEAT1 was associated with Akt/mTOR signalling pathway activation by increasing expression of p-Akt, p-mTOR, Bcl-2 and decreasing expression of Bax. In conclusion, these results demonstrated that NEAT1 underlay paclitaxel-resistance in NSCLC.	30782035	RID03417	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	NEAT1	p-mTOR	positively-E	western blot	upregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(+);chemoresistance(+)	NA	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 mediates paclitaxel-resistance of non-small cell of lung cancer through activation of Akt/mTOR signalling pathway.Development of paclitaxel-resistance is a main problem during non-small cell lung cancer (NSCLC) chemotherapy. Nuclear paraspeckle assembly transcript 1 (NEAT1) is an oncogenic long non-coding RNA (lncRNA) which has been proved to be aberrantly upregulated in many human malignancies. In this study, we investigated the mechanism by which NEAT1 contributed to paclitaxel-resistance in NSCLC. NEAT1 was upregulated significantly in paclitaxel-resistant NSCLC cell line, compared with other NSCLC cell lines and normal bronchial epithelial (BE) cell line. Knockdown of NEAT1 could reverse the paclitaxel-resistance through induction of apoptosis by increasing cleaved PARP and cleaved caspase-3 expression. Moreover, NEAT1 was associated with Akt/mTOR signalling pathway activation by increasing expression of p-Akt, p-mTOR, Bcl-2 and decreasing expression of Bax. In conclusion, these results demonstrated that NEAT1 underlay paclitaxel-resistance in NSCLC.	30782035	RID03418	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	NEAT1	BCL2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(+);chemoresistance(+)	NA	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171791	NA	283131	596	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	Bcl-2|PPP1R50	NEAT1 mediates paclitaxel-resistance of non-small cell of lung cancer through activation of Akt/mTOR signalling pathway.Development of paclitaxel-resistance is a main problem during non-small cell lung cancer (NSCLC) chemotherapy. Nuclear paraspeckle assembly transcript 1 (NEAT1) is an oncogenic long non-coding RNA (lncRNA) which has been proved to be aberrantly upregulated in many human malignancies. In this study, we investigated the mechanism by which NEAT1 contributed to paclitaxel-resistance in NSCLC. NEAT1 was upregulated significantly in paclitaxel-resistant NSCLC cell line, compared with other NSCLC cell lines and normal bronchial epithelial (BE) cell line. Knockdown of NEAT1 could reverse the paclitaxel-resistance through induction of apoptosis by increasing cleaved PARP and cleaved caspase-3 expression. Moreover, NEAT1 was associated with Akt/mTOR signalling pathway activation by increasing expression of p-Akt, p-mTOR, Bcl-2 and decreasing expression of Bax. In conclusion, these results demonstrated that NEAT1 underlay paclitaxel-resistance in NSCLC.	30782035	RID03419	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	NEAT1	BAX	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(+);chemoresistance(+)	NA	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000087088	NA	283131	581	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BCL2L4	NEAT1 mediates paclitaxel-resistance of non-small cell of lung cancer through activation of Akt/mTOR signalling pathway.Development of paclitaxel-resistance is a main problem during non-small cell lung cancer (NSCLC) chemotherapy. Nuclear paraspeckle assembly transcript 1 (NEAT1) is an oncogenic long non-coding RNA (lncRNA) which has been proved to be aberrantly upregulated in many human malignancies. In this study, we investigated the mechanism by which NEAT1 contributed to paclitaxel-resistance in NSCLC. NEAT1 was upregulated significantly in paclitaxel-resistant NSCLC cell line, compared with other NSCLC cell lines and normal bronchial epithelial (BE) cell line. Knockdown of NEAT1 could reverse the paclitaxel-resistance through induction of apoptosis by increasing cleaved PARP and cleaved caspase-3 expression. Moreover, NEAT1 was associated with Akt/mTOR signalling pathway activation by increasing expression of p-Akt, p-mTOR, Bcl-2 and decreasing expression of Bax. In conclusion, these results demonstrated that NEAT1 underlay paclitaxel-resistance in NSCLC.	30782035	RID03420	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Obesity	TMEM18-DT	TMEM18	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	NA	regulation	RNA-protein	NA	NA	NA	Disease of metabolism	Obesity	lncRNA	PCG	ENSG00000233296	GRCh38_2:677186-697382	ENSG00000151353	NA	105373354	129787	AC092159.2	DKFZp434C1714|lncND	The role and possible mechanism of lncRNA AC092159.2 in modulating adipocyte differentiation.Obesity is a major risk factor for metabolic diseases, while adipocyte differentiation is closely related to obesity occurrence. Long noncoding RNAs (lncRNAs) are a unique class of transcripts in regulation of various biological processes. Using lncRNA microarray, we found lncRNA AC092159.2 was highly expressed in differentiated HPA-v and located ~247 bp upstream of the TMEM18, which was associated with BMI and obesity. We aimed to explore the role of AC092159.2 in adipogenesis and the underlying mechanisms. The effects of AC092159.2 gain- and loss-of-function on HPA-v adipogenesis were determined with lentivirus and siRNA-mediated cell transduction, respectively. Lipid accumulation was evaluated by oil red O staining; the expression of AC092159.2, TMEM18 and several adipogenesis makers in HPA-v were analyzed by qPCR/western blot. We found that the expression of AC092159.2 gradually increased during HPA-v differentiation, and its expression in omental adipose tissue was positively related with BMI among 48 human subjects. Overexpression of AC092159.2 promoted adipocytes differentiation while knockdown of it led to an adipogenic defect. Moreover, the expression of AC092159.2 and TMEM18 were positively correlated during adipogenic differentiation. AC092159.2 overexpression boosted TMEM18 expression while AC092159.2 knockdown restrained TMEM18 expression. Further rescue experiments showed that TMEM18 knockdown partially restrained adipogenic differentiation in AC092159.2 overexpressed HPA-v and adipogenic defect caused by AC092159.2 knockdown could be rescued by TMEM18 overexpression. Luciferase reporter assays revealed that AC092159.2 had a transcriptional activation effect on TMEM18. We concluded that lncRNA AC092159.2 promoted human adipocytes differentiation possibly by regulating TMEM18.	30753134	RID03421	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Pre-eclampsia	HIF1A-AS2	PHLDA1	positively-E	CHIP;RIP	downregulation	qRT-PCR;RNA-seq;western blot	NA	NA	cell proliferation(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000139289	NA	100750247	22822	3'aHIF-1A|aHIF	DT1P1B11|PHRIP|TDAG51	lncRNA HIF1A Antisense RNA 2 Modulates Trophoblast Cell Invasion and Proliferation through Upregulating PHLDA1 Expression.Long noncoding RNAs (lncRNAs) have been reported to be involved in various human diseases, and increasing studies have revealed that lncRNAs can play a vital role in preeclampsia (PE). In our study, lncRNA hypoxia-inducible factor 1 alpha (HIF1A) antisense RNA 2 (HIF1A-AS2) was found to be significantly downregulated in placenta tissues of PE patients by quantitative real-time PCR analysis. Moreover, Cell Counting Kit-8 (CCK-8) assays showed that downregulation of HIF1A-AS2 can impede cell proliferation of HTR-8/SVneo and JAR trophoblasts cells. Ectopic overexpression of HIF1A-AS2 can increase the function of trophoblasts cell migration and invasion in<U+00A0>vitro. RNA-sequencing (RNA-seq), RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) experiments showed that HIF1A-AS2 can recruit lysine-specific demethylase 1 (LSD1) and epigenetically repress pleckstrin homology-like domain, family A, member 1 (PHLDA1) transcription in human trophoblasts cells. In summary, our findings suggest that downregulated HIF1A-AS2 may play a role in the pathogenesis and progression of PE, and has potential as a novel prognostic marker in PE.	31085354	RID03422	interact with protein	prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Senescence	RP11-670E13.6	CDK4	positively-E	RNA pull-down assay;RIP	downregulation	RNA-seq	NA	NA	senescence(-)	ceRNA(miR-663a)	regulation	RNA-protein	NA	NA	NA	Other	Senescence	lncRNA	PCG	NA	NA	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	LncRNA RP11-670E13.6, interacted with hnRNPH, delays cellular senescence by sponging microRNA-663a in UVB damaged dermal fibroblasts.Ultraviolet (UV) irradiation from the sunlight is a major etiologic factor for premature skin aging. Long noncoding RNAs (lncRNAs) are involved in various biological processes, and their roles in UV irradiation-induced skin aging have recently been described. Previously, we found that the lncRNA RP11-670E13.6 was up-regulated and delayed cellular senescence in UVB-irradiated primary human dermal fibroblasts. Here, we performed further investigations of RP11-670E13.6 function. The results showed that this lncRNA directly bound to miR-663a and functioned as a sponge for miR-663a to modulate the derepression of Cdk4 and Cdk6, thereby delaying cellular senescence during UV irradiation-induced skin photoaging. Moreover, we found that RP11-670E13.6 may facilitate DNA damage repair by increasing ATM and -GammaH2A.X levels. In addition, heterogeneous nuclear ribonucleoprotein H physically interacted with RP11-670E13.6 and blocked its expression. Collectively, our results suggested that the RP11-670E13.6/miR-663a/CDK4 and RP11-670E13.6/miR-663a/CDK6 axis, which may function as competitive endogenous RNA networks, played important roles in UVB-induced cellular senescence.	31444317	RID03423	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Senescence	RP11-670E13.6	CDK6	positively-E	RNA pull-down assay;RIP	downregulation	RNA-seq	NA	NA	senescence(-)	ceRNA(miR-663a)	regulation	RNA-protein	NA	NA	NA	Other	Senescence	lncRNA	PCG	NA	NA	ENSG00000105810	NA	NA	1021	NA	MCPH12|PLSTIRE	LncRNA RP11-670E13.6, interacted with hnRNPH, delays cellular senescence by sponging microRNA-663a in UVB damaged dermal fibroblasts.Ultraviolet (UV) irradiation from the sunlight is a major etiologic factor for premature skin aging. Long noncoding RNAs (lncRNAs) are involved in various biological processes, and their roles in UV irradiation-induced skin aging have recently been described. Previously, we found that the lncRNA RP11-670E13.6 was up-regulated and delayed cellular senescence in UVB-irradiated primary human dermal fibroblasts. Here, we performed further investigations of RP11-670E13.6 function. The results showed that this lncRNA directly bound to miR-663a and functioned as a sponge for miR-663a to modulate the derepression of Cdk4 and Cdk6, thereby delaying cellular senescence during UV irradiation-induced skin photoaging. Moreover, we found that RP11-670E13.6 may facilitate DNA damage repair by increasing ATM and -GammaH2A.X levels. In addition, heterogeneous nuclear ribonucleoprotein H physically interacted with RP11-670E13.6 and blocked its expression. Collectively, our results suggested that the RP11-670E13.6/miR-663a/CDK4 and RP11-670E13.6/miR-663a/CDK6 axis, which may function as competitive endogenous RNA networks, played important roles in UVB-induced cellular senescence.	31444317	RID03424	ceRNA or sponge	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Senescence	HNRNPH1	RP11-670E13.6	negatively-E	RNA pull-down assay;RIP	downregulation	RNA-seq	NA	NA	senescence(-)	NA	binding/interaction	protein-RNA	NA	NA	NA	Other	Senescence	PCG	lncRNA	ENSG00000169045	NA	NA	NA	3187	NA	HNRPH|HNRPH1|hnRNPH	NA	LncRNA RP11-670E13.6, interacted with hnRNPH, delays cellular senescence by sponging microRNA-663a in UVB damaged dermal fibroblasts.Ultraviolet (UV) irradiation from the sunlight is a major etiologic factor for premature skin aging. Long noncoding RNAs (lncRNAs) are involved in various biological processes, and their roles in UV irradiation-induced skin aging have recently been described. Previously, we found that the lncRNA RP11-670E13.6 was up-regulated and delayed cellular senescence in UVB-irradiated primary human dermal fibroblasts. Here, we performed further investigations of RP11-670E13.6 function. The results showed that this lncRNA directly bound to miR-663a and functioned as a sponge for miR-663a to modulate the derepression of Cdk4 and Cdk6, thereby delaying cellular senescence during UV irradiation-induced skin photoaging. Moreover, we found that RP11-670E13.6 may facilitate DNA damage repair by increasing ATM and -GammaH2A.X levels. In addition, heterogeneous nuclear ribonucleoprotein H physically interacted with RP11-670E13.6 and blocked its expression. Collectively, our results suggested that the RP11-670E13.6/miR-663a/CDK4 and RP11-670E13.6/miR-663a/CDK6 axis, which may function as competitive endogenous RNA networks, played important roles in UVB-induced cellular senescence.	31444317	RID03425	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Inflammatory bowel disease	GAS5	MMP2	negatively-E		downregulation	qRT-PCR	NA	NA	cell injury(-)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000087245	NA	60674	4313	NCRNA00030|SNHG2	CLG4|CLG4A|TBE-1	Long Non-Coding RNA GAS5 and Intestinal MMP2 and MMP9 Expression: A Translational Study in Pediatric Patients with IBD.Background: The long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) seems to be involved in the regulation of mediators of tissue injury, in particular matrix metalloproteinases (MMPs), implicated in the pathogenesis of inflammatory bowel disease (IBD). We investigated the role of GAS5 in regulating MMP2 and MMP9 expression in pediatric patients with IBD and in vitro.Methods: In total, 25 IBD patients were enrolled: For each patient paired inflamed and non-inflamed biopsies were collected. RNA was extracted and GAS5, MMP2, and MMP9 were quantified by TaqMan assay. The expression of GAS5 and MMPs was also determined in the human monocytic THP1 cells differentiated into macrophages and stimulated with lipopolysaccharide (LPS). The function of GAS5 was assessed by overexpressing the lncRNA and evaluating the MMPs levels.Results: Real-time PCR results demonstrated a downregulation of GAS5 and an upregulation of both MMPs in inflamed tissues. In vitro data confirmed the trend observed in patients for the three genes: The stimulation with LPS promoted a downregulation of GAS5 while an increase of MMPs was observed. Overexpression experiments showed that higher levels of GAS5 lead to a decrease of both enzymes.Conclusion: These results provide new information about the role of GAS5 in IBD: The lncRNA could mediate tissue damage by modulating the expression of MMPs.	31652976	RID03426	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Inflammatory bowel disease	GAS5	MMP9	negatively-E		downregulation	qRT-PCR	NA	NA	cell injury(-)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000100985	NA	60674	4318	NCRNA00030|SNHG2	CLG4B	Long Non-Coding RNA GAS5 and Intestinal MMP2 and MMP9 Expression: A Translational Study in Pediatric Patients with IBD.Background: The long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) seems to be involved in the regulation of mediators of tissue injury, in particular matrix metalloproteinases (MMPs), implicated in the pathogenesis of inflammatory bowel disease (IBD). We investigated the role of GAS5 in regulating MMP2 and MMP9 expression in pediatric patients with IBD and in vitro.Methods: In total, 25 IBD patients were enrolled: For each patient paired inflamed and non-inflamed biopsies were collected. RNA was extracted and GAS5, MMP2, and MMP9 were quantified by TaqMan assay. The expression of GAS5 and MMPs was also determined in the human monocytic THP1 cells differentiated into macrophages and stimulated with lipopolysaccharide (LPS). The function of GAS5 was assessed by overexpressing the lncRNA and evaluating the MMPs levels.Results: Real-time PCR results demonstrated a downregulation of GAS5 and an upregulation of both MMPs in inflamed tissues. In vitro data confirmed the trend observed in patients for the three genes: The stimulation with LPS promoted a downregulation of GAS5 while an increase of MMPs was observed. Overexpression experiments showed that higher levels of GAS5 lead to a decrease of both enzymes.Conclusion: These results provide new information about the role of GAS5 in IBD: The lncRNA could mediate tissue damage by modulating the expression of MMPs.	31652976	RID03427	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatitis B	LINC01149	MICA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000231836	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:31484113-31489410	ENSG00000233051	NA	101929111	100507436	XXbac-BPG181B23.4	PERB11.1	LINC01149 variant modulates MICA expression that facilitates hepatitis B virus spontaneous recovery but increases hepatocellular carcinoma risk.Interpreting disease-causing variants, especially in noncoding regions by genome-wide association studies (GWAS), has become one of the most challenging and demanding tasks. We hypothesized that functional lncRNAs variants in GWAS-identified loci might alter expression level of genes associated with persistent HBV infection and hepatocellular carcinoma (HCC). Integrated bioinformatics approaches were used to prioritize potentially functional variants and a two-stage case-control study (2473 HBV positive HCC patients, 2248 persistent HBV carriers and 2294 spontaneously recovered subjects) was performed to assess the roles of these variants. The rs2844512 G > C variant in LINC01149 was identified to facilitate HBV spontaneous recovery (OR = 0.84, 95% CI = 0.77-0.92) but increase the risk of HCC (OR = 1.21, 95% CI = 1.11-1.32) in combined samples. Subsequent biological assays indicated this variant created a binding site for miR-128-3p and upregulated MICA expression by serving as a miRNA sponge, which might recruit NK-cells to lyse infected cells, but release highly soluble MICA by shedding to induce NK-cells exhaustion and tumor immune evasion. These findings highlight a regulatory circuit between LINC01149 and MICA, mediating by miR-128-3p, and the important role of upregulated MICA in conferring susceptibility to persistent HBV infection and HCC.	31754211	RID03428	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC01149	MICA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231836	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:31484113-31489410	ENSG00000233051	NA	101929111	100507436	XXbac-BPG181B23.4	PERB11.1	LINC01149 variant modulates MICA expression that facilitates hepatitis B virus spontaneous recovery but increases hepatocellular carcinoma risk.Interpreting disease-causing variants, especially in noncoding regions by genome-wide association studies (GWAS), has become one of the most challenging and demanding tasks. We hypothesized that functional lncRNAs variants in GWAS-identified loci might alter expression level of genes associated with persistent HBV infection and hepatocellular carcinoma (HCC). Integrated bioinformatics approaches were used to prioritize potentially functional variants and a two-stage case-control study (2473 HBV positive HCC patients, 2248 persistent HBV carriers and 2294 spontaneously recovered subjects) was performed to assess the roles of these variants. The rs2844512 G > C variant in LINC01149 was identified to facilitate HBV spontaneous recovery (OR = 0.84, 95% CI = 0.77-0.92) but increase the risk of HCC (OR = 1.21, 95% CI = 1.11-1.32) in combined samples. Subsequent biological assays indicated this variant created a binding site for miR-128-3p and upregulated MICA expression by serving as a miRNA sponge, which might recruit NK-cells to lyse infected cells, but release highly soluble MICA by shedding to induce NK-cells exhaustion and tumor immune evasion. These findings highlight a regulatory circuit between LINC01149 and MICA, mediating by miR-128-3p, and the important role of upregulated MICA in conferring susceptibility to persistent HBV infection and HCC.	31754211	RID03429	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	CHRF	MIR146A	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+);JAK1/STAT3 signaling pathway(+);inflammatory response(-)	NA	regulation	protein-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	ENSG00000253522	NA	NA	406938	NA	MIRN146|MIRN146A|miR-146a|miRNA146A	Long noncoding RNA CHRF exacerbates IL-6-induced inflammatory damages by downregulating microRNA-146a in ATDC5 cells.Osteoarthritis (OA) is a frequent chronic musculoskeletal disorder which lacks applicably effective therapeutic strategy. In this study, we attempted to investigate whether long noncoding RNA (lncRNA) cardiac hypertrophy-related factor (CHRF) participated in mediating interleukin-6 (IL-6)-induced in vitro inflammatory damages as well as the regulatory mechanisms. ATDC5 cells were stimulated with IL-6, and then cellular damages were evaluated on the basis of cell viability by CCK-8, apoptotic cells by observation with flow cytometry, apoptosis-associated proteins by western blot and accumulation of inflammatory factors by quantitative reverse transcription polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and western blot Then, effects of lncRNA CHRF on IL-6-treated cells were evaluated. We further explored the downstream factor of lncRNA CHRF and demonstrated whether lncRNA CHRF functioned through the downstream factor. Afterwards, crucial signaling cascades were anatomized. We found that IL-6 reduced cell viability, elevated apoptosis, induced upregulation of inflammatory factors, as well as upregulated lncRNA CHRF and down-regulated miR-146a expression. Then, we found lncRNA CHRF overexpression aggravated IL-6-induced alterations, and lncRNA CHRF knockdown showed the opposite effects. Furthermore, miR-146a was identified to be negatively regulated by lncRNA CHRF, and its overexpression abrogated the roles of lncRNA CHRF in IL-6-treated cells. IL-6-induced the accumulation of IkBalpha, p65, JAK1, and STAT3 at phosphorylated level was further facilitated by lncRNA CHRF whereas repressed by miR-146a. In conclusion, lncRNA CHRF aggravated the IL-6-induced inflammatory damages in ATDC5 cells. We further outlined a possible mechanism that through downregulating miR-146a, lncRNA CHRF evoked the activation of NF-kB and JAK1/STAT3 signaling cascades.	31026064	RID03430	expression association	NA		
Colon cancer	WiNTRLINC1	ASCL2	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell viability(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000183734	NA	NA	430	NA	ASH2|bHLHa45|HASH2	WiNTRLINC1/ASCL2/c-Myc Axis Characteristics of Colon Cancer with Differentiated Histology at Young Onset and Essential for Cell Viability.Results: Real-time quantitative reverse transcriptase-polymerase chain reaction confirmed definite overexpression of WiNTRLINC1 mRNA in primary colon cancer compared with the corresponding normal colon mucosa tissues (p = 0.0005), such as ASCL2, c-Myc, and PRL-3 (p < 0.0001). The four gene expression signatures were tightly associated in the center of the ASCL2 gene (r = 0.72, p < 0.0001) in clinical samples. WiNTRLINC1 was not significantly associated with prognostic factors in colon cancer and other lncRNAs, while the WiNTRLINC1/ASCL2/c-Myc signatures were unique to young-onset colon cancer with differentiated histology. On the other hand, undifferentiated histology was significantly associated with H19 expression. Knockdown of the WiNTRLINC1 gene reduced the expression of ASCL2/c-Myc, but rather augmented PRL-3 at mRNA level, and robustly affected cell viability in colon cancer cell lines.	31549316	RID03431	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE67939,GSE86978)
Colon cancer	WiNTRLINC1	MYC	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell viability(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	WiNTRLINC1/ASCL2/c-Myc Axis Characteristics of Colon Cancer with Differentiated Histology at Young Onset and Essential for Cell Viability.Results: Real-time quantitative reverse transcriptase-polymerase chain reaction confirmed definite overexpression of WiNTRLINC1 mRNA in primary colon cancer compared with the corresponding normal colon mucosa tissues (p = 0.0005), such as ASCL2, c-Myc, and PRL-3 (p < 0.0001). The four gene expression signatures were tightly associated in the center of the ASCL2 gene (r = 0.72, p < 0.0001) in clinical samples. WiNTRLINC1 was not significantly associated with prognostic factors in colon cancer and other lncRNAs, while the WiNTRLINC1/ASCL2/c-Myc signatures were unique to young-onset colon cancer with differentiated histology. On the other hand, undifferentiated histology was significantly associated with H19 expression. Knockdown of the WiNTRLINC1 gene reduced the expression of ASCL2/c-Myc, but rather augmented PRL-3 at mRNA level, and robustly affected cell viability in colon cancer cell lines.	31549316	RID03432	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colon cancer	WiNTRLINC1	PTP4A3	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell viability(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000184489	NA	NA	11156	NA	PRL-3|PRL-R|PRL3	WiNTRLINC1/ASCL2/c-Myc Axis Characteristics of Colon Cancer with Differentiated Histology at Young Onset and Essential for Cell Viability.Results: Real-time quantitative reverse transcriptase-polymerase chain reaction confirmed definite overexpression of WiNTRLINC1 mRNA in primary colon cancer compared with the corresponding normal colon mucosa tissues (p = 0.0005), such as ASCL2, c-Myc, and PRL-3 (p < 0.0001). The four gene expression signatures were tightly associated in the center of the ASCL2 gene (r = 0.72, p < 0.0001) in clinical samples. WiNTRLINC1 was not significantly associated with prognostic factors in colon cancer and other lncRNAs, while the WiNTRLINC1/ASCL2/c-Myc signatures were unique to young-onset colon cancer with differentiated histology. On the other hand, undifferentiated histology was significantly associated with H19 expression. Knockdown of the WiNTRLINC1 gene reduced the expression of ASCL2/c-Myc, but rather augmented PRL-3 at mRNA level, and robustly affected cell viability in colon cancer cell lines.	31549316	RID03433	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Sepsis	MALAT1	BRCA1	negatively-E	RNA pull-down assay;CHIP;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000012048	NA	378938	672	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BRCC1|FANCS|PPP1R53|RNF53	lncRNA MALAT1 Accelerates Skeletal Muscle Cell Apoptosis and Inflammatory Response in Sepsis by Decreasing BRCA1 Expression by Recruiting EZH2.Sepsis is a serious and elusive syndrome caused by infection, which is accompanied by a high mortality worldwide. Recent evidence has documented the regulatory role of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) during the inflammatory process, the effects of which in the development of sepsis have become the focus of the current study. An in<U+00A0>vivo mouse model and in<U+00A0>vitro cell model of sepsis induced by lipopolysaccharide (LPS) were developed. High expression of lncRNA MALAT1 along with low expression of breast cancer susceptibility gene 1 (BRCA1) were identified in septic mice and human skeletal muscle cells of sepsis. Then, lncRNA MALAT1 expression was altered in<U+00A0>vivo and in<U+00A0>vitro to examine serum levels of inflammatory factors, as well as skeletal muscle cell apoptosis. lncRNA MALAT1 was noted to regulate the expression and export from the nucleus of BRCA1 by recruiting zeste homolog 2 (EZH2) in skeletal muscle cells of sepsis. Silencing lncRNA MALAT1 resulted in reduced serum levels of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha (TNF-alpha), neutrophil migration, skeletal muscle cell apoptosis, and AKT-1 phosphorylation. Taken together, lncRNA MALAT1 interacting with EZH2 stimulated AKT-1 phosphorylation and decreased BRCA1 expression, consequently aggravating the progression of sepsis, highlighting a promising therapeutic option for sepsis.	31830649	RID03434	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Cardiac hypertrophy	SYNE1-AS1	SP1	positively-E	RNA pull-down assay;luciferase activity assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-525-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	TF	ENSG00000234577	GRCh38_6:152380546-152381564	ENSG00000185591	NA	100505475	6667	NA	NA	SP1-SYNE1-AS1-miR-525-5p feedback loop regulates Ang-II-induced cardiac hypertrophy.Cardiac hypertrophy (CH) has become a huge threat to human health. Recent years, long noncoding RNAs (lncRNAs) have been studied in human diseases, including CH. According to bioinformatics analysis, 10 lncRNAs possibly involved in the progression of CH were screened out. Among which, lncRNA SYNE1 antisense RNA 1 (SYNE1-AS1) could be upregulated by Angiotensin II (Ang-II) in cardiomyocytes. Thus, we chose SYNE1-AS1 to do further study. To identify the biological function of SYNE1-AS1 in CH, SYNE1-AS1 was silenced in Ang-II-induced cardiomyocytes. Results of immunofluorescence staining demonstrated that increased cell surface area in Ang-II-induced cardiomyocytes was reduced by SYNE1-AS1 knockdown. Moreover, the hypertrophic responses were attenuated by SYNE1-AS1 knockdown. Mechanically, SYNE1-AS1 positively regulated Sp1 transcription factor (SP1) by sponging microRNA-525-5p (miR-525-5p). On the basis of previous reports, SP1 can transcriptionally activate lncRNAs. Therefore, we investigated the interaction between SP1 and SYNE1-AS1 promoter. Intriguingly, SYNE1-AS1 was activated by SP1. At last, rescue assays demonstrated the function of SP1-SYNE1-AS1 axis in CH. In conclusion, SP1-induced upregulation of lncRNA SYNE1-AS1 promoted CH via miR-525-5p/SP1 axis.	30652310	RID03435	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atrial fibrillation	LINC00472	JP2	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-24)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000211688	NA	79940	NA	C6orf155|dJ288M22.3|FLJ13189|P53RRA	JP2|TCRGJP2	LncRNA-LINC00472 contributes to the pathogenesis of atrial fibrillation (Af) by reducing expression of JP2 and RyR2 via miR-24.BACKGROUND: Dysregulated methylation of the promoter of lncRNA LINC00472 reduces the expression of LINC00472 and subsequently up-regulates the expression of its competing endogenous RNA miR-24. In addition, JP2 can stabilize the expression of RyR2, whereas the deregulation of RyR2 expression may contribute to the pathogenesis of atrial fibrillation (AF). In this study, we aimed to study the role of LINC00472 in the pathogenesis of AF.METHODS: 125 AF patients and 168 healthy controls were enrolled to compare their expression of miR-24, LINC00472, JP2 and RyR2. A dual-luciferase reporter gene assay accompanied by real-time PCR, western blot and IHC assay was subsequently conducted to evaluate the regulatory relationship among miR-24, LINC00472, JP2 and RyR2 in HCM and H9C2 cells.RESULTS: AF patients were associated with an increased level of miR-24 expression and reduced level of LINC00472 expression. Also, the level of DNA methylation in LINC00472 was increased in AF patients. MiR-24 could negatively regulate the expression of LINC00472 and JP2 by directly binding to them.CONCLUSIONS: LINC00472 could regulate the progression of AF via modulating the LINC00472/miR-24/JP2/RyR2 signaling pathway.	31562981	RID03436	ceRNA or sponge	NA		
Atrial fibrillation	LINC00472	RYR2	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-24)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000198626	NA	79940	6262	C6orf155|dJ288M22.3|FLJ13189|P53RRA	ARVC2|ARVD2|VTSIP	LncRNA-LINC00472 contributes to the pathogenesis of atrial fibrillation (Af) by reducing expression of JP2 and RyR2 via miR-24.BACKGROUND: Dysregulated methylation of the promoter of lncRNA LINC00472 reduces the expression of LINC00472 and subsequently up-regulates the expression of its competing endogenous RNA miR-24. In addition, JP2 can stabilize the expression of RyR2, whereas the deregulation of RyR2 expression may contribute to the pathogenesis of atrial fibrillation (AF). In this study, we aimed to study the role of LINC00472 in the pathogenesis of AF.METHODS: 125 AF patients and 168 healthy controls were enrolled to compare their expression of miR-24, LINC00472, JP2 and RyR2. A dual-luciferase reporter gene assay accompanied by real-time PCR, western blot and IHC assay was subsequently conducted to evaluate the regulatory relationship among miR-24, LINC00472, JP2 and RyR2 in HCM and H9C2 cells.RESULTS: AF patients were associated with an increased level of miR-24 expression and reduced level of LINC00472 expression. Also, the level of DNA methylation in LINC00472 was increased in AF patients. MiR-24 could negatively regulate the expression of LINC00472 and JP2 by directly binding to them.CONCLUSIONS: LINC00472 could regulate the progression of AF via modulating the LINC00472/miR-24/JP2/RyR2 signaling pathway.	31562981	RID03437	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Acute lymphocytic leukemia	NEAT1	ABCA3	positively-E	DIANA LncBase;LncACTdb	upregulation	qRT-PCR	NA	NA	prognosis(+);chemoresistance(+)	ceRNA(miR-335-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000167972	NA	283131	21	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ABC-C|ABC3|EST111653|LBM180	Dysregulation of miR-335-3p, targeted by NEAT1 and MALAT1 long non-coding RNAs, is associated with poor prognosis in childhood acute lymphoblastic leukemia.Acute lymphoblastic leukemia (ALL) is the most prevalent cancer among children, and multidrug efflux mediated by overexpression of ABC transporters is the major impediment to successful chemotherapy in this malignancy. The goal of this study is to identify the non-coding RNAs (ncRNAs) which may affect the expression levels of ABCA3; the previously identified prognostic biomarker for multidrug resistance (MDR) in childhood ALL (cALL). Bone marrow samples from 64 cALLs, including 46 de novo and 18 relapsed patients, in addition to 30 non-cancer controls were collected, and ncRNAs were nominated using in silico studies. Quantitative RT-PCRshowed low expression profiles of miR-335-3p in cALLs compared with the control group (P<U+202F>=<U+202F>0.018). Inverse correlation was determined between the miR-335-3p and ABCA3 mRNA expression profiles in cALL patients (r<U+202F>=<U+202F>0.5019, P<U+202F>=<U+202F>0.002). Moreover, it was shown that the expression levels of miR-335-3p was downregulated in the drug-resistant samples (MDR group) compared with the drug-sensitive patients (mrd- group), (P<U+202F>=<U+202F>0.0005, AUC<U+202F>=<U+202F>0.801). On the other hand, negative correlations were identified between the expression levels of miR-335-3p and the selected LncRNAs, NEAT1 and MALAT1, in the MDR group compared with the mrd- patients (P<U+202F>=<U+202F>0.009), suggesting a sponge effect for these LncRNAs. The current study showed a potential regulatory role for miR-335-3p in ABCA3 expression targeted by NEAT1 and MALAT1 long non-coding RNAs. This negative impact may possibly contribute to the development of chemoresistance in childhood ALL, and provide an exceptional insight to new therapeutic approaches.	30639603	RID03438	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065)
Acute lymphocytic leukemia	MALAT1	ABCA3	positively-E	DIANA LncBase;LncACTdb	upregulation	qRT-PCR	NA	NA	prognosis(+);chemoresistance(+)	ceRNA(miR-335-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000167972	NA	378938	21	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ABC-C|ABC3|EST111653|LBM180	Dysregulation of miR-335-3p, targeted by NEAT1 and MALAT1 long non-coding RNAs, is associated with poor prognosis in childhood acute lymphoblastic leukemia.Acute lymphoblastic leukemia (ALL) is the most prevalent cancer among children, and multidrug efflux mediated by overexpression of ABC transporters is the major impediment to successful chemotherapy in this malignancy. The goal of this study is to identify the non-coding RNAs (ncRNAs) which may affect the expression levels of ABCA3; the previously identified prognostic biomarker for multidrug resistance (MDR) in childhood ALL (cALL). Bone marrow samples from 64 cALLs, including 46 de novo and 18 relapsed patients, in addition to 30 non-cancer controls were collected, and ncRNAs were nominated using in silico studies. Quantitative RT-PCRshowed low expression profiles of miR-335-3p in cALLs compared with the control group (P<U+202F>=<U+202F>0.018). Inverse correlation was determined between the miR-335-3p and ABCA3 mRNA expression profiles in cALL patients (r<U+202F>=<U+202F>0.5019, P<U+202F>=<U+202F>0.002). Moreover, it was shown that the expression levels of miR-335-3p was downregulated in the drug-resistant samples (MDR group) compared with the drug-sensitive patients (mrd- group), (P<U+202F>=<U+202F>0.0005, AUC<U+202F>=<U+202F>0.801). On the other hand, negative correlations were identified between the expression levels of miR-335-3p and the selected LncRNAs, NEAT1 and MALAT1, in the MDR group compared with the mrd- patients (P<U+202F>=<U+202F>0.009), suggesting a sponge effect for these LncRNAs. The current study showed a potential regulatory role for miR-335-3p in ABCA3 expression targeted by NEAT1 and MALAT1 long non-coding RNAs. This negative impact may possibly contribute to the development of chemoresistance in childhood ALL, and provide an exceptional insight to new therapeutic approaches.	30639603	RID03439	ceRNA or sponge	chemoresistance,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065)
Colorectal cancer	HOTAIR	FUT6	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156413	NA	100124700	2528	HOXC-AS4|HOXC11-AS1|NCRNA00072	FCT3A|FLJ40754|FT1A|FucT-VI	HOTAIR/miR-326/FUT6 axis facilitates colorectal cancer progression through regulating fucosylation of CD44 via PI3K/AKT/mTOR pathwayMetastasis is the main cause of death in colorectal cancer (CRC) patients. Aberrant fucosylation, catalyzed by the specific fucosyltransferases (FUTs), is associated with malignant behaviors. Non-conding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), emerge as key molecules in cancer malignancy. The aim of this study was to investigate HOTAIR/miR-326/FUT6 axis modified fucosylation on sLeX-CD44 (HCELL), which served as E-selectin ligand during CRC progression. Higher levels of HOTAIR and FUT6 were verified in CRC tissues and cell lines, with a positive correlation. HOTAIR was associated with poor clinical prognosis of CRC. Altered HOTAIR levels influenced proliferation, aggressiveness, apoptosis and tumorigenesis of CRC cells. HOTAIR directly harbored miR-326 binding sites and regulated FUT6 expression. Further results corroborated that HOTAIR/miR-326/FUT6 axis modified alpha1, 3-fucosylation of CD44, which mediated CRC malignancy. Co-modulation of HOTAIR, miR-326 and FUT6 impacted alpha1, 3-fucosylated CD44, which further triggered PI3K/AKT/mTOR pathway. HOTAIR also mediated CRC tumorigenesis and liver metastasis in vivo. Thus, our findings indicated that HOTAIR/miR-326/FUT6 axis mediated CRC procession through alpha1, 3-fucosylated CD44 via PI3K/AKT/mTOR pathway. This work rendered new therapeutic targets for CRC.	30742932	RID03440	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD);DOWN(PRAD);DATA(GSE117623,GSE40174,GSE67980,GSE60407)
Diabetic retinopathy	FENDRR	VEGFA	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);angiogenesis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000112715	NA	400550	7422	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	VEGF|VEGF-A|VPF	LncRNA FENDRR promotes high-glucose-induced proliferation and angiogenesis of human retinal endothelial cells;FENDRR overexpression significantly promoted the high-glucose-induced proliferation, migration, capillary morphogenesis, and VEGF expression in HRECs;RT-qPCR analysis revealed that relative FENDRR level in blood from DR patients was significantly also upregulated compared with the normal subjects;FENDRR overexpression greatly increased the protein expression of VEGF (a pivotal marker of angiogenesis) in HRECs, whereas FENDRR knockdown exerted opposite effects;The overexpression and knockdown efficiency of FENDRR in HRECs was determined by RT-qPCR	30700211	RID03441	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Kidney injury	LINC00520	OSMR	positively-E	luciferase reporter assay;qRT-PCR	upregulation	microarray	GSE30718	NA	PI3K/AKT signaling pathway(+)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000145623	NA	645687	9180	C14orf34|LASSIE	OSMRB|OSMRbeta	LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway;LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI;RNA expression data were downloaded from the NCBI Gene Expression Omnibus (GEO, GSE30718, https://www.ncbi.nlm.nih.gov/geo/);microarray analysis was used to screen out differentially expressed mRNAs and lncRNAs to explore the molecular mechanism of kidney transplants acute injury. Figure 1a indicates top 10 upregulated and downregulated mRNAs in AKI. Besides, the results of the differential analysis showed that only CTSLP8 and LINC00520 were highly expressed in AKI; qRT-PCRwas performed to verify the expression of LINC00520, miR-27b-3p, and OSMR in normal and AKI renal tissues. The results suggested that LINC00520 and OSMR were observably upregulated in AKI renal tissues,while miR-27b-3p was markedly downregulated in AKI renal tissues (Figure 3d). Besides, dual luciferase reporter gene assays indicated that LINC00520-WT and OSMR-WT presented lower luciferase activity than the corresponding MUT group, confirming the binding relationship of LINC00520/miR-27b and miR-27b-3p/OSMR	30684280	RID03442	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827)
Osteosarcoma	DNAJC3-DT	DNAJC3	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);chemosensitivity(-)	NA	association	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000247400	GRCh38_13:95648711-95676973	ENSG00000102580	NA	100289274	5611	DNAJC3-AS1	ERdj6|HP58|P58|p58(IPK)|P58IPK|PRKRI	Long noncoding RNA DNAJC3-AS1 promotes osteosarcoma progression via its sense-cognate gene DNAJC3;We found that DNAJC3-AS1 expression was up-regulated in osteosarcoma;Mechanistically, DNAJC3-AS1 enhanced cell proliferation, migration, and invasion in vitro and in vivo and reduced sensitivity of osteosarcoma to cisplatin. These effects of DNAJC3-AS1 were reversed by down-regulation of its sense-cognate gene DNAJC3;Expression of DNAJC3-AS1 was examined in 30 pairsof OS specimens and pair-matched adjacent noncancerous tissues by using qRT-PCRNAJC3-AS1 associates positively with sense-cognate gene DNAJC3 in OS cells;we then performed biological information analysis, which showed that DNAJC3-AS1 and DNAJC3 constituted a 'head-to-head'-pairing pattern with DNAJC3-AS1 overlapping the promoter region of DNAJC3 completely (Figure 5A). Therefore, we detected the correlation between DNAJC3-AS1 and DNAJC3. We observed an increasing expression of DNAJC3 level in OS specimens compared with their corresponding noncancerous specimens (Figure 5B). Furthermore, OS cell lines also presented higher expression level of DNAJC3 compared with hFOB1.19 cells (Figure 5C). Importantly, correlation analysis revealed a positive relationship between DNAJC3-AS1 and DNAJC3 expression level over OS specimens (Figure 5D). These results were further more supported by western blot(Figures 5E and S1A). These results demonstrated that DNAJC3-AS1 may participate in the development and progression of osteosarcoma via regulating its sense-cognate gene DNAJC3	30652414	RID03443	expression association	chemoresistance		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE75367,GSE86978)
Osteoporosis	NEAT1	BMP1	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168487	NA	283131	649	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BMP-1|PCOLC	LncRNA NEAT1/miR-29b-3p/BMP1 axis promotes osteogenic differentiation in human bone marrow-derived mesenchymal stem cells;Firstly, the relative lower expression of BMP1 was detected in hBMSCs obtained from osteoporosis patients;The luciferase activity assay performed in HEK-293 T cell revealed that the inhibitory effect of miR-29b-3p mimics on the luciferase activity of BMP1-WT, indicating the binding relation between miR-29-3p and BMP1. Pull-down assay further demonstrated the interaction between miR-29b-3p and BMP1.Firstly, the relative lower expression of BMP1 was detected in hBMSCs obtained from osteoporosis patients.Mechanically, BMP1 was demonstrated to be the target mRNA of miR-29b-3p.Moreover, increasing studies indicate that long non-coding RNAs (lncRNAs) are crucial regulators in hBMSCs osteogenic differentiation by exerting ceRNA function.	30638953	RID03444	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	CASC15	TWIST1	positively-E	RIP;luciferase reporter assay;bioinformatics	upregulation	RT-qPCR	TCGA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	ceRNA(miR-33a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000122691	NA	401237	7291	LINC00340|lnc-SOX4-1	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	CASC15 promotes epithelial to mesenchymal transition and facilitates malignancy of hepatocellular carcinoma cells by increasing TWIST1 gene expression via miR-33a-5p sponging;Interaction between CASC15 and microRNA-33a-5p (miR-33a-5p) was verified by argonaute 2-RNA Immunoprecipitation (AGO2-RIP) and luciferase reporter assays;CASC15 promoted EMT in HCC cells by increasing N-cadherin and Vimentin protein level while decreasing that of E-cadherin through TWIST1. CASC15 facilitated HCC cell proliferation, migration and invasion while reducing cell apoptosis through TWIST1;Transcriptome sequencing data in the Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma dataset was accessed through www.cbioportal.org/study-id=lihc_tcga#summary	31401158	RID03445	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	CASC15	SOX4	positively-E	western blot;bioinformatics	upregulation	RT-qPCR	TCGA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000124766	NA	401237	6659	LINC00340|lnc-SOX4-1	NA	CASC15 promotes epithelial to mesenchymal transition and facilitates malignancy of hepatocellular carcinoma cells by increasing TWIST1 gene expression via miR-33a-5p sponging;TWIST1, sex-determining region Y-related high-mobility group box 4 (Sox4) and Versican were found as putative CASC15 co-expressing genes.-CASC15 positively regulated TWIST1 gene expression as well as protein level of Sox4 and Versican in HCC cells;The western blot results indicated that Sox4 and Versican protein expression level in HCC cells could also be increased by CASC15 OE or decreased by CASC15 KD (Fig. 2G K), suggesting that CASC15 might also regulate the expression of Sox4 and Versican genes in HCC cells;we propose that the possibility that CASC15 promotes HCC development by upregulating Sox4 and Versican gene expression should also be verified;;Transcriptome sequencing data in the Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma dataset was accessed through www.cbioportal.org/study-id=lihc_tcga#summary	31401158	RID03446	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	CASC15	VCAN	positively-E	western blot;bioinformatics	upregulation	RT-qPCR	TCGA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000038427	NA	401237	1462	LINC00340|lnc-SOX4-1	CSPG2|PG-M	CASC15 promotes epithelial to mesenchymal transition and facilitates malignancy of hepatocellular carcinoma cells by increasing TWIST1 gene expression via miR-33a-5p sponging;TWIST1, sex-determining region Y-related high-mobility group box 4 (Sox4) and Versican were found as putative CASC15 co-expressing genes.-CASC15 positively regulated TWIST1 gene expression as well as protein level of Sox4 and Versican in HCC cells; The western blot results indicated that Sox4 and Versican protein expression level in HCC cells could also be increased by CASC15 OE or decreased by CASC15 KD (Fig. 2G K), suggesting that CASC15 might also regulate the expression of Sox4 and Versican genes in HCC cells;;Transcriptome sequencing data in the Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma dataset was accessed through www.cbioportal.org/study-id=lihc_tcga#summary	31401158	RID03447	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	CASC15	CDH2	positively-E	bioinformatics	upregulation	RT-qPCR	TCGA	NA	epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000170558	NA	401237	1000	LINC00340|lnc-SOX4-1	CD325|CDHN|NCAD	CASC15 promotes epithelial to mesenchymal transition and facilitates malignancy of hepatocellular carcinoma cells by increasing TWIST1 gene expression via miR-33a-5p sponging;CASC15 promoted EMT in HCC cells by increasing N-cadherin and Vimentin protein level while decreasing that of E-cadherin through TWIST1;;Transcriptome sequencing data in the Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma dataset was accessed through www. cbioportal.org/study-id=lihc_tcga#summary	31401158	RID03448	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Hepatocellular carcinoma	CASC15	CDH1	negatively-E	bioinformatics	upregulation	RT-qPCR	TCGA	NA	epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000039068	NA	401237	999	LINC00340|lnc-SOX4-1	CD324|UVO|uvomorulin	CASC15 promotes epithelial to mesenchymal transition and facilitates malignancy of hepatocellular carcinoma cells by increasing TWIST1 gene expression via miR-33a-5p sponging;CASC16 promoted EMT in HCC cells by increasing N-cadherin and Vimentin protein l-	31401158	RID03449	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Diffuse large b-cell lymphoma	MYC	FIRRE	positively-F	JASPAR;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000213468	GRCh38_X:131688779-131830862	4609	286467	bHLHe39|c-Myc|MYCC	LINC01200	LncRNA FIRRE is activated by MYC and promotes the development of diffuse large B-cell lymphoma via Wnt/beta-catenin signaling pathway;qRT-PCRproved that lncRNA functional intergenic repeating RNA element (FIRRE) was up-regulated in DLBCL tissues and cells;The suppressive effect of FIRRE knockdown on DLBCL cell growth;We chose five of them for qRT-PCRanalysis due to they have been reported in human cancers as the transcriptional activators of lncRNAs. And we found that MYC was significantly highly expressed in five DLBCL cells when normalized to WIL2S (Fig. 3A). To analyze the potential regulation of MYC on FIRRE expression, we separately silenced and overexpressed MYC in DLBCL cells (Fig. 3B). Afterwards, the FIRRE expression was found to be downregulated in MYC-downregulated cells but was upregulated in MYC-overexpressed cells;We obtained the binding motif of MYC and the top two binding sequences between MYC and FIRRE promoter from JASPAR (http://jaspar.genereg.net/) (Fig. 3D). These two binding sequences (site1 and site2) were distributed in two parts of FIRRE promoter (P1 and P2). ChIP assay revealed that the binding of MYC in P2 fragment of FIRRE promoter (Fig. 3E). Luciferase activity showed that MYC overexpression led to the increased luciferase activity of P2 fragment (Fig. 3F). Therefore, we confirmed that site2 was responsible for the interaction between MYC and FIRRE.	30739786	RID03450	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Kidney injury	MGAT3-AS1	PTEN	positively-E	RNA pull-down assay;RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-22)	regulation	RNA-protein	NA	CSC	NA	Other	Injury	lncRNA	PCG	ENSG00000227188	GRCh38_22:39475807-39476822	ENSG00000171862	NA	104502417	5728	TapSAKI	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA TapSAKI promotes inflammation injury in HK -2 cells and urine derived sepsis-induced kidney injury;RNA precipitation and RNA pull-down were performed to confirm the interaction between TapSAKI and miR-22;TapSAKI interacted with miR-22, and negatively modulate miR-22 expression;TapSAKI was elevated in urine derived sepsis-induced kidney injury, and promoted HK-2 cell apoptosis and inflammatory response through miR-22/PTEN/TLR4/NF-jB pathway;QuantStudio 3 Real-Time PCR System (Applied Biosystems, New York, CA, USA) was used to analyze TapSAKI, miR-22 and PTEN expressions;These findings suggested TapSAKI promoted PTEN and TLR4/NF-jB pathway through miR-22 and proved TapSAKI could promote HK-2 cell apoptosis.	30666657	RID03451	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Kidney injury	MGAT3-AS1	TLR4	positively-E	RNA pull-down assay;RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-22)	regulation	RNA-protein	NA	CSC	NA	Other	Injury	lncRNA	PCG	ENSG00000227188	GRCh38_22:39475807-39476822	ENSG00000136869	NA	104502417	7099	TapSAKI	ARMD10|CD284|hToll|TLR-4	LncRNA TapSAKI promotes inflammation injury in HK -2 cells and urine derived sepsis-induced kidney injury;TapSAKI was elevated in urine derived sepsis-induced kidney injury, and promoted HK-2 cell apoptosis and inflammatory response through miR-22/PTEN/TLR4/NF-jB pathway;QuantStudio 3 Real-Time PCR System (Applied Biosystems, New York, CA, USA) was used to analyze TapSAKI, miR-22 and PTEN expressions;TapSAKI knockdown decreased PTEN, TLR4, and p-p65 expressions, and inhibited apoptosis protein cleaved-caspase-3 expression and HK-2 cell apoptosis	30666657	RID03452	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Kidney injury	MGAT3-AS1	NFKB1	positively-E	RNA pull-down assay;RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-22)	regulation	RNA-protein	NA	CSC	NA	Other	Injury	lncRNA	TF	ENSG00000227188	GRCh38_22:39475807-39476822	ENSG00000109320	NA	104502417	4790	TapSAKI	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	LncRNA TapSAKI promotes inflammation injury in HK -2 cells and urine derived sepsis-induced kidney injury;TapSAKI was elevated in urine derived sepsis-induced kidney injury, and promoted HK-2 cell apoptosis and inflammatory response through miR-22/PTEN/TLR4/NF-jB pathway;QuantStudio 3 Real-Time PCR System (Applied Biosystems, New York, CA, USA) was used to analyze TapSAKI, miR-22 and PTEN expressions;TapSAKI knockdown decreased PTEN, TLR4, and p-p65 expressions, and inhibited apoptosis protein cleaved-caspase-3 expression and HK-2 cell apoptosis	30666657	RID03453	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic retinopathy	MIAT	TGFB1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell viability(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000105329	NA	440823	7040	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Long Non-Coding RNA of Myocardial Infarction Associated Transcript (LncRNA-MIAT) Promotes Diabetic Retinopathy by Upregulating Transforming Growth Factor-beta1 (TGF-beta1) Signaling;MIAT lncRNA overexpression upregulated TGF-beta1 expression and promoted apoptosis of ARPE-19 cells-in vitro;The key findings of this study were that plasma levels of long non-coding RNA of myocardial infarction associated transcript (lncRNA-MIAT) were significantly increased in patients with diabetic retinopathy, and that in ARPE-19 human retinal pigment epithelial cells cultured in a high glues environment in vitro, increased expression of lncRNA-MIAT reduced cell viability by the activation of transforming growth factor-beta1 (TGF-beta1) signaling;To further investigate the potential interactions between MIAT lncRNA and TGF-beta1, the MIAT expression vector plasmid was transfected into ARPE-19 cells, and TGF-beta1 expression was measured by western blot. As shown in Figure 5A, significant differences were found in expression levels of TGF-beta1 between the groups. MIAT lncRNA overexpression led to significantly upregulated expression of TGF-beta1	30595603	RID03454	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetes mellitus	MALAT1	VEGFA	positively-E		downregulation	RT-qPCR	NA	NA	cell stemness(+)	ceRNA(miR-205-5p)	regulation	RNA-protein	NA	CSC	NA	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	VEGF|VEGF-A|VPF	Improved therapeutic effects on diabetic foot by human mesenchymal stem cells expressing MALAT1 as a sponge for microRNA-205-5p;our data suggest that MALAT1 functions as a sponge RNA for miR-205-5p to increase therapeutic effects of MSCs on DF;MALAT1 is a ceRNA for miR-205-5p, and is low expressed in human MSCs.Recently, genetically modified MSCs have been used in therapy and we have shown that depletion of micoRNA-205-5p (miR-205-5p) in human MSCs promotes VEGF-mediated therapeutic effects on DF.Here, we showed that a long non-coding RNA (lncRNA), MALAT1, is a competing endogenous RNA (ceRNA) for miR-205-5p, and is low expressed in human MSCs.Ectopic expression of MALAT1 in human MSCs significantly decreased miR-205-5p levels, resulting in upregulation of VEGF production and improved in vitro endothelial cell tube formation.	31866580	RID03455	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Myeloma	HOTAIR	NFKB1	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Effects of lncRNA HOTAIR on proliferation and apoptosis of myeloma cells through NF-kB pathway;The Reverse Transcription-Polymerase Chain Reaction (RT-PCR was performed to detect the expression of lncRNA HOTAIR in myeloma cells;LncRNA HOTAIR activates the expression of NF-kB in myeloma cells and promotes the proliferation of myeloma cellsThe protein expression of NF-kB was detected via western blot	31799674	RID03456	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	u50535	CCL20	positively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000115009	NA	NA	6364	NA	CKb4|exodus-1|LARC|MIP-3a|SCYA20|ST38	lncRNA-u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling;The results demonstrated that lncRNA-u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells;western blot and luciferase reporter gene assays demonstrated that lncRNA-u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA-u50535 decreased CCL20, CCR6 and p-ERK levels. The effects of lncRNA-u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced;Therefore, the present study hypothesized that lncRNA-u50535 might activate ERK signaling by upregulating CCL20 and CCR6, and this was confirmed by western blot analysis	31545478	RID03457	expression association	NA		UP(LIHC);DATA(GSE117623)
Lung cancer	u50535	ERK	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000133216	NA	NA	NA	NA	NA	lncRNA-u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling;The results demonstrated that lncRNA-u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells;western blot and luciferase reporter gene assays demonstrated that lncRNA-u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA-u50535 decreased CCL20, CCR6 and p-ERK levels. The effects of lncRNA-u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced;Therefore, the present study hypothesized that lncRNA-u50535 might activate ERK signaling by upregulating CCL20 and CCR6, and this was confirmed by western blot analysis	31545478	RID03458	expression association	NA		
Lung cancer	u50535	CCR6	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000112486	NA	NA	1235	NA	BN-1|CD196|CKR-L3|CMKBR6|DCR2|DRY-6|GPR-CY4|GPR29|STRL22	lncRNA-u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling;The results demonstrated that lncRNA-u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells;western blot and luciferase reporter gene assays demonstrated that lncRNA-u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA-u50535 decreased CCL20, CCR6 and p-ERK levels. The effects of lncRNA-u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced;Therefore, the present study hypothesized that lncRNA-u50535 might activate ERK signaling by upregulating CCL20 and CCR6, and this was confirmed by western blot analysis	31545478	RID03459	expression association	NA		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cholangiocarcinoma	RMRP	MIR217	negatively-E		upregulation	qRT-PCR;sequencing	NA	NA	cancer progression(+)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000207548	NA	6023	406999	CHH|NME1|RMRPR|RRP2	hsa-mir-217|miR-217|MIRN217	Long noncoding-RNA component of mitochondrial RNA processing endoribonuclease is involved in the progression of cholangiocarcinoma by regulating microRNA-217;Our findings indicated that RMRP can play a part in promoting cancer by regulating the expression of miR-217;qRT-PCRresults showed that compared with ENST00000601661.1 and ENST00000516869.1 (RPPH1), the difference of RMRP (NR_003051) expression in CCA and biliary epithelial cell lines was more significant;the results suggest that RMRP was highly expressed in CCA tissues and cell lines;qRT-PCRresults showed that the expression of miR 217 was negatively correlated with the expression of RMRP (Figure 6B), which was consistent with the above sequencing results	31111617	RID03460	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Atrial fibrillation	PVT1	SP1	positively-E	LncBase;luciferase reporter assay;qRT-PCR;RNAi	upregulation	qRT-PCR	NA	NA	TGF-beta1/SMAD signaling pathway(+);cell proliferation(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000185591	NA	5820	6667	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 regulates atrial fibrosis via miR-128-3p-SP1-TGF-beta1-Smad axis in atrial fibrillation;PVT1 acted as a sponge for miR-128-3p to facilitate Sp1 expression, thereby activating the TGF-beta1/Smad signaling pathway;qRT-PCRanalysis of PVT1 expression in human atrial muscle tissues;our bioinformatics analysis (DIANA TOOLS) revealed that PVT1 harbors putative binding sites of miR-128-3p (Fig. 3e), Moreover, RIP assays disclosed that PVT1 and miR-128-3p expressions were substantially enriched by Ago2 antibody compared with control IgG antibody (Fig. 3f ). Luciferase activity assay showed that miR-128-3p mimic led to a notable decrease in luciferase activity in PVT1-WT reporter compared with the mimic NC group, whereas had no obvious effect on luciferase activity in PVT1-MUT reporter (Fig. 3g). Together, these results verified PVT1 interacted directly with miR-128-3p; In addition, PVT1 overexpression significantly inhibited miR-128-3p expression (Fig. 3h), whereas induced Sp1 expression at both mRNA (Fig. 3i) and protein (Fig. 3j) levels. In contrast, PVT1 knockdown exerted the opposite;The predicted binding sites between PVT1 and miR-128-3p (DIANA TOOLS-LncBase v.2);PVT1 facilitates the Ang-II-induced fibroblasts proliferation, collagen production, and TGF-beta1/Smad signaling activation via miR-128-3p/Sp1 axis	30894138	RID03461	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	TP73-AS1	ALDH1A1	positively-E	CRISPRi	upregulation	qRT-PCR	TCGA;GTEx	NA	prognosis(-);chemosensitivity(-)	NA	association	RNA-protein	Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000165092	NA	57212	216	KIAA0495|PDAM	ALDH1|PUMB1|RALDH1	The lncRNA TP73-AS1 is linked to aggressiveness in glioblastoma and promotes temozolomide resistance in glioblastoma cancer stem cells;Using CRISPRi to downregulate our candidate lncRNA in gCSC, we demonstrate that TP73-AS1 promotes TMZ resistance in gCSC and is linked to regulation of the expression of metabolism- related genes and ALDH1A1, a protein known to be expressed in cancer stem cell markers and protects gCSC from TMZ treatment. Taken together, our results reveal that high TP73-AS1 predicts poor prognosis in primary GBM cohorts and that this lncRNA promotes tumor aggressiveness and TMZ resistance in gCSC;To assess whether TP73-AS1 is clinically relevant in GBM, we used GEPIA (http://gepia.cancer-pku.cn/index.html) where GBM expression data, obtained from the TCGA, are compared with normal brain tissue data, obtained from GTEx, in a standardized manner;TP73- AS1 expression is significantly higher in primary GBM vs. normal brain tissue; We found that DEAB increased the sensitivity of G7 cells to TMZ, confirming the protective functions of ALDH1 in gCSC and providing support to the model where TP73-AS1 enhances the resistance of gCSC to TMZ by promoting the expression of ALDH1A1	30867410	RID03462	expression association	prognosis,chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE67939,GSE75367,GSE86978)
Colon cancer	DLEU1	KPNA3	positively-E	RNAi	upregulation	qPCR	TCGA	NA	tumorigenesis(+);prognosis(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000102753	NA	10301	3839	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	hSRP1|IPOA4|SRP1gamma|SRP4	Upregulation of DLEU1 expression by epigenetic modification promotes tumorigenesis in human cancer;DLEU1 promotes SRP4 expression via increasing H3K27ac enrichment to SRP4 locus epigenetically; Finally, high expression of DLEU1 correlates with worse prognosis not only in specific cancer type patients but also in patients in the pan cancer cohort;DLEU1 was selected to validate the novel finding and result showed that it promoted tumorigenesis in vitro and in vivo;The genome-wide DLEU1 profiles in breast cancer, colon cancer, and pan-cancer were downloaded from TCGA;DLEU1 expression is upregulated in human cancer;Expression of DLEU1 is upregulated in breast cancer tissues (N = 250) than that in adjacent normal tissues (N = 250) via quantitative polymerase chain reaction assays. (b) Expression of DLEU1 is upregulated in colon cancer tissues (N = 50) than that in adjacent normal tissues (N = 50) via qPCR assays;As a nearby gene, SRP4 was decreased in its messenger RNA and protein level when knockdown of DLEU1 expression (Figure 4d,g). Moreover, H3K27ac modification was observed in SRP4 locus via analyzing ENCODE data (Figure 4e). Thus, we reasoned whether DLEU1 could promote SRP4 expression via increasing H3K27ac enrichment epigenetically in cis. As expected, knockdown of DLEU1 expression suppressed H3K27ac enrichment in SRP4 locus mechanistically	30793303	RID03463	epigenetic regulation	prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	DLEU1	KPNA3	positively-E	RNAi	upregulation	qPCR	TCGA	NA	tumorigenesis(+);prognosis(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000102753	NA	10301	3839	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	hSRP1|IPOA4|SRP1gamma|SRP4	Upregulation of DLEU1 expression by epigenetic modification promotes tumorigenesis in human cancer;DLEU1 promotes SRP4 expression via increasing H3K27ac enrichment to SRP4 locus epigenetically; Finally, high expression of DLEU1 correlates with worse prognosis not only in specific cancer type patients but also in patients in the pan cancer cohort;DLEU1 was selected to validate the novel finding and result showed that it promoted tumorigenesis in vitro and in vivo;The genome-wide DLEU1 profiles in breast cancer, colon cancer, and pan-cancer were downloaded from TCGA;DLEU1 expression is upregulated in human cancer;Expression of DLEU1 is upregulated in breast cancer tissues (N = 250) than that in adjacent normal tissues (N = 250) via quantitative polymerase chain reaction assays. (b) Expression of DLEU1 is upregulated in colon cancer tissues (N = 50) than that in adjacent normal tissues (N = 50) via qPCR assays;As a nearby gene, SRP4 was decreased in its messenger RNA and protein level when knockdown of DLEU1 expression (Figure 4d,g). Moreover, H3K27ac modification was observed in SRP4 locus via analyzing ENCODE data (Figure 4e). Thus, we reasoned whether DLEU1 could promote SRP4 expression via increasing H3K27ac enrichment epigenetically in cis. As expected, knockdown of DLEU1 expression suppressed H3K27ac enrichment in SRP4 locus mechanistically	30793303	RID03464	epigenetic regulation	prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Urinary bladder cancer	LINC01638	ROCK2	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);cancer recurrence(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000233521	GRCh38_22:27221349-27225134	ENSG00000134318	NA	105372978	9475	NA	NA	LINC01638 lncRNA mediates the postoperative distant recurrence of bladder cancer by upregulating ROCK2;In the present study, expression of LINC01638 and ROCK2 was analyzed using quantitative PCR, ELISA and western blot;Overexpression of LINC01638 and ROCK2 mediated the promoted migration and invasion of bladder cancer cells, and ROCK2 small interfering RNA silencing attenuated the enhancing effects of LINC01638 on cancer cell migration and invasion. Therefore, LINC01638 may mediate the postoperative distant recurrence of bladder cancer by upregulating ROCK2;RT-qPCR was performed to detect the plasma LINC01638 and ROCK2 mRNA in patients with bladder cancer and healthy controls;Plasma LINC01638 and ROCK2 mRNA is upregulated in patients with bladder cancer;Overexpression of LINC01638 and ROCK2 and reverse transcription-quantitative PCR experiments were performed to investigate the interaction between LINC01638 and ROCK2 in bladder cancer;overexpression of LINC01638 led to ROCK2 upregulation in the bladder cancer cell lines HT-1197 and HT-1376 at the mRNA (P<0.05; Fig. 5A) and protein levels (P<0.05; Fig. 5B).	31620199	RID03465	expression association	recurrence	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Head and neck squamous cell carcinoma	COMMD6	TEX41	positively-E	DIANA-microT;miRanda;miRWalk;Targetscan	upregulation	RT-PCR	TCGA	NA	cancer progression(+)	ceRNA(miR-340)	regulation	protein-RNA	NA	NA	NA	Cancer	Head and neck cancer	PCG	lncRNA	ENSG00000188243	NA	ENSG00000226674	GRCh38_2:144666312-145262988	170622	401014	Acrg	DKFZp686O1327|LINC00953	Prognosis and modulation mechanisms of COMMD6 in human tumours based on expression profiling and comprehensive bioinformatics analysis;the TEX41-miR-340-COMMD6 network was further verified based on the differential expression profiles in HNSC;To validate the prediction results, the expression levels of COMMD6 and the differentially predicted miRNAs and lncRNAs in the network were compared between normal and tumour samples in human HNSC obtained from TCGA database. A significantly higher level of COMMD6 was found in tumours compared to normal tissues (Fig. 4c), indicating a tumour promoting role of COMMD6 in HNSC;Indeed, we found the complementary sequences between the 3 untranslational region of COMMD6 and hsa-miR-340 (Fig. 4f). Moreover, complementary sequences were detected between lncRNA TEX41 and hsa-miR-340 (Fig. 4g). Based on the differential expression and complementary results, lncRNA TEX41 might promote COMMD6 expression by inhibiting the expression of has-miR-340 in HNSC (Fig. 4h)	31523056	RID03466	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE51827)
Rheumatoid arthritis	CYTOR	FOXM1	positively-F	RNAi;ChIP;luciferase reporter assay	upregulation	microarray;qRT-PCR	UCSC	NA	cell proliferation(+);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000111206	NA	112597	2305	C2orf59|LINC00152|MGC4677|NCRNA00152	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	FOXM1/LINC00152 feedback loop regulates proliferation and apoptosis in rheumatoid arthritis fibroblast-like synoviocytes via Wnt/beta-catenin signaling pathway;lncRNA microarray analysis was applied to screen out lncRNAs differentially expressed in RA FLS;we found that forkhead box M1 (FOXM1) transcriptionally activated LINC00152 in RA FLS; Gain- or loss-of function assays were further carried out in RA FLS, and the results revealed that LINC00152 promoted proliferation but induced apoptosis in RA FLS. Furthermore, up-regulation of LINC00152 may induce promotion of Wnt/beta-catenin signaling pathway in RA FLS;FOXM1 is predicted as the transcription regulator for LINC00152 in accordance with the ChIP-seq result of UCSC (http://genome.ucsc.edu/). Binding sequence between miR-194-5p and LINC00152 was predicted from DIANA (http://carolina.imis.athena-innovation.gr/diana_tools/web/index.php-r=lncbasev2%2Findex-predicted). Putative binding sites of miR-194-5p in 3 UTR of FOXM1 were obtained from starbase;As presented in Figure 1A, top 50 up-regulated lncRNAs were selected out due to their highest fold change (>5.0). Among which, LINC00152 presented the highest fold change. Up-regulation of LINC00152 in RA FLS was also proved by qRT-PCR(Figure 1B);As expected, silencing of FOXM1 led to the down-regulation of LINC00152, whereas overexpression of FOXM1 induced up-regulation of LINC00152 (Figure 3C). Furthermore, ChIP assay determined the affinity of FOXM1 to LINC00152 promoter in RA FLS (Figure 3D). The effect of FOXM1 on the luciferase activity of LINC00152 promoter was detected. Unsurprisingly, FOXM1 could enhance the luciferase activity of LINC00152 promoter (Figure 3E)	31854447	RID03467	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hypoxia-induced acute myocardial infarction	RMRP	TP53	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-214-5p)	regulation	NA	NA	NA	NA	Other	Acute myocardial infarction	lncRNA	TF	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000141510	NA	6023	7157	CHH|NME1|RMRPR|RRP2	LFS1|p53	LncRNA RMRP accelerates hypoxia-induced injury by targeting miR-214-5p in H9c2 cells; Hypoxia treatment significantly induced cell damage in H9c2 cells, accompanied with the upregulation of RMRP expressions;RMRP served as an endogenous sponge for miR-214-5p, and its expression was negatively regulated by RMRP. The effects of RMRP knockdown on hypoxia-induced injury were further enhanced with miR-214-5p overexpression, but significantly abrogated with miR-214-5p silence. Moreover, p53 was verified as a direct target of miR-214-5p, and functional investigation revealed that RMRP regulated hypoxia-induced injury via modulating p53 signaling pathway, which was partially mediated by miR-214-5p;qRT-PCRresults showed that compared to normonic treated group, the expression levels of RMRP in H9c2 cells was significantly;Accordingly, luciferase reporter vector containing wild-type (WT) RMRP or mutant (MT) RMRP was generated. The results showed that the luciferase activities in H9c2 cells were remarkably inhibited in miR-214-5p mimics and WT-RMRP co-transfected group when compared to NC group (P < 0.05, Fig. 3B). However, no significant change was observed in MT-RMRP transfected group. Furthermore, qRT-PCRassay displayed that the expression level of miR-214-5p was significantly reduced by hypoxia treatment in H9c2 cells compared with control group (P < 0.05, Fig. 3C), but was significantly up-regulated after hypoxia treatment in a timedependent manner;upregulated with knockdown of RMRP (P < 0.05). However, overexpression of RMRP showed an inhibitory effect on miR-214-5p expression in hypoxia-treated H9c2 cells (P < 0.05);	31839421	RID03468	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Osteoarthritis	CDKN2B-AS1	DUSP4	positively-E	luciferase reporter assay ;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(miR-122-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000120875	NA	100048912	1846	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	HVH2|MKP-2|TYP	LncRNA ANRIL impacts the progress of osteoarthritis via regulating proliferation and apoptosis of osteoarthritis synoviocytes;qRT-PCRwas used to detect the expression of lncRNA ANRIL in normal synoviocytes and osteoarthritis synoviocytes;western blot was used to analyze the possible mechanism that ANRIL regulated the cells' proliferation in osteoarthritis;We indicated that the expression of ANRIL was significantly improved in OAS compared to NS;ANRIL could regulate the proliferation and apoptosis of OAS via miR-122-5p/DUSP4 axis	31799639	RID03469	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Esophagus squamous cell carcinoma	HERES	EZH2	positively-F	RIP;ChIP	upregulation		ENCODE	NA	WNT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000106462	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	HERES, a lncRNA that regulates canonical and noncanonical Wnt signaling pathways via interaction with EZH2;To address this question, binding sites for possible epigenetic modulators that can drive the histone methylation of target genes were first examined using publicly available ChIPseq datasets from the ENCODE project;RNA immunoprecipitation (RIP) (Fig. 6B) and EZH2 IP (Fig. 6C) assays showed the interaction of HERES and CACNA2D3 with EZH2	31732666	RID03470	interact with protein	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Myocardial infarction	MEG3	TP53	positively-F	Immunofluorescence assay;luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	LFS1|p53	Long non-coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress-mediated apoptosis by targeting p53 following myocardial infarction;we firstly observed that the expression levels of the lncRNA MEG3 in infarct hearts and hypoxic neonatal mice ventricular myocytes (NMVMs) were up regulated by quantitative real time PCR (qRT-PCR;We therefore explored the association of lncRNA MEG3 with p53 in infarct hearts and hypoxic NMVMs by immunochemical, immunofluorescence and western blot assays;RNA binding protein immunoprecipitation (RIP) assay demonstrated that lncRNA MEG3 could directly bind to p53 in primary NMVMs; In accord with a previous study,28 we found that inhibition of p53 reduced lncRNA MEG3 levels in hypoxic NMVMs;-lncRNA MEG3 knockdown targeted and inhibited p53 protein	31631486	RID03471	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Polycystic ovary syndrome	MALAT1	TGFBR1	positively-E	miRcode;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	TGFbeta signaling pathway(+)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106799	NA	378938	7046	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	MALAT1 is involved in the pathophysiological process of PCOS by modulating TGFbeta signaling in granulosa cells;MALAT1 was confirmed to function as a competing endogenous RNA (ceRNA), interacting with miR-125b and miR-203a. Meanwhile, miR-125b and miR-203a was identified as two novel TGFbeta signaling negative regulators by targeting TGFBR1 and TGFBR2. Finally, MALAT1 knockdown was found to induce the upregulation of miR-125b and miR-203a, which further repressed TGFbeta signaling, changed some downstream gene expression, and resulted in a disordered cell cycle;The level of MALAT1 was determined by qRT-PCRo determine the mechanism by which MALAT1 regulates TGFbeta signaling, the miRNAs that directly interact with MALAT1 were predicted using bioinformatics tool miRcode (http://www.mircode.org/index.php). The direct interactions were confirmed by dual-luciferase assay using MALAT1 reporter vector in KGN cells. As shown in Fig. 3A, the luciferase activity was significantly repressed by miR-15, miR-23a, miR125b, miR-146b, and miR-203a, indicating the direct interactions with MALAT1;we predicted the direct targets of miR-125b and miR-203a using the bioinformatics tool TargetScan (http://www. targetscan.org/vert_70/). TGFBR1 is a predicted target of miR-125b; meanwhile, TGFBR2 is a predicted target of miR-203a;The results of dual luciferase assay and immunoblotting indicated that TGFBR2 is a direct target of miR-203a;the biological functions of siMALAT1 on cell viability and apoptosis were totally rescued by miR-125b and miR203a, indicating that siMALAT1 inhibits TGFbeta signaling through upregulating miR-125b and miR-203a;we observed MALAT1 reduction in GCs from patients with PCOS, and the downregulation of MALAT1 relates to upregulated proliferation and downregulated apoptosis of GCs	31557499	RID03472	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Polycystic ovary syndrome	MALAT1	TGFBR2	positively-E	miRcode;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	TGFbeta signaling pathway(+)	ceRNA(miR-203a)	regulation	RNA-protein	NA	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163513	NA	378938	7048	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MFS2|TBR-ii|TBRII	MALAT1 is involved in the pathophysiological process of PCOS by modulating TGFbeta signaling in granulosa cells;MALAT1 was confirmed to function as a competing endogenous RNA (ceRNA), interacting with miR-125b and miR-203a. Meanwhile, miR-125b and miR-203a was identified as two novel TGFbeta signaling negative regulators by targeting TGFBR1 and TGFBR2. Finally, MALAT1 knockdown was found to induce the upregulation of miR-125b and miR-203a, which further repressed TGFbeta signaling, changed some downstream gene expression, and resulted in a disordered cell cycle;The level of MALAT1 was determined by qRT-PCRo determine the mechanism by which MALAT1 regulates TGFbeta signaling, the miRNAs that directly interact with MALAT1 were predicted using bioinformatics tool miRcode (http://www.mircode.org/index.php). The direct interactions were confirmed by dual-luciferase assay using MALAT1 reporter vector in KGN cells. As shown in Fig. 3A, the luciferase activity was significantly repressed by miR-15, miR-23a, miR125b, miR-146b, and miR-203a, indicating the direct interactions with MALAT1;we predicted the direct targets of miR-125b and miR-203a using the bioinformatics tool TargetScan (http://www. targetscan.org/vert_70/). TGFBR1 is a predicted target of miR-125b; meanwhile, TGFBR2 is a predicted target of miR-203a;The results of dual luciferase assay and immunoblotting indicated that TGFBR2 is a direct target of miR-203a;the biological functions of siMALAT1 on cell viability and apoptosis were totally rescued by miR-125b and miR203a, indicating that siMALAT1 inhibits TGFbeta signaling through upregulating miR-125b and miR-203a	31557499	RID03473	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	FENDRR	CSNK1E	NA			microarray	GSE55945	NA	cell invasion(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000213923	NA	400550	1454	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	CKIE|CKIepsilon|HCKIE	FENDRR reduces tumor invasiveness in prostate cancer PC-3 cells by targeting CSNK1E;Prostate cancer samples were collected from the NCBI Gene Expression Omnibus (GEO) database including 13 gene expression profiles of prostate cancer samples and 8 normal samples, numbered GSE55945;	31539119	RID03474	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Malignant glioma	H19	miR-675	negatively-E	western blot	downregulation	RT-PCR	NA	NA	cancer progression(+)	NA	association	RNA-RNA	Cucurmin	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	A negative feedback loop of H19/miR-675/VDR mediates therapeutic effect of cucurmin in the treatment of glioma;The interaction between H19 and VDR was explored by the utilization of real time PCR and western blot as a target of miR 675 and a regulator of H19 transcription, VDR negatively regulated the expression of H19, which is a key regulator of biological activities in glioma cells. Therefore, H19, miR 675, and VDR formed a regulatory feedback loop, which could be involved in the development of glioma;We also found that miR 675 is located within the chromosome segment of H19, while the increase in H19 expression could inhibit the expression of miR 675	31468534	RID03475	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Malignant glioma	VDR	H19	negatively-E	western blot	downregulation	RT-PCR	NA	NA	cancer progression(+)	NA	association	NA	Cucurmin	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000111424	NA	ENSG00000130600	GRCh38_11:1995171-2001470	7421	283120	NR1I1|PPP1R163	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	A negative feedback loop of H19/miR-675/VDR mediates therapeutic effect of cucurmin in the treatment of glioma;The interaction between H20 and VDR was explored by the utilization of real time PCR and western blotsuggesting that H19 expression was negatively correlated with VDR expression;as a target of miR 675 and a regulator of H19 transcription, VDR negatively regulated the expression of H19, which is a key regulator of biological activities in glioma cells. Therefore, H19, miR 675, and VDR formed a regulatory feedback loop, which could be involved in the development of glioma	31468534	RID03476	expression association	NA	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE75367)	UP(NSCLC);DATA(GSE74639)
Cardiac hypertrophy	CHAR	PTEN	positively-E	RNAi	downregulation	qPCR	NA	NA	cardiac hypertrophy(+)	ceRNA(miR-20b)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	NA	NA	ENSG00000171862	NA	NA	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA cardiac hypertrophy-associated regulator governs cardiac hypertrophy via regulating miR-20b and the downstream PTEN/AKT pathway;CHAR was found markedly down regulated in both in vivo mouse model of cardiac hypertrophy induced by pressure overload and in vitro cellular model of cardiomyocyte hypertrophy induced by angiotensin II (AngII) insult;CHAR was found to act as a competitive endogenous RNA (ceRNA) to down regulate miR 20b that we established as a pro hypertrophic miRNA;We found that miR 20b induced CH by directly repressing PTEN expression and indirectly increas ing AKT activity. Moreover, CHAR overexpression mitigated the repression of PTEN and activation of AKT by miR 20b, and as such, it abrogated the deleterious effects of miR 20b on CH;Overexpression of CHAR reduced the hypertrophic responses;we first con ducted quantitative PCR on four lncRNAs (AK134605, AK028678, AK141772 and AK087652) that had been found to be down regu lated in our previous microarray analysis;we named AK134605 cardiac hypertrophy associated regulator (CHAR) in the rest of our manuscript	31465630	RID03477	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Cardiac hypertrophy	CHAR	AKT1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cardiac hypertrophy(+)	ceRNA(miR-20b)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	NA	NA	ENSG00000142208	NA	NA	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA cardiac hypertrophy-associated regulator governs cardiac hypertrophy via regulating miR-20b and the downstream PTEN/AKT pathway;CHAR was found markedly down regulated in both in vivo mouse model of cardiac hypertrophy induced by pressure overload and in vitro cellular model of cardiomyocyte hypertrophy induced by angiotensin II (AngII) insult;CHAR was found to act as a competitive endogenous RNA (ceRNA) to down regulate miR 20b that we established as a pro hypertrophic miRNA;We found that miR 20b induced CH by directly repressing PTEN expression and indirectly increas ing AKT activity. Moreover, CHAR overexpression mitigated the repression of PTEN and activation of AKT by miR 20b, and as such, it abrogated the deleterious effects of miR 20b on CH;Overexpression of CHAR reduced the hypertrophic responses;we first con ducted quantitative PCR on four lncRNAs (AK134605, AK028678, AK141772 and AK087652) that had been found to be down regu lated in our previous microarray analysis;we named AK134605 cardiac hypertrophy associated regulator (CHAR) in the rest of our manuscript	31465630	RID03478	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Intervertebral disc degeneration	HOTAIR	NOTCH1	positively-E	TargetScan;miR-base;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148400	NA	100124700	4851	HOXC-AS4|HOXC11-AS1|NCRNA00072	TAN1	Intervertebral disc degeneration (IDD) is a major cause of lower back pain, but the specific molecular mechanisms governing its development are poorly characterized.We therefore used real-time qPCR to measure HOTAIR and microRNA(miR)-34a-5p in degenerative NP cells, and then validated their functional relevance via overexpressing them in these NP cells.We further verified the targets of these RNA constructs in 293 T cells through the use of a dual-luciferase reporter assay.Our results indicated that IDD was linked with decreased HOTAIR expression relative to regular NP cells, and overexpressing this lncRNA was linked to reduced apoptotic NP cell death, whereas overexpressing miR-34a-5p had the opposite effect.We found that HOTAIR served as a miR-34a-5p sponge, sequestering this miRNA and thereby down regulating genes linked to apoptosis through the Notch signaling pathway.Together these results reveal that a HOTAIR/miR-34a-5p/Notch1 signaling pathway may regulate the development of IDD, potentially making HOTAIR a viable target for treatment of this disease.	31376409	RID03479	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hypercholesterolemia	BM450697	LDLR	negatively-E	ChIP;DRIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	regulation	RNA-protein	NA	NA	NA	Genetic disease	Familial hypercholesterolemia	lncRNA	PCG	NA	NA	ENSG00000130164	NA	NA	3949	NA	LDLCQ2	Control of LDL Uptake in Human Cells by Targeting the LDLR Regulatory Long Non-coding RNA BM450697;BM450697 Modulates LDLR mRNA Levels through Transcriptional Interference;We therefore performed chromatin immunoprecipitation (ChIP) assays with SREBP1a and Pol II (using the antibody toward the catalytically active phosphorylated serine 5 Pol II). We observed that when exogenous BM450697 RNA was transfected into Hep 3B cells, Pol II association at the LDLR promoter was significantly less compared with the control (scrambled, or a control lambda RNA; Figure 2B). Similarly, it appeared as if SREBP1a enrichment at the SREBP1 binding site was less than the control. However, this observation was not significant. Taken together, these data suggest that BM450697 decreases LDLR mRNA levels mechanistically by blocking interactions with Pol II and possibly SREBP1a at the promoter of LDLR;suggest that BM450697 is a transcriptional regulator of LDLR and can therefore serve as a convenient and potentially highly specific target to control LDLR expression via directed small RNAs;our ChIRP results suggest that lncRNA BM45069 is associated directly with the 30 end of the LDLR promoter, and our DRIP assay confirmed the presence of an DNA:RNA hybrid	31279228	RID03480	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE109761,GSE111065)
Ischemic stroke	CHRF	SOX6	positively-E	lnCeDB;luciferase reporter assay	upregulation		NA	NA	cell injury(+);apoptosis process(-)	ceRNA(miR-126)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	NA	NA	ENSG00000110693	NA	NA	55553	NA	HSSOX6|SOXD|TOLCAS	Long non-coding RNA CHRF modulates the progression of cerebral ischemia/reperfusion injury via miR-126/SOX6 signaling pathway;CHRF played as a competing endogenous RNA (ceRNA) and competed with Sex-determining region Y box 6 (SOX6) to direct binding with miR-126, subsequently regulating ischemic neuronal death;As shown in Figs. 1A and 3 putative-binding sites between CHRF and miR-126 were detected according to sequence assays and an open online database lnCeDB, indicating its ceRNA potential for miR-126. With the up-regulation of miR-126 doses, the reduction in luciferase reporter activities of the CHRF-MUT1 and CHRF-MUT2 was observed;CHRF competes with SOX6 for binding with miR-126 tomodulate ischemic neuronal injury;Suppression of CHRF alleviates cerebral I/R injury in vivo;In our study, we found that CHRF expression was markedly elevated in ischemic core of mice after MCAO operation at different time points;CHRF knockdown could alleviate the ischemic neuronal death by improving miR-126 expression and reducing SOX6	31060778	RID03481	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Osteosarcoma	NEAT1	HOXA13	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106031	NA	283131	3209	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	HOX1|HOX1J	Long noncoding RNA NEAT1 regulates the development of osteosarcoma through sponging miR-34a-5p to mediate HOXA13 expression as a competitive endogenous RNA; LncRNA NEAT1 expression remains high in osteosarcoma tissues;In this study, NEAT1 expression in osteosarcoma cells was detected by qRT-PCRe identified the potential target of NEAT1 through bioinformatics and dual-luciferase reporter gene assay. Furthermore, their interaction and functions in regulating the development of osteosarcoma were clarified by western blot and RIP assay;Overexpression of NEAT1 markedly accelerated proliferative and reduced apoptosis potentials of osteosarcoma cells	31044561	RID03482	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Alzheimer's disease	BACE1-AS	BACE1	positively-E	Miranda;luciferase reporter assay;qPCR	upregulation		GSE46131;GSE46579;GSE48552	NA	amyloid plaque formation(+)	ceRNA(miR-29,miR-107,miR-124,miR-761)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000278768	GRCh38_11:117288453-117293578	ENSG00000186318	NA	100379571	23621	BACE1-AS1|BACE1AS|FJ573250|NCRNA00177	BACE	BACE1-AS prevents BACE1 mRNA degradation through the sequestration of BACE1-targeting miRNAs;The overexpression of BACE1-AS results in the repression of miRNAs that target BACE1, thus preventing BACE1 mRNA from being degraded; our results also showed a novel mechanism by which BACE1-AS functions as a ceRNA to sequester the miRNAs it shares with BACE1, such as mir-29, mir-107, mir-124, mir-485 and mir-761, to increase BACE1 expression;These observations together establish that BACE1-AS regulates BACE1 expression and increases Abeta production in APP transgenic mice;For example, if the level of BACE1-AS increases, miRNAs targeting both BACE1 and BACE1-AS would be consumed, resulting in the derepression of BACE1 and subsequent overproduction of the beta-amyloid peptide;The expression levels of related microRNAs in the brains of AD patients compared with those of normal controls based on publicly available RNA-seq (GSE46131,GSE46579 and GSE48552) databases;Elevated BACE1-AS expression has been observed in the brains of Fig. 2. BACE1-AS shares regulatory miRNAs with BACE1. (A) The comparison of mir-29, mir-107, mir-124, mir-485 target sites in the full-length BACE1-AS sequence, as predicted using the bioinformatics tool Miranda. These miRNAs were previously reported to target BACE1;Target validation using luciferase reporters in HEK293 T cells. The relative luciferase activity of luciferase reporters containing wild-type BACE1-AS	30959172	RID03483	ceRNA or sponge	NA	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE51827)
Intracranial aneurysm	GASAL1	TGFB1	negatively-E	western blot	downregulation	microarray	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Intracranial aneurysm	lncRNA	PCG	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000105329	NA	401472	7040	GASL1	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Expression of a Novel Long Noncoding RNA (lncRNA), GASL1, is Downregulated in Patients with Intracranial Aneurysms and Regulates the Proliferation of Vascular Smooth Muscle Cells In Vitro;Preliminary microarray data in our laboratory indicated that the novel long noncoding RNA (lncRNA), GASL1, was downregulated in patients with intracranial aneurysms;Expression of the novel lncRNA, GASL1, was downregulated in patients with intracranial aneurysms and regulated the proliferation of VSMCs in vitro by targeting TGF-beta1;In human VSMCs, lncRNA GASL1 overexpression increased cell proliferation and downregulated TGF-beta1 expression, while treatment with TGF-beta1 reduced VSMC proliferation but showed no effects on GASL1 expression;Correlation analysis indicated a potential interaction between lncRNA GASL1 and TGF-beta1. To further investigate this interaction, lncRNA GASL1 overexpression in human vascular smooth muscle cells (VSMCs) were constructed and the effects on TGF-beta1 were explored by western blot;lncRNA GASL1 as an upstream negative regulator of TGF-beta1;Lasergene 6.0 software (DNASTAR Inc., Madison, WI, USA) was used to explore the potential binding site between PCED1B-AS1 and miR-155	30742604	RID03484	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Tuberculosis	PCED1B-AS1	miR-155	negatively-F	qPCR;Lasergene;luciferase reporter assay	downregulation	microarray	NA	NA	apoptosis process(-);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Other	Tuberculosis	lncRNA	miRNA	ENSG00000247774	GRCh38_12:47205896-47216460	NA	NA	100233209	NA	NA	NA	Long non-coding PCED1B-AS1 regulates macrophage apoptosis and autophagy by sponging miR-155 in active tuberculosis; It was found that PCED1B-AS1 expression was down-regulated in patients with active tuberculosis, accompanied by significant attenuated monocyte apoptosis and enhanced autophagy;microarray analysis of lncRNA expression profiles in human macrophages indicate that PCED1BAS1 levels were reduced by 19.25- and 16.67-fold in the H73Rainfected group and H73Rv-infected group, respectively [17]. Our data demonstrated a significant reduction in PCED1B-AS1 expression in monocytes from patients with active TB compared with that in monocytes from healthy controls;It is reported that lncRNAs serve as molecular sinks to modulate miRNA levels by direct binding [20,21]. qPCR was performed to verify the expression of miR-155 in monocytes from patients with active TB; Luciferase reporter assays indicated that miR-155 mimics significantly reduced the luciferase activity of wild-type recombinant plasmid but not mutant recombinant plasmid in macrophages	30621915	RID03485	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Poststroke depression	lncRNA SRA	PPARG	positively-E	western blot;RNAi;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	regulation	protein-RNA	NA	NA	NA	Disease of mental health	Mental depression	lncRNA	PCG	NA	NA	ENSG00000132170	NA	NA	5468	NA	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARG5|PPARgamma	Steroid receptor RNA activator affects the development of poststroke depression by regulating the peroxisome proliferator-activated receptor -Gamma signaling pathway;Reverse transcription-quantitative PCR (RT-PCR, western blot and luciferase dual reporter assay analyses were performed to detect the expression of peroxisome proliferatoractivated receptor -Gamma (PPAR-Gamma) expression following SRA small interfering RNA (siRNA) treatment;SRA upregulated PPAR-Gamma mRNA and protein expression, whereas SRA siRNA significantly downregulated its expression;SRA was more highly expressed in rats with PSD than rats without PSD;As demonstrated in Fig. 4, the luciferase activity of SRA was significantly increased in SRA overexpressed cells compared with the cells transfected with an empty vector [t(df=2)=13.9, P<0.01] (Fig. 4a);RT-qPCR and western blot were performed to examine the interaction between SRA and PPAR-Gamma;In conclusion, this is the first report to indicate that lncRNA SRA directly regulates the transcriptional activation of PPAR-Gamma and affects PSD through the coactivation of PPAR, which may affect the expression of inflammatory genes and the associated signal transduction	31714481	RID03486	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Pulmonary hypertension	TUG1	MIR328	negatively-F	luciferase reporter assay;microscale thermophoresis	upregulation	RT-PCR;Immunofluorescence assay	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000207948	NA	55000	442901	LINC00080|NCRNA00080|TI-227H	MIRN328|hsa-mir-328|mir-328	TUG1 Regulates Pulmonary Arterial Smooth Muscle Cell Proliferation in Pulmonary Arterial Hypertension;TUG1 expression and localization was detected by real-time polymerase chain reaction (PCR) and fluorescence in situ hybridization;All these functions of TUG1 were likely to be associated with miR-328;: TUG1 was upregulated in the pulmonary arteries of mice after a hypoxic assault and showed a significant increase in patients with PAH;To confirm this prediction, we constructed luciferase reporter assays, which contain miR-328-3p binding sites (5493-5512 nt). We found that miR-328-3p decreased luciferase levels, whereas a treatment with miR-328-3p inhibitor, AMO-328-3p, reversed this effect;microscale thermophoresis results further validated the binding of TUG1with miR-328-3p;these results imply that TUG1 inhibits miR-328 through a competitive endogenous RNA function in HPASMCs;MiR-328-3p reverses the effect of TUG1 on cell proliferation;TUG1 regulates PASMC proliferation and apoptosis, leading to pulmonary vascular remodelling	31679623	RID03487	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Aortic valve disease	MALAT1	ELAVL1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation		NA	NA	cell differentiation(+)	ceRNA(miR-191-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Hua|HUR|MelG	Novel mechanisms for osteogenic differentiation of human aortic valve interstitial cells;HuR is negatively regulated by miR-191-3p, and MALAT1, through sponging miR-191-3p, positively regulates HuR levels. Altogether, these results show the existence of a specific circuitry between MALAT1 and HuR to establish correct progression of in vitro osteogenic differentiation of VICs;Luciferase reporter assays validated human antigen R as the direct target of miR-191-3p;The results revealed a significant amount of miR-191-3p in the MALAT1 pulled-down pellet compared with the negative control group (Figure 5, C). We further performed an RIP assay and found that higher MALAT1 and miR-191-3p RNA levels were detected in Ago2 immunoprecipitates compared with the control immunoglobulin G group (Figure 5, D), suggesting that MALAT1 and miR-191-3p were in the same RNA-induced silencing complex. Together, these results support the bioinformatics predictions and indicate that MALAT1 can directly sponge miR-191-3p	31301902	RID03488	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Ulcerative colitis	CDKN2B-AS1	Claudin-2	positively-E	western blot;immunohistochemistry	downregulation	microarray	NA	NA	intestinal epithelial barrier(-)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Linear and circular CDKN2B-AS1 expression is associated with Inflammatory Bowel Disease and participates in intestinal barrier formation;Cells with down-regulated CDKN2B-AS1 exhibited increased proliferation and no alterations in apoptosis. Targeting both the linear and circular transcripts of CDKN2B-AS1 with short hairpin RNAs enhanced barrier function;We subsequently determined that Claudin-2, a leaky Claudin known to decrease barrier function, was decreased in CDKN2B-AS1 knockdown cells;To better understand the role for long non-coding RNAs in the pathogenesis of IBD we performed a lncRNA microarray of colonic biopsies from healthy controls and actively inflamed IBD patients. One of the most significantly decreased genes on the array was CDKN2B-AS1 with a 12.2-fold downregulation and p = 0.00087;Lastly, we measured Claudin-2 protein levels by western blot in control and CDKN2B-AS1 downregulated cells and observed an almost entire loss in Claudin-2 in CDKN2B-AS1 downregulated cells as compared to controls (Fig. 7b). We did not observe any differences in the tight Claudin, Claudin-4, in cells with downregulated CDKN2B-AS1 (Fig. 7b). As an alternative method to determine the relative levels of Claudin-2 immunohistochemistry was performed on cells that were lightly dissociated and pelleted as immunofluorescence staining for Claudin-2 was unsuccessful in Caco-2 BBE cells (data not shown). In control cells Claudin-2 staining was diffuse and dark brown whereas in both cell lines with down-regulated CDKN2B-AS1 a lighter brown was observed suggesting lower levels of Claudin-2 (Fig. 7c). The signal intensity for Occludin on serial sections was similar between all three conditions (Fig. 7c);Mechanistically, CKDN2B-AS1 down-regulation results in increased colonic barrier integrity possibly through decreases in Claudin-2 expression	31207308	RID03489	expression association	NA	UP(SKCM);DATA(GSE38495)	
Intervertebral disc degeneration	IQANK1	Col II	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	NA	NA	642574	NA	FAM83H-AS1|FAM83HAS1|onco-lncRNA-3	NA	LncRNA FAM83H-AS1 induces nucleus pulposus cell growth via targeting the Notch signaling pathway;;FAM83H-AS1 expression was increased by IL-1beta and TNF-alphatreatment in NP cells. Ectopic expression of FAM83H-AS1 induced cell growth and modulated extracellular matrix (ECM) expression in the NP cell. Elevated expression of FAM83H-AS1 promoted Notch1 and Hes1 expression in NP cells. Furthermore, FAM83H-AS1 induced NP cell growth and modulated ECM expression through targeting Notch 1;we demonstrated that elevated expression of FAM83H-AS1 reduced Col II expression (Figure 5a). Moreover, aggrecan expression was downregulated in NP cell after treatment with pcDNA-FAM83H-AS1 vector (Figure 5b). Ectopic expression of FAM83H-AS1 increased the expression of MMP-3 expression (Figure 5c), MMP-13 expression (Figure 5d);We first detected lncRNA FAM83H AS1 expression in five nondegenerated NP samples and 30 degenerative NP samples using qRT-PCRAM83H-AS1 promoted nucleus pulposus cell proliferation and modulated ECM expression through targeting Notch 1	31102263	RID03490	expression association	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	
Intervertebral disc degeneration	IQANK1	MMP\3	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	NA	NA	642574	NA	FAM83H-AS1|FAM83HAS1|onco-lncRNA-3	NA	LncRNA FAM83H-AS1 induces nucleus pulposus cell growth via targeting the Notch signaling pathway;;FAM83H-AS1 expression was increased by IL-1beta and TNF-alphatreatment in NP cells. Ectopic expression of FAM83H-AS1 induced cell growth and modulated extracellular matrix (ECM) expression in the NP cell. Elevated expression of FAM83H-AS1 promoted Notch1 and Hes1 expression in NP cells. Furthermore, FAM83H-AS1 induced NP cell growth and modulated ECM expression through targeting Notch 1;we demonstrated that elevated expression of FAM83H-AS1 reduced Col II expression (Figure 5a). Moreover, aggrecan expression was downregulated in NP cell after treatment with pcDNA-FAM83H-AS1 vector (Figure 5b). Ectopic expression of FAM83H-AS1 increased the expression of MMP-3 expression (Figure 5c), MMP-13 expression (Figure 5d);We first detected lncRNA FAM83H AS1 expression in five nondegenerated NP samples and 30 degenerative NP samples using qRT-PCRAM83H-AS1 promoted nucleus pulposus cell proliferation and modulated ECM expression through targeting Notch 1	31102263	RID03491	expression association	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	
Intervertebral disc degeneration	IQANK1	NOTCH1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000148400	NA	642574	4851	FAM83H-AS1|onco-lncRNA-3	TAN1	LncRNA FAM83H-AS1 induces nucleus pulposus cell growth via targeting the Notch signaling pathway;;FAM83H-AS1 expression was increased by IL-1beta and TNF-alphatreatment in NP cells. Ectopic expression of FAM83H-AS1 induced cell growth and modulated extracellular matrix (ECM) expression in the NP cell. Elevated expression of FAM83H-AS1 promoted Notch1 and Hes1 expression in NP cells. Furthermore, FAM83H-AS1 induced NP cell growth and modulated ECM expression through targeting Notch 1;We first detected lncRNA FAM83H AS1 expression in five nondegenerated NP samples and 30 degenerative NP samples using qRT-PCRlevated expression of FAM83H-AS1 promoted the expression of Notch1 and Hes1 in nucleus pulposus cells;FAM83H-AS1 promoted nucleus pulposus cell proliferation and modulated ECM expression through targeting Notch 1	31102263	RID03492	expression association	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Intervertebral disc degeneration	IQANK1	HES1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000114315	NA	642574	3280	FAM83H-AS1|onco-lncRNA-3	bHLHb39|FLJ20408|HES-1|HRY	LncRNA FAM83H-AS1 induces nucleus pulposus cell growth via targeting the Notch signaling pathway;;FAM83H-AS1 expression was increased by IL-1beta and TNF-alphatreatment in NP cells. Ectopic expression of FAM83H-AS1 induced cell growth and modulated extracellular matrix (ECM) expression in the NP cell. Elevated expression of FAM83H-AS1 promoted Notch1 and Hes1 expression in NP cells. Furthermore, FAM83H-AS1 induced NP cell growth and modulated ECM expression through targeting Notch 1;We first detected lncRNA FAM83H AS1 expression in five nondegenerated NP samples and 30 degenerative NP samples using qRT-PCRlevated expression of FAM83H-AS1 promoted the expression of Notch1 and Hes1 in nucleus pulposus cells;FAM83H-AS1 promoted nucleus pulposus cell proliferation and modulated ECM expression through targeting Notch 1	31102263	RID03493	expression association	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Myocardial ischemia	C2dat1	VEGFA	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+);JAK/STAT3 signaling pathway(+)	ceRNA(miR-22)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	NA	NA	ENSG00000112715	NA	NA	7422	NA	VEGF|VEGF-A|VPF	Long noncoding RNA C2dat1 protects H9c2 cells against hypoxia injury by downregulating miR-22;Finally, we found that silence of C2dat1 deactivated PI3K/AKT/mTOR and JAK/STAT3 pathways via regulating miR-22 and its downstream gene VEGF. C2dat1-miR-22-VEGF axis could regulate hypoxia injury in H9c2 cells. C2dat1 alleviated hypoxia injury possibly via downregulating miR-22, then upregulating VEGF, which further enhancing the activation of PI3K/AKT/mTOR and JAK/STAT3 pathways;Upregulating C2dat1 alleviated hypoxia-evoked injury through miR-22;Quantitative real time polymerase chain reaction (qRT-PCR data showed that miR 22 expression was downregulated following transfection pEX C2dat1, whereas it was upregulated by sh C2dat1 (both p < 0.01; Figure 3). It seems that miR 22 was negatively regulated by C2dat1.	31004350	RID03494	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Non-small cell lung cancer	SP1	NORAD	positively-E	ChIP;RT-qPCR;JASPAR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000260032	GRCh38_20:36045618-36051018	6667	647979	NA	LINC00657	Long noncoding RNA LINC00657 induced by SP1 contributes to the non-small cell lung cancer progression through targeting miR-26b-5p/COMMD8 axis;quantitative reverse-transcription polymerase chain reaction (RT-qPCR) revealed that LINC00657 level was apparently elevated in NSCLC cells; the chromatin immunoprecipitation result identified the transcription factor SP1 could bind with LINC00657 promoter, and RT-qPCR proved SP1 positively regulated LINC00657 expression in NSCLC cells; With the application of rescue assays, we uncovered that overexpression of COMMD8 partly mitigated the impairment of LINC00657 repression on NSCLC cell proliferation and migration. Together, our study illustrated that SP1-stimulated LINC00657 promoted NSCLC progression through targeting miR-26b-5p/COMMD8 axis;Based on the prediction by UCSC (http://genome. ucsc.edu/) and JASPAR database (http://jaspardev.genereg.net/), SP1 was a potential TF that modulated LINC00657 transcription. Of note, JASPAR suggested two putative SP1 binding sites in the LINC00657 promoter region, including the sites E1 ( 105 to 95 bp, CCTCCACCTCC) and E2 ( 431 to 421 bp, CCTCCACCTCC; Figure 2a). In addition, we found that the level of LINC00657 was apparently elevated in NCSCLC cells responding to SP1 overexpression (Figure 2b,c), further implying the positive regulation of SP1 on LINC00657 expression in NSCLC. Thereafter, the ChIP assay indicated that SP1 could bind to LINC00657 at E1 sites (Figure 2d). Besides, it was turned out that the luciferase activity of LINC00657 promoter containing wild type transcription factor binding sites (TFBS) was enhanced while no obvious change could be noticed in that of its promoter with the TFBS mutated (Figure 2e,f), implying that SP1 regulated LINC00657 transcription by binding to LINC00657 promoter at E1 site. To sum up, SP1 was an activator for LINC00675 transcription in NSCLC.	31566716	RID03495	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	NORAD	COMMD8	positively-E	RIP;starBase;RT-qPCR;western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000169019	NA	647979	54951	LINC00657	FLJ20502	Long noncoding RNA LINC00657 induced by SP1 contributes to the non-small cell lung cancer progression through targeting miR-26b-5p/COMMD8 axis;quantitative reverse-transcription polymerase chain reaction (RT-qPCR) revealed that LINC00657 level was apparently elevated in NSCLC cells; the mechanistic investigations unveiled that LINC00657 was an endogenous sponge of miR-26b-5p and therefore boosted the expression of copper metabolism MURR1 domain-containing 8 (COMMD8), one of the targets of miR-26b-5p;With the application of rescue assays, we uncovered that overexpression of COMMD8 partly mitigated the impairment of LINC00657 repression on NSCLC cell proliferation and migration. Together, our study illustrated that SP1-stimulated LINC00657 promoted NSCLC progression through targeting miR-26b-5p/COMMD8 axis;To further verify the interaction between LINC00657 and miR 26b 5p, RIP assay was employed;By the use of starBase (http://starbase.sysu.edu.cn), miR 26b 5p was found to have a high potential to bind with LINC00657;With the employment of starBase, COMMD8 was suggested as one of the targets of miR 26b 5p (Figure 4a), it was therefore selected to be a potential downstream effector of LLINC00657/miR 26b 5p axis. Besides, RT-qPCR exhibited that COMMD8 expression was distinctly upregulated in NSCLC cells (Figure 4b). Based on RT-qPCR and western blot, overexpression of miR 26b 5p or suppression of LINC00657 resulted in a predominant abrogation on COMMD8 expression at both messenger RNA and protein levels (Figure 4c,d). Furtherly, it was unveiled that the luciferase activity of COMMD8 WT was sharply reduced by miR 26b 5p mimics, while such reduction resulted from miR 26b 5p upregulation was partly regained under LINC00657 overexpression in both A549 and H1975 cells (Figure 4e f). What s more, the result of RIP assay indicated that LINC00657, miR 26b 5p, and COMMD8 were all abundant in anti Ago2 group rather than anti IgG group, suggesting the coexistence of them in RNA induced silencing complexes in NSCLC cells (Figure 4g). Taken together, LINC00657 regulated COMMD8 expression in NSCLC via sponging miR 26b 5p	31566716	RID03496	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	GAS5	miR-135a	negatively-F	Immunofluorescence assay;luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(-);lipid metabolic process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Silencing of GAS5 represses the malignant progression of atherosclerosis through upregulation of miR-135a;qRT-PCRwas used to assess the expression of GAS5 and miR-135a;The targeted interaction between GAS5 and miR-135a was determined by dual-luciferase reporter assay and RNA immunoprecipitation assay;GAS5 directly targeted miR-135a and repressed miR-135a expression. MiR-135a expression restoration abrogated the alleviative effects of GAS5 silencing on inflammation and lipid metabolic disorders in ox-LDL-treated macrophages;These data strongly pointed to a role of GAS5 as a molecular sponge for miR-135a;These predicted data by starBase v2.0 software revealed that GAS5 harbored a putative binding site for miR-135a (Fig. 5A);Silencing of GAS5 alleviated inflammation and lipid metabolic disorders by upregulating miR-135a	31545249	RID03497	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Hepatocellular carcinoma	CYTOR	CDK13	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-26b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000065883	NA	112597	8621	C2orf59|LINC00152|MGC4677|NCRNA00152	CDC2L|CDC2L5|CHED|KIAA1791	Insight into the molecular mechanism of LINC00152/miR-215/CDK13 axis in hepatocellular carcinoma progression;we observed LINC00152 was obviously upregulated in HCC cells;The mutations made in LINC00152 sequence were displayed in Figure 4B. Cotransfection of the WT LINC00152 with miR 152 mimics reduced the reporter activity (Figure 4C);Binding sites of miR 215 and CDK13 was manifested in Figure 5A. WT CDK13 and MUT CDK13 were displayed in Figure 5B. Cotransfection of WT CDK13 with miR 215 mimics repressed the reporter activity (Figure 5C). CDK13 was inhibited by miR 215 in vitro (Figure 5D). This indicated miR 215 directly targeted CDK13.	31297882	RID03498	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	ZEB2-AS1	PGF	positively-E	LncBase;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression;cell proliferation(-);cell invasion(-)	ceRNA(miR-149)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000119630	NA	100303491	5228	ZEB2-AS|ZEB2AS|ZEB2NAT	D12S1900|PGFL|PIGF|PLGF|PlGF-2|SHGC-10760	The decreased lncRNA ZEB2-AS1 in pre-eclampsia controls the trophoblastic cell line HTR-8/SVneo's invasive and migratory abilities via the miR-149/PGF axis;Downregulation of lncRNA ZEB2-AS1 was detected in placentas from patients with PE when compared with those from normal pregnancies;These findings indicate that ZEB2-AS1 contributes to PE progression by affecting cell proliferative and invasive capacities via the miR-149/PGF axis in HTR-8/SVneo cells;ZEB2-AS1 upregulation markedly promoted proliferative, migratory, and invasive potentials in HTR-8/SVneo cells, while knockdown of ZEB2-AS1 had the opposite effects;Total RNA from clinical samples or treated cells was extracted using TRIzol reagent;ZEB2 AS1 downstream targets were predicted by bioinformatics analyses (LncBase Predicted, V2.0). miR 149 was selected for further investigations as miR 149 has been well documented in regulating cell invasive and migratory potentials.13-15 The binding sites between miR 149 and ZEB2 AS1 are presented in Figure 3A;A reduction in the wild type vector luciferase activity was seen in the miR 149 overexpression group, and increased luciferase activity was seen in the miR 149 downregulation group (Figure 3C);	31148230	RID03499	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Endometrial cancer	CCAT1	CDK2	positively-E	RNAi	upregulation	RT-PCR	NA	NA	cell migration(+);cell cycle phase transition(G0/G1)(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000123374	NA	100507056	1017	CARLO5|CARLo-5|onco-lncRNA-40	CDKN2|p33(CDK2)	CARLo-5 as an oncogenic gene in endometrial carcinoma;Here, we measured the expression of CARLo-5 in EC cell lines, including HEC-1B, KLE, Ishikawa, RL95-2, and primary cultured normal endometrial cells by qPCR and RT-PCRCARLo-5 Is Highly Expressed in EC Tissues and EC Cell Lines;To further clarify the mechanism by which CARLo-5 regulates the function of EC cells, we examined the expression of CDK2 and CDKN1A and cancer cell migration-related proteins, MMP2 and MMP9 in EC cells with downregulation of CARLo-5; Overall, these data indicate that CARLo-5 may regulate the cell cycle and migration partly by regulating the expression of CDK2, CDKN1A, MMP2, and MMP9 in EC cells;Our results showed that knocking down CARLo-5 could inhibit the migration and invasion of EC cells by decreasing the level of MMP2 and MMP9 proteins;These results support the hypothesis that CARLo-5 leads to G0/G1 phase arrest by partly regulating the expression of CDK2 and CDKN1A;Moreover, the expression of CARLo-5 was positively related to CDK2 but negatively related to CDKN1A in EC tissues	31661565	RID03500	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Endometrial cancer	CCAT1	CDKN1A	negatively-E	RNAi	upregulation	RT-PCR	NA	NA	cell migration(+);cell cycle phase transition(G0/G2)(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000124762	NA	100507056	1026	CARLO5|CARLo-5|onco-lncRNA-40	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	CARLo-5 as an oncogenic gene in endometrial carcinoma;Here, we measured the expression of CARLo-5 in EC cell lines, including HEC-1B, KLE, Ishikawa, RL95-2, and primary cultured normal endometrial cells by qPCR and RT-PCRCARLo-5 Is Highly Expressed in EC Tissues and EC Cell Lines;To further clarify the mechanism by which CARLo-5 regulates the function of EC cells, we examined the expression of CDK2 and CDKN1A and cancer cell migration-related proteins, MMP2 and MMP9 in EC cells with downregulation of CARLo-5; Overall, these data indicate that CARLo-5 may regulate the cell cycle and migration partly by regulating the expression of CDK2, CDKN1A, MMP2, and MMP9 in EC cells;Our results showed that knocking down CARLo-5 could inhibit the migration and invasion of EC cells by decreasing the level of MMP2 and MMP9 proteins	31661565	RID03501	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Endometrial cancer	CCAT1	MMP2	positively-E	RNAi	upregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+);cell cycle phase transition(G0/G3)(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000087245	NA	100507056	4313	CARLO5|CARLo-5|onco-lncRNA-40	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	CARLo-5 as an oncogenic gene in endometrial carcinoma;Here, we measured the expression of CARLo-5 in EC cell lines, including HEC-1B, KLE, Ishikawa, RL95-2, and primary cultured normal endometrial cells by qPCR and RT-PCRCARLo-5 Is Highly Expressed in EC Tissues and EC Cell Lines;To further clarify the mechanism by which CARLo-5 regulates the function of EC cells, we examined the expression of CDK2 and CDKN1A and cancer cell migration-related proteins, MMP2 and MMP9 in EC cells with downregulation of CARLo-5; Overall, these data indicate that CARLo-5 may regulate the cell cycle and migration partly by regulating the expression of CDK2, CDKN1A, MMP2, and MMP9 in EC cells;Our results showed that knocking down CARLo-5 could inhibit the migration and invasion of EC cells by decreasing the level of MMP2 and MMP9 proteins	31661565	RID03502	expression association	NA		UP(PAAD);DATA(GSE40174)
Endometrial cancer	CCAT1	MMP9	positively-E	RNAi	upregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+);cell cycle phase transition(G0/G4)(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000100985	NA	100507056	4318	CARLO5|CARLo-5|onco-lncRNA-40	CLG4B|GELB|MANDP2|MMP-9	CARLo-5 as an oncogenic gene in endometrial carcinoma;Here, we measured the expression of CARLo-5 in EC cell lines, including HEC-1B, KLE, Ishikawa, RL95-2, and primary cultured normal endometrial cells by qPCR and RT-PCRCARLo-5 Is Highly Expressed in EC Tissues and EC Cell Lines;To further clarify the mechanism by which CARLo-5 regulates the function of EC cells, we examined the expression of CDK2 and CDKN1A and cancer cell migration-related proteins, MMP2 and MMP9 in EC cells with downregulation of CARLo-5; Overall, these data indicate that CARLo-5 may regulate the cell cycle and migration partly by regulating the expression of CDK2, CDKN1A, MMP2, and MMP9 in EC cells;Our results showed that knocking down CARLo-5 could inhibit the migration and invasion of EC cells by decreasing the level of MMP2 and MMP9 proteins	31661565	RID03503	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	CHRF	MIR211	negatively-F	RNA pull-down assay;immunoprecipitation	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);WNT/beta-catenin signaling pathway(+);cell viability(+);cell proliferation(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	NA	NA	ENSG00000207702	NA	NA	406993	NA	MIRN211|mir-211	The long noncoding RNA cardiac hypertrophy-related factor plays oncogenic roles in hepatocellular carcinoma by downregulating microRNA-211;The expression levels of CHRF and microRNA 211 (miR 211) in HCC tissues and/or cell lines HepG2 and Huh 7 were measured using quantitative reverse transcription polymerase chain reaction;The pull down assay and RNA immunoprecipitation were performed to analyze the association between CHRF and miR 211;CHRF negatively regulated the expression of miR 21, and miR 21 was a direct target of CHRF. Overexpression of miR 211 reversed the effects of CHRF on HepG2 and Huh 7 cell viability, proliferation, and EMT process. Furthermore, overexpression of CHRF activated the PI3K/AKT and Wnt/beta catenin pathways in HepG2 cells by downregulating miR 211; CHRF played oncogenic roles in HCC. The overexpression of CHRF promoted HepG2 and Huh 7 cell viability, proliferation, and EMT process by downregulating miR 211 and then activating the PI3K/AKT and Wnt/beta catenin pathways	30916824	RID03504	ceRNA or sponge	NA		
Myocardial ischemia	LINC01116	miR-21	negatively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell injury(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000199004	NA	375295	NA	TALNEC2	NA	Long noncoding RNA TALNEC2 regulates myocardial ischemic injury in H9c2 cells by regulating miR-21/PDCD4-medited activation of Wnt/beta-catenin pathway;TALNEC2 could negative regulate the miR 21 expression, and overexpression of TALNEC2 aggravated hypoxia injury by downregulation of miR 21. Moreover, miR 21 negatively regulated the PDCD4 expression, and PDCD4 was a target of miR 21;The quantitative real-time polymerase chain reaction (qRT-PCR analysis was subsequently performed to detect the expression levels of TALNEC2 and PDCD4 using the One Step SYBR- PrimeScript-PLUS RT-RNA PCR Kit (TaKaRa) and GAPDH was used for normalizing;TALNEC2 level is high in clinicalcases and hypoxia induces hypoxia injury in H9c2 cells;TALNEC2 negatively regulates miR-21 expression in H9c2 cells and overexpression of TALNEC2 aggravates hypoxia injury possible by downregulation of miR-21;Luciferase reporter assay confirmed the target relationship between TALNEC2 and miR 21, in detail, the luciferase activity of TALNEC2 wt was significantly inhibited in miR 21 overexpressing cells (P < 0.05), but the luciferase activities of TALNEC2 mut did not exhibit conspicuous change;miR 21 or TALNEC2 was enriched by the bio TALNEC2 or bio miR 21, respectively (P < 0.001, Figure 3E1; P < 0.01, Figure 3E2). Indicating that miR 21 was targeted by TALNEC2;E1 and E2, RNA pull down showed the enrichment of miR 21 and TALNEC2; As shown in Figure 4B, the binding sequence between miR 21 and PDCD4 was predicted by Targetscan software;Further luciferase reporter assay confirmed the target relationship between miR 21 and PDCD4, in detail, the luciferase activity of PDCD4 wt was significantly inhibited in miR 21 overexpressing H9c2 cells (P < 0.05), but the luciferase activities of PDCD4 mut did not exhibit	30861181	RID03505	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Cartilage damage	HOTAIR	WIF1	negatively-E			RT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Other	Cartilage damage	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156076	NA	100124700	11197	HOXC-AS4|HOXC11-AS1|NCRNA00072	WIF-1	LncRNA HOTAIR-mediated Wnt/beta-catenin network modeling to predict and validate therapeutic targets for cartilage damage;In Fig. 1a, the expression of WIF-1 obviously increases linearly without the introduction of HOTAIR which is not in a steady state. This result reveals that HOTAIR is important in controlling the dynamic behavior of WIF-1, dysfunction of HOTAIR may lead to the disturbance of downstream signal transmission;This result is in a good agreement with the experimental observation that HOTAIR directly inhibited the expression of WIF-1 through increasing H3K27 trimethylation in the promoter region and then activated Wnt/beta-catenin pathway [34];	31366320	RID03506	expression association	NA		
Cartilage damage	HOTAIR	MMP13	NA			RT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Other	Cartilage damage	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000137745	NA	100124700	4322	HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG3|MANDP1|MDST|MMP-13	LncRNA HOTAIR-mediated Wnt/beta-catenin network modeling to predict and validate therapeutic targets for cartilage damage;: A dynamic network of lncRNA HOTAIR-mediated Wnt/beta-catenin pathway regulating MMP-13 is developedto investigate the dynamic mechanism of the network involved in the pathogenesis of cartilage damage	31366320	RID03507	expression association	NA		UP(PAAD);DATA(GSE40174)
Lung cancer	LINC00922	CXCR4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000261742	GRCh38_16:65284496-65576345	ENSG00000121966	NA	283867	7852	Lnc-LALC	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis;Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction;Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction;Through dual-luciferase reporter gene assay and functional experiments, the potential function of LINC00922/miRNA-204/CXCR4 regulatory loop in mediating the progression of lung cancer was explored;CXCR4 was upregulated in lung cancer tissues and cells, which promoted lung cancer cells to migrate and invade. LINC00922 regulated the level of CXCR4 and directly bound to miRNA-204/CXCR4;LINC00922 was upregulated in lung cancer	31287095	RID03508	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic foot ulcers	lncRNA-ENST00000411554	MAPK1	negatively-E	FISH;RT-qPCR	downregulation	microarray;RT-qPCR	NA	NA	immune response(-)	NA	association	RNA-protein	NA	NA	Evading Immune Detection;Tumor Promoting Inflammation;Evading Immune Detection;Tumor Promoting Inflammation	Other	Diabetic foot ulcers	lncRNA	PCG	NA	NA	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|NS13|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Screening and preliminary validation of T lymphocyte immunoregulation-associated long non-coding RNAs in diabetic foot ulcers;A target regulatory association was identified between downregulated lncRNA-ENST00000411554 and upregulated mitogen-activated protein kinase (MAPK)1 in DFU tissues, and a negative correlation was detected between this RNA and protein;activation of the MAPK signal transduction pathway mediated by the lncRNA-ENST00000411554/MAPK1 axis may affect the DFU immune regulatory imbalance;To investigate the involvement of lncRNA in DFUs, lncRNA/mRNA gene chip technology was used to detect lncRNA and mRNA expression in the wound surface tissues obtained from the ulcer and control groups;Therefore, to investigate whether there was a negative correlation between lncRNA-ENST00000411554 and MAPK1 expression in control and DFU tissues, an additional 19 control and 36 ulcer wound surface tissue samples were investigated via lncRNA FISH and RT-qPCR. The results revealed that lncRNA-ENST00000411554 expression was significantly downregulated and MAPK1 expression was significantly upregulated in DFU tissues compared with the control tissues, and thus exhibited a negative correlation	30664216	RID03509	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Spontaneous abortion	H19	ITGB3	positively-E	qRT-PCR;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell invasion(-)	ceRNA(let-7)	regulation	RNA-protein	NA	NA	NA	Other	Spontaneous abortion	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000259207	NA	283120	3690	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CD61|GP3A|GPIIIa	H19 regulates trophoblastic spheroid adhesion by competitively binding to let-7;In the embryonic chorion tissue of spontaneous abortion (SA), the expressions of H19 and ITGB3 at both the mRNA and protein levels decreased;The results of quantitative RT-PCR western blot dual-luciferase report gene and functional miRNA let-7 rescue experiments, adhesion assay and in vitro transwell invasion assay confirmed that H19 regulated trophoblastic spheroid adhesion with endometrial stromal cells through the H19/let-7/ITGB3 axis, thereby providing an improved understanding of the molecular mechanism of SA;H19 regulated the expression of ITGB3 by competitively binding to miRNA let-7;H19 promoted HTR-8 adhesion and invasion by inhibiting miRNA let-7;In the present study, we showed that H19 knockdown decreased the expression of ITGB3 by acting as a molecular sponge that enabled let-7a-5p to avoid mRNA degradation on its target gene ITGB3, leading to the impaired adhesion and invasion of EVT cells	30780128	RID03510	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE75367)
Colorectal cancer	SNAI1	WiNTRLINC1	negatively-E	ChIP	downregulation	qRT-PCR	NA	NA	cell stemness(-);cell proliferation(-)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000124216	NA	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	NA	Genome-wide mapping of DNA-binding sites identifies stemness-related genes as directly repressed targets of SNAIL1 in colorectal cancer cells;SNAIL1 directly represses the proto-oncogene MYB, and the long noncoding RNA (lncRNA) WiNTRLINC1, a recently described regulator of ASCL2;SNAIL1-mediated downregulation of MYB and ISC markers like WiNTRLINC1 likely contributes to the decrease in proliferation known to be associated with EMT, while simultaneously abrogating stemness features of colorectal cancer cells	31391555	RID03511	expression association	NA	UP(PAAD);DATA(GSE40174)	
Lung cancer	LINC00922	CXCR4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000261742	GRCh38_16:65284496-65576345	ENSG00000121966	NA	283867	7852	Lnc-LALC	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	LINC00922 Accelerates the Proliferation, Migration and Invasion of Lung Cancer Via the miRNA-204/CXCR4 Axis;Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction;Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction;Through dual-luciferase reporter gene assay and functional experiments, the potential function of LINC00922/miRNA-204/CXCR4 regulatory loop in mediating the progression of lung cancer was explored;CXCR4 was upregulated in lung cancer tissues and cells, which promoted lung cancer cells to migrate and invade. LINC00922 regulated the level of CXCR4 and directly bound to miRNA-204/CXCR4;LINC00922 was upregulated in lung cancer	31287095	RID03512	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic foot ulcers	lncRNA-ENST00000411554	MAPK1	negatively-E	FISH;RT-qPCR	upregulation	microarray;RT-qPCR	NA	NA	immune response(-)	NA	association	RNA-protein	NA	NA	Evading Immune Detection;Tumor Promoting Inflammation;Evading Immune Detection;Tumor Promoting Inflammation	Other	Diabetic foot ulcers	lncRNA	PCG	NA	NA	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|NS13|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Screening and preliminary validation of T lymphocyte immunoregulation-associated long non-coding RNAs in diabetic foot ulcers;A target regulatory association was identified between downregulated lncRNA-ENST00000411554 and upregulated mitogen-activated protein kinase (MAPK)1 in DFU tissues, and a negative correlation was detected between this RNA and protein;activation of the MAPK signal transduction pathway mediated by the lncRNA-ENST00000411554/MAPK1 axis may affect the DFU immune regulatory imbalance;To investigate the involvement of lncRNA in DFUs, lncRNA/mRNA gene chip technology was used to detect lncRNA and mRNA expression in the wound surface tissues obtained from the ulcer and control groups;Therefore, to investigate whether there was a negative correlation between lncRNA-ENST00000411554 and MAPK1 expression in control and DFU tissues, an additional 19 control and 36 ulcer wound surface tissue samples were investigated via lncRNA FISH and RT-qPCR. The results revealed that lncRNA-ENST00000411554 expression was significantly downregulated and MAPK1 expression was significantly upregulated in DFU tissues compared with the control tissues, and thus exhibited a negative correlation	30664216	RID03513	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Spontaneous abortion	H19	ITGB3	positively-E	qRT-PCR;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell invasion(-)	ceRNA(let-7)	regulation	RNA-protein	NA	NA	NA	Other	Spontaneous abortion	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000259207	NA	283120	3690	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CD61|GP3A|GPIIIa	H19 regulates trophoblastic spheroid adhesion by competitively binding to let-7;In the embryonic chorion tissue of spontaneous abortion (SA), the expressions of H19 and ITGB3 at both the mRNA and protein levels decreased;The results of quantitative RT-PCR western blot dual-luciferase report gene and functional miRNA let-7 rescue experiments, adhesion assay and in vitro transwell invasion assay confirmed that H19 regulated trophoblastic spheroid adhesion with endometrial stromal cells through the H19/let-7/ITGB3 axis, thereby providing an improved understanding of the molecular mechanism of SA;H19 regulated the expression of ITGB3 by competitively binding to miRNA let-7;H19 promoted HTR-8 adhesion and invasion by inhibiting miRNA let-7;In the present study, we showed that H19 knockdown decreased the expression of ITGB3 by acting as a molecular sponge that enabled let-7a-5p to avoid mRNA degradation on its target gene ITGB3, leading to the impaired adhesion and invasion of EVT cells	30780128	RID03514	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE75367)
Colorectal cancer	SNAI1	WiNTRLINC1	negatively-E	ChIP	downregulation		NA	NA	cell stemness(-);cell proliferation(-)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000124216	NA	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	NA	Genome-wide mapping of DNA-binding sites identifies stemness-related genes as directly repressed targets of SNAIL1 in colorectal cancer cells;SNAIL1 directly represses the proto-oncogene MYB, and the long noncoding RNA (lncRNA) WiNTRLINC1, a recently described regulator of ASCL2;SNAIL1-mediated downregulation of MYB and ISC markers like WiNTRLINC1 likely contributes to the decrease in proliferation known to be associated with EMT, while simultaneously abrogating stemness features of colorectal cancer cells	31391555	RID03515	expression association	NA	UP(PAAD);DATA(GSE40174)	
Hepatoblastoma	H19	PTK2	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-138)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000169398	NA	283120	5747	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	FADK|FAK|FAK1|PPP1R71	H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2. Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR-138 and downregulated the expression of FADD via targeting miR-675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.	30367502	RID03516	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE75367)
Hepatoblastoma	H19	FADD	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-675)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168040	NA	283120	8772	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	GIG3|MORT1	Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR-138 and downregulated the expression of FADD via targeting miR-675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.	30367502	RID03517	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Gastric cancer	MALAT1	ATG5	negatively-E	western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-30b)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000057663	NA	378938	9474	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APG5|APG5L|ASP|hAPG5	LncRNA MALAT1 potentiates autophagy-associated cisplatin resistance by regulating the microRNA-30b/autophagy-related gene 5 axis in gastric cancer.Further investigations demonstrated that MALAT1 inhibited miR-30b expression by direct interaction. Moreover, miR-30b abolished MALAT1-induced CDDP resistance by inhibiting autophagy in AGS/CDDP and HGC-27/CDDP cells. Furthermore, ATG5 was found to be a target of miR-30b.Additionally, MALAT1 sequestered miR-30b from ATG5 to increase ATG5 expression in AGS/CDDP and HGC-27/CDDP cells.	30365113	RID03518	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	MALAT1	CCND1	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);cell migration(-)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000110092	NA	378938	595	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL1|D11S287E|PRAD1|U21B31	Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR-34a/cyclin D1 axis.In addition, MALAT1 promoted OS cell viability, invasion and migration, while MALAT1 silencing exhibited opposing effects. Moreover, MALAT1 functioned as a ceRNA to suppress miR-34a expression and in turn upregulate CCND1 in OS cells.	30365098	RID03519	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Sepsis	TFDP1	E-selectin	positively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	NA	NA	7027	NA	DILC|Dp-1|DP1|DRTF1	NA	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-0 siRNAs. Reverse transcription-quantitative polymerase chain reaction analysis and western blot were performed to evaluate the effects of lipopolysaccharide (LPS) on the expression of DILC, IL-6, STAT3, and TLR4, in addition to the effects of DILC and IL-6 on the synthesis of tumor necrosis factor (TNF-alpha), chemokine ligand 5 (CCL5), E-selectin and C-X-C motif chemokine receptor 1 (CXCR1). In addition, the regulatory association between DILC, IL-6, STAT3 and TLR4 was investigated.	30365067	RID03520	interact with protein	chemoresistance	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Sepsis	TFDP1	CXCR1	positively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000163464	NA	7027	3577	DILC|Dp-1|DP1|DRTF1	CD181|CDw128a|CKR-1|CMKAR1|IL8RA	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-1 siRNAs	30365067	RID03521	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Sepsis	TFDP1	CCL5	positively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000161570	NA	7027	6352	DILC|Dp-1|DP1|DRTF1	D17S136E|MGC17164|RANTES|SCYA5|SISd|TCP228	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-2 siRNAs	30365067	RID03522	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Sepsis	TFDP1	TNF	positively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000228978	NA	7027	7124	DILC|DP1|DRTF1|Dp-1	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-3 siRNAs	30365067	RID03523	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC);DATA(GSE117623)
Sepsis	TFDP1	TLR4	negatively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	interact with protein	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000136869	NA	7027	7099	DILC|Dp-1|DP1|DRTF1	ARMD10|CD284|hToll|TLR-4	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-4 siRNAs	30365067	RID03524	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Sepsis	TFDP1	STAT3	negatively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	interact with protein	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	TF	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000168610	NA	7027	6774	DILC|Dp-1|DP1|DRTF1	APRF	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-5 siRNAs	30365067	RID03525	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Sepsis	TFDP1	IL6	negatively-E	luciferase reporter assay;RT-qPCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	interact with protein	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000136244	NA	7027	3569	DILC|Dp-1|DP1|DRTF1	BSF2|HGF|HSF|IFNB2|IL-6	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-6 siRNAs	30365067	RID03526	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Squamous cell carcinoma	LOC441178	ROCK1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENST00000400831	NA	ENSG00000067900	NA	NA	6093	NA	p160ROCK	Long Noncoding RNA LOC441178 Reduces the Invasion and Migration of Squamous Carcinoma Cells by Targeting ROCK1.Previous studies suggested that dysregulation of lncRNA 441178 (LOC441178) is possibly associated with oral squamous cell carcinoma (OSCC). The postoperative survival time was significantly prolonged in the high-grade OSCC patients with high LOC441178 expression compared with those with low LOC441178 expression, which indicated that LOC441178 may act as a prognostic marker and as a potential tumor suppressor for OSCC.Furthermore, we found that rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) is one of the functionally relevant targets of LOC441178 in squamous cells, which is negatively correlated with LOC441178 in tumor tissues from OSCC patients.	30364063	RID03527	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Squamous cell carcinoma	UCA1	LC3-II	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA1 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID03528	expression association	NA	UP(PAAD);DATA(GSE40174)	
Squamous cell carcinoma	UCA1	p62	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000073792	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA2 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID03529	expression association	NA	UP(PAAD);DATA(GSE40174)	
Squamous cell carcinoma	UCA1	ATG5	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000057663	NA	652995	9474	CUDR|LINC00178|onco-lncRNA-36|UCAT1	APG5|APG5L|ASP|hAPG5	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA3 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID03530	expression association	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	H19	TWIST1	positively-E	RNA pull-down assay;RNAi;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	H19 downregulation can increase miR-326 expression in HCC cells. Meanwhile, miR-326 mimics can also inhibit HCC progression, whereas miR-326 inhibitors exhibited a reverse phenomenon by modulating H19 expression. In addition, a negative association between H19 and miR-326 was predicted and confirmed. Furthermore, the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression. Here, by performing bioinformatics analysis, TWIST1 was identified as a downstream target of miR-326. The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR-326 and modulate TWIST1 levels in HCC pathogenesis. Taken these together, these findings indicated that H19/miR-326/TWIST1 axis was involved in HCC development and can indicate a novel HCC target.	30362512	RID03531	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Pancreatic ductal adenocarcinoma	NEAT1	RELA	positively-E	Chip;luciferase reporter assay;RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-302a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000173039	NA	283131	5970	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NFKB3|p65	RELA/NEAT1/miR-302a-3p/RELA feedback loop modulates pancreatic ductal adenocarcinoma cell proliferation and migration.RELA overexpression promoted PDAC cell proliferation and migration, which could be partially attenuated by the NEAT1 knockdown. By binding to RELA, miR-302a-3p inhibited RELA expression, as well as PDAC cell proliferation and migration. RELA downstream NEAT1 expression was negatively regulated by miR-302a-3p; the suppressive effect of NEAT1 knockdown on PDAC cell proliferation and migration was partially attenuated by miR-302a-3p inhibition. Moreover, through direct binding, the expression of miR-302a-3p was also negatively regulated by NEAT1. The expression of miR-302a-3p was downregulated and negatively correlated with RELA or NEAT1 in tissue samples, indicating that rescuing miR-302a-3p expression may inhibit PDAC cell proliferation and migration through RELA/NEAT1. In summary, RELA, NEAT1, and miR-302a-3p form a feedback loop in PDAC to modulate PDAC cell proliferation and migration.	30362505	RID03532	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteoarthritis	DANCR	JAK2	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);inflammatory response(+)	ceRNA(miR-216a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000096968	NA	57291	3717	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	JTK10	In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.	30361290	RID03533	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Retinoblastoma	CDKN2B-AS1	ATM	negatively-F	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);ATM/E2F1 signaling pathway(+);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149311	NA	100048912	472	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	ATA|ATC|ATD|ATDC|TEL1|TELO1	The silencing of ANRIL or up-regulation of ATM exerted an inhibitory effect on the proliferation and invasion while improving the apoptosis of HXO-RB44 and Y79 cells. In conclusion, the key observations of our study demonstrated that ANRIL depletion could act to suppress retinoblastoma progression by activating the ATM-E2F1 signaling pathway. These results provide a potentially promising basis for the targetted intervention treatment of human retinoblastoma.	30355646	RID03534	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Osteosarcoma	BDNF-AS	Caspase3	negatively-F	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	NA	NA	497258	NA	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	NA	The in vitro studies indicated that BDNF-AS overexpression inhibits OS cell proliferation and promotes cell apoptosis through regulating cleaved caspase-3. In conclusion, BDNF-AS serves as a tumor suppressive lncRNA in OS.	30352834	RID03535	expression association	NA	UP(LIHC);DATA(GSE117623)	
Pancreatic ductal adenocarcinoma	MALAT1	ZEB1	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);cell invasion	ceRNA(miR-200c-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 upregulated SMAD3 expression to contribute to metastasis of cervical cancer by sponging miR-143-3p.Clinical data further indicated that MALAT-1 and ZEB1 expression was negatively correlated with miR-200c-3p transcript level of PDAC tissues. There was a positive correlation between MALAT-1 and ZEB1 level.	30352575	RID03536	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	OIP5-AS1	SMAD3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000166949	NA	729082	4088	cyrano|linc-OIP5	HsT17436|JV15-2|MADH3	Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 upregulated SMAD3 expression to contribute to metastasis of cervical cancer by sponging miR-143-3p.LncRNA OIP5-AS1 is demonstrated to mediate the physiological process of cervical cancer cells. Moreover, silencing SMAD3 via siRNA suppressed cell number, viability, migration and invasion, whereas overexpression of OIP5-AS1 promoted these abilities. Furthermore, lncRNA OIP5-AS1 exert its function via sponging miR-143-3p to regulate SMAD3 expression.	30341904	RID03537	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic carcinoma	PVT1	DGCR8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(-)	ceRNA(miR-1207-5p;miR-1207-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000128191	NA	5820	54487	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	C22orf12|DGCRK6|Gy1|pasha	Pvt1 oncogene (non-protein coding) (PVT1) has been reported to be an oncogenic long non-coding RNA in tumorigenesis. In the present study, we show that the expression of PVT1 is correlated with gemcitabine efficacy in PC therapy. Inhibition of PVT1 led to decreased cell growth in PC cells treated with gemcitabine. We also demonstrate that gemcitabine treatment decreases PVT1 levels and increases its encoded miRNAs, such as the miR-1207 pair (miR-1207-5p/3p).Mechanistic studies revealed that miR-1207-5p and miR-1207-3p target the SRC proto-oncogene (non-receptor tyrosine kinase) and ras homolog family member A in PC cells, respectively. In particular, we observed that gemcitabine induced Drosha ribonuclease III (Drosha) and DGCR8 microprocessor complex subunit (DGCR8) upregulation and then triggered PVT1 processing.	30341811	RID03538	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	NEAT1	SOX13	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000143842	NA	283131	9580	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ICA12|MGC117216|Sox-13	Overexpression of SOX13 was able to partially restore the inhibitory effect of NEAT1 on cell proliferation. Meanwhile, it was found that low expression of NEAT1 significantly inhibited tumor formation in vivo.	30338809	RID03539	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colon cancer	HOTAIR	IGF2BP2	negatively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(-);cell proliferation(-);cell migration(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000073792	NA	100124700	10644	HOXC-AS4|HOXC11-AS1|NCRNA00072	IMP-2|p62	LncRNA HOTAIR positively regulated IGF2BP2. Besides, the expressions of HOTAIR and E-cadherin and the apoptosis were increased, while the expressions of IGF2BP2 and vimentin, the growth, invasion and migration of LoVo cells, the average tumor weight, and microvessel density value were decreased.  Taken together, the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial-mesenchymal transition.Long noncoding RNA HOTAIR silencing inhibits invasion and proliferation of human colon cancer LoVo cells via regulating IGF2BP2	30335892	RID03540	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Clear cell renal cell carcinoma	MALAT1	ACVR2B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	ceRNA(miR-194-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000114739	NA	378938	93	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ActR-IIB	LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR-194-5p/ACVR2B signaling.This investigation was purposed to extrapolate whether and how lncRNA MALAT1, miR-194-5p, and ACVR2B altered development of clear cell kidney carcinoma (KIRC). We totally gathered 318 pairs of KIRC tissues and adjacent normal tissues, and also purchased human KIRC cell lines and normal human proximal tubular epithelial cell line. Besides, si-MALAT1, pcDNA-MALAT1, miR-194-5p mimic, miR-194-5p inhibitor, and negative control (NC) were, respectively, transfected into KIRC cells. The viability, proliferation, and apoptosis of the cells were determined with CCK-8 assay, colony formation assay, and flow cytometry. Dual-luciferase reporter gene assay was implemented to validate the targeted relationships between MALAT1 and miR-194-5p, as well as between miR-194-5p and ACVR2B. The results showed that highly expressed MALAT1, ACVR2B, and lowly expressed miR-194-5p were associated with larger tumor size (<<- cm), advanced TNM stage and poor prognosis of KIRC patients, when, respectively, compared with lowly expressed MALAT1, ACVR2B, and highly expressed miR-194-5p (P < 0.05). Transfection of pcDNA-MALAT1, miR-194-5p inhibitor, and pcDNA-ACVR2B conferred the KIRC cells with promoted viability and proliferation, as well as reduced apoptosis (P < 0.05). Treatment of rats with pcDNA-MALAT1, miR-194-5p inhibitor, or pcDNA-ACVR2B also contributed to larger tumor size growing in them (P < 0.05). Moreover, MALAT1 could directly target miR-194-5p to suppress its expression, and ACVR2B was the targeted molecule of miR-194-5p (P < 0.05). Finally, ACVR2B could reverse the effects exerted by miR-194-5p on viability, proliferation, and apoptosis of KIRC cells (P < 0.05). In conclusion, LncRNA MALAT1/miR-194-5p/ACVR2B signaling was regarded as a candidate pathway for modulating KIRC progression.	30334578	RID03541	ceRNA or sponge	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE86978)
Endometriosis	MALAT1	HIF1A	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell autophagy(+)	NA	regulation	NA	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100644	NA	378938	3091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA MALAT1 mediates hypoxia-induced pro-survival autophagy of endometrial stromal cells in endometriosis.In cultured human endometrial stromal cells, both lncRNA-MALAT1 and autophagy were induced by hypoxia in a time-dependent manner and lncRNA-MALAT1 up-regulation was dependent on HIF-1alpha signalling.Our analyses also show that knockdown of lncRNA-MALAT1 suppressed hypoxia induced autophagy. Furthermore, inhibiting autophagy with specific inhibitor 3-Methyladenine (3-MA) and Beclin1 siRNA enhanced apoptosis of human endometrial stromal cells under hypoxia condition.	30324652	RID03542	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	NNT-AS1	MIR363	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell cycle(+);cell invasion(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000207572	NA	100652772	574031	NA	MIR-363|MIRN363|hsa-mir-363	Long noncoding RNA NNT-AS1 promotes gastric cancer proliferation and invasion by regulating microRNA-363 expression .we showed that NNT-AS1 acted as a sponge competing endogenous RNA for microRNA-363 (miR-363), which was downregulated in the GC samples and cell lines. miR-363 expression was negatively related with NNT-AS1 expression in GC samples. Upregulated expression of miR-363 suppressed GC cell growth, cycle, and invasion. Furthermore, we reported that elevated expression of NNT-AS1 promoted GC cell proliferation, cycle, and invasion partly by suppressing miR-363 expression. These results indicated that lncRNA NNT-AS1 acted as an oncogene in the development of GC partly by inhibiting miR-363 expression.	30324628	RID03543	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Gastric cancer	LINC00460	KDM2A	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000173120	NA	728192	22992	NA	CXXC8|DKFZP434M1735|FBL11|FBL7|FBXL11|FLJ00115|JHDM1A|KIAA1004|LILINA	LINC00460 modulates KDM2A to promote cell proliferation and migration by targeting miR-342-3p in gastric cancer,Here, we found that LINC00460 was highly expressed in GC tissues and cell lines. Moreover, LINC00460 overexpression was found to promote GC cell proliferation, migration and invasion, whereas LINC00460 down-regulation significantly inhibited these processes. Notably, we confirmed that LINC00460 could up-regulate KDM2A expression by competitively binding to miR-342-3p in GC cells. Furthermore, the suppressive effects of LINC00460 down-regulation on GC cell proliferation, migration and invasion were partially reversed by a miR-342-3p inhibitor.	30323616	RID03544	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	GAS5	p62	positively-E	western blot;RNAi;siRNA	downregulation	qRT-PCR	NA	NA	cell autophagy(-);mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000073792	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA growth arrest-specific 5 facilitates glioma cell sensitivity to cisplatin by suppressing excessive autophagy in an mTOR-dependent manner.Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression.Functional assay confirmed that knockdown of GAS5 enhanced cell resistance to cisplatin in U87 cells, which had a relatively high expression of GAS5. Conversely, elevation of GAS5 increased cell sensitivity to cisplatin in U138 cells that had a relatively low expression of GAS5. Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression. In addition, GAS5 restored cisplatin-inhibited mammalian target of rapamycin (mTOR) activation. Preconditioning with mTOR antagonist rapamycin engendered not only mTOR inhibition but also abrogated GAS5-mediated depression in cisplatin-evoked autophagy.	30317677	RID03545	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	GAS5	LC3II	negatively-E	western blot;RNAi;siRNA	downregulation	qRT-PCR	NA	NA	cell autophagy(-);mTOR signaling pathway(+)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA growth arrest-specific 5 facilitates glioma cell sensitivity to cisplatin by suppressing excessive autophagy in an mTOR-dependent manner.Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression.Functional assay confirmed that knockdown of GAS5 enhanced cell resistance to cisplatin in U87 cells, which had a relatively high expression of GAS5. Conversely, elevation of GAS5 increased cell sensitivity to cisplatin in U138 cells that had a relatively low expression of GAS5. Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression. In addition, GAS5 restored cisplatin-inhibited mammalian target of rapamycin (mTOR) activation. Preconditioning with mTOR antagonist rapamycin engendered not only mTOR inhibition but also abrogated GAS6-mediated depression in cisplatin-evoked autophagy.	30317677	RID03546	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Osteosarcoma	APTR	YAP1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+)	ceRNA(miR-132-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696277	ENSG00000137693	NA	100505854	10413	RSBN1L-AS1	YAP65	Long noncoding RNA APTR contributes to osteosarcoma progression through repression of miR-132-3p and upregulation of yes-associated protein 1	30317613	RID03547	ceRNA or sponge	NA	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Malignant glioma	GACAT3	ELAVL1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+)	ceRNA(miR-330-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000066044	NA	104797537	1994	LINC01458|lncRNA-AC130710	Hua|HUR|MelG	Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)-3127-5p. Subsequently, ELAVL1 was identified as a direct target of miR-3127-5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR-3127-5p, leading to glioma progression. Long noncoding RNA gastric cancer-associated transcript 3 plays oncogenic roles in glioma through sponging miR-3127-5p	30317610	RID03548	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Atherosclerosis	MALAT1	SOCS1	positively-E	western blot;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(-);JAK-STAT signaling pathway(-)	ceRNA(miR-155)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185338	NA	378938	8651	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Cish1|JAB|SOCS-1|SSI-1|TIP3	The suppression of ox-LDL-induced inflammatory cytokine release and apoptosis of HCAECs by long non-coding RNA-MALAT1 via regulating microRNA-155/SOCS1 pathway.We found that the pro-inflammatory cytokine release and the apoptosis of HCAECs were elevated upon ox-LDL treatment, while MALAT1 expression was also up regulated. Knocking down of MALAT1 boosted ox-LDL-induced cytokine release and apoptosis of HCAECs. The binding site of miR-155 in MALAT1 sequence was confirmed by dual luciferase assay. Furthermore, miR-155 inhibition significantly repressed ox-LDL mediated inflammation and apoptosis of HCAECs via SOCS1. At last, we found that MALAT1 could suppress the inflammatory cytokine release and cell apoptosis via sponging miR-155 to increase SOCS1 level, which in turn restrained JAK-STAT pathway.	30314869	RID03549	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	FLVCR1-DT	E2F3	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-573)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000198468	GRCh38_1:212852105-212858138	ENSG00000112242	NA	642946	1871	FLVCR1-AS1|LQK1|NCRNA00292	NA	The suppression of ox-LDL-induced inflammatory cytokine release and apoptosis of HCAECs by long non-coding RNA-MALAT1 via regulating microRNA-155/SOCS1 pathway.Results revealed that FLVCR1-AS1 was markedly upregulated in NSCLC tissues and cell lines. Knockdown of FLVCR1-AS1 significantly inhibited the proliferation, migration, invasion and promoted apoptosis of NSCLC cells, and suppressed tumor growth of NSCLC in vivo. Moreover, we explored regulatory mechanism, and found that FLVCR1-AS1 functioned as a competing endogenous RNA (ceRNA) by directly binding to miRNA-573, and E2F transcription factor 3 (E2F3) was identified as a down-stream target of miR-573. FLVCR1-AS1 positively regulated E2F3 expression through inhibiting miR-573 in NSCLC cells.	30309647	RID03550	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Laryngeal squamous cell carcinoma	PVT1	miR-519d-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Upregulation of lncRNA PVT1 markedly facilitated proliferation suppressed apoptosis and promoted cell migration in LSCC cells. We further demonstrated that silencing PVT1 strikingly suppressed proliferation, promoted apoptosis, and reduced migration in LSCC cells. Further bioinformatic analysis and dual-luciferase reporter assay revealed that PVT1 could function as an oncogenic transcript partly through sponging miR-519d-3p. Besides, mechanistic investigations indicated that PVT1 could promote cell and migration through interacting with miR-519d-3p.	30304557	RID03551	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Gastric cancer	HOTAIRM1	PTEN	positively-E	luciferase reporter assay;western blot	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	ceRNA(miR-17-5p);PI3K signaling pathway;AKT signaling pathway	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000171862	NA	100506311	5728	HOXA-AS1|HOXA1-AS1|NCRNA00179	BZS|MHAM|MMAC1|PTEN1|TEP1	Long noncoding RNA HOTAIRM1 inhibits cell progression by regulating miR-17-5p/ PTEN axis in gastric cancer.HOTAIRM1 and phosphatase and tensin homolog (PTEN) were both downregulated in GC, whereas miR-17-5p was upregulated. Moreover, the PI3K/AKT pathway was found activated in GC. HOTAIRM1 targeted miR-17-5p, whereas PTEN was the downstream target gene of miR-17-5p. HOTAIRM1 suppressed proliferation and migration of GC cell line and induced their apoptosis, whereas miR-17-5p played the opposite role on GC cell line. HOTAIRM1 also postponed tumor growth in vivo and inhibited the PI3K/AKT pathway in GC.	30302796	RID03552	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	AFAP1-AS1	IGF1R	positively-E	western blot;luciferase reporter assay	downregulation	qRT-PCR	GSE16515;GSE32688	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+);tumor growth(+)	ceRNA(miR-133a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000140443	NA	84740	3480	AFAP1-AS|AFAP1AS|MGC10981	CD221|IGFIR|IGFR|JTK13|MGC18216	The long coding RNA AFAP1-AS1 promotes tumor cell growth and invasion in pancreatic cancer through upregulating the IGF1R oncogene via sequestration of miR-133a.Moreover, we demonstrated that knockdown of IGF1R by transfection with si-IGF1R suppressed cell proliferation, invasion and migration of PaCa-2 and SW1990 PC cells, suggesting that IGF1R may function as an oncogene in PC cells. In the present study, we found that the AFAP1-AS1 RNA gene was significantly upregulated in PC tissues and cell lines. Upregulation of AFAP1-AS1 was also found to be associated with poor prognosis in PC patients. Further, knockdown of AFAP1-AS1 suppressed cell proliferation and invasion, and induced cell apoptosis in vitro as well as inducing tumor growth in vivo. Further investigation revealed that AFAP1-AS1 could act as a ceRNA for miR-133a and thereby modulate the expression of the IGF1R oncogene. Taken together, these results implicate AFAP1-AS1 as being involved in the regulation of pancreatic carcinogenesis by acting as a ceRNA and therefore suggest that it may have potential as a therapeutic target for the treatment of PC.	30300116	RID03553	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Ovarian cancer	MALAT1	RBFOX2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100320	NA	378938	23543	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FOX-2|HNRBP2|HRNBP2|RBM9	The long non-coding RNA MALAT1 promotes ovarian cancer progression by regulating RBFOX2-mediated alternative splicing.Suppression of MALAT1 also resulted in decreased expression of RBFOX2, and alternative processing of the pro-apoptotic tumor suppressor gene KIF1B. MALAT1 knockdown resulted in decreased proliferation, invasion, anchorage-independent growth, and increased anoikis. Suppression of MALAT1 also resulted in decreased expression of RBFOX2, and alternative processing of the pro-apoptotic tumor suppressor gene KIF1B. RBFOX2 suppression resulted in preferential splicing of the pro-apoptotic isoform of KIF1B (KIFB1B-beta) and increased anoikis.	30294913	RID03554	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)
Gastric cancer	NBAT1	SOX9	positively-F	RNA pull-down assay;RNAi;luciferase reporter assay;western blot;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000125398	NA	729177	6662	CASC14|NBAT-1	CMD1|CMPD1|SRA1	A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.NBAT1 was found to be significantly down-regulated in GC tissue. Decreased NBAT1 expression was correlated with poor differentiation, higher tumor stage and lymph node metastasis, and poor prognosis. Functional assays showed that NBAT1 inhibited GC proliferation, migration, and invasion.A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.In the current research, we investigated the expression of NBAT1 in GC tissues and cells. NBAT1 was overexpressed and silenced in GC cells to determine the effect of NBAT1 in regulating GC cell proliferation, apoptosis, migration, and angiogenesis. Moreover, we found that NBAT1 exerted tumor-suppressive activity through degrading Sox9 protein. Our findings contributed to a better understanding of lncRNA functions in GC.	30287498	RID03555	expression association	metastasis,prognosis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Gallbladder cancer	MEG3	LATS2	positively-E	ChIP;RIP;western blot;RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150457	NA	55384	26524	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long noncoding RNA MEG3 regulates LATS2 by promoting the ubiquitination of EZH2 and inhibits proliferation and invasion in gallbladder cancer.We found that MEG3 was downregulated in GBC tissues and cells, and low expression of MEG3 was correlated with poor prognostic outcomes in patients. Overexpression of MEG3 inhibited GBC cell proliferation and invasion, induced cell apoptosis and decreased tumorigenicity in nude mice. Moreover, we found that MEG3 was associated with EZH2 and attenuated EZH2 by promoting its ubiquitination. Furthermore, MEG3 executed its functions via EZH2 to regulate the downstream target gene LATS2. Taken together, these findings suggest that MEG3 is an effective target for GBC therapy and may facilitate the development of lncRNA-directed diagnostics and therapeutics against GBC.	30282996	RID03556	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	LOXL1-AS1	CCND1	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	ceRNA(miR-541-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000110092	NA	100287616	595	NA	BCL1|D11S287E|PRAD1|U21B31	LOXL1-AS1 down-regulation inhibits the expression of CCND1 and cell cycle progression, whereas these effects are abolished upon miR-541-3p suppression.RNA sequencing analysis revealed that it regulates the expression of cell cycle-related genes. LOXL1-AS1 is predominantly distributed in the cytoplasm, where it interacts with miR-541-3p. In addition, miR-541-3p targets the cell cycle regulator CCND1 in prostate cancer cells. LOXL1-AS1 down-regulation inhibits the expression of CCND1 and cell cycle progression, whereas these effects are abolished upon miR-541-3p suppression. In summary, our study revealed that LOXL1-AS1 regulates prostate cancer cell proliferation and cell cycle progression through miR-541-3p and CCND1. Modulation of their levels may be used to treat prostate cancer.	30278884	RID03557	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	MEG3	HSPG2	positively-E	western blot	downregulation	qRT-PCR	NA	NA	angiogenesis(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000142798	NA	55384	3339	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	perlecan|PRCAN|SJS1	Mining Prognostic Significance of MEG3 in Human Breast Cancer Using Bioinformatics Analysis.We found that MEG3 was more frequently downregulated in breast cancer than in normal tissues and this correlated with prognosis. However, estrogen receptor and progesterone receptor status were found to be positively correlated with MEG3 expression. Conversely, basal-like status, triple-negative breast cancer status, and Scarff Bloom & Richardson grade criterion were negatively correlated with MEG3 expression. Following data mining in multiple big data databases, we confirmed a positive correlation between MEG3 and heparan sulfate proteoglycan 2 (HSPG2) expression in breast cancer tissues.	30278461	RID03558	expression association	prognosis		DOWN(BRCA);DATA(GSE86978)
Osteoarthritis	TP53COR1	MIR451A	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	ENSG00000284565	NA	102800311	574411	TRP53COR1|linc-p21|lincRNA-p21	MIR451|MIRN451|hsa-mir-451|hsa-mir-451a|mir-451a	LncRNA-p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR-451.Overexpression of lncRNA-p21 suppressed the expression of miR-451 while the silencing of lncRNA-p21 reversed this effect. MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. The increased cell viability and decreased apoptosis rate induced by lncRNA-p21 silencing was abolished by the miR-451 inhibitor. MiR-451 mimic effectively increased the downregulatory effect of pcDNA3.the level of lncRNA-p21 was significantly upregulated in OA cartilage when compared with the normal cartilage. Silencing of lncRNA-p21 increased cell viability and inhibited the apoptosis rate of chondrocytes in OA, while lncRNA-p21 overexpression decreased cell viability and increased the apoptosis rate of chondrocytes in OA. Overexpression of lncRNA-p21 suppressed the expression of miR-451 while the silencing of lncRNA-p21 reversed this effect. MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. The increased cell viability and decreased apoptosis rate induced by lncRNA-p21 silencing was abolished by the miR-451 inhibitor. MiR-451 mimic effectively increased the downregulatory effect of pcDNA3.1-lncRNA-p21 on miR-451. The decreased cell viability and increased apoptosis rate induced by the overexpression of lncRNA-p21 was abolished by the miR-451 mimic. Investigation into the underlying mechanism revealed that lncRNA-p21 interacted with miRNA-451. In addition, lncRNA-p21 negatively regulated the expression of miR-451. Furthermore, lncRNA-p21 promoted the apoptosis of chondrocytes in OA by acting as a sponge for miR-451. Thus, lncRNA-p21 was proposed as a promising target for the treatment of OA.	30272288	RID03559	ceRNA or sponge	NA		
Gastric adenocarcinoma	CCAT1-L	MYC	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001). There was a positive correlation between the expression level of CCAT1-L mRNA and c-MYC mRNA (r=0.863, P<0.001). CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01). Knockdown of CCAT1-L in MGC803 and MKN-28 cells markedly reduced the cell proliferation, migration, and invasion (P<0.001). CCAT1-L knockdown also evidently inhibited tumor growth and improved survival in nude mice (P<0.001). Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.lncRNA CCAT1-L and MYC are overexpressed in gastric adenocarcinoma. When CCAT1-L was knocked down, the proliferation, migration, and invasion abilities of gastric adenocarcinoma cells were decreased, and the mortality of mice with gastric adenocarcinoma cell line was also decreased. At the same time, the activity of epithelial-sesenchymal transition protein was also decreased. Therefore, the inhibition of CCAT1-L expression can inhibit the epithelial-sesenchymal transition of gastric adenocarcinoma cells and thus inhibits the metastasis of gastric adenocarcinoma, which has a positive effect in preventing the metastasis and treatment of gastric adenocarcinoma.	30254457	RID03560	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric adenocarcinoma	CCAT1-L	RAS	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001). There was a positive correlation between the expression level of CCAT1-L mRNA and c-MYC mRNA (r=0.863, P<0.001). CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01). Knockdown of CCAT1-L in MGC803 and MKN-28 cells markedly reduced the cell proliferation, migration, and invasion (P<0.001). CCAT1-L knockdown also evidently inhibited tumor growth and improved survival in nude mice (P<0.001). Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.lncRNA CCAT1-L and MYC are overexpressed in gastric adenocarcinoma. When CCAT1-L was knocked down, the proliferation, migration, and invasion abilities of gastric adenocarcinoma cells were decreased, and the mortality of mice with gastric adenocarcinoma cell line was also decreased. At the same time, the activity of epithelial-sesenchymal transition protein was also decreased. Therefore, the inhibition of CCAT2-L expression can inhibit the epithelial-sesenchymal transition of gastric adenocarcinoma cells and thus inhibits the metastasis of gastric adenocarcinoma, which has a positive effect in preventing the metastasis and treatment of gastric adenocarcinoma.	30254457	RID03561	expression association	metastasis		
Gastric adenocarcinoma	CCAT1-L	T-ERK	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001). There was a positive correlation between the expression level of CCAT1-L mRNA and c-MYC mRNA (r=0.863, P<0.001). CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01). Knockdown of CCAT1-L in MGC803 and MKN-28 cells markedly reduced the cell proliferation, migration, and invasion (P<0.001). CCAT1-L knockdown also evidently inhibited tumor growth and improved survival in nude mice (P<0.001). Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.lncRNA CCAT1-L and MYC are overexpressed in gastric adenocarcinoma. When CCAT1-L was knocked down, the proliferation, migration, and invasion abilities of gastric adenocarcinoma cells were decreased, and the mortality of mice with gastric adenocarcinoma cell line was also decreased. At the same time, the activity of epithelial-sesenchymal transition protein was also decreased. Therefore, the inhibition of CCAT1-L expression can inhibit the epithelial-sesenchymal transition of gastric adenocarcinoma cells and thus inhibits the metastasis of gastric adenocarcinoma, which has a positive effect in preventing the metastasis and treatment of gastric adenocarcinoma.	30254457	RID03562	expression association	metastasis		
Gastric adenocarcinoma	CCAT1-L	EIF2AK3	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000172071	NA	NA	9451	NA	PEK|PERK|WRS	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001). There was a positive correlation between the expression level of CCAT1-L mRNA and c-MYC mRNA (r=0.863, P<0.001). CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01). Knockdown of CCAT1-L in MGC803 and MKN-28 cells markedly reduced the cell proliferation, migration, and invasion (P<0.001). CCAT1-L knockdown also evidently inhibited tumor growth and improved survival in nude mice (P<0.001). Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.lncRNA CCAT1-L and MYC are overexpressed in gastric adenocarcinoma. When CCAT1-L was knocked down, the proliferation, migration, and invasion abilities of gastric adenocarcinoma cells were decreased, and the mortality of mice with gastric adenocarcinoma cell line was also decreased. At the same time, the activity of epithelial-sesenchymal transition protein was also decreased. Therefore, the inhibition of CCAT2-L expression can inhibit the epithelial-sesenchymal transition of gastric adenocarcinoma cells and thus inhibits the metastasis of gastric adenocarcinoma, which has a positive effect in preventing the metastasis and treatment of gastric adenocarcinoma.	30254457	RID03563	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Gastric adenocarcinoma	CCAT1-L	EIF2AK3	negatively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000172071	NA	NA	9451	NA	PEK|PERK|WRS	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001). There was a positive correlation between the expression level of CCAT1-L mRNA and c-MYC mRNA (r=0.863, P<0.001). CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01). Knockdown of CCAT1-L in MGC803 and MKN-28 cells markedly reduced the cell proliferation, migration, and invasion (P<0.001). CCAT1-L knockdown also evidently inhibited tumor growth and improved survival in nude mice (P<0.001). Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.lncRNA CCAT1-L and MYC are overexpressed in gastric adenocarcinoma. When CCAT1-L was knocked down, the proliferation, migration, and invasion abilities of gastric adenocarcinoma cells were decreased, and the mortality of mice with gastric adenocarcinoma cell line was also decreased. At the same time, the activity of epithelial-sesenchymal transition protein was also decreased. Therefore, the inhibition of CCAT2-L expression can inhibit the epithelial-sesenchymal transition of gastric adenocarcinoma cells and thus inhibits the metastasis of gastric adenocarcinoma, which has a positive effect in preventing the metastasis and treatment of gastric adenocarcinoma.	30254457	RID03564	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Colorectal cancer	ZFAS1	KDR	positively-E	RNA pull-down assay;RNAi;dual-luciferase reporter assay;western blot;dual-luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000128052	NA	441951	3791	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	CD309|FLK1|VEGFR|VEGFR2	SP1-induced lncRNA-ZFAS1 contributes to colorectal cancer progression via the miR-150-5p/VEGFA axis.We found that ZFAS1 expression was higher in CRC tissues, where it was associated with poor overall survival (OS), we also showed that ZFAS1 upregulation was induced by nuclear transcription factor SP1. Moreover, ZFAS1 and VEGFA are both targets of miR-150-5p, while ZFAS1 binds to miR-150-5p in an AGO2-dependent manner. Additionally, ZFAS1 upregulation markedly promoted as well as ZFAS1 knockdown significantly suppressed CRC cell proliferation, migration, invasion and angiogenesis, and the inhibitory effect caused by ZFAS1 knockdown could be reversed by antagomiR-150-5p. Lastly, we demonstrated that ZFAS1 knockdown inhibited EMT process and inactivated VEGFA/VEGFR2 and downstream Akt/mTOR signaling pathway in CRC. Our data demonstrated that SP1-induced ZFAS1 contributed to CRC progression by upregulating VEGFA via competitively binding to miR-150-5p, which acts as a tumor suppressor by targeting VEGFA in CRC.	30250022	RID03565	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	ZFAS1	VEGFA	positively-E	RNA pull-down assay;RNAi;dual-luciferase reporter assay;western blot;dual-luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000112715	NA	441951	7422	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	VEGF|VEGF-A|VPF	We found that ZFAS1 expression was higher in CRC tissues, where it was associated with poor overall survival (OS), we also showed that ZFAS1 upregulation was induced by nuclear transcription factor SP1. Moreover, ZFAS1 and VEGFA are both targets of miR-150-5p, while ZFAS1 binds to miR-150-5p in an AGO2-dependent manner. Additionally, ZFAS1 upregulation markedly promoted as well as ZFAS1 knockdown significantly suppressed CRC cell proliferation, migration, invasion and angiogenesis, and the inhibitory effect caused by ZFAS1 knockdown could be reversed by antagomiR-150-5p. Lastly, we demonstrated that ZFAS1 knockdown inhibited EMT process and inactivated VEGFA/VEGFR2 and downstream Akt/mTOR signaling pathway in CRC. Our data demonstrated that SP1-induced ZFAS1 contributed to CRC progression by upregulating VEGFA via competitively binding to miR-150-6p, which acts as a tumor suppressor by targeting VEGFA in CRC.	30250022	RID03566	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	CDKN2B-AS1	miR-191	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-191)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000207605	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Knockdown long non-coding RNA ANRIL inhibits proliferation, migration and invasion of HepG2 cells by down-regulation of miR-191.Knockdown of ANRIL inhibited proliferation, induced apoptosis, meanwhile suppressed migration and invasion of HepG2 cells. Additionally, the results showed that the expression level of miR-191 was down-regulated by ANRIL knockdown in HepG2 cells. Importantly, overexpression of miR-191 reversed the anti-tumor effect of ANRIL on cell proliferation, apoptosis, migration and invasion in HepG2 cells. Besides, we found that ANRIL knockdown inactivated NF-kB and Wnt/beta-catenin pathways by regulating miR-191.These data demonstrated that ANRIL knockdown suppressed proliferation, migration, invasion, and promoted apoptosis in HepG2 cells by down-regulating miR-191 and inactivating NF-kB and Wnt/beta-catenin signaling pathways.The knockdown expression vectors of ANRIL were transfected into HepG2 cells, and qRT-PCR CCK-8, flow cytometry, Transwell and western blot assays were performed to analyze the effect of ANRIL on cell proliferation, apoptosis, migration and invasion. The relative expression of miR-191 was then examined in ANRIL knockdown vector transfected cells. These experiments were repeated again for exploring the effect of miR-191 on HepG2 cells. NF-kB and Wnt/beta-catenin signaling pathways were examined by using western blot assay.	30249208	RID03567	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Hepatocellular carcinoma	CRNDE	MAPK1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000100030	NA	643911	5594	CRNDEP|LINC00180|LOC643911	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR-217/MAPK1 axis.CRNDE was up-regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary.	30246921	RID03568	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	NEAT1	SMC1A	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000072501	NA	283131	8243	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DXS423E|KIAA0178|SB1.8|SMC1L1|Smcb	Long noncoding RNA NEAT1 modulates cell proliferation and apoptosis by regulating miR-23a-3p/SMC1A in acute myeloid leukemia.The qRT-PCRillustrated that NEAT1 and SMC1A expression was decreased but that miR-23a-3p expression was increased in primary AML cells and THP-1 cells compared with that in normal cells. The RIP assay and dual-luciferase assay revealed the targeting relationship between miR-23a-3p and NEAT1 or SMC1A. The CCK-8 assay showed that the overexpression of NEAT1 and SMC1A or repression of miR-23a-3p inhibited cell proliferation. Flow cytometry showed that the upregulation of NEAT1 and SMC1A or repression of miR-23a-3p promoted apoptosis and affected the cell cycle. NEAT1 repressed the expression of miR-23a-3p, and therefore promoted SMC1A, which in turn suppressed myeloid leukemia cell proliferation and enhanced apoptosis.The expression of nuclear paraspeckle assembly transcript 1 (NEAT1), miR-23a-3p, and structural maintenance of chromosome 1 alpha (SMC1A) in primary AML cells and THP-1 cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR. A Cell Counting Kit-8 (CCK-8) assay was used to analyze proliferation. Cell cycle progression and apoptosis were examined by flow cytometry. RNA immunoprecipitation (RIP) and dual-luciferase assays were performed to determine the correlation between miR-23a-3p and NEAT1 or SMC1A. The qRT-PCRillustrated that NEAT1 and SMC1A expression was decreased but that miR-23a-3p expression was increased in primary AML cells and THP-1 cells compared with that in normal cells. The RIP assay and dual-luciferase assay revealed the targeting relationship between miR-23a-3p and NEAT1 or SMC1A. The CCK-8 assay showed that the overexpression of NEAT1 and SMC1A or repression of miR-23a-3p inhibited cell proliferation. Flow cytometry showed that the upregulation of NEAT1 and SMC1A or repression of miR-23a-3p promoted apoptosis and affected the cell cycle. NEAT1 repressed the expression of miR-23a-3p, and therefore promoted SMC1A, which in turn suppressed myeloid leukemia cell proliferation and enhanced apoptosis.	30246348	RID03569	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Pre-eclampsia	SNHG5	N-cadherin	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-26a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	NA	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	The lncRNA small nucleolar RNA host gene 5 regulates trophoblast cell proliferation, invasion, and migration via modulating miR-26a-5p/N-cadherin axis.Furthermore, miR-26a-5p was predicted to target the 3' untranslated region of N-cadherin, which was confirmed by luciferase reporter assay, and miR-26a-5p overexpression suppressed N-cadherin expression in HTR-8/SVneo cells. N-cadherin mRNA expression was downregulated in PE placental tissues and was positively correlated with SNHG5 expression. Both overexpression of miR-26a-5p and knockdown of N-cadherin suppressed HTR-8/SVneo cell invasion and migration, and also attenuated the effects of SNHG5 on the cellular functions of HTR-8/SVneo cells. In conclusion, our study suggested that SNHG5 promotes trophoblast cell proliferation, invasion, and migration at least partly via regulating the miR-26a-5p/N-cadherin axis.	30242892	RID03570	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Tongue squamous cell carcinoma	CRNDE	miR-384	negatively-E		upregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	CRNDE promotes cell tongue squamous cell carcinoma cell growth and invasion through suppressing miR-384.Overexpression of miR-384 suppressed TSCC cell proliferation, cell cycle, and invasion. Furthermore, we demonstrated that CRNDE promoted TSCC cell proliferation and invasion through inhibiting miR-384 expression. These results suggested that CRNDE acts as an oncogene in the development of TSCC, which partially occurs through inhibiting miR-384 expression.	30242873	RID03571	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Osteoarthritis	CIR	ATOH8	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000138433	GRCh38_2:174348022-174395712	ENSG00000168874	NA	NA	84913	NA	bHLHa21|FLJ14708|HATH6	Long non-coding RNA CIR inhibits chondrogenic differentiation of mesenchymal stem cells by epigenetically suppressing ATOH8 via methyltransferase EZH2.LncRNA CIR suppresses chondrogenic differentiation of hUC-MSCs. Mechanistically, lncRNA CIR could inhibit ATOH8 expression that functions to promote chondrogenic differentiation through EZH3-mediated epigenetic modifications.	33546582	RID03572	epigenetic regulation	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367,GSE86978)
Colorectal cancer	LINC01224	MIR2467	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000269416	GRCh38_19:23399097-23416075	ENSG00000264292	NA	104472717	100616360	NA	mir-2467	qRT-PCRwas performed to examine the expressions of LINC01224 and miR-2467. CCK-8 assay, colony formation assay and transwell invasion assay were used to examine the progression of breast cancer cells. Luciferase and RNA-binding protein immunoprecipitation (RIP) assay were applied to verify the binding site. Correlation analysis of miR-2467 and LINC01224 expression in lung cancer tissues was shown. Pancreatic cancer cells growth in vivo was evaluated using xenograft tumor assay.Finally, LINC01224 silence inhibited the growth CRC cells in vivo.</AbstractText>: LINC01224 expression was observed to be up-regulated in CRC tissues and cell lines. Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. Luciferase reporter assays illustrated that LINC01224 regulated miR-2467 directly, and RNA-binding protein immunoprecipitation (RIP) further confirmed that the suppression of LINC01224 by miR-2467 was in an RISC-dependent manner. Finally, LINC01224 silence inhibited the growth CRC cells in vivo.	33542656	RID03573	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Ovarian cancer	XIST	miR-149-3p	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell cycle(-);cell invasion(-);cell proliferation(-);cell migration(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	High XIST expression indicated a poor prognosis of OC. Inhibition of XIST or elevation of miR-149-3p repressed proliferation, invasion, migration, and colony formation ability, and promoted apoptosis and cell cycle arrest of HO-8910 cells. In SKOV3 cells upon treatment of overexpressed XIST or reduction of miR-149-3p, there exhibited an opposite tendency. Based on online website prediction, dual luciferase reporter gene, and RNA pull-down assays, we found that there was a negative relationship between XIST and miR-149-3p, and miR-149-3p downregulated FOXP3 expression. This study highlights that knockdown of XIST elevates miR-149-3p expression to suppress malignant behaviors of OC cells, thereby inhibiting OC development.	33542185	RID03574	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Colon cancer	CDKN2B-AS1	miR-181a-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	LncRNA ANRIL negatively regulated chitooligosaccharide-induced radiosensitivity in colon cancer cells by sponging miR-181a-5p.The overexpression of ANRIL reduced the cell apoptosis rate after irradiation. MiR-181a-5p directly bound to ANRIL and was upregulated by irradiation in a dose-dependent manner. The suppression of miR-181a-5p decreased cell apoptosis. The COS treatment notably downregulated cell survival and promoted apoptosis in cells exposed to irradiation. The overexpression of ANRIL partially reversed COS-induced apoptosis and the inhibition rate; the upregulation of miR-181a-5p could counteract the impact of ANRIL regulation in cells.The ANRIL expression in colon cancer cell lines was examined using real-time quantitative polymerase chain reaction (RT-qPCR), based on which we selected the cell line that presented the highest expression of ANRIL for radiosensitivity research. The cells were exposed to X-rays (0 Gy, 2 Gy, 4 Gy, and 6 Gy) and evaluated for changes in ANRIL and miR-181a-5p expression using RT-qPCR. Cell viability was evaluated using the CCK8 method, while apoptosis was detected with flow cytometry assays. Dual luciferase assays validated the binding between ANRIL and miR-181a-5p.	33529508	RID03575	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Japanese encephalitis	CCR1	SUSAJ1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	sponge	regulation	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Brain disease	PCG	lncRNA	ENSG00000163823	NA	NA	NA	1230	NA	CD191|CKR-1|CMKBR1|MIP1aR|SCYAR1	NA	Inhibition of Japanese encephalitis virus proliferation by long non-coding RNA SUSAJ1 in PK-15 cells.In this study, we demonstrated that swine lncRNA-SUSAJ1 could suppress JEV proliferation in PK-15 cells. We also found that CCR1 inhibited the expression of lncRNA-SUSAJ1 via the transcription factor SP1. In addition, knockdown of CCR1 could upregulated the expression of SP1 and lncRNA-SUSAJ1, resulting in resistance to JEV proliferation.These findings illustrate the importance of lncRNAs in virus proliferation, and reveal how this virus regulates lncRNAs in host cells to promote its proliferation.	33509198	RID03576	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE111842,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Kidney disease	SNHG15	ICAM1	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell viability(+)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000090339	NA	285958	3383	C7orf40|Linc-Myo1g|MYO1GUT	BB2|CD54|P3.58	SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.	33506255	RID03577	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367)
Prostate cancer	SNHG1	miR-383-5p	negatively-F	luciferase reporter assay;RNAi;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Long noncoding RNA SNHG1 promotes human prostate cancer progression by sponging miR-383-5p.MiR-383-5p was significantly downregulated in prostate cancer tissues and cells. Inhibition of miR-383-5p could partially restore the effects of SNHG1 knockdown on prostate cancer cell proliferation, apoptosis, migration and invasion. Furthermore, murine xenograft models were established to investigate the effects of SNHG1 and miR-383-5p in tumorigenesis in vivo. We found SNHG1 knockdown or miR-383-5p overexpression repressed tumor growth in vivo.	33470616	RID03578	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Lung adenocarcinoma	LINC00520	FOXR2	positively-E	luciferase reporter assay;RNAi;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1252-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000189299	NA	645687	139628	C14orf34|LASSIE	FOXN6|MGC21658	Long noncoding RNA LINC00520 accelerates lung adenocarcinoma progression via miR-1252-5p/FOXR2 pathway.Furthermore, knockdown of LINC00520 inhibited lung ADC cells proliferation, migration and invasion, while co-transfection with a miR-1252-5p inhibitor inverted these influences. Additionally, the findings also demonstrated that FOXR2 was a target of miR-1252-5p; thus, LINC00520 could regulate FOXR2 level. Moreover, LINC00520 silencing suppressed the tumor growth of lung ADC in vivo. In summary, our data indicated that LINC00520 may act as a ceRNA to modulated FOXR2 level by sponging miR-1252-5p, which might bring a potential and effective biomarker to lung ADC treatment.our results demonstrated the reciprocal repression influence between LINC00520 and miR-1252-5p. Moreover, luciferase reporter assays, RIP (RNA-binding protein immunoprecipitation) and pull down assays revealed that miR-1252-5p regulated LINC00520 in RISC-dependent.	33464477	RID03579	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Colorectal cancer	MCM3AP-AS1	FOXF2	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);	ceRNA(miR-19a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000137273	NA	114044	2295	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	FKHL6|FREAC2	lncRNA MCM3AP-AS1 inhibits the progression of colorectal cancer via the miR-19a-3p/FOXF2 axis.MCM3AP-AS1 expression was down-modulated in CRC, and its dysregulation was linked to unfavorable pathological characteristics. MCM3AP-AS1 significantly impeded the multiplication and migration of CRC cells. MCM3AP-AS1 was recognized as a molecular sponge to suppress miR-19a-3p expression, and FOXF2 was a target gene of miR-19a-3p. MCM3AP-AS1 positively modulated FOXF2 expression, and its biological effect was dependent the on miR-19a-3p/FOXF2 axis.	33450091	RID03580	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	HCP5	EPHA7	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-101)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000135333	NA	10866	2045	D6S2650E|P5-1	Hek11	Down-regulation of HCP5 inhibits cell proliferation, migration, and invasion through regulating EPHA7 by competitively binding miR-101 in osteosarcoma.miR-101 was targeted by HCP5 and its expression was decreased in OS. The inhibitor of miR-101 reversed the impact of HCP5 down-regulation on cell proliferation, apoptosis, and metastasis in OS. Ephrin receptor 7 (EPHA7) was proved to be a target of miR-101 and had ability to recover the effects of miR-101 inhibitor in OS. In conclusion, lncRNA HCP5 knockdown suppressed cell proliferation, migration, and invasion, and induced apoptosis through depleting the expression of EPHA7 by binding to miR-101, providing a potential therapeutic strategy of HCP5 in OS.HCP5 was up-regulated both in OS tissues and cell lines and high expression of HCP5 was associated to low survival in OS patients.	33439936	RID03581	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Nasopharynx carcinoma	LINC00312	PRKDC	negatively-F	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	MRN/ATM/CHK2 signaling pathway(-);ATR/CHK1 signaling pathway(-)	NA	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000237697	NA	ENSG00000253729	NA	29931	5591	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	DNA-PKC|DNA-PKcs|DNAPK|DNAPKc|DNPK1|HYRC|HYRC1|p350|p460|XRCC7	LncRNA linc00312 suppresses radiotherapy resistance by targeting DNA-PKcs and impairing DNA damage repair in nasopharyngeal carcinoma.Radioresistance is the main obstacle in the clinical management of nasopharyngeal carcinoma (NPC). linc00312 is deregulated in a number of human cancers, including NPC. However, the detailed functions and underlying mechanisms of linc00312 in regulating radiosensitivity of NPC remains unknown. In this study, cox regression analysis was used to assess the association between linc00312 and NPC patients' survival after radiotherapy. Our results reveal that linc00312 is significantly down-regulated in NPC tissues and patients with higher expression of linc00312 are significantly associated with longer overall survival and better short-term radiotherapy efficacy. Overexpression of linc00312 could increase the sensitivity of NPC cells to ionizing radiation, as indicated by clonogenic survival assay, comet assay, and flow cytometry. Mechanistically, RNA pull down and RNA immunoprecipitation were performed to investigate the binding proteins of linc00312. linc00312 directly binds to DNA-PKcs, hinders the recruitment of DNA-PKcs to Ku80, and inhibits phosphorylation of AKT-DNA-PKcs axis, therefore inhibiting the DNA damage signal sensation and transduction in the NHEJ repair pathway. In addition, linc00312 impairs DNA repair and cell cycle control by suppressing MRN-ATM-CHK2 signal and ATR-CHK1 signal. In summary, we identified DNA-PKcs as the binding protein of linc00312 and revealed a novel mechanism of linc00312 in the DNA damage response, providing evidence for a potential therapeutic strategy in NPC.	33431817	RID03582	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Triple-negative breast cancer	ZFAS1	STAT3	positively-F	western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000168610	NA	441951	6774	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	APRF	LncRNA ZFAS1 inhibits triple-negative breast cancer by targeting STAT3.we found that the expression of the lncRNA, ZFAS1, was significantly downregulated in blood samples of TNBC patients (n=40) compared to matched healthy controls (n=40).	33429003	RID03583	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	Linc-SCRG1	SKP2	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-[0-9]6a)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000145604	NA	NA	6502	NA	FBL1|FBXL1|FLB1|p45	Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2.LincSCRG1 was found to be strongly elevated in human HCC tissues and cell lines. Cotransfection of in-miR26a or overexpression of SKP2 (ov-SKP2) with sh-lincSCRG1 could rescue the anticancer functions of sh-lincSCRG1, including suppressing proliferation and migration of HCC cells. Additionally, sh-lincSCRG1 could effectively inhibit the growth of subcutaneous xenograft tumours and lung metastasis, while the anticancer effect of sh-lincSCRG1 could be reversed by cotransfection of in-miR26a.CONCLUSIONS: LincSCRG1 acts as a ceRNA of miR26a to restrict its ability to derepress SKP2, thereby inducing the proliferation and migration of HCC cells in vitro and in vivo. Depletion of lincSCRG1 could be used as a potential therapeutic approach in HCC.To explore the lincSCRG1 regulation axis, bioinformatics, RIP and luciferase reporter assay were performed. The expressions of lincSCRG1-miR26a-SKP2 were detected in HCC tissues and cell lines through qPCR and western blot. LincSCRG1 acts as a ceRNA of miR26a to restrict its ability to derepress SKP2, thereby inducing the proliferation and migration of HCC cells in vitro and in vivo.	33422101	RID03584	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	GAS5	SKP2	positively-E	western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(-);cell autophagy(-)	ceRNA(miR-[0-9]4a)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000145604	NA	60674	6502	NCRNA00030|SNHG2	FBL1|FBXL1|p45	lncRNA GAS5 inhibits malignant progression by regulating macroautophagy and forms a negative feedback regulatory loop with the miR-34a/mTOR/SIRT1 pathway in colorectal cancer.we explored the role of the negative feedback loop formed by the GAS5/miR-34a axis and mammalian target of rapamycin/sirtuin 1 (mTOR/SIRT1) pathway on macroautophagy and apoptosis in CRC. Expression of GAS5, miR-34a, SIRT1 and mTOR in CRC patients and cell lines was detected by quantitative reverse transcription polymerase chain reaction. Online bioinformatic analysis was used to predict the downstream miRs of GAS5. Luciferase assay and western blot were performed to demonstrate miR-34a as a downstream target gene of GAS5 in CRC cells.  Our results suggested that GAS5 was downregulated and acted as a molecular sponge of miR-34a during CRC progression. miR-34a participated in regulating GAS5-suppressed CRC cell macroautophagy and induced apoptosis through the mTOR/SIRT1 pathway. GAS5-mediated macroautophagy was maintained in an equilibrium state that might have a protective effect on CRC cell apoptosis. The mTOR signaling pathway suppressed GAS5 expression and formed a negative regulation feedback loop with miR-34a in CRC cells. Our results suggested that the GAS5/miR-34a/SIRT1/mTOR negative regulatory feedback loop mediated CRC cell macroautophagy, and maintained the cells in an autonomous equilibrium state, but not excessive activation state, which functions as a strong antiapoptotic phenotype during human CRC progression.	33416133	RID03585	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Inflammation	NEAT1	NLRP3	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell autophagy(+)	NA	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000162711	NA	283131	114548	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCU|MWS|NALP3|PYPAF1	lncRNA NEAT1 ameliorates LPS-induced inflammation in MG63 cells by activating autophagy and suppressing the NLRP3 inflammasome.For this purpose, MG63 cells were stimulated with various concentrations of lipopolysaccharide (LPS) for different periods of time to construct an optimal inflammatory model and RNA sequencing was then performed on these cells. The levels of nuclear enriched abundant transcript 1 (NEAT1), various inflammatory factors, Nod-like receptor protein 3 (NLRP3) protein and osteogenesis-related proteins, as well as the levels of cell apoptosis- and cell cycle-related markers were measured in MG63 cells stimulated with LPS, transfected with NEAT1 overexpression plasmid and treated with bexarotene by western blot RT-qPCR, immunofluorescence, FISH, TEM and flow cytometry. There were 427 differentially expressed genes in the LPS-stimulated MG63 cells, in which NEAT1 was significantly downregulated.	33416115	RID03586	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	LINC00963	CDC5L	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-612)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000096401	NA	100506190	988	MetaLnc9	CDC5|CEF1|hCDC5|PCDC5RP	Long Noncoding RNA LINC00963 Promotes CDC5L-Mediated Malignant Progression in Gastric Cancer.The expression levels of LINC00963, miR-612, and cell division cycle 5-like protein (CDC5L) were measured using quantitative real-time PCR or western blot. The biological functions of LINC00963, miR-612, and CDC5L in GC cells were analyzed by transwell and proliferation experiments. LINC00963 expression was higher in GC tissues than in adjacent normal tissues. Similar results were found in GC cell lines and normal human gastric epithelial cells. Upregulation of LINC00963 was related to the poor prognosis of patients with GC. Knockdown of LINC00963 inhibited the proliferation, invasion, and metastasis but promoted the apoptosis of GC cells. Furthermore, silencing of LINC00963 in GC cells significantly suppressed the tumor growth of GC. Bioinformatics analysis indicated that LINC00963 could target miR-612 by functioning as a competing endogenous RNA. The expression of miR-612 decreased in GC tissues and cell lines. Meanwhile, LINC00963 expression was negatively associated with miR-612. CDC5L was a direct target of miR-612. miR-612 suppressed the expression of CDC5L in GC tissues and cells. Moreover, LINC00963 inhibited the differentiation and maturation of DCs by regulating miR-612 expression in DCs.	33376349	RID03587	ceRNA or sponge	metastasis,prognosis	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Non-small cell lung cancer	FGF12-AS2	NCAPG2	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-188-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230126	GRCh38_3:192515022-192516573	ENSG00000146918	NA	100873987	54892	NA	CAP-G2|FLJ20311|hCAP-G2|LUZP5|MTB	Downregulation of lncRNA FGF12-AS2 suppresses the tumorigenesis of NSCLC via sponging miR-188-3p.Gene and protein expressions in NSCLC cells were measured by q-PCR and western blot, respectively. CCK-8 and immunofluorescence staining were performed to detect the cell proliferation. Cell apoptosis was tested by flow cytometry. Transwell assay was used to detect the cell migration and invasion. Finally, the dual luciferase report assay was used to verify the relation among FGF12-AS2, miR-188-3p, and NCAPG2.Downregulation of FGF12-AS2 significantly inhibited the proliferation of NSCLC cells via inducing apoptosis. In addition, FGF12-AS2 silencing notably suppressed the migration and invasion of A549 cells. Meanwhile, FGF12-AS2 modulated the progression of NSCLC via regulation of miR-188-3p/NCAPG2 axis. Finally, knockdown of FGF12-AS2 inhibited the tumorigenesis of NSCLC via suppressing the EMT process of NSCLC.Downregulation of lncRNA FGF12-AS2 suppressed the tumorigenesis of NSCLC via sponging miR-188-3p.	33344773	RID03588	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	XIST	NOTCH1	positively-E	luciferase reporter assay;western blot;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-137)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148400	NA	7503	4851	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	TAN1	Long non-coding RNA XIST promotes cell proliferation of pancreatic cancer through miR-137 and Notch1 pathway.PC tissues and cell lines were analyzed for XIST, miR-137 and Notch1 expressions through quantitative real-time polymerase chain reaction (qRT-PCR and western blot. Nude mouse xenograft tumor assay was used to detect XIST effects on pancreatic tumorigenesis in vivo. Cell Counting Kit (CCK-8) assay was performed to detect PC cell proliferation. dual-luciferase reporter assay, qRT-PCR RNA immunoprecipitation (RIP) and western blot assays were applied to validate the target relationship of XIST, miR-137 and Notch1.Results demonstrated that XIST expression was increased in PC tissues and cells. XIST knockdown inhibited PC cell proliferation in vitro and also repressed the tumor growth in vivo. XIST directly interacted with miR-137 and negatively regulated its expression. Notch1 was identified as a target gene of miR-137 and XIST acted as a competitive endogenous RNA (ceRNA) to positively regulate Notch1 expression by suppressing miR-137. In addition, we detected miR-137 was negatively correlated with XIST and Notch1 respectively, and a positive correlation between Notch1 and XIST expression in PC tissues. Furthermore, Notch1 overexpression could offset the suppressing effect of XIST knockdown or miR-137 overexpression on cell proliferation. Therefore, XIST may play an important role in promoting cell .these results proposed that XIST functioned as an endogenous sponge in promoting PC cell proliferation through competing for miR-137 to regulate Notch1 expression, and may provide more therapeutic targets for the patients with PC.	33336734	RID03589	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	ICMT-DT	CNN1	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+);tumorigenesis(+);	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225077	GRCh38_1:6234692-6239444	ENSG00000130176	NA	148645	1264	C1orf211|LINC00337|MGC40168|NCRNA00337	Sm-Calp|SMCC	LINC00337 promotes tumor angiogenesis in colorectal cancer by recruiting DNMT1, which suppresses the expression of CNN1.MTT-based method, Transwell migration/invasion assays, and tube formation assay were adopted to evaluate the cancer cell proliferation, migration/invasion, and proangiogenetic potency respectively in vitro. The tumor growth, microvascular density (MVD) and markers of proliferation (Ki67) and angiogenesis (VEGF) were quantified in nude mice xenografted with CRC cells. It was found that CNN1 downregulation and LINC00337 overexpression occurred in CRC tissues and cells. Besides, the CNN1 promoter region was hypermethylated in CRC. CNN1 overexpression or LINC00337 knockdown restricted CRC cell proliferation, migration/invasion, and proangiogenetic potency in vitro, which was substantiated by the in vivo experiments evidenced by facilitated tumor growth and MVD as well as elevated Ki67 and VEGF. Furthermore, our mechanistic evidence revealed that LINC00337 recruited DNMT1 to the promoter region of CNN1 and restricted the transcription of CNN1. Taken together, this study indicates that LINC00337 facilitates the tumorigenesis and angiogenesis in CRC via recruiting DNMT1 to inhibit the expression of CNN1.	33328585	RID03590	epigenetic regulation	NA		UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Acute myeloid leukemia	SNHG5	CCN2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-26b)	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000118523	NA	387066	1490	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	CTGF|IGFBP8	LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia.LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia.The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.	33318617	RID03591	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Lung cancer	AFAP1-AS1	HDGF	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-545-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000143321	NA	84740	3068	AFAP1-AS|AFAP1AS|MGC10981	HMG1L2	The knockdown of LncRNA AFAP1-AS1 suppressed cell proliferation, migration, and invasion, and promoted apoptosis by regulating miR-545-3p/hepatoma-derived growth factor axis in lung cancer.This study aimed to elucidate the functional mechanisms of AFAP1-AS1 and miR-545-3p in lung cancer. Quantitative real time polymerase chain reaction was carried out to determine the levels of AFAP1-AS1, miR-545-3p and hepatoma-derived growth factor (HDGF). Cell proliferation, apoptosis, migration and invasion were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry, and transwell migration and invasion assays, respectively. Furthermore, the interaction between miR-545-3p and AFAP1-AS1 or HDGF was predicted by bioinformatics analysis software starbase and confirmed by the dual-luciferase reporter assay. western blot assay was used to detect the protein level of HDGF. Besides, murine xenograft model was conducted through injecting A549 cells transfected with sh-AFAP1-AS1. The expression levels of AFAP1-AS1 and HDGF were increased, while miR-545-3p was decreased in lung cancer tissues and cells. AFAP1-AS1 knockdown suppressed lung cancer cell proliferation, migration, and invasion and induced apoptosis. Furthermore, AFAP1-AS1 mediated cell progression through regulating miR-545-3p expression. In addition, miR-545-3p negatively regulated the expression level of HDGF via binding 3'-untranslated region of HDGF. As expected, AFAP1-AS1 knockdown inhibited lung cancer progression via affecting miR-545-3p/HDGF axis. Besides, AFAP1-AS1 knockdown suppressed lung cancer tumor growth in vivo. Collectively, our results suggested that AFAP1-AS1 promoted the development of lung cancer via regulating miR-545-3p/HDGF axis, providing a potential target for the treatment of lung cancer.	33290312	RID03592	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Non-hodgkin lymphoma	CASC2	APC	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-155-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hematologic cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000134982	NA	255082	324	C10orf5	DP2|DP2.5|DP3|PPP1R46	[The Molecular Mechanism of LncRNA-CASC2/miR-155-5p/APC Axis Regulating the Progression of Non-Hodgkin Lymphoma]The expression level of CASC2 and miR-155-5p in NHL cell lines were examined by qRT-PCR Dual-luciferase reporter gene assay was used to verify the relationship between miR-155-5p, CASC2 and APC. The effects of CASC/miR-155-5p/APC axis to the proliferation, invasion and apoptosis of NK-92 cells were detected by MTT, Transwell assay and flow cytometry assay, respectively.CASC2 was downregulated in NHL cell lines. Overexpression of CASC2 could inhibit the proliferation and invasion of NK-92 cells, and promote its apoptosis. Dual-luciferase reporter gene assay confirmed that there was a targeting relationship between miR-155-5p, CASC2 and APC. The restoration experiments proved that knockdown of both miR-155-5p and CASC2 or APC could restore the inhibitory effect of miR-155-5p silencing to the biological behavior of NK-92 cells.Overexpression of CASC2 suppresses the proliferation and invasion of NK-92 cells, promote the apoptosis of NK-92 cells via targeting miR-155-5p and upregulating APC expression.	33283723	RID03593	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Uveal melanoma	GAS5	miR-21	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell viability(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Uveal cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Non-Coding RNA GAS5 Targeting microRNA-21 to Suppress the Invasion and Epithelial-Mesenchymal Transition of Uveal Melanoma.The expression levels of GAS5 and microRNA-21 (miR-21) in UM tissues and cells were detected by qRT-PCRanalysis. CCK-8 assay was performed to investigate the viability of UM cells after cell transfections, and the migration and invasion of UM cells were determined by transwell assay. The protein expression levels were detected by western blot assay. The relationship between miR-21 and GAS5 in UM cells was confirmed by bioinformatics prediction and luciferase report assay.Our experiments demonstrated that GAS5 was markedly downregulated in UM cells and clinical specimens. Overexpression of GAS5 inhibited, whereas knockdown of GAS5 promoted the viability, migration, and invasion of UM cells. The epithelial-to-mesenchymal transition (EMT) process of UM cells was also suppressed by upregulating of GAS5 and enhanced by downregulating of GAS5. Additionally, as a competitive endogenous RNA (ceRNA), GAS5 directly binded to the oncogenic miR-21 in UM cells, and overexpression of miR-21 attenuated the EMT-suppressing effect of GAS5.Taken together, our findings suggest that GAS5/miR-21 axis is implicated in the pathogenesis of UM and might serve as a potential therapeutic target.	33273862	RID03594	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	TMPO-AS1	miR-383-5p	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000257167	GRCh38_12:98512973-98516422	NA	NA	100128191	NA	NA	NA	LncRNA TMPO-AS1 Promotes Proliferation and Invasion by Sponging miR-383-5p in Glioma Cells.Expression levels of TMPO-AS1 and miR-383-5p in glioma cell lines were measured by real-time quantitative PCR (RT-qPCR). CCK-8, colony formation, wound-healing, and Transwell assays were conducted to determine cell proliferation, migration and invasion abilities, respectively. western blot was applied to detect the expression of corresponding proteins. Immunofluorescence assay was performed to measure the expression of Ki67. The binding condition between TMPO-AS1 and miR-383-5p was verified by dual-luciferase reporter assay.We found that TMPO-AS1 was up-regulated while miR-383-5p was down-regulated in glioma cell lines, and knockdown of TMPO-AS1 significantly suppressed glioma cell proliferation, migration and invasion abilities. miR-383-5p was demonstrated to be a direct target of TMPO-AS1. Besides, inhibition of miR-383-5p abolished the effects of TMPO-AS1 knockdown on glioma cells. our study revealed that inhibition of lncRNA TMPO-AS1 could suppress glioma progression through targeting miR-383-5p. TMPO-AS1 might be used as a therapeutic target for glioma treatment.	33262650	RID03595	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	
Atherosclerosis	H19	PAPPA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-599)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000182752	NA	283120	5069	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ASBABP2|DIPLA1|IGFBP-4ase|PAPA|PAPP-A|PAPPA1	Knockdown of H19 Attenuates Ox-LDL-induced Vascular Smooth Muscle Cell Proliferation, Migration, and Invasion by Regulating miR-599/PAPPA Axis.Our results showed that H19 expression was elevated in serum samples of AS patients and ox-LDL-treated HA-VSMC. H19 silence mitigated ox-LDL-induced proliferation, migration and invasion of HA-VSMC. H19 acted as a sponge for miR-599, and miR-599 knockdown reversed the suppressive effect of H19 silence on proliferation, migration and invasion of HA-VSMC. PAPPA was a target of miR-599, and attenuated the inhibitive role of miR-599 in HA-VSMC processes. H19 knockdown repressed PAPPA expression by increasing miR-599. Moreover, H19 interference alleviated hyperlipidemia response in HFD-treated ApoE mice. Collectively, knockdown of H19 inhibited proliferation, migration and invasion of ox-LDL-treated HA-VSMC and hyperlipidemia response in HFD-treated ApoE mice by regulating miR-599/PAPPA axis, indicating H19 might act as a potential target for the treatment of AS.	33235026	RID03596	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DOWN(PAAD);DATA(GSE117623,GSE40174)
Spermatogonia	AGO2	CBL	positively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-122-5p)	regulation	NA	NA	NA	Evading Apoptosis	Other	Spermatogonia	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000110395	NA	27161	867	CASC7|EIF2C2|hAGO2|LINC00980|Q10	c-Cbl|CBL2|RNF55	LncRNA CASC7 competed with miRNA-122-5p, and it suppressed the inhibition of CBL. Collectively, these results implicate that miRNA-122-5p enhances the proliferation and DNA synthesis and inhibits the early apoptosis of human SSCs by targeting CBL and competing with lncRNA CASC7. Therefore, this study provides novel insights into epigenetic regulation of fate determinations of human SSCs, and it offers new targets for gene therapy of male infertility that is associated with aging.	33231565	RID03597	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	GAS6-AS1	SETD1A	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	ceRNA(miR-324-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000233695	GRCh38_13:113815630-113845744	ENSG00000099381	NA	650669	9739	NA	KIAA0339|KMT2F|Set1|SET1A	LncRNA GAS6-AS1 facilitates the progression of breast cancer by targeting the miR-324-3p/SETD1A axis to activate the PI3K/AKT pathway.our findings showed that GAS6-AS1 expression was significantly elevated in breast cancer tissues and cell lines, and the high level of GAS6-AS1 reflected a poor prognosis of patients with breast cancer. Moreover, GAS6-AS1 knockdown suppressed cell proliferation, migration and invasion as well as facilitated cell apoptosis. We further found that the depletion of GAS6-AS1 suppressed the PI3K/AKT signaling pathway through inhibiting the levels of pathway-related proteins. Mechanically, GAS6-AS1 acted as a competing endogenous RNA (ceRNA) to sponge miR-324-3p and upregulate SETD1A expression. Besides, GAS6-AS1 activated the PI3K/AKT pathway by targeting the miR-324-3p/SETD1A axis. Rescue assays showed that SETD1A overexpression or 740Y-P treatment reversed the inhibitory effect of silenced GAS6-AS1 on cellular progresses of breast cancer. In summary, this work first explored the molecular regulatory mechanism of GAS6-AS1 in breast cancer cells and revealed that GAS6-AS1 facilitated the malignant behaviors of breast cancer cells by the miR-324-3p/SETD1A axis to activate the PI3K/AKT pathway.	33223203	RID03598	ceRNA or sponge	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	HCG11	PBX3	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000167081	NA	493812	5090	bK14H9.3|FLJ14049|FLJ30357	NA	Knockdown of lncRNA HCG11 suppresses cell progression in ovarian cancer by modulating miR-144-3p/PBX3.The upregulated of HCG11 was observed in OC tissues and OC cell lines. Moreover, miR-144-3p was down expressed in OC tissues and cell lines. Functionally, the knockdown of HCG11 prevented cell viability of SKOV3 cells, while miR-144-3p inhibitor abrogated the suppressor on cell progression. Furthermore, PBX3 was verified to be a target gene of miR-144-3p. In addition, PBX3 knockdown prevented the cell progression of SKOV3 cells.CONCLUSIONS: These data displayed that the knockdown of HCG11 prevented cell progression in OC by sponging miR-144-3p and downregulating PBX3. All results revealed that HCG11 can be a potential therapeutic target for OC therapy. RT-qPCR analysis was applied to detect the expression of HCG11, miR-144-3p and PBX3 in OC tissues and cell lines. MTT assay and transwell assay were opted to measure the cell viability of OC cells. The protein expression level of PBX3 was measured by western blot assay. dual-luciferase reporter assay was carried out to assess the correlation between HCG11, miR-144-3p and PBX3.	33215418	RID03599	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE111842,GSE55807)
Oral squamous cell carcinoma	XIST	miR-27b-3p	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	LncRNA XIST promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by downregulating miR-27b-3p.The results showed that lncRNA XIST was upregulated in OSCC tissues, cell lines, and CDDP-resistant OSCC cells. Functionally, upregulation of lncRNA XIST promoted cell proliferation, enhanced CDDP resistance, and inhibited apoptosis in OSCC cells. In addition, lncRNA XIST acts as a molecular sponge for miR-27b-3p in OSCC. Downregulation of miR-27b-3p partially reversed the tumor suppression effect and CDDP chemosensitivity of XIST knockdown in CDDP-resistant OSCC cells. In conclusion, lncRNA XIST promotes cell proliferation and enhances resistance to CDDP in OSCC by downregulating miR-27b-3p.	33191714	RID03600	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Rheumatoid arthritis	ZFAS1	MMP-15	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-)	ceRNA(miR-296-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 silencing alleviates rheumatoid arthritis via blocking miR-296-5p-mediated down-regulation of MMP-15.Herein, the RA mouse model and the human RA synoviocyte MH7A cell lines stimulated with TNF-alpha were established. ZFAS1 was next determined to be highly expressed in the mice with RA-like symptoms and TNF-alpha-stimulated MH7A cells while inhibiting ZFAS1 was demonstrated to promote proliferation and suppress apoptosis of MH7A cells. Furthermore, ZFAS1 knockdown exerted anti-inflammation effect in vitro and in vivo and reduced the arthritis index value. Moreover, RNA immunoprecipitation and dual-luciferase reporter assays identified the binding of ZFAS1 to microRNA (miR)-296-5p as well as the binding of miR-296-5p to matrix metalloproteinase-15 (MMP-15). Of note, ZFAS1 could bind miR-296-5p to up-regulate the expression of MMP-15. Our results from in vitro and in vivo experiments demonstrated silencing ZFAS1 mitigated RA-like symptoms such as inflammation and hyperplasia via miR-296-5p-dependent inhibition of MMP-15. Taken altogether, our study confirmed that ZFAS1 involved in RA progression by competitively binding to miR-296-5p and regulating MMP-15 expression.	33191176	RID03601	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Sepsis	MALAT1	miR-150	negatively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MicroRNA-150 affects endoplasmic reticulum stress via MALAT1-miR-150 axis-mediated NF-kB pathway in LPS-challenged HUVECs and septic mice.MiR-150 was downregulated in LPS-induced HUVECs. MiR-150 mimics restrained LPS-induced inflammatory response by reducing TNF-alpha and IL-6 levels, but increasing IL-10 level. Moreover, miR-150 mimics downregulated endoplasmic reticulum (ER) stress-related proteins, GRP78 and CHOP levels in LPS-exposed HUVECs. Additionally, LPS-induced apoptosis was suppressed by miR-150 mimics via decreasing cleaved caspase-3 and Bax levels, while enhancing Bcl-2 level. Mechanistically, MALAT1 could competitively bind to miR-150. LPS-induced apoptosis, ER stress and inflammation were promoted by MALAT1 overexpression, but reversed by siMALAT1. Furthermore, miR-150 inhibitor strengthened LPS-induced apoptosis, ER stress and inflammation, which could be attenuated by siMALAT1 via regulating NF-kB pathway. Finally, agomiR-150 repressed ER stress and inflammatory response in PAECs isolated from septic mice via decreasing MALAT1 level.SIGNIFICANCE: Our findings suggest that miR-150 affects sepsis-induced endothelial injury by regulating ER stress and inflammation via MALAT1-mediated NF-kB pathway.	33181172	RID03602	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	AC010789.1	ZEB1	positively-E	luciferase reporter assay;western blot;TCGA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-432-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA AC010789.1 Promotes Colorectal Cancer Progression by Targeting MicroRNA-432-3p/ZEB1 Axis and the Wnt/beta-Catenin Signaling Pathway.Moreover, AC010789.1 silencing inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as tumorigenesis and metastasis in vivo. Mechanistically, we demonstrated that repression of AC010789.1 promoted miR-432-3p expression, and miR-432-3p directly binds to ZEB1. We then proved the anti-tumor role of miR-432-3p in CRC, showing that the inhibitory effect of AC010789.1 knockdown on CRC cells was achieved by the upregulation of miR-432-3p but downregulation of ZEB1. We also established that silencing AC010789.1 suppressed the Wnt/beta-catenin signaling pathway. However, this inhibitory effect was partially counteracted by inhibition of miR-432-3p. In summary, these results reveal that silencing AC010789.1 suppresses CRC progression via miR-432-3p-mediated ZEB1 downregulation and suppression of the Wnt/beta-catenin signaling pathway, highlighting a potentially promising strategy for CRC treatment.	33178684	RID03603	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Adhesions of uterus	SNHG5	FOXF2	negatively-E	western blot;CHIP-seq	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Reproductive system disease	Uterine disease	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000137273	NA	387066	2295	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	FKHL6|FREAC2	si-SNHG5-FOXF2 inhibits TGF-beta1-induced fibrosis in human primary endometrial stromal cells by the Wnt/beta-catenin signalling pathway.FOXF2 was highly expressed in the endometrium of patients with IUA. Treatment of primary HESCs with 10<U+2009>ng/ml TGF-beta1 for 72<U+2009>h was found to be most effective for developing an IUA cell model. FOXF2 regulated multiple downstream target genes, including collagen, vimentin (VIM) and cyclin D2/DK4, by ChIP-seq and ChIP-PCR. FOXF2 downregulation inhibited TGF-beta1-mediated primary HESC fibrosis, including ECM formation, cell proliferation and Wnt/beta-catenin signalling pathway-related protein expression. We identified lncRNA SNHG5 as an upstream gene that directly regulates FOXF2 by RIP-seq, qRT-PCR WB and FISH. SNHG5 downregulation suppressed FOXF2 expression in the IUA cell model, resulting in synergistic repression of the Wnt/beta-catenin pathway, thereby altering TGF-beta1-mediated ECM aggregation in endometrial stromal cells ex vivo.Regulation of the Wnt/beta-catenin signalling pathway and ECM formation by si-SNHG5-FOXF2 effectively inhibited the profibrotic effect of TGF-beta1 on primary HESCs. This finding can provide a molecular basis for antagonizing TGF-beta1-mediated fibrosis in primary HESCs.</AbstractText>: Regulation of the Wnt/beta-catenin signalling pathway and ECM formation by si-SNHG5-FOXF2 effectively inhibited the profibrotic effect of TGF-beta1 on primary HESCs. This finding can provide a molecular basis for antagonizing TGF-beta1-mediated fibrosis in primary HESCs.We induced primary human endometrial stromal cells (HESCs) into myofibroblasts (MFs) to develop an IUA cell model with various concentrations of TGF-beta1 at various times. Downstream target genes of FOXF2 were screened by chromatin immunoprecipitation combined with whole-genome high-throughput sequencing (ChIP-seq). We investigated ECM formation, cell proliferation and Wnt/beta-catenin signalling pathway-related proteins in primary HESCs with FOXF2 downregulation by quantitative reverse transcription-polymerase chain reaction (qRT-PCR, western blot (WB), immunohistochemistry (IHC), flow cytometry, ethylenediurea (EdU) and CCK8 assays. We identified long noncoding RNAs (lncRNA) SNHG5 as the upstream regulatory gene of FOXF2 through RNA immunoprecipitation (RIP), RNA pull-down and fluorescence in situ hybridization (FISH).	33176855	RID03604	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(PAAD);DATA(GSE40174)
Acute myocardial infarction	FGD5	RORA	positively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000154783	GRCh38_3:14810853-14934571	ENSG00000069667	NA	152273	6095	FLJ00274|FLJ39957|ZFYVE23	NR1F1|ROR1|ROR2|ROR3|RZRA	FGD5 antisense RNA 1 (FGD5-AS1) is a long non-coding RNA in acute myocardial infarction (AMI), which is primarily caused by myocardial ischemia-hypoxia. Retinoid acid receptor-related orphan receptor alpha (RORA) is a key protector in maintaining heart function. However, the roles of FGD5-AS1 and RORA in AMI have not previously been elucidated. The present study investigated the effect and mechanism of FGD5-AS1 and RORA in human cardiomyocyte AC16 cells under hypoxia. Reverse transcription-quantitative PCR and western blot demonstrated that FGD5-AS1 and RORA were downregulated in the serum of patients with AMI and hypoxia-challenged AC16 cells. Functional experiments were performed via assays, flow cytometry and western blot. In response to hypoxia, superoxide dismutase (SOD) activity was inhibited, but apoptosis rate and levels of reactive oxygen species and malondialdehyde were promoted in AC16 cells, accompanied by increased Bax and cleaved caspase-3 expression levels, and decreased SOD2 and glutathione peroxidase 1 expression levels. However, hypoxia-induced oxidative stress and apoptosis in AC16 cells were attenuated by ectopic expression of FGD5-AS1 or RORA. Moreover, silencing RORA counteracted the suppressive role of FGD5-AS1 overexpression in hypoxic injury. FGD5-AS1 controlled RORA expression levels via microRNA-195-5p (miR-195), as confirmed by dual-luciferase reporter and RNA pull-down assays. Consistently, miR-195 knockdown suppressed hypoxia-induced oxidative stress and apoptosis in AC16 cells, which was abrogated by downregulating FGD5-AS1 or RORA. In conclusion, FGD5-AS1 modulated hypoxic injury in human cardiomyocytes partially via the miR-195/RORA axis, suggesting FGD5-AS1 as a potential target in interfering with the progression of AMI.	33174051	RID03605	ceRNA or sponge	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE86978)
Atherosclerosis	HIF1A-AS2	ATF2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(-)	NA	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000115966	NA	100750247	1386	3'aHIF-1A|aHIF	CRE-BP1|CREB2|HB16|TREB7	Inhibition of long noncoding RNA HIF1A-AS2 confers protection against atherosclerosis via ATF2 downregulation.Downregulating lncRNA HIF1A-AS2 in ox-LDL-exposed ECs, SMCs and HCAECs inhibited inflammation by reducing levels of pro-inflammatory factors and adhesion molecules. LncRNA HIF1A-AS2 bound to the transcription factor USF1 to elevate ATF2 expression. USF1 overexpression counteracted the suppressive effect of lncRNA HIF1A-AS2 silencing on ox-LDL-induced inflammation. Knockdown of lncRNA HIF1A-AS2 or ATF2 could also attenuate inflammation in atherosclerotic mice. Collectively, the present study demonstrates that downregulation of lncRNA HIF1A-AS2 represses the binding of USF1 to the ATF2 promoter region and then inhibits ATF2 expression, thereby suppressing atherosclerotic inflammation.This study suggests lncRNA HIF1A-AS2 as an promising therapeutic target for atherosclerosis.	33133688	RID03606	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Acute hepatic injury	LINC00472	TRIM8	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell viability(-)	ceRNA(miR-373-3p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000171206	NA	79940	81603	C6orf155|dJ288M22.3|FLJ13189|P53RRA	GERP|RNF27	Down-regulation of long noncoding RNA LINC00472 alleviates sepsis-induced acute hepatic injury by regulating miR-373-3p/TRIM8 axis.LINC00472 and TRIM8 were significantly upregulated in liver tissues and THLE-3 cells in sepsis-induced AHI models, while miR-373-3p was downregulated. Silencing of LINC00472 promoted cell viability and suppressed cell apoptosis in LPS-treated THLE-3 cells, whereas upregulation of LINC00472 had the opposite effect. Moreover, LINC00472 served as a sponge for miR-373-3p and negatively regulated its expression. miR-373-3p mimics could promote THLE-3 cell viability and suppress cell apoptosis. Additionally, TRIM8 was a direct target of miR-373-3p, which was downregulated in LINC00472-silenced cells and upregulated by the miR-373-3p inhibitor. Further, the co-transfection of miR-373-3p inhibitor reversed the effects of LINC00472 knockdown on cell viability and apoptosis. Downregulation of LINC00472 in rats restored the levels of ALT, AST, IL-6, IL-10, and TNF-alpha.Downregulation of LINC00472 ameliorates sepsis-induced AHI by regulating the miR-373-3p/TRIM8 axis.	33129786	RID03607	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	PCGEM1	LGMN	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-642a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000100600	NA	64002	5641	LINC00071|NCRNA00071|PCAT9	LGMN1|PRSC1	Down-regulation of lncRNA PCGEM1 inhibits cervical carcinoma by modulating the miR-642a-5p/LGMN axis.LncRNA PCGEM1 (PCGEM1) has been reported to exert essential effects on the development and progress of various tumors, while the detailed effects and possible mechanisms of PCGEM1 in cervical carcinoma remain unknown. In the present study, PCGEM1 was over-expressed in cervical carcinoma cells as evidenced by real-time quantitative polymerase chain reaction (RT-qPCR) assay. Knockdown of PCGEM1 significantly repressed proliferation, migration, and invasion, while induced G1 arrest in cervical carcinoma cells. In addition, PCGEM1 was predicted to target miR-642a-5p by bioinformatics software, which was further confirmed by luciferase reporter assay. Besides, RT-qPCR assay indicated that miR-642a-5p expression was decreased in cervical carcinoma cells and knockdown of PCGEM1 could accelerate miR-642a-5p expression. Moreover, inhibition of miR-642a-5p partly abolished the functions of PCGEM1 knockdown on proliferation, cell cycle, migration and invasion of cervical carcinoma cells. Furthermore, miR-642a-5p could bind to the 3'-UTR of LGMN, which was over-expressed in the cervical carcinoma cells. Suppression of LGMN partly restored the functions of miR-642a-5p inhibitor on proliferation, cell cycle distribution, migration and invasion in the cervical carcinoma cells treated with the PCGEM1 shRNA. Taken together, our data indicated that knockdown of PCGEM1 inhibited proliferation, migration and invasion in cervical carcinoma by modulating the miR-642a-5p/ LGMN axis.	33121976	RID03608	ceRNA or sponge	NA	UP(PAAD);DATA(GSE60407)	UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Osteosarcoma	GAS5	PTEN	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell growth(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	33121268	RID03609	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Colorectal cancer	MEG3	PDHB	positively-E	luciferase reporter assay;western blot;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-103a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168291	NA	55384	5162	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	PDHE1B	LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway.Furthermore, MEG3 overexpression hindered tumor growth and facilitated ER stress in vivo. Molecularly, miR-103a-3p was a target of MEG3, and further targeted PDHB. Similarly, in function, blocking miR-103a-3p suppressed CC in vitro by affecting proliferation, invasion, and ER stress; in addition, restoring miR-103a-3p partially counteracted the suppressive role of MEG3 in CC cells. MEG3 sponged miR-103a-3p to suppress CC malignancy by inducing ER stress and inhibiting cell proliferation and invasion via upregulating PDHB, suggesting a novel MEG3/miR-103a-3p/PDHB ceRNA pathway.Relative expression of MEG3, miRNA (miR)-103a-3p, and pyruvate dehydrogenase E1 subunit beta (PDHB) was detected by RT-qPCR and western blot. Cell proliferation was measured by CCK-8 assay, colony formation assay, and flow cytometry, as well as xenograft tumor assay. Transwell assay examined cell invasion. Endoplasmic reticulum (ER) stress was evaluated by western blot. dual-luciferase reporter assay and RNA immunoprecipitation determined the relationship between miR-103a-3p and MEG3 or PDHB.	33118833	RID03610	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Lung injury	MALAT1	FOXP2	positively-E	dual-luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Other	Injury	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000128573	NA	378938	93986	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CAGH44|SPCH1|TNRC10	Furthermore, inhibition of miR-194-5p exerted a rescue effect on MALAT1 knockdown of FOXP2, whereas the overexpression of FOXP2 reversed the effect of MALAT1 knockdown on viability and apoptosis of LPS-stimulated HPAEpiC.Our results demonstrated that MALAT1 knockdown alleviated HPAEpiC apoptosis by competitively binding to miR-194-5p and then elevating the inhibitory effect on its target FOXP2. These data provide a novel insight into the role of MALAT1 in the progression of ALI and potential diagnostic and therapeutic strategies for ALI patients.</AbstractText>: Our results demonstrated that MALAT1 knockdown alleviated HPAEpiC apoptosis by competitively binding to miR-194-5p and then elevating the inhibitory effect on its target FOXP2. These data provide a novel insight into the role of MALAT1 in the progression of ALI and potential diagnostic and therapeutic strategies for ALI patients.	33118280	RID03611	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Pre-eclampsia	FAM99A	YAP1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-134-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000205866	GRCh38_11:1665597-1667856	ENSG00000137693	NA	387742	10413	FLJ42833	YAP65	FAM99A and YAP1 were significantly up-regulated, and miR-134-5p was significantly down-regulated in PE tissues (n=30). miR-134-5p was verified as a candidate of FAM99A and YAP1. FAM99A promoted cell metastasis, but reduced apoptosis in HTR8/SVneo cells by regulating miR-134-5p. miR-134-5p down-regulated YAP1 expression to suppress cell metastasis, while it induced apoptosis in HTR8/SVneo cells. FAM99A positively modulated YAP1 expression by sponging miR-134-5p. FAM99A modulated YAP1 to accelerate cell migration and invasion, and inhibited cell apoptosis in PE cells by sponging miR-134-5p. The novel regulatory network may shed light on the pathogenesis of PE.	33111745	RID03612	ceRNA or sponge	metastasis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Lung squamous cell carcinoma	LINC00355	LYAR	positively-E	RNA pull-down assay;luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-466)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227674	GRCh38_13:63851197-64076044	ENSG00000145220	NA	144766	55646	NA	ZC2HC2|ZLYAR	LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis.The results showed that LINC00355 was upregulated in lung SCC and was positively associated with poor overall survival in lung SCC patients. he expression and subcellular location of LINC00355 were determined by qRT-PCRand RNA-FISH, respectively. The lung SCC cell growth was analyzed by CCK-8 assay, transwell invasion, wound healing, colony formation, and flow cytometry assays. Reactive oxygen species level was evaluated by DCFH-DA probes. Bioinformatics online websites, luciferase reporter assay, RNA binding protein immunoprecipitation (RIP), and RNA pull-down assays were utilized to investigate the interaction among LINC00355, miR-466, and Ly-1 antibody reactive clone (LYAR). The results showed that LINC00355 was upregulated in lung SCC and was positively associated with poor overall survival in lung SCC patients. LINC00355 was mainly located in the cytoplasm of SCC cells.	33111744	RID03613	ceRNA or sponge	NA	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Malignant glioma	LINC00707	miR-613	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000238266	GRCh38_10:6779549-6879450	NA	NA	100507127	NA	NA	NA	The Long Intergenic Noncoding RNA 00707 Sponges MicroRNA-613 (miR-613) to Promote Proliferation and Invasion of Gliomas.LINC00707 was up-regulated in gliomas. Up-regulated LINC00707 increased the proliferation, migration and invasion of glioma cells, and silenced LINC00707 reduced these abilities. The increase of the expression level of LINC00707 down-regulated miR-613 in glioma cells, while the inhibition of the expression level of LINC00707 up-regulated miR-613 in glioma cells. The high expression of LINC00707 was related to the Karnofsky performance status (KPS) score and WHO staging. LINC00707 could offset the ability of miR-613 to inhibit glioma proliferation and invasion.CONCLUSION: LINC00707 promotes proliferation and invasion of glioma cells by sponging miR-613. The regulatory axis of LINC00707/miR-613 provides new insights into the mechanism and treatment of gliomas.	33107401	RID03614	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Ovarian cancer	PTPRG-AS1	HDAC4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-545-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000241472	GRCh38_3:62221249-62369406	ENSG00000068024	NA	100506994	9759	NA	BDMR|HA6116|HD4|HDAC-4|HDAC-A|HDACA|KIAA0288	Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays.Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4.CONCLUSIONS: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.	33099316	RID03615	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Malignant glioma	DGCR5	SMAD7	positively-E	western blot	upregulation	microarray;qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000101665	NA	26220	4092	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	MADH7|MADH8	LncRNA DGCR5 plays a tumor-suppressive role in glioma via the miR-21/Smad7 and miR-23a/PTEN axes. LncRNA DGCR5 overexpression significantly inhibited the capacity of glioma cells to proliferate, migrate, and invade, whereas promoted the apoptosis of glioma cells. Moreover, lncRNA DGCR5 overexpression upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker VIM, as well as Snai2 and TWIST. Regarding the underlying molecular mechanisms, lncRNA DGCR5 could inhibit miR-21 and miR-23a expression, and miR-21 or miR-23a overexpression significantly reversed the tumor-suppressive effects of lncRNA DGCR5 overexpression. LncRNA DGCR5 exerted its tumor-suppressive effects through the DGCR5/miR-21/Smad7 and DGCR5/miR-23a/PTEN axes. In conclusion, lncRNA DGCR5 suppresses the capacity of glioma cells to migrate and invade via miR-21/Smad7, whereas it inhibits the proliferation and enhances the apoptosis of glioma cells through miR-23a/PTEN.	33085646	RID03616	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	DGCR5	PTEN	positively-E	western blot	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-23a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000171862	NA	26220	5728	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA DGCR5 plays a tumor-suppressive role in glioma via the miR-21/Smad7 and miR-23a/PTEN axes. LncRNA DGCR5 overexpression significantly inhibited the capacity of glioma cells to proliferate, migrate, and invade, whereas promoted the apoptosis of glioma cells. Moreover, lncRNA DGCR5 overexpression upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker VIM, as well as Snai2 and TWIST. Regarding the underlying molecular mechanisms, lncRNA DGCR5 could inhibit miR-21 and miR-23a expression, and miR-21 or miR-23a overexpression significantly reversed the tumor-suppressive effects of lncRNA DGCR5 overexpression. LncRNA DGCR5 exerted its tumor-suppressive effects through the DGCR5/miR-21/Smad7 and DGCR5/miR-23a/PTEN axes. In conclusion, lncRNA DGCR5 suppresses the capacity of glioma cells to migrate and invade via miR-21/Smad7, whereas it inhibits the proliferation and enhances the apoptosis of glioma cells through miR-24a/PTEN.	33085646	RID03617	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	NORAD	ABCB1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-202-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000085563	NA	647979	5243	LINC00657	ABC20|CD243|CLCS|GP170|MDR1|p-170|P-gp|PGY1	LncRNA NORAD/miR-202-5p regulates the drug resistance of A549/DDP to cisplatin by targeting P-gp.The MTT assay found that miR-202-5p inhibitor reversed the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Then, the western blot data showed that knockdown of NORAD reduced P-gp expression, and miR-202-5p inhibitor enhanced P-gp expression. ABCB1 overexpression reversed the inhibitory effect of NORAD knockdown on A549/DDP cells. Moreover, NORAD could directly bind to miR-202-5p, and ABCB1 was a target of miR-202-5p. Inhibition of miR-202-5p and overexpression of ABCB1 eliminated the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Overexpression of miR-202-5p suppressed P-gp expression in A549/DDP cells. Collectively, our data showed that NORAD could enhance the DDP resistance of A549/DDP cells and potentially increased P-gp expression by sponging the miR-202-5p.	33084601	RID03618	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Malignant glioma	MALAT1	ZEB2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	KIAA0569|SIP-1|SIP1|ZFHX1B	We further found that MALAT1 silencing significantly inhibited glioma cell proliferation while induced cell cycle arrest and apoptosis. In parallel, knockdown of MALAT1 decreased tumor volume in vivo. These results suggested that MALAT1 acts as a functional oncogene, resulting in the oncogenicity in glioma. Nevertheless, the tumor-suppressive effect of MALAT1 silencing was reversed by miR-124. Besides, the relevance of ZEB2 in tumor progression has been studied in several forms of human cancer, and ZEB2 was identified as a target of miR-124 and negatively regulated by miR-124. MALAT1 overexpression or miR-124 inhibitor led to increased expression of ZEB2. In summary, our study depicts a novel pathway of MALAT1/miR-124/ZEB2 that regulates the progression of glioma and might provide a promising strategy for glioma therapy.	33078370	RID03619	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatitis C	LINC01189	miR-155-5p	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Hepatitis	lncRNA	miRNA	ENSG00000232827	GRCh38_9:62452451-62522018	NA	NA	643648	NA	NA	NA	Long noncoding RNA LINC01189 is associated with HCV-hepatocellular carcinoma and regulates cancer cell proliferation and chemoresistance through hsa-miR-155-5p.In HCC cell lines of Huh7 and Hep3B, LINC01189 was upregulated to investigate its effects on cancer cell proliferation and 5-FU chemoresistance. The competing endogenous RNA (ceRNA) target of LINC01189, human microRNA-155-5p (hsa-miR-155-5p) was probed by dual-luciferase assay and qRT-PCR Hsa-miR-155-5p was upregulated in LINC01189-overexpessed Huh7 and Hep3B cells to investigate their epigenetic correlation on HCC development regulation.RESULTS: LINC01189 is downregulated in HCV-infected HCC tumors and cell lines. LINC01189 overexpression inhibited HCC cancer cell proliferation and 5-FU chemoresistance. Hsa-miR-155-5p was confirmed to be a ceRNA target of LINC01189 in HCC. Upregulating hsa-miR-155-5p reversed the LINC01189-mediated inhibition on HCC proliferation and 5-FU chemoresistance.CONCLUSIONS: LINC01189 downregulation is associated with HCV infection in HCC, and it has tumor-suppressing effects on HCC development through hsa-miR-155-5p. LINC01189 downregulation is associated with HCV infection in HCC, and it has tumor-suppressing effects on HCC development through hsa-miR-155-5p.	33059056	RID03620	ceRNA or sponge	chemoresistance		
Hepatocellular carcinoma	MIR503HG	PDCD4	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);angiogenesis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-15b)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000150593	NA	84848	27250	H19X|MGC16121	H731	LncRNA miR503HG inhibits epithelial-mesenchymal transition and angiogenesis in hepatocellular carcinoma by enhancing PDCD4 via regulation of miR-15b.The expressions of miR503HG, miR-15b and PDCD4 in HCC tissues and cell lines were measured. After cell transfection, Transwell assay tested the migration and invasion ability of HCC cells. qRT-PCRand western blot detected the expressions of EMT markers (E-cad, N-cad, Vim and Snail-1). Matrigel-based tube formation assay assessed the angiogenesis capacity of human umbilical vein endothelial cells (HUVECs) cultured in conditioned medium of treated HCC cells. ELISA detected the level of VEGF in supernatant of HUVECs. RIP, RNA pull-down and dual-luciferase reporter assay were applied to verify the binding of miR-15b to miR503HG or PDCD4. pcDNA3.1-miR503HG-BEL-7404 cells or pcDNA3.1-BEL-7404 cells were implanted into nude mice for construction of HCC model in vivo.miR503HG and PDCD4 were under-expressed and miR-15b was over-expressed in HCC cells and tissues. Up-regulation of miR503HG and PDCD4 or inhibition of miR-15b hindered migration, invasion and EMT of HCC cells and angiogenesis of HUVECs. Both miR503HG and PDCD4 could bind to miR-15b. Over-expression of miR503HG suppressed HCC growth and angiogenesis in nude mice. LncRNA miR503HG suppresses EMT and angiogenesis in HCC via miR-15b/PDCD4 axis.	33046427	RID03621	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Tongue squamous cell carcinoma	NEAT1	ITGA3	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000005884	NA	283131	3675	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CD49c|GAP-B3|MSK18|VCA-2|VLA3a	[LncRNA NEAT1 regulates proliferation, migration and invasion of tongue squamous cell carcinoma cells by regulating miR-339-5p/ITGA3 axis]. qRT-PCRand western blot were used to detect the expression of NEAT1, miR-339-5p, ITGA3 mRNA and ITGA3 protein in 25 cases of human tongue squamous cell carcinoma, its corresponding adjacent tissues, human normal oral mucosal cell line HOK and human tongue squamous cell carcinoma cell lines TSCCA, CAL27, SCC15 and HN13. CAL27 cell lines that inhibited NEAT1 and overexpressed miR-339-5p were constructed, respectively. Cell viability was detected by MTT assay, cell numbers of migration and invasion were detected by Transwell assay, and the expression of Cyclin D1 and MMP-9 proteins were detected by western blot. The dual luciferase reporter gene was used to verify the targeting relationship of NEAT1, miR-339-5p and ITGA3, and the regulatory relationship was detected by western blot and qRT-PCR SPSS 17.0 software package was used for statistical analysis of the data.Compared with normal human oral mucosal cell line HOK, the expression of NEAT1 and ITGA3 was up-regulated, while the expression of miR-339-5p was down-regulated in human tongue squamous cell carcinoma cell lines. Inhibition of NEAT1 or over-expression of miR-339-5p significantly inhibited proliferation, migration and invasion of CAL27 cells, and significantly inhibited expression of Cyclin D1 and MMP-9 proteins. Dual luciferase reporter gene assay confirmed that NEAT1 directly interacted with miR-339-5p and suppressed its expression. miR-339-5p negatively regulated ITGA3 expression. Inhibition of NEAT1 reversed the inhibitory effect of the inhibition of miR-339-5p on proliferation, migration and invasion of CAL27 cells.CONCLUSIONS: LncRNA NEAT1 promotes proliferation, migration and invasion of tongue squamous cell carcinoma cells by down-regulating miR-339-5p/ITGA3 axis.	33043343	RID03622	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Pre-eclampsia	GASAL1	SRSF1	positively-E	RNA pull-down assay;western blot;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000136450	NA	401472	6426	GASL1	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	LncRNA GASAL1 Interacts with SRSF1 to Regulate Trophoblast Cell Proliferation, Invasion, and Apoptosis Via the mTOR Signaling Pathway.RNA pull-down assays showed that GASAL1 directly binds with SRSF1 that could promote cell proliferation and invasion and suppress cell apoptosis. Further research showed that promoting effects of trophoblasts proliferation and invasion caused by co-transfecting GASAL1 and SRSF1 into HTR-8/SVneo and JAR cells were impaired by SRSF1 knockdown. Moreover, inhibition of the mammalian target of rapamycin (mTOR) activity by rapamycin influenced the effects of GASAL1 on cell proliferation, invasion, and apoptosis. Taken together, these findings suggest that lncRNA GASAL1 interacts with SRSF1 to regulate the proliferative, invasive, and apoptotic abilities of trophoblast cells via the mTOR signaling pathway.GASAL1 was significantly downregulated in the placentas' of tissues from primipara with PE and trophoblast cell lines. Then, the upregulation of GASAL1 dramatically decreased proliferation and invasion and enhanced apoptosis in HTR-8/SVneo and JAR cells. Bioinformatics tool predicated that there is a potential interaction between GASAL1 and serine/arginine splicing factor 1 (SRSF1). RNA pull-down assays showed that GASAL1 directly binds with SRSF1 that could promote cell proliferation and invasion and suppress cell apoptosis. Further research showed that promoting effects of trophoblasts proliferation and invasion caused by co-transfecting GASAL1 and SRSF1 into HTR-8/SVneo and JAR cells were impaired by SRSF1 knockdown. Moreover, inhibition of the mammalian target of rapamycin (mTOR) activity by rapamycin influenced the effects of GASAL1 on cell proliferation, invasion, and apoptosis. Taken together, these findings suggest that lncRNA GASAL1 interacts with SRSF1 to regulate the proliferative, invasive, and apoptotic abilities of trophoblast cells via the mTOR signaling pathway.	33028104	RID03623	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LINC01089	BTG2	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000212694	GRCh38_12:121795267-121803906	ENSG00000159388	NA	338799	7832	AK096174|LIMT	APRO1|MGC126063|MGC126064|PC3|TIS21	LINC01089 inhibits the progression of cervical cancer via inhibiting miR-27a-3p and increasing BTG2.The interactions between LINC01089 and miR-27a-3p were verified by bioinformatics, a dual luciferase reporter gene experiment and a RNA immunoprecipitation experiment, respectively.RESULTS: The expression of LINC01089 in CC was markedly down-regulated. The low expression of LINC01089 in CC was closely associated with a larger tumor size and positive lymph node metastasis. Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had the opposite biological functions. In terms of mechanism, LINC01089 could sponge miR-27a-3p and indirectly up-regulate BTG2 expression.CONCLUSIONS: LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.The expression of LINC01089 in CC was markedly down-regulated. The low expression of LINC01089 in CC was closely associated with a larger tumor size and positive lymph node metastasis. Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had the opposite biological functions. In terms of mechanism, LINC01089 could sponge miR-27a-3p and indirectly up-regulate BTG2 expression.LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.	33025678	RID03624	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	LUCAT1	KLF6	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000067082	NA	100505994	1316	SCAL1|SCAT5	BCD1|COPEB|CPBP|GBF|PAC1|ST12|Zf9	LncRNA LUCAT1/miR-181a-5p axis promotes proliferation and invasion of breast cancer via targeting KLF6 and KLF15.A total of 31 breast cancer patients who underwent tumor resection, but without chemo- or radiotherapy or acute lung/heart/kidney diseases, provided tumor and adjacent normal tissues. Bioinformatic analysis, qRT-PCR and luciferase reporter assay were carried out during the study.qRT-PCRanalysis indicated that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, LUCAT1 was markedly up-regulated in the breast cancer tissues and five BC cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7. The knockdown of LUCAT1, through the transfection of small interfering RNA (siRNA) specific to LUCAT1, resulted in inhibition of proliferation in breast cancer cells. The expression levels of miR-181a-5p were decreased in the breast cancer tissues and five BC cell lines. Bioinformatic analysis and luciferase reporter assay suggested the interaction between miR-181a-5p and LUCAT1. In addition, the effects of LUCAT1 on promoting cell proliferation were attenuated by overexpression of miR-181a-5p through the transfection of miR-181a-5p mimic. Moreover, bioinformatics and luciferase reporter assay confirmed that miR-181a-5p targeted the 3'-UTR region of KLF6 and KLF15 mRNA, which were two tumor suppressor genes. LUCAT1/miR-181a-5p axis regulated the expression of KLF6 and KLF15 both in vitro and in vivo.	32998707	RID03625	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE67939)
Kidney injury	MALAT1	HMGB1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-370-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Injury	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DKFZp686A04236|HMG1|HMG3|SBP-1	Lnc-MALAT1 was increased both in the serum of sepsis patients and cells injured by LPS, which could inhibit the cell proliferation, promote the cell apoptosis and increase the expression of TNF-alpha, IL-6 and IL-1beta caused by paclitaxel. Moreover, lnc-MALAT1 was sponged with miR-370-3p which had the inverse effects with lnc-MALAT1 in LPS induced HK-2 cells. What's more, miR-370-3p targeted HMGB1 which was induced in serum and cells of sepsis. Knockdown of miR-370-3p inhibited the expression of HMGB1 and suppressed the proliferation but promoted the apoptosis of HK-2 cells injured by LPS as well as the expression of TNF-alpha, IL-6 and IL-1beta. Besides, paclitaxel restrained the expression of HMGB1 via regulating lnc-MALAT1/miR-370-3p axis.SIGNIFICANCE: Paclitaxel could protect against LPS-induced AKI via the regulation of lnc-MALAT1/miR-370-3p/HMGB1 axis and the expression of TNF-alpha, IL-6 and IL-1beta, revealing that paclitaxel might act as a therapy drug in reducing sepsis-associated AKI.	32998017	RID03626	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Sepsis-induced myocardial injury	H19	SORBS2	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell injury(-)	ceRNA(miR-93-5p)	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000154556	NA	283120	8470	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ARGBP2|KIAA0777	LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis.H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury via regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury in vitro via modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.	32996061	RID03627	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065)
Urinary bladder cancer	TUG1	CAPN7	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-29c-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000131375	NA	55000	23473	FLJ20618|LINC00080|NCRNA00080	PalBH	[Mir-29c-3p targeting TUG1 affects migration and invasion of bladder cancer cells by regulating CAPN7 expression].Trans-well assay was used to detect the changes in migration and invasion abilities of bladder cancer T24 cells after TUG1 knockdown using RNA interference technique, and the alteration in the expression of CAPN7 was also detected. The expression of CAPN7 was examined in T24 cells overexpressing mir-29c-3p by western blot, and luciferase reporter assay was performed to confirm the targeting of miR-29c-3p to TUG1 and CAPN7. The effects of CAPN7 overexpression and sh-TUG1 on the migration and invasion of T24 cells were investigated.CONCLUSIONS: Mir-29c-3p targeting TUG1 affects the migration and invasion of bladder cancer cells by regulating the expression of CAPN7.The expression of TUG1 was up-regulated and mir-29c-3p was down-regulated significantly in bladder cancer tissue with a negative correlation between their expressions. TUG1 knockdown significantly inhibited the migration and invasion of T24 cells (P < 0.01). Overexpression of mir-29c-3p in T24 cells obviously down-regulated the expression of CAPN7 protein, whose expression was positively correlated with TUG1 expression (r=0.4081, P=0.0139). The results of luciferase reporter assay confirmed both TUG1 and CAPN7 as the targets of mir-29c-3p. CAPN7 overexpression could partially reverse the tumor suppressing effect of sh-TUG1 in T24 cells.Conclusions: Mir-29c-3p targeting TUG1 affects the migration and invasion of bladder cancer cells by regulating the expression of CAPN7.	32990242	RID03628	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE86978)
Hepatocellular carcinoma	TMPO-AS1	GOT1	positively-E	RNA pull-down assay;western blot;luciferase reporter assay;starBase database	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);	ceRNA(miR-429)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000120053	NA	100128191	2805	NA	AST1	LncRNA TMPO-AS1 Aggravates the Development of Hepatocellular Carcinoma via miR-429/GOT1 Axis.Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression of TMPO-AS1, miR-429 and GOT1 in HCC tissues and cell lines. Cell viability, proliferation, apoptosis, and stemness characteristics were detected by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, sphere formation and western blot assays, separately. The relationship among TMPO-AS1, miR-429 and GOT1 was predicted by starBase database and confirmed using luciferase reporter and RNA pull-down assays..In this study, our findings revealed that TMPO-AS1 expression was upregulated in HCC tissues and cell lines. TMPO-AS1 aggravated HCC progression via promoting cell proliferation, stemness as well as suppressing cell apoptosis. Further, molecular mechanism exploration discovered that TMPO-AS1 functioned as a molecular sponge for miR-429 and GOT1 served as a downstream target gene of miR-429 in HCC. Furthermore, there was a negative relationship between GOT1 and miR-429 as well as a positive correlation between GOT1 and TMPO-AS1 in HCC. Rescue assays suggested that overexpression of GOT1 partially reversed the inhibitory effects of TMPO-AS1 knockdown on HCC progression.Taken together, these findings indicated that TMPO-AS1 acted as a tumor motivator to expedite HCC progression via targeting miR-429/GOT1 axis, which may provide a fresh treatment strategy for HCC.</AbstractText>: Taken together, these findings indicated that TMPO-AS1 acted as a tumor motivator to expedite HCC progression via targeting miR-429/GOT1 axis, which may provide a fresh treatment strategy for HCC.	32988599	RID03629	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	UP(PAAD,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Hepatocellular carcinoma	CR594175	CTNNB1	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);tumor growth(-)	ceRNA(miR-142-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000168036	NA	NA	1499	NA	armadillo|beta-catenin|CTNNB	A study of the mechanism of lncRNA-CR594175 in regulating proliferation and invasion of hepatocellular carcinoma cells in vivo and in vitro.The results revealed that lncRNA-CR594175, as a RNA sponge, broke the negative regulation of hsa-miR-142-3p on Catenin, beta-1 (CTNNB1), and once lncRNA-CR594175 was silenced, the hsa-miR142-3p regained its negative regulation on CTNNB1 which can promote HCC progression by activating the wnt pathway.Our present study demonstrated for the first time that lncRNA-CR594175 silencing suppressed proliferation and invasion of HCC cells in vivo and in vitro by restoring the negative regulation of hsa-miR-142-3p on CTNNB1, laying a solid theoretical base for using lncRNA-CR594175 as genetic target therapy for HCC and offering a reasonable explanation for inactivation of miRNA in different tumors or in the tumor at different stages.</AbstractText>: Our present study demonstrated for the first time that lncRNA-CR594175 silencing suppressed proliferation and invasion of HCC cells in vivo and in vitro by restoring the negative regulation of hsa-miR-142-3p on CTNNB1, laying a solid theoretical base for using lncRNA-CR594175 as genetic target therapy for HCC and offering a reasonable explanation for inactivation of miRNA in different tumors or in the tumor at different stages.	32983253	RID03630	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Rheumatoid arthritis	NEAT1	YY1	positively-E	luciferase assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);	ceRNA(miR-410-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100811	NA	283131	7528	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	LncRNA NEAT1 Targets Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via the miR-410-3p/YY1 Axis.LncRNA NEAT1 functions as an oncogene in multiple human cancers. However, its expression and role in fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA) remain unclear. Thus, we investigated the expression of NEAT1 in synovial tissues and FLSs in RA, to determine its role in the development of RA. Quantitative real-time polymerase chain reaction was used to measure the expression of NEAT1. FLS proliferation was evaluated using cell proliferation assays. Flow cytometry was used to analyze cell cycle progression and apoptosis in FLSs. Binding between NEAT1 and miR-410-3p was demonstrated by dual-luciferase assays. We found that NEAT1 was upregulated in synovial tissues and FLSs in RA. Upregulation of NEAT1 promoted cell proliferation, induced S-to G2/M phase transition, and suppressed apoptosis in RA FLSs. NEAT1 directly bound to and negatively modulated miR-410-3p expression, while positively regulating YinYang 1(YY1; a miR-410-3p target). Inhibiting miR-410-3p and upregulating YY1 partially restored the inhibitory role in cell viability induced by the depletion of NEAT1 in RA FLSs. Besides pro-proliferative and anti-apoptotic roles, upregulation of NEAT1 promoted migration, invasion, and inflammatory cytokines secretion in RA FLSs. Taken together, our results suggest that the NEAT1 may serve as a novel diagnostic and therapeutic target for patients with RA.	32983133	RID03631	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Atherosclerosis	HOXA-AS3	CDKN1B	positively-E	RNA pull-down assay;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-455-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000254369	GRCh38_7:27129977-27155928	ENSG00000111276	NA	100133311	1027	HOXA6as	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Knockdown of lncRNA HOXA-AS3 Suppresses the Progression of Atherosclerosis via Sponging miR-455-5p.Finally, in vivo model of atherosclerosis was established to confirm the function of HOXA-AS3 during the development of atherosclerosis in vivo.LncRNA HOXA-AS3 was upregulated in oxLDL-treated HUVECs. In addition, oxLDL-induced growth inhibition of HUVECs was significantly reversed by knockdown of HOXA-AS3. Consistently, oxLDL notably induced G1 arrest in HUVECs, while this phenomenon was greatly reversed by HOXA-AS3 siRNA. Furthermore, downregulation of HOXA-AS3 notably inhibited the progression of atherosclerosis through mediation of miR-455-5p/p27 Kip1 axis. Besides, silencing of HOXA-AS3 notably relieved the symptom of atherosclerosis in vivo.</AbstractText>: LncRNA HOXA-AS3 was upregulated in oxLDL-treated HUVECs. In addition, oxLDL-induced growth inhibition of HUVECs was significantly reversed by knockdown of HOXA-AS3. Consistently, oxLDL notably induced G1 arrest in HUVECs, while this phenomenon was greatly reversed by HOXA-AS3 siRNA. Furthermore, downregulation of HOXA-AS3 notably inhibited the progression of atherosclerosis through mediation of miR-455-5p/p27 Kip1 axis. Besides, silencing of HOXA-AS3 notably relieved the symptom of atherosclerosis in vivo.Downregulation of HOXA-AS3 significantly suppressed the progression of atherosclerosis via regulating miR-455-5p/p27 Kip1 axis. Thus, HOXA-AS3 might serve as a potential target for the treatment of atherosclerosis.</AbstractText>: Downregulation of HOXA-AS3 significantly suppressed the progression of atherosclerosis via regulating miR-455-5p/p27 Kip1 axis. Thus, HOXA-AS3 might serve as a potential target for the treatment of atherosclerosis.	32982172	RID03632	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hypopharyngeal squamous cell carcinoma	MALAT1	ZEB1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-429)	regulation	NA	NA	NA	NA	Cancer	Squamous cell carcinoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Inhibition of long non-coding RNA MALAT1 elevates microRNA-429 to suppress the progression of hypopharyngeal squamous cell carcinoma by reducing ZEB1.The PI3K/Akt/mTOR signaling pathway-related proteins, proliferation-related proteins, cell cycle-related proteins, apoptosis-related proteins, and migration-related proteins were detected using western blot The cell growth in vivo was observed. The targeting relationships between MALAT1 and miR-429, and between miR-429 and ZEB1 were confirmed..MALAT1 and ZEB1 expression in HSCC was upregulated while miR-429 expression was downregulated. Reduced MALAT1 and ZEB1, and upregulated miR-429 inactivated the PI3K/Akt/mTOR signaling pathway, suppressed in vitro viability, colony formation ability, migration and invasion, as well as cell growth in vivo, and promoted the apoptosis of FaDu cells. Downregulated miR-429 reversed the role of MALAT1 inhibition in FaDu cell growth. LncRNA MALAT1 served as a sponge of miR-429, thus regulating ZEB1 expression.CONCLUSION: Inhibition of MALAT1 was able to elevate miR-429 to suppress the progression of HSCC via reducing ZEB1. Our research provided a potential therapeutic target for HSCC.	32980391	RID03633	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	BCYRN1	CUEDC2	positively-E	RNA pull-down assay;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-619-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000107874	NA	618	79004	BC200|BC200a|LINC00004|NCRNA00004	C10orf66|MGC2491	LncRNA BCYRN1 inhibits glioma tumorigenesis by competitively binding with miR-619-5p to regulate CUEDC2 expression and the PTEN/AKT/p21 pathway Differential RNA transcripts and BCYRN1 were identified by RT-qPCR in glioma samples and controls. CCK-8, colony formation assays, flow cytometry, TUNEL assays, cell migration assays, wound-healing assays, and xenograft model were established to investigate the biological function of BCYRN1 both in vitro and in vivo. Various bioinformatics analysis, dual-luciferase reporter assays, biotinylated RNA pull-down assays, and rescue experiments were conducted to reveal the underlying mechanisms of competitive endogenous RNAs (ceRNAs). 183 lncRNAs were identified with significant dysregulation in glioma and randomly selected differential RNAs were further confirmed by RT-qPCR. Among them, BCYRN1 was the most downregulated lncRNA, and its low expression positively correlated with glioma progression. Functionally, BCYRN1 overexpression inhibited cell proliferation, migration in glioma cell lines, whereas BCYRN1 depletion resulted in the opposite way. MiR-619-5p was further confirmed as the direct target of BCYRN1. Mechanistically, miR-619-5p specifically targeted the CUE domain containing protein 2 (CUEDC2), and BCYRN1/miR-619-5p suppressed glioma tumorigenesis by inactivating PTEN/AKT/p21 pathway in a CUEDC2-dependent manner. Overall, our data presented that the reduced expression of BCYRN1 was associated with poor patient outcome in glioma. BCYRN1 functioned as a ceRNA to inhibit glioma progression by sponging miR-619-5p to regulate CUEDC2 expression and PTEN/AKT/p21 pathway. Our results indicated that BCYRN1 exerted tumor suppressor potential and might be a candidate in the diagnosis and treatment of glioma.	32978519	RID03634	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Lung injury	Hsp4	DNAJB6	positively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-466m-3p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000105993	NA	NA	10049	NA	LGMD1D|MRJ	Long non-coding RNA Hsp4 alleviates lipopolysaccharide-induced apoptosis of lung epithelial cells via miRNA-466m-3p/DNAjb6 axis.In our research, we found that LPS treatment remarkably induced apoptosis of MLE-12 cells and decreased the expression of Hsp4. Overexpression of Hsp4 significantly reversed LPS-induced cell apoptosis through inhibiting mTOR signaling, while suppression of Hsp4 presented opposite effects. Further results showed that Hsp4 positively regulated the expression of miR-466m-3p. Knockdown of miR-466m-3p reversed LPS-induced cell apoptosis via increasing the levels of DNAjb6 which was confirmed to be the target gene of miR-466m-3p. This finding will be helpful for further understanding the critical roles of Hsp4 in ALI and may provide potential targets for ALI diagnosis and treatment.	32976821	RID03635	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Colon cancer	LINC02418	BCL2	positively-E	luciferase assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-34b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214039	GRCh38_12:130032928-130045057	ENSG00000171791	NA	100190940	596	NA	Bcl-2|PPP1R50	LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis.The expressional level of LINC02418 in CRC patients was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR. Kaplan-Meier analyses was used to investigate the correlation between LINC02418 and overall survival (OS) of CRC patients. Cell proliferative, migratory and invasive abilities were detected by CCK-8 assays, colony formation assays and trans-well assays in HCT116 and LoVo cells which were stably transduced with sh-LINC02418 or sh-NC. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assays. western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway.LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently affect BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth.LINC02418 was upregulated in human CRC samples and could be used as the indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.	32973404	RID03636	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	BANCR	IGF1R	positively-E	western blot;luciferase assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);IGF1R/RAF/MEK/ERK signaling pathway(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296678-69311111	ENSG00000140443	NA	100885775	3480	LINC00586	CD221|IGFIR|IGFR|JTK13|MGC18216	Long non-coding RNA BANCR mediates esophageal squamous cell carcinoma progression by regulating the IGF1R/Raf/MEK/ERK pathway via miR-338-3p.It was found that BANCR and IGF1R were upregulated, while miR<U+2011>338<U+2011>3p was downregulated in ESCC tissues and cells. Both BANCR and IGF1R knockdown suppressed the proliferation, migration, invasion and epithelial<U+2011>mesenchymal transition (EMT) of ESCC cells. IGF1R enhancement reversed BANCR knockdown<U+2011>mediated effects on the proliferation, migration, invasion and EMT of ESCC cells. BANCR regulated the Raf/MEK/ERK pathway by regulating IGF1R expression. Notably, BANCR regulated IGF1R expression by sponging miR<U+2011>338<U+2011>3p. Moreover, BANCR silencing inhibited tumor growth in<U+00A0>vivo. On the whole, the findings of the present study demonstrate that BANCR inhibition blocks ESCC progression by inactivating the IGF1R/Raf/MEK/ERK pathway by sponging miR<U+2011>338<U+2011>3p.	32945416	RID03637	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Non-small cell lung cancer	LUCAT1	ULK1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell autophagy(+);apoptosis process(+)	ceRNA(miR-514a-3p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000177169	NA	100505994	8408	SCAL1|SCAT5	ATG1|ATG1A	Long non-coding RNA LUCAT1 contributes to cisplatin resistance by regulating the miR-514a-3p/ULK1 axis in human non-small cell lung cancer.Drug resistance is a major obstacle in the therapy of malignant tumors, including non-small cell lung cancer (NSCLC). Long non-coding RNAs (lncRNAs) have been demonstrated to be involved in chemoresistance. The present study aimed to investigate the role of lung cancer-associated transcript 1 (LUCAT1) in cisplatin (DDP) resistance in NSCLC. By using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), it was found that the expression of LUCAT1 was elevated and that of microRNA-514a-3p (miR-514a-3p) was decreased in DDP-resistant NSCLC tissues and cells. Functionally, LUCAT1 upregulation enhanced cisplatin resistance by promoting the viability, autophagy and metastasis, and inhibiting the apoptosis of NSCLC cells, as demonstrated by Cell Counting kit-8 (CCK-8) assay, western blot Transwell assay and flow cytometric analysis. LUCAT1 was identified as a sponge of miR-514a-3p and uncoordinated-51-like kinase 1 (ULK1) was proven to be a target gene of miR-514a-3p by bioinformatics analysis, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The enhancing effect of miR-514a-3p on cisplatin sensitivity was reversed by the elevation of LUCAT1. ULK1 knockdown suppressed cisplatin resistance, while this effect was attenuated by miR-514a-3p inhibition. Moreover, LUCAT1 positively regulated ULK1 expression by targeting miR-514a-3p. In addition, LUCAT1 knockdown suppressed tumor growth in vivo. On the whole, the findings of the present study demonstrate that LUCAT1 contributes to the resistance of NSCLC cells to cisplatin by regulating the miR-514a-3p/ULK1 axis, elucidating a novel regulatory network in cisplatin resistance in NSCLC.	32945379	RID03638	ceRNA or sponge	metastasis,chemoresistance	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	FOXD2-AS1	S100A1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000160678	NA	84793	6271	MGC12982	S100-alpha|S100A	Long non-coding RNA FOXD2-AS1 regulates the tumorigenesis and progression of breast cancer via the S100 calcium binding protein A1/Hippo signaling pathway,The aim of the present study was to investigate the role of FOXD2-AS1 in breast cancer, and to clarify the underlying mechanisms. The expression of FOXD2-AS1 in breast cancer cell lines was first quantified by reverse transcription-quantitative PCR, and the biological function of FOXD2-AS1 was then determined. Cellular proliferative ability was determined by Cell Counting kit-8 assay, and wound healing and Transwell assays were conducted to assess the cell migratory and invasive ability. Corresponding protein expression levels were determined by western blot In addition, experimental animal models were established by the subcutaneous injection of MDA-MB-468 cells into the right axillary lymph nodes of BALB/c nude mice, and the effects of FOXD2-AS1 on tumor growth were observed. The results indicated that FOXD2-AS1 expression was upregulated in breast cancer cell lines, and that FOXD2-AS1 downregulation significantly inhibited the proliferation, migration and invasiveness of MCF-7 and MDA-MB-468 cells. S100 calcium binding protein A1 (S100A1) was also upregulated in breast cancer cell lines and was positively regulated by FOXD2-AS1. Furthermore, the inhibition of S100A1 and the overexpression of the serine/threonine-protein kinase, large tumor suppressor homolog 1 (LATS1), inhibited the FOXD2-AS1-induced cellular proliferation, migration and invasiveness in breast cancer. Experimental mouse models revealed that FOXD2-AS1 downregulation significantly inhibited tumor growth, and that the levels of phosphorylated (p-)YAP and p-LATS1 were upregulated by FOXD2-AS1 knockdown, indicating that the inhibition of FOXD2-AS1 activated Hippo/yes-associated protein signaling. On the whole, the findings of the present study suggest that the FOXD2-AS1/S100A1/Hippo axis is involved in the tumorigenesis and progression of breast cancer. In the future, these may contribution to the identification of more effective breast cancer treatments.	32945354	RID03639	expression association	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(SKCM);DATA(GSE38495)
Osteosarcoma	TUSC8	EHD2	positively-E	western blot;starBase;Luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-197-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237361	GRCh38_13:44400173-44405984	ENSG00000024422	NA	400128	30846	LINC01071|XLOC_010588	PAST2	TUSC8 inhibits the development of osteosarcoma by sponging miR-197-3p and targeting EHD2.  In the present study, it was observed that TUSC8 was markedly downregulated in OS tissues and cell lines. Functional experiments demonstrated that the overexpression of TUSC8 significantly suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), whereas it accelerated the apoptosis of OS cells. Mechanistically, TUSC8 served as a sponge for miR-197-3p, and EH-domain containing 2 (EHD2) was identified as a downstream target molecule of miR-197-3p. Further investigations indicated that EHD2 knockdown significantly reversed the effects on OS cellular processes induced by TUSC8 overexpression. On the whole, these findings indicate that TUSC8 functions as a competing endogenous RNA (ceRNA) to suppress OS cell growth and EMT via the miR-197-3p/EHD2 axis. TUSC8 may thus function as a potential therapeutic target in OS treatment.	32945345	RID03640	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	SNHG15	CD274	positively-E	luciferase assay;western blot	downregulation	qRT-PCR	NA	NA	immune evasion(+)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000120217	NA	285958	29126	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	LncRNA SNHG15 Contributes to Immuno-Escape of Gastric Cancer Through Targeting miR141/PD-L1.Further, our results suggested that SNHG15 acted as a competing endogenous RNA (CeRNA) to sponge miR-141, which was downregulated in gastric cancers and negatively correlated to PD-L1.Our results suggested that SNHG15 improved the expression of PD-L1 by inhibiting miR-141, which in turn promoted the resistance of stomach cancer cells to the immune responses.	32943878	RID03641	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Thyroid cancer	SLC26A4-AS1	DDX5	negatively-E	RNA pull-down assay;western blot;RIP	downregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233705	GRCh38_7:107650260-107662204	ENSG00000263077	NA	286002	1655	NA	G17P1|HLR1|p68	LncRNA SLC26A4-AS1 suppresses the MRN complex-mediated DNA repair signaling and thyroid cancer metastasis by destabilizing DDX5.Lymph node metastasis is the major adverse feature for recurrence and death of thyroid cancer patients. To identify lncRNAs involved in thyroid cancer metastasis, we systemically screened differentially expressed lncRNAs in lymph node metastasis, thyroid cancer, and normal tissues via RNAseq. We found that lncRNA SLC26A4-AS1 was continuously, significantly down-regulated in normal tissues, thyroid cancer, and lymph node metastasis specimens. Low SLC26A4-AS1 levels in tissues were significantly associated with poor prognosis of thyroid cancer patients. LncRNA SLC26A4-AS1 markedly inhibited migration, invasion, and metastasis capability of cancer cells in vitro and in vivo. Intriguingly, SLC26A4-AS1 could simultaneously interact with DDX5 and the E3 ligase TRIM25, which promoting DDX5 degradation through the ubiquitin-proteasome pathway. In particular, SLC26A4-AS1 inhibited expression of multiple DNA double-strand breaks (DSBs) repair genes, especially genes coding proteins in the MRE11/RAS50/NBS1 (MRN) complex. Enhanced interaction between DDX5 and transcriptional factor E2F1 due to silencing of SLC26A4-AS1 promoted binding of the DDX5-E2F1 complex at promoters of the MRN genes and, thus, stimulate the MRN/ATM dependent DSB signaling and thyroid cancer metastasis. Our study uncovered new insights into the biology driving thyroid cancer metastasis and highlights potentials of lncRNAs as future therapeutic targets again cancer metastasis.	32939012	RID03642	interact with protein	metastasis,recurrence,prognosis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Myocardial ischemia	TTTY15	let-7i-5p	negatively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);mitochondrial function(-)	NA	regulation	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000233864	NA	NA	NA	64595	NA	NCRNA00138	NA	Silencing TTTY15 mitigates hypoxia-induced mitochondrial energy metabolism dysfunction and cardiomyocytes apoptosis via TTTY15/let-7i-5p and TLR3/NF-kB pathways.Noncoding RNAs are interweaved in pathological processes in myocardial ischemia (MI), such as long noncoding RNA (lncRNA) and microRNAs (miRNAs). The aim of this study was to figure out the role of Testis-specific transcript Y-linked 15 (TTTY15) and let-7i-5p in cell model of MI in cardiomyocytes. Hypoxia-induced cell injury was assessed by Cell counting kit 8 assay, flow cytometry, commercial kits and western blot. As a result, hypoxia stress induced inhibition on cell proliferation, glucose uptake, and ATP production, and promotion on apoptosis, lactate dehydrogenase (LDH) release, and lactic acid production in human cardiomyocyte AC16 cells. During hypoxia injury, expression of TTTY15 and let-7i-5p was measured by real-time quantitative polymerase chain reaction, and TTTY15 was upregulated, accompanied with let-7i-5p downregulation. Functionally, either silencing TTTY15 or overexpressing let-7i-5p could attenuate hypoxia-induced apoptosis and mitochondrial energy metabolism dysfunction in AC16 cells. Moreover, there was an interaction between TTTY15 and let-7i-5p via target binding, as evidenced by dual-luciferase reporter assay and RNA immunoprecipitation assay. Knockdown of let-7i-5p could counteract the protective role of TTTY15 deletion in hypoxic AC16 cells. Meanwhile, toll-like receptor 3 (TLR3)/nuclear factor-kappa B (NF-kB) signaling was validated by western blot. Expression of TLR3, tumor necrosis factor receptor-associated factor 6 (TRAF6) and phosphorylated p65 was promoted in hypoxic AC16 cells, which was abrogated by TTTY15 silencing along with let-7i-5p upregulation. Collectively, TTTY15 knockdown protects cardiomyocytes against hypoxia-induced apoptosis and mitochondrial energy metabolism dysfunction in vitro through let-7i-5p/TLR3/NF-kB pathway to suppress.	32926961	RID03643	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Atherosclerosis	PEBP1P2	CDK9	negatively-E	western blot;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	NA	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000270532	GRCh38_2:85341281-85341838	ENSG00000136807	NA	647307	1025	NA	C-2k|CDC2L4|PITALRE|TAK	Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis.we found that PEBP1P2 represses proliferation, migration, and dedifferentiation during phenotype switching in VSMCs induced by platelet-derived growth factor BB (PDGF-BB). Mechanistically, cyclin-dependent kinase 9 (CDK9) was confirmed to be the direct target of PEBP1P2, which was proven to mediate phenotypic switching and proliferation of VSMCs and was rescued by PEBP1P2. Then, we explored the clinical significance, as we observed the decreased expression of PEBP1P2 in the serum of coronary heart disease (CHD) patients and human advanced carotid atherosclerotic plaques. Finally, PEBP1P2 overexpression distinctly suppressed neointima formation and VSMC phenotypic switching in vivo. Taken together, PEBP1P2 inhibits proliferation and migration in VSMCs by directly binding to CDK9, implying that it may be a promising therapeutic target for the treatment of proliferative vascular diseases.	32916601	RID03644	expression association	NA	UP(SKCM,BRCA);DATA(GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Breast cancer	OIP5-AS1	GLO1	positively-E	western blot;starBase2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-216a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000124767	NA	729082	2739	cyrano|linc-OIP5	GLOD1	The expression of OIP5-AS1 and miR-216a-5p was detected by quantitative real-time polymerase chain reaction. Cell proliferation, apoptosis, migration, or invasion was assessed by 4-5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, flow cytometry, or transwell assay, respectively. The binding sites were predicted by bioinformatics tool starBase2.0 (http://starbase.sysu.edu.cn/starbase2/index.php). The interaction between miR-216a-5p and OIP5-AS1 or glyoxalase 1 (GLO1) was confirmed by dual-luciferase reporter assay. The expression of GLO1 was quantified by western blot. Nude mouse tumorigenicity assays were conducted to verify the role of OIP5-AS1 in vivo. OIP5-AS1 and GLO1 were highly expressed in both clinical tumor tissues and cell lines, whereas miR-216a-5p was downregulated. Knockdown of OIP5-AS1 suppressed proliferation, migration, and invasion but promoted apoptosis of breast cancer cells. MiR-216a-5p was a target of OIP5-AS1 and interacted with GLO1. MiR-216a-5p inhibition or GLO1 overexpression reversed the effects of OIP5-AS1 knockdown on the development of breast cancer cells. OIP5-AS1 knockdown depleted tumor growth in vivo.OIP5-AS1 knockdown suppressed the progression of breast cancer by inducing GLO1 expression via competitively binding to miR-216a-5p, suggesting that OIP5-AS1 was a hopeful biomarker for the therapy of breast cancer.	32916503	RID03645	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807)
Endometrial cancer	RP11-395G23.3	PTEN	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-205-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000254615	NA	ENSG00000171862	NA	NA	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA RP11-395G23.3 suppresses the endometrial cancer progression via regulating microRNA-205-5p/PTEN axis.We discovered that low RP11-395G23.3 expression was significantly related to advanced histological grade and lymphovascular space invasion in EC patients. In addition, overexpression of RP11-395G23.3 significantly inhibited the proliferation, invasion, migration, and induced apoptosis of Ishikawa and HEC-1A cells in vitro. Our results also showed that RP11-395G23.3 could directly bind to miRNA-205-5p through its miRNA response elements and eliminate the inhibitory effect of targeting gene PTEN, thus leading to the signaling pathway of phosphatidylinositol-3-kinase/AKT inactivation. We demonstrated for the first time that RP11-395G23.3 may inhibit the development and pathogenesis of EC by acting as a sponge for miRNA-205-5p and increasing PTEN expression. RP11-395G23.3 may be a target for the diagnosis and treatment of EC.	32913516	RID03646	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Gastric cancer	FAM230B	TOP2A	positively-E	luciferase assay;western blot; LncBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-27a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000215498	GRCh38_22:21167758-21192156	ENSG00000131747	NA	642633	7153	FLJ46366	TOP2|TOP2alpha|TOPIIA	LncRNA FAM230B Promotes Gastric Cancer Growth and Metastasis by Regulating the miR-27a-5p/TOP2A Axis.We found that FAM230B was highly expressed in gastric cancer cell lines and mainly located in the cytoplasm. FAM230B overexpression promoted the proliferation, migration, and invasion of AGS cells and repressed their apoptosis; it also facilitated tumor growth in vivo. In contrast, FAM230B knockdown suppressed the proliferation, migration, and invasion of MGC0803 cells, but enhanced their apoptosis and inhibited tumor growth in vivo. MiR-27a-5p expression was suppressed by FAM230B overexpression in AGS cells. MiR-27a-5p inhibited the proliferation, migration, and invasion of gastric cancer cells, and promoted the apoptosis of gastric cancer cells by reducing TOP2A (topoisomerase 2 alpha) expression.CONCLUSION: Our study showed that lncRNA FAM230B might function to promote GC. FAM230B functioned as a ceRNA by sponging miR-27a-5p and enhancing TOP2A expression.	32910366	RID03647	ceRNA or sponge	metastasis	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Pituitary cancer	CASC9	APOBEC3G	positively-E	western blot	upregulation	qRT-PCR	NA	NA	glycolysis(+)	ceRNA(miR-590-3p)	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000239713	NA	101805492	60489	ESCCAL-1|linc-JPH1|LINC00981	bK150C2.7|CEM15|dJ494G10.1|FLJ12740|MDS019	Inhibition of lncRNA-UCA1 suppresses pituitary cancer cell growth and prolactin (PRL) secretion via attenuating glycolysis pathway.Consistent with other cancers, lncRNA-UCA1 was highly expressed in pituitary tumors. Meanwhile, we found glycolysis of pituitary tumors was higher than normal pituitary tissues. Overexpression of lncRNA-UCA1 in rat pituitary cancer cell lines, GH3 and MMQ, significantly promoted glucose uptake and lactate production. In addition, expressions of the glycolysis key enzymes, HK2 and LDHA, were significantly upregulated by exogenous overexpression of lncRNA-UCA1. Importantly, silencing lncRNA-UCA1 obviously inhibited pituitary cancer cells growth and prolactin (PRL) secretion. We report higher lncRNA-UCA1 expression is associated with higher serum PRL level in pituitary patients. Finally, by blocking the lncRNA-UCA1-promoted glycolysis of pituitary cancer cells by glycolysis inhibitor, 2-DG, we obtained recovery of cell growth rate and PRL secretion from an in vitro model. Taken together, our investigation revealed an oncogenic role of lncRNA-UCA1 through upregulating glycolysis of pituitary tumors. This study contributes to underlying molecular mechanisms of the tumorigenesis of pituitary tumors.	32909148	RID03648	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Neuropathic pain	H19	CDK5	positively-E	luciferase assay;western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-196a-5p)	regulation	RNA-protein	NA	NA	NA	Other	Neuropathic pain	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000164885	NA	283120	1020	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PSSALRE	Long Noncoding RNA H19 Induces Neuropathic Pain by Upregulating Cyclin-Dependent Kinase 5-Mediated Phosphorylation of cAMP Response Element Binding Protein.LncRNA H19 is upregulated in many human diseases, including NP. Cyclin-dependent kinase 5 (CDK5) aggressively worsens inflammatory action and nerve damage to cause severe NP. Phosphorylated cAMP response element binding protein (CREB) is detrimental to nerves and promotes NP progression. Herein, aim of our study was to assess the mechanism of lncRNA H19.Our study demonstrated that silencing H19 inhibited NP by suppressing CDK5/p35 and p-CREB phosphorylation via the miR-196a-5p/CDK5 axis, which may provide new insight into NP treatment.</AbstractText>: Our study demonstrated that silencing H19 inhibited NP by suppressing CDK5/p35 and p-CREB phosphorylation via the miR-196a-5p/CDK5 axis, which may provide new insight into NP treatment.Our study demonstrated that silencing H19 inhibited NP by suppressing CDK5/p35 and p-CREB phosphorylation via the miR-196a-5p/CDK5 axis, which may provide new insight into NP	32903807	RID03649	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807)
Gastric cancer	PART1	PDGFB	negatively-F	RIP;RNA pull-down assay;ChIP	downregulation	microarray;qRT-PCR	NA	NA	PDGFRbeta/PI3K/AKT signaling pathway(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000100311	NA	25859	5155	DKFZP586D0823|NCRNA00206	SIS|SSV	Long noncoding RNA PART1 restrains aggressive gastric cancer through the epigenetic silencing of PDGFB via the PLZF-mediated recruitment of EZH2.the clinical significance and underlying mechanism of PART1 function in gastric cancer remains undefined. Here, seven differential expression levels of noncoding RNAs (DE-lncRNAs) were screened from gastric cancer through a probe reannotation of a human exon array. PART1 was selected for further study because of its high fold change number. In our cohort, PART1 was identified as a significant downregulated lncRNA in gastric cancer tissues by qPCR and in situ hybridization (ISH), and its low expression was significantly correlated with postoperative metastasis and short overall survival time after surgery. Through the results of gain-of-function experiments, PART1 was confirmed as a tumor suppressor that can decrease not only cell viability, migration, and invasion in vitro but also tumorigenesis and tumor metastasis in vivo. Mechanistically, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) showed that PART1 interacts with androgen receptor (AR), and then, promyelocytic leukemia zinc finger (PLZF) is upregulated in an androgen-independent manner. In a chain reaction, chromatin immunoprecipitation (ChIP) assay additionally illustrated that PLZF upregulation increased the enrichment of EZH2 and H3K27 trimethylation in the platelet-derived growth factor (PDGFB) promotor, thereby inhibition of PDGFB and the subsequent PDGFRbeta/PI3K/Akt signaling pathway. Based on these findings, we showed PART1 plays a tumor suppressor role by promoting PLZF expression followed by recruitment of EZH2 to mediate epigenetic PDGFB silencing and downstream PI3K/Akt inhibition, suggesting that PART1 has a key role in restraining the aggressive ability of GC cells and providing a novel perspective on lncRNAs in GC progression.	32901105	RID03650	epigenetic regulation	metastasis	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	UP(LIHC);DATA(GSE117623)
Oral squamous cell carcinoma	MALAT1	MAGEA9	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000166008	NA	378938	4108	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CT1.9|MAGE9|MGC8421	Long Non-Coding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Cell Proliferation and Migration by Regulating miR-143-3p and MAGE Family Member A9 (MAGEA9) in Oral Squamous Cell Carcinoma.qRT-PCRresults showed that MALAT1 and MAGEA9 were expressed at higher levels and miR-143-3p was expressed at lower levels in OSCC tissues. Dramatic suppression of cell proliferation and migration abilities were caused by MALAT1 knockdown or miR-143-3p overexpression in CAL-27 cells. MALAT1 directly interacted with and negatively regulated miR-143-3p. Moreover, MAGEA9 was validated as a miR-143-3p target gene and was found to be negatively regulated by it. MALAT1 knockdown suppressed MAGEA9 protein expression and had the same effect as MAGEA9 knockdown. Additionally, MAGEA9 knockdown inhibited CAL-27 cell proliferation and migration abilities. Finally, in OSCC tissues, MALAT1 and miR-143-3p expression were negatively correlated and MALAT1 was positively correlated with MAGEA9 expression, while an inverse correlation between MAGEA9 and miR-143-3p expression was observed. CONCLUSIONS Taken together, our results suggest that MALAT1 functions as a competing endogenous RNA (ceRNA) in promoting OSCC cell proliferation and migration abilities through the miR-143-3p/MAGEA9 axis, thus providing new therapeutic targets for treatment of OSCC.We assessed levels of MALAT1, miR-143-3p, and MAGEA9 expression in OSCC tissues and cell lines by quantitative real-time polymerase chain reaction (qRT-PCR and western blot assay. Proliferation and migration of CAL-27 cells were detected via CCK-8 and transwell assays, respectively. To study the relationships among MALAT1, miR-143-3p, and MAGEA9, we performed dual-luciferase assay and assessed the results using Spearman correlation analysis.	32879299	RID03651	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	PWRN1	miR-214-5p	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	epigenetic regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000259905	GRCh38_15:24101827-24823365	NA	NA	791114	NA	NCRNA00198	NA	Long noncoding RNA PWRN1 is lowly expressed in osteosarcoma and modulates cancer proliferation and migration by targeting hsa-miR-214-5p.We found that PWRN1 was downregulated in both osteosarcoma cells and human tumors. PWRN1 downregulation was correlated with advanced stage, metastasis, and low survival rate in cancer patients. PWRN1 overexpression in osteosarcoma cells significantly inhibited their proliferation, cisplatin chemoresistance, and in vivo growth. In addition, we demonstrated that PWRN1 directly bound miR-214-5p and suppressed its expression in osteosarcoma cells. Furthermore, we showed that miR-214-5p overexpression reversed the anti-cancer effects of PWRN1 on osteosarcoma cell proliferation and cisplatin chemoresistance.CONCLUSION: Our data provide new insights into the epigenetic axis of PWRN1/miR-214-5p in regulating osteosarcoma progression and chemoresistance. PWRN1 may also be a biomarker to predicting cancer patients' poor prognosis and novel pharmaceutical targets for personalized medicine.	32870579	RID03652	epigenetic regulation	metastasis,chemoresistance,prognosis	UP(PAAD);DATA(GSE60407)	
Oral squamous cell carcinoma	DANCR	miR-216a-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	LncRNA DANCR regulates the growth and metastasis of oral squamous cell carcinoma cells via altering miR-216a-5p expression.Up-regulated DANCR expression and down-regulated miR-216a-5p expression were observed in both OSCC tissues and cells, and they were proven strongly correlated to the histological grade, clinical staging and lymph node metastasis of OSCC patients.The expression of DANCR and miR-216a-5p in OSCC patients and cells were measured. SCC15 and CAL-27 cells were selected to divide into Control, sh-NC, DANCR shRNA, DANCR, miR-216a-5p mimic, and DANCR + miR-216a-5p mimic groups. Dual-luciferase reporter gene assay was performed for the verification of the targeting relationship between miR-216a-5p and DANCR/Bcl-2/KLF12. We also quantified the abilities of OSCC cells regarding proliferation, invasion, migration and apoptosis, and the expression levels of apoptosis-related proteins were measured. Finally, the tumor-bearing nude mice were established to verify the effect of DANCR in vivo. Up-regulated DANCR expression and down-regulated miR-216a-5p expression were observed in both OSCC tissues and cells, and they were proven strongly correlated to the histological grade, clinical staging and lymph node metastasis of OSCC patients. Dual-luciferase reporter gene assay showed a target relationship between DANCR and miR-216a-5p, as well as between miR-216a-5p and Bcl-2/KLF12. Both DANCR shRNA and miR-216a-5p mimic decreased proliferative, migration and invasive abilities of OSCC cells with increased cell apoptosis. However, DANCR group showed completely opposite trends. Moreover, miR-216a-5p mimic could reverse the role of DANCR in promoting tumor growth. In-vivo experiment confirmed the inhibitory role of DANCR shRNA in tumor growth and metastasis. We concluded that DANCR may promote the growth and metastasis of OSCC cells and suppress OSCC cell apoptosis by sponging miR-216a-5p.	32860589	RID03653	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Cervical cancer	UCA1	KIF20A	positively-E	luciferase assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000112984	NA	652995	10112	CUDR|LINC00178|onco-lncRNA-36|UCAT1	RAB6KIFL	Long non-coding RNA UCA1 upregulates KIF20A expression to promote cell proliferation and invasion via sponging miR-204 in cervical cancer.We found that UCA1 expression was greatly up-regulated in cervical cancer tissues and cell lines. Our in vitro assays revealed that the suppressing of UCA1 could reduce cervical cancer cells proliferation, migration, and invasion. In addition, we found that lncRNA UCA1 could sponge miR-204 and promote the proliferation and invasion of cervical cancer cells via the up-regulating of KIF20A expression. As a result, the inhibiting of UCA1 could lower cervical cancer (CC) cells growth rate in vivo.Our results identified that UCA1 could serve as an oncogene in cervical cancer cell progression through the modulating of miR-204/KIF20A axis. It gives novel insights to the searching of novel therapeutic methods for cervical cancer.	32835591	RID03654	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Atherosclerosis	OIP5-AS1	miR-26a-5p	negatively-E	luciferase reporter assay;RIP;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Long Noncoding RNA OIP5-AS1 Contributes to the Progression of Atherosclerosis by Targeting miR-26a-5p Through the AKT/NF-kB Pathway.As a result, the expression of OIP5-AS1 was upregulated and miR-26a-5p was downregulated in ox-LDL-treated HUVECs. MiR-26a-5p was identified as a direct target of OIP5-AS1. OIP5-AS1 knockdown reversed the inhibitory effect on cell proliferation and the promotional effects on apoptosis and inflammation induced by ox-LDL treatment in HUVECs. Interestingly, the effects caused by OIP5-AS1 knockdown were further attenuated by miR-26a-5p inhibition. Furthermore, OIP5-AS1 knockdown blocked the AKT/NF-kB pathway by regulating miR-26a-5p expression. In conclusion, OIP5-AS1 knockdown promoted cell proliferation and suppressed apoptosis and inflammatory response in ox-LDL-treated HUVECs by targeting miR-26a-5p through blocking the AKT/NF-kB pathway, indicating a promising strategy for AS treatment.	32833899	RID03655	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Non-small cell lung cancer	RPPH1	WNT2B	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000259001	GRCh38_14:20343048-20343685	ENSG00000134245	NA	85495	7482	H1RNA|RPPH1-1	WNT13|XWNT2	lncRNA RPPH1 promotes non-small cell lung cancer progression through the miR-326/WNT2B axis.lncRNA RPPH1 promotes non-small cell lung cancer progression through the miR-326/WNT2B axis.The aim of the present study was to examine the role of ribonuclease P RNA component H1 (RPPH1) in non-small cell lung cancer (NSCLC). RPPH1 expression was assessed in datasets from The Cancer Genome Atlas, as well as lung cancer cell lines and patients with NSCLC. RPPH1 was significantly upregulated in NSCLC cell lines, compared with a normal lung epithelial cell line. Moreover, high RPPH1 expression was associated with poor overall survival and disease progression. RPPH1 was knocked down in A549 and H1299 cells using short hairpin (sh) RNA constructs, and the expressions of target genes and proteins were determined by reverse transcription-quantitative PCR and western blot. Cell invasion potential was also determined using Transwell Matrigel assays. Compared with the negative control, RPPH1 silencing significantly reduced the number of invading cells, increased E-cadherin expression and reduced vimentin protein expression. Cell resistance to cisplatin/cis-diamminedichloridoplatinum (CDDP) was also evaluated using Cell Counting Kit-8 and colony formation assays. RPPH1 overexpression increased the resistance of A549 and H1299 cells to CDDP. Moreover, the potential interactions between RPPH1, microRNA (miR)-326 and Wnt family member 2B (WNT2B) were investigated using luciferase reporter assays and co-transfection experiments. MiR-326 expression was directly inhibited by RPPH1. In A549 cells co-transfected with shRPPH1 and miR-326 inhibitor, the invading cell number significantly increased compared with cells transfected with shRPPH1 alone. In addition, E-cadherin expression levels were reduced, and vimentin was upregulated. MiR-326 overexpression partially reduced the resistance of A549 cells to CDDP induced by RPPH1 overexpression. WNT2B expression was directly suppressed using miR-326. A549 cells co-transfected with a miR-326 mimic and a WNT2B overexpression vector demonstrated increased invasion potential, reduced E-cadherin and increased vimentin protein expression levels, compared with cells transfected with the mimic alone. miR-326 overexpression reduced CDDP resistance in A549 cells. However, co-transfection with WNT2B partially enhanced CDDP resistance, compared with the mimic alone. In conclusion, RPPH1 promoted NSCLC progression and lung cancer cell resistance to CDDP through miR-326 and WNT2B.	32831924	RID03656	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	XIST	PAX5	positively-E	western blot;starBase;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-338-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000196092	NA	7503	5079	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BSAP	Long noncoding RNA XIST knockdown suppresses the growth of colorectal cancer cells via regulating microRNA-338-3p/PAX5 axis.The transcription level and protein level of genes were assessed by quantitative real-time PCR (qRT-PCR and western blot assay, respectively. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry analysis were used to determine cell proliferation ability and apoptosis rate, respectively. In addition, cell migratory ability and invasive ability were measured using transwell assay. Besides, the interaction between miR-338-3p and XIST or paired box 5 (PAX5) was predicted by starBase or TargetScan and then verified by the dual-luciferase reporter assay.	32826710	RID03657	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	KTN1-AS1	PDPK1	positively-E	luciferase assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);apoptosis process(-)	ceRNA(miR-130a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000186615	GRCh38_14:55496786-55580888	ENSG00000140992	NA	100129075	5170	C14orf33|MYCLo-3	PDK1	LncRNA KTN1-AS1 promotes the progression of non-small cell lung cancer via sponging of miR-130a-5p and activation of PDPK1.Long noncoding RNAs (lncRNAs) are known to play an important role in the aberrant regulation of gene expression in many cancers, including NSCLC. Here, we investigated the involvement of the lncRNA KTN1-AS1 in NSCLC. We found that KTN1-AS1 expression was upregulated in NSCLC tissue and was positively associated with poor prognosis. KTN1-AS1 knockdown inhibited cell growth and proliferation, increased apoptosis, and modulated the expression of cell cycle- and apoptosis-related proteins (cyclin A1, cyclin-dependent kinase 2, Bcl2, and Bax) in NSCLC cell lines and tumour xenografts in nude mice. KTN1-AS1 bound to and directly regulated the expression of miR-130a-5p. Notably, miR-130a-5p overexpression suppressed NSCLC cell proliferation and increased apoptosis in vitro and in vivo, and this effect was reversed by KTN1-AS1 overexpression. Finally, we showed that KTN1-AS1 modulated the expression of 3-phosphoinositide-dependent protein kinase 1 (PDPK1), a miR-130a-5p target and key regulator of autophagy in NSCLC cells. Taken together, our results suggest that the KTN1-AS1/miR-130a-5p/PDPK1 pathway may be a potential therapeutic target for NSCLC.	32820252	RID03658	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Renal cell carcinoma	CDKN2B-AS1	CCND1	positively-E	luciferase assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(-);apoptosis process(-)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000110092	NA	100048912	595	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	BCL1|D11S287E|PRAD1|U21B31	LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.Functionally, attenuation of CDKN2B-AS1 and/or overexpression of miR-141 inhibited proliferation, clonogenicity, migration/invasion, induced apoptosis in vitro and suppressed tumor growth in xenograft mouse model. Further, overexpression of CDKN2B-AS1 is positively correlated with poor overall survival of RCC patients. Expression of miR-141 also robustly discriminated malignant from non-malignant tissues and its inhibition in normal RPTEC cells induced pro-cancerous characteristics. CDKN2B-AS1 attenuation or miR-141 overexpression decreased CCND1/CCND2 expression, resulting in reduced RAC1/pPXN that are involved in migration, invasion and epithelial-mesenchymal transition. This study, for the first time, deciphered the role of CDKN2B-AS1/miR-141/Cyclin D axis in RCC and highlights this network as a promising therapeutic target for the regulation of EMT driven metastasis in RCC.	32814766	RID03659	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Renal cell carcinoma	CDKN2B-AS1	CCND2	positively-E	luciferase assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(-);apoptosis process(-)	ceRNA(miR-142)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000118971	NA	100048912	894	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.Functionally, attenuation of CDKN2B-AS1 and/or overexpression of miR-141 inhibited proliferation, clonogenicity, migration/invasion, induced apoptosis in vitro and suppressed tumor growth in xenograft mouse model. Further, overexpression of CDKN2B-AS1 is positively correlated with poor overall survival of RCC patients. Expression of miR-141 also robustly discriminated malignant from non-malignant tissues and its inhibition in normal RPTEC cells induced pro-cancerous characteristics. CDKN2B-AS1 attenuation or miR-141 overexpression decreased CCND1/CCND2 expression, resulting in reduced RAC1/pPXN that are involved in migration, invasion and epithelial-mesenchymal transition. This study, for the first time, deciphered the role of CDKN2B-AS1/miR-142/Cyclin D axis in RCC and highlights this network as a promising therapeutic target for the regulation of EMT driven metastasis in RCC.	32814766	RID03660	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Rheumatoid arthritis	H19	CDK2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-124a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000123374	NA	283120	1017	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Notably, lncRNA-H19 competitively bound to miR-124a, which directly targets CDK2 and MCP-1. It was confirmed that lncRNA-H19 regulates the proliferation of synoviocytes by acting as a sponge of miR-124a to modulate CDK2 and MCP-1 expression. Furthermore, the agonists of LXR inhibited lncRNA-H19-mediated miR-124a-CDK2/MCP-1 signalling pathway in synoviocytes. The 'lncRNA-H19-miR-124a-CDK2/MCP-1' axis plays an important role in LXR anti-arthritis.CONCLUSION: Regulation of the miR-124a-CDK2/MCP-1 pathway by lncRNA-H19 plays a crucial role in the proliferation of FLS. Targeting this axis has therapeutic potential in the treatment of RA and may represent a novel strategy for RA treatment.	32810279	RID03661	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Rheumatoid arthritis	H19	CCL2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-124a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000108691	NA	283120	6347	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	GDCF-2|HC11|MCAF|MCP-1|MCP1|MGC9434|SCYA2|SMC-CF	Notably, lncRNA-H19 competitively bound to miR-124a, which directly targets CDK2 and MCP-1. It was confirmed that lncRNA-H19 regulates the proliferation of synoviocytes by acting as a sponge of miR-124a to modulate CDK2 and MCP-1 expression. Furthermore, the agonists of LXR inhibited lncRNA-H19-mediated miR-124a-CDK2/MCP-1 signalling pathway in synoviocytes. The 'lncRNA-H19-miR-124a-CDK2/MCP-1' axis plays an important role in LXR anti-arthritis.CONCLUSION: Regulation of the miR-124a-CDK2/MCP-1 pathway by lncRNA-H19 plays a crucial role in the proliferation of FLS. Targeting this axis has therapeutic potential in the treatment of RA and may represent a novel strategy for RA treatment.	32810279	RID03662	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Breast cancer	CERS6-AS1	BAP1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-125a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227617	GRCh38_2:168771951-168786961	ENSG00000163930	NA	100861402	8314	NA	hucep-6|KIAA0272|UCHL2	lncRNA CERS6-AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR-125a-5p to upregulate BAP1 expression.Then we found CERS6-AS1 was upregulated in BC tissues. Long noncoding RNAs (lncRNAs) can act as oncogene and tumor suppressor genes in many types of cancers including breast cancer (BC). Our previous study has indicated microRNA (miR)-125a-5p was downregulated and function as a tumor suppressor in BC. However, its upstream regulation mechanism is still unclear. In this study, we used bioinformatics algorithms, RNA pull-down assay, and dual-luciferase reports assay to predict and confirm lncRNA CERS6-AS1 interacted with miR-125a-5p. Then we found CERS6-AS1 was upregulated in BC tissues. Experimental results of tumor growth in nude mice show that CERS6-AS1 promotes tumor growth. Furthermore, CERS6-AS1 regulated BC susceptibility gene 1-associated protein 1 (BAP1) expression via sponging miR-125a-5p via western blotand quantitative polymerase chain reaction arrays. Finally, we showed that miR-125a-5p had opposing effects to those of CERS6-AS1 on BC cells, demonstrating that CERS6-AS1 may promote cell proliferation and inhibit cell apoptosis via sponging miR-125a-5p. Our results indicated CERS6-AS1 promote BC cell proliferation and inhibit cell apoptosis via sponging miR-125a-5p to upregulate BAP1 expression.	32808708	RID03663	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Breast cancer	NEAT1	miR-146b-5p	negatively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long Non-Coding RNA NEAT1 Promotes the Proliferation, Migration, and Metastasis of Human Breast-Cancer Cells by Inhibiting miR-146b-5p Expression.Quantitative real time-polymerase chain reaction (qRT-PCR was used to measure expression of lncRNA NEAT1 and microRNA (miR)-146b-5p in BC tissues and cell lines. Cell Counting Kit (CCK)-8, cell colony-formation, wound-healing, and Transwell- assays were undertaken to determine the effects of lncRNA NEAT1 and miR-146b-5p on progression of BC cells. The interaction between lncRNA NEAT1 and miR-146b-5p was examined by luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and RNA-pull-down assays.Expression of lncRNA NEAT1 was upregulated in BC tissues and cell lines. High expression of lncRNA NEAT1 predicted poor overall survival in BC patients. Silencing of expression of lncRNA NEAT1 inhibited epithelial-sesenchymal transition (EMT) and suppressed the proliferation, migration and invasion of BC cells. Ectopic expression of lncRNA NEAT1 induced EMT and promoted BC progression. Mechanistic investigations revealed that miR-146b-5p was a direct target of lncRNA NEAT1, and its expression was correlated negatively with expression of lncRNA NEAT1 in BC tissues.	32801860	RID03664	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Non-small cell lung cancer	DUXAP8	HK2	positively-E	luciferase assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell viability(+);glycolysis(+)	ceRNA(miR-409-3p)	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000159399	NA	503637	3099	NA	NA	Long Non-Coding RNA DUXAP8 Facilitates Cell Viability, Migration, and Glycolysis in Non-Small-Cell Lung Cancer via Regulating HK2 and LDHA by Inhibition of miR-409-3p.Real-time quantitative PCR (RT-qPCR) was used to detect DUXAP8 and microRNA-409-3p (miR-409-3p) expression. CCK-8, cell colony formation assay, and Transwell migration assay were performed to measure cell growth and migration, respectively. The expression of the relative proteins was detected by western blot. Cell glycolysis was determined by glucose uptake, adenosine triphosphate (ATP) concentration, lactate generation, extracellular acidification rate and oxygen consumption rate assays. Bioinformatics analysis and dual-luciferase reporter assay were used to measure the interaction among DUXAP8, miR-409-3p, hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA). In vivo, subcutaneous tumor formation assay was performed in the nude mice.DUXAP8 was highly expressed in NSCLC, while miR-409-3p was downregulated. High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients. Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis. Besides, DUXAP8 sponged miR-409-3p to promote HK2 and LDHA expression. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. Moreover, DUXAP8 downregulation markedly inhibited tumor growth in vivo.	32801745	RID03665	ceRNA or sponge	metastasis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	DUXAP8	LDHA	positively-E	luciferase assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell viability(+);glycolysis(+)	ceRNA(miR-409-3p)	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000134333	NA	503637	3939	NA	NA	High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients. Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis. Besides, DUXAP8 sponged miR-409-3p to promote HK2 and LDHA expression. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. Moreover, DUXAP8 downregulation markedly inhibited tumor growth in vivo.</AbstractText>: DUXAP8 was highly expressed in NSCLC, while miR-409-3p was downregulated. High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients. Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis. Besides, DUXAP8 sponged miR-409-3p to promote HK2 and LDHA expression. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. Moreover, DUXAP8 downregulation markedly inhibited tumor growth in vivo.Our findings demonstrated that DUXAP8 served as an oncogene in the progression of NSCLC.</AbstractText>: Our findings demonstrated that DUXAP8 served as an oncogene in the progression of NSCLC.	32801745	RID03666	ceRNA or sponge	metastasis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Prostate cancer	EMX2OS	TCF12	positively-E	luciferase reporter assay;RNA pull-down assay;western blot;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	NA	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000229847	GRCh38_10:117473215-117545068	ENSG00000140262	NA	196047	6938	EMX2-AS1|NCRNA00045	bHLHb20|HEB|HsT17266|HTF4|p64	LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway.The EMX2OS expression was assessed in PCa tissues, paracancer tissues, PCa cells and normal prostate epithelial cells by qPCR. Gain- and loss-of-function experiments were performed to investigate the role of EMX2OS and FUS in cGMP-PKG (cyclic guanosine monophosphate-dependent protein kinase)-mediated proliferation, invasion, and migration in human PCa cell lines DU145 and PC3. Then, the interaction of transcription factor 12 (TCF12) with EMX2OS promoter was confirmed by using the dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RNA binding protein immunoprecipitation and RNA pull-down assays were used to verify the interaction between EMX2OS and FUS protein. Finally, the role of EMX2OS and FUS in tumor growth in vivo was validated in a xenograft nude mouse model.TCF12 and EMX2OS were both downregulated in PCa tissues and cells, and they negatively regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. TCF12 was a transcription factor of EMX2OS. TCF12 and EMX2OS overexpression both down-regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. Furthermore, EMX2OS directly bound with FUS protein and had a synergy effect with FUS protein on cGMP-PKG-mediated cell functions, which could be suppressed by (D)-DT-2 (a cGMP-PKG inhibitor). In addition, the overexpression of FUS or EMX2OS individually markedly decreased the volume and weight of tumors in vivo, and co-overexpression of them further inhibited tumor growth.	32801740	RID03667	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939)
Atherosclerosis	circ_0029589	STIM1	positively-E	luciferase reporter assay;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000167323	NA	NA	6786	NA	D11S4896E|GOK|IMD10|STRMK|TAM|TAM1	The relationship between miR-214-3p and circ_0029589 or STIM1 was tested via dual-luciferase reporter analysis and RNA immunoprecipitation.KEY FINDINGS: Circ_0029589 level was enhanced in ox-LDL-challenged VSMCs. Circ_0029589 interference constrained cell proliferation, migration and invasion in ox-LDL-challenged VSMCs. miR-214-3p was targeted by circ_0029589 and miR-214-3p knockdown weakened the suppressive function of circ_0029589 silence on VSMCs proliferation, migration and invasion. STIM1 was targeted via miR-214-3p and miR-214-3p could suppress VSMCs proliferation, migration and invasion via decreasing STIM1. Moreover, circ_0029589 modulated STIM1 level by miR-214-3p.SIGNIFICANCE: Circ_0029589 knockdown repressed proliferation, migration and invasion of VSMCs challenged via ox-LDL by regulating miR-214-3p and STIM1, indicating that circ_0029589 might play important role in atherosclerosis.Circ_0029589 knockdown repressed proliferation, migration and invasion of VSMCs challenged via ox-LDL by regulating miR-214-3p and STIM1, indicating that circ_0029589 might play important role in atherosclerosis.	32795540	RID03668	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	HCG11	GFI1	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-942-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000162676	NA	493812	2672	bK14H9.3|FLJ14049|FLJ30357	GFI-1|GFI1A|ZNF163	Long noncoding RNA HCG11 inhibited growth and invasion in cervical cancer by sponging miR-942-5p and targeting GFI1.Long noncoding RNAs (lncRNAs) act as essential regulators in cancer tumorigenesis. Our study aimed to explore the underlying mechanism of lncRNA human leukocyte antigen complex group 11 (HCG11) in cervical cancer (CC) progression. Long noncoding RNA HCG11 was downregulated in CC. Functional assays demonstrated that lncRNA HCG11 inhibited CC cell proliferation and invasion. Then, we confirmed that lncRNA HCG11 could directly bind to miR-942-5p. Moreover, inhibition of miR-942-5p suppressed the growth and invasion of CC cells, and growth factor-independent transcription repressor 1 (GFI1) gene was the target gene of miR-942-5p. Long noncoding RNA HCG11 increased the expression of GFI1 and suppressed cell proliferation and invasion by acting as a miR-942-5p sponge. Finally, the overexpression of lncRNA HCG11 suppressed the proliferation and metastasis of CC cells in vivo.	32794340	RID03669	ceRNA or sponge	metastasis	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	NORAD	AKR1B1	positively-E	western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000085662	NA	647979	231	LINC00657	ALDR1|AR	Silencing of Long Non-Coding RNA (LncRNA) Non-Coding RNA Activated by DNA Damage (NORAD) Inhibits Proliferation, Invasion, Migration, and Promotes Apoptosis of Glioma Cells via Downregulating the Expression of AKR1B1.Furthermore, the expression of proteins in extracellular signal-regulated kinase (ERK) signaling was tested using western blot. RESULTS The results revealed that NORAD and AKR1B1 were highly expressed in glioma cells. NORAD silencing inhibited proliferation, invasion and migration but promoted apoptosis of glioma cells, accompanied by the expression changes of migration- and apoptosis-related proteins. However, after co-transfection with AKR1B1 pcDNA3.1 in NORAD silencing cells, the effects of NORAD silencing on proliferation, invasion, migration, and apoptosis were attenuated. Consistently, the expression of phosphorylated ERK (p-ERK) was decreased after NORAD silencing, which were reversed following AKR1B1 overexpression. CONCLUSIONS These findings demonstrated that NORAD silencing suppressed proliferation, invasion, and migration and boosted apoptosis of glioma cells via downregulating the AKR1B1 expression, which may provide a potential therapeutic target for glioma treatment.	32778640	RID03670	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807)
Lung cancer	UCA1	miR-138	negatively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	miR-138 and miR-193 target long non-coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancermiR-138 and miR-193 specifically targeted and regulated lncRNA-UCA1. MiR-138 and miR-193 both suppressed cell proliferation and cell cycle progression. Moreover, miR-138 and miR-193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR-138 or miR-193. Furthermore, miR-138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR-138 and miR-193 common target. In human lung cancer tissues, our study showed a significant negative correlation betwemiRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR-138 and miR-193 on UCA1 and CDK6 were verified by luciferase reporter analysis. western blot was used to detect protein levels. The RNA level was evaluated using quantitative real-time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR-138 or miR-193 and UCA1 in lung cancer tissues was assessed using quantitative real-time PCR.en miR-138 or miR-193 and UCA1 in lung cancer tissues.CONCLUSIONS: Our results demonstrated that miR-138 and miR-193 affect cell function by directly targeting and regulating UCA1 in lung cancer.	32767514	RID03671	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Lung cancer	UCA1	MIR193A	negatively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000207614	NA	652995	406968	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MIRN193|MIRN193A|mir-193a	miR-138 and miR-193 specifically targeted and regulated lncRNA-UCA1. MiR-138 and miR-193 both suppressed cell proliferation and cell cycle progression. Moreover, miR-138 and miR-193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR-138 or miR-193. Furthermore, miR-138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR-138 and miR-193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR-138 or miR-193 and UCA1 in lung cancer tissues.CONCLUSIONS: Our results demonstrated that miR-138 and miR-193 affect cell function by directly targeting and regulating UCA1 in lung cancer.	32767514	RID03672	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Colorectal cancer	PGM5-AS1	SMAD4	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-100-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000265923	NA	ENSG00000141646	NA	572558	4089	FAM233A|LOC572558	DPC4|MADH4	Reduced long noncoding RNA PGM5-AS1 facilitated proliferation and invasion of colorectal cancer through sponging miR-100-5p.We found that both PGM5-AS1 and SMAD4 were downregulated in human colorectal cancer tissues and cells. qRT-PCRand CCK-8 assay showed that PGM5-AS1 expression is associated with the proliferation of colorectal cancer cells. Transwell assay showed that PGM5-AS1 regulated the migration ability of colorectal cancer cells. The bioinformatics prediction and Luciferase assay demonstrated that by sponging miR-100-5p, PGM5-AS1 can serve as a molecular sponge to further regulate the expression of SMAD4.CONCLUSIONS: In this study, we found that lncRNA-PGM5-AS1 was low expressed in human colorectal cancer cells, which could promote tumor proliferation, migration and invasion by serving as a molecular sponge and by modulating the inhibitory effect of miR-100-5p on tumor suppressor gene SMAD4.	32767323	RID03673	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Glioblastoma	PWRN1	miR-21-5p	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell growth(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000259905	GRCh38_15:24101827-24823365	NA	NA	791114	NA	NCRNA00198	NA	PWRN1 Suppressed Cancer Cell Proliferation and Migration in Glioblastoma by Inversely Regulating hsa-miR-21-5p.qRT-PCRwas applied to assess PWRN1 expression in human GBM tumors and GBM cell lines. PWRN1 was overexpressed by lentiviral infection in LN-229 and U-251 cells to evaluate its effect on GBM cell proliferation and migration in vitro, and xenograft in vivo. The endogenously competing target of PWRN1, human microRNA-21-5p (hsa-miR-21-5p) was evaluated by dual-luciferase activity assay and qRT-PCR Also, hsa-miR-21-5p was upregulated in PWRN1-overexpressed GBM cells to evaluate the functional involvement of hsa-miR-21-5p in PWRN1-mediated GBM cell proliferation and migration.PWRN1 was downregulated in both human GBM tumors and GBM cell lines. In LN-229 and U-251, PWRN1 overexpression suppressed cancer cell proliferation and migration in vitro, and xenograft growth in vivo. Hsa-miR-21-5p was demonstrated to be the downstream competing target of PWRN1 in GBM. Conversely, upregulating hsa-miR-21-5p in LN-229 and U-251 cells reversed the tumor-suppressing effects of PWRN1 overexpression.	32753949	RID03674	expression association	NA	UP(PAAD);DATA(GSE60407)	
Colorectal cancer	NEAT1	CEP55	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000138180	NA	283131	55165	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	C10orf3|CT111|FLJ10540	Evaluation of Potential of Long Noncoding RNA NEAT1 in Colorectal Cancer.Long noncoding RNAs (lncRNAs) have been reported to be involved in cancer initiation and evolution, including colorectal cancer (CRC). Nuclear-enriched abundant transcript 1 (NEAT1) exerts important functions in multiple cancers; however, the specific modulatory mechanism in CRC demands in-depth exploration. The expression levels of NEAT1, microRNA-195-5p (miR-195-5p), and centrosomal protein 55 (CEP55) were examined using quantitative real-time polymerase chain reaction (qRT-PCR, and protein expression of CEP55 was detected by western blot assay. Cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazole-2-y1)-2,5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry. Transwell migration and invasion assays were applied to evaluate cell metastasis ability. dual-luciferase reporter assay was used to analyze the correlation among NEAT1, miR-195-5p and CEP55. The expression of NEAT1 was up-regulated in CRC tissues and cells, and overall survival was lower with high expression of NEAT1. Knockdown of NEAT1 repressed cell proliferation, migration, and invasion, while inducing apoptosis in CRC cells. NEAT1 targeted miR-195-5p and inhibited the expression of miR-195-5p. Silence of NEAT1 inhibited CRC cell proliferation, migration, and invasion, and promoted apoptosis by up-regulating miR-195-5p. MiR-195-5p targeted and suppressed CEP55 expression, and CEP55 reverted the effects induced by miR-195-5p. NEAT1 regulated the expression of CEP55 through miR-195-5p. NEAT1 promotes colorectal cancer cellular processes by regulating CEP55 expression via the sponging of miR-195-5p. Therefore, NEAT1 might play a crucial role in CRC treatments.	32749120	RID03675	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Endometrial cancer	LNCOC1	CD274	positively-E	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell viability(-)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000253741	GRCh38_8:142701857-142727047	ENSG00000120217	NA	100288181	29126	Lnc-OC1	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	Inhibition of Lnc-OC1 Induced Cell Apoptosis and Decreased Cell Viability by Releasing miR-34a and Inhibiting PD-L1 in Endometrial Carcinoma.Now, there is a growing awareness of the role to long non-coding RNAs (lncRNAs) in tumorigenesis and progression of a variety of malignancies including endometrial carcinoma (EC). Here, we explored the potential molecular mechanism of Lnc-OC1, a novel lncRNA, in the development of EC. Our results suggested that Lnc-OC1 was significantly upregulated in EC tissues comparing with normal tissues. Besides, Lnc-OC1 was higher expressed in the more advanced stage of EC. Therefore, Lnc-OC1 might be a crucial regulator in the progress of EC. Moreover, knockdown of Lnc-OC1 leaded to an inhibition of cell viability and a raise of cell apoptosis. In addition, Lnc-OC1 could sponge miR-34a and thus decrease its expression. miR-34a was proved to be a tumor suppressor in different malignance, hence downregulating Lnc-OC1 helped to alleviate EC by releasing miR-34a. Furthermore, rescue experiments significantly indicated that knockdown of Lnc-OC1 inhibited cell growth through repressing PD-L1 expression at least partially. Concisely, our results proved that Lnc-OC1/miR-34a/PD-L1 axis might serve as a therapeutic target of EC.	32748220	RID03676	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Sepsis	TUG1	SLIT2	positively-E	luciferase reporter assay;western blot;RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(-);cell autophagy(-);inflammatory response(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000145147	NA	55000	9353	FLJ20618|LINC00080|NCRNA00080	SLIL3|Slit-2	TUG1 expression was decreased after the treatment of LPS in HUVECs. Overexpression of TUG1 decreased LPS-induced apoptosis, autophagy, and inflammatory response. TUG1 was a sponge of miR-27a-3p. Upregulation of miR-27a-3p reversed the suppressive effect of TUG1 overexpression on LPS-induced apoptosis, autophagy, and inflammatory response. SLIT2 was a target of miR-27a-3p. Knockdown of miR-27a-3p could inhibit LPS-induced injury by increasing SLIT2 in HUVECs. TUG1 could enhance SLIT2 expression by competitively sponging miR-27a-3p.CONCLUSIONS: TUG1 could repress cell apoptosis, autophagy, and inflammatory response in LPS-treated HUVECs by sponging miR-27a-3p to target SLIT2, providing a potential target for the treatment of sepsis.	32738556	RID03677	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Lupus nephritis	NEAT1	TRAF6	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell injury(+);NF-kB signaling pathway(+)	ceRNA(miR-146b)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Nephritis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000175104	NA	283131	7189	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	RNF85	LncRNA NEAT1 accelerates renal mesangial cell injury via modulating the miR-146b/TRAF6/NF-kB axis in lupus nephritis.Although growing advances have been made in the regulation of lupus nephritis recently, lupus nephritis is still one of the major causes of death in SLE patients and the pathogenesis remains largely unknown. Therefore, exploring the pathological mechanisms is urgently needed for designing and developing novel therapeutic strategies for lupus nephritis. Human renal mesangial cells (HRMCs) were transfected with sh-NEAT1, miR-146b mimic, pcDNA-NEAT1, miR-146b inhibitor, or sh-TRAF6 to modify their expression. Lipopolysaccharide (LPS) was used to induce inflammatory injury. Cell viability was examined with CCK8. Apoptosis was determined by flow cytometry and Hoechst staining. qRT-PCRand western blot were used to analyze gene expression. The secretion of inflammatory cytokines was examined with ELISA. The bindings of NEAT1 with miR-146b and miR-146b with TRAF6 were tested by dual-luciferase reporter assay. NEAT1 was upregulated in LPS-treated HRMCs. Both the knockdown of NEAT1 and TRAF6 suppressed the LPS-induced inflammatory injury in HRMCs. NEAT1 directly targeted miR-146b to control miR-146b-mediated regulation of TRAF6 expression in HRMCs. NEAT1 promoted the expression of TRAF6 via targeting miR-146b to accelerate the LPS-mediated renal mesangial cell injury in HRMCs. Moreover, TRAF6 activated the NF-kB signaling in HRMCs. NEAT1 accelerated renal mesangial cell injury via directly targeting miR-146b, promoting the expression of TRAF6, and activating the NF-kB signaling in lupus nephritis. Our investigation elucidated novel pathological mechanisms and provided potential therapeutic targets for lupus nephritis.	32710276	RID03678	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Neuroblastoma	NEAT1	FOXP1	positively-E	luciferase reporter assay;StarBase	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);ERK/AKT signaling pathway(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000114861	NA	283131	27086	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	12CC4|hFKH1B|HSPC215|QRF1	NEAT1 Negatively Regulates Cell Proliferation and Migration of Neuroblastoma Cells by miR-183-5p/FOXP1 Via the ERK/AKT Pathway.We observed that the expression of lncRNA nuclear-enriched abundant transcript-1 (NEAT1) was significantly decreased in human neuroblastoma tissues and cell lines, compared with the normal. We observed cell proliferation, migration, and invasion with Cell Counting Kit-8 assay, colony formation assay, and Transwell assay to investigate the effects of NEAT1, miR-183-5p, or FOXP1 on neuroblastoma cells. And we also used StarBase and luciferase reporter gene assay to predict and confirm the interaction of NEAT1, miR-183-5p, and FOXP1 in neuroblastoma cells. First, overexpression of NEAT1 suppressed cell proliferation and played a key role in cell migration and invasion. In addition, NEAT1 was demonstrated to directly interact with miR-183-5p and exerted its antioncogenic role in neuroblastoma by negatively regulating miR-183-5p expression. miR-183-5p suppressed the expression of FOXP1 and regulated cell proliferation and migration by directly targeting FOXP1 mRNA 3'-untranslated region. Moreover, FOXP1 antagonized the effect of miR-183-5p on the phosphorylation of extracellular-regulated kinase/protein kinase B (ERK/AKT), while FOXP1 siRNA increased the reduced phosphorylation of ERK/AKT caused by miR-183-5p inhibitor in neuroblastoma cells. Taken together, these data showed that NEAT1 negatively regulated cell proliferation and migration of neuroblastoma by the miR-183-5p/FOXP1 axis via suppression of the ERK/AKT pathway. Our findings may provide a new target for the study of pathogenesis and treatment of neuroblastoma.	32693640	RID03679	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)
Gallbladder cancer	PVT1	miR-30d-5p	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 regulates gallbladder cancer progression through miR-30d-5p.Gallbladder cancer (GBC) is a malignant tumors that develops insidiously and rapidly. In this work, we explored the function of long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) in modulating GBC development. PVT1 and miR-30d-5p expression were detected by real-time fluorescent quantitative polymerase chain reaction (qRT-PCR. The relationship of PVT1 and miR-30d-5p was analyzed by Dual luciferase activity and Spearman correlation analysis. The effect of PVT1 on GBC progression was detected by cell counting kit-8 (CCK-8) and Transwell assay. In GBC tissues and cell lines, upregulation of PVT1 and downregulation of miR-30d-5p were observed. PVT1 silencing suppressed cell proliferation and invasion of GBC cells. Based on the analysis of Dual luciferase activity and Spearman correlation, miR-30d-5p was confirmed as a target of PVT1, and their expression had a negative correlation in GBC tissues. Additionally, miR-30d-5p inhibitor could reverse the effects of PVT1 knockdown. These data demonstrated that PVT1 facilitated to GBC tumorigenesis by promoting cell proliferation and invasion via miR-30d-5p, indicating that PVT1 may be a potential biomarker of GBC diagnosis and treatment.	32689767	RID03680	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Gastric cancer	PCAT18	TP53INP1	positively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell viability(+);cell invasion(+);cell migration(+)	ceRNA(miR-301a)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265369	GRCh38_18:26687621-26703638	ENSG00000164938	NA	728606	94241	LINC01092	DKFZp434M1317|FLJ22139|P53DINP1|SIP|Teap|TP53INP1A|TP53INP1B	LncRNA PCAT18/miR-301a/TP53INP1 axis is involved in gastric cancer cell viability, migration and invasion.we found that PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion and migration of GC cells and tumour growth of GC xenograft tumours. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumour suppressor for GC and lncRNA PCAT18, miR-301a and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration and invasion.	32687182	RID03681	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	DMTF1	FUT4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-125a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000135164	GRCh38_7:87152409-87196337	ENSG00000196371	NA	9988	2526	DMP1|DMTF|hDMP1|MRUL	CD15|ELFT|FCT3A|FUC-TIV	Long Non-coding RNA MRUL Contributes to Osteosarcoma Progression Through the miR-125a-5p/FUT4 Axis.This research aimed to investigate the effect of a long non-coding RNA (lncRNA), MRUL, on OS and revealed its potential molecular mechanisms. The bioinformatics analysis demonstrated that lncRNA MRUL was involved in regulating nucleic acid-templated transcription, cellular macromolecule biosynthetic process, immune response, and inflammatory response. In this work, the expression of lncRNA MRUL was detected by quantitative real-time polymerase chain reaction (qRT-RCR) in both cancer tissues and cell lines. We found that lncRNA MRUL was up-regulated in cancer tissues and cell lines. Functional experiments showed that knockdown of lncRNA MRUL inhibited OS cell proliferation, and metastasis. At the same time, we found that lncRNA MRUL interacted with miR-125a-5p to suppress FUT4 expression. Moreover, inhibition of miR-125a-5p abrogated the biological roles of lncRNA MRUL knockdown on OS cell proliferation, migration, and invasion. In conclusion, these results demonstrated that OS-upregulated lncRNA MRUL promoted cell proliferation, and metastasis via negatively regulating miR-125a-5p, and imply that lncRNA MRUL may be a potential biomarker for OS.	32670359	RID03682	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)
Osteoporosis	FTX	MIR137	negatively-E	luciferase reporter assay;RIP;RNA pull-down assay;western blot	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000284202	NA	100302692	406928	FLJ33139|LINC00182|MIR374AHG|NCRNA00182	hsa-mir-137|miR-137|MIRN137	Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137.The expressions of FTX and miR-137 in bone and serum samples of patients with or without OP were measured. Bioinformatics analysis, RIP assays and luciferase reporter assays were performed to examine the upstream and downstream transactional factors of miR-137. Functional assays were conducted to check the roles of the Notching1 signaling pathway OP.FTX was suppressed in OP samples and serums, however, miR-137 was greatly elevated. FTX reduced osteoclast-genesis and inhibited osteogenic differentiation by targeting miR-137. This also inhibited the Notch1 signaling pathway.Our experiments and results pointed out that lncRNA FTX up-regulated miR-137 in OP through the Notch1 signaling pathway.	32660465	RID03683	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	
Pancreatic cancer	HULC	MIR622	negatively-F	luciferase reporter assay;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000251164	NA	ENSG00000207858	NA	728655	693207	HCCAT1|LINC00078|NCRNA00078	MIRN622|hsa-mir-622	The Interaction Between Long Non-coding RNA HULC and MicroRNA-622 via Transfer by Extracellular Vesicles Regulates Cell Invasion and Migration in Human Pancreatic Cancer.Moreover, some ncRNAs can be transferred by extracellular vesicles (EVs) from their donor cells to recipient cells. We previously verified that lncRNA HULC is up-regulated in PDAC cells and the intercellular transfer of HULC by EVs can promote PDAC cell invasion and migration through the induction of epithelial-sesenchymal transition (EMT). Therefore, we identified the miRNA that could target HULC and investigated the functional contributions of the miRNAULC interaction and EV transfer of miRNA to the EMT pathway in PDAC. microarray analysis revealed 187 miRNAs that were decreased to <0.87-fold in Panc-1 cells treated with TGF-beta compared with the control. Of these, miR-622 was predicted to target HULC directly by bioinformatics analysis. Expression of miR-622 was significantly down-regulated by TGF-beta in a panel of PDAC cells. miR-622 overexpression by a miRNA mimic significantly decreased HULC expression, increased E-cadherin expression, and decreased expression of Snail, N-cadherin, and vimentin. Moreover, overexpression of miR-622 significantly reduced cell invasion and migration whereas inhibition of miR-622 increased HULC expression and promoted EMT signaling, invasion, and migration of PDAC cells. Furthermore, incubation with miR-622-overexpressing EVs could transfer miR-622, which significantly elevated miR-622 expression and decreased cell invasion and migration via inhibition of the EMT pathway in recipient PDAC cells. These results provide mechanistic insights into the development of PDAC by demonstrating that miR-622, as a miRNA downregulated by TGF-beta, could target HULC and suppress invasion and migration by inhibiting EMT signaling via EV transfer. These observations may identify EV-encapsulated miRNA as a novel therapeutic target for human PDAC.	32656089	RID03684	ceRNA or sponge	NA		UP(BRCA);DATA(GSE51827,GSE55807)
Thoracic aortic aneurysm	HIF1A-AS1	APAF1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(let-7g)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Aortic disease	lncRNA	PCG	ENSG00000258777	GRCh38_14:61680723-61695892	ENSG00000120868	NA	100750246	317	5'aHIF-1A	APAF-1|CED4	HIF1A-AS1 regulated the proliferation, apoptosis ,and the activity of extracellular matrix proteins in VSMCs through modulating APAF1 by targeting let-7g, leading to the development of TAA.The expression of HIF1A-AS1, collagen I, collagen III, microRNA let-7g (let-7g) and apoptotic protease-activating factor 1 (APAF1) was detected by quantitative real-time polymerase chain reaction. Cell proliferation and cell apoptosis were assessed by Cell Counting Kit-8 and flow cytometry assays, respectively. The protein levels of proliferating cell nuclear antigen, Cleaved caspase-3 (Cleaved-cas3), B cell lymphoma/leukemia-2 (Bcl-2), Collagen I, Collagen III, and APAF1 were quantified by western blot. The relationship between let-7g and HIF1A-AS1 or APAF1 was predicted by the online bioinformatics tool and verified by dual-luciferase reporter assay and RNA pull-down assay.HIF1A-AS1 was upregulated in TAA tissues and was a valuable diagnostic marker of TAA. HIF1A-AS1 overexpression suppressed proliferation, induced apoptosis, and reduced the expression of extracellular matrix proteins in VSMCs. let-7 g was a target of HIF1A-AS1, and its inhibition functioned the same role as HIF1A-AS1 overexpression. APAF1 was a target of let-7g, and its knockdown played the opposite role with HIF1A-AS1 overexpression. The reintroduction of let-7g or APAF1 knockdown reversed the effects of HIF1A-AS1 overexpression in VSMCs.Conclusions: HIF1A-AS1 regulated the proliferation, apoptosis ,and the activity of extracellular matrix proteins in VSMCs through modulating APAF1 by targeting let-7g, leading to the development of TAA.	32653692	RID03685	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	HAGLR	CCND1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-526b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000110092	NA	401022	595	HOXD-AS1|Mdgt|MIR7704HG	BCL1|D11S287E|PRAD1|U21B31	Colorectal cancer (CRC) is one of the most common malignancies in the world. It has been reported that the abnormal expression of long noncoding RNA HOXD-AS1 promotes the development of CRC, while the mechanism is still unclear. The aim of this study is to investigate the effects of HOXD-AS1 on proliferation, migration, and invasion in CRC and explore the underlying mechanism.HOXD-AS1 was highly expressed in CRC, and high expression of HOXD-AS1 was related to the poor prognosis of patients with CRC. MiR-526b-3p could be targeted by HOXD-AS1. Function experiment results revealed that miR-526b-3p inhibitor could reverse the suppressive effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of CRC cells. Moreover, CCND1 was a target of miR-526b-3p, and its overexpression could reverse the inhibitory effect of miR-526b-3p overexpression on the proliferation, migration, and invasion of CRC cells. In addition, CCND1 overexpression reversed the suppressive effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of CRC.HOXD-AS1 upregulated the expression of CCND1 to promote the proliferation, migration, and invasion of CRC through targeting miR-526b-3p. This provided a new theoretical basis for clinical anticancer research of CRC.</AbstractText>: HOXD-AS1 upregulated the expression of CCND1 to promote the proliferation, migration, and invasion of CRC through targeting miR-526b-3p. This provided a new theoretical basis for clinical anticancer research of CRC.	32640404	RID03686	ceRNA or sponge	prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Gastric cancer	FEZF1-AS1	HMGA2	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	ceRNA(miR-363-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000149948	NA	154860	8091	NA	BABL|HMGIC|LIPO	LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2.Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. MiR-363-3p is used as a target of FEZF1-AS1, because its expression was suppressed by FEZF1-AS1 in GCSCs. FEZF1-AS1 could sponge miR-363-3p and increased the expression of high-mobility group AT-hook 2 (HMGA2). The expression of FEZF1-AS1 and miR-363-3p, as well as that of miR-363-3p and HMGA2, was negatively correlated in GC tissues. Finally, FEZF1-AS1 contributed to promotion of GCSCs progression partially through inhibition of miR-363-3p. Subcutaneous xenotransplanted tumor model revealed that silence of FEZF1-AS1 suppressed in vivo tumorigenic ability of GSCS via downregulation of HMGA2. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.	32638620	RID03687	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Melanoma	CAR10	RAB3D	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000148848	GRCh38_10:126012381-126388477	ENSG00000105514	NA	NA	9545	NA	D2-2|GOV|RAB16|RAD3D	Long Noncoding RNA CAR10 Contributes to Melanoma Progression By Suppressing miR-125b-5p to Induce RAB3D Expression.qRT-PCRwas utilized to analyze CAR10 in melanoma human tissues and cell lines while Kaplan-Meier curve was used to examine the survival rate. CCK8 assay and EdU assay were used to assess cell proliferation when Transwell assay was conducted to determine migration and invasion. And tumor xenograft assay was performed to evaluate tumor growth in vivo. Additionally, luciferase assay and RNA pull-down assay were performed to analyze the interactions among CAR10, miR-125b-5p and RAB3D..LncRNA CAR10 was upregulated in melanoma tissues and cell lines. Upregulation of CAR10 predicted a poor prognosis in patients with melanoma. CAR10 knockdown suppressed proliferation, migration and invasion of melanoma cells in vitro. CAR10 silencing attenuated tumor growth in vivo. CAR10 inhibited miR-125b-5p activity to upregulate RAB3D expression. And miR-125b-5p/RAB3D signaling is crucial for CAR10-dependent melanoma progression.</AbstractText>: LncRNA CAR10 was upregulated in melanoma tissues and cell lines. Upregulation of CAR10 predicted a poor prognosis in patients with melanoma. CAR10 knockdown suppressed proliferation, migration and invasion of melanoma cells in vitro. CAR10 silencing attenuated tumor growth in vivo. CAR10 inhibited miR-125b-5p activity to upregulate RAB3D expression. And miR-125b-5p/RAB3D signaling is crucial for CAR10-dependent melanoma progression.Our work suggests that lncRNA CAR10 promotes melanoma growth and metastasis through modulating miR-125b-5p/RAB3D axis.</AbstractText>: Our work suggests that lncRNA CAR10 promotes melanoma growth and metastasis through modulating miR-125b-5p/RAB3D axis.	32636644	RID03688	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE51827,GSE75367,GSE86978)
Malignant glioma	FLVCR1-DT	miR-30b-3p	negatively-F	luciferase reporter assay;RNA pull-down assay;miRDB	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000198468	GRCh38_1:212852105-212858138	NA	NA	642946	NA	FLVCR1-AS1|LQK1|NCRNA00292	NA	Long non-coding RNA FLVCR1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-30b-3p.Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults that originates from glial cells. The prognosis of patients with high-grade glioma is poor. It is therefore crucial to develop effective therapeutic strategies. Long non-coding RNAs (lncRNAs) have been reported as potential inducers or suppressors of tumor progression. Previous studies have indicated that the lncRNA Feline Leukemia Virus Subgroup C Cellular Receptor 1 Antisense RNA 1 (FLVCR1-AS1) is involved in the development and progression of gastric and lung cancer, as well as hepatocellular carcinoma and cholangiocarcinoma; however, the biological effect of FLVCR1-AS1 in glioma is not completely understood. The aim of the present study was to investigate how FLVCR1-AS1 modulates cell proliferation and invasion in glioma. FLVCR1-AS1 expression was significantly upregulated in GBM tissues compared with adjacent normal brain samples, and was higher in GBM cell lines compared with normal human astrocyte cells. Furthermore, the microRNA (miR)-30b-3p was revealed to be a putative target of FLVCR1-AS1, and the suppressive effects of miR-30b-3p on cellular proliferation and invasion were reversed following FLVCR1-AS1-knockdown. The results from Cell Counting Kit-8 and Transwell assays confirmed that FLVCR1-AS1-knockdown inhibited GBM cell proliferation and invasion ability. In addition, FLVCR1-AS1 was found to directly interact with miR-30b-3p, and a rescue experiment further established that FLVCR1-AS1 contributed to glioma progression by inhibiting miR-30b-3p. The results from the present study demonstrated that FLVCR1-AS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miR-30b-3p. These findings suggested that FLVCR1-AS1 may be considered as a novel therapeutic target and diagnostic biomarker for GBM.	32626942	RID03689	ceRNA or sponge	prognosis		
Non-small cell lung cancer	AGO2	miR-92a	negatively-F	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000123908	GRCh38_8:140520156-140635633	NA	NA	27161	NA	CASC7|EIF2C2|hAGO2|LINC00980|Q10	NA	The long non-coding RNA CASC7 inhibits growth and invasion of non-small cell lung cancer cells through phosphatase and tensin homolog upregulation via sequestration of miR-92a. However, to the best of our knowledge, the role of the lncRNA cancer susceptibility candidate 7 (CASC7) in NSCLC has not been clearly determined. The aim of the present study was to investigate the involvement of CASC7 in NSCLC. Marked downregulation of CASC7 was observed in NSCLC tissues and cell lines, and this downregulation of CASC7 was closely associated with distant metastasis, lymph node involvement and poor overall survival in NSCLC patients. Furthermore, overexpression of CASC7 significantly suppressed the proliferation, invasion and migration of the NSCLC cells A549 and H358, and promoted cell apoptosis in vitro. In addition, CASC7 was shown to act as a competing endogenous RNA by sponging miR-92a, which was proven to be an oncogenic miRNA in our previous study. The expression of miR-92a was upregulated in NSCLC tissues and cell lines, and was found to be inversely associated with CASC7 expression in NSCLC tissues. It was also demonstrated that CASC7 upregulated the expression of the tumor suppressor gene phosphatase and tensin homolog (a well-known target of miR-92a) by sequestration of miR-92a. Moreover, the tumor-suppressive effects of CASC7 were partly reversed by miR-92a overexpression in NSCLC cells. Collectively, the results of the present study indicated that CASC7 may act as a tumor-suppressive lncRNA that inhibits NSCLC progression by sponging miR-92a. These findings may improve our understanding of the potential mechanisms through which gain of CASC7 expression represses NSCLC progression.	32626930	RID03690	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Prostate cancer	PVT1	KIF23	positively-E	western blot;starBase v2.0;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-15a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000137807	NA	5820	9493	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	KNSL5|MKLP-1|MKLP1	Knockdown of lncRNA PVT1 inhibits prostate cancer progression in vitro and in vivo by the suppression of KIF23 through stimulating miR-15a-5p.The expression of PVT1 and KIF23 was enhanced, while miR-15a-5p expression was reduced in PCa tissues and cells. PVT1 interference inhibited proliferation, migration and invasion but promoted apoptosis of PCa cells. MiR-15a-5p was a target of PVT1, and KIF23 was a target of miR-15a-5p. The inhibition of miR-15a-5p reversed the effects of PVT1 interference and suppressed the roles of KIF23 knockdown. KIF23 expression was regulated by PVT1 through miR-15a-5p. PVT1 interference blocked PCa progression in vivo.PVT1 knockdown had effects on the progression of PCa by inhibiting the expression of KIF23 via enriching miR-15a-5p in vitro and in vivo, suggesting that PVT1 might be a novel biomarker for the treatment of PCa.</AbstractText>: PVT1 knockdown had effects on the progression of PCa by inhibiting the expression of KIF23 via enriching miR-15a-5p in vitro and in vivo, suggesting that PVT1 might be a novel biomarker for the treatment of PCa.The expression of PVT1, microRNA-15a-5p (miR-15a-5p) and kinesin family member 23 (KIF23) was detected by quantitative real-time polymerase chain reaction (qRT-PCR. Cell proliferation, apoptosis, migration and invasion were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry and transwell assays, respectively. The protein levels of KIF23 and proliferation, apoptosis, and epithelial-mesenchymal transition (EMT)-related markers were quantified by western blot. The relationship between miR-15a-5p and PVT1 or KIF23 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Xenograft assay was conducted to determine the role of PVT1 in vivo.	32624708	RID03691	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	PCGEM1	P4HA2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-129-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000072682	NA	64002	8974	LINC00071|NCRNA00071|PCAT9	C-P4Halpha(II)	LncRNA PCGEM1 enhances metastasis and gastric cancer invasion through targeting of miR-129-5p to regulate P4HA2 expression.Bioinformatics database and Ago2-RIP were performed to predict and verify the potential targets of lncRNA PCGEM1. Both gain- and loss-of-function experiments were carried out to dissect the biological functions of RNAs. Fluorescence in situ hybridization, dual-luciferase reporter assays, western blot, and real-time PCR (RT-PCR experiments were utilized to determine the pathophysiological pathways of competitive endogenous RNAs (ceRNAs).GC cells expressed high levels of cytoplasmic PCGEM1. Loss-of-function experiments displayed that the silencing of PCGEM1 suppressed metastatic and invasive cell qualities. PCGEM1 was also found to have associations with miR-129-5p. Subsequently, luciferase reporter and RIP experiments, together with RT-PCR verified that PCGEM1 functioned as a ceRNA of P4HA2 (Prolyl 4-Hydroxylase Subunit Alpha 2) via sponging miR-129-5p to up-regulate P4HA2 expression. Finally, the rescue assays determined that P4HA2 overexpression rescued the inhibited cell invasion and metastasis caused by PCGEM1 down-regulation.	32622013	RID03692	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE60407)	UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	CRNDE	CDK6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-33a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000105810	NA	643911	1021	CRNDEP|LINC00180|LOC643911	PLSTIRE	Long non-coding RNA CRNDE promotes malignant progression of hepatocellular carcinoma through the miR-33a-5p/CDK6 axis.Emerging evidence has suggested that long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) is upregulated in hepatocellular carcinoma (HCC) and is associated with cell invasion, migration, and growth. However, the potential modulation mechanism remains to be elucidated. MiR-33a-5p and cyclin-dependent kinase 6 (CDK6) also participate in the pathophysiology of HCC. This work aims to investigate the effect of CRNDE on HCC apoptosis, invasion, and migration and elucidate the role of miR-33a-5p and CDK6 therein. CRNDE and CDK6 were upregulated in HCC tissues and cells, while miR-33a-5p was downregulated. Inhibition of CRNDE suppressed the invasion, migration, and proliferation of HCC cells and enhanced apoptosis by modulating proteins associated with mitochondrial apoptosis (caspase 3, Bax, cytochrome-c, Bcl-2), which were the same as the function of miR-33a-5p overexpression. The dual-luciferase reporter assay demonstrated that miR-33a-5p was a target of CRNDE, and in turn, CRNDE inhibition enhanced the level of miR-33a-5p. CDK6 was also revealed as a target of miR-33a-5p, and both CRNDE inhibition and miR-33a-5p overexpression suppressed CDK6 expression and led to G0/G1 phase block in HCC cells. In vivo experiments using a mouse xenograft tumor model further verified the interaction between CRNDE and miR-33a-5p, showing that miR-33a-5p overexpression or CRNDE inhibition suppressed CDK6 expression and HCC tumorigenesis. Overall, the present work indicated that CRNDE plays an oncogenic function in HCC through regulating the miR-33a-5p/CDK6 axis, revealing a potential therapeutic target in HCC.	32621257	RID03693	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Breast cancer	LINC00839	LIN28B	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);PI3K/AKT signaling pathway(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000185904	GRCh38_10:42475480-42495337	ENSG00000187772	NA	84856	389421	NA	CSDD2|FLJ16517	A nuclear lncRNA Linc00839 as a Myc target to promote breast cancer chemoresistance via PI3K/AKT signaling pathway.Here, we reported that Linc00839 was localized in the nucleus and upregulated in chemoresistant breast cancer cells and tissues, and high level of Linc00839 was associated with a poor prognosis. Knockdown of Linc00839 significantly suppressed proliferation, invasion, and migration, sensitized cells to paclitaxel in vitro and inhibited transplant tumor development in vivo. Mechanistically, we found that Myc could directly bind to the promoter region of Linc00839 and activate its transcription. Furthermore, Linc00839 overexpression increased the expression of Myc and the RNA-binding protein Lin28B and activated the PI3K/AKT signaling pathway. We also discovered that Lin28B positively interacted with Linc00839 and was upregulated in breast cancer tissues. Taken together, for the first time, we showed that Linc00839 was activated by Myc and promoted proliferation and chemoresistance in breast cancer through binding with Lin28B. These findings provide new insight into the regulatory mechanism of Linc00839 and propose a Myc/Linc00839/Lin28B feedback loop that could be used as a novel therapeutic target for breast cancer.	32619088	RID03694	expression association	chemoresistance,prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Nasopharynx carcinoma	MCM3AP-AS1	miR-34a	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000215424	GRCh38_21:46229196-46259390	NA	NA	114044	NA	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	NA	MiR-34a Inhibits Cell Proliferation and Induces Apoptosis in Human Nasopharyngeal Carcinoma by Targeting lncRNA MCM3AP-AS1.In NPC cells, overexpression of MCM3AP-AS1 did not affect the expression of miR34a, while overexpression of miR-34a led to downregulated MCM3AP-AS1. Cell proliferation and apoptosis assay showed that overexpression of miR-34a reduced the enhancing effects of overexpressing MCM3AP-AS1 on cell proliferation and the inhibitory effects on cell apoptosis.</AbstractText>: Our bioinformatics analysis showed that MCM3AP-AS1 may be targeted by miR-34a, which is a well-studied tumor suppressor miRNA. In this study, we showed that miR-34a was downregulated and MCM3AP-AS1 was upregulated in NPC. An inverse correlation between the expression of MCM3AP-AS1 and miR-34a was found across NPC tissue samples. High expression level of MCM3AP-AS1 and low levels of miR-34a in NPC tissues predicted the poor survival. In NPC cells, overexpression of MCM3AP-AS1 did not affect the expression of miR34a, while overexpression of miR-34a led to downregulated MCM3AP-AS1. Cell proliferation and apoptosis assay showed that overexpression of miR-34a reduced the enhancing effects of overexpressing MCM3AP-AS1 on cell proliferation and the inhibitory effects on cell apoptosis.MiR-34a inhibits cell proliferation and induces apoptosis in human NPC by targeting MCM3AP-AS1.</AbstractText>: MiR-34a inhibits cell proliferation and induces apoptosis in human NPC by targeting MCM3AP-AS1.	32606969	RID03695	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	
Colorectal cancer	HCP5	PFN1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-)	ceRNA(miR-299-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000108518	NA	10866	5216	D6S2650E|P5-1	NA	Knockdown of lncRNA HCP5 Suppresses the Progression of Colorectal Cancer by miR-299-3p/PFN1/AKT Axis.The expression of HCP5 had a higher level in colorectal cancer samples and cells by qRT-PCR comparing with the normal colorectal tissues and human normal colon epithelial cell. It was revealed that knockdown of HCP5 inhibited viabilities, migration and invasion, while inducing apoptosis in SW480 and HCT-116 cells. Then, HCP5 negatively regulated the expressions of miR-299-3p, which negatively regulated the expressions of PFN1 by targeting PFN1. Furthermore, miR-299-3p inhibitor could alleviate the inhibiting effect by si-HCP5 on cell process of SW480 and HCT-116 cells. In addition, the lncHCP5/miR-299-3p/PFN1 axis could affect the progression of CRC through activating the AKT signaling. Last, we confirmed that knockdown of HCP5 inhibited the progression of CRC with an in vivo experiment.The experiments and analyses support our hypothesis that knockdown of lncRNA HCP5 suppresses the progression of colorectal cancer by miR-299-3p/PFN1/AKT axis.</AbstractText>: The experiments and analyses support our hypothesis that knockdown of lncRNA HCP5 suppresses the progression of colorectal cancer by miR-299-3p/PFN1/AKT axis.	32606965	RID03696	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	DSCAM-AS1	SOX4	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000124766	NA	100506492	6659	M41	NA	LncRNA DSCAM-AS1 Promotes Colon Cancer Cells Proliferation and Migration via Regulating the miR-204/SOX4 Axis.DSCAM-AS1 was significantly upregulated in CC and high expression of DSCAM-AS1 was associated with poor prognosis in patients with colon cancer. Knockdown of DSCAM-AS1 significantly suppressed CC cells proliferation and migration. In addition, DSCAM-AS acted as a molecular sponge for miR-204 and SOX4 was identified as a direct target of miR-204 in CC. Moreover, the rescue assay revealed that miR-204 inhibition partly abolished the effects of DSCAM-AS1 knockdown on CC cells proliferation, migration and SOX4 expression.</AbstractText>: DSCAM-AS1 was significantly upregulated in CC and high expression of DSCAM-AS1 was associated with poor prognosis in patients with colon cancer. Knockdown of DSCAM-AS1 significantly suppressed CC cells proliferation and migration. In addition, DSCAM-AS acted as a molecular sponge for miR-204 and SOX4 was identified as a direct target of miR-204 in CC. Moreover, the rescue assay revealed that miR-204 inhibition partly abolished the effects of DSCAM-AS1 knockdown on CC cells proliferation, migration and SOX4 expression.The present study demonstrated that DSCAM-AS1 acted as an oncogenic lncRNA in CC progression by regulating miR-204/SOX4 axis and DSCAM-AS1 may serve as a novel therapeutic target in the treatment of colon cancer.</AbstractText>: The present study demonstrated that DSCAM-AS1 acted as an oncogenic lncRNA in CC progression by regulating miR-204/SOX4 axis and DSCAM-AS1 may serve as a novel therapeutic target in the treatment of colon cancer.	32606930	RID03697	ceRNA or sponge	prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Adhesions of uterus	TUG1	FASLG	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-590-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Reproductive system disease	Uterine disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000117560	NA	55000	356	FLJ20618|LINC00080|NCRNA00080	APT1LG1|CD178|FasL|TNFSF6	lncRNA TUG1 promotes endometrial fibrosis and inflammation by sponging miR-590-5p to regulate Fasl in intrauterine adhesions.Here, we found that lncRNA TUG1 was upregulated in the endometrial tissues of IUA and TGF-beta1-treated human embryonic stem cells (hESCs). Moreover, lncRNA TUG1-silenced alleviated TGF-beta1-induced the proliferation and migration abilities of hESCs and enhanced inflammatory cytokines secretion in vitro. In vivo experiments showed that inhibition of lncRNA TUG1 promoted endometrium regeneration in IUA rats through downregulating inflammatory response and epithelial-to-mesenchymal transition (EMT) process. Mechanistically, lncRNA TUG1 suppression attenuated EMT process and inflammation through competitively binding miR-590-5p to downregulate Fasl expression. Collectively, our findings provide vital theoretical evidence for explaining the mechanisms of the lncRNA TUG1/miR-590-5p/Fasl axis in the progression of IUA, and may provide a new biomarker for the treatment of IUA patients.	32599321	RID03698	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ischemic stroke	MALAT1	PIK3CA	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);PI3K/AKT signaling pathway(-)	ceRNA(miR-126)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000121879	NA	378938	5290	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PI3K	LncRNA MALAT1 Promotes OGD-Induced Apoptosis of Brain Microvascular Endothelial Cells by Sponging miR-126 to Repress PI3K/Akt Signaling Pathway.Ischemic stroke (IS) is a common disease that seriously endangers human health. Patients with IS present with increased death of brain microvascular endothelial cells (BMECs). MALAT1 is found to be upregulated in IS patients. However, the function of MALAT1 in IS pathogenesis still remains unclear. This study aimed to investigate the role of MALAT1 in IS in vitro model and the related molecular mechanisms. The expressions of MALAT1 and miR-126 were detected by qPCR. The in vitro IS model was established by treating BMECs with oxygen-glucose deprivation (OGD). Cell viability and cell apoptosis were assessed by MTT assay and flow cytometry, respectively. Luciferase assay was conducted to examine the interplay between MALAT1 and miR-126. western blot was used to determine the protein levels of apoptosis-associated proteins (e.g. caspase 3, Bax and Bcl-2) and PI3K/Akt pathway-related proteins (e.g. PI3K, Akt, p-PI3K, p-Akt). OGD induced upregulation of MALAT1 and downregulation of miR-126 in HBMECs. MALAT1 knockdown promoted the proliferation of HBMECs and reduced the proportion of apoptotic HBMECs by regulating the expression of apoptosis-related proteins. MALAT1 targeted and negatively regulated miR-126 expression. Overexpression of miR-126 activated the PI3K/Akt pathway, which in turn affected the proliferation and apoptosis of HBMECs. MALAT1 negatively regulated PI3K/Akt pathway. MALAT1 inhibited the proliferation and induced the apoptosis of OGD-induced HBMECs through suppressing PI3K/AKT pathway by sponging miR-126, providing a potential therapeutic target for IS.	32591985	RID03699	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Gastric cancer	LINC00242	FOXC1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+)	ceRNA(miR-141)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000229214	GRCh38_6:169788790-169799549	ENSG00000054598	NA	401288	2296	C6orf122|dJ266L20.5|FLJ31451|NCRNA00242	ARA|FKHL7|FREAC3|IGDA|IHG1|IRID1	Activation of the LINC00242/miR-141/FOXC1 axis underpins the development of gastric cancer.LINC00242 was highly expressed in GC tissues and cells and contributed to poor prognosis. LINC00242 knockdown inhibited HGC27 cell viability, migration and invasion, and tube formation of HBMVECs. LINC00242 interacted with miR-141 and positively regulated FOXC1, a target gene of miR-141. LINC00242 knockdown was partially lost in HGC27 cells upon miR-141 inhibition or FOXC1 overexpression. The tumor-promoting effect of LINC00242 on GC was demonstrated in nude mice.Taken together, the present study demonstrates the oncogenic role of the LINC00242/miR-141/FOXC1 axis in GC, highlighting a theoretical basis for GC treatment.</AbstractText>: Taken together, the present study demonstrates the oncogenic role of the LINC00242/miR-141/FOXC1 axis in GC, highlighting a theoretical basis for GC treatment.	32587479	RID03700	ceRNA or sponge	prognosis		UP(SKCM);DATA(GSE38495)
Glioblastoma	FGD5-AS1	HNRNPK	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+);apoptosis process(-)	ceRNA(miR-129-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000225733	GRCh38_3:14920347-14948424	ENSG00000165119	NA	100505641	3190	NA	CSBP|HNRPK|TUNP	FGD5-AS1 facilitates glioblastoma progression by activation of Wnt/beta-catenin signaling via regulating miR-129-5p/HNRNPK axis.The expression of FGD5-AS1, miR-129-5p, and heterogeneous nuclear ribonucleoprotein K (HNRNPK) mRNA were measured by qRT-PCR Cell proliferation, invasion and apoptosis were determined by MTT, colony formation, transwell and flow cytometry assays. The protein levels of Ki-67, HNRNPK and Wnt signaling-associated genes were examined by western blot assay. The possible action mechanism of FGD5-AS1 was detected by bioinformatic tools, luciferase reporter, RIP and TOP/FOP Flash reporter assays. A nude mouse xenograft model was built to analyze the function of FGD5-AS1 in vivo.FGD5-AS1 expression was increased in GBM tumor tissues and cells. Knockdown of FGD5-AS1 inhibited cell proliferation and invasion in vitro, and slowed tumor growth in vivo. Mechanistically, FGD5-AS1 served as a sponge of miR-129-5p to relieve its suppression on HNRNPK. Moreover, down-regulation of HNRNPK repressed cell proliferation and invasion, while enhanced apoptosis. Additionally, si-FGD5-AS1-mediated suppression of cell proliferation and invasion was obviously reversed by the decrease of miR-129-5p or restoration of HNRNPK. Furthermore, FGD5-AS1 promoted cell growth and invasion by stimulating Wnt/beta-catenin signaling via regulation of miR-129-5p/HNRNPK.SIGNIFICANCE: FGD5-AS1 promoted GBM progression at least partly by regulating miR-129-5p/HNRNPK to activate Wnt/beta-catenin signaling, suggesting the potential of FGD5-AS1 as a candidate target to improve GBM therapy.	32585241	RID03701	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	XIST	PAX6	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-142-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000007372	NA	7503	5080	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	AN|AN1|AN2|D11S812E|WAGR	Knockdown of lncRNA XIST Suppresses Cell Tumorigenicity in Human Non-Small Cell Lung Cancer by Regulating miR-142-5p/PAX6 Axis.XIST was elevated in NSCLC, and XIST knockdown suppressed cell proliferation, migration, invasion and induced apoptosis in vitro as well as repressed tumor growth in vivo. MiR-142-5p was a target of XIST, and silencing miR-142-5p reversed the anti-tumor functions mediated by XIST knockdown in NSCLC cells. PAX6 was confirmed to be a target of miR-142-5p, and the inhibitory effects caused by miR-142-5p restoration in NSCLC cell malignant phenotypes were attenuated by PAX6 overexpression. Besides that, XIST could indirectly regulate PAX6 expression by sponging miR-142-5p in vivo and in vitro.XIST suppresses cell tumorigenicity in human NSCLC by regulating miR-142-5p/PAX6 axis, which indicates a novel insight into the pathogenesis of NSCLC and lays a foundation for the molecular therapy of NSCLC.</AbstractText>: XIST suppresses cell tumorigenicity in human NSCLC by regulating miR-142-5p/PAX6 axis, which indicates a novel insight into the pathogenesis of NSCLC and lays a foundation for the molecular therapy of NSCLC.	32581553	RID03702	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC);DATA(GSE117623)
Atherosclerosis	NORAD	WNT7B	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-30c-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000188064	NA	647979	7477	LINC00657	NA	Knockdown of LINC00657 inhibits ox-LDL-induced endothelial cell injury by regulating miR-30c-5p/Wnt7b/beta-catenin.Long noncoding RNAs (lncRNAs) play pivotal roles in the pathogenesis, development, and treatment of atherosclerosis (AS). The endothelial cell injury is a feature of AS. However, the role and mechanism of lncRNA LINC00657 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell injury remain unclear. The serum samples were collected from 32 AS patients and normal volunteers. Ox-LDL-treated human umbilical vein endothelial cells (HUVEC) were used for the experiments in vitro. The levels of LINC00657, microRNA (miR)-30c-5p and Wnt family member 7B (Wnt7b) were measured by quantitative real-time polymerase chain reaction or western blot. The expression levels of proteins in Wnt7b/beta-catenin pathway or endothelial-mesenchymal transition (EndMT) were detected by western blot. The secretion of inflammatory cytokine was examined by enzyme linked immunosorbent assay (ELISA). Cell viability and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, flow cytometry, and western blot. The target association of miR-30c-5p and LINC00657/Wnt7b was analyzed via dual-luciferase reporter assay and RNA pull-down assay. LINC00657 expression was increased in AS serum and ox-LDL-treated HUVEC cells. LINC00657 knockdown suppressed ox-LDL-induced Wnt7b/beta-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. MiR-30c-5p was bound to LINC00657 and it knockdown reversed the role of LINC00657 inhibition in ox-LDL-induced HUVEC cell injury. MiR-30c-5p targeted Wnt7b to inhibit ox-LDL-induced Wnt7b/beta-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. Silence of LINC00657 repressed ox-LDL-induced injury via inhibiting EndMT, inflammatory response, and apoptosis in HUVEC cells by regulating miR-30c-5p/Wnt7b/beta-catenin, indicating a potential target for treatment of AS.	32577947	RID03703	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE67939)
Atherosclerosis	NORAD	CTNNB1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-30c-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000168036	NA	647979	1499	LINC00657	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LINC00657 expression was increased in AS serum and ox-LDL-treated HUVEC cells. LINC00657 knockdown suppressed ox-LDL-induced Wnt7b/beta-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. MiR-30c-5p was bound to LINC00657 and it knockdown reversed the role of LINC00657 inhibition in ox-LDL-induced HUVEC cell injury. MiR-30c-5p targeted Wnt7b to inhibit ox-LDL-induced Wnt7b/beta-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. Silence of LINC00657 repressed ox-LDL-induced injury via inhibiting EndMT, inflammatory response, and apoptosis in HUVEC cells by regulating miR-30c-5p/Wnt7b/beta-catenin, indicating a potential target for treatment of AS.	32577947	RID03704	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Diabetic retinopathy	MIR497HG	SIRT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000267532	GRCh38_17:7015818-7019659	ENSG00000096717	NA	100506755	23411	MIR195HG	SIR2L1	LncRNA MIR497HG inhibits proliferation and migration of retinal endothelial cells under high-level glucose treatment via miRNA-128-3p/SIRT1 axis.Materials and methods: Relative expression levels of MIR497HG, microRNA-128-3p (miRNA-128-3p) and SIRT1 in HRECs treated with different doses of glucose and mannitol were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Dual-Luciferase reporter gene assay was conducted to assess the interaction among MIR497HG, miRNA-128-3p, and SIRT1. In addition, the potential effects of MIR497HG/miRNA-128-3p/SIRT1 axis on proliferative and migratory capacities in HRECs were evaluated by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU) and transwell assay, respectively.MIR497HG is downregulated after HG treatment. In addition, it suppresses the proliferation and migration of HRECs by targeting miRNA-128-3p/SIRT1 axis, thus influencing the progression of diabetic retinopathy.	32572899	RID03705	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	GATA3-AS1	COPS5	positively-E	RIP;western blot;luciferase reporter assay;RNA pull-down assay;ChIP	upregulation	qRT-PCR	NA	NA	immune evasion(+);cell growth(+)	ceRNA(miR-676-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000121022	NA	399717	10987	NA	CSN5|JAB1|MOV-34|SGN5	LncRNA GATA3-AS1 facilitates tumour progression and immune escape in triple-negative breast cancer through destabilization of GATA3 but stabilization of PD-L1.GATA3-AS1 expression in BC tissues and adjacent normal tissues was obtained from online databases. Loss-of-function assays were designed and conducted to verify the functional role of GATA3-AS1 in TNBC cells. Bioinformatic analysis and mechanism experiments were applied to explore the downstream molecular mechanism of GATA3-AS1. Similarly, the upstream mechanism which led to the upregulation of GATA3-AS1 in TNBC cells was also investigated..Results: GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Functionally, cell proliferation was repressed by silencing GATA3-AS1.Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.The interaction between endogenous PD-L1 and CSN5 was further demonstrated by Co-IP assay followed by western blotIn current study, we discovered that CSN5 expression was decreased by GATA3-AS1 deficiency.Briefly, GATA3-AS1 promoted PD-L1 deubiquitination by upregulating COPS5.GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.	32687248	RID03706	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Triple-negative breast cancer	GATA3-AS1	CD274	negatively-F	RIP;western blot;luciferase reporter assay;RNA pull-down assay;ChIP	upregulation	qRT-PCR	NA	NA	immune evasion(+);cell growth(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000120217	NA	399717	29126	NA	B7-H|B7H1|PD-L1|PDCD1L1|PDCD1LG1|PDL1|hPD-L1	LncRNA GATA3-AS1 facilitates tumour progression and immune escape in triple-negative breast cancer through destabilization of GATA3 but stabilization of PD-L1.Results: GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Functionally, cell proliferation was repressed by silencing GATA3-AS1.Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.The interaction between endogenous PD-L1 and CSN5 was further demonstrated by Co-IP assay followed by western blotIn current study, we discovered that CSN5 expression was decreased by GATA3-AS1 deficiency.Briefly, GATA3-AS1 promoted PD-L1 deubiquitination by upregulating COPS5.GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.	32687248	RID03707	expression association	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Triple-negative breast cancer	GATA3-AS1	GATA3	negatively-E	RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);prognosis	expression regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000107485	NA	399717	2625	NA	HDR|HDRS	LncRNA GATA3-AS1 facilitates tumour progression and immune escape in triple-negative breast cancer through destabilization of GATA3 but stabilization of PD-L1.GATA3-AS1 expression in BC tissues and adjacent normal tissues was obtained from online databases. Loss-of-function assays were designed and conducted to verify the functional role of GATA3-AS1 in TNBC cells. Bioinformatic analysis and mechanism experiments were applied to explore the downstream molecular mechanism of GATA3-AS1. Similarly, the upstream mechanism which led to the upregulation of GATA3-AS1 in TNBC cells was also investigated.Results: GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Functionally, cell proliferation was repressed by silencing GATA3-AS1.Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.The interaction between endogenous PD-L1 and CSN5 was further demonstrated by Co-IP assay followed by western blotIn current study, we discovered that CSN5 expression was decreased by GATA3-AS1 deficiency.Briefly, GATA3-AS1 promoted PD-L1 deubiquitination by upregulating COPS5.GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.	32687248	RID03708	expression association	prognosis	UP(BRCA);DATA(GSE55807)	UP(BRCA);DATA(GSE55807)
Triple-negative breast cancer	CBP	GATA3-AS1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation;histone modification	association	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000102076	NA	ENSG00000197308	GRCh38_10:8050450-8053484	NA	399717	NA	NA	LncRNA GATA3-AS1 facilitates tumour progression and immune escape in triple-negative breast cancer through destabilization of GATA3 but stabilization of PD-L1.Results: GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Functionally, cell proliferation was repressed by silencing GATA3-AS1.Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.The interaction between endogenous PD-L1 and CSN5 was further demonstrated by Co-IP assay followed by western blotIn current study, we discovered that CSN5 expression was decreased by GATA3-AS1 deficiency.Briefly, GATA3-AS1 promoted PD-L1 deubiquitination by upregulating COPS5.GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. GATA3-AS1 induced the deubiquitination of PD-L1 through miR-676-3p/COPS5 axis. GATA3-AS1 destabilized GATA3 protein by promoting GATA3 ubiquitination.	32687248	RID03709	epigenetic regulation	NA		UP(BRCA);DATA(GSE55807)
Nasopharynx carcinoma	LINC01503	FOSL1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000175592	NA	100506119	8061	NA	FRA|FRA1|fra-1	AR-induced long non-coding RNA LINC01503 facilitates proliferation and metastasis via the SFPQ-FOSL1 axis in nasopharyngeal carcinoma.Our previous lncRNA expression profiles identified that LINC01503 was overexpressed in NPC. Here, we verified that LINC01503 was highly expressed in NPC and correlated with poor prognosis. LINC01503 promoted NPC cell proliferation, migration, and invasion in vitro, and facilitated tumor growth and metastasis in vivo.Taken together, our findings reveal that AR-induced LINC01503 can promote NPC progression through the SFPQ-FOSL1 axis, which represents a novel prognostic biomarker and therapeutic target for NPC patients.	32661324	RID03710	expression association	metastasis,prognosis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	
Nasopharynx carcinoma	LINC01503	SFPQ	interact	luciferase reporter assay;RNA pull-down assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000116560	NA	100506119	6421	NA	POMP100|PPP1R140|PSF	AR-induced long non-coding RNA LINC01503 facilitates proliferation and metastasis via the SFPQ-FOSL1 axis in nasopharyngeal carcinoma.Our previous lncRNA expression profiles identified that LINC01503 was overexpressed in NPC. Here, we verified that LINC01503 was highly expressed in NPC and correlated with poor prognosis. LINC01503 promoted NPC cell proliferation, migration, and invasion in vitro, and facilitated tumor growth and metastasis in vivo.Taken together, our findings reveal that AR-induced LINC01503 can promote NPC progression through the SFPQ-FOSL1 axis, which represents a novel prognostic biomarker and therapeutic target for NPC patients.	32661324	RID03711	expression association	metastasis,prognosis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Osteosarcoma	FOXC1	HOTTIP	negatively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000054598	NA	ENSG00000243766	GRCh38_7:27198575-27207259	2296	100316868	ARA|FKHL7|FREAC3|IGDA|IHG1|IRID1	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	The Sp1/FOXC1/HOTTIP/LATS2/YAP/beta-catenin cascade promotes malignant and metastatic progression of osteosarcoma.Sp1 activated FOXC1 and they both directly transactivated HOTTIP, which recruited enhancer of zeste homolog 2 and lysine-specific demethylase 1 to silence LATS2 and thus activated YAP/beta-catenin signaling.In summary, we showed that the Sp1/FOXC1/HOTTIP/LATS2/YAP/beta-catenin cascade presented oncogenic activities in OS cells.Analyzing the promoter sequence of HOTTIP gene using JASPAR (http://jaspar.genereg.net/) revealed three potential binding sites (BS1, BS2, and BS3) to FOXC1 (Fig. 7B).ChIP assay showed that FOXC1 preferentially bound to BS1, but not to BS2 or BS3 (Fig. 7C).Furthermore, we performed luciferase assay and showed that when BS1 was mutated, FOXC1 failed to stimulate the luciferase activity driven by this binding sequence.Taken together, these data suggest that FOXC1 directly binds to the promoter (at BS1 site) and activates the transcription of HOTTIP in OS cells.	32634265	RID03712	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Osteosarcoma	SP1	HOTTIP	negatively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000243766	GRCh38_7:27198575-27207259	6667	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	The Sp1/FOXC1/HOTTIP/LATS2/YAP/beta-catenin cascade promotes malignant and metastatic progression of osteosarcoma.Sp1 bound to the promoters and activated the transcriptions of FOXC1 and HOTTIP in OS cells.Similarly, the expression of HOTTIP was robustly reduced in shSp1 cells.Luciferase assay showed that mutating BS2, but not BS1, completely nullified the binding of Sp1.Collectively, these data suggest that Sp1 binds to the promoters and directly activates the transcription of both FOXC1 and HOTTIP.	32634265	RID03713	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Osteosarcoma	HOTTIP	LATS2	negatively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000150457	NA	100316868	26524	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	NA	The Sp1/FOXC1/HOTTIP/LATS2/YAP/beta-catenin cascade promotes malignant and metastatic progression of osteosarcoma.HOTTIP suppressed the expression of LATS2 by functioning as a scaffold for EZH2 and LSD1.RIP assays further confirmed the interaction between HOTTIP and EZH2 or LSD1 in both SW1353 and 143B cells (Fig. 6C).It was reported that HOTTIP, by functioning as a scaffold for EZH2 and LSD1, repressing LATS2 expression [25] and LATS2 essentially controlled YAP activity [26].In addition, we detected significant down-regulation of beta-catenin and YAP1 that destined YAP to degradation, in both shHOTTIP cells (P < 0.05, when compared to shNC cells; Fig. 6E), suggesting that targeting HOTTIP was sufficient to inhibit the activation of YAP/beta-catenin signaling.	32634265	RID03714	expression association	metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Colorectal cancer	PRKCQ-AS1	YBX1	positively-E	starBase v3.0;RNAi;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-1287-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000237943	GRCh38_10:6580419-6616921	ENSG00000065978	NA	439949	4904	ENST00000414894.1	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA PRKCQ-AS1 promotes CRC cell proliferation and migration via modulating miR-1287-5p/YBX1 axis.Knockdown of PRKCQ-AS1 would induce a decrease in proliferative and migrating ability of CRC cells.Also, PRKCQ-AS1 enriched in cytoplasm of CRC cells and negatively regulated miR-1287-5p level.Furthermore, PRKCQ-AS1 could upregulate the mRNA and protein level of YBX1 targeted by miR-1287-5p.And YBX1 expression was elevated in CRC cells and tissues.Rescue assays in vitro and in vivo showed that overexpression of YBX1 could partly offset the effect of CRC progression induced by knocking down PRKCQ-AS1, demonstrating PRKCQ-AS1 mediating CRC progression via miR-1287-5p/YBX1 pathway.	32619070	RID03715	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Soft-tissue sarcomas	NEAT1	KHSRP	positively-F	RNA pull-down assay;western blot	upregulation	RT-qPCR;northern blot	NA	NA	cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Soft-tissue sarcomas	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000088247	NA	283131	8570	LINC00084|NCRNA00084|TncRNA|VINC	FBP2|FUBP2|KSRP|p75	The long non-coding RNA NEAT1 promotes sarcoma metastasis by regulating RNA splicing pathways.Using RNA sequencing (RNA-Seq) of matched primary KP tumors and lung metastases, we found that the long non-coding RNA (lncRNA) Neat1 is significantly upregulated in lung metastases.In particular, KH-Type Splicing Regulatory Protein (KHSRP) interacts with Neat1 and is associated with poor prognosis of human STS.Collectively, these results suggest that Neat1 and its interacting proteins which regulate RNA splicing are involved in mediating sarcoma metastasis.	32561656	RID03716	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Oesophageal cancer	TP53COR1	CDKN1A	positively-E				NA	NA	cell cycle(-);cell proliferation(+)	expression regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	NA	NA	ENSG00000124762	NA	102800311	1026	TRP53COR1|linc-p21|lincRNA-p21	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	An update on long intergenic noncoding RNA p21: a regulatory molecule with various significant functions in cancer.Actually, it seems that, lincRNA-p21 acts through enhancing the expression of p21 and reduces the expression of cyclin D, and as a result, cell-cycle were arrested [23].	32582435	RID03717	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Oesophageal cancer	TP53COR1	Cyclin D	negatively-E				NA	NA	cell cycle(-)	expression regulation	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	NA	NA	NA	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	An update on long intergenic noncoding RNA p21: a regulatory molecule with various significant functions in cancer.Actually, it seems that, lincRNA-p21 acts through enhancing the expression of p21 and reduces the expression of cyclin D, and as a result, cell-cycle were arrested [23].	32582435	RID03718	expression association	NA		
Hepatocellular carcinoma	TP53COR1	miR-9	negatively-E				NA	NA	cancer progression(-)	sponge	regulation	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	NA	NA	NA	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	An update on long intergenic noncoding RNA p21: a regulatory molecule with various significant functions in cancerIn this regard, lncRNA-p21 has been indicated to control the of microRNA-9 expression level negatively.Therefore, lincRNA-p21 could repress the development of hepatocellular carcinoma by the miR-9/E-cadherin signaling pathway [33].	32582435	RID03719	ceRNA or sponge	NA		
Liver cancer	TP53COR1	HIF1A	negatively-E				NA	NA	apoptosis process(+);cell proliferation(-);cell invasion(-)	expression regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000100644	NA	102800311	3091	TRP53COR1|linc-p21|lincRNA-p21	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	An update on long intergenic noncoding RNA p21: a regulatory molecule with various significant functions in cancer.Likewise, lincRNA-p21 can diminish the expression of HIF-1alpha, reduce the VEGF levels, prevent the cell proliferation and invasion, and finally increase the apoptosis of MHCC97H liver cancer cells [22].	32582435	RID03720	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	SNHG6	ZEB1	positively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000148516	NA	641638	6935	HBII-276HG|NCRNA00058|U87HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Another study demonstrated that SNHG6 plays an oncogenic role in liver tumorigenesis by activating the TGF-beta1/SMAD signaling pathway and upregulating zinc finger E-box-binding homeobox1 (ZEB1) via effectively sponging miR-101-3p, resulting in epithelial-sesenchymal transition (EMT) [9].	32518528	RID03721	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG6	MYC	positively-E		upregulation		NA	NA	cell proliferation(+);cancer progression(+)	ceRNA(let-7c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000136997	NA	641638	4609	HBII-276HG|NCRNA00058|U87HG	bHLHe39|c-Myc|MYCC	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Chen et al. recently showed that SNHG6 promotes HCC cell proliferation via competitively binding let-7c-5p and thereby regulating the expression of c-Myc [19].	32518528	RID03722	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	SNHG6	SERPINH1	positively-E		upregulation		NA	NA	cancer progression(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000149257	NA	641638	871	HBII-276HG|NCRNA00058|U87HG	CBP1|CBP2|HSP47|SERPINH2	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Besides, SNHG6 could also activate SERPINH1 expression by competitive binding to miR-139-5p in HCC, which is verified by Wu et al.	32518528	RID03723	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Colorectal cancer	SNHG6	MIR760	NA		upregulation		NA	NA	cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000211575	NA	641638	100126348	HBII-276HG|NCRNA00058|U87HG	MIRN760|hsa-mir-760|mir-760	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.They illustrated that miR-760, as a direct target of SNHG6, could reverse the inhibitory effect of SNHG6 knockdown on CRC progression by targeting forkhead box C1 [23].	32518528	RID03724	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Colorectal cancer	SNHG6	UPF1	NA		upregulation		NA	NA	TGF-beta/SMAD signaling pathway(+)	NA	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000005007	NA	641638	5976	HBII-276HG|NCRNA00058|U87HG	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumorsThey also proved that SNHG6 could activate the TGF-beta/Smad pathway by binding to UPF1 in CRC cells [10].	32518528	RID03725	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SNHG6	E2F5	positively-E		upregulation		NA	NA	cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000133740	NA	641638	1875	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.For miR-181a-5p, Yu et al.demonstrated that E2F5, as a direct target of this miRNA, is upregulated, resulting in increased CRC proliferation by regulating the cell cycle [25].	32518528	RID03726	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	SNHG6	ZEB1	NA		upregulation		NA	NA	cell migration(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000148516	NA	641638	6935	HBII-276HG|NCRNA00058|U87HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Yan et al.revealed that SNHG6-promoted cell growth could be due to its influence on cell cycle through interacting with PRC2 and epigenetic silencing p27, whereas SNHG6-accelerated migration could be through miR-101-3p sponging, thereby regulating ZEB1.	32518528	RID03727	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG6	CDKN1A	positively-E		upregulation		NA	NA	cancer progression(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Li  study indicated that SNHG6 facilitates GC progression by upregulating p21 through activation of the JNK pathway and suppression of EZH2 [30].	32518528	RID03728	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SNHG6	HIF1A	NA		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-186-5p)	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100644	NA	641638	3091	HBII-276HG|NCRNA00058|U87HG	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.In Du'-study, they demonstrated that SNHG6 promoted the proliferation, migration, and invasion of ESCC cells through regulating miR-186-5p/HIF1alpha axis [33].	32518528	RID03729	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Lung cancer	SNHG6	RSF1	positively-E		upregulation		NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000048649	NA	641638	51773	HBII-276HG|NCRNA00058|U87HG	HBXAP|p325|RSF-1|XAP8	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.In Dong'-study, SNHG6 significantly promoted proliferation and inhibited apoptosis of NSCLC cells.Mechanism research demonstrated that SNHG6 regulates miR-490-3p/RSF1 axis [35].	32518528	RID03730	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Lung cancer	SNHG6	CDYL	NA		upregulation		NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000153046	NA	641638	9425	HBII-276HG|NCRNA00058|U87HG	CDYL1|DKFZP586C1622	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Silencing SNHG6 expression repressed cell growth and invasion in vitro and in vivo.Mechanically, SNHG6 was identified to regulate CDYL expression by acting as a sponge of miR-101-3p [36].	32518528	RID03731	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Lung adenocarcinoma	SNHG6	E2F7	positively-E		upregulation		NA	NA	cell metastasis(+);cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+);cell cycle(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000165891	NA	641638	144455	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Functionally and mechanically, SNHG6 promotes cell cycle progression, cell proliferation, migration, invasion, and EMT by acting as ceRNA via competitively binding to miR-26a-5p, thereby activating E2F7 [37].	32518528	RID03732	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	SNHG6	Snail1/2	positively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+);	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Their data suggested that overexpressed SNHG6 induces EMT through upregulating Snail1/2 and promotes migration and invasion of bladder cancer cells by sponging miR-125b, thereby activating the target gene of miR-125b-novel (nua) kinase family 1 (NUAK1), also known as ARK5.Thus, SNHG6 accelerates bladder cancer cell progression through miR-125b/NUAK1 and miR-125b/Snail1/2 pathways.	32518528	RID03733	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Urinary bladder cancer	SNHG6	NUAK1	positively-E		upregulation		NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000074590	NA	641638	9891	HBII-276HG|NCRNA00058|U87HG	ARK5|KIAA0537	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.Their data suggested that overexpressed SNHG6 induces EMT through upregulating Snail1/2 and promotes migration and invasion of bladder cancer cells by sponging miR-125b, thereby activating the target gene of miR-125b-novel (nua) kinase family 1 (NUAK1), also known as ARK5.Thus, SNHG6 accelerates bladder cancer cell progression through miR-125b/NUAK1 and miR-125b/Snail1/2 pathways.	32518528	RID03734	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	SNHG6	miR-101-3p	negatively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.In their research, SNHG6 promotes glioma cell proliferation, migration, and EMT and reduces apoptosis by downregulating miR-101-3p.	32518528	RID03735	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Malignant glioma	SNHG6	Caspase3	NA		upregulation		NA	NA	apoptosis process(+);cell autophagy(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.In Zhu  study, they found that SNHG6 could competitively sponging miR-26a-5p thereby regulating ULK1, and induced cell apoptosis and autophagy by targeting caspase3 and ATF3 [49].	32518528	RID03736	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Malignant glioma	SNHG6	ATF3	NA		upregulation		NA	NA	apoptosis process(+);cell autophagy(+)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000162772	NA	641638	467	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors.In Zhu  study, they found that SNHG6 could competitively sponging miR-26a-5p thereby regulating ULK1, and induced cell apoptosis and autophagy by targeting caspase3 and ATF3 [49].	32518528	RID03737	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065)
Juvenile idiopathic arthritis	RP11-340F14.6	FOXP3	negatively-E		upregulation		NA	NA	immune response(+)	NA	NA	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	NA	NA	ENSG00000049768	NA	NA	50943	NA	AIID|DIETER|IPEX|JM2|PIDX|XPID	Long non-coding RNA RP11-340F14.6 promotes a shift in the Th17/Treg ratio by binding with P2X7R in juvenile idiopathic arthritis.Long non-coding RNA (lncRNAs) have been identified to play important roles in multiple human diseases via the regulation of cell proliferation, cell invasion, or cell death. However, little is known about the role of lncRNAs in the process of shifts in the Th17/Treg ratio during the progression of juvenile idiopathic arthritis (JIA). The aim of the present study was to determine the role of lncRNA RP11-340F14.6 in the shifting of the Th17/Treg ratio in JIA. The distribution of the T cell subgroup was detected by flow cytometry in peripheral blood mononuclear cells from patients with JIA and healthy controls. It was found that the expression of lncRNA RP11-340F14.6 was upregulated, and to positively correlate with that of retinoic acid-related orphan receptor gamma t (ROR-Gammat), and to negatively correlate with Foxp3 expression in patients with JIA. RP11-340F14.6 induced the expression of its neighbor, P2X7R. Through a P2X7R-independent approach, this lncRNA was also found to play a pivotal role in stimulating Th17 differentiation and simultaneously suppressing Treg distribution. Taken together, the findings of the present study demonstrate that RP11-340F14.6 specifically binds to P2X7R, which results in the continuous activation of P2X7R. Thus, RP11-340F14.6 may serve as a promising therapeutic target for the treatment of JIA.	32467993	RID03738	expression association	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Juvenile idiopathic arthritis	RP11-340F14.6	RORt	positively-E		upregulation		NA	NA	immune response(+)	NA	NA	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA RP11-340F14.6 promotes a shift in the Th17/Treg ratio by binding with P2X7R in juvenile idiopathic arthritis.Long non-coding RNA (lncRNAs) have been identified to play important roles in multiple human diseases via the regulation of cell proliferation, cell invasion, or cell death. However, little is known about the role of lncRNAs in the process of shifts in the Th17/Treg ratio during the progression of juvenile idiopathic arthritis (JIA). The aim of the present study was to determine the role of lncRNA RP11-340F14.6 in the shifting of the Th17/Treg ratio in JIA. The distribution of the T cell subgroup was detected by flow cytometry in peripheral blood mononuclear cells from patients with JIA and healthy controls. It was found that the expression of lncRNA RP11-340F14.6 was upregulated, and to positively correlate with that of retinoic acid-related orphan receptor gamma t (ROR-Gammat), and to negatively correlate with Foxp3 expression in patients with JIA. RP11-340F14.6 induced the expression of its neighbor, P2X7R. Through a P2X7R-independent approach, this lncRNA was also found to play a pivotal role in stimulating Th17 differentiation and simultaneously suppressing Treg distribution. Taken together, the findings of the present study demonstrate that RP11-340F14.6 specifically binds to P2X7R, which results in the continuous activation of P2X7R. Thus, RP11-340F14.6 may serve as a promising therapeutic target for the treatment of JIA.	32467993	RID03739	expression association	NA		
Juvenile idiopathic arthritis	RP11-340F14.6	P2X7R	positively-E		upregulation		NA	NA	immune response(+)	NA	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA RP11-340F14.6 promotes a shift in the Th17/Treg ratio by binding with P2X7R in juvenile idiopathic arthritis.Long non-coding RNA (lncRNAs) have been identified to play important roles in multiple human diseases via the regulation of cell proliferation, cell invasion, or cell death. However, little is known about the role of lncRNAs in the process of shifts in the Th17/Treg ratio during the progression of juvenile idiopathic arthritis (JIA). The aim of the present study was to determine the role of lncRNA RP11-340F14.6 in the shifting of the Th17/Treg ratio in JIA. The distribution of the T cell subgroup was detected by flow cytometry in peripheral blood mononuclear cells from patients with JIA and healthy controls. It was found that the expression of lncRNA RP11-340F14.6 was upregulated, and to positively correlate with that of retinoic acid-related orphan receptor gamma t (ROR-Gammat), and to negatively correlate with Foxp3 expression in patients with JIA. RP11-340F14.6 induced the expression of its neighbor, P2X7R. Through a P2X7R-independent approach, this lncRNA was also found to play a pivotal role in stimulating Th17 differentiation and simultaneously suppressing Treg distribution. Taken together, the findings of the present study demonstrate that RP11-340F14.6 specifically binds to P2X7R, which results in the continuous activation of P2X7R. Thus, RP11-340F14.6 may serve as a promising therapeutic target for the treatment of JIA.	32467993	RID03740	expression association	NA		
Glioma	NEAT1	CCT6A	positively-E	Starbase v2.0;TargetScan;luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-)	ceRNA(miR-152-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000146731	NA	283131	908	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CCT6|Cctz|HTR3|TCP20|TCPZ|TTCP20	Long non-coding RNA NEAT1 promotes human glioma tumor progression via miR-152-3p/CCT6A pathway.Methods: The levels of NEAT1, microRNA-152-3p (miR-152-3p) and chaperonin containing TCP1 subunit 6A (CCT6A) in glioma tissues and cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR.The interactions between miR-152-3p and NEAT1 or CCT6A were predicted by starBase v2.0 or TargetScan, then luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pull-down assay were performed to validate the interaction.Results: The levels of NEAT1, CCT6A were highly expressed, but miR-152-3p was decreased in glioma tissues and cells.NEAT1 depletion or miR-152-3p mimics suppressed cell viability, migrated and invaded abilities but induced apoptotic rate in A172 and U251 cells, while the introduction of CCT6A partly counteracted these impacts.In addition, NEAT1 silencing impeded xenograft tumor growth in vivo.MiR-152-3p was verified as a direct target of NEAT1 and directly targeted CCT6A.CCT6A expression was upregulated by NEAT1 and reversed by miR-152-3p.Conclusion: NEAT1 enhanced glioma progression, partially through miR-152-3p/CCT6A pathway.	32454145	RID03741	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Acute myeloid leukemia	ZNF407-AS1	MIR625	negatively-F	StarBase;luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell metastasis(+);apoptosis process(-)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000264247	GRCh38_18:74590317-74598885	ENSG00000207781	NA	400657	693210	LINC00909	hsa-mir-625|MIRN625	LncRNA LINC00909 promotes cell proliferation and metastasis in pediatric acute myeloid leukemia via miR-625-mediated modulation of Wnt/beta-catenin signaling.In this study, the levels of LINC00909 were observed to be distinctly upregulated in AML patients and cell lines.Higher levels of LINC00909 were associated with FAB classification, cytogenetics and poorer prognosis.Mechanistically, we demonstrated that LINC00909 functioned as a molecular sponge for miR-625.In addition, we observed that Wnt/beta-catenin signaling pathway was suppressed by LINC00909 knockdown.	32423818	RID03742	ceRNA or sponge	metastasis,prognosis		
Breast cancer	H19	YWHAZ	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cancer progression(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-340-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000164924	NA	283120	7534	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	14-3-3-zeta|KCIP-1|YWHAD	Long noncoding RNA H19 acts as a miR-340-3p sponge to promote epithelial-mesenchymal transition by regulating YWHAZ expression in paclitaxel-resistant breast cancer cells.Emerging references had indicated that the lncRNA H19 acts as significant roles in tumor progression and epithelial-mesenchymal transition (EMT).In this study, it was detected that the expression level of H19 was increased in BC paclitaxel-resistant (PR) cells subline (MCF-7/PR) in comparison with MCF-7 parental cells.In vitro, there were demonstrated that H19 overexpression promoted BC cells proliferation, metastasis, invasion and EMT procedures, and suppressed cells apoptosis.Besides, bioinformatics tools and dual-luciferase reporters assays indicated that miR-340-3p could act as a potential target gene of H19, the underlying mechanism studies proved that H19 could act as a competing endogenous RNA (ceRNA) via competitively binding miR-340-3p to promote BC cell proliferation, metastasis and EMT by regulating tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ) and potentiate the Wnt/beta-catenin signaling in BC cells.In summary, our findings demonstrated that H19 could act as a ceRNA in BC progression, metastasis and EMT through modulating miR-340-3p/YWHAZ axis and activating the canonical Wnt/beta-catenin signaling pathway, indicating that H19 might act as an underlying therapeutic target and prognostic biomarker for BC therapy.	32420678	RID03743	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Diffuse large b-cell lymphoma	FOXM1	OR3A4P	positively-E	luciferase reporter assays;	upregulation	RT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);tumorigenesis(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Lymphoma	TF	lncRNA	ENSG00000111206	NA	ENSG00000180068	GRCh38_17:3309986-3311446	2305	390756	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	OR3A4	FOXM1-induced upregulation of lncRNA OR3A4 promotes the progression of diffuse large B-cell lymphoma via Wnt/beta-catenin signaling pathway.In our study, it was revealed that the expression of OR3A4 was upregulated in DLBCL tumors and cell lines, and patients with high OR3A4 expression suffered from poor prognosis.Knockdown of OR3A4 suppressed cell proliferation and promoted cell apoptosis in DLBCL.Moreover, knockdown of OR3A4 inactivated Wnt/beta-catenin signaling pathway, and Riluzole treatment could partially rescue the inhibitive effect of OR3A4 silencing on DLBCL cell proliferation.Furthermore, FOXM1 expression was discovered to be upregulated in DLBCL tissues, and it positively modulated the expression of OR3A4 at transcriptional leve.It was also revealed that FOXM1 knockdown inactivated Wnt/beta-catenin signaling pathway.Taken together, FOXM1-induced upregulation of OR3A4 enhances the occurrence of DLBCL via Wnt/beta-catenin signaling pathway.	32417392	RID03744	transcriptional regulation	prognosis	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)	
Retinoblastoma	LINC00324	STAT3	positively-E	StarBase 3.0;luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	tumor growth(+);cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+)	ceRNA(miR-769-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000178977	GRCh38_17:8220624-8224043	ENSG00000168610	NA	284029	6774	C17orf44|FLJ34790|MGC104931|NCRNA00324	APRF	Long intergenic non protein-coding RNA 324 (LINC00324) is abnormally expressed in multiple human cancer types and plays an important role in cancer initiation and progression.This study showed that LINC00324 was expressed at higher levels in retinoblastoma (RB) tumors and cell lines than in control samples.Increased LINC00324 expression closely correlated with the TNM stage, optic nerve invasion, and shorter overall survival among patients with RB.The knockdown of LINC00324 decreased RB cell proliferation, colony formation, migration, and invasion, and promoted apoptosis and cell cycle arrest in vitro as well as hindered tumor growth in vivo.With respect to the mechanism, LINC00324 acted as a competing endogenous RNA for microRNA-769-5p (miR-769-5p) in RB cells.The mRNA of signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-769-5p in RB cells.Our findings describe a novel RB-related LINC00324-siR-769-5p-STAT3 axis that is implicated in the malignancy of RB in vitro and in vivo.	32369777	RID03745	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteogenic differentiation	LOC100506178	BMP2	positively-E	luciferase reporter assay;RNAi;LncBase Predicted v2;RIP	upregulation	qRT-PCR	NA	NA	cell differentiation	ceRNA(miR-214-5p)	regulation	NA	NA	CSC	NA	Other	Osteogenic differentiation	lncRNA	PCG	NA	NA	ENSG00000125845	NA	NA	650	NA	BDA2|BMP2A|SSFSC|SSFSC1	LncRNA LOC100506178 promotes osteogenic differentiation via regulating miR-214-5p-BMP2 axis in human bone marrow mesenchymal stem cells.LOC100506178 positively regulates BMP2 expression through sponging miR-214-5p.Quantitative real time PCR (qRT-PCR was used to examine the expression of LOC100506178, miR-214-5p, Runt-related transcription factor 2 (RUNX2), Osterix (Osx), and Alkaline Phosphatase (ALP) in BMP2-induced osteogenic differentiation of hBMSCs.Luciferase reporter assay was performed to assess the association between LOC100506178 and miR-214-5p, as well as miR-214-5p and BMP2.The miR-214-5p sponging potential of LOC100506178 was evaluated by RNA immunoprecipitation.In the present study, the expression of LOC100506178 was found to be increased in BMP2-induced osteogenic differentiation of hBMSCs, accompanied with decreased miR-214-5p expression and increased RUNX2, Osx and ALP expression.LOC100506178 significantly induced, while miR-214-5p suppressed the BMP2-induced osteogenic differentiation of hBMSCs.In conclusion, our data indicate a novel molecular pathway LOC100506178/miR-214-5p/BMP2 in relation to hBMSCs differentiation into osteoblasts, which may facilitate bone anabolism.	32328347	RID03746	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Gastric cancer	LINC00339	SRY-box9	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-539)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000218510	GRCh38_1:22024558-22031223	NA	NA	29092	NA	HSPC157|NCRNA00339	NA	Long noncoding RNA LINC00339 promotes the oncogenicity of gastric cancer by regulating SRY-box 9 expression via sponging of microRNA-539.Here, we found that LINC00339 expression was aberrantly high in gastric cancer and significantly associated with lymph node metastasis, invasive depth, and TNM stage.A knockdown of LINC00339 suppressed gastric cancer cell proliferation, migration, and invasion and induced apoptosis in vitro and slowed tumor growth in vivo.Our findings highlight the importance of the LINC00339-siR-539-SOX9 pathway in gastric cancer pathogenesis and may point to novel targets for the diagnosis, prognosis, and/or treatment of gastric cancer.Subsequently, the luciferase reporter assay was carried out to confirm the direct binding of LINC00339 to miR-539 in gastric cancer cells.The direct interaction between LINC00339 and miR-539 was further characterized by the RIP assay.	32308105	RID03747	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cervical cancer	DGUOK-AS1	EMSY	positively-E	luciferase reporter analysis;RIP;starBase v2.0	upregulation	RT-qPCR	NA	NA	cell proliferation;DNA damage(-)	ceRNA(miR-653-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237883	GRCh38_2:73947322-73982164	ENSG00000158636	NA	100874048	56946	NA	C11orf30	DGUOK-AS1 promotes cell proliferation in cervical cancer via acting as a ceRNA of miR-653-5p.We found that DGUOK-AS1 was aberrantly upregulated in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues through TCGA database.Real-time quantitative polymerase chain reaction (RT-qPCR) also verified the high expression of DGUOK-AS1 in CC cell lines.In addition, dual-luciferase reporter and RNA immunoprecipitation (RIP) experiments validated the binding relation between miR-653-5p and DGUOK-AS1 or EMSY.EMSY is required for DGUOK-AS1 to induce cell proliferation and repress DNA damage in CC.After transfection of miR-653-5p mimics, the expression of EMSY strikingly declined, while no significant change of PPP1CC expression was captured (Figure 3B).	32283566	RID03748	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	PVT1	LASP1	positively-E				NA	NA	cell migration(+)	ceRNA(miR-203)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000002834	NA	5820	3927	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Lasp-1|MLN50	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion. Overexpression of PVT1 in ESCC keep miR-203 away from LASP1 (LIM and SH3 domain protein 1) binding so releases LASP1 and promotes cell migration [30].	32185664	RID03749	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	CCAT1	HNRNPA1	positively-E				NA	NA	cell migration(+)	ceRNA(miR-490)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000135486	NA	100507056	3178	CARLO5|CARLo-5|onco-lncRNA-40	ALS20|hnRNP-A1|HNRPA1	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion. Likewise miRNA-218-5p and miR-490 both sponge to CCAT1, but, CCAT1/miR-490/hnRNPA1 axis appears to be more efective in promoting the migration of GC	32185664	RID03750	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	CCAT1	HMGA2	positively-E				NA	NA	cancer progression(+)	ceRNA(let-7)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000247844	NA	ENSG00000149948	NA	100507056	8091	CARLO5|CARLo-5|onco-lncRNA-40	BABL|HMGIC|LIPO	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.This c-Myc-induced lncRNA also acts as a sponge of let-7 tumor suppressor and therefore rescues expression of HMGA2, c-Myc, and then itself to promote hepatocellular carcinoma progression	32185664	RID03751	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	GAPLINC	CD44	positively-E				NA	NA	cell metastasis(+);cell proliferation(+);angiogenesis(+)	ceRNA(miR-[0-9]11-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000026508	NA	100505592	960	LINC01540|lncRNA-uc002kmd.1|RP11-838N2.4|TCONS_00026238	CD44R|CSPG8|HCELL|IN|MC56|MDU2|MDU3|MIC4|Pgp1	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.GAPLINC functions as miRNA sponge and competes with CD44 to decoy the miR211-3p, which targets both CD44 and GAPLINC, resulting in decreased degradation of CD44 mRNA and increased gastric cancer proliferation, migration and angiogenesis	32185664	RID03752	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	HIF1A	GAPLINC	positively-E				NA	NA	tumorigenesis(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000100644	NA	ENSG00000266835	GRCh38_18:3466250-3478978	3091	100505592	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LINC01540	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.The upregulation of GAPLINC under hypoxia revealed that HIF-1alpha controls transcriptional activation of GAPLINC via binding to its promoter region that leads to the acceleration of GC tumor progression and decreases its apoptosis	32185664	RID03753	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	GAPLINC	c-MET	positively-E				NA	NA	cell invasion(+)	ceRNA(miR-34a)	regulation	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540|lncRNA-uc002kmd.1|RP11-838N2.4|TCONS_00026238	NA	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.Besides, it can positively regulate the c-MET protooncogene through the GAPLINC/miR-34a/c-MET axis in CRC cells	32185664	RID03754	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Oral squamous cell carcinoma	SNHG20	LIN28A	positively-E				NA	NA	tumorigenesis(+)	ceRNA(miR-197)	regulation	NA	NA	CSC	NA	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000131914	NA	654434	79727	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	CSDD1|FLJ12457|LIN-28|LIN28|ZCCHC1	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.On the other hand, overexpression of this lncRNA in HCC and oral squamous cell carcinoma is associated with cancer progression and stemness [56, 59, 60]. Sequestered miR-197 by an excessive level of SNHG20 leads to the release of the LIN28 stem factor which promotes cancer stem cell (CSC) properties and oncogenesis in OSCC cells [56].	32185664	RID03755	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC);DATA(GSE117623)
Cancer	HAND2-AS1	KLF14	positively-E				NA	NA	tumorigenesis(-)	ceRNA(miR-21)	regulation	NA	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000266265	NA	79804	136259	DEIN|FLJ11539|NBLA00301	BTEB5	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.Functionally, this lncRNA attenuates tumor progression and invasion through sponging an oncogenic micro-RNA, miR-21, in ESCC [93], facilitating the expression of KLF14, as a member of Kruppel like factor family (KLF) of transcription factors in CRC [95]. Both KLF14 and HAND2-AS1 are the target of miR-1275, so overexpression of HAND2-AS1 suppresses the efect of miR-1275 on KLF14 and its downstream targets [93] to detract CRC tumor progression.	32185664	RID03756	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DATA(GSE40174)
Cancer	MIR22HG	MMP9	negatively-E				NA	NA	tumorigenesis(-)	ceRNA(miR-22-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000100985	NA	84981	4318	C17orf91|DKFZp686O06159|MGC14376	CLG4B	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.MIR22HG which is also known as C17orf91 inhibits HCC tumor progression by two mechanisms. The frst mechanism is mediated by HMGB1(High mobility group box 1) where MIR22HG promotes the expression of miR-22-3p to target the 3' UTR of theHMGB1 mRNA and inhibit the HMGB1-mediated gene expression of matrix metallopeptidase 9 (MMP9) and ERK[105] which are involved in epithelial to mesenchymal transition and cell proliferation, respectively (Fig. 2).	32185664	RID03757	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastrointestinal cancer	FER1L4	PTEN	positively-E				NA	NA	PI3K/AKT signaling pathway(-);cell proliferation(-)	ceRNA(miR-106a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastrointestinal cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	bA563A22B.1|C20orf124|dJ309K20.1	BZS|MHAM|MMAC1|PTEN1|TEP1	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion. This lncRNA acts as a ceRNA and inhibits the proliferation and invasion of the above-mentioned tumors mainly through the sponging of miR-106a-5p [110'-13]. MiR-106a-5p as an oncogenic micro-RNA suppresses the expression of tumor suppressor genes such asPTEN and RB, hence promoting cell growth by inducing the G0/G1 to S phase transition [111'-14]. Overall, the bestestablished mechanism of action of FER1L4 is the sequestration of miR-106a-5p and making the PTEN free to prevent the activation of PI3K/AKT pathway and cell proliferation in gastrointestinal cancers	32185664	RID03758	ceRNA or sponge	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Esophagus squamous cell carcinoma	NPTN-IT1	TP53	positively-E				NA	NA	cell proliferation(+);cell invasion(+)	expression regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000141510	NA	101241892	7157	lncRNA-LET	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor PromotionIn this axis, lncRNA LET acts as the regulator of p53 and NF90. Downregulation of this lncRNA decreases p53, one of the main regulators of gene expression which inhibits cell cycle and promotes cell death, and increases NF90 expression hence, promoting the proliferation and invasion of ESCC cells	32185664	RID03759	expression association	NA	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	NPTN-IT1	ILF3	positively-E				NA	NA	cell proliferation(+);cell invasion(+)	expression regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000129351	NA	101241892	3609	lncRNA-LET	CBTF|DRBF|DRBP76|MMP4|MPHOSPH4|MPP4|MPP4110|NF-AT-90|NF110|NF110b|NF90|NF90a|NF90b|NF90c|NF90ctv|NFAR|NFAR-1|NFAR-2|NFAR110|NFAR2|NFAR90|TCP110|TCP80	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor PromotionIn this axis, lncRNA LET acts as the regulator of p53 and NF90. Downregulation of this lncRNA decreases p53, one of the main regulators of gene expression which inhibits cell cycle and promotes cell death, and increases NF90 expression hence, promoting the proliferation and invasion of ESCC cells	32185664	RID03760	expression association	NA	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	DANCR	NPTN-IT1	negatively-E				NA	NA	cell migration(+)	expression regulation	association	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	lncRNA	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000281183	GRCh38_15:73567012-73569294	57291	101241892	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	lncRNA-LET	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion Downregulation of LET in gastric cancer [119, 122] resulted from overexpression of lncRNA DANCR stimulates the migration of GC cells	32185664	RID03761	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Gastric cancer	TINCR	PDK1	positively-E				NA	NA	tumorigenesis(+)	ceRNA(miR-375)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000152256	NA	257000	5163	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.Moreover, TINCR can act as a ceRNA and be targeted by miR-375. Sponging of miR375 by TINCR leads to the upregulation of PDK1 in gastric cancer cells, which highlights the oncogenic role of TINCR in gastric cancer pathogenesis	32185664	RID03762	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Colorectal cancer	TP73-AS1	PTEN	NA				NA	NA	PI3K/AKT signaling pathway(-);cancer progression(-)	ceRNA(miR-103)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000171862	NA	57212	5728	KIAA0495|PDAM	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion. Moreover,in colorectal cancer, it functions as a tumor suppressor by sponging of miR-103, which results in PTEN escape and halting of the PI3/AKT signaling pathway	32185664	RID03763	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	LINC00052	miR-330-3p	negatively-E				NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000259527	GRCh38_15:87576929-87579866	NA	NA	145978	NA	NCRNA00052|TMEM83	NA	Long Noncoding RNAs in Gastrointestinal Cancer: Tumor Suppression Versus Tumor Promotion.It triggers apoptosis and prevents G1 phase progression via sponging of miR-330-3p in pancreatic cancer	32185664	RID03764	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Cervical cancer	MEG3	miR-21-5p	negatively-E		downregulation		NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.MEG3 has shown to act as a cancer suppressor through its ability to down regulate the miR-21-5p levels in cervical cancer cell lines (147).	32154165	RID03765	ceRNA or sponge	NA		
Cervical cancer	GAS5	IER3	positively-E		downregulation		NA	NA	cell radiosensitivity(+)	ceRNA(miR-106b)	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000227231	NA	60674	8870	NCRNA00030|SNHG2	DIF-2|IEX-1|IEX-1L|PRG1	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.reported that GAS5 acts as miR-106b sponge causing up regulation of IER3 expression and enhanced radio-sensitivity of cervical cancer cells (144).	32154165	RID03766	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC);UP(BRCA);DATA(GSE117623,GSE109761,GSE55807)
Cervical cancer	SPYR4-IT1	ZEB1	NA		upregulation		NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.More recently, the silencing of SPRY4-IT1 in cervical cancer cell lines has shown to inhibit migration and invasion through the SPYR4-IT1/miR-101-3p/ZEB1 axis.	32154165	RID03767	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MALAT1	RBG2	NA		upregulation		NA	NA	cell invasion(-);cell metastasis(-)	ceRNA(miR-124)	regulation	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.Accordingly, down regulation of MALAT1 in cervical cancer cell lines and in cervical cancer tissues reduces invasion and metastasis through the inhibition of epidermal mesenchymal transition and modulation of the MALAT1-miR-124-RBG2 axis (141).	32154165	RID03768	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Cervical cancer	MALAT1	miR-206	NA		upregulation		NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.The MALAT1 is over expressed in cervical cancer cell lines and cancer tissues infected with high risk HPVs (177), acts as a sponge for several miRNAs, including miR-124, miR-145, and miR-206, and favors cervical cancer progression (178).	32154165	RID03769	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Cervical cancer	MALAT1	miR-145	NA		upregulation		NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000269936	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.The MALAT1 is over expressed in cervical cancer cell lines and cancer tissues infected with high risk HPVs (177), acts as a sponge for several miRNAs, including miR-124, miR-145, and miR-206, and favors cervical cancer progression (178).	32154165	RID03770	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Cervical cancer	MALAT1	miR-124	NA		upregulation		NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.The MALAT1 is over expressed in cervical cancer cell lines and cancer tissues infected with high risk HPVs (177), acts as a sponge for several miRNAs, including miR-124, miR-145, and miR-206, and favors cervical cancer progression (178).	32154165	RID03771	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Cervical cancer	HOTAIR	MMP9	positively-E		upregulation		NA	NA	cell invasion(+)	expression regulation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.HOTAIR expression causes the up regulation of the vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9) and EMT-related genes thus promoting tumor aggressiveness in cervical carcinoma (133).	32154165	RID03772	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	HOTAIR	VEGFA	positively-E		upregulation		NA	NA	cell invasion(+)	expression regulation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXC-AS4|HOXC11-AS1|NCRNA00072	VEGF|VEGF-A|VPF	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.HOTAIR expression causes the up regulation of the vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9) and EMT-related genes thus promoting tumor aggressiveness in cervical carcinoma (133).	32154165	RID03773	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cervical cancer	HOTAIR	MAPK1	NA		upregulation		NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-23b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.Indeed, HOTAIR has shown to alter the miR-143-3p/BCL2 axis favoring cervical cancer cell growth (130) and miR-23b/MAPK1 axis contributing to cell proliferation and metastasis (139).	32154165	RID03774	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	HOTAIR	BCL2	NA		upregulation		NA	NA	cell growth(+)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.Indeed, HOTAIR has shown to alter the miR-143-3p/BCL2 axis favoring cervical cancer cell growth (130) and miR-23b/MAPK1 axis contributing to cell proliferation and metastasis (139).	32154165	RID03775	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Atherosclerosis	ciRS-7	miR-26a-5p	negatively-E	qRT-PCR;siRNA	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);angiogenesis(+);apoptosis process(-);PI3K/AKT signaling pathway(+);JNK/p38 signaling pathway(-)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Circular RNA ciRS-7 promotes tube formation in microvascular endothelial cells through downregulation of miR-26a-5p.Silencing ciRS-7 suppressed viability, migration, and tube formation but promoted apoptosis.miR-26a-5p expression was elevated by silencing ciRS-7 and reduced by overexpressing ciRS-7.Moreover, overexpressing ciRS-7 facilitated viability, migration, and tube formation via upregulating miR-26a-5p.Conclusively, overexpressing ciRS-7 mobilized phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway and suppressed c-Jun N-terminal kinase (JNK)/p38 pathway.ciRS-7 exerted influence on apoptosis, viability, migration, and tube formation through mediating PI3K/AKT and JNK/p38 pathways by miR-26a-5p downregulation in HMEC-1 cells.The expression level of ciRS-7 was de_x0002_termined by using quantitative reverse transcription PCR (qRT-PCR.To assess the association between ciRS 7 and miR 26a 5p, miR 26a 5p expression was evaluated utilizing qRT-PCR First, the knockdown of ciRS 7 led to significant upregulation of miR 26a 5p (P < .01). On the contrary, miR 26a 5p expression was obviously declined by ciRS 7 overexpression (P <  .01; Figure 3).	32053286	RID03776	expression association	NA		
Senescence	MYC	SENEBLOC	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Other	Senescence	TF	lncRNA	ENSG00000136997	NA	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	NA	SENEBLOC, a long non-coding RNA suppresses senescence via p53-dependent and independent mechanisms.Long non-coding RNAs (lncRNAs) have emerged as important biological tuners. Here, we reveal the role of an uncharacterized lncRNA we call SENEBLOC that is expressed by both normal and transformed cells under homeostatic conditions. SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.Identification of SENEBLOC as a c-Myc responsive lncRNA involved in senescence.Eight cMyc responsive lncRNAs were validated using qPCR along with the previously characterized Glut1 gene.Collectively, these data support the trans_x0002_activation of SBLC by c-Myc.	32030426	RID03777	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Senescence	SENEBLOC	MDM2	interact	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	senescence(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Other	Senescence	lncRNA	PCG	NA	NA	ENSG00000135679	NA	NA	4193	NA	HDM2|MGC5370	Long non-coding RNAs (lncRNAs) have emerged as important biological tuners. Here, we reveal the role of an uncharacterized lncRNA we call SENEBLOC that is expressed by both normal and transformed cells under homeostatic conditions. SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.SBLC facilitates a ternary complex between p53 and MDM2 that promotes p53 degradation.Indeed, RNA pull-down assays revealed that both p53 and MDM2 were selectively recovered with SBLC.In support, the association of SBLC with p53 and MDM2 was confirmed using p53 and MDM2 immunoprecipitation (RIP) assays.	32030426	RID03778	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Senescence	SENEBLOC	TP53	interact	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	senescence(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Other	Senescence	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Long non-coding RNAs (lncRNAs) have emerged as important biological tuners. Here, we reveal the role of an uncharacterized lncRNA we call SENEBLOC that is expressed by both normal and transformed cells under homeostatic conditions. SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.Indeed, RNA pull-down assays revealed that both p53 and MDM2 were selectively recovered with SBLC.In support, the association of SBLC with p53 and MDM2 was confirmed using p53 and MDM2 immunoprecipitation (RIP) assays	32030426	RID03779	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Senescence	SENEBLOC	CDKN1A	negatively-E	ChIP	downregulation	qPCR	NA	NA	senescence(-)	histone modification	regulation	RNA-protein	NA	NA	NA	Other	Senescence	lncRNA	PCG	NA	NA	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Here, we reveal the role of an uncharacterized lncRNA we call SENEBLOC that is expressed by both normal and transformed cells under homeostatic conditions. SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.Con_x0002_versely, enforced expression of SBLC caused reduction in the levels of p21 protein.These data imply that the increased p21 observed af_x0002_ter SBLC silencing predominantly results from transcrip_x0002_tional regulation. Indeed, ChIP analysis after knockdown of HDAC5 confirmed that hyperacetylation of H3 and H4 histones were increased in the p21 proximal promoter, supporting the role of HDAC5 in p21 regulation.	32030426	RID03780	epigenetic regulation	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Senescence	SENEBLOC	HDAC5	positively-E	RNA pull-down assay	downregulation	qPCR	NA	NA	senescence(-)	ceRNA(miR-3175)	regulation	RNA-protein	NA	NA	NA	Other	Senescence	lncRNA	PCG	NA	NA	ENSG00000108840	NA	NA	10014	NA	FLJ90614|KIAA0600|NY-CO-9	SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.Bioinformatics examination revealed complementarity between SBLC and the seed region of miR-3175 . pull-down assays demonstrated miR- 3175 was recovered along with SBLC, indicating that SBLC binds to miR-3175 in the endogenous state.	32030426	RID03781	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Senescence	E2F1	SENEBLOC	positively-E	ChIP	downregulation	qPCR	NA	NA	senescence(-)	transcriptional regulation	regulation	NA	Rapamycin	NA	NA	Other	Senescence	TF	lncRNA	ENSG00000101412	NA	NA	NA	1869	NA	RBBP3|RBP3	NA	Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.Moreover, depletion of E2F1 by shRNA significantly decreased SBLC expression in the context of both vehicle and rapamycintreated cells.Supporting the involvement of E2F1 as a transcriptional driver contributing to SBLC expression after rapamycin treatment, ChIP analysis confirmed that E2F1 could bind to SBLC through motifs in the intergenic region between exons 1 and 2.	32030426	RID03782	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Retinoblastoma	DNM3OS	SMAD6	positively-E	dual-luciferase reporter analysis;Starbase v3.0;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-134-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000230630	GRCh38_1:172138397-172144840	ENSG00000137834	NA	100628315	4091	DNM3-AS1|MIR199A2HG	HsT17432|MADH6|MADH7	SMAD6, positively regulated by the DNM3OS-miR-134-5p axis, confers promoting effects to cell proliferation, migration and EMT process in retinoblastoma.Methods :The expression of SMAD6 mRNA, miR-134-5p and DNM3OS was measured by RT-qPCR. SMAD6 protein levels were measured by western blot. The effects of SMAD6 depletion on RB cells were analyzed using CCK-8 and transwell assays. The key proteins related to epithelial-mesenchymal transition (EMT) was determined by western blot. The localization of DNM3OS was detected by nuclear/cytoplasmic assay. In addition, the direct interaction between miR-134-5p and SMAD6 or DNM3OS was confirmed with the application of dual-luciferase reporter assay.Results:SMAD6 was upregulated in RB tissue samples and cell lines, and silencing SMAD6 suppressed cell proliferation, migration and EMT in RB. Mechanically, SMAD6 was positively regulated by lncRNA DNM3OS through competitively interacting with miR-134-5p. DNM3OS contributed to RB progression by SMAD6-mediated manner.Conclusions:This research unmasked a novel DNM3OS/miR-134-5p/SMAD6 pathway in RB, which might make contribution to treatment of RB.Using starBase v3.0, we found a cluster of lncRNAs capable of binding to miR-134-5p.	31992960	RID03783	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,BRCA);DATA(GSE40174,GSE41245)
Lung adenocarcinoma	ANKRD40CL	ETS1	positively-E	dual-luciferase reporter analysis;FISH;RIP	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-204-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000134954	NA	55018	2113	C17orf73|FLJ20694|LINC00483	ETS-1|EWSR2|FLJ10768	The long noncoding RNA LINC00483 promotes lung adenocarcinoma progression by sponging miR-204-3p.The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD).The expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR.The interaction between LINC00483 and miR-204-3p was analyzed using dual-luciferase, fluorescence in situ hybridization and RNA immunoprecipitation.Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown.LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p.ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483.This study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1.	31889958	RID03784	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Chronic hyperglycemia	MIR181A2HG	AKT2	positively-E	TargetScan;luciferase reporter assay;RNA pull-down assay;western blot	downregulation	RT-qPCR;FISH	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-6832-5p;miR-6842-5p;miR-8056)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Genetic disease	Hyperglycemia	lncRNA	PCG	ENSG00000224020	GRCh38_9:124658412-124698631	ENSG00000105221	NA	100379345	208	NA	PKB脙沤脗虏	Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.The persistent exposure of HUVECs to HG resulted in MIR181A2HG down-regulation and thus reduced its ability to sponge miR-6832-5p, miR-6842-5p and miR-8056, subsequently leading to an increase in miR-6832-5p, miR-6842-5p and miR-8056 levels.Mechanistically, miR-6832-5p, miR-6842-5p and miR-8056 were found to target the 3'UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2.On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis.The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG-induced endothelial dysfunction.To further validate the direct association of MIR181A2HG with these 3 miRNAs,RNA pull-down assay was performed, demonstrating that miR-6832-5p, miR-6842-5p and miR-8056 were enriched in the precipitates of 3'-biotinylated MIR181A2HG.	33537821	RID03785	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	TINCR	EGFR	positively-E	luciferase reporter assay;ChIP-PCR;RIP	upregulation	qRT-PCR	TCGA	NA	tumorigenesis(+);prognosis(-);tumor growth(+)	ceRNA(miR-503-5p);DNA methylation	NA	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000146648	NA	257000	1956	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	ERBB|ERBB1|ERRP	LncRNA TINCR favors tumorigenesis via STAT3-TINCR-EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer.The long noncoding RNA (lncRNA) TINCR has recently been found to be associated with the progression of human malignancies, but the molecular mechanism of TINCR action remains elusive, particularly in breast cancer. The oncogenic role of TINCR was examined in vitro and in vivo in breast cancer. Next, the interaction between TINCR, DNMT1, and miR-503-5p methylation was explored. Moreover, the mechanism by which TINCR enhances EGFR expression and downstream signaling via an RNA-RNA interaction was comprehensively investigated. Furthermore, upstream transcriptional regulation of TINCR expression by STAT3 was examined by performing chromatin immunoprecipitation. Finally, feedback signaling in the STAT3-TINCR-EGFR downstream cascade was also investigated. TINCR is upregulated in human breast cancer tissues, and TINCR knockdown suppresses tumorigenesis in vitro and in vivo. Mechanistically, TINCR recruits DNMT1 to the miR-503-5p locus promoter, which increases the methylation and suppresses the transcriptional expression of miR-503-5p. Furthermore, TINCR also functions as a competing endogenous RNA to upregulate EGFR expression by sponging miR-503-5p. In addition, TINCR stimulates JAK2-STAT3 signaling downstream from EGFR, and STAT3 reciprocally enhances the transcriptional expression of TINCR. Our findings broaden the current understanding of the diverse manners in which TINCR functions in cancer biology. The newly identified STAT3-TINCR-EGFR-feedback loop could serve as a potential therapeutic target for human cancer.TINCR promotes tumor growth in vivo and in vitro.	33446634	RID03786	ceRNA or sponge	prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Breast cancer	STAT3	TINCR	positively-E	JASPAR;ChIP-PCR	upregulation	qRT-PCR	TCGA	NA	tumorigenesis(+);prognosis(-);tumor growth(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000223573	GRCh38_19:5558167-5578349	6774	257000	APRF	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	To investigate the transcriptional regulation upstream of TINCR, we used the online database JASPAR (http://jaspar.genereg.net/) to search for transcription factors that might potentially be enriched at the promoter of the TINCR locus. The analysis yielded putative STAT3-binding sites in the region upstream of the TSS of TINCR (Fig. 7a). Moreover, there were obvious enrich_x0002_ment peaks of STAT3 in the promotor region (chr19-5572112'-573399) of TINCR in HCC70 cells in ENCODE database (Fig. 7b). Next, from the CCLE data_x0002_base, TINCR expression was found to be positively cor_x0002_related with STAT3 expression in human cancer cells(Fig. 7c). Last, STAT3 knockdown decreased the expres_x0002_sion of TINCR (Fig. 7d), and the results of ChIP-PCR assays indicated that STAT3 was highly enriched at the TINCR promoter relative to mock control (Fig. 7e). Col_x0002_lectively, our results indicate that TINCR stimulates the activation of EGFR and its key downstream-signaling effectors, including STAT3, which, reciprocally, promotes the transcriptional expression of TINCR.TINCR promotes tumor growth in vivo and in vitro	33446634	RID03787	transcriptional regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Gastric cancer	LINC00673	LATS2	negatively-E				NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000150457	NA	100499467	26524	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	A review of linc00673 as a novel lncRNA for tumor regulation.applied bioinformatics predictions and performed radioimmunoprecipitation assays and found that Linc00673 can bind to LSD1 and EZH2 19. Moreover, EZH2 and LSD1 were found to bind directly to the promoter regions of tumor suppressor genes LATS2 and KLF2, which induces the H3K27 trimethylation or H3K4 demethylation of these genes and downregulates their expression.This event ultimately promotes the proliferation, invasion, and migration of gastric cancer cells.	33390809	RID03788	transcriptional regulation	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00673	KLF2	negatively-E				NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000127528	NA	100499467	10365	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	LKLF	A review of linc00673 as a novel lncRNA for tumor regulation.applied bioinformatics predictions and performed radioimmunoprecipitation assays and found that Linc00673 can bind to LSD1 and EZH2 19. Moreover, EZH2 and LSD1 were found to bind directly to the promoter regions of tumor suppressor genes LATS2 and KLF2, which induces the H3K27 trimethylation or H3K4 demethylation of these genes and downregulates their expression.This event ultimately promotes the proliferation, invasion, and migration of gastric cancer cells.	33390809	RID03789	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	LINC00673	MARK4	positively-E				NA	NA	Hippo signaling pathway(+);cell proliferation(+)	ceRNA(miR-515-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000007047	NA	100499467	57787	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	FLJ90097|KIAA1860|MARKL1|Nbla00650|PAR-1D	A review of linc00673 as a novel lncRNA for tumor regulation.A past study found that Linc00673 can sponge-absorb miR-515-5p, relieve the inhibition of miR-515-5p on microtubule affinity regulating mitogen-activated protein kinase 4 (MARK4), and activate the hippo signal pathway participated by MARK4 in order to promote the proliferation of breast cancer cells 22.	33390809	RID03790	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978,GSE41245)
Systemic juvenile idiopathic arthritis	MALAT1	ZBTB4	positively-E	bioinformatics;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	JAK/STAT signaling pathway(+)	ceRNA(miR-150-5p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000174282	NA	378938	57659	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	KAISO-L1|KIAA1538|ZNF903	Suppression of lncRNA MALAT1 reduces pro-inflammatory cytokines production by regulating miR-150-5p/ZBTB4 axis through JAK/STAT signal pathway in systemic juvenile idiopathic arthritis.Systemic juvenile idiopathic arthritis (sJIA) is a common chronic disease occurring in children. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of diverse human diseases. This study aimed to explore the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and its mechanism in sJIA. We found that the expression of MALAT1, the plasma level of pro-inflammatory cytokines (IL-6, IL-17, IL-1beta, and TNF-alpha) as well as MMP-8 and MMP-9 production were significantly elevated in sJIA patients. Moreover, we observed that the production of these cytokines in peripheral blood mononuclear cells (PBMCs) from sJIA patients were reduced after MALAT1 knockdown. Furthermore, bioinformatics analysis predicted that MALAT1 might bind to miR-150-5p and ZBTB4 was a downstream target gene of miR-150-5p. Besides, rescue assays revealed that MALAT1 knockdown-mediated suppressive effects on cytokine production could be reversed by ZBTB4 overexpression. In addition, MALAT1 activated the JAK/STAT signaling by upregulating ZBTB4 expression. In summary, our findings demonstrated that MALAT1 promoted pro-inflammatory cytokine and MMP production by targeting the miR-150-5p/ZBTB4 axis through JAK/STAT signaling pathway in sJIA, suggesting that MALAT1 may have a potential diagnostic biomarker for the pathogenesis and therapy of sJIA. We first measured MALAT1 expression by RT-qPCR in PBMCs.As presented in Fig. 1A, there was a significant upregulation of MALAT1 expression in sJIA patients compared with healthy control, implying that MALAT1 might play a role in the pathogenesis of sJIA.To validate the interaction between MALAT1 and miR-150-5p, the luciferase reporter assay and RIP assay were conducted.	33341002	RID03791	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	HAND2-AS1	SOX7	positively-E		downregulation		NA	NA	cell proliferation(-)	ceRNA(miR-1275)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000171056	NA	79804	83595	DEIN|FLJ11539|NBLA00301	NA	Role of HAND2-AS1 in human tumors. Wang et al. [40] reported that the expression of HAND2-AS1 was downregulated in breast cancer tissues, especially in lumen A, lumen B, andbasal cell type, and they further found that HAND2-AS1 promoted the expression of SOX7 and inhibited the proliferation of breast cancer cells by downregulating the expression of miR-1275 in breast cancer. Wei et al. [41] found that HAND2-AS1 could inhibit the proliferation of cancer cells and serve as the tumor suppressor gene of triplenegative breast cancer	33096034	RID03792	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DATA(GSE117623)
Breast cancer	MAFG-DT	MYB	positively-E	Starbase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);prognosis	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000265688	GRCh38_17:81927829-81930753	ENSG00000118513	NA	92659	4602	MAFG-AS1	c-myb	Regulatory effect of the MAFG-AS1/miR-150-5p/MYB axis on the proliferation and migration of breast cancer cells.Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG-AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG-AS1 in breast cancer. To achieve this, the expression of MAFG-AS1, microRNA (miR)-150-5p and MYB was detected by reverse transcription-quantitative PCR. The binding between miR-150-5p and MAFG-AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG-AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG-AS1 expression promoted the proliferation, migration and epithelial-mesenchymal transition of breast cancer cells. By contrast, miR-150-5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR-150-5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG-AS1 served as a sponge of miR-150-5p, and that miR-150-5p bound to MYB. The functional rescue assay results demonstrated that MAFG-AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR-150-5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG-AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR-150-5p/MYB axis, which suggested that MAFG-AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.	33367930	RID03793	ceRNA or sponge	prognosis		
Gastric cancer	SNHG22	HMGA1	positively-E	dual-luciferase reporter analysis;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	prognosis;cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-361-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000267322	GRCh38_18:49813961-49851059	ENSG00000137309	NA	103091864	3159	SCARNA17HG	HMGIY	Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/beta-Catenin Axis.RT-qPCR was used to identify SNHG22 and microRNA-361-3p (miR-361-3p) in GC tissues and cells. Functional assays were implemented to measure changes on biological activities of GC cells under different transfections. Besides, after human umbilical vein endothelial cells (HUVECs) were co-cultured with supernatant of transfected GC cells, angiogenesis was assessed by tube formation assay in vitro. HMGA1 and beta-catenin expression were determined. Finally, mechanistic assays, including RNA pull-down assay and dual-luciferase reporter assay, were employed to assess relationships among SNHG22, miR-361-3p, and HMGA1.SNHG22 and HMGA1 were highly expressed but miR-361-3p was poorly expressed in GC tissues. Mechanistically, SNHG22 bound to miR-361-3p, and miR-361-3p targeted HMGA1 to disrupt the Wnt/beta-catenin pathway. Following SNHG22 or HMGA1 silencing or miR-361-3p upregulation, we observed a decline of proliferation, migration, and invasion of GC cells and HUVEC angiogenesis but acceleration of GC cell apoptosis and cell cycle arrest.Collectively, SNHG22 silencing possessed tumor-suppressing potentials in GC development via Wnt/beta-catenin pathway by binding to miR-361-3p and downregulating HMGA1, highlighting a new promising road for GC treatment development.	33364835	RID03794	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Colorectal cancer	SOX9	FARSA-AS1	positively-E	luciferase reporter assay;DNA pull-down assay;ChIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell stemness(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000125398	NA	ENSG00000266975	GRCh38_19:12930522-12933296	6662	106144598	CMD1|CMPD1|SRA1	NA	SOX9-activated FARSA-AS1 predetermines cell growth, stemness, and metastasis in colorectal cancer through upregulating FARSA and SOX9.In this study, we hypothesized that SOX9 could regulate the function of cancer stem/initiating cells (CSCs) to further facilitate the progression of colorectal cancer (CRC).Silencing of SOX9 suppressed cell growth, stemness, migration, and invasion.SOX9 silencing decreased the luciferase activity of wildtype FARSA-AS1 promoter, whereas that of FARSA-AS1 promoter with mutant binding site displayed no significant changes (Fig. 2G). Data from ChIP and DNA pull-down assays further confirmed the interactivity of SOX9 with FARSA-AS1 promoter (Fig. 2H, I). Conclusively, SOX9- transcriptionally activates FARSA-AS1 in CRC cells.	33318478	RID03795	transcriptional regulation	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)	
Colorectal cancer	FAFASA-AS1	SOX9	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell stemness(+);cell migration(+);cell invasion(+);tumor growth(+);cell metastasis(+)	ceRNA(miR-18b-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000125398	NA	NA	6662	NA	CMD1|CMPD1|SRA1	SOX9-activated FARSA-AS1 predetermines cell growth, stemness, and metastasis in colorectal cancer through upregulating FARSA and SOX9.Mechanistically, SOX9 activated the transcription of lncRNA phenylalanyl-tRNA synthetase subunit alpha antisense RNA 1 (FARSA-AS1), while FARSA-AS1 elevated SOX9 in turn by absorbing miR-18b-5p and augmented FARSA via sequestering miR-28-5p.Furthermore, loss of FARSA-AS1 hindered malignant phenotypes in vitro and blocked tumor growth and metastasis in vivo.Notably, we testified that FARSA-AS1 aggravated the malignancy in CRC by enhancing SOX9 and FARSA.In addition, RNA pull-down assay results confirmed the specific interaction of FARSA-AS1 with miR-18b-5p-WT rather than miR-18b-5p-Mut (Fig. 4H). Meanwhile, the combination between miR-18b-5p and SOX9 was testified similarly by such manners (Fig. 4I, J). Taken all together, FARSA-AS1 upregulates SOX9 in CRC by sponging miR-18b-5p.	33318478	RID03796	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Colorectal cancer	FAFASA-AS1	FARSA	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell stemness(+);cell migration(+);cell invasion(+);tumor growth(+);cell metastasis(+)	ceRNA(miR-28-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000179115	NA	NA	2193	NA	CML33|FARSL|FARSLA	Hence, we speculated that miR-28-5p might be implicated in the regulation of FARSA-AS1 on FARSA in CRC. The predicted binding sequences between miR-28-5p and FARSA-AS1 or FARSA were illustrated in Fig. 6F. Then, we overexpressed miR-28-5p in SW480 and SW1116 cells (Fig. 6G). As anticipated, the luciferase activity of FARSA-AS1-WT was considerably diminished with the transfection of miR-28- 5p mimics, while miR-28-5p overexpression did not impact the luciferase activity of FARSA-AS1-Mut (Fig. 6H). RNA pull-down assay data implied the remarkable enrichment of FARSA-AS1 specially by biotinylated miR-28-5p-WT (Fig. 6I). Furthermore, the interaction between miR-28-5p and FARSA was also validated by luciferase reporter assay and RNA pull-down assay (Fig. 6J, K). All data suggested that FARSA-AS1 upregulates FARSA via sequestering miR-28-5p.	33318478	RID03797	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842)
Breast cancer	SNHG3	ITGA5	positively-E		upregulation		NA	NA	cell viability(+);cell migration(-);cell invasion(-);Vav2/Rac1 signaling pathway(-)	ceRNA(miR-[0-9]26)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000161638	NA	8420	3678	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	CD49e|FNRA	LncRNA SNHG3, a potential oncogene in human cancers.SNHG3 expression in 60 pairs of breast cancer tissues and observed remarkable upregulation of SNHG3 expression in breast cancer tissues and cells.Moreover, SNHG3 expression is positively correlated with hepatoma-derived growth factor (HDGF) expression.Furthermore, SNHG3 acts as a competing endogenous RNA by directly binding to miR-384 in a sequence-specific manner.Meanwhile, HDGF is also a target gene of miR-384 and is regulated by SNHG3.In other words, SNHG3 functions as an endogenous sponge by sequestering miR-384, thus abolishing the miRNA-induced repressive effect on HDGF.SNHG3 uses a miR-330-5p sponge to positively regulate pyruvate kinase M1/M2 (PKM) expression, inhibit mitochondrial oxidative phosphorylation, and enhance breast cancer cell proliferation.SNHG3 silencing enhances apoptosis in triple-negative breast cancer (TNBC) cells through the miR-326/integrin alpha5 (ITGA5) axis and inhibits cell viability, migration, invasion and the Vav2/Rac1 signaling pathway.	33292213	RID03798	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Breast cancer	SNHG3	PKM	positively-E		upregulation		NA	NA	cell proliferation(+)	ceRNA(miR-330-5P)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000067225	NA	8420	5315	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	OIP3|PK3|PKM2|THBP1	LncRNA SNHG3, a potential oncogene in human cancers.SNHG3 expression in 60 pairs of breast cancer tissues and observed remarkable upregulation of SNHG3 expression in breast cancer tissues and cells.Moreover, SNHG3 expression is positively correlated with hepatoma-derived growth factor (HDGF) expression.Furthermore, SNHG3 acts as a competing endogenous RNA by directly binding to miR-384 in a sequence-specific manner.Meanwhile, HDGF is also a target gene of miR-384 and is regulated by SNHG3.In other words, SNHG3 functions as an endogenous sponge by sequestering miR-384, thus abolishing the miRNA-induced repressive effect on HDGF.SNHG3 uses a miR-330-5p sponge to positively regulate pyruvate kinase M1/M2 (PKM) expression, inhibit mitochondrial oxidative phosphorylation, and enhance breast cancer cell proliferation.SNHG3 silencing enhances apoptosis in triple-negative breast cancer (TNBC) cells through the miR-326/integrin alpha5 (ITGA5) axis and inhibits cell viability, migration, invasion and the Vav2/Rac1 signaling pathway.	33292213	RID03799	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Osteosarcoma	SNHG3	RAB22A	positively-E		upregulation		NA	NA	cell growth(+)	ceRNA(miR-151a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000124209	NA	8420	57403	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	NA	LncRNA SNHG3, a potential oncogene in human cancers.Expression of SNHG3 and Rab22a was upregulated in 54 OS tissues and OS cell lines (Saos2, MG63, U2OS and HOS) compared to paired normal tissues and normal osteoblasts, while miRNA-151a-3p was expressed at low levels.SNHG3 upregulates Rab22a expression, and SNHG3 binds to Rab22a and miRNA-151a-3p.A previous study demonstrated that the SNHG3/miRNA-151a-3p/Rab22a axis regulates invasion and migration of osteosarcoma.These results indicated that SNHG3 promotes the growth of OS cells by sponging the miRNA-196a-5p/homeobox c8 (HOXC8) axis, providing a potential marker in OS patients.	33292213	RID03800	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Malignant glioma	SNHG3	KLF2	negatively-E				NA	NA	cancer progression(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000127528	NA	8420	10365	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	LKLF	LncRNA SNHG3, a potential oncogene in human cancers.In addition, KLF2 and p21 were downregulated in glioma tissues.SNHG3 was negatively correlated with p21 and KLF2.These experiments revealed that SNHG3 accelerates the malignancy of glioma by inhibiting transcription of KLF2 and p21.	33292213	RID03801	transcriptional regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SNHG3	CDKN1A	negatively-E				NA	NA	cancer progression(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000124762	NA	8420	1026	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA SNHG3, a potential oncogene in human cancers.In addition, KLF2 and p21 were downregulated in glioma tissues.SNHG3 was negatively correlated with p21 and KLF2.These experiments revealed that SNHG3 accelerates the malignancy of glioma by inhibiting transcription of KLF2 and p21.	33292213	RID03802	transcriptional regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Laryngeal carcinoma	SNHG3	WEE1	positively-E		upregulation		NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-384)	regulation	RNA-protein	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000166483	NA	8420	7465	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	WEE1A	LncRNA SNHG3, a potential oncogene in human cancers.Expression of SNHG3 was upregulated in LC tissues and cell lines compared to normal tissues and cell lines.SNHG3 negatively regulates miR-384, improves wee1-like protein kinase (WEE1) expression, and promotes LC cell migration and invasion.Furthermore, SNHG3 acts as a ceRNA by directly binding to miR-384 to increase WEE1 expression.In summary, these results indicated that SNHG3 regulates the migration and invasion of LC cells via the miR-384/WEE1 axis.	33292213	RID03803	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Laryngeal carcinoma	SNHG3	YAP1	positively-E		upregulation		NA	NA	cancer progression(-)	ceRNA(miR-340-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000137693	NA	8420	10413	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	YAP65	LncRNA SNHG3, a potential oncogene in human cancers.Found that knock down of SNHG3 reduced the growth of LSCC xenograft tumors by regulating the miR-340-5p/yes-associated protein 1 (YAP1) axis and Wnt/beta-catenin pathway.	33292213	RID03804	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Colorectal cancer	SNHG3	RUNX2	positively-E		upregulation		NA	NA	cancer progression(+);prognosis	ceRNA(miR-539)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000124813	NA	8420	860	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	LncRNA SNHG3, a potential oncogene in human cancers.SNHG3 was highly expressed in CRC tumor tissues compared to adjacent normal tissues.Mechanistically, SNHG3 acts as the miRNA's ceRNA to bind miR-539, thereby regulating the expression of its target gene, runt-related transcription factor 2 (RUNX2), and promoting the occurrence and development of CRC.Upregulation of SNHG3 is correlated with poor prognosis, indicating that it may be an important biomarker of CRC.	33292213	RID03805	ceRNA or sponge	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	SNHG3	TOP2A	positively-E				NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000131747	NA	8420	7153	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	TOP2|TOP2alpha|TOPIIA	LncRNA SNHG3, a potential oncogene in human cancers.SNHG3 acts as a ceRNA of mir-139-5p and inhibits the activity of mir-139-5p.Expression of topoisomerase IIalpha (TOP2A), a target of miR-139-5p, was increased, which ultimately promoted proliferation and metastasis of renal cancer cells.These results confirmed that the SNHG3/miR-139-5p/TOP2A axis plays a crucial role in renal cell carcinoma and may represent a key target for diagnosis and treatment.	33292213	RID03806	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	SNHG3	ZEB1	positively-E		upregulation		NA	NA	tumorigenesis(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000148516	NA	8420	6935	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA SNHG3, a potential oncogene in human cancers.In conclusion, SNHG3 promotes hepatocellular tumorigenesis via the miR-326/SMAD3/ZEB1 axis.found that expression of SNHG3 in highly metastatic HCC cells was significantly higher than in low metastatic HCC cells.	33292213	RID03807	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	E2F1	SNHG3	positively-E		upregulation		NA	NA	STAT3 signaling pathway(+);cell proliferation(+);cell migration(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000242125	GRCh38_1:28505980-28510892	1869	8420	RBBP3|RBP3	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	LncRNA SNHG3, a potential oncogene in human cancers.showed that expression of SNHG3 in non-small-cell lung cancer (NSCLC) tissues and cells was higher than in normal tissues and cell lines.Mechanistically, SNHG3 is activated by E2F transcription factor 1 (E2F1), subsequently promoting proliferation and migration of NSCLC by activating the transforming growth factor-beta (TGF-beta), interleukin-6 (IL-6)/janus-activated kinase 2 (JAK2)/signal transducer activator of transcription 3 (STAT3) pathways [66].	33292213	RID03808	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)
Leukemia	SNHG3	SRGN	positively-E				NA	NA	cell growth(+)	ceRNA(miR-758-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000122862	NA	8420	5552	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	PPG|PRG|PRG1	LncRNA SNHG3, a potential oncogene in human cancers.Mechanistically, we found that SNHG3 regulates the expression of serglycin (SRGN) by competitively binding to miR-758-3p.In other words, SNHG3 promotes the growth of acute myeloid leukemia cells by regulating the miR-758-3p/SRGN axis, providing a new therapeutic direction for the treatment of AML.	33292213	RID03809	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	SNHG3	PSMD10	positively-E		downregulation		NA	NA	cell migration(-);cell invasion(-);cell proliferation(-);colony formation(-)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000101843	NA	8420	5716	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	p28	LncRNA SNHG3, a potential oncogene in human cancers.showed that SNHG3 can be used as the ceRNA of this miRNA to bind to miR-214-3p, actively regulating expression of the proteasome 26S subunit non-ATPase 10 (PSMD10) and significantly reducing PTC in vitro cell migration, invasion, proliferation and colony formation.found that lncRNA SNHG3 was significantly downregulated in PTC tissues and cell lines.	33292213	RID03810	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Prostate cancer	SNHG3	SMURF1	positively-E		upregulation		NA	NA	cancer progression(+)	ceRNA(miR-577)	regulation	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000198742	NA	8420	57154	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	KIAA1625	LncRNA SNHG3, a potential oncogene in human cancers.reported that SNHG3 is highly expressed in prostate cancer cell lines.Mechanistically, SNHG3 endogenously absorbs miR-577, thereby positively expressing smad ubiquitin regulatory factor 1 (SMURF1) and promoting the development of prostate cancer.	33292213	RID03811	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	SNHG3	GINS2	positively-E		upregulation		NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	ceRNA(miR-[0-9]15-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000131153	NA	8420	51659	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	Pfs2|PSF2	LncRNA SNHG3, a potential oncogene in human cancers. identified that lncRNA SNHG3 is upregulated in bladder cancer tissues, and lncRNA SNHG3 knockdown inhibits bladder cancer cell proliferation, migration, invasion and EMT processes both in vitro and in vivo.In addition, under the mechanism of ceRNA, SNHG3 sponges miR515-5p to escalate expression of the GINS complex subunit 2 (GINS2).	33292213	RID03812	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE55807,GSE67939)
Cervical cancer	ZFAS1	MIR647	negatively-F	RIP;Lncbase;luciferase reporter assay;miRNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);tumor growth(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000207554	NA	441951	693232	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	MIRN647|hsa-mir-647	qRT-PCRwas performed to examine the differential expression of ZFAS1 in CC tissues and adjacent normal cervical tissues. Gain- and loss-of-function experiments were constructed to test the functional role of ZFAS1 in CC by CCK-8, colony formation, transwell and xenograft models assays. Luciferase reporter, RNA immunoprecipitation (RIP), methylated RNA immunoprecipitation (MeRIP), RNA pull-down assays were used to reveal the underlying mechanisms.Results: We found that ZFAS1 was significantly upregulated in CC tissues. Elevation of ZFAS1 correlated with advanced FIGO stage, lymph node and distant metastasis, and also indicated poor overall survival in patients with CC. Functional experiments demonstrated that ZFAS1 promoted CC cell proliferation, migration and invasion in vitro, and facilitated tumor growth and metastasis in vivo. Mechanistic investigation revealed that ZAFS1 seques_x0002_tered miR-647, and this RNA-RNA interaction is regulated by METLL3-mediated m6A modification.Conclusion: Our findings elucidate the functional roles of ZFAS1 and its m6A modification in CC cells and indicate that ZFAS1 may be a promising target for CC treatment.In conclusion, we demonstrated ZFAS1 as an oncogenic lncRNA in CC. ZFAS1 promotes CC cell proliferation and metastasis by acting as a ceRNA that sponges miR-647, which is regulated by m6 A modification. Our findings indicated that ZFAS1 may be a prognostic indicator and promising therapeutic target for CC patients.	33235466	RID03813	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Sepsis	HULC	RAC1	positively-E	dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	CSC	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000251164	NA	ENSG00000136238	NA	728655	5879	HCCAT1|LINC00078|NCRNA00078	p21-Rac1|Rac-1|TC-25	Potential role of lncRNA HULC/miR-128-3p/RAC1 axis in the inflammatory response during LPS-induced sepsis in HMEC-1 cells.Sepsis is a serious clinical condition characterized by systemic inflammation. The long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) was validated to partake in the development of sepsis. The present study aimed to investigate the potential mechanism of HULC in lipopolysaccharide (LPS)-induced sepsis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotwas employed to examine the expression of HULC, microRNA (miR)-128-3p, Rac family small GTPase 1 (RAC1) and pro-inflammatory factors [IL-6, TNF-alpha, intercellular adhesion molecule (ICAM1) and vascular cell adhesion molecule (VCAM1)] in the serum of patients with sepsis or LPS-induced human dermal microvascular endothelial cells (HMEC-1). Flow cytometry and western blot assays were performed to detect cell apoptosis. The targeted relationship among HULC, miR-128-3p and RAC1 was confirmed by a dual-luciferase reporter assay, RNA binding protein immunoprecipitation (RIP) assay and RNA pull-down assay. HULC and RAC1 were found to be upregulated, and miR-128-3p was downregulated in the serum of patients with sepsis and LPS-stimulated HMEC-1 cells. LPS promoted apoptosis and inflammation, which were decreased by silencing of HULC. HULC targeted miR-128-3p and negatively regulated its expression. HULC knockdown protected HMEC-1 cells from LPS-induced injury by upregulating miR-128-3p. RAC1 was a target of miR-128-3p, and gain of RAC1 also relieved the silencing of HULC-mediated suppressive effects on apoptosis and inflammation in LPS-stimulated HMEC-1 cells. In conclusion, HULC knockdown partially reversed LPS-induced sepsis via the regulation of miR-128-3p/RAC1 axis.	33174038	RID03814	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	ROR1-AS1	STC2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell viability(+);cell proliferation(+);cell migration(+);cell invasion(+);cell autophagy(+);apoptosis process(-)	ceRNA(miR-670-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000223949	GRCh38_1:64094379-64171342	ENSG00000113739	NA	101927034	8614	NA	STC-2	In the current study, RT-qPCR analysis uncovered that ROR1-AS1 expression was evidently upregulated in CC tissues and cell lines. Functional experiments (CCK-8, EdU, TUNEL, wound healing and Transwell assays as well as western blot revealed that knockdown of ROR1-AS1 markedly suppressed the malignant phenotypes of CC cells via decreasing cell viability, proliferation, migration, invasion and autography, and facilitating cell apoptosis. Subsequently, by performing luciferase reporter and RNA pull-down assays, miR-670-3p was identified to be sponged by ROR1-AS1. Additionally, STC2 was disclosed to be targeted by miR-670-3p in CC cells. Rescue assays illuminated that upregulation of STC2 counteracted ROR1-AS1 knockdown-induced suppression on CC cell growth.	33081599	RID03815	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Nasopharynx carcinoma	DANCR	SOX2	positively-E	RNA-seq;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);tumorigenesis(+);prognosis(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000181449	NA	57291	6657	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	We found that DANCR is dramatically up-regulated in human NPC, and that it is an indicator for poor survival prognosis. DANCR knockdown suppressed cell proliferation, colony formation in vitro, and tumorigenicity in vivo. Mechanistic analyses demonstrated that DANCR could bind to RNA-binding protein 3 (RBM3) protein and stabilize SOX2 mRNA, resulting in NPC cell proliferation. Our findings indicate that DANCR functions as an oncogene and a potential therapeutic target for NPC.Furthermore, DANCR interacted with SOX2 mRNA (Figure 5F) and RBM3 depletion inhibited the association of DANCR with SOX2 mRNA (Figure 5G), indicating that RBM3 was needed for the binding between DANCR and SOX2 mRNA. Moreover, DANCR or RBM3 depletion significantly decreased the half-life of SOX2 mRNA (Figure 5H). In conclusion, DANCR regulates SOX2 mRNA stability and expression using RBM3.To probe the DANCR-associated downstream genes, RNASeq analysis was performed to compare the mRNA expression pattern influenced by DANCR knockdown. In addition, SOX2 was one of the top differentially expressed genes. SOX2 is required for NPC cell proliferation.RBM3 stabilizes YAP mRNA expression during cold stress.21 Hence, we studied whether SOX2 serves as a bona fide RBM3 target in NPC cells. RBM3 associated with SOX2 mRNA, using RNA immunoprecipitation assays. The RNA pull-down assay further demonstrated that DANCR bonded with RBM3 protein.	32971057	RID03816	interact with protein	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Cardiac cytotoxicity	SNHG16	hsa-miR-186-5p	negatively-E	dual-luciferase reporter assay;StarBase	upregulation	qRT-PCR	NA	NA	cytotoxicity(-)	sponge	binding/interaction	RNA-RNA	Propofol	CSC	NA	Other	Cardiac cytotoxicity	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes.PPF-induced SNHG6 expression change in HiPSC-CMs were monitored by qRT-PCRSNHG6 was downregulated in HiPSC-CMs to examine its role in PPF-induced cardiac cytotoxicity.The expression of competing endogenous RNA (ceRNA) candidate of SNHG6, human microRNA-186-5p (hsa-miR-186-5p) was also investigated in PPF-exposed HiPSC-CMs.Functions of hsa-miR-186-5p were further investigated in PPF-exposed and SNHG6-downregulated HiPSC-CMs.Results: PPF induced significant cytotoxicity, as well as SNHG6 upregulation in HiPSC-CMs.SNHG6 downregulation had rescuing effects on PPF-induced cardiac cytotoxicity.Dual-luciferase activity assay confirmed that hsa-miR-186-5p was the ceRNA candidate of SNHG6.qRT-PCR;ISHowed hsa-miR-186-5p expression was reversely correlated with SNHG6 in PPF-exposed HiPSC-CMs.Suppressing hsa-miR-186-5p reduced the rescuing effects of SNHG6-downregulation on PPF-induced cardiac cytotoxicity.Conclusions: SNHG6/hsa-miR-186-5p can modulate PPF-induced cardiac cytotoxicity in HiPSC-CMs, and thus may be a future drug target to prevent PPF infusion syndrome.	32968636	RID03817	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Hepatocellular carcinoma	IGFL2-AS1	BPY2C	positively-E	LncBase v.2;luciferase reporter assay;TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-7855-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000268621	GRCh38_19:46189029-46203160	ENSG00000185894	NA	645553	442868	AC006262.5	VCY2C	The AC006262.5-miR-7855-5p-BPY2C axis facilitates hepatocellular carcinoma proliferation and migration.Here, we identified an enriched long non-coding RNA, AC006262.5, associated with HCC, that promoted the proliferation, migration, and invasiveness of HCC cells, both in vitro and in vivo.In addition, our results revealed that AC006262.5 bound to and regulated miR-7855-5p, a tumor-suppressive miRNA, in HCC.Moreover, our data show that AC006262.5 regulates the expression of BPY2C via miR-7855-5p.Finally, we found that AC006262.5 and miR-7855-5p formed a regulatory loop.Upregulation of AC006262.5 resulted in decreased expression of miR-7855-5p, and downregulation of miR-7855-5p further facilitated the expression of AC006262.5.	32956593	RID03818	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Cervical cancer	Np63	PART1	positively-E	RNA-seq;shRNA;ChIP-seq	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	TF	lncRNA	NA	NA	ENSG00000152931	GRCh38_5:60487713-60548813	NA	25859	NA	NCRNA00206	lncRNA PART1 and MIR17HG as Np63alpha direct targets regulate tumor progression of cervical squamous cell carcinoma.In this study, we have identified 39 long noncoding RNAs as Np63alpha targets in CSCC through RNA sequencing and chromatin immunoprecipitation sequencing, in which we further confirmed and focused on the two tumor-related long noncoding RNAs, PART1 (lncPART1) and MIR17HG (lncMIR17HG).Experiments from stable overexpression/knockdown cell lines revealed that lncPART1 and lncMIR17HG regulated cell In vivo experiments further showed that lncPART1 suppresses tumor growth in CSCC-derived tumors.Examinations of clinical tissues indicated that the expression of lncPART1 was positively correlated with Np63alpha expression, while lncMIR17HG was negatively correlated with Np63alpha expression, suggesting that Np63alpha plays a central role via regulating its direct targets in the progression of CSCC.The expression of lncPART1 was significantly lower than that in normaltissues (Figure 1E). The correlation analyses revealed that lncPART1 expression was positively correlated with Np63alpha expression (Figure 1F).Overexpression of lncPART1 suppressed, while knockdown of lncPART1 promoted proliferation, migration, and invasion of cervical cancer cell lines.Np63alpha, as a transcription factor, can both activate the expression of target genes (eg, lncPART1) and inhibit the expression of some other target genes (eg, lncMIR17HG), which reveals its combinatory effects of tran_x0002_scriptional regulators.To investigate the transcriptional regulatory mechanisms of Np63alpha in CSCC, we performed RNA-seq in ME-180/shp63 cell lines. Totally, 394 lncRNAs were significantly affected (cutoff of two FCs and P < 10 5) compared with the no-knockdown control. To determine global direct targets of Np63alpha, we performed ChIP-seq of endogenous p63 in ME-180 cells.	32920922	RID03819	expression association	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Cervical cancer	Np63	MIR17HG	negatively-E	RNA-seq;shRNA;ChIP-seq	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	NA	NA	ENSG00000215417	GRCh38_13:91347820-91354579	NA	407975	NA	C13orf25|FGLDS2|LINC00048|MIHG1|MIRH1|MIRHG1|NCRNA00048|miR-17-92	lncRNA PART1 and MIR17HG as Np63alpha direct targets regulate tumor progression of cervical squamous cell carcinoma.In this study, we have identified 39 long noncoding RNAs as Np63alpha targets in CSCC through RNA sequencing and chromatin immunoprecipitation sequencing, in which we further confirmed and focused on the two tumor-related long noncoding RNAs, PART1 (lncPART1) and MIR17HG (lncMIR17HG).Experiments from stable overexpression/knockdown cell lines revealed that lncPART1 and lncMIR17HG regulated cell In vivo experiments further showed that lncPART1 suppresses tumor growth in CSCC-derived tumors.Examinations of clinical tissues indicated that the expression of lncPART1 was positively correlated with Np63alpha expression, while lncMIR17HG was negatively correlated with Np63alpha expression, suggesting that Np63alpha plays a central role via regulating its direct targets in the progression of CSCC.On the other hand, the expression of lncMIR17HG was significantly higher than that in normal tissues (Figure 1G). The correlation analyses revealed that MIR17HG expression was negatively correlated with Np63alpha expression (Figure 1H).Knockdown of lncMIR17HG markedly suppressed the proliferation, migration, and invasion of SiHa cells.Np63alpha, as a transcription factor, can both activate the expression of target genes (eg, lncPART1) and inhibit the expression of some other target genes (eg, lncMIR17HG), which reveals its combinatory effects of tran_x0002_scriptional regulators.To investigate the transcriptional regulatory mechanisms of Np63alpha in CSCC, we performed RNA-seq in ME-180/shp63 cell lines. Totally, 394 lncRNAs were significantly affected (cutoff of two FCs and P < 10 5) compared with the no-knockdown control. To determine global direct targets of Np63alpha, we performed ChIP-seq of endogenous p63 in ME-180 cells.	32920922	RID03820	expression association	NA		UP(LIHC);DATA(GSE117623)
Intervertebral disk degeneration	NEAT1	BCL2	negatively-E	Starbase;miRTarBase;dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-195a)	binding/interaction	RNA-protein	NA	NA	NA	Other	Intervertebral disk degeneration	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171791	NA	283131	596	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	Bcl-2|PPP1R50	Silencing of Long Non-coding RNA NEAT1 Upregulates miR-195a to Attenuate Intervertebral Disk Degeneration via the BAX/BAK Pathway.Quantitative real-time PCR was performed to detect the relative NEAT1 and miR-195a expressions and further confirmed the relationship between NEAT1 and miR-195a.The relative NEAT1 expression was significantly upregulated in the IVDD rat model and the denatured HNPC.Silencing of NEAT1 expression in HNPC significantly promoted the Collagen II and TIMP-1 expression induced by AGE while greatly suppressing the expressions of MMP-3 and cleaved caspase-3.Besides, downregulation of NEAT1 obviously reversed the AGE-induced apoptosis in HNPC.More interestingly, these effects of NEAT1 knockout on HNPC were largely reversed by silencing of miR-195a or overexpression of BAX under the AGE treatment.Mechanically, the direct combination of NEAT1 with miR-195a resulted in upregulation of MMP-3, cleaved caspase-3, BAX, and BAK, as well as downregulation of Collagen II and TIMP-1, which are associated with EMT and apoptosis.NEAT1 played its role in IVDD progression via partly by mediating the miR-195 expression and might be used as a potential target for IVDD therapy.	32850952	RID03821	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	GABPB1-AS1	NOTCH2	positively-E	FISH;Starbase;RIP;RNA pull-down assay	upregulation	qPCR;microarray	NA	NA	prognosis;cancer progression(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-519e-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000244879	GRCh38_15:50354950-50372202	ENSG00000134250	NA	100129387	4853	NA	NA	HPV16 E6 oncoprotein-induced upregulation of lncRNA GABPB1-AS1 facilitates cervical cancer progression by regulating miR-519e-5p/Notch2 axis.In the present study HPV16 E6-induced differential expression of lncRNAs, miRNA, and mRNA were identified using microarray-based analysis and verified in tumor r cell lines and tumor tissues, and the function of lncRNA in CC was investigated in vitro and in vivo.We found that an lncRNA, named GABPB1-AS1, was significantly upregulated in HPV16-positive CC tissues and cell lines.High expression of GABPB1-AS1 was correlated with a poor prognosis for HPV16-positive CC patients.Functionally, E6-induced GABPB1-AS1 overexpression facilitated CC cells proliferation and invasion in vitro and in vivo.Mechanistically, GABPB1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-519e-5p, resulting in the de-repression of its target gene Notch2 which is well known as an oncogene.Therefore, GABPB1-AS1 functioned as a tumor activator in CC pathogenesis by binding to miR-519e-5p and destroying its tumor suppressive function.The direct binding of miR-519e-5p to GABPB1-AS1 was further affirmed using RNA pull-down.	32844486	RID03822	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	LINC00973	Siglec-15	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	immune response(+)	ceRNA(miR-7109-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000240476	GRCh38_3:98981058-98983096	NA	NA	100506377	NA	CTD-2021J15.2	NA	LINC00973 is involved in cancer immune suppression through positive regulation of Siglec-15 in clear-cell renal cell carcinoma.Here we found that long non-coding RNA (lncRNA) LINC00973 was higher in Siglec-15-positive clear-cell renal cell carcinoma (ccRCC), and LINC00973 positively regulated Siglec-15 expression at transcriptional level.This effect was evidently dependent on miR-7109-3p (designated as miR-7109 hereafter), and we provided evidence that Siglec-15 is a direct target of miR-7109.Through sponging miR-7109, LINC00973 functioned as competing endogenous RNA (ceRNA) to control cell surface abundance of Siglec-15, and, consequently, was involved in cancer immune suppression.We further demonstrated that LINC00973 and miR-7109 expression in ccRCC antagonistically influenced immune activation of co-cultured Jurkat cells.For LINC00973 and Siglec-15 quantitation, total RNA was extracted using TRIzol (Invitrogen) and reverse-transcribed into cDNA with a High-Capacity cDNA Reverse Transcription Kit (ThermoFisher). Quantitation was performed with PowerUp SYBR Green Master Mix (Applied Biosystems). For miR-7109 quantitation, an All-in-One miRNA qRT-PCRDetection Kit (GeneCopoeia) was used and U6 served as endogenous control.	32780490	RID03823	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Gastric cancer	DDX11-AS1	IRS1	positively-E		upregulation		NA	NA	cancer progression(-)	ceRNA(miR-326)	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000169047	NA	100506660	3667	CONCR|SCAT4	HIRS-1	LncRNA DDX11-AS1: a novel oncogene in human cancer. Ren et-al found that the high expression of DDX11-AS1 was closely related to advanced TNM stage and lymph node metastasisand found that it was signifcantly highly expressed in GC tumour tissues and cells.  Mechanistically, DDX11-AS1 can directly target miR-326 and miR-326 and bind to IRS 1 inOXA-resistant GC cells. In terms of function, DDX11-AS1 silencing can inhibit the progression of OXA-resistant GC cells by targeting miR-326 and downregulating IRS1 expression. DDX11-AS1 is expected to be a novel target for diagnosis and treatment in GC.	32772230	RID03824	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Urinary bladder cancer	DDX11-AS1	CDK6	positively-E	shRNA	upregulation		NA	NA	cancer progression(+)	ceRNA(miR-499b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000105810	NA	100506660	1021	CONCR|SCAT4	PLSTIRE	LncRNA DDX11-AS1: a novel oncogene in human cancer. Li et-al. [33] showed that, compared with the levels in normal paracancerous tissues and cell lines, the expression of DDX11-AS1 was signifcantly upregulated in 108 BLCA tissues and 5 cell lines.DDX11-AS1 exacerbated BLCA progression by enhancing CDK6 expression through the suppression of miR-499b-5p.	32772230	RID03825	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Osteosarcoma	DDX11-AS1	DDX11	positively-E		upregulation		NA	NA	tumorigenesis(+)	ceRNA(miR-873-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000013573	NA	100506660	1663	CONCR|SCAT4	CHL1|ChlR1|KRG-2|WABS	LncRNA DDX11-AS1: a novel oncogene in human cancer.A subsequent study into its molecular mechanisms showed that DDX11-AS1 could upregulate the expression of DDX11 in osteosarcoma through miR-873-5p. In conclusion, DDX11-AS1 promotes the development of osteosarcoma by stabilizing DDX11	32772230	RID03826	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367)
Malignant glioma	CYTOR	CD164	positively-E	dual-luciferase reporter analysis;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell viability(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(-)	ceRNA(miR-613)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000135535	NA	112597	8763	C2orf59|LINC00152|MGC4677|NCRNA00152	DFNA66|MGC-24|MUC-24	Long non-coding RNA LINC00152/miR-613/CD164 axis regulates cell proliferation, apoptosis, migration and invasion in glioma via PI3K/AKT pathway.The level of LINC00152, microRNA-613 (miR-613) and the cluster of differentiation 164 (CD164) were measured by quantitative real-time polymerase chain reaction (qRT-PCR in glioma tissues and cell lines.Meanwhile, dual-luciferase reporter and RNA immunoprecipitation (RIP) assay were performed to examine the interrelation between miR-613 and LINC00152 or CD164.The levels of LINC00152 and CD164 were obviously increased while miR-613 was especially decreased in glioma tissues and cell lines.The downregulation of LINC00152 and CD164, as well as the upregulation of miR-613 induced cell apoptosis, repressed viability, migration, and invasion.Furthermore, miR-613 was a target gene of LINC00152, while targeted CD164.Low-expression of LINC00152 modified cell proliferation, apoptosis migration and invasion through LINC00152/miR-613/CD164 axis via PI3K/AKT signaling pathway in glioma, thus providing new therapeutic target in the clinical treatment of glioma.	32726126	RID03827	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	HOXA11-AS	ERBB2	NA				NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-331-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000141736	NA	221883	2064	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CD340|HER-2|HER2|NEU|NGL	Non-coding RNAs in gastric cancer.In addition, HOTAIR acts as a ceRNA for miR-331-3p to enhance the expression of HER2 (Erb-B2 receptor tyrosine kinase 2), which promotes theproliferation and invasion of gastric cancer cells [48].	32712234	RID03828	ceRNA or sponge	NA		UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Gastric cancer	HOXA11-AS	PRSS8	negatively-E				NA	NA	cell proliferation(+);cell invasion(+)	expression regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000052344	NA	221883	5652	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CAP1	Non-coding RNAs in gastric cancer.HOXA11-AS facilitates the proliferation and invasion of gastric cancer cells by recruiting the chromatin modification factors to inhibit the expression of PRSS8 (protease serine 8) and KLF2 (kruppel-like factor 2) [22]. Another study has shown that HOXA11-AS partially enhances the migration, invasion and metastasis of gastric cancer cells by promoting the protein expression of beta-catenin and KLF2 [19].	32712234	RID03829	expression association	metastasis		UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE55807,GSE75367)
Gastric cancer	HOXA11-AS	KLF2	negatively-E				NA	NA	cell proliferation(+);cell invasion(+)	expression regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000127528	NA	221883	10365	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	LKLF	Non-coding RNAs in gastric cancer.HOXA11-AS facilitates the proliferation and invasion of gastric cancer cells by recruiting the chromatin modification factors to inhibit the expression of PRSS8 (protease serine 8) and KLF2 (kruppel-like factor 2) [22]. Another study has shown that HOXA11-AS partially enhances the migration, invasion and metastasis of gastric cancer cells by promoting the protein expression of beta-catenin and KLF2 [19].	32712234	RID03830	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MALAT1	ATG12	positively-E				NA	NA	cell autophagy(+);chemoresistance(+)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000145782	NA	378938	9140	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APG12|APG12L	Non-coding RNAs in gastric cancer.In addition, MALAT1 acts as a sponge for miR-23b-3p to attenuate the inhibitory effect of miR-23b-3p on ATG12 (autophagy-related protein 12), inducing chemo-induced autophagy and chemoresistance in gastric cancer cells.	32712234	RID03831	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Gastric cancer	EFNA1	ephrin A1	positively-E				NA	NA	cell invasion(+);cell metastasis(+)	sponge	association	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000169242	GRCh38_1:155127876-155134899	NA	NA	1942	NA	B61|ECKLG|EFL1|EPLG1|GMAN|LERK-1|LERK1|TNFAIP4	NA	Non-coding RNAs in gastric cancer.GMAN promotes gastric cancer cell invasion and metastasis by increasing the translation of ephrin A1 mRNA via competitively binding to GMAN antisense lncRNA.	32712234	RID03832	ceRNA or sponge	metastasis	UP(NSCLC,BRCA);DATA(GSE74639,GSE55807)	
Gastric cancer	MEG3	BCL2	positively-E				NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-181a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Bcl-2|PPP1R50	Non-coding RNAs in gastric cancer. MEG3 hinders gastric cancer cell proliferation, migration and invasion by upregulating the expression of Bcl-2 (B cell lymphoma-2) through its ceRNA activity on oncogenic miR-181a [64].	32712234	RID03833	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	MEG3	miR-21	negatively-E				NA	NA	epithelial to mesenchymal transition(-)	expression regulation	association	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000199004	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Non-coding RNAs in gastric cancer.MEG3 also suppresses EMT process by negatively regulating miR-21 expression in gastric cancer cells [65].	32712234	RID03834	expression association	NA		
Gastric cancer	DLST	miR-502-3p	negatively-E		upregulation		NA	NA	NRAS/MEK1/ERK1/2 signaling pathway(+)	sponge	association	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000119689	GRCh38_14:74881891-74903743	NA	NA	1743	NA	DLTS|KGD2|OGDC-E2	NA	Non-coding RNAs in gastric cancer. For example, circDLST is dramatically upregulated in gastric cancer tissues, and its high expression is correlated with poor survival in patients with gastric cancer [154]. Mechanistically, circDLST has been shown to activate the NRAS/MEK1/ERK1/2 signaling pathway by acting as a sponge of miR-502-3p in gastric cancer cells.	32712234	RID03835	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	DONSON	SOX4	positively-E				NA	NA	tumorigenesis(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000159147	GRCh38_21:33559542-33588706	ENSG00000124766	NA	29980	6659	B17|C21orf60|C2TA|DKFZP434M035	NA	Non-coding RNAs in gastric cancer. Mechanistically, circ-DONSON is able to recruit NURF (nucleosome remodeling factor) complex to activate the transcription of SOX4 (SRY-box transcription factor 4) in the nucleus, which contributes to the malignant behaviors of gastric cancer cells.	32712234	RID03836	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Gastric cancer	NRIP1	AKT1	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-149-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000180530	GRCh38_21:14961235-15065936	ENSG00000142208	NA	8204	207	RIP140	AKT|PKB|PRKBA|RAC|RAC-alpha	Non-coding RNAs in gastric cancer.CircNRIP1 is also an oncogenic cicRNA that is highly expressed in gastric cancer. The upregulation of circNRIP1 is significantly correlated with larger tumor size, lymphatic invasion, shorter overall survival and disease-free survival of patients [160]. Knockdown of circNRIP1 impairs the proliferation, migration and invasion of gastric cancer cells via sponging of miR-149-5p to reduce AKT1 expression. However, whether circNRIP1 exerts its regulatory role in gastric cancer progression by interacting with RNA binding proteins remains unclear.	32712234	RID03837	ceRNA or sponge	NA	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	RBM33	IL6	NA		upregulation		NA	NA	apoptosis process(+);cell proliferation(-);cell invasion(-)	ceRNA(miR-149)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000184863	GRCh38_7:155644451-155781485	ENSG00000136244	NA	155435	3569	DKFZp434D1319|DKFZp686F102|MGC20460|PRR8	BSF2|HGF|HSF|IFNB2|IL-6	Non-coding RNAs in gastric cancer.CircRBM33 has been reported to be upregulated in gastric carcinoma tissues, and its upregulation is associated with advanced TNM stages, lymph node metastasis, and poor differentiation [163]. Silencing of circRBM33 increases apoptosis and decreases proliferation and invasion through enhancement of the circRBM33/miR-149/IL-6 axis in gastric cancer cells.	32712234	RID03838	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Gastric cancer	PSMC3	miR-296-5p	NA		downregulation		NA	NA	tumorigenesis(-)	sponge	association	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000165916	GRCh38_11:47418769-47426473	NA	NA	5702	NA	DCIDP|RPT5|TBP1	NA	Non-coding RNAs in gastric cancer.Circ-PSMC3 expression is significantly decreased in gastric cancer tissues and corresponding plasma [174]. The downregulation of Circ-PSMC3 is correlated with higher TNM stage and shorter overall survival of patients. Ectopic expression of circ-PSMC3 suppresses gastric cancer cell tumorigenesis by acting as a sponge of miR-296-5p, which further inhibits the expression of PTEN (phosphatase and tensin homolog).	32712234	RID03839	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)	
Gastric cancer	TINCR	STAU1	interact		upregulation		NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000124214	NA	257000	6780	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	PPP1R150|STAU	Expression of TINCR has been significantly higher in gastric cancer cell line compared with a human gastric epithelial cell line. Notably, in gastric cancer cell lines, the nuclear transcription factor SP1 has a prominent role in induction of expression of this lncRNA. The oncogenic role of TINCR in gastric cancer cells is mediated through its interaction with STAU1 protein. This interaction can modulate stability and expression of KLF2 and subsequently regulate expression of cyclindependent kinase genes [6]. Moreover, E2F1 enhances expression of TINCR in gastric cancer cells. Forced over-expression of E2F1 enhances gastric cancer cells proliferation, while its silencing reduces cell proliferation through hindering cell cycle progression in these cells. This transcription factor enhances growth of gastric cancer cells via induction of TINCR expression. TINCR interacts with STAU1 protein to affect stability and expression of the CDKN2B transcript, thus enhancing the proliferation of these cells.	32695943	RID03840	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Gastric cancer	E2F1	TINCR	positively-E		upregulation		NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000223573	GRCh38_19:5558167-5578349	1869	257000	RBBP3|RBP3	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	Expression of TINCR has been significantly higher in gastric cancer cell line compared with a human gastric epithelial cell line. Notably, in gastric cancer cell lines, the nuclear transcription factor SP1 has a prominent role in induction of expression of this lncRNA. The oncogenic role of TINCR in gastric cancer cells is mediated through its interaction with STAU1 protein. This interaction can modulate stability and expression of KLF2 and subsequently regulate expression of cyclindependent kinase genes [6]. Moreover, E2F1 enhances expression of TINCR in gastric cancer cells. Forced over-expression of E2F1 enhances gastric cancer cells proliferation, while its silencing reduces cell proliferation through hindering cell cycle progression in these cells. This transcription factor enhances growth of gastric cancer cells via induction of TINCR expression. TINCR interacts with STAU1 protein to affect stability and expression of the CDKN2B transcript, thus enhancing the proliferation of these cells.	32695943	RID03841	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Gastric cancer	TINCR	CDKN2B	NA		upregulation		NA	NA	cell proliferation(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000147883	NA	257000	1030	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	CDK4I|INK4B|MTS2|P15|p15INK4b|TP15	Expression of TINCR has been significantly higher in gastric cancer cell line compared with a human gastric epithelial cell line. Notably, in gastric cancer cell lines, the nuclear transcription factor SP1 has a prominent role in induction of expression of this lncRNA. The oncogenic role of TINCR in gastric cancer cells is mediated through its interaction with STAU1 protein. This interaction can modulate stability and expression of KLF2 and subsequently regulate expression of cyclindependent kinase genes [6]. Moreover, E2F1 enhances expression of TINCR in gastric cancer cells. Forced over-expression of E2F1 enhances gastric cancer cells proliferation, while its silencing reduces cell proliferation through hindering cell cycle progression in these cells. This transcription factor enhances growth of gastric cancer cells via induction of TINCR expression. TINCR interacts with STAU1 protein to affect stability and expression of the CDKN2B transcript, thus enhancing the proliferation of these cells.	32695943	RID03842	transcriptional regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	TINCR	BRAF	interact				NA	NA	MAPK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000157764	NA	257000	673	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	BRAF1	NSCLC is another cancer type in which mechanistic studies of TINCR showed conflicting results.-This lncRNA has been shown to interact with BRAF to enhance its kinase activity, therefore resulting in activation of MAPK pathway.-On the other hand, other have shown that this lncRNA decreases expression of miR-21 in NSCLC and suppresses cancer cell migration and invasion.	32695943	RID03843	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	TINCR	miR-21	negatively-E				NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000199004	NA	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	NSCLC is another cancer type in which mechanistic studies of TINCR showed conflicting results.-This lncRNA has been shown to interact with BRAF to enhance its kinase activity, therefore resulting in activation of MAPK pathway.-On the other hand, other have shown that this lncRNA decreases expression of miR-21 in NSCLC and suppresses cancer cell migration and invasion.	32695943	RID03844	transcriptional regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Hepatocellular carcinoma	TINCR	TP53	NA				NA	NA	apoptosis process(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000141510	NA	257000	7157	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	LFS1|p53	TINCR: An lncRNA with dual functions in the carcinogenesis process.In HCC, two distinct studies showed association between over-expression of this lncRNA and induction of apoptosis via regulation of P53 and enhancement of cell proliferation via modulation of the miR-214-5p/ROCK1 axis, respectively [16,17].	32695943	RID03845	transcriptional regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TINCR	ROCK1	NA				NA	NA	cell proliferation(+)	ceRNA(miR-214-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000067900	NA	257000	6093	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	p160ROCK	TINCR: An lncRNA with dual functions in the carcinogenesis process.In HCC, two distinct studies showed association between over-expression of this lncRNA and induction of apoptosis via regulation of P53 and enhancement of cell proliferation via modulation of the miR-214-5p/ROCK1 axis, respectively [16,17].	32695943	RID03846	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TINCR	DDX5	NA				NA	NA	cancer progression(-)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000263077	NA	257000	1655	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	G17P1|HLR1|p68	TINCR: An lncRNA with dual functions in the carcinogenesis process.Consistent with the latter study, depletion of this lncRNA in other HCC cell liens decreased oncogenic behavior through modulation of miR-218-5p/DDX5/AKT signaling [18].	32695943	RID03847	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cancer	TINCR	KLF4	NA				NA	NA	cancer progression(+)	ceRNA(miR-7)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000136826	NA	257000	9314	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	EZF|GKLF	TINCR: An lncRNA with dual functions in the carcinogenesis process.Notably, TINCR exerts its oncogenic role through competing with miR-7 and modulating KLF4 expression [19].	32695943	RID03848	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Cancer	TINCR	ERBB2	NA				NA	NA	apoptosis process(-)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000141736	NA	257000	2064	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	CD340|HER-2|HER2|NEU|NGL	TINCR: An lncRNA with dual functions in the carcinogenesis process.Another study in breast cancer demonstrated the role of TINCR in stimulation of tumorigenesis through modulating expression of miR-125b and its target gene ERBB2.Through this molecular axis, TINCR inhibits apoptosis in breast cancer cells [20].	32695943	RID03849	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Cancer	TINCR	ERBB2	NA				NA	NA	chemoresistance(+)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000141736	NA	257000	2064	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	CD340|HER-2|HER2|NEU|NGL	TINCR: An lncRNA with dual functions in the carcinogenesis process.Its interaction with miR-125b has been shown to release HER-2 and prompt trastuzumab resistance.	32695943	RID03850	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Heart failure	H19	PRC2	interact	ChIp-seq;ChIP-PCR	downregulation	qRT-PCR;microarray;sequencing	NA	NA	cancer progression(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 is highly conserved and down-regulated in failing hearts from mice, pigs and humans. H19 gene therapy pre_x0002_vents and reverses experimental pressure-overload-induced heart failure. H19 acts as an anti-hypertrophic lncRNA and represents a promising therapeutic target to combat pathological cardiac remodelling.Surprisingly, when interrogating the H3K27me3 signatures in the individual loci, we found no changes in the Nfatc3 locus, which was confirmed by ChIP-Seq and ChIP-PCR (Supplementary material online, Figure S6C E). This suggests a non-direct regulation of the Nfatc3 locus, by H19-mediated PRC2 regulation. Indeed, among the most differentially affected loci we identified the antihypertrophic NFAT mediator Tescalcin (Tesc) 25,26 locus to be heavily methylated upon H19 siRNA treatment (Figure 4D). This was confirmed in independent ChIP-qPCR experiments (Figure 4E).	32657324	RID03851	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	
Laryngeal squamous cell carcinoma	IGKJ2-MALLP2	CDKN1A	positively-E	dual-luciferase reporter analysis	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);angiogenesis(-)	ceRNA(miR-1911-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	NA	NA	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	lncRNA IGKJ2-MALLP2 suppresses LSCC proliferation, migration, invasion, and angiogenesis by sponging miR-1911-3p/p21.Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2-MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2-MALLP2 expression was confirmed by RT-qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2-MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual-luciferase reporter assay, the ability of miR-1911-3p to bind both IGKJ2-MALLP2 and p21 mRNA was demonstrated. IGKJ2-MALLP2 could upregulate p21 expression by competitively binding miR-1911-3p. Moreover, IGKJ2-MALLP2 effectively hindered the invasion, migration, and proliferation of AMC-HN-8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF-A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2-MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2-MALLP2, which mediates p21 expression by targeting miR-1911-3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC.	32639636	RID03852	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Esophageal cancer	SMIM45	BCL2L1	positively-E	dual-luciferase reporter analysis;LncBASE;TargetScan	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000205704	GRCh38_22:41952174-41958933	ENSG00000171552	NA	339674	598	LINC00634	Bcl-X|bcl-xL|bcl-xS|BCL2L|BCLX|PPP1R52	Long Noncoding RNA LINC00634 Functions as an Oncogene in Esophageal Squamous Cell Carcinoma Through the miR-342-3p/Bcl2L1 Axis.Many long noncoding RNAs reportedly have tumor suppressive roles or are oncogenic in esophageal cancer. We have previously performed a chip-based expression analysis of primary esophageal cancer tissues and found that the expression of LINC00634 in these tissues was higher than that in nontumor tissues. Quantitative real-time-polymerase chain reaction, cell counting kit-8, flow cytometry, caspase3/7 assay, dual-luciferase reporter assay, and restore assay were used to detect the proliferative and apoptotic effects of LINC00634 in esophageal cancer cells. The results showed that the expression of LINC00634 in these tissues was higher than that in nontumor tissues and associated with tumor-node-metastasis (TNM) stage of patients. Knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells. LINC00634 could target Bcl2L1 through miR-342-3p. In this study, we show that LINC00634 is upregulated in esophageal cancer. We also show that the knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells through the miR-342-3p/Bcl2L1 axis.Quanti_x0002_tative real-time polymerase chain reaction (qRT-PCR assay was used to detect the LINC00634 expression levels in EC cells.TargetScan was used to predict the targets of miR-342-3p,and results showed that the 30-UTR of Bcl2L1 harbors miR-342-3p binding sites.DIANA LncBASE Predicted was used to identify the miRNAs containing complementary bases with LINC00634, and LINC00634 was predicted to harbor miR-342-3p binding sites.	32583748	RID03853	ceRNA or sponge	metastasis		UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Cervical cancer	BBOX1-AS1	HOXC6	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;LncBase;starBase	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);tumorigenesis(+)	ceRNA(miR-361-3p);interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000254560	GRCh38_11:27047186-27220113	ENSG00000197757	NA	103695435	3223	NA	HOX3|HOX3C	LncRNA BBOX1-AS1 upregulates HOXC6 expression through miR-361-3p and HuR to drive cervical cancer progression.Over the past years, growing attention has been paid to deciphering the pivotal role of long non-coding RNAs (lncRNAs) in regulating the occurrence and development of human malignancies, cervical cancer (CC) included. Nonetheless, the regulatory role of lncRNA BBOX1 antisense RNA 1 (BBOX1-AS1) has not been explored as yet.Material and Methods The expression of BBOX1-AS1 was detected by reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8), colony formation, TUNEL, western blot, transwell and immunofluorescence assays testified the critical role of BBOX1-AS1 in CC. The relationship between RNAs (BBOX1-AS1, miR-361-3p, HOXC6 and HuR) was analysed by luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assays.BBOX1 antisense RNA 1 antisense RNA 1 was revealed to be highly expressed in CC. Decreased expression of BBOX1-AS1 had suppressive effects on CC cell growth and migration. Molecular mechanism assays verified that BBOX1-AS1 had negative interaction with miR-361-3p in CC. Additionally, homeobox C6 (HOXC6) was validated to be a downstream target of miR-361-3p in CC. Furthermore, ELAV-like RNA-binding protein 1, also known as HuR, was uncovered to be capable of regulating the mRNA stability of HOXC6 in CC. More importantly, rescue assays delineated that knockdown of HuR after overexpressing miR-361-3p could reverse BBOX1-AS1 upregulation-mediated effect on CC progression. Similarly, the function induced by BBOX1-AS1 upregulation on CC progression could be countervailed by HOXC6 depletion.BBOX1 antisense RNA 1 facilitates CC progression by upregulating HOXC6 expression via miR-361-3p and HuR.BBOX1-AS1 downregulation inhibits the in vivo tumorigenesis of CC.	32515533	RID03854	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	
Clear cell renal cell carcinoma	TTN-AS1	Cyclin D1	positively-E	dual-luciferase reporter analysis;Starbase;TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);cancer progression(+)	ceRNA(miR-195)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	Long Non-Coding RNA TTN-AS1 Serves as a Competing Endogenous RNA of miR-195 to Facilitate Clear Cell Renal Cell Carcinoma Progression.Introduction: Clear cell renal cell carcinoma (ccRCC) is an aggressive human malignancy. Long non-coding RNAs (lncRNAs) are critical regulators in many malignant tumors, including ccRCC. The aim of this study is to investigate the expression, functions and molecular mechanisms of lncRNA TTN-AS1 in ccRCC.Methods: A total of 145 paired cancer and normal tissues were collected from patients with ccRCC. The expression levels of TTN-AS1 and miR-195 in the tissues or cells were measured by RT-qPCR analysis. The expression levels of cyclin D1 protein were measured by western blot Cell proliferation and cell cycle distribution were detected by MTT assay and flow cytometer analysis, respectively. The binding relationship between miR-195 and TTN-AS1 or cyclin D1 mRNA was validated by dual-luciferase reporter assay.Results: Our results revealed that TTN-AS1 expression levels in human ccRCC tissues and cell lines were markedly increased. High expression of TTN-AS1 was closely associated with adverse clinicopathological characteristics of ccRCC patients. Gain- and loss-of-function experiments showed that TTN-AS1 overexpression promoted the proliferation and cell cycle transition of ccRCC cells, while the malignant traits were obviously suppressed after TTN-AS1 knockdown. Mechanistically, miR-195 was found to bind with and to be negatively regulated by TTN-AS1 in ccRCC cells. Further, we showed that cyclin D1 is a direct target of miR-195 in ccRCC, and rescue assays verified that restoration of miR-195 expression partially blocked the oncogenic effects of TTN-AS1 in ccRCC cells.Conclusion: Our study provides a novel mechanism of TTN-AS1/miR-195/cyclin D1 regulatory axis in ccRCC, which may become a breakthrough for ccRCC therapy in the future.As revealed by Figure 3A, TTN-AS1 was distributed mostly in the cytoplasm of ACHN and 786-O cells, and through the Starbase database , we identified the potential binding sites for miR-195 on TTN-AS1.By using the TargetScan database we noticed that the 3 -UTR region of cyclin D1 mRNA has the potential binding sites of miR-195.	32440207	RID03855	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Pancreatic adenocarcinoma	FOXA2	LINC00261	positively-E	luciferase reporter assay;ChIP-qPCR;siRNA	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Cancer	TF	lncRNA	ENSG00000125798	NA	ENSG00000259974	GRCh38_20:22547671-22578642	3170	140828	HNF3B	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	Extensive in silico analyses followed by in vitro experiments identified long intergenic non-coding RNA 261 (LINC00261) as a downregulated lncRNA in the squamous subtype of PDAC, which is generally associated with transforming growth factor beta (TGFbeta) signaling in human cancer cells. Its genomic neighbor, the transcription factor forkhead box protein A2 (FOXA2), regulated LINC00261 expression by direct binding of the LINC00261 promoter. CRISPR-mediated knockdown and promoter knockout validated the importance of LINC00261 in TGFbeta-mediated epithelial mesenchymal transition (EMT) and established the epithelial marker E-cadherin, an important cell adhesion protein, as a downstream target of LINC00261. Consequently, depletion of LINC00261 enhanced motility and invasiveness of PANC-1 cells in vitro. Altogether, our data suggest that LINC00261 is an important tumor-suppressive lncRNA in PDAC that is involved in maintaining a pro-epithelial state associated with favorable disease outcome.To investigate whether FOXA2 could regulate LINC00261 expression in pancreatic cancer cells, we manipulated FOXA2 levels in PANC-1 cells. Knockdown of FOXA2 using two different small interfering RNAs (siRNAs) led to a strong decrease of LINC00261 transcript levels.Interestingly, the transcription factor FOXA2 is a genomic neighbor of LINC00261, which was positively correlated (r = 0.72 0.91) with LINC00261 expression in all datasets analyzed.LINC00261 Downregulation Leads to Increased Cell Migration and Invasion.	32414223	RID03856	transcriptional regulation	NA		UP(LIHC);DATA(GSE117623)
Pancreatic adenocarcinoma	LINC00261	CDH1	positively-E	luciferase reporter assay;ChIP-qPCR	downregulation	qRT-PCR;sequencing	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	RNA-protein	NA	CSC	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000039068	NA	140828	999	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	CD324|UVO|uvomorulin	CRISPR-mediated knockdown and promoter knockout validated the importance of LINC00261 in TGFbeta-mediated epithelial mesenchymal transition (EMT) and established the epithelial marker E-cadherin, an important cell adhesion protein, as a downstream target of LINC00261. Consequently, depletion of LINC00261 enhanced motility and invasiveness of PANC-1 cells in vitro. Altogether, our data suggest that LINC00261 is an important tumor-suppressive lncRNA in PDAC that is involved in maintaining a pro-epithelial state associated with favorable disease outcome.To investigate whether FOXA2 could regulate LINC00261 expression in pancreatic cancer cells, we manipulated FOXA2 levels in PANC-1 cells. Knockdown of FOXA2 using two different small interfering RNAs (siRNAs) led to a strong decrease of LINC00261 transcript levels.The most interesting downstream target of LINC00261 was CDH1, which was robustly decreased in both systems. The CDH1 gene encodes E-cadherin, an important transmembrane cell adhesion molecule that plays a role in the formation of adherens junctions, thereby contributing to maintaining epithelial cell and tissue structures.Here, we cloned the promoter region of CDH1 in front of the luciferase gene and transfected this construct into PANC-1 wild-type or LINC00261-depleted cells and measured luciferase activity 48 h later. Intriguingly, the reduced expression level of LINC00261 in KO clones resulted in significantly lower CDH1 promoter activity as compared to WT clones (Figure 6e). Taken together, these results indicate that LINC00261 might be involved in the regulation of CDH1 transcription, thereby controlling the epithelial identity of pancreatic cancer cells.	32414223	RID03857	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Cerebral ischemia-reperfusion injury	SNHG16	LIMK1	positively-E	Starbase;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell injury(-);cell survival(+);apoptosis process(-)	ceRNA(miR-106b-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000106683	NA	100507246	3984	Nbla10727|Nbla12061|ncRAN	LIMK	Overexpression of long non-coding RNA SNHG16 against cerebral ischemia-reperfusion injury through miR-106b-5p/LIMK1 axis.Long non-coding RNA (LncRNA) involved in types of physiological insults and diseases via regulating the responses of complex molecular, including cerebral ischemia-reperfusion (I/R) injury. LncRNA SNHG16 played a potential role in ketamine-induced neurotoxicity. In this study, we utilized an in vitro cell model of I/R to examine the specific function and mechanism of LncRNA SNHG16 in oxygen-glucose deprivation and reperfusion (OGD/R) induced SH-SY5Y cells. After in vitro treatment of OGD/R, the lower the SH-SY5Y cell survival, the higher cell the apoptosis and increased caspase-3 activity was observed. Also, OGD/R induced endoplasmic reticulum stress (ERS) through increasing GRP78 and CHOP expressions and down-regulated LncRNA SNHG16 in SH-SY5Y cells. Conversely, LncRNA SNHG16 overexpression promoted OGD/R induced SH-SY5Y cell survival, suppressed its apoptosis, and caspase-3 activity. GRP78 and CHOP expressions were significantly suppressed in LncRNA SNHG16 overexpressing cells. MiR-106b-5p expression was increased and LIMK1 expression was down-regulated in OGD/R induced SH-SY5Y cells, and these effects were reversed by LncRNA SNHG16 overexpression, respectively. Moreover, LIMK1 is a direct target of MiR-106b-5p, and knockdown of LIMK1 reversed the effects of LncRNA SNHG16 on OGD/R-induced SH-SY5Y cells biology. Altogether, these results confirmed an important neuroprotection role of LncRNA SNHG16 in OGD/R induced SH-SY5Y cells injury, and miR-106b-5p/LIMK1 signal axis was involved in the action of LncRNA SNHG16.	32407850	RID03858	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	DSCAM-AS1	USP47	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+);AKT/mTOR signaling pathway(+)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000170242	NA	100506492	55031	M41	NA	Long non-coding RNA DSCAM-AS1 upregulates USP47 expression through sponging miR-101-3p to accelerate osteosarcoma progression.Osteosarcoma (OS) originating from mesenchyme is one of the most common invasive tumors of bone, and has an extremely high mortality rate. Previous studies have reported that long non-coding RNAs (lncRNAs) play essential roles in the tumorigenesis and progression of a multitude of human cancers. The lncRNA DSCAM-AS1 has been reported to be an oncogenic gene in many cancers. However, the roles and regulatory mechanisms of DSCAM-AS1 in OS have not been deeply investigated. In this study, our findings prove that DSCAM-AS1 is highly expressed in OS cells. Knockdown of DSCAM-AS1 suppressed cell proliferation, migration, and invasiveness, and induced cell apoptosis in OS. Additionally, knockdown of DSCAM-AS1 inactivated the Wnt-beta-catenin signaling pathway. Moreover, research into its molecular mechanisms confirmed that DSCAM-AS1 functions as a sponge for miR-101-3p, and that ubiquitin-specific peptidase 47 (USP47) is a target gene of miR-101-3p. Furthermore, a negative relationship between miR-101-3p and DSCAM-AS1 or USP47 was discovered. The results from our rescue assays suggest that DSCAM-AS1 regulates the progression of OS through binding with miR-101-3p to control the expression of USP47. Finally, we discovered that AKT-mTOR signaling pathway mediates the activity of DSCAM-AS1 in OS. Taken together, our results show that DSCAM-AS1 accelerates the progression of OS via the miR-101-3p-USP47 axis, which could present a new potential therapeutic treatment for OS.These data suggested that DSCAM-AS1 is positively correlated to AKT/mTOR pathway in OS.	32379981	RID03859	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE55807)
Breast cancer	HNF1A-AS1	TRIM32	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);cancer progression(+)	ceRNA(miR-20a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000119401	NA	283460	22954	C12orf27|FLJ38690|HAS1|NCRNA00262	BBS11|HT2A|LGMD2H|TATIP	Materials and Methods: Expression of HNF1A-AS1, miRNA (miR)-20a-5p, and tripartite motif containing 32 (TRIM32) was detected using quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis, migration, and invasion were measured by cellTiter 96 AQueous one solution cell proliferation assay kit, flow cytometry, and transwell assays, respectively.  Epithelial-mesenchymal transition (EMT) was evaluated by western blot, analyzing E-cadherin, N-cadherin, and vimentin expression. Mice xenograft model was generated to investigate tumor growth in vivo. The target binding among miR-20a-5p, HNF1A-AS1, and TRIM32 was confirmed by dual-luciferase reporter assay. Results: Expression of HNF1A-AS1 and TRIM32 was upregulated and miR-20a-5p was downregulated in breast cancer tumors and cell lines. Deletion of HNF1A-AS1 induced cell apoptosis rate, but suppressed cell proliferation, EMT, migration, and invasion in MDA-MB-231 and MCF-7 cells. Furthermore, HNF1A-AS1 downregulation impeded tumor growth in vivo. Interestingly, miR-20a-5p overexpression elicited the similar suppressive effects in MDA-MB-231 and MCF-7 cells, which was partially reversed by TRIM32 upregulation; besides, miR-20a-5p silencing could abolish the antitumor role of HNF1A-AS1 deletion. Notably, HNF1A-AS1 positively modulated TRIM32 expression through acting as a molecular sponge for miR-20a-5p. Conclusions: Knockdown of HNF1A-AS1 suppressed breast carcinogenesis presumably through targeting miR- 20a-5p/TRIM32 axis, suggesting that HNF1A-AS1 might be a promising therapy target for breast cancer.	32319789	RID03860	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Glioblastoma	LINC00467	IP6K2	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-339-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000068745	NA	84791	51447	C1orf97|MGC14801	IHPK2	Methods: The expression of LINC00467/miR-339-3p/IP6K2 glioblastoma tissues and cells was evaluated by RT-qPCR. The protein expression of genes (cleaved PARP, PARP, cleaved caspase 3, caspase 3, Bax, Bcl-2 and IP6K2) was measured by western blot assay. Then role of LINC00467 was demonstrated by EdU, colony formation, flow cytometry and TUNEL assays. The relationship between miR-339-3p and LINC00467/IP6K2 was validated by RNA pull down and luciferase reporter assays.Results: The expression of LINC00467 was upregulated in glioblastoma tissues and cells. LINC00467 knockdown suppressed cell proliferation but activated cell apoptosis. Further, LINC00467 high expression was associated with shorter overall survival rate in glioblastoma patients. Further, LINC00467 could bind with miR-339-3p, and IP6K2 was targeted by miR-339-3p. IP6K2 expression was regulated by LINC00467/miR-339-3p in a ceRNA pattern. Moreover, LINC00467 could regulate the development of glioblastoma via miR-339-3p/IP6K2 axis.Conclusions: LINC00467 knockdown repressed cell proliferation but stimulated cell apoptosis in glioblastoma via miR-339-3p/IP6K2 axis, which may enlighten to find a novel therapeutic tactic for glioblastoma patients.	32176627	RID03861	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE55807,GSE67939)
Chronic obstructive pulmonary disease	SNHG5	PTEN	positively-E	starBase;luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);inflammatory response(-)	ceRNA(miR-132)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000171862	NA	387066	5728	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA SNHG5 regulates cell apoptosis and inflammation by miR-132/PTEN axis in COPD.Long non-coding RNAs small nucleolar RNA host gene 5 (lncRNA SNHG5) plays well-defined roles in the malignant progression. However, the roles of SNHG5 in chronic obstructive pulmonary disease (COPD) progression remain unclear. In the present study, SNHG5 expression was low expressed in COPD tissues and positively correlated with low forced expiratory volume in one second (FEV1)% in patients. Subsequently, cigarette smoke extract (CSE) decreased SNHG5 expression in 16HBE cells, and SNHG5 overexpression in 16HBE cells mitigated the effects of CSE on the proliferation, apoptosis and inflammation (IL-1beta, IL-6 and TNF-a). Mechanistically, SNHG5 functioned as a competing endogenous RNA (ceRNA) for miR-132 in COPD, thereby increasing the expression of the miR-132 target PTEN. Moreover, rescue assays demonstrated that PTEN suppression (or miR-132 overexpression) attenuated the effects of SNHG5 upregulation on COPD progression. In conclusion, the SNHG5-miR-132-PTEN axis might play critical roles in COPD development, providing an effective target for the treatment of COPD.	32145584	RID03862	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hemangioma	CASC2	FBXL3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell growth(-)	ceRNA(miR-18a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000005812	NA	255082	26224	C10orf5	FBL3|FBL3A|FBXL3A	lncRNA CASC2 suppresses the growth of hemangioma cells by regulating miR-18a-5p/FBXL3 axis.Dysregulation of lncRNA cancer susceptibility candidate 2 (CASC2) is involved in the pathogenesis of multiple malignancies. However, the underlying mechanisms by which lncRNA CASC2 regulates the proliferation of hemangiomas (HAs) remain undocumented. Herein, the expression levels of lncRNA CASC2 and VEGF in proliferating or involuting phase HAs were assessed by qRT-PCRanalysis, and the effects of lncRNA CASC2 on HAs cell growth were evaluated by MTT, colony formation assays and western blot lncRNA CASC2 specific binding with miR-18a-5p was confirmed by luciferase report assay. Consequently, we found that the expression of lncRNA CASC2 was reduced in proliferating phase HAs as compared with the involuting phase HAs or normal tissues, and possessed a negative correlation with VEGF expression in proliferating phase HAs. Restored expression of lncRNA CASC2 repressed cell viability and colony formation and downregulated VEGF expression, while silencing lncRNA CASC2 showed the opposite effects. Moreover, lncRNA CASC2 was confirmed to bind with miR-18a-5p, which could reverse lncRNA CASC2-induced anti-proliferative effects by targeting FBXL3 in HAs cells. Altogether, our findings demonstrated that lncRNA CASC2 suppressed the growth of HAs cells by regulating miR-18a-5p/FBXL3 axis.lncRNA CASC2 reduced the proliferation and colony formation of HAs cells.	32138500	RID03863	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE41245)
Atherosclerosis	OIP5-AS1	OLR1	positively-E	starBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell viability(-)	ceRNA(miR-320a)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000173391	NA	729082	4973	cyrano|linc-OIP5	CLEC8A|LOX1|LOXIN|SCARE1|SLOX1	LNCRNA OIP5-AS1 regulates oxidative low-density lipoprotein-mediated endothelial cell injury via miR-320a/LOX1 axis.An increasing amount of research showed that endothelial cells (ECs) play crucial role in vascular disorders such as atherosclerosis (AS). LncRNA OIP5-AS1 and microRNA-320a (miR-320a) were reported to exert function in ECs. The purpose of this research was to investigate the functional mechanism of OIP5-AS1 and miR-320a in ox-LDL-treated HUVECs. The RNA levels of OIP5-AS1, miR-320a, and Lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR. The protein levels of LOX1 and cell apoptosis-related genes were determined by western blot assay. In addition, Cell Counting Kit-8 (CCK-8) and flow cytometry analysis were used to assess cell viability and apoptosis, respectively. Lactate dehydrogenase (LDH) activity was measured using LDH release assay. Besides, the interaction between miR-320a and OIP5-AS1 or LOX1 was predicted by starbase and verified by the dual-luciferase reporter assay. OIP5-AS1 expression was increased and miR-320a expression was decreased in oxidative low-density lipoprotein (ox-LDL)-treated HUVECs. OIP5-AS1 knockdown upregulated ox-LDL-treated HUVECs viability and suppressed apoptosis as well as LDH release. Interestingly, OIP5-AS1 elevated LOX1 level through downregulating miR-320a expression. As expected, miR-320a modulated LOX1 expression to mediate ox-LDL-treated HUVECs progression. Furthermore, OIP5-AS1 knockdown modulated cell progression via regulating miR-320a/LOX1 axis in ox-LDL-treated HUVECs. Our results demonstrated that the depletion of OIP5-AS1 enhanced cell viability and repressed apoptosis as well as LDH release in ox-LDL-treated HUVECs, providing potential target for the treatment of AS.	32072428	RID03864	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Sepsis	NEAT1	THBS1	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(+);cell proliferation(-)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000137801	NA	283131	7057	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	THBS|THBS-1|TSP|TSP-1|TSP1	Patients and methods: The abundance of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1), miR-370-3p, and thrombospondin-1 (TSP-1) were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR in sepsis patients and lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Enzyme-linked immunosorbent assay (ELISA) was performed to examine the concentration of cytokines in RAW 264.7 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry assay, and western blot assay were conducted to detect the proliferation and apoptosis of RAW 264.7 cells. dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA-pull down assay were conducted to confirm the combination between miR-370-3p and NEAT1 or TSP-1 in RAW 264.7 cells.Results: The enrichment of NEAT1 was enhanced in sepsis patients and LPS-stimulated RAW 264.7 cells. NEAT1 contributed to LPS-induced inflammation and apoptosis of RAW 264.7 cells. MiR-370-3p bound to NEAT1, and it was negatively regulated by NEAT1 in RAW 264.7 cells. LPS promoted the inflammation and apoptosis while restrained the proliferation of RAW 264.7 cells via NEAT1/miR-370-3p axis. TSP-1 was a target of miR-370-3p in RAW 264.7 cells, and miR-370-3p suppressed the inflammation and apoptosis while it facilitated the proliferation of LPS-induced RAW 264.7 cells via TSP-1.Conclusions: LncRNA NEAT1 promoted the inflammation and apoptosis while restrained the proliferation of LPS-stimulated RAW 264.7 cells through the miR-370-3p/TSP-1 axis.	31957847	RID03865	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Breast cancer	LINC00312	CDH1	positively-E	miRcode;RNA22;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);colony formation(-);cell migration(-);cell invasion(-)	ceRNA(miR-9)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237697	NA	ENSG00000039068	NA	29931	999	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	CD324|UVO|uvomorulin	Long non-coding RNAs (lncRNAs) are important mediators of the initiation and progression of tumors, including breast cancer (BC). The exact role of long intergenic non-coding RNA 00312 (LINC00312) in BC and its mechanism of action have not been reported to date. In the present study, LINC00312 was found to be downregulated in human BC tissues and cell lines by RT-qPCR. The findings of a functional study indicated that overexpression of LINC00312 suppressed the proliferation, colony forming ability, migration and invasiveness of BC cell lines. Mechanistically, LINC00312 was found to induce suppression of cell migration and invasion by directly binding to miR-9. Overexpression of LINC00312 increased the expression of cadherin 1 (CDH1), a direct target of miR-9, and decreased the expression of vimentin (VIM), a major cytoskeletal component of mesenchymal cells as determined by western blot miR-9 partly abrogated the upregulation of CDH1 and downregulation of VIM induced by LINC00312. Taken together, the results of the present study indicate a role for the LINC00312/miR-9/CDH1 axis in the progression of BC, and suggest a novel lncRNA-based diagnostic biomarker or therapeutic target for BC.To further explore the molecular mechanism of action of LINC00312 in BC, two different mRNA target-predicting algorithms, including miRcode and RNA22 , were used to predict the potential miRNAs that directly bind to LINC00312. miR 9, the level of which was found to be upregulated in BC cells , was identified as the most promising candidate. The potential binding sequences of miR-9 and LINC00312 are shown in Fig. 3A. RT-qPCR was first performed to examine the regulatory interconnection between LINC00312 and miR-9.A dual-luciferase reporter assay was performed to verify the direct interaction between LINC00312 and miR-9.	31894332	RID03866	ceRNA or sponge	NA		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Mycoplasma pneumoniae pneumonia	MALAT1	NFKB1	positively-F	dual-luciferase reporter analysis;western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Respiratory system disease	Bacterial pneumonia	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Our aim was to determine whether the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in Mycoplasma pneumoniae pneumonia (MPP), and its possible mechanism of action. MALAT1 expression in the bronchoalveolar lavage fluid of 50 hospitalized children with MPP was compared to its expression in 30 children with intrabronchial foreign bodies. MALAT1 expression was higher in children with MPP, accompanied by increased inflammatory mediators interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha), compared to the controls. In human airway epithelial cells infected with wild-type Mycoplasma pneumoniae (strain M129), MALAT1, IL-8, and TNF-alpha expression significantly increased, and increased expression of IL-8 and TNF-alpha could be suppressed by MALAT1 knockdown. Luciferase reporter gene assay and western blot showed that knockdown of MALAT1 reduced nuclear factor-kB (NF-kB) activation. In vivo, RNAi packaged with adenovirus (Adv) was nasally transfected into BALB/c mice to silence MALAT1, and an MP-infected mouse pneumonia model was prepared. The results demonstrated that the degree of pulmonary inflammatory injury, vascular permeability, secretion of inflammatory factors, and expression of phosphorylated p65 (pp65) in MP-infected mice were partly reversed after MALAT1 knockdown compared to those in the controls. In conclusion, MALAT1 is involved in the regulation of airway and pulmonary inflammation caused by MP infection via NF-kB regulation.By performing in vivo experiments, we found that downregulation of MALAT1 reduces pulmonary inflammation caused by MP infection.	33134293	RID03867	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ischemic stroke	PVT1	TP53	NA	dual-luciferase reporter analysis;starbase	upregulation	qPCR	NA	NA	ferroptosis(+)	ceRNA(miR-214)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000141510	NA	5820	7157	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	LFS1|p53	LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p53.Aim: The study aims to investigate the roles of LncRNA and miRNA in ferroptosis in brain ischemia/reperfusion (I/R) in vivo and in vitro.Materials and methods: qPCR assay was used to analyze lncRNA PVT1 and miR-214 expressions in acute ischemic stroke (AIS) patients. Then, we established brain I/R mice models and OGD/R PC12 cell models to analyze the mechanism of ferroptosis. I/R mice were treated by lncRNA PVT silencing or miR-214 overexpressing lentivirus via lateral ventricles. Infarct size was analyzed by TTC staining, accompanied by the detection of ferroptosis indicators through Perls'Prussian blue staining, iron kit, MDA kit, glutathione kit, GPx activities kit and western blot (WB). dual-luciferase reporter assay was used to assess whether miR-214 bound to PVT1, TP53 or TFR1. Co-IP analyzed the interplay of p53 with SLC7A11.Key findings: We found that the levels of PVT1 were upregulated and miR-214 levels were downregulated in plasma of AIS patients. NIHSS score was positively correlated with PVT1 levels but was negatively with miR-214 levels. PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.Conclusion: PVT1 regulated ferroptosis through miR-214-mediated TFR1 and TP53 expression. There was a positive feedback loop of lncRNA PVT1/miR-214/p53 possibly.	32827544	RID03868	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Ischemic stroke	PVT1	TFRC	NA	dual-luciferase reporter analysis;starbase	upregulation	qPCR	NA	NA	ferroptosis(+)	ceRNA(miR-214)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000072274	NA	5820	7037	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CD71|p90|TFR1	LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p53.Aim: The study aims to investigate the roles of LncRNA and miRNA in ferroptosis in brain ischemia/reperfusion (I/R) in vivo and in vitro.Materials and methods: qPCR assay was used to analyze lncRNA PVT1 and miR-214 expressions in acute ischemic stroke (AIS) patients. Then, we established brain I/R mice models and OGD/R PC12 cell models to analyze the mechanism of ferroptosis. I/R mice were treated by lncRNA PVT silencing or miR-214 overexpressing lentivirus via lateral ventricles. Infarct size was analyzed by TTC staining, accompanied by the detection of ferroptosis indicators through Perls'Prussian blue staining, iron kit, MDA kit, glutathione kit, GPx activities kit and western blot (WB). dual-luciferase reporter assay was used to assess whether miR-214 bound to PVT1, TP53 or TFR1. Co-IP analyzed the interplay of p53 with SLC7A11.Key findings: We found that the levels of PVT1 were upregulated and miR-214 levels were downregulated in plasma of AIS patients. NIHSS score was positively correlated with PVT1 levels but was negatively with miR-214 levels. PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.Conclusion: PVT1 regulated ferroptosis through miR-214-mediated TFR1 and TP53 expression. There was a positive feedback loop of lncRNA PVT1/miR-214/p53 possibly.	32827544	RID03869	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827)
Diabetic retinopathy	NEAT1	TGFB1	positively-E	siRNA; qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105329	NA	283131	7040	LINC00084|NCRNA00084|TncRNA|VINC	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Diabetic retinopathy (DR) is complication resulted from Type 2 diabetes mellitus. Accumulating evidence has proved the functions of long noncoding RNAs (lncRNAs) in the progression of DR. Recent reports exert the numerous regulatory functions of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in various diseases. However, its implications in DR remain barely known. Therefore, this study was carried out to explore the role of NEAT1 in high-glucose (HG)-triggered injury of human retinal endothelial cells (hRECs). Here, we found the NEAT1 level was significantly elevated in patients with DR, in the retina of diabetic rats and mice. Meanwhile, hRECs under HG stimuli also exhibited an increase of NEAT1. Moreover, the loss of NEAT1 enhanced hRECs proliferation and repressed HG-induced apoptosis, which was accompanied by an upregulation of Bcl-2 and a downregulation of Bax. Subsequently, the knockdown of NEAT1 obviously reduced HG-triggered oxidative stress injury in hRECs. It was reflected that intracellular reactive oxygen species and malondialdehyde level induced by HG were repressed by NEAT1 downregulation, while superoxide dismutase activity was increased. In addition, decreased NEAT1 repressed the inflammatory processes effectively as indicated by the inactivation of inflammatory cytokines Cox-2, interleukin-6, and tumor necrosis factor-alpha. Furthermore, vascular endothelial growth factor A (VEGF) and transforming growth factor-beta1 (TGF-beta1) expression in patients with DR, DR rats, and HG-incubated hRECs was obviously increased. The silence of NEAT1 could reduce the enhanced expression of VEGF and TGF-beta1 induced by HG. Hence, we concluded NEAT1 might contribute to the development of DR through activating TGF-beta1 and VEGF.Three different doses (10, 20, and 30 mM) of glucose were utilized to incubate hRECs with 10 mM glucose as the control. mRNA expression of TGF beta1 and VEGF in hRECs was tested by qRT-PCR In Figure 6a,b, glucose significantly increased the level of TGF beta1 and VEGF. Besides, we observed mRNA expression of TGF beta1 and VEGF was significantly inhibited by NEAT1 siRNA. Consistently, TGF beta1 and VEGF protein levels were also obviously repressed by the silence of NEAT1 in hRECs. These implied that TGF beta1 and VEGF could be highly inactivated by NEAT1 knockdown in DR.	32356340	RID03870	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic retinopathy	NEAT1	VEGFA	positively-E	siRNA; qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112715	NA	283131	7422	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	VEGF|VEGF-A|VPF	Diabetic retinopathy (DR) is complication resulted from Type 2 diabetes mellitus. Accumulating evidence has proved the functions of long noncoding RNAs (lncRNAs) in the progression of DR. Recent reports exert the numerous regulatory functions of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in various diseases. However, its implications in DR remain barely known. Therefore, this study was carried out to explore the role of NEAT1 in high-glucose (HG)-triggered injury of human retinal endothelial cells (hRECs). Here, we found the NEAT1 level was significantly elevated in patients with DR, in the retina of diabetic rats and mice. Meanwhile, hRECs under HG stimuli also exhibited an increase of NEAT1. Moreover, the loss of NEAT1 enhanced hRECs proliferation and repressed HG-induced apoptosis, which was accompanied by an upregulation of Bcl-2 and a downregulation of Bax. Subsequently, the knockdown of NEAT1 obviously reduced HG-triggered oxidative stress injury in hRECs. It was reflected that intracellular reactive oxygen species and malondialdehyde level induced by HG were repressed by NEAT1 downregulation, while superoxide dismutase activity was increased. In addition, decreased NEAT1 repressed the inflammatory processes effectively as indicated by the inactivation of inflammatory cytokines Cox-2, interleukin-6, and tumor necrosis factor-alpha. Furthermore, vascular endothelial growth factor A (VEGF) and transforming growth factor-beta1 (TGF-beta1) expression in patients with DR, DR rats, and HG-incubated hRECs was obviously increased. The silence of NEAT1 could reduce the enhanced expression of VEGF and TGF-beta1 induced by HG. Hence, we concluded NEAT1 might contribute to the development of DR through activating TGF-beta1 and VEGF.Three different doses (10, 20, and 30 mM) of glucose were utilized to incubate hRECs with 10 mM glucose as the control. mRNA expression of TGF beta1 and VEGF in hRECs was tested by qRT-PCR In Figure 6a,b, glucose significantly increased the level of TGF beta1 and VEGF. Besides, we observed mRNA expression of TGF beta1 and VEGF was significantly inhibited by NEAT1 siRNA. Consistently, TGF beta1 and VEGF protein levels were also obviously repressed by the silence of NEAT1 in hRECs. These implied that TGF beta1 and VEGF could be highly inactivated by NEAT1 knockdown in DR.	32356340	RID03871	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cardiomyopathy	NORAD	ZEB1	positively-E	dual-luciferase reporter analysis;StarBase	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Cardiomyopathy	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000148516	NA	647979	6935	LINC00657	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Materials and methods: Cell viability, 5-Ethynyl-2'-deoxyuridine (EdU)-positive ratio and apoptotic rate in human cardiomyocyte cell line AC16 undergoing treatment of normal-level (NG) or high-level glucose (HG) were assessed at first. NORAD level in HG-induced AC16 cells at different time points was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Subsequently, cell viability, EdU-positive ratio, and apoptotic rate in HG-induced AC16 cells overexpressing NORAD were evaluated. Next, subcellular distribution of NORAD was examined, and Dual-Luciferase reporter gene assay was performed to clarify the interaction among NORAD, miRNA-150-5p, and ZEB1. At last, rescue experiments were conducted to clarify the role of NORAD/miRNA-150-5p/ZEB1 axis in influencing the proliferation and apoptosis in HG-induced AC16 cells.Results: Results revealed that HG treatment suppressed the proliferative ability and stimulated apoptosis in AC16 cells. Besides, NORAD was time-dependently downregulated in HG-induced AC16 cells, and it was mainly distributed in cytoplasm. In addition, the overexpression of NORAD enhanced proliferative ability, attenuated apoptosis, and increased Bcl-2/Bax ratio in HG-induced AC16 cells. Finally, NORAD/miRNA-150-5p/ZEB1 axis was verified to protect the malignant progression of DCM.NORAD was Downregulated in Cardiomyocytes Undergoing High-Level Glucose Treatment.With the prolongation of HG treatment, ZEB1 was gradually downregulated in AC16 cells.	33215445	RID03872	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	LINC00589	CTNNB1	positively-E	knockdown;luciferase reporter assay;RIP	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000168036	NA	619351	1499	C8orf75|TSLNC8	armadillo|beta-catenin|CTNNB	Long noncoding RNA TSLNC8 enhances pancreatic cancer aggressiveness by regulating CTNNB1 expression via association with HuR.Pancreatic cancer (PC) is one of the most lethal malignancies worldwide. Tumor suppressor long noncoding RNA on chromosome 8p12 (TSLNC8) is a newly identified long noncoding RNA (lncRNA) and play an important role in human cancers. However, the function and molecular mechanism of TSLNC8 in PC progression remain to be elucidated. Our results showed a significant increase of TSLNC8 expression in PC tissues and cell lines. Upregulation of TSLNC8 expression in PC tissues was closely correlated with TNM stage, distant and lymph node metastasis, and poor prognosis of PC patients. Functional experiments demonstrated that TSLNC8 promoted PC cells proliferation and invasion in vitro, and enhanced PC growth and metastasis in vivo. Mechanistically, TSLNC8 associated with HuR, promoted the binding of HuR with CTNNB1 mRNA and increased the stability of CTNNB1 mRNA, thus activating WNT/beta-catenin signaling pathway. Taken together, our present study revealed that oncogenic lncRNA TSLNC8 positively regulate PC growth and metastasis via HuR-mediated mRNA stability of CTNNB1, extending the understanding of PC pathogenesis regulated by lncRNAs.TSLNC8 associates with-HuR to-stabilize CTNNB1 mRNA.	32951177	RID03873	interact with protein	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	LINC00589	ELAVL1	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	interact with protein	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000066044	NA	619351	1994	C8orf75|TSLNC8	Hua|HUR|MelG	Long noncoding RNA TSLNC8 enhances pancreatic cancer aggressiveness by regulating CTNNB1 expression via association with HuR.Pancreatic cancer (PC) is one of the most lethal malignancies worldwide. Tumor suppressor long noncoding RNA on chromosome 8p12 (TSLNC8) is a newly identified long noncoding RNA (lncRNA) and play an important role in human cancers. However, the function and molecular mechanism of TSLNC8 in PC progression remain to be elucidated. Our results showed a significant increase of TSLNC8 expression in PC tissues and cell lines. Upregulation of TSLNC8 expression in PC tissues was closely correlated with TNM stage, distant and lymph node metastasis, and poor prognosis of PC patients. Functional experiments demonstrated that TSLNC8 promoted PC cells proliferation and invasion in vitro, and enhanced PC growth and metastasis in vivo. Mechanistically, TSLNC8 associated with HuR, promoted the binding of HuR with CTNNB1 mRNA and increased the stability of CTNNB1 mRNA, thus activating WNT/beta-catenin signaling pathway. Taken together, our present study revealed that oncogenic lncRNA TSLNC8 positively regulate PC growth and metastasis via HuR-mediated mRNA stability of CTNNB1, extending the understanding of PC pathogenesis regulated by lncRNAs.Recently, RNA binding protein HuR has been found to stabilize CTNNB1 mRNA, which is regulated by some lncRNAs. We suspected that TSLNC8 might regulate CTNNB1 in this manner. To confrm this hypothesis, we performed a RIP assay using an anti-HuR antibody and found that TSLNC8 was significantly enriched by HuR.	32951177	RID03874	interact with protein	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Kidney failure	RPSAP52	GSTM1	positively-E	dual-luciferase reporter analysis;qPCR;western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-423-5p)	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000241749	GRCh38_12:65758020-65826997	ENSG00000134184	NA	204010	2944	NA	GST1|H-B|MU	This study aimed to investigate the roles of RPSAP52 in renal failure. Our results showed that RPSAP52 was upregulated in plasma of renal failure patients in comparison to healthy controls. dual-luciferase reporter assay showed that RPSAP52 could interact with miR-423-5p, while overexpression of RPSAP52 and miR-423-5p did not alter the expression of each other in human renal proximal tubular epithelial cells (HRPTEpCs). In addition, overexpression of RPSAP52 increased the expression levels of GSTM1 in HRPTEpCs. Cell apoptosis assay showed that overexpression of RPSAP52 and GSTM1 decreased the apoptotic rate of HRPTEpCs under hypoxia conditions. MiR-423-5p played an opposite role and attenuated the effects of overexpressing RPSAP52 and GSTM1. Therefore, RPSAP52 may regulate miR-423-5p/GSTM1 axis to suppress hypoxia-induced HRPTEpC apoptosis.GSTM1 has been reported to be a downstream target of miR-423-5p. In this study, the effects of overexpressing RPSAP52 and miR-423-5p on the expression of GSTM1 at both mRNA and protein  levels were evaluated by qPCR and western blot, respectively. Compared to the C and NC groups, overexpression of miR- 423-5p led to downregulated GSTM1, which confirmed the targeting of GSTM1 by miR-423-5p (p < .05). In addition, overexpression of RPSAP52 upregulated GSTM1 and attenuated effects of the overexpression of miR-423-5p on GSTM1 (p < .05).	32299250	RID03875	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Myocardial cell injury	1700020I14Rik	CGRP	positively-E	dual-luciferase reporter analysis	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-297a)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000262933	NA	NA	NA	NA	NA	The model of myocardial ischemia-reperfusion (I/R) injury and myocardial cells hypoxia/reoxygenation (H/R) injury were established and the expression of 1700020I14Rik, miR-297a or CGRP was analyzed by qRT-PCRor western blot. Moreover, myocardial cell apoptosis was assessed by TUNEL staining and the concentration of LDH in the mouse plasma sample or myocardial cell culture supernatant was measured by the LDH cytotoxicity test kit. Furthermore, the differences of myocardial cell survival rate after H/R treatment were assessed by MTT assay and the observation of CGRP expression was performed in HL-1 cells overexpressed or silenced with 1700020I14Rik or miR-297a. In addition, the regulating function of miR-297a on 1700020I14Rik and CGRP expression was analyzed by a dual-luciferase reporter assay.Results: The expressions of 1700020I14Rik and CGRP were abnormally down-regulated in a model of myocardial I/R injury and myocardial cells H/R injury, while miR-297a was up-regulated. By TUNEL staining, the apoptotic rate of myocardial cells in the model of myocardial I/R injury was significantly increased. Furthermore, the concentrations of LDH in the mouse plasma sample or myocardial cell culture supernatant were significantly increased after myocardial cell injury. By MTT assay, the survival rate of cells was decreased after myocardial cells were treated with H/R. In addition, overexpression of 1700020I14Rik or knockdown of miR-297a could up-regulate CGRP protein level, while interference with 1700020I14Rik or overexpression of miR-297a produced the opposite result. Further study confirmed that lncRNA 1700020I14Rik/miR-297a/CGRP axis suppressed myocardial cell apoptosis in myocardial I/R injury.Conclusion: Our results indicated that 1700020I14Rik was abnormally down-regulated in myocardial injury tissues. In-depth studies manifested that 1700020I14Rik/miR-297a/CGRP axis suppressed myocardial cell apoptosis in myocardial I/R injury.	32298875	RID03876	ceRNA or sponge	NA		
Pancreatic carcinoma	XIST	miR-124	NA				NA	NA	cell growth(+)	NA	NA	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Tumor suppressor and oncogenic role of long non-coding RNAs in cancer.XIST plays a role in the cell cycle through miR-140/miR-124, thereby promoting growth in pancreatic carcinoma [28].	32232211	RID03877	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Pancreatic carcinoma	XIST	miR-140	NA				NA	NA	cell growth(+)	NA	NA	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Tumor suppressor and oncogenic role of long non-coding RNAs in cancer.XIST plays a role in the cell cycle through miR-140/miR-124, thereby promoting growth in pancreatic carcinoma [28].	32232211	RID03878	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Cancer	HOTAIR	miR-141	NA				NA	NA	cancer progression(+)	NA	NA	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Tumor suppressor and oncogenic role of long non-coding RNAs in cancer.It was reported that mir-7 and mir-34a regulate the HOTAIR expression level, which interacts with mir-141 and mir-34a to reinforce cancer development [33].	32232211	RID03879	expression association	NA		
Cancer	HOTAIR	miR-34a	NA				NA	NA	cancer progression(+)	NA	NA	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Tumor suppressor and oncogenic role of long non-coding RNAs in cancer.It was reported that mir-7 and mir-34a regulate the HOTAIR expression level, which interacts with mir-141 and mir-34a to reinforce cancer development [33].	32232211	RID03880	expression association	NA		
Obesity	CLNK	PARP1	interact	RNA pull-down assay;RIP;ChIP;western blot	downregulation	RT-qPCR;sequencing;microarray	GSE126887;GSE126839	NA	immune response(-);inflammatory response(-)	interact with protein	binding/interaction	NA	NA	CSC	Evading Immune Detection;Tumor Promoting Inflammation;Evading Immune Detection;Tumor Promoting Inflammation	Disease of metabolism	Obesity	lncRNA	PCG	ENSG00000109684	GRCh38_4:10486395-10684768	ENSG00000143799	NA	116449	142	MIST	ADPRT|ARTD1|PARP|PPOL	Novel Long Noncoding RNA, Macrophage Inflammation-Suppressing Transcript ( MIST), Regulates Macrophage Activation During Obesity.Objective: Systemic low-grade inflammation associated with obesity and metabolic syndrome is a strong risk factor for the development of diabetes mellitus and associated cardiovascular complications. This inflammatory state is caused by release of proinflammatory cytokines by macrophages, especially in adipose tissue. Long noncoding RNAs regulate macrophage activation and inflammatory gene networks, but their role in macrophage dysfunction during diet-induced obesity has been largely unexplored. Approach and Results: We sequenced total RNA from peritoneal macrophages isolated from mice fed either high-fat diet or standard diet and performed de novo transcriptome assembly to identify novel differentially expressed mRNAs and long noncoding RNAs. A top candidate long noncoding RNA, macrophage inflammation-suppressing transcript (Mist), was downregulated in both peritoneal macrophages and adipose tissue macrophages from high-fat diet-fed mice. GapmeR-mediated Mist knockdown in vitro and in vivo upregulated expression of genes associated with immune response and inflammation and increased modified LDL (low-density lipoprotein) uptake in macrophages. Conversely, Mist overexpression decreased basal and LPS (lipopolysaccharide)-induced expression of inflammatory response genes and decreased modified LDL uptake. RNA-pull down coupled with mass spectrometry showed that Mist interacts with PARP1 (poly [ADP]-ribose polymerase-1). Disruption of this RNA-protein interaction increased PARP1 recruitment and chromatin PARylation at promoters of inflammatory genes, resulting in increased gene expression. Furthermore, human orthologous MIST was also downregulated by proinflammatory stimuli, and its expression in human adipose tissue macrophages inversely correlated with obesity and insulin resistance.Conclusions: Mist is a novel protective long noncoding RNA, and its loss during obesity contributes to metabolic dysfunction and proinflammatory phenotype of macrophages via epigenetic mechanisms.	32078363	RID03881	interact with protein	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Non-small cell lung cancer	GAS5	PTEN	positively-E	qPCR;western blot	upregulation	qPCR;sequencing	NA	NA	AKT signaling pathway(+);radiosensitivity(+);apoptosis process(-)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA GAS5 increases the radiosensitivity of A549 cells through interaction with the miR-21/PTEN/Akt axis.Radioresistance hinders the therapeutic outcomes of radiotherapy in non-small cell lung cancer (NSCLC). Although long non-coding RNAs (lncRNAs) have been demonstrated to participate in the regulation of multiple cell behaviors, whether they can modulate the radiosensitivity of NSCLC and the underlying molecular mechanisms have not been well investigated. In the present study, it was revealed that NSCLC NCI-H460 cells were more sensitive to ionizing radiation (IR) than A549 cells. Using the RNA-Seq method, four highly differentially expressed lncRNAs were identified, including the growth arrest-specific transcript 5 (GAS5), syntaxin binding protein 5 antisense RNA 1 (STXBP5-AS1), metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and X-inactive specific transcript (XIST), which were predicted to play roles in the acquisition of radiosensitivity. Using real-time quantitative PCR (qPCR), it was demonstrated that lncRNA GAS5 was significantly upregulated in NCI-H460 cells but not in A549 cells during IR. Mechanistically, it was demonstrated that overexpression of lncRNA GAS5 decreased the level of microRNA-21 (miR-21). Overexpression of lncRNA GAS5 or suppression of miR-21 markedly increased the IR-induced cell apoptosis of A549 cells. It was also demonstrated that overexpression of lncRNA GAS5 increased PTEN expression and suppressed Akt phosphorylation through the modulation of miR-21. Notably, it was revealed that IR enhanced the interaction between lncRNA GAS5 and the miR-21/PTEN/Akt axis. In summary, the present findings revealed that lncRNA GAS5 has a radiosensitization effect on NSCLC, indicating the potential application of lncRNA GAS5 in NSCLC radiotherapy.	32020207	RID03882	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Ovary adenocarcinoma	CYTOR	MCL1	positively-E		upregulation		NA	NA	apoptosis process(-)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000143384	NA	112597	4170	C2orf59|LINC00152|MGC4677|NCRNA00152	BCL2L3|Mcl-1	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.It has been reported that linc00152 might directly bind to miR-125b, up-regulate Mcl-1 (myeloid cell leukemia-1), and protect ovarian adenocarcinoma cells from apoptosis [13].	31896236	RID03883	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric adenocarcinoma	CYTOR	ETS1	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-193b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000134954	NA	112597	2113	C2orf59|LINC00152|MGC4677|NCRNA00152	ETS-1|EWSR2|FLJ10768	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.In addition, linc00152 may promote cell proliferation and increase cell migration in gastric adenocarcinoma cells by sponging miR-193b-3p, and thus, upregulating ETS1 [15].	31896236	RID03884	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	CYTOR	NOTCH1	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000148400	NA	112597	4851	C2orf59|LINC00152|MGC4677|NCRNA00152	TAN1	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.In another study, it was found that sponging of miR-139-5p by linc00152 up-regulated Notch1, which promoted cell proliferation, cell invasion, and migration in colorectal carcinoma cells [16].	31896236	RID03885	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	CYTOR	CDK14	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-1182)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000058091	NA	112597	5218	C2orf59|LINC00152|MGC4677|NCRNA00152	PFTAIRE1|PFTK1	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.In one study conducted using osteosarcoma cells, it was suggested that linc00152 transcriptionally activated by TCF3 (a transcription factor) might bind to miR-1182, up-regulate CDK14, and promote cell proliferation and migration [20].	31896236	RID03886	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	CYTOR	FYN	positively-E		upregulation		NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000010810	NA	112597	2534	C2orf59|LINC00152|MGC4677|NCRNA00152	MGC45350|SLK|SYN	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.In another study, results indicated that linc00152-dependent miR-153-3p down-regulation up-regulated Fyn (a proto-oncogene) and led to the induction of cell proliferation and the suppression of apoptosis in esophageal squamous cell carcinoma cells [24].	31896236	RID03887	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	CYTOR	CTNNB1	positively-E		upregulation		NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Bladder carcinoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000168036	NA	112597	1499	C2orf59|LINC00152|NCRNA00152	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.In addition, linc00152 caused the proliferation of bladder carcinoma cells by upregulating beta-catenin expression and directly activating the Wnt/beta-catenin pathway [28].	31896236	RID03888	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	CYTOR	DNMT1	positively-E		upregulation		NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000130816	NA	112597	1786	C2orf59|LINC00152|MGC4677|NCRNA00152	CXXC9|DNMT|MCMT	Long non-coding RNA linc00152 acting as a promising oncogene in cancer progression.It has also been reported that interaction between linc00152 and DNA methyltransferase (DNMT) may result in DNMT activation, the inhibitions of BRCA1 (breast cancer type 1 susceptibility protein) and PTEN, and increased cell proliferation and invasiveness in triple-negative breast adenocarcinoma and breast ductal carcinoma [33].	31896236	RID03889	interact with protein	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	H19	SNORA7A	negatively-E	AIG Assay	downregulation	qRT-PCR	PRJNA673185	NA	tumorigenesis(-)	NA	association	RNA-RNA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	snoRNA	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000207496	NA	283120	619563	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ACA7	LncRNA H19 Suppresses Osteosarcomagenesis by Regulating snoRNAs and DNA Repair Protein Complexes.Osteosarcoma is one of the most frequent common primary malignant tumors in childhood and adolescence. Long non-coding RNAs (lncRNAs) have been reported to regulate the initiation and progression of tumors. However, the exact molecular mechanisms involving lncRNA in osteosarcomagenesis remain largely unknown. Li-Fraumeni syndrome (LFS) is a familial cancer syndrome caused by germline p53 mutation. We investigated the tumor suppressor function of lncRNA H19 in LFS-associated osteosarcoma. Analyzing H19-induced transcriptome alterations in LFS induced pluripotent stem cell (iPSC)-derived osteoblasts, we unexpectedly discovered a large group of snoRNAs whose expression was significantly affected by H19. We identified SNORA7A among the H19-suppressed snoRNAs. SNORA7A restoration impairs H19-mediated osteogenesis and tumor suppression, indicating an oncogenic role of SNORA7A. TCGA analysis indicated that SNORA7A expression is associated with activation of oncogenic signaling and poor survival in cancer patients. Using an optimized streptavidin-binding RNA aptamer designed from H19 lncRNA, we revealed that H19-tethered protein complexes include proteins critical for DNA damage response and repair, confirming H19's tumor suppressor role. In summary, our findings demonstrate a critical role of H19-modulated SNORA7A expression in LFS-associated osteosarcomas.To validate our transcriptome results, we ectopically expressed H19 in LFS iPSC-derived osteoblasts and found that H19 significantly inhibits SNORA7A expression.To investigate whether the inhibition of SNORA7A plays a role in H19-mediated tumor suppression, we performed an in vitro AIG assay and found retarded clonal growth of H19-transduced LFS osteoblasts upon SNORA7A ectopic expression (Figure 2C). These results suggest that SNORA7A is negatively regulated by H19, and that SNORA7A functions as an onco-snoRNA by antagonizing H19  tumor suppressor function.	33519915	RID03890	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	HOTAIR	CCL2	positively-E				NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000108691	NA	100124700	6347	HOXC-AS4|HOXC11-AS1|NCRNA00072	GDCF-2|HC11|MCAF|MCP-1|MCP1|MGC9434|SCYA2|SMC-CF	MicroRNAs and lncRNAs-A New Layer of Myeloid-Derived Suppressor Cells RegulationIn the case of HCC cell lines, a recent study confirmed that HOTAIR-overexpressing cells release a high level of CCL2 and support macrophage/MDSC proliferation.	33133086	RID03891	expression association	NA		UP(PAAD);DATA(GSE40174)
Cancer	MIR124-1HG	DDIT3	positively-E		upregulation		NA	NA	cell differentiation(+);cell viability(+)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000284859	GRCh38_CHR_HG76_PATCH:10046775-10053583	ENSG00000175197	NA	157627	1649	LINC00599|neuroLNC|Rncr3	CHOP|CHOP10|GADD153	MicroRNAs and lncRNAs-A New Layer of Myeloid-Derived Suppressor Cells Regulation.Moreover, RNCR3 stimulates the differentiation and activity of MDSC through sponging miR-185-5p so as to produce its target gene named Chop (129).It is demonstrated that miR-185-5p affected the MDSCs expansion and reversed the impact of RNCR3 on MDSC differentiation and function by targeting Chop.Therefore, this study proposed a RNCR3/miR-185-5p/Chop autologously strengthening complex to support MDSC differentiation and suppressive activity in response to extracellular inflammatory and tumor-related signals (129).	33133086	RID03892	ceRNA or sponge	NA		DOWN(LIHC);DATA(GSE117623)
Cancer	lnc-C/EBPbeta	IL4I1	negatively-E				NA	NA	cell differentiation(-)	interact with protein	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000104951	NA	NA	259307	NA	FIG1|LAAO|LAO|hIL4I1	MicroRNAs and lncRNAs-A New Layer of Myeloid-Derived Suppressor Cells Regulation.They confirmed that lnc-C/EBPbeta controls numerous transcripts in MDSCs to regulate MDSC differentiation and suppressive activity in inflammatory and tumor milieus.lnc-C/EBPbeta can downregulate interleukin 4-induced gene-1 (IL4i1) to affect the MDSC differentiation by attaching with C/EBPbeta LIP and WD repeat-containing protein 5 (WDR5) (133).	33133086	RID03893	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG17	RFX1	positively-E	RIP;RNA pull-down assay;dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-3180-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000132005	NA	388796	5989	NA	EF-C	Hepatocellular carcinoma human samples and cell lines were subjected to qRT-PCRfor expression assessment. CCK-8 assay, Transwell migration and invasion assay, were applied for cell function detection. Animal experiment was used to measure the function of SNHG17 on cell growth in vivo. western blot was conducted to evaluate the level of EMT in cells. RIP, RNA pull-down and luciferase reporter assays were performed to assess the correlation between SNHG17, miR-3180-3p and RFX1.Results: Our study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. SNHG17 promoted HCC cell growth and metastasis in vivo. Furthermore, we investigated the downstream factor of SNHG17, SNHG17 acted as a molecular sponge for miR-3180-3p, and SNHG17 regulated RFX1 expression via miR-3180-3p. SNHG17 promotes tumor-like behavior in HCC cells via miR-3180-3p/RFX1.Conclusion: We determined RFX1 as the target of miR-3810-3p; SNHG17 enhanced the progression of HCC via the miR-3180-3p/RFX1 axis. Taken together, our findings may provide insight into the  mechanism involved in the progression of HCC and develop SNHG17 as a novel therapeutic target against HCC. SNHG17 promoted HCC cell proliferation (Figure 7A, migration (Figure 7B), invasion (Figure 7C), and EMT (Figures 7D,E) by sponging miR-3180-3p and upregulating RFX1.	33519911	RID03894	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Glioblastoma	MVIH	MIR302A	negatively-F	bioinformatics; Ago2 immunoprecipitation assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	NA	NA	ENSG00000207927	NA	NA	407028	NA	MIRN302|MIRN302A|hsa-mir-302|mir-302a	Glioblastoma (GB) is the most frequent and malignant type of brain tumor, for which no effective therapy exists. The high proliferative and invasive nature of GB, as well as its acquired resistance to chemotherapy, makes this type of cancer extremely lethal shortly after diagnosis. Long non-protein coding RNAs (lncRNA) are a class of regulatory RNAs whose levels can be dysregulated in the context of diseases, unbalancing several physiological processes. The lncRNA associated with microvascular invasion in hepatocellular carcinoma (lncRNA-MVIH), overexpressed in several cancers, was described to co-precipitate with phosphoglycerate kinase 1 (PGK1), preventing secretion of this enzyme to the extracellular environment and promoting cell migration and invasion. We hypothesized that, by silencing the expression of lncRNA-MVIH, the secretion of PGK1 would increase, reducing GB cell migration and invasion capabilities. We observed that lncRNA-MVIH silencing in human GB cells significantly decreased glycolysis, cell growth, migration, and invasion and sensitized GB cells to cediranib. However, no increase in extracellular PGK1 was observed as a consequence of lncRNA-MVIH silencing, and therefore, we investigated the possibility of a mechanism of miRNA sponge of lncRNA-MVIH being in place. We found that the levels of miR-302a loaded onto RISC increased in GB cells after lncRNA-MVIH silencing, with the consequent downregulation of several miR-302a molecular targets. Our findings suggest a new mechanism of action of lncRNA-MVIH as a sponge of miR-302a. We suggest that lncRNA-MVIH knockdown may be a promising strategy to address GB invasiveness and chemoresistance, holding potential towards its future application in a clinical context.LncRNA-MVIH and PGK1 mRNA levels in U87 and DBTRG cells (A) and in 34 GB tumor samples (B) were compared to those of NHA, by qRT-PCR	33438023	RID03895	ceRNA or sponge	chemoresistance		
Glioblastoma	MVIH	PGK1	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000102144	NA	NA	5230	NA	NA	Downregulation of long non-protein coding RNA MVIH impairs glioblastoma cell proliferation and invasion through an miR-302a-dependent mechanism.Glioblastoma (GB) is the most frequent and malignant type of brain tumor, for which no effective therapy exists. The high proliferative and invasive nature of GB, as well as its acquired resistance to chemotherapy, makes this type of cancer extremely lethal shortly after diagnosis. Long non-protein coding RNAs (lncRNA) are a class of regulatory RNAs whose levels can be dysregulated in the context of diseases, unbalancing several physiological processes. The lncRNA associated with microvascular invasion in hepatocellular carcinoma (lncRNA-MVIH), overexpressed in several cancers, was described to co-precipitate with phosphoglycerate kinase 1 (PGK1), preventing secretion of this enzyme to the extracellular environment and promoting cell migration and invasion. We hypothesized that, by silencing the expression of lncRNA-MVIH, the secretion of PGK1 would increase, reducing GB cell migration and invasion capabilities. We observed that lncRNA-MVIH silencing in human GB cells significantly decreased glycolysis, cell growth, migration, and invasion and sensitized GB cells to cediranib. However, no increase in extracellular PGK1 was observed as a consequence of lncRNA-MVIH silencing, and therefore, we investigated the possibility of a mechanism of miRNA sponge of lncRNA-MVIH being in place. We found that the levels of miR-302a loaded onto RISC increased in GB cells after lncRNA-MVIH silencing, with the consequent downregulation of several miR-302a molecular targets. Our findings suggest a new mechanism of action of lncRNA-MVIH as a sponge of miR-302a. We suggest that lncRNA-MVIH knockdown may be a promising strategy to address GB invasiveness and chemoresistance, holding potential towards its future application in a clinical context.	33438023	RID03896	expression association	chemoresistance		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Ovary adenocarcinoma	E7	lnc-FANCI-2	positively-E	luciferase reporter assay	upregulation	RT-qPCR;sequencing	NA	NA	tumorigenesis(+)	NA	association	protein-RNA	NA	CSC	NA	Cancer	Ovarian cancer	TF	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Long noncoding RNAs (lncRNAs) play diverse roles in biological processes, but their expression profiles and functions in cervical carcinogenesis remain unknown. By RNA-sequencing (RNA-seq) analyses of 18 clinical specimens and selective validation by RT-qPCR analyses of 72 clinical samples, we provide evidence that, relative to normal cervical tissues, 194 lncRNAs are differentially regulated in high-risk (HR)-HPV infection along with cervical lesion progression. One such lncRNA, lnc-FANCI-2, is extensively characterized because it is expressed from a genomic locus adjacent to the FANCI gene encoding an important DNA repair factor. Both genes are up-regulated in HPV lesions and in in vitro model systems of HR-HPV18 infection. We observe a moderate reciprocal regulation of lnc-FANCI-2 and FANCI in cervical cancer CaSki cells. In these cells, lnc-FANCI-2 is transcribed from two alternative promoters, alternatively spliced, and polyadenylated at one of two alternative poly(A) sites. About 10 copies of lnc-FANCI-2 per cell are detected preferentially in the cytoplasm. Mechanistically, HR-HPVs, but not low-risk (LR)-HPV oncogenes induce lnc-FANCI-2 in primary and immortalized human keratinocytes. The induction is mediated primarily by E7, and to a lesser extent by E6, mostly independent of p53/E6AP and pRb/E2F. We show that YY1 interacts with an E7 CR3 core motif and transactivates the promoter of lnc-FANCI-2 by binding to two critical YY1-binding motifs. Moreover, HPV18 increases YY1 expression by reducing miR-29a, which targets the 3' untranslated region of YY1 mRNA. These data have provided insights into the mechanisms of how HR-HPV infections contribute to cervical carcinogenesis.	33436409	RID03897	expression association	NA		
Ovary adenocarcinoma	YY1	lnc-FANCI-2	positively-E	luciferase reporter assay	upregulation	RT-qPCR;sequencing	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000100811	NA	NA	NA	7528	NA	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Long noncoding RNAs (lncRNAs) play diverse roles in biological processes, but their expression profiles and functions in cervical carcinogenesis remain unknown. By RNA-sequencing (RNA-seq) analyses of 18 clinical specimens and selective validation by RT-qPCR analyses of 72 clinical samples, we provide evidence that, relative to normal cervical tissues, 194 lncRNAs are differentially regulated in high-risk (HR)-HPV infection along with cervical lesion progression. One such lncRNA, lnc-FANCI-2, is extensively characterized because it is expressed from a genomic locus adjacent to the FANCI gene encoding an important DNA repair factor. Both genes are up-regulated in HPV lesions and in in vitro model systems of HR-HPV18 infection. We observe a moderate reciprocal regulation of lnc-FANCI-2 and FANCI in cervical cancer CaSki cells. In these cells, lnc-FANCI-2 is transcribed from two alternative promoters, alternatively spliced, and polyadenylated at one of two alternative poly(A) sites. About 10 copies of lnc-FANCI-2 per cell are detected preferentially in the cytoplasm. Mechanistically, HR-HPVs, but not low-risk (LR)-HPV oncogenes induce lnc-FANCI-2 in primary and immortalized human keratinocytes. The induction is mediated primarily by E7, and to a lesser extent by E6, mostly independent of p53/E6AP and pRb/E2F. We show that YY1 interacts with an E7 CR3 core motif and transactivates the promoter of lnc-FANCI-2 by binding to two critical YY1-binding motifs. Moreover, HPV18 increases YY1 expression by reducing miR-29a, which targets the 3' untranslated region of YY1 mRNA. These data have provided insights into the mechanisms of how HR-HPV infections contribute to cervical carcinogenesis.	33436409	RID03898	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	
Cervical cancer	TDRG1	SEMA4C	positively-E	dual-luciferase reporter analysis;bioinformatics	upregulation	RT-qPCR	NA	NA	cell invasion(+)	ceRNA(miR-214-5p)	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000168758	NA	732253	54910	LINC00532|lincRNA-NR_024015	Semacl1|Semaf|SEMAI	Long non-coding RNA TDRG1 promotes hypoxia-induced glycolysis by targeting the miR-214-5p/SEMA4C axis in cervical cancer cells.Long non-coding RNA (lncRNA) has been demonstrated as vital regulator in human cancer. However, the precise role of lnc-TDRG1 in cervical cancer (CC) remains unclear, so this study was aimed to clarify the role and underlying molecular mechanism of lnc-TDRG1 in CC. The real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to assess the expression levels of lnc-TDRG1, miR-214-5p and Semaphorin 4C (SEMA4C). Under hypoxia condition, the biological behaviors of CC cell, including invasion and glycolysis were determined by transwell assay and Glucose Assay Kit and Lactate Assay Kit, respectively. The western blot assay was employed to test the expression level of SEMA4C and hexokinase 2 (HK2) expression. The interaction relationship between miR-214-5p and lnc-TDRG1 or SEMA4C was analyzed bioinformatics database and confirmed by dual-luciferase reporter assay, respectively. A xenograft experiment in nude mice was established to clarify the functional role of lnc-TDRG1 in vivo. We found Lnc-TDRG1 was highly expressed in CC tissues and cells and it was upregulated in response to hypoxia. Loss-of-functional experiment suggested that knockdown of lnc-TDRG1 impede invasion, hypoxia-induced glycolysis in vitro and tumor growth in vivo, which was abolished by knockdown of miR-214-5p or overexpression of SEMA4C. Moreover, we confirmed that miR-214-5p specifically bound to SEMA4C and negatively correlated with SEMA4C expression. Collectively, lnc-TDRG1 regulated SEMA4C expression by sponging miR-214-5p in CC. Collectively, mechanistically, lnc-TDRG1 could act as a sponge of miR-214-5p to regulate the expression of SEMA4C, and further regulate invasion and hypoxia-glycolysis in CC cells.	33394293	RID03899	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE51827,GSE75367,GSE86978)
Modulates chromatin	MYOD1	LncMyoD	interact	luciferase reporter assay;RIP		qRT-PCR;sequencing	NA	NA	cell stemness(+)	interact with protein	binding/interaction	NA	NA	CSC	NA	Other	Modulates chromatin	TF	lncRNA	ENSG00000129152	NA	NA	NA	4654	NA	MYF3|MYOD|MYODRIF|PUM|bHLHc1	NA	A long noncoding RNA, LncMyoD, modulates chromatin accessibility to regulate muscle stem cell myogenic lineage progression.Epigenetics regulation plays a critical role in determining cell identity by controlling the accessibility of lineage-specific regulatory regions. In muscle stem cells, epigenetic mechanisms of how chromatin accessibility is modulated during cell fate determination are not fully understood. Here, we identified a long noncoding RNA, LncMyoD, that functions as a chromatin modulator for myogenic lineage determination and progression. The depletion of LncMyoD in muscle stem cells led to the down-regulation of myogenic genes and defects in myogenic differentiation. LncMyoD exclusively binds with MyoD and not with other myogenic regulatory factors and promotes transactivation of target genes. The mechanistic study revealed that loss of LncMyoD prevents the establishment of a permissive chromatin environment at myogenic E-box-containing regions, therefore restricting the binding of MyoD. Furthermore, the depletion of LncMyoD strongly impairs the reprogramming of fibroblasts into the myogenic lineage. Taken together, our study shows that LncMyoD associates with MyoD and promotes myogenic gene expression through modulating MyoD accessibility to chromatin, thereby regulating myogenic lineage determination and progression.	33293420	RID03900	interact with protein	NA		
Breast cancer	AGAP2-AS1	CPT1	positively-E	mass spectrometry;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell stemness(+);chemoresistance(+)	ceRNA(miR-15a-5p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000111666	NA	100130776	NA	LOC100130776|PUNISHER	NA	MSC-induced lncRNA AGAP2-AS1 promotes stemness and trastuzumab resistance through regulating CPT1 expression and fatty acid oxidation in breast cancer.Trastuzumab resistance has been becoming a major obstacle for treatment of HER-2-positive breast cancer patients. Increasing evidence suggests that mesenchymal stem cells (MSCs) play critical roles during the formation of drug resistance, however, the underlying mechanism is not well known. In this study, mass spectrometry, RNA pull-down and RNA immunoprecipitation assays were performed to verify the direct interactions among AGAP2-AS1 and other associated targets, such as human antigen R (HuR), miR-15a-5p, and carnitine palmitoyl transferase 1 (CPT1). In vitro and in vivo experimental assays were done to clarify the functional role of AGAP2-AS1 in trastuzumab resistance, stemness, and fatty acid oxidation (FAO). The results showed that MSC co-culture induced trastuzumab resistance. AGAP2-AS1 was upregulated in MSC-cultured cells, and knockdown of AGAP2-AS1 reversed the MSC-mediated trastuzumab resistance. Furthermore, MSC culture-induced AGAP2-AS1 regulates stemness and trastuzumab resistance via activating FAO. Mechanistically, AGAP2-AS1 is associated with HuR, and the AGAP2-AS1-HuR complex could directly bind to the CPT1, increasing its expression via improving RNA stability. In addition, AGAP2-AS1 could serve as ceRNA via sponging miR-15a-5p and releasing CPT1 mRNA. Clinically, increased expression of serum AGAP2-AS1 predicts poor response to trastuzumab treatment in breast cancer patients. In conclusion, MSC culture-induced AGAP2-AS1 caused stemness and trastuzumab resistance via promoting CPT1 expression and inducing FAO. Our results provide new insight of the role of MSCs in trastuzumab resistance and AGAP2-AS1 could be promising predictive biomarker and therapeutic target for HER-2+ breast cancer patients.	33273726	RID03901	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Breast cancer	AGAP2-AS1	ELAVL1	interact	RIP	upregulation	qRT-PCR	NA	NA	cell stemness(+);chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000066044	NA	100130776	1994	LOC100130776|PUNISHER	Hua|HUR|MelG	MSC-induced lncRNA AGAP2-AS1 promotes stemness and trastuzumab resistance through regulating CPT1 expression and fatty acid oxidation in breast cancer.Trastuzumab resistance has been becoming a major obstacle for treatment of HER-2-positive breast cancer patients. Increasing evidence suggests that mesenchymal stem cells (MSCs) play critical roles during the formation of drug resistance, however, the underlying mechanism is not well known. In this study, mass spectrometry, RNA pull-down and RNA immunoprecipitation assays were performed to verify the direct interactions among AGAP2-AS1 and other associated targets, such as human antigen R (HuR), miR-15a-5p, and carnitine palmitoyl transferase 1 (CPT1). In vitro and in vivo experimental assays were done to clarify the functional role of AGAP2-AS1 in trastuzumab resistance, stemness, and fatty acid oxidation (FAO). The results showed that MSC co-culture induced trastuzumab resistance. AGAP2-AS1 was upregulated in MSC-cultured cells, and knockdown of AGAP2-AS1 reversed the MSC-mediated trastuzumab resistance. Furthermore, MSC culture-induced AGAP2-AS1 regulates stemness and trastuzumab resistance via activating FAO. Mechanistically, AGAP2-AS1 is associated with HuR, and the AGAP2-AS1-HuR complex could directly bind to the CPT1, increasing its expression via improving RNA stability. In addition, AGAP2-AS1 could serve as ceRNA via sponging miR-15a-5p and releasing CPT1 mRNA. Clinically, increased expression of serum AGAP2-AS1 predicts poor response to trastuzumab treatment in breast cancer patients. In conclusion, MSC culture-induced AGAP2-AS1 caused stemness and trastuzumab resistance via promoting CPT1 expression and inducing FAO. Our results provide new insight of the role of MSCs in trastuzumab resistance and AGAP2-AS1 could be promising predictive biomarker and therapeutic target for HER-2+ breast cancer patients.	33273726	RID03902	interact with protein	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	MYLK-AS1	E2F7	positively-E	FISH;RIP;dual-luciferase reporter analysis;bioinformatics	upregulation	qRT-PCR	TCGA	NA	VEGFR-2 signaling pathway(+);cancer progression(+);angiogenesis(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000239523	GRCh38_3:123585300-123644568	ENSG00000165891	NA	100506826	144455	NA	NA	Bioinformatic analysis was performed to determine the potential relationship among MYLK-AS1, miRNAs and mRNAs. A total of 156 samples of normal liver and paired HCC tissues from HCC patients were used to evaluate MYLK-AS1 expression by qRT-PCR Human HCC cell lines were used to evaluate the colony formation, cell proliferation, migration, invasion, cell cycle and apoptosis after transfection of lentiviral short-hairpin RNAs (shRNAs) targeting MYLK-AS1 or MYLK-AS1 vectors. The competitive endogenous RNA (ceRNA) mechanism was clarified using fluorescence in situ hybridization (FISH), western blot, qPCR, RNA binding protein immunoprecipitation (RIP), and dual luciferase reporter analysis.Results: MYLK-AS1 up-regulation was detected in the HCC tumor tissues and cell lines associated with the enhancement of the angiogenesis and tumor progression. The down-regulation of MYLK-AS1 reversed the effects on angiogenesis, proliferation, invasion and metastasis in the HCC cells and in vivo. MYLK-AS1 acted as ceRNA, capable of regulating the angiogenesis in HCC, while the microRNA miR-424-5p was the direct target of MYLK-AS1. Promoting the angiogenesis and the tumor proliferation, the complex MYLK-AS1/miR-424-5p activated the VEGFR-2 signaling through E2F7, whereas the specific targeting of E2F transcription factor 7 (E2F7) by miR-424-5p, was indicated by the mechanism studies.Conclusions: MYLK-AS1 and E2F7 are closely related to some malignant clinicopathological features and prognosis of HCC, thus the MYLK-AS1/ miR-424-5p/E2F7 signaling pathway might represent a promising treatment strategy to combat HCC.The significant upregulation of MYLK-AS1 in HCC was confirmed in this study, promoting cancer cell proliferation and angiogenesis, both and in vivo and in vitro.	33168027	RID03903	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE111842)	UP(LIHC);DATA(GSE117623)
Parkinson's disease	OIP5-AS1	PLK2	NA	luciferase reporter assay;western blot;starbase			NA	NA	cell autophagy(+)	ceRNA(miR-126)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000145632	NA	729082	10769	cyrano|linc-OIP5	SNK	LncRNA OIP5-AS1 reduces alpha-synuclein aggregation and toxicity by targeting miR-126 to activate PLK2 in human neuroblastoma SH-SY5Y cells.It has been reported that many long noncoding RNAs (lncRNA) are abnormally expressed in Parkinson's disease (PD). However, the knowledge about the role of dysregulated lncRNA in the pathological process of PD and the potential molecular regulation mechanism is still limited. Our immunofluorescence data show that miR-126 enhances the aggregation and toxicity of synuclein, while lncRNA OIP5-AS1 reduces the aggregation and toxicity of MPP + induced alpha-synuclein by targeting miR-126. Luciferase experiments have found that miR-126 regulates alpha-synuclein by targeting PLK2. western blot and IP experimental analysis showed that this process is achieved by regulating PLK2/alpha-synuclein autophagy. In conclusion, our data indicate that OIP5-AS1 promotes the autophagy of PLK2-alpha-synuclein by targeting the miR-126 axis with pathogenic factors, thus reducing the aggregation toxicity of alpha-synuclein, which It will help better to understand the mechanism of dopaminergic neuron loss in PD and provide novel treatment options. western blotshowed that PLK2 was  negatively regulated by miR-126 (Fig. 2c).	33161106	RID03904	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Oral squamous cell carcinoma	PCGEM1	miR-148a	positively-E	starBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	TGF-beta2/SMAD2 signaling pathway(+);cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	A total of 60 OSCC cases were collected. Cancer tissues and normal tissues more than 2 cm away from cancer tissues were also collected. Real-time quantitative polymerase chain reaction (qRT-PCR was used to detect the expression of miR-148a and lncRNA PCGEM1 in OSCC, adjacent normal tissues, oral mucosa epithelial cells, KB, BcaCD885, SCC-4, CAL27, and SCC-15. The relationship between the expression of lncRNA PCGEM1 and miR-148a and the clinicopathological information of patients was analyzed. The lncRNA PCGEM1-silenced cell line KB-siPCGEM1 and negative control (KB-NC) group were constructed, and KB was used as the blank control group. The effects of lncRNA PCGEM1 on the proliferation, invasion, and migration of KB cells were determined via MTT, Transwell, and scratch assays. The bioinformatics website starBase was used to predict the complementary binding microRNA (miRNA) of lncRNA PCGEM1. Furthermore, the genes that the miRNA could target and bind were predicted in accordance with the website www.microRNA.org. western blotwas used to detect the expression of TGF beta2/Smad2 signaling pathway proteins.Results: qRT-PCRresults showed that the expression level of lncRNA PCGEM1 and miR-148a in OSCC tissues was higher than that in normal tissues (P<0.05). The expression of lncRNA PCGEM1 and miR-148a in the cancer tissues of patients with different TNM grades, lymph node metastasis, and tissue differentiation was statistically significant (P<0.05). Compared with those in the blank control group and the KB-NC group, OD492 nm value was significantly decreased and cell mobility was significantly reduced in the KB-siPCGEM1 group (P<0.05). Bioinformatics predictions showed that lncRNA PCGEM1 could bind to miR-148a in a complementary manner and that miR-148a had a targeted binding site with TGF beta2. qRT-PCRand western blotresults showed that the expression levels of miR-148a, TGF beta2, and p-Smad2 in the KB-siPCGEM1 group were significantly lower than those in the blank control and KB-NC groups (P<0.05), and no statistically significant difference between the blank control group and the KB-NC group was observed (P>0.05).Conclusions: LncRNA PCGEM1 is highly expressed in OSCC. The high expression of lncRNA PCGEM1 may enhance the TGF beta2/Smad2 signaling pathway by upregulating miR-148a, thus promoting the development of OSCC.	33085241	RID03905	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE60407)	
Esophagus squamous cell carcinoma	LOC440173	HDAC9	positively-E	dual-luciferase reporter analysis;RIP;bioinformatics	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);tumor growth(+)	ceRNA(miR-30d-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000048052	NA	NA	9734	NA	HD7|HDAC|HDAC7B|KIAA0744|MITR	A novel long noncoding RNA, LOC440173, promotes the progression of esophageal squamous cell carcinoma by modulating the miR-30d-5p/HDAC9 axis and the epithelial-mesenchymal transition.Countless evidence suggests that long noncoding RNAs (lncRNAs) are involved in human malignant cancers, including esophageal squamous cell carcinoma (ESCC), although their exact function remains unclear. In the present study, we aimed to investigate the roles and molecular mechanisms of the lncRNA LOC440173 in ESCC progression. microarray analysis and quantitative real-time polymerase chain reaction were conducted to measure the expression levels of LOC440173 and miR-30d-5p. The biological function of this lncRNA was investigated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, clone formation, and transwell assays, as well as flow cytometry and western blot The function of LOC440173 was validated in vivo using tumor xenografts. The regulatory network of LOC440173/miR-30d-5p/HDAC9 was established using bioinformatic analysis and verified with dual-luciferase reporter assays, RNA immunoprecipitation assay, and rescue experiments. The expression level of LOC440173 was significantly increased in ESCC tissues and esophageal carcinoma cells. High LOC440173 expression was correlated with histological grade, tumor invasion depth, lymph node metastasis, and TNM stage. Overexpression of LOC440173 promoted esophageal cancer cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT) process in vitro, and facilitated tumor growth in vivo. MicroRNA-30d-5p (miR-30d-5p) was downregulated in ESCC tissues and acted as a direct binding target of LOC440173 during the regulation of HDAC9 expression in esophageal carcinoma cells. In conclusion, LOC440173 exerts a promotive role in ESCC tumorigenesis by targeting the miR-30d-5p/HDAC9 axis and regulating the EMT process. LOC440173 might be a new therapeutic target for the treatment of ESCC.	33079409	RID03906	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE51827,GSE86978)
Colorectal cancer	SNHG11	HIF1A	positively-F	RNA pull-down assay;ChIP-seq;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000174365	GRCh38_20:38446343-38450940	ENSG00000100644	NA	128439	3091	C20orf198|LINC00101|NCRNA00101	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1alpha.Epigenetic alteration is one of the hallmarks of colorectal cancer (CRC). Many driver genes are regulated by DNA methylation in CRC. However, the role of DNA methylation regulating lncRNAs remain elusive. Here, we identify that SNHG11 (small nucleolar RNA host gene 11) is upregulated by promotor hypomethylation in CRC and is associated with poor prognosis in CRC patients. SNHG11 can promote CRC cell migration and metastasis under hypoxia. Interestingly, the DNA-binding motif of SNHG11 is similar to that of HIF-1alpha. In addition, SNHG11-associated genes are enriched with members of the HIF-1 signaling pathway in CRC. Mechanistically, SNHG11 binds to the pVHLrecognition sites on HIF-1alpha, thus blocking the interaction of pVHL with HIF-1alpha and preventing its ubiquitination and degradation. Moreover, SNHG11 upregulates the expression of HIF-1alpha target genes, i.e., AK4, ENO1, HK2, and Twist1. Notably, SNHG11 can bind to the HRE sites in the promoter of these genes and increase their transcription. In summary, these results identify a SNHG11/ HIF-1alpha axis that plays a pivotal role in tumor invasion and metastasis.The results showed that SNHG11 knockdown reduced HIF-1alpha protein levels, whereas MG132 treatment diminished this reduction (Fig. 4C and Supplementary Fig. 7B, C). In contrast, SNHG11 overexpression caused an increase in HIF-1alpha protein levels (Fig. 4D). SNHG11 overexpression under hypoxia did not change pVHL protein levels or HIF-1alpha mRNA levels.Mechanistically, SNHG11 binds to HIF-1alpha and regulates HIF-1alpha stability.	33060856	RID03907	interact with protein	metastasis,prognosis	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Bone disease	TUG1	CNR2	positively-E	dual-luciferase reporter analysis;RIP;LncBase Predicted v.2;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell differentiation(+)	ceRNA(miR-545-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000188822	NA	55000	1269	FLJ20618|LINC00080|NCRNA00080	CB2	Osteoblast differentiation is an effective way to promote bone formation. Long non-coding RNA taurine upregulated 1 (TUG1) has been identified as a crucial modulator of multiple biological processes. This study was designed to investigate the function of TUG1 in the proliferation and differentiation of osteoblast precursor cells hFOB1.19. In this study, we found that TUG1 promoted hFOB1.19 cell proliferation, while TUG1 knockdown hindered cell proliferation. TUG1 and cannabinoid receptor 2 (CNR2) were upregulated, while miR-545-3p was down-regulated in hFOB1.19 cells undergoing osteoblastic differentiation. TUG1 induced osteoblast differentiation by increasing alkaline phosphatase (ALP) activity and the expression of osteoblastic differentiation markers. TUG1 was a sponge of miR-545-3p and regulated osteoblastic differentiation by modulating miR-545-3p. Moreover, miR-545-3p directly targeted CNR2 and restored the effect of CNR2 on osteoblastic differentiation. In conclusion, TUG1 accelerated the proliferation and differentiation of osteoblasts by sponging miR-545-3p and increasing CNR2 expression, which might provide a new biomarker for bone diseases.LncBase Predicted v.2 online database  predicted that TUG1 contained the complementary binding sites of miR-545-3p. dual-luciferase reporter assay disclosed that the luciferase activity of TUG1-wt reporter was significantly decreased after transfection with miR-545- 3p mimic, but the luciferase activity of TUG1-mut reporter was not affected when the binding sites were mutated. Furthermore, RIP assay was performed to verify whether miR-545-3p was a target of TUG1.TargetScan online database predicted that miR-545-3p and CNR2 30 UTR had putative binding sites.	33053117	RID03908	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Polycystic ovary syndrome	H19	CCN2	positively-E	luciferase reporter assay;bioinformatics	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-19b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000118523	NA	283120	1490	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CTGF|IGFBP8	lncRNA H19 acts as a ceRNA to regulate the expression of CTGF by targeting miR-19b in polycystic ovary syndrome.The etiology of polycystic ovary syndrome (PCOS) is complex and the pathogenesis is not fully understood. Some studies have shown that dysregulation of ovarian granulosa cells may be related to abnormal follicles and excessive androgen in women with PCOS. Our team has also confirmed the high expression status of H19 in PCOS patients in the early stage. However, the relationship between H19 and miR-19b in the development of PCOS is still unknown. Therefore, we used bioinformatics to predict the binding sites of human H19 and miR-19b, and of miR-19b and CTGF genes. After the silencing and overexpression of H19, real-time polymerase chain reaction (PCR) was used to detect the expressions of H19, miR-19b, and CTGF. western blot was used to detect CTGF protein. Proliferation of KGN cells after H19 silencing was detected by CCK8. Flow cytometry was used to detect the apoptosis of KGN cells after H19 silencing. After the overexpression of H19, it was found that the expression of miR-19b gene decreased and the expression of CTGF increased, whereas silencing of H19 did the opposite. In addition, H19 could promote cell proliferation and decrease cell apoptosis. Finally, luciferase reporter assays showed that the 3'-end sequences of lncRNA H19 and CTGF contained the binding site of miR-19b. In conclusion, our study indicated that lncRNA H19 acted as a ceRNA to bind to miR-19b via a "sponge" to regulate the effect of CTGF on KGN cells, which may play a vital role in PCOS.	33053114	RID03909	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Oral squamous cell carcinoma	ELDR	ILF3	interact	RNA pull-down assay;RIP;western blot;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);EGFR signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000280890	GRCh38_7:55235965-55255635	ENSG00000129351	NA	102725541	3609	Fabl|LINC01156	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	Here, we show that ELDR is highly expressed in OSCC patient samples and in cell lines. Overexpression of ELDR in normal non-tumorigenic oral keratinocytes induces cell proliferation, colony formation, and PCNA expression.We also show that ELDR depletion reduces OSCC cell proliferation and PCNA expression. Proteomics data identifies the RNA binding protein ILF3 as an interacting partner of ELDR. We further show that the ELDR-ILF3 axis regulates Cyclin E1 expression and phosphorylation of the retinoblastoma (RB) protein.Intratumoral injection of ELDR-specific siRNA reduces OSCC and PDX tumor growth in mice. These findings provide molecular insight into the role of ELDR in oral cancer and demonstrate that targeting ELDR has promising therapeutic potential.We also did not detect ELDR in the RIP assay performed with unrelated antibody for HA-tagged methyltransferase like 3 (HA-METTL3; Fig EV3), further confirming the specific interaction between ELDR and ILF3. Thus, our data strongly demonstrate a direct interaction between ELDR and ILF3.We then examined the interaction by RNA pull-down assay followed by western blotand observed the presence of ILF3 in RNA-protein complex in both Cal27 and JHU022 cells (Fig 4C). Relative expression of ELDR in OSCC patient samples compared to adjacent non-tumor tissues (N = 20) analyzed by qRT-PCR.	33043604	RID03910	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	ELDR	EGFR	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+)	ceRNA(miR-7)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000280890	GRCh38_7:55235965-55255635	ENSG00000146648	NA	102725541	1956	Fabl|LINC01156	ERBB|ERBB1|ERRP	Since we did not observe involvement of ILF3 in EGFR regulation, next question was how ELDR regulates EGFR. miR-7 inhibits EGFR by binding its 30 UTR (Webster et al, 2009; Han et al, 2015). We therefore examined whether ELDR-miR-7 axis is involved to regulate EGFR. For this, Cal27 and JHU029 cells were transfected with control or siELDR and miR-7 expression was examined. We observed a significant upregulation of miR-7 upon knockdown of ELDR in the cells (Fig 6A). We also overexpressed ELDR in Cal27 and JHU029 cells (Fig EV4A) and observed significant downregulation of miR-7 in the cells (Fig 6B). This result indicates that ELDR inhibits miR-7 expression. Next, we overexpressed miR-7 mimic in Cal27 and JHU029 cells (Fig EV4B), however, we did not see any alteration in ELDR expression (Fig 6C). Interestingly, we observed reduced EGFR protein expression following overexpres_x0002_sion of mimic miR-7 in Cal27 and JHU029 cells, which can be rescued by exogenous ELDR (Figs 6D and EV4C). The expression of miR-7 in Cal27 and JHU029 cells was much lower as compared to control NOK (Fig 6E). These results suggested that ELDR induces EGFR signaling by inhibiting miR-7 (Fig 6F), although the underly_x0002_ing mechanism remains to be elucidated.	33043604	RID03911	ceRNA or sponge	NA		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	Linc-smad7	SIRT6	positively-E	dual-luciferase reporter analysis;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-125b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000077463	NA	NA	51548	NA	SIR2L6|hSIRT6	Long intergenic noncoding RNA smad7 (Linc-smad7) has been recently identified as a new long non-coding RNA (lncRNA). However, the role of Linc-smad7 in the tumourigenesis of human cancers remains unknown. This study uncovered that Linc-smad7 was increased in HCC samples and HCC cell lines using RT-qPCR assays. Furthermore, the overexpression of Linc-smad7 indicated poor clinicopathological features and outcomes for HCC patients. In addition, Linc-smad7 promoted HCC cells proliferation, migration, invasion and EMT, as determined by MTT, colony formation, Transwell assays and western blot Functionally, it was demonstrated that Linc-smad7 could bind with microRNA-125b (miR-125b), and the restoration of miR-125b rescued the promoting effects of Linc-smad7 on HCC cells. Finally, it was observed that sirtuin 6 (SIRT6) was positively regulated by Linc-smad7 in HCC as the direct target of miR-125b, and decreased SIRT6 reversed the effects of Linc-smad7 on promoting HCC. In conclusion, the current study first identified Linc-smad7 is increased in HCC, facilitating HCC cells proliferation, migration, invasion and EMT via regulating the miR-125b/SIRT6 axis.To confirm whether Linc-smad7 could directly bind with miR-125b, we constructed Linc-smad7-WT and Lincsmad7-MUT vectors. dual-luciferase reporter assay results demonstrated that the relative luciferase activities in HCC cells co-transfected with Linc-smad7-WT and miR-125b mimics were significantly reduced compared with those in HCC cells transfected with NC vector (p < 0.05, Figure 4G and H). While, the relative luciferase activities in HCC cells co-transfected with miR- 125b mimics and Linc-smad7-MUT did not decrease significantly (p < 0.05, Figure 4G and H). In addition,   biotin-labelled RNA pull-down assays showed that the bio-Linc-smad7 probe could pull down miR-125b in HCC cells, but the bio-Linc-smad7-MUT-probe did not affect miR-125b in HCC cells (p < 0.05, Figure 4I-K). Compared with that in cells transfected with mimic-NC  control, miR-125b expression was increased in Hep3B  cells (Figure 4L) and Huh7 cells (Figure 4M) transfected  with miR-125b mimics (p  <   0.01). In short, these data  strongly suggest that Linc-smad7 directly sponges miR- 125b in HCC cells.	33037850	RID03912	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SPRY4-IT1	PDK1	positively-E	RIP;Immunoblot	upregulation	qPCR	NA	NA	cell growth(+);cell survival(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000152256	NA	100642175	5163	SPRIGHTLY	NA	Colorectal cancer (CRC) becomes the third leading cause of cancer-related deaths worldwide recently. The prognosis of CRC is still poor in decades, and targeted therapy is still a potential effective treatment. Long non-coding RNAs (lncRNAs) could regulate series of cellular functions and developmental processes. LncRNA-SPRY4-IT1 (GenBank ID AK024556) is derived from an intron of the SPRY4 gene, which was highly expressed in melanoma cells and affected the progression of multiple types of cancers. However, the mechanism of SPRY4-IT1 in CRC progression remains unclear. Herein, we found the high level of SPRY4-IT1 in human colorectal cancer (CRC) tissues and cells, and correlated with patients' prognosis. We further noticed that SPRY4-IT1 regulated CRC cell growth and glycolysis, and promoting PDK1 expression. Our data further confirmed that SPRY4-IT1 regulated CRC progression targeting PDK1. We therefore thought SPRY4-IT1 could serve as a promising molecular target for the treatment of CRC.Through RIP assays, we found the antibody of PDK1 could significantly enrich SPRY4-IT1, indicating the possible interaction between PDK1 and SPRY4-IT1 (Figure 3 (C)). Subsequently, we performed Immunoblot assays to confirm the regulation of SPRY4-IT1 on PDK1 expression.	33029299	RID03913	expression association	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Hypoxic pulmonary hypertension	GAS5	KCNK3	positively-E	luciferase reporter assay;DIANA;starBase;Targetscan;miRDB	downregulation	qRT-PCR;ISH	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Pulmonary hypertension	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171303	NA	60674	3777	NCRNA00030|SNHG2	K2p3.1|TASK|TASK-1|TASK1	Pulmonary hypertension (PH) is a progressive and potentially serious lung disease, defined by an abnormal elevation of pulmonary arterial pressure. PH occurs for many reasons, and hypoxia is considered as an important stimulus for the disease. Proliferation and migration of pulmonary artery smooth muscular cells (PASMCs) in the small peripheral pulmonary arteries are common characteristic features in hypoxia-induced PH (HPH). However, the mechanisms involved in the hypoxia-induced cell proliferation and migration are not clear. The aim of the present study was to investigate the role of lncRNA Gas5 in the hypoxia-stimulated proliferation and migration of human PASMCs (hPASMCs). We found that the expression of Gas5 was down-regulated in a rat model with hypoxia and in cultured hypoxic hPASMCs, and silence of Gas5 significantly promoted hPASMCs proliferation and migration in both normal and hypoxia condition. Subsequent studies revealed that miR-23b-3p interacted with Gas5 by directly targeting the miRNA-binding site in the Gas5 sequence, and qRT-PCRresults showed miR-23b-3p and Gas5 could affect each other's expression, respectively. Further study demonstrated that Gas5 acted as a competing endogenous RNA (ceRNA) for miR-23b-3p to modulate the KCNK3 expression, and these interactions led to promotion of hPASMCs proliferation and migration. This study identified that Gas5/miR-23b-3p/KCNK3 axis may be a mechanism that hypoxia-induced PASMCs proliferation and migration, providing a strategy for clinical treatment of HPH in the future.Using miRNA predict databases (Targetscan, DIANA and miRDB), we found that miR-23b-3p has the potential to bind the 3 -UTR region of KCNK3.To address this, two bioinformatic databases (DIANA and starBase) were employed to predict the potential miRNAs that can be regulated by Gas5, and we found that there were 17 miRNAs were predicted by both DIANA and starBase.	33010302	RID03914	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteoporosis	GAS5	UPF1	positively-E	RNA pull-down assay;RIP;western blot	downregulation	qPCR	NA	NA	cell differentiation(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000005007	NA	60674	5976	NCRNA00030|SNHG2	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	Osteoporosis is a common systemic skeletal disorder resulting in bone fragility and increased fracture risk. It is still necessary to explore its detailed mechanisms and identify novel targets for the treatment of osteoporosis. Previously, we found that a lncRNA named GAS5 in human could negatively regulate the lipoblast/adipocyte differentiation. However, it is still unclear whether GAS5 affects osteoblast differentiation and whether GAS5 is associated with osteoporosis. Our current research found that GAS5 was decreased in the bones and BMSCs, a major origin of osteoblast, of osteoporosis patients. Mechanistically, GAS5 promotes the osteoblast differentiation by interacting with UPF1 to degrade SMAD7 mRNA. Moreover, a decreased bone mass and impaired bone repair ability were observed in Gas5 heterozygous mice, manifesting in osteoporosis. The systemic supplement of Gas5-overexpressing adenoviruses significantly ameliorated bone loss in an osteoporosis mouse model. In conclusion, GAS5 promotes osteoblast differentiation by targeting the UPF1/SMAD7 axis and protects against osteoporosis.Then, we performed an RNA pull-down assay to identify the interacting protein of GAS5. The mass spectrometry results indicatedthat UPF1, a DNA/RNA helicase at the crossroads of many critical cellular pathways for RNA and DNA maintenance (Fiorini et al., 2018), was identified in the GAS5 pull-down assay (Figure 4A). western blotof the GAS5 pull-down protein confirmed that GAS5 could interact with UPF1 specifically (Figure 4B), and a RIP assay using the anti-UPF1 antibody further confirmed this conclusion.	33006314	RID03915	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Sepsis	THRIL	TNF	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-19a)	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000228978	NA	102659353	7124	BRI3BP-AS1|BRI3BPAS1|Linc1992|TCONS_00020260	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	LncRNA THRIL is upregulated in sepsis and sponges miR-19a to upregulate TNF-alpha in human bronchial epithelial cells.Background: Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in various diseases. Our bioinformatics analysis showed that lncRNA TNFalpha and heterogenous nuclear ribonucleoprotein L (hnRNPL) related immunoregulatory LincRNA (THRIL) may interact with miR-19a, which targets TNF-alpha. This study aimed to explore the role of THRIL, an enhancer of LPS-induced inflammatory, in sepsis.Methods: Research subjects of the present study included 66 sepsis patients and 66 healthy volunteers. The expression levels of THRIL, miR-19a and TNF-alpha in plasma samples from these participants were determined by RT-qPCR. The interaction between THRIL and miR-19a was explored by performing overexpression experiments in human bronchial epithelial cells (HBEpCs). The roles of THRIL, miR-19a and TNF-alpha in regulating the apoptosis of HBEpCs were analyzed by cell apoptosis assay.Results: We found that THRIL was upregulated in sepsis patients. THRIL is predicted to interact with miR-19a, and the interaction was confirmed by dual-luciferase activity assay. However, THRIL and miR-19a did not affect the expression of each other. Instead, overexpression of THRIL resulted in the increased expression levels of TNF-alpha, a downstream target of miR-19a in HBEpCs. In HBEpCs, LPS treatment induced the overexpression of THRIL. Cell apoptosis analysis showed that overexpression of THRIL and TNF-alpha promoted the apoptosis of HBEpCs induced by LPS, while overexpression of miR-19a played an opposite role. Overexpression of THRIL attenuated the effects of overexpression of miR-19a.Conclusion: Therefore, THRIL is upregulated in sepsis and may sponge miR-19a to upregulate TNF-alpha, thereby promoting lung cell apoptosis.	32944003	RID03916	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Lung adenocarcinoma	lnc-REG3G-3-1	SLC2A5	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	GSE146461	NA	cell migration(+);cell invasion(+)	ceRNA(miR-215-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000142583	NA	NA	6518	NA	GLUT-5|GLUT5	lnc-REG3G-3-1/miR-215-3p Promotes Brain Metastasis of Lung Adenocarcinoma by Regulating Leptin and SLC2A5.This study aims to explore the role and mechanism of specific lncRNA in brain metastasis (BM) from lung adenocarcinoma (LADC), providing an effective biomarker for early diagnosis and targeted therapy of BM from LADC. Based on the gene expression profiles of lncRNA and mRNA in LADC and BM tissues detected by Gene Chip, lnc-REG3G-3-1 was selected, and the related genes, including miR-215-3p, leptin, and SLC2A5, were identified by data analysis. Human LADC cell lines A549 and H1299 were cultured. Dual-luciferase and endogenous validation experiments were used to confirm the regulation between these genes. Real-time quantitative reverse transcription-polymerase chain reaction and western blot were used to detect gene expression. The tumor metastasis-related gene function of lnc-REG3G-3-1 and miR-215-3p in H1299 cells was verified by Transwell invasion, migration assays, and scratch testing. Nude mice xenograft tumors constructed with decreased lnc-REG3G-3-1 confirmed the influences on gene expression in vivo. lnc-REG3G-3-1 was highly expressed in BM tissues that originated from LADC compared with that in primary cancer tissues. lnc-REG3G-3-1 reduced miR-215-3p expression, thereby regulating the target genes leptin and SLC2A5 and the signaling pathways, taking part in the lnc-REG3G-3-1/miR-215-3p axis in the process of BM from LADC. lnc-REG3G-3-1, leptin, and SLC2A5 through regulating signaling pathways may be jointly involved in the regulation of the biological process of BM in patients with LADC.The results showed that, compared with the control group, the overexpression of lnc-REG3G-3-1 can significantly enhance the migration and invasion abilities of cells, whereas the knockdown of lnc-REG3G- 3-1 can significantly reduce the migration and invasion abilities of cells.Based on these bioinformatics results, real-time RT-PCRwas used to detect the expression differences of lnc-REG3G-3-1, leptin, and SLC2A5 genes and the three miRNAs in A549 and H1299 cells and human normal lung epithelial cell line BEAS-2B as control.The results show that the expression of lnc-REG3G-3-1, leptin, and SLC2A5 in A549 and H1299 cells  was significantly increased compared with that in control cells, and the expression in H1299 cells was significantly increased compared with that in A549 cells.After SLC2A5-3 UTR mutation, the changes in miR-215-3p did not affect the activity of luciferase. The results show that miR-215-3p has a targeting effect on SLC2A5 (Figure 2F,b).	32903414	RID03917	ceRNA or sponge	metastasis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE75367,GSE86978)
Lung adenocarcinoma	lnc-REG3G-3-1	Leptin	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	GSE146461	NA	cell migration(+);cell invasion(+)	ceRNA(miR-215-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lnc-REG3G-3-1/miR-215-3p Promotes Brain Metastasis of Lung Adenocarcinoma by Regulating Leptin and SLC2A5.This study aims to explore the role and mechanism of specific lncRNA in brain metastasis (BM) from lung adenocarcinoma (LADC), providing an effective biomarker for early diagnosis and targeted therapy of BM from LADC. Based on the gene expression profiles of lncRNA and mRNA in LADC and BM tissues detected by Gene Chip, lnc-REG3G-3-1 was selected, and the related genes, including miR-215-3p, leptin, and SLC2A5, were identified by data analysis. Human LADC cell lines A549 and H1299 were cultured. Dual-luciferase and endogenous validation experiments were used to confirm the regulation between these genes. Real-time quantitative reverse transcription-polymerase chain reaction and western blot were used to detect gene expression. The tumor metastasis-related gene function of lnc-REG3G-3-1 and miR-215-3p in H1299 cells was verified by Transwell invasion, migration assays, and scratch testing. Nude mice xenograft tumors constructed with decreased lnc-REG3G-3-1 confirmed the influences on gene expression in vivo. lnc-REG3G-3-1 was highly expressed in BM tissues that originated from LADC compared with that in primary cancer tissues. lnc-REG3G-3-1 reduced miR-215-3p expression, thereby regulating the target genes leptin and SLC2A5 and the signaling pathways, taking part in the lnc-REG3G-3-1/miR-215-3p axis in the process of BM from LADC. lnc-REG3G-3-1, leptin, and SLC2A5 through regulating signaling pathways may be jointly involved in the regulation of the biological process of BM in patients with LADC.The results showed that, compared with the control group, the overexpression of lnc-REG3G-3-1 can significantly enhance the migration and invasion abilities of cells, whereas the knockdown of lnc-REG3G- 3-1 can significantly reduce the migration and invasion abilities of cells.Based on these bioinformatics results, real-time RT-PCRwas used to detect the expression differences of lnc-REG3G-3-1, leptin, and SLC2A5 genes and the three miRNAs in A549 and H1299 cells and human normal lung epithelial cell line BEAS-2B as control.The results show that the expression of lnc-REG3G-3-1, leptin, and SLC2A5 in A549 and H1299 cells  was significantly increased compared with that in control cells, and the expression in H1299 cells was significantly increased compared with that in A549 cells. The results show that miR-215-3p has a targeting effect on leptin.	32903414	RID03918	ceRNA or sponge	metastasis		
Colorectal cancer	SNHG16	CCL2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000108691	NA	100507246	6347	Nbla10727|Nbla12061|ncRAN	GDCF-2|HC11|MCAF|MCP-1|MCP1|MGC9434|SCYA2|SMC-CF	LncRNA SNHG16 promotes colorectal cancer cell proliferation, migration, and epithelial-mesenchymal transition through miR-124-3p/MCP-1.Colorectal cancer (CRC) has been the third leading cause of cancer-associated deaths. LncRNA SNHG16 is reported to be involved in metastasis of CRC cells. However, the mechanism by which SNHG16 regulates CRC progression is poorly understood. The proliferation of CRC cells was examined by MTT. Wound healing and transwell assay were used to measure migration and invasion ability. RT-qPCR and western blot were used to examine gene expression. Immunofluorescence was conducted to evaluate the EMT of CRC cells. Luciferase reporter assay were used to confirm direct interaction between miR-124-3p and SNHG16 or MCP-1. The interaction between miR-124-3p and SNHG16 was detected by RIP and RNA pull-down assay. H&E staining was used to test the histomorphological changes of hepatic metastatic nodules. Finally, xenograft tumor experiment was utilized to determine tumor growth in vivo. SNHG16 and miR-124-3p were dysregulated in human colorectal tumors or cells. Knockdown of SNHG16 led to attenuate cell proliferation, migration, invasion, and EMT of CRC cells. And xenograft tumor experiment showed that SNHG16 might influence tumor growth. In contrast, miR-124-3p exerted the antitumor effects. Knockdown of miR-124-3p can reverse the effect of sh-SNHG16 on CRC cells. miR-124-3p could directly bind to SNHG16 or MCP-1. More importantly, MCP-1 acts as a critical effector mediating the role of SNHG16/ miR-124-3p in CRC cells. In summary, our data suggest that SNHG16 plays a contributory role in proliferation, migration, and EMT of CRC cells via miR-124-3p/MCP-1 axis, which offers a rationale for targeting SNHG16 and developing therapeutic drugs to treat CRC.RTqPCR results showed that lncRNA SNHG16 level was increasingly elevated from colorectal tumor tissues compared with matched paracarcinoma tissues.	32859986	RID03919	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD);DATA(GSE40174)
Asthma	PVT1	MIR149	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell injury(+);inflammatory response(+);apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	NA	Respiratory system disease	Asthma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000207611	NA	5820	406941	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MIRN149|mir-149	LncRNA PVT1 exacerbates the inflammation and cell-barrier injury during asthma by regulating miR-149.Methods and materials: Human small airway epithelial cells (HSAECs) with PVT1 overexpressed or knocked down were constructed, and platelet activating factor (PAF) was used to treat HSAECs to mimic the pathological process of asthma in vitro. The expressions of prostaglandin E2 (PGE2), interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha) were measured by enzyme-linked immunosorbent assay (ELISA). The expressions of PKC, MyD88, and NF--B were measured by western blot. Monolayer permeability of HSAECs was also compared within different groups. Luciferase reporter gene assay was employed to detect the targeting relationship between PVT1 and miR-149.Results: The knockdown of PVT1 attenuated the levels of inflammatory factors induced by PAF and destruction of cell-barrier function. The overexpression of PVT1 facilitated the pathological development. Additionally, miR-149 was identified as a target microRNA of PVT1, and the overexpression of miR-149 could reverse the effects of PVT1 on PAF-induced HSAECs.Conclusion: These findings suggest that PVT1 may represent a novel potential target for treatment of asthma.Moreover, the apoptosis was detected using flow cytometry, and the results indicated that the apoptosis rate significantly increased following the overexpression of PVT1 and decreased when PVT1 was knocked down (Figure 3B).	32830409	RID03920	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Skin melanoma	lncRNA-TTN-AS1	TTR	positively-E		upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	NA	NA	ENSG00000118271	NA	NA	7276	NA	ATTR|CTS|CTS1|HEL111|HsT2651|PALB|TBPA|TTN	Long noncoding RNA TTN-AS1 facilitates tumorigenesis and metastasis by maintaining TTN expression in skin cutaneous melanoma.The antisense transcript, emanating from the opposite strand to a protein-coding or sense strand, has been reported to have critical roles in gene regulation. The perturbation of an antisense RNA can alter the expression of sense messenger RNAs. In this study, a long noncoding RNA TTN-AS1 (lncRNA-TTN-AS1), which is transcribed in the opposite direction of the human titin (TTN) gene, has been identified and explored in skin cutaneous melanoma (SKCM). We found that the expression of TTN and lncRNA-TTN-AS1 had a significantly positive correlation in SKCM cells. Functionally, ectopic expression of TTN and lncRNA-TTN-AS1 promoted SKCM tumorigenesis and metastasis both in vitro and in vivo. Moreover, knockdown of TTN partially abrogated lncRNA-TTN-AS1 induced SKCM tumorigenesis. Mechanistically, hypomethylation of transcription initiation site was responsible for lncRNA-TTN-AS1 high expression levels. LncRNA-TTN-AS1 facilitated SKCM progression by promoting TTN expression at both transcriptional and posttranscriptional levels. As detailed, lncRNA-TTN-AS1 had a significant effect on the increase of TTN promoter activity. Besides, lncRNA-TTN-AS1 also induced the accumulation of TTN in cytoplasm by increasing the stability of TTN mRNA. Clinically, we found that high TTN and lncRNA-TTN-AS1 expression were positively correlated with poor overall survival of SKCM patients, and may be considered as novel biomarkers and drug targets for SKCM patients.In addition, the results from the database showed that TTN was highly expressed in skin cancer tissues compared with adjacent normal tissues (Fig. S1a, b). Hence, these data showed that high TTN and lncRNA-TTN-AS1 expression levels in SKCM patients were related to poor outcome.TTN and lncRNA-TTN-AS1 induced SKCM cell proliferation, suppressed cell apoptosis, and promoted cell migration in vitro.However, whether lncRNA-TTN-AS1 could interact with TTN, and molecular mechanisms of lncRNA-TTN-AS1 in SKCM are still unknown.	32820147	RID03921	expression association	metastasis		UP(LIHC);DATA(GSE117623)
Cholangiocarcinoma	TTN-AS1	Neuropilin-1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+)	ceRNA(miR-320a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	Neuropilin-1 regulated by miR-320a participates in the progression of cholangiocarcinoma by serving as a co-receptor that activates multiple signaling pathways. The present study sought to investigate upstream lncRNAs that control the expression of miR-320a/neuropilin-1 axis and dissect some of the underlying mechanisms. Here we report lncRNA TTN-AS1 (titin-antisense RNA1) acts as a sponging ceRNA to downregulate miR-320a and is highly expressed in human cholangiocarcinoma tissues and cells. The expression of the above three molecules is correlated with the clinicopathologic parameters of cholangiocarcinoma patients. In this study, multiple bioinformatics tools and databases were employed to seek potential lncRNAs that have binding sites with miR-320a and TTN-AS1 was identified because it exhibited the largest folds of alteration between cholangiocarcinoma and normal bile duct epithelial cells. The regulatory role of TTN-AS1 on miR-320a was further evaluated by luciferase reporter and RNA pull-down assays, coupled with in situ hybridization and RNA immunoprecipitation analyses, which showed that TTN-AS1 bound to miR-320a through an argonaute2-dependent RNA interference pathway in the cytoplasm of cholangiocarcinoma cells. Knockdown and overexpression assays showed that the regulatory effect between TTN-AS1 and miR-320 was in a one-way manner. TTN-AS1 promoted the proliferation and migration of cholangiocarcinoma cells via the miR-320a/ neuropilin-1 axis. The function of TTN-AS1 on tumor growth and its interaction with miR-320a were confirmed in animal models. Further mechanistic studies revealed that TTA-AS1, through downregulating miR-320a, promoted cell cycle progression, epithelial-mesenchymal transition, and tumor angiogenesis by upregulating neuropilin-1, which co-interacted with the hepatocyte growth factor/c-Met and transforming growth factor (TGF)-beta/TGF-beta receptor I pathways. In conclusion, the present results demonstrate that lncRNA TTA-AS1 is a sponging ceRNA for miR-320a, which in turn downregulates neuropilin-1 in cholangiocarcinoma cells, indicating these three molecules represent potential biomarkers and therapeutic targets in the management of cholangiocarcinoma.The overexpression of NRP-1 in clinical CCA tissues was confirmed by using immunohistochemistry of tissue microarrays.	32801339	RID03922	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Ischemic stroke	MACC1-AS1	TWIST1	positively-E	luciferase reporter assay;RNA pull-down assay;bioinformatics	downregulation	RT-qPCR	NA	NA	angiogenesis(+);cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-6867-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000228598	GRCh38_7:20141916-20153531	ENSG00000122691	NA	100874041	7291	NA	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	LncRNA MACC1-AS1 attenuates microvascular endothelial cell injury and promotes angiogenesis under hypoxic conditions via modulating miR-6867-5p/TWIST1 in human brain microvascular endothelial cells.Background: Hypoxia following ischemic stroke is a common cause of brain insults. Mounting evidence suggests that long non-coding RNAs (lncRNAs) play a vital role in regulating certain physiological and pathological processes including ischemic stroke. For the first time, the present study investigated the effects and mechanism of LncRNA MACC1-AS1 on hypoxia-induced human brain microvascular endothelial cells (HBMECs).Methods: LncRNA MACC1-AS1 levels in HBMECs were detected via reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), were detected using their respective kits. Flow cytometry and clone formation assay were performed to evaluate the effects of lncRNA MACC1-AS1 on cell apoptosis and cell proliferation respectively. Angiogenesis capacity was evaluated via tube formation assay. Transwell migration assay was performed for assessment of cell migration, western blot assay was performed for measurement of Twist1 and VE-cadherin level, and permeability assay was performed for evaluation of the cell barrier function. The target gene was predicted via bioinformatics online tool and validated through luciferase reporter assay and RNA pull-down assay.Results: LncRNA MACC1-AS1 was downregulated in hypoxia-induced HBMECs. Overexpression of LncRNA MACC1-AS1 reduced cell apoptosis and oxidative stress, while promoting cell proliferation, migration, and angiogenesis. Moreover, LncRNA MACC1-AS1 overexpression reduced cell permeability and elevated VE-cadherin level, which contributed to maintaining cell barrier function. TWIST1 was validated as the target of miR-6867-5p which was further targeted by lncRNA MACC1-AS1. Thus, LncRNA MACC1-AS1 functions in hypoxia-induced HBMECs by regulating miR-6867-5p/TWIST1.Conclusions: In this study, we found that LncRNA MACC1-AS1 exerted a protective role in hypoxia-induced HBMECs via regulating miR-6867-5p/TWIST1, indicating a new therapeutic strategy for future ischemic stroke therapy.	32793720	RID03923	ceRNA or sponge	NA		UP(SKCM);DATA(GSE38495)
Neuropathic pain	ZRANB1	LPAR3	positively-E	luciferase reporter assay;RNA pull-down assay;bioinformatics	downregulation	qRT-PCR	NA	NA	WNT5a/beta-catenin signaling pathway(+)	ceRNA(miR-24-3p)	regulation	NA	NA	CSC	NA	Other	Neuropathic pain	lncRNA	PCG	ENSG00000019995	GRCh38_10:124942123-124988189	ENSG00000171517	NA	54764	23566	TRABID	Edg-7|EDG7|HOFNH30|LP-A3|LPA3|RP4-678I3	Downregulated circular RNA zRANB1 mediates Wnt5a/beta-Catenin signaling to promote neuropathic pain via miR-24-3p/LPAR3 axis in CCI rat models.Neuropathic pain, which results from impairment of the somatosensory system, has affected about 8% population around the world and leads to considerable burdens for patients and world health care system. However, its underlying mechanisms remain poorly understood. In this study, we hypothesized that miR-24-3p was involved in the progression of neuropathic pain in CCI rat models. By measuring miR-24-3p expression in CCI rats, we found that miR-24-3p expression was increased in CCI rats, suggesting miR-24-3p might participate in neuropathic pain progression. Next, by conducting a serial in vitro and vivo experiments, we found that miR-24-3p regulated Wnt5a/beta-Catenin Signaling levels to promote neuropathic pain progression via targeting LPAR3 in CCI rats. Furthermore, we explored the upstream regulator of miR-24-3p by conducting bioinformatics analysis, we found that circular RNA cZRANB1 might sponge to miR-24-3p. Then we applied biotinylated RNA pull-down and luciferase reporter assays to assess the association between cZRANB1 and miR-24-3p. It was found that cZRANB1 mediated LPAR3 expression via sponging miR-24-3p. Collectively, our study suggests that cZRNAB1 regulated Wnt5a/beta-Catenin Signaling expression via miR-24-3p/LPAR3 axis in CCI rat models.	32777532	RID03924	ceRNA or sponge	NA	UP(PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	UP(LIHC);DATA(GSE117623)
Breast cancer	XIST	NLRC5	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000140853	NA	7503	84166	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	CLR16.1|FLJ21709|NOD27	The lncRNA XIST promotes the progression of breast cancer by sponging miR-125b-5p to modulate NLRC5.X-inactivation-specific transcript (XIST) is a long noncoding RNA (lncRNA) that functions as an indicator of various human tumors, including those of breast cancer. This study was conducted to characterize a novel regulatory network involving XIST in breast cancer cells. The mRNAs of XIST, miR-125b-5p, and NOD-like receptor family CARD domain containing 5 (NLRC5) in breast cancer cells and tissues were analyzed using quantitative real-time polymerase chain reaction. Cell proliferation, apoptosis, migration, and invasion were separately detected via cell counting kit-8, flow cytometry, and Transwell assays. The relationships between XIST, miR-125b-5p, and NLRC5 were predicted and then confirmed using the dual-luciferase reporter assay. NLRC5 protein expression was quantitated using western blot assays. XIST was found to be overexpressed in breast cancer tissues and cells, which was accompanied by miR-125b-5p downregulation and NLRC5 upregulation. XIST knockdown significantly repressed cell proliferation, anti-apoptosis, migration, and invasion activities in breast cancer cells, and the loss of miR-125b-5p had a similar effect. XIST was shown to sponge miR-125b-5p, which in turn targeted NLRC5. NLRC5, a breast cancer promotor, is negatively regulated by miR-125b-5p. Moreover, the downregulation of NLRC5 induced by the loss of XIST was significantly reversed by miR-125b-5p knockdown. In conclusion, the lncRNA XIST promotes the malignancy of breast cancer cells partly by competitively binding to miR-125b-5p, which then led to increased NLRC5 expression. Our study suggests that targeting XIST may be a possible treatment for breast cancer.	32774715	RID03925	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Lung adenocarcinoma	SLCO4A1-AS1	NFE2L1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+);chemoresistance(+);WNT signaling pathway(+)	ceRNA(miR-4701-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000082641	NA	100127888	4779	NA	FLJ00380|LCR-F1|NRF1|TCF11	SLCO4A1-AS1 promotes cell growth and induces resistance in lung adenocarcinoma by modulating miR-4701-5p/NFE2L1 axis to activate WNT pathway.Long noncoding RNAs (lncRNAs) possessed essential functions in the biological behaviors of various human cancers. SLCO4A1 antisense RNA 1 (SLCO4A1-AS1) is a lncRNA that has been reported as a oncogenic regulator in colorectal cancer and bladder cancer. However, whether it exerted functions in the gene expression and cellular processes in lung adenocarcinoma (LUAD) remains still obscure. In the present research, we unveiled the high level of SLCO4A1-AS1 in LUAD tissues and cells. Moreover, functional assays indicated that SLCO4A-AS1 facilitated LUAD cell proliferation, motility, and cisplatin-resistance. Besides, mechanism investigation revealed that miR-4701-5p could interact with SLCO4A1-AS1 and directly target to NFE2L1. The expression correlation between miR-4701-5p and SLCO4A1-AS1 or NFE2L1 was found to be negative. Moreover, NFE2L1 was expressed at a same tendency with SLCO4A1-AS1 in LUAD tissues and cells. In addition, it was confirmed that NFE2L1 was involved in SLCO4A1-AS1-mediated activation of WNT pathway. According to rescue assays, NFE2L1 could involve in SLCO4A1-AS1-mediated LUAD cell growth. Conclusively, our study demonstrated that SLCO4A1-AS1 facilitated cell growth and enhanced the resistance of LUAD cells to chemotherapy via activating WNT pathway through miR-4701-5p/NFE2L1 axis.	32762035	RID03926	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Asthma	lnc-BAZ2B	BAZ2B	positively-E	knockdown	upregulation	RT-qPCR;microarray	NA	NA	cell viability(+);inflammatory response(+)	NA	association	NA	NA	NA	NA	Respiratory system disease	Asthma	lncRNA	TF	NA	NA	ENSG00000123636	NA	NA	29994	NA	WALp4	lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma through stabilizing BAZ2B pre-mRNA.Background: Dysregulation of long noncoding RNAs (lncRNAs) is associated with a variety of human diseases; however, whether they have a role in childhood asthma is unknown.Objective: We sought to determine the differential expression profiles of lncRNAs in PBMCs of children with asthma and the mechanisms underlying the effects of lncRNAs on the pathogenesis of asthma.Methods: The differential expression profiles of lncRNAs were analyzed by transcriptome microarray. The effects and mechanisms by which lncRNAs influence macrophage activation were detected by real-time quantitative PCR, western blot, RNase protection assay, and chromatin immunoprecipitation assay. The roles played by lncRNAs in asthma were tested in a cockroach allergen extract (CRE)-induced mouse model.Results: We identified 719 lncRNAs that were differentially expressed in PBMCs of children with asthma, 502 of which were upregulated and 217 were downregulated. An lncRNA of unknown function, lnc-BAZ2B, was dominantly expressed in monocytes and significantly upregulated in children with asthma. lnc-BAZ2B promotes M2 macrophage activation by enhancing BAZ2B expression and exacerbated lung inflammation in an M2 macrophage-associated CRE-induced asthma model. Mechanistically, lnc-BAZ2B promoted the expression of its cis target gene BAZ2B by stabilizing its pre-mRNA. BAZ2B, a reader of H3K14ac modification, enhanced the transcription of IRF4 and promoted M2 macrophage activation. lnc-BAZ2B expression was correlated with that of BAZ2B in PBMCs from children with asthma. Baz2b knockdown could alleviate asthma severity in a CRE-induced asthma model.Conclusion: lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma and may serve as a potential therapeutic and diagnostic target in children with asthma.	32712329	RID03927	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE75367)
Glioblastoma	LGMNP1	LGMN	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-495-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214269	GRCh38_13:64958097-64959396	ENSG00000100600	NA	122199	5641	LGMN2P	LGMN1|PRSC1	The LGMN pseudogene promotes tumor progression by acting as a miR-495-3p sponge in glioblastoma.Pseudogenes, which are long noncoding RNAs that originate from protein-coding genes, have been suggested to play important roles in disease. Although studies have revealed high expression of legumain (LGMN) in many types of tumors, the regulation of LGMN remains largely unknown. Here, we found that a novel LGMN pseudogene (LGMNP1) was upregulated in glioblastoma (GBM) tissues and high LGMNP1 expression in GBM cells enhanced proliferation and invasion. Biochemical analysis showed that cytoplasmic LGMNP1 functionally targeted miR-495-3p in a manner involving an RNA-induced silencing complex. dual-luciferase reporter assays demonstrated that LGMN was a target of miR-495-3p, and LGMN was upregulated and positively correlated with LGMNP1 in GBM. Moreover, miR-495-3p was downregulated and negatively correlated with LGMNP1 in GBM tissues. Notably, the tumor-promoting effects of LGMNP1 upregulation could be alleviated by miR-495-3p mimics. Furthermore, GBM cells overexpressing LGMNP1 exhibited more aggressive tumor progression and elevated LGMN expression in vivo. Thus, our data illustrate that LGMNP1 exerts its oncogenic activity, at least in part, as a competitive endogenous RNA (ceRNA) that elevates LGMN expression by sponging miR-495-3p. CeRNA-mediated miRNA sequestration might be a novel therapeutic strategy in GBM.	32711096	RID03928	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Osteoarthritis	JUND1	LOXL1-AS1	positively-E	JASPAR;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	TF	lncRNA	NA	NA	ENSG00000261801	GRCh38_15:73908071-73928248	NA	100287616	NA	NA	qRT-PCRassay was applied to detect gene expression, while western blot was performed to measure levels of apoptosis-related proteins. CCK-8, colony formation and TUNEL assays were conducted to explore the functional role of LOXL1-AS1 in OA. ChIP assay was utilized to assess the affinity between JunD proto-oncogene, AP-1 transcription factor subunit (JUND) and LOXL1-AS1 promoter. Mechanism experiments were implemented to investigate the underlying molecular mechanism of LOXL1-AS1.Key findings: LOXL1-AS1 was up-regulated in OA cartilage tissues. Silencing LOXL1-AS1 hampered proliferation and inflammation, yet promoting apoptosis in chondrocytes. LOXL1-AS1 was transcriptionally activated by JUND1. LOXL1-AS1 sequestered miR-423-5p and abolished miR-423-5p-mediated repression on lysine demethylase 5C (KDM5C), thus promoted the development of OA.Significance: LncRNA LOXL1-AS1 is transcriptionally activated by JUND and facilitates the proliferation and inflammation of chondrocytes via elevating miR-423-5p-mediated KDM5C in OA, which may provide potential therapeutic target for OA.As shown in Fig. 2C, the DNA motif of JUND in the promoter region of LOXL1-AS1 and several predicted binding sites were obtained from JASPAR. We divided the promoter region (upstream 2000 bp from transcription start site TSS) into five parts based on the distribution of binding sites.To further verify this conclusion, we cloned the full length of LOXL1-AS1 promoter (P FL) and the five divided regions (P1, P2, P3, P4, P5) into pGL3 luciferase reporter and performed luciferase reporter assay in HEK-293T cells .	32679142	RID03929	transcriptional regulation	NA		DOWN(BRCA);DATA(GSE111842)
Osteoarthritis	LOXL1-AS1	KDM5C	positively-E	StarBase;RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);inflammatory response(+);(+);apoptosis process(-)	ceRNA(miR-423-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000126012	NA	100287616	8242	NA	DXS1272E|JARID1C|MRX13|SMCX|XE169	qRT-PCRassay was applied to detect gene expression, while western blot was performed to measure levels of apoptosis-related proteins. CCK-8, colony formation and TUNEL assays were conducted to explore the functional role of LOXL1-AS1 in OA. ChIP assay was utilized to assess the affinity between JunD proto-oncogene, AP-1 transcription factor subunit (JUND) and LOXL1-AS1 promoter. Mechanism experiments were implemented to investigate the underlying molecular mechanism of LOXL1-AS1.Key findings: LOXL1-AS1 was up-regulated in OA cartilage tissues. Silencing LOXL1-AS1 hampered proliferation and inflammation, yet promoting apoptosis in chondrocytes. LOXL1-AS1 was transcriptionally activated by JUND1. LOXL1-AS1 sequestered miR-423-5p and abolished miR-423-5p-mediated repression on lysine demethylase 5C (KDM5C), thus promoted the development of OA.Significance: LncRNA LOXL1-AS1 is transcriptionally activated by JUND and facilitates the proliferation and inflammation of chondrocytes via elevating miR-423-5p-mediated KDM5C in OA, which may provide potential therapeutic target for OA. Eight potential miRNAs in the downstream of LOXL1-AS1 were predicted using the online bioinformatics tool starBase	32679142	RID03930	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	OIP5-AS1	FOXD1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+);ERK signaling pathway(+)	ceRNA(miR-429)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000251493	NA	729082	2297	cyrano|linc-OIP5	FKHL8|FREAC4	LncRNA OIP5-AS1 promotes the malignancy of pancreatic ductal adenocarcinoma via regulating miR-429/FOXD1/ERK pathway.Background: Pancreatic ductal adenocarcinoma (PDAC), a subtype of pancreatic cancer, is a malignant tumor with unfavorable prognosis. Despite accumulating researches have made efforts on finding novel therapeutic methods for this disease, the underlying mechanism of long non-coding RNAs (lncRNAs) remains elusive. OIP5 antisense RNA 1 (OIP5-AS1) has been reported to play important role in the occurrence and development of multiple human cancers. This study was aimed at unveiling the regulatory role of OIP5-AS1 in PDAC.Methods: RT-qPCR analysis revealed the OIP5-AS1 expression in PDAC tissues and adjacent normal ones. Kaplan-Meier method was applied to analyze the overall survival of patients with high or low level of OIP5-AS1. Gain- or loss-of function assays were performed to assess the effects of OIP5-AS1 knockdown on cell functions, including proliferation, migration and EMT process. Mechanism experiments, such as luciferase reporter and RNA pull-down assays proved the interaction between OIP5-AS1 and miR-429 as well as that between miR-429 and FOXD1.Results: OIP5-AS1 was up-regulated in PDAC tissues and cell lines, and high level of OIP5-AS1 indicated poor prognosis in PDAC patients. OIP5-AS1 knockdown hindered cell proliferation, migration and epithelial-mesenchymal transition (EMT) process, while overexpression of OIP5-AS1 caused the opposite results. OIP5-AS1 activated ERK pathway through up-regulating forkhead box D1 (FOXD1) expression by sponging miR-429. Furthermore, OIP5-AS1 facilitated cell growth in vivo.Conclusion: OIP5-AS1 exerted oncogenic function in PDAC cells through targeting miR-429/FOXD1/ERK pathway.	32669972	RID03931	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(BRCA);DATA(GSE55807)
Gastric cancer	RP11-323N12.5	YAP1	positively-E	luciferase reporter assay	upregulation	RT-PCR	TCGA	NA	tumor growth(+);immune response(-);cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000267601	GRCh38_17:78855478-78855844	ENSG00000137693	NA	NA	10413	NA	COB1|YAP|YAP-1|YAP2|YAP65|YKI	RP11-323N12.5 was identified using GEPIA. Its expression levels and their relationship with clinical features were investigated using clinical samples. The regulation of YAP1 transcription by RP11-323N12.5 was investigated in both GC and T cells, the tumor and immunosuppression promotion roles of RP11-323N12.5 were explored in vitro and in vivo.Results: RP11-323N12.5 was the most up-regulated lncRNA in human GC, based on data from the TCGA database. Its transcription was significantly positively correlated with YAP1 transcription, YAP1 downstream gene expression which contribute to tumor growth and immunosuppression. RP11-323N12.5 promoted YAP1 transcription by binding to c-MYC in the YAP1 promoter region. Meanwhile, transcription of RP11-323N12.5 was also regulated by YAP1/TAZ/TEADs activation in GC cells. RP11-323N12.5 had tumor- and immnosuppression-promoting effects by enhancing YAP1 downstream genes in GC cells. Excessive RP11-323N12.5 was also observed in tumor-infiltrating leukocytes (TILs), which may be exosome-derived and also be related to enhanced Treg differentiation as a result YAP1 up-regulation. Moreover, RP11-323N12.5 promoted tumor growth and immunosuppression via YAP1 up-regulation in vivo.Conclusions: RP11-323N12.5 was the most up-regulated lncRNA in human GC and it promoted YAP1 transcription by binding to c-MYC within the YAP1 promoter in both GC and T cells. RP11-323N12.5 is an ideal therapeutic target in human GC due to its tumor-promoting and immunosuppression characteristics.RP11 323N12.5 promoted GC cell proliferation and invasion, as well as immunosuppression, by increasing YAP1 expression.	32623586	RID03932	transcriptional regulation	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Glioblastoma	HULC	RRAS	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251164	NA	ENSG00000126458	NA	728655	6237	HCCAT1|LINC00078|NCRNA00078	R-Ras	Quantitative Proteomics Analysis Indicates That Upregulation of lncRNA HULC Promotes Pathogenesis of Glioblastoma Cells.Purpose: Glioblastoma (GBM) is an aggressive central nervous system (CNS) cancer and a serious threat to human health. The long noncoding RNA (lncRNA) HULC has been implicated in GBM, but the molecular mechanism is uncertain. This study used quantitative proteomic analysis for global identification of HULC-regulated proteins in glioblastoma cells and identification of potential biomarkers.Materials and methods: qRT-PCRwas used to determine the expression of HULC in U87 cells stably transfected with HULC or an empty vector (control). The CCK-8 assay, transwell assay, and wound-scratch assay were used to measure cell proliferation, invasion, and migration. Quantitative proteomics using Tandem Mass Tag (TMT) labeling, high-performance liquid chromatography (HPLC) fractionation, and liquid chromatography-mass spectrometry (LC-MS/MS) analysis were used to identify differentially expressed proteins (DEPs). Screened proteins were validated by parallel reaction monitoring (PRM) and western blot.Results: Overexpression of HULC led to increased cell proliferation, invasion, and migration. HULC overexpression also led to significant upregulation of 37 proteins and downregulation of 78 proteins. Bioinformatics analysis indicated these proteins had roles in cellular component, biological process, and molecular function. PRM results of 8 of these proteins (PTK2, TNC, ITGAV, LASP1, MAPK14, ITGA1, GNA13, RRAS) were consistent with the LC-MS/MS and western blot results.Conclusion: The results of present study suggest that lncRNA HULC promotes GBM cell proliferation, invasion, and migration by regulating RRAS expression, suggesting that RRAS may be a potential biomarker or therapeutic target for this cancer.	32606802	RID03933	expression association	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842)
Colorectal cancer	lnc-HSD17B11-1:1	MACC1	positively-E	dual-luciferase reporter analysis;RIP;bioinformatics	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000183742	NA	NA	346389	NA	7A5|SH3BP4L	Lnc-HSD17B11-1:1 Functions as a Competing Endogenous RNA to Promote Colorectal Cancer Progression by Sponging miR-338-3p to Upregulate MACC1.Background: Long non-coding RNAs (lncRNAs) play pivotal roles in various kinds of human diseases, especially in cancer. However, regulatory role, clinical significance and underlying mechanisms of lncRNAs in colorectal cancer (CRC) liver metastasis still remain largely unknown. This study aimed to report a novel lncRNA, lnc-HSD17B-11:1, and its functional role in CRC progression.Materials and methods: Differentially expressed lnc-HSD17B11-1:1 was screened and identified from a lncRNA profile microarray. Quantitative real-time PCR was used to determine the expression levels and prognostic values of lncRNA in CRC cohorts. In vitro and in vivo functional experiments were performed to investigate the effects of lnc-HSD17B11-1:1 on tumor growth and metastasis in CRC. Mechanistically, Base Scope, bioinformatics analyses, dual-luciferase reporter assay and RNA immunoprecipitation experiments were performed to confirm the association of lnc-HSD17B11-1:1 and miR-338-3p. dual-luciferase reporter assay, qRT-PCRand western blotwere performed to assess the relationships among lnc-HSD17B11-1:1, miR-338-3p, and MACC1.Results: Evidently up-regulation of lnc-HSD17B11-1:1 in CRC primary tissues was correlated with the depth of invasion (p = 0.043), clinical stage (p = 0.027), distant metastasis (p = 0.003) and poor prognosis of patients with CRC. lnc-HSD17B11-1:1 promoted CRC cell proliferation, mobility and invasion in vitro and in vivo. Mechanistic analysis revealed that lnc-HSD17B11-1:1 may act as a competing endogenous RNA (ceRNA) by acting as a sponge for miR-338-3p to upregulate the expression of MACC1.Conclusion: These findings suggest that lnc-HSD17B11-1:1 promotes CRC progression through lnc-HSD17B11-1:1/miR-338-3p/MACC1 axis and this might serve as a new diagnostic marker or target for treatment of CRC.	32595704	RID03934	ceRNA or sponge	metastasis,prognosis		UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807)
Oesophageal squamous cell carcinoma	IQANK1	Girdin	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-10a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	NA	NA	642574	NA	FAM83H-AS1|onco-lncRNA-3	NA	LncRNA FAM83H-AS1 promotes oesophageal squamous cell carcinoma progression via miR-10a-5p/Girdin axis.Long non-coding RNAs (lncRNAs) have been well demonstrated to emerge as crucial regulators in cancer progression, and they can function as regulatory network based on their interactions. Although the biological functions of FAM83H-AS1 have been confirmed in various tumour progressions, the underlying molecular mechanisms of FAM83H-AS1 in oesophageal squamous cell carcinoma (ESCC) remained poorly understood. To address this, we treated human oesophageal cancer cell line Eca109 cells with TGF-beta and found FAM83H-AS1 was notably overexpressed. In the present study, FAM83H-AS1 was observed to be significantly up-regulated in ESCC tissues and was associated with TNM stage, pathological differentiation and lymph node metastasis. FAM83H-AS1 reinforced oesophageal cancer cell proliferation, migration and invasion, and participated in epithelial-to-mesenchymal transition (EMT) process at mRNA and protein levels. In addition, a concordant regulation between FAM83H-AS1 and its sense strand FAM83H was detected at the transcriptional and translational levels. Furthermore, FAM83H-AS1 could act as competing endogenous RNA to affect the expression of Girdin by sponging miR-10a-5p verified by RIP and luciferase reporter assays. Consequently, the study provided a unique perspective of FAM83H-AS1 in ESCC progression, which may be considered as potential biomarker and therapeutic target for ESCC therapy.	32583631	RID03935	ceRNA or sponge	metastasis	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	
Hepatocellular carcinoma	LINC01419	EZH2	positively-E	ChIP;RNA pull-down assay;RIP;starBase 2.0	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253898	GRCh38_8:83403758-83408900	ENSG00000106462	NA	103352670	2146	PRLH1|TCONS_00014497	ENX-1|EZH1|KMT6|KMT6A	LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK.Long non-coding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis, for example, in hepatocellular carcinoma (HCC). This study explored the role of LINC01419, a new lncRNA, in HCC. In vitro study revealed that LINC01419 promotes growth and migration of HCC cells. Genes that affected cell proliferation and cell migration were identified using RNA-sequence. Subsequently, it was confirmed that LINC01419 binds to EZH2, leading to histone methylation of the RECK promoter. Interaction between LINC01419 and FUS stabilized EZH2 mRNA thereby enhancing EZH2 expression. Conclusively, the results of this study confirm that LINC01419 may serve as a potential target for HCC diagnosis and treatment.Expression of mRNA and protein levels of EZH2 decreased when LINC01419 was inhibited, whereas, it increased when LINC01419 was overexpressed (Figure 4A and 4B).From this, it was proved that LINC01419 positively regulates EZH2 inHCC.The RBP, FUS, was shown to interact with LINC01419 and EZH2- mRNA, this was verified with the starBase 2.0.	32522890	RID03936	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	LINC01419	RECK	negatively-E	ChIP	upregulation	qPCR	TCGA	NA	cell growth(+);cell migration(+)	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253898	GRCh38_8:83403758-83408900	ENSG00000122707	NA	103352670	8434	PRLH1|TCONS_00014497	hRECK|ST15	LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK.Long non-coding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis, for example, in hepatocellular carcinoma (HCC). This study explored the role of LINC01419, a new lncRNA, in HCC. In vitro study revealed that LINC01419 promotes growth and migration of HCC cells. Genes that affected cell proliferation and cell migration were identified using RNA-sequence. Subsequently, it was confirmed that LINC01419 binds to EZH2, leading to histone methylation of the RECK promoter. Interaction between LINC01419 and FUS stabilized EZH2 mRNA thereby enhancing EZH2 expression. Conclusively, the results of this study confirm that LINC01419 may serve as a potential target for HCC diagnosis and treatment.LINC01419 thus partially inhibits the apparent expression of RECK and promotes growth and migration of HCC cells.	32522890	RID03937	epigenetic regulation	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	JUN	LINC01419	positively-E	ChIP;UCSC;PROMO;q-PCR	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000177606	NA	ENSG00000253898	GRCh38_8:83403758-83408900	3725	103352670	AP-1|c-Jun	PRLH1|TCONS_00014497	LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK.Long non-coding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis, for example, in hepatocellular carcinoma (HCC). This study explored the role of LINC01419, a new lncRNA, in HCC. In vitro study revealed that LINC01419 promotes growth and migration of HCC cells. Genes that affected cell proliferation and cell migration were identified using RNA-sequence. Subsequently, it was confirmed that LINC01419 binds to EZH2, leading to histone methylation of the RECK promoter. Interaction between LINC01419 and FUS stabilized EZH2 mRNA thereby enhancing EZH2 expression. Conclusively, the results of this study confirm that LINC01419 may serve as a potential target for HCC diagnosis and treatment.When c-jun was overexpressed, luciferase activity in wild-type LINC01419 promoter increased (Figure 6C). Two bioinformatics software (UCSC and PROMO) were used to analyze the 1000bp region, upstream of the LINC01419 transcription initiation site.However, c-jun overexpression had no significant effect on luciferase activity when cjun binding sites on LINC01419 were mutated (Figure 6C). Based on these results, it was suggested that c-jun binding to the LINC01287 promoter positively regulates its expression.To confirm c-jun binding at the LINC01419 promoter,chromatin immune-precipitation and q-PCR assays were performed.	32522890	RID03938	transcriptional regulation	metastasis	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Kidney disease	OIP5-AS1	miR-30c-5p	negatively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);fibrotic((+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	LncRNA OIP5-AS1 induces epithelial-to-mesenchymal transition and renal fibrosis in diabetic nephropathy via binding to miR-30c-5p.NIn recent years, the incidence of diabetic nephropathy (DN) is rising, and is one of the most important complications of diabetic patients. In this study, the role and regulatory mechanism of lncRNA OIP5-AS1 in the regulation of DN were investigated. Here, the expressions of lncRNA OIP5-AS1 and miR-30c-5p were detected by RT-qPCR. western blotwas used to detect the protein expression of E-cadherin, N-cadherin, TGF-beta1, alpha-SMA. The relationship between OIP5-AS1 and miR-30c-5p was confirmed by dual-luciferase reporter assay. The results showed that the expression of lncRNA OIP5-AS1 was increased in db/db DN mice kidney tissue and high glucose-stimulated HK2 cells. lncRNA OIP5-AS1 promoted epithelial-to-mesenchymal transition (EMT) and renal fibrosis in high glucose-stimulated HK2 cells. In addition, lncRNA OIP5-AS1 directly targets miR-30c-5p, and lncRNA OIP5-AS1 negatively regulated miR-30c-5p expression in high glucose-stimulated HK2 cells. More importantly, overexpression of miR-30c-5p attenuated the promoting effect of OIP5-AS1 on EMT and renal fibrosis in high glucose-stimulated HK2 cells. In conclusion, lncRNA OIP5-AS1 induces EMT and renal fibrosis in DN via binding to miR-30c-5p.	32519534	RID03939	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Coronary atherosclerotic heart disease	CDKN2B-AS1	NOX1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Vascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000007952	NA	100048912	27035	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	GP91-2|MOX1|NOH-1|NOH1	LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype.Many studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases.Moreover, luciferase reporter assay using plasmid containing NOX1 promoter sequence suggested ANRIL promotes NOX1 transcription by interacting to its promoter region (Fig. 5c). The results showed the enhanced cell proliferation, ROS production and migration activity after ox-LDL treatment were all attenuated significantly by siRNA-mediated repression of NOX1 (Fig. 6a d). Similar change was observed in expression level of synthetic phenotype marker OPN, together suggesting the critical role of NOX1 to facilitate the phenotype switch of smooth muscle cells of LncRNA regulator ANRIL (Fig. 6e, f).	32513988	RID03940	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(SKCM);DATA(GSE38495)
Coronary atherosclerotic heart disease	CDKN2B-AS1	HDAC3	negatively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Vascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171720	NA	100048912	8841	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	HD3|KDAC3|RPD3|RPD3-2	LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype.Many studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases. The potential associations between ANRIL with WDR5 and HDAC3 were investigated by RNA pull-down and RNA immunoprecipitation assays.In HASMCs overexpressing ANRIL, the repression of both WDR5 and HDAC3 significantly reduced NOX1 expression (Fig. 7a).	32513988	RID03941	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Coronary atherosclerotic heart disease	CDKN2B-AS1	WDR5	negatively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Vascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000196363	NA	100048912	11091	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	CFAP89|SWD3	LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype.Many studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases.In HASMCs overexpressing ANRIL, the repression of both WDR5 and HDAC3 significantly reduced NOX1 expression (Fig. 7a).	32513988	RID03942	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	HIF1A	H19	positively-E	dual-luciferase reporter analysis;ChIP;RNA pull-down assay;RIP	upregulation	RT-qPCR;microarray	GSE45001;GSE32225	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	TF	lncRNA	ENSG00000100644	NA	ENSG00000130600	GRCh38_11:1995171-2001470	3091	283120	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Transcription factor HIF1alpha promotes proliferation, migration, and invasion of cholangiocarcinoma via long noncoding RNA H19/microRNA-612/Bcl-2 axis.Cholangiocarcinoma, which is the most common invasive malignant tumor of the biliary tract, has poor prognosis. There is evidence suggesting that hypoxia-inducible factor 1alpha (HIF1alpha) plays an important role in cholangiocarcinoma. Also, microRNA-612 (miR-612) is another key regulator of cholangiocarcinoma. In this study, we investigate the scantly documented interaction of HIF1alpha and miR-612 in cholangiocarcinoma. We first undertook microarray-based cholangiocarcinoma gene expression profiles to screen out the differentially expressed long noncoding RNAs (lncRNAs) and genes. We used reverse transcription quantitative polymerase chain reaction to detect the expression of HIF1alpha in normal bile duct and cholangiocarcinoma tissues, and in corresponding cells lines. Cell counting kit 8, scratch, and Transwell assays were used to detect the proliferation, migration and invasion of cholangiocarcinoma cells. Cell cycle distribution and apoptosis were detected by flow cytometry. ChIP, dual luciferase reporter gene assay, RNA pull-down, and RNA immunoprecipitation were used to verify relationship between HIF1alpha and lncRNA H19, and lncRNA H19 and miR-612. We also monitored tumor formation in nude mice to verify the effect of HIF1alpha on cholangiocarcinoma. HIF1alpha expression was elevated in cholangiocarcinoma tissues and cells. Silencing HIF1alpha reduced proliferation, migration, and invasion of cholangiocarcinoma cells. HIF1alpha transcriptionally activated the expression of lncRNA H19. Overexpression of miR-612 could rescue the proliferation, migration and invasion of cholangiocarcinoma cells caused by lncRNA H19 overexpression. Taken together, HIF1alpha activated lncRNA H19-mediated miR-612/Bcl-2 pathway to promote cholangiocarcinoma, suggesting a promising therapeutic target for cholangiocarcinoma.HIF1a transcriptionally activated the expression of lncRNA H19.	32505707	RID03943	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(NSCLC);DATA(GSE74639)
Cholangiocarcinoma	H19	BCL2	positively-E	dual-luciferase reporter analysis;ChIP;RNA pull-down assay;RIP	upregulation	RT-qPCR;microarray	GSE45001;GSE32225	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-612)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000171791	NA	283120	596	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Bcl-2|PPP1R50	Transcription factor HIF1alpha promotes proliferation, migration, and invasion of cholangiocarcinoma via long noncoding RNA H19/microRNA-612/Bcl-2 axis.Cholangiocarcinoma, which is the most common invasive malignant tumor of the biliary tract, has poor prognosis. There is evidence suggesting that hypoxia-inducible factor 1alpha (HIF1alpha) plays an important role in cholangiocarcinoma. Also, microRNA-612 (miR-612) is another key regulator of cholangiocarcinoma. In this study, we investigate the scantly documented interaction of HIF1alpha and miR-612 in cholangiocarcinoma. We first undertook microarray-based cholangiocarcinoma gene expression profiles to screen out the differentially expressed long noncoding RNAs (lncRNAs) and genes. We used reverse transcription quantitative polymerase chain reaction to detect the expression of HIF1alpha in normal bile duct and cholangiocarcinoma tissues, and in corresponding cells lines. Cell counting kit 8, scratch, and Transwell assays were used to detect the proliferation, migration and invasion of cholangiocarcinoma cells. Cell cycle distribution and apoptosis were detected by flow cytometry. ChIP, dual luciferase reporter gene assay, RNA pull-down, and RNA immunoprecipitation were used to verify relationship between HIF1alpha and lncRNA H19, and lncRNA H19 and miR-612. We also monitored tumor formation in nude mice to verify the effect of HIF1alpha on cholangiocarcinoma. HIF1alpha expression was elevated in cholangiocarcinoma tissues and cells. Silencing HIF1alpha reduced proliferation, migration, and invasion of cholangiocarcinoma cells. HIF1alpha transcriptionally activated the expression of lncRNA H19. Overexpression of miR-612 could rescue the proliferation, migration and invasion of cholangiocarcinoma cells caused by lncRNA H19 overexpression.	32505707	RID03944	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Endometrial cancer	AFAP1-AS1	VEGFA	positively-E	luciferase reporter assay;miRDB;RIP;Targetscan	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-545-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000112715	NA	84740	7422	AFAP1-AS|AFAP1AS|MGC10981	VEGF|VEGF-A|VPF	LncRNA AFAP1-AS1 contributes to the progression of endometrial carcinoma by regulating miR-545-3p/VEGFA pathway.Endometrial carcinoma (EC) accounts for 20%-30% of female reproductive tumors. Targeted therapy for EC has shown great advantages with small side effects. To improve the survival of EC patients, more new therapeutic targets need to be found. Long non-coding RNAs (lncRNAs) are series of RNAs with over 200 nucleotides that regulate various cellular functions. LncRNA actin filamentin-1 antisense RNA 1 (AFAP1-AS1) is involved in the development of a variety of cancers, such as pancreas ductal adenocarcinoma and esophageal adenocarcinoma. However, it is not clear whether AFAP1-AS1 has any effects on EC or the exact regulatory mechanism. Herein, we found the high expression of AFAP1-AS1 in human EC tissues, and AFAP1-AS1 was correlated with EC patients' prognosis and clinical features. AFAP-AS1 could affect EC cell proliferation, migration, and invasion, and contributed to endothelial cell angiogenesis. We further showed that AFAP-AS1 could promote the expression of VEGFA through the adsorption of miR-545-3p, thus promoting the angiogenesis and invasion of EC, and contribute to tumor growth and metastasis in vivo. Thus, we thought AFAP1-AS1 had the potential to serve as an EC therapeutic target.qPCR results displayed enhanced expression of AFAP1-AS1 in tumor tissues.	32504788	RID03945	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Melanoma	LINC00520	EIF5A2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;sequencing	GSE15605;GSE34460;GSE24996;TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000163577	NA	645687	56648	C14orf34|LASSIE	NA	Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis.Background: Long intergenic non-protein coding RNA 520 (LINC00520), a novel identified lncRNA, has been shown to modulate the malignant phenotype of tumor cells in some malignant tumors. However, the exact role and molecular mechanism of LINC00520 in malignant melanoma has not been studied.Methods: The expression of LINC00520 in melanoma tissues were detected by using RNA-seq analysis and qRT-PCR Melanoma cases from the public databases (The Cancer Genome Atlas (TCGA), GEO#GSE15605, GEO#GSE34460 and GEO#GSE24996) were included in this study. CCK-8 assay, EdU assay, transwell and scratch wound assay were used to explore the role of LINC00520 in melanoma cells. Luciferase reporter assays, MS2-RIP, RNA pull-down and RNA-ChIP assay were used to demonstrate the molecular biological mechanism of LINC00520 in melanoma.Results: We found that LICN00520 was found to be overexpressed in melanoma tissue. High expression of LICN00520 is a risk factor for the prognosis of melanoma patients. LINC00520 promotes the proliferation, invasion and migration of melanoma cells. LICN00520 exerted its oncogenic role by competitive binding miR-125b-5p to promote Eukaryotic initiation factor 5A2 (EIF5A2) expression. We also showed that LICN00520 promotes the growth and metastasis of melanoma in vivo through regulating miR-125b-5p/EIF5A2 axis.Conclusions: All results elucidated the role and molecular mechanism of LINC00520 in the malignant development of melanoma. LINC00520, a new oncogene in melanoma, maybe serve as a survival biomarkers or therapeutic target for melanoma patients.	32466797	RID03946	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE51827,GSE86978)
Cervical cancer	PITPNA-AS1	c-MET	positively-E	TargetScan;miRDB;RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-876-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000236618	GRCh38_17:1516877-1518101	NA	NA	100306951	NA	NA	NA	In the study, we found that PITPNA-AS1 was markedly increased in human cervical cancer tissues and cell lines. PITPNA-AS1 over-expression elevated the proliferation of cervical cancer cells, whereas PITPNA-AS1 knockdown reduced the cell proliferation. Moreover, PITPNA-AS1 knockdown markedly accelerated the G0/G1 and reduced the G2/M phase transitions through decreasing the cyclin-dependent kinase (CDK)-2/4/6 and CyclinD1 expression levels. In addition, apoptosis was significantly induced by PITPNA-AS1 knockdown in cervical cancer cells. Importantly, PITPNA-AS1 was identified as the sponge of miR-876-5p, and a negative correlation was detected between PITPNA-AS1 and miR-876-5p in cervical cancer samples. Moreover, tyrosine-protein kinase MET (c-MET) was identified to be a down-streaming target gene of miR-876-5p in cervical cancer cells. PITPNA-AS1 meditated the effects of c-MET on the proliferation, apoptosis and cell cycle in cervical cancer cells by adsorbing miR-876-5p. In summary, targeting the PITPNA-AS1-associated signaling could be a therapeutic strategy for the treatment of cervical cancer.Luciferase reporter assay displayed a significantly reduced luciferase activity of PITPNAAS1-WT induced by the miR-876-5p mimic in cervical cancer cells. However, miR-876-5p mimic had no influences on luciferase activity when the cervical cancer cells were co-transfected with PITPNA-AS1- MUT, indicating that PITPNA-AS1 directly bound to miR-876-5p (Fig. 3I). RIP analysis demonstrated that PITPNA-AS1 and miR-876-5p were preferentially enriched in the anti-AGO2 group compared to the IgG control group (Fig. 3J and K). Therefore, PITPNA-AS1 could sponge miR-876-5p, which was a tumor suppressor in cervical cancer.	32460193	RID03947	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)	
Gastric cancer	CircFOXO3	USP44	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);tumor growth(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	circRNA	PCG	NA	NA	ENSG00000136014	NA	NA	84101	NA	NA	CircFOXO3 functions as a molecular sponge for miR-143-3p to promote the progression of gastric carcinoma via upregulating USP44.Gastric carcinoma (GC) ranks fifth in terms of cancer morbidity and third in cancer-related death worldwide and imposes enormous health and economic burdens. The molecular mechanisms underlying GC formation and progression remain unclear. Our aim was to identify the involvement of circular RNA circFOXO3 in GC, and to determine the underlying mechanisms. In this study, we revealed a stimulatory role of circular RNA circFOXO3 in tumor growth in vivo. CircFOXO3 enhanced GC cell proliferation and migration in vitro and promoted tumor growth of GC cells in vivo. Bioinformatic analysis revealed that circFOXO3 might regulate USP44 expression by specifically binding to microRNA (miR)-143-3p. Existence of circFOXO3-miR-143-3p-USP44 axis in GC cells was confirmed by RNA-binding protein immunoprecipitation, luciferase reporter assay, and an RNA pull-down experiments. All the data indicate that circFOXO3 promotes GC cell proliferation and migration by upregulating USP44 expression via targeting of miR-143-3p.	32445925	RID03948	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	MYC	SNHG11	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000174365	GRCh38_20:38446343-38450940	4609	128439	bHLHe39|c-Myc|MYCC	C20orf198|LINC00101	SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc.Dysregulation of long non-coding RNAs (lncRNA) have long been linked to the onset and development of colorectal cancer (CRC), yet the underlying mechanisms remain elusive. Small nucleolar RNA host gene 11 (SNHG11) is a novel lncRNA with few information about its role in development and progression of CRC. Here, we found SNHG11, a highly conserved lncRNA, was commonly overexpressed in various cancer including CRC. High expression of SNHG11 correlated with poor prognosis in patients with CRC. Gain of function and loss-of function experiments showed that SNHG11 visibly promoted proliferation in CRC cells. Mechanistic assays revealed that SNHG11 interacted with Insulin-like growth factor 2 (IGF2) mRNA-binding protein 1 (IGF2BP1), thereby enhancing the interaction between IGF2BP1 and c-Myc mRNA, a well-known target of IGF2BP1. Consequently, c-Myc mRNA expression was stabilized and its downstream targets were significantly upregulated. Further investigation demonstrated that SNHG11 upregulated c-Myc which in turn transcriptionally upregulated SNHG11. Taken together, our findings suggested that reciprocal regulation of SNHG11 and c-Myc promotes cell proliferation in CRC. Luciferase activity from the wide type, but not the mutant reporter, was significantly increased by c-Myc overexpression (Fig. 4G). Conversely, luciferase activity from the wide type, but not the mutant reporter, was significantly decreased by c-Myc downregulation (Fig. 4G). These data demonstrate that SNHG11 is transcriptionally regulated by c-Myc.	32439170	RID03949	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842)
Colorectal cancer	SNHG11	MYC	positively-E	StarBase;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000174365	GRCh38_20:38446343-38450940	ENSG00000136997	NA	128439	4609	C20orf198|LINC00101	bHLHe39|c-Myc|MYCC	SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc.Dysregulation of long non-coding RNAs (lncRNA) have long been linked to the onset and development of colorectal cancer (CRC), yet the underlying mechanisms remain elusive. Small nucleolar RNA host gene 11 (SNHG11) is a novel lncRNA with few information about its role in development and progression of CRC. Here, we found SNHG11, a highly conserved lncRNA, was commonly overexpressed in various cancer including CRC. High expression of SNHG11 correlated with poor prognosis in patients with CRC. Gain of function and loss-of function experiments showed that SNHG11 visibly promoted proliferation in CRC cells. Mechanistic assays revealed that SNHG11 interacted with Insulin-like growth factor 2 (IGF2) mRNA-binding protein 1 (IGF2BP1), thereby enhancing the interaction between IGF2BP1 and c-Myc mRNA, a well-known target of IGF2BP1. Consequently, c-Myc mRNA expression was stabilized and its downstream targets were significantly upregulated. Further investigation demonstrated that SNHG11 upregulated c-Myc which in turn transcriptionally upregulated SNHG11. Taken together, our findings suggested that reciprocal regulation of SNHG11 and c-Myc promotes cell proliferation in CRC.	32439170	RID03950	interact with protein	prognosis	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Bone volume inadequacy	H19	APC	positively-E	dual-luciferase reporter analysis	upregulation	RT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell differentiation(+)	ceRNA(miR-675)	regulation	RNA-protein	NA	CSC	NA	Other	Bone volume inadequacy	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000134982	NA	283120	324	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	DP2|DP2.5|DP3|PPP1R46	Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of human bone marrow mesenchymal stem cells via H19/miR-675/APC axis.Bone volume inadequacy is an emerging clinical problem impairing the feasibility and longevity of dental implants. Human bone marrow mesenchymal stem cells (HBMSCs) have been widely used in bone remodeling and regeneration. This study examined the effect of long noncoding RNAs (lncRNAs)-H19 on the human amnion-derived mesenchymal stem cells (HAMSCs)-droved osteogenesis in HBMSCs. HAMSCs and HBMSCs were isolated from abandoned amniotic membrane samples and bone marrow. The coculture system was conducted using transwells, and H19 level was measured by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR. The mechanism was further verified. We here discovered that osteogenesis of HBMSCs was induced by HAMSCs, while H19 level in HAMSCs was increased during coculturing. H19 had no significant effect on the proliferative behaviors of HBMSCs, while its overexpression of H19 in HAMSCs led to the upregulated osteogenesis of HBMSCs in vivo and in vitro; whereas its knockdown reversed these effects. Mechanistically, H19 promoted miR-675 expression and contributed to the competitively bounding of miR-675 and Adenomatous polyposis coli (APC), thus significantly activating the Wnt/beta-catenin pathway. The results suggested that HAMSCs promote osteogenic differentiation of HBMSCs via H19/miR-675/APC pathway, and supply a potential target for the therapeutic treatment of bone-destructive diseases.	32434960	RID03951	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Hepatocellular carcinoma	HAGLR	SLC27A4	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000167114	NA	401022	10999	HOXD-AS1|Mdgt|MIR7704HG	ACSVL4|FATP4	LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4.Background: Mounting evidences have indicated that long non-coding RNA (lncRNA) HOXD cluster antisense RNA 1 (HOXD-AS1) is dysregulated and participates into the progression of cancers. This study aims to investigate the biological roles and mechanisms of HOXD-AS1 in the metastasis of hepatocellular carcinoma (HCC).western blotconfirmed the knockdown efficiency of SLC27A4 in two cell lines.Methods: The quantitative real-time PCR (qPCR) assay was used to assess the level of miR-326 and HOXD-AS1 in HCC tissues and cell lines. The growth of HCC cell was analyzed by using CCK-8 assay and colony formation assay. The migration and invasion of HCC cell were investigated by using wound healing and transwell invasion analysis. The expressions of SLC27A4, N-cadherin and E-cadherin were determined by western blot. The growth of HCC cell in vivo was assessed by using xenograft model.Results: Here, we elaborated that HOXD-AS1 was overexpressed in HCC tissues than that in the adjacent normal tissues and the level of HOXD-AS1 was related with the aggressive phenotypes of HCC. Functionally, downregulation of HOXD-AS1 repressed the proliferation, invasion abilities of HCC cell in vitro and the distant metastasis of HCC cell in vivo. Further investigations demonstrated that HOXD-AS1 directly bound with miR-326 and thereby regulated its endogenous target gene, solute carrier family 27 member 4 (SLC27A4).Conclusions: All these findings indicated that HOXD-AS1-miR-326-SLC27A4 axis participated into the progression of HCC.	32425696	RID03952	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Glaucoma	TGFbeta2-AS1	TGFB2	positively-E	knockdown	downregulation	qRT-PCR	NA	NA	ECM deposition(+);TGF-beta signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Glaucoma	lncRNA	PCG	NA	NA	ENSG00000092969	NA	NA	7042	NA	G-TSF|LDS4|TGF-beta2	lncRNA TGFbeta2-AS1 promotes ECM production via TGF-beta2 in human trabecular meshwork cells.Evidence indicates that long noncoding RNAs (lncRNAs) participate in the regulation of various physiological and pathological processes including organ fibrosis and eye-related diseases. The important pathological manifestations of open-angle glaucoma (OAG) are human trabecular meshwork cells (HTMCs) apoptosis and excessive deposition of extracellular matrix (ECM) components in TM, which can cause pathological changes in the outflow pathway. To investigate the role and regulation mechanism of lncRNA in HTMCs under oxidative stress, we established an oxidative stress model in HTMCs using hydrogen peroxide (H2O2) followed by RNA sequencing and found that subsets of lncRNAs and mRNAs that closely associate with TGF-beta signaling are differentially regulated in these cells. We then constructed a network with the TGF-beta2 -colocalized and -coexpressed lncRNAs, to investigate the effects and regulatory mechanisms of the potential lncRNAs on ECM deposition in HTMCs. The gain-of-function and loss-of-function experiments demonstrated that lnc-TGFbeta2-AS1 promotes ECM production via TGF-beta2 in HTMC, suggesting that lnc-TGFbeta2-AS1 may be a potential glaucoma treatment target.	32423825	RID03953	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	DSCAM-AS1	HMGB1	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-577)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000189403	NA	100506492	3146	M41	DKFZp686A04236|HMG1|HMG3|SBP-1	LncRNA DSCAM-AS1 promotes non-small cell lung cancer progression via regulating miR-577/HMGB1 axis.Non-small cell lung cancer (NSCLC) is a major source of cancer mortality. Long non-coding RNA DSCAM-AS1 has been certified to be involved in the pathogenesis of NSCLC. This study aimed to further investigate the potential mechanism of DSCAM-AS1 in NSCLC progression. The expressions of DSCAM-AS1, miR-577, and high mobility group box 1 (HMGB1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR or western blot assay. Cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. Flow cytometry assay was conducted to monitor cell apoptosis. Cell migration and invasion were measured by transwell assay. Wnt/beta-catenin pathway-related factors were detected by western blot assay. The relationship between DSCAM-AS1, miR-577, and HMGB1 was validated by bioinformatics analysis and dual-luciferase reporter assay. The xenograft mouse model was established to analyze tumor growth in vivo. DSCAM-AS1 and HMGB1 were upregulated, while miR-577 was downregulated in NSCLC tissues and cells. DSCAM-AS1 promoted cell proliferation, migration and invasion, and restrained cell apoptosis in NSCLC cells. Overexpression of HMGB1 reversed the effects of DSCAM-AS1 depletion on the progression of NSCLC. DSCAM-AS1 modulated HMGB1 expression by sponging miR-577. DSCAM-AS1 regulated the Wnt/beta-catenin pathway by regulating miR-577 and HMGB1. DSCAM-AS1 knockdown blocked the tumor growth in vivo. In conclusion, DSCAM-AS1 facilitated NSCLC progression by regulating the HMGB1-mediated Wnt/beta-catenin pathway, providing a promising therapeutic target for NSCLC.	32386483	RID03954	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Triple-negative breast cancer	AFAP1-AS1	NUDT1	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-145)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000106268	NA	84740	4521	AFAP1-AS|AFAP1AS|MGC10981	MTH1	lncRNA AFAP1-AS1 promotes triple negative breast cancer cell proliferation and invasion via targeting miR-145 to regulate MTH1 expression.The actin fiber-associated protein 1-antisense RNA1 (AFAP1-AS1) is upregulated in various cancers and associated with cancer proliferation and metastasis. Several cancer-related pathways have been linked to up-expression of this long non-coding (lnc)RNA, but the underlying mechanisms are yet unknown. In triple negative breast cancer (TNBC), AFAP1-AS1 expression is also significantly overexpressed compared to that in other subtypes of breast cancer from the TCGA dataset. In this study, we performed bioinformatic RNAhybrid analyses and identified that miR-145 is a potential target of AFAP1-AS1 and able to reduce MutT homolog-1 (MTH1) expression. Thus, this study investigated the oncogenic activity of AFAP1-AS1 in TNBC cells and the underlying mechanisms that are yet poorly understood. The results showed that miR-145 expression was low, whereas AFAP1-AS1 and MTH1 expression was high in TNBC cells and that miR-145 mimics reduced TNBC cell proliferation and invasion, whereas miR-145 knockdown exerted the opposite activity in TNBC cells. Moreover, knockdown of AFAP1-AS1 reduced tumor cell proliferation and invasion, but miR-145 co-transfection rescued tumor cell viability and colony formation ability. The dual-luciferase reporter assay showed that AFAP1-AS1 could directly target miR-145, while miR-145 could directly target MTH1. After knockdown of ATF6, AFAP1-AS1 was reduced along with AFAP1-AS1 promoter activity. This study revealed that AFAP1-AS1 could promote TNBC cell proliferation and invasion via regulation of MTH1 expression through targeting of miR-145.	32376943	RID03955	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE111842)
Osteogenic differentiation	LINC02349	SMAD5	positively-E	luciferase reporter analysis;RIP	upregulation	qPCR	NA	NA	cell differentiation(+);Dlx5/OSX signaling pathway(+)	ceRNA(miR-25-3p)	regulation	NA	NA	CSC	NA	Other	Osteogenic differentiation	lncRNA	TF	ENSG00000259284	GRCh38_15:61729765-61731389	ENSG00000113658	NA	100506530	4090	NA	Dwfc|JV5-1|MADH5	Linc02349 promotes osteogenesis of human umbilical cord-derived stem cells by acting as a competing endogenous RNA for miR-25-3p and miR-33b-5p.Objectives: Increasing evidences suggest that inducing mesenchymal stem cells to differentiate into osteoblasts has been as an especially important component in the prevention and therapy for degenerative bone disease. Here, we identify a novel lncRNA, linc02349, which increases significantly during osteogenic differentiation.Materials and methods: Human umbilical cord-derived stem cells (hUC-MSCs) and dental pulp mesenchymal stem cells were used. Overexpression and knockdown of linc02349 in cell lines were generated using lentiviral-mediated gene delivery method. Bioinformatics prediction, Ago2-RIP assay and dual-luciferase reporter system were employed to examine miRNA which interacts with linc02349. The RNA FISH assay was performed to identify the subcelluar location of linc02349. Alizarin Red S staining, ALP staining and qPCR were applied to identify the osteogenic differentiation. The potential linc02349-regulated genes, miR-25-3p and miR-33b-5p, were explored by ChIP, RIP and western blot assays. Micro-CT was used to measure the osteogenic content in bone formation assay in vivo.Results: Linc02349 overexpression improves osteogenic differentiation by in vitro and in vivo analysis. Mechanistically, linc02349 acts as a molecular sponge for miR-25-3p and miR-33b-5p to control expression abundance of SMAD5 and Wnt10b, respectively, which eventually activated Dlx5/OSX pathway and hence promoted osteogenic differentiation. In addition, we revealed that STAT3 interacts with linc02349 promoter region and positively regulates the linc02349 transcriptional activity.Conclusion: These findings identify that linc02349 modulates the osteogenic differentiation through acting as a sponge RNA of miR-25-3p and miR-33b-5p and regulating SMAD5 and Wnt10b, and proposed a new interaction between STAT3 and linc02349, which could be a potential target in the process the osteogenesis of hUC-MSCs for future clinical application.	32346990	RID03956	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Osteogenic differentiation	LINC02349	WNT10B	positively-E	luciferase reporter analysis;RIP	upregulation	qPCR	NA	NA	cell differentiation(+);Dlx5/OSX signaling pathway(+)	ceRNA(miR-33b-5p)	regulation	RNA-protein	NA	CSC	NA	Other	Osteogenic differentiation	lncRNA	PCG	ENSG00000259284	GRCh38_15:61729765-61731389	ENSG00000169884	NA	100506530	7480	NA	SHFM6|WNT-12	Linc02349 promotes osteogenesis of human umbilical cord-derived stem cells by acting as a competing endogenous RNA for miR-25-3p and miR-33b-5p.Objectives: Increasing evidences suggest that inducing mesenchymal stem cells to differentiate into osteoblasts has been as an especially important component in the prevention and therapy for degenerative bone disease. Here, we identify a novel lncRNA, linc02349, which increases significantly during osteogenic differentiation.Materials and methods: Human umbilical cord-derived stem cells (hUC-MSCs) and dental pulp mesenchymal stem cells were used. Overexpression and knockdown of linc02349 in cell lines were generated using lentiviral-mediated gene delivery method. Bioinformatics prediction, Ago2-RIP assay and dual-luciferase reporter system were employed to examine miRNA which interacts with linc02349. The RNA FISH assay was performed to identify the subcelluar location of linc02349. Alizarin Red S staining, ALP staining and qPCR were applied to identify the osteogenic differentiation. The potential linc02349-regulated genes, miR-25-3p and miR-33b-5p, were explored by ChIP, RIP and western blot assays. Micro-CT was used to measure the osteogenic content in bone formation assay in vivo.Results: Linc02349 overexpression improves osteogenic differentiation by in vitro and in vivo analysis. Mechanistically, linc02349 acts as a molecular sponge for miR-25-3p and miR-33b-5p to control expression abundance of SMAD5 and Wnt10b, respectively, which eventually activated Dlx5/OSX pathway and hence promoted osteogenic differentiation. In addition, we revealed that STAT3 interacts with linc02349 promoter region and positively regulates the linc02349 transcriptional activity.Conclusion: These findings identify that linc02349 modulates the osteogenic differentiation through acting as a sponge RNA of miR-25-3p and miR-33b-5p and regulating SMAD5 and Wnt10b, and proposed a new interaction between STAT3 and linc02349, which could be a potential target in the process the osteogenesis of hUC-MSCs for future clinical application.	32346990	RID03957	ceRNA or sponge	NA		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE67939,GSE75367,GSE86978)
Osteogenic differentiation	STAT3	LINC02349	positively-E	Chip-qPCR;luciferase reporter assay	upregulation	qPCR	NA	NA	cell differentiation(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Other	Osteogenic differentiation	TF	lncRNA	ENSG00000168610	NA	ENSG00000259284	GRCh38_15:61729765-61731389	6774	100506530	APRF	NA	Linc02349 promotes osteogenesis of human umbilical cord-derived stem cells by acting as a competing endogenous RNA for miR-25-3p and miR-33b-5p.Objectives: Increasing evidences suggest that inducing mesenchymal stem cells to differentiate into osteoblasts has been as an especially important component in the prevention and therapy for degenerative bone disease. Here, we identify a novel lncRNA, linc02349, which increases significantly during osteogenic differentiation.Materials and methods: Human umbilical cord-derived stem cells (hUC-MSCs) and dental pulp mesenchymal stem cells were used. Overexpression and knockdown of linc02349 in cell lines were generated using lentiviral-mediated gene delivery method. Bioinformatics prediction, Ago2-RIP assay and dual-luciferase reporter system were employed to examine miRNA which interacts with linc02349. The RNA FISH assay was performed to identify the subcelluar location of linc02349. Alizarin Red S staining, ALP staining and qPCR were applied to identify the osteogenic differentiation. The potential linc02349-regulated genes, miR-25-3p and miR-33b-5p, were explored by ChIP, RIP and western blot assays. Micro-CT was used to measure the osteogenic content in bone formation assay in vivo.Results: Linc02349 overexpression improves osteogenic differentiation by in vitro and in vivo analysis. Mechanistically, linc02349 acts as a molecular sponge for miR-25-3p and miR-33b-5p to control expression abundance of SMAD5 and Wnt10b, respectively, which eventually activated Dlx5/OSX pathway and hence promoted osteogenic differentiation. In addition, we revealed that STAT3 interacts with linc02349 promoter region and positively regulates the linc02349 transcriptional activity.Conclusion: These findings identify that linc02349 modulates the osteogenic differentiation through acting as a sponge RNA of miR-25-3p and miR-33b-5p and regulating SMAD5 and Wnt10b, and proposed a new interaction between STAT3 and linc02349, which could be a potential target in the process the osteogenesis of hUC-MSCs for future clinical application.	32346990	RID03958	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Sepsis-induced acute kidney injury<U+00A0>	B4GALT1-AS1	FOXA1	positively-E	dual-luciferase reporter analysis;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-96)	regulation	NA	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	TF	ENSG00000233554	GRCh38_9:33166948-33182865	ENSG00000129514	NA	101929639	3169	NA	HNF3A|TCF3A	SIKIAT1/miR-96/FOXA1 axis regulates sepsis-induced kidney injury through induction of apoptosis.Objective and design Nowadays, sepsis-induced acute kidney injury (AKI) has gradually become a global problem for its high incidence and increasing mortality. Previous study has reported lncRNA ENST00000452391.1 in sepsis patients. However, its potential biological function and downstream molecular mechanism are still mysterious. Methods and results Our study found that it was upregulated in sepsis-induced AKI patients, so it was identifed as "Sepsisinduced kidney injury associated transcript 1 (SIKIAT1)'- We used lipopolysaccharide (LPS) stimulated HK-2 cells as an in vitro model to demonstrated that SIKIAT1 acts as a ceRNA for miR-96-3p to enhance FOXA1 expression and promote HK-2 cell apoptosis. Conclusion Therefore, it could be a potential biomarker and therapeutic target for sepsis-induced AKI in the development of disease.	32342116	RID03959	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Asthma	MALAT1	CTLA4	NA		upregulation		NA	NA	cell differentiation(+)	ceRNA(miR-155)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163599	NA	378938	1493	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CD|CD152|CELIAC3|CTLA-4|GSE|IDDM12	Commentary on: The potency of lncRNA MALAT1/miR-155 in altering asthmatic Th1/Th2 balance by modulation of CTLA4.Asthma is a common, allergic respiratory disorder affecting over 350 million people worldwide. One of the key features of asthma is skewing of CD4+ cells toward Th2 responses. This promotes the production of cytokines like IL-4 that induce IgE production resulting in the hypersecretion of mucus and airway smooth muscle contraction. Understanding the factors that favor Th2 expansion in asthma would provide important insights into the underlying pathogenesis of this disorder. Asthma research has focused on signaling pathways that control the transcription of key asthma-related genes. However, increasing evidence shows that post-transcriptional factors also determine CD4+ cell fate and the enhancement of allergic airway responses. A recent paper published by Liang et al. (Bioscience Reports (2020) 40, https://doi.org/10.1042/BSR20190397) highlights a novel role for the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in Th2 development in asthma. MALAT1 modulates several biological processes including alternative splicing, epigenetic modification and gene expression. It is one of the most highly expressed lncRNAs in normal tissues and MALAT1 levels correlate with poor clinical outcomes in cancer. The mechanisms of action of MALAT1 in tumor progression and metastasis remain unclear and even less is known about its effects in inflammatory disease states like asthma. The work of Liang et al. demonstrates heightened MALAT1 expression in asthma and further shows that this lncRNA targets miR-155 to promote Th2 differentiation in this disease. This insight sets the stage for future studies to examine how MALAT1 manipulation could deter allergic immune responses in asthmatic airways.	32292999	RID03960	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pancreatic beta cell inflammation	Lnc13	STAT1	positively-E	RIP	upregulation	qPCR	NA	NA	inflammatory response(+)	interact with protein	regulation	NA	NA	NA	NA	Other	Pancreatic beta cell inflammation	lncRNA	TF	NA	NA	ENSG00000115415	NA	NA	6772	NA	ISGF-3|STAT91	The T1D-associated lncRNA Lnc13 modulates human pancreatic beta cell inflammation by allele-specific stabilization of STAT1 mRNA.Taking together, these results indicate that Lnc13 enhances STAT1 expression levels by stabilizing its mRNA in the cytoplasm through interaction with the RNA-binding protein PCBP2.	32284404	RID03961	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hypoxia/reoxygenation injury of cardiomyocytes	LINC-ROR	MST1	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-138)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000173531	NA	100885779	4485	lincRNA-RoR|lincRNA-ST8SIA3|ROR	D3F15S2|DNF15S2|HGFL|MSP|NF15S2	Long non-coding RNA ROR sponges miR-138 to aggravate hypoxia/reoxygenation-induced cardiomyocyte apoptosis via upregulating Mst1.Background: Hypoxia/reoxygenation (H/R) injury of cardiomyocytes causes an irreversible damage to heart and largely results in acute myocardial infarction. Study has indicated lncRNA ROR aggravates myocardial ischemia/reperfusion (I/R) injury. Also, lncRNA ROR sponges miR-138 to promote osteogenesis. MiR-138 involves in hypoxic pulmonary vascular remodelling by targeting Mst1. However, the interaction between lncRNA ROR, miR-138 and Mst1 involved in myocardial H/R injury is still unknown.Methods: H9C2 cells were used to establish H/R injury model. The expression levels of lncRNA ROR and miR-138 were modified by transfection with the miR-138 mimics or lncRNA ROR overexpression plasmid. MTT and flow cytometry analysis were performed to detect cell proliferation and apoptosis. dual-luciferase reporter assay was used to determine interaction between lncRNA ROR and miR-138 or miR-138 and Mst1. Expression levels of lncRNA ROR, miR-138, Mst1 and apoptosis-related markers were determined by qRT-PCRor western blot.Results: LncRNA ROR was significantly up-regulated, while miR-138 was obviously down-regulated in H/R-induced injury of H9C2 cells. Furthermore, miR-138 overexpression alleviated cardiac cell apoptosis induced by H/R injury. Mst1 was revealed to be a target of miR-138 and negatively regulated by miR-138. Mst1 overexpression reversed the protective effects of miR-138 on H/R injury of H9C2 cells. LncRNA ROR was identified as a sponge for miR-138. MiR-138 could protect H9C2 cells form H/R injury induced by lncRNA ROR overexpression.Conclusion: Our study provides that lncRNA ROR sponges miR-138 to aggravate H/R-induced myocardial cell injury by upregulating the expression of Mst1.	32240614	RID03962	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Intrahepatic cholangiocarcinoma	ZEB1-AS1	ZEB1	positively-E	RT-qPCR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);tumorigenesis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long non-coding RNA ZEB1-AS1 predicts a poor prognosis and promotes cancer progression through the miR-200a/ZEB1 signaling pathway in intrahepatic cholangiocarcinoma.Emerging evidence suggests that long non-coding RNAs (lncRNAs) play pivotal roles in cancer progression, including in intrahepatic cholangiocarcinoma (IHCC). The overexpression of lncRNA ZEB1 antisense 1 (ZEB1-AS1) has been discovered in several types of cancer; however, the clinical significance and functional role of ZEB1-AS1 in IHCC have not yet been determined. In the present study, ZEB1-AS1 was found to be upregulated in IHCC cell lines and tissues. A high ZEB1-AS1 expression was associated with clinical progression and a poor survival of patients with IHCC, and was identified as an independent risk factor for a poor prognosis. In addition, ZEB1-AS1 promoted the proliferation and metastasis of IHCC cells both in vitro and in vivo. ZEB1-AS1 was demonstrated to increase the expression of ZEB1 by sponging miR-200a and to thereby accelerate epithelial-mesenchymal transition (EMT). On the whole, the findings of the present study demonstrate that ZEB1-AS1 promotes proliferation and metastasis in IHCC, and induces EMT through the miR-200a/ZEB1 signaling pathway. ZEB1-AS1 may thus be a promising prognostic biomarker and essential therapeutic target for IHCC.	32236578	RID03963	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	CRNDE	RAP1A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-101)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000116473	NA	643911	5906	CRNDEP|LINC00180|LOC643911	KREV-1|SMGP21	Long noncoding RNA CRNDE promotes proliferation, migration and invasion in prostate cancer through miR-101/Rap1A.Prostate cancer (Pca) is the second frequent malignancy in men. Long noncoding RNAs (lncRNAs) have been reported to play essential roles in the progression of cancers, including Pca. LncRNA colorectal neoplasia differentially expressed (CRNDE) has been found to affect tumorigenesis in many cancers. However, the exact role and mechanism of CRNDE in Pca remain poorly understood. 64 Pca patients were recruited in this study. PC3 and 22RV1 cells were used in vitro experiments. The expressions of CRNDE, microRNA-101 (miR-101), and Ras-related protein 1A (Rap1A) were detected in vivo and in vitro by quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation, apoptosis, migration, and invasion were investigated through cell counting kit-8, flow cytometry, and Transwell assays, respectively. The interaction between miR-101 and CRNDE or Rap1A was explored by bioinformatics analysis and luciferase reporter assay. High expression of CRNDE was shown in Pca tissues and cells and predicted poor outcomes of patients. Overexpression of CRNDE promoted cell proliferation, migration, and invasion but decreased apoptosis in Pca cells, while its knockdown showed an opposite effect. CRNDE was a decoy of miR-101 and its effect on Pca progression was reversed by miR-101. Rap1A was identified as a target of miR-101 and it attenuated the effect of miR-101 on Pca development. Moreover, the Rap1A protein level was positively regulated by CRNDE, which was weakened by miR-101. CRNDE contributed to cell proliferation, migration, and invasion by regulating the miR-101/Rap1A axis in Pca, providing a novel strategy for Pca treatment.	32182086	RID03964	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Lower respiratory tract disease	NRAV	RAB5C	positively-E	qRT-PCR;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);vesicle transport(+)	ceRNA(miR-509-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Lower respiratory tract disease	lncRNA	PCG	ENSG00000248008	GRCh38_12:120488079-120495946	ENSG00000261378	NA	100506668	5878	DYNLL1-AS1	RAB5CL|RABL	Long Noncoding RNA NRAV Promotes Respiratory Syncytial Virus Replication by Targeting the MicroRNA miR-509-3p/Rab5c Axis To Regulate Vesicle Transportation.Respiratory syncytial virus (RSV) is an enveloped RNA virus which is responsible for approximately 80% of lower respiratory tract infections in children. Current lines of evidence have supported the functional involvement of long noncoding RNA (lncRNA) in many viral infectious diseases. However, the overall biological effect and clinical role of lncRNAs in RSV infection remain unclear. In this study, lncRNAs related to respiratory virus infection were obtained from the lncRNA database, and we collected 144 clinical sputum specimens to identify lncRNAs related to RSV infection. Quantitative PCR (qPCR) detection indicated that the expression of lncRNA negative regulator of antiviral response (NRAV) in RSV-positive patients was significantly lower than that in uninfected patients, but lncRNA psoriasis-associated non-protein coding RNA induced by stress (PRINS), nuclear paraspeckle assembly transcript 1 (NEAT1), and Nettoie Salmonella pas Theiler's (NeST) showed no difference in vivo and in vitro Meanwhile, overexpression of NRAV promoted RSV proliferation in A549 and BEAS-2B cells, and vice versa, indicating that the downregulation of NRAV was part of the host antiviral defense. RNA fluorescent in situ hybridization (FISH) confirmed that NRAV was mainly located in the cytoplasm. Through RNA sequencing, we found that Rab5c, which is a vesicle transporting protein, showed the same change trend as NRAV. Subsequent investigation revealed that NRAV was able to favor RSV production indirectly by sponging microRNA miR-509-3p so as to release Rab5c and facilitate vesicle transportation. The study provides a new insight into virus-host interaction through noncoding RNA, which may contribute to exploring potential antivirus targets for respiratory virus.IMPORTANCE The mechanism of interaction between RSV and host noncoding RNAs is not fully understood. In this study, we found that the expression of long noncoding RNA (lncRNA) negative regulator of antiviral response (NRAV) was reduced in RSV-infected patients, and overexpression of NRAV facilitated RSV production in vitro, suggesting that the reduction of NRAV in RSV infection was part of the host antiviral response. We also found that NRAV competed with vesicle protein Rab5c for microRNA miR509-3p in cytoplasm to promote RSV vesicle transport and accelerate RSV proliferation, thereby improving our understanding of the pathogenic mechanism of RSV infection.	32102886	RID03965	ceRNA or sponge	NA	UP(SKCM,BRCA);DATA(GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Myocardial injury	H19	IGF1	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	apoptosis process(-);cell injury(-);inflammatory response(-)	ceRNA(miR-29a)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000017427	NA	283120	3479	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	IGF|IGF-I|IGFI|MGF	Ghrelin protects against obesity-induced myocardial injury by regulating the lncRNA H19/miR-29a/IGF-1 signalling axis.Background: Obesity is associated with the impairment of cardiac fitness and consequent ventricular dysfunction and heart failure. Ghrelin has been largely documented to be cardioprotective against ischaemia/reperfusion injury. However, the role of ghrelin in obesity-induced myocardial injury is largely unknown. This study sought to determine the cardiac effect of ghrelin against obesity-induced injury and the underlying mechanisms.Methods: The effect of ghrelin was evaluated in a mouse model of obesity and a palmitic acid (PA)-treated cardiomyocyte cell line with or without ghrelin transfection. Gene and protein expression levels were determined by real-time PCR and western blot, respectively. Cell apoptosis was measured by flow cytometry analysis.Results: In the present study, we found that both a high-fat diet (HFD) and PA treatment caused myocardial injury by increasing apoptosis and the expression of inflammatory cytokines. Overexpression of ghrelin reversed the effects induced by HFD or PA treatment. Knockdown of lncRNA H19 or overexpression of miR-29a abrogated the cardioprotective effects of ghrelin against apoptosis and inflammation. We also found that IGF-1 was a target gene of miR-29a and that H19 regulated IGF-1 expression via miR-29a. Overexpression of IGF-1 partially reversed the apoptosis and inflammation promoting effects of miR-29a.Conclusions: Our findings suggested that ghrelin protected against obesity-induced myocardial injury by regulating the H19/miR-29a/IGF-1 signalling axis, providing further evidence for the clinical application of ghrelin.	32084395	RID03966	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DATA(GSE117623)
Myocardial injury	GHRL	H19	positively-E	western blot	upregulation	RT-PCR	NA	NA	apoptosis process(-);cell injury(-);inflammatory response(-)	transcriptional regulation	regulation	protein-RNA	NA	NA	Evading Apoptosis	Other	Injury	PCG	lncRNA	ENSG00000157017	NA	ENSG00000130600	GRCh38_11:1995171-2001470	51738	283120	ghrelin|MTLRP|obestatin	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Ghrelin protects against PA-induced injury in cardiomyocytes via upregulating the expression of lncRNA H19.To determine the role of H19 in the protection against PA-induced myocardial injury, we knocked down the H19 expression when ghrelin was overexpressed in HCM cells exposed to PA.	32084395	RID03967	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(NSCLC);DATA(GSE74639)
Osteosarcoma	OR3A4P	miR-1227-5p	negatively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell metastasis(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000180068	GRCh38_17:3309986-3311446	NA	NA	390756	NA	OR3A4	NA	Long noncoding RNA OR3A4 promotes the proliferation and invasion of osteosarcoma cells by sponging miR-1227-5p.Background: Long noncoding RNAs (lncRNAs) have been identified as key players in promoting tumourigenesis in osteosarcoma. LncRNA OR3A4 (OR3A4) has been reported as an oncogene in a number of tumours. However, the clinical value of OR3A4 in osteosarcoma and the role of OR3A4 in osteosarcoma progression are still unknown.Methods: The expression levels of OR3A4 in the tumour tissue of osteosarcoma patients and osteosarcoma cell lines were detected by RT-PCR Kaplan-Meier analysis and log-rank test were performed to evaluate the relationship between the level of OR3A4 expression and the prognosis of osteosarcoma patients. We investigated the association between the tissue expression levels of OR3A4 and different clinicopathological characteristics of osteosarcoma patients by Chi2 tests. Bioinformatic databases and luciferase reporter assays were used to predict and validate the target microRNA of OR3A4. Finally, the role of OR3A4 in the proliferation and invasion of osteosarcoma cells was tested by MTT and Transwell assays, respectively.Results: We observed that the expression level of OR3A4 was upregulated in the tumour tissue of osteosarcoma patients (p < 0.001) and osteosarcoma cell lines (p < 0.01) compared with the normal adjacent tissue and a normal human foetal osteoblastic cell line, respectively. The survival curve revealed that patients with high expression levels of OR3A4 had lower overall survival. Increased OR3A4 expression in osteosarcoma patients was associated with distant metastasis (p = 0.02) and advanced clinical stage (p < 0.001). In addition, bioinformatics analysis and luciferase reporter assays verified the complementary binding between OR3A4 and miR-1227-5p. Furthermore, we found that OR3A4 acted as a miR-1227-5p "sponge" to modulate osteosarcoma cell proliferation and invasion via downregulation of miR-1227-5p.Conclusion: OR3A4 promotes osteosarcoma cell proliferation and invasion by sponging miR-1227-5p, which might be related to the metastasis of osteosarcoma and could be used as a potential prognostic biomarker and therapeutic target in osteosarcoma.	32082982	RID03968	ceRNA or sponge	metastasis,prognosis		
Colorectal cancer	91H	IGF2	positively-E	RIP;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(-);cell invasion(-);cell autophagy(-)	interact with protein	association	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000167244	NA	NA	3481	NA	C11orf43|FLJ44734|IGF-II	Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer.91H, a long non-coding antisense transcripts located on the position of the H19/IGF2 locus had been suggested to play a critical role in tumour development. However, little study had proved the mechanism in colorectal cancer (CRC). Hence, we performed this study to deeply explore the mechanism of lncRNA 91H in tumour progression. The expression of lncRNA 91H was first detected in CRC tissues and cells which was higher in vitro and in vivo than normal cells or tissues and CRC patients with high lncRNA 91H expression usually had a high risk in tumour metastasis (p < .05). Then, monodansylcadaverine (MDC) staining, scratch wound, migration and invasion assays were conducted which showed to that reduced lncRNA 91H would greatly affect tumour migration, invasion and autophagy. Finally, by RNA pull down and RNA-binding protein immunoprecipitation (RIP) assay, a significant interaction was found between lncRNA 91H and IGF2BP2 which was proved to play an important role in CRC IGF2 expression. All these results suggested lncRNA 91H promotes IGF2 expression by interacting with IGF2BP2 which would provide a new strategy in finding potential CRC diagnostic biomarkers and therapeutic targets.	32070145	RID03969	interact with protein	metastasis		UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Diabetes mellitus	CASC15	miR-34c	negatively-E	transient cell transfections	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	Long Non-Coding RNA (LncRNA) CASC15 Is Upregulated in Diabetes-Induced Chronic Renal Failure and Regulates Podocyte Apoptosis.BACKGROUND CASC15 has been recently characterized as an oncogenic lncRNA. This study aimed to investigate the role of CASC15 in diabetic patients complicated with chronic renal failure (DCRF). MATERIAL AND METHODS Levels of CASC15 in plasma derived from 3 groups of participants were measured by qPCR and compared by ANOVA and Tukey test. The interaction between CASC15 and miR-34c was analyzed by performing cell transfections. Cell apoptosis assay was performed to analyze the effects of transfections on the apoptosis of CIHP-1 cells (podocytes). RESULTS We found that CASC15 in plasma was upregulated in DCRF compared with diabetic patients (no obvious complications) and healthy controls. Upregulation of CASC15 distinguished DCRF patients from healthy controls and diabetic patients. High D-glucose environment induced the upregulation of CASC15 in cells of the human podocyte cell line CIHP-1. Overexpression of CASC15 did not affect miR-34c in CIHP-1 cells, but bioinformatics analysis showed that CASC15 can sponge miR-34c. Overexpression of CASC15 led to an increased apoptotic rate of CIHP-1 cells, and miR-34c overexpression led to a decreased apoptotic rate of CIHP-1 cells. In addition, CASC15 overexpression attenuated the effects of miR-34c overexpression on cell apoptosis. CONCLUSIONS Therefore, CASC15 is upregulated in DCRF patients and promotes the apoptosis of podocytes by sponging miR-34c. Our study adds to our understanding of the pathogenesis of DCRF and suggests that CASC15 could serve as a potential therapeutic target of DCRF.	32053576	RID03970	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Breast cancer	AFAP1-AS1	ERBB2	positively-E	RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	interact with protein	association	RNA-protein	Trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000141736	NA	84740	2064	AFAP1-AS|AFAP1AS|MGC10981	CD340|HER-2|HER2|NEU|NGL	Exosome-mediated lncRNA AFAP1-AS1 promotes trastuzumab resistance through binding with AUF1 and activating ERBB2 translation.Background: Although trastuzumab provides significant clinical benefit for HER2-positive breast cancers, responses are limited by the emergence of resistance. Recent evidence suggests that long noncoding RNAs (lncRNAs) play important roles in tumorigenesis and chemoresistance. However, the regulatory mechanism of lncRNAs in trastuzumab resistance is not well established to date. In this research, we identified the differentially expressed lncRNA and investigated its regulatory role in trastuzumab resistance of breast cancer.Methods: LncRNA microarray and qRT-PCRwere performed to identify the dysregulated lncRNAs. Transmission electron microscopy, differential ultracentrifugation and qRT-PCRwere used to verify the existence of exosomal AFAP1-AS1 (actin filament associated protein 1 antisense RNA 1). Bioinformatics prediction, RNA fluorescence in situ hybridization (RNA-FISH) and immunoprecipitation assays were performed to identify the direct interactions between AFAP1-AS1 and other associated targets, such as AU-binding factor 1 (AUF1) and ERBB2. Finally, a series gain- or loss-functional assays were done to prove the precise role of AFAP1-AS1 in trastuzumab resistance.Results: AFAP1-AS1 was screened out due to its higher expression in trastuzumab-resistant cells compared to sensitive cells. Increased expression of AFAP1-AS1was associate with poorer response and shorter survival time of breast cancer patients. AFAP1-AS1 was upregulated by H3K27ac modification at promoter region, and knockdown of AFAP1-AS1 reversed trastuzumab resistance. Moreover, extracellular AFAP1-AS1 secreted from trastuzumab resistant cells was packaged into exosomes and then disseminated trastuzumab resistance of receipt cells. Mechanically, AFAP1-AS1 was associated with AUF1 protein, which further promoted the translation of ERBB2 without influencing the mRNA level.Conclusion: Exosomal AFAP1-AS1 could induce trastuzumab resistance through associating with AUF1 and promoting ERBB2 translation. Therefore, AFAP1-AS1 level may be useful for prediction of trastuzumab resistance and breast cancer treatment.	32020881	RID03971	interact with protein	chemoresistance	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Laryngeal squamous cell carcinoma	FOXD2-AS1	STAT3	positively-E	RNA pull-down;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	regulation	NA	Stattic	CSC	NA	Cancer	Larynx cancer	lncRNA	TF	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000168610	NA	84793	6774	MGC12982	APRF	Long noncoding RNA FOXD2-AS1 enhances chemotherapeutic resistance of laryngeal squamous cell carcinoma via STAT3 activation.Laryngeal squamous cell carcinoma (LSCC) is a common head and neck cancer. Despite recently improved management of LSCC, chemotherapy resistance of patients remains a challenge. In this study, we identified that long noncoding RNA FOXD2-AS1 regulates LSCC therapeutic resistance by augmenting LSCC stemness. LSCC chemotherapy-resistant patients showed increased FOXD2-AS1 expression compared with that in chemotherapy-sensitive patients, which predicted poor prognosis. Gain- or loss-of-function experiments showed that upregulated FOXD2-AS1 maintained cancer stemness, reducing the response to chemotherapy, while FOXD2-AS1 downregulation had the opposite effects. FOXD2-AS1 acted as a scaffold for STAT3 and PRMT5, promoting STAT3 transcriptional activity, which is essential to maintain cancer stemness and promote chemotherapeutic resistance. Interfering with FOXD2-AS1 using short hairpin RNA rescued LSCC's chemotherapeutic sensitivity. Thus, FOXD2-AS1 promotes LSCC chemotherapeutic resistance and is an upstream activator of STAT3, making FOXD2-AS1 a potential therapeutic target to improve the chemotherapy effect in LSCC patients.	31959918	RID03972	transcriptional regulation	chemoresistance,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophagus squamous cell carcinoma	LINC00963	RAB14	positively-E	luciferase reporter assay;western blot;immunochemistry	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-214-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000119396	NA	100506190	51552	MetaLnc9	FBP|RAB-14	LINC00963 predicts poor prognosis and promotes esophageal cancer cells invasion via targeting miR-214-5p/RAB14 axis.In mechanism, LINC00963 served as a sponge for miR-214-5p in ESCC progression.LINC00963 might promote ESCC cells proliferation and invasion via regulating the miR-214-5p/RAB14 axis and it might serve as a therapeutic target for ESCC treatment.LINC00963 might promote ESCC cells proliferation and invasion via regulating the miR-214-5p/RAB14 axis and it might serve as a therapeutic target for ESCC treatment.	31957829	RID03973	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Intervertebral disc degeneration	SLC20A1	MMP3	positively-E	luciferase reporter assay;starBase	upregulation	RT-qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-31-5p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000144136	GRCh38_2:112645939-112663825	ENSG00000263313	NA	6574	4314	Glvr-1|GLVR1|PiT-1|PiT1	STMY|STMY1	LincRNA-SLC20A1 (SLC20A1) promotes extracellular matrix degradation in nucleus pulposus cells in human intervertebral disc degeneration by targeting the miR-31-5p/MMP3 axis.MMP3 is a downstream target for miR-31-5p and is positively modulated by SLC20A1 in degenerative NP cells. The upregulation of SLC20A1 aggravates ECM degradation in degenerative human NP cells by targeting the miR-31-5p/MMP3 axis, suggesting that the SLC20A1/miR-31-5p/MMP3 pathway can contribute to IDD progression.	31934214	RID03974	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Ovarian cancer	OIP5-AS1	SNAI1	positively-E	RT-qPCR;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000124216	NA	729082	6615	cyrano|linc-OIP5	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	LncRNA OIP5-AS1 upregulates snail expression by sponging miR-34a to promote ovarian carcinoma cell invasion and migration.The expression of OIP5-AS1 and snail in paired tissues were determined by RT-qPCR. The interaction between OIP5-AS1 and miR-34a was predicted by IntaRNA2.0 and confirmed by dual-luciferase reporter assay.overexpression of miR-34a reduced the effects of overexpression of OIP5-AS1 on the expression of snail. In cell invasion and migration assay, overexpression of OIP5-AS1 and snail resulted in increased OC cell invasion and migration, while overexpression of miR-34a decreased OC cell invasion and migration. Moreover, overexpression of miR-34a attenuated the effects of OIP5-AS1 overexpression on OC cell invasion and migration.OIP5-AS1 may upregulate snail expression in OC by sponging miR-34a to promote OC cell invasion and migration.	33092644	RID03975	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD);DATA(GSE40174)
Alzheimer's disease	MALAT1	CNR1	positively-E	shRNA;luciferase reporter assay	upregulation	RT-qPCR;microarray	NA	NA	apoptosis process(-);PI3K/AKT signaling pathway(+)	ceRNA(miR-30b)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000118432	NA	378938	1268	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CANN6|CB-R|CB1|CB1A|CB1K5|CNR	Neuro-protective roles of long non-coding RNA MALAT1 in Alzheimer's disease with the involvement of the microRNA-30b/CNR1 network and the following PI3K/AKT activation. The phosphorylation of PI3K and AKT was stimulated when MALAT1 or CNR1 was overexpressed. To sum up, we found MALAT1 could promote neuronal recovery following AD through the miR-30b/CNR1 network and the PI3K/AKT signaling activation.	32976819	RID03976	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE75367,GSE86978)
Kidney disease	ARAP1-AS2	ARAP1	positively-E	RNA pull-down assay;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);fibrotic(+);EGFR/TGF-beta/SMAD3 signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000245148	GRCh38_11:72700474-72705607	ENSG00000186635	NA	100506020	116985	NA	CENTD2	LncRNA ARAP1-AS2 promotes high glucose-induced human proximal tubular cell injury via persistent transactivation of the EGFR by interacting with ARAP1. we found that overexpression or knockdown of ARAP1-AS2 could regulate fibrosis and HK-2 cell proliferation through EGFR/TGF-beta/Smad3 signalling. RNA pull-down assays revealed that ARAP1-AS2 directly interacts with ARAP1. Coimmunoprecipitation, dual-immunofluorescence and ubiquitination assays showed that ARAP1 may maintain persistent EGFR activation by reducing EGFR ubiquitination through competing with Cbl for CIN85 binding. Taken together, our results suggest that the lncRNA ARAP1-AS2 may promote high glucose-induced proximal tubular cell injury via persistent EGFR/TGF-beta/Smad3 pathway activation by interacting with ARAP1.	32969198	RID03977	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Osteosarcoma	SNHG8	miR-542-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000269893	GRCh38_4:118278705-118285316	NA	NA	100093630	NA	LINC00060|NCRNA00060	NA	Long noncoding RNA SNHG8 promotes the proliferation of osteosarcoma cells by downregulating miR-542-3p.The interplay between SNHG8 and miR-542-3p was affirmed by a luciferase report assay. The effects of SNHG8 on miR-542-3p expression were examined in MG-63 and SW-1353 cells by qRT-PCRanalysis.SNHG8 could negatively regulate miR-542-3p expression and bind with miR-542-3p, which attenuated SNHG8 induced cell proliferation. Taken together, these findings indicate that lncRNA SNHG8 promotes the proliferation of OS cells by downregulating miR-542-3p.	32450677	RID03978	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	
Lung non-small cell carcinoma	FEZF1-AS1	NOTCH1	positively-E	qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000148400	NA	154860	4851	NA	TAN1	LncRNA FEZF1-AS1 promotes non-small lung cancer cell migration and invasion through the up-regulation of NOTCH1 by serving as a sponge of miR-34a.FEZF1-AS1, miR-34a, and NOTCH-1 were overexpressed to analyze the relationship between them. FEZF1-AS1 was up-regulated in NSCLC patients.In NSCLC tissues, NOTCH-1 and FEZF1-AS1 were positively correlated. In NSCLC cells, over-expression of FEZF1-AS1 resulted in up-regulated expressions of NOTCH-1, while miR-34a over-expression mediated down-regulated expressions of NOTCH-1.MiR-34a played the opposite role and reduced the effects of FEZF1-AS1 over-expression.CONCLUSIONS: FEZF1-AS1 promoted NSCLC cell migration and invasion through the up-regulation of NOTCH1 by serving as a sponge of miR-34a.	32349744	RID03979	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Acute renal injury	CDKN2B-AS1	miR-199a	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);TLR4/NF-kB signaling pathway(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	It was predicted that miR-199a was a potential target for ANRIL by 3 miRNA databases (TargetScan, PicTar and miRanda; Fig. 1F). WT or MT miR-199a-3'-UTR was cloned to confirm whether ANRIL can directly bind to miR-199a and luciferase activity was assayed. As shown in Figure 1G, overexpression of miRNA-199a mimic can significantly reduce the activity of ANRIL-3'UTR luciferase (p < 0.01), but MT ANRIL-3'UTR luciferase activity has no significant change, which fully indicates that miRNA-199a is the direct target of ANRIL in laryngeal cancer cells.Overexpression of ANRIL increased apoptosis and promoted TLR4 (Toll-like receptor 4), NF-kB phosphorylation, and downstream transcription factor production.CONCLUSION: ANRIL/NF-kB pathway in LPS-induced apoptosis provided theoretical guidance for ANRIL in the treatment of AKI.	32069473	RID03980	transcriptional regulation	NA	UP(SKCM);DATA(GSE38495)	
Oral squamous cell carcinoma	SNHG17	ELF1	positively-E	DNA/RNA pull down;RIP; ChIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000120690	NA	388796	1997	NA	NA	SNHG17/miR-384/ELF1 axis promotes cell growth by transcriptional regulation of CTNNB1 to activate Wnt/beta-catenin pathway in oral squamous cell carcinoma.Further mechanistic studies, including DNA/RNA pull down, RIP, ChIP, and luciferase reporter gene assays, were conducted. It was confirmed that Wnt/beta-catenin signaling pathway was involved in the SNHG17-mediated OSCC cell growth.we were pleasantly surprised to find that SNHG17 and ELF1 functioned as ceRNAs in OSCC via competitively binding to microRNA-384 (miR-384). By using rescue assays, we revealed that SNHG17 facilitated OSCC cell growth through modulating miR-384/ELF1 axis. Importantly, we certified that ELF1 was indispensable for SNHG17-affected OSCC progression. Collectively, it can be concluded that SNHG17/miR-384/ELF1 axis contributed to OSCC cell growth via promoting CTNNB1 expression, thus activating Wnt/beta-catenin signaling pathway.	33531646	RID03981	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Radiation-induced lung injury	RP11	miR-29a	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell injury(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000105618	GRCh38_19:54115410-54131719	NA	NA	NA	NA	NA	NA	To validate the direct binding between miR-29a and LncRNA-RP11 at endogenous levels, the entire wild-type 3'-UTR of miR-29a or the mutant 3'-UTR in the seed region, where located the LncRNA-RP11 binding sites, was cloned downstream of the luciferase gene  open reading frame. Overexpression of miR-29a suppressed the luciferase activity of luciferase reporter harboring full length LncRNA-RP11, while miR-29a inhibitor elevated the luciferase activity. On the other hand, site-directed mutagenesis of the binding site successfully abolished the above effects in HLF-1 (Figure 3C) and WI-38 (Figure 3D), indicating LncRNA-RP11 could act as a ceRNA of miRNA-29a.	33117089	RID03982	ceRNA or sponge	NA		
Lung cancer	SNHG16	VEGFA	positively-E	RT-qPCR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-520)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000112715	NA	100507246	7422	Nbla10727|Nbla12061|ncRAN	VEGF|VEGF-A|VPF	LncRNA SNHG16 drives proliferation, migration, and invasion of lung cancer cell through modulation of miR-520/VEGF axis.RT-qPCR was used to analyze the expression patterns of SNHG16, miR-520 and VEGF. MTT and transwell methods were used to detect the effect of SNHG16 on cell migration. The association between SNHG16, miR-520 and VEGF was analyzed by bioinformatics analysis and Dual-Luciferase verification reporter analysis. LncRNA SNHG16 as ceRNA up-regulates VEGF in lung cancer cells by binding to miR-520. LncRNA SNHG16 as ceRNA promotes the migration of lung cancer cells by regulating the miR-520/VEGF axis.	33015794	RID03983	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Ovarian cancer	LINC00662	HIF1A	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);glycolysis(+)	ceRNA(miR-375)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000100644	NA	148189	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LINC00662 promotes glycolysis and cell survival by regulating miR- 375/HIF-1alpha axis in ovarian cancer.The interaction between LINC00662 and miR-375 was verified using luciferase assays and RNA immunoprecipitation. Results showed that LINC00662 was highly expressed in OC tissues and cells, and patients with increased expression of LINC00662 were associated with shorter overall survival. LINC00662 might regulate HIF-1alpha expression via miR-375. These findings suggested that LINC00662 has the potential to be explored as a diagnostic biomarker for OC.	32476381	RID03984	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	MACC1-AS1	LAST1/2	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell stemness(+);Hippo signaling pathway(-)	NA	regulation	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228598	GRCh38_7:20141916-20153531	NA	NA	100874041	NA	NA	NA	Long noncoding RNA MACC1-AS1 promotes the stemness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1/2. Additionally, it was found that MACC1-AS1 interacted with up-frameshift 1 (UPF1) to modulate mRNA decay of LATS1/2. Overexpression of LAST1/2 attenuated the promoting effects of MACC1-AS1 overexpression on the stemness of NSCLC cells. Therefore, our results demonstrate the effects of the novel MACC1-AS1/UPF1/LATS1/2 axis in NSCLC cell stemness. Notably, the expression of MACC1-AS1 and UPF1 exhibiteda positive correlation in lung cancer patients (Figure 4I), whileMACC1-AS1 expression displayed a negative correlation withLAST1/2 expression (Figure 4J,K).	32401390	RID03985	expression association	NA		
Myocardial ischemia and reperfusion injury	A2M-AS1	IL1R2	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	ENSG00000245105	GRCh38_12:9065163-9068689	ENSG00000115590	NA	144571	7850	NA	CD121b|IL1RB	LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2.qRT-PCRand western blot were adopted to test the levels of mRNA and protein.Besides, a negative correlation was showed between A2M-AS1 and IL1R2 expression. In H/R-treated cardiomyocytes, overexpression of IL1R2 weakened the promoting proliferation and anti-apoptosis effects caused by overexpressing A2M-AS1.This study demonstrates the potential regulatory role of A2M-AS1/ IL1R2 axis in cardiomyocytes suffered from H/R, and provides insight into the protection of MI/RI.	33057899	RID03986	expression association	NA	DOWN(BRCA);DATA(GSE67939)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nasopharynx carcinoma	AFAP1-AS1	KAT2B	interact	RNA pull-down assay;RIP;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000114166	NA	84740	8850	AFAP1-AS|AFAP1AS|MGC10981	GCN5|GCN5L|P/CAF|PCAF	Long Noncoding RNA AFAP1-AS1 Is a Critical Regulator of Nasopharyngeal Carcinoma Tumorigenicity.AFAP1-AS1 was required for NPC proliferation in vitro and tumorigenicityin vivo. Mechanistic investigations suggested that AFAP1-AS1 binds to KAT2B andpromotes acetyltransferase activation at two residues (E570/D610).	33330099	RID03987	transcriptional regulation	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	AFAP1-AS1	TIF1	interact	dual-luciferase reporter assay;CHIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	NA	NA	84740	NA	AFAP1-AS|AFAP1AS	NA	Long Noncoding RNA AFAP1-AS1 Is a Critical Regulator of Nasopharyngeal Carcinoma Tumorigenicity.AFAP1-AS1 was required for NPC proliferation in vitro and tumorigenicityin vivo. Mechanistic investigations suggested that AFAP1-AS1 binds to KAT2B andpromotes acetyltransferase activation at two residues (E570/D611).	33330099	RID03988	transcriptional regulation	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	
Abdominal aortic aneurysm	LBX2-AS1	LBX2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(-)	ceRNA(miR-4685-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	TF	ENSG00000257702	GRCh38_2:74502552-74505091	ENSG00000179528	NA	151534	85474	NA	NA	LncRNA LBX2-AS1 facilitates abdominal aortic aneurysm through miR-4685-5p/LBX2 feedback loop.Mechanically, the regulation role of LBX2-AS1 on miR-4685-5p or that of miR-4685-5p on LBX2 was investigated by quantitative real-time polymerase chain reaction (qRT-PCR. Additionally, the competing endogenous RNA (ceRNA) network was confirmed by luciferase reporter, RNA pull-down, and RNA immunoprecipitation (RIP) assays. LBX2-AS1 sequestered miR-4685-5p to release LBX2 expression via ceRNA mechanism.our data suggested that LBX2-AS1, miR-4685-5p and LBX2 constituted a positive feedback loop in promoting AAA development, implying a potential usage of LBX2-AS1/miR-4685-5p/LBX2 axis in AAA management.	32559617	RID03989	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Cardiovascular system disease	H19	TET1	positively-E	luciferase reporter assay;siRNA;CHIP-qPCR	upregulation	RT-qPCR	NA	NA	TGF-beta signaling pathway(+)	ceRNA(miR-let-7)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000138336	NA	283120	80312	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	bA119F7.1|CXXC6|KIAA1676|LCX	H19/TET1 axis promotes TGF-beta signaling linked to endothelial-to-mesenchymal transition.Further, we provide evidence that this H19/TET1-mediated regulation of TGF-beta signaling and EndMT occurs in mouse pulmonary microvascular ECs in vivo under hyperglycemic conditions.These results suggest that H19 positively regulates expression of TET1, TGFBR2, and TSP1 in ECs and that TNF-alpha upregulates these genes in a H19-dependent manner.	32374060	RID03990	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DATA(GSE117623)
Prostate cancer	LINC01611	GRIN2A	positively-E	RT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000231776	GRCh38_6:84421028-84556152	ENSG00000183454	NA	105377880	2903	RP1-90L14.1|TCONS_l2_00025430	GluN2A|NMDAR2A	Effects of long non-coding RNA RP1-90L14.1 on the biological behaviors of cancer prostate LNCaP cells and its regulating mechanisms.lncRNA RP1-90L14.1 may play important roles in the proliferation, migration and invasiveness of prostate cancer cells. RP1-90L14.1 can promote the expressions of GRIN2A and BACE2 and may have an endogenous competitive relation with GRIN2A and BACE2.	32216238	RID03991	transcriptional regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	RP1-90L14.1	BACE2	positively-E	RT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000231776	GRCh38_6:84421028-84556152	ENSG00000182240	NA	NA	25825	NA	AEPLC|ALP56|ASP1|ASP21|BAE2|CDA13|CEAP1|DRAP	Effects of long non-coding RNA RP1-90L14.1 on the biological behaviors of cancer prostate LNCaP cells and its regulating mechanisms.lncRNA RP1-90L14.1 may play important roles in the proliferation, migration and invasiveness of prostate cancer cells. RP1-90L14.1 can promote the expressions of GRIN2A and BACE2 and may have an endogenous competitive relation with GRIN2A and BACE3.	32216238	RID03992	transcriptional regulation	NA		UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE109761,GSE111065,GSE86978)
Triple-negative breast cancer	HIF1A	LncIHAT	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell survival(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000100644	NA	NA	NA	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	NA	LncIHAT Is Induced by Hypoxia-Inducible Factor 1 and Promotes Breast Cancer Progression.This study systematically identified hypoxia-induced lncRNA transcriptome in TNBC and sheds light on multiple layers of regulatory mechanisms of gene expression under hypoxia.	33380467	RID03993	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Triple-negative breast cancer	LncIHAT	PDPK1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell survival(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000140992	NA	NA	5170	NA	PDK1|PDPK2|PDPK2P|PRO0461	Consistently, levels of ITGA6 and PDK1 proteins were also reduced by either of the two lncIHAT shRNAs in MDA-MB-231 cells (Fig. 5C). In contrast, the distal neighboring gene RAPGEF4 mRNA expression was not affected by lncIHAT KD in MDA-MB-231 cells (Supplementary Fig. S3C). Similar results were found in SUM159 cells (Fig. 5D ; Supplementary Fig. S3D and S3E). These results indicate that lncIHAT is required for expression of its proximal neighboring genes ITGA6 and PDK1 in TNBC cells.	33380467	RID03994	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Triple-negative breast cancer	LncIHAT	ITGA6	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell survival(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000091409	NA	NA	3655	NA	CD49f|ITGA6B|JEB6|VLA-6	Consistently, levels of ITGA6 and PDK1 proteins were also reduced by either of the two lncIHAT shRNAs in MDA-MB-231 cells (Fig. 5C). In contrast, the distal neighboring gene RAPGEF4 mRNA expression was not affected by lncIHAT KD in MDA-MB-231 cells (Supplementary Fig. S3C). Similar results were found in SUM159 cells (Fig. 5D ; Supplementary Fig. S3D and S3E). These results indicate that lncIHAT is required for expression of its proximal neighboring genes ITGA6 and PDK1 in TNBC cells.	33380467	RID03995	transcriptional regulation	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	HCP5	miR-29b-3p	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	LncRNA HCP5 Promotes Cell Invasion and Migration by Sponging miR-29b-3p in Human Bladder Cancer.MiR-29b-3p mediated the effect of HCP5 on cell viability, proliferation, migration and invasion in RT4 cells. In addition, miR-29b-3p could regulate the expression of HMGB1 through interaction with HMGB1.The findings in this study supported that lncRNA HCP5 could promote cell invasion and migration by sponging miR-29b-3p in human BC.	33235469	RID03996	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Coronary slow flow	MALAT1	MEF2A	positively-E	dual-luciferase reporter assay;CHIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-181b-5p)	regulation	NA	NA	NA	NA	Other	Coronary slow flow	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000068305	NA	378938	4205	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	RSRFC4|RSRFC9	The lncRNA MALAT1 participates in regulating coronary slow flow endothelial dysfunction through the miR-181b-5p-MEF2A-ET-1 axis.While MEF2A was highly enriched in CSF-induced HUVECs, MEF2A knockdown reduced ET-1 and increased the endothelial function of CSF-induced HUVECs as a transcriptional regulator of ET-1. MALAT1 modulated MEF2A expression positively by sponging miR-181b-5p.CONCLUSIONS: Endothelial function is reduced in CSF. MALAT1 participates in regulating CSF endothelial dysfunction through the miR-181b-5p-MEF2A-ET-1 axis, and could provide a new target for CSF treatment.	33545365	RID03997	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Breast cancer	MaTAR25	Tensin1	positively-E	qRT-PCRmmunoblot;CRISPR/Cas9	upregulation	qRT-PCR;Sanger sequencing;northern blot	NA	NA	cell viability(+);cell migration(+);cell invasion(+);cancer progression(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	MaTAR25 lncRNA regulates the Tensin1 gene to impact breast cancer progression.MaTAR25 functions by interacting with purine rich element binding protein B (PURB), and associating with a major downstream target gene Tensin1 (Tns1) to regulate its expression in trans.	33353933	RID03998	transcriptional regulation	metastasis		
Sepsis	LUADT1	Pim-1	positively-E	RT-qPCR;western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-195)	regulation	RNA-RNA	NA	NA	Evading Apoptosis	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	NA	NA	106182249	NA	NA	NA	LncRNA LUADT1 sponges miR-195 to prevent cardiac endothelial cell apoptosis in sepsis.The interaction between miR-195 and LUADT1 was determined by overexpression experiments and luciferase activity assay. In addition, it was found that overexpression of LUADT1 and Pim-1 reduced the enhancement effects of miR-195 on LPS-induced cardiac endothelial cell apoptosis.In summary, LUADT1 may protect cardiac endothelial cells against apoptosis in sepsis by regulating the miR-195/Pim-1 axis.	33225891	RID03999	ceRNA or sponge	NA	UP(NSCLC,PRAD,SKCM);DATA(GSE74639,GSE104209,GSE38495)	
House dust mite-induced inflammatory response	OIP5-AS1	HMGB1	positively-E	co-transfection	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	NA	Other	House dust mite-induced inflammatory response	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000189403	NA	729082	3146	cyrano|linc-OIP5	DKFZp686A04236|HMG1|HMG3|SBP-1	OIP5-AS1 silencing resulted in a significant increase in miR-143-3p and a concomitant decrease in HMGB1 expression. However, co-transfection of si-OIP5-AS1 together with miR-143-3p inhibitor p-HMGB1 reversed these effects. Moreover, transfection miR-143-3p inhibitor alone or overexpression of HMGB1 both resulted in an increase in HMGB1. However, co-transfection with si-OIP5-AS1 downregulated HMGB1, compared with transfection with miR-143-3p inhibitor or pHMGB1 alone. Altogether, these findings suggested that OIP5-AS1 may regulate HMGB1 via miR-143-3p in Der p1-treated BEAS-2B cells (Fig. 7).	33174035	RID04000	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Non-small cell lung cancer	MALAT1	COMMD8	positively-E	starbase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-);glycolysis(+)	ceRNA(miR-613)	regulation	RNA-protein	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169019	NA	378938	54951	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FLJ20502	LncRNA MALAT1 Aggravates the Progression of Non-Small Cell Lung Cancer by Stimulating the Expression of COMMD8 via Targeting miR-613.The relationship between miR-613 and MALAT1 or COMMD8 was predicted by the bioinformatics tool starbase and verified by dual-luciferase reporter assay. MALAT1 and COMMD8 were aberrantly upregulated in NSCLC tissues and cells. We found that miR-613 was a target of MALAT1, and miR-613 could bind to the 3- untranslated region (3-UTR) of COMMD8. MALAT1 regulated the expression of COMMD8 by absorbing miR-613. MALAT1 promoted malignant activities of NSCLC cells through targeting miR-613/COMMD8 axis, and exosome-mediated transfer of NSCLC might be a novel approach for NSCLC treatment.	33149680	RID04001	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney disease	KCNQ1OT1	HMGA2	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-18b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000149948	NA	10984	8091	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	BABL|HMGIC|LIPO	KCNQ1OT1/miR-18b/HMGA2 axis regulates high glucose-induced proliferation, oxidative stress, and extracellular matrix accumulation in mesangial cells.The relationship between miR-18b and KCNQ1OT1 or HMGA2 was determined via dual-luciferase reporter analysis, RNA immunoprecipitation, and pull-down. KCNQ1OT1 expression was increased and miR-18b expression was decreased in DN patients and HG-challenged HMCs. miR-18b was targeted via KCNQ1OT1. Knockdown of KCNQ1OT1 weakened HG-caused proliferation, oxidative stress, and ECM accumulation of HMCs by increasing miR-18b.	32989627	RID04002	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	RP11-1094M14.8	CXCL9	positively-E	siRNA;qRT-PCR	upregulation	qRT-PCR	NA	NA	prognosis(+)	ceRNA(miR-1269a)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000267369	GRCh38_17:35498218-35499175	ENSG00000138755	NA	NA	4283	NA	CMK|Humig|MIG|SCYB9|crg-10	A ceRNA network and a potential regulatory axis in gastric cancer with different degrees of immune cell infiltration.qRT-PCRresults showed that RP11-1094M14.8 knockdown significantly reduced the expression of CXCL9, and RP11-1094M14.8 overexpression had the opposite effect. The results of clinical analysis of gastric cancer samples showed that RP11-1094M14.8 and CXCL9 were highly expressed in hot tumors, and CXCL9 was positively correlated with a better prognosis for patients.The RP11-1094M14.8/miR-1269a/CXCL9 axis may serve as a potential immune-therapeutic target for gastric cancer with different degrees of immune cell infiltration.	32860283	RID04003	ceRNA or sponge	prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Ovarian epithelial carcinoma	TONSL-AS1	CDK1	positively-E	IntaRNA;dual-luciferase reporter assay;qPCR;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000232600	GRCh38_8:144437675-144439971	ENSG00000170312	NA	100287098	983	NA	CDC2|CDC28A	LncRNA TONSL-AS1 regulates miR-490-3p/CDK1 to affect ovarian epithelial carcinoma cell proliferation.Dual luciferase assay and RNA interaction prediction showed the direct interaction between TONSL-AS1 and miR-490-3p. However, overexpression of miR-490-3p did not affect the expression of TONSL-AS1. Instead, overexpression of TONSL-AS1 resulted in the upregulation of CDK1, a target of miR-490-3p, in EOC cells. Overexpression of TONSL-AS1 and CDK1 resulted in increased proliferation rate of EOC cells. Overexpression of miR-490-3p played an opposite role and reduced the effects of overexpression of TONSL -AS1 and CDK1.CONCLUSIONS: Therefore, TONSL-AS1 may regulate miR-490-3p/CDK1 to affect EOC cell proliferation.	32414422	RID04004	ceRNA or sponge	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Prostate cancer	DPP10-AS1	FOXM1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(-)	interact with protein	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000235026	GRCh38_2:115126622-115161384	ENSG00000111206	NA	389023	2305	NA	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Tetramethylpyrazine reduces prostate cancer malignancy through inactivation of the DPP10-AS1/CBP/FOXM1 signaling pathway.Reverse transcription-quantitative PCR showed TMP treatment increased the expression of lncRNA DPP10-AS1 in PCa cells. DPP10-AS1 was associated with CREB binding protein, thereby induced H3K27ac enrichment at the promoter region of the FOXM1 gene. In conclusion, the present study showed that TMP may be a promising treatment agent for PCa and lncRNA DPP10-AS1 may be a promising therapeutic target for TMP treatment.	32319592	RID04005	interact with protein	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung adenocarcinoma	TMPO-AS1	SOX12	positively-E	qRT-PCR;dual-luciferase reporter assay;western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000177732	NA	100128191	6666	NA	SOX22	TMPO-AS1, a Novel E2F1-Regulated lncRNA, Contributes to the Proliferation of Lung Adenocarcinoma Cells via Modulating miR-326/SOX12 Axis.The transcription levels of TMPO-AS1, miR-326, and SOX12 in LUAD tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR.The target relationship among TMPO-AS1, miR-326, and SOX12 and promoter activity of TMPO-AS1 was measured using dual-luciferase reporter assay. we demonstrated that TMPO-AS1 could modulate the proliferation of LUAD cells through increasing SOX12 expression level via sponging miR-326 in accordance with bioinformatics analysis and experimental validation.TMPO-AS1 can modulate LUAD cell proliferation through E2F1/miR-326/ SOX12 pathway	33293866	RID04006	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	E2F1	TMPO-AS1	positively-E	qRT-PCR;ChIP-qPCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000257167	GRCh38_12:98512973-98516422	1869	100128191	RBBP3|RBP3	NA	We evaluated the regulatory effect of E2F1 on the expression of TMPO-AS1 in LUAD cells through overexpressing or silencing E2F1, and qRT-PCRresults indicated that overexpression of E2F1 could up-regulate the TMPO-AS1 expression level in both H838 and SK-LU-1 cells (Figure 5C), whereas E2F1 knockdown decreased TMPO-AS1 expression (Figure 5D). To confirm TMPO-AS1 was regulated by E2F1 at transcriptional level, TMPO-AS1 promoter was cloned into pGL3-basic vector and then co-transfected with E2F1 overexpression vector into HEK-293 cells, and we found luciferase activity could be facilitated by overexpression of E2F1 (Figure 5E). Furthermore, ChIP-qPCR assay was performed to validate the direct binding between E2F1 and TMPO-AS1 promoter, and the results showed a significant enrichment of E2F1 on TMPO-AS1 promoter in both H838 and SK-LU-1 cells (Figure 5F). These findings manifest that the up-regulation of TMPO-AS1 is mediated by E2F1 in LUAD.we evaluated the regulatory effect of E2F1 on the expression of TMPO-AS1 in LUAD cells through overexpressing or silencing E2F1, and qRT-PCRresults indicated that overexpression of E2F1 could up-regulate the TMPO-AS1 expression level in both H838 and SK-LU-1 cells (Figure 5C), whereas E2F1 knockdown decreased TMPO-AS1 expression (Figure 5D). To confirm TMPO-AS1 was regulated by E2F1 at transcriptional level, TMPO-AS1 promoter was cloned into pGL3-basic vector and then co-transfected with E2F1 overexpression vector into HEK-293 cells, and we found luciferase activity could be facilitated by overexpression of E2F1 (Figure 5E). Furthermore, ChIP-qPCR assay was performed to validate the direct binding between E2F1 and TMPO-AS1 promoter, and the results showed a significant enrichment of E2F1 on TMPO-AS1 promoter in both H838 and SK-LU-1 cells (Figure 5F). These findings manifest that the up-regulation of TMPO-AS1 is mediated by E2F1 in LUAD.	33293866	RID04007	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Atherosclerosis	MAARS	ELAVL1	positively-E	RNA pull-down;RT-qPCR	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000066044	NA	NA	1994	NA	ELAV1|HUR|Hua|MelG	A macrophage-specific lncRNA regulates apoptosis and atherosclerosis by tethering HuR in the nucleus. Overexpression and knockdown studies verified MAARS as a critical regulator of macrophage apoptosis and efferocytosis in vitro, in an HuR-dependent manner.These findings establish a mechanism by which a macrophage-specific lncRNA interacting with HuR regulates apoptosis, with implications for a broad range of vascular disease states.	33262333	RID04008	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Age-related cataract	NONHSAT143692.2	OGG1	positively-E	shRNA;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-4728-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Cataract	lncRNA	PCG	NA	NA	ENSG00000114026	NA	NA	4968	NA	HMMH|HOGG1|MUTM|OGH1	Long non-coding RNA NONHSAT143692.2 is involved in oxidative DNA damage repair in the lens by regulating the miR-4728-5p/OGG1 axis.miR-4728-5p was predicted to bind to NONHSAT143692.2 and OGG1 mRNA 3'UTR. The overexpression of miR-4728-5p downregulated the expression of NONHSAT143692.2 (P<0.001), OGG1 mRNA (P<0.001) and OGG1 protein (P<0.001). The knockdown of miR-4728-5p reversed the above-mentioned outcomes. Overall, the findings of the present study demonstrate that the NONHSAT143692.2/miR-4728-5p/OGG1 axis may play an important role in the development of ARC.	33000245	RID04009	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE55807)
Ovarian cancer	CHRF	MIR10B	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);STAT3 signaling pathway(+);chemoresistance(+)	NA	association	protein-RNA	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	NA	NA	ENSG00000207744	NA	NA	406903	NA	MIRN10B|hsa-mir-10b|miRNA10B|mir-10b	Novel role of lncRNA CHRF in cisplatin resistance of ovarian cancer is mediated by miR-10b induced EMT and STAT3 signaling.Induction of epithelial-to-mesenchymal-transition (EMT) and activation of STAT3 signaling were determined to be the mechanisms underlying the CHRF-miR-10b axis-mediated cisplatin resistance. Down-regulation of CHRF reversed EMT, STAT3 activation and the resulting cisplatin resistance, which could be attenuated by miR-10b. Our results support a novel role of lncRNA CHRF in cisplatin resistance of OC and establish CHRF-miR-10b signaling as a putative therapeutic target for sensitizing resistant OC cells.	32901049	RID04010	expression association	chemoresistance		
Lung adenocarcinoma	LINC00511	PKM	positively-E	RT-qPCR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-625-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000067225	NA	400619	5315	onco-lncRNA-12	OIP3|PK3|PKM2|THBP1	LncRNA LINC00511 plays an oncogenic role in lung adenocarcinoma by regulating PKM2 expression via sponging miR-625-5p.LINC00511 expression in LAC tissues and cell lines (H1299 and A549) were detected by real time-polymerase chain reaction (RT-qPCR).Overexpression of LINC00511 promoted proliferation, invasion and migration capacities of LAC cells. Moreover, LINC00511 promoted LAC progression via serving as a sponge of miR-625-5p and regulating PKM2 expression.CONCLUSIONS: The present study showed that LINC00511 was involved in LAC progression by targeting miR-625-5p/PKM2, indicating that LINC00511/miR-625-5p/PKM2 may function as promising therapeutic targets for LAC.	32716147	RID04011	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Leukemia	LncRNA-OBFC2A	SMAD3	interact	RNA-FISH;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell cycle(-);chemoresistance(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	NA	NA	ENSG00000166949	NA	NA	4088	NA	HSPC193|HsT17436|JV15-2|LDS1C|LDS3|MADH3|hMAD-3|hSMAD3|mad3	LncRNA-OBFC2A targeted to Smad3 regulated Cyclin D1 influences cell cycle arrest induced by 1,4-benzoquinone.In vitro study, results showed that benzene metabolic, 1,4-Benzoquinone (1,4-BQ), induced cell cycle arrest at the G1 phase accompanied with decreased expression of Cyclin D1 in a dose-dependently manner. Further, we found that lncRNA-OBFC2A can interact with Smad3 to control cell cycle via modulating Cyclin D1 expression. Thus, these findings indicate that lncRNA-OBFC2A targeted to Smad3 regulated cyclin D1 influences cell cycle arrest induced by 1,4-BQ. LncRNA-OBFC2A, Smad3 and Cyclin D1 as a set of biomarkers play important roles in benzene haematotoxicity.	32645459	RID04012	transcriptional regulation	chemoresistance		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	LINC01198	PTEN	negatively-E	qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000231817	GRCh38_13:46455131-46515958	ENSG00000171862	NA	101929344	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	LINC01198 facilitates gliomagenesis through activating PI3K/AKT pathway.Through mechanistic exploration, we illustrated that LINC01198 increased PIK3CA expression by sponging miR-129-5p in the cytoplasm. Furthermore, PTEN was transcriptionally repressed by REST/RCOR1/HDAC2 complex. LINC01198 activates PI3 K/AKT signalling to exert oncogenic function in gliomagenesis by regulating PIK3CA and PTEN, which highlights a new approach for glioma treatment.Firstly, the influence of LINC01198 on the expressions of several genes involving in PI3 K/AKT activation was examined by qRT-PCRand western blot. The results exhibited that LINC01198 had a positive effect on the expression (at both mRNA and protein levels) of PIK3CA but a negative impact on that of PTEN.	32378450	RID04013	transcriptional regulation	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Malignant glioma	LINC01198	PIK3CA	positively-E	qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000231817	GRCh38_13:46455131-46515958	ENSG00000121879	NA	101929344	5290	NA	PI3K	LINC01198 facilitates gliomagenesis through activating PI3K/AKT pathway.Through mechanistic exploration, we illustrated that LINC01198 increased PIK3CA expression by sponging miR-129-5p in the cytoplasm. Furthermore, PTEN was transcriptionally repressed by REST/RCOR1/HDAC2 complex. LINC01198 activates PI3 K/AKT signalling to exert oncogenic function in gliomagenesis by regulating PIK3CA and PTEN, which highlights a new approach for glioma treatment.Firstly, the influence of LINC01198 on the expressions of several genes involving in PI3 K/AKT activation was examined by qRT-PCRand western blot. The results exhibited that LINC01198 had a positive effect on the expression (at both mRNA and protein levels) of PIK4CA but a negative impact on that of PTEN.	32378450	RID04014	transcriptional regulation	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Dysregulation of angiogenesis	NORAD	miR-590-3p	negatively-E	RT-qPCR;dual-luciferase reporter assay;ELISA	upregulation	RT-qPCR	NA	NA	cell migration(+);cell viability(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Other	Dysregulation of angiogenesis	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	Long non-coding RNA NORAD regulates angiogenesis of human umbilical vein endothelial cells via miR-590-3p under hypoxic conditions.NORAD was identified to bind with miR-590-3p directly, and miR-590-3p was shown to target certain proangiogenic agents, such as vascular endothelial growth factor (VEGF)A, fibroblast growth factor (FGF)1 and FGF2 directly.  the present results suggested that lncRNA NORAD may bind with miR-590-3p to regulate the angiogenic ability of HUVECs via the regulation of several downstream proangiogenic factors under hypoxia.	32323787	RID04015	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Atherosclerosis	CDKN2B-AS1	FRS2	positively-E	luciferase reporter assay;RIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cancer progression(+)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000166225	NA	100048912	10818	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	FRS2A|FRS2alpha|SNT-1|SNT1	LncRNA ANRIL regulates cell proliferation and migration via sponging miR-339-5p and regulating FRS2 expression in atherosclerosis.Quantitative reverse transcriptase PCR (qRT-PCR and western blot were employed to investigate the mRNA and protein expression level.Cell proliferation and migration assays were demonstrated to evaluate the functional role of ANRIL in AS. Potential target of ANRIL was determined using Luciferase reporter assay and RNA immunoprecipitation (RIP).These results revealed the underlying mechanism that ANRIL promoted AS progression by sponging miR-399-5p and regulating RAS/RAF/ERK signal pathway, suggesting that ANRIL might be a potential target for the therapeutic strategy of AS.Luciferase reporter assay confirmed that miR-339-5p could bind to FRS2.	32141564	RID04016	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE86978,GSE41245)
Crohn's disease	lncRNACNN3-206	Caspase10	positively-E	RT-PCRimmunohistochemical;FISH;luciferase reporter assay;siRNA	upregulation	RT-PCR	NA	NA	cell invasion(+);cell migration(+);apoptosis process(+)	ceRNA(miR-212)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Crohn's disease	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lncRNACNN3-206 activates intestinal epithelial cell apoptosis and invasion by sponging miR-212, an implication for Crohn's disease.Activation of the lncRNACNN3-206-miR-212-Caspase10 regulatory network led to increased apoptosis, migration and invasion in intestinal epithelial cells. Knockdown of lncRNACNN3-206 expression alleviated intestinal mucosal inflammation and tissue damage in the CD mouse model.CONCLUSION: lncRNACNN3-206 may play a key role in CD pathogenesis. lncRNACNN3-206 could be a therapeutic target for CD treatment.As shown in Supplementary Figure 7, we found that overexpression of lncRNACNN3-206 led to decreased levels of miR-212 in cells, but increased levels of Caspase10 mRNA. After lncRNACNN3-206 expression was knocked down, miR-212 levels were increased, while Caspase10 mRNA levels were decreased. These observations provided further support for the proposed mechanism that lncRNACNN3-206 overexpression could absorb miR-212, leading to the degradation of miR-212, resulting in a decrease in intracellular free miR-212 levels, thereby alleviating the inhibition of Caspase10 by miR-212, and eventually significantly increasing mRNA levels of Caspase10.	32089625	RID04017	ceRNA or sponge	NA		
Tongue squamous cell carcinoma	SNHG17	SP1	positively-E	siRNA;starBase 3.0;miRDB;RIP;luciferase reporter assay;RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+)	ceRNA(miR-876)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000185591	NA	388796	6667	NA	NA	SNHG17 enhances the malignant characteristics of tongue squamous cell carcinoma by acting as a competing endogenous RNA on microRNA-876 and thereby increasing specificity protein 1 expression.The SNHG17 knockdown significantly decreased TSCC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Mechanism investigation revealed that SNHG17 acts as a competing endogenous RNA on microRNA-876 (miR-876) in TSCC cells. In addition, specificity protein 1 (SP1) was validated as a direct target gene of miR-876 in TSCC cells.	32089063	RID04018	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic retinopathy	TDRG1	VEGFA	positively-E	siRNA;immunofluorescence	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000112715	NA	732253	7422	LINC00532|lincRNA-NR_024015	VEGF|VEGF-A|VPF	LncRNA TDRG1-Mediated Overexpression of VEGF Aggravated Retinal Microvascular Endothelial Cell Dysfunction in Diabetic Retinopathy.LncRNA TDRG1 and VEGF were found to be co-expressed and significantly upregulated in fibrovascular membranes (FVMs) from DR patients compared to those from EM patients. In the in vitro model, hyperglycemic treatment markedly increased the expression of lncRNA TDRG1 and VEGF at the mRNA and protein levels, which promoted cell proliferation and migration, enhanced permeability, and disrupted tube formation of HRECs.	32082175	RID04019	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Osteoarthritis	LINC00662	miR-15b-5p	negatively-E	luciferase reporter assay;shRNA	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	Long noncoding RNA LINC00662-miR-15b-5p mediated GPR120 dysregulation contributes to osteoarthritis.Our results show that GPR120 was negatively regulated by miR-15b-5p through targeting 3' untranslated region (3'UTR), and that miR-15b-5p was negatively regulated by LINC00662. Further luciferase assay shows that LINC00662-miR-15b-5p signaling pathway contributed the regulation of GPR120 expression. Functionally, the decreased of LINC00662 caused increased miR-15b-5p, thereby leading to decreased GPR120. In summary, the present study shows that LINC00662-miR-15b-5p signaling pathway is involved in the regulation of GPR120, thereby contributing to arthritis.	32037689	RID04020	expression association	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Temporomandibular joint osteoarthritis	XIST	ADAMTS5	positively-E	dual-luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Osteoarthritis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000154736	NA	7503	11096	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ADAM-TS 11|ADAM-TS 5|ADAM-TS5|ADAMTS-11|ADAMTS-5|ADAMTS11|ADMP-2	Long non-coding RNA XIST regulates chondrogenic differentiation of synovium-derived mesenchymal stem cells from temporomandibular joint via miR-27b-3p/ADAMTS-5 axis.The direct interaction between miR-27b-3p and XIST or ADAMTS-5 was confirmed by dual-luciferase reporter assay or RNA immunoprecipitation (RIP) assay.Dual luciferase reporter and RIP assays identified that XIST acted as a sponge for miR-27b-3p. Moreover, XIST regulated ADAMTS-5 expression by directly binding miR-27b-3p. More importantly,miR-27b-3p/ADAMTS-5 rescued the effects of XIST on chondrogenic differentiation of SMSCs.CONCLUSION: The results suggest that XIST modulates SMSCs chondrogenic differentiation via the miR-27b-3p/ADAMTS-5 axis, which provides new targets for TMJOA treatment.	33128918	RID04021	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC);DATA(GSE117623)
Kidney disease	KCNQ1OT1	SORBS2	positively-E	starBase 3.0;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+);NF-kB signaling pathway(+)	ceRNA(miR-18b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000154556	NA	10984	8470	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	ARGBP2|KIAA0777	LncRNA KCNQ1OT1 affects cell proliferation, apoptosis and fibrosis through regulating miR-18b-5p/SORBS2 axis and NF-<U+0138>B pathway in diabetic nephropathy.Both knockdown of KCNQ1OT1 and silencing of SORBS2 restrained proliferation and fibrosis and induced apoptosis in DN cells. KCNQ1OT1 regulated DN cells proliferation, apoptosis and fibrosis via KCNQ1OT1/miR-18b-5p/SORBS2 axis and NF--B pathway.	32905431	RID04022	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065)
Colorectal cancer	LINC00460	SPHK1	negatively-E	dual-luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-613)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000176170	NA	728192	8877	NA	SPHK	Long Noncoding RNA LINC00460 Facilitates Colorectal Cancer Progression by Negatively Regulating miR-613.The relationship between LINC00460 and miR-613 expression was explored by dual-luciferase reporter assay.In vivo studies, LINC00460 knockdown attenuated tumour growth. MiR-613 downregulation and SphK1 upregulation in the CRC tissues, and LINC00460 expression levels were inversely correlated with miR-613 expression and positively correlated with the SphK1 mRNA expression. Overall, LINC00460 modulated cell proliferation, migration, invasion and sphingosine kinase 1 (SphK1) expression in HT29 and LOVO cells, at least in most part, by regulating miR-613.	32821121	RID04023	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Atherosclerosis	E2F1	SNHG7	positively-E	luciferase reporter assay;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	TF	lncRNA	ENSG00000101412	NA	ENSG00000233016	GRCh38_9:136721366-136728184	1869	84973	RBBP3|RBP3	MGC16037|NCRNA00061	E2F1/SNHG7/miR-186-5p/MMP2 axis modulates the proliferation and migration of vascular endothelial cell in atherosclerosis.RNA and protein levels were respectively measured using RT-qPCR and western blot. Molecular interaction was detected using luciferase reporter assay and chromatin immunoprecipitation (ChIP). results unveiled that lncRNA SNHG7 was remarkedly up-regulated in ox-LDL exposed HUVECs. Gain and loss of function experiments showed that the SNHG7 repressed the proliferation and migration of HUVECs. Mechanistically, transcription factor E2F1 was found to target the promoter region of lncRNA SNHG7 and accelerated its expression. Moreover, miR-186-5p was found to bind with the 3'-UTR of SNHG7, meanwhile miR-186-5p also bound with the MMP2 mRNA 3'-UTR.these results show the essential roles of E2F1/SNHG7/miR-186-5p/MMP2 axis on the proliferation and migration of endothelial cells, providing a potential therapeutic target for atherosclerosis.	32603818	RID04024	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)
Kidney disease	PVT1	WT1	positively-E	western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);fibrotic(+)	ceRNA(miR-23b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000184937	NA	5820	7490	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	AWT1|GUD|NPHS4|WAGR|WIT-2	Knockdown of lncRNA PVT1 alleviates high glucose-induced proliferation and fibrosis in human mesangial cells by miR-23b-3p/WT1 axis.The expression levels of PVT1, miR-23b-3p, and Wilms tumor protein 1 (WT1) mRNA were assessed by quantitative real-time polymerase chain reaction (qRT-PCR.The targeted correlation between miR-23b-3p and PVT1 or WT1 was verified by dual-luciferase reporter assay.PVT1 modulated WT1 expression through acting as a molecular sponge of miR-23b-3p. The miR-23b-3p/WT1 axis mediated the protective effect of PVT1 knockdown on HG-induced proliferation and fibrosis in MCs. Our study suggested that PVT1 knockdown ameliorated HG-induced proliferation and fibrosis in MCs at least partially by regulating the miR-23b-3p/WT1/NF-kB pathway. Targeting PVT1 might be a potential therapeutic strategy for DN treatment.	32322310	RID04025	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Laryngeal squamous cell carcinoma	DLEU2	PIK3CD	positively-E	qRT-PCR;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);prognosis(-);AKT signaling pathway(+)	ceRNA(miR-30c-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000171608	NA	8847	5293	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	p110D	Long noncoding RNA DLEU2 predicts a poor prognosis and enhances malignant properties in laryngeal squamous cell carcinoma through the miR-30c-5p/PIK3CD/Akt axis.We found that DLEU2 was significantly upregulated and predicted poor clinical outcomes in LSCC patients. In addition, ectopic overexpression of DLEU2 promoted the proliferation and migration of LSCC cells both in vivo and in vitro. Mechanistically, DLEU2 served as a competing endogenous RNA to regulate PIK3CD expression by sponging miR-30c-5p and subsequently activated the Akt signaling pathway.we found that the novel LSCC-related gene DLEU2 enhances the malignant properties of LSCCs via the miR-30c-5p/PIK3CD/Akt axis. DLEU2 and its targeted miR-30c-5p/PIK3CD/Akt axis may represent valuable prognostic biomarkers and therapeutic targets for LSCCs.	32555190	RID04026	ceRNA or sponge	prognosis	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Ischemic heart failure	SOX2-OT	TRAF6	negatively-E	RNA pull-down assay;immunoblotting;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(-);inflammatory response(-)	ceRNA(miR-455-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000175104	NA	347689	7189	DKFZp761J1324|NCRNA00043|SOX2OT	RNF85	LncRNA promoted inflammatory response in ischemic heart failure through regulation of miR-455-3p/TRAF6 axis.Online software program was used to identify miRNAs that target SOX2-OT, followed by validation using RNA pull-down.SOX2-OT contains binding sites for miR-455-3p, miR-5586-3p and miR-1252-5p. RNA pull-down confirmed the binding ability between SOX2-OT and miR-455-3p. TRAF6 is a direct target of miR-455-3p. Moreover, the regulatory activity of SOX2-OT on inflammatory response was partially through its negative regulation of miR-455-3p, which directly regulates TRAF6.SOX2-OT may be a driver of IHF through repression of miR-455-3p, and miR-455-3p alleviates IHF by targeting TRAF6.	32350569	RID04027	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Colorectal cancer	LINC00467	miR-451a	negatively-E	RNAhybrid	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000153363	GRCh38_1:211382736-211435570	NA	NA	84791	NA	C1orf97|MGC14801	NA	linc00467 was revealed to be overexpressed in human CRC tissues,In HT29 and HCT116 cells, linc00467-knockout was revealed to decrease cellular proliferation and increase apoptosis,Finally, the downstream target of linc00467 in CRC promotion was predicted using bioinformatics analysis.The results demonstrated that linc00467 targets and regulates the expression of microRNA (miR)-451a, promoting carcinogenesis and metastasis in CRC.increased linc00467 expression promotes metastasis by targeting miR-451a, which ultimately increases cellular proliferation and inhibits apoptosis in human CRC cells.	32934693	RID04028	ceRNA or sponge	metastasis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	
Breast cancer	PART1	MIR4516	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000265867	NA	25859	100616258	NCRNA00206	mir-4516	lncRNA PART1 Promotes Breast Cancer Cell Progression by Directly Targeting miR-4516.qRT-PCRwas performed to examine the expressions of PART1 and miR-4516.we showed that lncRNA PART1 was highly expressed in breast cancer cells. Knockdown of PART1 induced decreased proliferation, invasion and migration of breast cancer cells.we found that PART1 can bind to miR-4516 directly. We also found that inhibition of miR-4516 could rescue the decreased proliferation, migration and invasion of breast cancer cells induced by knockdown of PART1.	32922076	RID04029	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	
Retinoblastoma	XIST	NRP1	positively-E	qRT-PCRhRNA	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-200a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000099250	NA	7503	8829	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	CD304|NRP|VEGF165R	Carboplatin Inhibits the Progression of Retinoblastoma Through IncRNA XIST/miR-200a-3p/NRP1 Axis.he expression of XIST and miR-200a-3p in the samples were determined by qRT-PCR XIST was highly expressed while miR-200a-3p was lowly expressed in patients' tissues, XIST-siRNA (si-XIST), XIST-shRNA (sh-XIST), empty vector plasmid (siRNA-NC), miR-200a-3p-mimics and miR -200a-3p-inhibition were transfected into Y79 cells.Silencing XIST and over-expressed miR-200a-3p could inhibit cell epithelial-mesenchymal transition (EMT), proliferation, invasion, and promote apoptosis.	32904674	RID04030	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761)
Retinoblastoma	MALAT1	BCL2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Bcl-2|PPP1R50	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-9 and Bax.	32894536	RID04031	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	MALAT1	Clecaspase-3	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-10 and Bax.	32894536	RID04032	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Retinoblastoma	MALAT1	Clecaspase-9	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-11 and Bax.	32894536	RID04033	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Retinoblastoma	MALAT1	BAX	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL2L4	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-12 and Bax.	32894536	RID04034	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	NKILA	BCL2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000171791	NA	105416157	596	NA	Bcl-2|PPP1R50	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-9 and Bax.	32894536	RID04035	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	NKILA	Clecaspase-3	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-10 and Bax.	32894536	RID04036	expression association	NA		
Retinoblastoma	NKILA	Clecaspase-9	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-11 and Bax.	32894536	RID04037	expression association	NA		
Retinoblastoma	NKILA	BAX	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000087088	NA	105416157	581	NA	BCL2L4	Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.qRT-PCRwas adopted to detect the NKILA and MALAT1 levels in samples,Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-12 and Bax.	32894536	RID04038	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MIR99AHG	FOXP1	positively-E	luciferase reporter gene detection experiments	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-577)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000215386	GRCh38_21:15928296-16645467	ENSG00000114861	NA	388815	27086	C21orf34|C21orf35|FLJ38295|LINC00478|MONC	12CC4|hFKH1B|HSPC215|QRF1	Long noncoding RNA MIR99AHG promotes gastric cancer progression by inducing EMT and inhibiting apoptosis via miR577/FOXP1 axis.The expression level of MIR99AHG in GC cell lines and tissues was monitored via qPCR.a target of MIR99AHG was predicted and identified by luciferase reporter gene detection experiments.MIR99AHG was strongly up-regulated in human GC and contributed to cancer progression.Knockdown of MIR99AHG expression inhibited cell proliferation, invasion, migration and promoted cell apoptosis. Moreover, MIR99AHG worked as an oncogenic gene though competing for endogenous RNA (ceRNA) of miR-577.	32874129	RID04039	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)
Gastric cancer	XIST	JAK2	positively-E	bioinformatics;fluorescein reporter gene detection;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-337)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000096968	NA	7503	3717	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	JTK10	The lncRNA XIST promotes proliferation, migration and invasion of gastric cancer cells by targeting miR-337.Fluorescein reporter gene detection was used to determine the relationship between JAK2 and XIST.XIST expression was significantly up-regulated in AGS and HGC-27 cells.The proliferation, invasion and migration of GC cells were simultaneously inhibited by XIST knockdown, and the relationship between XIST and miR-337 was confirmed by bioinformatics analysis. JAK2 is expected to be the target gene of miR-337.	32830093	RID04040	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Esophageal cancer	METTL3	AKT1	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	phosphorylation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000165819	GRCh38_14:21498133-21511342	ENSG00000142208	NA	56339	207	M6A|MT-A70|Spo8	AKT|PKB|PRKBA|RAC|RAC-alpha	METTL3 promotes the proliferation and invasion of esophageal cancer cells partly through AKT signaling pathway.METTL3 knockdown reduced the proliferation, clonality, migration and invasion of Eca-109 and KY-SE150 cells, and induced cell apoptosis, which may be mediated by activation of the mitochondrial apoptotic pathway. Further, METTL3 overexpression promoted the proliferation, clonality, migration and invasion of Eca-109 and KY-SE150 cells, and inhibited cell apoptosis. In addition, METTL3 regulated the expression of Wnt/beta-catenin and AKT signaling pathway components. A double-effect inhibitor (BEZ235) inhibited AKT and mTOR phosphorylation and hindered the effect of METTL3 overexpression on the proliferation and migration of Eca-109 and KY-SE150 cells. Our data suggest that METTL3 plays a carcinogenic role in human EC progression partially through AKT signaling pathways, suggesting that METTL3 may serve as a potential therapeutic target for EC therapy.METTL3 is highly expressed in human EC cells., METTL3 knockdown resulted in decreased phosphorylation level of AKT (Ser-473) and mTOR	32825955	RID04041	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	METTL3	BAX	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000165819	GRCh38_14:21498133-21511342	ENSG00000087088	NA	56339	581	M6A|MT-A70|Spo8	BCL2L4	METTL3 promotes the proliferation and invasion of esophageal cancer cells partly through AKT signaling pathway.Knockdown of METTL3 also resulted in a significant up-regulation of pro-apoptotic protein Bax, Caspase 3 and Caspase 9, and a significant down-regulation of anti-apoptotic protein Bcl2. METTL3 overexpression has the opposite regulation effect on the expression of apoptosis-related proteins.METTL3 inhibits apoptosis and the mitochondrial apoptotic pathway in human EC cells.	32825955	RID04042	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	METTL3	Caspase3	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000165819	GRCh38_14:21498133-21511342	NA	NA	56339	NA	M6A|MT-A70|Spo8	NA	METTL3 promotes the proliferation and invasion of esophageal cancer cells partly through AKT signaling pathway.Knockdown of METTL3 also resulted in a significant up-regulation of pro-apoptotic protein Bax, Caspase 3 and Caspase 9, and a significant down-regulation of anti-apoptotic protein Bcl2. METTL3 overexpression has the opposite regulation effect on the expression of apoptosis-related proteins.METTL4 inhibits apoptosis and the mitochondrial apoptotic pathway in human EC cells.	32825955	RID04043	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Esophageal cancer	METTL3	Caspase9	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000165819	GRCh38_14:21498133-21511342	NA	NA	56339	NA	M6A|MT-A70|Spo8	NA	METTL3 promotes the proliferation and invasion of esophageal cancer cells partly through AKT signaling pathway.Knockdown of METTL3 also resulted in a significant up-regulation of pro-apoptotic protein Bax, Caspase 3 and Caspase 9, and a significant down-regulation of anti-apoptotic protein Bcl2. METTL3 overexpression has the opposite regulation effect on the expression of apoptosis-related proteins.METTL5 inhibits apoptosis and the mitochondrial apoptotic pathway in human EC cells.	32825955	RID04044	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Esophageal cancer	METTL3	BCL2	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000165819	GRCh38_14:21498133-21511342	ENSG00000171791	NA	56339	596	M6A|MT-A70|Spo8	Bcl-2|PPP1R50	METTL3 promotes the proliferation and invasion of esophageal cancer cells partly through AKT signaling pathway.Knockdown of METTL3 also resulted in a significant up-regulation of pro-apoptotic protein Bax, Caspase 3 and Caspase 9, and a significant down-regulation of anti-apoptotic protein Bcl2. METTL3 overexpression has the opposite regulation effect on the expression of apoptosis-related proteins.METTL6 inhibits apoptosis and the mitochondrial apoptotic pathway in human EC cells.	32825955	RID04045	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	EPIC1	AKT1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE98538	NA	AKT signaling pathway(+)	NA	regulation	RNA-protein	Rapamycin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000142208	NA	284930	207	Lnc-EPIC1	AKT|PKB|PRKBA|RAC|RAC-alpha	MYC-binding lncRNA EPIC1 promotes AKT-mTORC1 signaling and rapamycin resistance in breast and ovarian cancer.RNA-seq analysis of breast and ovarian cancer cells demonstrated that EPIC1-knockdown led to the downregulation of genes in the AKT-mTORC1 signaling pathway.EPIC1 (epigenetically-induced lncRNA 1) is a Myc-binding lncRNA, which has been previously demonstrated to be overexpressed in multiple cancer types.	32810332	RID04046	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	EPIC1	AKT1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE98538	NA	AKT signaling pathway(+)	NA	regulation	RNA-protein	Rapamycin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000142208	NA	284930	207	Lnc-EPIC1	AKT|PKB|PRKBA|RAC|RAC-alpha	MYC-binding lncRNA EPIC1 promotes AKT-mTORC1 signaling and rapamycin resistance in breast and ovarian cancer.RNA-seq analysis of breast and ovarian cancer cells demonstrated that EPIC1-knockdown led to the downregulation of genes in the AKT-mTORC1 signaling pathway.EPIC1 (epigenetically-induced lncRNA 2) is a Myc-binding lncRNA, which has been previously demonstrated to be overexpressed in multiple cancer types.	32810332	RID04047	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00205	FUS	positively-E	RT-qPCR;western blot;RNA pull-down assay;starBase2;RIP	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223768	GRCh38_21:45288035-45297806	ENSG00000089280	NA	642852	2521	NCRNA00205	ALS6|FUS1|hnRNP-P2|HNRNPP2|TLS	LINC00205 promotes malignancy in lung cancer by recruiting FUS and stabilizing CSDE1.we observed the elevated expression of LINC00205 in LC tissues and cells through real-time quantitative PCR (RT-qPCR).silencing LINC00205 inhibited LC cell growth and migration, but aggravated cell apoptosis.we found that LINC00205 recruited FUS to maintain the mRNA stability of cold shock domain containing E1 (CSDE1) and therefore up-regulated CSDE1 expression in LC.Cells were harvested and lysed for RIP process with the antibody against FUS or IgG (negative control). Input served as the positive control. RNA precipitated in indicated groups was evaluated by RT-qPCR.Bioinformatics from starBase2 (http://starbase.sysu.edu.cn/index.php) predicted FUS as a potential candidate which was capable of binding to LINC00205 with district stringency.  Since FUS was recognized as an RNA-binding protein (RBP) and lncRNAs generally interact with RBPs in cytoplasm, we then wondered whether LINC00205 could interact with FUS in LC.RNA pull down further confirmed the direct interaction between LINC00205 and FUS, since FUS bands could only be observed in Input and Bio-LINC00205 groups	32808651	RID04048	expression association	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00205	CSDE1	positively-E	starBase2;RIP;RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);apoptosis process(-)	mRNA stability	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000223768	GRCh38_21:45288035-45297806	ENSG00000009307	NA	642852	7812	NCRNA00205	D1S155E|UNR	LINC00205 promotes malignancy in lung cancer by recruiting FUS and stabilizing CSDE1.we observed the elevated expression of LINC00205 in LC tissues and cells through real-time quantitative PCR (RT-qPCR).silencing LINC00205 inhibited LC cell growth and migration, but aggravated cell apoptosis.we found that LINC00205 recruited FUS to maintain the mRNA stability of cold shock domain containing E1 (CSDE1) and therefore up-regulated CSDE1 expression in LC.Cells were harvested and lysed for RIP process with the antibody against FUS or IgG (negative control). Input served as the positive control. RNA precipitated in indicated groups was evaluated by RT-qPCR.Bioinformatics from starBase2 predicted FUS as a potential candidate which was capable of binding to LINC00205 with district stringency.  Since FUS was recognized as an RNA-binding protein (RBP) and lncRNAs generally interact with RBPs in cytoplasm, we then wondered whether LINC00205 could interact with FUS in LC.RNA pull down further confirmed the direct interaction between LINC00205 and FUS, since FUS bands could only be observed in Input and Bio-LINC00206 groups.RBPs, including FUS, have been featured with the ability of maintaining mRNA stability. Prediction from starBase2 indicated that CSDE1 was a potent gene whose mRNA was able to interact with FUS. Subsequent RIP assay confirmed such prediction, as CSDE1 mRNA was evidently precipitated by anti-FUS . Then we detected the expression of CSDE1 by performing RT-qPCR and western blot, and the results manifested the elevated mRNA and protein levels of CSDE1 in LC cells in comparison with control BEAS-2B cells.	32808651	RID04049	interact with mRNA	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	FOXCUT	FOXC1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell growth(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000054598	NA	101927703	2296	LINC01379|TCONS_00011636	ARA|FKHL7|FREAC3|IGDA|IHG1|IRID1	FOXCUT Promotes the Proliferation and Invasion by Activating FOXC1/PI3K/AKT Pathway in Colorectal Cancer.FOXC1 and FOXCUT lncRNA expression levels were detected in a panel of paired specimens obtained from 48 patients' tissues and cell lines with CRC using RT-qPCR.a novel long noncoding RNA (FOXCUT) was frequently overexpressed in CRC tissues and cell lines. In addition, the expressions of FOXCUT and FOXC1 were positively correlated.When the expression of FOXCUT was downregulated by small interfering RNA (siRNA), the expression of FOXC1 was also decreased. Moreover, knockdown of FOXCUT significantly inhibited proliferation and invasion of CRC cell lines and resulted in downregulated expression of the matrix metalloproteinase 1 (MMP-1).FOXCUT promotes the expression of FOXC1 to activate PI3K/AKT signaling pathway for its regulation of cell growth and proliferation.	32801872	RID04050	expression association	NA		UP(SKCM);DATA(GSE38495)
Colorectal cancer	LNCARSR	HK1	positively-E	RIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell invasion(+);cell migration(+);glucose metabolic process(+);cell metastasis(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000156515	NA	102723932	3098	lnc-TALC	NA	lncARSR sponges miR-34a-5p to promote colorectal cancer invasion and metastasis via hexokinase-1-mediated glycolysis.Here, we analyzed specimens from 89 patients with CRC and demonstrated that lncARSR was highly expressed in CRC tissues and negatively associated with survival.Cell overexpression or knockdown of lncARSR were used to perform RIP assay with AGO2 antibody in accordance with the instructions of Magna RIP- Kit (Millipore). Enrichment levels of lncARSR and HK1 were measured with qPCR assay.The 3'UTR of HK1 or lncARSR containing miR-34a-5p putative binding sites were amplified and cloned into pGL3 vector. QuikChange Site-Directed Mutagenesis kit (Stratagene) was applied to mutate miR-34-5p binding site on the 3'UTR of HK1. miR-34a-5p mimics or inhibitor and the wild-type or mutant type luciferase vectors were co-transfected into CRC cells. This assay was conducted with the dual-luciferase reporter gene assay system (Promega). Luciferase activity was measured and normalized to Renilla luciferase activity.	32798250	RID04051	ceRNA or sponge	metastasis		UP(LIHC,PAAD,BRCA);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE41245)
Non-small cell lung cancer	LINC00467	AKT1	NA	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);prognosis(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000142208	NA	84791	207	C1orf97|MGC14801	AKT|PKB|PRKBA|RAC|RAC-alpha	LINC00467 is up-regulated by TDG-mediated acetylation in non-small cell lung cancer and promotes tumor progression.LINC00467 highly expressed in NSCLC tissues and associated with advanced clinical stages and poor outcome. Knockdown of LINC00467 inhibited cell growth and metastasis via regulating the Akt signaling pathway.The identified LINC00467 may serve as a valuable diagnostic and prognostic biomarker as well as a therapeutic target for NSCLC.	32796958	RID04052	expression association	metastasis,prognosis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	LINC02418	KNL1	positively-E	luciferase reporter;RIP;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-4677-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214039	GRCh38_12:130032928-130045057	ENSG00000137812	NA	100190940	57082	NA	AF15Q14|CASC5|CT29|D40|hKNL-1|hSpc105|KIAA1570|MCPH4|PPP1R55|Spc7	LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression.Gene expression was examined by RT-qPCR or western blot. The interaction of miR-4677-3p with LINC02418 (or KNL1) was verified through luciferase reporter, RIP and RNA pull-down assays.High expression of LINC02418 was observed in LAD specimens and cells.Downregulation of LINC02418 obstructed the proliferation and motility of LAD cells. Moreover, LINC02418 negatively modulated miR-4677-3p expression and miR-4677-3p overexpression could repress cell proliferation and migration.	32795273	RID04053	ceRNA or sponge	NA		UP(SKCM,BRCA);DATA(GSE38495,GSE111842)
Papillary thyroid carcinoma	ENST	CDC25C	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000158402	NA	NA	995	NA	CDC25|PPP1R60	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH4 cells.	32791924	RID04054	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Papillary thyroid carcinoma	ENST	CHEK1	negatively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000149554	NA	NA	1111	NA	CHK1	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH5 cells.	32791924	RID04055	expression association	NA		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE67939)
Papillary thyroid carcinoma	ENST	PIK3CA	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000121879	NA	NA	5290	NA	PI3K	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH6 cells.	32791924	RID04056	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Papillary thyroid carcinoma	ENST	p-PI3K	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH7 cells.	32791924	RID04057	expression association	NA		
Papillary thyroid carcinoma	ENST	AKT1	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000142208	NA	NA	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH8 cells.	32791924	RID04058	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	ENST	p-AKT	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway.The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay.siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K.ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH9 cells.	32791924	RID04059	expression association	NA		
Malignant glioma	HNF1A-AS1	MAP2K4	positively-E	luciferase reporter assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	JNK signaling pathway(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000065559	NA	283460	6416	C12orf27|FLJ38690|HAS1|NCRNA00262	JNKK1|MEK4|MKK4|PRKMK4|SERK1	Long noncoding RNA HNF1A-AS1 regulates proliferation and apoptosis of glioma through activation of the JNK signaling pathway via miR-363-3p/MAP2K4.we confirmed that the expression level of HNF1A-AS1 was increased in glioma tissues and cells. Knockdown of HNF1A-AS1 inhibited cell proliferation and promoted cell apoptosis in glioma. We also found the regulatory effect of HNF1A-AS1 on the MAP2K4-dependent JNK signaling pathway. All findings indicated that HNF1A-AS1 induces the upregulation of MAP2K4 to activate the JNK signaling pathway to promote glioma cell growth by acting as a miR-363-3p sponge.In the be_x0002_ginning, starBase (http://starbase.sysu.edu.cn/) predicted eight can_x0002_didate miRNAs that could bind with HNF1A-AS1. Then, theluciferase activity of the HNF1A-AS1 reporter was examined fol_x0002_lowing the overexpression of these miRNAs in U87-MG and A172cells by luciferase reporter analysis. Results in qRT-PCRdemonstrated that MAP2K4 expressionwas overtly hindered in response to HNF1A-AS1 suppression(Figure 4c). Therefore, we selected MAP2K4 for the following experiments. Bioinformatics analysis revealed the binding site betweenMAP2K4 and miR-363-3p. Luciferase reporter assay wasapplied to evaluate the interaction between MAP2K4 3'-UTR andmiR-363-3p.	32779194	RID04060	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Malignant glioma	USF1	HAS2-AS1	positively-E	ChIP;dual-luciferase reporter assays	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000158773	NA	ENSG00000248690	GRCh38_8:121639293-121994185	7391	594842	bHLHb11|MLTFI|UEF	HAS2-AS|HAS2AS|HASNT|NCRNA00077	The transcription factor USF1 promotes glioma cell invasion and migration by activating lncRNA HAS2-AS1.qRT-PCRwas used to detect the expressions of HAS2-AS1 and USF1 in glioma tissues and cell lines.The chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were applied to demonstrate the binding of USF1 and HAS2-AS1 promoter region.USF1 was highly expressed in glioma and positively correlated with HAS2-AS1.	32776110	RID04061	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cervical cancer	ACTA2-AS1	SMAD3	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000166949	NA	100132116	4088	UC001kfo|uc001kfo.1|ZXF1	HsT17436|JV15-2|MADH3	A novel mechanism by which ACTA2-AS1 promotes cervical cancer progression: acting as a ceRNA of miR-143-3p to regulate SMAD3 expression.Quantitative real-time PCR (qRT-PCR was conducted to detect the expression level of messenger RNA of ACTA2-AS1, miR-143-3p and SMAD3 in tumor tissues and cells.ACTA2-AS1 was significantly increased in CC tissues and cells and miR-143-3p was down-regulated.dual-luciferase reporter assay and further mechanistic experiments confirmed that ACTA2-AS1 could sponge and regulate the expression of miR-143-3p.Loss-of-function assay revealed that silencing of ACTA2-AS1 inhibited cell proliferation, colony formation, migration and promoted apoptosis in CC.	32774166	RID04062	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gallbladder cancer	SNHG6	miR-26b-5p	negatively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell growth(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	LncRNA SNHG6 regulating Hedgehog signaling pathway and affecting the biological function of gallbladder carcinoma cells through targeting miR-26b-5p.it has been found that the expression of LncRNA SNHG6 is upregulated in gallbladder carcinoma tissues.For the detection of SNHG6 and miR-26b-5p in samples we used qRT-PCRSilencing of SNHG6 and upregulation of miR-26b-5p could promote cell apoptosis, inhibit cell growth, and epithelial-mesenchymal transition (ETM). Silencing of SNHG6 and upregulation of miR-26b-5p could inhibit Gli1, Gli2, Shh, Smo, N-cadherin, vimentin and Snail proteins, and promote upregulation of Gli3 and E-Cadherin expression. Dual-Luciferase report confirmed that SNHG6 and miR-26b-5p have targeted relationship.	32744686	RID04063	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Kidney injury	NEAT1	TRAF6	positively-E	starBase;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);inflammatory response(+)	ceRNA(let-7b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000175104	NA	283131	7189	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	RNF85	Long Non-Coding RNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)Relieves Sepsis-Induced Kidney Injury and Lipopolysaccharide (LPS)-Induced Inflammation in HK-2 Cells.We used real-time quantitative polymerase chain reaction (RT-qPCR) to analyze the expression of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1), let-7b-5p, and tumor necrosis factor receptor-associated factor 6 (TRAF6).The interaction relationship among NEAT1, TRAF6, and let-7b-5p was analyzed by the bioinformatics starBase database and dual-luciferase reporter assay.lncRNA NEAT1 was expressed at higher levels in kidney tissues from sepsis patients than in healthy kidney tissues. NEAT1 regulated TRAF6 expression by sponging let-7b-5p in HK-2 cells, which promotes LPS-induced injury and inflammation in HK-2 cells.	32724027	RID04064	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	RUSC1-AS1	NOTCH3	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);Notch signaling pathway(+)	ceRNA(miR-7-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225855	GRCh38_1:155316863-155324176	ENSG00000074181	NA	284618	4854	C1orf104|FLJ35976	CADASIL|CASIL	LncRNA RUSC1-AS1 promotes the proliferation of hepatocellular carcinoma cells through modulating NOTCH signaling.we found that RUSC1-AS1 was upregulated in HCC tissues and cells, and predicted unfavorable prognosis of HCC patients.mechanism assays including luciferase reporter assay and RIP assay demonstrated that RUSC1-AS1 could directly bind to hsa-miR-7-5p. Besides, hsa-miR-7-5p targeted and negatively regulated NOTCH3 expression.RUSC1-AS1 sponged hsa-miR-7-5p to upregulate NOTCH3 and to trigger the NOTCH signaling pathway.lncRNA RUSC1-AS1 promoted the proliferation and reduced the apoptosis of HCC cells through activation of NOTCH signaling via hsa-miR-7-5p/NOTCH3 axis.	32701359	RID04065	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807,GSE75367)
Kawasaki disease	SOCS2-AS1	CUEDC2	positively-E	luciferase reporter assay;RIP;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Immune system disease	Lymph node disease	lncRNA	PCG	ENSG00000246985	GRCh38_12:93542022-93571768	ENSG00000107874	NA	144481	79004	NA	C10orf66|MGC2491	Kawasaki disease: SOCS2-AS1/miR-324-5p/CUEDC2 axis regulates the progression of human umbilical vein endothelial cells.SOCS2-AS1 expression was examined via RT-qPCR.The interaction among RNAs (SOCS2-AS1, miR-324-5p and CUEDC2) was validated via luciferase reporter, RIP and RNA pull-down assays.SOCS2-AS1 was highly expressed in serum and tissues of KD patients.SOCS2-AS1 upregulates CUEDC2 via inhibiting miR-324-5p to promote the progression of HUVECs in KD.SOCS2-AS1 contributes to cell proliferation in HUVECs of KD through elevating CUEDC2 expression by sequestering miR-324-5p.	32688371	RID04066	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Breast cancer	SCAMP1-TV2	PUM2	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000055917	NA	NA	23369	NA	PUMH2|PUML2	Silencing SCAMP1-TV2 Inhibited the Malignant Biological Behaviors of Breast Cancer Cells by Interaction With PUM2 to Facilitate INSM1 mRNA Degradation.Cell Counting Kit-8 (CCK-8), RNA Immunoprecipitation (RIP), and RNA pull-down assays were employed to determine the interactions between SCAMP1-TV2 and Pumilio RNA binding family member 2 (PUM2).Silenced SCAMP1-TV2 inhibited the proliferation, migration, and invasion of breast cancer cells, and promoted cell apoptosis.As compared with paracancerous tissues, the expression of SCAMP1-TV2 was significantly increased in luminal A and triple negative breast cancer tissues .The bioinformatics software RBPMAP and Starbase 2.0 predicted that PUM2 can bind to SCAMP1-TV2, indicating that SCAMP1-TV2 may require PUM2 for its function.In order to validate the interaction between SCAMP1-TV2 and PUM2, RIP assay and RNA pull-down assay were performed.	32670859	RID04067	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	SCAMP1-TV2	INSM1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000173404	NA	NA	3642	NA	IA-1|IA1	Silencing SCAMP1-TV2 Inhibited the Malignant Biological Behaviors of Breast Cancer Cells by Interaction With PUM2 to Facilitate INSM1 mRNA Degradation.Cell Counting Kit-8 (CCK-8), RNA Immunoprecipitation (RIP), and RNA pull-down assays were employed to determine the interactions between SCAMP1-TV2 and Pumilio RNA binding family member 2 (PUM2).Silenced SCAMP1-TV2 inhibited the proliferation, migration, and invasion of breast cancer cells, and promoted cell apoptosis.As compared with paracancerous tissues, the expression of SCAMP1-TV2 was significantly increased in luminal A and triple negative breast cancer tissues .The bioinformatics software RBPMAP and Starbase 2.0 predicted that PUM2 can bind to SCAMP1-TV2, indicating that SCAMP1-TV2 may require PUM2 for its function.In order to validate the interaction between SCAMP1-TV2 and PUM3, RIP assay and RNA pull-down assay were performed.The luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were used to get to know the effect of human insulinoma-associated 1 (INSM1) directly on the SAM and SH3 domain containing 1 (SASH1) promoter.	32670859	RID04068	interact with protein	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Chronic obstructive pulmonary disease	RP11-86H7.1	NFKB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);NF-kB signaling pathway(+)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	TF	NA	NA	ENSG00000109320	NA	NA	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	LncRNA RP11-86H7.1 promotes airway inflammation induced by TRAPM2.5 by acting as a ceRNA of miRNA-9-5p to regulate NFKB1 in HBECS.After exposure to TRAPM2.5, the novel lncRNA RP11-86H7.1 was markedly upregulated in HBECs.the lncRNA RP11-86H7.1 can promote the inflammatory response by acting as a competing endogenous RNA of miR-9-5p, reversing the inhibitory effect of its target gene NFKB1, and sustaining NF-kB activation.	32665564	RID04069	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LOXL1-AS1	RHOXF2	positively-E	miRDB;TargetScan7;luciferase reporter assay;pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-3128)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000131721	NA	100287616	84528	NA	CT107|PEPP-2|PEPP2|THG1	LOXL1-AS1 Contributes to Non-Small Cell Lung Cancer Progression by Regulating miR-3128/RHOXF2 Axis.Gene expression was measured by qRT-PCR(quantitative real-time PCR). The bioinformatics databases (miRDB and TargetScan7) were used to predict target genes. Luciferase assay and pull-down assay were processed for verifying the binding sites.LncRNA LOXL1-AS1 was higher expressed in lung cancer tissues and cells.LOXL1-AS1 promotes the progression of NSCLC by regulating miR-3128/RHOXF2 axis, which might be a new potential target for the diagnosis and treatment of NSCLC.After knocking down LOXL1-AS1, proliferation, invasion and migration of H1299 and A549 cells were inhibited.	32636639	RID04070	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	
Atherosclerosis	CTBP1-DT	ATG14	positively-E	dual-luciferase reporter assay	downregulation		NA	NA	cell proliferation(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000196810	GRCh38_4:1249300-1288291	ENSG00000126775	NA	92070	22863	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	ATG14L|KIAA0831	CTBP1-AS2 inhibits proliferation and induces-autophagy in ox-LDL-stimulated vascular smooth muscle-cells by regulating miR-195-5p/ATG14.A dual-luciferase reporter assay confirmed that miR-195-5p is a downstream target miRNA of lncRNA CTBP1-AS2 and miR-195-5p was increased in AS.The expression levels of miR-195-5p and CTBP1-AS2 in the serums of patients with AS and human aorta vascular smooth muscle cells was increased or decreased, respectively, following treatment with oxidized low-density lipoprotein (ox-LDL). The present study revealed that lncRNA CTBP1-AS2 may serve a role in AS by inhibiting the proliferation and promoting the autophagy of VSMCs through ATG14 modulation via miR-195-5p. These data may provide a novel therapeutic target for AS.	32626936	RID04071	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Pancreatic cancer	H19	SOCS5	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+);chemoresistance(+);STAT3 signaling pathway(+)	ceRNA(miR-675-3p)	regulation	RNA-protein	Gemcitabine	CSC	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000171150	NA	283120	9655	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	LncRNA H19-Derived miR-675-3p Promotes Epithelial-Mesenchymal Transition and Stemness in Human Pancreatic Cancer Cells by targeting the STAT3 Pathway.H19 expression is remarkably upregulated in PC cell lines.The expression levels of H19 were positively correlated with miR-675-3p expression in PC cell. We subcloned 3'-UTR SOCS5 fragments containing wild-type (SOCS5-WT) and mutant (SOCS5-MUT) miR-675-3p-binding sites into a psi/check2 vector to confirm whether miR-675-3p directly targeted SOCS5. Based on these data, H19/miR-675-3p regulates SOCS5/STAT3 signaling through the direct targeting of SOCS5 by miR-675-3p.	32626524	RID04072	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Acute myeloid leukemia	CCAT1	MYC	positively-E	StarBase;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000247844	NA	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	bHLHe39|c-Myc|MYCC	lncRNA CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop drives progression of acute myeloid leukaemia.we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects.CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.In order to further explore the downstream molecular mechanism of CCAT1, we carried out bioinformatics analysis through StarBase (http://starbase.sysu.edu.cn/). We found that CCAT1 contained the target site of miR-490-3p .Next, we conducted bioinformatics analysis through StarBase (http://starbase.sysu.edu.cn/) and TargetScan (http://www.targetscan.org/) to search binding sites between miR-490-3p and downstream target genes, and we noticed that MAPK1 was a potential target of miR-490-3p.	32621182|31790145	RID04073	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Acute myeloid leukemia	KCNQ1OT1	MYC	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000136997	NA	10984	4609	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	bHLHe39|c-Myc|MYCC	LncRNA KCNQ1OT1 controls cell proliferation, differentiation and apoptosis by sponging miR-326 to regulate c-Myc expression in acute myeloid leukemia.The expressions of KCNQ1OT1, microRNA-326 (miR-326) and c-Myc were measured by quantitative real-time polymerase chain reaction and western blot, respectively.The interaction between miR-326 and KCNQ1OT1 or c-Myc was explored by luciferase activity, RNA immunoprecipitation or RNA pull-down assay.KCNQ1OT1 knockdown inhibited cell proliferation but promoted apoptosis and cell differentiation. KCNQ1OT1 was a decoy of miR-326 and c-Myc was a target of miR-326. c-Myc protein level was suppressed by KCNQ1OT1 interference and rescued by miR-326 abrogation. Our data showed that KCNQ1OT1 regulates proliferation, differentiation and apoptosis in AML cells by acting as a competing endogenous RNA (ceRNA) for miR-326 to regulate c-Myc, providing a novel avenue for AML treatment.	32621182|31390869	RID04074	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Multiple myeloma	UCA1	IL6R	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);JAK2/STAT3 signaling pathway(+)	ceRNA(miR-331-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000160712	NA	652995	3570	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CD126|gp80|IL-1Ra|IL-6R|IL6RA	Long noncoding RNA UCA1 regulates proliferation and apoptosis in multiple myeloma by targeting miR-331-3p/IL6R axis for the activation of JAK2/STAT3 pathway.The expression of UCA1, miR-331-3p, and IL6R in tumor tissues and cells was measured by qRT-PCRThe interaction among miR-331-3p, UCA1, and IL6R was determined by Luciferase reporter system. The expression of UCA1 and IL6R was up-regulated, while miR-331-3p was down-regulated in MM tumors and cell lines compared with normal tissues and cells. By calculation, miR-331-3p was correlated with UCA1 or IL6R inversely. UCA1 facilitated the activation of the JAK2/STAT3 signaling pathway by enhancing IL6R expression via targeting miR-331-3p. UCA1 accelerates proliferation and suppresses apoptosis in MM by targeting miR-331-3p/IL6R axis to activate JAK2/STAT3 pathway, providing potential targets for the diagnosis and therapy of MM.	32621182|31773675	RID04075	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Neuroblastoma	SNHG4	miR-377-3p	negatively-E		upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	miRNA	ENSG00000281398	GRCh38_5:139274102-139284899	NA	NA	724102	NA	NCRNA00059|U19H	NA	LncRNA SNHG4 promotes neuroblastoma proliferation, migration, and invasion by sponging miR-377-3p.the high expression of lncRNA small nucleolar RNA host gene 4 (SNHG4) in neuroblastoma was tested via quantitative reverse transcription-polymerase chain reaction (qRT-PCR. In mechanism, we found that SNHG4 acted as a competing endogenous RNA to sponge miR-377-3p, which was downregulated in neuroblastomas and inhibited cell proliferation and invasion.	32614236	RID04076	ceRNA or sponge	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	
Malignant glioma	SNHG6	LMO3	positively-E	StarBase;TargetScan;western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-543)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000048540	NA	641638	55885	HBII-276HG|NCRNA00058|U87HG	DAT1|RBTNL2|Rhom-3	LncRNA SNHG6 promotes LMO3 expression by sponging miR-543 in glioma.The levels of SNHG6, microRNA-543 (miR-543) and LIM-only protein 3 (LMO3) were detected in glioma tissues and cells by quantitative real-time polymerase chain reaction.The target relationships were predicted by StarBase v.2.0 and TargetScan and confirmed by dual-luciferase reporter assay. We found that SNHG6 was obviously upregulated in glioma tissues and cells. SNHG6 knockdown significantly repressed glioma cell proliferation, migration and invasion, and induced apoptosis.SNHG6 could competitively sponging miR-543 thereby modulating LMO3 in glioma cells. SNHG6 served as an oncogene and played a vital role in glioma development through miR-543/LMO3 axis.	32613482	RID04077	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE55807)
Acute myeloid leukemia	MROCKI	SOS1	positively-E	miRDB;TargetScan;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000227502	GRCh38_6:113868013-113873390	ENSG00000115904	NA	285758	6654	LINC01268|LOC285758|ROCKI	GF1|GINGF|HGF	Long non-coding RNA LINC01268 promotes cell growth and inhibits cell apoptosis by modulating miR-217/SOS1 axis in acute myeloid leukemia.The expression level of LINC01268 in AML was measured by quantitative PCR (qPCR).The interaction between LINC01268 and miR-217 were predicted by the miRDB website, and then verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay.The relationship between miR-217 and SOS1 was predicted by TargetScan website, and verified by luciferase reporter assay.LINC01268 functioned as a ceRNA via competitively binding to miR-217, and SOS1 was identified as a target of miR-217.	32609259	RID04078	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	TUG1	FLOT1	positively-E	starBase;TargetScan;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(MiR-31-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000223654	NA	55000	10211	FLJ20618|LINC00080|NCRNA00080	NA	Long Non-Coding RNA TUG1 Promotes Cell Proliferation and Inhibits Cell Apoptosis, Autophagy in Clear Cell Renal Cell Carcinoma via MiR-31-5p/FLOT1 Axis.The levels of TUG1, microRNA miR-31-5p and flotillin 1 (FLOT1) in ccRCC tissues and cells were detected by qRT-PCR The interactions between miR-31-5p and TUG1 or FLOT1 were predicted by starBase v2.0 and TargetScan, respectively, which were further validated by RIP assay and RNA pull-down assay.TUG1 was dramatically up-regulated in ccRCC tissues and cells. TUG1 silencing inhibited cell proliferation and promoted cell apoptosis, autophagy in 786-0 and A498 cells.ll data demonstrated that TUG1 promotes cell proliferation and inhibits cell apoptosis and autophagy in ccRCC by miR-31-5p/FLOT1 axis, which may provide a therapeutic target for ccRCC patients.	32606796	RID04079	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Papillary thyroid carcinoma	SBF2-AS1	CDK14	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell viability(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-431-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000058091	NA	283104	5218	NA	PFTAIRE1|PFTK1	Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer.result indicated a higher SBF2-AS1 expression in PTC tissues than adjacent normal tissues.SBF2-AS1 could bind with miR-431-5p and showed negative correlation with miR-431-5p in PTC patients.miR-431-5p bind with cyclin-dependent kinase (CDK) 14 and showed negative correlation with CDK14 in PTC patients.	32602632	RID04080	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	SNHG6	VPS45	positively-E	starBase;RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-485-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000136631	NA	641638	11311	HBII-276HG|NCRNA00058|U87HG	h-vps45|H1|VPS45A|VPS45B	SPI1-induced upregulation of lncRNA SNHG6 promotes non-small cell lung cancer via miR-485-3p/VPS45 axis.the expression of SNHG6 was abnormally high in NSCLC tissues and cells.loss of SNHG6 expression led to the inhibition on the growth, migration and invasion of NSCLC cells.miR-485-3p was necessary for the regulatory relation between SNHG6 and VPS45. we proved that SPI1/SNHG6/miR-485-3p/VPS45 axis exerted oncogenic role in the cellular process of NSCLC cells.	32590190	RID04081	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Atherosclerosis	TUG1	ROR2	positively-E	dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-141-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000169071	NA	55000	4920	FLJ20618|LINC00080|NCRNA00080	BDB|BDB1|NTRKR2	Long Noncoding RNA TUG1 Promotes the Function in ox-LDL-Treated HA-VSMCs via miR-141-3p/ROR2 Axis.the putative binding sites between miR-141-3p and TUG1 or ROR2 were predicted by starBase software online.While the low expression of miR-141-3p negatively correlated with that of TUG1 or ROR2 in AS tissues. Silencing of TUG1 inhibited the proliferation, migration, invasion, and metastasis in ox-LDL-treated HA-VSMCs.	32565910	RID04082	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	LINC00662	EGLN2	positively-E	bioinformatics;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000269858	NA	148189	112398	NA	HIFPH1|PHD1	Long non-coding RNA LINC00662 promotes proliferation and migration of breast cancer cells via regulating the miR-497-5p/EglN2 axis.The expression level of LINC00662 was determined in human breast cancer cell lines and tissues by real-time quantitative polymerase chain reaction (RT-qPCR).LINC00662-specific miRNA and miRNA-gene axis were examined in a dual-luciferase reporter assay and western blot.We found that LINC00662 was overexpressed in both breast cancer cell lines and tissue compared to normal breast cell lines and healthy breast tissue.Bioinformatics analysis predicted that LNC00662 binds to miR-497-5p.our results demonstrated that overexpression of LINC00662 accelerated the malignant growth of breast cancer cells via sponging miR-497-5p and upregulating EglN2 expression, and indicate that targeting LINC00662 may represent a novel strategy for breast cancer therapy.	32558530	RID04083	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	EWSAT1	CPEB4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-330-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000113742	NA	283673	80315	FLJ33768|LINC00277|NCRNA00277|TMEM84	KIAA1673	LncRNA EWSAT1 upregulates CPEB4 via miR-330-5p to promote cervical cancer development.EWSAT1 expression in cervical cancer was evaluated through qRT-PCRDownregulated EWSAT1 expression inhibited Hela cell migration, proliferation, and invasion. EWSAT1 targeted to miR-330-5p and upregulated cytoplasmic polyadenylation element-binding protein 4 (CPEB4) expression by sponging miR-330-5p.Our study revealed that EWSAT1 enhances CPEB4 expression through sponging miR-330-5p, thereby promoting cervical cancer development, which might provide potential therapeutic targets for clinically cervical cancer patients.Luciferase assay was employed to demonstrate EWSAT1 and miR-330-5p interaction. In cervical cancer, the expression of EWSAT1 was enhanced and contributed to the poor prognosis.	32556917	RID04084	ceRNA or sponge	prognosis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Ovarian cancer	THORLNC	STAT3	positively-E	shRNA;western blot	upregulation	RT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell metastasis(+);self-renewal(+)	ceRNA(IL-6)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000168610	NA	100506797	6774	THOR	APRF	Long non-coding RNA THOR promotes ovarian Cancer cells progression via IL-6/STAT3 pathway.RT-PCRand western blotwere used to detect the expression of THOR, p-STAT3 and IL-6.ur results find that THOR is markedly upregulated in human OC tissues and predicts the poor prognosis of OC patients. Functional studies have revealed that knockdown of THOR inhibits the growth, metastasis and self-renewal of OC cells.Our findings reveal that THOR could promote OC cells growth, metastasis and self-renewal by activating IL-6/STAT3 signaling and may be a good predictive factor and therapeutic target.	32552789	RID04085	ceRNA or sponge	metastasis,prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Chordoma	XIST	PPP1R13L	positively-E	siRNA;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Chordoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000104881	NA	7503	10848	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	IASPP|RAI	LncRNA XIST Promotes Growth of Human Chordoma Cells by Regulating miR-124-3p/iASPP Pathway..Quantitative real time-polymerase chain reaction (qRT-PCR was performed to determine lncRNA XIST expression in human chordoma tissues and matched-noncancerous tissues. Silencing and overexpression of lncRNA XIST were carried out by RNA interference (RNAi) and lentiviral transduction, respectively.We found that lncRNA XIST expression was upregulated in chordoma and strongly correlated with poor patient prognosis.lncRNA XIST promoted proliferation and inhibited apoptosis of chordoma cells.upregulation of lncRNA XIST led to a decrease in miR-124-3p expression, thereby promoting the expression of the miR-124-3p target gene, inhibitor of apoptosis-stimulating protein of p53 (iASPP).  Our findings demonstrate a key role for lncRNA XIST in chordoma progression by regulating miR124-3p/iAPSS pathway.	32547104	RID04086	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	ST8SIA6-AS1	HDAC11	positively-E	dual-luciferase reporter assay;western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-4656)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000204832	GRCh38_10:17386919-17445758	ENSG00000163517	NA	100128098	79885	APAL	NA	LncRNA ST8SIA6-AS1 promotes hepatocellular carcinoma cell proliferation and resistance to apoptosis by targeting miR-4656/HDAC11 axis.The expression of ST8SIA6-AS1 was studied by realtime PCR (RT-qPCR) and bioinformatic analysis.The target of ST8SIA6-AS1 was analyzed by bioinformatic analysis and validated by dual-luciferase reporter assay, western blot and RT-qPCR.In this study we demonstrated that ST8SIA6-AS1 was an upregulated lncRNA in hepatocellular carcinoma. SiRNA-mediated knockdown of ST8SIA6-AS1 repressed cell proliferation and induced cell apoptosis in HCC cells. In conclusion, our findings suggested that ST8SIA6-AS1 was a novel upregulated lncRNA in HCC and could facilitate cell proliferation and resistance to cell apoptosis via sponging miR-4656 and elevation of HDAC11, which might be a promising biomarker for patients with HCC.	32536820	RID04087	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495)
Tongue squamous cell carcinoma	FOXD2-AS1	p-p65	positively-E	western blot;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);prognosis(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	Upregulation of long non-coding RNA FOXD2-AS1 promotes progression and predicts poor prognosis in tongue squamous cell carcinoma.Expression of FOXD2-AS1 was detected in TSCC tissues and TCGA data. Compared to the normal tissues and samples, FOXD2-AS1 significantly highly expressed in TSCC tissues and in TSCC samples of TCGA data, and high expression of FOXD2-AS1 was associated with lymphatic metastasis and poor TNM stages.Downregulation of FOXD2-AS1 inhibited the migration and invasion of SCC-9 and CAL-27 cell lines. western blot showed that the expression of p-p44 and p-p65 downregulated after FOXD2-AS1 knockdown.	32531865	RID04088	expression association	metastasis,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Tongue squamous cell carcinoma	FOXD2-AS1	p-p44	positively-E	western blot;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);prognosis(-)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	Upregulation of long non-coding RNA FOXD2-AS1 promotes progression and predicts poor prognosis in tongue squamous cell carcinoma.Expression of FOXD2-AS1 was detected in TSCC tissues and TCGA data. Compared to the normal tissues and samples, FOXD2-AS1 significantly highly expressed in TSCC tissues and in TSCC samples of TCGA data, and high expression of FOXD2-AS1 was associated with lymphatic metastasis and poor TNM stages.Downregulation of FOXD2-AS1 inhibited the migration and invasion of SCC-9 and CAL-27 cell lines. western blot showed that the expression of p-p44 and p-p65 downregulated after FOXD2-AS2 knockdown.	32531865	RID04089	expression association	metastasis,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Malignant glioma	LIN28A	SNHG14	NA	RIP;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);glycolysis(+);cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Brain glioma	TF	lncRNA	ENSG00000131914	NA	ENSG00000224078	GRCh38_15:24978583-25420336	79727	104472715	CSDD1|FLJ12457|LIN-28|LIN28|ZCCHC1	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	Lin28A promotes IRF6-regulated aerobic glycolysis in glioma cells by stabilizing SNHG14.Quantitative real-time polymerase chain reaction and western blot showed that Lin28A and SNHG14 were overexpressed and IRF6 was downregulated in glioma.Taken together, our data revealed that the Lin28A/SNHG14/IRF6 axis is crucial for reprogramming glucose metabolism and stimulating tumorigenesis in glioma cells. Thus, targeting this axis might help in the development of a novel therapeutic strategy for glioma metabolism.	32527996	RID04090	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)
Pancreatic cancer	ZEB1-AS1	TRIB2	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);tumorigenesis(+)	ceRNA(miR-505-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000071575	NA	220930	28951	NA	GS3955|TRB2	LncRNA ZEB1-AS1 promotes pancreatic cancer progression by regulating miR-505-3p/TRIB2 axis.The expression of ZEB1-AS1 in PC tissues and cells was assessed by RT-qPCR.The association between ZEB1-AS1 and miR-505 was verified by dual-luciferase reporter assay.Our results revealed that ZEB1-AS1 expression was significantly upregulated in PC tissues and cells, and the high expression of ZEB1-AS1 indicated the low overall survival rate in PC patients.gain-of-function assays indicated that knockdown of ZEB1-AS1 inhibited the cell viability, migration and invasion of PC cells, while overexpression of ZEB1-AS1 promoted PC cell progression.These results confirmed that ZEB1-AS1 promoted the tumorigenesis of PC through the miR-505/TRIB2 axis, which indicated that ZEB1-AS1 might function as a biomarker for PC treatment and provide a new therapeutic direction in PC.	32513531	RID04091	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nephrotic syndrome	H19	COQ8B	negatively-E	RT-qPCR;western blot	downregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000123815	NA	283120	79934	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ADCK4|COQ8|FLJ12229	Absence of Long Noncoding RNA H19 Promotes Childhood Nephrotic Syndrome through Inhibiting ADCK4 Signal.The expression of H19 and ADCK4 (which are genes recently identified to play key roles in the development of nephrotic syndrome) in peripheral blood mononuclear cells (PBMCs), were detected by real-time quantitative polymerase chain reaction (RT-qPCR).The expression of ADCK4 was also detected by RT-qPCR or western blot when H19 was overexpressed or knocked down in human primary renal podocytes.Luciferase activity analysis was performed to measure whether H19 could regulate the promoter activity of ADCK4.Long noncoding RNA H19 (lncRNA H19) expression was downregulated in PBMCs of children with nephrotic syndrome. ADCK4 was also downregulated.	32489187	RID04092	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nephrotic syndrome	THAP1	H19	positively-E	Luciferase reporter assay;RNA pull-down;RNA immunoprecipitation assay	downregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Urinary system disease	Kidney disease	TF	lncRNA	ENSG00000131931	NA	ENSG00000130600	GRCh38_11:1995171-2001470	55145	283120	4833431A01Rik|DYT6|FLJ10477	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	We detected the THAP1 level in PBMCs of 30 healthy children and 30 NS children by RT-q-PCR and found that THAP1 level was increased (Supplementary Figure 2). Further study revealed that THAP1 promoted the expression of ADCK4 (Supplementary Figure 3). Luciferase reporter assay demonstrated that THAP1 overexpression promoted the activity of the luciferase reporter containing ADKC4 promoter (Supplementary Figure 4). These studies indicated that H19 may regulate ADCK4 through binding with the transcription factor THAP1.	32489187	RID04093	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(NSCLC);DATA(GSE74639)
Sepsis	HULC	TRPM7	positively-E	dual-luciferase reporter;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-204-5p)	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000251164	NA	ENSG00000092439	NA	728655	54822	HCCAT1|LINC00078|NCRNA00078	CHAK1|LTRPC7|TRP-PLIK	LPS promotes the progression of sepsis by activation of lncRNA HULC/miR-204-5p/TRPM7 network in HUVECs.Lipopolysaccharide (LPS) has been reported to induce inflammatory responses, and long non-coding RNA highly up-regulated in liver cancer (HULC) expression was associated with the progression of sepsis.HULC, microRNA-204-5p (miR-204-5p) and TRPM7 expressions in serum of sepsis patients and human umbilical vein endothelial cells (HUVECs) were examined by quantitative real-time polymerase chain reaction (qRT-PCR.Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between HULC and miR-204-5p, miR-204-5p and TRPM7.Mechanically, HULC positively regulated TRPM7 expression by sponging miR-204-5p in HUVECs. LPS impaired cell viability, and promoted cell apoptosis, inflammatory response and oxidative stress in HUVECs by regulating HULC/miR-204-5p/TRPM7 axis.	32484206	RID04094	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Lung squamous cell carcinoma	LINC00173.v1	VEGFA	positively-E	bioinformatics analysis;RNA immunoprecipitation ;luciferase reporter assays	upregulation	RT-qPCR	TCGA;The clinical profile of lung cancer dataset; RNA sequencing profile were downloaded from The Cancer Genome Atlas	NA	angiogenesis(+);cancer progression(+);cell proliferation(+);cell migration(+)	ceRNA(miR-511-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000112715	NA	NA	7422	NA	MVCD1|VEGF|VPF	LINC00173.v1 promotes angiogenesis and progression of lung squamous cell carcinoma by sponging miR-511-5p to regulate VEGFA expression.Differential lncRNA expression in SQC was analyzed in AE-meta and TCGA datasets, and further confirmed in lung cancer tissues and adjacent normal tissues with RT-qPCR and in-situ hybridization.Bioinformatics analysis, RNA immunoprecipitation and luciferase reporter assays were performed to elucidate the downstream target of LINC00173.v1.Our results further revealed that LINC00173.v1 promoted the proliferation and migration of vascular endothelial cells and the tumorigenesis of SQC cells by upregulating VEGFA expression by sponging miR-511-5p.our results showed that squamous cell carcinoma-specific factor Np63alpha contributed to LINC00173.v1 overexpression in SQC.LINC00173.v1 was specifically upregulated in SQC tissues, which predicted poorer overall and progression-free survival in SQC patients.	32473645	RID04095	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Head and neck squamous cell carcinoma	LINC00520	HOXA10	positively-E	dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000253293	NA	645687	3206	C14orf34|LASSIE	HOX1|HOX1H	Silencing of long non-coding RNA LINC00520 promotes radiosensitivity of head and neck squamous cell carcinoma cells.Interactions between LINC00520 and miR-195, homeobox A10 (HOXA10) and miR-195 were evaluated by dual-luciferase reporter gene assay, RNA Immunoprecipitation (RIP), and RNA pull-down assay.LINC00520 was upregulated while miR-195 was downregulated in HNSCC cells and tissues. Silencing LINC00520 or overexpressing miR-195 promoted radiosensitivity and inhibited cell proliferation, invasion, migration, and apoptosis in HNSCC.LINC00520/miR-195/HOXA10 is involved in the radiosensitivity mediation, providing potential therapeutic target for HNSCC treatment.	32462956	RID04096	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Myocardial infarction	ZNF667-AS1	miR-93	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	miRNA	ENSG00000166770	GRCh38_19:56477250-56504362	ENSG00000207757	NA	100128252	NA	MORT	NA	LncRNAMORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.Expression of MORT and miR-93 in hearth tissues and plasma of both MI mice and Sham mice and both MI patients and healthy controls was detected by RT-qPCR. MORT expression levels were also higher, while levels of miR-93 were also lower in plasma of MI patients compared with healthy controls.Therefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.	32450811	RID04097	ceRNA or sponge	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE51827,GSE86978)	
Gastric cancer	GCM1	miR-124	negatively-E	luciferase reporter assay;bioinformatics;ChIP	upregulation	RT-qPCR	NA	NA	cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000137270	GRCh38_6:53126961-53148841	NA	NA	8521	NA	GCMA|hGCMa	NA	SP1-activated long noncoding RNA lncRNA GCMA functions as a competing endogenous RNA to promote tumor metastasis by sponging miR-124 and miR-34a in gastric cancer.we identified a novel cancer-related lncRNA, termed lncRNA GCMA (Gastric Cancer metastasis-associated lncRNA), which was upregulated in GC tissues with lymph node metastasis (LNM) compared with tissues without LNM. High expression of GCMA was significantly associated with poor prognosis of patients with GC. Luciferase assays, bioinformatics analyses and chromatin immunoprecipitation (ChIP) assays indicated that SP1 transcription factor directly bound to the GCMA promoter region and activated its transcription. and activated its transcription. Functionally, upregulation of GCMA dramatically promoted GC cells proliferation, migration and invasion in vitro, whereas knockdown of GCMA elicited the opposite function. says, luciferase assays and western blot assays, GCMA was demonstrated to function as a competing endogenous RNA (ceRNA) via competitively absorbing miR-124 and miR-34a to upregulate slug and snail, thereby induced epithelial-mesenchymal transition (EMT) and GC cell metastasis in vitro and in vivo.these results demonstrate that GCMA functions as an oncogenic lncRNA that may serve as a potential prognostic biomarker for GC and shed new lights on targeted therapy of GC in the future.	32439864	RID04098	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Gastric cancer	GCM1	miR-34a	negatively-E	luciferase reporter assay;bioinformatics;ChIP	upregulation	RT-qPCR	NA	NA	cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000137270	GRCh38_6:53126961-53148841	NA	NA	8521	NA	GCMA|hGCMa	NA	SP1-activated long noncoding RNA lncRNA GCMA functions as a competing endogenous RNA to promote tumor metastasis by sponging miR-124 and miR-35a in gastric cancer.we identified a novel cancer-related lncRNA, termed lncRNA GCMA (Gastric Cancer metastasis-a	32439864	RID04099	ceRNA or sponge	metastasis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Gastric cancer	SNHG1	NOTCH1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-15b)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000148400	NA	23642	4851	LINC00057|lncRNA16|NCRNA00057|UHG	TAN1	LncRNA SNHG1 promotes EMT process in gastric cancer cells through regulation of the miR-15b/DCLK1/Notch1 axis.Gene expression of DCLK1, miR-15b and lncRNA SNHG1 was investigated by qRT-PCRthe correctness of the prediction results was confirmed by a dual-luciferase reporter assay.The expression of DCLK1, Notch1, and SNHG1 was increased in GC tissues, while the expression of miR-15b was decreased. Overexpression of lncRNA SNHG1 promoted the expression of DCLK1 and Nothc1 in GC cells. SNHG1 enhances the EMT process in GC cells through DCLK1-mediated Notch1 pathway, which can be a potential target for treating GC.	32423385	RID04100	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	SNHG1	DCLK1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-15b)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000133083	NA	23642	9201	LINC00057|lncRNA16|NCRNA00057|UHG	DCAMKL1|DCDC3A|DCLK|KIAA0369	LncRNA SNHG1 promotes EMT process in gastric cancer cells through regulation of the miR-15b/DCLK1/Notch1 axis.Gene expression of DCLK1, miR-15b and lncRNA SNHG2 was investigated by qRT-PCRthe correctness of the prediction results was confirmed by a dual-	32423385	RID04101	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Myocardial infarction	CDKN2B-AS1	AKT1	positively-E	RNA immunoprecipitation	upregulation	RT-qPCR	NA	NA	angiogenesis(+)	phosphorylation	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	AKT|PKB|PRKBA|RAC|RAC-alpha	Overexpression of long non-coding RNA ANRIL promotes post-ischaemic angiogenesis and improves cardiac functions by targeting Akt.adenovirus-mediated lncRNA-ANRIL overexpression increased the phosphorylated levels of Akt and eNOS, promoted post-ischaemic angiogenesis and improved heart functions in mice with MI surgery. LncRNA-ANRIL regulates Akt phosphorylation to improve endothelial functions, which promotes angiogenesis and improves cardiac functions in mice following MI. In this perspective, targeting lncRNA-ANRIL/Akt may be considered to develop a drug to treat angiogenesis-related diseases.	32400082	RID04102	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Myocardial infarction	MALAT1	miR-497	negatively-E	luciferase activity assay;RNA pull-down	upregulation	RNA-seq	NA	NA	angiogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Extracellular vesicles from human embryonic stem cell-derived cardiovascular progenitor cells promote cardiac infarct healing through reducing cardiomyocyte death and promoting angiogenesis.luciferase activity assay, RNA pull-down, and manipulation of miR-497 levels showed that MALAT1 improved NRCMs survival and HUVEC tube formation through targeting miR-497. The cardioprotective effects of hCVPC-EVs can be enhanced by hypoxia-conditioning of hCVPCs and are partially contributed by MALAT1 via targeting the miRNA.RNA-seq analysis revealed a high abundance of the lncRNA MALAT1 in the EV-H. Its abundance was upregulated in the infarcted myocardium and cardiomyocytes treated with hCVPC-EVs.	32393784	RID04103	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Pre-eclampsia	AK002210	NAIP	positively-E	luciferase activity assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-590)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000249437	NA	NA	4671	NA	BIRC1|NLRB1	AK002210 promotes the proliferation, migration and invasion of trophoblast cell through regulating miR-590/NAIP signal axis.Quantitative reverse transcription PCR was used to assess the gene expression.Luciferase assay and rescue experiment were carried out to verify the interaction between miR-590-3p and AK002210 as well as NLR family apoptosis inhibitory protein (NAIP).miR-590-3p also directly targets NAIP which served as a ceRNA of AK002210. AK002210 was proved to participated in the regulation of ERK/MMP-2 signal axis. In conclusion, we found that AK002210 knockdown may play a critical role in the progression of PE via miR-590-3p/NAIP and ERK/MMP signaling. It has potential to be a novel prognostic or therapeutic marker of PE.	32387473	RID04104	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Osteosarcoma	LINC-PINT	miR-524-5p	negatively-E	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000231721	GRCh38_7:130938963-131110176	NA	NA	378805	NA	FLJ43663|LincRNA-Pint|MKLN1-AS1|PINT	NA	LncRNA LINC-PINT regulating proliferation and apoptosis of osteosarcoma cells by targeting miR-524-5p.Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR was used to detect the expressions of LINC-PINT and miR-524-5p in normal osteoblast hFOB and human osteosarcoma cell lines HOS, MG63 and SAOS2 cells.The transcriptional activity was detected by double luciferase reporter assay.Compared with normal osteoblast hFOB cell (1.00 0.08 vs 1.00 0.06), the expressions of LINC-PINT were down-regulated (0.18 0.01; 0.33 0.01; 0.42 0.01), while the expressions of miR-524-5p were up-regulated (2.65 0.23; 1.68 0.14; 1.51 0.13) in human osteosarcoma cell lines HOS, MG63 and SAOS2 cells, respectively.Overexpression of LINC-PINT significantly inhibited the proliferation (0.41 0.05 vs. 0.62 0.05 for 48 h; 0.57 0.05 vs. 1.06 0.09 for 72 h, both P<0.05) while promoted the apoptosis (25.28 2.15 vs. 9.01 0.17, P<0.01) of HOS cells.Knockdown of LINC-PINT or overexpression of miR-524-5p can significantly promote the proliferation and inhibit apoptosis of HOS cells.Long non-coding RNA LINC-PINT can inhibit the proliferation and promote apoptosis of osteosarcoma cells through targeting miR-524-5p, which will provide a new target for the treatment of osteosarcoma.	32375449	RID04105	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Gastric cancer	LINC00511	EZH2	positively-E	luciferase activity assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000106462	NA	400619	2146	onco-lncRNA-12	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA LINC00511 promoted cell proliferation and invasion via regulating miR-124-3p/EZH2 pathway in gastric cancer.RT-PCRwas used to detect the expressions of LINC00511 and miR-124-3p in GC tumor tissues, adjacent tissues and GC cell lines.dual-luciferase reporter assay was performed to prove the potential binding sites between LINC00511 and miR-124-3p, miR-124-3p and EZH2.We found that LINC00511 was significantly increased in GC tissues and GC cell lines, which was associated with tumor growth, metastasis and predicted poor diagnosis of GC patients. We uncovered a previously unappreciated LINC00511/miR-124-3p/EZH2 signaling axis in promoting cell proliferation and invasion in GC patients and GC cell lines, which suggested that it might be a potential target for treating human GC.	32373959	RID04106	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MIR1258	LINC01278	negatively-E	LncBase v.2;dual-luciferase reporter assay;RIP	downregulation	sequencing	NA	NA	cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	ENSG00000221240	NA	ENSG00000235437	GRCh38_X:63222993-63561095	100302172	92249	MIRN1258|hsa-mir-1258|mir-1258	NA	The beta-catenin/TCF-4-LINC01278-miR-1258-Smad2/3 axis promotes hepatocellular carcinoma metastasis.We first identified that miR-1258 was downregulated in HCC tissues both in The Cancer Genome Atlas (TCGA) and Sun Yat-sen University Cancer Center (SYSUCC) dataset.Luciferase assays verified direct binding of miR-1258 to Smad2 and Smad3, thereby attenuating TGF-beta/Smad signaling. We further established that lncRNA LINC01278 was a negative regulator of miR-1258.miR-1258 downregulation in turn increased LINC01278 expression. We also observed that TCF-4 could bind to the LINC01278 promoter site.	32372060	RID04107	ceRNA or sponge	metastasis		DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827)
Hepatocellular carcinoma	LINC01278	SMAD2	positively-E	shRNA;overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	ceRNA(miR-1258)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000235437	GRCh38_X:63222993-63561095	ENSG00000175387	NA	92249	4087	NA	JV18-1|MADH2|MADR2	The beta-catenin/TCF-4-LINC01278-miR-1258-Smad2/3 axis promotes hepatocellular carcinoma metastasis.We first identified that miR-1258 was downregulated in HCC tissues both in The Cancer Genome Atlas (TCGA) and Sun Yat-sen University Cancer Center (SYSUCC) dataset.Luciferase assays verified direct binding of miR-1258 to Smad2 and Smad3, thereby attenuating TGF-beta/Smad signaling. We further established that lncRNA LINC01278 was a negative regulator of miR-1258.miR-1258 downregulation in turn increased LINC01278 expression. We also observed that TCF-4 could bind to the LINC01279 promoter site.	32372060	RID04108	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	LINC01278	SMAD3	positively-E	shRNA;overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	ceRNA(miR-1258)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000235437	GRCh38_X:63222993-63561095	ENSG00000166949	NA	92249	4088	NA	HsT17436|JV15-2|MADH3	The beta-catenin/TCF-4-LINC01278-miR-1258-Smad2/3 axis promotes hepatocellular carcinoma metastasis.We first identified that miR-1258 was downregulated in HCC tissues both in The Cancer Genome Atlas (TCGA) and Sun Yat-sen University Cancer Center (SYSUCC) dataset.Luciferase assays verified direct binding of miR-1258 to Smad2 and Smad3, thereby attenuating TGF-beta/Smad signaling. We further established that lncRNA LINC01278 was a negative regulator of miR-1258.miR-1258 downregulation in turn increased LINC01278 expression. We also observed that TCF-4 could bind to the LINC01280 promoter site.	32372060	RID04109	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00473	ROBO1	positively-E	dual-luciferase reporter assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell motility(+)	ceRNA(miR-1294)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223414	NA	ENSG00000169855	NA	90632	6091	C6orf176|LNC473|bA142J11.1	DUTT1|FLJ21882|SAX3	LINC00473 promotes lung adenocarcinoma progression by regulating miR-1294/ROBO1 axis.In this study, RT-qPCR was used to measure the expression of LINC00473, miR-1294 and ROBO1. The results showed that LINC00473 was up-regulated and miR-1294 was down-regulated in lung adenocarcinoma tissues and cells. LINC00473 promoted cell proliferation and motility in lung adenocarcinoma by downregulating miR-1294. In conclusion, LINC00473 acts as a tumor promoter in lung adenocarcinoma by regulating the miR-1294/ROBO1 axis.	32351100	RID04110	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Ovarian cancer	HOTAIR	EZH2	positively-E	dual-luciferase reporter assays	upregulation	RT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-138-5p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|EZH1|KMT6|KMT6A	Knockdown of long non-coding RNA HOTAIR reverses cisplatin resistance of ovarian cancer cells through inhibiting miR-138-5p-regulated EZH2 and SIRT1.The aim of this study was to explore the role of HOX transcript antisense RNA (HOTAIR) in DDP-resistant ovarian cancer cells.Real-time PCR, western blot, dual-luciferase reporter assay, and flow cytometry were then used to evaluate the effect of HOTAIR/miR-138-5p axis on chemoresistance of DDP-resistant ovarian cancer cells to DDP.We found that HOTAIR was upregulated in DDP-resistant cells, while miR-138-5p was downregulated. Knockdown of HOTAIR increased the expression of miR-138-5p in DDP-resistant cells and miR-138-5p is directly bound to HOTAIR.These data demonstrate that HOTAIR acts as a sponge of miR-138-5p to prevent its binding to EZH2 and SIRT1, thereby promoting DDP-resistance of ovarian cancer cells. Our work will shed light on the development of therapeutic strategies for ovarian cancer treatment.	32349783	RID04111	ceRNA or sponge	chemoresistance		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	HOTAIR	SIRT1	positively-E	dual-luciferase reporter assays	upregulation	RT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-138-5p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000096717	NA	100124700	23411	HOXC-AS4|HOXC11-AS1|NCRNA00072	SIR2L1	Knockdown of long non-coding RNA HOTAIR reverses cisplatin resistance of ovarian cancer cells through inhibiting miR-138-5p-regulated EZH2 and SIRT1.The aim of this study was to explore the role of HOX transcript antisense RNA (HOTAIR) in DDP-resistant ovarian cancer cells.Real-time PCR, western blot, dual-luciferase reporter assay, and flow cytometry were then used to evaluate the effect of HOTAIR/miR-138-5p axis on chemoresistance of DDP-resistant ovarian cancer cells to DDP.We found that HOTAIR was upregulated in DDP-resistant cells, while miR-138-5p was downregulated. Knockdown of HOTAIR increased the expression of miR-138-5p in DDP-resistant cells and miR-138-5p is directly bound to HOTAIR.These data demonstrate that HOTAIR acts as a sponge of miR-138-5p to prevent its binding to EZH2 and SIRT2, thereby promoting DDP-resistance of ovarian cancer cells. Our work will shed light on the development of therapeutic strategies for ovarian cancer treatment.	32349783	RID04112	ceRNA or sponge	chemoresistance		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	TUG1	miR-212-3p	negatively-E	bioinformatics software;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Effect of LncTUG1 on NK cell killing sensitivity in oral squamous cell carcinoma cells by targeting miR-212-3p.TUG1 siRNA was transfected,the expression of TUG1, cell proliferation, cell apoptosis and NK cell killing rate were detected by qRT-PCR MTT, flow cytometry and LDH. Bioinformatics software was used to predict that TUG1 and miR-212-3p will target and complement each other, so luciferase reporter vector was constructed and the targeting relationship was identified. Down-regulation of TUG1 targeting and negative regulation of miR-212-3p inhibits proliferation, induces apoptosis and improves NK cell killing sensitivity of oral squamous cell carcinoma cells.	32346696	RID04113	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Atherosclerosis	CDKN2B-AS1	CDKN2B	NA	RIP;ChIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	CDK4I|INK4B|MTS2|P15|p15INK4b|TP15	Long non-coding RNA CDKN2B-AS1 contributes to atherosclerotic plaque formation by forming RNA-DNA triplex in the CDKN2B promoter. RIP and ChIP assays were used to identify interactions between CDKN2B-AS1, CCCTC-binding factor (CTCF), enhancer of zeste homologue 2 (EZH2), and CDKN2B. Triplex formation was determined by RNA-DNA pull-down and capture assay as well as EMSA experiment.CDKN2B-AS1 showed high expression levels in atherosclerosis, whereas CDKN2B showed low expression levels. CDKN2B-AS1 is highly expressed in atherosclerosis whilst CDKN2B is poorly expressed.To evaluate the expression of CDKN2B-AS1 in atherosclerosis, we examined the expression levels of CDKN2B-AS1 at tissue and cell levels by RT-qPCR.These results indicated that knocking down CDKN2B-AS1 can reverse the inhibitory effects of CDKN2B knockdown on mRCT in THP-1 macrophage-derived and HPM-derived foam cells and the promoting effects on intracellular lipid accumulation. These findings suggest that CDKN2B-AS1 participates in THP-1 macrophage-derived and HPM-derived foam cell development through CDKN2B.	32335370	RID04114	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC);DATA(GSE117623)
Atherosclerosis	MALAT1	ABCA1	positively-E	western blot;bioinformatics;dual-luciferase reporter assay;RT-qPCR	downregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000165029	NA	378938	19	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ABC1|HDLDT1|TGD	Long noncoding RNA MALAT1 regulates cholesterol accumulation in ox-LDL-induced macrophages via the microRNA-17-5p/ABCA1 axis.the mRNA expression level of MALAT1 was measured using reverse transcription-quantitative PCR (RT-qPCR) and the protein expression level was detected via western blotBioinformatics, dual-luciferase reporter and RT-qPCR assays were used to investigate the relationship between MALAT1 and the microRNA (miR)-17-5p/ATP-binding cassette transporter-A1 (ABCA1) axis. the present results suggested that the MALAT1 expression level was significantly decreased in patients with AS.In summary, knockdown of MALAT1 may promote cholesterol accumulation by regulating the miR-17-5p/ABCA1 axis in ox-LDL-induced THP-1 macrophages.	32319624	RID04115	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	SNHG1	MAPK6	positively-E	miRBase;miRanda;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	ceRNA(miR-196a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000069956	NA	23642	5597	LINC00057|lncRNA16|NCRNA00057|UHG	ERK3|HsT17250|p97MAPK|PRKM6	LncRNA SNHG1 regulates vascular endothelial cell proliferation and angiogenesis via miR-196a. we found SNHG1 is upregulated in TNF-alpha-treated HUVECs.Then we demonstrated that SNHG1 may interact directly with miR-196a to act as a miR-196a sponge. Further, MAPK6 were predicted to be the target of miR-196a. So we blocked miR-196a, which increased expression level of MAPK6, enhanced cell proliferation, migration and angiogenesis. These data indicated that SNHG1/miR-196a/MAPK6 axis may take a part in autophagy regulation in TNF-alpha-treated HUVECs. The subsequent rescue experiments come to the results ascertained the specificity of SNHG1/miR-196a/MAPK6 axis in regulating MAPK6. Overall, our findings demonstrate a novel mechanism by which SNHG1 overexpression protects the function of HUVECs, which may delay the progression of AS. SNHG1/miR-196a/MAPK6 axis may be of therapeutic significance in AS.First, we predicted the potential miRNA binding sites in SNHG1 through bioinformatic database (miRBase and miRanda). n order to further verify the direct binding between miR-196a and SNHG1, RIP assay was performed in HUVECs lysate. W	32297149	RID04116	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Malignant glioma	NCK1-DT	TRIM24	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-138-2-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000122779	NA	101927597	8805	NCK1-AS1|SLC35G2-AS1	hTIF1|RNF82|TIF1|Tif1a	Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/beta-catenin axis.microarray analyses were performed to explore the lncRNAs/miRNAs/genes with differential expression in glioma. The interactions among NCK1-AS1, miR-138-2-3p and TRIM24 were validated through luciferase reporter, RNA immunoprecipitation and RNA pull-down assays.High expression of NCK1-AS1 was found in glioma tissues and cells, especially in U251 cells.Online predictions and the integrated experiments identified that NCK1-AS1 elevated the TRIM24 expression through sponging miR-138-2-3p, and further activated the Wnt/beta-catenin pathway.Artificial silencing of NCK1-AS1 or up-regulation of miR-138-2-3p led to inhibited proliferation, invasion and migration but promoted cell apoptosis of U251 cells, while up-regulation of TRIM24 reversed these changes, and it activated the Wnt/beta-catenin pathway.ur study suggested that NCK1-AS1 might elevate TRIM24 expression and further activate the Wnt/beta-catenin pathway via acting as a ceRNA for miR-138-2-3p. Silencing of NCK1-AS1 might inhibit the progression of glioma.	32293515	RID04117	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Rheumatoid arthritis	PVT1	SCUBE2	positively-E	western blot;RNA pull-down assays;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-543)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000175356	NA	5820	57758	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Cegb1|Cegf1|FLJ16792	Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis. PVT1 was overexpressed in synovial tissues from RA patients through microarray expression profiles.Overexpression of PVT1 or silencing of miR-543 enhanced SCUBE2 expression, thereby promoting proliferation and interleukin-1beta (IL-1beta) secretion, while inhibiting apoptosis rate of FLSs. Conversely, si-SCUBE2 reversed the role of miR-543 inhibitor.CONCLUSION: The key findings support that PVT1 knockdown has the potency to hinder RA progression by inhibiting SCUBE2 expression to sponge miR-543.	32293498	RID04118	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Pancreatic ductal adenocarcinoma	MALAT1	KRAS	positively-E	miRcode;RNAhybrid	upregulation	gene expression profile	NA	NA	cell growth(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000133703	NA	378938	3845	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	K-Ras4B|KRAS1|KRAS2	The lncRNA MALAT1 acts as a competing endogenous RNA to regulate KRAS expression by sponging miR-217 in pancreatic ductal adenocarcinoma.MALAT1 is expressed at higher levels in pancreatic ductal adenocarcinoma (PDAC) tissues than in nontumour tissues and in metastatic PDAC than in localized tumours. Moreover, MALAT1 knockdown inhibits cell cycle progression and impairs tumour cell migration and invasion. We found that miR-217 can bind MALAT1 and regulate its expression in PDAC cell lines. We also found MALAT1 knockdown attenuates the protein expression of KRAS, a known target of miR-217. After MALAT1 knockdown, KRAS protein expression levels can be rescued through inhibition of miR-217 expression. Data mining of the above gene profiling results showed that MALAT1 was expressed at higher levels in PDAC tissues than in nontumour tissues.Taken together, these results indicate that MALAT1 enhances pancreatic cancer cell growth and proliferation and inhibits cell apoptosis.Bioinformatics algorithms used for predicting miRNA targets, including miRcode32 and RNAhybrid33, identified miR-217 as one of the miRNAs specific for MALAT1. he decreases in KRAS levels resulting from MALAT1 knockdown could be partially rescued by the introduction of an miR-217 inhibitor .	32257946|28701723	RID04119	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Pancreatic ductal adenocarcinoma	PVT1	miR-448	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-448)	regulation	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA-PVT1 promotes pancreatic cancer cells proliferation and migration through acting as a molecular sponge to regulate miR-448.we first measured the level of PVT1 in the PC cell lines and tissues by quantitative real-time PCR (qRT-PCR, and then employed loss-of-function and gain-of-function approaches to explore the association between PVT1 expression levels and PC cell proliferation/migration ability. bioinformatics analysis was utilized to show that PVT1 contains binding site for miR-448 and an inverse correlation between PVT1 and miR-448 was obtained in PC specimens. dual-luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) and applied biotin-avidin pull-down system were applied to further confirm that PVT1 directly bind with microRNA binding site harboring in the PVT1 sequence. SERBP1 was identified as a target of miR-448 according to the gene expression array analysis of PC clinical samples. Together, we revealed that PVT1 functions as an endogenous "sponge" by competing for miR-448 binding to regulate the miRNA target SERBP1 and, therefore, promotes the proliferation and migration of PC cells.	32257946|28657147	RID04120	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Pancreatic ductal adenocarcinoma	PVT1	ULK1	positively-E	miRanda;PicTar;Targetscan;DIANA;StarBase v2.0	upregulation	sequencing	NA	NA	cell autophagy(+)	ceRNA(miR-20a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000177169	NA	5820	8408	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG1|ATG1A	LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis.PVT1 expression level was detected by quantitative real-time polymerase chain reaction (qRT-PCR and hybridization in situ (ISH). we found that PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression and the development of pancreatic ductal adenocarcinoma.we found that PVT1 was dramatically up-regulated in 20 PDA tissues compared with the corresponding non-tumor tissues .PVT1 induces autophagy by up-regulating ULK1 protein in vitro.to demonstrate whether PVT1 plays as a ceRNA, we first applied bioinformatics analysis to explore potential miRNAs targeting the ULK1 3'UTR (miRanda, PicTar and Targetscan, Additional file 1: Table S4) and targeting the PVT1 3'UTR (DIANA and StarBase v2.0, Additional file 1: Table S5).	32257946| 30001707	RID04121	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	H19	CDK14	positively-E	luciferase reporter assay;RIP	upregulation	sequencing	NA	NA	cell proliferation(+);cell migration(+);WNT signaling pathway(+)	ceRNA(miR-194)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000058091	NA	283120	5218	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PFTAIRE1|PFTK1	LncRNA H19/miR-194/PFTK1 axis modulates the cell proliferation and migration of pancreatic cancer.PDAC tissues, the expression of H19 and PFTK1 were upregulated; H19 knockdown suppressed the cell proliferation and migration of PDAC, while PFTK1 overexpression partially attenuated the suppressive effect of H19 knockdown.As analyzed by TCGA and predicted by online tools, miR-194 was negatively correlated with PFTK1 and might bind to both H19 and PFTK1, which was further confirmed by luciferase reporter and RNA immunoprecipitation assays.H19/miR-194 axis modulated PDAC cell proliferation and migration through PFTK1 downstream Wnt signaling. Results suggested that rescuing miR-194 expression in PDAC can inhibit lncRNA H19 and PFTK1 expression, subsequently suppressing PDAC cell proliferation and migration. Due to the complexity of the lncRNA-miRNA-mRNA network, further in vivo experiments examining potential side effects are needed in future study to explore the clinical application of these findings.	32257946| 30474270	RID04122	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	GAS5	RECK	positively-E	qRT-PCR;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell invasion(-)	ceRNA(miR-135b)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000122707	NA	60674	8434	NCRNA00030|SNHG2	hRECK|ST15	GAS5 Regulates RECK Expression and Inhibits Invasion Potential of HCC Cells by Sponging miR-135b.Expression of GAS5 and microRNA-135b (miR-135b) was analyzed by qRT-PCRin paired HCC tissue samples. Targeting of GAS5 and RECK by miR-135b was confirmed by qRT-PCR western blot, and luciferase reporter assays.Decreased GAS5 and increased miR-135b in HCC inversely correlate with each other and both correlate with poor prognosis of HCC patients. GAS5 is a target of miR-135b. Furthermore, GAS5 positively regulates expression of RECK, also a target of miR-135b, which further inhibits MMP-2 expression and contributes to invasion repression.GAS5 acted as a tumor suppressor in HCC invasion in a competing endogenous RNA manner. Our findings indicate that GAS5 is a promising therapeutic target for HCC treatment.	32257946| 30733959	RID04123	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CRNDE	POU2F1	positively-E	dual-luciferase reporter assay;qRT-PCR;western blot;Immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-539-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000143190	NA	643911	5451	CRNDEP|LINC00180|LOC643911	1-Oct|OTF1	lncRNA CRNDE promotes the proliferation and metastasis by acting as sponge miR-539-5p to regulate POU2F1 expression in HCC.We used qRT-PCRto detect the expression of lncRNA CRNDE in HCC cells, normal cells and clinical tissues.Online prediction software was used to predict the binding sites between lncRNA CRNDE and miR-539-5p, or miR-539-5p and POU2F1 3'UTR. dual-luciferase reporter assay, qRT-PCRand RNA pull-down were used to detect target-relationship between lncRNA CRNDE and miR-539-5p. lncRNA CRNDE was highly expressed in HCC cells and HCC tissues compared with normal cells and the corresponding adjacent normal tissues. lncRNA CRNDE promoted the cell viability, migration and invasion of HCC cells, while inhibited the apoptosis and promoted the EMT process of HCC cells.lncRNA CRNDE promotes the expression of POU2F1 by adsorbing miR-539-5p, thus promoting the progression of HCC.In HCC clinical tissues, miR-539-5p expression decreased and POU2F1 increased compared with the corresponding adjacent normal tissues.	32252678	RID04124	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807)
Hepatocellular carcinoma	CRNDE	BAX	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000087088	NA	643911	581	CRNDEP|LINC00180|LOC643911	BCL2L4	lncRNA CRNDE promotes the proliferation and metastasis by acting as sponge miR-539-5p to regulate POU2F1 expression in HCC.We used qRT-PCRto detect the expression of lncRNA CRNDE in HCC cells, normal cells and clinical tissues.Online prediction software was used to predict the binding sites between lncRNA CRNDE and miR-539-5p, or miR-539-5p and POU2F1 3'UTR. dual-luciferase reporter assay, qRT-PCRand RNA pull-down were used to detect target-relationship between lncRNA CRNDE and miR-539-5p. lncRNA CRNDE was highly expressed in HCC cells and HCC tissues compared with normal cells and the corresponding adjacent normal tissues. lncRNA CRNDE promoted the cell viability, migration and invasion of HCC cells, while inhibited the apoptosis and promoted the EMT process of HCC cells.lncRNA CRNDE promotes the expression of POU2F1 by adsorbing miR-539-5p, thus promoting the progression of HCC.In HCC clinical tissues, miR-539-5p expression decreased and POU2F2 increased compared with the corresponding adjacent normal tissues. western blot revealed that overexpression of lncRNA CRNDE decreased the expression of Bax and Cleaved Caspase 3, and enhanced the expression of Bcl-2.	32252678	RID04125	expression association	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CRNDE	Caspase3	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	lncRNA CRNDE promotes the proliferation and metastasis by acting as sponge miR-539-5p to regulate POU2F1 expression in HCC.We used qRT-PCRto detect the expression of lncRNA CRNDE in HCC cells, normal cells and clinical tissues.Online prediction software was used to predict the binding sites between lncRNA CRNDE and miR-539-5p, or miR-539-5p and POU2F1 3'UTR. dual-luciferase reporter assay, qRT-PCRand RNA pull-down were used to detect target-relationship between lncRNA CRNDE and miR-539-5p. lncRNA CRNDE was highly expressed in HCC cells and HCC tissues compared with normal cells and the corresponding adjacent normal tissues. lncRNA CRNDE promoted the cell viability, migration and invasion of HCC cells, while inhibited the apoptosis and promoted the EMT process of HCC cells.lncRNA CRNDE promotes the expression of POU2F1 by adsorbing miR-539-5p, thus promoting the progression of HCC.In HCC clinical tissues, miR-539-5p expression decreased and POU2F2 increased compared with the corresponding adjacent normal tissues. western blot revealed that overexpression of lncRNA CRNDE decreased the expression of Bax and Cleaved Caspase 3, and enhanced the expression of Bcl-3.	32252678	RID04126	expression association	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Hepatocellular carcinoma	CRNDE	BCL2	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000171791	NA	643911	596	CRNDEP|LINC00180|LOC643911	Bcl-2|PPP1R50	lncRNA CRNDE promotes the proliferation and metastasis by acting as sponge miR-539-5p to regulate POU2F1 expression in HCC.We used qRT-PCRto detect the expression of lncRNA CRNDE in HCC cells, normal cells and clinical tissues.Online prediction software was used to predict the binding sites between lncRNA CRNDE and miR-539-5p, or miR-539-5p and POU2F1 3'UTR. dual-luciferase reporter assay, qRT-PCRand RNA pull-down were used to detect target-relationship between lncRNA CRNDE and miR-539-5p. lncRNA CRNDE was highly expressed in HCC cells and HCC tissues compared with normal cells and the corresponding adjacent normal tissues. lncRNA CRNDE promoted the cell viability, migration and invasion of HCC cells, while inhibited the apoptosis and promoted the EMT process of HCC cells.lncRNA CRNDE promotes the expression of POU2F1 by adsorbing miR-539-5p, thus promoting the progression of HCC.In HCC clinical tissues, miR-539-5p expression decreased and POU2F2 increased compared with the corresponding adjacent normal tissues. western blot revealed that overexpression of lncRNA CRNDE decreased the expression of Bax and Cleaved Caspase 3, and enhanced the expression of Bcl-4.	32252678	RID04127	expression association	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	SNHG14	STAT3	positively-E	bioinformatics;luciferase reporter assay;RIP;RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+);cancer progression(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000168610	NA	104472715	6774	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	APRF	Long noncoding RNA SNHG14 promotes the aggressiveness of retinoblastoma by sponging microRNA-124 and thereby upregulating STAT3.SNHG14 expression levels in RB tissue samples and cell lines were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR).The target microRNA (miRNA) of SNHG14 was predicted by bioinformatics analysis and was subsequently validated by a luciferase reporter assay, RNA immunoprecipitation (RIP) assay, RT-qPCR, and western blotSNHG14 was identified to be significantly overexpressed in RB tissues and cell lines. SNHG14 served as a ceRNA to upregulate STAT3 by sponging miR-124. Therefore, targeting the SNHG14/miR-124/STAT3 pathway may be an effective therapeutic strategy against RB.	32236565	RID04128	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophageal cancer	ELFN1-AS1	GFPT1	positively-E	RNAi	upregulation	sequencing	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-183-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000236081	GRCh38_7:1738630-1742291	ENSG00000198380	NA	101927125	2673	MYCLo-2	GFA|GFAT|GFAT1|GFPT	LncRNA ELFN1-AS1 promotes esophageal cancer progression by up-regulating GFPT1 via sponging miR-183-3p.we discovered that higher ELFN1-AS1 expression indicated shorter patient survival in pan-cancer, including ESCA, using online The Cancer Genome Atlas (TCGA) tools. The lncRNA ELFN1-AS1 was significantly up-regulated in ESCA tissues and cell lines when compared with the counterparts. we found that the expression of microRNA-183-3p (miR-183-3p) and ELFN1-AS1 or glutamine-fructose-6-phosphate transaminase 1 (GFPT1) were inversely correlated in ESCA. Both ELFN1-AS1 and GFPT1 are direct targets of miR-183-3p in ESCA. The effects of ELFN1-AS1 knockdown on ESCA progression were partially rescued by inhibition of miR-183-3p or over-expression of GFPT1. In summary, the results of this study suggest that the lncRNA ELFN1-AS1 facilitates the progression of ESCA by acting as a competing endogenous RNA (ceRNA) to promote GFPT1 expression via sponging miR-183-3p.	32229685	RID04129	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(PRAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065)
Hypertension	MALAT1	NR3C2	positively-E	western blot;dual-luciferase reporter assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell metastasis(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000151623	NA	378938	4306	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MLR|MR	Long Non-Coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Hypertension by Modulating the Hsa-miR-124-3p/Nuclear Receptor Subfamily 3, Group C, Member 2 (NR3C2) and Hsa-miR-135a-5p/NR3C2 Axis.The mechanism for lncRNA MALAT1 modulating the proliferation and apoptosis of HUVECs was explored by cell transfection, Cell Counting Kit-8 (CCK-8), quantitative real-time polymerase chain reaction (qRT-PCR, western blot, and dual-luciferase reporter assays.MALAT1 was increased in the plasma of hypertensive patients. Additionally, after knocking down MALAT, the levels of hsa-miR-124-3p and hsa-miR-135a-5p in HUVECs were markedly increased, while the expression level of NR3C2 protein was decreased. MALAT1 regulates proliferation and apoptosis of HUVECs through the hsa-miR-124-3p/NR3C2 and/or hsa-miR-135a-5p/NR3C2 axis.	32222724	RID04130	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Polycystic ovary syndrome	NEAT1	miR-16	negatively-E	luciferase reporter gene assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long Non-coding RNA NEAT1 Drives the Development of Polycystic Ovary Syndrome via Sponging Multiple MicroRNAs.A line of evidences have validated that multiple microRNAs (including miR-16, miR-483 and miR-324-3p) were abnormally expressed in granulosa cells, which may be closely related with the pathogenesis of polycystic ovary syndrome (PCOS). RT-PCRwas performed to detect NEAT1 expression in PCOS tissues, and human ovarian granulosa cell line KGN were taken as the model to construct the cell line with high expression and low expression of NEAT1.we performed luciferase reporter gene assay and RNA binding protein immunoprecipitation (RIP) assay to verify the interaction between NEAT1, miR-16, miR-483 and miR-324-3p. We demonstrated that NEAT1 was highly expressed in PCOS tissues and cells.Over-expressed NEAT1 promoted the proliferation and inhibited the apoptosis.In conclusion, NEAT1 can promote the proliferation of ovarian granulosa cells and arrest apoptosis via impeding expressions of miR-16, miR-483 and miR-324-3p. Our research would shed new light on the molecular mechanism of ovarian granulosa cell disorder.	32222120	RID04131	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Polycystic ovary syndrome	NEAT1	MIR483	negatively-E	luciferase reporter gene assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000207805	NA	283131	619552	LINC00084|NCRNA00084|TncRNA|VINC	MIRN483|hsa-mir-483|mir-483	Long Non-coding RNA NEAT1 Drives the Development of Polycystic Ovary Syndrome via Sponging Multiple MicroRNAs.A line of evidences have validated that multiple microRNAs (including miR-16, miR-483 and miR-324-3p) were abnormally expressed in granulosa cells, which may be closely related with the pathogenesis of polycystic ovary syndrome (PCOS). RT-PCRwas performed to detect NEAT1 expression in PCOS tissues, and human ovarian granulosa cell line KGN were taken as the model to construct the cell line with high expression and low expression of NEAT1.we performed luciferase reporter gene assay and RNA binding protein immunoprecipitation (RIP) assay to verify the interaction between NEAT1, miR-16, miR-483 and miR-324-3p. We demonstrated that NEAT1 was highly expressed in PCOS tissues and cells.Over-expressed NEAT1 promoted the proliferation and inhibited the apoptosis.In conclusion, NEAT1 can promote the proliferation of ovarian granulosa cells and arrest apoptosis via impeding expressions of miR-16, miR-483 and miR-324-4p. Our research would shed new light on the molecular mechanism of ovarian granulosa cell disorder.	32222120	RID04132	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Polycystic ovary syndrome	NEAT1	miR-324-3p	negatively-E	luciferase reporter gene assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long Non-coding RNA NEAT1 Drives the Development of Polycystic Ovary Syndrome via Sponging Multiple MicroRNAs.A line of evidences have validated that multiple microRNAs (including miR-16, miR-483 and miR-324-3p) were abnormally expressed in granulosa cells, which may be closely related with the pathogenesis of polycystic ovary syndrome (PCOS). RT-PCRwas performed to detect NEAT1 expression in PCOS tissues, and human ovarian granulosa cell line KGN were taken as the model to construct the cell line with high expression and low expression of NEAT1.we performed luciferase reporter gene assay and RNA binding protein immunoprecipitation (RIP) assay to verify the interaction between NEAT1, miR-16, miR-483 and miR-324-3p. We demonstrated that NEAT1 was highly expressed in PCOS tissues and cells.Over-expressed NEAT1 promoted the proliferation and inhibited the apoptosis.In conclusion, NEAT1 can promote the proliferation of ovarian granulosa cells and arrest apoptosis via impeding expressions of miR-16, miR-483 and miR-324-5p. Our research would shed new light on the molecular mechanism of ovarian granulosa cell disorder.	32222120	RID04133	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Non-small cell lung cancer	SNHG6	RSF1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000048649	NA	641638	51773	HBII-276HG|NCRNA00058|U87HG	HBXAP|p325|RSF-1|XAP8	Long Noncoding RNA SNHG6 Promotes Proliferation and Inhibits Apoptosis in Non-small Cell Lung Cancer Cells by Regulating miR-490-3p/RSF1 Axis.he expression of SNHG6, miR-490-3p, and remodeling and spacing factor 1 (RSF1) in NSCLC tumors and cells was measured by quantitative real-time polymerase chain reaction.Luciferase reporter assay was employed for verifying the interaction between miR-490-3p and SNHG6 or RSF1.SNHG6 and RSF1 expression were upregulated, whereas miR-490-3p was downregulated in NSCLC tumors and cell lines compared with normal tissues and cells. Then, luciferase reporter assay confirmed the interaction between miR-490-3p and SNHG6 or RSF1.The authors demonstrated that SNHG6 promoted proliferation and inhibits apoptosis in NSCLC by regulating miR-490-3p/RSF1 axis, representing promising targeted therapeutic strategies against NSCLC.	32202941	RID04134	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Non-small cell lung cancer	SNHG6	BAX	negatively-E	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000087088	NA	641638	581	HBII-276HG|NCRNA00058|U87HG	BCL2L4	Long Noncoding RNA SNHG6 Promotes Proliferation and Inhibits Apoptosis in Non-small Cell Lung Cancer Cells by Regulating miR-490-3p/RSF1 Axis.he expression of SNHG6, miR-490-3p, and remodeling and spacing factor 1 (RSF1) in NSCLC tumors and cells was measured by quantitative real-time polymerase chain reaction.Luciferase reporter assay was employed for verifying the interaction between miR-490-3p and SNHG6 or RSF1.SNHG6 and RSF1 expression were upregulated, whereas miR-490-3p was downregulated in NSCLC tumors and cell lines compared with normal tissues and cells. Then, luciferase reporter assay confirmed the interaction between miR-490-3p and SNHG6 or RSF1.The authors demonstrated that SNHG6 promoted proliferation and inhibits apoptosis in NSCLC by regulating miR-490-3p/RSF2 axis, representing promising targeted therapeutic strategies against NSCLC. SNHG6 knockdown boostedexpression of apoptosis-related protein Bax, cleaved casp-3,and suppressed expression of antiapoptosis protein Bcl-2.	32202941	RID04135	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG6	Caspase3	negatively-E	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Long Noncoding RNA SNHG6 Promotes Proliferation and Inhibits Apoptosis in Non-small Cell Lung Cancer Cells by Regulating miR-490-3p/RSF1 Axis.he expression of SNHG6, miR-490-3p, and remodeling and spacing factor 1 (RSF1) in NSCLC tumors and cells was measured by quantitative real-time polymerase chain reaction.Luciferase reporter assay was employed for verifying the interaction between miR-490-3p and SNHG6 or RSF1.SNHG6 and RSF1 expression were upregulated, whereas miR-490-3p was downregulated in NSCLC tumors and cell lines compared with normal tissues and cells. Then, luciferase reporter assay confirmed the interaction between miR-490-3p and SNHG6 or RSF1.The authors demonstrated that SNHG6 promoted proliferation and inhibits apoptosis in NSCLC by regulating miR-490-3p/RSF2 axis, representing promising targeted therapeutic strategies against NSCLC. SNHG6 knockdown boostedexpression of apoptosis-related protein Bax, cleaved casp-3,and suppressed expression of antiapoptosis protein Bcl-3.	32202941	RID04136	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Non-small cell lung cancer	SNHG6	BCL2	positively-E	western blot;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000171791	NA	641638	596	HBII-276HG|NCRNA00058|U87HG	Bcl-2|PPP1R50	Long Noncoding RNA SNHG6 Promotes Proliferation and Inhibits Apoptosis in Non-small Cell Lung Cancer Cells by Regulating miR-490-3p/RSF1 Axis.he expression of SNHG6, miR-490-3p, and remodeling and spacing factor 1 (RSF1) in NSCLC tumors and cells was measured by quantitative real-time polymerase chain reaction.Luciferase reporter assay was employed for verifying the interaction between miR-490-3p and SNHG6 or RSF1.SNHG6 and RSF1 expression were upregulated, whereas miR-490-3p was downregulated in NSCLC tumors and cell lines compared with normal tissues and cells. Then, luciferase reporter assay confirmed the interaction between miR-490-3p and SNHG6 or RSF1.The authors demonstrated that SNHG6 promoted proliferation and inhibits apoptosis in NSCLC by regulating miR-490-3p/RSF2 axis, representing promising targeted therapeutic strategies against NSCLC. SNHG6 knockdown boostedexpression of apoptosis-related protein Bax, cleaved casp-3,and suppressed expression of antiapoptosis protein Bcl-4.	32202941	RID04137	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Rheumatoid arthritis	CASC2	IL17A	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000112115	NA	255082	3605	C10orf5	CTLA8|IL-17|IL-17A|IL17	lncRNA CASC2 downregulation participates in rheumatoid arthritis, and CASC2 overexpression promotes the apoptosis of fibroblast-like synoviocytes by downregulating IL-17.Our preliminary microarray data showed that lncRNA CASC2 was downregulated in the plasma of patients with rheumatoid arthritis.n the present study, lncRNA CASC2 and IL-17 in plasma were detected by reverse transcription-quantitative PCR and ELISA, respectively. downregulation of lncRNA CASC2 is involved in RA and lncRNA CASC2 overexpression may promote the apoptosis of HFLS by downregulating IL-17.	32186765	RID04138	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Acute myeloid leukemia	MAGI2-AS3	LRIG1	negatively-E	MethPrimer;RNA pull-down assay;RIP	downregulation	RT-qPCR	NA	NA	self-renewal(-)	DNA demethylation	regulation	RNA-protein	NA	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000144749	NA	100505881	26018	ENST00000414797	DKFZP586O1624|LIG-1|LIG1	LncRNA MAGI2-AS3 inhibits the self-renewal of leukaemic stem cells by promoting TET2-dependent DNA demethylation of the LRIG1 promoter in acute myeloid leukaemia.MAGI2-AS3 exhibited a poor expression level in LSCs than the normal human haematopoietic stem cells. MAGI2-AS3-overexpressed LSCs acquired the ability of self-renewal following lentivirus-mediated knockdown of LRIG1.Methylation-dependent inhibition of LRIG1 was evident in LSCs. MAGI2-AS3 was found to induce occupancy of TET2 at the LRIG1 promoter. Lentivirus-mediated downregulation of TET2 could impair MAGI2-AS3-mediated elevation of LRIG1 and neutralize the inhibitory effect of MAGI2-AS3 on LSCs self-renewal. In vivo analysis indicated an elevated overall survival of NOD/SCID mice injected with LSCs in the presence of MAGI2-AS3. Altogether, the key findings support the potential of lncRNA MAGI2-AS3 to serve as a novel candidate for the improvement of AML treatment.We downloaded the gene expression profile GSE17054, which consisted of 4 normal samples and 9 AML samples with normal samples as control [16] from the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). Analysis of the differentially expressed lncRNAs was conducted using the 'limma'-package of R language [17] with the screening criteria set as |log FoldChange| >1 and a p value <0.05. Our analysis of the dataset revealed the presence of a total of 3005 differentially expressed lncRNAs in LSCs of AML, among which lncRNA MAGI2-AS3 was significantly down-regulated .Our data clearly illustrated that lncRNA MAGI2-AS3 overexpression inhibited LSCs self-renewal;	32174258	RID04139	expression association	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827)
Cervical cancer	SNHG7	PAK4	positively-E	RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-485)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000130669	NA	84973	10298	MGC16037|NCRNA00061	NA	Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4.Reverse-transcription quantitative PCR was performed to measure SNHG7 expression in cervical cancer. SNHG7 was found to be markedly upregulated in cervical cancer tissues and cell lines.Higher SNHG7 expression significantly correlated with FIGO stage, lymph node metastasis, the depth of cervical invasion, and shorter overall survival in patients with cervical cancer. Functional experiments indicated that a SNHG7 knockdown attenuated proliferation, migration, and invasiveness and promoted apoptosis of cervical cancer cells in vitro. The SNHG7 knockdown also slowed tumor growth in vivo.Further investigation showed that SNHG7 acts as a competing endogenous RNA for microRNA-485 (miR-485) in cervical cancer cells, and the inhibitory actions of the SNHG7 knockdown on the malignant phenotype were reversed by miR-485 inhibition. P21-activated kinase 4 (PAK4) was identified as a direct target gene of miR-485 in cervical cancer, and PAK4 expression was promoted by SNHG7.	32158221	RID04140	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE75367)
Retinoblastoma	XIST	SOX4	positively-E	dual-luciferase reporter assay;Spearman's analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000124766	NA	7503	6659	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	XIST promotes cell proliferation and invasion by regulating miR-140-5p and SOX4 in retinoblastoma.Expressions of XIST, microRNA-140-5p (miR-140-5p), and sex-determining region Y-related high-mobility group box 4 (SOX4) were analyzed by qRT-PCRor western blot. Relationships of XIST, SOX4, and miR-140-5p were evaluated by dual-luciferase reporter assay and Spearman's analysis.In RB tissues, XIST and SOX4 expressions were obviously increased, but the miR-140-5p expression was markedly reduced. XIST overexpression or miR-140-5p inhibition could abrogate the inhibition of SOX4 silencing on cell proliferation and invasion of RB cells. XIST was obviously increased in RB tissues and cells, and XIST inhibition repressed the proliferation and invasion of RB cells by miR-140-5p/SOX4 axis, which may provide new understandings of the XIST molecular mechanism in RB.	32127028	RID04141	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Pancreatic ductal adenocarcinoma	HOTTIP	CHI3L1	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000133048	NA	100316868	1116	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	GP39|YK-40|YKL40	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04142	expression association	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE86978)
Pancreatic ductal adenocarcinoma	HOTTIP	CLIC5	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000112782	NA	100316868	53405	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	DFNB102	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04143	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Pancreatic ductal adenocarcinoma	HOTTIP	CYB5R2	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000166394	NA	100316868	51700	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	NA	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04144	expression association	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Pancreatic ductal adenocarcinoma	HOTTIP	CYP26B1	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000003137	NA	100316868	56603	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	P450RAI-2	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04145	expression association	NA		UP(PAAD);DATA(GSE40174)
Pancreatic ductal adenocarcinoma	HOTTIP	SULT1A1	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196502	NA	100316868	6817	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	P-PST|STP|STP1	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04146	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	HOTTIP	UCP2	positively-E	overexpression;RNA pull-down assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000175567	NA	100316868	7351	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	BMIQ4|SLC25A8	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 protein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC5 inhibited cell invasion. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04147	expression association	NA		DOWN(NSCLC,PAAD,SKCM,BRCA);DATA(GSE74639,GSE60407,GSE38495,GSE111842)
Pancreatic ductal adenocarcinoma	miR-497	HOTTIP	negatively-F	DIANA;LncBase v2;RNA pull-down assay;luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	Ectopic HOTTIP expression induces noncanonical transactivation pathways to promote growth and invasiveness in pancreatic ductal adenocarcinoma.HOXA transcript at the distal tip (HOTTIP), a long noncoding RNA, is upregulated in pancreatic ductal adenocarcinoma (PDAC).To investigate the roles of differentially expressed lncRNAs in PDAC, we profiled their expressions using microarray (Human LncRNA microarray V2.0), which analyzed 33,045 lncRNAs and 30,215 pro_x0002_tein-coding genes simultaneously, on four pairs of PDAC primary tumor and nontumor tissues. microarray analysis indicated that HOTTIP was upregulated by at least 2 old in all four patients. qRT-PCR confirmed that HOTTIP expression levels were fre_x0002_quently higher in PDAC primary tumors that in their adjacent nontumor tissues.]. Therefore, we focused on genes that were downregulated on inhibition of HOTTIP. We observed that the expression levels of CHI3L1, CLIC5, CYB5R2, CYP26B1, SULT1A1, and UCP2 were significantly decreased after HOTTIP knockdown , whereas they were upregulated when HOTTIP was overexpressed in HPDE cells. Knockdown of UCP2, CYB5R2,CLIC5, and CYP26B1 significantly inhibited PDAC cell growth. Moreover, depletion of CYB5R2, CHI3L1, SULT1A1, and CLIC11 inhibited cell invasion.To determine the mechanism by which miRNAs regulate HOTTIP expression, we first searched the HOTTIP exon regions for putative binding sites of cancer associated miRNAs using a bioinformatics pre_x0002_diction tool (Fig. 6A) [17]. Then, the cancer associated miRNAs that regulate HOTTIP in PDAC were validated by transfecting each miRNA mimic in PDAC cells. We observed that miR'-97 significantly reduced HOTTIP expression (Fig. 6B and C). Luciferase assay and miRNA pull-down assay also revealed the binding of miR'-97 to the HOTTIP exon region. Moreover, HOTTIP upregulation in PDAC cells promoted tumor growth and invasion.	32120024	RID04148	ceRNA or sponge	NA		
Hypertension	AK094457	NOS3	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell injury(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000164867	NA	NA	4846	NA	ECNOS|eNOS	Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury. western blot was performed to detect the endothelial nitric oxide synthase (eNOS), p-eNOS and endothelin-1 (ET-1).According to the results, we found that knockdown lncRNA AK094457 could alleviate the decrease of vascular endothelial cell viability induced by angiotensin II (Ang II). The knockdown of lncRNA AK094457 also relieved the downregulation of eNOS and p-eNOS, and the decreasing of NO release. All these results indicated that lncRNA AK094457 could promote Ang II-induced vascular endothelial cell injury. On the contrary, knockdown of lncRNA AK094457 could alleviate this damage. The knockdown of the lncRNA AK094457 relieved the Ang II-induced vascular endothelial injury.	32027625	RID04149	expression association	NA		DOWN(BRCA);DATA(GSE75367)
Hypertension	AK094457	p-eNOS	negatively-E	RNA pull-down assay	upregulation		NA	NA	cell injury(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury. western blot was performed to detect the endothelial nitric oxide synthase (eNOS), p-eNOS and endothelin-1 (ET-1).According to the results, we found that knockdown lncRNA AK094457 could alleviate the decrease of vascular endothelial cell viability induced by angiotensin II (Ang II). The knockdown of lncRNA AK094457 also relieved the downregulation of eNOS and p-eNOS, and the decreasing of NO release. All these results indicated that lncRNA AK094457 could promote Ang II-induced vascular endothelial cell injury. On the contrary, knockdown of lncRNA AK094457 could alleviate this damage. The knockdown of the lncRNA AK094458 relieved the Ang II-induced vascular endothelial injury.	32027625	RID04150	expression association	NA		
Hypertension	AK094457	ET-1	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell injury(+)	NA	association	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury. western blot was performed to detect the endothelial nitric oxide synthase (eNOS), p-eNOS and endothelin-1 (ET-1).According to the results, we found that knockdown lncRNA AK094457 could alleviate the decrease of vascular endothelial cell viability induced by angiotensin II (Ang II). The knockdown of lncRNA AK094457 also relieved the downregulation of eNOS and p-eNOS, and the decreasing of NO release. All these results indicated that lncRNA AK094457 could promote Ang II-induced vascular endothelial cell injury. On the contrary, knockdown of lncRNA AK094458 could alleviate this damage.	32027625	RID04151	expression association	NA		
Osteoarthritis	NKILA	SP1	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	NF-kB signaling pathway(-);inflammatory response(+);cell proliferation(-);apoptosis process(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000185591	NA	105416157	6667	NA	NA	The reduced lncRNA NKILA inhibited proliferation and promoted apoptosis of chondrocytes via miR-145/SP1/NF-kB signaling in human osteoarthritis.RT-PCRwas used to detect the expressions of NKILA and miR-145 in OA tissues.luciferase assay was performed to explore the binding site of NKILA and miR-145, miR-145 and SP1.According to the results, this study uncovers NKILA is reduced in human osteoarthritic cartilage tissues. Furthermore, we firstly uncover that the reduced NKILA could function as a ceRNA to improve miR-145, which inhibited SP1 expression and regulated NF-kB signaling pathway, thereby promoting tissue inflammation, and inhibiting proliferation and promoting apoptosis of chondrocytes. Thus, it may be used as a promising prognostic marker and a potential target for osteoarthritis. These results in_x0002_dicated that NKILA inhibited SP1/NF-kB signal_x0002_ing pathway in chondrocytes.	32016955	RID04152	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	BCYRN1	PKM	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+);glucose metabolic process(+)	ceRNA(miR-149)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000067225	NA	618	5315	BC200|BC200a|LINC00004|NCRNA00004	OIP3|PK3|PKM2|THBP1	Long non-coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR-149/PKM2 axis in non-small-cell lung cancer.BCYRN1 expression was detected in NSCLC cells and tissues using reverse transcription-uantitative PCR.The relationships between BCYRN1 and microRNA (miR)-149, and between miR-149 and pyruvate kinase M1/2 (PKM2) were measured using a dual-luciferase reporter assay.High BCYRN1 expression was observed in NSCLC tissues and cells compared with the corresponding controls.BCYRN1 induced glycolysis and upregulated the expression levels of PKM2 in NSCLC cells.PKM2 was involved in NSCLC cell proliferation and invasion, and BCYRN1 knockdown and miR-149 overexpression inhibited both processes. The present study suggested that BCYRN1 was involved in cell glycolysis, proliferation and invasion during NSCLC via regulating miR-149 and PKM2. Mechanistically, the results suggested that BCYRN1 induced cell glycolysis and tumor progression via the microRNA (miRNA/miR)-149/PKM2 signaling pathway.	32016455	RID04153	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Colorectal cancer	TUG1	TWIST1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000122691	NA	55000	7291	FLJ20618|LINC00080|NCRNA00080	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	The long noncoding RNA TUG1 is required for TGF-beta/TWIST1/EMT-mediated metastasis in colorectal cancer cells.we show that TGF-beta promotes CRC migration and upregulates the expression of long-noncoding RNA Taurine Upregulated Gene 1 (TUG1). TUG1 knockdown inhibited migration, invasion, and epithelial-mesenchymal transition (EMT) of CRC cells in vitro, and reduced CRC lung metastasis in vivo.TGF-beta induced metastasis, and TUG1 knockdown inhibited these effects. These data demonstrate that TUG1 is a downstream molecular of TGF-beta.Moreover, TWIST1 expression was increased with TGF-beta treatment, and TUG1 knockdown decreased TWIST1 expression in CRC cells. TWIST1 knockdown inhibited invasion and EMT in CRC cells; these effects were not changed by simultaneous TUG1 knockdown, indicating that TWIST1 is a downstream mediator of TUG1. Moreover, TUG1 was significantly overexpressed in CRC patients. In conclusion, TGF-beta promotes metastasis of CRC via a TUG1/TWIST1/EMT signaling pathway. TUG1 may be a promising drug target to inhibit TGF-beta pathway activation in the treatment of CRC.	31988275	RID04154	transcriptional regulation	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	TGFB1	TUG1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(+)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000253352	GRCh38_22:30969245-30979395	7040	55000	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LINC00080|NCRNA00080|TI-227H	The long noncoding RNA TUG1 is required for TGF-beta/TWIST1/EMT-mediated metastasis in colorectal cancer cells.we show that TGF-beta promotes CRC migration and upregulates the expression of long-noncoding RNA Taurine Upregulated Gene 1 (TUG1). TUG1 knockdown inhibited migration, invasion, and epithelial-mesenchymal transition (EMT) of CRC cells in vitro, and reduced CRC lung metastasis in vivo.TGF-beta induced metastasis, and TUG1 knockdown inhibited these effects. These data demonstrate that TUG1 is a downstream molecular of TGF-beta.Moreover, TWIST1 expression was increased with TGF-beta treatment, and TUG1 knockdown decreased TWIST1 expression in CRC cells. TWIST1 knockdown inhibited invasion and EMT in CRC cells; these effects were not changed by simultaneous TUG1 knockdown, indicating that TWIST1 is a downstream mediator of TUG1. Moreover, TUG1 was significantly overexpressed in CRC patients. In conclusion, TGF-beta promotes metastasis of CRC via a TUG1/TWIST1/EMT signaling pathway. TUG2 may be a promising drug target to inhibit TGF-beta pathway activation in the treatment of CRC. Transforming growth factor-beta (TGF-beta) has a central role not only in the regulation of the normal colon but also in the development and metastasis of CRC.	31988275	RID04155	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Urinary bladder cancer	TUG1	SMC2	positively-E	ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);colony formation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000136824	NA	55000	10592	FLJ20618|LINC00080|NCRNA00080	CAP-E|hCAP-E|SMC2L1	Structural maintenance of chromosomes 2 is identified as an oncogene in bladder cancer in vitro and in vivo.Taurine upregulated gene 1 (TUG1) has been found to promote bladder cancer cell growth in our recent research.Immunohistochemical staining was used to test the gene expression levels in tissues from bladder cancer patients. We found that deregulated genes were strongly enriched in cell cycle or pathways in cancer in TUG1-depleted bladder cancer cells.Structural maintenance of chromosomes 2 (SMC2) was inhibited after TUG1 knockdown.The depletion of TUG1 or SMC2 led to G2/M phase arrest in bladder cancer cells.SMC2 depletion inhibited bladder cancer cell proliferation, promoted apoptosis, decreased colony formation, and reduced tumor growth in xenograft nude mice. Overexpression of SMC2 restored the growth of TUG1-depleted cells. The expression levels of SMC2 were higher in human bladder cancer tissues than that in paired normal tissues. Our data suggest that SMC2 is an oncogene in bladder cancer and depletion of SMC2 might have potential therapeutical significance in bladder cancer. To identify vital players in bladder cancer that are regulated by TUG1, we profiled the transcriptome of TUG1-depleted bladder cancer T24 cells using Affymetrix GeneChip PrimeView Human Gene Expression Arrays.	31986889	RID04156	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,SKCM);DOWN(PRAD,PAAD);DATA(GSE117623,GSE104209,GSE60407,GSE38495)
Cardiac hypertrophy	MHRT	KLF4	positively-E	luciferase reporter assay;miRcode;overexpression	downregulation	RT-PCR	NA	NA	cardiac hypertrophy(-)	ceRNA(miR-145a-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	TF	NA	NA	ENSG00000136826	NA	104564225	9314	Myheart	EZF|GKLF	LncRNA-Mhrt regulates cardiac hypertrophy by modulating the miR-145a-5p/KLF4/myocardin axis.we find that Mhrt reduces myocardin expression through KLF4 in vivo and in vitro. Meanwhile, Mhrt promotes the expression of KLF4 through direct binding to miR-145a-5p or inhibiting phosphorylation of KLF4 by forming a complex with KLF4 to prevent the binding of ERK and KLF4, thereby inhibiting myocardin expression and the development of myocardial hypertrophy. Taken together, our findings reveal a new pathway, Mhrt-KLF4-myocardin, that regulates cardiac hypertrophy and revealed additional possible action modes of Mhrt in the occurrence and development of cardiac hypertrophy. The new regulatory pathway serves as a potential therapeutic avenue for cardiac hypertrophy. KLF4 mRNA and protein levels were significantly increased with Mhrt overexpression compared with the control group. Through bioinformatics prediction (using online miRcode software, available at http://www.mircode.org) and previous research reports, miR-145a-5p was identified. In hypertrophic, ischaemic or idiopathic cardiomyopathy tissues, Mhrt expression decreased by 82.8%, 72.8% and 65.9%, respectively.	31982428	RID04157	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Degenerative calcific aortic valve disease	AFAP1-AS1	SMAD5	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-155)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000113658	NA	84740	4090	AFAP1-AS|AFAP1AS|MGC10981	Dwfc|JV5-1|MADH5	LncRNA AFAP1-AS1 promotes osteoblast differentiation of human aortic valve interstitial cells through regulating miR-155/SMAD5 axis.This study aims to explore the function and underlying mechanism of long non-coding RNA (lncRNA) AFAP1-AS1 (actin filament-associated protein 1 antisense RNA 1) in the pathogenesis of DCAVD.AFAP1-AS1, miR-155 and mRNA levels were detected by qRT-PCR The interaction between AFAP1-AS1 and miR-155, as well as miR-155 and SMAD5 was evaluated using luciferase reporter assay.AFAP1-AS1 expression was increased both in calcified aortic valves from DCAVD patients and after osteogenic induction in human VICs.Mechanistically, AFAP1-AS1 acted as a sponge for miR-155 to elevate SMAD5 expression. Further functional assays revealed that miR-155 mimic and SMAD5 silencing effectively reversed AFAP1-AS1-promoted osteogenic differentiation of VICs.Collectively, AFAP1-AS1 promotes osteogenic differentiation of VICs, at least in part, by sponging miR-155 to upregulate SMAD5. This study sheds new light on lncRNA-directed therapeutics in DCAVD.	31945413	RID04158	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Breast cancer	CASC15	KLF5	positively-E	TargetScan;luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+)	ceRNA(miR-153-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000102554	NA	401237	688	LINC00340|lnc-SOX4-1	BTEB2|CKLF|IKLF	LncRNA cancer susceptibility candidate 15 accelerates the breast cancer cells progression via miR-153-3p/KLF5 positive feedback loop.This study uncovered that CASC15 expression level was aberrantly high-expressed in breast cancer tissue specimens and cells.the loss-of-functional experiments showed that knockdown of CASC15 suppressed the malignant behaviors of breast cancer cells, such as proliferation, invasion and tumor growth in vitro and vivo. Mechanically, we confirmed that CASC15 functioned as a competing endogenous RNA (ceRNA) of miR-153-3p, besides, miR-153-3p targeted the 3'-UTR of KLF5 mRNA utilizing the bioinformatics online tools, luciferase reporter assay and RNA immunoprecipitation. Interestingly, we confirmed that the transcription factor KLF5 binds with the promoter region of CASC15 and activates the transcription. In conclusion, we validated the positive feedback loop of KLF5/CASC15/miR-153-3p/KLF5 in the acceleration of breast cancer malignant behaviors and tumorigenesis, suggesting the important biologic roles of CASC15 on the breast cancer tumorigenesis.To measure the level of lncRNA CASC15 in breast cancer tissue and cells, RT-PCRwas performed. Data illustrated that CASC15 levels were high-expressed in breast cancer tissue compared with that of adjacent non-tumorous tissue.  Thus, above data concluded that lncRNA CASC15 and KLF5 are both high-expressed in breast cancer tissue and cells. Again, the online tools (TargetScan, http://www.targetscan.org/vert_71/) indicated that miR-153'-p also could share with the complementary sites with KLF5 mRNA 3'-UTR.	30389133	RID04159	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Nasopharynx carcinoma	HOTAIR	PTGS2	positively-E	TargetScan; luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-101)	regulation	RNA-RNA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000073756	NA	100124700	5743	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	COX-2|COX2|GRIPGHS|PGG/HS|PGHS-2|PHS-2|hCox-2	lncRNA HOTAIR upregulates COX-2 expression to promote invasion and migration of nasopharyngeal carcinoma by interacting with miR-101.We used RT-qPCR approach to examine genes expression and mRNA level. We predicted direct downstream targets of miR-101 by bioinformatic analysis, which was confirmed by dual-luciferase reporter assay.HOTAIR was upregulated in NPC tissues and cells. miR-101 inhibitor greatly enhanced HOTAIR knockdown-regulated cell proliferation, migration and invasion of CNE1 and CNE2 cells. miR-101 was shown to directly bind 3'-UTR of COX-2 and downregulate COX-2 expression. Finally, COX-2 overexpression was demonstrated to rescue the tumor phenotypes of nasopharyngeal carcinoma cells attenuated by HOTAIR knockdown or miR-101 mimic.Here, we highlight the importance of HOTAIR/miR-101/COX-2 axis in progression of nasopharyngeal carcinoma cells. Our findings provide a novel mechanism for explaining HOTAIR-induced nasopharyngeal carcinoma and help developing the therapeutical strategies by targeting HOTAIR. We used the online program TargetScan to predict the potential target genes of miR-101.	31943306|30314699	RID04160	ceRNA or sponge	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Aneurysm	TUG1	ATF2	negatively-E	bioinformatics analysis; luciferase assays;RIP;RNA pull-down	upregulation	RT-qPCR	NA	NA	cell migration(+);cell differentiation(+)	ceRNA(miR-6321)	regulation	NA	NA	NA	NA	Cancer	Aneurysm	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000115966	NA	55000	1386	FLJ20618|LINC00080|NCRNA00080	CRE-BP1|CREB2|HB16|TREB7	LncRNA TUG1 functions as a ceRNA for miR-6321 to promote endothelial progenitor cell migration and differentiation.Bioinformatics prediction, luciferase assays, western blots and RIP assays indicated that lncRNA TUG1 functions as a ceRNA (competing endogenous RNA) for miR-6321 and that miR-6321 inhibits EPC migration and differentiation through its target, ATF2. As a potential therapeutic target, lncRNA TUG1 may play a vital role in the pathogenesis of aneurysms. RNA pull-down and luciferase reporter assays showed the binding of lncRNA TUG1 with miR-6321.	31935381	RID04161	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Glioblastoma	HOTAIRM1	ZEB2	positively-E	luciferase reporter gene assay	downregulation	qRT-PCR	GSE103228	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-873-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000169554	NA	100506311	9839	HOXA-AS1|HOXA1-AS1|NCRNA00179	KIAA0569|SIP-1|SIP1|ZFHX1B	Long non-coding RNA HOTAIRM1 promotes proliferation and inhibits apoptosis of glioma cells by regulating the miR-873-5p/ZEB2 axis.We analyzed the most dysregulated microRNAs from the Gene Expression Omnibus (GEO) database and examined the expression of miR-873-5p in 20 glioblastoma tissues compared with ten normal brain tissues collected in the Zhejiang Tongde Hospital. We then overexpressed or inhibited miR-873-5p expression in U87 glioblastoma cell lines and analyzed the phenotype using the cell counting kit-8 assay, wound healing assay, and apoptosis. we predicted upstream and downstream genes of miR-873-5p in glioblastoma using bioinformatics analysis and tested our hypothesis in U87 cells using the luciferase reporter gene assay and western blot assay.The miR-873-5p was downregulated in glioblastoma tissues compared with that in normal brain tissues .the long non-coding RNA HOTAIRM1 was found to act as a sponge of miR-873-5p to activate ZEB2 expression in U87 cells.CONCLUSIONS: We uncovered a novel HOTAIRM1/miR-873-5p/ZEB2 axis in glioblastoma cells, providing new insight into glioblastoma progression and a theoretical basis for the treatment of glioblastoma. To explore the biological function of miRNAs in glioblastoma, we analyzed the GSE103228 data from the Gene Expression Omnibus (GEO) database. We further explored the mechanism of miR-873-5p in glioblastoma progression and found that miR-873-5p expression was inhibited in lncRNA HOTAIRM1 overexpressed U87 cells.	31929367	RID04162	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	TUG1	IGF2	positively-E	luciferase reporter assay;	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-148b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000167244	NA	55000	3481	FLJ20618|LINC00080|NCRNA00080	C11orf43|FLJ44734|IGF-II	LncRNA TUG1 regulates proliferation and apoptosis by regulating miR-148b/IGF2 axis in ox-LDL-stimulated VSMC and HUVEC.The expression levels of TUG1, microRNA (miR)-148b and insulin-like growth factor 2 (IGF2) were measured by quantitative real-time polymerase chain reaction or western blot.The target association among TUG1, miR-148b and IGF2 was determined by luciferase reporter assay and RNA immunoprecipitation. The expression of TUG1 was increased in ox-LDL-treated VSMC and HUVEC. Silence of TUG1 inhibited proliferation and promoted apoptosis in ox-LDL-treated VSMC but induced proliferation promotion and apoptosis inhibition in HUVEC stimulated by ox-LDL. miR-148b was a target of TUG1 and its knockdown reversed the effect of TUG1 silence on proliferation and apoptosis of VSMC and HUVEC challenged by ox-LDL. IGF2 was a target of miR-148b and miR-148b regulated proliferation and apoptosis in ox-LDL-treated VSMC and HUVEC by targeting IGF2. TUG1 promoted IGF2 protein expression by sponging miR-148b. TUG1 knockdown attenuated ox-LDL-induced injury through regulating proliferation and apoptosis of VSMC and HUVEC by miR-148b/IGF2 axis, providing a novel mechanism for pathogenesis of atherosclerosis.	31926240	RID04163	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Osteoporosis	miR-19b-3p	H19	negatively-F	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell differentiation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	MicroRNA-19b-3p promotes cell proliferation and osteogenic differentiation of BMSCs by interacting with lncRNA H19.The expression of miR-19b-3p and lncRNA H19 were measured in postmenopausal osteoporosis patients and BMP-22 induced BMSCs using qRT-PCRThe expression of miR-19b-3p was significantly up-regulated in postmenopausal osteoporosis patients and BMP-2 induced BMSCs.LncRNA H19 was obviously down-regulated in postmenopausal osteoporosis patients. H19 overexpression significantly decreased cell proliferation and differentiation by down-regulating miR-19b-3p.These data were the first to reveal the critical role of H19/miR-19b-3p in postmenopausal osteoporosis, and provided a new therapeutic target for OP.	31918667	RID04164	ceRNA or sponge	NA		UP(NSCLC);DATA(GSE74639)
Gastric cancer	HOTAIR	HOXC6	positively-E	siRNA;Genecards	upregulation	qRT-PCR	TCGA	NA	cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000197757	NA	100124700	3223	HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX3|HOX3C	HoxC6 Functions as an Oncogene and Isoform HoxC6-2 May Play the Primary Role in Gastric Carcinogenesis. Metastasis-related nucleotide lncRNA HOTAIR was selected by bioinformatics, and verification was carried out by in vitro researches.In vitro, HoxC6, HoxC6-1, and HoxC6-2 knockdown by small interference RNA was carried for evaluating the changes of malignant biological behaviors of gastric cancer cells, such as proliferation, migration, invasion, apoptosis, and cell cycle alternation.over-expression of HOTAIR, which is relevant with HoxC6 during gastric carcinogenesis, was detected in gastric cancerous tissues. Restored expression of HoxC6 partially reversed the decreased migration caused by down-regulating HOTAIR in gastric cancer cells.  According to the related literatures and Genecards analysis (http://www.genecards.org/), fifty-three genes including JunD, BMP7, Bcl-2, MKI67, and 22 nucleotides including long noncoding RNA (lncRNA) HOTAIR were screened. TCGA RNA-Seq data were downloaded from TCGA (http://cancergenome.nih.gov/) following the approval of this project by the consortium.	31900716	RID04165	expression association	metastasis		
Colorectal cancer	91H	HNRNPK	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000165119	NA	NA	3190	NA	CSBP|HNRPK|TUNP	Exosomal lncRNA 91H is associated with poor development in colorectal cancer by modifying HNRNPK expression.Then RNA pull-down and RIP were used to detect how lncRNA 91H affect CRC IGF2 express. We found that serum lncRNA 91H expression was closely related to cancer exosomes in vitro and vivo which may enhance tumor-cell migration and invasion in tumor development by modifying HNRNPK expression. Then the clinic pathological significance of exosomal 91H was evaluated which demonstrated that CRC patients with high lncRNA 91H expression usually showed a higher risk in tumor recurrence and metastasis than patients with low lncRNA 91H expression (P < 0.05).All these data suggested that exosomal lncRNA 91H enhancing CRC metastasis by modifying HNRNPK expression might be an early plasma-based biomarker for CRC recurrence or metastasis. Further large-scale studies are needed to confirm our findings.By performing qRT-PCR the expression of exosomal 91H in cell lines HCT-8, HCT-116 were 16.96 and 5.30-fold change higher than FHC with P < 0.05,We next investigated the molecular mechanism by which lncRNA 91 regulated tumor development. Pull down assays with cell lysate showed that heterogeneous nuclear ribonucleoprotein K (HNRNPK) protein might directly interact with lncRNA 91 by MS analysis. To further confirm the lncRNA 91H-protein interactions in vivo, RNA interference was used in this study which demonstrated that the HNRNPK protein expression significantly decreased compared with negative control.	31896067|29410604	RID04166	interact with protein	metastasis,recurrence		DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	H19	CTNNB1	positively-E	overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);chemoresistance(+);cell metastasis(+)	ceRNA(miR-141)	regulation	RNA-protein	Oxaliplatin	CSC	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168036	NA	283120	1499	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Carcinoma-associated fibroblasts promote the stemness and chemoresistance of colorectal cancer by transferring exosomal lncRNA H19.H19 was highly expressed in the tumor tissues of CAC mice compared with the expression in normal colon tissues. RNA-FISH and immunofluorescence assays were performed to assess the expression of H19 in tumor stroma and cancer nests. H19 activated the beta-catenin pathway via acting as a competing endogenous RNA sponge for miR-141 in CRC, while miR-141 significantly inhibited the stemness of CRC cells. H19 activated the beta-catenin pathway via acting as a competing endogenous RNA sponge for miR-141, while miR-141 inhibited the stemness of CRC cells. Our findings indicate that H19 expressed by CAFs of the colorectal tumor stroma contributes to tumor development and chemoresistance.The qRT-PCRresults showed increased expression of H19 in tumor tissues from CRC patients.Given that the Wnt/beta-catenin pathway is critical for the capability of intestinal stem cells 60-62, the maintenance of CSCs 63, 64 and the chemoresistance of cancer cells 65-67, we wondered whether the Wnt/beta-catenin pathway was regulated by H19 in CRC. We found that overexpression of H19 promoted Wnt luciferase reporter (TOPFlash) activity and significantly increased the protein level of beta-catenin. Overexpression of H19 also enhanced the expression of the downstream genes of the Wnt/beta-catenin pathway.CAFs enhances the level of H19, stemness and oxaliplatin resistance of colorectal cancer cells. HNRNPK was regulated by lncRNA 91H mediation so that it could further promote tumor development and metastasis.	31896067|30083271	RID04167	ceRNA or sponge	metastasis,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Oesophageal squamous cell carcinoma	PCAT1	miR-326	negatively-F	RegRNA;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	Long noncoding RNA PCAT1, a novel serum-based biomarker, enhances cell growth by sponging miR-326 in oesophageal squamous cell carcinoma.we confirmed that PCAT1 was highly expressed in ESCC tissues and cell lines. Knockdown of PCAT1 inhibited the growth of ESCC cells, whereas overexpression of PCAT1 showed the opposite effect both in vitro and in vivo.PCAT1 could bind to miR-326, a tumour suppressor in diverse human cancers. Thus, our data indicate that PCAT1 promotes ESCC cell proliferation by sponging miR-326 and may serve as a non-invasive biomarker for ESCC.was indeed highly expressed in ESCC specimens (Fig. -(Fig.1a).1a). Consistent results were obtained by analysis of the PCAT1 expression in oesophageal carcinoma using the Cancer Genome Atlas (TCGA) database.Total RNA was then isolated to detect the expression levels of PCAT1 and cMYC by RT-qPCR. To examine whether cytoplasm-localized PCAT1 can bind to endogenous miRNAs, we predicted its target miRNAs using RegRNA.A dual-luciferase reporter assay was performed to validate the interaction between them using a reporter plasmid with PCAT1 in the 3'UTR of the luciferase gene. To examine whether cytoplasm-localized PCAT1 can bind to endogenous miRNAs, we predicted its target miRNAs using RegRNA.	31896067|31273188	RID04168	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pancreatic ductal adenocarcinoma	SOX2-OT	SOX2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	microarray	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-200)	regulation	NA	NA	CSC	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	NCRNA00043|SOX2OT	ANOP3|MCOPS3	Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA in pancreatic ductal adenocarcinoma.We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC. we observed a decreased exosomal Sox2ot expression in postoperative blood samples of PDAC patients. The exosomal lncRNA Sox2ot plays important roles in tumor progression and may be a useful maker for pancreatic cancer prognosis.. Our RNA pull-down results showed that neither the Sox2ot sense RNA nor the antisense RNA could bind the Sox2 protein, and the RIP results showed that the complex precipitated with an antibody against Sox2 did not contain Sox2ot RNA . Furthermore, a dual-luciferase reporter gene assay showed that Sox2ot could not bind to the promoter region of Sox2. As both Sox2ot and Sox2 can regulate EMT and stemproperties, and Sox2ot can promote the expression of Sox2, we further investigated whether Sox2ot could regulate EMT and stem properties via Sox2.	31896067|29643475	RID04169	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Osteoarthritis	H19	miR-106a-5p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Long non-coding RNA H19 modulates proliferation and apoptosis in osteoarthritis via regulating miR-106a-5p. The expression levels of H19 and miR-106a-5p in OA samples from patients or cultured chondrocytes were examined by quantitative real time polymerase chain reaction. expression levels of PCNA, CyclinD1, Caspase 3 and Cleaved Caspase 3. StarBase database, luciferase assay and RNA immunoprecipitation were introduced to confirm the relationship between H19 and miR-106a-5p.H19 expression was upregulated, while miR-106a-5p level was downregulated in OA samples and IL-1b-treated chondrocytes. H19 overexpression inhibited the proliferation and induced apoptosis in IL-1b-treated chondrocytes, while H19 knockdown induced the opposite effect. Luciferase and RIP assay demonstrated that miR-106a-5p was a direct target of H19. miR-106a-5p overexpression led to proliferation promotion and apoptosis inhibition in chondrocytes treated by IL-1beta and it reversed the effect of H19 addition. We conclude that H19 could regulate proliferation and apoptosis of chondrocytes treated by IL-1beta in OA via sponging miR-106a-5p.	31894109	RID04170	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Papillary thyroid carcinoma	BGLT3	PTEN	positively-F	ChIP;Co-IP; RNA pull-down assay ;luciferase reporter assays	downregulation	qRT-PCR	NA	NA	cancer progression(-);PI3K/AKT signaling pathway(-)	NA	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260629	GRCh38_11:5244554-5245546	ENSG00000171862	NA	103344929	5728	BGL3|LINC01083|lncRNA-BGL3	BZS|MHAM|MMAC1|PTEN1|TEP1	BGL3 inhibits papillary thyroid carcinoma progression<U+00A0>via regulating PTEN stability.Expression of BGL3 was determined by quantitative real-time polymerase chain reaction (qRT-PCR.The molecular mechanism underlying BGL3 was tested by ChIP, Co-IP, RNA pull-down and luciferase reporter assays.BGL3 was significantly decreased in PTC tissues compared to adjacent normal thyroid tissues, and it was transcriptionally repressed by oncogene Myc.Overexpression of BGL3 inhibited PTC cell proliferation and migration in vitro, and reduced tumor size and lung metastasis nodules in vivo. Our data underscore the critical tumor-inhibiting role of BGL3 in PTC via post-translational regulation of PTEN protein stability, which may serve as a novel therapeutic target and prognostic biomarker in human PTC. BGL3 was mainly located in the cytoplasm, in which interacted with PTEN and recruited OTUD3, enhancing the de-ubiquitination effect of OTUD3 on PTEN, resulting in increasing PTEN protein stability and inactivating carcinogenic PI3K/AKT signaling.	33543443	RID04171	expression association	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Urinary bladder cancer	GACAT3	CDKN1A	negatively-E	CRISPR-Cas13	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000124762	NA	104797537	1026	LINC01458|lncRNA-AC130710	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer.Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues.The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues.Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3.A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT3 may be a novel target for diagnosis and treatment of bladder cancer. Knockdown of lncRNA-GACAT3 Induced Apoptosis and Inhibited Cell Migration	33537343	RID04172	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Urinary bladder cancer	GACAT3	BAX	negatively-E	CRISPR-Cas13	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000087088	NA	104797537	581	LINC01458|lncRNA-AC130710	BCL2L4	CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer.Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues.The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues.Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3.A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT4 may be a novel target for diagnosis and treatment of bladder cancer. Knockdown of lncRNA-GACAT3 Induced Apoptosis and Inhibited Cell Migration	33537343	RID04173	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	GACAT3	E-Cadherin	negatively-E	CRISPR-Cas13	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer.Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues.The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues.Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3.A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT5 may be a novel target for diagnosis and treatment of bladder cancer. Knockdown of lncRNA-GACAT3 Induced Apoptosis and Inhibited Cell Migration	33537343	RID04174	expression association	NA		
Urinary bladder cancer	GACAT3	miR-497	negatively-F	CRISPR-Cas13	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer.Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues.The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues.Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3.A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT6 may be a novel target for diagnosis and treatment of bladder cancer.  dual-luciferase reporter assay showed that co-transfection of lncRNA GACAT3-WT and miR-515-5p significantly inhibited luciferase activity than that of control group. It demonstrated the ceRNA mechanism for GACAT3.	33537343	RID04175	ceRNA or sponge	NA		
Melanoma	MIR205HG	VEGFA	positively-E	TargetScan;dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cancer progression(+)	ceRNA(miR-299-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000112715	NA	642587	7422	LINC00510	VEGF|VEGF-A|VPF	LncRNA MIR205HG regulates melanomagenesis via the miR-299-3p/VEGFA axis.Quantitative real-time PCR (qRT-PCR analysis showed that MIR205HG levels were significantly upregulated in melanoma cell lines compared to normal human melanocytes.Dual luciferase reporter and RNA pull-down assays confirmed that MIR205HG directly binds to microRNA (miR)-299-3p. Targetscan analysis and dual-luciferase reporter assays showed that miR-299-3p directly binds to the 3'UTR of VEGFA mRNA.These results demonstrate that MIR205HG supports melanoma growth via the miR-299-3p/VEGFA axis. This makes MIR205HG a potential therapeutic target for the treatment of melanoma.  MIR205HG-silenced melanoma cells showed increased miR-299-3p expression and lower levels of both VEGFA mRNA and protein.	33535182	RID04176	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Spinal cord injury	ZFAS1	PTEN	positively-E	RIP; luciferase reporter assay	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(-)	ceRNA(miR-1953)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000171862	NA	441951	5728	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	BZS|MHAM|MMAC1|PTEN1|TEP1	Long noncoding RNA ZFAS1 aggravates spinal cord injury by binding with miR-1953 and regulating the PTEN/PI3K/AKT pathway.RIP and luciferase reporter assay were applied to detect binding capacity among RNAs. Next, ZFAS1 was identified to be upregulated in spinal cord tissues of SCI mice. ZFAS1 knockdown promoted functional recovery and inhibited cell apoptosis and the inflammatory response in SCI mice. ZFAS1 bound with microRNA 1953 (miR-1953), and miR-1953 was downregulated in spinal cord tissues of SCI mice. Furthermore, we confirmed that ZFAS1 promoted SCI progression via binding with miR-1953.In addition, phosphatase and tensin homolog (PTEN) was verified to be a downstream target for miR-1953 in vitro, and PTEN was upregulated in spinal cord tissues of SCI mice. Finally, we illustrated that ZFAS1 inactivated the PI3K/AKT pathway through upregulation of PTEN. In conclusion, our study revealed that ZFAS1 facilitated SCI by binding with miR-1953 and regulating the PTEN/PI3K/AKT pathway, which may provide a potential novel insight for treatment of SCI.  The level of ZFAS1 in spinal cord tissues of SCI mice at one, three, seven and fourteen days was detected by RT-qPCR analysis.	33524472	RID04177	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Aortic dissection	H19	miR-193b-3p	negatively-F	StarBase v2.0;dual luciferase assay;RNA pull-down assay;RIP; Pearson correlation coefficient	upregulation	qRT-PCR	GSE92427	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Aortic aneurysm	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	LncRNA H19 regulates smooth muscle cell functions and participates in the development of aortic dissection through sponging miR-193b-3p.The expressions of related genes in human aortic smooth muscle cells (HASMCs) induced by platelet-derived growth factor BB (PDGF-BB) or in the aortic tissue of AD patients/mice were identified by western blot and quantitative real-time polymerase chain reaction.The targeting relationship between H19 and miR-193b-3p was predicted and verified by bioinformatics analysis, dual luciferase assay, RNA pull-down assay, RNA immunoprecipitation (RIP), and Pearson correlation coefficient.LncRNA H19 was abnormally high-expressed in thoracic aorta tissues of AD patients, and it could competitively bind to and inhibit miR-193b-3p.H19 regulated smooth muscle cell function by sponging miR-193b-3p and it participated in the development of AD. The GEO database (https://www.ncbi.nlm.nih.gov/geo/) (GSE92427) was used to analyze the expression of related miRNA in the aortic dissection of AD patients and healthy controls. starBase v2.0 software was used to predict the potential targeted binding sites of H19 and miR-193b-3p.	33403385	RID04178	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	TTN-AS1	Cyclin E1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PTEN/AKT signaling pathway(-);chemoresistance(+)	ceRNA(miR-16-5p)	regulation	RNA-protein	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	LncRNA TTN-AS1 intensifies sorafenib resistance in hepatocellular carcinoma by sponging miR-16-5p and upregulation of cyclin E1.To investigate the potential role of lncRNA TTN-AS1 in HCC cells with sorafenib (SOR) resistance, and explore the underlying pathways, quantitative real time polymerase chain reaction (qRT-PCR was used to test the expression of TTN-AS1 in HCC tissues and cells.Expression levels of the downstream target of TTN-AS1, miR-16-5p were studied by dual-luciferase binding assay, cell proliferation, and western blotAs the results revealed, TTN-AS1 silencing in HCC cells induced apoptosis by enhancing the sensitivity of cells to SOR, and the tumor in nude mice became smaller. The mechanism study showed that miR-16-5p was affected by TTN-AS1 sponge, up-regulated cyclin E1 expression, and regulated PTEN/Akt signaling pathway, thereby significantly alleviating the inhibition of apoptosis of HCC cells induced by TTN-AS1 gene. Collectively, our results provided TTN-AS1 as a potential therapeutic target for sorafenib resistance in HCC. LncRNA TTN-AS1 intensifies sorafenib resistance in HCC by sponging miR-16-5p and upregulations of cyclin E1 via regulating PTEN/Akt signaling pathway. In-depth study of the mechanism found that TTN-AS1 effectively inhibited the activation of PTEN/Akt signaling pathway, and miR-16-5p inhibitor or overexpression of cyclin E1 reversed the inactivation.	33378944	RID04179	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Intervertebral disc degeneration	PART1	miR-190a-3p	negatively-F	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell viability(-);apoptosis process(-);inflammatory response(-);ECM degradation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000152931	GRCh38_5:60487713-60548813	NA	NA	25859	NA	DKFZP586D0823|NCRNA00206	NA	Role of lncRNA PART1 in intervertebral disc degeneration and associated underlying mechanism.Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure lncRNA PART1 expression levels in 10 ng/ml LPS-stimulated NP cells and normal cells.dual-luciferase reporter assays were conducted to verify the possible binding sites of microRNA (miR)-190a-3p on lncRNA PART1.Expression levels of lncRNA PART1 in LPS-treated NP cells were found to be higher compared with those in the control groups. miR-190a-3p directly targeted lncRNA PART1. PART1 knockdown enhanced cell viability, reduced cell apoptosis, inhibited inflammatory factor secretion and promoted ECM degradation in LPS-stimulated NP cells.these results suggest that PART1 accelerates the progression of IDD by directly targeting miR-190a-3p, which provides a novel target for IDD diagnosis and treatment.	33376513	RID04180	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	
Chronic obstructive pulmonary disease	MEG3	miR-149-3p	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-3p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD. The ratio of p-p65/t-p65 and p-IkBalpha/t-IkBalpha was increased when the expression of miR-149-3p was inhibited by miR-149-3p inhibitor, compared with the negative control group; however, it would be reversed when MEG3 was downregulated with miR-149-3p inhibitor in CSE-induced HBE cells.	33365060	RID04181	ceRNA or sponge	NA		
Chronic obstructive pulmonary disease	MEG3	IL6	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136244	NA	55384	3569	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BSF2|HGF|HSF|IFNB2|IL-6	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-4p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.	33365060	RID04182	expression association	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Chronic obstructive pulmonary disease	MEG3	TNF	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000228978	NA	55384	7124	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-5p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.	33365060	RID04183	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Chronic obstructive pulmonary disease	MEG3	BCL2	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Bcl-2|PPP1R50	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-6p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.	33365060	RID04184	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Chronic obstructive pulmonary disease	MEG3	Caspase3	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-7p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.	33365060	RID04185	expression association	NA		
Chronic obstructive pulmonary disease	MEG3	Caspase9	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR.Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples.MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-alpha, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3.The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-kB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-kB signal pathway via miR-149-8p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.	33365060	RID04186	expression association	NA		
Posterior capsule opacification	MALAT1	SMAD4	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Other	Posterior capsule opacification	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141646	NA	378938	4089	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DPC4|MADH4	LncRNA-MALAT1/miRNA-204-5p/Smad4 Axis Regulates Epithelial-Mesenchymal Transition, Proliferation and Migration of Lens Epithelial Cells.RNA levels of MALAT1 and miR-204-5p were analyzed by RT-qPCR.dual-luciferase reporter assays in LECs were conducted to verify whether miRNA-204-5p was negatively regulated by MALAT1 and Smad4 was a direct target of miR-204-5p.The expression of MALAT1 was upregulated in PCO specimens.the knockdown of MALAT1 could inhibit the EMT, proliferation, and migration of LECs; however, those can be reversed by anti-miR-204-5p.Conclusions: Our findings reveal that MALAT1 may regulate EMT, proliferation, and migration of LECs as a ceRNA by "sponging" miR-204-5p and targeting Smad4, and serve as a promising therapeutic target in preventing PCO. Besides, the upregulation of MALAT1 was correlated with the downregulation of miR-204-5p and upregulation of Smad4.	33327804	RID04187	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colorectal cancer	RAD51-AS1	NDRG2	positively-E	StarBase;luciferase reporter assay	downregulation	sequencing	TCGA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245849	GRCh38_15:40686183-40695107	ENSG00000165795	NA	100505648	57447	TODRA	KIAA1248|SYLD	LncRNA RAD51-AS1/miR-29b/c-3p/NDRG2 crosstalk repressed proliferation, invasion and glycolysis of colorectal cancer.RAD51-AS1 expression was observed to be lower in CRC cell lines compared with normal cell line (NCM460).In the meanwhile, both the levels of miR-29b-3p and miR-29c-3p were prominently elevated in CRC cells.RAD51-AS1 functioned as a competing endogenous RNA (ceRNA) for sponging miR-29b-3p and miR-29c-3p, leading to enhancement of their common target N-myc downstream-regulated gene 2 (NDRG2). these findings provide comprehensive evidence that RAD51-AS1 repressed cell proliferation, migration, invasion and glycolysis process, ultimately contributing to the progression of CRC by repressing the miR-29b/c-3p/NDRG2 signaling axis, insinuating the putative potential of RAD51-AS1/miR-29b/c-3p/NDRG2 interaction network in unraveling CRC pathology and hopefully contributed to the treatment of CRC patients.we used the online tools StarBase toexplore the potential miRNAs that interact with RAD51-AS1.To further testify the relationship between RAD51-AS1 and miR-29b/c-3p, we conducted a luciferase reporter assay. According to the TCGA data, we found that RAD51-AS1 expression was predominantly downregulated in COAD specimens in contrast to that in normal tissues.	33314669	RID04188	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC);DATA(GSE117623,GSE74639,GSE104209,GSE51827,GSE55807,GSE86978)
Colorectal cancer	RAD51-AS1	NDRG2	positively-E	StarBase;luciferase reporter assay	downregulation	sequencing	TCGA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-29c-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245849	GRCh38_15:40686183-40695107	ENSG00000165795	NA	100505648	57447	TODRA	KIAA1248|SYLD	LncRNA RAD51-AS1/miR-29b/c-3p/NDRG2 crosstalk repressed proliferation, invasion and glycolysis of colorectal cancer.RAD51-AS1 expression was observed to be lower in CRC cell lines compared with normal cell line (NCM460).In the meanwhile, both the levels of miR-29b-3p and miR-29c-3p were prominently elevated in CRC cells.RAD51-AS1 functioned as a competing endogenous RNA (ceRNA) for sponging miR-29b-3p and miR-29c-3p, leading to enhancement of their common target N-myc downstream-regulated gene 2 (NDRG2). these findings provide comprehensive evidence that RAD51-AS1 repressed cell proliferation, migration, invasion and glycolysis process, ultimately contributing to the progression of CRC by repressing the miR-29b/c-3p/NDRG2 signaling axis, insinuating the putative potential of RAD51-AS1/miR-29b/c-3p/NDRG2 interaction network in unraveling CRC pathology and hopefully contributed to the treatment of CRC patients.we used the online tools StarBase toexplore the potential miRNAs that interact with RAD51-AS1.To further testify the relationship between RAD51-AS1 and miR-29b/c-3p, we conducted a luciferase reporter assay. According to the TCGA data, we found that RAD51-AS2 expression was predominantly downregulated in COAD specimens in contrast to that in normal tissues.	33314669	RID04189	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC);DATA(GSE117623,GSE74639,GSE104209,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	CBR3-AS1	SMAD3	positively-E	Miranda	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell invasion(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000166949	NA	100506428	4088	PlncRNA-1	HsT17436|JV15-2|MADH3	Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis.PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues.PlncRNA-1 modulated the expression of smad3 and has-miR-136-5p (miR-136).miR-136 regulated the expression of PlncRNA-1 and smad3. PlncRNA-1 mimics competitive endogenous RNA (ceRNA) in its regulation of smad3 expression by binding miR-136. Rescue analysis further revealed that modulation of miR-136 could reverse the expression of smad3 and epithelial-mesenchymal transition (EMT) marker proteins impaired by PlncRNA-1. In summary, PlncRNA-1 has important clinical predictive values and is involved in the post-transcriptional regulation of smad3. The PlncRNA-1/miR-136/smad3 axis provides insights into the regulatory mechanism of BC, thus may serve as a potential therapeutic target and prognostic biomarker for cancer. This study revealed that the interference of PlncRNA-1 expression significantly inhibits the migration and invasion of bladder cancer cells and smad3 was related to tumor migration and invasion.	33288752	RID04190	ceRNA or sponge	prognosis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Choriocarcinoma	LOXL1-AS1	miR-515-5p	negatively-F	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);NF-kB signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Choriocarcinoma	lncRNA	miRNA	ENSG00000261801	GRCh38_15:73908071-73928248	NA	NA	100287616	NA	NA	NA	Targeted-regulating of miR-515-5p by LncRNA LOXL1-AS1 on the proliferation and migration of trophoblast cells.Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of LOXL1-AS1 and miR-515-5p.and the luciferase assay was used to detected the targeting relationship of LOXL1-AS1 and miR-515-5p.Our results showed that human placental trophoblast cells had higher level of LOXL1-AS1 in comparison to human choriocarcinoma cells, however, human placental trophoblast cells had lower level of miR-515-5p.Compared with the miR-NC group, the expression level of miR-515-5p in JeG-3 cells in the miR-515-5p group was significantly increased. In addition, the expression levels of CyclinD1, MMP2 and MMP9 were significantly decreased, and the cell survival rate was significantly decreased; also, and the number of migrated cells was significantly decreased. In this study, LOXL1-AS1 expression was low, and expression levels of p-p65 and p-IkBalpha were reduced, indicating that low LOXL1-AS1 expression inhibited NF-kB signaling pathway. Low expression of miR-515-5p partially reversed the inhibition effect of low expression of LOXL1-AS1 on NF-kB signaling pathway, and the low expression of LOXL1-AS1 inhibited cell proliferation and migration.	33278425	RID04191	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	
Choriocarcinoma	LOXL1-AS1	Cyclin D1	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell migration(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	NA	NA	100287616	NA	NA	NA	Targeted-regulating of miR-515-5p by LncRNA LOXL1-AS1 on the proliferation and migration of trophoblast cells.Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of LOXL1-AS1 and miR-515-5p.and the luciferase assay was used to detected the targeting relationship of LOXL1-AS1 and miR-515-5p.Our results showed that human placental trophoblast cells had higher level of LOXL1-AS1 in comparison to human choriocarcinoma cells, however, human placental trophoblast cells had lower level of miR-515-5p. t-test analysis showed that the expression level of LOXL1-AS1 in JeG-3 cells in the si-LOXL1-AS1 group was significantly reduced, and the expression levels of CyclinD1, MMP2 and MMP9 were significantly reduced, the cell survival rate was significantly reduced, and the number of migrated cells was significantly reduced	33278425	RID04192	expression association	NA	DOWN(BRCA);DATA(GSE111842)	
Choriocarcinoma	LOXL1-AS1	MMP2	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell migration(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000087245	NA	100287616	4313	NA	CLG4|CLG4A|TBE-1	Targeted-regulating of miR-515-5p by LncRNA LOXL1-AS1 on the proliferation and migration of trophoblast cells.Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of LOXL1-AS1 and miR-515-5p.and the luciferase assay was used to detected the targeting relationship of LOXL1-AS1 and miR-515-5p.Our results showed that human placental trophoblast cells had higher level of LOXL1-AS1 in comparison to human choriocarcinoma cells, however, human placental trophoblast cells had lower level of miR-515-5p. t-test analysis showed that the expression level of LOXL1-AS1 in JeG-3 cells in the si-LOXL1-AS1 group was significantly reduced, and the expression levels of CyclinD1, MMP2 and MMP9 were significantly reduced, the cell survival rate was significantly reduced, and the number of migrated cells was significantly reduced	33278425	RID04193	expression association	NA	DOWN(BRCA);DATA(GSE111842)	UP(PAAD);DATA(GSE40174)
Choriocarcinoma	LOXL1-AS1	MMP9	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell migration(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000100985	NA	100287616	4318	NA	CLG4B	Targeted-regulating of miR-515-5p by LncRNA LOXL1-AS1 on the proliferation and migration of trophoblast cells.Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of LOXL1-AS1 and miR-515-5p.and the luciferase assay was used to detected the targeting relationship of LOXL1-AS1 and miR-515-5p.Our results showed that human placental trophoblast cells had higher level of LOXL1-AS1 in comparison to human choriocarcinoma cells, however, human placental trophoblast cells had lower level of miR-515-5p. t-test analysis showed that the expression level of LOXL1-AS1 in JeG-3 cells in the si-LOXL1-AS1 group was significantly reduced, and the expression levels of CyclinD1, MMP2 and MMP9 were significantly reduced, the cell survival rate was significantly reduced, and the number of migrated cells was significantly reduced	33278425	RID04194	expression association	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Skin squamous cell carcinoma	EZR-AS1	PTK2	positively-E	LncTar	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000169398	NA	101409257	5747	NA	FADK|FAK|FAK1|PPP1R71	lncRNA EZR-AS1 knockdown represses proliferation, migration and invasion of cSCC via the PI3K/AKT signaling pathway.EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR.EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively.EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The analysis of LncTar identified FAK as a target of EZR-AS1. Furthermore, the RT-qPCR results suggested that FAK expression was significantly higher in cSCC tissues compared with healthy tissues. In summary, EZR-AS1 knockdown inhibited the PI3K/AKT signaling pathway by suppressing FAK expression in cSCC cells.	33236153	RID04195	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE75367)
Skin squamous cell carcinoma	EZR-AS1	MMP2	positively-E	LncTar	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000087245	NA	101409257	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	lncRNA EZR-AS1 knockdown represses proliferation, migration and invasion of cSCC via the PI3K/AKT signaling pathway.EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR.EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively.EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The analysis of LncTar identified FAK as a target of EZR-AS1. Furthermore, the RT-qPCR results suggested that FAK expression was significantly higher in cSCC tissues compared with healthy tissues. In summary, EZR-AS1 knockdown inhibited the PI3K/AKT signaling pathway by suppressing FAK expression in cSCC cells. Compared with the si-NC group, EZR-AS1 knockdown significantly reduced the protein expression levels of MMP-2, MMP-9 and Bcl-2, but significantly increased the protein expression levels of Bax.	33236153	RID04196	expression association	NA		UP(PAAD);DATA(GSE40174)
Skin squamous cell carcinoma	EZR-AS1	MMP9	positively-E	LncTar	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000100985	NA	101409257	4318	NA	CLG4B|GELB|MANDP2|MMP-9	lncRNA EZR-AS1 knockdown represses proliferation, migration and invasion of cSCC via the PI3K/AKT signaling pathway.EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR.EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively.EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The analysis of LncTar identified FAK as a target of EZR-AS1. Furthermore, the RT-qPCR results suggested that FAK expression was significantly higher in cSCC tissues compared with healthy tissues. In summary, EZR-AS1 knockdown inhibited the PI3K/AKT signaling pathway by suppressing FAK expression in cSCC cells. Compared with the si-NC group, EZR-AS1 knockdown significantly reduced the protein expression levels of MMP-2, MMP-9 and Bcl-2, but significantly increased the protein expression levels of Bax.	33236153	RID04197	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Skin squamous cell carcinoma	EZR-AS1	BCL2	positively-E	LncTar	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000171791	NA	101409257	596	NA	Bcl-2|PPP1R50	lncRNA EZR-AS1 knockdown represses proliferation, migration and invasion of cSCC via the PI3K/AKT signaling pathway.EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR.EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively.EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The analysis of LncTar identified FAK as a target of EZR-AS1. Furthermore, the RT-qPCR results suggested that FAK expression was significantly higher in cSCC tissues compared with healthy tissues. In summary, EZR-AS1 knockdown inhibited the PI3K/AKT signaling pathway by suppressing FAK expression in cSCC cells. Compared with the si-NC group, EZR-AS1 knockdown significantly reduced the protein expression levels of MMP-2, MMP-9 and Bcl-2, but significantly increased the protein expression levels of Bax.	33236153	RID04198	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Skin squamous cell carcinoma	EZR-AS1	BAX	negatively-E	LncTar	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000087088	NA	101409257	581	NA	BCL2L4	lncRNA EZR-AS1 knockdown represses proliferation, migration and invasion of cSCC via the PI3K/AKT signaling pathway.EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR.EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively.EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The analysis of LncTar identified FAK as a target of EZR-AS1. Furthermore, the RT-qPCR results suggested that FAK expression was significantly higher in cSCC tissues compared with healthy tissues. In summary, EZR-AS1 knockdown inhibited the PI3K/AKT signaling pathway by suppressing FAK expression in cSCC cells. Compared with the si-NC group, EZR-AS1 knockdown significantly reduced the protein expression levels of MMP-2, MMP-9 and Bcl-2, but significantly increased the protein expression levels of Bax.	33236153	RID04199	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney disease	MALAT1	KLF5	positively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(let-7f)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102554	NA	378938	688	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BTEB2|CKLF|IKLF	LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy.MALAT1 and KLF5 are upregulated, and let-7f is downregulated in renal tissues of DN mice.Inhibited MALAT1 and elevated let-7f promote proliferation, but decelerate apoptosis of HG-induced podocytes.It was predicted that MALAT1 could particularly bind to let-7f (Fig. 9A), and it was confirmed that (Fig. 9B) compared with the mimic NC group, the luciferase activity of MALAT1-Wt was abated in the let-7f mimic group (P < 0.05), while that of MALAT1-Mut was not broadly changed (P > 0.05), suggesting that let-7f could particularly bind with MALAT1. The target relation between let-7f and KLF5 was predicted at https://cm.jefferson.edu/rna22/Precomputed/ (Fig. 9D), and it was confirmed that (Fig. 9E) the cell luciferase activity was decreased after KLF5-Wt plasmid and let-7f mimic were co-transfected into the MPC5 cells, indicating that KLF5 was targeted by let-7f.	33232688	RID04200	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Kidney disease	MALAT1	NPHS1	negatively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000161270	NA	378938	4868	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CNF|NPHN|nephrin	LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy.MALAT1 and KLF5 are upregulated, and let-7f is downregulated in renal tissues of DN mice.Inhibited MALAT1 and elevated let-7f promote proliferation, but decelerate apoptosis of HG-induced podocytes.It was predicted that MALAT1 could particularly bind to let-7f (Fig. 9A), and it was confirmed that (Fig. 9B) compared with the mimic NC group, the luciferase activity of MALAT1-Wt was abated in the let-7f mimic group (P < 0.05), while that of MALAT1-Mut was not broadly changed (P > 0.05), suggesting that let-7f could particularly bind with MALAT1. The target relation between let-7f and KLF5 was predicted at https://cm.jefferson.edu/rna22/Precomputed/ (Fig. 9D), and it was confirmed that (Fig. 9E) the cell luciferase activity was decreased after KLF5-Wt plasmid and let-7f mimic were co-transfected into the MPC5 cells, indicating that KLF5 was targeted by let-7f. Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues.	33232688	RID04201	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Kidney disease	MALAT1	podocin	negatively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy.MALAT1 and KLF5 are upregulated, and let-7f is downregulated in renal tissues of DN mice.Inhibited MALAT1 and elevated let-7f promote proliferation, but decelerate apoptosis of HG-induced podocytes.It was predicted that MALAT1 could particularly bind to let-7f (Fig. 9A), and it was confirmed that (Fig. 9B) compared with the mimic NC group, the luciferase activity of MALAT1-Wt was abated in the let-7f mimic group (P < 0.05), while that of MALAT1-Mut was not broadly changed (P > 0.05), suggesting that let-7f could particularly bind with MALAT1. The target relation between let-7f and KLF5 was predicted at https://cm.jefferson.edu/rna22/Precomputed/ (Fig. 9D), and it was confirmed that (Fig. 9E) the cell luciferase activity was decreased after KLF5-Wt plasmid and let-7f mimic were co-transfected into the MPC5 cells, indicating that KLF5 was targeted by let-7f. Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues.	33232688	RID04202	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Kidney disease	MALAT1	desmin	positively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy.MALAT1 and KLF5 are upregulated, and let-7f is downregulated in renal tissues of DN mice.Inhibited MALAT1 and elevated let-7f promote proliferation, but decelerate apoptosis of HG-induced podocytes.It was predicted that MALAT1 could particularly bind to let-7f (Fig. 9A), and it was confirmed that (Fig. 9B) compared with the mimic NC group, the luciferase activity of MALAT1-Wt was abated in the let-7f mimic group (P < 0.05), while that of MALAT1-Mut was not broadly changed (P > 0.05), suggesting that let-7f could particularly bind with MALAT1. The target relation between let-7f and KLF5 was predicted at https://cm.jefferson.edu/rna22/Precomputed/ (Fig. 9D), and it was confirmed that (Fig. 9E) the cell luciferase activity was decreased after KLF5-Wt plasmid and let-7f mimic were co-transfected into the MPC5 cells, indicating that KLF5 was targeted by let-7f. Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues.	33232688	RID04203	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Kidney disease	MALAT1	Caspase3	positively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy.MALAT1 and KLF5 are upregulated, and let-7f is downregulated in renal tissues of DN mice.Inhibited MALAT1 and elevated let-7f promote proliferation, but decelerate apoptosis of HG-induced podocytes.It was predicted that MALAT1 could particularly bind to let-7f (Fig. 9A), and it was confirmed that (Fig. 9B) compared with the mimic NC group, the luciferase activity of MALAT1-Wt was abated in the let-7f mimic group (P < 0.05), while that of MALAT1-Mut was not broadly changed (P > 0.05), suggesting that let-7f could particularly bind with MALAT1. The target relation between let-7f and KLF5 was predicted at https://cm.jefferson.edu/rna22/Precomputed/ (Fig. 9D), and it was confirmed that (Fig. 9E) the cell luciferase activity was decreased after KLF5-Wt plasmid and let-7f mimic were co-transfected into the MPC5 cells, indicating that KLF5 was targeted by let-7f. Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues.	33232688	RID04204	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Hepatocellular carcinoma	PCED1B-AS1	CD274	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);colony formation(+);tumorigenesis(+)	ceRNA(miR-194-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000247774	GRCh38_12:47205896-47216460	ENSG00000120217	NA	100233209	29126	NA	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	Dual targeting of PD-L1 and PD-L2 by PCED1B-AS1 via sponging hsa-miR-194-5p induces immunosuppression in hepatocellular carcinoma.The interaction between PCED1B-AS1 and hsa-miR-194-5p was measured by microRNA pull down and in vitro binding assay.The effects of PCED1B-AS1 knockdown and over-expression on hsa-miR-194-5p and PD-Ls expression were investigated in HCC cell lines.PD-L1 expression was highly correlated with PD-L2 expression in HCC. PCED1B-AS1 and hsa-miR-194-5p expression was up-regulated in HCC.CED1B-AS1 was positively correlated with PD-Ls but negatively correlated hsa-miR-194-5p in HCC. These correlations were cross-validated by TCGA-LIHC dataset. PCED1B-AS1 interacted with hsa-mir-194-5p which inhibited PD-Ls expression.PCED1B-AS1 enhanced the expression of PD-Ls via sponging hsa-mir-194-5p.PCED1B-AS1 promoted cell proliferation, colony formation and in vivo tumor formation in xenografted nude mice while inhibited apoptosis.PCED1B-AS1 enhances the expression and function of PD-Ls via sponging hsa-miR-194-5p to induce immunosuppression in HCC.	33219943	RID04205	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Hepatocellular carcinoma	PCED1B-AS1	PDCD1LG2	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);colony formation(+);tumorigenesis(+)	ceRNA(miR-194-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000247774	GRCh38_12:47205896-47216460	ENSG00000197646	NA	100233209	80380	NA	B7-DC|bA574F11.2|Btdc|CD273|PD-L2|PDL2	Dual targeting of PD-L1 and PD-L2 by PCED1B-AS1 via sponging hsa-miR-194-5p induces immunosuppression in hepatocellular carcinoma.The interaction between PCED1B-AS1 and hsa-miR-194-5p was measured by microRNA pull down and in vitro binding assay.The effects of PCED1B-AS1 knockdown and over-expression on hsa-miR-194-5p and PD-Ls expression were investigated in HCC cell lines.PD-L1 expression was highly correlated with PD-L2 expression in HCC. PCED1B-AS1 and hsa-miR-194-5p expression was up-regulated in HCC.CED1B-AS1 was positively correlated with PD-Ls but negatively correlated hsa-miR-194-5p in HCC. These correlations were cross-validated by TCGA-LIHC dataset. PCED1B-AS1 interacted with hsa-mir-194-5p which inhibited PD-Ls expression.PCED1B-AS1 enhanced the expression of PD-Ls via sponging hsa-mir-194-5p.PCED1B-AS1 promoted cell proliferation, colony formation and in vivo tumor formation in xenografted nude mice while inhibited apoptosis.PCED1B-AS1 enhances the expression and function of PD-Ls via sponging hsa-miR-194-6p to induce immunosuppression in HCC.	33219943	RID04206	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	DUXAP10	E-cadherin	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	NA	NA	503639	NA	LNMAT1	NA	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP5 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04207	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Renal cell carcinoma	DUXAP10	Cyclin D	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	NA	NA	503639	NA	LNMAT1	NA	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP6 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04208	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Renal cell carcinoma	DUXAP10	Cyclin E	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	NA	NA	503639	NA	LNMAT1	NA	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP7 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04209	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Renal cell carcinoma	DUXAP10	CDK4	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	ENSG00000135446	NA	503639	1019	NA	PSK-J3	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP8 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04210	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Renal cell carcinoma	DUXAP10	N-cadherin	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	NA	NA	503639	NA	NA	NA	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP9 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04211	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Renal cell carcinoma	DUXAP10	vimentin	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000257227	NA	NA	NA	503639	NA	NA	NA	Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR to evaluate DUXAP10 expression in human RCC tissues and cell lines.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP10 may serve as a novel predictive biomarker and therapeutic target for RCC.	33215419	RID04212	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Cerebral ischemia-reperfusion injury	NEAT1	AKT1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000142208	NA	283131	207	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	AKT|PKB|PRKBA|RAC|RAC-alpha	Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion.Real-time quantitative PCR (qRT-PCR was used to measure the expression of phenotypic markers of classically activated (M1) and alternatively activated (M2) microglia, and western blot was performed to detect the levels of proteins related to the AKT/STAT3 pathway.The expression of the lncRNA NEAT1 was significantly upregulated in patients with ischaemic stroke, and knockdown of the lncRNA NEAT1 alleviated OGD/R-induced apoptosis and increased neuronal viability.the lncRNA NEAT1 may inhibit microglial polarization towards the M1 phenotype to reduce the damage caused by OGD/R and reduce the activity of the AKT/STAT3 pathway. In conclusion, the lncRNA NEAT1 may be a potential target for new therapeutic interventions for cerebral I/R.Both AKT and STAT3 play important roles in many physiological processes. The AKT/STAT3 pathway was analysed using western blot. As shown in Fig. 5a, c, the levels of the total STAT3 and AKT proteins were unchanged. Moreover,the phosphorylation of both AKT and STAT3 was reduced in the NEAT1 knockdown BV-2 cells compared with the control cells after OGD/R.	33184298	RID04213	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cerebral ischemia-reperfusion injury	NEAT1	STAT3	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APRF	Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion.Real-time quantitative PCR (qRT-PCR was used to measure the expression of phenotypic markers of classically activated (M1) and alternatively activated (M2) microglia, and western blot was performed to detect the levels of proteins related to the AKT/STAT3 pathway.The expression of the lncRNA NEAT1 was significantly upregulated in patients with ischaemic stroke, and knockdown of the lncRNA NEAT1 alleviated OGD/R-induced apoptosis and increased neuronal viability.the lncRNA NEAT1 may inhibit microglial polarization towards the M1 phenotype to reduce the damage caused by OGD/R and reduce the activity of the AKT/STAT3 pathway. In conclusion, the lncRNA NEAT1 may be a potential target for new therapeutic interventions for cerebral I/R.Both AKT and STAT3 play important roles in many physiological processes. The AKT/STAT3 pathway was analysed using western blot. As shown in Fig. 5a, c, the levels of the total STAT3 and AKT proteins were unchanged. Moreover,the phosphorylation of both AKT and STAT3 was reduced in the NEAT1 knockdown BV-3 cells compared with the control cells after OGD/R.	33184298	RID04214	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteoporosis	HCG18	NOTCH1	positively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell differentiation(-)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000148400	NA	414777	4851	Em:AB014087.1|FLJ25550|FLJ31598	TAN1	Long noncoding RNA HCG18 inhibits the differentiation of human bone marrow-derived mesenchymal stem cells in osteoporosis by targeting miR-30a-5p/NOTCH1 axis.RT-qPCR was performed to detect the expression of HCG18 and miR-30a-5p in BMSCs.The interaction between HCG18 and miR-30a-5p was analyzed by dual luciferase assay and RNA pull-down assay. During the differentiation from BMSCs to osteoblasts, the expression of HCG18 was significantly downregulated, and the expression of miR-30a-5p was significantly upregulated. miR-30a-5p partially abolished the effect of HCG18 on osteogenic differentiation of BMSCs. NOTCH1 was a target protein of miR-30a-5p, and upregulation of NOTCH1 reversed the effect of miR-30a-5p on osteogenic differentiation of BMSCs.HCG18 inhibited osteogenic differentiation of BMSCs induced by OP via the miR-30a-5p/NOTCH1 axis. HCG18 can be identified as a regulator of osteogenic differentiation of BMSCs.	33176682	RID04215	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	FEZF1-AS1	ITGA11	positively-E	RIP; luciferase reporter assay	upregulation	microarray	GSE137445	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-516b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000137809	NA	154860	22801	NA	HsT18964	Long non-coding RNA FEZF1-AS1 facilitates non-small cell lung cancer progression via the ITGA11/miR-516b-5p axis.FEZF1-AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC.Via integrating Arraystar Human mRNA microarray data and miRNA bioinformatics analysis, it was revealed that ITGA11 expression was decreased with loss of FEZF1-AS1 and increased with gain of FEZF1-AS1 expression, and microRNA (miR)-516b-5p inhibited the expression levels of both FEZF1-AS and ITGA11.RNA-binding protein immunoprecipitation and RNA pull-down assays further demonstrated that FEZF1-AS1 could bind to miR-516b-5p and that ITGA11 was a direct target of miR-516b-5p by luciferase reporter assay. The samples included eight frozen tissues of NSCLCs (four samples of squamous cell carcinoma and four of adenocarcinoma) and paired normal lung tissues (GSE137445). Inhibiting ITGA11 or overexpressing miR-516b-5p inhibits cell proliferation and invasion in NSCLC.	33174014	RID04216	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colon cancer	EPIC1	MYC	positively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136997	NA	284930	4609	Lnc-EPIC1	bHLHe39|c-Myc|MYCC	Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression.RNA-immunoprecipitation and RNA pull-down results confirmed that Lnc-EPIC1 directly binds MYC protein in colon cancer cells. MYC target proteins, including cyclin A, cyclin D and CDK9, were downregulated with Lnc-EPIC1 silencing, but upregulated after Lnc-EPIC1 overexpression in colon cancer cells. Further Lnc-EPIC1 silencing or overexpression failed to alter functions of MYC-knockout colon cancer cells. Collectively, overexpressed Lnc-EPIC1 is important for the progression of human colon cancer cells. Total RNA was subjected to qPCR analyses. Results in Figure 1A demonstrated that Lnc-EPIC1 expression increased over seven folds in colon cancer tissues, when compared to it in the normal colon tissues. Lnc-EPIC1 siRNA inhibits colon cancer cell growth, proliferation, migration and invasion.	33170148	RID04217	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colon cancer	EPIC1	Cyclin A	positively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	NA	NA	284930	NA	Lnc-EPIC1	NA	Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression.RNA-immunoprecipitation and RNA pull-down results confirmed that Lnc-EPIC1 directly binds MYC protein in colon cancer cells. MYC target proteins, including cyclin A, cyclin D and CDK9, were downregulated with Lnc-EPIC1 silencing, but upregulated after Lnc-EPIC1 overexpression in colon cancer cells. Further Lnc-EPIC1 silencing or overexpression failed to alter functions of MYC-knockout colon cancer cells. Collectively, overexpressed Lnc-EPIC1 is important for the progression of human colon cancer cells. Total RNA was subjected to qPCR analyses. Results in Figure 1A demonstrated that Lnc-EPIC1 expression increased over seven folds in colon cancer tissues, when compared to it in the normal colon tissues. Lnc-EPIC2 siRNA inhibits colon cancer cell growth, proliferation, migration and invasion.	33170148	RID04218	expression association	NA		
Colon cancer	EPIC1	Cyclin D	positively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	NA	NA	284930	NA	Lnc-EPIC1	NA	Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression.RNA-immunoprecipitation and RNA pull-down results confirmed that Lnc-EPIC1 directly binds MYC protein in colon cancer cells. MYC target proteins, including cyclin A, cyclin D and CDK9, were downregulated with Lnc-EPIC1 silencing, but upregulated after Lnc-EPIC1 overexpression in colon cancer cells. Further Lnc-EPIC1 silencing or overexpression failed to alter functions of MYC-knockout colon cancer cells. Collectively, overexpressed Lnc-EPIC1 is important for the progression of human colon cancer cells. Total RNA was subjected to qPCR analyses. Results in Figure 1A demonstrated that Lnc-EPIC1 expression increased over seven folds in colon cancer tissues, when compared to it in the normal colon tissues. Lnc-EPIC3 siRNA inhibits colon cancer cell growth, proliferation, migration and invasion.	33170148	RID04219	expression association	NA		
Colon cancer	EPIC1	CDK9	positively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136807	NA	284930	1025	Lnc-EPIC1	C-2k|CDC2L4|PITALRE|TAK	Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression.RNA-immunoprecipitation and RNA pull-down results confirmed that Lnc-EPIC1 directly binds MYC protein in colon cancer cells. MYC target proteins, including cyclin A, cyclin D and CDK9, were downregulated with Lnc-EPIC1 silencing, but upregulated after Lnc-EPIC1 overexpression in colon cancer cells. Further Lnc-EPIC1 silencing or overexpression failed to alter functions of MYC-knockout colon cancer cells. Collectively, overexpressed Lnc-EPIC1 is important for the progression of human colon cancer cells. Total RNA was subjected to qPCR analyses. Results in Figure 1A demonstrated that Lnc-EPIC1 expression increased over seven folds in colon cancer tissues, when compared to it in the normal colon tissues. Lnc-EPIC4 siRNA inhibits colon cancer cell growth, proliferation, migration and invasion.	33170148	RID04220	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Myocardial ischemia	TUG1	miR-29a-3p	negatively-F	StarBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	LncRNA TUG1 Contributes to Hypoxia-Induced Myocardial Cell Injury Through Downregulating miR-29a-3p in AC16 Cells.Quantitative real-time polymerase chain reaction was applied to measure the enrichment of TUG1 and miR-29a-3p. MiR-29a-3p was predicted as a target of TUG1 by StarBase bioinformatic software, and the target relationship between TUG1 and miR-29a-3p was verified by dual-luciferase reporter assay.TUG1 was markedly upregulated while the level of miR-29a-3p was notably decreased in hypoxia-stimulated AC16 cells.TUG1 silencing-mediated influences in hypoxia-induced AC16 cells were partly reversed by the interference of miR-29a-3p. In conclusion, TUG1 accelerated hypoxia-induced AC16 injury through inversely modulating the level of miR-29a-3p. TUG1/miR-29a-3p axis might be an underlying therapeutic target for myocardial ischemia.	33165134	RID04221	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Hepatocellular carcinoma	FBXL19-AS1	miR-342-3p	negatively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	Flavonoids of Sophorae Fructus	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000260852	GRCh38_16:30919319-30923269	NA	NA	283932	NA	MGC125469|MGC125470|MGC125472|NCRNA00095	NA	Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway. qRT-PCRwas used to detect the effect of flavonoids of Sophorae Fructus on the expression levels of FBXL19-AS1 and miR-342-3 p in Huh7 cells. The dual-luciferase reporter assay was used to detect whether FBXL19-AS1 targeted at miR-342-3 p.The expression level of FBXL19-AS1 was significantly decreased in Huh7 cells treated with flavonoids of Sophorae Fructus, whereas the expression level of miR-342-3 p was significantly increased. 	33164374	RID04222	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	
Hepatocellular carcinoma	FBXL19-AS1	Cyclin D1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	Flavonoids of Sophorae Fructus	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	NA	NA	283932	NA	MGC125469|MGC125470|MGC125472|NCRNA00095	NA	Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway. qRT-PCRwas used to detect the effect of flavonoids of Sophorae Fructus on the expression levels of FBXL19-AS1 and miR-342-3 p in Huh7 cells. The dual-luciferase reporter assay was used to detect whether FBXL19-AS1 targeted at miR-342-3 p.The expression level of FBXL19-AS1 was significantly decreased in Huh7 cells treated with flavonoids of Sophorae Fructus, whereas the expression level of miR-342-3 p was significantly increased. 	33164374	RID04223	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	
Hepatocellular carcinoma	FBXL19-AS1	MMP2	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	Flavonoids of Sophorae Fructus	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000087245	NA	283932	4313	MGC125469|MGC125470|MGC125472|NCRNA00095	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway. qRT-PCRwas used to detect the effect of flavonoids of Sophorae Fructus on the expression levels of FBXL19-AS1 and miR-342-3 p in Huh7 cells. The dual-luciferase reporter assay was used to detect whether FBXL19-AS1 targeted at miR-342-3 p.The expression level of FBXL19-AS1 was significantly decreased in Huh7 cells treated with flavonoids of Sophorae Fructus, whereas the expression level of miR-342-3 p was significantly increased. 	33164374	RID04224	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	FBXL19-AS1	MMP9	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	Flavonoids of Sophorae Fructus	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000100985	NA	283932	4318	NCRNA00095	CLG4B|GELB|MANDP2|MMP-9	Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway. qRT-PCRwas used to detect the effect of flavonoids of Sophorae Fructus on the expression levels of FBXL19-AS1 and miR-342-3 p in Huh7 cells. The dual-luciferase reporter assay was used to detect whether FBXL19-AS1 targeted at miR-342-3 p.The expression level of FBXL19-AS1 was significantly decreased in Huh7 cells treated with flavonoids of Sophorae Fructus, whereas the expression level of miR-342-3 p was significantly increased. 	33164374	RID04225	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	FBXL19-AS1	CDKN1A	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	Flavonoids of Sophorae Fructus	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000124762	NA	283932	1026	NCRNA00095	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway. qRT-PCRwas used to detect the effect of flavonoids of Sophorae Fructus on the expression levels of FBXL19-AS1 and miR-342-3 p in Huh7 cells. The dual-luciferase reporter assay was used to detect whether FBXL19-AS1 targeted at miR-342-3 p.The expression level of FBXL19-AS1 was significantly decreased in Huh7 cells treated with flavonoids of Sophorae Fructus, whereas the expression level of miR-342-3 p was significantly increased. 	33164374	RID04226	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Diffuse large b-cell lymphoma	HCP5	MET	positively-E	lnCAR;luciferase reporter assay;Starbase	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-27b-3p)	regulation	RNA-protein	Geniposide	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000105976	NA	10866	4233	D6S2650E|P5-1	DFNB97|HGFR|RCCP2	Geniposide inhibits proliferation and induces apoptosis of diffuse large B-cell lymphoma cells by inactivating the HCP5/miR-27b-3p/MET axis. we tried to explore the potential mechanism underlying the role of HCP5 in DLBCL. According to the lnCAR (https://lncar.renlab.org/) website30, miR-27b-3p, which was previously reported to be a tumor suppressor in DLBCL, was predicted as a candidate target of HCP5.a luciferase reporter assay demonstrated that miR-27b-3p overexpression remarkably reduced the luciferase activity of the plasmid carrying WT HCP5 but not MUT HCP5.Moreover, analysis of the TCGA data using starBase webtool28 confirmed the negative correlation between HCP5 and miR-27b-3p expression in DLBCL tissues.  HCP5 expression was revealed to be upregulated in DLBCL tissues and cell lines.	33162801	RID04227	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Pancreatic cancer	CASC19	E2F7	positively-E	StarBase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-148b)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000254166	GRCh38_8:127072694-127227541	ENSG00000165891	NA	103021165	144455	CARLo-6|LINC01245	NA	LncRNA CASC19 contributed to the progression of pancreatic cancer through modulating miR-148b/E2F7 axis.RT-qPCR assay was adopted to analyze CASC19 expression in PC tissues and cell lines. Bioinformatics analysis and Luciferase reporter assay were utilized to confirm the interaction between miR-148b and CASC19 or E2F7.The results elucidated that CASC19 expression was markedly increased in PC tissues and cell lines.The inhibitory effect of CASC19 knockdown on the progression of PC was reversed by the down-regulation of miR-148b or up-regulation of E2F7.CONCLUSIONS: These results demonstrated that CASC19 participated in the development of PC. The CASC19/miR-148b/E2F7 axis might be a new study direction for PC treatment. Binding sequences between CASC19 and miR-148b were predicted by starBase bioinformatic analysis website	33155202	RID04228	ceRNA or sponge	NA	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Temporal lobe epilepsy	MEG3	PIK3CA	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+);apoptosis process(-);cell viability(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000121879	NA	55384	5290	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	PI3K	LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE.overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI3K/AKT/mTOR pathway in SREDs.MEG3 reduced proinflammatory cytokines, oxidative stress, and apoptosis rate of hippocampal neuron and enhanced cell viability through the activation of the PI3K/AKT/mTOR pathway in SREDs and rats with TLE. Our findings may contribute to find a new therapeutic target for the treatment of epilepsy.	33149593	RID04229	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Temporal lobe epilepsy	MEG3	IL-1	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(-);apoptosis process(-);cell viability(+)	NA	association	RNA-RNA	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE.overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI3K/AKT/mTOR pathway in SREDs.MEG3 reduced proinflammatory cytokines, oxidative stress, and apoptosis rate of hippocampal neuron and enhanced cell viability through the activation of the PI4K/AKT/mTOR pathway in SREDs and rats with TLE. Our findings may contribute to find a new therapeutic target for the treatment of epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE. Overexpression of MEG3 reduced the expression of IL-1beta, IL-6, and TNF-alpha, MDA content, apoptosis rate of hippocampal neuron, increased SOD activity, and inhibited the PI3K/AKT/mTOR pathway in rats with TLE. In addition, overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI3K/AKT/mTOR pathway in SREDs.	33149593	RID04230	expression association	NA		
Temporal lobe epilepsy	MEG3	IL6	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(-);apoptosis process(-);cell viability(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136244	NA	55384	3569	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BSF2|HGF|HSF|IFNB2|IL-6	LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE.overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI3K/AKT/mTOR pathway in SREDs.MEG3 reduced proinflammatory cytokines, oxidative stress, and apoptosis rate of hippocampal neuron and enhanced cell viability through the activation of the PI4K/AKT/mTOR pathway in SREDs and rats with TLE. Our findings may contribute to find a new therapeutic target for the treatment of epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE. Overexpression of MEG3 reduced the expression of IL-1beta, IL-6, and TNF-alpha, MDA content, apoptosis rate of hippocampal neuron, increased SOD activity, and inhibited the PI3K/AKT/mTOR pathway in rats with TLE. In addition, overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI4K/AKT/mTOR pathway in SREDs.	33149593	RID04231	expression association	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Temporal lobe epilepsy	MEG3	TNF	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(-);apoptosis process(-);cell viability(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000228978	NA	55384	7124	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE.overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI3K/AKT/mTOR pathway in SREDs.MEG3 reduced proinflammatory cytokines, oxidative stress, and apoptosis rate of hippocampal neuron and enhanced cell viability through the activation of the PI4K/AKT/mTOR pathway in SREDs and rats with TLE. Our findings may contribute to find a new therapeutic target for the treatment of epilepsy.MEG3 expression was downregulated in SREDs and rats with TLE. Overexpression of MEG3 reduced the expression of IL-1beta, IL-6, and TNF-alpha, MDA content, apoptosis rate of hippocampal neuron, increased SOD activity, and inhibited the PI3K/AKT/mTOR pathway in rats with TLE. In addition, overexpression of MEG3 enhanced cell viability and inhibited apoptosis through the activation of the PI5K/AKT/mTOR pathway in SREDs.	33149593	RID04232	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Breast cancer	MIR99AHG	Cyclin D1	positively-E	RNA pull-down assay	upregulation	qPCR	(SRA) database (accession codes:?PRJNA611025)	NA	chemoresistance(+)	protein stability	binding/interaction	RNA-protein	Tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000215386	GRCh38_21:15928296-16645467	NA	NA	388815	NA	C21orf34|C21orf35|DILA1|LINC00478|MONC	NA	LncRNA DILA1 inhibits Cyclin D1 degradation and contributes to tamoxifen resistance in breast cancer.we identify a lncRNA, DILA1, which-interacts with Cyclin D1 and is overexpressed in tamoxifen-resistant breast cancer cells.DILA1 inhibits the phosphorylation of Cyclin D1 at Thr286 by directly interacting with Thr286 and blocking its subsequent degradation, leading to overexpressed Cyclin D1 protein in breast cancer. Knocking down DILA1 decreases Cyclin D1 protein expression, inhibits cancer cell growth and restores tamoxifen sensitivity both in vitro and in vivo.his study shows the previously unappreciated importance of post-translational dysregulation of Cyclin D1 contributing to tamoxifen resistance in breast cancer. Moreover, it reveals the novel mechanism of DILA1 in regulating Cyclin D1 protein stability and suggests DILA1 is a specific therapeutic target to downregulate Cyclin D1 protein and reverse tamoxifen resistance in treating breast cancer.	33139730	RID04233	interact with protein	chemoresistance	UP(LIHC);DATA(GSE117623)	
Parkinson's disease	AK039862	PAFAH1B1	positively-E	RPISeq	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell migration(-)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000007168	NA	NA	5048	NA	LIS1|MDCR|MDS|NudF|PAFAH	Inflammatory lncRNA AK039862 regulates paraquat-inhibited proliferation and migration of microglial and neuronal cells through the Pafah1b1/Foxa1 pathway in co-culture environments.RNA-Protein Interaction Prediction (RPISeq) (http://pridb.gdcb.iastate.edu/RPISeq/index.html) predicted that there might be an interaction between AK039862 and Pafah1b1/Foxa1 (Supplementary Fig. 1). Then, we chose AK039862  homologous genes Pafah1b1 and transcription factor Foxa1 as potential targets of AK039862 to be evaluated in PQ-induced neuronal damage process. AK039862 overexpression exacerbates cell death and knockdown rescues microglial migration inhibition induced by PQ exposure .The expression of lncRNA AK039862 and AK048895 increased at more than 6-folds in PQ-exposed mice as compared to the control in the microarray database.Overexpression of AK039862 could up-regulate the expression of Pafah1b1 and Foxa1 mRNA with PQ treatment .	33120262	RID04234	expression association	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Parkinson's disease	AK039862	FOXA1	positively-E	RPISeq	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell migration(-)	NA	association	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	TF	NA	NA	ENSG00000129514	NA	NA	3169	NA	HNF3A	Inflammatory lncRNA AK039862 regulates paraquat-inhibited proliferation and migration of microglial and neuronal cells through the Pafah1b1/Foxa1 pathway in co-culture environments.RNA-Protein Interaction Prediction (RPISeq) (http://pridb.gdcb.iastate.edu/RPISeq/index.html) predicted that there might be an interaction between AK039862 and Pafah1b1/Foxa1 (Supplementary Fig. 1). Then, we chose AK039862  homologous genes Pafah1b1 and transcription factor Foxa1 as potential targets of AK039862 to be evaluated in PQ-induced neuronal damage process. AK039862 overexpression exacerbates cell death and knockdown rescues microglial migration inhibition induced by PQ exposure .The expression of lncRNA AK039862 and AK048895 increased at more than 6-folds in PQ-exposed mice as compared to the control in the microarray database.Overexpression of AK039862 could up-regulate the expression of Pafah1b1 and Foxa1 mRNA with PQ treatment .	33120262	RID04235	expression association	NA		UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	FBXL19-AS1	PIN1	positively-E	RIP;dual-luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000127445	NA	283932	5300	MGC125469|MGC125470|MGC125472|NCRNA00095	dod	Long Noncoding RNA FBXL19-AS1 Expedites Cell Growth, Migration and Invasion in Cervical Cancer by miR-193a-5p/PIN1 Signaling.RT-qPCR was utilized to test gene expression.Moreover, RIP, RNA pull-down and luciferase reporter assays were utilized for detecting the correlations among FBXL19-AS1, miR-193a-5p and PIN1 (peptidylprolyl cis/trans isomerase, NIMA-interacting 1).FBXL19-AS1 exhibited elevated expression in cervical cancer tissues and cells. Silencing FBXL19-AS1 repressed cell proliferation through arresting cell cycle and stimulating apoptosis, and losing FBXL19-AS1 also restrained cell migration and invasion. Also, we discovered FBXL19-AS1 as a miR-193a-5p sponge, while miR-193a-5p was a tumor inhibitor in cervical cancer. Further, PIN1 was proved as the miR-193a-5p target, and FBXL19-AS1 augmented PIN1 expression in cervical cancer via sequestering miR-193a-5p. Of note, PIN1 accelerated the progression of cervical cancer, and its upregulation counteracted the impacts of depleted FBXL19-AS1 on cervical cancer cell functions.	33116834	RID04236	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Cervical cancer	LINC00511	DRAM1	positively-E	RIP;dual-luciferase reporter assay;	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000136048	NA	400619	55332	onco-lncRNA-12	DRAM|FLJ11259	Long Non-Coding RNA LINC00511 Accelerates Proliferation and Invasion in Cervical Cancer Through Targeting miR-324-5p/DRAM1 Axis.The expression of LINC00511 in cervical cancer and cell lines was examined by RT-PCRDual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to identify the target of LINC00511.the results showed that LINC00511 was significantly up-regulated in cervical cancer and cell lines and mainly distributed in the cytoplasm of cervical cancer cells.Bioinformatic analysis, dual-luciferase reporter, and RIP assays showed that LINC00511 was a target of miR-324-5p, while DRAM1 was a direct target of miR-324-5p.DRAM1 overexpression promoted both HPV-negative and HPV-positive cervical cancer cell proliferation and invasion, which could be reversed by miR-324-5p mimics or si-LINC00511.DRAM1 overexpression promoted both HPV-negative and HPV-positive cervical cancer cell proliferation and invasion, which could be reversed by miR-324-5p mimics or si-LINC00511.Collectively, these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.	33116605	RID04237	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Malignant glioma	LINC00210	MIR328	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000231814	GRCh38_1:217892900-217920804	ENSG00000207948	NA	100885798	442901	NCRNA00210	MIRN328|hsa-mir-328|mir-328	LINC00210 exerts oncogenic roles in glioma by sponging miR-328.The present study demonstrated that LINC00210 was significantly upregulated in glioma tissues, and high expression of LINC00210 was significantly associated with advanced clinical stage and poor prognosis in patients with glioma.he results of luciferase reporter assays indicated that LINC00210 could directly target microRNA (miR)-328 in glioma cells, and miR-328 expression was negatively correlated with LINC00210 expression in glioma tissues. LINC00210 knockdown significantly promoted the expression of miR-328 in U251 and T98G cells. Moreover, silencing miR-328 impaired the inhibitory effects of LINC00210 knockdown on the proliferation and migration of U251 and T98G cells. Therefore, the present results suggested that LINC00210 may exert an oncogenic role in glioma via sponging miR-328.	33110451	RID04238	ceRNA or sponge	prognosis		
Hepatocellular carcinoma	Lnc-ATG9B-4	CDK5	positively-E		upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cancer progression(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000164885	NA	NA	1020	NA	LIS7|PSSALRE	Lnc-ATG9B-4 aggravates progress of hepatocellular carcinoma through cell proliferation and migration by upregulating CDK5.lnc AC010973.1 (lnc-ATG9B-4) was first identified by microarray analysis from 8 patients with hepatocellular carcinoma and confirmed by quantitative PCR in 176 patients with hepatocellular carcinoma.In hepatocellular carcinoma cells, overexpression of lnc-ATG9B-4 promoted proliferation, invasion, as well as migration, while inhibiting lnc-ATG9B-4 by siRNA significantly attenuated the proliferation, invasion, as well as migration.lnc-ATG9B-4 increased the expression of cyclin-dependent kinase 5 (CDK5), which was closely related to the development and chemotherapy sensitivity of hepatocellular carcinoma. In summary, our results revealed that lnc-ATG9B-4 suggests an unfavorable prognosis of hepatocellular carcinoma and facilitates the proliferation, invasion, as well as migration of hepatocellular carcinoma cells by upregulating CDK5. This research suggests that lnc-ATG9B-4 may be a new biomarker for predicting the prognosis of hepatocellular carcinoma; meanwhile, targeting lnc-ATG9B-4 might serve as a potential strategy for the treatment hepatocellular carcinoma.	33023330	RID04239	expression association	chemoresistance,prognosis		DOWN(LIHC,PRAD,PAAD);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807)
Non-small cell lung cancer	B4GALT1-AS1	SOX9	positively-E	RIP;StarBase v3.0	upregulation	RT-qPCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-30e)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000233554	GRCh38_9:33166948-33182865	ENSG00000125398	NA	101929639	6662	NA	CMD1|CMPD1|SRA1|SRXX2|SRXY10	Long non-coding RNA B4GALT1-Antisense RNA 1/microRNA-30e/SRY-box transcription factor 9 signaling axis contributes to non-small cell lung cancer cell growth.Reverse transcription-quantitative PCR was performed to detect B4GALT1-AS1 levels in NSCLC tissues and cell lines.Potential influences of B4GALT1-AS1 on biological functions of NSCLC were assessed through a series of in vitro experiments, and the molecular mechanism was determined via RNA immunoprecipitation (RIP) and bioinformatics analyses.In the present study, B4GALT1-AS1 competed as an endogenous RNA by sequestering microRNA-30e (miR-30e) leading to an enhanced expression of SRY-box transcription factor 9 (SOX9). The effects of silencing B4GALT1-AS1 on NSCLC cells proliferation could be ameliorated by inhibiting miR-30e or restoring SOX9. Hence, B4GALT1-AS1 acted as a lncRNA that drives tumor progression in NSCLC via the regulation of the miR-30e/SOX9 axis. The findings of the present study indicated that the B4GALT1-AS1/miR-30e/SOX9 axis maybe an effective target for NSCLC treatment and management. Subsequently, on performing the CCK-8 assay, pc-SOX9 co-transfection was found to reverse the decline in proliferation of A549 and H1299 cells caused by the silencing of B4GALT1-AS1. Next, StarBase version 3.0, a publicly available algorithm was used to predict the miRNAs that interact directly with B4GALT1-AS1.	33014162	RID04240	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Atherosclerosis	HCG11	FOXF1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000103241	NA	493812	2294	bK14H9.3|FLJ14049|FLJ30357	FKHL5|FREAC1	LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis in atherosclerosis.Quantitative Real-time Polymerase Chain Reaction (qRT-PCR was used to detect the expression of HCG11 and miR-144 in the serum of AS patients and healthy volunteers. Luciferase gene reporter and RNA pull down experiments confirmed the relationship between HCG11 and miR-144, miR-144 and FOXF1.LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis.Overexpression of HCG11 promoted the proliferation and inhibited apoptosis of VSMCs.This study showed that HCG11 was significantly upregulated in patients with AS, while miR-144 was down-regulated in patients with AS.	33008472	RID04241	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	TINCR	MTOR	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-7)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000198793	NA	257000	2475	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	lncRNA TINCR facilities bladder cancer progression via regulating miR-7 and mTOR.The present study found that the expression of TINCR was significantly increased in bladder cancer tissues and cell lines, when compared with that in adjacent normal tissues and normal urinary tract epithelial cell line SV-HUC-1, respectively.Silencing of TINCR expression significantly increased miR-7 expression and reduced bladder cancer cell proliferation, migration and invasion, while knockdown of miR-7 expression reversed the inhibitory effects of TINCR downregulation on bladder cancer cells. mTOR was then identified as a target gene of miR-7 in bladder cancer, and it was demonstrated that overexpression of mTOR reversed the inhibitory effects of miR-7 on bladder cancer cells. In conclusion, this study suggests that TINCR/miR-7/mTOR signaling may be a potential therapeutic target for bladder cancer.	33000269	RID04242	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Cerebrovascular disease	OIP5-AS1	HMGB1	positively-E	StarBase 3.0;TargetScan;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	TLR4/NF-kB signaling pathway(+);cell proliferation(-);apoptosis process(+);inflammatory response(+);oxidative stress(+)	ceRNA(miR-98-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Brain disease	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000189403	NA	729082	3146	cyrano|linc-OIP5	DKFZp686A04236|HMG1|HMG3|SBP-1	LncRNA OIP5-AS1 facilitates ox-LDL-induced endothelial cell injury through the miR-98-5p/HMGB1 axis.The expression of OIP5-AS1, miR-98-5p and High-mobility group protein box-1 (HMGB1) was detected by quantitative real-time polymerase chain reaction (qRT-PCR.The targets of OIP5-AS and miR-98-5p were predicted by starBase 3.0 and TargetScan and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The expression of OIP5-AS1 was upregulated, while miR-98-5p was downregulated in ox-LDL-induced human umbilical vein endothelial cells (HUVECs). knockdown of OIP5-AS1 induced proliferation and inhibited apoptosis, inflammatory injury and oxidative stress injury in ox-LDL-induced HUVEC cells. Interestingly, miR-98-5p was a target of OIP5-AS1 and miR-98-5p inhibition abolished the effects of OIP5-AS1 downregulation on ox-LDL-induced HUVECs injury.More importantly, miR-98-5p directly targeted HMGB1, and OIP5-AS1 regulated the expression of HMGB1 by sponging miR-98-5p. Finally, OIP5-AS1 regulated the TLR4/nuclear factor-kappa B (NF-kB) signaling pathway through miR-98-5p/HMGB1 axis. LncRNA OIP5-AS1 accelerates ox-LDL-induced endothelial cell injury through regulating HMGB1 mediated by miR-98-5p via the TLR4/NF-kB signaling pathway. In conclusion, our study indicated that the expression of OIP5-AS1 was increased, while OIP5-AS1 knockdown induced proliferation and inhibited apoptosis, inflammatory injury and oxidative stress injury of ox-LDL-induced HUVEC cells.	32990894	RID04243	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Malignant glioma	HOTAIR	NLK	negatively-E	IHC	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087095	NA	100124700	51701	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.4, fold in GBM cell lines, respectively.-The 5'-domain ofHOTAIR binds to the PRC2 complex, containing EZH2, SUZ12, andEED. The PRC2 complex induces H3K27me3, thereby inhibiting theexpression of various target genes. The 3'-domain binds to theLSD1/CoREST/REST complex, resulting in the removal of H3K4me2,leading to gene silencing. The target genes of HOTAIR involve NLK,PDCD4, CDK2, CDK4, E2F1, p21, p16, CDC6, NCAPG, PLK4,CENPE, NUSAP1, NCAPH, ASPM, CEP55, and KIF4A among others.In this way, HOTAIR plays a pro-oncogenic role in gliomagenesis, pro_x0002_moting glioma cell proliferation, migration, invasion, and epithelialmesenchymal transition, as well as the tumorigenicity of GSCs	32978667	RID04244	epigenetic regulation	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Malignant glioma	HOTAIR	PDCD4	negatively-E	western blot;ChIP	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000150593	NA	100124700	27250	HOXC-AS4|HOXC11-AS1|NCRNA00072	H731	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.5, fold in GBM cell lines, respectively	32978667	RID04245	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Malignant glioma	HOTAIR	CDK2	negatively-E	siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000123374	NA	100124700	1017	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.6, fold in GBM cell lines, respectively	32978667	RID04246	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	HOTAIR	CDK4	negatively-E	siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000135446	NA	100124700	1019	HOXC-AS4|HOXC11-AS1|NCRNA00072	PSK-J3	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.7, fold in GBM cell lines, respectively	32978667	RID04247	epigenetic regulation	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Malignant glioma	HOTAIR	E2F1	negatively-E	siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000101412	NA	100124700	1869	HOXC-AS4|HOXC11-AS1|NCRNA00072	RBBP3|RBP3	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.8, fold in GBM cell lines, respectively	32978667	RID04248	epigenetic regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	HOTAIR	CDKN1A	negatively-E		upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.9, fold in GBM cell lines, respectively	32978667	RID04249	epigenetic regulation	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Malignant glioma	HOTAIR	p16	negatively-E	siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000147889	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.10, fold in GBM cell lines, respectively	32978667	RID04250	epigenetic regulation	NA		
Malignant glioma	HOTAIR	CDC6	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000094804	NA	100124700	990	HOXC-AS4|HOXC11-AS1|NCRNA00072	CDC18L	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.11, fold in GBM cell lines, respectively	32978667	RID04251	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Malignant glioma	HOTAIR	NCAPG	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109805	NA	100124700	64151	HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP-G|FLJ12450|hCAP-G|YCG1	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.12, fold in GBM cell lines, respectively	32978667	RID04252	epigenetic regulation	NA		UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Malignant glioma	HOTAIR	PLK4	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000142731	NA	100124700	10733	HOXC-AS4|HOXC11-AS1|NCRNA00072	Sak|STK18	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.13, fold in GBM cell lines, respectively	32978667	RID04253	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM);DOWN(NSCLC);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Malignant glioma	HOTAIR	CENPE	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000138778	NA	100124700	1062	HOXC-AS4|HOXC11-AS1|NCRNA00072	KIF10|PPP1R61	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.14, fold in GBM cell lines, respectively	32978667	RID04254	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Malignant glioma	HOTAIR	NUSAP1	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000137804	NA	100124700	51203	HOXC-AS4|HOXC11-AS1|NCRNA00072	ANKT|BM037|FLJ13421|LNP|PRO0310p1|Q0310|SAPL	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.15, fold in GBM cell lines, respectively	32978667	RID04255	epigenetic regulation	NA		UP(PAAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842,GSE55807)
Malignant glioma	HOTAIR	NCAPH	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000121152	NA	100124700	23397	HOXC-AS4|HOXC11-AS1|NCRNA00072	BRRN1|CAP-H|hCAP-H	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.16, fold in GBM cell lines, respectively	32978667	RID04256	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Malignant glioma	HOTAIR	ASPM	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000066279	NA	100124700	259266	HOXC-AS4|HOXC11-AS1|NCRNA00072	ASP|Calmbp1|FLJ10517|FLJ10549|MCPH5	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.17, fold in GBM cell lines, respectively	32978667	RID04257	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Malignant glioma	HOTAIR	CEP55	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000138180	NA	100124700	55165	HOXC-AS4|HOXC11-AS1|NCRNA00072	C10orf3|CT111|FLJ10540	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.18, fold in GBM cell lines, respectively	32978667	RID04258	epigenetic regulation	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Malignant glioma	HOTAIR	KIF4A	negatively-E	western blot;Immunofluorescence analysis	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000090889	NA	100124700	24137	HOXC-AS4|HOXC11-AS1|NCRNA00072	FLJ12530|FLJ12655|FLJ14204|FLJ20631|HSA271784|KIF4|KIF4-G1|MRX100	Critical role of HOX transcript antisense intergenic RNA (HOTAIR)in gliomas.We found that primary tumours in GBMdisplaying tumour progression were characterized by increased MEG3,HOTAIR expression levels. The lncRNAs MEG3, HOTAIR showed high expressions (Fig. 1a). These lncRNAs showed a significant increased 5.3,2.19, fold in GBM cell lines, respectively	32978667	RID04259	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Malignant glioma	HOTAIR	FGF1	positively-E	Starbase;shRNA;dual-luciferase reporter assay;overexpression;knockdown	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113578	NA	100124700	2246	HOXC-AS4|HOXC11-AS1|NCRNA00072	AFGF|ECGF|ECGF-beta|ECGFA|ECGFB|FGF-alpha|FGFA|GLIO703|HBGF1	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-125a/mTOR, thereby affecting gliom development and progression.	32978667	RID04260	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Malignant glioma	HOTAIR	SKA2	positively-E	luciferase assays	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000182628	NA	100124700	348235	HOXC-AS4|HOXC11-AS1|NCRNA00072	FAM33A|FLJ12758	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-126a/mTOR, thereby affecting gliom development and progression.	32978667	RID04261	ceRNA or sponge	NA		DOWN(PRAD,PAAD);UP(SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE55807)
Malignant glioma	HOTAIR	USF1	positively-E	dual-luciferase reporter assays;overexpression;siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	ceRNA(miR-148b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000158773	NA	100124700	7391	HOXC-AS4|HOXC11-AS1|NCRNA00072	bHLHb11|MLTFI|UEF	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-127a/mTOR, thereby affecting gliom development and progression.	32978667	RID04262	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	HOTAIR	glutaminase	positively-E	RNA pull-down assay	upregulation	qPCR;RT-PCR	NA	NA	cell invasion(+);chemoresistance(+);angiogenesis(+)	ceRNA(miR-126-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-128a/mTOR, thereby affecting gliom development and progression.	32978667	RID04263	ceRNA or sponge	chemoresistance		
Malignant glioma	HOTAIR	MTOR	positively-E	western blot;overexpression;siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-125a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000198793	NA	100124700	2475	HOXC-AS4|HOXC11-AS1|NCRNA00072	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-129a/mTOR, thereby affecting gliom development and progression.	32978667	RID04264	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Malignant glioma	HOTAIR	MIR219A1	negatively-E	siRNA	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000199036	NA	100124700	407002	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MIR219-1|MIRN219-1|MRI219-1|hsa-mir-219a-1|mir-219|mir-219a-1	Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.HOTAIR can regulate several miR-related pathways, such as miR-326/FGF1, miR-141/SKA2, miR-148b-3p, miR-15b/p53, miR_x0002_126-5p/glutaminase, and miR-130a/mTOR, thereby affecting gliom development and progression.	32978667	RID04265	ceRNA or sponge	NA		
Osteosarcoma	SNHG22	NKIRAS2	positively-E	RNA pull-down assay;RIP;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-4492)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000267322	GRCh38_18:49813961-49851059	ENSG00000260770	NA	103091864	28511	SCARNA17HG	DKFZP434N1526|kappaB-Ras2|KBRAS2	Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma.we confirmed that SNHG22 was downregulated in OS, and the overexpression of SNHG22 significantly inhibited OS progression in vivo and in vitro.overexpression of SNHG22 also inhibited the migration and proliferation of human umbilical vein endothelial cells (HUVECs) and prevented the epithelial-to-mesenchymal transition (EMT) in OS.the interaction between miR-4492 and SNHG22 we previously predicted was validated by RNA pull-down assays and RNA immunoprecipitation assays. dual-luciferase reporter assays showed that SNHG22 could directly interact with miR-4492 and upregulate the expression of NK-kB inhibitor-interacting Ras-like 2 (NKIRAS2) by its competing endogenous RNA (ceRNA) activity on miR-4492. In conclusion, our study has clarified the function of SNHG22 in OS progression and suggests a novel therapeutic target for OS.	32950969	RID04266	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE55807,GSE67939)
Diabetic cataract	KCNQ1OT1	ITGAV	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	TGF-beta/Smad3 signaling pathway(-);cell viability(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-26a-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000138448	NA	10984	3685	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CD51|MSK8|VNRA|VTNR	LncRNA KCNQ1OT1 knockdown inhibits viability, migration and epithelial-mesenchymal transition in human lens epithelial cells via miR-26a-5p/ITGAV/TGF-beta/Smad3 axis.The levels of KCNQ1OT1, miR-26a-5p, integrin alphaV (ITGAV), TGF-beta, Smad3 and phosphorylated (p)-Smad3 were measured via quantitative real-time polymerase chain reaction or western blot.The target relationship between miR-26a-5p and KCNQ1OT1 or ITGAV was determined via luciferase reporter assay.KCNQ1OT1 was up-regulated and miR-26a-5p level was reduced in diabetic cataract tissues and HG-treated SRA01/04 cells. Silence of KCNQ1OT1 or miR-26a-5p up-regulation repressed cell viability, migration and EMT in SRA01/04 cells stimulated via HG.KCNQ1OT1 could target miR-26a-5p and controlled cell viability, migration and EMT via regulating miR-26a-5p. ITGAV was targeted via miR-26a-5p and positively regulated via KCNQ1OT1. ITGAV overexpression promoted cell viability, migration and EMT in HG-treated SRA01/04 cells, which were mitigated by KCNQ1OT1 silence.KCNQ1OT1 knockdown mitigated HG-induced the activation of TGF-beta/Smad3 signaling by regulating miR-26a-5p.CONCLUSION: KCNQ1OT1 knockdown represses cell viability, migration and EMT through miR-26a-5p/ITGAV/TGF-beta/Smad3 axis in SRA01/04 cells under HG condition, providing a new target for the treatment of diabetic cataract.	32950535	RID04267	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Pituitary adenoma	H19	ATG7	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(+);cancer progression(-)	ceRNA(miR-93a)	regulation	RNA-protein	Dopamine agonists	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000197548	NA	283120	10533	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	APG7L|DKFZp434N0735|GSA7	The long noncoding RNA-H19/miRNA-93a/ATG7 axis regulates the sensitivity of pituitary adenomas to dopamine agonists.ur previous study demonstrated that long noncoding RNA H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumor progression. H19 promoted ATG7 expression in pituitary tumor cells by inhibiting miR-93a expression.a potential binding site between miR-93 and H19 was confirmed, and low expression of miR-93 was previously found in DA-resistant prolactinomas. Furthermore, we showed that miR-93a regulates ATG7 expression by targeting ATG7 mRNA. In conclusion, our study has identified the role of the H19-miR-93-ATG7 axis in DA treatment of prolactinomas, which may be a potential therapeutic target for human prolactinomas.	32946927	RID04268	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Colorectal cancer	BCYRN1	KRAS	positively-E	TargetScan;dual-luciferase reporter gene assay	upregulation	RT-PCR	NA	NA	cell growth(+)	ceRNA(miR-204-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000133703	NA	618	3845	BC200|BC200a|LINC00004|NCRNA00004	K-Ras4B|KRAS1|KRAS2	Long non-coding RNA BCYRN1 exerts an oncogenic role in colorectal cancer by regulating the miR-204-3p/KRAS axis.RT-PCRwas used to detect the expression level of BCYRN1 in tumour tissues and CRC cell lines.The dual luciferase reporter gene detects the competitive binding of BCYRN1 to miR-204-3p. TargetScan analysis and dual luciferase reporter gene assays were applied to detect the target gene of miR-204-3p. Rescue experiments verified that BCYRN1 affects CRC by regulating the effect of miR-204-3p on KRAS.We found that compared with normal tissues and human intestinal epithelial cells (HIECs), CRC tumour tissues and cell lines had significantly increased BCYRN1 levels.n addition, bioinformatics analysis and dual-luciferase reporter assay showed that BCYRN1 served as a competitive endogenous RNA (ceRNA) to regulate the development of CRC through competitively binding to miR-204-3p. Further studies proved that overexpression of miR-204-3p reversed the effects of BCYRN1 on CRC. Next, TargetScan analysis and dual-luciferase reporter assay indicated that KRAS is a target gene of miR-204-3p and is negatively regulated by miR-204-3p. A series of rescue experiments showed that BCYRN1 affected the occurrence and development of CRC by regulating the effects of miR-204-3p on KRAS.tumorigenesis experiments in a CRC mouse model confirmed that BCYRN1 downregulation effectively inhibited tumour growth.Our findings suggest that BCYRN1 plays a carcinogenic role in CRC by regulating the miR-204-3p/KRAS axis.	32944001	RID04269	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Chronic heart failure	GAS5	miR-223-3P	negatively-F	dual-luciferase reporter gene assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	sponge	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Heart failure	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Low-expressed GAS5 injure myocardial cells and progression of chronic heart failure via regulation of miR-223-3P.In this study, the expression of GAS5 and miR-223-3p in peripheral blood of CHF patients and healthy subjects was first detected, GAS5 was low in CHF while miR-223-3p was high.Through dual luciferase reporter and RNA immunoprecipitation experiment, we found that miR-223-3p was regulated by GAS5 in a targeted manner.we found that inhibition of GAS5 with elevated expression of miR-223-3p decreased the proliferative capacity of cardiomyocytes and increased apoptotic capacity and inflammatory factors.	32926880	RID04270	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Rheumatoid arthritis	PVT1	miR-145-5p	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long non-coding RNA PVT1 can regulate the proliferation and inflammatory responses of rheumatoid arthritis fibroblast-like synoviocytes by targeting microRNA-145-5p.Quantitative real-time polymerase chain reaction (qRT-PCR was performed to determine mRNA level. The binding sites between PVT1 and miR-145-5p were verified by a dual-luciferase reporter assay.PVT1 was significantly increased and miR-145-5p was decreased in synovial tissues of RA patients.knockdown of PVT1 inhibited TNF-alpha-induced production of interleukin (IL)-1beta and IL-6 and the activation of NF-kB through miR-145-5p. PVT1 can regulate apoptosis and inflammatory responses in RA-FLSs by targeting miR-145-5p. Knockdown of PVT1 inhibited TNF-alpha-induced RA-FLS over-proliferation and reversed TNF-alpha-induced RA-FLS apoptosis reduction.	32918701	RID04271	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Breast cancer	MALAT1	ABCB1	negatively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-485-3p)	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000085563	NA	378938	5243	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ABC20|CD243|CLCS|GP170|MDR1|p-170|P-gp|PGY1	Long-chain non-coding RNA MALAT1 regulates paclitaxel resistance of breast cancer cells by targeting miR-485-3p.To investigate the role of long-chain non-coding RNA MALAT1 in modulating paclitaxel resistance in breast cancer cells.CONCLUSIONS: MALAT1 can modulate paclitaxel resistance in breast cancer cells possibly by targeting miR-485-3p to down-regulate P-gp and Bcl-2 and up-regulate Bax. Compared with paclitaxel-sensitive SK-BR-3 cells, paclitaxel-resistant SK-BR-3 cells showed significantly increased the IC50 of paclitaxel with up-regulated MALAT1 expression and down-regulated miR-485-3p expression. 	32897218	RID04272	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Breast cancer	MALAT1	BCL2	negatively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-485-3p)	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Bcl-2|PPP1R50	Long-chain non-coding RNA MALAT1 regulates paclitaxel resistance of breast cancer cells by targeting miR-485-3p.To investigate the role of long-chain non-coding RNA MALAT1 in modulating paclitaxel resistance in breast cancer cells.CONCLUSIONS: MALAT1 can modulate paclitaxel resistance in breast cancer cells possibly by targeting miR-485-3p to down-regulate P-gp and Bcl-2 and up-regulate Bax. Compared with paclitaxel-sensitive SK-BR-3 cells, paclitaxel-resistant SK-BR-3 cells showed significantly increased the IC50 of paclitaxel with up-regulated MALAT1 expression and down-regulated miR-485-3p expression. 	32897218	RID04273	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	MALAT1	BAX	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-485-3p)	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL2L4	Long-chain non-coding RNA MALAT1 regulates paclitaxel resistance of breast cancer cells by targeting miR-485-3p.To investigate the role of long-chain non-coding RNA MALAT1 in modulating paclitaxel resistance in breast cancer cells.CONCLUSIONS: MALAT1 can modulate paclitaxel resistance in breast cancer cells possibly by targeting miR-485-3p to down-regulate P-gp and Bcl-2 and up-regulate Bax. Compared with paclitaxel-sensitive SK-BR-3 cells, paclitaxel-resistant SK-BR-3 cells showed significantly increased the IC50 of paclitaxel with up-regulated MALAT1 expression and down-regulated miR-485-3p expression. 	32897218	RID04274	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	PSMA3-AS1	RAB22A	positively-E	luciferase reporter assay;StarBase	upregulation	microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-302a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000257621	GRCh38_14:58265365-58298134	ENSG00000124209	NA	379025	57403	FLJ31306	NA	Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma. it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines.PSMA3-AS1 bound to miR-302a-3p directly reduced the expression of miR-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis.these assays also confirmed that RAB22A was a target of miR-302a-3p.therefore, the PSMA3-AS1/miR-302a-3p/RAB22A pathway regulatory axis may be revealed in the pathogenesis of glioma, and PSMA3-AS1 can be used as an underlying target for the treatment and prognosis of glioma. Briefly, it can be concluded that miR-302a-3p targets RAB22A, and RAB22A expression may be adjusted by PSMA3-AS1 in a positive manner via sponging miR-302a-3p, evidencing the role of the PSMA3-AS1/miR-302a-3p/RAB22A pathway.  StarBase revealed that miR-302a-3p and 3'UTR of PSMA3-AS1 were complementary as they shared binding sites.	32894281	RID04275	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Ovarian cancer	LINC00858	RAD18	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell motility(+);epithelial to mesenchymal transition(+);apoptosis process(-)	ceRNA(miR-134-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000070950	NA	170425	56852	CRCAL-2	RNF73	Long non-coding RNA LINC00858 aggravates the oncogenic phenotypes of ovarian cancer cells through miR-134-5p/RAD18 signaling.we focused on the function and probable mechanisms of LINC00858 in ovarian cancer.Real-time quantitative polymerase chain reaction (RT-qPCR) was employed for detecting the expression of LINC00858, miR-134-5p and RAD18 E3 ubiquitin protein ligase (RAD18). Interplays between LINC00858, miR-134-5p and RAD18 were detected by RNA immunoprecipitation (RIP), RNA pull down and luciferase reporter assays.LINC00858 were up-regulated in ovarian cancer tissues and cells, and its expression was elevated in advanced samples compared to early ones. Knocking down LINC00858 inhibited cell proliferation, motility and EMT, but accelerated cell apoptosis in ovarian cancer.LINC00858 sequestered miR-134-5p to elevate RAD18 expression, resulting in aggravated development of ovarian cancer. This might provide promising targets for treating patients with ovarian cancer.	32875345	RID04276	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Kidney disease	CTBP1-DT	FOXO1	positively-E	StarBase;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);ECM accumulation(-);inflammatory response(-)	ceRNA(miR-155-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000196810	GRCh38_4:1249300-1288291	ENSG00000150907	NA	92070	2308	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	FKH1|FKHR|FOXO1A	LncRNA CTBP1-AS2 alleviates high glucose-induced oxidative stress, ECM accumulation, and inflammation in diabetic nephropathy via miR-155-5p/FOXO1 axis.The expression of CTBP1-AS2, miR-155-5p and FOXO1 was detected by real-time PCR and western blot.The target association between miR-155-5p and CTBP1-AS2 or FOXO1 was confirmed by dual-luciferase reporter assays.The expression of CTBP1-AS2 was downregulated, and miR-155-5p was highly expressed in peripheral blood of DN patients and HG-treated HGMCs.Further investigation revealed that CTBP1-AS2 overexpression inhibited proliferation, oxidative stress, ECM accumulation and inflammatory response in HG-induced HGMCs. Mechanical analysis revealed that CTBP1-AS2 regulated FOXO1 expression via sponging miR-155-5p.Taken together, this study revealed CTBP1-AS2 attenuated HG-induced HGMC proliferation, oxidative stress, ECM accumulation, and inflammation through miR-155-5p/FOXO1 signaling. StarBase predicted the putative binding sites of CTBP1-AS2 and miR-155-5p. Furthermore, the enforced expression of miR-155-5p or the knockdown of FOXO1 could significantly reverse the inhibitory effects of CTBP1-AS2 on the proliferation, oxidative stress, ECM accumulation, and inflammatory response of HGMCs.  Therefore, our results suggest that CTBP1-AS2 may act as a ceRNA to upregulate FOXO1 expression by sponging miR-155-5p in the regulation of HGMCs.	32868076	RID04277	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	PICSAR	EIF6	positively-E	starBase v3.0;LncBase	upregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-588)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000242372	NA	378825	3692	C21orf113|LINC00162|NCRNA00162|NLC1-C|PRED74	b(2)gcn|EIF3A|ITGB4BP|p27BBP	Long noncoding RNA PICSAR/miR-588/EIF6 axis regulates tumorigenesis of hepatocellular carcinoma by activating PI3K/AKT/mTOR signaling pathway.we found that PICSAR was upregulated in HCC tissues and cells and correlated with progression and poor prognosis in HCC patients.PICSAR could function as a competing endogenous RNA by sponging microRNA (miR)-588 in HCC cells. Mechanically, miR-588 inhibited HCC progression and alternation of miR-588 reversed the promotive effects of PICSAR on HCC cells. In addition, we confirmed that eukaryotic initiation factor 6 (EIF6) was a direct target of miR-588 in HCC and mediated the biological effects of miR-588 and PICSAR in HCC, resulting in PI3K/AKT/mTOR pathway activation.Our data identified PICSAR as a novel oncogenic lncRNA associated with malignant clinical outcomes in HCC patients. To confirm whether PICSAR could act as a ceRNA, we used the bioinformatics platforms starBase version 3.0 and LncBase version 2 to search for miRNAs that potentially interact with PICSAR (Figure 4A).PICSAR played an oncogenic role by targeting miR-588 and subsequently promoted EIF6 expression and PI3K/AKT/mTOR activation in HCC. Our results revealed that PICSAR could be a potential prognostic biomarker and therapeutic target for HCC. western blot assay showed that restoration of miR-155-5p significantly reduced FOXO1 protein expression.	32860321	RID04278	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,PAAD);UP(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Acute pancreatitis	MEG3	FGFR2	positively-E	starBase v2.0;dual-luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);inflammatory response(-);cell apoptosis(-)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	NA	Endocrine system disease	Pancreatitis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000066468	NA	55384	2263	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BEK|CD332|CEK3|CFD1|ECT1|JWS|K-SAM|KGFR|TK14|TK25	LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-kB Pathway.The expression of MEG3, miR-195-5p, and fibroblast growth factor receptor 2 (FGFR2) was measured using quantitative real-time polymerase chain reaction (qRT-PCR.The targeted relationship between miR-195-5p and MEG3 or FGFR2 was forecasted by the online software starBase v2.0 and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.the expression of MEG3 and FGFR2 was decreased in caerulein-induced HPDE cells, while the expression of miR-195-5p was increased. MEG3 overexpression inhibited cell apoptosis and inflammatory responses that were induced by caerulein. FGFR2 was a target of miR-195-5p, and MEG3 regulated the expression of FGFR2 by sponging miR-195-5p. FGFR2 overexpression abolished miR-195-5p enrichment-aggravated inflammatory injuries. Moreover, the NF-kB signaling pathway was involved in the MEG3/miR-195-5p/FGFR2 axis. Collectively, MEG3 participates in caerulein-induced inflammatory injuries by targeting the miR-195-5p/FGFR2 regulatory axis via mediating the NF-kB pathway in HPDE cells. The purpose of this study was to ensure the function and action mode of lncRNA maternally expressed gene 3 (MEG3) in caerulein-induced AP cell model.	32856219	RID04279	ceRNA or sponge	NA		UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE55807)
Pre-eclampsia	KCNQ1OT1	miR-146a-3p	negatively-F	bioinformatics analysis;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000269821	GRCh38_11:2608328-2699994	NA	NA	10984	NA	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	Regulatory relationship between lncRNA KCNQ1OT1 and miR-146a-3p in preeclampsia.The expression level of KCNQ1OT1 mRNA and miR-146a-3p in the placenta tissues between two groups were detected by using quantitative real time (qRT)-PCR.The targeting relationship between KCNQ1OT1 and miR-146a-3p were predicted by bioinformatics software and confirmed by luciferase assay. The mRNA expression level of KCNQ1OT1 in the placenta of PE group was lower than that of control group.Luciferase assay showed that there was a targeting relationship between KCNQ1OT1 and mir-146a-3p.the expression level of KCNQ1OT1 mRNA (0.78 0.04 vs 0.50 0.03) increased, and the expression level of miR-146a-3p (0.42 0.03 vs 0.46 0.03) decreased, the cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 were all increased .KCNQ1OT1 could target the regulation of miR-146a-3p through CXCL12/CXCR4 pathway in the proliferation, invasion an migration of HTR8/SVneo cells, which may be involved in the pathogenesis of PE.	32854478	RID04280	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	
Pre-eclampsia	KCNQ1OT1	CXCL12	positively-E	bioinformatics analysis;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000107562	NA	10984	6387	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	PBSF|SCYB12|SDF-1a|SDF-1b|SDF1|SDF1A|SDF1B|TLSF-a|TLSF-b|TPAR1	Regulatory relationship between lncRNA KCNQ1OT1 and miR-146a-3p in preeclampsia.The expression level of KCNQ1OT1 mRNA and miR-146a-3p in the placenta tissues between two groups were detected by using quantitative real time (qRT)-PCR.The targeting relationship between KCNQ1OT1 and miR-146a-3p were predicted by bioinformatics software and confirmed by luciferase assay. The mRNA expression level of KCNQ1OT1 in the placenta of PE group was lower than that of control group.Luciferase assay showed that there was a targeting relationship between KCNQ1OT1 and mir-146a-3p.the expression level of KCNQ1OT1 mRNA (0.78 0.04 vs 0.50 0.03) increased, and the expression level of miR-146a-3p (0.42 0.03 vs 0.46 0.03) decreased, the cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 were all increased .KCNQ1OT1 could target the regulation of miR-146a-3p through CXCL12/CXCR4 pathway in the proliferation, invasion an migration of HTR9/SVneo cells, which may be involved in the pathogenesis of PE.	32854478	RID04281	expression association	NA	UP(BRCA);DATA(GSE111842)	
Pre-eclampsia	KCNQ1OT1	CXCR4	positively-E	bioinformatics analysis;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000121966	NA	10984	7852	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	Regulatory relationship between lncRNA KCNQ1OT1 and miR-146a-3p in preeclampsia.The expression level of KCNQ1OT1 mRNA and miR-146a-3p in the placenta tissues between two groups were detected by using quantitative real time (qRT)-PCR.The targeting relationship between KCNQ1OT1 and miR-146a-3p were predicted by bioinformatics software and confirmed by luciferase assay. The mRNA expression level of KCNQ1OT1 in the placenta of PE group was lower than that of control group.Luciferase assay showed that there was a targeting relationship between KCNQ1OT1 and mir-146a-3p.the expression level of KCNQ1OT1 mRNA (0.78 0.04 vs 0.50 0.03) increased, and the expression level of miR-146a-3p (0.42 0.03 vs 0.46 0.03) decreased, the cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 were all increased .KCNQ1OT1 could target the regulation of miR-146a-3p through CXCL12/CXCR4 pathway in the proliferation, invasion an migration of HTR10/SVneo cells, which may be involved in the pathogenesis of PE.	32854478	RID04282	expression association	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Coronary atherosclerotic heart disease	NEAT1	MAPK1	positively-E	dual-luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell viability(+);apoptosis process(-)	ceRNA(miR-140-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100030	NA	283131	5594	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	NEAT1/miR-140-3p/MAPK1 mediates the viability and survival of coronary endothelial cells and affects coronary atherosclerotic heart disease.RT-PCRand western blotwere carried out to examine the expressions of related RNAs.Colony formation assay, cell proliferation assay, apoptosis assay, and dual-luciferase reporter assay were conducted to investigate the abilities of colony migration, cell proliferation, apoptosis, and targeting.The results showed that NEAT1 was up-regulated in CAD blood samples and in human coronary endothelial cells (HCAECs). NEAT1 directly targeted miR-140-3p, and the expression of miR-140-3p was inversely correlated with the expression of NEAT1 in CAD patients.Our results revealed that lncRNA NEAT1 increased cell viability and inhibited CAD cell apoptosis possibly by activating the miR-140-3p/MAPK1 pathway, and lncRNA NEAT1 might serve as a potential therapeutic target for CAD.	32844995	RID04283	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	HCG11	SOCS5	negatively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell viability(-);cell migration(-);cell invasion(-);tumorigenesis(-)	ceRNA(miR-522-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000171150	NA	493812	9655	bK14H9.3|FLJ14049|FLJ30357	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	Long non-coding RNA HCG11 sponging miR-522-3p inhibits the tumorigenesis of non-small cell lung cancer by upregulating SOCS5.The mRNA expression of HCG11, miR-522-3p and SOCS5 was detected by RT-qPCR.The regulatory mechanism of lncRNA HCG11 was investigated by CCK-8, transwell and dual-luciferase reporter assays.Downregulation of lncRNA HCG11 and upregulation of miR-522-3p were found in NSCLC tissues and cells, and abnormal expressions of lncRNA HCG11 and miR-522-3p were related to adverse clinical outcomes of NSCLC patients. LncRNA HCG11 acted as a molecular sponge for miR-522-3p.lncRNA HCG11 inhibited cell viability, migration and invasion in NSCLC by downregulating miR-522-3p.LncRNA HCG11 inhibits cell viability, migration and invasion in NSCLC by functioning as a ceRNA of miR-522-3p to upregulate SOCS5.	32844573	RID04284	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Congenital heart disease	SAP30-2:1	HAND2	positively-E	RIP	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Heart disease	lncRNA	TF	NA	NA	ENSG00000164107	NA	NA	9464	NA	DHAND2|Hed|Thing2|bHLHa26|dHand	Long non-coding RNA SAP30-2:1 is downregulated in congenital heart disease and regulates cell proliferation by targeting HAND2.We used Gene Expression Omnibus data mining, bioinformatics analysis, and analysis of clinical tissue samples and observed that the novel lncRNA SAP30-2:1 with unknown function was significantly downregulated in damaged cardiac tissues from patients with CHD. Knockdown of lncRNA SAP30-2:1 inhibited the proliferation of human embryonic kidney and AC16 cells and decreased the expression of heart and neural crest derivatives expressed 2 (HAND2).lncRNA SAP30-2:1 was associated with HAND2 by RNA immunoprecipitation. Overall, these results suggest that lncRNA SAP30-2:1 may be involved in heart development through affecting cell proliferation via targeting HAND2 and may thus represent a novel therapeutic target for CHD. To validate whether lncRNA SAP30-2:1 is related to CHD or heart development, we detected its expression in 53 samples of damaged heart tissue from patients with CHD and 11 normal heart tissue samples using qPCR.	32820380	RID04285	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE41245)
Lung injury	THRIL	ROCK2	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	inflammatory response(-);apoptosis process(+)	ceRNA(miR-424)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000134318	NA	102659353	9475	BRI3BP-AS1|Linc1992|TCONS_00020260	NA	LncRNA THRIL aggravates sepsis-induced acute lung injury by regulating miR-424/ROCK2 axis.MPVECs were transfected with Ad-shTHRIL or NC, followed by lipopolysaccharide (LPS) treatment. MiR-424 and Rho-associated kinase 2 (ROCK2) were predicted and verified as direct targets of THRIL and miR-424, respectively, by using dual-luciferase reporter assay.Our results showed that THRIL was highly expressed in the lung of sepsis mice.The effect of THRIL on inflammatory response and apoptosis in the lung was confirmed in sepsis cell model. Moreover, mechanistic studies have shown that THRIL up-regulated ROCK2 level through sponging miR-424. Furthermore, ROCK2 overexpression reversed the inhibitory effects of THRIL knockdown on LPS-induced inflammatory response and apoptosis. Overall, in vivo and in vitro results suggested that THRIL accelerates sepsis-induced lung injury by sponging miR-424 and further restoring ROCK2.	32818819	RID04286	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Esophageal cancer	EIF3J-DT	AKT1	positively-E	StarBase;targetscan3.0	upregulation	qRT-PCR	NA	NA	cell invasion(+)	ceRNA(miR-373-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000179523	GRCh38_15:44527257-44537046	ENSG00000142208	NA	645212	207	EIF3J-AS1	AKT|PKB|PRKBA|RAC|RAC-alpha	LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p.Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage.Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients.We next investigated EIF3J-AS1 levels in ECa vs. non-cancer cells and tissues via qRT-PCRanalysis. To investigate this, the starBase tool (https://starbase.sysu.edu.cn/) was applied to screen the potential miRNAs that interact with B4GALT1-AS1 and the potential target miRNA of EIF3J-AS1 was miR-373-3p.Furthermore, targetscan3.0 identified miR-373-3p as a putative binding target for AKT1 based on sequence complementarity (Fig. 4C), indicating that EIF3J-AS1 may act as ceRNA to sponge miR-373-3p to enhance to AKT1 inducing ECa progression.	32811869	RID04287	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometriosis	MALAT1	CREB1	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(+);apoptosis process(-)	ceRNA(miR-126-5p)	regulation	NA	NA	CSC	Evading Apoptosis	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000118260	NA	378938	1385	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.MALAT1, miR-126-5p, and CREB1 levels in human endometrial stromal cells (HESCs) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR).The interactivity between miR-126-5p and MALAT1 (or CREB1) was assessed by dual luciferase reporter system.Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results.miR-126-5p directly regulated CREB1 expression via binding to its 3' non-coding region. Finally, miR-126-5p inhibitor-mediated apoptosis inhibition was restrained by CREB1 silencing via inactivation of PI3K-AKT pathway in HESCs. Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI3K/AKT pathway. Our findings explained the pathogenesis of endometriosis and offered promising therapeutic option for endometriosis. To evaluate the functional roles of lncRNA MALAT1 in HESCs, we knocked down MALAT1 by transfection with si-MALAT1.  Furthermore, recent research demonstrated that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression was increased in ectopic endometrial tissues and participated in the progression of endometriosis.	32809092	RID04288	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Endometriosis	MALAT1	Caspase3	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.MALAT1, miR-126-5p, and CREB1 levels in human endometrial stromal cells (HESCs) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR).The interactivity between miR-126-5p and MALAT1 (or CREB1) was assessed by dual luciferase reporter system.Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results.miR-126-5p directly regulated CREB1 expression via binding to its 3' non-coding region. Finally, miR-126-5p inhibitor-mediated apoptosis inhibition was restrained by CREB1 silencing via inactivation of PI3K-AKT pathway in HESCs. Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI4K/AKT pathway. Our findings explained the pathogenesis of endometriosis and offered promising therapeutic option for endometriosis.	32809092	RID04289	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Endometriosis	MALAT1	BAX	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL2L4	LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.MALAT1, miR-126-5p, and CREB1 levels in human endometrial stromal cells (HESCs) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR).The interactivity between miR-126-5p and MALAT1 (or CREB1) was assessed by dual luciferase reporter system.Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results.miR-126-5p directly regulated CREB1 expression via binding to its 3' non-coding region. Finally, miR-126-5p inhibitor-mediated apoptosis inhibition was restrained by CREB1 silencing via inactivation of PI3K-AKT pathway in HESCs. Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI5K/AKT pathway. Our findings explained the pathogenesis of endometriosis and offered promising therapeutic option for endometriosis.	32809092	RID04290	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometriosis	MALAT1	BCL2	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Bcl-2|PPP1R50	LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.MALAT1, miR-126-5p, and CREB1 levels in human endometrial stromal cells (HESCs) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR).The interactivity between miR-126-5p and MALAT1 (or CREB1) was assessed by dual luciferase reporter system.Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results.miR-126-5p directly regulated CREB1 expression via binding to its 3' non-coding region. Finally, miR-126-5p inhibitor-mediated apoptosis inhibition was restrained by CREB1 silencing via inactivation of PI3K-AKT pathway in HESCs. Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI6K/AKT pathway. Our findings explained the pathogenesis of endometriosis and offered promising therapeutic option for endometriosis.	32809092	RID04291	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	CASC2	KANK1	positively-E	dual-luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);apoptosis process(+)	ceRNA(miR-31-5p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000107104	NA	255082	23189	C10orf5	ANKRD15|KANK|KIAA0172	Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis.Expression levels of CASC2, miR-31-5p, and KANK1 in OSCC tissues and cells were determined by qRT-PCRThe relationship between CASC2 or KANK1 and miR-31-5p was verified with a dual-luciferase reporter or RIP assays.We observed that CASC2A and KANK1 were downregulated while miR-31-5p was upregulated in DDP-resistant OSCC tissues and cells.CASC2 overexpression enhanced cell DDP sensitivity and accelerated cell apoptosis in DDP-resistant OSCC cells in vivo and in vitro.To conclude, CASC2 boosted the DDP sensitivity and apoptosis of DDP-resistant OSCC cells by upregulating KANK1 via sponging miR-31-5p, and CASC2 might be a potential target for DDP-resistant OSCC treatment.	32787433	RID04292	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE51827)
Pulmonary arterial hypertension	SMILR	RHOA	positively-E	DIANA;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);vascular remodeling(+);RhoA/ROCK signaling pathway(+)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Pulmonary hypertension	lncRNA	PCG	ENSG00000255364	GRCh38_8:122414332-122428551	ENSG00000067560	NA	105375734	387	NA	ARH12|ARHA|Rho12|RHOH12	SMILR activated RhoA/ROCK signaling by targeting miR-141 to disinhibit its downstream target RhoA.SMILR, microRNA-141 (miR-141), and RhoA were identified by qRT-PCRin PAH patients' serum.We also performed bioinformatical prediction, luciferase reporter assay, and RNA-binding protein immunoprecipitation (RIP) to assess the interaction among SMILR, miR-141, and RhoA.SMILR and RhoA expression were upregulated, while miR-141 expression was downregulated in PAH patients.SMILR directly interacted with miR-141 and negatively regulated its expression.SMILR knockdown or miR-141 overexpression inhibited hypoxia-induced cell proliferation and migration via repressing RhoA/ROCK signaling in pulmonary arterial smooth muscle cells (PASMCs), which was confirmed in vivo experiments that knockdown of SMILR inhibited vascular remodeling and alleviated PAH in rats.	32559140	RID04293	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Cervical cancer	DINOL	TP53	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);ATM/CHK2 signaling pathway(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000285244	GRCh38_6:36677609-36678559	ENSG00000141510	NA	108783646	7157	DINO	LFS1|p53	Expression of the Long Noncoding RNA DINO in Human Papillomavirus-Positive Cervical Cancer Cells Reactivates the Dormant TP53 Tumor Suppressor through ATM/CHK2 Signaling.The damage-induced long noncoding RNA, DINO (DINOL), is a TP53 transcriptional target that has been reported to bind to and stabilize TP53, thereby amplifying TP53 signaling.We show that HPV-positive cervical carcinoma cells contain low levels of DINO because of HPV E6/UBE3A-mediated TP53 degradation.This causes a marked sensitization to chemotherapy agents and renders cells vulnerable to metabolic stress.Acute DINO expression in HPV-positive cervical cancer cells induces hallmarks of DNA damage response signaling, and TP53 activation involves ATM/CHK2 signaling.Hence, strategies that target DINO may be useful for restoring TP53 tumor suppressor activity in HPV-positive cancers and other tumor types that retain wild-type TP53.	32546626	RID04294	transcriptional regulation	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	SNHG3	YAP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-340-5p)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000137693	NA	8420	10413	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	YAP65	The knockdown of SNHG3 inhibits the progression of laryngeal squamous cell carcinoma by miR-340-5p/YAP1 axis and Wnt/beta-catenin pathway.The expression levels of SNHG3, Yes-associated protein 1 (YAP1), and microRNA-340-5p (miR-340-5p) were measured via quantitative real-time polymerase chain reaction or western blot.The association between SNHG3 and miR-340-5p or miR-340-5p and YAP1 was assessed by dual-luciferase reporter assay.We found that the levels of SNHG3 and YAP1 were increased but the miR-340-5p expression was decreased in LSCC tissues and cells.SNHG3 could regulate YAP1 expression by competitively binding with miR-340-5p.The knockdown of SNHG3 or YAP1 inhibited cell viability and glycolysis but induced apoptosis in LSCC cells.Knockdown of SNHG3 repressed Wnt/beta-catenin pathway by regulating miR-340-5p and YAP1.In conclusion, knockdown of SNHG3 inhibited LSCC progression via inactivating Wnt/beta-catenin pathway by regulating the miR-340-5p/YAP1 axis.	32538668	RID04295	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Gastric cancer	GAS5	miR-18a	negatively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cytotoxicity(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long non-coding RNA GAS5 promotes natural killer cell cytotoxicity against gastric cancer by regulating miR-18a.The expressions of GAS5 and miR-18a in NK cells were measured by qRT-PCRThe interaction between GAS5 and miR-18a was determined by the luciferase reporter system and RIP assay, respectively.We found that GAS5 expression was downregulated while miR-18a expression was upregulated in primary NK cells isolated from GC patient compared with the healthy controls.The deficiency of GAS5 significantly suppressed the secretion of IFN--Gamma and TNF-alpha as well as the killing effect of NK cells. GAS5 acts as a molecular sponge of miR-18a.	32538667	RID04296	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Esophageal cancer	LINC00460	miR-1224-5p	negatively-F	luciferase reporter assay;LncBase v2.0	upregulation	bioinformatics analysis(starBase,GEPIA);qRT-PCR	TCGA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	LncRNA linc00460 sponges miR-1224-5p to promote esophageal cancer metastatic potential and epithelial-mesenchymal transition.Bioinformatics analysis and quantitative real time polymerase chain reaction (qRT-PCR were used to detect linc00460 expression in ESCA.The direct binding effect between linc00460 and microRNA-1224-5p (miR-1224-5p) was evaluated by the dual-luciferase reporter assay.In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines.Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells.miR-1224-5p, a potential tumor suppressor, was negatively correlated with linc00460 in ESCA.Linc00460 and miR-1224-5p could bind directly in ESCA cells.Taken together, linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. The online The Cancer Genome Atlas (TCGA) analysis database GEPIA was used to observe the expression of linc00460 in ESCA. The online TCGA analysis database starBase was utilized to observe the expression of linc00460 and miR-1224-5p in ESCA, and analyze the correlation between linc00460 and its miRNA targets in ESCA. LncBase Predicted v2.0 [19] was used for predicting miRNA targets of linc00460.	32534700	RID04297	ceRNA or sponge	metastasis		
Non-small cell lung cancer	FGD5-AS1	WEE1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell autophagy(+);chemoresistance(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000225733	GRCh38_3:14920347-14948424	ENSG00000166483	NA	100505641	7465	NA	WEE1A	Elevation of FGD5-AS1 contributes to cell progression by improving cisplatin resistance against non-small cell lung cancer cells through regulating miR-140-5p/WEE1 axis.FGD5-AS1 and WEE1 expression were up-regulated in DDP-resistant tumors and cells compared with DDP-sensitive ones.we discovered that FGD5-AS1 was able to enhance WEE1 expression by interacting with miR-140-5p.Overexpression of FGD5-AS1 accelerated cell proliferation, migration, invasion and autophagy by enhancing cisplatin resistance against NSCLC cells through miR-140-5p/WEE1 axis, presenting promising biomarkers for the diagnosis of DDP-resistant NSCLC patients.  The interaction among FGD5-AS1, miR-140-5p and WEE1-like protein kinase (WEE1) was evaluated by dual-luciferase reporter assay. The potential role of FGD5-AS1 in cisplatin-resistant NSCLC patients was evaluated by qRT-PCR	32534055	RID04298	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Lung cancer	ACTA2-AS1	MAPK	positively-E	RNA knockdown;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);prognosis(-)	NA	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	NA	NA	100132116	NA	UC001kfo|uc001kfo.1|ZXF1	NA	Enhanced expression of lncRNA ZXF1 promotes cisplatin resistance in lung cancer cell via MAPK axis.We found that ZXF1 overexpression in lung cancer tissue increased the risk of treatment failure and tumor recurrence.In contrast, deactivating MAPK pathway by ZXF1 silencing enhanced cisplatin-induced cell cycle arrest and apoptosis by activating p53/p21 axis.Taken together, our study revealed that lncRNA ZXF1 contributes to cisplatin resistance and leads to the poor prognosis of lung cancer via activating MAPK pathway, which represents as a promising target to optimize lung cancer treatment.  As evaluated by real-time PCR, the expression of ZXF1 was largely inhibited on siRNA treatment.	32533982	RID04299	expression association	recurrence,prognosis,chemoresistance	UP(LIHC);DATA(GSE117623)	
Gastric cancer	LATS2-AS1-001	LATS2	positively-E	RIP	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell viability(+)	interact with protein	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000150457	NA	NA	26524	NA	NA	The novel long non-coding RNA LATS2-AS1-001 inhibits gastric cancer progression by regulating the LATS2/YAP1 signaling pathway via binding to EZH2. qRT-PCRwas applied to evaluate LATS2-AS1-001 expression and correlation with LATS2 in GC.RNA immunoprecipitation (RIP) was performed to assess the interaction between EZH2 and LATS2-AS1-001.Decreased expression levels of LATS2-AS1-001 and LATS2 were confirmed in 357 GC tissues compared with the normal mucosa.A strong positive correlation between LATS2-AS1-001 and LATS mRNA expression was found in Pearson Correlation analysis Moreover, ectopic expression of LATS2-AS1-001 decreased cell viability, induced G0/G1 phase arrest, and inhibited cell migration and invasion in GC cells.Mechanistically, overexpressing LATS2-AS1-001 upregulated LATS2 and induced YAP1 phosphorylation via binding to EZH2.	32514249	RID04300	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric cancer	LATS2-AS1-001	YAP1	negatively-E	RIP	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell viability(+)	phosphorylation	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000137693	NA	NA	10413	NA	YAP65	The novel long non-coding RNA LATS2-AS1-001 inhibits gastric cancer progression by regulating the LATS2/YAP1 signaling pathway via binding to EZH2. qRT-PCRwas applied to evaluate LATS2-AS1-001 expression and correlation with LATS2 in GC.RNA immunoprecipitation (RIP) was performed to assess the interaction between EZH2 and LATS2-AS1-001.Decreased expression levels of LATS2-AS1-001 and LATS2 were confirmed in 357 GC tissues compared with the normal mucosa.A strong positive correlation between LATS2-AS1-001 and LATS mRNA expression was found in Pearson Correlation analysis Moreover, ectopic expression of LATS2-AS1-001 decreased cell viability, induced G0/G1 phase arrest, and inhibited cell migration and invasion in GC cells.Mechanistically, overexpressing LATS2-AS1-001 upregulated LATS2 and induced YAP1 phosphorylation via binding to EZH2. As shown above, LATS2 mRNA and protein levels were significantly increased after LATS2-AS1-001 overexpression, while total YAP1 amounts were decreased both at the mRNA and protein levels. LATS2-AS1-001 overexpression promotes YAP1 phosphorylation and downregulates Cyclin D1 in GC cells.	32514249	RID04301	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Gastric cancer	LATS2-AS1-001	Cyclin D1	negatively-E	RIP	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell viability(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	The novel long non-coding RNA LATS2-AS1-001 inhibits gastric cancer progression by regulating the LATS2/YAP1 signaling pathway via binding to EZH2. qRT-PCRwas applied to evaluate LATS2-AS1-001 expression and correlation with LATS2 in GC.RNA immunoprecipitation (RIP) was performed to assess the interaction between EZH2 and LATS2-AS1-001.Decreased expression levels of LATS2-AS1-001 and LATS2 were confirmed in 357 GC tissues compared with the normal mucosa.A strong positive correlation between LATS2-AS1-001 and LATS mRNA expression was found in Pearson Correlation analysis Moreover, ectopic expression of LATS2-AS1-001 decreased cell viability, induced G0/G1 phase arrest, and inhibited cell migration and invasion in GC cells.Mechanistically, overexpressing LATS2-AS1-001 upregulated LATS2 and induced YAP1 phosphorylation via binding to EZH2. LATS2-AS1-001 overexpression promotes YAP1 phosphorylation and downregulates Cyclin D1 in GC cells.	32514249	RID04302	expression association	NA		
Gastric cancer	LINC00511	KDM2A	positively-E	StarBase;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-);cancer progression(+)	ceRNA(miR-29b)	regulation	RNA-protein	Epigallocatechin Gallate	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000173120	NA	400619	22992	onco-lncRNA-12	CXXC8|DKFZP434M1735|FBL11|FBL7|FBXL11|FLJ00115|JHDM1A|KIAA1004|LILINA	Epigallocatechin gallate reverses gastric cancer by regulating the long noncoding RNA LINC00511/miR-29b/KDM2A axis.LINC00511 was discovered to be suppressed by EGCG and highly expressed in GC cells and tissues.our data suggested LINC00511 could decrease the expression of miR-29b, followed by inducing GC development. Knockdown of LINC00511 inhibited cell growth and promoted cell death ratio in GC. We performed luciferase reporter assays, which showed that LINC00511 competitively bond to miR-29b with KDM2A, thereby restoring plasmid activity. We further validated the probable binding sites of LINC00511 to miRNAs using starBase database. Furthermore, luciferase reporter assays showed that miR-29b specifically bond to LINC00511.	32512188	RID04303	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetes mellitus	MALAT1	SOCS3	positively-E	luciferase reporter assay;StarBase	upregulation	RT-qPCR	NA	NA	cell injury(+);apoptosis process(+)	ceRNA(miR-361-3p)	regulation	RNA-protein	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000184557	NA	378938	9021	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CIS3|Cish3|SOCS-3|SSI-3	Long noncoding RNA MALAT1 promotes high glucose-induced inflammation and apoptosis of vascular endothelial cells by regulating miR-361-3p/SOCS3 axis.Furthermore, through bioinformatics analysis and dual luciferase assay, we found that MALAT1 directly sponges miR-361-3p to counteract its suppression on SOCS3 expression.We found that HG treatment significantly promotes MALAT1 and SOCS3 expressions, but inhibits miR-361-3p expression in HUVECs.In conclusion, our results indicate that knockdown of MALAT1 inhibits HG-induced vascular endothelial injury through regulating miR-361-3p/SOCS3 axis, suggesting that inhibition of MALAT1 as a potential target for endothelial injury therapy for DM. To understand whether MALAT1 or SOCS3 is the potential target gene of miR-361-3p, we used Starbase (http://starbase.sysu.edu.cn/) for analysis.	32509100	RID04304	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Osteosarcoma	lncRNA-SARCC	MIR143	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	RNA-RNA	Cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	NA	NA	ENSG00000208035	NA	NA	406935	NA	MIRN143|mir-143	LncRNA-SARCC sensitizes osteosarcoma to cisplatin through the miR-143-mediated glycolysis inhibition by targeting Hexokinase2.In this study, we reported the significant down-regulation of the long noncoding RNA-Suppressing Androgen Receptor in Renal Cell Carcinoma (lncRNA-SARCC) in the cells of osteosarcoma and in the specimens from osteosarcoma patients.Overexpression of the lncRNA-SARCC sensitizes osteosarcoma cells to cisplatin.From microarray analysis, we screened several miRNAs, which are significantly regulated by the lncRNA-SARCC in osteosarcoma cells, and revealed that lncRNA-SARCC promoted microRNA-43 (miR-143) expression in osteosarcoma.	32508321	RID04305	expression association	chemoresistance		
Oral squamous cell carcinoma	SNHG12	E2F1	positively-E	ChIP;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000101412	NA	85028	1869	ASLNC04080|C1orf79|LINC00100|PNAS-123	RBBP3|RBP3	SNHG12/miR-326/E2F1 feedback loop facilitates the progression of oral squamous cell carcinoma.qRT-PCRmanifested the upregulation of SNHG12 expression in OSCC tissues and cells.E2F1 was found to be a transcription factor of SNHG12 to stimulate its expression.SNHG12 deficiency reduced E2F1 expression in turn.MiR-326 was found to be shared between SNHG12 and E2F1. SNHG12 augmented E2F1 in OSCC through miR-326 sequestration.rescue assays demonstrated that overexpressed E2F1 restored the inhibitory effect resulted from SNHG12 silence, indicating that SNHG12 promoted the progression of OSCC by E2F1-dependent way.	32506729	RID04306	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	p-p65	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04307	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	TNF	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000228978	NA	378938	7124	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04308	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	IL6	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136244	NA	378938	3569	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BSF2|HGF|HSF|IFNB2|IL-6	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04309	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	BAX	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL2L4	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04310	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	Clecaspase-3	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04311	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Apoptosis and inflammation in human umbilical vein endothelial cells	MALAT1	Clecaspase-9	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Apoptosis and inflammation in human umbilical vein endothelial cells	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kB signaling pathway.The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using western blot.The expression levels of MALAT1, TNF-alpha, and IL-6 in HUVECs were increased in the HG environment;when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-alpha, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased.Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-kB signaling pathway.	32502356	RID04312	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Hepatocellular carcinoma	H19	TP53	negatively-E	knockdown	upregulation	sequencing	NA	NA	apoptosis process(-)	NA	regulation	NA	Galangin	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LFS1|p53	Galangin promotes cell apoptosis through suppression of H19 expression in hepatocellular carcinoma cells.Using RNA sequencing, the differential expression of lncRNA in human HCC cell line with highly metastatic potential (MHCC97H) cells treated with galangin was investigated.the expression of H19 was markedly reduced following treatment with galangin in MHCC97H cells.Notably, the results indicated that knockdown of H19 and miR675 induced the expression of p53, eventually promoting cell apoptosis in MHCC97H cells.	32485786	RID04313	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Vascular smooth muscle cell calcification/senescence	BHLHE40	LINC00458	negatively-E	luciferase reporter assay;CHIP	upregulation	qRT-PCR	NA	NA	senescence(-)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Other	Vascular smooth muscle cell calcification/senescence	TF	lncRNA	ENSG00000134107	NA	ENSG00000234787	GRCh38_13:54115783-54142319	8553	100507428	BHLHB2|Clast5|1-Dec|SHARP2|STRA13	ES3|LncRNA-ES3	LncRNA-ES3 inhibition by Bhlhe40 is involved in high glucose-induced calcification/senescence of vascular smooth muscle cells.Moreover, we identified that Bhlhe40 regulates lncRNA-ES3 in HA-VSMCs by binding to the promoter region of the lncRNA-ES3 gene (LINC00458).Upregulation or inhibition of lncRNA-ES3 expression significantly promoted or reduced calcification/senescence of HA-VSMCs, respectively.The results demonstrate that lncRNA-ES3 triggers gene silencing of multiple miRNAs by binding to Bhlhe40, leading to calcification/senescence of VSMCs.	32483833	RID04314	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Renal fibrosis	NEAT1	miR-129	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	fibrotic(+);epithelial to mesenchymal transition(+);inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long noncoding RNA NEAT1 sponges miR-129 to modulate renal fibrosis by regulation of collagen type I.Our results indicated that NEAT1 and collagen type I levels were significantly upregulated, whereas miR-129 was obviously downregulated, in the progression of renal fibrosis.NEAT1 directly targeted miR-129, and miR-129 directly bound to collagen type I. Downregulation of miR-129 reversed inhibition of renal fibrosis induced by NEAT1 silencing, and upregulation of collagen type I also reversed inhibition of renal fibrosis caused by miR-129 overexpression.In conclusion, NEAT1 sponged miR-129 to modulate the epithelial-mesenchymal transition process and inflammation response of renal fibrosis by regulation of collagen type I. Our study indicates a novel role in the regulation of renal fibrosis and provides a new potential treatment target for renal fibrosis. Meanwhile, NEAT1 knockdown or miR-129 overexpression inhibited collagen type I deposition, the epithelial-mesenchymal transition process, and the inflammation response to suppress renal fibrosis. Overexpression of miR-129 suppressed and silencing of miR-129 induced luciferase activity of wild-type NEAT1 significantly, which was confirmed by a dual-luciferase reporter assay.	32475133	RID04315	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Diabetic retinopathy	MEG3	miR-93	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);inflammatory response(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000207757	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long Noncoding RNA MEG3 Inhibits Apoptosis of Retinal Pigment Epithelium Cells Induced by High Glucose via the miR-93/Nrf2 Axis.Long noncoding (lnc) RNA MEG3 and miR-93 expression was detected by real-time quantitative PCR.The relationships among MEG3, miR-93, and Nrf2 (also known as NFE2L2) were explored via dual-luciferase reporter assay.lncRNA MEG3 and Nrf2 were decreased and miR-93 was increased in blood samples of DR patients and HG-treated human RPE and ARPE-19 cells.Overexpression of miR-93 inhibited cell proliferation and promoted apoptosis, whereas overexpression of Nrf2 or MEG3 promoted proliferation and suppressed apoptosis and inflammation.MEG3 targeted miR-93 and down-regulated miR-93. miR-93 directly targeted Nrf2 and negatively regulated Nrf2.	32473920	RID04316	expression association	NA		
Diabetic retinopathy	MEG3	Nrf2	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);inflammatory response(-)	ceRNA(miR-93)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long Noncoding RNA MEG3 Inhibits Apoptosis of Retinal Pigment Epithelium Cells Induced by High Glucose via the miR-93/Nrf2 Axis.Long noncoding (lnc) RNA MEG3 and miR-93 expression was detected by real-time quantitative PCR.The relationships among MEG3, miR-93, and Nrf2 (also known as NFE2L2) were explored via dual-luciferase reporter assay.lncRNA MEG3 and Nrf2 were decreased and miR-93 was increased in blood samples of DR patients and HG-treated human RPE and ARPE-19 cells.Overexpression of miR-93 inhibited cell proliferation and promoted apoptosis, whereas overexpression of Nrf2 or MEG3 promoted proliferation and suppressed apoptosis and inflammation.MEG3 targeted miR-93 and down-regulated miR-93. miR-93 directly targeted Nrf2 and negatively regulated Nrf3.	32473920	RID04317	ceRNA or sponge	NA		
Gastric cancer	NMRAL2P	ACOT7	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(-);cell migration(-);apoptosis process(+)	DNA methylation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000097021	NA	344887	11332	LOC344887|NMRAL1P1	ACH1|ACT|BACH|CTE-II|hBACH|LACH1|MGC1126	Interaction between ACOT7 and LncRNA NMRAL2P via Methylation Regulates Gastric Cancer Progression.The expressions of ACOT7 and NMRAL2P were detected by real-time quantitative PCR and western blot.NMRAL2P was downregulated in tumor tissues and GC cell lines.NMRAL2P indirectly methylated ACOT7 by binding to DNMT3b, thereby suppressing ACOT7 expression. ACOT7 was upregulated in gastric tumor tissues and GC cell lines. ACOT7 gene silencing induced a less malignant phenotype and was closely correlated to reduced cell proliferation and migration, altered cell cycle, and increased apoptosis.	32469171	RID04318	epigenetic regulation	NA		UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Diabetic retinopathy	GAS5	SERCA2b	positively-E	western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(-);inflammatory response(-)	NA	regulation	RNA-RNA	NA	NA	Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses ER stress-induced apoptosis and inflammation by regulating SERCA2b in HG-treated retinal epithelial cell.Hyperglycemia impairs the retinal functions in patients with diabetic retinopathy (DR).the present study aimed to investigate the roles of lncRNA GAS5 and SERCA2 in retinal pigment epithelium cells exposed to HG. GAS5 expression levels were detected using reverse transcription-quantitative PCR.the expression levels of SERCA2b, ER stress-related proteins, pro-inflammatory factors and apoptotic proteins were determined by western blot ELISA or flow cytometry.GAS5 and SERCA2b overexpression significantly decreased ER stress-related apoptosis and inflammation, whereas SERCA2b knockdown significantly reversed the inhibitory effect of GAS5 on ER stress, apoptosis and inflammation.The results of the present study indicated that GAS5 may suppress ER stress-induced apoptosis and inflammation by regulating SERCA2b in HG-treated cells. GAS5 and SERCA2b expression levels decrease in HG-treated ARPE-19 cells.	32467994	RID04319	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral cavity cancer	DNM3OS	HIP1	positively-E	microarray analysis;RNA-sequencing;luciferase reporter assay	upregulation	qPCR	NA	NA	cell viability(+);cell migration(+)	ceRNA(miR-204-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000230630	GRCh38_1:172138397-172144840	ENSG00000127946	NA	100628315	3092	DNM3-AS1|MIR199A2HG	ILWEQ	Long non-coding RNA DNM3OS/miR-204-5p/HIP1 axis modulates oral cancer cell viability and migration.The microarray profiling and RNA-sequencing analysis were performed to identify lncRNAs related to oral cancer development, and lncRNA DNM3OS was selected.DNM3OS was upregulated in oral cancer tissues and cells.DNM3OS targeted miR-204-5p to inhibit miR-204-5p expression.miR-204-5p targeted HIP1 to inhibit HIP1 expression.Within oral carcinoma tissue samples, expression of DNM3OS and HIP1 was increased whereas the miR-204-5p expression was downregulated;miR-204-5p had a negative correlation with DNM3OS and HIP1, respectively, while DNM3OS and HIP1 were positively correlated with each other. HIP1 knockdown inhibited oral cancer cell viability and migration.	32463958	RID04320	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Atherosclerosis	LOXL1-AS1	STAT3	positively-E	JASPAR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-515-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000168610	NA	100287616	6774	NA	APRF	LOXL1-AS1/miR-515-5p/STAT3 Positive Feedback Loop Facilitates Cell Proliferation and Migration in Atherosclerosis.In this research, we detected through reverse transcription-quantitative polymerase chain reaction that LOXL1-AS1 expression was markedly upregulated in patients with AS.The role of LOXL1-AS1 in vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) was unmasked by functional assays.knockdown of LOXL1-AS1 exerted suppressive effect on proliferation and migration whereas accelerated apoptosis in VSMCs and HUVECs.LOXL1-AS1 could elevate STAT3 expression by sponging miR-515-5p in VSMCs and HUVECs.rescue assays delineated that inhibited expression of miR-515-5p or elevated expression of STAT3 could reverse the restraining effect of LOXL1-AS1 depletion on the progression of AS in HUVECs.  Afterward, the DNA motif of STAT3 and the binding site between LOXL1-AS1 and STAT3 were obtained from JASPAR (http://jaspar.genereg.net/) and shown in Figure 3E. Moreover, the luciferase reporter assay revealed that the luciferase activity of LOXL1-AS1 promoter-WT could be increased by overexpressing STAT3, whereas decreased by knocking down STAT3 in VSMCs and HUVECs.	32453072	RID04321	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Glioblastoma	miR-370-3p	NEAT1	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	miRNA	lncRNA	NA	NA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	Mir-370-3p Impairs Glioblastoma Stem-Like Cell Malignancy Regulating a Complex Interplay between HMGA2/HIF1A and the Oncogenic Long Non-Coding RNA (lncRNA) NEAT1.Among the genes downregulated by the restored expression of miR-370-3p, we found the EMT-inducer high-mobility group AT-hook 2 (HMGA2), the master transcriptional regulator of the adaptive response to hypoxia, Hypoxia-inducible factor (HIF)1A, and the long non-coding RNAs (lncRNAs) Nuclear Enriched Abundant Transcript (NEAT)1.the expression levels of miR-370-3p and NEAT1 were inversely related in both GBM tumor specimens and GSCs, and a dual-luciferase reporter assay proved the direct binding between miR-370-3p and the lncRNAs NEAT1.Our results identify a critical role of miR-370-3p in the regulation of GBM development, indicating that miR-370-3p acts as a tumor-suppressor factor inhibiting glioma cell growth, migration and invasion by targeting the lncRNAs NEAT1, HMGA2, and HIF1A, thus, providing a potential candidate for GBM patient treatment. As shown in Figure 4C, the expression level of NEAT1 was significantly elevated in GBM tissues (p < 0.0001, Student  t-test) and GSCs (p < 0.017, Student  t-test) compared to normal brain tissues and normal NSCs, respectively.	32443824	RID04322	transcriptional regulation	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Colorectal cancer	SOCS2-AS1	SOCS2	positively-E	luciferase reporter assay;RIP;TANRIC	downregulation	qRT-PCR	TCGA	NA	cancer progression(-);cell metastasis(-)	ceRNA(miR-1264)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000246985	GRCh38_12:93542022-93571768	ENSG00000120833	NA	144481	8835	NA	CIS2|Cish2|SOCS-2|SSI-2|SSI2|STATI2	LncRNA SOCS2-AS1 inhibits progression and metastasis of colorectal cancer through stabilizing SOCS2 and sponging miR-1264.We showed that SOCS2-AS1 was lowly expressed in CRC tissues and cells.we discovered that SOCS2-AS1 was positively correlated with SOCS2 expression in CRC tissues.SOCS2-AS1 contributes to SOCS2 expression through restraining miR-1264. To investigate the functional mechanism of SOCS2-AS1, we used TANRIC tool (https://ibl.mdanderson.org/tanric/_design/basic/summary.html) and performed bioinformatics analysis to search target genes which are correlated with SOCS2-AS1 level in CRC tissues. TCGA data using GEPIA tool also indicated that SOCS2-AS1 and SOCS2 expressions were positively correlated in CRC tissues (Figure 4B), which was validated by qRT-PCR	32437330	RID04323	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC);DATA(GSE117623)
Malignant glioma	NNT-AS1	PRMT1	positively-E	luciferase reporter assay;	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	ceRNA(miR-494-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000126457	NA	100652772	3276	RP11-159F24.1	ANM1|HCP1|HRMT1L2	LncRNA NNT-AS1 promote glioma cell proliferation and metastases through miR-494-3p/PRMT1 axis.mRNA expression was tested using RT-qPCR.The results showed that lncNNT-AS1 is significantly up-regulated during the early stages of glioma.high levels of NNT-AS1 are observed in glioma cell lines compared to human astrocyte (HA) cells.the inhibition of NNT-AS1 directly interacted with miRNA-494-3p, and positively regulated the downstream target PRMT1 in vitro. our results indicated that the miR-494-3p-PRMT1 axis is involved the tumor-suppressive effects of NNT-AS1 inhibition, which sheds new light on lncRNA-directed diagnostics and the therapeutics of glioma. Further study proved that the overexpression of miRNA-494-3p and the inhibition of PRMT1 could attenuate both glioma cell proliferation and metastases. Moreover, si-NNT-AS1 remarkably down-regulated the protein expression level of PRMT1; this effect was attenuated by the miR-494-3p inhibitor (Figure 4(c-e)).	32420808	RID04324	ceRNA or sponge	metastasis	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE67939)
Malignant glioma	MEG3	SMARCB1	positively-E	luciferase reporter assay;DIANA;StarBase	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);epithelial to mesenchymal transition(-)	ceRNA(miR-6088)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000099956	NA	55384	6598	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BAF47|hSNFS|Ini1|PPP1R144|RDT|Sfh1p|SNF5|SNF5L1|Snr1	Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis.Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1.MEG3 and SMARCB1 expressions were downregulated in glioma cells.MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088.Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. DIANA and Starbase showed possible binding sites between MEG3 and miR-6088 as well as miR-6088 and SMARCB1.	32420340	RID04325	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Pancreatic cancer	HCP5	CDK8	positively-E	luciferase reporter assay;starBase;TargetScan	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000132964	NA	10866	1024	D6S2650E|P5-1	K35	LncRNA HCP5 Regulates Pancreatic Cancer Progression by miR-140-5p/CDK8 Axis.Quantitative real-time polymerase chain reaction was performed to detect the expression levels of HCP5, microRNA (miR)-140-5p, and cyclin-dependent kinase 8 (CDK8) in PC tissues and cells.The interaction between miR-140-5p and HCP5 or CDK8 was predicted by starBase or TargetScan, respectively.The dual-luciferase reporter assay was conducted to corroborate the interaction.HCP5 and CDK8 were significantly upregulated in PC tissues and cells, opposite to the expression of miR-140-5p.Downregulation of HCP5 impeded PC progression by downregulating CDK8 via sponging miR-140-5p.	32407143	RID04326	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Cervical cancer	LINC00173	FBXW7	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-182-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000196668	GRCh38_12:116533422-116536518	ENSG00000109670	NA	100287569	55294	FLJ42957|NCRNA00173	AGO|CDC4|FBW7|FBX30|FBXW6|FLJ11071|SEL-10|SEL10	Long noncoding RNA LINC00173 is downregulated in cervical cancer and inhibits cell proliferation and invasion by modulating the miR-182-5p/FBXW7 axis.Here, for the first time, we found that the expression of LINC00173 was decreased in CC tissues compared with that in nontumor tissues.LINC00173 functioned as a molecular sponge for miR-182-5p and inversely regulated the miR-182-5p level in CC cells.LINC00173 overexpression enhanced the FBXW7 level via regulation of miR-182-5p in HeLa Cells.	32402537	RID04327	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367)
Cervical cancer	FENDRR	TUBA1A	positively-E	Gain or loss of function experiments;RIP;pull down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell invasion(-)	ceRNA(miR-15a/b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000167552	NA	400550	7846	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	B-ALPHA-1|FLJ25113|TUBA3	FENDRR suppresses cervical cancer proliferation and invasion by targeting miR-15a/b-5p and regulating TUBA1A expression.In this study, quantitative real-time polymerase chain reaction (qRT-PCR analysis detected gene expression in tissues and cells.Gain- or loss-of-function experiments revealed the biological effects of FENDRR and miR-15a/b-5p on CC cell functions.Mechanism experiments including RNA immunoprecipitation (RIP) assay, pull down assay and luciferase reporter assay depicted the binding situation and coexistence of indicated genes.FENDRR was downregulated in CC tissues and cells, which suppressed CC progression.MiR-15a-5p and miR-15b-5p shared binding sites with FENDRR and had interaction with FENDRR.Tubulin alpha1A (TUBA1A) was downregulated in CC tissues and positively modulated by FENDRR.TUBA1A was the target of miR-15a/b-5p.FENDRR inhibits CC progression through upregulating TUBA1A in a miR-15a/b-5p-dependent manner.	32398968	RID04328	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE75367)
Tongue squamous cell carcinoma	TUG1	CXCR4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumor growth(+);chemoresistance(+)	ceRNA(miR-133b)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000121966	NA	55000	7852	FLJ20618|LINC00080|NCRNA00080	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	TUG1/miR-133b/CXCR4 axis regulates cisplatin resistance in human tongue squamous cell carcinoma.The levels of TUG1, microRNA-133b (miR-133b) and cysteine-X-cysteine chemokine receptor 4 (CXCR4) were measured by quantitative real-time polymerase chain reaction or western blot.The interactions among TUG1, miR-133b and CXCR4 were evaluated by luciferase reporter assay and RNA immunoprecipitation.TUG1 expression was elevated in cisplatin-resistant TSCC tissues and cells compared with that in sensitive group and its knockdown inhibited cisplatin resistance to SCC25/CDDP and CAL27/CDDP cells.miR-133b was targeted via TUG1 and its overexpression suppressed cisplatin resistance. CXCR4 was a target of miR-133b.interference of TUG1 attenuated tumor growth by regulating miR-133b and CXCR4 in vivo.Downregulation of TUG1 impeded cisplatin resistance in TSCC-resistant cells by mediating miR-133b and CXCR4, indicating TUG1 as a promising target for TSCC chemotherapy.	32390763	RID04329	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	LINC00313	FOSL2	positively-E	StarBase;TargetScan;luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+);cell proliferation(+);apoptosis process(-);cell autophagy(-)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000185186	GRCh38_21:43461960-43479534	ENSG00000075426	NA	114038	2355	C21orf84|CH507-42P11.5|NCRNA00313	FRA2	LncRNA LINC00313 Knockdown Inhibits tumorigenesis and Metastasis in Human Osteosarcoma by Upregulating FOSL2 through Sponging miR-342-3p. We evaluated mRNA and protein expression using real-time quantitative PCR and western blot.Potential target sites for LINC00313 and miR-342-3p were predicted with starBase v.2.0 and TargetScan Human, and verified using luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay.LINC00313 was upregulated and miR-342-3p was downregulated in OS tissues and cells.miR-342-3p, sponged by LINC00313, inversely modulated FOSL2 by targeting MG-63 cells, and FOSL2 expression was positively controlled by LINC00313. FOSL2 downregulation and miR-342-3p overexpression suppressed cell proliferation and migratory and invasive abilities while promoting apoptosis and autophagy, all of which were consistent with the effects of LINC00313 knockdown.	32390359	RID04330	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoarthritis	CTBP1-DT	miR-130a	negatively-E	methylation-specific PCR	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	DNA methylation	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000196810	GRCh38_4:1249300-1288291	NA	NA	92070	NA	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	NA	LncRNA CTBP1-AS2 is upregulated in osteoarthritis and increases the methylation of miR-130a gene to inhibit chondrocyte proliferation. CTBP1-AS2 was inversely correlated with miR-130a.RT-qPCR was performed to determine the expression levels of CTBP1-AS2 and miR-130a in synovial fluid.The results showed that CTBP1-AS2 was upregulated in OA and inversely correlated with miR-130a.In chondrocytes of OA patients, overexpression of CTBP1-AS2 led to increased methylation of miR-130a gene and downregulated expression of miR-130a, while overexpression of miR-130a did not affect the expression of CTBP1-AS2.CTBP1-AS2 is overexpressed in OA and may downregulate miR-130a through methylation to suppress the proliferation of chondrocytes. To investigate the interactions between CTBP1-AS2 and miR-130a, the two types of chondrocytes were transfected with CTBP1-AS2 expression vector or miR-130a mimic.	32388751	RID04331	epigenetic regulation	NA		
Breast cancer	SNHG12	SALL4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-15a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000101115	NA	85028	57167	ASLNC04080|C1orf79|LINC00100|PNAS-123	dJ1112F19.1|ZNF797	Upregulation of SNHG12 accelerates cell proliferation, migration, invasion and restrain cell apoptosis in breast cancer by enhancing regulating SALL4 expression via sponging miR-15a-5p.The levels of SNHG12, miR-15a-5p, and Sal-like 4 (SALL4) in BC tumor tissues and cells were measured by qRT-PCRThe interaction between miR-15a-5p and SNHG12 or SALL4 was evaluated by dual-luciferase reporter assay.SNHG12 and SALL4 expressions were upregulated whereas miR-15a-5p was downregulated in BC tumors compared with normal tissues.SNHG12 was found to accelerate BC cell progression by absorbing miR-15a-5p to enhance SALL4 expression.	32386479	RID04332	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	NEAT1	miR-153-3p	negatively-F	luciferase reporter assay;RIP;MiRcode;MiRBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Downregulation of NEAT1 Suppresses Cell Proliferation, Migration, and Invasion in NSCLC Via Sponging miR-153-3p.Quantitative real-time polymerase chain reaction was applied to examine the expression of NEAT1 and miR-153-3p.The interaction between NEAT1 and miR-153-3p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay.NEAT1 directly interacts with miR-153-3p in NSCLC.Knockdown of NEAT1 could suppress cell proliferation, migration, and invasion of NSCLC while promoting cell apoptosis through sponging miR-153-3p. These data showed that NEAT1 is highly expressed in NSCLC tissues and cell lines. In addition, upregulation of miR-153-3p inhibits the cell progression, and miR-153-3p inhibitor recovers the inhibition effect of si-NEAT1 in NSCLC cell lines. Subsequently, si-NEAT1 inhibits Wnt/beta-catenin signaling pathway, which is reactivated by miR-153-3p inhibitor. To demonstrate whether miR-153-3p were regulated by lncRNA NEAT1, the online bioinformatic tools of MiRcode and MiRBase were used to predict the binding site. A significant negative correlation between NEAT1 and miR-153-3p was also presented in NSCLC tissues.	32380843	RID04333	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Cholangiocarcinoma	CDKN2B-AS1	ERRFI1	negatively-E	RIP;RPISeq;ChIP	upregulation	qRT-PCR	TCGA;GSE76297	NA	cell migration(+);cell proliferation(+);cell metastasis(+)	histone modification	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000116285	NA	100048912	54206	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	GENE-33|MIG-6|RALT	Long noncoding RNA ANRIL promotes the malignant progression of cholangiocarcinoma by epigenetically repressing ERRFI1 expression.By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.ERRFI1 expression was suppressed in CCA cells. Overexpression of ERRFI1 suppresses CCA cell proliferation and metastasis, and ERRFI1 is a confirmed target of ANRIL. In addition, the probability of interaction between EZH2 and ANRIL was predicted on the RNA-Protein Interaction Prediction website, and the result showed that EZH2 could bind well with ANRIL. As revealed in Figure 6C, endogenous ANRIL was amplified in the anti-EZH2 RIP fraction relative to the input; the IgG fraction of HuCCT1 and RBE cell lines with an Ab against enhancer of EZH2 was used for comparison. To further determine whether ANRIL suppressed the expression of ERRFI1 by interacting with EZH2, a ChIP analysis was carried out. The ChIP assays revealed that ANRIL knockdown reduced the binding of EZH2 to the promoters of ERRFI1 as well as H3K27me3 levels. These results indicated that EZH2 could bind directly to the promoter of ERRFI1 and then repress ERRFI1 expression directly by mediating H3K27me3 demethylation modifications. To comprehensively characterize aberrantly expressed lncRNAs in CCA, we analyzed TCGA CCA and normal tissue RNA sequencing data (9 normal and 36 cancer samples) and 1 independent microarray dataset from the Gene Expression Omnibus database (GSE76297; 92 cancer tissue samples and 91 normal tissue samples).	32378752	RID04334	epigenetic regulation	metastasis	UP(SKCM);DATA(GSE38495)	UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Atherosclerosis	NEAT1	PRKG1	positively-E	RIP;luciferase reporter assay;bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);AKT/mTOR signaling pathway(+)	ceRNA(miR-638)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000185532	NA	283131	5592	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	PGK|PKG|PKG1|PRKG1B|PRKGR1B	NEAT1 knockdown suppresses endothelial cell proliferation and induces apoptosis by regulating miR-638/AKT/mTOR signaling in atherosclerosis.The levels of lncRNA-NEAT1 and miR-638 expression in clinical samples and cells were explored via quantitative reverse transcription polymerase chain reaction.the proportion of cells and correlations among phosphoglycerate kinase 1 (PGK1), NEAT1, and miR-638 were determined through RNA immunoprecipitation and luciferase assays and bioinformatics analysis.In the serum of patients with AS and HAECs induced by oxidized low-density lipoprotein (ox-LDL), the expression level of miR-638 was decreased, whereas that of NEAT1 was increased.NEAT1 inhibited miR-638 expression through direct mutual action.The following mechanical investigations revealed that PGK1 was a miR-638 target, whose expression was increased by NEAT1, a competing endogenous RNA of miR-638. To sum up, the present study confirmed that NEAT1 downregulation restrained ox-LDL-triggered HAECs from proliferating and induced their apoptosis by inactivating AKT/mTOR signaling via miR-638.	32377692	RID04335	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Nasopharynx carcinoma	SNHG7	ELAVL1	positively-E	RNA pull-down;RIP;luciferase reporter assay;StarBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-514a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000066044	NA	84973	1994	MGC16037|NCRNA00061	Hua|HUR|MelG	LncRNA SNHG7 promotes the proliferation of nasopharyngeal carcinoma by miR-514a-5p/ELAVL1 axis.The interactions between SNHG7/ELAVL1 and miR-514a-5p were confirmed by RNA pull down, RT-qPCR, RIP and luciferase reporter assays.SNHG7 was confirmed to bind with miR-514a-5p and negatively modulate miR-514a-5p expression.LncRNA SNHG7 promotes the proliferation and migration of nasopharyngeal carcinoma by miR-514a-5p/ ELAVL1 axis. By browsing Starbase, 2 miRNAs (miR-668-3p and miR-514a-5p) were found to potentially bind with SNHG7. In the present study, we firstly verified that ELAVL1 was a downstream gene of miR-514a-5p, and the expression level of ELAVL1 was negatively regulated by miR-514a-5p and positively regulated by SNHG7.	32370736	RID04336	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Non-small cell lung cancer	WT1-AS	TGFB1	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell stemness(-)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000183242	GRCh38_11:32435518-32500632	ENSG00000105329	NA	51352	7040	WIT-1|WIT1|WT1-AS1|WT1AS	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA WT1-AS over-expression inhibits non-small cell lung cancer cell stemness by down-regulating TGF-beta1.WT1-AS and TGF-beta1 mRNA in two types of tissues of 74 NSCLC patients were detected by performing RT-qPCR experiments.We found that WT1-AS was down-regulated, while TGF-beta1 was upregulated in NSCLC tissues.WT1-AS and TGF-beta1 were inversely correlated in NSCLC tissues.WT1-AS over-expression resulted in inhibited cancer cell stemness. It is worth noting that TGF-beta1 and WT1-AS were not significantly correlated across normal tissues, indicating that the interaction between TGF-beta1 and WT1-AS is likely mediated by certain NSCLC-related factors.	32349718	RID04337	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Bone disease	H19	SATB2	positively-E	TargetScan;luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-140-5p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone diseases	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000119042	NA	283120	23314	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	FLJ21474|KIAA1034	Long non-coding RNA H19 promotes osteogenic differentiation of human bone marrow-derived mesenchymal stem cells by regulating microRNA-140-5p/SATB2 axis.RT-qPCR assay was conducted to examine the expression of H19, miR-140-5p and SATB2.The relationships among H19, miR-140-5p and SATB2 were examined through bioinformatics analyses, luciferase reporter assay, RIP assay and RNA pull-down assay.H19 expression was remarkably increased and miR-140-5p expression was dramatically reduced during osteogenic differentiation of BMMSCs. bioinformatics analyses suggest that miR-140-5p have the potential to bind with H19 and SATB homeobox 2 (SATB2). H19 knockdown reduced SATB2 expression by upregulating miR-140-5p. Next, we further demonstrated that H19 knockdown resulted in the significant reduction of SATB2 protein expression in BM-MSCs, while this effect was abol_x0002_ished by miR-140-5p deficiency (figure 8), suggesting that H19 functioned as a ceRNA of miR-140-5p to sequester miR-140-5p from its target SATB2. Next, bioinformatics prediction analysis by TargetScanonline website shows that SATB2 is a potential target of miR-140-5p.	32345782	RID04338	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
The failure of hair follicle regeneration	PCAT1	WNT10B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-329)	regulation	RNA-protein	NA	NA	NA	Other	The failure of hair follicle regeneration	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000169884	NA	100750225	7480	PCA1|PCAT-1|PiHL	SHFM6|WNT-12	LncRNA-PCAT1 maintains characteristics of dermal papilla cells and promotes hair follicle regeneration by regulating miR-329/Wnt10b axis. The failure of hair follicle regeneration is the major cause of alopecia, which is a highly prevalent disease worldwide.qRT-PCRand western blot were used to detect gene and protein expression, respectively.Luciferase assay was used to examine the relationship among PCAT1, miR-329 and Wnt10b.Up-regulation of PCAT1 and Wnt10b, however, down-regulation of miR-329 were found in the in vitro 3D dermal papilla.Bioinformatics analysis and luciferase assays demonstrated that PCAT1 promoted Wnt10b expression by sponging miR-329.PCAT1 maintains characteristics of DP cells by targeting miR-329 to activating Wnt/beta-catenin signaling pathway, thereby promoting hair follicle regeneration.	32339605	RID04339	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE67939,GSE75367,GSE86978)
Kidney injury	CASC2	miR<U+2011>155	negatively-F	luciferase reporter assay;StarBase 3.0	downregulation	RT-qPCR	NA	NA	cell injury(-);cell viability(+);inflammatory response(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	Evading Apoptosis	Other	Injury	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long non-coding RNA CASC2 ameliorates sepsis-induced acute kidney injury by regulating the miR-155 and NF-kB pathway.Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI).The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects.the CASC2 level was negatively associated with the severity of AKI. the current study observed that CASC2 was negatively associated with a pro-inflammatory microRNA (miR)-155. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide-stimulated human renal tubular epithelial HK-2 cells. In addition, bioinformatics predictions showed that CASC2 can directly bind to miR-155, as demonstrated by the luciferase reporter assay. The prediction of the interaction between CASC2 and miR-155 was performed using Starbase 3.0.	32323747	RID04340	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pneumonia	CRNDE	miR-141	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+);inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	Long Non-Coding RNA (lncRNA) CRNDE Regulated Lipopolysaccharides (LPS)-Induced MRC-5 Inflammation Injury Through Targeting MiR-141.Pneumonia is a common disease with high morbidity and even death.Quantitative real-time polymerase chain reaction (qRT-PCR was applied to detect the expression of CRNDE and miR-141 in lipopolysaccharides (LPS)-induced MRC-5 cells and pneumonia tissues.luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to prove the relationship between CRNDE and miR-141.e found that CRNDE expression was induced in LPS-induced MRC-5 cells and pneumonia tissues.miR-141 expression was low in LPS-induced MRC-5 cells and was verified was a target miRNA of CRNDE by using luciferase reporter assay and RIP assay.In this study, we found that downregulation of CRNDE and upregulation of miR-141 inhibited cell apoptosis and inflammation response and promoted cell viability in LPS-induced MRC-5 cells.	32317619	RID04341	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Hepatocellular carcinoma	HOTAIR	miR-217-5p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long Noncoding RNA HOTAIR Contributes to Progression in Hepatocellular Carcinoma by Sponging miR-217-5p. The expression of HOTAIR and miR-217-5p in 35 HCC patients and HCC cells was measured by quantitative real-time polymerase chain reaction.The interaction between HOTAIR and miR-217-5p was determined by luciferase reporter system.The expression of HOTAIR was upregulated, whereas miR-217-5p was downregulated in HCC tumor tissues and cell lines (Hep3B and Huh-7) compared with normal tissues and human normal liver cell line MIHA.HOTAIR expression was negatively correlated with miR-217-5p expression in HCC.HOTAIR knockdown induced apoptosis and inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).luciferase reporter system confirmed the interaction between HOTAIR and miR-217-5p.HOTAIR contributes to cell progression in HCC by sponging miR-217-5p, representing promising biomarkers for HCC treatment. miR-217-5p inhibitor attenuated the suppression of HOTAIR silencing on HCC cell proliferation, migration, invasion, and EMT.	32315535	RID04342	ceRNA or sponge	NA		
Renal cell carcinoma	lncRNA 00312	miR-34a-5p	negatively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA 00312 Attenuates Cell Proliferation and Invasion and Promotes Apoptosis in Renal Cell Carcinoma via miR-34a-5p/ASS1 Axis.RT-PCRwas performed to determine lncRNA 00312, miR-34a-5p, and ASS1 mRNA expression.lncRNA was significantly downregulated in RCC cells such as A498 and ACHN;Our study found that miR-34a-5p had the potential binding site with lncRNA 00312 and revealed the role of miR-34a-5p in RCC. lncRNA 00312 can inhibit RCC proliferation and invasion and promote apoptosis in vitro by suppressing miR-34a-5p and overexpressing ASS1.	32308805	RID04343	expression association	NA		
Renal cell carcinoma	lncRNA 00312	ASS1	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000130707	NA	NA	445	NA	ASS|CTLN1	lncRNA 00312 Attenuates Cell Proliferation and Invasion and Promotes Apoptosis in Renal Cell Carcinoma via miR-34a-5p/ASS1 Axis.RT-PCRwas performed to determine lncRNA 00312, miR-34a-5p, and ASS1 mRNA expression.lncRNA was significantly downregulated in RCC cells such as A498 and ACHN;Our study found that miR-34a-5p had the potential binding site with lncRNA 00312 and revealed the role of miR-34a-5p in RCC. lncRNA 00312 can inhibit RCC proliferation and invasion and promote apoptosis in vitro by suppressing miR-34a-5p and overexpressing ASS2.	32308805	RID04344	ceRNA or sponge	NA		UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Nasopharynx carcinoma	EBV-miR-BART6-3p	MIR3936HG	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	miRNA	lncRNA	NA	NA	ENSG00000233006	NA	NA	553103	NA	SLC22A5-AS1	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell proliferation through the LOC553103-STMN1 axis.Epstein-Barr virus (EBV) is a tumorigenic virus that can cause various human malignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).we report that EBV-miR-BART6-3p inhibits the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-coding RNA (lncRNA), LOC553103. via RNA immunoprecipitation and luciferase reporter assay, we confirmed that LOC553103 directly binds and stabilizes the 3'UTR region of STMN1 mRNA.These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expression of cell cycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation. In addition, knockdown of LOC553103 downregulated the STMN1 protein expression, while LOC553103 overexpression upregulated STMN1 protein expression. Interestingly, the RNAhybrid software predicted multiple binding sites between LOC553103 and the STMN1 mRNA 3'UTR. RIP assay was then used to detect whether LOC553103 directly binds the 3'UTR region of STMN1 mRNA. The results of the MTT assay showed that STMN1 knockdown significantly inhibited proliferation of 5-8F, HNE2, AGS, and C666-1 cells.	32306460	RID04345	expression association	NA		DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	MIR3936HG	STMN1	positively-E	RNAhybrid;RIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233006	GRCh38_5:132311285-132370170	ENSG00000117632	NA	553103	3925	LOC553103|SLC22A5-AS1	C1orf215|FLJ32206|Lag|LAP18|OP18|PP17|PP19|PR22|SMN	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell proliferation through the LOC553103-STMN1 axis.Epstein-Barr virus (EBV) is a tumorigenic virus that can cause various human malignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).we report that EBV-miR-BART6-3p inhibits the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-coding RNA (lncRNA), LOC553103. via RNA immunoprecipitation and luciferase reporter assay, we confirmed that LOC553103 directly binds and stabilizes the 3'UTR region of STMN1 mRNA.These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expression of cell cycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation. In addition, knockdown of LOC553103 downregulated the STMN1 protein expression, while LOC553103 overexpression upregulated STMN1 protein expression. Interestingly, the RNAhybrid software predicted multiple binding sites between LOC553103 and the STMN1 mRNA 3'UTR. RIP assay was then used to detect whether LOC553103 directly binds the 3'UTR region of STMN1 mRNA. The results of the MTT assay showed that STMN1 knockdown significantly inhibited proliferation of 5-8F, HNE2, AGS, and C666-1 cells. These results indicate that LOC553103 may directly target the mRNA 3'UTR region of STMN1 and upregulate the STMN1 expression.	32306460	RID04346	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Kidney disease	ZEB1-AS1	BMP7	positively-E	MiRcode;starBase 2.0;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);fibrotic(-)	ceRNA(miR-216-5p)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000101144	NA	220930	655	NA	OP-1	lncRNA ZEB1-AS1 inhibits high glucose-induced EMT and fibrogenesis by regulating the miR-216a-5p/BMP7 axis in diabetic nephropathy.Quantitative polymerase chain reaction (qRT-PCR was utilized to detect the expression levels of ZEB1-AS1, microRNA-216a-5p (miR-216a-5p), and bone morphogenetic protein 7 (BMP7).Additionally, the interaction among ZEB1-AS1, miR-216a-5p, and BMP7 was predicted by MiRcode (http://www.mircode.org) and starBase 2.0 (omics_06102, omicX), and confirmed by luciferase reporter assay.ZEB1-AS1 and BMP7 were down-regulated, while miR-216a-5p was highly expressed in kidney tissues of DN patients.ZEB1-AS1 directly targeted miR-216a-5p, and overexpression of miR-216a-5p restored the inhibitory effects of ZEB1-AS1 overexpression on EMT and fibrogenesis.lncRNA ZEB1-AS1 inhibited high glucose-induced EMT and fibrogenesis via regulating miR-216a-5p/BMP7 axis in diabetic nephropathy, providing a potential target for DN therapy.	32294702	RID04347	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE55807)
Osteoporosis	MCF2L-AS1	RUNX2	positively-E	microarray analysis;luciferase reporter assay	upregulation	q-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-33a)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000235280	GRCh38_13:112967484-112968824	ENSG00000124813	NA	100289410	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	The lncRNA MCF2L-AS1 controls osteogenic differentiation by regulating miR-33a.We found high lncRNA MCF2L-AS1 expression in human bone marrow mesenchymal stem cells, and used bioinformatics analysis to analyze its function.Silencing of MCF2L-AS1 increased the expression of miR-33a and subsequently inhibited Runx2 expression at the post-transcriptional level.MCF2L-AS1 knockdown induced inhibition of osteoblast differentiation.MCF2L-AS1 directly interacted with miR-33a, and downregulation of miR-33a efficiently reversed the suppression of Runx2 induced by MCF2L-AS1 short hairpin RNA (shRNA).MCF2L-AS1 positively regulated the expression of Runx2 by sponging miR-33a, and promoted osteogenic differentiation in BMSCs. Bone homeostasis is maintained by balanced osteoblast-mediated tissue production and osteoclast-mediated tissue destruction, and is disrupted in pathological conditions such as osteoporosis.	32255731	RID04348	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	DLX6-AS1	ERP44	positively-E	StarBase v2.0;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-149-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000023318	NA	285987	23071	Evf-2|FLJ34048|NCRNA00212	KIAA0573|PDIA10|TXNDC4	The regulatory network of lncRNA DLX6-AS1/miR-149-5p/ERP44 is possibly related to the progression of preeclampsia.The levels of DLX6-AS1, microRNA-149-5p (miR-149-5p) and endoplasmic reticulum protein 44 (ERP44) were measured by quantitative real-time polymerase chain reaction (qRT-PCR.The target relationship was predicted by StarBase v2.0 and confirmed by dual-luciferase reporter assay.Higher levels of DLX6-AS1 and ERP44, lower level of miR-149-5p were observed in PE placenta tissues.We also found that DLX6-AS1 could enhance ERP44 expression by sponging miR-149-5p.DLX6-AS1 inhibited proliferation and invasion of trophoblast cells, and suppressed angiogenesis of HUVEC cells by miR-149-5p/ERP44 pathway.	32250737	RID04349	ceRNA or sponge	NA		UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Type 1 diabetes mellitus	MALAT1	PDX1	negatively-E	ChIP-qPCR	upregulation	RT-PCR	NA	NA	insulin synthesis(-)	histone modification	regulation	NA	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000139515	NA	378938	3651	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	IDX-1|IPF1|MODY4|PDX-1|STF-1	LncRNA MALAT1 induces the dysfunction of beta cells via reducing the histone acetylation of the PDX-1 promoter in type 1 diabetes.The expression of MALAT1 was determined using real-time PCR, while the PDX-1 protein expression was determined using western blot.ChIP-qPCR was carried out to determine the histone acetylation of the PDX-1 promoter.In NOD islets and IL-1beta-stimulated Min6 cells, the expression of MALAT1 was increased, while the mRNA and protein levels of PDX-1 were decreased at an age/time-dependent manner.MALAT1 induces the dysfunction of beta cells via reducing the H3 histone acetylation of the PDX-1 promoter and subsequently inhibiting the expression of PDX-1, thus suppressing the insulin secretion.	32243891	RID04350	epigenetic regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Melanoma	AFAP1-AS1	RAI14	positively-E	RNA pull down;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor growth(+);cancer progression(+)	ceRNA(miR-653-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000039560	NA	84740	26064	AFAP1-AS|AFAP1AS|MGC10981	DKFZp564G013|KIAA1334|NORPEG|RAI13	Long non-coding RNA AFAP1-AS1 accelerates the progression of melanoma by targeting miR-653-5p/RAI14 axis.The expression of AFAP1-AS1 was detected by qRT-PCRThe interaction among AFAP1-AS1, miR-653-5p and RAI14 was investigated by RNA pull down, RIP and luciferase reporter assays.AFAP1-AS1 was highly expressed in melanoma cell lines. AFAP1-AS1 was a ceRNA of RAI14 by competitively binding with miR-653-5p.miR-653-5p overexpression or RAI14 inhibition could repress tumor growth.AFAP1-AS1 exerts its oncogenic function in melanoma by targeting miR-653-5p/RAI14 axis. AFAP1-AS1 was highly expressed in melanoma cell lines.	32228518	RID04351	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE55807)
Septic acute kidney injury	DANCR	miR-214	negatively-F	ELISA;western blot;recovery experiment;StarBase v2.0;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	Long Noncoding RNA DANCR Suppressed Lipopolysaccharide-Induced Septic Acute Kidney Injury by Regulating miR-214 in HK-2 Cells.We used qRT-PCRto examine the level of DANCR in patient blood serum samples and in HK-2 cells.Enzyme linked immunosorbent assay (ELISA), western blot and recovery experiments were performed to elucidate the further mechanism.We found that DANCR was decreased in the serum of AKI patients and HK-2 cells treated with LPS.Bioinformatics analysis showed that DANCR served as a sponge for miR-214.DANCR inhibited the expression of KLF6.Our study suggests that AKI development could be alleviated by sponging miR-214 and regulating KLF6 expression, which provides a novel potential mechanism involved in the diagnosis and treatment of sepsis-induced AKI patients. A luciferase reporter assay verified the binding with decreased fluorescence in cells transfected with the miR-214 mimic and DANCR wild type construct	32222722	RID04352	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Septic acute kidney injury	DANCR	KLF6	negatively-E	ELISA;western blot;recovery experiment;StarBase v2.0;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000067082	NA	57291	1316	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	BCD1|COPEB|CPBP|GBF|PAC1|ST12|Zf9	Long Noncoding RNA DANCR Suppressed Lipopolysaccharide-Induced Septic Acute Kidney Injury by Regulating miR-214 in HK-2 Cells.We used qRT-PCRto examine the level of DANCR in patient blood serum samples and in HK-2 cells.Enzyme linked immunosorbent assay (ELISA), western blot and recovery experiments were performed to elucidate the further mechanism.We found that DANCR was decreased in the serum of AKI patients and HK-2 cells treated with LPS.Bioinformatics analysis showed that DANCR served as a sponge for miR-214.DANCR inhibited the expression of KLF6.Our study suggests that AKI development could be alleviated by sponging miR-214 and regulating KLF6 expression, which provides a novel potential mechanism involved in the diagnosis and treatment of sepsis-induced AKI patients.	32222722	RID04353	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE67939)
Myocardial infarction	HIF1A-AS2	TRIM44	positively-E	luciferase reporter assay;RNA pull down;RIP	upregulation	qRT-PCR	NA	NA	cell injury(-)	ceRNA(miR-623)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000166326	NA	100750247	54765	3'aHIF-1A|aHIF	DIPB|MC7	Knockdown of HIF1A-AS2 suppresses TRIM44 to protect cardiomyocytes against hypoxia-induced injury.Myocardial infarction (MI) is a common cardiovascular disease characterized by an interruption of blood and oxygen supply to the heart, which results in gradual damage to the myocardial tissue and ultimately heart failure. we report that HIF1A-AS2 is upregulated in hypoxia-treated human cardiomyocytes (HMCs) compared with normal cardiomyocytes, and that silenced HIF1A-AS2 inhibited apoptosis and facilitated viability, migration, and invasion of HMCs.Our data suggested that in MI, HIF1A-AS2 upregulation was associated with miR-623, which promoted expression of tripartite motif containing 44 (TRIM44).we conclude that cardiomyocytes can be protected against hypoxic-treated injury by knockdown of HIF1A-AS2, which suppresses TRIM44, and that HIF1A-AS2 overexpression is a prognostic indicator of MI. HIF1A-AS2/miR-623/TRIM44 formed a functional ceRNA network in MI.	32222118	RID04354	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE75367)
Neuroblastoma	HNF4A-AS1	CTCF	positively-E	luciferase reporter assay;ChIP;overexpression;knockdown	upregulation	qRT-PCR	GSE143896	NA	glucose metabolic process(+);cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000229005	GRCh38_20:44372746-44395706	ENSG00000102974	NA	101927219	10664	uc002xlx	CFAP108|FAP108	HNF4A-AS1/hnRNPU/CTCF axis as a therapeutic target for aerobic glycolysis and neuroblastoma progression.Mechanistically, transcription factor HNF4A increased the expression of hexokinase 2 (HK2) and solute carrier family 2 member 1 (SLC2A1), while HNF4A-AS1 bound to heterogeneous nuclear ribonucleoprotein U (hnRNPU) to facilitate its interaction with CCCTC-binding factor (CTCF),resulting in transactivation of CTCF and transcriptional alteration of HNF4A and other genes associated with tumor progression.In clinical NB cases, high expression of HNF4A-AS1, hnRNPU, CTCF, or HNF4A was associated with poor survival of patients.These findings suggest that therapeutic targeting of HNF4A-AS1/hnRNPU/CTCF axis inhibits aerobic glycolysis and NB progression. HNF4A-AS1 facilitates aerobic glycolysis and aggressiveness of NB cells via hnRNPU-mediated transactivation of CTCF. Sequencing results have been deposited in GEO database (accession code GSE143896).	32216806	RID04355	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Colon adenocarcinoma	LINC00342	MDM2	positively-E	StarBase v2.0;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;ISH	TCGA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	ceRNA(miR-545-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232931	GRCh38_2:95807052-95835003	ENSG00000135679	NA	150759	4193	NCRNA00342	HDM2|MGC5370	LINC00342 regulates cell proliferation, apoptosis, migration and invasion in colon adenocarcinoma via miR-545-5p/MDM2 axis. The LINC00342 expressions in COAD tissues were detected via qRT-PCRand in situ hybridization analysis.The target miRNA of LINC00342 were predicted and verified by online bioinformatics tools and luciferase reporter assay and RNA pull-down assay.LINC00342 was over-expressed in COAD tissues and LINC00342 overexpression was related to the poor prognosis of COAD patients.LINC00342 knockdown inhibited cell proliferation, migration and invasion and promoted apoptosis of COAD cells.LINC00342 targeted to miR-545-5p/murine double minute 2 (MDM2) in COAD.In COAD tissues and cell lines, LINC00342 expression was positively correlated to MDM2 expression, while it was negatively correlated to miR-545-5p expression. Given that lncRNAs serve as molecular sponges for miRNAs in many diseases, we used starBase v2.0 to predict the candidate target miRNAs binding with DANCR. LINC00342 acted as a sponge for miR-545-5p in COAD. The expression levels of LINC00342 in COAD tumor samples (n = 471) and in normal samples (n = 41) were downloaded from the TCGA database.	32213297	RID04356	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colon adenocarcinoma	LINC00342	miR-545-5p	negatively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;ISH	NA	NA	cell proliferation(+);apoptosis process(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000232931	GRCh38_2:95807052-95835003	NA	NA	150759	NA	NCRNA00342	NA	LINC00342 regulates cell proliferation, apoptosis, migration and invasion in colon adenocarcinoma via miR-545-5p/MDM2 axis. The LINC00342 expressions in COAD tissues were detected via qRT-PCRand in situ hybridization analysis.The target miRNA of LINC00342 were predicted and verified by online bioinformatics tools and luciferase reporter assay and RNA pull-down assay.LINC00342 was over-expressed in COAD tissues and LINC00342 overexpression was related to the poor prognosis of COAD patients.LINC00342 knockdown inhibited cell proliferation, migration and invasion and promoted apoptosis of COAD cells.LINC00342 targeted to miR-545-5p/murine double minute 2 (MDM2) in COAD.In COAD tissues and cell lines, LINC00342 expression was positively correlated to MDM2 expression, while it was negatively correlated to miR-545-5p expression.	32213297	RID04357	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	
Ovarian cancer	DUXAP9	miR-29c-3p	negatively-E	StarBase;luciferase reporter assay	upregulation	qRT-PCR	GSE119055;GSE83693	NA	tumor malignant transformation(+);cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225210	GRCh38_14:19062316-19131167	NA	NA	503638	NA	FLJ39632|LINC01296|lncRNA-CTD903|LNMAT1	NA	MiR-29c-3p, a target miRNA of LINC01296, accelerates tumor malignancy: therapeutic potential of a LINC01296/miR-29c-3p axis in ovarian cancer.Through online software prediction, miR-29c-3p has been discriminated as the target miRNA of LINC01296 for further research, and subsequent luciferase assay confirmed bioinformatics prediction. the qRT-PCRdata revealed that the miR-29c-3p expression in OC cell lines (SKOV-3 and OVCAR-3) was markedly declined than that in normal control cells (IOSE80).the functional experiments, such as CCK8, colony formation and Transwell assays, prompted that inhibition of miR-29c-3p can obviously increase the proliferation, invasion and migration of OVCAR3 and SKOV3 cells compared with control group, while downregulation of LINC01296 showed an opposite result.It is worth noting that downregulation of LINC01296 can reverse the effect of miR-29c-3p suppression on OC cells.we detected the changes of EMT-related proteins by western blot experiment, and reached a similar conclusion that knockdown of LINC01296 reversed the EMT caused by miR-29c-3p inhibition.the cancer-promoting function of LINC01296 was achieved by regulating the expression of miR-29c-3p, and LINC01296/miR-29c-3p axis mediates the mechanical regulation of EMT in OC cells, hoping to provide the novel biomarkers and possibilities for OC therapy. Gene expression profiles of OC patients were downloaded from the two independent datasets (the accessing number of GSE119055, and GSE83693) of Gene Expression Omnibus (GEO, http://www.ncbi.nlm.nih.gov/geo/). Firstly, StarBase website (http://starbase.sysu.edu.cn/) was used to predict the target miRNA of LINC01296. LINC01296 directly targets miR-29c-3p and negatively regulated its expression. Loss of E-cad is a marker of EMT [17], and inhibition of miR-29c-3p can significantly decrease its expression in OVCAR3 and SKOV3 cells, while induce the expression of N-cadherin and Vimentin.	32192508	RID04358	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Lung adenocarcinoma	ZNF667-AS1	MIR223	negatively-E	cell transfection	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000166770	GRCh38_19:56477250-56504362	ENSG00000207939	NA	100128252	407008	MORT	MIRN223|miRNA223|mir-223	Mortal Obligate RNA Transcript Inhibits Cancer Cell Invasion and Migration in Lung Adenocarcinoma by Downregulating miRNA-223.Mortal obligate RNA transcript (MORT), a long noncoding RNA, has been reported as a potential tumor suppressor in many types of cancer.Quantitative reverse transcription-polymerase chain reaction was used to assess gene expression.Cell transfections were used to analyze gene interactions.MORT was downregulated, whereas miRNA-223 was upregulated in LUAD.Expression of miRNA-223 and MORT was inversely correlated in LUAD tissue samples.Therefore, MORT may inhibit cancer cell invasion and migration in LUAD by downregulating miRNA-223.	32160014	RID04359	expression association	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE51827,GSE86978)	
Osteoarthritis	LINC00461	miR-30a-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell cycle(+);inflammatory response(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000245526	GRCh38_5:88507546-88691057	NA	NA	645323	NA	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	NA	Long noncoding RNA LINC00461 induced osteoarthritis progression by inhibiting miR-30a-5p.A CCK-8 assay was performed to detect cell viability, and qRT-PCRanalysis was used to measure mRNA expression.The targeting by miR-30a-5p of the LINC00461 3'UTR was detected using a luciferase reporter assay.Our data indicated that the inflammatory mediators IL-6 and TNF-alpha induced LINC00461 expression in chondrocytes and that the expression of LINC00461 was upregulated in OA tissues.The expression level of miR-30a-5p in OA tissues was negatively related to LINC00461 expression.we showed that LINC00461 directly interacted with miR-30a-5p in chondrocytes.we found that overexpression of LINC00461 enhanced chondrocyte proliferation, cell cycle progression, inflammation, and ECM degradation by downregulating miR-30a-5p.	32155130	RID04360	expression association	NA	UP(LIHC);DATA(GSE117623)	
Pre-eclampsia	AGAP2-AS1	JDP2	negatively-E	luciferase reporter assay;CHIP	downregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(-);apoptosis process(-);cell invasion(-)	ceRNA(miR-574)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000140044	NA	100130776	122953	LOC100130776|PUNISHER	JUNDM2	Down-regulated lncRNA AGAP2-AS1 contributes to pre-eclampsia as a competing endogenous RNA for JDP2 by impairing trophoblastic phenotype.we found that lncRNA AGAP2-AS1 is abnormally down-regulated in severe PE placenta tissues. AGAP2-AS1 promoted the suppressor protein, Jun dimerization protein 2 (JDP2), by sponging miR-574-5p. further impairment of the trophoblastic phenotype was achieved by way of inhibiting cell growth, apoptosis and invasion.Our results showed that the down-regulated expression of lncRNA AGAP2-AS1 might serve as a key suppressor in PE via inhibition of JDP2 at the post-transcriptional level by competing for miR-574;	32150333	RID04361	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Rheumatoid arthritis	GAS5	HIPK2	negatively-E		downregulation		NA	NA	cell proliferation(-);inflammatory response(-)	DNA methylation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000064393	NA	60674	28996	NCRNA00030|SNHG2	NA	Long non-coding RNA growth arrest-specific transcript 5 regulates rheumatoid arthritis by targeting homeodomain-interacting protein kinase 2.In this study, we test the hypothesis that GAS5 might inhibit proliferation and inflammatory response of FSs in RA.The expression of GAS5 was significantly reduced in RA synovial tissues and RA FSs, whereas the expression of homeodomain-interacting protein kinase 2 (HIPK2) was increased, indicating that it plays a critical role in inflammation and autoimmune diseases.We found that overexpression of GAS5 decreased the level of HIPK2, TNF-alpha and IL-6.treatment with methylation inhibitor 5-aza-2-deoxycytidine (5-azadC) inhibited hypermethylation of GAS5 promoter and expression of HIPK2.These results indicated that GAS5 regulates RA via potentially targeting HIPK2.	32141429	RID04362	epigenetic regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE55807)
Renal cell carcinoma	LINC01939	MIR154	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000228799	GRCh38_2:899462-905539	ENSG00000207978	NA	101060385	406946	NA	MIRN154|mir-154	Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154.LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCRassay.LINC01939 was down-regulated in RCC tissues.Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression.Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.	32138544	RID04363	expression association	NA		
Hepatocellular carcinoma	MALAT1	SNAI1	positively-E	luciferase reporter assay;RNA pull down;RIP	upregulation	q-PCR	NA	NA	cancer progression(+)	ceRNA(miR-22)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124216	NA	378938	6615	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 cooperates with enhancer of zeste homolog 2 to promote hepatocellular carcinoma development by modulating the microRNA-22/Snail family transcriptional repressor 1 axis.aberrantly elevated levels of MALAT1 were detected in both HCC specimens and cell lines. Mechanistic investigations showed that Snail family transcriptional repressor 1 (SNAI1) is a direct target of microRNA (miR)-22 and that MALAT1 modulates SNAI1 expression by acting as a competing endogenous RNA for miR-22.Cooperating with EZH2, MALAT1 positively regulated SNAI1 by repressing miR-22 and inhibiting E-cadherin expression, playing a vital role in epithelial to mesenchymal transition.	32129914	RID04364	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Nephroblastoma	LINC00667	IKBKB	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-200b/c/429)	regulation	RNA-protein	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000263753	GRCh38_18:5237826-5290608	ENSG00000104365	NA	339290	3551	NA	IKK-beta|IKK2|IKKB|IMD15|IMD15A|IMD15B|NFKBIKB	LINC00667 promotes Wilms' tumor metastasis and stemness by sponging miR-200b/c/429 family to regulate IKK-beta.And data from three independent analyses of quantitative real-time polymerase chain reaction revealed that the expression of miR-200b/c/429 was downregulated in Wilms' tumor cell lines.Moreover, miR-200b/c/429 was sponged by LINC00667 in Wilms' tumor cells.LINC00667 competitively bound with miR-200b/c/429 to regulate IKK-beta expression and then activated NF-kB pathway in Wilms' tumor.LINC00667 promoted Wilms' tumor progression by sponging miR-200b/c/429 family to regulate IKK-beta.	32129525	RID04365	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Hepatocellular carcinoma	SNHG1	miR-377-3p	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	LncRNA SNHG1 promotes cell progression and metastasis via sponging miR-377-3p in hepatocellular carcinoma.The expression levels of SNHG1 and miR-377-3p were detected by qRT-PCRin HCC tissues and cells.The binding sites of SNHG1 and miR-377-3p were predicted by the online software and confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay.We found that SNHG1 was markedly upregulated in HCC tissues and cells.SNHG1 directly bound to miR-377-3p.SNHG1 inhibited apoptosis and induced proliferation, migration, invasion, and EMT by sponging miR-377-3p in HCC, which indicated that SNHG1 may be a potential biomarker and therapeutic target for HCC treatment.	32122143	RID04366	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Glioblastoma	MALAT1	miR-101	negatively-E		downregulation		NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 induces protective autophagy and suppresses apoptosis in GBM cells via sponging miRNA-101 and increases temozolomide chemoresistance via enhancing epithelial-mesenchymal transition, suppressing miR-203 and promoting thymidilate synthase.	32119915	RID04367	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Papillary thyroid carcinoma	CDKN2B-AS1	miR-320a	negatively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell viability(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Propofol upregulates miR-320a and reduces HMGB1 by downregulating ANRIL to inhibit PTC cell malignant behaviors.Dual-luciferase reporter gene assay and RNA pull-down assay were applied to verify ANRIL/miR-320a/HMGB1 relation.ANRIL was upregulated in TPC-1 and BCPAP cells.miR-320a targeted HMGB1, and ANRIL bound to miR-320a.Propofol upregulated miR-320a and reduced HMGB1 by downregulating ANRIL and inactivating the Wnt/beta-catenin and NF-kB pathways, thus preventing PTC cell malignant behaviors.	32098696	RID04368	expression association	NA	UP(SKCM);DATA(GSE38495)	
Lung cancer	LINC00511	MMP2/9/12	negatively-E	western blot;RNAi	upregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	NA	NA	400619	NA	LCAL5|onco-lncRNA-12	NA	Knockdown of Linc00511 inhibits TGF-beta-induced cell migration and invasion by suppressing epithelial-mesenchymal transition and down-regulating MMPs expression.Our results showed that knockdown of linc00511 significantly inhibited TGF-beta1-induced migration and invasion and down-regulated the mRNA and protein levels of MMP2, MMP9 and MMP12 in TGF-beta1 treated SPCA1 and H1975 cells.Some evidences have been provided to verify up-regulation of linc00511 in multiple cancers and oncogenic roles during cancer malignant process.	32092827	RID04369	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Infantile hemangioma	MALAT1	VEGFA	positively-E	bioinformatics analysis;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	VEGF|VEGF-A|VPF	The knockdown of MALAT1 inhibits the proliferation, invasion and migration of hemangioma endothelial cells by regulating MiR-206 / VEGFA axis.Quantitative real-time (qRT)-PCR was performed to detect the expressions of MALAT1, miR-206 and VEGFA.The correlations among MALAT1, miR-206 and VEGFA were confirmed by bioinformatics analysis and dual-luciferase reporter assay.The results showed that MALAT1 and VEGFA were high-expressed and miR-206 was low-expressed in IH tissues.MALAT1 directly targeted and inhibited the expression of miR-206, and VEGFA was predicted to be the target gene for miR-206.	32084582	RID04370	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Atherosclerosis	HOTTIP	miR-490-3p	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	NA	HOTTIP knockdown inhibits cell proliferation and migration via regulating miR-490-3p/HMGB1 axis and PI3K-AKT signaling pathway in ox-LDL-induced VSMCs.Atherosclerosis (AS) is a common cardiovascular disease with complicated pathogenesis.Quantitative real-time polymerase chain reaction (qRT-PCR was performed to detect the expression of HOTTIP, miR-490-3p and high mobility group B 1 (HMGB1) in AS patients' sera and oxidized low-density lipoprotein (ox-LDL) induced human aortic vascular smooth muscle cells (HA-VSMCs).dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to verify the targeting association between HOTTIP and miR-490-3p, as well as miR-490-3p and HMGB1.HOTTIP and HMGB1 were upregulated and miR-490-3p was downregulated in the sera of AS patients and ox-LDL-stimulated HA-VSMCs.MiR-490-3p was identified as a target of HOTTIP and HOTTIP overexpression abolished the inhibition on cell proliferation and migration mediated by miR-490-3p in ox-LDL-induced HA-VSMCs.	32081664	RID04371	expression association	NA		
Prostate cancer	SNHG1	miR-377-3p	negatively-E	bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Long Noncoding RNA SNHG1 Contributes to the Promotion of Prostate Cancer Cells Through Regulating miR-377-3p/AKT2 Axis.Abnormal expression of SNHG1, survival analysis, and target gene were determined or predicted by bioinformatics techniques.Gene expressions at transcriptional and translational levels were determined by Quantitative Real-time PCR and western blot, respectively.The results showed that SNHG1 was highly expressed in PCa tissues, which was accompanied by decreased miR-377-3p expression and poor overall survival rate, and that miR-377-3p was predicted as the target of SNHG1 in PCa cells.SNHG1 counteracted the effects of miR-377-3p on inhibiting cell growth and promoting apoptosis of PCa cells.	32077748	RID04372	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Osteoarthritis	SNHG7	SYVN1	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell autophagy(-)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000162298	NA	84973	84447	MGC16037|NCRNA00061	DER3|HRD1	LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferation, apoptosis and autophagy in osteoarthritis.The expression of SNHG7, miR-34a-5p and SYVN1 was detected using qRT-PCRin tissues, serum and cells.The RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays were used to verify the relationship between SNHG7, miR-34a-5p and SYVN1.SNHG7 and SYVN1 expression were down-regulated, but miR-34a-5p was up-regulated in OA tissues and IL-1beta treated cells compared with normal tissues and chondrocyte.SNHG7 regulated SYVN1 through sponging miR-34a-5p.More than that, RIP, pull-down and luciferase reporter assay was applied to determine that miR-34a-5p was a target miRNA of SNHG7 and SYVN1 was a target mRNA of miR-34-5p.SNHG7 sponged miR-34a-5p to affect cell proliferation, apoptosis and autophagy through targeting SYVN1 which provides a novel sight into the pathogenesis of OA.	32066502	RID04373	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Neuropathic pain	MALAT1	miR-129-5p	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Other	Neuropathic pain	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	lncRNA MALAT1 contributes to neuropathic pain development through regulating miR-129-5p/HMGB1 axis in a rat model of chronic constriction injury.Bilateral sciatic nerves were ligated to induce chronic constriction injury (CCI) in order to establish the neuropathic pain rat model followed by behavioral tests, RT-qPCR;western blot, and ELISA.Dual luciferase activity assay was performed to determine the binding effect between MALAT1 or HMGB1 and miR-129-5p.The mRNA levels of MALAT1 were significantly enhanced in CCI rats.MALAT1 inhibition repressed the development of neuropathic pain and neuroinflammation.Additionally, miR-129-5p was decreased and HMGB1 was increased, both of which could be rectified by MALAT1 inhibition.MALAT1 targeted miR-129-5p/HMGB1 axis.	32065547	RID04374	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Neuropathic pain	MALAT1	HMGB1	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	binding/interaction	NA	NA	NA	NA	Other	Neuropathic pain	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DKFZp686A04236|HMG1|HMG3|SBP-1	lncRNA MALAT1 contributes to neuropathic pain development through regulating miR-129-5p/HMGB1 axis in a rat model of chronic constriction injury.Bilateral sciatic nerves were ligated to induce chronic constriction injury (CCI) in order to establish the neuropathic pain rat model followed by behavioral tests, RT-qPCR;western blot, and ELISA.Dual luciferase activity assay was performed to determine the binding effect between MALAT1 or HMGB1 and miR-129-5p.The mRNA levels of MALAT1 were significantly enhanced in CCI rats.MALAT1 inhibition repressed the development of neuropathic pain and neuroinflammation.Additionally, miR-129-5p was decreased and HMGB1 was increased, both of which could be rectified by MALAT1 inhibition.MALAT1 targeted miR-129-5p/HMGB1 axis.	32065547	RID04375	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Lung cancer	NORAD	ADAM19	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000135074	NA	647979	8728	LINC00657	MLTNB	Long noncoding RNA NORAD regulates lung cancer cell proliferation, apoptosis, migration, and invasion by the miR-30a-5p/ADAM19 axis.The expression levels of NORAD, miR-30a-5p and a disintegrin and metalloproteinase 19 (ADAM19) were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR.The interaction between miR-30a-5p and NORAD or ADAM19 was predicted by online software and confirmed by the dual-luciferase reporter assay.The expression levels of NORAD and ADAM19 were increased and the expression level of miR-30a-5p was decreased in lung cancer tissues and cells.NORAD directly interacted with miR-30a-5p and its overexpression reversed the anti-cancer role of miR-30a-5p in lung cancer.NORAD functioned as a competing endogenous RNA (ceRNA) through sponging miR-30a-5p to regulate ADAM19 expression.NORAD knockdown suppressed cell proliferation, migration and invasion but promoted cell apoptosis in lung cancer cells by regulating miR-30a-5p/ADAM19, providing a possible therapeutic strategy for lung cancer patients.	32055266	RID04376	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	DDX11-AS1	SEC11A	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-873-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000140612	NA	100506660	23478	CONCR|SCAT4	SEC11L1|sid2895|SPC18|SPCS4A	Long non-coding RNA DDX11-AS1 facilitates gastric cancer progression by regulating miR-873-5p/SPC18 axis.we found that DDX11-AS1 expression was up-regulated in GC tumour tissues and cells. DDX11-AS1 enhanced SPC18 expression through acting as a ceRNA for miR-873-5p.DDX11-AS1 may serve as an oncogene in GC progression by sponging miR-873-5p and promoting SPC18 expression, providing a new insight into the mechanisms of DDX11-AS1 and elucidating a promising therapy target in GC.	32054332	RID04377	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939)
Pancreatic cancer	LINC00261	FOXO3	positively-E	TargetScan;luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);WNT signaling pathway(-)	ceRNA(miR-552-5p)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000118689	NA	140828	2309	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	AF6q21|FKHRL1|FOXO2|FOXO3A	Linc00261 inhibits metastasis and the WNT signaling pathway of pancreatic cancer by regulating a miR-552-5p/FOXO3 axis.The expression of Linc00261 in patients with PC and PC cell lines was assessed using reverse transcription-quantitative PCR and the association of Linc00261 expression with survival was analyzed in the online database, GEPIA.The relationship between Linc00261, the miR-552-5p/forkhead box O3 (FOXO3) axis and the Wnt signaling pathway were determined using bioinformatics analysis, dual luciferase assay and western blot.Linc00261 expression was significantly decreased in PC tissues and cell lines, and reduced expression was associated with less favorable outcomes in patients with PC.Linc00261 was revealed to directly bind to microRNA (miR)-552-5p and to decrease the expression of miR-552-5p.Linc00261 overexpression increased the expression of FOXO3, a target gene of miR-552-5p, as well as inhibited the Wnt signaling pathway.Target miRNAs of Linc00261 were predicted using TargetScan, and the analysis revealed that miR-552-5p possessed potential binding sites for Linc00261 (Fig. 5A). A dual-luciferase reporter assay was performed and the results revealed that luciferase activity was decreased in PANC-1 and MIA-PaCa2 cells co-transfected with miR-552-5p mimic and Linc00261-WT plasmid compared with cells co-transfected with NC mimic and the Linc00261-WT plasmid (Fig. 5B; P<0.05).	32020223	RID04378	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE51827,GSE86978)
Kidney disease	CASC2	MIR133B	negatively-E	luciferase reporter assay;RNA pull-down	downregulation	qRT-PCR	NA	NA	cell proliferation(-);extracellular matrix accumulation(-);oxidative stress(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000199080	NA	255082	442890	C10orf5	MIRN133B|miRNA133B|mir-133b	LncRNA CASC2 regulates high glucose-induced proliferation, extracellular matrix accumulation and oxidative stress of human mesangial cells via miR-133b/FOXP1 axis.The expression level of CASC2 and miR-133b was detected by quantitative real-time polymerase chain reaction (qRT-PCR.The relationship between miR-133b and CASC2 or FOXP1 was predicted by online bioinformatics tools and verified by dual-luciferase reporter assay or RNA pull-down.The expression of CASC2 was reduced in serum from DN patients and HG-induced HMCs.MiR-133b was a target of CASC2 with a high level in serum from DN patients and HG-induced HMCs, and its enrichment reversed the effects of CASC2 upregulation.CASC2 upregulation inhibited HG-induced HMCs proliferation, ECM accumulation and oxidative stress.CASC2 upregulation suppressed HG-induced proliferation, ECM accumulation and oxidative stress of HMCs through miR-133b /FOXP1 regulatory axis, suggesting that CASC2 was a novel biomarker for DN treatment.	32016985	RID04379	expression association	NA	UP(LIHC);DATA(GSE117623)	
Endothelial dysfunction	SNHG9	TRADD	negatively-E	RNA pull-down assay;RIP	downregulation	RT-qPCR	NA	NA	inflammatory response(-);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Other	Endothelial dysfunction	lncRNA	PCG	ENSG00000255198	GRCh38_16:1964899-1965509	ENSG00000102871	NA	735301	8717	DKFZp686N06141|NCRNA00062	Hs.89862	SNHG9, delivered by adipocyte-derived exosomes, alleviates inflammation and apoptosis of endothelial cells through suppressing TRADD expression.we proved that adipocytes-derived exosomal SNHG9 were downregulated in obese persons and further decreased in obese individuals with endothelial dysfunction.RNA-binding protein immunoprecipitation assay based on Ago2 antibody and ribonuclease protection assay demonstrated that exosomal SNHG9 directly bound to a specific region in TRADD mRNA sequence and formed an RNA dimeric inducible silencing complex.SNHG9 could prevent endothelial dysfunction in obese patients by suppressing inflammation and apoptosis, indicating that SNHG9 may be a potential therapeutic target for obese patients with endothelial dysfunction.	32007500	RID04380	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Autoimmune disease	GAS5	STAT3	negatively-E	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell differentiation(-)	ubiquitination	binding/interaction	NA	NA	NA	NA	Immune system disease	Primary immunodeficiency disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000168610	NA	60674	6774	NCRNA00030|SNHG2	APRF	LncRNA GAS5 inhibits Th17 differentiation and alleviates immune thrombocytopenia via promoting the ubiquitination of STAT3. The expression of GAS5 in peripheral blood mononuclear cells (PBMCs) of ITP patients and spleen tissues of ITP mice was measured by qRT-PCRThe combination between GAS5 and STAT3 was confirmed by RNA pull-down assay and RNA Binding Protein Immunoprecipitation (RIP).GAS5 expression was downregulated both in PBMCs of ITP patients and spleen tissues of ITP mice.RNA pull-down and RNA immunoprecipitation assays confirmed the interaction between GAS5 and STAT3.Further studies showed GAS5 accelerated the degradation of STAT3 via promoting TRAF6-mediated ubiquitination.LncRNA GAS5 inhibited Th17 differentiation through promoting the TRAF6-mediated ubiquitination of STAT3, thus relieving ITP.	31978798	RID04381	epigenetic regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Myocardial infarction	LncDACH1	YAP1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cardiac repair(+);cardiomyocyte regeneration(+)	phosphorylation	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	NA	NA	ENSG00000137693	NA	NA	10413	NA	COB1|YAP|YAP-1|YAP2|YAP65|YKI	Targeting LncDACH1 promotes cardiac repair and regeneration after myocardium infarction.We have reported that a highly conserved long noncoding RNA (lncRNA) LncDACH1 was overexpressed in the failing hearts.LncDACH1 enhanced yes-associated protein 1 (YAP1) phosphorylation and reduced its nuclear translocation by binding PP1A.LncDACH1 governs heart regeneration in postnatal and ischemic hearts via regulating PP1A/YAP1 signal, which confers a novel therapeutic strategy for ischemic heart diseases.	31969690	RID04382	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Liver fibrosis	DNMT3A	CDKN2B-AS1	negatively-E	immunohistochemistry;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	AMPK signaling pathway(-);cancer progression(-)	NA	association	protein-RNA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	PCG	lncRNA	ENSG00000119772	NA	ENSG00000240498	GRCh38_9:21994139-22128103	1788	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	Epigenetic silencing of LncRNA ANRIL enhances liver fibrosis and HSC activation through activating AMPK pathway.The expression levels of DNA methyltransferases 3A (DNMT3A), ANRIL, alpha-Smooth muscle actin (alpha-SMA), Type I collagen (Col1A1), adenosine monophosphate-activated protein kinase (AMPK) and p-AMPK in rat and human liver fibrosis were detected by immunohistochemistry, qRT-PCRand western blot.our study demonstrated that ANRIL was significantly decreased in activated HSC and liver fibrosis tissues, while Col1A1, alpha-SMA and DNMT3A were significantly increased in activated HSC and liver fibrosis tissues.Reduction in DNMT3A elevated ANRIL expression in activated HSC.our study found that epigenetic DNMT3A silencing of ANRIL enhances liver fibrosis and HSC activation through activating AMPK pathway.The expression levels of DNA methyltransferases 3A (DNMT3A), ANRIL, alpha-Smooth muscle actin (alpha-SMA), Type I collagen (Col1A1), adenosine monophosphate-activated protein kinase (AMPK) and p-AMPK in rat and human liver fibrosis were detected by immunohistochemistry, qRT-PCRand western blot.	31961061	RID04383	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)	UP(SKCM);DATA(GSE38495)
Cardiac hypertrophy	Ahit	MEF2A	negatively-E	catRAPID;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(-)	DNA methylation	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	TF	NA	NA	ENSG00000068305	NA	NA	4205	NA	RSRFC4|RSRFC9	Long Noncoding RNA Ahit Protects Against Cardiac Hypertrophy Through SUZ12 (Suppressor of Zeste 12 Protein Homolog)-Mediated Downregulation of MEF2A (Myocyte Enhancer Factor 2A).Using catRAPID program, an interaction between Ahit and SUZ12 (suppressor of zeste 12 protein homolog) was predicted and validated by RNA immunoprecipitation and immunoblotting following RNA pull-down.the expression of human Ahit (leukemia-associated noncoding IGF1R activator RNA 1 [LUNAR1]) in the serum samples from patients of hypertrophic cardiomyopathy was tested by quantitative real-time polymerase chain reaction.A previously unannotated lncRNA, antihypertrophic interrelated transcript (Ahit), was identified to be upregulated in the mouse hearts after transverse aortic constriction.Mechanistically, Ahit directly bound and recruited SUZ12, a core PRC2 (polycomb repressive complex 2) protein, to the promoter of MEF2A, triggering its trimethylation on H3 lysine 27 (H3K27me3) residues and mediating the downregulation of MEF2A, thereby preventing cardiac hypertrophy.	31957467	RID04384	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	CYTOR	PIK3CA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-139)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000121879	NA	112597	5290	C2orf59|LINC00152|MGC4677|NCRNA00152	PI3K	Long Intergenic Nonprotein Coding RNA 0152 Promotes Hepatocellular Carcinoma Progression by Regulating Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway through miR-139/PIK3CA.we identified a significant up-regulation of LINC00152 in both HCC tissues and cell lines.LINC00152 functioned as an efficient miR-139 sponge, thereby releasing the suppression of PIK3CA (a target gene of miR-139).	31954697	RID04385	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Colon cancer	STAT3	HOTAIR	positively-E	RNA interference	upregulation	qRT-PCR	NA	NA	cell invasion(-);apoptosis process(+)	NA	regulation	NA	Propofol	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6774	100124700	APRF	HOXC-AS4|HOXC11-AS1|NCRNA00072	Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF-1 and suppressing Wnt pathway.RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer.Quantitative real-time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial-mesenchymal transition-related markers, respectively.STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol.Taken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF-1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future.	31953926	RID04386	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Atherosclerosis	MALAT1	TOX	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(-);oxidative stress(-)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198846	NA	378938	9760	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	KIAA0808|TOX1	LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX.AS tissues were collected to determine the level of MALAT1 expression in AS patients, together with determination of miR-181b expression.Luciferase activity assay was conducted to evaluate the potential target sites of miR-181b on MALAT1 and TOX.we demonstrated that MALAT1 was upregulated in patients with AS.MALAT1 silencing significantly downregulated the expression of the miR-181b target gene TOX via reversing the effect of miR181b.MALAT1 suppression protects the endothelium from oxLDL-induced inflammation and oxidative stress in endothelial cells by upregulation of miR-181b and downregulation of TOX.	31949884	RID04387	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Osteosarcoma	SNHG14	FBXO22	positively-E	luciferase reporter assay;bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-433-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000167196	NA	104472715	26263	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	FBX22|FISTC1	Long noncoding RNA SNHG14 promotes osteosarcoma progression via miR-433-3p/FBXO22 axis.In this present study, we found that SNHG14 was significantly upregulated in osteosarcoma tissues and cell lines.Bioinformatics analysis and luciferase assays identified that microRNA-433-3p (miR-433-3p) was a direct target of SNHG14, and directly targeted F-box only protein 22 (FBXO22).Mechanistic analysis demonstrated that SNHG14 acted as a ceRNA in modulating osteosarcoma proliferation, migration and invasion by decoying miR-433-3p to upregulate FBXO22 expression.	31948764	RID04388	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Epilepsy	NEAT1	miR-129-5p	negatively-E	luciferase reporter assay	upregulation	RT-qPCR;western blot	NA	NA	inflammatory response(+)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Brain disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 affects inflammatory response by targeting miR-129-5p and regulating Notch signaling pathway in epilepsy.The expression levels of RNA and protein in temporal lobe tissues and epilepsy cell model were determined by RT-qPCR;western blot or ELISA, respectively.dual-luciferase reporter assay was used to explore the interaction relationship between lncRNA NEAT1, miR-129-5p and Notch1.The overexpression of NEAT1 suppressed the expression level of miR-129-5p.The present study verified that lncRNA NEAT1 affected inflammatory response of epilepsy by suppressing miR-129-5p and further regulating Notch signaling pathway in IL-1beta-induced epilepsy cell model.	31948324	RID04389	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Malignant glioma	LINC00520	TFAP4	positively-E	RIP;CHIP	upregulation	qRT-PCR	NA	NA	cell migration(-)	ceRNA(miR-520f-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000090447	NA	645687	7023	C14orf34|LASSIE	AP-4|bHLHc41	Transcription factor AP-4 (TFAP4)-upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA-520f-3p feedback loop.Both TFAP4-66aa-uORF and miR-520f-3p were downregulated, and TFAP4, LASP1, and LINC00520 were highly expressed in glioma tissues and cells.LINC00520 could promote the expression of TFAP4 by competitively binding to miR-520f-3p.Our findings together indicated that TFAP4-66aa-uORF inhibited the TFAP4/LINC00520/miR-520f-3p feedback loop by directly inhibiting TFAP4 expression, subsequently leading to inhibition of glioma malignancy.	31943575	RID04390	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	BDNF-AS	TP53	positively-E	RIP;RNA pull-down;ChIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000141510	NA	497258	7157	BDNF-AS1|BDNFAS|BDNFOS|BT2A|BT2B|BT2C|BT2D|NCRNA00049	LFS1|p53	Activation of BDNF-AS/ADAR/p53 Positive Feedback Loop Inhibits Glioblastoma Cell Proliferation.qRT-PCRwas used to determine BDNF-AS expression in GBM cells.RIP and RNA pull-down were conducted to detect the interactions among BDNF-AS, ADAR, and p53.ChIP and luciferase reporter assays were performed to detect transcriptional activation of BDNF-AS by p53.Importantly, we illustrated that BDNF-AS coupled with ADAR protein to potentiate stability of p53 mRNA and thus upregulate p53.We found that BDNF-AS was significantly downregulated in GBM cell lines, and its overexpression inhibited GBM cell growth, and promoted apoptosis.	31939089	RID04391	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Malignant glioma	NEAT1	MIR92B	negatively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000271748	NA	283131	693235	LINC00084|NCRNA00084|TncRNA|VINC	MIRN92B|hsa-mir-92b|mir-92b	Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes Apoptosis of Glioma Cells Via Downregulating MiR-92b. The expression of NEAT1 was compared between glioma tissues and adjacent tissues as well as between glioma cells and normal astrocytes using quantitative real-time polymerase chain reaction. The expression of NEAT1 was low in glioma tissues and cells compared to the normal ones.The interaction between NEAT1 and miR-92b was confirmed using RNA immunoprecipitation, RNA pull-down assay, and luciferase reporter assay.Our findings indicated that NEAT1 acts as a tumor suppressor in glioma cells, which provides a novel target in overcoming glioma growth.	31933377	RID04392	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Hypoxia-induced cardiomyocytes injury	TUG1	miR-133a	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Other	Injury	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Knockdown of TUG 1 suppresses hypoxia-induced apoptosis of cardiomyocytes by up-regulating miR-133a.TUG 1 and miR-133a expression levels in hypoxia-cultured human AC16 cardiomyocytes were examined by RT-qPCR.The expression levels of cleaved poly ADP ribose polymerase (PARP) and cleaved caspase-3 were evaluated by western blotWe found that TUG 1 expression was elevated, while miR-133a expression was reduced under hypoxic condition in AC16 cells.We identified that TUG 1 acted as a competing endogenous RNA to suppress miR-133a expression.TUG 1 knockdown relieved hypoxia-induced reduction of proliferation and repressed hypoxia-induced AC16 cell apoptosis by up-regulating miR-133a expression.	31926162	RID04393	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Epilepsy	miR-138-5p	KCNQ1OT1	negatively-E	luciferase reporter assay;StarBase	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Brain disease	miRNA	lncRNA	NA	NA	ENSG00000269821	GRCh38_11:2608328-2699994	NA	10984	NA	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	Long Non-coding RNA KCNQ1OT1 Contributes to Antiepileptic Drug Resistance Through the miR-138-5p/ABCB1 Axis in vitro.The results revealed that expression of P-glycoprotein (P-gp) and KCNQ1OT1 was significantly elevated in phenytoin-resistant HBMECs (HBMEC/PHT).Interestingly, bioinformatics prediction tools indicated miR-138-5p could directly target the transcripts of KCNQ1OT1 and NF-kB p65, and these results were confirmed by luciferase assays.our results suggested that KCNQ1OT1 contributes to AED resistance through the miR-138-5p/NF-kB/ABCB1 axis in HBMEC/PHT cells, and these results provide a promising therapeutic target for the treatment of medically intractable epilepsy.Interestingly, KCNQ1OT1 and NF-kB p65 harbored putative binding sites of miR-138-5p according to the StarBase2.0 bioinformatics database1. Luciferase assays were used to confirm the functional binding sites among KCNQ1OT1, NF-kB p65, and miR-138-5p.	31920517	RID04394	transcriptional regulation	chemoresistance		UP(BRCA);DATA(GSE111842)
Hepatocellular carcinoma	MALAT1	FOXA1	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	angiogenesis(-)	ceRNA(miR-3064-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000129514	NA	378938	3169	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HNF3A	MicroRNA-3064-5p sponged by MALAT1 suppresses angiogenesis in human hepatocellular carcinoma by targeting the FOXA1/CD24/Src pathway.miR-3064-5p was inversely correlated with lncRNA MALAT1 and FOXA1.MiR-3064-5p played an antiangiogenic role by inhibiting the FOXA1/CD24/Src pathway, whereas oncogenic MALAT1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-3064-5p to alleviate the suppressive effect on the FOXA1 pathway.HCC patients with high miR-3064-5p, low MALAT1, or low FOXA1 expression had a better prognosis with longer overall survival and recurrence-free survival.Taken together, miR-3064-5p exerts an antiangiogenic role by targeting the FOXA1/CD24/Src pathway but oncogenic lncRNA MALAT1 acts as a ceRNA to sponge miR-3064-5p.	31914639	RID04395	ceRNA or sponge	recurrence,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	PTENP1	PTEN	positively-E	bioinformatics analysis;luciferase reporter assay;RNA-pull down assay	upregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);epithelial to mesenchymal transition(-);apoptosis process(+)	ceRNA(miR-106b)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA PTENP1 inhibits cervical cancer progression by suppressing miR-106b.Bioinformatics analysis, luciferase reporter assay and RNA-pull down assay were performed to verify the association of miR-106b, PTEN, and PTENP1.It was found that the expressions of PTENP1 and PTEN were up-regulated and that of miR-106b were down-regulated in cervical cancer tissues and cells.Our results suggest that LncRNA PTENP1 inhibits cervical cancer progression by competitively binding to miR-106b, leading to promote PTEN expression, inhibit cell proliferation and EMT and induce cell apoptosis in cervical cancer cells.	31913710	RID04396	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Uveal melanoma	MALAT1	HOXC4	positively-E	bioinformatics analysis;luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(-)	sponge	regulation	NA	NA	NA	NA	Cancer	Uveal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198353	NA	378938	3221	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HOX3|HOX3E	Suppression of long noncoding RNA MALAT1 inhibits the development of uveal melanoma via microRNA-608-mediated inhibition of HOXC4.HOXC4 was found to be a gene upregulated in uveal melanoma, while knockdown of its expression resulted in suppression of uveal melanoma cell migration, proliferation, and invasion, as well as cell cycle progression.MALAT1 could upregulate the HOXC4 by binding to miR-608.MALAT1 downregulation functions to restrain the development of uveal melanoma via miR-608-mediated inhibition of HOXC4.	31913701	RID04397	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Parkinson's disease	SNHG1	PTEN	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cytotoxicity(+)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000171862	NA	23642	5728	LINC00057|lncRNA16|NCRNA00057|UHG	BZS|MHAM|MMAC1|PTEN1|TEP1	SNHG1 promotes MPP +-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p.Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCRThe interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis.Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. PTEN was identified as a direct target of miR-153-3p, and SNHG1 could serve as a competing endogenous RNA (ceRNA) of miR-153-3p to improve the expression of PTEN.SNHG1 aggravates MPP+-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.SNHG1 was found to activate PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p.	31907031	RID04398	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Myocardial infarction	NEAT1	ATG12	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-378a-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000145782	NA	283131	9140	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APG12|APG12L	Suppression of long noncoding RNA NEAT1 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-378a-3p.RT-qPCR was used to detect the expression of lncRNA NEAT1 and miR-378a-3p in peripheral blood and mouse cardiomyocytes of patients with myocardial infarction.Target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lncRNA NEAT1 and miR-378a-3p.lncRNA NEAT1 was highly expressed in peripheral blood and mouse cardiomyocytes of patients with myocardial infarction.lncRNA NEAT1 inhibited miR-378a-3p expression, and miR-378a-3p inhibited Atg12 expression, while lncRNA NEAT1 regulated expression of Atg12 and related autophagic factors via miR-378a-3p. lncRNA NEAT1 can regulate the proliferation of cardiomyocytes by regulating miR-378-3p/Atg12 axis, thus accelerating the occurrence and development of cardiomyocytes.	31904498	RID04399	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Cervical cancer	LINC00240	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cytotoxicity(-)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000224843	GRCh38_6:26956932-27059749	ENSG00000168610	NA	100133205	6774	bA373D17.1|C6orf41|NCRNA00240	APRF	Natural killer T cell cytotoxic activity in cervical cancer is facilitated by the LINC00240/microRNA-124-3p/STAT3/MICA axis.we found that LINC00240 expression was markedly increased in cervical cancer.LINC00240 expression was able to induce STAT3 expression via sponging of miR-124-3p, and showed a positive association with STAT3 expression in cervical cancer tissues.The target of LINC00240 was confirmed as microRNA(miR)-124-3p.Inhibition of miR-124-3p significantly enhanced cervical cancer progression via targeting of STAT3, which is greatly activated in tumor-infiltrating immune cells.LINC00240 overexpression suppressed the cytotoxic activity of NKT cells by affecting the STAT3/MICA axis.we found that LINC00240 expression promoted cervical cancer progression via induction of miR-124-3p/STAT3/MICA-mediated NKT cell tolerance.	31904481	RID04400	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Multiple myeloma	PVT1	MIR486-1	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Myeloma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000274705	NA	5820	619554	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MIR486|MIRN486|hsa-mir-486|hsa-mir-486-1|mir-486-1	Knockdown of long non-coding RNA plasmacytoma variant translocation 1 inhibits cell proliferation while promotes cell apoptosis via regulating miR-486-mediated CDK4 and BCAS2 in multiple myeloma.Lnc-Pvt1 expression was increased in MM cell lines (NCI-H929, U-266 and LP-1 cell lines) compared with human normal plasma cells.lnc-Pvt1 shRNA increased miR-486 expression compared with control shRNA.Lnc-Pvt1 knockdown inhibits cell proliferation and induces cell apoptosis through potentially regulating miR-486-mediated CDK4 and BCAS2 in MM.	31900844	RID04401	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Gastric cancer	LINC00163	AKAP12	positively-E	western blot;luciferase reporter assays;bioinformatics analysis	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-183)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234880	GRCh38_21:44989864-44994086	ENSG00000131016	NA	727699	9590	C21orf134|NCRNA00163|NLC1-A|NLC1A	AKAP250|SSeCKS	LINC00163 inhibits the invasion and metastasis of gastric cancer cells as a ceRNA by sponging miR-183 to regulate the expression of AKAP12.Real-time PCR (RT-qPCR), western blot dual-luciferase reporter assays and fluorescence in situ hybridization were conducted to explore the underlying mechanisms of competitive endogenous RNAs (ceRNAs).LINC00163 can be used as a ceRNA to inhibit the expression of miR-183, thus enhancing the anticancer effect of AKAP12.Our results demonstrated that weak LINC00163 expression in GC can sponge miR-183 to promote AKAP12.We established that the LINC00163/miR-183/AKAP12 axis plays an important role in GC invasion and metastasis and may be a potential biomarker and target for GC treatment.Based on TCGA data and bioinformatics analysis, we identified the LINC00163/miR-183/A-Kinase Anchoring Protein 12 (AKAP12) axis.	31894433	RID04402	ceRNA or sponge	metastasis		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Polycystic ovary syndrome	CYCSP5	IGF1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Reproductive system disease	Ovarian dysfunction	lncRNA	PCG	ENSG00000227735	GRCh38_1:244598391-244598687	ENSG00000017427	NA	360158	3479	HCP5	IGF|IGF-I|IGFI|MGF	LncRNA HCP5 promotes cell proliferation and inhibits apoptosis via miR-27a-3p/IGF-1 axis in human granulosa-like tumor cell line KGN.The results showed that downregulation of HCP5 suppressed cell proliferation through arresting cell cycle progression at G1 phase, and induced the apoptosis via activating mitochondrial pathway, while overexpression of HCP5 played the opposite effects in KGN cells.We predicted and confirmed miR-27a-3p was a directly target to HCP5 and it could directly bind with insulin-like growth factor-1 (IGF-1).The results demonstrated that downregulation and upregulation of miR-27a-3p could block the effects on the proliferation and apoptosis mediated by silencing and overexpressing HCP5 in KGN cellsmiR-27a-3p inhibitor remarkably reversed the IGF-1 decrease regulated by knocking down HCP5 and miR-27a-3p mimics inhibited the IGF-1 increase modulated by overexpressing HCP5 in KGN cells.	31891769	RID04403	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Ovarian cancer	NEAT1	FGF9	positively-E	luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);angiogenesis(+)	ceRNA(miR-365)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000102678	NA	283131	2254	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 promotes proliferation of ovarian cancer cells and angiogenesis of co-incubated human umbilical vein endothelial cells by regulating FGF9 through sponging miR-365: An experimental study.qRT-PCRand western blot tested the expressions of vascular endothelial growth factor (VEGF), angiogenin 1 (Ang-1) and matrix metalloproteinase 2 (MMP2).dual-luciferase reporter assay determined the targeted binding of NEAT1 and FGF9 to miR-365.LncRNA NEAT1 and FGF9 are over-expressed in OC cells.NEAT1 can down-regulate the expression of miR-365 while up-regulating that of FGF9.dual-luciferase reporter assay determined that NEAT1 competes with FGF9 for binding to miR-365.LncRNA NEAT1 up-regulates FGF9 by sponging miR-365, thus promoting OC cell proliferation and angiogenesis of HUVECs.	33545926	RID04404	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Breast cancer	XIC	CEBPA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000245848	NA	7502	1050	SXI1|XCE|XIST	C/EBP-alpha|CEBP	lncRNA-Xist/miR-101-3p/KLF6/C/EBPalpha axis promotes TAM polarization to regulate cancer cell proliferation and migration.In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)alpha, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1).Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPalpha and KLF6 expression. the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPalpha and KLF6 expression.	33510942	RID04405	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	XIC	CEBPA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	NA	NA	ENSG00000245848	NA	7502	1050	SXI1|XCE|XIST	C/EBP-alpha|CEBP	lncRNA-Xist/miR-101-3p/KLF6/C/EBPalpha axis promotes TAM polarization to regulate cancer cell proliferation and migration.In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)alpha, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1).Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPalpha and KLF6 expression. the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPalpha and KLF6 expression.	33510942	RID04406	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	PCAT1	DKC1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000130826	NA	100750225	1736	PCA1|PCAT-1|PiHL	Cbf5|DKC|dyskerin|NAP57|NOLA4|XAP101	LncRNA PCAT1 Interacts with DKC1 to Regulate Proliferation, Invasion and Apoptosis in NSCLC Cells via the VEGF/AKT/Bcl2/Caspase9 Pathway.we observed that lncRNA PCAT1 expression was upregulated in both human NSCLC tissues and cell lines, which was determined by qualitative polymerase chain reaction analysis.RNA pull-down assays with biotinylated probes and transcripts both confirmed that PCAT1 directly bounds with DKC1 that could also promote NSCLC cell proliferation and invasion and inhibit cell apoptosis.Moreover, the effects of PCAT1 and DKC1 on NSCLC functions are synergistic. lncRNA PCAT1 interacts with DKC1 to regulate proliferation, invasion, and apoptosis in NSCLC cells via the VEGF/AKT/Bcl-2/caspase9 pathway.	33461333	RID04407	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Lung cancer	SOX2-OT	SOX2	positively-E	gene silencing;ChIP-qPCR assay	upregulation	RT-qPCR	NA	NA	prognosis(-);chemoresistance(+)	NA	association	NA	Cisplatin;Erlotinib	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	NCRNA00043|SOX2OT	ANOP3|MCOPS3	LncRNA SOX2-OT regulates AKT/ERK and SOX2/GLI-1 expression, hinders therapy, and worsens clinical prognosis in malignant lung diseases.We evaluated the role of SOX2-OT/SOX2 and SOX2-OT/SOX2/GLI-1 axes using RT-qPCR;western blot, immunofluorescence analyses, gene silencing, cellular cytotoxic, and ChIP-qPCR assays on human cell lines, solid lung malignant tumors, and normal lung tissue. we identified that inhibition of SOX2-OT and reduced expression of SOX2/GLI-1 sensitizes lung cancer cells to EGFR/TKI-erlotinib or cisplatin-based treatment.we show that high co-expression of SOX2-OT/SOX2 transcripts and SOX2/GLI-1 proteins appears to correlate with a poor clinical prognosis and lung malignant phenotype.We detected that the SOX2-OT/SOX2/GLI-1 axis promotes resistance to tyrosine kinase inhibitor (TKI)-erlotinib and cisplatin-based therapy.	33433063	RID04408	expression association	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Renal fibrosis	LUCAT1	ZEB1	positively-E	siRNA transfection	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000148516	NA	100505994	6935	SCAL1|SCAT5	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Knockdown of the Long Noncoding RNA LUCAT1 Inhibits High-Glucose-Induced Epithelial-Mesenchymal Transition through the miR-199a-5p-ZEB1 Axis in Human Renal Tubular Epithelial Cells.The results of the quantitative reverse transcription PCR indicated that the LUCAT1 level in the HG group was increased, whereas the miR-199a-5p level was decreased.LUCAT1 and ZEB1 mRNA comprised the same microRNA response elements of miR-199a-5p.LUCAT1 knockdown had no effect on the miR-199a-5p level but decreased the HG-induced upregulation of ZEB1.LUCAT1 likely promotes HG-induced EMT through ZEB1 by sponging miR-199a-5p.	33426083	RID04409	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	HYOU1-AS	HYOU1	positively-E		upregulation		NA	NA	cancer progression(+)	interact with protein	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000262812	NA	NA	10525	NA	GRP-170|Grp170|HSP12A|IMD59|ORP-150|ORP150	Long non-coding antisense RNA HYOU1-AS is essential to human breast cancer development through competitive binding hnRNPA1 to promote HYOU1 expression.We identified an antisense lncRNA, HYOU1-AS, which is transcribed from the opposite strand of the hypoxia up-regulated 1 (HYOU1) gene, enriched in the nucleus and highly expressed in TNBC.we found that HYOU1-AS could promote the expression of HYOU1, a proliferative gene, through competitively binding to hnRNPA1, an RNA-binding protein, to relieve its post-transcriptional inhibition of the HYOU1 mRNA.our data indicated that the lncRNA HYOU1-AS promoted TNBC progression through upregulating HYOU1.	33422616	RID04410	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)
Osteonecrosis	NORAD	miR-26a-5p	negatively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell differentiation(-);apoptosis process(+)	NA	regulation	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	LncRNA NORAD promotes bone marrow stem cell differentiation and proliferation by targeting miR-26a-5p in steroid-induced osteonecrosis of the femoral head.Steroid-induced osteonecrosis of the femoral head (SONFH) is a devastating orthopedic disease, which seriously affects the quality of life of patients.The mRNA expression of NORAD, miR-26a-5p, OPG, RANK, and RANKL was detected by RT-qPCR.The dual-luciferase reporter gene assay was performed to confirm the binding between NORAD and miR-26a-5p.NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated.NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated.NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis by regulation of miR-26a-5p in hBMSCs.	33413642	RID04411	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Hepatocellular carcinoma	NEAT1	SMO	positively-E	StarBase;TargetScan;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell viability(+);cell migration(+);cell invasion(+);apoptosis process(+)	ceRNA(miR-503)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000128602	NA	283131	6608	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	FZD11|SMOH	Silencing of long non-coding RNA NEAT1 inhibits hepatocellular carcinoma progression by downregulating SMO by sponging microRNA-503.Reverse transcription-quantitative PCR was used to detect the expression levels of NEAT1, microRNA (miR)-503 and Smoothened (SMO) mRNA in HCC tissues and cells.StarBase and TargetScan were utilized to predict the target sequence between miR-503 and NEAT1 or SMO, the results of which were verified using a dual-luciferase reporter assay.The RNA expression level of NEAT1 and SMO was significantly elevated in HCC tissues and cells compared with that in the corresponding healthy tissues and cells, which was contrary to miR-503 expression level.Further studies found that miR-503 expression was negatively correlated with NEAT1 or SMO.It was also confirmed that NEAT1 directly interacted with miR-503 and miR-503 could bind to the 3'-untranslated region of SMO.These results demonstrated that downregulation of NEAT1 impeded the viability, migration, invasion and induced apoptosis through the NEAT1/miR-503/SMO axis in the HCC cell line.	33398379	RID04412	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Malignant glioma	NEAT1	BZW1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-98-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000082153	NA	283131	9689	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BZAP45|KIAA0005	LncRNA NEAT1 promotes glioma cancer progression via regulation of miR-98-5p/BZW1.Quantitative real-time PCR technology was used to determine the expression levels of relevant genes in tumor tissues and cell lines.A luciferase reporter assay was used to determine the interactions of the genes.We demonstrated that NEAT1 was upregulated glioma cells and negatively correlated with miR-98-5p in glioma tissues.BZW1 was identified as a direct target of miR-98-5p.We also identified that BZW1 was positively correlated with NEAT1 in glioma tissues.	33393590	RID04413	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761)
Primary ovarian insufficiency	PVT1	FOXO3	positively-E	RNA pull-down;RIP;luciferase reporter assay	downregulation	methylation-specific polymerase chain reaction	NA	NA	apoptosis process(+)	phosphorylation	binding/interaction	NA	NA	NA	NA	Reproductive system disease	Ovarian disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000118689	NA	5820	2309	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	AF6q21|FKHRL1|FOXO2|FOXO3A	Hypermethylation-mediated downregulation of lncRNA PVT1 promotes granulosa cell apoptosis in premature ovarian insufficiency via interacting with Foxo3a.The methylation level in the PVT1 promoter region was detected by methylation-specific polymerase chain reaction.The interaction between PVT1 and forkhead box class O3A (Foxo3a) was confirmed by RNA pull-down and RNA immunoprecipitation assays.The effect of PVT1 on transcription activity of Foxo3a was detected by luciferase reporter assay.The expression of PVT1 was low in the POI ovarian tissues compared with the controls, and such a low expression was related to the hypermethylation of the PVT1 promoter.We determined that PVT1 could bind with Foxo3a and that downregulating PVT1 by small interfering RNAs inhibited Foxo3a phosphorylation by promoting SCP4-mediated Foxo3a dephosphorylation, resulting in an increase in Foxo3a transcription activity.	33393111	RID04414	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(BRCA);DATA(GSE51827,GSE86978)
Colorectal cancer	THCYTX	miR-590-5p	negatively-E	luciferase report assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	NA	NA	NA	NA	84434	NA	FTX	NA	LncRNA FTX Promotes Colorectal Cancer Cells Migration and Invasion by miRNA-590-5p/RBPJ Axis.In this study, qRT-PCRwas performed to detect the expression of FTX, miR-590-5p and Recombination signal binding protein for immunoglobulin kappa J region (RBPJ) in CRC tissues or cells.Luciferase report assay was performed to verify the relation between miR-590-5p and FTX or RBPJ.It was found that FTX was upregulated in CRC tissues and cells.Knockdown of FTX or overexpression of miR-590-5p can inhibit the proliferation, migration, and invasion of CRC cells.Meanwhile, miR-590-5p was the target of FTX, and RBPJ was the direct target of miR-590-5p.proliferation, migration, and invasion	33389283	RID04415	expression association	NA		
Renal cell carcinoma	HCP5	MAPK1	positively-E	RIP;western blot	upregulation	qRT-PCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000100030	NA	10866	5594	D6S2650E|P5-1	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Effects of LncRNA HCP5/miR-214-3p/MAPK1 Molecular Network on Renal Cell Carcinoma Cells.The expression of HCP5 in human renal cell carcinoma (RCC) was detected by real-time quantitative PCR.The molecular mechanism of LncRNAs was explored by RNA immunoprecipitation and western blot.qRT-PCRrevealed that HCP5 was enhanced in neoplasm tissues of ccRCC patients and correlated with the metastatic characteristics of RCC.Mechanically, HCP5 inhibited the growth and metastasis of ccRCC cells by regulating miR-214-3p/MAPK1 axis.LncRNA or ceRNA regulates gene expression by competitively binding microRNA (miR).miR-214-3p Mediated by HCP5 Regulated the Expression of MAPK1	33380840	RID04416	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	MIR205HG	SOX4	positively-E	cell transfection	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-214)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000124766	NA	642587	6659	LINC00510	NA	LncRNA MIR205HG Drives Esophageal Squamous Cell Carcinoma Progression by Regulating miR-214/SOX4 Axis.We used qRT-PCRto detect the expression level of MIR205HG, miR-214, and SOX4 in human ESCC tissues and cell lines. Here, we found MIR205HG was substantially up-regulated in ESCC, and there was a positive correlation between MIR205HG expression and tumor size and lymphatic metastasis of ESCC patients.We also found that SOX4 was a direct target mRNA of miR-214, and MIR205HG could act as a molecular sponge to regulate SOX4 expression in ESCC.Taken together, our findings demonstrate that MIR205HG promotes ESCC progression by regulating the miR-214/SOX4 axis.MIR205HG Promotes ESCC Cell Migration via Targeting miR-214.MIR205HG Upregulates SOX4 Expression by miR-214.	33376358	RID04417	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	CASC9	miR-424-5p	negatively-E	DIANA-LncBase V2;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000249395	GRCh38_8:75120409-75352327	NA	NA	101805492	NA	ESCCAL-1|linc-JPH1|LINC00981	NA	LncRNA CASC9 promotes proliferation, migration and inhibits apoptosis of hepatocellular carcinoma cells by down-regulating miR-424-5p.Higher expression of CASC9 was observed in HCC tissues/ cells than in adjacent normal tissues/ human hepatic epithelial cells, and was closely linked to poor prognosis of HCC, tumor size, TNM stage, differentiation degree, lymph node metastasis and alpha-fetoprotein (AFP).CASC9 was negatively correlated with miR-424-5p.CASC9 promoted proliferation, invasion and migration and inhibited apoptosis in HCC cells by inhibiting miR-424-5p.	33346094	RID04418	expression association	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	
Esophagus squamous cell carcinoma	XIST	CCND1	positively-E	starBase v2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000110092	NA	7503	595	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA XIST promotes the progression of esophageal squamous cell carcinoma through sponging miR-129-5p and upregulating CCND1 expression.qRT-PCRassay was used to determine the levels of XIST and miR-129-5p.Bioinformatic analysis was performed using starBase v2.0 software.Dual-luciferase reporter and RNA immunoprecipitation assays were employed to confirm the interaction between XIST and miR-129-5p or miR-129-5p and CCND1.Our results indicated that XIST was upregulated and miR-129-5p was downregulated in ESCC.Moreover, XIST directly interacted with miR-129-5p and repressed miR-129-5p expression.MiR-129-5p mediated the regulatory effect of XIST on ESCC cell progression in vitro, and XIST promoted CCND1 expression by sponging miR-129-5p.Our findings suggested that XIST silencing repressed the progression of ESCC at least partly through regulating the miR-129-5p/CCND1 axis.	33345719	RID04419	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	XIST	miR-129-5p	negatively-E	starBase v2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Long non-coding RNA XIST promotes the progression of esophageal squamous cell carcinoma through sponging miR-129-5p and upregulating CCND1 expression.qRT-PCRassay was used to determine the levels of XIST and miR-129-5p.Bioinformatic analysis was performed using starBase v2.0 software.Dual-luciferase reporter and RNA immunoprecipitation assays were employed to confirm the interaction between XIST and miR-129-5p or miR-129-5p and CCND1.Our results indicated that XIST was upregulated and miR-129-5p was downregulated in ESCC.Moreover, XIST directly interacted with miR-129-5p and repressed miR-129-5p expression.MiR-129-5p mediated the regulatory effect of XIST on ESCC cell progression in vitro, and XIST promoted CCND1 expression by sponging miR-129-5p.Our findings suggested that XIST silencing repressed the progression of ESCC at least partly through regulating the miR-129-5p/CCND1 axis.	33345719	RID04420	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Esophageal cancer	LINC-ROR	LMNB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000176619	NA	100885779	84823	lincRNA-RoR|lincRNA-ST8SIA3|ROR	LMN2	ROR promotes the proliferation and migration of esophageal cancer through regulating miR-145/LMNB2 signal axis.This study performed dual-luciferase reporter assay to evaluate the binding between miR-145 and ROR as well as miR-145 and LMNB2.Gene expression in EC tissues and cells were detected using quantitative real-time PCR (qRT-PCR assay.ROR and LMNB2 were up-regulated and miR-145 was down-regulated in EC tissues and cells.LMNB2 which is regulated by ROR and miR-145 was highly expressed in EC and promoted the proliferation and migration of EC in vitro and in vivo.The proliferation and migration of EC cells were promoted by overexpression of of ROR or LMNB2.	33312362	RID04421	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	ZFPM2-AS1	TRIM24	positively-E	miRBase;luciferase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	cancer progression(+)	sponge	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000122779	NA	102723356	8805	SCAT3	PTC6|RNF82|TF1A|TIF1|TIF1A|TIF1ALPHA|hTIF1	Long non-coding RNA ZFPM2-AS1 promotes colorectal cancer progression by sponging miR-137 to regulate TRIM24.Expression levels of ZFPM2-AS1 in tissue and CRC cells were measured by reverse transcription-quantitative PCR.bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation assay and western blot were performed to explore the possible underlying mechanism.The expression levels of ZFPM2-AS1 were significantly upregulated in tissue samples from patients with CRC and CRC cell lines compared with normal tissue and normal human colorectal mucosa cell line. it was found that ZFPM2-AS1 positively regulated tripartite motif containing 24 (TRIM24) expression by sponging miR-137.ZFPM2-AS1 in CRC progression, miRBase was used to predict potential target miRNAs for ZFPM2-AS1.	33300060	RID04422	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Malignant glioma	DANCR	EZH2	positively-E	RIP;RNA pull-down;ChIP	upregulation	RT-PCR;western blot	NA	NA	cell invasion(+);cell migration(+);cell proliferation(+);apoptosis process(-)	interact with protein	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000106462	NA	57291	2146	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	ENX-1|EZH1|KMT6|KMT6A	LncRNA ANCR promotes glioma cells invasion, migration, proliferation and inhibits apoptosis via interacting with EZH2 and repressing PTEN expression.Expression of lncRNA ANCR, enhancer of zeste homolog 2 (EZH2), and phosphatase and tensin homolog (PTEN) in glioma tissues and cells was determined by RT-PCRor western blot assay.The relationships between ANCR and EZH2, and between EZH2 and PTEN were confirmed through RIP, RNA pull-down, and chromatin immunoprecipitation assays.Our results indicated that ANCR and EZH2 were upregulated and PTEN was downregulated in glioma tissues and cell lines.ANCR expression was positively related to EZH2 expression, while PTEN expression was negatively related to ANCR/EZH2 expression.EZH2 interacted with ANCR in glioma cells.we have found that restrained ANCR could repress invasion, migration, and proliferation, as well as promote apoptosis of glioma cells through interacting with EZH2 and regulating the expression of PTEN, offering an effective therapeutic target for patients with glioma.	33293663	RID04423	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Thyroid cancer	MAPKAPK5-AS1	YWHAH	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000234608	GRCh38_12:111839758-111842902	ENSG00000128245	NA	51275	7533	C12orf47|FLJ39616	YWHA1	IncRNA MAPKAPK5-AS1 promotes proliferation and migration of thyroid cancer cell lines by targeting miR-519e-5p/YWHAH.Results of RT-qPCR analysis demonstrated that MAPKAPK5-AS1 was more highly expressed in thyroid cancer cells compared to normal cells.Mechanistically, we found that miR-519e-5p was negatively regulated by MAPKAPK5-AS1 and that tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta (YWHAH) was a target of miR-519e-5p. rescue assays demonstrated that downregulation of MAPKAPK5-AS1 expression inhibited cell proliferation, migration, and invasion and promoted apoptosis by sponging miR-519e-5p, thereby increasing YWHAH expression.	33272009	RID04424	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE75367)
Lung cancer	LINC00485	MYC	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000258169	GRCh38_12:102809280-102824399	ENSG00000136997	NA	283432	4609	NA	bHLHe39|c-Myc|MYCC	Long intergenic non-coding RNA Linc00485 promotes lung cancer progression by modulating miR-298/c-Myc axis.we found that the expression of Linc00485 was significantly increased in human lung cancer tissue and associated with malignant phenotypes, including tumour-node-metastasis (TNM) stage, metastasis and relapse.Mechanistically, Linc00485 regulated the expression of c-Myc by directly binding to miR-298;Overall, these findings indicate that Linc00485 overexpression down-regulates miR-298, resulting in the up-regulation of c-Myc and thereby promoting the development of lung cancer.	33237626	RID04425	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Osteoarthritis	GAS5	MIR137	negatively-E		upregulation		NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Arthritis	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000284202	NA	60674	406928	NCRNA00030|SNHG2	hsa-mir-137|miR-137|MIRN137	LncRNA GAS5 induces chondrocyte apoptosis by down-regulating miR-137.GAS5 was up-regulated in serum and cartilage tissues of KOA patients, and down-regulation of GAS5 could inhibit the apoptosis process of chondrocytes and promote proliferation.MiR-137 was down-regulated in samples of KOA patients and was negatively regulated by GAS5.GAS5 induced apoptosis of chondrocytes and inhibited its proliferation through targeted down-regulating miR-137.GAS5 is up-regulated in KOA serum, cartilage tissues and cells, and can induce chondrocyte apoptosis through down-regulating miR-137.	33215412	RID04426	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	ROR1-AS1	MIR4686	negatively-E	microarray;luciferase assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000223949	GRCh38_1:64094379-64171342	ENSG00000265258	NA	101927034	100616126	NA	NA	Exosomal lncRNA ROR1-AS1 Derived from Tumor Cells Promotes Glioma Progression via Regulating miR-4686.microarray is used to identify the lncRNAs that are differentially expressed in glioma.The expression of long non-coding RNA (lncRNA) ROR1-AS1 and miR-4686 was detected by qRT-PCR Luciferase assay and RIP assay were used to identify the relationship between lncRNA ROR1-AS1 and miR-4686. ROR1-AS1 was up-regulated in glioma tissues, and the high expression of ROR1-AS1 indicated a poor prognosis in glioma patients.Furthermore, ROR1-AS1 acted as a sponge of miR-4686 and inhibited its expression.Our study suggested tumor cells derived exo-ROR1-AS1 promoted glioma progression by inhibiting miR-4686, which might be a potential therapeutic target for glioma clinical treatment.	33204092	RID04427	ceRNA or sponge	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Gastric cancer	SUMO1P3	WNT1	positively-E	cell transfection	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000235082	GRCh38_1:160317403-160317706	ENSG00000125084	NA	474338	7471	NA	INT1	LncRNA SUMO1P3 regulates the invasion, migration and cell cycle of gastric cancer cells through Wnt/beta-catenin signaling pathway.The expression of SUMO1P3 in GC tissues and cells were detected by RT-qPCR.The expression of SUMO1P3 was significantly upregulated in GC tissues and cell lines.Further study showed that downregulation of SUMO1P3 significantly reduced the expressions of Wnt1, beta-catenin, c-myc, and Cyclin D1 in SGC-7901 and MKN45 cells.UMO1P3 may promote invasion, migration, and cycle progression of SGC-7901 and MKN45 cells by enhancing the Wnt/beta-catenin pathway.	33179980	RID04428	expression association	NA	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	
Gastric cancer	SUMO1P3	CTNNB1	positively-E	cell transfection	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000235082	GRCh38_1:160317403-160317706	ENSG00000168036	NA	474338	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA SUMO1P3 regulates the invasion, migration and cell cycle of gastric cancer cells through Wnt/beta-catenin signaling pathway.The expression of SUMO1P3 in GC tissues and cells were detected by RT-qPCR.The expression of SUMO1P3 was significantly upregulated in GC tissues and cell lines.Further study showed that downregulation of SUMO1P3 significantly reduced the expressions of Wnt1, beta-catenin, c-myc, and Cyclin D1 in SGC-7901 and MKN45 cells.UMO1P3 may promote invasion, migration, and cycle progression of SGC-7901 and MKN45 cells by enhancing the Wnt/beta-catenin pathway.	33179980	RID04429	expression association	NA	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Kidney injury	MEG3	HMGB1	positively-E	luciferase reporter assay;qRT-PCR;western blot analysis	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000189403	NA	55384	3146	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DKFZp686A04236|HMG1|HMG3|SBP-1	MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR-129-5p/HMGB1 axis.In HK-2 cells, expression of MEG3 detected using quantitative real-time polymerase chain reaction (qRT-PCR, was significantly upregulated after CoCl2 treatment and hypoxia/reoxygenation treatment.Together with qRT-PCRand western blot a dual-luciferase reporter gene assay was used to verify the interactions among MEG3, miR-129-5p, and HMGB1.The results demonstrated that in HK-2 cells, miR-129-5p was a target of MEG3, and HMGB1 served as a target gene of miR-129-5p.compared with the control group, the expression levels of MEG3 and HMGB1 in samples derived from AKI patients were remarkably upregulated, and the expression of miR-129-5p was downregulated. taken together, we conclude that the overexpression of MEG3 induced by I/R promotes apoptosis of TECs via regulating the miR-129-5p/HMGB1 axis.	33175458	RID04430	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Osteoporosis	LINC01535	BMP2	positively-E		upregulation		NA	NA	cell differentiation(+)	sponge	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226686	GRCh38_19:37251867-37265547	ENSG00000125845	NA	101927667	650	NA	BMP2A	Osteoporosis is a debilitating skeletal disease that causes bones to collapse and is accompanied by a high risk of bone fracture.lncRNA LINC01535 upregulates BMP2 expression levels to promote osteogenic differentiation via sponging miR-3619-5p.The present study showed that the expression levels of LINC01535 were upregulated upon increasing osteogenic differentiation time.Using bioinformatics analysis, LINC01535 was discovered to have complementary binding sites for microRNA (miR)-3619-5p, and further experiments demonstrated that LINC01535 functioned as a sponge of miR-3619-5p. bone morphogenetic protein 2 (BMP2) was confirmed to be a target of miR-3619-5p.The results revealed that LINC01535 regulated the expression levels of BMP2 via sponging miR-3619-5p.the findings of the present study suggested that LINC01535 may accelerate the osteogenic process of hBMSCs via targeting the miR-3619-5p/BMP2 axis, which may offer an innovative therapeutic method for osteoporosis.	33174047	RID04431	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Cholangiocarcinoma	TUG1	miR-29a	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	LncRNA TUG1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells by Inhibiting miR-29a.qRT-PCRwas performed to detect TUG1 and miR-29a expression in the cholangiocarcinoma tissues and cells.Dual luciferase reporter gene assay (DLRGA) was performed to confirm the correlation of TUG1 with miR-29a. TUG1 was highly expressed while miR-29a was poorly expressed in cholangiocarcinoma cells.TUG1 expression was negatively correlated with miR-29a expression, and TUG1 had a relatively high diagnostic value for cholangiocarcinoma.It can promote the growth and metastasis of cholangiocarcinoma cells by inhibiting miR-29a, so it may be a new target for diagnosing and treating cholangiocarcinoma.	33173343	RID04432	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Cervical cancer	GATA6-AS	MIR205	negatively-E	transient transfection	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	miRNA	NA	NA	ENSG00000284485	NA	NA	406988	NA	MIRN205|mir-205	LncRNA GATA6-AS inhibits cancer cell proliferation and promotes cancer cell apoptosis in cervical cancer by down-regulating miR-205.To explore the expression of GATA6-AS, RT-qPCR was performed to detect GATA6-AS in plasma of 65 CSCC patients and 58 healthy females.We found that plasma GATA6-AS expression was down-regulated in CSCC patients than that in healthy females, and HPV infection did not significantly affect the plasma expression of GATA6-AS.The expression of miR-205 in plasma was also found to be up-regulated in CSCC patients than that in healthy females and inversely correlated with the expression of GATA6-AS in CSCC patients.Taken together, these results suggest that GATA6-AS may inhibit cell proliferation and promote cell apoptosis in CSCC by down-regulating miR-205.	33167959	RID04433	expression association	NA		
Breast cancer	LL22NC03-N64E9.1	EZH2	positively-E	RIP;CHIP;rescue experiment	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000271127	GRCh38_22:15794901-15797909	ENSG00000106462	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	Upregulated Long Non-Coding RNA LL22NC03-N64E9.1 Promotes the Proliferation and Migration of Human Breast Cancer Cells by Silencing Kruppel-Like Factor 2 Expression.qRT-PCRwas used to assess the relative expression of LL22NC03-N64E9.1 in BC tissues.RNA immunoprecipitation, chromosome immunoprecipitation assay and rescue experiments were performed to analyze the association of LL22NC03-N64E9.1 with target proteins and genes in BC cells.We identified that LL22NC03-N64E9.1 is an oncogene, upregulated in BC, which was verified in a cohort of 48 pairs of BC tissues.In terms of the mechanism, LL22NC03-N64E9.1 acted on the enhancer of zeste homolog 2 (EZH2) by direct binding, which promoted BC cell growth.Furthermore, in the promoters of KLF2, the trimethylation of H3K27 could be regulated by LL22NC03-N64E9.1 as the mediator.Relying on the LL22NC03-N64E9.1/EZH2/KLF2 pathway, the lncRNA LL22NC03-N64E9.1 was significantly associated with BC development and could, therefore, be a potential therapeutic target to block BC growth.	33149681	RID04434	expression association	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	SNHG3	TRPC3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;cell transfection	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-339-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000138741	NA	8420	7222	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	NA	Long-Chain Non-Coding RNA SNHG3 Promotes the Growth of Ovarian Cancer Cells by Targeting miR-339-5p/TRPC3 Axis.A qRT-PCRassay was carried out to detect the level of SNHG3 in OC tissues, serum and cells, a CCK-8 assay to measure the proliferation of OC cells, a transwell assay to measure the invasion and migration of OC cells, and a flow cytometry to detect the cell cycle distribution and apoptosis rate of OC cells.SNHG3 was overexpressed in OC tissues, serum, and cells, and the overexpression in serum indicated a poor prognosis of patients.SNHG3 can be adopted as a marker for diagnosis and prognosis evaluation of OC and it plays a role in the progression of OC by enabling the miR-339-5p sponge to regulate TRPC3 expression.MiR-339-5p is the Inhibitory Target of SNHG3	33149611	RID04435	ceRNA or sponge	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Tongue squamous cell carcinoma	HEIH	HDGF	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-3619-5p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831618	ENSG00000143321	NA	100859930	3068	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	HMG1L2	Exosomal lncRNA HEIH promotes cisplatin resistance in tongue squamous cell carcinoma via targeting miR-3619-5p/HDGF axis.HEIH expression was significantly upregulated in SCC4/DDP cells.HEIH acted as a competing endogenous RNA (ceRNA) for miR-3619-5p to upregulate HDGF expression.Exosomal HEIH acted as a ceRNA for miR-3619-5p to upregulate HDGF, thereby promoting DDP resistance in TSCC cells.	33130420	RID04436	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Malignant glioma	KCNQ1OT1	YY1AP1	positively-E	luciferase reporter assay	upregulation	RT-qPCR;western blot	NA	NA	cell proliferation(+);cell invasion(+)	sponge	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000163374	NA	10984	55249	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	HCCA2|YAP|YY1AP	lncRNA KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the miR-375/YAP pathway.Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription-quantitative PCR and western blot were used to investigate the expression profiles of key molecules.The results indicated that KCNQ1OT1 was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis.The effects of KCNQ1OT1 on migration and invasion were partially attributed to enhanced Yes-associated protein (YAP) expression levels and epithelial-mesenchymal transition (EMT) signaling.Furthermore, microRNA (miR)-375 functioned as a link between KCNQ1OT1 and YAP in regulating cell proliferation.	33125099	RID04437	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Chronic obstructive pulmonary disease	HOXA-AS2	NOTCH1	positively-E	cell transfection	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000148400	NA	285943	4851	HOXA3as	TAN1	microarray Analysis of Long Non-Coding RNAs in Lung Tissues of Patients with COPD and HOXA-AS2 Promotes HPMECs Proliferation via Notch1.We analyzed lncRNA profiles of three non-COPD and seven COPD patients' lungs via microarray and then validated the expression of the top differentially expressed lncRNAs by using real-time polymerase chain reaction (PCR).real-time PCR confirmed that HOXA-AS2 was downregulated in COPD patients.Knocking down HOXA-AS2 inhibited HPMECs proliferation and the expression of Notch1 in HPMECs.Our results demonstrated that differentially expressed lncRNAs may act as potential molecular biomarkers for the diagnosis of COPD, and HOXA-AS2 was involved in the pathogenesis of COPD by regulating HPMECs proliferation via Notch1, which may provide a new approach for COPD treatment.	33116460	RID04438	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nephroblastoma	DLEU1	RANBP2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000153201	NA	10301	5903	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	ADANE|ANE1|NUP358	[Deleted in lymphocytic leukemia 1 promoted proliferation and apoptosis of nephroblastoma cells through regulating miR-513a-5p and RANBP2 pathway].Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expressions of DLEU1, miR-513a-5p, RANBP2 in nephroblastoma tissues, normal adjacent tissues, normal kidney cell HK2, and hemangioblastoma cell GHINK-1.Dual luciferase report test was used to detect the luciferase activity of cells.The expression levels of DLEU1, miR-513a-5p and RANBP2 in adjacent tissues were 1.02 0.08, 1.01 0.06, 1.00 0.05, respectively, significantly lower than 5.16 0.24, 0.23 0.02, 1.67 0.09 in nephroblasts tumor tissues .Overexpression of DLEU1 significantly reduced the apoptosis rate .Overexpression of RANBP2 significantly reduced the apoptosis rate.Compared with the miR-NC group , the luciferase activity of DLEU1-WT  and RANBP2-WT  in miR-513a-5p group were significantly reduced .Simultaneous overexpression of pcDNA-DLEU1 and miR-513a-5p in GHINK-1 cells significantly reduced the apoptosis rate .Simultaneous overexpression of miR-513a-5p and RANBP2 in GHINK-1 cells significantly reduced the apoptosis rate .The long-chain non-coding RNA (lncRNA) DLEU1 can promote the proliferation and inhibit the apoptosis of nephroblastoma cells.	33113626	RID04439	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE67939,GSE86978,GSE41245)
Nephroblastoma	DLEU1	miR-513a-5p	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	[Deleted in lymphocytic leukemia 1 promoted proliferation and apoptosis of nephroblastoma cells through regulating miR-513a-5p and RANBP2 pathway].Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expressions of DLEU1, miR-513a-5p, RANBP2 in nephroblastoma tissues, normal adjacent tissues, normal kidney cell HK2, and hemangioblastoma cell GHINK-1.Dual luciferase report test was used to detect the luciferase activity of cells.The expression levels of DLEU1, miR-513a-5p and RANBP2 in adjacent tissues were 1.02 0.08, 1.01 0.06, 1.00 0.05, respectively, significantly lower than 5.16 0.24, 0.23 0.02, 1.67 0.09 in nephroblasts tumor tissues .Overexpression of DLEU1 significantly reduced the apoptosis rate .Overexpression of RANBP2 significantly reduced the apoptosis rate.Compared with the miR-NC group , the luciferase activity of DLEU1-WT  and RANBP2-WT  in miR-513a-5p group were significantly reduced .Simultaneous overexpression of pcDNA-DLEU1 and miR-513a-5p in GHINK-1 cells significantly reduced the apoptosis rate .Simultaneous overexpression of miR-513a-5p and RANBP2 in GHINK-1 cells significantly reduced the apoptosis rate .The long-chain non-coding RNA (lncRNA) DLEU1 can promote the proliferation and inhibit the apoptosis of nephroblastoma cells.	33113626	RID04440	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Gastric cancer	miR-103a	NEAT1	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	The Long Non-Coding RNA NEAT1 Promotes Gastric Cancer Cell Proliferation and Invasion by Regulating miR-103a/ STAMBPL1 Axis.The correlation between NEAT1, miR-103a and STAMBPL1 was determined by luciferase reporter assay.LncRNA NEAT1 was found to be up-regulated in GC cell lines.NEAT1 was targeted and inhibited by miR-103a and acted as an oncogene, which promoted the malignant behavior of GC cells.	33111649	RID04441	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Renal cell carcinoma	SNHG4	RUNX2	positively-E	Lnclocator;StarBase;UALCAN plotter;luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell invasion(+);cell proliferation(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000124813	NA	724102	860	NCRNA00059|U19H	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Long noncoding RNA SNHG4 promotes renal cell carcinoma tumorigenesis and invasion by acting as ceRNA to sponge miR-204-5p and upregulate RUNX2.Quantitative real-time polymerase chain reaction (qRT-PCR was performed to examine expression levels of SNHG4 in RCC tissue samples and cell lines.The interaction among SNHG4, miR-204-5p, and RUNX2 was verified by bioinformatic analysis, a luciferase gene report, qRT-PCR western blot and RNA immunoprecipitation assays.SNHG4 was highly expressed in RCC tissue samples and cell lines, and its upregulation was significantly involved in node involvement, distant metastasis, and reduced overall and relapse-free survival of patients with RCC.Mechanistically, SNHG4 functioned as a competing endogenous RNA (ceRNA) for sponging miR-204-5p, leading to the upregulation of its target RUNX2 to promote RCC cell proliferation and invasion.Data mining analyses were conducted following the Lnclocator [23], StarBase 3.0 (http://starbase.sysu.edu.cn/), and UALCAN plotter (http://ualcan.path. uab.edu/index.html) databases.	33088220	RID04442	ceRNA or sponge	metastasis	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic retinopathy	MIAT	CASP1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell pyroptosis(+)	sponge	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000137752	NA	440823	834	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ICE|IL1BC	MIAT and CASP1 expression were substantially increased, while that of miR-342-3p was decreased in AGE-BSA-treated HRPCs.Long noncoding RNA MIAT regulates primary human retinal pericyte pyroptosis by modulating miR-342-3p targeting of CASP1 in diabetic retinopathy.Luciferase reporter assay results demonstrated binding between MIAT and miR-342-3p, as well as between miR-342-3p and CASP1.MIAT antagonized the effect of miR-342-3p on the depression of its target CASP1 and promoted AGE-BSA-induced pericyte pyroptosis.	33065089	RID04443	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Rheumatoid arthritis	NEAT1	MDM2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	sponge	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000135679	NA	283131	4193	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	HDM2|MGC5370	Delivery of Long Non-coding RNA NEAT1 by Peripheral Blood Monouclear Cells-Derived Exosomes Promotes the Occurrence of Rheumatoid Arthritis via the MicroRNA-23a/MDM2/SIRT6 Axis.LncRNA NEAT1 was found to be highly expressed in RA, and PBMCs-derived exos contributed to RA development by delivering lncRNA NEAT1.LncRNA NEAT1 shuttled by PBMC-derived exos promoted FLS proliferation and inflammation through regulating the MDM2/SIRT6 axis.This study highlights that lncRNA NEAT1 shuttled by PBMC-derived exos contributes to RA development with the involvement of the miR-23a/MDM2/SIRT6 axis.It is known that lncRNA NEAT1 can inhibit the expression of miR-23a .miR-23a Inhibits Inflammation in RA by Suppressing MDM2	33042992	RID04444	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lumbar disc herniation	TUG1	miR-26a	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Lumbar disc herniation	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	LncRNA TUG1 promotes the intervertebral disc degeneration and nucleus pulposus cell apoptosis though modulating miR-26a/HMGB1 axis and regulating NF-kB activation.The expression of TUG1 and HMGB1 protein in human degenerative disc NP tissues and NPCs was significantly increased, while the level of miR-26a was significantly decreased.TUG1 acted as an endogenous sponge to down-regulate the expression of miR-26a in NPCs by direct binding to miR-26a.TUG1 could promote the apoptosis and ECM degradation of degenerated intervertebral disc NPCs by regulating the miR-26a/HMGB1, which may be involved in the activation of NF-kB pathway.	33042430	RID04445	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Skin melanoma	TPT1-AS1	miR-671-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	binding/interaction	RNA-RNA	Guizhi Fuling Pills	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000170919	GRCh38_13:45341345-45417975	NA	NA	100190939	NA	NA	NA	Guizhi Fuling pills inhibit the proliferation, migration and invasion of human cutaneous malignant melanoma cells by regulating the molecular axis of LncRNA TPT1-AS1 / miR-671-5p.qRT-PCRwas used to detect the expression of TPT1-AS1 and miR-671-5p.The dual-luciferase report experiment verified the targeting relationship of TPT1-AS1, miR-671-5p.Guizhi Fuling Pill may reduce the proliferation, migration and invasion of human cutaneous malignant melanoma cells by down-regulating the expression of TPT1-AS1 and up-regulating the expression of miR-671-5p.The dual-luciferase report experiment confirmed that TPT1-AS1 could target and bind to miR-671-5p and could regulate the expression and activity of miR-671-5p.	33040829	RID04446	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	
Osteoarthritis	NEAT1	PLA2G4A	positively-E	TargetScan;starBase;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000116711	NA	283131	5321	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	cPLA2-alpha|PLA2G4	LncRNA NEAT1 regulates chondrocyte proliferation and apoptosis via targeting miR-543/PLA2G4A axis.The targeted relationship among nuclear enriched abundant transcript 1 (NEAT1), microRNA-543 (miR-543) and PLA2G4A was predicted on TargetScan V7.2 and starBase and validated by performing dual-luciferase reporter assay.High-expressed NEAT1 was detected in OA cartilage and chondrocytes.NEAT1 was negatively correlated with miR-543 and was low-expressed in OA cartilage and PLA2G4A was negatively correlated with miR-543 and was high-expressed in OA cartilage.NEAT1 could sponge miR-543 to induce PLA2G4A expression, inhibit chondrocyte proliferation and promote apoptosis.	33040229	RID04447	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE51827)
Atherosclerosis	MALAT1	STAT3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168610	NA	378938	6774	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APRF	LncRNA MALAT1 Promotes STAT3-Mediated Endothelial Inflammation by Counteracting the Function of miR-590.The interactions among MALAT1, miR-590, and STAT3 were predicted by bioinformatics analysis and verified by qRT-PCR western blot, or dual-luciferase reporter assay.MALAT1 was upregulated in ECs treated with ox-LDL, and knockdown of MALAT1 significantly inhibited ox-LDL-induced inflammation.Mechanistically, MALAT1 could directly downregulate miR-590, and miR-590 could bind to the 3'-UTR of STAT3 to repress its expression.Thus, MALAT1 serves as a proinflammatory lncRNA in ECs through regulating the miR-590/STAT3 axis, suggesting that MALAT1 may be a promising therapeutic target during the treatment of atherosclerosis.	33022677	RID04448	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	LINC00858	RABL3	negatively-E	bioinformatic analysis;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000144840	NA	170425	285282	CRCAL-2	MGC23920	Long non-coding RNA LINC00858 promotes cells proliferation and invasion through the miR-153-3p/Rabl3 axis in hepatocellular carcinoma.The relative expression levels of LINC00858 in HCC samples and adjacent non-tumor samples were determined by qRT-PCRBioinformatic analysis and the following Luciferase activity reporter assay were utilized to explore the downstream molecules of LINC00858.Our results showed that LINC00858 was highly expressed in both HCC tissues and cell lines. LINC00858 was found to act as a sponge of miR-153-3p, which directly bound to Rabl3 and regulated the Rabl3 expression.inhibition of miR-153-3p counteracted the effects of LINC00858 knockdown on proliferation and invasion of HCC cells. the overexpression of Rabl3 rescued the effects of miR-153-3p on cell proliferation and invasion of HCC cells.	33015775	RID04449	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)
Esophagus squamous cell carcinoma	LINC00673	CDKN2C	negatively-E	western blot;ChIP;ChIP-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000123080	NA	100499467	1031	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	INK4C|p18	LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation.The expression levels of LINC00673 and its potential target genes were assessed by quantitative real-time polymerase chain reaction (qPCR) in ESCC surgical specimens and ESCC cell lines.The molecular mechanisms underlying LINC00673 were explored via western blot, chromatin immunoprecipitation (ChIP), and ChIP-PCR.Up-regulated LINC00673 was associated with poor prognosis in ESCC patients and promoted the proliferation of ESCC cells both in vitro and in vivo.The present findings are the first to reveal that LINC00673 represses CDKN2C expression and promotes ESCC cell proliferation by elevating EZH2-mediated H3K27me3 levels.	33014799	RID04450	epigenetic regulation	prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	MKLN1<U+2011>AS	HDGF	positively-E	luciferase reporter assay;RIP;western blot;rescue experiment	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-654-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000143321	NA	NA	3068	NA	HMG1L2	Long non-coding RNA MKLN1-AS aggravates hepatocellular carcinoma progression by functioning as a molecular sponge for miR-654-3p, thereby promoting hepatoma-derived growth factor expression.MKLN1-AS expression in HCC tissues and cell lines was detected using reverse-transcription quantitative PCR (RT-qPCR).The interaction among microRNA-654-3p (miR-654-3p), MKLN1-AS and hepatoma-derived growth factor (HDGF) in HCC was investigated using luciferase reporter assay, RNA immunoprecipitation assay, RT-qPCR;western blot and rescue experiments.MKLN1-AS was upregulated in HCC tissues and cell lines, and a high MKLN1-AS expression was associated with shorter overall survival and disease-free survival in patients with HCC.The results indicated that MKLN1-AS functioned as a competing endogenous RNA by sponging miR-654-3p in HCC cells.MKLN1-AS induced pro-oncogenic effects during HCC progression by serving as a molecular sponge for miR-654-3p to increase HDGF expression.	33000222	RID04451	ceRNA or sponge	NA		UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Cervical cancer	HAGLR	FGF2	positively-E	luciferase reporter assay;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-877-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000138685	NA	401022	2247	HOXD-AS1|Mdgt|MIR7704HG	FGFB	HOXD-AS1 facilitates cell migration and invasion as an oncogenic lncRNA by competitively binding to miR-877-3p and upregulating FGF2 in human cervical cancer.The targeting relationship between miRNA and mRNA/lncRNA was determined by dual luciferase reporter, qRT-PCRand western blot assays.HOXD-AS1 was overexpressed in CC tissues and cell lines.Mechanistically, HOXD-AS1 acted as a competing endogenous RNA (ceRNA) to sponge miR-877-3p and led to upregulation of FGF2, a target of miR-877-3p.	32977766	RID04452	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hirschsprung's disease	AFAP1-AS1	E2F3	positively-E	microarray analysis;luciferase reporter assay;RIP	downregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	ceRNA(miR-195)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000112242	NA	84740	1871	AFAP1-AS|AFAP1AS|MGC10981	NA	Involvement of the lncRNA AFAP1-AS1/microRNA-195/E2F3 axis in proliferation and migration of enteric neural crest stem cells of Hirschsprung's disease.AFAP1-AS1 was reduced in HSCR patients.E2F3 was diminished when miR-195 was upregulated, and AFAP1-AS1 inhibition reduced its ability to bind to miR-195.Altogether, AFAP1-AS1 silencing acts as an endogenous RNA by interacting with miR-195 to alter E2F3 expression, thus conferring repressive effects on ENCSC activity and promoting HSCR progression.	32959905	RID04453	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	PVT1	SLC2A1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000117394	NA	5820	6513	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CSE|DYT17|DYT18|DYT9|EIG12|GLUT|GLUT-1|GLUT1|GLUT1DS|HTLVR|PED|SDCHCN	Long noncoding RNA PVT1 promotes tumor cell proliferation, invasion, migration and inhibits apoptosis in oral squamous cell carcinoma by regulating miR-150-5p/GLUT-1.we found that the expression of PVT1 was increased in human OSCC tumor tissues and it was related to reduced survival of the patients.Furthermore, miR-150-5p expression was downregulated in OSCC tumor tissues and it was negatively related with PVT1.In addition, luciferase gene reporter assay verified the miR-150-5p directly binds with PVT1, which regulates the biological functions of OSCC.GLUT-1 protein expression was upregulated in human OSCC tumor tissues.Additionally, luciferase gene reporter assay confirmed that GLUT-1 was a target for miR-150-5p.	32945498	RID04454	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD,PRAD);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE67939)
Ischemic stroke	SNHG16	BCL2	positively-E	luciferase reporter assay;immunoprecipitation assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	interact with miR	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000171791	NA	100507246	596	Nbla10727|Nbla12061|ncRAN	Bcl-2|PPP1R50	Long non-coding RNA SNHG16 inhibits the oxygen-glucose deprivation and reoxygenation-induced apoptosis in human brain microvascular endothelial cells by regulating miR-15a-5p/bcl-2.Following OGD-R, proliferation, apoptosis and miR-15a-5p, SNHG16 and Bcl-2 expression levels were determined using MTT, flow cytometry, reverse transcription-quantitative PCR or western blot.The potential interaction of SNHG16 with miR-15a-5p was analyzed by pull-down, luciferase and immunoprecipitation assays.SNHG16 was pulled-down by miR-15a-5p and anti-Ago2.miR-15a-5p overexpression significantly decreased SNHG16-regulated luciferase activity and hBMEC survival by increasing apoptosis.SNHG16 overexpression decreased miR-15a-5p expression levels in hBMECs.SNHG16 gradually decreased following OGD-R and its overexpression decreased miR-15a-5p expression levels and promoted the proliferation of hBMECs by decreasing apoptosis.SNHG16 enhanced Bcl-2 expression levels in hBMECs, which was abrogated by miR-15a-5p.Bioinformatics suggest that SNHG16 may antagonize the binding of miR-15a-5p to the 3'UTR of Bcl-2 mRNA.These findings suggest that SNHG16 may protect hBMECs from OGD-R-induced apoptosis by antagonizing the miR-15a-5p/bcl-2 axis.	32945414	RID04455	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	ZFPM2-AS1	MIF	positively-F	mass spectrometry;western blot;RNA pull-down assay;RIP	upregulation	qPCR;microarray;sequencing	GSE1279;TCGA	NA	cancer progression(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000240972	NA	102723356	4282	SCAT3	GIF|GLIF	ZFPM2-AS1, a novel lncRNA, attenuates the p53 pathway and promotes gastric carcinogenesis by stabilizing MIF;tumor-activated ZFPM2-AS1 could bind to and protect the degradation of macrophage migration inhibitory factor (MIF);Knockdown of MIF expression diminished ZFPM2-AS1's impact on p53 expression in gastric cancer cells.	29985481	RID04456	interact with protein	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Cervical cancer	HAGLR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-130a-3p)	regulation	NA	Cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000148516	NA	401022	6935	HOXD-AS1|Mdgt|MIR7704HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	HOXD-AS1 Exerts Oncogenic Functions and Promotes Chemoresistance in Cisplatin-Resistant Cervical Cancer Cells;These results collectively show that HOXD-AS1 can act as a competing endogenous RNA to upregulate ZEB1 expression via miR-130a-3p	29896986	RID04457	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial cancer	TDRG1	VEGFA	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000112715	NA	732253	7422	LINC00532|lincRNA-NR_024015	VEGF|VEGF-A|VPF	LncRNA TDRG1 enhances tumorigenicity in endometrial carcinoma by binding and targeting VEGF-A protein;RNA binding protein immunoprecipitation (RIP) assays confirmed that lncRNA TDRG1 directly binds to VEGF-A protein;knockdown of VEGFA in lncRNA TDRG1-overexpressing endometrial carcinoma cells reversed the effects of lncRNA TDRG1 on cell proliferation, invasion, migration and apoptosis.RNA binding protein immunoprecipitation (RIP) assays confirmed that lncRNA TDRG1 directly binds to VEGF-A protein. Furthermore, knockdown of VEGFA in lncRNA TDRG1-overexpressing endometrial carcinoma cells reversed the effects of lncRNA TDRG1 on cell proliferation, invasion, migration and apoptosis.	29920344	RID04458	interact with protein	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Colorectal cancer	LIFR-AS1	TNFAIP3	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	microarray;qRT-PCR	NA	NA	photodynamic therapy resistance(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-29a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000118503	NA	100506495	7128	NA	A20|OTUD7C	Functional role of a long non-coding RNA LIFR-AS1/miR-29a/TNFAIP3 axis incolorectal cancer resistance to pohotodynamic therapy;LIFR-AS1 serves as a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of CRC to PDT	29807108	RID04459	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC00339	FOXM1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000111206	NA	29092	2305	HSPC157|NCRNA00339	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Long non-coding RNA LINC00339 facilitates the tumorigenesis of non-small cell lung cancer by sponging miR-145 through targeting FOXM1;Luciferase reporter assay and RNA immunoprecipitation (RIP) revealed that LINC00339 promoted the NSCLC progression via FOXM1 via targeting miR-145	29906749	RID04460	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Lung adenocarcinoma	NNT-AS1	miR-129-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR;sequencing	TCGA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	NA	NA	100652772	NA	RP11-159F24.1	NA	LncRNA NNT-AS1 promotes the proliferation, and invasion of lung cancer cells via regulating miR-129-5p expression;we identified that NNT-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-129-5p in lung cancer	29857296	RID04461	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Breast cancer	CBR3-AS1	TGFB1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000105329	NA	100506428	7040	PlncRNA-1	CED|DPD1|TGFB|TGFbeta	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-beta1 and downregulating PHGDH;Upregulation of PlncRNA-1 promoted the expression of TGF-beta1, but inhibited the expression of PHGDH;LncRNA PlncRNA-1 overexpression reduced the proliferation rate, but increased the apoptosis rate of breast cancer cells, while treatment with TGF-beta inhibitor reduced those effects of PlncRNA-1 overexpression	29626321	RID04462	expression association	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	FUNDC2P4	CDH1	positively-E	western blot	downregulation	microarray;qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227009	GRCh38_22:39155525-39155945	ENSG00000039068	NA	100127979	999	NA	CD324|UVO|uvomorulin	LncRNA FUNDC2P4 down-regulation promotes epithelial-mesenchymal transition by reducing E-cadherin expression in residual hepatocellular carcinoma after insufficient radiofrequency ablation;overexpression of FUNDC2P4 inhibited proliferation, invasion and migration potential and up-regulated E-cadherin expression in SMMC-7721 cells, whereas silencing FUNDC2P4 promoted these potentials	29295626	RID04463	expression association	NA		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Malignant glioma	SNHG12	ELAVL1	interact	RIP;qRT-PCR;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000066044	NA	85028	1994	ASLNC04080|C1orf79|LINC00100|PNAS-123	Hua|HUR|MelG	Long non-coding RNA SNHG12 promotes the proliferation and migration of glioma cells by binding to HuR;RIP and RNA pull-down assays demonstrated that SNHG12 was associated with and was stabilized by HuR	30015836	RID04464	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Melanoma	LNCRNA-ATB	YAP1	positively-E	RNA pull-down assay;RT-qPCR;western blot	upregulation	microarray;qRT-PCR	GSE3189	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-590-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	NA	NA	ENSG00000137693	NA	114004396	10413	NA	YAP65	lncRNA-ATB functions as a competing endogenous RNA to promote YAP1 by sponging miR-590-5p in malignant melanoma;lncRNA-ATB functions as a competing endogenous RNA (ceRNA) to enhance Yes associated protein 1 expression by competitively sponging microRNA miR-590-5p;lncRNA-ATB functions as a ceRNA to promote MM proliferation and invasion	29956757	RID04465	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	FOXO1	GAPLINC	negatively-E	ChIP;bioinformatics analysis	upregulation	microarray;RT-PCR	NA	NA	chemoresistance(+)	histone modification	binding/interaction	NA	Erlotinib	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000150907	NA	ENSG00000266835	GRCh38_18:3466250-3478978	2308	100505592	FKH1|FKHR|FOXO1A	LINC01540|lncRNA-uc002kmd.1|RP11-838N2.4|TCONS_00026238	Exosome-mediated transfer of lncRNA RP11-838N2.4 promotes erlotinib resistance in non-small cell lung cancer.forkhead box protein O1 (FOXO1) could bind to the promoter region of lncRNA RP11-838N2.4, resulting in its silencing through the recruitment of histone deacetylase.Furthermore, bioinformatics analysis and chromatin immunoprecipitation revealed that forkhead box protein O1 (FOXO1) could bind to the promoter region of lncRNA RP11-838N2.4, resulting in its silencing through the recruitment of histone deacetylase.	29845246	RID04466	epigenetic regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(SKCM);DATA(GSE38495)
Prostate cancer	PCSEAT	EZH2	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	NA	cell proliferation(+)	ceRNA(miR-143-3p;miR-24-2-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000286027	GRCh38_21:41580475-41582887	ENSG00000106462	NA	105372808	2146	PRCAT38	ENX-1|EZH1|KMT6|KMT6A	The long non-coding RNA PCSEAT exhibits an oncogenic property in prostate cancer and functions as a competing endogenous RNA that associates with EZH2;PCSEAT promotes cell proliferation, at least in part by affecting miR-143-3p- and miR-24-2-5p-mediated regulation of EZH2, suggesting that PCSEAT and EZH2 competitively sponge miR-143-3p and miR-24-2-5p	29803673	RID04467	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic ductal adenocarcinoma	PVT1	ULK1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR;ISH	GSE15471;GSE16515	NA	cell autophagy(+);cancer progression(+)	ceRNA(miR-20a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000177169	NA	5820	8408	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG1|ATG1A	LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis;PVT1 promoted cyto-protective autophagy and cell growth by targeting ULK1;PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression	30001707	RID04468	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Melanoma	CCAT1	miR-33a	negatively-F	luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	The lncRNA CCAT1 Upregulates proliferation and Invasion in Melanoma Cells via Suppressing miR-33a.Bioinformatics analysis predicted that miR-33a acted as a target of CCAT1, which was confirmed by dual-luciferase reporter assay.CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma.With the aid of bioinformatics analysis (starBase, www.starbase.sysu.edu.cn), we discovered the target miR-33a, which had been verified to be a tumor suppressor in the oncogenesis of melanoma13.	28409554	RID04469	ceRNA or sponge	NA		
Renal cell carcinoma	CCAT1	BIRC7	positively-F	RNA pull-down assay;RIP	upregulation	qRT-PCR;western blot	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000101197	NA	100507056	79444	CARLO5|CARLo-5|onco-lncRNA-40	KIAP|ML-IAP|mliap|RNF50	LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein.RNA pull-down and RIP assays showed that CCAT1 was physically associated with Livin protein. Livin was significantly inhibited by CCAT1 silencing;CCAT1 silencing could inhibit the growth of RCC in vivo that was accompanied by the reduction of Livin in RCC tissues. CCAT1 inhibits RCC cell apoptosis and increases cell viability through up-regulation of Livin.In this study, the expression of CCAT1 and Livin of RCC tissues or cells was determined using qRT-PCR(quantitative real-time PCR) and western blot, respectively.	28470345	RID04470	interact with protein	NA		
Lung adenocarcinoma	CCAT1	BCL2L1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(let-7c)	regulation	RNA-protein	Docetaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000171552	NA	100507056	598	CARLO5|CARLo-5|onco-lncRNA-40	Bcl-X|bcl-xL|bcl-xS|BCL2L|BCLX|PPP1R52	Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells.the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells.	27566568	RID04471	ceRNA or sponge	chemoresistance		UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Non-small cell lung cancer	EGFR-AS1	miR-223	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.Bioinformatics analysis and a luciferase reporter assay confirmed that EGFR-AS1 mediated cell proliferation and chemoresistance through directly binding to microRNA-223. Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.	30431074	RID04472	ceRNA or sponge	chemoresistance,prognosis		
Cervical cancer	MNX1-AS1	MAPK3	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000102882	NA	645249	5595	CCAT5|LOC645249|MAYA	ERK1|p44erk1|p44mapk|PRKM3	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID04473	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MNX1-AS1	MAPK1	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000100030	NA	645249	5594	CCAT5|LOC645249|MAYA	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID04474	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MNX1-AS1	MAPK8	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000107643	NA	645249	5599	CCAT5|LOC645249|MAYA	JNK|JNK1|PRKM8|SAPK1	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID04475	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	UCA1	CTNNB1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	chromatin looping;enhancer	regulation	RNA-protein	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168036	NA	652995	1499	CUDR|LINC00178|onco-lncRNA-36|UCAT1	armadillo|beta-catenin|CTNNB	Long Noncoding RNA CUDR Regulates HULC and beta-Catenin to Govern Human Liver Stem Cell Malignant Differentiation. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like cells by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On the other hand, excessive CUDR triggers hepatocyte-like cells malignant transformation. Mechanistically, we identify CUDR causes highly upregulated in liver cancer (HULC) and beta-catenin abnormal expression by inhibiting HULC promoter methylation and promoting beta-catenin promoter-enhancer chromatin looping formation mediated by CUDR-ccctc-binding factor (CTCF) complex, which recruits more RNA polII and P300. Strikingly, HULC and beta-catenin activity are crucial for CUDR oncogenic function.	26347501	RID04476	chromatin looping	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	NBAT1	SOX7	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	prognosis(-);cell proliferation(+);cell migration(+);cell invasion(+);	ceRNA(miR-21)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000171056	NA	729177	83595	CASC14|NBAT-1	NA	Long non-coding RNA NBAT1 inhibits the progression of glioma through the miR-21/SOX7 axis.The results revealed that NBAT1 expression was significantly decreased in patients with metastatic glioma compared with the controls (patients with non-metastatic glioma.The CCK-8 assay demonstrated that the proliferative ability of o/e-NBAT1-transfected A172 and AM38 cells significantly decreased compared with that of the control (P<0.05; Fig. 2B and C). In addition, the Transwell assay results revealed that the migratory and invasive abilities of o/e-NBAT1-transfected A172 and AM38 cells were significantly inhibited compared with those of the control groups (P<0.05; Fig. 2D-G). Collectively, these results suggested that overexpression of NBAT1 may suppress the proliferation, migration and invasion of glioma cells. Luciferase reporter vectors containing WT-NBAT1 and MUT-NBAT1 sequences of predicted miR-21 binding sites were constructed. The results demonstrated that miR-21 mimics significantly attenuated the activity of the luciferase plasmid containing the WT binding sites compared with that of the MUT control (P<0.05; Fig. 3B). To identify the putative targets of miR-21, the complementary sequence of miR-21 in SOX7 transcripts was predicted (Fig. 6A). The interaction between SOX7 and miR-21 was confirmed using a dual-luciferase assay. Luciferase reporter plasmids containing SOX7-WT) and SOX7-MUT fragments of the predicted miR-21 binding sites were constructed.	32782620	RID04477	ceRNA or sponge	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Colorectal cancer	LINC00665	ATF1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell migration(+);cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000123268	NA	100506930	466	CIP2A-BP	TREB36	LINC00665/miR-9-5p/ATF1 is a novel axis involved in the progression of colorectal cancer.The results showed that the expres-sions of LINC00665 and ATF1 mRNA in CRC were signifi-cantly higher than that in normal tissues adjacent to cancer, while the expression of miR-9-5p was significantly lower (Fig. 1a-c).We found that the high expression of LINC00665 in tumor tissues was significantly correlated with local lymph node metastasis and poor differentiation of the CRC tissue in patients, instead of gender, age, tumor size and T stage (Table 1). This also suggested that high expression of LINC00665 could probably be involved in the progression of CRC. We found that miR-9-5p was one of the candidate targets of LINC00665, and  the  predicted  binding  site  is  shown  in  Fig. 2a.To further clarify the targeted binding relationship between LINC00665 and miR-9-5p, RIP experiments were also conducted. As was shown (Fig. 2g), miR-9-5p mimics observably increased the enriched LINC00665 by anti-Ago2 antibody compared with in the control anti-IgG. Further-more, dual-luciferase reporter assay showed that miR-9-5p inhibitors could significantly increase the luciferase activity of wild-type LINC00665 reporter in DLD-1 cells (Fig. 2h). On  the  other  hand,  miR-9-5p  mimics  could  remarkably  reduce  the  luciferase  activity  of  wild-type  LINC00665  reporter in SW620 cells (Fig. 2i). These results suggested that LINC00665 could negatively regulate the expression of miR-9-5p by directly sponging it.Functional  experiments showed that LINC00665 overexpression sig-nificantly promoted cell proliferation and inhibited cell apoptosis, whereas knockdown of LINC00665 exerted the opposite effects (Fig. 3d ; Supplementary Fig. 3). Com-pared with in the over-expressed LINC00665 group, co-transfection of miR-9-5p mimics reversed the effects of LINC00665 (Fig. 3d ). Consistently, compared with in the LINC00665 knockdown group, co-transfection of miR-9-5p inhibitors also reversed the effects of LINC0066 shRNA#1 and shRNA#2 (Fig. 3d-f, Supplementary Fig. 3).The results showed that over-expres-sion of LINC00665 significantly promoted the movemen of DLD-1 cells compared with in the control group, and the scratch healing rate of DLD-1 cells was significantly reduced after transfection of miR-9-5p. By contrast, knockdown of LINC00665 decreased the cell motility significantly, and the inhibitors of miR-9-5p partially reversed the inhibitory effect caused by knockdown of LINC00665 (Fig. 4a; Sup-plementary Fig. 3).To further investigate the downstream molecular mechanism of miR-9-5p, we predicted the target genes of miR-9-5p with TargetScan (https ://www.targe tscan .org/vert_72/), and found that ATF1 was a candidate target gene of miR-9-5p (Fig. 5a). Furthermore, the results of qRT-PCRand western blot showed that ATF1 expression was significantly increased in DLD-1 cells transfected with miR-9-5p inhibitors on both mRNA and protein expression levels (Fig. 5b, c). On the other hand, over-expression of miR-9-5p observably inhibited ATF1 expres-sion in SW620 cells (Fig. 5b, c). Importantly, dual-luciferase reporter  assay  showed  that  miR-9-5p  mimics  markedly  reduced the luciferase activity of wide-type ATF1 reporter, but possessed no significant effect on the luciferase activity of mutated ATF1 reporter (Fig. 5d). Additionally, western blot also showed that ATF1 expression was significantly up-regu-lated after transfection of LINC00665 overexpression plasmid; conversely, down-regulation of ATF1 expression in SW620 cells was induced by LINC00665 knockdown (Fig. 5e, Sup-plementary Fig. 6). These results suggested that ATF1 was a downstream gene of miR-9-5p, and LINC00665 indirectly and positively regulated its expression level.	32776307	RID04478	ceRNA or sponge	metastasis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Head and neck squamous cell carcinoma	FKBP9P1	PIK3CA	positively-E	shRNA;knockdown	upregulation	qRT-PCR	NA	NA	prognosis(-);cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000176826	GRCh38_7:55681074-55713252	ENSG00000121879	NA	360132	5290	FKBP9L|MGC20531	PI3K	Silencing novel long non-coding RNA FKBP9P1 represses malignant progression and inhibits PI3K/AKT signaling of head and neck squamous cell carcinoma in vitro.Initially, FKBP9P1 expression was measured in all 114 HNSCC tissue samples and paired adjacent normal tissues using qRT-PCR As shown in Figure -Figure1A,1A, we found that FKBP9P1 expression was significantly higher in HNSCC tissues than in adjacent normal tissues (tumor vs. normal, 1.914   1.430 vs. 0.957   1.430, t-=-7.746, P-<-0.001). We also detected FKBP9P1 expression in cell lines [Figure -[Figure1B],1B], and its expression in HNSCC cells (FaDu, Cal-27, SCC4, and SCC9) was significantly higher than that in normal control cell line HaCaT (all P-<-0.01). These results indicate that FKBP9P1 may play an oncogene role in HNSCC.Additionally, survival analysis using the Kaplan-Meier method demonstrated that a higher FKBP9P1 level was associated with poor OS (P-=-0.002) [Figure -[Figure1C]1C] and poor DFS (P-<-0.0001) [Figure -[Figure1D].1D]. These results suggest that FKBP9P1 could be a potential effective prognostic biomarker for HNSCC patients.To determine the effect of FKBP9P1 knockdown on the migration and invasion of HNSCC cells, wound healing assay [Figure -[Figure2D]2D] and trans-well assay [Figure -[Figure2E]2E] were performed. As shown in the figures, after FKBP9P1 knockdown, the migratory, and invasion abilities of Cal-27 and SCC9 cells were both remarkably impaired (all P-<-0.01). The results suggest that FKBP9P1 knockdown significantly inhibits HNSCC cell migration and invasion.As shown in Figure -Figure3,3, FKBP9P1 knockdown suppressed the p-PI3K and p-AKT, while PI3K and AKT expression had no significant difference between FKBP9P1 knockdown cells and control cells. Our data indicate that FKBP9P1 knockdown suppresses the PI3K/AKT signaling pathway and this pathway may be the underlying mechanism of FKBP9P1 in HNSCC progression.	32769488	RID04479	expression association	prognosis	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Head and neck squamous cell carcinoma	FKBP9P1	AKT1	positively-E	shRNA;knockdown	upregulation	qRT-PCR	NA	NA	prognosis(-);cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000176826	GRCh38_7:55681074-55713252	ENSG00000142208	NA	360132	207	FKBP9L|MGC20531	AKT|PKB|PRKBA|RAC|RAC-alpha	Silencing novel long non-coding RNA FKBP9P1 represses malignant progression and inhibits PI3K/AKT signaling of head and neck squamous cell carcinoma in vitro.Initially, FKBP9P1 expression was measured in all 114 HNSCC tissue samples and paired adjacent normal tissues using qRT-PCR As shown in Figure -Figure1A,1A, we found that FKBP9P1 expression was significantly higher in HNSCC tissues than in adjacent normal tissues (tumor vs. normal, 1.914   1.430 vs. 0.957   1.430, t-=-7.746, P-<-0.001). We also detected FKBP9P1 expression in cell lines [Figure -[Figure1B],1B], and its expression in HNSCC cells (FaDu, Cal-27, SCC4, and SCC9) was significantly higher than that in normal control cell line HaCaT (all P-<-0.01). These results indicate that FKBP9P1 may play an oncogene role in HNSCC.Additionally, survival analysis using the Kaplan-Meier method demonstrated that a higher FKBP9P1 level was associated with poor OS (P-=-0.002) [Figure -[Figure1C]1C] and poor DFS (P-<-0.0001) [Figure -[Figure1D].1D]. These results suggest that FKBP9P1 could be a potential effective prognostic biomarker for HNSCC patients.To determine the effect of FKBP9P1 knockdown on the migration and invasion of HNSCC cells, wound healing assay [Figure -[Figure2D]2D] and trans-well assay [Figure -[Figure2E]2E] were performed. As shown in the figures, after FKBP9P1 knockdown, the migratory, and invasion abilities of Cal-27 and SCC9 cells were both remarkably impaired (all P-<-0.01). The results suggest that FKBP9P1 knockdown significantly inhibits HNSCC cell migration and invasion.As shown in Figure -Figure3,3, FKBP9P1 knockdown suppressed the p-PI3K and p-AKT, while PI3K and AKT expression had no significant difference between FKBP9P1 knockdown cells and control cells. Our data indicate that FKBP9P1 knockdown suppresses the PI3K/AKT signaling pathway and this pathway may be the underlying mechanism of FKBP9P1 in HNSCC progression.	32769488	RID04480	expression association	prognosis	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	DUXAP8	YAP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-590-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000137693	NA	503637	10413	NA	YAP65	Long noncoding RNA DUXAP8 regulates proliferation and apoptosis of ovarian cancer cells via targeting miR-590-5p.The results in (Fig. 1) clearly showed that the expression of DUXAP8 was clearly decreased after transfection of siRNA-1# and siRNA-2# (p <   0.05). Further, the interference effect of siRNA-2# on DUXAP8 in SKOV3 and OVCAR3 cells was significantly stronger than that of siRNA-1# (p < 0.05).Figure 2a  showed  that  the  expression  of  DUXAP8  was  significantly down-regulated in DUXAP8 siRNA-1# and siRNA-2#group, and the expression of DUXAP8 was sig-nificantly up-regulated in DUXAP8 mimic group (p < 0.05). The cell proliferation ability and colony formation were sig-nificantly decreased after DUXAP8 interference in SKOV3 and OVCAR3 cells (Fig. 2b, c, p <   0.05). The flow cytometry results showed that DUXAP8 interference promoted apop-tosis (Fig. 2d, p <   0.05). By contrast, the DUXAP8 mimic group showed diametrically opposite results. These results indicated that DUXAP8 could regulate the proliferation and apoptosis of ovarian cancer cells. As shown in  (Fig. 3c,  d),  compared  with  the  siRNA-NC  group,  the growth rate, volume, and the weight of tumor were significantly reduced in siRNA-1# and siRNA-2#grou(p  <    0.05).Furthermore,  TUNEL  assay  showed  that  DUXAP8  interference  promoted  apoptosis  in  cells  (Fig. 3e).These results indicated that DUXAP8 could regulate the proliferation and apoptosis of ovarian cancer cells in nude mice trans-planted tumor model.To further verify whether DUXAP8 targeted miR-590-5p, a dual luciferase reporter system was used. The results showed that miR-590-5p reduced luciferase activity of DUXAP8 containing WT 3'UTR (p <   0.05), but did not decrease luciferase activ-ity of DUXAP8 containing Mut 3'UTR (p >  0.05),  which demonstrating that miR-590-5p is a target gene of DUXAP8 in cells (Fig. 4b).The results showed that after DUXAP interfer-ence, the cell proliferation ability and colony formation were inhibited, and apoptosis rate was increased. Those biological behaviors in DUXAP8 +   miR inhibitor NC group were simi-lar with DUXAP8 siRNA group. However, the treatment of miR inhibitor can attenuate the above effects of DUXAP8 on cells. All these findings suggested that DUXAP8 regulates the proliferation and apoptosis of ovarian cancer cells by regulating miR-590-5p.Dual luciferase reported  that  miR-590-5p  reduced  luciferase  activity  of  YAP1 containing WT 3'UTR, but did not reduce the lucif-erase activity of YAP1 containing Mut 3'UTR (p < 0.05), which demonstrating that YAP1 is a target gene of miR-590-5p in cells (Fig. 6a).	32749665	RID04481	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Colorectal cancer	ADIPOQ	TP53	positively-E	luciferase reporter assay;StarBase	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-219c-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000181092	GRCh38_3:186842704-186858463	ENSG00000141510	NA	9370	7157	ACDC|ACRP30|adiponectin|apM1|GBP28	LFS1|p53	Decreased long noncoding RNA ADIPOQ promoted cell proliferation and metastasis via miR-219c-3p/TP53 pathway in colorectal carcinoma.We then performed qRT-PCRto detect those gene expressions in our clinical samples (n=10). The results showed that ADIPOQ was significantly reduced in colorectal cancer tissues (Figure 1B), while no differences had been found in other three lncRNAs (Figure 1C-E). To verify the role of ADIPOQ on cell proliferation, CCK8 assay was performed on Caco-2 cells after regulation of ADIPOQ expression. The results revealed that overexpression of ADIPOQ significantly reduced colorectal cancer cells proliferation compared with the control group, whereas inhibition of ADIPOQ expression remarkably increased the cell proliferation number at 3 days (Figure 2C, 2D).The results revealed that after ADIPOQ upregulation, the number of Caco-2 cells that transferred through transwell chambers was significantly reduced in response to fetal bovine serum compared with control group (Figure 3A). Besides, after inhibition of ADIPOQ expression, the number of Caco-2 cells transferred through transwell chambers was significantly increased (Figure 3B). These data suggested that ADIPOQ alteration regulated the migration ability of human colorectal cancer cells; upregulated ADIPOQ can effectively inhibit the migration and invasion of colorectal cancer cells, making ADIPOQ a potential target for tumor therapy.Therefore, we assumed that ADIPOQ could modulate the migration and invasion of colorectal carcinoma through interacting with miR-219c-3p. To further confirm this, ADIPOQ-wt Luciferase reporter vector and ADIPOQ-mut 3'UTR Luciferase reporter vector were synthesized, and Luciferase reporter assay was performed (Figure 4D). Compared with the control, the Luciferase activity of Caco-2 cells that co-transfected with wild type ADIPOQ (ADIPOQ-wt) and miR-219c-3p mimic was significantly decreased (p < 0.01), and it was reversely increased after mutation at the binding site of ADIPOQ (ADIPOQ-mut) compared with ADIPOQ-wt (p < 0.01) (Figure 4E). These results demonstrated that ADIPOQ could directly bind to miR-219c-3p.We observed decreased TP53 expression after Caco-2 cells were transfected with the miR-219c3p mimics, which suggested that miR-219c-3p could downregulate TP53 expression (Figure 5A).As expected, Dual-Luciferase report results showed that miR-219c-3p mimics significantly downregulated the TP53 expression whereas point mutations in the TP53 3'-UTR abrogated the suppressed effect of miR-219c-3p (Figure 5C). Then, we validated whether ADIPOQ can regulate TP53 expression via sponging with miR-219c-3p. The results showed that ADIPOQ could significantly increase TP53 expression; however, mutation of the binding site with ADIPOQ of miR-219c-3p eliminated the function effectively (Figure 5D). Conversely, inhibition of miR-219c-3p overcame the suppression of TP53 by ADIPOQ knockdown (Figure 5E). Taken together, these data demonstrated that ADIPOQ could serve as ceRNA for the miR-219c-3p to further modulate TP53. To investigate whether ADIPOQ was correlated miRNA, we used StarBase 2.0 to predict the target miRNA of ADIPOQ and found that miR_x0002_219c-3p is a target miRNA of ADIPOQ.	32744690	RID04482	ceRNA or sponge	metastasis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Osteosarcoma	MALAT1	MIR202	positively-F	transfection	upregulation	qPCR	NA	NA	cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Bone sarcoma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000284219	NA	378938	574448	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MIRN202|hsa-mir-202|mir-202	LncRNA MALAT1 facilitates lung metastasis of osteosarcomas through miR-202 sponging.We compared lncRNAs in samples of patients with lung metastases versus samples of patients with no metastasis. A number of lncRNAs were shortlisted for evaluation based on the published reports. Some lncRNAs have been evaluated earlier in osteosarcoma models while the other tested lncRNAs have been reported in other cancer models. Several lncRNAs were significantly upregulated (Fig. 1) as well as downregulated (Fig. 2) in lung metastatic osteosarcomas.MALAT1 was revealed to be the most significantly upregulated lncRNA with a p value of?<?0.0001. LncRNAs function via sponging their target microRNAs (miRNAs)15. Therefore, we were interested in finding a miRNA that was functionally involved in lncRNA MALAT1's actions towards promoting lung metastasis of osteosarcoma. We turned to both published reports as well as online tools to predict miRNA targets of MALAT1. Many such potential miRNAs were evaluated as presented in Fig. 4. Two miRNAs, miR-202 and miR-34a stood out as the most significantly (p?<?0.0001) upregulated miRNAs in KRIB cells that had MALAT1 downregulated. In addition, several other miRNAs, such as, miR-205, miR-142, miR-129, miR-144 and miR-509 were also significantly upregulated but the levels of miR-202 were found to be the highest~?eightfolds higher than the control cells. miR-140-5p was also elevated but did not reach statistical significance (Fig. 4).Moreover, since miR-202 was the most significantly regulated miRNA by MALAT1, we downregulated this miRNA in MALAT1 downregulated KRIB cells. Such decrease in the levels of miR-202 mimicked rescue of MALAT1 and attenuated the effects of MALAT1 downregulation significantly (p?<?0.0007, Fig. 5A). Since miR-202 is tumor suppressive, as per the results presented so far, we transfected miR-202 in the cells before injecting them in mice and found that higher miR-202 levels by themselves significantly decreased the lung metastatic nodules (Fig. 5A). Finally, as presented above, miR-34a is another miRNA that is regulated by MALAT1 (Fig. 4). We checked if this miRNA could also similarly impact lung metastasis. When we injected cells with ectopic miR-34a, we found a decrease in the lung metastatic nodules but the change was not found to be statistically significant (Fig. 5A).	32728178	RID04483	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Retinoblastoma	RBAT1	E2F3	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	GSE111168	NA	cell proliferation(+);tumorigenesis(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	NA	NA	ENSG00000112242	NA	NA	1871	NA	NA	A novel LncRNA transcript, RBAT1, accelerates tumorigenesis through interacting with HNRNPL and cis-activating E2F3.We found 10 differential expressed genes (|log2(Fold_change)|->-1.5, p-<-0.05) which were previously reported to be the driver/suppressor genes of retinoblastoma, and 14 differentials expressed lncRNAs (|log2FC|->-1.5, p-<-0.05) were then identified which shared overlap region with these coding genes. Among these lncRNAs, we focused on the prominent one with highest expression of log2FC-=-4.898, termed as ENST00000433182 (Supplementary Table 4).To determine the role of RBAT1 in tumor progression, we silenced RBAT1 in tumor cell lines using LNA-modified antisense oligonucleotides (GapmeRs).CCK8 assays showed that cell proliferation was significantly inhibited in RBAT1-silenced tumor cell lines (Fig. -(Fig.2b).2b). Consistently, the colony formation of tumor cell lines was decreased after silencing RBAT1 (Fig. -(Fig.2c).2c). We also observed that the RBAT1-silenced cell lines formed smaller colonies (Fig. -(Fig.2d).2d).To further explore the functional role of E2F3 in Rb and BCa cell lines, we first tested its expression. Here, we found that E2F3 expression is significantly higher in Rb and BCa cell lines than that in normal cell lines (Fig. -(Fig.4a4a and b). As expected, the colony formation of tumor cell lines was decreased after E2F3 silencing (Fig. -(Fig.4c,4c, d). We also observed that the E2F3-silenced cell lines formed smaller colonies (Fig. -(Fig.4e).4e). CCK8 assays demonstrated inhibited proliferation after interfering E2F3 (Fig. -(Fig.4f).4f). To further evaluate the effects of E2F3 on Rb cell tumorigenesis in vivo, we performed orthotopic xenograft after E2F3 knockdown. Consistently, E2F3-silencing significantly reduced the tumor volumes and weights (Fig. -(Fig.4g4g and h). Similarly, in a patient-derived xenograft (PDX) Rb model (Fig. 5a and b), RBAT1 inhibition had therapeutic effects (Fig. -(Fig.5c5c and d) with decreased expression of E2F3 (Fig. -(Fig.5e5e and f). Taken together, these data suggested that RBAT1 sustains tumor cell oncogenicity by activating E2F3 signaling.Given that the first exon of RBAT1 was in the E2F3 promoter and that a 209-bp complete complementary sequence is found in this region, the E2F3 promoter was chosen as the candidate site for detection. The GAPDH promoter served as a negative control. We analyzed a 2-kb locus upstream from the transcription start site (TSS) of the E2F3 gene to confirm the promoter region (Supplementary Fig. 9A). Through luciferase reporter assays, we identified a---500 to --1000-bp segment upstream from the TSS as the promoter region of E2F3 with high transcriptional activity (Supplementary Fig. 9B). Specifically, ChIRP-PCR showed that RBAT1 was enriched in the E2F3 promoter region in three tumor cell lines, whereas a weak RBAT1 enrichment was observed at the E2F3 promoter after RBAT1 suppression (Fig. -(Fig.6e-g);6e-g); suggesting that the promoter region of E2F3 was the binding site for lncRNA RBAT1. These data indicate that RBAT1 binds directly to HNRNPL and the E2F3 promoter region with high affinity.To determine whether RBAT1 could activate E2F3 by recruiting HNRNPL to its promoter, we evaluated the status of E2F3 promoter transcriptional activity in tumor cell lines with different RBAT1 and HNRNPL expression levels using luciferase assays. We observed that E2F3 promoter activation was suppressed in RBAT1 or HNRNPL knockdown tumor cell lines (Fig. -(Fig.7e).7e). Also, we examined the DNA copy number variations (CNV) in tumor cell lines. We observed an increased E2F3 copy number in Rb and BCa cell lines. However, there was no obvious changes in the copy number of E2F3 gene after RBAT1 silenced (Supplementary Fig. 10 and 11). Furthermore, we have also tested HT1376, a bladder cancer cell line without E2F3 locus amplification (Supplementary Fig. 12A). We found that RBAT1 was also highly expressed in HT-1376 (Supplementary Fig. 12B) which indicates the RBAT1 was not upregulated by copy number amplification of E2F3 locus. In addition, after knockdown RBAT1 (Supplementary Fig. 12C), the expression of E2F3 was largely reduced (Supplementary Fig. 12D) and the tumor proliferation was also suppressed (Supplementary Fig. 12E). Our results indicating that RBAT1 was not upregulated by copy number amplification of E2F3 locus, could also epigenetically regulate E2F3 expression. To sum up, our data showed that RBAT1 recruits HNRNPL to E2F3 promoter and activates its expression.	32669100	RID04484	expression association	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	RBAT1	E2F3	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	GSE111168	NA	cell proliferation(+);tumorigenesis(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	NA	NA	ENSG00000112242	NA	NA	1871	NA	NA	A novel LncRNA transcript, RBAT1, accelerates tumorigenesis through interacting with HNRNPL and cis-activating E2F3.We found 10 differential expressed genes (|log2(Fold_change)|->-1.5, p-<-0.05) which were previously reported to be the driver/suppressor genes of retinoblastoma, and 14 differentials expressed lncRNAs (|log2FC|->-1.5, p-<-0.05) were then identified which shared overlap region with these coding genes. Among these lncRNAs, we focused on the prominent one with highest expression of log2FC-=-4.898, termed as ENST00000433182 (Supplementary Table 4).To determine the role of RBAT1 in tumor progression, we silenced RBAT1 in tumor cell lines using LNA-modified antisense oligonucleotides (GapmeRs).CCK8 assays showed that cell proliferation was significantly inhibited in RBAT1-silenced tumor cell lines (Fig. -(Fig.2b).2b). Consistently, the colony formation of tumor cell lines was decreased after silencing RBAT1 (Fig. -(Fig.2c).2c). We also observed that the RBAT1-silenced cell lines formed smaller colonies (Fig. -(Fig.2d).2d).To further explore the functional role of E2F3 in Rb and BCa cell lines, we first tested its expression. Here, we found that E2F3 expression is significantly higher in Rb and BCa cell lines than that in normal cell lines (Fig. -(Fig.4a4a and b). As expected, the colony formation of tumor cell lines was decreased after E2F3 silencing (Fig. -(Fig.4c,4c, d). We also observed that the E2F3-silenced cell lines formed smaller colonies (Fig. -(Fig.4e).4e). CCK8 assays demonstrated inhibited proliferation after interfering E2F3 (Fig. -(Fig.4f).4f). To further evaluate the effects of E2F3 on Rb cell tumorigenesis in vivo, we performed orthotopic xenograft after E2F3 knockdown. Consistently, E2F3-silencing significantly reduced the tumor volumes and weights (Fig. -(Fig.4g4g and h). Similarly, in a patient-derived xenograft (PDX) Rb model (Fig. 5a and b), RBAT1 inhibition had therapeutic effects (Fig. -(Fig.5c5c and d) with decreased expression of E2F3 (Fig. -(Fig.5e5e and f). Taken together, these data suggested that RBAT1 sustains tumor cell oncogenicity by activating E2F3 signaling.Given that the first exon of RBAT1 was in the E2F3 promoter and that a 209-bp complete complementary sequence is found in this region, the E2F3 promoter was chosen as the candidate site for detection. The GAPDH promoter served as a negative control. We analyzed a 2-kb locus upstream from the transcription start site (TSS) of the E2F3 gene to confirm the promoter region (Supplementary Fig. 9A). Through luciferase reporter assays, we identified a---500 to --1000-bp segment upstream from the TSS as the promoter region of E2F3 with high transcriptional activity (Supplementary Fig. 9B). Specifically, ChIRP-PCR showed that RBAT1 was enriched in the E2F3 promoter region in three tumor cell lines, whereas a weak RBAT1 enrichment was observed at the E2F3 promoter after RBAT1 suppression (Fig. -(Fig.6e-g);6e-g); suggesting that the promoter region of E2F3 was the binding site for lncRNA RBAT1. These data indicate that RBAT1 binds directly to HNRNPL and the E2F3 promoter region with high affinity.To determine whether RBAT1 could activate E2F3 by recruiting HNRNPL to its promoter, we evaluated the status of E2F3 promoter transcriptional activity in tumor cell lines with different RBAT1 and HNRNPL expression levels using luciferase assays. We observed that E2F3 promoter activation was suppressed in RBAT1 or HNRNPL knockdown tumor cell lines (Fig. -(Fig.7e).7e). Also, we examined the DNA copy number variations (CNV) in tumor cell lines. We observed an increased E2F3 copy number in Rb and BCa cell lines. However, there was no obvious changes in the copy number of E2F3 gene after RBAT1 silenced (Supplementary Fig. 10 and 11). Furthermore, we have also tested HT1376, a bladder cancer cell line without E2F3 locus amplification (Supplementary Fig. 12A). We found that RBAT1 was also highly expressed in HT-1376 (Supplementary Fig. 12B) which indicates the RBAT1 was not upregulated by copy number amplification of E2F3 locus. In addition, after knockdown RBAT1 (Supplementary Fig. 12C), the expression of E2F3 was largely reduced (Supplementary Fig. 12D) and the tumor proliferation was also suppressed (Supplementary Fig. 12E). Our results indicating that RBAT1 was not upregulated by copy number amplification of E2F3 locus, could also epigenetically regulate E2F3 expression. To sum up, our data showed that RBAT1 recruits HNRNPL to E2F3 promoter and activates its expression.	32669100	RID04485	expression association	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Esophageal cancer	DRAIC	NFIB	positively-E	luciferase reporter assay;RNA pull-down	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);cell autophagy(-)	ceRNA(miR-149-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000245750	GRCh38_15:69462921-69843120	ENSG00000147862	NA	145837	4781	NA	NFI-RED|NFIB2|NFIB3	Regulatory effect of LncRNA DRAIC/miR-149-5p/NFIB molecular network on autophagy of esophageal cancer cells and its biological behavior.The  DRAIC  expression  levels in  EC  cells werehigher  than  thosein  normal  esophageal epithelial cells(Figure 1-A, p -.050). Eca-109 and EC9706 cells with highest expression level were selected for subsequent tests. After transfection,proliferation and invasion of the si-DRAIC group  were  lower  than  the  NC-DRAIC  group,  while  apoptosis  and  autophagy  were  higher  than the NC-DRAIC group (Figures1-B, C, D, E, F, p -.050).The  miR-149-5p  expression  levelsin  EC  cells  werelower  than  thosein  normal  esophageal epithelial  cells (Figure  2-A, p -.050). Aftertransfection, cell  proliferation  and  invasion  in  the miR-mimics group were lower than those in the miR-NC group, while apoptosis and autophagy were higher than those in the miR-NC group (Figure 2-B, C, D, E, F, p -.050).The starbase online website discoveredthatDRAIC and miR-149-5phad binding sites(Figure 3-A), and dual-luciferase report showed that the fluorescence activity of DRAIC-wt was inhibited by  transfected  miR-149-5p  mimetic (Figure  3-B,  p -.050).  In  the  pull-down  experiment, DRAIC  was  only  pulled  down  by  biotin-labeled  miR-149-5p-wt  (Figure  3-C,  p -.050). However,  the  miR-149-5  pexpression  levelsin  Eca-109  and  EC9706  cells  transfected  with  low expression plasmid and empty vector of DRAIC werehigher in the si-DRAIC group thanthosein the NC-DRAIC group.The low expression plasmidof DRAIC and miR-149-5p inhibitor were co-transfected into Eca-109 and EC9706 cells and set as group A; the low expression plasmid of DRAIC was transfected and  set  as  group  B;  the  empty  vector  of  DRAIC  was  transfected  separately  and  set  as  group  C. Proliferation, invasion, apoptosis and autophagy of group A and group C had no difference (P > 0.050), while those of group B werelower than thoseof the other two groups, and apoptosis and autophagy werehigher than thoseof bothgroups (P < 0.050). (Figure 4)The  online  website  Targetscan7.2 discoveredthatmiR-149-5p  and  NFIBhad binding  sites(Figure 6-A), and dual-luciferase report signified that the fluorescence activity of miR-149-5p-wt was  inhibited  by  transfected  NFIB  high  expression  plasmid  (Figure  6-B,  p -.050).  After detecting the NFIB protein expressionlevelsin Eca-109 and EC9706 cells transfected with miR-149-5p inhibitor and negative control, we found thatthe levels ofthe miR-inhibition group werehigher than those of the miR-NC group(Figure 6-C,p -.050)	32659236	RID04486	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Osteoporosis	LOXL1-AS1	HMGA2	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-196a-5p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000149948	NA	100287616	8091	NA	BABL|HMGIC|LIPO	LncRNA LOXL1-AS1 controls osteogenic and adipocytic differentiation of bone marrow mesenchymal stem cells in postmenopausal osteoporosis through regulating the miR-196a-5p/Hmga2 axis.The levels of LOXL1-AS1, miR-196a-5p and Hmga2 in peripheral blood from postmenopausal osteoporosis patients and healthy postmenopausal females (control) were deter-mined using RT-qPCR. As shown in Fig. a, b and c, com-pared with the control group, LOXL1-AS1 and Hmga2 in postmenopausal osteoporosis had a higher level, while the level of miR-196a-5p in osteoporosis was lower than that in the control group.o measure the effect of LOXL1-AS1 on the osteogenic and adipocytic differentiation of hBMMSCs, LOXL1-AS1 overexpression  plasmid,  plasmid  control,  shRNAs  of  LOXL1-AS1 (shRNA1#, shRNA2#), and scramble shRNA were, respectively, transfected into hBMMSCs.Compared with the control group, LOXL1-AS1 overexpression plasmid group revealed the lower activ-ity of ALP and the less of mineralized nodules formation (Fig. 3a). However, LOXL1-AS1 knockdown increased the ALP activity and mineralized nodules formation in compari-son to the scramble group, as shown in Fig. 3a. Additionally, the overexpression of LOXL1-AS1 decreased the levels of ALP, OPN, and Runx-2 as compared to the control, whereas LOXL1-AS1 knockdown increased the levels of ALP, OPN, and Runx-2 in comparison to the scramble group (Fig. 3b). Hence, the high level of LOXL1-AS1 inhibited the osteo-genic differentiation of hBMMSCs.In addition, the adipocytic differentiation of hBMMSCs was measured using oil red O staining assay. Figure 3a sug-gests that LOXL1-AS1 overexpression promoted adipocytic differentiation of hBMMSCs compared with the control group, while LOXL1-AS1 knockdown suppressed adipo-genesis.  Collectively,  LOXL1-AS1  inhibited  osteogenic  differentiation but promoted adipocytic differentiation.The potential binding sites of miR-196a-5p with LOXL1-AS1 was shown in Fig. 4a. The relationship between miR-196a-5p and LOXL1-AS1 was detected via luciferase reporter assay and RIP assay. The luciferase activity of LOXL1-AS1-WT was obviously down-regulated by the introduction of miR-196a-5p mimic, and yet the activity in LOXL1-AS1-MUT group had no obvious change (Fig. 4b). As compared to the control groups, RIP assay revealed the higher enrich-ment value of Ago2-bound LOXL1-AS1 and miR-196a-5p (Fig. 4c). These findings indicated the direct binding rela-tionship between miR-196a-5p and LOXL1-AS1.miR-196a-5p mimic considerably decreased the luciferase activity of Hmga2-WT and yet had no effect on the activity of Hmga2-MUT, which con-firmed the direct target relationship between miR-196A-5p and Hmga2 (Fig. 5b).Based on the above results, we speculated that LOXL1-AS1 sponged miR-196a-5p to regulate Hmga2 expression, which might affect the osteogenic and adipocytic differ-entiation of hBMMSCs.	32651705	RID04487	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Pancreatic cancer	LINC00261	miR-23a-3p	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000259974	GRCh38_20:22547671-22578642	NA	NA	140828	NA	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	NA	LINC00261 inhibits progression of pancreatic cancer by down-regulating miR-23a-3p.To  explore  the  function  of  LINC00261 in  vitro, LINC00261 expression was measured in pancreatic cancer cell lines. As displayed in Figure 1B,  lower  level  of  LINC00261  was  found  in  four  pancreatic  cancer  cells  lines  than  control (HPDE6-C7) cells. To  analyze  the  effect  of  LINC00261  on  pancreatic  cancer  development in  vitro,  the viability, invasion and apoptosis of CFPAC-1 and BxPC-3 cells were examined. As shown in  Figure 2A and B, overexpression of LINC00261 decreased cell viability at 48 and 72 h, but it did  not  affect  the  viability  at  24  h.  The  invasive ability  of  CFPAC-1  and  BxPC-3  cells  was detected  at  24  h.  The  data  of  transwell  analysis  showed  that  up-regulation  of  LINC00261 repressed  cell  invasion  (Figure  3A  and  B).  Moreover,  epithelial-mesenchymal  transition,  a key  event  involved  in  cell  invasion,  was  investigated  in  the  two  cell  lines  via  detecting  the related  biomarkers. To  analyze  the  potential  action  mechanism  of  LINC00261,  the  targeted  miRNA  of LINC00261 was analyzed. After analysis of TCGA database from LinkedOmics, we selected 5 miRNAs (miR-21,  miR-222, miR-193b, miR-221 and miR-23a-3p) of which expression in pancreatic  cancer  was  negatively  correlated  with  LINC00261  (Figure  5A  and  B).  By analyzing the target association between LINC00261 and the 5 miRNAs using starBase online, there  was  only  complementary  sequence  between  miR-23a-3p  and  LINC00261  (Figure  5C). TCGA  database  from  LinkedOmics  also showed  that there  was  a  slightly inverse  correlation (r  =  -0.3794, P<0.0001)  between  the  amounts  of  LINC00261  and  miR-23a-3p  in  pancreatic cancer (Figure 5D). These data indicated that miR-23a-3p was a potential candidate target of LINC00261.   To   identify   the   target   association   between   LINC00261   and   miR-23a-3p, dual-luciferase  reporter  and  RIP  assays  were  conducted  in  CFPAC-1  cells.  Addition  of miR-23a-3p obviously declined the luciferase activity in LINC00261-WT group, while it did not affect the activity in LINC00261-MUT group (Figure 6A).To  analyze  if  miR-23a-3p  was  needed  for  the  action mechanism  of  LINC00261  in pancreatic  cancer,  CFPAC-1  and  BxPC-3  cells  were  transfected  with  Vector  +  miR-con, LINC00261  overexpression  vector  +  miR-con,  or  LINC00261  overexpression  vector  + miR-23a-3p.   As   displayed   in   Figure   7A   and   B,   addition   of   miR-23a-3p   attenuated LINC00261-induced  inhibition  of  viability  in  CFPAC-1  and  BxPC-3  cells  at  48  and  72  h. miR-23a-3p  addition  weakened  the  suppressive  role  of  LINC00261  in  invasion  of  CFPAC-1 and   BxPC-3   cells   (Figure   7C   and   D).   Restoration   of miR-23a-3p   protected   against LINC00261-mediated apoptosis of the two cell lines (Figure 7E and F). These data suggested that  LINC00261  mediated  pancreatic  cancer  cell  viability,  invasion  and  apoptosis  at  least partially via modulating miR-23a-3p.	32590069	RID04488	expression association	NA	UP(LIHC);DATA(GSE117623)	
Hepatocellular carcinoma	FOXD2-AS1	MAP3K1	positively-E	luciferase reporter assay;RIP;RNA pull-down	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000095015	NA	84793	4214	MGC12982	MAPKKK1|MEKK|MEKK1	Long noncoding RNA FOXD2-AS1 aggravates hepatocellular carcinoma tumorigenesis by regulating the miR-206/MAP3K1 axis.We first examined the level of FOXD2-AS1 in the serum of HCC patients. FOXD2-AS1 expression was markedly elevated in HCC patients compared to that in healthy controls (Figure 1A).Next, FOXD2-AS1 expression was examined in 60 pairs of HCC tumors and adjacent nontumor tissues. Consistently, we observed that FOXD2-AS1 was also significantly upregulated in tumor tissues (Figure 1B).Next, to determine whether FOXD2-AS1 affected HCC cell proliferation, CCK8 assay was performed. Hepatocellular carcinoma cells were infected with sh-NC, sh-FOXD2-AS1, sh01, sh02, or sh03 for 48 hours. qRT-PCRanalysis indicated that sh02 exhibited the strongest effect on FOXD2-AS1 levels (Figure 2A). Hepatocellular carcinoma cell survival was repressed in response to decreased FOXD2-AS1 expression in HCC cells (Figure 2B). EdU assays proved that cell proliferation was inhibited by LV-shFOXD2-AS1 (Figure 2C). In addition, the knockdown of FOXD2-AS1 strongly triggered apoptosis of HepG2 and MHCC-97L cells (Figure 2D). The migration and invasion capacity of HCC cells was restrained by LV-shFOXD2-AS1 (Figure 2E,F). These findings indicate that loss of FOXD2-AS1 inhibits HCC cell growth, migration, and invasion.To examine the interaction between FOXD2-AS1 and miR-206, HCC cells were infected with LV-shFOXD2-AS1. miR-206 expression was elevated in response to LV-shFOXD2-AS1 (Figure 3A). A schematic of the interaction between miR-206 and FOXD2-AS1 is indicated in Figure 3B. In addition, RIP assays evidenced that FOXD2-AS1 and miR-206 were abundant in Ago2 pellets (Figure 3C). Moreover, RNA pull-down assays showed an interaction between FOXD2-AS1 and miR-206 (Figure 3D). These findings imply that miR-206 is a target of FOXD2-AS1.MAP3K1 was also predicted as a target of miR-206, and a schematic of their interaction was described in Figure 4A. WT-MAP3K1 and MUT-MAP3K1 were shown in Figure 4B. Cotransfection of WT-MAP3K1 with miR-206 markedly suppressed reporter activity (Figure 4C). MAP3K1 mRNA expression was strongly induced in HCC cells compared to that in LO2 cells (Figure 4D). We then showed that MAP3K1 was inhibited by miR-206 mimics (Figure 4E,F). Next, as shown in Figure 4G,H MAP3K1 expression was inhibited by LV-shFOXD2-AS1 infection in HCC cells. These data suggest that FOXD2-AS1 can modulate HCC progression by targeting miR-206/MAP3K1.Subsequently, an in vivo assay was employed to confirm the effect of FOXD2-AS1 on HCC progression. Six mice were injected in the front dorsum with parental HepG2 cells and the other six were injected with HepG2 cells infected with LV-shFOXD2-AS1. Inhibition of FOXD2-AS1 profoundly inhibited tumor growth (Figure 5A). HE staining and IHC showed Ki-67 was depressed by LV-shFOXD2-AS1 (Figure 5B). Loss of FOXD2-AS1 repressed MAP3K1 through sponging miR-206 (Figure 5C-F). Thus, the downregulation of FOXD2-AS1 inhibits HCC development in vivo.Kaplan-Meier analysis was conducted to identify the correlation between FOXD2-AS1 and HCC patient survival. We detected the expression level of FOXD2-AS1 in HCC serum in all patients. FOXD2-AS1 were high expressed in HCC with an AUC of 0.866 (Figure 6). These results suggest that FOXD2-AS1 is an appropriate biomarker for HCC diagnostic prediction.	32558350	RID04489	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	CYTOR	YAP1	positively-E	luciferase reporter assay;RIP;RNA pull-down	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(+);cell autophagy(-);chemoresistance(-)	ceRNA(miR-613)	regulation	RNA-protein	Carboplatin;Adriamycin	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000137693	NA	112597	10413	C2orf59|LINC00152|MGC4677|NCRNA00152	YAP65	LncRNA LINC00152 Increases the Aggressiveness of Human Retinoblastoma and Enhances Carboplatin and Adriamycin Resistance by Regulating MiR-613/Yes-Associated Protein 1 (YAP1) Axis.To begin with, RT-qPCR was used to reveal the expression level of LINC00152 in retinoblastoma tissues. As shown in Figure 1A, the data suggested that LINC00152 was prominently overexpressed in retinoblastoma tissues compared with normal retina tissues.Meanwhile, a negative correlation between LINC00152 and miR-613 in retinoblastoma tissues was confirmed using Pearson correlation analysis (Figure 1D). Consistently, LINC00152 expression level was lower in ARPE-19 cells than that in 4 human retinoblastoma cell lines (RBL-13, Y79, Weri-RB-1, and SO-RB50), while miR-613 was overexpressed in ARPE-19 cells than that in human retinoblastoma cell lines (Figure 1E). From these data, we concluded that LINC00152 was associated with poor prognosis of retinoblastoma and negatively correlated with miR-613 expression in retinoblastoma tissues and cells.To understand the relationship between LINC00152 and miR-613, we first screened the target genes of LINC00152 by prediction of bioinformatics software starBase (http://starbase.sysu.edu.cn/). The results indicated that miR-613 was a target of LINC00152 (Figure 2A). Next, dual-luciferase report experiment was performed and showed that miR-613 mimic significantly repressed the luciferase activity of LINC00152-WT reporter, but the luciferase activity in LINC00152-MUT reporter had no significant change (Figure 2B).The data of CCK-8 assay showed that knockdown of miR-613 reverted the reduction of cell viability in Y79 and Weri-RB-1 cells caused by LINC00152 silencing (Figure 3C, 3D). Flow cytometry assay results revealed that apoptosis rate of retinoblastoma cells was significantly upregulated in retinoblastoma cells transfected with si-LINC00152#1 compared to si-NC group, while retinoblastoma cells transfected with anti-miR-613 led to lower apoptosis rate than anti-miR-NC group, and it is worth noted that LINC00152 silencing effects could be counteracted by introducing anti-miR-613 into Y79 and Weri-RB-1 cells (Figure 3E). Consistent with cell viability results, LINC00152 silencing remarkably inhibited invasion of retinoblastoma cells, while miR-613 knockdown induced opposite effects, interestingly, miR-613 silencing abolished the inhibition effect of LINC00152 silencing on cells invasion (Figure 3F). All data indicated that LINC00152 regulated cell proliferation, apoptosis, invasion and autophagy of retinoblastoma cells by directly targeting miR-613.As shown in Figure 4A'-D, the results of the CCK-8 assay indicated that Y79 and Weri-RB-1 cells infected with si-LINC00152#1 exhibited a maximal sensitivity to carboplatin (IC50, 17.26 ug/mL, 21.78 ug/mL) and adriamycin (IC50, 6.167 ug/mL, 21.3 ug/mL). Furthermore, the IC50 was ranked as follows: si-NC group > si-LINC00152#1 group, anti-miR-613 group > anti-miR-NC group, interestingly, anti-miR-613 group > si-LINC00152#1+anti-miR-613 group > si-LINC00152#1 group. Thus, LINC00152 regulated chemoresistance to carboplatin and adriamycin in Y79 and Weri-RB-1 cells by regulating miR-613 expression.Bioinformatics software starBase (http://starbase.sysu.edu.cn/) analysis implied that miR-613 had binding sites with 3'UTR of YAP1 (Figure 5A). The luciferase reporter vector assay was used to confirm the prediction. Following the results suggested that elevated expression of miR-613 effectively decreased the luciferase activity of YAP1-WT reporter, however, luciferase activity of YAP1-MUT almost unchanged by miR-613 mimic (Figure 5B, 5C). To clarify the regulatory impact between miR-613 and YAP1, we first examined the relative expression level of YAP1 in retinoblastoma cells transfected with miR-613, miR-NC, anti-miR-613 or anti-miR-NC by RT-qPCR assay. The results indicated that the mRNA expression level of YAP1 was significantly downregulated in miR-613 group when compared with matched miR-NC group, conversely, miR-613 knockdown effectively enhanced YAP1 expression (Figure 5D, 5E). The same results were found in Figure 5F and 5G, as certificated by western blot assay. As shown in Figure 5H, YAP1 was enhanced in retinoblastoma tissues than control group. Finally, we also proved that the negative correlation relationship between miR-613 and YAP1 was existed in retinoblastoma tissues (Figure 5I). These results suggested that miR-613 negatively regulated YAP1 expression in retinoblastoma cells.The RT-qPCR and western blot assay were utilized to evaluate the mRNA and protein expression levels of YAP1 in Y79 and Weri-RB-1 cells. The data exhibited that the expression level of YAP1 was obviously downregulated in cells transfected with si-LINC00152#1 than si-NC control group, while miR-613 silencing effectively eliminated downregulation of YAP1 caused by LINC00152 knockdown (Figure 7A'-C). In the end, a positive correlation between YAP1 and LINC00152 in retinoblastoma tissues was confirmed using RT-qPCR assay (Figure 7D). In short, LINC00152 knockdown inhibited YAP1 expression by targeting miR-613 in vitro.As shown in Figure 8A and 8B compared with the sh-NC group, the volume and weight of tumor in sh-LINC00152 group were significantly decreased. Moreover, RT-qPCR assay indicated that compared with sh-NC group, LINC00152 and YAP1 were declined, while miR-613 was highly expressed in sh-LINC00152 group (Figure 8C'-E). western blot assay indicated that downregulation of LINC00152 inhibited protein level of YAP1 (Figure 8F). Thus, these results indicated that downregulation of LINC00152 inhibited tumor development in vivo.	32541644	RID04490	ceRNA or sponge	chemoresistance,prognosis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Triple-negative breast cancer	DGCR5	WNT3A	positively-E	western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000154342	NA	26220	89780	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	NA	Long non-coding RNA DGCR5 incudes tumorigenesis of triple-negative breast cancer by affecting Wnt/beta-catenin signaling pathway.RT-qPCR was conducted for detecting DGCR5 expression in 57 patients'-tissues and 4 TNBC cell lines. DGCR5 was significantly upregulated in tu-mor tissue samples than that in adjacent tissues (Figure 1A). Analysis of clinicopathological features in those patients demonstrated that downregulated DGCR5 was obviously correlated to lymph node metastasis and tumor stage (Table 1). Compared with the expression in MCF-10A, DGCR5 level was significantly higher in TNBC cells (Figure 1B). Moreover, MTT assay showed that the cell growth ability was significantly repressed after DGCR5 was knocked down (Figure 2B). Transwell assay showed that the number of migrated cells was significantly decreased after DGCR5 was knocked down (Figure 2C). Furthermore, transwell assay showed that the number of invaded cells was significantly reduced after DGCR5 was knocked down (Figure 2D). Then, the ability of DGCR5 in tumor forma-tion and metastasis was detected in vivo. The tu-mor size in sh-DGCR5 group was smaller compared with negative control shRNA group (Figure 3A). The weight of dissected tumors in sh-DGCR5 group was smaller compared with negative control shR-NA group (Figure 3B). The number of metastatic nodules in the lung from the sh-DGCR5 group was significantly reduced compared to negative control shRNA group (Figure 3C). Moreover, the expres-sion level of DGCR5 in dissected tumor tissues was detected by RT-qPCR and the results showed that DGCR5 was lower-expressed in sh-DGCR5 group compared with negative control shRNA group (Fig-ure 3D). To explore the underlying mechanism of DGCR5 function in TNBC, RT-qPCR and western blot assay were conducted to detect the target pro-teins in Wnt/beta-catenin signaling pathway such as Wnt3a, beta-catenin, C-myc and Survivin. RT-qPCR results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4A). western blot assay results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4B). These results suggested that DGCR5 participated in the regulation of Wnt/beta-catenin signaling pathway and further promoted TNBC development and metastasis.	32521856	RID04491	expression association	metastasis		UP(PAAD);DATA(GSE40174)
Triple-negative breast cancer	DGCR5	CTNNB1	positively-E	western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000168036	NA	26220	1499	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA DGCR5 incudes tumorigenesis of triple-negative breast cancer by affecting Wnt/beta-catenin signaling pathway.RT-qPCR was conducted for detecting DGCR5 expression in 57 patients'-tissues and 4 TNBC cell lines. DGCR5 was significantly upregulated in tu-mor tissue samples than that in adjacent tissues (Figure 1A). Analysis of clinicopathological features in those patients demonstrated that downregulated DGCR5 was obviously correlated to lymph node metastasis and tumor stage (Table 1). Compared with the expression in MCF-10A, DGCR5 level was significantly higher in TNBC cells (Figure 1B). Moreover, MTT assay showed that the cell growth ability was significantly repressed after DGCR5 was knocked down (Figure 2B). Transwell assay showed that the number of migrated cells was significantly decreased after DGCR5 was knocked down (Figure 2C). Furthermore, transwell assay showed that the number of invaded cells was significantly reduced after DGCR5 was knocked down (Figure 2D). Then, the ability of DGCR5 in tumor forma-tion and metastasis was detected in vivo. The tu-mor size in sh-DGCR5 group was smaller compared with negative control shRNA group (Figure 3A). The weight of dissected tumors in sh-DGCR5 group was smaller compared with negative control shR-NA group (Figure 3B). The number of metastatic nodules in the lung from the sh-DGCR5 group was significantly reduced compared to negative control shRNA group (Figure 3C). Moreover, the expres-sion level of DGCR5 in dissected tumor tissues was detected by RT-qPCR and the results showed that DGCR5 was lower-expressed in sh-DGCR5 group compared with negative control shRNA group (Fig-ure 3D). To explore the underlying mechanism of DGCR5 function in TNBC, RT-qPCR and western blot assay were conducted to detect the target pro-teins in Wnt/beta-catenin signaling pathway such as Wnt3a, beta-catenin, C-myc and Survivin. RT-qPCR results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4A). western blot assay results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4B). These results suggested that DGCR5 participated in the regulation of Wnt/beta-catenin signaling pathway and further promoted TNBC development and metastasis.	32521856	RID04492	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Triple-negative breast cancer	DGCR5	MYC	positively-E	western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000136997	NA	26220	4609	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	bHLHe39|c-Myc|MYCC	Long non-coding RNA DGCR5 incudes tumorigenesis of triple-negative breast cancer by affecting Wnt/beta-catenin signaling pathway.RT-qPCR was conducted for detecting DGCR5 expression in 57 patients'-tissues and 4 TNBC cell lines. DGCR5 was significantly upregulated in tu-mor tissue samples than that in adjacent tissues (Figure 1A). Analysis of clinicopathological features in those patients demonstrated that downregulated DGCR5 was obviously correlated to lymph node metastasis and tumor stage (Table 1). Compared with the expression in MCF-10A, DGCR5 level was significantly higher in TNBC cells (Figure 1B). Moreover, MTT assay showed that the cell growth ability was significantly repressed after DGCR5 was knocked down (Figure 2B). Transwell assay showed that the number of migrated cells was significantly decreased after DGCR5 was knocked down (Figure 2C). Furthermore, transwell assay showed that the number of invaded cells was significantly reduced after DGCR5 was knocked down (Figure 2D). Then, the ability of DGCR5 in tumor forma-tion and metastasis was detected in vivo. The tu-mor size in sh-DGCR5 group was smaller compared with negative control shRNA group (Figure 3A). The weight of dissected tumors in sh-DGCR5 group was smaller compared with negative control shR-NA group (Figure 3B). The number of metastatic nodules in the lung from the sh-DGCR5 group was significantly reduced compared to negative control shRNA group (Figure 3C). Moreover, the expres-sion level of DGCR5 in dissected tumor tissues was detected by RT-qPCR and the results showed that DGCR5 was lower-expressed in sh-DGCR5 group compared with negative control shRNA group (Fig-ure 3D). To explore the underlying mechanism of DGCR5 function in TNBC, RT-qPCR and western blot assay were conducted to detect the target pro-teins in Wnt/beta-catenin signaling pathway such as Wnt3a, beta-catenin, C-myc and Survivin. RT-qPCR results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4A). western blot assay results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4B). These results suggested that DGCR5 participated in the regulation of Wnt/beta-catenin signaling pathway and further promoted TNBC development and metastasis.	32521856	RID04493	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Triple-negative breast cancer	DGCR5	BIRC5	positively-E	western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000089685	NA	26220	332	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	API4|EPR-1|survivin	Long non-coding RNA DGCR5 incudes tumorigenesis of triple-negative breast cancer by affecting Wnt/beta-catenin signaling pathway.RT-qPCR was conducted for detecting DGCR5 expression in 57 patients'-tissues and 4 TNBC cell lines. DGCR5 was significantly upregulated in tu-mor tissue samples than that in adjacent tissues (Figure 1A). Analysis of clinicopathological features in those patients demonstrated that downregulated DGCR5 was obviously correlated to lymph node metastasis and tumor stage (Table 1). Compared with the expression in MCF-10A, DGCR5 level was significantly higher in TNBC cells (Figure 1B). Moreover, MTT assay showed that the cell growth ability was significantly repressed after DGCR5 was knocked down (Figure 2B). Transwell assay showed that the number of migrated cells was significantly decreased after DGCR5 was knocked down (Figure 2C). Furthermore, transwell assay showed that the number of invaded cells was significantly reduced after DGCR5 was knocked down (Figure 2D). Then, the ability of DGCR5 in tumor forma-tion and metastasis was detected in vivo. The tu-mor size in sh-DGCR5 group was smaller compared with negative control shRNA group (Figure 3A). The weight of dissected tumors in sh-DGCR5 group was smaller compared with negative control shR-NA group (Figure 3B). The number of metastatic nodules in the lung from the sh-DGCR5 group was significantly reduced compared to negative control shRNA group (Figure 3C). Moreover, the expres-sion level of DGCR5 in dissected tumor tissues was detected by RT-qPCR and the results showed that DGCR5 was lower-expressed in sh-DGCR5 group compared with negative control shRNA group (Fig-ure 3D). To explore the underlying mechanism of DGCR5 function in TNBC, RT-qPCR and western blot assay were conducted to detect the target pro-teins in Wnt/beta-catenin signaling pathway such as Wnt3a, beta-catenin, C-myc and Survivin. RT-qPCR results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4A). western blot assay results showed that Wnt3a, beta-catenin, C-myc and Survivin could be downregulated via knockdown of DGCR5 (Figure 4B). These results suggested that DGCR5 participated in the regulation of Wnt/beta-catenin signaling pathway and further promoted TNBC development and metastasis.	32521856	RID04494	expression association	metastasis		UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Kidney disease	SNHG16	CCND1	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);fibrotic(+)	ceRNA(miR-141-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000110092	NA	100507246	595	Nbla10727|Nbla12061|ncRAN	BCL1|D11S287E|PRAD1|U21B31	LncRNA SNHG16 induces proliferation and fibrogenesis via modulating miR-141-3p and CCND1 in diabetic nephropathy.Firstly, to explore the effect of SNHG16 in DN progression,we tested expression of SNHG16 in renal cortex of db/db mice and normal control C57BL/Ks mice at 24 weeks using real-time PCR. As showed in Fig.1a, we observed thatSNHG16 was obviously increased in db/db mice. In Fig.3b, the CCK-8 assay displayed that SNHG16 silencing significantly inhibited the survival of mesangial cells. Loss of SNHG16 repressed PCNA and CCND1 protein expres-sion as evidenced by western blot assays (Fig.3c, d). Inaddition, in Fig.3e, f, the EdU assay implied that cell proliferation was  also greatly restrained by SNHG16 knockdown. These indicated that SNHG16 contributed tomesangial cell proliferation.Moreover,flow cytometry analysis indicated that highglucose inhibited mesangial cell apoptosis than the normal concentration  of  glucose.  LV-shSNHG16  could  sig-nificantly induce cell apoptosis as exhibited in Fig.4a, b. In addition, we observed high glucose contributed to cell cycle progression while LV-shSNHG16 transfection could inhibit that (Fig.4c, d). These illustrated that down regulation of SNHG16 induced mesangial cells apoptosis and repressed progression of cell cycle.Mesangial cells were incubated with low and high glucose,respectively, and then transfected with LV-shSNHG1.Then, western blotwas applied to test the expres-sion levels of Fibronectin and alpha-SMA. Fibronectin and alpha-SMA protein level was higher under high glucose and loss of SNHG16 suppressed Fibronectin and alpha-SMA protein expression (Fig.5a, b). These suggested that silencing of SNHG16 depressed mesangial cellsfibrogenesis.miR-141-3p was predicted as a direct of SNHG16. Thebinding regions between them were exhibited in Fig.6a.Then, luciferase reporter plasmids of WT-SNHG16 and MUT-SNHG16-binding sites were manifested in Fig.6b.Then, co-transfection of the luciferase reporter plasmid containing WT-SNHG16 with miR-141-3p mimics repres-sed the reporter activity (Fig.6c). Then, the RIP assay was employed and miR-141-3p and SNHG16 were much moreenriched in Ago2 pellet (Fig.6d). Meanwhile, down-regulation  of  SNHG16  greatly  induced  miR-141-3p expression  as  shown  in  Fig.6e.  miR-141-3p  was decreased in the renal cortex of db/db mice as indicated in Fig.6f. These implied  miR-141-3p was a direct of SNHG16.Furthermore, CCND1 can act as a direct target of miR-141-3p. Figure7a exhibited the binding sites between CCND1and miR-141-3p. Luciferase reporter plasmids of WT-CCND1 and MUT-CCND1-binding sites were displayed inFig.7b. Co-transfection of the luciferase reporter plasmidcontaining WT-CCND1 with miR-141-3p mimics greatlyreduced the reporter activity in mesangial cells (Fig.7c).Addition of WT-SNHG16 rescued the inhibition effect ofmiR-141-3p on the CCND1 3'UTR activity.	32504027	RID04495	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Atherosclerosis	MIAT	PAPPA	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-148b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000182752	NA	440823	5069	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ASBABP2|DIPLA1|IGFBP-4ase|PAPA|PAPP-A|PAPPA1	Long non-coding RNA MIAT/miR-148b/PAPPA axis modifies cell proliferation and migration in ox-LDL-induced human aorta vascular smooth muscle cells.Owing to  the  high  expression  of  MIAT  in  ox-LDL-induced  AS  cell  model,  our study    detected    how    MIAT    contributing    to    proliferation    and    migration    in ox-LDL-induced   HA-VSMCs.   Firstly,   si-MIAT1   or   si-NC   was   transfected   into ox-LDL  induced  HA-VSMCs.  Level  of  MIAT  was  substantially  decreased  and  the results  were  showed  in  Fig.  2A.  Meanwhile,  cell  proliferation  was  identified  by CCK-8  assay, andresults  showed  that silencedMIAT  markedly  attenuated  cell proliferation  (Fig.  2B).  The  expression  of  Ki-67  and  PCNA  was  employed  to  verify cell  proliferation  at  protein  level,  from  the  results,  the  repressed  expression  of  them meant   that   knockdown   of   MIAT1   remarkably   hindered   cell   proliferation   in ox-LDL-induced  HA-VSMCs in  vitro (Fig.  2C). Meanwhile, thetendency  of  these proteins to  changewas  verified through Flow  Cytometry(Sup Fig. 1). What  more, wound-healing  assay  was  performed  to  determine  cell  migration  capacity,  the  results exhibited  that  the  cell  migration  distance  was  effectively  impeded  in  si-MIAT  group (Fig.  2D).  Besides,  levels  of  MMP-2  and  MMP-9  were  also  used  to  clarify  the capacity  of  cell  migration, and western  blot  assay  results  revealed  that  transfection with  si-MIAT1  led  a  significant  curb  influence  on  the  expression  of  MMP-2  and MMP-9   in   ox-LDL-induced   HA-VSMCs(Fig.   2E).   All   data   implied   that   cell proliferation  and migration were both inhibited by  MIAT silence in ox-LDL-induced HA-VSMCs.To clarify the results, luciferase reporter assay was carried out to verify the interaction between MIAT and miR-148b, and the inhibitory effect  of  miR-148b  mimics  and  the  promotor  effect  of  miR-148b  inhibitor  on luciferase  activities  in  wild-type  groups  suggested  that  miR-148b  was  targeted  by MIAT  (Fig.  3B).  Additionally,  the  interrelation  between  miR-148b  and  MIAT  was further confirmed by RIP assay, the results demonstrated that the enrichment of MIAT was  improved  by  miR-148b,  and  miR-148b  was  also  increased  by  MIAT,  these evidences  further  expound  that  MIAT  directly  targeted  miR-148b  (Fig.  3C).From the above, the evidences suggested that the role of MIAT was exerted by sponging miR-148b.On the  account  of  miR-148b  participated  in  the  modulation  of  AS  progression, the study detected the role of miR-148b in this process subsequently. Firstly, miR-NC or   miR-148b   was   transfected   into   ox-LDL-induced   HA-VSMCs,   the   promotor efficiency  was  measured  by  qRT-PCR  and  the  results  were  exhibited  in  Fig.  4A.  At the  same  time,  cell  proliferation  was  determined  by  CCK-8  assay,  the  results discovered  that  miR-148b  notably  suppressed  cell  proliferation  in  ox-LDL  induced AS cell model (Fig. 4B). The conclusion of cell proliferation was confirmed through measuring  levels  of  Ki-67  and  PCNA,  the  significant  low-expression  of  them supported  the  above  CCK-8  assay  conclusion  (Fig.  4C).These data explored that cell migration capacity was dramatically hampered by miR-148b mimics.The   inhibitory   effect   of   MIAT   downregulationon   cell proliferation  was  regained  by  miR-148b  inhibitor  in  ox-LDL-induced  HA-VSMCs (Fig.  5B).  What   more,  the  expression  of  MMP-2  and  MMP-9  recovered  by miR-148b  inhibitor  also  confirmed  that  miR-148b  ameliorated  the  effect  of  si-MIAT on  cell  proliferation  in  ox-LDL  induced  AS  cell  model  (Fig.  5C).  Furthermore, wound-healing assay was carried out to identify cell migration capacity, the migration distance  was  restored  by  co-transfectionwithsi-MIAT  and  miR-148b  inhibitor compared  with  only  transfected  with  si-MIAT  (Fig.  5D).  Meanwhile,  the  increased expression   of   MMP-2   and   MMP-9   in   cells   co-transfected   with   si-MIAT   and anti-miR-148b also demonstrated that the suppressor role of MIAT knockdown in cell migration was relieved by miR-148b inhibitor (Fig. 5E). In brief, the inhibitory effects of  MIAT  knockdown  on  cell  behaviors  of  proliferation  and  migration  were  reverted by miR-148b inhibitor.In order to verify the regulatory mechanism between miR-148b and  PAPPA,  dual-luciferase  reporter  assay  and  RIP  assay  were  conducted.  The inhibitory  effect  of  miR-148b  mimics  and  promotor  effect  of  miR-148b  inhibitor  on fluorescence  intensity  in  wild-type  group  initially  judged  that  miR-148b  targeted PAPPA (Fig. 6B). Additionally, the higher enrichment of relative RNA in Ago2 groups than  that  of  IgG  groups  further  proved  that  PAPPA  was  targeted  by  miR-148b  (Fig. 6C). The   results discovered  that  the  augment  effect  of  MIAT  on  the  expression  of  PAPPA  was  partial overturned  by  miR-148b  mimics  (Fig.  8A).  Synchronously,  level  of  PAPPA  was repressed  by  MIAT  knockdown,  whereas  the  inhibiting  effect  of  si-MIAT  on  PAPPA expression  was  abrogated  by  co-transfectionwith  miR-148b  inhibitor  (Fig.  8B).  In summary, these evidences emerged that PAPPA expression was co-regulated by MIAT and miR-148b, it was positively related to MIAT, while was contrary to miR-148b.	32470448	RID04496	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC);DOWN(PAAD);DATA(GSE117623,GSE40174)
Acute myeloid leukemia	PVT1	MYC	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell viability(-)	NA	regulation	NA	NA	NA	NA	Reproductive system disease	Primary ovarian insufficiency	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	bHLHe39|c-Myc|MYCC	Reduce proliferation of human bone marrow cells from acute myeloblastic leukemia with minimally differentiation by blocking lncRNA PVT1.After the transfection of antisense LNA GapmeRs into the cells, the transfection efficiency was determined by fluores-cence microscopy due to the FAM group in the oligonucleo-tide strands. The transfection level was determined by more than 90% by flow cytometry (Fig. 1). q-RT PCR was per-formed to measure the expression of PVT1 in four different cell groups (control, mock group, ALGNC, Antisense LNA GapmeRs) 24, 48, and 72 h after transfection. PVT1 expres-sion was decreased significantly in the antisense LNA Gap-meRs group at all of the three-time points compared to other groups (p < 0.001)  (Fig. 2).To evaluate the effect of PVT1 inhibition on cell viability, the MTT test was performed at 24, 48, and 72 h after trans-fection. Compared to the control group, the viability in all other groups was reduced, but the reduction in antisense LNA GapmeRs group was notably significant (Fig. 3).To determine the effect of PVT1 inhibition on apoptosis and necrosis Annexin-V/PI double staining was carried out after transfection at 24, 48, and 72 h. Due to the transfection reagent toxicity, the apoptotic ratio was high in all groups, but  it  was  more  significant  in  the  antisense  LNA  group  (p < 0.001). The highest amount of apoptosis was in the LNA GapmeRs group compared to other groups. Generally, the results reveal that PVT1 degradation induced apoptosis in the cells. (Fig. 4). Simultaneously, necrosis was measured as well. The necrosis ratio was significantly higher in the LNA GapmeRs group at all three-time points, which explains why apoptosis rate was lower in the LNA GapmeRs group com-pared to other time points results, the cells were entered in necrosis phase. This result represents that PVT1 blockage by antisense LNA GapmeRs may have induced necrosis in human cancerous blast cells (Fig. 5).qRT-PCRwas performed for c-Myc as well as PVT1 in con-trol, mock group, ALGNC, and antisense LNA GapmeRs group at three-time points after transfection. The expres-sion of c-Myc was lower in the LNA GapmeRs group as compared to others. In this group, c-Myc expression was almost the same amount at 24 and 72 h and it was a little more in 48 h post-transfection. It can be concluded that the expression of PVT1 can influence c-Myc expression (Fig. 6).	32406010	RID04497	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	LINC00665	E2F3	positively-E	luciferase reporter assay;bioinformatics analysis	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-138-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000112242	NA	100506930	1871	CIP2A-BP	NA	Downregulation of LINC00665 confers decreased cell proliferation and invasion via the miR-138-5p/E2F3 signaling pathway in NSCLC.A lncRNA microarray was used to analyze paired NSCLC and ad-jacent normal lung tissues. The results can be seen in theFig. 1A.LINC00665 was markedly upregulated in tumor tissues compare to thenormal tissues with a greater thanfive-fold changes.We used the CCK-8 assay for analyzing cell growth and found that the OD 450 valuein sh-lncRNA groups of A549 and H1299 cells was markedly decreased when compared with the NC group (Fig. 2B,p< 0.05). The results demonstrated  the  inhibitory  effects  of  downregulated  lncRNA LINC00665 on cell growth in A549 and H1299 cells. As shown in Fig. 2C, the relative number of invading cells was markedly decreased(p< 0.05) in the sh-lncRNA group when compared with the NC group,which suggested that down regulated lncRNA LINC00665 could forbid cell invasion in vitro.We constructed xenograft experiments in nude mice in which weinjected transfected A549 cells. From these xenograft experiments, we collected the tumors from the nude mice (Fig. 3A) and compared the volume of tumors between the sh-lncRNA group and NC group in three weeks. As shown inFig. 3B, the tumor volume in sh-lncRNA LINC00665 group was significantly smaller than that of the NC group in the third week (p< 0.05); the tumor weight in sh-lncRNA group was also found lighter (Fig. 3C,p< 0.05). Using RT-qPCR, we proved that LINC00665 was downregulated in the xenograft tissues of the sh-lncRNA group(Fig. 3D,p< 0.05). InFig. 3E, the number of Ki67-positive cells was significantly decreased in sh-lncRNA group demonstrating that down-regulated LINC00665 could inhibit A549 cell prolifer.In the following dual-luciferase reporter assay, luciferase activity in miR-138-5p mimics and wild-typeLINC00665-pmirGLO co-transfected cells was the lowest among theother three experimental groups (Fig. 4B,p< 0.05). Additionally, asshown in Fig. 4C, miR-138-5p level was significantly upregulated incells transfected with sh-lncRNA LINC00665 (p< 0.05). Conversely,miR-138-5p was in relatively lower expression in 37 NSCLC tissues compared to that in normal lung tissues (Fig. 4D,p< 0.05). Finally, we compared the expression of miR-138-5p and LINC00665 in tissues andthe results of spearman rank correlation test showed that the two sideshad a significant negative linear correlation with one another (Fig. 4E,R2= 0.326,p< 0.05). The achievements above point out that LINC00665 regulates the expression of miR-138-5p.We operated dual-luciferase reporter experi-ments invitro. Relative luciferase activity was decreased only in cellsco-transfected with miR-138-5p mimics and wt-E2F3 3'UTR-pmirGLO,which was significantly different to that of the other three experimentalgroups (Fig. 5B,p< 0.05). Consequently, E2F3 was one of the targets ofmiR-138-5p. The results of western blotdemonstrated thatE2F3 protein expression was downregulated (Fig. 5C,p< 0.05) in miR-138-5p mimics group. Similarly, in cells transfected with shRNA-LINC00665, the E2F3 protein expression was also decreased (Fig. 5 p< 0.05). No statistical difference occurred in the two groups(p> 0.05). In the results above, we suspected that there may exist LINC00665/miR-138-5p/E2F3 axis that could influence cell proliferation and in-vasion in A549 and H1299 cells. In order to verify the theory, weconstructed pcDNA3.1-E2F3 (Ex-E2F3, E2F3 without 3'UTR, SangonBiotech Co., Ltd, shanghai) and transfect it into A549 and H1299 cellsrespectively. Then CCK-8 assay and transwell experiment were per-formed to test the effects of pcDNA3.1-E2F3; cells transfected withnothing served as normal control. As shown inFig. 6A and B, comparedwith only miR-138-5p mimic-transfected or shRNA-LINC00665-trans-fected cells, the OD 450 value was recovered (p< 0.05), and thenumber of invasive cells was mounting (p< 0.05) in cells both trans-fected with shRNA-LINC00665 and Ex-E2F3. These results underscoredthat E2F3 without 3'UTR could counteract the effects of downregulatedLINC00665 on cell proliferation and invasion	32403047	RID04498	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Essential hypertension	LOC646616	WNT3	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000249142	GRCh38_5:32522758-32523865	ENSG00000108379	NA	646616	7473	NA	INT4|MGC131950|MGC138321|MGC138323	Identification of candidate lncRNAs and circRNAs regulating WNT3/beta-catenin signaling in essential hypertension. Next, we investigated the expression of LOC646616, LAP3P2, hsa_circ_0039388, and hsa_circ_0038648 in human aortic smooth muscle cells (HASMCs) and in Human embryonic kidney 293T (HEK293T) cells using qRT-PCR Results showed high expression of all these transcripts in HASMCs (Figure 3E). To verify the subcellular localization of the above ncRNAs, we employed qRT-PCR This analysis demonstrated that LOC646616 was mainly located in the cytoplasm (Figure 3F). Consistent with qRT-PCRresults, single-molecule RNA-FISH analysis revealed a relatively high expression and a predominantly cytoplasmic distribution for both LOC646616 and hsa_circ_0038648 in HASMCs (Figure 3G).To confirm the interaction between LOC646616 and miR-637, we performed RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. RIP results revealed that LOC646616 and miR-637 were co-immunoprecipitated by an Ago2 antibody in HASMCs, indicating that both ncRNAs were in the same RNA-induced silencing complex (RISC). Subsequently, we confirmed through qRT-PCRthat the precipitated products were indeed LOC646616 and miR-637 (Figure 5F). Considering the effect of miR-637 transfection, we conducted dual-luciferase reporter assays on HEK293T cells co-transfected with miR-637 mimics or mimic NC and luciferase constructs containing wild-type LOC646616 (Luc-LOC646616-wt) or a mutated transcript form (Luc-LOC646616-mut) (Figure 5G, left panel). Results showed that miR-637 expression suppressed luciferase activity driven by LOC646616-wt, and it had a much lower effect on its mutated form (Figure 5G, right panel). These results revealed that LOC646616 inhibits the expression of miR-637 by direct binding.Using qRT-PCRand western blot, we verified that WNT3 and beta-catenin expression was considerably increased in hypertensive subjects (Figure 6A, -,6B).6B). Based on results of our ceRNA network analysis, we performed dual-luciferase reporter assays in HEK293T cells to confirm the interaction between miR-637 and WNT3. Results revealed that in the presence of miR-637 mimics the wild-type 3'-UTR of WNT3 exhibited a low translation level compared to the mutant 3'-UTR (Figure 6C, -,6D).6D).To verify that LOC646616 interacts with miR-637 to activate the expression of WNT3, we measured WNT3 mRNA and protein levels in HASMCs transfected with siRNAs targeting the corresponding ncRNAs. As shown in Figure 7E and -and7F,7F, WNT3 expression was significantly reduced by LOC646616 knockdown, and significantly increased by miR-637 inhibition. Confirming opposite regulatory roles for these ncRNAs on WNT3 expression, further expression assays showed that concurrent inhibition of miR-637 counteracted the inhibitory effect of LOC646616 silencing on WNT3 expression (Figure 7E and -and7F).7F). These results strongly suggest that LOC646616 increases WNT3 expression by sponging miR-637.Based on the results of our ceRNA network predicting a regulatory module composed of LOC646616-miR-637-CAMK2N2, we assessed CAMK2N2 expression and conducted correlation analyses for this ceRNA triplet. Both qRT-PCRand western blot showed that CAMK2N2 expression was significantly higher in hypertensive subjects compared to normotensive controls (Supplementary Figure 7A, 7B). Meanwhile, bivariate correlation analysis demonstrated that CAMK2N2 was positively correlated with LOC646616 (Supplementary Figure 7C) and inversely correlated with miR-637 (Supplementary Figure 7D). These data strongly suggest that LOC646616 and miR-367 exert mutual regulation on both WNT3 and CAMK2N2, and indicate that LOC646616 upregulation inhibits miR-637 expression to activate the WNT3/beta-catenin axis in hypertension.	32392180	RID04499	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Essential hypertension	LOC646616	CAMK2N2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000249142	GRCh38_5:32522758-32523865	ENSG00000163888	NA	646616	94032	NA	CaM-KIIN	Identification of candidate lncRNAs and circRNAs regulating WNT3/beta-catenin signaling in essential hypertension. Next, we investigated the expression of LOC646616, LAP3P2, hsa_circ_0039388, and hsa_circ_0038648 in human aortic smooth muscle cells (HASMCs) and in Human embryonic kidney 293T (HEK293T) cells using qRT-PCR Results showed high expression of all these transcripts in HASMCs (Figure 3E). To verify the subcellular localization of the above ncRNAs, we employed qRT-PCR This analysis demonstrated that LOC646616 was mainly located in the cytoplasm (Figure 3F). Consistent with qRT-PCRresults, single-molecule RNA-FISH analysis revealed a relatively high expression and a predominantly cytoplasmic distribution for both LOC646616 and hsa_circ_0038648 in HASMCs (Figure 3G).To confirm the interaction between LOC646616 and miR-637, we performed RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. RIP results revealed that LOC646616 and miR-637 were co-immunoprecipitated by an Ago2 antibody in HASMCs, indicating that both ncRNAs were in the same RNA-induced silencing complex (RISC). Subsequently, we confirmed through qRT-PCRthat the precipitated products were indeed LOC646616 and miR-637 (Figure 5F). Considering the effect of miR-637 transfection, we conducted dual-luciferase reporter assays on HEK293T cells co-transfected with miR-637 mimics or mimic NC and luciferase constructs containing wild-type LOC646616 (Luc-LOC646616-wt) or a mutated transcript form (Luc-LOC646616-mut) (Figure 5G, left panel). Results showed that miR-637 expression suppressed luciferase activity driven by LOC646616-wt, and it had a much lower effect on its mutated form (Figure 5G, right panel). These results revealed that LOC646616 inhibits the expression of miR-637 by direct binding.Using qRT-PCRand western blot, we verified that WNT3 and beta-catenin expression was considerably increased in hypertensive subjects (Figure 6A, -,6B).6B). Based on results of our ceRNA network analysis, we performed dual-luciferase reporter assays in HEK293T cells to confirm the interaction between miR-637 and WNT3. Results revealed that in the presence of miR-637 mimics the wild-type 3'-UTR of WNT3 exhibited a low translation level compared to the mutant 3'-UTR (Figure 6C, -,6D).6D).To verify that LOC646616 interacts with miR-637 to activate the expression of WNT3, we measured WNT3 mRNA and protein levels in HASMCs transfected with siRNAs targeting the corresponding ncRNAs. As shown in Figure 7E and -and7F,7F, WNT3 expression was significantly reduced by LOC646616 knockdown, and significantly increased by miR-637 inhibition. Confirming opposite regulatory roles for these ncRNAs on WNT3 expression, further expression assays showed that concurrent inhibition of miR-637 counteracted the inhibitory effect of LOC646616 silencing on WNT3 expression (Figure 7E and -and7F).7F). These results strongly suggest that LOC646616 increases WNT3 expression by sponging miR-637.Based on the results of our ceRNA network predicting a regulatory module composed of LOC646616-miR-637-CAMK2N2, we assessed CAMK2N2 expression and conducted correlation analyses for this ceRNA triplet. Both qRT-PCRand western blot showed that CAMK2N2 expression was significantly higher in hypertensive subjects compared to normotensive controls (Supplementary Figure 7A, 7B). Meanwhile, bivariate correlation analysis demonstrated that CAMK2N2 was positively correlated with LOC646616 (Supplementary Figure 7C) and inversely correlated with miR-637 (Supplementary Figure 7D). These data strongly suggest that LOC646616 and miR-367 exert mutual regulation on both WNT3 and CAMK2N2, and indicate that LOC646616 upregulation inhibits miR-637 expression to activate the WNT3/beta-catenin axis in hypertension.	32392180	RID04500	ceRNA or sponge	NA		UP(BRCA);DATA(GSE55807)
Hepatocellular carcinoma	TRIM52-AS1	MRPS18A	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-514a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000248275	GRCh38_5:181261169-181272307	ENSG00000096080	NA	100507602	55168	NA	FLJ10548|MRPS18-3	Long Noncoding RNA TRIM52-AS1 Sponges miR-514a-5p to Facilitate Hepatocellular Carcinoma Progression Through Increasing MRPS18A.Previous studies reported thatTRIM52-AS1was involvedin renal cell carcinoma, so the authors applied GEPIA da-tabase and found that TRIM52-AS1expression was notablyupregulated in LIHC (liver HCC) tissue samples (T=369) compared  with  normal  liver  tissue  samples  (n=160)(Fig. 1A).The au-thors selected sh-TRIM52-AS1#1 for further use as it presentedbetter knockdown efficiency. Later on, the authors analyzedthe function ofTRIM52-AS1inHCC.AsshowninCCK-8assay, cell viability was inhibited byTRIM52-AS1down-regulation (Fig. 1D). Consistently, colony formation assayverified that cell proliferation was attenuated by reduction ofTRIM52-AS1(Fig. 1E).So the authors searched star-Base and found that there were 20 miRNAs that had po-tential binding abilities toTRIM52-AS1(Fig. 2B). Amongthem, 13 miRNAs haven't been explored in HCC. More-over, RNA pull-down assay unveiled that onlymiR-514a-5pwas greatly enriched in bio-TRIM52-AS1-WT group ratherthan in bio-NC and bio-TRIM52-AS1-Mut groups (Fig. 2C).RT-qPCR detected the expression ofmiR-514a-5p, dis-closing thatmiR-514a-5pwas downregulated in HCC cells(Fig. 2D).In addition,miR-514a-5pexpression was inversely reg-ulated byTRIM52-AS1(Fig. 2E). RIP manifested the en-richment ofTRIM52-AS1, andmiR-514a-5pwas observed inAgo2 group instead of IgG group (Fig. 2F). Then RT-qPCRobtained the satisfactory overexpression efficacy ofmiR-514a-5pin HCC cells (Fig. 2G). The putative binding siteforTRIM52-AS1andmiR-514a-5pwas  presented  inFigure 2H. Luciferase reporter assay showed thatmiR-514a-5pupregulation reduced the luciferase activity ofTRIM52-AS1-WT, but didn't influence that ofTRIM52-AS1-Mut(Fig. 2I). All the data indicated thatTRIM52-AS1boundwithmiR-514a-5p.Next, the authors analyzed the downstream ofmiR-514a-5p. Two programs (including miRmap and RNA22) selectedfrom starBase revealed that CYP2S1, BCL2L13, ATP2C1,USP11, andMRPS18Awere potentially targeted bymiR-514a-5p(Fig. 3A, B). RT-qPCR disclosed thatmiR-514a-5poverexpression markedly decreased the mRNA and proteinexpression ofMRPS18A, whereas had no obvious effectson the expression of others in both HepG2 and Huh7 cells(Fig. 3C, D). In addition,MRPS18Aexpression was evidentlyenhanced in HCC cells in comparison with normal livercells (Fig. 3E).In addition,TRIM52-AS1, miR-518a-5p, andMRPS18Awere identified to be enriched in Ago2-precipitated com-plexes (Fig. 3F), suggesting that miR-518a-5p might bindwithMRPS18Ain RNA-induced silencing complexes inHCC.  The  binding  sites  between  miR-518a-5p  andMRPS18Afrom starBase are shown in Figure 3G. Lucifer-ase reporter assays further confirmed that miR-518a-5pcould bind with and silenceMRPS18A, proved by overex-pression of miR-518a-5p that markedly reduced the lucifer-ase activity ofMRPS18A-WT, not that ofMRPS18A-Mut(Fig. 3H). In summary,MRPS18Aserved as a downstreamtarget ofmiR-514a-5pin HCC.Finally, the authors performed rescue assays to validate whether TRIM52-AS1accelerated HCC progression by regulating MRPS18A.To beginwith,MRPS18Awas overexpressedin HepG2 cells by pcDNA3.1/MRPS18A, which resulted in amarked enhancement of MRPS18A expression (Fig. 4A).CCK-8 and colony formation assays uncovered that MRPS18A upregulation recovered TRIM52-AS1-mediated suppression oncell proliferation in HCC (Fig. 4B, C). What  more, enhancedcell apoptosis byTRIM52-AS1silence was reversed by MRPS18A overexpression (Fig. 4D, E).Transwell assays revealed that cell migration and inva-sion repressed byTRIM52-AS1depletion was rescued as a result of MRPS18A enhancement (Fig. 4F, G). western blotmanifested that over expression of MRPS18A neutralized the promoting effect on E-cadherin, as well as the inhibitory effects on N-cadherin and Vimentin causedbyTRIM52-AS1 ablation (Fig. 4H). Altogether,TRIM52-AS1accelerated HCC development through modulating MRPS18A.	32391716	RID04501	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Tetralogy of fallot	TBX5-AS1:2	TBX5	positively-E	luciferase reporter assay;RNA pull-down assay;GEO data mining;bioinformatics analysis	downregulation	qPCR	NA	NA	cell proliferation(-);	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Congenital heart disease	lncRNA	TF	NA	NA	ENSG00000089225	NA	NA	6910	NA	HOS	Hypermethylation-mediated down-regulation of lncRNA TBX5-AS1:2 in Tetralogy of Fallot inhibits cell proliferation by reducing TBX5 expression.To validate the role of lncRNA TBX5-AS1:2 in heart development or TOF and to determine whether lncRNA TBX5-AS1:2 affected the expression of TBX5 in TOF, we detected lncRNA TBX5-AS1:2 and TBX5 expression in 53 samples of injured heart tissue from patients with TOF and 13 normal heart samples using qPCR. The results confirmed that lncRNA TBX5-AS1:2 and TBX5 expression were significantly down-regulated in TOF compared with normal control (NC) (Figure 1E,F).Abnormal cell proliferation and apoptosis is a key feature of TOF. To investigate the effects of lncRNA TBX5-AS1:2 on cell proliferation and apoptosis, lncRNA TBX5-AS1:2 was successfully down-regulated by stable transfection of shRNA2 lentivirus with the most interference efficiency and up-regulated separately in HEK293T cells (Figure 2A,B). CCK8 assay showed that lncRNA TBX5-AS1:2 knock-down significantly inhibited cell proliferation, consistent with the tendency in cells overexpressing lncRNA TBX5-AS1:2 (Figure 2C,D). However, flow cytometry analysis revealed that lncRNA TBX5-AS1:2 dysregulation did not affect apoptosis of HEK293T cells (Figure 2E,F).Previous bioinformatics prediction indicated that lncRNA TBX5-AS1:2 may be co-expressed with its sense gene TBX5. We therefore detected TBX5 mRNA and protein expression levels by qPCR and western blot (WB) in HEK293T cells with down-regulated and up-regulated lncRNA TBX5-AS1:2. TBX5 mRNA and protein levels were both significantly down-regulated after lncRNA TBX5-AS1:2 knock-down (Figure 3C,D) and up-regulated after lncRNA TBX5-AS1:2 overexpression (Figure 3E,F).Considering that lncRNA TBX5-AS1:2 regulated TBX5 expression, we performed TBX5 rescue experiment to determine whether lncRNA TBX5-AS1:2 influencing cell proliferation was mediated by TBX5. TBX5 was overexpressed successfully in HEK293T cells with lncRNA TBX5-AS1:2 knock-down, and then, CCK8 assay showed that TBX5 rescued the cell proliferation suppressed by lncRNA TBX5-AS1:2 knock-down (Figure 3G). Therefore, it indicated that lncRNA TBX5-AS1:2 knoc-kdown may inhibit cell proliferation by TBX5.DNA methylation is an important factor regulating the expression of lncRNAs. We further explored the mechanism by which lncRNA TBX5-AS1:2 was down-regulated in injured heart tissues from TOF patients by predicting the distribution of CpG islands in the lncRNA TBX5-AS1:2 regulatory sequence using MethPrimer online. Four CpG islands were identified (Figure 4A), of which islands 2 and 3 located in the basal core promoter were selected for investigation of their methylation status in human heart samples. BSP for clones revealed that CpG island 2 was remarkably hypermethylated in the injured heart tissues of TOF patients compared with normal heart tissue (P = .001) (Figure 4B and Table S3), but there was no significant difference in CpG island 3 (Table S4).Hypermethylation of CpG islands can inhibit the transcriptional activity of lncRNAs. We therefore transfected methylated and unmethylated lncRNA TBX5-AS1:2 reporter plasmids containing CpG island 2 into HEK293T cells. The unmethylated construct was digested by MRSEs whereas the methylated construct was not (Figure 4C). BSP revealed that the methylation efficiency of CpG island 2 was increased in HEK293T cells when the construct was methylated (Figure 4D,E). dual-luciferase reporter assay revealed that the methylated construct decreased the transcriptional activity of lncRNA TBX5-AS1:2 in HEK293T cells compared with the unmethylated construct (Figure 4F).	32368852	RID04502	epigenetic regulation	NA		UP(LIHC);DATA(GSE117623)
Atherosclerosis	SMILR	KLF5	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-10b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000255364	GRCh38_8:122414332-122428551	ENSG00000102554	NA	105375734	688	NA	BTEB2|CKLF|IKLF	SMILR Aggravates the Progression of Atherosclerosis by Sponging miR-10b-3p to Regulate KLF5 Expression.First, we investigatedthe expression of SMILR in AS by RT-qPCR. The resultsshowed that the expression of SMILR was much higher inthe serum of AS patients than healthy volunteers (Fig.1a).It has been reported that ox-LDL can induce AS.Next, theCCK-8 assay indicated that the proliferation of VSMCsand U937 cells was inhibited by the knockdown of SMILRcompared with that in the NC group (Fig.2b, c). In addi-tion, the western blot assay indicated that SMILR knock-down suppressed the protein expression of the followingcell proliferation-associated genes: PCNA (proliferatingcell nuclear antigen), CDK2 (cyclin-dependent kinase 2),and Cyclin A1 in VSMCs and U937 cells (Fig.2d, e).Subsequently, the flow cytometry assay showed thatSMILR knockdown elevated cell apoptosis in VSMCsand U937 cells (Fig.2f, g). After that, the western blotassay was performed to observe the protein levels of cellapoptosis-associated genes (Bax and Bcl-2) in VSMCs andU937 cells, and the results showed that SMILR knock-down increased the protein level of Bax while inhibitingBcl-2 protein levels in VSMCs and U937 cells (Fig.2h, i).In conclusion, SMILR knockdown inhibited cell prolifer-ation while increasing cell apoptosis in AS.To confirm the relationship between SMILR and miR-10b-3p, the lucifer-ase assay was performed. The luciferase assay showed that the luciferase activity of pmirGLO-SMILR-WT was re-duced by miR-10b-3p overexpression, while it was pro-moted by the knockdown of miR-10b-3p in VSMCs andU937 cells, and there was no obvious change in the lucif-erase activity of pmirGLO-SMILR-MUT (Fig.3c, d). Tofurther verify the relationship between SMILR and miR-10b-3p, RIP assay was conducted and the results showedthat the expression of SMILR and miR-10b-3p was enriched in the Ago2 pellet compared with the IgG controlpellet (Fig.3e, f). Next, an RT-qPCR experiment showed that miR-10b-3p overexpression inhibited SMILR expres-sion, while miR-10b-3p knockdown resulted in a clear increase in SMILR expression (Fig.3g). Similarly, the introduction of si-SMILR#1 and si-SMILR#2 vectors re-sulted in a remarkable increase in miR-10b-3p expression in VSMCs and U937 cells (Fig.3h). Moreover, it could beseen from the RT-qPCR assay that SMILR was obviously overexpressed upon transfection of the pcDNA3.1/SMILR vector in VSMCs and U937 cells (Fig.3i), and SMILR overexpression inhibited the relative miR-10b-3p level(Fig.3j).First, CCK-8 assays suggested that miR-10b-3p knockdown reversed the inhibitory influence of SMILR knockdown on the prolif-eration ability of VSMCs and U937 cells (Fig.4a, b).Subsequently, the western blot assay was carried out todetect the protein expression of PCNA, CDK2, and CyclinA1. From Fig.4c , it can be concluded that the deficiencyin miR-10b-3p rescued the downregulation of PCNA,CDK2, and Cyclin A1 protein expression caused by SMILR knockdown in VSMCs and U937 cells. Moreover,the flow cytometry assay showed that silencing miR-10b-3p reversed the increase in the percentage of apoptotic cells induced by the deficiency of SMILR in VSMCs and U937cells (Fig.4g, h). Furthermore, the western blot assay was performed to detect the protein expression of Bax and Bcl-2. From Fig.4i , it can be seen that miR-10b-3p knock-down restored the upregulated Bax protein expression affected by silencing SMILR in VSMCs and U937 cells.In contrast, the knockdown of miR-10b-3p reversed the decrease in Bcl-2 protein expression induced by the defi-ciency of SMILR in VSMCs and U937 cells. All these data suggested that miR-10b-3p counteracted SMILR-mediated regulation of AS. o determine the downstream targets of miR-10b-3p, we searched theTargetScan online database and found that miR-10b-3p could regulate the expression of many target genes.Hence, we reviewed the literature and found a study showing that the KLF5 was regulated by miR-152 inthe progression of AS [27]. Thus, the KLF5 was cho-sen as a candidate gene for the following investigation.First, we obtained the predicated binding site of miR-10b-3p on the KLF5 3'UTR from TargetScan (Fig.5a).A luciferase reporter assay was carried out to furtherconfirm the relationship among SMILR, miR-10b-3p,and KLF5. As demonstrated in Fig.5b, c,thelucifer-ase assay of VSMCs and U937 cells showed thatSMILR overexpression reversed the inhibitory influ-ence of miR-10b-3p overexpression on the luciferaseactivity of pmirGLO-KLF5-WT, while there was nosignificant change in the pmirGLO-KLF5-MUT group.Subsequently, the RT-qPCR and western blot assays suggested that SMILR upregulation counteracted theinhibitory influence of miR-10b-3p overexpression onthe mRNA and protein expression of KLF5 in VSMCs and U937 cells (Fig.5d, e). Furthermore, the western blot assay showed that the KLF5 overexpression restored the upregulated Bax protein expression affectedby miR-10b-3p overexpression. In contrast, the KLF5 overexpression reversed the inhibition of Bcl-2 protein expression mediated by the overexpression of miR-10b-3p (Fig.6i ). Collectively, the results indicated that miR-10b-3p-modulated cell proliferation and apoptosis in AS by targeting the KLF5.	32367412	RID04503	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Hepatocellular carcinoma	TERF1	TERRA	positively-E	knockdown;overexpression	downregulation	FISH	NA	NA	cell metastasis(+);cell survival(+);prognosis	NA	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000147601	NA	NA	NA	7013	NA	PIN2|TRBF1|TRF|TRF1	NA	Noncoding telomeric repeat-containing RNA inhibits the progression of hepatocellular carcinoma by regulating telomerase-mediated telomere length.To investigate the functional roles of TERRA in human HCC, we first examined the expression level of TERRA in paired HCC and peritumor tissues by FISH. Our results showed that the expression of TERRA was significantly decreased in HCC tissues (n = 176) when compared with the corresponding peritumor tissues (Figure 1A). We further found that HCC patients with low expression of TERRA (C/P < 1, where C is the foci of TERRA in cancer tissues, and P is the foci of TERRA in peritumor tissues) had significantly poorer DFS and OS than those with high expression of TERRA (C/P>1) (log-rank, P < .01) (Figure 1B). To explore the expression of TERRA in HCC cells, we systematically detected the expression level of TERRA in 5 HCC cell lines (SNU-739, SNU-368, HLE, HLF, and SNU-878) and 1 normal liver cell line (BEL-7702) by FISH. Our results further confirmed that the expression of TERRA in HCC cells was significantly lower than that in normal liver cells (Figure 2A). Then we constructed HCC cell lines with stable TRF1 and TRF2 knockdown and overexpression, which were confirmed by western blot(Figure S1A), to elucidate the role of TRF1 and TRF2 in regulating the expression of TERRA. As shown in Figure 2B, the expression of TERRA was positively correlated with TRF1 expression but negatively correlated with TRF2 expression. These results indicate that the expression of TERRA is mainly regulated by TRF1 and TRF2 (*P < .05; **P < .005).In vitro viability, cell proliferation, and apoptosis of HCC cells with different TERRA expression levels were analyzed. As shown in Figure 3A-C, both cell viability and cell proliferation ability were significantly increased, whereas cell apoptosis was significantly inhibited, in HCC cells with TERRA knockdown compared with the control group. Furthermore, cell models with downregulated or upregulated expression of TERRA were also established by stable knockdown of TRF1 or TRF2, respectively. As shown in Figure 3D,E, cell viability and cell proliferation abilities were significantly increased in HCC cells with TRF1 knockdown, whereas opposite effects were observed in HCC cells with TRF2 knockdown. In contrast, cell apoptosis was significantly inhibited by TRF1 knockdown in both SNU-368 and SNU-739 cells, whereas it was increased by TRF2 knockdown (Figure 3F). Therefore, these results indicate that TERRA expression is correlated with the viability of HCC cells (*P < .05; **P < .005).We next examined the effect of TERRA on HCC growth and metastasis in vivo by constructing a xenograft nude mouse model using HCC cell lines with stable TRF1 and TRF2 knockdown. As shown in Figure 7A-C, xenograft tumors developed from SNU-739 cells with stable TRF1 knockdown and TRF2 knockdown showed a significant increase and decrease in growth capacity, respectively, when compared with control cells.We next examined the role of TERRA in HCC metastasis in vivo. Our results indicated that TERRA downregulation mediated by TRF1 knockdown significantly increased the incidence of intrahepatic metastasis and lung metastasis compared with control mice. These effects caused by TERRA downregulation were significantly reversed by TMPyP4 treatment. In contrast, the incidence of intrahepatic metastasis and lung metastasis were remarkably decreased by TRF2 knockdown in mice with xenografts developed from SNU-739 cells. Opposite results were obtained in xenograft mice treated with TA-65 or TERRA knockdown (Figure 8A-E).	32357278	RID04504	expression association	metastasis,prognosis	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)	
Hepatocellular carcinoma	TRF2	TERRA	negatively-E	knockdown;overexpression	downregulation	FISH	NA	NA	cell metastasis(+);cell survival(+);prognosis	NA	regulation	protein-RNA	NA	CSC	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000132604	NA	NA	NA	NA	NA	NA	NA	Noncoding telomeric repeat-containing RNA inhibits the progression of hepatocellular carcinoma by regulating telomerase-mediated telomere length.To investigate the functional roles of TERRA in human HCC, we first examined the expression level of TERRA in paired HCC and peritumor tissues by FISH. Our results showed that the expression of TERRA was significantly decreased in HCC tissues (n = 176) when compared with the corresponding peritumor tissues (Figure 1A). We further found that HCC patients with low expression of TERRA (C/P < 1, where C is the foci of TERRA in cancer tissues, and P is the foci of TERRA in peritumor tissues) had significantly poorer DFS and OS than those with high expression of TERRA (C/P>1) (log-rank, P < .01) (Figure 1B). To explore the expression of TERRA in HCC cells, we systematically detected the expression level of TERRA in 5 HCC cell lines (SNU-739, SNU-368, HLE, HLF, and SNU-878) and 1 normal liver cell line (BEL-7702) by FISH. Our results further confirmed that the expression of TERRA in HCC cells was significantly lower than that in normal liver cells (Figure 2A). Then we constructed HCC cell lines with stable TRF1 and TRF2 knockdown and overexpression, which were confirmed by western blot(Figure S1A), to elucidate the role of TRF1 and TRF2 in regulating the expression of TERRA. As shown in Figure 2B, the expression of TERRA was positively correlated with TRF1 expression but negatively correlated with TRF2 expression. These results indicate that the expression of TERRA is mainly regulated by TRF1 and TRF2 (*P < .05; **P < .005).In vitro viability, cell proliferation, and apoptosis of HCC cells with different TERRA expression levels were analyzed. As shown in Figure 3A-C, both cell viability and cell proliferation ability were significantly increased, whereas cell apoptosis was significantly inhibited, in HCC cells with TERRA knockdown compared with the control group. Furthermore, cell models with downregulated or upregulated expression of TERRA were also established by stable knockdown of TRF1 or TRF2, respectively. As shown in Figure 3D,E, cell viability and cell proliferation abilities were significantly increased in HCC cells with TRF1 knockdown, whereas opposite effects were observed in HCC cells with TRF2 knockdown. In contrast, cell apoptosis was significantly inhibited by TRF1 knockdown in both SNU-368 and SNU-739 cells, whereas it was increased by TRF2 knockdown (Figure 3F). Therefore, these results indicate that TERRA expression is correlated with the viability of HCC cells (*P < .05; **P < .005).We next examined the effect of TERRA on HCC growth and metastasis in vivo by constructing a xenograft nude mouse model using HCC cell lines with stable TRF1 and TRF2 knockdown. As shown in Figure 7A-C, xenograft tumors developed from SNU-739 cells with stable TRF1 knockdown and TRF2 knockdown showed a significant increase and decrease in growth capacity, respectively, when compared with control cells.We next examined the role of TERRA in HCC metastasis in vivo. Our results indicated that TERRA downregulation mediated by TRF1 knockdown significantly increased the incidence of intrahepatic metastasis and lung metastasis compared with control mice. These effects caused by TERRA downregulation were significantly reversed by TMPyP4 treatment. In contrast, the incidence of intrahepatic metastasis and lung metastasis were remarkably decreased by TRF2 knockdown in mice with xenografts developed from SNU-739 cells. Opposite results were obtained in xenograft mice treated with TA-65 or TERRA knockdown (Figure 8A-E).	32357278	RID04505	expression association	metastasis,prognosis		
Parkinson's disease	H19	PIK3R3	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(+);	ceRNA(miR-585-3p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000117461	NA	283120	8503	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	p55	LncRNA H19 Attenuates Apoptosis in MPTP-Induced Parkinson's Disease Through Regulating miR-585-3p/PIK3R3.As shown in Fig. 1c, the transcription of H19 was decreased from day 0 to day 7, which indicated that H19 was down-regulated in PD mice.Cell prolifera-tion was examined by BrdU assay. The results showed that H19 overexpression reversed MPP-induced the proliferation inhibition (Fig. 2d). Besides, cell apoptosis was analyzed by TUNEL staining. The number of TUNEL-positive cells was increased about four times compared with control, and overexpression of H19 significantly inhibited MPP+ induced apoptosis  of  SH-SY5Y  cells  (p < 0.01  vs.  MPP+cector) (Fig. 2e). we predicted the potential miR-NAs binding sequence for H19 by using miRDB database (http://mirdb .org/). As shown in Fig. 3a, miR-585-3p could complementally bind to the 3'-UTR of H19 (H19 wt), but not H19 mutation sequence. To further investigate the target-ing relationship between H19 and miR-585-3p, luciferase reporter plasmids containing the wild-type or mutant-H19 for miR-585-3p-binding site and miR-585-3p mimics were co-transfected into HEK293 cells. The transfection efficacy was confirmed by qPCR (Fig. 3b). The level of miR-585-3p was significantly increased in HEK-293 cells (p <   0.01 vs. miR  NC).  Furthermore,  the  luciferase  activities  of  H19  were  markedly  inhibited  in  miR-585-3p  over-expressed  HEK-293 cells (p <   0.01 vs. miR NC) while there was no significant change for the H19 mutation (Fig. 3c). The RIP assay revealed that H19 was enriched in Ago-2 contain-ing miR-595-3p compared with negative control immuno-globulin G (IgG) (p < 0.01)  (Fig. 3d). The H19 knockdown  markedly  increased  miR-585-3p  expression  (Fig. 3f). Taken together, miR-585-3p was a direct target of H19 interacted and its expression was negatively modulated by H19.miR-585-3p  could  complementally bind to the 3'-UTR of PIK3R3 wild type sequence. To investigate the regulatory effect of miR-585-3p on PIK3R3, miR-585-3p over-expressed plasmid was co-transfected with PIK3R3 wild type or PIK3R3 mutation type sequence to HEK-293 cells. The level of luciferase activ-ity of PIK3R3 wild type group was significantly decreased in miR-585-3p wild type group (p <   0.01 vs. miR NC), but not PIK3R3 mutation group (Fig. 4b. Further, miR-585-3p over-expression plasmid or inhibitor or negative control was transfected to SH-SY5Y cells. The transfection efficiency was  confirmed  by  qPCR  (Fig. 4c),  which  showed  that  miR-585-3p inhibitor significantly inhibited the transcrip-tion of miRNA. PIK3R3 level was negatively regulated by miR-585-3p (Fig. 4d).The cell proliferation and apoptosis were analyzed by BrdU and TUNEL staining assays. The results demonstrated that H19 overexpression increased the cell proliferation (Fig. 5b) and reduced apoptosis (Fig. 5c) (p < 0.01  vs. vector +   miR NC), whereas miR-585-3p overexpression reversed the proliferation and apoptosis induced by H19 (p <   0.01 vs. H19 +   miR NC). Furthermore, the apopto-sis and proliferation associated proteins were analyzed by western blot. The level of anti-apoptotic protein Bcl-2 was increased in H19 overexpression cells, while inhib-ited by miR-585-3p. The expression of pro-apoptotic pro-teins (Bax and cleaved-caspase3) and poly ADP-ribose polymerase (PARP, DNA repair enzyme) was decreased in H19 overexpression cells, while reversed by miR-585-3p overexpression (Fig. 5d). These results indicated that H19 could inhibit apoptosis through miR-585-3p.	32356199	RID04506	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Vascular calcification	GAS5	PTEN	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell differentiation(+);calcium signaling pathway(+)	ceRNA(miR-26b-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Vascular calcification	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	The lncRNA GAS5 Inhibits the Osteogenic Differentiation and Calcification of Human Vascular Smooth Muscle Cells.HASMCs were stimulated with 3 mM Pi to induce osteo-blastic differentiation. As indicated by RT-PCR there was a marked increase in the mRNA expression of Runx2 from 0 to 14 days (Fig. 1a). However, as shown in Fig. 1b, stimula-tion with Pi clearly attenuated the expression of GAS5 in HASMCs in a time-dependent manner.To explore the effect of GAS5 on the osteoblastic differentia-tion of HASMCs, HASMCs were infected with Lv-GAS5 and Lv-NC. qRT-PCRanalysis revealed clearly increased expression of GAS5 in the Lv-GAS5 group (Fig. 2a). The mRNA expression of Runx2 and activity of ALP were sig-nificantly  decreased  in  the  GAS5-overexpressing  group  (Fig. 2b and c). As shown in Fig. 2d, von Kossa staining revealed fewer calcified nodules in the Lv-GAS5 group. Transfection with Lv-GAS5 significantly decreased cell cal-cification in HASMCs based on the quantification of intra-cellular calcium deposition (Fig. 2e). western blotshowed that Lv-GAS5 reduced the expression of Runx2 and promoted the expression of alpha-SMA compared with the Lv-NC group in Pi-stimulated HASMCs (Fig. 2f). These results suggest an inhibitory effect of GAS5 on HASMC osteoblastic differentiation and calcification.To further explore the molecular mechanisms underlying the inhibitory effect of GAS5 on the osteoblastic differentiation of HASMCs, we identified a potential miR-26b-5p bind-ing site in GAS5 through the ENCORI platform (https ://starb ase.sysu.edu.cn) (Fig. 3a). As demonstrated in Fig. 3b, luciferase activity was obviously reduced in HASMCs trans-fected with miR-26b-5p mimics and GAS5-WT reporter. In addition, the expression of miR-26-5p was significantly decreased in GAS5-overexpressing HASMCs (Fig. 3c). We also found that the expression of miR-26-5p time-depend-ently increased after Pi stimulation of HASMCs.The TargetScan bioinformatics algorithm (https ://www.targe tscan .org) was used to predict the downstream targets of miR-26b-5p, and PTEN was selected due to the target sequences at the 3'-untranslated region of PTEN (Fig. 4a). Moreover, the results of a dual-luciferase reporter assay revealed  that  cotransfection  with  miR-26b-5p clearly inhibited the luciferase activity of the PTEN-WT reporter in HASMCs, while the activity of the PTEN-MUT reporter is almost unaffected (Fig. 4b). To verify the transfection efficiency, the expression of miR-26b-5p in HASMCs after their transfection was detected by qRT-PCRanalysis (Fig. 4c). The PTEN level was also clearly decreased  in  miR-26b-5p-overexpressing  HASMCs  (Fig. 4d). Downregulation of PTEN after Pi stimulation of HASMCs at different time points was also analyzed by western blot (Fig.4c).Rescue experiments were performed to confirm whether the effect of GAS5 on Pi-stimulated HASMCs is at least partly mediated by the miR-26b-5p/PTEN axis. As shown in Fig. 5a, cotransfection of miR-26b-5p mimics markedly reduced PTEN protein level in GAS5-overexpressing HASMCs. In addition, we also found that the inhibitory effects of GAS5 on osteo-blastic differentiation were partially rescued following miR-26b-5p overexpression, based on mRNA expression of Runx2 and activation of ALP (Fig. 5b and c). miR-26b-5p overexpres-sion also rescued the inhibitory effect of GAS5 on calcification through intracellular calcium deposition quantification and von Kossa staining (Fig. 5d and e).	32347320	RID04507	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Oral submucous fibrosis	LINC00312	YBX1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell viability(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	TF	ENSG00000237697	NA	ENSG00000065978	NA	29931	4904	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	LINC00312/YBX1 Axis Regulates Myofibroblast Activities in Oral Submucous Fibrosis.To detect the key lncRNA involved in the fibrogenesis, the two collected normal and OSF tissueswere subjected to RNA sequencing analysis.  Our results revealed that LINC00312 was one of thelncRNAs with differential expression and the expression of LINC00312 was elevated in OSF tissuescompared  to  the  normal  counterparts  (Figure  1A).  The  expression  of  LINC00312  was  positivelyassociated with myofibroblast markers using Pearson correlation analysis (Supplementary FigureS1A). Our results also showed that LINC00312 was overexpressed in fBMFs compared to normalBMFs (Figure 1B). In  order  to  investigate  the  effect  of  LINC00312  on  the  myofibroblast  transdifferentiation,we employed a small hairpin to silence the expression of LINC00312 in two lines of OSF patient-derivedfibrtic buccal mucosal fibroblasts (fBMFs) (Figure 2A). The proliferation rate was not changed inLINC00312-knockdown fBMFs (Figure 2B). The expression of myofibroblast and fibrosis markers,alpha-SMA and p-Smad2 (Figure 2C and Supplementary Figure S1B) was downregulated. We also foundthat the ability of collagen gel contraction was reduced (Figure 2D). In addition, the cell motilityof fBMFs toward a chemo-attractant gradient was diminished in the LINC00312-reduced fBMFs(Figure 2E). Moreover,  the wound healing capacity of fBMFs was downregulated after a silence of LINC00312 (Figure 2F). These results indicated that the expression of LINC00312 affected thephenotypes and markers of myofibroblasts.The increased expression levels of LINC00312 (Figure 3B)and YBX1 (Figure 3C) in OSF specimens were validated using qRT-PCRanalysis. We carried out an RIP assay using a YBX1-specific antibody followed by qRT-PCRwith primers specific for LINC00312 toverify their interaction. As expected, LINC00312 was enriched in the anti-YBX1 group, compared to thecontrol IgG group (Figure 3D). Moreover, we observed a positive correlation between the expressionof LINC00312 and YBX1 (Figure 3E), which also was in favor of our hypothesis that YBX1 interactswith LINC00312.To investigate whether LINC00312 modulated the features of myofibroblasts through YBX1,we sought to examine the effect of YBX1 on myofibroblast activities.  Our results showed that theknockdown of YBX1 inhibited the expression ofalpha-SMA and phosphorylated Smad2 (Figure 4A andSupplementary Figure S1C). In addition to the reduced expression of fibrosis markers, collagen gelcontractility of fBMFs was decreased as well (Figure 4B). In addition, the transwell migration ability(Figure 4C) and wound healing abilities (Figure 4D) were both declined. Altogether, these findingssuggested that the expression of YBX1 regulated the myofibroblast activities of fBMFs.After confirming the effect of YBX1 and LINC00312 on myofibroblast activities, the last step wasto verify that LINC00312 regulated the activation of myofibroblasts through YBX1. We demonstratedthat overexpression of LINC00312 (Figure 4E) increased the transwell migration ability of BMFs, whilethe knockdown of YBX1 reverted this effect (Figure 5A). Likewise, the elevation of LINC00312 inBMFs induced the invasion capacity, whereas the silencing of YBX1 reversed the LINC00312-enhancedinvasion ability (Figure 5B). We found that YBX1 suppression reverted the induced p-Smad2 andalpha-SMA by LINC00312 overexpression in BMFs (Figure 6). Collectively, these results showed that theincreased expression of LINC00312 stimulated the transdifferentiation of BMFs into myofibroblasts viainteracting with YBX1.	32340273	RID04508	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pre-eclampsia	HOTAIR	miR-106	negatively-E	RIP;Bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR modulates the progression of preeclampsia through inhibiting miR-106 in an EZH2-dependent manner.To validate whether the abnormal expression  of  HOTAIR  in  PE  placenta  exist,  the  HOTAIR  expression  was  analyzed  by  real-time QPCR  in 30paired  placental  tissues  from  PE  patients  and  the  healthy  controls.  We  found  that  the expression  patternof  HOTAIR wassignificantly  higher  in  placentas  from  PE  patients,  compared with  that  in  normal  pregnancies  (Fig.  1A).he results revealed that knockdown of HOTAIR significantlyenhanced the migration and invasion ofHTR-8/SVneotrophoblasts.  Meanwhile,  HOTAIR  overexpression  noticeablyrepressed  the number  of  migratory  and  invasive JEG-3trophoblasts  compared  with  control  group  (Fig.  2D).  In addition, we also  assessedthe  effect  of  HOTAIR  on migration  using wound  healing analysis.Similarly,  as  shown  in  Fig.  2E,  in  comparison  with  the  negative  control  groups,  the  knockdown groups exhibited a shorterhealing distance in HTR-8/SVneo trophoblasts whereas over-expression of HOTAIR showed a longerhealing distance in JEG-3trophoblasts, indicating HOTAIR repressedthe  cell  migration. Taken  together,  these  results support  the  crucial  role  of HOTAIR  for  the progression of PE. As shown in Fig. 3A, miR-106a showed the grea tes tincrease after HOTAIR knockdown in  both  HTR-8/SVneo  and  JEG-3  cell  lines.  Moreover,  the  expression  of  miR-106a  was  markedly decreased  in  cells  transefected  with  pcDNA-HOTAIR  (Fig.  3B),indicating  that  HOTAIR  might negatively  regulate miR-106a expressionin  trophoblast  cells.Additionally,  we  investigated  the expression  pattern of  miR-106a in  vivoand  the  results  demonstrated  that the  expression  of miR-106a  in  the  chorionic  plates  of  placenta  from  PE  patients wassignificantly  lower  than  that from normal pregnancies, which was negatively correlated with HOTAIR (Fig.    3C). Furthermore, the  Pearson  correlated  analysis  also  indicated  an  inverse  correlation  between  HOTAIR  and miR-106a (Fig. 3D). Taken together, our results suggest that miR-106a may serve as a downstream target gene of HOTAIR in the progression.On  the  other  hand,  in  a  transwell  assay,  increased  miR-106a  expression  showed  an enhanced  effect  on  the  migration  and  invasion,  however,  reduced  miR-106a  expression  showed  a decreased  effect  on  the  migration  and  invasion(Fig.  4D).  In  addition,  miR-106a over-expression also exhibited enhanced   wound   healing   function.   In   consistent   with   former   observation, knock-down of miR-106a showed declined wound healing functioncompared in control cells(Fig. 4E), These  findings  suggest  that  HOTAIR  might repressPE  progression  via  repressing  miR-106a expression.Moreover, we evaluated the effect of EZH2 on HOTAIR-mediated miR-106a expression. As shown in Fig. 5E, in consistent  with  previous  observations,  while  HOTAIR  overexpression  significantly  reduced  the mRNA  level  of  miR-106a,  in  combination  with  knockdown  of  EZH2  could  remarkablyattenuate the  effect  of  down-regulated  miR-106a  mRNA  level,  both  inHTR-8/SVneo  and  JEG-3  cell  lines. These  data  suggest  that  that the  regulation  of miR-106abyHOTAIR  isdependent  on  thedirect binding between HOTAIR andEZH2.We  further  investigated  whether  the  modulation  of  trophoblast  function  by  HOTAIR  was dependent on EZH2, we also performed the transwell assay in HTR-8/SVneo and JEG-3 cell lines. As shown in Fig. 5F, knockdown of HOTAIR significantlyenhanced the migration and invasion of both celllines, whereas the improvement effects were almost abolished by overexpression of EZH2 in  trophoblast  cells.  Hence,  our  data  suggest  that  HOTAIR  modulates  miR-106a  transcription  and trophoblast cell function in an EZH2 dependent manner.	32320706	RID04509	expression association	NA		
Pre-eclampsia	EZH2	miR-106	negatively-E	RIP;Bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	binding/interaction	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	PCG	miRNA	ENSG00000106462	GRCh38_7:148807257-148884321	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	NA	Long non-coding RNA HOTAIR modulates the progression of preeclampsia through inhibiting miR-106 in an EZH2-dependent manner.To validate whether the abnormal expression  of  HOTAIR  in  PE  placenta  exist,  the  HOTAIR  expression  was  analyzed  by  real-time QPCR  in 30paired  placental  tissues  from  PE  patients  and  the  healthy  controls.  We  found  that  the expression  patternof  HOTAIR wassignificantly  higher  in  placentas  from  PE  patients,  compared with  that  in  normal  pregnancies  (Fig.  1A).he results revealed that knockdown of HOTAIR significantlyenhanced the migration and invasion ofHTR-8/SVneotrophoblasts.  Meanwhile,  HOTAIR  overexpression  noticeablyrepressed  the number  of  migratory  and  invasive JEG-3trophoblasts  compared  with  control  group  (Fig.  2D).  In addition, we also  assessedthe  effect  of  HOTAIR  on migration  using wound  healing analysis.Similarly,  as  shown  in  Fig.  2E,  in  comparison  with  the  negative  control  groups,  the  knockdown groups exhibited a shorterhealing distance in HTR-8/SVneo trophoblasts whereas over-expression of HOTAIR showed a longerhealing distance in JEG-3trophoblasts, indicating HOTAIR repressedthe  cell  migration. Taken  together,  these  results support  the  crucial  role  of HOTAIR  for  the progression of PE. As shown in Fig. 3A, miR-106a showed the grea tes tincrease after HOTAIR knockdown in  both  HTR-8/SVneo  and  JEG-3  cell  lines.  Moreover,  the  expression  of  miR-106a  was  markedly decreased  in  cells  transefected  with  pcDNA-HOTAIR  (Fig.  3B),indicating  that  HOTAIR  might negatively  regulate miR-106a expressionin  trophoblast  cells.Additionally,  we  investigated  the expression  pattern of  miR-106a in  vivoand  the  results  demonstrated  that the  expression  of miR-106a  in  the  chorionic  plates  of  placenta  from  PE  patients wassignificantly  lower  than  that from normal pregnancies, which was negatively correlated with HOTAIR (Fig.    3C). Furthermore, the  Pearson  correlated  analysis  also  indicated  an  inverse  correlation  between  HOTAIR  and miR-106a (Fig. 3D). Taken together, our results suggest that miR-106a may serve as a downstream target gene of HOTAIR in the progression.On  the  other  hand,  in  a  transwell  assay,  increased  miR-106a  expression  showed  an enhanced  effect  on  the  migration  and  invasion,  however,  reduced  miR-106a  expression  showed  a decreased  effect  on  the  migration  and  invasion(Fig.  4D).  In  addition,  miR-106a over-expression also exhibited enhanced   wound   healing   function.   In   consistent   with   former   observation, knock-down of miR-106a showed declined wound healing functioncompared in control cells(Fig. 4E), These  findings  suggest  that  HOTAIR  might repressPE  progression  via  repressing  miR-106a expression.Moreover, we evaluated the effect of EZH2 on HOTAIR-mediated miR-106a expression. As shown in Fig. 5E, in consistent  with  previous  observations,  while  HOTAIR  overexpression  significantly  reduced  the mRNA  level  of  miR-106a,  in  combination  with  knockdown  of  EZH2  could  remarkablyattenuate the  effect  of  down-regulated  miR-106a  mRNA  level,  both  inHTR-8/SVneo  and  JEG-3  cell  lines. These  data  suggest  that  that the  regulation  of miR-106abyHOTAIR  isdependent  on  thedirect binding between HOTAIR andEZH2.We  further  investigated  whether  the  modulation  of  trophoblast  function  by  HOTAIR  was dependent on EZH2, we also performed the transwell assay in HTR-8/SVneo and JEG-3 cell lines. As shown in Fig. 5F, knockdown of HOTAIR significantlyenhanced the migration and invasion of both celllines, whereas the improvement effects were almost abolished by overexpression of EZH2 in  trophoblast  cells.  Hence,  our  data  suggest  that  HOTAIR  modulates  miR-106a  transcription  and trophoblast cell function in an EZH2 dependent manner.	32320706	RID04510	expression association	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	
Acute myeloid leukemia	SNHG4	PTEN	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-10a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000171862	NA	724102	5728	NCRNA00059|U19H	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA SNHG4 regulates miR-10a/PTEN to inhibit the proliferation of acute myeloid leukemia cells.The differential expression of SNHG4 in AML was first explored by analyzing the TCGA dataset. It was observed that the expression level of SNHG4 was lower in AMLtissues (16.07) than in non-tumor tissues (56.27). Thedownregulation of SNHG4 in AML was confirmed bymeasuring its expression levels in bone marrow mono-nuclear cells (BMMCs) from both AML patients (n= 60)and healthy participants (n= 60) by performing qPCR.Comparing the control group, the unpairedt-testshowed that expression levels of SNHG4 were signifi-cantly lower in the AML group (Figure 1,p< 0.05). It isworth noting that miR-10 was significantly upregulatedin the AML group (Supplemental Figure 1B,p< 0.05),while PTEN mRNA was significantly downregulated inthe AML group (Supplemental Figure 1B,p< 0.05). The potential-based pairs formed by SNHG4 and miR-10a were predicted using an online RNA-RNA inter-action program IntaRNA [14]. It was observed thatSNHG4 and miR-10a can form strong base pairingbetween them (Figure 2A). Dual-luciferase assay wasperformed to further analyze the interaction betweenSNHG4 and miR-10a. Comparing to cells transfectedwith SNHG4 vector and NC miRNA (NC group), cellstransfected with SNHG4 vector and miR-10a mimic(miR-10a group) showed significantly reduced lucifer-ase activity (Figure 2B,p< 0.05).Kasumi-6 cells were transfected with SNHG4 vector ormiR-10a mimic to further analyze the interaction between them. Overexpression of SNHG4 and miR-10a was confirmed by qPCR at 24 h post-transfection(Figure 3A,p< 0.05). Comparing to C and NC groups,overexpression of SNHG4 and miR-10a failed to signifi-cantly affect the expression of each other (Figure 3B).PTEN has been proved as a direct target of miR-10a.The effects of SNHG4 and miR-10a overexpression onthe expression of PTEN were analyzed by qPCR andwestern blot at mRNA (Figure 3C) and protein (Figure3D) levels, respectively. Comparing to the C group,miR-10a overexpression led to downregulated PTEN(p< 0.05). SNHG4 overexpression played the oppositerole and attenuated the effects of miR-10a overexpres-sion (p< 0.05).The CCK-8 assay was performed to analyze the effectsof SNHG4, miR-10a and PTEN overexpression on theproliferation of Kasumi-6 cells. Comparing to the Cgroup, cell proliferation analysis showed that SNHG4and PTEN overexpression led to decreased proliferationrates of AML cells and reduced enhancing effects ofmiR-10a on cell proliferation (Figure 4,p< 0.05)	32319862	RID04511	ceRNA or sponge	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Aortic dissection	XIST	PTEN	positively-E	luciferase reporter assay;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(-);apoptosis process(+)	ceRNA(miR-17)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Aortic disease	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171862	NA	7503	5728	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BZS|MHAM|MMAC1|PTEN1|TEP1	Long Noncoding RNA XIST/miR-17/PTEN Axis Modulates the Proliferation and Apoptosis of Vascular Smooth Muscle Cells to Affect Stanford Type A Aortic Dissection.To identify the expression level of XIST in patients with TAAD, qRT-PCRwas applied to check XIST expression in aortic wall tissues of patients with TAAD and compared with NA tissues. It was evident that XIST was significantly increased in aortic wall tissues versus in NA tissues of patients with TAAD (Fig. 1A). To investigate the role of XIST in the prognosis of patients with TAAD, the Kaplan-Meier survival curve analysis was performed. The findings displayed that patients with a higher XIST expression had a lower survival time than patients with low expression of XIST (Fig. 1B). Thus, we concluded that the upregulation of XIST was associated with poor prognosis of patients with TAAD.Results showed that miR-17 was remarkably increased in the si-XIST group compared with the si-NC group, but it was markedly decreased in the pcDNA-XIST group compared with the pcDNA-NC group (Fig. 3B), implying a negative interaction between XIST and miR-17. In addition, luciferase reporters containing wild-type or mutant XIST was constructed. Restoration of miR-17 considerably reduced the luciferase activity of the wild-type XIST reporter vector, but not of the mutant-type XIST reporter vector (Fig. 3C). Meanwhile, miR-17 expression was significantly downregulated in aortic wall tissues compared with NA tissues of patients with TAAD (Fig. 3D). Pearson correlation analysis revealed that the expression of XIST and miR-17 was negatively correlated in aortic wall tissues of patients with TAAD (Fig. 3E). Thesefindings strongly suggest that XIST directly interacted with miR-17 in TAAD.The luciferase assay showed that the luciferase activity of PTEN-WT was reduced significantly in miR-17 mimic-transfected VSMCs. However, there was no significant change in the luciferase activity of PTEN-MuT( F i g .5 B ) ,i n d i c a t i n gt h a t PTEN could interact with miR-17. Moreover, qRT-PCRand western blot results discovered that miR-17 regulated PTEN expression inversely (Figs. 5C, D). Then, we explored the interplay between XIST, miR-17, and PTEN, and results showed that PTEN expression was increased by miR-17 inhibitors but attenuated after being cotransfected with miR-17 inhibitors and si-XIST (Figs. 5E, F). However, PTEN expression reduced by the miR-17 mimic could be rescued by the incorporation of pcDNA-XIST (Figs. 5G, H), indicating that XIST regulated PTEN expression through targeting miR-17. Moreover, PTEN expressionin aortic wall tissues was higher than that in NA tissues of patients with TAAD (Fig. 5I).	32282501	RID04512	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pre-eclampsia	lncZBTB39	THSD7A	positively-E	transcriptomic microarray;RT-qPCR	upregulation	RT-qPCR;microarray;FISH	NA	NA	cell invasion(-);cell migration(+)	ceRNA(miR-210)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000005108	NA	NA	221981	NA	KIAA0960	Upregulated LncZBTB39 in pre-eclampsia and its effects on trophoblast invasion and migration via antagonizing the inhibition of miR-210 on THSD7A expression.Further validation in another set of placenta samples using RT-qPCR suggested that the expression of lncZBTBT39 was significantly elevated in PE-complicated human placentas (Fig. 1B).Next, the lncZBTB39 overexpressing and lncZBTB39-KD HTR8/SVneo cells were subjected to migration and invasion assays. Knockdown of lncZBTB39 strongly promoted HTR8/SVneo cell migration, while overexpression of lncZBTB39 resulted in a significant loss of trophoblast cell motility (Fig. 2B).Further validation by RT-qPCR confirmed that THSD7A transcription is regulated by lncZBTB39 (Fig. 3C).The levels of the THSD7A mRNA were significantly increased in PE placentas (Fig. 4A), showing a similar trend to that of lncZBTB39 expression. Unexpectedly, the elevation of THSD7A expression observed in response to lncZBTB39 transfection was further diminished by additional miR210 mimics in a dose-dependent manner (Fig. 4B).We next investigated the relationship between LncZTBT39 and miR210 in HTR8/SVneo cell. The RT-PCRresults showed that overexpression of lncZBTB39 up-regulated miR210 expression in HTR8/SVneo cell (Fig. 4C), while Knockdown of lncZBTB39 strongly decreased miR210 expression in HTR8/SVneo cell (Fig. 4C).	32222649	RID04513	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Pre-eclampsia	GAS5	miR-21	negatively-E	knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(-);cell invasion(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Non-coding RNA Gas5 Is Associated With Preeclampsia and Regulates Biological Behaviors of Trophoblast via MicroRNA-21.We examined a total of 72 placentas for the expression of GAS5 using qRT-PCR As shown inFigure 1AandTable 1, expression of GAS5 elevated in PE groups. The expression of GAS5 was significantly elevated in ePE compared to lCON(P<0.001) and eCON (P<0.05), respectively. The level of GAS5 also elevated significantly in lPE compared to lCON(P<0.05).The results (shown inSupplementary Table S3) indicated that the proliferation ability of JEG-3 cells in KD(GAS5) continuously increased compared with the NCKD(GAS5) (P<0.001) while the proliferation ability of HTR-8/SVneo in KD(GAS5) increased on day 2 (P<0.001). On the contrary, OE (GAS5) inhibited the proliferation of HTR-8/SVneo persistently compared with control (P<0.001) while the proliferation of JEG-3 is decreased on day 2 in OE (GAS5) (P<0.05) (shown inFigure 3A).As depicted inFigure 4A, overexpression of GAS5 significantly reduced the migration ability of JEG-3 cells compared with the NCOE(GAS5).At 24h post-scratch,the migration rate of OE(GAS5) decreased(P<0.05), and at 48 h post-scratch, the migration rate of the cells was persistently decreased (P<0.001).The results of Transwell assay showed that overexpression of GAS5 significantly (P<0.001) reduced the invasion ability of JEG-3 cells, meanwhile, HTR-8/SVneo cell line demonstrated the same trends. The invasion ability of HTR-8/SVneo cells was significantly reduced after overexpression of GAS5 (P<0.001).After GAS5 lentivirus vectors infected the trophoblast cells, the expression level of miR-21 was firstlydetected.Theresults showed(Figure 5A), in JEG-3 cells, knockdown of GAS5 elevated the expression of miR-21 (P<0.05) compared with the control NCKD (GAS5). Overexpression of GAS5 declined miR-21 expression (P<0.05) compared with the control conversely. In HTR-8/SVneo cells, after knocking down GAS5, the level of miR-21 was also increased (P<0.05). However, the overexpression of GAS5 didn't alter the level of miR-21 (P>0.05) in HTR-8/SVneo.Further, HTR-8/SVneo cell line was selected which was closer to the villous cells in first-trimester placenta.According to the prediction of KEGG (Kyoto Encyclopedia of Genesand Genomes)bioinformatics database,we detected the alteration of the PI3K/AKT signaling pathway downstream proteins MMP9 and TP53,which were closely related with preeclampsia (Gao et al.,2016;Chen and Khalil,2017), after GAS5 expression changed. The results showed that the expressions of MMP9 and TP53 were all regulated up and down statistically according to the activation of PI3K/AKT signaling pathway by qRTPCR (Figure 6C). However, due to the low expression level of this two downstream protein in HTR-8/SVneo, no target band was detected in WB.	32194641	RID04514	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Pre-eclampsia	GAS5	MMP9	negatively-E	knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000100985	NA	60674	4318	NCRNA00030|SNHG2	CLG4B	Long Non-coding RNA Gas5 Is Associated With Preeclampsia and Regulates Biological Behaviors of Trophoblast via MicroRNA-21.We examined a total of 72 placentas for the expression of GAS5 using qRT-PCR As shown inFigure 1AandTable 1, expression of GAS5 elevated in PE groups. The expression of GAS5 was significantly elevated in ePE compared to lCON(P<0.001) and eCON (P<0.05), respectively. The level of GAS5 also elevated significantly in lPE compared to lCON(P<0.05).The results (shown inSupplementary Table S3) indicated that the proliferation ability of JEG-3 cells in KD(GAS5) continuously increased compared with the NCKD(GAS5) (P<0.001) while the proliferation ability of HTR-8/SVneo in KD(GAS5) increased on day 2 (P<0.001). On the contrary, OE (GAS5) inhibited the proliferation of HTR-8/SVneo persistently compared with control (P<0.001) while the proliferation of JEG-3 is decreased on day 2 in OE (GAS5) (P<0.05) (shown inFigure 3A).As depicted inFigure 4A, overexpression of GAS5 significantly reduced the migration ability of JEG-3 cells compared with the NCOE(GAS5).At 24h post-scratch,the migration rate of OE(GAS5) decreased(P<0.05), and at 48 h post-scratch, the migration rate of the cells was persistently decreased (P<0.001).The results of Transwell assay showed that overexpression of GAS5 significantly (P<0.001) reduced the invasion ability of JEG-3 cells, meanwhile, HTR-8/SVneo cell line demonstrated the same trends. The invasion ability of HTR-8/SVneo cells was significantly reduced after overexpression of GAS5 (P<0.001).After GAS5 lentivirus vectors infected the trophoblast cells, the expression level of miR-21 was firstlydetected.Theresults showed(Figure 5A), in JEG-3 cells, knockdown of GAS5 elevated the expression of miR-21 (P<0.05) compared with the control NCKD (GAS5). Overexpression of GAS5 declined miR-21 expression (P<0.05) compared with the control conversely. In HTR-8/SVneo cells, after knocking down GAS5, the level of miR-21 was also increased (P<0.05). However, the overexpression of GAS5 didn't alter the level of miR-21 (P>0.05) in HTR-8/SVneo.Further, HTR-8/SVneo cell line was selected which was closer to the villous cells in first-trimester placenta.According to the prediction of KEGG (Kyoto Encyclopedia of Genesand Genomes)bioinformatics database,we detected the alteration of the PI3K/AKT signaling pathway downstream proteins MMP9 and TP53,which were closely related with preeclampsia (Gao et al.,2016;Chen and Khalil,2017), after GAS5 expression changed. The results showed that the expressions of MMP9 and TP53 were all regulated up and down statistically according to the activation of PI3K/AKT signaling pathway by qRTPCR (Figure 6C). However, due to the low expression level of this two downstream protein in HTR-8/SVneo, no target band was detected in WB.	32194641	RID04515	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pre-eclampsia	GAS5	TP53	negatively-E	knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	LFS1|p53	Long Non-coding RNA Gas5 Is Associated With Preeclampsia and Regulates Biological Behaviors of Trophoblast via MicroRNA-21.We examined a total of 72 placentas for the expression of GAS5 using qRT-PCR As shown inFigure 1AandTable 1, expression of GAS5 elevated in PE groups. The expression of GAS5 was significantly elevated in ePE compared to lCON(P<0.001) and eCON (P<0.05), respectively. The level of GAS5 also elevated significantly in lPE compared to lCON(P<0.05).The results (shown inSupplementary Table S3) indicated that the proliferation ability of JEG-3 cells in KD(GAS5) continuously increased compared with the NCKD(GAS5) (P<0.001) while the proliferation ability of HTR-8/SVneo in KD(GAS5) increased on day 2 (P<0.001). On the contrary, OE (GAS5) inhibited the proliferation of HTR-8/SVneo persistently compared with control (P<0.001) while the proliferation of JEG-3 is decreased on day 2 in OE (GAS5) (P<0.05) (shown inFigure 3A).As depicted inFigure 4A, overexpression of GAS5 significantly reduced the migration ability of JEG-3 cells compared with the NCOE(GAS5).At 24h post-scratch,the migration rate of OE(GAS5) decreased(P<0.05), and at 48 h post-scratch, the migration rate of the cells was persistently decreased (P<0.001).The results of Transwell assay showed that overexpression of GAS5 significantly (P<0.001) reduced the invasion ability of JEG-3 cells, meanwhile, HTR-8/SVneo cell line demonstrated the same trends. The invasion ability of HTR-8/SVneo cells was significantly reduced after overexpression of GAS5 (P<0.001).After GAS5 lentivirus vectors infected the trophoblast cells, the expression level of miR-21 was firstlydetected.Theresults showed(Figure 5A), in JEG-3 cells, knockdown of GAS5 elevated the expression of miR-21 (P<0.05) compared with the control NCKD (GAS5). Overexpression of GAS5 declined miR-21 expression (P<0.05) compared with the control conversely. In HTR-8/SVneo cells, after knocking down GAS5, the level of miR-21 was also increased (P<0.05). However, the overexpression of GAS5 didn't alter the level of miR-21 (P>0.05) in HTR-8/SVneo.Further, HTR-8/SVneo cell line was selected which was closer to the villous cells in first-trimester placenta.According to the prediction of KEGG (Kyoto Encyclopedia of Genesand Genomes)bioinformatics database,we detected the alteration of the PI3K/AKT signaling pathway downstream proteins MMP9 and TP53,which were closely related with preeclampsia (Gao et al.,2016;Chen and Khalil,2017), after GAS5 expression changed. The results showed that the expressions of MMP9 and TP53 were all regulated up and down statistically according to the activation of PI3K/AKT signaling pathway by qRTPCR (Figure 6C). However, due to the low expression level of this two downstream protein in HTR-8/SVneo, no target band was detected in WB.	32194641	RID04516	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LBX2-AS1	IRS1	positively-E	luciferase reporter assay;RIP;bioinformatics analysis	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-384)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257702	GRCh38_2:74502552-74505091	ENSG00000169047	NA	151534	3667	NA	HIRS-1	Long noncoding RNA LBX2-AS1 drives the progression of hepatocellular carcinoma by sponging microRNA-384 and thereby positively regulating IRS1 expression.To elucidate the association ofLBX2-AS1expression with HCC, total RNA was extracted from 45 pairs of HCC tissue samples and matched adjacent normal tissues. RT-qPCR analysis was performed to measure LBX2-AS1expression and revealed thatLBX2-AS1expression was significantly higher in HCC tissue samples compared with that in the adjacent normal tissues (Fig. 1A). Similarly, all three HCC cell lines (Huh7, Hep3B, and SK-HEP-1) manifested higherLBX2-AS1expression than that in the immortalized normal human liver epithelial cell line (LO2;Fig. 1B).The high expression ofLBX2-AS1in HCC tissues and cell lines prompted us to assess the contribution ofLBX2-AS1to HCC progression. Huh7 and Hep3B cells, which presented relatively higher expression among the three HCC cell lines, were transfected with either si-LBX2AS1 or si-NC.LBX2-AS1was found to be significantly downregulated in Huh7 and Hep3B cells after the transfection with si-LBX2-AS1 (Fig. 2A). Results of the CCK-8 assay revealed that theLBX2-AS1downregulation impeded the proliferation of Huh7 and Hep3B cells compared with the cells transfected with si-NC (Fig. 2B). In addition, significant induction of apoptosis in theLBX2-AS1-efficient Huh7 and Hep3B cells was detected byflow-cytometric analysis (Fig. 2C). The regulatory effects of theLBX2-AS1knockdown on the migratory and invasive abilities of HCC cells were examined in Transwell migration and invasion assays. The numbers of migratory (Fig. 2D) and invading (Fig. 2E) Huh7 and Hep3B cells were much lower in theLBX2-AS1knockdown groups than in the si-NC groups. These results meant thatLBX2-AS1may play a cancer-promoting part in HCC progression.Before the luciferase reporter assay to illustrate the potential interaction betweenLBX2-AS1and miR-384, the efficiency of miR-384 transfection was confirmed via RT-qPCR analysis, and the results were satisfactory (Fig. 3C). Next, the luciferase reporter assay was performed on Huh7 and Hep3B cells that were cotransfected with either the miR-384 mimics or miR-NC and either plasmid LBX2-AS1-wt or LBX2-AS1-mut. The results suggested that the luciferase activity was significantly lower in Huh7 and Hep3B cells cotransfected with LBX2AS1-wt and the miR-384 mimics; however, no significant effect was observed in LBX2-AS1-mut groups (Fig. 3D). The RIP assay uncovered obvious enrichment ofLBX2-AS1and miR-384 in the AGO2 group, thus confirming thatLBX2-AS1can bind to miR-384 in HCC cells (Fig. 3E). We next attempted to investigate the correlation betweenLBX2-AS1 and miR-384 expression levels in HCC tissue samples. MiR-384 expression in the 45 pairs of HCC tissue samples and matched adjacent normal tissues was quantitated by RT-qPCR. The HCC tissues showed a significantly lower miR-384 level than that in the adjacent normal tissues (Fig. 3F).Rescue experiments were conducted to determine whether the increase in miR-384 expression was responsible for the effects of the LBX2-AS1knockdown on HCC cells. Huh7 and Hep3B cells transfected with si-LBX2-AS1 were treated with either the miR-384 inhibitor or NC inhibitor. Functional experiments revealed that the inhibition of miR384 abrogated the effects of theLBX2-AS1downregulation on the proliferation (Fig. 5A), apoptosis (Fig. 5B), migration (Fig. 5C), and invasiveness (Fig. 5D) of Huh7 and Hep3B cells. These results suggested thatLBX2-AS1exerted its tumor-promoting action in HCC cells at least in part by downregulating miR-384.	32143907	RID04517	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Chronic obstructive pulmonary disease	MIR155HG	BRD4	positively-E	luciferase reporter assay;RIP;DIANA-LncBaseV2;DianaTools	upregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000234883	GRCh38_21:25561810-25575168	ENSG00000141867	NA	114614	23476	BIC|miPEP155|MIRHG2|NCRNA00172	CAP|HUNK1|HUNKI|MCAP	LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis.The expression of MIR155HG in 49 cases of lung tissue specimens was measured using qRT-PCRand we found that compared with samples from non-smoker without COPD group, the expression level of MIR155HG was significantly elevated in lung tissues of smokers without or with COPD, especially in smokers with COPD group (Figure 1A). In addition, after exposure to a varying concentration of CSE (0, 0.5, 1, 2, 2.5, 5%) for 24 h, the expression of MIR155HG in HPMECs was discovered to be increased in a dose-dependent manner (Figure 1B). Furthermore, the expression of MIR155HG was also time-dependently up-regulated in HPMECs by 2.5% CSE exposure at 0, 6, 12, 24 and 36 h (Figure 1C).To explore the potential biological functions of MIR155HG in CSE-induced apoptosis and inflammation, HPMECs exposed with 2.5% CSE were transfected with si-NC or si-MIR155HG, and then the transfection efficiency was demonstrated using qRT-PCRwith the results of decreased MIR155HG expression in HPMECs transfected with si-MIR155HG (Figure 2A). Subsequently, flow cytometry results showed CSE treatment markedly increased the apoptosis, while silencing of MIR155HG could significantly alleviate CSE-induced apoptosis of HPMECs (Figure 2B). Moreover, western blot indicated that the increase of Bax and cleaved-caspase3 protein and decrease of Bcl-2 protein induced by 2.5% CSE exposure in HPMECs was attenuated by si-MIR155HG transfection in HPMECs (Figure 2C), further validating that MIR155HG deletion suppressed CSE-induced apoptosis. According to the prediction of DIANA-LncBaseV2 prediction program, miR-218-5p might be a potential target of MIR155HG (Figure 3A). To verify this prediction, luciferase reporter assay was performed and we found miR-218-5p mimic transfection reduced the luciferase activity of the MIR155HG-WT reporter vector but not MIR155HG-MUT reporter vector in HPMECs (Figure 3B). However, miR-218-5p inhibitor transfection enhanced the luciferase activity of the MIR155HG-WT reporter vector and there was no obvious change in MIR155HG -MUT reporter after reduction of miR-218-5p in HPMECs (Figure 3C). Meanwhile, RIP assay further confirmed the direct interaction between miR-218-5p and MIR155HG because of significant enrichment of MIR155HG in HPMECs (Figure 3D). Additionally, a negatively between MIR155HG and miR-218-5p in the tissues of smokers with COPD was observed (Figure 3E), and MIR155HG overexpression inhibited miR-218-5p expression, while MIR155HG deletion promoted miR-218-5p expression in HPMECs (Figure 3F). Thus, MIR155HG was a sponge of miR-218-5p and negatively regulated its expression.The potential target gene of miR-218-5p was predicted using DianaTools program, and BRD4 was found that might be a target of miR-218-5p (Figure 5A). Then luciferase reporter analysis exhibited that the relative luciferase activity of the BRD4-WT reporter vector was dramatically inhibited by miR-218-5p overexpression, whereas was increased by miR-218-5p inhibition in HPMECs, meanwhile, no significance was observed in BRD4-MUT reporter vector co-transfection groups (Figure 5B,C). All these data suggested the direct interaction of miR-218-5p and BRD4.	32129458	RID04518	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Chronic hyperglycemia	XIC	hsa-miR21-5p	negatively-F	dual-luciferase assay;qRT-PCR	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Genetic disease	Hyperglycemia	lncRNA	miRNA	NA	NA	NA	NA	7502	NA	SXI1|XCE|XIST	NA	Long non-coding RNA XIST regulates hyperglycemia-associated apoptosis and migration in human retinal pigment epithelial cells.Again, quantification confirmedthat, migration capability was severely inhibited by HG treatment in APRE19 cells (Fig. 1D,p< 0.05). In addition, qRT-PCRanalysis showed that, as compared to NG condition, HG condition significantly reduced the expression level of lncRNA XIST in APRE-19 cells (Fig. 1E, * p< 0.05).Transfected ARPE-19 cells were then exposed to HG to mimic hyperglycemia insult, followed by measurements on apoptosis and migration. The TUNEL assay showed that TUNEL activity was markedly reduced in cells transfected with pc/XIST, rather than in cells transfected with pc/C (Fig. 2B). In addition, quantitative measurement confirmed that, XIST overexpression significantly reduced hyperglycemia-induced apoptosis in ARPE-19 cells (Fig. 2C, *p< 0.05). In the wound-healing assay, it indicated that markedly more wound area was recovered in hyperglycemia-insulted APRE-19 cells if they were transfected with pc/XIST, as compared to cells transfected with pc/C (Fig. 2D). Moreover, quantification confirmed that, migration capability in hyperglycemia-insulted APRE-19 cells was significantly restored by XIST overexpression (Fig. 2E, *p< 0.05).We thus constructed two luciferase reporter vectors, one containing the wild type XIST 3'-UTR (XIST_WildType, with hsa-miR-21-5p binding region) and the other containing a mutant XIST 3'-UTR (XIST_Mutant, without hsa-miR-21-5p binding region). Then, a dual-luciferase reporter assay was performed. It showed that significant luciferase activity reduction was monitored in cells co-transfected with hsa-miR-21-5p mimics and XIST_WildType (Fig. 3B, *p< 0.05), indicating that XIST could bind hsa-miR-21-5p.Then, double-transfected ARPE-19 cells were exposed to HG. After that, a TUNEL assay demonstrated that TUNEL activity was markedly increased in cells double-transfected with pc/XIST + hsa-miR21-5p, than in cells double-transfected with pc/XIST + hsa-miR (Fig. 4B). This observation was confirmed by quantitative measurement, showing that cells double-transfected with pc/XIST + hsa-miR21-5p were more prone to hyperglycemia-induced apoptosis (Fig. 4C, *p< 0.05). Finally, in the wound-healing assay, it showed that markedly less wound area was recovered in hyperglycemia-insulted APRE-19 cells if they were double-transfected with pc/XIST + hsa-miR21-5p, rather than double-transfected with pc/XIST + hsa-miR (Fig. 4D). Again, quantification confirmed that, migration capability in hyperglycemia-insulted APRE-19 cells was significantly reduced in cells double-transfected with pc/XIST + hsa-miR21-5p (Fig. 4E, *p< 0.05).Overall, these data indicated that hsa-miR-21-5p upregulation reversed the protective effects of XIST overexpression in hyperglycemiainsulted ARPE-19 cells.	32106367	RID04519	ceRNA or sponge	NA		
Septic acute kidney injury	TCONS_00016233	AIFM1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-22-3p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000156709	NA	NA	9131	NA	AIF|AUNX1|CMTX4|DFNX5|NAMSD|PDCD8	The Biomarker TCONS_00016233 Drives Septic AKI by Targeting the miR-22-3p/AIFM1 Signaling Axis.Quantitative real-time PCR (qRT-PCR analysis confirmed that TCONS_00016233 was indeed induced in septic AKI and non-AKI patients when compared to healthy controls (2.25- and 1.3-fold change in septic AKI and non-AKI versus control, respectively; Figure 1D).Taken together, our data indicate an increased detection of TCONS_00016233 in the plasma of septic AKI and non-AKI patients.qRT-PCRanalysis has showed that LPS-induced TCONS_00016233 expression in HK-2 cells was markedly suppressed by transient gene silencing using TCONS_00016233 siRNA (Figure 4A). Additionally, flow cytometry (FCM) results indicate that TCONS_00016233 gene silencing notably inhibits the LPS-induced apoptosis of siRNA-transfected HK-2 cells (Figures 4B and 4C). Consistently, immunoblot analysis shows that the siRNA-mediated TCONS_00016233 knockdown significantly reduced LPS-induced accumulation of cleaved caspase-3 (Figures 4D and 4E). These data suggest that TCONS_00016233 can mediate LPS-induced apoptosis in vitro.To verify whether increased TCONS_00016233 levels would also impact LPS-induced apoptosis in vitro, a TCONS_00016233 expression vector was transfected into HK-2 cells for further functional analyses. qRT-PCRanalysis showed that LPS-induced TCONS_00016233 expression can be further enhanced by TCONS_00016233 overexpression in HK-2 cells (Figure 5A). Moreover, FCM results reiterated that TCONS_00016233 overexpression markedly aggravates LPS-induced renal cell apoptosis in HK-2 cells (Figures 5B and 5C). Consistently, immunoblot analysis demonstrated that TCONS_00016233 overexpression can markedly augment LPS-caused accumulation of the cleaved caspase-3 protein (Figures 5D and 5E). Finally, overexpression of TCONS_00016233 enhances LPS-induced expression of IL-1beta and TNF-alpha (Figures 5F'-I). These data agree with previous knockdown experiments, supporting the notion that TCONS_00016233 acts as an apoptotic and inflammation inducer in LPS-treated HK-2 cells.Functional analysis, based on a luciferase reporter gene assay, indicates that a miR-22-3p mimic can markedly suppress the luciferase activity of TCONS_00016233-wild-type (WT) but not TCONS_00016233-mutant (MUT) (Figure 6B). Indeed, colocalization analysis indicated that TCONS_00016233 may interact with miR-22-3p in the cytosolic compartment of both untreated and LPS-stimulated HK-2 cells (Figure 6C).By performing computational analysis (using the miRBase database), we have predicted that AIFM1 is a putative miR-22-3p target gene (Figure 8A). In fact, reporter assays here demonstrate that the miR-22-3p mimic suppresses the luciferase activity of AIFM1-WT but not AIFM1-MUT (Figure 8B). qRT-PCRand immunoblot results show that the miR-22-3p mimic significantly decreases AIFM1 mRNA and protein levels (Figures 8C and 8D). FCM results indicate that AIFM1 knockdown markedly suppresses LPS-induced renal cell apoptosis in HK-2 cells (Figures 8E and 8F). Immunoblot results demonstrated that silencing of AIFM1 expression can notably suppress LPS-induced accumulation of the cleaved caspase-3 (Figures 8G and 8H). Altogether, these data demonstrate that AIFM1 might be a direct target gene of miR-22-3p.The FISH analysis demonstrated that TCONS_00016233 was mainly expressed in the tubular cells of the kidney after CLP with injection of TCONS_00016233 (Figure S4B). The qRT-PCRdata indicated that transfection of TCONS_00016233 can enhance the CLP-mediated suppression of miR-22-3p (Figures S3A and S3B). Immunoblot analysis showed that CLP can upregulate the expression levels of cleaved caspase-3 and AIFM1, which were further enhanced by TCONS_00016233 overexpression (Figures S3C and S3D). Finally, the immunoblot and qRT-PCRanalysis demonstrated that overexpression of TCONS_00016233 enhanced CLP-induced expression of IL-1beta and TNF-alpha (Figures S1E-S1H). These conclusive data further confirmed that TCONS_00016233 can mediate the CLP-dependent AKI progression.	32059335	RID04520	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842)
Septic acute kidney injury	TCONS_00016233	IL-1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	The Biomarker TCONS_00016233 Drives Septic AKI by Targeting the miR-22-3p/AIFM1 Signaling Axis.Quantitative real-time PCR (qRT-PCR analysis confirmed that TCONS_00016233 was indeed induced in septic AKI and non-AKI patients when compared to healthy controls (2.25- and 1.3-fold change in septic AKI and non-AKI versus control, respectively; Figure 1D).Taken together, our data indicate an increased detection of TCONS_00016233 in the plasma of septic AKI and non-AKI patients.qRT-PCRanalysis has showed that LPS-induced TCONS_00016233 expression in HK-2 cells was markedly suppressed by transient gene silencing using TCONS_00016233 siRNA (Figure 4A). Additionally, flow cytometry (FCM) results indicate that TCONS_00016233 gene silencing notably inhibits the LPS-induced apoptosis of siRNA-transfected HK-2 cells (Figures 4B and 4C). Consistently, immunoblot analysis shows that the siRNA-mediated TCONS_00016233 knockdown significantly reduced LPS-induced accumulation of cleaved caspase-3 (Figures 4D and 4E). These data suggest that TCONS_00016233 can mediate LPS-induced apoptosis in vitro.To verify whether increased TCONS_00016233 levels would also impact LPS-induced apoptosis in vitro, a TCONS_00016233 expression vector was transfected into HK-2 cells for further functional analyses. qRT-PCRanalysis showed that LPS-induced TCONS_00016233 expression can be further enhanced by TCONS_00016233 overexpression in HK-2 cells (Figure 5A). Moreover, FCM results reiterated that TCONS_00016233 overexpression markedly aggravates LPS-induced renal cell apoptosis in HK-2 cells (Figures 5B and 5C). Consistently, immunoblot analysis demonstrated that TCONS_00016233 overexpression can markedly augment LPS-caused accumulation of the cleaved caspase-3 protein (Figures 5D and 5E). Finally, overexpression of TCONS_00016233 enhances LPS-induced expression of IL-1beta and TNF-alpha (Figures 5F'-I). These data agree with previous knockdown experiments, supporting the notion that TCONS_00016233 acts as an apoptotic and inflammation inducer in LPS-treated HK-2 cells.Functional analysis, based on a luciferase reporter gene assay, indicates that a miR-22-3p mimic can markedly suppress the luciferase activity of TCONS_00016233-wild-type (WT) but not TCONS_00016233-mutant (MUT) (Figure 6B). Indeed, colocalization analysis indicated that TCONS_00016233 may interact with miR-22-3p in the cytosolic compartment of both untreated and LPS-stimulated HK-2 cells (Figure 6C).By performing computational analysis (using the miRBase database), we have predicted that AIFM1 is a putative miR-22-3p target gene (Figure 8A). In fact, reporter assays here demonstrate that the miR-22-3p mimic suppresses the luciferase activity of AIFM1-WT but not AIFM1-MUT (Figure 8B). qRT-PCRand immunoblot results show that the miR-22-3p mimic significantly decreases AIFM1 mRNA and protein levels (Figures 8C and 8D). FCM results indicate that AIFM1 knockdown markedly suppresses LPS-induced renal cell apoptosis in HK-2 cells (Figures 8E and 8F). Immunoblot results demonstrated that silencing of AIFM1 expression can notably suppress LPS-induced accumulation of the cleaved caspase-3 (Figures 8G and 8H). Altogether, these data demonstrate that AIFM1 might be a direct target gene of miR-22-3p.The FISH analysis demonstrated that TCONS_00016233 was mainly expressed in the tubular cells of the kidney after CLP with injection of TCONS_00016233 (Figure S4B). The qRT-PCRdata indicated that transfection of TCONS_00016233 can enhance the CLP-mediated suppression of miR-22-3p (Figures S3A and S3B). Immunoblot analysis showed that CLP can upregulate the expression levels of cleaved caspase-3 and AIFM1, which were further enhanced by TCONS_00016233 overexpression (Figures S3C and S3D). Finally, the immunoblot and qRT-PCRanalysis demonstrated that overexpression of TCONS_00016233 enhanced CLP-induced expression of IL-1beta and TNF-alpha (Figures S1E-S1H). These conclusive data further confirmed that TCONS_00016233 can mediate the CLP-dependent AKI progression.	32059335	RID04521	expression association	NA		
Septic acute kidney injury	TCONS_00016233	TNF	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000228978	NA	NA	7124	NA	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	The Biomarker TCONS_00016233 Drives Septic AKI by Targeting the miR-22-3p/AIFM1 Signaling Axis.Quantitative real-time PCR (qRT-PCR analysis confirmed that TCONS_00016233 was indeed induced in septic AKI and non-AKI patients when compared to healthy controls (2.25- and 1.3-fold change in septic AKI and non-AKI versus control, respectively; Figure 1D).Taken together, our data indicate an increased detection of TCONS_00016233 in the plasma of septic AKI and non-AKI patients.qRT-PCRanalysis has showed that LPS-induced TCONS_00016233 expression in HK-2 cells was markedly suppressed by transient gene silencing using TCONS_00016233 siRNA (Figure 4A). Additionally, flow cytometry (FCM) results indicate that TCONS_00016233 gene silencing notably inhibits the LPS-induced apoptosis of siRNA-transfected HK-2 cells (Figures 4B and 4C). Consistently, immunoblot analysis shows that the siRNA-mediated TCONS_00016233 knockdown significantly reduced LPS-induced accumulation of cleaved caspase-3 (Figures 4D and 4E). These data suggest that TCONS_00016233 can mediate LPS-induced apoptosis in vitro.To verify whether increased TCONS_00016233 levels would also impact LPS-induced apoptosis in vitro, a TCONS_00016233 expression vector was transfected into HK-2 cells for further functional analyses. qRT-PCRanalysis showed that LPS-induced TCONS_00016233 expression can be further enhanced by TCONS_00016233 overexpression in HK-2 cells (Figure 5A). Moreover, FCM results reiterated that TCONS_00016233 overexpression markedly aggravates LPS-induced renal cell apoptosis in HK-2 cells (Figures 5B and 5C). Consistently, immunoblot analysis demonstrated that TCONS_00016233 overexpression can markedly augment LPS-caused accumulation of the cleaved caspase-3 protein (Figures 5D and 5E). Finally, overexpression of TCONS_00016233 enhances LPS-induced expression of IL-1beta and TNF-alpha (Figures 5F'-I). These data agree with previous knockdown experiments, supporting the notion that TCONS_00016233 acts as an apoptotic and inflammation inducer in LPS-treated HK-2 cells.Functional analysis, based on a luciferase reporter gene assay, indicates that a miR-22-3p mimic can markedly suppress the luciferase activity of TCONS_00016233-wild-type (WT) but not TCONS_00016233-mutant (MUT) (Figure 6B). Indeed, colocalization analysis indicated that TCONS_00016233 may interact with miR-22-3p in the cytosolic compartment of both untreated and LPS-stimulated HK-2 cells (Figure 6C).By performing computational analysis (using the miRBase database), we have predicted that AIFM1 is a putative miR-22-3p target gene (Figure 8A). In fact, reporter assays here demonstrate that the miR-22-3p mimic suppresses the luciferase activity of AIFM1-WT but not AIFM1-MUT (Figure 8B). qRT-PCRand immunoblot results show that the miR-22-3p mimic significantly decreases AIFM1 mRNA and protein levels (Figures 8C and 8D). FCM results indicate that AIFM1 knockdown markedly suppresses LPS-induced renal cell apoptosis in HK-2 cells (Figures 8E and 8F). Immunoblot results demonstrated that silencing of AIFM1 expression can notably suppress LPS-induced accumulation of the cleaved caspase-3 (Figures 8G and 8H). Altogether, these data demonstrate that AIFM1 might be a direct target gene of miR-22-3p.The FISH analysis demonstrated that TCONS_00016233 was mainly expressed in the tubular cells of the kidney after CLP with injection of TCONS_00016233 (Figure S4B). The qRT-PCRdata indicated that transfection of TCONS_00016233 can enhance the CLP-mediated suppression of miR-22-3p (Figures S3A and S3B). Immunoblot analysis showed that CLP can upregulate the expression levels of cleaved caspase-3 and AIFM1, which were further enhanced by TCONS_00016233 overexpression (Figures S3C and S3D). Finally, the immunoblot and qRT-PCRanalysis demonstrated that overexpression of TCONS_00016233 enhanced CLP-induced expression of IL-1beta and TNF-alpha (Figures S1E-S1H). These conclusive data further confirmed that TCONS_00016233 can mediate the CLP-dependent AKI progression.	32059335	RID04522	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Parkinson's disease	AL049437	MAPK1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;western blot	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-205-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000100030	NA	NA	5594	NA	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Knockdown of long non-coding RNA AL049437 mitigates MPP+<U+202F>-induced neuronal injury in SH-SY5Y cells via the microRNA-205-5p/MAPK1 axis.Compared with that in control mice, AL049437 expression was markedly increased in mice injected with MPTP, while miR-205-5p expression was markedly decreased (Fig. 1A and 1B).Since AL049437 expression was upregulated in thein vivoandin vitromodels of PD, we performed AL049437 knockdown by siAL049437 in SH-SY5Y cells to explore its role in PD. As expected, downregulation of AL049437 expression was observed in si-AL049437transfected cells (Fig. 2A). Further, CCK-8 assay showed that MPP + treatment caused a reduction in the viability of SH-SY5Y cells; however, this effect was mitigated by silencing of AL049437 (Fig. 2B). Flow cytometry analysis revealed that treatment of SH-SY5Y cells with MPP + caused an increase in cell apoptosis, and this effect was abrogated by AL049437 knockdown (Fig. 2C). Simultaneously, an obvious increase in TNF-alphaand IL-6 levels was observed in SH-SY5Y cells stimulated with MPP+, and this increase was attenuated following AL049437 knockdown (Fig. 2D and 2E).Hence, to investigate the interaction between AL049437 and miR-205-5p, luciferase reporter and RNA pull-down assays were performed in SH-SY5Y cells. Overexpression of miR-205-5p, but not miRNC, markedly decreased the luciferase activity of reporter containing AL049437-WT. However, the luciferase activity of reporter containing AL049437-MUT was unaffected following miR-205-5p mimic or miRNC transfection (Fig. 3C). As detected by the RNA pull-down assay, the expression of AL049437 was much higher in the Bio-miR-205-5p group than that in the Bio-NC group (Fig. 3D). Additionally, knockdown of AL049437 significantly increased the expression of miR-205-5p, while overexpression of AL049437 decreased the expression of miR-205-5p in SH-SY5Y cells (Fig. 3E).To validate the binding of MAPK1 and miR-205-5p, we co-transfected SH-SY5Y cells with MAPK1-WT or MAPK1-MUT and miR-205-5p or miR-NC. Compared with the miR-NC group, upregulation of miR-205-5p strikingly decreased the luciferase activity of reporters containing MAPK1-WT. However, the luciferase activity of reporters containing MAPK1-MUT was not significantly altered following miR-205-5p or miR-NC transfection (Fig. 4B). Likewise, upregulation of miR-205-5p decreased, while downregulation of miR-205-5p increased the mRNA and protein expression of MAPK1, as determined by qRT-PCRand western blot, respectively (Fig. 4C and 4D).	32057949	RID04523	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	GPNCA	GSK3B	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000082701	NA	NA	2932	NA	NA	Upregulation of GPNCA is associated with poor prognosis through enhancement of tumor growth via regulating GSK3B.We examined the expression of lncRNA GPNCA using the normal human liver cell L02, human liver cancer cell HepG2, human normal renal cell HK2 and human renal cancer cell 769 by SYBR-green relative quantity RT-PCR which was often used for gene expression detection amongst different cells or tissues. qRT-PCRrevealed that GPNCA was overexpressed in the cancer cells (Fig. 7A). In addition, we also did absolute qPCR to detect the copy number of GPNCA and the results also revealed that GPNCA was upregulated in cancer cells (Fig. 7B and Supplemental Fig. S3A).To investigate the role of GPNCA during cell proliferation, HepG2 and HCT116 GPNCA knockdown cells were established using lentivirus shRNA infections. The knockdown efficiency of lncRNA GPNCA was measured by qRT-PCRand showed high efficiency in HepG2 and HCT116 cells (Fig. 7F,G). To elucidate the role of lncRNA GPNCA during tumor cell proliferation, CCK-8 (cell counting kit-8) cell viability assays were performed. The results showed that GPNCA silencing inhibited cell proliferation both in HepG2 and HCT116 cells (Fig. 7H,I). These findings were confirmed in colony formation assays (Fig. 7J,K). Taken together, these data demonstrate that GPNCA silencing inhibits tumor cell growth.To make sure, qPCR assays were conducted to detect GSK3B RNA levels in GPNCA stable knockdown HCT116 and HepG2 cells, whose results showed that the mRNA levels of GSK3B were markedly decreased in GPNCA stable knockdown cells (Fig. 8F). Besides, western blot assays were also carried out and the results showed that GSK3B protein were reduced both in HCT116 and HepG2 cells with GPNCA stable knockdown (Fig. 8G and Supplemental Fig. S5A). However, the expressions of GPNCA were not influenced by GSK3B knockdown both in HCT116 and HepG2 cells (Fig. 8H). These data demonstrated that GPNCA regulated tumor cells proliferation by targeting to its nearby protein-coding gene GSK3B and high GPNCA expression was responsible for the upregulation of GSK3B in many tumors.	32029792	RID04524	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cancer	GPNCA	GSK3B	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000082701	NA	NA	2932	NA	NA	Upregulation of GPNCA is associated with poor prognosis through enhancement of tumor growth via regulating GSK3B.We examined the expression of lncRNA GPNCA using the normal human liver cell L02, human liver cancer cell HepG2, human normal renal cell HK2 and human renal cancer cell 769 by SYBR-green relative quantity RT-PCR which was often used for gene expression detection amongst different cells or tissues. qRT-PCRrevealed that GPNCA was overexpressed in the cancer cells (Fig. 7A). In addition, we also did absolute qPCR to detect the copy number of GPNCA and the results also revealed that GPNCA was upregulated in cancer cells (Fig. 7B and Supplemental Fig. S3A).To investigate the role of GPNCA during cell proliferation, HepG2 and HCT116 GPNCA knockdown cells were established using lentivirus shRNA infections. The knockdown efficiency of lncRNA GPNCA was measured by qRT-PCRand showed high efficiency in HepG2 and HCT116 cells (Fig. 7F,G). To elucidate the role of lncRNA GPNCA during tumor cell proliferation, CCK-8 (cell counting kit-8) cell viability assays were performed. The results showed that GPNCA silencing inhibited cell proliferation both in HepG2 and HCT116 cells (Fig. 7H,I). These findings were confirmed in colony formation assays (Fig. 7J,K). Taken together, these data demonstrate that GPNCA silencing inhibits tumor cell growth.To make sure, qPCR assays were conducted to detect GSK3B RNA levels in GPNCA stable knockdown HCT116 and HepG2 cells, whose results showed that the mRNA levels of GSK3B were markedly decreased in GPNCA stable knockdown cells (Fig. 8F). Besides, western blot assays were also carried out and the results showed that GSK3B protein were reduced both in HCT116 and HepG2 cells with GPNCA stable knockdown (Fig. 8G and Supplemental Fig. S5A). However, the expressions of GPNCA were not influenced by GSK3B knockdown both in HCT116 and HepG2 cells (Fig. 8H). These data demonstrated that GPNCA regulated tumor cells proliferation by targeting to its nearby protein-coding gene GSK3B and high GPNCA expression was responsible for the upregulation of GSK3B in many tumors.	32029792	RID04525	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Tongue squamous cell carcinoma	CISAL	BRCA1	negatively-E	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	mitochondrial fission(-);apoptosis process(-);chemosensitivity(-)	NA	binding/interaction	RNA-protein	Cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	NA	NA	ENSG00000012048	NA	NA	672	NA	BRCC1|FANCS|PPP1R53|RNF53	lncRNA CISAL Inhibits BRCA1 Transcription by Forming a Tertiary Structure at Its Promoter.Notably, one lncRNA (RefSeq accession number LINC01011) was mostly upregulated in chemosensitive tumors (Figures 1C and S1C). Thus, we focused on this uncharacterized lncRNA and named it CISAL (cisplatin sensitivity-associated lncRNA). We tested whether CISAL could regulate mitochondrial fission and cisplatin sensitivity in TSCC cells. CISAL knockdown by shRNA attenuated mitochondrial fission and cell apoptosis upon cisplatin treatment in TSCC cells (Figures 2A, 2B, S3E, and S3F). Moreover, the release of cytochrome c (CYT c) from the intermembrane space of the mitochondria to the cytosol and caspase-3/7 activity were attenuated upon CISAL silencing in TSCC cells under cisplatin treatment (Figures 2A and S3G).As expected, we found that GABPA knockdown reduced BRCA1 levels in CAL-27 and SCC-9 cells (Figures S9A and S9B), whereas overexpression of GABPA upregulated BRCA1 levels in both cell lines (Figure S9C). ChIP and luciferase reporter assays identified the transcriptional functionality of GABPA as well (Figures 4E'-G).RNA immunoprecipitation (RIP) assays revealed that CISAL could interact with endogenous GABPA in TSCC cells (Figure 5A). RNA pull-down assay also identified that CISAL could interact with recombinant GABPA and endogenous GABPA in TSCC cells (Figure 5B).	32000125	RID04526	expression association	chemoresistance		UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Tongue squamous cell carcinoma	CISAL	GABPA	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	mitochondrial fission(-);apoptosis process(-);chemosensitivity(-)	NA	binding/interaction	NA	Cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	TF	NA	NA	ENSG00000154727	NA	NA	2551	NA	E4TF1-60|E4TF1A|NFT2|NRF2|NRF2A	lncRNA CISAL Inhibits BRCA1 Transcription by Forming a Tertiary Structure at Its Promoter.Notably, one lncRNA (RefSeq accession number LINC01011) was mostly upregulated in chemosensitive tumors (Figures 1C and S1C). Thus, we focused on this uncharacterized lncRNA and named it CISAL (cisplatin sensitivity-associated lncRNA). We tested whether CISAL could regulate mitochondrial fission and cisplatin sensitivity in TSCC cells. CISAL knockdown by shRNA attenuated mitochondrial fission and cell apoptosis upon cisplatin treatment in TSCC cells (Figures 2A, 2B, S3E, and S3F). Moreover, the release of cytochrome c (CYT c) from the intermembrane space of the mitochondria to the cytosol and caspase-3/7 activity were attenuated upon CISAL silencing in TSCC cells under cisplatin treatment (Figures 2A and S3G).As expected, we found that GABPA knockdown reduced BRCA1 levels in CAL-27 and SCC-9 cells (Figures S9A and S9B), whereas overexpression of GABPA upregulated BRCA1 levels in both cell lines (Figure S9C). ChIP and luciferase reporter assays identified the transcriptional functionality of GABPA as well (Figures 4E'-G).RNA immunoprecipitation (RIP) assays revealed that CISAL could interact with endogenous GABPA in TSCC cells (Figure 5A). RNA pull-down assay also identified that CISAL could interact with recombinant GABPA and endogenous GABPA in TSCC cells (Figure 5B).	32000125	RID04527	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	UCA1	miR-185-5p	negatively-E	bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);tumorigenesis(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Silencing of long noncoding RNA UCA1 inhibits colon cancer invasion, migration and epithelial-mesenchymal transition and tumour formation by upregulating miR-185-5p in vitro and in vivo.The expression levels of UCA1 and miR-185-5p were detected by RTqPCR. As shown in Figure 1A,B, the expression level of UCA1 was significantly increased in colon cancer cell lines (SW480, SW620 and HT-29) compared to CCD-18Co and HIEC-6, while the level of miR185-5p was significantly decreased. These results indicate that the expression of UCA1 is upregulated in colon cancer cells, while the expression of miR-185-5p is downregulated. In these colon cancer cell lines, changes in SW480 and HT-29 were more pronounced, and thus SW480 and HT-29 cell lines were used for subsequent studies.Besides, knockdown of UCA1 by shRNA (sh-UCA1) significantly reduced the expression level of UCA1, while increasing the expression level of miR-185-5p (Figure 2B,C). Moreover, miR-185-5p was significantly overexpressed in HIEC-6 and SW480 cells transfected with the miR-185-5p mimic. However, the increase of miR185-5p in HIEC-6 cells was higher than that in SW480 cells (Figure 2D,E). Furthermore, dual-luciferase assay showed that cotransfection of miR-185-5p mimic and UCA1 wt significantly reduced luciferase activity in HIEC-6 and SW480 cells (Figure 2F,G). These results indicated that UCA1 negatively regulated the level of miR185-5p in colon cancer cells.Transwell assays, wound healing assay and western blot were performed to investigate the effects of UCA1 on cell invasion, migration and epithelial-mesenchymal transition (EMT), respectively. As shown in Figure 3A, sh-UCA1 significantly increased the expression level of miR-185-5p, whereas miR-185-5p inhibitor showed the opposite effect. Besides, Transwell experiments showed that UCA1 knockdown significantly inhibited the invasion of SW480 and HT-29 cells, while miR-185-5p inhibitor reversed the inhibitory effect of sh-UCA1 on cell invasion. Notably, sh-UCA1 had no significant effect on the invasiveness of HIEC-6 cells (Figure 3B). western blot assay showed that UCA1 knockdown significantly reduced the protein level of VEGF, while miR-185-5p inhibitor reversed the inhibitory effect of sh-UCA1 on VEGF expression. Likewise, sh-UCA1 had no significant effect on the expression of VEGF in HIEC-6 cells (Figure 3C). Similarly, knockdown of UCA1 significantly inhibited the migration of SW480 and HT-29 cells. In contrast, the downregulation of miR-185-5p significantly promoted cell migration (Figure 3D).	31989667	RID04528	expression association	NA	UP(PAAD);DATA(GSE40174)	
Primary graft dysfunction	XIST	IL12A	positively-E	luciferase reporter assay;RNA pull-down;RIP	upregulation	RT-qPCR;western blot	NA	NA	apoptosis process(-)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Other	Primary graft dysfunction	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000168811	NA	7503	3592	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	CLMF|IL-12A|NFSK|NKSF1|p35	Long non-coding RNA X-inactive specific transcript silencing ameliorates primary graft dysfunction following lung transplantation through microRNA-21-dependent mechanism.To assess the consequence of lung transplantation on miR-21 expression levels in the context of PGD, we performed RT-qPCR. Intriguingly, in comparison to the non-PGD cohort, miR-21 expression was significantly decreased in the PGD patient cohort after lung transplantation, and expression levels were negatively associated with the PGD grade (Fig. 1a, b). It was predicted that there existed binding sites between miR-21 and XIST (Fig. 5a). We again utilized the dual-luciferase reporter assay to show that in XIST-Wt cells, mimic-NC had no effect on luciferase activity of XIST, but after miR-21 mimic transfection, the luciferase activity of XIST was significantly inhibited. In XIST-Mut, both treatments had no effect on luciferase activity of XIST, indicating that there were specific binding sites between miR-21 and XIST (Fig. 5b). We then sought to explore the interaction between miR-21 and XIST by conducting RNA pull-down and RIP assays. Encouragingly, we found an enriched level of XIST pulled down by miR-21-Wt over miR-21-Mut, which also validated a binding interaction of miR-21 with XIST (Fig. 5c). Next, the RIP assay showed that the expression of XIST and miR-21 bound with Ago2 was elevated compared to those bound with IgG, again demonstrating that miR-21 interacts with XIST (Fig. 5d). Further we also detected a high expression of XIST in the BALF of PGD patients (Fig. 5e). We then demonstrated that the deletion of XIST by transfection of sh-XIST enhanced miR-21 expression but suppressed IL-12A expression (Fig. 5f). Finally, the correlation analysis indicated that XIST was negatively correlated with miR-21, but positively correlated with IL-12A (Fig. 5g, h). In summary, the above results provide evidence that XIST can competitively bind to miR-21 to upregulate the expression of IL-12A.To further evaluate the mechanistic underpinnings of the effects of XIST/miR-21/IL-12A axis on NET formation we used a series of in vitro assays. First, we introduced the sh-XIST, IL-12A overexpression vector and miR-21 inhibitor respectively into the PMA-treated PMNs and found that the content of NET-DNA was remarkably elevated by the combined treatment with sh-XIST and miR-21 inhibitor or sh-XIST plus IL-12A overexpression vector in comparison with the combined treatment with sh-XIST plus inhibitor-NC or sh-XIST plus vector-NC, respectively (Fig. 7a). The results of immunofluorescence staining showed that XIST silencing along with miR-21 inhibition or XIST silencing plus IL-12A overexpression led to an increased number of filamentous and green-stained intercellular DNA than XIST silencing alone (Fig. 7b). Next, using flow cytometry, we measured the apoptosis rate in PMA-treated PMNs and showed that PMA-treated PMNs transfected with sh-XIST and miR-21 inhibitor or those transfected with sh-XIST and IL-12A overexpression vector exhibited lower apoptosis rates in comparison to those transfected with sh-XIST and inhibitor-NC or sh-XIST and vector-NC, independently (Fig. 7c). Taken together, these results support the conclusion that inhibition of miR-21 or elevation of IL-12A reverses the effects of XIST silencing on NET formation.	31981974	RID04529	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)
Myocardial ischemia and reperfusion injury	FTX	FMR1	positively-E	luciferase reporter assay;	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);oxidative stress(+)	ceRNA(miR-410-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Injury	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000102081	NA	100302692	2332	FLJ33139|LINC00182|MIR374AHG|NCRNA00182	FMRP|FRAXA|MGC87458|POF|POF1	Long non-coding RNA FTX alleviates hypoxia/reoxygenation-induced cardiomyocyte injury via miR-410-3p/Fmr1 axis.To investigate the role of FTX in myocardial I/R injury, the expression level of FTX in the serum of myocardial I/R injury patients was determined via qRT-PCR The data indicated that the level of FTX was conspicuously reduced in the serum of myocardial I/R injury patients compared to that in normal group (Figure 1A). Besides, the expression of FTX was drastically decreased in H9c2 cells treated with H/R when compared to cells under the condition of normoxia (Figure 1B). These findings suggested that FTX might be involved in the progression of I/R-induced myocardial injury.CCK-8 assay implicated that H/R treatment led to a remarkable reduction in cell proliferation, while FTX overexpression distinctly reversed this reduction in H9c2 cells (Figure 2B). Flow cytometry analysis data showed that the apoptosis of H9c2 cells was evidently enhanced after H/R treatment, whereas this impact on cell apoptosis was partly restored by the transfection of FTX (Figure 2C). The protein levels of apoptosis-associated factors (Bcl-2, Bax and cleaved-casp-3) were examined through western blot assay. The results implied that Bcl-2 was decreased, and Bax and cleaved-casp-3 were increased under the treatment of H/R in H9c2 cells, while the elevation of FTX abolished these influences (Figure 2D).Next, dual-luciferase reporter assay was employed to verify this prediction. The results implicated the luciferase activity was suppressed in H9c2 cells co-transfected with FTX WT and miR-410-3p in reference to that in H9c2 cells co-transfected with FTX WT and miR-NC, while the luciferase activity was not affected in FTX MUT group (Figure 3B). Subsequently, H9c2 cells were treated with H/R+pcDNA, H/ R+FTX, H/R+si-NC or H/R+si-FTX and then the expression of miR-410-3p was determined by qRT-PCR The results exhibited that FTX overexpression significantly inhibited the expression of miR-410-3p and FTX knockdown distinctly promoted the expression of miR410-3p in H/R-induced H9c2 cells (Figure 3C).Taken together, FTX negatively regulated miR-410-3p expression by direct interaction in H/R-induced H9c2 cells.To verify it, we performed dual-luciferase reporter assay. The data showed that compared to miR-NC and Fmr1 3'-UTR-WT co-transfected group, co-transfection of miR-410-3p and Fmr1 3'-UTR-WT led to an effective inhibition in the luciferase activity in H9c2 cells, while the luciferase activity was not affected in Fmr1 3'-UTR-MUT group (Figure 5B). Then we treated H9c2 cells with H/ R+miR-NC, H/R+miR-410-3p, H/R+anti-miRNC or H/R+anti-miR-410-3p to explore the association between miR-410-3p and Fmr1. As exhibited in Figure 5C and D, the mRNA and protein levels of Fmr1 were decreased in H/R-induced H9c2 cells following miR-410-3p transfection and were increased after anti-miR-4103p transfection. As we expected, the mRNA and protein levels of Fmr1 in myocardial I/R injury patients'-serum and H/R-stimulated H9c2 cells were dramatically reduced compared to control groups (Figure 5E-H).As shown in Figure 7A, Fmr1 mRNA expression was positively correlated with FTX expression in the serum of myocardial I/R injury patients. Next, to further confirm the association among FTX, miR-410-3p and Fmr1, H9c2 cells were treated with H/R+si-NC, H/R+si-FTX, H/ R+si-FTX+anti-miR-NC or H/R+si-FTX+antimiR-410-3p and then the mRNA and protein levels of Fmr1 were detected. The results exhibited that FTX depletion resulted in distinct reduction in the mRNA and protein levels of Fmr1 in H/R-induced H9c2 cell compared to control group, while the administration of antimiR-410-3p markedly overturned the influences (Figure 7B and C). These findings demonstrated that FTX could modulate Fmr1 expression by sponging miR-410-3p in H/R-stimulated H9c2 cells.	31957854	RID04530	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Chronic heart failure	LUCAT1	HOXA13	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);apoptosis process(-)	ceRNA(miR-612)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000106031	NA	100505994	3209	SCAL1|SCAT5	HOX1|HOX1J	Downregulated long noncoding RNA LUCAT1 inhibited proliferation and promoted apoptosis of cardiomyocyte via miR-612/HOXA13 pathway in chronic heart failure.To explore the roles and functions of LUCAT1 in patients with CHF, we first used qRT-PCRto detect the expressions of LUCAT1 in serum samples from 60 patients and 60 healthy volunteers. Results showed that LUCAT1 was significantly decreased for about 1.7 folds in patients with CHD (Figure 1A) (p<0.05), compared with healthy control.CCK8 assay revealed that LUCAT1 downregulation significantly inhibited cell proliferation after 3 d and 7 d, compared with si-control group (Figure 2B) (p<0.01). Moreover, flow cytometry (FACS) results indicated that LUCAT1 silence significantly increased the apoptotic rate of AC16 cells (Figure 2C) (p<0.01). To confirm whether LUCAT1 could directly bind with miR-612, WT-LUCAT1 and MUT-LUCAT1 sequences were constructed to explore further the association between LUCAT1 and miR-612 in AC16 cells and the luciferase gene reporter assay was performed (Figure 3E). Results showed that the relative luciferase activity in AC16 cells co-transfected with WT-LUCAT1 and miR612 mimic was significantly repressed compared with that in cells transfected with miR-NC. However, the relative luciferase activity was reversed in cells co-transfected with MUT-PVT1 and miR-612 mimic (Figure 3F) (p<0.01). These findings indicated that LUCAT1 could function as a ceRNA to competitively bind with miR-612 in AC16 cells.We detected HOXA13 protein expression in AC16 cells transfected with miR-612 mimic or si-LUCAT1. Results showed that the protein level of HOXA13 was repressed in miR-612 mimic group, compared with miR-NC (Figure 5A,B) (p<0.01). Furthermore, protein level of HOXA13 was increased in si-LUCAT1 group, compared with si-control (Figure 5C,D) (p<0.01). These results indicated that LUCAT1 positively interacted with HOXA13 and miR-612 was negatively interacted with HOXA13, which was predicted to be a target of miR-612. To detect whether miR-612 could target at HIG2 in AC16 cells, WT-HOXA13 and MUT-HOXA13 sequences were constructed into GLO vectors and the luciferase gene reporter assay was performed (Figure 5E). Luciferase gene reporter assay revealed that miR612 overexpression could repress the luciferase activity of WT-HOXA13 but not in MUT-HOXA13 reporter in AC16 cells (Figure 5F) (p<0.01). Above all, these results suggested that miR-612 directly binds with HOXA13 in AC16 cells. Collectively, we assumed that LUCAT1 could directly bind with miR-612, targeting at repressing HOXA13 expression, thereby promoting cell proliferation and cell apoptosis in CHF patients.Furthermore, CCK8 assays showed that the cell proliferation abilities of AC16 cells with si-LUCAT1 were repressed, while they were reversed after adding miR-612 inhibitor (Figure 6B) (p<0.01). Moreover, FACS results revealed that the cell apoptotic rate was increased in AC16 cells with si-LUCAT1, while it was reversed after adding miR-612 inhibitor (Figure 6C) (p<0.01). In addition, WB results showed that Bcl-2 protein level was decreased; however, the levels of HOXA13, Bax, Bad and cleaved caspase-3 were increased in si-LUCAT1 group, while they were all reversed after miR612 inhibitor transfection (Figure 6D,E) (p<0.01). Collectively, these data revealed that LUCAT1 promoted cell proliferation and inhibited apoptosis via miR-612/HOXA13 axis in CHF.	31957853	RID04531	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Kidney disease	SPAG5-AS1	YY1	positively-E	luciferase reporter assay;RNA pull-down;RIP;co-IP;CHIP	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell autophagy(-)	ceRNA(miR-769-5p)	regulation	NA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000227543	GRCh38_17:28598790-28617377	ENSG00000100811	NA	100506436	7528	NA	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	SPAG5-AS1 inhibited autophagy and aggravated apoptosis of podocytes via SPAG5/AKT/mTOR pathway.Since lncRNAs could regulate their target genes at different levels such as transcriptional level, post-transcriptional level and post-translational level,26, 27, 28 we detected at which level SPAG5-AS1 regulated SPAG5 expression. Luciferase activity of SPAG5 promoter reporter was attenuated by the knockdown of SPAG5-AS1 silence in HG-treated HPCs (Figure -(Figure2I).2I). However, the half-life of SPAG5 mRNA stability presented no significant variation under SPAG5-AS1 depletion compared to control in HG-treated HPCs (Figure -(Figure2J).2J). The protein degradation of SPAG5 was monitored after the addition of CHX, the inhibitor of protein production. Results showed that silence of SPAG5-AS1 facilitated the degradation of SPAG5 protein in HG-treated HPCs (Figure -(Figure2K).2K). Collectively, these results indicated that SPAG5-AS1 positively regulated SPAG5 expression by inducing its transcription and protein stability.The function of SPAG5-AS1 in HG-induced damage of HPCs was examined as well. As shown by the results of flow cytometry analysis, knockdown of SPAG5-AS1 countervailed the pro-apoptotic effect of HG treatment in HPCs (Figure -(Figure3A).3A). Silence of SPAG5-AS1 impaired the high expression of cleaved caspase 3, cleaved caspase 9 and Bax and reversed the low expression of Bcl-2 in HG-treated HPCs (Figure -(Figure3B).3B). Depletion of SPAG5-AS1 recovered the fluorescence intensity of LC-3 and podocin that were reduced by HG treatment in HPCs (Figure -(Figure3C).3C). The GFP-mRFP-LC3 assay exhibited that silencing SPAG5-AS1 restored the autophagic flux that was blocked by HG in HPCs (Figure S1B). The decrease of LC-3II/LC-3I and Beclin 1 levels and increase of p62 level under HG treatment were reversed by SPAG5-AS1 knockdown in HPCs (Figure -(Figure3D).3D). Jointly, these results implied that SPAG5-AS1 knockdown attenuated the HG-induced podocyte damage by inhibiting apoptosis and inducing autophagy.ChIP analysis illustrated that the DNA fragments with binding sites 1 and 3, rather than site 2, were enriched in the precipitated products of YY1 (Figure -(Figure4E).4E). In concordance, in HG-treated HPCs, YY1 protein was detectable in the pull-down of WT SPAG5-AS1/SPAG5 promoter and SPAG5-AS1/SPAG5 promoter with site 1 or site 3; however, SPAG5-AS1/SPAG5 promoter with only site 2 failed to pull down YY1 (Figure -(Figure4F).4F). Luciferase reporter analysis elucidated that in HG-treated HPCs, the silence of YY1 reduced the luciferase activity of SPAG5-AS1/SPAG5 promoter, and mutation of site 1 or site 3, instead of site 2, could partly restore the luciferase activity (Figure -(Figure4G).4G). These data proved that YY1 targeted the promoter of SPAG5-AS1/SPAG5 at site 1 and site 3.RT-qPCR data depicted that among the 10 miRNAs, only miR-769-5p and miR-378f exhibited significant downregulation under the treatment of HG compared to HG and MA in HPCs (Figure -(Figure5D),5D), indicating the participation of the 2 miRNAs in HG-induced HPC injury. However, pull-down assay showed that only miR-769-5p was pulled down by SPAG5-AS1 biotin probe rather than no-biotin probe (Figure -(Figure5E),5E), indicating that miR-769-5p was a target for SPAG5-AS1. Moreover, we confirmed that the silence of SPAG5-AS1 had no influence on the expression of miR-769-5p in HG-treated HPCs (Figure -(Figure5F).5F). RIP analysis confirmed that miR-769-5p was co-immunoprecipitated with SPAG5-AS1 and YY1 by Ago2 antibody (Figure -(Figure5G).5G). The predicted miR-769-5p sites on SPAG5-AS1 and YY1 were substituted with complementary sequences to generate SPAG5-AS1 Mut and YY1 Mut reporters (Figure -(Figure5H).5H). Luciferase reporter assay confirmed that miR-769-5p overexpression abrogated luciferase activity of SPAG5-AS1 WT and YY1 WT in HG-treated HPCs (Figure -(Figure55H).	31957155	RID04532	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Kidney disease	SPAG5-AS1	SPAG5	positively-E	luciferase reporter assay;RNA pull-down;RIP;co-IP;CHIP	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell autophagy(-)	NA	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000227543	GRCh38_17:28598790-28617377	ENSG00000076382	NA	100506436	10615	NA	DEEPEST|hMAP126|MAP126	SPAG5-AS1 inhibited autophagy and aggravated apoptosis of podocytes via SPAG5/AKT/mTOR pathway.Since lncRNAs could regulate their target genes at different levels such as transcriptional level, post-transcriptional level and post-translational level,26, 27, 28 we detected at which level SPAG5-AS1 regulated SPAG5 expression. Luciferase activity of SPAG5 promoter reporter was attenuated by the knockdown of SPAG5-AS1 silence in HG-treated HPCs (Figure -(Figure2I).2I). However, the half-life of SPAG5 mRNA stability presented no significant variation under SPAG5-AS1 depletion compared to control in HG-treated HPCs (Figure -(Figure2J).2J). The protein degradation of SPAG5 was monitored after the addition of CHX, the inhibitor of protein production. Results showed that silence of SPAG5-AS1 facilitated the degradation of SPAG5 protein in HG-treated HPCs (Figure -(Figure2K).2K). Collectively, these results indicated that SPAG5-AS1 positively regulated SPAG5 expression by inducing its transcription and protein stability.The function of SPAG5-AS1 in HG-induced damage of HPCs was examined as well. As shown by the results of flow cytometry analysis, knockdown of SPAG5-AS1 countervailed the pro-apoptotic effect of HG treatment in HPCs (Figure -(Figure3A).3A). Silence of SPAG5-AS1 impaired the high expression of cleaved caspase 3, cleaved caspase 9 and Bax and reversed the low expression of Bcl-2 in HG-treated HPCs (Figure -(Figure3B).3B). Depletion of SPAG5-AS1 recovered the fluorescence intensity of LC-3 and podocin that were reduced by HG treatment in HPCs (Figure -(Figure3C).3C). The GFP-mRFP-LC3 assay exhibited that silencing SPAG5-AS1 restored the autophagic flux that was blocked by HG in HPCs (Figure S1B). The decrease of LC-3II/LC-3I and Beclin 1 levels and increase of p62 level under HG treatment were reversed by SPAG5-AS1 knockdown in HPCs (Figure -(Figure3D).3D). Jointly, these results implied that SPAG5-AS1 knockdown attenuated the HG-induced podocyte damage by inhibiting apoptosis and inducing autophagy.ChIP analysis illustrated that the DNA fragments with binding sites 1 and 3, rather than site 2, were enriched in the precipitated products of YY1 (Figure -(Figure4E).4E). In concordance, in HG-treated HPCs, YY1 protein was detectable in the pull-down of WT SPAG5-AS1/SPAG5 promoter and SPAG5-AS1/SPAG5 promoter with site 1 or site 3; however, SPAG5-AS1/SPAG5 promoter with only site 2 failed to pull down YY1 (Figure -(Figure4F).4F). Luciferase reporter analysis elucidated that in HG-treated HPCs, the silence of YY1 reduced the luciferase activity of SPAG5-AS1/SPAG5 promoter, and mutation of site 1 or site 3, instead of site 2, could partly restore the luciferase activity (Figure -(Figure4G).4G). These data proved that YY1 targeted the promoter of SPAG5-AS1/SPAG5 at site 1 and site 3.RT-qPCR data depicted that among the 10 miRNAs, only miR-769-5p and miR-378f exhibited significant downregulation under the treatment of HG compared to HG and MA in HPCs (Figure -(Figure5D),5D), indicating the participation of the 2 miRNAs in HG-induced HPC injury. However, pull-down assay showed that only miR-769-5p was pulled down by SPAG5-AS1 biotin probe rather than no-biotin probe (Figure -(Figure5E),5E), indicating that miR-769-5p was a target for SPAG5-AS1. Moreover, we confirmed that the silence of SPAG5-AS1 had no influence on the expression of miR-769-5p in HG-treated HPCs (Figure -(Figure5F).5F). RIP analysis confirmed that miR-769-5p was co-immunoprecipitated with SPAG5-AS1 and YY1 by Ago2 antibody (Figure -(Figure5G).5G). The predicted miR-769-5p sites on SPAG5-AS1 and YY1 were substituted with complementary sequences to generate SPAG5-AS1 Mut and YY1 Mut reporters (Figure -(Figure5H).5H). Luciferase reporter assay confirmed that miR-769-5p overexpression abrogated luciferase activity of SPAG5-AS1 WT and YY1 WT in HG-treated HPCs (Figure -(Figure55H).	31957155	RID04533	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE51827,GSE55807)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE55807)
Non-small cell lung cancer	VPS9D1-AS1	HMGA2	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-532-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000261373	GRCh38_16:89711856-89718165	ENSG00000149948	NA	100128881	8091	MYU	BABL|HMGIC|LIPO	Long noncoding RNA VPS9D1-AS1 augments the malignant phenotype of non-small cell lung cancer by sponging microRNA-532-3p and thereby enhancing HMGA2 expression.Expression profiles of VPS9D1-AS1 in 51 pairs of NSCLC samples and corresponding normal lung tissues were evaluated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). VPS9D1-AS1 expression was higher in NSCLC tissue samples than in normal lung tissues (Figure 1A, P < 0.05). By using the median level of VPS9D1-AS1 expression in the NSCLC tissue samples as a cutoff, all samples from the 51 NSCLC patients were classified into either VPS9D1-AS1 high-expression or VPS9D1-AS1 low-expression groups. The analysis of the correlation between VPS9D1-AS1 expression level and clinicopathological characteristics revealed that increased VPS9D1-AS1 expression correlated significantly with tumor size (P = 0.025), TNM stage (P = 0.002), and lymph node metastasis (P = 0.012; Table 1). In particular, patients with NSCLC in the VPS9D1-AS1 high-expression group showed shorter overall survival than patients in the VPS9D1-AS1 low-expression group (Figure 1B, P = 0.030). The observed relationship between VPS9D1-AS1 expression level and malignancy prompted us to investigate the biological effects of VPS9D1-AS1 on the malignant phenotype of NSCLC H460 and A549 cells, which showed the highest expression of VPS9D1-AS1 among the five NSCLC cell lines. H460 and A549 cells were transfected with the small interfering RNA (siRNA) si-VPS9D1-AS1 targeting VPS9D1-AS1 or negative control siRNA (si-NC). Successful knock-down of VPS9D1-AS1 after transfecting H460 and A549 cells with si-VPS9D1-AS1 was confirmed by RT-qPCR (Figure 2A, P < 0.05).Direct binding of miR-532-3p to VPS9D1-AS1 in NSCLC cells was verified by the luciferase reporter assay. Luciferase reporter plasmids carrying the wild-type (wt) or mutant (mut) binding site for miR-532-3p were constructed (VPS9D1-AS1-wt and VPS9D1-AS1-mut, respectively) and separately co-transfected with agomir-532-3p, an miR-532-3p mimic increasing its expression, or agomir-NC into H460 and A549 cells. Agomir-532-3p transfection-mediated upregulation of miR-532-3p (Figure 3F, P < 0.05) dramatically decreased VPS9D1-AS1-wt luciferase activity (P < 0.05) in H460 and A549 cells, whereas no such change was detected in cells transfected with VPS9D1-AS1-mut (Figure 3G). An RNA immunoprecipitation (RIP) assay confirmed that VPS9D1-AS1 and miR-532-3p were substantially enriched in the immunoprecipitated AGO2 protein complex, suggesting that AGO2 bound to VPS9D1-AS1 and miR-532-3p directly in NSCLC cells (Figure 3H, P < 0.05). Collectively, these data provided sufficient evidence that VPS9D1-AS1 directly interacts with miR-532-3p in NSCLC cells.A luciferase reporter assay was then performed to demonstrate the possibility of miR-532-3p binding to the 3'-UTR of HMGA2 mRNA in NSCLC cells. The luciferase activity of the HMGA2-wt reporter plasmid, which contained a wild-type miR-532-3p-binding site in the HMGA2 3'-UTR driving the expression of the luciferase gene, was notably weakened upon co-transfection of H460 and A549 cells with agomir-532-3p (P < 0.05). In contrast, the luciferase activity of HMGA2-mut was not altered by miR-532-3p upregulation (Figure 4G).As we established that HMGA2 was a direct target gene of miR-532-3p in NSCLC cells, we next explored whether VPS9D1-AS1 could modulate HMGA2 expression in NSCLC cells. mRNA (Figure 5A, P < 0.05) and protein (Figure 5B, P < 0.05) levels of HMGA2 were low in H460 and A549 cells deficient in VPS9D1-AS1, as revealed by RT-qPCR and western blot, respectively. To investigate whether miR-532-3p sponging mediated the positive effect of VPS9D1-AS1 on HMGA2 expression, rescue experiments were conducted in H460 and A549 cells by co-transfecting them with si-VPS9D1-AS1 and antagomir-532-3p (inhibitor of miR-532-3p) or antagomir-NC. Transfection with antagomir-532-3p potently silenced miR-532-3p expression in H460 and A549 cells, as evidenced by RT-qPCR data (Figure 5C, P < 0.05). VPS9D1-AS1 knockdown significantly increased miR-532-3p expression and decreased HMGA2 mRNA and protein levels in H460 and A549 cells.We finally investigated the impact of VPS9D1-AS1 knockdown on tumor growth in vivo in the xenograft experiment. H460 cells transfected with si-VPS9D1-AS1 or si-NC were subcutaneously injected into nude mice. Tumor xenograft volume was much smaller in the si-VPS9D1-AS1 group than in the si-NC group (Figure 8A, -,8B;8B; P < 0.05). In addition, tumor weight was significantly lower in the si-VPS9D1-AS1 group than in the si-NC group (Figure 8C, P < 0.05) at 4 weeks after the injection of cells. VPS9D1-AS1 expression was significantly downregulated in tumor xenografts from the si-VPS9D1-AS1 group, compared with that in xenografts from the si-NC group (Figure 8D, P < 0.05). Meanwhile, RT-qPCR revealed that miR-532-3p expression was higher in tumor xenografts derived from H460 cells transfected with si-VPS9D1-AS1 cells (Figure 8E, P < 0.05). Furthermore, HMGA2 protein expression was significantly lower in the si-VPS9D1-AS1 group relative to that in the si-NC group (Figure 8F, P < 0.05). These results indicated that VPS9D1-AS1 knockdown attenuated tumor growth of NSCLC cells through the downregulation of the miR-532-3p-HMGA2 axis output	31902794	RID04534	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Ankylosing spondylitis	MEG3	miR-146a	negatively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Spinal disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000253522	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 inhibits the inflammatory response of ankylosing spondylitis by targeting miR-146a.In AS, inflammatory response is an important indicator to determine the course of disease. To assess the levels of inflammatory and lncRNA MEG3 in AS patients, ELISA and qRT-PCRanalyses were performed in the study. ELISA results showed that the levels of IL-1beta, IL-6, and TNF-alpha were significantly increased in the serum of AS patients (n = 33) when compared with non-AS normal people (n = 16) (Fig. 1a-c). Also, as qRT-PCR;ISHowed, the level of MEG3 in the serum of AS patients was markedly lower than that in non-AS normal people (Fig. 1d). These results indicated that inflammatory cytokines were highly expressed and MEG3 was poorly expressed in AS patients.The results showed that the expression of MEG3 was remarkably negatively correlated with the contents of inflammatory cytokine IL-1beta, IL-6, and TNF-alpha (Fig. 2a-c), indicating that MEG3 expression was related to the inflammatory response in AS patients.To understand the anti-inflammatory mechanism of MEG3, we used LncBase v.2 tool to make bioinformatics prediction, and the results disclosed that miR-146a has a binding site with MEG3. MEG3-WT and MEG3-MUT luciferase reporters were generated containing miR-146a binding sites and mutant binding sites, respectively (Fig. 4a). dual-luciferase reporter assay showed that the overexpression of miR-146a markedly decreased the luciferase activity of MEG3-WT reporter, while miR-146a inhibitor (in-miR-146a) significantly enhanced its luciferase activity, but they had no effect on MEG3-MUT reporter (Fig. 4b). Also, RIP assay results indicated that MEG3 and miR-146a were remarkably enriched in Anti-Ago2 complex compared with IgG (Fig. 4c). Finally, through qRT-PCR we found that overexpression of MEG3 significantly inhibited the level of miR146a, and the expression of miR-146a obviously increased after MEG3 knockdown (Fig. 4d). These results showed that lncRNA MEG3 could directly bind with miR-146a.ELISA and qRT-PCRresults revealed that overexpression of miR-146a obviously promoted the levels of IL-1beta, IL-6, and TNF-alpha, while the inhibition of miR-146a showed the opposite inhibitory effect (Fig. 6b ). It suggested that miR-146a had a pro-inflammatory effect in AS.The results showed that MEG3 markedly blocked the expression of miR-146a, while the addition of miR-146a mimic restored its expression (Fig. 7a). ELISA and qRT-PCRresults indicated that aberrant expression of miR-146a reversed the suppression effect of overexpressed MEG3 on IL-1beta, IL-6, and TNF-alpha levels in HFLS cells (Fig. 7b ). These results confirmed that the anti-inflammatory effect of MEG3 was achieved by inhibiting the expression of miR-146a.	31894531	RID04535	ceRNA or sponge	NA		
Osteoarthritis	GAS5	BCL2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171791	NA	60674	596	NCRNA00030|SNHG2	Bcl-2|PPP1R50	Silencing of long-chain non-coding RNA GAS5 in osteoarthritic chondrocytes is mediated by targeting the miR-34a/Bcl-2 axis.The expression of GAS5 in primary cultured chondrocytes was detected by RT-qPCR. GAS5 was expressed in both articular and normal chondrocytes and its expression levels in the osteoarthritic chondrocytes was significantly higher than those noted in normal chondrocytes (2.37 1.12 vs. 1.07 0.22) (P<0.05, data not shown).During that process, chondrocyte proliferation and apoptosis play an important role (10). MTT assay demonstrated that the proliferation of cells in the si-GAS5 group was significantly increased compared with that of the control group (P<0.05). western blotindicated that the expression levels of proliferating cell nuclear antigen (PCNA) and Ki-67 in the si-GAS5 group were significantly higher than those of the control group (P<0.05, Fig. 3A). The results suggested that GAS5 silencing could promote the proliferation of OACs.ELISA indicated that the levels of TNF-alpha and IL-6 in the si-GAS5 group were significantly lower than those of the control group (P<0.05, Fig. 4B), indicating that GAS5 silencing could reduce the severity of the inflammatory response of OACs.It was predicted by TargetScan that miR-34a may be a target of GAS5 and Bcl-2 a candidate target gene of miR-34a (Fig. 5A). The results of the dual-luciferase reporter assay demonstrated that luciferase activity was significantly decreased in cells co-transfected with GAS5-WT and miR-34a mimic (P<0.05, Fig. 5B). Bcl-2-WT and miR-34a mimic co-transfection resulted in a significant decrease in luciferase activity (P<0.05). GAS5 overexpression or knockout cell lines were established. Moreover, miR-34a overexpression was achieved by transfection of miR-34a to the cells, and miR-34a inhibition by addition of a miR-34a inhibitor. The results indicated that miR-34a was downregulated in the GAS5 group (Fig. 5C), while the expression levels of the Bcl-2 protein were increased compared with those of the control group (P<0.05, Fig. 5C). The effect noted in the sh-GAS5 group was contradictory to these findings. The expression levels of Bcl-2 in the miR-34a mimic and miR-34a inhibitor groups were lower and higher than those of the control group, respectively (P<0.05, Fig. 5D). These results indicated that GAS5 could indirectly regulate the expression levels of Bcl-2 by targeting miR-34a.Cell lines that were co-transfected with GAS5 and miR-34a were established. The results of the FCM analysis indicated that the apoptotic rate of the GAS5 group was significantly increased compared with that of the control group (P<0.05, Fig. 6A), suggesting that GAS5 overexpression promoted the induction of apoptosis. The apoptotic rate in the miR-34a mimic with GAS5 overexpression group was lower than that of the GAS5 group alone and higher than that of the miR-34a mimic group alone (P<0.05). Consequently, the expression levels of Bcl-2 were significantly increased and significantly decreased in the GAS5 and in the miR-34a mimic groups, respectively (P<0.05, Fig. 6B). These findings indicated that the induction of OAC apoptosis by GAS5 was reduced by miR-34a and that the Bcl-2-mediated inhibition of miR-34a expression was reduced by GAS5. Collectively, the data indicated that GAS5 regulated the induction of OAC apoptosis by targeting the miR-34a/Bcl-2 axis.	31894330	RID04536	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	TMEM238L	GFI1	positively-E	luciferase reporter assay;RNA pull-down;RIP	downregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-942_5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000162676	NA	100289255	2672	FORCP|LINC00675	GFI-1|GFI1A|ZNF163	GFI1-Mediated Upregulation of LINC00675 as a ceRNA Restrains Hepatocellular Carcinoma Metastasis by Sponging miR-942-5p.Firstly, we investigated the expression of GFI1 in HCC tissue samples and adjacent tissues. It was shown that GFI1 was obviously reduced in HCC tissues as displayed in Figure 1A. In Figure 1B, it was indicated that GFI1 was decreased in advanced HCC tissues (stages T3-T4) compared to T1-T2 stages. In addition, in Figure 1C, we found that GFI1 LINC00675 was greatly decreased in HCC tissues with lymphatic metastasis compared. Next, we confirmed that GFI1 was also decreased in HCC cells (Hep3B, QGY-7703, SMCC-7721 and MHCC-97L) compared with the QSG-7701 cells in Figure 1D.Moreover, to study the effect of LINC00675 on HCC cell proliferation, QGY-7703 and SMCC-7721 cells were transfected with LINC00675 overexpression plasmid. EdU assay indicated that overexpression of LINC00675 significantly inhibited QGY-7703, SMCC-7721 cell proliferation compared with the control groups in Figures 3A, B. As shown in Figure 3C, QGY-7703 and SMCC-7721 cell apoptosis was obviously triggered by the overexpressed LINC00675. In addition, in Figure 3D, HCC cell cycle distribution was blocked in G1 phase significantly by LINC00675. Transwell migration and invasion assay implied that the migrated and invaded cells in LINC00675 overexpression groups were notably less than the cells in the LV-NC group in Figures 3E, F. Then, we implanted either control or QGY-7703 cells with stable overexpressed LINC00675. In Figure 3G, it was shown that LINC00675 overexpression significantly depressed the number of metastatic lung nodules. Subsequently, we confirmed that LINC00675 and GFI1 expression was greatly increased in mice lung tissues (Figures 3H, I).Then, by using bioinformatics analysis, the binding sites between LINC00675 and miR-942-5p was exhibited in Figure 4A. Luciferase reporter plasmids of WT-LINC00675 and MUT-LINC00675 binding sites were displayed in Figure 4A. In addition, a negative correlation between LINC00675 and miR-942-5p was shown in HCC tissues (Figure 4B). Co-transfection of the WT-LINC00675 with miR-924-5p inhibitors induced the reporter activity while the mimics reduced the reporter activity (Figure 4C). In Figure 4D, LINC00675 was most abundantly pulled down by miR-942-5p in QGY-7703 and SMCC-7721 cells.In order to study the mechanism of LINC00675 down-regulation in HCC, bioinformatical software program JASPAR (http://jaspar.genereg.net/cgi-bin/jaspar_db.pl) was carried out to analyze the promoter regions of LINC00675, and three potential sites of GFI1 binding were predicted. In Figure 2A, the DNA motif of GFI1 in UBE4B promoter was demonstrated. QGY-7703 and SMCC-7721 cells were transfected with GFI1 siRNA. LINC00675 expression was significantly decreased after GFI1 was reduced in HCC cells (Figures 2B, C). The LINC00675 promoter region including three binding sites of GFI1 was inserted into a PGL3 vector as displayed in Figure 2D. As shown in Figures 2E, F, GFI1 significantly enhanced the luciferase activity in HCC cells.Moreover, by using bioinformatics analysis, the binding sites between GFI1 and miR-942-5p was displayed in Figure 6A. Luciferase reporter plasmids of WT-GFI1 and MUT-GFI1 binding sites were demonstrated in Figure 6A. Co-transfection of the WT-GFI1 with miR-924-5p inhibitors enhanced the reporter activity while the mimics of miR-924-5p inhibited the reporter activity (Figure 6B). In addition, miR-924-5p mimics reduced GFI1 mRNA, and protein expression significantly in QGY-7703 and SMCC-7721 cells (Figures 6C, D).	33489916	RID04537	ceRNA or sponge	metastasis		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	GFI1	TMEM238L	positively-E	luciferase reporter assay;RNA pull-down;RIP	downregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000162676	NA	ENSG00000263429	GRCh38_17:10794913-10804099	2672	100289255	GFI-1|GFI1A|ZNF163	FORCP|LINC00675	GFI1-Mediated Upregulation of LINC00675 as a ceRNA Restrains Hepatocellular Carcinoma Metastasis by Sponging miR-942-5p.Firstly, we investigated the expression of GFI1 in HCC tissue samples and adjacent tissues. It was shown that GFI1 was obviously reduced in HCC tissues as displayed in Figure 1A. In Figure 1B, it was indicated that GFI1 was decreased in advanced HCC tissues (stages T3-T4) compared to T1-T2 stages. In addition, in Figure 1C, we found that GFI1 LINC00675 was greatly decreased in HCC tissues with lymphatic metastasis compared. Next, we confirmed that GFI1 was also decreased in HCC cells (Hep3B, QGY-7703, SMCC-7721 and MHCC-97L) compared with the QSG-7701 cells in Figure 1D.Moreover, to study the effect of LINC00675 on HCC cell proliferation, QGY-7703 and SMCC-7721 cells were transfected with LINC00675 overexpression plasmid. EdU assay indicated that overexpression of LINC00675 significantly inhibited QGY-7703, SMCC-7721 cell proliferation compared with the control groups in Figures 3A, B. As shown in Figure 3C, QGY-7703 and SMCC-7721 cell apoptosis was obviously triggered by the overexpressed LINC00675. In addition, in Figure 3D, HCC cell cycle distribution was blocked in G1 phase significantly by LINC00675. Transwell migration and invasion assay implied that the migrated and invaded cells in LINC00675 overexpression groups were notably less than the cells in the LV-NC group in Figures 3E, F. Then, we implanted either control or QGY-7703 cells with stable overexpressed LINC00675. In Figure 3G, it was shown that LINC00675 overexpression significantly depressed the number of metastatic lung nodules. Subsequently, we confirmed that LINC00675 and GFI1 expression was greatly increased in mice lung tissues (Figures 3H, I).Then, by using bioinformatics analysis, the binding sites between LINC00675 and miR-942-5p was exhibited in Figure 4A. Luciferase reporter plasmids of WT-LINC00675 and MUT-LINC00675 binding sites were displayed in Figure 4A. In addition, a negative correlation between LINC00675 and miR-942-5p was shown in HCC tissues (Figure 4B). Co-transfection of the WT-LINC00675 with miR-924-5p inhibitors induced the reporter activity while the mimics reduced the reporter activity (Figure 4C). In Figure 4D, LINC00675 was most abundantly pulled down by miR-942-5p in QGY-7703 and SMCC-7721 cells.In order to study the mechanism of LINC00675 down-regulation in HCC, bioinformatical software program JASPAR (http://jaspar.genereg.net/cgi-bin/jaspar_db.pl) was carried out to analyze the promoter regions of LINC00675, and three potential sites of GFI1 binding were predicted. In Figure 2A, the DNA motif of GFI1 in UBE4B promoter was demonstrated. QGY-7703 and SMCC-7721 cells were transfected with GFI1 siRNA. LINC00675 expression was significantly decreased after GFI1 was reduced in HCC cells (Figures 2B, C). The LINC00675 promoter region including three binding sites of GFI1 was inserted into a PGL3 vector as displayed in Figure 2D. As shown in Figures 2E, F, GFI1 significantly enhanced the luciferase activity in HCC cells.Moreover, by using bioinformatics analysis, the binding sites between GFI1 and miR-942-5p was displayed in Figure 6A. Luciferase reporter plasmids of WT-GFI1 and MUT-GFI1 binding sites were demonstrated in Figure 6A. Co-transfection of the WT-GFI1 with miR-924-5p inhibitors enhanced the reporter activity while the mimics of miR-924-5p inhibited the reporter activity (Figure 6B). In addition, miR-924-5p mimics reduced GFI1 mRNA, and protein expression significantly in QGY-7703 and SMCC-7721 cells (Figures 6C, D).	33489916	RID04538	expression association	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Colon cancer	PCAT1	BAX	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);chemosensitivity(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000087088	NA	100750225	581	PCA1|PCAT-1|PiHL	BCL2L4	LncRNA-PCAT1 controls the growth, metastasis and drug resistance of human colon cancer cells.qRT-PCRmethod was used to determine the expression of lncRNA-PCAT1 in the tissue samples and colon cell lines (normal and cancerous). The results indicated that the cancer tissues and cell lines (DLD-1, HT-29 and HCT-116) exhibited significantly higher expression levels of lnc-PCAT1 than the normal tissues and epithelial cell line (Figure 1A and 1B). Among the cancer cell lines, HCT-116 showed highest expression of lncRNA-PCAT1 and was thus chosen for further experimentations.The decline in cell viability was shown to be due to cell apoptosis owing to the modification of Bax/Bcl-2 ratio. The protein concentration of Bax was seen to be increasing while that of Bcl-2 decreased in cancer cells transfected with lncRNA-PCAT1 (Figure 3B).The effects of downregulation of lncRNAPCAT1 in HCT-116 cancer cells were also evident in the reduction of their migration rates (Figure 4A). Similar observation was drawn for the invasion of the colon cancer cells transfected with the silencing constructs of lncRNA-PCAT1 (Figure 4B). Together, these findings highlight the potential of lncRNA-PCAT1 in controlling the metastasis of human colon cancer.The values suggested that repression of lncRNA-PCAT1 expression led to significant decline in the proliferation rates of colon cancer cells (Figure 5). Moreover, the downregulation of lncRNA-PCAT1 in colon cancer cells enhanced their chemosensitivity to 5-flourouracil, implicating the molecular anticancer role of lncRNA-PCAT1 against the growth and proliferation of human colon cancer.	33277833	RID04539	expression association	metastasis,chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	PCAT1	BCL2	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);chemosensitivity(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000171791	NA	100750225	596	PCA1|PCAT-1|PiHL	Bcl-2|PPP1R50	LncRNA-PCAT1 controls the growth, metastasis and drug resistance of human colon cancer cells.qRT-PCRmethod was used to determine the expression of lncRNA-PCAT1 in the tissue samples and colon cell lines (normal and cancerous). The results indicated that the cancer tissues and cell lines (DLD-1, HT-29 and HCT-116) exhibited significantly higher expression levels of lnc-PCAT1 than the normal tissues and epithelial cell line (Figure 1A and 1B). Among the cancer cell lines, HCT-116 showed highest expression of lncRNA-PCAT1 and was thus chosen for further experimentations.The decline in cell viability was shown to be due to cell apoptosis owing to the modification of Bax/Bcl-2 ratio. The protein concentration of Bax was seen to be increasing while that of Bcl-2 decreased in cancer cells transfected with lncRNA-PCAT1 (Figure 3B).The effects of downregulation of lncRNAPCAT1 in HCT-116 cancer cells were also evident in the reduction of their migration rates (Figure 4A). Similar observation was drawn for the invasion of the colon cancer cells transfected with the silencing constructs of lncRNA-PCAT1 (Figure 4B). Together, these findings highlight the potential of lncRNA-PCAT1 in controlling the metastasis of human colon cancer.The values suggested that repression of lncRNA-PCAT1 expression led to significant decline in the proliferation rates of colon cancer cells (Figure 5). Moreover, the downregulation of lncRNA-PCAT1 in colon cancer cells enhanced their chemosensitivity to 5-flourouracil, implicating the molecular anticancer role of lncRNA-PCAT1 against the growth and proliferation of human colon cancer.	33277833	RID04540	expression association	metastasis,chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Liver cancer	MEG3	TP53	positively-E	CHIP;luciferase reporter assay;RNA pull-down assay	downregulation	RT-PCR	NA	NA	cell proliferation(+)	DNA methylation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	LFS1|p53	Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically.Ultimately, H3K27me1, H3K27me2, and H3K27me3 were significantly increased in the pCMV6-A-GFP-MEG3 group compared to the pCMV6-A-GFP group and reduced in the pGFP-V-RS-MEG3 group compared to the pGFP-V-RS group (Fig. 2J (a, b)). Collectively, these results suggest that MEG3 enhances the methylation modification of histone H3 at the lysine 27 through P53 in human liver cancer stem cells.Collectively, these observations suggest that MEG3 inhibits the growth of human liver cancer stem cells.Collectively, these results suggest that excessive TERT or TRF2 abrogates the inhibitory effect of MEG3 on the growth of human liver cancer stem cells.Collectively, these results suggest that MEG3 inhibits telomere elongation dependent on both P53 and HULC in liver cancer stem cells.Our results indicate that MEG3 enhances the P53 expression by triggering the loading of P300 and RNA polymerase II onto its promoter regions dependent on HP1alpha. Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Furthermore, MEG3 inhibits the expression of TERT by increasing the H3K27me3 in TERT promoter regions, thereby inhibiting the activity of telomerase by reducing the binding of TERT to TERC. Furthermore, MEG3 also increases the expression of TERRA; therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibits the activity of telomerase in hLCSCs. Strikingly, MEG3 reduces the length of telomere by blocking the formation of complex maintaining telomere length (POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere by increasing the interplay between P53 and HULC. Ultimately, MEG3 inhibits the growth of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2).	33256840	RID04541	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Liver cancer	MEG3	TERT	negatively-E	CHIP;luciferase reporter assay;RNA pull-down assay	downregulation	RT-PCR	NA	NA	cell proliferation(+)	DNA methylation	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000164362	NA	55384	7015	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	EST2|hEST2|TCS1|TP2|TRT	Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically.Ultimately, H3K27me1, H3K27me2, and H3K27me3 were significantly increased in the pCMV6-A-GFP-MEG3 group compared to the pCMV6-A-GFP group and reduced in the pGFP-V-RS-MEG3 group compared to the pGFP-V-RS group (Fig. 2J (a, b)). Collectively, these results suggest that MEG3 enhances the methylation modification of histone H3 at the lysine 27 through P53 in human liver cancer stem cells.Collectively, these observations suggest that MEG3 inhibits the growth of human liver cancer stem cells.Collectively, these results suggest that excessive TERT or TRF2 abrogates the inhibitory effect of MEG3 on the growth of human liver cancer stem cells.Collectively, these results suggest that MEG3 inhibits telomere elongation dependent on both P53 and HULC in liver cancer stem cells.Our results indicate that MEG3 enhances the P53 expression by triggering the loading of P300 and RNA polymerase II onto its promoter regions dependent on HP1alpha. Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Furthermore, MEG3 inhibits the expression of TERT by increasing the H3K27me3 in TERT promoter regions, thereby inhibiting the activity of telomerase by reducing the binding of TERT to TERC. Furthermore, MEG3 also increases the expression of TERRA; therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibits the activity of telomerase in hLCSCs. Strikingly, MEG3 reduces the length of telomere by blocking the formation of complex maintaining telomere length (POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere by increasing the interplay between P53 and HULC. Ultimately, MEG3 inhibits the growth of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2).	33256840	RID04542	epigenetic regulation	NA		UP(PAAD);DATA(GSE40174)
Liver cancer	MEG3	TERRA	positively-E	CHIP;luciferase reporter assay;RNA pull-down assay	downregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically.Ultimately, H3K27me1, H3K27me2, and H3K27me3 were significantly increased in the pCMV6-A-GFP-MEG3 group compared to the pCMV6-A-GFP group and reduced in the pGFP-V-RS-MEG3 group compared to the pGFP-V-RS group (Fig. 2J (a, b)). Collectively, these results suggest that MEG3 enhances the methylation modification of histone H3 at the lysine 27 through P53 in human liver cancer stem cells.Collectively, these observations suggest that MEG3 inhibits the growth of human liver cancer stem cells.Collectively, these results suggest that excessive TERT or TRF2 abrogates the inhibitory effect of MEG3 on the growth of human liver cancer stem cells.Collectively, these results suggest that MEG3 inhibits telomere elongation dependent on both P53 and HULC in liver cancer stem cells.Our results indicate that MEG3 enhances the P53 expression by triggering the loading of P300 and RNA polymerase II onto its promoter regions dependent on HP1alpha. Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Furthermore, MEG3 inhibits the expression of TERT by increasing the H3K27me3 in TERT promoter regions, thereby inhibiting the activity of telomerase by reducing the binding of TERT to TERC. Furthermore, MEG3 also increases the expression of TERRA; therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibits the activity of telomerase in hLCSCs. Strikingly, MEG3 reduces the length of telomere by blocking the formation of complex maintaining telomere length (POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere by increasing the interplay between P53 and HULC. Ultimately, MEG3 inhibits the growth of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2).	33256840	RID04543	expression association	NA		
Vascular cognitive impairment	TUG1	BDNF	negatively-E	RNA pull-down experiment;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Disease of mental health	Cognitive disorder	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000176697	NA	55000	627	FLJ20618|LINC00080|NCRNA00080	NA	Knockdown of lncRNA TUG1 inhibits hippocampal neuronal apoptosis and participates in aerobic exercise-alleviated vascular cognitive impairment.To investigate whether TUG1 and BDNF were differentially expressed during VCI, we detected the levels of TUG1 and BDNF in the serum of healthy people (n-=-20) and VCI patients (n-=-20). The results of qRT-PCR;ISHowed that compared with healthy people, the level of TUG1 was observably elevated in the serum of VCI patients, which was 2.9 times higher than that in healthy people (Fig. 1a), while the mRNA level of BDNF was 0.52 times lower than that in healthy people (Fig. 1b). Meanwhile, ELISA results showed that serum BDNF levels were markedly reduced in VCI patients (Fig. 1c). Besides, the serum CRP (Fig. 1d) and IL-6 (Fig. 1e) levels in the VCI patients were upregulated in comparison with the healthy controls, indicating the brain injury of the VCI patients. These results indicated that TUG1 and BDNF may be involved in the pathological process of VCI.To further explore the relationship between TUG1 and BDNF, we detected whether TUG1 binds to BDNF via RIP and RNA pull-down analysis. RIP results showed that TUG1 was enriched in the anti-BDNF immunoprecipitants (Fig. 3a), and BDNF was enriched in the TUG1-pulled down compounds (Fig. 3b). These results indicated that TUG1 could bind to BDNF protein. Moreover, under the OGD treatment, the knockdown of TUG1 elevated mRNA and protein levels of BDNF, and the lentivirus-mediated BDNF knockdown reversed such effect (Fig. 3c, d). Furthermore, the lentivirus-mediated BDNF knockdown reduced the elevation of cell apoptosis which was caused by TUG1 knockdown in OGD-induced HT22 cells (Fig. 3e ). The trends of protein expressions of cleaved-Caspase 3 and Bcl-2 were consistent with the apoptotic results (Fig. 3e ). These results indicated that TUG1 negatively regulates BDNF expression by binding to BDNF, thus affecting the apoptosis of OGD-induced hippocampal neurons.	33213523	RID04544	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Malignant glioma	LINC00525	miR-338-3p	negatively-F	bioinformatics analysis;RT-PCR	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000146666	GRCh38_7:47761476-47766772	NA	NA	84847	NA	NA	NA	Long non-coding RNA LINC00525 regulates the proliferation and epithelial to mesenchymal transition of human glioma cells by sponging miR-338-3p.To know about the expression of lncRNA-LINC00525 in human glioma, the RT-PCRwas performed for analyzing its transcript abundance in glioma cell lines (U87, MO59K, U118, Hs683 and LN-18) in comparison to the normal astrocyte cell line. It was seen that all the cancer cell lines exhibited significantly (P-<-0.05) higher lncRNA-LINC00525 expression than the normal astrocytes (Fig. 1a). The upregulation of lncRNA-LINC00525 was upto 6.6 folds in glioma cells. Highest expression levels were noted from the U87 and U187 cell lines and thus these were taken for the further characterization of role lncRNA-LINC00525 in glioma. The results are thus indicative of dysregulation of lncRNA-LINC00525 in glioma suggesting its probable molecular regulatory role in the malignancy.The U87 and U187cell lines were transfected with si-LINC00525 construct to perform the experimental gene silencing of lncRNA-LINC00525 in these cell lines. The RT-PCRexpression study of lncRNA-LINC00525 showed that the si-LINC00525 transfected cells exhibited significant transcriptional repression (5.3-fold) of lncRNA-LINC00525 in comparison to the respective normal control cell lines transfected with si-NC (Fig. 1b). The proliferation of cancer cells under lncRNA-LINC00525 knockdown was shown to be significantly (P-<-0.05) lower in comparison to the control cells, as deduced by MTT assay (Fig. 1c).The effects of lncRNA-LINC00525 was assessed by colony formation assay. The results showed that U118 and U87 glioma cell colonies decreased significantly upon RNA-LINC00525 silencing (Fig. 2a, b). The colonies were inhibited by almost 60% in both U118 and U87 glioma cells. These results suggest that lncRNA-LINC00525 regulates the growth of glioma cancer cells and its intentional silencing might serve a therapeutic role against the human glioma.The metastasis of cancer cells is one of the crucial aspects of aggressiveness of a particular human cancer (Steeg 2016). Thus, scientists are continuously looking for the measures to contain the motility of cancer cells. The assessment of the migration of glioma cells showed that the cancer cells showed significantly lower migration under lncRNA-LINC00525 knockdown (Fig. 3). The invasion of the glioma cells was also seen to significantly fall under lncRNA-LINC00525 knockdown (Fig. 4). Together the results show that lncRNA-LINC00525 might be positively regulating the metastasis of glioma cells and thus its molecular targeting may assist is restricting the glioma spread.To specifically predict the microRNA targeting lncRNA-LINC00525 in glioma, in silico analysis was used. The bioinformatics showed that miR-338-3p is interacting with lncRNA-LINC00525 in a sequence specific manner in glioma (Fig. 6a). The prediction was supported by the RT-PCRstudy of miR-338-3p in glioma cell lines. The cancer cell lines exhibited significantly lower miR-338-3p expression corresponding to higher lncRNA-LINC00525 levels in comparison to the normal astrocytes (Fig. 6b). miR-338-3p was over-expressed in U87 and U118 cell lines (Fig. 7a). The miR-338-3p over-expression further reduced the proliferation of glioma cancer cells, in vitro (Fig. 7b). The results thus suggest that lncRNA-LINC00525 might be regulating the mechanics of growth and proliferation of glioma cancer cells via its sponging of miR-338-3p.	32857271	RID04545	expression association	metastasis	UP(LIHC);DATA(GSE117623)	
Psoriasis	TUSC7	GATA3	positively-E	dual-luciferase reporter assay;miRDB	downregulation	RT-PCR;western blot	NA	NA	cell viability(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-616)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Integumentary system disease	Skin disease	lncRNA	TF	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000107485	NA	285194	2625	LINC00902|LOC285194|LSAMP-AS3|NCRNA00295	HDR	LOC285194 inhibits proliferation of human keratinocytes through regulating miR-616/GATA3 pathway.To test the relationship between LOC285194 and psoriasis, the expression of LOC285194 in the skin lesion samples from patients with psoriasis was assessed. Results from the qRT-PCR;ISHowed that LOC285194 expression was significantly reduced in the skin lesion samples from psoriasis patients compared to the normal skin tissues from healthy subjects (Fig. 1A).Results from the CCK-8 assay revealed that overexpression of LOC285194 significantly reduced cell viability of Hacat cells, whereas LOC285194 silencing enhanced cell viability (Fig 2B). Furthermore, flow cytometry results demonstrated that LOC285194 overexpression led to increased proportion of cells in the G1 phase and reduced cells in the S phase. This was in contrast to cells treated with siLOC285194-#1, which displayed opposite effects (Fig 2C). Consistently, investigation of the protein levels of cell cycle regulators (PCNA and p21) by western blot showed that LOC285194 overexpression in Hacat cells resulted in decreased PCNA and increased p21 protein levels, while knockdown of LOC285194 caused an opposite effect (Fig 2D).These findings are important and suggest that exogenous overexpression of LOC285194 could suppress growth of keratinocytes via inducing S phase arrest. To verify their relationship, dual-luciferase reporter assays were performed in HEK-293 cells. Results from the dual-luciferase reporter assay demonstrated that co-transfection of LOC285194-wt and miR-616 mimics (miR-616) inhibited luciferase activity in relative to the LOC285194-wt+miR-NC group. However, this inhibitory effect was diminished when LOC285194-mut plasmid was used (Fig. 4C). The transfection efficiency of miR-616 mimics (miR-616) in HEK-293 cells was verified before performing the luciferase assays (Fig. 4B). Moreover, RIP assay displayed that LOC285194 and miR-616 were all enriched in Ago2-containing microribonucleoproteins (Fig. 4D), further supporting that miR-616 is a direct target of LOC285194.Results from the dual-luciferase reporter assays demonstrated that co-transfection of miR-616 mimics (miR-616) and GA TA3-wt led to a significant reduction in luciferase activity (Fig. 5B), whereas no difference in luciferase activity was observed when GA TA3-mut plasmid was used. These indicate a direct binding site between miR-616 and GA TA3. Next, to further validate their relationship, we used a miR-616 inhibitor (miR-616 inh). The transfection efficiency of miR-616 inh in Hacat cells was validated (Fig. 5C). The results confirmed a negative regulatory relationship between miR-616 and GA TA3, in which overexpression of miR-616 reduced GA TA3 protein level and miR-616 inhibition led to an opposite effect in GA TA3 expression (Fig. 5D).	32439362	RID04546	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(BRCA);DATA(GSE55807)
Abdominal aortic aneurysm	CRNDE	SMAD3	positively-E	RNA pull-down;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000166949	NA	643911	4088	CRNDEP|LINC00180|LOC643911	HsT17436|JV15-2|MADH3	LncRNA CRNDE affects the proliferation and apoptosis of vascular smooth muscle cells in abdominal aortic aneurysms by regulating the expression of Smad3 by Bcl-3.The results showed that the expression of LncRNA CRNDE was significantly down-regulated in AAA tissues (Figure 1(a)). Mouse vascular smooth muscle cells (VSMCs) were treated with 1 uM AngII for 48 h [25]. According to the results of MTT and EdU assays, it was found that AngII stimulation significantly inhibited the proliferation of mouse VSMCs and reduced the percentage of EdU positive cells (Figure 1(b)). From the results of flow cytometry, we found that AngII stimulation significantly promoted the apoptosis of mouse VSMCs (Figure 1(e,f)). In addition, it could be seen from the results of qRT-PCRthat the expression of LncRNA CRNDE was significantly down-regulated after AngII stimulation (Figure 1(g)). In summary, the expression of LncRNA CRNDE was down-regulated in AAA tissues and AngII-stimulated VSMCs.From the results of qRT-PCR it could be seen that the expression of LncRNA CRNDE was markedly down-regulated after the AngII stimulation. Compared with the AngII+pcDNA group, the expression of LncRNA CRNDE was significantly up-regulated in the AngII+pcDNA-CRNDE group (Figure 2(a)). The results of MTT and EdU assays indicated that the AngII stimulation inhibited VSMCs proliferation and reduced the percentage of EdU positive cells. Besides, compared with the AngII+pcDNA group, the proliferation of VSMCs was promoted and the percentage of EdU positive cells was increased in the AngII+pcDNA-CRNDE group (Figure 2(b )). From the results of flow cytometry, we found that the AngII stimulation promoted the apoptosis of VSMCs. In addition, compared with the AngII+pcDNA group, the apoptosis of VSMCs was repressed in the AngII+pcDNA-CRNDE group (Figure 2(e,f)). From the above experimental results, the overexpression of LncRNA CRNDE could promote the proliferation of VSMCs and repress the apoptosis of cells.Subsequently, we explored the interaction between LncRNA CRNDE and Bcl-3 by RNA pull-down and RIP experiments. From the RNA pull-down detection data, it was found that the expression of Bcl-3 was detected in the CRNDE pull-down complex (Figure 3(a) and Supplemental Figure 1a). RIP experiments revealed that LncRNA CRNDE was accumulated in Bcl-3 precipitated protein samples (Figure 3(b)). Furthermore, we transfected si-control or si-CRNDE into mouse VSMCs, respectively. western blotshowed that the transfection of si-CRNDE down-regulated the protein level of Bcl-3 (Figure 3(c) and Supplemental Figure 1b,C). Besides, in order to elucidate the interaction between Bcl-3 and Smad3, we performed a Co-immunoprecipitation (Co-IP) experiment. From the results of this experiment, it was found that there is an interaction between Bcl-3 and Smad3 protein (Figure 3(d) and Supplemental Figure 1d,E). Subsequently, we transfected pcDNA-CRNDE or pcDNA-CRNDE+si-Bcl-3 into mouse VSMCs and treated the cells with 20 ug/mL CHX, and then detected the stability of Smad3 protein at 0, 4, and 8 h, respectively. western blotindicated that Smad3 protein in cells transfected with pcDNA-CRNDE alone was much more stable than cells transfected with pcDNA-CRNDE+si-Bcl-3 (Figure 3(e) and Supplemental Figure 2a,B). Furthermore, we transfected pcDNA-CRNDE or si-CRNDE into mouse VSMCs and treated the cells with 100 mM MG132 for 6 h. From the results of western blot the interference with LncRNA CRNDE increased the ubiquitination degradation of Smad3 protein, while the overexpression of LncRNA CRNDE produced the opposite effect (Figure 3(F) and Supplemental Figure 2c and Supplemental Figure 3a). Taken together, the above experimental results indicated that LncRNA CRNDE bound to Bcl-3 and LncRNA CRNDE could regulate the ubiquitination of Smad3 via Bcl-3.	32240036	RID04547	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Leukemia	FAS-AS1	FAS	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000026103	NA	100302740	355	FAS-AS|FASAS|SAF	APO-1|APT1|CD95|FAS1|TNFRSF6	Regulatory loop between lncRNA FAS-AS1 and DNMT3b controls FAS expression in hydroquinone-treated TK6 cells and benzene-exposed workers.To examine whether these lncRNAs are abnormally expressed in HQ-TK6 cells, we detected their expression levels by qRT-PCR Compared with that in PBS-TK6 cells, FAS-AS1 and BC035666 expression was decreased significantly, while NALT and LUNAR1 expression was increased significantly (Fig. 1a).To confirm the biological function of FAS-AS1 in HQ-TK6 cells, we generated HQ-TK6 cells overexpressing FAS-AS1 by transducing a cloned pLVX-Puro vector overexpressing FASAS1. FAS-AS1 expression was increased 7.5-fold compared to that in the NC control cells (Supplementary Figs. 2a and b). Restoration of FAS-AS1 promoted cell apoptosis in the starvation state (Fig. 2a and b). Moreover, the mRNA expression of the proapoptotic genes Caspase-3 and Caspase-9 was increased. However, the mRNA expression of the antiapoptotic protein Bcl-2 was decreased (Fig. 2b). However, restoration of FAS-AS1 did not affect cell proliferation (Supplementary Fig. 2c).To determine whether FAS-AS1 regulates epigenetic factors, we examined the expression of epigenetic factors associated with DNA methylation and histone acetylation after restoration of FAS-AS1 (Fig. 5a and b). Restoration of FAS-AS1 mediated the downregulation of DNMT3b but not that of several other methylation-related molecules. Furthermore, restoration of FASAS1 upregulated the expression of H3ac and H3K27ac but downregulated the expression of SIRT1 (Fig. 5c). Moreover, IHC assays showed that the expression of these molecules was identical to that in HQ-TK6 cells overexpressing FAS-AS1, and the expression of FAS was upregulated in tumor tissues obtained after tumor formation in nude mice (Fig. 5d). These results demonstrated that FAS-AS1 mediated the downregulation of DNMT3b and SIRT1.Moreover, the expression of FAS in HQ-TK6 cells, FAS-AS1-overexpressing cells and DNMT3b knockout cells was downregulated, upregulated and upregulated, respectively (Fig. 6a, b and 6c). The expression change of FAS was opposite to the change in SIRT1 expression. We also found that the enrichment of H3K27ac in the FAS promoter region was increased in FAS-AS1-overexpressing cells (Fig. 6d) and was attenuated in DNMT3b knockout cells (Fig. 6e). This evidence confirmed that FASAS1 and DNMT3b form a mutual suppression loop and may be involved in regulating the expression of FAS through regulation of SIRT1 by changing the level of acetylation at the H3k27 site.	32088430	RID04548	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Leukemia	FAS-AS1	DNMT3B	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000088305	NA	100302740	1789	FAS-AS|FASAS|SAF	NA	Regulatory loop between lncRNA FAS-AS1 and DNMT3b controls FAS expression in hydroquinone-treated TK6 cells and benzene-exposed workers.To examine whether these lncRNAs are abnormally expressed in HQ-TK6 cells, we detected their expression levels by qRT-PCR Compared with that in PBS-TK6 cells, FAS-AS1 and BC035666 expression was decreased significantly, while NALT and LUNAR1 expression was increased significantly (Fig. 1a).To confirm the biological function of FAS-AS1 in HQ-TK6 cells, we generated HQ-TK6 cells overexpressing FAS-AS1 by transducing a cloned pLVX-Puro vector overexpressing FASAS1. FAS-AS1 expression was increased 7.5-fold compared to that in the NC control cells (Supplementary Figs. 2a and b). Restoration of FAS-AS1 promoted cell apoptosis in the starvation state (Fig. 2a and b). Moreover, the mRNA expression of the proapoptotic genes Caspase-3 and Caspase-9 was increased. However, the mRNA expression of the antiapoptotic protein Bcl-2 was decreased (Fig. 2b). However, restoration of FAS-AS1 did not affect cell proliferation (Supplementary Fig. 2c).To determine whether FAS-AS1 regulates epigenetic factors, we examined the expression of epigenetic factors associated with DNA methylation and histone acetylation after restoration of FAS-AS1 (Fig. 5a and b). Restoration of FAS-AS1 mediated the downregulation of DNMT3b but not that of several other methylation-related molecules. Furthermore, restoration of FASAS1 upregulated the expression of H3ac and H3K27ac but downregulated the expression of SIRT1 (Fig. 5c). Moreover, IHC assays showed that the expression of these molecules was identical to that in HQ-TK6 cells overexpressing FAS-AS1, and the expression of FAS was upregulated in tumor tissues obtained after tumor formation in nude mice (Fig. 5d). These results demonstrated that FAS-AS1 mediated the downregulation of DNMT3b and SIRT1.Moreover, the expression of FAS in HQ-TK6 cells, FAS-AS1-overexpressing cells and DNMT3b knockout cells was downregulated, upregulated and upregulated, respectively (Fig. 6a, b and 6c). The expression change of FAS was opposite to the change in SIRT1 expression. We also found that the enrichment of H3K27ac in the FAS promoter region was increased in FAS-AS1-overexpressing cells (Fig. 6d) and was attenuated in DNMT3b knockout cells (Fig. 6e). This evidence confirmed that FASAS1 and DNMT3b form a mutual suppression loop and may be involved in regulating the expression of FAS through regulation of SIRT1 by changing the level of acetylation at the H3k27 site.	32088430	RID04549	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Leukemia	FAS-AS1	SIRT1	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000096717	NA	100302740	23411	FAS-AS|FASAS|SAF	SIR2L1	Regulatory loop between lncRNA FAS-AS1 and DNMT3b controls FAS expression in hydroquinone-treated TK6 cells and benzene-exposed workers.To examine whether these lncRNAs are abnormally expressed in HQ-TK6 cells, we detected their expression levels by qRT-PCR Compared with that in PBS-TK6 cells, FAS-AS1 and BC035666 expression was decreased significantly, while NALT and LUNAR1 expression was increased significantly (Fig. 1a).To confirm the biological function of FAS-AS1 in HQ-TK6 cells, we generated HQ-TK6 cells overexpressing FAS-AS1 by transducing a cloned pLVX-Puro vector overexpressing FASAS1. FAS-AS1 expression was increased 7.5-fold compared to that in the NC control cells (Supplementary Figs. 2a and b). Restoration of FAS-AS1 promoted cell apoptosis in the starvation state (Fig. 2a and b). Moreover, the mRNA expression of the proapoptotic genes Caspase-3 and Caspase-9 was increased. However, the mRNA expression of the antiapoptotic protein Bcl-2 was decreased (Fig. 2b). However, restoration of FAS-AS1 did not affect cell proliferation (Supplementary Fig. 2c).To determine whether FAS-AS1 regulates epigenetic factors, we examined the expression of epigenetic factors associated with DNA methylation and histone acetylation after restoration of FAS-AS1 (Fig. 5a and b). Restoration of FAS-AS1 mediated the downregulation of DNMT3b but not that of several other methylation-related molecules. Furthermore, restoration of FASAS1 upregulated the expression of H3ac and H3K27ac but downregulated the expression of SIRT1 (Fig. 5c). Moreover, IHC assays showed that the expression of these molecules was identical to that in HQ-TK6 cells overexpressing FAS-AS1, and the expression of FAS was upregulated in tumor tissues obtained after tumor formation in nude mice (Fig. 5d). These results demonstrated that FAS-AS1 mediated the downregulation of DNMT3b and SIRT1.Moreover, the expression of FAS in HQ-TK6 cells, FAS-AS1-overexpressing cells and DNMT3b knockout cells was downregulated, upregulated and upregulated, respectively (Fig. 6a, b and 6c). The expression change of FAS was opposite to the change in SIRT1 expression. We also found that the enrichment of H3K27ac in the FAS promoter region was increased in FAS-AS1-overexpressing cells (Fig. 6d) and was attenuated in DNMT3b knockout cells (Fig. 6e). This evidence confirmed that FASAS1 and DNMT3b form a mutual suppression loop and may be involved in regulating the expression of FAS through regulation of SIRT1 by changing the level of acetylation at the H3k27 site.	32088430	RID04550	expression association	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pneumonia	NKILA	miR-21	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell injury(+);NF-kB signaling pathway(+);JNK signaling pathway(+)	NA	regulation	RNA-RNA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000199004	NA	105416157	NA	NA	NA	Long non-coding RNA NKILA weakens TNF-alpha-induced inflammation of MRC-5 cells by miR-21 up-regulation.To determine the effect of NKILA on IP, we overexpressed NKILA in MRC5 cells. It turned out to be that when pc-NKILA was transfected into MRC5 cells, NKILA expression was notably up-regulated (p-<-.001, Figure 2(A)). Besides, cell viability was remarkably increased (p-<-.05, Figure 2(B)) and apoptosis was reduced (p-<-.01, Figure 2(C)) after NKILA overexpression. Meanwhile, apoptosis-related Bcl-2 expression was increased, while Bax and Cleaved-PARP expression was reduced (all p-<-.01, Figure 1(D,E)). Further ELISA and western blot results discovered that inflammatory cytokines IL-1beta and IL-6 expression was remarkably down-regulated (both p-<-.01, Figure 1(F,G)). In conclusion, TNF-alpha-induced injury was remitted by NKILA overexpression.In order to further understand the regulating mechanism of NKILA in IP, we further explored the expression of miR-21 in NKILA overexpressed MRC5 cells. Fortunately, we found that compared to pcDNA3.1 transfected group, miR-21 level was remarkably enhanced in pc-NKILA transfected group (p-<-.01, Figure 3), indicating that miR-21 expression was positively correlated with NKILA expression.Undertaking Figure 3, we transfected miR-21 inhibitor into MRC5 cells and results showed that miR-21 expression was remarkably decreased (p-<-.001, Figure 4(A)). Based on this, miR-21 inhibitor was transfected into NKILA overexpressed cells, and following results showed that NKILA overexpression-triggered effects on cell viability and cell apoptosis were both notably remitted by miR-21 inhibition (both p-<-.05, Figure 4(B,C)). Meanwhile, apoptosis-related Bcl-2 expression was reduced, while Bax and Cleaved-PARP expression was increased after miR-21 inhibition (p-<-.05 or p-<-.01, Figure 4(D,E)). Further ELISA and western blot results discovered that inflammatory cytokines IL-1beta and IL-6 expression was remarkably up-regulated (p-<-.01, Figure 4(F,G)). In conclusion, NKILA overexpression-induced protective effects were weakened by miR-21 inhibition.At first, TNF-alpha treatment remarkably increased the ratios of p/t-IkBalpha, p/t-p65 (both p-<-.001, Figure 5(A,B)) and p/t-JNK (p-<-.001, Figure 5(C,D)). After pc-NKILA was transfected into TNF-alpha-injured cells, these ratios were reduced (all p-<-.01). Further, miR-21 inhibition remarkably recovered NKILA overexpression-triggered impacts (all p-<-.05). In conclusion, NKILA overexpression inhibited NF-kB and JNK pathways by modulating miR-21 expression.	32013579	RID04551	expression association	NA		
Meningioma	MEG3	AKAP12	positively-E	dual-luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell migration(+);cell invasion(+);cell proliferation(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Meningioma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000131016	NA	55384	9590	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	AKAP250|SSeCKS	Long Non-Coding RNA MEG3 Modifies Cell-Cycle, Migration, Invasion, and Proliferation Through AKAP12 by Sponging miR-29c in Meningioma Cells.The expression of MEG3 was determined in MEN specimens. Compared with normal control, a low level of MEG3 was observed in MEN tissues (Figure 1A). In addition, relative operating characteristic curves (ROC) analysis was carried out, and the area under the ROC curves (AUC; 0.85) showed that MEG3 might be a potential marker in MEN progression (Figure 1B). Moreover, miR-29c was increased in MEN tissues (Figure 1C). Similarly, the ROC curves implied the apparent isolation between MEN and match healthy donators, with an AUC of 0.875 for miR-29c (Figure 1D). From all subjects, we displayed that miR-29c was inversely correlated with MEG3 in clinical MEN tissues (Figure 1E). Collectively, MEG3 and miR-29c acted as strict factors in the process of MEN.Then, dual-luciferase reporter assay and RIP assay were performed to verify the interrelation between them. We found that the luciferase activity of MEG3-WT reporter was remarkably decreased (about 70%) in miR-29c-transfected IOMM-Lee and CH157-MN cells, whereas miR-29c had no statistical impact on the luciferase activity of mutant reporter (Figures 2B, C). As shown in Figures 2D, E, the levels of MEG3 and miR-29c were augmented in the Ago2-treated group. Next, MEG3 or si-MEG3 was transfected into IOMM-Lee and CH157-MN cells, respectively. qRT-PCRanalysis exhibited that MEG3 passively regulated miR-29c in the two MEN cells (Figures 2F, G). All the results demonstrated that MEG3 served as the upstream of miR-29c in MEN cells.Given the molecular mechanism between miR-29c and MEG3, we investigated the biological function of them in MEN cells. First, MEG3 alone or combined with miR-29c was transfected into IOMM-Lee and CH157-MN cells. As depicted in Figures 3A, B, MEG3 increase could impede the level of miR-29c in the two MEN cells, and reintroduction with miR-29c could overturn this effect. The triggered ability of cell-cycle arrest resulted from MEG3 augment was distinctly hindered via co-transfection with MEG and miR-29c in the two MEN cells (Figures 3C, D). Moreover, cell migration was assessed using wound healing assay, and the results determined that miR-29c supplement relieved the inhibitory effect of MEG3 on cell migration in vitro (Figures 3E, F). Also, cell invasion was restrained as a result of MEG3 increase, which was regained by miR-29c supplement in IOMM-Lee and CH157-MN cells (Figures 3G, H). MEG3 overexpression inhibited cell proliferation, which was reversed by miR-29c upregulation (Figure 3I). In brief, MEG3 regulated cell-cycle arrest, migration, invasion, and proliferation via miR-29c in MEN cells.Results from dual-luciferase reporter analysis showed that the luciferase activity of AKAP12-WT reporter was significantly diminished by miR-29c, but miR-29c had no statistical effect on changing luciferase activity of the mutant reporter system in IOMM-Lee and CH157-MN cells (Figures 4B, C). Levels of miR-29c and AKAP12 were notably upregulated in Ago2-treated IOMM-Lee and CH157-MN cells (Figures 4D, E). As shown in Figures 4F, G, miR-29c could inversely regulate the level of AKAP12 at the aspect of protein expression. Overall, we could conclude that AKAP12 acted as the downstream of miR-29c.As described in Figure 6A, an inverse correlation between miR-29c and AKAP12 was observed in clinical MEN tissues. On the contrary, AKAP12 was positively associated with MEG3 in MEN samples (Figure 6B). Then, MEG3 alone or combined with miR-29c was transfected into IOMM-Lee and CH157-MN cells, and the high level of AKAP12, caused by MEG3 increase, was apparently decreased after co-transfection with miR-29c and MEG3 in the two MEN cells (Figure 6C). Similarly, the declined level of AKAP12 induced by si-MEG3 was restored by anti-miR-29c (Figure 6D). Collectively, AKAP12 was co-regulated by MEG3 and miR-29c in the process of MEN.	33251130	RID04552	ceRNA or sponge	NA		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Laryngeal squamous cell carcinoma	IUR	TP53	positively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-24)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	LncRNA-IUR Sponges miR-24 to Upregulate P53 in Laryngeal Squamous Cell Carcinoma.Differential expression of IUR in LSCC was determined by measuring the expression levels of IUR, p53 and miR-24 in both LSCC and non-tumor tissues collected from the 60 patients with LSCC. Paired t-test showed that the expression levels of IUR and p53 were significantly lower in LSCC tissues than that in non-tumor tissues (Figure 1A and -andC,C, p < 0.001), while the expression levels of miR-24 were higher in LSCC tissues than that in non-tumor tissues. Survival curves showed that the overall survival rate of patients in the low IUR level group was significantly lower than that of patients in the high IUR level group (Figure 1B, p < 0.05). And Chi-squared test showed that the expression levels of IUR were not significantly correlated with clinical stages (p = 0.87). See Table 1 for details.The potential base pairs formed by IUR and miR-24 were predicted using IntaRNA (http://rna.informatik.uni-freiburg.de/IntaRNA/Input.jsp). It was observed that IUR and miR-24 can form strong base pairs between each other (Figure 2A). dual-luciferase reporter assay was performed to further analyze the interaction between IUR and miR-24. Compared to cells transfected with IUR and miRNA NC (NC group), cells transfected with IUR and miR-24 mimic (miR-24 group) showed significantly lower relative luciferase activity (Figure 2B, p < 0.05).Wound healing assay (Figure 3A and -andC)C) and transwell assay (Figure 3B and -andD)D) were performed to study the effects of the interactions between IUR and miR-24 of cell migration and invasion. Compared to C, NC miRNA and PcDNA3.1, overexpression of miR-24 led to promoted, while overexpression of IUR inhibited the cell migration and invasion. In addition, overexpression of miR-24 reduced the inhibited effects of IUR to LSCC cells.UM-SCC-17A cells were transfected with IUR expression vector or miR-24 mimic to further evaluate the interaction between IUR and miR-24. Overexpression of IUR and miR-24 was confirmed by qPCR at 24 h post-transfection (Figure 4A, p < 0.05). Comparing to C and NC groups, overexpression of IUR and miR-24 did not alter the expression of each other (Figure 4B). Then, the effects of IUR and miR-24 on the expression of p53 in UM-SCC-17A cells were assessed by qPCR and western blot at mRNA (Figure 4C) and protein (Figure 4D) levels, respectively. Comparing to C and NC groups, overexpression of miR-24 led to downregulated p53. In contrast, overexpression of IUR played an opposite role and reduced the effects of overexpression of miR-24 (p < 0.05).	33235495	RID04553	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Kidney disease	CASC2	SOCS2	positively-E	luciferase assay;western blot assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);fibrotic(+)	ceRNA(miR-144)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000120833	NA	255082	8835	C10orf5	CIS2|Cish2|SOCS-2|SSI-2|SSI2|STATI2	LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis.The relative expression of CASC2 in DN mice and HRMCs was assessed by qRT-PCR As expected, CASC2 had lower expression in DN mice and HG-induced HRMCs than in control mice (p < 0.05; Fig. 1E, F). These data suggest that CASC2 could play an important role in regulating the process of DN.To detect the effect of CASC2 on HG-induced HRMCs in different pathological processes, a CASC2 overexpression vector (pcDNA3.1-CASC2) was transfected into HRMCs. The level of CASC2 was downregulated after HG induct(p < 0.05), while the overexpression of CASC2 significantly upregulated CASC2 expression (p < 0.01, Fig. 2A). Subsequently, flow cytometry was used to detect the apoptosis rate. The results showed that HG significantly promoted apoptosis (p < 0.01) and overexpression of CASC2 clearly attenuated HG-induced apoptosis (p < 0.05; Fig. 2B). To uncover the downstream targets of CASC2, we used DIANA software to predict the downstream-targeted miRNAs that could bind and interact with CASC2. As shown in Figure 3A, miR-144 was selected as the target downstream miRNA for further study. Next, a dual-luciferase reporter assay revealed that the luciferase activity of cells co-transfected with miR-144 mimics and wild-type CASC2 vector was notably decreased compared to that of cells co-transfected with miR-144 mimics and mutant CASC2 vector (p < 0.01; Fig. 3B). Further qRT-PCRdetection showed that knockdown of CASC2 was directly related to upregulated miR-144 expression, whereas overexpression of CASC2 obviously downregulated miR-144 expression (Fig. 3C). Together, these results demonstrated that CASC2 directly interacts with miR-144.Luciferase activity assays provided further evidence that SOCS2 could be a downstream target of miR-144. The results demonstrated that decreased luciferase activity was observed in cells co-transfected with miR-144 mimics and SOCS2-WT, compared to cells co-transfected with SOCS2-WT and mimics NC. There was no significant change in luciferase activity in cells co-transfected with SOCS2-MUT vector (p < 0.05; Fig. 4B). Moreover, qRT-PCRand Wterblotting showed that overexpression of miR-144 decreased the mRNA and protein expression of SOCS2, while knockdown of miR-144 increased the expression of SOCS2 at both the mRNA and protein levels (Fig. 4C, D), suggesting that miR-144 negatively regulated the expression of SOCS2.	33227790	RID04554	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Breast cancer	FERRE	EZH2	positively-E	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000106462	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	Upregulation of long noncoding RNA FERRE promoted growth and invasion of breast cancer through modulating miR-19a-5p/EZH2 axis.For validation, we detected the expressions of FERRE and EZH2 in tumor samples acquired from breast cancer patients. Total RNA of breast cancer tissues and adjacent normal tissues were extracted, and the expressions of FERRE and EZH2 were revealed by qRT-PCR Results showed that both FERRE and EZH2 were significantly upregulated in breast cancer tissues (Figure 1B, 1C). To further illustrate the biological function of FERRE in breast cancer, qRT-PCRanalysis was performed to detect FERRE expression in human breast cancer cell lines MCF-7. Results showed that expressions of FERRE and EZH2 were remarkably increased in MCF-7 cells compared with human epithelia cells HEK293 (p < 0.01) (Figure 1D, 1E). From these data, we suggested that FERRE might play a biological role in breast cancer.To explore the functions of FERRE in breast cancer progression, we constructed FERRE overexpressing lentiviral and transfected it into MCF-7 cells. In addition, we also synthesized small interfering RNA of FERRE to inhibit its expression before it was transfected into MCF-7 cells. After that, the expression of FERRE was detected by qRT-PCRand the results showed that the expression of FERRE in the FERRE overexpressed group was significantly enhanced compared with the control (p < 0.05), while the expression levels of FERRE were reduced in the FERRE inhibition group compared with the control group (p < 0.05) (Figure 2A, 2B).The results disclosed that overexpressing FERRE significantly increased cell proliferation of MCF-7 compared with the control, whereas inhibition of FERRE expression remarkably reduced the cell proliferation number (Figure 3A, 3B). Besides, qRT-PCRanalysis showed that the expression of apoptotic related genes such as Bax and cleaved caspase-3 were significantly decreased whereas the expression of anti-apoptotic gene Bcl-2 was remarkably increased after upregulation of FERRE expression (Figure 3C), and it was reversed after FERRE inhibition (Figure 3D). These results suggested that changing the expression of FERRE can regulate the proliferation ability of breast cancer cells.We constructed FERRE-wt Luciferase reporter vector and FERRE-mut 3'UTR Luciferase reporter vector and performed Luciferase reporter assay (Fig-ure 4D). The results showed that compared with the control, the Luciferase activity of MCF-7 cells that co-transfected with wide type FERRE (FERRE-wt) and miR-19a-5p mimic was significantly decreased (p < 0.01), and it was reversely increased after mutation at the binding site of FERRE (FERRE-mut) compared with FERREwt (p < 0.01) (Figure 4E). These results identified that FERRE could directly bind to miR-19a5p. In addition, overexpression of FERRE significantly inhibited miR-19a-5p expression and FERRE downregulation reversely supported miR-19a-5p expression in MCF-7 cells (Figure 4F, 4G). We also transfected miR-19a-5p mimic and miR-19a-5p inhibitor into MCF-7 cells; the results revealed that miR-19a-5p mimic inhibited FERRE expression and miR-19a-5p inhibitor increased FERRE expression (Figure 4H, 4I). Taken together, these findings demonstrated that FERRE can directly sponge with miR-19a-5p.To validate this mechanism, mice EZH2 3'-UTR were cloned into the Luciferase reporter vector and miR-19a5p binding mutants were constructed in which the putative miR-19a-5p binding sites GUACU in the EZH2 3'-UTR were mutated into CAUGA (Figure 5B). As expected, Dual-Luciferase report results showed that miR-19a-5p mimics significantly decreased the EZH2 expression whereas point mutations in the EZH2 3'-UTR alleviate the inhibited effect of miR-19a-5p (Figure 5C). Furthermore, we investigate whether FERRE can regulate EZH2 expression via sponging with miR-19a-5p. The results showed that FERRE could significantly increase EZH2 expression; nevertheless, mutation of the binding site with FERRE of miR-19a-5p eliminated the function effectively (Figure 5D).Bioinformatics prediction was made to detect the binding site of FERRE and miR-19a-5p	33215433	RID04555	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	LINC02381	miR-21	negatively-F	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000199004	NA	400043	NA	LOC400043	NA	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway. Furthermore, LINC02381 expression level was investigated in gastric cancer and adjacent normal tissues, using RT-qPCR, and the results indicated that LINC02381 lncRNA expression level was significantly lower in gastric cancer, compared with the adjacent normal tissues (Figure 2C).dual-luciferase reporter assay was performed to investigate whether direct interaction could occur between LINC02381 and these candidate microRNAs. Results indicated that miR-21, miR-590, and miR-27a all were capable of reducing the Renilla:LINC02381 luciferase activity, compared to that in control groups (Figure 3B). These data suggest that LINC02381 may play a tumor-suppressive role in gastric cancer progression by sponging the oncogenic microRNAs (and de-repressing their target genes).To examine the effect of LINC02381-mediated sponging of the candidate miRNAs on Wnt signaling pathway, TOPflash assay was performed. As expected, miR-21, miR-590, and miR-27a overexpression elevated the activity of pGL3-TopFlash reporter, drastically (Figure 4C). On the other hand, LINC02381 overexpression reduced the luciferase activity of pGL3-TopFlash reporter (Figure 4C). Consistently, as shown in Figure 4D, the protein expression of beta-catenin was significantly suppressed by LINC02381 upregulation of gastric cancer cells, compared with the control group. Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.As shown in Figures 5C,D, the proportions of apoptotic cells following the LINC02381 overexpression were significantly increased, compared with those in the control group. Moreover, consistent with aforementioned data, overexpression of LINC02381 elevated caspase 3/7 activity level in both tested cell lines (Figure 5E). Taken together, these data indicated that LINC02381 treatment could arrest cell progression in the G0/G1 phase of the cell cycle and induce apoptosis.To investigate the impact of LINC02381 on the survival of gastric cell lines, the MTT assay was performed. The results showed that the viability of the cells transfected with pcDNA-LINC02381 was significantly inhibited, compared with that of control cells (Figure 5F). Furthermore, a dramatic decrease in the number of colonies was detected following the overexpression of LINC02381 in AGS and MKN45 cells, compared to control cells (Figures 5G,H). These findings suggested that LINC02381 acts as a tumor suppressor and inhibits gastric cell proliferation.These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.	33194632	RID04556	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	
Gastric cancer	LINC02381	MIR590	negatively-F	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000207741	NA	400043	693175	NA	MIRN590|hsa-mir-590|mir-590	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway. Furthermore, LINC02381 expression level was investigated in gastric cancer and adjacent normal tissues, using RT-qPCR, and the results indicated that LINC02381 lncRNA expression level was significantly lower in gastric cancer, compared with the adjacent normal tissues (Figure 2C).dual-luciferase reporter assay was performed to investigate whether direct interaction could occur between LINC02381 and these candidate microRNAs. Results indicated that miR-21, miR-590, and miR-27a all were capable of reducing the Renilla:LINC02381 luciferase activity, compared to that in control groups (Figure 3B). These data suggest that LINC02381 may play a tumor-suppressive role in gastric cancer progression by sponging the oncogenic microRNAs (and de-repressing their target genes).To examine the effect of LINC02381-mediated sponging of the candidate miRNAs on Wnt signaling pathway, TOPflash assay was performed. As expected, miR-21, miR-590, and miR-27a overexpression elevated the activity of pGL3-TopFlash reporter, drastically (Figure 4C). On the other hand, LINC02381 overexpression reduced the luciferase activity of pGL3-TopFlash reporter (Figure 4C). Consistently, as shown in Figure 4D, the protein expression of beta-catenin was significantly suppressed by LINC02381 upregulation of gastric cancer cells, compared with the control group. Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.As shown in Figures 5C,D, the proportions of apoptotic cells following the LINC02381 overexpression were significantly increased, compared with those in the control group. Moreover, consistent with aforementioned data, overexpression of LINC02381 elevated caspase 3/7 activity level in both tested cell lines (Figure 5E). Taken together, these data indicated that LINC02381 treatment could arrest cell progression in the G0/G1 phase of the cell cycle and induce apoptosis.To investigate the impact of LINC02381 on the survival of gastric cell lines, the MTT assay was performed. The results showed that the viability of the cells transfected with pcDNA-LINC02381 was significantly inhibited, compared with that of control cells (Figure 5F). Furthermore, a dramatic decrease in the number of colonies was detected following the overexpression of LINC02381 in AGS and MKN45 cells, compared to control cells (Figures 5G,H). These findings suggested that LINC02381 acts as a tumor suppressor and inhibits gastric cell proliferation.	33194632	RID04557	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	
Gastric cancer	LINC02381	miR-27a	negatively-F	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000250742	GRCh38_12:54126053-54147485	NA	NA	400043	NA	LOC400043	NA	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway. Furthermore, LINC02381 expression level was investigated in gastric cancer and adjacent normal tissues, using RT-qPCR, and the results indicated that LINC02381 lncRNA expression level was significantly lower in gastric cancer, compared with the adjacent normal tissues (Figure 2C).dual-luciferase reporter assay was performed to investigate whether direct interaction could occur between LINC02381 and these candidate microRNAs. Results indicated that miR-21, miR-590, and miR-27a all were capable of reducing the Renilla:LINC02381 luciferase activity, compared to that in control groups (Figure 3B). These data suggest that LINC02381 may play a tumor-suppressive role in gastric cancer progression by sponging the oncogenic microRNAs (and de-repressing their target genes).To examine the effect of LINC02381-mediated sponging of the candidate miRNAs on Wnt signaling pathway, TOPflash assay was performed. As expected, miR-21, miR-590, and miR-27a overexpression elevated the activity of pGL3-TopFlash reporter, drastically (Figure 4C). On the other hand, LINC02381 overexpression reduced the luciferase activity of pGL3-TopFlash reporter (Figure 4C). Consistently, as shown in Figure 4D, the protein expression of beta-catenin was significantly suppressed by LINC02381 upregulation of gastric cancer cells, compared with the control group. Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.As shown in Figures 5C,D, the proportions of apoptotic cells following the LINC02381 overexpression were significantly increased, compared with those in the control group. Moreover, consistent with aforementioned data, overexpression of LINC02381 elevated caspase 3/7 activity level in both tested cell lines (Figure 5E). Taken together, these data indicated that LINC02381 treatment could arrest cell progression in the G0/G1 phase of the cell cycle and induce apoptosis.To investigate the impact of LINC02381 on the survival of gastric cell lines, the MTT assay was performed. The results showed that the viability of the cells transfected with pcDNA-LINC02381 was significantly inhibited, compared with that of control cells (Figure 5F). Furthermore, a dramatic decrease in the number of colonies was detected following the overexpression of LINC02381 in AGS and MKN45 cells, compared to control cells (Figures 5G,H). These findings suggested that LINC02381 acts as a tumor suppressor and inhibits gastric cell proliferation.	33194632	RID04558	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	
Gastric cancer	LINC02381	MYC	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000136997	NA	400043	4609	LOC400043	bHLHe39|c-Myc|MYCC	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway. Furthermore, LINC02381 expression level was investigated in gastric cancer and adjacent normal tissues, using RT-qPCR, and the results indicated that LINC02381 lncRNA expression level was significantly lower in gastric cancer, compared with the adjacent normal tissues (Figure 2C).dual-luciferase reporter assay was performed to investigate whether direct interaction could occur between LINC02381 and these candidate microRNAs. Results indicated that miR-21, miR-590, and miR-27a all were capable of reducing the Renilla:LINC02381 luciferase activity, compared to that in control groups (Figure 3B). These data suggest that LINC02381 may play a tumor-suppressive role in gastric cancer progression by sponging the oncogenic microRNAs (and de-repressing their target genes).To examine the effect of LINC02381-mediated sponging of the candidate miRNAs on Wnt signaling pathway, TOPflash assay was performed. As expected, miR-21, miR-590, and miR-27a overexpression elevated the activity of pGL3-TopFlash reporter, drastically (Figure 4C). On the other hand, LINC02381 overexpression reduced the luciferase activity of pGL3-TopFlash reporter (Figure 4C). Consistently, as shown in Figure 4D, the protein expression of beta-catenin was significantly suppressed by LINC02381 upregulation of gastric cancer cells, compared with the control group. Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.As shown in Figures 5C,D, the proportions of apoptotic cells following the LINC02381 overexpression were significantly increased, compared with those in the control group. Moreover, consistent with aforementioned data, overexpression of LINC02381 elevated caspase 3/7 activity level in both tested cell lines (Figure 5E). Taken together, these data indicated that LINC02381 treatment could arrest cell progression in the G0/G1 phase of the cell cycle and induce apoptosis.To investigate the impact of LINC02381 on the survival of gastric cell lines, the MTT assay was performed. The results showed that the viability of the cells transfected with pcDNA-LINC02381 was significantly inhibited, compared with that of control cells (Figure 5F). Furthermore, a dramatic decrease in the number of colonies was detected following the overexpression of LINC02381 in AGS and MKN45 cells, compared to control cells (Figures 5G,H). These findings suggested that LINC02381 acts as a tumor suppressor and inhibits gastric cell proliferation.Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.	33194632	RID04559	expression association	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LINC02381	CCND1	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000110092	NA	400043	595	LOC400043	BCL1|D11S287E|PRAD1|U21B31	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway. Furthermore, LINC02381 expression level was investigated in gastric cancer and adjacent normal tissues, using RT-qPCR, and the results indicated that LINC02381 lncRNA expression level was significantly lower in gastric cancer, compared with the adjacent normal tissues (Figure 2C).dual-luciferase reporter assay was performed to investigate whether direct interaction could occur between LINC02381 and these candidate microRNAs. Results indicated that miR-21, miR-590, and miR-27a all were capable of reducing the Renilla:LINC02381 luciferase activity, compared to that in control groups (Figure 3B). These data suggest that LINC02381 may play a tumor-suppressive role in gastric cancer progression by sponging the oncogenic microRNAs (and de-repressing their target genes).To examine the effect of LINC02381-mediated sponging of the candidate miRNAs on Wnt signaling pathway, TOPflash assay was performed. As expected, miR-21, miR-590, and miR-27a overexpression elevated the activity of pGL3-TopFlash reporter, drastically (Figure 4C). On the other hand, LINC02381 overexpression reduced the luciferase activity of pGL3-TopFlash reporter (Figure 4C). Consistently, as shown in Figure 4D, the protein expression of beta-catenin was significantly suppressed by LINC02381 upregulation of gastric cancer cells, compared with the control group. Overexpression of LINC02381 in both AGS and MKN45 cells also repressed the expression of Cyclin D1 (35) and c-MYC (36), which are well-documented downstream target genes of Wnt/beta-catenin signaling pathway (Figure 3E). These data show that LINC02381, by binding to the candidate microRNAs, can de-repress Wnt signaling inhibitors and inhibit Wnt/beta-catenin signaling.As shown in Figures 5C,D, the proportions of apoptotic cells following the LINC02381 overexpression were significantly increased, compared with those in the control group. Moreover, consistent with aforementioned data, overexpression of LINC02381 elevated caspase 3/7 activity level in both tested cell lines (Figure 5E). Taken together, these data indicated that LINC02381 treatment could arrest cell progression in the G0/G1 phase of the cell cycle and induce apoptosis.To investigate the impact of LINC02381 on the survival of gastric cell lines, the MTT assay was performed. The results showed that the viability of the cells transfected with pcDNA-LINC02381 was significantly inhibited, compared with that of control cells (Figure 5F). Furthermore, a dramatic decrease in the number of colonies was detected following the overexpression of LINC02381 in AGS and MKN45 cells, compared to control cells (Figures 5G,H). These findings suggested that LINC02381 acts as a tumor suppressor and inhibits gastric cell proliferation.	33194632	RID04560	expression association	NA	UP(BRCA);DATA(GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Osteoarthritis	PVT1	HMGB1	positively-E	dual-luciferase reporter assay;starBase v2.0	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell viability(+);apoptosis process(+);inflammatory response(+);TLR4/NF-kB signaling pathway(+)	ceRNA(miR-93-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000189403	NA	5820	3146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	DKFZp686A04236|HMG1|HMG3|SBP-1	Knockdown of exosome-mediated lnc-PVT1 alleviates lipopolysaccharide-induced osteoarthritis progression by mediating the HMGB1/TLR4/NF-kB pathway via miR-93-5p.miR-93-5p in the serum of patients with osteoarthritis was decreased compared with the serum of healthy volunteers (Fig. 1G). In addition, miR-93-5p was significantly downregulated in LPS (5 and 10 ug/ml)-treated C28/I2 cells (Fig. 1H). Pearson correlation analysis demonstrated that the expression of miR-93-5p and PVT1 was negatively correlated in the serum of patients with osteoarthritis (Fig. 1I). Collectively, these results indicated that the upregulation of PVT1 mediated by exosomes and the reduction of miR-93-5p may be associated with the pathogenesis of osteoarthritis.A CCK-8 assay demonstrated that PVT1 downregulation reversed the suppressive influence of LPS on the viability of C28/I2 cells (Fig. 3B). The increase of apoptosis in LPS-treated C28/I2 cells was reversed by the downregulation of PVT1 (Fig. 3C). In addition, the enhancement of Bax and cleaved caspase-3 proteins and the decrease of Bcl-2 protein in LPS-induced C28/I2 cells were overturned by PVT1 inhibition (Fig. 3D). ELISA revealed that reduced PVT1 expression abrogated the increase in IL-6, IL-1beta and TNF-alpha in C28/I2 cells treated with LPS (Fig. 3E). western blotalso demonstrated that PVT1 silencing reversed LPS-mediated effects on the protein levels of IL-6, IL-1beta, TNF-alpha, aggrecan and MMP13 in C28/I2 cells (Fig. 3F). In brief, PVT1 downregulation abolished LPS-mediated viability, apoptosis, inflammation responses and collagen degradation in C28/I2 cells. miR-93-5p was revealed to be a possible target for PVT1 (Fig. 4A). Subsequently, the luciferase reporter vectors WT-PVT1 and MUT-PVT1 were constructed to verify the potential binding sites between PVT1 and miR-93-5p. dual-luciferase reporter assay demonstrated that miR-93-5p introduction suppressed the luciferase activity of WT-PVT1 when compared with the miR-NC, while no significant difference was observed in luciferase activity between the miR-NC and MUT-PVT1 groups (Fig. 4B). RT-qPCR demonstrated that PVT1 expression level was decreased in LPS-stimulated C28/I2 cells transfected with si-PVT1, but the expression of PVT1 was enhanced in LPS-stimulated C28/I2 cells transfected with PVT1 (Fig. 4C).As illustrated in Fig. 5A, miR-93-5p possessed latent binding sites in HMGB1. The luciferase reporter vectors HMGB1 3'UTR-WT and HMGB1 3'UTR-MUT were then established and a dual-luciferase reporter assay demonstrated a significant suppression of luciferase activity of HMGB1 3'UTR-WT in C28/I2 cells transfected with miR-93-5p compared with the negative control group, while HMGB1 3'UTR-MUT luciferase activity was not noticeably altered (Fig. 5B). In addition, the mRNA and protein levels of HMGB1 were significantly upregulated in the serum of osteoarthritis patients (Fig. 5C). The mRNA and protein levels of HMGB1 were significantly increased in LPS (5 ug/ml)-treated C28/I2 cells, implying that HMGB1 may be associated with LPS-induced osteoarthritis (Fig. 5D and E).Inhibition of PVT1 reversed the increase of TLR4, p-p65 and p-IkB-alpha proteins in C28/I2 cells induced by LPS. However, inhibition of miR-93-5p and HMGB1 upregulation abolished the suppressive impact of PVT1 suppression on p-p65, TLR4 and p-IkB-alpha protein expression levels in LPS-stimulated C28/I2 cells (Fig. 7B). Additionally, the data indicated that LPS-induced PVT1 accelerated osteoarthritis by activating the TLR4/NF-kB pathway through the miR-93-5p/HMGB1 axis in C28/I2 cells (Fig. 7C). These findings indicated that PVT1 regulated the TLR4/NF-kB pathway through the miR-93-5p/HMGB1 axis.HMGB1 serves as a target for miR-93-5p To further investigate the molecular mechanism of miR-93-5p in osteoarthritis, the latent target for miR-93-5p was explored in starBase v2.0. A CCK-8 assay demonstrated that the promotion of proliferation of LPS-stimulated C28/I2 cells caused by PVT1 silencing was reversed by the inhibition of miR-93-5p	33174011	RID04561	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Lung adenocarcinoma	LINC00472	YBX1	negatively-F	RNA pull-down assay;RIP;RPISeq	downregulation	microarray	GSE31210; GSE27262;GSE27262;GSE31210	NA	cell migration(+);cel invasion(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000065978	NA	79940	4904	C6orf155|dJ288M22.3|FLJ13189|P53RRA	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	LncRNA LINC00472 regulates cell stiffness and inhibits the migration and invasion of lung adenocarcinoma by binding to YBX1.SAM microarray analysis software identified 3658 differentially expressed probes in GSE31210 and 6172 differentially expressed probes in GSE27262. Analysis of these probes revealed that 1995 probes were differentially expressed in both groups: 403 were highly expressed and 1592 were lowly expressed in lung cancers (Supplementary Fig. 1a). Based on NetAffx, Refseq and Ensembl non-coding RNA annotations, we identified 14 overlapping probes representing 13 lncRNAs, including 1 highly expressed lncRNA and 12 lowly expressed lncRNAs in lung cancer samples (Supplementary Fig. 1b, c). Among the 12 lowly expressed lncRNAs, one probe, LINC00472, attracted our attention. LINC00472 expression was also low in lung adenocarcinoma tissues compared to noncancerous lung epithelium tissues according to the GEO database (GSE27262 and GSE31210) (Fig. -(Fig.1a).1a). The TCGA data also showed that LINC00472 expression was significantly lower in lung adenocarcinoma tissues (Fig. -(Fig.1a1a).The results showed a lower expression of LINC00472 in A549 and PC-9 tumor cells compared to the human normal lung epithelial cells BEAS-2B (Fig. -(Fig.2a).2a). As shown in Fig. -Fig.2b,2b, LINC00472 was successfully overexpressed in the A549 and PC-9 cells. The results of the scratch test showed that the migration abilities of A549 and PC-9 cells transfected with the LINC00472 overexpressed vector were significantly weaker than the empty vector (Fig. -(Fig.2c).2c). Invasion assay results showed that A549 and PC-9 cells transfected with the overexpressing LINC00472 vector had a weaker invasive ability compared to cells transfected with the empty vector (Fig. -(Fig.2d).2d). These results indicated that LINC00472 inhibited cell migration and invasion.The results showed a lower expression of LINC00472 in A549 and PC-9 tumor cells compared to the human normal lung epithelial cells BEAS-2B (Fig. -(Fig.2a).2a). As shown in Fig. -Fig.2b,2b, LINC00472 was successfully overexpressed in the A549 and PC-9 cells. The results of the scratch test showed that the migration abilities of A549 and PC-9 cells transfected with the LINC00472 overexpressed vector were significantly weaker than the empty vector (Fig. -(Fig.2c).2c). Invasion assay results showed that A549 and PC-9 cells transfected with the overexpressing LINC00472 vector had a weaker invasive ability compared to cells transfected with the empty vector (Fig. -(Fig.2d).2d). These results indicated that LINC00472 inhibited cell migration and invasion.To confirm this interaction, we performed an RNA pull-down assay and found that LINC00472 specifically bound to the YBX1 protein using western blot (Fig. -(Fig.4a).4a). A RIP assay using a YBX1-specific antibody was also performed to confirm whether the YBX1 specifically bound to LINC00472 (Fig. -(Fig.4b).4b). As expected, LINC00472 was enriched in the anti-YBX1 group compared to the control IgG group. These results indicated that LINC00472 bound to the YBX1 protein.RNA pull down and RIP assays identified that LINC00472 interacted with the transcription factor Y-box binding protein 1 (YBX1), which partially reversed the inhibition of cell migration and invasion and increased LINC00472-induced cell stiffness and adhesion.To explore the possible mechanism underlying the biological function of LINC00472, we used website predictions (http://pridb.gdcb.iastate.edu/RPISeq/ index.html) to identify potential combinations of LINC00472. The prediction showed an interaction between LINC00472 and YBX1.	33144579	RID04562	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteoarthritis	ARFRP1	TLR4	positively-E	miRcode;PITA;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+);cell injury(+)	ceRNA(miR-15a-5p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000101246	GRCh38_20:63698642-63708025	ENSG00000136869	NA	10139	7099	ARL18|ARP|Arp1	ARMD10|CD284|hToll|TLR-4	LncRNA ARFRP1 knockdown inhibits LPS-induced the injury of chondrocytes by regulation of NF-kB pathway through modulating miR-15a-5p/TLR4 axis.Firstly, we analyzed the expression level of ARFRP1 in 83 OA cartilage tissues and 29 normal tissue using qRT-PCRassay, and found that ARFRP1 expression was increased in OA cartilage tissues (Fig. 1A). Subsequently, ARFRP1 level was detected in LPS-induced chondrocytes. The results suggested that ARFRP1 level was significantly upregulated by LPS treatment in a dose-dependent manner (Fig. 1B). This means that the construction of OA cell model is successful. Moreover, ARFRP1 may be involved in LPS-regulated OA development.Next, CCK-8 assay was carried out to assess cell viability. As shown inFig. 2B, LPS treatment significantly inhibited cell viability, whereas this action was weakened by the downregulation of ARFRP1. Through flow cytometry analysis, we found that ARFRP1 knockdown suppressed cell apoptosis promoted by LPS treatment in chondrocytes (Fig. 2C and D). Consistent with this result, negative effect of ARFRP1 knockdown on LPS-regulated the levels of apoptosisrelated proteins, including Cyclin D1, Bcl-2, and Bax, was observed in chondrocytes (Fig. 2E). These data revealed that ARFRP1 depletion repressed LPS-induced the injury of chondrocytes.Then, the dual-luciferase reporter assay was performed to verify this interaction. Firstly, qRT-PCRassay confirmed that the transfection of miR-15a-5p strongly increased miR15a-5p expression (Fig. 3B). Subsequently, luciferase activity was determined. As indicated inFig. 3C, the cell transfected with miR-15a-5p and ARFRP1-Wt, but not miR-15a-5p and ARFRP1-Mut, exhibited lower luciferase activity compared with the control cells, revealing that miR15a-5p interacted with ARFRP1. Meanwhile, this interaction was confirmed by pull down assay (Fig. 3D and E). Next, ARFRP1 or si-ARFRP1 was transfected into chondrocytes to explore the effect of ARFRP1 on miR-15a-5p expression. We confirmed that the transfection of ARFRP1 increased ARFRP1 expression as well as the transfection of si-ARFRP1 decreased ARFRP1 expression first (Fig. 3F), and then suggested that ARFRP1 overexpression significantly downregulated miR-15a-5p level as well as ARFRP1 knockdown dramatically upregulated miR-15a-5p level (Fig. 3G). Taken together, ARFRP1, as a miR-15a-5p sponge, negatively regulated miR-15a-5p expression.In this study, TLR4 3'UTR was predicted as potential target gene of miR-15a-5p by online tool PITA (Fig. 5A). We next performed the dual-luciferase reporter assay to confirm this prediction. The results suggested that miR-15a-5p strongly reduced the luciferase activity of TLR4 3'UTR-Wt, but not TLR4 3'UTR-Mut (Fig. 5B). Confirming the interaction between miR-15a-5p and TLR4. Then, the effect of miR-15a-5p on TLR4 expression was investigated in chondrocytes. As demonstrated in Fig. 5C and D, the mRNA level and protein level of TLR4 were downregulated by miR-15a-5p overexpression and upregulated by miR-15a5p knockdown. Therefore, miR-15a-5p negatively modulated TLR4 expression. Furthermore, we confirmed that ARFRP1 upregulation increased TLR4 level, whereas this change was weakened by miR-15a-5p overexpression (Fig. 5E and F), which indicated that ARFRP1 regulated miR-15a-5p expression to mediate TLR4 level in chondrocytes. Besides, increased TLR4 expression was observed in OA cartilage tissues (Fig. 5G).To further identify the activation of NF-kB signal pathway, nuclear protein P65 and cytoplasm P65 in chondrocyte were tested. Nuclear protein P65 expression obviously increased when stimulated by LPS, while it was dramatically down-regulated when knockdown the expression of ARFRP1, yet inhibited the expression of miR-15a-5p reversed the nuclear translocation of p65 (Fig. 6C). Consistent with these data, ARFRP1 knockdown suppressed NF-kB-driven luciferase activity induced by LPS, whereas this inhibitory effect was weakened by miR-15a-5p depletion (Fig. 6D). Therefore, ARFRP1 exerted function through modulating NF-kB pathway via regulation of miR-15a-5p/TLR4 axis in LPS-induced chondrocytes. The interaction between miR-15a-5p and ARFRP1 or Toll-like receptor 4 (TLR4) was predicted by miRcode or PITA, and then confirmed by the dual-luciferase reporter assay or pull down assay.	32931797	RID04563	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Large intestine cancer	TTN-AS1	PAK3	positively-E	siRNA;knockdown;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	radiosensitivity;apoptosis process(-)	ceRNA(miR-134-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Intestinal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000077264	NA	100506866	5063	NA	bPAK|hPAK3|MRX30|MRX47	LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human large intestine cancer cells through the P21 pathway and AKT/GSK-3beta/beta-catenin pathway.TTN-AS1 expression was increased in SW620 and HT29 cells after X-ray treatment for 24 hr. Remarkably, the higher the X-ray dose, the greater the TTN-AS1 expression. The expression of TTN-AS1 in large intestine cancer cells that were exposed to a 4 Gy dose was significantly higher than in those that were exposed to a 2 Gy dose (Figure1a). Then, the TTN-AS expression in SW620 and HT29 cells was regulated by si-TTN-AS1 and up-TTN-AS1 transfection. In fact, si- TTN-AS1 and up-TTN-AS1 transfection was able to knockdown the expression and overexpress TTN-AS1, respectively, both in SW620 and HT29 cells (Figure1b).The knockdown of TTN-AS1 expression using si-TTN-AS1 transfection significantly increased the miR-134-5p expression, whereas TTN-AS1 overexpression induced by up-TTN-AS1 transfection significantly decreased its expression in large intestine cancer cells (Figure3a). In addition, dual-luciferase reporter assay results suggested that, in the WT-TNN-AS1 transfected cells, miR-134-5p- mimic transfection significantlydecreased the luciferase activity, while miR-134-5p-inhibitor transfection significantly increased it, compared with miR-134-5p-NC transfected HT29 cells (Figure3b). However, miR-134-5p-mimic and miR-134-5p-inhibitor transfection did not affect the luciferase activity in the MUT-TNN-AS1 transfected cells. Moreover, compared with HT29 cells transfected with miR-134-5p-NC, the miR-134-5p-mimic transfection significantly decreased the expression of TTN-AS1 and p21-activated kinase 3 (PAK3) while miR-134-5p transfection significantly increased their expression (Figure3c). PAK3 protein expression increased in HT29 cells after they were exposed to a 4 Gy X-ray dose for 24 hr. Moreover, TTN-AS1 knockdown significantly decreased the PAK3 protein expression and TTN- AS1 overexpression significantly increased the expression of that protein with or without X-ray treatment (Figure4a,b). However, TTN-AS1 knockdown and overexpression significantly decreased or increased, respectively, the expression of cyclin-dependent kinase inhibitor 1A (P21) in HT29 cells, only after exposition to a 4 Gy X-ray dose for 24 hr (Figures4aand4c). Without X-ray treatment, P21 protein expression in HT29 cells was very low and did not show significant changes after regulating TTN-AS1 expression. The knockdown of P21 expression by si-P21 transfection caused a decrease in protein expression only in X-ray treated cells as the absence of protein expression was verified in non-X-ray exposed cells (Figure4d).	32749739	RID04564	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Large intestine cancer	TTN-AS1	CDKN1A	positively-E	siRNA;knockdown;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	radiosensitivity;apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Intestinal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000124762	NA	100506866	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human large intestine cancer cells through the P21 pathway and AKT/GSK-3beta/beta-catenin pathway.TTN-AS1 expression was increased in SW620 and HT29 cells after X-ray treatment for 24 hr. Remarkably, the higher the X-ray dose, the greater the TTN-AS1 expression. The expression of TTN-AS1 in large intestine cancer cells that were exposed to a 4 Gy dose was significantly higher than in those that were exposed to a 2 Gy dose (Figure1a). Then, the TTN-AS expression in SW620 and HT29 cells was regulated by si-TTN-AS1 and up-TTN-AS1 transfection. In fact, si- TTN-AS1 and up-TTN-AS1 transfection was able to knockdown the expression and overexpress TTN-AS1, respectively, both in SW620 and HT29 cells (Figure1b).The knockdown of TTN-AS1 expression using si-TTN-AS1 transfection significantly increased the miR-134-5p expression, whereas TTN-AS1 overexpression induced by up-TTN-AS1 transfection significantly decreased its expression in large intestine cancer cells (Figure3a). In addition, dual-luciferase reporter assay results suggested that, in the WT-TNN-AS1 transfected cells, miR-134-5p- mimic transfection significantlydecreased the luciferase activity, while miR-134-5p-inhibitor transfection significantly increased it, compared with miR-134-5p-NC transfected HT29 cells (Figure3b). However, miR-134-5p-mimic and miR-134-5p-inhibitor transfection did not affect the luciferase activity in the MUT-TNN-AS1 transfected cells. Moreover, compared with HT29 cells transfected with miR-134-5p-NC, the miR-134-5p-mimic transfection significantly decreased the expression of TTN-AS1 and p21-activated kinase 3 (PAK3) while miR-134-5p transfection significantly increased their expression (Figure3c). PAK3 protein expression increased in HT29 cells after they were exposed to a 4 Gy X-ray dose for 24 hr. Moreover, TTN-AS1 knockdown significantly decreased the PAK3 protein expression and TTN- AS1 overexpression significantly increased the expression of that protein with or without X-ray treatment (Figure4a,b). However, TTN-AS1 knockdown and overexpression significantly decreased or increased, respectively, the expression of cyclin-dependent kinase inhibitor 1A (P21) in HT29 cells, only after exposition to a 4 Gy X-ray dose for 24 hr (Figures4aand4c). Without X-ray treatment, P21 protein expression in HT29 cells was very low and did not show significant changes after regulating TTN-AS1 expression. The knockdown of P21 expression by si-P21 transfection caused a decrease in protein expression only in X-ray treated cells as the absence of protein expression was verified in non-X-ray exposed cells (Figure4d).	32749739	RID04565	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Diabetic retinopathy	OIP5-AS1	MYC	positively-E	luciferase reporter assay;miRcode;TargetScan;miRTarBase;miRDB	downregulation	qRT-PCR	GSE122189	NA	cell viability(-)	ceRNA(miR-449c)	regulation	NA	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000136997	NA	729082	4609	cyrano|linc-OIP5	bHLHe39|c-Myc|MYCC	Integrative analysis of competitive endogenous RNA network reveals the regulatory role of non-coding RNAs in high-glucose-induced human retinal endothelial cells.We selected the top 5 DE lncRNAs and hub genes as candidate RNAs and verified their expression levels using the qRT-PCRmethod. The results suggested that ZNRD1-AS1, MEG3, OIP5-AS1, TPTEP1, MYC and SQSTM1 were significantly decreased and MAPK1 was significantly increased in the HG group (Figs. 6A and -and6B6B). Next, we discovered that the expressions of lncRNA OIP5-AS1 and the hub gene MYC were the most significantly down-regulated genes, and that miR-449c was the common target of both genes. We performed miR-449c expression verification and found that its expression was increased in the HG group (Fig. 6C). Finally, we performed a luciferase reporter assay to confirm that miR-449c was a common target of both genes and reconstructed a key ceRNA subnetwork (OIP5-AS1/miR-449c/MYC) (Fig. 7).We tested the levels of miR-449c in the HG transfection miR-449c inhibitor group and HG transfection inhibitor NC group by qRT-PCRto ensure that the miR-449c inhibitor effectively reduced the expression of miR-449c in HRECs. The results showed that miR-449c in the HG transfection miR-449c inhibitor group was significantly lower than in the NG, HG and HG transfection inhibitor NC groups at 48 h, respectively. The levels of miR-449c in the HG group and HG transfection inhibitor NC group were higher than that in the NG group at 48 h (Fig. 8A). The expressions of OIP5-AS1 and MYC were measured by qRT-PCRto determine the levels of lncRNA OIP5-AS1 and hub gene MYC regulated by miR-449c in vitro. The results showed that OIP5-AS1 and MYC in the HG transfection miR-449c inhibitor group were significantly higher than in the NG, HG and HG transfection inhibitor NC groups at 48 h, respectively. The OIP5-AS1, MYC in the HG group, and HG transfection inhibitor NC group were lower than in the NG group at 48 h (Figs. 8B and -and8C8C).The viability and apoptosis of HRECs affected by miR-449c were analyzed by CCK-8 analysis and flow cytometry, respectively, to investigate the in-vitro biological behavior of miR-449c-regulated HRECs. The results showed that the cell viability of the HG group, HG transfection inhibitor NC group, and HG transfection miR-449c inhibitor group were all lower than that of the NG group at 12, 24 and 48 h. The cell viability of HRECs in the HG transfection miR-449c inhibitor group under hyperglycemic culture conditions was significantly greater than that of HRECs in the HG group and the HG transfection inhibitor NC group at 24 and 48 h. However, the cell viability of the three HG groups was not statistically significant at 6 and 12 h (Fig. 9A). Similarly, the cell apoptosis of the HG group, HG transfection inhibitor NC group and HG transfection miR-449c inhibitor group were all higher than that of the NG group at 48 h. Cell apoptosis of HRECs in the HG transfection miR-449c inhibitor group under hyperglycemic culture conditions was significantly lower than that of HRECs in the HG group and HG transfection inhibitor NC group at 48 h, respectively. However, cell apoptosis of HRECs in the HG group and HG transfection inhibitor NC group was not statistically significant at 48 h (Figs. 9B and -and9C9C).The ceRNA network was screened using intersecting prediction results from miRcode, TargetScan, miRTarBase and miRDB. The results showed that the cell viability of the HG group, HG transfection inhibitor NC group, and HG transfection miR-449c inhibitor group were all lower than that of the NG group at 12, 24 and 48 h.	32655995	RID04566	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 6D).	32321151	RID04567	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 6D).	32321151	RID04568	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-370-3p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 6D).	32321151	RID04569	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-620)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 7D).	32321151	RID04570	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-620)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 8D).	32321151	RID04571	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-620)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 9D).	32321151	RID04572	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-665)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 10D).	32321151	RID04573	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-665)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 11D).	32321151	RID04574	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-665)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 12D).	32321151	RID04575	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-1270)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 13D).	32321151	RID04576	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-1270)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 14D).	32321151	RID04577	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-1270)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 15D).	32321151	RID04578	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-3064-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 16D).	32321151	RID04579	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-3064-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 17D).	32321151	RID04580	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-3064-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 18D).	32321151	RID04581	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS2	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-6504-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111335	NA	378938	4939	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 19D).	32321151	RID04582	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OAS3	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-6504-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111331	NA	378938	4940	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 20D).	32321151	RID04583	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Systemic lupus erythematosus	MALAT1	OASL	positively-E	knockdown;PITA;RNA22;miRmap;mircoT;miRanda;PicTar;Targetscan	upregulation	RT-qPCR	GSE10325	NA	inflammatory response(+)	ceRNA(miR-6504-5p)	regulation	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135114	NA	378938	8638	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OASL1|p59OASL|TRIP14	MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.To confirm the data of OAS2, OAS3, and OASL from the GSE10325 data set, we performed a PCR assay in PBMCs, CD19+ B, and CD4+ T cells in patients with active SLE and healthy participants. OAS2, OAS3, and OASL were up-regulated in PBMCs in active SLE patients compared to healthy participants (P<0.05, Figure 2). OASL expression in CD19+ B cells showed no significant difference between active SLE patients and healthy participants, but OAS2 and OAS3 expression in CD19+ B were notably up-regulated in active SLE patients (P<0.05). CD4+ T cells from active SLE patients showed increased expression of all OAS2, OAS3, and OASL compared to healthy participants (P<0.05).To confirm the regulatory effect of MALAT1 on OAS2, OAS3, and OASL, we knocked down MALAT1 in CD4+ T cells. PCR analysis showed that OAS2, OAS3, and OASL expression was also decreased with knockdown (P<0.05, Figure 3E). We also evaluated the correlation of MALAT1 with OAS2, OAS3, and OASL in their expression in PBMCs cells, CD19+ B cells, and CD4+ T cells from SLE patients. OAS2, OAS3, and OASL expression had no correlation with that of MALAT1 in PBMCs cells (Figure 4). However, OAS2 expression in CD19+ B cells as well as OAS3 and OASL expression in CD4+ T cells were positively correlated with MALAT1 expression in these cells (P<0.05).Treatment with IFN-alpha-2a increased MALAT1 expression in CD4+ T cells, but transfection with siRNA-MALAT1 before IFN-alpha-2a treatment conversely down-regulated MALAT1 expression (P<0.01 vs IFN-alpha-2a treatment group, Figure 6A). The down-regulation of MALAT1 attenuated the increase of OAS2 (P<0.05), OAS3 (P<0.05), and OASL (P<0.05) expression caused by IFN-alpha-2a (Figure 6B). To determine the role of OAS2, OAS3, and OASL in IFN-alpha-2a-mediated inflammation, we silenced them alone in CD4+ T cells (P<0.01, Figure 6C). Depletion of MALAT1, OAS2, OAS3, and OASL decreased TNF-alpha (P<0.05, P<0.01) and IL-1beta (P<0.05, P<0.01) expression in CD4+ T cells upon IFN-alpha-2a treatment, while it had no effect on IFNalpha expression (Figure 21D).	32321151	RID04584	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE111842,GSE86978)
Cataract	CDKN2B-AS1	miR-21	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell injury(+)	NA	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Cataract	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000199004	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	Long non-coding RNA ANRIL alleviates H 2 O 2-induced injury by up-regulating microRNA-21 in human lens epithelial cells.In the in vivo experiment, we found that in contrast with normal tissues, lncRNA ANRIL and miR-21 had low expression level in cataract patient tissues (P < 0.05 or P < 0.01, Figure 7A, -,7B).7B). Those data further demonstrated that H2O2 stimulation caused same results with the in vivo assay in which lncRNA ANRIL and miR-21 were down-regulated.In Figure 2A, the expression level of lncRNA ANRIL in cells transfected with pc-ANRIL was observably higher than that in cells transfected with pcDNA3.1 (P < 0.01), suggesting that lncRNA ANRIL was overexpressed successfully after cell transfection. Then, transfected or untransfected HLEC SRA01/04 cells were treated with H2O2, and cell injury was evaluated. Results showed that H2O2-induced cell injury was alleviated by overexpression of lncRNA ANRIL, presenting increased cell viability (P < 0.05, Figure 2B), down-regulated p53 as well as up-regulated cyclinD1 and CDK4 (all P < 0.05, Figure 2C, -,2D),2D), also the decreased apoptotic cells (P < 0.05, Figure 2E, -,2F),2F), and down-regulated Bax and cleaved caspase-3 as well as up-regulated Bcl-2 (Figure 2G), when compared to the H2O2 + pcDNA3.1 group. Results indicated that lncRNA ANRIL might attenuate H2O2-induced cell injury in HLECs.Moreover, lncRNA ANRIL silencing vector was constructed, leading to down-regulation of lncRNA ANRIL (P < 0.001, Figure 3E). Silencing lncRNA ANRIL inhibited miR-21 (P < 0.01, Figure 3F), while H2O2 induction down-regulated the expression of lncRNA ANRIL (P < 0.001) and inhibited miR-21 (P < 0.01) (Figure 3G), representing the close involvement of miR-21 and lncRNA ANRIL in the regulation of H2O2 damage.The involvements of AMPK and beta-catenin in lncRNA ANRIL-associated modulation were finally investigated. In Figure 6A, -,6B,6B, phosphorylated levels of AMPK were significantly up-regulated by H2O2 stimulation (P < 0.05), and the up-regulation was further increased by lncRNA ANRIL overexpression (P < 0.01). In the meantime, phosphorylated levels of AMPK were significantly reduced by miR-21 inhibition relative to the H2O2 + pc-ANRIL + inhibitor-NC group (P < 0.05). The alteration of beta-catenin expression after H2O2 stimulation and ANRIL overexpression with or without miR-21 inhibition was consistent with AMPK phosphorylation (Figure 6C, -,6D).6D).Above all, results indicated that lncRNA ANRIL could activate AMPK and beta-catenin via up-regulation of miR-21. The activation of AMPK and beta-catenin promoted the antioxidant function and proliferation of cells.Overexpression of lncRNA ANRIL up-regulated miR-21 expression	32310822	RID04585	expression association	NA	UP(SKCM);DATA(GSE38495)	
Cataract	CDKN2B-AS1	PRKAA2	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell injury(+)	phosphorylated	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000162409	NA	100048912	5563	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	AMPK|AMPKa2|PRKAA	Long non-coding RNA ANRIL alleviates H 2 O 2-induced injury by up-regulating microRNA-21 in human lens epithelial cells.In the in vivo experiment, we found that in contrast with normal tissues, lncRNA ANRIL and miR-21 had low expression level in cataract patient tissues (P < 0.05 or P < 0.01, Figure 7A, -,7B).7B). Those data further demonstrated that H2O2 stimulation caused same results with the in vivo assay in which lncRNA ANRIL and miR-21 were down-regulated.In Figure 2A, the expression level of lncRNA ANRIL in cells transfected with pc-ANRIL was observably higher than that in cells transfected with pcDNA3.1 (P < 0.01), suggesting that lncRNA ANRIL was overexpressed successfully after cell transfection. Then, transfected or untransfected HLEC SRA01/04 cells were treated with H2O2, and cell injury was evaluated. Results showed that H2O2-induced cell injury was alleviated by overexpression of lncRNA ANRIL, presenting increased cell viability (P < 0.05, Figure 2B), down-regulated p53 as well as up-regulated cyclinD1 and CDK4 (all P < 0.05, Figure 2C, -,2D),2D), also the decreased apoptotic cells (P < 0.05, Figure 2E, -,2F),2F), and down-regulated Bax and cleaved caspase-3 as well as up-regulated Bcl-2 (Figure 2G), when compared to the H2O2 + pcDNA3.1 group. Results indicated that lncRNA ANRIL might attenuate H2O2-induced cell injury in HLECs.Moreover, lncRNA ANRIL silencing vector was constructed, leading to down-regulation of lncRNA ANRIL (P < 0.001, Figure 3E). Silencing lncRNA ANRIL inhibited miR-21 (P < 0.01, Figure 3F), while H2O2 induction down-regulated the expression of lncRNA ANRIL (P < 0.001) and inhibited miR-21 (P < 0.01) (Figure 3G), representing the close involvement of miR-21 and lncRNA ANRIL in the regulation of H2O2 damage.The involvements of AMPK and beta-catenin in lncRNA ANRIL-associated modulation were finally investigated. In Figure 6A, -,6B,6B, phosphorylated levels of AMPK were significantly up-regulated by H2O2 stimulation (P < 0.05), and the up-regulation was further increased by lncRNA ANRIL overexpression (P < 0.01). In the meantime, phosphorylated levels of AMPK were significantly reduced by miR-21 inhibition relative to the H2O2 + pc-ANRIL + inhibitor-NC group (P < 0.05). The alteration of beta-catenin expression after H2O2 stimulation and ANRIL overexpression with or without miR-21 inhibition was consistent with AMPK phosphorylation (Figure 6C, -,6D).6D).Above all, results indicated that lncRNA ANRIL could activate AMPK and beta-catenin via up-regulation of miR-21. The activation of AMPK and beta-catenin promoted the antioxidant function and proliferation of cells.	32310822	RID04586	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807)
Cataract	CDKN2B-AS1	CTNNB1	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell injury(+)	NA	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000168036	NA	100048912	1499	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA ANRIL alleviates H 2 O 2-induced injury by up-regulating microRNA-21 in human lens epithelial cells.In the in vivo experiment, we found that in contrast with normal tissues, lncRNA ANRIL and miR-21 had low expression level in cataract patient tissues (P < 0.05 or P < 0.01, Figure 7A, -,7B).7B). Those data further demonstrated that H2O2 stimulation caused same results with the in vivo assay in which lncRNA ANRIL and miR-21 were down-regulated.In Figure 2A, the expression level of lncRNA ANRIL in cells transfected with pc-ANRIL was observably higher than that in cells transfected with pcDNA3.1 (P < 0.01), suggesting that lncRNA ANRIL was overexpressed successfully after cell transfection. Then, transfected or untransfected HLEC SRA01/04 cells were treated with H2O2, and cell injury was evaluated. Results showed that H2O2-induced cell injury was alleviated by overexpression of lncRNA ANRIL, presenting increased cell viability (P < 0.05, Figure 2B), down-regulated p53 as well as up-regulated cyclinD1 and CDK4 (all P < 0.05, Figure 2C, -,2D),2D), also the decreased apoptotic cells (P < 0.05, Figure 2E, -,2F),2F), and down-regulated Bax and cleaved caspase-3 as well as up-regulated Bcl-2 (Figure 2G), when compared to the H2O2 + pcDNA3.1 group. Results indicated that lncRNA ANRIL might attenuate H2O2-induced cell injury in HLECs.Moreover, lncRNA ANRIL silencing vector was constructed, leading to down-regulation of lncRNA ANRIL (P < 0.001, Figure 3E). Silencing lncRNA ANRIL inhibited miR-21 (P < 0.01, Figure 3F), while H2O2 induction down-regulated the expression of lncRNA ANRIL (P < 0.001) and inhibited miR-21 (P < 0.01) (Figure 3G), representing the close involvement of miR-21 and lncRNA ANRIL in the regulation of H2O2 damage.The involvements of AMPK and beta-catenin in lncRNA ANRIL-associated modulation were finally investigated. In Figure 6A, -,6B,6B, phosphorylated levels of AMPK were significantly up-regulated by H2O2 stimulation (P < 0.05), and the up-regulation was further increased by lncRNA ANRIL overexpression (P < 0.01). In the meantime, phosphorylated levels of AMPK were significantly reduced by miR-21 inhibition relative to the H2O2 + pc-ANRIL + inhibitor-NC group (P < 0.05). The alteration of beta-catenin expression after H2O2 stimulation and ANRIL overexpression with or without miR-21 inhibition was consistent with AMPK phosphorylation (Figure 6C, -,6D).6D).Above all, results indicated that lncRNA ANRIL could activate AMPK and beta-catenin via up-regulation of miR-21. The activation of AMPK and beta-catenin promoted the antioxidant function and proliferation of cells.	32310822	RID04587	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ischemic stroke	DANCR	XBP1s	positively-E	luciferase reporter assay;overexpression		qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);angiogenesis(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-33a-5p)	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	LncRNA DANCR attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through regulating of miR-33a-5p/XBP1s.From the results (Figure 2B), it can be concluded that BMECs were successfully transfected with DANCR and at a higher rate than that of the OGD-treated BMECs transfected with the negative control (ov-NC). Next, MTS assay showed that cell viability of the DANCR group was significantly increased compared with that of the ov-NC groups, whereas that of the si-DANCR group was significantly decreased compared with that of the si-NC group (Figure 2C). It can be concluded from our results that DANCR overexpression can effectively inhibit apoptosis of OGD-treated BMECs, while silenced DANCR can effectively enhance apoptosis (Figures 2D and -and2E).2E). To further evaluate the effect of DANCR on BMECs, cell migration and tube formation assays were performed. From Figure 3A, it can be observed that the migration ability of cells in the DANCR group was much higher than that of cells in the ov-NC group, while silenced DANCR significantly decreased the migration ability. Moreover, angiogenesis was also promoted in the DANCR group and inhibited in the si-DANCR group, as shown in Figure 3B.Therefore, we chose miR-33a-5p for further experiments. The results showed that miR-33a-5p expression was the lowest at 4 h and the highest at 10 h after OGD treatment (Figure 7B). Furthermore, miR-33a-5p expression negatively correlated with DANCR and XBP1s expression (Figure 7C). Additionally, DANCR overexpression significantly inhibited miR-33a-5p expression in OGD-treated BMECs (Figure 7D). Moreover, luciferase reporter assay showed that miR-33a-5p overexpression significantly decreased the WT-XBP1-associated luciferase activity compared to that in the NC group, whereas it had no obvious effect on the luciferase activity of MUT-XBP1 compared with that in the NC group (Figure 7E). These results also showed that miR-33a-5p overexpression significantly decreased the WT-DANCR-associated luciferase activity compared with that in the NC group, whereas it had no obvious effect on the luciferase activity of MUT-DANCR compared with that in the NC group (Figure 7F).A previous study found that DANCR activates Wnt/beta-catenin signaling to promote glioma proliferation [13]. In the present study, we found that beta-catenin expression was significantly promoted by DANCR overexpression, whereas it was significantly inhibited by silencing DANCR expression in OGD-treated BMECs (Figure 12A). Additionally, beta-catenin expression was significantly inhibited in the DANCR+si-XBP1s and DANCR+miR-33a-5p mimic groups compared with the DANCR+si-NC and DANCR+NC mimic groups, respectively (Figures 12B and 12C). Finally, we found that beta-catenin expression was significantly promoted in the miR-33a-5p mimic+ov-XBP1s group compared with the miR-33a-5p mimic+ov-NC group (Figure 12D).	31986122	RID04588	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Cholangiocarcinoma	ZEB1-AS1	HOXB8	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+);cell stemness(+)	ceRNA(miR-133b)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000120068	NA	220930	3218	NA	HOX2|HOX2D	AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma and facilitates tumor stemness, proliferation and invasion through mediating miR-133b/HOXB8.The expression of ZEB1-AS1 was detected in CCA tissues by using quantitative real-time polymerase chain reaction (qRT-PCR. Results showed that ZEB1-AS1 was significantly overexpressed in CCA tissues compared with that in paired adjacent nontumor bile duct tissues (Figure 1A).For assessing proliferative ability, we performed cell counting kit-8 (CCK-8) assay. The proliferation curves displayed that knocking down ZEB1-AS1 inhibited proliferation of CCA cells in comparison with controls (Figure 2C). 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay was also carried out to measure cellular viability, and proliferation activity was suppressed in si-ZEB1-AS1 cells (Figure 2D). Afterwards, we detected clonogenic capacity of CCA cells through performing colony formation assay. As displayed in Figure 2E, silencing ZEB1-AS1 restrained colony-forming ability of QBC939 and CCLP-1 cells. More importantly, spheroid formation assay verified that ZEB1-AS1 knockdown attenuated tumor stemness in CCA cells (Figure 2F). To sum up, these findings illustrated that ZEB1-AS1 promoted malignant proliferation and tumor stemness in CCA.As confirmed by wound healing assay, cellular motility was repressed by knocking down ZEB1-AS1 in CCA cells (Figure 3A). Moreover, transwell assay was conducted to investigate metastatic ability of CCA cells in this study. As shown in Figure 3B, silencing ZEB1-AS1 reduced migratory numbers of CCA cells demonstrated through transwell assay without Matrigel. Subsequently, we confirmed that ZEB1-AS1 knockdown caused a decrease of invasive cells in transwell assay with Matrigel (Figure 3C). Studies confirmed that tumor metastasis mainly depended on EMT process [14]. Accordingly, we measured the epithelial and mesenchymal markers of EMT in QBC939 and CCLP-1 cells via western blot. Results confirmed that knocking down ZEB1-AS1 decreased snail and vimentin expression, whereas E-cadherin expression was increased in CCA cells (Figure 3D). In summary, ZEB1-AS1 contributed to migration and invasion of CCA cells in part by promoting EMT. In addition, miR-133b expression was also assessed in CCA cells, and the result was consistent with detection in tumor tissues (Figure 5E). Subsequently, dual luciferase reporter gene assays were conducted to demonstrate the binding of ZEB1-AS1 to miR-133b through cloning miR-133b-binding site region of ZEB1-AS1 sequence into luciferase reporter plasmids, including ZEB1-AS1 wild type and mutant type (Figure 5F). As expected, upregulated miR-133b caused by cotransfected with miR-133b mimics suppressed luciferase activity of ZEB1-AS1 wild type rather than mutant type (Figure 5G), suggesting that ZEB1-AS1 bound to miR-133b through the binding site. RNA immunoprecipitation (RIP) assays were performed for further verifying their target binding. Results displayed that ZEB1-AS1 enrichment was higher in Argonaute 2 (AGO2) groups with miR-133b mimics than controls (Figure 5H). Above findings elucidated that ZEB1-AS1 inhibited miR-133b by serving as a sponge in CCA cells.The qRT-PCRanalysis revealed that upregulated miR-133b restrained HOXB8 expression both at mRNA and protein levels (Figure 6A, -,6B).6B). HOXB8 mRNA expression was markedly increased in CCA tissues and inversely related to miR-133b expression (r = -0.4227, P < 0.01; Figure 6C, -,6D).6D). Furthermore, both mRNA and protein of HOXB8 were overexpressed in CCA cells (Figure 6E, -,6F).6F). Luciferase reporter assays confirmed that upregulated miR-133b repressed luciferase activity of HOXB8 wild type, while luciferase activity of HOXB8 mutant type was not significantly affected (Figure 6G, -,6H).6H). In addition, AGO2 RIP assays further confirmed that miR-133b enriched HOXB8 mRNA in CCA cells (Figure 6I). Overall, miR-133b repressed HOXB8 in CCA cells by interacting with the binding site of HOXB8 3'UTR.Finally, the effect of ZEB1-AS1/miR-133b/HOXB8 in nude mice was investigated via subcutaneous tumor formation experiments. As shown in Figure 8A'-D, knocking down ZEB1-AS1 not only depressed tumor volumes throughout the course of cancer growth, but also remarkably inhibited tumor weights. Notably, the inhibitory effect caused by silencing ZEB1-AS1 was partly rescued through miR-133b knockdown. HOXB8 expression in xenograft tumors was detected via qRT-PCRand western blot. Results displayed that HOXB8 expression was restrained both at mRNA and protein levels by silencing ZEB1-AS1. More importantly, restoration of miR-133b expression saved the downexpression of HOXB8 generated through ZEB1-AS1 knockdown (Figure 8E, -,8F).8F). These findings indicated that ZEB1-AS1 promoted tumor growth of CCA by regulating miR-133b/HOXB8 not only in vitro but also in vivo.	31978895	RID04589	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	
Hypertension	MALAT1	BMPR2	positively-E	luciferase reporter assay;TargetScan	downregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(has-miR-539-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204217	NA	378938	659	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BMPR-II|BMPR3|BRK-3|PPH1|T-ALK	Correlation Between Single Nucleotide Polymorphisms of the rs664589 Locus in the Long-Chain Noncoding RNA Lung Adenocarcinoma Metastasis-Associated Gene 1, Hypertension, and Its Mechanism.We analyzed the correlation between the SBP and DBP in different MALAT1 gene rs664589 locus genotypes. The results showed that the SBP and DBP were significantly higher in patients with the G allele than those with the C allele (p-<-0.01; Fig. 1).We detected the expression levels of lncRNA MALAT1, hsa-miR-539-3p, and hsa-miR-485-3p in the plasma of participants by qRT-PCR We found that lncRNA MALAT1 was lower in the plasma of patients with hypertension compared with that in the controls (Fig. 2A), while the hsa-miR-539-3p and hsa-miR-485-3p were higher in the plasma of patients with hypertension compared with that in the controls (Fig. 2B, C). We found that there were targeted binding sites for hsa-miR-539-3p and hsa-miR-485-3p on MALAT1 (Fig. 5A), and there were targeted binding sites for the hsa-miR-539-3p and hsa-miR-485-3p on the 3'UTR of the BMPR2 through the TargetScan 3.1 online prediction software (Fig. 5B). In 293T cells after cotransfection of hsa-miR-539-3p or hsa-miR-485-3p with MALAT1 WT or MALAT1 MT, the dual-luciferase reporter assay revealed that in the MALAT1 group, the dual luciferase activity was significantly decreased in the hsa-miR-539-3p mimic and hsa-miR-485-3p mimic groups compared with that in the hsa-miR-539-3p NC and hsa-miR-485-3p NC groups. However, the dual luciferase activity was significantly increased in the hsa-miR-539-3p inhibitor and hsa-miR-485-3p inhibitor groups compared with that in the hsa-miR-539-3p NC and hsa-miR-485-3p NC groups (p-<-0.05; Fig. 5C, D). These findings indicated that hsa-miR-539-3p and hsa-miR-485-3p are targets of MALAT1 WT, not targets of MALAT1 MT.	32109146	RID04590	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE51827,GSE86978)
Hypertension	MALAT1	BMPR2	positively-E	luciferase reporter assay;TargetScan	downregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(has-miR-485-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204217	NA	378938	659	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BMPR-II|BMPR3|BRK-3|PPH1|T-ALK	Correlation Between Single Nucleotide Polymorphisms of the rs664589 Locus in the Long-Chain Noncoding RNA Lung Adenocarcinoma Metastasis-Associated Gene 1, Hypertension, and Its Mechanism.We analyzed the correlation between the SBP and DBP in different MALAT1 gene rs664589 locus genotypes. The results showed that the SBP and DBP were significantly higher in patients with the G allele than those with the C allele (p-<-0.01; Fig. 1).We detected the expression levels of lncRNA MALAT1, hsa-miR-539-3p, and hsa-miR-485-3p in the plasma of participants by qRT-PCR We found that lncRNA MALAT1 was lower in the plasma of patients with hypertension compared with that in the controls (Fig. 2A), while the hsa-miR-539-3p and hsa-miR-485-3p were higher in the plasma of patients with hypertension compared with that in the controls (Fig. 2B, C). We found that there were targeted binding sites for hsa-miR-539-3p and hsa-miR-485-3p on MALAT1 (Fig. 5A), and there were targeted binding sites for the hsa-miR-539-3p and hsa-miR-485-3p on the 3'UTR of the BMPR2 through the TargetScan 3.1 online prediction software (Fig. 5B). In 293T cells after cotransfection of hsa-miR-539-3p or hsa-miR-485-3p with MALAT1 WT or MALAT1 MT, the dual-luciferase reporter assay revealed that in the MALAT1 group, the dual luciferase activity was significantly decreased in the hsa-miR-539-3p mimic and hsa-miR-485-3p mimic groups compared with that in the hsa-miR-539-3p NC and hsa-miR-485-3p NC groups. However, the dual luciferase activity was significantly increased in the hsa-miR-539-3p inhibitor and hsa-miR-485-3p inhibitor groups compared with that in the hsa-miR-539-3p NC and hsa-miR-485-3p NC groups (p-<-0.05; Fig. 5C, D). These findings indicated that hsa-miR-539-3p and hsa-miR-485-3p are targets of MALAT1 WT, not targets of MALAT1 MT.	32109146	RID04591	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	HAND2-AS1	ROCK2	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000134318	NA	79804	9475	DEIN|NBLA00301|UPH	ROCK-II	lncRNA HAND2-AS1 mediates the downregulation of ROCK2 in hepatocellular carcinoma and inhibits cancer cell proliferation, migration and invasion.The present study first detected the expression of HAND2-AS1 and ROCK2 in the serum of all 3 groups of participants. Results showed that serum levels of HAND2-AS1 were significantly downregulated (P<0.05; Fig. 1A), while serum levels of ROCK2 were significantly increased (P<0.05; Fig. 1B) in HCC patients compared with in HB patients and healthy controls. However, no significant differences in serum levels of HAND2-AS1 and ROCK2 were found between HB patients and healthy controls. It is worth noting that, HAND2-AS1 expression levels decreased, while ROCK2 expression levels increased with the increase of clinical stages, however the changes were not statistically significant (data not shown).In this experiment, the control (C) group was the untransfected cells and the negative control (NC) group was the cells transfected with empty vectors. Compared with C and NC, HAND2-AS1 overexpression led to significantly inhibited ROCK2 expression in cells of SNU-398 human HCC cell line (P<0.05) but not in cells of THLE-3 human normal liver epithelial cell line (Fig. 4A). In contrast, ROCK2 overexpression did not significantly affect HAND2-AS1 expression in cells of those two cell lines (Fig. 4B).In this experiment, the control group was the untransfected cells and NC group was the cells transfected with empty vectors. Compared with C (untransfected cells) and NC (empty vector transfection), HAND2-AS1 overexpression significantly inhibited, while ROCK2 overexpression significantly promoted the proliferation (P<0.05; Fig. 5A), migration (P<0.05; Fig. 5B) and invasion (P<0.05; Fig. 5C) of SNU-398 human HCC cell line, but not cells of THLE-3 human normal liver epithelial cell line. In addition, compared with SNU-398 cells with HAND2-AS1 overexpression only, SNU-398 cells with both HAND2-AS1 and ROCK2 overexpression showed significantly promoted proliferation (P<0.05; Fig. 5A), migration (P<0.05; Fig. 5B) and invasion (P<0.05; Fig. 5C).	31922232	RID04592	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Cerebral ischemia-reperfusion injury	SNHG1	miR-424	negatively-F	dual-luciferase reporter assay;StarBase	upregulation	RT-qPCR	NA	NA	apoptosis process(+);mitochondrial function(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Knockdown of lncRNA SNHG1 alleviates oxygen-glucose deprivation/reperfusion-induced cell death by serving as a ceRNA for miR-424 in SH-SY5Y cells.First, we assessed cell viability by MTT assay and observed that 6 h of OGD followed by 24 h of reperfusion resulted in a significant decrease in the viability of SH-SY5Y cells (Figure 1(a)). In addition, as determined byflow cytometric analysis, the number of SH-SY5Y cells undergoing apoptosis was also remarkably increased upon OGD/R treatment (Figure 1(b)). RTqPCR analysis was then carried out to indicate that SNHG1 was markedly overexpressed in OGD/ R-treated SH-SY5Y cells (Figure 1(c)).As measured by RT-qPCR analysis, SNHG1 expression was successfully knocked down by transfection with si-SNHG1 in OGD/R-treated SHSY5Y cells (Figure 2(a)). We further observed that knockdown of SNHG1 largely increased the viability and decreased the apoptosis of OGD/R-treated SHSY5Y cells (Figure 2(b,c)).dual-luciferase reporter assay was then carried out to confirm the prediction, and the results showed that, in SH-SY5Y cells, miR-424 mimics but not the NC significantly inhibited the luciferase activity of SNHG1-WT; however, miR-424 mimics did not obviously alter the luciferase activity of SNHG1MUT (Figure 3(b)). The loss of MMP is regarded as a vital event during cellapoptosis. Through JC-1 staining, we confirmed that the impaired MMP in OGD/R-treated SH-SY5Y cells was ameliorated by SNHG1 knockdown, but this effect was diminished by co-transfection with miR424 inhibitor (Figure 5(a)). Also, co-transfection with miR-424 inhibitor blocked the inhibitory effect of SNHG1 knockdown on the release of cytochrome c from mitochondria in OGD/R-treated SH-SY5Y cells (Figure 5(b)).Subsequently, we proposed that SNHG1 might func_x0002_tion as a ceRNA to regulate miRNAs. Through the Starbase database (http://starbase.sysu.edu.cn/index.php), miR-424 was found to potentially bind toSNHG1 with binding sites shown in Figure 3(a)	31900069	RID04593	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Cerebral ischemia-reperfusion injury	SNHG15	TP53INP1	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;StarBase	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(+);inflammatory response(+)	ceRNA(miR-455-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000164938	NA	285958	94241	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	DKFZp434M1317|FLJ22139|P53DINP1|SIP|Teap|TP53INP1A|TP53INP1B	LncRNA SNHG15 Knockdown Protects Against OGD/R-Induced Neuron Injury by Downregulating TP53INP1 Expression via Binding to miR-455-3p.	33528807	RID04594	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	LINC00426	MIR4319	negatively-F	RNA pull-down assay;miRcode	upregulation	RT-PCR	NA	NA	chemoresistance(+);prognosis;cell viability(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	Doxorubicin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000238121	GRCh38_13:30340267-30377145	ENSG00000265957	NA	100188949	100422829	NA	NA	Long non-coding RNA LINC00426 contributes to doxorubicin resistance by sponging miR-4319 in osteosarcoma.We first determined the relative expression of LINC00426 in three established doxorubicin-resistant OS cell lines in comparison with the sensitive parental cells. As shown in Fig. 1a, dramatic increases of LINC00426 transcript were observed in all of three cell lines, which indicated the intimate linkage between high abundance of LINC00426 with doxorubicin resistance at least in vitro. The up-regulation of LINC00426 in OS patients was further confirmed in 50 paired OS clinical samples (Fig. -(Fig.1b).1b).Two independent siRNAs were employed to specifically silenced LINC00426 in both MG63/DXR and KHOS/DXR cells, and the knockdown efficiency was experimentally confirmed by real-time PCR (Fig. 2a). Cell viability measured with CCK-8 kit unambiguously was greatly compromised by LINC00426 depletion in both cells (Fig. -(Fig.2b,2b, c). Furthermore, the cell proliferation was significantly suppressed by LINC00426-specific siRNAs in both cell lines as well in comparison with scrambled negative control (Fig. -(Fig.2d).2d). Most importantly, the relative sensitivity to doxorubicin was markedly restored upon LINC00426 knockdown as indicated by the decrease of IC50 value (Fig. -(Fig.2e),2e), which was accompanied by the remarkable increase of caspase-3 activity in LINC00426-deficient cells (Fig. -(Fig.2f).2f). Therefore, our data clearly demonstrated that LINC00426-silencing fundamentally contributed to the re-sensitization of resistant cells to doxorubicin treatments.To interrogate the potentially regulatory effects of miR-4319 on LINC00426, we constructed LINC00426-fused luciferase reporter plasmids. Co-transfection with miR-4319 greatly suppressed the LINC00426-driven luciferase activity in MG63/DXR cells in comparison with negative control, which was readily abolished by the mutation introduced into the putative recognizing site in LINC00426 transcript (Fig. -(Fig.3b).3b). Similar observation was confirmed in KHOS/DXR cells as shown in Fig. -Fig.3c.3c. The binding between LINC00426 and miR-4319 was directly analyzed by pull-down assay with biotin-labelled probes. As shown in Fig. -Fig.3d3d and e, remarkable enrichments of both LINC00426 and miR-4319 were observed with antisense DNA probe other than sense DNA probe in both cell lines. Reciprocally, LINC00426 transcripts were significantly enriched in the miR-4319 pull-down complex in comparison with biotin-labelled negative control (Fig. -(Fig.3f).3f). We further noticed that endogenous miR-4319 was greatly up-regulated in LINC00426-deficient cells and inhibited by exogenously introduced LINC00426 expression (Fig. -(Fig.3g,3g, h). Taken together, we provided evidences in support of the sponging function of LINC00426 against miR-4319 in osteosarcoma.Although we demonstrated the sponging function of LINC00426 against miR-4319 and improving effects of miR-4319 on Dox resistance in OS cells, whether miR-4319 predominantly contributed to doxorubicin resistance downstream LINC00426 was still to be addressed. To this end, we specifically inhibited miR-4319 in the LINC00426-deficient cells, the relative expression of miR-4319 in this scenario was validated by real-time PCR (Fig. 5a). The compromised cell viability elicited by LINC00426 deficiency was almost completely restored by miR-4319-inhibitor in both MG63/DXR and KHOS/DXR cells (Fig. -(Fig.5b,5b, c). Similarly, the cell proliferation inhibited by si-LINC00426 was stimulated by co-transfection with miR-4319-inhibitor (Fig. -(Fig.5d).5d). Further analysis demonstrated that miR-4319 inhibition in the LINC00426-silenced cells remarkably increased IC50 value of Dox, which suggested the re-occurrence of drug resistance under this condition (Fig. -(Fig.5e).5e). Consistently, the activation of caspase-3 was dramatically suppressed by miR-4319-inhibitor in both cell lines (Fig. -(Fig.5f).5f). Taken together, our data indicated that LINC00426 promoted Dox resistance in OS via sponging miR-4319.To better understand the mechanistic involvements of LINC00426 in osteosarcoma, we next employed the bioinformatic tool miRcode (http://www.mircode.org/mircode) to predict and discover the possible target microRNA of LINC00426.	32620145	RID04595	ceRNA or sponge	chemoresistance,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Hepatocellular carcinoma	lincNMR	YBX1	positively-E	luciferase reporter assay;RBPmap	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000065978	NA	NA	4904	NA	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer.To identify long noncoding RNAs (lncRNAs) deregulated in hepatocellular carcinoma (HCC), lncRNA expression was analyzed genome-wide based on the TCGA RNA sequencing dataset of liver cancer patients (tumor-=-200 samples, normal-=-50 samples). Out of 12,727 annotated lncRNAs in the TANRIC liver cancer dataset32, 217 lncRNAs were found to be significantly (P-<-0.05) induced by at least fivefold (median tumor/normal). In total, 49 lncRNAs were selected based on their genomic location, repeat content, pseudogene content, and association with clinical properties, and their expression was validated in nine liver cancer cell lines (Supplementary Data 1). Nine expressed lncRNAs were further selected based on expression levels, coding potential, and novelty for RNAi-based phenotypic analysis using siPOOLs33. Among these candidates, the uncharacterized transcript RP6-65G23.3 yielded the strongest decrease of cell viability as determined by ATP content measurement in liver cancer cells, comparable with the effect of PLK134 or HULC35 knockdown (Fig. 1a). For reasons described below, we named this lncRNA lincNMR (long intergenic noncoding RNA-nucleotide metabolism regulator).To elucidate the cellular function of lincNMR, we depleted lincNMR using two independent siPOOLs for additional specificity and to exclude any off-target effects observed with single siRNAs33 in multiple cancer cell lines. Both siPOOLs knocked down lincNMR efficiently in multiple liver (Supplementary Fig. 2a), breast (Supplementary Fig. 2b), and lung (Supplementary Fig. 2c) cancer cell lines. Since lincNMR knockdown decreased cell viability in liver cancer cells (Fig. 1a), cell proliferation was determined by performing BrdU incorporation assays. LincNMR silencing with two independent siPOOLs resulted in 30'-0% decrease in cell proliferation in four liver cancer cell lines (HLE, HLF, SNU-387, and FLC-4) (Fig. 1b). Depletion of lincNMR also impaired cell proliferation in three breast (MCF-7, KPL-1, and T47D) (Supplementary Fig. 2d) and three lung (A549, NCI-H460, and NCI-H1299) cancer cell lines (Supplementary Fig. 2e). The overexpression of lincNMR rescued the proliferation defect caused by lincNMR depletion attesting to its specificity (Fig. 1c). Furthermore, a cell cycle analysis using flow cytometry confirmed an increase of cells in the G0/G1 phase of the cell cycle after depletion of lincNMR in multiple cell lines (Figs. 1d and Supplementary S2f, g).The arrest of cells in the G0 / G1 phase prompted us to evaluate the induction of senescence. Depletion of lincNMR triggered senescence in three liver cancer cells with two independent siPOOLs as evident by beta-GAL-positive blue cells in SA-beta-GAL assay (Fig. 1e, f). The induction of senescence was supported by the induction of the pro-inflammatory cytokines IL-1a and IL-1b, which are bona fide markers of the senescence-associated secretary phenotype (SASP) as well as the senescence-associated proteins EDN and IGFBP7 (Fig. 1g). The direct interaction of lincNMR and YBX1 protein prompted us to assess the activity of YBX1 upon lincNMR depletion using luciferase assays for YBX1 transactivational activity. Knockdown of lincNMR significantly decreased the YBX1 activity in two independent liver cancer cell lines (Fig. 3f). In turn, overexpression of YBX1 partially rescued the proliferation deficit caused by lincNMR knockdown (Fig. 3g). Together, these data show that lincNMR interacts with and regulates YBX1, YBX1 mimics the impact of lincNMR on cell proliferation, and the regulation of lincNMR by YBX1 generates a feedforward loop leading to the correlation of expression in liver cancer.This decrease of RRM2, TK1, and TYMS proteins after lincNMR depletion was validated by western blot (Fig. 4c) in good accordance with the independent triple-label SILAC-MS approach (Fig. 4d). In addition, a decrease of RRM2, TK1, and TYMS mRNAs was also observed after lincNMR depletion with both siPOOLs (Supplementary Fig. 5d). Since we identified lincNMR as a regulator of the transcription factor YBX1, we tested whether also YBX1 depletion would affect RRM2, TK1, and TYMS expression levels. Indeed, loss of YBX1 induced a significant decrease of RRM2, TK1, and TYMS protein levels (Fig. 4e, f) establishing the lincNMR-YBX1-RRM2 / TK1 / TYMS axis. Depletion of RRM2, TK1, and TYMS with siPOOLs significantly impaired cell proliferation mimicking the phenotype observed after lincNMR depletion (Fig. 5a) with a knockdown efficiency in the range of 95'-9% (Supplementary Fig. 5e). Similarly, the RRM2 inhibitor triapine45 induced an arrest of cell cycle progression in the G1 phase similar to lincNMR knockdown (Fig. 5b).Also, the expression of YBX1 mRNA significantly positively correlated with RRM2, TK1, and TYMS mRNA expression in 374 human hepatocellular carcinoma samples (TCGA, Fig. 6a-c). The YBX1 protein interacted with the promoter regions of the RRM2, TK1, and TYMS genes as revealed by chromatin immunoprecipitation (ChIP, Fig. 6d). Lastly, we performed luciferase assays with the promoter regions of RRM2, TK1, and TYMS fused to firefly luciferase. Knockdown of lincNMR or YBX1 significantly decreased the luciferase activity for all three promoters (Fig. 6e), further corroborating the regulatory interaction of lincNMR and YBX1 with RRM2, TK1, and TYMS.In addition, we searched for predicted RBP binding sites in the target genes using RBPmap43 and found three YBX1 sites and two SRSF3 sites (P-<-0.001) in the lincNMR transcript. UV-RIP followed by RT-qPCR validated the interaction between lincNMR RNA and YBX1 protein.	32587247	RID04596	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	lincNMR	RRM2	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);senescence(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000171848	NA	NA	6241	NA	C2orf48|FLJ25102	The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer.To identify long noncoding RNAs (lncRNAs) deregulated in hepatocellular carcinoma (HCC), lncRNA expression was analyzed genome-wide based on the TCGA RNA sequencing dataset of liver cancer patients (tumor-=-200 samples, normal-=-50 samples). Out of 12,727 annotated lncRNAs in the TANRIC liver cancer dataset32, 217 lncRNAs were found to be significantly (P-<-0.05) induced by at least fivefold (median tumor/normal). In total, 49 lncRNAs were selected based on their genomic location, repeat content, pseudogene content, and association with clinical properties, and their expression was validated in nine liver cancer cell lines (Supplementary Data 1). Nine expressed lncRNAs were further selected based on expression levels, coding potential, and novelty for RNAi-based phenotypic analysis using siPOOLs33. Among these candidates, the uncharacterized transcript RP6-65G23.3 yielded the strongest decrease of cell viability as determined by ATP content measurement in liver cancer cells, comparable with the effect of PLK134 or HULC35 knockdown (Fig. 1a). For reasons described below, we named this lncRNA lincNMR (long intergenic noncoding RNA-nucleotide metabolism regulator).To elucidate the cellular function of lincNMR, we depleted lincNMR using two independent siPOOLs for additional specificity and to exclude any off-target effects observed with single siRNAs33 in multiple cancer cell lines. Both siPOOLs knocked down lincNMR efficiently in multiple liver (Supplementary Fig. 2a), breast (Supplementary Fig. 2b), and lung (Supplementary Fig. 2c) cancer cell lines. Since lincNMR knockdown decreased cell viability in liver cancer cells (Fig. 1a), cell proliferation was determined by performing BrdU incorporation assays. LincNMR silencing with two independent siPOOLs resulted in 30'-0% decrease in cell proliferation in four liver cancer cell lines (HLE, HLF, SNU-387, and FLC-4) (Fig. 1b). Depletion of lincNMR also impaired cell proliferation in three breast (MCF-7, KPL-1, and T47D) (Supplementary Fig. 2d) and three lung (A549, NCI-H460, and NCI-H1299) cancer cell lines (Supplementary Fig. 2e). The overexpression of lincNMR rescued the proliferation defect caused by lincNMR depletion attesting to its specificity (Fig. 1c). Furthermore, a cell cycle analysis using flow cytometry confirmed an increase of cells in the G0/G1 phase of the cell cycle after depletion of lincNMR in multiple cell lines (Figs. 1d and Supplementary S2f, g).The arrest of cells in the G0 / G1 phase prompted us to evaluate the induction of senescence. Depletion of lincNMR triggered senescence in three liver cancer cells with two independent siPOOLs as evident by beta-GAL-positive blue cells in SA-beta-GAL assay (Fig. 1e, f). The induction of senescence was supported by the induction of the pro-inflammatory cytokines IL-1a and IL-1b, which are bona fide markers of the senescence-associated secretary phenotype (SASP) as well as the senescence-associated proteins EDN and IGFBP7 (Fig. 1g). The direct interaction of lincNMR and YBX1 protein prompted us to assess the activity of YBX1 upon lincNMR depletion using luciferase assays for YBX1 transactivational activity. Knockdown of lincNMR significantly decreased the YBX1 activity in two independent liver cancer cell lines (Fig. 3f). In turn, overexpression of YBX1 partially rescued the proliferation deficit caused by lincNMR knockdown (Fig. 3g). Together, these data show that lincNMR interacts with and regulates YBX1, YBX1 mimics the impact of lincNMR on cell proliferation, and the regulation of lincNMR by YBX1 generates a feedforward loop leading to the correlation of expression in liver cancer.This decrease of RRM2, TK1, and TYMS proteins after lincNMR depletion was validated by western blot (Fig. 4c) in good accordance with the independent triple-label SILAC-MS approach (Fig. 4d). In addition, a decrease of RRM2, TK1, and TYMS mRNAs was also observed after lincNMR depletion with both siPOOLs (Supplementary Fig. 5d). Since we identified lincNMR as a regulator of the transcription factor YBX1, we tested whether also YBX1 depletion would affect RRM2, TK1, and TYMS expression levels. Indeed, loss of YBX1 induced a significant decrease of RRM2, TK1, and TYMS protein levels (Fig. 4e, f) establishing the lincNMR-YBX1-RRM2 / TK1 / TYMS axis. Depletion of RRM2, TK1, and TYMS with siPOOLs significantly impaired cell proliferation mimicking the phenotype observed after lincNMR depletion (Fig. 5a) with a knockdown efficiency in the range of 95'-9% (Supplementary Fig. 5e). Similarly, the RRM2 inhibitor triapine45 induced an arrest of cell cycle progression in the G1 phase similar to lincNMR knockdown (Fig. 5b).Also, the expression of YBX1 mRNA significantly positively correlated with RRM2, TK1, and TYMS mRNA expression in 374 human hepatocellular carcinoma samples (TCGA, Fig. 6a-c). The YBX1 protein interacted with the promoter regions of the RRM2, TK1, and TYMS genes as revealed by chromatin immunoprecipitation (ChIP, Fig. 6d). Lastly, we performed luciferase assays with the promoter regions of RRM2, TK1, and TYMS fused to firefly luciferase. Knockdown of lincNMR or YBX1 significantly decreased the luciferase activity for all three promoters (Fig. 6e), further corroborating the regulatory interaction of lincNMR and YBX1 with RRM2, TK1, and TYMS.Among the strongly downregulated proteins upon lincNMR knockdown, we identified RRM2 (si-lincNMR-A-=--68%, si-lincNMR-B-=--67%), TK1 (si-lincNMR-A-=--52%, si-lincNMR-B-=--58%), and TYMS (si-lincNMR-A-=--43%, si-lincNMR-B-=--57%) and other key enzymes in nucleotide metabolism pathways (Fig. 4a, b), which were also part of the enriched gene ontology terms (Supplementary Fig. 5c).	32587247	RID04597	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	lincNMR	TYMS	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);senescence(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000176890	NA	NA	7298	NA	HsT422|TMS|TS|Tsase	The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer.To identify long noncoding RNAs (lncRNAs) deregulated in hepatocellular carcinoma (HCC), lncRNA expression was analyzed genome-wide based on the TCGA RNA sequencing dataset of liver cancer patients (tumor-=-200 samples, normal-=-50 samples). Out of 12,727 annotated lncRNAs in the TANRIC liver cancer dataset32, 217 lncRNAs were found to be significantly (P-<-0.05) induced by at least fivefold (median tumor/normal). In total, 49 lncRNAs were selected based on their genomic location, repeat content, pseudogene content, and association with clinical properties, and their expression was validated in nine liver cancer cell lines (Supplementary Data 1). Nine expressed lncRNAs were further selected based on expression levels, coding potential, and novelty for RNAi-based phenotypic analysis using siPOOLs33. Among these candidates, the uncharacterized transcript RP6-65G23.3 yielded the strongest decrease of cell viability as determined by ATP content measurement in liver cancer cells, comparable with the effect of PLK134 or HULC35 knockdown (Fig. 1a). For reasons described below, we named this lncRNA lincNMR (long intergenic noncoding RNA-nucleotide metabolism regulator).To elucidate the cellular function of lincNMR, we depleted lincNMR using two independent siPOOLs for additional specificity and to exclude any off-target effects observed with single siRNAs33 in multiple cancer cell lines. Both siPOOLs knocked down lincNMR efficiently in multiple liver (Supplementary Fig. 2a), breast (Supplementary Fig. 2b), and lung (Supplementary Fig. 2c) cancer cell lines. Since lincNMR knockdown decreased cell viability in liver cancer cells (Fig. 1a), cell proliferation was determined by performing BrdU incorporation assays. LincNMR silencing with two independent siPOOLs resulted in 30'-0% decrease in cell proliferation in four liver cancer cell lines (HLE, HLF, SNU-387, and FLC-4) (Fig. 1b). Depletion of lincNMR also impaired cell proliferation in three breast (MCF-7, KPL-1, and T47D) (Supplementary Fig. 2d) and three lung (A549, NCI-H460, and NCI-H1299) cancer cell lines (Supplementary Fig. 2e). The overexpression of lincNMR rescued the proliferation defect caused by lincNMR depletion attesting to its specificity (Fig. 1c). Furthermore, a cell cycle analysis using flow cytometry confirmed an increase of cells in the G0/G1 phase of the cell cycle after depletion of lincNMR in multiple cell lines (Figs. 1d and Supplementary S2f, g).The arrest of cells in the G0 / G1 phase prompted us to evaluate the induction of senescence. Depletion of lincNMR triggered senescence in three liver cancer cells with two independent siPOOLs as evident by beta-GAL-positive blue cells in SA-beta-GAL assay (Fig. 1e, f). The induction of senescence was supported by the induction of the pro-inflammatory cytokines IL-1a and IL-1b, which are bona fide markers of the senescence-associated secretary phenotype (SASP) as well as the senescence-associated proteins EDN and IGFBP7 (Fig. 1g). The direct interaction of lincNMR and YBX1 protein prompted us to assess the activity of YBX1 upon lincNMR depletion using luciferase assays for YBX1 transactivational activity. Knockdown of lincNMR significantly decreased the YBX1 activity in two independent liver cancer cell lines (Fig. 3f). In turn, overexpression of YBX1 partially rescued the proliferation deficit caused by lincNMR knockdown (Fig. 3g). Together, these data show that lincNMR interacts with and regulates YBX1, YBX1 mimics the impact of lincNMR on cell proliferation, and the regulation of lincNMR by YBX1 generates a feedforward loop leading to the correlation of expression in liver cancer.This decrease of RRM2, TK1, and TYMS proteins after lincNMR depletion was validated by western blot (Fig. 4c) in good accordance with the independent triple-label SILAC-MS approach (Fig. 4d). In addition, a decrease of RRM2, TK1, and TYMS mRNAs was also observed after lincNMR depletion with both siPOOLs (Supplementary Fig. 5d). Since we identified lincNMR as a regulator of the transcription factor YBX1, we tested whether also YBX1 depletion would affect RRM2, TK1, and TYMS expression levels. Indeed, loss of YBX1 induced a significant decrease of RRM2, TK1, and TYMS protein levels (Fig. 4e, f) establishing the lincNMR-YBX1-RRM2 / TK1 / TYMS axis. Depletion of RRM2, TK1, and TYMS with siPOOLs significantly impaired cell proliferation mimicking the phenotype observed after lincNMR depletion (Fig. 5a) with a knockdown efficiency in the range of 95'-9% (Supplementary Fig. 5e). Similarly, the RRM2 inhibitor triapine45 induced an arrest of cell cycle progression in the G1 phase similar to lincNMR knockdown (Fig. 5b).Also, the expression of YBX1 mRNA significantly positively correlated with RRM2, TK1, and TYMS mRNA expression in 374 human hepatocellular carcinoma samples (TCGA, Fig. 6a-c). The YBX1 protein interacted with the promoter regions of the RRM2, TK1, and TYMS genes as revealed by chromatin immunoprecipitation (ChIP, Fig. 6d). Lastly, we performed luciferase assays with the promoter regions of RRM2, TK1, and TYMS fused to firefly luciferase. Knockdown of lincNMR or YBX1 significantly decreased the luciferase activity for all three promoters (Fig. 6e), further corroborating the regulatory interaction of lincNMR and YBX1 with RRM2, TK1, and TYMS.Among the strongly downregulated proteins upon lincNMR knockdown, we identified RRM2 (si-lincNMR-A-=--68%, si-lincNMR-B-=--67%), TK1 (si-lincNMR-A-=--52%, si-lincNMR-B-=--58%), and TYMS (si-lincNMR-A-=--43%, si-lincNMR-B-=--57%) and other key enzymes in nucleotide metabolism pathways (Fig. 4a, b), which were also part of the enriched gene ontology terms (Supplementary Fig. 5c).	32587247	RID04598	expression association	NA		UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	lincNMR	TK1	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);senescence(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000167900	NA	NA	7083	NA	NA	The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer.To identify long noncoding RNAs (lncRNAs) deregulated in hepatocellular carcinoma (HCC), lncRNA expression was analyzed genome-wide based on the TCGA RNA sequencing dataset of liver cancer patients (tumor-=-200 samples, normal-=-50 samples). Out of 12,727 annotated lncRNAs in the TANRIC liver cancer dataset32, 217 lncRNAs were found to be significantly (P-<-0.05) induced by at least fivefold (median tumor/normal). In total, 49 lncRNAs were selected based on their genomic location, repeat content, pseudogene content, and association with clinical properties, and their expression was validated in nine liver cancer cell lines (Supplementary Data 1). Nine expressed lncRNAs were further selected based on expression levels, coding potential, and novelty for RNAi-based phenotypic analysis using siPOOLs33. Among these candidates, the uncharacterized transcript RP6-65G23.3 yielded the strongest decrease of cell viability as determined by ATP content measurement in liver cancer cells, comparable with the effect of PLK134 or HULC35 knockdown (Fig. 1a). For reasons described below, we named this lncRNA lincNMR (long intergenic noncoding RNA-nucleotide metabolism regulator).To elucidate the cellular function of lincNMR, we depleted lincNMR using two independent siPOOLs for additional specificity and to exclude any off-target effects observed with single siRNAs33 in multiple cancer cell lines. Both siPOOLs knocked down lincNMR efficiently in multiple liver (Supplementary Fig. 2a), breast (Supplementary Fig. 2b), and lung (Supplementary Fig. 2c) cancer cell lines. Since lincNMR knockdown decreased cell viability in liver cancer cells (Fig. 1a), cell proliferation was determined by performing BrdU incorporation assays. LincNMR silencing with two independent siPOOLs resulted in 30'-0% decrease in cell proliferation in four liver cancer cell lines (HLE, HLF, SNU-387, and FLC-4) (Fig. 1b). Depletion of lincNMR also impaired cell proliferation in three breast (MCF-7, KPL-1, and T47D) (Supplementary Fig. 2d) and three lung (A549, NCI-H460, and NCI-H1299) cancer cell lines (Supplementary Fig. 2e). The overexpression of lincNMR rescued the proliferation defect caused by lincNMR depletion attesting to its specificity (Fig. 1c). Furthermore, a cell cycle analysis using flow cytometry confirmed an increase of cells in the G0/G1 phase of the cell cycle after depletion of lincNMR in multiple cell lines (Figs. 1d and Supplementary S2f, g).The arrest of cells in the G0 / G1 phase prompted us to evaluate the induction of senescence. Depletion of lincNMR triggered senescence in three liver cancer cells with two independent siPOOLs as evident by beta-GAL-positive blue cells in SA-beta-GAL assay (Fig. 1e, f). The induction of senescence was supported by the induction of the pro-inflammatory cytokines IL-1a and IL-1b, which are bona fide markers of the senescence-associated secretary phenotype (SASP) as well as the senescence-associated proteins EDN and IGFBP7 (Fig. 1g). The direct interaction of lincNMR and YBX1 protein prompted us to assess the activity of YBX1 upon lincNMR depletion using luciferase assays for YBX1 transactivational activity. Knockdown of lincNMR significantly decreased the YBX1 activity in two independent liver cancer cell lines (Fig. 3f). In turn, overexpression of YBX1 partially rescued the proliferation deficit caused by lincNMR knockdown (Fig. 3g). Together, these data show that lincNMR interacts with and regulates YBX1, YBX1 mimics the impact of lincNMR on cell proliferation, and the regulation of lincNMR by YBX1 generates a feedforward loop leading to the correlation of expression in liver cancer.This decrease of RRM2, TK1, and TYMS proteins after lincNMR depletion was validated by western blot (Fig. 4c) in good accordance with the independent triple-label SILAC-MS approach (Fig. 4d). In addition, a decrease of RRM2, TK1, and TYMS mRNAs was also observed after lincNMR depletion with both siPOOLs (Supplementary Fig. 5d). Since we identified lincNMR as a regulator of the transcription factor YBX1, we tested whether also YBX1 depletion would affect RRM2, TK1, and TYMS expression levels. Indeed, loss of YBX1 induced a significant decrease of RRM2, TK1, and TYMS protein levels (Fig. 4e, f) establishing the lincNMR-YBX1-RRM2 / TK1 / TYMS axis. Depletion of RRM2, TK1, and TYMS with siPOOLs significantly impaired cell proliferation mimicking the phenotype observed after lincNMR depletion (Fig. 5a) with a knockdown efficiency in the range of 95'-9% (Supplementary Fig. 5e). Similarly, the RRM2 inhibitor triapine45 induced an arrest of cell cycle progression in the G1 phase similar to lincNMR knockdown (Fig. 5b).Also, the expression of YBX1 mRNA significantly positively correlated with RRM2, TK1, and TYMS mRNA expression in 374 human hepatocellular carcinoma samples (TCGA, Fig. 6a-c). The YBX1 protein interacted with the promoter regions of the RRM2, TK1, and TYMS genes as revealed by chromatin immunoprecipitation (ChIP, Fig. 6d). Lastly, we performed luciferase assays with the promoter regions of RRM2, TK1, and TYMS fused to firefly luciferase. Knockdown of lincNMR or YBX1 significantly decreased the luciferase activity for all three promoters (Fig. 6e), further corroborating the regulatory interaction of lincNMR and YBX1 with RRM2, TK1, and TYMS.Among the strongly downregulated proteins upon lincNMR knockdown, we identified RRM2 (si-lincNMR-A-=--68%, si-lincNMR-B-=--67%), TK1 (si-lincNMR-A-=--52%, si-lincNMR-B-=--58%), and TYMS (si-lincNMR-A-=--43%, si-lincNMR-B-=--57%) and other key enzymes in nucleotide metabolism pathways (Fig. 4a, b), which were also part of the enriched gene ontology terms (Supplementary Fig. 5c).	32587247	RID04599	expression association	NA		UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE111842,GSE55807,GSE67939)
Osteoarthritis	H19	miR-140-5p	negatively-E		upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Regulation of lncRNA-H19/miR-140-5p in cartilage matrix degradation and calcification in osteoarthritis.Compared with healthy tissues, the expression of H19 in OA cartilage tissue increased significantly (P<0.05, Figure 1A). T ransient transfection of si-H19 into could inhibit the expression of H19 significantly (P<0.05, Figure 1B), which could promote cell proliferation significantly and maintained for at least 72 h due to the silence of H19 (P<0.05, Figure 1C). The result of flow cytometry showed that silencing H19 by transfection of si-H19 could inhibit apoptosis significantly (P<0.05) (Figure 1D). Also, si-H19 in HC-A cells could lead to low expression of Bax and high expression of Bcl-2 (Figure 1E), with the difference statistically significant (P<0.05).Compared with healthy tissues, the expression of miR-1405p was decreased in OA cartilage tissues significantly (P<0.05, Figure 4A). It was shown that the expression of H19 and miR-140-5p was negatively correlated (r=0.98, P<0.001, Figure 4B). The expression of miR-140-5p could also be upregulated by si-H19 significantly (P<0.05, Figure 4C). The expression of miR-140-5p could be increased by transfection of miR-140-5p mimic, while it could be inhibited by transfection of miR-140-5p inhibitor (Figure 4C).	32576007	RID04600	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Thoracic aortic aneurysm	AK131850	TGFB1	negatively-E	siRNA;overexpression;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Aortic disease	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA AK131850 is downregulated in thoracic aortic aneurysm and negatively affects the levels of TGF-beta1 in aortic smooth muscle cells.The differential expression of AK131850 and TGF-b1 mRNA in TAA was analysed by measuring the expression levels of AK131850 and TGF-b1 mRNA in aortic media specimens from 60 TAA patients and 60 healthy controls. Unpairedt-test showed that, comparing to control group, levels of AK131850 expression were significantly lower in TAA group (Figure 1(A),p<.05). In contrast, levels of TGF-b1 mRNA expression were significantly overexpressed in TAA comparing to controls (Figure 1(B),p<.05).The correlations between levels of AK131850 and TGF-b1 mRNA expression were analysed by linear regression. It was observed that expression levels of AK131850 and TGF-b1 mRNA were significantly and inversely correlated across TAA samples (Figure 2(A)). In addition, levels of AK131850 and TGF-b1 mRNA were also inversely and significantly correlated across control samples (Figure 2(B)).Comparing to C and NC groups, AK131850 overexpression led to the downregulated TGF-b1 at both mRNA and protein levels (Figure 3(B),p<.05). In addition, AK131850 siRNA caused the upregulated expression of TGFb1 mRNA and protein (Figure 3(C),p<.05). RNA-IP analysis showed that TGF-b1 and AK131850 may bind each other (Figure 3(D)).Effects of transfections on the proliferation of HAOSMCs were analysed by CCK-8 assay. Comparing to C and NC groups, AK131850 overexpression resulted in promoted proliferation of HAOSMCs (Figure 4(A),p<.05). In addition, K131850 siRNA silencing led to reduced proliferation rate of HAOSMC (Figure 4(B),p<.05).	32501722	RID04601	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	TMPO-AS1	TMEFF2	positively-E	StarBase;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell metastasis(+);chemoresistance(+);epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-200c)	regulation	RNA-protein	5-fluorouracil	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000144339	NA	100128191	23671	NA	CT120.2|HPP1|TENB2|TPEF|TR	Roles of a TMPO-AS1/microRNA-200c/TMEFF2 ceRNA network in the malignant behaviors and 5-FU resistance of ovarian cancer cells.Subsequently, we downloaded the expression of lncRNA TMPO-AS1 in 414 patients with OC and normal ovarian tissues in GTEx database through Xena platform (Fig. 1E). We found that lncRNA TMPO-AS1 had significant higher expression in OC tissues.Then, we detected the role of TMPO-AS1 in the resistance of SKOV3 cells to 5-FU. The parental SKOV3 cells transfected with overexpression vector containing TMPO-AS1 showed augmented resistance to 5-FU while the SKOV3/5-FU cells transfected with siRNAs targeted TMPOAS1 showed weakened resistance to 5-FU (Fig. 2A). Later, we detected the epithelial-mesenchymal transition (EMT)-related protein expression of the cells. TMPO-AS1 knockdown inhibited the EMT of the SKOV3/5-FU cells, while TMPO-AS1 overexpression accelerated the EMT of the parental SKOV3 cells (Fig. 2D). After that, we tested the invasionand migration abilities of cells by Transwell assay. Overexpression of TMPO-AS1 evidently strengthened the invasion and migration abilities of the parental SKOV3 cells, while inhibition of TMPOAS1 expression significantly reduced the invasion and migration ability of SKOV3/5-FU cells (Fig. 2F).Through the dual-luciferase reporter gene assay, we found that there were binding sites between miR-200c and TMPO-AS1 (Fig. 3F).Through the dualluciferase reporter gene assay, we found that miR-200c could target TMEFF2 (Fig. 3J). After that, we measured the mRNA expression of TMEFF2 in the parental OC cells and SKOV3/5-FU cells. mRNA expression of TMEFF2 was increased in SKOV3/5-FU cells, and TMPOAS1 overexpression increased the mRNA expression of TMEFF2 (Fig. 3K).Cells were treated with overexpressed TMPO-AS1 and miR-200c mimic or treated with si-TMPO-AS1 and miR-200c inhibitor. The results presented that overexpression of miR-200c partially reversed the cell resistance and metastasis caused by overexpression of TMPO-AS1, while transfection of miR-200c inhibitor restored the resistance and metastasis of SKOV3/5-FU cells treated with si-TMPO-AS1 (Fig. 4A).Subsequently, changes of PI3K/Akt signaling pathway in each group of cells were detected using western blot The activation degree of PI3K/Akt in SKOV3/5-FU cells was evidently higher than that in parental SKOV3 cells, while inhibition/overexpression of TMPO-AS1 inhibited/promoted the extent of PI3K/Akt phosphorylation, and overexpression of miR-200c also inhibited the extent of PI3K/Akt phosphorylation in parental cells overexpressing TMPO-AS1 (Fig. 5A). The 15 differentially ex_x0002_pressed miRNAs and TMPO-AS1 targeted miRNAs predicted by the StarBase database were intersected, from which miR-200c was obtained (Fig. 3E). Through the dual-luciferase reporter gene assay, we found that there were binding sites between miR-200c and TMPO-AS1(Fig. 3F).	32497621	RID04602	ceRNA or sponge	metastasis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE60407,GSE67939)
Prostate cancer	PDE10A	SEPTIN6	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);JAK/STAT signaling pathway(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000112541	NA	ENSG00000125354	GRCh38_X:119615724-119693370	10846	23157	ADSD2|HSPDE10A|IOLOD|LINC00473|PDE10A19	SEP2|SEPT2|SEPT6	The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer.The high expression of LINC00473 has been observed in a couple of cancers including breast cancer, esophageal squamous cell carcinoma and colorectal cancer [16,17,22], while the expression of LINC00473 in prostate cancer remains unknown. The result of RT-qPCR assay showed that LINC00473 expression was higher in prostate cancer cells (PC3, DU145 and LNCaP) than that in human normal prostate epithelial cells (P69) (Figure 1A).To deeply explore the molecular mechanism of LINC00473 administrating proliferation of prostate cancer cells, starBase (http://starbase.sysu.edu.cn) was employed to seek putative miRNA that could bind to LINC00473. As shown in Figure 2A, miR-195-5p had several binding sites for LINC00473. Additionally, compared with normal prostate cells (P69), prostate cancer cells indicated lower expression of miR-195-5p (Figure 2B). According to RIP assay, not only LINC00473 but also miR-195-5p was abundant in anti-Ago2 group rather than anti-IgG group (Figure 2C), delineating that LINC00473 and miR-195-5p coexisted in RNA-induced silencing complexes (RISCs). Luciferase reporter assay using PC3 and DU145 cells demonstrated that miR-195-5p amplification led to an obvious attenuation of luciferase activity in LINC00473-WT vectors and no alteration was noticed in LINC00473-Mut vectors (Figure 2D). Finally, miR-195-5p expression was decreased by LINC00473 inhibition and miR-195-5p overexpression down-regulated LINC00473 expression (Figure 2E). To conclude, LINC00473 interacts with miR-195-5p and negatively modulates miR-195-5p expression.Abundant reports proposed that miRNAs could modulate expression of target genes by specifically binding with the 3'UTR of target genes [23,24], so we predicted that miR-195-5p also worked in this pattern in prostate cancer. Based on the prediction of starBase, SEPT2 was discovered to combine with miR-195-5p (Figure 3A). Then, prostate cancer cells (PC3, DU145 and LNCaP) displayed higher SEPT2 expression than P69 cells (Figure 3B). The result of luciferase reporter assay elucidated that the luciferase activity of SEPT-WT vectors in PC3 and DU145 cells was attenuated by transfection of miR-195-5p mimics whereas no apparent changes of luciferase activity were observed in SEPT2-Mut group (Figure 3C). RNA pull-down assay depicted that both LINC00473 and SEPT2 were enriched by biotin-labeled miR-195-5p probe but not by no-biotin miR-195-5p probe (Figure 3D). Nuclear-cytoplasmic fractionation assay indicated that LINC00473, miR-195-5p and SEPT2 were all predominantly located in cytoplasm (Figure 3E). Either LINC00473 inhibition or miR-195-5p overexpression decreased SEPT2 expression (Figure 3F). To sum up, SEPT2 is the target gene downstream of LINC00473/miR-195-5p pathway in prostate cancer.To validate whether LINC00473 exerted the oncogenic impacts on prostate cancer via miR-195-5p/SEPT2 axis, rescue assays were performed. At the beginning, the down-regulation of mRNA and protein expression of SEPT2 resulting from LINC00473 suppression was reversed by overexpressing SEPT2 (Figure 4A,B). Subsequently, EdU and colony formation assays using PC3 cells uncovered that the inhibitive effect on proliferative capability of LINC00473 silence was partially rescued by transfection of pcDNA3.1/SEPT2 (Figure 4C,D). Last but not least, the protein expression of phosphorylated JAK2 and STAT3 down-regulated by LINC00473 knockdown was restored by SEPT2 overexpression (Figure 4E). In a word, LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer.	32440687	RID04603	ceRNA or sponge	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)	
Atherosclerosis	TUG1	PRKAA2	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);AMPK/mTOR signaling pathway(-);cell autophagy(-)	NA	regulation	RNA-protein	Metformin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000162409	NA	55000	5563	FLJ20618|LINC00080|NCRNA00080	AMPK|AMPKa2|PRKAA	Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis.To investigate the correlation between lncRNA TUG1 and AS, qRT-PCRwas used to detect TUG1 expression in the peripheral blood of healthy controls and patients with CHD. The results suggested that TUG1 expression was robustly upregulated in patients with CHD, compared with that in healthy controls (Figure 1A). Then, cells were incubated with metformin (10 mmol/L) for 24, 48, or 72 h. As shown in Figure 1B, the expression of TUG1 was downregulated in a time-dependent manner.Next, HUVECs were transfected with si-TUG1(#1, #2) to knock down the expression of TUG1. Following transfection, TUG1 expression decreased sharply in the si-TUG1 groups compared with that in the si-NC group (Figure 3A). Similar to the results of metformin treatment, we found that knockdown of TUG1 expression by siRNA inhibited proliferation (Figure 3B, -,CC and -andF)F) and migration (Figure 3D and -andG),G), while promoted autophagy (Figure 3E, -,HH and -andI)I) in HUVECs.western blot was then used to detect the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, ATG3, p62, and LC3 after cells were transfected with si-TUG1 (#2, 50 nm). si-TUG1 (#2) resulted in better knockdown efficiency and was thus selected for subsequent experiments. As expected, the expression of p-AMPK/AMPK, ATG3, and LC3II/LC3I was upregulated, whereas that of p-mTOR/mTOR and p62 was downregulated by si-TUG1 (Figure 5A ). However, the effect of si-TUG1 on the AMPK/mTOR pathway was reversed by treatment with Compound C (C.C, 50 umol/L, an AMPK inhibitor), which suggested that TUG1 knockdown could activate the AMPK/mTOR pathway in HUVECs. In addition, as shown in Figure 5G and -andH,H, C.C reversed the effects on proliferation and migration induced by si-TUG1. Figure 5I shows the technical rote of metformin and lncRNA TUG1 in AS.	32099330	RID04604	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807)
Atherosclerosis	TUG1	LC3II	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-RNA	Metformin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis.To investigate the correlation between lncRNA TUG1 and AS, qRT-PCRwas used to detect TUG1 expression in the peripheral blood of healthy controls and patients with CHD. The results suggested that TUG1 expression was robustly upregulated in patients with CHD, compared with that in healthy controls (Figure 1A). Then, cells were incubated with metformin (10 mmol/L) for 24, 48, or 72 h. As shown in Figure 1B, the expression of TUG1 was downregulated in a time-dependent manner.Next, HUVECs were transfected with si-TUG1(#1, #2) to knock down the expression of TUG1. Following transfection, TUG1 expression decreased sharply in the si-TUG1 groups compared with that in the si-NC group (Figure 3A). Similar to the results of metformin treatment, we found that knockdown of TUG1 expression by siRNA inhibited proliferation (Figure 3B, -,CC and -andF)F) and migration (Figure 3D and -andG),G), while promoted autophagy (Figure 3E, -,HH and -andI)I) in HUVECs.western blot was then used to detect the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, ATG3, p62, and LC3 after cells were transfected with si-TUG1 (#2, 50 nm). si-TUG1 (#2) resulted in better knockdown efficiency and was thus selected for subsequent experiments. As expected, the expression of p-AMPK/AMPK, ATG3, and LC3II/LC3I was upregulated, whereas that of p-mTOR/mTOR and p62 was downregulated by si-TUG1 (Figure 5A ). However, the effect of si-TUG1 on the AMPK/mTOR pathway was reversed by treatment with Compound C (C.C, 50 umol/L, an AMPK inhibitor), which suggested that TUG1 knockdown could activate the AMPK/mTOR pathway in HUVECs. In addition, as shown in Figure 5G and -andH,H, C.C reversed the effects on proliferation and migration induced by si-TUG1. Figure 5I shows the technical rote of metformin and lncRNA TUG1 in AS.	32099330	RID04605	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Atherosclerosis	TUG1	LC3I	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	Metformin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis.To investigate the correlation between lncRNA TUG1 and AS, qRT-PCRwas used to detect TUG1 expression in the peripheral blood of healthy controls and patients with CHD. The results suggested that TUG1 expression was robustly upregulated in patients with CHD, compared with that in healthy controls (Figure 1A). Then, cells were incubated with metformin (10 mmol/L) for 24, 48, or 72 h. As shown in Figure 1B, the expression of TUG1 was downregulated in a time-dependent manner.Next, HUVECs were transfected with si-TUG1(#1, #2) to knock down the expression of TUG1. Following transfection, TUG1 expression decreased sharply in the si-TUG1 groups compared with that in the si-NC group (Figure 3A). Similar to the results of metformin treatment, we found that knockdown of TUG1 expression by siRNA inhibited proliferation (Figure 3B, -,CC and -andF)F) and migration (Figure 3D and -andG),G), while promoted autophagy (Figure 3E, -,HH and -andI)I) in HUVECs.western blot was then used to detect the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, ATG3, p62, and LC3 after cells were transfected with si-TUG1 (#2, 50 nm). si-TUG1 (#2) resulted in better knockdown efficiency and was thus selected for subsequent experiments. As expected, the expression of p-AMPK/AMPK, ATG3, and LC3II/LC3I was upregulated, whereas that of p-mTOR/mTOR and p62 was downregulated by si-TUG1 (Figure 5A ). However, the effect of si-TUG1 on the AMPK/mTOR pathway was reversed by treatment with Compound C (C.C, 50 umol/L, an AMPK inhibitor), which suggested that TUG1 knockdown could activate the AMPK/mTOR pathway in HUVECs. In addition, as shown in Figure 5G and -andH,H, C.C reversed the effects on proliferation and migration induced by si-TUG1. Figure 5I shows the technical rote of metformin and lncRNA TUG1 in AS.	32099330	RID04606	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Atherosclerosis	TUG1	MTOR	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);AMPK/mTOR signaling pathway(-);cell autophagy(-)	NA	regulation	RNA-protein	Metformin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000198793	NA	55000	2475	FLJ20618|LINC00080|NCRNA00080	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis.To investigate the correlation between lncRNA TUG1 and AS, qRT-PCRwas used to detect TUG1 expression in the peripheral blood of healthy controls and patients with CHD. The results suggested that TUG1 expression was robustly upregulated in patients with CHD, compared with that in healthy controls (Figure 1A). Then, cells were incubated with metformin (10 mmol/L) for 24, 48, or 72 h. As shown in Figure 1B, the expression of TUG1 was downregulated in a time-dependent manner.Next, HUVECs were transfected with si-TUG1(#1, #2) to knock down the expression of TUG1. Following transfection, TUG1 expression decreased sharply in the si-TUG1 groups compared with that in the si-NC group (Figure 3A). Similar to the results of metformin treatment, we found that knockdown of TUG1 expression by siRNA inhibited proliferation (Figure 3B, -,CC and -andF)F) and migration (Figure 3D and -andG),G), while promoted autophagy (Figure 3E, -,HH and -andI)I) in HUVECs.western blot was then used to detect the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, ATG3, p62, and LC3 after cells were transfected with si-TUG1 (#2, 50 nm). si-TUG1 (#2) resulted in better knockdown efficiency and was thus selected for subsequent experiments. As expected, the expression of p-AMPK/AMPK, ATG3, and LC3II/LC3I was upregulated, whereas that of p-mTOR/mTOR and p62 was downregulated by si-TUG1 (Figure 5A ). However, the effect of si-TUG1 on the AMPK/mTOR pathway was reversed by treatment with Compound C (C.C, 50 umol/L, an AMPK inhibitor), which suggested that TUG1 knockdown could activate the AMPK/mTOR pathway in HUVECs. In addition, as shown in Figure 5G and -andH,H, C.C reversed the effects on proliferation and migration induced by si-TUG1. Figure 5I shows the technical rote of metformin and lncRNA TUG1 in AS.	32099330	RID04607	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Atherosclerosis	TUG1	p62	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	Metformin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000073792	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis.To investigate the correlation between lncRNA TUG1 and AS, qRT-PCRwas used to detect TUG1 expression in the peripheral blood of healthy controls and patients with CHD. The results suggested that TUG1 expression was robustly upregulated in patients with CHD, compared with that in healthy controls (Figure 1A). Then, cells were incubated with metformin (10 mmol/L) for 24, 48, or 72 h. As shown in Figure 1B, the expression of TUG1 was downregulated in a time-dependent manner.Next, HUVECs were transfected with si-TUG1(#1, #2) to knock down the expression of TUG1. Following transfection, TUG1 expression decreased sharply in the si-TUG1 groups compared with that in the si-NC group (Figure 3A). Similar to the results of metformin treatment, we found that knockdown of TUG1 expression by siRNA inhibited proliferation (Figure 3B, -,CC and -andF)F) and migration (Figure 3D and -andG),G), while promoted autophagy (Figure 3E, -,HH and -andI)I) in HUVECs.western blot was then used to detect the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, ATG3, p62, and LC3 after cells were transfected with si-TUG1 (#2, 50 nm). si-TUG1 (#2) resulted in better knockdown efficiency and was thus selected for subsequent experiments. As expected, the expression of p-AMPK/AMPK, ATG3, and LC3II/LC3I was upregulated, whereas that of p-mTOR/mTOR and p62 was downregulated by si-TUG1 (Figure 5A ). However, the effect of si-TUG1 on the AMPK/mTOR pathway was reversed by treatment with Compound C (C.C, 50 umol/L, an AMPK inhibitor), which suggested that TUG1 knockdown could activate the AMPK/mTOR pathway in HUVECs. In addition, as shown in Figure 5G and -andH,H, C.C reversed the effects on proliferation and migration induced by si-TUG1. Figure 5I shows the technical rote of metformin and lncRNA TUG1 in AS.	32099330	RID04608	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Non-small cell lung cancer	CCAT1	FOXO1	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	Hyperoside	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000247844	NA	ENSG00000150907	NA	100507056	2308	CARLO5|CARLo-5|onco-lncRNA-40	FKH1|FKHR|FOXO1A	Hyperoside exhibits anticancer activity in non-small cell lung cancer cells with T790M mutations by upregulating FoxO1 via CCAT1.FoxO1 is a key protein that plays a crucial role in tumor cell apoptosis, and the results of the present study revealed that the expression of FoxO1 was downregulated and CCAT1 was upregulated in the T790M-positive H1975 cells compared with the wild-type PC-9 cells (Fig. S1). However, FoxO1 protein expression was observed to be upregulated following hyperoside (150 uM) treatment (Fig. 3A) in the H1975 cells, demonstrating that hyperoside-induced apoptosis was associated with FoxO1 upregulation. Meanwhile, hyperoside (150 uM) significantly downregulated the level of CCAT1 expression at 48 h (Fig. 3B). The present study further investigated whether CCAT1 regulates FoxO1 expression in T790M-positive H1975 cells. CCAT1 knockdown or overexpressing H1975 cells were established and the CCAT1 expression level was determined (Fig. 3C). It was revealed that FoxO1 protein expression was upregulated in the CCAT1-knockdown H1975 cells, while FoxO1 protein expression was downregulated in the CCAT1-overexpressing H1975 cells (Fig. 3D).MTT assay and Annexin V/PI apoptosis analysis were performed in order to investigate the anticancer activity of hyperoside in CCAT1-knockdown or -overexpressing and FoxO1-knockdown or -overexpressing H1975 cells (Figs. 3C and 4A). The results revealed that hyperoside did not decrease the cell proliferation or increase the apoptosis rate in the CCAT1-overexpressing or FoxO1-knockdown H1975 cells (Fig. 4B and C), suggesting that CCAT1-mediated FoxO1 signaling was essential for hyperoside in treating T790M-positive NSCLC.A xenograft tumor model was established by transplanting H1975 cells into nude mice in order to investigate the anticancer effect of hyperoside in vivo. Hyperoside significantly inhibited the growth of H1975 Xenograft tumors (Fig. 5A), and the nude mice did not exhibit significant weight loss in the hyperoside group compared with the control group (Fig. 5B). Finally, tumor tissues were removed and prepared for RT-qPCR analysis, immunohistochemistry staining and western blot The results revealed that FoxO1was highly expressed in the hyperoside group compared with the control group, and the level of CCAT1 was significantly downregulated by hyperoside treatment (Fig. 5C-E).	31894285	RID04609	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Oesophageal squamous cell carcinoma	SNHG5	MTA2	negatively-E	RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastroesophageal cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000149480	NA	387066	9219	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	MTA1-L1|MTA1L1	SNHG5 inhibits the progression of EMT through the ubiquitin-degradation of MTA2 in oesophageal cancer.We performed quantitative RT-PCR(q-PCR) to detect the expression of SNHG5 in 100 paired cancer and para-cancer oesophageal specimens from patients with ESCC. Among the 100 paired tissues, the SNHG5 levels in the ESCC tissues were decreased compared with those in the corresponding paracancer tissues (Fig. 1A). To further confirm the decreased expression of SNHG5 in ESCC, we also detected the expression level of SNHG5 in precancerous lesions. The results showed that SNHG5 expression was also decreased in ESCC tissues compared with precancerous lesions (Fig. 1B). We then screened ESCC data from TCGA, and SNHG5 was expressed at lower levels in ESCC tissues (Fig. 1C).To determine the mechanisms by which SNHG5 influences the biological function of ESCC cells, we first observed the morphological changes of cells. We found that the KYSE30 cells overexpressing SNHG5 exhibited a round, epithelial morphology while the control KYSE-30 cells exhibited an elongated, mesenchymal morphology (Fig. 2D); these results suggested that SNHG5 was involved in the progression of EMT in ESCC cells. Furthermore, immunofluorescence showed that overexpression of SNHG5 substantially increased the levels of the epithelial marker E-cadherin but decreased the levels of the mesenchymal markers N-cadherin and vimentin in KYSE-30 cells (Fig. 2E). Moreover, western blot and qPCR assays demonstrated that overexpression of SNHG5 decreased the levels of the mesenchymal markers N-cadherin, vimentin, CD24, MYLK and IGF2BP1, but increased the levels of the epithelial marker E-cadherin (Fig. 2F, Supplementary Fig. C). Taken together, these results indicated that SNHG5 influenced the growth, migration, invasion and EMT of ESCC cells.Next, the effect of SNHG5 expression on ESCC metastasis was evaluated. Histochemical analysis confirmed that the SNHG5-overexpressing cells formed fewer lung metastatic nodules than the control ESCC cells when these two types of cells were injected into the tail veins of nude mice (Fig. 3F). Taken together, these data indicated that SNHG5 strongly inhibited tumour growth and metastasis and might be a potential target for ESCC therapy.Similarly, knockdown of SNHG5 with siRNA increased the mRNA level of MTA2 (Fig. 4C). Then, we treated KYSE-30 cells with actinomycin D for different time points, and there was no significant difference at the different time points between the SNHG5 overexpression group and the control group. The results revealed that SNHG5 influenced the transcription, rather than degradation of MTA2 mRNA (Fig. 4E).To further investigate the effect of SNHG5 on MTA2, we evaluated the protein level of MTA2 with overexpression of SNHG5. Our results demonstrated that overexpression of SNHG5 decreased the total expression of MTA2 (Fig. 5A). We further investigated MTA2 expression in the cytoplasm and nucleus respectively. The results also demonstrated that MTA2 expression was downregulated in both the cytoplasm and nucleus (Fig. 5B). Next, we evaluated how SNHG5 affected MTA2 protein expression. First, pre-treatment of KYSE-30 cells with CHX, an established inhibitor of protein synthesis, decreased the MTA2 levels induced by the overexpression of SNHG5. Following treatment with the proteasome inhibitor MG132, the accumulation of endogenous MTA2 in the cells overexpressing SNHG5 was greater (Fig. 5C), indicating that SNHG5 might promote the proteasome-dependent degradation of MTA2 in ESCC cells. To confirm this hypothesis, we performed an IP assay. The results showed that MTA2 was immunoprecipitated by ubiquitination (Fig. 5D). Furthermore, we found that overexpression of SNHG5 decreased the protein levels of MTA2 by enhancing its ubiquitination. In addition, incubation of cells with MG132, prevented the degradation of the MTA2 protein induced by overexpression of SNHG5 (Fig. 5E, F).These results suggested that SNHG5 downregulated the MTA2 protein level by enhancing MTA2 protein ubiquitination in KYSE-30 cells.We also found that SNHG5 reversed the epithelial-mesenchymal transition by interacting with MTA2.	33095847	RID04610	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hypertrophic scar	HSRL	SNX9	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	Tanshinone IIA	NA	NA	Other	Hypertrophic scar	lncRNA	PCG	NA	NA	ENSG00000130340	NA	NA	51429	NA	SDP1|SH3PX1|SH3PXD3A	Tanshinone IIA down-regulated p-Smad3 signaling to inhibit TGF-beta1-mediated fibroblast proliferation via lncRNA-HSRL/SNX9.Results of quantitative real time PCR showed that treatment with TGF-beta1 alone upregulated HSRL and SNX9 (Figure 2A) mRNA levels in the HSF, which was reversed by TSIIA treatment in a dose-dependent manner. In line with this, the increased SNX9 protein level by TGF-beta1 treatment was reversed by TSIIA dose-dependently (Figure 2B).In addition, we also detected that TSIIA treatment for 24h inhibited HSRL and SNX9 gene transcription in comparison with TGF-beta1 group (Supplementary data 1A). Simultaneously, SNX9 and Smad2/3 signaling protein levels were downregulated 24h after TSIIA treatment in a dose-dependent manner (Supplementary data 1B). Our data demonstrated that at the two time points of 24 h and 48 h, TSIIA treatment could suppressed expression of HSRL, SNX9 and Smad2/3 signaling proteins.To validate our inference, TGF-beta1-stimulated HSF were transfected with siRNA targeting SNX9, followed by TSIIA (20 uM) treatment. Quantitative real time PCR analysis showed that siRNA targeting SNX9 inhibited the expression of SNX9 mRNA in TGF-beta1-stimulated HSF, which was enhanced by TSIIA treatment (Figure 4A).Then, the interaction between HSRL and SNX9 was validated by RNA pull-down assay in HSF. As shown in Figure 6A, SNX9 was specifically pulled down in TGF-beta1 and TGFbeta1+TSIIA treatment groups, rather than in control group. Compared with TGF-beta1 group, SNX9 was down-regulated in TGF-beta1+TSIIA group, as indicated by western blot	33049375	RID04611	expression association	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842)
Clear cell renal cell carcinoma	PCED1B-AS1	ZEB1	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	prognosis(-);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-484)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000247774	GRCh38_12:47205896-47216460	ENSG00000148516	NA	100233209	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long Non-Coding RNA PCED1B-AS1 Promotes the Progression of Clear Cell Renal Cell Carcinoma Through miR-484/ZEB1 Axis.We also measured the expression level of PCED1B-AS1 in ccRCC tissues and cell lines using qRT-PCR and the results revealed that the expression level of PCED1B-AS1 in ccRCC tissues was remarkably higher than normal kidney tissue (Figure 1C). ccRCC patients were divided into low expression group (n=20) and high expression group (n=20). The results showed that high expression of PCED1B-AS1 was associated with high tumor stage and high Fuhrman grade, but not related to age, gender, tumor diameter, and lymph node metastasis. The data indicated that PCED1B-AS1 may play a tumor-promoting role in ccRCC.We measured cell proliferation using CCK-8 and EdU assays. The results showed that PCED1B-AS1 knockdown markedly suppressed the proliferation of A498 and Caki-1 cells (Figure 2B and -andC).C). Wound healing experiments were used to examine the effect of PCED1B-AS1 on cell migration, the results of which demonstrated that the migration ccRCC cells with PCED1B-AS1 silenced was significantly inhibited (Figure 2D). western blot was used to detect the expression of EMT-related proteins, and the data demonstrated that silencing of PCED1B-AS1 significantly increased E-cadherin expression and decreased N-cadherin expression in ccRCC cells (Figure 2E).To verify the targeting relationship between them, we co-transfected PCED1B-AS1-WT luciferase reporter vector or PCED1B-AS1-MUT luciferase reporter vector and miR-484 mimics or NC mimics into A498 and Caki-1 cells. The results revealed that the luciferase activity in PCED1B-AS1-WT group was remarkably inhibited after transfection with miR-484 mimics, while the luciferase activity in PCED1B-AS1-MUT-transfected cells remained unchanged (Figure 3C). Additionally, RIP analysis showed that anti-Ago2 antibodies were able to immunoprecipitate PCED1B-AS1 and miR-484 in both A498 and Caki-1 cell lysates (Figure 3D). Moreover, qRT-PCRfound that miR-484 was markedly down-regulated in ccRCC tissues compared with normal kidney tissues (Figure 3E), and Pearson correlation analysis indicated that there was a negative correlation between PCED1B-AS1 expression and miR-484 expression in ccRCC tissues (Figure 3F). Additionally, compared with HK-2 cells, miR-484 expression in ccRCC cells was down-regulated (Figure 3G). These data suggested that PCED1B-AS1 could sponge miR-484 and inhibit its expression in ccRCC.The dual-luciferase reporter experiment revealed that transfection of miR-484 mimics reduced luciferase activity of ZEB1-WT reporter, but had no significant effect on the luciferase activity in ZEB1-MUT group (Figure 5B). western blot indicated that ZEB1 protein expression was markedly inhibited in miR-484 mimics-transfected cells (Figure 5C). In addition, we found that ZEB1 expression was remarkably higher in ccRCC tissues than in normal kidney tissues (Figure 5D), and correlation analysis showed that ZEB1 was positively correlated with PCED1B-AS1 expression (Figure 5E). The data indicated that ZEB1 was a direct target of miR-484 in ccRCC cells, and could probably be regulated by PCED1B-AS1.	33469315	RID04612	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Retinoblastoma	HEIH	WEE1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-194-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831618	ENSG00000166483	NA	100859930	7465	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	WEE1A	Long Noncoding RNA HEIH Promotes Proliferation, Migration and Invasion of Retinoblastoma Cells Through miR-194-5p/WEE1 Axis.We first determined the expression level of HEIH in normal retinal epithelial cell line ARPE-19 and retinoblastoma cell lines (Y79 and SO-Rb50). As shown in Figure 1A, HEIH was up-regulated 2.2-fold and 2.5-fold in Y79 and SO-Rb50 relative to ARPE-19. Then, we validated HEIH expression in 35 retinoblastoma tissues and 7 normal retinal tissues. Consistently, HEIH exhibited a mean 2.3-fold increase in retinoblastoma tissues (Figure 1B).Notably, a higher level of HEIH was observed in advanced tumor ICRB stage patients than that of early tumor stage (Figure 1C). Interestingly, HEIH expression was significantly related to retinoblastoma optic nerve invasion (Figure 1D) as well as choroidal invasion (Figure 1E). Furthermore, up-regulated HEIH predicted an unfavorable survival of retinoblastoma patients (P=0.0255; Figure 1F). Thus, HEIH might play an important regulatory role in retinoblastoma carcinogenesis.Loss-of-function assays were performed to establish the functional role of HEIH by transfecting si-HEIH into Y79 and SO-Rb50 cells. qRT-PCRresults showed that HEIH expression was significantly decreased after si-HEIH transfection (Figure 2A). As shown in Figure 2B, HEIH knockdown obviously reduced the number of viable cells. In addition, a similar effect was observed in colony formation assays (Figure 2C and -andD).D). We also evaluated the effects of HEIH on the migration and invasion of retinoblastoma cells. Wound-healing experiment proved that the migratory distance was markedly reduced by HEIH silence (Figure 2E and -andF).F). Transwell assay result showed that HEIH knockdown resulted in a smaller number of invasive cells than negative control (Figure 2G and -andH).H). Therefore, HEIH down-regulation suppressed proliferation and metastasis of retinoblastoma cells.We then constructed mutant and wild type luciferase reporter of HEIH for miR-194-5p. The results showed that wt-HEIH overexpression remarkably reduced the luciferase activity when co-transfection with miR-194-5p mimics compared with miRNA negative, but no obvious change for mutant HEIH (Figure 3B and -andC).C). We also assessed the regulatory relationship between HEIH and miR-194-5p. HEIH knockdown could up-regulate miR-194-5p expression (Figure 3D). These data suggest that miR-194-5p was a downstream target of HEIH in retinoblastoma.As shown in Figure 4A, we identified that the conserved 3- UTR of WEE1 contained complementary sequence of miR-194-5p at the position of 225'-31. Luciferase reporter assay was performed to validate whether miR-194-5p could directly interact with WEE1 3-UTR. In both Y79 and SO-Rb50 cells, luciferase activity of wt-WEE1+miR-194-5p mimics group was evidently decreased compared to mut-WEE1+miR-194 mimics (Figure 4B and -andC).C). We also performed western blot to test whether HEIH could regulate WEE1 expression through interacting with miR-194-5p. We found that HEIH knockdown could down-regulate WEE1 expression, but miR-194-5p inhibitor transfection reversed the effects of HEIH knockdown on WEE1 level (Figure 4D and -andE).E).We conclude that HEIH serves as a sponge of miR-194-5p to up-regulate WEE1 expression in retinoblastoma.To test whether HEIH exerted its oncogenic roles through regulating WEE1 expression, we first constructed WEE1 overexpressing vector pcDNA 3.1-WEE1 and its control vector pcDNA 3.1. western blotvalidated the up-regulation of WEE1 by pcDNA3.1-WEE1 transfection (Figure 5A and -andB).B). The proliferation of si-HEIH+pcDNA3.1-WEE1 was significantly increased compared with si-HEIH+pcDNA3.1-NC group (Figure 5D and -andE).E). Besides, ectopic expression of WEE1 also rescued the migrative and invasive capability of retinoblastoma cells (Figure 5F). Taken together, these findings indicate that HEIH promotes retinoblastoma cell proliferation, migration and invasion through up-regulating WEE1 expression.	33262604	RID04613	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Periodontitis	LINC01126	HIF1A	positively-E	dual-luciferase reporter assay;starBase;starBaseV2;LncBase;miRcode;miRWalk;TargetScan;miRTar	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+);MAPK signaling pathway(+)	ceRNA(miR-518a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Periodontitis	lncRNA	TF	ENSG00000279873	GRCh38_2:43227210-43228855	ENSG00000100644	NA	100129726	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA 01126 promotes periodontitis pathogenesis of human periodontal ligament cells via miR-518a-5p/HIF-1alpha/MAPK pathway.hPDLCs were treated in 3 different O2 concentrations to imitate the hypoxia environment during the periodontitis pathogenesis. Compare to the normoxia group, hypoxia decreased the proliferative ability while increased the apoptosis rate in a concentration dependent manner (Figure 2A, B). Hypoxic condition also promoted the expression of inflammatory cytokines including IL-1beta,IL-6, IL-8 and TNF-alpha (Figure 2C-F). The expression level of LINC01126 was found to be significantly upregulated in 1% and 5% O2 group and reached peak at 48 h (Figure 2G, H). Moreover, the protein expression of HIF-1, which is the most sensitive indicator to hypoxia was significantly upregulated under hypoxia (Figure 2I). Taken together, we disposed the cells in hypoxic conditions for 48 h in further experiment. These results indicate that hypoxia decreases the proliferation while increases apoptosis and inflammation, and LINC01126 is upregulated in hypoxia-induced hPDLCs.To determine the effect of LINC01126 in periodontitis, pCDH vector (pCDH-01126) was transfected to overexpress LINC01126 and shRNA targeting LINC01126 (sh-01126) was used to knock down LINC01126 expression. The transfection efficiency was more than-75% (Figure S2C,D). qRT-PCRresults were used to confirm the transfection effects in hPDLCs (Figure 3A). The proliferative capacity in each O2 concentration group was significantly suppressed after overexpression of LINC01126, and dramatically enhanced after knockdown of LINC01126 enhanced (Figure 3B-D). Moreover, we found that hypoxia induced the secretion of inflammatory cytokines IL-1beta,IL-6, IL-8 and TNF-alpha. Overexpression of linc01126 promoted the secretion of inflammatory cytokines while knockdown of LINC01126 suppressed the secretion of these inflammatory cytokines (Figure 3E).FISH results further verified our hypothesis that both LINC01126 and miR-518a-5p mainly localized in cytoplasm, indicating their interaction (Figure 4B). Then, luciferase reporters containing the wide-type (LINC01126-WT) or mutant type (LINC01126-MU) target site on LINC01126 were constructed to further identify whether miR-518a-5p could bind to LINC01126. LINC01126-WT reporter activity was remarkably inhibited by miR-518a-5p in 293T while LINC01126-MU reporter was not affected (Figure 4C, E).Moreover, qRT-PCRresults confirmed the transfection effects of miR-518a-5p mimic and miR-518a-5p inhibitor in hPDLCs (Figure 4G).All of these three predictions showed that the 3'-UTR of hypoxia-inducible factor-1alpha (HIF-1alpha) contained a miR-518a-5p binding site (Figure 5C). HIF-1alpha is one of the most sensitive and important molecule in response to Hypoxic conditions in hPDLCs. Therefore, we identified HIF-1alpha as a putative miR-518a-5p target. Then, HIF-1alpha 3- UTR and its mutant containing the putative miR-518a-5p binding sites were cloned into the downstream luciferase reporter. Compared with the control group, luciferase reporter activity was significantly reduced in miR-518a-5p transfected hPDLCs, and this reduction was relieved in mutated HIF-1alpha 3'UTR (Figure 5D). Moreover, after transfection of miR-518a-5p mimics, the expression of HIF-1alpha decreased, while the level of HIF-1alpha increased after transfection of miR-518a-5p inhibitors in hPDLCs (Figure 5E). Additionally, the expression of HIF-1alpha was significantly upregulated in cells overexpressed LINC01126, whereas co-transfection with pCDH-01126 and miR-518a-5p inhibitor significantly reversed HIF-1alpha expression levels. Downregulation of LINC01126 significantly downregulated the expression of HIF-1alpha,while transfection with sh-01126 and miR-518a-5p mimic synchronous had a reversed effect (Figure 5F).Altogether, these data indicate that HIF-1alpha acts as a downstream target of LINC01126/ miR-518a-5p axis.Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38-MAPK, are an important pathway in cell proliferation and inflammation 28 . The GSEA analysis predicted that MAPK pathway was associated with a majority of differentially expressed genes including LINC01126 in periodontitis. To investigate whether LINC01126/HIF-1alpha aggravates periodontitis development via accelerated MAPK pathway, we first use the western blot to measure the protein expression of the total p38, ERK1/2, and JNK in sh-HIF-1alpha, pCDH-01126/HIF-1alpha-treated hPDLCs. The results indicated that MAPK pathway was markedly decreased in HIF-1alpha knockdown group, while increased in the HIF-1alpha overexpressed group (Figure 7A-C). Moreover, we co-transfected PDCLs with pCDH-01126 and sh-HIF-1alpha. The results showed that overexpression of lnc01126 activated the MAPK pathway. However, co-transfection with pCDH-01126 and sh-HIF-1alpha alleviated the activation of MAPK pathway (Figure 7D-F).	33231338	RID04614	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteoporosis	SNHG16	BMP7	positively-E	dual-luciferase reporter assay;StarBase;TargetScan7.2;miRDB;PicTar	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-485-5p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000101144	NA	100507246	655	Nbla10727|Nbla12061|ncRAN	OP-1	SNHG16/miR-485-5p/BMP7 axis modulates osteogenic differentiation of human bone marrow-derived mesenchymal stem cells.hBMSCs were collected (Supplementary Fig. 1A). Flow cytometry highlighted that the percentage of CD90 positive cells was more than 99 % and that of CD45 positive cells was less than 1 % in the collected cells (Fig. 1A), indicating the hBMSCs met the experimental requirement. Subsequently, it was demonstrated that SNHG16 and BMP7 expressions in hBMSCs of OP group were lower than that in NC group, while miR-485-5p expression was markedly increased (Fig. 1B-D). In osteogenic induction experiment, qRT-PCRindicated that ALP , OPN and OCN expressions were gradually up-regulated (Fig. 1E-G); additionally, ALP staining assay also suggested that ALP expression in the cells was significantly up-regulated after the induction (Supplementary Fig. 1B). Meanwhile, SNHG16 and BMP7 expressions were enhanced gradually on the 0, 7 and 14 d, while miR-485-5p expression was declined in a time-dependent manner (Fig. 1H-J). Additionally, western blot indicated that BMP7 protein expression was increased in a time-dependent manner, accompanied by the increased expressions of ALP , OPN and OCN (Supplementary Fig. 1C).qRT-PCRdepicted that SNHG16 expression was suppressed greatly after transfection of sh-SNHG16 in hBMSCs (Fig. 2A). The MTT assay depicted that sh-SNHG16 greatly restrained the viability of hBMSCs, and induced the apoptosis of hBMSCs (Fig. 2B-D). Importantly, we observed that SNHG16 knockdown considerably elevated miR-485-5p expressions, but repressed BMP7 expressions (Fig. 2E-F). qRT-PCRuncovered that SNHG16 knockdown repressed ALP , OPN and OCN expressions in hBMSCs (Fig. 2G-I). ELISA assay showed that SNHG16 knockdown induced IL-6, IL-8 and TNF-alpha released by hBMSCs (Fig. 2J-L). These data revealed that knockdown of SNHG16 suppresses osteogenic differentiation of hBMSCs and probably induced inflammatory response.Then luciferase reporters containing SNHG16 wild type (wt) or mutant (mut) sequence were constructed to figure out whether miR-485-5p was the target of SNHG16. The results indicated that the over-expression of miR-485-5p suppressed the luciferase activity of SNHG16-wt reporter, and the mutation of site 1 abolished this effect, which validated that site 1 was a binding site between SNHG16 and miR-485-5p (Fig. 3B). Next, TargetScan, miRDB and PicTar databases implied that BMP7 was the target gene of miR-485-5p and there were three candidate binding sites (Fig. 3C). The target region 1 was validated as an effective binding site (Fig. 3D), indicating that BMP7 was a direct target of miR-485-5p. Collectively, SNHG16 raises BMP7 expression in hBMSCs by repressing miR-485-5p.To further explore whether SNHG16 could regulate the osteogenic differentiation of hBMSC by regulating miR-485-5p. MiR-485-5p inhibitors and sh-SNHG16 were co-transfected into hBMSC (Fig. 4A-B). qRT-PCRresults manifested that knockdown of SNHG16 remarkably up-regulated miR-485-5p expressions, but inhibited BMP7 expression and osteogenesis related genes ALP , OPN and OCN; when hBMSCs were co-transfected with miR-485-5p inhibitors, the above changes induced by SNHG16 knockdown were partly reversed (Fig. 4C-E). Consistently, at the protein level, it was verified that miR-485-5p inhibitors could reverse the down-regulation of BMP7 and osteogenesis-related genes ALP , OPN and OCN caused by knockdown of SNHG16 (Fig. 4F).	33179372	RID04615	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE55807)
Gastric cancer	LINC01436	APEX1	positively-E	luciferase reporter assay;RIP;StarBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);radioresistance(+)	ceRNA(miR-513a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231106	GRCh38_21:36005137-36007838	ENSG00000100823	NA	100996609	328	NA	APE|APE1|APEN|APEX|APX|HAP1|REF1	LINC01436 Promotes the Progression of Gastric Cancer via Regulating miR-513a-5p/APE1 Axis.To investigate the expression characteristics of LINC01436 in GC, we examined the LINC01436 expression in 40 cases of cancerous tissues from GC patients and compared it with the LINC01436 expression in corresponding adjacent tissues. qRT-PCRanalysis revealed that the LINC01436 expression in tumor tissues was observably higher than that in non-tumor tissues (Figure 1A).To assess the effect of LINC01436 on GC cells, the LINC01436 low expression and overexpression models were established with AGS cells and BGC-823 cells, respectively (Figure 2A). CCK-8 assay implied that the transfection of LINC01436 siRNA markedly reduced the viability of GC cells, while LINC01436 overexpression notably increased the proliferation of GC cells compared to NC group (Figure 2B). Furthermore, flow cytometry analysis revealed that LINC01436 knockdown enhanced the apoptosis of GC cells, while LINC01436 overexpression exerted the opposite function (Figure 2C). To further elaborate the effect of LINC01436 on GC cell metastasis, Transwell assay was carried out, the results of which unveiled that LINC01436 knockdown reduced GC cell migration and invasion, while LINC01436 overexpression enhanced these processes (Figure 2D). Additionally, colony formation assay implied that LINC01436 knockdown increased the radiosensitivity of GC cells, whereas LINC01436 overexpression had the opposite effect (Figure 2E).To further clarify the targeting relationship between LINC01436 and miR-513a-5p, the luciferase activity assay was performed and showed that miR-513a-5p mimics significantly repressed the luciferase activity of wild-type LINC01436 sequence, while overexpression of LINC01436 markedly reversed these effects (Figure 3E). In addition, there was no effect on the mutant LINC01436 sequence (Figure 3E). Consistently, RIP experiments showed that in AGS cells, LINC01436 and miR-513a-5p were significantly enriched in anti-Ago2 group compared with anti-IgG group (Figure 3F). Additionally, qRT-PCRresults revealed that LINC01436 overexpression suppressed the miR-513a-5p expression, while LINC01436 knockdown facilitated the expression of miR-513a-5p in GC cells (Figure 3G). Based on these results mentioned above, we identified that miR-513a-5p was a target of LINC01436.western blot was then adopted to detect the APE1 expression after selective regulation of LINC01436 and miR-513a-5p. The results revealed that miR-513a-5p overexpression or LINC01436 knockdown suppressed the APE1 expression, while miR-513a-5p repression or LINC01436 overexpression up-regulated APE1 expression (Figure 5C and -andD).D). Therefore, it could be concluded that APE1 expression was negatively regulated by miR-513a-5p, and could be indirectly and positively regulated by LINC01436.The LINC01436 and miR-513a-5p expressions were detected by qRT-PCR and the APE1 expression was detected by western blot. The results revealed that LINC01436 overexpression up-regulated APE1 protein expression and down-regulated miR-513a-5p expression in comparison with the NC group, and miR-513a-5p overexpression down-regulated APE1 expression (vs LINC01436 group) (Figure 6A). These results further indicated that LINC01436 could promote the expression of APE1 via repressing miR-513a-5p in GC cells. The results of rescue experiments showed that co-transfection of miR-513a-5p or si-APE1 into BGC-823 cells partly reversed the promotive effects of LINC01436 on the malignant phenotypes of BGC-823 cells (Figure 6D). In brief, LINC01436 participated in GC cell proliferation, apoptosis, metastasis and radioresistance via regulating miR-513a-5p and APE1 expressions.To further probe the downstream mechanism of LINC01436, we turned to StarBase database (http://starbase.sysu.edu.cn/) to predict potential downstream targets of LINC01436 and found that miR-513a-5p was one of its potential targets (Figure 3A).	33116638	RID04616	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE67939,GSE41245)
Osteoporosis	SNHG5	RUNX3	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-582-5p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000020633	NA	387066	864	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	AML2|CBFA3|PEBP2A3	SNHG5/miR-582-5p/RUNX3 feedback loop regulates osteogenic differentiation and apoptosis of bone marrow mesenchymal stem cells.Most importantly, we observed that the levels of SNHG5 and RUNX3 were gradually elevated due to the prolongation of osteogenic induction (Figure 1f). The tendencies of SNHG5 and RUNX3 were further confirmed by fluorescent in situ hybridization (FISH; Figure 1g). On the whole, these findings revealed that SNHG5 and RUNX3 might participate in the regulation of hBMSC osteogenic differentiation.Then, we tried to explore the role of SNHG5 in the progression of osteoporosis. SNHG5 was knocked down in hBMSCs by utilization of sh-SNHG5#1/2/3 plasmids and cells transfected with sh-SNHG5#1 vector presented the lowest SNHG5 expression (Figure 2a). Our results showed that the messenger RNA (mRNA) and protein expression levels of OCN, OSX, and COL1A were prominently dropped after 14 days of osteogenic induction attributable to SNHG5 depletion (Figure 2b,c). Meanwhile, the silencing of SNHG5 dramatically weakened ALP activity on Day 14 of hBMSC osteogenic differentiation (Figure 2d). Similarly, SNHG5 inhibition caused the dramatic reduction of matrix mineralization as validated by Alizarin Red S staining (Figure 2e).pull-down assay revealed that miR-582-5p could be pulled down by bio-SNHG5-WT and bio-RUNX3-WT, but not bio-NC, bio-SNHG5-Mut or bio-RUNX3- Mut (Figure 3g). Luciferase reporter assay elucidated that only the luciferase activities of SNHG5-WT and RUNX3-WT were decreased by miR-582-5p mimic, whereas those of SNHG5-Mut and RUNX3-Mut had no overt changes (Figure 3h). Concordantly, RIP experiments unraveled that SNHG5, miR-582-5p, and RUNX3 were highly expressed in Ago2 precipitates, certifying the interaction of miR-582-5p with SNHG5 and RUNX3 (Figure 3i).To testify the potential binding capacity of RUNX3 to SNHG5 promoter, ChIP assay was carried out and illuminated that the SNHG5 promoter was abundant in complexes enriched by the RUNX3 antibody, suggesting that RUNX3 directly bound to SNHG5 promoter (Figure 4b). Thereafter, RUNX3 was overexpressed by transfection with pcDNA3.1/RUNX3 vector (Figure 4c). Luciferase reporter assay elucidated that the upregulation of RUNX3 fortified the luciferase activity of the SNHG5 promoter (Figure 4d). In addition, the expression of SNHG5 was increased on account of RUNX3 overexpression (Figure 4e). In a word, we concluded that RUNX3 worked as a transcriptional activator of SNHG5.	33111341	RID04617	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Glioblastoma	SRC-1	XIST	positively-E	luciferase reporter assay;RNA pull-down assay;overexpression	upregulation	RT-qPCR	GSE4271;GSE44412;GSE2223;GSE4058	NA	cell stemness(+)	NA	regulation	protein-RNA	NA	CSC	NA	Cancer	Brain glioma	PCG	lncRNA	NA	NA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	Steroid receptor coactivator-1 enhances the stemness of glioblastoma by activating long noncoding RNA XIST/miR-152/KLF4 pathway.western blot and IF were used to detect the expression and distribution of SRC-1 in glioma tumor tissue and GBM cell lines. Together, our findings indicate that SRC-1 expression is positively correlated with clinical glioma malignant grade and inversely correlated with patient  prognosis.To explore the possible functions of SRC-1 in GBM, SRC-1 knockdown and overexpression cells were developed and named as U251-shSRC1, U87-shSRC1, C6-shSRC1, and LN229-SRC1. These cells were used to investigate the effects of SRC-1 on cell proliferation and migration in GBM cells. First, the results of MTT and colony formation revealed that SRC-1 knockdown significantly suppressed U251, U87, and C6 cell proliferation, whereas SRC-1 overexpression increased cell proliferation in LN229 cells (Figure 2A-F). SRC-1 knockdown increased the percentage of U251 cells in the G0/G1 phase with a concomitant decrease in S and G2/M phase (Figure 2G). Furthermore, SRC-1 knockdown suppressed the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, and cyclin-dependent kinase 4 (CDK4) (Figure 2H). In contrast, SRC-1 overexpression significantly reduced the percentage of LN229 cells in the G0/G1 phase and upregulated the expression of PCNA, cyclin D1, and CDK4 (Figure 2I,J).Silencing SRC-1 remarkably reduced the proliferation of U251 cells treated with TMZ or SOR (Figure 2K,L).As shown in Figure 3A-D, SRC-1 knockdown significantly reduced U251, U87, and C6 cell migration rates, and the reverse was shown in LN229-SRC1 and LN229-EV cells. To verify the roles of SRC-1 on the epithelial-mesenchymal transition (EMT) process, the protein expression of N-cadherin, E-cadherin, Vimentin, and TWIST1 was detected by western blot and IF. Our data confirmed that SRC-1 plays an important role in promoting EMT of GBM cells (Figure 3E-H). Together, these data suggest that SRC-1 promotes GBM cell proliferation and migration.In further efforts to investigate the downstream target genes for SRC-1 in GBM, we extracted total RNA from both U251-EV and U251-shSRC1 cells and generated the global gene expression profile by RNA-seq (Figure 6A). The RNA expression level of lncRNA XIST was less than eightfold in U251-shSRC1 cells compared with U251-EV cells (Figure 6B and Table S5).We validated the RNA-seq data by using RT-qPCR analysis. The results confirmed that XIST expression was robustly inhibited following SRC-1 knockdown and that XIST expression was increased following SRC-1 overexpression (Figure 6F,G).The expression of KLF4 and miR-152 was detected by RT-qPCR and western blot. The results revealed that KLF4 expression was inhibited and miR-152 expression was upregulated by SRC-1 knockdown, whereas overexpression of SRC-1 increased KLF4 expression and decreased miR-152 expression (Figure 6K,L). Then XIST expression was reverse rescued by transient siRNA transfection in LN229-SRC1 cells. The RT-qPCR results revealed that XIST reversed the expression of miR-152 but not KLF4 at RNA level, and western blotshowed that KLF4 protein expression was significantly decreased (Figure 7A,B). Furthermore, knockdown of XIST by siRNA abolished the induced sphere-forming ability of SRC-1 in LN229-SRC1 cells (Figure 7C). Next, to further confirm the role of miR-152 for SRC-1-regulated KLF4 and SRC-1-mediated stem-like characteristics in GBM cells, miR-152 expression was rescued by transient transfection of miR-152 mimic in LN229-SRC1 cell. The results revealed that miR-152 reversed the expression of KLF4 and XIST, and that miR-152 mimic abolished the induced sphere-forming ability of SRC-1/XIST in LN229-SRC1 cells (Figure 7D-F).To this end, we cloned the sequence of XIST promoter (-1982, +219) by PCR and inserted the sequence into luciferase reporter pGL3-basic plasmid. Dual-luciferase reporter results showed that firefly luciferase did not significantly change after SRC-1 overexpression in 293T cells, which suggested that SRC-1 does not influence the proximal XIST promoter activity (Figure 7G). These results implied that SRC-1 might posttranscriptionally regulate XIST. Moreover, patients with high expression of SRC-1 showed poorer overall survival than those with low expression (GSE44412, GSE4271) (Figure 1F).The results confirmed that XIST expression was robustly inhibited following SRC-1 knockdown and that XIST expression was increased following SRC-1 overexpression (Figure 6F,G).	33090636	RID04618	expression association	prognosis		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Glioblastoma	XIST	KLF4	positively-E	luciferase reporter assay;RNA pull-down assay;overexpression	upregulation	RT-qPCR	GSE4271;GSE44412;GSE2223;GSE4058	NA	cell stemness(+)	ceRNA(miR-152)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136826	NA	7503	9314	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	EZF|GKLF	Steroid receptor coactivator-1 enhances the stemness of glioblastoma by activating long noncoding RNA XIST/miR-152/KLF4 pathway.western blot and IF were used to detect the expression and distribution of SRC-1 in glioma tumor tissue and GBM cell lines. Together, our findings indicate that SRC-1 expression is positively correlated with clinical glioma malignant grade and inversely correlated with patient  prognosis.To explore the possible functions of SRC-1 in GBM, SRC-1 knockdown and overexpression cells were developed and named as U251-shSRC1, U87-shSRC1, C6-shSRC1, and LN229-SRC1. These cells were used to investigate the effects of SRC-1 on cell proliferation and migration in GBM cells. First, the results of MTT and colony formation revealed that SRC-1 knockdown significantly suppressed U251, U87, and C6 cell proliferation, whereas SRC-1 overexpression increased cell proliferation in LN229 cells (Figure 2A-F). SRC-1 knockdown increased the percentage of U251 cells in the G0/G1 phase with a concomitant decrease in S and G2/M phase (Figure 2G). Furthermore, SRC-1 knockdown suppressed the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, and cyclin-dependent kinase 4 (CDK4) (Figure 2H). In contrast, SRC-1 overexpression significantly reduced the percentage of LN229 cells in the G0/G1 phase and upregulated the expression of PCNA, cyclin D1, and CDK4 (Figure 2I,J).Silencing SRC-1 remarkably reduced the proliferation of U251 cells treated with TMZ or SOR (Figure 2K,L).As shown in Figure 3A-D, SRC-1 knockdown significantly reduced U251, U87, and C6 cell migration rates, and the reverse was shown in LN229-SRC1 and LN229-EV cells. To verify the roles of SRC-1 on the epithelial-mesenchymal transition (EMT) process, the protein expression of N-cadherin, E-cadherin, Vimentin, and TWIST1 was detected by western blot and IF. Our data confirmed that SRC-1 plays an important role in promoting EMT of GBM cells (Figure 3E-H). Together, these data suggest that SRC-1 promotes GBM cell proliferation and migration.In further efforts to investigate the downstream target genes for SRC-1 in GBM, we extracted total RNA from both U251-EV and U251-shSRC1 cells and generated the global gene expression profile by RNA-seq (Figure 6A). The RNA expression level of lncRNA XIST was less than eightfold in U251-shSRC1 cells compared with U251-EV cells (Figure 6B and Table S5).We validated the RNA-seq data by using RT-qPCR analysis. The results confirmed that XIST expression was robustly inhibited following SRC-1 knockdown and that XIST expression was increased following SRC-1 overexpression (Figure 6F,G).The expression of KLF4 and miR-152 was detected by RT-qPCR and western blot. The results revealed that KLF4 expression was inhibited and miR-152 expression was upregulated by SRC-1 knockdown, whereas overexpression of SRC-1 increased KLF4 expression and decreased miR-152 expression (Figure 6K,L). Then XIST expression was reverse rescued by transient siRNA transfection in LN229-SRC1 cells. The RT-qPCR results revealed that XIST reversed the expression of miR-152 but not KLF4 at RNA level, and western blotshowed that KLF4 protein expression was significantly decreased (Figure 7A,B). Furthermore, knockdown of XIST by siRNA abolished the induced sphere-forming ability of SRC-1 in LN229-SRC1 cells (Figure 7C). Next, to further confirm the role of miR-152 for SRC-1-regulated KLF4 and SRC-1-mediated stem-like characteristics in GBM cells, miR-152 expression was rescued by transient transfection of miR-152 mimic in LN229-SRC1 cell. The results revealed that miR-152 reversed the expression of KLF4 and XIST, and that miR-152 mimic abolished the induced sphere-forming ability of SRC-1/XIST in LN229-SRC1 cells (Figure 7D-F).To this end, we cloned the sequence of XIST promoter (-1982, +219) by PCR and inserted the sequence into luciferase reporter pGL3-basic plasmid. Dual-luciferase reporter results showed that firefly luciferase did not significantly change after SRC-1 overexpression in 293T cells, which suggested that SRC-1 does not influence the proximal XIST promoter activity (Figure 7G). These results implied that SRC-1 might posttranscriptionally regulate XIST.	33090636	RID04619	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Cervical cancer	LINC01133	FOXD1	positively-E	luciferase reporter assay;StarBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000251493	NA	100505633	2297	lncRNA-PAGBC	FKHL8|FREAC4	LINC01133 promotes the progression of cervical cancer via regulating miR-30a-5p/FOXD1.T o figure out the expression characteristics of LINC01133, we detected the expression of LINC01133 in CC tissues and normal tissues adjacent to cancer by qRT-PCR The results showed that the expression of LINC01133 in CC tissue was dramatically upregulated compared with the normal group (Figure1A).Consistently, we found that the expression of LINC01133 in CC was significantly higher than that in normal tissues (Figure1C). T o understand the significance of LINC01133 upregulation in CC, we explored the correlation between LINC01133 expression and clinical characteristics of patients with CC. According to the median expression level of LINC01133, 50 patients were divided into LINC01133 high-expression group and LINC01133 low-expression group. Our data suggested that the high expression of LINC01133 in CC tissues was associated with higher T stage and negative HPV infection, but not with age, histological type, lymph node metastasis and differentiation (T able2).The results showed that overexpression of LINC01133 inhibited the apoptosis of CC cells, whereas its knockdown promoted cell apoptosis (Figures2Dand S2). Transwell assay was done to detect the migration and invasion of CC cells. The results showed that overexpression of LINC01133 promoted the migration and invasion of CC cells, whereas knockdown of LINC01133 inhibited the migration and invasion of CC cells (Figure2E, F). Collectively, we concluded that LINC01133 could modulate the malignant phenotypes of CC cells.dual-luciferase reporter assay showed that the luciferase activity of the vector containing LINC01133-wt sequence was significantly reduced by the mimics of miR-30a-5p, but the luciferase activity of the LINC01133-MUT vector was not affected by the transfection of miR-30a-5p (Figure3B). In addition, qRT-PCRdemonstrated that the expression of miR-30a5p in CC tissues and cell lines was significantly downregulated compared with normal tissues and cervical epidermal cells (Figure3C,D). Collectively, these results validated that miR-30a-5p was a target of LINC01133 and could be negatively regulated by it. Flow cytometry analysis showed that overexpression of miR-30a-5p promoted the apoptosis of CC cells, whereas inhibitors of miR-30a-5p inhibited the apoptosis (Figures4Dand S4). Transwell assay was done to detect the invasion and migration of CC cells. Overexpression of miR-30a5p inhibited the migration and invasion of CC cells compared with NC group. Compared with NC-inhibitor group, inhibition of miR-30a-5p promoted the migration and invasion of CC cells, whereas miR-30a-5p inhibited the metastatic potential of CC cells (Figure4E,F).Based on these results, we concluded that miR-30a-5p was a tumor suppressor in CC.In addition, as shown, overexpression of miR30a-5p decreased FOXD1 expression, whereas the transfection of miR-30a-5p inhibitors increased FOXD1 expression (Figure5C). Overexpression of LINC01133 upregulated FOXD1 expression, whereas knockdown of LINC01133 downregulated FOXD1 (Figure5D). Thus, we concluded that LINC01133/miR-30a-5p axis could target FOXD1 to regulate the progression of CC.The results proved that overexpression of LINC01133 increased the expression of FOXD1 and downregulated the expression of miR-30a5p compared with Vector group; further overexpression of miR-30a-5p resulted in the downregulation of FOXD1 expression (vsLINC01133 group; Figure6A). Overexpression of LINC01133 promoted the proliferation of CC cells, and the cotransfection of miR-30a-5p mimics partly reversed this effect (Figure6D, E). Then the apoptosis of CC cells was detected by flow cytometry. The results showed that overexpression of LINC01133 could inhibit the apoptosis of CC cells, and miR-30a-5p mimics abolished the effect (Figure6F). Transwell assay showed that the overexpression of LINC01133 could promote the migration and invasion of CC cells, and miR-30a-5p mimics reversed these effects (Figure6. G, H). In conclusion, LINC01133 could regulate the proliferation, migration and invasion of CC cells by regulating the miR-30a-5p/FOXD1 axis.To explore the downstream mechanism of LINC01133 in CC, we predicted the downstream target of LINC01133 through StarBase database (http://starbase.sysu.edu.cn) and found that miR-30a-5p was one of its potential targets (Figure 3A). In conclusion, LINC01133 could regulate the proliferation, migration and invasion of CC cells by regulating themiR-30a-5p/FOXD1 axis.	33078907	RID04620	ceRNA or sponge	metastasis	UP(BRCA);DATA(GSE111065)	UP(BRCA);DATA(GSE55807)
Malignant glioma	LINC00466	CHEK1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-)	ceRNA(miR-508)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000224209	GRCh38_1:63159083-63317274	ENSG00000149554	NA	199899	1111	NA	CHK1	YY1-mediated up-regulation of lncRNA LINC00466 facilitates glioma progression via miR-508/CHEK1.	33037684	RID04621	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE67939)
Malignant glioma	YY1	LINC00466	positively-E	luciferase reporter assay;JASPAR;siRNA;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000100811	NA	ENSG00000224209	GRCh38_1:63159083-63317274	7528	199899	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	YY1-mediated up-regulation of lncRNA LINC00466 facilitates glioma progression via miR-508/CHEK1.qRT-PCRwas utilized to analyze LINC00466 in human glioma tissues and cell lines. Luciferase reporter assays were performed to explore whether YY1 could bind to the promoter region of LINC00466. We report that LINC00466 expression is increased in glioma cells and tissues. YY1 transcription factor (YY1) can bind directly to the LINC00466 promoter region. YY1 activates LINC00466 expression in the glioma cells.Therefore, we next sought to investigate whether YY1 could exactly bind to LINC00466 promoter and induce its expression. Two Jaspar algorithms predicting binding sites (with high predicting scores) were shown in Figure 2E.We next respectively transfected siRNAs targeting YY1 (si-YY1) and pcDNA3.1-YY1 into LN229 cells, and found that repressing YY1 expression significantly reduces LINC00466 levels, while LINC00466 expression is elevated depending on YY1 overexpression (Figure 2F). Then, ChIP assays demonstrated that YY1 can bind to P1 site of LINC00466 promoter (Figure 2G). Luciferase assays also validated that YY1 is capable to bind to LINC00466 promoter (Figure 2H).these data demonstrate that the silence of LINC00466 depresses the proliferation and induces apoptosis of glioma cells in vitro.Hence, we demonstrate that LINC00466 depletion impairs the metastatic abilities of glioma cells.	33037684	RID04622	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Chordoma	LINC00525	HMGB1	positively-E	luciferase reporter assay;RIP;StarBase 3.0;miRDB;TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-505-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Chordoma	lncRNA	TF	ENSG00000146666	GRCh38_7:47761476-47766772	ENSG00000189403	NA	84847	3146	NA	DKFZp686A04236|HMG1|HMG3|SBP-1	Long Noncoding RNA LINC00525 Promotes the Aggressive Phenotype of Chordoma Through Acting as a microRNA-505-3p Sponge and Consequently Raising HMGB1 Expression.First, GEPIA (http://gepia.cancer-pku.cn/) was used to identify the expression of LINC00525 in human cancers. Notably, LINC00525 was upregulated in the majority of human cancer types (Figure 1A). To address the dysregulation of LINC00525 in chordoma, RT-qPCR was conducted to detect the expression of this lncRNA in 33 chordoma tissues and 17 nucleus pulposus tissues. LINC00525 was shown to be overexpressed in chordoma tissues relative to pulposus tissues (Figure 1B).CCK-8 assay was performed to test the effect of LINC00525 knockdown on the proliferation of chordoma cells. The results indicated that downregulation of LINC00525 strikingly suppressed the proliferative capacities of U-CH1 and U-CH2 cells (Figure 1D). In addition, transfection with si-LINC00525 led to an increased frequency of apoptosis in U-CH1 and U-CH2 cells, as demonstrated by the flow cytometric analysis (Figure 1E). Furthermore, migration and invasion assays revealed that the loss of LINC00525 restricted both the migration (Figure 1F) and invasion (Figure 1G) of U-CH1 and U-CH2 cells. These results suggest that LINC00525 is upregulated and executes cancer-promoting roles in chordomas.Luciferase reporter assay was performed to explore the binding between LINC00525 and miR-505-3p in chordoma cells. Notably, the luciferase activity of wt-LINC00525 was clearly decreased in U-CH1 and U-CH2 cells after the introduction of miR-505-3p mimic. However, the luciferase activity of mut-LINC00525 was not altered significantly in response to co-transfection with miR-505-3p mimic (Figure 2D). RIP assay demonstrated the increased enrichment of both LINC00525 and miR-505-3p in the Ago2-immunoprecipitated pellet (Figure 2E), which further supported a direct interaction between LINC00525 and miR-505-3p in chordoma. Next, RT-qPCR analysis illustrated that miR-505-3p was weakly expressed in chordoma tissues (Figure 2F) and was negatively associated with LINC00525 expression (Figure 2G; r = -0.6844, P < 0.0001). To further verify the potential involvement of LINC00525 in modulating miR-505-3p expression, RT-qPCR analysis was performed to detect the expression of this miRNA in LINC00525-depleted U-CH1 and U-CH2 cells. Here, the downregulation of LINC00525 obviously promoted the expression of miR-505-3p in U-CH1 and U-CH2 cells (Figure 2H). In summary, these results proved that LINC00525 could act as a ceRNA in chordoma by directly sponging miR-505-3p.Next, we attempted to address whether LINC00525 could control HMGB1 expression in chordoma cells. U-CH1 and U-CH2 cells were transfected with si-LINC00525 or si-NC, and HMGB1 expression was measured. Notably, the levels of both HMGB1 mRNA (Figure 4G) and protein (Figure 4H) were decreased in U-CH1 and U-CH2 cells after the knockdown of LINC00525. A correlation analysis revealed a positive correlation between HMGB1 mRNA and LINC00525 expression in chordoma tissues (Figure 4I; r = 0.6394, P < 0.0001). To illustrate the interaction of miR-505-3p with LINC00525 and HMGB1 in chordoma cells, U-CH1 and U-CH2 cells were co-transfected with si-LINC00525 and either the miR-505-3p inhibitor or NC inhibitor. RT-qPCR and western blot verified that si-LINC00525 downregulated the expression of HMGB1 mRNA (Figure 4J) and protein (Figure 4K) in U-CH1 and U-CH2 cells, whereas this expression was partly recovered by co-transfection with the miR-505-3p inhibitor. Collectively, these data illustrate that LINC00525 positively regulates HMGB1 expression in chordoma cells by binding competitively to miR-505-3p.Meanwhile, western blot was employed to evaluate the transfection efficiency of HMGB1 overexpression plasmid pcDNA3.1-HMGB1, and the results indicated that transfection with pcDNA3.1-HMGB1 resulted in an obvious increase of HMGB1 protein expression in U-CH1 and U-CH2 cells (Figure 6A). The si-LINC00525 in parallel with pcDNA3.1-HMGB1 or pcDNA3.1 was introduced into U-CH1 and U-CH2 cells. The LINC00525 knockdown-induced suppression of U-CH1 and U-CH2 cell proliferation (Figure 6B) and enhancement of cell apoptosis (Figure 6C) were reversed by HMGB1 reintroduction. Furthermore, the hindered migration (Figure 6D) and invasion (Figure 6E) of U-CH1 and U-CH2 cells after LINC00525 silencing was recovered with the co-transfection of pcDNA3.1-HMGB1. Taken together, these results suggest that LINC00525 promotes chordoma progression through the miR-505-3p/HMGB1 axis.bioinformatics Analysis StarBase 3.0 (http://starbase.sysu.edu.cn/) was used to predict the potential miRNA(s) that would bind to LINC00525. The potential target mRNA(s) of miR-505-3p were identified using the miRDB tool (http://mirdb.org/miRDB/index.html), starBase 3.0, and TargetScan (http://www.targetscan.org/vert_60/).	32982292	RID04623	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Osteosarcoma	LINC00511	E2F1	positively-E	dual-luciferase reporter assay;siRNA;RNA pull-down assay;StarBase;TargetScan	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-185-3p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000101412	NA	400619	1869	onco-lncRNA-12	RBBP3|RBP3	LINC00511 Promotes Osteosarcoma tumorigenesis and Invasiveness through the miR-185-3p/E2F1 Axis.In our previous research, we obtained the expression profile of differentially expressed lncRNAs in osteosarcoma and found that many lncRNAs were abnormally expressed between osteosarcoma and nontumor tissues, and a new lncRNA LINC00511 was significantly upregulated in osteosarcoma samples. For determining the effect of LINC00511 knockdown on osteosarcoma cell proliferation, CCK-8 assay was used. The results of the CCK-8 assay indicated that the proliferation rate of SW1353 and U2OS cells transfected with si-LINC00511 was reduced by at least two times compared to the control (Figures 2(e) and 2(f)). It could be known that the LINC00511 knockdown could inhibit osteosarcoma cell proliferation.Next, we tested whether the knockdown of LINC00511 influenced the osteosarcoma cell metastatic abilities. As shown in Figures -Figures33 and -and4,4, the osteosarcoma cells (SW1353, U2OS) with LINC00511 knockdown had a smaller number of the nucleus relative to the negative control group. This directly indicated that the osteosarcoma cells knocked down of LINC00511 had much weaker migration and invasion ability. In conclusion, knockdown of LINC00511 inhibited osteosarcoma cell migration and invasion.LINC00511 is a lncRNA that can exert its functions as a "Sponge'-of relevant miRNAs, thus affecting the translation of target genes. To explore the mechanism of how LINC00511 played an important role in osteosarcoma cells, we performed a bioinformatics analysis of LINC00511. The prediction combining with previous reports showed miR-185-3p as the potential miRNA was associated with LINC00511. In order to confirm this, we first used qRT-PCRto measure the expression of miR-185-3p, and LINC00511 under different treatments. The expression level of miR-185-3p in SW1353 and U2OS cells with si-LINC00511 was nearly three times higher than that in the negative control groups (Figure 5(b)). That indicated knockdown of LINC00511 promoted miR-185-3p expression. In another set of experiments, osteosarcoma cells transfected with miR-185-3p showed lower LINC00511 expression than controls which showed that the expression of LINC00511 could be reduced by miR-185-3p (Figure 5(a)).In addition, we used a dual-luciferase reporter assay to further ascertain the binding affinity between miR-185-3p and LINC00511 or 3'-UTR of E2F1. It was shown that the transfection of miR-185-3p mimic reduced the luciferase activities in the original LINC00511 and 3'-UTR of E2F1, but not in the mutant (Figures 5(e) and 5(f)). All the data demonstrated that LINC00511 promoted osteosarcoma cell progression by regulating the miR-185-3p/E2F1 axis.By using the Starbase and TargetScan databases, we predicted E2F1 was a potential target of LINC00511/miR-185-3p.All the data demonstrated that LINC00511 promoted osteosarcoma cell progression by regulating the miR-185-3p/E2F1 axis.	32964019	RID04624	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	PCNAP1	SOX4	positively-E	luciferase reporter assay;TargetScan;miRcode	upregulation	qRT-PCR	NA	NA	prognosis(-);cell metastasis(+);cell migration(+);cell invasion(+)	ceRNA(miR-340-5p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000249065	GRCh38_4:99160514-99161645	ENSG00000124766	NA	359806	6659	p1PCNA	NA	lncRNA PCNAP1 predicts poor prognosis in breast cancer and promotes cancer metastasis via miR-340-5p-dependent upregulation of SOX4.We then performed RT-qPCR to check the relative expression levels of lncRNA PCNAP1. We found that the basal expression level of lncRNA PCNAP1 in BC was 0.217, which was significantly higher than that in corresponding adjacent healthy tissues (P<0.001) (Fig. 1A). Intriguingly, patients with metastasis had higher lncRNA PCNAP1 levels compared with those without metastasis (P<0.001) (Fig. 1B). To explore the role of lncRNA PCNAP1 in BC progression, loss-of-function experiments using siRNAs (siPCNAP1#a and siPCNAP1#b) and CCK-8 assays were performed in breast cancer cell lines MDA-MB-231 and MCF7. Levels of lncRNA PCNAP1 expression were markedly decreased in both cell types; by ~80% or ~70%, respectively, compared with the scrambled controls (P<0.001 in MDA-MB-231; P<0.01 in MCF7) (Fig. 2A and B). However, no significant effect of lncRNA PCNAP1 knockdown on BC cell viability was observed, consistent with the results of the CCK-8 assays (Fig. 2C and D). Given that lncRNA PCNAP1 levels were increased in metastatic samples, we conducted cell migration, invasion, and wound healing assays to determine whether there was an effect on BC cell metastasis. Loss of lncRNA PCNAP1 significantly decreased the speed of scratch closure in the two BC cell lines: By ~64% (P<0.01) in MDA-MB-231 and by ~82% (P<0.001) in MCF7 (Fig. 2E-H). In addition, inhibition of lncRNA PCNAP1 decreased invasion dramatically, as shown by the Transwell invasion assay results (P<0.01) (Fig. 2I-K). Furthermore, we cloned wild-type (WT) lncRNA PCNAP1 luciferase plasmids containing potential miR-340-5p binding sites or mutants (MUT) for each site. Luciferase assays were performed to confirm the interaction between miR-340-5p and lncRNA PCNAP1 after transfecting the plasmids with miR-340-5p mimics into MBA-MD-231 and MCF7 cells. The miR-340-5p mimics substantially inhibited the luciferase activity of WT lncRNA PCNAP1, by ~60% (P<0.01); however, they did not affect the luciferase activity of the lncRNA PCNAP1-MUT (Fig. 3D and E). To confirm these results, lncRNA PCNAP1 was knocked down in both MBA-MD-231 and MCF7 cells; the knockdown of lncRNA PCNAP1 increased the level of miR-340-5p 2-fold (P<0.01) as expected (Fig. 3F and G).To verify this result, we performed luciferase reporter assays in both MDA-MB-231 and MCF7 cells, and the reported luciferase contained SOX4-WT as well as SOX4-MUT without potential binding sites. The vector was co-transfected into MDA-MB-231 and MCF7 cells with miR-340-5p mimics and miR-340-5p inhibitor. The miR-340-5p mimics inhibited the luciferase activity of SOX4-WT by ~60 and ~64% in MDA-MB-231 and MCF7 cells, respectively, but did not inhibit the luciferase activity of SOX4-MUT (P<0.01 in MDA-MB-231; P<0.01 in MCF7) (Fig. 5C and D), indicating that miRNA-340-5p can directly target SOX4.To test whether lncRNA PCNAP1 promotes the metastasis of BC cells by regulating SOX4, we first analyzed the clinical organization of BC. Immunohistochemistry results showed that SOX4 expression was upregulated in BC tissues relative to adjacent tissues (Fig. 6A), and RT-qPCR results confirmed this finding (Fig. 6B). Furthermore, the expression of SOX4 was significantly upregulated in tissues of metastatic patients compared with those of non-metastatic patients (Fig. 6C). This result was consistent with those obtained for lncRNA PCNAP1 in BC tissues. Therefore, we performed a correlation analysis for lncRNA PCNAP1 and SOX4 expression in tumor tissues of metastatic patients. The results showed a significant positive correlation between lncRNA PCNAP1 and SOX4 expression in metastatic tissues (Fig. 6D). The expression of SOX4 was also significantly downregulated after knockdown of lncRNA PCNAP in the MDA-MB-231 and MCF7 cells, which confirmed the correlation between the two (Fig. 6E-G). By contrast, miR-340-5p expression was negatively correlated with SOX4 expression in metastatic tissues (Fig. 6H). western blotconfirmed that overexpression of miR-340-5p mimics in MDA-MB-231 and MCF7 cells resulted in a significant downregulation of SOX4 expression; by contrast, the miRNA inhibitor upregulated the expression of SOX4 (Fig. 6I-K). The Transwell assay results also confirmed that invasion of MCF7 was significantly decreased by the knockdown of lncRNA PCNAP1 and restored by the overexpression of SOX4 (Fig. 6L-O). Thus, the above results indicate that the lncRNA promotes the metastasis of breast cancer by downregulating miR-340-5p and consequently upregulating SOX4.To further explore the molecular mechanisms, we used bioinformatic tools to predict miRNAs that could bind lncRNA PCNAP1. Surprisingly, the first four miRNAs identified using the TargetScan software were all predicted to target SOX4 directly (Fig. 3B). The association between SOX4 and BC migration has been investigated previously (12,23). Of these four miRNA candidates, we focused on miR-340-5p, which could bind lncRNA PCNAP1 according to miRcode predictions (Fig. 3C). Furthermore, we cloned wild-type (WT) lncRNA PCNAP1 luciferase plasmids containing potential miR-340-5p binding sites or mutants (MUT) for each site.	32945462	RID04625	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	DUXAP8	BUB1	positively-E	luciferase reporter assay;StarBase	upregulation	qRT-PCR	GSE84402;GSE121248	NA	cell proliferation(+)	ceRNA(miR-490-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000169679	NA	503637	699	NA	BUB1A|BUB1L|hBUB1	Pseudogene DUXAP8 Promotes Cell Proliferation and Migration of Hepatocellular Carcinoma by Sponging MiR-490-5p to Induce BUB1 Expression.In order to understand the prognostic value of DUXAP8 in HCC, we performed an integrative analysis of HCC microarray profiles, including GSE84402 and GSE121248 datasets. As shown in Figures 1A,B, the results showed that DUXAP8 was overexpressed in HCC samples compared to normal tissues using GSE84402 (p < 0.001) and GSE121248 datasets (p < 0.001). Subsequently, the TCGA dataset was also used to determine the expression pattern of DUXAP8 in HCC. We also found upregulated DUXAP8 expression in HCC samples versus adjacent normal tissues (Figure 1C, p < 0.05). Very interestingly, we observed that DUXAP8 was upregulated in Stage II/III HCC samples compared to Stage I HCC samples (Figure 1D, p < 0.0 and p < 0.005). These results suggested that lncRNA DUXAP8 may play a regulatory role in HCC tumorigenesis and development.Next, the association between DUXAP8 expression and OS time and relapse-free survival (RFS) time were calculated by using the KM survival Plotter database. Kaplan-Meier survival curve analysis indicated that higher expression of DUXAP8 was significantly correlated with shorter OS time in patients with HCC (Figure 2A).Bioinformatics analysis showed that DUXAP8 was involved in regulating cancer proliferation in HCC. To further validate the biological function of DUXAP8 in HCC cells, we conducted loss-of-function assays by using specific siRNAs against DUXAP8. As shown in Figure 5, we found that the endogenous DUXAP8 expressions in Huh-7 and HepG2 cells transfected with siDUXAP8 were reduced by 53.4% (Figure 5A, p < 0.05) and 47.6% (Figure 5C, p < 0.05), respectively. Furthermore, CCK-8 assay was applied to detect the effect of DUXAP8 on cell proliferation in HCC. The results showed that the silencing of DUXAP8 significantly suppressed cell proliferation in both Huh-7 (Figure 5B, p < 0.01) and HepG2 (Figure 5D, p < 0.05).Furthermore, direct interaction between miR-490-5p and BUB1 or DUXAP8 was detected using luciferase assays (Figure 8D). The luciferase reporter assay revealed that luciferase activity was significantly repressed in the constructs of DUXAP8 (Figure 8E, p < 0.001)- and BUB1-3'UTR (Figure 8F, p < 0.001) when co-transfected with the corresponding miRNAs compared with NC, whereas the mutated 3'UTR did not show a significant response to miR-490-5p. Moreover, the results showed that BUB1 was suppressed after DUXAP8 knockdown and that the DUXAP8 knockdown-mediated suppression of BUB1 was reversed by miR-490-5 inhibitors in HCC cells (Figures 8G,H). Thus, these results showed that DUXAP8 sponges miR-490-5p to enhance BUB1 expression.In order to understand the prognostic value of DUXAP8 in HCC, we performed an integrative analysis of HCC microarray profiles, including GSE84402 and GSE121248 datasets. As shown in Figures 1A,B, the results showed that DUXAP8 was overexpressed in HCC samples compared to normal tissues using GSE84402 (p < 0.001) and GSE121248 datasets (p < 0.001).Starbase was then used to predict the potential miRNAs mediating the connection between BUB1 and DUXAP8, and MiR-490-5p was identified as the candidate miRNA involved in regulating both BUB1 and DUXAP8.Moreover, this study confirmed that DUXAP8 regulated HCC proliferation through BUB1.	32849765	RID04626	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Nasopharynx carcinoma	MIR924HG	SOCS1	negatively-E	RNA pull-down assay;catRAPID;RIP;siRNA	upregulation	qPCR	GSE12452;GSE53819	NA	cell proliferation(+);cell invasion(+);cell migration(+);JAK/STAT signaling pathway(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000267374	GRCh38_18:39206917-39800322	ENSG00000185338	NA	647946	8651	LINC00669	Cish1|JAB|SOCS-1|SSI-1|TIP3	LINC00669 insulates the JAK/STAT suppressor SOCS1 to promote nasopharyngeal cancer cell proliferation and invasion.None of the other lncRNAs showed significant difference in the survival curve analysis except for three classical lncRNAs of LINC00669, AFAP1-AS1 and CT75, whose upregulation are negatively correlated to the overall survival of NPC patients (Fig. -(Fig.1b,1b, c). Since LINC0069 was a novel lncRNA whose function was completely unknown, we made it the focus in our current study. Consistently, LINC00669 was confirmed by qPCR to be significantly upregulated in the patient-derived NPC tumors (Fig. -(Fig.1d)1d) Next, we conducted gain- and loss- of function assays to explore the functions of LINC00669 in NPC. Consistent in both CNE-2 and 5-8F cell lines, forced expression of LINC00669 dramatically promoted cell proliferation (Fig. 2a), invasion (Fig. -(Fig.2b)2b) and migration (Fig. -(Fig.2c),2c), while its depletion by small interfering RNA (siRNA) exhibited the opposite effects. Meanwhile, LINC00669 is essential for the survival of NPC cells as indicated by the strikingly induced spontaneous apoptosis upon loss of LINC00669 (Fig. -(Fig.2d).2d). Together, these data indicated that LINC00669 profoundly endows carcinogenic properties of NPC cells.Inspired by the cytoplasmic localization of LINC00669 (Fig. -(Fig.1e),1e), we speculated that it might participate in the translational or signaling regulations. To identify its target proteins, we incubated CNE-2 cell lysates with a biotin-labeled LINC00669, and proceeded with electrophoresis followed by silver staining. Mass spectrum analysis of the unique protein bands detected only in the sense but not anti-sense LINC00669-incubated cell lysates by silver staining indicated SOCS1 as a potential LINC00669-targeting protein (Fig. 3a). The direct interaction between LINC00669 and SOCS1 was further confirmed by western blot on LINC00669 pull-down cell lysates using an antibody against SOCS1 (Fig. -(Fig.3b).3b). Vice versa, RNA-immunoprecipitation (RIP) assay using SOCS1 antibody followed by qPCR analysis demonstrated that SOCS1 specifically precipitated LINC00669 in both CNE-2 and 5-8F cell lysates, and the enrichment of LINC00669 was largely decreased upon siRNA-mediated depletion of LINC00669 (Fig. -(Fig.33c).Aberrant activation of the JAK/STAT pathway has been found in many tumors [10]. Indeed, most of the component genes of this signaling pathway were upregulated in human NPC tumors at the transcription level (Fig. 5a). Unexpectedly, this was concurrent with upregulation of the negative feedback regulator SOCS1. We further examined the expression of SOCS1 and STAT1 proteins in NPC tumors and para-carcinoma tissues by IHC. Although SOCS1 levels were comparative between the normal and cancerous tissues, it was NPC tumors instead of para-carcinoma tissues that exhibited a strong immunostaining signal of STAT1 (Fig. -(Fig.5b),5b), indicating the interrupted Inhibition of SOCS1 on STAT1 in NPC tumors. Given the fact that SOCS1 strongly interacts with LINC00669, which is highly expressed in NPC tumors, we investigated how changes of LINC00669 and then its interaction with SOCS1 would affect SOCS1/STAT1 network. Obviously, transcription of SOCS1 and STAT1 did not vary with the expression of LINC00669 (Fig. -(Fig.5c).5c). Nor did SOCS1 protein change accordingly (Fig. -(Fig.5d).5d). Instead, STAT1 protein was increased when LINC00669 was overexpressed and was decreased when LINC00669 was depleted (Fig. -(Fig.5d).5d). Concomitantly, loss of LINC00669 also led to an increase in ubiquitination of STAT1 (Fig. -(Fig.5e),5e), which could be reversed upon forced expression of LINC00669 (Fig. -(Fig.55f).to explore novel lncRNAs that play key roles in NPC, we retrieved and interrogated the expression profiles of lncRNAs in two independent NPC mRNA expression profiling databases of GSE12452 [14] and GSE53819 [15] to have identified 153 commonly upregulated signatures (Fig. 1a)LINC00669 physically interacts with SOCS1. The direct interaction between LINC00669 and SOCS1 was further confirmed by western blot on LINC00669 pull-down cell lysates using an antibody against SOCS1 (Fig. -(Fig.3b).3b). Vice versa, RNA-immunoprecipitation (RIP) assay using SOCS1 antibody followed by qPCR analysis demonstrated that SOCS1 specifically precipitated LINC00669 in both CNE-2 and 5-8F cell lysates, and the enrichment of LINC00669 was largely decreased upon siRNA-mediated depletion of LINC00669.Consistent with the predication by catRAPID, only the constructs encompassing region of 190'-83-nt were able to pull-down SOCS1 (Fig. -(Fig.3g).3g). Taken together, these data indicated SOCS1 is an immediate target of LINC00669 for executing its oncogenic functions in NPC cells.	32831137	RID04627	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	MIR924HG	STAT1	positively-E	overexpression	upregulation	qPCR	GSE12452;GSE53820	NA	cell proliferation(+);cell invasion(+);cell migration(+);JAK/STAT signaling pathway(+);apoptosis process(-)	ubiquitination	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000267374	GRCh38_18:39206917-39800322	ENSG00000115415	NA	647946	6772	LINC00669	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	LINC00669 insulates the JAK/STAT suppressor SOCS1 to promote nasopharyngeal cancer cell proliferation and invasion.None of the other lncRNAs showed significant difference in the survival curve analysis except for three classical lncRNAs of LINC00669, AFAP1-AS1 and CT75, whose upregulation are negatively correlated to the overall survival of NPC patients (Fig. -(Fig.1b,1b, c). Since LINC0069 was a novel lncRNA whose function was completely unknown, we made it the focus in our current study. Consistently, LINC00669 was confirmed by qPCR to be significantly upregulated in the patient-derived NPC tumors (Fig. -(Fig.1d)1d) Next, we conducted gain- and loss- of function assays to explore the functions of LINC00669 in NPC. Consistent in both CNE-2 and 5-8F cell lines, forced expression of LINC00669 dramatically promoted cell proliferation (Fig. 2a), invasion (Fig. -(Fig.2b)2b) and migration (Fig. -(Fig.2c),2c), while its depletion by small interfering RNA (siRNA) exhibited the opposite effects. Meanwhile, LINC00669 is essential for the survival of NPC cells as indicated by the strikingly induced spontaneous apoptosis upon loss of LINC00669 (Fig. -(Fig.2d).2d). Together, these data indicated that LINC00669 profoundly endows carcinogenic properties of NPC cells.Inspired by the cytoplasmic localization of LINC00669 (Fig. -(Fig.1e),1e), we speculated that it might participate in the translational or signaling regulations. To identify its target proteins, we incubated CNE-2 cell lysates with a biotin-labeled LINC00669, and proceeded with electrophoresis followed by silver staining. Mass spectrum analysis of the unique protein bands detected only in the sense but not anti-sense LINC00669-incubated cell lysates by silver staining indicated SOCS1 as a potential LINC00669-targeting protein (Fig. 3a). The direct interaction between LINC00669 and SOCS1 was further confirmed by western blot on LINC00669 pull-down cell lysates using an antibody against SOCS1 (Fig. -(Fig.3b).3b). Vice versa, RNA-immunoprecipitation (RIP) assay using SOCS1 antibody followed by qPCR analysis demonstrated that SOCS1 specifically precipitated LINC00669 in both CNE-2 and 5-8F cell lysates, and the enrichment of LINC00669 was largely decreased upon siRNA-mediated depletion of LINC00669 (Fig. -(Fig.33c).Aberrant activation of the JAK/STAT pathway has been found in many tumors [10]. Indeed, most of the component genes of this signaling pathway were upregulated in human NPC tumors at the transcription level (Fig. 5a). Unexpectedly, this was concurrent with upregulation of the negative feedback regulator SOCS1. We further examined the expression of SOCS1 and STAT1 proteins in NPC tumors and para-carcinoma tissues by IHC. Although SOCS1 levels were comparative between the normal and cancerous tissues, it was NPC tumors instead of para-carcinoma tissues that exhibited a strong immunostaining signal of STAT1 (Fig. -(Fig.5b),5b), indicating the interrupted Inhibition of SOCS1 on STAT1 in NPC tumors. Given the fact that SOCS1 strongly interacts with LINC00669, which is highly expressed in NPC tumors, we investigated how changes of LINC00669 and then its interaction with SOCS1 would affect SOCS1/STAT1 network. Obviously, transcription of SOCS1 and STAT1 did not vary with the expression of LINC00669 (Fig. -(Fig.5c).5c). Nor did SOCS1 protein change accordingly (Fig. -(Fig.5d).5d). Instead, STAT1 protein was increased when LINC00669 was overexpressed and was decreased when LINC00669 was depleted (Fig. -(Fig.5d).5d). Concomitantly, loss of LINC00669 also led to an increase in ubiquitination of STAT1 (Fig. -(Fig.5e),5e), which could be reversed upon forced expression of LINC00669 (Fig. -(Fig.55f). Instead, STAT1 protein was increased when LINC00669 was overexpressed and was decreased when LINC00669 was depleted (Fig. -(Fig.5d).5d). Concomitantly, loss of LINC00669 also led to an increase in ubiquitination of STAT1 (Fig. -(Fig.5e),5e), which could be reversed upon forced expression of LINC00669 (Fig. -(Fig.55f).	32831137	RID04628	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	NFIA-AS2	ZFX	positively-E	dual-luciferase reporter assay;RIP;DIANA;Targetscan 7.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-655-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000237928	GRCh38_1:60912675-61056885	ENSG00000005889	NA	100996570	7543	NA	ZNF926	LncRNA NFIA-AS2 promotes glioma progression through modulating the miR-655-3p/ZFX axis.We firstly analyzed The Cancer Genome Atlas (TCGA) RNA sequencing data of NFIA-AS2 by bioinformatic website GEPIA (https ://www.gepia .cance r-pku.cn). As shown in Fig. 1a, lncRNA NFIA-AS2 was the most upregulated in glioma tissues among the different kinds of tumor tissues. The glioma tissues (n = 163) showed significant overexpression of lncRNA NFIA-AS2 compared with the adjacent normal tissues (n = 207) (Fig. 1b, P < 0.05). Similarly, the significant overexpression of NFIA-AS2 was also observed in glioma tissues compared to adjacent normal tissues from the clinical collection at our hospital (Fig. 1c, P < 0.01).Subsequently, the CCK8 assay revealed that downregulation of NFIA-AS2 strikingly alleviated the proliferation of U87 and U251 cells (Fig. 2b, c). Similarly, downregulation of NFIA-AS2 could significantly inhibit anchor-independent growth ability of U87 and U251 cells via colony formation assay (Fig. 2d). Also, the impact of NFIA-AS2 on glioma cell apoptosis was determined through carrying out the flow cytometric analysis. As shown in Fig. 2e, the data disclosed that the apoptosis degrees of U87 and U251 cells were remarkably augmented in the sh-NFIA-AS2 group compared with the sh-NC group. In addition, transwell migration and invasion assays revealed that the inhibition of NFIA-AS2 notably undermined the migration and invasion of glioma cells (Fig. 2f, g). Thus, NFIA-AS2 might play an oncogenic role by influencing the proliferation, migration and invasion of glioma cells.Lately, dual-luciferase reporter assay confirmed that the upregulation of miR-655-3p outstandingly arrested the luciferase activity of the NFIA-AS2-Wt in U87 and U251 cells; nevertheless, the change of luciferase activity of NFIA-AS2-Mut was not observed in miR-655-3p-transfected glioma cells (Fig. 3e). What is more, RIP analysis found a considerable enrichment of NFIA-AS2 and miR-655-3p in the anti-Ago2 group, further authenticating that NFIAAS2 could bind with miR-655-3p in U87 and U251 cells (Fig. 3f).The miR-655-3p inhibition or ZFX overexpression could neutralize the silencing of NFIA-AS2mediated suppressive function on cell proliferation (Fig. 4a, b). Besides, the reduced migration and invasion capacity of U87 cells, resulting from NFIA-AS2 deficiency, could be counteracted by miR-655-3p downregulation or ZFX upregulation (Fig. 4c, d). Taken together, NFIA-AS2 modulated glioma cell proliferaion, migration and invasion by sponging miR-655-3p/ZFX axis.Subsequently, the prediction of DIANA databases proved that miR-655-3p contained complementary binding sites with NFIA-AS2 as shown in Fig. 3b. Next, ZFX was predicted to possess binding sites with miR-655-3p using Targetscan 7.0 (Fig. 3g).	32779154	RID04629	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE67939,GSE41245)
Osteoporosis	GAS5	miR-21	negatively-E	RNA pull-down assay;IntaRNA	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	lncRNA GAS5 Is Upregulated in Osteoporosis and Downregulates miR-21 to Promote Apoptosis of Osteoclasts.The differential expression of GAS5 and miR-21 in osteoporosis patients was assessed by measuring the expression levels of GAS5 and miR-21 in plasma derived from both osteoporosis patients (n = 66) and healthy controls (n = 66). Unpaired t-test analysis showed that GAS5 was significantly upregulated (Figure 1A) in plasma of osteoporosis patients, while miR-21 was downregulated (Figure 1B) in plasma of osteoporosis patients compared to that in healthy controls (p < 0.05).Correlations between the expression levels of GAS5 and miR-21 were analyzed by Pearson correlation coefficient. It showed that the expression levels of GAS5 were significantly and inversely correlated with the expression levels of miR-21 across plasma samples in osteoporosis patients (Figure 2A). In contrast, the correlation between GAS5 and miR-21 was not significant across plasma samples in healthy controls (Figure 2B).From RNAs interaction detected by IntaRNA (http://rna.informatik.uni-freiburg.de/IntaRNA/), we obtained that lncRNA GAS5 might bind with miR-21 (Figure 4A) at 3--UTR. To confirm our finding from IntaRNA database, RNA pull-down assay was conducted to detect this interaction. lncRNA GAS5 could only be precipitated by miR-21 probe but it was undetectable in the product precipitated by control probe (Figure 4B, p < 0.001), indicating that miR-21 directly interacts with lncRNA GAS5 in osteoblasts.Compared to untransfected cells (C) and cells transfected with miRNA mimic or empty expression vector, overexpression of GAS5 led to promoted, while overexpression of miR-21 led to suppressed apoptosis of osteoclasts. In addition, overexpression of miR-21 attenuated the effects of overexpressing GAS5 (Figure 6, p < 0.05).From RNAs interaction detected by IntaRNA (http://rna.informatik.uni-freiburg.de/IntaRNA/), we obtained that lncRNA GAS5 might bind with miR-21 (Figure 4A) at 3--UTR. To confirm our finding from IntaRNA database, RNA pull-down assay was conducted to detect this interaction. lncRNA GAS5 could only be precipitated by miR-21 probe but it was undetectable in the product precipitated by control probe (Figure 4B, p < 0.001), indicating that miR-21 directly interacts with lncRNA GAS5 in osteoblasts.	32764903	RID04630	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Osteosarcoma	LINC01535	KCNC4	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;StarBase	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226686	GRCh38_19:37251867-37265547	ENSG00000116396	NA	101927667	3749	NA	C1orf30|HKSHIIIC|Kv3.4	LINC01535 Promotes the Development of Osteosarcoma Through Modulating miR-214-3p/KCNC4 Axis.First of all, we examined LINC01535 expression in OS tissues and cell lines (MG63, Saos2, HOS and U2OS) by qRT-PCR The adjacent normal tissues and human normal osteoblasts (hFOB1.19) were taken as control, separately. As depicted in Figure 1A, the expression of LINC01535 was significantly higher in OS tissues compared with adjacent normal tissues.Then, we implemented colony formation assay, EdU assay and CCK-8 assay to assess the effect of silenced LINC01535-1 on OS cell proliferation. These results all indicated the descending proliferative ability of Saos2 and U2OS cells after LINC01535 knockdown (Figure 1E). In addition, we detected the capacity of cell apoptosis by flow cytometry analysis in Saos2 and U2OS cells. The consequence indicated that cell apoptotic ability was remarkably enhanced after silencing LINC01535 (Figure 1H). Later, the levels of cell migration-associated proteins (MMP2, MMP7, MMP9, Slug and Twist) were tested by western blot to determine cell migration upon LINC01535 knockdown. As the result demonstrated, cell migration-associated protein levels were all decreased by LINC01535 deficiency (Figure 1I). Furthermore, wound healing assay further revealed that LINC01535 silencing curbed the migratory ability of Saos2 and U2OS cells (Figure 1J). In transwell assay, we observed that the invasion was also hindered in Saos2 and U2OS cells transfected with sh-LINC01535-1 (Figure 1K).To further filtrate, we checked expressions of predicted eleven miRNAs in normal human osteoblasts and OS cells. The results revealed that miR-214-3p expression was significantly down-regulated in OS cells, while other miRNAs did not exhibit expression difference (Figure S2A ). Most interestingly, we also found the binding site between LINC01535 and miR-214-3p (Figure 2C). In addition, we conducted luciferase reporter assay via co-transfecting LINC01535-WT/Mut and miR-214-3p mimics or NC mimics into Saos2 and U2OS cells. The results presented that the luciferase activity of LINC01535-WT was eminently declined by miR-214-3p overexpression, whereas no change was observed in LINC01535-Mut group (Figure 2D). Moreover, to certify the direct interaction between LINC01535 and miR-214-3p, RIP assay and RNA pull-down assay were carried out. According to the results of RNA pull-down experiment, we discovered that the enrichment of LINC01535 was significantly elevated by biotinylated miR-214-3p-WT instead of biotinylated miR-214-3p-Mut (Figure 2E).Subsequently, we explored the target genes of miR-214-3p and screened out five mRNAs, which could bind to miR-214-3p by using starBase (Figure 3A). Additionally, we performed luciferase reporter assay to estimate the luciferase activity of KCNC4 3-UTR, TBCID10B 3-UTR, SNX12 3-UTR, SPTBN2 3-UTR and REPIN1 3-UTR after transfecting miR-214-3p mimics. It was shown that KCNC4 3-UTR activity was prominently decreased by miR-214-3p mimics, while there was no alteration in other groups (Figure 3B). Hence, KCNC4 was predicted as a target gene of miR-214-3p.Finally, we carried out a battery of functional rescue experiments to explore whether LINC01535 modulated OS progression by regulating KCNC4. Colony formation assay, EdU assay and CCK-8 assay were conducted to detect cell proliferation ability. The results displayed that cell proliferation was attenuated after silencing LINC01535, while this phenomenon was recovered by overexpressing KCNC4 (Figure 4A). In addition, flow cytometry analysis unveiled that cell apoptosis elevated by LINC01535 interference was subsequently restored by KCNC4 overexpression (Figure 4D). Through western blot we observed levels of migration-related proteins were descending remarkably by reducing LINC01535. However, the protein levels were ascending upon KCNC4 overexpression (Figure 4E). As demonstrated in wound healing assay, KCNC4 overexpression recovered the inhibitory role of LINC01535 depletion in the migratory capacity of OS cells (Figure 4F). Finally, transwell assay confirmed the restorative effect of KCNC4 up-regulation on the suppressive invasion of sh-LINC01535-1 transfected cells (Figure 4G). Above experimental data demonstrated that LINC01535 regulated KCNC4 to promote cell growth, migration and invasion in OS.To find out the specific miRNA, we employed starBase (http://starbase.sysu.edu.cn/index.php) and found eleven miRNAs that could bind to LINC01535.  Moreover, to certify the direct interaction between LINC01535 and miR-214-3p, RIP assay and RNA pull-down assay were carried out.we performed luciferase reporter assay to estimate the luciferase activity of KCNC4 3-UTR, TBCID10B 3-UTR, SNX12 3-UTR, SPTBN2 3-UTR and REPIN1 3-UTR after transfecting miR-214-3p mimics.LINC01535 Facilitates Cell Growth, Migration and Invasion in OS by Regulating KCNC4	32753970	RID04631	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827)
Tongue squamous cell carcinoma	UCA1	CCR7	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000126353	NA	652995	1236	CUDR|LINC00178|onco-lncRNA-36|UCAT1	BLR2|CD197|CDw197|CMKBR7|EBI1	Long noncoding RNA UCA1 regulates CCR7 expression to promote tongue squamous cell carcinoma progression by sponging miR-138-5p.Firstly, we tested the expression of UCA1 and CCR7 in TSCC tissues. As presented in Table 2, we found that UCA1 and CCR7 were remarkably overexpressed in TSCC tissues compared with that in adjacent normal tissues. Interestingly, we uncovered that miR-138-5p was significantly lower expressed in TSCC tissues. Additionally, correlation analysis revealed that miR-138-5p was negatively correlated with UCA1 expression, while CCR7 was positively correlated with UCA1 expression in TSCC tissues (Figures 1A, 1B). To investigate the role of UCA1 in TSCC, we used si-UCA1 to knock down its expression in CAL-27 cells. qRT-PCRresults revealed that si-UCA1 could effectively inhibit UCA1 expression, indicating a good transfection efficiency (Figure 2A). Thus, we explored the effect of UCA1 silencing on the proliferation, migration, invasion, and glycolysis of CAL-27 cells. Colony formation assay results indicated that the number of cloned CAL-27 cells was obviously decreased in the si-UCA1 group compared with the si-NC group (Figure 2B).Colony formation assay results suggested that silenced CCR7 inhibited the number of cloned CAL-27 cells (Figure 3C), and WB analysis indicated that the protein levels of c-myc, PCNA, and Ki-67 were markedly decreased in the si-CCR7 group, which indicated that CCR7 knockdown restrained the proliferation of TSCC cells (Figure 3D). Furthermore, the number of migrated and invaded CAL-27 cells was obviously hindered in the CCR7 silencing group (Figures 3E, 3F), suggesting that knockdown of CCR7 suppressed the migration and invasion of TSCC cells, as evidenced by decreased the protein levels of MMP2, MMP9, and Vimentin, and increased E-cadherin level in the si-CCR7 group (Figure 3G). In addition, we also discovered that the silencing of CCR7 restrained the ECAR level, ATP level, glucose uptake, and lactate production of CAL-27 cells (Figures 3H'-K), revealing that CCR7 knockdown suppressed the glycolytic metabolism of TSCC cells. Furthermore, we also found similar results in UM1 cells transfected with si-CCR7 (Supplementary Figure S2).Besides, dual-luciferase reporter assay results revealed that the overexpression of miR-138-5p remarkably suppressed the luciferase activity of WT-UCA1 and WT-CCR7 3'UTR vectors, while had no effect on the luciferase activity of MUT-UCA1 and MUT-CCR7 3'UTR vectors in CAL-27 cells (Figures 5B, 5C), which confirmed the interaction between miR-138-5p and UCA1 or CCR7. Also, the expression of miR-138-5p was increased by UCA1 knockdown and decreased by UCA1 overexpression (Figure 5D).Through the detection of the CCR7 protein level, we discovered that the protein level of CCR7 was inhibited by miR-138-5p overexpression, while promoted by miR-138-5p inhibition (Figure 5F). Furthermore, overexpressed UCA1 increased CCR7 protein level, whereas this promotion effect could be reversed by miR-138-5p overexpression, indicating that CCR7 expression was regulated by UCA1 and miR-138-5p (Figure 5G). Additionally, these results were also confirmed in UM1 cells (Supplementary Figure S4). Therefore, we concluded that UCA1 promoted CCR7 expression through sponging miR-138-5p.	32749849	RID04632	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteoarthritis	MEG3	FOXO1	positively-E	siRNA;RIP;dual-luciferase reporter assay;starBase	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-361-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150907	NA	55384	2308	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	FKH1|FKHR|FOXO1A	MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axisCartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate constructs, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCRwas used to detect the expression of MEG3, miR-361-5p and FOXO1.western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model.Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes.Moreover, using western blot and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix.	31888661	RID04633	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Liver cancer	HULC	SIRT1	positively-E	RIP;CRISPR-Cas9	upregulation	RT-PCR	NA	NA	cell autophagy(+)	ceRNA(miR-675)	regulation	RNA-protein	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000096717	NA	728655	23411	HCCAT1|LINC00078|NCRNA00078	SIR2L1	Long noncoding RNA HULC accelerates the growth of human liver cancer stem cells by upregulating CyclinD1 through miR675-PKM2 pathway via autophagyLiver cancer stem cells were isolated from Huh7 cells; gene infection and tumorigenesis test in vitro and in vivo were performed.We demonstrate that HULC promotes growth of liver cancer stem cells in vitro and in vivo.Mechanistically, HULC enhances the expression of Sirt1 dependent on miR675 and then induces the cellular autophagy through Sirt1. HULC enhances CyclinD1 and thereby increases pRB and inhibited P21 WAF1/CIP 1 via autophagy-miR675-PKM2 pathway in human liver cancer stem cells. Ultimately, our results demonstrate that CyclinD1 is required for the oncogenic functions of HULC in liver cancer stem cells.It reveals the key molecular signaling pathways for HULC and provides important basic information for finding effective tumor therapeutic targets based on HULC.HULC increases the autophagy through Sirt1	31900225	RID04634	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	HULC	Cyclin D1	positively-E		upregulation	RT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long noncoding RNA HULC accelerates the growth of human liver cancer stem cells by upregulating CyclinD1 through miR675-PKM2 pathway via autophagyLiver cancer stem cells were isolated from Huh7 cells; gene infection and tumorigenesis test in vitro and in vivo were performed.We demonstrate that HULC promotes growth of liver cancer stem cells in vitro and in vivo.Mechanistically, HULC enhances the expression of Sirt1 dependent on miR675 and then induces the cellular autophagy through Sirt1. HULC enhances CyclinD1 and thereby increases pRB and inhibited P21 WAF1/CIP 1 via autophagy-miR675-PKM2 pathway in human liver cancer stem cells. Ultimately, our results demonstrate that CyclinD1 is required for the oncogenic functions of HULC in liver cancer stem cells.It reveals the key molecular signaling pathways for HULC and provides important basic information for finding effective tumor therapeutic targets based on HULC.HULC increases the autophagy through Sirt2. Collectively, these observations suggest thatHULC enhances CyclinD1 to increase pRB and inhibit P21 WAF1/CIP 1 via autophagy-PKM2 pathway in human liver cancer stem cells.findings suggest that HULC accelerates progression of human liver cancer stem cells dependent on CyclinD1. Therefore, the expres_x0002_sion of CyclinD1 was significantly increased in the pCMV6-A-GFP-HULC group compared to the pCMV6-A-GFP group.	31900225	RID04635	expression association	NA		
Prostate cancer	GAS5	HMGB1	positively-E	IHC;Targetscan;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);angiogenesis(+)	ceRNA(miR-1284)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000189403	NA	60674	3146	NCRNA00030|SNHG2	DKFZp686A04236|HMG1|HMG3|SBP-1	Rs145204276 and rs4759314 affect the prognosis of prostate cancer by modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathwaysThis study aims to characterize the role of GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms in the pathogenesis of PC. Both INS allele of GAS5 rs145204276 and A allele of HOTAIR rs4759314 were identified to increase the survival of PC patients. And patients carrying DEL/DELtAG genotypes tend to present higher levels of HMGB1, GAS5, HOTAIR and lower levels of miR-1284 and miR-22. In addition, the transcription activity of GAS5 promoter was increased by the deletion allele of rs145204276 polymorphism,while the G allele of rs4759314 polymorphism increased the transcription activity of HOTAIR promoter.GAS5 and HOTAIR could bind to miR-1284 and miR-22, respectively, while miR-1284 and miR-22 could bind to the 30UTR of HMGB1. Compared with the control group, the expressions of miR-1284 or miR-22 were decreased with the presence of GAS5 or HOTAIR, and the expression of HMGB1 was the highest in the GAS5tHOTAIR group.The overexpression of miR-22 can suppress the expression of HMGB1 while inhibiting HMGB1-induced autophagy of osteosarcoma cells, and the inhibition of HMGB1 expression by miR-22 in osteosarcoma cells renders the cells more sensitive to the treatments by Cis and Dox by reducing the potential of cancer cell invasion, migration, and proliferation.In summary, the findings of this study demonstrated that both GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms could affect the prognosis of PC by modulating the expression of HMGB1 via modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathways.HMGB1 was initially identified as a protein with the chro_x0002_matin-binding ability. However, HMGB1 has been implicated in the process of cancer cell metastasis, proliferation, and angiogenesis during the development of cancers	31916466	RID04636	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Prostate cancer	HOTAIR	HMGB1	positively-E	IHC;Targetscan;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);angiogenesis(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000189403	NA	100124700	3146	HOXC-AS4|HOXC11-AS1|NCRNA00072	DKFZp686A04236|HMG1|HMG3|SBP-1	Rs145204276 and rs4759314 affect the prognosis of prostate cancer by modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathwaysThis study aims to characterize the role of GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms in the pathogenesis of PC. Both INS allele of GAS5 rs145204276 and A allele of HOTAIR rs4759314 were identified to increase the survival of PC patients. And patients carrying DEL/DELtAG genotypes tend to present higher levels of HMGB1, GAS5, HOTAIR and lower levels of miR-1284 and miR-22. In addition, the transcription activity of GAS5 promoter was increased by the deletion allele of rs145204276 polymorphism,while the G allele of rs4759314 polymorphism increased the transcription activity of HOTAIR promoter.GAS5 and HOTAIR could bind to miR-1284 and miR-22, respectively, while miR-1284 and miR-22 could bind to the 30UTR of HMGB1. Compared with the control group, the expressions of miR-1284 or miR-22 were decreased with the presence of GAS5 or HOTAIR, and the expression of HMGB1 was the highest in the GAS5tHOTAIR group.The overexpression of miR-22 can suppress the expression of HMGB1 while inhibiting HMGB1-induced autophagy of osteosarcoma cells, and the inhibition of HMGB1 expression by miR-22 in osteosarcoma cells renders the cells more sensitive to the treatments by Cis and Dox by reducing the potential of cancer cell invasion, migration, and proliferation.In summary, the findings of this study demonstrated that both GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms could affect the prognosis of PC by modulating the expression of HMGB1 via modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathways.	31916466	RID04637	ceRNA or sponge	prognosis,metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Acute-on-chronic liver failure	NEAT1	TRAF6	positively-E	RNA pull-down assay;western blot;RIP	upregulation	RT-PCR	NA	NA	inflammatory response(-)	histone modification	binding/interaction	RNA-protein	NA	NA	NA	Other	Liver failure	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000175104	NA	283131	7189	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	RNF85	Long Non-coding RNA NEAT1 Alleviates Acute-on-Chronic Liver Failure Through Blocking TRAF6 Mediated Inflammatory Response.Acute-on-chronic liver failure (ACLF)model was established by challenging D-galactosamine (D-GalN)/lipopolysaccharide (LPS) i.p. in rats with cirrhosis. The serum levels of IL-1, IL-6, and HMGB1 were determined using ELISA. Quantitative real time-PCR and western blot were performed to evaluate RNA and protein levels of inflammatory response. RNA immunoprecipitation assay was performed to confirm protein that interacts with NEAT1.Over-expression of NEAT1 could interact with TRAF6 and decrease its ubiquitination level, and significantly reduced the expression levels of IL-6, IL-22. Importantly, in ACLF rat model, NEAT1 over-expression reduced several cytokines expression and alleviated the pathological status in contrast to the control group.Additionally, NEAT1 was increased and positively correlated with IL-22 and IL-6 levels in PBMCs from the ACLF patients.NEAT1 can suppress inflammatory response through blockade of TRAF6 ubiquitination in ACLF rat model, suggesting that lncRNA NEAT1 might play protective roles in the pathogenesis of ACLF and provide promising novel target for pharmacological intervention.Furthermore, an RNA immunoprecipitation experiment wascarried out to verify the specific interaction	31920708	RID04638	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Systemic lupus erythematosus	SLEAR	ILF2	positively-F	RNA pull-down assay;westerm blot;RIP	upregulation	qRT-PCR	GSE104480	NA	apoptosis process(+)	NA	binding/interaction	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	NA	NA	ENSG00000143621	NA	NA	3608	NA	NF45	Association of the Polymorphism rs13259960 in SLEAR With Predisposition to Systemic Lupus ErythematosusIn this study, we identified a significant SLE risk locus in the intron of SLEAR at 8q22. SLEAR was found to be expressed at significantly lower levels in SLE patients compared to healthy controls in the present study, as has also been indicated in publicly reported data.Our data demonstrate that SLEAR regulates the expression of target genes involved in cell apoptosis by interacting with proteins and/or chromatins. The molecular mechanism by which SLEAR modulates the activities of these anti-and proapoptotic genes warrants further study.Taken together, we have carried out a GWAS and a functional study, and identified a lncRNA, SLEAR, as an anti-SLE factor acting through regulation of apoptosis. The A>G variation at rs13259960 weakens this role of SLEAR and predisposes individuals to SLE.We therefore performed RNA pull-down assays by incubating nuclear extracts from Jurkat cells with in vitro-transcribed biotinylated SLEAR in the sense or antisense (neg_x0002_ative control) direction. western blot identified 5 protein candidates specifically pulled down with biotinylated SLEAR in all biologic experiments (con_x0002_ducted in triplicate): EWS, FUS, TAF15, hnRNP F, and ILF2 (Fig_x0002_ure  4B). RNA immunoprecipitation assays of the RNA binding proteins TAF15, hnRNP F, and ILF2 showed significant enrich_x0002_ment of SLEAR RNA, but not of beta-actin or GAPDH, as compared to IgG isotype controls (Figure 4C). These results thus confirm that SLEAR binds to these 3 proteins.	31930717	RID04639	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Systemic lupus erythematosus	SLEAR	HNRNPF	positively-F	RNA pull-down assay;westerm blot;RIP	upregulation	qRT-PCR	GSE104480	NA	apoptosis process(+)	NA	binding/interaction	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	NA	NA	ENSG00000169813	NA	NA	3185	NA	HNRPF	Association of the Polymorphism rs13259960 in SLEAR With Predisposition to Systemic Lupus ErythematosusIn this study, we identified a significant SLE risk locus in the intron of SLEAR at 8q22. SLEAR was found to be expressed at significantly lower levels in SLE patients compared to healthy controls in the present study, as has also been indicated in publicly reported data.Our data demonstrate that SLEAR regulates the expression of target genes involved in cell apoptosis by interacting with proteins and/or chromatins. The molecular mechanism by which SLEAR modulates the activities of these anti-and proapoptotic genes warrants further study.Taken together, we have carried out a GWAS and a functional study, and identified a lncRNA, SLEAR, as an anti-SLE factor acting through regulation of apoptosis. The A>G variation at rs13259960 weakens this role of SLEAR and predisposes individuals to SLE.We therefore performed RNA pull-down assays by incubating nuclear extracts from Jurkat cells with in vitro-transcribed biotinylated SLEAR in the sense or antisense (neg_x0002_ative control) direction. western blot identified 5 protein candidates specifically pulled down with biotinylated SLEAR in all biologic experiments (con_x0002_ducted in triplicate): EWS, FUS, TAF15, hnRNP F, and ILF2 (Fig_x0002_ure  4B). RNA immunoprecipitation assays of the RNA binding proteins TAF15, hnRNP F, and ILF2 showed significant enrich_x0002_ment of SLEAR RNA, but not of beta-actin or GAPDH, as compared to IgG isotype controls (Figure 4C). These results thus confirm that SLEAR binds to these 4 proteins.	31930717	RID04640	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Systemic lupus erythematosus	SLEAR	TAF15	positively-F	RNA pull-down assay;westerm blot;RIP	upregulation	qRT-PCR	GSE104480	NA	apoptosis process(+)	NA	binding/interaction	RNA-protein	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	NA	NA	ENSG00000172660	NA	NA	8148	NA	hTAFII68|Npl3|RBP56|TAF2N	Association of the Polymorphism rs13259960 in SLEAR With Predisposition to Systemic Lupus ErythematosusIn this study, we identified a significant SLE risk locus in the intron of SLEAR at 8q22. SLEAR was found to be expressed at significantly lower levels in SLE patients compared to healthy controls in the present study, as has also been indicated in publicly reported data.Our data demonstrate that SLEAR regulates the expression of target genes involved in cell apoptosis by interacting with proteins and/or chromatins. The molecular mechanism by which SLEAR modulates the activities of these anti-and proapoptotic genes warrants further study.Taken together, we have carried out a GWAS and a functional study, and identified a lncRNA, SLEAR, as an anti-SLE factor acting through regulation of apoptosis. The A>G variation at rs13259960 weakens this role of SLEAR and predisposes individuals to SLE.We therefore performed RNA pull-down assays by incubating nuclear extracts from Jurkat cells with in vitro-transcribed biotinylated SLEAR in the sense or antisense (neg_x0002_ative control) direction. western blot identified 5 protein candidates specifically pulled down with biotinylated SLEAR in all biologic experiments (con_x0002_ducted in triplicate): EWS, FUS, TAF15, hnRNP F, and ILF2 (Fig_x0002_ure  4B). RNA immunoprecipitation assays of the RNA binding proteins TAF15, hnRNP F, and ILF2 showed significant enrich_x0002_ment of SLEAR RNA, but not of beta-actin or GAPDH, as compared to IgG isotype controls (Figure 4C). These results thus confirm that SLEAR binds to these 5 proteins.	31930717	RID04641	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ischemic stroke	H19	ROCK2	positively-E	dual-luciferase reporter assay;siRNA;overexpression;starBase	upregulation	RT-PCR	NA	NA	HO-1/NRF2 signaling pathway(-)	ceRNA(miR-148a-3p)	regulation	RNA-protein	Metformin	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000134318	NA	283120	9475	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 AxisThis study is aimed at investigating the effect and mechanism of metformin in an experimental model of oxidative stress induced by ischemia/reperfusion (I/R) in vivo and oxygen glucose deprivation/reperfusion (OGD/R) in vitro. Metformin (100, 200, and 300 mg/kg) was administered intraperitoneally immediately after induction of cerebral ischemia. The indicators of oxidative stress selected were antioxidant enzyme activities of catalase, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione peroxidation enzyme (GSHPx). First, we demonstrated that metformin can significantly alleviate acute and chronic cerebral I/R injury and it has a strong regulatory effect on stroke-induced oxidative stress. It can reduce the elevated activities of MDA and NO and increase the levels of GSHPx and SOD in the cerebrum of mice and N2a cells exposed to I/R. Furthermore, real-time PCR and western blot were used to detect the expression of long noncoding RNA H19 (lncRNA-H19), microRNA-148a-3p (miR-148a-3p), and Rho-associated protein kinase 2 (Rock2). The direct interaction of lncRNA-H19, miR-148a-3p, and Rock2 was tested using a dual-luciferase reporter assay. lncRNA-H19 altered OGD/R-induced oxidative stress by modulating miR-148a-3p to increase Rock2 expression. The expression of lncRNAH19 and Rock2 could be downregulated with metformin in vivo and in vitro. In conclusion, our study confirmed that metformin exerts neuroprotective effects by regulating ischemic stroke-induced oxidative stress injury via the lncRNAH19/miR-148a-3p/Rock2 axis. These results provide new evidence that metformin may represent a potential treatment for stroke-related brain injury.	31934270	RID04642	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Cholestatic liver injury	H19	IL6	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000136244	NA	283120	3569	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BSF2|HGF|HSF|IFNB2|IL-6	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04643	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Cholestatic liver injury	H19	IL1B	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000125538	NA	283120	3553	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	IL-1B|IL1-BETA|IL1F2	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04644	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Cholestatic liver injury	H19	COX2	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000198712	NA	283120	4513	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	COII|MTCO2	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04645	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	
Cholestatic liver injury	H19	CCL5	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000161570	NA	283120	6352	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	D17S136E|MGC17164|RANTES|SCYA5|SISd|TCP228	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04646	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Cholestatic liver injury	H19	TNF	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000228978	NA	283120	7124	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	DIF|TNF-alpha|TNFA|TNFSF2	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04647	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC);DATA(GSE117623)
Cholestatic liver injury	H19	CXCL10	positively-E	overexpression	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000169245	NA	283120	3627	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	C7|crg-2|gIP-10|IFI10|INP10|IP-10|mob-1|SCYB10	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04648	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE86978)
Cholestatic liver injury	H19	CCL2	positively-E	western blot	upregulation	qPCR	NA	NA	macrophage polarization(+)	NA	association	RNA-protein	Bindarit	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000108691	NA	283120	6347	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	GDCF-2|HC11|MCAF|MCP-1|MCP1|MGC9434|SCYA2|SMC-CF	Cholangiocyte-Derived Exosomal lncRNA H19 Promotes Macrophage Activation and Hepatic Inflammation under Cholestatic ConditionsExosomal H19 derived from cholangiocytes was rapidly taken up by Kupffer cells. However, the mechanistic links between exosomal lncRNA H19 and macrophage-driven inflammation in cholestasis remain unclear.Here, we reported that the hepatic H19 level was closely correlated with macrophage activation and hepatic fibrosis in both M dr2-/- and bile duct ligation (BDL) cholestatic mouse models, as well as in human primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) patients. Exosomal H19 significantly i nduced t he e xpression a nd s ecretion o f c hemokine ( C motif) ligand 2 (CCL-2) and interleukin 6 (IL-6) in Kupffer cells. H19-enriched exosomes enhanced the activation M1 polarization of Kupffer cells and promoted the recruitment and differentiation of bone marrow-derived macrophages, which were inhibited by a CCL-2 pharmacological inhibitor.In conclusion, Cholangiocyte-derived exosomal H19 played a critical role in macrophage activation, differentiation, and chemotaxis through CCL-2/CCR-2 signaling pathways, which represent a therapeutic target for cholestatic liver diseases.	31940841	RID04649	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	LINC00460	CCND1	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000110092	NA	728192	595	NA	BCL1|D11S287E|PRAD1|U21B31	Long intergenic non-protein coding RNA 00460 predicts a poor prognosis and promotes tumorigenesis of human osteosarcomaTo discover more effective molecular targets for the treatment of OS, the association between LINC 00460 and OS prognosis was analyzed using the Gene Expression Profiling Interactive Analysis database. Additionally, small interfering RNA was used to knockdown LINC 00460 gene expression in vitro to verify its biological effects on the viability, invasive and migratory potential of OS cells. LINC00460 knockdown significantly reduced the viability of OS cells and initiated cell cycle arrest within the G0/G1 phase through the decreased expression of cyclin D1 and CD K4/CD K6. In addition, LINC 00460 knockdown promoted apoptosis of OS cells, and inhibited the migratory and invasive abilities of OS cells through the inhibition of the epithelial-mesenchymal transition pathway. In conclusion, the present study reported that LINC 00460 may predict OS prognosis, and may serve an important role in mediating the viability, invasive and migratory potential of OS cells. Based on these findings, LINC00460 demonstrated promising potential as a future therapeutic target for OS treatment.	31974626	RID04650	expression association	prognosis		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Osteosarcoma	LINC00460	CDK4	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000135446	NA	728192	1019	NA	PSK-J3	Long intergenic non-protein coding RNA 00460 predicts a poor prognosis and promotes tumorigenesis of human osteosarcomaTo discover more effective molecular targets for the treatment of OS, the association between LINC 00460 and OS prognosis was analyzed using the Gene Expression Profiling Interactive Analysis database. Additionally, small interfering RNA was used to knockdown LINC 00460 gene expression in vitro to verify its biological effects on the viability, invasive and migratory potential of OS cells. LINC00460 knockdown significantly reduced the viability of OS cells and initiated cell cycle arrest within the G0/G1 phase through the decreased expression of cyclin D1 and CD K4/CD K6. In addition, LINC 00460 knockdown promoted apoptosis of OS cells, and inhibited the migratory and invasive abilities of OS cells through the inhibition of the epithelial-mesenchymal transition pathway. In conclusion, the present study reported that LINC 00460 may predict OS prognosis, and may serve an important role in mediating the viability, invasive and migratory potential of OS cells. Based on these findings, LINC00460 demonstrated promising potential as a future therapeutic target for OS treatment.	31974626	RID04651	expression association	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	LINC00460	CDK6	positively-E	siRNA;western blot	upregulation	RT-qPCR	NA	NA	cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000105810	NA	728192	1021	NA	PLSTIRE	Long intergenic non-protein coding RNA 00460 predicts a poor prognosis and promotes tumorigenesis of human osteosarcomaTo discover more effective molecular targets for the treatment of OS, the association between LINC 00460 and OS prognosis was analyzed using the Gene Expression Profiling Interactive Analysis database. Additionally, small interfering RNA was used to knockdown LINC 00460 gene expression in vitro to verify its biological effects on the viability, invasive and migratory potential of OS cells. LINC00460 knockdown significantly reduced the viability of OS cells and initiated cell cycle arrest within the G0/G1 phase through the decreased expression of cyclin D1 and CD K4/CD K6. In addition, LINC 00460 knockdown promoted apoptosis of OS cells, and inhibited the migratory and invasive abilities of OS cells through the inhibition of the epithelial-mesenchymal transition pathway. In conclusion, the present study reported that LINC 00460 may predict OS prognosis, and may serve an important role in mediating the viability, invasive and migratory potential of OS cells. Based on these findings, LINC00460 demonstrated promising potential as a future therapeutic target for OS treatment.	31974626	RID04652	expression association	prognosis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Breast cancer	LINC00963	HMGA1	positively-E	RIP;luciferase reporter assay;starBase;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);tumor growth(+);cell metastasis(+);cancer progression(+)	ceRNA(miR-625)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000137309	NA	100506190	3159	MetaLnc9	HMGIY	LINC00963 was found to be overexpressed in breast cancer samples, and its overexpression was correlated with lymph node metastasis, TNM stage and differentiation grade. Patients with breast cancer harboring higher LINC00963 expression showed shorter overall survival than did the patients with lower LINC00963 expression. Functional experiments revealed that depletion of LINC00963 inhibited breast cancer cell proliferation, migration, and invasion and facilitated apoptosis in vitro and impaired tumor growth in vivo. Mechanism investigation revealed that LINC00963 can interact with microRNA-625 (miR-625). LINC00963 worked as a competitive endogenous RNA for miR-625 to weaken the suppressive effect of miR-625 on high mobility group AT-hook 1 (HMGA1) in breast cancer cells. Furthermore, miR-625 inhibition and HMGA1 restoration both abrogated the effects of LINC00963 silencing on breast cancer cells. Our findings indicate that the LINC00963-siR-625'-HMGA1 pathway plays an important role in the malignancy of breast cancer in vitro and in vivo. Hence, targeting this pathway may be a novel strategy against breast cancer. The luciferase reporter assay was conducted to dissect the direct interaction between LINC00963 and miR-625 in breast cancer cells. In addition, the RIP assay indicated that LINC00963 and miR-625 were preferentially enriched by the anti-AGO2 antibody after the immunoprecipitation in the lysates of MCF-7 and MDA-MB-231 cells, suggesting that miR-625 is a target of LINC00963 in breast cancer cells.HMGA1 has been previously validated as a direct target gene of miR-625 in breast cancer cells [35]. Hence, we next tested whether LINC00963 participates in the regulation of HMGA1 expression in breast cancer cells. The LINC00963 knockdown notably decreased the HMGA1 protein expression in MCF-7 and MDA-MB-231 cells (Figure 3i, ***P < 0.001). Taken together, these findings suggested that LINC00963 functioned as a ceRNA for miR-625 in breast cancer cells and thereby upregulated HMGA1.	32052688	RID04653	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Lung injury	NEAT1	HMGB1	positively-F	RNA pull-down assay;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+);inflammatory response(+);cell injury(+)	NA	NA	NA	NA	NA	NA	Other	Injury	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000189403	NA	283131	3146	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DKFZp686A04236|HMG1|HMG3|SBP-1	Depression of lncRNA NEAT1 Antagonizes LPS-Evoked Acute Injury and Inflammatory Response in Alveolar Epithelial Cells via HMGB1-RAGE SignalingHigh levels of the long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) have been positively correlated with increased severity and unfavorable prognoses in patients with sepsis. Nevertheless, the function and molecular mechanism of NEAT1 in ALI remain elusive. In the current study, high levels of NEAT1 were confirmed in lipopolysaccharide- (LPS-) induced ALI mice models and in LPS-stimulated cells from the alveolar epithelial A549 cell line. Intriguingly, cessation of NEAT1 led to increased cell viability and decreased lactate dehydrogenase release, apoptosis, and caspase-3/9 activity, which conferred protection against LPS-induced injury in these cells. NEAT1 inhibition also restrained LPS-evoked transcripts and production of inflammatory cytokines IL-6, IL-1beta, and TNF-alpha. A mechanism analysis corroborated the activation of high-mobility group box1 (HMGB1)/receptors for advanced glycation end products (RAGE) and NF-kB signaling in LPS-treated A549 cells. NEAT1 suppression reversed the activation of this pathway. Notably, reactivating HMGB1/RAGE signaling via HMGB1 overexpression blunted the anti-injury and anti-inflammation effects of NEAT1 knockdown. These findings suggest that NEAT1 may aggravate the progression of ALI and ARDS by inducing alveolar epithelial cell injury and inflammation via HMGB1/RAGE signaling, implying a promising treatment target for these conditions.NEAT1 knockdown also had a significant effect on the expression of HMGB1 (F(2, 12) = 18.03, P < 0.05), RAGE (F-(2, 12) = 4.2, P < 0.05), and p-p65 (F(2, 12) = 9.02, P < 0.05) in A549 cells.	32089649	RID04654	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Primary ovarian insufficiency	HCP5	YBX1	positively-F	RNA pull-down assay;western blot;catRAPID;RIP	downregulation	RT-qPCR	GSE135697	NA	DNA repair(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Reproductive system disease	Ovarian disease	lncRNA	TF	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000065978	NA	10866	4904	D6S2650E|P5-1	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA HCP5 participates in premature ovarian insufficiency by transcriptionally regulating MSH5 and DNA damage repair via YB1In this study, we identified a down-expressed lncRNA HCP5 in granulosa cells (GCs) from biochemical POI (bPOI) patients, which impaired DNA damage repair and promoted apoptosis of GCs. Mechanistically, we discovered that HCP5 stabilized the interaction between YB1 and its partner ILF2, which could mediate YB1 transferring into the nucleus of GCs. HCP5 silencing affected the localization of YB1 into nucleus and reduced the binding of YB1 to the promoter ofMSH5 gene, thereby diminishing MSH5 expression. Taken together, we identified that the decreased expression of HCP5 in bPOI contributed to dysfunctional GCs by regulating MSH5 transcription and DNA damage repair via the interaction with YB1, providing a novel epigenetic mechanism for POI pathogenesis.HCP5 directly binds to YB1.To investigate the protein partner of HCP5, RNA pull-down assay combined with MS was conducted with biotin-labeled HCP5 full-length transcript and its antisense transcript.  In addition, the potential binding fragments of HCP5 to YB1 were predicted by the catRAPID algorithm.Since RNA pull-down assay uncovered HCP5-YB1 interaction in vitro, we performed RNA-binding protein immunoprecipitation (RIP) to detect the endogenous association between HCP5 and YB1.	32112110	RID04655	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Primary ovarian insufficiency	HCP5	MSH5	positively-E	RNA pull-down assay;ChIP	downregulation	RT-qPCR	GSE135697	NA	DNA repair(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Reproductive system disease	Ovarian disease	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000237333	NA	10866	4439	D6S2650E|P5-1	G7	Long noncoding RNA HCP5 participates in premature ovarian insufficiency by transcriptionally regulating MSH5 and DNA damage repair via YB1In this study, we identified a down-expressed lncRNA HCP5 in granulosa cells (GCs) from biochemical POI (bPOI) patients, which impaired DNA damage repair and promoted apoptosis of GCs. Mechanistically, we discovered that HCP5 stabilized the interaction between YB1 and its partner ILF2, which could mediate YB1 transferring into the nucleus of GCs. HCP5 silencing affected the localization of YB1 into nucleus and reduced the binding of YB1 to the promoter ofMSH5 gene, thereby diminishing MSH5 expression. Taken together, we identified that the decreased expression of HCP5 in bPOI contributed to dysfunctional GCs by regulating MSH5 transcription and DNA damage repair via the interaction with YB1, providing a novel epigenetic mechanism for POI pathogenesis.Knockdown of HCP5 reduced YB1 binding to MSH5 promoter and inhibited the transcriptional activation of MSH5Notably, nuclear YB1 could locate to the promoters or other key regulatory regions of target genes, where the transcription is initiated (33). We further explored whether HCP5 knockdown affected YB1 occupancy to the MSH5 promoter. Chromatin immunoprecipitation (ChIP) assay followed by qPCR demonstrated significant enrichment of YB1 on MSH5 promoter (Figure -(Figure6A).6A). Furthermore, knockdown of HCP5 significantly reduced the binding of YB1 to the promoter of MSH5 (Figure -(Figure6B6B).	32112110	RID04656	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	GNAS	TPTEP1	negatively-F	immunoblot;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000087460	NA	ENSG00000100181	GRCh38_22:16601887-16698742	2778	387590	GNAS1|GNASXL|GPSA|NESP|NESP55|SCG6|SgVI	psiTPTE22	GNAS promotes inflammation-related hepatocellular carcinoma progression by promoting STAT3 activationImmunoblot showed that GNAS was mainly distributed in the cytoplasm, which indi- cates that GNAS interacts with STAT3 in the cytoplasm, but not in the nucleus. Our recent study reported that long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by interacting and suppressing STAT3 phosphorylation . Furthermore, we investigated whether GNAS would affect the interaction between TPTEP1 and STAT3 in HCC cells.GNAS knockout significantly promoted the interaction of TPTEP1 and STAT3 in LPS-stimulated HCC cells, and GNAS overexpression evidently inhibited it, as detected by RIP. Consistently, RNA pull-down assays also confirmed that GNAS knockout promoted, and GNAS overexpression inhibited, the interaction of biotin-tagged TPTEP1 and STAT3 in HCC cells. Overall, GNAS promotes LPS-induced STAT3 activation in HCC cells through inhibiting long non-coding RNA TPTEP1 interacting with STAT3.	32123532	RID04657	expression association	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	TPTEP1	STAT3	negatively-F	RNA pull-down assay;mass spectrometry	downregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000100181	GRCh38_22:16601887-16698742	ENSG00000168610	NA	387590	6774	psiTPTE22	APRF	Our recent study reported that long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by interacting and suppressing STAT3 phosphorylation.To further explore the mechanism underlying TPTEP1 suppresses HCC cell proliferation and invasion, biotin-labeled RNA pull-down accompanied by mass spectrometric assays were performed to investigate the TPTEP1-interacting proteins in HCC cells. Among the potential interacting proteins, a specific protein band at approximately 90-kDa in TPTEP1 pull-down samples was observed and then identified as STAT3 protein by mass spectrometry	32123532	RID04658	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Kaposi's sarcoma	ORF50	PAN RNA	positively-E	ChIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	enhencer	regulation	protein-RNA	NA	NA	NA	Disease by infectious agent	Kaposi's sarcoma	PCG	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	PAN RNA: transcriptional exhaust from a viral engineKaposi  sarcoma-associated herpesvirus (KSHV) genomes are maintained as episomes within infected cells and the virus exhibits a biphasic life cycle consisting of a life-long latent phase during which only a few viral genes are expressed and no viral progeny are produced and a transient lytic reactivation phase .Lytic replication is initiated by a single viral protein, K-Rta (ORF50), which activates more than 80 viral genes from multiple resident viral episomes (i.e., viral chromosomes). One of the major targets of K-Rta is a long non-coding nuclear RNA, PAN RNA (polyadenylated nuclear RNA), a lncRNA that accumulates to exceedingly high levels in the nucleus during viral reactivation. K-Rta directly binds to the PAN RNA promoter and robustly activates PAN RNA expression. ORF57 binds and recruits 3'-UTR genomic regions to the PAN RNA 5'-region through recognition of the PAN RNA MRE [ORF57/Mta responsive element (hairpin)] and/or physical interaction with K-Rta bound on a promoter. Increased numbers of genomic loops will then be formed at the PAN RNA genomic region through recruitment of 3'-UTR elements of distal genomic sites to the PAN RNA genomic region. This mechanism also facilitates recycling of assembled RNA Pol II complexes, accumulation of RNA Pol II at the genomic region, and increases accessibility to distal viral promoters in an active transcription-dependent manner. Closely clustered KSHV ORFs should also facilitate viral gene expression, because poly(A) sites and promoter regions are localized physically next to each other in the KSHV genome. Accordingly, K-Rta acts as the "Starter'- ORF57 acts as fuel to feed K-Rta-mediated gene activation, and the non-coding RNA genomic locus functions as the engine to drive transcription of the entire KSHV genome with PAN RNA emitted as exhaust material.The resulting accumulation of high levels of nuclear PAN RNA created by this process is an inducible enhancer-derived (eRNA) by-product that litters the infected cell nucleus.	32143650	RID04659	chromatin looping	NA		
Glioblastoma	HOTAIR	MIR219A1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000199036	NA	100124700	407002	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MIR219-1|MIRN219-1|MRI219-1|hsa-mir-219a-1|mir-219|mir-219a-1	HOTAIR inhibits the proliferation of glioblastoma cells by targeting miR-219With glioblastoma cell line U87 as the object, the changes in expression levels of HOTAIR and miR-219 in each group were detected via quantitative real-time polymerase chain reaction (qRT-PCR after HOTAIR in U87 cell lines was knocked down using small interfering RNA (siRNA). Then the cell proliferation in each group was determined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied to detect the cell apoptosis, and western blot assay was adopted to measure the changes in protein levels of Cyclin D1 and Bcl-2-associated X protein (Bax). After miR-219 knockdown with siRNA, the changes in expression levels of HOTAIR and miR-219 in each group were examined through qRT-PCR and the cell proliferation was tested by CCK-8 assay.After interference inHOTAIR using siRNA, compared with those in control group, the RNA expression level of HOTAIR was decreased remarkably (p < 0.05), the RNA expression level of miR-219 was increased notably (p < 0.05), the cell proliferation rate was inhibited evidently (p < 0.05), the apoptosis rate was enhanced obviously (p < 0.05), the protein expression level of Cyclin D1 declined markedly (p < 0.05), and the protein expression level of Bax rose distinctly (p < 0.05) in HOTAIR-siRNA group. After miR-219 knockdown with siRNA, the cell proliferation rate was raised remarkably (p < 0.05),but there was no significant change in the RNA expression level of HOTAIR (p > 0.05).	32176624	RID04660	ceRNA or sponge	NA		
Glioblastoma	HOTAIR	CCND1	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	HOTAIR inhibits the proliferation of glioblastoma cells by targeting miR-219With glioblastoma cell line U87 as the object, the changes in expression levels of HOTAIR and miR-219 in each group were detected via quantitative real-time polymerase chain reaction (qRT-PCR after HOTAIR in U87 cell lines was knocked down using small interfering RNA (siRNA). Then the cell proliferation in each group was determined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied to detect the cell apoptosis, and western blot assay was adopted to measure the changes in protein levels of Cyclin D1 and Bcl-2-associated X protein (Bax). After miR-219 knockdown with siRNA, the changes in expression levels of HOTAIR and miR-219 in each group were examined through qRT-PCR and the cell proliferation was tested by CCK-8 assay.After interference inHOTAIR using siRNA, compared with those in control group, the RNA expression level of HOTAIR was decreased remarkably (p < 0.05), the RNA expression level of miR-219 was increased notably (p < 0.05), the cell proliferation rate was inhibited evidently (p < 0.05), the apoptosis rate was enhanced obviously (p < 0.05), the protein expression level of Cyclin D1 declined markedly (p < 0.05), and the protein expression level of Bax rose distinctly (p < 0.05) in HOTAIR-siRNA group. After miR-219 knockdown with siRNA, the cell proliferation rate was raised remarkably (p < 0.05),but there was no significant change in the RNA expression level of HOTAIR (p > 0.05).	32176624	RID04661	expression association	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Glioblastoma	HOTAIR	BAX	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087088	NA	100124700	581	HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL2L4	HOTAIR inhibits the proliferation of glioblastoma cells by targeting miR-219With glioblastoma cell line U87 as the object, the changes in expression levels of HOTAIR and miR-219 in each group were detected via quantitative real-time polymerase chain reaction (qRT-PCR after HOTAIR in U87 cell lines was knocked down using small interfering RNA (siRNA). Then the cell proliferation in each group was determined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied to detect the cell apoptosis, and western blot assay was adopted to measure the changes in protein levels of Cyclin D1 and Bcl-2-associated X protein (Bax). After miR-219 knockdown with siRNA, the changes in expression levels of HOTAIR and miR-219 in each group were examined through qRT-PCR and the cell proliferation was tested by CCK-8 assay.After interference inHOTAIR using siRNA, compared with those in control group, the RNA expression level of HOTAIR was decreased remarkably (p < 0.05), the RNA expression level of miR-219 was increased notably (p < 0.05), the cell proliferation rate was inhibited evidently (p < 0.05), the apoptosis rate was enhanced obviously (p < 0.05), the protein expression level of Cyclin D1 declined markedly (p < 0.05), and the protein expression level of Bax rose distinctly (p < 0.05) in HOTAIR-siRNA group. After miR-219 knockdown with siRNA, the cell proliferation rate was raised remarkably (p < 0.05),but there was no significant change in the RNA expression level of HOTAIR (p > 0.05).	32176624	RID04662	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	MALAT1	SIRT1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell autophagy(+);apoptosis process(-);p38/MAPK signaling pathway(-);NF-kB signaling pathway(-)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000096717	NA	378938	23411	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	SIR2L1	LncRNA MALAT1 Enhances ox-LDL-Induced Autophagy through the SIRT1/MAPK/NF-kB Pathway in MacrophagesAtherosclerosis is the main cause of cardiovascular and cerebrovascular diseases. In advanced atherosclerotic plaque, macrophage apoptosis coupled with inflammatory cytokine secretion promotes the formation of necrotic cores. It has also been demonstrated that the long-noncoding Ribonucleic Acid (lnc RNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), with its potent function on gene transcription modulation, maintains oxidized low-density lipoprotein (ox-LDL)- induced macrophage autophagy (i.e., helps with cholesterol efflux). It also showed that MALAT1 activated Sirtuin 1 (SIRT1), which subsequently inhibited the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-kB) signaling pathways. ox-LDL has been used to incubate human myeloid leukemia mononuclear cells (THP-1)-derived macrophages to establish an in vitro foam cell model. Quantitative reverse-transcription polymerase chain reaction and western blot confirmed the increased expression level of MALAT1 and the autophagy-related protein Microtubuleassociated protein light chain 3 (LC-3), beclin-1. The small interfering RNA study showed a significant decrease in autophagy activity and an increase in apoptotic rate when knocking down MALAT1. Further study demonstrated that MALAT1 inhibited the expression of MAPK and NF-kB (p65) by upregulating SIRT1.	32183682	RID04663	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pregnancy-induced hypertension	MALAT1	ET-1	positively-E	IHC;luciferase reporter assay;StarBase;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	NF-kB signaling pathway(+)	ceRNA(miR-150-5p)	regulation	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 contributes to pregnancy-induced hypertension development by enhancing oxidative stress and inflammation through the regulation of the miR-150-5p/ET-1 axisHerein, we aim to explore the functional relevance of MALAT1 in PIH and to explain the potential underlying mechanisms.We found that the levels of ET-1 and MALAT1 were upregulated and that of miR-150-5p were downregulated in the serum of pregnant women with PIH and the aortic endothelial cells (ECs) of reduced uterine perfusion pressure (RUPP)-induced rat models. In aortic ECs, MALAT1 could competitively bind to miR-150-5p to upregulate the expression of ET-1. The MALAT1/miR-150-5p/ET-1 axis regulated the expression of endothelin B receptor (ETBR) in aortic ECs leading to oxidative stress imbalance and increased the release of proinflammatory cytokines (IL-18 and IL-1beta), which concurrently activated the NF-kB pathway to regulate the ETBR expression and to stimulate smooth muscle cell (SMC) contraction. Furthermore, silencing MALAT1 could alleviate the hypertensive symptoms of RUPP-induced rat models. Taken conjointly, the upregulation of MALAT1 can reduce the expression of ET-1 by competitively binding to miR-150-5p, which enhances the expression of ETBR via the activation of the NF-kB pathway in SMCs, thus exacerbating the hypertensive symptoms in the RUPP-induced rat models.Additionally, a bioinformatics website (http://starbase.sysu.edu.cn/index.php) predicted specific binding sites be_x0002_tween miR-150-5p and ET-1 (Figure 2D) and dual-luciferase reporter assay was performed to confirm the target relation_x0002_ship between miR-150-5p and ET-1. The luciferase activity of wt-ET-1 was reduced in cells transfected with miR-150-5p mimic (P > .05), but that of mut-ET-1 exhibited no significant changes following miR-150-5p mimic transfection (P < .05) (Figure 2E).Then the target relationship between miR-150-5p and MALAT1 was verified by dual-luciferase reporter assay.	32246794	RID04664	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Chronic heart failure	PVT1	miR-190a-5p	negatively-E	luciferase reporter assay;overexperssion;Targetscan	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart failure	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 contributes to vascular endothelial cell proliferation via inhibition of miR-190a-5p in diagnostic biomarker evaluation of chronic heart failureThe present study aimed to investigate the effects of lncRNA plasmacytoma variant translocation 1 (PVT1) and miR-190a-5p on vascular endothelial cell (EC) proliferation and assess their clinical value in the diagnosis of chronic heart failure (CHF). The expression of PVT1 and miR-190a-5p was investigated using reverse transcription-quantitative PCR. The interaction between PVT1 and miR-190a-5p was confirmed using a luciferase reporter assay. A Cell Counting Kit-8 assay was performed to examine EC proliferation. A receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of PVT1 and miR-190a-5p. PVT1 directly decreased the expression of miR-190a-5p in ECs. Overexpression of miR-190a-5p in ECs led to inhibited cell proliferation and miR-190a-5p antagonized the promotive effect of PVT1 on EC proliferation. Serum expression of PVT1 increased, while serum expression of miR-190a-5p decreased in patients with CHF compared with healthy controls (all P<0.001). The ROC curves indicated that PVT1 and miR-190a-5p were two diagnostic biomarkers of CHF, and the combination of PVT1 and miR-190a-5p showed better diagnostic accuracy compared with using PVT1 or miR-190-5p alone. In conclusion, the present study demonstrated that PVT1 promoted EC proliferation by directly suppressing miR-190a-5p. Circulating PVT1 and miR-190a-5p are possible two candidate diagnostic biomarkers of CHF, and the combined detection of the two indicators may provide a novel approach for CHF diagnosis.	32266032	RID04665	ceRNA or sponge	circulating	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Atherosclerosis	RAPIA	ITGB1	positively-E	dual-luciferase reporter assay;RIP;Targetscan;miRanda	upregulation	sequencing;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-183-5p)	regulation	RNA-protein	Atorvastatin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000150093	NA	NA	3688	NA	CD29|FNRB|GPIIA|MDF2|MSK12	Macrophage-Enriched lncRNA RAPIAWhether long noncoding RNAs (lncRNAs) affect the progression of atherosclerosis and whether they are potential targets for the treatment of advanced atherosclerosis are poorly understood.The progression of atherosclerotic lesions was accompanied by dynamic alterations in lncRNA expression, as revealed by RNA sequencing and quantitative polymerase chain reaction. Among the dynamically changing lncRNAs, we identified a novel lncRNA, lncRNA Associated with the Progression and Intervention of Atherosclerosis (RAPIA),that was highly expressed in advanced atherosclerotic lesions and in macrophages. Inhibition of RAPIA in vivo not only repressed the progression of atherosclerosis but also exerted atheroprotective effects similar to those of atorvastatin on advanced atherosclerotic plaques that had already formed. In vitro assays demonstrated that RAPIA promoted proliferation and reduced apoptosis of macrophages. A molecular sponge interaction between RAPIA and microRNA-183-5p was demonstrated by dual-luciferase reporter and RNA immunoprecipitation assays. Rescue assays indicated that RAPIA functioned at least in part by targeting the microRNA-183-5p/ITGB1 (integrin beta1) pathway in macrophages. In addition, the transcription factor FoxO1 (forkhead box O1) could bind to the RAPIA promoter region and facilitate the expression of RAPIA.	32268789	RID04666	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Atherosclerosis	FOXO1	RAPIA	positively-E	JASPAR;dual-luciferase reporter assay;ChIP;siRNA	upregulation	sequencing;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	enhencer	binding/interaction	NA	Atorvastatin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	TF	lncRNA	ENSG00000150907	NA	NA	NA	2308	NA	FKH1|FKHR|FOXO1A	NA	Macrophage-Enriched lncRNA RAPIAWhether long noncoding RNAs (lncRNAs) affect the progression of atherosclerosis and whether they are potential targets for the treatment of advanced atherosclerosis are poorly understood.The progression of atherosclerotic lesions was accompanied by dynamic alterations in lncRNA expression, as revealed by RNA sequencing and quantitative polymerase chain reaction. Among the dynamically changing lncRNAs, we identified a novel lncRNA, lncRNA Associated with the Progression and Intervention of Atherosclerosis (RAPIA),that was highly expressed in advanced atherosclerotic lesions and in macrophages. Inhibition of RAPIA in vivo not only repressed the progression of atherosclerosis but also exerted atheroprotective effects similar to those of atorvastatin on advanced atherosclerotic plaques that had already formed. In vitro assays demonstrated that RAPIA promoted proliferation and reduced apoptosis of macrophages. A molecular sponge interaction between RAPIA and microRNA-183-5p was demonstrated by dual-luciferase reporter and RNA immunoprecipitation assays. Rescue assays indicated that RAPIA functioned at least in part by targeting the microRNA-183-5p/ITGB1 (integrin beta1) pathway in macrophages. In addition, the transcription factor FoxO1 (forkhead box O1) could bind to the RAPIA promoter region and facilitate the expression of RAPIA.	32268789	RID04667	chromatin looping	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Kidney injury	LINC00963	miR-128-3p	negatively-F	dual-luciferase reporter assay;RNA pull-down assay;overexpression;siRNA;RegRNA 2.0	upregulation	qRT-PCR	NA	NA	cell injury(+);JAK2/STAT1 signaling pathway(+);cell cycle(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	miRNA	ENSG00000204054	GRCh38_9:129476946-129513687	NA	NA	100506190	NA	MetaLnc9	NA	LINC00963 targeting miR-128-3p promotes acute kidney injury process by activating JAK2/STAT1 pathway In this study, we established rat acute kidney injury (AKI) models by ischaemia and reperfusion (I/R) treatment. Urea and creatinine levels were determined, and histological features of kidney tissues were examined following HE staining. CCK8 assay was chosen to assess the viability of hypoxia-induced HK-2 cells. Dual-luciferase reporter gene assays were performed to verify the target relationship between LINC00963 and microRNA. The mRNA and protein levels were assayed by RT-qPCR and western blot, respectively. Annexin V-FITC/PI and TUNEL staining were used to evaluate apoptosis. LINC00963 was highly expressed in the cell and rat models, and miR-128-3p was predicted and then verified as a target gene of LINC00963. Knockdown of LINC00963 reduced acute renal injury both in vitro and in vivo. LINC00963 activated the JAK2/STAT1 pathway to aggravate renal I/R injury. LINC00963 could target miR-128-3p to reduce G1 arrest and apoptosis through JAK2/STAT1 pathway to promote the progression of AKI.	32270599	RID04668	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	
Non-small cell lung cancer	LCTS5	INO80	negatively-F	RNA pull-down assay;shRNA;immunoblot;ChIP-qPCR	downregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);tumor growth(+);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000128908	NA	NA	54617	NA	hINO80|INO80A|INOC1|KIAA1259	Long noncoding RNA LCTS5 inhibits non-small cell lung cancer by interacting with INO80 LncRNA profiling was used to identify the novel lncRNA LCTS5. Viability and migration assays were implemented to evaluate the in vitro effect of LCTS5. Transplantation study was designed to investigate the in vivo role. Short hairpin RNA (shRNA) and lentiviral vector were used to alter LCTS5 expression.  We identified a novel lncRNA named LCTS5 whose abundance is dramatically decreased in NSCLC. Overexpressing LCTS5 effectively inhibits viability and migration. Meanwhile, LCTS5 overexpression retards xenograft tumor growth and proliferation. LCTS5 interacts with INO80 to reduce INO80 occupancy at enhancer regions of multiple lung cancer related genes without affecting INO80 decay.The newly identified lncRNA LCTS5 impairs NSCLC progression and provides a compelling target for therapeutic intervention during NSCLC treatments. RNA pull-down assays were performed to identify potential bindingpartners of LCTS5.	32305524	RID04669	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Chronic myeloid leukemia	PANTR1	MDR	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	NA	association	RNA-protein	Imatinib	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233639	GRCh38_2:104764932-104853183	NA	NA	100506421	NA	linc-Brn1a|linc-POU3F3|LINC01158	NA	Relationship between PANTR1 and Imatinib Resistance of Chronic Myeloid Leukemia Cell Line K562 and Its Related MechanismsK562 control cells (Control) and K562 imatinib resistant cells (ImR) were cultured. Two siRNA vectors targeting PANTR1 and control vectors were transfected into K562-ImR cells by lentivirus as ImR-siPA#1, ImR-siPA#2 and ImR-siControl cells, respectively. Imatinib semi-inhibitory concentration (IC50) was detected by CCK-8 kit. The expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 mRNA were detected by fluorescence quantitative PCR RT-qPCR - and the expression level of BCR/ABL, MDR, CD44 and CD133 protein were detected by western blot.Imatinib IC50 in ImR cells was significantly higher than that in control cells (P -.01), that of ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than that in ImR-sicontrol cells (P -.01), but still significantly higher than that in control cells (P -.01). The mRNA expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells (P -.01). The mRNA expression level of PANTR1, MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than those in ImR-siControl cells (P -.01), while the expression level of BCR/ABL mRNA was not significantly different (P -.05). The protein expression level of BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells, while the protein expression level of MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 were significantly lower than those in ImR-siControl cells.LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.	32319374	RID04670	expression association	chemoresistance		
Chronic myeloid leukemia	PANTR1	CD44	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	NA	association	RNA-protein	Imatinib	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233639	GRCh38_2:104764932-104853183	ENSG00000026508	NA	100506421	960	linc-Brn1a|linc-POU3F3|LINC01158	CD44R|CSPG8|HCELL|IN|MC56|MDU2|MDU3|MIC4|Pgp1	Relationship between PANTR1 and Imatinib Resistance of Chronic Myeloid Leukemia Cell Line K562 and Its Related MechanismsK562 control cells (Control) and K562 imatinib resistant cells (ImR) were cultured. Two siRNA vectors targeting PANTR1 and control vectors were transfected into K562-ImR cells by lentivirus as ImR-siPA#1, ImR-siPA#2 and ImR-siControl cells, respectively. Imatinib semi-inhibitory concentration (IC50) was detected by CCK-8 kit. The expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 mRNA were detected by fluorescence quantitative PCR RT-qPCR - and the expression level of BCR/ABL, MDR, CD44 and CD133 protein were detected by western blot.Imatinib IC50 in ImR cells was significantly higher than that in control cells (P -.01), that of ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than that in ImR-sicontrol cells (P -.01), but still significantly higher than that in control cells (P -.01). The mRNA expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells (P -.01). The mRNA expression level of PANTR1, MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than those in ImR-siControl cells (P -.01), while the expression level of BCR/ABL mRNA was not significantly different (P -.05). The protein expression level of BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells, while the protein expression level of MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 were significantly lower than those in ImR-siControl cells.LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.	32319374	RID04671	expression association	chemoresistance		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Chronic myeloid leukemia	PANTR1	PROM1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	NA	association	RNA-protein	Imatinib	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233639	GRCh38_2:104764932-104853183	ENSG00000007062	NA	100506421	8842	linc-Brn1a|linc-POU3F3|LINC01158	AC133|CD133|CORD12|MCDR2|PROML1|RP41|STGD4	Relationship between PANTR1 and Imatinib Resistance of Chronic Myeloid Leukemia Cell Line K562 and Its Related MechanismsK562 control cells (Control) and K562 imatinib resistant cells (ImR) were cultured. Two siRNA vectors targeting PANTR1 and control vectors were transfected into K562-ImR cells by lentivirus as ImR-siPA#1, ImR-siPA#2 and ImR-siControl cells, respectively. Imatinib semi-inhibitory concentration (IC50) was detected by CCK-8 kit. The expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 mRNA were detected by fluorescence quantitative PCR RT-qPCR - and the expression level of BCR/ABL, MDR, CD44 and CD133 protein were detected by western blot.Imatinib IC50 in ImR cells was significantly higher than that in control cells (P -.01), that of ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than that in ImR-sicontrol cells (P -.01), but still significantly higher than that in control cells (P -.01). The mRNA expression level of PANTR1, BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells (P -.01). The mRNA expression level of PANTR1, MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 cells were significantly lower than those in ImR-siControl cells (P -.01), while the expression level of BCR/ABL mRNA was not significantly different (P -.05). The protein expression level of BCR/ABL, MDR, CD44 and CD133 in ImR cells were significantly higher than those in control cells, while the protein expression level of MDR, CD44 and CD133 in ImR-siPA#1 and ImR-siPA#2 were significantly lower than those in ImR-siControl cells.LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.	32319374	RID04672	expression association	chemoresistance		UP(BRCA);DATA(GSE109761)
Ovarian cancer	CCEPR	CCND1	positively-E	western blot	upregulation		NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000110092	NA	105682749	595	CCHE1|lncRNA-CCHE1	BCL1|D11S287E|PRAD1|U21B31	Upregulation of long non-coding RNA CCEPR is associated with poor prognosis and contributes to the progression of ovarian cancer through regulating the Wnt/beta-catenin signaling pathwayThe aim of the present study was to determine the clinical significance of CCEPR in OC and to investigate its biological roles.Cell Counting Kit-8 assay was used to analyze cell proliferation, Transwell assay was used to assess invasion, flow cytometric analysis was used to analyze apoptosis, and western blot was used to perform mechanistic studies. CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non-cancer tissues. Similarly, significant increases in CCEPR expression were observed in OC cell lines (SK-OV-3 and OVCAR-3) compared with the ovarian surface epithelial cell line, HOSEpiC. The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis. CCEPR-silenced OC cells also demonstrated decreased expression levels of four proteins involved in the Wnt/beta-catenin signaling pathway: Cyclin D1, beta-catenin, Myc and matrix metallopeptidase-7. In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/beta-catenin signaling pathway.	32319633	RID04673	expression association	prognosis		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Ovarian cancer	CCEPR	CTNNB1	positively-E	western blot	upregulation		NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000168036	NA	105682749	1499	CCHE1|lncRNA-CCHE1	armadillo|beta-catenin|CTNNB	Upregulation of long non-coding RNA CCEPR is associated with poor prognosis and contributes to the progression of ovarian cancer through regulating the Wnt/beta-catenin signaling pathwayThe aim of the present study was to determine the clinical significance of CCEPR in OC and to investigate its biological roles.Cell Counting Kit-8 assay was used to analyze cell proliferation, Transwell assay was used to assess invasion, flow cytometric analysis was used to analyze apoptosis, and western blot was used to perform mechanistic studies. CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non-cancer tissues. Similarly, significant increases in CCEPR expression were observed in OC cell lines (SK-OV-3 and OVCAR-3) compared with the ovarian surface epithelial cell line, HOSEpiC. The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis. CCEPR-silenced OC cells also demonstrated decreased expression levels of four proteins involved in the Wnt/beta-catenin signaling pathway: Cyclin D1, beta-catenin, Myc and matrix metallopeptidase-7. In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/beta-catenin signaling pathway.	32319633	RID04674	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	CCEPR	MYC	positively-E	western blot	upregulation		NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	105682749	4609	CCHE1|lncRNA-CCHE1	bHLHe39|c-Myc|MYCC	Upregulation of long non-coding RNA CCEPR is associated with poor prognosis and contributes to the progression of ovarian cancer through regulating the Wnt/beta-catenin signaling pathwayThe aim of the present study was to determine the clinical significance of CCEPR in OC and to investigate its biological roles.Cell Counting Kit-8 assay was used to analyze cell proliferation, Transwell assay was used to assess invasion, flow cytometric analysis was used to analyze apoptosis, and western blot was used to perform mechanistic studies. CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non-cancer tissues. Similarly, significant increases in CCEPR expression were observed in OC cell lines (SK-OV-3 and OVCAR-3) compared with the ovarian surface epithelial cell line, HOSEpiC. The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis. CCEPR-silenced OC cells also demonstrated decreased expression levels of four proteins involved in the Wnt/beta-catenin signaling pathway: Cyclin D1, beta-catenin, Myc and matrix metallopeptidase-7. In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/beta-catenin signaling pathway.	32319633	RID04675	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Ovarian cancer	CCEPR	MMP7	positively-E	western blot	upregulation		NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000137673	NA	105682749	4316	CCHE1|lncRNA-CCHE1	MPSL1|PUMP-1	Upregulation of long non-coding RNA CCEPR is associated with poor prognosis and contributes to the progression of ovarian cancer through regulating the Wnt/beta-catenin signaling pathwayThe aim of the present study was to determine the clinical significance of CCEPR in OC and to investigate its biological roles.Cell Counting Kit-8 assay was used to analyze cell proliferation, Transwell assay was used to assess invasion, flow cytometric analysis was used to analyze apoptosis, and western blot was used to perform mechanistic studies. CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non-cancer tissues. Similarly, significant increases in CCEPR expression were observed in OC cell lines (SK-OV-3 and OVCAR-3) compared with the ovarian surface epithelial cell line, HOSEpiC. The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis. CCEPR-silenced OC cells also demonstrated decreased expression levels of four proteins involved in the Wnt/beta-catenin signaling pathway: Cyclin D1, beta-catenin, Myc and matrix metallopeptidase-7. In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/beta-catenin signaling pathway.	32319633	RID04676	expression association	prognosis		UP(LIHC);DATA(GSE117623)
Cervical cancer	PTENP1	MTUS1	positively-E	dual-luciferase reporter assay;overexpression;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-19b)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000129422	NA	11191	57509	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	ATBP|ATIP1|ATIP3|DKFZp586D1519|FLJ14295|ICIS|KIAA1288|MP44|MTSG1	Reduced long non-coding RNA PTENP1 contributed to proliferation and invasion via miR-19b/MTUS1 axis in patients with cervical cancerIn this study, we mainly investigate the functions of lncRNA PTENP1 in the progression of human cervical cancer (CC).Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was performed to detect expression levels of PTENP1, miR-19b and MTUS1 in CC tissues,the adjacent tissues and CC cell lines. The correlations between PTENP1 with miR-19b, miR-19b with MTUS1 and PTENP1 with MTUS1 were analyzed. Overall survival (OS) of patients was analyzed using Kaplan-Meier method. Proliferation capacity was measured by CCK-8 assay and the invasion ability in CC cell line was detected by transwell assay. western blot (WB) assay was performed to measure protein levels of tissues and CC cell lines. Finally, dual-luciferase reporter assay was performed to prove the potential binding sites between PTENP1 and miR-19b,miR-19b and MTUS1.We found that PTENP1 was reduced in CC tissues and CC cell lines, which predicted the poor diagnosis of CC patients. MiR-19b was increased in CC tissues, which was negatively correlated with PTENP1 in CC tis-sues. MTUS1 was reduced in CC tissues, which was negatively correlated with miR-19b and positively correlated within PTENP1 CC tissues. Furthermore, PTENP1 overexpression inhibited cell proliferation ability and invasion capacity in HeLa cells, as well as repressed expressions of Cyclin D1, N-cadherin, and Vimentin. Moreover,Luciferase gene reporter assays verified that miR-19b was a direct target miRNA of PTENP1,and MTUS1 was identified as a direct target of miR-19b. In addition, the inhibited cell proliferation and invasion abilities in HeLa cells with p-PTENP1 were eliminated following with miR-19b mimic transfection. According to the results,this study showed that PTENP1 was reduced in CC patients and it was a prognostic factor for CC patients. Furthermore, we firstly uncovered that PTENP1 could inhibit cell proliferation and invasion via miR-19b/MTUS1 in CC patients,which uncovered the tumor-suppressive role of PTENP1 in CC and suggested that it might be a potential target for treating human CC.	32373949	RID04677	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Cervical cancer	PTENP1	Cyclin D1	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	NA	NA	11191	NA	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	NA	Reduced long non-coding RNA PTENP1 contributed to proliferation and invasion via miR-19b/MTUS1 axis in patients with cervical cancerIn this study, we mainly investigate the functions of lncRNA PTENP1 in the progression of human cervical cancer (CC).Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was performed to detect expression levels of PTENP1, miR-19b and MTUS1 in CC tissues,the adjacent tissues and CC cell lines. The correlations between PTENP1 with miR-19b, miR-19b with MTUS1 and PTENP1 with MTUS1 were analyzed. Overall survival (OS) of patients was analyzed using Kaplan-Meier method. Proliferation capacity was measured by CCK-8 assay and the invasion ability in CC cell line was detected by transwell assay. western blot (WB) assay was performed to measure protein levels of tissues and CC cell lines. Finally, dual-luciferase reporter assay was performed to prove the potential binding sites between PTENP1 and miR-19b,miR-19b and MTUS1.We found that PTENP1 was reduced in CC tissues and CC cell lines, which predicted the poor diagnosis of CC patients. MiR-19b was increased in CC tissues, which was negatively correlated with PTENP1 in CC tis-sues. MTUS1 was reduced in CC tissues, which was negatively correlated with miR-19b and positively correlated within PTENP1 CC tissues. Furthermore, PTENP1 overexpression inhibited cell proliferation ability and invasion capacity in HeLa cells, as well as repressed expressions of Cyclin D1, N-cadherin, and Vimentin. Moreover,Luciferase gene reporter assays verified that miR-19b was a direct target miRNA of PTENP1,and MTUS1 was identified as a direct target of miR-19b. In addition, the inhibited cell proliferation and invasion abilities in HeLa cells with p-PTENP1 were eliminated following with miR-19b mimic transfection. According to the results,this study showed that PTENP1 was reduced in CC patients and it was a prognostic factor for CC patients. Furthermore, we firstly uncovered that PTENP1 could inhibit cell proliferation and invasion via miR-19b/MTUS1 in CC patients,which uncovered the tumor-suppressive role of PTENP2 in CC and suggested that it might be a potential target for treating human CC.	32373949	RID04678	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	
Cervical cancer	PTENP1	N-cadherin	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	NA	NA	11191	NA	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	NA	Reduced long non-coding RNA PTENP1 contributed to proliferation and invasion via miR-19b/MTUS1 axis in patients with cervical cancerIn this study, we mainly investigate the functions of lncRNA PTENP1 in the progression of human cervical cancer (CC).Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was performed to detect expression levels of PTENP1, miR-19b and MTUS1 in CC tissues,the adjacent tissues and CC cell lines. The correlations between PTENP1 with miR-19b, miR-19b with MTUS1 and PTENP1 with MTUS1 were analyzed. Overall survival (OS) of patients was analyzed using Kaplan-Meier method. Proliferation capacity was measured by CCK-8 assay and the invasion ability in CC cell line was detected by transwell assay. western blot (WB) assay was performed to measure protein levels of tissues and CC cell lines. Finally, dual-luciferase reporter assay was performed to prove the potential binding sites between PTENP1 and miR-19b,miR-19b and MTUS1.We found that PTENP1 was reduced in CC tissues and CC cell lines, which predicted the poor diagnosis of CC patients. MiR-19b was increased in CC tissues, which was negatively correlated with PTENP1 in CC tis-sues. MTUS1 was reduced in CC tissues, which was negatively correlated with miR-19b and positively correlated within PTENP1 CC tissues. Furthermore, PTENP1 overexpression inhibited cell proliferation ability and invasion capacity in HeLa cells, as well as repressed expressions of Cyclin D1, N-cadherin, and Vimentin. Moreover,Luciferase gene reporter assays verified that miR-19b was a direct target miRNA of PTENP1,and MTUS1 was identified as a direct target of miR-19b. In addition, the inhibited cell proliferation and invasion abilities in HeLa cells with p-PTENP1 were eliminated following with miR-19b mimic transfection. According to the results,this study showed that PTENP1 was reduced in CC patients and it was a prognostic factor for CC patients. Furthermore, we firstly uncovered that PTENP1 could inhibit cell proliferation and invasion via miR-19b/MTUS1 in CC patients,which uncovered the tumor-suppressive role of PTENP3 in CC and suggested that it might be a potential target for treating human CC.	32373949	RID04679	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	
Cervical cancer	PTENP1	Vimentin	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	NA	NA	11191	NA	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	NA	Reduced long non-coding RNA PTENP1 contributed to proliferation and invasion via miR-19b/MTUS1 axis in patients with cervical cancerIn this study, we mainly investigate the functions of lncRNA PTENP1 in the progression of human cervical cancer (CC).Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was performed to detect expression levels of PTENP1, miR-19b and MTUS1 in CC tissues,the adjacent tissues and CC cell lines. The correlations between PTENP1 with miR-19b, miR-19b with MTUS1 and PTENP1 with MTUS1 were analyzed. Overall survival (OS) of patients was analyzed using Kaplan-Meier method. Proliferation capacity was measured by CCK-8 assay and the invasion ability in CC cell line was detected by transwell assay. western blot (WB) assay was performed to measure protein levels of tissues and CC cell lines. Finally, dual-luciferase reporter assay was performed to prove the potential binding sites between PTENP1 and miR-19b,miR-19b and MTUS1.We found that PTENP1 was reduced in CC tissues and CC cell lines, which predicted the poor diagnosis of CC patients. MiR-19b was increased in CC tissues, which was negatively correlated with PTENP1 in CC tis-sues. MTUS1 was reduced in CC tissues, which was negatively correlated with miR-19b and positively correlated within PTENP1 CC tissues. Furthermore, PTENP1 overexpression inhibited cell proliferation ability and invasion capacity in HeLa cells, as well as repressed expressions of Cyclin D1, N-cadherin, and Vimentin. Moreover,Luciferase gene reporter assays verified that miR-19b was a direct target miRNA of PTENP1,and MTUS1 was identified as a direct target of miR-19b. In addition, the inhibited cell proliferation and invasion abilities in HeLa cells with p-PTENP1 were eliminated following with miR-19b mimic transfection. According to the results,this study showed that PTENP1 was reduced in CC patients and it was a prognostic factor for CC patients. Furthermore, we firstly uncovered that PTENP1 could inhibit cell proliferation and invasion via miR-19b/MTUS1 in CC patients,which uncovered the tumor-suppressive role of PTENP4 in CC and suggested that it might be a potential target for treating human CC.	32373949	RID04680	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	
Osteosarcoma	RHPN1-AS1	SNAI2	positively-E	siRNA;starBase;dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-506)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000254389	GRCh38_8:143366631-143368548	ENSG00000019549	NA	78998	6591	C8orf51|MGC3113	SLUG|SLUGH|SLUGH1|SNAIL2	Long noncoding RNA RHPN1-AS1 exerts prooncogenic actions in osteosarcoma by functioning as a molecular sponge of miR-506 to positively regulate SNAI2 expressionThe expression of RHPN1-AS1 in OS was measured by RTqPCR.The effects of the RHPN1-AS1 silencing in OS cells were studied both in vitro (in a Cell Counting Kit-8 assay, apoptosis analysis, and Transwell migration and invasion assays) and in vivo (by means of tumor xenografts in nude mice). Herein, RHPN1-AS1 expression was found to be significantly upregulated in OS tissues and cell lines.The elevated expression of RHPN1-AS1 closely correlated with the tumor size, TNM stage, distal metastasis and shorter overall survival in patients with OS. The depletion of RHPN1-AS1 restrained OS cell proliferation, migration, and invasion, and exerted proapoptotic effects in vitro.Furthermore, the knockdown of RHPN1-AS1 effectively reduced the tumor growth of OS cells in vivo. As for the mechanism, RHPN1-AS1 increased snail family zinc finger 2 (SNAI2 also known as SNAIL2) expression by acting as a competing endogenous RNA of miR-506. Notably, increasing the amount of miR-506 partially reversed the effects of the RHPN1-AS1 downregulation on OS cells. In conclusion, RHPN1-AS1 contributes to the malignancy of OS cells in vitro and in vivo, largely via upregulation of the miR-506-SNAI2 axis output.The luciferase reporter assay was performed to verify whether RHPN1-AS1 was capable of binding to miR-506 in OS cells. the RIP assay was applied to test whether RHPN1-AS1 is associated with miR-506 within the AGO2-containing complex. RHPN1-AS1 and miR-506 turned out to be enriched in the AGO2-containing complex as compared with the IgG control .The mRNA (Figure 4(a)) and protein (Figure 4(b)) expression of SNAI2 in HOS and SAOS-2 cells was reduced by the transfection with si-RHPN1-AS1.These results collectively meant that RHPN1-AS1 functions as a ceRNA and positively modulates SNAI2 expression by sequestering miR-506.	32401134	RID04681	ceRNA or sponge	metastasis		
Temporal lobe epilepsy	ILF3-DT	IL-1	positively-E	overexpression;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-212)	regulation	RNA-RNA	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expressionIn this paper,we found that both hippocampal and serum ILF3-AS1 levels are higher in TLE patients than matched control individuals. In addition, we also found that overexpression of ILF3-AS1 promoted expression of MMP2, MMP3, MMP9, and MMP14. The inflammatory cytokines IL-1beta and TNF-alpha each enhanced ILF3-AS1 expression in astrocytes, and that ectopic expression of ILF3-AS1 induced expression of IL-6 and TNF-alpha.  perform a luciferase reporter analysis,  which  showed  that  miR-212 overexpression leads to a decrease in ILF3-AS1-luciferase activity in astrocytes. Moreover, forced ILF3-AS1 expression suppressed miR-212 expression in the astrocytes, and hippocampal and serum miR-212 expression was lower in TLE patients than in their control group. Taken together these results suggest ILF3-AS1 targets miR-212 to induce inflammatory cytokine and MMP3 and MMP9 expression. To determine whether ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by suppressing miR-212, a series of rescue experiments were performed. Forced miR-212 expression reduced expression of IL-1beta (Figure 7A), IL-6 (Figure 7B), and TNF-alpha (Figure 7C) in astrocytes overexpressing ILF3-AS1. Likewise, elevated miR-212 expression decreased expression of MMP3 (Figure 7D) and MMP9 (Figure 7E) in the ILF3-AS2-overexpressing cells.	32404536	RID04682	ceRNA or sponge	NA		
Temporal lobe epilepsy	ILF3-DT	IL6	positively-E	overexpression;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-213)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000136244	NA	147727	3569	ILF3-AS1	BSF2|HGF|HSF|IFNB2|IL-6	LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expressionIn this paper,we found that both hippocampal and serum ILF3-AS1 levels are higher in TLE patients than matched control individuals. In addition, we also found that overexpression of ILF3-AS1 promoted expression of MMP2, MMP3, MMP9, and MMP14. The inflammatory cytokines IL-1beta and TNF-alpha each enhanced ILF3-AS1 expression in astrocytes, and that ectopic expression of ILF3-AS1 induced expression of IL-6 and TNF-alpha.  perform a luciferase reporter analysis,  which  showed  that  miR-212 overexpression leads to a decrease in ILF3-AS1-luciferase activity in astrocytes. Moreover, forced ILF3-AS1 expression suppressed miR-212 expression in the astrocytes, and hippocampal and serum miR-212 expression was lower in TLE patients than in their control group. Taken together these results suggest ILF3-AS1 targets miR-212 to induce inflammatory cytokine and MMP3 and MMP9 expression. To determine whether ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by suppressing miR-212, a series of rescue experiments were performed. Forced miR-212 expression reduced expression of IL-1beta (Figure 7A), IL-6 (Figure 7B), and TNF-alpha (Figure 7C) in astrocytes overexpressing ILF3-AS1. Likewise, elevated miR-212 expression decreased expression of MMP3 (Figure 7D) and MMP9 (Figure 7E) in the ILF3-AS3-overexpressing cells.	32404536	RID04683	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Temporal lobe epilepsy	ILF3-DT	TNF	positively-E	overexpression;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-214)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000228978	NA	147727	7124	ILF3-AS1	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expressionIn this paper,we found that both hippocampal and serum ILF3-AS1 levels are higher in TLE patients than matched control individuals. In addition, we also found that overexpression of ILF3-AS1 promoted expression of MMP2, MMP3, MMP9, and MMP14. The inflammatory cytokines IL-1beta and TNF-alpha each enhanced ILF3-AS1 expression in astrocytes, and that ectopic expression of ILF3-AS1 induced expression of IL-6 and TNF-alpha.  perform a luciferase reporter analysis,  which  showed  that  miR-212 overexpression leads to a decrease in ILF3-AS1-luciferase activity in astrocytes. Moreover, forced ILF3-AS1 expression suppressed miR-212 expression in the astrocytes, and hippocampal and serum miR-212 expression was lower in TLE patients than in their control group. Taken together these results suggest ILF3-AS1 targets miR-212 to induce inflammatory cytokine and MMP3 and MMP9 expression. To determine whether ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by suppressing miR-212, a series of rescue experiments were performed. Forced miR-212 expression reduced expression of IL-1beta (Figure 7A), IL-6 (Figure 7B), and TNF-alpha (Figure 7C) in astrocytes overexpressing ILF3-AS1. Likewise, elevated miR-212 expression decreased expression of MMP3 (Figure 7D) and MMP9 (Figure 7E) in the ILF3-AS4-overexpressing cells.	32404536	RID04684	ceRNA or sponge	NA		DOWN(LIHC);DATA(GSE117623)
Temporal lobe epilepsy	ILF3-DT	MMP3	positively-E	overexpression;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-215)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000263313	NA	147727	4314	ILF3-AS1	STMY|STMY1	LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expressionIn this paper,we found that both hippocampal and serum ILF3-AS1 levels are higher in TLE patients than matched control individuals. In addition, we also found that overexpression of ILF3-AS1 promoted expression of MMP2, MMP3, MMP9, and MMP14. The inflammatory cytokines IL-1beta and TNF-alpha each enhanced ILF3-AS1 expression in astrocytes, and that ectopic expression of ILF3-AS1 induced expression of IL-6 and TNF-alpha.  perform a luciferase reporter analysis,  which  showed  that  miR-212 overexpression leads to a decrease in ILF3-AS1-luciferase activity in astrocytes. Moreover, forced ILF3-AS1 expression suppressed miR-212 expression in the astrocytes, and hippocampal and serum miR-212 expression was lower in TLE patients than in their control group. Taken together these results suggest ILF3-AS1 targets miR-212 to induce inflammatory cytokine and MMP3 and MMP9 expression. To determine whether ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by suppressing miR-212, a series of rescue experiments were performed. Forced miR-212 expression reduced expression of IL-1beta (Figure 7A), IL-6 (Figure 7B), and TNF-alpha (Figure 7C) in astrocytes overexpressing ILF3-AS1. Likewise, elevated miR-212 expression decreased expression of MMP3 (Figure 7D) and MMP9 (Figure 7E) in the ILF3-AS5-overexpressing cells.	32404536	RID04685	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Temporal lobe epilepsy	ILF3-DT	MMP9	positively-E	overexpression;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-216)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Epilepsy	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000100985	NA	147727	4318	ILF3-AS1	CLG4B	LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expressionIn this paper,we found that both hippocampal and serum ILF3-AS1 levels are higher in TLE patients than matched control individuals. In addition, we also found that overexpression of ILF3-AS1 promoted expression of MMP2, MMP3, MMP9, and MMP14. The inflammatory cytokines IL-1beta and TNF-alpha each enhanced ILF3-AS1 expression in astrocytes, and that ectopic expression of ILF3-AS1 induced expression of IL-6 and TNF-alpha.  perform a luciferase reporter analysis,  which  showed  that  miR-212 overexpression leads to a decrease in ILF3-AS1-luciferase activity in astrocytes. Moreover, forced ILF3-AS1 expression suppressed miR-212 expression in the astrocytes, and hippocampal and serum miR-212 expression was lower in TLE patients than in their control group. Taken together these results suggest ILF3-AS1 targets miR-212 to induce inflammatory cytokine and MMP3 and MMP9 expression. To determine whether ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by suppressing miR-212, a series of rescue experiments were performed. Forced miR-212 expression reduced expression of IL-1beta (Figure 7A), IL-6 (Figure 7B), and TNF-alpha (Figure 7C) in astrocytes overexpressing ILF3-AS1. Likewise, elevated miR-212 expression decreased expression of MMP3 (Figure 7D) and MMP9 (Figure 7E) in the ILF3-AS6-overexpressing cells.	32404536	RID04686	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	ILF3-DT	SMAD2	positively-E	dual-luciferase reporter assay;LncBase Predicted v2;Targetscan ;starBase;miRcode;miR-TarBase;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-132?p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000175387	NA	147727	4087	ILF3-AS1	JV18-1|MADH2|MADR2	The long non-coding RNA ILF3-AS1 increases the proliferation and invasion of retinoblastoma through the miR-132'-p/SMAD2 axisIn the present study, our work revealed that the lncRNA ILF3-AS1 was increased in both RB tissues and cell lines. Repression of ILF3-AS1 suppressed both RB cell proliferation and invasion in vitro. ILF3-AS1 also promoted tumor growth in vivo. While exploring the mechanisms behind ILF3-AS1 in RB, we identified that ILF3-AS1 sponges with miR-132'-p that is expressed at low levels in RB tissues as well as attenuates RB progression. Furthermore, SMAD2 was confirmed to be a miR-132'-p target. Finally, we found that SMAD2 overexpression or miR-132'-p inhibitors recover the inhibitory effects of ILF3-AS1 suppression on RB progression. Collectively, these data indicate that ILF3-AS1 is involved in RB progression through the miR-132'-p/SMAD2 axis, providing a novel and promising biomarker that can be used for the treatment of RB.To investigate the mechanisms behind ILF3-AS1 in the development of RB, potential targets of ILF3-AS1 were predicted using programs including targetscan, starBase and LncBase Predicted v2. Prediction results revealed miR-132'-p forms complementary base pairing with ILF3-AS1 (Fig. 3A-C). The dual-luciferase reporter assay showed miR-132'-p mimics suppress luciferase activity of WT-ILF3-AS1, but not the mutant form (Fig. 3D). We next explored the target genes of miR-132'-p. According to the StarBase, miRcode, miR-TarBase, and Targetscan databases.The correlation between ILF3-AS1 and miR-132'-p was confirmed by RIP assay.	32407730	RID04687	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	DANCR	KLF5	positively-E	starBase;siRNA;dual-luciferase reporter assay;Targetscan		qRT-PCR	NA	NA	cell viability(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-214)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000102554	NA	57291	688	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	BTEB2|CKLF|IKLF	Knockdown of DANCR Suppressed the Biological Behaviors of Ovarian Cancer Cells Treated with Transforming Growth Factor-b (TGF-b) by Sponging MiR-214Here, we attempted to evaluate the effect of DANCR on the biological behavior of transforming growth factor-b (TGF-b) stimulated ovarian cancer cells.The expression of DANCR in ovarian cancer cells (A2780 and SKOV3) treated with TGF-b were detected by quantitative real-time polymerase chain reaction (qRT-PCR. DANCR silencing was constructed using lentiviral transfection in ovarian cancer cells. The Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays were performed to measure some cytology index. western blot was utilized to explore the effect of DANCR on  KLF5 expression. The expression of DANCR in cancer cells (A2780 and SKOV3) treated with TGF-b was significantly higher. DANCR silencing suppressed cell viability, migration and invasion, and induced cell apoptosis of TGF-b treated ovarian cancer cells. Bioinformatics analysis showed that DANCR served as a sponge for miR-214, and also showed that KLF5 was targeted by miR-214. In addition, DANCR could inhibit the expression of KLF5.We are the first to report that knockdown of DANCR could affect the biological process of ovarian cancer cells treated with TGF-b by sponging miR-214, which may provide new therapeutic ideas of ovarian cancer.We observed miR-214 had a potential binding site with DANCR using starBase v2.0.DANCR silencing could elevate miR-214 expression level significantly in A2780 and SKOV3 cells treated with TGF-beta, which was reversed by miR-214 inhibitor.A highly conserved putative binding site was identified at KLF5 3'-UTR using TargetScan .	32417846	RID04688	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Malignant glioma	WT1-AS	AKT1	positively-E	DIANA;RIP;dual-luciferase reporter assay;overexpression	downregulation	qRT-PCR	NA	NA	AKT signaling pathway(+)	ceRNA(miR-494-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000183242	GRCh38_11:32435518-32500632	ENSG00000142208	NA	51352	207	WIT-1|WIT1|WT1-AS1|WT1AS	AKT|PKB|PRKBA|RAC|RAC-alpha	Long Noncoding RNA WT1-AS Inhibit Cell Malignancy via miR-494-3p in GliomaWe explore the role of aberration of microRNA namely miR-494-3p through long noncoding RNA WT1-AS in the development of gliomas. In this study, we found that, levels of WT1-AS were significantly reduced in glioma tissues and cell lines. The miR-494-3p levels were negatively correlated with WT1-AS levels. The cellular proliferation and invasiveness decreased in WT1-AS transfected cell lines. Further the half maximal inhibitory concentration (IC50) of chemotherapeutic agent temozolomide was significantly reduced in the presence of WT1-AS. The cotransfection of WT1-AS and miR-494-3p reduced activation of phospho-AKT (p-AKT). Expression of miR-494-3p is modulated by binding to long noncoding RNA WT1-AS.Deregulation of WT1-AS leads to aberrant expression of miR-494-3p leading to hyperactivation of AKT. This malformation may result in altering protective immune responses in malignancies. Targeting of WT1-AS, miR-494-3p, and AKT may be novel therapeutic options in treatment of glioma. Based on the prediction from DIANA Tools, miR-494-3p was predicted binding with WT1-AS (Figure 5A) and confirmed promoting glioma cells.WT1-AS Regulates Akt Signaling via miR-494-3p in Glioma Cells	32419643	RID04689	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	DANCR	MDM2	positively-E	Starbase;siRNA;dual-luciferase reporter assay;RNA pull-down assay	upregulation	microarray;RT-qPCR	NA	NA	cell proliferation(+);cell viability(+);cell metastasis(+);tumorigenesis(+)	ceRNA(miR-518a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000135679	NA	57291	4193	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	HDM2|MGC5370	Roles of DANCR/microRNA-518a-3p/MDMA ceRNA network in the growth and malignant behaviors of colon cancer cellsDifferentially expressed lncRNAs between CC and paracancerous tissues were analyzed using microarrays and RT-qPCR. Follow-up studies were conducted to evaluate the correlation between DANCR expression and prognosis of CC patients. Loss-of-functions of DANCR were performed to identify its role in the malignant behaviors of CC cells. Sub-cellular localization of DANCR and the potential targets of DANCR were predicted and validated.Cells with inhibited DANCR were implanted into nude mice to evaluate the tumor formation and metastasis in vivo.DANCR was highly-expressed in CC tissues and cell lines, and higher levels of DANCR were linked with worse prognosis and less survival time of CC patients. Silencing of DANCR inhibited proliferation, viability, metastasis and resistance to death of CC cells. DANCR was found to be sub-localized in cytoplasmic matrix and to mediate murine double minute 2 (MDM2) expression through sponging miR-518a-3p in CC cells, during which the Smad2/3 signaling was activated. Likewise, silencing of DANCR in CC cells inhibited tumor formation and metastasis in vivo.This study provided evidence that silencing of DANCR might inhibit the growth and metastasis of CC cells through the DANCR/miR-518a-3p/MDM2 ceRNA network and the defect of Smad2/3 while activation of the p53 signaling pathways. This study may offer novel insights in CC treatment.miR-518a-3p was selected as a DANCR target according to the predictions on StarBase, The binding relationship between DANCR and miR-518a-3p was validated through the dual luciferase reporter gene assay	32423468	RID04690	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	LINC00665	YBX1	positively-F	RNA pull-down assay;overexpression;RIP;western blot;	upregulation	qRT-PCR	TCGA	NA	angiogenesis(+)	histone modification	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000065978	NA	100506930	4904	CIP2A-BP	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinomaHere we found that linc00665 depletion could markedly depressed proliferation and capillary tube formation of HUVECs in vitro. Mechanistically, linc00665 directly interacted with YB-1 protein,enhanced its stability through inhibiting ubiquitination-dependent proteolysis and stimulated its nuclear translocation in LUAD cells. The accumulated nuclear YB-1 activated expression of ANGPT4, ANGPTL3 and VEGFA by binding to their promoters, contributing to tumor-related angiogenesis in vitro and in vivo.Collectively, we conclude that linc00665 induces tumor-related angiogenesis in LUAD by directly interacting with YB-1 and activating YB-1-ANGPT4/ANGPTL3/VEGFA axis, which provides promising anti-angiogenic targets for cancer therapy.To identify linc00665 interacting proteins, RNA pull-down assays were performed using biotin-labeled linc00665 and A549 whole cell lysates. The presence of YB-1 in linc00665 specifically precipitated samples was then confirmed by western blot (Fig. 3B). The physical inter_x0002_action between linc00665 and YB-1 was further validated by RIP, as YB-1 antibody enriched linc00665 enormously from cell extracts versus nonspecific IgG control (Fig. 3C). These results indicated specific interaction between linc00665 and YB-1.Linc00665 induced tumor-related angiogenesis via YB-1	32423800	RID04691	epigenetic regulation	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00665	ANGPT4	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	angiogenesis(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000101280	NA	100506930	51378	CIP2A-BP	NA	Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinomaHere we found that linc00665 depletion could markedly depressed proliferation and capillary tube formation of HUVECs in vitro. Mechanistically, linc00665 directly interacted with YB-1 protein,enhanced its stability through inhibiting ubiquitination-dependent proteolysis and stimulated its nuclear translocation in LUAD cells. The accumulated nuclear YB-1 activated expression of ANGPT4, ANGPTL3 and VEGFA by binding to their promoters, contributing to tumor-related angiogenesis in vitro and in vivo.Collectively, we conclude that linc00665 induces tumor-related angiogenesis in LUAD by directly interacting with YB-1 and activating YB-1-ANGPT4/ANGPTL3/VEGFA axis, which provides promising anti-angiogenic targets for cancer therapy.linc00665-induced high expression of ANGPT4, ANGPTL3 andVEGFA was also significantly blocked by YBX1 silencing in A549tumors (Fig. 4H). In short, these results highlighted YB-1 as a criticaleffector of linc00665-induced angiogenesis both in vitro andin vivo.	32423800	RID04692	transcriptional regulation	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	LINC00665	ANGPTL3	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	angiogenesis(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000132855	NA	100506930	27329	CIP2A-BP	ANGPT5	Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinomaHere we found that linc00665 depletion could markedly depressed proliferation and capillary tube formation of HUVECs in vitro. Mechanistically, linc00665 directly interacted with YB-1 protein,enhanced its stability through inhibiting ubiquitination-dependent proteolysis and stimulated its nuclear translocation in LUAD cells. The accumulated nuclear YB-1 activated expression of ANGPT4, ANGPTL3 and VEGFA by binding to their promoters, contributing to tumor-related angiogenesis in vitro and in vivo.Collectively, we conclude that linc00665 induces tumor-related angiogenesis in LUAD by directly interacting with YB-1 and activating YB-1-ANGPT4/ANGPTL3/VEGFA axis, which provides promising anti-angiogenic targets for cancer therapy.linc00665-induced high expression of ANGPT4, ANGPTL3 andVEGFA was also significantly blocked by YBX1 silencing in A549tumors (Fig. 4H). In short, these results highlighted YB-1 as a criticaleffector of linc00666-induced angiogenesis both in vitro andin vivo.	32423800	RID04693	transcriptional regulation	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	LINC00665	VEGFA	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA	NA	angiogenesis(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000112715	NA	100506930	7422	CIP2A-BP	VEGF|VEGF-A|VPF	Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinomaHere we found that linc00665 depletion could markedly depressed proliferation and capillary tube formation of HUVECs in vitro. Mechanistically, linc00665 directly interacted with YB-1 protein,enhanced its stability through inhibiting ubiquitination-dependent proteolysis and stimulated its nuclear translocation in LUAD cells. The accumulated nuclear YB-1 activated expression of ANGPT4, ANGPTL3 and VEGFA by binding to their promoters, contributing to tumor-related angiogenesis in vitro and in vivo.Collectively, we conclude that linc00665 induces tumor-related angiogenesis in LUAD by directly interacting with YB-1 and activating YB-1-ANGPT4/ANGPTL3/VEGFA axis, which provides promising anti-angiogenic targets for cancer therapy.linc00665-induced high expression of ANGPT4, ANGPTL3 andVEGFA was also significantly blocked by YBX1 silencing in A549tumors (Fig. 4H). In short, these results highlighted YB-1 as a criticaleffector of linc00667-induced angiogenesis both in vitro andin vivo.	32423800	RID04694	transcriptional regulation	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Breast cancer	IGF1	SNHG7	negatively-E	siRNA	upregulation	microarray;sequencing;qPCR	TCGA	NA	cell proliferation(+)	transcriptional regulation	association	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000017427	NA	ENSG00000233016	GRCh38_9:136721366-136728184	3479	84973	IGF|IGF-I|IGF1A|IGFI	MGC16037|NCRNA00061	SNHG7 is a lncRNA oncogene controlled by Insulin-like Growth Factor signaling through a negative feedback loop to tightly regulate proliferationSubstantial evidence implicates IGF1 signaling in the initiation and development of a number of cancers including breast cancer.Here, we demonstrate through whole transcriptome RNAseq that IGF1 signaling regulates a subset of lncRNAs that are altered in breast cancer, including the known but unstudied lncRNA, SNHG7, which is amplified or overerxpressed in ~5% of breast tumors in TCGA. Further, we show that SNHG7 is downregulated by IGF via a post-transcriptional mechanism through MAPK and controls proliferation in a dose-dependent manner. SNHG7, in part, tightly controls proliferation by altering mRNA levels of both IGF1 signaling intermediates and downstream IGF1 regulated genes. Thereby, we identified a novel fine-tuning feedback mechanism of growth factor induced proliferation and gene expression response that is disrupted in the tumors of a subset of breast cancer patients.	32444795	RID04695	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)
Intrahepatic cholangiocarcinoma	HAGLROS	FAS	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000026103	NA	102800310	355	NA	APO-1|APT1|CD95|FAS1|TNFRSF6	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .05). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04696	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Intrahepatic cholangiocarcinoma	HAGLROS	ACACA	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000132142	NA	102800310	31	NA	ACAC|ACC|ACC1	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .06). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04697	expression association	prognosis		UP(LIHC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Intrahepatic cholangiocarcinoma	HAGLROS	SCD1	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000099194	NA	102800310	NA	NA	NA	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .07). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04698	expression association	prognosis		
Intrahepatic cholangiocarcinoma	HAGLROS	CPT11	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	NA	NA	102800310	NA	NA	NA	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .08). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04699	expression association	prognosis		
Intrahepatic cholangiocarcinoma	HAGLROS	SREBF1	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000072310	NA	102800310	6720	NA	HMD|IFAP2|SREBP1|bHLHd1	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .09). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04700	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Intrahepatic cholangiocarcinoma	HAGLROS	PPARG	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	metabolic process(+)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000132170	NA	102800310	5468	NA	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARG5|PPARgamma	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cellsafter intervention of HAGLROS through RT-qPCR and western blotanalysis. After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1(SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatoryelement binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressingHAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .10). To sum up, knockdown of HAGLROSreduced the levels of lipid metabolism-related genes in ICC cells.	32446859	RID04701	expression association	prognosis		UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Intrahepatic cholangiocarcinoma	HAGLROS	MTOR	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000198793	NA	102800310	2475	NA	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cells after intervention of HAGLROS through RT-qPCR and western blot After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1 (SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatory element binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressing HAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .11). To sum up, knockdown of HAGLROS reduced the levels of lipid metabolism-related genes in ICC cells. Knocking down HAGLROS inhibits the activation of mTOR pathway and promotes autophagy of ICC cells.It has been reported that knocking down HAGLROS in GC cells in_x0002_hibits the activation of mTOR pathway, thereby increasing the expression of autophagy-related gene (ATG) ATG9A and ATG9B	32446859	RID04702	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Intrahepatic cholangiocarcinoma	HAGLROS	ATG9A	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell autophagy(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000198925	NA	102800310	79065	NA	APG9L1|FLJ22169	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cells after intervention of HAGLROS through RT-qPCR and western blot After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1 (SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatory element binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressing HAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .11). To sum up, knockdown of HAGLROS reduced the levels of lipid metabolism-related genes in ICC cells. Knocking down HAGLROS inhibits the activation of mTOR pathway and promotes autophagy of ICC cells.It has been reported that knocking down HAGLROS in GC cells in_x0002_hibits the activation of mTOR pathway, thereby increasing the expression of autophagy-related gene (ATG) ATG9A and ATG10B	32446859	RID04703	expression association	prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Intrahepatic cholangiocarcinoma	HAGLROS	ATG9B	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell autophagy(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000181652	NA	102800310	285973	NA	APG9L2|FLJ14885|NOS3AS|SONE	Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathwayIn this study, the sh-HAGLROS-1 or sh-HAGLROS-2 was transfected into QBC939 cells, and overexpressing HAGLROS vector was transfected into KMCH cells. HAGLROS expression in ICC tissues and cell lines was detected, and its association with ICC prognosis was further analyzed. Lipid accumulation and lipid-related indicators (TG, LDL-C, TC and HDLeC) in QBC939 and KMCH cells were measured. ICC cell viability, invasion and migration were measured. western blotwas used to detect levels of the mTOR axis-related proteins and autophagy-related proteins (LC3I, LC3II, Beclin and P62). The levels of serum lipids and SREBP1 positive expression in transplanted tumors of nude mice were detected. HAGLROS was highly expressed in ICC and negatively correlated with prognosis. QBC939 cells with knocking down HAGLROS exhibited reduced lipid-related protein levels, blocked ICC cellular processes, inactivated mTOR axis, and increased autophagy.Furthermore, after HAGLROS knockdown, the expression of FAS, ACC,SCD1, CPT11, SREBP1, and PPAR-Gamma in QBC939 cells decreased significantly. QBC939 cells with overexpressing HAGLROS showed opposite trends. The lipid-related protein levels in serum of nude mice and SREBP1 positive expression in transplanted tumors were diminished. Taken together, sh-HAGLROS inactivated the mTOR axis and promoted autophagy, thereby improving lipid metabolism reprogramming in ICC. This study may offer novel ICC treatments.To evaluate the effect of HAGLROS on lipid metabolism in ICC cells,we detected the levels of lipid metabolism related genes in ICC cells after intervention of HAGLROS through RT-qPCR and western blot After HAGLROS knockdown, levels of fatty acid synthase(FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA Desaturase1 (SCD1), carnitine palmitoyl transferase 11 (CPT11), sterol-regulatory element binding protein 1 (SREBP1), and peroxisome proliferator-ac_x0002_tivated receptor gamma (PPAR-Gamma) in QBC939 cells were decreased sig_x0002_nificantly, while those levels in KMCH cells with overexpressing HAGLROS showed opposite trends, compared with the control and NCgroups (Fig. 3A-B) (all p < .11). To sum up, knockdown of HAGLROS reduced the levels of lipid metabolism-related genes in ICC cells. Knocking down HAGLROS inhibits the activation of mTOR pathway and promotes autophagy of ICC cells.It has been reported that knocking down HAGLROS in GC cells in_x0002_hibits the activation of mTOR pathway, thereby increasing the expression of autophagy-related gene (ATG) ATG9A and ATG11B	32446859	RID04704	expression association	prognosis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367)
Renal fibrosis	LNCRNA-ATB	TGFB1	positively-F	overexpression;RNA pull-down assay		qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(+);senescence(+);TGF-beta/SMAD signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	PCG	NA	NA	ENSG00000105329	NA	114004396	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Long Non-Coding RNA (LncRNA)-ATB Promotes Inflammation, Cell Apoptosis and Senescence in Transforming Growth Factor-b1 (TGF-b1) Induced Human Kidney 2 (HK-2) Cells via TGFb/SMAD2/3 Signaling PathwayIn this study, we investigated the effects and mechanism of long non-coding RNA (LncRNA)-ATB in TGF-b1 induced human kidney 2 (HK-2) cells.We investigated the effects of either overexpression or knockdown of LncRNA-ATB on inflammation, cell apoptosis, and senescence in TGF-b1 induced HK-2 cells. TGF-b1 induced HK-2 cells served as the cell model. The gene level was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR and protein expressions by western blot. Cell Counting Kit-8 (CCK-8) assay was performed for assessment of cell viability. Flow cytometry was applied for detection of cell apoptosis. Tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and IL-6 were measured by corresponding kits.LncRNA-ATB was highly expressed in TGF-b1 induced HK-2 cells. Inflammation, cell apoptosis, and senescence were enhanced by TGF-b1 and these effects were all reduced by knockdown of LncRNA-ATB. Whereas overexpression of LncRNA-ATB had the opposite effects with knockdown of LncRNA-ATB. The TGFb/SMAD2/3 signaling pathway was activated by TGF-b1 and this effect was further enhanced by LncRNA-ATB overexpression.Silencing LncRNA-ATB inhibited the TGFb/SMAD2/3 signaling pathway in TGF-b1 induced cells. The effects of LncRNA-ATB overexpression aforementioned in TGF-b1 induced cells were abolished by blockage of the TGFb/S0MAD2/3 signaling pathway.Furthermore, after overexpression of LncRNA-ATB, the effects of TGF-beta1 on bcl2, p53, p21, and p16 were promoted and after knockdown of LncRNA-ATB, the opposite results were found. These results confirmed that LncRNA-ATB played a vital role in TGF-beta1 induced cell apoptosis and senescence.	32447340	RID04705	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	HCP5	PRC1	positively-E	dual-luciferase reporter assay;starBase;siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-525-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000198901	NA	10866	9055	D6S2650E|P5-1	ASE1	Role of lncRNAHCP5/microRNA-525-5p/PRC1 crosstalk in the malignant behaviors of ovarian cancer cellsThe study was intended to figure out the function of long non-coding RNA (lncRNA) HCP5 in OC metastasis.microarray analysis was conducted to probe aberrantly expressed lncRNAs in OC tissues. Artificial silencing of lncRNA HCP5 was introduced in OC cells to identify its role in cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT). The potential downstream targets of lncRNA HCP5 were predicted by bio-information system and validated through dual luciferase reporter gene assays. Silencing of microRNA-525-5p (miR-525-5p) was introduced in cells to probe its role in cell behaviors. Xenograft tumors were induced in nude mice for in vivo experiments.High expression of lncRNA HCP5 was found in OC tissues and cells. Silencing of lncRNA HCP5 led to a decrease in cell proliferation, invasion, migration and EMT process. LncRNA HCP is mainly sub-localized in cytoplasm. LncRNA HCP could act as a sponge for miR-525-5p, which could further bind to polycomb repressive complex 1 (PRC1). Knockdown of miR-525-5p partly recovered the biological behaviors of OC cells inhibited by HCP5 silencing. In addition, HCP5 promotes Wnt/beta-catenin signaling pathway activity. Silencing of lncRNA HCP5 also impedes growth and metastasis of tumor in mice.The study suggested that lncRNA HCP5 might promote malignant behaviors of OC cells through the miR-525-5p/PRC1 crosstalk and the Wnt/beta-catenin pathway. Silencing of HCP5 might serve as a novel option for OC treatment.	32511950	RID04706	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD,SKCM);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842)
Myocardial infarction	SOX2-OT	TGFBR1	positively-E	DIANA;Targetscan;luciferase reporter assay;overexpression;RNA pull-down assay;RIP;shRNA	upregulation	RT-qPCR	GSE66360	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-27a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000106799	NA	347689	7046	DKFZp761J1324|NCRNA00043|SOX2OT	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFbetaR1 AxisThe current research was aimed to explore the role of SOX2-OT in Myocardial infarction(MI).Bioinformatics analysis (DIANA tools and Targetscan) and a wide range of experiments (CCK-8, flow cytometry, RT-qPCR, luciferase reporter, RIP, caspase-3 activity, trans-well, and western blot assays) were adopted to investigate the function and mechanism of SOX2-OT.We discovered that hypoxia treatment decreased cell viability but increased cell apoptosis. Besides, lncRNA SOX2-OT expression was upregulated in hypoxic HCMs. Hereafter, we confirmed that SOX2-OT could negatively regulate miR-27a-3p levels by directly binding with miR-27a-3p, and miR-27a-3p also could negatively regulate SOX2-OT levels. Furthermore, knockdown of SOX2-OT promoted cell proliferation, migration, and invasion, but limited cell apoptosis. However, these effects were reversed by anti-miR-27a-5p. Besides, we verified that miR-27a-3p binding with the 3'UTR of TGFBR1 and SOX2-OTregulated TGFbetaR1 level by collaborating with miR-27a-3p in HCMs. Eventually, rescue assays validated that the influence of SOX2-OT silence or miR-27a-3p overexpression on cellular processes in cardiomyocytes injury was counteracted by TGFBR1 overexpression. Conclusions. Long noncoding RNA SOX2-OT exacerbated hypoxia-induced cardiomyocytes injury by regulating miR-27a-3p/TGFbetaR1 axis, which may provide a novel insight for heart failure treatment.	32528555	RID04707	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Retinoblastoma	ZFPM2-AS1	HOXA1	positively-E	dual-luciferase reporter assay;StarBase; miRDIP; RNA22;miRSearch;Targetscan;miRanda	upregulation	microarray;RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+)	ceRNA(miR-515)	regulation	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000105991	NA	102723356	3198	SCAT3	HOX1|HOX1F	Long Noncoding RNA ZFPM2-AS1 Knockdown Restrains the Development of Retinoblastoma by Modulating the MicroRNA-515/HOXA1/Wnt/beta-Catenin AxisFirst, comparing the differentially expressed lncRNAs in normal retinal tissues as well as retinoblastoma (RB) tissues, the target lncRNA ZFPM2-AS1 was screened out. We then assayed the ZFPM2-AS1 expression in three RB cell lines, and carried out methylthiazol tetrazolium (MTT), transwell assays, and flow cytometric analyses to examine the role of si-ZFPM2-AS1 on cell behaviors. Following online database predication, the correlations between ZFPM2-AS1 and microR-515 (miR-515) or homeobox A1 (HOXA1) were corroborated by dual-luciferase reporter gene assays. Quantitative real-time PCR along with western blot assays was fulfilled to ascertain the expression of relevant genes. ZFPM2-AS1 was significantly overexpressed in RB tissues and cell lines, and ZFPM2-AS1 silencing curtailed the growth and metastasis of RB cells both in vitro and in vivo. Bioinformatic websites and dual-luciferase reporter gene assays disclosed that ZFPM2-AS1 might perform as a competing endogenous RNA for miR-515 and positively correlate with HOXA1 to activate the Wnt/beta-catenin signaling pathway.Altogether, these data demonstrated that ZFPM2-AS1 interacted with HOXA1 to promote RB development via mediating miR-515, establishing a promising therapeutic biomarker for RB and prognosis.Through the StarBase, miRDIP, and RNA22 databases, miRNAs containing binding sites with ZFPM2-AS1 were screened out, among which miR-515 was confirmed as a putative target of ZFPM2-AS1 by a luciferase reporter assay.Moreover, overexpression or silencing of ZFPM2-AS1 negatively regulated the expression of miR-515 in Y79 and WRI-RB1 cells.In order to further determine the downstream regulatory mechanism for miR-515, HOXA1, a target of miR-515 was predicted using miRSearch, TargetScan, and Miranda bioinformatics website prediction and confirmed using dual-luciferase reporter gene assays (Fig. 3H). In addition, HOXA1 also shared a positive correlation with ZFPM2-AS1 expression in 51 RB tissues (Figs. 3I, 3J). Taken together, ZFPM2-AS1 interacted with miR-515 to promote HOXA1 expression.MiR-515 Overexpression Inhibits the Activity of RB Cells	32561925	RID04708	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Gallbladder cancer	MEG3	MANF	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000259880	NA	55384	7873	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ARMET|ARP	Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-kB signaling pathwayThe relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRTPCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using western blot, and the changes in nuclear factor-kB (NF-kB) protein in the nucleus were determined after overexpression of lncRNA MEG3.The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-kB signal in GBC cells was activated by lncRNA MEG3.LncRNA MEG3 activates the NF-kB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.The potential molecular pathways of lncRNA MEG3 in inhibiting proliferation and promoting apoptosis of GBC cells were explored. Previous studies12,13 have showed that lncRNA MEG3 plays a key role in the ERS pathway, which is directly related to tumor growth and apoptosis. Therefore, the effect of lncRNA MEG3 on the ERS pathway was studied. As shown in Figure 5, the ERS-re_x0002_lated proteins (MANF, GRP78, and caspase-3) were evidently upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by ln_x0002_cRNA MEG63 overexpression.	32633352	RID04709	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)
Gallbladder cancer	MEG3	HSPA5	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000044574	NA	55384	3309	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BiP|GRP78	Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-kB signaling pathwayThe relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRTPCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using western blot, and the changes in nuclear factor-kB (NF-kB) protein in the nucleus were determined after overexpression of lncRNA MEG3.The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-kB signal in GBC cells was activated by lncRNA MEG3.LncRNA MEG3 activates the NF-kB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.The potential molecular pathways of lncRNA MEG3 in inhibiting proliferation and promoting apoptosis of GBC cells were explored. Previous studies12,13 have showed that lncRNA MEG3 plays a key role in the ERS pathway, which is directly related to tumor growth and apoptosis. Therefore, the effect of lncRNA MEG3 on the ERS pathway was studied. As shown in Figure 5, the ERS-re_x0002_lated proteins (MANF, GRP78, and caspase-3) were evidently upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by ln_x0002_cRNA MEG64 overexpression.	32633352	RID04710	expression association	NA		UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Gallbladder cancer	MEG3	Caspase3	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-kB signaling pathwayThe relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRTPCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using western blot, and the changes in nuclear factor-kB (NF-kB) protein in the nucleus were determined after overexpression of lncRNA MEG3.The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-kB signal in GBC cells was activated by lncRNA MEG3.LncRNA MEG3 activates the NF-kB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.The potential molecular pathways of lncRNA MEG3 in inhibiting proliferation and promoting apoptosis of GBC cells were explored. Previous studies12,13 have showed that lncRNA MEG3 plays a key role in the ERS pathway, which is directly related to tumor growth and apoptosis. Therefore, the effect of lncRNA MEG3 on the ERS pathway was studied. As shown in Figure 5, the ERS-re_x0002_lated proteins (MANF, GRP78, and caspase-3) were evidently upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by ln_x0002_cRNA MEG65 overexpression.	32633352	RID04711	expression association	NA		
Gallbladder cancer	MEG3	NFKB1	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000109320	NA	55384	4790	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	It was found that the NF-kB protein in the nucleus was remarkably upregulat_x0002_ed after overexpression of lncRNA MEG3 (Fig_x0002_ure 6A), indicating that lncRNA MEG3 overex_x0002_pression activates the NF-kB signal.	32633352	RID04712	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pulmonary hypertension	TYKRIL	PDGFRB	positively-E	RNA pull-down assay;CRISPR-Cas9	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000113721	NA	NA	5159	NA	CD140b|JTK12|PDGFR|PDGFR1	Long Noncoding RNA TYKRIL Plays a Role in Pulmonary Hypertension via the p53-Mediated Regulation of PDGFRbetaUsing RNAseq data, LncRNA TYKRIL (Tyrosine kinase receptor inducing lncRNA) was identified to be consistently upregulated in pericytes and pulmonary arterial smooth muscles cells (PASMCs) exposed to hypoxia and derived from IPAH patients. TYKRIL knockdown reversed the pro-proliferative (n=3) and anti-apoptotic (n=3) phenotype induced under hypoxic and IPAH conditions. Due to the poor species conservation of TYKRIL, exvivo studies were carried out in precision cut lung slices (PCLS) from PH patients. Knockdown of TYKRIL in PCLS decreased the vascular remodeling (n=5). The number of PCNA positive cells in the vessels were decreased and number of TUNEL positive cells in the vessels were increased in LNA treated group compared to control. Expression of PDGFRbeta, a key player in PH, was found to strongly correlate with TYKRIL expression in the patient samples (n=12) and TYKRIL knockdown decreased PDGFRbeta expression (n=3). From the transcription factor-screening array, it was observed that TYKRIL knock down increased the p53 activity, a known repressor of PDGFRbeta. RNA immunoprecipitation (RIP) using various p53 mutants demonstrated that TYKRIL binds to the Nterminal of p53 (an important region for p300 interaction with p53). The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n=3) and regulates p53 nuclear translocation.	32634060	RID04713	expression association	NA		UP(LIHC);DATA(GSE117623)
Pulmonary hypertension	TYKRIL	TP53	negatively-F	RIP;RNA pull-down assay	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Long Noncoding RNA TYKRIL Plays a Role in Pulmonary Hypertension via the p53-Mediated Regulation of PDGFRbetaUsing RNAseq data, LncRNA TYKRIL (Tyrosine kinase receptor inducing lncRNA) was identified to be consistently upregulated in pericytes and pulmonary arterial smooth muscles cells (PASMCs) exposed to hypoxia and derived from IPAH patients. TYKRIL knockdown reversed the pro-proliferative (n=3) and anti-apoptotic (n=3) phenotype induced under hypoxic and IPAH conditions. Due to the poor species conservation of TYKRIL, exvivo studies were carried out in precision cut lung slices (PCLS) from PH patients. Knockdown of TYKRIL in PCLS decreased the vascular remodeling (n=5). The number of PCNA positive cells in the vessels were decreased and number of TUNEL positive cells in the vessels were increased in LNA treated group compared to control. Expression of PDGFRbeta, a key player in PH, was found to strongly correlate with TYKRIL expression in the patient samples (n=12) and TYKRIL knockdown decreased PDGFRbeta expression (n=3). From the transcription factor-screening array, it was observed that TYKRIL knock down increased the p53 activity, a known repressor of PDGFRbeta. RNA immunoprecipitation (RIP) using various p53 mutants demonstrated that TYKRIL binds to the Nterminal of p53 (an important region for p300 interaction with p53). The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n=3) and regulates p53 nuclear translocation.	32634060	RID04714	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	SNHG12	SP1	positively-E	catRAPID;overexpression;RIP	upregulation	qRT-PCR	TCGA;GSE64052;GSE53757	NA	cell proliferation(+);cell invasion(+);cell migration(+);cancer progression(+);chemoresistance(+)	protein stability	binding/interaction	NA	Sunitinib	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000185591	NA	85028	6667	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinomaIn this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis. SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro. Mechanically, SNHG12 bound to SP1 and prevented the ubiquitylation-dependent proteolysis of SP1.Luciferase activity analysis showed that the luciferase activity of the vector containing the WT CDCA3 promoter could be promoted by SP1 overexpression in 293T cells.In addition, RNA-binding protein immunoprecipitation (RIP) assays were conducted to validate the interaction between SNHG12 and SP1. Stabilised SP1 bound to a specific region in the promoter of CDCA3 and increased CDCA3 expression. Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance. Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.SNHG12 bound to and stabilised SP1, which activated CDCA3 transcription.According to published articles, the transcription factors SP1 and HOXB3 could bind to the promoter sequence of CDCA323,25. Studies have reported that nucleus-located lncRNAs could regulate protein transcription by binding to transcription factors28,29. To assess the possibility of SNHG12 interacting with these transcription factors, the catRAPID algorithm was used. Interestingly, the interaction strength between SNHG12 and SP1 was relatively higher, and potential binding sequences were predicted (Supplementary Fig. 7a, b). Thus, we mainly focused on SP1.In addition, RNA-binding protein immunoprecipitation (RIP) assays were conducted to validate the interaction between SNHG12 and SP1. Moreover, when SNHG12 was overexpressed, SP1 tended to be more stable (Fig. -(Fig.6i).6i).	32641718	RID04715	interact with protein	prognosis,chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	SNHG12	CDCA3	positively-E	overexpression;RNA pull-down assay;IHC;qRT-PCR;western blot	upregulation	qRT-PCR	TCGA;GSE64052;GSE53757	NA	cell proliferation(+);cell invasion(+);cell migration(+);cancer progression(+);chemoresistance(+)	transcriptional regulation	regulation	RNA-protein	Sunitinib	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000111665	NA	85028	83461	ASLNC04080|C1orf79|LINC00100|PNAS-123	GRCC8|TOME-1	Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinomaIn this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis. SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro. Mechanically, SNHG12 bound to SP1 and prevented the ubiquitylation-dependent proteolysis of SP1.Luciferase activity analysis showed that the luciferase activity of the vector containing the WT CDCA3 promoter could be promoted by SP1 overexpression in 293T cells.In addition, RNA-binding protein immunoprecipitation (RIP) assays were conducted to validate the interaction between SNHG12 and SP1. Stabilised SP1 bound to a specific region in the promoter of CDCA3 and increased CDCA3 expression. Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance. Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.Next, immunohistochemistry (IHC), qRT-PCRand western blot were performed to further verify that CDCA3 was highly expressed in RCC tissues at both the mRNA and protein levels (Fig. 4f, g). Furthermore, after knocking down or overexpressing CDCA3 (Supplementary Fig. 4a), we studied the biological functions of CDCA3 in RCC cells. According to the results of CCK8 assays, transwell assays and cell cycle analysis, we found that CDCA3 had the capacity to enhance the proliferation, invasion and migration of RCC cells. Overall, we found that SNHG12 promoted tumour progression via CDCA3 in RCC cells.we concluded that SNHG12 increased sunitinib resistance in RCC cells through CDCA3.	32641718	RID04716	transcriptional regulation	prognosis,chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Esophageal cancer	HOTAIR	MTHFR	negatively-E	dual-luciferase reporter assay;overexpression;ChIP	upregulation	RT-qPCR	GSE100942	NA	chemosensitivity(-)	DNA methylation	binding/interaction	RNA-protein	5-fluorouracil	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000177000	NA	100124700	4524	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR-mediated MTHFR methylation inhibits 5-fluorouracil sensitivity in esophageal cancer cellsIn the present study, we focus on exploring the role of long non-coding RNA (lncRNA) HOTAIR in EC progression and sensitivity of  Esophageal cancer (EC) cells to 5-FU.Paired cancerous and pre-cancerous tissues surgically resected from EC patients were collected in this study. Promoter methylation of the MTHFR was assessed by methylation-specific PCR. RIP and ChIP assays were adopted to examine the interaction of DNA methyltransferases (DNMTs) with lncRNA HOTAIR and MTHFR,respectively. EC cells resistant to 5-FU were induced by step-wise continuous increasing concentrations of 5-FU. The sensitivity of EC cells to 5-FU in vivo was evaluated in nude mice treated with xenografts of EC cells followed by injection with 5-FU (i.p.).We found reciprocal expression patterns of lncRNA HOTAIR and MTHFR in EC tissues and human EC cells.Interference with lncRNA HOTAIR enhanced 5-FU-induced apoptosis, exhibited anti-proliferative activity, and reduced promoter methylation of the MTHFR in EC cells. Besides, overexpression of MTHFR attenuated the acquired chemoresistance induced by overexpression of lncRNA HOTAIR in EC cells. At last, enhanced chemosensitivity was observed in vivo once nude mice xenografted with lncRNA HOTAIR-depleted EC cells.Together, our study proposes that pharmacologic targeting of lncRNA HOTAIR sensitizes EC cells to 5-FU-based chemotherapy by attenuating the promoter hypermethylation of the MTHFR in EC.Dual luciferase reporter gene assay displayed that the luciferase activity of MTHFR-WT was reduced in the presence of HOTAIR as compared to that of MTHFR-MUT (p-<-0.05) (Fig. 4e), suggesting that HOTAIR can bind to the promoter region of the MTHFR gene, which was consistent with bioinformatic prediction.In addition, CHIP was performed to determine enrichment of methyltransferases within the MTHFR promoter region, which showed that the methyltransferases were remarkably enriched in the MTHFR promoter region in TE-1/5-FU cells overexpressing HOTAIR (Fig. 4g).	32653028	RID04717	epigenetic regulation	chemoresistance		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Colon cancer	CASC2	miR-214	negatively-F	IHC;overexpressioon;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(-);cell autophagy(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long non-coding RNA CASC2 induces apoptosis and autophagy in human colon cancer cells via modulation of TRIM16 expressionThe gene expression analysis showed that LncRNA CASC2 is significantly suppressed in colon cancer tissues and cell lines. The immunohistochemistry also showed considerable increase of the Ki67 in colon cancer tissues suggestive of their aggressiveness. Overexpression of CASC2 inhibited the growth of HT-29 cells. The inhibition of HT-29 growth was due to the induction of apoptosis which was accompanied by upsurge of Bax, depletion of Bcl-2 and activation of caspase-3 cleavage. Electron microscopic analysis showed CASC2 overexpression also induced autophagy in the HT-29 cells which was associated with increase in LC3B II and Beclin 1 expression. Bioinformatic approaches and dual luciferase assay showed that CASC2 controls the TRIM16 via microRNA-214 axis. TRIM16 was found to be overexpressed in all the colon cancer tissues and cell lines. Overexpression of CASC2 caused significant inhibition of TRIM16. Additionally, silencing of TRIM16 resulted in the inhibition of HT-29 cell growth similar to that of CASC2 overexpression. Taken together, CASC2 may prove to be an important therapeutic target for colon cancer treatment.	32655801	RID04718	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Colon cancer	CASC2	TRIM16	negatively-E	IHC;overexpressioon;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(-);cell autophagy(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000221926	NA	255082	10626	C10orf5	EBBP	Long non-coding RNA CASC2 induces apoptosis and autophagy in human colon cancer cells via modulation of TRIM16 expressionThe gene expression analysis showed that LncRNA CASC2 is significantly suppressed in colon cancer tissues and cell lines. The immunohistochemistry also showed considerable increase of the Ki67 in colon cancer tissues suggestive of their aggressiveness. Overexpression of CASC2 inhibited the growth of HT-29 cells. The inhibition of HT-29 growth was due to the induction of apoptosis which was accompanied by upsurge of Bax, depletion of Bcl-2 and activation of caspase-3 cleavage. Electron microscopic analysis showed CASC2 overexpression also induced autophagy in the HT-29 cells which was associated with increase in LC3B II and Beclin 1 expression. Bioinformatic approaches and dual luciferase assay showed that CASC2 controls the TRIM16 via microRNA-214 axis. TRIM16 was found to be overexpressed in all the colon cancer tissues and cell lines. Overexpression of CASC2 caused significant inhibition of TRIM16. Additionally, silencing of TRIM16 resulted in the inhibition of HT-29 cell growth similar to that of CASC2 overexpression. Taken together, CASC2 may prove to be an important therapeutic target for colon cancer treatment.Additionally, it was found that silencing of TRIM16 could also inhibit the viability of the HT-29 cells similar to that of CASC2 silencing (Figure 6H).	32655801	RID04719	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065)
Colorectal cancer	TINCR	miR-31	negatively-F	luciferase reporter assay;miRcode;starBase	downregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000199177	NA	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	Decreased lncRNA, TINCR, promotes growth of colorectal carcinoma through upregulating microRNA-31Here, by a set of bioinformatics studies, we found that microRNA-31 (miR-31), the oncogenic miRNA that robustly upregulates in CRC, was a sponge miRNA for TINCR. TINCR and miR-31 levels were inversely correlated in both CRC tissues and CRC cell lines. Luciferase reporter assay revealed a specific binding site on TINCR for miR-31. Suppression of TINCR promoted CRC cell growth and migration in vitro, while overexpression of TINCR inhibited CRC cell growth and migration in vitro. TINCR depletion increased tumor xenograft growth in vivo, while TINCR overexpression inhibited it. Together, our study suggests that re-expressing TINCR may suppress invasive outgrowth of CRC through miR-31.	32681722	RID04720	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Breast cancer	SATB2-AS1	BRMS1L	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RNA22;StarBase;TargetScan;microRNA.org	downregulation	RT-qPCR	NA	NA	cell growth(-);cell metastasis(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-155-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000225953	GRCh38_2:199457697-199476935	ENSG00000100916	NA	150538	84312	NA	BRMS1|FLJ39177|MGC11296	Long non-coding RNA SATB2-AS1 inhibits microRNA-155-3p to-suppress breast cancer cell  growth by-promoting breast cancer metastasis  suppressor 1-likeLevels of SATB2-AS1, miR-155-3p and breast cancer metastasis suppressor 1-like (BRMS1L) in BC were determined. The prognostic role of SATB2-AS1 in BC patients was assessed. The screened cells were respectively  introduced with altered SATB2-AS1 or miR-155-3p to figure out their roles in malignant phenotypes of BC cells. The effect of varied SATB2-AS1 and miR-155-3p on BC cells in vivo was observed. Dual luciferase reporter gene assay and RNA-pull down assay were implemented to detect the targeting relationship of SATB2-AS1, miR-155-3p, and BRMS1L.SATB2-AS1 and BRMS1L were decreased while miR-155-3p was increased in BC cells and tissues. Patients with lower SATB2-AS1 expression had poor prognosis. Elevated SATB2-AS1 and inhibited miR-155-3p were able to restrain malignant behaviors of BC cells in vitro, as well as decelerate tumor growth in vivo. Oppositely, inhibited SATB2-AS1 and amplified miR-155-3p had converse effects on BC cell growth. MiR-155-3p mimic abrogated the impact of overexpressed SATB2-AS1. SATB2-AS1 could sponge miR-155-3p, and BRMS1L was the target gene of miR-155-3p.Elevated SATB2-AS1 and inhibited miR-155-3p could suppress the malignant phenotypes of BC cells, thereby restricting the development of BC.Dual luciferase reporter gene assay and RNA-pull down assay were implemented to detect the targeting relationship of SATB2-AS1, miR-155-3p, and BRMS1L.RNA22 and starBase online websites were employed to search for miRNAs possessing a chance to interact with SATB2-AS1. Among candidate miRNAs, miR-155-3p (Fig. 5a) was selected by virtue of its oncogenic effect in multiple cancers .Prediction tools, including TargetScan and microRNA.org were used to identify potential target genes of miR-155-3p. Among candidate genes, BRMS1L was selected due to its antitumor effect in human cancers	32694943	RID04721	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD);DOWN(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE60407,GSE111842,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	YY1	CASC9	positively-E	ChIP;RNA pull-down assay	upregulation	RT-PCR	TCGA	NA	tumor growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000249395	GRCh38_8:75120409-75352327	7528	101805492	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	ESCCAL-1|linc-JPH1|LINC00981	Multi-faceted epigenetic dysregulation of gene expression promotes esophageal squamous cell carcinomaPreviously, we showed that the lncRNA ESCCAL-1 was overexpressed in ESCC21, and overexpression of ESCCAL-1 has been reported in other cancer types.We found ESCCAL-1 is one of the most notable candidates for increased gene expression in C2 in association with decreased methylation.Furthermore, increased expression of ESCCAL-1 was a biomarker of worse overall survival time and progressionfree survival in ESCC patients.Knockdown of ESCCAL-1 reduced growth of patient-derived ESCC cells in vitro and in vivo, suggesting a cancer-promoting function. To identify a possible mechanism of ESCCAL-1 upregulation,we examined sequence motifs of known TFs in the ESCCAL-1 hypomethylated promoter region in silico and found a predicted binding site for YY1. YY1 is an TF belonging to the GLI-Kruppel class of zinc-finger proteins and contributes to tumorigenesis. Using ChIP-PCR, we validated YY1 binding at the hypomethylated promoter region of ESCCAL-1. RNA-seq profiling in cells with YY1 knockdown also revealed ESCCAL-1 as a YY1-regulated target-gene. RT-PCRassays also showed decreased expression of ESCCAL-1 in cells with YY1 deficiency, indicating YY1 transcriptionally regulates ESCCAL-1 in ESCC.Therefore, epigenetic dysregulation promotes ESCC through divergent and multi-factorial mechanisms.	32699215	RID04722	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)
Gastric cancer	PBX3	SNHG10	positively-E	JASPAR;ChIP;dual-luciferase reporter assay;RIP;RNA pull-down assay;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000167081	NA	ENSG00000247092	GRCh38_14:95521943-95534889	5090	283596	NA	C14orf62|FLJ40557|LINC00063|NCRNA00063	SNHG10/DDX54/PBX3 Feedback Loop Contributes to Gastric Cancer Cell GrowthOur study was conducted to investigate the function and molecular mechanism of SNHG10 in gastric cancer(GC).SNHG10 expression was detected by qRT-PCR The effect of SNHG10 on GC cell growth was assessed by colony formation, EdU, JC-1, flow cytometry, and wound-healing assays. The interaction between SNHG10 and PBX3 was confirmed through ChIP and luciferase reporter assay. RIP and RNA pull-down assays was used to define the binding of DEAD-box helicase 54 (DDX54) to SNHG10 or PBX homeobox 3 (PBX3).Results SNHG10 was expressed at a high level in GC cells. SNHG10 knockdown resulted in the inhibition on GC cell proliferation, migration but induced cell apoptosis. PBX3 could interact with SNHG10 promoter and thereby activate the expression of SNHG10. Subsequently, it was confirmed that SNHG10 positively modulated the expression of PBX3. Based on this, we found that DDX54 could bind to SNHG10 and PBX3, suggesting that SNHG10 maintained PBX3 mRNA stability through recruiting DDX54. Restoration assays indicated that PBX3 overexpression recovered SNHG10 silencing-induced inhibition on GC cell growth.SNHG10 facilitates cell growth by affecting DDX54-mediated PBX3 mRNA stability in GC.Then, we used JASPAR software to predict the binding motif of PBX3, and we found two sites (P1, P2) between PBX3 and SNHG10 promoter (Fig. 2f). The results of ChIP assays manifested that PBX3 combined with P2 site in the pro_x0002_moter regions of SNHG10 (Fig. 2g). Additionally, luciferase reporter assay elucidated that the luciferase activity of wild type SNHG10 promoter was weakened in PBX3-downregu_x0002_lated cells while increased upon PBX3 overexpression.	32712782	RID04723	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE111842,GSE55807)	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)
Gastric cancer	SNHG10	DDX54	positively-F	ChIP;dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);cell growth(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000247092	GRCh38_14:95521943-95534889	ENSG00000123064	NA	283596	79039	C14orf62|FLJ40557|LINC00063|NCRNA00063	5-Apr|DP97|MGC2835	SNHG10/DDX54/PBX3 Feedback Loop Contributes to Gastric Cancer Cell GrowthOur study was conducted to investigate the function and molecular mechanism of SNHG10 in gastric cancer(GC).SNHG10 expression was detected by qRT-PCR The effect of SNHG10 on GC cell growth was assessed by colony formation, EdU, JC-1, flow cytometry, and wound-healing assays. The interaction between SNHG10 and PBX3 was confirmed through ChIP and luciferase reporter assay. RIP and RNA pull-down assays was used to define the binding of DEAD-box helicase 54 (DDX54) to SNHG10 or PBX homeobox 3 (PBX3).Results SNHG10 was expressed at a high level in GC cells. SNHG10 knockdown resulted in the inhibition on GC cell proliferation, migration but induced cell apoptosis. PBX3 could interact with SNHG10 promoter and thereby activate the expression of SNHG10. Subsequently, it was confirmed that SNHG10 positively modulated the expression of PBX3. Based on this, we found that DDX54 could bind to SNHG10 and PBX3, suggesting that SNHG10 maintained PBX3 mRNA stability through recruiting DDX54. Restoration assays indicated that PBX3 overexpression recovered SNHG10 silencing-induced inhibition on GC cell growth.SNHG10 facilitates cell growth by affecting DDX54-mediated PBX3 mRNA stability in GC.	32712782	RID04724	transcriptional regulation	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Osteonecrosis	DANCR	FOXO1	negatively-F		downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell differentiation(-)	NA	regulation	NA	Bisphosphonates	CSC	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000150907	NA	57291	2308	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	FKH1|FKHR|FOXO1A	Altered Long Noncoding RNA Expression Profile in Multiple Myeloma Patients with Bisphosphonate-Induced Osteonecrosis of the JawBisphosphonates (BPs) are inhibitors of osteoclast-mediated bone resorption used for the treatment of multiple myeloma (MM) patients with osteolytic lesions. Bisphosphonate-induced osteonecrosis of the jaw (BONJ) is an infrequent drug-caused adverse event of these agents.Our study was aimed at evaluating 17 lncRNAs, whose  targets were previously validated as key elements in MM, bone metabolism, and angiogenesis in MM subjects without BONJ (MM group), in MM subjects with BONJ (BONJ group), and a group of healthy controls (CTRL group). . Our results demonstrated a different lncRNA profile in BONJ patients compared to MM patients and controls. Two lncRNAs (DANCR and MALAT1) were both downregulated compared to controls and MM, twelve (HOTAIR, MEG3, TP73-AS1, HOTTIP, HIF1AAS2, MANTIS, CTD-2201E18, CTD1-2003C8, R-471B22, RP1-43E13, RP11-553L6.5, and RP1-286D6) were overexpressed in MM with BONJ, and one (H19) was upregulated compared with only MM. Two lncRNAs (JHDMD1 and MTMR9LP) had higher expression, but these differences were not statistically significant. The examined lncRNAs target several genes and metabolic pathways. An altered lncRNA signature could contribute to the onset of BONJ or have a protective action. Targeting these lncRNAs could offer a possibility for the prevention or therapy of BONJ. Regarding the influence of DANCR (Differentiation Antagonizing Nonprotein Coding RNA) on bone metabolism, it decreases osteogenic differentiation blocking the p38MAPK pathway and inhibiting the Wnt/beta-catenin pathway. Moreover, this lncRNA decreases the expression of the transcription factor FOXO1, which in turn increases osteoblast differentiation and reduces osteoblast proliferation. A study aimed at evaluating DANCR expression in human periodontal ligament stem cells demonstrated that downregulation of DANCR was crucial for osteogenesis. Our results show reduced expression of DANCR in MM patients with BONJ. Lower lncRNA levels in MM patients with BONJ could correlate with the inhibition in osteoblast differentiation, which in turn affects the jaws during the development of lesions.	32714991	RID04725	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Osteonecrosis	MALAT1	miR-124	negatively-F		downregulation	RT-qPCR	NA	NA	cell differentiation(+)	NA	regulation	RNA-RNA	Bisphosphonates	NA	NA	Musculoskeletal system disease	Ischemic bone disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Altered Long Noncoding RNA Expression Profile in Multiple Myeloma Patients with Bisphosphonate-Induced Osteonecrosis of the JawBisphosphonates (BPs) are inhibitors of osteoclast-mediated bone resorption used for the treatment of multiple myeloma (MM) patients with osteolytic lesions. Bisphosphonate-induced osteonecrosis of the jaw (BONJ) is an infrequent drug-caused adverse event of these agents.Our study was aimed at evaluating 17 lncRNAs, whose  targets were previously validated as key elements in MM, bone metabolism, and angiogenesis in MM subjects without BONJ (MM group), in MM subjects with BONJ (BONJ group), and a group of healthy controls (CTRL group). . Our results demonstrated a different lncRNA profile in BONJ patients compared to MM patients and controls. Two lncRNAs (DANCR and MALAT1) were both downregulated compared to controls and MM, twelve (HOTAIR, MEG3, TP73-AS1, HOTTIP, HIF1AAS2, MANTIS, CTD-2201E18, CTD1-2003C8, R-471B22, RP1-43E13, RP11-553L6.5, and RP1-286D6) were overexpressed in MM with BONJ, and one (H19) was upregulated compared with only MM. Two lncRNAs (JHDMD1 and MTMR9LP) had higher expression, but these differences were not statistically significant. The examined lncRNAs target several genes and metabolic pathways. An altered lncRNA signature could contribute to the onset of BONJ or have a protective action. Targeting these lncRNAs could offer a possibility for the prevention or therapy of BONJ. The downregulation of MALAT1 (Metastasis-Associated Lung Adenocarcinoma Transcript 1) could have a similar meaning. It controls concentrations of integrins, such as ITGB1, which perform a relevant action in osteoclast genesis and cytoskeletal structure. MALAT1 regulates miR-124 which in turn negatively controls bone formations and osteogenic differentiation by working with Dlx transcription factors . Our data revealed significant downexpression ofMALAT1 compared to both the controls and MM patients, probably related to increased osteoclast genesis associated with bone lesions.	32714991	RID04726	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Osteonecrosis	HOTAIR	COL1A1	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	NA	NA	RNA-protein	Bisphosphonates	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000108821	NA	100124700	1277	HOXC-AS4|HOXC11-AS1|NCRNA00072	OI4	Altered Long Noncoding RNA Expression Profile in Multiple Myeloma Patients with Bisphosphonate-Induced Osteonecrosis of the JawBisphosphonates (BPs) are inhibitors of osteoclast-mediated bone resorption used for the treatment of multiple myeloma (MM) patients with osteolytic lesions. Bisphosphonate-induced osteonecrosis of the jaw (BONJ) is an infrequent drug-caused adverse event of these agents.Our study was aimed at evaluating 17 lncRNAs, whose  targets were previously validated as key elements in MM, bone metabolism, and angiogenesis in MM subjects without BONJ (MM group), in MM subjects with BONJ (BONJ group), and a group of healthy controls (CTRL group). . Our results demonstrated a different lncRNA profile in BONJ patients compared to MM patients and controls. Two lncRNAs (DANCR and MALAT1) were both downregulated compared to controls and MM, twelve (HOTAIR, MEG3, TP73-AS1, HOTTIP, HIF1AAS2, MANTIS, CTD-2201E18, CTD1-2003C8, R-471B22, RP1-43E13, RP11-553L6.5, and RP1-286D6) were overexpressed in MM with BONJ, and one (H19) was upregulated compared with only MM. Two lncRNAs (JHDMD1 and MTMR9LP) had higher expression, but these differences were not statistically significant. The examined lncRNAs target several genes and metabolic pathways. An altered lncRNA signature could contribute to the onset of BONJ or have a protective action. Targeting these lncRNAs could offer a possibility for the prevention or therapy of BONJ. HOTAIR (HOX Transcript Antisense RNA) can inhibit osteogenic differentiation. It was observed that the expression of HOTAIR was greater in patients with nontraumatic osteonecrosis of the femoral head (ONFH) compared with osteoarthritis samples. The concentration of osteogenic differentiation biomarkers, comprising COL1A1 and RUNX2 mRNA levels, was increased by si-HOTAIR. Moreover, HOTAIR is mechanoresponsive and therefore may have an action in mechanically controlled calcification. HOTAIR revealed higher expression in MM patients with BONJ compared to both controls and MM patients. These results were in line with the findings found in nontraumatic osteonecrosis of the femur, indicating that this lncRNA could negatively control osteogenic proliferation and differentiation .	32714991	RID04727	expression association	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Osteonecrosis	HOTAIR	RUNX2	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell differentiation(-)	interact with mRNA	binding/interaction	NA	Bisphosphonates	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124813	NA	100124700	860	HOXC-AS4|HOXC11-AS1|NCRNA00072	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	HOTAIR (HOX Transcript Antisense RNA) can inhibit osteogenic differentiation. It was observed that the expression of HOTAIR was greater in patients with nontraumatic osteonecrosis of the femoral head (ONFH) compared with osteoarthritis samples. The concentration of osteogenic differentiation biomarkers, comprising COL1A1 and RUNX2 mRNA levels, was increased by si-HOTAIR [50]. Moreover, HOTAIR is mechanoresponsive and therefore may have an action in mechanically controlled calcification.HOTAIR revealed higher expression in MM patients with BONJ compared to both controls and MM patients.These results were in line with the findings found in nontraumatic osteonecrosis of the femur, indicating that this lncRNAcould negatively control osteogenic proliferation and differentiation [50].	32714991	RID04728	interact with mRNA	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteonecrosis	HOTTIP	WDR5	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	interact with mRNA	binding/interaction	RNA-protein	Bisphosphonates	CSC	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196363	NA	100316868	11091	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	CFAP89|SWD3	Regarding the particular meaning that the overexpression of lncRNA HOTTIP (HOXA transcript at the distaltip) could assume, some findings suggest that systemic bisphosphonate treatment influences the activity of chondrocytes [57]. HOTTIP has been reported to interact with WDR5, forming a complex with TWIST1 [58]. In cranial bones, Twist1 induces a reduction of chondrogenesis via beta-catenin [59]. Moreover, this lncRNA is an enhancer thatcontrols the activity of 5'-HOXA genes to regulate the elongation of skeletal components via epigenetic mechanisms. Data obtained from the present study revealed that HOTTIP was significantly overexpressed in MM patients with BONJ compared to either the controls or MM, indicating a possible inhibiting effect on chondrogenesis and osteogenesis.Finally, it is worth noting that a change in the expression of some lncRNAs may have a protective action against the onset of BONJ.	32714991	RID04729	interact with mRNA	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Osteonecrosis	HOTTIP	TWIST1	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	interact with mRNA	binding/interaction	NA	Bisphosphonates	CSC	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Ischemic bone disease	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000122691	NA	100316868	7291	HOXA-AS6|HOXA13-AS1|NCRNA00213	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Regarding the particular meaning that the overexpression of lncRNA HOTTIP (HOXA transcript at the distaltip) could assume, some findings suggest that systemic bisphosphonate treatment influences the activity of chondrocytes [57]. HOTTIP has been reported to interact with WDR5, forming a complex with TWIST1 [58]. In cranial bones, Twist1 induces a reduction of chondrogenesis via beta-catenin [59]. Moreover, this lncRNA is an enhancer thatcontrols the activity of 5'-HOXA genes to regulate the elongation of skeletal components via epigenetic mechanisms. Data obtained from the present study revealed that HOTTIP was significantly overexpressed in MM patients with BONJ compared to either the controls or MM, indicating a possible inhibiting effect on chondrogenesis and osteogenesis.Finally, it is worth noting that a change in the expression of some lncRNAs may have a protective action against the onset of BONJ.	32714991	RID04730	interact with mRNA	NA		UP(SKCM);DATA(GSE38495)
Osteonecrosis	HIF1A-AS2	miR-153-3p	negatively-F	siRNA	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	sponge	binding/interaction	RNA-RNA	Bisphosphonates	NA	NA	Musculoskeletal system disease	Ischemic bone disease	lncRNA	miRNA	ENSG00000258667	GRCh38_14:61707564-61751099	NA	NA	100750247	NA	3'aHIF-1A|aHIF	NA	Finally, it is worth noting that a change in the expression of some lncRNAs may have a protective action against the onset of BONJ.	32714991	RID04731	ceRNA or sponge	NA		
Melanoma	DBH-AS1	miR-233-3p	positively-E	dual-luciferase reporter assay;western blot;starBase;RIP;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-223-3p)	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000225756	GRCh38_9:133654586-133657313	NA	NA	138948	NA	NCRNA00118	NA	LncRNA DBH-AS1 facilitates the tumorigenesis of melanoma by targeting miR-233-3p via IGF-1R/Akt signalingThe study will investigate the role of DBH-AS1 in melanoma cell. The expression profiles of DBH-AS1, miR-223-3p, and IGF-1R in melanoma tissues and cell lines were determined by RT-qPCR analysis. CCK-8 assay, colony assays and transwell assay were employed to analyze the effects of DBH-AS1 on the proliferation, migration, and invasion in GC cells. Bioinformatics analysis and dual-luciferase reporter assay determined the direct binding relation between DBH-AS1, miR-223-3p and IGF- 1 R in GC. Herein, we observed significant reductions in DBH-AS1 expression in melanoma tumor tissues and cell lines. Knockdown DBH-AS1 in melanoma cells impaired their proliferative, migratory, and invasive potential. We determined that DBH-AS1 was able to modulate insulin growth factor receptor (IGF-1R) expression as a competing endogenous RNA for DBH-AS1. In line with this finding, the knockdown DBH-AS1 was associated with decreases in the expression of glucose transporter (GLUT)-1 and a consequent inhibition of glucose uptake, lactate production, and ATP generation by melanoma cells.  These findings therefore suggest that DBH-AS1 can enhance glycolytic activity in melanoma cells, thereby disrupting melanoma progression via miR-223-3p/EGFR/AKT axis. As such this signaling axis may be a viable therapeutic target for melanoma treatment in human patients. We next sought to identify potential miR-223-3p target genes using TargetScan, identify_x0002_ing IGF1R as one such target candidate (Figure 4A). We, then, used a Luciferase reporter assay approach to determine whether miR-223-3p was able to bind to its predicted target sequence in the IGF-1R 3'-untranslated region (UTR). We found that miR-223-3p mimic transfection was able to inhibit the activity of a wild-type (WT) IGF-1R 3'-UTR Luciferase reporter, whereas it had no effect on a reporter in which its putative binding site had been mutated, consistent with the abili_x0002_ty of miR-223-3p to directly bind to this 3'-UTR region (Figure 4B and C). We further found that miR-223-3p overexpression was associated with marked decreases in IGF-1R mRNA and protein level expression as measured via qRT-PCRand western blot (Figure 4D and E). As such, these findings confirmed the ability of miR-223-3p to inhibit IGF-1R expression.	32744696	RID04732	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	
Colon cancer	LINC00858	WNK2	positively-E	immunoprecipitation;RNA pull-down assay;shRNA;western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(-);senescence(-);cell autophagy(-);tumor growth(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000165238	NA	170425	65268	CRCAL-2	KIAA1760|NY-CO-43|PRKWNK2|SDCCAG43	Long non-coding RNA LINC00858 inhibits colon cancer cell apoptosis,autophagy, and senescence by activating WNK2 promoter methylationAfter examining the expression of LINC00858 in colon cancer tissues and cell lines, we then identified the possible interaction between LINC00858 and WNK lysine deficient protein kinase 2 (WNK2) by fluorescence in situ hybridization, RNA immunoprecipitation, chromatin immunoprecipitation, and RNA pull-down assays. Next, the role of the LINC00858/WNK2 axis was explored by evaluating the apoptosis, autophagy,and senescence of colon cancer cells in vitro after ectopic expression and depletion experiments in HCT116 cells. Moreover, a mouse xenograft model of HCT116 cells was established to verify the function of the LINC00858/WNK2 axis in vivo. There was high expression of LINC00858 and low expression of WNK2 in colon cancer tissues and cell lines. Silencing of LINC00858 promoted apoptosis, senescence, and autophagy in colon cancer cells. Additionally, the enrichment of WNK2 was promoted when LINC00858 bound to DNA methyltransferases.Furthermore, in vivo assays demonstrated that silencing of LINC00858 resulted in inhibited tumor growth by upregulating WNK2. In summary, LINC00858 acts as a tumor-promoting lncRNA in colon cancer by downregulating WNK2. Our results may provide novel targets for the treatment for colon cancer.	32768499	RID04733	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Prostate cancer	UCA1	CDH1	positively-E	luciferase reporter assay;Co-immunoprecipitation;RIP;RNA pull-down assay;shRNA	downregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-296-3p);histone modification	association	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000039068	NA	652995	999	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CD324|UVO|uvomorulin	LncRNA UCA1 maintains the low-tumorigenic and nonmetastatic status by stabilizing E-cadherin in primary prostate cancer cellsIn this study, we revealed a novel biological function of UCA1, which was different from that reported by previous studies, was responsible for maintaining the low-tumorigenic, nonmetastatic phenotypes in primary prostate epithelial cells. UCA1 could stabilize E-cadherin protein by preventing the interaction between E-cadherin and its E3 ligase MDM2, which suppressed MDM2-mediated ubiquitination and degradation of E-cadherin. In addition, we also found that UCA1 acted as a sponge of miR-296-3p, which targeted E-cadherin gene CDH1 messenger RNA at the posttranscription level. Taken together, these findings demonstrated that UCA1 had a new important role in effectively keeping E-cadherin at a high level through a dual mechanism, which maintained primary prostate cancer cells at the low-tumorigenic and nonmetastatic status.	32805084	RID04734	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Malignant glioma	SNHG1	FTMT	positively-E	shRNA;overexpression;luciferase reporter assay;RIP;starBase;Targetscan;immunohistochemistry	upregulation	qRT-PCR	NA	NA	cell proliferation(+);angiogenesis(+);apoptosis process(-);tumorigenesis(+)	ceRNA(miR-9-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000181867	NA	23642	94033	LINC00057|lncRNA16|NCRNA00057|UHG	MtF	FtMt promotes glioma tumorigenesis and angiogenesis via lncRNA SNHG1/miR-9-5p axisFtMt expression was detected in glioma tissues and cells as well as in nude mouse tissues. Cell proliferation and apoptosis rate were observed following transfection of LV-FtMt or sh-FtMt in glioma cell line.Moreover, glioma cells with FtMt over-expression/knockdown were co-cultured with human umbilical veinendothelial cells (HUVECs) to observe its function on HUVEC proliferation, angiogenic ability and the vascular endothelial growth factor (VEGF) content. Gain and loss of function of small nucleolar RNA host gene 1 (SNHG1) and miR-9-5p were performed in glioma cells and GBM nude mice to observe its effect on glioma cell proliferation and HUVEC angiogenic ability. Luciferase reporter gene and RIP assay were employed to inspect the interactions among SNHG1, FtMt and miR-9-5p. Additionally, a xenograft mouse model was applied to determine the role of FtMt in glioma.In this work, FtMt was strongly expressed in glioma tissues and cells as well as in nude mouse tumor tissues. The employment of the loss-of and gain-of functions assays illustrated that FtMt enhanced glioma tumorigenesis and angiogenesis. Mechanistically, our findings showed that FtMt positively related to SNHG1 while negatively correlated with miR-9-5p, and both SNHG1 and FtMt can competitively bind with miR-9-5p. Besides,the inhibition effects of sh-FtMt on glioma were surveyed in vivo experiments.Evidence in this study suggested that FtMt promotes glioma tumorigenesis and angiogenesis via SNHG1 mediated miR-9-5p expression, which may provide a theoretical basis for glioma treatment.	32858123	RID04735	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Lung disease	lncRNA-5657	SPNS2	positively-E	shRNA;dual-luciferase reporter assay;overexpression;siRNA	upregulation	sequencing;qRT-PCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lower respiratory tract disease	lncRNA	PCG	NA	NA	ENSG00000183018	NA	NA	124976	NA	SLC63A2	LncRNA-5657 silencing alleviates sepsis-induced lung injury by suppressing the expression of spinster homology protein 2High-throughput sequencing was used to detect the changes in lncRNA expression profile in alveolar macrophages after LPS stimulation. The BALF of patients with sepsis-induced lung injury was collected. Rats with CLP-induced septic lung injury were treated with sh-lncRNA-5657 via intravenous injection. NR8383 cells were transfected with lentiviral vectors expressing lncRNA-5657, lncRNA-5657 smart silencer, or si-spns2. The BALF cells expression levels of lncRNA-5657 and proinflammatory cytokines in BALF of patients and rats as well as in rat macrophages were measured. Changes in histopathologic score, lung wet/dry weight ratio, and spns2 expression in macrophages were examined. The relationship between lncRNA-5657 and its potential target gene spns2 was validated using a dual-luciferase reporter assay.The lncRNA expression profile of LPS-stimulated macrophages demonstrated that lncRNA-5657 showed the greatest fold-change. The BALF cells of patients with sepsis-induced ARDS and the lung tissue of rats with CLP-induced sepsis had significantly increased lncRNA-5657 levels. LncRNA-5657 silencing alleviated CLP-induced lung inflammation in rats. In NR8383 cells, lncRNA-5657 overexpression enhanced, whereas lncRNA-5657 silencing attenuated the expression of proinflammatory cytokines and spns2. A dual-luciferase reporter assay showed that lncRNA-5657 interacted with the promoter of the spns2 gene. Spns2 silencing alleviated LPS-induced inflammatory response and blocked the proinflammatory function of lncRNA-5657 in alveolar macrophages.LncRNA-5657 is closely associated with sepsis-induce lung injury. In vitro and in vivo data demonstrated that LncRNA-5657 silencing alleviates sepsis-induced lung injury by inhibiting lung inflammatory response via suppressing spns2 expression.	32866783	RID04736	transcriptional regulation	NA		DOWN(BRCA);DATA(GSE86978)
Cervical cancer	SNHG6	STYX	positively-E	RNA pull-down assay;luciferase reporter assay;RIP;shRNA;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);radioresistance(+);cell growth(+)	ceRNA(miR-485-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000198252	NA	641638	6815	HBII-276HG|NCRNA00058|U87HG	NA	LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3pqRT-PCRanalysis was implemented to evaluate the expression levels of SNHG6, miR-485-3p and STYX in CC cells. RNA pull-down assay and luciferase reporter assay were conducted to verify the interaction between miR-485-3p and SNHG6 or STYX. Functional assays, such as colony formation assay, JC-1 assay and TUNEL assay were applied to detect the biological behaviors of CC cells. The resistance of CC cells to radiation was evaluated by colony formation assay.SNHG6 was expressed at a high level in CC cells. Silenced SNHG6 suppressed cell proliferation but promoted cell apoptosis. Additionally, silenced SNHG6 could sensitize CC cells to radiation treatment. miR-485-3p could bind to both SNHG6 and STYX. Knockdown of miR-485-3p or overexpression of STYX could abolish the effects of SNHG6 silencing on CC cell growth.LncRNA SNHG6 enhances the radioresistance of CC cells and promotes CC cell growth by sponging miR-485-3p to release STYX.	32884447	RID04737	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	SNHG7	ELK1	positively-E	shRNA;immunohistochemistry;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	sponge	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000126767	NA	84973	2002	MGC16037|NCRNA00061	NA	ELK1/lncRNA-SNHG7/miR-2682-5p feedback loop enhances bladder cancer cell growthThe expression of SNHG7 in BCa cells was uncovered by qRT-PCR The biological functions of SNHG7 in BCa cells were explored by CCK-8 assay, colony formation assay, flow cytometry analysis, wound healing assay and transwell assay. Luciferase reporter assay and RIP assay were applied to analyze the interaction of ELK1 with SNHG7 or miR-2682-5p.SNHG7 was conspicuously highly expressed in BCa tissues and cells. The upregulated expression of SNHG7 was related with poor prognosis in BCa patients. Moreover, SNHG7 exerted oncogenic functions in BCa through enhancing cell growth, migration and invasion. ELK1 increased the level of SNHG7 by binding with the promoter region of SNHG7. SNHG7 strengthened the expression of ELK1 via acting as a sponge of miR-2682-5p.Both ELK1 and miR-2682-5p involved in the SNHG7-mediated BCa progression.	32898531	RID04738	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	ELK1	SNHG7	positively-E	ChIP;shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	TF	lncRNA	ENSG00000126767	NA	ENSG00000233016	GRCh38_9:136721366-136728184	2002	84973	NA	MGC16037|NCRNA00061	ELK1/lncRNA-SNHG7/miR-2682-5p feedback loop enhances bladder cancer cell growthThe expression of SNHG7 in BCa cells was uncovered by qRT-PCR The biological functions of SNHG7 in BCa cells were explored by CCK-8 assay, colony formation assay, flow cytometry analysis, wound healing assay and transwell assay. Luciferase reporter assay and RIP assay were applied to analyze the interaction of ELK1 with SNHG7 or miR-2682-5p.SNHG7 was conspicuously highly expressed in BCa tissues and cells. The upregulated expression of SNHG7 was related with poor prognosis in BCa patients. Moreover, SNHG7 exerted oncogenic functions in BCa through enhancing cell growth, migration and invasion. ELK1 increased the level of SNHG7 by binding with the promoter region of SNHG7. SNHG7 strengthened the expression of ELK1 via acting as a sponge of miR-2682-5p.Both ELK1 and miR-2682-5p involved in the SNHG7-mediated BCa progression.	32898531	RID04739	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)
Gastric cancer	HOTAIR	MIR217	positively-E	overexpression;dual-luciferase reporter assay;shRNA;siRNA	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);colony formation(+);cell invasion(+)	ceRNA(miR-217)	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000207548	NA	100124700	406999	HOXC-AS4|HOXC11-AS1|NCRNA00072	hsa-mir-217|miR-217|MIRN217	Long Noncoding RNA HOTAIR Promotes Epithelial-Mesenchymal Transition and Is a Suitable Target to Inhibit Peritoneal Dissemination in Human Scirrhous Gastric CancersWe previously established an original cell line, HSC-60, from a scirrhous gastric cancer patient and isolated a peritoneal-metastatic cell line, 60As6,in nude mice following orthotopic inoculations. In the present study, we focused on the expression of long noncoding ribonucleic acid (RNA) (lncRNA) in the cell lines and investigated the mechanism on peritoneal dissemination.We demonstrated that an lncRNA, HOX transcript antisense RNA (HOTAIR), is expressed significantly more highly in 60As6 than HSC-60 cells. Then, using both HOTAIR knockdown and overexpression experiments, we showed that high-level expression of HOTAIR promotes epithelial-mesenchymal transition (EMT) in 60As6 cells. By luciferase assay,we found that HOTAIR directly targets and binds to miR-217,and that miR-217 directly binds to Zinc finger E-box-binding homeobox 1 (ZEB1). The knockdown of HOTAIR in 60As6 cells significantly reduced the invasion activity and peritoneal dissemination- and significantly prolonged the survival in the orthotopic tumor mouse model.An EMT-associated pathway (the HOTAIR-miR-217-ZEB1 axis) appears to inhibit peritoneal dissemination and could lead to a novel therapeutic strategy against scirrhous gastric cancer in humans.	32937635	RID04740	ceRNA or sponge	metastasis		
Papillary thyroid carcinoma	AGAP2-AS1	MMP2	positively-E	siRNA;western blot;Targetscan;MirDB;knockdown;overexpression;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-424-5p)	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000087245	NA	100130776	4313	LOC100130776|PUNISHER	CLG4|CLG4A|TBE-1	Long non-coding RNA AGAP2-AS1 increases the invasiveness of papillary thyroid cancerUsing qRT-PCR we analyzed AGAP2-AS1 expression in 110 paired PTC tissues and adjacent non-cancerous tissues. We found that AGAP2-AS1 expression was significantly higher in human PTC tissues than adjacent noncancerous tissues (n=110; p<0.01) and correlated with lymph node metastasis (p=0.01) and tumor-node-metastasis stage (p=0.006). AGAP2-AS1 downregulation decreased migration and invasion by PTC cells, and reduced expression of matrix metalloproteinase-2 (MMP2). AGAP2-AS1 upregulated MMP2 expression by competitively binding to microRNA-425-5p. In addition, miR-424-5p expression was decreased in PTC tissues and correlates negatively with the AGAP2-AS1 levels. These results demonstrate that AGAP2-AS1 expression is significantly elevated in PTC tissues and that, by binding to miRNA-425-5p, it upregulates the MMP2 expression, thereby increasing the invasiveness and migration capacity of PTC cells.	32960785	RID04741	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	NSUN2	H19	positively-E	CRISPR-Cas9;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);tumorigenesis(+);cancer progression(+)	RNA methylation	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000037474	NA	ENSG00000130600	GRCh38_11:1995171-2001470	54888	283120	FLJ20303|Misu|MRT5|TRM4	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Aberrant NSUN2-mediated m5C modification of H19 lncRNA is associated with poor differentiation of hepatocellular carcinomaNSUN2 is an RNA methyltransferase responsible for the m5C modification of multiple RNAs. In this study, we knocked down the NSUN2 gene in HepG2 cells by CRISPR/Cas9 technology and performed high-throughput RNA-BisSeq. An important tumor-related lncRNA H19 was identified to be targeted by NSUN2. Studies have shown that the expression of H19 lncRNA is abnormally elevated and has a carcinogenic effect in many types of tumors. Our results demonstrated that m5C modification of H19 lncRNA can increase its stability. Interestingly, m5C-modified H19 lncRNA can be specifically bound by G3BP1, a well-known oncoprotein which further leads to MYC accumulation. This may be a novel mechanism by which lncRNA H19 exerts its oncogenic effect. Besides, both the m5C methylation level and the expression level of H19 lncRNA in hepatocellular carcinoma tissues were significantly higher than those in adjacent non-cancer tissues, which were closely associated with poor differentiation of hepatocellular carcinoma (HCC). In conclusion, we found that H19 RNA is a specific target for the NSUN2 modifier. The m5C-modified H19 lncRNA may promote the occurrence and development of tumors by recruiting the G3BP1 oncoprotein. Our findings may provide a potential target and biomarker for the diagnosis and treatment of HCC.	32978516	RID04742	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	UP(NSCLC);DATA(GSE74639)
Hepatocellular carcinoma	G3BP1	H19	positively-F	RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);tumorigenesis(+);cancer progression(+)	RNA methylation	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000145907	NA	ENSG00000130600	GRCh38_11:1995171-2001470	10146	283120	G3BP|HDH-VIII	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Aberrant NSUN2-mediated m5C modification of H19 lncRNA is associated with poor differentiation of hepatocellular carcinomaNSUN2 is an RNA methyltransferase responsible for the m5C modification of multiple RNAs. In this study, we knocked down the NSUN3 gein HepG2 cells by CRISPR/Cas9 technology and performed high-throughput RNA-BisSeq. An important tumor-related lncRNA H19 was identified to be targeted by NSUN2. Studies have shown that the expression of H19 lncRNA is abnormally elevated and has a carcinogenic effect in many types of tumors. Our results demonstrated that m5C modification of H19 lncRNA can increase its stability. Interestingly, m5C-modified H19 lncRNA can be specifically bound by G3BP1, a well-known oncoprotein which further leads to MYC accumulation. This may be a novel mechanism by which lncRNA H19 exerts its oncogenic effect. Besides, both the m5C methylation level and the expression level of H19 lncRNA in hepatocellular carcinoma tissues were significantly higher than those in adjacent non-cancer tissues, which were closely associated with poor differentiation of hepatocellular carcinoma (HCC). In conclusion, we found that H19 RNA is a specific target for the NSUN2 modifier. The m5C-modified H19 lncRNA may promote the occurrence and development of tumors by recruiting the G3BP1 oncoprotein. Our findings may provide a potential target and biomarker for the diagnosis and treatment of HCC.	32978516	RID04743	epigenetic regulation	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	UP(NSCLC);DATA(GSE74639)
Lung cancer	BLACAT1	TIMM8A	positively-E	siRNA	upregulation	qPCR	NA	NA	cell migration(+);apoptosis process(+);chemoresistance(+)	interact with mRNA	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000126953	NA	101669762	1678	linc-UBC1|LINC00912|onco-lncRNA-30	DDP|DFN1|MTS	Effect of lncRNA-BLACAT1 on drug resistance of non-small cell lung cancer cells in DDP chemotherapy by regulating cyclin D1 expressionThe aim of this study was to investigate the effect of long noncoding ribonucleic acid (lncRNA)-bladder cancer associated  transcript  1  (BLACAT1)  on  the  drug  resistance of non-small cell lung cancer (NSCLC) cells  in  cisplatin  (DDP)  chemotherapy  by  regulating the expression of Cyclin D1. The expression level of lncRNA-BLACAT1 in normal human lung bronchial epithelial cell line BEAS-2B, NSCLC cell line A549, and DDP-resistant cell line A549 (A549/DDP) was detected by quantitative Poly- merase Chain Reaction (qPCR). LncRNA-BLA- CAT1 small interfering RNA (siRNA) (si-BLA- CAT1) and lncRNA-BLACAT1 negative control (si- NC) were transfected into A549/DPP cells. Then, qPCR was carried out to detect the changes in the expression of lncRNA-BLACAT1 before and after transfection. Thereafter, cell cycle and cell growth rate were detected by flow cytometry and the cell growth curve. Besides, the changes in cell migration, cell apoptosis, and Cyclin D1 were detected via wound healing assay, flow cytome- try, and western blot (WB).In GEO database, lncRNA-BLA- CAT1 was significantly overexpressed in NS- CLC (p<0.05), and the prognosis of NSCLC in BLACAT1 low-expression group was bet- ter than that in the BLACAT1 high-expression group (p<0.0001). Compared with that in BE- AS-2B cells, BLACAT messenger RNA (mRNA) was notably highly expressed in A549 cells (p<0.05), and compared with that in A549 cells, BLACAT1 mRNA in A549/DPP was significant- ly highly expressed in A549/DDP cells (p<0.05). Additionally, in comparison with that in the si- NC group, the content of lncRNA-BLACAT1 in si-BLACAT1 group was remarkably decreased (p<0.01). Moreover, flow cytometry detection of cell cycle revealed that compared with those in si-NC group, G0/G1 phase was markedly pro- longed and S phase  was shortened in si-BLACAT1 group. MTS assay manifested that the absorbance at 450 nm in si-BLACAT1 group was evidently decreased on the 3rd day compared with that in the si-NC group (p<0.05), and the difference between the two groups was the most significant on the 5th day (p<0.001). According to wound healing assay, compared with those in si-NC group, the distance between cells became larger, the cell migration ability was remarkably weakened (p<0.05), and cell apoptosis was prominently reduced in si-BLACAT1 group (p<0.05). WB results showed that compared with si-NC group, si-BLACAT1 group had significantly reduced Cyclin D1 (p<0.05) .LncRNA-BLACAT1  regulates  the expression of Cyclin D1, reduces the malignant  phenotype  of  drug-resistant  cells,  and  increases  the  sensitivity  of  lung  cancer  cells  to  DDP.	33015788	RID04744	interact with mRNA	chemoresistance,prognosis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Malignant glioma	SUMO1P3	CTNNB1	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);WNT/beta-catenin signaling pathway(+)	interact with mRNA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000235082	GRCh38_1:160317403-160317706	ENSG00000168036	NA	474338	1499	NA	armadillo|beta-catenin|CTNNB	Long non-coding RNA SUMO1P3 promotes glioma progression via the Wnt/beta-catenin pathwayThe present study examined SUMO1P3 expression in glioma tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 (CCK-8) and transwell assays were used to examine the effects of SUMO1P3 on the proliferation and invasion of glioma cells, respectively. Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.The expression level of SUMO1P3 was higher in glioma tissues compared with corresponding adjacent normal tissues. In addition,a high expression level of SUMO1P3 was significantly associated with clinical progression and poor survival for patients with glioma. Furthermore, the knockdown of SUMO1P3 inhibited the proliferation, migration and invasion of U87 and U251 cells. In addition, the knockdown of SUMO1P3 inhibits glioma growth in vivo. Finally, the knockdown of SUMO1P3 inhibited the epithelial-mesenchymal transition and reduced the expression levels of active beta-catenin, C-myc,and cyclin D1 in U87 and U251 cells. By contrast,the overexpression of SUMO1P3 promoted glioma cell proliferation, migration, and invasion. SUMO1P3 promotes glioma cell proliferation, migration, and invasion, and may be involved in Wnt/beta-catenin signaling.	33015800	RID04745	interact with mRNA	NA	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	SUMO1P4	MYC	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);WNT/beta-catenin signaling pathway(+)	interact with mRNA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000235555	GRCh38_19:49275119-49275420	ENSG00000136997	NA	101290502	4609	NA	bHLHe39|c-Myc|MYCC	Long non-coding RNA SUMO1P3 promotes glioma progression via the Wnt/beta-catenin pathwayThe present study examined SUMO1P3 expression in glioma tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 (CCK-8) and transwell assays were used to examine the effects of SUMO1P3 on the proliferation and invasion of glioma cells, respectively. Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.The expression level of SUMO1P3 was higher in glioma tissues compared with corresponding adjacent normal tissues. In addition,a high expression level of SUMO1P3 was significantly associated with clinical progression and poor survival for patients with glioma. Furthermore, the knockdown of SUMO1P3 inhibited the proliferation, migration and invasion of U87 and U251 cells. In addition, the knockdown of SUMO1P3 inhibits glioma growth in vivo. Finally, the knockdown of SUMO1P3 inhibited the epithelial-mesenchymal transition and reduced the expression levels of active beta-catenin, C-myc,and cyclin D1 in U87 and U251 cells. By contrast,the overexpression of SUMO1P3 promoted glioma cell proliferation, migration, and invasion. SUMO1P3 promotes glioma cell proliferation, migration, and invasion, and may be involved in Wnt/beta-catenin signaling.	33015800	RID04746	interact with mRNA	NA	UP(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Malignant glioma	SUMO1P5	CCND1	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);WNT/beta-catenin signaling pathway(+)	interact with mRNA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000110092	NA	474341	595	NA	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA SUMO1P3 promotes glioma progression via the Wnt/beta-catenin pathwayThe present study examined SUMO1P3 expression in glioma tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 (CCK-8) and transwell assays were used to examine the effects of SUMO1P3 on the proliferation and invasion of glioma cells, respectively. Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.The expression level of SUMO1P3 was higher in glioma tissues compared with corresponding adjacent normal tissues. In addition,a high expression level of SUMO1P3 was significantly associated with clinical progression and poor survival for patients with glioma. Furthermore, the knockdown of SUMO1P3 inhibited the proliferation, migration and invasion of U87 and U251 cells. In addition, the knockdown of SUMO1P3 inhibits glioma growth in vivo. Finally, the knockdown of SUMO1P3 inhibited the epithelial-mesenchymal transition and reduced the expression levels of active beta-catenin, C-myc,and cyclin D1 in U87 and U251 cells. By contrast,the overexpression of SUMO1P3 promoted glioma cell proliferation, migration, and invasion. SUMO1P3 promotes glioma cell proliferation, migration, and invasion, and may be involved in Wnt/beta-catenin signaling.	33015800	RID04747	interact with mRNA	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Pulmonary tuberculosis	MEG3	miR-145-5p	negatively-F	dual-luciferase reporter assay;siRNA;Targetscan;shRNA	downregulation	qRT-PCR	NA	NA	colony formation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 control Mycobacterium Tuberculosis  infection via controlled MiR-145-5p expression and modulation of Macrophages proliferationThis study explore the role of MEG3 in the proliferation and apoptosis of Mtb-infected macrophages. Between September 2017 and September 2019, 84 consecutive pulmonary Mtd patients admitted to our hospital were selected as the observation group (OG), and concurrently, 88 healthy controls were selected as the control group (CG). MEG3 and miR-145-5p in peripheral blood of the two groups were detected, and their diagnostic value in pulmonary tuberculosis (PTB) was analyzed by receiver operating characteristic (ROC) curves. In addition, Bacillus Calmette-Guerin (BCG) and mouse Raw264.7 macrophage strains were purchased to establish the Mtb-infected macrophage model. Colony forming unit (CFU) and flow cytometry were employed to determine the effects of MEG3 and miR-145-5p on macrophages, and the correlation between the two was performed by dual-luciferase reporter (DLR) assay. MEG3 was highly expressed in PTB, while miR-145-5p was lowly expressed (P<0.050).ROC analysis demonstrated that both MEG3 and miR-145-5p enjoyed favorable predictive value for the occurrence of PTB (P<0.001). In the Mtb-infected macrophage model, MEG3 decreased (P<0.050) while miR-145-5p increased with the time of infection (P<0.050). Inhibited MEG3 and overexpressed miR-145-5p resulted in increased CFU and decreased apoptosis ability of macrophages (P<0.050). The DLR assay identified a targeting relationship between miR-145-5p and MEG3 (P<0.050). The increase of MEG3 could inhibit the expression of in miR-145-5p (P<0.050). MEG3 affects the biological activity of Mtb-infected macrophages by targeting miR-145-5p,which may be the key to the diagnosis and treatment of PTB and even all kinds of tuberculosis in the future.	33035634	RID04748	ceRNA or sponge	NA		
Sepsis	MEG3	BAX	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000087088	NA	55384	581	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BCL2L4	LncRNA MEG3 expression in sepsis and its effect on LPS-induced macrophage function60 sepsis patients admitted to our hospital from February 2017 to September 2018 were selected as the sepsis group, and 50 non-septic patients diagnosed and treated in our hospital during the same period were selected as the control group. qRT-PCRwas used to detect the expression level of MEG3. ROC curve was used to analyze the diagnostic value of serum MEG3 in sepsis. The human macrophage cell line U937 was cultured in vitro and randomly divided into NC group, LPS group, LPS + pcDNA group, and LPS + pcDNA-MEG3 group. Flow cytometry was applied to detect the apoptosis rate. The levels of IL-1beta and TNF-alpha were detected by ELISA. western blot was used to detect the expression of Bax, Bcl-2 and NF-kB signaling pathway-related proteins p65 and p-p65. The expression level of serum MEG3 in the sepsis group was significantly lower than that in the control group (P <0.05). ROC curve analysis showed that the AUC area was 0.856, the sensitivity was 0.700, and the specificity was 0.883. Compared with the NC group, the macrophage apoptosis rate in the LPS group was increased (P <0.05), the levels of Bax and p-p65 protein were significantly increased (P <0.05), and the level of Bcl-2 protein was decreased (P <0.05), the levels of IL-1beta and TNF-alpha were increased (P <0.05). Compared with the LPS + pcDNA group, the apoptosis rate of the LPS + pcDNA-MEG3 group was significantly reduced (P <0.05), the levels of Bax and p-p65 protein were reduced (P <0.05), and the level of Bcl-2 protein was significantly increased (P <0.05), the levels of IL-1beta and TNF-alpha were reduced (P <0.05).The low expression of LncRNA MEG3 in the serum of patients with sepsis can predict the occurrence of sepsis. Overexpression of MEG3 can inhibit LPS-induced macrophage apoptosis and secretion of inflammatory factors by inhibiting the activation of the NF-kB signaling pathway.	33040826	RID04749	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Sepsis	MEG3	BCL2	positively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Bcl-2|PPP1R50	LncRNA MEG3 expression in sepsis and its effect on LPS-induced macrophage function60 sepsis patients admitted to our hospital from February 2017 to September 2018 were selected as the sepsis group, and 50 non-septic patients diagnosed and treated in our hospital during the same period were selected as the control group. qRT-PCRwas used to detect the expression level of MEG3. ROC curve was used to analyze the diagnostic value of serum MEG3 in sepsis. The human macrophage cell line U937 was cultured in vitro and randomly divided into NC group, LPS group, LPS + pcDNA group, and LPS + pcDNA-MEG3 group. Flow cytometry was applied to detect the apoptosis rate. The levels of IL-1beta and TNF-alpha were detected by ELISA. western blot was used to detect the expression of Bax, Bcl-2 and NF-kB signaling pathway-related proteins p65 and p-p65. The expression level of serum MEG3 in the sepsis group was significantly lower than that in the control group (P <0.05). ROC curve analysis showed that the AUC area was 0.856, the sensitivity was 0.700, and the specificity was 0.883. Compared with the NC group, the macrophage apoptosis rate in the LPS group was increased (P <0.05), the levels of Bax and p-p65 protein were significantly increased (P <0.05), and the level of Bcl-2 protein was decreased (P <0.05), the levels of IL-1beta and TNF-alpha were increased (P <0.05). Compared with the LPS + pcDNA group, the apoptosis rate of the LPS + pcDNA-MEG3 group was significantly reduced (P <0.05), the levels of Bax and p-p65 protein were reduced (P <0.05), and the level of Bcl-2 protein was significantly increased (P <0.05), the levels of IL-1beta and TNF-alpha were reduced (P <0.05).The low expression of LncRNA MEG3 in the serum of patients with sepsis can predict the occurrence of sepsis. Overexpression of MEG3 can inhibit LPS-induced macrophage apoptosis and secretion of inflammatory factors by inhibiting the activation of the NF-kB signaling pathway.	33040826	RID04750	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Sepsis	MEG3	IL1B	negatively-E	ELISA	downregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000125538	NA	55384	3553	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	IL-1B|IL1-BETA|IL1F2	LncRNA MEG3 expression in sepsis and its effect on LPS-induced macrophage function60 sepsis patients admitted to our hospital from February 2017 to September 2018 were selected as the sepsis group, and 50 non-septic patients diagnosed and treated in our hospital during the same period were selected as the control group. qRT-PCRwas used to detect the expression level of MEG3. ROC curve was used to analyze the diagnostic value of serum MEG3 in sepsis. The human macrophage cell line U937 was cultured in vitro and randomly divided into NC group, LPS group, LPS + pcDNA group, and LPS + pcDNA-MEG3 group. Flow cytometry was applied to detect the apoptosis rate. The levels of IL-1beta and TNF-alpha were detected by ELISA. western blot was used to detect the expression of Bax, Bcl-2 and NF-kB signaling pathway-related proteins p65 and p-p65. The expression level of serum MEG3 in the sepsis group was significantly lower than that in the control group (P <0.05). ROC curve analysis showed that the AUC area was 0.856, the sensitivity was 0.700, and the specificity was 0.883. Compared with the NC group, the macrophage apoptosis rate in the LPS group was increased (P <0.05), the levels of Bax and p-p65 protein were significantly increased (P <0.05), and the level of Bcl-2 protein was decreased (P <0.05), the levels of IL-1beta and TNF-alpha were increased (P <0.05). Compared with the LPS + pcDNA group, the apoptosis rate of the LPS + pcDNA-MEG3 group was significantly reduced (P <0.05), the levels of Bax and p-p65 protein were reduced (P <0.05), and the level of Bcl-2 protein was significantly increased (P <0.05), the levels of IL-1beta and TNF-alpha were reduced (P <0.05).The low expression of LncRNA MEG3 in the serum of patients with sepsis can predict the occurrence of sepsis. Overexpression of MEG3 can inhibit LPS-induced macrophage apoptosis and secretion of inflammatory factors by inhibiting the activation of the NF-kB signaling pathway.	33040826	RID04751	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Sepsis	MEG3	TNF	negatively-E	ELISA	downregulation	qRT-PCR	NA	NA	apoptosis process(+);inflammatory response(+);NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000228978	NA	55384	7124	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DIF|TNF-alpha|TNFA|TNFSF2	LncRNA MEG3 expression in sepsis and its effect on LPS-induced macrophage function60 sepsis patients admitted to our hospital from February 2017 to September 2018 were selected as the sepsis group, and 50 non-septic patients diagnosed and treated in our hospital during the same period were selected as the control group. qRT-PCRwas used to detect the expression level of MEG3. ROC curve was used to analyze the diagnostic value of serum MEG3 in sepsis. The human macrophage cell line U937 was cultured in vitro and randomly divided into NC group, LPS group, LPS + pcDNA group, and LPS + pcDNA-MEG3 group. Flow cytometry was applied to detect the apoptosis rate. The levels of IL-1beta and TNF-alpha were detected by ELISA. western blot was used to detect the expression of Bax, Bcl-2 and NF-kB signaling pathway-related proteins p65 and p-p65. The expression level of serum MEG3 in the sepsis group was significantly lower than that in the control group (P <0.05). ROC curve analysis showed that the AUC area was 0.856, the sensitivity was 0.700, and the specificity was 0.883. Compared with the NC group, the macrophage apoptosis rate in the LPS group was increased (P <0.05), the levels of Bax and p-p65 protein were significantly increased (P <0.05), and the level of Bcl-2 protein was decreased (P <0.05), the levels of IL-1beta and TNF-alpha were increased (P <0.05). Compared with the LPS + pcDNA group, the apoptosis rate of the LPS + pcDNA-MEG3 group was significantly reduced (P <0.05), the levels of Bax and p-p65 protein were reduced (P <0.05), and the level of Bcl-2 protein was significantly increased (P <0.05), the levels of IL-1beta and TNF-alpha were reduced (P <0.05).The low expression of LncRNA MEG3 in the serum of patients with sepsis can predict the occurrence of sepsis. Overexpression of MEG3 can inhibit LPS-induced macrophage apoptosis and secretion of inflammatory factors by inhibiting the activation of the NF-kB signaling pathway.	33040826	RID04752	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Lung adenocarcinoma	AKT1	LINC01546	positively-E	siRNA;RIP;RNA pull-down assay;shRNA	upregulation	RT-PCR	TCGA	NA	cell invasion(+);cell metastasis(+)	histone modification	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000142208	NA	ENSG00000228459	GRCh38_X:3271544-3290158	207	100129464	AKT|PKB|PRKBA|RAC|RAC-alpha	CXorf28|VAL	AKT-induced lncRNA VAL promotes EMT-independent metastasis through diminishing Trim16-dependent Vimentin degradationBased on long non-coding RNA (lncRNA) profiling induced by active AKT, we identify that VAL (Vimentin associated lncRNA, LINC01546), which is directly induced by AKT/STAT3 signaling, functions as a potent pro-metastatic molecule and is essential for active AKT-induced tumor invasion, metastasis and anoikis resistance in lung adenocarcinoma (LAD). Impressively, chemosynthetic siRNAs against VAL shows great therapeutic potential in AKT overactivation-driven metastasis. Interestingly, similar to activated AKT in LAD cells, although unable to induce epithelial-mesenchymal transition (EMT), VAL exerts potent pro-invasive and pro-metastatic effects through directly binding to Vimentin and competitively abrogating Trim16-depedent Vimentin poly-ubiquitination and degradation. Taken together, our study provides an interesting demonstration of a lncRNA-mediated mechanism for active AKT-driven EMT-independent LAD metastasis and indicates the great potential of targeting VAL or Vimentin stability as a therapeutic approach.	33046716	RID04753	epigenetic regulation	metastasis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Lung cancer	LSINCT5	AKT1	positively-E	shRNA;western blot;immunoprecipitation	upregulation	qPCR	NA	NA	chemosensitivity(-)	transcriptional regulation	binding/interaction	RNA-protein	Erlotinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000142208	NA	101234261	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Effect of long non-coding RNA long stress-induced noncoding transcript 5 on erlotinib resistance to lung cancer cells and the underlying mechanismsHuman lung cancer cell line A549, H520, H358, H1299, SPCA1, and PC9 were collected and cultured. Epidermal growth factor receptor (EGFR) mutant lung cancer cell line PC9 was divided into a control group, a resistance group, a interference group I and II.The control group was treated with dimethylsulfoxide (DMSO) for 10 weeks and then was transfected with control target sequence expression vector. The resistant group was treated with erlotinib at gradient concentration (0.1, 0.2, 0.4, 0.8, and 1.6 umol/L, respectively) for 2 weeks and then transfected with control target sequence expression vector. Interference group I and II were treated with erlotinib at gradient concentration (0.1, 0.2, 0.4, 0.8, and 1.6 umol/L, respectively) for 2 weeks and then transfected with the shRNA targeting expression vectors 1 and 2. 50% inhibitory concentration (IC50) of erlotinib was detected by cell counting kit-8 (CCK-8) assay. The mRNA expressions of LSINCT5,phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) were measured by realtime PCR. The protein levels of PI3K, Akt, and phospho-Akt (p-Akt) were detected by western blot. The divergences of Akt and IgG binding to LSINCT5 were detected by RNA immunoprecipitation (RNA-IP) experiment.The expression of LSINCT5 in PC9 cells was significantly higher than that in other lung cancer cell lines (all P<0.05). Compared with the control group, the IC50 of erotinib and the expression of LSINCT5, PI3K, and Akt mRNA and protein in the resistance group were significantly higher (all P<0.05), and the IC50 of erotinib and the expression of LSINCT5, Akt, and p-Akt in the interference group I and II were significantly lower (all P<0.05). Compared with IgG, LSINCT5 binding to Akt was increased significantly (P<0.05).The expression of LSINCT5 is high in the erlotinib-resistant cells. Interference with LSINCT5 may inhibit the expression and activity of Akt and promote the cell sensitivity to erlotinib.	33053528	RID04754	transcriptional regulation	chemoresistance	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	CASC2	EIF2AK3	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell survival(+);apoptosis process(-);radiosensitivity(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000172071	NA	255082	9451	C10orf5	PEK|PERK	Long non-coding RNA CASC2 enhances irradiation-induced endoplasmic reticulum stress in NSCLC cells through PERK signalingThe present study investigated the effects and molecular mechanisms of CASC2 on radiosensitivity and ER stress in NSCLC cells. The overexpression of CASC2 markedly decreased cell survival and increased apoptosis, expression of PERK, phosphorylated-eIF2alpha and CHOP in irradiated human NSCLC cells, whereas knocking down PERK reversed these effects. Moreover, CASC2 considerably promoted the stability of PERK mRNA, but had no effect on the activity of PERK gene promoter in irradiated NSCLC cells. Strikingly, CASC2 exhibited no apparent effect on non-irradiated NSCLC cells. This study demonstrated that lncRNA CASC2 increases the stability of PERK mRNA, which consequently triggers the PERK/eIF2alpha/CHOP ER stress pathway and promotes radiosensitivity or apoptosis in irradiated NSCLC cells. Results of the present study suggest that CASC2 can act as an effective therapeutic target to enhance the efficacy of radiotherapy in the treatment of NSCLC.	33062578	RID04755	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Gastric cancer	NUTM2A-AS1	HIF1A	positively-E	shRNA;dual-luciferase reporter assay;Immunoprecipitation;RNA pull-down assay;RIP	upregulation	RT-qPCR;western blot	TCGA	NA	cell viability(+);cell invasion(+);chemoresistance(+);tumorigenesis(+)	ceRNA(miR-376a)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000223482	GRCh38_10:87189773-87342612	ENSG00000100644	NA	728190	3091	FAM22A-AS1	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	LncRNA NUTM2A-AS1 positively modulates TET1 and HIF-1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR-376aThe purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A-AS1 in gastric cancer. mRNA and protein levels were measured by RT-qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dualluciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR-376a and NUTM2A-AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A-AS1 in vivo and human clinical setting. Our results suggested that NUTM2A-AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR-376a. More interestingly, TET1 and HIF-1A were negatively regulated by miR-376a. TET1 could interact with HIF-1A to modulate PD-L1. Finally, we revealed that PD-L1 was key to NUTM2A-AS1- and miR-376a-mediated tumorigenesis and drug resistance.In summary, our research provides another strategy for GC diagnosis and treatment by targeting NUTM2A-AS1/miR-376a/TET1/PD-L1 axis. Combinatorial utilization of traditional chemotherapy and immunotherapy will be more effective than single treatment for GC.	33089970	RID04756	ceRNA or sponge	chemoresistance	DOWN(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	NUTM2A-AS1	TET1	positively-E	shRNA;dual-luciferase reporter assay;Immunoprecipitation;RNA pull-down assay;RIP	upregulation	RT-qPCR;western blot	TCGA	NA	cell viability(+);cell invasion(+);chemoresistance(+);tumorigenesis(+)	ceRNA(miR-376a)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223482	GRCh38_10:87189773-87342612	ENSG00000138336	NA	728190	80312	FAM22A-AS1	bA119F7.1|CXXC6|KIAA1676|LCX	LncRNA NUTM2A-AS1 positively modulates TET1 and HIF-1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR-376aThe purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A-AS1 in gastric cancer. mRNA and protein levels were measured by RT-qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dualluciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR-376a and NUTM2A-AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A-AS1 in vivo and human clinical setting. Our results suggested that NUTM2A-AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR-376a. More interestingly, TET1 and HIF-1A were negatively regulated by miR-376a. TET1 could interact with HIF-1A to modulate PD-L1. Finally, we revealed that PD-L1 was key to NUTM2A-AS1- and miR-376a-mediated tumorigenesis and drug resistance.In summary, our research provides another strategy for GC diagnosis and treatment by targeting NUTM2A-AS1/miR-376a/TET1/PD-L1 axis. Combinatorial utilization of traditional chemotherapy and immunotherapy will be more effective than single treatment for GC.	33089970	RID04757	ceRNA or sponge	chemoresistance	DOWN(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Gastric cancer	NUTM2A-AS1	CD274	positively-E	shRNA;dual-luciferase reporter assay;Immunoprecipitation;RNA pull-down assay;RIP	upregulation	RT-qPCR;western blot	TCGA	NA	cell viability(+);cell invasion(+);chemoresistance(+);tumorigenesis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223482	GRCh38_10:87189773-87342612	ENSG00000120217	NA	728190	29126	FAM22A-AS1	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	LncRNA NUTM2A-AS1 positively modulates TET1 and HIF-1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR-376aThe purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A-AS1 in gastric cancer. mRNA and protein levels were measured by RT-qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dualluciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR-376a and NUTM2A-AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A-AS1 in vivo and human clinical setting. Our results suggested that NUTM2A-AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR-376a. More interestingly, TET1 and HIF-1A were negatively regulated by miR-376a. TET1 could interact with HIF-1A to modulate PD-L1. Finally, we revealed that PD-L1 was key to NUTM2A-AS1- and miR-376a-mediated tumorigenesis and drug resistance.In summary, our research provides another strategy for GC diagnosis and treatment by targeting NUTM2A-AS1/miR-376a/TET1/PD-L1 axis. Combinatorial utilization of traditional chemotherapy and immunotherapy will be more effective than single treatment for GC.	33089970	RID04758	expression association	chemoresistance	DOWN(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Gastric cancer	EGR1	LINC01503	positively-E	ChIP;immunofluorescence;RIP;overexpression;shRNA	upregulation	RT-qPCR	TCGA;GSE54129	NA	cell proliferation(+);tumorigenesis(+);apoptosis process(-);cell cycle(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000120738	NA	ENSG00000233901	GRCh38_9:129332300-129359541	1958	100506119	225|AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268	lnc-PPP2R4-5|RP11-65J3.1	EGR1-mediated linc01503 promotes cell cycle progression and tumorigenesis in gastric cancerBioinformatics analysis and quantitative reverse transcription polymerase chain reaction (qRT-PCR assays were implicated to detect linc01503 level in GC. The role of linc01503 was detected by in vitro functional assays and in vivo xenograft tumour models. The association between linc01503 and its upstream effector was identified by chromatin immunoprecipitation (ChIP) assays. The mechanistic model of linc01503 was clarified using subcellular separation,fluorescence in situ hybridization, RNA-sequencing, RNA immunoprecipitation (RIP)and ChIP assays.Linc01503 was remarkably elevated in GC and tightly linked with the overall survival of patients with GC. The key transcription factor early growth response protein 1 (EGR1) critically activated the transcription of linc01503. Functionally,linc01503 knockdown resulted in the activation of apoptosis and G1/G0 phase arrest in GC. Mechanistically, linc01503 interacted with histone modification enzyme enhancer of zeste 2 (EZH2) and lysine (K)-specific demethylase 1A (LSD1), thereby mediating the transcriptional silencing of dual-specificity phosphatase 5 (DUSP5) and cyclin-dependent kinase inhibitor 1A (CDKN1A) in GC.EGR1-activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicatingit as a prospective target for GC therapeutics.	33145887	RID04759	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)
Ovarian cancer	HOXB-AS3	LDHA	positively-E	siRNA;western blot	upregulation	qPCR	TCGA;GTEx	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+)	ceRNA(miR-378a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000134333	NA	404266	3939	NA	NA	LncRNA HOXB-AS3 Promotes Growth, invasion and Migration of Epithelial Ovarian Cancer by Altering GlycolysisChi-square test, Kaplan-Meier(KM) analysis and Cox regression analysis were used to analyze the clinicopathological features of HOXB-AS3 in EOC patients. CCK8, transwell and wound healing assay were used to test the function of HOXB-AS3. Luciferase reporter assay, western blot and glycolysis rate assay were used for further mechanistic studies.HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status. EOC patients with high levels of HOXB-AS3 had strikingly shorter disease-free survival (DFS) and overall survival (OS) times than those with low levels. HOXB-AS3 also might as an independent prognostic factor.Further study revealed knockdown of HOXB-AS3 significantly inhibited the proliferation, invasion and migration of EOC cells. Mechanistic investigations suggested that knockdown of HOXB-AS3 could decrease lactate dehydrogenase A (LDHA) expression and the extracellular acidification rate (ECAR) by sponging miR-378a-3p.To our knowledge, this is the first study to suggest that HOXB-AS3 could crosstalk with miRNA in the cytoplasm and alter glycolysis in cancer cells. Our results improve our understanding of the mechanism of HOXB-AS3 and suggest that HOXB-AS3 can act as a predictor of OS and a target for EOC therapies.	33148416	RID04760	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Clear cell renal cell carcinoma	SNHG6	HIF1A	positively-E	siRNA;RIP;RNA pull-down assay;immunoblot	upregulation	qRT-PCR	TCGA	NA	cancer progression(+);cell proliferation(+);cell migration(+);colony formation(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100644	NA	641638	3091	HBII-276HG|NCRNA00058|U87HG	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	Long noncoding RNA SNHG6 promotes carcinogenesis by enhancing YBX1-mediated translation of HIF1alpha in clear cell renal cell carcinoma In this study, we screened an oncogenic lncRNA termed SNHG6 using RNA-Seq data of ccRCC from The Cancer Genome Atlas (TCGA). Quantitative real-time PCR was then used to demonstrate the expression of SNHG6 in ccRCC tissues. SNHG6 overexpression is highly associated with malignant features in patients and is a prognostic indicator. SNHG6 significantly promotes ccRCC cell proliferation and metastasis in vitro and in vivo. Mechanistic investigations identified that SNHG6 exerts oncogenic effects by interacting with YBX1, and then, enhancing HIF1alpha translation. RNA immunoprecipitation (RIP) with an anti-YBX1 antibody demonstrated that YBX1 bound HIF1alpha transcripts directly in ACHN cells.Moreover, knockdown of SNHG6 attenuated the binding of YBX1 and the HIF1alpha transcript.This result suggests that SNHG6/YBX1 may form a complex to regulate HIF1alpha expression in ccRCC cells.	33150667	RID04761	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Atherosclerosis	BANCR	miR<U+2011>34c	negatively-F	dual-luciferase reporter assay;shRNA;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	DNA methylation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000278910	GRCh38_9:69296678-69311111	NA	NA	100885775	NA	LINC00586	NA	LncRNA BANCR induced vascular smooth muscle cell proliferation by downregulating miR-34c methylation in atherosclerosisThis study was to investigate the relationship between BANCR and miR-34c in atherosclerosis. Blood (5 ml) was obtained from 56 patients with atherosclerosis and 56 healthy volunteers after they were fasted overnight, and plasma was extracted from the blood. Human Aortic Smooth Muscle Cells (HASMCs) were used to perform in vitro cell experiments.RT-qPCR was performed to measure the expression of BANCR and miR-34c in plasma and HASMCs. dual-luciferase reporter assay detected the interaction between BANCR and miR-34c. CCK-8 assay was used to assess the effects of BANCR and miR-34c overexpression on the proliferation of HASMCs. western blot was used to assess the effects of BANCR and miR-34c overexpression on the protein expression of HMGB1, TNF-alpha and Bcl-2. In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis. Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation. In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-alpha and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. Therefore given BANCR upregulation in atherosclerosis, its expression may be considered as a novel and useful biomarker for atherosclerosis prevention and prognosis. However considering the possible effects of other underlying diseases on both BANCR expression and miR-34c in atherosclerosis, further investigation is suggested for future research.	33151462	RID04762	epigenetic regulation	prognosis	UP(SKCM);DATA(GSE38495)	
Kidney disease	CDKN2B-AS1	TXNIP	positively-E	dual-luciferase reporter assay;shRNA;starBase	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cell pyroptosis(+)	ceRNA(miR-497)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000117289	NA	100048912	10628	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	ARRDC6|EST01027|HHCPA78|THIF|VDUP1	LncRNA-antisense non-coding RNA in the INK4 locus promotes pyroptosis via miR-497/thioredoxin-interacting protein axis in diabetic nephropathyKidney tissues were collected from diagnosed DN patients. High glucose (HG) treatment of human renal tubular epithelial cell cells (HK-2) was used as the cell model of DN. qRT-PCRand western blot were performed to measure levels of ANRIL, miR-497, TXNIP, IL-1beta, IL-18, caspase-1, and NLRP3. LDH leakage and cell viability were determined with commercial LDH activity kit and MTT assay. ELISA was employed to examine secreted IL-1beta and IL-18 levels. Flow cytometry was used to examine caspase-1 activity. Dual luciferase assay was performed to validate interactions of ANRIL/miR-497 and miR-497/TXNIP.  ANRIL and TXNIP were elevated in DN kidney tissues and HG-treated HK-2 cells while miR-497 was reduced. ANRIL bound miR-497 while miR-497 directly targeted TXNIP. Knockdown of ANRIL suppressed HG-induced LDH leakage, TXNIP/NLRP3/caspase-1 activation,  and increases of IL-1beta and IL-18 secreted levels. miR-497 knockdown or TXNIP overexpression reversed the effects of ANRIL knockdown on LDH leakage and pyroptosis-related signaling. miR-497 mimics inhibited caspase-1-dependent pyroptosis while co-overexpression of TXNIP blocked its effects in HG-treated HK-2 cells.	33160992	RID04763	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thoracic aortic dissection	CDKN2B-AS1	STAT3	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);AKT signaling pathway(+)	ceRNA(miR-320d)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Aortic dissection	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000168610	NA	100048912	6774	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	APRF	CDKN2B-AS1 Aggravates the Pathogenesis of Human Thoracic Aortic Dissection by Sponge to miR-320d The expression of CDKN2B-AS1 in human thoracic aortic dissection(TAD) and normal aortic tissues of donors were examined by quantitative real-time polymerase chain reaction. RNA pull-down assay and a series of luciferase reporter assays were performed to predict the relationships between CDKN2B-AS1, miR-320d, and STAT3. Cell counting kit 8 (CCK-8), TUNEL, and western blot assays were applied to validate the biological functions of CDKN2B-AS1 in rat aortic vascular smooth muscle cells. Results showed that CDKN2B-AS1 was expressed at a higher level in human TAD than in normal aortic tissues. CDKN2B-AS1 overexpression significantly promoted apoptosis and suppressed the proliferation of vascular smooth muscle cells. CDKN2B-AS1 silence exhibited the opposite effects. Mechanistically, CDKN2B-AS1 was identified as a molecular sponge for miR-320d and positively modulated STAT3 expression via repressing miR-320d. In conclusion, our study revealed that CDKN2B-AS1 was dysregulated and displayed multiple potential functions in human TAD. These findings suggested that CDKN2B-AS1 was a novel potential therapeutic target for human TAD.	33165136	RID04764	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Breast cancer	TMPO-AS1	miR<U+2011>140<U+2011>5p	negatively-F	dual-luciferase reporter assay;siRNA;shRMA	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);colony formation(+);cell viability(+);cell migration(+)	sponge	regulation	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000257167	GRCh38_12:98512973-98516422	NA	NA	100128191	NA	NA	NA	Long non-coding RNA TMPO-AS1 promotes tumor progression  via sponging miR-140-5p in breast cancerTMPO-AS1 levels were measured in human cancer tissues and breast cancer cell lines, and the functional roles of TMPO-00AS1 in breast cancer cells were investigated by performing in vitro and in vivo assays. Additionally, luciferase reporter assays were conducted to detect the association between microRNA (miR)-140-5p and TMPO-AS1. TMPO-AS1 expression levels were significantly increased in breast cancer tissues and cell lines compared with adjacent non-cancerous tissues and MCF-10A cells, respect ively. In vitro and in vivo studies indicated that TMPO-AS1 knockdown significantly suppressed breast cancer cell viability at 48 and 72 h compared with the small interfering (si)RNA negative control group (NC; siNC). TMPO-AS1 knockdown in vitro inhibited MCF-7 and T47D cell migration and invasion compared with the siNC group. TMPO-AS1 knockdown in metastatic breast cancer cells also decreased metastatic colonization in the mouse lung compared with the short hairpin RNA NC group. Mechanistically, TMPO-AS1 promoted cellular viability and migration as a competing endogenous RNA by sponging miR-140-5p. The results suggested that TMPO-AS1 may serve as a potential therapeutic target in patients with breast cancer.	33235626	RID04765	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	
Cervical cancer	HIF1A-AS2	NANOG	positively-E	shRNA;western blot	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000111704	NA	100750247	79923	3'aHIF-1A|aHIF	FLJ12581|FLJ40451	Silencing long non-coding RNA HIF1A-AS2 inhibits proliferation, invasion and migration of cervical cancer cells in vitroWe designed 3 shRNA constructs for silencing HIF1A-AS2 in CaSki cells, and the shRNA with the strongest interference effect was selected for subsequent experiment. CaSki cells were transfected with shRNA-NC or Sh-HIF1A-AS2, and the changes in cell viability ,invasion ability , EMT, expressions of EMT-related proteins, formation of cell spheres and expressions of stem cell markers were detected. Transfection with shRNA-NC and Sh-HIF1A-AS2 did not significantly affected the viability of CaSki cells (P> 0.05). Compared with the cells transfected with shRNA-NC, the cells transfected with Sh- HIF1A-AS2 showed significantly reduced invasion ability , expressions of vimentin N-cadherin, and cell sphere formation ability . HIF1A-AS2 silencing obviously lowered the rate of ABCG2-positive cells, significantly reduced the mRNA and protein expressions of Nanog, OCT4, and SOX2, and strongly enhanced the expression of E-cadherin in CaSki cells (P<0.05). Conclusion Silencing HIF1A-AS2 can inhibit proliferation, invasion and migration of cervical cancer cells in vitro.	33243752	RID04766	expression association	NA		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Cervical cancer	HIF1A-AS3	POU5F1	positively-E	shRNA;western blot	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000233911	NA	105370526	5460	NA	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	Silencing long non-coding RNA HIF1A-AS2 inhibits proliferation, invasion and migration of cervical cancer cells in vitroWe designed 3 shRNA constructs for silencing HIF1A-AS2 in CaSki cells, and the shRNA with the strongest interference effect was selected for subsequent experiment. CaSki cells were transfected with shRNA-NC or Sh-HIF1A-AS2, and the changes in cell viability ,invasion ability , EMT, expressions of EMT-related proteins, formation of cell spheres and expressions of stem cell markers were detected. Transfection with shRNA-NC and Sh-HIF1A-AS2 did not significantly affected the viability of CaSki cells (P> 0.05). Compared with the cells transfected with shRNA-NC, the cells transfected with Sh- HIF1A-AS2 showed significantly reduced invasion ability , expressions of vimentin N-cadherin, and cell sphere formation ability . HIF1A-AS2 silencing obviously lowered the rate of ABCG2-positive cells, significantly reduced the mRNA and protein expressions of Nanog, OCT4, and SOX2, and strongly enhanced the expression of E-cadherin in CaSki cells (P<0.05). Conclusion Silencing HIF1A-AS2 can inhibit proliferation, invasion and migration of cervical cancer cells in vitro.	33243752	RID04767	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cervical cancer	HIF1A-AS4	SOX2	positively-E	shRNA;western blot	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	NA	NA	ENSG00000181449	NA	NA	6657	NA	NA	Silencing long non-coding RNA HIF1A-AS2 inhibits proliferation, invasion and migration of cervical cancer cells in vitroWe designed 3 shRNA constructs for silencing HIF1A-AS2 in CaSki cells, and the shRNA with the strongest interference effect was selected for subsequent experiment. CaSki cells were transfected with shRNA-NC or Sh-HIF1A-AS2, and the changes in cell viability ,invasion ability , EMT, expressions of EMT-related proteins, formation of cell spheres and expressions of stem cell markers were detected. Transfection with shRNA-NC and Sh-HIF1A-AS2 did not significantly affected the viability of CaSki cells (P> 0.05). Compared with the cells transfected with shRNA-NC, the cells transfected with Sh- HIF1A-AS2 showed significantly reduced invasion ability , expressions of vimentin N-cadherin, and cell sphere formation ability . HIF1A-AS2 silencing obviously lowered the rate of ABCG2-positive cells, significantly reduced the mRNA and protein expressions of Nanog, OCT4, and SOX2, and strongly enhanced the expression of E-cadherin in CaSki cells (P<0.05). Conclusion Silencing HIF1A-AS2 can inhibit proliferation, invasion and migration of cervical cancer cells in vitro.	33243752	RID04768	expression association	NA		UP(LIHC);DATA(GSE117623)
Gastric cancer	KDM7A-DT	PRAF2	positively-E	dual-luciferase reporter assay;siRNA;western blot;Immunofluorescence	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);cancer progression(+)	ceRNA(miR-450a-2-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260231	GRCh38_7:140177184-140179640	ENSG00000243279	NA	100134229	11230	JHDM1D-AS1	JM4|Yip6a	JHDM1D-AS1 aggravates the development of gastric cancer through miR-450a-2-3p-PRAF2 axisThe qPCR assay was used to detect the JHDM1D-AS1 and miR-450a-2-3p expression levels in GC tissues and cell lines. Bioinformatics analysis was used for exploring the lncRNA-microRNA-mRNA interaction network. We performed dual-luciferase reporter assay and qPCR assay in order to validate the direct interactions. We explored the JHDM1D-AS1 and miR-450a-2-3p on GC progression by using JHDM1D-AS1  siRNA and miR-450a-2-3p inhibitor; in vitro CCK-8 assay, colony formation assay, and invasion assay were conducted. Further, in vivo animal experiments were performed, and the expression levels of miR-450a-2-3p and PRAF2 in the tumor tissues were detected using qPCR and western blot The expression levels of JHDM1D-AS1 and miR-450a-2-3p in GC tissues and cell lines were higher and lower as compared to those in the corresponding normal controls, respectively. Moreover, high levels of JHDM1D-AS1 were closely related with metastasis and the GC TNM stage. Functionally, JHDM1D-AS1 depletion caused an obvious reduction in cell proliferation and invasion both in vitro and in vivo, while the addition of miR-450a-2-3p inhibitor could nullify these effects. Mechanically, JHDM1D-AS1 promoted GC progression via the sponging of miR-450a-2-3p in order to increase PRAF2 expression. The present results showed that the increased expression of JHDM1D-AS1 was closely associated with tumor progression of GC. JHDM1D-AS1/miR-450a-2-3p/PRAF2 axis may be a promising target for GC treatment.	33245963	RID04769	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761)
Gallbladder cancer	lncGALM	ZEB1	positively-E	shRNA;overexpression;siRNA;dual-luciferase reporter assay;RNA pull-down assay;RIP;Immunofluorescence	upregulation	sequencing;microarray;qRT-PCR;northern blot	GSE132223;GSE106671	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1beta-dependent liver arrest and tumor extravasationA novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1beta mRNA and stabilized the IL-1beta gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis.lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.	33252861	RID04770	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gallbladder cancer	lncGALM	ZEB2	positively-E	shRNA;overexpression;siRNA;dual-luciferase reporter assay;RNA pull-down assay;RIP;Immunofluorescence	upregulation	sequencing;microarray;qRT-PCR;northern blot	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	NA	NA	ENSG00000169554	NA	NA	9839	NA	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1beta-dependent liver arrest and tumor extravasationA novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1beta mRNA and stabilized the IL-1beta gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis.lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.	33252861	RID04771	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Gallbladder cancer	lncGALM	IL-1	negatively-E	overexpression;RNA pull-down assay;knockdown	upregulation	sequencing;microarray;qRT-PCR;northern blot	NA	NA	apoptosis process(+)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1beta-dependent liver arrest and tumor extravasationA novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1beta mRNA and stabilized the IL-1beta gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis.lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.	33252861	RID04772	transcriptional regulation	metastasis		
Lung adenocarcinoma	DUXAP8	miR-26b-5p	negatively-E	siRNA;shRNA;dual-luciferase reporter assay;RNA pull-down assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000271672	GRCh38_22:15826566-15827187	NA	NA	503637	NA	NA	NA	Silencing lncRNA DUXAP8 inhibits lung adenocarcinoma progression by targeting miR-26b-5pLoss-of-function experiments were performed to assess the function of DUXAP8 proliferation and apoptosis of H1975 and A549 cells. Functionally, silencing DUXAP8 inhibited proliferation and induced apoptosis of LUAD cells. Mechanistically, further correlation assay indicated a negative association between miR-26b-5p and DUXAP8 expression. Subsequently, we testified that DUXAP8 exerted its role in the progression and development of LUAD through targeting miR-26b-5p. In summary, our results elucidated that that DUXAP8 promoted tumor progression in LUAD by targeting miR-26b-5p, which provide a novel therapeutic target for diagnosis and therapy of LUAD.	33269379	RID04773	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	
Urinary bladder cancer	SOX2-OT	SOX2	positively-E	luciferase reporter assay;overexpression	upregulation	RT-qPCR	NA	NA	cell metastasis(-);cell stemness(+)	ceRNA(miR-200)	association	NA	NA	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX2-OT) is an evolutionarily conserved long noncoding RNA. Its intronic region contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Mechanistic investigations have revealed that SOX2-OT upregulates or downregulates the SOX2 expression through diverse pathways. Two studies demonstrated that SOX2-OT upregulates the SOX2 expression via the miR-200 family members in cancer cells. SOX2-OT acts as a miRNA sponge that competitively binds to miR-200 family members in order to upregulate the expression of SOX2 in cancer cells . One study revealed that the luciferase activity of the SOX2 promoter is significantly increased when SOX2-OT is overexpressed in pancreatic ductal adenocarcinoma cells, suggesting that SOX2-OT is a transcriptional activator of the SOX2 gene. However, a study on central nervous system development showed that SOX2-OT physically interacts with the multifunctional transcriptional regulator YY1, which binds to several CpG islands in the SOX2 locus in a SOX2-OT-dependent manner and downregulates SOX2 expression in neural stem cells. Another study showed that SOX2-OT impairs the formation of the chromatin promoter-enhancer loop upstream of the SOX2 gene and disrupts SOX2 transcription in neural stem cells. Although few studies have investigated the mechanism by which SOX2-OT regulates the SOX2 expression in cancer cells or neural stem cells, the regulation of the SOX2 expression by SOX2-OT in tumor cells follows a pattern opposite to that in neural stem cells.	33294436	RID04774	ceRNA or sponge	prognosis,metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Pancreatic ductal adenocarcinoma	SOX2-OT	SOX2	positively-E	luciferase reporter assay;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);tumor growth(+)	ceRNA(miR-200)	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX3-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r	33294436	RID04775	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Esophagus squamous cell carcinoma	SOX2-OT	SOX2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell metastasis(-);cell stemness(+)	transcriptional regulation	association	NA	NA	CSC	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX4-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------	33294436	RID04776	transcriptional regulation	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Septic cardiomyopathy	SOX2-OT	SOX2	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	mitochondrial function(-)	transcriptional regulation	association	NA	NA	NA	NA	Cardiovascular system disease	Cardiomyopathy	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX5-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------	33294436	RID04777	transcriptional regulation	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Cancer	SOX2-OT	SOX2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	transcriptional regulation	NA	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX6-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------	33294436	RID04778	transcriptional regulation	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Osteosarcoma	SOX2-OT	SOX2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell stemness(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX7-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------	33294436	RID04779	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Cancer	SOX2-OT	SOX2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX8-OT) is an evolutionarily conserved long noncoding RNA. Its intronic r--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------	33294436	RID04780	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Nasopharynx carcinoma	SOX2-OT	HNRNPA2B1	positively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	ceRNA(miR-146b-5p)	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000122566	NA	347689	3181	DKFZp761J1324|NCRNA00043|SOX2OT	HNRPA2B1	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX2-OT) is an evolutionarily conserved long noncoding RNA. Its intronic region contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04781	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	SOX2-OT	CFL2	positively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-369-3p)	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000165410	NA	347689	1073	DKFZp761J1324|NCRNA00043|SOX2OT	NEM7	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX2-OT) is an evolutionarily conserved long noncoding RNA. Its intronic region contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04782	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Ewing's sarcoma	SOX2-OT	FOXP4	positively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-363)	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Sarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000137166	NA	347689	116113	DKFZp761J1324|NCRNA00043|SOX2OT	FLJ40908	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX3-OT) is an evolutionarily conserved long noncoding RNA. Its intronic ron contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04783	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Non-small cell lung cancer	SOX2-OT	ZEB2	positively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-132)	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000169554	NA	347689	9839	DKFZp761J1324|NCRNA00043|SOX2OT	KIAA0569|SIP-1|SIP1|ZFHX1B	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX4-OT) is an evolutionarily conserved long noncoding RNA. Its intronic ron contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04784	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Pheochromocytoma	SOX2-OT	MCL-1 isoform 2	positively-E		upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);cell autophagy(-);apoptosis process(-)	ceRNA(miR-211)	association	RNA-RNA	NA	CSC	NA	Disease of cellular proliferation	Endocrine organ benign neoplasm	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	NA	NA	347689	NA	NCRNA00043|SOX2OT	NA	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX5-OT) is an evolutionarily conserved long noncoding RNA. Its intronic ron contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04785	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Gastric cancer	SOX2-OT	AKT2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-194-5p)	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000105221	NA	347689	208	DKFZp761J1324|NCRNA00043|SOX2OT	PKB脙沤脗虏	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX6-OT) is an evolutionarily conserved long noncoding RNA. Its intronic ron contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04786	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SOX2-OT	SOX3	positively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-194-5p, miR-122)	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000134595	NA	347689	6658	DKFZp761J1324|NCRNA00043|SOX2OT	PHP	Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic ComplicationsSRY-box transcription factor 2 (SOX2) overlapping transcript (SOX7-OT) is an evolutionarily conserved long noncoding RNA. Its intronic ron contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells.Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.Research has suggested that some lncRNAs are involved in the competitive binding of miRNAs . The members of this major subset of lncRNAs are called competing endogenous RNAs (ceRNAs), or miRNA sponges, and they form a regulatory network that controls the expression of proteincoding genes. In this network, lncRNAs positively regulate the expression of protein-coding genes by competitively binding to their miRNAs. SOX2-OT has been identifiedas an important ceRNA that affects cancer progression. An omics study revealed that SOX2-OT interacted with 6 differentially expressed miRNAs (hsamir-192-5p, hsa-mir-215-5p, hsa-mir-204-5p, hsa-mir-205-5p, hsa-mir-338-3p, hsa-mir-375) among 96 esophageal squamous cell carcinoma samples and 13 normal tissue samples. In addition, numerous studies have demonstrated that SOX2-OT can bind to unique miRNAs in various cancers, and almost no overlapping miRNAs have been identified among those cancers. miR-200c is the only exception, as SOX2-OT can target miR-200c in both bladder cancer and pancreatic ductal adenocarcinoma.Although SOX2-OT can target various miRNAs, it regulates similar cellular functions and behaviors, such as cancer cell proliferation, migration, invasion, metastasis, epithelialmesenchymal transition (EMT), and stemness maintenance.In addition to acting as a miRNA sponge, SOX2-OT acts as a regulator of transcription by serving as a bridge between epigenetic factors and DNA to affect gene expression. A recent study revealed that SOX2-OT interacts with EZH2, recruits EZH2 to DNA to form the polycomb repressive complex 2 (PRC2), induces H3K27me3, and epigenetically inhibits PTEN expression in laryngeal squamous cell carcinoma cells. Studies have demonstrated that SOX2-OT binds to nervous system polycomb 1 (NSPc1), a key component of polycomb repressive complex 1 (PRC1), in H4 glioma cells and U87 glioma cells, and regulates cancer cell proliferation and apoptosis. SOX2-OT can also act as a destabilizer of transcription factors to control gene expression. A study suggested that SOX2-OT directly binds to the transcription factor FUS and that FUS protein stability is altered by this binding. Thus, SOX2-OT acts as a tumor promoter in pancreatic ductal adenocarcinoma by physically binding to FUS to regulate its downstream cell cycle-associated factors CCND1 and p27.	33294436	RID04787	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DATA(GSE40174)
Chronic obstructive pulmonary disease	LINC00987	SIRT1	positively-E	lncBase;miRWalk;dual-luciferase reporter assay;siRNA	downregulation	RT-qPCR	NA	NA	cell viability(+);inflammatory response(-);cell autophagy(+);apoptosis process(+)	ceRNA(let-7b-5p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000237248	GRCh38_12:9240003-9257960	ENSG00000096717	NA	100499405	23411	NA	SIR2L1	LINC00987 Ameliorates COPD by Regulating LPS-Induced Cell Apoptosis, Oxidative Stress, Inflammation and Autophagy Through Let-7b-5p/SIRT1 AxisThe expression levels of LINC00987 and let-7b-5p were detected by real-time quantitativepolymerase chain reaction (RT-qPCR). The expression of apoptosis-associated proteins, oxidative stress (ROS)-related proteins, autophagy-related proteins and sirtuin1 (SIRT1) protein was determined by western blot. Cell viability was illustrated by cell counting kit-8 (CCK-8) assay. Cell apoptosis was investigated by caspase3 activity and apoptosis analysis assays. ROS, inflammation and autophagy were demonstrated by detecting reactive ROS level and superoxide dismutase (SOD) activity, enzyme-linked immunosorbent assay (ELISA) and western blot respectively. The binding sites between let-7b-5p and LINC00987 or SIRT1 were predicted by lncBase or miRWalk online database, and identified by dual-luciferase reporter assay.LINC00987 expression was strikingly downregulated and let-7b-5p expression was obviously upregulated in COPD tissues and LPS-induced BEAS-2B cells compared with control groups. LINC00987 overexpression promoted BEAS-2B cells against LPS-mediated viability, apoptosis, oxidative stress, inflammation and autophagy, whereas these effects were attenuated by let-7b-5p mimic or SIRT1 knockdown. Furthermore, LINC00987 sponged let- 7b-5p and let-7b-5p bound to SIRT1.	33311978	RID04788	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Coronary artery disease	MALAT1	CD36	positively-E		downregulation	qRT-PCR	NA	NA	inflammatory response(+);chemoresistance(+)	transcriptional regulation	binding/interaction	RNA-protein	Vitamin D	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135218	NA	378938	948	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FAT|GP3B|GP4|GPIV|SCARB3	Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls Blood samples were taken from 15 patients with coronary artery disease (CAD) and 15 non-CAD participants (NCAD )individuals. The plasma was used for biochemical analyses. MALAT1 and CD36 expressions were evaluated in the isolated peripheral blood mononuclear cells (PBMCs) by real-time PCR. Furthermore, the levels of inflammatory cytokines e.g. interleukin (IL)-6, IL-10, and IL-22 were measured in the supernatants of the cultured PBMCs by flow cytometry.The levels of MALAT1 and CD36 were not significantly different between the CAD and NCAD groups. However, a lower level of MALAT1 and CD36 was observed in PBMCs of vitamin D deficient (<15 ng/ml) CAD and NCAD participants. Furthermore, the vitamin D deficient (<15 ng/ml) group showed a significantly higher plasma level of IL-6, IL-10, and IL-22 compared to the non-deficient (<<-5 ng/ml) group. In addition, significant positive correlations were found between CD36, IL-22, and fasting blood sugar (FBS) with MALAT1. Given that in vitamin D deficient individuals a decreased level of MALAT1 was associated with CD36 expression and increased IL-22 production, vitamin D supplementation may play a role in reducing MALAT1/CD36/IL-22 mediated complications such as T2DM and CAD, especially in vitamin D deficiency.	33331582	RID04789	transcriptional regulation	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827)
Coronary artery disease	MALAT1	IL22	negatively-E		downregulation	qRT-PCR	NA	NA	inflammatory response(+);chemoresistance(+)	NA	association	RNA-protein	Vitamin D	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127318	NA	378938	50616	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	IL-21|IL-22|IL-D110|IL-TIF|ILTIF|MGC79382|MGC79384|TIFa|TIFIL-23|zcyto18	Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls Blood samples were taken from 15 patients with coronary artery disease (CAD) and 15 non-CAD participants (NCAD )individuals. The plasma was used for biochemical analyses. MALAT1 and CD36 expressions were evaluated in the isolated peripheral blood mononuclear cells (PBMCs) by real-time PCR. Furthermore, the levels of inflammatory cytokines e.g. interleukin (IL)-6, IL-10, and IL-22 were measured in the supernatants of the cultured PBMCs by flow cytometry.The levels of MALAT1 and CD36 were not significantly different between the CAD and NCAD groups. However, a lower level of MALAT1 and CD36 was observed in PBMCs of vitamin D deficient (<15 ng/ml) CAD and NCAD participants. Furthermore, the vitamin D deficient (<15 ng/ml) group showed a significantly higher plasma level of IL-6, IL-10, and IL-22 compared to the non-deficient (<<-5 ng/ml) group. In addition, significant positive correlations were found between CD36, IL-22, and fasting blood sugar (FBS) with MALAT1. Given that in vitamin D deficient individuals a decreased level of MALAT1 was associated with CD36 expression and increased IL-22 production, vitamin D supplementation may play a role in reducing MALAT1/CD36/IL-22 mediated complications such as T2DM and CAD, especially in vitamin D deficiency.	33331582	RID04790	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	XIST	MIR137	negatively-F	siRNA	upregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);chemosensitivity(-)	sponge	association	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000284202	NA	7503	406928	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	hsa-mir-137|miR-137|MIRN137	LncRNA XIST/miR-137 axis strengthens chemo-resistance and glycolysis of colorectal cancer cells by hindering transformation from PKM2 to PKM1 Altogether 212 pairs of tumor tissues and adjacent normal tissues were collected from CRC patients. Moreover, human CRC epithelial cell lines, including HT29, SW480, SW620 and LoVo, were purchased in advance, and their activity was estimated after transfection of si-XIST or miR-137 mimic. Furthermore, 5-FU/cisplatin-resistance of CRC cells was determined through MTT assay, and glycolytic potential of CRC cells was appraised based on oxygen consumption rate (OCR) and extracellular acidification rate (ECAR).Highly-expressed XIST were predictive of severe symptoms and unfavorable 3-year survival of CRC patients (P< 0.05). Besides, silencing of XIST not only diminished proliferative, migratory and invasive power of CRC cells (P< 0.05), but also enhanced sensitivity of CRC cells responding to 5-FU/cisplatin (P< 0.05). Glycolytic potency of CRC cells was also undermined by si-XIST, with decreased maximal respiration and maximal glycolytic capacity in the si-XIST group as relative to NC group (P< 0.05). Nevertheless, miR-137 mimic attenuated the facilitating effect of pcDNA3.1-XIST on proliferation, migration, invasion, 5-FU/cisplatin-resistance and glycolysis of CRC cells (P< 0.05). Ultimately, ratio of PKM2 mRNA and PKM1 mRNA, despite being up-regulated by pcDNA3.1-XIST, was markedly lowered when miR-137 mimic was co-transfected (P< 0.05).LncRNA XIST/miR-137 axis reinforced glycolysis and chemo-tolerance of CRC by elevating PKM2/PKM1 ratio, providing an alternative to boost chemo-therapeutic efficacy of CRC patients.	33386794	RID04791	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Hepatocellular carcinoma	NBAT1	MYC	negatively-E	overexpression	downregulation		NA	NA	tumorigenesis(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000136997	NA	729177	4609	CASC14|NBAT-1	bHLHe39|c-Myc|MYCC	Long noncoding RNA NBAT1 suppresses hepatocellular carcinoma progression via competitively associating with IGF2BP1 and decreasing c-Myc expressionHere, we found that the expression of NBAT1 was decreased in HCC tissues and cells; as well, the decreased expression of NBAT1 was also associated with tumor size and clinical TNM stages. NBAT1 overexpression, both in vitro and in vivo studies, inhibited tumorigenesis through apoptosis augmentation and cell cycle blockade. Mechanistically, NBAT1 bound to IGF2BP1 and inhibited the interaction between IGF2BP1 and c-Myc mRNA, thus suppressing the stability of c-Myc mRNA. Collectively, NBAT1 is associated with HCC tumorigenesis and could be a therapeutic target for HCC treatment.	33387362	RID04792	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LIFR-AS1	COL1A2	positively-E	shRNA;dual-luciferase reporter assay;immunohistochemistry;starBase;Targetscan;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-29a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000164692	NA	100506495	1278	NA	OI4	LncRNA LIFR-AS1 promotes proliferation and invasion of gastric cancer cell via miR-29a-3p/COL1A2 axisThe aim of this study was to investigate the function of LIFR-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer.qRT-PCRwas used to evaluate the expression of LIFR-AS1, miR-29a-3p and COL1A2 in gastric tumor tissues and cells. western blot was used to evaluate the protein expression of COL1A2 in gastric tumor cells. CCK-8 assay, transwell assay and flow cytometry were used to evaluate the roles of LIFR-AS1, miR-29a-3p and COL1A2 in cell proliferation, invasion, migration and apoptosis. The relationship among LIFR-AS1, miR-29a-3p and COL1A2 was assessed by bioinformatics analyses and luciferase reporter assay.The expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased. The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor.LIFR-AS1 plays an important role as a competing endogenous RNA in gastric tumor pathogenesis and may be a potential target for the diagnosis and treatment of gastric tumor.	33407453	RID04793	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Type 2 diabetes mellitus	EPB41L4A-AS1	MYD88	negatively-E	knockdown;shRNA;western blot;Immunofluorescence assay;ChIP	downregulation	microarray;qRT-PCR	GDS3875;GDS3874;GDS2856;ENCODE	NA	NF-kB signaling pathway(+);inflammatory response(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000224032	GRCh38_5:112160526-112164818	ENSG00000172936	NA	114915	4615	C5orf26|NCRNA00219|TIGA1	NA	Downregulation of lncRNA EPB41L4A-AS1 Mediates Activation of MYD88-Dependent NF-kB Pathway in Diabetes-Related InflammationTo explore the relationships between the expression of EPB41L4A-AS1 and inflammatory factors in the blood of T2DM patients, we analyzed peripheral blood mononuclear cell (PBMC) expression microarrays of T2DM patients and expression microarrays of PBMC treated with lipopolysaccharide (LPS) from the GEO database. The relationship between EPB41L4A-AS1 and phospho-p65 was explored by western blot (WB) and immunofluorescence. The interactions between EPB41L4A-AS1 and myeloid differentiation factor 88 (MYD88) were also verified through quantitative real-time PCR, WB, and chromatin immunoprecipitation. Glycolysis and mitochondrial stress were detected by Seahorse.EPB41L4A-AS1 showed very low expression.Knockdown of EPB41L4A-AS1 led to the phosphorylation and nuclear translocation of p65 and thus activated the NF-kB signaling pathway; it also reduced the enrichment of H3K9me3 in the MYD88 promoter and increased expression of MYD88. Overall, EPB41L4A-AS1 knockdown promoted the level of glycolysis and ultimately enhanced the inflammatory response.These results demonstrate that EPB41L4A-AS1 is closely associated with inflammation in T2DM, and that low expression of EPB41L4A-AS1 may be used as an indicator of chronic inflammation and possible diabetic vascular complications in T2DM patients.	33505165	RID04794	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	TANAR	TWIST1	positively-E	mirPath;shRNA;RNA pull-down assay;ChIP;luciferase reporter assay	upregulation	microarray;qRT-PCR	TCGA;GSE69535	NA	cancer progression(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	TF	NA	NA	ENSG00000122691	NA	NA	7291	NA	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Androgen receptor promotes renal cell carcinoma (RCC)vasculogenic mimicry (VM) via altering TWIST1 nonsense-mediated decay through lncRNA-TANARBased on TCGA online database UALCAN,we found elevating TWIST1 levels led to a significantly lower survival rate in ccRCC patients.AR-mediated TANAR signals might play a crucial role in ccRCC VM formation and metastasis, and targeting this newly identified AR/TANAR/TWIST1 signaling may help in the development of a novel anti-angiogenesis therapy to better suppress the ccRCC progression. In this study, we identified a novel lncRNA-TANAR, as an AR-transcriptionally-regulated lncRNA, is able to promote TWIST1 mRNA stability by suppressing NMD via competitive binding with UPF1 to the TWIST1 mRNA 5'UTR.Intriguingly, previous studies showed that UPF1 mostly targets 3'-untranslated region of mRNA to exert NMD function [60] while TANAR binds to the 5'UTR region of the TWIST1 mRNA. To further validate the role of NMD in regulating TWIST1 mRNA, we scrutinized iCLIP-seq data and found 12 confirmed UPF1 protein-TWIST1 mRNA binding sites [26], partly overlapping with the predicted TANAR-TWIST1 mRNA interaction region. Based on our RIP assays and luciferase analyzes (Fig. 6a k), we show lncRNA-TANAR increases TWIST1 mRNA stability via directly binding to its 5'UTR with disruption of UPF1 initiating nonsense-mediate TWIST1 mRNA decay. This suggests a role of 5'UTR in regulating NMD likely through the loop formation between the 5'UTR and 3'UTR of mRNA. In conclusion, we characterized a new long noncoding RNA TANAR transcriptionally regulated by AR, which influences VM formation by decreasing TWIST1 mRNA nonsense-mediated decay. Targeting the AR/lncRNA- TANAR/TWIST1 axis could be a promising strategy for the development of better treatment of ccRCC.	33510354	RID04795	transcriptional regulation	metastasis		UP(SKCM);DATA(GSE38495)
Ischemic stroke	OIP5-AS1	C1QTNF3	positively-E	RIP;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-186-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000082196	NA	729082	114899	cyrano|linc-OIP5	2310005P21Rik|Corcs|Cors|Cors-26|CTRP3	Up-regulating lncRNA OIP5-AS1 protects neuron injury against cerebral hypoxia-ischemia induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5pWe observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis.Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	33516048	RID04796	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE86978)
Colorectal cancer	LINC00460	IGF2BP2	positively-F	siRNA;shRNA;immunohistochemistry;RNA pull-down assay;RIP;western blot;overexpression	upregulation	qRT-PCR	GSE40967	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	interact with mRNA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000073792	NA	728192	10644	NA	IMP-2|p62	LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modificationThe expression levels of LINC00460 were analyzed by using a tissue microarray containing 498 CRC tissues and their corresponding non-tumor adjacent tissues. The correlations between the LINC00460 expression level and clinicopathological features were evaluated. The functional characterization of the role and molecular mechanism of LINC00460 in CRC was investigated through a series of in vitro and in vivo experiments. LINC00460 expression was increased in human CRC, and high LINC00460 expression was correlated with poor five-year overall survival and disease-free survival. LINC00460 overexpression sufficiently induced the epithelial-sesenchymal transition and promoted tumor cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. In addition, LINC00460 enhanced the protein expression of high-mobility group AT-hook 1 (HMGA1) by directly interacting with IGF2BP2 and DHX9 to bind the 3'-untranslated region (UTR) of HMGA1 mRNA and increased the stability of HMGA1 mRNA. In addition, the N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC. Finally, it suggested that HMGA1 was essential for LINC00460-induced cell proliferation, migration, and invasion.	33526059	RID04797	interact with mRNA	metastasis		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Colorectal cancer	LINC00460	DHX9	positively-F	siRNA;shRNA;immunohistochemistry;RNA pull-down assay;RIP;western blot;overexpression	upregulation	qRT-PCR	GSE40967	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	interact with mRNA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000135829	NA	728192	1660	NA	DDX9|LKP|RHA	LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modificationThe expression levels of LINC00460 were analyzed by using a tissue microarray containing 498 CRC tissues and their corresponding non-tumor adjacent tissues. The correlations between the LINC00460 expression level and clinicopathological features were evaluated. The functional characterization of the role and molecular mechanism of LINC00460 in CRC was investigated through a series of in vitro and in vivo experiments. LINC00460 expression was increased in human CRC, and high LINC00460 expression was correlated with poor five-year overall survival and disease-free survival. LINC00460 overexpression sufficiently induced the epithelial-sesenchymal transition and promoted tumor cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. In addition, LINC00460 enhanced the protein expression of high-mobility group AT-hook 1 (HMGA1) by directly interacting with IGF2BP2 and DHX9 to bind the 3'-untranslated region (UTR) of HMGA1 mRNA and increased the stability of HMGA1 mRNA. In addition, the N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC. Finally, it suggested that HMGA1 was essential for LINC00460-induced cell proliferation, migration, and invasion.	33526059	RID04798	interact with mRNA	metastasis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	LINC00460	HMGA1	positively-E	knockdown;overexpression;RIP	upregulation	qRT-PCR	GSE40967	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000137309	NA	728192	3159	NA	HMGIY	LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modificationThe expression levels of LINC00460 were analyzed by using a tissue microarray containing 498 CRC tissues and their corresponding non-tumor adjacent tissues. The correlations between the LINC00460 expression level and clinicopathological features were evaluated. The functional characterization of the role and molecular mechanism of LINC00460 in CRC was investigated through a series of in vitro and in vivo experiments. LINC00460 expression was increased in human CRC, and high LINC00460 expression was correlated with poor five-year overall survival and disease-free survival. LINC00460 overexpression sufficiently induced the epithelial-sesenchymal transition and promoted tumor cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. In addition, LINC00460 enhanced the protein expression of high-mobility group AT-hook 1 (HMGA1) by directly interacting with IGF2BP2 and DHX9 to bind the 3'-untranslated region (UTR) of HMGA1 mRNA and increased the stability of HMGA1 mRNA. In addition, the N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC. Finally, it suggested that HMGA1 was essential for LINC00460-induced cell proliferation, migration, and invasion.	33526059	RID04799	transcriptional regulation	metastasis		DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Atherosclerosis	XIST	PAPPA	positively-E	dual-luciferase reporter assay;Immunoprecipitation;RNA pull-down assay;siRNA	downregulation	qPCR	NA	NA	cell proliferation(+);inflammatory response(-);apoptosis process(-)	ceRNA(miR-98-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000182752	NA	7503	5069	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ASBABP2|DIPLA1|IGFBP-4ase|PAPA|PAPP-A|PAPPA1	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECsThe real-time quantitative polymerase chain reaction (qPCR) was used to determine alpha-smooth muscle actin, smooth muscle protein 22-alpha, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5pinduced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.	33542956	RID04800	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC);DOWN(PAAD);DATA(GSE117623,GSE40174)
Acute myeloid leukemia	HOTAIR	WT1	positively-E	western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell cycle(-);chemoresistance(+)	ceRNA(miR-20a-5p)	regulation	NA	Adriamycin	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000184937	NA	100124700	7490	HOXC-AS4|HOXC11-AS1|NCRNA00072	AWT1|GUD|NPHS4|WAGR|WIT-2	[Curcumin attenuates Adriamycin-resistance of acute myeloid leukemia by inhibiting the lncRNA HOTAIR/miR-20a-5p/WT1 axis.]This study aimed to investigate the mechanism by which curcumin affects the resistance of AML to Adriamycin by regulating HOX transcript antisense RNA (HOTAIR) expression. Cell viability, colony-formation, flow cytometry, and Transwell assays were used to assess cell proliferation, apoptosis, and migration. A dual-luciferase reporter assay was used to verify the interaction between microRNA (miR)-20a-5p and HOTAIR or Wilms' tumor 1 (WT1). RT-qPCR and western blot assays were performed to detect gene and protein expression. The results showed that curcumin suppressed the resistance to Adriamycin, inhibited the expression of HOTAIR and WT1, and promoted the expression of miR-20a-5p in human acute leukemia cells (HL-60) or Adriamycin-resistant HL-60 cells (HL-60/ADR). Furthermore, curcumin suppressed proliferation and promoted apoptosis of HL-60/ADR cells. Overexpression of HOTAIR reversed the regulatory effect of curcumin on apoptosis and migration and restored the effect of curcumin on inducing the expression of cleaved caspase3, Bax, and P27. In addition, HOTAIR upregulated WT1 expression by targeting miR-20a-5p, and inhibition of miR-20a-5p reversed the regulation of Adriamycin resistance by curcumin in AML cells. Finally, curcumin inhibited Adriamycin resistance by suppressing the HOTAIR/miR-20a-5p/WT1 pathway in vivo. In short, curcumin suppressed the proliferation and migration, blocked the cell cycle progression of AML cells, and sensitized AML cells to Adriamycin by regulating the HOTAIR/miR-20a-5p/WT1 axis. These findings suggest a potential role of curcumin and HOTAIR in AML treatment.	34282279	RID04801	ceRNA or sponge	chemoresistance		UP(LIHC);DATA(GSE117623)
Endometrial cancer	LINC01224	AKT3	positively-E	western blotLuciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-485-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000269416	GRCh38_19:23399097-23416075	ENSG00000117020	NA	104472717	10000	NA	PKBG|PRKBG|RAC-gamma	[Long non-coding RNA LINC01224 promotes cell proliferation and inhibits apoptosis by regulating AKT3 expression via targeting miR-485-5p in endometrial carcinoma]A total of 50 pairs of tumor and adjacent normal tissue from patients with EC, three EC cell lines and one human normal endometrial stromal cell (ESC) line were subjected to reverse transcription-quantitative PCR assay to evaluate the expression levels of LINC01224. Cell Counting Kit-8, colony formation and flow cytometry assays were used to assess cell proliferation and apoptosis. western blot was used to measure expression levels of apoptosis- and proliferation-associated proteins and AKT3 protein. A xenograft model of HEC1A cells was established to validate the in vivo function of LINC01224 in EC tumor growth. Starbase 3.0 database prediction and luciferase reporter and RNA pull-down assays were performed to verify the binding sites between LINC01224 and microRNA (miR)-485-5p and miR-485-5p and AKT3. LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. The upregulation of LINC01224 was negatively associated with survival of patients with EC. Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells; LINC01224 directly bound to and downregulated miR-485-5p to elevate the expression levels of AKT3, thereby promoting EC progression. LINC01224 depletion in EC cells hindered tumor growth in a xenograft model. The tumor suppressing effect of LINC01224-knockdown on EC progression was partly rescued by treatment with miR-485-5p inhibitor. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR-485-5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.	34278482	RID04802	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Glioma	TCONS_00004099	PTPRF	positively-E	western blot	upregulation	PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	ceRNA(miR-TCONS_00004099)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000142949	NA	NA	5792	NA	LAR	[LncRNA TCONS_00004099-derived microRNA regulates oncogenesis through PTPRF in gliomas.]western blots were carried out to verify the mechanisms related to PTPRF (Protein Tyrosine Phosphatase Receptor Type F). LncRNA TCONS_00004099 was significantly increased in glioma tissues and glioma cell lines. A novel miRNA (miRNA TCONS_00004099) derived from the lncRNA was identified by qPCR. Knockdown of this lncRNA suppressed cell proliferation, migration, invasion and enhanced TMZ-induced apoptosis in U87 and U251 cell lines  in vitro  and  in vivo . The miRNA mimics or inhibitor of miRNA TCONS_00004099 was used to reverse the effects of knockdown or overexpression of lncRNA TCONS_00004099, respectively. western blot verified that PTPRF is one of the downstream targets of lncRNA TCONS_00004099. These results demonstrated that lncRNA TCONS_00004099 promoted malignant behaviors in gliomas, including proliferation, metastasis, and anti-apoptosis. The effect of lncRNA TCONS_00004099 was mediated through miRNA TCONS_00004099 and its target PTPRF. Thus, the lncRNA TCONS_00004099/miRNA/PTPRF axis may be a potential therapeutic target for gliomas.	34277823	RID04803	ceRNA or sponge	metastasis		UP(LIHC,NSCLC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Esophagus squamous cell carcinoma	THAP9-AS1	SGMS2	positively-E	western blot;RNA pull-down assay ;dual-luciferase reporter assay;RNA immunoprecipitation (RIP) assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);epithelial to mesenchymal transition(-);apoptosis process(+)	ceRNA(miR-335-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251022	GRCh38_4:82893009-82900960	ENSG00000164023	NA	100499177	166929	NA	MGC26963|SMS2	[LncRNA THAP9-AS1 accelerates cell growth of esophageal squamous cell carcinoma through sponging miR-335-5p to regulate SGMS2.] We discovered that THAP9-AS1 was highly expressed in ESCC cell lines and that the knockdown of THAP9-AS1 inhibited proliferation, migration, and invasion as well as EMT of ECSS cells but enhanced cell apoptosis. Furthermore, miR-335-5p was proved to be sponged by THAP9-AS1 and its up-regulation could repress ESCC progression. Additionally, SGMS2 was verified to be the target gene of miR-335-5p. In rescue assay, SGMS2 overexpression could offset the suppressive role of THAP9-AS1 depletion on ESCC progression. In short, THAP9-AS1 accelerated cell growth of ESCC through sponging miR-335-5p to regulate SGMS2.	34273804	RID04804	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367,GSE86978)
Non-syndromic cleft lip and palate	ZFAS1	WNT	negatively-E	RNA pull-down assay-;RNA pull-down assay;RNA Immunoprecipitation Assay;western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	beta-catenin signaling pathway(-);cell proliferation(-);cell migration(-);cell differentiation(-)	NA	regulation	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Syndrome	Orofacial cleft	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	[SP1-Mediated Upregulation of Long Noncoding RNA ZFAS1 Involved in Non-syndromic Cleft Lip and Palate via Inactivating WNT/beta-Catenin Signaling Pathway.]This study aimed to investigate how dysregulated lncRNAs contribute to NSCLP. Using lncRNA sequencing, bioinformatics analysis, and clinical tissue sample detection, we identified that lncRNA ZFAS1 was significantly upregulated in NSCLP. The upregulation of ZFAS1 mediated by SP1 transcription factor (SP1) inhibited expression levels of Wnt family member 4 ( WNT4 ) through the binding with CCCTC-binding factor (CTCF), subsequently inactivating the WNT/beta-catenin signaling pathway, which has been reported to play a significant role on the development of lip and palate. Moreover,  in vitro , the overexpression of ZFAS1 inhibited cell proliferation and migration in human oral keratinocytes and human umbilical cord mesenchymal stem cells (HUC-MSCs) and also repressed chondrogenic differentiation of HUC-MSCs.  In vivo , ZFAS1 suppressed cell proliferation and numbers of chondrocyte in the zebrafish ethmoid plate. In summary, these results indicated that ZFAS1 may be involved in NSCLP by affecting cell proliferation, migration, and chondrogenic differentiation through inactivating the WNT/beta-catenin signaling pathway.	34268302	RID04805	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Liver cancer	LOXL1-AS1	NFIB	positively-E	western blotstarBase database;RNA pull-down assay;Luciferase reporter assays	upregulation	RT-qPCR	NA	NA	glucose metabolic process(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-377-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000147862	NA	100287616	4781	NA	NFI-RED|NFIB2|NFIB3	[lncRNA LOXL1-AS1 promotes liver cancer cell proliferation and migration by regulating the miR-377-3p/NFIB axis.] In the present study, LOXL1-AS1 expression was significantly upregulated in liver cancer tissues and cells compared with in normal liver tissues and cells, respectively. High LOXL1-AS1 expression was associated with poor clinical outcomes in patients with liver cancer. Furthermore, LOXL1-AS1-knockdown suppressed glucose metabolism, proliferation, migration and epithelial-mesenchymal transition (EMT) of liver cancer cells. Subsequently, LOXL1-AS1 acted as a microRNA (miR)-377-3p sponge, and nuclear factor I B (NFIB) was confirmed as the downstream target of miR-377-3p in liver cancer cells. Additionally, rescue assays suggested that NFIB overexpression countervailed the inhibitory influence of LOXL1-AS1 silencing on liver cancer cellular processes. The present study demonstrated that LOXL1-AS1 promoted glucose metabolism, proliferation, migration and EMT of liver cancer cells by sponging miR-377-3p and modulating NFIB, which may provide a novel insight for the treatment of liver cancer.	34267816	RID04806	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Oral squamous cell carcinoma	HOXA-AS2	CDK8	positively-E	Luciferase report assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-567)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000132964	NA	285943	1024	HOXA3as	K35	[LncRNA HOXA-AS2 Promotes Tumor Progression by Suppressing miR-567 Expression in Oral Squamous Cell Carcinoma.]LncRNA HOXA-AS2 Promotes Tumor Progression by Suppressing miR-567 Expression in Oral Squamous Cell Carcinoma.Growing evidence suggests that long non-coding RNAs (lncRNAs), such as lncRNA HOXA-AS2, are critical regulators involved in human cancer. However, the biological functions and detailed mechanisms underlying how lncRNA HOXA-AS2 affects oral squamous cell carcinoma (OSCC) remain unexplored. The expression of lncRNA HOXA-AS2 and miR-567 was determined in OSCC cell lines and clinical tissues by quantitative real-time PCR (qRT-PCR. Target site prediction and luciferase report assays were used to explore their potential interaction and binding sites between lncRNA HOXA-AS2 and miR-567. Overexpression or silencing expression of lncRNA HOXA-AS2 was performed to confirm that miR-567 was suppressed by lncRNA HOXA-AS2. WST-1 assay, crystal staining assay, and cell cycle analysis were used to assess the cell viability and proliferation ability. The target gene of miR-567 was predicted by Targetscan and validated by luciferase report assay as well as qRT-PCRand western blot. Xenograft nude mice model was done to demonstrate that lncRNA HOXA-AS2 promoted cell proliferation via targeting miR-567/CDK8 in vivo. LncRNA HOXA-AS2 was up-regulated in OSCC cells and tissues with the expression of miR-567 decreased. The tissue lncRNA HOXA-AS2 expression was found to positively correlate with the TNM stage and lymph node metastasis of OSCC patients. In terms of the mechanism, we found that lncRNA HOXA-AS2 negatively regulates miR-567 expression via a direct interaction. Functionally, overexpression of lncRNA HOXA-AS2 significantly promoted OSCC cell proliferation, while knockdown of lncRNA HOXA-AS2 significantly inhibited it. We also observed that miR-567 directly targets the 3' UTR of CDK8. Moreover, silencing lncRNA HOXA-AS2 inhibited tumor growth with the expression of miR-567 increased and CDK8 decreased in vivo. LncRNA HOXA-AS2 was up-regulated in OSCC, and its up-regulation correlated with poor clinical outcomes. The lncRNA also promoted OSCC cell proliferation by directly binding to miR-567, leading to an increase in CDK8 expression. The potential prognostic value of lncRNA HOXA-AS2 should be explored in future studies.	34267554	RID04807	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Nasopharynx carcinoma	FAM225B	CCND2	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-613)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000225684	GRCh38_9:113102117-113111543	ENSG00000118971	NA	100128385	894	C9orf110|LINC00256B|NCRNA00256B	NA	[Long noncoding RNA FAM225B facilitates proliferation and metastasis of nasopharyngeal carcinoma cells by regulating miR-613/CCND2 axis.]Growing evidence has suggested that abnormally expressed long non-coding RNAs (lncRNAs) play critical regulatory roles in nasopharyngeal carcinoma (NPC) pathogenesis. Family with sequence similarity 225 member B (FAM225B) is a novel lncRNA that has been implicated in several human cancers, yet its role in the context of NPC remains largely unclear. The aim of this study was to determine the expression level of FAM225B and its clinical significance in NPC patients. We observed a remarkable increase of FAM225B in NPC tissues and cell lines compared with controls. Also, highly expressed FAM225B was closely correlated with advanced TNM stage, distant metastasis, and poor overall survival. Interestingly, loss-of-function analysis revealed that FAM225B knockdown significantly inhibited tumor growth in vitro and in vivo, and decreased the migratory and invasive capacity of NPC cells. Mechanically, FAM225B functioned as an endogenous sponge by competing for miR-613 binding to up-regulate CCND2 expression. More importantly, rescue experiments further demonstrated that the suppressive impacts of FAM225B knockdown on cell proliferation, migration and invasion were significantly reversed after CCND2 overexpression. Taken all together, these findings highlight FAM225B as an oncogene that promotes NPC proliferation and metastasis through miR-613/CCND2 axis.	34255617	RID04808	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Colon cancer	NEAT1	BACH1	negatively-E		downregulation		NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000156273	NA	283131	571	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BACH-1|BTBD24	[Long non-coding RNA NEAT1 absorbs let-7 g-5p to induce epithelial-mesenchymal transition of colon cancer cells through upregulating BACH1.]Long noncoding RNAs (lncRNAs) are critical regulators in diverse human cancers. However, the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in colon cancer remains to be further investigated. We aimed to verify the role of NEAT1/let-7 g-5p/BTB and CNC homology 1 (BACH1) axis in colon cancer development. Expression of NEAT1, let-7 g-5p and BACH1 in colon cancer tissues and cells was determined. The interactions between NEAT1 and let-7 g-5p, and between let-7 g-5p and BACH1 were assessed. The colon cancer cell lines were treated with plasmids or oligonucleotides to alter NEAT1, BACH1 and let-7 g-5p expression. Then, viability, migration, invasion, and apoptosis of colon cells were evaluated, and the cell growth in vivo was observed as well. NEAT1 and BACH1 were upregulated while let-7 g-5p was downregulated in colon cancer tissues and cells. NEAT1/BACH1 silencing or let-7 g-5p elevation suppressed colon cancer cell growth in vivo and in vitro. The effects of silenced NEAT1 on colon cancer cells and xenografts were reversed by downregulating let-7 g-5p. Down-regulation of BACH1 reversed the effect of NEAT1 overexpression on colon cancer cells. NEAT1 directly bound to let-7 g-5p and let-7 g-5p targeted BACH1. Downregulated NEAT1 elevated let-7 g-5p to suppress EMT of colon cancer cells through inhibiting BACH1. This research may contribute to treatment of colon cancer.	34238666	RID04809	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Colon cancer	NEAT1	let-7g-5p	positively-E		downregulation		NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	[Long non-coding RNA NEAT1 absorbs let-7 g-5p to induce epithelial-mesenchymal transition of colon cancer cells through upregulating BACH1.]Long noncoding RNAs (lncRNAs) are critical regulators in diverse human cancers. However, the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in colon cancer remains to be further investigated. We aimed to verify the role of NEAT1/let-7 g-5p/BTB and CNC homology 1 (BACH1) axis in colon cancer development. Expression of NEAT1, let-7 g-5p and BACH1 in colon cancer tissues and cells was determined. The interactions between NEAT1 and let-7 g-5p, and between let-7 g-5p and BACH1 were assessed. The colon cancer cell lines were treated with plasmids or oligonucleotides to alter NEAT1, BACH1 and let-7 g-5p expression. Then, viability, migration, invasion, and apoptosis of colon cells were evaluated, and the cell growth in vivo was observed as well. NEAT1 and BACH1 were upregulated while let-7 g-5p was downregulated in colon cancer tissues and cells. NEAT1/BACH1 silencing or let-7 g-5p elevation suppressed colon cancer cell growth in vivo and in vitro. The effects of silenced NEAT1 on colon cancer cells and xenografts were reversed by downregulating let-7 g-5p. Down-regulation of BACH1 reversed the effect of NEAT1 overexpression on colon cancer cells. NEAT1 directly bound to let-7 g-5p and let-7 g-5p targeted BACH1. Downregulated NEAT1 elevated let-7 g-5p to suppress EMT of colon cancer cells through inhibiting BACH2. This research may contribute to treatment of colon cancer.	34238667	RID04810	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Cervical cancer	DANCR	ZEB1	positively-E	western blot;dual-luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-145-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000148516	NA	57291	6935	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long non-coding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) participates in the development of diverse cancers. Nevertheless, the impact of DANCR on cervical cancer (CC) remains largely unknown. This study aims to explore the effects of DANCR sponging microRNA-145-3p (miR-145-3p) on CC. Expression of KLF5, DANCR, miR-145-3p, and zinc finger E-box binding homeobox 1 (ZEB1) in CC and adjacent normal tissues was determined. Human CC cell lines were, respectively, treated with silenced DANCR or miR145-3p mimic/inhibitor. Then, the viability, migration, invasion, and apoptosis of CC cells were measured. The cell growth  in vivo  was observed as well. Chromatin immunoprecipitation assay was performed to analyze the binding of KLF5 and DANCR promoter. Interaction among DANCR, miR-145-3p, and ZEB1 was assessed. KLF5, DANCR, and ZEB1 were upregulated but miR-145-3p was downregulated in CC tissues. KLF5 activated DANCR expression and the high DANCR expression was related to tumor staging, infiltrating muscle depth and lymphatic metastasis of CC patients. Reduced DANCR or elevated miR-145-3p repressed malignant behaviors of CC cells. The tumor diameter and weight were also repressed by DANCR silencing or miR-145-3p elevation. The effect of DANCR knockdown on CC cells could be reversed by miR-145-3p inhibitor. MiR-145-3p was targeted by DANCR and ZEB1 was targeted by miR-145-3p. KLF5-induced overexpression of DANCR promotes CC progression via suppressing miR-145-3p to target ZEB1. This study may provide potential targets for CC treatment.	34233586	RID04811	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic carcinoma	HCG11	MDM2	positively-E	western blot;Dual luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-579-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000135679	NA	493812	4193	bK14H9.3|FLJ14049|FLJ30357	HDM2|MGC5370	[LncRNA HCG11/miR-579-3p/MDM2 axis modulates malignant biological properties in pancreatic carcinoma via Notch/Hes1 signaling pathway.]Increasing reports have revealed that dysregulated expression of long non-coding RNAs (lncRNAs) is involved in pancreatic carcinoma progression. This study intends to explore the function and molecular mechanism of lncRNA HLA complex group 11 (HCG11) in pancreatic carcinoma. The expression profiles of HCG11 in pancreatic carcinoma samples were detected by qPCR. Bioinformatics analysis was applied to detect the associations among HCG11/miR-579-3p/MDM2. The malignant properties of pancreatic carcinoma cells were measured by numerous biological assays. Xenograft model was exploited to detect the effect of HCG11 on tumor growth. A significant increase of HCG11 was occurred in pancreatic carcinoma samples. Knockdown of HCG11 suppressed the progression of pancreatic carcinoma cells. Bioinformatics analysis revealed that HCG11 upregulated MDM2 expression by competitively targeting miR-579-3p. The rescue assays showed that miR-579-3p reversed cell behaviors caused by HCG11, and MDM2 reversed cell properties induced by miR-579-3p. The Notch1 intracellular domain (NICD) and Hes1 protein levels were increased by overexpression of HCG11/MDM2. The tumor growth was suppressed after depletion of HCG11, followed by suppressing Ki67, PCNA and Vimentin expression, increasing TUNEL-positive cells and E-cadherin expression. Our observations highlighted that HCG11 contributed to the progression of pancreatic carcinoma by promoting growth and aggressiveness, and inhibiting apoptosis via miR-579-3p/MDM2/Notch/Hes1 axis.	34230221	RID04812	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colon cancer	CYTOR	SERPINE1	positively-E	TCGA;lncATLAS;lncBase database;TargetScan ;miRWalk ;western blot assay;Dual-luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-378a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000106366	NA	112597	5054	C2orf59|LINC00152|MGC4677|NCRNA00152	PAI|PAI1|PLANH1	[LncRNA CYTOR drives L-OHP resistance and facilitates the epithelial-mesenchymal transition of colon carcinoma cells via modulating miR-378a-5p/SERPINE1.]Long non-coding RNAs (lncRNAs) play a vital regulatory role in many human cancers. However, their underlying effect and molecular mechanism in chemoresistance need to be fully researched. This study found that lncRNA CYTOR expression was significantly up-regulated in colon carcinoma tissue and cells. Silencing lncRNA CYTOR  in vitro  facilitated L-OHP sensitivity of colon carcinoma cells and restrained epithelial-mesenchymal transition (EMT). Furthermore, lncRNA CYTOR could inhibit miR-378a-5p expression, while suppressing miR-378a-5p could attenuate the inhibition of lncRNA CYTOR silencing on L-OHP resistance and EMT. The downstream target mRNA of miR-378a-5p was further explored, and it was discovered that miR-378a-5p restrained SERPINE1 expression. Rescue assay indicated that overexpressing miR-378a-5p or silencing SERPINE1 expression counteracted the promotion of lncRNA CYTOR overexpression on L-OHP resistance and EMT of colon carcinoma cells.  In vivo  experiment exhibited that silencing lncRNA CYTOR repressed colon carcinoma growth, while miR-378a-5p inhibition diminished the suppression of silencing lncRNA CYTOR on colon carcinoma. These results testified that lncRNA CYTOR enhanced L-OHP drug resistance and induced EMT in colon carcinoma. It was also suggested that lncRNA CYTOR/miR-378a-5p/SERPINE1 axis was a regulatory pathway of L-OHP resistance in colon carcinoma. They could be potential therapeutic targets and prognostic biomarkers. Abbreviations: ATG: autophagy related; EPG: ectopic PGL granules; GFP: green fluorescent protein; LGG-1: LC3, GABARAP and GATE-16 family; LPLA-2: lysosomal phospholipase A2; PGL: P granule abnormality protein; PLA2: phospholipase A2; SD: standard deviation; SEPA-1: suppressor of ectopic P granules in autophagy mutant; SQST-1: sequestosome related.	34224332	RID04813	ceRNA or sponge	chemoresistance,prognosis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Ovarian cancer	SDCBP2-AS1	EPDR1	positively-E	western blot assay;RIP;Dual luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell viability(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-100-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234684	GRCh38_20:1325400-1378735	ENSG00000086289	NA	100507495	54749	NA	EPDR|MERP-1|MERP1|UCC1	[Long non-coding RNA SDCBP2-AS1 delays the progression of ovarian cancer via microRNA-100-5p-targeted EPDR1.]Dysregulation of long non-coding RNAs has been implied to connect with cancer progression. This research was to decipher the mechanism of long non-coding RNA SDCBP2-AS1 in ovarian cancer (OC) through regulation of microRNA (miR)-100-5p and ependymin-related protein 1 (EPDR1). LncRNA SDCBP2-AS1 and EPDR1 levels in OC were assessed by Gene Expression Profiling Interactive Analysis. lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 levels in OC tissues and cells were determined. SKOV3 and A2780 cells were transfected with lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1-related plasmids or sequences, and then their functions in cell viability, apoptosis, migration, and invasion were evaluated. The interplay of lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 was clarified. LncRNA SDCBP2-AS1 and EPDR1 levels were suppressed whilst miR-100-5p level was elevated in OC. After upregulating lncRNA SDCBP2-AS1 or EPDR1, viability, migration, and invasion of OC cells were impaired, and apoptosis rate was increased. Downregulating EPDR1 or upregulating miR-100-5p partially mitigated upregulated lncRNA SDCBP2-AS1-induced impacts on the biological functions of OC cells. LncRNA SDCBP2-AS1 sponged miR-100-5p, and EPDR1 was targeted by miR-100-5p. It is illustrated that lncRNA SDCBP2-AS1 regulates EPDR1 by sponge adsorption of miR-100-5p to inhibit the progression of OC.	34218800	RID04814	ceRNA or sponge	NA	DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	MIR29B2CHG	miR-29c	negatively-E	UCSC	downregulation	qRT-PCR	NA	NA	cell migration(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000203709	GRCh38_1:207801518-207879115	NA	NA	100128537	NA	C1orf132|FLJ35650	NA	[Expression and Function of C1orf132 Long-Noncoding RNA in Breast Cancer Cell Lines and Tissues.]miR-29b2 and miR-29c play a suppressive role in breast cancer progression.  C1orf132  (also named  MIR29B2CHG ) is the host gene for generating both microRNAs. However, the region also expresses longer transcripts with unknown functions. We employed bioinformatics and experimental approaches to decipher  C1orf132  expression and function in breast cancer tissues. We also used the CRISPR/Cas9 technique to excise a predicted  C1orf132  distal promoter and followed the behavior of the edited cells by real-time PCR, flow cytometry, migration assay, and RNA-seq techniques. We observed that  C1orf132  long transcript is significantly downregulated in triple-negative breast cancer. We also identified a promoter for the longer transcripts of  C1orf132  whose functionality was demonstrated by transfecting MCF7 cells with a  C1orf132  promoter-GFP construct. Knocking-out the promoter by means of CRISPR/Cas9 revealed no alterations in the expression of the neighboring genes  CD46  and  CD34 , while the expression of miR-29c was reduced by half. Furthermore, the promoter knockout elevated the migration ability of the edited cells. RNA sequencing revealed many up- and downregulated genes involved in various cellular pathways, including epithelial to mesenchymal transition and mammary gland development pathways. Altogether, we are reporting here the existence of an additional/distal promoter with an enhancer effect on miR-29 generation and an inhibitory effect on cell migration.	34201896	RID04815	expression association	NA		
Osteoarthritis	MIR22HG	ADAMTS5	positively-E	western blot;Targetscan ;Luciferase Reporter Assay;RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-9-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000154736	NA	84981	11096	C17orf91|DKFZp686O06159|MGC14376	ADAMTS11|ADMP-2	[LncRNA MIR22HG promotes osteoarthritis progression via regulating miR-9-3p/ADAMTS5 pathway.]Dysregulation of long non-coding RNAs (lncRNAs) plays a fundamental role in the development and progression of osteoarthritis (OA), but the potential functions of lncRNAs in OA were not fully clarified. In the present work, we want to clarify the underlying functions and mechanisms of MIR22HG in OA. qRT-PCRwas employed to detect the mRNA expression of MIR22HG, miR-9-3p, and ADAMTS5, while the protein expressions were measured using western blot. The cell proliferation was examined through CCK8, while apoptosis was used in flow cytometry. Luciferase reporter assay and RNA immunoprecipitation (RIP) assays were undertaken to investigate the binding relationship among MIR22HG, ADAMTS5, and miR-9-3p. MIR22HG was significantly overexpressed in OA cartilages, OA chondrocytes and IL-1beta-induced chondrocytes. Functionally, MIR22HG knockdown promoted cell proliferation, suppressed apoptosis, and contributed to downregulation of MMP13 and ADAMTS5 and upregulation of COL2A1 and ACAN in IL-1beta-stimulated chondrocytes. Mechanistically, bioinformatic analysis indicated that MIR22HG may serve as a sponge for miR-9-3p and ADAMTS5 may be a potential targeted gene for miR-9-3p, which were subsequently verified through a dual-luciferase reporter assay. Moreover, rescue experiments showed that MIR22HG participated in the regulation of chondrocytes proliferation, apoptosis, and degradation of extracellular matrix via miR-9-3p/ADAMTS5 pathway. In conclusion, our findings illuminated that inhibition of MIR22HG ameliorated IL-1beta-induced apoptosis and ECM degradation of human chondrocytes through miR-9-3p/ADAMTS5 pathway, which may provide a potentially promising target for OA treatment.	34187303	RID04816	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC);DATA(GSE117623)
Triple-negative breast cancer	BRE-AS1	miR-21	negatively-E	RNA pull-down assay;RIP assay;western blot analysis	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	ENSG00000199004	NA	NA	NA	NA	NA	[Long non-coding RNA BRE-AS1 inhibits the proliferation, migration, and invasion of cancer cells in triple-negative breast cancer and predicts patients' survival by downregulating miR-21.]Results: BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21 suppressed the role of BRE-AS1 in cancer cell behaviors.Conclusion: Therefore, BRE-AS1 may inhibit TNBC by downregulating miR-21.	34182945	RID04817	expression association	NA		
Gastric cancer	SNHG1	SOCS2	positively-E	western blot;RIP	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000120833	NA	23642	8835	LINC00057|lncRNA16|NCRNA00057|UHG	CIS2|Cish2|SOCS-2|SSI-2|SSI2|STATI2	[Long non-coding RNA SNHG1 suppresses cell migration and invasion and upregulates SOCS2 in human gastric carcinoma.]Gastric carcinoma (GC) is one of the most common malignancies and the third leading cause of cancer-related deaths worldwide. Long noncoding RNAs (lncRNAs) may be an important class of functional regulators involved in human gastric cancers development. In this study, we investigated the clinical significance and function of lncRNA SNHG1 in GC. SNHG1 was significantly downregulated in GC tumor tissues compared with adjacent noncancerous tissues. Overexpression of SNHG1 in BGC-823 cells remarkably inhibited not only cell proliferation, migration, invasion in vitro, but also tumorigenesis and lung metastasis in the chick embryo chorioallantoic membrane (CAM) assay in vivo. Conversely, inhibition of SNHG1 by transfection of siRNA in AGS cells resulted in opposite phenotype changes. Mechanically, SNHG1 was found interacted with ILF3, NONO and SFPQ. RNA-seq combined with bioinformatic analysis identified a serial of downstream genes of SNHG1, including SOCS2, LOXL2, LTBP3, LTBP4. Overexpression of SNHG1 induced SOCS2 expression whereas knockdown of SNHG1 decreased SOCS2 expression. In addition, knockdown of SNHG1 promoted the activation of JAK2/STAT signaling pathway. Taken together, our data suggested that SNHG1 suppressed aggressive phenotype of GC cells and regulated SOCS2/JAK2/STAT pathway.	34179518	RID04818	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Endometrial cancer	DLEU2	HK2	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);glycolysis(+)	ceRNA(miR-455)	regulation	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000159399	NA	8847	3099	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	NA	[Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway.]Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined. We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression. HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a. This study identified DLEU2 as an upstream activator of HK2-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.	34174908	RID04819	ceRNA or sponge	metastasis	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Endometrial cancer	DLEU2	EZH2	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);glycolysis(+)	NA	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000106462	NA	8847	2146	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	ENX-1|EZH1|KMT6|KMT6A	[Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway.]Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined. We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression. HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a. This study identified DLEU2 as an upstream activator of HK3-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.	34174909	RID04820	expression association	metastasis	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteoarthritis	KCNQ1OT1	TRPS1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell autophagy(-)	ceRNA(miR-126-5p)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000104447	NA	10984	7227	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	GC79|LGCR	[Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis.] Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic.	34108052	RID04821	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE67939)
Hypertensive disorder	NEAT1	miR-205-5p	negatively-F	western blot;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-RNA	Baicalin	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	[Baicalin enhances the proliferation and invasion of trophoblasts and suppresses vascular endothelial damage by modulating long non-coding RNA NEAT1/miRNA-205-5p in hypertensive disorder complicating pregnancy.]the production of reactive oxygen species (ROS) was determined by DCFH-DA staining. Furthermore, long non-coding RNA (lncRNA) NEAT1 and miRNA-205-5p levels were detected using real-time quantitative polymerase chain reaction and the binding relationship between lncRNA NEAT1 and miRNA-205-5p was verified by dual-luciferase reporter assay. Moreover, interactions among lncRNA NEAT1, miRNA-205-5p, and MMP9 or vascular endothelial growth factor (VEGF) were confirmed by RNA immunoprecipitation assay. Baicalin visibly improved cell viability, reduced the apoptosis of Ang II-stimulated HTR-8/SVneo and HUVEC cells, and repressed overproduction of ROS. Additionally, baicalin promoted the invasion of Ang II-stimulated HTR-8/SVneo cells and induced a stronger in vitro angiogenesis of Ang II-stimulated HUVECs. What's more, baicalin upregulated lncRNA NEAT1 expression and downregulated miR-205-5p expression. LncRNA NEAT1 sponged miR-205-5p and inhibited the combination of miR-205-5p and MMP9 or VEGF. Baicalin can facilitate the proliferation and invasion of trophoblasts and alleviate vascular endothelial damage by upregulating lncRNA NEAT1 to impede the interaction between miR-205-5p and MMP9 or VEGF.	34101306	RID04822	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Oral cavity cancer	HAR1A	ALPK1	positively-E	western blot	downregulation	microarray;RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000225978	GRCh38_20:63102205-63104386	ENSG00000073331	NA	768096	80216	HAR1F|LINC00064|NCRNA00064	FLJ22670|KIAA1527|Lak	[Long noncoding RNA HAR1A regulates oral cancer progression through the alpha-kinase 1, bromodomain 7, and myosin IIA axis.] The inflammatory and epithelial-to-mesenchymal transition marker expressions were analyzed using enzyme-linked immunosorbent assay and western blot. Phenotypic experiments were verified by colony formation assay, transwell migration assay, and Annexin V-apoptotic assay. In the nuclei of cancer cells, HAR1A functions upstream of signaling pathways and knockdown of HAR1A promoted ALPK1 expression and downregulated BRD7 resulting in inflammation and oral cancer progression. In monocytes, the expressions of TNF-alpha and CCL2 were increased following HAR1A knockdown and reduced following ALPK1 knockdown. HAR1A knockdown upregulated the expression of ALPK1, slug, vimentin, fibronectin, and N-cadherin but reduced the expression of E-cadherin in oral cancer cells. Myosin IIA was primarily located in the cytoplasm and that its decrease in the nuclei of oral cancer cells was likely to demonstrate suppressive ability in late-stage cancer. Our findings suggest that the HAR1A, BRD7, and myosin IIA are tumor suppressors while ALPK1 has oncogene-like property in the nucleus and is involved in inflammation and oral cancer progression. More research for HAR1A activators or ALPK1 inhibitors is required to develop potential therapeutic agents for advanced oral cancer. KEY MESSAGES: lncRNA HAR1A, BRD7, and myosin IIA are tumor suppressors whereas ALPK1 has an oncogenic-like property in the nucleus. lncRNA HAR1A/ALPK1/BRD7/myosin IIA axis plays a critical role in the progression of oral cancer. lncRNA HAR1A localizes upstream of signaling pathways to inhibit ALPK1 expression and then upregulated BRD7. lncRNA HAR1A and ALPK1 are involved in cancer progression via epithelial-to-mesenchymal transition regulations. ALPK1 inhibitors are potential kinase-targeted therapeutic agents for patients with advanced oral cancer.	34097087	RID04823	expression association	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral cavity cancer	HAR2A	BRD7	negatively-E	western blot	downregulation	microarray;RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	NA	NA	ENSG00000166164	NA	NA	29117	NA	BP75|CELTIX1|SMARCI1	[Long noncoding RNA HAR1A regulates oral cancer progression through the alpha-kinase 1, bromodomain 7, and myosin IIA axis.] The inflammatory and epithelial-to-mesenchymal transition marker expressions were analyzed using enzyme-linked immunosorbent assay and western blot. Phenotypic experiments were verified by colony formation assay, transwell migration assay, and Annexin V-apoptotic assay. In the nuclei of cancer cells, HAR1A functions upstream of signaling pathways and knockdown of HAR1A promoted ALPK1 expression and downregulated BRD7 resulting in inflammation and oral cancer progression. In monocytes, the expressions of TNF-alpha and CCL2 were increased following HAR1A knockdown and reduced following ALPK1 knockdown. HAR1A knockdown upregulated the expression of ALPK1, slug, vimentin, fibronectin, and N-cadherin but reduced the expression of E-cadherin in oral cancer cells. Myosin IIA was primarily located in the cytoplasm and that its decrease in the nuclei of oral cancer cells was likely to demonstrate suppressive ability in late-stage cancer. Our findings suggest that the HAR1A, BRD7, and myosin IIA are tumor suppressors while ALPK1 has oncogene-like property in the nucleus and is involved in inflammation and oral cancer progression. More research for HAR1A activators or ALPK1 inhibitors is required to develop potential therapeutic agents for advanced oral cancer. KEY MESSAGES: lncRNA HAR1A, BRD7, and myosin IIA are tumor suppressors whereas ALPK1 has an oncogenic-like property in the nucleus. lncRNA HAR1A/ALPK1/BRD7/myosin IIA axis plays a critical role in the progression of oral cancer. lncRNA HAR1A localizes upstream of signaling pathways to inhibit ALPK1 expression and then upregulated BRD7. lncRNA HAR1A and ALPK1 are involved in cancer progression via epithelial-to-mesenchymal transition regulations. ALPK2 inhibitors are potential kinase-targeted therapeutic agents for patients with advanced oral cancer.	34097088	RID04824	expression association	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Ovarian cancer	ACTA2-AS1	CXCL2	positively-E	dual-luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	ceRNA(miR-532-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000081041	NA	100132116	2920	UC001kfo|uc001kfo.1|ZXF1	CINC-2a|GRO2|GROb|MGSA-b|MIP-2a|SCYB2	[Mechanism underlying the regulation of lncRNA ACTA2-AS1 on CXCL2 by absorbing miRNA-532-5p as ceRNA in the development of ovarian cancer.]To explore the mechanism underlying the regulation of long non-coding RNA (LncRNA) ACTA2-AS1 on CXCL2 as a ceRNA of miR-532-5p in the progression of ovarian cancer (OC). A qRT-PCRassay was carried out for analyzing the expression changes of ACTA2-AS1, miR-532-5p, as well as CXCL2 in OC tissues and corresponding healthy paracancerous tissues HOSEpiC (human ovarian epithelial cells), and OC cells. OC cells were grouped and transfected, and the fluorescent in situ hybridization was adopted for evaluating ACTA2-AS1 in the cells. Additionally, a dual luciferase reporter (DLR) assay was carried out for verifying the correlation of ACTA2-AS1 with miR-532-5p and of miR-532-5p with CXCL2. Cells were transfected with si-ACTA2-AS1, miR-532-5p, or CXCL2 overexpression plasmids, and then the cell proliferation, invasion, and apoptosis were determined using MTT, Transwell, and flow cytometry assays, respectively. Compared with paracancerous tissues and HOSEpiC cells, OC tissues and cells showed increased ACTA2-AS1 and CXCL2 expression and decreased miR-532-5p expression (all P<0.05). ACTA2-AS1 acted as ceRNA in OC by negatively regulating miR-532-5p. Additionally, upregulating ACTA2-AS1 intensified the proliferation and invasion of cancer cells and suppressed their apoptosis (all P<0.05), and inhibition of it resulted in opposite results. In contrast, overexpressing miR-532-5p suppressed the proliferation, invasion, and clone formation of the cells and promoted their apoptosis (all P<0.05). The effect of ACTA2-AS1 on OC cells can be partially reversed by overexpressing miR-532-5p. Moreover, CXCL2, positively correlated with ACTA2-AS1 in expression (P<0.0001, r=0.7385), was the target of miR-532-5p, and its overexpression could partially offset the influence of miR-532-5p on OC cells. LncRNA ACTA2-AS1 can act as a tumor promoter in OC by absorbing miR-532-5p as ceRNA and regulating CXCL2, and ACTA2-AS1 inhibitor is expected to play a role in targeted therapy of OC.	34093945	RID04825	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	
Hepatocellular carcinoma	W42	DBN1	positively-E	RNA immunoprecipitation;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000113758	NA	NA	1627	NA	D0S117E	[Upregulation of long noncoding RNA W42 promotes tumor development by binding with DBN1 in hepatocellular carcinoma. ]We measured the expression of lncRNA W42 in HCC tissues and cells (Huh7 and SMMC-7721) by quantitative reverse transcriptase polymerase chain reaction. Receiver operating characteristic curves were used to assess the sensitivity and specificity of lncRNA W42 expression. HCC cells were transfected with pcDNA3.1-lncRNA W42 or shRNA-lncRNA W42. Cell functions were detected by cell counting Kit-8 (CCK-8), colony formation, flow cytometry and Transwell assays. The interaction of lncRNA W42 and DBN1 was confirmed by RNA immunoprecipitation and RNA pull-down assays. An HCC xenograft model was used to assess the role of lncRNA W42 on tumor growth  in vivo . The Kaplan-Meier curve was used to evaluate the overall survival and recurrence-free survival after surgery in patients with HCC. In this study, we identified a novel lncRNA (lncRNA W42), and investigated its biological functions and clinical significance in HCC. LncRNA W42 expression was upregulated in HCC tissues and cells. Overexpression of lncRNA W42 notably promoted the proliferative and invasion of HCC, and inhibited cell apoptosis. LncRNA W42 directly bound to DBN1 and activated the downstream pathway. LncRNA W42 knockdown suppressed HCC xenograft tumor growth  in vivo . The clinical investigation revealed that HCC patients with high lncRNA W42 expression exhibited shorter survival times. In vitro  and  in vivo  results suggested that the novel lncRNA W42, which is upregulated in HCC, may serve as a potential candidate prognostic biomarker and therapeutic target in HCC patients.	34092977	RID04826	interact with protein	recurrence,prognosis,metastasis		DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827)
Septic acute kidney injury	PVT1	miR-17-5p	negatively-F	western blot;dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell viability(-);inflammatory response(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	[LncRNA PVT1 accelerates LPS-induced septic acute kidney injury through targeting miR-17-5p and regulating NF-kB pathway.]The septic AKI model was constructed through lipopolysaccharide (LPS) treatment. PVT1 and miR-17-5p levels were measured using qRT-PCRanalysis. The concentrations of inflammatory cytokines were determined with ELISA kits. Cell viability and apoptosis were assessed using CCK-8 assay and flow-cytometric analysis, respectively. Protein levels were examined using western blot assay. The targeting association between miR-17-5p and PVT1 was verified by dual-luciferase reporter, RIP and RNA pull-down assays. PVT1 level was elevated and miR-17-5p level was declined in septic AKI patients' serum and LPS-stimulated HK-2 cells. Cell viability was suppressed and cell apoptosis and inflammation were promoted after LPS treatment. PVT1 knockdown or miR-17-5p elevation restored LPS-mediated HK-2 cell injury. MiR-17-5p was sponged by PVT1, and its inhibition weakened the impact of PVT1 deficiency on LPS-mediated injury of HK-2 cells. In addition, PVT1 knockdown inactivated NF-kB pathway mediated by LPS treatment, but miR-17-5p inhibition further reversed this effect. PVT1 knockdown promoted cell viability, suppressed inflammatory response and apoptosis by regulating miR-17-5p expression and NF-kB pathway in LPS-stimulated HK-2 cells.	34089461	RID04827	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Cancer	E2F	LAPAS1	positively-E	knockdown		qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cancer	PCG	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	[A novel E2F1-regulated lncRNA, LAPAS1, is required for S phase progression and cell proliferation.]The transcription factor E2F1 induces both proliferation and apoptosis and is a critical downstream target of the tumor suppressor RB. Long non-coding RNAs (lncRNAs) are major regulators of many cellular processes, including cell cycle progression and cell proliferation. However, the mode of action as well as the transcriptional regulation of most lncRNAs are only beginning to be understood. Here, we report that a novel human lncRNA, LAPAS1, is an E2F1- regulated lncRNA that affects S phase progression. Inhibition of LAPAS1 expression increases percentage of S phase cells, and its silencing in synchronized cells delays their progression through S phase. In agreement with its suggested role in cell cycle progression, prolonged inhibition of LAPAS1 attenuates proliferation of human cancer cells. Our data demonstrate that LAPAS1 predominantly functions in trans to repress expression of Sphingolipid Transporter 2 (SPNS2). Importantly, knockdown of SPNS2 rescues the effect of LAPAS1 silencing on cell cycle and cell proliferation. Notably, low levels of LAPAS1 are associated with increased survival of kidney cancer patients. Summarily, we identify LAPAS1 as a novel E2F-regulated lncRNA that has a potential role in human cancer and regulates cell-cycle progression and cell proliferation, at least in part, via regulation of SPNS2.Our study shows that silencing the lncRNA LAPAS1 upregulates SPNS2 levels.	34084281	RID04828	transcriptional regulation	NA		
Cancer	LAPAS1	SPNS2	negatively-E	knockdown		qRT-PCR	NA	NA	cell proliferation(-)	transcriptional regulation	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000183018	NA	NA	124976	NA	SLC63A2	[A novel E2F1-regulated lncRNA, LAPAS1, is required for S phase progression and cell proliferation.]The transcription factor E2F1 induces both proliferation and apoptosis and is a critical downstream target of the tumor suppressor RB. Long non-coding RNAs (lncRNAs) are major regulators of many cellular processes, including cell cycle progression and cell proliferation. However, the mode of action as well as the transcriptional regulation of most lncRNAs are only beginning to be understood. Here, we report that a novel human lncRNA, LAPAS1, is an E2F1- regulated lncRNA that affects S phase progression. Inhibition of LAPAS1 expression increases percentage of S phase cells, and its silencing in synchronized cells delays their progression through S phase. In agreement with its suggested role in cell cycle progression, prolonged inhibition of LAPAS1 attenuates proliferation of human cancer cells. Our data demonstrate that LAPAS1 predominantly functions in trans to repress expression of Sphingolipid Transporter 2 (SPNS2). Importantly, knockdown of SPNS2 rescues the effect of LAPAS1 silencing on cell cycle and cell proliferation. Notably, low levels of LAPAS1 are associated with increased survival of kidney cancer patients. Summarily, we identify LAPAS1 as a novel E2F-regulated lncRNA that has a potential role in human cancer and regulates cell-cycle progression and cell proliferation, at least in part, via regulation of SPNS2.Our study shows that silencing the lncRNA LAPAS1 upregulates SPNS2 levels.	34084281	RID04829	transcriptional regulation	NA		DOWN(BRCA);DATA(GSE86978)
Hepatoblastoma	TUG1	miR-204-5p	negatively-F	western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	JAK2/STAT3 signaling pathway(+);angiogenesis(+)	transcriptional regulation	association	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	[lncRNA TUG1 regulates angiogenesis via the miR-204-5p/JAK2/STAT3 axis in hepatoblastoma]In recent decades, emerging evidence has proven that long non-coding RNAs (lncRNAs) serve an important oncogenic role in the pathogenesis of hepatoblastoma. However, the underlying mechanism of lncRNA taurine upregulated 1 (TUG1) in the angiogenesis of hepatoblastoma remains unknown. The expression patterns of TUG1 and microRNA (miR)-204-5p were detected in hepatoblastoma tissues and cell lines via reverse transcription-quantitative PCR and were analysed using a Pearson's correlation test. A tube formation assay was performed using human umbilical vein endothelial cells to assess the vasculogenic activity of treated HuH-6 cells. ELISA was used to detect the level of the secretory proangiogenic factor VEGFA in the culture media of HuH-6 cells. A dual-luciferase reporter assay was performed to validate the binding relationships of TUG1/miR-204-5p and miR-204-5p/Janus kinase 2 (JAK2). Moreover, western blot was conducted to measure the protein expression levels of VEGFA, phosphorylated (p)-JAK2, JAK2, p-STAT3 and STAT3. It was identified that TUG1 was upregulated, while miR-204-5p was downregulated in hepatoblastoma tissues and cells. TUG1 knockdown inhibited angiogenesis induced by hepatoblastoma cells. Furthermore, miR-204-5p was identified as a target of TUG1. The results demonstrated that TUG1 attenuated the inhibitory effect of miR-204-5p on the JAK2/STAT3 pathway and promoted angiogenesis in hepatoblastoma cells. In summary, TUG1 was upregulated in hepatoblastoma and suppressed miR-204-5p, thereby activating the downstream signalling pathway of JAK2/STAT3 to facilitate angiogenesis. The present findings will provide novel targets for the treatment of hepatoblastoma.Altogether, these data suggest that TINCR enhances cell growth and represses apoptosis through TCPTP.	34080023	RID04830	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Hepatocellular carcinoma	TINCR	PTPN2	positively-F	RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+);apoptosis process(-);cell migration(+);	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000175354	NA	257000	5771	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	PTPT|TC-PTP|TCELLPTP|TCPTP	Long non-coding RNA TINCR promotes hepatocellular carcinoma proliferation and invasion via STAT3 signaling by direct interacting with T-cell protein tyrosine phosphatase (TCPTP).The long non-coding RNAs (lncRNAs) participate in modulating numerous important cancer phenotypes via formation of RNA-protein complex. TINCR (terminal differentiation-induced lncRNA) modulates cancer cell behavior in many human malignancies, such as hepatocellular carcinoma (HCC). Herein, we proposed to investigate the underlying mechanism by which TINCR regulates HCC progression via formation of RNA-protein. RNA pull-down, LC-MS/MS, bioinformatics analysis, and RNA immunoprecipitation (RIP) assays were employed to identify TINCR-interacting protein TCPTP in HCC cells. The siRNAs for TINCR and TCPTP were transfected into HCC cells. The plasmids encoding full length or the 1-360 nt deletion of TINCR were generated and applied to cell transfection. The CCK-8, colony formation, EdU, wound healing along with transwell assays were employed to examine cell proliferation, apoptosis, migration, and infiltration. Real-time PCR, as well as western blot assays were employed to assess the levels of STAT3 phosphorylation and its target genes. We identified 1-360 nt region of TINCR, which directly bound with the phosphatase domain of TCPTP to inhibit its tyrosine phosphatase activity. Then, the results showed that the increasing of cell growth, migration, infiltration, and the reducing of apoptosis in TINCR-knockdown HCC cells was remarkably reversed with TCPTP silence. Additionally, 1-360 TINCR overexpression did not affect HCC cell growth, apoptosis, migration, infiltration, and STAT3 target genes expression. Our data revealed that TINCR directly bound TCPTP and suppressed the dephosphorylation of STAT3, thus promoting STAT3 activation and its downstream target genes in HCC progression and tumorigenicity.HighlightsLncRNA TINCR interacted with protein TCPTPLncRNA TINCR maintained STAT3 phosphorylationLncRNA TINCR affected STAT3 signaling in HCCAbbreviations:lncRNAs: long non-coding RNAs; TINCR: terminal differentiation-induced lncRNA; TCPTP: T cell protein tyrosine phosphatase; siRNA: small-interfering RNA; HCC: hepatocellular carcinoma; nt: nucleotide; LC-MS/MS: Liquid Chromatography - Tandem Mass Spectrometry; RIP: RNA immunoprecipitation; ANOVA: analysis of variance; EdU: 5-ethynyl-2'-deoxyuridine; real-time PCR: real-time polymerase chain reaction; CCK-8: cell counting kit-8; aa: amino acids; STAT3: signal transducer and activator of transcription	34057016	RID04831	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978,GSE41245)
Hepatocellular carcinoma	TINCR	STAT3	positively-E	RNA pull-down;RIP;	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell invasion(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000168610	NA	257000	6774	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	APRF	Long non-coding RNA TINCR promotes hepatocellular carcinoma proliferation and invasion via STAT3 signaling by direct interacting with T-cell protein tyrosine phosphatase (TCPTP).The long non-coding RNAs (lncRNAs) participate in modulating numerous important cancer phenotypes via formation of RNA-protein complex. TINCR (terminal differentiation-induced lncRNA) modulates cancer cell behavior in many human malignancies, such as hepatocellular carcinoma (HCC). Herein, we proposed to investigate the underlying mechanism by which TINCR regulates HCC progression via formation of RNA-protein. RNA pull-down, LC-MS/MS, bioinformatics analysis, and RNA immunoprecipitation (RIP) assays were employed to identify TINCR-interacting protein TCPTP in HCC cells. The siRNAs for TINCR and TCPTP were transfected into HCC cells. The plasmids encoding full length or the 1-360 nt deletion of TINCR were generated and applied to cell transfection. The CCK-8, colony formation, EdU, wound healing along with transwell assays were employed to examine cell proliferation, apoptosis, migration, and infiltration. Real-time PCR, as well as western blot assays were employed to assess the levels of STAT3 phosphorylation and its target genes. We identified 1-360 nt region of TINCR, which directly bound with the phosphatase domain of TCPTP to inhibit its tyrosine phosphatase activity. Then, the results showed that the increasing of cell growth, migration, infiltration, and the reducing of apoptosis in TINCR-knockdown HCC cells was remarkably reversed with TCPTP silence. Additionally, 1-360 TINCR overexpression did not affect HCC cell growth, apoptosis, migration, infiltration, and STAT3 target genes expression. Our data revealed that TINCR directly bound TCPTP and suppressed the dephosphorylation of STAT3, thus promoting STAT3 activation and its downstream target genes in HCC progression and tumorigenicity.HighlightsLncRNA TINCR interacted with protein TCPTPLncRNA TINCR maintained STAT3 phosphorylationLncRNA TINCR affected STAT3 signaling in HCCAbbreviations:lncRNAs: long non-coding RNAs; TINCR: terminal differentiation-induced lncRNA; TCPTP: T cell protein tyrosine phosphatase; siRNA: small-interfering RNA; HCC: hepatocellular carcinoma; nt: nucleotide; LC-MS/MS: Liquid Chromatography - Tandem Mass Spectrometry; RIP: RNA immunoprecipitation; ANOVA: analysis of variance; EdU: 5-ethynyl-2'-deoxyuridine; real-time PCR: real-time polymerase chain reaction; CCK-8: cell counting kit-8; aa: amino acids; STAT4: signal transducer and activator of transcription	34057017	RID04832	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	HCG11	BRMS1	positively-E	dual-luciferase reporter assay;starBase 2.0	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-942-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000174744	NA	493812	25855	bK14H9.3|FLJ14049|FLJ30357	DKFZP564A063	Long Noncoding RNA HCG11 Acts as a Tumor Suppressor in Gastric Cancer by Regulating miR-942-5p/BRMS1 Axis.The functions of long noncoding RNAs (lncRNAs) have been widely investigated in human cancers, including gastric cancer (GC). The purpose of this study was to elucidate the role of lncRNA HCG11 in GC. In this study, mRNA and protein expressions were detected by quantitative real-time polymerase chain reaction assays (RT-qPCR) and western blot The proliferation ability of GC<U+2009>cells was examined by (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyl Tetrazolium Bromide) MTT assays. The invasion and migration abilities of GC cells were evaluated by Transwell assays. The binding sites between miR-942-5p and HCG11/BRMS1 were confirmed by dual-luciferase reporter assays. Results showed that LncRNA HCG11 was downregulated in GC cells. Functionally, overexpression of HCG11 inhibited GC<U+2009>cell proliferation, migration, and invasion. In addition, lncRNA HCG11 was found to act as a molecular sponge of miR-942-5p. Furthermore, miR-942-5p promoted GC progression by suppressing lncRNA HCG11 expression. Besides that, BRMS1 was confirmed as a direct target of miR-942-5p. More importantly, breast cancer metastasis suppressor 1 (BRMS1) inhibited GC progression by upregulating lncRNA HCG11 and downregulating miR-942-5p. In conclusion, LncRNA HCG11 inhibited cell proliferation, migration, and invasion in GC by sponging miR-942-5p and upregulating BRMS1.	34054958	RID04833	ceRNA or sponge	metastasis	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Ovarian cancer	Rg3	H19	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	transcriptional regulation	association	protein-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	PCG	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Ginsenoside Rg3 suppresses ovarian cancer cell proliferation and invasion by inhibiting the expression of lncRNA H19.Ovarian cancer (OC) is the most malignant disease of the female reproductive system and accounts for a large proportion of gynecological cancer-related deaths. Emerging evidence has indicated that ginsenoside Rg3, one of the tetracyclic triterpenoid saponins in ginseng, plays crucial roles in regulating cancer progression, yet its role and mechanisms in regulating the proliferation and invasion of OC are still elusive. In this study, the cell viability, proliferation, migration and invasion of OC were assessed by using methyl thiazol tetrazolium (MTT), colony formation, wound healing and Transwell assays, respectively. The protein levels of E-cadherin and N-cadherin were analyzed by western blot assay. The expression of long noncoding RNA (lncRNA) H19 was analyzed by quantitative real-time polymerase chain reaction (RT-qPCR). The results revealed that ginsenoside Rg3 significantly inhibited the viability of OC cells (SKOV3 and A2780) in a concentration<U+2011>dependent manner. Ginsenoside Rg3 (50 ug/ml) had almost no significant effect on the activity of human ovarian epithelial cells (HOSEpiCs). Thus, this dose was selected for the subsequent experiments. Furthermore, Rg3 markedly decreased the colony formation, migration and invasion of OC cells. In addition, the expression of N-cadherin was downregulated, and the expression of E-cadherin was upregulated with Rg3 treatment. Moreover, lncRNA H19 was upregulated in OC cells, and Rg3 negatively regulated H19 expression in a concentration-dependent manner. In terms of the mechanism, knockdown of H19 inhibited cell proliferation, migration and invasion, while overexpression of H19 reversed the inhibitory effect of Rg3 on the OC cells. In conclusion, ginsenoside Rg3 suppresses the proliferation, migration and invasion of OC cells by partially inhibiting the expression of lncRNA H19.	34038042	RID04834	transcriptional regulation	NA		UP(NSCLC);DATA(GSE74639)
Triple-negative breast cancer	SNHG6	BMPR1B	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000138696	NA	641638	658	HBII-276HG|NCRNA00058|U87HG	ALK6|CDw293	LncRNA SNHG6/miR-125b-5p/BMPR1B Axis: A New Therapeutic Target for Triple-Negative Breast Cancer.Triple-negative breast cancer (TNBC) is a significant cause of patient morbidity. The exactly pathobiological features of this condition has yet to be completely elucidated. Breast cancer data obtained from The Cancer Genome Atlas (TCGA) database were evaluated for lncRNA SNHG6 expression. Normal human breast epithelial cell line (MCF-10A) and other breast cancer cell lines (BT-549, MDA-MB-231, Hs 578t, ZR-75-30, SK-BR-3, MCF-7) were also assessed for lncRNA SNHG6 expressions. Cellular proliferative ability was evaluated with colony formation and CCK-8 assays. The ability of cells to migrate was scrutinized with the wound healing and Boyden chamber cell migration assays. qRT-PCRenabled for detection of lncRNA SNHG6, miR-125b-5p and BMPR1B mRNA expressions. Protein BMPR1B expressions were further assessed using western blot. Direct binding sites between transcripts were determined using dual-luciferase reporter assays. We also constructed a xenograft mouse model to further dissect the vivo implications of lncRNA SNHG6. Ki-67 and c-Caspase-3 expressions were detected using immunohistochemistry staining. Breast cancer cell lines demonstrated higher lncRNA SNHG6 expressions, particularly TNBC cell lines, in contrast to normal breast epithelial cell lines. This finding coincided with those noted on analysis of TCGA breast cancer data. lncRNA SNHG6 knockdown inhibited TNBC cell proliferation, migration, while promoted cell apoptosis. Furthermore, suppressed lncRNA SNHG6 expressions resulted in lower tumor weights and volumes in a xenograft mouse model, as evidenced by Ki-67 and c-Caspase-3 expression profiles in tumor tissues. miR-125b-5p and lncRNA SNHG6/BMPR1B both possessed direct binding sites for each other which was validated utilizing a dual-luciferase reporter assay. Decreasing lncRNA SNHG6 expression in TNBC cells upregulated miR-125b-5p expression. Another side, inhibiting miR-125b-5p upregulated BMPR1B expression in these cells. Moreover, knocking down lncRNA SNHG6 downregulated BMPR1B expression in TNBC cells, and the finding was rescued in cells which were exposed to miR-125b-5p inhibitor. Downregulating miR-125b-5p mitigated the effect of suppressing lncRNA SNHG6 on TNBC cell proliferation, migration, and apoptosis. Downregulation of lncRNA SNHG6 could inhibit TNBC cell proliferative, migratory capabilities and promote apoptosis capability, likely through modulation of the miR-125b-5p/BMPR1B axis. This axis may be targeted in formulating new therapies for TNBC.	34026654	RID04835	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Hepatocellular carcinoma	KCNQ1OT1	CBX3	positively-E	Starbase;Targetscan;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(+)	ceRNA(miR-29a-3p)	regulation	RNA-protein	Sevoflurane	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000122565	NA	10984	11335	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	HP1Hs-gamma	lncRNA KCNQ1OT1 reverses the effect of sevoflurane on hepatocellular carcinoma progression via regulating the miR-29a-3p/CBX3 axis.Sevoflurane (SEVO) is widely applied as an anesthetic, which exerts antitumor capacity in various cancers, including hepatocellular carcinoma (HCC). Previous studies indicated that long non-coding RNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) was upregulated, while microRNA-29a-3p (miR-29a-3p) was downregulated in HCC. Thus, we aimed to explore the roles of KCNQ1OT1 and miR-29a-3p in HCC cells exposed to SEVO. Cell proliferation, apoptosis, migration, and invasion were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and transwell assays, respectively. The levels of genes were determined by quantitative real-time polymerase chain reaction (qRT-PCR or western blot. Furthermore, the interaction between miR-29a-3p and KCNQ1OT1 or chromebox protein homolog 3 (CBX3) was predicted by Starbase or Targetscan, and then confirmed by dual-luciferase reporter assay. We found that the levels of KCNQ1OT1 and CBX3 were decreased, while miR-29a-3p was increased in SEVO-treated HCC cells. KCNQ1OT1 overexpression weakened the inhibitory effects of SEVO on HCC cell proliferation, apoptosis, migration, and invasion. Interestingly, KCNQ1OT1 bound to miR-29a-3p, and miR-29a-3p targeted CBX3. KCNQ1OT1 upregulated CBX3 level by repressing miR-29a-3p expression. Furthermore, KCNQ1OT1 exerted tumor promotion in HCC cells via suppressing miR-29a-3p to regulate CBX3 expression. Collectively, our findings demonstrated that KCNQ1OT1 regulated the antitumor effects of SEVO on HCC cells through modulating the miR-29a-3p/CBX3 axis, providing a theoretical basis for the treatment of HCC.	34008749	RID04836	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE86978)
Pancreatic cancer	TP73-AS1	GOLM1	positively-E	ENCORI;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(+);cancer progression(+);cell metastasis(+)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000135052	NA	57212	51280	KIAA0495|PDAM	bA379P1.3|C9orf155|FLJ23608|GOLPH2|GP73	Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis.Previous studies have suggested that long non-coding RNAs (lncRNA) TP73-AS1 is significantly upregulated in several cancers. However, the biological role and clinical significance of TP73-AS1 in pancreatic cancer (PC) remain unclear. To investigate the role of TP73-AS1 in the growth and metastasis of PC. The expression of lncRNA TP73-AS1, miR-128-3p, and  GOLM1  in PC tissues and cells was detected by quantitative real-time polymerase chain reaction. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation, migration, and invasion abilities were verified by Cell Counting Kit-8, wound-healing, and transwell assays, as well as flow cytometry and western blot The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and western blot. The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells. High TP73-AS1 expression was correlated with a poor prognosis. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion  in vitro  as well as suppressed tumor growth  in vivo . Mechanistically, TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p. Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis, which might provide a potential treatment strategy for patients with PC.	34007135	RID04837	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Clear cell renal cell carcinoma	MAGI2-AS3	HEY1	negatively-F	dual-luciferase reporter assay;RIP;ChIP	downregulation		NA	NA	tumorigenesis(-);angiogenesis(-)	interact with protein	binding/interaction	NA	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	TF	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000164683	NA	100505881	23462	ENST00000414797	bHLHb31|CHF-2|CHF2|HERP2|HESR-1|HESR1|HRT-1	LncRNA MAGI2-AS3 inhibits tumor progression and angiogenesis by regulating ACY1 via interacting with transcription factor HEY1 in clear cell renal cell carcinoma.Clear cell renal cell carcinoma (ccRCC) represents the most common type of RCC in adults, characterized by hyper-vascularization and metastatic relapse. Surgical resection is the main treatment due to poor response of ccRCC to radio-and chemotherapy. However, the high complexity of tumor vasculature in ccRCC has thwarted effects to develop new therapeutic strategies for ccRCC. In this study, we identify the anti-angiogenic activity of MAGI2-AS3 in ccRCC. 86 paired samples of tumor tissues and adjacent no-tumor tissues were collected from ccRCC patients. dual-luciferase reporter assay, RIP, and ChIP assays were employed to confirm interactions between MAGI2-AS3, transcription factor HEY1, and the ACY1 gene. In other studies, we assayed human ccRCC cells RLC-310 for their viability, migration and invasion using CCK-8 detection and transwell chamber systems. Angiogenesis was evaluated in the Matrigel-based human umbilical vein endothelial cell (HUVEC)-RLC-310 coculture model and immunohistochemical staining for vascular endothelial growth factor (VEGF) and CD31 in tumor tissues collected from a xenograft ccRCC mouse model. MAGI2-AS3 and ACY1 expression was downregulated in ccRCC tissues, and low expression of MAGI2-AS3 was associated with poor patient survival. Overexpression of MAGI2-AS3 could reduce ccRCC cell viability and migration, inhibit vessel-like tube formation of HUVECs in vitro, and repress tumor growth and angiogenesis in vivo. MAGI2-AS3 bound with HEY1 and reduced the HEY1 enrichment at the ACY1 promoter region, thus increasing ACY1 gene transcription. HEY1 knockdown or ACY1 overexpression that resisted MAGI2-AS3 knockdown was found in the in vivo and in vitro settings. The present study demonstrates that MAGI2-AS3 exerts tumor-suppressive, anti-angiogenic activities in ccRCC by modulating the HEY1/ACY1 pathway, thus lending support for conducting further investigations of anti-angiogenesis therapy for ccRCC.	34002044	RID04838	interact with protein	metastasis,chemoresistance	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE51827,GSE86978)
Clear cell renal cell carcinoma	MAGI2-AS3	ACY1	positively-E	dual-luciferase reporter assay;RIP;ChIP	downregulation		NA	NA	tumorigenesis(-);angiogenesis(-)	transcriptional regulation	regulation	RNA-protein	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000243989	NA	100505881	95	ENST00000414797	NA	LncRNA MAGI2-AS3 inhibits tumor progression and angiogenesis by regulating ACY1 via interacting with transcription factor HEY1 in clear cell renal cell carcinoma.Clear cell renal cell carcinoma (ccRCC) represents the most common type of RCC in adults, characterized by hyper-vascularization and metastatic relapse. Surgical resection is the main treatment due to poor response of ccRCC to radio-and chemotherapy. However, the high complexity of tumor vasculature in ccRCC has thwarted effects to develop new therapeutic strategies for ccRCC. In this study, we identify the anti-angiogenic activity of MAGI2-AS3 in ccRCC. 86 paired samples of tumor tissues and adjacent no-tumor tissues were collected from ccRCC patients. dual-luciferase reporter assay, RIP, and ChIP assays were employed to confirm interactions between MAGI2-AS3, transcription factor HEY1, and the ACY1 gene. In other studies, we assayed human ccRCC cells RLC-310 for their viability, migration and invasion using CCK-8 detection and transwell chamber systems. Angiogenesis was evaluated in the Matrigel-based human umbilical vein endothelial cell (HUVEC)-RLC-310 coculture model and immunohistochemical staining for vascular endothelial growth factor (VEGF) and CD31 in tumor tissues collected from a xenograft ccRCC mouse model. MAGI2-AS3 and ACY1 expression was downregulated in ccRCC tissues, and low expression of MAGI2-AS3 was associated with poor patient survival. Overexpression of MAGI2-AS3 could reduce ccRCC cell viability and migration, inhibit vessel-like tube formation of HUVECs in vitro, and repress tumor growth and angiogenesis in vivo. MAGI2-AS3 bound with HEY1 and reduced the HEY1 enrichment at the ACY1 promoter region, thus increasing ACY1 gene transcription. HEY1 knockdown or ACY1 overexpression that resisted MAGI2-AS3 knockdown was found in the in vivo and in vitro settings. The present study demonstrates that MAGI2-AS3 exerts tumor-suppressive, anti-angiogenic activities in ccRCC by modulating the HEY1/ACY2 pathway, thus lending support for conducting further investigations of anti-angiogenesis therapy for ccRCC.	34002044	RID04839	transcriptional regulation	metastasis,chemoresistance	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	SOX2-OT	SOX5	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR;ISH	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000134532	NA	347689	6660	DKFZp761J1324|NCRNA00043|SOX2OT	L-SOX5|MGC35153	A novel lncRNA SOX2OT promotes the malignancy of human colorectal cancer by interacting with miR-194-5p/SOX5 axis.Long noncoding RNAs (lncRNAs) show emerging roles in colorectal cancer (CRC) development and are considered to be involved in the potential mechanism of tumor malignancy. While Sox2 overlapping transcript (SOX2OT) has been implicated in the progression of multiple cancers, its role in CRC remains to be explored. In this study, in situ hybridization (ISH) and qRT-PCRwere performed to establish the functional relationships between SOX2OT and CRC deranged in CRC tissue and cells. Subsequently, SOX2OT shRNAs vectors were transfected into CRC cells to performed loss-of-function assays to detect the potential role of SOX2OT on proliferation and metastasis in vitro and vivo. The results showed SOX2OT was an oncogene that was up-regulated in human CRC tissues and cell lines. SOX2OT silencing suppressed cell proliferation, migration, and invasion in CRC cells in vitro, and inhibited tumorigenesis in the mouse xenografts. Bioinformatic predictive analysis coupled with the dual-luciferase reporter, RNA immunoprecipitation (RIP), and functional rescue assay elucidated the mechanistic network of the SOX2OT-miR-194-5p-SOX5 axis in CRC. Mechanistically, SOX2OT acted as a competing endogenous RNA (ceRNA) to upregulate SOX5 by sponging miR-194-5p. Downregulated SOX2OT boosted miR-194-5p expression, thus decreased the protein level of SOX5, which suppresses tumorgenesis of CRC.	33993197	RID04840	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	LINC01535	miR-761	negatively-F	dual-luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+);chemosensitivity(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000226686	GRCh38_19:37251867-37265547	NA	NA	101927667	NA	NA	NA	LncRNA LINC01535 promotes colorectal cancer development and chemoresistance by sponging miR-761.Colorectal cancer (CRC) is one of the most common human cancer types and a leading cause of cancer-related death. Accumulating evidence has confirmed that long non-coding RNAs have crucial roles in CRC progression. In the present study, the biological roles of LINC01535 were investigated and the interaction between long intergenic non-coding RNA (LINC)01535 and microRNA (miR)-761 in CRC was explored. LINC01535 expression was observed to be upregulated in CRC tissues and cell lines. A functional study suggested that LINC01535 silencing inhibited CRC cell proliferation and invasion but enhanced cisplatin sensitivity of CRC cells, while co-transfection with a miR-761 inhibitor reversed these biological effects. A luciferase reporter assay demonstrated that LINC01535 regulated miR-761 directly and RNA-binding protein immunoprecipitation further confirmed that the suppression of LINC01535 by miR-761 was via an RNA-induced silencing complex. Finally, knockdown of LINC01535 inhibited the growth of CRC cells  in vivo . Collectively, the results suggested that LINC01535 exerts oncogenic functions in CRC by sponging miR-761. In conclusion, the present study indicated that LINC01535 promoted CRC progression through sponging miR-761, and may serve as a potential diagnostic biomarker and therapeutic target for CRC.	33986850	RID04841	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	
Retinoblastoma	TRPM2-AS	WEE1	positively-E	Starbase;luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(+)	ceRNA(miR-497)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000166483	NA	101928607	7465	TRPM2-AS1	WEE1A	Long Noncoding RNA TRPM2-AS Promotes the Growth, Migration, and Invasion of Retinoblastoma via miR-497/WEE1 Axis.Long noncoding RNAs (lncRNAs) exhibit vital roles in many types of cancer, including retinoblastoma (RB), the most common primary intraocular malignancy tumor of infancy. A novel lncRNA TRPM2-AS has been demonstrated to be related to multiple cancers; however, its role in RB remains unclear. Here, we aimed to investigate the function of TRPM2-AS in RB. In this study, TRPM2-AS expression in 35 human RB tissues and RB cell lines was detected by real-time PCR. And, the relationship between its expression and clinicopathological characteristics of RB patients was analyzed. RB cells' proliferation, migration, invasion, apoptosis, and cell cycle were explored after silencing TRPM2-AS. The mechanism of TRPM2-AS in RB was focused on miR-497/WEE1 axis. Additionally, the role and mechanism of TRPM2-AS were confirmed in a xenograft mouse model. We found TRPM2-AS expression was enhanced in RB tissues and cells. And, higher TRPM2-AS expression was related to advanced clinical stage and optic nerve invasion in patients. Downregulation of TRPM2-AS significantly inhibited proliferation, migration, and invasion, elevated apoptosis, attenuated G2/M phase arrest in RB cells, and suppressed tumor growth  in vivo . TRPM2-AS acted as a ceRNA for miR-497 to positively regulate WEE1 expression. miR-497 inhibitor or WEE1 overexpression dramatically reversed the effects of TRPM2-AS downregulating on the malignant phenotypes of RB cells. Therefore, TRPM2-AS is an oncogenic lncRNA in RB, and it functions largely through the miR-497/WEE1 pathway. Despite the limited sample size, this study indicates that TRPM2-AS may be a candidate target in RB therapies.	33986660	RID04842	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Osteoporosis	TUG1	RUNX2	positively-E	dual-luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-23b)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124813	NA	55000	860	FLJ20618|LINC00080|NCRNA00080	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Long non-coding RNA taurine upregulated gene 1 is downregulated in osteoporosis and influences the osteogenic differentiation of bone marrow mesenchymal stem cells.With aging, an imbalance in bone remodeling leading to increased bone resorption and decreased bone formation is thought to contribute to osteoporosis. Osteoblastic differentiation of bone marrow mesenchymal stem cells (BMMSCs) plays a vital role in the pathogenesis of osteoporosis. However, the detailed molecular mechanisms of osteoporosis remain incompletely understood. Given that long non-coding RNA taurine upregulated gene 1 (lnc TUG1) plays a critical role in the osteogenic differentiation, and microRNA-23b (miR-23b) as a putative sponge for lnc TUG1 has upregulated expression in osteoporosis. Therefore, this study investigated the roles of TUG1/miR-23b in osteoporotic pathology. TUG1 and miR-23b expression in the plasma of osteoporotic patients were evaluated by quantitative real-time PCR (qRT-PCR. The osteogenic differentiation in human BMMSCs was evaluated by qRT-PCR western blot, Alizarin red staining after knockdown of TUG1 by small interfering RNA (siRNA) treatment. Decreased expression of TUG1 and increased expression of miR-23b evident in the plasma of patients with osteoporosis than in that of age- and sex-matched healthy controls. Additionally, increased miR-23b expression inhibited runt-related transcription factor 2 (RUNX2), osteocalcin, and osteopontin expression and reduced calcified nodule formation based on the results of qRT-PCR western blot, and Alizarin Red S staining. The study for the first time reported that silence of lncRNA TUG1 significantly suppressed the osteogenic differentiation of BMMSCs possibly by targeting the miR-23b/RUNX2 signaling pathway. This mechanism of TUG1/miR-23b/RUNX2 signaling within the osteogenic differentiation of BMMSCs might provide new insight for the development of lncRNA-directed diagnostic and therapeutic strategies for osteoporosis.Knockdown of TUG1 expression via RNA interference.	33976977	RID04843	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	MIAT	RAB22A	positively-E	Wound healing assay;western blot;enzyme-linked;immunosorbent; assay;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);cell migration(-);epithelial to mesenchymal transition(-)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000124209	NA	440823	57403	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	LncRNA MIAT Mediates ox-LDL-Induced Endothelial Cell Injury Via miR-206/RAB22A Axis.Long non-coding RNA myocardial infarction associated transcript (MIAT) has exerted significant effects on atherosclerosis (AS). The biological roles of MIAT in endothelial cell dysfunction are not thoroughly elucidated. The expression of MIAT, microRNA (miR)-206 and Ras-related protein Rab-22A (RAB22A) was detected by quantitative real-time polymerase chain reaction and western blot. The injury of human umbilical vein endothelial cells (HUVECs) was evaluated by testing cell viability, invasion, migration, apoptosis, epithelial-mesenchymal transition capacities and inflammatory response using cell counting kit-8, transwell, wound healing assays, flow cytometry, western blot and enzyme-linked immunosorbent assay, respectively. The binding interaction between miR-206 and MIAT or RAB22A was confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. The expression of MIAT was up-regulated in ox-LDL-treated HUVECs, and knockdown of MIAT in ox-LDL-treated HUVECs remarkably promoted cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT), as well as suppressed cell apoptosis and the levels of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and endothelial nitric oxide synthase (eNOS). In a mechanical study, MIAT directly targeted miR-206, and miR-206 inhibition attenuated the protective effects of MIAT knockdown on ox-LDL-triggered HUVEC injury. Besides that, RAB22A was a target of miR-206, and RAB22A overexpression reversed the biological effects of miR-206 on ox-LDL-treated HUVECs. Additionally, we also proved MIAT could regulate RAB22A via miR-206 in HUVECs. MIAT knockdown impaired ox-LDL-induced HUVEC injury via regulating miR-206/RAB22A axis, suggesting the potential impacts of MIAT on AS occurrence, which revealed a potential therapeutic strategy for future clinic intervention in AS.	33965771	RID04844	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Gastric cancer	PINK1-AS	Gi1	positively-E	RNA fluorescence in situ hybridization assay;RIP;RNA pull-down assay	upregulation	ISH;FISH	NA	NA	cell viability(+);cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-200a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000117242	GRCh38_1:20642657-20652193	NA	NA	100861548	NA	NAPINK1|PINK1-AS1|PINK1AS	NA	LncRNA PINK1-AS promotes Galphai1-driven gastric cancer tumorigenesis by sponging microRNA-200a.Gastric cancer (GC) is one of the leading causes of human mortality around the world. We have previously shown that Galphai1 (the inhibitory subunit 1 of the heterotrimeric guanine nucleotide-binding protein) recruitment to ligand-activated receptor tyrosine kinases (RTKs) is essential for signaling. Testing its role in GC cancer-promoting functions, we found that Galphai1 is upregulated in human GC, correlating with poor overall survival. In established and primary human GC cells, Galphai1 shRNA (small hairpin RNA) or knockout produced significant anti-GC cell activity, proliferation and migration was inhibited, and apoptosis was activated. Conversely, ectopic Galphai1 overexpression promoted proliferation and migration of GC cells in vitro. By examining the tumor-suppressive miRNA microRNA-200a (miR-200a), we found that miR-200a directly silenced Galphai1 to induce anti-GC cell activity. The expression of miR-200a was downregulated in human GC, correlating with upregulation of a novel miR-200a-targeting long non-coding RNA (LncRNA), PINK1 (PTEN Induced Kinase 1)-AS. RNA immunoprecipitation, RNA-pull down, and RNA fluorescence in situ hybridization assays confirmed that PINK1-AS directly binds to miR-200a. Silencing PINK1-AS in GC cells led to miR-200a accumulation, Galphai1 downregulation, and inhibition of GC cell progression in vitro, whereas PINK1-AS upregulation produced the converse results. Significantly, anti-GC cell activity induced by PINK1-AS shRNA was ameliorated by the expression of miR-200a antisense or the 3'-UTR (untranslated region)-depleted Galphai1. In vivo, the growth of subcutaneous MGC-803 xenografts in nude mice was inhibited by PINK1-AS shRNA, but accelerated by PINK1-AS overexpression. Patient-derived GC xenograft growth in nude mice was largely inhibited after intratumoral injection of PINK1-AS shRNA lentivirus. In conclusion, PINK1-AS promotes Galphai1-driven GC progression by sponging miR-200a.	33958720	RID04845	ceRNA or sponge	NA	DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Enterovirus 71	AK097647	IFN-1	negatively-E	RNAi	upregulation	RT-qPCR	NA	NA	immune response(+) 	transcriptional regulation	association	RNA-RNA	NA	NA	NA	Other	Enterovirus 71	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	The Upregulation of a Novel Long Noncoding RNA AK097647 Promotes Enterovirus 71 Replication and Decreases IFN-Lambda1 Secretion.Enterovirus 71 (EV71) infects millions of children every year in China and has become a challenge to public health. However, there is no effective treatment for EV71 infection. Long noncoding RNAs (lncRNAs) have been found to play various roles in virus replication and infection. We aimed to explore the role of a novel long noncoding RNA AK097647 (lncRNA-AK097647) during EV71 infection. To assess the role of lncRNA-AK097647 during EV71 infection, siRNAs were used to silence lncRNA-K097647 expression. RT-qPCR assay and western blot were applied to measure the mRNA and protein levels of EV71 VP1 and the phosphorylation of NF-kB. ELISA was used to detect the level of IFN-Lambda1 expression. The novel lncRNA-AK097647 was upregulated in human rhabdomyosarcoma cells and the blood of hand, foot, and mouth disease patients infected with EV71, as demonstrated by RT-qPCR. Interestingly, RNAi-mediated knockdown of lncRNA-AK097647 dramatically increased the level of IFN-Lambda1 expression, resulting in the suppression of EV71 replication. In contrast, overexpression of lncRNA-AK097647 decreased the level of IFN-Lambda1 expression and resulted in increased EV71 replication. In addition, we found that lncRNA-AK097647 could inhibit the phosphorylation of NF-kB. These results suggest a novel mechanism by which EV71 evades the IFN-mediated host antiviral response by increasing lncRNA-AK097647 expression.	33951637	RID04846	transcriptional regulation	NA		
Sepsis	Mirt2	MIR1246	positively-E	Methylation-specific PCR	downregulation	RT-qPCR	NA	NA	apoptosis process(-)	DNA methylation	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Disease by infectious agent	Bacterial infectious disease	lncRNA	miRNA	NA	NA	ENSG00000283203	NA	NA	100302142	NA	MIRN1246|hsa-mir-1246	lncRNA Mirt2 upregulates miR-1246 through methylation to suppress LPS-induced lung cell apoptosis/Methods:Forty sepsis patients (sepsis group; 23 males and 17 females; 40'-5 years, 48.6- -6.3 years), 40 sepsis patients with acute lung injury (sepsis-ALI group, 23 males and 17 females; 40'-5 years, 48.7- -6.4 years), and 40 healthy controls (control group, 23 males and 17 females; 40'-5 years, 48.6- -6.1 years) were included. Mirt2 and miR-1246 expression in plasma samples from these patients were determined by a reverse transcription-quantitative polymerase chain reaction (PCR). Overexpression of Mirt2 and miR-1246 was achieved in human bronchial epithelial cells (HBEpCs) to explore the interaction between them. The effects of Mirt2 overexpression on miR-1246 methylation were analyzed by methylation-specific PCR. Cell apoptosis analysis was performed to analyze the role of Mirt2 and miR-1246 in the apoptosis of HBEpCs.Mirt2 expression was downregulated in sepsis and was further downregulated in patients with sepsis-ALI. Mirt2 and miR-1246 found to be positively correlated. Downregulation of Mirt2 and miR-1246 was observed in HBEpCs with LPS treatment. In HBEpCs, Mirt2 overexpression increased miR-1246 expression but decreased its gene methylation. Cell apoptosis analysis showed that Mirt2 and miR-1246 negatively regulated the apoptosis of HBEpCs induced by LPS. In addition, miR-1246 inhibition reduced the inhibitory effects of Mirt2 overexpression on cell apoptosis.	33943017	RID04847	epigenetic regulation	NA		
Sepsis-induced acute kidney injury<U+00A0>	NKILA	CLDN2	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+);cell autophagy(+);inflammatory response(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000165376	NA	105416157	9075	NA	NA	LncRNA NKILA knockdown promotes cell viability and represses cell apoptosis, autophagy and inflammation in lipopolysaccharide-induced sepsis model by regulating miR-140-5p/CLDN2 axis.Long non-coding RNAs (lncRNAs) play vital roles in human diseases, including sepsis-induced acute kidney injury (AKI). Here, we aimed to investigate the functions of lncRNA NKILA in sepsis-engendered AKI. HK2 cells stimulated with LPS were used to mimic sepsis-induced AKI in<U+00A0>vitro. qRT-PCRwas conducted for lncRNA NKILA and miR-140-5p levels. Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis were employed to analyze cell viability and apoptosis. western blot assay was utilized to measured protein levels. ELISA kits were used to examine the concentrations of IL-6, IL-1beta and TNF-alpha. dual-luciferase reporter assay was utilized to analyze the relationships among lncRNA NKILA, miR-140-5p and claudin 2 (CLDN2). LPS restrained HK2 cell viability and accelerated cell apoptosis and autophagy. LncRNA NKILA was increased in LPS-treated HK2 cells. LncRNA NKILA silencing reversed the promotional influence of LPS on cell progression in HK2 cells. miR-140-5p inhibition ameliorated lncRNA NKILA knockdown-mediated cell injury in LPS-mediated HK2 cells. CLDN2 was the target of miR-140-5p. MiR-140-5p elevation promoted cell viability and suppressed cell apoptosis, autophagy and inflammation in LPS-induced HK2 cells, with CLDN2 elevation overturned the effects. LncRNA NKILA silencing protected HK2 cells from LPS-induced impairments by reducing CLDN2 through sponging miR-140-5p.	33932903	RID04848	ceRNA or sponge	NA		
Non-small cell lung cancer	BBOX1-AS1	MELK	positively-E	ChIP;ChIP;GEO;GEPIA;starBase;Meier Plotter;JASPAR;JASPAR;TargetScan	upregulation	qRT-PCR	GSE18842;GSE19188;GSE135918;GSE29250;GSE33532	NA	prognosis;cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-27a-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000254560	GRCh38_11:27047186-27220113	ENSG00000165304	NA	103695435	9833	NA	KIAA0175	KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway.Non-small cell lung cancer (NSCLC) is a major histological subtype of lung cancer with high mortality and morbidity. A substantial amount of evidence demonstrates long non-coding RNAs (lncRNA) as critical regulators in tumorigeneis and malignant progression of human cancers. The oncogenic role of BBOX1 anti-sense RNA 1 (BBOX1-AS1) has been reported in several tumors. As yet, the potential functions and mechanisms of BBOX1-AS1 in NSCLC are obscure. The gene and protein expression was detected by qRT-PCRand western blot. Cell function was determined by CCK-8, colony forming, would healing and transwell assays. Bioinformatics tools, ChIP assays, dual luciferase reporters system and RNA pull-down experiments were used to examine the interaction between molecules. Subcutaneous tumor models in nude mice were established to investigate in vivo NSCLC cell behavior. BBOX1-AS1 was highly expressed in NSCLC tissues and cells. High BBOX1-AS1 expression was associated with worse clinical parameters and poor prognosis. BBOX1-AS1 up-regulation was induced by transcription factor KLF5. BBOX1-AS1 deficiency resulted in an inhibition of cell proliferation, migration, invasion and EMT in vitro. Also, knockdown of BBOX1-AS1 suppressed NSCLC xenograft tumor growth in mice in vivo. Mechanistically, BBOX1-AS1 acted act as a competetive "sponge" of miR-27a-5p to promote maternal embryonic leucine zipper kinase (MELK) expression and activate FAK signaling. miR-27a-5p was confirmed as a tumor suppressor in NSCLC. Moreover, BBOX1-AS1-induced increase of cell proliferation, migration, invasion and EMT was greatly reversed due to the overexpression of miR-27a-5p. In addition, the suppressive effect of NSCLC progression owing to BBOX1-AS1 depletion was abated by the up-regulation of MELK. Consistently, BBOX1-AS1-mediated carcinogenicity was attenuated in NSCLC after treatment with a specific MELK inhibitor OTSSP167. KLF5-induced BBOX1-AS1 exerts tumor-promotive roles in NSCLC via sponging miR-27a-5p to activate MELK/FAK signaling, providing the possibility of employing BBOX1-AS1 as a therapeutic target for NSCLC patients.	33931086	RID04849	ceRNA or sponge	prognosis	UP(PRAD);DATA(GSE104209)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Non-small cell lung cancer	KLF5	BBOX1-AS1	positively-E	JASPAR;ChIP;dual-luciferase reporter assay	upregulation	qRT-PCR	GSE18842;GSE19188;GSE135918;GSE29250;GSE33532	NA	prognosis	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000102554	NA	ENSG00000254560	GRCh38_11:27047186-27220113	688	103695435	BTEB2|CKLF|IKLF	NA	KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway.Non-small cell lung cancer (NSCLC) is a major histological subtype of lung cancer with high mortality and morbidity. A substantial amount of evidence demonstrates long non-coding RNAs (lncRNA) as critical regulators in tumorigeneis and malignant progression of human cancers. The oncogenic role of BBOX1 anti-sense RNA 1 (BBOX1-AS1) has been reported in several tumors. As yet, the potential functions and mechanisms of BBOX1-AS1 in NSCLC are obscure. The gene and protein expression was detected by qRT-PCRand western blot. Cell function was determined by CCK-8, colony forming, would healing and transwell assays. Bioinformatics tools, ChIP assays, dual luciferase reporters system and RNA pull-down experiments were used to examine the interaction between molecules. Subcutaneous tumor models in nude mice were established to investigate in vivo NSCLC cell behavior. BBOX1-AS1 was highly expressed in NSCLC tissues and cells. High BBOX1-AS1 expression was associated with worse clinical parameters and poor prognosis. BBOX1-AS1 up-regulation was induced by transcription factor KLF5. BBOX1-AS1 deficiency resulted in an inhibition of cell proliferation, migration, invasion and EMT in vitro. Also, knockdown of BBOX1-AS1 suppressed NSCLC xenograft tumor growth in mice in vivo. Mechanistically, BBOX1-AS1 acted act as a competetive "sponge" of miR-27a-5p to promote maternal embryonic leucine zipper kinase (MELK) expression and activate FAK signaling. miR-27a-5p was confirmed as a tumor suppressor in NSCLC. Moreover, BBOX1-AS1-induced increase of cell proliferation, migration, invasion and EMT was greatly reversed due to the overexpression of miR-27a-5p. In addition, the suppressive effect of NSCLC progression owing to BBOX1-AS1 depletion was abated by the up-regulation of MELK. Consistently, BBOX1-AS1-mediated carcinogenicity was attenuated in NSCLC after treatment with a specific MELK inhibitor OTSSP167. KLF5-induced BBOX1-AS1 exerts tumor-promotive roles in NSCLC via sponging miR-27a-5p to activate MELK/FAK signaling, providing the possibility of employing BBOX1-AS1 as a therapeutic target for NSCLC patients.	33931086	RID04850	transcriptional regulation	prognosis	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)	UP(PRAD);DATA(GSE104209)
Cervical cancer	MIR503HG	CEBPB	positively-E		downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-191)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000172216	NA	84848	1051	H19X|MGC16121	C/EBP-beta|CRP2|IL6DBP|LAP|NFIL6|TCF5	LncRNA MIR503HG regulated cell viability, metastasis and apoptosis of cervical cancer via miR-191/CEBPB axis.<U+00A0> The long non-coding RNA MIR503 host gene (MIR503HG) plays a role in suppressing or promoting cancer in many types of human malignant tumors. The role of MIR503HG in cervical cancer is still unknown. The expression level of MIR503HG in cervical cancer tissues and cell lines was accessed using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR assay. The Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis were performed to assess cell proliferation and apoptosis in cervical cancer. The nude mouse xenograft experiment was used to examine the ability of MIR503HG in tumor formation. In our study, we found that the expression of MIR503HG was significantly reduced in cervical cancer tissues and cell lines. In vitro studies have shown that MIR503HG inhibited cell proliferation and invasion, and enhanced cell apoptosis in cervical cancer through the miR-191/CEBPB axis. MIR503HG regulated the expression of miR-191 via directly binding to miR-191. The expression of MIR503HG had a negative correlation with miR-191 expression in cervical cancer tissues. MiR-191 regulated the expression of CEBPB by directly targeting 3'-UTR of CEBPB mRNA. Overexpression of MIR503HG inhibited cell proliferation, invasion and apoptosis in vitro, and inhibited tumor growth in vivo. MIR503HG plays a role in suppressing tumors in cervical cancer and is a long-term non-coding RNA.	33928605	RID04851	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	KCNQ1	MIR133B	negatively-F	western blot;dual-luciferase reporter;RIP	upregulation	qRT-PCR	NA	NA	EGFR/PI3K/AKT signaling pathway(+);cell metastasis(+);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000053918	GRCh38_11:2444684-2849105	ENSG00000199080	NA	3784	442890	ATFB1|ATFB3|JLNS1|KCNA8|KCNA9|KVLQT1|Kv1.9|Kv7.1|LQT|LQT1|RWS|SQT2|WRS	MIRN133B|miRNA133B|mir-133b	Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b.The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR. Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.KCNQ1OT1 enhanced the proliferation and metastasis of ESCC cells by adsorbing miR-133b and impeded their apoptosis.	33909822	RID04852	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cardiomyopathy	KCNQ1OT1	PDCD4	positively-E	RIP;dual-luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-181a-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000150593	NA	10984	27250	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	H731	Long non-coding RNA KCNQ1OT1 increases the expression of PDCD4 by targeting miR-181a-5p, contributing to cardiomyocyte apoptosis in diabetic cardiomyopathy.Diabetic cardiomyopathy (DCM) is a specific myocardial alteration in patients with diabetics. LncRNA KCNQ1OT1 has been previously demonstrated to be involved in various diabetic complications. Our aims are to further investigate the underlying regulatory mechanisms/pathways of KCNQ1OT1 in DCM. In vitro and in vivo models of DCM were established in high glucose (HG)-treated human cardiomyocytes and in streptozotocin (STZ)-induced diabetic mice, respectively. Gene and protein expressions were examined by qPCR;western blot and ELISA. Cell proliferation and apoptosis were determined by CCK8 assay, flow cytometry and TUNEL staining. The association between KCNQ1OT1<U+00A0>and miR-181a-5p, miR-181a-5p and PDCD4 was predicted using bioinformatics methods and subsequently confirmed by dual luciferase reporter and RNA immunoprecipitation assays. Mouse cardiac tissues were collected and analysed using HE staining, Masson's staining and immunohistochemical analysis. KCNQ1OT1 and PDCD4 were upregulated in HG-treated human cardiomyocytes, while miR-181a-5p was downregulated. In addition, KCNQ1OT1 could negatively regulate miR-181a-5p expression; meanwhile, miR-181a-5p also negatively regulated PDCD4 expression. KCNQ1OT1 silencing suppressed the expression of inflammatory cytokines and cell apoptosis in vitro, whereas inhibition of miR-181a-5p abrogated those effects of KCNQ1OT1 knockdown. Moreover, overexpressed PDCD4 abolished the inhibition on inflammation and apoptosis caused by miR-181a-5p overexpression. Finally, KCNQ1OT1 knockdown reduced the expression of PDCD4 via regulating miR-181a-5p and inhibited myocardial inflammation and cardiomyocyte apoptosis in the in vivo DCM model. Our findings suggest that KCNQ1OT1 and its target gene miR-181a-5p regulate myocardial inflammation and cardiomyocyte apoptosis by modulating PDCD4 in DCM.	33907874	RID04853	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Liver cancer	PCAT6	HNRNPA2B1	positively-E	GEPIA;western blot;Starbase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+)	ceRNA(miR-326)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000122566	NA	100506696	3181	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	HNRPA2B1	lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR-326/hnRNPA2B1 axis in liver cancer.Liver cancer is one of the most common malignant human tumors with the highest morbidity and mortality rates of all cancer types in China. Evidence suggests that long non-coding RNA prostate cancer-associated transcript 6 (PCAT6) plays an essential role in tumor progression. However, the roles and mechanism of PCAT6 in liver cancer remain unclear. The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells  in vitro  and  in vivo . A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. Mechanistically, silenced PCAT6 suppressed the malignant phenotype of liver cancer cells through upregulating the inhibitory effect of miR-326 on hnRNPA2B1 expression. Taken together, these data demonstrated that knockdown of PCAT6 inhibited liver cancer progression through regulation of the miR-326/hnRNPA2B1 axis, suggesting that PCAT6 functions as an oncogene and may be a useful biomarker for the future diagnosis and treatment of liver cancer.	33907581	RID04854	ceRNA or sponge	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Kidney injury	NEAT1	TXNIP	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell injury(+)	ceRNA(miR-93-5p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000117289	NA	283131	10628	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ARRDC6|EST01027|HHCPA78|THIF|VDUP1	Long non-coding RNA NEAT1 promotes lipopolysaccharide-induced injury in human tubule epithelial cells by regulating miR-93-5p/TXNIP axis.Many long non-coding RNAs (lncRNAs) have been found to play crucial roles in sepsis-induced acute kidney injury (AKI), including lncRNA nuclear-enriched abundant transcript 1 (NEAT1). We aimed to further elucidate the functions and molecular mechanism of NEAT1 in sepsis-induced AKI. Sepsis-induced AKI cell model was established by treatment with lipopolysaccharide (LPS) in human tubule epithelial (HK2) cells. Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. western blot assay was performed to measure all protein levels. The concentrations of inflammatory factors were evaluated using enzyme-linked immunosorbent assay (ELISA). The expression levels of inflammatory factors, NEAT1, microRNA-93-5p (miR-93-5p), and thioredoxin-interacting protein (TXNIP) were measured by quantitative real-time polymerase chain reaction (qRT-PCR. The oxidative stress factors were detected using corresponding kits. The interaction between miR-93-5p and NEAT1 or TXNIP was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. NEAT1 was upregulated in serum of sepsis patients and LPS-induced HK2 cells. NEAT1 silence alleviated LPS-induced HK2 cell injury by inhibiting apoptosis, inflammation and oxidative stress. Moreover, miR-93-5p was a direct target of NEAT1, and suppression of NEAT1 weakened LPS-induced injury by upregulating miR-93-5p in HK2 cells. Furthermore, TXNIP was a downstream target of miR-93-5p, and miR-93-5p attenuated LPS-induced HK2 cell injury by downregulating TXNIP. In addition, NEAT1 regulated TXNIP expression by acting as a sponge of miR-93-5p. NEAT1 might aggravate LPS-induced injury in HK2 cells by regulating miR-93-5p/TXNIP axis, providing a potential therapeutic strategy for sepsis-associated AKI.	33885954	RID04855	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	PART1	MIR122	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000207778	NA	25859	406906	DKFZP586D0823|NCRNA00206	hsa-mir-122|hsa-mir-122a|miR-122|MIRN122|MIRN122A	Long non-coding RNA PART1 predicts a poor prognosis and promotes the malignant progression of pancreatic cancer by sponging miR-122.Long non-coding RNA PART1 predicts a poor prognosis and promotes the malignant progression of pancreatic cancer by sponging miR-122.Long non-coding RNA (lncRNA) prostate androgen-regulated transcript 1 (PART1) was previously shown to exert an oncogenic role in several human cancers. However, whether PART1 is associated with the malignant progression of pancreatic cancer remains unclear. In the current study, we aimed to identify the role and potential mechanism of PART1 in pancreatic cancer. qRT-PCRwas applied to detect PART1 expression in 45 cases of pancreatic cancer patients. The chi-square test was performed to assess the association between PART1 expression and clinicopathologic features, and Kaplan-Meier method was applied to evaluate overall survival. In vitro CCK-8, transwell invasion, and flow cytometry assays were applied to detect the effects of PART1 on cell proliferation, invasion, and apoptosis, respectively. Luciferase reporter and RNA immunoprecipitation assays were used to identify the regulatory mechanism between PART1 and miR-122. PART1 expression was upregulated in pancreatic cancer tissues and cell lines. High PART1 expression was closely correlated with tumor size, T classification, clinical stage, and vascular invasion, and predicted a poor overall survival. PART1 knockdown significantly suppressed cell proliferation and invasion abilities of pancreatic cancer but promoted cell apoptosis. PART1 was found to serve as a molecular sponge of miR-122, and miR-122 inhibition partially reversed the inhibitory phenotypes of PART1 knockdown on pancreatic cancer cells. PART1 promotes the malignant progression of pancreatic cancer by sponging miR-122. The PART1/miR-122 axis might be a promising target for anticancer therapy in patients with pancreatic cancer.	33865422	RID04856	ceRNA or sponge	prognosis	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	
Esophagus squamous cell carcinoma	THAP9-AS1	SOX4	positively-E	western blot;RIP;dual-luciferase reporter assay; assay;ChIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-133b)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251022	GRCh38_4:82893009-82900960	ENSG00000124766	NA	100499177	6659	NA	NA	THAP9-AS1/miR-133b/SOX4 positive feedback loop facilitates the progression of esophageal squamous cell carcinoma.Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors in the digestive system with a high incidence and poor prognosis. Long non-coding RNAs (LncRNA) have been reported to be closely associated with the occurrence and development of various human cancers. Data from GSE89102 shows an increase of THAP9-AS1 expression in ESCC. However, its functions and mechanisms underlying ESCC progression remain to be investigated. In this study, we found that THAP9-AS1 was overexpressed in ESCC tissues and cells. High THAP9-AS1 expression was positively correlated with tumor size, TNM stage, lymph node metastasis, and worse prognosis. Functionally, depletion of THAP9-AS1 suppressed cell proliferation, migration, and invasion, while enhanced apoptosis in vitro. Consistently, knockdown of THAP9-AS1 inhibited xenograft tumor growth in vivo. Mechanistically, THAP9-AS1 could serve as a competing endogenous RNA (ceRNA) for miR-133b, resulting in the upregulation of SOX4. Reciprocally, SOX4 bound to the promoter region of THAP9-AS1 to activate its transcription. Moreover, the anti-tumor property induced by THAP9-AS1 knockdown was significantly impaired due to miR-133b downregulation or SOX4 overexpression. Taken together, our study reveals a positive feedback loop of THAP9-AS1/miR-133b/SOX4 to facilitate ESCC progression, providing a potential molecular target to fight against ESCC.	33854048	RID04857	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Colon adenocarcinoma	ACTA2-AS1	BCL2L11	positively-E	dual-luciferase reporter assay;RNA pull-down assay;western blot;TCGA;GEPIA;lncBASE	downregulation	qRT-PCR	NA	NA	cell proliferation(-);prognosis;apoptosis process(+)	ceRNA(miR-4428)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000153094	NA	100132116	10018	UC001kfo|uc001kfo.1|ZXF1	BIM|BimEL|BimL|BimS|BOD	LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11.Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3' untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.	33845844	RID04858	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Pneumonia	SNHG16	SUSD2	positively-E	dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell autophagy(+);inflammatory response(+);cell proliferation(-)	ceRNA(miR-141-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000099994	NA	100507246	56241	Nbla10727|Nbla12061|ncRAN	BK65A6.2|FLJ22778|W5C5	LncRNA small nucleolar RNA host gene 16 (SNHG16) silencing protects lipopolysaccharide (LPS)-induced cell injury in human lung fibroblasts WI-38 through acting as miR-141-3p sponge.Long noncoding RNA (LncRNA) small nucleolar RNA host gene 16 (SNHG16) is correlated with cell injuries, including pneumonia. However, its role and mechanism remain vague in pneumonia. The interplay among genes was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. SNHG16 and sushi domain containing 2 (SUSD2) were upregulated, and miRNA (miR)-141-3p was downregulated in the serum of acute pneumonia patients and lipopolysaccharide (LPS)-challenged human lung fibroblasts WI-38. LPS induced apoptosis, autophagy, and inflammatory response in WI-38 cells, which was significantly attenuated by SNHG16 knockdown and/or miR-141-3p overexpression. Notably, both SNHG16 and SUSD2 were identified as target genes of miR-141-3p. Besides, the suppressive role of SNHG16 knockdown in LPS-induced in WI-38 cells was partially abolished by miR-141-3p silencing, and the similar inhibition of miR-141-3p overexpression was further blocked by SUSD2 restoration. In conclusion, knockdown of SNHG16 could alleviate LPS-induced apoptosis, autophagy, and inflammation in WI-38 cells partially though the SNHG16/miR-141-3p/SUSD2 pathway.	33836533	RID04859	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(BRCA);DATA(GSE55807)
Glioblastoma	OXCT1-AS1	CDC25A	positively-E	GEO;LncBase Predicted v.2;dual-luciferase reporter assay	upregulation	qRT-PCR	GSE4290;GSE90603;GSE104267	NA	cell proliferation(+);cell migration(+);cell invasion(+);prognosis	ceRNA(miR-195)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000248668	GRCh38_5:41869927-41872241	ENSG00000164045	NA	100874002	993	SARRAH	NA	Novel LncRNA OXCT1-AS1 indicates poor prognosis and contributes to tumorigenesis by regulating miR-195/CDC25A axis in glioblastoma.Long noncoding RNAs (lncRNAs) contribute to multiple biological processes in human glioblastoma (GBM). However, identifying a specific lncRNA target remains a challenge. In this study, bioinformatics methods and competing endogenous RNA (ceRNA) network regulatory rules were used to identify GBM-related lncRNAs and revealed that OXCT1 antisense RNA 1 (OXCT1-AS1) is a potential therapeutic target for the treatment of glioma. Based on the Gene Expression Omnibus (GEO) dataset, we identified differential lncRNAs, microRNAs and mRNAs and constructed an lncRNA-associated ceRNA network. The novel lncRNA OXCT1-AS1 was proposed to function as a ceRNA, and its potential target miRNAs were predicted through the database LncBase Predicted v.2. The expression patterns of OXCT1-AS1 in glioma and normal tissue samples were measured. The effect of OXCT1-AS1 on glioma cells was checked using the Cell Counting Kit 8 assay, cell colony formation assay, Transwell assay and flow cytometry in vitro. The dual-luciferase activity assay was performed to investigate the potential mechanism of the ceRNA network. Finally, orthotopic mouse models of glioma were created to evaluate the influence of OXCT1-AS1 on tumour growth in vivo. In this study, it was found that the expression of lncRNA OXCT1-AS1 was upregulated in both The Cancer Genome Atlas (TCGA) GBM patients and GBM tissue samples, and high expression of OXCT1-AS1 predicted a poor prognosis. Suppressing OXCT1-AS1 expression significantly decreased GBM cell proliferation and inhibited cell migration and invasion. We further investigated the potential mechanism and found that OXCT1-AS1 may act as a ceRNA of miR-195 to enhance CDC25A expression and promote glioma cell progression. Finally, knocking down OXCT1-AS1 notably attenuated the severity of glioma in vivo. OXCT1-AS1 inhibits glioma progression by regulating the miR-195-5p/CDC25A axis and is a specific tumour marker and a novel potential therapeutic target for glioma treatment.In summary, OXCT1-AS1 promotes GBM cell proliferation by competitively binding miR-195 and negatively regulating the miR-195/CDC25A axis.	33832517	RID04860	ceRNA or sponge	prognosis		UP(LIHC);DATA(GSE117623)
Gastric cancer	MSC-AS1	DDX5	positively-E	luciferase assays;RIP;TargetScan	upregulation	RT-qPCR	NA	NA	cell growth(+);inflammatory response(+);cell cycle(+)	ceRNA(miR-142-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000235531	GRCh38_8:71828167-72118393	ENSG00000263077	NA	100132891	1655	NA	G17P1|HLR1|p68	MSC-AS1 induced cell growth and inflammatory mediators secretion through sponging miR-142-5p/DDX5 in gastric carcinoma.Emerging studies have noted that dysregulated lncRNAs are implicated in cancer progression and tumorigenesis. We first showed that MSC-AS1 was overexpressed in gastric cancer (GC) cells (HGC-27, MKN-45, SGC-7901 and MGC-803 cells) compared with GES cells. We observed that MSC-AS1 was upregulated in GC specimens compared with paired normal specimens. MSC-AS1 increased cell growth and cycle progression. Moreover, the overexpression of MSC-AS1 enhanced the secretion of the inflammatory mediators IL-1beta, IL-6 and TNF-alpha. We found that the overexpression of MSC-AS1 inhibited the expression of miR-142-5p in HGC-27 cells. We noted that DDK5 was a target gene of miR-142-5p. The overexpression of miR-142-5p suppressed the luciferase activity of wild-type DDX5, but the luciferase activity of the mutant DDX5 was not changed. We showed that miR-142-5p was downregulated in GC specimens compared with paired normal specimens. MSC-AS1 expression was inversely correlated with miR-142-5p expression in GC specimens. MSC-AS1 induced cell growth, cell cycle progression and inflammatory mediator secretion by modulating DDX5. These results showed that MSC-AS1 functions as a key oncogene in the development of GC.	33819916	RID04861	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hypertrophic scar	MIR503HG	SMAD3	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Other	Hypertrophic scar	lncRNA	TF	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000166949	NA	84848	4088	H19X|MGC16121	HsT17436|JV15-2|MADH3	LncRNA MIR503HG promotes hypertrophic scar progression via miR-143-3p-mediated Smad3 expression.Hypertrophic scars (HSs) form due to unchecked proliferation of fibrous tissue after an injury to the skin. Recently, lncRNA MIR503HG was shown to be involved in HS. However, the mechanism by which MIR503HG affects the formation and progression of HS still needs further study. qRT-PCRwas applied to examine the levels of MIR503HG and miR-143-3p in HS tissues and human hypertrophic scar fibroblasts (hHSFs). The relationships of MIR503HG, miR-143-3p and Smad3 were explored with a dual-luciferase reporter assay. Cell proliferation, apoptosis, and invasion were measured by CCK-8 assay, flow cytometry and transwell assay, respectively. The protein level of Smad3 was tested via western blot. MIR503HG was upregulated and miR-143-3p was downregulated in HS versus normal skin tissues. The knockdown of MIR503HG and the overexpression of miR-143-3p suppressed the proliferation and invasion of hHSF, and promoted cell apoptosis. MIR503HG bound to miR-143-3p while miR-143-3p directly targeted Smad3 to inhibit its expression. Suppression of miR-143-3p and overexpression of Smad3, respectively, reversed these effects of knockdown of MIR503HG and overexpression of miR-143-3p on hHSFs. Our research supports a model in which the MIR503HG/miR-143-3p/Smad3 axis serves as a critical regulator of HS, highlighting a promising therapeutic option for HS.	33819360	RID04862	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	PVT1	ARL2	positively-E	dual-luciferase reporter assay;TargetScanHuman 7.2	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(-);tumorigenesis(+)	ceRNA(miR-503)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000213465	NA	5820	402	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ARFL2	LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression.Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual-luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1  in vivo . PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth  in vivo . PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.	33817293	RID04863	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE51827)
Osteosarcoma	ELAVL1	XIST	negatively-E	RIP	downregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	PCG	lncRNA	ENSG00000066044	NA	ENSG00000229807	GRCh38_X:73820649-73852723	1994	7503	Hua|HUR|MelG	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	Silencing of HuR Inhibits Osteosarcoma Cell Epithelial-Mesenchymal Transition via AGO2 in Association With Long Non-Coding RNA XIST.Osteosarcoma (OS) is a highly malignant and aggressive bone tumor. This study was performed to explore the mechanisms of HuR (human antigen R) in the progression of OS. HuR expression levels in OS tissues and cells were detected by immunohistochemistry and western blot. HuR siRNA was transfected into SJSA-1 OS cells to downregulate HuR expression, and then cell proliferation, migration, and epithelial-mesenchymal transition (EMT) were evaluated. RNA immunoprecipitation was performed to determine the association of the long non-coding RNA (lncRNA) XIST and argonaute RISC catalytic component (AGO) 2 with HuR. Fluorescence  in situ  hybridization analysis was performed to detect the expression of lncRNA XIST. western blot and immunofluorescence assays were performed to observe AGO2 expression after HuR or/and lncRNA XIST knockdown. Knockdown of HuR repressed OS cell migration and EMT. AGO2 was identified as a target of HuR and silencing of HuR decreased AGO2 expression. The lncRNA XIST was associated with HuR-mediated AGO2 suppression. Moreover, knockdown of AGO2 significantly inhibited cell proliferation, migration, and EMT in OS. Our findings indicate that HuR knockdown suppresses OS cell EMT by regulating lncRNA XIST/AGO2 signaling.	33816232	RID04864	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Osteosarcoma	XIST	AGO2	positively-E	FISH	downregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000123908	NA	7503	27161	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	CASC7|EIF2C2|hAGO2|LINC00980|Q10	Silencing of HuR Inhibits Osteosarcoma Cell Epithelial-Mesenchymal Transition via AGO2 in Association With Long Non-Coding RNA XIST.Osteosarcoma (OS) is a highly malignant and aggressive bone tumor. This study was performed to explore the mechanisms of HuR (human antigen R) in the progression of OS. HuR expression levels in OS tissues and cells were detected by immunohistochemistry and western blot. HuR siRNA was transfected into SJSA-1 OS cells to downregulate HuR expression, and then cell proliferation, migration, and epithelial-mesenchymal transition (EMT) were evaluated. RNA immunoprecipitation was performed to determine the association of the long non-coding RNA (lncRNA) XIST and argonaute RISC catalytic component (AGO) 2 with HuR. Fluorescence  in situ  hybridization analysis was performed to detect the expression of lncRNA XIST. western blot and immunofluorescence assays were performed to observe AGO2 expression after HuR or/and lncRNA XIST knockdown. Knockdown of HuR repressed OS cell migration and EMT. AGO2 was identified as a target of HuR and silencing of HuR decreased AGO2 expression. The lncRNA XIST was associated with HuR-mediated AGO2 suppression. Moreover, knockdown of AGO2 significantly inhibited cell proliferation, migration, and EMT in OS. Our findings indicate that HuR knockdown suppresses OS cell EMT by regulating lncRNA XIST/AGO2 signaling.	33816232	RID04865	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Papillary thyroid carcinoma	HCG18	PPP2R2A	positively-E	ENCORI;TargetScan v7.2;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-);apoptosis process(+)	ceRNA(miR-106a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000221914	NA	414777	5520	Em:AB014087.1|FLJ25550|FLJ31598	B55A|B55alpha|PR52A|PR55A|PR55alpha	LncRNA-HCG18 regulates the viability, apoptosis, migration, invasion and epithelial-mesenchymal transition of papillary thyroid cancer cells via regulating the miR-106a-5p/PPP2R2A axis.The incidence of papillary thyroid cancer (PTC) has experienced a rapid increase in recent years. Long non-coding RNA-homo sapiens HLA complex group (HCG) 18 plays a regulatory role in cancers, but its role in PTC remained unknown. This study determined the expressions of HCG18, microRNA (miR)-106a-5p, and protein phosphatase 2 regulatory subunit B alpha (PPP2R2A) in PTC tissues and cells by qRT-PCR ENCORI predicted the targeting relation between HCG18 and miR-106a-5p. TargetScan v7.2 predicted the targeting relation between miR-106a-5p and PPP2R2A. dual-luciferase reporter assay was performed to validate the two targeting relations. The viability, migration, and invasion of PTC cells were detected by Cell Counting Kit-8, wound healing assay, and Transwell assay, respectively. The expressions of matrix metalloproteinase 2 (MMP-2), MMP-9, E-cadherin, N-cadherin, and Vimentin in TPC-1 and MDA-T68 cells were assessed by qRT-PCRand western blot. It was found that HCG18 was down-regulated in PTC. Overexpressing HCG18 suppressed viability, migration, and invasion, promoted apoptosis, and inhibited miR-106a-5p expression in PTC cells. HCG18 interacted with miR-106a-5p, the expression of which was upregulated in PTC. Upregulating miR-106a-5p expression by lentivirus infection promoted viability, migration and invasion and inhibited apoptosis of PTC cells, reversed the effect of HCG18 on the biological behaviors of PTC cells, and promoted the expressions of MMP-2, MMP-9, E-cadherin, and Vimentin and downregulated E-cadherin expression in PTC cells. PPP2R2A, a direct target of miR-106a-5p, was downregulated in PTC, and HCG18 promoted PPP2R2A expression in PTC cells by sponging miR-106a-5p. Furthermore, PPP2R2A reversed the effects of miR-106a-5p on PTC cells. In conclusion, HCG18 suppressed viability, migration, invasion and epithelial-mesenchymal transition and promoted apoptosis of PTC cells via regulating the miR-106a-5p/PPP2R2A axis.	33798913	RID04866	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE75367)
Non-small cell lung cancer	MCF2L-AS1	miR-873-5p	negatively-F	RNA-pull down assay;luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell stemness(+)	NA	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000235280	GRCh38_13:112967484-112968824	NA	NA	100289410	NA	NA	NA	Long noncoding RNA MCF2L-AS1 promotes the cancer stem cell-like traits in non-small cell lung cancer cells through regulating miR-873-5p level.The roles of long noncoding RNA (lncRNA) MCF2L-AS1 have been identified in colorectal cancer, however, its roles in lung cancer progression have never been revealed. Here, we found that lncRNA MCF2L-AS1 was highly expressed in lung cancer tissues and cells, especially in non-small cell lung cancer (NSCLC). Functional experiments showed that MCF2L-AS1 knockdown suppressed the cancer stem cell (CSC)-like traits of NSCLC cells through qRT-PCR western blot, tumor-sphere formation, and ALDH activity detection. Additionally, bioinformatic assay combined with RNA pull down and luciferase reporter analysis confirmed that MCF2L-AS1 downregulated miR-873-5p level. Furthermore, miR-873-5p expression exhibited a lower level in lung cancer tissues and cells, and a negative correlation with MCF2L-AS1 expression in lung cancer tissues. Moreover, miR-873-5p inhibition partially reversed the suppression of MCF2L-AS1 on the CSC-like traits on NSCLC cells. Thus, this work identifies a novel MCF2L-AS1/miR-873-5p regulatory axis responsible for the CSC-like traits of NSCLC cells.	33783940	RID04867	expression association	NA		
Pancreatic cancer	OIP5-AS1	FOXM1	positively-E		upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);apoptosis process(-);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-320b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000111206	NA	729082	2305	cyrano|linc-OIP5	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	OPA Interacting Protein 5 Antisense RNA 1 Expedites Cell Migration and Invasion Through FOXM1/ Wnt/beta-Catenin Pathway in Pancreatic Cancer.Pancreatic cancer (PC) is a digestive tract malignancy with poor prognosis. Long noncoding RNA (lncRNA) OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was regarded to be correlated with human malignancy, working as tumor suppressor or promoter on the basis of tumor types. However, the function of OIP5-AS1 in PC remained unclear. The study focused on the function and regulatory mechanism of OIP5-AS1 in PC. OIP5-AS1 expression was assessed by the quantitative reverse transcription PCR (RT-qPCR) in tumor tissues and PC cell lines. 5-ethynyl-2'-deoxyuridine (EdU) incorporation and cell counting kit-8 (CCK-8) assays were applied to detect cell proliferation ability. Through wound healing and transwell assays, cell migration and invasion capacities were estimated. Flow cytometry analysis was performed to examine apoptosis capability of PC cells. OIP5-AS1 downregulating inhibited cell proliferation, migration, and invasion capacities, while promoting cell apoptosis rates. As a competing endogenous RNA (ceRNA), OIP5-AS1 competed with Forkhead Box M1 (FOXM1) for the binding sites on microRNA-320b (miR-320b). OIP5-AS1 was able to upregulate FOXM1 expression via silencing miR-320b. Furthermore, FOXM1 served as an activator of Wnt/beta-catenin pathway and mediated the effect of OIP5-AS1 on Wnt/beta-catenin pathway. OIP5-AS1 expedites the proliferative, migrated, and invasive capability of PC cells, while repressing cell apoptosis through regulating miRNA-320b/FOXM1 axis and FOXM1/Wnt/beta-catenin pathway in PC. OIP5-AS1 regulation on FOXM1/Wnt/beta-catenin pathway may offer novel efficient markers for PC treatments.	33782807	RID04868	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Oral squamous cell carcinoma	H19	PFKFB3	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	MAPK signaling pathway(+);glycolysis signaling pathway(+)	ceRNA(miR-675-5p)	regulation	RNA-protein	NA	CSC	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000170525	NA	283120	5209	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Glycolysis reprogramming in cancer-associated fibroblasts promotes the growth of oral cancer through the lncRNA H19/miR-675-5p/PFKFB3 signaling pathway.As an important component of the tumor microenvironment, cancer-associated fibroblasts (CAFs) secrete energy metabolites to supply energy for tumor progression. Abnormal regulation of long noncoding RNAs (lncRNAs) is thought to contribute to glucose metabolism, but the role of lncRNAs in glycolysis in oral CAFs has not been systematically examined. In the present study, by using RNA sequencing and bioinformatics analysis, we analyzed the lncRNA/mRNA profiles of normal fibroblasts (NFs) derived from normal tissues and CAFs derived from patients with oral squamous cell carcinoma (OSCC). LncRNA H19 was identified as a key lncRNA in oral CAFs and was synchronously upregulated in both oral cancer cell lines and CAFs. Using small interfering RNA (siRNA) strategies, we determined that lncRNA H19 knockdown affected proliferation, migration, and glycolysis in oral CAFs. We found that knockdown of lncRNA H19 by siRNA suppressed the MAPK signaling pathway, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) and miR-675-5p. Furthermore, the lncRNA H19/miR-675-5p/PFKFB3 axis was involved in promoting the glycolysis pathway in oral CAFs, as demonstrated by a luciferase reporter system assay and treatment with a miRNA-specific inhibitor. Our study presents a new way to understand glucose metabolism in oral CAFs, theoretically providing a novel biomarker for OSCC molecular diagnosis and a new target for antitumor therapy.	33762576	RID04869	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	OIP5-AS1	CCNG1	positively-E	dual-luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);glycolysis(+);apoptosis process(-)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000113328	NA	729082	900	cyrano|linc-OIP5	CCNG	Long non-coding RNA OIP5-AS1 facilitates the progression of ovarian cancer via the miR-128-3p/CCNG1 axis.Long non-coding RNA (LncRNA) o-phthalaldehyde-interacting protein 5 antisense transcript 1 (OIP5-AS1) serves major roles in the progression of various types of cancer. The present study investigated its biological function in ovarian cancer (OC) and its mechanisms. The levels of OIP5-AS1, microRNA-128-3p (miR-128-3p) and cyclin G1 (CCNG1) were examined by reverse transcription-quantitative PCR. Cell viability, apoptosis, migration and invasion were detected to analyze cellular progression. Glycolytic metabolism was assessed by detecting the levels of glucose consumption and lactate production. CCNG1 and hexokinase 2 protein levels were measured by western blot. dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assays were performed to affirm the interaction between two molecules. OIP5-AS1 was found to be upregulated in OC tissues and cells. Knockdown of OIP5-AS1 suppressed cell viability, migration, invasion and glycolysis while promoting apoptosis in OC cells. OIP5-AS1 interacted with miR-128-3p and functioned as an oncogene by sequestering miR-128-3p. In addition, CCNG1 was a target gene for miR-128-3p and miR-128-3p regulated the CCNG1-induced effects on OC cells by downregulating CCNG1. OIP5-AS1 upregulated the expression of CCNG1 via targeting miR-128-3p. OIP5-AS1 knockdown also inhibited tumor growth of OC in vivo by modulating the expression of miR-128-3p and CCNG1. Collectively, these data illustrated that the oncogenic role of OIP5-AS1 in OC was associated with the miR-128-3p/CCNG1 axis at least in part. OIP5-AS1 might be a probable diagnostic and therapeutic biomarker for the treatment of OC patients.	33760168	RID04870	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842)
Hepatocellular carcinoma	LINC-ROR	TWIST1	positively-E	western blot;immunofluorescence	upregulation	RT-qPCR	NA	NA	chemoresistance(+)	NA	binding/interaction	NA	Doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000122691	NA	100885779	7291	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	linc-ROR facilitates hepatocellular carcinoma resistance to doxorubicin by regulating TWIST1-mediated epithelial-mesenchymal transition.Long non-coding RNAs are associated with cancer progression. Long intergenic non-protein coding RNA (linc)-regulator of reprogramming (ROR) enhances tumor development in hepatocellular carcinoma (HCC). However, the effect of chemoresistance and its underlying mechanisms in HCC are not completely understood. The present study aimed to identify the effect of ROR on sensitivity to doxorubicin (DOX) in HCC cells. In the present study, Cell Counting Kit-8 and EdU assays were performed to assess cell viability and proliferation, respectively. In addition, E-cadherin and vimentin protein expression levels were assessed via western blot and immunofluorescence. The results of the present study demonstrated that HCC cells with high linc-ROR expression levels were more resistant to DOX, and linc-ROR knockdown increased HCC cell DOX sensitivity compared with the control group. The results indicated that compared with the NC siRNA group, linc-ROR knockdown notably suppressed epithelial-mesenchymal transition by downregulating twist family bHLH transcription factor 1 (TWIST1) expression. TWIST1 knockdown displayed a similar effect on HCC cell DOX sensitivity to linc-ROR knockdown. Moreover, linc-ROR knockdown-induced HCC cell DOX sensitivity was inhibited by TWIST1 overexpression. The present study provided evidence that linc-ROR promoted HCC resistance to DOX by inducing EMT via interacting with TWIST1. Therefore, linc-ROR might serve as a therapeutic target for reducing DOX resistance in HCC.	33760121	RID04871	expression association	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	PINT87aa	FOXM1	negatively-F	dual-luciferase reporter gene assay;western blot;ChIP	downregulation	RT-qPCR	NA	NA	cell growth(-);senescence(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000111206	NA	NA	2305	NA	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Cellular senescence in hepatocellular carcinoma induced by a long non-coding RNA-encoded peptide PINT87aa by blocking FOXM1-mediated PHB2.Rationale:  Recently, long non-coding RNAs (lncRNAs), known to be involved in human cancer progression, have been shown to encode peptides with biological functions, but the role of lncRNA-encoded peptides in cellular senescence is largely unexplored. We previously reported the tumor-suppressive role of PINT87aa, a peptide encoded by the long intergenic non-protein coding RNA, p53 induced transcript ( LINC-PINT).  Here, we investigated PINT87aa's role in hepatocellular carcinoma (HCC) cellular senescence.  Methods:  We examined PINT87aa and truncated PINT87aa functions  in vitro  by monitoring cell proliferation and performed flow cytometry, senescence-associated beta-galactosidase staining, JC-1 staining indicative of mitochondrial membrane potential, the ratio of the overlapping area of light chain 3 beta (LC3B) and mitochondrial probes and the ratio of lysosomal associated membrane protein 1 (LAMP1) overlapping with cytochrome c oxidase subunit 4I1 (COXIV) denoting mitophagy. PINT87aa and truncated PINT87aa functions  in vivo  were verified by subcutaneously transplanted tumors in nude mice. The possible binding between PINT87aa and forkhead box M1 (FOXM1) was predicted through structural analysis and verified by co-immunoprecipitation and immunofluorescence co-localization. Rescue experiments were performed  in vivo and in vitro  following FOXM1 overexpression. Further, chromatin immunoprecipitation, polymerase chain reaction, and dual-luciferase reporter gene assay were conducted to validate FOXM1 binding to the  prohibitin 2  ( PHB2 ) promoter.  Results:  PINT87aa was significantly increased in the hydrogen peroxide-induced HCC cell senescence model. Overexpression of PINT87aa induced growth inhibition, cellular senescence, and decreased mitophagy  in vitro  and  in vivo . In contrast, FOXM1 gain-of-function could partially reduce the proportion of senescent HCC cells and enhance mitophagy. PINT87aa overexpression did not affect the expression of FOXM1 itself but reduced that of its target genes involved in cell cycle and proliferation, especially  PHB2,  which was involved in mitophagy and transcribed by FOXM1. Structural analysis indicated that PINT87aa could bind to the DNA-binding domain of FOXM1, which was confirmed by co-immunoprecipitation and immunofluorescence co-localization. Furthermore, we demonstrated that the 2 to 39 amino acid truncated form of the peptide exerted effects similarly to the full form.  Conclusion:  Our study established the role of PINT87aa as a novel biomarker and a key regulator of cellular senescence in HCC and identified PINT87aa as a potential therapeutic target for HCC.	33754036	RID04872	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Psoriasis	HOTAIR	miR-126	negatively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Integumentary system disease	Skin disease	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Role of the long non-coding RNA HOTAIR/miR-126 axis in an in vitro psoriasis model.Psoriasis is a T-cell-mediated inflammatory skin disease that is characterized by excessive keratinocyte proliferation and persistent skin inflammation. Accumulating evidence suggests that long non-coding RNAs (lncRNAs) are dysregulated in a number of inflammatory conditions. In the present study, an  in vitro  psoriasis cell model was established. Human HaCaT keratinocytes were activated using the inflammatory factor IL-22. Briefly, HaCaT cells were starved in serum-free DMEM for 24 h and then stimulated with 100 ng/ml IL-22 in serum-free DMEM for 24 h. Previous research indicated that HOX transcript antisense RNA (HOTAIR) may participate in the development of psoriasis. First, reverse transcription-quantitative PCR (RT-qPCR) analysis was performed to detect HOTAIR expression. The results indicated that HOTAIR expression was reduced in IL-22-stimulated HaCaT cells. Subsequently, a dual-luciferase reporter assay was performed to verify the binding site between HOTAIR and microRNA (miR)-126. The RT-qPCR results indicated that miR-126 expression was increased in IL-22-stimulated HaCaT cells. Moreover, the effects of HOTAIR and miR-126 on IL-22-stimulated HaCaT cell proliferation and apoptosis were assessed. HaCaT cells were transfected with control-plasmid, HOTAIR-plasmid, HOTAIR-plasmid + mimic control or HOTAIR-plasmid + miR-126 mimic for 24 h. At 24 h post-transfection, the cells were stimulated with 100 ng/ml IL-22 for 24 h and experiments were conducted. IL-22 induced cell proliferation and suppressed apoptosis. However, HOTAIR-plasmid inhibited cell viability and induced apoptosis in IL-22-stimulated HaCaT cells. In addition, the western blot results indicated that HOTAIR-plasmid increased cleaved caspase-3 expression and the cleaved caspase-3/caspase-3 ratio, whereas the HOTAIR-plasmid-mediated effects were reversed by miR-126 mimic. Collectively, the results of the present study demonstrated that the lncRNA-HOTAIR/miR-126 axis may be implicated in the regulation of psoriasis progression and may serve as a potential therapeutic target for psoriasis.	33747185	RID04873	transcriptional regulation	NA		
Hepatocellular carcinoma	SLC16A1-AS1	miR-141	negatively-E	Linear regression	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	DNA methylation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000226419	GRCh38_1:112956415-113047055	NA	NA	100506392	NA	ENST00000421157.1	NA	LncRNA SLC16A1-AS1 is upregulated in hepatocellular carcinoma and predicts poor survival.Long non-coding RNAs (LncRNAs) are broadly transcribed in the genome of human and animals, they play critical roles in cellular process, and participate in the progression of multiple diseases, including cancer. SLC16A1-AS1 is a tumor suppressive lncRNA in lung cancer. This study aimed to investigate the involvement of lncRNA SLC16A1-AS1 in hepatocellular carcinoma (HCC). A total of 64 HCC patients were subjected to biopsy to obtain paired HCC and non-tumor tissues. Expression of SLC16A1-AS1 and miR-141 in paired tissues was determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of SLC16A1-AS1 and miR-141 were achieved in HCC cells to explore the interactions between them. The methylation of the gene encoding miR-141 in HCC cells was detected by methylation-specific PCR (MSP). CCK-8 assay was performed for cell proliferation assay. SLC16A1-AS1 was upregulated in HCC and its high expression levels predicted poor survival of HCC patients. Expression levels of miR-141 were lower in HCC patients and were inversely correlated with the expression levels of SLC16A1-AS1. In HCC cells, overexpression of SLC16A1-AS1 led to downregulation of miR-141, while overexpression of miR-141 did not regulate the expression of SLC16A1-AS1. In addition, overexpression of SLC16A1-AS1 led to increased methylation of miR-141. And overexpression of SLC16A1-AS1 attenuated the inhibitory effects of miR-141 on HCC cell proliferation. SLC16A1-AS1 is upregulated in HCC and predicts poor survival. In addition, SLC16A1-AS1 may downregulate miR-141 through methylation to promote cancer cell proliferation.	33744723	RID04874	epigenetic regulation	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE51827,GSE86978)	
Parkinson's disease	MALAT1	GPNMB	positively-E	western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-135b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136235	NA	378938	10457	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HGFIN|NMB	Long non-coding RNA MALAT1 regulates cell proliferation and apoptosis via miR-135b-5p/GPNMB axis in Parkinson's disease cell model.Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. SK-N-SH and SK-N-BE cells were treated with MPP +  to establish the MPP + -stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP + -stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP + -stimulated cell model of PD were explored. MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP + -stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP + -stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.	33726823	RID04875	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Kidney injury	H19	BCL2L11	positively-E	dual-luciferase reporter assay;Starbase	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell injury(+);cell proliferation(-)	ceRNA(miR-130a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Injury	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000153094	NA	283120	10018	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BIM|BimEL|BimL|BimS|BOD	Long Non-coding RNA H19 Augments Hypoxia/Reoxygenation-Induced Renal Tubular Epithelial Cell Apoptosis and Injury by the miR-130a/BCL2L11 Pathway.Acute kidney injury (AKI) is a severe kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the lncRNA H19/miR-130a axis for the regulation of inflammation, proliferation, and apoptosis in kidney epithelial cells. Human renal proximal tubular cells (HK-2) were induced by hypoxia/reoxygenation to replicate the AKI model  in vitro . After treatment, the effects of LncRNA H19 and miR-130a on proliferation and apoptosis of HK-2 cells were investigated by CCK-8 and flow cytometry. Meanwhile, the expressions of LncRNA H19, miR-130a, and inflammatory cytokines were detected by qRT-PCR western blot, and ELISA assays. The results showed that downregulation of LncRNA H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway. Taken together, our findings indicated that LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic biomarkers for the treatment of AKI.	33716779	RID04876	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	MITA1	MAP1LC3A	positively-E	qRT-PCR;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell viability(+)	NA	regulation	RNA-protein	Gefitinib	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000101460	NA	NA	84557	NA	ATG8E|LC3|LC3A|MAP1ALC3|MAP1BLC3	LncRNA MITA1 promotes gefitinib resistance by inducing autophagy in lung cancer cells.Lung cancer is a major health challenge worldwide. Gefitinib, a tyrosine kinase inhibitor (TKI), is the common therapeutic drug used in advanced non-small-cell lung cancer (NSCLC). However, it is eventually bound to face the problem of acquired drug resistance. In this work, we investigated the role of lncRNA MITA1 in the acquisition of gefitinib resistance in NSCLC and uncovered the possible underlying molecular mechanism of the same. Experiments were carried out using the HCC827 and HCC827GR cells. These were transfected with pcDNA-MITA1 or si-MITA1 and treated with gefitinib. Subsequently, lncRNA MITA1 mediated effect on cell viability and apoptosis were studied using the MTT and flow cytometry assays. Furthermore, using qRT-PCR western blot, and immunofluorescence assays, the regulatory association between lncRNA MITA1 and markers of autophagy (LC3, Beclin-1, and p62) were examined by estimating their cellular protein levels. Also, these results were verified in the presence of an autophagy inhibitor bafilomycin A1. We found that MITA1 was highly upregulated in the gefitinib-resistant NSCLC cells, indicating the regulatory role of MITA1 in gefitinib resistance. Mechanistically, upregulated MITA1 led to gefitinib resistance by suppressing apoptosis, increasing cell viability, and inducing autophagy. Furthermore, these results were true when tested in the presence of bafilomycin A1. Our results suggest that MITA1 by inducing autophagy could be a key regulator of gefitinib resistance in NSCLC.	33714755	RID04877	expression association	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	MITA1	Beclin-1	positively-E	qRT-PCR;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell viability(+)	NA	regulation	RNA-protein	Gefitinib	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA MITA1 promotes gefitinib resistance by inducing autophagy in lung cancer cells.Lung cancer is a major health challenge worldwide. Gefitinib, a tyrosine kinase inhibitor (TKI), is the common therapeutic drug used in advanced non-small-cell lung cancer (NSCLC). However, it is eventually bound to face the problem of acquired drug resistance. In this work, we investigated the role of lncRNA MITA1 in the acquisition of gefitinib resistance in NSCLC and uncovered the possible underlying molecular mechanism of the same. Experiments were carried out using the HCC827 and HCC827GR cells. These were transfected with pcDNA-MITA1 or si-MITA1 and treated with gefitinib. Subsequently, lncRNA MITA1 mediated effect on cell viability and apoptosis were studied using the MTT and flow cytometry assays. Furthermore, using qRT-PCR western blot, and immunofluorescence assays, the regulatory association between lncRNA MITA1 and markers of autophagy (LC3, Beclin-1, and p62) were examined by estimating their cellular protein levels. Also, these results were verified in the presence of an autophagy inhibitor bafilomycin A1. We found that MITA1 was highly upregulated in the gefitinib-resistant NSCLC cells, indicating the regulatory role of MITA1 in gefitinib resistance. Mechanistically, upregulated MITA1 led to gefitinib resistance by suppressing apoptosis, increasing cell viability, and inducing autophagy. Furthermore, these results were true when tested in the presence of bafilomycin A1. Our results suggest that MITA2 by inducing autophagy could be a key regulator of gefitinib resistance in NSCLC.	33714755	RID04878	expression association	NA		
Non-small cell lung cancer	MITA1	p62	positively-E	qRT-PCR;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell viability(+)	NA	regulation	RNA-protein	Gefitinib	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000073792	NA	NA	NA	NA	NA	LncRNA MITA1 promotes gefitinib resistance by inducing autophagy in lung cancer cells.Lung cancer is a major health challenge worldwide. Gefitinib, a tyrosine kinase inhibitor (TKI), is the common therapeutic drug used in advanced non-small-cell lung cancer (NSCLC). However, it is eventually bound to face the problem of acquired drug resistance. In this work, we investigated the role of lncRNA MITA1 in the acquisition of gefitinib resistance in NSCLC and uncovered the possible underlying molecular mechanism of the same. Experiments were carried out using the HCC827 and HCC827GR cells. These were transfected with pcDNA-MITA1 or si-MITA1 and treated with gefitinib. Subsequently, lncRNA MITA1 mediated effect on cell viability and apoptosis were studied using the MTT and flow cytometry assays. Furthermore, using qRT-PCR western blot, and immunofluorescence assays, the regulatory association between lncRNA MITA1 and markers of autophagy (LC3, Beclin-1, and p62) were examined by estimating their cellular protein levels. Also, these results were verified in the presence of an autophagy inhibitor bafilomycin A1. We found that MITA1 was highly upregulated in the gefitinib-resistant NSCLC cells, indicating the regulatory role of MITA1 in gefitinib resistance. Mechanistically, upregulated MITA1 led to gefitinib resistance by suppressing apoptosis, increasing cell viability, and inducing autophagy. Furthermore, these results were true when tested in the presence of bafilomycin A1. Our results suggest that MITA3 by inducing autophagy could be a key regulator of gefitinib resistance in NSCLC.	33714755	RID04879	expression association	NA		
Malignant glioma	RP11-279C4.1	CBX3	positively-E	Wound-Healing Assay;TargetScan database	upregulation	TANRIC;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);self-renewal(+)	ceRNA(miR-1273g-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000122565	NA	NA	11335	NA	HECH|HP1-GAMMA|HP1Hs-gamma	The LncRNA RP11-279C4.1 Enhances the Malignant Behaviour of Glioma Cells and Glioma Stem-Like Cells by Regulating the miR-1273g-3p/CBX3 Axis.Glioma is the most common type of solid tumour affecting the central nervous system, and the survival rate of patients with glioma is low. However, the mechanism associated with glioma progression remains unclear. Growing evidence suggests that lncRNAs play essential roles in the initiation and progression of tumours, including gliomas. In the present study, we identified and verified the expression of the novel lncRNA RP11-279C4.1 by analyzing the TANRIC database and performing qRT-PCRassays, the results of which revealed its upregulation in glioma tissues and cell lines. The results of multiple functional experiments demonstrated that RP11-279C4.1 knockdown inhibited glioma malignant phenotypes, including cell proliferation, migration, invasion and cell self-renew ability in vitro. In addition, RP11-279C4.1 downregulation suppressed tumour growth in vivo. Mechanistically, RP11-279C4.1 induced CBX3 activation via competitively sponging miR-1273g-3p, and rescue assay results confirmed the importance of the RP11-279C4.1/miR-1273g-3p/CBX3 axis. Overall, the results of our present study demonstrated that RP11-279C4.1 functions as an oncogene that promotes tumour progression by modulating the miR-1273g-3p/CBX3 axis in glioma, suggesting that RP11-279C4.1 may be a novel therapeutic target for glioma.	33694060	RID04880	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE86978)
Pulmonary hypertension	HOXA-AS3	PDE5A	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR;western blot	NA	NA	cell growth(+);cell migration(+);apoptosis process(-)	ceRNA(miR-675-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000254369	GRCh38_7:27129977-27155928	ENSG00000138735	NA	100133311	8654	HOXA6as	NA	LncRNA HOXA-AS3 Promotes the Progression of Pulmonary Arterial Hypertension through Mediation of miR-675-3p/PDE5A Axis.Pulmonary arterial hypertension (PAH) seriously threatens the elder people. Long non-coding RNAs (lncRNAs) are involved in multiple diseases. However, the study of the lncRNAs in the occurrence of PAH is just beginning. For this, we sought to explore the biological function of lncRNA HOXA cluster antisense RNA 3 (HOXA-AS3) in PAH. Hypoxia (HYP) was used to mimic in vitro model of PAH. Gene and protein expressions in cells were detected by q-PCR and western blot, respectively. In addition, cell proliferation and viability were tested by CCK-8 and MTT assay. Cell apoptosis was measured by flow cytometry. Wound healing was used to detect cell migration. Furthermore, the connection of HOXA-AS3, miR-675-3p, and phosphodiesterase 5A (PDE5A) was verified by dual-luciferase report assay. HOXA-AS3 and PDE5A were upregulated in human pulmonary artery smooth muscle cells (HPASMCs) in the presence of HYP, while miR-675-3p was downregulated. Moreover, knockdown of HOXA-AS3 suppressed the growth and migration of HPASMCs, but induced the apoptosis. Overexpression of miR-675-3p achieved the same effect. MiR-675-3p inhibitor or overexpression of PDE5A notably reversed the inhibitory effect of HOXA-AS3 knockdown on PAH. Finally, HOXA-AS3 could sponge miR-675-3p, and PDE5A was directly targeted by miR-675-3p. HOXA-AS3 increased the development of PAH via regulation of miR-675-3p/PDE5 axis, which could be the potential biomarker for treatment of PAH.	33687636	RID04881	ceRNA or sponge	NA		UP(LIHC,PRAD);DOWN(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE55807)
Cervical cancer	RPL34-DT	RPL34	positively-E	RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell migration(-);cell invasion(-);cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234492	GRCh38_4:108538190-108620460	ENSG00000109475	NA	285456	6164	FLJ37673|RP11-462C24.1|RPL34-AS1	L34	RPL34-AS1-induced RPL34 inhibits cervical cancer cell tumorigenesis via the MDM2-P53 pathway.Ribosomal proteins (RPs) are important components of ribosomes and related to the occurrence and development of tumors. However, little is known about the effects of the RP network on cervical cancer (CC). In this study, we screened differentially expressed RPL34 in CC by high-throughput quantitative proteome assay. We found that RPL34 acted as a tumor suppressor and was downregulated in CC and inhibited the proliferation, migration, and invasion abilities of CC cells. Next, we verified that RPL34 regulated the CC through the MDM2-P53 pathway by using Act D medicine, MDM2 inhibitor, and a series of western blot assays. Moreover, an antisense lncRNA, RPL34-AS1, regulated the expression of RPL34 and participated in the tumorigenesis of CC. RPL34 can reverse the effect of RPL34-AS1 in CC cells. Finally, by RNA-binding protein immunoprecipitation (RIP) assay we found that eukaryotic initiation factor 4A3 (EIF4A3), which binds to RPL34-AS1, regulated RPL34-AS1 expression in CC. Therefore, our findings indicate that RPL34-AS1-induced RPL34 inhibits CC cell proliferation, invasion, and metastasis through modulation of the MDM2-P53 signaling pathway, which provides a meaningful target for the early diagnosis and treatment of CC.	33675124	RID04882	expression association	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Cervical cancer	EIF4A3	RPL34-DT	positively-E	starBase;RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell migration(-);cell invasion(-);cell proliferation(-)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	PCG	lncRNA	ENSG00000141543	NA	ENSG00000234492	GRCh38_4:108538190-108620460	9775	285456	DDX48|EIF4AIII|Fal1|KIAA0111	FLJ37673|RP11-462C24.1|RPL34-AS1	RPL34-AS1-induced RPL34 inhibits cervical cancer cell tumorigenesis via the MDM2-P53 pathway.Ribosomal proteins (RPs) are important components of ribosomes and related to the occurrence and development of tumors. However, little is known about the effects of the RP network on cervical cancer (CC). In this study, we screened differentially expressed RPL34 in CC by high-throughput quantitative proteome assay. We found that RPL34 acted as a tumor suppressor and was downregulated in CC and inhibited the proliferation, migration, and invasion abilities of CC cells. Next, we verified that RPL34 regulated the CC through the MDM2-P53 pathway by using Act D medicine, MDM2 inhibitor, and a series of western blot assays. Moreover, an antisense lncRNA, RPL34-AS1, regulated the expression of RPL34 and participated in the tumorigenesis of CC. RPL34 can reverse the effect of RPL34-AS1 in CC cells. Finally, by RNA-binding protein immunoprecipitation (RIP) assay we found that eukaryotic initiation factor 4A3 (EIF4A3), which binds to RPL34-AS1, regulated RPL34-AS1 expression in CC. Therefore, our findings indicate that RPL34-AS1-induced RPL34 inhibits CC cell proliferation, invasion, and metastasis through modulation of the MDM2-P53 signaling pathway, which provides a meaningful target for the early diagnosis and treatment of CC.In this study, we found that EIF4A3 could bind to the region of RPL34-AS1 and regulate its expression. Synthetically, we concluded that EIF4A3 can induce RPL34-AS1 transcription.	33675124	RID04883	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761)	
Triple-negative breast cancer	LINC00472	MCM6	negatively-E	western blot;RIP;RNA pull-down assay;ChIP	downregulation	RT-qPCR	GSE61724	NA	apoptosis process(+);cell migration(-);cell invasion(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000076003	NA	79940	4175	C6orf155|dJ288M22.3|FLJ13189|P53RRA	Mis5	Methylation-dependent MCM6 repression induced by LINC00472 inhibits triple-negative breast cancer metastasis by disturbing the MEK/ERK signaling pathway.Long noncoding RNAs (lncRNAs) have been identified to be dysregulated in multiple cancer types, which are speculated to be of vital significance in regulating several hallmarks of cancer biology. Triple-negative breast cancer (TNBC) is acknowledged as an aggressive subtype of breast cancer. In this study, we found the lncRNA LINC00472 was poorly expressed in TNBC tissues and cells. Overexpression of LINC00472 could inhibit the proliferation, invasion and migration of MDA-MB-231 cells. On the contrary, minichromosome maintenance complex component 6 (MCM6) was highly expressed in TNBC tissues and MDA-MB-231 cells due to suppressed methylation. LINC00472 induced site-specific DNA methylation and reduced the MCM6 expression by recruiting DNA methyltransferases into the MCM6 promoter. Since the restoration of MCM6 weakened the tumor-suppressive effect of LINC00472 on MDA-MB-231 cells, LINC00472 potentially acted as a tumor suppressor by inhibiting MCM6. In addition,  in vivo  experiments further substantiated that overexpression of LINC00472 inhibited tumor growth and metastasis to lungs by decreasing the expression of MCM6. Overall, the present study demonstrated that LINC00472-mediated epigenetic silencing of MCM6 contributes to the prevention of tumorigenesis and metastasis in TNBC, providing an exquisite therapeutic target for TNBC.	33668040	RID04884	epigenetic regulation	metastasis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	H19	MTOR	negatively-F		upregulation		NA	NA	apoptosis process(-);cell migration(-);cell invasion(-);cell autophagy(-)	phosphorylation	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long noncoding RNA H19 contributes to the proliferation and autophagy of glioma cells through mTOR/ULK1 pathway.Long noncoding RNA (LncRNA) H19 has been proven to be involved in many kinds of cancers including glioma, and a previous study has shown an autophagy regulation of H19. The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in autophagy and Unc-51 like autophagy activating kinase 1 (ULK1) is also thought to be involved in autophagy signaling. In our study, we investigated the role of mTOR/ULK1 autophagy signaling in the H19-mediated promotion of glioma proliferation. Human glioma cells U87 and U251 and normal human astrocytes HA1800 were used in the study. First, the expression of H19 was determined in U87, U251, and HA1800 cells. Then, the cell proliferation and migration of glioma cells were detected, while the protein levels of main molecules of the mTOR/ULK1 pathway and autophagy-related proteins were also examined. Rapamycin, an inhibitor of mTOR, was used to further study the role of H19 in autophagy. We observed that overexpressed H19 promoted the proliferation and migration in glioma cells. The autophagy of U87 cells was suppressed when H19 was overexpressed and enhanced when H19 was silenced. H19 overexpression inhibited mTOR phosphorylation and promoted ULK1 phosphorylation. H19 promoted proliferation, migration, and autophagy by regulating mTOR signaling. In conclusion, we validate that H19 contributes to the proliferation and autophagy of glioma cells through the mTOR/ULK1 pathway.	33661803	RID04885	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Malignant glioma	H19	ULK1	positively-F		upregulation		NA	NA	apoptosis process(-);cell migration(-);cell invasion(-);cell autophagy(-)	phosphorylation	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000177169	NA	283120	8408	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ATG1|ATG1A	Long noncoding RNA H19 contributes to the proliferation and autophagy of glioma cells through mTOR/ULK1 pathway.Long noncoding RNA (LncRNA) H19 has been proven to be involved in many kinds of cancers including glioma, and a previous study has shown an autophagy regulation of H19. The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in autophagy and Unc-51 like autophagy activating kinase 1 (ULK1) is also thought to be involved in autophagy signaling. In our study, we investigated the role of mTOR/ULK1 autophagy signaling in the H19-mediated promotion of glioma proliferation. Human glioma cells U87 and U251 and normal human astrocytes HA1800 were used in the study. First, the expression of H19 was determined in U87, U251, and HA1800 cells. Then, the cell proliferation and migration of glioma cells were detected, while the protein levels of main molecules of the mTOR/ULK1 pathway and autophagy-related proteins were also examined. Rapamycin, an inhibitor of mTOR, was used to further study the role of H19 in autophagy. We observed that overexpressed H19 promoted the proliferation and migration in glioma cells. The autophagy of U87 cells was suppressed when H19 was overexpressed and enhanced when H19 was silenced. H19 overexpression inhibited mTOR phosphorylation and promoted ULK1 phosphorylation. H19 promoted proliferation, migration, and autophagy by regulating mTOR signaling. In conclusion, we validate that H19 contributes to the proliferation and autophagy of glioma cells through the mTOR/ULK2 pathway.	33661803	RID04886	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	LINC-ROR	MLL1	negatively-E	RNA pull-down assay;RIP;ChIP;western blot analysis	upregulation	RT-qPCR	NA	NA	cell growth(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000118058	NA	100885779	NA	lincRNA-RoR|lincRNA-ST8SIA3|ROR	NA	Long non-coding RNA ROR recruits histone transmethylase MLL1 to up-regulate TIMP3 expression and promote breast cancer progression.As a significant cause of cancer deaths worldwide, breast cancer continues to be a troublesome malignancy. Long non-coding RNAs (lncRNAs) have been implicated in the development of breast cancer. Abnormal methylation has been associated with unfavorable breast cancer prognosis. Herein, the current study aimed to elucidate the role of lncRNA ROR in breast cancer. RT-qPCR was performed to determine whether lncRNA ROR was highly expressed in breast cancer tissues, while lncRNA ROR expression was detected in both the nuclear and cytoplasm of breast cancer cells. MCF-7 cells were subsequently introduced with oe-lncRNA ROR, sh-lncRNA ROR to explore the effects of lncRNA ROR on cell proliferation, invasion and apoptosis. RIP, RNA pull-down and ChIP assays provided evidence suggesting that lncRNA ROR recruited transmethylase MLL1 to promote H3K4 trimethylation that enhanced TIMP3 transcription. The rescue experiments demonstrated that<U+00A0>lncRNA ROR knockdown could inhibit the progression of breast cancer via the downregulation of TIMP3. Finally, the in vivo experiment findings consistently highlighted the suppressive effects of lncRNA ROR silencing on tumor growth. Taken together, our study demonstrates that silencing of lncRNA ROR inhibits breast cancer progression via repression of transmethylase MLL1 and TIMP3, emphasizing the potential of lncRNA ROR as a novel target against breast cancer.	33653378	RID04887	expression association	prognosis	UP(LIHC);DATA(GSE117623)	
Breast cancer	LINC-ROR	TIMP3	positively-E	RNA pull-down assay;RIP;ChIP;western blot analysis	upregulation	RT-qPCR	NA	NA	cell growth(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000100234	NA	100885779	7078	lincRNA-RoR|lincRNA-ST8SIA3|ROR	SFD	Long non-coding RNA ROR recruits histone transmethylase MLL1 to up-regulate TIMP3 expression and promote breast cancer progression.As a significant cause of cancer deaths worldwide, breast cancer continues to be a troublesome malignancy. Long non-coding RNAs (lncRNAs) have been implicated in the development of breast cancer. Abnormal methylation has been associated with unfavorable breast cancer prognosis. Herein, the current study aimed to elucidate the role of lncRNA ROR in breast cancer. RT-qPCR was performed to determine whether lncRNA ROR was highly expressed in breast cancer tissues, while lncRNA ROR expression was detected in both the nuclear and cytoplasm of breast cancer cells. MCF-7 cells were subsequently introduced with oe-lncRNA ROR, sh-lncRNA ROR to explore the effects of lncRNA ROR on cell proliferation, invasion and apoptosis. RIP, RNA pull-down and ChIP assays provided evidence suggesting that lncRNA ROR recruited transmethylase MLL1 to promote H3K4 trimethylation that enhanced TIMP3 transcription. The rescue experiments demonstrated that<U+00A0>lncRNA ROR knockdown could inhibit the progression of breast cancer via the downregulation of TIMP3. Finally, the in vivo experiment findings consistently highlighted the suppressive effects of lncRNA ROR silencing on tumor growth. Taken together, our study demonstrates that silencing of lncRNA ROR inhibits breast cancer progression via repression of transmethylase MLL1 and TIMP4, emphasizing the potential of lncRNA ROR as a novel target against breast cancer.	33653378	RID04888	transcriptional regulation	prognosis	UP(LIHC);DATA(GSE117623)	UP(SKCM);DATA(GSE38495)
Nasopharynx carcinoma	OIP5-AS1	miR-203	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000207568	NA	729082	NA	cyrano|linc-OIP5	NA	Long Noncoding RNA OIP5-AS1 Promotes the Disease Progression in Nasopharyngeal Carcinoma by Targeting miR-203.Nasopharyngeal carcinoma (NPC) is a kind of malignancy generated from the nasopharyngeal epithelium. Recently, long noncoding RNA (lncRNA) has been shown to be involved in the regulation of many signaling pathways and is closely associated with carcinogenesis and tumor progression. However, the precise role of lncRNA Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in NPC is not well understood. Here, we find that OIP5-AS1 is overexpressed in NPC patient specimens and NPC cell lines. Further investigations reveal that knockdown of OIP5-AS1 significantly inhibits the proliferation, migration, and invasion and accelerates the apoptosis of NPC cells  in vitro.  Consistent with these findings, NPC progression is significantly slowed in mice when OIP5-AS1 is knocked down. Interestingly, there is a functional link between OIP5-AS1 and microRNA-203 (miR-203), a tumor suppressor, in NPC cells. In conclusion, our data demonstrate that OIP5-AS1 plays an important role in the development and progression of NPC by targeting miR-203 and therefore provide a promising target for the treatment of NPC.	33628831	RID04889	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Hcc bone metastasis	H19	PPP1CA	negatively-F		upregulation		NA	NA	cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Hepatocellular carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000172531	NA	283120	5499	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PP-1A|PP1A|PP1alpha|PPP1A	H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen-Activated Protein Kinase-Dependent Manner and Sponging microRNA 200b-3p.Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p. H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA-induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR-200b-3p.	33615520	RID04890	expression association	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Hcc bone metastasis	H19	PPP2CA	negatively-F		upregulation		NA	NA	cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Hepatocellular carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000113575	NA	283120	5515	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PP2AC|PP2Calpha	H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen-Activated Protein Kinase-Dependent Manner and Sponging microRNA 200b-3p.Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p. H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA-induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR-200b-4p.	33615520	RID04891	expression association	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065)
Hcc bone metastasis	H19	miR-200b-3p	positively-E		upregulation		NA	NA	apoptosis process(+);cell migration(+);cell invasion(+)	sponge	regulation	RNA-protein	NA	NA	NA	Cancer	Hepatocellular carcinoma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen-Activated Protein Kinase-Dependent Manner and Sponging microRNA 200b-3p.Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p. H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA-induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR-200b-5p.	33615520	RID04892	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	
Rheumatoid arthritis	GAS5	HDAC4	positively-E	RNA pull-down assay;RIP;TargetScan;dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	apoptosis process(+);cell migration(-);cell invasion(-);inflammatory response(-)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000068024	NA	60674	9759	NCRNA00030|SNHG2	BDMR|HA6116|HD4|HDAC-4|HDAC-A|HDACA|KIAA0288	Long non-coding RNA GAS5 suppresses rheumatoid arthritis progression via miR-128-3p/HDAC4 axis.Rheumatoid arthritis (RA) is a highly relevant public health problem. RA fibroblast-like synoviocytes (RAFLSs) play an important role in RA progression. Long non-coding RNA growth arrest-specific transcript 5 (GAS5) could improve RA by inducing RAFLSs apoptosis. However, the mechanism of GAS5 in RA remains unclear. RT-qPCR detected the expressions of GAS5, microRNA-128-3p (miR-128-3p), and histone deacetylase 4 (HDAC4) in RA synovial tissues and RAFLSs. Proliferation, apoptosis, migration, and invasion were measured by Cell Counting Kit-8 assay (CCK-8), flow cytometry, and transwell assays, severally. The protein levels of B-cell lymphoma-2 (Bcl-2), C-caspase 3, Bcl-2 related X protein (Bax), Tumor Necrosis factor-alpha (TNF-alpha), Interleukin 6 (IL-6), Interleukin 17 (IL-17), HDAC4, phosphorylation-protein kinase B (p-AKT), AKT, a phosphorylation-mechanistic target of rapamycin (p-mTOR), and mTOR were assessed by western blot assay. The interaction between miR-128-3p and GAS5 or HDAC4 was predicted by ENCORI or TargetScan Human and verified by the dual-luciferase reporter, RNA Immunoprecipitation (RIP), and RNA pull-down assays. GAS5 and HDAC4 were downregulated, and miR-128-3p was upregulated in RA synovial tissues and RAFLSs. Function analysis indicated that GAS5 curbed proliferation, migration, invasion, inflammation, and facilitated apoptosis of RAFLSs. Rescue assay confirmed that miR-128-3p overexpression or HDAC4 knockdown weakened the inhibitory effect of GAS5 or anti-miR-128-3p on RA development. GAS5 acted as a miR-128-3p sponge to upregulate HDAC4 expression. Besides, GAS5/miR-128-3p/HDAC4 axis regulated RA progression partially through the AKT/mTOR pathway. Our studies disclosed that GAS5 restrained inflammation in synovial tissue partly through regulating HDAC4 via miR-128-3p, suggesting a potential lncRNA-targeted therapy for RA treatment.	33611674	RID04893	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Diabetic retinopathy	SNHG7	XBP1	positively-E	dual-luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	CSC	NA	Nervous system disease	Diabetic retinopathy	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000100219	NA	84973	7494	MGC16037|NCRNA00061	XBP2	MSC-derived exosomal lncRNA SNHG7 suppresses endothelial-mesenchymal transition and tube formation in diabetic retinopathy via miR-34a-5p/XBP1 axis.Diabetic retinopathy (DR) is the most common complication of type 2 diabetes mellitus, which could result in visual impairment. Accumulating studies have shown the implication of long non-coding RNAs (lncRNAs) in the pathogenesis of DR. Our aims are to investigate whether lncRNA SNHG7 plays a role during DR pathogenesis. Human retinal microvascular endothelial cells (HRMECs) were treated with high glucose (HG) to build cell model. Relative expression of RNAs were examined using qPCR, and western blot or immunofluorescence analysis was adopted to detect the protein expression. Cell viability, migration and angiogenic capacity of HRMECs were estimated through CCK-8, transwell and tube formation experiments, respectively. Dual-luciferase reporter and RNA pull-down assays were employed to verify the interplay between miR-34a-5p and SNHG7 or XBP1. Mesenchymal stem cells (MSCs) were identified by examining typical surface makers using flow cytometry and the differentiation abilities via Alizarin red, Oil red O and Alcian blue staining. MSC-derived exosomes were verified by transmission electron microscopy and western blot. LncRNA SNHG7 sponged to and negatively regulated miR-34a-5p. SNHG7 overexpression repressed HG induced endothelial-mesenchymal transition (EndMT) and tube formation of HRMECs, while miR-34a-5p overexpression could reverse this effect. miR-34a-5p targeted and negative regulated XBP1. Knockdown of miR-34a-5p repressed HG induced EndMT and tube formation, which were partially blocked by XBP1 inhibition. MSC-derived exosomes could transfer SNHG7 to HRMECs and modulated EndMT and tube formation. The MSC-derived exosomal lncRNA SNHG7 suppresses EndMT and tube formation in HRMECs via miR-34a-5p/XBP1 axis.	33600866	RID04894	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Nasopharynx carcinoma	HEIH	CDK8	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831618	ENSG00000132964	NA	100859930	1024	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	K35	Long non-coding RNA HEIH modulates CDK8 expression by inhibiting miR-193a-5p to accelerate nasopharyngeal carcinoma progression.Nasopharyngeal carcinoma (NPC) is the commonest malignant tumor. In this article, we aimed to examine the molecular role of lncRNA HEIH in the progression of NPC. We assessed the expression of HEIH, miR-193a-5p and CDK8 in NPC tissues and cells by real-time PCR. The cell proliferation, invasion and migration of SUNE-1 cells were examined by CCK-8 and transwell assay. western blot assay was adopted to measure the protein expression level of CDK8. dual-luciferase reporter assay was adopted to evaluate the correlation between HEIH, miR-193a-5p and CDK8. We discovered that HEIH was high expressed and miR-193a-5p was reduced in both NPC tissues and cells. The upregulation of HEIH facilitated cell proliferation, migration and invasion of SUNE-1 cells. In addition, overexpression of miR-193a-5p restrained cell progression of SUNE-1 cells. Moreover, HEIH was proved to be a molecular sponge of miR-193a-5p in NPC. Besides that, CDK8 was found to be a direct target gene of miR-193a-5p in NPC. Furthermore, CDK8 knockdown suppressed cell progression of SUNE-1 cells. Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8.	33577031	RID04895	ceRNA or sponge	NA	DOWN(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	AND2-AS1	RUNX2	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000124813	NA	NA	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	lncRNA HAND2-AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression.The long non-coding RNA HAND2 antisense RNA 1 (HAND2-AS1) acts as a tumor suppressor in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the function of HAND2-AS1 in HCC. The expression levels of HAND2-AS1 and runt-related transcription factor 2 (RUNX2) were determined in patients with HCC and HCC cell lines using quantitative real-time polymerase chain reaction and western blot. Cell proliferation was determined using Cell Counting Kit-8 assay, and the correlation between HAND2-AS1 and RUNX2 expression was also investigated. The plasma level of HAND2-AS1 was downregulated and that of RUNX2 was upregulated in patients with early-stage HCC compared with those in healthy controls. No significant differences in the plasma levels of HAND2-AS1 and RUNX2 were found among hepatitis B virus (HBV)-positive, hepatitis C virus (HCV)-positive, and HBV- and HCV-negative patients with HCC. The plasma levels of HAND2-AS1 and RUNX2 were inversely correlated in the patient groups but not in the control group. HAND2-AS1 overexpression led to the downregulation of RUNX2 expression in human HCC cells, whereas RUNX2 failed to significantly affect HAND2-AS1 expression. HAND2-AS1 overexpression inhibited and RUNX2 overexpression promoted the proliferation of HCC cells. RUNX2 overexpression attenuated the inhibitory effects of HAND2-AS1 overexpression on cancer cell proliferation. HAND2-AS1 overexpression inhibits cancer cell proliferation in HCC by downregulating RUNX2 expression.	33566427	RID04896	transcriptional regulation	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	MT1JP	FBP1	positively-E	western blot;dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	apoptosis process(+);cell migration(-);cell invasion(-);cell proliferation(-)	ceRNA(miR-18a-5p)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000165140	NA	4498	2203	MT1|MT1J|MT1NP|MTB	FBP	LncRNA MT1JP plays a protective role in intrahepatic cholangiocarcinoma by regulating miR-18a-5p/FBP1 axis.Cholangiocarcinoma is a common malignant tumor of digestive system. LncRNA metallothionein 1<U+2009>J, pseudogene (MT1JP) has been reported to play tumor-suppressing roles in multiple cancers. However, its effect on cholangiocarcinoma has not been evaluated. The expression of MT1JP in intrahepatic cholangiocarcinoma specimens and paired para-carcinoma tissues were detected by real-time PCR. The overexpression plasmid and siRNA of MT1JP were transfected into intrahepatic cholangiocarcinoma cells to change the expression levels of MT1JP. CCK-8, flow cytometry and transwell assays were performed to measure proliferation, cell cycle transition, apoptosis, migration and invasion. dual-luciferase reporter assay, real-time PCR and western blot were carried out to screen the miRNA bound by MT1JP. In addition, xenograft experiment was used to determine the tumorigenesis of cholangiocarcinoma cells in nude mice. MT1JP was downregulated in intrahepatic cholangiocarcinoma specimens, and its expression was related with TNM stage and lymph node metastasis. Overexpression of MT1JP inhibited proliferation, cell cycle transition, migration and invasion, and induced apoptosis in intrahepatic cholangiocarcinoma cells. The knockdown of MT1JP led to opposite results. MT1JP bound to miR-18a-5p to facilitate the expression of fructose-1,6-bisphosphatase 1 (FBP1). MiR-18a-5p was increased in intrahepatic cholangiocarcinoma samples, and its expression was negatively correlated with that of MT1JP. In addition, MT1JP also suppressed tumorigenesis in nude mice. MT1JP alleviated proliferation, migration and invasion, and induced apoptosis in cholangiocarcinoma cells by regulating miR-18a-5p/FBP1 axis. These findings may provide novel insights for clinical diagnosis and treatment of cholangiocarcinoma.	33557774	RID04897	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Ovarian cancer	PVT1	AGO1	positively-E	western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+);cell proliferation(+);cell viability(+);TGF-beta signaling pathway(+)	ceRNA(miR-148a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000092847	NA	5820	26523	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	EIF2C1|hAGO1	LncRNA PVT1 promotes the progression of ovarian cancer by activating TGF-beta pathway via miR-148a-3p/AGO1 axis.Ovarian cancer is a lethal gynaecologic malignancy with poor diagnosis and prognosis. The long non-coding RNA plasmacytoma variant translocation1 (PVT1) and argonaute 1 (AGO1) are associated with carcinogenesis and chemoresistance; however, the relationship between PVT1 and AGO1 and the downstream mechanisms in ovarian cancer remains poorly known. PVT1 and AGO1 expression was assessed through RT-qPCR and western blot in both human tissues and cell lines. The viability and proliferation of ovarian cancer cells were determined by CCK-8 assay and TUNEL assay in vitro and immunohistochemistry in vivo. Cell invasion and migration were investigated through transwell and wound-healing assays. The roles and mechanisms of AGO1 on cell functions were further probed via gain- and loss-of-function analysis. We reveal that PVT1 expression was significantly increased in ovarian cancer tissues which is associated with advanced FIGO stage, lymph-node metastasis, poor survival rate, and high expression of AGO1. PVT1 or AGO1 knockdown significantly reduced the cell viability and increased the cell apoptosis and inhibited ovarian tumour growth and proliferation. Furthermore, we discovered that PVT1 up-regulated the expression of AGO1 and thus regulated the transforming growth factor-beta (TGF-beta) pathway to promote ovarian cancer progression through sponging miR-148a-3p. Additionally, the activation of ERK1/2, smad2 and smad4 is observed to be related to the PVT1/miR-148a-3p/AGO1/TGF-beta pathway-induced cascades. Taken together, the present study reveals that PVT1/miR-148a/AGO1 axis plays an important role in the progression of ovarian cancer and emphasize the potential as a target of value for ovarian cancer therapy.	34288373	RID04898	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Gestational diabetes mellitus	SNX17	IGF1	positively-E	western blot;luciferase Reporter Assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-517a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000115234	GRCh38_2:27370496-27377535	ENSG00000017427	NA	9784	3479	NA	IGF|IGF-I|IGFI|MGF	LncRNA-SNX17 Promotes HTR-8/SVneo Proliferation and Invasion Through miR-517a/IGF-1 in the Placenta of Diabetic Macrosomia.Gestational diabetes mellitus (GDM) has become a worldwide problem in recent years. Macrosomia, a primary consequence of GDM, has short-term and life-long consequences in the offspring of mothers with GDM. Our previous study showed that miR-517a was dysregulated in placenta and plasma of fetal growth restriction through inhibiting invasion of trophoblast and might be closely related with the regulation of birth weight by the placenta. To further investigate the mechanism of miR-517a, we conducted genome-wide microarray profile of lncRNAs. lncRNA-SNX17 was found to be significantly upregulated in the placenta of diabetic macrosomia by qRT-PCR and the expression of miR-517a and IGF-1 were measured by qRT-PCRand western blot. Interestingly, significant inverse correlations of the miR-517a with both lncRNA-SNX17 and IGF-1 expression were revealed in the placenta of diabetic macrosomia. Bioinformatic prediction also revealed that both lncRNA-SNX17 and IGF-1 possessed binding sites for miR-517a, which were then confirmed by luciferase report assay. LncRNA-SNX17 overexpression reduced the expression of miR-517a and increased the IGF-1 expression in HTR-8/SVneo human trophoblast cell line and thus enhanced the proliferation of HTR-8/SVneo. The enhancement of HTR-8/SVneo proliferation by lncRNA-SXN17 could be nullified by co-transfection of miR-517a mimics. The data suggested that lncRNA-SNX17 might promote the trophoblast proliferation through miR-517a/IGF-1 pathway and might play a role in the placentation of diabetic macrosomia.	34270000	RID04899	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC);DATA(GSE117623)
Cervical cancer	SNHG3	N-cadherin	positively-E	western blot	upregulation	RT-qPCR	GSE27678;GSE9750	NA	cell migration(+);cell invasion(+);cell proliferation(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	NA	NA	8420	NA	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	NA	[Role of long noncoding RNA SNHG3 in regulating proliferation, migration and invasion of cervical cancer SiHa cells].To investigate the regulatory role of the long non-coding RNA (lncRNA) small nucleolar host gene 3 (SNHG3) in proliferation, migration and invasion of human cervical cancer cell line SiHa. Array data were retrieved from GEO database to analyze the expression levels of SNHG3 in cervical cancer and adjacent normal tissues. SiHa cells were transfected with a small interfering RNA (siRNA) targeting SNHG3, and the changes in the transcriptional levels of lncRNA SNHG3 and the epithelial-mesenchymal transition (EMT) markers N-cadherin, Snail, vimentin and E-cadherin were detected using real-time quantitative PCR; the protein expressions of N-cadherin, Snail, vimentin and E-cadherin were determined using western blot. Cell counting kit-8 (CCK8) assay was utilized to assess the proliferation capacity of the transfected cells. Wound healing assay and Transwell assay were performed to evaluate the transversal and longitudinal migration and invasion abilities of the cells. SNHG3 was over-expressed in cervical cancer tissues and SiHa cells. In SiHa cells, knocking down SNHG3 significantly inhibited the proliferation ( P  < 0.001), migration ( P  < 0.01) and invasion abilities ( P  < 0.001) of the cells, down-regulated the expression levels of N-cadherin, Snail and vimentin ( P  < 0.001) and up-regulated the expression of E-cadherin ( P  < 0.001). SNHG3 may promote the proliferation, migration and invasion of SiHa cells by activating the EMT signaling pathway.	34238747	RID04900	transcriptional regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Cervical cancer	SNHG3	Snai	positively-E	western blot	upregulation	RT-qPCR	GSE27678;GSE9750	NA	cell migration(+);cell invasion(+);cell proliferation(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	NA	NA	8420	NA	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	NA	[Role of long noncoding RNA SNHG3 in regulating proliferation, migration and invasion of cervical cancer SiHa cells].To investigate the regulatory role of the long non-coding RNA (lncRNA) small nucleolar host gene 3 (SNHG3) in proliferation, migration and invasion of human cervical cancer cell line SiHa. Array data were retrieved from GEO database to analyze the expression levels of SNHG3 in cervical cancer and adjacent normal tissues. SiHa cells were transfected with a small interfering RNA (siRNA) targeting SNHG3, and the changes in the transcriptional levels of lncRNA SNHG3 and the epithelial-mesenchymal transition (EMT) markers N-cadherin, Snail, vimentin and E-cadherin were detected using real-time quantitative PCR; the protein expressions of N-cadherin, Snail, vimentin and E-cadherin were determined using western blot. Cell counting kit-8 (CCK8) assay was utilized to assess the proliferation capacity of the transfected cells. Wound healing assay and Transwell assay were performed to evaluate the transversal and longitudinal migration and invasion abilities of the cells. SNHG3 was over-expressed in cervical cancer tissues and SiHa cells. In SiHa cells, knocking down SNHG3 significantly inhibited the proliferation ( P  < 0.001), migration ( P  < 0.01) and invasion abilities ( P  < 0.001) of the cells, down-regulated the expression levels of N-cadherin, Snail and vimentin ( P  < 0.001) and up-regulated the expression of E-cadherin ( P  < 0.001). SNHG4 may promote the proliferation, migration and invasion of SiHa cells by activating the EMT signaling pathway.	34238747	RID04901	transcriptional regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Cervical cancer	SNHG3	E-cadherin	negatively-E	western blot	upregulation	RT-qPCR	GSE27678;GSE9750	NA	cell migration(+);cell invasion(+);cell proliferation(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	NA	NA	8420	NA	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	NA	[Role of long noncoding RNA SNHG3 in regulating proliferation, migration and invasion of cervical cancer SiHa cells].To investigate the regulatory role of the long non-coding RNA (lncRNA) small nucleolar host gene 3 (SNHG3) in proliferation, migration and invasion of human cervical cancer cell line SiHa. Array data were retrieved from GEO database to analyze the expression levels of SNHG3 in cervical cancer and adjacent normal tissues. SiHa cells were transfected with a small interfering RNA (siRNA) targeting SNHG3, and the changes in the transcriptional levels of lncRNA SNHG3 and the epithelial-mesenchymal transition (EMT) markers N-cadherin, Snail, vimentin and E-cadherin were detected using real-time quantitative PCR; the protein expressions of N-cadherin, Snail, vimentin and E-cadherin were determined using western blot. Cell counting kit-8 (CCK8) assay was utilized to assess the proliferation capacity of the transfected cells. Wound healing assay and Transwell assay were performed to evaluate the transversal and longitudinal migration and invasion abilities of the cells. SNHG3 was over-expressed in cervical cancer tissues and SiHa cells. In SiHa cells, knocking down SNHG3 significantly inhibited the proliferation ( P  < 0.001), migration ( P  < 0.01) and invasion abilities ( P  < 0.001) of the cells, down-regulated the expression levels of N-cadherin, Snail and vimentin ( P  < 0.001) and up-regulated the expression of E-cadherin ( P  < 0.001). SNHG5 may promote the proliferation, migration and invasion of SiHa cells by activating the EMT signaling pathway.	34238747	RID04902	transcriptional regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Pre-eclampsia	AFAP1-AS1	DUSP5	negatively-E		downregulation		NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000138166	NA	84740	1847	AFAP1-AS|AFAP1AS|MGC10981	HVH3	Silencing of AFAP1-AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression in pre-eclampsia.As a unique and common obstetric complication of pregnant women, pre-eclampsia (PE) has been the first leading cause of maternal and perinatal morbidity and mortality in the world. Mounting studies have demonstrated that an abnormality of long noncoding RNA (lncRNA) expression was related to the pathological process of PE. Here, we showed that lncRNA AFAP1-AS1 was markedly downregulated in pre-eclamptic placentas. We further investigated the mechanism underlying the regulatory role of AFAP1-AS1 in PE using human trophoblast cells. In vitro functional assays revealed that AFAP1-AS1 knockdown inhibited trophoblast proliferation, migration, and invasion. Moreover, AFAP1-AS1 interacts with EZH2 and inhibits DUSP5 expression through modulating H3K27m3 in the DUSP5 promoter of trophoblast cells, thus being involved in PE pathogenesis. Overall, these findings suggest that AFAP1-AS1 could potentially become a prognostic biomarker as well as a new therapeutic target for PE.	34192359	RID04903	expression association	prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Abdominal aortic aneurysm	SNHG5	SMAD4	positively-E	dual-luciferase reporter assay;RIP;knockdown	downregulation	qRT-PCR	GSE57691	NA	apoptosis process(+);cell migration(-);cell proliferation(-)	ceRNA(miR-205-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000141646	NA	387066	4089	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	DPC4|MADH4	Based on bioinformatics analysis lncrna SNHG5 modulates the function of vascular smooth muscle cells through mir-205-5p/SMAD4 in abdominal aortic aneurysm.The aim of this study was to explore expression profiles of long noncoding RNA (lncRNA)-messenger RNA (mRNA) in abdominal aortic aneurysm (AAA) patients. Further, we explored the mechanisms by which lncRNA SNHG5 modulates the function of vascular smooth muscle cells (VSMC) in AAA. Human gene expression profile GSE57691 dataset, was retrieved from Gene Expression Omnibus database. The dataset included gene expression array data of 49 AAA patients and 10 control aortic specimens from organ donors. To explore the main roles of the biological network, differentially expressed lncRNA and mRNAs in the aortic aneurysm (AAA) and normal aortic specimens were determined. Differentially expressed lncRNA and mRNAs were then used to construct a competing endogenous RNA (ceRNA) network using Cytoscape software, and the five key lncRNA were identified. SNHG5 which was significantly downregulated in the AAA was chosen and analysis showed that it regulates mir-205-5p and SMAD4 by binding to mir-205-5p. Double luciferase reporter gene assays, RNA immunoprecipitation, and RNA knockdown studies were used to establish the relationship between SNHG5 and mir-205-5p. Apoptosis rate was determined using flow cytometry, whereas cell proliferation was evaluated using Edu, and 24 well Transwell assay. western blotwas used to determine protein expression levels. The five differentially expressed lncRNAs were significantly correlated with 34 microRNAs and 112 mRNAs. mRNAs in the ceRNA network are implicated in protein binding, signal transduction, DNA and RNA transcription, development, and cell differentiation. SNHG5 was downregulated in the AAA and acts as a molecular sponge for mir-205. Downregulation of SNHG5 induces expression of mir-205-5p. Increased mir-205-5p expression level inhibits SMAD4 production, thus inhibiting proliferation and migration and promotes apoptosis of smooth muscle cells. Bioinformatics were used to explore molecular mechanism of AAA progression. The findings of this study show that lncRNA SNHG5 regulates proliferation and apoptosis of VSMC cells through modulation of the mir-205-5p/SMAD4 axis. Therefore, SNHG5 is a potential therapeutic target for AAA disease.	34185955	RID04904	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Renal cancer	DUXAP9	IGF2BP2	positively-F	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000073792	NA	503638	10644	FLJ39632|LINC01296|lncRNA-CTD903|LNMAT1	IMP-2|p62	N6-Methyladenosine Modification of LncRNA DUXAP9 Promotes Renal Cancer Cells Proliferation and Motility by Activating the PI3K/AKT Signaling Pathway.Most localized human renal clear cell carcinoma (ccRCC)-related deaths result from cancer recurrence and metastasis. However, the precise molecular mechanisms largely remain unknown. In recent years, an increasing number of long noncoding RNAs (lncRNAs) have been shown to be vital regulators of tumorigenesis. In this study, we characterized a lncRNA DUXAP9 and the upregulation of DUXAP9 was analyzed by quantitative real-time PCR in 112 pairs of localized ccRCC tumor tissues compared with adjacent normal tissues. Kaplan-Meier curves showed that patients of localized ccRCC with high DUXAP9 expression had poorer overall survival (P<0.01) and progression-free survival (P<0.05) than cases with low DUXAP9 expression. Multivariate Cox regression analysis also showed that high DUXAP9 expression was an independent risk factor for poor prognosis in localized ccRCC (p<0.05). DUXAP9 knockdown in renal cancer cells inhibited renal cancer cells proliferation and motility capacities  in vitro  and reversed epithelial-mesenchymal transition (EMT), whereas overexpression of DUXAP9 promoted renal cancer cells proliferation and motility capacities  in vitro  and induced EMT. Pull-down, RNA immunoprecipitation and RNA stability assays (involving actinomycin D) showed that DUXAP9 was methylated at N6-adenosine and binds to IGF2BP2, which increases its stability. DUXAP9 activate PI3K/AKT pathway and Snail expression in renal cancer cells. DUXAP9 may be useful as a prognostic marker and/or therapeutic target in localized ccRCC.	34168980	RID04905	epigenetic regulation	metastasis,recurrence,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Pancreatic ductal adenocarcinoma	LINC00842	PPARGC1A	negatively-F	RNA pull-down assay;RIP;ChIP;western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+);cell viability(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000223477	NA	ENSG00000109819	NA	643650	10891	NA	LEM6|PGC-1(alpha)|PGC-1alpha|PGC-1v|PGC1|PGC1A|PPARGC1	LINC00842 inactivates transcription co-regulator PGC-1alpha to promote pancreatic cancer malignancy through metabolic remodelling.The molecular mechanism underlying pancreatic ductal adenocarcinoma (PDAC) malignancy remains unclear. Here, we characterize a long intergenic non-coding RNA LINC00842 that plays a role in PDAC progression. LINC00842 expression is upregulated in PDAC and induced by high concentration of glucose via transcription factor YY1. LINC00842 binds to and prevents acetylated PGC-1alpha from deacetylation by deacetylase SIRT1 to form PGC-1alpha, an important transcription co-factor in regulating cellular metabolism. LINC00842 overexpression causes metabolic switch from mitochondrial oxidative catabolic process to fatty acid synthesis, enhancing the malignant phenotypes of PDAC cells. High LINC00842 levels are correlated with elevated acetylated- PGC-1alpha levels in PDAC and poor patient survival. Decreasing LINC00842 level and inhibiting fatty acid synthase activity significantly repress PDAC growth and invasiveness in mouse pancreatic xenograft or patient-derived xenograft models. These results demonstrate that LINC00842 plays a role in promoting PDAC malignancy and thus might serve as a druggable target.	34158490	RID04906	expression association	NA		UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Diabetic retinopathy	UCA1	VEGFC	positively-E	RIP;RNA pull-down assay;dual-luciferase reporter assay;western blot analysis	upregulation	RT-qPCR;microarray	GSE60436	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	ceRNA(miR-624-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000150630	NA	652995	7424	CUDR|LINC00178|onco-lncRNA-36|UCAT1	VEGF-C|VRP	Long noncoding RNA UCA1 promotes high glucose-induced human retinal endothelial cells angiogenesis via regulating miR-624-3p/VEGF-C.Emerging evidences have indicated that lncRNAs play important roles in the development and progression of Diabetic retinopathy (DR). It is reported that UCA1 was highly expressed in diabetic lymphoendothelial cells and influences glucose metabolism in rats with DR. The aim of the present study was to explore the role of UCA1 in the mechanism of DR. Gene expression analyses in fibrovascular membranes excised from patients with DR using public microarray datasets (GSE60436). RT-PCRwas performed to detect UCA1, miR-624-3p and VEGF-C expressions in blood of patients and human retinal endothelial cells (HRECs). Moreover, CCK-8, transwell assay, and tube formation assay were used to identify biological effects of UCA1 on HRECs proliferation, migration ability and angiogenesis in vitro. UCA1 and VEGF-C was elevated in DR patients and high glucose-induced HRECs cell lines, while miR-624-3p was decreased. UCA1 inhibition inhibited proliferation, angiogenesis and migration of HRECs cells under high glucose condition. Luciferase reporter assay indicated that UCA1 could sponge with miR-624-3p, which could directly target at VEGF-C. Finally, we proved a pathway that UCA1 promoted cell proliferation, migration and angiogenesis through sponging with miR-624-3p thereby upregulating VEGF-C in high glucose-induced HRECs. We identified UCA1 as an important factor associated with DR, which could regulate the expression of VEGF-C by sponging miR-624-3p in human retinal endothelial cells. Our results pay the way for further studies on diagnostic and therapeutic studies related to UCA1 in DR patients.	34137197	RID04907	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC);DATA(GSE117623)
Coronary slow flow	NEAT1	ICAM1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell proliferation(-)	ceRNA(miR-148b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Coronary slow flow	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000090339	NA	283131	3383	LINC00084|NCRNA00084|TncRNA|VINC	BB2|CD54|P3.58	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis.Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown. Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCRor western blot. Cell proliferation was measured by 5-Ethynyl-2'-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay. This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis. This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.	34135616	RID04908	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367)
Malignant glioma	SNHG16	TLR7	interact	RIP	upregulation	qRT-PCR	NA	NA	MyD88/NF-kB/c-Myc signaling pathway(+);prognosis	NA	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000196664	NA	100507246	51284	Nbla10727|Nbla12061|ncRAN	NA	Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7.Glioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors. However, the clinical treatment of glioma is limited. It is of great significance to seek new therapeutic methods for glioma via gene therapy. Long non-coding RNA (lncRNA) SNHG16 expression level was measured by microarray and qRT-PCRassay; ISH was used to identify the location of SNHG16. Cancer stem cells (CSCs) were separated from glioma tissues and identified using immunofluorescence. Exosomes were isolated from CSCs and cancer cells and identified by TEM and western blot. MTT, wound healing, transwell, and colony formation assay were performed to explore the role of SNHG16 or si-SNHG16 from CSCs on progression of glioma cells. RIP was used to verify the interaction between SNHG16 and TLR7. The experiment of Xenograft used for exploring the function of SNHG16/ TLR7/MyD88/NFkB/c-Myc on growth on glioma in vivo. microarray assay showed long non-coding RNA (lncRNA) SNHG16 was upregulated in glioma. Followed qRT-PCRalso showed an increase of SNHG16 in glioma tissues; high expression of SNHG16 indicated a poor prognosis in glioma patients. Interestingly, SNHG16 was packaged into exosomes and derived from CSCs. Functional analysis showed exo-SNHG16 secreted by CSCs promoted the progression of glioma cell lines SHG44 and U251. Furthermore, SNHG16 interacted with TLR7 and activated NFkB/c-Myc signaling in glioma cells. And the silencing of TLR7 inhibited the progression of SHG44 and U251 cells by exo-SNHG16 from CSCs. In vivo tumorigenesis experiments showed that exo-SNHG16 induced glioma progression by activating TLR7/MyD88/NFkB/c-Myc signaling. Our study suggested CSC-derived exo-SNHG16 promoted cancer progression by activating TLR7/MyD88/NFkB/c-Myc signaling pathway.	34134771	RID04909	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE111842,GSE51827,GSE75367,GSE86978)
Atherosclerosis	TP73-AS1	AKT3	positively-E	western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-654-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000117020	NA	57212	10000	KIAA0495|PDAM	PKBG|PRKBG|RAC-gamma	LncRNA TP73-AS1 promotes oxidized low-density lipoprotein-induced apoptosis of endothelial cells in atherosclerosis by targeting the miR-654-3p/AKT3 axis.Although lncRNA TP73-AS1 has been shown to play important roles in various human diseases, its function in atherosclerosis (AS) remains unclear. Human aortic endothelial cells (HAECs) were treated with 50<U+00A0>ug/ml oxidized low-density lipoprotein (ox-LDL) to establish an atherosclerotic cell model. The expression of TP73-AS1, miR-654-3p and AKT3 was detected by qRT-PCR Cell functions were evaluated CCK-8 assay and flow cytometry. The protein levels of apoptosis-related proteins were evaluated by western blot. The binding relationship among TP73-AS1, miR-654-3p and AKT3 was determined by bioinformatics analysis and luciferase reporter assay. TP73-AS1 was upregulated and miR-654-3p was downregulated in ox-LDL treated HAECs. TP73-AS1 silencing and miR-654-3p mimics decreased the viability and inhibited apoptosis of ox-LDL treated HAECs, decreased the expression levels of c-caspase-9, c-caspase-3 and Bax, and increased Bcl-2 expression. In addition, miR-654-3p inhibitor significantly reversed the inhibitory effects of si-TP73-AS1 on cell viability and apoptosis. TP73-AS1 could positively regulate AKT3 through directly sponging miR-654-3p. TP73-AS1 promoted apoptosis of ox-LDL stimulated endothelial cells by targeting the miR-654-3p/AKT3 axis, suggesting that TP73-AS1 might be a potential target for AS treatment.	34103010	RID04910	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Cervical cancer	ILF3-DT	PTEN	positively-E	western blot;dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	apoptosis process(+);cell migration(-);cell invasion(-);cell proliferation(-)	ceRNA(miR-454-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000171862	NA	147727	5728	ILF3-AS1	BZS|MHAM|MMAC1|PTEN1|TEP1	Mechanism underlying long non-coding RNA ILF3-AS1-mediated inhibition of cervical cancer cell proliferation, invasion and migration, and promotion of apoptosis,Long non-coding RNA ILF3 divergent transcript (ILF3-AS1) displays a tumor-suppressing effect. StarBase predicted that the potential target microRNA (miR) of ILF3-AS1 was miR-454-3p; therefore, the present study investigated the effect of ILF3-AS1 and its target miR-454-3p on cervical cancer (CC). Gene Expression Profiling Interactive Analysis was used to predict the expression of ILF3-AS1 in CC and the overall survival rate of patients. The present study demonstrated that ILF3-AS1 expression was significantly downregulated in human CC tissues and cells compared with adjacent tissues (ANTs) and normal cervical epithelial cells (NCEs), respectively. Patients with CC with high ILF3-AS1 expression displayed higher survival rates compared with patients with low ILF3-AS1 expression. Cell viability, apoptosis, migration and invasion were detected by performing Cell Counting Kit-8, flow cytometry, wound healing and Transwell assays, respectively. Compared with the negative control (NC) group, ILF3-AS1 overexpression significantly inhibited CC cell viability and migration, but significantly increased CC cell apoptosis. Moreover, ILF3-AS1 overexpression significantly upregulated E-Cadherin expression levels, but significantly downregulated N-Cadherin and snail family transcriptional repressor 1 expression levels compared with the NC group. miR-454-3p expression was negatively correlated with ILF3-AS1, and highly expressed in CC tissues and cells compared with ANTs and NCEs, respectively. PTEN, which was predicted and verified as the target gene for miR-454-3p, was significantly downregulated in CC tissues and cells compared with ANTs and NCEs, respectively. ILF3-AS1 expression was positively correlated with PTEN expression, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression. In conclusion, the present study indicated that ILF3-AS1 inhibited CC cell proliferation and migration, and promoted CC cell apoptosis by inhibiting epithelial-mesenchymal transition, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression.	34080029	RID04911	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Basal-like breast cancer	KLF5	IGFL2-AS1	positively-E		upregulation		NA	NA	cell growth(+);cell survival(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000102554	NA	ENSG00000268621	GRCh38_19:46189029-46203160	688	645553	BTEB2|CKLF|IKLF	AC006262.5	KLF5-induced lncRNA IGFL2-AS1 promotes basal-like breast cancer cell growth and survival by upregulating the expression of IGFL1.KLF5-induced lncRNA IGFL2-AS1 promotes basal-like breast cancer cell growth and survival by upregulating the expression of IGFL1.Basal-like breast cancer (BLBC) is the most malignant subtype of breast cancer and has a poor prognosis. Kruppel-like factor 5 (KLF5) is an oncogenic transcription factor in BLBCs. The mechanism by which KLF5 promotes BLBC by regulating the transcription of lncRNAs has not been fully elucidated. In this study, we discovered that lncRNA IGFL2-AS1 is a downstream target gene of KLF5 and that IGFL2-AS1 mediates the pro-proliferation and pro-survival functions of KLF5. Additionally, we demonstrated that IGFL2-AS1 functions by upregulating the transcription of its neighboring gene IGFL1 via two independent mechanisms. On the one hand, nuclear IGFL2-AS1 promotes the formation of a KLF5/TEAD4 transcriptional complex at the IGFL1 gene enhancer. On the other hand, cytoplasmic IGFL2-AS1 inhibits the expression of miR4795-3p, which targets the IGFL1 gene. TNFalpha induces the expression of IGFL2-AS1 and IGFL1 through KLF5. Taken together, the results of this study indicate that IGFL2-AS1 and IGFL1 may serve as new therapeutic targets for BLBCs.	34052325	RID04912	transcriptional regulation	prognosis	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)	UP(NSCLC);DATA(GSE74639)
Basal-like breast cancer	IGFL2-AS1	IGFL1	positively-E		upregulation		NA	NA	cell growth(+);cell survival(+)	ceRNA(miR-[0-9]795-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000268621	GRCh38_19:46189029-46203160	ENSG00000188293	NA	645553	374918	AC006262.5	UNQ644	KLF5-induced lncRNA IGFL2-AS1 promotes basal-like breast cancer cell growth and survival by upregulating the expression of IGFL1.KLF5-induced lncRNA IGFL2-AS1 promotes basal-like breast cancer cell growth and survival by upregulating the expression of IGFL1.Basal-like breast cancer (BLBC) is the most malignant subtype of breast cancer and has a poor prognosis. Kruppel-like factor 5 (KLF5) is an oncogenic transcription factor in BLBCs. The mechanism by which KLF5 promotes BLBC by regulating the transcription of lncRNAs has not been fully elucidated. In this study, we discovered that lncRNA IGFL2-AS1 is a downstream target gene of KLF5 and that IGFL2-AS1 mediates the pro-proliferation and pro-survival functions of KLF5. Additionally, we demonstrated that IGFL2-AS1 functions by upregulating the transcription of its neighboring gene IGFL1 via two independent mechanisms. On the one hand, nuclear IGFL2-AS1 promotes the formation of a KLF5/TEAD4 transcriptional complex at the IGFL1 gene enhancer. On the other hand, cytoplasmic IGFL2-AS1 inhibits the expression of miR4795-3p, which targets the IGFL1 gene. TNFalpha induces the expression of IGFL2-AS1 and IGFL1 through KLF5. Taken together, the results of this study indicate that IGFL2-AS1 and IGFL1 may serve as new therapeutic targets for BLBCs.	34052325	RID04913	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	
Prostate cancer	OIP5-AS1	SLC7A11	positively-E	dual-luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell viability(-)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000151012	NA	729082	23657	cyrano|linc-OIP5	xCT	LncRNA OIP5-AS1 inhibits ferroptosis in prostate cancer with long-term cadmium exposure through miR-128-3p/SLC7A11 signaling.Previous studies suggest that cadmium (Cd) is one of the causative factors of prostate cancer (PCa), but the effect of chronic Cd exposure on PCa progression remains unclear. Besides, whether long noncoding RNAs (lncRNAs) are involved in the regulation of prolonged exposure to Cd in PCa needs to be elucidated. In the present study, we found that the serum concentration of Cd in PCa patients was positively correlated with the Gleason score and tumor-node-metastasis (TNM) classification. To simulate chronic Cd exposure in PCa, we subjected PC3 and DU145 cells to long-term, low-dose Cd exposure and further examined tumor behavior. Functional studies identified that chronic Cd exposure promoted cell growth and ferroptosis resistance in vitro and in vivo. Furthermore, we found that lncRNA OIP5-AS1 expression was greatly elevated in PC3 and DU145 cells upon chronic Cd exposure. Dysregulation of OIP5-AS1 expression mediated cell growth and Cd-induced ferroptosis. Mechanistically, we demonstrated that OIP5-AS1 served as an endogenous sponge of miR-128-3p to regulate the expression of SLC7A11, a surrogate marker of ferroptosis. Moreover, miR-128-3p decreased cell viability by enhancing ferroptosis. Taken together, our data indicate that lncRNA OIP5-AS1 promotes PCa progression and ferroptosis resistance through miR-128-3p/SLC7A11 signaling.	34051661	RID04914	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteosarcoma	RUSC1-AS1	miR-340-5p	negatively-F	western blot;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000225855	GRCh38_1:155316863-155324176	NA	NA	284618	NA	C1orf104|FLJ35976	NA	LncRNA RUSC1-AS1 promotes osteosarcoma progression through regulating the miR-340-5p and PI3K/AKT pathway.Dysregulation of long noncoding RNA (lncRNA) is frequently involved in the progression and development of osteosarcoma. LncRNA RUSC1-AS1 is reported to be upregulated and acts as an oncogene in hepatocellular carcinoma, cervical cancer and breast cancer. However, its role in osteosarcoma has not been studied yet. In the present study, we investigated the role of RUSC1-AS1 in osteosarcoma both  in vitro  and  in vivo . The results showed that the expression of RUSC1-AS1 was significantly upregulated in osteosarcoma cell line U2OS and HOS compared to that in human osteoblast cell line hFOB1.19. Similar results were found in human samples. Silencing RUSC1-AS1 by siRNA significantly inhibited U2OS and HOS cell proliferation and invasion, measured by CCK-8 and transwell assay. Besides, knockdown of RUSC1-AS1 increased cell apoptosis in osteosarcoma cell lines. In addition, RUSC1-AS1 promoted the epithelial-mesenchymal transition (EMT) process of osteosarcoma cells.  In vivo  experiments confirmed that RUSC1-AS1 knockdown had an inhibitory effect on osteosarcoma tumor growth. Mechanically, we showed that RUSC1-AS1 directly binds to and inhibits miR-340-5p and activates the PI3K/AKT signaling pathway. In conclusion, our study demonstrated that RUSC1-AS1 promoted osteosarcoma development both  in vitro  and  in vivo  through sponging to miR-340-5p and activating the PI3K/AKT signaling pathway. Therefore, RUSC1-AS1 becomes a potential therapeutic target for osteosarcoma.	34048366	RID04915	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)	
Ovarian cancer	PART1	CHRAC1	positively-E		upregulation		NA	NA	apoptosis process(-);cell migration(+);cell invasion(+);cell proliferation(+)	ceRNA(miR-512-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000104472	NA	25859	54108	DKFZP586D0823|NCRNA00206	CHRAC15|YCL1	YY1-Induced lncRNA PART1 Enhanced Resistance of Ovarian Cancer Cells to Cisplatin by Regulating miR-512-3p/CHRAC1 Axis.Chemoresistance is one of the major obstacles encountered in ovarian cancer (OC) therapy. Long noncoding RNA  PART1  has been reported to be involved in the tumorigenesis of several types of cancers. However, the biological role of  PART1  in the chemoresistance of OC is still unclear. In this study, it was found that the expression levels of  PART1  and  CHRAC1  were increased and  miR-512-3p  expression was decreased in cisplatin (DDP)-resistant OC cell lines. The depletion of  PART1  enhanced the DDP sensitivity of DDP-resistant OC cells, as indicated by the inhibition of cell proliferation, migration, and invasion, and promotion of cell apoptosis. In the upstream mechanism exploration, we discovered that  PART1  was induced by  YY1  transcription factor. Moreover, it was identified that  miR-512-3p  was a target of  PART1 , and  PART1  regulated the DDP resistance of OC through  miR-512-3p.  In addition, we screened the candidate genes of  miR-512-3p. , and confirmed that  CHRAC1  was the downstream gene of  miR-512-3p.  Furthermore, the knockdown of  CHRAC1  inhibited proliferation, migration, and invasion, and accelerated apoptosis of DDP-resistant OC cells, which was counteracted after the inhibition of  miR-512-3p.  Finally, we observed that  PART1  regulated the expression of  CHRAC1  through  miR-512-3p.  In conclusion, we demonstrated that  YY1 -induced  PART1  accelerated DDP resistance of OC through  miR-512-3p/CHRAC1  axis, suggesting  PART1  may be a promising therapeutic target for DDP-resistant OC patients.	34030482	RID04916	ceRNA or sponge	chemoresistance	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	YY1	PART1	positively-E		upregulation		NA	NA	apoptosis process(-);cell migration(+);cell invasion(+);cell proliferation(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000152931	GRCh38_5:60487713-60548813	7528	25859	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	DKFZP586D0823|NCRNA00206	YY1-Induced lncRNA PART1 Enhanced Resistance of Ovarian Cancer Cells to Cisplatin by Regulating miR-512-3p/CHRAC1 Axis.Chemoresistance is one of the major obstacles encountered in ovarian cancer (OC) therapy. Long noncoding RNA  PART1  has been reported to be involved in the tumorigenesis of several types of cancers. However, the biological role of  PART1  in the chemoresistance of OC is still unclear. In this study, it was found that the expression levels of  PART1  and  CHRAC1  were increased and  miR-512-3p  expression was decreased in cisplatin (DDP)-resistant OC cell lines. The depletion of  PART1  enhanced the DDP sensitivity of DDP-resistant OC cells, as indicated by the inhibition of cell proliferation, migration, and invasion, and promotion of cell apoptosis. In the upstream mechanism exploration, we discovered that  PART1  was induced by  YY1  transcription factor. Moreover, it was identified that  miR-512-3p  was a target of  PART1 , and  PART1  regulated the DDP resistance of OC through  miR-512-3p.  In addition, we screened the candidate genes of  miR-512-3p. , and confirmed that  CHRAC1  was the downstream gene of  miR-512-3p.  Furthermore, the knockdown of  CHRAC1  inhibited proliferation, migration, and invasion, and accelerated apoptosis of DDP-resistant OC cells, which was counteracted after the inhibition of  miR-512-3p.  Finally, we observed that  PART1  regulated the expression of  CHRAC1  through  miR-512-3p.  In conclusion, we demonstrated that  YY1 -induced  PART1  accelerated DDP resistance of OC through  miR-512-3p/CHRAC1  axis, suggesting  PART1  may be a promising therapeutic target for DDP-resistant OC patients.	34030482	RID04917	transcriptional regulation	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Pediatric burns	HULC	TLR4	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	ECM synthesis(-);cell invasion(-);cell proliferation(-)	ceRNA(miR-663b)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Burn	lncRNA	PCG	ENSG00000251164	NA	ENSG00000136869	NA	728655	7099	HCCAT1|LINC00078|NCRNA00078	ARMD10|CD284|hToll|TLR-4	Long non-coding RNA HULC regulates TLR4 expression by acting as ceRNA to attract miR-663b in skin fibroblasts of pediatric burns.The study aims to elucidate the impact of LncRNA HULC in human skin fibroblasts (HSF) after burns in children. HULC might act as endogenous sponges for miR-663b to regulate the gene expression of TLR4. This study included 46 children with deep second-degree burns. On the 5th day after the injury, eligible samples from all patients were collected. HSF cells were selected to establish a thermal-injured model. qRT-PCRwas applied to detect the expression of HULC, miR-663b, and TLR4 mRNA in burn wound and normal skin tissue. The dual-luciferase reporter and RIP assay were performed to explore a targeted binding relationship between HULC and miR-663b, or miR-663b and TLR4. Cell proliferation and invasion were evaluated through the assay of CCK-8 and transwell assay. The expression levels of alpha-SMA, Collagen I, MMP-1, and TIMP-1, which are associated with extracellular matrix (ECM) production, were examinated by western blot. HULC and TLR4 mRNA expression were reduced on the 5th day after thermal injury in burn wounds, while miR-663b expression increased significantly (P<0.05), when compared to expression in the normal tissue. HULC and TLR4 mRNA concentration in HSF cells showed a transient increase after thermal injury, and a gradual decline with time was observed subsequently when compared to the control group. An inverse expression of miR-663b with the expression of HULC and TLR4 mRNA was observed simultaneously (P<0.05). A deficiency of HULC promotes the proliferation, invasion, and ECM synthesis of HSF cells with thermal injury; HULC functions as a ceRNA of miR-663b. Inhibitors of miR-663b partially rescued the effects on thermal-injured HSF cells induced by HULC deficiency (P<0.05). TLR4 is a target gene of miR-663b. The up-regulation of TLR4 also partially reversed the effect on the thermal-injury of HSF cells resulting from HULC deficiency (P<0.05). LncRNA HULC may function as a molecular sponge to regulate the expression of the miR-663b/TLR4, and thereby inhibit the proliferation, invasion, and ECM synthesis of thermal-injured HSF cells. HULC knockdown might significantly promote wound healing in children after burns.	34017408	RID04918	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LOC146880	FSCN1	positively-E	dual-luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	ceRNA(miR-328-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000075618	NA	NA	6624	NA	FLJ38511|p55|SNL	LncRNA LOC146880 promotes esophageal squamous cell carcinoma progression via miR-328-5p/FSCN1/MAPK axis.	34016787	RID04919	ceRNA or sponge	NA		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Hepatocellular carcinoma	EIF2AK3	RMRP	negatively-E	western blot;qRT-PCR;northern blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	protein-RNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000172071	NA	ENSG00000269900	GRCh38_9:35657751-35658018	9451	6023	PEK|PERK	CHH|NME1|RMRPR|RRP2	The expression of RMRP was correlated with the expression of PERK in experiments with the siRNA and PERK plasmid in both HCC cell lines and human HCC tissue. Furthermore, RMRP downregulation induced apoptotic cell death. RMRP is downregulated by PERK, which induces apoptosis in HCC.	33846370	RID04920	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)
Colorectal cancer	DANCR	NRAS	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	prognosis	ceRNA(miR-145-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000213281	NA	57291	4893	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	N-ras	It was demonstrated that DANCR could regulate NRAS expression by sponging miR-145-5 in colorectal cancer patients. Furthermore, the mean expression of miR-145-5p (p-<-0.001) and NRAS (p-<-0.001) was significantly different between tumor and normal tissue. A significant correlation was observed between DANCR and miR-145-5p (p-=-0.001), and also between miR-145-5p and NRAS (p-<-0.001) Our results are in line with other studies that have shown miR-145-5p decreased in colorectal cancer cells and associated with poor prognosis	33956301	RID04921	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Aortic dissection	LINC01278	ACTG2	positively-E	western blot;qRT-PCR;dual-luciferase reporter assay	downregulation	qRT-PCR	GSE52093	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-500b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Aortic disease	lncRNA	PCG	ENSG00000235437	GRCh38_X:63222993-63561095	ENSG00000163017	NA	92249	72	NA	ACTA3|ACTL3|ACTSG	Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD. These results suggest that linc01278 inhibits the proliferation and migrations of VSMCs.	33910387	RID04922	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Pneumonia	LINC00707	miR-223-5p	negatively-F		upregulation		NA	NA	cell injury(+)	sponge	binding/interaction	RNA-RNA	Lipopolysaccharide	NA	NA	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000238266	GRCh38_10:6779549-6879450	NA	NA	100507127	NA	NA	NA	LINC00707 knockdown relieved LPS-triggered injury in MRC-5 cells. LINC00707 directly interacted with miR-223-5p through acting as a miR-223-5p sponge. Moreover, miR-223-5p mediated the regulation of LINC00707 silencing on LPS-stimulated cytotoxicity in MRC-5 cells. p38 mitogen-activated protein kinases and nuclear factor-kB signaling pathways were modulated by the LINC00707/miR-223-5p axis in LPS-induced MRC-5 cells. Our present study indicated that LINC00707 depletion alleviated LPS-induced injury in MRC-5 cells at least partly by acting as a sponge of miR-223-5p, highlighting a new potential therapeutic avenue for pneumonia treatment.	33604647	RID04923	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Atherosclerosis	TCONS_00034812	miR-21	positively-E	RT-qPCR;MSP	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	DNA methylation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	NA	NA	ENSG00000199004	NA	NA	NA	NA	NA	Overexpression of TCONS_00034812 resulted in miR-21 upregulation and a decrease of miR-21 gene methylation. In contrast, silencing of TCONS_00034812 caused miR-21 downregulation and an increase of miR-21 gene methylation. Cell proliferation analysis indicated that the overexpression of TCONS_00034812 and miR-21 promoted cell proliferation, while silencing of TCONS_00034812 played an opposite role. Moreover, miR-21 overexpression weakened the effects of silencing TCONS_00034812 on cell proliferation.Conclusions: In summary, LncRNA-TCONS_00034812 is upregulated in atherosclerotic samples, and its overexpression upregulates miR-21 through methylation in human aortic smooth muscle cells (HAOSMCs). Our study indicates that LncRNA-TCONS_00034812 could serve as a potential biomarker for diagnosis of atherosclerosis.	34277805	RID04924	epigenetic regulation	NA		
Atherosclerosis	OIP5-AS1	miR-30c-5p	negatively-F	qRT-PCRIP;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+);NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The levels of lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were detected by corresponding detection kits, respectively. Quantitative real-time PCR (qRT-PCR was conducted to measure the expression of OIP5-AS1 or microRNA-30c-5p (miR-30c-5p) in HUVECs. Binding between OIP5-AS1 and miR-30c-5p was predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). western blot was used to analyze p-IkB, IkB, p-p65 and p65 levels. RESULTS:In HUVECs, exposure to ox-LDL led to a decrease in cell viability and an increase in LDH release and apoptosis with concomitant enhancement of oxidative stress, as evidenced by increased ROS and MDA generation, as well as decreased SOD activity and NO levels, while OIP5-AS1 knockdown or miR-30c-5p upregulation could rescue these effects above. Mechanically, OIP5-AS1 functioned as a sponge of miR-30c-5p. OIP5-AS1-induced injury and apoptosis, oxidative stress and activation of NF-kB pathway were reversed by miR-30c-5p in ox-LDL-treated HUVECs. CONCLUSION:OIP5-AS1 contributed to ox-LDL-treated HUVECs injury by activation of NF-kB pathway via miR-30c-5p.	33867356	RID04925	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Atherosclerosis	AK136714	ELAVL1	positively-F	RIP;RNA pull-down assay;Silver staining;Mass spectrometry	upregulation	microarray	GEO	NA	cell injury(+);apoptosis process(+);inflammatory response(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000066044	NA	NA	1994	NA	Hua|HUR|MelG	We used RNA pull-down, silver staining, and mass spectrometry to analyze the proteins that interacted with AK136714, FOXO3 and HuR (Figure 5A). RNA pull-down confirmed that AK136714 was able to bind HuR (Figure 5B).Cell immunofluorescence colocalization experiments showed that AK136714 was able to colocalize with HuR (Figure 5G). After AK136714 overexpression or suppression, RIP assay was performed and RT-PCRwas used to detect the expression of inflammatory factors (TNF-alpha, IL-1beta and IL-16) in the product pulled down by anti-HuR antibody. AK136714 inhibition reduces the binding of HuR to inflammatory factors (Figure 5H).RNA pull-down experiments and RIP experiments also verified that AK136714 was binding to FOXO3 (Figure 5J'-L). We explored whether AK136714 could bind with FOXO3 and modulate the transcription of Bim. The luciferase assay results indicated that AK136714 overexpression promoted Bim transcription, while AK136714 silencing inhibited Bim transcription (Figure 5M). qPCR was used to evaluate the mRNA expression of Bim, which indicated that AK136714 promoted the expression of Bim while AK136714 knockdown inhibited Bim expression (Figure 5N).	34015766	RID04926	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Atherosclerosis	AK136714	FOXO3	positively-F	RIP;RNA pull-down assay;Silver staining;Mass spectrometry	upregulation	microarray	GEO	NA	cell injury(+);apoptosis process(+);inflammatory response(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	NA	NA	ENSG00000118689	NA	NA	2309	NA	AF6q21|FKHRL1|FOXO2|FOXO3A	We used RNA pull-down, silver staining, and mass spectrometry to analyze the proteins that interacted with AK136714, FOXO3 and HuR (Figure 5A). RNA pull-down confirmed that AK136714 was able to bind HuR (Figure 5B).Cell immunofluorescence colocalization experiments showed that AK136714 was able to colocalize with HuR (Figure 5G). After AK136714 overexpression or suppression, RIP assay was performed and RT-PCRwas used to detect the expression of inflammatory factors (TNF-alpha, IL-1beta and IL-16) in the product pulled down by anti-HuR antibody. AK136714 inhibition reduces the binding of HuR to inflammatory factors (Figure 5H).RNA pull-down experiments and RIP experiments also verified that AK136714 was binding to FOXO3 (Figure 5J'-L). We explored whether AK136714 could bind with FOXO3 and modulate the transcription of Bim. The luciferase assay results indicated that AK136714 overexpression promoted Bim transcription, while AK136714 silencing inhibited Bim transcription (Figure 5M). qPCR was used to evaluate the mRNA expression of Bim, which indicated that AK136714 promoted the expression of Bim while AK136714 knockdown inhibited Bim expression (Figure 5N).	34015766	RID04927	interact with protein	NA		UP(BRCA);DATA(GSE51827,GSE86978)
Breast cancer	SNHG6	LAMC1	positively-E	qRT-PCR;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(-);cell invasion(+);cell migration(+);cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-543)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000135862	NA	641638	3915	HBII-276HG|NCRNA00058|U87HG	LAMB2	Transfection of miR-543 mimics remarkably upregulated miR-543 level, while miR-543 inhibitor downregulated (Fig. 2b). Concomitantly, we observed a reduction of LAMC1 following overexpression of miR-543 and an elevation of LAMC1 level in miR-543 inhibitor-transfected cells (Fig. 2c), suggesting that miR-543 negatively regulated LAMC1 expression. Through bioinformatic analysis, we detected potential binding sites between SNHG6 and miR-543, as well as between miR-543 and LAMC1 mRNA 3'-UTR (Fig. 2d-e). To directly confirm these interactions, we performed dual luciferase activity assay. MiR-543 mimics substantially diminished the relative luciferase activities of WT-SNHG6 and WT-LAMC1, but had no effects on the activities of MUT-SNHG6 and MUT-LAMC1 where in the predicted binding sites with miR-543 were mutated (Fig. 2d-e). These data demonstrate that SNHG6 directly binds miR-543 to inhibit its expression, while miR-543 targets LAMC1 and negatively regulates its expression.	33782812	RID04928	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DATA(GSE40174)
Pancreatic cancer	THCYTX	miR-513b-5p	negatively-F	RIP;western blot;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(-);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	NA	NA	NA	NA	84434	NA	FTX	NA	The expression levels of FTX were increased in PC cell lines, and silencing of FTX remarkably suppressed the invasion ability and cell viability. Besides, FTX could bind to miR-513b-5p as a competitive endogenous RNA, thus promoting the invasion and proliferation ability of PC cells. Moreover, knockdown of FTX inhibited the tumor growth and increased the expression levels of miR-513b-5p and apoptosis-related proteins in vivo. We therefore concluded that silencing of FTX may inhibit cell proliferation and promote apoptosis by regulating cell cycle. The expressions of FTX and miR-513b-5p in PC cell lines were determined by qRT-PCR As shown in Fig.-1a, compared with HPDE6-C7 cells, FTX was remarkably up-regulated in PC cell lines (P-<-0.05).These results demonstrated that silencing of FTX suppressed the pathogenesis of PC by inhibiting the migration and invasion of PC cells.	33736615	RID04929	ceRNA or sponge	NA		
Triple-negative breast cancer	DUXAP8	SAPCD2	positively-E	qRT-PCR;dual-luciferase reporter assay;western blo;CHIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-29a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000186193	NA	503637	89958	NA	C9orf140|p42.3	Intriguingly, DUXAP8 expression was higher in human TNBC cells than that in human breast cells	33683171	RID04930	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Triple-negative breast cancer	YY1	DUXAP8	positively-E	JASPAR;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000271672	GRCh38_22:15826566-15827187	7528	503637	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	Intriguingly, DUXAP8 expression was higher in human TNBC cells than that in human breast cells.YY1 binds to DUXAP8 promoter and activates the transcription of DUXAP8.The binding sites of YY1 and DUXAP8 promoter were predicted via UCSC and JASPAR.ChIP assay showed that the enrichment of DUXAP8 promoter in the complexes conjugated with anti-YY1 showed that YY1 can bind with DUXAP8 promoter.	33683171	RID04931	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Laryngeal squamous cell carcinoma	MIAT	miR-613	negatively-F	RT-qPCR;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Knocking down MIAT expression significantly reduced LSCC cell proliferation and inhibited colony formation, a shown by MTT and colony formation assays, respectively. MIAT knockdown also substantially inhibited the migratory and invasive abilities of LSCC cells, as shown by wound healing and Transwell invasion assays, respectively. Subsequently, luciferase reporter assays verified that MIAT could bind to miR-613, where a negative correlation was observed between the expression of MIAT and miR-613 in LSCC tissues. Suppression of miR-613 partially reversed the inhibitory effects of MIAT knockdown on the proliferation, migration and invasion of LSCC cells. Taken together, the present study identified that MIAT may function as an oncogenic lncRNA to promote LSCC progression, which provides a potential therapeutic target or as a novel diagnostic biomarker for LSCC.	33603840	RID04932	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Colorectal cancer	DLEU1	PRPS1	positively-E	qRT-PCR;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-320b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000147224	NA	10301	5631	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	CMTX5|DFN2|DFNX1	Moreover, knockdown of DLEU1 inhibited cell migration and invasion. Mechanistically, through interacting with miR-320b in CRC, DLEU1 promoted the level of PRPS1 which was a target of miR-320b. The rescue experiment confirmed that knockdown of DLEU1 repressed cell proliferation, migration and invasion while stimulated cell apoptosis via miR-320b/phosphoribosyl pyrophosphate synthetase 1 (PRPS1) axis. Meanwhile, the data of xenograft model exhibited that inhibition of DLEU1 suppressed tumor growth in vivo. In summary, DLEU1 knockdown may repress PRPS1 expression via miR-320b, and then repress cell proliferation, migration and invasion while stimulate cell apoptosis. Our research may provide a novel target for the treatment of CRC. The expression profile exhibited that DLEU1 level was observably increased in CRC tissues compared to non-tumor tissues	34113562	RID04933	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	CCAT2	CCN4	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000270132	NA	101805488	8840	LINC00873|NCCP1	WISP-1|WISP1|WISP1-OT1|WISP1-UT1	Results: CCAT2 was overexpressed in ESCC tissues compared with corresponding adjacent tissues. CCAT2 knockdown could suppress cell proliferation and invasion in vitro. Furthermore, knockdown of CCAT2 could suppress the mRNA and protein levels of beta-catenin and Wnt-induced-secreted-protein-1 (WISP1), as well as the mRNA levels of their downstream targets VEGF-A, MMP2, and ICAM-1. High expression of CCAT2 and WISP1 were associated with poor prognosis of ESCC patients.Conclusions: In conclusion, a novel CCAT2/beta-catenin/WISP1 axis was revealed in ESCC progression and may provide a promising therapeutic target against ESCC. CCAT2 and WISP1 are potential molecular biomarkers for predicting prognosis of ESCC.	34057837	RID04934	transcriptional regulation	prognosis		
Pancreatic cancer	TP73-AS1	MMP14	positively-E	RT-qPCR;dual-luciferase reporter assay;western blo;FISH	upregulation	RT-qPCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+)	ceRNA(miR-200a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000157227	NA	57212	4323	KIAA0495|PDAM	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	The overexpression of TP-73-AS1 was found to correlate with both PDAC stage and lymph node metastasis. To reveal its role in PDCA, we targeted TP73-AS1 using LnRNA inhibitors in a range of pancreatic cancer (PC) cell lines. We found that the inhibition of TP73-AS1 led to a loss of MMP14 expression in PC cells and significantly inhibited their migratory and invasive capacity. No effects of TP73-AS1 on cell survival or proliferation were observed. Mechanistically, we found that TP73-AS1 suppressed the expression of the known oncogenic miR-200a. Taken together, these data highlight the prognostic potential of TP73-AS1 for PC patients and highlight it as a potential anti-PDAC therapeutic target.	33683827	RID04935	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Intervertebral disc degeneration	MT1DP	miR-365	positively-E	qRT-PCRIP;western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000205361	GRCh38_16:56643610-56644942	NA	NA	326343	NA	MTM	NA	The expression of NRF-2 in LDH (as the IDD group) was significantly down-regulated compared to the NC group (P<0.05; Figure 1A). Meanwhile the expression of MT1DP and miR-365 in the LDH group was significantly up-regulated compared to the NC group (P<0.05; Figure 1B,C). The interaction between MT1DP and miR-365 was examined. The results of the RNA immunoprecipitation (RIP) assay revealed a direct interaction between MT1DP and miR-365 (P<0.05; Figure 1D).	33569453	RID04936	expression association	NA		
Gastric cancer	NCK1-DT	BCL9	positively-E	qRT-PCRIP;western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-22-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000116128	NA	101927597	607	NCK1-AS1|SLC35G2-AS1	NA	In vitro assays including MTT, colony formation, Transwell, wound healing and sphere formation assays indicated that NCK1-AS1 depletion inhibited cell proliferation, migration, invasion and stemness maintenance. Luciferase reporter and RIP assays suggested that NCK1-AS1 functioned as a competitive endogenous RNA (ceRNA) for miR-22-3p to positively modulate BCL9 expression. BCL9 was a target gene of miR-22-3p. According to western blotand TOP/FOP flash assay, NCK1-AS1 activated the Wnt/beta-catenin signaling via the miR-22-3p/BCL9 axis. Furthermore, rescue experiments verified that NCK1-AS1 affected cellular processes by activating the Wnt/beta-catenin signaling pathway via the miR-22-3p/BCL9 axis. Tumor xenograft model validated that NCK1-AS1 promoted tumor growth in vivo via the Wnt/beta-catenin signaling by upregulating BCL9 expression. Overall, NCK1-AS1 functions as an oncogene and promotes gastric cancer progression via the miR-22-3p/BCL9-Wnt/beta-catenin signaling pathway.	33974352	RID04937	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SNHG16	miR-1285-3p	negatively-F	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Results: The present study demonstrated that SNHG16 is highly expressed in both the tissues of patients with OS, as well as OS cell lines, and its expression level was positively correlated with clinical stage and poor overall survival. Functional assays revealed that the depletion of SNHG16 inhibits OS growth, OS cell progression and promotes apoptosis both in vivo and in vitro. In addition, the present study revealed that microRNA-1285-3p expression levels can be decreased by SNHG16 acting as a 'sponge', and that this pathway takes part in OS tumor growth in vivo, and OS cell proliferation, invasion, migration and apoptosis in vitro.Conclusions: The results from the present study demonstrate the role of lncRNA SNHG16 in OS progression, which is SNHG16 might exert oncogenic role in osteosarcoma (OS) by acting as a ceRNA of miR-1285-3p, and it may become a novel target in OS therapy.	33823834	RID04938	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Osteosarcoma	LIFR-AS1	NFIA	positively-E	qRT-PCRIP;western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell invasion(+)	ceRNA(miR-29a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000162599	NA	100506495	4774	NA	KIAA1439|NFI-L	Methods: TAMs were differentiated from human mononuclear cells THP-1, and a high-throughput microarray assay was used to analyze the dysregulated lncRNAs and miRNAs in osteosarcoma cells co-cultured with macrophages-derived exosomes. western blot, qRT-PCRassays, and dual-luciferase reporter assay were used to verify the interaction among LIFR-AS1, miR-29a, and NFIA. Cck-8, EdU, colony formation assay, wound-healing, and transwell assay were performed to explore the characterize the proliferation and metastasis ability of OS cells. And qPCR;western blots, immunohistochemistry, and cell immunofluorescence were used to detect the expression of relative genes or proteins.Results: In this study, we found that THP-1-induced macrophage-derived exosomes could facilitate osteosarcoma cell progression both in vitro and in vivo. Then, the results of the high-throughput microarray assay showed that LIFR-AS1 was highly expressed and miR-29a was lowly expressed. Furthermore, LIFR-AS1 was identified as a miR-29a sponge, and NFIA was validated as a direct target of miR-29a. Functional assays demonstrated that knockdown of exosomal LIFR-AS1 could attenuate the promotion effects of macrophages-derived exosomes on osteosarcoma cell progression and miR-29a inhibition could reserve the effect of LIFR-AS1-knockdown exosomes. Correspondingly, NFIA-knockdown could partially reverse the tumor inhibition effect of miR-29a on osteosarcoma cells.Conclusions: Taken together, macrophages-derived exosomal lncRNA LIFR-AS1 can promote osteosarcoma cell proliferation, invasion, and restrain cell apoptosis via miR-29a/NFIA axis, which can act as a potential novel therapeutic target for osteosarcoma therapy.	33794884	RID04939	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	LINC00173	RAB14	positively-E	qRT-PCR;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	chemoresistance(+);prognosis	ceRNA(miR-641)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000196668	GRCh38_12:116533422-116536518	ENSG00000119396	NA	100287569	51552	FLJ42957|NCRNA00173	FBP|RAB-14	Reverse transcription-quantitative PCR analysis indicated that LINC00173 was highly expressed in DDP-resistant HCC tissues and cell lines, and high expression levels of LINC00173 were found to be associated with poor prognosis in patients with HCC. Moreover, LINC00173-knockdown improved the DDP sensitivity of DDP-resistant HCC cells. A luciferase reporter assay also demonstrated that microRNA (miR)-641 was a direct target of LINC00173. miR-641 inhibition restored the promoting effect of LINC00173 knockdown on DDP sensitivity in HCC cells. Furthermore, RAB14 was identified as a target of miR-641, and RAB14 overexpression restrained the inducing effect of LINC00173 knockdown on HCC cell DDP sensitivity. The findings of the present study demonstrated that LINC00173 increased DDP resistance in HCC via the miR-641/RAB14 axis, which may represent a promising therapeutic strategy for HCC.	33777195	RID04940	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Diffuse large b-cell lymphoma	SNHG14	miR-152-3p	negatively-F	qRT-PCRIP;western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	miRNA	ENSG00000224078	GRCh38_15:24978583-25420336	NA	NA	104472715	NA	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	NA	The results showed that SNHG14 expression increased and miR-152-3p expression decreased in DLBCL tissues and cell lines, indicating a negative correlation between miR-152-3p and SNHG14 expression. Moreover, SNHG14 was found to promote DLBCL growth, migration, and EMT-like processes in-vitro, and directly inhibits miR-152-3p gene expression via sequestration of the miR-152-3p transcripts in DLBCL. Additionally, SNHG14/miR-152-3p inhibits apoptosis and promotes cell proliferation on cytotoxic T lymphocytes (CTLs) in DLBCL via the PD-1/PD-L1 checkpoint. Furthermore, both the immune escape and progression of DLBCL are advanced by SNHG14 expression via its interactions with miR-152-3p. Collective, this suggests that SNHG14 is a potential diagnostic, prognostic, and therapeutic target for DLBCL.	33682607	RID04941	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	
Ovarian cancer	PRKAR1B-AS2	PI3K-110alpha	positively-E	western blot;RIP	upregulation	microarray	TCGA	NA	prognosis;cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	Cisplatin	CSC	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229380	GRCh38_7:561958-565619	NA	NA	101927000	NA	NA	NA	Analysis of The Cancer Genome Atlas OC dataset, in vitro experiments, proteomic analysis, and a xenograft OC mouse model were implemented. Our findings indicated that overexpression of PRKAR1B-AS2 is negatively correlated with overall survival in OC patients. Furthermore, PRKAR1B-AS2 knockdown-attenuated proliferation, migration, and invasion of OC cells and ameliorated cisplatin and alpelisib resistance in vitro. In proteomic analysis, silencing PRKAR1B-AS2 markedly inhibited protein expression of PI3K-110alpha and abrogated the phosphorylation of PDK1, AKT, and mTOR, with no significant effect on PTEN. The RNA immunoprecipitation detected a physical interaction between PRKAR1B-AS2 and PI3K-110alpha. Moreover, PRKAR1B-AS2 knockdown by systemic administration of 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine nanoparticles loaded with PRKAR1B-AS2-specific small interfering RNA enhanced cisplatin sensitivity in a xenograft OC mouse model. In conclusion, PRKAR1B-AS2 promotes tumor growth and confers chemoresistance by modulating the PI3K/AKT/mTOR pathway. Thus, targeting PRKAR1B-AS2 may represent a novel therapeutic approach for the treatment of OC patients.	33668685	RID04942	interact with protein	chemoresistance,prognosis		
Pre-eclampsia	NEAT1	PTEN	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-411-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171862	NA	283131	5728	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BZS|MHAM|MMAC1|PTEN1|TEP1	Methods: NEAT1 and miR-411-5p levels were detected by quantitative real-time PCR. Colony formation assay detected cell proliferation and transwell assay detected cell migration and invasion. dual-luciferase reporter assay detected the binding between NEAT1 and miR-411-5p as well as the binding between miR-411-5p and PTEN. RNA pull-down assay detected the combination between NEAT1 and miR-411-5p.Result: NEAT1 was increased and miR-411-5p was reduced in PE patients and human trophoblasts (HTR8/SVneo cells) that were induced with H2O2. Interference with NEAT1 promoted cell proliferation, migration, and invasion, and the miR-411-5p inhibitor reversed the effect of siRNA-NEAT1. The expression of PTEN was promoted in PE patients and HTR8/SVneo cells that were induced with H2O2, while the miR-411-5p mimic inhibited PTEN expression, and the plasmid-mediated PTEN overexpression reversed the effect of the miR-411-5p mimic. Besides, under H2O2 induction, the miR-411-5p mimic promoted cell proliferation, migration, and invasion, and the plasmid-mediated PTEN overexpression reversed the effect of the miR-411-5p mimic.Conclusion: Interference with lncRNA NEAT1 promoted the proliferation, migration, and invasion of trophoblasts and alleviated the development of PE, which was partly mediated by upregulating miR-411-5p and inhibiting PTEN expression.	33876722	RID04943	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	SNHG17	miR-942	negatively-F	qRT-PCR;dual-luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000196756	GRCh38_20:38419638-38435409	NA	NA	388796	NA	NA	NA	Methods: First, the mRNA expression levels of various genes were quantified in PC tissues and cell lines using quantitative reverse-transcription PCR (qRT-PCR. The interaction between SNHG17 and miR-942 was explored by bioinformatics prediction as well as a dual-luciferase reporter assay. The proliferation and viability of pancreatic carcinoma cells were examined using cell counting kit-8 and MTT assays, respectively. Cellular migratory and invasive properties were evaluated using transwell migration and wound healing assays. Cell death was measured using flow cytometry. Protein expression was quantified by western blot.Results: SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual-luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition.	33841638	RID04944	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Chronic obstructive pulmonary disease	TUG1	NFKB1	positively-E	qRT-PCR;dual-luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	ceRNA(miR-145-5p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000109320	NA	55000	4790	LINC00080|NCRNA00080|TI-227H	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-kBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-kBp65, NF-kBp65, TNF-alpha, and (Interleukin) IL-1beta were examined with qRT-PCR western blot, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-kB were verified with luciferase reporter assay. Results: The expressions of lncRNA TUG1, phospho-NF-kBp65, TNF-alpha, and IL-1beta were increased significantly in pHBECs after being infected with IAV for 24 h (all p0.05). The detailed time analysis revealed that the NF-kBp65 in DHBE was activated earlier than that in NHBE by western blot and immunofluorescence. Knockdown of lncRNA TUG1 and miR-145-5p mimic attenuated the expressions of NF-kBp65, TNF-alpha, and IL-1beta significantly. The miR-145-5p inhibitor and NF-kBp65 transfection reversed the attenuated expressions of NF-kBp65, TNF-alpha, and IL-1beta. Conclusion: The IAV causes the hypersusceptibility of airway inflammatory response, which may be closely associated with more severe symptoms in AECOPD patients. The lncRNA TUG1 inhibitor may be a promising therapeutic strategy for AECOPD caused by IAV.	33841139	RID04945	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiac arrest	MEG3	SIRT1	positively-E	DIANA;dual-luciferase reporter assay;Targetscan	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-34a-3p)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cardiovascular system disease	Congestive heart failure	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000096717	NA	55384	23411	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	SIR2L1	The effect and underlying mechanism of MEG3 on the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury were analyzed by methyl thiazolyl tetrazolium (MTT) assays, Annexin V-FITC/PI apoptosis detection kit, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, quantitative polymerase chain reaction (qPCR) assays, western blot luciferase reporter gene assays, transepithelial electrical resistance (TEER) measurements, immunofluorescence analysis, and enzyme-linked immunosorbent assay (ELISA) assays. Interestingly, we found that MEG3 could protect Caco-2 cells from oxygen-glucose deprivation (OGD)/reoxygenation-induced I/R injury by modulating cell proliferation and apoptosis. Moreover, MEG3 relieved OGD-induced intestinal barrier dysfunction  in vitro , as demonstrated by its significant rescue effect on transepithelial electrical resistance and the expression of tight junction proteins such as occludin and claudin-1 (CLDN1), which were impaired in OGD-treated Caco-2 cells. Mechanistically, MEG3 inhibited the expression of inflammatory factors including interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, interferon-gamma (IFN)--Gamma, inflammatory factors including interleukin (IL)-10, and transforming growth factor beta (TGFb)-1, as well as nuclear factor-kappa B (NF-kB) signaling. In response to OGD treatment  in vitro , MEG3 also activated the expression of sirtuin 1 (SIRT1) by Caco-2 cells via sponging miR-34a-3p. Furthermore, MEG3 relieved CA-induced intestinal barrier dysfunction through NF-kB signaling  in vivo . LncRNA MEG3 can protect the intestinal barrier from cardiac arrest-induced I/R injury via miR-34a-3p/SIRT1/NF-kB signaling. This finding provides new insight into the mechanism by which MEG3 restores intestinal barrier function following I/R injury, presenting it as a potential therapeutic candidate or strategy in intestinal injury.	33569424	RID04946	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	KIMAT1	KRAS	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay	upregulation	microarray	TCGA	NA	tumorigenesis(+)	transcriptional regulation	NA	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000133703	NA	NA	3845	NA	K-Ras4B|KRAS1|KRAS2	Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.	33795683	RID04947	transcriptional regulation	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Lung cancer	MYC	KIMAT1	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay	upregulation	microarray	TCGA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000136997	NA	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	NA	Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.	33795683	RID04948	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Lung cancer	KIMAT1	DHX9	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay	upregulation	microarray	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000135829	NA	NA	1660	NA	DDX9|LKP|RHA	Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.	33795683	RID04949	transcriptional regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	KIMAT1	NPM1	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay	upregulation	microarray	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000181163	NA	NA	4869	NA	B23|NPM	Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.	33795683	RID04950	transcriptional regulation	NA		DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Lung adenocarcinoma	LINC01006	CTNNB1	positively-E	RT-qPCR;RNA pull-down assay;RIP;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-129-2-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000182648	GRCh38_7:156388922-156640654	ENSG00000168036	NA	100506380	1499	C7orf13|MY040	armadillo|beta-catenin|CTNNB	This study is to explore the role of LINC01006 in LUAD. Quantitative real-time PCR (RT-qPCR) analysis and western blot were used to determine the expression levels and protein levels, respectively. Functional assays and animal experiments investigated the role of LINC01006 both in vivo and in vitro. Moreover, TOP/FOP assay was performed to detect the activation of the Wnt/beta-catenin signaling pathway. The interaction between LINC01006 and microRNA 29-2-3-p (miR-29-2-3-p)/catenin beta 1 (CTNNB1) was explored by RNA binding protein immunoprecipitation (RIP), RNA pull-down, luciferase reporter assays, and rescue experiments. According to the results, LINC01006 was highly expressed in LUAD tissues and cell lines. LINC01006 knockdown significantly suppressed cell proliferative, migratory, and epithelial-mesenchymal transition (EMT) capacities and tumor development. Moreover, LINC01006 enhanced CTNNB1 via sequestering miR-129-2-3p and activated the Wnt/beta-catenin pathway in LUAD. Overall, LINC01006 promotes LUAD development via activating the Wnt/beta-catenin pathway, implying that LINC01006 might be a promising biomarker for LUAD treatment.	33753463	RID04951	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Intrahepatic cholangiocarcinoma	lncRNA-PAICC	miR-141-3p	negatively-F	RT-PCRdual-luciferase reporter assay;MS2-RIP;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	To investigate the biological function of lncRNA-PAICC in ICC cell lines, we detected the expression of lncRNA-PAICC in ICC cell lines and normal human intrahepatic bile duct epithelial cells (HIBECs) by RT-PCR and we confirmed that lncRNA-PAICC expression in ICC cell lines was significantly higher than that in HIBECs.Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-3p.	33552968	RID04952	ceRNA or sponge	NA		
Intrahepatic cholangiocarcinoma	lncRNA-PAICC	miR-27a-3p	negatively-F	RT-PCRdual-luciferase reporter assay;MS2-RIP;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	To investigate the biological function of lncRNA-PAICC in ICC cell lines, we detected the expression of lncRNA-PAICC in ICC cell lines and normal human intrahepatic bile duct epithelial cells (HIBECs) by RT-PCR and we confirmed that lncRNA-PAICC expression in ICC cell lines was significantly higher than that in HIBECs.Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-4p.	33552968	RID04953	ceRNA or sponge	NA		
Cholangiocarcinoma	LINC00184	ANXA2	positively-E	qRT-PCR;RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);metabolic process(+)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000224939	GRCh38_1:234629311-234634780	ENSG00000182718	NA	100302691	302	HANC|NCRNA00184	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	We used bioinformatics to analyze the expression of LINC00184, microRNA (miR)-23b-3p and ANXA2 in cholangiocarcinoma tissues. The levels of LINC00184, miR-23b-3p, and ANXA2 were detected by qRT-PCR Cell proliferation was tested by CCK8. Transwell assay was used to detect cell invasion and migration. The target connection between LINC00184, miR-23b-3p, or ANXA2 was probed by luciferase reporter assay. RNA pull-down method was employed to test the relationship among LINC00184/miR-23b-3p/ANXA2 in cholangiocarcinoma cells. The Pearson correlation coefficient analyzed was applied to analyze the correlation among LINC00184, miR-23b-3p, and ANXA2. LC-MS/M analysis was used to explore whether the changes of adenine metabolism was affected by LINC00184 in cholangiocarcinoma cells. We discovered that LINC00184 expression was heightened in cholangiocarcinoma patients and cells. Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p. Moreover, ANXA2 was positively modulated by LINC00184 via sponging miR-23b-3p. In short, silencing of LINC00184 suppressed cell proliferation, invasion and migration through over-expression of miR-23b-3p and reducing of ANXA2 in cholangiocarcinoma cells.	33913242	RID04954	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	PRR34-AS1	E2F2	positively-E	qRT-PCR;RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+)	ceRNA(miR-296-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000241990	GRCh38_22:46053705-46057210	ENSG00000007968	NA	150381	1870	NA	E2F-2	Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process  in<U+00A0>vitro  and facilitated tumor growth  in<U+00A0>vivo . In addition, western blotand TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/beta-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/beta-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.	34168917	RID04955	ceRNA or sponge	NA	DOWN(LIHC,PAAD,BRCA);UP(PRAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Hepatocellular carcinoma	PRR34-AS1	SOX12	positively-E	qRT-PCR;RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+)	ceRNA(miR-296-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000241990	GRCh38_22:46053705-46057210	ENSG00000177732	NA	150381	6666	NA	SOX22	Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process  in<U+00A0>vitro  and facilitated tumor growth  in<U+00A0>vivo . In addition, western blotand TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/beta-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/beta-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.	34168917	RID04956	ceRNA or sponge	NA	DOWN(LIHC,PAAD,BRCA);UP(PRAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	E2F2	PRR34-AS1	positively-E	qRT-PCR;RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000007968	NA	ENSG00000241990	GRCh38_22:46053705-46057210	1870	150381	E2F-2	NA	Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process  in<U+00A0>vitro  and facilitated tumor growth  in<U+00A0>vivo . In addition, western blotand TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/beta-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/beta-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.	34168917	RID04957	transcriptional regulation	NA	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)	DOWN(LIHC,PAAD,BRCA);UP(PRAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Acute myeloid leukemia	HOXBLINC	NPM1c+	positively-E	qRT-PCRIP;CHIP;CHRIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	NPM1c +  maintains a unique leukemic gene expression program, characterized by activation of HOXA/B clusters and MEIS1 oncogene to facilitate leukemogenesis. However, the mechanisms by which NPM1c +  controls such gene expression patterns to promote leukemogenesis remain largely unknown. Here, we show that the activation of HOXBLINC, a HOXB locus-associated long non-coding RNA (lncRNA), is a critical downstream mediator of NPM1c + -associated leukemic transcription program and leukemogenesis. HOXBLINC loss attenuates NPM1c + -driven leukemogenesis by rectifying the signature of NPM1c +  leukemic transcription programs. Furthermore, overexpression of HoxBlinc (HoxBlincTg) in mice enhances HSC self-renewal and expands myelopoiesis, leading to the development of AML-like disease, reminiscent of the phenotypes seen in the Npm1 mutant knock-in (Npm1 c/+ ) mice. HoxBlincTg and Npm1 c/+  HSPCs share significantly overlapped transcriptome and chromatin structure. Mechanistically, HoxBlinc binds to the promoter regions of NPM1c +  signature genes to control their activation in HoxBlincTg HSPCs, via MLL1 recruitment and promoter H3K4me3 modification. Our study reveals that HOXBLINC lncRNA activation plays an essential oncogenic role in NPM1c +  leukemia. HOXBLINC and its partner MLL1 are potential therapeutic targets for NPM1c +  AML.	33782403	RID04958	transcriptional regulation	NA		
Hepatocellular carcinoma	LINC01133	ANXA2	positively-E	qRT-PCR;RNA pull-down assay;western blot;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+)	ceRNA(miR-199a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000182718	NA	100505633	302	lncRNA-PAGBC	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	We preformed Kaplan-Meier analysis and log-rank test to identify lncRNA CNV with prognostic value. We conducted loss- and gain-of-function studies to explore the biological functions of LINC01133 in vitro and in vivo. The competing endogenous RNAs (ceRNAs) mechanism was clarified by microRNA sequencing (miR-seq), quantitative real-time PCR (qRT-PCR, western blot, and dual-luciferase reporter assays. We confirmed the binding mechanism between lncRNA and protein by RNA pull-down, RNA immunoprecipitation, qRT-PCR and western blot. Genomic copy numbers of LINC01133 were increased in HCC, which were positively related with the elevated expression of LINC01133. Increased copy number of LINC01133 predicted the poor prognosis in HCC patients. LINC01133 overexpression in HCC cells promoted proliferation and aggressive phenotypes in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. LINC01133 sponged miR-199a-5p, resulting in enhanced expression of SNAI1, which induced epithelial-to-mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate the ANXA2/STAT3 signaling pathway. LINC01133 promotes HCC progression by sponging miR-199a-5p and interacting with ANXA2. LINC01133 CNV gain is predictive of poor prognosis in patients with HCC.	34047479	RID04959	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Gastric cancer	STAT1	DLEU2	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000115415	NA	ENSG00000231607	GRCh38_13:49956670-50125720	6772	8847	ISGF-3|STAT91	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	Quantitative real-time PCR (RT-qPCR) and western blotwere conducted to evaluate the expression levels and protein levels of related genes in GC cells. Functional assays were implemented to explore the effect of deleted in lymphocytic leukemia 2 (DLEU2). The upstream and downstream mechanisms of DLEU2 were verified by mechanism investigations. The expression of long non-coding RNA (lncRNA) DLEU2 was observably high in GC cells and tissues. DLEU2 silence depressed the capacities of proliferation, migration and invasion but promoted apoptosis in GC cells. Moreover, DLEU2 was activated by signal transducer and activator of transcription 1 (STAT1) and sequestered microRNA-23b-3p (miR-23b-3p) to modulate the expression of notch receptor 2 (NOTCH2), thereby stimulating Notch signaling pathway. More importantly, DLEU2 contributed to GC progression via targeting miR-23b-3p/NOTCH2 axis. In summary, our research identified the STAT1/DLEU2/miR-23b-3p/NOTCH2/Notch axis in GC development, indicating that DLEU2 might function as a novel biomarker in GC.	33785336	RID04960	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)
Gastric cancer	DLEU2	NOTCH2	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000134250	NA	8847	4853	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	NA	Quantitative real-time PCR (RT-qPCR) and western blotwere conducted to evaluate the expression levels and protein levels of related genes in GC cells. Functional assays were implemented to explore the effect of deleted in lymphocytic leukemia 2 (DLEU2). The upstream and downstream mechanisms of DLEU2 were verified by mechanism investigations. The expression of long non-coding RNA (lncRNA) DLEU2 was observably high in GC cells and tissues. DLEU2 silence depressed the capacities of proliferation, migration and invasion but promoted apoptosis in GC cells. Moreover, DLEU2 was activated by signal transducer and activator of transcription 1 (STAT1) and sequestered microRNA-23b-3p (miR-23b-3p) to modulate the expression of notch receptor 2 (NOTCH2), thereby stimulating Notch signaling pathway. More importantly, DLEU2 contributed to GC progression via targeting miR-23b-3p/NOTCH2 axis. In summary, our research identified the STAT1/DLEU2/miR-23b-3p/NOTCH2/Notch axis in GC development, indicating that DLEU2 might function as a novel biomarker in GC.	33785336	RID04961	ceRNA or sponge	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ulcerative colitis	UCA1	BRD4	positively-E	RT-qPCR;western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell injury(+)	ceRNA(miR-331-3p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000141867	NA	652995	23476	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CAP|HUNK1|HUNKI|MCAP	These data implied that UCA1 level was enhanced in UC patients and LPS treatment could induce injury in FHCs.The interaction between UCA1 and miR-331-3p or BRD4 was confirmed by luciferase reporter assay. The expressions of key factors involved in NF-kB pathway were assessed by western blot. LncRNA UCA1 level was elevated in colonic mucosa tissues of UC patients. LPS stimulation restrained cell viability and promoted the apoptosis and inflammatory factors levels, thus inducing FHCs inflammatory injury, while these effects were partially abolished by UCA1 knockdown. Moreover, it was found that UCA1 silence improved LPS-triggered cell injury via miR-331-3p. In addition, BRD4 was directly targeted by miR-331-3p, and BRD4 deficiency neutralized the effects of miR-331-3p repression on LPS-triggered injury in LPS-treated FHCs. Our data determined that UCA1 knockdown attenuated UC development via targeting the miR-331-3p/BRD4/NF-kB pathway.	34140798	RID04962	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Leukemia	UCA1	miR-613	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);chemoresistance(+);cell viability(+);cell cycle(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	Daunorubicin	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	LncRNA UCA1 elevates the resistance of human leukemia cells to daunorubicin by the PI3K/AKT pathway via sponging miR-613.Acute leukemia is a hematological malignant tumor. Long non-coding RNA urothelial cancer-associated 1 (UCA1) is involved in the chemo-resistance of diverse cancers, but it is unclear whether UCA1 is associated with the sensitivity of acute leukemia cells to daunorubicin (DNR). DNR (100 nM) was selected for functional analysis. The viability, cell cycle progression, apoptosis, and invasion of treated acute leukemia cells (HL-60 and U-937) were evaluated by cell counting kit-8 (CCK-8) assay, flow cytometry assay, or transwell assay. Protein levels were detected with western blot Expression patterns of UCA1 and miR-613 were assessed by quantitative real-time polymerase chain reaction (qRT-PCR. The relationship between UCA1 and microRNA-613 (miR-613) was verified by dual-luciferase reporter assay. We observed that UCA1 expression was elevated in HL-60 and U-937cells. DNR constrained viability, cell cycle progression, invasion, and facilitated apoptosis of HL-60 and U-937 cells in a dose-dependent manner, but these impacts mediated by DNR were reverted after UCA1 overexpression. MiR-613 was down-regulated in HL-60 and U-937 cells, and UCA1 was verified as a miR-613 sponge. MiR-613 inhibitor reversed DNR treatment-mediated effects on viability, cell cycle progression, apoptosis, and invasion of HL-60 and U-937 cells, but these impacts mediated by miR-613 inhibitor were counteracted after UCA1 inhibition. Notably, the inactivation of the PI3K/AKT pathway caused by DNR treatment was reversed after miR-613 inhibitor introduction, but this influence mediated by miR-613 inhibitor was offset after UCA1 knockdown. In conclusion, UCA1 up-regulation facilitated the resistance of acute leukemia cells to DNR via the PI3K/AKT pathway by sponging miR-613.	33969374	RID04963	ceRNA or sponge	chemoresistance	UP(PAAD);DATA(GSE40174)	
Triple-negative breast cancer	AFAP1-AS1	miR-195	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	Formononetin	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000272620	GRCh38_4:7754077-7778928	NA	NA	84740	NA	AFAP1-AS|AFAP1AS|MGC10981	NA	Formononetin relieves the facilitating effect of lncRNA AFAP1-AS1-miR-195/miR-545 axis on progression and chemo-resistance of triple-negative breast cancer.This investigation attempted to discern whether formononetin restrained progression of triple-negative breast cancer (TNBC) by blocking lncRNA AFAP1-AS1-miR-195/miR-545 axis. We prepared TNBC cell lines (i.e. MDA-MB-231 and BT-549) and normal human mammary epithelial cell line (i.e. MCF-10A) in advance, and the TNBC cell lines were, respectively, transfected by pcDNA3.1-lncRNA AFAP1-AS1, si-lncRNA AFAP1-AS1, pcDNA6.2/GW/EmGFP-miR-545 or pcDNA6.2/GW/EmGFP-miR-195. Resistance of TNBC cells in response to 5-Fu, adriamycin, paclitaxel and cisplatin was evaluated through MTT assay, while potentials of TNBC cells in proliferation, migration and invasion were assessed via CCK8 assay and Transwell assay. Consequently, silencing of lncRNA AFAP1-AS1 impaired chemo-resistance, proliferation, migration and invasion of TNBC cells ( P <0.05), and over-expression of miR-195 and miR-545, which were sponged and down-regulated by lncRNA AFAP1-AS1 ( P <0.05), significantly reversed the promoting effect of pcDNA3.1-lncRNA AFAP1-AS1 on proliferation, migration, invasion and chemo-resistance of TNBC cells ( P <0.05). Furthermore, CDK4 and Raf-1, essential biomarkers of TNBC progression, were, respectively, subjected to target and down-regulation of miR-545 and miR-195 ( P <0.05), and they were promoted by pcDNA3.1-lncRNA AFAP1-AS1 at protein and mRNA levels ( P <0.05). Additionally, formononetin significantly decreased expressions of lncRNA AFAP1-AS1, CDK4 and Raf-1, while raised miR-195 and miR-545 expressions in TNBC cells ( P <0.05), and exposure to it dramatically contained malignant behaviors of TNBC cells ( P <0.05). In conclusion, formononetin alleviated TNBC malignancy by suppressing lncRNA AFAP1-AS1-miR-195/miR-545 axis, suggesting that molecular targets combined with traditional Chinese medicine could yield significant clinical benefits in TNBC.	34289449	RID04964	ceRNA or sponge	chemoresistance	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	
Triple-negative breast cancer	AFAP1-AS2	miR-545	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	Formononetin	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Formononetin relieves the facilitating effect of lncRNA AFAP1-AS1-miR-195/miR-545 axis on progression and chemo-resistance of triple-negative breast cancer.This investigation attempted to discern whether formononetin restrained progression of triple-negative breast cancer (TNBC) by blocking lncRNA AFAP1-AS1-miR-195/miR-545 axis. We prepared TNBC cell lines (i.e. MDA-MB-231 and BT-549) and normal human mammary epithelial cell line (i.e. MCF-10A) in advance, and the TNBC cell lines were, respectively, transfected by pcDNA3.1-lncRNA AFAP1-AS1, si-lncRNA AFAP1-AS1, pcDNA6.2/GW/EmGFP-miR-545 or pcDNA6.2/GW/EmGFP-miR-195. Resistance of TNBC cells in response to 5-Fu, adriamycin, paclitaxel and cisplatin was evaluated through MTT assay, while potentials of TNBC cells in proliferation, migration and invasion were assessed via CCK8 assay and Transwell assay. Consequently, silencing of lncRNA AFAP1-AS1 impaired chemo-resistance, proliferation, migration and invasion of TNBC cells ( P <0.05), and over-expression of miR-195 and miR-545, which were sponged and down-regulated by lncRNA AFAP1-AS1 ( P <0.05), significantly reversed the promoting effect of pcDNA3.1-lncRNA AFAP1-AS1 on proliferation, migration, invasion and chemo-resistance of TNBC cells ( P <0.05). Furthermore, CDK4 and Raf-1, essential biomarkers of TNBC progression, were, respectively, subjected to target and down-regulation of miR-545 and miR-195 ( P <0.05), and they were promoted by pcDNA3.1-lncRNA AFAP1-AS1 at protein and mRNA levels ( P <0.05). Additionally, formononetin significantly decreased expressions of lncRNA AFAP1-AS1, CDK4 and Raf-1, while raised miR-195 and miR-545 expressions in TNBC cells ( P <0.05), and exposure to it dramatically contained malignant behaviors of TNBC cells ( P <0.05). In conclusion, formononetin alleviated TNBC malignancy by suppressing lncRNA AFAP1-AS1-miR-195/miR-545 axis, suggesting that molecular targets combined with traditional Chinese medicine could yield significant clinical benefits in TNBC.	34289449	RID04965	ceRNA or sponge	chemoresistance		
Lung adenocarcinoma	LINC00942	FZD1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-5006-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249628	GRCh38_12:1500525-1504424	ENSG00000157240	NA	100292680	8321	NA	DKFZp564G072	LINC00942 Promotes Tumor Proliferation and Metastasis in Lung Adenocarcinoma via FZD1 Upregulation.Long non-coding RNAs (lncRNAs) have been reported to play important roles in the progression of human cancers. Herein, bioinformatic analysis identified that LINC00942 was a highly overexpressed lncRNA in lung adenocarcinoma (LUAD). The present study aimed to explore the roles and possible molecular mechanisms of LINC00942 in LUAD. First, on the basis of TCGA database, the expression and prognosis of LINC00942 were analyzed in LUAD tissues. Then, si-LINC00942 was transfected into A549 and H1299 cells to knockdown the expression of LINC00942. Cell viability was detected by MTT assay. Flow cytometry was used to analyze cell apoptosis. The expressions of PCNA, Bax, Bcl-2, and wnt/beta-catenin pathway proteins were detected by western blot. dual-luciferase reporter assay was used to evaluate the regulatory relationship between LINC00942 and miR-5006-5p, or miR-5006-5p and FZD1. We discovered that LINC00942 was up-regulated in LUAD tissues compared with adjacent tissues. Besides, we found the increased LINC00942 expression was associated with poor survival. In addition, silencing of LINC00942 suppressed the proliferation, migration, invasion and facilitated the apoptosis of A549 and H1299 cells. Moreover, silencing of LINC00942 repressed the expression of PCNA, Bcl-2, and enhanced Bax expression in A549 and H1299 cells. Mechanically, LINC00942 exerted its effects via enhancing Wnt signaling. LINC00942 functioned as competing endogenous RNA (ceRNA) by binding to miR-5006-5p, upregulating the expression of FZD1, which was a direct target of miR-5006-5p. Our findings indicated that LINC00942/miR-5006-5p/FZD1 axis played important roles in LUAD growth through enhancing Wnt signaling. LINC00942/miR-5006-5p/FZD1 axis might serve as a potential biomarker and therapeutic target for LUAD treatment.	34253104	RID04966	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	GAU1	GALNT8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);chemoresistance(+);prognosis	NA	regulation	RNA-protein	Oxaliplatin	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255474	GRCh38_12:4700417-4720102	ENSG00000130035	NA	101929549	26290	GALNT8-DT	GALNAC-T8	lncRNA GAU1 Induces GALNT8 Overexpression and Potentiates Colorectal Cancer Progression.lncRNA is a key epigenetic regulator in biological processes. In the human cancer transcriptome library MiTranscriptome, we identified  GAU1  as the top upregulated lncRNA in colorectal cancer (CRC) by sample set enrichment analysis (overexpression ranking percentile = 99.75%,  P  < 10 -50 ), which is coexpressed with the potential oncogene  GALNT8  (Spearman rho = 0.67,  P  = 2.44 X 10 -23 , TCGA dataset  n  = 184). Experimental data revealed that  GAU1  regulates the expression of  GALNT8 . The overexpression of either  GAU1  or  GALNT8  significantly promotes the cell cycle and proliferation of CRC cell lines and correlates with poor prognosis in patients with CRC ( P  = 3.04 X 10 -2 ), while silencing of  GAU1  or  GALNT8  suppressed the cancer cell proliferation and induced the CRC cell line resistance to oxaliplatin  in vitro  treatment. Our results suggested that the previously less studied  GAU1  and  GALNT8  may play as CRC prognosis markers and potential targets for chemotherapy treatment.	34239555	RID04967	expression association	chemoresistance,prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	GLCC1	IGF2BP1	positively-E	RNA pull-down assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000159217	NA	NA	10642	NA	IMP-1	An oncogenic lncRNA, GLCC1, promotes tumorigenesis in gastric carcinoma by enhancing the c-Myc/IGF2BP1 interaction.Accumulating evidence has shown that long non-coding RNAs (lncRNAs) are vital regulators of the expression of various genes in multiple human diseases. The aim of this study was to investigate the role of glycolysis-associated lncRNA of colorectal cancer (GLCC1) in the progression of gastric carcinoma as well as the underlying mechanism. The expression levels of GLCC1 and c-Myc were determined in 47 pairs of gastric carcinoma tissues and cell lines using qRT-PCR(quantitative real-time polymerase chain reaction). Next, the functional roles of GLCC1 and c-Myc in the proliferation, apoptosis, migration and invasion of gastric carcinoma cells (BGC823 and SGC7901 cells) were determined by siRNA-mediated knockdown of these molecules, and the cells were evaluated by Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays. In addition, RIP and RNA pull-down assays were used to examine the interaction between GLCC1 and c-Myc/IGF2BP1. Further mechanistic studies were conducted using western blot. lncRNA GLCC1 and c-Myc were observed to be significantly increased in both gastric carcinoma tissues and cell lines. Knockdown of GLCC1 or c-Myc suppressed cell proliferation, migration and invasion but promoted apoptosis in both the BGC823 and SGC7901 cell lines. Mechanistically, c-Myc was identified as a downstream regulator involved in the GLCC1-mediated biological effects in gastric carcinoma. The RNA pull-down and PIP assays further showed that the up-regulation of lncRNA GLCC1 enhanced the interaction of the IGF2BP1 protein with c-Myc RNA, thus promoting the stabilization of c-Myc mRNA. Altogether, we demonstrated that lncRNA GLCC1 modulates gastric cancer cell migration and invasion by enhancing the c-Myc/IGF2BP1 interaction, and lncRNA GLCC1 may serve as a potential therapeutic target for preventing the development and progression of human gastric carcinoma.	34196212	RID04968	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	GLCC1	MYC	positively-E	RNA pull-down assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	An oncogenic lncRNA, GLCC1, promotes tumorigenesis in gastric carcinoma by enhancing the c-Myc/IGF2BP1 interaction.Accumulating evidence has shown that long non-coding RNAs (lncRNAs) are vital regulators of the expression of various genes in multiple human diseases. The aim of this study was to investigate the role of glycolysis-associated lncRNA of colorectal cancer (GLCC1) in the progression of gastric carcinoma as well as the underlying mechanism. The expression levels of GLCC1 and c-Myc were determined in 47 pairs of gastric carcinoma tissues and cell lines using qRT-PCR(quantitative real-time polymerase chain reaction). Next, the functional roles of GLCC1 and c-Myc in the proliferation, apoptosis, migration and invasion of gastric carcinoma cells (BGC823 and SGC7901 cells) were determined by siRNA-mediated knockdown of these molecules, and the cells were evaluated by Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays. In addition, RIP and RNA pull-down assays were used to examine the interaction between GLCC1 and c-Myc/IGF2BP1. Further mechanistic studies were conducted using western blot. lncRNA GLCC1 and c-Myc were observed to be significantly increased in both gastric carcinoma tissues and cell lines. Knockdown of GLCC1 or c-Myc suppressed cell proliferation, migration and invasion but promoted apoptosis in both the BGC823 and SGC7901 cell lines. Mechanistically, c-Myc was identified as a downstream regulator involved in the GLCC1-mediated biological effects in gastric carcinoma. The RNA pull-down and PIP assays further showed that the up-regulation of lncRNA GLCC1 enhanced the interaction of the IGF2BP1 protein with c-Myc RNA, thus promoting the stabilization of c-Myc mRNA. Altogether, we demonstrated that lncRNA GLCC1 modulates gastric cancer cell migration and invasion by enhancing the c-Myc/IGF2BP1 interaction, and lncRNA GLCC1 may serve as a potential therapeutic target for preventing the development and progression of human gastric carcinoma.	34196212	RID04969	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	HCP5	DNMT3A	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);epithelial to mesenchymal transition(+)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000119772	NA	10866	1788	D6S2650E|P5-1	NA	Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A.Multiple studies have revealed that long non-coding RNA (lncRNAs) served as regulatory factors in modulating tumorigenesis of hepatocellular carcinoma (HCC). In the present study, we demonstrated that lncRNA HCP5 was overexpressed in HCC tissues and cell lines, and these findings were obvious even in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis, and invasion both  in vitro  and  in vivo  through promoting apoptosis and by inactivating the epithelial-mesenchymal transition (EMT) progress. Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, and served as a tumor suppressor of HCC to prevent cell proliferation, migration, and invasion. Subsequently, DNMT3A was identified as a downstream regulatory factor of miR-29b-3p, and acted as a participated element of HCC progression by activating AKT phosphorylation. Taken together, our study elucidated for the first time that HCP5 plays a crucial role in HCC via the HCP5/miR-29b-3p/DNMT3A/AKT axis and our findings demonstrated a novel diagnostic and therapeutic strategy with potentiality to treat HCC.	34148029	RID04970	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Osteosarcoma	LINC02620	FGF7	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell growth(+)	ceRNA(miR-1303)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225768	GRCh38_10:104474939-104480274	ENSG00000140285	NA	101927523	2252	BCRT1	KGF	LncRNA BCRT1 facilitates osteosarcoma progression via regulating miR-1303/FGF7 axis.Growing studies noted that lncRNA was closely related with the initiation and progression of tumors. However, the role of BCRT1 in the progression of osteosarcoma remains unknown. We noted that BCRT1 is significantly upregulated in osteosarcoma specimens and cells. Elevated expression of BCRT1 promotes cell growth and cell cycle in osteosarcoma cell. Moreover, BCRT1 induces EMT and secretion of inflammatory mediators in osteosarcoma cell. We illustrated that elevated expression of BCRT1 decreases miR-1303 expression in MG-63 cell. The expression of miR-1303 is lower in osteosarcoma specimens than in non-tumor specimens. There is an inverse interrelation between miR-1303 levels and BCRT1 levels in osteosarcoma specimens. Furthermore, we identified FGF7 is one direct target gene of miR-1303 in osteosarcoma cell. Ectopic expression of miR-1303 suppresses FGF7 expression and elevated expression of BCRT1 enhanced FGF7 expression in MG-63 cell. Finally, we illustrated that BCRT1 induces osteosarcoma cell cycle and proliferation and promotes EMT progression and inflammatory mediators secretion via modulating FGF7 expression. Our study suggested that BCRT1 acts as one oncogene in osteosarcoma progression.	34102610	RID04971	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Cervical cancer	UCA1	SOX2	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-122-5p)	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000181449	NA	652995	6657	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Exosomal lncRNA UCA1 modulates cervical cancer stem cell self-renewal and differentiation through microRNA-122-5p/SOX2 axis.There is growing evidence discussing the role of long non-coding RNAs (lncRNAs) in cervical cancer (CC). We performed this study to explore the impact of exosomal lncRNA urothelial cancer-associated 1 (UCA1) in CC stem cells by sponging microRNA-122-5p (miR-122-5p) and regulating SOX2 expression. CC stem cells (CD133 + CaSki) and exosomes were extracted and identified. The synthesized UCA1- and miR-122-5p-related sequences were transfected into CaSki cells, CaSki cells-derived exosomes were extracted and then co-cultured with CD133 + CaSki cells. The functional roles of UCA1 and miR-122-5p in self-renewal and differentiation ability of CC stem cells were determined using ectopic expression, knockdown/depletion and reporter assay experiments. An in vivo experiment was performed to verify the in vitro results. Up-regulated UCA1 and SOX2 and down-regulated miR-122-5p were found in CaSki-Exo. Exosomes promoted invasion, migration, proliferation and restrained apoptosis of CD133 + CaSki cells. Silencing UCA1 or up-regulating miR-122-5p degraded SOX2 expression, and reduced invasion, migration and proliferation of CD133 + CaSki cells while advanced apoptosis and suppressed the tumor volume and weight in nude mice. Our study provides evidence that CaSki-Exo can promote the self-renewal and differentiation ability of CC stem cells while silencing UCA1 or up-regulating miR-122-5p restrains self-renewal and differentiation of CC stem cells.	34053467	RID04972	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	NRAD1	c-Met	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis	ceRNA(miR-27a)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233725	GRCh38_13:43908669-44030461	ENSG00000105976	NA	121838	NA	LINC00284|NCRNA00284	NA	Oncogenic long intervening noncoding RNA Linc00284 promotes c-Met expression by sponging miR-27a in colorectal cancer.Emerging evidences suggest that long noncoding RNA (lncRNA) plays a vital role in tumorigenesis and cancer progression. Here, the aim of this study is to investigate the biological function of long intervening noncoding RNA Linc00284 in colorectal cancer (CRC). The expression levels of Linc00284, miR-27a and c-Met were evaluated by qPCR and/or western blot. Immunohistochemistry was used to detect the expression of Ki67 and Phh3 in tumor tissues. The interaction between Linc00284, miR-27a and c-Met was validated by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell function experiments, including CCK-8, wound-healing and transwell invasion assays, were conducted. The in vivo studies were performed with the subcutaneous tumor xenograft mouse models. Our findings reveal that Linc00284 is upregulated in CRC tissues and colorectal cancer cell lines HCT116 and SW480 in comparison with corresponding para-carcinoma tissues and human fetal colonic mucosa cells FHC. High expression of Linc00284 in tumor tissues is associated with tumor metastasis and predicts a poor clinical outcome in CRC patients. Serum Linc00284 is increased, while miR-27a is decreased in CRC patients compared to healthy controls. ROC curve analysis indicates that serum Linc00284 and miR-27a produce the area under the curve (AUC) value of at 0.8151 and 0.7316 in patients with colorectal cancer compared to healthy individuals, respectively. Additionally, results in vitro and in vivo experiments suggest that Linc00284 silencing significantly suppresses CRC cell proliferation and/or invasion. Mechanistically, Linc00284 promotes c-Met expression by acting as miR-27a sponge, leading to the activation of downstream signaling pathways, thereby causing malignant phenotypes of CRC cells. Taken together, Linc00284 exhibits oncogenic function and the disturbance of Linc00284/miR-27a/c-Met regulatory axis contributes to CRC progression, providing new insight into the pathogenesis of colorectal cancer. Importantly, the expression levels of serum Linc00284 and miR-27a may serve as clinical biomarkers for CRC diagnosis.	34050266	RID04973	ceRNA or sponge	metastasis,prognosis		
Squamous cell carcinoma	LINC01929	FOXC1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-137-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Squamous cell carcinoma	lncRNA	TF	ENSG00000267013	GRCh38_18:55105904-55124306	ENSG00000054598	NA	101927229	2296	CTD-2171N6.1	ARA|FKHL7|FREAC3|IGDA|IHG1|IRID1	Long Non-Coding RNA LINC01929 Accelerates Progression of Oral Squamous Cell Carcinoma by Targeting the miR-137-3p/FOXC1 Axis.Recently, additional long noncoding RNAs (lncRNAs) have been identified and their possible roles were investigated in a variety of human tumors. One of these lncRNAs, LINC01929, promoted the progression of some cancers, whereas its expression and biological function in human oral squamous cell carcinoma (OSCC)<U+2002>remains still mostly uncertain. The LINC01929 expression in OSCC tissues or cell lines was identified  via  quantitative real-time polymerase chain reaction. The cell counting kit-8, transwell migration, wound-healing, and flow cytometry assays were utilized to characterize the functions of LINC01929 in OSCC cells. The interactive relationships between LINC01929 and miR-137-3p, miR-137-3p and Forkhead box C1 (FOXC1) were investigated by the dual-luciferase activity assay. Our findings demonstrated that LINC01929 was highly expressed in OSCC tissue samples and cell lines, whereas miR-137-3p expression was downregulated. LINC01929 acted as a carcinogenic lncRNA with accelerated OSCC cell proliferation, migration and invasion, and suppression of apoptosis. We further indicated that LINC01929 facilitated tumor growth in xenograft mouse models. Mechanistically, LINC01929 acted as a sponge for miR-137-3p to elevate FOXC1 expression, which is the target of miR-137-3p. In addition, downregulated miR-137-3p expression rescued the suppressive behaviors of LINC01929 knockdown on the biological behaviors of OSCC cells. Taken together, LINC01929 functioned as a tumor-promoting lncRNA  via  the miR-137-3p/FOXC1 axis in OSCC, suggesting novel targets for OSCC therapy.	33968763	RID04974	ceRNA or sponge	NA		UP(SKCM);DATA(GSE38495)
Miscarriage	Lnc-HZ08	CBL	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/p-AKT/p-P21/CDK2 signaling pathway(-);cell proliferation(-);cell invasion(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Miscarriage	lncRNA	PCG	NA	NA	ENSG00000110395	NA	NA	867	NA	C-CBL|CBL2|FRA11B|NSLL|RNF55	Lnc-HZ08 regulates BPDE-induced trophoblast cell dysfunctions by promoting PI3K ubiquitin degradation and is associated with miscarriage.Increasing evidences have shown that pregnant women might miscarry after exposure with environmental BaP (benzo(a)pyrene). Additionally, BPDE (benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide), the ultimate metabolite of BaP, could induce dysfunctions of human trophoblast cells. However, it is rarely correlated between miscarriage and trophoblast dysfunctions. Moreover, their underlying mechanisms are still largely unidentified. In this study, a novel lncRNA (long non-coding RNA), lnc-HZ08, was identified to be highly expressed in human recurrent miscarriage (RM) tissues and in BPDE-treated human trophoblast cells. Lnc-HZ08 acts as a RNA scaffold to interact with both PI3K and its ubiquitin ligase CBL (Cbl proto-oncogene), enhances their protein interactions, and promotes PI3K ubiquitin degradation. In RM tissues and BPDE-treated trophoblast cells, DNA methylation level in lnc-HZ08 promoter region was reduced, which promotes estrogen receptor 1 (ER)-mediated lnc-HZ08 transcription. Subsequently, this upregulated lnc-HZ08 downregulated PI3K level, suppressed PI3K/p-AKT/p-P21/CDK2 pathway, and thus weakened proliferation, migration, and invasion of human trophoblast cells, which further induces miscarriage. These results may provide novel scientific and clinical insights in the occurrence of unexplained miscarriage. A novel lncRNA (lnc-HZ08) regulates the functions of human trophoblast cells and affects miscarriage. Lnc-HZ08 promotes PI3K ubiquitin degradation by enhancing CBL and PI3K interactions, downregulates PI3K/p-AKT/p-P21/CDK2 pathway, and weakens proliferation, migration, and invasion of trophoblast cells. BPDE exposure reduces the DNA methylation level in lnc-HZ08 promoter region and promotes estrogen receptor 1 (ER)-mediated lnc-HZ08 transcription. The suppressed PI3K/p-AKT/p-P21/CDK2 pathway regulated by increased lnc-HZ08 is associated with miscarriage. These results provide novel insights in the occurrence of unexplained miscarriage. Graphical Headlights <U+2022> Lnc-HZ08 downregulates PI3K/p-AKT/p-P21/CDK2 pathway to suppress proliferation, migration, and invasion of human trophoblast cells, and affects miscarriage. <U+2022> Lnc-HZ08 acts as a RNA scaffold to enhance the protein interaction of PI3K and its ubiquitin ligase CBL, which increases PI3K ubiquitination and degradation. <U+2022> Lnc-HZ08 transcription is associated with DNA methylation on its promoter region and transcription factor ER.	33864160	RID04975	interact with protein	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Miscarriage	Lnc-HZ08	PIK3CA	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/p-AKT/p-P21/CDK2 signaling pathway(-);cell proliferation(-);cell invasion(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Miscarriage	lncRNA	PCG	NA	NA	ENSG00000121879	NA	NA	5290	NA	CCM4|CLAPO|CLOVE|CWS5|MCAP|MCM|MCMTC|PI3K|PI3K-alpha|p110-alpha	Lnc-HZ08 regulates BPDE-induced trophoblast cell dysfunctions by promoting PI3K ubiquitin degradation and is associated with miscarriage.Increasing evidences have shown that pregnant women might miscarry after exposure with environmental BaP (benzo(a)pyrene). Additionally, BPDE (benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide), the ultimate metabolite of BaP, could induce dysfunctions of human trophoblast cells. However, it is rarely correlated between miscarriage and trophoblast dysfunctions. Moreover, their underlying mechanisms are still largely unidentified. In this study, a novel lncRNA (long non-coding RNA), lnc-HZ08, was identified to be highly expressed in human recurrent miscarriage (RM) tissues and in BPDE-treated human trophoblast cells. Lnc-HZ08 acts as a RNA scaffold to interact with both PI3K and its ubiquitin ligase CBL (Cbl proto-oncogene), enhances their protein interactions, and promotes PI3K ubiquitin degradation. In RM tissues and BPDE-treated trophoblast cells, DNA methylation level in lnc-HZ08 promoter region was reduced, which promotes estrogen receptor 1 (ER)-mediated lnc-HZ08 transcription. Subsequently, this upregulated lnc-HZ08 downregulated PI3K level, suppressed PI3K/p-AKT/p-P21/CDK2 pathway, and thus weakened proliferation, migration, and invasion of human trophoblast cells, which further induces miscarriage. These results may provide novel scientific and clinical insights in the occurrence of unexplained miscarriage. A novel lncRNA (lnc-HZ08) regulates the functions of human trophoblast cells and affects miscarriage. Lnc-HZ08 promotes PI3K ubiquitin degradation by enhancing CBL and PI3K interactions, downregulates PI3K/p-AKT/p-P21/CDK2 pathway, and weakens proliferation, migration, and invasion of trophoblast cells. BPDE exposure reduces the DNA methylation level in lnc-HZ08 promoter region and promotes estrogen receptor 1 (ER)-mediated lnc-HZ08 transcription. The suppressed PI3K/p-AKT/p-P21/CDK2 pathway regulated by increased lnc-HZ08 is associated with miscarriage. These results provide novel insights in the occurrence of unexplained miscarriage. Graphical Headlights <U+2022> Lnc-HZ08 downregulates PI3K/p-AKT/p-P21/CDK2 pathway to suppress proliferation, migration, and invasion of human trophoblast cells, and affects miscarriage. <U+2022> Lnc-HZ08 acts as a RNA scaffold to enhance the protein interaction of PI3K and its ubiquitin ligase CBL, which increases PI3K ubiquitination and degradation. <U+2022> Lnc-HZ08 transcription is associated with DNA methylation on its promoter region and transcription factor ER.	33864160	RID04976	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Hepatocellular carcinoma	HOTAIR	DHX33	positively-E	starbase;dual-luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);cell growth(+)	ceRNA(miR-526b-3p)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000005100	NA	100124700	56919	HOXC-AS4|HOXC11-AS1|NCRNA00072	DDX33|DKFZp762F2011|FLJ21972	Long non-coding RNA HOTAIR promotes hepatocellular carcinoma progression by regulating miR-526b-3p/DHX33 axis.Hepatocellular carcinoma (HCC) is one of the most common human cancers. Long non-coding RNAs (lncRNAs) play pivotal roles in progression of various cancers, including HCC. We aimed to explore the exact role and underlying mechanism of lncRNA HOX transcript antisense intergenic RNA (HOTAIR) in HCC. Quantitative real time polymerase chain reaction (qRT-PCR was carried out to determine the levels of HOTAIR, DEAH-box helicase 33 (DHX33) and miR-526b-3p. western blot assay was used to detect the protein level of DHX33. Besides, cell proliferation and apoptosis were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Cell migration and invasion were detected by transwell assay. The interaction between miR-526b-3p and HOTAIR or DHX33 was predicted by starbase and confirmed by the dual-luciferase reporter assay. Murine xenograft model was established through injecting Huh7 cells transfected with sh-NC or sh-HOTAIR. The levels of HOTAIR and DHX33 were increased in HCC tissues and cells. Knockdown of either HOTAIR or DHX33 suppressed proliferation, migration and invasion but increased apoptosis in HCC cells. Moreover, DHX33 overexpression reversed the suppressive effect of HOTAIR knockdown on progression of HCC cells. Interestingly, miR-526b-3p could directly bind to HOTAIR, and DHX33 was a direct target of miR-526b-3p. Additionally, interference of HOTAIR restrained the tumor growth by upregulating miR-526b-3p and downregulating DHX33 in vivo. HOTAIR knockdown suppressed cell proliferation, migration and invasion, and promoted apoptosis via regulating miR-526b-3p/DHX33 axis in HCC cells, providing a potential avenue for treatment of HCC.	33843021	RID04977	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	H19	LDHA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);immune evasion(+)	ceRNA(miR-519d-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000134333	NA	283120	3939	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 promotes aerobic glycolysis, proliferation, and immune escape of gastric cancer cells through the microRNA-519d-3p/lactate dehydrogenase A axis.Long noncoding RNAs (lncRNAs) have been investigated in multiple human cancers including gastric cancer (GC). Our research aims to explore the role of H19 in aerobic glycolysis, proliferation, and immune escape of GC cells. The expression of H19 in GC samples was analyzed using Gene Expression Profiling Interactive Analysis, Gene Expression Omnibus data, and real-time quantitative PCR analysis. Relative quantification of glucose consumption and lactate production from cell supernatant were applied to assess the aerobic glycolysis of GC cells. Subcellular fractionation, luciferase reporter, and western blot assays certified the binding between genes. Cell Counting Kit-8 and colony formation assays were used to determine GC cell proliferation. Flow cytometry, ELISA, and real-time quantitative PCR assays were applied to analyze the immunosuppressive effect of H19. H19 was highly expressed in samples of patients with GC, and associated with tumor growth in vivo. H19 knockdown suppressed glucose consumption, lactate production, and proliferation of GC cells by regulating the microRNA (miR)-519d-3p/lactate dehydrogenase A (LDHA) axis. Both miR-519d-3p depletion and LDHA overexpression could reverse the H19 knockdown-induced decrease in aerobic glycolysis and proliferation. Moreover, conditioned medium from stable knockdown H19 GC cells modulated the activity of immune cells including -GammadeltaT cells, Jurkat cells, and tumor-associated macrophages in a miR-519d-3p/LDHA/lactate axis-dependent manner. The H19/miR-519d-3p/LDHA axis mainly contributed to aerobic glycolysis, proliferation, and immune escape of GC cells.	33756038	RID04978	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Laryngeal squamous cell carcinoma	LINC01638	BATF3	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell growth(+)	ceRNA(miR-523-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	ENSG00000233521	GRCh38_22:27221349-27225134	ENSG00000123685	NA	105372978	55509	NA	JDP1|JUNDM1|SNFT	Long noncoding RNA LINC01638 contributes to laryngeal squamous cell cancer progression by modulating miR-523-5p/BATF3 axis.Long noncoding RNA (lncRNA) plays a critical role in tumorigenesis. How lncRNA regulates laryngeal squamous cell carcinoma (LSCC) progression remains poorly understood. In the present study, we found that LINC01638 was highly expressed in LSCC tissues. And LINC01638 expression was positively correlated with clinical stage and lymph node metastasis. Patients with LINC01638 high expression displayed a low survival rate. Results from CCK8, colony formation, and transwell assays showed that LINC01638 knockdown suppressed the proliferation, migration and invasion of LSCC cells  in vitro . Animal experiments indicated that LINC01638 silencing attenuated tumor growth  in vivo . In terms of mechanism, LINC01638 was found to sponge miR-523-5p and promote BATF3 expression. In summary, our results demonstrated that LINC01638/miR-523-5p/BATF3 axis plays a crucial function in initiating LSCC development and may be a potential target for tumor therapy.	33714208	RID04979	ceRNA or sponge	metastasis	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842,GSE51827,GSE75367,GSE86978)
Gastric cancer	LINC00641	NOTCH1	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-)	ceRNA(miR-429)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000258441	GRCh38_14:21200079-21206900	ENSG00000148400	NA	283624	4851	NA	AOS5|AOVD1|TAN1|hN1	Linc00641 promotes the progression of gastric carcinoma by modulating the miR-429/Notch-1 axis.Linc00641 plays different roles in various types of human cancers. However, the function of linc00641 and its underlying mechanism of action in gastric cancer have not been fully elucidated. Therefore, the aim of our current study was to explore the molecular mechanism of linc00641 in gastric cancer. MTT assays, flow cytometry, wound healing assays, and Transwell invasion assays were utilized to measure cell viability, apoptosis, migration and invasion, respectively. western blot and RT-PCRassays were carried out to explore the mechanism of linc00641 in gastric cancer cells. We found that silencing linc00641 suppressed the viability and stimulated the apoptosis of gastric cancer cells, while linc00641 overexpression had the opposite effects. Moreover, linc00641 sponged the expression of miR-429 and subsequently upregulated Notch-1 expression in gastric cancer cells. We concluded that linc00641 promoted the malignant progression of gastric cancer by modulating the miR-429/Notch-1 axis.	33714199	RID04980	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	AC005592.2	OLFM4	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000231185	GRCh38_5:142325293-142672001	ENSG00000102837	NA	NA	10562	NA	GC1|GW112|OLM4|OlfD|UNQ362|bA209J19.1|hGC-1|hOLfD	Super-enhancer-associated long noncoding RNA AC005592.2 promotes tumor progression by regulating OLFM4 in colorectal cancer.Super-enhancer-associated long noncoding RNAs (SE-lncRNAs) have been reported to play essential roles in tumorigenesis, but the fundamental mechanism of SE-lncRNAs in colorectal cancer (CRC) remains largely unknown. A microarray was performed to identify the differentially expressed SE-lncRNAs between CRC tissues and peritumoral tissues. A novel SE-lncRNA, AC005592.2, was selected from these differentially expressed SE-lncRNAs to explore its effects on CRC development. Fluorescence quantitative real-time PCR (qRT-PCR was used to assay the expression of AC005592.2 in CRC tissues and cell lines. Functional assays were applied to identify the biological effects of AC005592.2 in CRC cells. Furthermore, RNA-seq was employed to predict potential targets of AC005592.2. AC005592.2 was significantly increased in CRC tissues and cells. High expression of AC005592.2 was significantly associated with TNM stage and tumor differentiation in CRC patients. Knockdown of AC005592.2 suppressed CRC cell proliferation, invasion and migration but promoted apoptosis, while AC005592.2 overexpression exerted the opposite effects on CRC cells. In addition, AC005592.2 positively regulated the expression of olfactomedin 4 (OLFM4), which was also upregulated in CRC tissues. The findings suggested that AC005592.2 is a crucial promoter of CRC progression and may serve as an attractive therapeutic target for CRC.	33622275	RID04981	transcriptional regulation	NA		UP(LIHC);DATA(GSE117623)
Melanoma	TINCR	ATF4	negatively-E	western blot;shRNA	downregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+)	NA	regulation	NA	BRAF-V600E	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000128272	NA	257000	468	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	CREB-2|TAXREB67|TXREB	Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation.Transition from proliferative-to-invasive phenotypes promotes metastasis and therapy resistance in melanoma. Reversion of the invasive phenotype, however, is challenged by the poor understanding of mechanisms underlying its maintenance. Here, we report that the lncRNA TINCR is down-regulated in metastatic melanoma and its silencing increases the expression levels of invasive markers, in vitro migration, in vivo tumor growth, and resistance to BRAF and MEK inhibitors. The critical mediator is ATF4, a central player of the integrated stress response (ISR), which is activated in TINCR-depleted cells in the absence of starvation and eIF2alpha phosphorylation. TINCR depletion increases global protein synthesis and induces translational reprogramming, leading to increased translation of mRNAs encoding ATF4 and other ISR proteins. Strikingly, re-expression of TINCR in metastatic melanoma suppresses the invasive phenotype, reduces numbers of tumor-initiating cells and metastasis formation, and increases drug sensitivity. Mechanistically, TINCR interacts with mRNAs associated with the invasive phenotype, including ATF4, preventing their binding to ribosomes. Thus, TINCR is a suppressor of the melanoma invasive phenotype, which functions in nutrient-rich conditions by repressing translation of selected ISR RNAs.Strikingly, western blot of shTINCR WM902B and MMC70 melanoma cells showed marked down-regulation of MITF and increased expression of ATF4 and its transcriptional target CHOP (DDIT3), as compared to control cells (Fig 5A). Consistently, MITF and ATF4 target genes were, respectively, depleted and enriched in the transcriptome of shTINCR WM902B cells .	33586907	RID04982	expression association	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)
Aortic dissection	OIP5-AS1	TUB	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	microarray	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Aortic disease	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000166402	NA	729082	7275	cyrano|linc-OIP5	rd5	Lnc-OIP5-AS1 exacerbates aorta wall injury during the development of aortic dissection through upregulating TUB via sponging miR-143-3p.Dysfunction of major cells constituting the aortic wall is the pathological basis for AD development. Determining whether non-coding RNAs can influence AD progression by regulating these cellular functions and identifying some specific non-coding RNAs is of great significance in uncovering molecular mechanisms of the development of AD. microarray analyses and hierarchical clustering analysis were used to select candidate lncRNAs and miRNAs associated with AD. dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay were performed to verify the direct bonding relationship between genes. The regulatory effects of genes on cell function were examined in a series of experiments. We found that lnc-OIP5-AS1 was upregulated, whereas miR-143-3p was downregulated in cells treated with angiotensin II (AngII) and AD tissues. Lnc-OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) of miR-143-3p to suppress the proliferation and mobility, but promote apoptosis of HAECs and HASMCs, and simultaneously result in the imbalances between MMP-2/9 and TIMP-2/1 in HASMCs and the excessive secretion of IL-6, IL-1beta, and IL-17A of HAAFs. Moreover, overexpression or silence of TUB, a target gene of miR-143-3p, counteracted the influence of miR-143-3p or lnc-OIP5-AS1 on cells, respectively. Our findings revealed that lncRNA OIP5-AS1 exacerbates aorta intima, media, and adventitia injury in the development of AD through upregulating TUB via sponging miR-143-3p and also support more detailed future studies by providing a novel molecular basis underlying AD formation.	33577845	RID04983	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	DANCR	ERBB2	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-1225-3p)	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000141736	NA	57291	2064	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CD340|HER-2|HER2|NEU|NGL	Long non-coding RNA DANCR promoted non-small cell lung cancer cells metastasis via modulating of miR-1225-3p/ErbB2 signal.Currently, we aimed to illustrate the role of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) and erb-b2 receptor tyrosine kinase 2 (ErbB2) in non-small cell lung cancer (NSCLC). Expression of DANCR, microRNA-1225-3p (miR-1225-3p) and ErbB2 mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR assays. The clinical value of DANCR was checked by a ROC curve analysis, a Kaplan-Meier analysis and a Pearson Chi-Square test. Transwell chamber assays were performed to determine the migration and invasion ability changes of SPCA1 and A549 cells. The protein expression of ErbB2 was tested by western blot assays. The targeted binding effect between miR-1225-3p and DANCR or ErbB2 was confirmed by a dual-luciferase reporter assay and an RNA pull-down assay, respectively. In the current study, it was found that DANCR was upregulated and correlated with poor prognosis in patients with NSCLC. DANCR promoted NSCLC cells migration and invasion via upregulation of ErbB2. DANCR regulated ErbB2 at posttranscriptional level. Mechanically, it was illustrated that miR-1225-3p negatively regulated ErbbB2 and it-mediated migration and invasion via directly targeting in NSCLC cells. Meanwhile, it was showed that DANCR interacted with miR-1225-3p in a reciprocal suppression manner. Even further, through a RIP assay and a luciferase assay, we showed that DANCR interacted with miR-1225-3p through a microRNA response element (MRE-1225-3p) via directly binding. Finally, it was demonstrated that DANCR served as a miR-1225-3p sponge to promote ErbB2 expression and to facilitate ErbB2-mediated migration and invasion in NSCLC cells. In the current study, it was illustrated that DNACR promoted ErbB2-mediated migration and invasion via working as a ceRNA of miR-1225-3p in NSCLC cells.	33577030	RID04984	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Polycystic ovary syndrome	CCNL1	FOXO1	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	TF	ENSG00000163660	GRCh38_3:157146508-157160760	ENSG00000150907	NA	57018	2308	ania-6a	FKH1|FKHR|FOXO1A	Long non-coding RNA lnc-CCNL1-3:1 promotes granulosa cell apoptosis and suppresses glucose uptake in women with polycystic ovary syndrome.Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disease in premenopausal women. Long non-coding RNAs (lncRNAs) constitute important factors in numerous biological processes. However, their roles in PCOS pathogenesis require further clarification. Our study aims to elucidate the roles of lncRNA lnc-CCNL1-3:1 (CCNL) in PCOS.  CCNL  expression in human luteinized granulosa cells (hLGCs) derived from women with and without PCOS was detected. The full length of CCNL was obtained by 5' and 3' rapid amplification of cDNA ends. CCNL roles in granulosa cell apoptosis, mitochondrial function, and glucose uptake were evaluated. The binding relationship between CCNL and forkhead box O1 (FOXO1) was determined by RPISeq, RNA immunoprecipitation, subcellular fractionation, and immunofluorescence. In KGN cells and hLGCs,  CCNL  overexpression upregulated FOXO1 expression, promoted cell apoptosis, reduced glucose transport capability, and impaired mitochondrial function, and these effects were partially abolished by silencing FOXO1. The interaction of CCNL with FOXO1 might prevents FOXO1 exclusion from the nucleus and subsequent degradation in the cytosol. We determined that CCNL serve as a facilitator in the processes of PCOS. CCNL might participate in PCOS pathologies such as follicular atresia and insulin resistance.	33552682	RID04985	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Endometrioid carcinoma	MCM3AP-AS1	VEGFA	positively-E	IntaRNA;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-126)	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000112715	NA	114044	7422	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	VEGF|VEGF-A|VPF	The MCM3AP-AS1/miR-126/VEGF axis regulates cancer cell invasion and migration in endometrioid carcinoma.Long non-coding RNA (lncRNA) MCM3AP-AS1 plays an oncogenic role in several malignancies, but its role in endometrioid carcinoma (EC) is unclear. This study was carried out to explore the role of MCM3AP-AS1 in EC. A total of 60 EC patients were enrolled in this study. Expression levels of MCM3AP Antisense RNA 1 (MCM3AP-AS1), microRNA-126 (miR-126), and vascular endothelial growth factor (VEGF) in tissues and transfetced cells were measured by RT-qPCR. Cell transfections were performed to explore the interaction among MCM3AP-AS1, miR-126 and VEGF. Transwell assays were perfromed to evaluate the invasion and migration abilities of HEC-1 cells after transfection. MCM3AP-AS1 was upregulated in EC and predicted poor survival. MCM3AP-AS1 directly interacted with miR-126. In EC cells, overexpression of MCM3AP-AS1 and miR-126 did not significantly affect the expression of each other. In addition, overexpression of MCM3AP-AS1 increased the expression levels of VEGF, a target of miR-126. Moreover, overexpression of MCM3AP-AS1 and VEGF increased the migration and invasion rates of EC cells, while overexpression of miR-126 suppressed these cell behaviors. Overexpression of MCM3AP-AS1 attenuated the role of miR-126 in cell invasion and migration. Therefore, MCM3AP-AS1 may serve as a competing endogenous RNA (ceRNA) of miR-126 to upregulate VEGF, thereby regulating cancer cell behaviors in EC.	34256796	RID04986	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Osteoarthritis	HOTAIR	ADAM10	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-222-3p)	binding/interaction	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000137845	NA	100124700	102	HOXC-AS4|HOXC11-AS1|NCRNA00072	CD156C|HsT18717|kuz|MADM	Blocking HOTAIR protects human chondrocytes against IL-1beta-induced cell apoptosis, ECM degradation, inflammatory response and oxidative stress via regulating miR-222-3p/ADAM10 axis.Long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) contributes to cartilage damages including osteoarthritis (OA). While, its role and mechanism in chondrocytes is incompletely clear. HOTAIR, microRNA (miR)-222-3p and ADAM metalloproteinase-like domain 10 (ADAM10) expressions were detected by real-time quantitative PCR and western blot. The interaction between miR-222-3p and HOTAIR or ADAM10 was confirmed by dual-luciferase reporter assay. Cell injury was measured by MTS method, flow cytometry, western blot, enzyme-linked immunosorbent assay for collagen Type II, type<U+00A0>X,<U+00A0>sex determining region Y-box 9 (SOX9), matrix metalloproteinase (MMP)-13, interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-alpha, and special assay kits for malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD). HOTAIR was highly expressed in human OA cartilages and IL-1beta-induced OA model in immortalized chondrocytes (C-28/I2). Under IL-1beta stress, blocking HOTAIR was responsible to high mitochondrial activity and low early apoptosis rate, accompanied with increased B cell lymphoma (Bcl)-2 and LC3B-II/I proteins, boosted IL-10 and SOD productions, suppressed cleaved caspase-3 and p62 proteins, and decreased MDA and ROS levels, as well as elevated secretions of Type II collagen, Type<U+00A0>X<U+00A0>collagen, SOX9, MMP-13, IL-6, and TNF-alpha. Moreover, miR-222-3p was a target of HOTAIR, and its overexpression and knockdown could suppress and aggravate IL-1beta-induced chondrocytes injury. Furthermore, restoring ADAM10, a target gene of miR-222-3p, counteracted the protective role of miR-222-3p upregulation. HOTAIR might contribute to IL-1beta-induced chondrocytes death, inflammation, extracellular matrix degradation, and oxidative stress in OA via miR-222-3p/ADAM10 axis.	34192661	RID04987	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	CYTOR	RAB10	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-103)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000084733	NA	112597	10890	C2orf59|LINC00152|MGC4677|NCRNA00152	NA	Long noncoding RNA CYTOR triggers gastric cancer progression by targeting miR-103/RAB10.Growing evidence has indicated that the long noncoding RNA (lncRNA) CYTOR is involved in the initiation and progression of malignancies, including gastric cancer. Nevertheless, the mechanisms of CYTOR in gastric cancer development are not fully understood. In the present study, we aimed to clarify the association of CYTOR, miR-103, and RAB10 in gastric cancer progression. We found that CYTOR expression was increased in metastatic gastric cancer biopsies compared with that in primary samples. CYTOR expression was significantly positively correlated with the invasiveness, lymph node metastasis, and advanced stages of gastric cancer. In addition, downregulation of CYTOR expression hampered cell proliferation and migration but induced cell apoptosis. Furthermore, CYTOR sponged miR-103 and diminished miR-103 expression, thus rescuing oncogene RAB10 expression. Knockdown of CYTOR suppressed tumor growth in human BGC823 mouse models. These findings suggest that the CYTOR/miR-103/RAB10 axis is a novel signaling pathway that facilitates gastric cancer progression. CYTOR-targeted interventions provide a rationale to improve therapies targeting gastric cancer progression.	34110382	RID04988	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	DNM3OS	MAP3K3	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-193a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230630	GRCh38_1:172138397-172144840	ENSG00000198909	NA	100628315	4215	DNM3-AS1|MIR199A2HG	MAPKKK3|MEKK3	DNM3OS Facilitates Ovarian Cancer Progression by Regulating miR-193a-3p/MAP3K3 Axis.Long non-coding RNAs (lncRNAs) are essential regulators in the development of ovarian cancer (OC). Nonetheless, the function of lncRNA DNM3 opposite strand/antisense RNA (DNM3OS) in OC remains unclear. This work aimed to investigate the biological roles and underlying mechanisms of DNM3OS in OC. Quantitative real-time polymerase chain reaction was conducted to examine DNM3OS, microRNA (miR)-193a-3p, and mitogen-activated protein kinase 3 (MAP3K3) mRNA expression in OC tissues and cell lines. Kaplan-Meier survival analysis was employed to analyze the relationship between DNM3OS expression and the prognosis of OC patients. Cell counting kit-8, 5-ethynyl-2'-deoxyuridine, and transwell experiments were conducted to monitor cell proliferation, migration, and invasion, respectively. western blot was applied to examine epithelial-mesenchymal transition associated protein (E-cadherin and N-cadherin) expression. Luciferase reporter gene and RNA immunoprecipitation experiments were performed to confirm the relationships among DNM3OS, miR-193a-3p, and MAP3K3. Pearson's correlation analysis was adopted to analyze the correlations among DNM3OS, miR-193a-3p, and MAP3K3 mRNA. DNM3OS expression was remarkably increased in OC tissues and cell lines, which was associated with the unfavorable prognosis of the patients. DNM3OS overexpression enhanced OC cell proliferation, migration, and invasion; suppressed E-cadherin protein expression; and facilitated N-cadherin protein expression, while the transfection of miR-193a-3p mimics had the opposite effects. DNM3OS directly interacted with miR-193a-3p, and miR-193a-3p targeted MAP3K3 by directly binding to 3'UTR. DNM3OS could up-regulate the expression of MAP3K3 via repressing miR-193a-3p expression. DNM3OS, as an oncogenic lncRNA, increases the malignancy of OC cells via regulation of an miR-193a-3p/MAP3K3 axis.	34027641	RID04989	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Colorectal cancer	LEF1-AS1	LEF1	positively-E	dual-luciferase reporter assay;RIP;EMSA;CHIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000138795	NA	641518	51176	NA	TCF10|TCF1ALPHA|TCF7L3	LncRNA LEF1-AS1/LEF1/FUT8 Axis Mediates Colorectal<U+00A0>Cancer Progression by Regulating alpha1, 6-Fucosylationvia Wnt/beta-Catenin Pathway.Fucosylation alteration is involved in several steps of human cancer pathogenesis. Dysregulated long non-coding RNA (lncRNA) often leads to malignancy in colorectal cancer (CRC). Differential levels of LEF1-AS1, LEF1 and FUT8 are analyzed by qRT-PCRand western blot. Chip, RIP, EMSA and luciferase reporter assay confirm the direct interaction among LEF1-AS1, MLL1, H3K4me3, LEF1 and FUT8. Functionally, CRC cell proliferation, migration and invasion are analyzed by CCK8 assay, colony formation assay, transwell assay and flow cytometry. The xenografts nude mice models, lung metastasis and liver metastasis are established to determine the effect of LEF1-AS1/LEF1/FUT8 axis on CRC progression in vivo. Here, we identify that LEF1-AS1 and LEF1 are higher in CRC tissues than that in adjacent tissues, as well as upregulated in CRC cell lines than that in normal colorectal cells. Altered levels of LEF1-AS1 modulate LEF1 expression, while altered LEF1 could not regulate LEF1-AS1. LEF1-AS1 recruits MLL1 to the promoter region of LEF1, induces H3K4me3 methylation modification and mediates LEF1 transcription. Furthermore, alpha1-6 fucosyltransferase FUT8 is overexpressed in CRC tissues and positively correlated to LEF1. FUT8 is a direct target of transcription factor LEF1, which regulates FUT8 level. Altered FUT8 also regulates the core fucosylation of CRC cells, and LEF1-AS1 mediates FUT8 level through activation of Wnt/beta-catenin/LEF1 pathway, thereby resulting in beta-catenin nuclear translocation. In addition, LEF1-AS1 mediates the proliferation, migration and invasion of CRC cells in vitro. LEF1-AS1 silence hinders the tumorigenesis, liver and lung metastasis of SW620 cells in vivo, while overexpressed FUT8 abolishes the suppressive impact of LEF1-AS1 repression on the biological behavior of SW620 cells. Our studies uncovered a novel mechanism for constitutive LEF1-AS1/LEF1/FUT8 axis in CRC progression by regulating alpha1, 6-fucosylation via Wnt/beta-catenin pathway, and consequently, as a potential therapeutic target in CRC.	34021424	RID04990	interact with protein	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	LEF1-AS1	FUT8	positively-E	dual-luciferase reporter assay;RIP;EMSA;CHIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000033170	NA	641518	2530	NA	NA	LncRNA LEF1-AS1/LEF1/FUT8 Axis Mediates Colorectal<U+00A0>Cancer Progression by Regulating alpha1, 6-Fucosylationvia Wnt/beta-Catenin Pathway.Fucosylation alteration is involved in several steps of human cancer pathogenesis. Dysregulated long non-coding RNA (lncRNA) often leads to malignancy in colorectal cancer (CRC). Differential levels of LEF1-AS1, LEF1 and FUT8 are analyzed by qRT-PCRand western blot. Chip, RIP, EMSA and luciferase reporter assay confirm the direct interaction among LEF1-AS1, MLL1, H3K4me3, LEF1 and FUT8. Functionally, CRC cell proliferation, migration and invasion are analyzed by CCK8 assay, colony formation assay, transwell assay and flow cytometry. The xenografts nude mice models, lung metastasis and liver metastasis are established to determine the effect of LEF1-AS1/LEF1/FUT8 axis on CRC progression in vivo. Here, we identify that LEF1-AS1 and LEF1 are higher in CRC tissues than that in adjacent tissues, as well as upregulated in CRC cell lines than that in normal colorectal cells. Altered levels of LEF1-AS1 modulate LEF1 expression, while altered LEF1 could not regulate LEF1-AS1. LEF1-AS1 recruits MLL1 to the promoter region of LEF1, induces H3K4me3 methylation modification and mediates LEF1 transcription. Furthermore, alpha1-6 fucosyltransferase FUT8 is overexpressed in CRC tissues and positively correlated to LEF1. FUT8 is a direct target of transcription factor LEF1, which regulates FUT8 level. Altered FUT8 also regulates the core fucosylation of CRC cells, and LEF1-AS1 mediates FUT8 level through activation of Wnt/beta-catenin/LEF1 pathway, thereby resulting in beta-catenin nuclear translocation. In addition, LEF1-AS1 mediates the proliferation, migration and invasion of CRC cells in vitro. LEF1-AS1 silence hinders the tumorigenesis, liver and lung metastasis of SW620 cells in vivo, while overexpressed FUT8 abolishes the suppressive impact of LEF1-AS1 repression on the biological behavior of SW620 cells. Our studies uncovered a novel mechanism for constitutive LEF1-AS1/LEF1/FUT8 axis in CRC progression by regulating alpha1, 6-fucosylation via Wnt/beta-catenin pathway, and consequently, as a potential therapeutic target in CRC.	34021424	RID04991	interact with protein	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	LEF1-AS1	MLL1	positively-E	dual-luciferase reporter assay;RIP;EMSA;CHIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000118058	NA	641518	NA	NA	NA	LncRNA LEF1-AS1/LEF1/FUT8 Axis Mediates Colorectal<U+00A0>Cancer Progression by Regulating alpha1, 6-Fucosylationvia Wnt/beta-Catenin Pathway.Fucosylation alteration is involved in several steps of human cancer pathogenesis. Dysregulated long non-coding RNA (lncRNA) often leads to malignancy in colorectal cancer (CRC). Differential levels of LEF1-AS1, LEF1 and FUT8 are analyzed by qRT-PCRand western blot. Chip, RIP, EMSA and luciferase reporter assay confirm the direct interaction among LEF1-AS1, MLL1, H3K4me3, LEF1 and FUT8. Functionally, CRC cell proliferation, migration and invasion are analyzed by CCK8 assay, colony formation assay, transwell assay and flow cytometry. The xenografts nude mice models, lung metastasis and liver metastasis are established to determine the effect of LEF1-AS1/LEF1/FUT8 axis on CRC progression in vivo. Here, we identify that LEF1-AS1 and LEF1 are higher in CRC tissues than that in adjacent tissues, as well as upregulated in CRC cell lines than that in normal colorectal cells. Altered levels of LEF1-AS1 modulate LEF1 expression, while altered LEF1 could not regulate LEF1-AS1. LEF1-AS1 recruits MLL1 to the promoter region of LEF1, induces H3K4me3 methylation modification and mediates LEF1 transcription. Furthermore, alpha1-6 fucosyltransferase FUT8 is overexpressed in CRC tissues and positively correlated to LEF1. FUT8 is a direct target of transcription factor LEF1, which regulates FUT8 level. Altered FUT8 also regulates the core fucosylation of CRC cells, and LEF1-AS1 mediates FUT8 level through activation of Wnt/beta-catenin/LEF1 pathway, thereby resulting in beta-catenin nuclear translocation. In addition, LEF1-AS1 mediates the proliferation, migration and invasion of CRC cells in vitro. LEF1-AS1 silence hinders the tumorigenesis, liver and lung metastasis of SW620 cells in vivo, while overexpressed FUT8 abolishes the suppressive impact of LEF1-AS1 repression on the biological behavior of SW620 cells. Our studies uncovered a novel mechanism for constitutive LEF1-AS1/LEF1/FUT8 axis in CRC progression by regulating alpha1, 6-fucosylation via Wnt/beta-catenin pathway, and consequently, as a potential therapeutic target in CRC.	34021424	RID04992	interact with protein	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Glaucoma	LINC01518	miR-216b-5p	negatively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Nervous system disease	Glaucoma	lncRNA	miRNA	ENSG00000233515	GRCh38_10:42644445-42691723	NA	NA	101929397	NA	NA	NA	Long Noncoding RNA LINC01518 Modulates Proliferation and Migration in TGF-beta1-Treated Human Tenon Capsule Fibroblast Cells Through the Regulation of hsa-miR-216b-5p.In this study, we investigated the expression and functions of long noncoding RNAs (LncRNAs) of LINC01518 in an in vitro model of TGF-beta1-treated human Tenon capsule fibroblast (HTF) cells. qRT-PCRwas used to examine LINC01518 expression in in situ human glaucoma tissues, and in vitro HTF cells treated with TGF-beta1. Lentivirus-mediated LINC01518 knockdown was performed in HTF cells to investigate its effect on TGF-beta1-induced cell proliferation, migration and autophagy signaling pathway. The potential ceRNA candidate of LINC01518, hsa-miR-216b-5p, was probed by dual-luciferase assay and qRT-PCR Hsa-miR-216b-5p was also knocked down in LINC01518-downregulated HTF cells to investigate the function of this lncRNA-miRNA epigenetic axis in TGF-beta1-treated HTF cells. LINC01518 was upregulated in human glaucoma tissues and cultured HTF cells. LINC01518 downregulation significantly suppressed TGF-beta1-induced cell proliferation, migration and autophagy signaling pathway in HTF cells. Hsa-miR-216b-5p was confirmed to be a ceRNA target of LINC01518. Knocking down hsa-miR-216b-5p reversed the suppressing effects of LINC01518 downregulation in TGF-beta1-treated HTF cells. Our study demonstrated that LINC01518 is a functional factor in regulating proliferation and migration in TGF-beta1-treated HTF cells, and hsa-miR-216b -5p may also be involved. Targeting the epigenetic axis of LINC01518/hsa-miR-216b-5p may provide new insight into the pathological development of human glaucoma.	33993456	RID04993	ceRNA or sponge	NA		
Hypertrophic scar	INHBA	MCL1	positively-E	LncBase;dual-luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Other	Hypertrophic scar	lncRNA	PCG	ENSG00000122641	GRCh38_7:41667168-41705834	ENSG00000143384	NA	3624	4170	NA	BCL2L3|Mcl-1	Silencing of long noncoding INHBA antisense RNA1 suppresses proliferation, migration, and extracellular matrix deposition in human hypertrophic scar fibroblasts via regulating microRNA-141-3p/myeloid cell leukemia 1 axis.Long noncoding RNAs (lncRNAs) play vital roles in the progression of hypertrophic scar (HS). We aimed to explore the effect of lncRNA INHBA Antisense RNA1 (INHBA-AS1) in the formation of HS and identify the potential mechanisms. INHBA-AS1 and microRNA (miR)-141-3p expression in human HS fibroblasts (hHSFs) was determined using RT-qPCR. LncBase online database predicted that miR-141-3p could be a putative target of INHBA-AS1, and the interaction of them was verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Subsequently, following INHBA-AS1 silencing, cell proliferation and migration were evaluated using CCK-8, wound healing and Transwell assays. And rescue experiments were conducted to analyze the impact of INHBA-AS1 and miR-141-3p on HS formation. Immunofluorescence assay was employed to examine the expression of extracellular matrix (ECM)-related proteins. Then, StarBase database predicated that myeloid cell leukemia 1 (MCL1) was a potential target of miR-141-3p, which was verified with luciferase reporter- and RIP assays. Finally, cell function and ECM deposition were determined after MCL1-downregulation. INHBA-AS1 was significantly elevated while miR-141-3p was notably reduced in hHSFs. And it was confirmed that miR-141-3p was directly targeted by INHBA-AS1. Moreover, INHBA-AS1 silencing markedly attenuated the proliferation, migration and ECM accumulation of hHSFs, which were restored after miR-141-3p silencing. Additionally, MCL1 was confirmed as a direct target of miR-141-3p, and MCL1-knockdown remarkably alleviated the proliferation, migration and ECM accumulation of hHSFs. INHBA-AS1-knockdown suppresses the formation of HS by regulating miR-141-3p/MCL1 pathway, suggesting a promising therapeutic target for HS treatment.	33977869	RID04994	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	LINC01123	GLI1	positively-E	TargetScan;dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-516b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000204588	GRCh38_2:109987063-109996140	ENSG00000111087	NA	440894	2735	NA	GLI	LINC01123 enhances osteosarcoma cell growth by activating the Hedgehog pathway via the miR-516b-5p/Gli1 axis.The lncRNA LINC01123 has been reported to act as an oncogene in many human cancers. Nevertheless, the function and underlying mechanism of LINC01123 in osteosarcoma (OS) remain unclear. This study aimed to explore the roles and mechanisms of LINC01123 in OS progression. In this study, the expression of LINC01123 was significantly upregulated in OS cell lines than in a human osteoblast cell line. Furthermore, in vitro and in vivo experiments confirmed that knockdown of LINC01123 suppressed cell progression. Mechanistically, LINC01123 acted as a competing endogenous RNA by sponging miR-516b-5p, thus, increasing Gli1 expression by directly targeting its 3'UTR. Taken together, LINC01123 enhances OS proliferation and metastasis via the miR-516b-5p/Gli1 axis. Therefore, LINC01123 may be a potential therapeutic target for OS treatment.	33837611	RID04995	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral submucous fibrosis	H19	COL1A1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	fibrotic(-)	ceRNA(miR-29b)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000108821	NA	283120	1277	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	OI4	Targeting lncRNA H19/miR-29b/COL1A1 Axis Impedes Myofibroblast Activities of Precancerous Oral Submucous Fibrosis.Oral submucous fibrosis (OSF) is known as a potentially malignant disorder, which may result from chemical irritation due to areca nuts (such as arecoline). Emerging evidence suggests that fibrogenesis and carcinogenesis are regulated by the interaction of long noncoding RNAs (lncRNAs) and microRNAs. Among these regulators, profibrotic lncRNA  H19  has been found to be overexpressed in several fibrosis diseases. Here, we examined the expression of  H19  in OSF specimens and its functional role in fibrotic buccal mucosal fibroblasts (fBMFs). Our results indicate that the aberrantly overexpressed  H19  contributed to higher myofibroblast activities, such as collagen gel contractility and migration ability. We also demonstrated that  H19  interacted with  miR - 29b , which suppressed the direct binding of  miR - 29b  to the 3'-untranslated region of type I collagen (COL1A1). We showed that ectopic expression of  miR - 29b  ameliorated various myofibroblast phenotypes and the expression of alpha-smooth muscle actin (alpha-SMA), COL1A1, and fibronectin (FN1) in fBMFs. In OSF tissues, we found that the expression of  miR - 29b  was downregulated and there was a negative correlation between  miR - 29b  and these fibrosis markers. Lastly, we demonstrate that arecoline stimulated the upregulation of  H19  through the transforming growth factor (TGF)-beta pathway. Altogether, this study suggests that increased TGF-beta secretion following areca nut chewing may induce the upregulation of  H19 , which serves as a natural sponge for  miR - 29b  and impedes its antifibrotic effects.	33672311	RID04996	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Osteosarcoma	LINC02381	CDCA4	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-503-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000170779	NA	400043	55038	LOC400043	FLJ20764|Hepp	ELK1-induced upregulation lncRNA LINC02381 accelerates the osteosarcoma tumorigenesis through targeting CDCA4 via sponging miR-503-5p.Long noncoding RNAs (lncRNAs) have been identified as functional modulators in human tumors. The purpose of our study was to determine the expressing trend, clinical significance and functions of lncRNA LINC02381(LINC02381) in osteosarcoma. We observed that the expression of LINC02381 and cell division cycle-associated protein 4 (CDCA4) were distinctly increased in osteosarcoma specimens and cells, while miR-503-5p expression was decreased. Additionally, ETS transcription factor ELK1 (ELK1) could bind directly to the LINC02381 promoter region and activate its transcription. Clinical assays revealed that high LINC02381 was associated with advanced clinical progress and poor clinical outcome. Functionally, knockdown of LINC02381 suppressed the proliferation, migration and invasion of osteosarcoma cells. What's more, LINC02381 could down-regulate CDCA4 via sponging miR-503-5p, and there existed a negative correlation between LINC02381 expression and miR-503-5p expression in 92 osteosarcoma samples. Rescue experiments proved the carcinogenic role of LINC02381/miR-503-5p/CDCA4 axis in osteosarcoma progression. Overall, our data illustrated how LINC02381 played an oncogenic role in osteosarcoma and might offer a novel diagnostic and prognostic biomarker and potential therapeutic target for osteosarcoma.	33640603	RID04997	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE55807)	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE111842)
Diabetic retinopathy	TPTEP1	STAT3	negatively-E	luciferase reporter assay;RNA pull-down assay;CHIP	upregulation	RT-qPCR	NA	NA	cell migration(-);angiogenesis(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	TF	ENSG00000100181	GRCh38_22:16601887-16698742	ENSG00000168610	NA	387590	6774	psiTPTE22	APRF	TPTEP1 suppresses high glucose-induced dysfunction in retinal vascular endothelial cells by interacting with STAT3 and targeting VEGFA.Diabetic retinopathy (DR) is a vascular complication of diabetes mellitus that causes visual impairment and blindness. Long noncoding RNAs (lncRNAs) have been revealed to be involved in biological processes of several diseases including DR. We designed this study to investigate the specific role of TPTEP1 in DR. First, we mimicked diabetic conditions with high glucose (HG) stimulation of human retinal vascular endothelial cells (HRVECs) and measured TPTEP1 expression in HG-stimulated HRVECs using RT-qPCR analysis. Then, CCK-8, Transwell, and Matrigel tube formation assays as well as western blotwere performed to reveal the biological functions of TPTEP1 in HG-stimulated HRVECs. Subsequently, bioinformatics analysis, RNA pull down, luciferase reporter and ChIP assays as well as western blotevaluated the relationship of TPTEP1, signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor A (VEGFA) in HG-stimulated HRVECs. Finally, to verify the regulation of the TPTEP1/STAT3/VEGFA axis in HG-stimulated HRVECs, rescue experiments were carried out in HG-stimulated HRVECs. TPTEP1 presented a significant downregulation in HG-stimulated HRVECs. Additionally, TPTEP1 overexpression reduced viability, migration, and angiogenesis in HG-stimulated HRVECs. Moreover, TPTEP1 suppressed phosphorylation and nuclear translocation of STAT3, and thereby downregulated VEGFA mRNA and protein levels. Furthermore, TPTEP1 overexpression-mediated suppression of HG-induced dysfunction in HRVECs was countervailed by STAT3 upregulation or VEGFA upregulation. TPTEP1 alleviated HG-induced dysfunction in HRVECs via interacting with STAT3 and targeting VEGFA.	33576890	RID04998	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Diabetic retinopathy	TPTEP1	VEGFA	negatively-E	luciferase reporter assay;RNA pull-down assay;CHIP	upregulation	RT-qPCR	NA	NA	cell migration(-);angiogenesis(-)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000100181	GRCh38_22:16601887-16698742	ENSG00000112715	NA	387590	7422	psiTPTE22	VEGF|VEGF-A|VPF	TPTEP1 suppresses high glucose-induced dysfunction in retinal vascular endothelial cells by interacting with STAT3 and targeting VEGFA.Diabetic retinopathy (DR) is a vascular complication of diabetes mellitus that causes visual impairment and blindness. Long noncoding RNAs (lncRNAs) have been revealed to be involved in biological processes of several diseases including DR. We designed this study to investigate the specific role of TPTEP1 in DR. First, we mimicked diabetic conditions with high glucose (HG) stimulation of human retinal vascular endothelial cells (HRVECs) and measured TPTEP1 expression in HG-stimulated HRVECs using RT-qPCR analysis. Then, CCK-8, Transwell, and Matrigel tube formation assays as well as western blotwere performed to reveal the biological functions of TPTEP1 in HG-stimulated HRVECs. Subsequently, bioinformatics analysis, RNA pull down, luciferase reporter and ChIP assays as well as western blotevaluated the relationship of TPTEP1, signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor A (VEGFA) in HG-stimulated HRVECs. Finally, to verify the regulation of the TPTEP1/STAT3/VEGFA axis in HG-stimulated HRVECs, rescue experiments were carried out in HG-stimulated HRVECs. TPTEP1 presented a significant downregulation in HG-stimulated HRVECs. Additionally, TPTEP1 overexpression reduced viability, migration, and angiogenesis in HG-stimulated HRVECs. Moreover, TPTEP1 suppressed phosphorylation and nuclear translocation of STAT3, and thereby downregulated VEGFA mRNA and protein levels. Furthermore, TPTEP1 overexpression-mediated suppression of HG-induced dysfunction in HRVECs was countervailed by STAT3 upregulation or VEGFA upregulation. TPTEP1 alleviated HG-induced dysfunction in HRVECs via interacting with STAT3 and targeting VEGFA.	33576890	RID04999	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Osteosarcoma	miR-129-5p	GSTP1P1	negatively-E	IntaRNA 2.0	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	sponge	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000257569	GRCh38_12:55900300-55900618	NA	2951	NA	GST3L|GSTP1P|GSTPL|GSTPP|Lnc712	MiR-129-5p Suppresses Cell Proliferation of Human Osteosarcoma Cancer by Down-Regulating LncRNA Lnc712.Lnc712 has been characterized as an oncogenic lncRNA in breast cancer. This study aimed to investigate the role of Lnc712 in osteosarcoma (OS). OS and paired non-tumor tissues were collected from 58 OS patients. Expression of Lnc712 and miR-129-5p in paired tissue samples was determined by RT-qPCR. Lnc712 and miR-129-5p expression was achieved in OS cells to study the interaction between them. Cell proliferation was analyzed by CCK-8 assay. Lnc712 was upregulated in OS and was inversely correlated with miR-129-5p. In OS cells, Lnc712 overexpression failed to significantly affect miR-129-5p, while miR-129-5p overexpression led to downregulated Lnc712. Cell proliferation showed that Lnc712 overexpression resulted in increased cell proliferation rate. MiR-129-5p overexpression played an opposite role and reversed the effect of Lnc712 overexpression. MiR-129-5p may suppress cell proliferation of OS by down-regulating Lnc712.	33732018	RID05000	ceRNA or sponge	NA		
Gouty arthritis	MALAT1	NLRP3	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	inflammatory response(-)	ceRNA(miR-876-5p)	regulation	RNA-protein	Total glucosides of paeony	NA	NA	Musculoskeletal system disease	Arthritis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000162711	NA	378938	114548	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCU|MWS|NALP3|PYPAF1	Total glucosides of paeony protects THP-1 macrophages against monosodium urate-induced inflammation via MALAT1/miR-876-5p/NLRP3 signaling cascade in gouty arthritis.Monosodium urate (MSU)-mediated inflammatory response is a crucial inducing factor in gouty arthritis. Here, we explored the underlying mechanism of total glucosides of paeony (TGP) in MSU-induced inflammation of THP-1 macrophages in gouty arthritis. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability. Enzyme-linked immunosorbent assay (ELISA) was utilized to measure the production of interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot assay were conducted to determine RNA and protein expression. dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were used to confirm the interaction between miR-876-5p and MALAT1 or NLR family pyrin domain containing 3 (NLRP3). MSU-induced damage and inflammatory response in THP-1 macrophages were alleviated by the treatment of TGP in a dose-dependent manner. Overexpression of NLRP3 or MALAT1 reversed the protective effects of TGP in MSU-induced THP-1 macrophages. The binding relation between miR-876-5p and MALAT1 or NLRP3 was identified in THP-1 macrophages. MALAT1 up-regulated the expression of NLRP3 by sponging miR-876-5p in THP-1 macrophages. TGP suppressed MSU-induced inflammation in THP-1 macrophages through regulating MALAT1/miR-876-5p/NLRP3 axis. TGP suppressed MSU-induced activation of TLR4/MyD88/NF-kB pathway through regulating MALAT1/miR-876-5p/NLRP3 axis. In conclusion, TGP suppressed MSU-induced inflammation in THP-1 macrophages through regulating MALAT1/miR-876-5p/NLRP3 axis and TLR4/MyD88/NF-kB pathway, suggesting that TGP was a promising active ingredient for gouty arthritis treatment.	33677310	RID05001	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Malignant glioma	LINC02381	CBX5	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000094916	NA	400043	23468	LOC400043	HP1|HP1-ALPHA|HP1Hs-alpha	LINC02381 contributes to cell proliferation and hinders cell apoptosis in glioma by transcriptionally enhancing CBX5.Glioma, featured with high incidence and low survival rate, is the most common type of primary brain tumor, severely affecting human life worldwide. LINC02381 is an interesting lncRNA functioning as oncogenic lncRNA in some cancers but as tumor-suppressor in others, but no report demonstrates its association with and function in glioma. Intriguingly, we found in a bioinformatics website LncRNADisease that LINC02381 was closely related to malignant glioma, so this study aimed to figure out the expression and function of LINC02381 in glioma. By RT-qPCR, we confirmed LINC02381 upregulation in glioma cells. Functional experiments demonstrated that LINC02381 knockdown repressed glioma cell proliferation and induced apoptosis. Boinformatics tools and RT-qPCR revealed the positive correlation between LINC02381 and CBX5 in glioma cells. More importantly, we confirmed that LINC02381 could interact and work synergistically with CEBPbeta to bind to CBX5 promoter and activate CBX5 transcriptionally. Additionally, rescue experiments indicated that CBX5 up-regulation reversed the decline in cell proliferation and the augment in cell apoptosis caused by LINC02381 knockdown. To conclude, LINC02381 could facilitate CBX5 transcription via interaction with CEBPbeta, thus exerting its oncogenic role in glioma cells, which could contribute to better understanding of glioma.	34274429	RID05002	expression association	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842)
Thyroid cancer	ZFAS1	MMP3	positively-E	luciferase reporter assay;CHIP;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000263313	NA	441951	4314	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	STMY|STMY1	CREB3 Transactivates lncRNA ZFAS1 to Promote Papillary Thyroid Carcinoma Metastasis by Modulating miR-373-3p/MMP3 Regulatory Axis.The incidence rate of thyroid carcinoma ranks ninth among human malignancies, and it accounts for the most frequent malignancy in endocrine-related tumors. This study aimed to investigate the role of long noncoding RNA (lncRNA) ZFAS1 in the metastasis of papillary thyroid carcinoma (PTC) and the potential molecular mechanisms. Both ZFAS1 and MMP3 were highly expressed in thyroid carcinoma and PTC cell, as measured by the q-PCR and TCGA database. In addition, ZFAS1 induced TPC-1 metastasis through inducing the epithelial-mesenchymal transition (EMT) process. Besides, ZFAS1 knockdown by siRNA induced miR-373-3 p  expression and reduced MMP3 expression, as quantified by q-PCR and western blot. According to the luciferase assay, both ZFAS1 and MMP3 were classified as the direct targets of miR-373-3 p . However, MMP3 itself did not affect ZFAS1. Using the online prediction tool, CREB3 was predicted as the transcription factor (TF) of ZFAS1 that contained two binding sites on its promoter region, and CREB3 was positively correlated with ZFAS1 in thyroid carcinoma cohorts. Results from the dual-luciferase assay and ChIP-qPCR indicated that both the two binding sites were essential for the transcription of ZFAS1. In conclusion, CREB3 activated lncRNA ZFAS1 at the transcriptional level to promote PTC metastasis by modulating miR-373-3 p /MMP3.	34249125	RID05003	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Thyroid cancer	CREB3	ZFAS1	positively-E	luciferase reporter assay;CHIP;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000107175	NA	ENSG00000177410	GRCh38_20:49278178-49299600	10488	441951	Luman|LZIP|sLZIP	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	CREB3 Transactivates lncRNA ZFAS1 to Promote Papillary Thyroid Carcinoma Metastasis by Modulating miR-373-3p/MMP3 Regulatory Axis.The incidence rate of thyroid carcinoma ranks ninth among human malignancies, and it accounts for the most frequent malignancy in endocrine-related tumors. This study aimed to investigate the role of long noncoding RNA (lncRNA) ZFAS1 in the metastasis of papillary thyroid carcinoma (PTC) and the potential molecular mechanisms. Both ZFAS1 and MMP3 were highly expressed in thyroid carcinoma and PTC cell, as measured by the q-PCR and TCGA database. In addition, ZFAS1 induced TPC-1 metastasis through inducing the epithelial-mesenchymal transition (EMT) process. Besides, ZFAS1 knockdown by siRNA induced miR-373-3 p  expression and reduced MMP3 expression, as quantified by q-PCR and western blot. According to the luciferase assay, both ZFAS1 and MMP3 were classified as the direct targets of miR-373-3 p . However, MMP3 itself did not affect ZFAS1. Using the online prediction tool, CREB3 was predicted as the transcription factor (TF) of ZFAS1 that contained two binding sites on its promoter region, and CREB3 was positively correlated with ZFAS1 in thyroid carcinoma cohorts. Results from the dual-luciferase assay and ChIP-qPCR indicated that both the two binding sites were essential for the transcription of ZFAS1. In conclusion, CREB3 activated lncRNA ZFAS1 at the transcriptional level to promote PTC metastasis by modulating miR-373-3 p /MMP3.	34249125	RID05004	interact with protein	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Skin squamous cell carcinoma	HCP5	EZH2	positively-E	TargetScan;mirDIP;miRSearch;miRDB;RNA22;dual-luciferase reporter assay;RNA pull-down assay;RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000106462	NA	10866	2146	D6S2650E|P5-1	ENX-1|EZH1|KMT6|KMT6A	lncRNA HCP5 acts as a ceRNA to regulate EZH2 by sponging miR-138-5p in cutaneous squamous cell carcinoma.Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are essential for the progression of tumors, including cutaneous squamous cell carcinoma (CSCC). The present study aimed to examine the competing endogenous RNA (ceRNA) network in CSCC. Differentially expressed genes in CSCC were analyzed using the GSE66359 microarray data set, and the upstream miRNAs and lncRNAs were predicted using online database analysis (TargetScan 7.1, mirDIP 4.1, miRSearch V3.0, miRDB and RNA22 2.0) and were verified in clinical tissues. RNA pull-down and dual luciferase reporter gene assays were used to verify the targeting relationships among lncRNA human histocompatibility leukocyte antigen complex P5 (HCP5), miR-138-5p and enhancer of zeste homolog 2 (EZH2). Cell lines with a high and low HCP5 expression were screened, and a pcDNA-3.1-HCP5 overexpression vector, small interfering RNA against HCP5, miR-138-5p mimics and miR-138-5p inhibitors were transfected into the CSCC cells. Cell viability, invasion, migration, apoptotic rate and autophagy were evaluated. The effects of HCP5 on autophagy and apoptosis of CSCC cells were verified in vivo using Ki67 and TUNEL staining. EZH2 was demonstrated to be upregulated in CSCC cells. miR-138-5p target sequences were identified in HCP5 and EZH2. HCP5 was revealed to function as a putative ceRNA of miR-138-5p to positively regulate EZH2, and EZH2 was shown to regulate autophagy and apoptosis of CSCC cells through the STAT3/VEGFR2 pathway. HCP5 overexpression decreased miR-138-5p levels, increased EZH2 levels and promoted cell malignant behaviors and autophagy but decreased the apoptosis rate. These trends were opposite when HCP5 was silenced. In conclusion, HCP5 may competitively bind to miR-138-5p to regulate EZH2 in CSCC cells, promoting autophagy and reducing apoptosis through the STAT3/VEGFR2 pathway. This study may provide a new perspective for understanding the molecular mechanism and treatment of CSCC.	34195851	RID05005	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteoporosis	LINC00963	ETS1	positively-E	luciferase reporter assay;RNAi;RIP	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-760)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000134954	NA	100506190	2113	MetaLnc9	ETS-1|EWSR2|FLJ10768	LncRNA LINC00963 promotes osteogenic differentiation of hBMSCs and alleviates osteoporosis progression by targeting miRNA-760/ETS1 axis.Although long non-coding RNA LINC00963 has been reported to play a crucial regulatory role in osteoporosis (OP), its specific mechanism has not been well studied. Cell viability of human bone marrow mesenchymal stem cells (hBMSCs) transfected with short hairpin RNA targeting LINC00963 (sh-LINC00963) and negative control (sh-NC) was analysed by cell counting kit-8 (CCK-8) assay. Alkaline phosphatase (ALP) activity in hBMSCs transfected with sh-LINC00963 and sh-NC after induction by osteogenic medium (OM) on day 7 was detected. The protein expression levels of osteocalcin (OCN) and osteopontin (OPN) in hBMSCs transfected with sh-LINC00963 and sh-NC during OM induction on day 3 were detected by western blot. The relationship among LINC00963, miR-760, and E26 transformation specific-1 (ETS1) was determined by bioinformatics analysis, luciferase reporter assay, and RNA-binding protein immunoprecipitation (RIP) assay. A rat model with OP was established to confirm the role of LINC00963  in<U+00A0>vivo . The expression level of LINC00963 was much lower in hBMSCs isolated from the discarded femoral head tissues of OP patients compared with that in health patients. Meanwhile, the expression level of LINC00963 was significantly increased and the expression level of miR-760 was decreased in hBMSCs during osteogenic induction. LINC00963 could bind to the 3'-untranslated region (3'-UTR) of miR-760 and negatively regulate the expression of miR-760, then promote the osteogenic differentiation in hBMSCs. ETS1 was identified as a target of miR-760. Moreover, overexpression of LINC00963 obviously reduced bone mineral density (BMD) of the left femur in OP rats and alleviated OP progression  in<U+00A0>vivo.  Our results demonstrated that LINC00963 positively regulated the expression of ETS1 by directly targeting miR-760, and then promoted osteogenic differentiation of hBMSCs  in<U+00A0>vitro , and also attenuated OP progression  in<U+00A0>vivo , suggesting that LINC00963 might be a potential therapeutic target for OP.	34184952	RID05006	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Osteoporosis	IGF2-AS	KLK4	positively-E	TargetScan;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-3,126-5p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000167749	NA	51214	9622	IGF2-AS1|IGF2AS|PEG8	EMSP|EMSP1|KLK-L1|PRSS17|PSTS	lncRNA IGF2-AS promotes the osteogenic differentiation of bone marrow mesenchymal stem cells by sponging miR-3,126-5p to upregulate KLK4.Osteoporosis (OP) is a bone disease characterized by reduced amount and quality of bone. This study was designed to explore the role and mechanism of lncRNA IGF2-AS in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Human lncRNA and miRNA microarray analyses were performed to measure the differential expression levels of lncRNAs and miRNAs in undifferentiated and osteogenically differentiated BMSCs. lncRNA IGF2-AS, miR-3,126-5p, and KLK4 levels were measured by real-time quantitative polymerase chain reaction (RT-qPCR). Osteogenic differentiation of BMSCs was assessed by alkaline phosphatase (ALP) staining and Alizarin Red staining (ARS). Protein levels of osterix (Osx), osteocalcin (OCN), and runt-related transcription factor 2 (RUNX2) were examined by RT-PCRand western blot assays. The binding relationship between miR-3,126-5p and lncRNA IGF2-AS or KLK4 was predicted by TargetScan (http://www.targetscan.org/vert_72/) and then verified with a dual-luciferase reporter assay. lncRNA IGF2-AS and KLK4 were highly expressed and miR-3,126-5p was weakly expressed in osteogenically differentiated BMSCs. Moreover, lncRNA IGF2-AS overexpression enhanced the osteogenic differentiation of BMSCs. In contrast, lncRNA IGF2-AS knockdown showed the opposite trend. Moreover, miR-3,126-5p overexpression abolished the lncRNA IGF2-AS-mediated osteogenic differentiation of BMSCs. lncRNA IGF2-AS functions as a sponge of miR-3,126-5p to regulate KLK4 expression. lncRNA IGF2-AS enhances the osteogenic differentiation of BMSCs by modulating the miR-3,126-5p/KLK4 axis, suggesting a promising therapeutic target for bone-related diseases.	34101307	RID05007	ceRNA or sponge	NA		
Gastric cancer	LINC00659	IQGAP3	positively-E	bioinformatics method	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228705	GRCh38_20:62772980-62776996	ENSG00000183856	NA	100652730	128239	NA	NA	Upregulation of LINC00659 expression predicts a poor prognosis and promotes migration and invasion of gastric cancer cells.Long non-coding RNAs (lncRNAs) serve an important role in the progression of cancer. LINC00659 was recently identified as a novel oncogenic lncRNA involved in colon cancer cell proliferation via modulating the cell cycle. However, the function of LINC00659 in other types of cancer, especially in gastric cancer (GC), remains unknown. In the present study, bioinformatics analysis combined with cell experiments were performed to explore the function of LINC00659 in GC. It was revealed that LINC00659 expression was significantly upregulated in GC tissues and cell lines. Increased levels of LINC00659 were associated with advanced tumor stage and unfavorable prognosis of patients with GC. Additionally, upregulated LINC00659 expression promoted the migration and invasion of GC cells. Further analysis using a bioinformatics method revealed that matrix metalloproteinase 15 and IQ motif-containing GTPase activating protein 3 were potential downstream targets of LINC00659 involved in tumor metastasis, although the precise underlying mechanism requires further exploration.	34084224	RID05008	expression association	metastasis,prognosis		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Gastric cancer	LINC00659	MMP3	positively-E	bioinformatics method	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228705	GRCh38_20:62772980-62776996	ENSG00000263313	NA	100652730	4314	NA	STMY|STMY1	Upregulation of LINC00659 expression predicts a poor prognosis and promotes migration and invasion of gastric cancer cells.Long non-coding RNAs (lncRNAs) serve an important role in the progression of cancer. LINC00659 was recently identified as a novel oncogenic lncRNA involved in colon cancer cell proliferation via modulating the cell cycle. However, the function of LINC00659 in other types of cancer, especially in gastric cancer (GC), remains unknown. In the present study, bioinformatics analysis combined with cell experiments were performed to explore the function of LINC00659 in GC. It was revealed that LINC00659 expression was significantly upregulated in GC tissues and cell lines. Increased levels of LINC00659 were associated with advanced tumor stage and unfavorable prognosis of patients with GC. Additionally, upregulated LINC00659 expression promoted the migration and invasion of GC cells. Further analysis using a bioinformatics method revealed that matrix metalloproteinase 15 and IQ motif-containing GTPase activating protein 3 were potential downstream targets of LINC00659 involved in tumor metastasis, although the precise underlying mechanism requires further exploration.	34084224	RID05009	expression association	metastasis,prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	NR2F2-AS1	PLEKHO2	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-106b)	regulation	RNA-protein	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000247809	GRCh38_15:96110040-96327361	ENSG00000241839	NA	644192	80301	NA	DKFZp761K2312|PLEKHQ1|PP1628|pp9099	The miR-106b/NR2F2-AS1/PLEKHO2 Axis Regulates Migration and Invasion of Colorectal Cancer through the MAPK Pathway.Increasing numbers of miRNAs have been observed as oncogenes or tumor suppressors in colorectal cancer (CRC). It was recently reported that hsa-miR-106b-5p (miR-106b) promoted CRC cell migration and invasion. However, there were also studies showing contradictory results. Therefore, in the present study, we further explore the role of miR-106b and its downstream networks in the carcinogenesis of CRC. We observed that the expression of miR-106b is significantly increased in Pan-Cancer and CRC tissues compared with normal tissues from The Cancer Genome Atlas (TCGA) database. Furthermore, we used Transwell, Cell Counting Kit-8, and colony formation assays to clarify that miR-106b promotes the migratory, invasive, and proliferative abilities of CRC cells. For the first time, we systematically screened the target mRNAs and lncRNAs of miR-106b using TCGA database and the bioinformatics algorithms. dual-luciferase reporter assay confirmed that NR2F2-AS1 and PLEKHO2 are the direct targets of miR-106b. Furthermore, NR2F2-AS1 acts as a competing endogenous RNA (ceRNA) to regulate PLEKHO2 expression by sponging miR-106b. The results of Gene set enrichment analysis (GSEA) and western blot indicated that they play important roles in CRC progression by regulating MAPK pathway. Thus, miR-106b/NR2F2-AS1/PLEKHO2/MAPK signaling axis may suggest the potential usage in CRC treatment.	34070923	RID05010	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Prostate cancer	PCA3	SREBF1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-132-3P)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000072310	NA	50652	6720	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	bHLHd1|SREBP-1c|SREBP1|SREBP1a	LncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.Antimony is a common environmental contaminant that causes biological toxicity in exposed populations worldwide. Previous studies have revealed that antimony promotes prostate cancer growth by stabilizing the c-Myc protein and mimicking androgen activity. However, the role of lncRNAs in the regulation of antimony-induced carcinogenesis remains unknown, and the precise mechanisms need to be explored. In the present study, we found that chronic exposure to antimony promoted cell growth and lipid metabolic disequilibrium in prostate cancer. Mechanistically, we identified a long noncoding RNA molecule, PCA3, that was substantially upregulated in LNCaP cells in response to long-term antimony exposure. Functional studies indicated that abnormal PCA3 expression modulated antimony-induced proliferation and cellular triglyceride and cholesterol levels. In addition, PCA3 levels were found to be inversely correlated with MIR-132-3 P levels by acting as a decoy for MIR-132-3P. Besides, SREBP1 directly interacted with MIR-132-3 P to increase cell growth and disrupt lipid metabolism by targeting its 3'UTR regions. Taken together, our results revealed that lncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.	34052307	RID05011	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	DLGAP1-AS1	MARK4	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-515-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000007047	NA	649446	57787	FLJ35776|HsT914	FLJ90097|KIAA1860|MARKL1|Nbla00650|PAR-1D	Long non-coding RNA DLGAP1-AS1 promotes the progression of gastric cancer via miR-515-5p/MARK4 axis.Long non-coding RNA (lncRNA) is an essential regulator of carcinogenesis and cancer progression. In the study, we explored the role of lncRNA DLGAP1-AS1 in gastric cancer (GC). qRT-PCRwas carried out to detect DLGAP1-AS1 expression in GC tissues and cell lines. CCK-8 assay, EdU assay, and transwell experiments were employed to detect the malignant biological behaviors of GC cells with DLGAP1-AS1 knockdown or overexpression. Bioinformatics and dual-luciferase report assay were used to confirm the binding relationship between DLGAP1-AS1 and miR-515-5p. MARK4 expression was detected by western blot after DLGAP1-AS1/miR-515-5p was selectively regulated. DLGAP1-AS1 was up-regulated in GC tissues and cell lines, and its high expression was closely associated with larger tumor size, higher TNM stage, and lymph node metastasis. Furthermore, DLGAP1-AS1 overexpression enhanced cell proliferation, migration, and invasion, and miR-515-5p could reverse these effects. DLGAP1-AS1 participated in the regulation of the MARK4 signaling pathway by targeting miR-515-5p. DLGAP1-AS1 promoted GC progression through miR-515-5p/MARK4 signaling pathway.	34037089	RID05012	ceRNA or sponge	metastasis	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978,GSE41245)
Non-small cell lung cancer	LINC00847	IFITM1	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell growth(+)	ceRNA(miR-147a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245060	GRCh38_5:180830326-180839742	ENSG00000185885	NA	729678	8519	NA	9?7日|CD225|DSPA2a|IFI17	Long Non-coding RNA LINC00847 Induced by E2F1 Accelerates Non-small Cell Lung Cancer Progression Through Targeting miR-147a/IFITM1 Axis.Background:  Long non-coding RNAs (lncRNAs) can remarkably regulate human malignancies in terms of the development and the progression. Previously, lncRNA LINC00847 (LINC00847) has been reported to present dysregulation in several tumors. However, the expression and function of LINC00847 in non-small cell lung cancer (NSCLC) have not been investigated.  Methods:  RT-qPCR was performed to determine the expressions of LINC00847 in collected tissue samples and cell lines. The clinical significance of LINC00847 was statistically analyzed. CCK-8 test, cell scratch test and trans-well test were used to evaluate the proliferation, invasion and migration abilities of NSCLC cells, respectively. The xenograft tumor model was constructed to confirm the effects of LINC00847 knockdown on NSCLC  in vivo . Further, luciferase reporter assays and western blot were performed to explore molecular mechanisms underlying the functions of LINC00847.  Results:  Increased expressions of LINC00847 were observed in NSCLC samples as well as cell lines. Additionally, E2F1 could be capable of directly binding to the LINC00847 promoter region, followed by promoting its expression. Clinically, LINC00847 high-expression could lead to poor prognosis of NSCLC patients. Functionally, LINC00847 knockdown noticeably repressed NSCLC cell growth and metastasis. Mechanically, miR-147a/IFITM1 axis was a downstream target of LINC00847, and silencing of miR-147a could rescue the anti-cancer effects of LINC00847 knockdown on NSCLC cell behaviors.  Conclusion:  Overall, up regulation of LINC00847 induced by E2F1 promoted the progression of NSCLC by modulating miR-147a/IFITM1 axis, representing a novel regulatory mechanism for NSCLC progression.	33968966	RID05013	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367)
Colorectal cancer	UCA1	SP1	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RNAi;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-495)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000185591	NA	652995	6667	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	lncRNA UCA1 induced by SP1 and SP3 forms a positive feedback loop to facilitate malignant phenotypes of colorectal cancer via targeting miR-495.Long noncoding RNA (LncRNA) urothelial cancer associated 1 (UCA1) was dysregulated in colorectal cancers (CRC) and promoted tumor progression of CRC. The aims of this study are to further investigate the underlying mechanism. Short hairpin RNAs (shRNAs) were applied for gene knockdown. microRNA mimic and pcDNA-UCA1 plasmids were transfected for miR-495 and UCA1 overexpression, respectively. MTT was applied to determine cell viability and sensitivity of 5-fluorouracil (FU). Transwell assays were performed to evaluate cell migration/invasion. Angiogenesis was evaluated by tube formation. western blot and quantitative PCR were utilized for protein and mRNA detection, respectively. The interaction of UCA1, miR-495 and SP1/SP3 were explored by dual-luciferase assay. RNA pull-down was adopted to determine the UCA1/miR-495 interaction. UCA1 was significantly upregulated in CRC tissues. UCA1 enhanced cell proliferation, migration/invasion, angiogenesis, epithelial-mesenchymal transition, and resistance to 5-FU in CRC cell lines. MiR-495 was inversely correlated to the expression of UCA1. The results indicated that UCA1 sponged miR-495, leading to the disinhibition of SP1/SP3 expression. SP1/SP3 induced the expression of DNA methyltransferases and, in turn, contributed to UCA1 mediated tumor-promoting actions. Reduction of SP1/SP3 exerted anti-cancer effects, which can be reversed by forced expression of UCA1. UCA1-miR-495-SP1/SP3 axis is dysregulated in CRC and contributed to malignant phenotypes of CRC. UCA1-SP1/SP3 may form a positive feedback loop in CRC.	33961855	RID05014	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	UCA1	SP3	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-495)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000172845	NA	652995	6670	CUDR|LINC00178|onco-lncRNA-36|UCAT1	SPR-2	lncRNA UCA1 induced by SP1 and SP3 forms a positive feedback loop to facilitate malignant phenotypes of colorectal cancer via targeting miR-495.Long noncoding RNA (LncRNA) urothelial cancer associated 1 (UCA1) was dysregulated in colorectal cancers (CRC) and promoted tumor progression of CRC. The aims of this study are to further investigate the underlying mechanism. Short hairpin RNAs (shRNAs) were applied for gene knockdown. microRNA mimic and pcDNA-UCA1 plasmids were transfected for miR-495 and UCA1 overexpression, respectively. MTT was applied to determine cell viability and sensitivity of 5-fluorouracil (FU). Transwell assays were performed to evaluate cell migration/invasion. Angiogenesis was evaluated by tube formation. western blot and quantitative PCR were utilized for protein and mRNA detection, respectively. The interaction of UCA1, miR-495 and SP1/SP3 were explored by dual-luciferase assay. RNA pull-down was adopted to determine the UCA1/miR-495 interaction. UCA1 was significantly upregulated in CRC tissues. UCA1 enhanced cell proliferation, migration/invasion, angiogenesis, epithelial-mesenchymal transition, and resistance to 5-FU in CRC cell lines. MiR-495 was inversely correlated to the expression of UCA1. The results indicated that UCA1 sponged miR-495, leading to the disinhibition of SP1/SP3 expression. SP1/SP3 induced the expression of DNA methyltransferases and, in turn, contributed to UCA1 mediated tumor-promoting actions. Reduction of SP1/SP3 exerted anti-cancer effects, which can be reversed by forced expression of UCA1. UCA1-miR-495-SP1/SP3 axis is dysregulated in CRC and contributed to malignant phenotypes of CRC. UCA1-SP1/SP3 may form a positive feedback loop in CRC.	33961855	RID05015	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00518	MECP2	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell cycle(+)	ceRNA(miR-185-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000183674	GRCh38_6:10429255-10435015	ENSG00000169057	NA	221718	4204	C6orf218|MGC40222	MRX16|MRX79|RTT	LINC00518 Promotes Cell Proliferation by Regulating the Cell Cycle of Lung Adenocarcinoma Through miR-185-3p Targeting MECP2.Previous studies have shown that long intergenic non-protein coding RNA 00518 (LINC00518) are essential for the cell growth and metastasis of human cancer. However, the role of LINC00518 in lung adenocarcinoma (LUAD) is still unknown. This research put emphasis on the function of LINC00518 on the cell growth of LUAD. The lncRNA, miRNA and mRNA expression were measured by using qRT-PCR Protein levels were measured by using western blot. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Bioinformatic analysis and luciferase reporter assays were chosen to confirm the mechanism of LINC00518 in LUAD. We found that LINC00518 was highly expressed in LUAD specimens and the high-expression was negatively correlated with the overall survival rates. This finding was also proved in the LUAD cell lines. Through a series of  in vitro and in vivo  experiments, we proved that LICN00518 promoted the cell growth of LUAD by regulating the cell cycle. Moreover, LICN00518 upregulated the expression of MECP2 by mutagenesis of miR-185-3p. The results suggested that LICN00518 could be used as a survival indicator and potential therapeutic target for LUAD patients.	33937054	RID05016	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Osteoporosis	SNHG14	CCN5	positively-E	StarBase;miRanda;Luciferase reporter assay;RNA pull-down assay;RNAi;	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-185-5p)	regulation	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000064205	NA	104472715	8839	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	CT58|CTGF-L|WISP-2|WISP2	LncRNA SNHG14 promotes osteogenic differentiation of human bone marrow-derived mesenchymal stem cells via regulating miR-185-5p/WISP2 axis.Osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs) is vital for bone formation, and its dysfunction is linked to osteoporosis (OP). In this work, we explored the function of long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) in regulating osteogenic differentiation of hBMSCs. In the present study, the expression of SNHG14 in hBMSCs obtained from OP patients was measured by quantitative real-time polymerase chain reaction (qRT-PCR. SNHG14 was over-expressed or knocked down in hBMSCs, and the expression levels of OP-related genes (ALP, OCN, and OPN) in hBMSCs were detected by qRT-PCRand western blot. StarBase database and miRanda database were used to predict the binding sites between SNHG14 and miR-185-5p, and between miR-185-5p and 3'UTR of WNT1 inducible signaling pathway protein 2 (WISP2), respectively. Luciferase reporter gene assay was used to validate the binding relationship between SNHG14 and miR-185-5p, and miR-185-5p and 3'UTR of WISP2, respectively. Here, we report that SNHG14 was significantly down-regulated in hBMSCs obtained from patients with OP. Overexpression of SNHG14 promoted osteogenic differentiation, while knockdown of SNHG14 worked oppositely. Mechanistically, miR-185-5p was demonstrated to be a target of SNHG14, and could reverse the function of SNHG14. Additionally, WISP2 was identified as a target gene of miR-185-5p in hBMSCs and could be indirectly regulated by SNHG14. Taken together, down-regulation of SNHG14 in hBMSCs accelerated the progression of OP via regulating miR-185-5p/WISP2 axis.	33928771	RID05017	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	
Oral squamous cell carcinoma	PANDAR	SRSF7	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000115875	NA	101154753	6432	PANDA	9G8|AAG3|HSSG1|RBM37|SFRS7|ZCCHC20|ZCRB2	Knockdown of LncRNA PANDAR by CRISPR-dCas9 Decreases Proliferation and Increases Apoptosis in Oral Squamous Cell Carcinoma.Oral squamous cell carcinoma (OSCC) is the most common malignant epithelial tumor in the oral cavity. Emerging evidence has demonstrated the important function roles of long noncoding RNAs (lncRNAs) in human cancers. LncRNA promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) functions as an oncogene in multiple carcinomas, whereas its function in OSCC has not been investigated yet. The aim of our study is to investigate the possible regulatory mechanism of PANDAR in OSCC. First of all, PANDAR was highly expressed in OSCC cells and loss-of-function assays mediated by CRISPR-dCas9 observed that PANDAR silencing restrained cell proliferation and promoted cell apoptosis. Then we found and confirmed the interaction between PANDAR and serine and arginine rich splicing factor 7 (SRSF7). Subsequently, serine/threonine-protein kinase pim-1 (PIM1) was proved to be regulated by PANDAR in SRSF7-dependant way. Rescue experiments validated that PANDAR modulated the proliferation and apoptosis in OSCC through PIM1. In conclusion, PANDAR bound with SRSF7 to increase PIM1 expression, hence promoting the development of OSCC. These data shed new lights into the seeking for effective diagnostic biomarkers and therapeutic targets for OSCC patients.	33842552	RID05018	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)
Oral squamous cell carcinoma	PANDAR	PIM1	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000137193	NA	101154753	5292	PANDA	PIM	Knockdown of LncRNA PANDAR by CRISPR-dCas9 Decreases Proliferation and Increases Apoptosis in Oral Squamous Cell Carcinoma.Oral squamous cell carcinoma (OSCC) is the most common malignant epithelial tumor in the oral cavity. Emerging evidence has demonstrated the important function roles of long noncoding RNAs (lncRNAs) in human cancers. LncRNA promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) functions as an oncogene in multiple carcinomas, whereas its function in OSCC has not been investigated yet. The aim of our study is to investigate the possible regulatory mechanism of PANDAR in OSCC. First of all, PANDAR was highly expressed in OSCC cells and loss-of-function assays mediated by CRISPR-dCas9 observed that PANDAR silencing restrained cell proliferation and promoted cell apoptosis. Then we found and confirmed the interaction between PANDAR and serine and arginine rich splicing factor 7 (SRSF7). Subsequently, serine/threonine-protein kinase pim-1 (PIM1) was proved to be regulated by PANDAR in SRSF7-dependant way. Rescue experiments validated that PANDAR modulated the proliferation and apoptosis in OSCC through PIM1. In conclusion, PANDAR bound with SRSF7 to increase PIM1 expression, hence promoting the development of OSCC. These data shed new lights into the seeking for effective diagnostic biomarkers and therapeutic targets for OSCC patients.	33842552	RID05019	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Lung cancer	CRYBG3	EEF1A1	positively-E	RIP;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233280	NA	ENSG00000156508	NA	131544	1915	DKFZp667G2110	EE1A1|EEF1A|EF1A|LENG7	Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis.The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells' metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.	33809929	RID05020	interact with protein	metastasis,prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Lung cancer	CRYBG3	MDM2	positively-E	RIP;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell metastasis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233280	NA	ENSG00000135679	NA	131544	4193	DKFZp667G2110	HDM2|MGC5370	Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis.The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells' metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.	33809929	RID05021	expression association	metastasis,prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	CRYBG3	MTBP	positively-E	RIP;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell metastasis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233280	NA	ENSG00000172167	NA	131544	27085	DKFZp667G2110	NA	Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis.The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells' metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.	33809929	RID05022	expression association	metastasis,prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE51827,GSE67939)
Lung cancer	CRYBG3	ACTN4	negatively-E	RIP;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell metastasis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233280	NA	ENSG00000130402	NA	131544	81	DKFZp667G2110	FSGS1	Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis.The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells' metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.	33809929	RID05023	expression association	metastasis,prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	GAS5	miR-1297	negatively-E	miRDB14;DIANA IncBase;RegRNA;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Accelerates Cholangiocarcinoma Progression by Regulating hsa-miR-1297.Long noncoding RNAs (lncRNAs) have been reported as important molecules in cholangiocarcinoma (CCA) occurrence and development. A previous study showed that lncRNA GAS5 (GAS5) was an oncogene in some tumors. But the role of GAS5 in CCA progression reminds unclear. This research was designed to study the expression and potential effects of GAS5 in the progression of CCA. The expression of GAS5 in CCA tissues was evaluated through mining of the TCGA and GEPIA databases. qRT-PCRwas applied to validate the results in our clinical samples.  Chi   2  test was used to analyze the association between the expression level of tissue GAS5 and different clinicopathological parameters of CCA patients. The target gene of GAS5 was predicted by bioinformatic databases, and further verified by luciferase reporter assays. Finally, the role of GAS5 in CCA cells invasion and proliferation was detected by Transwell assay and CCK-8 assay. Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. In addition, the function study showed that GAS5 acted as a "sponge" to downregulate hsa-miR-1297, thus modulating CCA cell proliferation and invasion. GAS5 acts as an endogenous sponge of hsa-miR-1297 to promote CCA cell proliferation and invasion, which might be a potential biomarker and therapeutic target for CCA.	33790648	RID05024	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Triple-negative breast cancer	lnc005620	ITGB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Epirubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000150093	NA	NA	3688	NA	CD29|FNRB|GPIIA|MDF2|MSK12	Novel Long Noncoding RNA 005620 Induces Epirubicin Resistance in Triple-Negative Breast Cancer by Regulating ITGB1 Expression.Triple-negative breast cancer (TNBC) is often treated with anthracyclines (e.g., epirubicin or doxorubicin), but very little is known about anthracycline resistance, especially epirubicin resistance in TNBC. To identify novel long noncoding RNAs (lncRNAs) involved in epirubicin resistance in TNBC, we established a new TNBC MDA-MB-231 cell line that was resistant to epirubicin (Epi-R). A total of 12 differentially expressed lncRNAs were identified using RNA sequencing analysis of Epi-R cells. Among these lncRNAs, we found a novel intronic lncRNA, lnc005620, was highly expressed in Epi-R cells and human TNBC tissues. Further gain- and loss-of-function studies demonstrated that lnc005620 played an oncogenic role and partially abrogated the effects of epirubicin on TNBC cells. Using iTRAQ proteomics analysis, we found that three members of the integrin family, integrin beta4, integrin beta1 and integrin alpha6, were all upregulated in Epi-R MDA-MB-231 cells. Integrin beta1, encoded by the ITGB1 gene, was validated to be a downstream target of lnc005620 in Epi-R MDA-MB-231 cells. Our study demonstrates that novel lnc005620 promotes TNBC progression and chemoresistance to epirubicin  via  integrin beta1 both  in vitro  and  in vivo  and provides a promising therapeutic target for TNBC patients in terms of enhancing the benefits of epirubicin treatment.	33747911	RID05025	expression association	chemoresistance		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Prostate cancer	PTTG3P	PTTG1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-146a-3p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000213005	GRCh38_8:66767400-66768005	ENSG00000164611	NA	26255	9232	PTTG3	EAP1|HPTTG|PTTG|securin|TUTR1	The lncRNA PTTG3P promotes the progression of CRPC via upregulating PTTG1.Overexpression of certain long non-coding RNAs (lncRNAs) promotes the progression of castration-resistant prostate cancer (CRPC). The significance and potential role of the lncRNA designated pituitary tumour-transforming 3, pseudogene (PTTG3P) in CRPC is unknown. We detected PTTG3P expression by qPCR. Upregulated PTTG3P expression was performed to explore the role of PTTG3P in PCa cells resistant to ADT (androgen deprivation therapy). The relationship among PTTG3P, mir-146a-3p and PTTG1 were validated by qPCR;western blot and luciferase assay. PTTG3P levels were significantly increased in the androgen-independent PC cell lines, as well as in CRPC tissues compared with those of the androgen-dependent prostate cancer cell line LNCaP and tumour tissues of patients with hormone-naive prostate cancers. Enforced expression of PTTG3P in androgen-deprived LNCaP cells significantly enhanced survival, clonogenicity, and tumorigenicity. Further, PTTG3P acted as a competing endogenous RNA (ceRNA, natural miRNA sponge) to upregulate PTTG1 expression by competing for mir-146a-3p in the progression to CRPC. Our findings suggest that PTTG3P promotes the resistance of prostate cancer cells to androgen-deprivation therapy via upregulating PTTG1. PTTG3P may therefore represent a potential target for therapy of CRPC.	33743960	RID05026	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(NSCLC,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)
Hepatocellular carcinoma	SNHG6	HIF1A	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-6509-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100644	NA	641638	3091	HBII-276HG|NCRNA00058|U87HG	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	LncRNA-SNHG6 promotes the progression of hepatocellular carcinoma by targeting miR-6509-5p and HIF1A.Accumulating evidences have been reported that long noncoding RNAs play crucial roles in the progression of hepatocellular carcinoma (HCC). SnoRNA host gene 6 (SNHG6) is believed to be involved in several human cancers, but the specific molecular mechanism of SNHG6 in HCC is not well studied. In this study, we experimentally down-regulated the SNHG6 in two hepatocellular carcinoma cell lines in vitro, and then measured the proliferation, migration and invasion abilities and the apoptotic levels. Also, we performed the xenograft assay to investigate the function of SNHG6 during the tumor growth in vivo. We found SNHG6 was highly expressed in HCC tissues. Next, using Hep3B and Huh7 cells, we confirmed knockdown of SNHG6 reduced the proliferation, migration and invasion abilities in vitro. Also, by bioinformatics analysis, further molecular and cellular experiments, we found miR-6509-5p bound to SNHG6 directly, and the expression level of HIF1A was regulated through SNHG6/miR-6509-5p axis. Finally, we found that down-regulation of SNHG6 dramatically reduced the tumor growth ability of Huh7 cells in vivo. We concluded that SNHG6/miR-6509-5p/HIF1A axis functioned in the progression of hepatocellular carcinoma, and could be the promising therapeutic targets during the development of hepatocellular carcinoma drugs.	33663502	RID05027	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Urinary bladder cancer	ELNAT1	UBE2I	negatively-E	RNA pull-down assay	upregulation	sequencing	NA	NA	cell metastasis(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	NA	ENSG00000103275	NA	NA	7329	NA	UBC9	SUMOylation promotes extracellular vesicle-mediated transmission of lncRNA ELNAT1 and lymph node metastasis in bladder cancer.Small ubiquitin-like modifier (SUMO) binding (termed SUMOylation) emerged as the inducer for the sorting of bioactive molecules into extracellular vesicles (EVs), triggering lymphangiogenesis and further driving tumor lymph node (LN) metastasis, but the precise mechanisms remain largely unclear. Here, we show that bladder cancer (BCa) cell-secreted EVs mediated intercellular communication with human lymphatic endothelial cells (HLECs) through transmission of the long noncoding RNA ELNAT1 and promoted lymphangiogenesis and LN metastasis in a SUMOylation-dependent manner in both cultured BCa cell lines and mouse models. Mechanistically, ELNAT1 induced UBC9 overexpression to catalyze the SUMOylation of hnRNPA1 at the lysine 113 residue, which mediated recognition of ELNAT1 by the endosomal sorting complex required for transport (ESCRT) and facilitated its packaging into EVs. EV-mediated ELNAT1 was specifically transmitted into HLECs and epigenetically activated SOX18 transcription to induce lymphangiogenesis. Importantly, blocking the SUMOylation of tumor cells by downregulating UBC9 expression markedly reduced lymphatic metastasis in EV-mediated, ELNAT1-treated BCa in vivo. Clinically, EV-mediated ELNAT1 was correlated with LN metastasis and a poor prognosis for patients with BCa. These findings highlight a molecular mechanism whereby the EV-mediated ELNAT1/UBC9/SOX18 regulatory axis promotes lymphangiogenesis and LN metastasis in BCa in a SUMOylation-dependent manner and implicate ELNAT1 as an attractive therapeutic target for LN metastatic BCa.	33661764	RID05028	expression association	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)
Urinary bladder cancer	ELNAT1	SOX18	positively-E	RNA pull-down assay	upregulation	sequencing	NA	NA	cell metastasis(+);cell metastasis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	NA	NA	ENSG00000203883	NA	NA	54345	NA	NA	SUMOylation promotes extracellular vesicle-mediated transmission of lncRNA ELNAT1 and lymph node metastasis in bladder cancer.Small ubiquitin-like modifier (SUMO) binding (termed SUMOylation) emerged as the inducer for the sorting of bioactive molecules into extracellular vesicles (EVs), triggering lymphangiogenesis and further driving tumor lymph node (LN) metastasis, but the precise mechanisms remain largely unclear. Here, we show that bladder cancer (BCa) cell-secreted EVs mediated intercellular communication with human lymphatic endothelial cells (HLECs) through transmission of the long noncoding RNA ELNAT1 and promoted lymphangiogenesis and LN metastasis in a SUMOylation-dependent manner in both cultured BCa cell lines and mouse models. Mechanistically, ELNAT1 induced UBC9 overexpression to catalyze the SUMOylation of hnRNPA1 at the lysine 113 residue, which mediated recognition of ELNAT1 by the endosomal sorting complex required for transport (ESCRT) and facilitated its packaging into EVs. EV-mediated ELNAT1 was specifically transmitted into HLECs and epigenetically activated SOX18 transcription to induce lymphangiogenesis. Importantly, blocking the SUMOylation of tumor cells by downregulating UBC9 expression markedly reduced lymphatic metastasis in EV-mediated, ELNAT1-treated BCa in vivo. Clinically, EV-mediated ELNAT1 was correlated with LN metastasis and a poor prognosis for patients with BCa. These findings highlight a molecular mechanism whereby the EV-mediated ELNAT1/UBC9/SOX18 regulatory axis promotes lymphangiogenesis and LN metastasis in BCa in a SUMOylation-dependent manner and implicate ELNAT1 as an attractive therapeutic target for LN metastatic BCa.	33661764	RID05029	expression association	metastasis,prognosis		
Endometriosis	CCDC80	HOXA10	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-135b)	regulation	NA	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000091986	GRCh38_3:112596797-112649530	ENSG00000253293	NA	151887	3206	CL2|DRO1|LINC01279|SSG1|TCONS_00006930|URB	HOX1|HOX1H	Lnc-RNA LINC01279 induces endometriosis via targeting of HOXA10.To explore the regulatory role and molecular mechanism of lncRNA-LINC01279 in endometriosis (EMs). Between September 2018 and July 2019, 20 EMs patients and 20 healthy subjects were recruited to detect the expression of lncRNA-LINC01279 in EMs and in normal endometrium via qRT-PCR Autograft was used to establish EMs models on Spraque-Dawley (SD) rats, which was followed by taking volume measurements of EMs endometrium and observing pathological changes in the morphology of EMs via hematoxylin and eosin (H&E) staining. The qRT-PCRtechnique was further carried out to determine mRNA expression of lncRNA-LINC01279 and HOXA10 in the serum of EMs rats and LINC01279 shRNA-transfected rats, while the protein expression of HOXA10 was determined using a western blot. EMs patients presented with upregulation of lncRNA-LINC01279 and downregulation of HOXA10 (p<U+2009>< 0.01 or 0.001). Online predictions further revealed that lncRNA-LINC01279 regulated the expression of HOXA10 via miRNA-135b. In EMs models, it was observed that there were a significantly enlarged endometrium and poor pathological morphology, significant upregulation of lncRNA-LINC01279, and downregulation of miR-135b and HOXA10 in serum (p<U+2009>< 0.05, 0.01 or 0.001). In the lncRNA-LINC01279 shRNA group, EMs rats, following treatment, had a sharp decrease in the volume of EMs endometrium, and an improvement in pathological morphology, while lncRNA-LINC01279 was downregulated, with upregulation of miR-135b and HOXA10 (p<U+2009>< 0.05, 0.01 or 0.001). LncRNA-LINC01279, by the mechanism of targeting miR-135b, has the potential to downregulate the expression of HOXA10, and therefore, can promote the development and progression of EMs.	33657670	RID05030	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Acute myeloid leukemia	DANCR	ATG16L1	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-874-3P)	regulation	RNA-protein	Ara-C	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000085978	NA	57291	55054	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	APG16L|ATG16A|ATG16L|FLJ10035|WDR30	Long noncoding RNA DANCR confers cytarabine resistance in acute myeloid leukemia by activating autophagy via the miR-874-3P/ATG16L1 axis.Autophagy is an important mechanism involved in the regulation of acute myeloid leukemia (AML) chemoresistance. The long noncoding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) exhibits oncogenic activity in several types of human cancers, including AML, but it remains unclear whether it regulates autophagy and chemoresistance in AML. We report here that cytarabine (Ara-C) treatment elevates DANCR expression in human AML cells. In addition, DANCR overexpression confers and its knockdown diminishes Ara-C resistance in human AML cells, suggesting that DANCR positively regulates AML chemoresistance to Ara-C. Moreover, DANCR promotes autophagy in Ara-C-treated human AML cells and acts as a sponge to decrease miR-20a-5p expression, thereby upregulating the expression of ATG16L1, a critical component of the autophagy machinery. Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells. Together, this study identifies DANCR as a positive regulator of Ara-C resistance in human AML cells, suggesting this lncRNA as a potential target for overcoming Ara-C resistance in AML chemotherapy.	33638615	RID05031	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Papillary thyroid carcinoma	FAM230B	WNT5A	positively-E	RNA pull-down assay	upregulation	qRT-PCR	TCGA;GEO	NA	cell invasion(+);cell migration(+);cell metastasis(+)	ceRNA(miR-378a-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000215498	GRCh38_22:21167758-21192156	ENSG00000114251	NA	642633	7474	FLJ46366	hWNT5A	LncRNA FAM230B promotes the metastasis of papillary thyroid cancer by sponging the miR-378a-3p/WNT5A axis.Emerging evidence indicates that the dysregulation of long non-coding RNAs (lncRNAs) plays critical roles in the progression of papillary thyroid cancer (PTC). In this study, we found consistently elevated expression levels of the lncRNA FAM230B in PTC tissues, both in newly generated RNA-seq data and in datasets from the GEO and TCGA databases. We demonstrated that the expression of FAM230B can be used for the diagnosis of PTC and is also strongly associated with lymph node metastasis. The potential biological functions of FAM230B and molecular mechanisms by which it regulates PTC progression were investigated. Functionally, FAM230B promoted the migration and invasion of PTC cells in<U+00A0>vitro and in<U+00A0>vivo. Mechanistically, FAM230B sponged miR-378a-3p and showed competitive binding to the 3'-UTR of WNT5A. FAM230B overexpression resulted in elevated WNT5A expression and thereby regulated the epithelial-mesenchymal transition in PTC cells. Finally, we verified that both miR-378a-3p overexpression and WNT5A silencing effectively offset the impacts of FAM230B on PTC cell migration and invasion. In conclusion, our study demonstrated the oncogenic function of the lncRNA FAM230B in PTC cells, providing a novel target for PTC diagnosis and therapy.	33578293	RID05032	ceRNA or sponge	metastasis	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Pancreatic cancer	CCAT1	HMGA1	positively-E	RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);angiogenesis(+)	ceRNA(miR-138-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000247844	NA	ENSG00000137309	NA	100507056	3159	CARLO5|CARLo-5|onco-lncRNA-40	HMGIY	Pancreatic cancer cells-derived exosomal long non-coding RNA CCAT1/microRNA-138-5p/HMGA1 axis promotes tumor angiogenesis.Pancreatic cancer (PC) cells-derived exosomes could mediate angiogenesis of human microvascular endothelial cells (HUVECs) in PC. Considering that, this research was implemented to figure out the concrete role of PC cells-derived exosomal long non-coding RNA colon cancer-associated transcript-1 (CCAT1) in PC with its regulation on microRNA-138-5p/high mobility group A1 (miR-138-5p/HMGA1) axis. PC tissues and normal tissues were resected. PC cells (PANC-1) were interfered with plasmids to change CCAT1 and/or miR-138-5p expression. Exosomes were isolated from PANC-1 cells and co-cultured with HUVECs. The proliferation and apoptosis of PANC-1 and HUVECs were examined. The angiogenic ability of HUVECs was tested in vivo in xenografted tumors and in vitro. CCAT1, miR-138-5p and HMGA1 expression were determined, as well as their interactions. CCAT1 and HMGA1 expression were raised while miR-138-5p expression was reduced in PC. Silencing CCAT1 disrupted cell proliferation and stimulated apoptosis of PANC-1 cells. Knocked down CCAT1 from PANC-1 cells-derived exosomes promoted apoptosis and repressed proliferation of HUVECs. Down-regulated/up-regulated CCAT1 from PANC-1 cells-derived exosomes destroyed/enhanced the angiogenic ability of HUVECs in vivo and in vitro. CCAT1 mediated HMGA1 through competitively binding to miR-138-5p. Overexpression of miR-138-5p antagonized the effects of up-regulated CCAT1 on angiogenesis of HUVECs in vitro. It is informative that PANC-1 cells-derived exosomal CCAT1 strengthens angiogenesis of HUVECs through binding to miR-138-5p to elevate HMGA1 expression.	33872661	RID05033	ceRNA or sponge	NA		DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Inflammatory bowel disease	NEAT1	TNFRSF1B	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	inflammatory response(-)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000028137	NA	283131	7133	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CD120b|p75|TNF-R-II|TNF-R75|TNFBR|TNFR2|TNFR80	LncRNA NEAT1 mediates intestinal inflammation by regulating TNFRSF1B.Inflammatory bowel disease (IBD) is a chronic nonspecific intestinal disease. Our previous work showed that long non-coding RNA (LncRNA) nuclear enriched abundant transcript 1 (NEAT1) plays an important role in IBD. In the current study, we aimed to explore the underlying mechanism by which NEAT1 participates in the development of the disease. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to detect the expression of NEAT1 and tumor necrosis factor superfamily member 1B (TNFRSF1B) in clinical specimens and dextran sulfate sodium (DSS) colitis mice. Inflammatory cell models were established by stimulating human normal intestinal epithelial cell line NCM460 and human colon cancer cell line HT-29 with tumor necrosis factor alpha (TNF-alpha). Expressions of inflammatory cytokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were detected by enzyme-linked immunosorbent assay (ELISA) or RT-qPCR, TNFRSF1B, NF-kB p65 and p-NF-kB p65 followed by the knockdown or overexpression of NEAT1 and TNFRSF1B were analyzed by western blot, and the regulatory effects of NEAT1 on TNFRSF1B were detected by RNA pull-down experiments and RNA-decay assay. The translocation of NF-kB p65 to the nucleus was detected by immunofluorescence. In patients' specimens and DSS colitis mouse models, NEAT1 and TNFRSF1B expression were up-regulated compared with the control group. TNF-alpha stimulation increased NEAT1 and TNFRSF1B expression and activated NF-kB signaling pathway by increasing the translocation of NF-kB p65 to the nucleus. In the presence of TNF-alpha stimulation, NEAT1 knockdown reduces the expression of TNFRSF1B and the translocation of NF-kB p65, thereby relieves cell inflammation. These effects can be reversed by the overexpression of TNFRSF1B.In addition, NEAT1 is involved in inflammatory response by up-regulating the mRNA levels of TNFRSF1B, and knocking down NEAT1 can alleviate inflammation by down-regulating TNFRSF1B. Moreover, NEAT1 co-precipitates TNFRSF1B mRNA in RNA-pull-down assay, and the presence of NEAT1 stabilizes the mRNA of TNFRSF1B. Our results showed that LncRNA NEAT1 promotes NF-kB p65 translocation and mediates intestinal inflammation by regulating TNFRSF1B.	34268386	RID05034	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Oral squamous cell carcinoma	LINC00662	EZH2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-144-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000106462	NA	148189	2146	NA	ENX-1|EZH1|KMT6|KMT6A	LINC00662 Promotes Oral Squamous Cell Carcinoma Cell Growth and Metastasis through miR-144-3p/EZH2 Axis.Long non-coding RNA (lncRNA) is identified as an important regulator involved in oral squamous cell carcinoma (OSCC) tumorigenesis. This study aimed to investigate the functional role and underlying mechanism of LINC00662 in OSCC. The expression levels of LINC00662, miR-144-3p, and enhancer of zeste homolog 2 (EZH2) mRNA were quantified with quantitative real-time polymerase chain reaction in OSCC tissues and cell lines. western blotwas used to assay the expression levels of E-cadherin, Vimentin, and EZH2. Cell proliferation, migration, and invasion were monitored by cell counting kit-8 and Transwell assays. Dual-luciferase reporter and RNA immunoprecipitation assays were employed to verify the regulatory relationship between LINC00662 and miR-144-3p. The expression of LINC00662, positively associated with the increased TNM stage and lymph node metastasis of the patients, was up-regulated in OSCC tissues and cells. The overexpression of LINC00662 facilitated the proliferation, migration, and invasion of OSCC cells. MiR-144-3p could bind to LINC00662, and the promoting effect of LINC00662 overexpression was counteracted by miR-144-3p mimic. Moreover, EZH2 expression was negatively regulated by miR-144-3p and positively regulated by LINC00662. The silencing of EZH2 attenuated the promoting effects of overexpression of LINC00662 on cell proliferation, migration, invasion, and epithelial-mesenchymal transition. LINC00662, as an oncogenic lncRNA of OSCC, accelerates OSCC progression by repressing miR-144-3p expression and increasing EZH2 expression.	34164962	RID05035	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Liver cancer	XIST	ZEB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA XIST promotes liver cancer progression by acting as a molecular sponge of miR-200b-3p to regulate ZEB1/2 expression.To evaluate the predictive value of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) for survival, and determine the involvement of miRNA(miR)-200b-3p and zinc finger E-box-binding homeobox (ZEB) 1/2 in the pro-tumor effect of lncRNA XIST in liver cancer. We evaluated lncRNA XIST expression in liver cancer tissues and cell lines by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and analyzed the correlation between its expression and overall survival of liver cancer patients by Kaplan-Meier analysis. Its effects on cell proliferation, migration, and invasion were analyzed by Cell-Counting Kit-8 and Transwell assays. The association between lncRNA XIST and miR-200b-3p, and the effects of lncRNA XIST on ZEB1/2 expression were explored using luciferase reporter assays, real-time PCR, and western blot. The lncRNA XIST was significantly upregulated in liver cancer, and increased lncRNA XIST expression was associated with a poor prognosis. The lncRNA XIST promoted liver cancer cell proliferation, migration, and invasion  in vitro , and acted as a molecular sponge for miR-200b-3p, and also regulated the expression of ZEB1/2 via miR-200b-3p. The lncRNA XIST is an oncogenic lncRNA that promotes liver cancer metastasis, and its pro-metastatic phenotype can be partially attributed to the lncRNA XIST/miR-200b-3p/ZEB1/2 signaling axis.	34018840	RID05036	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	XIST	ZEB2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169554	NA	7503	9839	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA XIST promotes liver cancer progression by acting as a molecular sponge of miR-200b-3p to regulate ZEB1/2 expression.To evaluate the predictive value of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) for survival, and determine the involvement of miRNA(miR)-200b-3p and zinc finger E-box-binding homeobox (ZEB) 1/2 in the pro-tumor effect of lncRNA XIST in liver cancer. We evaluated lncRNA XIST expression in liver cancer tissues and cell lines by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and analyzed the correlation between its expression and overall survival of liver cancer patients by Kaplan-Meier analysis. Its effects on cell proliferation, migration, and invasion were analyzed by Cell-Counting Kit-8 and Transwell assays. The association between lncRNA XIST and miR-200b-3p, and the effects of lncRNA XIST on ZEB1/2 expression were explored using luciferase reporter assays, real-time PCR, and western blot. The lncRNA XIST was significantly upregulated in liver cancer, and increased lncRNA XIST expression was associated with a poor prognosis. The lncRNA XIST promoted liver cancer cell proliferation, migration, and invasion  in vitro , and acted as a molecular sponge for miR-200b-3p, and also regulated the expression of ZEB1/2 via miR-200b-3p. The lncRNA XIST is an oncogenic lncRNA that promotes liver cancer metastasis, and its pro-metastatic phenotype can be partially attributed to the lncRNA XIST/miR-200b-3p/ZEB1/2 signaling axis.	34018840	RID05037	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Early pregnancy loss	NR026833.1	BMP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+)	NA	regulation	RNA-protein	NA	CSC	NA	Other	Miscarriage	lncRNA	PCG	NA	NA	ENSG00000125845	NA	NA	650	NA	BDA2|BMP2A|SSFSC|SSFSC1	The BMP2 Signaling Axis Promotes Invasive Differentiation of Human Trophoblasts.Embryo implantation and trophoblast invasion are principal limiting factors of pregnancy establishment. Aberrant embryo development or improper trophoblast differentiation and invasion may lead to various unfavorable pregnancy-related outcomes, including early pregnancy loss (EPL). Our clinical data show that the serum BMP2 levels were significantly increased during the first trimester of pregnancy and that the serum and BMP2 expression levels were lower in women with EPL than in women with normal early pregnancies. Moreover, we observed that BMP2 was expressed in oocytes and trophoblast cells of cleaved embryos and blastocysts prior to implantation in both humans and mice. Exogenous BMP2 promoted embryonic development by enhancing blastocyst formation and hatching in mice. LncRNA NR026833.1 was upregulated by BMP2 and promoted SNAIL expression by competitively binding to miR-502-5p. SNAIL induced MMP2 expression and promoted cell invasion in primary extravillous trophoblast cells. BMP2 promotes the invasive differentiation of mouse trophoblast stem cells by downregulating the expression of TS cell marker and upregulating the expression of trophoblast giant cell marker and labyrinthine/spongiotrophoblast marker. Our findings provide significant insights into the regulatory roles of BMP2 in the development of the placenta, which may give us a framework to explore new therapeutic strategies to pregnancy-related complications.	33614644	RID05038	expression association	NA		UP(LIHC);DATA(GSE117623)
Early pregnancy loss	NR026833.1	SNAI1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+)	ceRNA(miR-502-5p)	regulation	NA	NA	CSC	NA	Other	Miscarriage	lncRNA	TF	NA	NA	ENSG00000124216	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The BMP2 Signaling Axis Promotes Invasive Differentiation of Human Trophoblasts.Embryo implantation and trophoblast invasion are principal limiting factors of pregnancy establishment. Aberrant embryo development or improper trophoblast differentiation and invasion may lead to various unfavorable pregnancy-related outcomes, including early pregnancy loss (EPL). Our clinical data show that the serum BMP2 levels were significantly increased during the first trimester of pregnancy and that the serum and BMP2 expression levels were lower in women with EPL than in women with normal early pregnancies. Moreover, we observed that BMP2 was expressed in oocytes and trophoblast cells of cleaved embryos and blastocysts prior to implantation in both humans and mice. Exogenous BMP2 promoted embryonic development by enhancing blastocyst formation and hatching in mice. LncRNA NR026833.1 was upregulated by BMP2 and promoted SNAIL expression by competitively binding to miR-502-5p. SNAIL induced MMP2 expression and promoted cell invasion in primary extravillous trophoblast cells. BMP2 promotes the invasive differentiation of mouse trophoblast stem cells by downregulating the expression of TS cell marker and upregulating the expression of trophoblast giant cell marker and labyrinthine/spongiotrophoblast marker. Our findings provide significant insights into the regulatory roles of BMP2 in the development of the placenta, which may give us a framework to explore new therapeutic strategies to pregnancy-related complications.	33614644	RID05039	ceRNA or sponge	NA		UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	LINC00355	ABCB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);chemoresistance(+)	ceRNA(miR-34b-5p)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000227674	GRCh38_13:63851197-64076044	ENSG00000085563	NA	144766	5243	NA	ABC20|CD243|CLCS|GP170|MDR1|p-170|P-gp|PGY1	Exosomal LINC00355 derived from cancer-associated fibroblasts promotes bladder cancer cell resistance to cisplatin by regulating miR-34b-5p/ABCB1 axis.Cisplatin resistance is a major challenge for bladder cancer (BC). Evidence indicates that exosome derived from cancer-associated fibroblasts (CAF-Exo) can promote chemotherapy resistance in various human tumors by delivering bioactive molecules. We have previously demonstrated that CAF-derived exosomal LINC00355 promotes BC cell proliferation and invasion. However, the underlying mechanisms are still unclear. In this study, we aimed to investigate the role and mechanisms of CAF-derived exosomal LINC00355 in BC cell resistance to cisplatin. Exosomes were isolated from normal fibroblasts (NFs) and BC tumor-derived CAFs, namely, NF-Exo and CAF-Exo. CAFs were transfected with si-Ctrl or si-LINC00355 and then different exosomes were isolated, namely, CAFsi-Ctrl-Exo and CAFsi-LINC00355-Exo. The human BC cell lines (T24 and 5367) were incubated with NF-Exo, CAF-Exo, CAFsi-Ctrl-Exo, and CAFsi-LINC00355-Exo in the presence of cisplatin. MTT proliferation assay and flow cytometric analysis showed that CAF-Exo promoted BC cell resistance to cisplatin and upregulated ABCB1 expression in BC cells by transferring LINC00355 to BC cells. Luciferase activity assay confirmed the interaction between miR-34b-5p and LINC00355 or ABCB1. qRT-PCRand western blotfurther showed that LINC00355 sponged miR-34b-5p to upregulate ABCB1 expression. However, the promoting effects of CAF-Exo on BC cell resistance to cisplatin were abolished by miR-34b-5p overexpression and ABCB1 silencing. In conclusion, exosomal LINC00355 derived from CAFs promotes BC cell resistance to cisplatin by regulating the miR-34b-5p/ABCB1 axis.	33720323	RID05040	ceRNA or sponge	chemoresistance	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Glioblastoma	TP73-AS1	YY1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	NA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000100811	NA	57212	7528	KIAA0495|PDAM	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	TP73-AS1 is induced by YY1 during TMZ treatment and highly expressed in the aging brain.Aging is a factor associated with poor prognosis in glioblastoma (GBM). It is therefore important to understand the molecular features of aging contributing to GBM morbidity.  TP73-AS1  is a long noncoding RNA (lncRNA) over expressed in GBM tumors shown to promote resistance to the chemotherapeutic temozolomide (TMZ), and tumor aggressiveness. How the expression of  TP73-AS1  is regulated is not known, nor is it known if its expression is associated with aging. By analyzing transcriptional data obtained from natural and pathological aging brain, we found that the expression of  TP73-AS1  is high in pathological and naturally aging brains. YY1 physically associates with the promoter of  TP73-AS1  and we found that along with  TP73-AS1 ,  YY1  is induced by TMZ. We found that the  TP73-AS1  promoter is activated by TMZ, and by YY1 over expression. Using CRISPRi to deplete YY1, we found that YY1 promotes up regulation of  TP73-AS1  and the activation of its promoter during TMZ treatment. In addition, we identified two putative YY1 binding sites within the  TP73-AS1  promoter, and used mutagenesis to find that they are essential for TMZ mediated promoter activation. Together, our data positions YY1 as an important  TP73-AS1  regulator, demonstrating that  TP73-AS1  is expressed in the natural and pathological aging brain, including during neurodegeneration and cancer. Our findings advance our understanding of  TP73-AS1  expression, bringing forth a new link between TMZ resistance and aging, both of which contribute to GBM morbidity.	34115613	RID05041	interact with protein	chemoresistance,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Diabetic retinopathy	SNHG16	IRAK1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+);NF-kB signaling pathway(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-146a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000184216	NA	100507246	3654	Nbla10727|Nbla12061|ncRAN	IRAK|pelle	Upregulation of long non-coding RNA SNHG16 promotes diabetes-related RMEC dysfunction via activating NF-kB and PI3K/AKT pathways.Diabetic retinopathy (DR) is a severe diabetes-induced eye disease, in which its pathological phenomena basically include abnormal proliferation, migration, and angiogenesis of microvascular endothelial cells in the retina. Long non-coding RNAs (lncRNAs) have been proven to be important regulators in various biological processes, but their participation in DR remains largely undiscovered. In the present study, we aimed to unveil the role of lncRNA small nucleolar RNA host gene 16 (SNHG16) in regulating the functions of human retinal microvascular endothelial cells (hRMECs) under a high-glucose (HG) condition. We found that SNHG16 expression was significantly upregulated in hRMECs treated with HG. Functionally, SNHG16 could facilitate hRMEC proliferation, migration, and angiogenesis. Moreover, SNHG16 was associated with nuclear factor kB (NF-kB) and phosphatidylinositol 3-kinase (PI3K)/AKT pathways. Mechanistically, SNHG16 could promote hRMEC dysfunction by sequestering microRNA (miR)-146a-5p and miR-7-5p to act as a competing endogenous RNA (ceRNA) with interleukin-1 receptor-associated kinase 1 (IRAK1) and insulin receptor substrate 1 (IRS1). In conclusion, our results illustrated the potential role of SNHG16 in facilitating hRMEC dysfunction under HG treatment, providing a novel approach for DR therapy.	33898104	RID05042	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Osteosarcoma	LOC100129620	CDK6	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+);NF-kB signaling pathway(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-335-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	NA	ENSG00000105810	NA	NA	1021	NA	PLSTIRE	LncRNA LOC100129620 promotes osteosarcoma progression through regulating CDK6 expression, tumor angiogenesis, and macrophage polarization.Osteosarcoma is a malignant tumor with high mortality in children and adolescents. The mechanism of osteosarcoma metastasis is currently unclear. Abnormal expression of long non-coding RNA (lncRNA) plays an important role in tumor metastasis. We used bioinformatics to analyze the differences in gene expression between osteosarcoma  in situ  and osteosarcoma lung metastases. CCK-8 was used to detect the effect of lncRNA LOC100129620 on the proliferation of osteosarcoma cells. The effect of LOC100129620 on the invasion of osteosarcoma cells was assessed by Transwell assay. The regulatory effect of LOC100129620 on miR-335-3p was examined using RNA pull-down and luciferase reporter gene assays. The effect of LOC100129620 on the polarization of macrophages was detected by quantitative real-time fluorescent PCR. The results show that LOC100129620 can promote the proliferation and migration of osteosarcoma cells. LOC100129620 can promote the proliferation of osteosarcoma  in vivo . LOC100129620 can bind to miR-335-3p and regulate its function. MiR-335-3p mediates the regulatory effects of LOC100129620 on CDK6. LOC100129620 promotes the formation of blood vessels and the polarization of macrophages. The LOC100129620/miR-335-3p/CDK6 signaling pathway promotes the metastasis of osteosarcoma by regulating the proliferation of osteosarcoma cells, angiogenesis, and macrophage polarization.	34015762	RID05043	ceRNA or sponge	metastasis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Esophageal cancer	EMSLR	WTAP	positively-E	luciferase reporter assay;TargetScan;PITA;microT_CDS;miRmap;starBase	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-758-3p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000232445	GRCh38_7:101308270-101314800	ENSG00000146457	NA	101927746	9589	EMS	KIAA0105|MGC3925|Mum2	Hypoxia induces chemoresistance of esophageal cancer cells to cisplatin through regulating the lncRNA-EMS/miR-758-3p/WTAP axis.Hypoxia contributes significantly to the development of chemoresistance of many malignancies including esophageal cancer (EC). Accumulating studies have indicated that long non-coding RNAs play important roles in chemotherapy resistance. Here, we identified a novel lncRNA-EMS/miR-758-3p/WTAP axis that was involved in hypoxia-mediated chemoresistance to cisplatin in human EC. Hypoxia induced the expressions of lncRNA EMS and WTAP, and reduced the expression of miR-758-3p in EC cell line ECA-109. In addition, the expressions of EMS and WTAP were required for the hypoxia-induced drug resistance to cisplatin in EC cells, while overexpression of miR-758-3p reversed such chemoresistance. The targeting relationships between EMS and miR-758-3p, as well as miR-758-3p and WTAP, were verified by luciferase-based reporter assays and multiple quantitative assays after gene overexpression/knockdown. Moreover, we found significant correlations between tumor expressions of these molecules. Notably, higher levels of EMS/WTAP, or lower levels of miR-758-3p in tumors predicted worse survivals of EC patients. Furthermore, in a xenograft mouse model, targeted knockdown of EMS and WTAP in ECA-109 cells markedly attenuated the resistance of tumors to cisplatin treatments. Our study uncovers a critical lncRNA-EMS/miR-758-3p/WTAP axis in regulating hypoxia-mediated drug resistance to cisplatin in EC.	34081626	RID05044	ceRNA or sponge	chemoresistance		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Non-small cell lung cancer	NEAT1	ACSL4	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Erastin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000068366	NA	283131	2182	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ACS4|FACL4|LACS4|MRX63|MRX68	Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer.Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays of NEAT1 function were used to determine its roles in cell death (by TUNEL staining) and lipid peroxidation (by malondialdehyde levels). Expression of ferroptosis-related proteins (SLCA11, GPX4, and TFR4) was evaluated by western blot in NSCLC cells treated or not with the ferroptosis inducer erastin. Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone. NEAT1 regulates ferroptosis and ferroptosis sensitivity, with the latter depending on ACSL4, suggesting that targeting NEAT1 or ACSL4 may be a viable therapeutic approach to the treatment of NSCLC.	33730930	RID05045	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	NEAT1	SLC7A11	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Erastin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000151012	NA	283131	23657	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	xCT	Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer.Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays of NEAT1 function were used to determine its roles in cell death (by TUNEL staining) and lipid peroxidation (by malondialdehyde levels). Expression of ferroptosis-related proteins (SLCA11, GPX4, and TFR4) was evaluated by western blot in NSCLC cells treated or not with the ferroptosis inducer erastin. Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone. NEAT1 regulates ferroptosis and ferroptosis sensitivity, with the latter depending on ACSL4, suggesting that targeting NEAT1 or ACSL4 may be a viable therapeutic approach to the treatment of NSCLC.	33730930	RID05046	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	NEAT1	GPX4	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Erastin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000167468	NA	283131	2879	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	MCSP|PHGPx	Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer.Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays of NEAT1 function were used to determine its roles in cell death (by TUNEL staining) and lipid peroxidation (by malondialdehyde levels). Expression of ferroptosis-related proteins (SLCA11, GPX4, and TFR4) was evaluated by western blot in NSCLC cells treated or not with the ferroptosis inducer erastin. Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone. NEAT1 regulates ferroptosis and ferroptosis sensitivity, with the latter depending on ACSL4, suggesting that targeting NEAT1 or ACSL4 may be a viable therapeutic approach to the treatment of NSCLC.	33730930	RID05047	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	NEAT1	TFR4	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-protein	Erastin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer.Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays of NEAT1 function were used to determine its roles in cell death (by TUNEL staining) and lipid peroxidation (by malondialdehyde levels). Expression of ferroptosis-related proteins (SLCA11, GPX4, and TFR4) was evaluated by western blot in NSCLC cells treated or not with the ferroptosis inducer erastin. Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone. NEAT1 regulates ferroptosis and ferroptosis sensitivity, with the latter depending on ACSL4, suggesting that targeting NEAT1 or ACSL4 may be a viable therapeutic approach to the treatment of NSCLC.	33730930	RID05048	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Bacterial meningitis	lncRSPH9-4	MMP3	positively-E	dual-luciferase reporter assay;FISH	upregulation	qRT-PCR	NA	NA	blood-tumor barrier(-)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Bacterial meningitis	lncRNA	PCG	NA	NA	ENSG00000263313	NA	NA	4314	NA	STMY|STMY1	LncRSPH9-4 Facilitates Meningitic Escherichia coli-Caused Blood-Brain Barrier Disruption via miR-17-5p/MMP3 Axis.Brain microvascular endothelial cells (BMECs) constitute the structural and functional basis for the blood-brain barrier (BBB) and play essential roles in bacterial meningitis. Although the BBB integrity regulation has been under extensive investigation, there is little knowledge regarding the roles of long non-coding RNAs (lncRNAs) in this event. The present study aimed to investigate the roles of one potential lncRNA,  lncRSPH9-4 , in meningitic  E. coli  infection of BMECs.  LncRSPH9-4  was cytoplasm located and significantly up-regulated in meningitic  E. coli -infected hBMECs. Electrical cell-substrate impedance sensing (ECIS) measurement and western blot assay demonstrated  lncRSPH9-4  overexpression in hBMECs mediated the BBB integrity disruption. By RNA-sequencing analysis, 639 mRNAs and 299 miRNAs were significantly differentiated in response to lncRSPH9-4 overexpression. We further found  lncRSPH9-4  regulated the permeability in hBMECs by competitively sponging  miR-17-5p , thereby increasing MMP3 expression, which targeted the intercellular tight junctions. Here we reported the infection-induced  lncRSPH9-4  aggravated disruption of the tight junctions in hBMECs, probably through the  miR-17-5p /MMP3 axis. This finding provides new insights into the function of lncRNAs in BBB integrity during meningitic  E. coli  infection and provides the novel nucleic acid targets for future treatment of bacterial meningitis.	34198485	RID05049	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	MALAT1	SRSF1	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-202-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136450	NA	378938	6426	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	CCL21 activation of the MALAT1/SRSF1/mTOR axis underpins the development of gastric carcinoma.As a significant cause of malignancy mortality, gastric carcinoma (GC) has been well documented to be an often-fatal diagnosis. Despite the limitations of effective therapy, immunotherapy has emerged as a promising therapeutic approach capable of killing cancer cells via the immune system. The current study was conducted to investigate the effect of cytokine C-C motif chemokine ligand 21 (CCL21) on GC progression through the metastasis-associated lung adenocarcinoma transcript 1/serine arginine-rich splicing factor 1/mammalian target of rapamycin (MALAT1/SRSF1/mTOR) axis. Bioinformatics analysis was conducted to identify the key genes associated with GC and to subsequently predict their downstream genes. The effect of CCL21, MALAT1, and SRSF1 on the malignant phenotypes and epithelial-mesenchymal transition (EMT) of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo were assessed by expression determination and plasmid transfection. Additionally, RNA pull-down and RNA binding protein immunoprecipitation experiments were performed to determine the MALAT1-microRNA-202-3p (miR-203-3p) interaction and miR-202-3p-SRSF1 interaction followed by the analysis of their effect on the mTOR pathway. CCL21 was identified as a key GC immune gene. Overexpressed CCL21, MALAT1, and SRSF1 along with poorly expressed miR-202-3p were identified in the GC cells. CCL21 induced the MALAT1 expression in a time- and dose-dependent manner. Functionally, MALAT1 targeted miR-202-3p but upregulated SRSF1 and activated mTOR. Crucially, evidence was obtained indicating that CCL21 promoted both the malignant phenotypes and EMT of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo by increasing the MALAT1-induced upregulation of SRSF1. Taken together, the key observations of our study provide evidence that CCL21 enhances the progression of GC via the MALAT1/SRSF1/mTOR axis, providing a novel therapeutic target for the treatment of GC.	34001131	RID05050	ceRNA or sponge	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MALAT1	MTOR	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-202-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198793	NA	378938	2475	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	CCL21 activation of the MALAT1/SRSF1/mTOR axis underpins the development of gastric carcinoma.As a significant cause of malignancy mortality, gastric carcinoma (GC) has been well documented to be an often-fatal diagnosis. Despite the limitations of effective therapy, immunotherapy has emerged as a promising therapeutic approach capable of killing cancer cells via the immune system. The current study was conducted to investigate the effect of cytokine C-C motif chemokine ligand 21 (CCL21) on GC progression through the metastasis-associated lung adenocarcinoma transcript 1/serine arginine-rich splicing factor 1/mammalian target of rapamycin (MALAT1/SRSF1/mTOR) axis. Bioinformatics analysis was conducted to identify the key genes associated with GC and to subsequently predict their downstream genes. The effect of CCL21, MALAT1, and SRSF1 on the malignant phenotypes and epithelial-mesenchymal transition (EMT) of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo were assessed by expression determination and plasmid transfection. Additionally, RNA pull-down and RNA binding protein immunoprecipitation experiments were performed to determine the MALAT1-microRNA-202-3p (miR-203-3p) interaction and miR-202-3p-SRSF1 interaction followed by the analysis of their effect on the mTOR pathway. CCL21 was identified as a key GC immune gene. Overexpressed CCL21, MALAT1, and SRSF1 along with poorly expressed miR-202-3p were identified in the GC cells. CCL21 induced the MALAT1 expression in a time- and dose-dependent manner. Functionally, MALAT1 targeted miR-202-3p but upregulated SRSF1 and activated mTOR. Crucially, evidence was obtained indicating that CCL21 promoted both the malignant phenotypes and EMT of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo by increasing the MALAT1-induced upregulation of SRSF1. Taken together, the key observations of our study provide evidence that CCL21 enhances the progression of GC via the MALAT1/SRSF1/mTOR axis, providing a novel therapeutic target for the treatment of GC.	34001131	RID05051	ceRNA or sponge	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Gastric cancer	MALAT1	CCL21	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-202-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137077	NA	378938	6366	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	6Ckine|CKb9|ECL|exodus-2|SCYA21|SLC|TCA4	CCL21 activation of the MALAT1/SRSF1/mTOR axis underpins the development of gastric carcinoma.As a significant cause of malignancy mortality, gastric carcinoma (GC) has been well documented to be an often-fatal diagnosis. Despite the limitations of effective therapy, immunotherapy has emerged as a promising therapeutic approach capable of killing cancer cells via the immune system. The current study was conducted to investigate the effect of cytokine C-C motif chemokine ligand 21 (CCL21) on GC progression through the metastasis-associated lung adenocarcinoma transcript 1/serine arginine-rich splicing factor 1/mammalian target of rapamycin (MALAT1/SRSF1/mTOR) axis. Bioinformatics analysis was conducted to identify the key genes associated with GC and to subsequently predict their downstream genes. The effect of CCL21, MALAT1, and SRSF1 on the malignant phenotypes and epithelial-mesenchymal transition (EMT) of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo were assessed by expression determination and plasmid transfection. Additionally, RNA pull-down and RNA binding protein immunoprecipitation experiments were performed to determine the MALAT1-microRNA-202-3p (miR-203-3p) interaction and miR-202-3p-SRSF1 interaction followed by the analysis of their effect on the mTOR pathway. CCL21 was identified as a key GC immune gene. Overexpressed CCL21, MALAT1, and SRSF1 along with poorly expressed miR-202-3p were identified in the GC cells. CCL21 induced the MALAT1 expression in a time- and dose-dependent manner. Functionally, MALAT1 targeted miR-202-3p but upregulated SRSF1 and activated mTOR. Crucially, evidence was obtained indicating that CCL21 promoted both the malignant phenotypes and EMT of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo by increasing the MALAT1-induced upregulation of SRSF1. Taken together, the key observations of our study provide evidence that CCL21 enhances the progression of GC via the MALAT1/SRSF1/mTOR axis, providing a novel therapeutic target for the treatment of GC.	34001131	RID05052	ceRNA or sponge	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Laryngeal squamous cell carcinoma	MNX1-AS1	BCL9	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(+);angiogenesis(+);beta-catenin signaling pathway(+);cell growth(+)	ceRNA(miR-744-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000116128	NA	645249	607	CCAT5|LOC645249|MAYA	NA	LncRNA MNX1-AS1 Contributes to Laryngeal Squamous Cell Carcinoma Growth and Migration by Regulating mir-744-5p/bcl9/beta-Catenin Axis.Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the progression of laryngeal squamous cell carcinoma (LSCC). Here, we aimed to disclose the role of MNX1-AS1 in LSCC progression, and explore whether MNX1-AS1 participates in LSCC progression via targeting miR-744-5p to active BCL9/beta-catenin signaling. Sixty-five human LSCC tissues and the paracancerous normal tissues were recruited to determine the levels of MNX1-AS1, miR-744-5p and BCL9 using qRT-PCR The interaction of miR-744-5p and MNX1-AS1/BCL9 was determined by using the RNA immunoprecipitation (RIP) assay and/or luciferase gene reporter assay. Cell viability,  in vivo  tumor formation, invasion and migration abilities were detected by MTT, Xenograft models and Transwell assays. MNX1-AS1 level was increased significantly in human LSCC tissues as compared with the normal tissues, which showed a positive correlation with BCL9 level while a negative correlation with miR-744-5p level. High level of MNX1-AS1 predicted a poor prognosis and an advanced clinical process in LSCC patients. miR-744-5p targeted upregulation weakened the luciferase activity of MNX1-AS1 and /BCL9, and downregulated their expression levels-wt, while showed no effect when the binding sites were mutated. Knockdown of MNX1-AS1 markedly weakened cell viability, migration, and invasion abilities, while BCL9 overexpression abolished these tendencies. In addition, MNX1-AS1 downregulation induced decreases in tumor volumes and weights  in vivo , accompanied by reductions in BCL9, Ki-67 and beta-catenin expression and an increase in miR-744-5p expression. Collectively, this study reveals that MNX1-AS1 contributes to cell growth and migration by regulating miR-744-5p/BCL9/beta-catenin axis in LSCC.	33821684	RID05053	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Aids	GAS5	MIR21	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	regulation	RNA-RNA	NA	NA	NA	Disease by infectious agent	Viral infectious disease	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	406991	NCRNA00030|SNHG2	hsa-mir-21|MIR-21|MIRN21	Long Non-coding RNA GAS5 Regulates T Cell Functions via miR21-Mediated Signaling in People Living With HIV.T cells are critical for the control of viral infections and T cell responses are regulated by a dynamic network of non-coding RNAs, including microRNAs (miR) and long non-coding RNAs (lncRNA). Here we show that an activation-induced decline of lncRNA growth arrest-specific transcript 5 (GAS5) activates DNA damage response (DDR), and regulates cellular functions and apoptosis in CD4 T cells derived from people living with HIV (PLHIV) via upregulation of miR-21. Notably, GAS5-miR21-mediated DDR and T cell dysfunction are observed in PLHIV on antiretroviral therapy (ART), who often exhibit immune activation due to low-grade inflammation despite robust virologic control. We found that GAS5 negatively regulates miR-21 expression, which in turn controls critical signaling pathways involved in DNA damage and cellular response. The sustained stimulation of T cells decreased GAS5, increased miR-21 and, as a result, caused dysfunction and apoptosis in CD4 T cells. Importantly, this inflammation-driven T cell over-activation and aberrant apoptosis in ART-controlled PLHIV and healthy subjects (HS) could be reversed by antagonizing the GAS5-miR-21 axis. Also, mutation of the miR-21 binding site on exon 4 of GAS5 gene to generate a GAS5 mutant abolished its ability to regulate miR-21 expression as well as T cell activation and apoptosis markers compared to the wild-type GAS5 transcript. Our data suggest that GAS5 regulates TCR-mediated activation and apoptosis in CD4 T cells during HIV infection through miR-21-mediated signaling. However, GAS5 effects on T cell exhaustion during HIV infection may be mediated by a mechanism beyond the GAS5-miR-21-mediated signaling. These results indicate that targeting the GAS5-miR-21 axis may improve activity and longevity of CD4 T cells in ART-treated PLHIV. This approach may also be useful for targeting other infectious or inflammatory diseases associated with T cell over-activation, exhaustion, and premature immune aging.	33776993	RID05054	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Psoriasis	NORAD	CDC6	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000094804	NA	647979	990	LINC00657	CDC18L	LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation.Psoriasis is a chronic, inflammatory skin disease. It was reported that lncRNA Non-coding RNA-activated by DNA damage (NORAD) has potential regulatory effects on skin diseases. Our previous studies found that lncRNA NORAD was highly expressed and its potential target miR-26a was down-regulated in psoriasis model mice. Here, we aimed to investigate the role of NORAD in the development of psoriasis. IL-22/LPS (interleukin-22/lipopolysaccharide)-stimulated HaCaT (human immortalized keratinocytes) cell model and imiquimod-induced mouse model were established. Keratin 6 (K6), Keratin 16 (K16), Keratin 17 (K17), and Cell division cycle 6 (CDC6) levels were detected by western blot. Cell activity was detected by CCK-8, MTT, and EdU assays. Quantitative real-time PCR was performed to examine the levels of NORAD, miR-26a, CDC6, K6, K16, and K17. Haematoxylin-eosin staining was applied to observe the degree of skin thickening and hyperplasia. Fluorescence  in situ  hybridization detects the location of NORAD. RNA immunoprecipitation, RNA pull-down, and Luciferase test were performed to detect the interaction between NORAD and miR-26a. In IL-22/LPS-stimulated HaCaT cells, NORAD, CDC6, and keratinocyte proliferation-related proteins (K6, K16, and K17) were up-regulated and miR-26a was down-regulated. Cell survival and proliferation were also increased. However, the results were reversed after interference with NORAD. Also,  in<U+00A0>vitro  experiments revealed that NORAD negatively regulated miR-26a. In IL-22/LPS-stimulated HaCaT cells and skin of imiquimod-induced mice, we found that lower NORAD resulted in an increase of miR-26a and a decrease of CDC6, further decreased levels of keratinocyte proliferation-related proteins (K6, K16, and K17).	33759666	RID05055	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Psoriasis	NORAD	K6	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation.Psoriasis is a chronic, inflammatory skin disease. It was reported that lncRNA Non-coding RNA-activated by DNA damage (NORAD) has potential regulatory effects on skin diseases. Our previous studies found that lncRNA NORAD was highly expressed and its potential target miR-26a was down-regulated in psoriasis model mice. Here, we aimed to investigate the role of NORAD in the development of psoriasis. IL-22/LPS (interleukin-22/lipopolysaccharide)-stimulated HaCaT (human immortalized keratinocytes) cell model and imiquimod-induced mouse model were established. Keratin 6 (K6), Keratin 16 (K16), Keratin 17 (K17), and Cell division cycle 6 (CDC6) levels were detected by western blot. Cell activity was detected by CCK-8, MTT, and EdU assays. Quantitative real-time PCR was performed to examine the levels of NORAD, miR-26a, CDC6, K6, K16, and K17. Haematoxylin-eosin staining was applied to observe the degree of skin thickening and hyperplasia. Fluorescence  in situ  hybridization detects the location of NORAD. RNA immunoprecipitation, RNA pull-down, and Luciferase test were performed to detect the interaction between NORAD and miR-26a. In IL-22/LPS-stimulated HaCaT cells, NORAD, CDC6, and keratinocyte proliferation-related proteins (K6, K16, and K17) were up-regulated and miR-26a was down-regulated. Cell survival and proliferation were also increased. However, the results were reversed after interference with NORAD. Also,  in<U+00A0>vitro  experiments revealed that NORAD negatively regulated miR-26a. In IL-22/LPS-stimulated HaCaT cells and skin of imiquimod-induced mice, we found that lower NORAD resulted in an increase of miR-26a and a decrease of CDC6, further decreased levels of keratinocyte proliferation-related proteins (K6, K16, and K17).	33759666	RID05056	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Psoriasis	NORAD	KRT7	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000135480	NA	647979	3855	LINC00657	CK7|K2C7|K7|SCL	LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation.Psoriasis is a chronic, inflammatory skin disease. It was reported that lncRNA Non-coding RNA-activated by DNA damage (NORAD) has potential regulatory effects on skin diseases. Our previous studies found that lncRNA NORAD was highly expressed and its potential target miR-26a was down-regulated in psoriasis model mice. Here, we aimed to investigate the role of NORAD in the development of psoriasis. IL-22/LPS (interleukin-22/lipopolysaccharide)-stimulated HaCaT (human immortalized keratinocytes) cell model and imiquimod-induced mouse model were established. Keratin 6 (K6), Keratin 16 (K16), Keratin 17 (K17), and Cell division cycle 6 (CDC6) levels were detected by western blot. Cell activity was detected by CCK-8, MTT, and EdU assays. Quantitative real-time PCR was performed to examine the levels of NORAD, miR-26a, CDC6, K6, K16, and K17. Haematoxylin-eosin staining was applied to observe the degree of skin thickening and hyperplasia. Fluorescence  in situ  hybridization detects the location of NORAD. RNA immunoprecipitation, RNA pull-down, and Luciferase test were performed to detect the interaction between NORAD and miR-26a. In IL-22/LPS-stimulated HaCaT cells, NORAD, CDC6, and keratinocyte proliferation-related proteins (K6, K16, and K17) were up-regulated and miR-26a was down-regulated. Cell survival and proliferation were also increased. However, the results were reversed after interference with NORAD. Also,  in<U+00A0>vitro  experiments revealed that NORAD negatively regulated miR-26a. In IL-22/LPS-stimulated HaCaT cells and skin of imiquimod-induced mice, we found that lower NORAD resulted in an increase of miR-26a and a decrease of CDC6, further decreased levels of keratinocyte proliferation-related proteins (K6, K16, and K17).	33759666	RID05057	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807,GSE75367)
Psoriasis	NORAD	K17	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000128422	NA	647979	NA	LINC00657	NA	LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation.Psoriasis is a chronic, inflammatory skin disease. It was reported that lncRNA Non-coding RNA-activated by DNA damage (NORAD) has potential regulatory effects on skin diseases. Our previous studies found that lncRNA NORAD was highly expressed and its potential target miR-26a was down-regulated in psoriasis model mice. Here, we aimed to investigate the role of NORAD in the development of psoriasis. IL-22/LPS (interleukin-22/lipopolysaccharide)-stimulated HaCaT (human immortalized keratinocytes) cell model and imiquimod-induced mouse model were established. Keratin 6 (K6), Keratin 16 (K16), Keratin 17 (K17), and Cell division cycle 6 (CDC6) levels were detected by western blot. Cell activity was detected by CCK-8, MTT, and EdU assays. Quantitative real-time PCR was performed to examine the levels of NORAD, miR-26a, CDC6, K6, K16, and K17. Haematoxylin-eosin staining was applied to observe the degree of skin thickening and hyperplasia. Fluorescence  in situ  hybridization detects the location of NORAD. RNA immunoprecipitation, RNA pull-down, and Luciferase test were performed to detect the interaction between NORAD and miR-26a. In IL-22/LPS-stimulated HaCaT cells, NORAD, CDC6, and keratinocyte proliferation-related proteins (K6, K16, and K17) were up-regulated and miR-26a was down-regulated. Cell survival and proliferation were also increased. However, the results were reversed after interference with NORAD. Also,  in<U+00A0>vitro  experiments revealed that NORAD negatively regulated miR-26a. In IL-22/LPS-stimulated HaCaT cells and skin of imiquimod-induced mice, we found that lower NORAD resulted in an increase of miR-26a and a decrease of CDC6, further decreased levels of keratinocyte proliferation-related proteins (K6, K16, and K17).	33759666	RID05058	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Lipid metabolic disorder	NEAT1	AGPS	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	lipid homeostasis(-)	ceRNA(miR-372-3p)	regulation	RNA-protein	Rapamycin	NA	NA	Disease of metabolism	Lipid metabolism disorder	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000018510	NA	283131	8540	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ADAP-S|ADAS|ADHAPS|ADPS|ALDHPSY	NEAT1/hsa-miR-372-3p axis participates in rapamycin-induced lipid metabolic disorder.Rapamycin is a crucial immunosuppressive regimen for patients that have undergone liver transplantation (LT). However, one of the major side effects of rapamycin include metabolic disorders such as dyslipidemia, and the mechanism remains unknown. This study aims to explore the biomolecules that are responsible for rapamycin-induced dyslipidemia and the control strategies that can reverse the lipid metabolism disorder. In this study, data collected from LT patients, cell and mouse models treated with rapamycin were analyzed. Results showed an increase of triglycerides (TGs) induced by rapamycin. MicroRNAs (miRNAs) play important roles in many vital biological processes including TG metabolism. hsa-miR-372-3p was filtered using RNA sequencing and identified as a key regulator in rapamycin-induced TGs accumulation. Using bioinformatics and experimental analyses, target genes of hsa-miR-372-3p were predicted. These genes were alkylglycerone phosphate synthase (AGPS) and apolipoprotein C4 (APOC4), which are reported to be involved in TG metabolism. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was also identified as an upstream regulatory factor of hsa-miR-372-3p. From the results of this study, NEAT1/hsa-miR-372-3p/AGPS/APOC4 axis plays a vital role in rapamycin-disruption of lipid homeostasis. Therefore, targeting this axis is a potential therapeutic target combating rapamycin-induced dyslipidemia after LT.	33705959	RID05059	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Lipid metabolic disorder	NEAT1	APOC4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	lipid homeostasis(-)	ceRNA(miR-372-3p)	regulation	RNA-protein	Rapamycin	NA	NA	Disease of metabolism	Lipid metabolism disorder	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000267467	NA	283131	346	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1/hsa-miR-372-3p axis participates in rapamycin-induced lipid metabolic disorder.Rapamycin is a crucial immunosuppressive regimen for patients that have undergone liver transplantation (LT). However, one of the major side effects of rapamycin include metabolic disorders such as dyslipidemia, and the mechanism remains unknown. This study aims to explore the biomolecules that are responsible for rapamycin-induced dyslipidemia and the control strategies that can reverse the lipid metabolism disorder. In this study, data collected from LT patients, cell and mouse models treated with rapamycin were analyzed. Results showed an increase of triglycerides (TGs) induced by rapamycin. MicroRNAs (miRNAs) play important roles in many vital biological processes including TG metabolism. hsa-miR-372-3p was filtered using RNA sequencing and identified as a key regulator in rapamycin-induced TGs accumulation. Using bioinformatics and experimental analyses, target genes of hsa-miR-372-3p were predicted. These genes were alkylglycerone phosphate synthase (AGPS) and apolipoprotein C4 (APOC4), which are reported to be involved in TG metabolism. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was also identified as an upstream regulatory factor of hsa-miR-372-3p. From the results of this study, NEAT1/hsa-miR-372-3p/AGPS/APOC4 axis plays a vital role in rapamycin-disruption of lipid homeostasis. Therefore, targeting this axis is a potential therapeutic target combating rapamycin-induced dyslipidemia after LT.	33705959	RID05060	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Pancreatic ductal adenocarcinoma	CERS6-AS1	FGFR1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-15a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000227617	GRCh38_2:168771951-168786961	ENSG00000077782	NA	100861402	2260	NA	BFGFR|CD331|CEK|FLG|FLT2|H2|H3|H4|H5|KAL2|N-SAM	Long non-coding RNA CERS6-AS1 facilitates the oncogenicity of pancreatic ductal adenocarcinoma by regulating the microRNA-15a-5p/FGFR1 axis.The long non-coding RNA CERS6 antisense RNA 1 (CERS6-AS1) has critical regulatory roles in breast cancer progression. Here, we determined CERS6-AS1 expression in pancreatic ductal adenocarcinoma (PDAC) and the roles of CERS6-AS1 in PDAC carcinogenesis. The mechanisms underlying the regulatory actions of CERS6-AS1 in PDAC cells were elucidated in detail. CERS6-AS1 expression was evidently increased in PDAC tissues and cell lines. Patients with PDAC having high CERS6-AS1 expression had shorter overall survival periods than those having low CERS6-AS1 expression. Functionally, the knockdown of CERS6-AS1 attenuated the proliferation, migration, and invasion and stimulated apoptosis of PDAC cells  in vitro . Additionally, CERS6-AS1 depletion decreased PDAC tumor growth  in vivo.  Mechanistically, CERS6-AS1 could competitively bind to microRNA-15a-5p (miR-15a-5p) and effectively work as a molecular sponge in PDAC cells, resulting in the upregulation of fibroblast growth factor receptor 1 (FGFR1), a direct target of miR-15a-5p. Rescue experiments revealed that miR-15a-5p downregulation or FGFR1 restoration rescued the effects of CERS6-AS1 knockdown on the behaviors of PDAC cells. In conclusion, CERS6-AS1 promoted the oncogenicity of PDAC by serving as a competing endogenous RNA to sequester miR-15a-5p and increase FGFR1 expression, which highlights the potential of the CERS6-AS1/miR-15a-5p/FGFR1 pathway as an effective target for cancer therapy.	33581689	RID05061	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Periodontal disease	PWAR6	BMP2	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-106a-5p)	regulation	RNA-protein	NA	CSC	NA	Gastrointestinal system disease	Periodontal disease	lncRNA	PCG	ENSG00000257151	NA	ENSG00000125845	NA	100506965	650	HBT8|PAR-6	BMP2A	PWAR6 interacts with miR-106a-5p to regulate the osteogenic differentiation of human periodontal ligament stem cells.Human periodontal ligament stem cells (hPDLSCs) associated with bone regeneration serve an important role in the treatment of periodontal disease. Long non-coding RNAs are involved in the osteogenesis of multiple stem cells and can act as a sponge of microRNAs (miRs). The present study aimed to investigate the interaction between Prader Willi/Angelman region RNA 6 (PWAR6) and miR-106a-5p, as well as their influences on the osteogenic differentiation of hPDLSCs. hPDLSCs were isolated and cultured in osteogenic medium (OM) or growth medium (GM) for 7 days prior to transfection with PWAR6 overexpression vector, short hairpin RNA PWAR6 or miR-106a-5p mimic. The expression levels of runt-related transcription factor 2, osteocalcin and bone morphogenetic protein 2 (BMP2) were detected by western blot and reverse transcription-quantitative PCR (RT-qPCR), and the expression levels of PWAR6, miR-106a-5p and alkaline phosphatase (ALP) were determined by RT-qPCR. ALP activity assays and Alizarin red staining were performed to detect osteogenesis and mineralization, respectively. Luciferase activities of wild-type and mutant PWAR6 and BMP2 were assessed by conducting a dual-luciferase reporter assay. The results indicated that PWAR6 expression was upregulated in OM-incubated hPDLSCs compared with GM-incubated hPDLSCs, and PWAR6 overexpression increased the osteogenic differentiation and mineralization of hPDLSCs compared with the corresponding control group. By contrast, miR-106a-5p expression was downregulated in OM-incubated hPDLSCs compared with GM-incubated hPDLSCs. PWAR6 acted as a sponge of miR-106a-5p and PWAR6 overexpression promoted the osteogenesis of miR-106a-5p mimic-transfected hPDLSCs. BMP2 was predicted as a target gene of miR-106a-5p. Collectively, the results indicated that PWAR6 displayed a positive influence on the osteogenic differentiation of hPDLSCs. The results of the present study demonstrated that the PWAR6/miR-106a-5p interaction network may serve as a potential regulatory mechanism underlying hPDLSCs osteogenesis.	33576453	RID05062	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	UP(LIHC);DATA(GSE117623)
Neuroblastoma	MIAT	MYCN	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000134323	NA	440823	4613	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	bHLHe37|MYCNOT|N-myc|NMYC	MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines.Neuroblastoma (NBL) is the most common extracranial childhood malignant tumor and represents a major cause of cancer-related deaths in infants.  NMYC  amplification or overexpression is associated with the malignant behavior of NBL tumors. In the present study, we revealed an association between long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) and  NMYC  amplification in NBL cell lines and MIAT expression in NBL tissue samples. MIAT silencing induces cell death only in cells with  NMYC  amplification, but in NBL cells without  NMYC  amplification it decreases only the proliferation. MIAT downregulation markedly reduces the NMYC expression in  NMYC -amplified NBL cell lines and c-Myc expression in  NMYC  non-amplified NBL cell lines, but the ectopic overexpression or downregulation of NMYC did not affect the expression of MIAT. Moreover, MIAT downregulation results in decreased ornithine decarboxylase 1 (ODC1), a known transcriptional target of  MYC  oncogenes, and decreases the glycolytic metabolism and respiratory function. These results indicate that MIAT is an upstream regulator of NMYC and that MIAT/NMYC axis disruption induces cell death in  NMYC -amplified NBL cell lines. These findings reveal a novel mechanism for the regulation of NMYC in NBL, suggesting that MIAT might be a potential therapeutic target, especially for those with  NMYC  amplification.	33806217	RID05063	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Neuroblastoma	MIAT	ODC1	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000115758	NA	440823	4953	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ODC	MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines.Neuroblastoma (NBL) is the most common extracranial childhood malignant tumor and represents a major cause of cancer-related deaths in infants.  NMYC  amplification or overexpression is associated with the malignant behavior of NBL tumors. In the present study, we revealed an association between long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) and  NMYC  amplification in NBL cell lines and MIAT expression in NBL tissue samples. MIAT silencing induces cell death only in cells with  NMYC  amplification, but in NBL cells without  NMYC  amplification it decreases only the proliferation. MIAT downregulation markedly reduces the NMYC expression in  NMYC -amplified NBL cell lines and c-Myc expression in  NMYC  non-amplified NBL cell lines, but the ectopic overexpression or downregulation of NMYC did not affect the expression of MIAT. Moreover, MIAT downregulation results in decreased ornithine decarboxylase 1 (ODC1), a known transcriptional target of  MYC  oncogenes, and decreases the glycolytic metabolism and respiratory function. These results indicate that MIAT is an upstream regulator of NMYC and that MIAT/NMYC axis disruption induces cell death in  NMYC -amplified NBL cell lines. These findings reveal a novel mechanism for the regulation of NMYC in NBL, suggesting that MIAT might be a potential therapeutic target, especially for those with  NMYC  amplification.	33806217	RID05064	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE86978)
Neuroblastoma	MIAT	MYC	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000136997	NA	440823	4609	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	bHLHe39|c-Myc|MYCC	MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines.Neuroblastoma (NBL) is the most common extracranial childhood malignant tumor and represents a major cause of cancer-related deaths in infants.  NMYC  amplification or overexpression is associated with the malignant behavior of NBL tumors. In the present study, we revealed an association between long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) and  NMYC  amplification in NBL cell lines and MIAT expression in NBL tissue samples. MIAT silencing induces cell death only in cells with  NMYC  amplification, but in NBL cells without  NMYC  amplification it decreases only the proliferation. MIAT downregulation markedly reduces the NMYC expression in  NMYC -amplified NBL cell lines and c-Myc expression in  NMYC  non-amplified NBL cell lines, but the ectopic overexpression or downregulation of NMYC did not affect the expression of MIAT. Moreover, MIAT downregulation results in decreased ornithine decarboxylase 1 (ODC1), a known transcriptional target of  MYC  oncogenes, and decreases the glycolytic metabolism and respiratory function. These results indicate that MIAT is an upstream regulator of NMYC and that MIAT/NMYC axis disruption induces cell death in  NMYC -amplified NBL cell lines. These findings reveal a novel mechanism for the regulation of NMYC in NBL, suggesting that MIAT might be a potential therapeutic target, especially for those with  NMYC  amplification.	33806217	RID05065	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	MALAT1	ST8SIA4	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell migration(+);angiogenesis(+)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000113532	NA	378938	7903	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PST|PST1|SIAT8D	lncRNA MALAT1/miR-26a/26b/ST8SIA4 axis mediates cell invasion and migration in breast cancer cell lines.Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA that is overexpressed in various human cancers, including breast cancer. Evidence has associated the function of the alpha-2,8-sialyltransferase (ST8SIA) family with breast cancer. The present study aimed to investigate the potential roles of MALAT1 in breast cancer development and progression using analyses of both breast cancer tissues and cell lines. The mRNA levels of MALAT1, microRNA (miR)-26a/26b and ST8SIA4 were detected by reverse transcription-quantitative PCR (RT-qPCR) and the protein level of ST8SIA4 was assessed by western blot Cell proliferation, invasion and migration were detected by CCK-8, wound healing and Transwell assays, respectively. Interactions between MALAT1 and miR-26a/26b were assessed using fluorescence in situ hybridization, RNA immunoprecipitation and luciferase reporter assays. Herein, different levels of MALAT1 were primarily observed in human breast cancer samples and cells. Upregulated MALAT1 was a crucial predictor of poor breast cancer prognosis. Altered MALAT1 modulated cell progression in breast cancer. Moreover, miR-26a/26b was confirmed as a direct regulator of MALAT1, and ST8SIA4 was predicted as a target of miR-26a/26b. Functional analysis in human breast cancer cell lines demonstrated that MALAT1 modulated breast cancer cell tumorigenicity by acting as a competing endogenous lncRNA (ceRNA) to regulate ST8SIA4 levels by sponging miR-26a/26b. The identification of the MALAT1/miR-26a/26b/ST8SIA4 axis which contributes to breast cancer progression may constitute a potential new therapeutic target.	34278507	RID05066	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	MALAT1	ST8SIA4	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell migration(+);angiogenesis(+)	ceRNA(miR-26b)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000113532	NA	378938	7903	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PST|PST1|SIAT8D	lncRNA MALAT1/miR-26a/26b/ST8SIA4 axis mediates cell invasion and migration in breast cancer cell lines.Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA that is overexpressed in various human cancers, including breast cancer. Evidence has associated the function of the alpha-2,8-sialyltransferase (ST8SIA) family with breast cancer. The present study aimed to investigate the potential roles of MALAT1 in breast cancer development and progression using analyses of both breast cancer tissues and cell lines. The mRNA levels of MALAT1, microRNA (miR)-26a/26b and ST8SIA4 were detected by reverse transcription-quantitative PCR (RT-qPCR) and the protein level of ST8SIA4 was assessed by western blot Cell proliferation, invasion and migration were detected by CCK-8, wound healing and Transwell assays, respectively. Interactions between MALAT1 and miR-26a/26b were assessed using fluorescence in situ hybridization, RNA immunoprecipitation and luciferase reporter assays. Herein, different levels of MALAT1 were primarily observed in human breast cancer samples and cells. Upregulated MALAT1 was a crucial predictor of poor breast cancer prognosis. Altered MALAT1 modulated cell progression in breast cancer. Moreover, miR-26a/26b was confirmed as a direct regulator of MALAT1, and ST8SIA4 was predicted as a target of miR-26a/26b. Functional analysis in human breast cancer cell lines demonstrated that MALAT1 modulated breast cancer cell tumorigenicity by acting as a competing endogenous lncRNA (ceRNA) to regulate ST8SIA4 levels by sponging miR-26a/26b. The identification of the MALAT1/miR-26a/26b/ST8SIA4 axis which contributes to breast cancer progression may constitute a potential new therapeutic target.	34278507	RID05067	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00958	NUDT19	positively-E	StarBase	upregulation		TCGA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000213965	NA	100506305	390916	NA	RP2	LncRNA LINC00958 Activates mTORC1/P70S6K Signalling Pathway to Promote Epithelial-Mesenchymal Transition Process in the Hepatocellular Carcinoma;The LINC00958 was up-regulated in HCC tissues and cell lines;The analysis of TCGA and StarBase showed that NUDT19 was a direct target of LINC00958 and was positively regulated by LINC00958;LINC00958 silencing inhibited the proliferation, migration, and EMT process of HCC via inhibiting NUDT19 mediated mTORC1/P70S6K signalling pathway	33979257	RID05068	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Pneumonia	NEAT1	MIR146B	negatively-F	Starbase;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000202569	NA	283131	574447	LINC00084|NCRNA00084|TncRNA|VINC	MIRN146B|miRNA146B|mir-146b	LncRNA NEAT1 Regulates Infantile Pneumonia by Sponging miR-146b;The lncRNA NEAT1 and miR-146b expression levels were detected by qPCR in both groups;Starbase predicted the binding site between lncRNA NEAT1 and miR-146b, and the targeted relationship between them was detected by dual luciferase reporter gene;the relative expression of miR-146b in serum of infantile pneumonia decreased, and over-expressing it could promote LPS-induced cell viability and reduce apoptosis;Knocking down lncRNA NEAT1 promotes cell growth and reduces apoptosis in LPS-induced HFL1 cells	33978942	RID05069	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Atherosclerosis	TUG1	RUNX2	negatively-F	hTFtarget database;shRNA	upregulation	microarray	GEO	NA	cell proliferation(-);cell migration(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124813	NA	55000	860	FLJ20618|LINC00080|NCRNA00080	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis;microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples;TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs);TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs;TUG1 bound to Runt-related transcription factor 2 (Runx2);TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration	33971184	RID05070	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	TUG1	ANPEP	positively-E	hTFtarget database;shRNA	upregulation	microarray	GEO	NA	cell proliferation(-);cell migration(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000166825	NA	55000	290	FLJ20618|LINC00080|NCRNA00080	CD13|gp150|LAP1|p150|PEPN	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis;microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples;TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs);TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs;TUG1 bound to Runt-related transcription factor 2 (Runx2);TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration;Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration	33971184	RID05071	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	SAMD12-AS1	DNMT1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000281641	GRCh38_8:118620498-118906155	ENSG00000130816	NA	552860	1786	C8orf26|NCRNA00252	CXXC9|DNMT|MCMT	LncRNA SAMD12-AS1 promotes the progression of gastric cancer via DNMT1/p53 axis;qRT-PCRwas performed to analyze the expression of lncRNA SAMD12-AS1 in GC tissues and cell lines;SAMD12-AS1 was highly up-regulated in human gastric cancer tissues and cell lines compared to their normal counterparts;Binding of RNA and proteins were detected via RNA binding protein immunoprecipitation (RIP) assay;SAMD12-AS1 was also found to promote the oncogenic role of GC cells via inhibiting the P53 signaling pathway;SAMD12-AS1 might performed its biological roles in GC via directly interacting with DNMT1 and facilitating DNMT1 repress the P53 signaling pathway	33962804	RID05072	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Diffuse large b-cell lymphoma	LINC00908	miR-671-5p	negatively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	miRNA	ENSG00000263812	NA	NA	NA	284276	NA	ASRPS	NA	LINC00908 Promotes Diffuse Large B-Cell Lymphoma Development by Down-Regulating miR-671-5p;LINC00908 and miR-671-5p expression were evaluated in DLBCL tissues and cell lines using RT-qPCR;The physical interaction between LINC00908 and miR-671-5p was confirmed using bioinformatics analysis and a dual luciferase assay, RIP and RNA pull down;The expression of LINC00908 was markedly up-regulated in diffuse large B-cell lymphoma tissues and cell lines, and the decreased expression of LINC00908 significantly inhibited diffuse large B-cell lymphoma cell proliferation and invasion;we revealed that LINC00908 directly interacted with miR-671-5p, which was down-regulated in diffuse large B-cell lymphoma cells and highly expressed with LINC00908 knockdown	33958893	RID05073	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Hepatocellular carcinoma	lnc-LYZ-2	FUBP1	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000162613	NA	NA	8880	NA	FBP|FUBP|hDH V	Differentially Expressed Long Noncoding RNAs Involved in FUBP1 Promoting Hepatocellular Carcinoma Cells Proliferation;Coexpression analysis of dysregulated lncRNAs-mRNAs network showed that lnc-LYZ-2 was the lncRNA most relevant to FUBP1. Inhibition of lnc-LYZ-2 could significantly relieve the proproliferation effect of FUBP1 on HCC cells, suggesting that lnc-LYZ-2 was partially involved in proproliferation regulation of FUBP1;The expression of target genes was detected by quantitative reverse transcription-PCR (RT-PCR and western blot assays.	33954195	RID05074	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Osteosarcoma	MIR205HG	TWIST2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+)	ceRNA(miR-2114-3p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000233608	NA	642587	117581	LINC00510	bHLHa39|Dermo-1|DERMO1	MIR205 host gene (MIR205HG) drives osteosarcoma metastasis via regulating the microRNA 2114-3p (miR-2114-3p)/twist family bHLH transcription factor 2 (TWIST2) axis;we found that MIR205 host gene (MIR205HG) was significantly elevated in human OS tissues, especially in metastatic OS tissues;The vast majority of MIR205HG was situated in the cytosol, and served as a competing endogenous RNA (ceRNA) that directly bound to microRNA 2114-3p (miR-2114-3p), resulting in increased twist family bHLH transcription factor 2 (TWIST2) level;the attenuated cell invasion caused by MIR205HG knockdown was effectively rescued by miR-2114-3p silencing or TWIST2 overexpression;The levels of MIR205HG in OS and normal tissues were tested by qRT-PCR MIR205HG was shown to be evidently elevated in OS as compared to normal tissues;RNA pull-down assay showed that only miR-2114-3p was significantly enriched by MIR205HG probe in both HOS and MG63 cells (Figure 3(b)). Consistently, miR-2114-3p probe could also pull down endogenous MIR205HG, but this effect disappeared by mutated probe;overexpression of miR-2114-3p substantially reduced the luciferase activity of wild-type MIR205HG vector, while had no effect on the mutant one; Luciferase reporter assay results showed that miR-2114-3p overexpression significantly weakened the luciferase activity of wild-type TWIST2 3`-UTR vector, but this effect was blocked by mutant vector	33949284	RID05075	ceRNA or sponge	metastasis		
Endometriosis	AFAP1-AS1	STAT3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000168610	NA	84740	6774	AFAP1-AS|AFAP1AS|MGC10981	APRF	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-beta/Smad signaling via miR-424-5p;Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR and western blot;Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3);AFAP1-AS1 activated the STAT3/transforming growth factor-beta1 (TGF-beta1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression	33949053	RID05076	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Myocardial injury	SNHG1	XIAP	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-)	ceRNA(miR-181a-5p)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000101966	NA	23642	331	LINC00057|lncRNA16|NCRNA00057|UHG	API3|BIRC4|hILP|ILP-1	Long Non-Coding RNA Small Nucleolar RNA Host Gene 1 Alleviates Sepsis-Associated Myocardial Injury by Modulating the miR-181a-5p/XIAP Axis in vitro;A quantitative real-time polymerase chain reaction was executed to determine the expression of SNHG1 and microRNA (miR)-181a-5p;The targeted interrelations among SNHG1, miR-181a-5p, and X-linked inhibitor of apoptosis protein (XIAP) were verified by dual-luciferase reporter assay;Relative protein expression of XIAP was detected by western blot;SNHG1 and XIAP were down-regulated, and miR-181a-5p was up-regulated in LPS-induced H9c2 cells;Overexpression of SNHG1 or inhibition of miR-181a-5p facilitated cell viability and repressed inflammation and oxidative stress in LPS-treated H9c2 cells;MiR-181a-5p was a target of and negatively regulated by SNHG1;At the same time, XIAP was a target gene of and inversely modulated by miR-181a-5p;XIAP was positively regulated by SNHG1	33941563	RID05077	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	OIP5-AS1	MTDH	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000147649	NA	729082	92140	cyrano|linc-OIP5	3D3|AEG-1|LYRIC	Long noncoding RNA OIP5-AS1 exhibits oncogenic activity in bladder cancer through miR-217 and MTDH;OIP5-AS1, miR-217 and MTDH expressions in BCa tissues and cells were detected by qRT-PCRor Western;OIP5-AS1 was upregulated in BCa tissues and cells, and OIP5-AS1 knockdown could inhibit the proliferation and invasion of BCa cells. MiR-217 was a direct-acting target of OIP5-AS1, and MTDH was a target of miR-217. OIP5-AS1 knockdown inhibits human BCa cell proliferation and invasion through miR-217/MTDH axis;The correlation between OIP5-AS1 and miR-217, miR-217 and MTDH, and OIP5-AS1 and MTDH were studied by Luciferase reporter assay and Spearman correlation analysis	33928606	RID05078	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Hepatocellular carcinoma	SNHG9	GSTP1	negatively-E	RIP;luciferase reporter assay;CHIP	upregulation	RT-qPCR	GSE19915;GSE13507;GSE3167;TCGA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255198	GRCh38_16:1964899-1965509	ENSG00000084207	NA	735301	2950	DKFZp686N06141|NCRNA00062	FAEES3|GST3|GSTP	lncRNA SNHG9 Promotes Cell Proliferation, Migration, and Invasion in Human Hepatocellular Carcinoma Cells by Increasing GSTP1 Methylation, as Revealed by CRISPR-dCas9; Histological data analysis, CRISPR-dCas9, and cytological function experiment were used to study the expression level and biological function of SNHG9 in HCC. There was an upregulated expression of SNHG9 in HCC;Knockdown of SNHG9 can inhibit cell proliferation, block cell cycle progression, and inhibit cell migration and invasion by upregulating GSTP1;LncRNA SNHG9 recruits methylated enzymes (DNMT1, DNMT3A, and DNMT3B) to increase GSTP1 promoter methylation, a common event in the development of HCC	33898523	RID05079	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE86978)
Colorectal cancer	LINC00665	PAK2	positively-E	starBase;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-126-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000180370	NA	100506930	5062	CIP2A-BP	PAK65|PAKgamma	Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p;LINC00665 was significantly upregulated in CRC;Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3;We then evaluated the levels of LINC00665 expression in CRC tumor tissues via qPCR, which showed significant upregulation of this lincRNA specifically in CRC samples	33878735	RID05080	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	LINC00665	FZD3	positively-E	starBase;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-126-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000104290	NA	100506930	7976	CIP2A-BP	NA	Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p;LINC00665 was significantly upregulated in CRC;Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3;We then evaluated the levels of LINC00665 expression in CRC tumor tissues via qPCR, which showed significant upregulation of this lincRNA specifically in CRC samples	33878735	RID05081	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Non-small cell lung cancer	LINC00473	miR-497-5p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223414	NA	NA	NA	90632	NA	C6orf176|LNC473|bA142J11.1	NA	lncRNA LINC00473 promotes proliferation, migration, invasion and inhibition of apoptosis of non-small cell lung cancer cells by acting as a sponge of miR-497-5p;Reverse transcription-quantitative PCR was conducted to detect the level of LINC00473 and miR-497-5p;RNA immunoprecipitation and a luciferase reporter assay were performed to verify the regulatory relationship between lncRNA-LINC00473 and miR-497-5p;LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression	33868467	RID05082	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Lung adenocarcinoma	PD-L1-lnc	MYC	positively-F	shRNA;siRNA	upregulation	qRT-PCR;sequencing	NA	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	PD-L1 lncRNA splice isoform promotes lung adenocarcinoma progression via enhancing c-Myc activity;Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFN-Gamma;Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity;Employing qRT-PCR Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1	33849634	RID05083	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Laryngeal carcinoma	LINC01303	TIMP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell metastasis(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-200c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000250548	GRCh38_14:61556273-61570653	ENSG00000035862	NA	101927780	7077	NA	CSC-21K	LINC01303 promotes the proliferation and migration of laryngeal carcinoma by regulating miR-200c/TIMP2 axis;Real-time quantitative PCR (qRT-PCR was applied for the determination of LINC01303, miR-200c and TIMP metallopeptidase inhibitor 2 (TIMP2) expression in LSCC tissues and cell lines;The interaction between LINC01303 and miR-200c was analyzed with bioinformatics analysis and luciferase activity analysis;LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues;LINC01303 plays a carcinogenic part in LSCC carcinogenesis through regulating miR-200c/TIMP2 axis, which may become a promising target of LSCC therapy;High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration	33841686	RID05084	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	TRERNA1	NRAS	positively-E	RNA-seq;RIP;bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+);chemoresistance(+);cell proliferation(+)	ceRNA(miR-22-3p)	regulation	RNA-protein	Sorafenib	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000213281	NA	100887755	4893	LINC00651|ncRNA-a7|treRNA	N-ras	TRERNA1 upregulation mediated by HBx promotes sorafenib resistance and cell proliferation in HCC via targeting NRAS by sponging miR-22-3p;RNA sequencing (RNA-seq) analysis indicated that NRAS proto-oncogene (NRAS) is a potential target of TRERNA1 that mediates aspects of hepatocellular carcinogenesis. TRERNA1 acts as a ceRNA to regulate NRAS expression by sponging microRNA (miR)-22-3p;Via co-expression network analysis of upregulated lncRNAs and mRNAs, 6 relevant lncRNAs were identified as candidates for further validation using quantitative reverse-transcriptase PCR (qRT-PCR. TRERNA1 was considered a potential candidate because of its relatively high expression level after transfection with HBx;we performed bioinformatics analysis, which predicted that miR-22-3p harbors a common target binding site for both TRERNA1 and the NRAS 30UTR (Figures 5H and 5I). miRNAs degrade their binding targets in a manner dependent on Ago2, the core component of the RNA-induced silencing complex.27We performed an anti-Ago2 RNA immunoprecipitation (RIP) assay to confirm this effect of miRNAs.	33839325	RID05085	ceRNA or sponge	chemoresistance		UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Hepatocellular carcinoma	HBX	TRERNA1	positively-E	RNA-seq	upregulation	qRT-PCR	NA	NA	cancer progression(+);chemoresistance(+);cell proliferation(+);prognosis(+)	NA	association	protein-RNA	Sorafenib	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	NA	NA	ENSG00000231265	GRCh38_20:50040716-50041504	NA	100887755	NA	LINC00651|ncRNA-a7|treRNA	TRERNA1 upregulation mediated by HBx promotes sorafenib resistance and cell proliferation in HCC via targeting NRAS by sponging miR-22-3p;In this study, we found that translation regulatory lncRNA 1 (TRERNA1) upregulation by HBx not only promoted HCC cell proliferation by regulating the cell cycle in vitro and in vivo but also correlated positively with poor prognosis in HCC	33839325	RID05086	expression association	prognosis,chemoresistance		
Ewing's sarcoma	TUG1	MSI2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-199a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Sarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000153944	NA	55000	124540	FLJ20618|LINC00080|NCRNA00080	NA	LncRNA TUG1 promotes Ewing's sarcoma cell proliferation, migration, and invasion via the miR-199a-3p-MSI2 signaling pathway;RT-qPCR was used to detect the expression of TUG1, microRNA-199a-3p (miR-199a-3p), and musashi2 (MSI2) in Ewing's sarcoma tissues and cell lines;The interaction between TUG1/MSI2 and miR-199a-3p was validated by the dual-luciferase reporter assay;The levels of TUG1 and MSI2 were increased, while the level of miR-199a-3p was decreased in Ewing's sarcoma tissues and cells;TUG1 functioned as a competing endogenous RNA to regulate MSI2 expression by sponging miR-199a-3p	33780263	RID05087	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Pulmonary hypertension	CEBPB	HAS2-AS1	positively-E	JASPAR;luciferase reporter assay;ChIP;western blot	upregulation	qRT-PCR;microarray	GEO	NA	cell proliferation(+);cell migration(+);inflammatory response(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	TF	lncRNA	ENSG00000172216	NA	ENSG00000248690	GRCh38_8:121639293-121994185	1051	594842	C/EBP-beta|IL6DBP|NF-IL6|TCF5	HAS2-AS|HAS2AS|HASNT|NCRNA00077	The Transcription Factor C/EBPbeta Promotes HFL-1 Cell Migration, Proliferation, and Inflammation by Activating lncRNA HAS2-AS1 in Hypoxia;The upstream transcription factor of HAS2-AS1 was predicted by JASPAR website, and the binding site between C/EBPbeta and HAS2-AS1 was predicted by JASPAR, too. In order to verify the association between C/EBPbeta and the HAS2 promoter region, we used chromatin immunoprecipitation (ChIP) and dual luciferase reporter gene detection, western blot to detect the expression of inflammation-related proteins, and qRT-PCRto detect the expression of HAS2-AS1 and HAS2;Idiopathic pulmonary fibrosis (IPF) with HPH patient microarray data was downloaded from the GEO database and analyzed by R software. Our study showed that HAS2-AS1 and C/EBPbeta were highly expressed in hypoxic HFL-1 cells, and the knockdown of HAS2-AS1 expression could inhibit the proliferation, migration, and inflammatory response of HFL-1 cells;C/EBPbeta binds to the promoter region of HAS2-AS1 and has a positive regulation effect on the transcription of HAS2-AS1;This study suggested that C/EBPbeta could upregulate HAS2-AS1 expression and induce HFL-1 cell proliferation, migration, and inflammation response	33777961	RID05088	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Malignant glioma	LINC01116	MDM2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-744-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000135679	NA	375295	4193	TALNEC2	HDM2|MGC5370	LINC01116 promotes the proliferation and invasion of glioma by regulating the microRNA-744-5p-MDM2-p53 axis;The expression of LINC01116 and microRNA (miR)-744-5p in glioma tissues and cells was detected by reverse transcription quantitative PCR;A dual luciferase reporter system was used to locate common binding sites between miR-744-5p and LINC01116 or the 3' untranslated region of E3 ubiquitin protein ligase Mdm2 (MDM2);RNA immunoprecipitation was used to determine the interactions between RNAs and proteins;LINC01116 was found to be highly expressed in glioma tissues, which was associated with a malignant phenotype. LINC01116 promoted the proliferation and invasiveness of glioma cells, and inhibited the p53 pathway by preserving the expression of MDM2 mRNA via miR-744-5p sponging	33760190	RID05089	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Pneumonia	GAS5	TIMP3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-);inflammatory response(+)	ceRNA(miR-222-3p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000100234	NA	60674	7078	NCRNA00030|SNHG2	SFD	Long non-coding RNA GAS5 protects against Mycoplasma pneumoniae pneumonia by regulating the microRNA-222-3p/TIMP3 axis;The expression of GAS5, microRNA 222 3p, (miR-222-3p) and tissue inhibitor of metalloproteinases 3 (TIMP3) in MPP was investigated using reverse transcription quantitative PCR;A dual-luciferase reporter assay assessed the associations among GAS5, miR-222-3p and TIMP3;The expression of GAS5 and TIMP3 was downregulated in MPP;GAS5 directly interacted with miR-222-3p. TIMP3 was a target of miR-222-3p;GAS5 overexpression increased the viability and decreased the inflammation of LAMP induced THP 1 cells by regulating the miR 222 3p/TIMP3 axis	33760178	RID05090	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	DQ786243	WNT3A	positively-E	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	ceRNA(miR-15p-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000154342	NA	NA	89780	NA	NA	lncRNA DQ786243 promotes hepatocellular carcinoma cell invasion and proliferation by regulating the miR-15p-5p/Wnt3A axis; lncDQ, miR-15p-5p and Wnt3A expression levels were characterized in HCC and portal vein tumor thrombus tissue samples and for liver cancer and liver cancer cell lines using reverse transcription quantitative PCR;Bioinformatics software was used for the analysis of interactions between lncDQ and miR-15p-5p, miR-15p-5p and Wnt3A. Luciferase assays confirmed the binding relationships between miR 15b 5p and the 3' untranslated region (UTR) of Wnt3A;lncDQ was able to bind with miR-15b-5p and served as a competing endogenous RNA. As the target gene of miR-15b-5p, Wnt3A was correlated with poor prognoses for patients with HCC;lncDQ and Wnt3A expression were significantly increased in HCC tissues	33760109	RID05091	ceRNA or sponge	prognosis		UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	NORAD	PEAK1	positively-E	luciferase reporter assay;bioinformatics;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+);ERK signaling pathway(+)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000173517	NA	647979	79834	LINC00657	KIAA2002|sgk269	LncRNA NORAD, sponging miR-363-3p, promotes invasion and EMT by upregulating PEAK1 and activating the ERK signaling pathway in NSCLC cells;We found that lncRNA NORAD was highly expressed in human NSCLC tissues and cell lines;Then bioinformatics analysis was used to screen for candidate miRNA bound with lncRNA NORAD and the target gene of miRNA in NSCLC. The luciferase reporter gene assay and RNA pull-down assay were used to verify the relationship;the expression levels of NORAD in clin ical tissue specimens and different NSCLC cell lines were determined by RT-qPCR	33742335	RID05092	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE67980,GSE111842,GSE51827,GSE55807,GSE86978)
Colon adenocarcinoma	ILF3-DT	CAMK1D	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-619-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000183049	NA	147727	57118	ILF3-AS1	CKLiK	LncRNA ILF3-AS1 Promotes the Progression of Colon Adenocarcinoma Cells Through the miR-619-5p/CAMK1D Axis;In the present study, we investigated the expression of ILF3-AS1 in COAD cell lines, human normal colon epithelial cell line, patient tumor tissues and adjacent normal tissues by real-time quantitative PCR (RT-qPCR);The direct binding of ILF3-AS1 and miR-619-5p/CAMK1D was validated by the luciferase reporter assay;The results showed that the expression of ILF3-AS1 was significantly higher in COAD tissue than in normal adjacent samples, and this conclusion was confirmed in the available public datasets;After further exploring the mechanisms, we found that ILF3-AS1 serves as a competitive endogenous RNA of mir-619-5p. It can bind to mir-619-5p and reduce its expression, thus regulating the target gene CAMK1D	33737811	RID05093	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Lung cancer	UNC5B-AS1	miR-218-5p	negatively-F	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000237512	GRCh38_10:71217220-71218294	NA	NA	728978	NA	UASR1	NA	Effects of LncRNA UNC5B-AS1 on adhesion, invasion and migration of lung cancer cells and its mechanism;Real-time quantitative PCR (qRT-PCR was used to detect the expressions of UNC5B-AS1 in human bronchial epithelial cells HBE and different lung cancer cells of A549, H1437, H1975, H1299 and H460;The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells ( P <0.05);qRT-PCRand dual-luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression;lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT	33719270	RID05094	ceRNA or sponge	NA		
Lung cancer	UNC5B-AS1	CDH1	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237512	GRCh38_10:71217220-71218294	ENSG00000039068	NA	728978	999	UASR1	CD324|UVO|uvomorulin	Effects of LncRNA UNC5B-AS1 on adhesion, invasion and migration of lung cancer cells and its mechanism;Real-time quantitative PCR (qRT-PCR was used to detect the expressions of UNC5B-AS1 in human bronchial epithelial cells HBE and different lung cancer cells of A549, H1437, H1975, H1299 and H460;The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells ( P <0.05);qRT-PCRand dual-luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression;lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT	33719270	RID05095	expression association	NA		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Lung cancer	UNC5B-AS1	VIM	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237512	GRCh38_10:71217220-71218294	ENSG00000026025	NA	728978	7431	UASR1	NA	Effects of LncRNA UNC5B-AS1 on adhesion, invasion and migration of lung cancer cells and its mechanism;Real-time quantitative PCR (qRT-PCR was used to detect the expressions of UNC5B-AS1 in human bronchial epithelial cells HBE and different lung cancer cells of A549, H1437, H1975, H1299 and H460;The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells ( P <0.05);qRT-PCRand dual-luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression;lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT	33719270	RID05096	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Lung cancer	UNC5B-AS1	TWIST1	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000237512	GRCh38_10:71217220-71218294	ENSG00000122691	NA	728978	7291	UASR1	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Effects of LncRNA UNC5B-AS1 on adhesion, invasion and migration of lung cancer cells and its mechanism;Real-time quantitative PCR (qRT-PCR was used to detect the expressions of UNC5B-AS1 in human bronchial epithelial cells HBE and different lung cancer cells of A549, H1437, H1975, H1299 and H460;The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells ( P <0.05);qRT-PCRand dual-luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression;lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT	33719270	RID05097	expression association	NA		UP(SKCM);DATA(GSE38495)
Ovarian cancer	FOXD2-AS1	MIR4492	negatively-F	miRDB database;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000264211	NA	84793	100616376	NA	mir-4492	Long non-coding RNA FOXD2-AS1 promotes proliferation, migration and invasion of ovarian cancer cells via regulating the expression of miR-4492;The expression of lncRNA FOXD2-AS1 and miR-4492 was detected by reverse transcription-quantitative PCR;The mutual binding site of lncRNA FOXD2-AS1 and miR-4492 was predicted with the miRDB database and verified by a luciferase reporter assay;The results suggested that lncRNA FOXD2-AS1 was upregulated in ovarian cancer tissues and cell lines	33717250	RID05098	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Brain injury	NKILA	NLRX1	positively-E	RNA22;luciferase reporter assay;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell injury(-)	ceRNA(miR-195)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000160703	NA	105416157	79671	NA	CLR11.3|NOD9	Long noncoding RNA NKILA transferred by astrocyte-derived extracellular vesicles protects against neuronal injury by upregulating NLRX1 through binding to mir-195 in traumatic brain injury;It was revealed that NKILA was downregulated in injured neurons;NKILA could competitively bind to miR-195 that directly targeted NLRX1. Next, the upregulation of NLRX1 or NKILA relived neuronal injury by promoting neuronal proliferation but inhibiting apoptosis;the reverse transcription-quantitative polymerase chain reaction (RT-qPCR) results confirmed that NKILA expression was downregulated in injured neurons;the RNA22 website predicted binding sites between NKILA and miR-195 (Figure 3C). Dual-luciferase reporter gene assay further validated that when compared with the treatment of vector, the luciferase activity of miR-195-wild type (WT) was inhibited by the treatment of oe-NKILA;RNA pull-down displayed that compared with the treatment of Bio-probe NC, the enrichment of miR-195 remained unchanged following the treatment of Bio-MUT-NKILA	33686956	RID05099	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Colorectal cancer	MCM3AP-AS1	SENP1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000079387	NA	114044	29843	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	NA	Long noncoding RNA MCM3AP-AS1 enhances cell proliferation and metastasis in colorectal cancer by regulating miR-193a-5p/SENP1;The expression of MCM3AP-AS1 was detected by quantitative reverse transcription PCR (RT-qPCR) in CRC tissues and matched noncancerous tissues (NCTs);The binding relationship between MCM3AP-AS1, miR-193a-5p and sentrin-specific peptidase 1 (SENP1) were screened and identified by databases, RT-qPCR, dual-luciferase reporter assay and western blot; we got that the expression of MCM3AP-AS1 was higher in CRC tissues than in paired NCTs, and increased MCM3AP-AS1 expression was associated with adverse outcomes in CRC patients	33686713	RID05100	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Hepatocellular carcinoma	BACE1-AS	CELF1	positively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-377-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000278768	GRCh38_11:117288453-117293578	ENSG00000149187	NA	100379571	10658	BACE1-AS1|BACE1AS|FJ573250|NCRNA00177	BRUNOL2|CUG-BP|CUGBP|CUGBP1|EDEN-BP|hNab50|NAB50|NAPOR	LncRNA BACE1-AS enhances the invasive and metastatic capacity of hepatocellular carcinoma cells through mediating miR-377-3p/CELF1 axis;qRT-PCRconfirmed the abnormal BACE1-AS level in HCC tissues and cells;Databases prediction suggested that miR-377-3p might be a modulatory target of BACE1-AS and luciferase assay confirmed this hypothesis;This study found that BACE1-AS was overexpressed in HCC tissues and cell lines;MiR-377-3p was negatively modulated by BACE1-AS in HCC tumor tissues and cells;CELF1 was identified as a downstream regulator of miR-377-3p and served as an oncogene in HCC cells	33667514	RID05101	ceRNA or sponge	metastasis	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Vitreoretinopathy	TCF4	ERLR	positively-E	ChIP	upregulation	microarray;RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Nervous system disease	Retinal disease	TF	lncRNA	ENSG00000196628	NA	NA	NA	6925	NA	bHLHb19|E2-2|ITF2|SEF2-1B	NA	Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy;we found that ERLR is upregulated in RPE cells stimulated with transforming growth factor (TGF)-beta1 as detected by lncRNA microarray and RT-PCRMechanistically, chromatin immunoprecipitation (ChIP) assays indicated that the transcription factor TCF4 directly binds to the promoter region of ERLR and promotes its transcription	33664479	RID05102	interact with protein	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)	
Vitreoretinopathy	ERLR	MYH9	positively-E		upregulation	microarray;RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Nervous system disease	Retinal disease	lncRNA	PCG	NA	NA	ENSG00000100345	NA	NA	4627	NA	DFNA17|EPSTS|FTNS|MHA|NMHC-II-A|NMMHCA	Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy;we found that ERLR is upregulated in RPE cells stimulated with transforming growth factor (TGF)-beta1 as detected by lncRNA microarray and RT-PCRMechanistically, chromatin immunoprecipitation (ChIP) assays indicated that the transcription factor TCF4 directly binds to the promoter region of ERLR and promotes its transcription;ERLR mediates EMT by directly binding to MYH9 protein and increasing its stability	33664479	RID05103	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Skin squamous cell carcinoma	H19	miR-675	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Roles of the H19/microRNA-675 axis in the proliferation and epithelial-mesenchymal transition of human cutaneous squamous cell carcinoma cells;The mRNA expression levels of H19 and miR-675 were analyzed using reverse transcription quantitative PCR, and Cell Counting Kit 8, wound healing and Transwell assays were performed to analyze the cell proliferation, migration and invasion of cSCC cells, respectively;a dual-luciferase reporter assay was performed to determine the interactions between H19, miR-675 and p53;The results of the present study revealed that the expression levels of H19 and miR 675 were upregulated in cSCC tissues and cSCC cell lines;The knockdown of H19 or miR 675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis;The overexpression of H19 upregulated the expression levels of its predicted target, miR 675, which subsequently promoted the EMT process and downregulated the expression levels of p53	33649811	RID05104	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Skin squamous cell carcinoma	H19	TP53	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LFS1|p53	Roles of the H19/microRNA-675 axis in the proliferation and epithelial-mesenchymal transition of human cutaneous squamous cell carcinoma cells;The mRNA expression levels of H19 and miR-675 were analyzed using reverse transcription quantitative PCR, and Cell Counting Kit 8, wound healing and Transwell assays were performed to analyze the cell proliferation, migration and invasion of cSCC cells, respectively;a dual-luciferase reporter assay was performed to determine the interactions between H19, miR-675 and p53;The results of the present study revealed that the expression levels of H19 and miR 675 were upregulated in cSCC tissues and cSCC cell lines;The knockdown of H19 or miR 675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis;The overexpression of H19 upregulated the expression levels of its predicted target, miR 675, which subsequently promoted the EMT process and downregulated the expression levels of p53	33649811	RID05105	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Recurrent miscarriage	LNC-HZ01	MXD1	positively-E	PROMO;MeRIP; RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Recurrent miscarriage	lncRNA	TF	NA	NA	ENSG00000059728	NA	NA	4084	NA	BHLHC58|MAD|MAD1	Lnc-HZ01 with m6A RNA methylation inhibits human trophoblast cell proliferation and induces miscarriage by up-regulating BPDE-activated lnc-HZ01/MXD1 positive feedback loop;In this work, we identified a novel lncRNA HZ01 (lnc-HZ01) that is up-regulated in both RM tissues and BPDE-exposed trophoblast cells;Mechanistically, lnc-HZ01 promotes MXD1 mRNA transcription by up-regulating its transcription factor c-JUN and also enhances MXD1 protein stability by up-regulating its deubiquitin enzyme USP36;RT-qPCR analysis showed that lnc-HZ01 was significantly up-regulated in the RM tissues relative to those in the HC tissues;Using PROMO software, c-JUN was predicted to bind with the promoter sequence of MXD1	33647641	RID05106	epigenetic regulation	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Recurrent miscarriage	LNC-HZ01	JUN	positively-F	PROMO;MeRIP; RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Recurrent miscarriage	lncRNA	TF	NA	NA	ENSG00000177606	NA	NA	3725	NA	AP-1|AP1|c-Jun|cJUN|p39	Lnc-HZ01 with m6A RNA methylation inhibits human trophoblast cell proliferation and induces miscarriage by up-regulating BPDE-activated lnc-HZ01/MXD1 positive feedback loop;In this work, we identified a novel lncRNA HZ01 (lnc-HZ01) that is up-regulated in both RM tissues and BPDE-exposed trophoblast cells;Mechanistically, lnc-HZ01 promotes MXD1 mRNA transcription by up-regulating its transcription factor c-JUN and also enhances MXD1 protein stability by up-regulating its deubiquitin enzyme USP36;RT-qPCR analysis showed that lnc-HZ01 was significantly up-regulated in the RM tissues relative to those in the HC tissues;Using PROMO software, c-JUN was predicted to bind with the promoter sequence of MXD1	33647641	RID05107	expression association	NA		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)
Recurrent miscarriage	LNC-HZ01	USP36	positively-F	PROMO;MeRIP; RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Recurrent miscarriage	lncRNA	PCG	NA	NA	ENSG00000055483	NA	NA	57602	NA	DUB1	Lnc-HZ01 with m6A RNA methylation inhibits human trophoblast cell proliferation and induces miscarriage by up-regulating BPDE-activated lnc-HZ01/MXD1 positive feedback loop;In this work, we identified a novel lncRNA HZ01 (lnc-HZ01) that is up-regulated in both RM tissues and BPDE-exposed trophoblast cells;Mechanistically, lnc-HZ01 promotes MXD1 mRNA transcription by up-regulating its transcription factor c-JUN and also enhances MXD1 protein stability by up-regulating its deubiquitin enzyme USP36;RT-qPCR analysis showed that lnc-HZ01 was significantly up-regulated in the RM tissues relative to those in the HC tissues;Using PROMO software, c-JUN was predicted to bind with the promoter sequence of MXD1	33647641	RID05108	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE75367)
Recurrent miscarriage	MXD1	LNC-HZ01	positively-E	PROMO;MeRIP; RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Recurrent miscarriage	TF	lncRNA	ENSG00000059728	NA	NA	NA	4084	NA	BHLHC58|MAD|MAD1	NA	Lnc-HZ01 with m6A RNA methylation inhibits human trophoblast cell proliferation and induces miscarriage by up-regulating BPDE-activated lnc-HZ01/MXD1 positive feedback loop;In this work, we identified a novel lncRNA HZ01 (lnc-HZ01) that is up-regulated in both RM tissues and BPDE-exposed trophoblast cells;Mechanistically, lnc-HZ01 promotes MXD1 mRNA transcription by up-regulating its transcription factor c-JUN and also enhances MXD1 protein stability by up-regulating its deubiquitin enzyme USP36;RT-qPCR analysis showed that lnc-HZ01 was significantly up-regulated in the RM tissues relative to those in the HC tissues;Using PROMO software, c-JUN was predicted to bind with the promoter sequence of MXD1	33647641	RID05109	epigenetic regulation	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Polycystic ovary syndrome	LINC00477	miR-128	negatively-F	luciferase reporter assay;bioinformatics;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(-);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	miRNA	ENSG00000197503	GRCh38_12:24566964-24584168	NA	NA	144360	NA	C12orf67|FAM191B|FLJ32894	NA	The LINC00477/miR-128 axis promotes the progression of polycystic ovary syndrome by regulating ovarian granulosa cell proliferation and apoptosis;qRT-PCRanalysis was performed to examine the expression pattern of LINC00477 in serum samples of PCOS patients as well as PCOS animal models;The correlation between LINC00477 and miR-128 was verified by bioinformatics analysis and dual-luciferase reporter and RNA pull-down assays;LINC00477 was significantly upregulated in the serum of PCOS patients as well as PCOS mouse models; LINC00477 may function as a ceRNA to inhibit proliferation and apoptosis of granulosa cells by modulating miR-128 expression	33622342	RID05110	ceRNA or sponge	NA		
Lung adenocarcinoma	SLC2A1-DT	miR-508-5p	negatively-F	bioinformatics;luciferase reporter assay	upregulation	sequencing	NA	NA	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227533	GRCh38_1:42959049-42996814	NA	NA	440584	NA	SLC2A1-AS1	NA	TFAP2A-induced SLC2A1-AS1 promotes cancer cell proliferation; it was revealed that lncRNA SLC2A1-AS1 was notably over-expressed in LUAD and was closely correlated with patients' overall survival (OS);SLC2A1-AS1 enriched in the cytoplasm of LUAD cells could directly bind to miR-508-5p and negatively regulate its level;The inhibitory effect of miR-508-5p on LUAD cell proliferation was in part abrogated by SLC2A1-AS1 manipulation;To explore the differential expressed lncRNAs (DElncRNAs) associated with LUAD, we analyzed the RNA-seq data from 151 cases of lung cancer tissues and 51 cases of normal tissues from the Cancer RNA-Seq Nexus database;We obtained 701 and 85 miRNAs that may interact with SLC2A1-AS1 from LncBase v2.0 and lncRNASNP2, respectively;we confirmed that SLC2A1-AS1 was a direct target of miR-508-5p in LUAD cells using the dualluciferase reporter assay	33580997	RID05111	ceRNA or sponge	NA		
Lung adenocarcinoma	TFAP2A	SLC2A1-DT	positively-E	ChIP-PCR;western blot;bioinformatics	upregulation	sequencing	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000137203	NA	ENSG00000227533	GRCh38_1:42959049-42996814	7020	440584	AP-2|AP-2alpha|AP2TF|TFAP2	SLC2A1-AS1	TFAP2A-induced SLC2A1-AS1 promotes cancer cell proliferation; it was revealed that lncRNA SLC2A1-AS1 was notably over-expressed in LUAD and was closely correlated with patients' overall survival (OS);SLC2A1-AS1 enriched in the cytoplasm of LUAD cells could directly bind to miR-508-5p and negatively regulate its level;The inhibitory effect of miR-508-5p on LUAD cell proliferation was in part abrogated by SLC2A1-AS1 manipulation;To explore the differential expressed lncRNAs (DElncRNAs) associated with LUAD, we analyzed the RNA-seq data from 151 cases of lung cancer tissues and 51 cases of normal tissues from the Cancer RNA-Seq Nexus database;we used JASPAR tool online to predict transcription factors (TFs) that may bind to the promoter region of SLC2A1-AS1 encoding gene;Result from the ChIP-PCR demonstrated that TFAP2A could bind directly to the promoter region of SLC2A1-AS1 encoding gene (Figure 6B). The silencing effect of two siRNAs targeting TFAP2A was confirmed by western blot	33580997	RID05112	interact with protein	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)	
Atherosclerosis	PCA3	miR-140-5p	negatively-F	luciferase reporter assay;ChIP	downregulation	qPCR	GEO	NA	lipid metabolic process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000225937	GRCh38_9:76691980-76863307	NA	NA	50652	NA	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	NA	Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis;The expression of PCA3, miR-140-5p, RFX7 and ABCA1 were determined by qPCR or western blot in ox-LDL-treated macrophages;Target relationships among PCA3, miR-140-5p, RFX7, and ABCA1 promoter area were validated via dual-luciferase reporter gene assay or chromatin immunoprecipitation assay;PCA3 was down-regulated in foam cells, whereas miR-140-5p was highly expressed;PCA3 up-regulated ABCA1 expression by binding to miR-140-5p to up-regulate RFX7 and ABCA1 expression in macrophages;lncRNA PCA3 promotes ABCA1-mediated cholesterol efflux to inhibit atherosclerosis through sponging miR-140-5p and up-regulating RFX7	33578049	RID05113	ceRNA or sponge	NA		
Atherosclerosis	PCA3	RFX7	positively-E	luciferase reporter assay;ChIP	downregulation	qPCR	GEO	NA	lipid metabolic process(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000181827	NA	50652	64864	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	FLJ12994|RFXDC2	Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis;The expression of PCA3, miR-140-5p, RFX7 and ABCA1 were determined by qPCR or western blot in ox-LDL-treated macrophages;Target relationships among PCA3, miR-140-5p, RFX7, and ABCA1 promoter area were validated via dual-luciferase reporter gene assay or chromatin immunoprecipitation assay;PCA3 was down-regulated in foam cells, whereas miR-140-5p was highly expressed;PCA3 up-regulated ABCA1 expression by binding to miR-140-5p to up-regulate RFX7 and ABCA1 expression in macrophages;lncRNA PCA3 promotes ABCA1-mediated cholesterol efflux to inhibit atherosclerosis through sponging miR-140-5p and up-regulating RFX7	33578049	RID05114	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Atherosclerosis	PCA3	ABCA1	positively-E	luciferase reporter assay;ChIP	downregulation	qPCR	GEO	NA	lipid metabolic process(+)	promoter	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000165029	NA	50652	19	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	ABC1|HDLDT1|TGD	Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis;The expression of PCA3, miR-140-5p, RFX7 and ABCA1 were determined by qPCR or western blot in ox-LDL-treated macrophages;Target relationships among PCA3, miR-140-5p, RFX7, and ABCA1 promoter area were validated via dual-luciferase reporter gene assay or chromatin immunoprecipitation assay;PCA3 was down-regulated in foam cells, whereas miR-140-5p was highly expressed;PCA3 up-regulated ABCA1 expression by binding to miR-140-5p to up-regulate RFX7 and ABCA1 expression in macrophages;miR-140-5p also inhibit ABCA1 expression via downregulation of RFX7 to impede RCT and aggravate atherosclerosis;lncRNA PCA3 promotes ABCA1-mediated cholesterol efflux to inhibit atherosclerosis through sponging miR-140-5p and up-regulating RFX7;Overexpression of PCA3 promoted ABCA1-mediated cholesterol efflux and reduced lipid accumulation in macrophages	33578049	RID05115	expression association	NA		UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	FOXD2-AS1	miR-143	negatively-E	western blot;RNAi;siRNA	upregulation	RT-PCR	NA	NA	chemoresistance(+);apoptosis process(-);cell invasion(+);cell migration(+)	NA	association	RNA-RNA	Cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin by inhibiting miR-143 expression;western blot results demonstrated that the knockdown of FOXD2-AS1 remarkably upregulated the expression of pro-apoptotic protein Bax and repressed that of anti-apoptotic protein Bcl-2 in drug-resistant human osteosarcoma cells (p<0.05); it was found that the expression level of miR-143 was distinctly elevated in drug-resistant human osteosarcoma cells after knockdown of FOXD2-AS1 (p<0.05);LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin, promotes their apoptosis and weakens their invasion and migration abilities	33577022	RID05116	expression association	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Osteosarcoma	FOXD2-AS1	BAX	negatively-E	western blot;RNAi;siRNA	upregulation	RT-PCR	NA	NA	chemoresistance(+);apoptosis process(-);cell invasion(+);cell migration(+)	NA	association	RNA-protein	Cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000087088	NA	84793	581	MGC12982	BCL2L4	LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin by inhibiting miR-143 expression;western blot results demonstrated that the knockdown of FOXD2-AS1 remarkably upregulated the expression of pro-apoptotic protein Bax and repressed that of anti-apoptotic protein Bcl-2 in drug-resistant human osteosarcoma cells (p<0.05); it was found that the expression level of miR-143 was distinctly elevated in drug-resistant human osteosarcoma cells after knockdown of FOXD2-AS1 (p<0.05);LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin, promotes their apoptosis and weakens their invasion and migration abilities	33577022	RID05117	expression association	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	FOXD2-AS1	BCL2	positively-E	western blot;RNAi;siRNA	upregulation	RT-PCR	NA	NA	chemoresistance(+);apoptosis process(-);cell invasion(+);cell migration(+)	NA	association	RNA-protein	Cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000171791	NA	84793	596	MGC12982	Bcl-2|PPP1R50	LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin by inhibiting miR-143 expression;western blot results demonstrated that the knockdown of FOXD2-AS1 remarkably upregulated the expression of pro-apoptotic protein Bax and repressed that of anti-apoptotic protein Bcl-2 in drug-resistant human osteosarcoma cells (p<0.05); it was found that the expression level of miR-143 was distinctly elevated in drug-resistant human osteosarcoma cells after knockdown of FOXD2-AS1 (p<0.05);LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin, promotes their apoptosis and weakens their invasion and migration abilities	33577022	RID05118	expression association	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Type 1 diabetes mellitus	lncRNA SRA	MIR146B	negatively-F	RNAi;immunoblot	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	protein-RNA	NA	NA	NA	Endocrine system disease	Diabetes mellitus	lncRNA	miRNA	NA	NA	ENSG00000202569	NA	NA	574447	NA	MIRN146B|miRNA146B|mir-146b	Long, Noncoding RNA SRA Induces Apoptosis of beta-Cells by Promoting the IRAK1/LDHA/Lactate Pathway;LncRNA SRAs were highly expressed in plasma samples and peripheral blood mononuclear cells (PBMCs) from T1D patients;LncRNA SRA acts as a microRNA (miR)-146b sponge through direct sequence-structure interactions;LncRNA SRA contributed to T1D pathogenesis through the inhibition of miR-146b in beta-cells, with activating signaling transduction of interleukin-1 receptor-associated kinase 1 (IRAK1)/LDHA/pLDHA;Silencing of lncRNA SRA increased the functional genes of Tregs, resulting in metabolic reprogramming, such as decreased lactate levels, repressed lactate dehydrogenase A (LDHA)/phosphorylated LDHA (pLDHA at Tyr10) expression, decreased reactive oxygen species (ROS) production, increased ATP production, and finally, decreased beta-cell apoptosis in vitro;The plasma levels of lncRNA SRA and miR-146b were determined using real-time qPCR;To investigate the possible interaction between lncRNA SRA and miR-146b, we performed a crossover study;The effects of the miR-146b mimic and shSRA knockdown on the IRAK1/AKT/mammalian Target Of Rapamicyn (mTOR) signaling network were further investigated using select mediators in the immunoblotting analysis	33572095	RID05119	ceRNA or sponge	NA		
Atherosclerosis	XIST	TLR4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-599)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136869	NA	7503	7099	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ARMD10|CD284|hToll|TLR-4	LncRNA XIST Promotes Atherosclerosis by Regulating miR-599/TLR4 Axis;The levels of XIST, miR-599, and TLR4 were tested by RT-qPCR;A dual-luciferase reporter assay was employed to investigate the interaction between miR-599 and XIST or TLR4;In this research, we uncovered that the XIST level was elevated in the serum of AS patients and ox-LDL-treated AS cell models;Functional analysis revealed that XIST depletion restrained cell proliferation, while induced the apoptosis in AS cell models;miR-599 was verified to be a direct downstream target of XIST and miR-599 inhibitor reversed the effects of XIST knockdown on AS progression;we demonstrated that XIST increased TLR4 expression by serving as a ceRNA of miR-599	33566259	RID05120	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Prostate cancer	RAMS11	CBX4	positively-F	RIP;ChIP;RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	NA	NA	ENSG00000141582	NA	NA	8535	NA	hPC2|NBP16|PC2	Long Non-Coding RNA (lncRNA) RAMS11 Promotes Metastatis and Cell Growth of Prostate Cancer by CBX4 Complex Binding to Top2alpha;microarray experiments and real-time polymerase chain reaction (PCR) measured the expression of lncRNA;The expression of lncRNA RAMS11 was up-regulated in prostate cancer tissue samples;We also demonstrated that lncRNA RAMS11 bound to CBX4 to activate expression of Top2alpha;RNA immunoprecipitation (RIP) showed that enrichment levels of lncRNA RAMS11 binding to CBX4 in PC3 and DU145 cells were higher than those of lncRNA RAMS11 binding to lgG (Figure 5A). Chip assay showed that Top2alpha promoter levels of lncRNA RAMS11 binding to CBX4 or si-CBX4 binding to CBX4 were lower than those of WT binding to CBX4 or WT binding to CBX4 in LNCap or DU145 cells	33564266	RID05121	interact with protein	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	RAMS11	TOP2A	positively-E	RIP;ChIP;RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);cell growth(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	NA	NA	ENSG00000131747	NA	NA	7153	NA	TOP2|TOP2alpha|TOPIIA|TP2A	Long Non-Coding RNA (lncRNA) RAMS11 Promotes Metastatis and Cell Growth of Prostate Cancer by CBX4 Complex Binding to Top2alpha;microarray experiments and real-time polymerase chain reaction (PCR) measured the expression of lncRNA;The expression of lncRNA RAMS11 was up-regulated in prostate cancer tissue samples;We also demonstrated that lncRNA RAMS11 bound to CBX4 to activate expression of Top2alpha;Our results indicated that lncRNA RAMS11 promoted cell growth and metastasis of prostate cancer by CBX4 complex via binding to Top2alpha, and might be developed for the treatment of prostate cancer	33564266	RID05122	expression association	metastasis		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Liver fibrosis	NEAT1	CYTH3	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	GSE77271	NA	fibrotic(-)	ceRNA(miR-148a-3p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000008256	NA	283131	9265	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ARNO3|cytohesin-3|GRP1|PSCD3	LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate Cyth3;Upregulation of Neat1 and cytohesin 3 ( Cyth3 ) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues;Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate Cyth3 expression;Knockdown of Neat1 inhibited Cyth3 expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation;Knockdown of Neat1 or Cyth3 attenuated liver fibrosis and collagen deposition in vivo and the activation of HSCs in vitro;Then, the outcomes of the qPCR assay showed that miR- 148a-3p and miR-22-3p were the most substantially downregulated miRNAs in CCl4-induced mice compared with other miRNAs in the top 10 downregulated miRNAs;Both miR-22-3p and miR-148a-3p directly interacted with the corresponding Neat1 3'UTR in mice and the Neat1 3-UTR in humans. Luciferase activity assays revealed that miR-148a-3p or miR-22-3p mimics decreased the luciferase activity of Neat1-wt, while the miR-148a-3p or miR-22-3p inhibitor significantly increased the luciferase activity of Neat1-wt. However, none of the transfection groups affected the luciferase activity of Neat1-mut	33550894	RID05123	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Liver fibrosis	NEAT1	CYTH3	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	GSE77272	NA	fibrotic(-)	ceRNA(miR-22-3p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000008256	NA	283131	9265	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ARNO3|cytohesin-3|GRP1|PSCD3	LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate Cyth3;Upregulation of Neat1 and cytohesin 3 ( Cyth3 ) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues;Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate Cyth3 expression;Knockdown of Neat1 inhibited Cyth3 expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation;Knockdown of Neat1 or Cyth3 attenuated liver fibrosis and collagen deposition in vivo and the activation of HSCs in vitro;Then, the outcomes of the qPCR assay showed that miR- 148a-3p and miR-22-3p were the most substantially downregulated miRNAs in CCl4-induced mice compared with other miRNAs in the top 10 downregulated miRNAs;Both miR-22-3p and miR-148a-3p directly interacted with the corresponding Neat1 3'UTR in mice and the Neat1 3-UTR in humans. Luciferase activity assays revealed that miR-148a-3p or miR-22-3p mimics decreased the luciferase activity of Neat1-wt, while the miR-148a-3p or miR-22-3p inhibitor significantly increased the luciferase activity of Neat1-wt. However, none of the transfection groups affected the luciferase activity of Neat1-mut	33550894	RID05124	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Chronic obstructive pulmonary disease	TUG1	BCL2L11	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-9a-5p)	regulation	RNA-protein	NA	CSC	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000153094	NA	55000	10018	FLJ20618|LINC00080|NCRNA00080	BIM|BimEL|BimL|BimS|BOD	lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR-9a-5p/BCL2L11 axis in chronic obstructive pulmonary disease;Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure the expression of TUG1 mRNA levels in the treated cells;The association between TUG1, the miR-9a-5p/BCL2L11 axis and with miR-9a-5p were predicted and verified using a dual-luciferase reporter assay system;miR-9a-5p mimic reversed the increase in cell apoptosis induced by CSE by inhibiting BCL2L11 expression in HPMECs	34257718	RID05125	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Myocardial infarction	LINC00261	TNRC6A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	ceRNA(miR-522-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000090905	NA	140828	27327	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	CAGH26|GW182|KIAA1460|TNRC6	Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis;qRT-PCRwas performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells;The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay;LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI;LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p;Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis	34239606	RID05126	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Esophageal cancer	WDFY3-AS2	PTEN	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-18a)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000180769	GRCh38_4:84965534-85011277	ENSG00000171862	NA	404201	5728	C4orf12|FBI4|NCRNA00247	BZS|MHAM|MMAC1|PTEN1|TEP1	Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis;RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells;The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN;WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC;Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients	34194502	RID05127	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Kidney disease	HCP5	HMGA2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	AKT/mTOR signaling pathway(+);cell proliferation(+);fibrotic(+);inflammatory response(+)	ceRNA(miR-93-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000149948	NA	10866	8091	D6S2650E|P5-1	BABL|HMGIC|LIPO	LncRNA HCP5 knockdown inhibits high glucose-induced excessive proliferation, fibrosis and inflammation of human glomerular mesangial cells by regulating the miR-93-5p/HMGA2 axis;he expression of HCP5, miR-93-5p and high mobility group AT-hook 2 (HMGA2) mRNA was detected using quantitative polymerase chain reaction (QPCR);The predicted relationship between miR-93-5p and HCP5 or HMGA2 was verified using dual-luciferase reporter assay, pull-down assay or RNA immunoprecipitation (RIP) assay;The expression of HCP5 and HMGA2 was enhanced, while the expression of miR-93-5p was declined in DN serum samples and HG-treated HGMCs;MiR-93-5p was a target of HCP5, and miR-93-5p inhibition reversed the effects caused by HCP5 knockdown. Moreover, HMGA2 was a target of miR-93-5p, and HMGA2 overexpression abolished the effects of miR-93-5p restoration;HCP5 knockdown inhibited the AKT/mTOR signaling pathway	34187448	RID05128	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Papillary thyroid carcinoma	OIP5-AS1	XIAP	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-429)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000101966	NA	729082	331	cyrano|linc-OIP5	API3|BIRC4|hILP|ILP-1	Long non-coding RNA OIP5-AS1 serves as a competing endogenous RNA to modulate X-linked inhibitor of apoptosis protein expression via adsorbing miR-429 in papillary thyroid cancer;OIP5-AS1 and miR-429 expression levels in PTC tissues and cells were examined using qRT-PCR dual-luciferase reporter gene experiment was employed to validate the relationship for miR-429 and XIAP, miR-429 and OIP5-AS1;In this work we reported that OIP5-AS1 expression was up-modulated in PTC tissues and cell lines;OIP5-AS1 overexpression enhanced the proliferation and metastasis of PTC cells, but the transfection of miR-429 mimics reversed the functions of OIP5-AS1 on the proliferation, migration, and invasion of PTC cells. Additionally, OIP5-AS1 was identified as a competitive endogenous RNA (ceRNA) that repressed miR-429, thereby increasing the expression level of XIAP	34155880	RID05129	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	OIP5-AS1	ATG5	positively-E	Starbase;Targetscan;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	angiogenesis(+);cell autophagy(+)	ceRNA(miR-153)	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000057663	NA	729082	9474	cyrano|linc-OIP5	APG5|APG5L|ASP|hAPG5	Highly enriched exosomal lncRNA OIP5-AS1 regulates osteosarcoma tumor angiogenesis and autophagy through miR-153 and ATG5;The gene expression levels of lncRNA OIP5-AS1, miR-153 and autophagy-related protein 5 (ATG5) were quantified by real-time quantitative PCR (RT-PCR;The binding sites of lncRNA OIP5-AS1 and miR-153 were predicted by Starbase3.0, and the binding sites of miR-153 and ATG5 were predicted by Targetscan7.2. The gene binding sites were verified by luciferase reporter gene detection or RNA immunoprecipitation (RIP);The results of RT-PCRshowed that lncRNA OIP5-AS1 levels were elevated in OS cells and exosomes secreted by cells.	34150009	RID05130	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Atherosclerosis	MIAT	CASP1	positively-E		upregulation	RT-PCR	NA	NA	cell viability(-);apoptosis process(+)	ceRNA(miR-214-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000137752	NA	440823	834	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ICE|IL1BC	LncRNA Miat knockdown alleviates endothelial cell injury through regulation of miR-214-3p/Caspase-1 signaling during atherogenesis;Real-time PCR was used to measure the expression of lncRNA Miat, miR-214, Caspase-1 and IL-1beta;The results found that lncRNA Miat was upregulated in ox-LDL induced atherosclerosis model in vitro;LncRNA Miat and miR-214 has binding site. And CASP1, which encode Caspase-1, is a target of miR-214;the expression of miR-214-3p was upregulated and Caspase-1 was downregulated after knockdown of lncRNA Miat;The inhibition of lncRNA Miat protects against ox-LDL induced HAEC injury, presented as increased cell viability and decreased apoptosis	34137063	RID05131	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Systemic lupus erythematosus	H19	IL2	negatively-F	gain-of-function and loss-of-function using mimic-H19 (H19-OE) and inhibitor-H19 (H19-KD)	upregulation	RT-qPCR	NA	NA	cell cycle(-);cell proliferation(-)	sponge	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000109471	NA	283120	3558	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	IL-2|TCGF	LncRNA H19 induces immune dysregulation of BMMSCs, at least partly, by inhibiting IL-2 production;In this study, we first examined H19 expression in SLE patients by RT-qPCR and found that H19 expression was significantly upregulated in the serum and bone marrow-derived mesenchymal stem cells (BMMSCs) of SLE patients and positively associated with SLE disease activity index;dual-luciferase reporter assay confirmed the in silico prediction of interaction between H19 and IL-2. Furthermore, RT-qPCR showed that H19 directly inhibited IL-2 transcription in BMMSCs	34130625	RID05132	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Follicular thyroid carcinoma	GAS5	CDKN2B	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell cycle(-);cell proliferation(-)	ceRNA(miR-221-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000147883	NA	60674	1030	NCRNA00030|SNHG2	CDK4I|INK4B|MTS2|P15|p15INK4b|TP15	Long Noncoding RNA GAS5 Targeting miR-221-3p/Cyclin-Dependent Kinase Inhibitor 2B Axis Regulates Follicular Thyroid Carcinoma Cell Cycle and Proliferation;Quantitative real-time polymerase chain reaction (qRT-PCR was employed to detect GAS5 and miR-221-3p expression in the FTC tissues and cells;The dual-luciferase reporter assay was employed to validate the binding relationship of GAS5/miR-221-3p and miR-221-3p/cyclin-dependent kinase inhibitor 2B (CDKN2B);Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells;GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p;GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression. GAS5 induced G0/G1 phase arrest and inhibited cell proliferation via targeting miR-221-3p/CDKN2B axis in FTC	34130294	RID05133	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Pulmonary hypertension	SFTA3	STK4	positively-E	luciferase activity assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-23a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000229415	GRCh38_14:36473288-36513829	ENSG00000101109	NA	253970	6789	NANCI|PAHRF|SFTPH|SP-H|SPH	KRS2|MST1|YSK3	The lncRNA PAHRF functions as a competing endogenous RNA to regulate MST1 expression by sponging miR-23a-3p in pulmonary arterial hypertension;LncRNA PAHRF was down-regulated in both the PAs of PAH patients and hypoxic human pulmonary artery smooth muscle cells (PASMCs);LncRNA PAHRF expression and localization were analyzed by realtime PCR and fluorescence in situ hybridization;The overexpression of PAHRF inhibited the proliferation and promoted the apoptosis of PASMCs;Luciferase activity assay proved molecular binding between PAHRF and hsa-miR-23a-3p. Moreover, MST1 was confirmed to be the putative target gene and regulated by PAHRF/miR-23a-3p;we explored the molecular mechanism regulating the expression of miR-23a-3p, and found that lncRNA PAHRF acted as an endogenous sponge for miR-23a-3p, and silencing lncRNA PAHRF could up-regulate the expression of miR-23a-3p	34126237	RID05134	ceRNA or sponge	NA	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE86978)
Chronic obstructive pulmonary disease	LUCAT1	miR-181a-5p	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR;ELISA	NA	NA	cell proliferation(+);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	NA	NA	100505994	NA	SCAL1|SCAT5	NA	Expression of long non-coding RNA LUCAT1 in patients with chronic obstructive pulmonary disease and its potential functions in regulating cigarette smoke extract-induced 16HBE cell proliferation and apoptosis; qRT-PCRand ELISA assays were performed to detect the expression levels of lncRNA LUCAT1, miR-181a-5p, and inflammatory cytokines;The dual-luciferase reporter and RNA pull-down assays were used to detect the binding relationship between lncRNA LUCAT1 and miR-181a-5p; meanwhile, Spearman's correlation assay was used to verify the correlation between lncRNA LUCAT1 and miR-181a-5p;a western blot assay was utilized to determine the mechanism of lncRNA LUCAT1/miR-181a-5p/Wnt/beta-catenin axis in COPD;LncRNA LUCAT1 was upregulated in the serums of COPD patients;Cell proliferation and apoptosis assays showed that LUCAT1 silencing alleviated CSE's effects on 16HBE cell proliferation and apoptosis. Mechanically, rescue assays demonstrated that miR-181a-5p inhibition could partially counteract the impact of LUCAT1 on COPD progression through the Wnt/beta-catenin pathway	34125980	RID05135	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Intervertebral disc degeneration	JPX	HIF1A	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation		GSE132182	NA	cell proliferation(+);apoptosis process(-);Hippo/YAP signaling pathway(-)	ceRNA(miR-18a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000100644	NA	554203	3091	DCBALD06|ENOX|LINC00183|NCRNA00183	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA JPX regulates proliferation and apoptosis of nucleus pulposus cells by targeting the miR-18a-5p/HIF-1alpha/Hippo-YAP pathway;Our study revealed that lncRNA JPX is expressed at low levels in HNPCs under normoxic conditions;Luciferase and RNA pull-down assays were used to verify that lncRNA JPX directly bound to miR-18a-5p and influenced HNPC proliferation and apoptosis;a luciferase assay confirmed the direct binding of miR-18a-5p to HIF-1alpha and demonstrated a negative correlation between miR-18a-5p and HIF-1alpha;overexpression of lncRNA JPX upregulated HIF-1alpha by inhibiting the expression of miR-18a-5p, thereby inhibiting the Hippo-YAP pathway;NPCs cultured for 2.5 and 21 months were used, which simulated IDD development in vitro. There were 2044 differentially expressed lncRNAs/mRNAs in 21month NPCs compared to 2.5-month NPCs (Fig. 1A). Among them, lncRNA JPX was substantially downregulated in 21-month NPCs, and its functional importance and mechanism of action have not been reported in IDD. Therefore, JPX was selected to study the mechanism in HNPCs cultured under Hx/Nx conditions. The results showed that JPX expression was downregulated in the Nx group compared with that in the Hx group (Fig. 1B), which was consistent with the GEO analysis. Additionally, cell proliferation in the Nx group decreased (Fig. 1C), and apoptosis increased;Effects of Nx on the proliferation and apoptosis of HNPCs and expression of lncRNA JPX. (A) Differential expression of lncRNA/mRNA, conforming to the log2 |FC|>1.5 and P<0.05 standard genetic variations of heat map. (B) Differences in JPX expression under Hx and Nx conditions determined by RT-qPCR. (C) The effect of Nx conditions on HNPC proliferation was analyzed by CCK-8. (D) The effect of Nx on HNPC apoptosis was analyzed by FCM. (E) RT-qPCR verified the efficacy of the JPX overexpression plasmid. (F) Effect of overexpression of JPX on expression of high glucose induced expression of JPX. (G) The effect of JPX overexpression on HNPC proliferation was analyzed by CCK-8. (H) The effect of JPX overexpression on HPNC apoptosis was analyzed by FCM.	34111667	RID05136	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gallbladder cancer	TTN-AS1	HMGA1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-107)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000137309	NA	100506866	3159	NA	HMGIY	LncRNA TTN-AS1 acts as a tumor promoter in gallbladder carcinoma by regulating miR-107/HMGA1 axis;The expression levels of lncRNA TTN-AS1, miR-107, and HMGA1 in tissues and cell lines were assessed by RT-qPCR;The relationship between miR-107 and lncRNA TTN-AS1 or HMGA1 was confirmed by luciferase reporter assay;Upregulation of lncRNA TTN-AS1 and downregulation of miR-107 were detected in GBC;lncRNA TTN-AS1 promoted cell viability and motility in GBC by sponging miR-107. In addition, miR-107 directly targets HMGA1;HMGA1 promoted GBC progression by interacting with lncRNA TTN-AS1/miR-107 axis	34090483	RID05137	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Ovarian cancer	XIST	BCL2L2	NA	luciferase reporter assay		RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-335)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000129473	NA	7503	599	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BCL-W|KIAA0271|PPP1R51	Long non-coding RNA XIST regulates ovarian cancer progression via modulating miR-335/BCL2L2 axis;RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues;The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay;These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2;The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells	34090463	RID05138	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Lung adenocarcinoma	EGR1	LINC01116	positively-E	JASPAR;qRT-PCR;luciferase reporter assay;ChIP	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000120738	NA	ENSG00000163364	GRCh38_2:176611464-176637931	1958	375295	225|AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268	TALNEC2	Long non-coding RNA LINC01116 is activated by EGR1 and facilitates lung adenocarcinoma oncogenicity via targeting miR-744-5p/CDCA4 axis;qRT-PCRand western blot were applied for quantifying the expression of RNAs and proteins;LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1;LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells;Subsequent qRT-PCRdemonstrated an elevation in the expression of LINC01116 induced by overexpressing EGR1 (Fig. 2C), which indicated that EGR1 may stimulate the transcription of LINC01116. We then found the DNA motif of EGR1 and acquired three specific binding sites in the sequence of human LINC01116 promoter from JASPAR, as illustrated in Fig. 2D. We divided the promoter of LINC01116 into four parts according to the predicted binding sites (Fig. 2E). ChIP assay manifested that the LINC01116 promoter was remarkably pulled down by specific antibody targeting EGR1 only in P4 sectional part (Fig. 2F). To further testify this finding, we sub-cloned the full promoter region of LINC01116 (P FL) and P4-deleted promoter region into pGL3 vector (Fig. 2G). Luciferase reporter assay revealed that the luciferase activity of P FL was distinctively enhanced by overexpressing EGR1 in HEK-293 T, whereas no luciferase activity change in the deletion of P4 sectional part (Fig. 2H). This observation represented that EGR1 interacted with LINC01116 promoter at about 1400 to 2000 bp downstream the transcription start site	34090440	RID05139	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)
Lung adenocarcinoma	LINC01116	CDCA4	positively-E	starBase;qRT-PCR;luciferase reporter assay;RNA pull down;RNAi	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-335)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000170779	NA	375295	55038	TALNEC2	FLJ20764|Hepp	Long non-coding RNA LINC01116 is activated by EGR1 and facilitates lung adenocarcinoma oncogenicity via targeting miR-744-5p/CDCA4 axis;qRT-PCRand western blot were applied for quantifying the expression of RNAs and proteins;LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1;MiR-744-5p could bind to LINC01116;cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p;LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells;Subcellular fraction and FISH assays revealed that LINC01116 was predominantly distributed in cytoplasm (Fig. 3A, B). Next, we utilized starBase (http://starbase.sysu.edu.cn/) bioinformatics analysis to find the potential miRNAs that could bind with LINC01116. Only miR-744-5p was found to be significantly enriched in biotin LINC01116-WT rather than biotin LINC01116-Mut (Fig. 3C). Later, qRT-PCRwas carried out to evaluate the effect of LINC01116 knockdown on miR-744-5p in A549 and PC9 cells (Additional file 1: Figure S1C). The results indicated LINC01116 knockdown had no influence on miR-744-5p expression, showing that LINC01116 could competitively bind with miR-744-5p. In addition, starBase indicated putative binding sites between miR-744-5p and LINC01116 (Fig. 3D). Moreover, we found that the expression of miR-744-5p was markedly lower in LAD cell than that in HBE (Fig. 3E). dual-luciferase reporter assays suggested that the transfection of miR-744-5p mimics restrained the luciferase activity of LINC01116-WT, yet eliciting no variation in that of LINC01116-Mut (Fig. 3F). Additionally, RNA pull-down assay manifested that LINC01116 was pulled down and enriched by Biotin miR-744-5p-WT probe (Fig. 3G). These data indicated that miR-744-5p could bind to LINC01116. Later, the function of miR-744-5p was investigated. We firstly silenced miR-744-5p utilizing miR-744-5p inhibitor (Fig. 3H). It was showed that miR-744-5p inhibitor obviously promoted A549 cell proliferation in EdU and colony formation, and counteracted the anti-proliferation effects of LINC01116 silencing (Fig. 3I, J). Furthermore, miR-744-5p inhibitor diminished apoptotic cells relative to control group, and reversed the pro-apoptosis influence exerted by LINC01116 silencing (Fig. 3K). Additionally, miR-744-5p inhibitor exerted positive impacts on migrating and invasive abilities of A549 cells, and offset the inhibitory impacts on migration and invasion induced by LINC01116 silencing (Fig. 3L, M). MiR-744-5p mimics elicited opposite outcomes in these cellular activities;qRT-PCRanalysis showed that CDCA4 was significantly down-regulated by transfection of miR-744-5p mimics into A549 cells (Fig. 4A). Subsequent qRT-PCRdetected an abnormal overexpression pattern of CDCA4 in LAD cells (Fig. 4B). We then obtained putative binding sites between miR-744-5p and CDCA4 (Fig. 4C). dual-luciferase reporter assays showed that the luciferase activity of CDCA4-WT was notably decreased in A549 and PC9 by miR-744-5p overexpression	34090440	RID05140	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE111842)
Lung adenocarcinoma	SGMS1-AS1	MYLI9	positively-E	ENCORI;luciferase reporter assay;RNAi	downregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-744-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226200	GRCh38_10:50623466-50641451	NA	NA	104355295	NA	NA	NA	LncRNA SGMS1-AS1 regulates lung adenocarcinoma cell proliferation, migration, invasion, and EMT progression via miR-106a-5p/MYLI9 axis;The ENCORI and GEPIA databases were used to analyze the differences in SGMS1, miR-106a-5p, and MYLIP between LUAD and normal tissue. Their expression levels were examined by RT-PCRSGMS1-AS1 was downregulated in LUAD tissue as well as cells;miR-106a-5p was the direct target of SGMS1-AS1 and transfecting miR-106a-5p inhibitor could reversed the impact induced by knockdown of SGMS1-AS1. Subsequently, we found that MYLIP was the target of miR-106a-5p, which was negatively correlated with miR-106a-5p, but had high positive correlation with SGMS1-AS1;MiR-106a-5p was stated to be the direct target of SGMS1 AS1 by the ENCORI database (Figure 3(a)). This database also showed that the expression of SGMS1 AS1 was negatively related with that of miR-106a-5p;To verify the relationship between the two genes, we employed the luciferase reporter assay and the data illustrated that heterotopic expression of miR 106A 5p had no obvious effect on the luciferase activity of mutant SGMS1 AS1 but significantly depressed that of wild type SGMS1 AS1;the mRNA level of miR 106a 5p increased dramatically in A549 and PC9 after transfecting with siSGMS1 AS1	34061466	RID05141	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pituitary adenoma	TUG1	TESC	positively-E		upregulation		NA	NA	NF-kB signaling pathway(-);cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-)	ceRNA(miR-187-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000088992	NA	55000	54997	FLJ20618|LINC00080|NCRNA00080	CHP3|FLJ20607|TSC	Long non-coding RNA TUG1/microRNA-187-3p/TESC axis modulates progression of pituitary adenoma via regulating the NF-kB signaling pathway;We observed that TUG1 was upregulated in PA tissues and was associated with invasion, knosp grade and tumor size;TUG1 particularly bound to miR-187-3p;TUG1 inhibition downregulated TESC, which was targeted by miR-187-3p;In conclusion, this study suggests that TUG1 sponges miR-187-3p to affect PA development by elevating TESC and regulating the NF-kB signaling pathway;TUG1 knockdown inhibited cell proliferation, invasion, migration, and epithelial-mesenchymal transition, promoted apoptosis, and regulated the expression of NF-kB p65 and inhibitor of kB (IkB)-alpha in PA cells lines in vitro, and also inhibited tumor growth in vivo, and these effects were reversed by miR-187-3p reduction;We detected the expression of TUG1 in PA tissues and normal pituitary tissues using RT-qPCR to verify its abnormal expression in PA, and the results suggested that versus the normal pituitary tissues, the expression of TUG1 was heightened in PA tissues; It was predicted at the online analysis website RNA22 (https://cm.jefferson.edu/rna22/Precomputed/) that there existed particular binding region between the sequences of TUG1 and miR-187-3p;we detected the expression of miR-187-3p in PA tissues. The results showed that miR-187-3p was downregulated in PA tissues versus normal pituitary tissues;TUG1 luciferase reporter plasmids with Wt and predicted mutant sites for miR-187-3p were constructed. We found that miR-187-3p mimic repressed the luciferase activity of the Wt plasmid whereas did not affect the luciferase activity of the mutant plasmid;the results of RNA pull-down assay illustrated that TUG1 was pulled down by the target oligos	34021124	RID05142	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842,GSE109761)
Atherosclerosis	SNHG12	EIF5A	negatively-F	starBase;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-766-5p)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000132507	NA	85028	1984	ASLNC04080|C1orf79|LINC00100|PNAS-123	EIF-5A|EIF5A1|MGC104255|MGC99547	Silencing of lncRNA SNHG12 inhibits proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/EIF5A axis;Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) was employed to determine the expression of SNHG12, miR-766-5p and eukaryotic translation initiation factor 5A (EIF5A) in oxidized low-density lipoprotein (ox-LDL)-induced hVSMCs;To further investigate the regulatory mechanisms, binding sites between SNHG12 and miR-766-5p, and EIF5A and miR-766-5p were predicted using starBase database and validated using luciferase reporter gene assays;SNHG12 silencing inhibited ox-LDL-induced proliferation and migration of hVSMCs. Moreover, SNHG12 acted as a sponge of miR-766-5p, and miR-766-5p also interacted with EIF5A. EIF5A plasmids promoted the capacities of proliferation and migration in ox-LDL-induced hVSMCs	34018346	RID05143	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)
Atherosclerosis	MIAT	STIM1	positively-E	starBase;dual-luciferase reporter and RNA immunoprecipitation assays.	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-641)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000167323	NA	440823	6786	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	D11S4896E|GOK	Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells;The RNA levels of MIAT, microRNA-641 (miR-641) and stromal interaction molecule 1 (STIM1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR;The putative binding relationships between miR-641 and MIAT or STIM1 were predicted by starbase online database, and identified by dual-luciferase reporter and RNA immunoprecipitation assays;MIAT and STIM1 expression were substantially upregulated, whereas miR-641 expression was downregulated in ox-LDL-induced VSMCs compared with control groups;MIAT acted as a sponge for miR-641, and miR-641 was associated with STIM1	34016053	RID05144	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	SNHG12	CUL4B	positively-E	luciferase reporter assay;RNA pull-down assay		qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000158290	NA	85028	8450	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	LncRNA SNHG12 regulates the miR-101-3p/CUL4B axis to mediate the proliferation, migration and invasion of non-small cell lung cancer;The expression levels of SNHG12, miR-101-3p, and CUL4B in collected human NSCLC tumor tissues and NSCLC cell lines were tested via qRT-PCR;dual-luciferase reporter assays and RNA pull-down assays were adopted to explore the target site;CUL4B was confirmed as a functional target of miR-101-3p;we found that SNHG12 regulated miR-101-3p to modulate the PI3K/AKT pathway mediated by CUL4B	34002487	RID05145	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioma	HCP5	miR-128	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	Knockdown of Long Non-Coding RNA HCP5 Increases Radiosensitivity Through Cellular Senescence by Regulating microRNA-128 in Gliomas;The levels of HCP5 and microRNA (miR)-128 were detected using qRT-PCRuciferase reporter and RNA immunoprecipitation (RIP) assays were performed to determine the correlation between HCP5 and miR-128;HCP5 level of glioma cells was significantly higher than human astrocytes, whereas miR-128 level was lower in glioma cells;It was demonstrated that HCP5 directly bound to miR-128 and regulated its expression in glioma cells;These findings suggested that interaction between lncRNA HCP5 and microRNA-128 could regulate the radiosensitivity of glioma cells by intervening in cellular senescence;Knockdown of HCP5 inhibited cell proliferation and increased radiosensitivity in glioma cells	33994812	RID05146	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Glioma	NEAT1	KCTD20	positively-E	luciferase reporter assay;immunoprecipitation;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);prognosis(-)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112078	NA	283131	222658	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	C6orf69|dJ108K11.3|MGC14254	Long non-coding RNA NEAT1 regulates glioma cell proliferation and apoptosis by competitively binding to microRNA-324-5p and upregulating KCTD20 expression;By reverse transcription quantitative PCR and fluorescence in situ hybridization analysis, NEAT1 expression was upregulated in glioma tissues compared with in adjacent normal brain tissues, and elevated NEAT1 levels were associated with poor prognosis;Using bioinformatics analysis, RNA immunoprecipitation experiments and luciferase reporter assays, it was demonstrated that NEAT1 may competitively bind to microRNA (miR)-324-5p, thus blocking its interaction with target mRNAs;the inhibition of NEAT1 resulted in the downregulation of KCTD20 through competitive binding with miR 324 5p, decreased cell proliferation and increased apoptosis	33982764	RID05147	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE55807)
Melanoma	DUXAP8	NUPR1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-3182)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000176046	NA	503637	26471	NA	COM1|p8	DUXAP8 knockdown inhibits the development of melanoma by regulating the miR-3182/NUPR1 pathway;The expression levels of DUXAP8 were determined in 43 samples from patients with melanoma in different stages, as well as human epidermal melanocytes cells and malignant melanoma cell lines using reverse transcription-quantitative PCR (RT-qPCR);The relationship between lncRNA DUXAP8 expression and microRNA (miR)-3182 or nuclear protein 1 transcriptional regulator (NUPR1) levels was analyzed using Pearson's correlation. Luciferase reporter and RNA pull-down were used to examine the interactions between these molecules;lncRNA DUXAP8 was upregulated in melanoma tissue and cells compared with normal tissues and cells;Knockdown of lncRNA DUXAP8 inhibited proliferation, migration and invasion of melanoma cells	33981357	RID05148	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807,GSE75367)
Pulmonary fibrosis	PFI	SRSF1	negatively-E	ChIRP-MS;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	fibrotic(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	PCG	NA	NA	ENSG00000136450	NA	NA	6426	NA	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	The long non-coding RNA PFI protects against pulmonary fibrosis by interacting with splicing regulator SRSF1;We used a qRT-PCRassay to identify dysregulated lncRNAs in the lungs of mice with experimental, bleomycin (BLM)-induced pulmonary fibrosis, and a series of molecular assays to assess the role of the novel lncRNA NONMMUT060091, designated as pulmonary fibrosis inhibitor (PFI), which was significantly downregulated in lung fibrosis;Mechanistically, using chromatin isolation by RNA purification-mass spectrometry (ChIRP-MS) and an RNA pull-down assay, PFI was found to directly bind Serine/arginine-rich splicing factor 1 (SRSF1), and to repress its expression and pro-fibrotic activity	33981019	RID05149	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	AGAP2-AS1	NOTCH2	positively-E	lncatlas;FISH;luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	radioresistance(+)	ceRNA(miR-296)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000134250	NA	100130776	4853	LOC100130776|PUNISHER	NA	M2 macrophage-derived exosomal long non-coding RNA AGAP2-AS1 enhances radiotherapy immunity in lung cancer by reducing microRNA-296 and elevating NOTCH2;AGAP2-AS1 and NOTCH2 increased while miR-296 decreased in radioresistant patients and lung cancer cells;AGAP2-AS1 negatively regulated miR-296, and NOTCH2 was targeted by miR-296;M2 macrophage-derived exosomal AGAP2-AS1 enhances radiotherapy immunity in lung cancer by reducing miR-296 and elevating NOTCH2;AGAP2-AS1, miR-296, and NOTCH2 levels in lung cancer tissues and adjacent tissues were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR);An online analysis website (http://lncatlas.crg.eu/) was used to investigate the functional mechanism of AGAP2-AS1, and it was found that (Supplementary Fig. 3A) AGAP2-AS1 mainly distributed in the cytoplasm. This result was confirmed by RNA-FISH assay; It was further confirmed that (Supplementary Fig. 3E) relative to the mimic NC group, the luciferase activity of cells with the AGAP2-AS1-WT in the miR-296 mimic group was repressed. Results of RNA pull-down assay (Supplementary Fig. 3F) reflected that in relation to the Bio-NC group, the enrichment of AGAP2-AS1 was enhanced in the Bio-miR-296-WT group, further indicating that miR-296 particularly bound to AGAP2-AS1. RIP assay was conducted to explore the regulatory role of miRNA in Ago2 protein	33972506	RID05150	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pre-eclampsia	ATB	YY1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-651-3p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	TF	NA	NA	ENSG00000100811	NA	NA	7528	NA	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	Effect of lncRNA-ATB/miR-651-3p/Yin Yang 1 pathway on trophoblast-endothelial cell interaction networks;the binding site of lncRNA-ATB and miR-651-3p was verified using dual-luciferase reporter assay, and the rescue experiment was used to study the effects of these two on the biological function;LncRNA-ATB was found to be down-regulated in the placenta of preeclampsia patients;MiR-651-3p was a direct target of lncRNA-ATB and they had opposite effects;MiR-651-3p has been confirmed to directly target the 3' untranslated region of YY1;western blotshowed that lncRNA-ATB could regulate YY1 expression by sponging miR-651-3p;LncRNA-ATB knockdown decreased trophoblast migration, invasion and colocalisation with human umbilical vein endothelial cells;The qRT-PCRresults showed that the expression of placental lncRNA-ATB in PE patients was lower than that in normal pregnant women, which was consistent with our previous study;potential target miRNA of lncRNA was predicted using miRDB and the specific wild and mutant type sequences are shown in Figure 3A. dual-luciferase reporter assay was then used to verify this prediction;qRT-PCRresults showed that overexpression of lncRNA ATB led to a decrease in miR 651 3p expression while transfection with si ATB led to an increase in miR 651 3p expression;qRT-PCRresults showed that overexpression of lncRNA ATB led to a decrease in miR 651 3p expression while transfection with si ATB led to an increase in miR 651 3p expression;	33942988	RID05151	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Pancreatic cancer	CERS6-AS1	HMGA1	positively-E	luciferase reporter assay;immunoprecipitation;RNA pull down	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-15a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000227617	GRCh38_2:168771951-168786961	ENSG00000137309	NA	100861402	3159	NA	HMGIY	Long Noncoding RNA CERS6-AS1 Accelerates the Proliferation and Migration of Pancreatic Cancer Cells by Sequestering MicroRNA-15a-5p and MicroRNA-6838-5p and Modulating HMGA1;Quantitative real-time polymerase chain reaction analysis was used to examine the expression of CERS6-AS1 in PC cell lines;RNA pull-down, RNA immunoprecipitation, and luciferase reporter assays were implemented to delve into the regulatory mechanism of CERS6-AS1 in PC;CERS6-AS1 was significantly upregulated in PC;CERS6-AS1 sponged microRNA-15a-5p (miR-15a-5p) and microRNA-6838-5p (miR-6838-5p) to regulate HMGA1	33939677	RID05152	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Parkinson's disease	SNHG1	MAPK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	apoptosis process(+);inflammatory response(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000100030	NA	23642	5594	LINC00057|lncRNA16|NCRNA00057|UHG	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Long Noncoding RNA SNHG1 Knockdown Ameliorates Apoptosis, Oxidative Stress and Inflammation in Models of Parkinson's Disease by Inhibiting the miR-125b-5p/MAPK1 Axis;The levels of SNHG1, miR-125b-5p and mitogen-activated protein kinase 1 (MAPK1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR or western blot;dual-luciferase reporter assay was performed to identify the relationship between miR-125b-5p and SNHG1 or MAPK1;SNHG1 and MAPK1 were significantly up-regulated while miR-125b-5p was down-regulated in the MPTP-induced PD mouse model and MPP + -induced PD cell models;SNHG1 silence or miR-125b-5p overexpression protected against MPP + -evoked apoptosis, oxidative stress and inflammation in SK-N-SH and MN9D cells. Moreover, SNHG1 acted as a molecular sponge of miR-125b-5p, and the protective impact of SNHG1 silence on MPP + -evoked cell damage was reversed by miR-125b-5p inhibition	33911864	RID05153	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thyroid eye disease	LPAL2	EGFR	positively-E	miRDB;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	EGFR/AKT signaling pathway(+)	ceRNA(miR-1287-5p)	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000213071	GRCh38_6:160453428-160520269	ENSG00000146648	NA	80350	1956	APOAL|APOARGC	ERBB|ERBB1|ERRP	LncRNA LPAL2/miR-1287-5p/EGFR Axis Modulates TED-Derived Orbital Fibroblast Activation Through Cell Adhesion Factors;Long noncoding RNA LPAL2 level was also upregulated in orbital tissues and positively correlated with ICAM-1 and ICAM-4 expression;miR-1287-5p was directly bound to the epidermal growth factor receptor (EGFR) 3' untranslated region and LPAL2, and LPAL2 modulated EGFR/protein kinase B (AKT) signaling through targeting miR-1287-5p;The LPAL2/miR-1287-5p axis modulated TGF-beta1-induced increases in cell adhesion factor levels and TED orbital fibroblast activation through EGFR/AKT signaling	33877318	RID05154	ceRNA or sponge	NA	UP(PAAD,PRAD);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	ZEB1-AS1	MIR23C	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000264566	NA	220930	100500809	NA	hsa-mir-23c|mir-23c	LncRNA ZEB1-AS1 regulates hepatocellular carcinoma progression by targeting miR-23c;qRT-PCRresults indicated ZEB1-AS1 was upregulated and miR-23c was downregulated in HCC tissues and cell lines;dual-luciferase reporter assay showed that miR-23c is a target of ZEB1-AS1, and ZEB1-AS1 was significantly negatively correlated with the miR-23c expression in HCC tissues;	33865414	RID05155	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	
Hepatocellular carcinoma	XIST	TRIM25	positively-E	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-192)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000121060	NA	7503	7706	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	EFP|RNF147|ZNF147	LncRNA XIST upregulates TRIM25 via negatively regulating miR-192 in hepatitis B virus-related hepatocellular carcinoma;qRT-PCRresults showed that the expression levels of lncRNA XIST were remarkably increased in HBV-related HCC tissues and HepG2.2.15 cells;Biological information and luciferin gene reporter assay were performed to detect the interaction among lncRNA XIST, miR-192 and TRIM25;TRIM25 was a direct target of miR-192, and lncRNA XIST could up-regulate the expression of TRIM25 by targeting miR-192;overexpression of miR-192 observably inhibited the proliferation and migration of HCC cells, while overexpression of lncRNA XIST showed an opposite effect	33858324	RID05156	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hypertrophic scar	NORAD	TGF-betaR2	positively-E	Starbase;luciferase reporter assay;RIP	downregulation	qPCR;ELISA	NA	NA	cell proliferation(-)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	LncRNA NORAD regulates scar hypertrophy via miRNA-26a mediating the regulation of TGFbetaR1/2;Hypertrophic scar tissues were collected and assayed for LncRNA NORAD, miR-26a, transforming growth factor beta receptor I (TGF-betaR1) and TGF-betaR2, with enzyme-linked immunosorbent assay (ELISA) or qualitative polymerase chain reaction (qPCR);The binding sites of miRNA-26a and LncRNA NORAD, TGF-betaR2, or UBE3A were predicted using Starbase and confirmed with dual-luciferase reporter assay. RNA immunoprecipitation (RIP) was utilized to explore the interplay of miR-26a with its target genes;LncRNA NORAD is decreased, miR-26a is increased and TGF-beta receptors show abnormal expression in scar tissue;LncRNA NORAD may act as a sponge, binding miR-26a and changing its expression. Finally, RIP shows that miR-26a targets the 3'UTRs of TGF-betaR2 and UBE3A;LncRNA NORAD regulates HSF proliferation via miR-26a mediating the regulation of TGF-betaR2/R1	33857357	RID05157	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Hypertrophic scar	NORAD	UBE3A	positively-E	Starbase;luciferase reporter assay;RIP	downregulation	qPCR;ELISA	NA	NA	cell proliferation(-)	ceRNA(miR-26a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000114062	NA	647979	7337	LINC00657	ANCR|AS|E6-AP|EPVE6AP|FLJ26981|HPVE6A	LncRNA NORAD regulates scar hypertrophy via miRNA-26a mediating the regulation of TGFbetaR1/2;Hypertrophic scar tissues were collected and assayed for LncRNA NORAD, miR-26a, transforming growth factor beta receptor I (TGF-betaR1) and TGF-betaR2, with enzyme-linked immunosorbent assay (ELISA) or qualitative polymerase chain reaction (qPCR);The binding sites of miRNA-26a and LncRNA NORAD, TGF-betaR2, or UBE3A were predicted using Starbase and confirmed with dual-luciferase reporter assay. RNA immunoprecipitation (RIP) was utilized to explore the interplay of miR-26a with its target genes;LncRNA NORAD is decreased, miR-26a is increased and TGF-beta receptors show abnormal expression in scar tissue;LncRNA NORAD may act as a sponge, binding miR-26a and changing its expression. Finally, RIP shows that miR-26a targets the 3'UTRs of TGF-betaR2 and UBE3A;LncRNA NORAD regulates HSF proliferation via miR-26a mediating the regulation of TGF-betaR2/R1	33857357	RID05158	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD);DATA(GSE40174,GSE104209)
Urinary bladder cancer	SYNE3	CDKN1A	negatively-E	western blot;CRISPR-CasRx	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000176438	GRCh38_14:95407266-95516650	ENSG00000124762	NA	161176	1026	C14orf139|C14orf49|KASH3|LINC00341|NCRNA00341|NET53|Nesp3	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	CRISPR-CasRx Targeting LncRNA LINC00341 Inhibits Tumor Cell Growth in vitro and in vivo;qRT-PCRwas employed to quantify the levels of expression of LINC00341 in tumor tissues along with the matched non-tumor tissues;The expression of p21, Bax as well as E-cadherin were assayed using western blot;The results demonstrated that LINC00341 was overexpressed in bladder cancer in contrast with the healthy tissues;In T24 as well as 5637-cell lines harboring LINC00341-sgRNA, inhibition of cell proliferation ( in vitro and in vivo ), elevated apoptosis rate and diminished migration ability;silencing LINC00341 upregulated the expressions of p21, Bax as well as E-cadherin. Knockout of these genes could eliminate the phenotypic changes caused by sgRNA targeting LINC00341	33855047	RID05159	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Urinary bladder cancer	SYNE3	BAX	negatively-E	western blot;CRISPR-CasRx	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000176438	GRCh38_14:95407266-95516650	ENSG00000087088	NA	161176	581	C14orf139|C14orf49|FLJ25605|LINC00341|NCRNA00341|Nesp3|Nesprin-3|NET53	BCL2L4	CRISPR-CasRx Targeting LncRNA LINC00341 Inhibits Tumor Cell Growth in vitro and in vivo;qRT-PCRwas employed to quantify the levels of expression of LINC00341 in tumor tissues along with the matched non-tumor tissues;The expression of p21, Bax as well as E-cadherin were assayed using western blot;The results demonstrated that LINC00341 was overexpressed in bladder cancer in contrast with the healthy tissues;In T24 as well as 5637-cell lines harboring LINC00341-sgRNA, inhibition of cell proliferation ( in vitro and in vivo ), elevated apoptosis rate and diminished migration ability;silencing LINC00341 upregulated the expressions of p21, Bax as well as E-cadherin. Knockout of these genes could eliminate the phenotypic changes caused by sgRNA targeting LINC00341	33855047	RID05160	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	SYNE3	CDH1	negatively-E	western blot;CRISPR-CasRx	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000176438	GRCh38_14:95407266-95516650	ENSG00000039068	NA	161176	999	C14orf139|C14orf49|FLJ25605|LINC00341|NCRNA00341|Nesp3|Nesprin-3|NET53	CD324|UVO|uvomorulin	CRISPR-CasRx Targeting LncRNA LINC00341 Inhibits Tumor Cell Growth in vitro and in vivo;qRT-PCRwas employed to quantify the levels of expression of LINC00341 in tumor tissues along with the matched non-tumor tissues;The expression of p21, Bax as well as E-cadherin were assayed using western blot;The results demonstrated that LINC00341 was overexpressed in bladder cancer in contrast with the healthy tissues;In T24 as well as 5637-cell lines harboring LINC00341-sgRNA, inhibition of cell proliferation ( in vitro and in vivo ), elevated apoptosis rate and diminished migration ability;silencing LINC00341 upregulated the expressions of p21, Bax as well as E-cadherin. Knockout of these genes could eliminate the phenotypic changes caused by sgRNA targeting LINC00341	33855047	RID05161	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	LINC00221	MMP11	positively-E	luciferase reporter assay;RNA pull-down assay;bioinformatics;RIP	upregulation		NA	NA	cancer progression(+)	ceRNA(let-7a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000187156	NA	ENSG00000099953	NA	338005	4320	C14orf98|NCRNA00221	STMY3	LINC00221 silencing prevents the progression of hepatocellular carcinoma through let-7a-5p-targeted inhibition of MMP11;microarray profiles of hepatocellular carcinoma (HCC) identified that long intergenic noncoding RNA 00221 (LINC00221) was upregulated;Online prediction showed the potential binding relationship between LINC00221 and let-7a-5p, as well as that between let-7a-5p and matrix metalloproteinase 11 (MMP11). The results of luciferase, RNA immunoprecipitation, and RNA pull-down assays identified that LINC00221 interacted with let-7a-5p to increase expression of MMP11. Furthermore, we demonstrated that LINC00221 silencing increased let-7a-5p and inhibited MMP11 expression, thereby delaying the progression of HCC in vitro	33836753	RID05162	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Gastric cancer	MAGI1-IT1	IGF1	positively-E	Starbase;luciferase reporter assay;RIP;bioinformatics;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272610	GRCh38_3:65872815-65954558	ENSG00000017427	NA	151877	3479	NA	IGF|IGF-I|IGF1A|IGFI	The Long Noncoding RNA MAGI1-IT1 Regulates the miR-302d-3p/IGF1 Axis to Control Gastric Cancer Cell Proliferation;120 pairs of GC patient tumor, paracancerous tissues, human GES-1 control cells and human AGS, MKN-74, MKN-45, and MGC-803 GC cell lines were used to detected MAGI1-IT1, miR-302d-3p, and IGF1 expression by a qPCR approach;Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival;Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target;IGF1 was subsequently identified as a miR-302d-3p target gene that was upregulated by MAGI1-IT1 through miR-302d-3p;Starbase v2.0 was next employed to identify miR-302d-3p as a putative target for MAGI1-IT1 (Figure 3A). Luciferase reporter assays confirmed the ability of MAGI1-IT1 and miR-302d-3p to interact with one another (Figure 3B), and MAGI1-IT1 knockdown resulted in miR-302d-3p upregulation (Figure 3C). Anti-Ago2 RIP assays additionally confirmed MAGI1 IT1 and miR-302d-3p enrichment in Ago2 complexes (Figure 3D). When we assessed miR-302d-3p expression in GC tissues, we determined that this miRNA was expressed at lower levels in GC patient tumor tissues relative to paracancerous tissues (Figure 3E). Pearson correlation analyses further confirmed MAGI1-IT1 and miR-302d-3p levels to be negatively correlated with one another in GC tissues (Figure 3F).	33833579	RID05163	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Gastric cancer	MAGI1-IT1	miR-302d-3p	negatively-E	Starbase;luciferase reporter assay;RIP;bioinformatics;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000272610	GRCh38_3:65872815-65954558	NA	NA	151877	NA	NA	NA	The Long Noncoding RNA MAGI1-IT1 Regulates the miR-302d-3p/IGF1 Axis to Control Gastric Cancer Cell Proliferation;120 pairs of GC patient tumor, paracancerous tissues, human GES-1 control cells and human AGS, MKN-74, MKN-45, and MGC-803 GC cell lines were used to detected MAGI1-IT1, miR-302d-3p, and IGF1 expression by a qPCR approach;Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival;Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target;IGF1 was subsequently identified as a miR-302d-3p target gene that was upregulated by MAGI1-IT1 through miR-302d-3p;Starbase v2.0 was next employed to identify miR-302d-3p as a putative target for MAGI1-IT1 (Figure 3A). Luciferase reporter assays confirmed the ability of MAGI1-IT1 and miR-302d-3p to interact with one another (Figure 3B), and MAGI1-IT1 knockdown resulted in miR-302d-3p upregulation (Figure 3C). Anti-Ago2 RIP assays additionally confirmed MAGI1 IT1 and miR-302d-3p enrichment in Ago2 complexes (Figure 3D). When we assessed miR-302d-3p expression in GC tissues, we determined that this miRNA was expressed at lower levels in GC patient tumor tissues relative to paracancerous tissues (Figure 3E). Pearson correlation analyses further confirmed MAGI1-IT1 and miR-302d-3p levels to be negatively correlated with one another in GC tissues (Figure 4F).	33833579	RID05164	expression association	NA	UP(LIHC);DATA(GSE117623)	
Lung adenocarcinoma	MSC-AS1	GPAM	positively-E		upregulation		NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-33b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000235531	GRCh38_8:71828167-72118393	ENSG00000119927	NA	100132891	57678	NA	GPAT1|KIAA1560|MGC26846	LncRNA MSC-AS1 facilitates lung adenocarcinoma through sponging miR-33b-5p to up-regulate GPAM;We found that the expression of MSC-AS1 was significantly higher in LUAD tissues and cells than that in normal ones;we confirmed that the proliferation of LUAD cells was significantly restrained by down-regulation of MSC-AS1 and the rate of cell apoptosis was accelerated;The results from our mechanistic experiments showed that MSC-AS1 interacts with microRNA-33b-5p (miR-33b-5p);glycerol-3-phosphate acyltransferase, mitochondrial (GPAM) was found to be a direct target gene of miR-33b-5p, and it has similar functions to MSC-AS1;inhibition of miR-33b-5p or overexpression GPAM reversed the inhibitory effects of MSC-AS1 silencing on LUAD cell growth	33821667	RID05165	ceRNA or sponge	NA		UP(LIHC);DOWN(NSCLC);DATA(GSE117623,GSE74639)
Non-small cell lung cancer	SNHG4	KDM3A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);colony formation(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-let-7e)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000115548	NA	724102	55818	NCRNA00059|U19H	JHMD2A|JMJD1|JMJD1A|KIAA0742|TSGA	The long non-coding RNA SNHG4/microRNA-let-7e/KDM3A/p21 pathway is involved in the development of non-small cell lung cancer;A dual-luciferase reporter gene assay was used to examine lncRNA SNHG4 binding with miR-let-7e and miR-let-7e binding with lysine demethylase 3A (KDM3A);lncRNAs SNHG4 and KDM3A were both upregulated in NSCLC tissues;lncRNA SNHG4 was found to bind to miR-let-7e that negatively targeted KDM3A. KDM3A inhibited p53-K372me1, thus reducing p21 expression.  The NSCLC development was inhibited by downregulating lncRNA SNHG4 in nude mice;The knockdown of lncRNA SNHG4 or KDM3A inhibited H1299 cell viability, colony formation, invasion, migration, and cycle progression while inducing apoptosis;we initially identified the expression of lncRNA SNHG4 in 50 cancerous tissues and matched noncancerous lung tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR	33816782	RID05166	ceRNA or sponge	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	VESTAR	ELAVL1	positively-F		upregulation		NA	NA	prognosis(-)	NA	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000066044	NA	NA	1994	NA	Hua|HUR|MelG	Mechanistically, VESTAR directly bound and stabilized VEGFC mRNA. VESTAR also interacted with HuR, a positive regulator of VEGFC mRNA stability, and increased HuR binding to VEGFC mRNA.	33771898	RID05167	expression association	prognosis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	VESTAR	ELAVL1	positively-F		upregulation		NA	NA	prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000066044	NA	NA	1994	NA	Hua|HUR|MelG	Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability;VESTAR was overexpressed in ESCC tissues and was predictive of poor prognosis in patients with ESCC;VESTAR directly bound and stabilized VEGFC mRNA. VESTAR also interacted with HuR, a positive regulator of VEGFC mRNA stability, and increased HuR binding to VEGFC mRNA;In ESCC, NXF1 and SRSF3 facilitated nuclear export of VESTAR to the cytoplasm, which was associated with lymph node metastasis	33771898	RID05168	interact with protein	metastasis,prognosis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	NXF1	VESTAR	positively-F		upregulation		NA	NA	prognosis(-);cell metastasis(+)	NA	association	protein-RNA	NA	NA	NA	Cancer	Esophageal cancer	PCG	lncRNA	ENSG00000162231	NA	NA	NA	10482	NA	DKFZp667O0311|Mex67|TAP	NA	Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability;VESTAR was overexpressed in ESCC tissues and was predictive of poor prognosis in patients with ESCC;VESTAR directly bound and stabilized VEGFC mRNA. VESTAR also interacted with HuR, a positive regulator of VEGFC mRNA stability, and increased HuR binding to VEGFC mRNA;In ESCC, NXF1 and SRSF3 facilitated nuclear export of VESTAR to the cytoplasm, which was associated with lymph node metastasis	33771898	RID05169	expression association	metastasis,prognosis	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)	
Esophagus squamous cell carcinoma	SRSF3	VESTAR	positively-F		upregulation		NA	NA	prognosis(-);cell metastasis(+)	NA	association	protein-RNA	NA	NA	NA	Cancer	Esophageal cancer	PCG	lncRNA	ENSG00000112081	NA	NA	NA	6428	NA	SFRS3|SRp20	NA	Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability;VESTAR was overexpressed in ESCC tissues and was predictive of poor prognosis in patients with ESCC;VESTAR directly bound and stabilized VEGFC mRNA. VESTAR also interacted with HuR, a positive regulator of VEGFC mRNA stability, and increased HuR binding to VEGFC mRNA;In ESCC, NXF1 and SRSF3 facilitated nuclear export of VESTAR to the cytoplasm, which was associated with lymph node metastasis	33771898	RID05170	expression association	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Hepatocellular carcinoma	MROCKI	MAP3K7	positively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227502	GRCh38_6:113868013-113873390	ENSG00000135341	NA	285758	6885	LINC01268|LOC285758|ROCKI	MEKK7|TAK1	High Expression of LINC01268 is Positively Associated with Hepatocellular Carcinoma Progression via Regulating MAP3K7;Expression level and localization of LINC01268 in human liver cancer cells and HCC tissues were investigated using RT-qPCR and fluorescent in situ hybridization (FISH), respectively;we identified that LINC01268 was highly expressed in HCC cell lines and tissues;Co-expression analysis implied an interaction between LINC01268 and MAP3K7. Similar to LINC01268, MAP3K7 was highly expressed in HCC cells, and positively correlated with moderate/poor differentiation as well as poor prognosis;Knockdown of LINC01268 in HCC cell lines led to reduction of MAP3K7 at both mRNA and protein levels;Knockdown of LINC01268 inhibited the proliferation of HCC cells, which was enhanced by overexpression of LINC01268	33727826	RID05171	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Multiple myeloma	RP11-301G19.1	HMGB2	positively-E	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-582-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	TF	ENSG00000227706	GRCh38_6:67878316-67889339	ENSG00000164104	NA	NA	3148	NA	HMG2	The LncRNA RP11-301G19.1/miR-582-5p/HMGB2 axis modulates the proliferation and apoptosis of multiple myeloma cancer cells via the PI3K/AKT signalling pathway;Our results demonstrated that RP11-301G19.1 was upregulated in MM cell lines and that its downregulation inhibited the proliferation and cell cycle progression and promoted the apoptosis of MM cells;Bioinformatic analysis and luciferase reporter assay results revealed that RP11-301G19.1 can upregulate the miR-582-5p-targeted gene HMGB2 as a competing endogenous RNA (ceRNA);The levels of RP11-301G19.1 in the MM cells and nPCs were assessed by qRT-PCR RP11-301G19.1 expression was significantly higher in the MM cells than in the nPCs	33707625	RID05172	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatoblastoma	ARID1B	HOXA-AS2	positively-E	ChIP;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000049618	NA	ENSG00000253552	GRCh38_7:27107777-27134302	57492	285943	6A3-5|BAF250b|DAN15|ELD/OSA1|KIAA1235|p250R|SMARCF2	HOXA3as	ARID1B/SUB1-activated lncRNA HOXA-AS2 drives the malignant behaviour of hepatoblastoma through regulation of HOXA3;In our previous study, genome-wide analysis with a lncRNA microarray found that lncRNA HOXA-AS2 was up-regulated in HB;Mechanistic investigations indicated that HOXA-AS2 was modulated by chromatin remodelling factor ARID1B and transcription co-activator SUB1, thereby protecting HOXA3 from degradation. Therefore, HOXA-AS2 positively regulates HOXA3, which might partly demonstrate the involvement of HOXA3 in HOXA-AS2-mediated HB carcinogenesis;Our data revealed knockdown of HOXA-AS2 increased cell apoptosis and inhibited cell proliferation, migration and invasion in HB;The qRT-PCRresults showed that HOXA-AS2 expression was obviously up-regulated in HB tissues;With the use of the University of California, Santa Cruz Genome Browser database, we found that ARID1B may bind to the HOXA AS2 promoter region. Chromatin immunoprecipitation coupled with qRT-PCRconfirmed that ARID1B combined with the HOXA AS2 promoter region at a position located 1 400 bp upstream of the transcription start site (Figure 6B,C). Immunoprecipitation of ARID1B identified SUB1, a transcriptional co factor (Figure 6D). To explore the influence of ARID1B and SUB1 on HOXA AS2, shRNA and overexpression assays were performed, respectively (Figure 6E H). The qRT-PCRresults demonstrated that knockdown of ARID1B or overexpression of SUB1 induced the expression of HOXA AS2 (Figure 6I,J). Consistent with these findings, immunohistochemistry results found that ARID1B was down regulated in HB, while HOXA3 was up regulated, as compared with adjacent normal liver tissues	33683826	RID05173	expression association	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(NSCLC);DATA(GSE74639)
Hepatoblastoma	SUB1	HOXA-AS2	positively-E	ChIP;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000113387	NA	ENSG00000253552	GRCh38_7:27107777-27134302	10923	285943	p14|p15|PC4	HOXA3as	ARID1B/SUB1-activated lncRNA HOXA-AS2 drives the malignant behaviour of hepatoblastoma through regulation of HOXA3;In our previous study, genome-wide analysis with a lncRNA microarray found that lncRNA HOXA-AS2 was up-regulated in HB;Mechanistic investigations indicated that HOXA-AS2 was modulated by chromatin remodelling factor ARID1B and transcription co-activator SUB1, thereby protecting HOXA3 from degradation. Therefore, HOXA-AS2 positively regulates HOXA3, which might partly demonstrate the involvement of HOXA3 in HOXA-AS2-mediated HB carcinogenesis;Our data revealed knockdown of HOXA-AS2 increased cell apoptosis and inhibited cell proliferation, migration and invasion in HB;The qRT-PCRresults showed that HOXA-AS2 expression was obviously up-regulated in HB tissues;	33683826	RID05174	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807,GSE67939)	UP(NSCLC);DATA(GSE74639)
Hepatoblastoma	HOXA-AS2	HOXA3	positively-E	ChIP;qRT-PCR	upregulation	microarray;qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000105997	NA	285943	3200	HOXA3as	HOX1|HOX1E	ARID1B/SUB1-activated lncRNA HOXA-AS2 drives the malignant behaviour of hepatoblastoma through regulation of HOXA3;In our previous study, genome-wide analysis with a lncRNA microarray found that lncRNA HOXA-AS2 was up-regulated in HB;Mechanistic investigations indicated that HOXA-AS2 was modulated by chromatin remodelling factor ARID1B and transcription co-activator SUB1, thereby protecting HOXA3 from degradation. Therefore, HOXA-AS2 positively regulates HOXA3, which might partly demonstrate the involvement of HOXA3 in HOXA-AS2-mediated HB carcinogenesis;Our data revealed knockdown of HOXA-AS2 increased cell apoptosis and inhibited cell proliferation, migration and invasion in HB;The qRT-PCRresults showed that HOXA-AS2 expression was obviously up-regulated in HB tissues;The results of qRT-PCRand western blot showed that knockdown of HOXA AS2 decreased HOXA3 expression, while overexpression of HOXA AS2 increased HOXA3 expression	33683826	RID05175	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Colorectal cancer	XIST	miR-125b-2-3p	negatively-F	luciferase reporter assay;bioinformatics;western blot	upregulation		NA	NA	cell proliferation(+);chemoresistance(+);epithelial to mesenchymal transition(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	The lncRNA XIST/miR-125b-2-3p axis modulates cell proliferation and chemotherapeutic sensitivity via targeting Wee1 in colorectal cancer;Based on multiple databases, the upstream competitive endogenous RNAs (ceRNAs) and the downstream genes for miR-125b-2-3p were predicted by bioinformatic analysis, followed by the experiments including luciferase reporter assays, western blot assays, and so on;miR-125b-2-3p was absorbed by long noncoding RNA (lncRNA) XIST regulating WEE1 G2 checkpoint kinase (WEE1) expression. The upregulation of miR-125b-2-3p inhibited the proliferation and epithelial-mesenchymal transition (EMT) of CRC induced by lncRNA XIST;LncRNA XIST promoted CRC metastasis acting as a ceRNA for miR-125b-2-3p to mediate WEE1 expression;Based on our previous studies, lncRNA XIST was significantly upregulated and promoted proliferation and metastasis in CRC and gastric cancer (GC)	33666372	RID05176	ceRNA or sponge	metastasis,chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Cerebral ischemia-reperfusion injury	XIST	GAB2	positively-E	luciferase reporter assay;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell viability(-);apoptosis process(+)	ceRNA(miR-486-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000033327	NA	7503	9846	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	KIAA0571	Long noncoding RNA XIST enhances cerebral ischemia-reperfusion injury by regulating miR-486-5p and GAB2;RT-qPCR assay was performed to detect the mRNA expression of XIST, GAB2 and miR-486-5p. The correlation between XIST and miR-486-5p, miR-486-5p and GAB2 were verified by RT-qPCR assay and dual-luciferase reporter assay;XIST and GAB2 were significantly highly expressed, while miR-486-5p was low expressed in SH-SY5Y cells under I/R; For our experiment, miR-486-5p was a target of XIST, and GAB2 was a downstream gene of miR-486-5p;Moreover, XIST was found to restrain cell viability and induce cell apoptosis	33660813	RID05177	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatitis	TUG1	TNF	positively-E	miRanda;Targetscan;luciferase reporter assay;RNAi;RIP	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Liver disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000228978	NA	55000	7124	FLJ20618|LINC00080|NCRNA00080	DIF|TNF-alpha|TNFA|TNFSF2	Silencing lncRNA TUG1 Alleviates LPS-Induced Mouse Hepatocyte Inflammation by Targeting miR-140/TNF;microarray showed that lncRNA TUG1 was upregulated in LPS-induced hepatocyte inflammation;TUG1 acted as a sponge of miR-140, and miR-140 directly targeted TNFalpha (TNF);Functional analysis showed that si-TUG1 inhibited LPS-induced inflammation response in mice liver, inhibited apoptosis level, and protected liver function;qRT-PCRalso indicated that TUG1 was upregulated in LPS-treated liver tissues compared with saline-treated liver tissues;we used miRanda database and found a potential binding between TUG1 and miR-140-5p (miR-140) (Figure 4A). Then, luciferase assay showed miR-140 inhibited activity of WT TUG1 not mut TUG1 in HEK293 cells (Figure 4B). Overexpression of TUG1 inhibited miR-140 level, while silencing of TUG1 promoted miR-140 level in AML12 cells;Through Targetscan, we found base pairing of miR-140 and TNFalpha (TNF) (Figure 5A). The following luciferase analysis suggested miR-140 directly inhibited TNF expression (Figure 5B). Furthermore, miR-140 suppressed TNF mRNA and protein expression, but AMO-140 increased TNF level in AML12 cells (Figures 5C,D). RIP assay showed enrichment of miR-140 in biotinylated TNF cells (Figure 5E).	33644034	RID05178	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Kidney injury	RMRP	DDX5	positively-E		upregulation	RT-qPCR	NA	NA	inflammatory response(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000263077	NA	6023	1655	CHH|NME1|RMRPR|RRP2	G17P1|HLR1|p68	Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury;RMRP was upregulated in sera from patients with AKI and in LPS-induced cells;We found that microRNA 206 (miR-206) binds with and is negatively regulated by RMRP: miR-206 directly targets the 3' untranslated region of DEAD-box helicase 5 (DDX5) and negatively regulates DDX5 expression. By binding with miR-206, RMRP upregulated DDX5 expression;The lncRNA RMRP contributes to sepsis-induced AKI through upregulation of DDX5 in a miR-206 dependent manner and through activation of NLRP3 inflammasome; According to the results of RT-qPCR, RMRP expression was upregulated in the sera of septic patients with AKI, compared with that from healthy individuals;Searching the starBase website, we found that seven miRNAs (miR-206, miR-766-5p, miR-1-3p, miR-613, miR-580-3p, miR-3142, and miR-1245b-5p) harbored binding sites on RMRP. Subsequent RT-qPCR analysis showed that only miR-206 was downregulated in response to LPS stimulation in HK-2 cells;We discovered that luciferase activity of pmirGLO-RMRP-Wt was significantly decreased by miR-206 mimics, while no significant change was observed in pmirGLO-RMRP-Mut groups (Fig. 4C), indicating that miR-206 can bind with RMRP at the predicted sites	33635017	RID05179	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney injury	RMRP	NLRP3	positively-E		upregulation	RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000162711	NA	6023	114548	CHH|NME1|RMRPR|RRP2	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCU|MWS|NALP3|PYPAF1	Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury;RMRP was upregulated in sera from patients with AKI and in LPS-induced cells;We found that microRNA 206 (miR-206) binds with and is negatively regulated by RMRP: miR-206 directly targets the 3' untranslated region of DEAD-box helicase 5 (DDX5) and negatively regulates DDX5 expression. By binding with miR-206, RMRP upregulated DDX5 expression;The lncRNA RMRP contributes to sepsis-induced AKI through upregulation of DDX5 in a miR-206 dependent manner and through activation of NLRP3 inflammasome; According to the results of RT-qPCR, RMRP expression was upregulated in the sera of septic patients with AKI, compared with that from healthy individuals	33635017	RID05180	expression association	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Chronic periodontitis	MALAT1	HIF3A	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(-);inflammatory response(+);apoptosis process(+)	ceRNA(miR-769-5p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Periodontitis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124440	NA	378938	64344	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	bHLHe17|IPAS|MOP7|PASD7	Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis;Quantitative real-time PCR (qRT-PCR was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs;Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A;The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs;MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression;miR-769-5p targeted HIF3A and negatively modulated HIF3A expression;MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs	33604388	RID05181	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Endometrial cancer	MCTP1-AS1	miR-650	negatively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000249545	GRCh38_5:94979151-94980893	NA	NA	113523641	NA	NA	NA	LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis;MTCP1-AS1 expression level was determined in human EC tissues and cell lines by qRT-PCR;luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR-650, MCTP1-AS1 and SMAD7 in EC cells;MCTP1-AS1 was proved to be the target of miR-650 and reversely correlated with its expression;Our data showed that MCTP1-AS1 expression was downregulated in EC tissues and cell lines	33568915	RID05182	ceRNA or sponge	NA		
Glioblastoma	GAS8-AS1	NEAT1	negatively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(-)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	lncRNA	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000245532	GRCh38_11:65422774-65445540	750	283131	C16orf3	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	LncRNA GAS8-AS1 downregulates lncRNA NEAT1 to inhibit glioblastoma cell proliferation;The expression levels of GAS8-AS1 and NEAT1 in GBM patients and the healthy controls were measured by performing RT-qPCR;GAS8-AS1 was downregulated, while lncRNA NEAT1 was upregulated in the plasma of GBM patients;The expression of GAS8-AS1 and NEAT1 was inversely correlated only in GBM patients. Overexpression of GAS8-AS1 reduced the expression levels of NEAT1 in GBM cells, while knock-down of GAS8-AS1 increased the expression levels of NEAT1.  However, overexpression of NEAT1 showed no significant effects on the expression of GAS8-AS1. Knock-down of GAS8-AS1 promoted GBM cell proliferation and invasion and enhanced the activation of the Wnt/beta-catenin pathway. However, the effects of knock-down of GAS8-AS1 were alleviated by the knock-down of NEAT1. Overexpression of GAS8-AS1 inhibits GBM cell proliferation and invasion by downregulating NEAT1	33942556	RID05183	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Hemangioma	MEG8	NOTCH2	positively-E	luciferase reporter assay			NA	NA	cell proliferation(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000258399	GRCh38_14:100836269-100947194	ENSG00000134250	NA	79104	4853	AL132709.8|Bsr|Irm|LINC00024|lnc-MGC|NCRNA00024|Rian|SNHG23|SNHG24	NA	Silencing long non-coding RNA MEG8 inhibits the proliferation and induces the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis;Using a dual-luciferase assay, we confirmed the binding between MEG8 and miR-497-5p, and between the miR-497-5p and 3'UTR of NOTCH2;	33839417	RID05184	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	ATP2B1-AS1	ZC3H12A	positively-E	RT-qPCR;luciferase reporter assay;RNA pull-down assay;bioinformatics;	downregulation	RT-qPCR;western blot	NA	NA	immune evasion(+);cell invasion(+);apoptosis process(-);cytotoxicity(-)	ceRNA(miR-425-3p)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000271614	GRCh38_12:89708959-89712590	ENSG00000163874	NA	338758	80149	LINC00936	FLJ23231|MCPIP1|Regnase-1	Elevated linc00936 or silenced microRNA-425-3p inhibits immune escape of gastric cancer cells via elevation of ZC3H12A;Elevated miR-425-3p and reduced linc00936, and ZC3H12A expression levels were found in GC tissues and cells;Up-regulating linc00936 or down-regulating miR-425-3p inhibited immune escape, migration, promoted apoptosis of GC cells, as well induced CIK cell cytotoxicity to GC cells;The study concludes that up-regulated linc00936 or silenced miR-425-3p inhibits immune escape of GC cells via elevation of ZC3H12A;Linc00936, miR-425-3p and ZC3H12A expression in GC tissues and adjacent tissues were detected by RT-qPCR and western blotLinc00936, miR-425-3p and ZC3H12A expression levels in MKN-45 cells were detected by RT-qPCR and western blot(Fig. 3G I). As indicated, down-regulating linc00936 reduced linc00936 and ZC3H12A and increased miR-425-3p levels. Up-regulating miR-425-3p elevated miR-425-3p and decreased ZC3H12A levels. Inhibition of miR- 425-3p weakened linc00936 suppression-induced effects on miR-425-3p and ZC3H12A levels;Linc00936 competitively binds with miR-425-3p to regulate ZC3H12A;The results of dual luciferase reporter gene assay in BGC-823 and MKN-45 cells exhibited that (Fig. 6B, C) the luciferase activity of linc00936-WT in the miR-425-3p mimic group was decreased, while the luciferase activity of linc00936-MUT in the miR-425-3p mimic group had no apparent changes. RNA-pull down assay results showed that (Fig. 6D, E) the enrichment level of linc00936 was clearly increased in the Bio-miR-425-3p-WT group, while no clear difference exhibited in the enrichment level of linc00936 in the Bio-miR-425-3p-MUT group. These results indicated that linc00936 could competitively bind with miR-425-3p, thereby affecting miR-425-3p expression	33756228	RID05185	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	TCONS_00023297	MIR608	negatively-F	luciferase reporter assay;RIP	upregulation	microarray;qRT-PCR	NA	NA	cell differentiation(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	ENSG00000207551	NA	NA	693193	NA	MIRN608|hsa-mir-608	LncRNA TCONS_00023297 Regulates the Balance of Osteogenic and Adipogenic Differentiation in Bone Marrow Mesenchymal Stem Cells and the Coupling Process of Osteogenesis and Angiogenesis;The expression of lncRNAs in the osteogenic differentiation of hBMSCs was detected by lncRNA microarray. Real-time quantitative PCR was used to detect the expression changes of lncRNA and osteogenic genes during hBMSC osteogenic and adipogenic differentiation;The ceRNA mechanisms were detected by RIP and luciferase reporter gene assays;TCONS_00023297 increased expression during osteogenic differentiation;TCONS_00023297 regulated miR-608 via a ceRNA mechanism;TCONS_00023297 regulates osteogenic differentiation, adipogenic differentiation, and osteogenic-angiogenic coupling of hBMSCs via the TCONS_00023297/miR-608/RUNX2/SHH signaling axis	34262909	RID05186	ceRNA or sponge	NA		
Sinonasal squamous cell carcinoma	LINC02200	NFKB1	positively-F	western blot;ChIP;RIP	upregulation	RNAscope	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Squamous cell carcinoma	lncRNA	TF	ENSG00000250358	GRCh38_5:112628436-112682077	ENSG00000109320	NA	102467214	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	The function and mechanism of long non-coding RNA RP11-159K7.2 in sinonasal squamous cell carcinoma;The expression of RP11-159K7.2 in SNSCC tissue was significantly higher than that in adjacent tissues;RP11-159K7.2 directly bound to nuclear factor-kB (NF-kB) in SNSCC cells, and the regulation of RP11-159K7.2 on the proliferation and invasion of SNSCC cells depended on NF-kB;Mechanically, the protein chip, western blot and RNA immunoprecipitation were performed to identify the proteins bound by RP11-159K7.2;he expression of RP11-159K7.2 in SNSCC and adjacent tissues was detected by RNAscope in situ hybridization to observe its association with prognosis	34256488	RID05187	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Mycoplasma pneumoniae pneumonia	NKILA	NFKB1	positively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Respiratory system disease	Bacterial pneumonia	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Attenuated lncRNA NKILA Enhances the Secretory Function of Airway Epithelial Cells Stimulated by Mycoplasma pneumoniae via NF-kB;The results suggested that NKILA was downregulated in children with MPP, while IL-8 and TNF-alpha levels increased;we detected NKILA in the BALF of 38 hospitalized children with MPP and 30 children with FB using qRT-PCRhe effects of NKILA on NF-kB activity were examined by the dual-luciferase reporter assay. The results showed that MP treatment increased NF-kB transcriptional activity, while knockdown of NKILA further increased NF-kB activity;We observed roughly sevenfold enrichment of IkBalpha in the immunoprecipitates compared to the IgG control (Figure 4(c)), indicating that NKILA physically associates with IkBalpha;we conclude that attenuating lncRNA NKILA enhances the secretory function of airway epithelial cells stimulated by MP via regulation of NF-kB signaling	33855076	RID05188	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Mycoplasma pneumoniae pneumonia	NKILA	IkBalpha	positively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+)	interact with protein;phosphorylation	binding/interaction	RNA-protein	NA	NA	NA	Respiratory system disease	Bacterial pneumonia	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	Attenuated lncRNA NKILA Enhances the Secretory Function of Airway Epithelial Cells Stimulated by Mycoplasma pneumoniae via NF-kB;The results suggested that NKILA was downregulated in children with MPP, while IL-8 and TNF-alpha levels increased;we detected NKILA in the BALF of 38 hospitalized children with MPP and 30 children with FB using qRT-PCRhe effects of NKILA on NF-kB activity were examined by the dual-luciferase reporter assay. The results showed that MP treatment increased NF-kB transcriptional activity, while knockdown of NKILA further increased NF-kB activity;We observed roughly sevenfold enrichment of IkBalpha in the immunoprecipitates compared to the IgG control (Figure 4(c)), indicating that NKILA physically associates with IkBalpha	33855076	RID05189	interact with protein	NA		
Liver cancer	ADAMTS9-AS2	ADAMTS9	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000163638	NA	100507098	56999	NA	KIAA1312	Long non-coding RNA ADAMTS9-AS2 inhibits liver cancer cell proliferation, migration and invasion;The results indicated that ADAMTS9-AS2 overexpression and knockdown increased and decreased ADAMTS9 mRNA and protein expression levels, respectively, indicating that alterations in ADAMTS9 expression corresponded with ADAMTS9-AS2 expression;the expression of ADAMTS9-AS2 was detected in a normal liver cell line (MIHA) and three liver cancer cell lines (HepG2, MHCC97-H and Hep 3B2.1-7) via RT-qPCR;Compared with MIHA cells, ADAMTS9-AS2 expression levels were significantly upregulated in Hep 3B2.1-7 cells (P<0.001) and significantly downregulated in HepG2 and MHCC97-H cells (both P<0.01);The results indicated that ADAMTS9-AS2 overexpression or knockdown resulted in increased and decreased ADAMTS9 expression levels, respectively;ADAMTS9-AS2 inhibits liver cancer cell proliferation, migration and invasion	33850531	RID05190	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DATA(GSE117623)
Coronary artery disease	TONSL-AS1	MIR197	negatively-F	IntaRNA2.0	downregulation	qRT-PCR	NA	NA	cell migration(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000232600	GRCh38_8:144437675-144439971	ENSG00000207709	NA	100287098	406974	NA	MIRN197|miR-197|miRNA197	LncRNA TONSL-AS1 participates in coronary artery disease by interacting with miR-197;The interaction between TONSL-AS1 and miR-197 was predicted by IntaRNA2.0;TONSL-AS1 was downregulated in CAD;Overexpression experiments showed that TONSL-AS1 and miR-197 had no significant effect on the expression of each other. We speculated that MAFG-AS1 may sponge miR-145;overexpression of TONSL-AS1 attenuated the effects of overexpression of miR-197 on migration and apoptosis of HCAECs;The expression levels of TONSL-AS1 and miR-197 in plasma samples of CAD patients (n =60) and healthy controls (n =60) were measured by RT-qPCR. Compared with the control group, the expression levels of TONSL-AS1 were significantly lower in CAD group (Fig. 1A, p <0.05). In contrast, the expression levels of miR-197 were significantly higher in CAD group than that in the control group (Fig. 1B, p <0.05).	33662410	RID05191	ceRNA or sponge	NA		
Colorectal cancer	LINC00922	LZTS1	negatively-E	RNAi;qRT-PCRSP	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000261742	GRCh38_16:65284496-65576345	ENSG00000061337	NA	283867	11178	Lnc-LALC	FEZ1	Long non-coding RNA Lnc-LALC facilitates colorectal cancer liver metastasis via epigenetically silencing LZTS1;We found that upregulated Lnc-LALC in CRC was negatively correlated with LZTS1 expression, and Lnc-LALC could regulate LZTS1 expression in both mRNA and protein level in our study;Lnc-LALC enhanced the CRC cells metastasis ability in vitro and vivo through inhibiting the expression of LZTS1;the precise mechanisms exploration showed that lnc-LALC could recruit DNA methyltransferases (DNMTs) to the LZTS1 promoter by combining with Enhancer of zeste homolog 2(EZH2) and then altered the expression of LZTS1 via DNMTs-mediated DNA methylation;qRT-PCRresults revealed that LZTS1 was downregulated in CRC cell lines when the NCM460 cells were used as a control;A Methylation specific PCR (MSP) revealed that the promoter region of LZTS1 was hypermethylated in CRC cells but hypomethylated in the NCM460 cells	33637680	RID05192	epigenetic regulation	metastasis		UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Colon cancer	SLCO4A1-AS1	SLCO4A1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay		RT-qPCR;western blot	NA	NA	cancer progression(+)	ceRNA(miR-150-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000101187	NA	100127888	28231	NA	OATP-E|OATP4A1|SLC21A12	LncRNA SLCO4A1-AS1 modulates colon cancer stem cell properties by binding to miR-150-3p and positively regulating SLCO4A1;and the expression of SLCO4A1-AS1 and SLCO4A1 in colon cancer tissues was determined using reverse transcription quantitative polymerase chain reaction and western blotThe interaction among SLCO4A1-AS1, microRNA-150-3p (miR-150-3p) and SLCO4A1 was verified using dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down;SLCO4A1-AS1 was confirmed to competitively bind to miR-150-3p to elevate SLCO4A1 expression;these findings provide evidence demonstrating that depleting SLCO4A1-AS1 competitively binds to miR-150-3p, which downregulates SLCO4A1 expression, thus hindering colon cancer progression	33958701	RID05193	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(SKCM);DATA(GSE38495)
Esophageal cancer	ENST00000437781.1	SIX4	negatively-E	RNAi;bioinformatics	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	NA	NA	ENSG00000100625	NA	NA	51804	NA	AREC3	Identification of crucial long non-coding RNAs and mRNAs along with related regulatory networks through microarray analysis in esophageal carcinoma;2052 lncRNAs and 3240 mRNAs were found to be differentially expressed in 5 EC tumor tissues versus adjacent normal tissues by microarray analysis;we demonstrated that ENST00000437781.1 knockdown inhibited cell proliferation and facilitated cell apoptosis by downregulating SIX homeobox 4 (SIX4) and ENST00000524987.1 knockdown had no influence on anoctamin 1 calcium activated chloride channel (ANO1) expression in EC cells;Considering the high expression of ENST00000437781.1 (p39026_v4 probe; 14.6-fold upregulation) and SIX4 (A_32_P204205 probe; 10.5-fold upregulation) in EC tissues (Excel 1A and Excel 4B sheet 1) and strong positive association between ENST00000437781.1 and SIX4 in EC tissues along with their putative trans-regulation relationships (miRNA sequestration) (Excel 4B sheet 2), the effect of ENST00000437781.1 knockdown on SIX4 (a carcinoma-related gene annotated by KEGG pathway database) expression was measured by RT-qPCR assay in Eca-109 cells. Transfection efficiency analysis showed that the transfection of ENST00000437781.1-siRNA1 and ENST00000437781.1-siRNA2 could remarkably reduce ENST00000437781.1 expression in Eca-109 cells (Fig. 5a). RT-qPCR assay showed that the depletion of ENST00000437781.1 mediated by ENST00000437781.1siRNA1 led to the notable reduction of SIX4 mRNA level;RT-qPCR assay demonstrated that ENST00000524987.1, ANO1, ENST00000437781.1, and SIX4 expression levels were noticeably increased in 20 cases of EC tissues than those in adjacent normal tissues;correlation analysis validated that ENST00000437781.1 expression level was positively associated with SIX4 expression level (Fig. 6f), whereas there was no significant association between ENST00000524987.1 and	33864185	RID05194	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065)
Atherosclerosis	ZEB1-AS1	ETS1	positively-E			qRT-PCR	NA	NA	TGF-beta/SMAD signaling pathway(+);cell injury(+)	ceRNA(miR-590-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000134954	NA	220930	2113	NA	ETS-1|EWSR2|FLJ10768	Exosomes-Mediated LncRNA ZEB1-AS1 Facilitates Cell Injuries by miR-590-5p/ETS1 Axis Through the TGF-beta/Smad Pathway in Oxidized Low-density Lipoprotein-induced Human Umbilical Vein Endothelial Cells;Quantitative real-time polymerase chain reaction was conducted to measure the expression of ZEB1-AS1, microRNA-590-5p (miR-590-5p), or erythroblastosis virus E26 oncogene homolog 1 (ETS1) in cells or exosomes;ZEB1-AS1 sponged miR-590-5p to regulate ETS1 expression;our findings demonstrated that exosomes-mediated ZEB1-AS1 enhanced cell injuries by miR-590-5p/ETS1 axis through the TGF-beta/Smad pathway in ox-LDL-induced HUVECs, suggesting that inhibiting ZEB1-AS1 might be an effective way for atherosclerosis treatment	33818551	RID05195	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	LUCAT1	CDK4	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	AKT signaling pathway(+);MAPK signaling pathway(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000135446	NA	100505994	1019	SCAL1|SCAT5	PSK-J3	The progression of pancreatic cancer cells is promoted by a long non-coding RNA LUCAT1 by activating AKT phosphorylation;Pancreatic cancer and adjacent tissues were collected, and the expression of LUCAT1, one potential involved LucRNA, was measured using real-time qPCR (RT-qPCR);In comparison to normal cells, LUCAT1 was highly expressed in human pancreatic cancer cell lines (p<0.05);The higher expression of LUCAT1 resulted in enhanced pathogenesis of PDA cells and motivated the development to S phase by regulation of cyclin D1, CDK4. Furthermore, LUCAT1 promoted PDA cells development by inducing AKT's and p38 MAPK's phosphorylation. LUCAT1, as the key factor, played a positive role in the proliferation and invasion of pancreatic cells via AKT/MAPK signaling;To confirm these results, western blot and RTPCR were performed to measure cell cycle checkpoint-associated proteins. CDK4, Cyclin D1 and cyclin E2 showed significantly reduced expression after down-regulating LUCAT1, yet the expression of p21 protein was enhanced	33577028	RID05196	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Pancreatic cancer	LUCAT1	CCND1	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	AKT signaling pathway(+);MAPK signaling pathway(+);cell cycle(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000110092	NA	100505994	595	SCAL1|SCAT5	BCL1|D11S287E|PRAD1|U21B31	The progression of pancreatic cancer cells is promoted by a long non-coding RNA LUCAT1 by activating AKT phosphorylation;Pancreatic cancer and adjacent tissues were collected, and the expression of LUCAT1, one potential involved LucRNA, was measured using real-time qPCR (RT-qPCR);In comparison to normal cells, LUCAT1 was highly expressed in human pancreatic cancer cell lines (p<0.05);The higher expression of LUCAT1 resulted in enhanced pathogenesis of PDA cells and motivated the development to S phase by regulation of cyclin D1, CDK4. Furthermore, LUCAT1 promoted PDA cells development by inducing AKT's and p38 MAPK's phosphorylation. LUCAT1, as the key factor, played a positive role in the proliferation and invasion of pancreatic cells via AKT/MAPK signaling;To confirm these results, western blot and RTPCR were performed to measure cell cycle checkpoint-associated proteins. CDK4, Cyclin D1 and cyclin E2 showed significantly reduced expression after down-regulating LUCAT1, yet the expression of p21 protein was enhanced	33577028	RID05197	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Pancreatic cancer	LUCAT1	AKT1	positively-F	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	AKT signaling pathway(+);MAPK signaling pathway(+);cell cycle(+)	phosphorylation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000142208	NA	100505994	207	SCAL1|SCAT5	AKT|PKB|PRKBA|RAC|RAC-alpha	The progression of pancreatic cancer cells is promoted by a long non-coding RNA LUCAT1 by activating AKT phosphorylation;Pancreatic cancer and adjacent tissues were collected, and the expression of LUCAT1, one potential involved LucRNA, was measured using real-time qPCR (RT-qPCR);In comparison to normal cells, LUCAT1 was highly expressed in human pancreatic cancer cell lines (p<0.05);The higher expression of LUCAT1 resulted in enhanced pathogenesis of PDA cells and motivated the development to S phase by regulation of cyclin D1, CDK4. Furthermore, LUCAT1 promoted PDA cells development by inducing AKT's and p38 MAPK's phosphorylation. LUCAT1, as the key factor, played a positive role in the proliferation and invasion of pancreatic cells via AKT/MAPK signaling;To confirm these results, western blot and RTPCR were performed to measure cell cycle checkpoint-associated proteins. CDK4, Cyclin D1 and cyclin E2 showed significantly reduced expression after down-regulating LUCAT1, yet the expression of p21 protein was enhanced	33577028	RID05198	interact with protein	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	LUCAT1	MAPK	positively-F	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	AKT signaling pathway(+);MAPK signaling pathway(+);cell cycle(+)	phosphorylation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	NA	NA	100505994	NA	SCAL1|SCAT5	NA	The progression of pancreatic cancer cells is promoted by a long non-coding RNA LUCAT1 by activating AKT phosphorylation;Pancreatic cancer and adjacent tissues were collected, and the expression of LUCAT1, one potential involved LucRNA, was measured using real-time qPCR (RT-qPCR);In comparison to normal cells, LUCAT1 was highly expressed in human pancreatic cancer cell lines (p<0.05);The higher expression of LUCAT1 resulted in enhanced pathogenesis of PDA cells and motivated the development to S phase by regulation of cyclin D1, CDK4. Furthermore, LUCAT1 promoted PDA cells development by inducing AKT's and p38 MAPK's phosphorylation. LUCAT1, as the key factor, played a positive role in the proliferation and invasion of pancreatic cells via AKT/MAPK signaling;To confirm these results, western blot and RTPCR were performed to measure cell cycle checkpoint-associated proteins. CDK4, Cyclin D1 and cyclin E2 showed significantly reduced expression after down-regulating LUCAT1, yet the expression of p21 protein was enhanced	33577028	RID05199	interact with protein	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Cholangiocarcinoma	SNHG3	ERG	positively-E	knockdown;RNA pull-down assay;dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell proliferation(+)	ceRNA(miR-3173-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000157554	NA	8420	2078	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	erg-3|p55	LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173-5p/ERG Axis.The expression of SNHG3 and miR-3173-5p was evaluated using qRT-PCRanalysis.Knockdown of SNHG3 was achieved by shRNA.Furthermore, using RNA pull-down and dual luciferase assays, the interactions between SNHG3 and miR-3173-5p and between miR-3173-5p and ERG in CCA cells were validated.Results: SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells.Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells.Mechanistically, SNHG3-sponged miR-3173-5p, thus releasing the repression of ERG by miR-3173-5p.Rescue experiments showed that the miR-3173-5p/ERG axis mediated the oncogenic effect of SNHG3.	34647226	RID05200	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	DRAIC	SLBP	positively-E	Transwell assays	upregulation	qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-432-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245750	GRCh38_15:69462921-69843120	ENSG00000163950	NA	145837	7884	NA	HBP	DRAIC promotes growth of breast cancer by sponging miR-432-5p to upregulate SLBP.To be specific, qRT-PCRassay was conducted to measure the expression of DRAIC and other downstream target genes.It was uncovered that DRAIC was expressed at a high level in BRCA cells.In addition, cell apoptosis was promoted due to DRAIC knockdown.The inhibitory effect of DRAIC reduction on BRCA cell migration and invasion was proven by transwell assays.Mechanistically, DRAIC was confirmed to predominantly distribute in the cytoplasm and could interact with miR-432-5p.In addition, stem-loop binding protein (SLBP) was verified to be a downstream target of miR-432-5p and was positively regulated by DRAIC.Taken together, DRAIC sponged miR-432-5p to enhance SLBP expression, by which malignant behaviors of BRCA cells were promoted.	34645975	RID05201	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Hepatocellular carcinoma	GAS5	DDIT3	positively-F	RNA pull-down assay;mass spectrometry	downregulation	qRT-PCR	NA	NA	apoptosis process(+);tumor growth(-);CHOP signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000175197	NA	60674	1649	NCRNA00030|SNHG2	CHOP|CHOP10|GADD153	Long noncoding RNA Gas5 induces cell apoptosis and inhibits tumor growth via activating the CHOP-dependent endoplasmic reticulum stress pathway in human hepatoblastoma HepG2 cells.Lower expression levels of Gas5 were determined in HCC tissues and cells by quantitative reverse transcription-polymerase chain reaction.Protein complexes that bound to Gas5 were isolated from HepG2 cells through pull-down experiments and analyzed by mass spectrometry.Gas5 inhibited HepG2 cell growth and induced cell apoptosis via upregulating CHOP to activate the ER stress signaling pathway.Further studies indicated that the knockdown of CHOP by shRNA partially reversed Gas5-mediated apoptosis in HepG2 cells.These findings suggest that Gas5 functions as a tumor suppressor and induces apoptosis through activation of ER stress by targeting the CHOP signal pathway in HCC.	34636091	RID05202	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	CRNDE	NASP	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	prognosis	ceRNA(miR-29c-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000132780	NA	643911	4678	CRNDEP|LINC00180|LOC643911	DKFZp547F162|FLB7527|FLJ31599|FLJ35510|MGC19722|MGC20372|MGC2297|PRO1999	Knockdown of long noncoding RNA colorectal neoplasia differentially expressed inhibits hepatocellular carcinoma progression by mediating the expression of nuclear autoantigenic sperm protein.Expression levels of CRNDE in HCC tissues and cell lines were detected by reverse transcription-quantitative (RT-q) PCR, and Cell Counting kit 8, wound-healing and Transwell assays were used to evaluate the influences of CRNDE on in vitro cellular proliferation, migration and invasiveness, respectively.The interaction between CRNDE and microRNA (miR)-29c-3p was determined by dual-luciferase reporter assay, and rescue experiments were conducted to evaluate the interactive relationships between CRNDE and miR-29c-3p or nuclear autoantigenic sperm protein (NASP).CRNDE was found to be upregulated in HCC tissues and cells, and to be positively associated with the poor prognosis of patients with HCC.Furthermore, CRNDE-knockdown suppressed cell proliferation, migration and invasion abilities.Bioinformatics and RT-qPCR analysis indicated miR-29c-3p as a potential target of CRNDE.In line with previous reports, as a tumor suppressor, downregulated expression of miR-29c-3p was observed in HCC.In addition, the present study revealed that miR-29c-3p directly targeted NASP.NASP expression was markedly elevated following transfection with an miR-29c-3p inhibitor, while knocking down CRNDE inhibited NASP expression.Collectively, the results of the present study revealed that CRNDE was upregulated and exerted an oncogenic role in HCC by targeting miR-29c-3p, and that the upregulation of CRNDE also promoted NASP expression.	34633056	RID05203	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842)
Hepatocellular carcinoma	miR-135a	TONSL-AS1	negatively-E	Overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000232600	GRCh38_8:144437675-144439971	NA	100287098	NA	NA	MicroRNA-135a expression is upregulated in hepatocellular carcinoma and targets long non-coding RNA TONSL-AS1 to suppress cell proliferation.Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of TONSL-AS1 and microRNA (miRNA/miR)-135a in HCC tissues and paired adjacent normal tissues.The results demonstrated that TONSL-AS1 expression was downregulated in HCC tissues, which was associated with a lower survival rate in patients with HCC.TONSL-AS1 and miR-135a were predicted to interact with each other, whereby overexpression of miR-135a downregulated TONSL-AS1 expression.The results demonstrated that TONSL-AS1 and miR-135a were inversely correlated with each other.Notably, overexpression of TONSL-AS1 inhibited HCC cell proliferation, while overexpression of miR-135a promoted HCC cell proliferation and decreased the effect of overexpression of TONSL-AS1 on cell proliferation.Taken together, the results of the present study suggest that miR-135a expression is upregulated in HCC and targets lncRNA TONSL-AS1 to suppress cell proliferation.	34630715	RID05204	transcriptional regulation	NA		
Lung adenocarcinoma	METTL14	HCG11	negatively-E		downregulation		NA	NA	tumor growth(-)	transcriptional regulation	regulation	protein-RNA	NA	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000145388	NA	ENSG00000228223	GRCh38_6:26521709-26527404	57721	493812	KIAA1627	bK14H9.3|FLJ14049|FLJ30357	LncRNA HCG11 mediated by METTL14 inhibits the growth of lung adenocarcinoma via IGF2BP2/LATS1.Our data revealed that lncRNA HCG11 expression was downregulated in LUAD, which was modulated by the hypermethylation of HCG11 promoter and Methyltransferase Like 14 (METTL14) mediated N6-methyladenosine (m6A) modification.	34624573	RID05205	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	HCG11	LATS1	positively-E		downregulation		NA	NA	tumor growth(-);cancer progression(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000131023	NA	493812	9113	bK14H9.3|FLJ14049|FLJ30357	WARTS	LncRNA HCG11 mediated by METTL14 inhibits the growth of lung adenocarcinoma via IGF2BP2/LATS1.Our data revealed that lncRNA HCG11 expression was downregulated in LUAD, which was modulated by the hypermethylation of HCG11 promoter and Methyltransferase Like 14 (METTL14) mediated N6-methyladenosine (m6A) modification.The m6A modification of HCG11 promoted its nuclear exportation and binding by Insulin Like Growth Factor 2 MRNA Binding Protein 2 (IGF2BP2), resulting in increased stability.HCG11 could recruit IGF2BP2 to target Large Tumor Suppressor Kinase 1 (LATS1) mRNA to enhance the stability and promote the expression of LATS1.HCG11 served as a tumor suppressor to restrain tumor growth in LUAD by regulating LATS1.In summary, this study demonstrated that HCG11 mediated by METTL14 inhibited the growth of lung adenocarcinoma via IGF2BP2/LATS1.	34624573	RID05206	transcriptional regulation	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	HCG11	IGF2BP2	positively-F		downregulation		NA	NA	cancer progression(-)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000073792	NA	493812	10644	bK14H9.3|FLJ14049|FLJ30357	IMP-2|p62	LncRNA HCG11 mediated by METTL14 inhibits the growth of lung adenocarcinoma via IGF2BP2/LATS1.Our data revealed that lncRNA HCG11 expression was downregulated in LUAD, which was modulated by the hypermethylation of HCG11 promoter and Methyltransferase Like 14 (METTL14) mediated N6-methyladenosine (m6A) modification.The m6A modification of HCG11 promoted its nuclear exportation and binding by Insulin Like Growth Factor 2 MRNA Binding Protein 2 (IGF2BP2), resulting in increased stability.HCG11 could recruit IGF2BP2 to target Large Tumor Suppressor Kinase 1 (LATS1) mRNA to enhance the stability and promote the expression of LATS1.HCG11 served as a tumor suppressor to restrain tumor growth in LUAD by regulating LATS1.In summary, this study demonstrated that HCG11 mediated by METTL14 inhibited the growth of lung adenocarcinoma via IGF2BP2/LATS1.	34624573	RID05207	transcriptional regulation	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Breast cancer	SNHG1	STAT6	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	macrophage polarization(+);cell growth(+);cell metastasis(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000166888	NA	23642	6778	LINC00057|lncRNA16|NCRNA00057|UHG	D12S1644|IL-4-STAT	LncRNA-SNHG1 promotes macrophage M2-like polarization and contributes to breast cancer growth and metastasis.Silencing of SNHG1 inhibited the phosphorylation of STAT6.To explore whether lncRNA-SNHG1 mediated M2 macrophage polarization via STAT pathway, western blotwas performed to detect protein levels of STAT1 and STAT6 and their phosphorylation level.And knockdown of lncRNA-SNHG1 by siRNA transfection attenuated that effect and decreasing the phosphorylation level of STAT6.These results indicated that lncRNA-SNHG1 regulated phosphorylation of STAT6 to mediated M2 macrophage polarization.	34618681	RID05208	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Lung adenocarcinoma	LINC00968	CDC14A	positively-E		downregulation		NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-22-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246430	GRCh38_8:56494923-56559823	ENSG00000079335	NA	100507632	8556	NA	cdc14|Cdc14A1|Cdc14A2|DFNB105|DFNB32	Long noncoding RNA LINC00968 inhibits proliferation, migration and invasion of lung adenocarcinoma through targeting miR-22-5p/CDC14A axis.In the present study, we found that lncRNA LINC00968 was significantly down-regulated in LUAD tissues and cell lines.In conclusion, our study demonstrated that LINC00968 inhibited proliferation, migration and invasion of LUAD by sponging miR-22-5p and further restoring CDC14A.	34603911	RID05209	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Atherosclerosis	XIST	GDF2	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);BMP9/ALK1/endoglin signaling pathway(+)	ceRNA(miR-761)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000128802	NA	7503	2658	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BMP-9|BMP9	The proliferation and migration of atherosclerosis-related HVSMCs were inhibited by downregulation of lncRNA XIST via regulation of the miR-761/BMP9 axis.A dual-luciferase reporter assay was employed to verify the binding relationships between XIST and miR-761, miR-761, and BMP9.Ox-LDL induced the proliferation and migration of HVSMCs, upregulated the expression of XIST, downregulated miR-761 expression, and activated the BMP9/ALK1/endoglin pathway.Luciferase assays revealed that XIST sponged miR-761.Our findings suggested that XIST knockdown suppressed the proliferation and migration of HVSMCs by promoting miR-761, which targeted-inhibited the BMP9/ALK1/endoglin pathway.	34595819	RID05210	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DATA(GSE40174)
Mantle cell lymphoma	LUADT1	TRIM11	positively-E	western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-24-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000154370	NA	106182249	81559	NA	BIA1|RNF92	LncRNA LUADT1 is Upregulated in Mantle Cell Lymphoma and Modulates TRIM11 by Sponging miR-24-3p to Inhibit Cell Apoptosis.We found LUADT1 may form base pairing with miR-24-3p.Then, quantitative polymerase chain reaction and western blot were used to detect the level of relative messenger RNA and protein expression, respectively.Bioinformatics analysis showed that LUADT1 may bind miR-24-3p, which can target TRIM11.Correlation analysis showed that LUADT1 was not significantly correlated with miR-24-3p.In MCL cells, LUADT1 overexpression led to upregulated TRIM11, whereas miR-24-3p overexpression led to downregulated TRIM11.Therefore, LUADT1 was upregulated in MCL and could modulate TRIM11 by sponging miR-24-3p to inhibit cancer cell apoptosis.	34591388	RID05211	ceRNA or sponge	NA	UP(NSCLC,PRAD,SKCM);DATA(GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939,GSE75367)
Malignant glioma	RP1-86C11.7	TFRC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(-)	ceRNA(miR-144-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000272468	GRCh38_6:27122657-27123221	ENSG00000072274	NA	NA	7037	NA	CD71|IMD46|T9|TFR|TFR1|TR|TRFR|p90	LncRNA RP1-86C11.7 exacerbates the glioma progression and oncogenicity by hsa-miR-144-3p/TFRC signaling.The TFRC level was higher in glioma cell lines, and elevated TFRC expression promoted the proliferation and survival of glioma cells.Further study showed that hsa-miR-144a-3p bound to the 3'-UTR of TFRC mRNA and inhibited its expression, preventing the malignant properties of glioma cells, such as proliferation and survival.We also found that the lncRNA RP1-86C11.7 sponges hsa-miR-144-3p to suppress its protective role in glioma.RP1-86C11.7 overexpression in glioma cells elevated TFRC expression, increased the intracellular free iron level, and deteriorated oncogenicity, with a significant reduction in hsa-miR-144-3p.However, the effect of silencing RP1-86C11.7 was reversed with simultaneous hsa-miR-144-3p inhibitor treatment: the TFRC level, intracellular iron level and proliferation in glioma cells increased.	34571345	RID05212	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827)
Colorectal cancer	MIR155HG	ANXA2	positively-E	RNAi;RNA pull-down assay;dual-luciferase reporter analysis	upregulation		NA	NA	macrophage polarization(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-650)	regulation	RNA-protein	Oxaliplatin	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234883	GRCh38_21:25561810-25575168	ENSG00000182718	NA	114614	302	BIC|miPEP155|MIRHG2|NCRNA00172	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	LncRNA MIR155HG induces M2 macrophage polarization and drug resistance of colorectal cancer cells by regulating ANXA2.RNA immunoprecipitation, RNA pull-down and dual-luciferase reporter assays were applied to verify the targeting relationships among MIR155HG, miR-650 and ANXA2.Results: MIR155HG and ANXA2 were highly expressed in CRC tissues/cells and of prognostic values for CRC patients.Knockdown of MIR155HG or ANXA2 suppressed M2 macrophage polarization, and proliferation, migration, invasion and oxaliplatin resistance of CRC cells.MIR155HG competed with ANXA2 for binding miR-650 and can also directly target ANXA2.Conclusion: This study highlighted that MIR155HG, by regulating the miR-650/ANXA2 axis, promotes CRC progression and enhances oxaliplatin resistance in CRC cells through M2 macrophage polarization.	34562123	RID05213	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Lung cancer	LINC01089	HPDG	positively-E	ChIP;luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-301b-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000212694	GRCh38_12:121795267-121803906	NA	NA	338799	NA	AK096174|LIMT	NA	LINC01089, suppressed by YY1, inhibits lung cancer progression by targeting miR-301b-3p/HPDG axis.Methods: YY1, LINC01089, and miR-301b-3p levels in lung cancer tissues and cells were assessed using qRT-PCRBioinformatics analysis and luciferase reporter, ChIP, and RIP assays were carried out for determining the relationships among YY1, LINC01089, miR-301b-3p, and HPGD.Results: LINC01089 was decreased in lung cancer tissues and cells, and low LINC01089 level predicted a poor clinical outcome.YY1 directly bound to LINC01089 promoter region and inhibited its transcription.LINC01089 knockdown thwarted the proliferation, invasion, and migration capacity of H1299 and A549 cells and aggravated tumor growth.	34561789	RID05214	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)	
Lung cancer	YY1	LINC01089	negatively-E	ChIP;luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000212694	GRCh38_12:121795267-121803906	7528	338799	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	AK096174|LIMT	LINC01089, suppressed by YY1, inhibits lung cancer progression by targeting miR-301b-3p/HPDG axis.Methods: YY1, LINC01089, and miR-301b-3p levels in lung cancer tissues and cells were assessed using qRT-PCRBioinformatics analysis and luciferase reporter, ChIP, and RIP assays were carried out for determining the relationships among YY1, LINC01089, miR-301b-3p, and HPGD.Results: LINC01089 was decreased in lung cancer tissues and cells, and low LINC01089 level predicted a poor clinical outcome.YY1 directly bound to LINC01089 promoter region and inhibited its transcription.LINC01089 knockdown thwarted the proliferation, invasion, and migration capacity of H1299 and A549 cells and aggravated tumor growth.	34561789	RID05215	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Non-small cell lung cancer	CYTOR	PTMA	positively-E	dual-luciferase reporter analysis;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	prognosis	ceRNA(miR-20)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000187514	NA	112597	5757	C2orf59|LINC00152|MGC4677|NCRNA00152	TMSA	lncRNA cytoskeleton regulator reduces non-small cell lung cancer radiosensitivity by downregulating miRNA-206 and activating prothymosin alpha.CYTOR was overexpressed in NSCLC and was associated with poor prognosis.Mechanistically, CYTOR specifically bound to miR-206 and silencing CYTOR promoted miR-206 to enhance the radiosensitivity of NSCLC cells.PTMA is a target of miR-206 and silencing CYTOR inhibited PTMA expression via miR-206, thus promoting radiosensitivity of NSCLC cells.	34558643	RID05216	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Osteosarcoma	JPX	MYC	positively-E	western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+)	transcriptional regulation	association	NA	Melatonin	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000136997	NA	554203	4609	DCBALD06|ENOX|LINC00183|NCRNA00183	bHLHe39|c-Myc|MYCC	Anticancer effects of melatonin via regulating lncRNA JPX-Wnt/beta-catenin signalling pathway in human osteosarcoma cells.The expression of relevant lncRNAs in OS cells was determined by real-time qPCR analysis.western blot results showed that lncRNA JPX overexpression significantly increased the expression of beta -catenin, MYC, Axin2 and Cyclin D1 proteins in MG63 cells, suggesting that lncRNA JPX activated the Wnt/beta -catenin pathway.	34547170	RID05217	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Osteosarcoma	JPX	AXIN2	positively-E	western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+)	transcriptional regulation	association	RNA-protein	Melatonin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000168646	NA	554203	8313	DCBALD06|ENOX|LINC00183|NCRNA00183	DKFZp781B0869|MGC126582	Anticancer effects of melatonin via regulating lncRNA JPX-Wnt/beta-catenin signalling pathway in human osteosarcoma cells.The expression of relevant lncRNAs in OS cells was determined by real-time qPCR analysis.western blot results showed that lncRNA JPX overexpression significantly increased the expression of beta -catenin, MYC, Axin2 and Cyclin D1 proteins in MG63 cells, suggesting that lncRNA JPX activated the Wnt/beta -catenin pathway.	34547170	RID05218	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Osteosarcoma	JPX	Cyclin D1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+)	transcriptional regulation	association	RNA-protein	Melatonin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225470	GRCh38_X:73944182-74070408	NA	NA	554203	NA	DCBALD06|ENOX|LINC00183|NCRNA00183	NA	Anticancer effects of melatonin via regulating lncRNA JPX-Wnt/beta-catenin signalling pathway in human osteosarcoma cells.The expression of relevant lncRNAs in OS cells was determined by real-time qPCR analysis.western blot results showed that lncRNA JPX overexpression significantly increased the expression of beta -catenin, MYC, Axin2 and Cyclin D1 proteins in MG63 cells, suggesting that lncRNA JPX activated the Wnt/beta -catenin pathway.	34547170	RID05219	transcriptional regulation	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	
Colon cancer	HCG11	PDK4	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation		NA	NA	chemosensitivity(-)	ceRNA(miR-144-3p)	regulation	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000004799	NA	493812	5166	bK14H9.3|FLJ14049|FLJ30357	NA	LncRNA HCG11 promotes 5-FU resistance of colon cancer cells through reprogramming glucose metabolism by targeting the miR-144-3p-PDK4 axis.Methods and results: This study uncovers that HCG11 was significantly upregulated in CRC tumors tissues and cell lines.Moreover, HCG11 was elevated in 5-FU resistant CRC tumors.Furthermore, microRNA-microarray, RNA pull-down and luciferase assays demonstrated that HCG11 inhibited miR-144-3p which displays suppressive roles in colon cancer via sponging it to form a ceRNA network.We identified pyruvate dehydrogenase kinase 4 (PDK4), which is a glucose metabolism key enzyme, was directly targeted by miR-144-3p in CRC cells.Finally, restoration of miR-144-3p in HCG11-overexpressing DLD-1 5-FU resistant cells successfully overcame the HCG11-faciliated 5-FU resistance via targeting PDK4.	34542064	RID05220	ceRNA or sponge	chemoresistance	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE86978)
Glioblastoma	FEZF1-AS1	NOB1	positively-E		upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000141101	NA	154860	28987	NA	ART-4|MST158|NOB1P|PSMD8BP1	LncRNA FEZF1-AS1 aggravates cell proliferation and migration in glioblastoma.Materials & methods: The expression pattern of FEZF1-AS1 was firstly figured out in GBM cells using RT-qPCR.Results: FEZF1-AS1 possessed high expression in GBM cells.With the help of bioinformatics prediction and mechanism assays, FEZF1-AS1 was found to bind to miR-363-3p and NOB1 was determined to be the downstream gene.Finally, results of rescue assays verified that the suppressive function of FEZF1-AS1 inhibition on GBM development were restored by miR-363-3p depletion or overexpression of NOB1.Conclusion: FEZF1-AS1 had oncogenic function in the advancement of GBM by targeting miR-363-3p/NOB1, which made FEZF1-AS1 a potential biomarker for GBM treatment.	34530115	RID05221	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Cancer	MEG3	CDKN1A	positively-E		downregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	transcriptional regulation	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000124762	NA	55384	1026	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	The long non-coding RNA (lncRNA) microarray analysis showed that the expression level of a tumor suppressive lncRNA maternally expressed 3 (MEG3) is significantly down-regulated in Cd-transformed cells, which is confirmed by further q-PCR analysis.Further mechanistic studies revealed that the cell cycle inhibitor p21 level is reduced and retinoblastoma protein (Rb) phosphorylation is increased in Cd-transformed cells to promote cell cycle progression.In contrast, stably overexpressing MEG3 increased p21 levels and reduced Rb phosphorylation and Bcl-xL levels in Cd-exposed cells and reduced their cell cycle progression and apoptosis resistance.Together, these findings suggest that MEG3 down-regulation may play important roles in Cd-induced cell transformation and CSC-like property by promoting cell cycle progression and apoptosis resistance.	34520792	RID05222	transcriptional regulation	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Cancer	MEG3	BCL2L1	negatively-E		downregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	transcriptional regulation	association	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171552	NA	55384	598	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Bcl-X|bcl-xL|bcl-xS|BCL2L|BCLX|PPP1R52	The long non-coding RNA (lncRNA) microarray analysis showed that the expression level of a tumor suppressive lncRNA maternally expressed 3 (MEG3) is significantly down-regulated in Cd-transformed cells, which is confirmed by further q-PCR analysis.Further mechanistic studies revealed that the cell cycle inhibitor p21 level is reduced and retinoblastoma protein (Rb) phosphorylation is increased in Cd-transformed cells to promote cell cycle progression.In contrast, stably overexpressing MEG3 increased p21 levels and reduced Rb phosphorylation and Bcl-xL levels in Cd-exposed cells and reduced their cell cycle progression and apoptosis resistance.Together, these findings suggest that MEG3 down-regulation may play important roles in Cd-induced cell transformation and CSC-like property by promoting cell cycle progression and apoptosis resistance.	34520792	RID05223	transcriptional regulation	NA		UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Oral squamous cell carcinoma	HOXA-AS2	EZH2	positively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000106462	NA	285943	2146	HOXA3as	ENX-1|EZH1|KMT6|KMT6A	LncRNA HOXA-AS2 Promotes Oral Squamous Cell Proliferation, Migration, and Invasion via Upregulating EZH2 as an Oncogene.RT-qPCR was performed to analyze the HOXA-AS2 expressions in human immortalized oral epithelial cell (HIOEC) line, human OSCC cell lines, and plasma.The interaction between HOXA-AS2 and EZH2 was validated by RNA immunoprecipitation assay.Compared with HIOEC cells, HOXA-AS2 expression in OSCC cells was upregulated.HOXA-AS2 knockdown significantly inhibited Tca-8113 cell proliferation, blocked the cell cycle by arresting cells in the G0/G1 phase, promoted apoptosis, and suppressed migration and invasion.In addition, HOXA-AS2 was predicted to directly target EZH2 and positively regulate EZH2 expression.In summary, the findings suggested that HOXA-AS2 may inhibit cell proliferation, invasion, and migration, induce cell cycle arrest in the G0/G1 phase, and increase cell apoptosis by targeting EZH2.	34519570	RID05224	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	EZH2	H19	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);WNT/beta-catenin signaling pathway(-)	transcriptional regulation	association	protein-RNA	Curcumin;N-n-butyl haloperidol iodide	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000130600	GRCh38_11:1995171-2001470	2146	283120	ENX-1|EZH1|KMT6|KMT6A	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Combination of curcumin with N-n-butyl haloperidol iodide inhibits hepatocellular carcinoma malignant proliferation by downregulating enhancer of zeste homolog 2 (EZH2) - lncRNA H19 to silence Wnt/beta-catenin signaling.In order to investigate the molecular pathways, various experiments such as western blot, qPCR, RNA-seq, immunostaining and transfection were performed.The F2C treatment downregulates enhancer of zeste homolog 2 (EZH2) transcription and protein expression, which is key epigenetic regulator responsible for HCC development.Moreover, the inhibition of EZH2 by F2C led to Wnt/beta-catenin signaling inhibition by decreasing tri-methylation of histone H3 at lysine 27 (H3K27me3) and long non-coding RNA H19 expression.Conclusion: These findings suggested that, F2C inhibited HCC formation, migration and its modulatory mechanism seemed to be associated with downregulation of EZH2, silencing Wnt/beta-catenin signaling by interacting with H19, suggesting that F2C may be a promising drug in the clinical treatment of HCC.	34517264	RID05225	transcriptional regulation	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	UP(NSCLC);DATA(GSE74639)
Gastric cancer	SNHG7	miR-485-5p	negatively-E	dual-luciferase reporter analysis;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	LncRNA SNHG7 Regulates Gastric Cancer Progression by miR-485-5p.Methods: SNHG7 and microRNA-485-5p (miR-485-5p) expressions in gastric cancer tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR.The dual-luciferase reporter assay, RNA immunoprecipitation (RIP) experiment, and Pearson's correlation analysis were used to confirm the relationship between SNHG7 and miR-485-5p.Results: SNHG7 expression was increased in human gastric cancer tissues and cells.Knockdown of SNHG7 could notably inhibit the gastric cancer cells proliferation, migration, and invasion.The dual-luciferase reporter assay and RIP experiments proved that miR-485-5p was a direct target of SNHG7.At the same time, further experiments demonstrated that miR-485-5p inhibition reversed the suppression of SNHG7 knockdown on gastric cancer cells proliferation, migration, and invasion.Conclusions: SNHG7 knockdown could hamper gastric cancer progression via inhibiting miR-485-5p expression, providing a novel understanding for gastric cancer development.	34512753	RID05226	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Colorectal cancer	DUXAP8	ZNF277	positively-E	dual-luciferase reporter analysis;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-519b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000198839	NA	503637	11179	NA	NRIF4|ZNF277P	Long Non-Coding RNA Duxap8 Facilitates Cell Proliferation and Induces Apoptosis in Colorectal Cancer via miR-519b/ZNF277 Axis.Methods: Reverse transcription quantitative PCR (RT-qPCR), cell counting kit-8 (CCK-8), 5-ethynyl-20-deoxyuridine (EdU), colony formation assay, flow cytometry, TdT-mediated dUTP nick-end labeling (TUNEL), western blot, hematoxylin-eosin staining (HE), in situ hybridization (ISH) analysis, immunohistochemistry (IHC) and tumor transplantation experiment were performed to investigate the function and mechanism of Duxap8 in colorectal cancer.Then, we proved that the expression level of Duxap8 was significantly increased in human colorectal cancer tissues and cell lines.Functionally, Duxap8 knockdown inhibited the proliferation and induced the apoptosis of colorectal cancer cells, while Duxap8 overexpression facilitated the proliferation and suppressed the apoptosis in colorectal cancer in vitro.Furthermore, Duxap8 functioned as a competing endogenous RNA to induce the development and progression of colorectal cancer through sponging miR-519b-3p to upregulate ZNF277.Discussion: Taken together, our results demonstrated that Duxap8 enhanced the expression level of ZEB1 to promote via competing for miR-519b-3p, which might be a promising molecular therapeutic target of colorectal cancer.	34511937	RID05227	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Laryngeal squamous cell carcinoma	YY1	GAS5	negatively-E	RIP;ChIP;dual-luciferase reporter analysis	downregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Larynx cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000234741	GRCh38_1:173858559-173868882	7528	60674	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NCRNA00030|SNHG2	YY1 Promotes Telomerase Activity and Laryngeal Squamous Cell Carcinoma Progression Through Impairment of GAS5-Mediated p53 Stability.YY1 mRNA and protein expression in human LSCC cell lines was detected by RT-qPCR and western blotAn interaction of YY1, GAS5, and p53 protein stability was predicted and confirmed by bioinformatics, ChIP, Co-IP, RIP, and FISH assays.LSCC cell lines presented with upregulated expression of YY1, downregulated GAS5 expression, and decreased p53 stability.YY1 inhibited the expression of GAS5, which in turn recruited p300 and bound to p53, thus stabilizing it.Moreover, YY1 could directly interact with p300 and suppressp53 stability, leading to enhancement of cell proliferation, telomere length and telomerase activity in vitro along with tumor growth in vivo.Collectively, YY1 can stimulate proliferation and telomerase activity of LSCC cells through suppression of GAS5-dependent p53 stabilization or by decreasing p53 stability via a direct interaction with p300, suggesting that YY1 presents a therapeutic target as a potential oncogene in LSCC development and progression.	34497757	RID05228	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Laryngeal squamous cell carcinoma	GAS5	TP53	positively-F	RIP;ChIP;dual-luciferase reporter analysis	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	LFS1|p53	YY1 Promotes Telomerase Activity and Laryngeal Squamous Cell Carcinoma Progression Through Impairment of GAS5-Mediated p53 Stability.YY1 mRNA and protein expression in human LSCC cell lines was detected by RT-qPCR and western blotAn interaction of YY1, GAS5, and p53 protein stability was predicted and confirmed by bioinformatics, ChIP, Co-IP, RIP, and FISH assays.LSCC cell lines presented with upregulated expression of YY1, downregulated GAS5 expression, and decreased p53 stability.YY1 inhibited the expression of GAS5, which in turn recruited p300 and bound to p53, thus stabilizing it.Moreover, YY1 could directly interact with p300 and suppressp53 stability, leading to enhancement of cell proliferation, telomere length and telomerase activity in vitro along with tumor growth in vivo.Collectively, YY1 can stimulate proliferation and telomerase activity of LSCC cells through suppression of GAS5-dependent p53 stabilization or by decreasing p53 stability via a direct interaction with p300, suggesting that YY1 presents a therapeutic target as a potential oncogene in LSCC development and progression.	34497757	RID05229	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Ischemic cerebral injury	ALMS1-IT1	RELA	positively-E		upregulation		NA	NA	NF-kB signaling pathway(+)	transcriptional regulation	association	NA	NA	NA	NA	Cardiovascular system disease	Brain ischemia	lncRNA	TF	ENSG00000230002	GRCh38_2:73456764-73459482	ENSG00000173039	NA	100874291	5970	NA	NFKB3|p65	Upregulated Long Non-coding RNA ALMS1-IT1 Promotes Neuroinflammation by Activating NF-kB Signaling in Ischemic Cerebral Injury.Mechanistically, ALMS1-IT1 knockdown suppressed the activation of NF-kB signaling in vitro and in vivo, as evidenced by decreased p65 expression and p65 nuclear translocation.Conclusion: These data demonstrated that ALMS1-IT1 inhibition improved neurological function of MCAO rats, at least in part by repressing NF-kB-dependent neuro-inflammation.	34455967	RID05230	transcriptional regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Neonatal pneumonia	SNHG4	METTL3	negatively-E	RIP	downregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Respiratory system disease	Pneumonia	lncRNA	PCG	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000165819	NA	724102	56339	NCRNA00059|U19H	M6A|MT-A70|Spo8	Long noncoding RNA SNHG4 remits lipopolysaccharide-engendered inflammatory lung damage by inhibiting METTL3 - Mediated m 6 A level of STAT2 mRNA.Methods: RT-qPCR was used to determine the expression of SNHG4 and METTL3 in the serum from NP patients and normal volunteers, as well as in LPS treated-WI-38 cells.The enrichment of SNHG4 in the METTL3 promoter region was assessed with RIP assay.Results: SNHG4 was downregulated, and METTL3 was upregulated in NP patients and LPS-treated cells.SNHG4 overexpression facilitated cell proliferation, migration and SOD concentration, as well as inhibited cell apoptosis and production of IL-6, TNF-alpha and MDA, and suppressed the expression of NF-kB pathway proteins.Mechanistically, SNHG4 bound with METTL3 and downregulated METTL3 expression.Besides, total m6A level was lower in the SNHG4 overexpressed or METTL3 inhibited cells.Conclusions: This study reveals that SNHG4 promotes LPS induced inflammation in human lung fibroblasts and mouse lung tissues in vitro and in vivo by inhibiting METTL3-mediated m6A level of STAT2 mRNA, which may provide a potential therapeutic mechanism for NP.	34450538	RID05231	transcriptional regulation	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	TG2-lncRNA	RXRA	interact		upregulation	RT-qPCR	NA	NA	prognosis	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000186350	NA	NA	6256	NA	NR2B1|RXR-alpha|RXRalpha	Inhibition of the lncRNA Coded within Transglutaminase 2 Gene Impacts Several Relevant Networks in MCF-7 Breast Cancer Cells.Moreover, our experiments strongly suggest the ability of TG2-lncRNA to directly interact with important transcription factors, such as RXRalpha and TP53, paving the way for several regulatory loops that can potentially influence the phenotypic behaviour of MCF-7 cells.	34449674	RID05232	transcriptional regulation	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	TG2-lncRNA	TP53	interact		upregulation	RT-qPCR	NA	NA	prognosis	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	Inhibition of the lncRNA Coded within Transglutaminase 2 Gene Impacts Several Relevant Networks in MCF-7 Breast Cancer Cells.Moreover, our experiments strongly suggest the ability of TG2-lncRNA to directly interact with important transcription factors, such as RXRalpha and TP53, paving the way for several regulatory loops that can potentially influence the phenotypic behaviour of MCF-7 cells.	34449674	RID05233	transcriptional regulation	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Gastric adenocarcinoma	TSIX	RAD51	positively-E				NA	NA	apoptosis process(+);ATF6 signaling pathway(+)	ceRNA(miR-320a)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000270641	GRCh38_X:73792205-73829231	ENSG00000051180	NA	9383	5888	LINC00013|NCRNA00013|XIST-AS1	BRCC5|FANCR|HsRad51|HsT16930|RAD51A|RECA	Cation Lipid-Assisted PEG6-PLGA Polymer Nanoparticles Encapsulated Knocking Down Long ncRNAs Reverse Non-Coding RNA of Xist Through the Support Vector Machine Model to Regulate the Molecular Mechanisms of Gastric Cancer Cell Apoptosis.Knocking down lncRNA TSIX restored the suppression role of miR-320a on Rad51 and inhibited the Rad51 expression.Simultaneously, this ceRNA network activated the ATF6 signaling pathway after endoplasmic reticulum stress to promote GAC cells' apoptosis and inhibit the disease.TSIX/miR-320a/Rad51 network may be a potential biological target of GAC disease and provides a new strategy for treating GAC disease.	34446134	RID05234	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Kidney disease	CASC2	TIMP3	positively-E	dual-luciferase reporter analysis	downregulation	RT-qPCR	NA	NA	cell proliferation(-);inflammatory response(-);fibrotic(-)	ceRNA(miR-135a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000100234	NA	255082	7078	C10orf5	SFD	Long non-coding RNA CASC2 restrains high glucose-induced proliferation, inflammation and fibrosis in human glomerular mesangial cells through mediating miR-135a-5p/TIMP3 axis and JNK signaling.Methods: The expression of CASC2 and microRNA-135a-5p (miR-135a-5p) was determined by real-time quantitative polymerase chain reaction (RT-qPCR).dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the target relationship between miR-135a-5p and CASC2 or tissue inhibitors of metalloproteinase 3 (TIMP3).miR-135a-5p was validated as a target of CASC2, and CASC2 restrained HG-induced influences in HMCs partly by down-regulating miR-135a-5p.CASC2 overexpression suppressed HG-induced activation of Jun N-terminal Kinase (JNK) signaling partly through mediating miR-135a-5p/TIMP3 signaling.Conclusions: In conclusion, CASC2 alleviated proliferation, inflammation and fibrosis in DN cell model by sponging miR-135a-5p to induce TIMP3 expression.	34446088	RID05235	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(SKCM);DATA(GSE38495)
Endometriosis	LINC01133	CDKN1A	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell cycle(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124762	NA	100505633	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.We found that LINC01133 is upregulated in ectopic endometriotic lesions.We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle.These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways.	34445100	RID05236	transcriptional regulation	NA	UP(BRCA);DATA(GSE111065)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Endometriosis	LINC01133	Cyclin A	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell cycle(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	NA	NA	100505633	NA	NA	NA	LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.We found that LINC01133 is upregulated in ectopic endometriotic lesions.We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle.These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways.	34445100	RID05237	transcriptional regulation	NA	UP(BRCA);DATA(GSE111065)	
Oral carcinoma	MIR31HG	LBH	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000171889	GRCh38_9:21453802-21559900	ENSG00000213626	NA	554202	81606	hsa-lnc-31|LncHIFCAR|LOC554202	NA	LncRNA MIR31HG Drives Oncogenicity by Inhibiting the Limb-Bud and Heart Development Gene ( LBH) during Oral Carcinoma.Overexpression of MIR31HG and of miR-31 occurs during oral squamous cell carcinoma (OSCC).The present study identifies up-regulation of MIR31HG expression during the potentially premalignant disorder stage of oral carcinogenesis.In addition, the decreased proliferation, invasion and colony formation capability of the KO4 cell subclone was reversed by knockdown of LBH.	34445087	RID05238	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	CDKN2B-AS1	DUSP1	negatively-E	RNA pull-down assay			NA	NA	cancer progression(-)	interact with protein	association	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000120129	NA	100048912	1843	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	CL100|HVH1|MKP-1|PTPN10	CDKN2B antisense RNA 1 suppresses tumor growth in human colorectal cancer by targeting MAPK inactivator dual-specificity phosphatase 1.RNA pull-down assay was conducted to identify the target of CDKN2B-AS1 in CRC cells.CDKN2B-AS1 bound to mitogen-activated protein kinase (MAPK) inactivator dual-specificity phosphatase 1 (DUSP1) in CRC cells.In contrast to CDKN2B-AS1, DUSP1 promoted CRC cell proliferation, suppressed apoptosis and inactivated MEK/ERK/p38 signaling in CRC cells.Furthermore, CDKN2B-AS1 overexpression attenuated DUSP1 expression in normal colonic myofibroblasts and CRC cells.	34436551	RID05239	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Ovarian cancer	LINC00858	TRIM44	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-134-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000166326	NA	170425	54765	CRCAL-2	DIPB|MC7	Long noncoding RNA LINC00858 promotes the progression of ovarian cancer via regulating the miR-134-5p/TRIM44 axis.The qRT-PCRwas used to measure the expression levels of LINC00858 and miR-134-5p in ovarian cancer tissue specimens and cell lines.Biological information analysis and luciferase report gene assay were used to verify potential downstream genes of LINC00858.Our results showed that LINC00858 was highly expressed in human ovarian cancer tissues and cell lines.Knockdown of LINC00858 inhibited cell proliferation, migration and invasion of SKOV3 cells, and suppressed tumor growth in mouse xenograft models.Mechanistic studies revealed that LINC00858 acted as a sponge of miR-134-5p and then regulated TRIM44 expression in SKOV3 cells.Furthermore, rescue experiments illustrated that inhibition of miR-134-5p restored the inhibitory effects of LINC00858 knockdown on cell proliferation, migration and invasion.In conclusion, these findings demonstrated that LINC00858 exerted oncogenic role in ovarian cancer, which was mediated by miR-134-5p/TRIM44 axis.	34423728	RID05240	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE75367)
Breast cancer	MALAT1	HMGA2	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+)	ceRNA(miR-26b)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000149948	NA	378938	8091	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BABL|HMGIC|LIPO	The m6A methyltransferase METTL3 controls epithelial-mesenchymal transition, migration and invasion of breast cancer through the MALAT1/miR-26b/HMGA2 axis.Here, our study investigated the effects of the novel m6A methyltransferase METTL3 on epithelial-mesenchymal transition (EMT) in BC via the MALAT1/miR-26b/HMGA2 axis.Methods: Firstly, we collected clinical BC samples and cultured BC cells, and detected mRNA and protein levels in the human samples and human cell lines by RT-qPCR and western blot, respectively.Then, the binding of MALAT1 and miR-26b and the targeting relationship between miR-26b and HMGA2 were examined by dual-luciferase assay.Moreover, the binding of MALAT1 and miR-26b was tested by RNA pull down and RNA immunoprecipitation (RIP) assays.Results: In BC, the level of miR-26b was consistently low, while the levels of METTL3, MALAT1 and HMGA2 were high.Further experiments showed that METTL3 up-regulated MALAT1 expression by modulating the m6A modification of MALAT1, and that MALAT1 could promote the expression of HMGA2 by sponging miR-26b.Furthermore, MALAT1 mediated miR-26b to target HMGA2 and promote EMT, migration, and invasion.In summary, METTL3 promoted tumorigenesis of BC via the MALAT1/miR-26b/HMGA2 axis.	34419065	RID05241	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hypertrophic scar	NEAT1	FRS2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	fibrotic(+)	ceRNA(miR-29-3p)	regulation	RNA-protein	NA	NA	NA	Other	Hypertrophic scar	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000166225	NA	283131	10818	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	FRS2A|FRS2alpha|SNT-1|SNT1	Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts.Expression of lncRNAs, miRNAs, and genes were detected by polymerase chain reaction; protein expression was evaluated using western blot.The interaction between microRNA (miR)-29-3p and NEAT1 or fibroblast growth factor receptor substrate 2 (FRS2) was verified by luciferase and RNA pull-down assays.The results showed that NEAT1 was overexpressed in the hypertrophic dermis and in HSFs.Moreover, NEAT1 functioned as a competing endogenous RNA to upregulate FRS2 by sponging miR-29-3p.In conclusion, NEAT1 knockdown protected against hypertrophic scarring by modulating the miR-29-3p/FRS2 axis, which is a viable target in scar treatment.	34414852	RID05242	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE86978,GSE41245)
Corneal angiogenesis	TUG1	VEGFA	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	ceRNA(miR-505-3p)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Corneal neovascularization	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Knockdown of lncRNA TUG1 suppresses corneal angiogenesis through regulating miR-505-3p/VEGFA.qRT-PCRand western blot were performed to examine gene expression and protein levels.dual-luciferase reporter assay was used for functional interaction validation between miR-505-3p and its targets.Results: TUG1 and VEGFA were upregulated in CRNV tissues and VEGFA-treated HUVECs.TUG1 regulated the angiogenesis of HUVECs by modulating VEGFA expression through targeting miR-505-3p.Conclusions: Our results suggest that lncRNA TUG1 promotes the angiogenesis of HUVECs through modulating miR-505-3p/VEGFA axis.	34411571	RID05243	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Gastric cancer	LOC100505817	WT1	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);epithelial to mesenchymal transition(-);cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-20a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000184937	NA	NA	7490	NA	AWT1|GUD|NPHS4|WAGR|WIT-2	Tumor Inhibitory Effect of Long Non-coding RNA LOC100505817 on Gastric Cancer.We also proposed a hypothesis that the regulation of Wnt/beta-catenin pathway by LOC100505817 was regulated by miR-20a-mediated WT1.After the collection of cancer tissues and adjacent tissues were obtained from GC patients, expression of LOC100505817, Wnt/beta-catenin pathway- and EMT-related genes was quantified.Then interactions among LOC100505817, miR-20a and WT1 were explored by dual luciferase reporter gene assay, RNA pull-down assay and RNA binding protein immunoprecipitation (RIP) assay.The results found poor expression LOC100505817 was poorly expressed in GC cells and tissues.Wnt/beta-catenin pathway and EMT in GC cells were suppressed by LOC100505817 through miR-20a-inhibted WT1.In summary, our results provided evidence suggesting that LOC100505817 inhibits GC through LOC100505817-mediated inhibition of Wnt/beta-catenin pathway, that leads to the overall restraining of GC cell proliferation, migration and invasion through miR-20a-reduced WT1.	34385891	RID05244	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Breast cancer	CDKN2B-AS1	STK39	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-122-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000198648	NA	100048912	27347	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	DCHT|SPAK	Knockdown of long non-coding RNA CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.Twenty-eight pairs of breast cancer tissue and adjacent normal tissue from breast cancer patients were used to investigate the expression of CDKN2B-AS1 by qRT-PCRAs for the results, there is a relative rich expression of CDKN2B-AS1 in breast cancer tissues compared with the corresponding adjacent normal tissues.Compared with the human breast epithelial cell line, the abundant expression of CDKN2B-AS1 in breast cancer cells were revealed as well.In mechanism, CDKN2B-AS1 sponged the miR-122-5p to regulate STK39 expression.Last, an in vivo model also confirmed that knockdown CDKN2B-AS1 retarded the growth of breast cancer.Our data concluded that knockdown of CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.	34374638	RID05245	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD,BRCA);DOWN(PRAD,PAAD);DATA(GSE40174,GSE104209,GSE60407,GSE55807)
Breast cancer	ARHGAP5-AS1	SMAD7	interact	RNA pull-down assay;RIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(-)	interact with protein	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000258655	GRCh38_14:32074946-32076793	ENSG00000101665	NA	84837	4092	C14orf128|MGC15504	MADH7|MADH8	Long non-coding RNA ARHGAP5-AS1 inhibits migration of breast cancer cell via stabilizing SMAD7 protein.RNA pull-down assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7.dual-luciferase reporter assays were performed to evaluate the activation of TGF-beta signaling.Results: We analyzed the RNA-seq data of MDA-MB-231 and its highly metastatic derivative MDA-MB-231-LM2 cell lines (referred to as LM2) and identified a novel lncRNA (NR_027263) named as ARHGAP5-AS1, which expression was significantly downregulated in LM2 cells.Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2.Conclusion: ARHGAP5-AS1 inhibits breast cancer cell migration via stabilization of SMAD7 protein and could serve as a novel biomarker and a potential target for breast cancer in the future.	34370213	RID05246	interact with protein	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	LOC550643	miR-125b-2-3p	negatively-E	knockdown	upregulation	RT-PCR	NA	NA	prognosis;cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	LOC550643, a Long Non-coding RNA, Acts as Novel Oncogene in Regulating Breast Cancer Growth and Metastasis.Among the cell lines, a novel lncRNA, LOC550643, was highly expressed in breast cancer cells.Furthermore, the high expression of LOC550643 was significantly correlated with the poor prognosis of breast cancer patients, especially those with triple-negative breast cancer.Knockdown of LOC550643 inhibited cell proliferation of breast cancer cells by blocking cell cycle progression at S phase.Furthermore, LOC550643 could inhibit miR-125b-2-3p expression to promote breast cancer cell growth and invasiveness.Overall, our study shows that LOC550643 plays an important role in breast cancer cell metastasis and growth, and LOC550643 could be a potential diagnosis biomarker and therapeutic target for breast cancer.	34354991	RID05247	transcriptional regulation	metastasis,prognosis		
Triple-negative breast cancer	PITPNA-AS1	SIK2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;ChIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-520d-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236618	GRCh38_17:1516877-1518101	ENSG00000170145	NA	100306951	23235	NA	DKFZp434K1115|KIAA0781|LOH11CR1I|QIK|SNF1LK2	MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54.Methods: PITPNA-AS1 expression in TNBC tissues and cells was determined by RT-qPCR.The molecular mechanism of PITPNA-AS1 was explored by RNA pull down, luciferase reporter, RIP and ChIP assays.Results: PITPNA-AS1 showed high expression levels in TNBC tissues and cells.Mechanistically, PITPNA-AS1 upregulated SIK2 expression by sponging miR-520d-5p and recruiting DDX54 protein.More importantly, we found that the upregulation of PITPNA-AS1 in TNBC cells was attributed to transcription factor MYBL2.Conclusion: PITPNA-AS1 activated by MYBL2 plays an oncogenic role in TNBC through upregulating SIK2.	34353336	RID05248	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE55807,GSE75367)
Triple-negative breast cancer	MYBL2	PITPNA-AS1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;ChIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000101057	NA	ENSG00000236618	GRCh38_17:1516877-1518101	4605	100306951	B-MYB|BMYB	NA	MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54.Methods: PITPNA-AS1 expression in TNBC tissues and cells was determined by RT-qPCR.The molecular mechanism of PITPNA-AS1 was explored by RNA pull down, luciferase reporter, RIP and ChIP assays.Results: PITPNA-AS1 showed high expression levels in TNBC tissues and cells.Mechanistically, PITPNA-AS1 upregulated SIK2 expression by sponging miR-520d-5p and recruiting DDX54 protein.More importantly, we found that the upregulation of PITPNA-AS1 in TNBC cells was attributed to transcription factor MYBL2.Conclusion: PITPNA-AS1 activated by MYBL2 plays an oncogenic role in TNBC through upregulating SIK2.	34353336	RID05249	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Non-small cell lung cancer	LINC00852	KLF4	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemosensitivity(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000231177	GRCh38_3:10284419-10285746	ENSG00000136826	NA	84657	9314	C3orf42|GHRL-AS2|GHRLOS2|NAG73	EZF|GKLF	LINC00852 is associated with poor prognosis in non-small cell lung cancer patients and its inhibition suppresses cancer cell proliferation and chemoresistance via the hsa-miR-145-5p/KLF4 axis.Methods: LINC00852 expression was examined by quantitative real-time PCR (qRT-PCR in both NSCLC clinical samples and in vitro NSCLC cell lines.The potential downstream target of LINC00852, the axis of human microRNA-145-5p (hsa-miR-145-5p) and Kruppel-like factor 4 (KLF4) gene, was investigated in NSCLC, by dual-luciferase assay, qRT-PCRand genetic knockdown functional assays.Results: LINC00852 is up-regulated in both NSCLC tumors and NSCLC cell lines.Moreover, the hsa-miR-145-5p/KLF4 axis was demonstrated to be directly regulated by LINC00852 in NSCLC.Inhibiting hsa-miR-145-5p or overexpressing KLF4 could reverse the LINC00852-down-regulation-induced anti-cancer effects on NSCLC cancer cell proliferation and chemoresistance.The epigenetic signaling pathway of LINC00852/hsa-miR-145-5p/KLF4 may be considered as a novel molecular target for fighting NSCLC.	34342374	RID05250	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Oral cavity cancer	MROS-1	PRUNE2	positively-E		upregulation		NA	NA	JAK/STAT signaling pathway(+);cell migration(+)	transcriptional regulation	association	RNA-protein	Melatonin	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	NA	NA	ENSG00000106772	NA	NA	158471	NA	A214N16.3|bA214N16.3|BMCC1|BNIPXL|C9orf65|KIAA0367	A novel melatonin-regulated lncRNA suppresses TPA-induced oral cancer cell motility through replenishing PRUNE2 expression.In this study, we identified a melatonin-attenuated lncRNA acting as a potential melatonin-regulated oral cancer stimulator (MROS-1).Downregulation of MROS-1 by melatonin suppressed TPA-induced oral cancer migration through replenishing the protein expression of prune homolog 2 (PRUNE2), which functioned as a tumor suppressor in oral cancer.Melatonin-mediated MROS-1/PRUNE2 expression and cell motility in oral cancer were regulated largely through the activation of JAK-STAT pathway.In addition, MROS-1, preferentially localized in the nuclei, promoted oral cancer migration in an epigenetic mechanism in which it modulates PRUNE2 expression by interacting with a member of the DNA methylation machinery, DNA methyltransferase 3A (DNMT3A).Higher methylation levels of PRUNE2 promoter were associated with nodal metastases and inversely correlated with PRUNE2 expression in head and neck cancer.Collectively, these findings suggest that MROS-1, serving as a functional mediator of melatonin signaling, could predispose patients with oral cancer to metastasize and may be implicated as a potential target for antimetastatic therapies.	34339541	RID05251	transcriptional regulation	metastasis		UP(LIHC);DOWN(NSCLC);DATA(GSE117623,GSE74639)
Colorectal cancer	ELFN1-AS1	MTA1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-1250)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000236081	GRCh38_7:1738630-1742291	ENSG00000182979	NA	101927125	9112	MYCLo-2	NA	A long non-coding RNA, ELFN1-AS1, sponges miR-1250 to upregulate MTA1 to promote cell proliferation, migration and invasion, and induce apoptosis in colorectal cancer.Patients and methods: First, we found that ELFN1-AS1 was highly abundant in the human CRC tissues and cell lines.Silence of ELFN1-AS1 expression reduced cell proliferation, colony formation, migration and invasion, while inducing apoptosis in vitro; moreover, knockdown of ELFN1-AS1 decreased the size and weight of tumor in vivo.Results: Luciferase reporter assay revealed that ELFN1-AS1 interacted with miR-1205 and suppressed its expression.Conclusions: In sum, our study demonstrated that ELFN1-AS1 sponges miR-1205 to upregulate MTA1, which is essential for CRC cell proliferation, migration, and invasion as well as apoptosis induction.	34337713	RID05252	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	NR2F1-AS1	MAP3K2	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-493-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000169967	NA	441094	10746	FLJ42709	MEKK2|MEKK2B	The Effect and Mechanism of lncRNA NR2F1-As1/miR-493-5p/MAP3K2 Axis in the Progression of Gastric Cancer.Methods: The expression patterns of NR2F1-AS1, MAP3K2, and miR-493-5p in GC tissues and cells were detected by RT-qPCR.The relationship between NR2F1-AS1, MAP3K2, and miR-493-5p was verified by a dual-luciferase reporter assay.Results: The increased NR2F1-AS1 and MAP3K2 expressions were discovered in GC tissues and cells compared with control groups.Knockdown of NR2F1-AS1 and MAP3K2 dramatically suppressed cell proliferation and migration, while it enhanced cell apoptosis in GC cells.In addition, NR2F1-AS1 was found to be a sponge of miR-493-5p, and MAP3K2 was a downstream gene of miR-493-5p.Moreover, the expression of MAP3K2 was notably reduced by miR-493-5p, and NR2F1-AS1 counteracted the inhibition of miR-493-5p.Conclusion: Thus, NR2F1-AS1 was verified to regulate GC cell progression by sponging miR-493-5p to upregulate MAP3K2 expression.	34335755	RID05253	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	AFAP1-AS1	VEGFC	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell stemness(-)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000150630	NA	84740	7424	AFAP1-AS|AFAP1AS|MGC10981	VEGF-C|VRP	LncRNA AFAP1-AS1/miR-27b-3p/VEGF-C axis modulates stemness characteristics in cervical cancer cells.The levels of AFAP1-AS1 were measured by quantitative real-time PCR (qRT-PCR.RNA pull-down and luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor (VEGF)-C.Conclusions: LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.	34334630	RID05254	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	Lnc-STYK1-2	ITGA2	positively-E	dual-luciferase reporter analysis	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);tumorigenesis(-);AKT/STAT3/NF-kB signaling pathway(-)	ceRNA(miR-146b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	NA	ENSG00000164171	NA	NA	3673	NA	BR|CD49B|GPIa|HPA-5|VLA-2|VLAA2	Lnc-STYK1-2 regulates bladder cancer cell proliferation, migration, and invasion by targeting miR-146b-5p expression and AKT/STAT3/NF-kB signaling.Methods: Differential lncRNA and mRNA profiles were characterized by high-throughput RNA sequencing combined with validation via quantitative PCR.The dual-luciferase reporter assay verified the association of miR-146b-5p with lnc-STYK1-2 and the target gene.Results: Alterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues.lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice.lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells.Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association.Conclusion: lnc-STYK1-2 inhibited bladder cancer cell proliferation, migration, and tumorigenesis by targeting miR-146b-5p to regulate ITGA2 expression and AKT/STAT3/NF-kB signaling.	34332611	RID05255	ceRNA or sponge	NA		UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE40174)
Multiple myeloma	HCP5	PLAGL2	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin/cyclin D1 signaling pathway(+);cancer progression(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000126003	NA	10866	5326	D6S2650E|P5-1	ZNF900	LncRNA HCP5 acts as a miR-128-3p sponge to promote the progression of multiple myeloma through activating Wnt/beta-catenin/cyclin D1 signaling via PLAGL2.Methods: HCP5 level in MM was assessed through qRT-PCRBioinformatics analysis and RIP/RNA pull-down assays were carried out to determine the relationships among HCP5, miR-128-3p, and PLAGL2.Results: HCP5 was significantly increased in MM. HCP5 knockdown effectively thwarted the proliferative rate and cell cycle of MM cell lines and suppressed tumor growth.HCP5 regulated PLAGL2 expression by sponging miR-128-3p.Conclusion: Our study revealed that HCP5/miR-128-3p/PLAGL2 is closely correlated to MM development by modulating Wnt/beta-catenin/cyclin D1 signaling.HCP5 promoted cell proliferation and tumor formation of MM cells by activating the Wnt/beta-catenin/CCND1 signaling pathway by sponging miR-128-3p to increase PLAGL2 expression.	34331612	RID05256	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807,GSE75367)
Gastric cancer	IGF2-AS	CREB1	positively-E	dual-luciferase reporter analysis;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);prognosis;glycolysis(-)	ceRNA(miR-195)	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Gastric cancer	lncRNA	TF	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000118260	NA	51214	1385	IGF2-AS1|IGF2AS|PEG8	NA	IGF2-AS knockdown inhibits glycolysis and accelerates apoptosis of gastric cancer cells through targeting miR-195/CREB1 axis.The expression levels of IGF2-AS, miR-195 and cAMP responsive element binding protein 1 (CREB1) mRNA were assessed by qRT-PCRThe targeted interaction between miR-195 and IGF2-AS or CREB1 was validated using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays.Our data revealed that IGF2-AS was upregulated in GC tissues and predicted poor prognosis.Moreover, IGF2-AS acted as a sponge of miR-195 and CREB1 was a direct target of miR-195.In conclusion, our study suggested that IGF2-AS knockdown suppressed glycolysis and facilitated apoptosis in GC cells at least partly through sponging miR-195 and modulating CREB1 expression, highlighting a novel therapeutic strategy for GC treatment.	34321174	RID05257	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Atherosclerosis	TUG1	miR-382-5p	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	association	RNA-RNA	Taurine	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	lncRNA TUG1 promotes atherosclerosis progression by targeting miR-382-5p.Methods: The levels of TUG1 and miR-382-5p in atherosclerotic serum samples and a cell model were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).Moreover, the interaction between TUG1 and miR-382-5p was confirmed by luciferase assay.Results: TUG1 and miR-382-5p expressions were significantly increased and decreased, respectively, in both atherosclerotic serum samples and a cell model.In addition, the expression of TUG1 was negatively correlated with the level of miR-382-5p in atherosclerotic serum samples.Moreover, silencing of TUG1 reduced cell growth and enhanced the apoptosis of ox-LDL-treated VSMCs.Conclusion: TUG1 can aggravate atherosclerosis progression by reducing the expression of miR-382-5p.	34646415	RID05258	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Myocardial infarction	SNHG1	MYC	positively-E	luciferase reporter assay;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000136997	NA	23642	4609	LINC00057|lncRNA16|NCRNA00057|UHG	bHLHe39|c-Myc|MYCC	LncRNA Snhg1-driven self-reinforcing regulatory network promoted cardiac regeneration and repair after myocardial infarction.We aimed to determine whether the lncRNA small nucleolar RNA host gene 1 Snhg1 (Snhg1) could form a positive feedback loop with c-Myc to induce cardiac regeneration.Methods: Quantitative PCR and in situ hybridization experiments were performed to determine the Snhg1 expression patterns in fetal and myocardial infarction (MI) hearts.RNA sequencing and RNA pull-down were performed to explore how Snhg1 mediated cardiac regeneration.Chromatin immunoprecipitation and luciferase reporter assays were used to demonstrate the positive feedback loop between Snhg1 and c-Myc.Results: Snhg1 expression was increased in human and mouse fetal and myocardial infarction (MI) hearts, particularly in CMs.Overexpression of Snhg1 promoted CM proliferation, angiogenesis, and inhibited CM apoptosis after myocardial infarction, which further improved post-MI cardiac function.Mechanistically, Snhg1 directly bound to phosphatase and tensin homolog (PTEN) and induced PTEN degradation, activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway to promote CM proliferation.The c-Myc protein, one of downstream targets of PI3K/AKT signaling, functioned as a transcription factor by binding to the promoter regions of Snhg1.Perturbation of the positive feedback between Snhg1 and c-Myc by mutation of the binding sequence significantly affected Snhg1-induced CM proliferation.Conclusions: Snhg1 effectively elicited CM proliferation and improved cardiac function post-MI by forming a positive feedback loop with c-Myc to sustain PI3K/Akt signaling activation, and thus may be a promising cardiac regeneration strategy in treating heart failure post-MI.	34646377	RID05259	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Myocardial infarction	SNHG1	PTEN	negatively-E	luciferase reporter assay;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000171862	NA	23642	5728	LINC00057|lncRNA16|NCRNA00057|UHG	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA Snhg1-driven self-reinforcing regulatory network promoted cardiac regeneration and repair after myocardial infarction.We aimed to determine whether the lncRNA small nucleolar RNA host gene 1 Snhg1 (Snhg1) could form a positive feedback loop with c-Myc to induce cardiac regeneration.Methods: Quantitative PCR and in situ hybridization experiments were performed to determine the Snhg1 expression patterns in fetal and myocardial infarction (MI) hearts.RNA sequencing and RNA pull-down were performed to explore how Snhg1 mediated cardiac regeneration.Chromatin immunoprecipitation and luciferase reporter assays were used to demonstrate the positive feedback loop between Snhg1 and c-Myc.Results: Snhg1 expression was increased in human and mouse fetal and myocardial infarction (MI) hearts, particularly in CMs.Overexpression of Snhg1 promoted CM proliferation, angiogenesis, and inhibited CM apoptosis after myocardial infarction, which further improved post-MI cardiac function.Mechanistically, Snhg1 directly bound to phosphatase and tensin homolog (PTEN) and induced PTEN degradation, activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway to promote CM proliferation.The c-Myc protein, one of downstream targets of PI3K/AKT signaling, functioned as a transcription factor by binding to the promoter regions of Snhg1.Perturbation of the positive feedback between Snhg1 and c-Myc by mutation of the binding sequence significantly affected Snhg1-induced CM proliferation.Conclusions: Snhg1 effectively elicited CM proliferation and improved cardiac function post-MI by forming a positive feedback loop with c-Myc to sustain PI3K/Akt signaling activation, and thus may be a promising cardiac regeneration strategy in treating heart failure post-MI.	34646377	RID05260	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Glioblastoma	IGF2BP2	CASC9	interact	knockdown	upregulation	qPCR	NA	NA	glucose metabolic process(+)	transcriptional regulation	association	protein-RNA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Brain glioma	PCG	lncRNA	ENSG00000073792	NA	ENSG00000249395	GRCh38_8:75120409-75352327	10644	101805492	IMP-2|p62	ESCCAL-1|linc-JPH1|LINC00981	m 6 A reader IGF2BP2-stabilized CASC9 accelerates glioblastoma aerobic glycolysis by enhancing HK2 mRNA stability.Moreover, the m6A-related lncRNA CASC9 expression was significantly elevated in the GBM tissue and its ectopic high expression was associated with poor survival, acting as an independent prognostic factor for GBM patients.Functionally, the aerobic glycolysis was promoted in the CASC9 overexpression transfection, which was inhibited in CASC9 knockdown in GBM cells.Mechanistically, m6A reader IGF2BP2 (insulin-like growth factor 2 mRNA binding protein 2) could recognize the m6A site of CASC9 and enhance its stability, then CASC9 cooperated with IGF2BP2, forming an IGF2BP2/CASC9 complex, to increase the HK2 (Hexokinase 2) mRNA stability.Our findings reveal that CASC9/IGF2BP2/HK2 axis promotes the aerobic glycolysis of GBM.	34645788	RID05261	transcriptional regulation	prognosis	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)
Malignant glioma	LINC01138	SP1	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000215863	NA	ENSG00000185591	NA	388685	6667	FLJ39739|LINC00875	NA	Silencing long noncoding RNA LINC01138 inhibits aerobic glycolysis to reduce glioma cell proliferation by regulating the microRNA-375/SP1 axis.The aim of the present study was to investigate the mechanism by which long intergenic non-protein coding RNA (LINC) 01138 affects glycolysis and proliferation in glioma cells via the microRNA (miR)-375/specificity protein 1 (SP1) axis.LINC01138 expression was assessed in glioma tissues and cells using reverse transcription-quantitative PCR and the association between LINC01138 and patient clinicopathological features was analyzed.miR-375 and SP1 expression levels were also assessed, and the distribution of LINC01138 in the nucleus and cytoplasm was investigated using subcellular fractionation localization.Furthermore, the binding relationships between LINC01138 and miR-375, and between miR-375 and SP1 were assessed via dual-luciferase experiment, RIP and RNA pull-down assays.LINC01138 was highly expressed in glioma, which was independent of patient sex or age but was significantly related to tumor diameter, the World Health Organization tumor grade and lymph node metastasis.Moreover, LINC01138 acted as a competing endogenous RNA to sponge miR-375 and promote SP1 expression.The present study demonstrated that silencing LINC01138 inhibited aerobic glycolysis and thus reduced glioma cell proliferation, potentially by modulating the miR-375/SP1 axis.	34643249	RID05262	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	RP11-84C13.1	RUNX2	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	cancer progression(-)	ceRNA(miR-23b-3p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000271359	NA	ENSG00000124813	NA	NA	860	NA	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	Long non-coding RNA RP11-84C13.1 promotes osteogenic differentiation of bone mesenchymal stem cells and alleviates osteoporosis progression via the miR-23b-3p/RUNX2 axis.Runt-related transcription factor 2 (RUNX2) and RP11-84C13.1 serum levels were assessed by reverse transcription-quantitative (RT-q)PCR.Following transfection of pcDNA-RP11-84C13.1, si-RP11-84C13.1, microRNA (miRNA)-23b-3p mimic and miRNA-23b-3p inhibitor, the expression levels of RUNX2 and RP11-84C13.1 were determined by RT-qPCR.The binding of RP11-84C13.1 to miRNA-23b-3p and the binding of miRNA-23b-3p to RUNX2 was confirmed by dual-luciferase reporter gene assay.The osteogenic differentiation-related genes RUNX2 and RP11-84C13.1 were markedly upregulated in a time-dependent manner, while the miRNA-23b-3p level gradually decreased in hBMSCs with the prolongation of osteogenesis.Furthermore, RP11-84C13.1 regulated RUNX2 expression by targeting miRNA-23b-3p.In conclusion, lncRNA RP11-84C13.1 upregulated RUNX2 by absorbing miRNA-23b-3p, and thus induced hBMSC osteogenesis to alleviate osteoporosis.	34630694	RID05263	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	MALAT1	MAT2A	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-485-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168906	NA	378938	4144	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MATA2|MATII|SAMS2	MALAT1 Inhibits Proliferation of HPV16-Positive Cervical Cancer by Sponging miR-485-5p to Promote Expression of MAT2A.In the current study, we documented that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA, is upregulated in HPV16-positive cervical cancer tissue and cell lines.Mechanistically, our results suggested that MALAT1 upregulates Methionine adenosyltransferase 2A (MAT2A) by sponging miR-485-5p.Taken together, our results demonstrated that MALAT1 acts as a competitive endogenous RNA (ceRNA) to regulate MAT2A by sponging miR-485-5p in HPV16-positive cervical cancer, suggesting that MALAT1 may act as a potential therapeutic target for HPV16-positive cervical cancer.	34610246	RID05264	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	PSMA3-AS1	CD274	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000257621	GRCh38_14:58265365-58298134	ENSG00000120217	NA	379025	29126	FLJ31306	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	lncRNA PSMA3-AS1 promotes the progression of non-small cell lung cancer through targeting miR-17-5p/PD-L1.Material and methods: The expression of PSMA3-AS1, miR-17-5p and PD-L1 in a human bronchial epithelial cell line, BEAS-2B, and NSCLC cell lines, H226 and A549, were detected with quantitative real-time polymerase chain reaction (qRT-PCR or western blot.Double fluorescent enzyme reporting was used to detect the relationship between PSMA3-AS1, miR-17-5p and PD-L1.Results: The expression of PSMA3-AS1 in NSCLC cells was significantly higher than in human bronchial epithelial cells.In addition, double fluorescent enzyme results showed that PSMA3-AS1 could competitively bind miR-17-5p to PD-L1.The expression of miR-17-5p is low in lung cancer cells, while the expression of PD-L1 in them is high.Overexpression of PD-L1 reversed the inhibitory effect of PSMA3-AS1 knockdown on the proliferation, migration and invasion of lung cancer cells.Conclusions: Generally speaking, PSMA3-AS1 is highly expressed in NSCLC.The PSMA3-AS1 can promote the proliferation, migration and invasion of NSCLC cells by regulating miR-17-5p/PD-L1.	34610219	RID05265	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Atherosclerosis	AL355711	ABCG1	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cancer progression(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000160179	NA	NA	9619	NA	ABC8	Long non-coding RNA AL355711 promotes smooth muscle cell migration through the ABCG1/MMP3 pathway.The expression of lncRNAs or mRNAs was detected using reverse transcription-quantitative polymerase chain reaction.The expression of lncRNA AL355711, ABCG1 and MMP3 was found to be higher in human atherosclerotic plaques or in patients with atherosclerotic CAD.The correlation analysis revealed that ABCG1 may be involved in the regulation between lncRNA AL355711 and MMP3 in atherosclerotic CAD.The knockdown of lncRNA AL355711 inhibited ABCG1 transcription and smooth muscle cell migration.In addition, lncRNA AL355711 was found to regulate MMP3 expression through the ABCG1 pathway.The expression of ABCG1 and MMP3 was found to be high in an animal model of atherosclerosis.The results indicated that lncRNA AL355711 promoted VSMC migration and atherosclerosis partly via the ABCG1/MMP3 pathway.	34608503	RID05266	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE51827,GSE75367,GSE86978,GSE41245)
Steroid-induced necrosis of femoral head	NEAT1	CYP1A2	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-23b-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Osteonecrosis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000140505	NA	283131	1544	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CP12|P3-450	lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis.The aim of this article was to investigate the role of lncRNA NEAT1 as a molecular sponge to adsorb miR-23b-3p and regulate CYP1A2 in SNFH.Compared to the control group, the lncRNA NEAT1 and CYP1A2 expression in the SNFH group was increased, while miR-23b-3p expression was decreased.GCs could inhibit the osteogenic differentiation of hBMSCs and upregulate the expression of lncRNA NEAT1.Knockdown of lncRNA NEAT1 could promote the proliferation and osteogenic differentiation of hBMSCs in the SNFH group.In conclusion, lncRNA NEAT1 as a ceRNA can adsorb miR-23b-3p and promote the expression of CYP1A2, which then inhibits the osteogenic differentiation of hBMSCs and promotes the progress of SNFH.	34595348	RID05267	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatoblastoma	SNHG9	WNT3A	positively-E	dual luciferase reporter activity; RNA immunoprecipitation (RIP); biotin RNA pull down;Spemann's Pearson correlation coefficient assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-23a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255198	GRCh38_16:1964899-1965509	ENSG00000154342	NA	735301	89780	DKFZp686N06141|NCRNA00062	NA	SNHG9 promotes Hepatoblastoma tumorigenesis via miR-23a-5p/Wnt3a Axis.Methods: In this study, we estimated SNHG9 expression in hepatoblastoma tissue and cell lines by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR.Next, we downregulated and upregulated SNHG9 expression in hepatoblastoma cell lines and then determined cell proliferation (CCK-8), colony formation, and cellular apoptosis activity.The dual luciferase reporter activity, RNA immunoprecipitation (RIP), biotin RNA pull down and Spemann's Pearson correlation coefficient assay were performed to establish the interaction between SNHG9, WNt3a and miR- 23a-5p.A xenograft in-vivo tumorgenicity test was performed to elucidate the role of SNHG9 hepatoblastoma in tumorigenesis.Results: SNHG9 was significantly upregulated in hepatoblastoma tissue and cell lines.Dual luciferase activity, RNA immunoprecipitation and biotin pull down confirmed the direct interaction of miR-23a-5p with SNHG9.The xenograft tumorgenicity test showed SNHG9 downregulation significantly inhibited the tumor growth in BALB/c mice.Conclusion: We concluded that SNHG9/miR-23a-5p/Wnt3a axis promotes the progression hepatoblastoma tumor.	34539877	RID05268	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(PAAD);DATA(GSE40174)
Pancreatic cancer	SNHG11	VEGFA	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);angiogenesis(+)	ceRNA(miR-324-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000174365	GRCh38_20:38446343-38450940	ENSG00000112715	NA	128439	7422	C20orf198|LINC00101	VEGF|VEGF-A|VPF	Exosome-mediated lncRNA SNHG11 regulates angiogenesis in pancreatic carcinoma through miR-324-3p/VEGFA axis.LncRNA SNHG11 (SNHG11) has been found to display high expression in serum of PC patients, which implies that dysregulated SNHG11 may be related to the development of PC.After conducting experiments with constructed models in vitro or in vivo, we found that exosomal SNHG11 promoted cell proliferation, migration, and angiogenesis but impeded cell apoptosis in PC in vitro, and additionally, it facilitated tumor growth in vivo.Exosome-mediated SNHG11 regulated the expression of VEGFA through sponging miR-324-3p.Rescue assays validated that the inhibitory effect of SNHG11 depletion on cell proliferation, migration, and angiogenesis could be reversed by miR-324-3p downregulation or VEGFA upregulation, and the promoting effect of SNHG11 silence on cell apoptosis could be rescued by transfection of miR-324-3p inhibitor or pcDNA3.1-VEGFA.To conclude, exosomal-mediated SNHG11 could regulate PC progression via miR-324-3p/VEGFA axis.	34519129	RID05269	ceRNA or sponge	NA	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Liver cancer	NKILA	miR-485-5p	negatively-E	dual-luciferase reporter analysis	upregulation	PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	LncRNA NKILA Promotes Epithelial-Mesenchymal Transition of Liver Cancer Cells by Targeting miR-485-5p.The LncRNA NKILA and miR-485-5p level in cancer and adjacent tissues, LC, and normal liver cells of patients was tested by PCR.At last, the relationship between LncRNA NKILA and miR-485-5p was assessed by a dual-luciferase reporter assay.Results: The LncRNA NKILA expression was high in LC tissues and cells (P < 0.050), while miR-485-5p was low compared with the normal adjacent tissues (P < 0.050).Prognostic follow-up manifested that high LncRNA NKILA or low miR-485-5p could predict the poor prognosis and high mortality risk of the patients (P < 0.050).LC cells with downregulated LncRNA NKILA documented inhibited proliferation, invasion, and EMT, while the apoptosis level of the cells increased (P < 0.050).The proliferation, invasion, and EMT were inhibited by miR-485-5p increase, while the apoptosis of the cells decreased after upregulating miR-485-5p (P < 0.050).Online websites predicted that LncRNA NKILA had a binding site with miR-485-5p, and dual-luciferase reporter assay confirmed that LncRNA NKILA could directly target with miR-485-5p (P < 0.050).Conclusion: The LncRNA NKILA with high expression advances LC cell proliferation, invasion, and EMT by targeting miR-485-5p.	34512751	RID05270	expression association	prognosis		
Airway hyper-reactivity	TUG1	CELF1	positively-E	dual-luciferase reporter analysis;RNA immunoprecipitation assay (RIP) analysis	upregulation	qRT-PCR	NA	NA	cell cycle(+)	ceRNA(miR-222-3p)	regulation	RNA-protein	Taurine	NA	Self Sufficiency in Growth Signals	Immune system disease	Respiratory allergy	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000149187	NA	55000	10658	FLJ20618|LINC00080|NCRNA00080	BRUNOL2|CUG-BP|CUGBP|CUGBP1|EDEN-BP|hNab50|NAB50|NAPOR	lncRNA TUG1 as a ceRNA promotes PM exposure-induced airway hyper-reactivity.Alterations in messenger RNA (RNA), microRNA and long non-coding RNA (lncRNA) profiles of human bronchial epithelial (HBE) cells treated with PM were analyzed by microarray assays.Next, we identified that lncRNA taurine upregulated gene 1 (TUG1) acted as a competing endogenous RNA for microRNA-222-3p (miR-222-3p) and subsequently attenuated the inhibitory effect of miR-222-3p on CUGBP elav-like family member 1 (CELF1).The binding potency among ceRNAs was verified by RNA immunoprecipitation (RIP) assay and dual-luciferase reporter assay.Knockdown of TUG1 attenuated HBE cell apoptosis and cell cycle arrest by downregulation of CELF1 and protein 53 (p53).In summary, our novel findings revealed that TUG1 triggered dysfunction of pulmonary cells followed by PM exposure by serving as a sponge for miR-222-3p and thereby upregulating the expression of CELF1and p53.	34492818	RID05271	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteomyelitis	NONHSAT009986	WNT3A	negatively-F			qRT-PCR	NA	NA	tumorigenesis(-)	transcriptional regulation	association	RNA-protein	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000154342	NA	NA	89780	NA	NA	LncRNA NONHSAT009968 inhibits the osteogenic differentiation of hBMMSCs in SA-induced inflammation via Wnt3a.In our previous study, we found that long non-coding RNA (lncRNA) NONHSAT009968 inhibited the ability of osteogenic differentiation in staphylococcal protein A (SPA)-treated human bone marrow mesenchymal stem cells (hBMMSCs), but the underlying mechanism remains unclear.In addition, NONHSAT009968 inhibited osteogenic differentiation of hBMMSCs treated with SPA via Wnt3a, both in vivo and in vitro.In sum, the results suggested that lncNONHSAT009968 inhibited osteogenic differentiation of hBMMSCs in SA-induced inflammation through Wnt3a, which may have affected the occurrence and development of osteomyelitis.	34492499	RID05272	transcriptional regulation	NA		UP(PAAD);DATA(GSE40174)
Unexplained recurrent spontaneous abortion	RP11-115N4.1	HNRNPH3	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	inflammatory response	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Other	Miscarriage	lncRNA	PCG	ENSG00000243144	GRCh38_7:91311368-91515427	ENSG00000096746	NA	NA	3189	NA	2H9|HNRPH3	Long Noncoding RNA RP11-115N4.1 Promotes Inflammatory Responses by Interacting With HNRNPH3 and Enhancing the Transcription of HSP70 in Unexplained Recurrent Spontaneous Abortion.Results: RP11-115N4.1 was identified as the most differentially expressed lncRNA which was highly upregulated in peripheral blood of non-pregnant URSA patients (P = 3.63E-07, Fold change = 2.96), and this dysregulation was further validated in approximately 26.67% additional patients (4/15).Furthermore, heat-shock HSP70 genes (HSPA1A and HSPA1B) were found to be significantly upregulated upon RP11-115N4.1 overexpression by transcriptome analysis (HSPA1A (P = 4.39E-08, Fold change = 4.17), HSPA1B (P = 2.26E-06, Fold change = 2.99)).RNA pull down and RNA immunoprecipitation assay (RIP) analysis demonstrated that RP11-115N4.1 bound to HNRNPH3 protein directly, which in turn activate heat-shock proteins (HSP70) analyzed by protein-protein interaction and HNRNPH3 knockdown assays.Conclusion: Our results demonstrated that the activation of RP11-115N4.1 can significantly increase the protein level of HSP70 via binding to HNRNPH3, which may modulate the immune responses and related to URSA.	34484222	RID05273	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Breast cancer	SNHG1	TERT	positively-E		upregulation		NA	NA	prognosis(-)	ceRNA(miR-18b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000164362	NA	23642	7015	LINC00057|lncRNA16|NCRNA00057|UHG	EST2|hEST2|TCS1|TP2|TRT	Long noncoding RNA SNHG1 promotes TERT expression by sponging miR-18b-5p in breast cancer.Results: LncRNA SNHG1 was upregulated and had a positive relationship with poor prognosis according to bioinformatics analysis in pan-cancer including breast cancer.Mechanistically, SNHG1 functioned as a competing endogenous RNA (ceRNA) to promote TERT expression by sponging miR-18b-5p in breast cancer.Finally, E2F1 as a transcription factor, binding to SNHG1 promoter and enhanced SNHG1 transcription in breast cancer.	34465388	RID05274	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Breast cancer	SNHG1	TERT	positively-E	luciferase reporter assay;CoIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis	ceRNA(miR-18b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000164362	NA	23642	7015	LINC00057|lncRNA16|NCRNA00057|UHG	EST2|hEST2|TCS1|TP2|TRT	Long noncoding RNA SNHG1 promotes TERT expression by sponging miR-18b-5p in breast cancer.Results: LncRNA SNHG1 was upregulated and had a positive relationship with poor prognosis according to bioinformatics analysis in pan-cancer including breast cancer.Mechanistically, SNHG1 functioned as a competing endogenous RNA (ceRNA) to promote TERT expression by sponging miR-18b-5p in breast cancer.Finally, E2F1 as a transcription factor, binding to SNHG1 promoter and enhanced SNHG1 transcription in breast cancer.	34465388	RID05275	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Breast cancer	E2F1	SNHG1	positively-E	luciferase reporter assay;CoIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000255717	GRCh38_11:62851978-62855953	1869	23642	RBBP3|RBP3	LINC00057|lncRNA16|NCRNA00057|UHG	Long noncoding RNA SNHG1 promotes TERT expression by sponging miR-18b-5p in breast cancer.Results: LncRNA SNHG1 was upregulated and had a positive relationship with poor prognosis according to bioinformatics analysis in pan-cancer including breast cancer.Mechanistically, SNHG1 functioned as a competing endogenous RNA (ceRNA) to promote TERT expression by sponging miR-18b-5p in breast cancer.Finally, E2F1 as a transcription factor, binding to SNHG1 promoter and enhanced SNHG1 transcription in breast cancer.	34465388	RID05276	transcriptional regulation	prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	GSTM3TV2	FOSL2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-597)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000075426	NA	NA	2355	NA	FLJ23306|FRA2	LncRNA GSTM3TV2 Promotes Cell Proliferation and Invasion via miR-597/FOSL2 Axis in Hepatocellular Carcinoma.We observed that the expression of lncRNA GSTM3TV2 and FOSL2 were upregulated in HCC.Meanwhile, the migration and invasion of HCC cells were greatly decreased by the downregulated lncRNA GSTM3TV2.The luciferase reporter assays showed that lncRNA GSTM3TV2 could be directly bound to miR-597, and the level of miR-597 was also decreased in the tumor tissues.lncRNA GSTM3TV2 could stabilize FOSL2 expression, resulting in the oncogenic properties of lncRNA GSTM3TV2 in HCC.	34458365	RID05277	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	SP7	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-96)	regulation	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170374	NA	378938	121340	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	osterix|OSX	Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes the Osteoblast Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells by Targeting the microRNA-96/Osterix Axis.Metastasis-associated lung adenocarcinoma transcript 1, miR-96, and osteogenesis-related Messenger RNA expression was assessed by Quantitative Real-time Polymerase Chain Reaction (qRT-PCR.The interactions between miR-96 and osterix (Osx), MALAT1, and miR-96 were determined by luciferase reporter assay.Results: The expression of MALAT1 was upregulated whereas that of miR-96 was downregulated in osteogenic hBMSCs.In addition, the expression of MALAT1 significantly decreased whereas that of miR-96 increased in the hBMSCs of osteoporosis (OP) patients.Dual luciferase report assay verified that miR-96 is a regulatory target of MALAT1 and that Osx is a gene target of miR-96.Conclusions: Taken together, the results demonstrate that MALAT1 promotes the osteogenic differentiation of hBMSCs by regulating the miR-96/Osx axis.	34456284	RID05278	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Parkinson's disease	HAGLR	MECP2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000169057	NA	401022	4204	HOXD-AS1|Mdgt|MIR7704HG	MRX16|MRX79|RTT	HAGLR promotes neuron differentiation through the miR-130a-3p-MeCP2 axis.By microarray analysis, lncRNA HAGLR was observed to be significantly upregulated during the RA-induced SH-SY5Y differentiation.The RNA-pull down assay and luciferase assay demonstrated that HAGLR functioned as a ceRNA of miR-130a-3p in SH-SY5Y cells.We identified MeCP2, a vital molecule in neuronal diseases, to be a direct target of miR-130a-3p in SH-SY5Y cells by western blot and luciferase assays.In summary, this study reveals a potential molecular mechanism for the lncRNA-HAGLR-promoted in vitro neuron differentiation by targeting the miR-130a-3p-MeCP2 axis, contributing to the understanding of the pathogenesis and progression of PD.	34430707	RID05279	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Gastric cancer	HDAC3	LOC101928316	negatively-E				NA	NA	cell viability(+);cell invasion(+);cell migration(+);PI3K/AKT/mTOR signaling pathway(+);chemosensitivity(-)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000171720	NA	NA	NA	8841	NA	HD3|KDAC3|RPD3|RPD3-2	NA	HDAC3-mediated lncRNA-LOC101928316 contributes to cisplatin resistance in gastric cancer via activating the PI3K-Akt-mTOR pathway.We revealed that HDAC3 expression in cisplatin-resistant cell lines was significantly higher than that of GC parental cell lines.To our surprise, silencing HDAC3 inhibited the transcription of LOC101928316 by promoting the level of acetylation of H3K4 on the LOC101928316 promoter, thus promoting the LOC101 expression in GC cisplatin-resistant cell lines.Together, the overexpression of HDAC3 mediated LOC101928316 to promote GC resistance to cisplatin by activating the PI3K-Akt-mTOR pathway.	34427099	RID05280	transcriptional regulation	chemoresistance	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)	
Non-small cell lung cancer	LINC01224	MIR2467	negatively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000269416	GRCh38_19:23399097-23416075	ENSG00000264292	NA	104472717	100616360	NA	mir-2467	Long non-coding RNA LINC01224 promotes progression and cisplatin resistance in non-small lung cancer by sponging miR-2467.Presently, LINNC01224 expression was elevated and miR-2467 expression was down-regulated in NSCLC, compared with standard control.Afterward, the dual-luciferase reporter assay, RIP assay and RNA pull-down assay validated the base-pair interaction between LINC01224 and miR-2467.Moreover, our findings demonstrated that the silence of LINC01224 inhibited cell proliferation and invasion in NSCLC and enhanced cisplatin (CDDP) sensitivity in vitro.To sum up, LINC01224 can promote tumor progression and CDDP resistance in NSCLC via sponging miR-2467, suggesting a promising therapeutic target for better diagnosis and prognosis of NSCLC patients.	34403779	RID05281	ceRNA or sponge	prognosis,chemoresistance	UP(LIHC);DATA(GSE117623)	
Gallbladder cancer	MYLK-AS1	EZH2	positively-E	luciferase reporter assay;Starbase 3.0	upregulation	qPCR	NA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-217)	regulation	RNA-protein	Gemcitabine	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000239523	GRCh38_3:123585300-123644568	ENSG00000106462	NA	100506826	2146	NA	ENX-1|EZH1|KMT6|KMT6A	Long Non-Coding RNA Myosin Light Chain Kinase Antisense 1 Plays an Oncogenic Role in Gallbladder Carcinoma by Promoting Chemoresistance and Proliferation.Methods: Quantitative polymerase chain reaction (qPCR) was used to verify the expression of lncRNA myosin light chain kinase antisense RNA 1 (MYLK-AS1) in 120 pairs of GBC tissues and paired adjacent non-tumour tissues, as well as in six different GBC cell lines (NOZ, EH-GB1, OCUG-1, GBC-SD, SGC-996 and QBC-939).The target miRNAs (miR) of MYLK-AS1 and downstream target genes were predicted using Starbase 3.0 software and confirmed by double luciferase reporting test.Results: Here, we demonstrated that MYLK-AS1 was significantly upregulated and correlated with a poor prognosis and poor clinical characteristics in GBC.Mechanistically, MYLK-AS1 functioned as an efficient miR-217 sponge, thereby releasing the inhibition of enhancer of zeste 2 polycomb repressive complex 2 (EZH2) subunit expression.MYLK-AS1 promoted GBC cell proliferation and resistance to gemcitabine by upregulating EZH2 expression, and EZH2 was confirmed as a direct target of miR-217.	34393514	RID05282	ceRNA or sponge	chemoresistance,prognosis	DOWN(BRCA);DATA(GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	AU021063	TRIB3	positively-F			qPCR	NA	NA	MEK/ERK signaling pathway(+);cell invasion(+);cell metastasis(+)	stabilize	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000101255	NA	NA	57761	NA	C20orf97|dJ1103G7.3|TRB3	The novel long noncoding RNA AU021063, induced by IL-6/Arid5a signaling, exacerbates breast cancer invasion and metastasis by stabilizing Trib3 and activating the Mek/Erk pathway.Interleukin (IL-6) is a pleotropic cytokine with both tumor-promoting and -inhibitory effects on breast cancer growth.We found that IL-6 induced the expression of AU021063 predominantly in breast cancer compared to other cancer types.Mechanistically, IL-6 induced AT-rich interactive domain 5a (Arid5a) expression, which promotes the transcription of AU021063.In turn, AU021063 promotes breast cancer metastasis through stabilizing tribbles homolog 3 (Trib3) and activating Mek/Erk signaling pathwayOverall, our study highlights the importance of IL-6-Arid5a-AU021063 axis in regulating breast cancer invasiveness and metastasis, which may provide potential novel therapeutics for breast cancer.	34389433	RID05283	expression association	metastasis		UP(PAAD,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	IL6	AU021063	positively-E			qPCR	NA	NA	cell invasion(+);cell metastasis(+)	transcriptional regulation	association	protein-RNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000136244	NA	NA	NA	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	NA	The novel long noncoding RNA AU021063, induced by IL-6/Arid5a signaling, exacerbates breast cancer invasion and metastasis by stabilizing Trib3 and activating the Mek/Erk pathway.Interleukin (IL-6) is a pleotropic cytokine with both tumor-promoting and -inhibitory effects on breast cancer growth.We found that IL-6 induced the expression of AU021063 predominantly in breast cancer compared to other cancer types.Mechanistically, IL-6 induced AT-rich interactive domain 5a (Arid5a) expression, which promotes the transcription of AU021063.In turn, AU021063 promotes breast cancer metastasis through stabilizing tribbles homolog 3 (Trib3) and activating Mek/Erk signaling pathwayOverall, our study highlights the importance of IL-6-Arid5a-AU021063 axis in regulating breast cancer invasiveness and metastasis, which may provide potential novel therapeutics for breast cancer.	34389433	RID05284	transcriptional regulation	metastasis	DOWN(BRCA);DATA(GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	CCAT2	IGF2BP2	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-200b)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000073792	NA	101805488	10644	LINC00873|NCCP1	IMP-2|p62	Long Non-Coding RNA CCAT2 Promotes the Development of Esophageal Squamous Cell Carcinoma by Inhibiting miR-200b to Upregulate the IGF2BP2/TK1 Axis.RT-qPCR was adopted to detect CCAT2 expression in collected clinical samples, ESCC cell lines, and a normal cell line.Bioinformatics analysis, dual-luciferase reporter assay, and RIP were conducted for the target relationship profiling.Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues.CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression.IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification.Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.	34386421	RID05285	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Colorectal cancer	SNHG22	E2F3	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000267322	GRCh38_18:49813961-49851059	ENSG00000112242	NA	103091864	1871	SCARNA17HG	NA	lncRNA SNHG22 sponges miR-128-3p to promote the progression of colorectal cancer by upregulating E2F3.SNHG22 expression was detected in colorectal adenoma, CRC tumor tissues (TTs) and adjacent non-cancerous tissues (ANTs) using reverse transcription-quantitative PCR (RT-qPCR).The interaction between SNHG22 and microRNA-128-3p (miR-128-3p), and the target genes of miR-128-3p were explored using online tools, RT-qPCR;western blot and a dual-luciferase reporter assay.The present study revealed that SNHG22 expression was most highly expressed in TTs followed by adenoma tissues and ANTs.In addition, high SNHG22 expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC.The mechanistic study revealed that SNHG22 bound to miR-128-3p and attenuated its inhibitory effects on E2F transcription factor 3 (E2F3) expression levels and activity.Rescue experiments demonstrated that inhibiting miR-128-3p or upregulating E2F3 offset the effects of SNHG22 knockdown on CRC cells.The present findings support the existence of an interactive regulatory network involving SNHG22, miR-128-3p and E2F3 in CRC cell lines, indicating that the SNHG22/miR-128-3p/E2F3 axis may be considered a novel diagnostic and therapeutic target in CRC.	34368861	RID05286	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Infantile hemangioma	TUG1	IGFBP5	positively-E	luciferase reporter assay;Starbase	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-137)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hemangioma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000115461	NA	55000	3488	FLJ20618|LINC00080|NCRNA00080	NA	LncRNA-TUG1 promotes the progression of infantile hemangioma by regulating miR-137/IGFBP5 axis.The expression of TUG1 in IH tissues was assessed by quantitative reverse transcriptase PCR (qRT-PCR.The underlying molecular mechanism of TUG1 was investigated by Starbase prediction and luciferase reporter assay and further determined by loss- and gain-of-function approaches.Results: TUG1 was significantly upregulated in infant hemangioma tissues compared with normal adjacent subcutaneous tissues.Specifically, TUG1 could compete with IGFBP5 for miR137 binding.Conclusion: TUG1 was closely associated with the progression of IH by regulating the miR-137/IGFBP5 axis, which might be a potential target for IH treatment.	34362467	RID05287	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Pre-eclampsia	TUG1	VEGFA	positively-E	luciferase reporter assay;Starbase	downregulation	qRT-PCR	NA	NA	angiogenesis(+);ANG2/TIE2 signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-29a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Long noncoding TUG1 promotes angiogenesis of HUVECs in PE via regulating the miR-29a-3p/VEGFA and Ang2/Tie2 pathways.TUG1, miR-29a-3p and vascular endothelial growth factor A (VEGFA) were detected via qRT-PCRThe binding relationship was analyzed via Starbase, Jefferson and dual-luciferase reporter analysis.Results: TUG1 and VEGFA levels were downregulated, and levels of miR-29a-3p, sFLT1 and sENG were increased in PE patients.TUG1 sponged miR-29a-3p, and miR-29a-3p overexpression reversed the function of TUG1 on H/R-induced HUVECs dysfunction.Conclusion: TUG1 facilitates proliferation, migration, invasion and angiogenesis in H/R-stimulated HUVECs via activating the VEGFA and Ang2/Tie2 signaling by regulating miR-29a-3p.	34352236	RID05288	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Aging	NONHSAT069381	mCASP3	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-124-5p)	regulation	NA	NA	NA	NA	Other	Aging	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA NONHSAT069381 and NONHSAT140844 Increase in Aging Human Blood, Regulating Cardiomyocyte Apoptosis.The results indicated that lncRNA (NONHSAT069381 and NONHSAT140844) and miRNA (hsa-miR-124-5p and hsa-miR-6507-5p) were increased in aging human blood, confirmed by both bioinformatics analysis and polymerase chain reaction (PCR).Furthermore, luciferase reporter assay revealed that hsa-miR-124-5p might be a mediator between NONHSAT069381 and mCASP3 and hsa-miR-6507-5p might be a mediator between NONHSAT140844 and mXIAP.Overexpression of hsa-miR-124-5p decreased caspase-3 levels and overexpression of hsa-miR-6507-5p decreased XIAP content in AC16 cells.	34336120	RID05289	ceRNA or sponge	NA		
Aging	NONHSAT140844	mXIAP	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-6507-5p)	regulation	RNA-protein	NA	NA	NA	Other	Aging	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA NONHSAT069381 and NONHSAT140844 Increase in Aging Human Blood, Regulating Cardiomyocyte Apoptosis.The results indicated that lncRNA (NONHSAT069381 and NONHSAT140844) and miRNA (hsa-miR-124-5p and hsa-miR-6507-5p) were increased in aging human blood, confirmed by both bioinformatics analysis and polymerase chain reaction (PCR).Furthermore, luciferase reporter assay revealed that hsa-miR-124-5p might be a mediator between NONHSAT069381 and mCASP3 and hsa-miR-6507-5p might be a mediator between NONHSAT140844 and mXIAP.Overexpression of hsa-miR-124-5p decreased caspase-3 levels and overexpression of hsa-miR-6507-5p decreased XIAP content in AC16 cells.	34336120	RID05290	ceRNA or sponge	NA		
Papillary thyroid carcinoma	CASC15	WNT7A	positively-E		upregulation		NA	NA	cell proliferation(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-7151-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000154764	NA	401237	7476	LINC00340|lnc-SOX4-1	Wnt-7a	LncRNA CASC15 promotes the proliferation of papillary thyroid carcinoma cells by regulating the miR-7151-5p/WNT7A axis.The present study results showed that CASC15 was overexpressed in PTC tissues compared with normal tissues and acted as a potent oncogene to promote the proliferation and tumorigenesis of PTC cells both in vitro and in vivo.Mechanistic studies demonstrated that CASC15 could serve as an endogenous miRNA sponge to absorb and downregulate miR-7151-5p, thereby preventing the inhibition of WNT7A during PTC progression.Furthermore, the study demonstrated that CASC15 activated the WNT/beta-catenin signaling pathway by upregulating WNT7A in PTC.	34325316	RID05291	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	BCYRN1	WNT5A	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	enhancer	association	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000114251	NA	618	7474	BC200|BC200a|LINC00004|NCRNA00004	hWNT5A	Tumor-derived exosomal BCYRN1 activates WNT5A/VEGF-C/VEGFR3 feedforward loop to drive lymphatic metastasis of bladder cancer.RNA pull-down assays, luciferase assays, and actinomycin assays were conducted to detect the regulatory mechanism of exosomal BCYRN1.Results: LncRNA BCYRN1 was substantially upregulated in urinary-EXO from patients with BCa, and associated with the LN metastasis of BCa.Mechanistically, BCYRN1 epigenetically upregulated WNT5A expression by inducing hnRNPA1-associated H3K4 trimethylation in WNT5A promoter, which activated Wnt/beta-catenin signaling to facilitate the secretion of VEGF-C in BCa.Conclusion: Our results uncover a novel mechanism by which exosomal BCYRN1 synergistically enhances VEGF-C/VEGFR3 signaling-induced lymphatic metastasis of BCa, indicating that BCYRN1 may serve as an encouraging therapeutic target for patients with BCa.	34323412	RID05292	chromatin looping	metastasis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Esophageal cancer	LINC00667	SLC2A3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-200b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000263753	GRCh38_18:5237826-5290608	ENSG00000059804	NA	339290	6515	NA	GLUT3	LINC00667 Promotes Progression of Esophageal Cancer Cells by Regulating miR-200b-3p/SLC2A3 Axis.Methods: Quantitative real-time PCR was used to investigate the levels of LINC00667, miR-200b-3p, and SLC2A3.Interaction between LINC00667 and miR-200b-3p or miR-200b-3p and SLC2A3 were confirmed using a luciferase reporter assay.Results: In this work, we found that LINC00667 expression was up-regulated in EC cell lines, and LINC00667 knockdown inhibited cell proliferation, migration, and invasion in EC cells.Our results demonstrated that LINC00667 plays a critical role in metastatic EC by mediating sponge regulatory axis miR-200b-3p/SLC2A3.To explore function of LINC00667/miR-200b-3p/SLC2A3 axis may provide an informative biomarker of malignancy and a highly selective anti-EC therapeutic target.	34313922	RID05293	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065)
Lung cancer	HHIP<U+2011>AS1	PCDHGA9	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(-);cell stemness(-)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000261934	NA	NA	56107	NA	PCDH-GAMMA-A9	Long non-coding RNA HHIP-AS1 inhibits lung cancer epithelial-mesenchymal transition and stemness by regulating PCDHGA9.The aim of the present study was to investigate the effect of hedgehog-interacting protein antisense RNA 1 (HHIP-AS1) on epithelial-mesenchymal transition (EMT) and cellular stemness of human lung cancer cells by regulating the microRNA (miR)-153-3p/PCDHGA9 axis.Reverse transcription-quantitative PCR was used to compare the expression of HHIP-AS1 in lung cancer and adjacent normal lung tissues.The associations among HHIP-AS1, miR-153-3p and PCDHGA9 were predicted by bioinformatics analysis and verified by a dual-luciferase reporter system.The results showed that the expression of HHIP-AS1 in lung cancer tissues was significantly lower than that in normal tissues (P<0.001).The luciferase reporter system verified that HHIP-AS1 could adsorb miR-153-3p and that PCDHGA9 was the target gene of miR-153-3p.In conclusion, HHIP-AS1 inhibits the EMT and stemness of lung cancer cells by regulating the miR-153-3p/PCDHGA9 axis.	34643245	RID05294	ceRNA or sponge	NA		
Osteogenic differentiation	KCNQ1OT1	miR-24-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Other	Osteogenic differentiation	lncRNA	miRNA	ENSG00000269821	GRCh38_11:2608328-2699994	NA	NA	10984	NA	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	Long non-coding RNA potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 regulates the proliferation and osteogenic differentiation of human periodontal ligament stem cells by targeting miR-24-3p.The down-regulation of lncRNA KCNQ1OT1, the overexpression of anti-miR-24-3p on the proliferation and the levels of osteocalcin (OCN), osteopontin (OPN) and alkaline phosphatase (ALP) of hPDLSCs were investigated.Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the levels of lncRNA KCNQ1OT1, miR-24-3p, OCN, OPN, and ALP.The targeted relationship between lncRNA KCNQ1OT1 and miR-24-3p was detected by double-luciferase experiment.Results: The expression level of lncRNA KCNQ1OT1 increased, and that of miR-24-3p decreased during the osteogenesis of hPDLSCs (P<0.05).Conclusions: Down-regulation of lncRNA KCNQ1OT1 inhibited the proliferation and osteogenic differentiation of hPDLSCs by targeting the up-regulated expression of miR-24-3p.	34636202	RID05295	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	
Coronary heart disease	LOXL1-AS1	SNX16	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell pyroptosis(+)	ceRNA(miR-16-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000104497	NA	100287616	64089	NA	NA	Differential Expression of LOXL1-AS1 in Coronary Heart Disease and its Regulatory Mechanism in ox-LDL-Induced Human Coronary Artery Endothelial Cell Pyroptosis.LOXL1-AS1, miR-16-5p, and SNX16 expressions in ox-LDL-treated HCAECs were determined using RT-qPCR.NLPR3, cleaved-caspase-1, and GSDMD-N protein levels were measured using western blot.The binding relationships between LOXL1-AS1 and miR-16-5p and miR-16-5p and SNX16 were verified.Results: LOXL1-AS1 was highly expressed in CHD patients.Conclusion: LOXL1-AS1 was elevated in CHD patients with a good diagnostic value for CHD and predictive value for MACE.LOXL1-AS1 downregulated miR-16-5p expression by binding to miR-16-5p to enhance ox-LDL-induced HCAEC pyroptosis, which may be associated with upregulation of SNX16 transcription.	34633594	RID05296	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	XIST	PIK3CA	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-320a)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000121879	NA	7503	5290	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	PI3K	Long non-coding RNA XIST accelerates hepatic carcinoma progression by targeting the microRNA-320a/PIK3CA axis.Reverse transcription-quantitative polymerase chain reaction was conducted to detect lncRNA-XIST, miR-320a and PIK3CA expression.Moreover, the binding of lncRNA XIST, PIK3CA and miR-320a were verified by luciferase reporter experiment and pull-down assay.lncRNA XIST was highly expressed in hepatic carcinoma tissues and cells.The lncRNA XIST negatively targeted miR-320a, and miR-320a negatively regulated the expression of PIK3CA.lncRNA XIST accelerates hepatic carcinoma progression by targeting the miR-320a/PIK3CA axis, which might provide the theoretical basis for the potential targeted therapy of hepatic carcinomas.	34630708	RID05297	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Atherosclerosis	PVT1	GRB2	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	ERK1/2 signaling pathway(+);cell injury(+);cancer progression(+)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000177885	NA	5820	2885	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NCKAP2	Background and aims: LncRNA plasmacytoma variant translocation 1 (PVT1) plays a regulatory role in some cardiovascular diseases, but its role in atherosclerosis (AS) remains barely explored.Dual-luciferase reporter gene and RNA immunoprecipitation assays were used to confirm the interaction between miR-153-3p and PVT1 or growth factor receptor binding protein 2 (GRB2).PVT1 acted as a sponge of miR-153-3p, and GRB2 was confirmed as a target of miR-153-3p.MiR-153-3p overexpression attenuated the enhanced effects of PVT1 on ox-LDL-induced cell damage.Inhibiting PVT1 restrained the activation of ERK1/2 and p38 pathway via miR-153-3p/GRB2 axis.Conclusion: PVT1 knockdown alleviated ox-LDL-induced vascular endothelial cell injury and atherosclerosis through miR-153-3p/GRB2 axis via ERK1/2 and p38 pathway.	34627697	RID05298	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Kidney disease	MIAT	GPRC5A	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	NF-kB signaling pathway(+);cell injury(+)	ceRNA(miR-182-5p)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000013588	NA	440823	9052	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	PEIG-1|RAI3|RAIG1|TIG1	Long noncoding RNA MIAT inhibits the progression of diabetic nephropathy and the activation of NF-kB pathway in high glucose-treated renal tubular epithelial cells by the miR-182-5p/GPRC5A axis.MIAT, microRNA-182-5p (miR-182-5p), and G protein-coupled receptor class C group 5 member A (GPRC5A) levels were all examined via reverse transcription-quantitative polymerase chain reaction (RT-qPCR).Intergenic binding was verified using dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays.Mechanistically, MIAT was proved as a miR-182-5p sponge and regulated the expression of GPRC5A that was a miR-182-5p target.The rescued experiments demonstrated that MIAT downregulation or miR-182-5p upregulation aggravated the HG-induced cell damages and activated the NF-kB pathway via the respective regulation of miR-182-5p or GPRC5A.Conclusion: Taken together, MIAT functioned as an inhibitory factor in the pathogenesis to impede the development of DN and inactivate the NF-kB pathway via regulating the miR-182-5p/GPRC5A axis.	34553078	RID05299	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE55807)
Gastric cancer	KLF5	DANCR	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell autophagy(+);cancer progression(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000102554	NA	ENSG00000226950	GRCh38_4:52712325-52723623	688	57291	BTEB2|CKLF|IKLF	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	KLF5 activates lncRNA DANCR and inhibits cancer cell autophagy accelerating gastric cancer progression.The expression of KLF5, DANCR, and AKT2 in GC tissue was upregulated, and the expression of miR-194 was downregulated.The mechanistic investigations revealed that KLF5 activated the transcription of DANCR in the promoter region and elevated its expression.DANCR acted as a miR-194 sponge to repress its expression in GC.MiR-194 targeted and inhibited AKT2 expression.Silencing KLF5 augmented GC cell autophagy, apoptosis and impeded its viability through the DANCR/miR-194/AKT2 axis.The tumor-inhibiting properties of KLF5 knockdown were substantiated in vivo.Together, our study uncovered the oncogenic role of KLF5-dependent lncRNA DANCR transcription in GC in vivo and in vitro, which implicates the miR-194/AKT2 axis in tumor growth regulation, and it may be a potential therapeutic target for human GC.	34548487	RID05300	transcriptional regulation	NA	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)
Gastric cancer	DANCR	AKT2	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-194)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000105221	NA	57291	208	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	PKB脙沤脗虏	KLF5 activates lncRNA DANCR and inhibits cancer cell autophagy accelerating gastric cancer progression.The expression of KLF5, DANCR, and AKT2 in GC tissue was upregulated, and the expression of miR-194 was downregulated.The mechanistic investigations revealed that KLF5 activated the transcription of DANCR in the promoter region and elevated its expression.DANCR acted as a miR-194 sponge to repress its expression in GC.MiR-194 targeted and inhibited AKT2 expression.Silencing KLF5 augmented GC cell autophagy, apoptosis and impeded its viability through the DANCR/miR-194/AKT2 axis.The tumor-inhibiting properties of KLF5 knockdown were substantiated in vivo.Together, our study uncovered the oncogenic role of KLF5-dependent lncRNA DANCR transcription in GC in vivo and in vitro, which implicates the miR-194/AKT2 axis in tumor growth regulation, and it may be a potential therapeutic target for human GC.	34548487	RID05301	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atrial fibrillation	TUG1	TGFB1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Heart disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000105329	NA	55000	7040	LINC00080|NCRNA00080|TI-227H	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA TUG1 Regulates Proliferation of Cardiac Fibroblast via the miR-29b-3p/TGF-beta1 Axis.qRT-PCRwas used for the measurement of gene levels.Luciferase reporter assay was performed for target gene analysis.Results: Elevated levels of TUG1 and low expression of miR-29b-3p were detected in the serum of AF patients compared with the healthy controls.Taurine upregulated gene 1 (TUG1) functions as a competing endogenous RNA (ceRNA) for miR-29b-3p, and downregulation of miR-29b-3p reversed the role of TUG1 in CF proliferation.TGF-beta1 is a direct target gene of miR-29b-3p.Conclusions: Long non-coding RNA taurine upregulated gene 1 is a key regulator in the occurrence of AF.Slicing TUG1 inhibits CF proliferation by regulating the miR-29b-3p/TGF-beta1 axis.	34540908	RID05302	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	EPIST	miR-149-5p	negatively-F	luciferase reporter assay;StarBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000249082	GRCh38_5:135038831-135040047	NA	NA	101927953	NA	C5orf66-AS1|CTC-276P9.1|Epist	NA	Knockdown of lncRNA C5orf66-AS1 inhibits osteosarcoma cell proliferation and invasion via miR-149-5p upregulation.Expression levels of C5orf66-AS1 and microRNA (miRNA/miR)-149-5p in tissues from patients with OS and OS cells lines were evaluated using reverse transcription quantitative (RT-q)PCR.The miRNA target interaction between C5orf66-AS1 and miR-149-5p was predicted and verified using StarBase and dual-luciferase reporter assays.In addition, the expression levels of migration- and apoptosis-associated proteins [matrix metalloproteinase-9 (MMP-9), Bcl-2 and Bax] were determined using western blot and RT-qPCR.The results demonstrated that C5orf66-AS1 was significantly upregulated and miR-149-5p was significantly downregulated in OS tissues and cells (MG63 and U2OS).Furthermore, it was revealed that C5orf66-AS1 negatively regulated the expression of miR-149-5p in OS cells, as confirmed by the inhibition of C5orf66-AS1 expression and miR-149-5p upregulation in cells transfected with small interfering (si RNA targeting C5orf66-AS1.Bioinformatics analysis further confirmed that miR-149-5p could directly bind to C5orf66-AS1.In summary, the results from the present study indicated that C5orf66-AS1 knockdown inhibits OS cell proliferation and invasion via the upregulation of miR-149-5p.	34539861	RID05303	ceRNA or sponge	NA		
Osteoarthritis	LINC01385	TLR4	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-140-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000251604	GRCh38_5:73451498-73453395	ENSG00000136869	NA	106144542	7099	TCONS_00009424	ARMD10|CD284|hToll|TLR-4	Knockdown of LINC01385 inhibits osteoarthritis progression by modulating the microRNA-140-3p/TLR4 axisThe mRNA expression level of LINC01385, microRNA(miR)-140-3p, and Toll-like receptor 4 (TLR4) was detected using reverse transcription-quantitative PCR, while ELISA was used to determine the concentration of different inflammatory factors [tumor necrosis factor-alpha (TNF-alpha), IL-6, and prostaglandin E2 (PGE2)].The associations between miR-140-3p and LINC01385/TLR4 were confirmed using a dual-luciferase reporter assay.LINC01385 mRNA expression level was increased in OA tissues and IL-1beta-induced HC-a.In addition, it was confirmed that LINC01385 targeted miR-140-3p, while TLR4 was a target gene of miR-140-3p.Negative correlations between LINC01385 and miR-140-3p, and between miR-140-3p and TLR4 were observed in OA tissues.LINC01385 knockdown reduced the progression of OA by modulating the miR-140-3p/TLR4 axis in vitro; thus, LINC01385 may be a therapeutic target for OA.	34539840	RID05304	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Glioblastoma	DLGAP1-AS1	ROCK1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	WNT signaling pathway(+);cell proliferation(+)	ceRNA(miR-515-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000067900	NA	649446	6093	FLJ35776|HsT914	p160ROCK	LncRNA DLGAP1-AS1 accelerates glioblastoma cell proliferation through targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.Methods: DLGAP1-AS1 expression in GBM cells was detected by RT-qPCR.RIP, RNA pull down, and luciferase reporter assay were applied for measuring the interplay of DLGAP1-AS1 with other RNAs.Results: DLGAP1-AS1 was distinctly upregulated in GBM cells.DLGAP1-AS1 depletion inhibited cell proliferation, but induced apoptosis. MiR-515-5p could be sponged by DLGAP1-AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho-associated coiled-coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid-2 like 1 (NFE2L1) were confirmed as the target gene of miR-515-5p. Wnt signaling pathway could be activated by DLGAP1-AS1 via regulating ROCK1 and NFE2L1 expression. Rescue assays proved that overexpression of both ROCK1 and NFE2L1 could totally reverse the inhibitory effect of silencing DLGAP1-AS1 on GBM cell proliferation.Conclusion: LncRNA DLGAP1-AS1 accelerated cell proliferation in GBM via targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.	34536977	RID05305	ceRNA or sponge	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	DLGAP1-AS1	NFE2L1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	WNT signaling pathway(+);cell proliferation(+)	ceRNA(miR-515-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000082641	NA	649446	4779	FLJ35776|HsT914	FLJ00380|LCR-F1|NRF1|TCF11	LncRNA DLGAP1-AS1 accelerates glioblastoma cell proliferation through targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.Methods: DLGAP1-AS1 expression in GBM cells was detected by RT-qPCR.RIP, RNA pull down, and luciferase reporter assay were applied for measuring the interplay of DLGAP1-AS1 with other RNAs.Results: DLGAP1-AS1 was distinctly upregulated in GBM cells.DLGAP1-AS1 depletion inhibited cell proliferation, but induced apoptosis. MiR-515-5p could be sponged by DLGAP1-AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho-associated coiled-coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid-2 like 1 (NFE2L1) were confirmed as the target gene of miR-515-5p. Wnt signaling pathway could be activated by DLGAP1-AS1 via regulating ROCK1 and NFE2L1 expression. Rescue assays proved that overexpression of both ROCK1 and NFE2L1 could totally reverse the inhibitory effect of silencing DLGAP1-AS1 on GBM cell proliferation.Conclusion: LncRNA DLGAP1-AS1 accelerated cell proliferation in GBM via targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.	34536977	RID05306	ceRNA or sponge	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
End-stage renal disease	GAS5	PTEN	positively-E	western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA GAS5 Competitively Combined With miR-21 Regulates PTEN and Influences EMT of Peritoneal Mesothelial Cells via Wnt/beta-Catenin Signaling Pathway.Objective: Epithelial-mesenchymal transition (EMT) is an important factor leading to peritoneal fibrosis (PF) in end-stage renal disease (ESRD) patients. The current research aimed to evaluate the effect of long non-coding RNA growth arrest-specific 5 (lncRNA GAS5) in human peritoneal mesothelial cells (HPMCs) EMT and explore the potential molecular mechanisms.Materials and methods: HPMCs were cultured under control conditions or with high glucose (HG). The cells were then treated with lncRNA GAS5, lncRNA GAS5 siRNA, with or without miR-21 inhibitor and PTEN transfection. Expression of lncRNA GAS5, miR-21, alpha-SMA, Vimentin, E-cadherin, phosphatase and tensin homolog deleted on chromosome ten (PTEN), Wnt3a, and beta-catenin were measured by real time PCR and western blot. Bioinformatics analyses were used to test the specific binding sites between the 3' UTR of the PTEN gene, miR-21, and lncRNA GAS5. Rescue experiments were performed to confirm the lncRNA GAS5/miR-21/PTEN axis in HPMC EMT.Results: We found that HG-induced EMT decreased lncRNA GAS5 and that overexpression of lncRNA GAS5 can attenuate EMT in HPMCs. In addition, lncRNA GAS5 regulated HG-induced EMT through miR-21/PTEN. Cotransfection of miR-21 inhibitors remarkably increased PTEN expression and attenuated EMT in lncRNA GAS5 knockdown HPMCs. Moreover, rescue experiments showed that overexpression of PTEN attenuated the EMT effects of lncRNA GAS5 siRNA in HPMCs. We also confirmed that the Wnt/beta-catenin pathway was stimulated in lncRNA GAS5/miR-21/PTEN-mediated EMT.Conclusion: Our research showed that lncRNA GAS5 competitively combined with miR-21 to regulate PTEN expression and influence EMT of HPMCs via the Wnt/beta-catenin signaling pathway. This study provides novel evidence that lncRNA GAS5 may be a potential therapeutic target for HPMC EMT.	34526907	RID05307	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Neuropathic pain	PCAT19	KDM3A	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-182-5p)	regulation	RNA-protein	NA	NA	NA	Other	Neuropathic pain	lncRNA	PCG	ENSG00000267107	GRCh38_19:41449520-41501255	ENSG00000115548	NA	100505495	55818	LINC01190|LOC100505495	JHMD2A|JMJD1|JMJD1A|KIAA0742|TSGA	LncRNA PCAT19 Regulates Neuropathic Pain via Regulation of miR-182-5p/JMJD1A in a Rat Model of Chronic Constriction Injury.mRNA expression of PCAT19, neuroinflammatory factor, microRNA (miR)-182-5p, and Jumonji domain containing 1A (JMJD1A) were detected by quantitative real-time PCR.dual-luciferase reporter assay was used to evaluate the targeting relationship between genes.Results: PCAT19 was continuously upregulated in CCI rats.Conclusion: This study shows that PCAT19 plays a role in NP by targeting the miR-182-5p/JMJD1A axis, and PCAT19 can be used as a new therapeutic target for NP.	34518490	RID05308	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Pre-eclampsia	NR_002794	TIE1	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	transcriptional regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000066056	NA	NA	7075	NA	JTK14|TIE	Identification of downstream targets and signaling pathways of long non-coding RNA NR_002794 in human trophoblast cells.western blot assay demonstrated that NR_002794 inactivated protein kinase B (AKT) and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways and activated cell apoptotic signaling in SWAN71 cells.Both RNA-seq and reverse transcription-quantitative PCR (RT-qPCR) outcomes showed that NR_002794 up-regulation could notably inhibit the expression of C-C motif chemokine ligand 4 like 2 (CCL4L2), interleukin 15 receptor subunit alpha (IL15RA), interleukin 32 (IL32), and tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE1), while NR_002794 knockdown induced these gene expressions in SWAN71 cells.In conclusion, lncRNA NR_002794 could exert its functions by regulating AKT and ERK1/2 pathways and TIE1 expression in human trophoblast cells.	34516352	RID05309	transcriptional regulation	chemoresistance		UP(LIHC);DATA(GSE117623)
Coronary artery disease	MIAT	JAK2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	JAK2/STAT3 signaling pathway(+);apoptosis process(-);inflammatory response(-)	ceRNA(miR-181a-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000096968	NA	440823	3717	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	JTK10	LncRNA MIAT knockdown alleviates oxygen-glucose deprivation-induced cardiomyocyte injury by regulating JAK2/STAT3 pathway via miR-181a-5p.Gene and protein expressions were identified by quantitative real time-polymerase chain reaction or western blot.The interaction of MIAT, miR-181a-5p, and janus kinase 2 (JAK2) was identified by dual-luciferase report assay.Results: Expression of MIAT and JAK2 were increased in OGD-treated HCM and mice of I/R model group, and miR-181a-5p was decreased.Moreover, MIAT targeted miR-181a-5p to enhance the expression of JAK2 and signal Transducer and Activator of Transcription 3 (STAT3), and miR-181a-5p overexpression promoted proliferation, whereas it inhibited apoptosis in OGD-induced cardiomyocytes.Furthermore, the regulatory effects of MIAT knockdown in cell proliferation, apoptosis, and inflammatory injury was reversed by inhibition of miR-181a-5p or overexpression of JAK2 in OGD-treated HCM.Conclusion: MIAT knockdown inhibited apoptosis and inflammation by regulating JAK2/STAT3 signaling pathway via targeting miR-181a-5p in myocardial ischemia model.	34489160	RID05310	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Esophageal cancer	OIP5-AS1	FOXD1	positively-E		upregulation		NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000251493	NA	729082	2297	cyrano|linc-OIP5	FKHL8|FREAC4	Long Non-Coding RNA OIP5-AS1 Inhibits the Proliferation and Migration of Esophageal Squamous Carcinoma Cells by Targeting FOXD1/miR-30a-5p Axis and the Effect of Micro- and Nano-Particles on Targeting Transfection System.lnc RNA OIP5-AS1 was highly expressed in human ESCC tissues and cells, targeted miR-30a-5p, and inhibited miR-30a-5p expression.Additionally, in human ESCC tissues, miR-30a-5p was poorly expressed, whereas FOXD1 mRNA and protein were highly expressed, with a negative correlation between miR-30a-5p and FOXD1 expression.FOXD1 promoted the proliferation and invasion of ESCC and was related to the ERK1/2 signaling pathway; ERK1/2 inhibitors (LY-3214996) reversed the biological function of FOXD1.	34446141	RID05311	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(BRCA);DATA(GSE55807)
Idiopathic pulmonary fibrosis	FENDRR	CTNNB1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000168036	NA	400550	1499	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Noncoding RNA FENDRR Inhibits Lung Fibroblast Proliferation via a Reduction of beta-Catenin.Silencing SRSF9 reduced fibroblast proliferation.FENDRR reduced beta-catenin protein, but not mRNA levels.The reduction of beta-catenin protein levels in lung fibroblasts by gene silencing or chemical inhibitor decreased fibroblast proliferation.In conclusion, FENDRR inhibits fibroblast proliferation and functions as an anti-fibrotic lncRNA.Silencing and Overexpression of beta-Catenin Reduces or Increases Fibroblast Proliferation.RNA Sequencing Analysis Identifies Seven Cell Proliferation-Related Genes That Are Up-Regulated by Asbestos, but Attenuated by FENDRR	34445242	RID05312	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Asthma	NEAT1	SLC26A2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-9-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000155850	NA	283131	1836	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DTD|DTDST	Role of NEAT1/MiR-9-5p/SLC26A2 Pathway on Human Airway Smooth Muscle Cell.Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses.Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample.PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs.Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs.Conclusion: These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs.	34427073	RID05313	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	lncBCAS1-4_1	ZEB1	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A Newly Identified lncBCAS1-4_1 Associated With Vitamin D Signaling and EMT in Ovarian Cancer Cells.We further assessed the potential lncRNAs that linked vitamin D signaling with EMT, and lncBCAS1-4_1 was identified in the first time.Moreover, we found that the most upregulated lncBCAS1-4_1 showed 75% same transcripts with CYP24A1 (metabolic enzyme of 1alpha,25(OH)2D3).Furthermore, lncBCAS1-4_1 could resist the antitumor effect of 1alpha,25(OH)2D3, which was associated with upregulated ZEB1.	34422647	RID05314	transcriptional regulation	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Anaplastic thyroid carcinoma	RP11-395G23.3	RORA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000254615	NA	ENSG00000069667	NA	NA	6095	NA	IDDECA|NR1F1|ROR1|ROR2|ROR3|RZR-ALPHA|RZRA	Long Non-coding RNA RP11-395G23.3 Acts as a Competing Endogenous RNA of miR-124-3p to Regulate ROR1 in Anaplastic Thyroid Carcinoma.The upregulation of RP11-395G23.3 in ATC cells was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR.Mechanically, RP11-395G23.3 could increase ROR1 via sponging miR-124-3p as a ceRNA.In the loss of function assays, results suggested silencing of RP11-395G23.3 inhibited cell proliferation and induced cell apoptosis.Moreover, ROR1 expression was decreased with the downregulation of RP11-395G23.3, but was rescued by the co-transfection of the miR-124-3p inhibitor in ATC cells.	34421987	RID05315	ceRNA or sponge	NA		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE86978)
Chronic myelogenous leukemia	LNC000093	RUNX1	positively-E	knockdown	downregulation	RT-qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-675-5p)	regulation	NA	Imatinib	NA	NA	Cancer	Chronic myeloid leukemia	lncRNA	TF	NA	NA	ENSG00000159216	NA	NA	861	NA	AML1|AMLCR1|CBFA2|PEBP2A2	The Tyrosine Kinase-Driven Networks of Novel Long Non-coding RNAs and Their Molecular Targets in Myeloproliferative Neoplasms.The newly identified LNC000093 served as a competitive endogenous RNA for miR-675-5p and reversed the imatinib resistance in CML cells through regulating RUNX1 expression.LNC000093 Is a Novel Downregulated lncRNA in Imatinib-Resistant CML Cells Differentia	34414175	RID05316	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	MEG3	IDO1	positively-E	luciferase reporter assay;RIP	downregulation	PCR	NA	NA	prognosis	ceRNA(miR-543)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000131203	NA	55384	3620	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	IDO|INDO	Effects of LncRNA MEG3 on immunity and autophagy of non-small cell lung carcinoma through IDO signaling pathway.Results: LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05).However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05).Conclusion: MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.	34399782	RID05317	ceRNA or sponge	prognosis		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	Linc8087	COL4A2	positively-E	ChIP	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000134871	NA	NA	1284	NA	DKFZp686I14213|FLJ22259	Linc8087 predicts favorable prognosis and inhibits cell migration and invasion in NSCLC.RT-qPCR was used to confirm the expression of linc8087 in tumor tissues.Results: We found that linc8087 expression was obviously decreased in both NSCLC tissues and cell lines compared with paired normal tissues and a normal bronchial epithelium cell line.The Human Tumor Metastasis RT2 Profiler PCR Array was used to detect and analyze the mRNA levels of 84 genes involved in metastasis.Low expression of linc8087 was significantly associated with poor survival.Overexpressed linc8087 inhibited cell migration and invasion in A549 and PC9 cell lines.The result of RT2 Profiler PCR Array showed that overexpressed linc8087 upregulated the expression of the COL4A2, CST7 and FAT1 genes and led to the downregulation of SERPINE1.Conclusions: These results indicate that linc8087 plays a key role in the progression of NSCLC, and it may serve as a meaningful prognostic biomarker as well as a latent therapeutic target in NSCLC patients.	34391179	RID05318	transcriptional regulation	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	Linc8087	CST7	positively-E	ChIP	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000077984	NA	NA	8530	NA	NA	Linc8087 predicts favorable prognosis and inhibits cell migration and invasion in NSCLC.RT-qPCR was used to confirm the expression of linc8087 in tumor tissues.Results: We found that linc8087 expression was obviously decreased in both NSCLC tissues and cell lines compared with paired normal tissues and a normal bronchial epithelium cell line.The Human Tumor Metastasis RT2 Profiler PCR Array was used to detect and analyze the mRNA levels of 84 genes involved in metastasis.Low expression of linc8087 was significantly associated with poor survival.Overexpressed linc8087 inhibited cell migration and invasion in A549 and PC9 cell lines.The result of RT2 Profiler PCR Array showed that overexpressed linc8087 upregulated the expression of the COL4A2, CST7 and FAT1 genes and led to the downregulation of SERPINE1.Conclusions: These results indicate that linc8087 plays a key role in the progression of NSCLC, and it may serve as a meaningful prognostic biomarker as well as a latent therapeutic target in NSCLC patients.	34391179	RID05319	transcriptional regulation	metastasis,prognosis		DOWN(BRCA);DATA(GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)
Non-small cell lung cancer	Linc8087	FAT1	positively-E	ChIP	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000083857	NA	NA	2195	NA	CDHF7|CDHR8|FAT	Linc8087 predicts favorable prognosis and inhibits cell migration and invasion in NSCLC.RT-qPCR was used to confirm the expression of linc8087 in tumor tissues.Results: We found that linc8087 expression was obviously decreased in both NSCLC tissues and cell lines compared with paired normal tissues and a normal bronchial epithelium cell line.The Human Tumor Metastasis RT2 Profiler PCR Array was used to detect and analyze the mRNA levels of 84 genes involved in metastasis.Low expression of linc8087 was significantly associated with poor survival.Overexpressed linc8087 inhibited cell migration and invasion in A549 and PC9 cell lines.The result of RT2 Profiler PCR Array showed that overexpressed linc8087 upregulated the expression of the COL4A2, CST7 and FAT1 genes and led to the downregulation of SERPINE1.Conclusions: These results indicate that linc8087 plays a key role in the progression of NSCLC, and it may serve as a meaningful prognostic biomarker as well as a latent therapeutic target in NSCLC patients.	34391179	RID05320	transcriptional regulation	metastasis,prognosis		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Non-small cell lung cancer	Linc8087	SERPINE1	negatively-E	ChIP	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000106366	NA	NA	5054	NA	PAI|PAI1|PLANH1	Linc8087 predicts favorable prognosis and inhibits cell migration and invasion in NSCLC.RT-qPCR was used to confirm the expression of linc8087 in tumor tissues.Results: We found that linc8087 expression was obviously decreased in both NSCLC tissues and cell lines compared with paired normal tissues and a normal bronchial epithelium cell line.The Human Tumor Metastasis RT2 Profiler PCR Array was used to detect and analyze the mRNA levels of 84 genes involved in metastasis.Low expression of linc8087 was significantly associated with poor survival.Overexpressed linc8087 inhibited cell migration and invasion in A549 and PC9 cell lines.The result of RT2 Profiler PCR Array showed that overexpressed linc8087 upregulated the expression of the COL4A2, CST7 and FAT1 genes and led to the downregulation of SERPINE1.Conclusions: These results indicate that linc8087 plays a key role in the progression of NSCLC, and it may serve as a meaningful prognostic biomarker as well as a latent therapeutic target in NSCLC patients.	34391179	RID05321	transcriptional regulation	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Glioblastoma	LINC00511	miR-126-5p	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72290091-72640472	NA	NA	400619	NA	onco-lncRNA-12	NA	LINC00511 facilitates Temozolomide resistance of glioblastoma cells via sponging miR-126-5p and activating Wnt/beta-catenin signaling;The potential functions of LINC00511 were evaluated by quantitative real-time polymerase chain reaction, cell viability assay, colony formation assay, western blot, soft agar assay, flow cytometry, tumor xenograft model, immunofluorescence, sphere formation assay, fluorescent in situ hybridization, luciferase reporter assay, and RNA pull-down assay. We found that LINC00511 was upregulated in U87-R cells and GBM samples, and correlated with poor prognosis of GBM patients.Furthermore, LINC00511 was mainly distributed in the cytoplasm of GBM cells and regulated Wnt/beta-catenin activation by acting as a molecular sponge for miR-126-5p. Multiple genes of Wnt/beta-catenin signaling such as DVL3, WISP1, and WISP2 were targeted by miR-126-5p. MiR-126-5p restoration impaired TMZ resistance of GBM cells.	34328678	RID05322	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Hepatocellular carcinoma	EPIST	DUSP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-127-3p)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249082	GRCh38_5:135038831-135040047	ENSG00000120129	NA	101927953	1843	C5orf66-AS1|CTC-276P9.1|Epist	CL100|HVH1|MKP-1|PTPN10	Mesenchymal stem cell-derived exosomes block malignant behaviors of hepatocellular carcinoma stem cells through a lncRNA C5orf66-AS1/microRNA-127-3p/DUSP1/ERK axis.The CSCs were treated with Exo, and then the proliferation, migration, invasion, angiogenesis-stimulating and self-renewal abilities of the Hep3B-CSCs and HuH7-CSCs were significantly reduced.The integrated bioinformatic analyses and luciferase assays suggested that C5orf66-AS1 upregulated DUSP1 expression through sequestering microRNA-127-3p (miR-127-3p). To conclude, this research reported that MSC-derived Exo block malignant behaviors of HCC-sourced CSCs through a C5orf66-AS1/miR-127-3p/DUSP1/ERK axis.	34431063	RID05323	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Parkinson's disease	MEG3	LRRK2	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell viability(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000188906	NA	55384	120892	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DKFZp434H2111|FLJ45829|PARK8|RIPK7|ROCO2	Downregulation of lncRNA MEG3 is involved in Parkinson's disease.RT-qPCR was performed to measure the expression of MEG3 and LRRK2. Overexpression of MEG3 increased the expression levels of leucine-rich repeat kinase 2 (LRRK2) in SH-SY5Y cells. In contrast, overexpression of LRRK2 showed no significant effects on MEG3. Overexpression of MEG3 improved the viability and inhibited the apoptosis of SH-SY5Y cells pretreated with MPP + .In conclusion, lncRNA MEG3 is downregulated in PD and may affect the expression of LRRK2 to regulate cell viability and apoptosis involved in PD.	34643842	RID05324	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hirschsprung's disease	DRAIC	ITGA6	positively-E	luciferase reporter assay;siRNA;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000245750	GRCh38_15:69462921-69843120	ENSG00000091409	NA	145837	3655	NA	CD49f	LncRNA DRAIC regulates cell proliferation and migration by affecting the miR-34a-5p/ITGA6 signal axis in Hirschsprung's disease.Quantitative reverse transcription-polymerase chain reaction (qRT-PCR was used to detect the expression of DRAIC in HSCR bowel stenosis tissues and normal colon tissues.RNA pull-down and dual-luciferase reporter assays were used to confirm the competitive relationship of DRAIC and integrin subunit alpha 6 (ITGA6) through their association with miR-34a-5p. The lncRNA DRAIC was significantly increased in colon tissue from HSCR patients.The RNA pull-down and dual-luciferase reporter assays have proven the competitive relationship between DRAIC and ITGA6 through their association with miR-34a-5p. Further rescue experiments have confirmed that DRAIC regulates cell proliferation and migration by affecting the miR-34a-5p/ITGA6 signal axis in HSCR. DRAIC promoted cell proliferation and migration by regulating the miR-34a-5p/ITGA6 signal axis in HSCR.	34471485	RID05325	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Acute graft versus host disease	IFN	IFNG-AS1	positively-E	GraphPad Prism 6	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	transcriptional regulation	association	NA	NA	NA	NA	Other	Acute graft versus host disease	PCG	lncRNA	NA	NA	ENSG00000255733	GRCh38_12:67989445-68234686	NA	100885789	NA	GS1-410F4.2|NEST|Tmevpg1	IFNG-AS1 and MAF4 long non-coding RNAs are upregulated in acute leukemia patients who underwent bone marrow transplantation. The expression of lncRNA levels was measured using the qRT-PCRtechnique.However, the aGVHD group showed an overt up-regulation of the two lncRNAs on samples taken at day 28 and 52 8 compared to non-GVHD patients. Since the intracellular pathway of these lncRNAs shows a direct relationship with the IFN-Gamma cytokine production resulting in differentiation to TH1 cells and inhibition of differentiation to TH2 cells, they can be, therefore, considered as suitable molecular candidates for the prediction of aGVHD in patients receiving HSCT.	34380104	RID05326	transcriptional regulation	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Acute graft versus host disease	IFN	MAFTRR	positively-E	GraphPad Prism 6	upregulation	qRT-PCR	NA	NA	cell differentiation(-)	transcriptional regulation	association	NA	NA	NA	NA	Other	Acute graft versus host disease	TF	lncRNA	NA	NA	ENSG00000261390	GRCh38_16:79715220-79770651	NA	102467146	NA	linc-MAF-4|lincMAF4	IFNG-AS1 and MAF4 long non-coding RNAs are upregulated in acute leukemia patients who underwent bone marrow transplantation. The expression of lncRNA levels was measured using the qRT-PCRtechnique.However, the aGVHD group showed an overt up-regulation of the two lncRNAs on samples taken at day 28 and 52 8 compared to non-GVHD patients. Since the intracellular pathway of these lncRNAs shows a direct relationship with the IFN-Gamma cytokine production resulting in differentiation to TH1 cells and inhibition of differentiation to TH3 cells, they can be, therefore, considered as suitable molecular candidates for the prediction of aGVHD in patients receiving HSCT.	34380104	RID05327	transcriptional regulation	NA		
Gastric cancer	SP1	THAP7-AS1	positively-E	shRNA	upregulation	microarray	NA	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000230513	GRCh38_22:21001886-21010342	6667	439931	NA	NA	lncRNA THAP7-AS1, transcriptionally activated by SP1 and post-transcriptionally stabilized by METTL3-mediated m6A modification, exerts oncogenic properties by improving CUL4B entry into the nucleus.SP1, a transcription factor, could bind directly to the THAP7-AS1 promoter region and activate its transcription. Taken together, our results show that THAP7-AS1, transcriptionally activated by SP1 and then modified by METTL3-mediated m6A, exerts oncogenic functions, by promoting interaction between NLS and importin alpha1 and then improving the CUL4B protein entry into the nucleus to repress the transcription of miR-22-3p and miR-320a.	34608273	RID05328	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	METTL3	THAP7-AS2	positively-E	shRNA	upregulation	microarray	NA	NA	cancer progression(+)	interact with protein;histone modification	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000165819	NA	NA	NA	56339	NA	M6A|MT-A70|Spo8	NA	lncRNA THAP7-AS1, transcriptionally activated by SP1 and post-transcriptionally stabilized by METTL3-mediated m6A modification, exerts oncogenic properties by improving CUL4B entry into the nucleus.Moreover, the m6A modification of THAP7-AS1 by METTL3 enhanced its expression depending on the "reader" protein IGF2BP1-dependent pathway. THAP7-AS1 promoted GC cell progression. Taken together, our results show that THAP7-AS1, transcriptionally activated by SP1 and then modified by METTL3-mediated m6A, exerts oncogenic functions, by promoting interaction between NLS and importin alpha1 and then improving the CUL4B protein entry into the nucleus to repress the transcription of miR-22-3p and miR-320a.	34608273	RID05329	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	THAP7-AS2	miR-22-3p	negatively-E	shRNA	upregulation	microarray	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(+)	interact with protein;histone modification	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA THAP7-AS1, transcriptionally activated by SP1 and post-transcriptionally stabilized by METTL3-mediated m6A modification, exerts oncogenic properties by improving CUL4B entry into the nucleus.Mechanistically, THAP7-AS1 interacted with the 1-50 Amino Acid Region (nuclear localization signal) of CUL4B through its 1-442 nt Sequence, and it promoted interaction between nuclear localization signal (NLS) and importin alpha1, and improved the CUL4B protein entry into the nucleus, repressing miR-22-3p and miR-320a expression by CUL4B-catalyzed H2AK119ub1 and the EZH2-mediated H3K27me3, subsequently activating PI3K/AKT signaling pathway to promote GC progression. Moreover, LV-sh-THAP7-AS1 treatment could suppress GC growth, invasion and metastasis, indicating that THAP7-AS1 may act as a promising molecular target for GC therapies. Taken together, our results show that THAP7-AS1, transcriptionally activated by SP1 and then modified by METTL3-mediated m6A, exerts oncogenic functions, by promoting interaction between NLS and importin alpha1 and then improving the CUL4B protein entry into the nucleus to repress the transcription of miR-22-3p and miR-320a.	34608273	RID05330	interact with protein	metastasis		
Gastric cancer	THAP7-AS2	miR-320a	negatively-E	shRNA	upregulation	microarray	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(+)	interact with protein;histone modification	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA THAP7-AS1, transcriptionally activated by SP1 and post-transcriptionally stabilized by METTL3-mediated m6A modification, exerts oncogenic properties by improving CUL4B entry into the nucleus.Mechanistically, THAP7-AS1 interacted with the 1-50 Amino Acid Region (nuclear localization signal) of CUL4B through its 1-442 nt Sequence, and it promoted interaction between nuclear localization signal (NLS) and importin alpha1, and improved the CUL4B protein entry into the nucleus, repressing miR-22-3p and miR-320a expression by CUL4B-catalyzed H2AK119ub1 and the EZH2-mediated H3K27me3, subsequently activating PI3K/AKT signaling pathway to promote GC progression. Moreover, LV-sh-THAP7-AS1 treatment could suppress GC growth, invasion and metastasis, indicating that THAP7-AS1 may act as a promising molecular target for GC therapies. Taken together, our results show that THAP7-AS1, transcriptionally activated by SP1 and then modified by METTL3-mediated m6A, exerts oncogenic functions, by promoting interaction between NLS and importin alpha1 and then improving the CUL4B protein entry into the nucleus to repress the transcription of miR-22-3p and miR-321a.	34608273	RID05331	interact with protein	metastasis		
Hepatocellular carcinoma	VPS9D1-AS1	CDK4	positively-E	shRNA;siRNA	upregulation	microarray;qRT-PCR	GSE65485;TCGA	NA	cell proliferation(+);apoptosis process(-)	RNA stability;interact with protein	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261373	GRCh38_16:89711856-89718165	ENSG00000135446	NA	100128881	1019	MYU	PSK-J3	The lncRNA VPS9D1-AS1 Promotes Hepatocellular Carcinoma Cell Cycle Progression by Regulating the HuR/CDK4 Axis.Using microarray data from the NCBI Gene Expression Omnibus (GEO) database (GSE65485) and The Cancer Genome Atlas (TCGA) database, VPS9D1-AS1 expression in HCC and normal liver tissue sample HCC were compared. Relative lncRNA expression was also measured through real-time quantitative PCR (qPCR) in 80 pairs of HCC tumor and paracancerous tissues and in human HCC cell lines. Knocking down VPS9D1-AS1 impaired the proliferative and colony formation activity of HepG2 cells while promoting their apoptotic death. Consistently, VPS9D1-AS1 silencing suppressed HCC tumor growth in vivo. Mechanistically, VPS9D1-AS1 was able to bind to the HuR protein and thereby influence the stability and expression of the CDK4 mRNA, thus impacting HCC cell proliferation. The VPS9D1-AS1/HuR/CDK4 signaling axis regulates HCC tumor cell oncogenic activity, highlighting this pathway as a promising therapeutic target.	34558987	RID05332	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Breast cancer	AC012213.3	RAD54B	positively-E	DESeq2 package	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000197275	NA	NA	25788	NA	RDH54	Overexpression of the lncRNA AC012213.3 Promotes Proliferation, Migration and Invasion of Breast Cancer via RAD54B/PI3K/AKT Axis and is Associated with Worse Patient Prognosis.We then used the DESeq2 package to profile the expression of the lncRNAs between the patients and normal samples.Besides, in vitro assays demonstrated that downregulation of AC012213.3 suppresses the proliferation and invasion of breast cancer cells. Further analysis showed that RAD54B is a downstream AC012213.3 target gene and was upregulated in breast cancer. Interestingly, RAD54B expression was associated with shorter survival in breast cancer. In addition, AC012213.3 was shown to facilitate breast cancer progression through the RAD54B/PI3K/AKT axis. Taken together, our data demonstrated that lncRNA AC012213.3 is upregulated in breast cancer and could enhance breast cancer progression through RAD54B/PI3K/AKT axis.	34557038	RID05333	transcriptional regulation	prognosis		DOWN(NSCLC,BRCA);UP(SKCM);DATA(GSE74639,GSE38495,GSE111842,GSE86978)
Pancreatic cancer	ZFAS1	HMGA2	positively-E	RIP;CHIP;RNA pull-down assay;luciferase reporter assay;siRNA	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-497-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000149948	NA	441951	8091	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	BABL|HMGIC|LIPO	Long non-coding RNA ZFAS1 promotes pancreatic cancer proliferation and metastasis by sponging miR-497-5p to regulate HMGA2 expression.The expression of ZFAS1, miR-497-5p and HMGA2 in pancreatic cancer tissues was detected by qRT-PCR Pancreatic cancer data in The Cancer Genome Atlas were also included in this study. MS2-RIP, RNA pull-down, RNA-ChIP and luciferase reporter assays were used to clarify the molecular biological mechanisms of ZFAS1 in pancreatic cancer.ZFAS1 promoted the growth and metastasis of pancreatic cancer cells, and miR-497-5p acted as a tumour suppressor gene in pancreatic cancer by targeting HMGA2. We also demonstrated that ZFAS1 exerts its effects by promoting HMGA2 expression through decoying miR-497-5p. We also found that ZFAS1 promoted the progression of pancreatic cancer in vivo by modulating the miR-497-5p/HMGA2 axis.	34552050	RID05334	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Atherosclerosis	TP53COR1	SIRT1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	ceRNA(miR-221)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	NA	ENSG00000096717	NA	102800311	23411	TRP53COR1|linc-p21|lincRNA-p21	SIR2|SIR2L1|SIR2alpha	LincRNA-p21 alleviates atherosclerosis progression through regulating the miR-221/SIRT1/Pcsk9 axis.The binding of LincRNA-p21 and miR-221 or miR-221 and SIRT1 was measured using a dual luciferase reporter gene assay and RIP. miR-221 was highly expressed while SIRT1 was poorly expressed in AS. LincRNA-p21 acted as a sponge for miR-221. miR-221 targeted and negatively regulated the expression of SIRT1. LincRNA-p21 promoted the deacetylation of Pcsk9 by SIRT1 by competitively binding to miR-221, whereby promoting HAEC proliferation, migration and tube formation. In conclusion, LincRNA-p21 acted as a molecular sponge for miR-221 to promote deacetylation of the promoter region of Pcsk9 by SIRT1, therefore preventing the development of AS.	34541816	RID05335	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Atherosclerosis	SIRT1	PCSK9	negatively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(-)	deacetylation	association	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000096717	GRCh38_10:67884656-67918390	ENSG00000169174	NA	23411	255738	SIR2L1	FH3|HCHOLA3|NARC-1	LincRNA-p21 alleviates atherosclerosis progression through regulating the miR-221/SIRT1/Pcsk9 axis.The binding of LincRNA-p21 and miR-221 or miR-221 and SIRT1 was measured using a dual luciferase reporter gene assay and RIP. miR-221 was highly expressed while SIRT1 was poorly expressed in AS. LincRNA-p21 acted as a sponge for miR-221. miR-221 targeted and negatively regulated the expression of SIRT1. LincRNA-p21 promoted the deacetylation of Pcsk9 by SIRT1 by competitively binding to miR-221, whereby promoting HAEC proliferation, migration and tube formation. In conclusion, LincRNA-p21 acted as a molecular sponge for miR-221 to promote deacetylation of the promoter region of Pcsk9 by SIRT2, therefore preventing the development of AS.	34541816	RID05336	epigenetic regulation	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Colorectal cancer	YY1	LINC01224	positively-E	luciferase reporter assay;RIP;CHIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000269416	GRCh38_19:23399097-23416075	7528	104472717	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	LINC01224 promotes colorectal cancer progression through targeting miR-485-5p/MYO6 axis.Dual-luciferase reporter, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation, and pull-down assays were conducted to analyze the binding interaction. LINC01224 was upregulated via the transcription factor YY1. LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. YY1-induced LINC01224 regulates CRC development via modulating miR-485-5p/MYO6 axis.	34535152	RID05337	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	LINC01224	MYO6	positively-E	luciferase reporter assay;RIP;CHIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-485-5p)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000269416	GRCh38_19:23399097-23416075	ENSG00000196586	NA	104472717	4646	NA	DFNA22|DFNB37|KIAA0389	LINC01224 promotes colorectal cancer progression through targeting miR-485-5p/MYO6 axis.Dual-luciferase reporter, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation, and pull-down assays were conducted to analyze the binding interaction. LINC01224 was upregulated via the transcription factor YY1. LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. YY1-induced LINC01224 regulates CRC development via modulating miR-485-5p/MYO6 axis.LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. MiR-485-5p was sponged by LINC01224, and miR-485-5p downregulation relieved the influence of LINC01224 interference on CRC progression. MYO6 was targeted via miR-485-5p and regulated via LINC01224/miR-485-5p axis. MiR-485-5p overexpression suppressed CRC cell proliferation, migration, and invasion and facilitated apoptosis. MYO6 upregulation mitigated the role of miR-485-5p. LINC01224 knockdown decreased xenograft tumor growth. YY1-induced LINC01224 regulates CRC development via modulating miR-485-5p/MYO6 axis.	34535152	RID05338	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807,GSE75367)
Psoriasis	KCNQ1OT1	GAB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-183-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Immune system disease	Psoriasis	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000109458	NA	10984	2549	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	DFNB26	KCNQ1OT1 promotes the proliferation and migration of psoriatic keratinocytes by regulating miR-183-3p/GAB1.Target miRNA of KCNQ1OT1 was identified by luciferase activity and RNA immunoprecipitation (RIP) assays.KCNQ1OT1 was bound to microRNA-183-3p (miR-183-3p) and negatively regulated its expression. Over-expression of growth factor receptor binding 2-associated binding protein 1 (GAB1) counteracted with the suppressive effects of KCNQ1OT1-induced silence on the viability and migration of TNF-alpha-treated HaCaT cells.KCNQ1OT1 silence suppressed the proliferation and migration of TNF-alpha-treated HaCaT cells through regulation of miR-183-3p/GAB1.	34476933	RID05339	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807)
Breast cancer lung metastatic dormancy	NR2F1-AS1	NR2F1	positively-E	RIP;CHIP;shRNA	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);tumorigenesis(-);cell metastasis(+);cell proliferation(-)	interact with protein;interact with mRNA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000175745	NA	441094	7025	FLJ42709	COUP-TFI|COUPTF1|EAR-3|ERBAL3|SVP44|TCFCOUP1|TFCOUP1	Long non-coding RNA-NR2F1-AS1-induces breast cancer lung metastatic dormancy by regulating NR2F1 and Np63.The long non-coding RNA (lncRNA) NR2F1-AS1 (NAS1) is up-regulated in the dormant mesenchymal-like BCSCs, and functionally promotes tumor dissemination but reduces proliferation in lungs. NAS1 binds to NR2F1 mRNA and recruits the RNA-binding protein PTBP1 to promote internal ribosome entry site (IRES)-mediated NR2F1 translation, thus leading to suppression of Np63 transcription by NR2F1. Furthermore, Np63 downregulatio results in epithelial-mesenchymal transition, reduced tumorigenicity and enhanced dormancy of cancer cells in lungs.	34475402	RID05340	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	
Pancreatic ductal adenocarcinoma	NEAT1	PRKDC	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-101)	regulation	RNA-protein	Gemcitabine	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000253729	NA	283131	5591	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DNA-PKC|DNA-PKcs|DNAPK|DNAPKc|DNPK1|HYRC|HYRC1|p350|p460|XRCC7	NEAT1/miR-101-dependent Up-regulation of DNA-PKcs Enhances Malignant Behaviors of Pancreatic Ductal Adenocarcinoma Cells.The levels of miRNA-101 and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) were detected by real-time PCR. The regulatory relationship between NEAT1 and miR-101 was determined by a luciferase assay.Further study showed that miRNA-101 level was decreased in PDAC tissues and cells, which could be responsible for DNA-PKcs overexpression and DNA-PKcs mediated oncogenic actions in PDAC cells. Moreover, NEAT1 functions as an oncogene influencing cell proliferation, migration and invasion in part by serving as a competing endogenous RNA (ceRNAs) modulating miR-101 expression, leading to up-regulation of DNA-PKcs.These findings suggest that NEAT1/miR-101-dependent up-regulation of DNA-PKcs promotes the malignant behaviors of PDAC cells. The NEAT1/miR-101/DNA-PKcs axis may serve as a viable prognostic marker and therapeutic target for PDAC.	34405022	RID05341	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Esophageal cancer	OIP5-AS1	VOPP1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-30a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000154978	NA	729082	81552	cyrano|linc-OIP5	DKFZp564K0822|ECop|FLJ20532|GASP|WBP1L2	Long non-coding RNA OIP5-AS1 promotes the progression of esophageal cancer by regulating miR-30a/VOPP1 expression. Furthermore, dual-luciferase reporter and RNA immunoprecipitation assays were used to study the interaction between miRNA and lncRNA or genes. The results revealed that OIP5-AS1 expression in EC tissues and cultured EC cells was upregulated, microRNA-30a (miR-30a) expression was downregulated. Vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) was verified as the direct target of miR-30a. VOPP1 expression was positively correlated with OIP5-AS1 expression in EC cells. In conclusion, OIP5-AS1 promoted the proliferation, migration and invasion of EC cells by increasing VOPP1 expression by sponging miR-30a.	34386073	RID05342	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Atherosclerosis	SNHG12	IGF2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell injury(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000167244	NA	85028	3481	ASLNC04080|C1orf79|LINC00100|PNAS-123	C11orf43|FLJ44734|IGF-II	LncRNA SNHG12 regulates ox-LDL-induced endothelial cell injury by the miR-218-5p/IGF2 axis in atherosclerosis.RT-qPCR determined the levels of SNHG12, microRNA-218-5p (miR-218-5p) and insulin-like growth factor-II (IGF2). The molecular mechanisms were investigated using luciferase reporter and RNA pull-down assays. We found that SNHG12 and IGF2 expression levels were high and miR-218-5p expression levels were low in AS patients and ox-LDL-treated HUVECs.SNHG12 upregulated IGF2 expression by sponging miR-218-5p. More importantly, SNHG12 increased proinflammatory cytokine production and augmented atherosclerotic lesions in vivo. Overall, SNHG12 promotes the development of AS by the miR-218-5p/IGF2 axis.	34313533	RID05343	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Retinoblastoma	MIAT	LASP1	positively-E	luciferase reporter assay;shRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-665)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000002834	NA	440823	3927	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	Lasp-1|MLN50	Downregulation of MIAT reduces the proliferation and migratory and invasive abilities of retinoblastoma cells by sponging miR-665 and regulating LASP1.To do so, the expression levels of MIAT, microRNA (miR)-665, and LIM and SH3 protein 1 (LASP1) in Rb tissues from patients or Rb cells were analysed using reverse transcription quantitative PCR. The interactions between miR-665 and MIAT/LASP1 were confirmed by the dual-luciferase reporter assay.In addition, LASP1 was identified as a target gene of miR-665. Both the decreased expression of miR-665 and the elevated expression of LASP1 reversed the suppressive effects of MIAT knockdown on the proliferation and migratory and invasive abilities of Y79 cells. Furthermore, MIAT silencing attenuated the development of Rb by regulating the miR-665/LASP1 axis. Taken together, these findings suggested that MIAT may be considered as a possible therapeutic target for Rb.	34630696	RID05344	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	LINC00662	ITPR1	positively-E	luciferase reporter assay;RNA pull-down assay;FISH	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-16-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000150995	NA	148189	3708	NA	ACV|Insp3r1|IP3R1|PPP1R94|SCA15|SCA16|SCA29	LncRNA LINC00662 Exerts an Oncogenic Effect on Osteosarcoma by the miR-16-5p/ITPR1 Axis.Experiments including RT-qPCR, MTT, western blot, FISH, RNA pull-down, luciferase reporter, colony formation, transwell invasion and migration, and sphere formation assay were performed to investigate the regulatory role of LINC00662 in OS. Through a series of  in vivo  assays, LINC00662 knockdown suppressed OS cell proliferation, invasion, migration, and stemness property maintenance. Further mechanistical investigations indicated that LINC00662 functioned as a competing endogenous RNA (ceRNA) for sponging microRNA-16-5p (miR-16-5p) to upregulate the expression of IP receptor type 1 (ITPR1) in OS cells. Restoration assays validated the involvement of ITPR1 in LINC00662-mediated regulation of cell functions in OS. LINC00662 exerts oncogenic functions in OS by targeting the miR-16-5p/ITPR1 axis.	34621314	RID05345	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939)
Lung adenocarcinoma	SNX20AR	SNX20	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	hypermethylation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000167208	NA	NA	124460	NA	SLIC-1|SLIC1	SNX20AR/MiRNA-301a-3p/SNX20 Axis Associated With Cell Proliferation and Immune Infiltration in Lung Adenocarcinoma.e found that over-expression of SNX20 significantly restrain NSCLC cell proliferation and migration. Subsequently, we discover a network regulating SNX20 in LUAD, further study found that the decreased of the SNX20 likely caused by DNA hypermethylation. Furthermore, we identified that SNX20AR/miRNA-301a-3p mediated decreased of SNX20 correlated with lung cancer progression and cancer immune infiltration in LUAD. Our findings suggested that ncRNAs play a crucial role in the regulatory network of SNX20. Collectively, our findings demonstrate the suppressor roles of the SNX20AR/miRNA-301a-3p/SNX20 axis in Lung Adenocarcinoma, represent that SNX20 have the potential of as an effective therapeutic target in future.	34604311	RID05346	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Primordial dwarfism	7SK	CDC6	negatively-E	CRISPR/Cas9;shRNA	upregulation	PCR	NA	NA	cell proliferation(-)	interact with protein	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Osteochondrodysplasia	lncRNA	PCG	ENSG00000271818	GRCh38_13:45123093-45123414	ENSG00000094804	NA	NA	990	NA	CDC18L	7SK truncation at 128-179 nt suppresses embryonic stem cell proliferation-in vitro-by downregulating CDC6.We identified a novel deletion mutation of 7SK at 128-179 nt in the ESCs, which resulted in deficiency of cell proliferation. 7SK truncation at 128-179 nt significantly reduced the protein expressions of La-related protein 7 (LARP7) and CDC6.7SK truncation at 128-179 nt can significantly impair proliferation of ESCs by downregulating CDC6. 7SK is a key regulator of proliferation and mediates the growth of ESCs through a mechanism dependent on CDK9 activity, suggesting the value of 7SK truncation at 128-179 nt as a potential target for early diagnosis and treatment of PD.	34549701	RID05347	interact with protein	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	NEAT1	GSDME	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell pyroptosis(+);cell viability(+)	ceRNA(miR-448)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105928	NA	283131	1687	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DFNA5|ICERE-1	Long non-coding RNA nuclear paraspeckle assembly transcript 1 regulates ionizing radiation-induced pyroptosis via microRNA-448/gasdermin E in colorectal cancer cells.The binding association between miR-448 and GSDME was assessed using the dual-luciferase reporter assay.GSDME was identified as a downstream target of miR-448. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was upregulated in response to IR and enhanced GSDME expression by negatively regulating miR-448 expression. Notably, NEAT1 knockdown suppressed IR-induced pyroptosis, full-length GSDME expression and GSDME cleavage compared with that in irradiated cells. In addition, NEAT1 knockdown rescued the IR-induced decrease in cell viability in HCT116 cells. The findings of the present study indicated that lncRNA NEAT1 modulates IR-induced pyroptosis and viability in HCT116 cells via miR-448 by regulating the expression, but not activation of GSDME. The present study provides crucial mechanistic insight into the potential role of lncRNA NEAT1 in IR-induced pyroptosis.	34476497	RID05348	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Osteosarcoma	YY1	HCG11	interact	luciferase reporter assay;JASPAR;ChIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000100811	NA	ENSG00000228223	GRCh38_6:26521709-26527404	7528	493812	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	bK14H9.3|FLJ14049|FLJ30357	lncRNA HCG11 suppresses human osteosarcoma growth through upregulating p27 Kip1.Our data revealed that HCG11 expression is decreased in OS, which is a result of transcriptional repression of YY1.In conclusion, HCG11 is downregulated in OS, and restrains OS growth both  in vitro  and  in vivo  by raising p27 Kip1 expression via binding to miR-942-5p and IGF2BP2.	34518440	RID05349	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Osteosarcoma	HCG11	CDKN1B	positively-E	shRNA;starBase;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell growth(+)	interact with protein	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000111276	NA	493812	1027	CTA-14H9.3|bK14H9.3	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	lncRNA HCG11 suppresses human osteosarcoma growth through upregulating p27 Kip1.Low HCG11 level is closely associated with larger tumor size and shorter overall survival of OS patients. HCG11 negatively regulates cell proliferation, cell cycle, DNA replication  in vitro  and tumor growth  in vivo . HCG11 can raise p27 Kip1 expression via binding to miR-942-5p and IGF2BP2, and p27 Kip1 acts as a key effector for HCG11 exerting biological functions. In conclusion, HCG11 is downregulated in OS, and restrains OS growth both  in vitro  and  in vivo  by raising p27 Kip1 expression via binding to miR-942-5p and IGF2BP2.	34518440	RID05350	interact with protein	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	METTL3	FOXD2-AS1	interact	MeRIP-qPCR	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	RNA stability	association	protein-RNA	NA	NA	NA	Cancer	Cervical cancer	PCG	lncRNA	ENSG00000165819	NA	ENSG00000237424	GRCh38_1:47432133-47434641	56339	84793	M6A|MT-A70|Spo8	MGC12982	m6A methyltransferase METTL3-mediated lncRNA FOXD2-AS1 promotes the tumorigenesis of cervical cancer.Mechanistically, m6A methyltransferase methyltransferase-like 3 (METTL3) enhanced the stability of FOXD2-AS1 and maintained its expression. Moreover, FOXD2-AS1 recruited lysine-specific demethylase 1 (LSD1) to the promoter region of p21 to silence its transcription abundance. In conclusion, these findings support that METTL3/FOXD2-AS1 accelerates cervical cancer progression via a m6A-dependent modality, which may serve as a potential therapeutic target for cervical cancer.	34589576	RID05351	interact with mRNA	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)
Atherosclerosis	LINC-ROR	let-7b-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	oxidative metabolic process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	lincRNA-RoR|lincRNA-ST8SIA3|ROR	NA	Overexpressed lncRNA ROR Promotes the Biological Characteristics of ox-LDL-Induced HUVECs via the let-7b-5p/HOXA1 Axis in Atherosclerosis.The expression of let-7b-5p, which bound to lncRNA ROR, was downregulated in AS, indicating that the two genes were negatively correlated.In AS, lncRNA ROR promoted the biological characteristics of oxidation of low-density lipoprotein-induced HUVECs  via  the let-7b-5p/HOXA1 axis.	34589524	RID05352	expression association	NA	UP(LIHC);DATA(GSE117623)	
Gastric cancer	GRASLND	LOX	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);angiogenesis(+)	ceRNA(miR-30c-2-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228203	GRCh38_2:6911754-6918734	ENSG00000113083	NA	386597	4015	RNF144A-AS1	NA	RNF144A-AS1, a TGF-beta1- and hypoxia-inducible gene that promotes tumor metastasis and proliferation via targeting the miR-30c-2-3p/LOX axis in gastric cancer.The expression of RNF144A-AS1, miR-30c-2-3p, and Lysyl oxidase (LOX) was detected by quantitative real-time PCR assay. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation (RIP) assay explored the interactions among RNF144A-AS1, miR-30c-2-3p, and LOX. The expression of RNF144A-AS1 was significantly upregulated in GC tissues and was associated with poor prognosis and later-stage diseases. Mechanism exploration indicated RNF144A-AS1 served as a microRNA decoy of miR-30c-2-3p to release LOX. Gene Set Enrichment Analysis further suggested LOX and RNF144A-AS1 were enriched in the same gene sets, emphasizing the internal mechanism connection between these two genes.TGF-beta1- and hypoxia-inducible RNF144A-AS1 promoted tumor metastasis, angiogenesis, and proliferation through targeting the miR-30c-2-3p/LOX axis in GC, highlighting the value of the RNF144A-AS1/miR-30c-2-3p/LOX axis in therapeutic interventions of GC.	34583752	RID05353	ceRNA or sponge	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Gastric cancer	TGFB1	GRASLND	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);angiogenesis(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000228203	GRCh38_2:6911754-6918734	7040	386597	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	RNF144A-AS1	RNF144A-AS1, a TGF-beta1- and hypoxia-inducible gene that promotes tumor metastasis and proliferation via targeting the miR-30c-2-3p/LOX axis in gastric cancer.Cells were treated with recombinant human TGF-beta1 (Transforming Growth Factor beta1) to explore the effect of TGF-beta1 on RNF144A-AS1.  The expression of RNF144A-AS1 was significantly upregulated in GC tissues and was associated with poor prognosis and later-stage diseases.  Additionally, RNF144A-AS1 was also induced by TGF-beta1.	34583752	RID05354	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Parkinson's disease	NEAT1	SP1	positively-E	luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-519a-3p)	regulation	NA	1-methyl-4-phenylpyridine	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000185591	NA	283131	6667	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long Noncoding RNA NEAT1 Knockdown Ameliorates 1-Methyl-4-Phenylpyridine-Induced Cell Injury Through MicroRNA-519a-3p/SP1 Axis in Parkinson Disease.The targeting relationship between miR-519a-3p and NEAT1 or SP1 was predicted by starBase online database and verified by a dual-luciferase reporter assay. NEAT1 and SP1 expressions were significantly upregulated.NEAT1 served as a sponge of miR-519a-3p and regulated MPP+-caused cell injury by interacting with miR-519a-3p. Also, SP1, a target gene of miR-519a-3p, rescued miR-519a-3p-mediated actions under MPP+ treatment. Importantly, NEAT1 stimulated SP1 expression through interaction with miR-519a-3p.NEAT1 silencing protected against MPP+-induced neuroblastoma cell injury by regulating the miR-519a-3p/SP1 pathway. This finding provides a novel direction for the development of therapeutic strategies for Parkinson disease.	34508910	RID05355	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	NEAT1	RUNX2	positively-E	luciferase reporter assay;RNA pull-down assay;FISH;RIP;shRNA	upregulation	RT-qPCR	GSE38241	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-205-5p);interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000124813	NA	283131	860	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	LncRNA nuclear-enriched abundant transcript 1 shuttled by prostate cancer cells-secreted exosomes initiates osteoblastic phenotypes in the bone metastatic microenvironment via miR-205-5p/runt-related transcription factor 2/splicing factor proline- and glutamine-rich/polypyrimidine tract-binding protein 2 axis.Further gain- and loss-of-function experimentation revealed that NEAT1 acted as a competing endogenous RNA (ceRNA) of microRNA (miR)-205-5p to upregulate the runt-related transcription factor 2 (RUNX2) levels.  Collectively, our findings indicated that PCa-derived exosomes-loaded NEAT1 upregulated RUNX2 to facilitate the osteogenesis of hBMSCs by competitively binding to miR-205-5p via the SFPQ/PTBP2 axis, therefore providing a potential therapeutic target to treat osteogenesis of hBMSCs in PCa. NEAT1 shuttled by PCa-derived exosomes could be transferred into hBMSCs, where NEAT1 exerted inductive properties in osteogenic differentiation of hBMSCs through the upregulation of RUNX2 by competitively binding to miR-205-5p and regulating SFPQ/PTBP2 in vitro and in vivo.	34459124	RID05356	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Intrahepatic cholangiocarcinoma	FAM66C	KCND2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);glycolysis(+)	ceRNA(miR-23b-3p)	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000226711	GRCh38_12:8180209-8216151	ENSG00000184408	NA	440078	3751	NA	KIAA1044|Kv4.2|RK5	Long noncoding RNA FAM66C promotes tumor progression and glycolysis in intrahepatic cholangiocarcinoma by regulating hsa-miR-23b-3p/KCND2 axis.The dual-luciferase reporter and RNA pull-down assays were conducted as a means of confirming the interactions between FAM66C, miR-23b-3p, and KCND2.Mechanistic analyses revealed that FAM66C regulated the downstream target gene KCND2 by sponging miR-23b-3p. FAM66C effect on ICC was further validated in murine xenograft assays. FAM66C knockdown cells gave rise to tumors that were smaller in size, consistent with the role of FAM66C as a promoter of in vivo tumor growth. These data revealed that FAM66C was able to drive ICC tumor progression and glycolytic activity via the miR-23b-3p/KCND2 axis, indicating FAM66C may be a viable target for treating ICC.	34418280	RID05357	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE111065,GSE51827,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Sepsis acute kidney injury	CASC9	miR-424-5p	interact	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(+)	NA	regulation	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000249395	GRCh38_8:75120409-75352327	NA	NA	101805492	NA	ESCCAL-1|linc-JPH1|LINC00981	NA	The lncRNA CASC9 alleviates lipopolysaccharide-induced acute kidney injury by regulating the miR-424-5p/TXNIP pathway.CASC9 was significantly downregulated in the LPS-induced AKI model. CASC9 attenuated cell inflammation and apoptosis and enhanced the antioxidant capacity of cells. Regarding the mechanism, miR-424-5p was identified as the downstream target of CASC9, and the interaction between CASC9 and miR-424-5p promoted thioredoxin-interacting protein (TXNIP) expression.CASC9 alleviates LPS-induced AKI in vivo and in vitro, and CASC9 directly targets miR-424-5p and further promotes the expression of TXNIP.	34407684	RID05358	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	
Cervical cancer	HOXC-AS3	miR-105-5p	negatively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251151	GRCh38_12:53981509-53985519	NA	NA	100874365	NA	NA	NA	Long noncoding RNA HOXC-AS3 enhances the progression of cervical cancer via activating ErbB signaling pathway.dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to test the regulatory interaction of HOXC-AS3, miR-105-5p and SOS1. MiR-105-5p was a downstream target of HOXC-AS3, and it mediated the HOXC-AS3-induced oncogenic effects. Mechanistically, the bioinformatic analysis illustrated that SOS1 was targeted by miR-105-5p. Up-regulating SOS1 heightened the growth, migration and invasion of CC cells by enhancing the ErbB signaling pathway, which was reversed by miR-105-5p. Up-regulated HOXC-AS3 aggravates CC by promoting SOS1 expression via targeting miR-105-5p.	34387789	RID05359	transcriptional regulation	NA		
Cervical cancer	HOXC-AS3	SOS1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251151	GRCh38_12:53981509-53985519	ENSG00000115904	NA	100874365	6654	NA	GF1|GINGF|HGF	Long noncoding RNA HOXC-AS3 enhances the progression of cervical cancer via activating ErbB signaling pathway.dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to test the regulatory interaction of HOXC-AS3, miR-105-5p and SOS1. MiR-105-5p was a downstream target of HOXC-AS3, and it mediated the HOXC-AS3-induced oncogenic effects. Mechanistically, the bioinformatic analysis illustrated that SOS1 was targeted by miR-105-5p. Up-regulating SOS1 heightened the growth, migration and invasion of CC cells by enhancing the ErbB signaling pathway, which was reversed by miR-105-5p. Up-regulated HOXC-AS3 aggravates CC by promoting SOS1 expression via targeting miR-105-6p.	34387789	RID05360	expression association	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	OXCT1-AS1	LEF1	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	stability;ubiquitination	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000248668	GRCh38_5:41869927-41872241	ENSG00000138795	NA	100874002	51176	SARRAH	TCF10|TCF1ALPHA|TCF7L3	lncRNA OXCT1-AS1 Promotes Metastasis in Non-Small-Cell Lung Cancer by Stabilizing LEF1, In Vitro and In Vivo.Further, the protective effect of lncRNA OXCT1-AS1 on lymphoid enhancer factor 1 (LEF1) was examined using RNA pull-down and RNA immunoprecipitation assays. Mechanistically, through direct interaction, lncRNA OXCT1-AS1 maintained LEF1 stability by blocking NARF-mediated ubiquitination. Furthermore, LEF1 knockdown impaired invasion and migration of NSCLC  in vitro  and  in vivo . Collectively, these data highlight the ability of lncRNA OXCT1-AS1 to promote NSCLC metastasis by stabilizing LEF1 and suggest that lncRNA OXCT1-AS1 represents a novel therapeutic target in NSCLC.	34337014	RID05361	epigenetic regulation	metastasis		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ischemic heart disease	SCDAL	GDF6	positively-E	shRNA;siRNA	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	NA	NA	ENSG00000156466	NA	NA	392255	NA	BMP13|KFS|KFS1|SGM1	A Novel Human Long Noncoding RNA SCDAL Promotes Angiogenesis through SNF5-Mediated GDF6 Expression.Mechanistically, SCDAL induces growth differentiation factor 6 (GDF6) expression via direct interaction with SNF5 at GDF6 promoter. Secreted GDF6 promotes endothelial angiogenesis via non-canonical vascular endothelial growth factor receptor 2 activation. Furthermore, SCDAL-GDF6 is expressed in human endothelial cells, and directly enhances endothelial angiogenesis in vitro and in vivo. Thus, these findings uncover a previously unknown lncRNA-dependent regulatory circuit for angiogenesis. Targeted intervention of the SCDAL-GDF6 pathway has potential as a therapy for ischemic heart diseases.	34319658	RID05362	interact with protein	NA		
Colorectal cancer	MALAT1	SMAD1	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170365	NA	378938	4086	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	JV4-1|MADH1|MADR1	Long noncoding RNA MALAT1 sponging miR-26a-5p to modulate Smad1 contributes to colorectal cancer progression by regulating autophagy.Mechanistically, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) may act as a competing endogenous RNA by binding with miR-26a-5p competitively and thus modulating the de-repression of downstream target Smad1. Furthermore, clinical analysis results show that Smad1 is positively correlated with MALAT1 and negatively correlated with miR-26a-5p in CRC samples. In conclusion, our results demonstrated that Smad1 may serve as an oncogene in CRC through autophagy.	34313719	RID05363	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	FOXD1-AS1	FOXD1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	interact with RNA	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000247993	GRCh38_5:73446357-73446984	ENSG00000251493	NA	106144539	2297	TCONS_00009423	FKHL8|FREAC4	FOXD1-AS1 upregulates FOXD1 to promote oral squamous cell carcinoma progression.FOXD1-AS1 expression was detected via RT-qPCR. FOXD1-AS1 was expressed at a high level in head and neck squamous cell carcinoma (HNSC). Knockdown of FOXD1-AS1 exerted repressive impacts on OSCC cell proliferation, migration, invasion, and EMT. Moreover, FOXD1-AS1 positively regulated its nearby gene FOXD1 via interacting with miR-369-3p. In addition, adenosine deaminase RNA specific (ADAR), known as a RNA-binding protein (RBP), was capable to bind with FOXD1-AS1 and FOXD1 simultaneously, and could regulate the stability of FOXD1 mRNA. Aside from that, rescue assays delineated that FOXD1-AS1 promoted OSCC progression via upregulating FOXD1.FOXD1-AS1 elevates FOXD1 expression to promote OSCC malignant phenotypes through miR-369-3p and ADAR.	34403535	RID05364	interact with mRNA	NA	UP(BRCA);DATA(GSE55807)	UP(BRCA);DATA(GSE55807)
Ischemic heart disease	LncHrt	SIRT2	interact	RIP;RNA pull-down assay;shRNA	upregulation	qRT-PCR;microarray	NA	NA	LKB1/AMPK signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Heart disease	lncRNA	PCG	NA	NA	ENSG00000068903	NA	NA	22933	NA	SIR2|SIR2L|SIR2L2	LncRNA LncHrt preserves cardiac metabolic homeostasis and heart function by modulating the LKB1-AMPK signaling pathway.RNA-pull down followed by mass spectrometry and RNA immunoprecipitation (RIP) identified SIRT2 as a LncHrt-interacting protein involved in cardiac metabolic regulation. Mechanistically, we established that LncHrt interacts with SIRT2 to preserve SIRT2 deacetylase activity by interfering with the CDK5 and SIRT2 interaction. This increases downstream LKB1-AMPK kinase signaling, which ameliorates functional and metabolic deficits. Importantly, we found the expression of the human homolog of mouse LncHrt was decreased in patients with dilated cardiomyopathy. Together, these studies identify LncHrt as a cardiac metabolic regulator that plays an essential role in preserving heart function by regulating downstream metabolic signaling pathways. Consequently, LncHrt is a potentially novel RNA-based therapeutic target for ischemic heart disease.	34379189	RID05365	transcriptional regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Colorectal cancer	MCF2L-AS1	RAB22A	positively-E	luciferase reporter assay;RNA pull-down assay;FISH;RIP	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-105-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000235280	GRCh38_13:112967484-112968824	ENSG00000124209	NA	100289410	57403	NA	NA	LncRNA MCF2L-AS1 aggravates the malignant development of colorectal cancer via targeting miR-105-5p/RAB22A axis.MCF2L-AS1 expression in CRC cells was tested via RT-qPCR assay. MCF2L-AS1 was highly expressed in CRC cells, and it could enhance the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of CRC cells. MiR-105-5p was sponged by MCF2L-AS1 in CRC cells and Ras-related protein Rab-22A (RAB22A) was verified to be the downstream target of miR-105-5p. It was verified through rescue assays that RAB22A overexpression or miR-105-5p silencing could reverse the repressive impact of MCF2L-AS1 silencing on CRC progression.MCF2L-AS1 accelerated the malignant development of CRC cells by targeting the miR-105-5p/RAB22A axis.	34592939	RID05366	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Gallbladder cancer	LINC01410	STAT5A	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	GSE76633	NA	cell proliferation(+);cell migration(+);cell invasion(+);ErbB signaling pathway(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000238113	GRCh38_9:62801461-62813486	ENSG00000126561	NA	103352539	6776	NA	MGF|STAT5	Long Non-Coding RNA LINC01410 Promoted Tumor Progression via the ErbB Signaling Pathway by Targeting STAT5 in Gallbladder Cancer.RNA pull-down, RNA immune-precipitation (RIP), and western blot assay were conducted to investigate the mechanisms underlying the biological function of LINC01410 in GBC.LINC01410 was significantly upregulated in the GBC tissues compared to adjacent non-tumor tissues. Overexpression of LINC01410 promoted GBC cell proliferation, migration, and invasion in vitro and GBC progression in vivo, whereas LINC01410 downregulation rescued these effects in vitro. From RNA pull-down and RIP assay, we identified that STAT5 was a critical downstream target of LINC01410. Furthermore, ErbB signaling pathway was involved in the malignant phenotypes of GBC mediated by LINC01410.Our results suggested that LINC01410 was an important lncRNA that promoted GBC progression via targeting STAT5 and activating ErbB signaling pathway.	34322379	RID05367	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	RMRP	NRP2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-613)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000118257	NA	6023	8828	CHH|NME1|RMRPR|RRP2	VEGF165R2	lncRNA RMRP predicts poor prognosis and mediates tumor progression of esophageal squamous cell carcinoma by regulating miR-613/ neuropilin 2 (NRP2) axis.RMRP was significantly upregulated in ESCC, which was associated with the lymph node metastasis status, the TNM stage of patients, and a poor outcome of ESCC patients. Moreover, RMRP promoted the proliferation, migration, and invasion of ESCC cells via regulating miR-613/NRP2.RMRP was involved in the progression of ESCC through regulating the miR-613/NRP2 axis, which provides a potential target for the treatment of ESCC.	34516335	RID05368	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	ILF3-DT	ILF3	interact	knockdown	upregulation	qRT-PCR	NA	NA	cancer progression(+)	RNA stability;interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000129351	NA	147727	3609	ILF3-AS1	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	Long non-coding RNA ILF3-AS1 facilitates hepatocellular carcinoma progression by stabilizing ILF3 mRNA in an m6A-dependent manner.Here, we found that ILF3-AS1 expression was significantly elevated in HCC tissues and also associated with prognosis of patients with HCC.  Mechanistically, ILF3-AS1 associated with ILF3 mRNA and inhibited its degradation. ILF3-AS1 increased ILF3 m6A level via recruiting N6-methyladenosine (m6A) RNA methyltransferase METTL3. Moreover, IFL3-AS1 enhanced the interaction between ILF3 mRNA and m6A reader IGF2BP1. Overall, our study revealed the function and mechanism of ILF3-AS1 in the malignant phenotypes of HCC cells, which provides a novel therapeutic target for HCC.	34491544	RID05369	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteoporosis	PART1	RUNX3	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell differentiation(+);apoptosis process(-)	ceRNA(miR-185-5p)	regulation	NA	NA	CSC	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000020633	NA	25859	864	DKFZP586D0823|NCRNA00206	AML2|CBFA3|PEBP2A3	LncRNA PART1/miR-185-5p/RUNX3 feedback loop modulates osteogenic differentiation of bone marrow mesenchymal stem cells.PART1, miR-185-5p, and RUNX3 levels were assessed  via  RT-qPCR. The relationship between miR-185-5p and PART1 or RUNX3 was validated by luciferase reporter, RIP assays.Moreover, PART1 served as a ceRNA to influence the RUNX3 level  via  targeting miR-185-5p. In addition, RUNX3 was verified to activate the transcription of PART1 in hBMSCs.Our study elaborated that PART1/miR-185-5p/RUNX3 feedback contributed to osteogenic differentiation and inhibited the hBMSCs apoptosis, suggesting that PART1 might be a novel target for OP treatment.	34431433	RID05370	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Colorectal cancer	SNHG10	MIR3690	positively-E	luciferase reporter assay;starBase	upregulation	RT-qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000247092	GRCh38_14:95521943-95534889	ENSG00000265658	NA	283596	100500894	C14orf62|LINC00063|NCRNA00063	MIR3690-1|MIR3690-2|hsa-mir-3690-1|hsa-mir-3690-2|mir-3690-1|mir-3690-2	Long noncoding RNA SNHG10 promotes colorectal cancer cells malignant progression by targeting miR-3690.Expression levels of genes in colorectal cancer tissues and cell lines were detected by Starbase and reverse transcription quantitative PCR (RT-qPCR) Cell Counting Kit-8 (CCK-8).In addition, the interaction of SNHG10 and miR-3690 was analyzed by dual-luciferase reporter assays.dual-luciferase reporter assay confirmed that miR-3690 directly targeted SNHG10.More importantly, the silencing of miR-3690 reversed the effect of the SNHG10 knockdown on the cell viability, proliferation, migration and invasion of HCT116 and DXH-1 cells. The present results demonstrated that SNHG10 promotes colorectal cancer cells the malignant progression by targeting miR-3690.	34477483	RID05371	transcriptional regulation	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)	
Lung cancer	SOX21-AS1	PIM2	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-24-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000102096	NA	100507533	11040	NA	NA	Long non-coding RNA SOX21-AS1 modulates lung cancer progress upon microRNA miR-24-3p/PIM2 axis.The relationships between  miR-24-3p  and  SOX21-AS1  or PIM2 were predicted using bioinformatics tools and confirmed using a luciferase reporter assays. SOX21-AS1  expression levels were high in lung cancer tissues and cells. PIM2 was targeted by  miR-24-3p  and showed increased levels in tumor tissues and cells. Furthermore,  miR-24-3p  overexpression inhibited the proliferation and promoted the apoptosis of lung cancer cells. In lung cancer cells,  SOX21-AS1  negatively modulated the  miR-24-3p /PIM2 axis to facilitate their proliferation, migration, and invasion. These findings offer a novel idea for future research on treating lung cancer at the molecular level.	34511042	RID05372	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	PCGEM1	miR-152-3p	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	LncRNA PCGsEM1 contributes to the Proliferation, Migration and Invasion of Non-small Cell Lung Cancer Cells via acting as a Sponge for miR-152-3p Short title: The PCGEM1/miR-152-3p axis in NSCLC.The expression of LncRNA PCGEM1 and miR-152-3p in NSCLC tissues and cells was analyzed using quantitative real-time RT-PCR The further luciferase reporter assay and expression results showed that miR-152-3p might be a target gene of PCGEM1 and mediate the effects of PCGEM1 on cell proliferation, migration and invasion in NSCLC.Thus, the findings from the present study indicate that the NSCLC patients have significantly increased PCGEM1 and decreased miR-152-3p expression and that the knockdown of PCGEM1 may inhibit NSCLC cell proliferation, migration and invasion by sponging miR-152-3p. The PCGEM1/miR-152-3p axis may provide novel therapeutic targets for NSCLC treatment.	34455968	RID05373	ceRNA or sponge	NA	UP(PAAD);DATA(GSE60407)	
Cholangiocarcinoma	PVT1	KLF5	positively-E	luciferase reporter assay;siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(KLF5)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000102554	NA	5820	688	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BTEB2|CKLF|IKLF	Effect of lncRNA PVT1/miR186/KLF5 Axis on the Occurrence and Progression of Cholangiocarcinoma. Additionally, lncRNA PVT1 and KLF5 were proved to be highly expressed in CCA tissues and cell lines.Cotransfection of lncRNA PVT1 and miR186 increased the expression of KLF5 compared with controls. Overall, these results demonstrated that the lncRNA PVT1/miR186/KLF5 axis might exert a key role in the occurrence and progression of CCA, and this axis might provide a new target for treating CCA.	34337058	RID05374	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Breast cancer	PCDHB17P	MELK	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell metastasis(+);angiogenesis(+);cell migration(-);cell invasion(-)	ceRNA(miR-145-3p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255622	GRCh38_5:141155996-141159061	ENSG00000165304	NA	54661	9833	PCDH-psi1|PCDHB17	KIAA0175	PCDHB17P/miR-145-3p/MELK/NF-kB Feedback Loop Promotes Metastasis and Angiogenesis of Breast Cancer.Mechanistic investigation indicated that PCDHB17P acted as a cancer-promoting competing endogenous RNA (ceRNA) by binding miR-145-3p and upregulating MELK. Overall, the results demonstrated that the constitutive activation of PCDHB17P/miR-145-3p/MELK/NF-kB feedback loop promotes the metastasis and angiogenesis of breast cancer, suggesting that this lncRNA might be a promising prognostic biomarker and therapeutic target for breast cancer.	34350110	RID05375	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Breast cancer	NFKB1	PCDHB17P	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell metastasis(+);angiogenesis(+);cell migration(-);cell invasion(-)	transcriptional regulation	association	NA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000109320	NA	ENSG00000255622	GRCh38_5:141155996-141159061	4790	54661	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	ME4|PCDH-psi1|PCDHB17	PCDHB17P/miR-145-3p/MELK/NF-kB Feedback Loop Promotes Metastasis and Angiogenesis of Breast Cancer.Interestingly, MELK could in turn increase the promoter activity and expression of PCDHB17P via NF-kB, thus forming a positive feedback loop that drives the metastasis and angiogenesis of breast cancer. Overall, the results demonstrated that the constitutive activation of PCDHB17P/miR-145-3p/MELK/NF-kB feedback loop promotes the metastasis and angiogenesis of breast cancer, suggesting that this lncRNA might be a promising prognostic biomarker and therapeutic target for breast cancer.	34350110	RID05376	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Renal cell carcinoma	SNHG17	H2AX	positively-E	luciferase reporter assay;RIP;siRNA	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-328-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000188486	NA	388796	3014	NA	H2AFX	LncRNA SNHG17 promotes tumor progression and predicts poor survival in human renal cell carcinoma via sponging miR-328-3p.The interaction between SNHG17, miR-328-3p, and Histone'sH2Avariant (H2AX) was verified by bioinformatics, dual-luciferase reporter gene, and RNA immunoprecipitation (RIP). Highly expressed SNHG17 was evident in RCC tissue samples and cell lines, and SNHG17 overexpression was related to advanced TNM stage and reduced relapse-free and overall survival of patients with RCC.More importantly, SNHG17 could upregulate the expression of H2AX by acting as a miR-328-3p sponge.  In vivo  experiments confirmed that SNHG17 promoted the growth of RCC tumors. SNHG17/miR-328-3p/H2AXaxis might be involved in RCC progression, which provided a potential therapeutic target for RCC.	34497156	RID05377	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Gastric cancer	FOXC2-AS1	FOXC2	interact	knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	RNA stability;interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260944	GRCh38_16:86565145-86567845	ENSG00000176692	NA	103752587	2303	ODRUL	FKHL14|MFH-1	FOXC2-AS1 stabilizes FOXC2 mRNA via association with NSUN2 in gastric cancer cells.Here, we found that FOXC2-AS1 expression was significantly elevated in GC tissues and cells. Functionally, knockdown of FOXC2-AS1 attenuated the proliferation, migration and invasion of GC cells, whereas overexpression of FOXC2-AS1 showed the opposite effects. Further investigation revealed that FOXC2-AS1 interacted with FOXC2 mRNA and repressed its degradation. FOXC2-AS1 recruited RNA methyltransferase NSUN2 to FOXC2 mRNA, increasing its m5C level and association with YBX1. Taken together, our findings suggested that FOXC2-AS1 acted as an oncogenic lncRNA by stabilizing FOXC2 mRNA in an m5C-dependent manner, which may provide a novel therapeutic target for GC.	34324140	RID05378	interact with protein	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	AC016745.3	NONO	negatively-E	ChIP;qRT-PCR;RNA pull-down assay	upregulation	RIP	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000234997	GRCh38_2:113325009-113430988	ENSG00000147140	NA	NA	4841	NA	MRXS34|NMT55|NRB54|P54|P54NRB|PPP1R114	[AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO.]The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examines the function and mechanisms of action of lncRNA  AC016745.3  in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of  AC016745.3  expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of  AC016745.3  inhibits the proliferation and migration of PCa cells, and suppresses the expression of AR target genes. This research also demonstrates that the protein NONO interacts with AR and functions as an AR co-activator, promoting AR transcriptional activity. Furthermore, using RNA immunoprecipitation (RIP)-PCR experiments, the study demonstrates that both NONO and AR can bind  AC016745.3 . Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that  AC016745.3  can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that  AC016745.3  can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of  AC016745.3  expression can enhance NONO's promotion effect on AR.	34833084	RID05379	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Prostate cancer	AC016745.3	AR	negatively-E	ChIP;qRT-PCR;RNA pull-down assay	upregulation	RIP	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000234997	GRCh38_2:113325009-113430988	ENSG00000169083	NA	NA	367	NA	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	[AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO.]The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examines the function and mechanisms of action of lncRNA  AC016745.3  in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of  AC016745.3  expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of  AC016745.3  inhibits the proliferation and migration of PCa cells, and suppresses the expression of AR target genes. This research also demonstrates that the protein NONO interacts with AR and functions as an AR co-activator, promoting AR transcriptional activity. Furthermore, using RNA immunoprecipitation (RIP)-PCR experiments, the study demonstrates that both NONO and AR can bind  AC016745.3 . Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that  AC016745.3  can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that  AC016745.3  can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of  AC016745.4  expression can enhance NONO's promotion effect on AR.	34833084	RID05380	expression association	NA		UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Gastric cancer	FEZF1-AS1	ATG5	positively-E	RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell autophagy(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000057663	NA	154860	9474	NA	APG5|APG5L|ASP|hAPG5	[LncRNA FEZF1-AS1 Promotes Multi-Drug Resistance of Gastric Cancer Cells via Upregulating ATG5.]	34790665	RID05381	expression association	NA		UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Triple-negative breast cancer	LINC01234	SYNJ1	positively-E	RIP;Luciferase Reporter Assay;western blot;AnnoLnc database;TargetScan ; miRTarBase;	upregulation	RT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell proliferation(+)	ceRNA(miR-429)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000159082	NA	100506465	8867	onco-lncRNA-32	INPP5G|PARK20	[ln RNA LINC01234 promotes triple-negative breast cancer progression through regulating the miR-429/SYNJ1 axis.]Emerging evidence has illustrated that long noncoding RNA 01234 (LINC01234) has played a pivotal role in the development and progression of human cancer. The regulatory role and underlying mechanisms of LINC01234 in triple-negative breast cancer (TNBC) remains unknown. In this study, we analyzed the expression level of LINC01234 in several breast cancer cell lines. CCK-8, EdU, flow cytometry analysis, wound healing assay, and transwell assay were carried out to investigate the effect of LINC01234 on tumor proliferation, apoptosis, and migration. Bioinformatic analysis and luciferase reporter assays were performed to confirm the molecular binding. We found that LINC01234 was dramatically upregulated in breast cancer cell lines, especially in TNBC. The loss and gain-of functional experiments revealed that LINC01234 significantly promoted proliferation, migration, and suppressed cell apoptosis of MDA-MB-231 cells  in vitro  and inhibited tumorigenesis  in vivo . Mechanistic investigations demonstrated that LINC01234 might act as a competing endogenous RNA (ceRNA) for miR-429 to regulate the SYNJ1 expression. The effects of miR-429 and SYNJ1 in MDA-MB-231 cells were also analyzed. Our results revealed that the novel LINC01234/miR-429/SYNJ1 axis played a critical role in progression of TNBC cell line MDA-MB-231, and it may serve as a therapeutic target for TNBC.	34786067	RID05382	ceRNA or sponge	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	LINC01554	G3BP2	positively-E	luciferase reporter assay	upregulation	sequencing	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000236882	GRCh38_5:95838245-95860133	ENSG00000138757	NA	202299	9908	C5orf27|FIS|FLJ38821	KIAA0660	[G3BP2 regulated by the lncRNA LINC01554 facilitates esophageal squamous cell carcinoma metastasis through stabilizing HDGF transcript.]Metastasis is the leading cause of death of patients with esophageal squamous cell carcinoma (ESCC). Although an increasing number of studies have demonstrated the involvement of G3BP2 in several human cancers, how G3BP2 interacts with long noncoding RNAs and regulates mRNA transcripts in mediating ESCC metastasis remains unclear. In this study, we uncovered that G3BP2 was upregulated in ESCC. Further analysis revealed that upregulation of G3BP2 was significantly correlated with lymph node metastasis, depth of tumor invasion and unfavorable outcomes in ESCC patients. Both in vitro and in vivo functional assays demonstrated that G3BP2 dramatically enhanced ESCC cell migration and invasion. Mechanistically, LINC01554 maintained the high G3BP2 expression in ESCC by protecting G3BP2 from degradation through ubiquitination and the interaction domains within LINC01554 and G3BP2 were identified. In addition, RNA-seq revealed that HDGF was regulated by G3BP2. G3BP2 bound to HDGF mRNA transcript to stabilize its expression. Ectopic expression of HDGF effectively abolished the G3BP2 depletion-mediated inhibitory effect on tumor cell migration. Intriguingly, introduction of compound C108 which can inhibit G3BP2 remarkedly suppressed ESCC cell metastasis in vitro and in vivo. Collectively, this study describes a newly discovered regulatory axis, LINC01554/G3BP2/HDGF, that facilitates ESCC metastasis and will provide novel therapeutic strategies for ESCC.	34782720	RID05383	expression association	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Childhood pneumonia	GAS5	INPP5D	positively-E		upregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-155)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Respiratory system disease	Pneumonia	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000168918	NA	60674	3635	NCRNA00030|SNHG2	SHIP|SHIP-1|SHIP1|SIP-145|hp51CN|p150Ship	[LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.]LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and miR-155 in childhood pneumonia. GAS5 and miR-155 levels in plasma samples from pneumonia patients and controls were detected using RT-qPCR. The role of GAS5 in miR-155 RNA gene methylation in human bronchial epithelial cells (HBEpCs) was analyzed by methylation analysis. Flow cytometry and RT-qPCR were applied to analyze cell apoptosis and SHIP-1 expression, respectively. GAS5 was downregulated in pneumonia, and miR-155 was upregulated in pneumonia. GAS5 and miR-155 were inversely correlated. GAS5 overexpression decreased miR-155 expression in HBEpCs, while miR-155 overexpression showed no significant effects on GAS5 expression. In addition, GAS5 suppressed LPS-induced HBEpC apoptosis, promoted SHIP-1 expression, and reduced the enhancing effect of miR-155 on cell apoptosis and SHIP-1 expression. GAS5 may participate in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.	34758804	RID05384	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	PAX8-AS1	PKN2	positively-E	western blot;Luciferase Reporter Assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(-);	ceRNA(miR-96-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000189223	GRCh38_2:113211421-113276581	ENSG00000065243	NA	654433	5586	NA	Pak-2|PRK2|PRKCL2|STK7	[Overexpression of PAX8-AS1 Inhibits Malignant Phenotypes of Papillary Thyroid Carcinoma Cells via miR-96-5p/PKN2 Axis.]Thyroid carcinoma (THCA) is the most frequent endocrine malignancy. Papillary thyroid carcinoma (PTC) is the major subtype of THCA, accounting for over 80% of all THCA cases. LncRNA PAX8-AS1, a tumor suppressor associated with various human cancers, has been reported to be relevant to the regulation of all sorts of cellular processes. The purpose of this study was to verify the role of PAX8-AS1 in PTC. Three human PTC cell lines (K1, TPC-1, and IHH4) and one normal human thyroid cell line, Nthy-ori3-1, were used in our study. The expression of genes was detected by qRT-PCR The bioinformatic analysis and luciferase reporter assay were used to confirm the binding relationship of PAX8-AS1 to miR-96-5p, and the targeting relationship of miR-96-5p to PKN2 was also predicted. Cell proliferation and apoptosis capacities were assessed by MTT and flow cytometry, respectively. EdU assay was used to detect cell proliferation. western blot assay was employed to examine protein expression. The expression of PAX8-AS1 was decreased in PTC tissues and cells. PAX8-AS1 overexpression inhibited the proliferation of PTC cells and promoted cell apoptosis. In addition, PAX8-AS1 bonds with miR-96-5p, whose downregulation elevated the expression of PKN2 in PTC cells. Importantly, according to the rescue experiments, PKN2 silencing partially reversed the inhibitory effects of PAX8-AS1 expression on PTC cell proliferation and apoptosis. We found that the PAX8-AS1/miR-96-5p/PKN2 axis was closely related to the progression of PTC, which could be a potential target for treating PTC patients.	34745257	RID05385	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Myeloma	HDAC1	NONHSAT113026	positively-E	western blot;Luciferase Reporter Assay	downregulation	RT-qPCR	NA	NA	cell migration(-)	NA	regulation	protein-RNA	NA	NA	NA	Cancer	Myeloid neoplasm	PCG	lncRNA	ENSG00000116478	NA	NA	NA	3065	NA	GON-10|HD1|KDAC1|RPD3|RPD3L1	NA	[HDAC1 promotes the migration of human myeloma cells via regulation of the lncRNA/Slug axis]	34738621	RID05386	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)	
Gastric cancer	TFAP2A-AS1	NISCH	positively-E	western blot;luciferase reporter assay;RNA pull-down assay;RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(-);cell proliferation(-)	ceRNA(miR-3657)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229950	GRCh38_6:10409340-10416446	ENSG00000010322	NA	100130275	11188	NA	I-1|IRAS|KIAA0975	[Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis.]Recently, overwhelming evidence supports that long noncoding RNAs (lncRNAs) play crucial roles in the occurrence and progression of tumors. However, the role and mechanism of lncRNA TFAP2A-AS1 in human gastric cancer (GC) remains unclear. Thus, the biological role and regulatory mechanisms of TFAP2A-AS1 in GC were explored. Quantitative real-time PCR (qPCR) was applied to detect gene expression. western blot was used to measure protein expression. Cell proliferation and migration were determined by functional assays. Fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular distribution of TFAP2A-AS1 in GC. Mechanism investigations were conducted to explore the downstream genes of TFAP2A-AS1 and the upstream transcription factor of TFAP2A-AS1 in GC cells. TFAP2A-AS1 inhibits the proliferation and migration of GC cells. In the downstream regulation mechanism, miR-3657 was verified as the downstream gene of TFAP2A-AS1 and NISCH as the target of miR-3657. NISCH also suppresses cell proliferation and migration in GC. In the upstream regulation mechanism, transcription factor KLF15 positively mediates TFAP2A-AS1 to suppress GC cell proliferation and migration. KLF15-mediated TFAP2A-AS1 hampers cell proliferation and migration in GC via miR-3657/NISCH axis.	34727954	RID05387	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Otitis	NEAT1	p38	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	inflammatory response(+);apoptosis process(+)	ceRNA(miR-495)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Otitis	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100591	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	[Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes the inflammation and apoptosis of otitis media with effusion through targeting microRNA (miR)-495 and activation of p38 MAPK signaling pathway.]Long non-coding RNA (lncRNA) plays a vital role in human inflammatory diseases. Our study aimed to investigate the function of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in otitis media with effusion (OME). The mRNA levels of NEAT1 and miR-495 were measured by RT-qPCR. The protein levels of p38 MAPK were detected by western blot. The levels of inflammatory cytokines were examined by ELISA. CCK-8 and flow cytometry assays were used to evaluate the cell viability and apoptosis, respectively. The interaction between NEAT1 and miR-495 was determined by luciferase reporter and RIP assays. NEAT1 was highly expressed in OME, and silencing of NEAT1 facilitated the cell proliferation and suppressed levels of inflammatory cytokines and cell apoptosis in LPS-induced HMEECs. Moreover, miR-495 was confirmed as a downstream target of NEAT1. Functional assays revealed that NEAT1 promoted the OME by targeting miR-495. It was further demonstrated that NEAT1 could activate the p38 MAPK signaling pathway by regulating miR-495, and the p38 MAPK inhibitor restored the effects of NEAT1 overexpression on the inflammation levels, cell proliferation, and apoptosis. Our study revealed that lncRNA NEAT1 served as a ceRNA to activate p38 MAPK signaling by targeting miR-495 in OME, which may offer a new target for OME treatment.	34723778	RID05388	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Atherosclerosis	RP11-531A24.3	ANXA2	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell migration(+);	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000260838	GRCh38_8:72947150-72950445	ENSG00000182718	NA	NA	302	NA	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	[lncRNA RP11-531A24.3 inhibits the migration and proliferation of vascular smooth muscle cells by downregulating ANXA2 expression.]	34721681	RID05389	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Septic acute kidney injury	NONRATG019935.2	TP53	positively-E	RIP;luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+);	NA	regulation	NA	NA	NA	NA	Other	Injury	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	[Upregulation of lncRNA NONRATG019935.2 suppresses the p53-mediated apoptosis of renal tubular epithelial cells in septic acute kidney injury.]Although increasing evidence has confirmed that the apoptosis of renal tubular epithelial cells (RTECs) is a crucial contributor to the onset and development of septic acute kidney injury (AKI), the pathological mechanism by which RTEC apoptosis is upregulated during septic AKI is not entirely clear. In this study, a rat model of septic AKI was induced by a cecal ligation puncture procedure or lipopolysaccharide (LPS) injection. Four differentially expressed long noncoding RNAs (DE-Lncs) in the rat model of septic AKI were determined using RNA-sequencing and verified by qRT-PCR Among the four DE-Lncs, the expression level of lncRNA NONRATG019935.2 (9935) exhibited the most significant reduction in both septic AKI rats and LPS-treated NRK-52E cells (a rat RTEC line). The overexpression of 9935 suppressed cell apoptosis and p53 protein level in LPS-treated NRK-52E cells, and retarded septic AKI development in the rat model of septic AKI. Mechanistically, 9935 decreased the human antigen R (HuR)-mediated Tp53 mRNA stability by limiting the combination of HuR and the 3'UTR region of Tp53 mRNA in RTECs. The overexpression of HuR abrogated the inhibitory effect of pcDNA-9935 on the LPS-induced apoptosis of NRK-52E and rat primary RTECs. In conclusion, 9935 exerts its role in septic AKI by suppressing the p53-mediated apoptosis of RTECs, and this essential role of 9935 relies on its destructive effect on HuR-mediated Tp53 mRNA stability.	34719669	RID05390	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hemangioma	MEG8	Notch	positively-E	western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell invasion(-);cell proliferation(-)	ceRNA(miR-495)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000258399	GRCh38_14:100836269-100947194	NA	NA	79104	NA	Bsr|Irm|LINC00024|NCRNA00024|Rian|SNHG23|SNHG24|lnc-MGC	NA	Knockdown of lncRNA MEG8 inhibits cell proliferation and invasion, but promotes cell apoptosis in hemangioma, via miR-203-induced mediation of the Notch signaling pathway;As a member of the long non-coding (lnc)RNA family, lncRNA maternally expressed 8, small nucleolar RNA host gene (MEG8), has been reported to serve an oncogenic role in several types of malignancies, including hepatocellular carcinoma, non-small cell lung cancer and pancreatic cancer. The current study aimed to investigate the effect of the knockdown of MEG8 on human hemangioma endothelial cell (HemEC) proliferation, apoptosis and invasion, in addition to determining the underlying molecular mechanism. The knockdown of lncRNA MEG8 was achieved by transfecting lncRNA MEG8 small interfering (si)RNA into HemECs, while the combined knockdown of lncRNA MEG8 knockdown and microRNA (miR)-203 was established by co-transfecting lncRNA MEG8 siRNA and a miR-203 inhibitor into HemECs. The cell proliferation, apoptosis and invasion and the expression levels of miR-34a, miR-200b, miR-200b and Notch signaling pathway-related factors were detected via CCK-8 Kit, flow cytometry, Transwell, reverse transcription-quantitative PCR and western blot assay, respectively. The knockdown of lncRNA MEG8 significantly inhibited proliferation (P<0.05) and invasion (P<0.05), but promoted apoptosis (P<0.01) in HemECs. Furthermore, lncRNA MEG8 knockdown upregulated miR-203 (P<0.01) expression, but did not alter miR-34a or miR-200b expression (both P>0.05). Subsequent experiments revealed that miR-203 silencing exerted no significant effect on the expression levels of lncRNA MEG8 (P>0.05) in HemECs. In addition, miR-203 silencing increased cell proliferation (P<0.05) and invasion (P<0.01), but suppressed apoptosis (P<0.05). miR-203 silencing also reversed the effect of lncRNA MEG8 knockdown on the proliferation (P<0.05), apoptosis (P<0.001) and invasion (P<0.01) of HemECs. Moreover, lncRNA MEG8 knockdown downregulated jagged canonical notch ligand 1 (JAG1; P<0.05) and Notch1 (P<0.05) expression levels, while miR-203 silencing upregulated JAG1 (P<0.01) and Notch1 (P<0.01) expression levels and reversed the effects of lncRNA MEG8 knockdown on JAG1 (P<0.01) and Notch1 (P<0.01) expression in HemECs. In conclusion, the findings of the present study suggested that lncRNA MEG8 knockdown may inhibit cell proliferation and invasion, but promote cell apoptosis in hemangioma via miR-203-induced mediation of the Notch signaling pathway.	34713294	RID05391	ceRNA or sponge	NA		
Cancer	SNHG1	VEGFA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell migration(-);cell proliferation(-)	ceRNA(miR-195-5)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000112715	NA	23642	7422	LINC00057|lncRNA16|NCRNA00057|UHG	VEGF|VEGF-A|VPF	Knockdown of LncRNA SNHG1 Suppresses Corneal Angiogenesis by the Regulation of miR-195-5p/VEGF-A.LncRNA SNHG1 (SNHG1) has been widely studied as the causative factor of angiogenesis and proliferative agent in gastric, lung, cervical, and hepatocellular carcinomas. However, its significance of angiogenesis and progression of corneal neovascularization (CRNV) is least understood. This study focuses on the molecular mechanisms followed by SNHG1 to establish CRNV and its angiogenesis. Bioinformatics analysis to identify potential miRNA targets of SNHG1 and vascular endothelial growth factor A (VEGF-A) was conducted using StarBase and was subsequently confirmed by the luciferase reporter assay. Relative quantitative expression of SNHG1 in human umbilical vein endothelial cells (HUVECs) was detected through qRT-PCRand western blot Cell proliferation was detected through CCK-8 assay, whereas migratory abilities of the cells were determined with transwell assay. A capillary-like tube formation assay was performed to detect the tube formation ability of the cells. Following this, relative expression of miR-195-5p and VEGF-A was determined through qRT-PCRand western blot Results from the experiments manifested upregulated levels of SNHG1 and VEGF-A in HUVECs and CRNV tissues as compared with the control group, whereas downregulated levels of miR-195-5p were measured in the CRNV tissues and HUVECs, suggesting the negative correlation between lncRNA and miRNA. Overexpressed vascular endothelial growth factor promoted cell proliferation and tube formation; however, its silencing leads to inhibition in angiogenesis and proliferation. Potential binding sites of SNHG1 showed miR-195-5p as its direct target and SNHG1 as a sponge for this miRNA. Knockdown and downregulated levels of SNHG1 showed a notable decrease and inhibition in angiogenesis and migration of CRNV cells. The study showed that SNHG1 inhibition significantly reduced cell proliferation, migration, and tube formation in HUVECs transfect with lncRNA SNHG1. Mechanistic insights into the SNHG1 showed that SNHG1 acts as a sponge for miR-195-5p and upregulates the levels of VEGF-A.	34712495	RID05392	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Pancreatic cancer	IPO7	MALAT1	positively-E	luciferase reporter assay;western blot;qPCR;RIP	upregulation	qPCR	NA	NA	apoptosis process(+);cell migration(-);cell proliferation(-)	ceRNA(MiR-129-5p)	regulation	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000205339	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10527	378938	Imp7|RANBP7	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Pancreatic Cancer Progression Is Regulated by IPO7/p53/LncRNA MALAT1/MiR-129-5p Positive Feedback Loop.Background:  Pancreatic cancer is a malignancy with poor prognosis. Importin 7 (IPO7) is a soluble nuclear transport factor, which has been linked to the pathogenesis of several human diseases. However, its role and underlying mechanism in pancreatic cancer are still obscure.  Methods:  Immunohistochemical staining and quantitative real-time polymerase chain reaction (qPCR) were performed to determine IPO7 expression in pancreatic cancer tissues and adjacent tissues. western blot was used to measure IPO7 expression at the protein level in cell lines. Cell Counting Kit-8 (CCK-8), 5-bromo-2'-deoxyuridine (BrdU), flow cytometry, and Transwell assays were employed to explore the biological functions of IPO7. Subcutaneous xenograft transplanted tumor model and caudal vein injection model in mice were also established to validate the oncogenic role of IPO7. western blot and qPCR were utilized to detect the regulatory function of IPO7 on p53 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), respectively. Interaction between MALAT1 and miR-129-5p and interaction between miR-129-5p and IPO7 were verified by bioinformatics prediction, qPCR, dual-luciferase reporter gene experiment, RNA immunoprecipitation (RIP), and pull-down assay.  Results:  Upregulation of IPO7 in pancreatic cancer tissues was associated with adverse prognosis of the patients with pancreatic cancer. Knocking down IPO7 remarkably suppressed cancer cell proliferation and metastasis, while it promoted apoptosis. Overexpression of IPO7 facilitated the malignant phenotypes of pancreatic cancer cells. Mechanistically, IPO7 could repress the expression of p53 and induce the expression of MALAT1 but reduce miR-129-5p expression. Furthermore, miR-129-5p was identified as a posttranscriptional regulator for IPO7, and its inhibition led to IPO7 overexpression in pancreatic cancer cells.  Conclusion:  IPO7 is a novel oncogene for pancreatic cancer, and IPO7/p53/MALAT1/miR-129-5p positive feedback loop facilitates the progression of this deadly disease.	34660566	RID05393	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	TMEM220-AS1	TMEM220	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell invasion(-);cell proliferation(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000263400	GRCh38_17:10729777-10815164	ENSG00000187824	NA	101101775	388335	NA	NA	LncRNA TMEM220-AS1 suppresses hepatocellular carcinoma cell proliferation and invasion by regulating the TMEM220/beta-catenin axis.Long non-coding RNAs (lncRNAs) are critical drivers and suppressors of human hepatocellular carcinoma (HCC). The downregulation of transmembrane protein 220 antisense RNA 1 (TMEM220-AS1) is correlated with poor prognosis in HCC. Nevertheless, the role of TMEM220-AS1 in HCC and the underlying mechanism remains unclear. In this study, TMEM220-AS1 levels were markedly reduced in HCC tissues compared with noncancerous tissues. TMEM220-AS1 downregulation was confirmed in HCC cell lines. TMEM220-AS1 expression was associated with tumor stage, venous infiltration, tumor size, and survival of HCC patients. TMEM220-AS1 overexpression suppressed the migration, invasion, and proliferation of HCC cells. Interestingly, ectopic expression of TMEM220-AS1 increased TMEM220 levels in HCC cells. Decreased TMEM220 levels were observed in HCC tissues and cell lines. TMEM220 expression was positively correlated with TMEM220-AS1 levels in HCC tissue samples and TMEM220 downregulation was significantly correlated with reduced patient survival. TMEM220 overexpression suppressed HCC cell proliferation and mobility. TMEM220 knockdown eliminated the suppressive effect of TMEM220-AS1 in HCCLM3 cells. Mechanistically, TMEM220 overexpression reduced the nuclear accumulation of beta-catenin and decreased MYC, Cyclin D1, and Snail1 mRNA levels in HCCLM3 cells. BIO, a GSK3beta inhibitor, eliminated TMEM220-induced Wnt/beta-catenin pathway inactivation and inhibited HCC cell proliferation and mobility. In conclusion, TMEM220-AS1 and TMEM220 were expressed at low levels in HCC patients. TMEM220-AS1 inhibited the malignant behavior of HCC cells by enhancing TMEM220 expression and subsequently inactivating the Wnt/beta-catenin pathway.	34659569	RID05394	expression association	prognosis		DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	HAGLR	LDHA	positively-E	ENCORI;Kaplan-Meier Plotter survival analysis;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	5-fluorouracil	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000134333	NA	401022	3939	HOXD-AS1|Mdgt|MIR7704HG	NA	Long noncoding RNA HAGLR sponges miR-338-3p to promote 5-Fu resistance in gastric cancer through targeting the LDHA-glycolysis pathway;Gastric cancer (GC) is one of the most common human malignancies due to its invasiveness and metastasis. 5-Fu is a widely applied chemotherapeutic agent against GC. Although 5-Fu therapy has achieved improvements in GC treatment, a large fraction of patients developed drug resistance which significantly limited its clinical applications. Recent studies revealed the pivotal roles of long noncoding RNAs (lncRNAs) in tumorigenesis and progressions of various tumors, including GC. However, the biological roles and molecular mechanisms of lncRNA HAGLR in GC remain unclear. Here, we report HAGLR was upregulated in both GC tissues and cell lines. In addition, HAGLR was associated with a poorly survival rate of GC patients. Blocking HAGLR inhibited GC cells proliferation and sensitized GC cells to 5-Fu. Bioinformatical analysis and luciferase assay demonstrated that HAGLR sponged microRNA (miR)-338-3p, which functions as a tumor suppressor in GC to downregulate its expressions. Moreover, from the established 5-Fu resistant GC cell line (HGC27 5-Fu R), we detected significantly elevated HAGLR, downregulated miR-338-3p, and glucose metabolism compared with parental HGC27 cells. We identified lactate dehydrogenase-A (LDHA), a glucose metabolism key enzyme, was the direct target of miR-338-3p in GC cells. Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Taken together, this study revealed essential roles and molecular mechanisms for the HAGLR-mediated 5-Fu resistance in GC, contributing to the development of new noncoding RNA-based therapeutic strategies against chemoresistant GC.	34658120	RID05395	ceRNA or sponge	metastasis,chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Ovarian cancer	SNHG20	ROCK1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-148a)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000067900	NA	654434	6093	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	p160ROCK	LncRNA SNHG20 promotes migration and invasion of ovarian cancer via modulating the microRNA-148a/ROCK1 axis.Ovarian cancer (OC) is characterized by early metastasis and poor prognosis, which threatens the health of women worldwide. Small nucleolar RNA host gene 20 (SNHG20), a long noncoding RNA (lncRNA), has been verified to be significantly up-regulated in several tumors, including OC. MicroRNA-148a (miR-148a)/rho-kinase1 (ROCK1) axis plays an important role in the modulation of tumor development. However, whether SNHG20 can regulate OC progression through miR-148a/ROCK1 axis remains unclear. Normal human ovarian epithelial cell line and four OC cell lines were adopted for in vitro experiments. Real-time PCR was performed to assess the levels of SNHG20 and miR-148a. OC cell proliferation, apoptosis, invasion and migration were detected using clone formation, flow cytometry, transwell, and wound healing assays, respectively. Tumor xenograft assay was applied to evaluate the effect of SNHG20 on tumor growth in vivo. Significant higher expression of SNHG20 was observed in OC cell lines. SNHG20 markedly promoted the invasion, migration, proliferation and inhibited the apoptosis of OC cells. SNHG20 enhanced ROCK1 expression by sponging miR-148a, and the direct binding between SNHG20/ROCK1 and miR-148a was identified. SNHG20 promoted invasion and migration of OC via targeting miR-148a/ROCK1 axis. The present research may provide a novel insight for the therapeutic strategies of OC.	34836544	RID05396	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	CRNDE	MCM5	positively-E	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	ceRNA(miR-136-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000100297	NA	643911	4174	CRNDEP|LINC00180|LOC643911	CDC46	Identification of a TGF-beta/SMAD/lnc-UTGF positive feedback loop and its role in hepatoma metastasis.Aberrant activation of the TGF-beta/SMAD signaling pathway is often observed in hepatocellular carcinoma (HCC). Whether lncRNA regulates the TGF-beta/SMAD signaling remains largely unknown. Here, we identified an oncogenic lncRNA that was upregulated in HCC and was transcriptionally induced by TGF-beta (named lnc-UTGF, lncRNA upregulated by TGF-beta). Upon TGF-beta stimulation, SMAD2/3 bound to the lnc-UTGF promoter and activated lnc-UTGF expression. In turn, the TGF-beta/SMAD signaling was augmented by overexpressing lnc-UTGF, but was inhibited by silencing lnc-UTGF. Mechanism investigations revealed that lnc-UTGF interacted with the mRNAs of SMAD2 and SMAD4 via complementary base-pairing, resulting in enhanced stability of SMAD2/4 mRNAs. These data suggest a novel TGF-beta/SMAD/lnc-UTGF positive feedback circuitry. Subsequent gain- and loss-of-function analyses disclosed that lnc-UTGF promoted the migration and invasion of hepatoma cells, and this effect of lnc-UTGF was attenuated by repressing SMAD2/4 expression or by mutating the SMAD2/4-binding sites in lnc-UTGF. Studies using mouse models further confirmed that in vivo metastasis of hepatoma xenografts was inhibited by silencing lnc-UTGF, but was enhanced by ectopic expression of lnc-UTGF. The lnc-UTGF level was positively correlated with the SMAD2/4 levels in xenografts. Consistently, we detected an association of lnc-UTGF upregulation with increase of SMAD2, SMAD4, and their metastasis effector SNAIL1 in human HCC. And high lnc-UTGF level was also significantly associated with enhanced metastasis potential, advanced TNM stages, and worse recurrence-free survival. Conclusion: there exists a lnc-UTGF-mediated positive feedback loop of the TGF-beta signaling and its deregulation promotes hepatoma metastasis. These findings may provide a new therapeutic target for HCC metastasis.	34809738	RID05397	ceRNA or sponge	metastasis,recurrence	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SNHG17	Trim23-PES1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	tumor growth(+);cell metastasis(+)	ceRNA(miR-339-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	NA	NA	388796	NA	NA	NA	SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop.Small nucleolar RNA host gene (SNHG) long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers and involved in tumorigenesis and progression. SNHG17 has been reported as a candidate oncogene in several cancer types, however, its regulatory role in colorectal cancer (CRC) is unclear. SNHG17 expression in multiple CRC cohorts was assessed by RT-qPCR or bioinformatic analyses. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell mobility and invasiveness were assessed by Transwell assays. Tumor xenograft and metastasis models were applied to confirm the effects of SNHG17 on CRC tumorigenesis and metastasis in vivo. Immunohistochemistry staining was used to measure protein expression in cancer tissues. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and dual luciferase assays were used to investigate the molecular mechanism of SNHG17 in CRC. Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop. We identified SNHG17 as an oncogenic lncRNA in CRC and identified abnormal upregulation of SNHG17 as a prognostic risk factor for CRC. Our mechanistic investigations demonstrated, for the first time, that SNHG17 promotes tumor growth and metastasis through two different regulatory mechanisms, SNHG17-Trim23-PES1 axis and SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop, which may be exploited for CRC therapy.	34782005	RID05398	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Colorectal cancer	SNHG18	FOSL2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	tumor growth(+);cell metastasis(+)	ceRNA(miR-339-5p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000250786	GRCh38_5:9546170-9550725	ENSG00000075426	NA	100505806	2355	NA	FLJ23306|FRA2	SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop.Small nucleolar RNA host gene (SNHG) long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers and involved in tumorigenesis and progression. SNHG17 has been reported as a candidate oncogene in several cancer types, however, its regulatory role in colorectal cancer (CRC) is unclear. SNHG17 expression in multiple CRC cohorts was assessed by RT-qPCR or bioinformatic analyses. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell mobility and invasiveness were assessed by Transwell assays. Tumor xenograft and metastasis models were applied to confirm the effects of SNHG17 on CRC tumorigenesis and metastasis in vivo. Immunohistochemistry staining was used to measure protein expression in cancer tissues. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and dual luciferase assays were used to investigate the molecular mechanism of SNHG17 in CRC. Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop. We identified SNHG17 as an oncogenic lncRNA in CRC and identified abnormal upregulation of SNHG17 as a prognostic risk factor for CRC. Our mechanistic investigations demonstrated, for the first time, that SNHG17 promotes tumor growth and metastasis through two different regulatory mechanisms, SNHG17-Trim23-PES1 axis and SNHG17-miR-339-5p-FOSL2-SNHG18 positive feedback loop, which may be exploited for CRC therapy.	34782005	RID05399	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gallbladder cancer	TMPO-AS1	E2F2	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+);cell invasion(+);cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-1179)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000007968	NA	100128191	1870	NA	E2F-2	Long non-coding RNA TMPO-AS1 promotes cell proliferation, migration, invasion and epithelial-to-mesenchymal transition in gallbladder carcinoma by regulating the microRNA-1179/E2F2 axis.Gallbladder carcinoma (GBC), which is a common tumor of the biliary system, poses a serious threat to human life and health. The present study aimed to investigate the molecular mechanism of the long non-coding (lnc)RNA thymopoietin antisense transcript 1 (TMPO-AS1)/microRNA (miRNA/miR)-1179/E2F transcription factor 2 (E2F2) axis in GBC. The viability, proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of GBC cell lines were assessed via the Cell Counting Kit-8, colony formation, Transwell migration and invasion, immunofluorescence and western blot assays. In the present study, lncRNA TMPO-AS1 was significantly upregulated in clinical GBC tissues and cell lines, and was highly expressed in stage III+IV patients with GBC compared with stage I+II patients with GBC. In addition, the overall survival rate of patients with low TMPO-AS1 expression levels was higher than those with high TMPO-AS1 expression levels. Furthermore, TMPO-AS1 knockdown inhibited the viability, proliferation, migration, invasion and EMT of GBC cell lines. In addition, miR-1179 expression was downregulated in clinical GBC tissues and cell lines, and negatively correlated with TMPO-AS1 expression. The results revealed that miR-1179 is a target of TMPO-AS1, which was confirmed via the dual-luciferase reporter assay and RNA pull-down analysis. Overexpression of miR-1179 inhibited the viability, proliferation, migration, invasion and EMT of GBC cell lines. Furthermore, E2F2 was verified as a direct target of miR-1179 by binding to its 3'-untranslated region. E2F2 expression was significantly upregulated in clinical GBC tissues and cell lines, and negatively correlated with miR-1179 expression. Notably, E2F2 knockdown partially hindered the effects of TMPO-AS1/miR-1179 on the proliferation and metastasis of GBC cell lines. Taken together, the results of the present study suggest that TMPO-AS1 potentially plays a tumor-promoting role in the occurrence and development of GBC, which may be achieved by regulating the miR-1179/E2F2 axis.	34777589	RID05400	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Oesophageal squamous cell carcinoma	SNHG6	EZH2	negatively-F		upregulation		NA	NA	tumorigenesis(+)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA SNHG6 promotes oesophageal squamous cell carcinoma by downregulating the miR-101-3p/EZH2 pathway.Long noncoding RNAs (LncRNAs) have been reported to play a vital role in the development of oesophageal squamous cell carcinoma (OSCC). Our previous study revealed that the significant upregulation of the LncRNA small nucleolar RNA host gene 6 (SNHG6) in OSCC promotes OSCC tumourigenesis. However, the mechanisms underlying the dynamics of SNHG6 expression in OSCC have rarely been studied. In this study, we verified the tumour-promoting effect of SNHG6 through sponging miR-101-3p, and their levels were negatively correlated in human samples of OSCC. In addition, miR-101-3p overexpression reversed the effect of SNHG6. Moreover, we confirmed that SNHG6/miR-101-3p affects OSCC by regulating the expression of the enhancer of zeste 2 (EZH2). The effect of EZH2 silencing resembled closely that of SNHG6 knockdown. EZH2 silencing inhibited the expression of protein cyclin D1 and beta-catenin, but in contrast, it enhanced the expression of E-cadherin. These findings demonstrated the oncogenic role of SNHG6, which promotes OSCC progression by regulating the expression of EZH2 through its interaction with miR-101-3p. These findings may help in improving the diagnosis and treatment methods of OSCC.	34766670	RID05401	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	LINC01050	SPZ1	positively-E	Luciferase assay;ChIP;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis	ceRNA(miR-7161-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000271216	GRCh38_13:42810366-42814897	ENSG00000164299	NA	103689845	84654	NA	FLJ25709|NYD-TSP1|PPP1R148	C-Myc-activated long non-coding RNA LINC01050 promotes gastric cancer growth and metastasis by sponging miR-7161-3p to regulate SPZ1 expression.Growing evidence shows that long non-coding RNAs (lncRNAs) play significant roles in cancer development. However, the functions of most lncRNAs in human gastric cancer are still not fully understood. Here, we explored the role of a novel c-Myc-activated lncRNA, LINC01050, in gastric cancer progression. The expression of LINC01050 in the context of gastric cancer was assessed using The Cancer Genome Atlas datasets. Its functions in gastric cancer were investigated through gain- and loss-of-function experiments combined with the Cell Counting Kit-8 assays, colony-forming assays, Transwell assays, flow cytometry, western blot, and xenograft tumor and mouse metastasis models. Potential LINC01050 transcription activators were screened via bioinformatics and validated by chromatin immunoprecipitation and luciferase assays. The interaction between LINC01050 and miR-7161-3p and the targets of miR-7161-3p were predicted by bioinformatics analysis and confirmed by a luciferase assay, RNA immunoprecipitation, RNA pull-down, and rescue experiments. LINC01050 was significantly up-regulated in gastric cancer, and its high expression was positively correlated with a poor prognosis. The transcription factor c-Myc was found to directly bind to the LINC01050 promoter region and activate its transcription. Furthermore, overexpression of LINC01050 was confirmed to promote gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition in vitro and tumor growth in vivo. At the same time, its knockdown inhibited gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition in vitro along with tumor growth and metastasis in vivo. Moreover, mechanistic investigations revealed that LINC01050 functions as a molecular sponge to absorb cytosolic miR-7161-3p, which reduces the miR-7161-3p-mediated translational repression of SPZ1, thus contributing to gastric cancer progression. Taken together, our results identified a novel gastric cancer-associated lncRNA, LINC01050, which is activated by c-Myc. LINC01050 may be considered a potential therapeutic target for gastric cancer.	34749766	RID05402	ceRNA or sponge	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
T-cell acute lymphocytic leukemia	PPM1A-AS	NOTCH4	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000206312	NA	NA	4855	NA	INT3	LncRNA PPM1A-AS Regulate Tumor Development Through Multiple Signal Pathways in T-Cell Acute Lymphoblastic Leukemia.ALL (Acute lymphoblastic leukemia) is the most common pediatric malignancy and T-ALL (T-cell acute lymphoblastic leukemia) comprises about 15% cases. Compared with B-ALL (B-cell acute lymphoblastic leukemia), the prognosis of T-ALL is poorer, the chemotherapy is easier to fail and the relapse rate is higher. Previous studies mainly focused in Notch1-related long non-coding RNAs (lncRNAs) in T-ALL. Here, we intend to investigate lncRNAs involved in T-ALL covering different subtypes. The lncRNA PPM1A-AS was screened out for its significant up-regulation in 10 T-ALL samples of different subtypes than healthy human thymus extracts. Besides, the PPM1A-AS expression levels in 3 T-ALL cell lines are markedly higher than that in CD45 +  T cells of healthy human. We further demonstrate that PPM1A-AS can promote cell proliferation and inhibit cell apoptosis  in vitro  and can influence T-ALL growth  in vivo . Finally, we verified that PPM1A-AS can regulate core proteins, Notch4, STAT3 and Akt, of 3 important signaling pathways related to T-ALL. These results confirm that lncRNA PPM1A-AS can act as an oncogene in T-ALL and maybe a potential clinical target of patients resistant to current chemotherapy or relapsed cases.	34746000	RID05403	expression association	chemoresistance,prognosis		UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
T-cell acute lymphocytic leukemia	PPM1A-AS	STAT3	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	NA	NA	ENSG00000168610	NA	NA	6774	NA	APRF	LncRNA PPM1A-AS Regulate Tumor Development Through Multiple Signal Pathways in T-Cell Acute Lymphoblastic Leukemia.ALL (Acute lymphoblastic leukemia) is the most common pediatric malignancy and T-ALL (T-cell acute lymphoblastic leukemia) comprises about 15% cases. Compared with B-ALL (B-cell acute lymphoblastic leukemia), the prognosis of T-ALL is poorer, the chemotherapy is easier to fail and the relapse rate is higher. Previous studies mainly focused in Notch1-related long non-coding RNAs (lncRNAs) in T-ALL. Here, we intend to investigate lncRNAs involved in T-ALL covering different subtypes. The lncRNA PPM1A-AS was screened out for its significant up-regulation in 10 T-ALL samples of different subtypes than healthy human thymus extracts. Besides, the PPM1A-AS expression levels in 3 T-ALL cell lines are markedly higher than that in CD45 +  T cells of healthy human. We further demonstrate that PPM1A-AS can promote cell proliferation and inhibit cell apoptosis  in vitro  and can influence T-ALL growth  in vivo . Finally, we verified that PPM1A-AS can regulate core proteins, Notch4, STAT3 and Akt, of 3 important signaling pathways related to T-ALL. These results confirm that lncRNA PPM2A-AS can act as an oncogene in T-ALL and maybe a potential clinical target of patients resistant to current chemotherapy or relapsed cases.	34746000	RID05404	expression association	chemoresistance,prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
T-cell acute lymphocytic leukemia	PPM1A-AS	AKT1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000142208	NA	NA	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	LncRNA PPM1A-AS Regulate Tumor Development Through Multiple Signal Pathways in T-Cell Acute Lymphoblastic Leukemia.ALL (Acute lymphoblastic leukemia) is the most common pediatric malignancy and T-ALL (T-cell acute lymphoblastic leukemia) comprises about 15% cases. Compared with B-ALL (B-cell acute lymphoblastic leukemia), the prognosis of T-ALL is poorer, the chemotherapy is easier to fail and the relapse rate is higher. Previous studies mainly focused in Notch1-related long non-coding RNAs (lncRNAs) in T-ALL. Here, we intend to investigate lncRNAs involved in T-ALL covering different subtypes. The lncRNA PPM1A-AS was screened out for its significant up-regulation in 10 T-ALL samples of different subtypes than healthy human thymus extracts. Besides, the PPM1A-AS expression levels in 3 T-ALL cell lines are markedly higher than that in CD45 +  T cells of healthy human. We further demonstrate that PPM1A-AS can promote cell proliferation and inhibit cell apoptosis  in vitro  and can influence T-ALL growth  in vivo . Finally, we verified that PPM1A-AS can regulate core proteins, Notch4, STAT3 and Akt, of 3 important signaling pathways related to T-ALL. These results confirm that lncRNA PPM3A-AS can act as an oncogene in T-ALL and maybe a potential clinical target of patients resistant to current chemotherapy or relapsed cases.	34746000	RID05405	expression association	chemoresistance,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	FOXD3-AS1	CDK6	positively-E	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	ceRNA(miR-135a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000105810	NA	100996301	1021	pasFOXD3	PLSTIRE	lncRNA FOXD3-AS1 promotes the progression of non-small cell lung cancer by regulating the miR-135a-5p/CDK6 axis.Long non-coding RNA (lncRNA) is essential to the development and progression of malignant human cancer. Growing evidence suggests that the lncRNA forkhead box D3 antisense 1 (FOXD3-AS1) is a crucial regulatory effector for multiple cancer types and is closely associated with poor prognosis. However, in most cases, the molecular mechanism underlying the role of FOXD3-AS1 in cancer development has not yet been fully elucidated. The present study focused on non-small cell lung cancer (NSCLC) in order to gain insight into how FOXD3-AS1 drives cancer progression. First, FOXD3-AS1 expression in NSCLC tissue samples was detected using reverse transcription-quantitative (RT-qPCR). Moreover, cell proliferation and apoptosis were determined using Cell Counting Kit-8 assays and flow cytometry, respectively. A luciferase reporter assay was then performed to determine whether there was a direct binding association between FOXD3-AS1 and microRNA (miR)-135a-5p. Lastly, a tumor subcutaneous xenograft model was established to examine the role of FOXD3-AS1 in tumor growth. FOXD3-AS1 was significantly overexpressed in NSCLC tissue samples and cell lines compared with normal tissue samples and cells. FOXD3-AS1 silencing expression significantly inhibited A549 and H1229 cell proliferation while inducing apoptosis compared with sh-NC group. The luciferase reporter assay demonstrated the direct binding interaction between FOXD3-AS1 and miR-135a-5p. Moreover, FOXD3-AS1 silencing led to the upregulation of miR-135a-5p in A549 and H1229 cells compared with sh-NC group. It was also demonstrated that miR-135a-5p could bind to the 3' untranslated region of cyclin-dependent kinase 6 (CDK6) and negatively modulate its transcription. miR-135a-5p knockdown or CDK6 overexpression reversed the inhibition on cell proliferation and apoptosis following FOXD3-AS1 knockdown. Altogether, the present study suggests that FOXD3-AS1 sponges miR-135a-5p to promote cell proliferation and concomitantly inhibit apoptosis by regulating CDK6 expression in NSCLC cells.	34733371	RID05406	ceRNA or sponge	prognosis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Prostate cancer	AY927529	CXCL14	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000145824	NA	NA	9547	NA	BMAC|bolekine|BRAK|Kec|KS1|MIP-2g|NJAC|SCYB14	Exosomal lncAY927529 enhances prostate cancer cell proliferation and invasion through regulating bone microenvironment.Exosomes mediate the interaction between cancer cells and their microenvironment, and play a key role in tumor development. Although exosomes can package lncRNAs to mediate extracellular communication, the role of exosomal lncRNA AY927529 in prostate cancer (PCa) remains unclear. Exosomes were extracted from normal human prostatic epithelial cell lines (BPH-1 and RWPE-1) and PCa cell lines (VCaP and LNCaP, DU145, PC3) by ultrahigh speed centrifugation. Results of western blot indicated that Alix, HSC70 and TSGl01 protein levels were upregulated in exosomes derived from PCa cells. LncAY927529 level was upregulated in PCa cells and exosomes derived from PCa patient serum and human PCa cells. CCK-8, Transwell and Flow cytometry assays demonstrated that bone marrow stromal cell line (ST2) conditioned medium (ST2-CM), treated with exosomes derived from PCa cells with high lncAY927529 level, promoted proliferation and invasion of PC3 and DU145 cells, and inhibited cell apoptosis. RT-qPCR assay indicated that lncAY927529 level was downregulated in PC3 and DU145 cells, exosomes derived from PCa cells (PCa-Exo) and ST2-CM treated with PCa-Exo with low expression of lncAY927529, and overexpression of lncAY927529 had the opposite results. In addition, western blot assay showed that the autophagy related protein LC3II level was increased in ST2 cells treated with exosomes derived from DU145 cells with high expression of lncAY927529, and LC3I protein level was decreased. CXCL14 acted as a RNA-binding protein of lncAY927529, and exosome-mediated lncAY927529 positively regulated CXCL14 levels in ST2 cells. In general, exosome-mediated lncAY927529 could promote PCa cell proliferation and invasion by regulating bone microenvironment, suggesting that exosomal lncAY927529 may be a potential molecular diagnostic marker of PCa.	34724861	RID05407	expression association	NA		UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE74639,GSE60407,GSE38495,GSE55807)
Diabetic retinopathy	THRIL	ATG4D	positively-E	luciferase activity assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell proliferation(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Nervous system disease	Retinal disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000130734	NA	102659353	84971	BRI3BP-AS1|Linc1992|TCONS_00020260	APG4-D|APG4D|AUTL4	LncRNA THRIL promotes high glucose-induced proliferation and migration of human retina microvascular endothelial cells through enhancing autophagy.Diabetes retinopathy (DR) is associated with retinal microvascular system injury induced by high glucose (HG). This study aims to explore the role and mechanism of long non-coding RNA THRIL in regulating cell proliferation and migration of human retina microvascular endothelial cells (hRMECs) under HG condition. The gene and protein expression were detetced by RT-PCRand western blot, respectively. Cell proliferation and migration of hRMECs were examined using MTT assay and Transwell assay, respectively. The interaction between miR-125b-5p and THRIL or autophagy-related gene 4D (ATG4D) was analyzed using luciferase activity assay. THRIL expression was induced by HG in hRMECs. THRIL overexpression enhanced the proliferation and migration of hRMECs induced by HG, whereas THRIL silencing yielded the opposite results. Furthermore, THRIL overexpression induced autophagy activation, and inhibition of autophagy by 3-methyladenine abrogated the promotory effects of THRIL overexpression on cell proliferation and migration of hRMECs. Mechanismly, THRIL inhibited miR-125b-5p to upregulate the expression of ATG4D (an important autophagy-related gene), thereby promoting autophagy. Moreover, miR-125b-5p overexpression or ATG4D silencing alone abolished the promoting effects of THRIL overexpression on HG-induced autophagy, proliferation and migration of hRMECs. THRIL promotes HG-induced cell proliferation and migration of hRMECs through activation of autophagy via the miR-125b-5p/ATG4D axis. THRIL may serve as a potential therapeutic target for DR.	34718852	RID05408	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	LINC01094	CHSY1	positively-E		upregulation		NA	NA	cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-224-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251442	GRCh38_4:78638780-78683185	ENSG00000131873	NA	100505702	22856	CTEPHA1	CSS1|KIAA0990	A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties.Cancer stem cells (CSCs) are considered as the major cause to tumor initiation, recurrence, metastasis, and drug resistance, driving poor clinical outcomes in patients. Long noncoding RNAs (lncRNAs) have emerged as crucial regulators in cancer development and progression. However, limited lncRNAs involved in CSCs have been reported. The novel lncROPM (a regulator of phospholipid metabolism) in breast CSCs (BCSCs) was identified by microarray and validated by qRT-PCRin BCSCs from breast cancer cells and tissues. The clinical significance of lncROPM was evaluated in two breast cancer cohorts and TANRIC database (TCGA-BRCA, RNAseq data). Gain- and loss-of-function assays were performed to examine the role of lncROPM on BCSCs both in vitro and in vivo. The regulatory mechanism of lncROPM was investigated by bioinformatics, RNA FISH, RNA pull-down, luciferase reporter assay, and actinomycin D treatment. PLA2G16-mediated phospholipid metabolism was determined by UHPLC-QTOFMS system. Cells' chemosensitivity was assessed by CCK8 assay. LncROPM is highly expressed in BCSCs. The enhanced lncROPM exists in clinic breast tumors and other solid tumors and positively correlates with malignant grade/stage and poor prognosis in breast cancer patients. Gain- and loss-of-function studies show that lncROPM is required for the maintenance of BCSCs properties both in vitro and in vivo. Mechanistically, lncROPM regulates PLA2G16 expression by directly binding to 3'-UTR of PLA2G16 to increase the mRNA stability. The increased PLA2G16 significantly promotes phospholipid metabolism and the production of free fatty acid, especially arachidonic acid in BCSCs, thereby activating PI3K/AKT, Wnt/beta-catenin, and Hippo/YAP signaling, thus eventually involving in the maintenance of BCSCs stemness. Importantly, lncROPM and PLA2G16 notably contribute to BCSCs chemo-resistance. Administration of BCSCs using clinic therapeutic drugs such as doxorubicin, cisplatin, or tamoxifen combined with Giripladib (an inhibitor of cytoplasmic phospholipase A2) can efficiently eliminate BCSCs and tumorigenesis. Our study highlights that lncROPM and its target PLA2G16 play crucial roles in sustaining BCSC properties and may serve as a biomarker for BCSCs or other cancer stem cells. Targeting lncROPM-PLA2G16 signaling axis may be a novel therapeutic strategy for patients with breast cancer.	34716872	RID05409	ceRNA or sponge	metastasis,recurrence,chemoresistance,prognosis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Oral squamous cell carcinoma	HOXA-AS3	LPCAT1	positively-E	RIP;Luciferase Reporter Assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000254369	GRCh38_7:27129977-27155928	ENSG00000153395	NA	100133311	79888	HOXA6as	AGPAT10|AGPAT9|AYTL2|FLJ12443	Long non-coding RNA HOXA-AS3 promotes cell proliferation of oral squamous cell carcinoma through sponging microRNA miR-218-5p.Increasing evidence demonstrated long non-coding RNAs (lncRNAs) play important roles in the occurrence and development of oral squamous cell carcinoma (OSCC). This study aimed to explore the role and molecular mechanism of lncRNA HOXA-AS3 in the progression of OSCC. Here, we found that  t he expression of lncRNA HOXA-AS3 was upregulated in OSCC tissues and cell lines compared with the para-cancerous tissues and normal human oral keratinocyte (NHOK), respectively. Inhibition of HOXA-AS3 significantly inhibited the proliferation and colony formation of OSCC cells. Further, the luciferase reporter assay showed that HOXA-AS3 was directly bound to miR-218-5p. Moreover, the expression of miR-218-5p was negatively regulated by HOXA-AS3, and miR-218-5p could inhibit the expression of collagen type I alpha1 (COL1A1) and lysophosphatidylcholine acyltransferase 1 (LPCAT1). In addition, silencing miR-218-5p reversed the inhibitory effect of HOXA-AS3 knockdown on the proliferative potential of OSCC cells. In summary, our study illustrated that HOXA-AS3 promoted cancer cell proliferation in OSCC, possibly by sponging miR-218-5p for the first time, which provides a new target or a potential diagnostic biomarker for OSCC.	34698001	RID05410	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	SNHG17	NETO2	positively-E	luciferase activity assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(-);cell proliferation(-)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000171208	NA	388796	81831	NA	FLJ10430|NEOT2	Long non-coding RNA SNHG17 promotes lung adenocarcinoma progression by targeting the microRNA-193a-5p/NETO2 axis.Long non-coding RNAs (lncRNAs) play vital roles in human cancers. It has been reported that lncRNA SNHG17 expression is dysregulated in different types of cancer and involved in cancer progression. However, the role of SNHG17 in lung adenocarcinoma (LUAD) remains unclear. The present study aimed to investigate the role of SNHG17 in LUAD. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect SNHG17 expression in LUAD tissues and cells. The effects of SNHG17 on cancer cell migration, invasion, proliferation and epithelial-to-mesenchymal transition (EMT) were assessed via Transwell, MTT and western blot assays, respectively. The interactions between SNHG17 and microRNA (miRNA/miR)-193a-5p, miR-193a-5p and neuropilin and tolloid-like 2 (NETO2) were assessed via the dual-luciferase reporter assay. NETO2 expression and its potential role in LUAD were analyzed via RT-qPCR analysis and the UALCAN database. The results demonstrated that SNHG17 expression was significantly upregulated in LUAD tissues and cells, and high SNHG17 expression was associated with tumor-node-metastasis stage and poor prognosis of patients with LUAD. SNHG17 knockdown inhibited cell migration, invasion, proliferation and the EMT process. In addition, the results revealed that SNHG17 functions as a competing endogenous RNA of miR-193a-5p. The results of the dual-luciferase reporter assay confirmed that miR-193a-5p can directly target SNHG17. NETO2 was also predicted as a target protein of miR-193a-5p, which was confirmed via the dual-luciferase reporter assay. The roles of NETO2 knockdown in cancer cells were rescued following transfection with miR-193a-5p inhibitor or overexpression of SNHG17. Notably, high NETO2 expression was associated with poor prognosis of patients with LUAD. Bioinformatics analysis demonstrated that the promoter methylation level of NETO2 decreased in LUAD. Taken together, the results of the present study suggest that SNHG17 expression is upregulated in LUAD tissues and cells, and SNHG17 exerts tumor promoting effect by targeting the miR-193a-5p/NETO2 axis.	34671432	RID05411	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE111842,GSE67939)
Cancer	SNHG17	LRPPRC	positively-E	RNA pull-down assay;RIP; ATGpr;GEPIA;TANRIC;UCSC	upregulation		NA	NA	cell cycle phase transition (+);cell proliferation(+);cell growth(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000138095	NA	388796	10128	NA	GP130|LRP130|LSFC	LncRNA SNHG17 interacts with LRPPRC to stabilize c-Myc protein and promote G1/S transition and cell proliferation.Oncogenic c-Myc is a master regulator of G1/S transition. Long non-coding RNAs (lncRNAs) emerge as new regulators of various cell activities. Here, we found that lncRNA SnoRNA Host Gene 17 (SNHG17) was elevated at the early G1-phase of cell cycle. Both gain- and loss-of function studies disclosed that SNHG17 increased c-Myc protein level, accelerated G1/S transition and cell proliferation, and consequently promoted tumor cell growth in vitro and in vivo. Mechanistically, the 1-150-nt of SNHG17 physically interacted with the 1035-1369-aa of leucine rich pentatricopeptide repeat containing (LRPPRC) protein, and disrupting this interaction abrogated the promoting role of SNHG17 in c-Myc expression, G1/S transition, and cell proliferation. The effect of SNHG17 in stimulating cell proliferation was attenuated by silencing c-Myc or LRPPRC. Furthermore, silencing SNHG17 or LRPPRC increased the level of ubiquitylated c-Myc and reduced the stability of c-Myc protein. Analysis of human hepatocellular carcinoma (HCC) tissues revealed that SNHG17, LRPPRC, and c-Myc were significantly upregulated in HCC, and they showed a positive correlation with each other. High level of SNHG17 or LRPPRC was associated with worse survival of HCC patients. These data suggest that SNHG17 may inhibit c-Myc ubiquitination and thus enhance c-Myc level and facilitate proliferation by interacting with LRPPRC. Our findings identify a novel SNHG17-LRPPRC-c-Myc regulatory axis and elucidate its roles in G1/S transition and tumor growth, which may provide potential targets for cancer therapy.	34671012	RID05412	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Cancer	SNHG18	MYC	positively-E	RNA pull-down assay;RIP; ATGpr;GEPIA;TANRIC;UCSC	upregulation		NA	NA	cell cycle phase transition (+);cell proliferation(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000250786	GRCh38_5:9546170-9550725	ENSG00000136997	NA	100505806	4609	NA	bHLHe39|c-Myc|MYCC	LncRNA SNHG17 interacts with LRPPRC to stabilize c-Myc protein and promote G1/S transition and cell proliferation.Oncogenic c-Myc is a master regulator of G1/S transition. Long non-coding RNAs (lncRNAs) emerge as new regulators of various cell activities. Here, we found that lncRNA SnoRNA Host Gene 17 (SNHG17) was elevated at the early G1-phase of cell cycle. Both gain- and loss-of function studies disclosed that SNHG17 increased c-Myc protein level, accelerated G1/S transition and cell proliferation, and consequently promoted tumor cell growth in vitro and in vivo. Mechanistically, the 1-150-nt of SNHG17 physically interacted with the 1035-1369-aa of leucine rich pentatricopeptide repeat containing (LRPPRC) protein, and disrupting this interaction abrogated the promoting role of SNHG17 in c-Myc expression, G1/S transition, and cell proliferation. The effect of SNHG17 in stimulating cell proliferation was attenuated by silencing c-Myc or LRPPRC. Furthermore, silencing SNHG17 or LRPPRC increased the level of ubiquitylated c-Myc and reduced the stability of c-Myc protein. Analysis of human hepatocellular carcinoma (HCC) tissues revealed that SNHG17, LRPPRC, and c-Myc were significantly upregulated in HCC, and they showed a positive correlation with each other. High level of SNHG17 or LRPPRC was associated with worse survival of HCC patients. These data suggest that SNHG17 may inhibit c-Myc ubiquitination and thus enhance c-Myc level and facilitate proliferation by interacting with LRPPRC. Our findings identify a novel SNHG17-LRPPRC-c-Myc regulatory axis and elucidate its roles in G2/S transition and tumor growth, which may provide potential targets for cancer therapy.	34671012	RID05413	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	LIFR-AS1	VEGFA	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000112715	NA	100506495	7422	NA	VEGF|VEGF-A|VPF	M6A-mediated up-regulation of LncRNA LIFR-AS1 enhances the progression of pancreatic cancer via miRNA-150-5p/ VEGFA/Akt signaling.N 6 -methyladenosine (m 6 A) modification, the most abundant internal methylation of eukaryotic RNA transcripts, is critically implicated in RNA processing. There is extensive evidence indicating that long non-coding RNAs (lncRNAs) serve as key regulators of oncogenesis and tumor progression in humans. Through prior study has assessed that LIFR-AS1 plays a key role in various kinds of malignant tumors. However, the exact role of m 6 A induced LIFR-AS1 in pancreatic cancer (PC) and its potential molecular mechanisms remain largely unknown. In this study, we determined that PC cell lines and tumors exhibit increased LIFR-AS1 expression that correlates with larger tumor size, lymph node metastasis, and more advanced TNM stage. Functionally, loss-of-function studies indicated that LIFR-AS1 knockdown decreased the proliferation, migration, and invasion of PC cells in vitro. Mechanistically, we found that METTL3 induced m 6 A hyper-methylation on the 3' UTR of LIFR-AS1 to enhance its mRNA stability and LIFR-AS1 could directly interact with miR-150-5p, thereby indirectly up-regulating VEGFA expressions within cells. Through rescue experiments, we were able to confirm that the unfavorable impact of LIFR-AS1 knockdown on VEGFA /PI3K/Akt Signaling could be reversed via the inhibition of miR-150-5p expression. Together, these findings indicate that a noval m6A-LIFR-AS1 axis promotes PC progression at least in part via regulation of the miR-150-5p/VEGFA axis, indicating that this regulatory axis may be a viable clinical target for the treatment of PC.	34658294	RID05414	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	LINC00839	miR-3666	positively-E	luciferase activity assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(-);cell proliferation(-);cell invasion(-)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000185904	GRCh38_10:42475480-42495337	NA	NA	84856	NA	NA	NA	[Effects of LINC00839 targeting miR-3666 on proliferation, migration and invasion of hepatocellular carcinoma cells].Objective:  To investigate the effects of lncRNA LINC00839 on the proliferation, migration and invasion of hepatocellular carcinoma cells and its mechanism.  Methods:  Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of LINC00839 and miR-3666 in hepatocellular carcinoma tissues and adjacent tissues. Pearson correlation was used to analyze the correlation between LINC00839 and miR-3666 expression in liver cancer tissues. Hepatocellular carcinoma cells MHCC97H were cultured in vitro and divided into si-NC group, si-LINC00839 group, miR-NC group, miR-3666 group, si-LINC00839+ anti-miR-NC group, and si-LINC00839+ anti-miR-3666 group. Methylthiazoletrazolium (MTT) method and clone formation experiment were used to detect cell proliferation. Transwell array was used to detect the cell migration and invasion. western blot was used to detect the protein expressions of p21, E-cadherin and MMP-2. The double luciferase reporter gene experiment was used to verify the regulatory relationship between LINC00839 and miR-3666.  Results:  Compared with adjacent tissues, the expression level of LINC00839 in hepatocellular carcinoma tissues increased (2.82 0.27 vs. 0.96 0.10,  P <0.001), but the expression level of miR-3666 decreased (0.23 0.02 vs. 1.01 0.10,  P <0.001). The expression levels of LINC00839 and miR-3666 in liver cancer tissue were negatively correlated (r=-0.658,  P <0.001). The survival rate of MHCC97H cells in the si-LINC00839 group [(53.91 5.41)% vs. (100.53 10.22)%], the number of clones formed (92.0 8.0 vs. 164.0 14.3), the number of migration (131.0 12.7 vs. 247.0 22.4), the number of invasion (66.0 6.4 vs. 120.0 11.6) and the protein level of MMP-2 (0.20 0.02 vs. 0.67 0.06) were lower than those in the si-NC group ( P <0.001). However, the protein levels of p21 (0.76 0.07 vs. 0.25 0.02) and E-cadherin (0.78 0.08 vs. 0.14 0.01) were higher than those in the si-NC group ( P <0.001). LINC00839 targeted and negatively regulated the expression of miR-3666. The survival rate of MHCC97-H cells in the miR-3666 group [(47.93 4.86)% vs. (100.11 10.21)%], the number of clone formation (78.0 7.7 vs. 166.0 15.9), the number of migration (117.0 12.1 vs. 250.0 25.0), the number of invasion (57.0 5.7 vs. 121.0 12.3) and the protein level of MMP-2 (0.16 0.01 vs. 0.69 0.07) were lower than those in the miR-NC group (all  P <0.001). However, the protein levels of p21 (0.83 0.08 vs. 0.24 0.02) and E-cadherin (0.87 0.09 vs. 0.13 0.01)were higher than those in the miR-NC group (all  P <0.001). The survival rate of MHCC97-H cells in the si-LINC00839+ anti-miR-3666 group [(89.94 9.05)% vs. (54.12 5.39)%], the number of clones (143.0 13.8 vs. 94.0 9.4), the number of migration (208.0 19.8 vs. 129.0 12.6), the number of invasion (108.0 10.1 vs. 65.0 6.4) and the protein level of MMP-2 (0.31 0.03 vs 0.66 0.06) were higher than those in the si-LINC00839+ anti-miR-NC group ( P <0.001). However, the protein levels of p21 (0.31 0.03 vs. 0.74 0.07) and E-cadherin (0.28 0.03 vs. 0.80 0.08) were lower than those int the si-LINC00839+ anti-miR-NC group ( P <0.001).  Conclusion:  Inhibition of LINC00839 expression may inhibit the proliferation, migration and invasion of hepatocellular carcinoma cells by targeting up-regulation of miR-3666 expression.	34794216	RID05415	expression association	NA	UP(SKCM);DATA(GSE38495)	
Liver disease	MEG3	PPARG	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-145)	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Liver disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000132170	NA	55384	5468	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARG5|PPARgamma	lncRNA MEG3 modulates hepatic stellate cell activation by sponging miR-145 to regulate PPAR-Gamma is important to determine the mechanism of liver fibrosis for targeted therapy and the development of targeted therapies for liver fibrosis may offer promise for patients with liver disease. Long non-coding RNAs (lncRNAs) serve a role in hepatic fibrosis. The lncRNA maternally expressed gene 3 (MEG3) has been confirmed to inhibit liver fibrosis. The present study investigated the role of the MEG3 in healthy patients and patients with liver fibrosis. The expression levels of MEG3 and microRNA (miR)-145 in the serum of healthy volunteers and patients with liver fibrosis and in LX-2 cells were detected using reverse transcription-quantitative PCR. A dual-luciferase reporter assay was used to determine the targeting relationship between MEG3 and miR-145, and the targeting relationship between miR-145 and peroxisome proliferator-activated receptor Gamma (PPAR-Gamma). The protein expression levels of PPAR-Gamma, alpha-smooth muscle actin (alpha-SMA) and collagen I (COL1A1) were detected using western blot. The expression levels of alpha-SMA and COL1A1 were also determined using immunofluorescence. Finally, a Cell Counting Kit-8 assay was performed to assess the proliferative ability of LX-2 cells. A significantly reduced MEG3 expression level was demonstrated in serum from patients with liver fibrosis compared with serum from healthy controls. TGF-beta1 induced a significantly decreased MEG3 expression level in LX-2 human hepatic stellate cells in vitro. The TGF-beta1-induced increases in cell proliferation and alpha-SMA and COL1A1 protein expression levels were reversed following MEG3 overexpression. The results also demonstrated that MEG3 sponged miR-145 and competed endogenously with miR-145 to regulate PPAR-Gamma. In summary, the present study identified MEG3 as an anti-fibrotic lncRNA and provided new information regarding the role of MEG3 in liver fibrosis. MEG3 may therefore be a potential target in the treatment of liver fibrosis.	34738631	RID05416	ceRNA or sponge	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Hemangioma	HNF1A-AS1	IL6	positively-E	luciferase activity assay	upregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000136244	NA	283460	3569	C12orf27|FLJ38690|HAS1|NCRNA00262	BSF2|HGF|HSF|IFNB2|IL-6	[HNF1A-AS1 inhibits proliferation, migration and invasion of IL-6-induced hemangioma endothelial cells by targeting miR-363-3p].To explore the effect of HNF1A-AS1 on the proliferation, migration and invasion of IL-6-induced hemangioendothelial cells (HemEC) and possible mechanism. RT-qPCR was used to detect the expression level of HNF1A-AS1 and miR-363-3p in the tumor tissue and adjacent normal skin tissue from 35 patients with hemangioma. Pearson correlation was used to analyze the correlation between the expression of HNF1A-AS1 and miR-363-3p in tumor tissues. HemEC were isolated and cultured in vitro.Dual luciferase reporter gene experiment was used to study the regulatory effect between HNF1A-AS1 and miR-363-3p. IL-6 was added to HemEC transfected with si-NC, si-HNF1A-AS1, si-HNF1A-AS1 and anti-miR-NC, or si-HNF1A-AS1 and anti-miR-363-3p, respectively. CCK-8 method and clone formation experiment were used to detect cell proliferation in each group. Transwell method was used to detect cell migration and invasion in each group. western blot was used to detect the expression of Ki67, MMP-2 and MMP-9 proteins in each group. Compared with normal skin tissues, the expression of IL-6 mRNA in hemangioma tissues was increased (P<0.05), and the expression of IL-6 mRNA in the proliferative phase was lower than that in the degenerative phase (P<0.05). Expression of HNF1A-AS1 in hemangioma tissue was increased (P<0.05), while that of miR-363-3p was decreased (P<0.05), and the two were negatively correlated (r=-0.758, P<0.05). HNF1A-AS1 down-regulated the expression of miR-363-3p in HemEC.IL-6 promoted the expression of HNF1A-AS1, OD value, number of colonies, number of migration and invasion of HemEC cells, and the expression of Ki67, MMP-2 and MMP-9proteins (P<0.05), while reduced the expression of miR-363-3p (P<0.05). Down-regulating si-HNF1A-AS1 reduced the IL-6-induced HemEC cell OD value, colony numbers, migration and invasion and the expression of Ki67, MMP-2 and MMP-9 proteins (P<0.05). Down-regulating miR-363-3p attenuated the inhibitory effect of down-regulating si-HNF1A-AS1 on the proliferation, migration and invasion of HemEC cells induced by IL-6 (P<0.05). Expression of HNF1A-AS1 is increased in hemangioma tissues. Down-regulating HNF1A-AS1 may inhibit proliferation, migration and invasion of IL-6-induced hemangioma endothelial cells by targeted up-regulation of miR-363-3p.	34729750	RID05417	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Colon adenocarcinoma	KCNQ1OT1	MFAP2	positively-E		upregulation		NA	NA	apoptosis process(+);cell migration(-);cell proliferation(-)	ceRNA(miR-423-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000117122	NA	10984	4237	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	MAGP|MAGP-1	Long non-coding RNA-KCNQ1OT1 mediates miR-423-5p/microfibril-associated protein 2 axis in colon adenocarcinoma.Long non-coding RNAs (lncRNAs) function as competing endogenous RNAs (ceRNAs) that contribute to carcinogenesis. Herein, we plan to explore whether lncRNA KCNQ1OT1 modulated miR-423-5p/microfibril-associated protein 2 (MFAP2) signaling axis is implicated in the progression of human colon adenocarcinoma. Clinical specimens were collected for histologic examination and gene expression analysis. In vitro experimental measurements, including CCK8, transwell and TUNEL staining, were performed to evaluate cell proliferation, migration and apoptosis. up-regulation of KCNQ1OT1 and MFAP2 and down-regulation of miR-423-5p in COAD tissues were substantiated by The Cancer Genome Atlas (TCGA) database and our clinical specimens. In vitro experimental measurements exhibited that knockdown of KCNQ1OT1 facilitated miR-423-5p expression and inhibited MFAP2 expression, simultaneously. Transfection of si-KCNQ1OT1, miR-423-5p mimics or si-MFAP2 had the ability to repress malignant phenotypes of COAD cells. Intriguingly, overexpression of MFAP2 restrained si-KCNQ1OT1- or miR-423-5p mimics-induced the inhibition of cell proliferation and migration and elevation of the apoptotic proportion of COAD cells. KCNQ1OT1 serves as a molecular sponge of miR-423-5p to accelerate the expression of MFAP2 that may be involved in the development of COAD. Our findings present a novel signaling axis KCNQ1OT1/miR-423-5p/MFAP2, which provides a theoretical basis and therapeutic target for the treatment of COAD.	34704601	RID05418	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	HOXA-AS3	SPNS2	negatively-E	luciferase activity assay	downregulation		NA	NA	cell cycle(-);cell proliferation(-);apoptosis process(+)	ceRNA(miR-4319)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000254369	GRCh38_7:27129977-27155928	ENSG00000183018	NA	100133311	124976	HOXA6as	SLC63A2	Long non-coding RNA HOXA-AS3 facilitates the malignancy in colorectal cancer by miR-4319/SPNS2 axis.Growing evidence has shown the oncogenic role of long non-coding RNA HOXA-AS3 in the progression of several types of cancers, while the effect of HOXA-AS3 on colorectal cancer (CRC) remains unclear. In this study, HOXA-AS3 was significantly over-expressed in CRC clinical samples and human CRC cell lines (SW480, SW620, HCT116, COLO205, and LOVO). HOXA-AS3 knockdown was further achieved by specific siRNAs in COLO205 and LOVO cell lines. The depletion of HOXA-AS3 remarkably inhibited cell proliferation, induced cell cycle arrest, and promoted cell apoptosis in CRC cell lines. Additionally, HOXA-AS3 knockdown was determined to facilitate miR-4319 expression and reduce expression level of sphingolipid transporter 2 (SPNS2) in CRC cell lines. The dual-luciferase reporter assay suggested that HOXA-AS3 acted as a sponge of miR-4319, and miR-4319 further directly targeted SPNS2 for expression regulation. Besides, HOXA-AS3 was determined to mediate CRC cell proliferation and apoptosis via miR-4319/SPNS2 axis. Moreover, tumorigenesis experiment validated that HOXA-AS3 promoted CRC progression in vivo by regulating miR-4319, SPNS2, and protein kinase B (AKT) signaling. In summary, this study reveals the novel role of HOXA-AS3 in pathogenesis of CRC and provides a candidate for CRC therapeutic target.	34671931	RID05419	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE86978)
Gastric cancer	GRIK1-AS1	IFIT2	positively-E	luciferase activity assay;western blot;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell invasion(-);cell proliferation(-)	ceRNA(miR-375)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000174680	GRCh38_21:29748175-29764002	ENSG00000119922	NA	642976	3433	C21orf9|GRIK1-AS|GRIK1AS|NCRNA00110	cig42|G10P2|GARG-39|IFI-54|IFI54|ISG-54|ISG-54K	Long Non-Coding RNA GRIK1-AS1 Inhibits the Proliferation and Invasion of Gastric Cancer Cells by Regulating the miR-375/IFIT2 Axis.Long non-coding RNAs (lncRNAs) play important roles in various biological processes and human diseases, including cancer. In this study, we demonstrated a regulatory relationship between lncRNA GRIK1-AS1 and miR-375/IFIT2 axis in gastric cancer. Our results show a decreased expression of GRIK1-AS1 in gastric cancer tissues compared to adjacent normal gastric tissues. Gastric cell lines also have reduced levels of GRIK1-AS1 compared to gastric epithelial cell line GES-1. Ectopic expression of GRIK1-AS1 in gastric cancer cell lines significantly inhibits cellular viability, migration, and invasion. RNA-pull down and the luciferase activity assays show that GRIK1-AS1 mainly interacts specifically with miR-375. We further demonstrate a negatively regulatory relationship between lncRNA GRIK1-AS1 and miR-375. We discovered that IFIT2 was one of the direct key downstream target genes of miR-375, and established the important role of the GRIK1-AS1/miR-375/IFIT2 axis in the progression of gastric cancer. Taken together, our results revealed a novel mechanism of GRIK1-AS1 as a sponge to miR-375 that impacts gastric cancer progression  via  modulating target mRNA IFIT2 translation, and as a result, opens a new strategy to future GRIK1-AS1 based therapeutic development.	34660323	RID05420	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Malignant glioma	PCAT1	miR-129-5p	negatively-E	shRNA;RT-qPCR	upregulation	RT-qPCR;microarray	NA	NA	cell proliferation(+);radioresistance(+);DNA damage(+);apoptosis process(+)	NA	association	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	Knockdown of long non-coding RNA PCAT1 in glioma stem cells promotes radiation sensitivity.microarray was carried out to detect that expressed PCAT1, and it was testified by RT-qPCR. PCAT1 had higher expression in GSCs. PCAT1 knockdown restrained the sphere-formation ability, increased the apoptosis rate and DNA damage under the treatment of radiation. Moreover, knockdown of PCAT1 inhibited the cell proliferation. In addition, silencing PCAT1 could increase the expression of miR-129-5p and decrease the expression of HMGB1. PCAT1 was overexpressed in GSCs and played a facilitating role in radiation resistance.	30564876	RID05421	expression association	NA	UP(LIHC);DATA(GSE117623)	
Malignant glioma	PCAT1	HMGB1	positively-E	shRNA;RT-qPCR	upregulation	RT-qPCR;microarray	NA	NA	cell proliferation(+);radioresistance(+);DNA damage(+);apoptosis process(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000189403	NA	100750225	3146	PCA1|PCAT-1|PiHL	DKFZp686A04236|HMG1|HMG3|SBP-1	Knockdown of long non-coding RNA PCAT1 in glioma stem cells promotes radiation sensitivity.microarray was carried out to detect that expressed PCAT1, and it was testified by RT-qPCR. PCAT1 had higher expression in GSCs. PCAT1 knockdown restrained the sphere-formation ability, increased the apoptosis rate and DNA damage under the treatment of radiation. Moreover, knockdown of PCAT1 inhibited the cell proliferation. In addition, silencing PCAT1 could increase the expression of miR-129-5p and decrease the expression of HMGB1. PCAT1 was overexpressed in GSCs and played a facilitating role in radiation resistance.	30564876	RID05422	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Gastric cancer	XLOC_006753	Caspase9	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+);apoptosis process(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 was highly expressed in GC patients and MDR GC cell lines (SGC-7901/5-FU and SGC-7901/DDP cell lines), and its high expression was positively associated with metastasis, TNM stage, tumor size, and poor survival in GC patients. Next, we used immunoblotting analysis to monitor expression changes in apoptosis-associated proteins in SGC-7901/5-FU and SGC-7901/DDP cells with ablation of XLOC_006753. When compared with control cells, caspase9 protein levels were increased (Fig.-5E). These results revealed that XLOC_006753 overexpression promoted apoptosis in SGC-7901/5-FU and SGC-7901/DDP cells by inhibiting expression of caspase 9.	30481766	RID05423	expression association	metastasis,chemoresistance		
Gastric cancer	XLOC_006753	EIF4EBP1	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000187840	NA	NA	1978	NA	4E-BP1|PHAS-I	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05424	expression association	chemoresistance		DOWN(LIHC,PRAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Gastric cancer	XLOC_006753	PIK3CA	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000121879	NA	NA	5290	NA	PI3K	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05425	expression association	chemoresistance		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Gastric cancer	XLOC_006753	AKT1	positively-F	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000142208	NA	NA	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05426	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	XLOC_006753	MTOR	positively-F	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000198793	NA	NA	2475	NA	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05427	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Gastric cancer	XLOC_006753	RPS6KB1	positively-F	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000108443	NA	NA	6198	NA	p70(S6K)-alpha|PS6K|S6K|S6K1|STK14A	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05428	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Gastric cancer	XLOC_006753	RPS6	positively-F	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000137154	NA	NA	6194	NA	S6	Long Non-Coding RNA XLOC_006753 Promotes the Development of Multidrug Resistance in Gastric Cancer Cells Through the PI3K/AKT/mTOR Signaling Pathway. XLOC_006753 promotes MDR by activation of the PI3K/AKT/mTOR signaling pathway. the expression levels of PI3K, p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), P70 S6 kinase/p-P70 S6 kinase (Thr389), p-S6 (Ser235/236), and p-4E-BP1 (Thr37/46) were reduced by siRNA-XLOC_006753 transfection.XLOC_006753 knockdown also promoted apoptosis. Furthermore, western blots showed that XLOC_006753 knockdown decreased some markers of MDR, G1/S transition, and EMT expression, while increasing caspase9 expression and inhibiting the PI3K/AKT/mTOR signaling pathway in SGC-7901/5-FU and SGC-7901/DDP cells.	30481766	RID05429	expression association	chemoresistance		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE67939,GSE75367,GSE86978)
Osteosarcoma	B4GALT1-AS1	ELAVL1	positively-F	RIP;luciferase reporter assay;knockdown	upregulation	RT-qPCR	NA	NA	cell stemness(+);cell migration(+);chemoresistance(+)	interact with protein	regulation	RNA-protein	Adriamycin	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233554	GRCh38_9:33166948-33182865	ENSG00000066044	NA	101929639	1994	NA	Hua|HUR|MelG	LncRNA B4GALT1-AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity.LncRNA B4GALT1-AS1 expression was significantly increased in OS tissues and cells spheres. Knockdown of B4GALT1-AS1 inhibited OS cells proliferation, migration, stemness and chemotherapeutic sensitivity.RNA immunoprecipitation (RIP) and Luciferase reporter assays were performed to determine the binding site of RNA-binding protein HuR on B4GALT1-AS1 and transcriptional factor YAP. Notably, RIP assay showed that B4GALT1-AS1 abundance was significantly increased in RNA immunoprecipitated with HuR antibody (Figure 4H), indicating that HuR could directly bind to B4GALT1-AS1.We indicate that lncRNA B4GALT1-AS1 promotes OS cells stemness and migration via recruiting HuR to enhance YAP activity.	30182452	RID05430	interact with protein	chemoresistance	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	B4GALT1-AS1	YY1AP1	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell stemness(+);cell migration(+);chemoresistance(+)	NA	association	RNA-protein	Adriamycin	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233554	GRCh38_9:33166948-33182865	ENSG00000163374	NA	101929639	55249	NA	HCCA2|YAP|YY1AP	LncRNA B4GALT1-AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity.LncRNA B4GALT1-AS1 expression was significantly increased in OS tissues and cells spheres. Knockdown of B4GALT1-AS1 inhibited OS cells proliferation, migration, stemness and chemotherapeutic sensitivity. B4GALT1-AS1 knockdown enhances adriamycin sensitivity in OS cells dependent on YAP expression.We indicate that lncRNA B4GALT1-AS1 promotes OS cells stemness and migration via recruiting HuR to enhance YAP activity.	30182452	RID05431	expression association	chemoresistance	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Esophageal cancer	LINC00261	DPYD	negatively-E	shRNA;RIP;luciferase reporter assay	downregulation	qRT-PCR	TCGA	NA	apoptosis process(+);cell cycle(-);chemosensitivity(+)	DNA methylation;transcriptional regulation	binding/interaction	RNA-protein	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000188641	NA	140828	1806	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	DHPDHase|DPD	Long noncoding RNA LINC00261 induces chemosensitization to 5-fluorouracil by mediating methylation-dependent repression of DPYD in human esophageal cancer.A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2'-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells.  BLAST comparison results provided evidence suggesting the existence of a binding site of complementary base pairing between LINC00261 and DPYD promoter region (Fig. 6C). The luciferase reporter gene assay indicated that, when compared to the NC group, the luciferase activity was significantly decreased in the DPYD-WT group (P < 0.05). Our study highlighted the potential of LINC00261 as a novel target capable of improving the chemotherapeutic response and survival of patients with esophageal cancer.	30226808	RID05432	epigenetic regulation	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Myocardial infarction	MEG3	HMGB1	positively-E	RNAi;western blot;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell injury(-)	ceRNA(miR-22)	regulation	NA	Atorvastatin	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000189403	NA	55384	3146	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DKFZp686A04236|HMG1|HMG3|SBP-1	Atorvastatin protects cardiac progenitor cells from hypoxia-induced cell growth inhibition via MEG3/miR-22/HMGB1 pathway.qRT-PCRresults demonstrated that miR-22 and miR-361 were significantly elevated after MEG3 knockdown (Fig. 3A). As miR-22 was reported to be involved in the pathological process of heart disease [24], we next focused on the biological function of miR22 in CPCs. As depicted in Fig. 3B, dual-luciferase reporter assay illustrated that MEG3 and miR-22 indeed had intermolecular binding. In addition, miR-22 expression level was increased after MEG3 suppression in CPCs under hypoxia condition and further, the overexpression of MEG3 inhibited the atorvastatin-induced restoration of miR22 expression in CPCs under hypoxia condition (Fig. 3C). These data confirmed that miR-22 was a target of MEG3 in the role of atorvastatin in CPCs under hypoxia condition. We found that hypoxia inhibits CPC viability and proliferation through modulating MEG3 expression, while atorvastatin application can protect CPCs from hypoxia-induced injury through inhibiting MEG3 expression.	30481260	RID05433	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Osteosarcoma	HOTAIR	ZEB1	positively-E	RNAi;qRT-PCR;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-217)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148516	NA	100124700	6935	HOXC-AS4|HOXC11-AS1|NCRNA00072	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	HOTAIR promotes osteosarcoma development by sponging miR-217 and targeting ZEB1.ZEB1 was identified as a downstream gene of miR-217 and we found that HOTAIR can mediate osteosarcoma progress by upregulating ZEB1 expression via acting as a competitive endogenous RNA (ceRNA) via miR-217.In addition, the subsequent functional assay exhibited that silencing HOTAIR could significantly repress osteosarcoma cell growth, migration, invasion, and induce cell apoptosis capacity, which indicated that HOTAIR exerted an oncogenic role in osteosarcoma.	30367466	RID05434	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC01433	STAT3	positively-E	RNA pull-down assay;RIP;RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell invasion(+)	ceRNA(miR-1301)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000230176	GRCh38_20:4192932-4195953	ENSG00000168610	NA	728228	6774	LOC728228	APRF	LINC01433 promotes hepatocellular carcinoma progression via modulating the miR-1301/STAT3 axis.In addition, the binding correlation between them was validated by performing RNA pull-down experiments and RIP assay. Moreover, STAT3 was predicted and validated as a target of miR-1301, and it was shown that miR-1301 mimics significantly suppressed STAT3 in HCC cells.Then, knockdown of LINC01433 was able to restrain HCC cell proliferation and cell colony formation and greatly induced cell apoptosis. On the contrary, overexpression of LINC01433 promoted HCC cell proliferation, increased cell colony formation, and enhanced cell invasion capacity.	30317567	RID05435	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	MALAT1	NEDD9	positively-E	shRNA;RNA pull-down assay;luciferase reporter assay			NA	NA	angiogenesis(+);cell invasion(+)	ceRNA(miR-145-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111859	NA	378938	4739	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CAS-L|CASS2|HEF1	Estrogen receptor beta promotes the vasculogenic mimicry (VM) and cell invasion via altering the lncRNA-MALAT1/miR-145-5p/NEDD9 signals in lung cancer.we applied the RNA pull-down assay with biotinylated MALAT1 antisense-oligo 5'- GGGAGTTACTTGCCAACTTG-3'-to pull-down MALAT1, and the results revealed that miR-145-5p was enriched in the pull-down product (Fig. 5c), suggesting the direct binding of miR-145-5p with MALAT1.Together, results from the above studies demonstrated thatERbetacan promote NSCLC VM formation and cell invasion via altering the ERbeta/MALAT1/miR145-5p/NEDD9 signaling.	30250297	RID05436	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	ESR2	MALAT1	positively-E	luciferase reporter assay;ChIP			NA	NA	angiogenesis(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000140009	NA	ENSG00000251562	GRCh38_11:65497688-65506516	2100	378938	ER-beta|Erb|NR3A2	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Estrogen receptor beta promotes the vasculogenic mimicry (VM) and cell invasion via altering the lncRNA-MALAT1/miR-145-5p/NEDD9 signals in lung cancer.Molecular mechanism dissection suggested that ERbeta could increase the lncRNA-MALAT1 (MALAT1) expression via directly binding to the estrogen response elements (EREs) located on the promoter of MALAT1.Together, results from the above studies demonstrated thatERbetacan promote NSCLC VM formation and cell invasion via altering the ERbeta/MALAT1/miR145-5p/NEDD9 signaling.	30250297	RID05437	transcriptional regulation	NA	UP(LIHC,PAAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Malignant glioma	LNCRNA-ATB	miR-204-3p	negatively-F	RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	NA	NA	NA	NA	114004396	NA	NA	NA	Exosomal lncRNA-ATB activates astrocytes that promote glioma cell invasion.We found that glioma cell-derived exosomes promoted the activation of astrocytes and had the ability to shuttle long non-coding RNA (lncRNA) activated by TGF-beta (lncRNA-ATB) to astrocytes. The results of RT-qPCR demonstrated that the exosomes derived from the A172 and U251 glioma cells contained higher levels of lncRNA-ATB when compared with those derived from the parent glioma cells More importantly, lncRNA-ATB activated astrocytes through the suppression of microRNA (miRNA or miR)-204-3p in an Argonaute 2 (Ago2)-dependent manner. Furthermore, astrocytes activated by lncRNA-ATB in turn promoted the migration and invasion of glioma cells.	30483768	RID05438	ceRNA or sponge	NA		
Triple-negative breast cancer	DANCR	RXRA	positively-F	RIP-qPCR;RNA pull-down assay;western blot	upregulation	RT-qPCR;microarray;sequencing	TCGA	NA	tumorigenesis(+);PI3K/AKT signaling pathway(+)	phosphorylation	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000186350	NA	57291	6256	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NR2B1	LncRNA DANCR upregulates PI3K/AKT signaling through activating serine phosphorylation of RXRA. Here, we found that lncRNA DANCR was significantly overregulated in TNBC tissues and cell lines compared with normal breast tissues or other type of breast cancer. Knockdown of DANCR suppressed TNBC proliferation both in vitro and in vivo. Further study of underlying mechanisms demonstrated that DANCR bound with RXRA and increased its serine 49/78 phosphorylation via GSK3beta, resulting in activating PIK3CA transcription, and subsequently enhanced PI3K/AKT signaling and TNBC tumorigenesis.	30518934	RID05439	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Triple-negative breast cancer	DANCR	PIK3CA	positively-E	shRNA;western blot;luciferase reporter assay	upregulation	RT-qPCR;microarray;sequencing	TCGA	NA	tumorigenesis(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000121879	NA	57291	5290	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	PI3K	LncRNA DANCR upregulates PI3K/AKT signaling through activating serine phosphorylation of RXRA. Here, we found that lncRNA DANCR was significantly overregulated in TNBC tissues and cell lines compared with normal breast tissues or other type of breast cancer. Knockdown of DANCR suppressed TNBC proliferation both in vitro and in vivo. Further study of underlying mechanisms demonstrated that DANCR bound with RXRA and increased its serine 49/78 phosphorylation via GSK3beta, resulting in activating PIK3CA transcription, and subsequently enhanced PI3K/AKT signaling and TNBC tumorigenesis.  knockdown of DANCR significantly inhibited PIK3CA protein and mRNA expression levels in both TNBC cells.	30518934	RID05440	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Non-small cell lung cancer	DUXAP9-206	CBLB	positively-F	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell migration(+);EGFR signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000114423	NA	NA	868	NA	Cbl-b|RNF56	LncRNA DUXAP9-206 directly binds with Cbl-b to augment EGFR signaling and promotes non-small cell lung cancer progression. DUXAP9-206 is up-regulated in NSCLC and correlates with patients survival. We reveal that DUXAP9-206 induced NSCLC cell proliferation and metastasis by directly interacting with Cbl-b, an E3 ubiquitin ligase, and reducing the degradation of epidermal growth factor receptor (EGFR) and thereby augmenting EGFR signaling in NSCLC.	30515972	RID05441	interact with protein	metastasis,prognosis		UP(LIHC);DOWN(PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367)
Non-small cell lung cancer	DUXAP9-206	EGFR	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell migration(+);EGFR signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|ERRP	LncRNA DUXAP9-206 directly binds with Cbl-b to augment EGFR signaling and promotes non-small cell lung cancer progression. DUXAP9-206 is up-regulated in NSCLC and correlates with patients survival. We reveal that DUXAP9-206 induced NSCLC cell proliferation and metastasis by directly interacting with Cbl-b, an E3 ubiquitin ligase, and reducing the degradation of epidermal growth factor receptor (EGFR) and thereby augmenting EGFR signaling in NSCLC.The results of western blotshowed that stable overexpression of DUXAP9-206 increased the expression level of EGFR and downstream ERK/Akt activation, while knockdown of DUXAP9-206 showed the opposite results	30515972	RID05442	expression association	metastasis,prognosis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	H19	SIRT1	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell autophagy(+)	ceRNA(miR-194-5p)	regulation	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000096717	NA	283120	23411	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	SIR2L1	Long non-coding RNA H19 confers 5-Fu resistance in colorectal cancer by promoting SIRT1-mediated autophagy.Quantitative analysis indicated that H19 was significantly increased in recurrent CRC patient samples. Furthermore, bioinformatics analysis showed that miR-194-5p could directly bind to H19, suggesting H19 might work as a ceRNA to sponge miR-194-5p, which was confirmed by dual-luciferase reporter assay and Immunoprecipitation assay. Extensively, our study also showed that SIRT1 is the novel direct target of miR-194-5p in CRC cells.Our finding provides a novel mechanistic role of H19 in CRC chemoresistance, suggesting that H19 may function as a marker for prediction of chemotherapeutic response to 5-Fu.	30451820	RID05443	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	PCAT6	MKRN3	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-30)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000179455	NA	100506696	7681	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	D15S9|MGC88288|RNF63|ZFP127|ZNF127	PCAT6 participates in the development of gastric cancer through endogenously competition with microRNA-30.PCAT6 was overexpressed in gastric cancer tissues than those of paracancerous tissues. PCAT6 expression was negatively correlated to prognosis, tumor size, TNM (tumor node metastasis) stage and metastasis of gastric cancer. For in vitro experiments, overexpression of PCAT6 increased proliferation, migration, and invasion, whereas decreased apoptosis of gastric cancer cells. MicroRNA-30 was predicted as the target gene of TCAT6. Furthermore, microRNA-30 was found to bind to TCAT6 via targeting MKRN3.	30178843	RID05444	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	LNCBRM	TPT1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-204-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249436	GRCh38_5:57574027-57619816	ENSG00000133112	NA	100996645	7178	LINCR-0003	fortilin|TCTP	Long noncoding RNA lncBRM promotes proliferation and invasion of colorectal cancer by sponging miR-204-3p and upregulating TPT1.And also, we showed that high expression of lncBRM predicted poor prognosis. Furthermore, we found that knockdown of lncBRM impaired the proliferation, migration and invasion of CRC cells while overexpressing of lncBRM promotes the proliferation, migration and invasion of CRC cells. Mechanically, we found that lncBRM served as a sponge of miR-204-3p that targeted TPT1. Highly expressed TPT1 can promote the proliferation, migration and invasion of CRC cells.	30563768	RID05445	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Osteosarcoma	DLX6-AS1	DLK1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	prognosis;WNT signaling pathway(+);cell stemness(+)	ceRNA(miR-129-5p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000185559	NA	285987	8788	Evf-2|FLJ34048|NCRNA00212	Delta1|FA1|pG2|Pref-1|ZOG	LncRNA DLX6-AS1/miR-129-5p/DLK1 axis aggravates stemness of osteosarcoma through Wnt signaling.Moreover, DLX6-AS1 competitively interacted with miR-129-5p to DLK1, resulting in activation of Wnt signaling and promotion of stemness in osteosarcoma. DLX6-AS1 functionally interplayed with miR-129-5p to form a reciprocal feedback loop to activate Wnt signaling. High DLX6-AS1 expression was observed in osteosarcoma tissues, and predicted a poor prognosis for osteosarcoma patients.	30442366	RID05446	ceRNA or sponge	prognosis		
Melanoma	SAMMSON	CARF	negatively-F	RNA pull-down assay;RIP;catRAPID	upregulation	RT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000138380	NA	101927152	79800	LINC01212	ALS2CR8|FLJ21579|NYD-SP24	SAMMSON fosters cancer cell fitness by concertedly enhancing mitochondrial and cytosolic translation.SAMMSON interferes with XRN2 binding to CARF in the nucleus by favoring the formation of an aberrant cytoplasmic RNA-protein complex containing CARF and p32, a mitochondrial protein required for the processing of the mitochondrial rRNAs.-	30374086	RID05447	interact with protein	NA	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Melanoma	SAMMSON	XRN2	positively-E	RNA pull-down assay;RIP;catRAPID	upregulation	RT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000088930	NA	101927152	22803	LINC01212	NA	SAMMSON fosters cancer cell fitness by concertedly enhancing mitochondrial and cytosolic translation.SAMMSON interferes with XRN2 binding to CARF in the nucleus by favoring the formation of an aberrant cytoplasmic RNA-protein complex containing CARF and p32, a mitochondrial protein required for the processing of the mitochondrial rRNAs.-	30374086	RID05448	interact with protein	NA	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Urinary bladder cancer	ELF3-AS1	KLF8	positively-F	RNA pull-down assay;RIP;western blot;shRNA	upregulation	microarray;qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000234678	GRCh38_1:201995696-202010463	ENSG00000102349	NA	102723465	11279	ENST00000415582|SCAT7	BKLF3|DXS741|ZNF741	The lncRNA ELF3-AS1 promotes bladder cancer progression by interaction with Kruppel-like factor 8.ELF3-AS1 was highly expressed in bladder cancer and correlated with poor prognosis. ELF3-AS1 could increase viability and migration of bladder cancer cells in vitro and promoted xenograft tumor growth in vivo. Furthermore, ELF3-AS1 could interact with KLF8 to stabilize KLF8 by protecting it from proteasome-mediated degradation.KLF8 in turn could bind ELF3-AS1 promoter and transactivate ELF3-AS1 expression. The positive feedback loop between ELF3-AS1 and KLF8 enhanced KLF8 signaling by increasing MMP9 expression. Collectively, our study has unraveled a novel mechanism of ELF3-AS1-mediated oncogenesis in bladder cancer by reinforcement of ELF3-AS1/KLF8 signaling with potential implications for therapeutic intervention.	30528231	RID05449	interact with protein	prognosis	DOWN(PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)	
Urinary bladder cancer	KLF8	ELF3-AS1	positively-E	RNA pull-down assay;RIP;western blot;shRNA;luciferase reporter assay	upregulation	microarray;qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Urinary bladder cancer	TF	lncRNA	ENSG00000102349	NA	ENSG00000234678	GRCh38_1:201995696-202010463	11279	102723465	BKLF3|DXS741|ZNF741	ENST00000415582|SCAT7	The lncRNA ELF3-AS1 promotes bladder cancer progression by interaction with Kruppel-like factor 8.ELF3-AS1 was highly expressed in bladder cancer and correlated with poor prognosis. ELF3-AS1 could increase viability and migration of bladder cancer cells in vitro and promoted xenograft tumor growth in vivo. Furthermore, ELF3-AS1 could interact with KLF8 to stabilize KLF8 by protecting it from proteasome-mediated degradation.KLF8 in turn could bind ELF3-AS1 promoter and transactivate ELF3-AS1 expression. The positive feedback loop between ELF3-AS1 and KLF8 enhanced KLF8 signaling by increasing MMP9 expression. Collectively, our study has unraveled a novel mechanism of ELF3-AS1-mediated oncogenesis in bladder cancer by reinforcement of ELF3-AS1/KLF8 signaling with potential implications for therapeutic intervention.	30528231	RID05450	transcriptional regulation	prognosis		DOWN(PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Obesity	H19	MBD1	positively-F	CHART-MS;siRNA	downregulation	sequencing	NA	NA	adipogenesis(+);oxidative metabolic process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Disease of metabolism	Obesity	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141644	NA	283120	4152	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CXXC3|PCM1	LincRNA H19 protects from dietary obesity by constraining expression of monoallelic genes in brown fat.Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. This has implications for our understanding how monoallelic gene expression affects metabolism in rodents and, potentially, humans.	30190464	RID05451	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TNK2-AS1	STAT3	positively-F	RIP;western blot	upregulation	RT-qPCR;microarray	NA	NA	angiogenesis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000224614	GRCh38_3:195908076-195913986	ENSG00000168610	NA	100128262	6774	NA	APRF	The positive feedback between lncRNA TNK2-AS1 and STAT3 enhances angiogenesis in non-small cell lung cancer;TNK2-AS1 was significantly upregulated in NSCLC and correlated with poor prognosis;Evidence has shown the importance of long non-coding RNAs (lncRNAs) during angiogenesis and lung cancer progression;TNK2-AS1 could interact with STAT3 to increase its protein stability by protecting it from proteasome-mediated degradation;Independent western blot showed that TNK2-AS1 could bind STAT3 directly (Fig. 3B). RNA immunoprecipitation (RIP) assay further confirmed the binding between STAT3 and TNK2-AS1;our work has elucidated a novel mechanism of TNK2-AS1-mediated angiogenesis by enforcing STAT3/VEGFA signaling;TNK2-AS1 was significantly upregulated in NSCLC and correlated with poor prognosis. We found that TNK2-AS1 could increase viability and migration of NSCLC cells in vitro. TNK2-AS1 also promoted NSCLC xenograft tumor growth and metastasis in vivo.	30454892	RID05452	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	STAT3	TNK2-AS1	positively-E	luciferase reporter assay;ChIP	upregulation	RT-qPCR;microarray	NA	NA	angiogenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000224614	GRCh38_3:195908076-195913986	6774	100128262	APRF	NA	The positive feedback between lncRNA TNK2-AS1 and STAT3 enhances angiogenesis in non-small cell lung cancer;STAT3 could also bind TNK2- AS1 promoter to trigger its transcription. The positive feedback loop between STAT3 and TNK2-AS1 therefore augmented STAT3 signaling by elevating VEGFA expression to facilitate angiogenesis	30454892	RID05453	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TNK2-AS1	VEGFA	positively-F	siRNA;overexpression	upregulation	RT-qPCR;microarray	NA	NA	angiogenesis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224614	GRCh38_3:195908076-195913986	ENSG00000112715	NA	100128262	7422	NA	VEGF|VEGF-A|VPF	The positive feedback between lncRNA TNK2-AS1 and STAT3 enhances angiogenesis in non-small cell lung cancer; We found that TNK2-AS1 level indeed positively affected VEGFA expression (Figs. S1A and S1B). VEGFA secretion was augmented by TNK2-AS1 overexpression (Fig. S1C) and attenuated via TNK2-AS1 knockdown (Fig. S1D). STAT3 inhibitor treatment strongly abolished enhanced VEGFA promoter activity and transcription induced by TNK2-AS1 overexpression	30454892	RID05454	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Gastric cancer	SNHG1	ADAM10	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000137845	NA	23642	102	LINC00057|lncRNA16|NCRNA00057|UHG	CD156C|HsT18717|kuz|MADM	LncRNA SNHG1 promoted HGC-27 cell growth and migration via the miR-140/ADAM10 axis;we reported that SNHG1 expression was significantly increased in GC cell lines and tissues;To examine the expression level of SNHG1 in primary GC tissue and their normal counterparts, RT-PCRassay was performed; To test whether SNHG1 and miR-140 are in the same RISC complex, RIP experiments were performed;As determined by the luciferase assay, miR-140 could bind to SNHG1 directly via putative miRNA response element.Mechanismly, it was found that SNHG1 functioned as a competing endogenous RNA to repress miR-140 expression and thereby elevated its down-stream target ADAM10.	30391432	RID05455	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Myasthenia gravis	MALAT1	MSL2	positively-E	Starbase;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	DNA damage(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	NA	Immune system disease	Autoimmune disease of the nervous system	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000174579	NA	378938	55167	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FLJ10546|KIAA1585|msl-2|MSL2L1|RNF184	The long noncoding RNA MALAT-1 functions as a competing endogenous RNA to regulate MSL2 expression by sponging miR-338-3p in myasthenia gravis;Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) has been associated with gene regulation and alternative splicing. It has shown relationship with proliferation, apoptosis, migration, and invasion;MSL2 is involved in chromatin organization and maintenance of normal histone profiles through its ligase activity, which may contribute to the DNA damage response	30362606	RID05456	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
T-cell leukemia	CDKN2B-AS1	CDKN1A	negatively-E	ChIP;siRNA	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000124762	NA	100048912	1026	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	Long Noncoding RNA ANRIL Supports Proliferation of Adult T-Cell Leukemia Cells through Cooperation with EZH2;E2F1 induced ANRIL transcription by enhancing its promoter activity; Knockdown of ANRIL in ATL cells repressed cellular proliferation and increased apoptosis in vitro and in vivo;we observed that the ANRIL/EZH2 complex repressed p21/CDKN1A transcription through H3K27 trimethylation of the p21/CDKN1A promoter.A chromatin immunoprecipitation assay revealed that ANRIL/EZH2 enhanced p65 DNA binding capability	30258010	RID05457	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Newborn respiratory distress syndrome	MALAT1	NFKB1	negatively-F	siRNA;ChIP	upregulation	RT-PCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	Knockdown of LncRNA MALAT1 contributes to cell apoptosis via regulating NF-KB/CD80 axis in neonatal respiratory distress syndrome;we report a critical role of lncRNA MALAT1 in regulating CD80 transcription in the NRDS-associated apoptosis via binding with NF-KB;Then we demonstrated knockdown of MALAT1 promoted CD80 transcription in A549 cells. Furthermore, we confirmed that MALAT1 downregulated transcriptional expression of CD80 by interfering with NF-KB activation and disrupting its binding efficiency with the CD80 promoter in the cell nucleus; We first showed MALAT1 and CD80 were highly expressed in the peripheral blood mononuclear cells of NRDS with infection exposure;Then we performed RIP from subcellular extracts of LPS-stimulated A549 cells using the p65 antibody. We observed a seven-fold enrichment of nuclear MALAT1, but not cytoplasmic MALAT1, in the anti-p65 immunoprecipitates compared with the IgG control (Fig. 5C), indicating that, in the nucleus, MALAT1 physically associates with p65. Based on these observations, we conclude that MALAT1 binds the nuclear p65 and thus prevents the binding of NF-KB to the promoter of CD80.Our data showed MALAT1 could directly interact with NF-KB. ChIP assay showed that knockdown of MALAT1 enanced the binding of NF-KB to CD80 promoter;MALAT1 level was observed in RDS peripheral blood mononuclear cells by RT-qPCR	30243953	RID05458	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Newborn respiratory distress syndrome	MALAT1	CD80	negatively-E	siRNA;ChIP	upregulation	RT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000121594	NA	378938	941	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	B7-1|B7.1|CD28LG|CD28LG1	Knockdown of LncRNA MALAT1 contributes to cell apoptosis via regulating NF-KB/CD80 axis in neonatal respiratory distress syndrome;we report a critical role of lncRNA MALAT1 in regulating CD80 transcription in the NRDS-associated apoptosis via binding with NF-KB;Then we demonstrated knockdown of MALAT1 promoted CD80 transcription in A549 cells. Furthermore, we confirmed that MALAT1 downregulated transcriptional expression of CD80 by interfering with NF-KB activation and disrupting its binding efficiency with the CD80 promoter in the cell nucleus; We first showed MALAT1 and CD80 were highly expressed in the peripheral blood mononuclear cells of NRDS with infection exposure;Then we performed RIP from subcellular extracts of LPS-stimulated A549 cells using the p65 antibody. We observed a seven-fold enrichment of nuclear MALAT1, but not cytoplasmic MALAT1, in the anti-p65 immunoprecipitates compared with the IgG control (Fig. 5C), indicating that, in the nucleus, MALAT1 physically associates with p65. Based on these observations, we conclude that MALAT1 binds the nuclear p65 and thus prevents the binding of NF-KB to the promoter of CD80.Our data showed MALAT1 could directly interact with NF-KB. ChIP assay showed that knockdown of MALAT1 enanced the binding of NF-KB to CD80 promoter.	30243953	RID05459	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE86978)
Newborn respiratory distress syndrome	MALAT1	P65	positively-F	RIP;ChIP;siRNA	upregulation	RT-PCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067715	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Knockdown of LncRNA MALAT1 contributes to cell apoptosis via regulating NF-KB/CD80 axis in neonatal respiratory distress syndrome;we report a critical role of lncRNA MALAT1 in regulating CD80 transcription in the NRDS-associated apoptosis via binding with NF-KB;Then we demonstrated knockdown of MALAT1 promoted CD80 transcription in A549 cells. Furthermore, we confirmed that MALAT1 downregulated transcriptional expression of CD80 by interfering with NF-KB activation and disrupting its binding efficiency with the CD80 promoter in the cell nucleus; We first showed MALAT1 and CD80 were highly expressed in the peripheral blood mononuclear cells of NRDS with infection exposure;Then we performed RIP from subcellular extracts of LPS-stimulated A549 cells using the p65 antibody. We observed a seven-fold enrichment of nuclear MALAT1, but not cytoplasmic MALAT1, in the anti-p65 immunoprecipitates compared with the IgG control (Fig. 5C), indicating that, in the nucleus, MALAT1 physically associates with p65. Based on these observations, we conclude that MALAT1 binds the nuclear p65 and thus prevents the binding of NF-KB to the promoter of CD80.Our data showed MALAT1 could directly interact with NF-KB. ChIP assay showed that knockdown of MALAT1 enanced the binding of NF-KB to CD80 promoter.	30243953	RID05460	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Cervical cancer	XLOC_006390	miR-331-3p	negatively-F	LncBase;siRNA	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+)	sponge	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p;Expression of miRNAs and lncRNA in cervical cancer cells and tissues was detected by reverse transcription polymerase chain reaction;XLOC_006390 was found to facilitate cervical cancer tumorigenesis and metastasis by downregulating miR-331-3p and miR-338-3p expression.	30207103	RID05461	ceRNA or sponge	metastasis		
Cervical cancer	XLOC_006390	miR-338-3p	negatively-F	LncBase;siRNA	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p;Expression of miRNAs and lncRNA in cervical cancer cells and tissues was detected by reverse transcription polymerase chain reaction;XLOC_006390 was found to facilitate cervical cancer tumorigenesis and metastasis by downregulating miR-331-3p and miR-338-4p expression.	30207103	RID05462	ceRNA or sponge	metastasis		
Cervical cancer	XLOC_006390	NRP2	positively-E	siRNA	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27193503-27200091	ENSG00000118257	NA	NA	8828	NA	VEGF165R2	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p;Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006390 was knocked down.	30207103	RID05463	expression association	metastasis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Cervical cancer	XLOC_006390	PKM	positively-E	siRNA	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27193503-27200091	ENSG00000067225	NA	NA	5315	NA	OIP3|PK3|PKM2|THBP1	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p;Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006391 was knocked down.	30207103	RID05464	expression association	metastasis		UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Cervical cancer	XLOC_006390	EYA2	positively-E	siRNA	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27193503-27200091	ENSG00000064655	NA	NA	2139	NA	EAB1	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p;Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006392 was knocked down.	30207103	RID05465	expression association	metastasis		
Nasopharynx carcinoma	HOXC13-AS	HMGA2	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR;sequencing	TCGA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-383-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000249641	GRCh38_12:53935328-53939643	ENSG00000149948	NA	100874366	8091	HOXC-AS5	BABL|HMGIC|LIPO	Long noncoding RNA HOXC13-AS positively affects cell proliferation and invasion in nasopharyngeal carcinoma via modulating miR-383-3p/HMGA2 axis;functional assay revealed that knockdown of HOXC13-AS impaired cell proliferation, migration, and invasion. Mechanistically, RIP and luciferase reporter analysis confirmed that miR-383-3p was a target of HOXC13-AS;rescue assays demonstrated that HOXC13-AS functioned as a competing endogenous RNAs to enhance the expression of HMGA2 via sponging miR-383-3p.	30536950	RID05466	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Liver cancer	LncHOXA10	HOXA10	positively-E	RNA pull-down assay;western blot;RAP assay	upregulation	RT-PCR;microarray	GSE14520	NA	tumorigenesis(+);self-renewal(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000253293	NA	NA	3206	NA	HOX1|HOX1.8|HOX1H|PL	LncHOXA10 drives liver TICs self-renewal and tumorigenesis via HOXA10 transcription activation;LncHOXA10 interacted with SNF2L and recruited NURF chromatin remodeling complex to HOXA10 promoter, and thus initiated the transcription of HOXA10;HOXA10 was the highest expressed HOX transcription factor in liver cancer;Through realtime PCR, we found lncHOXA10 was highly expressed in liver cancer	30545354	RID05467	expression association	NA		
Liver cancer	LncHOXA10	SMARCA1	interact	RNA pull-down assay;western blot;RIP	upregulation	RT-PCR;microarray	GSE14520	NA	tumorigenesis(+);self-renewal(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000102038	NA	NA	6594	NA	ISWI|NURF140|SNF2L|SNF2L1|SNF2LB|SNF2LT|SWI|SWI2|hSNF2L	LncHOXA10 drives liver TICs self-renewal and tumorigenesis via HOXA10 transcription activation;LncHOXA10 interacted with SNF2L and recruited NURF chromatin remodeling complex to HOXA10 promoter, and thus initiated the transcription of HOXA11;RNA pull-down showed a specific band in lncHOXA10 eluate, which was identified as SNF2L by mass spectrum, indicating the combination of lncHOXA10 and SNF2L (Fig. 5a). The interaction of lncHOXA10 and SNF2L was confirmed by western blot (Fig. 5b). To further confirm the combination of lncHOXA10 and SNF2L, we performed RAP (RNA antisense purification) assay (Fig. 5c). RAP assay also validated the interaction of lncHOXA10 and SNF2L, which was confirmed by western blot (Fig. 5d, e)	30545354	RID05468	interact with protein	NA		UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761)
Liver fibrosis	H19	USP4	positively-E	Starbase;dual-luciferase reporter assay;qRT-PCRite directed mutagenesis	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+)	ceRNA(miR-148a)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000114316	NA	283120	7375	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	UNP|Unph	H19/miR-148a/USP4 axis facilitates liver fibrosis by enhancing TGF-B signaling in both hepatic stellate cells and hepatocytes;H19 functioned as a competing endogenous RNA to sponge miR-148a and subsequently sustained the level of ubiquitin-specific protease 4 (USP4), which was an identified target of miR-148a and was able to stabilize TGF-B receptor I;With the bioinformatic analysis by Starbase 2.0, putative binding sites for miR-148a in H19 was designated;we found copy numbers of H19 and miR 148a were comparable (data not shown) and verified the binding between H19 and miR 148a using qRT-PCR dual-luciferase reporter assay and site directed mutagenesis	30362572	RID05469	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cancer	CamK-A	PNCK	interact	RNA pull-down assay;RIP	upregulation		NA	NA	tumor microenvironment remodeling(+);macrophage recruitment(+);angiogenesis(+);cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000130822	NA	NA	139728	NA	BSTK3|CaMK1b	LncRNA CamK-A Regulates Ca2+-SignalingMediated Tumor Microenvironment Remodeling;CamK-A is highly expressed in multiple human cancers and involved in cancer microenvironment remodeling via activation of Ca2+-triggered signaling;We performed an RNA pull-down assay followed by mass spectrometry (MS) (Lin et al., 2016; Xing et al., 2014) to identify CamKA-associated proteins that might be involved in CamK-A-related cytoplasmic processes. Interestingly, the sense CamK-A, but not the antisense or beads control, specifically bound to PNCK (also known as calcium/calmodulin-dependent protein kinase type 1B [PNCK I beta]) and IkBa (Figures 2A, S2A, and S2B; Table S3). An RNA protein binding assay using recombinant PNCK and IkBa confirmed that CamK-A directly associated with these two proteins both in vivo and in vitro (Figures 2A, 2B, and S2C). The specific interaction between CamK-A and PNCK or IkBa was also confirmed by using the RNA immunoprecipitation (RIP) assay (Figure 2C); Under hypoxia condition, the increased cytosolic Ca2+ induces the complex formation between CamK-A and PNCK, which activates PNCK. Activated CaMK, together with the apical CamK-A, further phosphorylates IkBa at Ser32 and triggers calcium-induced NF-kB signaling activity. The activated Ca2+-dependent NF-kB pathway favors tumor progression by increasing the downstream cytokines production, tumor energy metabolic uptake, and the infiltrated macrophage recruitment, thus promoting cancer glycolysis, angiogenesis, microenvironment reprogramming, and cancer development.	30220561	RID05470	interact with protein	NA		UP(BRCA);DATA(GSE55807)
Cancer	CamK-A	NFKBIA	interact	RNA pull-down assay;RIP	upregulation		NA	NA	tumor microenvironment remodeling(+);macrophage recruitment(+);angiogenesis(+);cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000100906	NA	NA	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	LncRNA CamK-A Regulates Ca2+-SignalingMediated Tumor Microenvironment Remodeling;CamK-A is highly expressed in multiple human cancers and involved in cancer microenvironment remodeling via activation of Ca2+-triggered signaling;We performed an RNA pull-down assay followed by mass spectrometry (MS) (Lin et al., 2016; Xing et al., 2014) to identify CamKA-associated proteins that might be involved in CamK-A-related cytoplasmic processes. Interestingly, the sense CamK-A, but not the antisense or beads control, specifically bound to PNCK (also known as calcium/calmodulin-dependent protein kinase type 1B [PNCK I beta]) and IkBa (Figures 2A, S2A, and S2B; Table S3). An RNA protein binding assay using recombinant PNCK and IkBa confirmed that CamK-A directly associated with these two proteins both in vivo and in vitro (Figures 2A, 2B, and S2C). The specific interaction between CamK-A and PNCK or IkBa was also confirmed by using the RNA immunoprecipitation (RIP) assay (Figure 2C); Under hypoxia condition, the increased cytosolic Ca2+ induces the complex formation between CamK-A and PNCK, which activates PNCK. Activated CaMK, together with the apical CamK-A, further phosphorylates IkBa at Ser32 and triggers calcium-induced NF-kB signaling activity. The activated Ca2+-dependent NF-kB pathway favors tumor progression by increasing the downstream cytokines production, tumor energy metabolic uptake, and the infiltrated macrophage recruitment, thus promoting cancer glycolysis, angiogenesis, microenvironment reprogramming, and cancer development.	30220561	RID05471	interact with protein	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Cancer	CamK-A	NFKB1	positively-E	siRNA	upregulation		NA	NA	tumor microenvironment remodeling(+);macrophage recruitment(+);angiogenesis(+);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cancer	lncRNA	TF	NA	NA	ENSG00000109320	NA	NA	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	LncRNA CamK-A Regulates Ca2+-SignalingMediated Tumor Microenvironment Remodeling;CamK-A is highly expressed in multiple human cancers and involved in cancer microenvironment remodeling via activation of Ca2+-triggered signaling;We performed an RNA pull-down assay followed by mass spectrometry (MS) (Lin et al., 2016; Xing et al., 2014) to identify CamKA-associated proteins that might be involved in CamK-A-related cytoplasmic processes. Interestingly, the sense CamK-A, but not the antisense or beads control, specifically bound to PNCK (also known as calcium/calmodulin-dependent protein kinase type 1B [PNCK I beta]) and IkBa (Figures 2A, S2A, and S2B; Table S3). An RNA protein binding assay using recombinant PNCK and IkBa confirmed that CamK-A directly associated with these two proteins both in vivo and in vitro (Figures 2A, 2B, and S2C). The specific interaction between CamK-A and PNCK or IkBa was also confirmed by using the RNA immunoprecipitation (RIP) assay (Figure 2C); Under hypoxia condition, the increased cytosolic Ca2+ induces the complex formation between CamK-A and PNCK, which activates PNCK. Activated CaMK, together with the apical CamK-A, further phosphorylates IkBa at Ser32 and triggers calcium-induced NF-kB signaling activity. The activated Ca2+-dependent NF-kB pathway favors tumor progression by increasing the downstream cytokines production, tumor energy metabolic uptake, and the infiltrated macrophage recruitment, thus promoting cancer glycolysis, angiogenesis, microenvironment reprogramming, and cancer development.	30220561	RID05472	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon adenocarcinoma	E2F1	MNX1-AS1	positively-E	JASPAR;luciferase reporter assay;ChIP	upregulation		NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000243479	GRCh38_7:157010805-157016426	1869	645249	RBBP3|RBP3	CCAT5|LOC645249|MAYA	E2F1-mediated MNX1-AS1-miR-218-5p-SEC61A1 feedback loop contributes to the progression of colon adenocarcinoma;JASPAR prediction tool showed that E2F1 could bind to the promoter region of MNX1-AS1. The chromatin immunoprecipitation assay and luciferase reporter assay were used to verify the interactions between MNX1-AS1 and E2F1	30362161	RID05473	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(BRCA);DATA(GSE55807)
Colon adenocarcinoma	MNX1-AS1	SEC61A1	positively-E	luciferase reporter assay	upregulation		NA	NA	cancer progression(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000058262	NA	645249	29927	CCAT5|LOC645249|MAYA	NA	E2F1-mediated MNX1-AS1-miR-218-5p-SEC61A1 feedback loop contributes to the progression of colon adenocarcinoma; Bioinformatics analysis and luciferase reporter assay indicated that MNX1-AS1 could sponge microRNA-218-5p (miR-218-5p). Furthermore, we discovered that SEC61A1 was downstream target of miR-218-5p, and MNX1-AS1 acted as a ceRNA to upregulate the expression of SEC61A1 through sponging miR-218-5p	30362161	RID05474	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	DCXR-DT	RAC3	positively-E	siRNA	upregulation	qRT-PCR;microarray	NA	NA	oncogenic role(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000264569	GRCh38_17:82037872-82039380	ENSG00000169750	NA	113523640	5881	RP13-650J16.1	NA	Specific expression of lncRNA RP13-650J16.1 and TCONS_00023979 in prostate cancer. RP13-650J16.1 and RAC3 expression was up-regulated, and TCONS_00023979 and PML expression was down-regulated in PCa tissues. Silencing RP13-650J16.1 could decrease RAC3 expression, and knockout of TCONS_00023979 also reduced PML expression. Moreover, the ability of proliferation, migration, and colony formation of DU145 cells was decreased after transfected with si-RP13-650J16.1, while these abilities were increased after transfected with si-TCONS_00023979. Collectively, our findings demonstrated that RP13-650J16.1 might be an oncogene and TCONS_00023979 might be an antioncogene in PCa.	30279207	RID05475	expression association	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065)
Prostate cancer	TCONS_00023979	PML	positively-E	siRNA	downregulation	qRT-PCR;microarray	NA	NA	tumor-suppressive function(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	NA	NA	ENSG00000140464	NA	NA	5371	NA	MYL|RNF71|TRIM19	Specific expression of lncRNA RP13-650J16.1 and TCONS_00023979 in prostate cancer. RP13-650J16.1 and RAC3 expression was up-regulated, and TCONS_00023979 and PML expression was down-regulated in PCa tissues. Silencing RP13-650J16.1 could decrease RAC3 expression, and knockout of TCONS_00023979 also reduced PML expression. Moreover, the ability of proliferation, migration, and colony formation of DU145 cells was decreased after transfected with si-RP13-650J16.1, while these abilities were increased after transfected with si-TCONS_00023979. Collectively, our findings demonstrated that RP13-650J16.1 might be an oncogene and TCONS_00023979 might be an antioncogene in PCa.	30279207	RID05476	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	KCNQ1OT1	HSP90AA1	positively-E	siRNA;luciferase reporter assay	upregulation	RT-PCR;microarray	GSE50081;GSE30219	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-27b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000080824	NA	10984	3320	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	FLJ31884|Hsp89|Hsp90|HSP90N|HSPC1|HSPCA	KCNQ1OT1 facilitates progression of non-small-cell lung carcinoma via modulating miRNA-27b-3p/HSP90AA1 axis.We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines. Furthermore, knockdown of KCNQ1OT1 reduced the expression of HSP90AA1. KCNQ1OT1 presented a positive correlation with HSP90AA1 which predicted the tumor progression in NSCLC from The Cancer Genome Atlas database. Intriguingly, KCNQ1OT1 modulated HSP90AA1 expression by sponging miR-27b-3p.We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines.KCNQ1OT1 facilitated proliferation, migration, and invasion in H460 cells.	30471108	RID05477	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Ovarian cancer	PANDAR	SRSF2	interact;negatively-E	RIP	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	interact with protein	binding/interaction	RNA-protein	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000161547	NA	101154753	6427	PANDA	PR264|SC-35|SC35|SFRS2|SFRS2A	The cisplatin-induced lncRNA PANDAR dictates the chemoresistance of ovarian cancer via regulating SFRS2-mediated p53 phosphorylation. We also proved that PANDAR exhibited higher expression in cisplatin-resistant ovarian cancer tissues and cells, compared with cisplatin-sensitive ones. Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15). This feedback regulation of PANDAR-SFRS2-p53 leads to a reduced transactivation of p53-related pro-apoptotic genes, such as PUMA (p53-upregulated modulator of apoptosis). Data showed that the levels of SFRS2 and p53 reduced in PANDAR-overexpressing cells compared with control group	30375398	RID05478	interact with protein	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE75367)
Ovarian cancer	PANDAR	TP53	negatively-E	overexpresion	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	NA	association	NA	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000141510	NA	101154753	7157	PANDA	LFS1|p53	The cisplatin-induced lncRNA PANDAR dictates the chemoresistance of ovarian cancer via regulating SFRS2-mediated p53 phosphorylation. We also proved that PANDAR exhibited higher expression in cisplatin-resistant ovarian cancer tissues and cells, compared with cisplatin-sensitive ones. Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15). This feedback regulation of PANDAR-SFRS2-p53 leads to a reduced transactivation of p53-related pro-apoptotic genes, such as PUMA (p53-upregulated modulator of apoptosis). Data showed that the levels of SFRS2 and p53 reduced in PANDAR-overexpressing cells compared with control group	30375398	RID05479	expression association	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Recurrent pregnancy loss	MALAT1	CCND1	positively-E	dual-luciferase reporter assay;overexpression;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-15;miR-383)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Recurrent pregnancy loss	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000110092	NA	378938	595	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL1|D11S287E|PRAD1|U21B31	Downregulated MALAT1 relates to recurrent pregnancy loss via sponging miRNAs. It is known that CCND1 is the direct target of miR-15 and miR-383, meanwhile, the expression of CCND2 is repressed by miR-375.Two days after transfection, cells were lysed and luciferase activity was detected. As shown in Fig. 2B, the relative luciferase activity was significantly repressed by miR-146a, -146b,- 15, -375, -383 and miR-205, indicating these miRNAs repressed luciferase expression via targeting MALAT1.In this study, we found a reduced MALAT1 level in the villus samples of 36 RPL patients.Predicted by bioinformatics tool and confirmed by dual luciferase assay, we identified that MALAT1 directly interacts with miRNAs.In conclusion, MALAT1 as a functional lncRNA controls cell proliferation, apoptosis, migration, invasion and modulates blood vessel formation.	30173780	RID05480	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Recurrent pregnancy loss	MALAT1	VEGFA	positively-E	dual-luciferase reporter assay;overexpression;siRNA	downregulation	qRT-PCR	NA	NA	angiogenesis(+)	ceRNA(miR-205;miR-15;miR-383)	regulation	RNA-protein	NA	NA	NA	Other	Recurrent pregnancy loss	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	VEGF|VEGF-A|VPF	Downregulated MALAT1 relates to recurrent pregnancy loss via sponging miRNAs.It is known that CCND1 is the direct target of miR-15 and miR-383, meanwhile, the expression of CCND2 is repressed by miR-375.Two days after transfection, cells were lysed and luciferase activity was detected. As shown in Fig. 2B, the relative luciferase activity was significantly repressed by miR-146a, -146b,- 15, -375, -383 and miR-205, indicating these miRNAs repressed luciferase expression via targeting MALAT1.In this study, we found a reduced MALAT1 level in the villus samples of 36 RPL patients.Predicted by bioinformatics tool and confirmed by dual luciferase assay, we identified that MALAT1 directly interacts with miRNAs.In conclusion, MALAT1 as a functional lncRNA controls cell proliferation, apoptosis, migration, invasion and modulates blood vessel formation.	30173780	RID05481	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Recurrent pregnancy loss	MALAT1	CCND2	positively-E	dual-luciferase reporter assay;overexpression;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-375)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Recurrent pregnancy loss	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000118971	NA	378938	894	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Downregulated MALAT1 relates to recurrent pregnancy loss via sponging miRNAs.It is known that CCND1 is the direct target of miR-15 and miR-383, meanwhile, the expression of CCND2 is repressed by miR-375.Two days after transfection, cells were lysed and luciferase activity was detected. As shown in Fig. 2B, the relative luciferase activity was significantly repressed by miR-146a, -146b,- 15, -375, -383 and miR-205, indicating these miRNAs repressed luciferase expression via targeting MALAT1.In this study, we found a reduced MALAT1 level in the villus samples of 36 RPL patients.Predicted by bioinformatics tool and confirmed by dual luciferase assay, we identified that MALAT1 directly interacts with miRNAs.In conclusion, MALAT1 as a functional lncRNA controls cell proliferation, apoptosis, migration, invasion and modulates blood vessel formation.	30173780	RID05482	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Estrogen-receptor positive breast cancer	H19	ESR1	positively-E	shRNA	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	Tamoxifen;Fulvestrant	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000091831	NA	283120	2099	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ER-alpha|Era|ESR|NR3A1	Long Non-Coding RNA H19 Acts as an Estrogen Receptor Modulator that is Required for Endocrine Therapy Resistance in ER+ Breast Cancer Cells.Lastly, we demonstrate that H19 regulates ERa expression at the transcript and protein levels in the endocrine therapy resistance (ETR) cells and that H19 protects ERa against Fulvestrant-mediated downregulation of ERa protein. Here we report that treating ETR cells with Tam or Fulvestrant increases H19 expression and that it's decreased expression overcomes resistance to Tam and Fulvestrant in these cells.Our data suggest that in the ETR cells, H19 expression acts as an ER modulator and that its levels and subsequently ERa levels can be substantially decreased by blocking Notch and c-MET receptor signaling. Consequently, treating ETR cells with these pharmacological inhibitors helps overcome resistance to Fulvestrant and Tamoxifen.We therefore examined ERa expression in LCC9 cells showing effective H19 knockdown (>70%, LCC9H19low) or ineffective H19 knockdown (30%, LCC9H19high) and found that ERa protein and transcript levels were both significantly decreased in the LCC9H19low cells but not in the LCC9H19high compared to control cells	30497079	RID05483	expression association	chemoresistance	UP(NSCLC);DATA(GSE74639)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Colorectal cancer	CCHE1	MAPK3	positively-E	Pearson correlation	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000102882	NA	NA	5595	NA	ERK1|p44erk1|p44mapk|PRKM3	Expression of long non-coding RNA CCHE1 in colorectal carcinoma: correlations with clinicopathological features and ERK/COX-2 pathway.both p-ERK1/2 levels and COX-2 expression showed a significant positive correlation with lncRNA-CCHE1 expression levels.LncRNA-CCHE1 relative expression was assessed using quantitative real-time RT-PCR P-ERK - and cyclin D1 levels were estimated by ELISA. COX-2 and proliferating cell nuclear antigen (PCNA) expression were assessed immunohistochemically. lncRNA-CCHE1 expression was upregulated in CRC tissues compared to adjacent non-cancerous tissues, and was significantly associated with larger tumor size, less differentiated histology, advanced dukes stage, positive lymph node involvement and vascular invasion.These findings signify that lncRNA-CCHE1 is a key oncogene possibly involved in CRC development and progression by modulating ERK/COX-2 pathway and cell proliferation activity. -	30484108	RID05484	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CCHE1	COX2	positively-E	Pearson correlation	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000198712	NA	NA	4513	NA	COII|MTCO2	Expression of long non-coding RNA CCHE1 in colorectal carcinoma: correlations with clinicopathological features and ERK/COX-2 pathway.both p-ERK1/2 levels and COX-2 expression showed a significant positive correlation with lncRNA-CCHE1 expression levels.LncRNA-CCHE1 relative expression was assessed using quantitative real-time RT-PCR P-ERK - and cyclin D1 levels were estimated by ELISA. COX-2 and proliferating cell nuclear antigen (PCNA) expression were assessed immunohistochemically. lncRNA-CCHE1 expression was upregulated in CRC tissues compared to adjacent non-cancerous tissues, and was significantly associated with larger tumor size, less differentiated histology, advanced dukes stage, positive lymph node involvement and vascular invasion.These findings signify that lncRNA-CCHE1 is a key oncogene possibly involved in CRC development and progression by modulating ERK/COX-2 pathway and cell proliferation activity. -	30484108	RID05485	expression association	NA		
Colorectal cancer	CCHE1	MAPK1	positively-E	Pearson correlation	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000100030	NA	NA	5594	NA	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Expression of long non-coding RNA CCHE1 in colorectal carcinoma: correlations with clinicopathological features and ERK/COX-2 pathway.both p-ERK1/2 levels and COX-2 expression showed a significant positive correlation with lncRNA-CCHE1 expression levels.LncRNA-CCHE1 relative expression was assessed using quantitative real-time RT-PCR P-ERK - and cyclin D1 levels were estimated by ELISA. COX-2 and proliferating cell nuclear antigen (PCNA) expression were assessed immunohistochemically. lncRNA-CCHE1 expression was upregulated in CRC tissues compared to adjacent non-cancerous tissues, and was significantly associated with larger tumor size, less differentiated histology, advanced dukes stage, positive lymph node involvement and vascular invasion.These findings signify that lncRNA-CCHE1 is a key oncogene possibly involved in CRC development and progression by modulating ERK/COX-2 pathway and cell proliferation activity. -	30484108	RID05486	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Liver cancer	LncHDAC2	PTCH1	negatively-E	ChIRP;EMSA;luciferase reporter assay	upregulation	northern blot;microarray	GSE122420	NA	self-renewal(+);Hedgehog signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000185920	NA	NA	5727	NA	BCNS|NBCCS|PTC|PTC1|PTCH	The long non-coding RNA LncHDAC2 drives the self-renewal of liver cancer stem cells via activation of Hedgehog signaling.Moreover, HDAC2 expression levels are positively related to HCC severity and PTCH1 levels are negatively related to HCC severity. Additionally, the Smo inhibitor cyclopamine was shown to impair the self-renewal of liver CSCs and suppress tumor propagation.LncHDAC2 is highly expressed in HCC tumors and liver CSCs. LncHDAC2 promotes the self-renewal of liver CSCs and tumor propagation.In liver CSCs, lncHDAC2 recruits the NuRD complex onto the promoter of PTCH1 to inhibit its expression, leading to activation of Hedgehog signaling.Our findings reveal that lncHDAC2 promotes the self-renewal of liver CSCs and tumor propagation by activating the Hedgehog signaling pathway.	30582981	RID05487	transcriptional regulation	NA		DOWN(BRCA);DATA(GSE51827,GSE86978)
Liver cancer	LncHDAC2	HDAC2	interact	RIP;western blot	upregulation	northern blot;microarray	GSE122420	NA	self-renewal(+);Hedgehog signaling pathway(+)	interact with protein	binding/interaction	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000196591	NA	NA	3066	NA	HD2|KDAC2|RPD3|YAF1	The long non-coding RNA LncHDAC2 drives the self-renewal of liver cancer stem cells via activation of Hedgehog signaling.Moreover, HDAC2 expression levels are positively related to HCC severity and PTCH1 levels are negatively related to HCC severity. Additionally, the Smo inhibitor cyclopamine was shown to impair the self-renewal of liver CSCs and suppress tumor propagation.LncHDAC2 is highly expressed in HCC tumors and liver CSCs. LncHDAC2 promotes the self-renewal of liver CSCs and tumor propagation.In liver CSCs, lncHDAC2 recruits the NuRD complex onto the promoter of PTCH1 to inhibit its expression, leading to activation of Hedgehog signaling.Our findings reveal that lncHDAC2 promotes the self-renewal of liver CSCs and tumor propagation by activating the Hedgehog signaling pathway.	30582981	RID05488	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	TP53COR1	SMOC1	positively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	tumor growth(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000198732	NA	102800311	64093	TRP53COR1|linc-p21|lincRNA-p21	OAS	lincRNA-p21 inhibits the progression of non-small cell lung cancer via targeting miR-17-5p. there was a significant low-expression of lincRNA-p21 in NSCLC tumor tissues, and lincRNA-p21 effectively inhibited the progression of lung cancer cells by suppressing cell proliferation and migration and promoting cell apoptosis. An evident negative association between lincRNA-p21 and miR-17-5p expression was observed, and the inhibitory effect of overexpressed lincRNA-p21 on lung cancer cells was counteracted by miR-17-5p. Bioinformatics and luciferase reporter analysis results confirmed that miR-17-5p is a direct targetfor lincRNA-p21. The present study provides evidence for lincRNA-p21 to inhibit the progression of NSCLC via direct targeting of a miR-17-5p associated signaling pathway. Nevertheless, miR-17 mimics were able to reverse the elevation in SMOC1 expression induced by lincRNA-p21 overexpression in the tumor tissue. These results demonstrated that lincRNA-p21 inhibited lung tumor growth via regulating SMOC1 in vivo.	30535441	RID05489	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	TP53COR1	BCL2	negatively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000171791	NA	102800311	596	TRP53COR1|linc-p21|lincRNA-p21	Bcl-2|PPP1R50	lincRNA-p21 inhibits the progression of non-small cell lung cancer via targeting miR-17-5p. there was a significant low-expression of lincRNA-p21 in NSCLC tumor tissues, and lincRNA-p21 effectively inhibited the progression of lung cancer cells by suppressing cell proliferation and migration and promoting cell apoptosis. Furthermore, the knockdown of si-lincRNA-p21 resulted in a significant increase in Bcl-2 and MMP9 levels compared with the NC group, whereas the addition of miR-17-5p inhibitors caused a reduction in the expression levels of Bcl-2 and MMP9 compared with that in the si-lincRNA-p21+miR-17-5p NC group. These results indicated that lincRNA-p21 affected lung cancer cells through altering the expression of Bcl-2 and MMP9.	30535441	RID05490	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	TP53COR1	MMP9	negatively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000100985	NA	102800311	4318	TRP53COR1|linc-p21|lincRNA-p21	CLG4B|GELB|MANDP2|MMP-9	lincRNA-p21 inhibits the progression of non-small cell lung cancer via targeting miR-17-5p. there was a significant low-expression of lincRNA-p21 in NSCLC tumor tissues, and lincRNA-p21 effectively inhibited the progression of lung cancer cells by suppressing cell proliferation and migration and promoting cell apoptosis. Furthermore, the knockdown of si-lincRNA-p21 resulted in a significant increase in Bcl-2 and MMP9 levels compared with the NC group, whereas the addition of miR-17-5p inhibitors caused a reduction in the expression levels of Bcl-2 and MMP9 compared with that in the si-lincRNA-p21+miR-17-5p NC group. These results indicated that lincRNA-p21 affected lung cancer cells through altering the expression of Bcl-2 and MMP9.	30535441	RID05491	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	GAS8-AS1	MLL1	interact	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000118058	NA	750	NA	C16orf3	NA	The long noncoding RNA GAS8-AS1 suppresses hepatocarcinogenesis by epigenetically activating the tumor suppressor GAS8.Moreover, we identified two GAS8-AS1-interacting proteins, mixed-lineage leukemia 1 (MLL1), a histone 3 Lys-4 (H3K4) methyltransferase, and its partner WD-40 repeat protein 5 (WDR5). RNA pull-down, ChIP, and RNA immunoprecipitation assays revealed that GAS8-AS1 is required for maintaining the GAS8 promoter in an open chromatin state by recruiting the MLL1/WDR5 complex and for enhancing RNA polymerase II activity and GAS8 transcription.We found that expression of GAS8-AS1 or GAS8 is significantly decreased in HCC tissues and is associated with a poor prognosis among HCC patients.Our results provide important insights into how lncRNA GAS8-AS1 suppresses HCC development and suggest potential strategies for treating patients with liver cancer.	30228180	RID05492	interact with protein	prognosis		
Hepatocellular carcinoma	GAS8-AS1	WDR5	interact	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000196363	NA	750	11091	C16orf3	CFAP89|SWD3	The long noncoding RNA GAS8-AS1 suppresses hepatocarcinogenesis by epigenetically activating the tumor suppressor GAS8.Moreover, we identified two GAS8-AS1-interacting proteins, mixed-lineage leukemia 1 (MLL1), a histone 3 Lys-4 (H3K4) methyltransferase, and its partner WD-40 repeat protein 5 (WDR5). RNA pull-down, ChIP, and RNA immunoprecipitation assays revealed that GAS8-AS1 is required for maintaining the GAS8 promoter in an open chromatin state by recruiting the MLL1/WDR5 complex and for enhancing RNA polymerase II activity and GAS8 transcription.We found that expression of GAS8-AS1 or GAS8 is significantly decreased in HCC tissues and is associated with a poor prognosis among HCC patients.Our results provide important insights into how lncRNA GAS8-AS1 suppresses HCC development and suggest potential strategies for treating patients with liver cancer.	30228180	RID05493	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	GAS8-AS1	GAS8	positively-E	siRNA;ChIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-);tumor growth(-)	histone modification	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000141013	NA	750	2622	C16orf3	DRC4|GAS11	The long noncoding RNA GAS8-AS1 suppresses hepatocarcinogenesis by epigenetically activating the tumor suppressor GAS8.Moreover, we identified two GAS8-AS1-interacting proteins, mixed-lineage leukemia 1 (MLL1), a histone 3 Lys-4 (H3K4) methyltransferase, and its partner WD-40 repeat protein 5 (WDR5). RNA pull-down, ChIP, and RNA immunoprecipitation assays revealed that GAS8-AS1 is required for maintaining the GAS8 promoter in an open chromatin state by recruiting the MLL1/WDR5 complex and for enhancing RNA polymerase II activity and GAS8 transcription.We found that expression of GAS8-AS1 or GAS8 is significantly decreased in HCC tissues and is associated with a poor prognosis among HCC patients.Our results provide important insights into how lncRNA GAS8-AS1 suppresses HCC development and suggest potential strategies for treating patients with liver cancer.LncRNA GAS8-AS1 recruits MLL1/WDR5 complex to modulate H3K4 methylation of GAS8 promoter and activates its expression. After knockdown expression of endogenous lncRNA GAS8-AS1, significantly reduced H3K4me3 at the GAS8 promoter was observed.LncRNA GAS8-AS1 and GAS8 inhibit HCC growth in vivo.	30228180	RID05494	epigenetic regulation	prognosis		DOWN(PRAD,PAAD);UP(BRCA);DATA(GSE104209,GSE60407,GSE109761,GSE111065)
Colorectal cancer	NEAT1	KRAS	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-193a-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000133703	NA	283131	3845	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	K-Ras4B|KRAS1|KRAS2	Knockdown long noncoding RNA nuclear paraspeckle assembly transcript 1 suppresses colorectal cancer through modulating miR-193a-3p/KRAS. As found, the expression level of NEAT1 increased in CRC samples in contrast with NAT samples. miR-193a-3p was reported as a target of NEAT1 through transfecting luciferase reporter plasmids of wild-type/mutant NEAT1-miR-193a-3p binding sites to 293T cell.KRAS acts as a target of miR-193a-3p.Knockdown NEAT1 circuitously modulate KRAS expression through miR-193a-3p both in vitro and in vivo. Generally, lncRNA NEAT1/hsa-miR-193a-3p/KRAS axis was substantiated in CRC cells and could provide novel insight into both diagnostic and therapeutic advancement in CRC.	30575330	RID05495	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Polycystic ovary syndrome	LINC-01572:28	CDKN1B	positively-E	siRNA;overexpression	upregulation	qRT-PCR;microarray	GSE114419	NA	cell proliferation(-);cell cycle(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	NA	NA	ENSG00000111276	NA	NA	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA LINC-01572:28 inhibits granulosa cell growth via a decrease in p27 (Kip1) degradation in patients with polycystic ovary syndrome.The expression levels of LINC-01572:28, lnc-EIF2B5-7-1, lnc-SIK2-1, lnc-CCNL1-3-1, and lnc-LYZL-9-1 were increased in patients with PCOS.We examined whether the overexpression of LINC-01572:28 affects the expression of these two factors. LINC-01572:28 had no effect on p21 (CDKN1A) mRNA and protein or p27 (CDKN1B) mRNA expression (Fig. 4A), but significantly induced an abundance of p27 protein in KGN and SVOG cells (Fig. 4B).These results suggest that LINC-01572:28 inhibits granulosa cell proliferation at least in part due to an increase in p27 protein abundance. RIP results showed a more significant enrichment of LINC-01572:28 using the SKP2 antibody compared with both the EZH2 antibody and the non-specific IgG control antibody.Our findings, therefore, suggest that LINC-01572:28 suppresses cell proliferation and cell cycle progression by reducing the degradation of p27 protein via SKP2 binding.	30293818	RID05496	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Polycystic ovary syndrome	LINC-01572:28	SKP2	interact	RIP	upregulation	qRT-PCR;microarray	GSE114419	NA	cell proliferation(-);cell cycle(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	NA	NA	ENSG00000145604	NA	NA	6502	NA	FBL1|FBXL1|FLB1|p45	siRNA;overexpression	30293818	RID05497	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	PTENP1	PTEN	positively-E	RNAi;bioinformatics analysis	downregulation	qRT-PCR	NA	NA	tumor growth(-);cancer progression(-)	ceRNA(miR-17)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	BZS|MHAM|MMAC1|PTEN1|TEP1	Exosome-transmitted long non-coding RNA PTENP1 suppresses bladder cancer progression.Furthermore, exosomal PTENP1 mediated the expression of PTEN by competitively binding to microRNA-17. PTENP1 was significantly reduced in BC tissues and in exosomes from plasma of patients with BC (P < 0.05).Normal cells secreted exosomal PTENP1 and transmitted it to BC cells, thus inhibiting the biological malignant behavior of BC cells by increasing cell apoptosis and reducing the ability to invade and migrate (P < 0.05). Exosomal PTENP1 could suppress tumor growth in vivo. Furthermore, exosomal PTENP1 mediated the expression of PTEN by competitively binding to microRNA-17.Exosomes derived from normal cells transfer PTENP1 to BC cells, which reduce the progression of BC both in vitro and in vivo and suggest that exosomal PTENP1 participates in normal-cell-to-bladder-cell communication during the carcinogenesis of BC.	30285771	RID05498	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	AFAP1-AS1	EGFR	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-146b-5p)	regulation	RNA-protein	Cucurbitacin B	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000146648	NA	84740	1956	AFAP1-AS|AFAP1AS|MGC10981	ERBB|ERBB1|ERRP	Cucurbitacin B suppresses proliferation of pancreatic cancer cells by ceRNA: Effect of miR-146b-5p and lncRNA-AFAP1-AS1.Insights into the mechanisms of competing endogenous RNAs (ceRNAs) gained from bioinformatics analysis and luciferase activity assays showed that the epidermal growth factor receptor (EGFR) and AFAP1-AS1 directly compete for miR-146b-5p binding. CuB-induced high miR-146b-5p expression and inhibited the expression of AFAP1-AS1. In summary, reducing the expression of endogenous AFAP1-AS1 effectively increased the available concentration of miR-146b-5p in PC, whereas miR-146b-5p overexpression prevented the expression of endogenous AFAP1-AS1.	30206930	RID05499	ceRNA or sponge	chemoresistance	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Triple-negative breast cancer	BORG	RPA1	interact	RNAi;mass-spectrometry	upregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	Doxorubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000132383	NA	NA	6117	NA	HSSB|REPA1|RF-A|RP-A|RPA70	The lncRNA BORG facilitates the survival and chemoresistance of triple-negative breast cancers;The chemoresistant traits of BORG depend upon its robust activation of the NF-kB signaling axis via a novel BORG-mediated feed-forward signaling loop, and via its ability to bind and activate RPA1. Indeed, genetic and pharmacologic inhibition of NF-kB signaling or the DNA-binding activity of RPA1 abrogates the pro-survival features of BORG and renders BORG-expressing TNBCs sensitive to doxorubicin-induced cytotoxicity.we identified the protein RPA1 as a strong binding partner of BORG in D2.OR cells.Taken together, these results establish RPA1 as an essential BORG-interacting molecule that participates in the acquisition of chemoresistant phenotypes by BORG.	30467380	RID05500	interact with protein	chemoresistance		UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE55807)
Malignant glioma	CASC9	STAT3	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	tumor growth(+);tumorigenesis(+)	ceRNA(miR-519d)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000168610	NA	101805492	6774	ESCCAL-1|linc-JPH1|LINC00981	APRF	Long noncoding RNA CASC9/miR-519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis.Results revealed that CASC9 expression was markedly overexpressed in the collected glioma tissue specimens compared with adjacent normal tissue. Mechanical studies revealed that miR-519d both targeted the 3'-UTR of CASC9 and STAT3 mRNA, which was identified by luciferase reporter assay and RNA immunoprecipitation (RIP).Functional studies found that siRNA-mediated CASC9 silencing inhibited the proliferative ability, invasion in vitro, and impaired the tumour growth in vivo.Moreover, chromatin immunoprecipitation (ChIP) and luciferase reporter assay revealed that STAT3, an oncogenic transcription factor, could bind with the promoter of CASC9 and activate its transcriptional level. In conclusion, our results concluded that CASC9 promotes STAT3 expression via sponging miR-519d, in return, STAT3 activate CASC9 transcription, forming a positive feedback loop of CASC9/miR-519d/STAT3. The novel finding provides a potential therapeutic target for glioma.	30270508	RID05501	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	STAT3	CASC9	positively-E	ChIP	upregulation	RT-PCR	NA	NA	tumor growth(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000168610	NA	ENSG00000249395	GRCh38_8:75120409-75352327	6774	101805492	APRF	ESCCAL-1|linc-JPH1|LINC00981	Long noncoding RNA CASC9/miR-519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis.Mechanical studies revealed that miR-519d both targeted the 3'-UTR of CASC9 and STAT3 mRNA, which was identified by luciferase reporter assay and RNA immunoprecipitation (RIP).Functional studies found that siRNA-mediated CASC9 silencing inhibited the proliferative ability, invasion in vitro, and impaired the tumour growth in vivo.Moreover, chromatin immunoprecipitation (ChIP) and luciferase reporter assay revealed that STAT3, an oncogenic transcription factor, could bind with the promoter of CASC9 and activate its transcriptional level. In conclusion, our results concluded that CASC9 promotes STAT3 expression via sponging miR-519d, in return, STAT3 activate CASC9 transcription, forming a positive feedback loop of CASC9/miR-519d/STAT3. The novel finding provides a potential therapeutic target for glioma.	30270508	RID05502	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)
Non-small cell lung cancer	HAND2-AS1	TGFB1	negatively-E	overexpression;correlation analysis	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell stemness(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000105329	NA	79804	7040	DEIN|NBLA00301|UPH	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA HAND2-AS1 inhibits non-small cell lung cancer migration, invasion and maintains cell stemness through the interactions with TGF-beta1. In our study, we observed that levels of HAND2-AS1 were lower in tumor tissues than that in adjacent healthy tissues. A significant negative correlation between plasma levels of HAND2-AS1 and TGF-beta1 was found in NSCLC patients but not in healthy controls. LncRNA HAND2-AS1 overexpression inhibits, while exogenous TGF-beta1 treatment promotes cell migration and invasion ability and cancer cell stemness. Cancer cells with lncRNA HAND2-AS1 overexpression showed down-regulated TGF-beta1, while TGF-beta1 treatment showed no significant effects on lncRNA HAND2-AS1 expression. TGF-beta1 attenuated the inhibitory effects of lncRNA HAND2-AS1 overexpression on cell migration, invasion and stemness. We concluded that lncRNA HAND2-AS1 may regulate the migration, invasion and stemness of NSCLC cells through interactions with TGF-beta1.	30509963	RID05503	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	RUNX1-IT1	PCNA	positively-E	siRNA;overexpression;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000132646	NA	80215	5111	C21orf96	NA	Long non-coding RNA RUNX1-IT1 plays a tumour-suppressive role in colorectal cancer by inhibiting cell proliferation and migration.In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis.The proliferation markers (PCNA, Ki67), apoptosis markers (cleaved-PARP, cleaved-caspase3), and MMP9 are detected by western blot.Moreover, the proliferative and migration potential of CRC cells were inhibited by overexpressing lncRNA RUNX1-IT1, which could be obviously improved by knocking down lncRNA RUNX1-IT1. The protein levels of PCNA, Ki67, and MMP9 were upregulated by overexpressing lncRNA RUNX1-IT1 and down regulated in si-RUNX1-IT1 cells. Besides, lncRNA RUNX1-IT1 could also promote the apoptosis of CRC cells. In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis. SIGNIFICANCE OF THE STUDY: We demonstrated that lncRNA RUNX1-IT1 was down regulated both in CRC tissues and cell lines. Besides, lncRNA RUNX1-IT1 could serve as a potential diagnostic biomarker and play a tumour-suppressive role owing to its good diagnostic efficacy and inhibition of CRC cell proliferation and migration.	30499136	RID05504	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Colorectal cancer	RUNX1-IT1	Ki67	positively-E	siRNA;overexpression;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	NA	NA	80215	NA	C21orf96	NA	Long non-coding RNA RUNX1-IT1 plays a tumour-suppressive role in colorectal cancer by inhibiting cell proliferation and migration.In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis.The proliferation markers (PCNA, Ki67), apoptosis markers (cleaved-PARP, cleaved-caspase3), and MMP9 are detected by western blot.Moreover, the proliferative and migration potential of CRC cells were inhibited by overexpressing lncRNA RUNX1-IT1, which could be obviously improved by knocking down lncRNA RUNX1-IT1. The protein levels of PCNA, Ki67, and MMP9 were upregulated by overexpressing lncRNA RUNX1-IT1 and down regulated in si-RUNX1-IT1 cells. Besides, lncRNA RUNX1-IT1 could also promote the apoptosis of CRC cells. In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis. SIGNIFICANCE OF THE STUDY: We demonstrated that lncRNA RUNX1-IT1 was down regulated both in CRC tissues and cell lines. Besides, lncRNA RUNX1-IT1 could serve as a potential diagnostic biomarker and play a tumour-suppressive role owing to its good diagnostic efficacy and inhibition of CRC cell proliferation and migration.	30499136	RID05505	expression association	NA		
Colorectal cancer	RUNX1-IT1	MMP9	positively-E	siRNA;overexpression;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000100985	NA	80215	4318	C21orf96	CLG4B	Long non-coding RNA RUNX1-IT1 plays a tumour-suppressive role in colorectal cancer by inhibiting cell proliferation and migration.In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis.The proliferation markers (PCNA, Ki67), apoptosis markers (cleaved-PARP, cleaved-caspase3), and MMP9 are detected by western blot.Moreover, the proliferative and migration potential of CRC cells were inhibited by overexpressing lncRNA RUNX1-IT1, which could be obviously improved by knocking down lncRNA RUNX1-IT1. The protein levels of PCNA, Ki67, and MMP9 were upregulated by overexpressing lncRNA RUNX1-IT1 and down regulated in si-RUNX1-IT1 cells. Besides, lncRNA RUNX1-IT1 could also promote the apoptosis of CRC cells. In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis. SIGNIFICANCE OF THE STUDY: We demonstrated that lncRNA RUNX1-IT1 was down regulated both in CRC tissues and cell lines. Besides, lncRNA RUNX1-IT1 could serve as a potential diagnostic biomarker and play a tumour-suppressive role owing to its good diagnostic efficacy and inhibition of CRC cell proliferation and migration.	30499136	RID05506	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	NNT-AS1	CTNNB1	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000168036	NA	100652772	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05507	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	NNT-AS1	RUNX2	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000124813	NA	100652772	860	RP11-159F24.1	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05508	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	NNT-AS1	IGF1R	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000140443	NA	100652772	3480	NA	CD221|IGFIR|IGFR|JTK13	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05509	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Osteosarcoma	NNT-AS1	MYC	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000136997	NA	100652772	4609	RP11-159F24.1	bHLHe39|c-Myc|MYCC	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05510	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Osteosarcoma	NNT-AS1	Cyclin D1	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	NA	NA	100652772	NA	NA	NA	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05511	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Osteosarcoma	NNT-AS1	MMP13	positively-E	overexpression;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000137745	NA	100652772	4322	RP11-159F24.1	CLG3	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.	30489194	RID05512	expression association	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	UP(PAAD);DATA(GSE40174)
Osteosarcoma	NNT-AS1	miR-320a	interact;negatively-F	DIANA-LncBase V2	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell survival(+);cell motility(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	NA	NA	100652772	NA	RP11-159F24.1	NA	Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a. Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo.NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.Our preliminary research using DIANA-LncBase V2 found that NNT-AS1 might promote cancer development by sponging miR-320a and other miR-320 family miRNAs.	30489194	RID05513	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Hepatocellular carcinoma	LINC00707	CDK14	positively-E	shRNA;dual-luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000058091	NA	100507127	5218	NA	PFTAIRE1|PFTK1	LINC00707 contributes to hepatocellular carcinoma progression via sponging miR-206 to increase CDK14.Subsequently, LINC00707 was significantly decreased in HepG2 and Huh7 cells. The in vitro functional assays demonstrated that knockdown of LINC00707 significantly reduced HCC cell proliferation, induced cell apoptosis, and blocked the cell cycle progression. In addition, HCC cell migration and invasion was also greatly inhibited by downregulation of LINC00707.The binding correlation between LINC00707 and miR-206 was confirmed by dual-luciferase reporter assay, RNA pull down and RNA immunoprecipitation assay in our study.Finally, in vivo assays were used and it was proved that silence of LINC00707 can restrain HCC development through modulating miR-206 to upregulate CDK14.	30488589	RID05514	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Osteosarcoma	FER1L4	PTEN	positively-E	starBase v2.0;dual-luciferase reporter assay;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration;(-);cell invasion(-);cell growth(-)	ceRNA(miR-18a-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	bA563A22B.1|C20orf124|dJ309K20.1	BZS|MHAM|MMAC1|PTEN1|TEP1	Long Noncoding RNA FER1L4 Suppresses tumorigenesis by Regulating the Expression of PTEN Targeting miR-18a-5p in Osteosarcoma.We found that the expression of FER1L4 was significantly downregulated in OS tissues and cell lines; moreover, low expression of FER1L4 was associated with advanced tumor-nude-metastasis (TNM) stage, lymph node metastases, and poor overall survival. Functional assays showed that upregulation of FER1L4 significantly inhibited OS cell proliferation, colony formation, migration, and invasion in vitro, as well as suppressed tumor growth in vivo. Assays performed to determine the underlying mechanism, indicated that FER1L4 interacted directly with miR-18a-5p. Subsequently, we found that FER1L4 significantly increased PTEN expression, a known target of miR-18a-5p, in OS cells. Furthermore, PTEN was found to be down-regulated, and positively correlated with FER1L4 in OS tissues.	30481787	RID05515	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic ductal adenocarcinoma	H19	CDK14	positively-E	RIP;luciferase reporter	upregulation	sequencing;qPCR	TCGA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-194)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000058091	NA	283120	5218	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PFTAIRE1|PFTK1	LncRNA H19/miR-194/PFTK1 axis modulates the cell proliferation and migration of pancreatic cancer.In the current study, upregulated lncRNAs positively correlated with PFTK1 were analyzed and selected using The Cancer Genome Atlas (TCGA) database. Of them, lncRNA H19 can activate Wnt signaling in cancers. In PDAC tissues, the expression of H19 and PFTK1 were upregulated; H19 knockdown suppressed the cell proliferation and migration of PDAC, while PFTK1 overexpression partially attenuated the suppressive effect of H19 knockdown. As analyzed by TCGA and predicted by online tools, miR-194 was negatively correlated with PFTK1 and might bind to both H19 and PFTK1, which was further confirmed by luciferase reporter and RNA immunoprecipitation assays. Moreover, the effect of H19 knockdown on PFTK1 protein and the cell proliferation and migration could be partially reversed by miR-194 inhibition; H19/miR-194 axis modulated PDAC cell proliferation and migration through PFTK1 downstream Wnt signaling. Results suggested that rescuing miR-194 expression in PDAC can inhibit lncRNA H19 and PFTK1 expression, subsequently suppressing PDAC cell proliferation and migration. Due to the complexity of the lncRNA-miRNA-mRNA network, further in vivo experiments examining potential side effects are needed in future study to explore the clinical application of these findings.	30474270	RID05516	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	ANKRD40CL	FMNL2	positively-E	luciferase reporter assay;siRNA;overexpression	upregulation	microarray;qRT-PCR	GSE84983	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-204-3p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000157827	NA	55018	114793	C17orf73|FLJ20694|LINC00483	FHOD2|KIAA1902	A novel long noncoding RNA, LINC00483 promotes proliferation and metastasis via modulating of FMNL2 in CRC be found a novel lncRNA, long intergenic non-protein coding RNA 483 (LINC00483), which was upregulated in CRC. Through a luciferase assay, we showed the direct binding effect between LINC00483 and miR-204-3p. Even further, we revealed that LINC00483 and formin like 2 (FMNL2) shared a similar miR-204-3p response elements (MREs-204-3p). FMNL2 was a direct target of miR-204-3p. FMNL2 was a downstream gene of LINC00483 and participated in LINC00483 mediated proliferation and metastasis. ;the outcomes of this study illustrated that LINC00483 promoted CRC cells proliferation and metastasis via modulating of FMNL2 by acting as a ceRNA of miR-204-3p.	30594388	RID05517	ceRNA or sponge	metastasis		UP(LIHC,PAAD,SKCM);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	HULC	MIR15A	negatively-E	siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000251164	NA	ENSG00000283785	NA	728655	406948	HCCAT1|LINC00078|NCRNA00078	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Long non-coding RNA HULC promotes proliferation, migration and invasion of pancreatic cancer cells by down-regulating microRNA-15a overexpression of HULC promoted the proliferation, migration and invasion of Panc-1 cells. Suppression of HULC had opposite effects and dramatically induced cell apoptosis. Moreover, HULC negatively regulated the expression of miR-15a in Panc-1 cells;HULC exerted oncogenic role in pancreatic cancer. Overexpression of HULC promoted the proliferation, migration and invasion of pancreatic cancer cells by down-regulating miR-15a and then activating PI3K/AKT pathway.	30593805	RID05518	expression association	NA		
Osteosarcoma	SNHG1	ROCK1	negatively-E	dual-luciferase reporter assay;siRNA;miRDB	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(-);epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000067900	NA	23642	6093	LINC00057|lncRNA16|NCRNA00057|UHG	p160ROCK	lncRNA SNHG1 negatively regulates miRNA-101-3p to enhance the expression of ROCK1 and promote cell proliferation, migration and invasion in osteosarcoma;lncRNA SNHG1 was upregulated and miRNA-101-3p was downregulated in OS tissues and cell lines. miRNA-101-3p was found to be a target of the lncRNA SNHG1 in OS, which further regulated the expression of Rho-associated coiled-coil-containing protein kinase 1 (ROCK1);It was found that the phosphoinositide 3-kinase/ATK pathway was inactivated and that epithelial-mesenchymal transition was activated in OS cell lines with overexpression of the lncRNA SNHG1;The lncRNA SNHG1 promoted OS cell proliferation, migration and invasion by downregulating the expression of miRNA-101-3p, which enhanced the expression of ROCK1.Phosphoinositide 3-kinase (PI3K)/AKT pathway is activated and EMT is induced.Overexpression of miR-101-3p inhibited the PI3K/AKT pathway via the downregulation of ROCK1.	30592267	RID05519	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	MYC	LINC00319	positively-E	ChIP;shRNA	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	TF	lncRNA	ENSG00000136997	NA	ENSG00000188660	GRCh38_21:43446601-43453902	4609	284836	bHLHe39|c-Myc|MYCC	C21orf125|FLJ38036|NCRNA00319|PRED49	MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6;Firstly, the low expression level of LINC00319 in whole blood of healthy individuals was obtained from UCSC, and its upregulation was detected in AML patients as well as AML cell lines. LINC00319 expression was demonstrated proportional to MYC level in AML samples and transcriptionally regulated by MYC; Mechanistically, we identified FUS as a shared RNA binding protein (RBP) interacting with both LINC00319 and SIRT6. And LINC00319 regulated SIRT6 expression at post-transcriptional level through FUS-dependent pathway. our findings unveiled that LINC00319 contributed to AML leukemogenesis via elevating SIRT6 expression, indicating a possible molecular target of LINC00319 for AML treatment.	30587342	RID05520	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Acute myeloid leukemia	LINC00319	SIRT6	positively-E;interact	shRNA;starBase  2.0;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	RNA stability;interact with mRNA	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000077463	NA	284836	51548	C21orf125|FLJ38036|NCRNA00319|PRED49	NA	MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6;Firstly, the low expression level of LINC00319 in whole blood of healthy individuals was obtained from UCSC, and its upregulation was detected in AML patients as well as AML cell lines. LINC00319 expression was demonstrated proportional to MYC level in AML samples and transcriptionally regulated by MYC; Mechanistically, we identified FUS as a shared RNA binding protein (RBP) interacting with both LINC00319 and SIRT6. And LINC00319 regulated SIRT6 expression at post-transcriptional level through FUS-dependent pathway. our findings unveiled that LINC00319 contributed to AML leukemogenesis via elevating SIRT6 expression, indicating a possible molecular target of LINC00319 for AML treatment.	30587342	RID05521	interact with mRNA	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	LINC00319	FUS	interact	shRNA;starBase  2.0;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000089280	NA	284836	2521	C21orf125|FLJ38036|NCRNA00319|PRED49	ALS6|FUS1|hnRNP-P2|HNRNPP2|TLS	MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6;Firstly, the low expression level of LINC00319 in whole blood of healthy individuals was obtained from UCSC, and its upregulation was detected in AML patients as well as AML cell lines. LINC00319 expression was demonstrated proportional to MYC level in AML samples and transcriptionally regulated by MYC; Mechanistically, we identified FUS as a shared RNA binding protein (RBP) interacting with both LINC00319 and SIRT6. And LINC00319 regulated SIRT6 expression at post-transcriptional level through FUS-dependent pathway. our findings unveiled that LINC00319 contributed to AML leukemogenesis via elevating SIRT6 expression, indicating a possible molecular target of LINC00319 for AML treatment.	30587342	RID05522	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	PCAT1	LRIG2	positively-E	luciferase reporter assay;RIP;shRNA	upregulation	qRT-PCR	NA	NA	cell growth(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-149-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000198799	NA	100750225	9860	PCA1|PCAT-1|PiHL	KIAA0806	LncRNA-PCAT-1 promotes non-small cell lung cancer progression by regulating miR-149-5p/LRIG2 axis;we also found that the knockdown of PCAT-1 remarkably suppressed cell growth by inducing cell cycle arrest and apoptosis promotion in NSCLC cells. Moreover, the bioinformatics analysis and luciferase reporter assay revealed that PCAT-1 directly bound to the miR-149-5p, which has been reported to act as a tumor suppressor in diverse cancers. In addition, our results confirmed that the tumor-promoting effects of PCAT-1 in NSCLC cells are at least partly through negative modulation of miR-149-5p. Finally, mechanistic investigations showed that PCAT-1 upregulated the expression of miR-149-5p target gene leucine-rich repeats and immunoglobulin (Ig)-like domains 2 (LRIG2) through competitively "spongeing" miR-149-5p. Therefore, we concluded that PCAT-1 may promote the development of NSCLC through the miR-149-5p/LRIG2 axis.	30569478	RID05523	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	IRF4	SOX2-OT	positively-E	luciferase reporter assay;JASPAR;ChIP	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	TF	lncRNA	ENSG00000137265	NA	ENSG00000242808	GRCh38_3:180989762-181836880	3662	347689	LSIRF|MUM1	DKFZp761J1324|NCRNA00043|SOX2OT	IRF4-induced upregulation of lncRNA SOX2-OT promotes cell proliferation and metastasis in cholangiocarcinoma by regulating SOX2 and PI3K/AKT signaling;The expression level of lncRNA SOX2-OT was significantly upregulated in cholangiocarcinoma tissues. Functional assays were further conducted to prove the oncogenic role of SOX2-OT on the proliferation and metastasis of cholangiocarcinoma cells. Furthermore, mechanism investigations manifested that transcription factor IRF4 upregulates SOX2-OT by promoting the transcriptional activity of SOX2-OT. SOX2-OT could positively regulate the nearby gene SOX2. SOX2-OT suppressed the nuclear transcription of PTEN, thereby activating PI3K/AKT signaling. lncRNA SOX2-OT upregulated by IRF4 promotes cell proliferation and metastasis in cholangiocarcinoma via upregulating SOX2 and activating PI3K/AKT signaling pathway.	30556855	RID05524	transcriptional regulation	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Cholangiocarcinoma	SOX2-OT	SOX2	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	IRF4-induced upregulation of lncRNA SOX2-OT promotes cell proliferation and metastasis in cholangiocarcinoma by regulating SOX2 and PI3K/AKT signaling;The expression level of lncRNA SOX2-OT was significantly upregulated in cholangiocarcinoma tissues. Functional assays were further conducted to prove the oncogenic role of SOX2-OT on the proliferation and metastasis of cholangiocarcinoma cells. Furthermore, mechanism investigations manifested that transcription factor IRF4 upregulates SOX2-OT by promoting the transcriptional activity of SOX2-OT. SOX2-OT could positively regulate the nearby gene SOX2. SOX2-OT suppressed the nuclear transcription of PTEN, thereby activating PI3K/AKT signaling. lncRNA SOX2-OT upregulated by IRF4 promotes cell proliferation and metastasis in cholangiocarcinoma via upregulating SOX2 and activating PI3K/AKT signaling pathway. The  positive  correla-tion  between  SOX2-OT expression and SOX2 expression in CCA tissues was then analyzed by the Spearman's correlation analysis.	30556855	RID05525	expression association	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Cholangiocarcinoma	SOX2-OT	PTEN	negatively-E	overexpression	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000171862	NA	347689	5728	DKFZp761J1324|NCRNA00043|SOX2OT	BZS|MHAM|MMAC1|PTEN1|TEP1	IRF4-induced upregulation of lncRNA SOX2-OT promotes cell proliferation and metastasis in cholangiocarcinoma by regulating SOX2 and PI3K/AKT signaling;The expression level of lncRNA SOX2-OT was significantly upregulated in cholangiocarcinoma tissues. Functional assays were further conducted to prove the oncogenic role of SOX2-OT on the proliferation and metastasis of cholangiocarcinoma cells. Furthermore, mechanism investigations manifested that transcription factor IRF4 upregulates SOX2-OT by promoting the transcriptional activity of SOX2-OT. SOX2-OT could positively regulate the nearby gene SOX2. SOX2-OT suppressed the nuclear transcription of PTEN, thereby activating PI3K/AKT signaling. lncRNA SOX2-OT upregulated by IRF4 promotes cell proliferation and metastasis in cholangiocarcinoma via upregulating SOX2 and activating PI3K/AKT signaling pathway.	30556855	RID05526	expression association	metastasis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Nasopharynx carcinoma	DANCR	ILF3	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR;microarray	GSE89804	NA	cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000129351	NA	57291	3609	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	Long non-coding RNA DANCR stabilizes HIF-1a and promotes metastasis by interacting with NF90/NF45 complex in nasopharyngeal carcinoma;Here, we found that DANCR was upregulated in NPC, especially in those with lymph lode metastasis, and its upregulation could predict poor survival.DANCR could increase HIF-1a mRNA stability through interacting with the NF90/NF45 complex;overexpression of HIF-1a in DANCR knockdown cells restored its suppressive effects on NPC cell migration and invasion.Taken together, our results suggest that DANCR acts as a prognostic biomarker and increases HIF-1a mRNA stability by interacting with NF90/NF45, leading to metastasis and disease progression of NPC.	30555573	RID05527	interact with protein	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	DANCR	ILF2	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR;microarray	GSE89805	NA	cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000143621	NA	57291	3608	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NF45	Long non-coding RNA DANCR stabilizes HIF-1a and promotes metastasis by interacting with NF90/NF45 complex in nasopharyngeal carcinoma;Here, we found that DANCR was upregulated in NPC, especially in those with lymph lode metastasis, and its upregulation could predict poor survival.DANCR could increase HIF-1a mRNA stability through interacting with the NF90/NF45 complex;overexpression of HIF-1a in DANCR knockdown cells restored its suppressive effects on NPC cell migration and invasion.Taken together, our results suggest that DANCR acts as a prognostic biomarker and increases HIF-1a mRNA stability by interacting with NF90/NF45, leading to metastasis and disease progression of NPC.	30555573	RID05528	interact with protein	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Nasopharynx carcinoma	DANCR	HIF1A	positively-E;interact	siRNA;shRNA;RIP;RNA pull-down assay	upregulation	qRT-PCR;microarray	GSE89806	NA	cell metastasis(+);cancer progression(+)	RNA stability;interact with mRNA	binding/interaction	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000100644	NA	57291	3091	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA DANCR stabilizes HIF-1a and promotes metastasis by interacting with NF90/NF45 complex in nasopharyngeal carcinoma;Here, we found that DANCR was upregulated in NPC, especially in those with lymph lode metastasis, and its upregulation could predict poor survival.DANCR could increase HIF-1a mRNA stability through interacting with the NF90/NF45 complex;overexpression of HIF-1a in DANCR knockdown cells restored its suppressive effects on NPC cell migration and invasion.Taken together, our results suggest that DANCR acts as a prognostic biomarker and increases HIF-1a mRNA stability by interacting with NF90/NF45, leading to metastasis and disease progression of NPC. Actually, a substantial subset of genes involved in hypoxia pathways were dysregulated after DANCR knockdown, including HIF-1a. we firstly did quantitative RT-PCRand western blot assays, and found that both the mRNA and protein of HIF-1a were obviously decreased in HONE1 and SUNE1 cells after knockdown of DANCR under hypoxic environment.	30555573	RID05529	interact with mRNA	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Malignant glioma	FOXD2-AS1	AKT1	positively-E	dual-luciferase reporter assay;overexpression;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-185)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000142208	NA	84793	207	MGC12982	AKT|PKB|PRKBA|RAC|RAC-alpha	Long noncoding FOXD2-AS1 is activated by CREB1 and promotes cell proliferation and metastasis in glioma by sponging miR-185 through targeting AKT1;luciferase reporter indicated that CREB1 could bind directly to FOXD2-AS1 promoter region and activate its transcription. Functional investigations revealed that knockdown of FOXD2-AS1 significantly suppressed glioma cells proliferation, migration, invasion and EMT, and promoted apoptosis;FOXD2-AS1 may act as an endogenous sponge by competing for miR-185, thereby regulating the targets of this miRNA;our data firstly demonstrated that CREB1-induced FOXD2-AS1 contributed to glioma progression by upregulating AKT1 via competitively binding to miR-185.LncRNA FOXD2-AS1 promoted glioma cells proliferation, migration and invasion through miR-185/AKT1 axis.	30553445	RID05530	ceRNA or sponge	metastasis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	CREB1	FOXD2-AS1	positively-E	ChIP;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000118260	NA	ENSG00000237424	GRCh38_1:47432133-47434641	1385	84793	NA	MGC12982	Long noncoding FOXD2-AS1 is activated by CREB1 and promotes cell proliferation and metastasis in glioma by sponging miR-185 through targeting AKT1;luciferase reporter indicated that CREB1 could bind directly to FOXD2-AS1 promoter region and activate its transcription. Functional investigations revealed that knockdown of FOXD2-AS1 significantly suppressed glioma cells proliferation, migration, invasion and EMT, and promoted apoptosis;FOXD2-AS1 may act as an endogenous sponge by competing for miR-185, thereby regulating the targets of this miRNA;our data firstly demonstrated that CREB1-induced FOXD2-AS1 contributed to glioma progression by upregulating AKT1 via competitively binding to miR-185.LncRNA FOXD2-AS1 promoted glioma cells proliferation, migration and invasion through miR-185/AKT1 axis.	30553445	RID05531	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)
Osteosarcoma	ELK1	MIR100HG	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	Hippo signaling pathway(-);cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000126767	NA	ENSG00000255248	GRCh38_11:122028325-122556721	2002	399959	NA	AGD1|linc-NeD125|lncRNA-N2	ELK1-induced upregulation of long non-coding RNA  predicts poor prognosis and promotes the progression of osteosarcoma by epigenetically silencing LATS1 and LATS2; At first, we measured the high expression of MIR100HG in OS tissues and cell lines by qRT-PCR Functionally, MIR100HG knockdown suppressed cell proliferation, cell cycle progression while promoted cell apoptosis. Mechanistically, MIR100HG was upregulated by the transcription factor ELK1. The upregulation of MIR100HG led to the inactivation of Hippo pathway. Furthermore, we found that MIR100HG inactivated Hippo pathway in OS cells by epigenetically silencing LATS1 and LATS2. MIR100HG was overexpressed in OS tissues and cell lines andpredicted poor prognosis in OS patients.	30551532	RID05532	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)
Osteosarcoma	MIR100HG	LATS1	negatively-F	ChIP;luciferase reporter assay;shRNA;overexpression	upregulation	qRT-PCR	NA	NA	Hippo signaling pathway(-);cancer progression(+)	histone modification	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000131023	NA	399959	9113	AGD1|linc-NeD125|lncRNA-N2	WARTS	ELK1-induced upregulation of long non-coding RNA  predicts poor prognosis and promotes the progression of osteosarcoma by epigenetically silencing LATS1 and LATS2;MIR100HG inactivated Hippo pathway in OS cells by epigenetically silencing LATS1 and LATS2. Rescue assays demonstrated that LATS1/2 involved in MIR100HG-mediated OS progression;ELK1-induced upregulation of MIR100HG promoted OS progression by epigenetically silencing LATS1 and LATS2 and inactivating Hippo pathway.ChIP assay was applied toanalyze the regulatory mechanism among MIR100HG, EZH2 and LATS1/2. The results obviously showed that silenced MIR100HG inhibited the binding ability of EZH2 to LATS1/2 promoter region(P = 0.019, P = 0.015) and mediated the demethylation of H3K27me3.MIR100HG was overexpressed in OS tissues and cell lines andpredicted poor prognosis in OS patients.	30551532	RID05533	epigenetic regulation	prognosis	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	MIR100HG	LATS2	negatively-F	ChIP;luciferase reporter assay;shRNA;overexpression	upregulation	qRT-PCR	NA	NA	Hippo signaling pathway(-);cancer progression(+)	histone modification	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000150457	NA	399959	26524	AGD1|linc-NeD125|lncRNA-N2	NA	ELK1-induced upregulation of long non-coding RNA  predicts poor prognosis and promotes the progression of osteosarcoma by epigenetically silencing LATS1 and LATS2;MIR100HG inactivated Hippo pathway in OS cells by epigenetically silencing LATS1 and LATS2. Rescue assays demonstrated that LATS1/2 involved in MIR100HG-mediated OS progression;ELK1-induced upregulation of MIR100HG promoted OS progression by epigenetically silencing LATS1 and LATS2 and inactivating Hippo pathway.ChIP assay was applied toanalyze the regulatory mechanism among MIR100HG, EZH2 and LATS1/2. The results obviously showed that silenced MIR100HG inhibited the binding ability of EZH2 to LATS1/2 promoter region(P = 0.019, P = 0.015) and mediated the demethylation of H3K27me3	30551532	RID05534	epigenetic regulation	prognosis	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Osteosarcoma	MIR100HG	EZH2	interact	RIP	upregulation	qRT-PCR	NA	NA	Hippo signaling pathway(-);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000106462	NA	399959	2146	AGD1|linc-NeD125|lncRNA-N2	ENX-1|EZH1|KMT6|KMT6A	ELK1-induced upregulation of long non-coding RNA  predicts poor prognosis and promotes the progression of osteosarcoma by epigenetically silencing LATS1 and LATS2; Results of RIP assay validated the interaction between MIR100HG and EZH2 inMG-63 (P = 0.004) and 143B (P = 0.004) cells. Taken together, we confirmed that ELK1-induced upregulation of MIR100HG epigenetically silenced LATS1/2 by binding with EZH2. MIR100HG was overexpressed in OS tissues and cell lines andpredicted poor prognosis in OS patients	30551532	RID05535	interact with protein	prognosis	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	circPVT1	E2F2	positively-E	luciferase reporter assay;RIP;siRNA;miRanda	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);E2F2 signaling pathway(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	circRNA	TF	NA	NA	ENSG00000007968	NA	NA	1870	NA	E2F-2	Circular RNA circPVT1 Promotes Proliferation and Invasion Through Sponging miR-125b and Activating E2F2 Signaling in Non-Small Cell Lung Cancer;We found that circPVT1 was upregulated in NSCLC specimens and cells. The transcription factor c-Fos binded to the promoter region of circPVT1, resulting in the overexpression of circPVT1 in NSCLC. Knockdown of circPVT1 suppressed NSCLC cell proliferation, migration and invasion, and increased apoptosis. In addition, circPVT1 mediated NSCLC progression via the regulation of E2F2 signaling pathway. More importantly, circPVT1 was predominantly abundant in the cytoplasm of NSCLC cells, and circPVT1 could serve as a competing endogenous RNA to regulate E2F2 expression and tumorigenesis in a miR-125b-dependent manner, which is further verified by using an in vivo xenograft model. CircPVT1 mediates tumorigenesis through sponging miR-125b and upregulating E2F2 in vivo.	30537738	RID05536	ceRNA or sponge	NA		UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Non-small cell lung cancer	FOS	circPVT1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);E2F2 signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	circRNA	ENSG00000170345	NA	NA	NA	2353	NA	AP-1|c-fos	NA	Circular RNA circPVT1 Promotes Proliferation and Invasion Through Sponging miR-125b and Activating E2F2 Signaling in Non-Small Cell Lung Cancer;We found that circPVT1 was upregulated in NSCLC specimens and cells. The transcription factor c-Fos binded to the promoter region of circPVT1, resulting in the overexpression of circPVT1 in NSCLC. Knockdown of circPVT1 suppressed NSCLC cell proliferation, migration and invasion, and increased apoptosis. In addition, circPVT1 mediated NSCLC progression via the regulation of E2F2 signaling pathway. More importantly, circPVT1 was predominantly abundant in the cytoplasm of NSCLC cells, and circPVT1 could serve as a competing endogenous RNA to regulate E2F2 expression and tumorigenesis in a miR-125b-dependent manner, which is further verified by using an in vivo xenograft model.	30537738	RID05537	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Hepatocellular carcinoma	P5848	ENO1	positively-E	siRNA;luciferase reporter assay;immune-fluorescence assay	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell survival(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000074800	NA	NA	2023	NA	ENO1L1|MBP-1|MPB1|PPH	Targetting an LncRNA P5848-ENO1 axis inhibits tumor growth in hepatocellular carcinoma.Here we showed that LncRNA P5848, whose up-regulation can lead to HCC cancer cell proliferation and migration. we have found that ENO1 was the target of LncRNA P5848. LncRNA P5848 up-regulated the gene and protein expression level of ENO1, promoting tumor growth and cell survival.Mechanistically, we have found that ENO1 was the target of LncRNA P5848. LncRNA P5848 up-regulated the gene and protein expression level of ENO1, promoting tumor growth and cell survival. However, siRNA-mediated knockdown of ENO1 counteracted the effects of LncRNA P5848 on cancer cell growth, cell survival, and migration. Taken together, LncRNA P5848 promotes HCC development by up-regulating ENO1, indicating that LncRNA P5848-ENO1 axis is a potential therapeutic target for the treatment of HCC.	30541900	RID05538	transcriptional regulation	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	ABHD11-AS1	WNT11	positively-E	siRNA;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-1254)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000085741	NA	171022	7481	LINC00035|NCRNA00035|WBSCR26	NA	Long noncoding RNA ABHD11-AS1 promote cells proliferation and invasion of colorectal cancer via regulating the miR-1254-WNT11 pathway.In the study, we found that ABHD11-AS1 was highly expressed in CRC tissues and cell lines. High ABHD11-AS1 expression was correlated with poor overall survival of patients with CRC. ABHD11-AS1 knockdown reduced CRC cell proliferation, in vitro invasion, and in vivo tumor growth. Investigation of the underlying mechanism showed that ABHD11-AS1 could act as a molecular sponge of miR-1254, and WNT11 was a downstream target of miR-1254 in CRC. Moreover, there was a negative association between ABHD11-AS1 expression (or WNT11) and miR-1254 in CRC tissues. The rescue assays showed that WNT11 overexpression partially rescued the effects of ABHD11-AS1 inhibition on CRC progression. Thus, we demonstrated that ABHD11-AS1 promotes CRC progression through the miR-1254-WNT11 pathway, which provides a new insight into the therapeutic strategies for CRC.	30537177	RID05539	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC);DATA(GSE117623)
Renal cell carcinoma	LNCRNA-ATB	DNMT1	interact	RIP;ChIP;siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	interact with protein;protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000130816	NA	114004396	1786	NA	CXXC9|DNMT|MCMT	Long noncoding RNA ATB participates in the development of renal cell carcinoma by downregulating p53 via binding to DNMT1.Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and migration-related assays were conducted to access the regulatory effects of lncRNA ATB on proliferative and migratory capacities of RCC cells. RIP and ChIP assays confirmed that lncRNA ATB can bind to DNMT1 and stabilize its expression; meanwhile, it can promote the binding of DNMT1 to p53. our study revealed that high expression of lncRNA ATB could accelerate the proliferative and migratory rates of RCC cells and inhibit cell apoptosis through downregulating p53 via binding to DNMT1. The ChIP assaydemonstrated that DNMT1 could bind to the DNA in the p53 promoterregion.	30536843	RID05540	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Renal cell carcinoma	LNCRNA-ATB	TP53	negatively-E	ChIP;siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	114004396	7157	NA	LFS1|p53	Long noncoding RNA ATB participates in the development of renal cell carcinoma by downregulating p53 via binding to DNMT1.Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and migration-related assays were conducted to access the regulatory effects of lncRNA ATB on proliferative and migratory capacities of RCC cells. RIP and ChIP assays confirmed that lncRNA ATB can bind to DNMT1 and stabilize its expression; meanwhile, it can promote the binding of DNMT1 to p53. our study revealed that high expression of lncRNA ATB could accelerate the proliferative and migratory rates of RCC cells and inhibit cell apoptosis through downregulating p53 via binding to DNMT1. The ChIP assaydemonstrated that DNMT1 could bind to the DNA in the p53 promoterregion.	30536843	RID05541	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Parkinson's disease	UCA1	SNCA	positively-E	knockdown;overexpression	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000145335	NA	652995	6622	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NACP|PARK1|PARK4|PD1	Expression levels of lncRNA-UCA1 and SNCA in brain tissues extracted from PD mice and MPP+-induced SH-SY5Y cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR.UCA1 and SNCA were highly expressed in brain tissues extracted from PD mice and MPP+-induced SH-SY5Y cells.LncRNA-UCA1 promotes the occurrence and progression of PD by upregulating SNCA expression.	30536337	RID05542	expression association	NA	UP(PAAD);DATA(GSE40174)	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE75367,GSE86978,GSE41245)
Breast cancer	SNHG7	MIR186	interact;negatively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000207721	NA	84973	406962	NCRNA00061	MIRN186|miR-186	LncRNA SNHG7 promotes development of breast cancer by regulating microRNA-186.The expression of SNHG7 in 72 pairs of BC tissues and paracancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR.Dual-luciferase reporter gene assay was conducted to verify the binding condition between SNHG7 and microRNA-186.SNHG7 expression was higher in BC tissues than that of paracancerous tissues.Both mRNA and protein levels of microRNA-186 were negatively correlated to SNHG7 in BC tissues.SNHG7 could promote malignant progression of BC by regulating microRNA-186.	30536320	RID05543	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Cervical cancer	MALAT1	BRWD1	positively-E;interact	starbase;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	Cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185658	NA	378938	54014	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	C21orf107|DCAF19|FLJ11315|N143|WDR9	MALAT1 promotes cisplatin resistance in cervical cancer by activating the PI3K/AKT pathway.We used bioinformatics methods to predict the downstream genes of MALAT1 and examined the expression relationship between the target gene BRWD1 and MALAT1 by quantitative Real-time polymerase chain reaction (qRT-PCR.Over-expression of MALAT1 in cells showed the opposite results.Over-expression of MALAT1 significantly up-regulated the mRNA expression of BRWD1 in HeLa and C-33A cells. Results: After MALAT1 was knocked down, cisplatin showed an inhibited effect on the proliferation of HeLa and C-33A cells in a concentration-dependent manner. After treatment of cervical cancer cells with 5 uM cisplatin, MALAT1 knockdown enhanced the apoptosis of HeLa and C-33A cells, and up-regulated expression of cleaved caspase-3. Over-expression of MALAT1 in cells showed the opposite results. Starbase website was used to predict that MALAT1 might regulate BRWD1 expression. Over-expression of MALAT1 significantly up-regulated the mRNA expression of BRWD1 in HeLa and C-33A cells. After knockdown of BRWD1, cisplatin markedly decreased the proliferation of HeLa and C-33A cells, and promoted cell apoptosis and cleaved caspase-3 expression. Besides, HeLa and C-33A cells showed increased expressions of p-PI3K and p-AKT after MALAT1 was up-regulated.Conclusions: MALAT1 promoted the cisplatin resistance of cervical cancer, which might be related to regulation of cell apoptosis via BRWD1 and PI3K/AKT pathway.	30536307	RID05544	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE55807)
Cervical cancer	DLX6-AS1	miR-199a	negatively-E	starBase v2.0;siRNA;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000231764	GRCh38_7:96955141-97014088	NA	NA	285987	NA	Evf-2|FLJ34048|NCRNA00212	NA	Long non-coding RNA DLX6-AS1 promotes proliferation by acting as a ceRNA targeting miR-199a in cervical cancer.In the present study, DLX6-AS1 expression was identified to be significantly upregulated in cervical cancer tissues and cell lines by reverse transcription-quantitative polymerase chain reactions.Overexpression of miR-199a counteracted the role of DLX6-AS1 in facilitating proliferation and inhibiting apoptosis in invitro rescue assays.The present results suggest that DLX6-AS1 acting as a sponge for miR-199a may serve a critical role in the development and progression of cervical cancer.	30535431	RID05545	ceRNA or sponge	NA		
Diabetic retinopathy	MEG3	SIRT1	positively-E	dual-luciferase reporter assay;overexpression	downregulation	qRT-PCR;western blot	NA	NA	apoptosis process(-);NF-kB signaling pathway(-);inflammatory response(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000096717	NA	55384	23411	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	SIR2L1	LncRNA-MEG3 alleviates high glucose induced inflammation and apoptosis of retina epithelial cells via regulating miR-34a/SIRT1 axis.LncRNA-MEG3 is associated with multiple biological processes including proliferation, apoptosis and inflammation response, and is dramatically decreased in DR.The expression level was detected by qRT-PCRand western blot.The targeted regulatory relationship was analyzed by dual luciferase assay.MEG3 could promote SIRT1 expression by targeting miR-34a.MEG3 could alleviate HG-inducing apoptosis and inflammation via inhibiting NF-kB signaling pathway by targeting miR-34a/SIRT1 axis.MEG3 promotes the expression of SIRT1 via sponging miR-34a.Next, we used bioinformatics methods to find that MEG3 and 3-UTR of SIRT1 have potential binding site of miR-34a (Fig. 2E-2F).	30529346	RID05546	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	TMEM238L	BCL2	positively-E	shRNA;overexpresion	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000171791	NA	100289255	596	FORCP|LINC00675	Bcl-2|PPP1R50	The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/beta-catenin signaling in cervical cancer. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer.In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells. Overexpression of LINC00675 also increased the activity of Wnt/beta-catenin signaling in cervical cancer cells, whereas knockdown of LINC00675 suppressed the activity of Wnt/beta-catenin signaling.	30372871	RID05547	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	TMEM238L	BAX	negatively-E	shRNA;overexpresion	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000087088	NA	100289255	581	FORCP|LINC00675	BCL2L4	LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer.In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells. Overexpression of LINC00675 also increased the activity of Wnt/beta-catenin signaling in cervical cancer cells, whereas knockdown of LINC00675 suppressed the activity of Wnt/beta-catenin signaling.In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells.	30372871	RID05548	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	TMEM238L	GSK-3beta	negatively-E	shRNA;overexpresion	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	NA	NA	100289255	NA	FORCP|LINC00675	NA	The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/beta-catenin signaling in cervical cancer. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer.In vivo tumor growth study showed that knockdown of LINC00675 suppressed tumor growth, increased the protein levels of Bax and GSK-3beta, and decreased the protein levels of Bcl-2 and beta-catenin in isolated tumor tissues. In conclusion, our results implied that LINC00675 promoted cancer cell proliferation, migration, and invasion, and inhibit apoptosis likely by modulating the Wnt/beta-catenin pathway.	30372871	RID05549	expression association	prognosis		
Cervical cancer	TMEM238L	CTNNB1	positively-E	shRNA;overexpresion	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000168036	NA	100289255	1499	FORCP|LINC00675	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/beta-catenin signaling in cervical cancer. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer.In vivo tumor growth study showed that knockdown of LINC00675 suppressed tumor growth, increased the protein levels of Bax and GSK-3beta, and decreased the protein levels of Bcl-2 and beta-catenin in isolated tumor tissues. In conclusion, our results implied that LINC00675 promoted cancer cell proliferation, migration, and invasion, and inhibit apoptosis likely by modulating the Wnt/beta-catenin pathway.	30372871	RID05550	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Calcification of the ligamentum flavum	DANCR	EZH2	positively-E;interact	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell differentiation(-);calcium signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Other	Calcification of the ligamentum flavum	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000106462	NA	57291	2146	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	ENX-1|EZH1|KMT6|KMT6A	Downregulation of antidifferentiation noncoding RNA promotes chondrogenic differentiation and calcification of ligamentum flavum-derived mesenchymal stem cells. We found that ANCR was downregulated in human CLF tissues.Mechanistically, we detected a positive correlation between ANCR and enhancer of zeste homolog 2 (EZH2) in human CLF tissues. In cultured LF-MSCs, ANCR knockdown decreased while ANCR overexpression increased EZH2 expression. In addition, physical association between ANCR and EZH2 was revealed by an RNA pull-down assay. Functionally, EZH2 overexpression prevented chondrogenic differentiation and calcification enhanced by ANCR knockdown. These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF-MSCs to suppress chondrogenic differentiation and calcification.	30368870	RID05551	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophagus squamous cell carcinoma	GAS5	PIK3CA	negatively-E	overexpresion	downregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway;cell proliferation(-);cell migration(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000121879	NA	60674	5290	NCRNA00030|SNHG2	PI3K	Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. GAS5 expression level was lower in tumor tissues than in adjacent healthy tissues. GAS5 overexpression inhibited tumor cell proliferation and migration, while treatment with PI3K activator reduced the inhibitory effects. GAS5 overexpression decreased the expression level of PI3K and phosphorylation levels of Akt and mTOR in esophageal cancer cells, while PI3K activator treatment showed no significant effects on GAS5 expression. GAS5 was downregulated in esophageal cancer patients compared to healthy controls, and GAS5 overexpression suppressed proliferation and migration of esophageal cancer cells by inactivating the PI3K/AKT/mTOR pathway.	30368517	RID05552	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Esophagus squamous cell carcinoma	GAS5	AKT1	negatively-F	overexpresion	downregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway;cell proliferation(-);cell migration(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000142208	NA	60674	207	NCRNA00030|SNHG2	AKT|PKB|PRKBA|RAC|RAC-alpha	Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. GAS5 expression level was lower in tumor tissues than in adjacent healthy tissues. GAS5 overexpression inhibited tumor cell proliferation and migration, while treatment with PI3K activator reduced the inhibitory effects. GAS5 overexpression decreased the expression level of PI3K and phosphorylation levels of Akt and mTOR in esophageal cancer cells, while PI3K activator treatment showed no significant effects on GAS5 expression. GAS5 was downregulated in esophageal cancer patients compared to healthy controls, and GAS5 overexpression suppressed proliferation and migration of esophageal cancer cells by inactivating the PI3K/AKT/mTOR pathway.	30368517	RID05553	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	GAS5	MTOR	negatively-F	overexpresion	downregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway;cell proliferation(-);cell migration(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000198793	NA	60674	2475	NCRNA00030|SNHG2	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. GAS5 expression level was lower in tumor tissues than in adjacent healthy tissues. GAS5 overexpression inhibited tumor cell proliferation and migration, while treatment with PI3K activator reduced the inhibitory effects. GAS5 overexpression decreased the expression level of PI3K and phosphorylation levels of Akt and mTOR in esophageal cancer cells, while PI3K activator treatment showed no significant effects on GAS5 expression. GAS5 was downregulated in esophageal cancer patients compared to healthy controls, and GAS5 overexpression suppressed proliferation and migration of esophageal cancer cells by inactivating the PI3K/AKT/mTOR pathway.	30368517	RID05554	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Breast cancer	lncRNACCDC6	CDC6	positively-E	RIP;luciferase reporter assay;western blot;shRNA	upregulation	qPCR	TANRIC	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-215)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000094804	NA	NA	990	NA	CDC18L|HsCDC18|HsCDC6|MGORS5	LncRNA-CDC6 promotes breast cancer progression and function as ceRNA to target CDC6 by sponging microRNA-215. TCGA database contains RNA sequencing data for multiple types of cancer. The RNA-seq and clinical profiles of 105 normal and 837 breast cancer tissues were downloaded and analyzed based on the Atlas of Noncoding RNAs in Cancer (TANRIC) database.Anti-Ago2 RIP assay verified the combination between miR-215 and lncRNADC6. (d) Effect of lncRNADC6 knockdown or overexpression on miR-215 expression. (e) The wild-type (Wt) and mutant type (Mut) of binding sites and luciferase reporter assay in MDA-MB-231 and MCF-7 cells demonstrated combination between miR-215 and lncRNADC6.Then both mRNA and protein expression level of CDC6 was detected with real-time PCR and western blot assay. Clinically, lncRNADC6 was highly expressed in tumor tissues and was positively correlated with clinical stages of breast cancers. Functionally, the ectopic expression of lncRNADC6 promoted proliferation via regulation of G1 phase checkpoint, and further promoting the migration capability. Moreover, lncRNADC6 could function as competitive endogenous RNA (ceRNA) via directly sponging of microRNA-215 (miR-215), which further regulating the expression of CDC6. Taken together, our results proved that lncRNADC6 could function as ceRNA and promote the proliferation and metastasis of breast cancer cells, which provided a novel prognostic marker for breast cancers in clinic.	30362551	RID05555	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Lung adenocarcinoma	LIN28B-AS1	LIN28B	positively-E	RIP;RNA pull-down assay;knockout;western blot;siRNA	upregulation	qRT-PCR	GTEx;TCGA	NA	cell proliferation(+);cell metastasis(+)	RNA stability	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000203809	GRCh38_6:104864464-104941447	ENSG00000187772	NA	100113403	389421	C6orf220|dJ439I14.1|LINC00577	CSDD2|FLJ16517	A cancer-testis non-coding RNA LIN28B-AS1 activates driver gene LIN28B by interacting with IGF2BP1 in lung adenocarcinoma. Firstly, we presented the CT expression pattern of LIN28B. Using transcriptomics data from the GTEx project, we found that LIN28B exhibits a testis-specific expression pattern among normal adult tissues.LIN28B and LIN28B-AS1 showed a special high expression in the testis.Upon integrating the expression profiles from the The Cancer Genome Atlas (TCGA) projects and our 24 LUAD tumor tissues, we observed that LIN28B is commonly activated in LUAD, clarifying that LIN28B is a CT gene.Interestingly, LIN28B-AS1- knockout NCI-H1299 cells expressed decreasing expression of LIN28B.In addition, the protein expression of LIN28B was deceased after depletion of LIN28B-AS1.As expected, functional assays suggested that LIN28B-AS1-knockout NCI-H1299 cells exhibited a significant decrease in cell proliferation, colony formation, and migration.Then CCND2 and FMN2 were validated by quantitative PCR assays.we performed an RNA pull-down assay followed by a proteomic analysis of the LIN28B-AS1-associated protein complex in NCI-H1299 cells to identify the mechanism by which LIN28B-AS1 increased LIN28B expression.we performed RNA pull-down followed by western blot with IGF2BP1 antibodies. IGF2BP1 was readily detected in the LIN28B-AS1 RNA pull-down complex but not in the control samples, including LIN28B-AS1 antisense RNA.We also performed RNA immunoprecipitation (RIP) for the RNA-IGF2BP1 complex using IGF2BP1 antibodies and measured the amount of LIN28B-AS1 associated with IGF2BP1 immunoprecipitates.We performed real-time quantitative reverse reaction (qRT-PCR and western blot assays to show that expression of IGF2BP1 was suppressed by IGF2BP1 small interfering RNA (siRNA) in NCI-H1299 cells.LIN28B-AS1 alters the LIN28B mRNA stability by interacting with IGF2BP1. In vitro and In vivo experiments confirmed that the activation of LIN28B could promote the proliferation and metastasis of LUAD cells and can influence cell cycle, DNA damage repair, and genome instability.We applied the same STAR-HTSeqDESeq2 pipeline and reference to quantify gene expressionand used 5 as the cutoff to define activation. In sum, we identify that LIN28B is an 'epi-driver'-of LUAD and clarify a new lncRNA-activated mechanism of LIN28B, which provide new candidate targets for precise anticancer therapy in the future.	30353165	RID05556	interact with mRNA	metastasis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Nasopharynx carcinoma	AFAP1-AS1	RAB11B	positively-E	RNAhybrid;RNA22;PITA;Targetscan;RegRNA;luciferase activity assay;western blot;siRNA;overexpression	upregulation	qPCR	GSE73460;GSE32906;GSE70970	NA	cell metastasis(+);cell migration(+);cell invasion(+)	ceRNA(miR-423-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000185236	NA	84740	9230	AFAP1-AS|AFAP1AS|MGC10981	H-YPT3	Long noncoding RNA AFAP1-AS1 acts as a competing endogenous RNA of miR-423-5p to facilitate nasopharyngeal carcinoma metastasis through regulating the Rho/Rac pathway.The overexpressing AFAP1- AS1 vector was constructed and transfected into the NPC cell lines 5-8F and HNE2, and the expression of AFAP1-AS1 was confirmed by real-time PCR.To identify the mechanism of AFAP1-AS1 in NPC, we used four programs (PITA, RNAhybrid, RNA22, and RNAreg2.0) to predict potential lncRNA-miRNA interactions involving AFAP1-AS1.AFAP1-AS1 was negatively regulated by miR-423-5p in NPC cells.Moreover, transfection with miR-423-5p inhibitors increased the luciferase activity of the wild type AFAP1-AS1 reporter (WT, Fig. 2e), suggesting that miR-423-5p binds with AFAP1-AS1 through this site.Based on the above findings, we screened online published miRNA datasets and found that miR-423-5p expression was low-expressed in NPC clinical samples compared with nontumor nasopharyngeal epithelium tissues in a gene expression profiling (GEP) dataset, GSE73460 (Additional file 2: Figure S1a), and another NPC GEP dataset, GSE32906 showed that the expression of miR-423-5p was tightly associated with the TNM stages of NPC patients (Additional file 2: Figure S1b). In the GSE70970 dataset, decreased miR-423-5p expression was also associated with poor overall survival and poor relapse-free survival.Taken together, these results indicated that AFAP1-AS1 might promote NPC cell migration and invasion via mutually regulated with miR-423-5p.We first confirmed that AFAP1-AS1 regulates the small GTPase family members at the mRNA level. After AFAP1-AS1 knockdown (siRNA) or overexpression in 5-8F and HNE2 cells, multiple members of the Rho/Rac pathway were affected at the mRNA level, as determined by real-time PCR.we found that the expression of RAC1, RHOC, LASP1, and RAB11B was reduced by miR-423-5p mimics and induced by miR-423-5p inhibitors at both the mRNA and protein levels.The 3'-UTR sequences of these genes were analyzed using the TargetScan software.Next, the vectors containing the wild type or mutant (mutations targeting the seed miR-423-5p sequence) RAB11B, LASP1, and RAC1 3'-UTR sequences were constructed, and luciferase analysis showed that miR-423-5p mimics reduced luciferase activity in 5-8F and HNE2 when transfected with vectors containing the wild type RAB11B.AFAP1-AS1 acts AS a ceRNA regulating FOSL2 expression in NPC.FOSL2 activates transcription of LASP1 by binding its promoter.The observations in this study identify an important role for AFAP1-AS1 as a competing endogenous RNA (ceRNA) in NPC pathogenesis and indicate that it may serve as a potential target for cancer diagnosis and treatment.	30326930	RID05557	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Nasopharynx carcinoma	AFAP1-AS1	LASP1	positively-E	RNAhybrid;RNA22;PITA;Targetscan;RegRNA;luciferase activity assay;western blot;siRNA;overexpression	upregulation	qPCR	GSE73460;GSE32906;GSE70970	NA	cell metastasis(+);cell migration(+);cell invasion(+)	ceRNA(miR-423-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000002834	NA	84740	3927	AFAP1-AS|AFAP1AS|MGC10981	Lasp-1|MLN50	Long noncoding RNA AFAP1-AS1 acts as a competing endogenous RNA of miR-423-5p to facilitate nasopharyngeal carcinoma metastasis through regulating the Rho/Rac pathway.The overexpressing AFAP1- AS1 vector was constructed and transfected into the NPC cell lines 5-8F and HNE2, and the expression of AFAP1-AS1 was confirmed by real-time PCR.To identify the mechanism of AFAP1-AS1 in NPC, we used four programs (PITA, RNAhybrid, RNA22, and RNAreg2.0) to predict potential lncRNA-miRNA interactions involving AFAP1-AS1.AFAP1-AS1 was negatively regulated by miR-423-5p in NPC cells.Moreover, transfection with miR-423-5p inhibitors increased the luciferase activity of the wild type AFAP1-AS1 reporter (WT, Fig. 2e), suggesting that miR-423-5p binds with AFAP1-AS1 through this site.Based on the above findings, we screened online published miRNA datasets and found that miR-423-5p expression was low-expressed in NPC clinical samples compared with nontumor nasopharyngeal epithelium tissues in a gene expression profiling (GEP) dataset, GSE73460 (Additional file 2: Figure S1a), and another NPC GEP dataset, GSE32906 showed that the expression of miR-423-5p was tightly associated with the TNM stages of NPC patients (Additional file 2: Figure S1b). In the GSE70970 dataset, decreased miR-423-5p expression was also associated with poor overall survival and poor relapse-free survival.Taken together, these results indicated that AFAP1-AS1 might promote NPC cell migration and invasion via mutually regulated with miR-423-5p.We first confirmed that AFAP1-AS1 regulates the small GTPase family members at the mRNA level. After AFAP1-AS1 knockdown (siRNA) or overexpression in 5-8F and HNE2 cells, multiple members of the Rho/Rac pathway were affected at the mRNA level, as determined by real-time PCR.we found that the expression of RAC1, RHOC, LASP1, and RAB11B was reduced by miR-423-5p mimics and induced by miR-423-5p inhibitors at both the mRNA and protein levels.The 3'-UTR sequences of these genes were analyzed using the TargetScan software.Next, the vectors containing the wild type or mutant (mutations targeting the seed miR-423-5p sequence) RAB11B, LASP1, and RAC1 3'-UTR sequences were constructed, and luciferase analysis showed that miR-423-5p mimics reduced luciferase activity in 5-8F and HNE2 when transfected with vectors containing the wild type RAB11B.AFAP1-AS1 acts AS a ceRNA regulating FOSL2 expression in NPC.FOSL2 activates transcription of LASP1 by binding its promoter.The observations in this study identify an important role for AFAP1-AS1 as a competing endogenous RNA (ceRNA) in NPC pathogenesis and indicate that it may serve as a potential target for cancer diagnosis and treatment.	30326930	RID05558	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	AFAP1-AS1	FOSL2	positively-E	RNAhybrid;RNA22;PITA;Targetscan;RegRNA;luciferase activity assay;western blot;siRNA;overexpression	upregulation	qPCR	GSE73460;GSE32906;GSE70970	NA	cell metastasis(+);cell migration(+);cell invasion(+)	ceRNA(miR-423-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000075426	NA	84740	2355	AFAP1-AS|AFAP1AS|MGC10981	FLJ23306|FRA2	LncRNA HULC promotes non-small cell lung cancer cell proliferation and inhibits the apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and its downstream PI3K/Akt pathway.	30326930	RID05559	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	NEAT1	SIRT1	positively-E	western blot;luciferase reporter assay;starBase;microT;RNA22;PicTar;microRNA.org;siRNA	upregulation	RT-qPCR	GSE20916;GSE9348	NA	cell proliferation(+);cell viability(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);cell growth(+);cell metastasis(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000096717	NA	283131	23411	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	SIR2L1	The expression of HULC in tumor tissues and adjacent healthy tissues of 102 patients with NSCLC was detected by qRT-PCR As shown in Figure 1, expression of HULC was significantly higher in tumor tissues than that in adjacent healthy tissues in 84 out of 102 patients.HULC overexpression significantly increased the expression level of both SPHK1 and phosphorylation level of Akt in both NSCLC cell lines.These results indicate that HULC may serve as a positive upstream regulator of SPHK1, which can activate downstream PI3K/Akt pathway in NSCLC cells.Effects on HULC Overexpression, SPHK1 Inhibitor and PI3K/Akt Inhibitor on Proliferation and Apoptosis of NSCLC Cells.CONCLUSIONS: LncRNA HULC overexpression can promote NSCLC cell proliferation and inhibit cell apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and further induce the activation of its downstream PI3K/Akt pathway.	30312725	RID05560	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	GCAWKR	WDR5	positively-F	western blot;RNA pull-down assay;RIP;Co-immunoprecipitation;ChIP;shRNA	upregulation	qRT-PCR	GSE50710;GSE112586	NA	cell proliferation(+);cell invasion(+);colony formation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272808	GRCh38_15:100849831-100876836	ENSG00000196363	NA	105369201	11091	NA	CFAP89|SWD3	lncRNA GCAWKR Promotes Gastric Cancer Development by Scaffolding the Chromatin Modification Factors WDR5 and KAT2A.The lncRNA and mRNA profiling data in 10 GC and paired normal tissues that we previously reported14 can be accessed via Gene Expression Omnibus (GEO): GSE50710.lncRNA GCAWKR Was Upregulated in GC Tissues.qRT-PCRanalysis demonstrated that the expression level of GCAWKR increased from normal gastric tissue to intestinal metaplasia (IM), to dysplasia, and to GC.To elucidate the potential role involved in the oncogenic function of GCAWKR, an RNA transcriptome-sequencing analysis was performed in SGC7901 cells that were transfected with GCAWKR short hairpin RNA (shRNA) or control shRNA (Figure 2A; data are available via GEO: GSE112586).The results demonstrated that the invasive ability in SGC7901 and BGC823 cells was decreased when GCAWKR expression was knocked down (Figure 2E), while GCAWKR-overexpressing SGC7901 and BGC823 cells exhibited higher invasive ability.RNA pull-down assay confirmed that GCAWKR specifically binds to WDR5 and KAT2A. WDR5, a key component of SET/MLL (SET-domain/mixed-lineage leukemia) histone-methyltransferase complexes, have an essential role in histone H3 Lys 4 (H3K4) trimethylation and subsequent transcriptional activation.To further consolidate the interaction, we analyzed the interaction between GCAWKR and WDR5/ KAT2A in the nucleus, and the radioimmunoprecipitation (RIP) assays showed that GCAWKR specifically binds to WDR5 and KAT2A.Our data illustrated that GCAWKR mediated the interaction between WDR5 and KAT2A.The chromatin IP (ChIP) assay confirmed the binding of WDR5 and KAT2A to the promoter region of PTP4A1. GCAWKR silencing markedly suppressed the binding ability of WDR5 and KAT2A.GCAWKR overexpression significantly promoted the GC cell proliferation, colony formation, and invasion in GC cells, and PTP4A1 knockdown attenuated the oncogenic effect induced by the GCAWKR overexpression.GCAWKR Promotes GC Development by Upregulating PTP4A1 Expression.GCAWKR affected cell proliferation and cell invasion in multiple GC models. Mechanistically, GCAWKR bound WDR5 and KAT2A and acted as a molecular scaffold of WDR5/KAT2A complexes, modulating the affinity for WDR5/KAT2A complexes in the target gene  promoter region. Thus, our data defined a mechanism of lncRNA-mediated carcinogenesis in GC, suggesting new therapeutic targets in GC.	30274785	RID05561	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	GCAWKR	KAT2A	positively-F	western blot;RNA pull-down assay;RIP;Co-immunoprecipitation;ChIP;shRNA	upregulation	qRT-PCR	GSE50710;GSE112586	NA	cell proliferation(+);cell invasion(+);colony formation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272808	GRCh38_15:100849831-100876836	ENSG00000259958	NA	105369201	2648	NA	GCN5|GCN5L2|PCAF-b	lncRNA GCAWKR Promotes Gastric Cancer Development by Scaffolding the Chromatin Modification Factors WDR5 and KAT2A.The lncRNA and mRNA profiling data in 10 GC and paired normal tissues that we previously reported14 can be accessed via Gene Expression Omnibus (GEO): GSE50710.lncRNA GCAWKR Was Upregulated in GC Tissues.qRT-PCRanalysis demonstrated that the expression level of GCAWKR increased from normal gastric tissue to intestinal metaplasia (IM), to dysplasia, and to GC.To elucidate the potential role involved in the oncogenic function of GCAWKR, an RNA transcriptome-sequencing analysis was performed in SGC7901 cells that were transfected with GCAWKR short hairpin RNA (shRNA) or control shRNA (Figure 2A; data are available via GEO: GSE112586).The results demonstrated that the invasive ability in SGC7901 and BGC823 cells was decreased when GCAWKR expression was knocked down (Figure 2E), while GCAWKR-overexpressing SGC7901 and BGC823 cells exhibited higher invasive ability.RNA pull-down assay confirmed that GCAWKR specifically binds to WDR5 and KAT2A. WDR5, a key component of SET/MLL (SET-domain/mixed-lineage leukemia) histone-methyltransferase complexes, have an essential role in histone H3 Lys 4 (H3K4) trimethylation and subsequent transcriptional activation.To further consolidate the interaction, we analyzed the interaction between GCAWKR and WDR5/ KAT2A in the nucleus, and the radioimmunoprecipitation (RIP) assays showed that GCAWKR specifically binds to WDR5 and KAT2A.Our data illustrated that GCAWKR mediated the interaction between WDR5 and KAT2A.The chromatin IP (ChIP) assay confirmed the binding of WDR5 and KAT2A to the promoter region of PTP4A1. GCAWKR silencing markedly suppressed the binding ability of WDR5 and KAT2A.GCAWKR overexpression significantly promoted the GC cell proliferation, colony formation, and invasion in GC cells, and PTP4A1 knockdown attenuated the oncogenic effect induced by the GCAWKR overexpression.GCAWKR Promotes GC Development by Upregulating PTP4A1 Expression.GCAWKR affected cell proliferation and cell invasion in multiple GC models. Mechanistically, GCAWKR bound WDR5 and KAT2A and acted as a molecular scaffold of WDR5/KAT2A complexes, modulating the affinity for WDR5/KAT2A complexes in the target gene  promoter region. Thus, our data defined a mechanism of lncRNA-mediated carcinogenesis in GC, suggesting new therapeutic targets in GC.	30274785	RID05562	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	GCAWKR	PTP4A1	positively-E	western blot;RNA pull-down assay;RIP;Co-immunoprecipitation;ChIP;shRNA	upregulation	qRT-PCR	GSE50710;GSE112586	NA	cell proliferation(+);cell invasion(+);colony formation(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272808	GRCh38_15:100849831-100876836	ENSG00000112245	NA	105369201	7803	NA	PRL-1|PRL1|PTPCAAX1	lncRNA GCAWKR Promotes Gastric Cancer Development by Scaffolding the Chromatin Modification Factors WDR5 and KAT2A.The lncRNA and mRNA profiling data in 10 GC and paired normal tissues that we previously reported14 can be accessed via Gene Expression Omnibus (GEO): GSE50710.lncRNA GCAWKR Was Upregulated in GC Tissues.qRT-PCRanalysis demonstrated that the expression level of GCAWKR increased from normal gastric tissue to intestinal metaplasia (IM), to dysplasia, and to GC.To elucidate the potential role involved in the oncogenic function of GCAWKR, an RNA transcriptome-sequencing analysis was performed in SGC7901 cells that were transfected with GCAWKR short hairpin RNA (shRNA) or control shRNA (Figure 2A; data are available via GEO: GSE112586).The results demonstrated that the invasive ability in SGC7901 and BGC823 cells was decreased when GCAWKR expression was knocked down (Figure 2E), while GCAWKR-overexpressing SGC7901 and BGC823 cells exhibited higher invasive ability.RNA pull-down assay confirmed that GCAWKR specifically binds to WDR5 and KAT2A. WDR5, a key component of SET/MLL (SET-domain/mixed-lineage leukemia) histone-methyltransferase complexes, have an essential role in histone H3 Lys 4 (H3K4) trimethylation and subsequent transcriptional activation.To further consolidate the interaction, we analyzed the interaction between GCAWKR and WDR5/ KAT2A in the nucleus, and the radioimmunoprecipitation (RIP) assays showed that GCAWKR specifically binds to WDR5 and KAT2A.Our data illustrated that GCAWKR mediated the interaction between WDR5 and KAT2A.The chromatin IP (ChIP) assay confirmed the binding of WDR5 and KAT2A to the promoter region of PTP4A1. GCAWKR silencing markedly suppressed the binding ability of WDR5 and KAT2A.GCAWKR overexpression significantly promoted the GC cell proliferation, colony formation, and invasion in GC cells, and PTP4A1 knockdown attenuated the oncogenic effect induced by the GCAWKR overexpression.GCAWKR Promotes GC Development by Upregulating PTP4A1 Expression.GCAWKR affected cell proliferation and cell invasion in multiple GC models. Mechanistically, GCAWKR bound WDR5 and KAT2A and acted as a molecular scaffold of WDR5/KAT2A complexes, modulating the affinity for WDR5/KAT2A complexes in the target gene  promoter region. Thus, our data defined a mechanism of lncRNA-mediated carcinogenesis in GC, suggesting new therapeutic targets in GC.	30274785	RID05563	epigenetic regulation	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE86978)
Ovarian cancer	ADAMTS9-AS2	FOXF2	positively-E	western blot;RIP;RNA pull-down assay;luciferase reporter assay;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000137273	NA	100507098	2295	NA	FKHL6|FREAC2	LncRNA ADAMTS9-AS2 regulates ovarian cancer progression by targeting miR-182-5p/FOXF2 signaling pathway.To explore the role of ADAMTS9-AS2 in OC progression, we first determined ADAMTS9-AS2 expression in OC cell lines by qRT-PCR Results showed that ADAMTS9-AS2 expression was significantly decreased in OC cell lines.qRT-PCR;ISHowed that miR- 182-5p expression was significantly increased in OC cell lines and tissues.dual-luciferase reporter assay showed that the relative luciferase activity of ADAMTS9-AS2-Wt was evidently reduced by miR-182-5p mimics.Moreover, RIP assay showed that ADAMTS9-AS2 was enriched in Ago2 group relative to the IgG group. In addition, pull-down assay revealed that miR-182-5p obtained a great enrichment in ADAMTS9-AS2 pull-down pellets.Then,we explore the downstreamofmiR-182-5p via the TargetScan prediction software database. FOXF2was identified to be a potential target of miR-182-5p (Fig. 5A). To further verify the prediction, luciferase reporter assay was used.Moreover, we showed that FOXF2 expression was significantly decreased and inversely correlated with miR-182-5p expression in OC tissues.Next,we explore the effects of ADAMTS9-AS2 on FOXF2 expression in OC. qRT-PCRandwestern blot results showed that ADAMTS9-AS2 overexpression significantly increased FOXF2 expression in OVCAR cells, while ADAMTS9-AS2 inhibition have opposite effects on FOXF2 expression in SKOV3 cells.Furthermore, rescue assays showed that FOXF2 inhibition could abolish the effects of ADAMTS9- AS2 on OVCAR cells proliferation and invasion.To further determine the effects of ADAMTS9-AS2 on tumorigenesis in vivo, we constructed ADAMTS9-AS2 overexpression cell lines, which were subcutaneously injected into the BALB/c nude mice. Results showed that ADAMTS9-AS2 overexpression reduced tumor growth in vivo.Taken together, our data suggested that lncRNA ADAMTS9-AS2 decreased OC progression by regulating miR- 182-5p/FOXF2 axis, indicating ADAMTS9-AS2 could serve as a potential therapeutic target for OC treatment.	30268751	RID05564	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DATA(GSE40174)
Lung cancer	lnc-MMP2-2	MMP2	positively-E	luciferase reporter assay;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	TGF-beta- mediated exosomal lnc-MMP2- 2 regulates migration and invasion of lung cancer cells to the vasculature by promoting MMP2 expression.Using lncRNA microarray analysis, we screened for differentially expressed exosomal lncRNAs related to TGF-beta- mediated EMT.We next confirmed the high levels of lnc-MMP2- 2 in TGF-beta- mediated exosomes by qRT-PCRSubsequently, with qRT-PCRand western blot assay, we observed that lnc-MMP2- 2 and MMP2 were both up-regulated in Texo treated A549 cells.Additionally, to investigate the relationship between lnc-MMP2- 2 and MMP2, MMP2 promoter-Luciferase asssay, qRT-PCRand western blot assays were performed.Transcriptional analysis also revealed that lnc-MMP2- 2 was highly enriched in TGF-beta- mediated exosomes and might function by increasing the expression of matrix metalloproteinase (MMP)2 through its enhancer activity, with ectopic expression and silencing of lnc-MMP2- 2 affecting lung cancer invasion and vascular permeability. Additionally, lnc-MMP2- 2 and MMP2 expression was assessed semiquantitatively, and tissue-specific correlations between lnc-MMP2- 2 and MMP2 expression were evaluated. These results suggested that exosomal lnc-MMP2- 2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer.	30256540	RID05565	expression association	metastasis		UP(PAAD);DATA(GSE40174)
Coronary syndrome	TCONS_00024652	MIR21	negatively-F	starBase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Artery disease	lncRNA	miRNA	NA	NA	ENSG00000199004	NA	NA	406991	NA	MIRN21|hsa-mir-21|miR-21|miRNA21	Long noncoding RNA TCONS_00024652 regulates vascular endothelial cell proliferation and angiogenesis via microRNA-21.During the initial phase of the current study, HUVECs were stimulated with TNF-alpha and levels of lncRNAs associated with the regulation of vascular function (25,26) and atherosclerosis (27) were assessed using RT-qPCR. The results revealed that expression of a majority of lncRNAs was significantly increased in these HUVECs following TNF-alpha treatment.Putative complementary sites within miR-21 and the 3'-untranslated region of TCONS_00024652 were predicted using starBase.Relative expression of miR-21 in HUVECs transfected with si-TCONS_00024652.Relative expression of TCONS_00024652 mRNA levels following transfection with miR-21 mimic or inhibitor, as determined using reverse transcription-quantitative polymerase chain reaction.Luciferase activity in HUVECs following co-transfection with miR-21 and luciferase reporters containing WT- or mut-TCONS_00024652 transcript.TCONS_00024652 knockdown inhibits the proliferation, migration and angiogenesis of HUVECs.miR-21 inhibition reverses the inhibitory effect of TCONS_00024652 knockdown on proliferation, migration and angiogenesis in HUVECs.The results of the present study suggest that the targeting of TCONS_00024652 by miR-21 may be a potential method of improving vascular endothelial dysfunction, neovascularization maturation and plaque stabilization.	30233677	RID05566	ceRNA or sponge	NA		
Non-small cell lung cancer	H19	NF1	positively-E	luciferase reporter assay;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-107)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000196712	NA	283120	4763	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NFNS|VRNF|WSS	LncRNA H19 serves as a ceRNA and participates in non-small cell lung cancer development by regulating microRNA-107.Overexpressed H19 increased proliferative and migratory abilities of A549 cells. Dual-luciferase reporter gene assay demonstrated that H19 regulates NF1 expression through competitive binding to microRNA-107, thereafter participating in NSCLC development.H19 is highly expressed in NSCLC, which promotes NSCLC development by regulating NF1 via competitive binding to microRNA- 107.	30280776	RID05567	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Rheumatoid arthritis	CEBPB	NTT	positively-E	ChIP;siRNA	upregulation	RT-PCR	NA	NA	cell cycle(-);cell differentiation(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	TF	lncRNA	ENSG00000172216	NA	ENSG00000006210	GRCh38_16:57372477-57385044	1051	7956	C/EBP-beta|CRP2|IL6DBP|LAP|NFIL6|TCF5	NA	lncRNA NTT/PBOV1 Axis Promotes Monocyte Differentiation and Is Elevated in Rheumatoid Arthritis.By examining the promoter sequence of NTT, we identified the potential binding motif of C/EBP , a key transcription factor in monocytes. To further check if C/EBP  binds to the NTT promoter and regulates NTT expression, we performed a chromatin immunoprecipitation assay (ChIP) and siRNA knockdown for C/EBP  in the THP-1 cell line. C/EBP  binding was detected on three positions of the NTT promoter, and C/EBP  knockdown in THP-1 resulted in decreased NTT expression.NTT expression in THP-1 was knocked down by si-RNA and the relative mRNA levels of nearby genes were analyzed.NTT knockdown showed the greatest impact on PBOV1 expression.An RNA immunoprecipitation assay showed that NTT could bind to hnRNP-U. DNA ChIP showed that hnRNP-U binds to two positions of the PBOV1 promoter, and the hnRNP-U binding became undetectable after NTT knockdown, suggesting NTT might enhance PBOV1 expression by interacting with hnRNP-U binding to the promoter of PBOV1.C/EBPb, NTT, and PBOV1 Expression Levels Were Highly Elevated in Fresh Rheumatoid Arthritis (RA) Patients.Overexpression of PBOV1 in THP-1 Cells Led to Cell Cycle Arrest and Differentiation to Macrophages.In conclusion, our study suggests that the lncRNA NTT is a regulator of inflammation in monocytes, and its activation participates in monocyte/macrophage differentiation and the pathogenesis of RA.	30231487	RID05568	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Rheumatoid arthritis	NTT	PBOV1	positively-E	RIP;ChIP	upregulation	RT-PCR	NA	NA	cell cycle(-);cell differentiation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000006210	GRCh38_16:57372477-57385044	ENSG00000254440	NA	7956	59351	NA	UC28|UROC28	lncRNA NTT/PBOV1 Axis Promotes Monocyte Differentiation and Is Elevated in Rheumatoid Arthritis.By examining the promoter sequence of NTT, we identified the potential binding motif of C/EBP , a key transcription factor in monocytes. To further check if C/EBP  binds to the NTT promoter and regulates NTT expression, we performed a chromatin immunoprecipitation assay (ChIP) and siRNA knockdown for C/EBP  in the THP-1 cell line. C/EBP  binding was detected on three positions of the NTT promoter, and C/EBP  knockdown in THP-1 resulted in decreased NTT expression.NTT expression in THP-1 was knocked down by si-RNA and the relative mRNA levels of nearby genes were analyzed.NTT knockdown showed the greatest impact on PBOV1 expression.An RNA immunoprecipitation assay showed that NTT could bind to hnRNP-U. DNA ChIP showed that hnRNP-U binds to two positions of the PBOV1 promoter, and the hnRNP-U binding became undetectable after NTT knockdown, suggesting NTT might enhance PBOV1 expression by interacting with hnRNP-U binding to the promoter of PBOV1.C/EBPb, NTT, and PBOV1 Expression Levels Were Highly Elevated in Fresh Rheumatoid Arthritis (RA) Patients.Overexpression of PBOV1 in THP-1 Cells Led to Cell Cycle Arrest and Differentiation to Macrophages.In conclusion, our study suggests that the lncRNA NTT is a regulator of inflammation in monocytes, and its activation participates in monocyte/macrophage differentiation and the pathogenesis of RA.	30231487	RID05569	transcriptional regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Cancer	PNCTR	PTBP1	negatively-F	RIP;FISH;siRNA	upregulation	qRT-PCR	NA	NA	cell survival(+)	alternative splicing	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	NA	NA	ENSG00000011304	NA	NA	5725	NA	HNRNP-I|HNRPI|pPTB|PTB|PTB-1|PTB2|PTB3|PTB4	A Short Tandem Repeat-Enriched RNA Assembles a Nuclear Compartment to Control Alternative Splicing and Promote Cell Survival.PNCTR is markedly overexpressed in a variety of cancer cells and its downregulation is sufficient to induce programmed cell death at least in part by stimulating PTBP1 splicing regulation activity.Nuclear and cytoplasmic fractions from control and DRB-treated HeLa cells (Figure S2F) were analyzed by RT-PCRwith primers designed to amplify three large STRcontaining fragments of PNCTR.As a direct test for PTBP1/PNCTR interaction, we analyzed HeLa cell lysate by RNA immunoprecipitation (RIP) with a PTBP1-specific antibody. qRT-PCRanalysis of the RIP samples showed a robust association of PTBP1 with PNCTR.To gain further insights into PNCTR localization, we co-stained HeLa cells with an RNA fluorescence in situ hybridization (FISH) probe spanning the entire PNCTR sequence and PTBP1-specific antibody. PNCTR signal typically occurred as one or two prominent dots adjacent to nucleoli.As expected, cells treated with a PTBP1-specific siRNA mixture (siPTBP1) had substantially reduced PTBP1 staining in the nucleoplasm and the PNC as compared to a non-targeting siRNA (siControl).PNCTR Is Required for Cell Survival.PNCTR Antagonizes PTBP1 Splicing Regulation Function.This work expands our understanding of the repeat-containing fraction of the human genome and illuminates a novel mechanism driving malignant transformation of cancer cells.	30318443	RID05570	interact with mRNA	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	lnc-RAB1A-2	FGF1	positively-E	western blot	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);PI3K/AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000113578	NA	NA	2246	NA	AFGF|ECGF|ECGF-beta|ECGFA|ECGFB|FGF-1|FGF-alpha|FGFA|GLIO703|HBGF-1|HBGF1	Upregulation of long non-coding RNA RAB1A-2 induces FGF1 expression worsening lung cancer prognosis.lnc-RAB1A-2 expression was significantly up-regulated in cancerous tissues compared with adjacent normal tissues.To explore the underlying mechanism by which lnc-RAB1A-2 affects lung cancer development, we performed a whole human genome oligo microarray, the results of which were analyzed for lncRNA-associated gene transcriptional changes by assessing the gene expression profiles of lnc-RAB1A-2 overexpression in A549 cells and control cells. By comparing RNA transcriptional levels of lnc-RAB1A-2-over-expressing A549 cells and that of the control cells, we found that 257 genes exhibited exerted obviously altered expression.We further conducted qPCR to validate the genes and found that FGF1 expression levels were correlated with those of lnc-RAB1A-2.We conducted another Agilent whole human genome oligo microarray using lnc-RAB1A-2 silenced PC-9 cell lines and control cell lines, and found the PI3K/AKT/mTOR gene FGF1 was downregulated at a 0.107- fold level in lnc-RAB1A-2 silenced cell lines compared with the control cell lines.Further analyses using digital gene expression tag profiling revealed that lnc-RAB1A-2 could affect the expression of fibroblast growth factor 1 (FGF1), a gene involved in the PI3K/AKT/mTOR pathway that is largely activated by RAB1A. FGF1 was confirmed to be a down-stream gene of lnc-RAB1A-2. Collectively, our study demonstrated that lnc-RAB1A-2 is associated with poor lung cancer prognosis by promoting lung cancer development.	30217564	RID05571	expression association	prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Traumatic brain injury	lncRNA2448-11	TNF	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000228978	NA	NA	7124	NA	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05572	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Traumatic brain injury	lncRNA2448-11	IL1B	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000125538	NA	NA	3553	NA	IL-1|IL1-BETA|IL1F2|IL1beta	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05573	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Traumatic brain injury	lncRNA2448-11	TGFB1	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05574	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Traumatic brain injury	lncRNA2448-11	THBD	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000178726	NA	NA	7056	NA	AHUS6|BDCA-3|BDCA3|CD141|THPH12|THRM|TM	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05575	expression association	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Traumatic brain injury	lncRNA1403	TNF	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000228978	NA	NA	7124	NA	DIF|TNF-alpha|TNFA|TNFSF2	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05576	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Traumatic brain injury	lncRNA1403	IL1B	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000125538	NA	NA	3553	NA	IL-1B|IL1-BETA|IL1F2	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05577	expression association	NA		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Traumatic brain injury	lncRNA1403	TGFB1	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|TGFB|TGFbeta	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05578	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Traumatic brain injury	lncRNA1403	THBD	positively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Other	Injury	lncRNA	PCG	NA	NA	ENSG00000178726	NA	NA	7056	NA	BDCA-3|CD141|THRM	Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate-to-severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs.Both 7.5 and 3% HS treatment decreased the expression levels of lncRNA2448-11 and lncRNA1403.The expression levels of lncRNA5189-2 were not significantly different following HS treatment (data not shown). The expression levels of lncRNA-related genes were also measured. Both 7.5 and 3% HS treatment significantly inhibited the expression levels of TNF-alpha and IL-1beta. Compared with the before group, 7.5% HS treatment significantly decreased the expression levels of thrombomodulin (P<0.05), whereas 3% HS treatment did not affect the expression levels of thrombomodulin. For TGF-beta, 7.5% HS treatment significantly increased its expression levels compared with the before group (P<0.05), while 3% HS treatment significantly decreased its expression at 24 h.These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.	30569101	RID05579	expression association	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	miR-675	H19	negatively-F		upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Co-expression profiling of plasma miRNAs and long noncoding RNAs in gastric cancer patients.The non-coding RNA levels were assessed by real-time PCR.Our results showed that the H19 level was significantly (P=0.008) elevated and MEG3 expression was significantly (P=0.002) down-regulated in GC patients compared to healthy participants. Furthermore, it was revealed that the miR-675-5p level was increased, while miR-141-3p plasma levels were significantly reduced in GC patients.A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC cells.Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors.It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues.H19 and miR-141 could compete with each other and affect their targets in GC cells.Furthermore, the clinicopathological analysis revealed that the expression level of MEG3 is significantly associated with lymph-node metastasis (P=0.028), and GC patients with advanced stages (III+IV) had a lower level of miR-148a-3p than early stages.The results of current study demonstrated that combination of H19, MEG3 and miR-675-5p expression levels could provide a potential diagnostic panel for GC.	30447342	RID05580	ceRNA or sponge	metastasis		UP(NSCLC);DATA(GSE74639)
Gastric cancer	H19	miR-141	negatively-F		upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Co-expression profiling of plasma miRNAs and long noncoding RNAs in gastric cancer patients.The non-coding RNA levels were assessed by real-time PCR.Our results showed that the H19 level was significantly (P=0.008) elevated and MEG3 expression was significantly (P=0.002) down-regulated in GC patients compared to healthy participants. Furthermore, it was revealed that the miR-675-5p level was increased, while miR-141-3p plasma levels were significantly reduced in GC patients.A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC cells.Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors.It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues.H19 and miR-141 could compete with each other and affect their targets in GC cells.Furthermore, the clinicopathological analysis revealed that the expression level of MEG3 is significantly associated with lymph-node metastasis (P=0.028), and GC patients with advanced stages (III+IV) had a lower level of miR-148a-3p than early stages.The results of current study demonstrated that combination of H19, MEG3 and miR-675-5p expression levels could provide a potential diagnostic panel for GC.	30447342	RID05581	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	
Gastric cancer	MEG3	miR-181a	negatively-F		downregulation	RT-PCR	NA	NA	tumor malignant transformation(+);prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Co-expression profiling of plasma miRNAs and long noncoding RNAs in gastric cancer patients.The non-coding RNA levels were assessed by real-time PCR.Our results showed that the H19 level was significantly (P=0.008) elevated and MEG3 expression was significantly (P=0.002) down-regulated in GC patients compared to healthy participants. Furthermore, it was revealed that the miR-675-5p level was increased, while miR-141-3p plasma levels were significantly reduced in GC patients.A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC cells.Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors.It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues.H19 and miR-141 could compete with each other and affect their targets in GC cells.Furthermore, the clinicopathological analysis revealed that the expression level of MEG3 is significantly associated with lymph-node metastasis (P=0.028), and GC patients with advanced stages (III+IV) had a lower level of miR-148a-3p than early stages.The results of current study demonstrated that combination of H19, MEG3 and miR-675-5p expression levels could provide a potential diagnostic panel for GC.	30447342	RID05582	ceRNA or sponge	metastasis,prognosis		
Gastric cancer	MEG3	miR-148a	negatively-F		downregulation	RT-PCR	NA	NA	tumor malignant transformation(+);prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Co-expression profiling of plasma miRNAs and long noncoding RNAs in gastric cancer patients.The non-coding RNA levels were assessed by real-time PCR.Our results showed that the H19 level was significantly (P=0.008) elevated and MEG3 expression was significantly (P=0.002) down-regulated in GC patients compared to healthy participants. Furthermore, it was revealed that the miR-675-5p level was increased, while miR-141-3p plasma levels were significantly reduced in GC patients.A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC cells.Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors.It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues.H19 and miR-141 could compete with each other and affect their targets in GC cells.Furthermore, the clinicopathological analysis revealed that the expression level of MEG3 is significantly associated with lymph-node metastasis (P=0.028), and GC patients with advanced stages (III+IV) had a lower level of miR-148a-3p than early stages.The results of current study demonstrated that combination of H19, MEG3 and miR-675-5p expression levels could provide a potential diagnostic panel for GC.	30447342	RID05583	ceRNA or sponge	metastasis,prognosis		
Gastric cancer	MEG3	miR-141	negatively-F		downregulation	RT-PCR	NA	NA	tumor malignant transformation(+);prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Co-expression profiling of plasma miRNAs and long noncoding RNAs in gastric cancer patients.The non-coding RNA levels were assessed by real-time PCR.Our results showed that the H19 level was significantly (P=0.008) elevated and MEG3 expression was significantly (P=0.002) down-regulated in GC patients compared to healthy participants. Furthermore, it was revealed that the miR-675-5p level was increased, while miR-141-3p plasma levels were significantly reduced in GC patients.A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC cells.Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors.It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues.H19 and miR-141 could compete with each other and affect their targets in GC cells.Furthermore, the clinicopathological analysis revealed that the expression level of MEG3 is significantly associated with lymph-node metastasis (P=0.028), and GC patients with advanced stages (III+IV) had a lower level of miR-148a-3p than early stages.The results of current study demonstrated that combination of H19, MEG3 and miR-675-5p expression levels could provide a potential diagnostic panel for GC.	30447342	RID05584	ceRNA or sponge	metastasis,prognosis		
Cmv infection	NRON	NFAT	negatively-E	qPCR	downregulation	microarray;qPCR	GSE88767	NA	senescence(-)	NA	association	RNA-protein	NA	NA	NA	Other	Cmv infection	lncRNA	PCG	ENSG00000253079	GRCh38_9:126408041-126408410	NA	NA	641373	NA	NCRNA00194	NA	Reduced expression of the lncRNA NRON is a potential hallmark of the CMV-amplified CD8+ T cell accumulations commonly seen in older humans. The profiling of microarray-detected lncRNAs and genes from five nonagenarians is found at https://www.ncbi.nlm.nih.gov/pubmed/ GEO (GSE88767).We used qPCR to re-validate the expression of NFAT1 in the CD28nullCD8+ T cell subset compared to that in the CD28bearingCD8+ T cell subset. In those cells, we found increased NFAT1 expression, which was inversely related to the reduction of NRON level. Subsequent cross-validation in CMVpp65CD8+ T cells compared to their sorted counterparts displayed a similar inverse relationship. We concluded that expression of an age-accumulated lncRNA (NRON) was decreased, whereas that of its immunity-related target gene (NFAT) was increased, in both CD28nullCD8+ T cells and CMVpp65CD8+ T cells of elderly individuals with persistent CMV infection. The identification of NRON as a potential biomarker suggests that NRON contributes to CMV-enhanced CD28nullCD8+ T cell aging by modulating phosphorylation and/or IL-4-dependent NFAT signaling.	30415066	RID05585	expression association	NA		
Breast cancer	H19	STAT3	positively-E	luciferase reporter assay;starBase;Targetscan;overexpression;siRNA;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-93-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168610	NA	283120	6774	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	APRF	LongnoncodingRNAH19competitively bindsmiR-93-5p to regulate STAT3 expression in breast cancer. The expression of STAT3 in MCF-7 cells and MDA-MB-231 cells were examined by qRT-PCRand western blot(WB). The results showed that the expression level of STAT3 in MDA-MB-231 cells was higher than that in MCF-7 cells.The potential mRNA-binding sites of H19 were predicted by using starbase v2.0.To investigate whether miR-93-5p affect STAT3 expression, we first checked and predicted the target sites of miR-93-5p in the 3'-UTR of STAT3 by TargetScanHuman release 7.2.To validate whether STAT3 was a direct target of miR-93-5p, luciferase reporters containing either the wild-type (WT) full-length STAT3 3'-UTR (STAT3-WT-luc) or the mutant (mut) miR-93-5p binding sites STAT3 3'-UTR (STAT3-mut-luc) were constructed.An RIP assay was used to pull down endogenous AGO2-containing miRNP complexes and their associated miRNAs in MDA-MB-231 cells.Our results indicated that H19 was a target of miR-93-5p and could probably modulate the expression of STAT3, which was a target of and was downregulated by miR-93-5p.The proliferation ability of MCF-7 cells increased when cotransfected with miR-93-5p mimics and pCDNA3.1-H19 compared cotransfected with miR-93-5p mimics and pCDNA3.1 and the proliferation ability of MCF-7 cells decreased when cotransfected with miR-93-5p mimics and Si-H19 compared with cotransfection with miR-93-5p mimics and Si-NC.Our study revealed a new network in the expression of STAT3 involving H19 and miR-93-5p, which may contribute to a better understanding of breast cancer pathogenesis and provide new insights into the treatment of this disease.	30256448	RID05586	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Rheumatoid arthritis	LERFS	SYNCRIP	positively-F	siRNA;immunoblot;RNA pull-down assay;overexpression	downregulation	RT-qPCR;microarray	GSE103578	NA	cell migration(+);cell invasion(+);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234665	GRCh38_9:62856999-62898095	ENSG00000135316	NA	403323	10492	NA	dJ3J17.2|GRY-RBP|hnRNP-Q|HNRNPQ|HNRPQ1|NSAP1	Long noncoding RNA LERFS negatively regulates rheumatoid synovial aggression and proliferation.Quantitative reverse transcription PCR (RT-qPCR) confirmed the significant decrease in LERFS expression in RA FLSs compared with that in HC FLSs.lncRNA LERFS has lower-than-normal expression in FLSs and synovial tissues from patients with RA.lncRNA LERFS is a negative regulator of RA FLS migration and invasion.LERFS represses the proliferation of RA FLSs.To evaluate how LERFS regulates the migration, invasion, and proliferation of RA FLSs, we sought to identify intracellular LERFS-binding factors using an RNA-pull-down assay. We transcribed full-length LERFS in vitro with biotinylated nucleotides, incubated the biotinylated LERFS (or antisense LERFS as a NC) with total cell lysates from high LERFS expressing RA FLSs, and pulled them down with streptavidin.To confirm that hnRNP Q binds specifically to LERFS, we repeated the pull-down assay with biotinylated LERFS and probed for hnRNP Q using immunoblot analysis.To corroborate these findings, we used an anti-anRNP Q antibody to immunoprecipitate endogenous hnRNP Q from total lysates of RA FLSs expressing high levels of LERFS and then extracted and analyzed the RNA bound to hnRNP Q.We also observed binding of LERFS to hnRNP Q in HC FLSs, which was evidenced by increased binding of the LERFS-hnRNP Q complex compared with that observed in RA FLSs.Next, we evaluated whether hnRNP Q helps modulate the migration, invasion, and proliferation of RA FLSs. We knocked down hnRNP Q expression using siRNA.Accordingly, we used hnRNP Q siRNA-3 (sihn- RNP Q) for subsequent experiments. Interestingly, hnRNP Q knockdown resulted in significant increases in migration, invasion, and proliferation (Figure 4, F). Conversely, overexpression of hnRNP Q decreased migration, invasion, and proliferation (Figure 4, I ). Our results suggest that hnRNP Q negatively regulates the migration, invasion, and proliferation of RA FLSs.We observed that overexpression of LERFS downregulated Rac1 mRNA expression but did not affect the mRNA expression of RhoA or CDC42 (Figure 5A). Interestingly, we showed that LERFS overexpression reduced the protein expression and activation of RhoA, Rac1, and CDC42 (Figure 5, B and C). Consistent with what we observed with LERFS, hnRNP Q knockdown by siRNA increased Rac1 mRNA expression, but it did not affect mRNA expression of RhoA or CDC42 (Figure 5D), and it increased the protein expression and activation of RhoA, Rac1, and CDC42.These data suggest that LERFS and hnRNP Q regulate Rho protein expression through different modes of action. In other words, LERFS and hnRNP Q might modulate the stability or translation of Rac1 mRNA but might regulate only the mRNA translation of RhoA and CDC42.western blotshowed that LERFS overexpression did not affect hnRNP Q expression (Figure 5G). The RNA immunoprecipitation (RIP) assay showed that hnRNP Q could bind RhoA, Rac1, and CDC42 mRNAs which was promoted by the overexpression of LERFS.Furthermore, we found that the LERFS overexpression'-induced decrease in RA FLS migration, invasion, and proliferation was reversed by knockdown of hnRNP Q (Supplemental Figure 14). Intriguingly, bioinformatics analysis revealed no Alu element in the LERFS sequence, suggesting that LERFS could not bind directly to the mRNAs of RhoA, Rac1, or CDC42.Therefore, our results indicate that LERFS regulates the protein expression of RhoA, Rac1, and CDC42 through its interaction with hnRNP Q in the cytoplasm, forming a cytoplasmic LERFS-hnRNP Q complex, which then anchors to RhoA, Rac1, and CDC42 to decrease the stability or translation of target mRNAs.	30198906	RID05587	interact with protein	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE55807,GSE86978)
Rheumatoid arthritis	LERFS	CDC42	negatively-E	RIP;overexpression;siRNA;western blot	downregulation	RT-qPCR;microarray	GSE103578	NA	cell migration(+);cell invasion(+);cell proliferation(+)	RNA stability;transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234665	GRCh38_9:62856999-62898095	ENSG00000070831	NA	403323	998	NA	CDC42Hs|G25K	Long noncoding RNA LERFS negatively regulates rheumatoid synovial aggression and proliferation.Quantitative reverse transcription PCR (RT-qPCR) confirmed the significant decrease in LERFS expression in RA FLSs compared with that in HC FLSs.lncRNA LERFS has lower-than-normal expression in FLSs and synovial tissues from patients with RA.lncRNA LERFS is a negative regulator of RA FLS migration and invasion.LERFS represses the proliferation of RA FLSs.To evaluate how LERFS regulates the migration, invasion, and proliferation of RA FLSs, we sought to identify intracellular LERFS-binding factors using an RNA-pull-down assay. We transcribed full-length LERFS in vitro with biotinylated nucleotides, incubated the biotinylated LERFS (or antisense LERFS as a NC) with total cell lysates from high LERFS-expressing RA FLSs, and pulled them down with streptavidin.To confirm that hnRNP Q binds specifically to LERFS, we repeated the pull-down assay with biotinylated LERFS and probed for hnRNP Q using immunoblot analysis.To corroborate these findings, we used an anti-hnRNP Q antibody to immunoprecipitate endogenous hnRNP Q from total lysates of RA FLSs expressing high levels of LERFS and then extracted and analyzed the RNA bound to hnRNP Q.We also observed binding of LERFS to hnRNP Q in HC FLSs, which was evidenced by increased binding of the LERFS-hnRNP Q complex compared with that observed in RA FLSs.Next, we evaluated whether hnRNP Q helps modulate the migration, invasion, and proliferation of RA FLSs. We knocked down hnRNP Q expression using siRNA.Accordingly, we used hnRNP Q siRNA-3 (sihn- RNP Q) for subsequent experiments. Interestingly, hnRNP Q knockdown resulted in significant increases in migration, invasion, and proliferation (Figure 4, F). Conversely, overexpression of hnRNP Q decreased migration, invasion, and proliferation (Figure 4, I ). Our results suggest that hnRNP Q negatively regulates the migration, invasion, and proliferation of RA FLSs.We observed that overexpression of LERFS downregulated Rac1 mRNA expression but did not affect the mRNA expression of RhoA or CDC42 (Figure 5A). Interestingly, we showed that LERFS overexpression reduced the protein expression and activation of RhoA, Rac1, and CDC42 (Figure 5, B and C). Consistent with what we observed with LERFS, hnRNP Q knockdown by siRNA increased Rac1 mRNA expression, but it did not affect mRNA expression of RhoA or CDC42 (Figure 5D), and it increased the protein expression and activation of RhoA, Rac1, and CDC42.These data suggest that LERFS and hnRNP Q regulate Rho protein expression through different modes of action. In other words, LERFS and hnRNP Q might modulate the stability or translation of Rac1 mRNA but might regulate only the mRNA translation of RhoA and CDC42.western blotshowed that LERFS overexpression did not affect hnRNP Q expression (Figure 5G). The RNA immunoprecipitation (RIP) assay showed that hnRNP Q could bind RhoA, Rac1, and CDC42 mRNAs which was promoted by the overexpression of LERFS.Furthermore, we found that the LERFS overexpression'-induced decrease in RA FLS migration, invasion, and proliferation was reversed by knockdown of hnRNP Q (Supplemental Figure 14). Intriguingly, bioinformatics analysis revealed no Alu element in the LERFS sequence, suggesting that LERFS could not bind directly to the mRNAs of RhoA, Rac1, or CDC42.Therefore, our results indicate that LERFS regulates the protein expression of RhoA, Rac1, and CDC42 through its interaction with hnRNP Q in the cytoplasm, forming a cytoplasmic LERFS-hnRNP Q complex, which then anchors to RhoA, Rac1, and CDC42 to decrease the stability or translation of target mRNAs.	30198906	RID05588	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Rheumatoid arthritis	LERFS	RAC1	negatively-E	RIP;overexpression;siRNA;western blot	downregulation	RT-qPCR;microarray	GSE103578	NA	cell migration(+);cell invasion(+);cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234665	GRCh38_9:62856999-62898095	ENSG00000136238	NA	403323	5879	NA	p21-Rac1|Rac-1|TC-25	Long noncoding RNA LERFS negatively regulates rheumatoid synovial aggression and proliferation.Quantitative reverse transcription PCR (RT-qPCR) confirmed the significant decrease in LERFS expression in RA FLSs compared with that in HC FLSs.lncRNA LERFS has lower-than-normal expression in FLSs and synovial tissues from patients with RA.lncRNA LERFS is a negative regulator of RA FLS migration and invasion.LERFS represses the proliferation of RA FLSs.To evaluate how LERFS regulates the migration, invasion, and proliferation of RA FLSs, we sought to identify intracellular LERFS-binding factors using an RNA-pull-down assay. We transcribed full-length LERFS in vitro with biotinylated nucleotides, incubated the biotinylated LERFS (or antisense LERFS as a NC) with total cell lysates from high LERFS-expressing RA FLSs, and pulled them down with streptavidin.To confirm that hnRNP Q binds specifically to LERFS, we repeated the pull-down assay with biotinylated LERFS and probed for hnRNP Q using immunoblot analysis.To corroborate these findings, we used an anti-hnRNP Q antibody to immunoprecipitate endogenous hnRNP Q from total lysates of RA FLSs expressing high levels of LERFS and then extracted and analyzed the RNA bound to hnRNP Q.We also observed binding of LERFS to hnRNP Q in HC FLSs, which was evidenced by increased binding of the LERFS-hnRNP Q complex compared with that observed in RA FLSs.Next, we evaluated whether hnRNP Q helps modulate the migration, invasion, and proliferation of RA FLSs. We knocked down hnRNP Q expression using siRNA.Accordingly, we used hnRNP Q siRNA-3 (sihn- RNP Q) for subsequent experiments. Interestingly, hnRNP Q knockdown resulted in significant increases in migration, invasion, and proliferation (Figure 4, F). Conversely, overexpression of hnRNP Q decreased migration, invasion, and proliferation (Figure 4, I ). Our results suggest that hnRNP Q negatively regulates the migration, invasion, and proliferation of RA FLSs.We observed that overexpression of LERFS downregulated Rac1 mRNA expression but did not affect the mRNA expression of RhoA or CDC42 (Figure 5A). Interestingly, we showed that LERFS overexpression reduced the protein expression and activation of RhoA, Rac1, and CDC42 (Figure 5, B and C). Consistent with what we observed with LERFS, hnRNP Q knockdown by siRNA increased Rac1 mRNA expression, but it did not affect mRNA expression of RhoA or CDC42 (Figure 5D), and it increased the protein expression and activation of RhoA, Rac1, and CDC42.These data suggest that LERFS and hnRNP Q regulate Rho protein expression through different modes of action. In other words, LERFS and hnRNP Q might modulate the stability or translation of Rac1 mRNA but might regulate only the mRNA translation of RhoA and CDC42.western blotshowed that LERFS overexpression did not affect hnRNP Q expression (Figure 5G). The RNA immunoprecipitation (RIP) assay showed that hnRNP Q could bind RhoA, Rac1, and CDC42 mRNAs which was promoted by the overexpression of LERFS.Furthermore, we found that the LERFS overexpression'-induced decrease in RA FLS migration, invasion, and proliferation was reversed by knockdown of hnRNP Q (Supplemental Figure 14). Intriguingly, bioinformatics analysis revealed no Alu element in the LERFS sequence, suggesting that LERFS could not bind directly to the mRNAs of RhoA, Rac1, or CDC42.Therefore, our results indicate that LERFS regulates the protein expression of RhoA, Rac1, and CDC42 through its interaction with hnRNP Q in the cytoplasm, forming a cytoplasmic LERFS-hnRNP Q complex, which then anchors to RhoA, Rac1, and CDC42 to decrease the stability or translation of target mRNAs.	30198906	RID05589	transcriptional regulation	NA		DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Colorectal cancer	ENSG00000231881	VEGFC	positively-E	western blot;luciferase reporter assay;Targetscan;PicTar;miRanda	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-133b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000150630	NA	NA	7424	NA	VEGF-C|VRP	Facilitating colorectal cancer cell metastasis by targeted binding of long non-coding RNA ENSG00000231881 with miR-133b via VEGFC signaling pathway.The correlation between ENSG00000231881 and CRC in clinical samples was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database. Possible binding points among miR-133b, VEGFC, and ENSG00000231881 were analyzed and predicted via the TargetScan, PicTar, and Miranda softwares.The GEPIA database is a database mining analysis website based on The Cancer Genome Atlas (TCGA). In this study, we analyzed the expression of lncRNA in CRC using the GEPIA database. The results showed that ENSG00000231881 presented a relatively high expression level in CRC patients.To verify the results from the database, clinical cancer tissues and paracancerous normal tissues were collected from 20 CRC patients for qPCR assay.The software prediction revealed the binding points between ENSG00000231881 and miR-133b.Dual luciferase assay was employed to verify this relationship.miR-133b overexpression inhibits multiple functional changes caused by ENSG00000231881 overexpression.miR-133b mimics inhibited the increase in cell proliferation caused by ENSG00000231881 overexpression.miR-133b mimics could inhibit the increase in cell metastasis caused by ENSG00000231881 overexpression.ENSG00000231881 binds to miR-133b via competitive endogenous RNA (ceRNA) mechanism and regulates the VEGFC signaling pathway, consequently leading to the metastasis of colorectal cancer cells. Our study provides a theoretical basis for the use of ENSG00000231881 as a therapeutic target for gene-targeted therapy in colorectal cancer.	30581003	RID05590	ceRNA or sponge	metastasis		UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	NEAT1_2	WEE1	positively-E	overexpression;western blot;luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	radiosensitivity(-);apoptosis process(+)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000166483	NA	NA	7465	NA	WEE1A	Downregulation of lncRNA NEAT1_2 radiosensitizes hepatocellular carcinoma cells through regulation of miR-101-3p/WEE1 axis.Compared to human hepatocyte cells (LO2), NEAT1_2 and WEE1 mRNA were markedly upregulated, and miR-101-3p was strikingly downregulated in HCC cell lines.Downregulation of WEE1 enhances the radiosensitivity of HCC cells.Bioinformatics analysis predicts that the 3'UTR of WEE1 harbors a putative miR-101-3p binding site.At 48 h post transfection, the luciferase activity of luciferase reporter containing WEE1-WT-3'UTR was strikingly reduced by miR-199-3p overexpression. However, the luciferase activity of luciferase reporter containing WEE1-MUT-3'UTR was unaffected (Figure 4B). In addition, upregulation of miR-101-3p obviously decreased the mRNA and protein levels of WEE1 compared with that in the miR-NC group, while transfection of anta-miR-101-3p presented the opposite effects.According to bioinformatics predictions, there was a direct interaction between NEAT1_2 and miR-29c.The luciferase activity of luciferase reporter containing NEAT1_2-WT was decreased in Huh7 cells transfected with miR-101-3p, but increased in Huh7 cells transfected with anta-miR-101-3p.Afterwards, Huh7 cells were transfected with pcDNA-NEAT1_2-WT, pcDNA-NEAT1_2-MUT, pcDNA, si-NEAT1_2 or si-NC, and the expression of miR-101-3p was determined by qRT-PCR The results confirmed that overexpression of wild type NEAT1_2 markedly reduced the expression of miR-101-3p, whereas NEAT1_2 silencing strikingly increased the expression of miR-101-3p.To conclude, our results support the concept that downregulation of lncRNA NEAT1_2 radiosensitizes hepatocellular carcinoma cells through regulation of miR-101-3p/WEE1 axis.	30488993	RID05591	ceRNA or sponge	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Pancreatic ductal adenocarcinoma	NONHSAT105177	CLU	negatively-E		downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	Melittin	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	NA	NA	ENSG00000120885	NA	NA	1191	NA	APOJ|CLI|CLU1|CLU2|KUB1|SGP-2|SP-40|TRPM-2	Melittin-induced long non-coding RNA NONHSAT105177 inhibits proliferation and migration of pancreatic ductal adenocarcinoma.To verify the microarray results, we performed quantitative reverse transcription polymerase chain reaction (qRT-PCR and obtained consistent results for six selected lncRNAs.Next, we further analyzed NONHSAT105177 expression in paired tumor and para-tumor tissue, finding that the expression of NONHSAT105177 was lower in the tumor tissue than in the para-tumor tissue.Upregulation of NONHSAT105177 suppressed the growth and migration of PDAC cells.NONHSAT105177 inhibited epithelial-sesenchymal transition (EMT) progression in PDAC cells.Furthermore, CLU protein levels were also reduced by NONHSAT105177 overexpression (Fig. 6b, c). Taken together, these data indicated that melittin inhibited PDAC by targeting CLU, in a manner mediated by NONHSAT105177 induction.NONHSAT105177 overexpression downregulated the cholesterol biosynthesis pathway in PDAC cells.The combined findings of our current and previous studies suggest that NONHSAT105177 mediated the melittin-induced inhibition of PDAC cell growth and metastasis, which indicated a potential target for developing new strategies.	30237397	RID05592	expression association	metastasis		UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Colorectal cancer	HOTTIP	CDKN1A	negatively-E		upregulation		NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000124762	NA	100316868	1026	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	LncRNA HOTTIP mediated DKK1 downregulation confers metastasis and invasion in colorectal cancer cells.Previous studies demonstrated that HOTTIP could promote colorectal cancer (CRC) cell proliferation via silencing of p21 expression. However, the potential role of HOTTIP in CRC metastasis has not yet been discussed. Here, cwe found that HOTTIP level was significantly higher in CRC than in corresponding adjacent normal tissues, and patients with a larger tumor size, advanced pathological stage, or distant metastasis had higher HOTTIP expression. Moreover, silencing HOTTIP expression by siRNA or shRNA could inhibit CRC cell migration and invasion in vitro and in vivo, whereas HOTTIP overexpression promoted cell metastasis, as documented in the SW480 cell lines. Mechanistic analyses indicated that HOTTIP regulates CRC cell metastasis partly through the downregulation of tumor suppressor DKK1 expression. Collectively, our results suggest that tumor expression of lncRNA HOTTIP plays an important role in CRC metastasis. HOTTIP may serve as a candidate biomarker in this disease.	30229808	RID05593	expression association	metastasis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	HOTTIP	DKK1	negatively-E	siRNA;shRNA	upregulation		NA	NA	cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000107984	NA	100316868	22943	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	DKK-1|SK	LncRNA HOTTIP mediated DKK1 downregulation confers metastasis and invasion in colorectal cancer cells.Previous studies demonstrated that HOTTIP could promote colorectal cancer (CRC) cell proliferation via silencing of p21 expression. However, the potential role of HOTTIP in CRC metastasis has not yet been discussed. Here, cwe found that HOTTIP level was significantly higher in CRC than in corresponding adjacent normal tissues, and patients with a larger tumor size, advanced pathological stage, or distant metastasis had higher HOTTIP expression. Moreover, silencing HOTTIP expression by siRNA or shRNA could inhibit CRC cell migration and invasion in vitro and in vivo, whereas HOTTIP overexpression promoted cell metastasis, as documented in the SW480 cell lines. Mechanistic analyses indicated that HOTTIP regulates CRC cell metastasis partly through the downregulation of tumor suppressor DKK1 expression. Collectively, our results suggest that tumor expression of lncRNA HOTTIP plays an important role in CRC metastasis. HOTTIP may serve as a candidate biomarker in this disease.	30229808	RID05594	expression association	metastasis		UP(LIHC);DATA(GSE117623)
Gastric cancer	MET	SNHG5	positively-E	overexpression;siRNA;luciferase reporter assay;RIP;western blot	downregulation	qPCR	NA	NA	apoptosis process(+);cell autophagy(+)	NA	regulation	protein-RNA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105976	NA	ENSG00000203875	GRCh38_6:85650491-85678932	4233	387066	DFNB97|HGFR|RCCP2	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	METase promotes cell autophagy via promoting SNHG5 and suppressing miR-20a in gastric cancer.The expression of SNHG5 was significantly decreased in tumor tissues when comparing with the expression in non-tumor tissues.In addition, GC cells transfected with METase promoted the expression of SNHG5, but decreased the expression of miR-20a.To determine the interaction between miR-20a and SNHG5, GC cell lines of SGC7901 and MKN45 were transfected with pcDNA-SNHG5 of si-SNHG5. As is presented in Fig. 3A, overexpressed SNHG5 significantly suppressed the expression of miR-20a, while down-regulated SNHG5 promoted the expression of miR-20a. Online prediction revealed that miR-20a could bind with the SNHG5-WT but not SNHG5-MUT. In addition, the luciferase reporter assay revealed that SGC7901 cell line transfected with miR-20a mimic significantly suppressed SNHG5-WT luciferase activity, while with miR-20a inhibitor significantly promoted SNHG5-WTluciferase activity. RIP revealed that the expression of SNHG5 and miR-20a was significantly increased in Ago complex. western blot revealed that GC cell lines SGC7901 and MKN45 transfected with pcDNA-SNHG5 significantly promoted the expression of Atg7, while transfected with si-SNHG5 dramatically suppressed the expression of Atg7.SNHG5 promoted GC cell apoptosis and autophage by suppressing the expression of miR-20a.To determine the mechanism of METase on cell apoptosis and autophage, GC cell lines SGC7901 and MKN45 were divided into four groups, including LV-ctrl, LV-METase, LV-METase + si-NC and LVMETase + si-SNHG5. We found that cells transfected with LV-METase significantly promoted apoptosis, while down-regulated SNHG5 abolished the results of LV-METase.Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC.	30227213	RID05595	expression association	NA	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)
Gastric cancer	SNHG5	miR-20a	negatively-F	overexpression;siRNA	downregulation	qPCR	NA	NA	apoptosis process(+);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000203875	GRCh38_6:85650491-85678932	NA	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	METase promotes cell autophagy via promoting SNHG5 and suppressing miR-20a in gastric cancer.The expression of SNHG5 was significantly decreased in tumor tissues when comparing with the expression in non-tumor tissues.In addition, GC cells transfected with METase promoted the expression of SNHG5, but decreased the expression of miR-20a.To determine the interaction between miR-20a and SNHG5, GC cell lines of SGC7901 and MKN45 were transfected with pcDNA-SNHG5 of si-SNHG5. As is presented in Fig. 3A, overexpressed SNHG5 significantly suppressed the expression of miR-20a, while down-regulated SNHG5 promoted the expression of miR-20a. Online prediction revealed that miR-20a could bind with the SNHG5-WT but not SNHG5-MUT. In addition, the luciferase reporter assay revealed that SGC7901 cell line transfected with miR-20a mimic significantly suppressed SNHG5-WT luciferase activity, while with miR-20a inhibitor significantly promoted SNHG5-WTluciferase activity. RIP revealed that the expression of SNHG5 and miR-20a was significantly increased in Ago complex. western blot revealed that GC cell lines SGC7901 and MKN45 transfected with pcDNA-SNHG5 significantly promoted the expression of Atg7, while transfected with si-SNHG5 dramatically suppressed the expression of Atg7.SNHG5 promoted GC cell apoptosis and autophage by suppressing the expression of miR-20a.To determine the mechanism of METase on cell apoptosis and autophage, GC cell lines SGC7901 and MKN45 were divided into four groups, including LV-ctrl, LV-METase, LV-METase + si-NC and LVMETase + si-SNHG5. We found that cells transfected with LV-METase significantly promoted apoptosis, while down-regulated SNHG5 abolished the results of LV-METase.Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC.	30227213	RID05596	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Renal cell carcinoma	COMETT	CCND1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000110092	NA	100996266	595	COMET|LINC01510	BCL1|D11S287E|PRAD1|U21B31	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05597	expression association	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Renal cell carcinoma	COMETT	CCNE1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000105173	NA	100996266	898	COMET|LINC01510	CCNE	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05598	expression association	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Renal cell carcinoma	COMETT	MMP2	negatively-E	western blot;overexpression	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000087245	NA	100996266	4313	COMET|LINC01510	CLG4|CLG4A|TBE-1	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05599	expression association	NA		UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	COMETT	MMP7	negatively-E	western blot;overexpression	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000137673	NA	100996266	4316	COMET|LINC01510	MPSL1|PUMP-1	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05600	expression association	NA		UP(LIHC);DATA(GSE117623)
Renal cell carcinoma	COMETT	MMP9	negatively-E	western blot;overexpression	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000100985	NA	100996266	4318	COMET|LINC01510	CLG4B	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05601	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	COMETT	CTNNB1	negatively-E	western blot;overexpression	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000168036	NA	100996266	1499	COMET|LINC01510	armadillo|beta-catenin|CTNNB	LINC01510 suppresses cell proliferation and invasion by inhibiting Wnt/b-catenin signaling in renal cell carcinoma.We firstly analyzed the expression of LINC01510 in RCC from the Cancer Genome Atlas (TCGA) and found that LINC01510 is downregulated in RCC tissues.Overexpression of LINC01510 inhibits cell proliferation, tumor growth and cell invasion.We then examined the expression of CCND1 and CCNE1, which play a key role in the transition of G0/G1 to S stage.To indentify the alteration of MMP2, MMP7 and MMP9, we observed these protein indeed decrease in Caki-1 when overexpressed LINC01510 through qRT-PCRAs CCND1 and CCNE1 are well-accepted target of Wnt/b-catenin signaling, we then asked whether LINC01510 regulates Wnt/bcatenin signaling then subsequently modulates cell proliferation and invasion. dual-luciferase reporter assays revealed that ectopic expression of LINC01510 leads to inhibition of Wnt/b-catenin signaling in 786-O, Caki-2and Caki-1. To confirm it, we performed western blot assay to examine the protein level of nuclear b-catenin, as illustrated in Fig. 4D, overexpression of LINC01510 significantly decreases its level. In addition, we ectopic expressed b-catenin in 786-O and Caki-1 stably cell lines and then performed CCK-8 cell viability assays and transwell assays, as shown in Fig. 4E and F, we found that overexpression of b-catenin partly rescues the inhibition of cell proliferation and invasion caused by LINC01510 overexpression. Taken together, these findings suggest that LINC01510 promotes cell proliferation through Wnt/b-catenin signaling.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/b-catenin signaling in RCC.	30224058	RID05602	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	FTH1P3	miR-224-5p	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000213453	GRCh38_2:27392784-27393367	NA	NA	2498	NA	FTHL3	NA	Long non-coding RNA ferritin heavy polypeptide 1 pseudogene 3 controls glioma cell proliferation and apoptosis via regulation of the microRNA-224-5p/tumor protein D52 axis.LncRNA FTH1P3 is upregulated in glioma tissues, and its upregulation promotes the proliferation and inhibits the apoptosis of glioma cells.miR-224-5p expression was significantly decreased in glioma tissues compared with normal tissues.In addition, miR-224-5p expression was significantly decreased in the pc-FTH1P3 group and increased in the siRNA-FTH1P3 group, compared with the corresponding control groups.To further examine the downstream regulatory mechanism of miR-224-5p, the target genes of miR-224-5p were predicted by TargetScanHuman. The results revealed that TPD52 was a potential target of miR-224-5p (Fig. 3A). The luciferase reporter assay demonstrated that miR-224-5p mimic decreased the luciferase activity of TPD52 3'-UTR-WT (P<0.05), although not that of TPD52 3'-UTR-MUT.protein expression of TPD52 was significantly decreased following overexpression of miR-224-5p.These data indicated that TPD52 was a target of miR-224-5p, and TPD52 expression was negatively regulated by miR-224-5p.The expression of TPD52 in glioma tissues was further determined by western blotFTH1P3 may exert its effects in glioma via the miR-224-5p/TPD52 axis.The findings of the present study may provide a theoretical basis for the study of the treatment of glioma in the future.	30221720	RID05603	ceRNA or sponge	NA	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Malignant glioma	FTH1P3	TPD52	negatively-E	luciferase reporter assay;siRNA;Targetscan;overexpression;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-224-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000076554	NA	2498	7163	FTHL3	D52|hD52|N8L	Long non-coding RNA ferritin heavy polypeptide 1 pseudogene 3 controls glioma cell proliferation and apoptosis via regulation of the microRNA-224-5p/tumor protein D52 axis.LncRNA FTH1P3 is upregulated in glioma tissues, and its upregulation promotes the proliferation and inhibits the apoptosis of glioma cells.miR-224-5p expression was significantly decreased in glioma tissues compared with normal tissues.In addition, miR-224-5p expression was significantly decreased in the pc-FTH1P3 group and increased in the siRNA-FTH1P3 group, compared with the corresponding control groups.To further examine the downstream regulatory mechanism of miR-224-5p, the target genes of miR-224-5p were predicted by TargetScanHuman. The results revealed that TPD52 was a potential target of miR-224-5p (Fig. 3A). The luciferase reporter assay demonstrated that miR-224-5p mimic decreased the luciferase activity of TPD52 3'-UTR-WT (P<0.05), although not that of TPD52 3'-UTR-MUT.protein expression of TPD52 was significantly decreased following overexpression of miR-224-5p.These data indicated that TPD52 was a target of miR-224-5p, and TPD52 expression was negatively regulated by miR-224-5p.The expression of TPD52 in glioma tissues was further determined by western blotFTH1P3 may exert its effects in glioma via the miR-224-5p/TPD52 axis.The findings of the present study may provide a theoretical basis for the study of the treatment of glioma in the future.	30221720	RID05604	ceRNA or sponge	NA	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	DOWN(LIHC);UP(BRCA);DATA(GSE117623,GSE55807)
Breast cancer	DSCAM-AS1	EPS8	positively-E	miRcode;Targetscan;luciferase reporter assay;siRNA	upregulation	qRT-PCR;microarray	GSE5840	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-);cell cycle(+);tumor growth(+)	ceRNA(miR-137)	regulation	RNA-protein	Tamoxifen	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000151491	NA	100506492	2059	M41	NA	LncRNA DSCAM-AS1 acts as a sponge of miR-137 to enhance Tamoxifen resistance in breast cancer.microarray analysis assays were carried out through GSE5840 gene chip.The data of four WT breast cancer cell lines and four RT breast cancer cell lines from GSE5840 were used to analyze lncRNA dysregulation.Moreover, the expression of DSCAM-AS1 was upregulated in TR breast cancer tissues in comparison with WT breast cancer tissues determined by qRT-PCRDSCAM-AS1 enhanced Tamoxifen resistance of breast cancer cell.The target of DSCAM-AS1 was predicted with miRcode, and we found that miR-137 was a potential target of DSCAM-AS1. qRT-PCRresults displayed that the expression of miR-137 in TR breast cancer tissues was relatively lower than that in WT breast cancer tissues (p < 0.01, Figure 6a). Using the miRcode database, we found that there was some potential binding sites between DSCAM-AS1 and miR-137, and hence miR-137 was chosen for the subsequent experiments (Figure 6b). Furthermore, dual-luciferase reporter assay also manifested that the luciferase acticity of the cells transfected with DSCAM-AS1-wild type in the miR-137 mimics group was remarkably weaker than in the miR-NC group.The binding sites of miR-137 on the 3'-UTR of EPS8 were predicted by TargetScan 7.1 (Figure 8b). Meanwhile, the results of dual-luciferase reporter assay exhibited that the luciferase activity of TR MCF7 cells cotransfected with miR-137 mimics and EPS8 wild-type recombinant vector was significantly lower compared with the mimics NC group.The qRT-PCRalso revealed that the expression of EPS8 in TR breast cancer tissues was dramatically downregulated after transfection with si-DSCAM-AS1.EPS8 could increase proliferation ability and suppress cell apoptosis and affect cell cycle of TR breast cancer cells.DSCAM-AS1 and EPS8 could facilitate breast cancer tumor growth in vivo.LncRNA DSCAM-AS1 acts as a competing endogenous RNA of miR-137 and regulates EPS8 to promote cell reproduction and suppresses cell apoptosis in TR breast cancer.	30203615	RID05605	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065)
Hepatocellular carcinoma	RAD51-AS1	RAD51	negatively-E	western blot;immunohistochemical staining;siRNA;overexpression	downregulation	RT-qPCR	NA	NA	chemosensitivity(-);radiosensitivity(-)	transcriptional regulation	regulation	RNA-protein	Melatonin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245849	GRCh38_15:40686183-40695107	ENSG00000051180	NA	100505648	5888	TODRA	BRCC5|FANCR|HsRad51|HsT16930|RAD51A|RECA	Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair.Formation of DNA damage- induced RAD51 foci was significantly reduced at every time point after melatonin treatment. To understand the mechanism by which melatonin inhibits HR, we used western blot to analyze expression of HR-associated proteins (Supplementary Figure S4, Figure 4F) and found significant decreases in RAD51, a key protein in HR, after cells were treated with melatonin (Figure 4F). In addition, immunohistochemical staining of mouse tumor tissue slices revealed that melatonin significantly inhibited expression and nuclear transport of RAD51 in tissues (Figure 4G). The above results prove that melatonin can suppress HR in HCC cells by inhibiting RAD51 expression, thereby increasing the cytotoxicity of chemotherapy and radiotherapy. Expression of a recently discovered lncRNA, RAD51-AS1, was significantly increased after melatonin treatment. We then confirmed this finding by real-time PCR and found that lncRNA RAD51-AS1 expression in cells treated with melatonin increased 1 .8 fold compared with that of the control group (vehicle only) and that RAD51 mRNA levels significantly decreased (Figure 5A,B). To determine whether binding of IncRNA RAD51-AS1 to RAD51 mRNA and the corresponding formation of double-stranded RNA can induce mRNA interference and result in RAD51 mRNA degradation, we used siRNA to silence expression of IncRNA RAD51-AS1 and then performed real-time PCR and western blot to assess RAD51 mRNA and protein expression. After RAD51-AS1 was silenced, RAD51 protein expression increased significantly (Figure 5G). Conversely, overexpression of lncRNA RAD51-AS1 decreased cellular RAD51 protein expression levels by 85% at 48 h (Figure 5H). However, RAD51 mRNA levels were not changed (Figure 5E,F). The above results indicate that lIncRNA RAD51-AS1 can suppress RA D51 protein expression, possibly by inhibiting translation initiation. Our results show that melatonin is a potential adjuvant treatment for chemotherapy and radiotherapy in HCC.	30201872	RID05606	transcriptional regulation	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	HOTAIR	MIR122	negatively-E	siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);tumorigenesis(+)	DNA methylation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000207778	NA	100124700	406906	HOXC-AS4|HOXC11-AS1|NCRNA00072	hsa-mir-122|hsa-mir-122a|miR-122|MIRN122|MIRN122A	LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.Our results showed that HOTAIR was highly expressed in HCC tissues, as compared with the peri-tumor tissues.Additionally, miR-122 expression was decreased in HCC tissues.An inverse relationship between HOTAIR and miR-122 in HCC would be observed.To further investigate the negative regulatory role of HOTAIR on miR-122 expression, we used the specific siRNAs (siHOTAIR) to silence HOTAIR. We found that HOTAIR expression was effectively knocked down by siHOTAIR-1 and siHOTAIR-2.Our results showed that knockdown of HOTAIR by siHOTAIR-1 dramatically increased the expression of miR-122 in HepG2 and Huh7 cells (Fig. 1e). On the other hand, overexpression of HOTAIR by pHOTAIR decreased miR-122 expression in HepG2 and Huh7 cells (Fig. 1f). These data indicated that HOTAIR negatively regulated miR-122 expression in HCC cells.HOTAIR promoted cell growth through downregulating miR-122 expression in vitro.HOTAIR mediated tumorigenicity through miR-122 downregulation in vivo.HOTAIR regulated DNA methylation of miR-122 promoter region.Our results showed that DNMT1, DNMT3A, and DNMT3B were upregualted in HCC cells.DNMT1, DNMT3A, and DNMT3B were suppressed by siHOTAIR-1 and promoted by pHOTAIR at both mRNA and protein levels (Fig. 5a ), indicating that HOTAIR are capable of inducing the upregulation of DNMTs in HCC cells, contributing to regulation of DNA methylation.Our results showed that either siDNMT1, or siDNMT3A, or siDNMT3B increased the expression level ofmiR-122.In addition, to assess whether HOTAIR is required for DNMTs binding to the miR-122 promoter region, ChIP was performed and our results showed that knockdown of HOTAIR caused a significant reduction of DNMTs binding to the promoter region of miR-122 (Fig. 5j). These data suggested that HOTAIR may epigenetically suppress miR-122 through DNMTsmediated DNA methylation.Our previous results have demonstrated that knockdown of HOTAIR by siHOTAIR-1 or excess miR-122 induced cell cycle arrest (Fig. 2c ). Moreover, it has been proved that Cyclin G1 (CCNG1) is a functional target ofmiR-122,which contributes to cell proliferation and cell cycle progression.HOTAIR upregulated Cyclin G1 via repressing miR-122.HOTAIR expression negatively correlated with miR-122 and positively correlated with Cyclin G1 in HCC.Taken together, our data suggested that lncRNA HOTAIR, upregulating DNMTs by EZH2, may epigenetically suppress miR-122 expression via DNA methylation, therefore leading to activation of CCNG1 and promotion of tumorigenicity in HCC	30195653	RID05607	epigenetic regulation	NA		
Hepatocellular carcinoma	HOTAIR	DNMT1	positively-F	siRNA;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);tumorigenesis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXC-AS4|HOXC11-AS1|NCRNA00072	CXXC9|DNMT|MCMT	LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.Our results showed that HOTAIR was highly expressed in HCC tissues, as compared with the peri-tumor tissues.Additionally, miR-122 expression was decreased in HCC tissues.An inverse relationship between HOTAIR and miR-122 in HCC would be observed.To further investigate the negative regulatory role of HOTAIR on miR-122 expression, we used the specific siRNAs (siHOTAIR) to silence HOTAIR. We found that HOTAIR expression was effectively knocked down by siHOTAIR-1 and siHOTAIR-2.Our results showed that knockdown of HOTAIR by siHOTAIR-1 dramatically increased the expression of miR-122 in HepG2 and Huh7 cells (Fig. 1e). On the other hand, overexpression of HOTAIR by pHOTAIR decreased miR-122 expression in HepG2 and Huh7 cells (Fig. 1f). These data indicated that HOTAIR negatively regulated miR-122 expression in HCC cells.HOTAIR promoted cell growth through downregulating miR-122 expression in vitro.HOTAIR mediated tumorigenicity through miR-122 downregulation in vivo.HOTAIR regulated DNA methylation of miR-122 promoter region.Our results showed that DNMT1, DNMT3A, and DNMT3B were upregualted in HCC cells.DNMT1, DNMT3A, and DNMT3B were suppressed by siHOTAIR-1 and promoted by pHOTAIR at both mRNA and protein levels (Fig. 5a), indicating that HOTAIR are capable of inducing the upregulation of DNMTs in HCC cells, contributing to regulation of DNA methylation.Our results showed that either siDNMT1, or siDNMT3A, or siDNMT3B increased the expression level ofmiR-122.In addition, to assess whether HOTAIR is required for DNMTs binding to the miR-122 promoter region, ChIP was performed and our results showed that knockdown of HOTAIR caused a significant reduction of DNMTs binding to the promoter region of miR-122 (Fig. 5j). These data suggested that HOTAIR may epigenetically suppress miR-122 through DNMTsmediated DNA methylation.Our previous results have demonstrated that knockdown of HOTAIR by siHOTAIR-1 or excess miR-122 induced cell cycle arrest (Fig. 2c). Moreover, it has been proved that Cyclin G1 (CCNG1) is a functional target ofmiR-122,which contributes to cell proliferation and cell cycle progression.HOTAIR upregulated Cyclin G1 via repressing miR-122.HOTAIR expression negatively correlated with miR-122 and positively correlated with Cyclin G1 in HCC.Taken together, our data suggested that lncRNA HOTAIR, upregulating DNMTs by EZH2, may epigenetically suppress miR-122 expression via DNA methylation, therefore leading to activation of CCNG1 and promotion of tumorigenicity in HCC	30195653	RID05608	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	HOTAIR	DNMT3A	positively-F	siRNA;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);tumorigenesis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000119772	NA	100124700	1788	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.Our results showed that HOTAIR was highly expressed in HCC tissues, as compared with the peri-tumor tissues.Additionally, miR-122 expression was decreased in HCC tissues.An inverse relationship between HOTAIR and miR-122 in HCC would be observed.To further investigate the negative regulatory role of HOTAIR on miR-122 expression, we used the specific siRNAs (siHOTAIR) to silence HOTAIR. We found that HOTAIR expression was effectively knocked down by siHOTAIR-1 and siHOTAIR-2.Our results showed that knockdown of HOTAIR by siHOTAIR-1 dramatically increased the expression of miR-122 in HepG2 and Huh7 cells (Fig. 1e). On the other hand, overexpression of HOTAIR by pHOTAIR decreased miR-122 expression in HepG2 and Huh7 cells (Fig. 1f). These data indicated that HOTAIR negatively regulated miR-122 expression in HCC cells.HOTAIR promoted cell growth through downregulating miR-122 expression in vitro.HOTAIR mediated tumorigenicity through miR-122 downregulation in vivo.HOTAIR regulated DNA methylation of miR-122 promoter region.Our results showed that DNMT1, DNMT3A, and DNMT3B were upregualted in HCC cells.DNMT1, DNMT3A, and DNMT3B were suppressed by siHOTAIR-1 and promoted by pHOTAIR at both mRNA and protein levels (Fig. 5a ), indicating that HOTAIR are capable of inducing the upregulation of DNMTs in HCC cells, contributing to regulation of DNA methylation.Our results showed that either siDNMT1, or siDNMT3A, or siDNMT3B increased the expression level ofmiR-122.In addition, to assess whether HOTAIR is required for DNMTs binding to the miR-122 promoter region, ChIP was performed and our results showed that knockdown of HOTAIR caused a significant reduction of DNMTs binding to the promoter region of miR-122 (Fig. 5j). These data suggested that HOTAIR may epigenetically suppress miR-122 through DNMTsmediated DNA methylation.Our previous results have demonstrated that knockdown of HOTAIR by siHOTAIR-1 or excess miR-122 induced cell cycle arrest (Fig. 2c ). Moreover, it has been proved that Cyclin G1 (CCNG1) is a functional target ofmiR-122,which contributes to cell proliferation and cell cycle progression.HOTAIR upregulated Cyclin G1 via repressing miR-122.HOTAIR expression negatively correlated with miR-122 and positively correlated with Cyclin G1 in HCC.Taken together, our data suggested that lncRNA HOTAIR, upregulating DNMTs by EZH2, may epigenetically suppress miR-122 expression via DNA methylation, therefore leading to activation of CCNG1 and promotion of tumorigenicity in HCC	30195653	RID05609	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	HOTAIR	DNMT3B	positively-F	siRNA;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);tumorigenesis(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000088305	NA	100124700	1789	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.Our results showed that HOTAIR was highly expressed in HCC tissues, as compared with the peri-tumor tissues.Additionally, miR-122 expression was decreased in HCC tissues.An inverse relationship between HOTAIR and miR-122 in HCC would be observed.To further investigate the negative regulatory role of HOTAIR on miR-122 expression, we used the specific siRNAs (siHOTAIR) to silence HOTAIR. We found that HOTAIR expression was effectively knocked down by siHOTAIR-1 and siHOTAIR-2.Our results showed that knockdown of HOTAIR by siHOTAIR-1 dramatically increased the expression of miR-122 in HepG2 and Huh7 cells (Fig. 1e). On the other hand, overexpression of HOTAIR by pHOTAIR decreased miR-122 expression in HepG2 and Huh7 cells (Fig. 1f). These data indicated that HOTAIR negatively regulated miR-122 expression in HCC cells.HOTAIR promoted cell growth through downregulating miR-122 expression in vitro.HOTAIR mediated tumorigenicity through miR-122 downregulation in vivo.HOTAIR regulated DNA methylation of miR-122 promoter region.Our results showed that DNMT1, DNMT3A, and DNMT3B were upregualted in HCC cells.DNMT1, DNMT3A, and DNMT3B were suppressed by siHOTAIR-1 and promoted by pHOTAIR at both mRNA and protein levels (Fig. 5a ), indicating that HOTAIR are capable of inducing the upregulation of DNMTs in HCC cells, contributing to regulation of DNA methylation.Our results showed that either siDNMT1, or siDNMT3A, or siDNMT3B increased the expression level ofmiR-122.In addition, to assess whether HOTAIR is required for DNMTs binding to the miR-122 promoter region, ChIP was performed and our results showed that knockdown of HOTAIR caused a significant reduction of DNMTs binding to the promoter region of miR-122 (Fig. 5j). These data suggested that HOTAIR may epigenetically suppress miR-122 through DNMTsmediated DNA methylation.Our previous results have demonstrated that knockdown of HOTAIR by siHOTAIR-1 or excess miR-122 induced cell cycle arrest (Fig. 2c ). Moreover, it has been proved that Cyclin G1 (CCNG1) is a functional target ofmiR-122,which contributes to cell proliferation and cell cycle progression.HOTAIR upregulated Cyclin G1 via repressing miR-122.HOTAIR expression negatively correlated with miR-122 and positively correlated with Cyclin G1 in HCC.Taken together, our data suggested that lncRNA HOTAIR, upregulating DNMTs by EZH2, may epigenetically suppress miR-122 expression via DNA methylation, therefore leading to activation of CCNG1 and promotion of tumorigenicity in HCC	30195653	RID05610	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	HOTAIR	CCNG1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113328	NA	100124700	900	HOXC-AS4|HOXC11-AS1|NCRNA00072	CCNG	LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.Our results showed that HOTAIR was highly expressed in HCC tissues, as compared with the peri-tumor tissues.Additionally, miR-122 expression was decreased in HCC tissues.An inverse relationship between HOTAIR and miR-122 in HCC would be observed.To further investigate the negative regulatory role of HOTAIR on miR-122 expression, we used the specific siRNAs (siHOTAIR) to silence HOTAIR. We found that HOTAIR expression was effectively knocked down by siHOTAIR-1 and siHOTAIR-2.Our results showed that knockdown of HOTAIR by siHOTAIR-1 dramatically increased the expression of miR-122 in HepG2 and Huh7 cells (Fig. 1e). On the other hand, overexpression of HOTAIR by pHOTAIR decreased miR-122 expression in HepG2 and Huh7 cells (Fig. 1f). These data indicated that HOTAIR negatively regulated miR-122 expression in HCC cells.HOTAIR promoted cell growth through downregulating miR-122 expression in vitro.HOTAIR mediated tumorigenicity through miR-122 downregulation in vivo.HOTAIR regulated DNA methylation of miR-122 promoter region.Our results showed that DNMT1, DNMT3A, and DNMT3B were upregualted in HCC cells.DNMT1, DNMT3A, and DNMT3B were suppressed by siHOTAIR-1 and promoted by pHOTAIR at both mRNA and protein levels (Fig. 5a ), indicating that HOTAIR are capable of inducing the upregulation of DNMTs in HCC cells, contributing to regulation of DNA methylation.Our results showed that either siDNMT1, or siDNMT3A, or siDNMT3B increased the expression level ofmiR-122.In addition, to assess whether HOTAIR is required for DNMTs binding to the miR-122 promoter region, ChIP was performed and our results showed that knockdown of HOTAIR caused a significant reduction of DNMTs binding to the promoter region of miR-122 (Fig. 5j). These data suggested that HOTAIR may epigenetically suppress miR-122 through DNMTsmediated DNA methylation.Our previous results have demonstrated that knockdown of HOTAIR by siHOTAIR-1 or excess miR-122 induced cell cycle arrest (Fig. 2c ). Moreover, it has been proved that Cyclin G1 (CCNG1) is a functional target ofmiR-122,which contributes to cell proliferation and cell cycle progression.HOTAIR upregulated Cyclin G1 via repressing miR-122.HOTAIR expression negatively correlated with miR-122 and positively correlated with Cyclin G1 in HCC.Taken together, our data suggested that lncRNA HOTAIR, upregulating DNMTs by EZH2, may epigenetically suppress miR-122 expression via DNA methylation, therefore leading to activation of CCNG1 and promotion of tumorigenicity in HCC	30195653	RID05611	expression association	NA		UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842)
Gastric cancer	H19	PRKAA1	negatively-E	western blot;shRNA	upregulation	microarray;qPCR	TCGA	NA	cell invasion(+);cell migration(+);chemosensitivity(-)	NA	regulation	RNA-protein	Metformin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000132356	NA	283120	5562	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	AMPKa1	Long noncoding RNA H19 participates in metformin-mediated inhibition of gastric cancer cell invasion.Based on TCGA analysis, H19 overexpression related to advanced pathological tumor stage (p < 0.01) and pathological tumor node metastasis (TNM) stage (p < 0.01) in data from 274 gastric cancer patients.Metformin acts through H19 downregulation to inhibit the invasion and migration, but not proliferation, of AGS and SGC7901 cells.We evaluated the mechanism behind the metformin-induced inhibition of invasion and migration via western blotfor protein levels of AMPKalpha and the metastasis-related protein MMP9. In AGS and SGC7901, metformin or shH19 alone could significantly increase the level of active pAMPKalpha and MMP9; however, total AMPKalpha was unchanged regardless of the presence of metformin or H19.AMPK and MMP9 are potential target genes of H19 in metformin-induced inhibition of invasion and migration.Metformin suppresses metastasis in vivo through decreasing H19.Moreover, H19 depletion increased AMPK activation and decreased MMP9 expression, and metformin could not further activate AMPK or decrease MMP9 in H19 knocked-down gastric cancer cells. In summary, metformin has a profound antitumor effect on gastric cancer cells, and H19 is a key component in the process of metformin suppressing gastric cancer cell invasion.	30192003	RID05612	expression association	metastasis,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Gastric cancer	H19	MMP9	negatively-E	western blot	upregulation	microarray;qPCR	TCGA	NA	cell invasion(+);cell migration(+);chemosensitivity(-)	NA	regulation	RNA-protein	Metformin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000100985	NA	283120	4318	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CLG4B	Long noncoding RNA H19 participates in metformin-mediated inhibition of gastric cancer cell invasion.Based on TCGA analysis, H19 overexpression related to advanced pathological tumor stage (p < 0.01) and pathological tumor node metastasis (TNM) stage (p < 0.01) in data from 274 gastric cancer patients.Metformin acts through H19 downregulation to inhibit the invasion and migration, but not proliferation, of AGS and SGC7901 cells.We evaluated the mechanism behind the metformin-induced inhibition of invasion and migration via western blotfor protein levels of AMPKalpha and the metastasis-related protein MMP9. In AGS and SGC7901, metformin or shH19 alone could significantly increase the level of active pAMPKalpha and MMP9; however, total AMPKalpha was unchanged regardless of the presence of metformin or H19.AMPK and MMP9 are potential target genes of H19 in metformin-induced inhibition of invasion and migration.Metformin suppresses metastasis in vivo through decreasing H19.Moreover, H19 depletion increased AMPK activation and decreased MMP9 expression, and metformin could not further activate AMPK or decrease MMP9 in H19 knocked-down gastric cancer cells. In summary, metformin has a profound antitumor effect on gastric cancer cells, and H19 is a key component in the process of metformin suppressing gastric cancer cell invasion.	30192003	RID05613	expression association	metastasis,chemoresistance	UP(NSCLC);DATA(GSE74639)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	OIP5-AS1	ITGA6	positively-E	DIANA;luciferase reporter assay;siRNA;RIP;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000091409	NA	729082	3655	cyrano|linc-OIP5	CD49f	Long noncoding RNA opa-interacting protein 5 antisense transcript 1 promotes proliferation and invasion through elevating integrin alpha6 expression by sponging miR-143-3p in cervical cancer.LncRNA OIP5-AS1 expression was increased in CC.To explore the molecular mechanism of lncRNA OIP5-AS1 on CC progression, DIANA was used to predict OIP5-AS1 targeting miRNAs. As shown in Figure 4A, miR-143-3p was a predicted target of OIP5-AS1. dual-luciferase reporter assay showed that the relative luciferase activity of OIP5- AS1-Wt was evidently reduced by miR-143-3p mimics (Figure 4B, P<0.05). Si-OIP5-AS1 remarkably increased the miR-143-3p expression in SiHa and CaSki cells.To explore whether OIP5-AS1 was regulated by miR-143-3p in an AGO2-dependent manner, RIP assay was performed. The results showed that OIP5-AS1 and miR-143-3p were preferentially enriched in Ago2-containing microribonucleoproteins.To identify the target genes of miR-143-3p, Targetscan software was used. ITGA6 was found to be a potential target of miR-143-3p (Figure 5A). To further verify the prediction, dual-luciferase reporter assay was used.Furthermore, qRT-PCR;ISHowed that the ITGA6 expression was noticeably increased and negatively correlated with the miR-143-3p expression in CC tissues.In conclusion, we demonstrated that OIP5-AS1 promoted proliferation and invasion of CC cells via increasing the ITGA6 expression by sponging miR-143-3p, which might be an effective therapeutic target for the treatment of patients with CC.	30188591	RID05614	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Idiopathic pulmonary fibrosis	MEG3	TP63	positively-E	immunoblot	upregulation	sequencing	GSE86618;GSE94555	NA	cell migration(+)	alternative splicing	binding/interaction	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000073282	NA	55384	8626	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	EEC3|KET|NBP|OFC8|p51|p53CP|p63|p73H|p73L|SHFM4|TP53CP|TP53L|TP73L	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05615	interact with mRNA	NA		UP(LIHC);DATA(GSE117623)
Idiopathic pulmonary fibrosis	MEG3	KRT14	positively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell migration(+)	NA	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000186847	NA	55384	3861	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	EBS3|EBS4	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05616	expression association	NA		UP(SKCM);DATA(GSE38495)
Idiopathic pulmonary fibrosis	MEG3	STAT3	positively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell migration(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168610	NA	55384	6774	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	APRF	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05617	interact with protein	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Idiopathic pulmonary fibrosis	MEG3	YAP1	positively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000137693	NA	55384	10413	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	YAP65	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05618	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Idiopathic pulmonary fibrosis	MEG3	TP73	negatively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000078900	NA	55384	7161	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	P73	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05619	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Idiopathic pulmonary fibrosis	MEG3	SOX2	negatively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000181449	NA	55384	6657	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05620	expression association	NA		UP(LIHC);DATA(GSE117623)
Idiopathic pulmonary fibrosis	MEG3	HES1	negatively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000114315	NA	55384	3280	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	bHLHb39|FLJ20408|HES-1|HRY	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05621	expression association	NA		UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Idiopathic pulmonary fibrosis	MEG3	HEY1	negatively-E		upregulation	sequencing	GSE86618;GSE94555	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000164683	NA	55384	23462	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	bHLHb31|CHF-2|CHF2|HERP2|HESR-1|HESR1|HRT-1	MEG3 is increased in idiopathic pulmonary fibrosis and regulates epithelial cell differentiation.RNA-sequencing (RNA-seq) data from epithelial cells isolated from normal and IPF lung tissue (GEO GSE86618) were reanalyzed.MEG3 RNA is highly expressed in IPF basal-like cells.Immunofluorescence colocalization demonstrated increased MEG3 RNA in IPF epithelial cells expressing basal cell markers TP63 and KRT5.Spearman correlation analysis of MEG3 with RNA profiles from IPF and donor EPCAM-sorted single cells demonstrated that normal AT2 epithelial cell markers (STFPC, SFTPB, SFTPA1, SFTPD, and NAPSA) and normal AT1 markers (HOPX) were negatively correlated with MEG3 RNA. In contrast, MEG3 RNA was positively correlated with basal cell associated transcripts, TP63, ITGB4, KRT17, and KRT5 (Figure 3A and Supplemental Table 1). Spearman correlation of bulk RNA sequences from CD326/HTII-280 FACS-sorted normal and IPF epithelial cells (GEO GSE94555) demonstrated that MEG3 positively correlated with basal cell markers TP63, KRT5, KRT17, KRT14, and ITGB4.MEG3 expression induced AXL, KRT14, and TP63 in the 3 cell lines tested. Expression of MEG3 inhibited FOXA2 and TP73 and increased STAT3 and YAP1 RNA in certain cell lines.Taken together, these data demonstrate that the LncRNA MEG3 regulates a number of genes (TP63, STAT3, KRT14, YAP1, and AXL) associated with basal cell identity and increased epithelial cell migration.To test the potential role of MEG3 in regulation of TP63 splicing, TP63 isoforms were detected by immunoblotting in HBEC3KT cells, which actively express multiple TP63 isoforms (24). Expression of MEG3 inhibited NTP63 protein variants, while TATP63 splice variants were not altered.TP63 splice isoforms were not altered in HBEC cells, consistent with total TP63 being unaltered in these cells.Promoter regions of genes associated with basal cell differentiation, i.e., SOX2, STAT3, FOXN4, FOXA1, TP73, and HEY1, and genes involved in EMT (SNAI2, SNAI1, and CDH1) contained predicted MEG3-binding sites (Figure 5B and Supplemental Table 2B). Taken together these data support a potential role for MEG3 in regulating basal cell differentiation and promoting EMT in IPF.Genes associated with basal cell differentiation; TP73, a regulator of ciliated cell differentiation; and the Notch target HEY1 were inhibited by MEG3 (Figure 6). In donor DD011L, TP73 was expressed at low levels at baseline and was not significantly altered by MEG3. Other Notch targets, NRARP and HEY1, were inhibited by MEG3 T16. In certain donors, MEG3 induced SNAI2, a gene associated with EMT, and regulated SOX2 depending on MEG3 expression levels (Supplemental Figure 5). Genes associated with basal cells that were induced in HBEC3KTs, BEAS2B, and H441, i.e., TP63 and KRT14, were not altered by MEG3 expression in primary HBEC cultures.Our current data predicts interactions between MEG3 and genes in the IPF TRN (green lines, Figure 7), wherein MEG3 positively regulates TP63, YAP1, SNAI2, and STAT3 and negatively regulates FOXA2 and TP73.Expression of MEG3 in human pulmonary epithelial cell lines increased basal cell associated RNAs, including TP63, KRT14, STAT3, and YAP1, and enhanced cell migration, consistent with a role for MEG3 in regulating basal cell identity. MEG3 reduced expression of TP73, SOX2, and Notchassociated RNAs HES1 and HEY1, in primary human bronchial epithelial cells, demonstrating a role for MEG3 in the inhibition of genes influencing basal cell differentiation into club, ciliated, or goblet cells. MEG3 induced basal cell genes and suppressed genes associated with terminal differentiation of airway cells, supporting a role for MEG3 in regulation of basal progenitor cell functions, which may contribute to tissue remodeling in IPF.	30185671	RID05622	expression association	NA		UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE51827,GSE86978)
Melanoma	LINC00963	NACC1	positively-E	miRDB;Targetscan;luciferase reporter assay;overexpression;RNA pull-down assay;siRNA	upregulation	qRT-PCR	GSE3189	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-608)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000160877	NA	100506190	112939	MetaLnc9	BEND8|BTBD14B|BTBD30|NAC-1|NAC1	Upregulation of LINC00963 facilitates melanoma progression through miR-608/NACC1 pathway and predicts poor prognosis.To identify critical lncRNAs involved in melanoma progression, the GEO dataset (GSE3189) about gene expression patterns in melanoma tissues and normal tissues was analyzed.We found that the expression of LINC00963 was upregulated nearly 3 times in melanoma tissues, compared to normal tissues.Afterward, the molecular mechanism of LINC00963 was explored. Through bioinformatics analysis using two independent tools (http://mirdb.org/miRDB/index.html and http://www. targetscan.org/vert_71/), we identified miR-608 as a possible target of LINC00963 while NACC1 targeted by miR-608. There were two potential binding sites in LINC00963 and seven potential sites in the 30-UTR of NACC1 for miR-608 (Fig. 3A). Luciferase reporter assay was utilized to verify their interaction. As shown, miR-608 overexpression suppressed the activity of LINC00963-reporter and NACC1-reporter (Fig. 3B). Moreover, RNA pull-down also indicated that LINC00963 interacted with endogenous miR-608 in A375 and A2058 cells (Fig. 3C). Above results confirmed their direct interaction. qRT-PCRanalysis showed that LINC00963 knockdown led to elevated expression of miR-608 in A375 and A2058 cells (Fig. 3D), whereas miR-608 ectopic expression inhibited NACC1 expression (Fig. 3E). To determine whether LINC00963 could promote NACC1 expression via inhibiting miR-608, we performed luciferase reporter assay, qRT-PCRand western blot. Results showed that LINC00963 knockdown suppressed the luciferase activity and NACC1 expression via suppression of miR-608 (Fig. 3FeH). Taken together, LINC00963 promotes NACC1 expression through targeting miR-608.Silencing NACC1 or overexpressing miR-608 inhibited the proliferation, migration and invasion of melanoma cells (Fig. 4BeE). The effects of LINC00963 silence on proliferation, migration and invasion were rescued by miR-608 inhibition (Fig. 4BeE). Overall, our results demonstrated that LINC00963 facilitates melanoma progression through sponging miR-608 to modulate NACC1 expression.	30180950	RID05623	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	CALML3-AS1	ZBTB2	positively-E	luciferase reporter assay;FISH;RNA pull-down assay;siRNA;overexpression	upregulation	qRT-PCR	GSE89006	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-4316)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000205488	GRCh38_10:5510036-5526246	ENSG00000181472	NA	100132159	57621	NA	bA351K16.2|KIAA1483|ZNF437	LncRNA CALML3-AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of microRNA-4316.To identify key lncRNAs implicated in BCa progression, we analyzed lncRNAs profiles (GSE89006) with pairs of BCa tissues and adjacent normal tissues in GEO database.As shown, CALML3-AS1 is the most upregulated one (Fig. 1A). qRT-PCRanalysis using 55 pairs of BCa tissues and adjacent normal tissues also verified the high expression of CALML3- AS1 in BCa tissues.Through bioinformatics analysis, we identified CALML3-AS1 may also interact with miR- 4316. Four potential binding sites for miR-4316 in CALML3-AS1 were predicted.Then luciferase reporter assay was carried out to verify their interaction. Results showed that miR- 4316 mimics significantly repressed the activity ofWT-reporter #1, #2 and #4, and vice versa.RNA-FISH also showed that CALML3-AS1 co-localizes with miR-4316 in T24 cells (Fig. 3E). Besides, RNA pull-down assay indicated that CALML3-AS1 could precipitate miR-4316 in T24 and SW780 cells (Fig. 3F). All these results demonstrated the direct interaction between CALML3-AS1 and miR-4316 in BCa cells. Finally, we also observed that CALML3- AS1 knockdown significantly promoted miR-4316 expression (Fig. 3G). Taken together, CALML3-AS1 sponges miR-4316 to inhibit its level in BCa cells.Furthermore, the target genes of miR-4316 were analyzed by bioinformatics approach and ZBTB2 was identified. A potential binding site for miR-4316 exists in the 30-UTR region of ZBTB2 mRNA (Fig. 4A). Luciferase reporter assay showed that overexpression of miR-4316 suppressed the activity of ZBTB2 WTreporter, and vice versa.We found that knockdown of CALML3- AS1 also led to decreased luciferase activity of ZBTB2 WT-reporter while inhibition of miR-4316 rescued it (Fig. 4C), suggesting CALML3-AS1 abrogates the inhibition of miR-4316 on ZBTB2. qRTPCR and western blot also demonstrated that miR-4316 suppressed ZBTB2 expression while CALML3-AS1 abolished miR-4316- mediated repression.In conclusion, our findings demonstrate a novel CALML3-AS1-mediated process involved in BCa progression and indicate it might be a promising therapeutic target.	30177388	RID05624	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Papillary thyroid carcinoma	CASC2	CDH1	positively-E	western blot	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000039068	NA	255082	999	C10orf5	CD324|UVO|uvomorulin	LncRNA CASC2 expression is downregulated in papillary thyroid cancer and promotes cell invasion by affecting EMT pathway.In the study, qRT-PCRanalysis was performed to  examine the expression of lncRNA CASC2 in the  plasma samples from 68 PTC patients and 39 pa-  tients with nodular goiter (NG). Our results demon-  strated that lncRNA CASC2 expression was signifi-  cantly lower in plasma samples and tumor tissues in  PTC patients compared to patients with nodular goi-  ter.To further investigate the under195 lying molecular mechanisms of lncRNA CASC2 in volved in tumor invasion, we detected the EMT path way related makers ZEB1, E-cadherin and N-cadherin  after lncRNA CASC2 overexpression. qRT-PCRas says results showed that overexpression of lncRNA CASC2 significantly reduced the mRNA expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the mRNA expression of the epithelial cell marker E-cadherin in TPC-1 and BCPAP cells (Fig. 3A and B). western blotresults showed that overexpression of lncRNA CASC2 significantly reduced the protein expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the protein expression of the epithelial cell marker E cadherin in TPC-1 and BCPAP cells (Fig. 3C and D).  These results indicated that overexpression of lncRNA  CASC2 expression inhibited EMT pathway.	30175973	RID05625	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Papillary thyroid carcinoma	CASC2	ZEB1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000148516	NA	255082	6935	C10orf5	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA CASC2 expression is downregulated in papillary thyroid cancer and promotes cell invasion by affecting EMT pathway.In the study, qRT-PCRanalysis was performed to  examine the expression of lncRNA CASC2 in the  plasma samples from 68 PTC patients and 39 pa-  tients with nodular goiter (NG). Our results demon-  strated that lncRNA CASC2 expression was signifi-  cantly lower in plasma samples and tumor tissues in  PTC patients compared to patients with nodular goi-  ter.To further investigate the under195 lying molecular mechanisms of lncRNA CASC2 in volved in tumor invasion, we detected the EMT path way related makers ZEB1, E-cadherin and N-cadherin  after lncRNA CASC2 overexpression. qRT-PCRas says results showed that overexpression of lncRNA CASC2 significantly reduced the mRNA expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the mRNA expression of the epithelial cell marker E-cadherin in TPC-1 and BCPAP cells (Fig. 3A and B). western blotresults showed that overexpression of lncRNA CASC2 significantly reduced the protein expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the protein expression of the epithelial cell marker E cadherin in TPC-1 and BCPAP cells (Fig. 3C and D).  These results indicated that overexpression of lncRNA  CASC2 expression inhibited EMT pathway.	30175973	RID05626	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	CASC2	CDH2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000170558	NA	255082	1000	C10orf5	CD325|CDHN|NCAD	LncRNA CASC2 expression is downregulated in papillary thyroid cancer and promotes cell invasion by affecting EMT pathway.In the study, qRT-PCRanalysis was performed to  examine the expression of lncRNA CASC2 in the  plasma samples from 68 PTC patients and 39 pa-  tients with nodular goiter (NG). Our results demon-  strated that lncRNA CASC2 expression was signifi-  cantly lower in plasma samples and tumor tissues in  PTC patients compared to patients with nodular goi-  ter.To further investigate the under195 lying molecular mechanisms of lncRNA CASC2 in volved in tumor invasion, we detected the EMT path way related makers ZEB1, E-cadherin and N-cadherin  after lncRNA CASC2 overexpression. qRT-PCRas says results showed that overexpression of lncRNA CASC2 significantly reduced the mRNA expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the mRNA expression of the epithelial cell marker E-cadherin in TPC-1 and BCPAP cells (Fig. 3A and B). western blotresults showed that overexpression of lncRNA CASC2 significantly reduced the protein expression of the mesenchymal cell markers ZEB1 and N-cadherin, but increased the protein expression of the epithelial cell marker E cadherin in TPC-1 and BCPAP cells (Fig. 3C and D).  These results indicated that overexpression of lncRNA  CASC2 expression inhibited EMT pathway.	30175973	RID05627	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DOWN(COAD);DATA(GSE117623,GSE74369)
Lung cancer	MEG3	TP53	positively-E	siRNA;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	regulation	NA	Paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	LFS1|p53	Paclitaxel promotes lung cancer cell apoptosis via MEG3-P53 pathway activation.PTX up-regulated the expression of MEG3 and P53 in A549 cell line.To prove our hypothesis that MEG3 participates in the antitumor effect of PTX by regulating the expression of P53, MEG3 siRNAs were employed to downregulate MEG3 expression. As shown in Fig. 2A, MEG3 was downregulated after transfection of siRNAs.Then, relationship between MEG3 and apoptosiswas determined via flow apoptosis assay, and the knockdown of MEG3 could significantly inhibit the PTX-induced apoptosis of A549 cells.To further explore the related molecular mechanism, western blotwas employed to determine apoptosisrelated protein P53 expression level. As shown in Fig. 2E and F, the expression of P53 in the siRNA group decreased by 25% compared with the control group (p - 0.012) and decreased by 20% in the siRNA t PTX group compared with the PTX group.Inhibition of MEG3 attenuated the antitumor activity of PTX.the level of MEG3 expression increased significantly after transfection.These results indicate that MEG3 inhibited the proliferation of A549 cells by activating p53.Overexpression of MEG3 enhanced the anti-tumor activity of PTX.P53 inhibitor had no effect on the expression of MEG3.Our results suggest that the MEG3-P53 pathway is involved in the apoptosis of A549 cells induced by PTX.	30173893	RID05628	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC000607	TP53	positively-E	western blot;RIP;overexpression	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Long non-coding RNA 00607 as a tumor suppressor by modulating NF-kB p65/p53 signaling axis in hepatocellular carcinoma.We performed lncRNA expression profiling by microarray in MHCC97H liver cancer cells treated with TNF-alpha and IL-6.To examine the clinicopathological significance of lncRNA 00607 expression in HCC, we performed quantitative real-time (qRT)-PCR assays to examine lncRNA 00607 expression levels on 27 cases of HCC and paired paratumor liver tissues. Interestingly, lncRNA 00607 was downregulated in majority of tumors.To elucidate the underlying molecular mechanism by which lncRNA 00607 overexpression decreased HCC cell proliferation,tumor growth whereas increased chemotherapy efficacy, we first examined the expression and phosphorylation status of NF-kB p65, p53, Stat1, ATF-2 and C-Myc by western blots in MHCC97H and HCCLM3 cells. Interestingly, lncRNA 00607 overexpression led to decreased p65 and its phosphorylation, a critical catalytic subunit of NF-kB (Figure 3A and C). Conversely, depletion of lncRNA 00607 by the specific siRNA led to increased p65 and its phosphorylation (Figure 3B). In further analyses, we observed that elevated lncRNA 00607 led to an increase in the protein and mRNA levels of p53 (Figure 3A and D) whereas depletion of lncRNA 00607 led to decreased p53 levels.The results showed a significantly negative correlation of NF-kB p65 with lncRNA 00607 while displaying a significantly positive correlation between p53 and lncRNA 00607 (Figure 3G). In summary, lncRNA 00607 may regulate NF-kB p65 and p53 expression.Our results showed that there was no significant difference in mRNA stability between lncRNA 00607 knockdown and control cells, suggesting that lncRNA 00607 may regulate p65 transcriptionally.we performed ChIP experiment to examine the potential binding of lncRNA 00607 on the p65 gene promoter.4C). RNA FISH technology combined with immunofluorescence analysis confirmed the co-localization of lncRNA 00607 and NF-kB p65 protein in the MHCC97H cells (Figure 4D). RNA immunoprecipitation experiments demonstrated that lncRNA 00607 was markedly directly bound by the NF-kB p65 protein but not by p53 (Figure 4E and Supplementary Figure 4, available at Carcinogenesis Online). Given that RNA immunoprecipitation experiments suggested lncRNA 00607 cannot bind with p53 directly, we aimed to determine whether p53 was regulated by NF-kB p65 activation in our setting. lncRNA 00607 induced p53 activation in HCC, which could be ameliorated by NF-kB p65 overexpression (Figure 4F). Thus, we found that lncRNA 00607 promoted p53 expression though repressing NF-kB p65 transcriptionally.Our result showed that lncRNA 00607 overexpression led to decreased cell growth in HCC, the effect rescued by p53 knockdown (Figure 5C). Consistently, knockdown p53 also blunted the effect of lncRNA 00607 overexpression on apoptosis in HCC cells (Figure 5D). These data suggest that the effects of lncRNA 00607 on cell proliferation and apoptosis were mediated by NF-kB p65/p53 signaling.Taken together, the findings of this study show that the TNF-alpha/IL-6-lncRNA 00607-NF-kB p65/p53 signaling axis represents a novel therapeutic avenue in cancer chemotherapy.	30169594	RID05629	expression association	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC000607	RELA	negatively-E	western blot;overexpression;siRNA;ChIP;FISH;immunofluorescence assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000173039	NA	NA	5970	NA	NFKB3|p65	Long non-coding RNA 00607 as a tumor suppressor by modulating NF-kB p65/p53 signaling axis in hepatocellular carcinoma.We performed lncRNA expression profiling by microarray in MHCC97H liver cancer cells treated with TNF-alpha and IL-6.To examine the clinicopathological significance of lncRNA 00607 expression in HCC, we performed quantitative real-time (qRT)-PCR assays to examine lncRNA 00607 expression levels on 27 cases of HCC and paired paratumor liver tissues. Interestingly, lncRNA 00607 was downregulated in majority of tumors.To elucidate the underlying molecular mechanism by which lncRNA 00607 overexpression decreased HCC cell proliferation,tumor growth whereas increased chemotherapy efficacy, we first examined the expression and phosphorylation status of NF-kB p65, p53, Stat1, ATF-2 and C-Myc by western blots in MHCC97H and HCCLM3 cells. Interestingly, lncRNA 00607 overexpression led to decreased p65 and its phosphorylation, a critical catalytic subunit of NF-kB (Figure 3A and C). Conversely, depletion of lncRNA 00607 by the specific siRNA led to increased p65 and its phosphorylation (Figure 3B). In further analyses, we observed that elevated lncRNA 00607 led to an increase in the protein and mRNA levels of p53 (Figure 3A and D) whereas depletion of lncRNA 00607 led to decreased p53 levels.The results showed a significantly negative correlation of NF-kB p65 with lncRNA 00607 while displaying a significantly positive correlation between p53 and lncRNA 00607 (Figure 3G). In summary, lncRNA 00607 may regulate NF-kB p65 and p53 expression.Our results showed that there was no significant difference in mRNA stability between lncRNA 00607 knockdown and control cells, suggesting that lncRNA 00607 may regulate p65 transcriptionally.we performed ChIP experiment to examine the potential binding of lncRNA 00607 on the p65 gene promoter.4C). RNA FISH technology combined with immunofluorescence analysis confirmed the co-localization of lncRNA 00607 and NF-kB p65 protein in the MHCC97H cells (Figure 4D). RNA immunoprecipitation experiments demonstrated that lncRNA 00607 was markedly directly bound by the NF-kB p65 protein but not by p53 (Figure 4E and Supplementary Figure 4, available at Carcinogenesis Online). Given that RNA immunoprecipitation experiments suggested lncRNA 00607 cannot bind with p53 directly, we aimed to determine whether p53 was regulated by NF-kB p65 activation in our setting. lncRNA 00607 induced p53 activation in HCC, which could be ameliorated by NF-kB p65 overexpression (Figure 4F). Thus, we found that lncRNA 00607 promoted p53 expression though repressing NF-kB p65 transcriptionally.Our result showed that lncRNA 00607 overexpression led to decreased cell growth in HCC, the effect rescued by p53 knockdown (Figure 5C). Consistently, knockdown p53 also blunted the effect of lncRNA 00607 overexpression on apoptosis in HCC cells (Figure 5D). These data suggest that the effects of lncRNA 00607 on cell proliferation and apoptosis were mediated by NF-kB p65/p53 signaling.Taken together, the findings of this study show that the TNF-alpha/IL-6-lncRNA 00607-NF-kB p65/p53 signaling axis represents a novel therapeutic avenue in cancer chemotherapy.	30169594	RID05630	transcriptional regulation	chemoresistance		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cancer	LINC02303	PSMD9	negatively-E	shRNA;RNA pull-down assay;RIP;luciferase reporter assay	upregulation	microarray	NA	NA	cell proliferation(+);cell cycle(+);tumor growth(+)	post-transcriptional level	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000258616	GRCh38_14:45706250-45715952	ENSG00000110801	NA	105370479	5715	TRMP	p27|Rpn4	TRMP, a p53-inducible long noncoding RNA, regulates G1/S cell cycle progression by modulating IRES-dependent p27 translation.To identify novel lncRNAs that involve in the regulation of p53 function, doxycycline-treated or untreated H1299 cells carrying a p53 tet-on system were used to determine the lncRNA expression profile via microarray analysis. Ten p53-upregulated lncRNAs identified by lncRNA microarray (fold change above 10) were selected for further validation using real-time RT-PCRanalysis.To explore the mechanism whereby TRMP regulates G1/S cell cycle progression, we examined whether TRMP could modulate the mRNA levels of G1-related cyclins and CDKs genes, such as p21, p27, cyclin D1, cyclin E1, CDK2, CDK4, and CDK6. The results showed that the mRNA levels of these G1 cell cycle-related genes were not affected by either knockdown or ectopic expression of TRMP.However, intriguingly, knockdown of TRMP increased, whereas ectopic expression of TRMP decreased the protein levels of p27, implying that TRMP regulates p27 protein expression at the post-transcriptional level.TRMP does not interfere with p27 protein turnover. We went on to test whether TRMP could regulate p27 protein expression via interacting with p27 mRNA. The results from the biotinylated oligonucleotide pull-down experiment showed no interaction between TRMP and p27 mRNA.Proteins pulled down by sense and antisense DNA oligomers corresponding to TRMP were separated by SDS-PAGE and analyzed by mass spectrometry.PTBP1 is a well-known RNA binding protein. Although a major role of PTBP1 is involved in mRNA splicing43, PTBP1 can also serve as a regulator of gene expression by binding to 5'-UTR of the target mRNAs and promoting their IRES-dependent translation44,45.More importantly, it has been previously shown that PTBP1 enhances p27 translation via binding to the p27 5'- UTR IRES site45. We therefore hypothesized that TRMP may regulate p27 translation though competing with p27 mRNA for PTBP1 binding. To further validate the interaction of PTBP1 with TRMP, an immunoprecipitation-reverse transcription polymerase chain reaction (IP-RT-PCR assay was performed. TRMP was readily detected in the Flag-PTBP1 immunoprecipitates, but not in the control immunoprecipitates (Fig. 5b). The PTBP1-TRMP interaction was also verified by affinity pull-down of endogenous TRMP using a biotin-labeled antisense DNA oligomer against TRMP.PTBP1 is directly associated with TRMP (Fig. 5e). Together, these data indicate PTBP1 as an interacting partner for TRMP. We next examined whether TRMP regulates the binding of PTBP1 to p27 mRNA. The results showed that knockdown of TRMP increased, whereas ectopic expression of TRMP decreased the binding of PTBP1 to p27 mRNA.the interaction between PTBP1 and p27 5'-UTR in a dose-dependent manner (Fig. 5h), suggesting TRMP competes with p27 mRNA for PTBP1 binding.the interaction between PTBP1 and p27 5'-UTR in a dose-dependent manner (Fig. 5h), suggesting TRMP competes with p27 mRNA for PTBP1 binding.To further determine the role of PTBP1 in TRMP-regulated p27 protein expression, TRMP and PTBP1 were knocked down individually or combined in A549 and U2OS cells. The results consistently showed that knockdown of TRMP resulted in increased protein expression of p27, however, which was greatly reversed by the simultaneous knockdown of PTBP1.indicating that TRMP regulates p27 protein expression via PTBP1. Taken together, these data suggest that TRMP regulates p27 protein levels by competing p27 mRNA for PTBP1 binding.TRMP regulates cell proliferation, G1/S cell cycle progression, and tumor xenograft growth via p27.Taken together, these findings suggest lncRNA as a new layer to fine-tune the p53 response and reveal TRMP as an important downstream effector of p53 activity.	30166522	RID05631	transcriptional regulation	NA		UP(PAAD,PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939)
Polycystic ovary syndrome	BANCR	BAX	positively-E	western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	Insulin	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296678-69311111	ENSG00000087088	NA	100885775	581	LINC00586	BCL2L4	LncRNA BANCR participates in polycystic ovary syndrome by promoting cell apoptosis.The mRNA expression levels of BANCR in GCs derived from patients with PCOS and healthy controls were detected by RT-qPCR. As shown in Fig. 1, the expression levels of BANCR were significantly higher in GCs from patients with PCOS than in controls.KGN cells were also transfected with a BANCR expression vector, after which, cell proliferation, apoptosis and the expression levels of pro-apoptotic B-cell lymphoma 2-associated X protein (Bax) and p53 were detected by Cell Counting kit-8 assay, MTT assay and western blot, respectively. The results revealed that the expression levels of lncRNA BANCR in GCs were significantly higher in patients with PCOS compared with in non-PCOS patients. In addition, insulin treatment significantly upregulated the expression of BANCR in GCs and KGN cells. Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of pro-apoptotic Bax and p53. Therefore, it may be concluded that lncRNA BANCR participates in PCOS by promoting cell apoptosis through the upregulation of Bax and p53.	30592281	RID05632	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Polycystic ovary syndrome	BANCR	TP53	positively-E	western blot	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	Insulin	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	TF	ENSG00000278910	GRCh38_9:69296678-69311111	ENSG00000141510	NA	100885775	7157	LINC00586	LFS1|p53	LncRNA BANCR participates in polycystic ovary syndrome by promoting cell apoptosis.The mRNA expression levels of BANCR in GCs derived from patients with PCOS and healthy controls were detected by RT-qPCR. As shown in Fig. 1, the expression levels of BANCR were significantly higher in GCs from patients with PCOS than in controls.KGN cells were also transfected with a BANCR expression vector, after which, cell proliferation, apoptosis and the expression levels of pro-apoptotic B-cell lymphoma 2-associated X protein (Bax) and p53 were detected by Cell Counting kit-8 assay, MTT assay and western blot, respectively. The results revealed that the expression levels of lncRNA BANCR in GCs were significantly higher in patients with PCOS compared with in non-PCOS patients. In addition, insulin treatment significantly upregulated the expression of BANCR in GCs and KGN cells. Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of pro-apoptotic Bax and p53. Therefore, it may be concluded that lncRNA BANCR participates in PCOS by promoting cell apoptosis through the upregulation of Bax and p53.	30592281	RID05633	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	NR2F2-AS1	BMI1	positively-E	microRNA;luciferase reporter assay;siRNA;Targetscan;western blot;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-320b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000247809	GRCh38_15:96110040-96327361	ENSG00000168283	NA	644192	648	NA	PCGF4|RNF51	LncRNA NR2F2-AS1 promotes tumourigenesis through modulating BMI1 expression by targeting miR-320b in non-small cell lung cancer.In order to disclose the role of LncRNA NR2F2-AS1 in NSCLC carcinogenesis, the expression of LncRNA NR2F2-AS1 in NSCLC samples and cell lines was analysed through qRT-PCR As shown in Figure 1A and Table 1, LncRNA NR2F2-AS1 expression in 39 surgically resected NSCLC tissues was significantly higher than that of the corresponding normal tissues.The bioinformatics analysis of microRNA database found the putative binding sites between LncRNA NR2F2-AS1 and miR-320b (Figure 3A). To further test this kind of relationship, a luciferase report assay was performed and as seen in Figure 3B, miR- 320b mimic lessened the luciferase activity of pmirGLO-wt-LncRNA NR2F2-AS1 but not of pmirGLO-wt-LncRNA NR2F2-AS1.Moreover, we examined the expression level of miR-320b in A549 and SPC-A-1 cells transfected with si-LncRNA NR2F2-AS1 and the level of LncRNA NR2F2-AS1 in cells transfected with miR-320b mimic respectively. The results showed that miR-320b was significantly up-regulated when decreasing the expression of LncRNA NR2F2-AS1.The bioinformatics analysis of microRNA database and Target Scan was applied to search the putative binding sites of target genes. As indicated in Figure 5A, miR-320b may regulate BMI1 by binding to its 3-UTR. To identify this hypothesis, a mutant BMI1 3-UTR was designed (Figure 5A) and amplified using PCR. After successfully constructing wild and mutant type of BMI1 3-UTR vector (pmirGLOWt- BMI1 3-UTR and pmirGLO-Mt-BMI1 3-UTR), the dual-luciferase report assay was performed in A549 and SPC-A-1 cells.The expression of BMI1 protein was also measured using western blot assay and was suppressed by overexpression of miR-320b (P < 0.05, Figure 5B). All these results indicated that miR-320b could down-regulate the expression of BMI1 for the fact that BMI1 is a direct target of miR- 320b.Down-regulated LncRNA NR2F2-AS1, upregulated miR-320b and si-BMI1 shared similar effects in cell proliferation, invasion and apoptosis.Combined with the following cellular experiments, the data showed that NR2F2-AS1 may influence the NSCLC cell proliferation, invasion and apoptosis through regulating miR-320b targeting BMI1.	30592135	RID05634	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	LUCAT1	ANXA2	negatively-F	RNA pull-down assay;western blot;FISH;immunofluorescence assay;overexpression;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000182718	NA	100505994	302	SCAL1|SCAT5	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	Long non-coding RNA LUCAT1 promotes tumourigenesis by inhibiting ANXA2 phosphorylation in hepatocellular carcinoma.To confirm the elevated expression of LUCAT1 in HCC tissues, we first examined its expression levels in 90 pairs of liver cancer and adjacent non-cancerous tissues by qRT-PCR An increase in LUCAT1 expression was found in the HCC samples.We used RNA pull-down assays followed by silver staining and MS to identify LUCAT1-binding proteins.Moreover, RNA-FISH and immunofluorescence assays indicated that LUCAT1 colocalized with ANXA2 in the cytoplasm of HCC cells.we conducted ANXA2-overexpressing HepG2 cell lines.the binding of ANXA2 and S100A10 in HCC cell lines using co-immunoprecipitation (Co-IP) assays.As LUCAT1 could bind to ANXA2, we wonder whether the expression or phosphorylation status of ANXA2 could be affected by LUCAT1 in HCC cell lines.Taken together, these results show that LUCAT1 inhibits the phosphorylation of ANXA2 at Ser-25, and then suppresses the degradation of AIIt, thereby promoting the stable expression of AIIt on the cell surface, resulting in the generation of plasmin and subsequently activating the MMP proteins.	30588744	RID05635	interact with protein	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Chronic pancreatitis	MIAT	COX2	positively-E	western blot;luciferase reporter assay;siRNA	upregulation	qRT-PCR	GSE24279	NA	cell proliferation(+)	ceRNA(miR-216a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Endocrine system disease	Pancreatitis	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000198712	NA	440823	4513	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	COII|MTCO2	Long noncoding RNA myocardial infarction associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis.Using miRNA microarray data derived from the National Center for Biotechnology Information (NCBI)  Gene Expression Omnibus (GEO) database (accession no. GSE24279), we searched the differentially expressed miRNAs in 27 pancreatitis and 22 normal control samples.The expression status of MIAT, miR-216a- 3p, and COX-2 were detected by qRT-PCRand western blot and the results indicated that the expressions of MIAT and COX-2 (Figure 1B and 1C) were elevated and miR-216a-3p (Figure 1B) was reduced in TGF-beta1-stimulated HPaSteCs compared with the control group.By bioinformatics analysis, we found that lncRNA MIAT and COX-2 shared the regulatory sites for miR-216a-3p. To determine whether miR-216a-3p directly bond to the predicted sites of MIAT and the 3'-UTR of COX-2, we performed dual-luciferase reporter assays.However, knockdown of miR-216a-3p in HPaSteCs led to significant reduction of miR-216a-3p mRNA levels and resulted in an increase of COX-2 levels (Figure 2D and 2E). Taken together, these results suggested that MIAT positively regulated the derepression of COX-2 by sponging miR-216a-3p in HPaSteCs.Our data indicated that miR-216a-3p was upregulated and COX-2 expression at mRNA and protein levels were obviously decreased in miR-216a-3p mimic-transfected HPaSteCs after TGF-beta1 induction.si-COX-2 could significantly suppress the expression of COX-2 both at mRNA and protein levels (Figure 5A and 5B), the protein levels of alpha-SMA and collagen I (Figure 5C) and cell proliferation (Figure 5D) in TGF-beta1-activated HPaSteCs, while pcDNA-MIAT observably overturned these effects.Our study provided mechanistic insights into a critical role for MIAT as a miRNA sponge in CP.	30582203	RID05636	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Non-small cell lung cancer	HULC	SPHK1	positively-E	western blot;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000176170	NA	728655	8877	HCCAT1|LINC00078|NCRNA00078	SPHK	LncRNA HULC promotes non-small cell lung cancer cell proliferation and inhibits the apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and its downstream PI3K/Akt pathway.The expression of HULC in tumor tissues and adjacent healthy tissues of 102 patients with NSCLC was detected by qRT-PCR As shown in Figure 1, expression of HULC was significantly higher in tumor tissues than that in adjacent healthy tissues in 84 out of 102 patients.HULC overexpression significantly increased the expression level of both SPHK1 and phosphorylation level of Akt in both NSCLC cell lines.These results indicate that HULC may serve as a positive upstream regulator of SPHK1, which can activate downstream PI3K/Akt pathway in NSCLC cells.Effects on HULC Overexpression, SPHK1 Inhibitor and PI3K/Akt Inhibitor on Proliferation and Apoptosis of NSCLC Cells.CONCLUSIONS: LncRNA HULC overexpression can promote NSCLC cell proliferation and inhibit cell apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and further induce the activation of its downstream PI3K/Akt pathway.	30575912	RID05637	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	HULC	AKT1	positively-F	western blot;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	phosphorylation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000142208	NA	728655	207	HCCAT1|LINC00078|NCRNA00078	AKT|PKB|PRKBA|RAC|RAC-alpha	LncRNA HULC promotes non-small cell lung cancer cell proliferation and inhibits the apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and its downstream PI3K/Akt pathway.The expression of HULC in tumor tissues and adjacent healthy tissues of 102 patients with NSCLC was detected by qRT-PCR As shown in Figure 1, expression of HULC was significantly higher in tumor tissues than that in adjacent healthy tissues in 84 out of 102 patients.HULC overexpression significantly increased the expression level of both SPHK1 and phosphorylation level of Akt in both NSCLC cell lines.These results indicate that HULC may serve as a positive upstream regulator of SPHK1, which can activate downstream PI3K/Akt pathway in NSCLC cells.Effects on HULC Overexpression, SPHK1 Inhibitor and PI3K/Akt Inhibitor on Proliferation and Apoptosis of NSCLC Cells.CONCLUSIONS: LncRNA HULC overexpression can promote NSCLC cell proliferation and inhibit cell apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and further induce the activation of its downstream PI3K/Akt pathway.	30575912	RID05638	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colon cancer	PCAT6	ARC	positively-E	shRNA;RIP;ChIP	upregulation	microarray	TCGA;GSE21510;GSE32323;GSE36070;GSE85766	NA	apoptosis process(-);cell growth(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000198576	NA	100506696	23237	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	Arg3.1|KIAA0278	Long noncoding RNA PCAT6 inhibits colon cancer cell apoptosis by regulating anti-apoptotic protein ARC expression via EZH2.Online-available datasets were downloaded from Gene Expression Omnibus (GEO, https://www.ncbi. nlm.nih.gov/geo/) and The Cancer Genome Atlas (TCGA, https://portal.gdc.cancer.gov/). R language and Bioconductor were used for data quality control, expression normalization, calculation, and annotation [16]. Five public cohorts were used in this study: GSE21510 and GSE32323 showed microarray expression profiling containing normal colonic epithelium tissues and colon cancer tissues. GSE36070 showed analysis of the EZH2-interacting RNAs in HCT116 cells using an in vivo cross-linking and immunoprecipitation strategy (iCLIP). GSE85766 showed H3K4me3, H3K27me3, and H3K79me3 CHIPsequencing data performed in colon cancer cell lines.PCAT6 is highly expressed in colon cancer and is associated with a poor patient prognosis.Our results showed that knocked down PCAT6 in colon cancer cells significantly decreased ARC expression at both the transcriptional and translation levels.To test the functional roles of PCAT6 and ARC in colon cancer cells, we performed rescue assays. We first designed two shRNAs against ARC and confirmed the interference efficiency in colon cancer cells (Supplementary Figure 1C). Our data showed that the introduction of PCAT6 significantly promoted cell growth, while the knockdown of ARC by shRNAs rescued the PCAT6-induced increase in cell growth (Figure 5(e)). Additionally, the upregulation of PCAT6 inhibited cell apoptosis and decreased cleaved caspase 3, while knocked down ARC expression by shRNAs remarkably abolished the inhibition of exogenous PCAT6 on cell apoptosis and reversed the inactivation of PCAT6 on cleaved caspase 3.By analyzing the data set of EZH2-interacting RNAs in HCT116 cells provided by Guil S [23], we identif-ied PCAT6 (RP11-480I12.3, ENST00000417262, Ensembl) as a potential EZH2- linked lncRNA. Indeed, our RNA immunoprecipitation assay using EZH2 antibody further verified the interaction of PCAT6 and EZH2 in HCT116 cells (Figure 6(a)). Therefore, we hypothesized that PCAT6 might regulate ARC expression via EZH2-mediated gene expression. To assess our hypothesis, we first designed two shRNAs against EZH2 to confirm whether EZH2 affects the expression of ARC. As expected, the results showed silenced EZH2 significantly reduced ARC expression at both the mRNA and protein levels in colon cancer cells, as well as increased the activation of cleaved caspase 3.Previous analyzes performed by Rokavec M combining the chromatin immunoprecipitation (ChIP) assay with sequencing showed histone 3 lysine 4 trimethylation (H3K4me3) occupancy over the ARC genomic loci in colon cancer cells.Because H3K4me3 is critical for gene activation, while H3K9 and H3K27 methylation is associated with gene silencing [25], we speculated that EZH2 might act as an activator in ARC transcriptional activation but not as a suppressor. Next, we performed CHIP assays to verify our hypothesis. Consistent with our hypothesis, the results showed that the occupancy of EZH2 and H3K4me3 was significantly reduced across the ARC gene region in HCT116 cells upon the knockdown of PCAT6 (Figure 6(c)). By contrast, enforcing PCAT6 expression increased the binding of EZH2 and H3K4me3 across the ARC genomic region in SW620 cells (Figure 6(d)). Together, these data support a model whereby PCAT6 acts as a coactivator with EZH2 occupancy and activity tomodulate ARC expression.	30569799	RID05639	transcriptional regulation	prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	UP(PAAD);DATA(GSE40174)
Nasopharynx carcinoma	DANCR	PTEN	negatively-E	western blot;siRNA;RIP;ChIP	upregulation	qRT-PCR	NA	NA	radiosensitivity(-);cell growth(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000171862	NA	57291	5728	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA ANCR promotes proliferation and radiation resistance of nasopharyngeal carcinoma by inhibiting PTEN expression.To explore the biological function of lncRNA ANCR in NPC, we first examined the mRNA level of ANCR in NPC tissues and corresponding adjacent normal tissues from 30 patients using qRT-PCR The expression of ANCR was significantly upregulated in NPC tissues.We analyzed the expression of a series of proliferation-related genes, including p16, p21, p27, p57, PTEN, and p53 in SUNE-1 cells by qRT-PCR We found that the expression of PTEN, a famous tumor suppressor, was greatly increased in ANCR knockdown SUNE-1 cells compared with NC control cell (Figure 4A). Then we preformed western blotto confirm this effect of ANCR on PTEN expression at the protein level. The results suggested that PTEN expression levels were increased in ANCR knockdown cells (Figure 4B and C). Further, qRT-PCRdata in NPC tissues exhibited a significant inverse correlation between ANCR and PTEN mRNA levels (Figure 4D). These results suggest that ANCR suppresses PTEN expression in NPC cells.To investigate their interaction in NPC cells, we did RIP assay in FLAG-tagged EZH2 overexpressed SUNE-1 cells. As shown in Figure 5A, FLAG-EZH2 was detected in the immunoprecipitates using western blot assay, and ANCR was also detected by qRT-PCR Then, to explore the potential mechanism of ANCR and EZH2 in PTEN regulation, we did (ChIP) assay using SUNE-1 cells transfected with NC or siANCR1. The result suggested that ANCR knockdown resulted in decreased EZH2 binding and H3K27me3 enrichment on PTEN promoter. In addition, we found that RNA polII binding and active histone marker H3K4me3 level was increased on PTEN promoter in ANCR knockdown cells. This result was consistent with activated PTEN expression (Figure 5B). Thus, it is believed that ANCR is required for EZH2 binding on PTEN promoter. It was reported that ANCR can regulate EZH2 expression and degradation.13,14 To examine this possibility in NPC cells, we used western blot to check the protein level of EZH2 and the result showed that ANCR did not affect EZH2 expression in NPC cells.Taken together, these results suggest that EZH2 and ANCR synergistically regulate PTEN expression and EZH2 is necessary for ANCR to repress the transcription of PTEN in SUNE-1 cells.	30568463	RID05640	transcriptional regulation	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Gastric cancer	HOTAIR	TUBGCP5	positively-E	miRanda;luciferase reporter assay;overexpression;siRNA	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+);cell growth(+);cell metastasis(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000153575	NA	100124700	114791	HOXC-AS4|HOXC11-AS1|NCRNA00072	GCP5|KIAA1899	Long non-coding RNA Hotair promotes gastric cancer progression via miR- 217-GPC5 axis.To better understand which lncRNA contributes to GC carcinogenesis, lncRNA microarray analysis was applied to screen differentially expressed lncRNAs between GC tissues and corresponding adjacent non-tumor tissues from 5 pair patients.lncRNA Hotair exhibits the highest expression level in GC tissues samples as compared with their matching adjacent normal tissues.In order to clarify the underlying mechanism which contributes to the oncogenic function roles of Hotari, computer algorithm miRanda was applied to predict the potential miRNA targets of Hotair in GC.A dual-luciferase reporter assay was applied to further confirm our prediction that miR-217 was a potential target for Hotair in GC cells.overexpression of miR-217 effectively reduced the luciferase activity of psi Hotair WT.Next, we detected the expression level of miR-217 in GC tissues and cell lines using qTR-PCR, and then analyzed the correlation between Hotair level and miR-217 expression using Spearman's correlation analysis. Our previous studies revealed that miR-217 expression was notably lower in GC tissues than correspondingly adjacent normal tissues.In addition, the level of miR-217 in Hotair siRNA, siRNA control, pcDNA3.1-Hotair or empty vector transfected SGC7901 and BGC823 cells was examined by qTR-PCR.Co-transfected SGC7901 and BGC823 cells with pcDNA3.1- Hotair, and miR-217 mimic or control vector, then examined the change on GC cells proliferative and metastatic capacity.Nevertheless, the influence of pcDNA3.1-Hotair on cell proliferation, apoptosis, migration, invasion, and EMT marker genes expression was effectively rescued by miR-217 mimic in GC cells.Collectively, abovementioned findings indicated that Hotair controls GC growth and metastasis through acting as a ceRNA to sponge miRNA-217 and directly increased the expression level of GCP5, which subsequently promotes GC progression and metastasis.Hotair could serve as a potentially prognostic indicator and provide new light into its underlying biological-molecular mechanism in GC.	30557546	RID05641	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Malignant glioma	ELL2	MAPK14	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	phosphorylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000118985	GRCh38_5:95885098-95961851	ENSG00000112062	NA	22936	1432	MRCCAT1	CSBP1|CSBP2|CSPB1|Mxi2|p38|PRKM14|PRKM15	Upregulation of long noncoding RNA MRCCAT1 predicts poor prognosis and functions as an oncogene in glioma.We measured the MRCCAT1 expression in these tissues by qPCR. As shown in Figure 1A, the MRCCAT1 expression was significantly upregulated in glioma tissues compared with that in normal brain tissues.p38- MAPK signaling is well known to potentiate cell proliferation and migration in various cancers, including glioma.p38 phosphorylation levels were measured by western blot in MRCCAT1 stably overexpressed and control U87 cells, and MRCCAT1 stably silenced and control U251 cells.The ectopic expression of MRCCAT1 increased phosphorylation levels of p38 in glioma cells. Conversely, knockdown of MRCCAT1 decreased phosphorylation levels of p38 in glioma cells.These results suggested that MRCCAT1 activates p38-MAPK signaling in glioma cells.MRCCAT1 is upregulated in glioma. Increased expression of MRCCAT1 predicts poor outcome of glioma patients. MRCCAT1 promotes glioma cell proliferation and migration via activating p38-MAPK signaling. MRCCAT1 may be a potential prognostic biomarker and therapeutic target for glioma.	30556882	RID05642	interact with protein	prognosis	UP(LIHC,PAAD);DOWN(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE60407,GSE111842,GSE67939)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Lung adenocarcinoma	LINC00324	AKT1	positively-E	luciferase reporter assay;western blot;siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell metastasis(+)	ceRNA(miR-615-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000178977	GRCh38_17:8220624-8224043	ENSG00000142208	NA	284029	207	C17orf44|FLJ34790|MGC104931|NCRNA00324	AKT|PKB|PRKBA|RAC|RAC-alpha	LINC00324 exerts tumor-promoting functions in lung adenocarcinoma via targeting miR-615-5p/AKT1 axis.We detected LINC00324 expression in 87 paired of LAC tissues and matched para-tumor tissues using qRT-PCR Figure 1A showed higher expression of LINC00324 in LAC samples than the para-tumor group.Considering the ceRNA role of lncRNAs, miR- 615-5p was found to be a target for LINC00324 through database searching. We constructed dual-luciferase reporter assay to verify our speculation.MiR-615-5p expression was markedly reduced in A549 cells overexpressing LINC00324, but increased in H1299 cells with LINC00324 knockdown. These data demonstrated LINC00324 could act as a sponge for miR-615-5p in LAC.Furthermore, we found that AKT1 can function as a target gene for LINC00324/miR-615-5p through bioinformatics prediction.The wild-type group showed a remarkable decrease in Luciferase activity, whereas the mutant group had no significant change compared to the control group.It is suggested AKT1 may act as a direct target for miR-615-5p in LAC cells. Next, the protein of AKT1 in LVLINC00324 transfected A549 cells and siRNAA LINC00324 transfected H1299 cells was detected using western blot.All these elucidated that LINC00324 promoted LAC progression via miR-615-5p/AKT1 axis.LINC00324 was significantly over-expressed in LAC tissues and cells. It promoted proliferation and metastasis but inhibited cell apoptosis of LAC cells via sponging miR- 615-5p to promote AKT1 expression. Our results demonstrated LINC00324 as a novel diagnostic and therapeutic target for LAC.	30556874	RID05643	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	MEG3	miR-21	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000199004	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Low expression of lncRNA MEG3 promotes the progression of oral squamous cell carcinoma by targeting miR-21.We first detected the expression of MEG3 in 45 OSCC tissues and normal control tissues by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Results showed that the expression of MEG3 was significantly decreased in OSCC tissues.We used bioinformatics to predict the miRNAs that could bind to MEG3 and performed functional analysis. Subsequently, miR-21 was selected (Figure 3A). Luciferase reporter gene assay showed that the Luciferase activity in cells of the MEG3-WT 3'UTR group was significantly reduced after transfection of miR-21.Similarly, ROC curve analysis demonstrated that miR-21 could be used as a marker for early diagnosis of OSCC.Low expression of MEG3 can promote the proliferation and migration of OSCC cells through targeted binding to miR-21.	30556872	RID05644	ceRNA or sponge	NA		
Colorectal adenocarcinoma	MEG3	TGFB1	negatively-E	western blot;siRNA;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105329	NA	55384	7040	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CED|DPD1|TGFB|TGFbeta	Down regulation of lncRNA MEG3 promotes colorectal adenocarcinoma cell proliferation and inhibits the apoptosis by up-regulating TGF-beta1 and its downstream sphingosine kinase 1.Expression of MEG3 in tumor tissues and adjacent healthy tissues of 84 patients with colorectal adenocarcinoma was detected by qRT-PCR As shown in Figure 1, the expression of MEG3 was significantly downregulated in tumor tissues compared with adjacent healthy tissues in 69 out of 84 patients.MEG3 knockdown and SPHK1 overexpression cell lines were confirmed by measuring the expression level of MEG3 and SPHK1 by qRT-PCRSPHK1 overexpression, and TGF-beta1 treatment all promoted tumor cell proliferation, and SPHK1 overexpression showed the strongest enhancing effect, followed by TGF-beta1 treatment, and the enhancing effect of MEG3 knockdown was the weakest.MEG3 knockdown significantly increased the expression level of both SPHK1 and TGF-beta1 in all the three cell lines.Treatment with TGF-beta1 showed no significant effects on MEG3 expression but significantly promoted the expression of SPHK1 (p < 0.05, Figure 5b). SPHK1 overexpression showed no significant effects on the expression of MEG3 and SPHK1 (p > 0.05, Figure 5c). These data suggest that MEG3 is in the upstream of TGF-beta1, and SPHK1 is in the downstream of TGF-beta1.Downregulation of lncRNA MEG3 can promote colorectal adenocarcinoma cell proliferation and inhibit the apoptosis by up-regulating TGF-beta1 and its downstream sphingosine kinase 1.	30556866	RID05645	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal adenocarcinoma	MEG3	SPHK1	negatively-E	western blot;siRNA;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000176170	NA	55384	8877	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	SPHK	Down regulation of lncRNA MEG3 promotes colorectal adenocarcinoma cell proliferation and inhibits the apoptosis by up-regulating TGF-beta1 and its downstream sphingosine kinase 1.Expression of MEG3 in tumor tissues and adjacent healthy tissues of 84 patients with colorectal adenocarcinoma was detected by qRT-PCR As shown in Figure 1, the expression of MEG3 was significantly downregulated in tumor tissues compared with adjacent healthy tissues in 69 out of 84 patients.MEG3 knockdown and SPHK1 overexpression cell lines were confirmed by measuring the expression level of MEG3 and SPHK1 by qRT-PCRSPHK1 overexpression, and TGF-beta1 treatment all promoted tumor cell proliferation, and SPHK1 overexpression showed the strongest enhancing effect, followed by TGF-beta1 treatment, and the enhancing effect of MEG3 knockdown was the weakest.MEG3 knockdown significantly increased the expression level of both SPHK1 and TGF-beta1 in all the three cell lines.Treatment with TGF-beta1 showed no significant effects on MEG3 expression but significantly promoted the expression of SPHK1 (p < 0.05, Figure 5b). SPHK1 overexpression showed no significant effects on the expression of MEG3 and SPHK1 (p > 0.05, Figure 5c). These data suggest that MEG3 is in the upstream of TGF-beta1, and SPHK1 is in the downstream of TGF-beta1.Downregulation of lncRNA MEG3 can promote colorectal adenocarcinoma cell proliferation and inhibit the apoptosis by up-regulating TGF-beta1 and its downstream sphingosine kinase 1.	30556866	RID05646	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	FALEC	PTEN	negatively-E	western blot;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000171862	NA	100874054	5728	FAL1|LINC00568|ncRNA-a1	BZS|MHAM|MMAC1|PTEN1|TEP1	Highly expressed lncRNA FAL1 promotes the progression of gastric cancer by inhibiting PTEN.qRT-PCRresults showed that the expression of FAL1 in GC tissues was significantly higher than that of adjacent tissues.Previous studies have shown that FAL1 overexpression promotes tumorigenesis via inhibiting PTEN expression. In the present study, we found that the expression of PTEN was significantly decreased in GC tissues.Transfection of FAL1-NC or FAL1-OE downregulated PTEN expression, whereas FAL1-siRNA transfection upregulated PTEN expression (Figure 3B and 3C). western blot results demonstrated that the protein level of PTEN was negatively regulated by FAL1.Moreover, PTEN expression in GC tissues was also negatively correlated with FAL1 expression.To explore the regulatory effect of FAL1 on PTEN, rescue experiments were conducted. Results showed that the overexpression of FAL1 significantly promoted the proliferation of GC cells, which could be partially reversed by PTEN overexpression (Figure 4A and 4B). Similarly, promoted cell cycle induced by FAL1 overexpression was partially reversed after the overexpression of PTEN.The overexpression of FAL1 can promote cell proliferation and cell cycle of GC via inhibiting PTEN.	30556865	RID05647	expression association	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic adenocarcinoma	SNHG8	CASP3	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000164305	NA	100093630	836	LINC00060|NCRNA00060	apopain|CPP32|CPP32B|Yama	LncRNA SNHG8 promotes the development and chemo-resistance of pancreatic adenocarcinoma.The expression of SNHG8 in 40 pairs of pancreatic adenocarcinoma tissues and para-cancerous tissues, as well as 10 normal pancreas tissues was detected by qRT-PCR Results showed that SNHG8 expression in pancreatic adenocarcinoma tissues was significantly higher than that of para-cancerous tissues.The regulatory role of SNHG8 in the apoptosis of pancreatic adenocarcinoma cells was accessed by flow cytometry and western blot, respectively. Results showed that SNHG8 knockdown significantly increased the apoptotic rate of Hs766T and PANC-1 cells (Figure 3A). western blot results demonstrated that downregulation of SNHG8 remarkably upregulated the protein expression levels of cleaved caspase-3 and cleaved PARP, indicating the promotion of cell apoptosis.To further explore whether SNHG8 could regulate chemotherapy resistance in pancreatic adenocarcinoma, Hs766T and PANC-1 cells were transfected with SNHG8 siRNA and induced with 0.2, 2, 20, and 200 uM gemcitabine, respectively. CCK-8 results demonstrated that SNHG8 knockdown significantly decreased chemotherapy resistance in pancreatic adenocarcinoma cells, indicating an elevated chemo-sensitivity to gemcitabine.SNHG8 is highly expressed in pancreatic adenocarcinoma tissues and is negatively correlated with its prognosis. Moreover, SNHG8 promotes cell proliferation and cell cycle, whereas inhibits cell apoptosis and reduces the chemo-sensitivity of pancreatic adenocarcinoma cells.	30556854	RID05648	expression association	chemoresistance,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Pancreatic adenocarcinoma	SNHG8	PARP1	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000143799	NA	100093630	142	LINC00060|NCRNA00060	ADPRT|ARTD1|PARP|PPOL	LncRNA SNHG8 promotes the development and chemo-resistance of pancreatic adenocarcinoma.The expression of SNHG8 in 40 pairs of pancreatic adenocarcinoma tissues and para-cancerous tissues, as well as 10 normal pancreas tissues was detected by qRT-PCR Results showed that SNHG8 expression in pancreatic adenocarcinoma tissues was significantly higher than that of para-cancerous tissues.The regulatory role of SNHG8 in the apoptosis of pancreatic adenocarcinoma cells was accessed by flow cytometry and western blot, respectively. Results showed that SNHG8 knockdown significantly increased the apoptotic rate of Hs766T and PANC-1 cells (Figure 3A). western blot results demonstrated that downregulation of SNHG8 remarkably upregulated the protein expression levels of cleaved caspase-3 and cleaved PARP, indicating the promotion of cell apoptosis.To further explore whether SNHG8 could regulate chemotherapy resistance in pancreatic adenocarcinoma, Hs766T and PANC-1 cells were transfected with SNHG8 siRNA and induced with 0.2, 2, 20, and 200 uM gemcitabine, respectively. CCK-8 results demonstrated that SNHG8 knockdown significantly decreased chemotherapy resistance in pancreatic adenocarcinoma cells, indicating an elevated chemo-sensitivity to gemcitabine.SNHG8 is highly expressed in pancreatic adenocarcinoma tissues and is negatively correlated with its prognosis. Moreover, SNHG8 promotes cell proliferation and cell cycle, whereas inhibits cell apoptosis and reduces the chemo-sensitivity of pancreatic adenocarcinoma cells.	30556854	RID05649	expression association	chemoresistance,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Ovarian cancer	JPX	PIK3CA	positively-E	western blot;overexpression	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	phosphorylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000121879	NA	554203	5290	DCBALD06|ENOX|LINC00183|NCRNA00183	PI3K	Long noncoding RNA-JPX predicts the poor prognosis of ovarian cancer patients and promotes tumor cell proliferation, invasion and migration by the PI3K/Akt/mTOR signaling pathway.32 cases ovarian cancer tissues and para-carcinoma tissues were extracted, and the expressions of JPX were detected by RT-PCR Expression of JPX was significantly upregulated in ovarian cancer tissues compared with para-carcinoma tissues.We screened a signaling pathway PI3K/Akt/ mTOR associated with JPX-promoting ovarian cancer OVCAR-3 cell proliferation by signaling pathway inhibitors.The JPX expression was significantly increased after pcDNA-JPX transfection, compared with the control (p < 0.01) (Figure 3A). western blot showed the expressions of p-PI3K, p-Akt and p-mTOR were significantly increased after transfected with pcDNA-JPX, compared to the control (p < 0.05) and the expressions of p-PI3K, p-Akt and p-mTOR were significantly decreased after adding PI3K/mTOR inhibitor into pcDNA-JPX group.These results indicated that JPX could activate the PI3K/Akt signaling pathway.JPX Promoted Cell Proliferation, Invasion and Migration of Ovarian Cancer Cells Through PI3K/Akt/mTOR Signaling Pathway.JPX could predict the poor prognosis in patients with ovarian cancer, which could promote the tumor cell proliferation, invasion and migration in human ovarian cancer cell lines and inhibited the cell apoptosis through activating PI3K/Akt/mTOR signaling pathway.	30556851	RID05650	interact with protein	prognosis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Ovarian cancer	JPX	AKT1	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	phosphorylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000142208	NA	554203	207	DCBALD06|ENOX|LINC00183|NCRNA00183	AKT|PKB|PRKBA|RAC|RAC-alpha	Long noncoding RNA-JPX predicts the poor prognosis of ovarian cancer patients and promotes tumor cell proliferation, invasion and migration by the PI3K/Akt/mTOR signaling pathway.32 cases ovarian cancer tissues and para-carcinoma tissues were extracted, and the expressions of JPX were detected by RT-PCR Expression of JPX was significantly upregulated in ovarian cancer tissues compared with para-carcinoma tissues.We screened a signaling pathway PI3K/Akt/ mTOR associated with JPX-promoting ovarian cancer OVCAR-3 cell proliferation by signaling pathway inhibitors.The JPX expression was significantly increased after pcDNA-JPX transfection, compared with the control (p < 0.01) (Figure 3A). western blot showed the expressions of p-PI3K, p-Akt and p-mTOR were significantly increased after transfected with pcDNA-JPX, compared to the control (p < 0.05) and the expressions of p-PI3K, p-Akt and p-mTOR were significantly decreased after adding PI3K/mTOR inhibitor into pcDNA-JPX group.These results indicated that JPX could activate the PI3K/Akt signaling pathway.JPX Promoted Cell Proliferation, Invasion and Migration of Ovarian Cancer Cells Through PI3K/Akt/mTOR Signaling Pathway.JPX could predict the poor prognosis in patients with ovarian cancer, which could promote the tumor cell proliferation, invasion and migration in human ovarian cancer cell lines and inhibited the cell apoptosis through activating PI3K/Akt/mTOR signaling pathway.	30556851	RID05651	interact with protein	prognosis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	JPX	MTOR	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	phosphorylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000198793	NA	554203	2475	DCBALD06|ENOX|LINC00183|NCRNA00183	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long noncoding RNA-JPX predicts the poor prognosis of ovarian cancer patients and promotes tumor cell proliferation, invasion and migration by the PI3K/Akt/mTOR signaling pathway.32 cases ovarian cancer tissues and para-carcinoma tissues were extracted, and the expressions of JPX were detected by RT-PCR Expression of JPX was significantly upregulated in ovarian cancer tissues compared with para-carcinoma tissues.We screened a signaling pathway PI3K/Akt/ mTOR associated with JPX-promoting ovarian cancer OVCAR-3 cell proliferation by signaling pathway inhibitors.The JPX expression was significantly increased after pcDNA-JPX transfection, compared with the control (p < 0.01) (Figure 3A). western blot showed the expressions of p-PI3K, p-Akt and p-mTOR were significantly increased after transfected with pcDNA-JPX, compared to the control (p < 0.05) and the expressions of p-PI3K, p-Akt and p-mTOR were significantly decreased after adding PI3K/mTOR inhibitor into pcDNA-JPX group.These results indicated that JPX could activate the PI3K/Akt signaling pathway.JPX Promoted Cell Proliferation, Invasion and Migration of Ovarian Cancer Cells Through PI3K/Akt/mTOR Signaling Pathway.JPX could predict the poor prognosis in patients with ovarian cancer, which could promote the tumor cell proliferation, invasion and migration in human ovarian cancer cell lines and inhibited the cell apoptosis through activating PI3K/Akt/mTOR signaling pathway.	30556851	RID05652	interact with protein	prognosis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Age-related hearing loss	MIAT	miR-29b	negatively-E	RT-PCR;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Nervous system disease	Inner ear disease	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1alpha signaling.Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator-activated receptor -Gamma coactivator 1alpha (PGC-1alpha) was downregulated in aged mice, with microRNA-29b (miR-29b) being highly expressed.To explore the possible signaling pathways of MIAT present in AHL, bioinformatics analyses were conducted to evaluate the regulatory relationships among MIAT, miR-29b, and SIRT1.In addition, the luciferase activity in SK-N-MC (Figure 4B) and SH-SY5Y cells (Figure 4C) cotransfected with wild-type MIAT and miR-29b was significantly reduced. Similarly, a putative target site of miR-29b was located in the 3'-UTR of SIRT1 (Figure 5A). In addition, the luciferase activity in SK-N-MC (Figure 5B) and SH-SY5Y cells (Figure 5C) cotransfected with wild-type SIRT1 and miR-29b was evidently decreased. Therefore, a MIAT/miR-29b/SIRT1/PGC-1alpha signaling pathway was established.On the contrary, SIRT1 mRNA (Figure 6B) and PGC-1alpha mRNA (Figure 6C) were both significantly reduced in the negative control group compared with those in the MIAT or anti-miR-29b group.Similar results were also obtained in SH-SY5Y cells (Figures 8 and 9), confirming the role of MIAT as an activator of SIRT1/PGC-1alpha expression via downregulating miR-29b expression. In addition, the downregulated SIRT/PGC-1alpha expression would in return increase the incidence of AHL via promoting the apoptosis of cochlear hair cells.MIAT could elevate the expression of SIRT1/PGC-1alpha via downregulating miR-29b. And the downregulated SIRT/PGC-1alpha increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.	30556210	RID05653	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Age-related hearing loss	MIAT	SIRT1	positively-E	RT-PCR;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-29b)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Inner ear disease	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000096717	NA	440823	23411	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	SIR2L1	Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1alpha signaling.Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator-activated receptor -Gamma coactivator 1alpha (PGC-1alpha) was downregulated in aged mice, with microRNA-29b (miR-29b) being highly expressed.To explore the possible signaling pathways of MIAT present in AHL, bioinformatics analyses were conducted to evaluate the regulatory relationships among MIAT, miR-29b, and SIRT1.In addition, the luciferase activity in SK-N-MC (Figure 4B) and SH-SY5Y cells (Figure 4C) cotransfected with wild-type MIAT and miR-29b was significantly reduced. Similarly, a putative target site of miR-29b was located in the 3'-UTR of SIRT1 (Figure 5A). In addition, the luciferase activity in SK-N-MC (Figure 5B) and SH-SY5Y cells (Figure 5C) cotransfected with wild-type SIRT1 and miR-29b was evidently decreased. Therefore, a MIAT/miR-29b/SIRT1/PGC-1alpha signaling pathway was established.On the contrary, SIRT1 mRNA (Figure 6B) and PGC-1alpha mRNA (Figure 6C) were both significantly reduced in the negative control group compared with those in the MIAT or anti-miR-29b group.Similar results were also obtained in SH-SY5Y cells (Figures 8 and 9), confirming the role of MIAT as an activator of SIRT1/PGC-1alpha expression via downregulating miR-29b expression. In addition, the downregulated SIRT/PGC-1alpha expression would in return increase the incidence of AHL via promoting the apoptosis of cochlear hair cells.MIAT could elevate the expression of SIRT1/PGC-1alpha via downregulating miR-29b. And the downregulated SIRT/PGC-1alpha increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.	30556210	RID05654	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Age-related hearing loss	MIAT	PPARGC1A	positively-E	RT-PCR;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-29b)	regulation	RNA-protein	NA	NA	NA	Nervous system disease	Inner ear disease	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000109819	NA	440823	10891	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	PGC-1alpha|PGC1|PGC1A|PPARGC1	Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1alpha signaling.Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator-activated receptor -Gamma coactivator 1alpha (PGC-1alpha) was downregulated in aged mice, with microRNA-29b (miR-29b) being highly expressed.To explore the possible signaling pathways of MIAT present in AHL, bioinformatics analyses were conducted to evaluate the regulatory relationships among MIAT, miR-29b, and SIRT1.In addition, the luciferase activity in SK-N-MC (Figure 4B) and SH-SY5Y cells (Figure 4C) cotransfected with wild-type MIAT and miR-29b was significantly reduced. Similarly, a putative target site of miR-29b was located in the 3'-UTR of SIRT1 (Figure 5A). In addition, the luciferase activity in SK-N-MC (Figure 5B) and SH-SY5Y cells (Figure 5C) cotransfected with wild-type SIRT1 and miR-29b was evidently decreased. Therefore, a MIAT/miR-29b/SIRT1/PGC-1alpha signaling pathway was established.On the contrary, SIRT1 mRNA (Figure 6B) and PGC-1alpha mRNA (Figure 6C) were both significantly reduced in the negative control group compared with those in the MIAT or anti-miR-29b group.Similar results were also obtained in SH-SY5Y cells (Figures 8 and 9), confirming the role of MIAT as an activator of SIRT1/PGC-1alpha expression via downregulating miR-29b expression. In addition, the downregulated SIRT/PGC-1alpha expression would in return increase the incidence of AHL via promoting the apoptosis of cochlear hair cells.MIAT could elevate the expression of SIRT1/PGC-1alpha via downregulating miR-29b. And the downregulated SIRT/PGC-1alpha increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.	30556210	RID05655	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Chronic renal failure	miR-19b-3p	LINC00667	negatively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);epithelial to mesenchymal transition(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	miRNA	lncRNA	NA	NA	ENSG00000263753	GRCh38_18:5237826-5290608	NA	339290	NA	NA	Effects of long non-coding RNA LINC00667 on renal tubular epithelial cell proliferation, apoptosis and renal fibrosis via the miR-19b-3p/LINC00667/CTGF signaling pathway in chronic renal failure;In response to LINC00667 silencing, the renal tubular epithelial cells displayed increased proliferation and migration accompanied by reduced apoptosis based on upregulated miR-19b-3p, along with inhibited renal fibrosis and EMT detected. Taken together, the key findings of our study demonstrated that decreased lncRNA LINC00667 could promote renal tubular epithelial cell proliferation and ameliorate renal fibrosis in CRF via the miR-19b-3p/LINC00667/CTGF signaling pathway.	30555030	RID05656	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)
Osteosarcoma	SP1	HCP5	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000206337	GRCh38_6:31463170-31478936	6667	10866	NA	D6S2650E|P5-1	SP1-induced upregulation of long non-coding RNA HCP5 promotes the development of osteosarcoma; CCK-8 and colony formation assay revealed the inhibitory effect of HCP5 knockdown on cell proliferation. Cell apoptosis was found to be increased in cells transfected with sh-HCP5#1. Moreover, cell invasion and epithelial-mesenchymal transition (EMT) were reversed by the silencing of HCP5. The results of functional assays showed that HCP5 acted as an oncogene in osteosarcoma. Mechanically, HCP5 was found to be activated by the transcription factor SP1. Finally, rescue assays were conducted to demonstrate the function of SP1/HCP5 axis in osteosarcoma. In conclusion, we confirmed that SP1-induced upregulation of long non-coding RNA HCP5 promotes the development of osteosarcoma.	30554864	RID05657	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	CRNDE	miR-338-3p	negatively-F	RNAi;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	Long noncoding RNA CRNDE promotes non-small cell lung cancer progression via sponging microRNA-338-3p;RESULTS:CRNDE expression is remarkably upregulated in NSCLC tissues and cell lines. Upregulated CRNDE expression was positively associated with advanced tumor-node-metastasis (TNM) stage, lymph node metastasis and poor overall survival of patients with NSCLC. Function assays demonstrated that knockdown of CRNDE significantly inhibited NSCLC cell proliferation, colony formation, migration and invasionin vitro, and decreased the xenograft tumor volume and weight in vitro. We uncovered that miR-338-3p is a downstream target of CRNDE and that miR-338-3p inhibition partially reversed the CRNDE depletion-mediated inhibitory effect on cell proliferation, colony formation, migration and invasion in NSCLC cells.                 CONCLUSION:These findings indicated that CRNDE functions as an oncogene that exerts important regulatory roles in NSCLC progression via sponging miR-338-3p.	30554121	RID05658	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Breast cancer	LINC01116	CDKN1C	negatively-E		upregulation		NA	NA	cell viability(+);colony formation(+);cell cycle(+);apoptosis process(-);cell autophagy(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000129757	NA	375295	1028	TALNEC2	BWCR|BWS|KIP2|WBS|p57|p57Kip2	The results showed that TALNEC2 was highly expressed in breast cancer tissues and cells. Knockdown of TALNEC2 significantly inhibited the malignant behaviors of MCF-7 and MDA-MB-231 cells, including inhibiting cell viability and colony forming, arresting cell cycle at G0/G1 phase, inducing cell apoptosis, and promoting cell autophagy.The expressions of p-p38, RelA, and RelB in MCF-7 cells were decreased after knockdown of TALNEC2 or EZH2, which were reversed by knockdown of p57 KIP2 concurrently. In conclusion, TALNEC2 may play an oncogenic role in breast cancer by binding to EZH2 to target p57 KIP2 .	30378143	RID05659	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Chronic myelogenous leukemia	MALAT1	MIR328	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	sponge	binding/interaction	RNA-RNA	Imatinib	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Chronic myeloid leukemia	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000207948	NA	378938	442901	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MIRN328|hsa-mir-328|mir-328	LncRNA MALAT1 promotes cell proliferation and imatinib resistance by sponging miR-328 in chronic myelogenous leukemia.The expression of MALAT1 was significantly increased in CML cells compared with peripheral blood cells from health donors. Silencing of MALAT1 significantly inhibited the proliferation and arrested cell cycle of CML cells by targeting miR-328. Moreover, MALAT1 knockdown enhanced imatinib sensitivity of K562<U+202F>cells, while silencing of miR-328 abolished this effect.	30366670	RID05660	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Breast cancer	LINC01585	CAMP	positively-E	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245479	GRCh38_15:90660207-90664967	ENSG00000164047	NA	101929765	820	NA	CAP18|FALL-39|FALL39|LL37	LINC01585 functions as a regulator of gene expression by the CAMP/CREB signaling pathway in breast cancer.we found that LINC01585 overexpression inhibited breast cancer proliferation and growth by prototypical experiments. Mechanistically, LINC01585 was located in nuclear and binding with NONO protein. Interestingly, when LINC01585 was down-expressed, NONO separated from LINC01585 and then interacted with CRTC. The complex promotes CAMP/CREB target gene transcription and thus promotes the growth of breast cancer.	30366079	RID05661	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	LINC01585	CREB	positively-E	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245479	GRCh38_15:90660207-90664967	ENSG00000118260	NA	101929765	NA	NA	NA	LINC01585 functions as a regulator of gene expression by the CAMP/CREB signaling pathway in breast cancer.we found that LINC01585 overexpression inhibited breast cancer proliferation and growth by prototypical experiments. Mechanistically, LINC01585 was located in nuclear and binding with NONO protein. Interestingly, when LINC01585 was down-expressed, NONO separated from LINC01585 and then interacted with CRTC. The complex promotes CAMP/CREB target gene transcription and thus promotes the growth of breast cancer.	30366079	RID05662	expression association	NA		
Ischemic heart disease	MALAT1	MEF2A	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-155)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000068305	NA	378938	4205	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	RSRFC4|RSRFC9	MALAT1 promoted cell proliferation and migration via MALAT1/miR-155/MEF2A pathway in hypoxia of cardiac stem cells.we demonstrated that MALAT1 regulated the MEF2A expression and exerted its role via modulation of the MALAT1/miR-155/MEF2A pathway. Taken together, our study illustrated that MALAT1 promoted the cell proliferation and migration in CoCl2 -induced CSCs hypoxia model, acting mechanistically by promoting MEF2A expression via "sponging" miR-155.	30362213	RID05663	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colorectal cancer	MAFG-DT	NDUFA4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-147b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000265688	GRCh38_17:81927829-81930753	ENSG00000189043	NA	92659	4697	MAFG-AS1	CI-9k|COXFA4|MISTR1|MLRQ|MRCAF1	LncRNA MAFG-AS1 promotes the progression of colorectal cancer by sponging miR-147b and activation of NDUFA4.overexpression of MAFG-AS1 promoted cell proliferation, cell cycle progression, and invasion, and inhibited apoptosis, while transduction of miR-147b partially reversed the effect of MAFG-AS1 on cellular processes.	30348529	RID05664	ceRNA or sponge	NA		UP(PAAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Colorectal cancer	MAPKAPK5-AS1	CDKN1A	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234608	GRCh38_12:111839758-111842902	ENSG00000124762	NA	51275	1026	C12orf47	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA MAPKAPK5-AS1 promotes colorectal cancer proliferation by partly silencing p21 expression.Knockdown of MAPKAPK5-AS1 significantly inhibited proliferation and caused apoptosis in CRC cells. We also found that p21 is a target of MAPKAPK5-AS1.	30343528	RID05665	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	RPL13AP20	EZH2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-214)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234498	GRCh38_12:12875499-12876107	ENSG00000106462	NA	387841	2146	HANR	ENX-1|EZH1|KMT6|KMT6A	HANR promotes hepatocellular carcinoma progression via miR-214/EZH2/TGF-beta axis.HANR knockdown induces attenuated cell proliferation, migration, invasion of HCC cells.we found that miR-214 was the downstream target of HANR. Furthermore, miR-214 inhibitor largely enhanced tumor phenotypes of HCC cells regulated by HANR knockdown. HANR and miR-214 regulated the EZH2, then affecting TGFBR2 level.	30342849	RID05666	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Nasopharynx carcinoma	LINC00210	NOTCH3	positively-E	luciferase reporter assay;RNA pull-down assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-328-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000231814	GRCh38_1:217892900-217920804	ENSG00000074181	NA	100885798	4854	NCRNA00210|RP11-72L13.1	CADASIL|CASIL	LINC00210 as a miR-328-5p sponge promotes nasopharyngeal carcinoma tumorigenesis by activating NOTCH3 pathway.Based on functional experiments, we revealed that LINC00210 contributed to NPC cell proliferation and invasion in vitro, and promotes tumor growth in vivo Mechanistically, we identified that LINC00210 was located in the cytoplasm of NPC cells and served as the miR-328-5p sponge. Furthermore, we showed that miR-328-5p targets the 3' untranslated region (3'-UTR) of NOTCH3. Through inhibiting miR-328-5p activity, LINC00210 promoted NOTCH3 expression in NPC, leading to activation of NOTCH3 signaling pathway.	30341249	RID05667	ceRNA or sponge	NA		UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807,GSE75367)
Colon cancer	NORAD	CAPN7	positively-E		downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);PI3K/AKT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000131375	NA	647979	23473	LINC00657	PalBH	LINC00657 promotes the development of colon cancer by activating PI3K/AKT pathway.LINC00657 had a low expression in colon cancer tissues, which could accelerate cell proliferation and invasion by activating PI3K/AKT pathway and inhibiting CAPN7 expression.	30338799	RID05668	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE86978)
Pre-eclampsia	EGFR-AS1	EGFR,	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Lowly expressed EGFR-AS1 promotes the progression of preeclampsia by inhibiting the EGFR-JAK/STAT signaling pathway.CCK-8 assay and colony formation assay showed that knockdown of EGFR-AS1 in HTR-8 cells inhibited cell proliferation. Flow cytometry results showed that knockdown of EGFR-AS1 blocked the cell cycle of HTR-8 cells.western blot results showed that the protein expressions of EGFR, p-JAK and p-STAT were decreased after knockdown of EGFR-AS1.	30338781	RID05669	expression association	NA		
Pre-eclampsia	EGFR-AS1	p-JAK	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Lowly expressed EGFR-AS1 promotes the progression of preeclampsia by inhibiting the EGFR-JAK/STAT signaling pathway.CCK-8 assay and colony formation assay showed that knockdown of EGFR-AS1 in HTR-8 cells inhibited cell proliferation. Flow cytometry results showed that knockdown of EGFR-AS1 blocked the cell cycle of HTR-8 cells.western blot results showed that the protein expressions of EGFR, p-JAK and p-STAT were decreased after knockdown of EGFR-AS1.	30338781	RID05670	expression association	NA		
Pre-eclampsia	EGFR-AS1	p-STAT	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Lowly expressed EGFR-AS1 promotes the progression of preeclampsia by inhibiting the EGFR-JAK/STAT signaling pathway.CCK-8 assay and colony formation assay showed that knockdown of EGFR-AS1 in HTR-8 cells inhibited cell proliferation. Flow cytometry results showed that knockdown of EGFR-AS1 blocked the cell cycle of HTR-8 cells.western blot results showed that the protein expressions of EGFR, p-JAK and p-STAT were decreased after knockdown of EGFR-AS1.	30338781	RID05671	expression association	NA		
Cervical cancer	CRNDE	PIK3CA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000121879	NA	643911	5290	CRNDEP|LINC00180|LOC643911	PI3K	Long non-coding RNA CRNDE may be associated with poor prognosis by promoting proliferation and inhibiting apoptosis of cervical cancer cells through targeting PI3K/AKT.Loss-of-function assays revealed that CRNDE influences proliferation and apoptosis in cervical cancer cells, and western blot assays revealed that the PI3K/AKT pathway was inactivated in response to CRNDE knockdown.	30334449	RID05672	expression association	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Cervical cancer	CRNDE	AKT1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000142208	NA	643911	207	CRNDEP|LINC00180|LOC643911	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA CRNDE may be associated with poor prognosis by promoting proliferation and inhibiting apoptosis of cervical cancer cells through targeting PI3K/AKT.Loss-of-function assays revealed that CRNDE influences proliferation and apoptosis in cervical cancer cells, and western blot assays revealed that the PI3K/AKT pathway was inactivated in response to CRNDE knockdown.	30334449	RID05673	expression association	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	HOTAIR	PTGS2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-101)	regulation	RNA-RNA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000073756	NA	100124700	5743	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	COX-2|COX2|GRIPGHS|PGG/HS|PGHS-2|PHS-2|hCox-2	lncRNA HOTAIR upregulates COX-2 expression to promote invasion and migration of nasopharyngeal carcinoma by interacting with miR-101.	30314699	RID05674	ceRNA or sponge	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	MEG3	BRCA1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-7-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000012048	NA	55384	672	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BRCC1|FANCS|PPP1R53|RNF53	High expression of lncRNA MEG3 participates in non-small cell lung cancer by regulating microRNA-7-5p.Overexpression of lncRNA MEG3 and BRCA1 in A549 and HCC823 cell lines resulted in increased apoptosis of lung cancer cells. dual-luciferase reporter assay demonstrated that lncRNA MEG3 can regulate the expression of BRCA1 through competitively binding to microRNA-7-5p to form the lncRNA MEG3/microRNA-7-5p/BRCA1 regulatory network. Besides, lncRNA MEG3 could inhibit the apoptosis inhibitory protein Bcl-2 and promote the expression of apoptosis-promoting factor Bax.	30280775	RID05675	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Colorectal cancer	CDKN2B-AS1	ABCC1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);chemoresistance(-)	ceRNA(let-7a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000103222	NA	100048912	4363	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	GS-X|MRP|MRP1	ANRIL promotes chemoresistance via disturbing expression of ABCC1 by regulating the expression of Let-7a in colorectal cancer.Results revealed that ANRIL was up-regulated in tumor tissues samples from patients with CRC and CRC cell lines.In vitro experiments revealed that ANRIL knockdown significantly inhibited CRC cell proliferation, improved the sensitivity of chemotherapy and promoted apoptosis. Further functional assays indicated that ANRIL overexpression significantly promoted cell chemoresistance by regulating ATP-binding cassette subfamily C member 1 through binding Let-7a.	30279206	RID05676	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	OGFRP1	LYPD3	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000182057	GRCh38_22:42269703-42279534	ENSG00000124466	NA	388906	27076	NA	C4.4A	Long non-coding RNA OGFRP1 regulates LYPD3 expression by sponging miR-124-3p and promotes non-small cell lung cancer progression.Loss-of-function assay indicated that knockdown of OGFRP1 inhibited proliferation, migration and invasion, and induced apoptosis in vitro. Mechanistically, OGFRP1 could directly bind to miR-124-3p and effectively act as a competing endogenous RNA (ceRNA) for miR-124-3p to promote the expression of the target gene LYPD3.	30274775	RID05677	ceRNA or sponge	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Melanoma	CRNDE	CCL18	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-205)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000006074	NA	643911	6362	CRNDEP|LINC00180|LOC643911	AMAC-1|CKb7|DC-CK1|DCCK1|MIP-4|PARC|SCYA18	The long non-coding RNA CRNDE competed endogenously with miR-205 to promote proliferation and metastasis of melanoma cells by targeting CCL18.the lncRNA CRNDE and CCL18 expression in melanoma tissues and cell lines were examined. It was determined that they were both overexpressed in melanoma tissues and cell lines. The down-regulation of lncRNA CRNDE and CCL18 induced melanoma cell apoptosis and inhibited cell viability. Then, miR-205 which had binding site with lncRNA CRNDE and CCL18 was involved in the next experiment, and it was down-regulated in melanoma that negatively correlated with lncRNA CRNDE expression.	30257602	RID05678	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Endometrial cancer	PCGEM1	STAT3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000168610	NA	64002	6774	LINC00071|NCRNA00071|PCAT9	APRF	The relationship between lncRNA PCGEM1 and STAT3 during the occurrence and development of endometrial carcinoma. The upregulation of PCGEM1 promoted the proliferation, migration, and invasive ability of EC cells while inhibiting apoptosis. The silencing of PCGEM1 had the opposite effects.we confirmed that PCGEM1 could upregulate the expression of STAT3 by acting as a competing endogenous RNA for miR-129-5p, thereby affecting the occurrence and development of EC.	30257404	RID05679	ceRNA or sponge	NA	UP(PAAD);DATA(GSE60407)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	PRNCR1	HEY2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-448)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224722	GRCh38_8:127086263-127087510	ENSG00000135547	NA	101867536	23493	PCAT8	bHLHb32|HERP1|HESR2	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer.Functional assays revealed the anti-oncogenic function of miR-448 in NSCLC by inhibiting cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT).we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448.	30257372	RID05680	ceRNA or sponge	NA		UP(SKCM);DATA(GSE38495)
Gastric cancer	SNHG17	p15	negatively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000086504	NA	388796	NA	NA	NA	LncRNA SNHG17 promotes gastric cancer progression by epigenetically silencing of p15 and p57. Gain- and loss-of-function of SNHG17 revealed that SNHG17 promoted GC cell proliferation, cell cycle progression, invasion, and migration and inhibited apoptosis. Mechanistic investigations showed that SNHG17 was associated with polycomb repressive complex 2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15 and p57, thus contributing to the regulation of GC cell cycle and proliferation.	30256413	RID05681	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Gastric cancer	SNHG17	CDKN1C	negatively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000129757	NA	388796	1028	NA	BWCR|BWS|KIP2|P57	LncRNA SNHG17 promotes gastric cancer progression by epigenetically silencing of p15 and p57. Gain- and loss-of-function of SNHG17 revealed that SNHG17 promoted GC cell proliferation, cell cycle progression, invasion, and migration and inhibited apoptosis. Mechanistic investigations showed that SNHG17 was associated with polycomb repressive complex 2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15 and p57, thus contributing to the regulation of GC cell cycle and proliferation.	30256413	RID05682	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Cervical cancer	SNHG12	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000168610	NA	85028	6774	ASLNC04080|C1orf79|LINC00100|PNAS-123	APRF	Long noncoding RNA SNHG12 promotes the progression of cervical cancer via modulating miR-125b/STAT3 axis. SNHG12 inhibition restrained the proliferation, migration, and invasion of cervical cancer cells. Meanwhile, miR-125b mimics repressed the expression of signal transducer and activator of transcription 3 (STAT3). SNHG12 modulated STAT3 by sponging miR-125b in cervical cancer and played an important role in the development of cervical cancer.	30246459	RID05683	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	MIF-AS1	NDUFA4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-212-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000281335	GRCh38_CHR_HSCHR22_1_CTG7:23894426-23898930	ENSG00000189043	NA	284889	4697	LOC284889|MIF-AS	CI-9k|COXFA4|MISTR1|MLRQ|MRCAF1	Long non-coding RNA MIF-AS1 promotes gastric cancer cell proliferation and reduces apoptosis to upregulate NDUFA4. MiR-212-5p was identified as the most important miRNA linker between lncMIF-AS1 and NDUFA4, which was negatively regulated by lncMIF-AS1 and its depletion is the main cause of NDUFA4 overexpression.the present study implies that inhibition of lncMIF-AS1/miR-212-5p/NDUFA4 signal transduction may provide a promising therapeutic target for the treatment of gastric cancer.	30238562	RID05684	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(PAAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Rheumatoid arthritis	GAS5	Caspase3	positively-E	RNAi;western blot	downregulation	RT-PCR	NA	NA	apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Tanshinone IIA promotes the apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis by up-regulating lncRNA GAS5.GAS5 knockdown down-regulated the expression of cleaved caspase-3 and caspase-9 in the RAFLS cells and activated the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway. These data indicate that Tan IIA promotes RAFLS apoptosis by up-regulating lncRNA GAS5, with enhanced expression of cleaved caspase-3/caspase-9 and inhibited PI3K/AKT signaling.	30232236	RID05685	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Rheumatoid arthritis	GAS5	Caspase9	positively-E	RNAi;western blot	downregulation	RT-PCR	NA	NA	apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Tanshinone IIA promotes the apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis by up-regulating lncRNA GAS5.GAS5 knockdown down-regulated the expression of cleaved caspase-3 and caspase-9 in the RAFLS cells and activated the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway. These data indicate that Tan IIA promotes RAFLS apoptosis by up-regulating lncRNA GAS5, with enhanced expression of cleaved caspase-3/caspase-9 and inhibited PI3K/AKT signaling.	30232236	RID05686	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Hepatocellular carcinoma	CRNDE	BCAT1	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-203)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000060982	NA	643911	586	CRNDEP|LINC00180|LOC643911	BCATc|BCT1	LncRNA CRNDE promotes hepatocellular carcinoma cell proliferation, invasion, and migration through regulating miR-203/ BCAT1 axis.LncRNA CRNDE could enhance HCC tumorgenesis by sponging miR-203 and mediating BCAT1. LncRNA CRNDE might facilitate HCC cell propagation, invasiveness, and migration through regulating miR-203/ BCAT1 axis.	30230527	RID05687	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE51827)
Colon cancer	TP53COR1	E-cadherin	positively-F	RIP;western blot	downregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	ubiquitination	binding/interaction	RNA-protein	Extract of Ginkgo biloba 761	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	NA	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	lincRNA-p21 Mediates the Anti-Cancer Effect of Ginkgo Biloba Extract EGb 761 by Stabilizing E-Cadherin Protein in Colon Cancer.Furthermore, lincRNA-p21 was localized in cytoplasm of colon cells and regulated E-cadherin expression at a post-transcriptional level.	30594943	RID05688	epigenetic regulation	NA		
Triple-negative breast cancer	CYTOR	PTEN	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ubiquitination	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171862	NA	112597	5728	C2orf59|LINC00152|MGC4677|NCRNA00152	BZS|MHAM|MMAC1|PTEN1|TEP1	YY1-regulated LINC00152 promotes triple negative breast cancer progression by affecting on stability of PTEN protein.Our further experiments showed up-regulated LINC00152 in TNBC obviously enhanced NEDD4-1 mediated ubiquitination and degradation of PTEN protein.	30594392	RID05689	epigenetic regulation	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Adenomyosis	TUG1	TIMP2	negatively-E	luciferase reporter assay;RIP;	upregulation	RT-PCR	NA	NA	cell invasion(+);cell migration(+)	enhancer	regulation	RNA-protein	NA	NA	NA	Reproductive system disease	Uterine disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000035862	NA	55000	7077	FLJ20618|LINC00080|NCRNA00080	CSC-21K	Upregulation of long noncoding RNA TUG1 by EGR1 promotes adenomyotic epithelial cell migration and invasion through recruiting EZH2 and suppressing TIMP2.The mechanistic experiments demonstrated that the function of TUG1 in adenomyotic epithelial cell invasion is, at least in part, through recruiting the enhancer of zeste homolog 2 (EZH2) to the promoter of tissue inhibitor of metalloproteinases 2 (TIMP2) and negatively regulating its expression.	30593723	RID05690	chromatin looping	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Atherosclerosis	NEXN-AS1	NEXN	positively-E	luciferase reporter assay;RIP;	downregulation	qRT-PCR	NA	NA	inflammatory response(+)	chromatin remodel	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000235927	GRCh38_1:77881348-77889539	ENSG00000162614	NA	374987	91624	C1orf118|FLJ90637	NELIN|nexilin	Long noncoding RNA NEXN-AS1 mitigates atherosclerosis by regulating the actin-binding protein NEXN.In vitro experiments revealed that NEXN-AS1 interacted with the chromatin remodeler BAZ1A and the 5' flanking region of the NEXN gene and that it also upregulated NEXN expression. Augmentation of NEXN-AS1 expression inhibited TLR4 oligomerization and NF-kB activity, downregulated the expression of adhesion molecules and inflammatory cytokines by endothelial cells, and suppressed monocyte adhesion to endothelial cells.	30589415	RID05691	chromatin looping	NA	UP(LIHC,PRAD,PAAD);DATA(GSE117623,GSE104209,GSE60407)	UP(LIHC,PAAD,PRAD,BRCA);DOWN(PRAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE75367)
Cervical cancer	DDN-AS1	TCF3	positively-E	luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-15a;miR-16)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000257913	GRCh38_12:48998367-49019241	ENSG00000071564	NA	105369758	6929	CAT1507	bHLHb21|E2A|E47|ITF1|MGC129647|MGC129648|p75|VDIR	DDN-AS1-miR-15a/16-TCF3 feedback loop regulates tumor progression in cervical cancer.Moreover, DDN-AS1 increased the expression of TCF3 by competitively binding miR-15a and miR-16. In conclusion, DDN-AS1-miR-15a/16-TCF3 feedback loop contributes to cell proliferation, migration, and invasion in CC.	30582201	RID05692	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE55807,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nasopharynx carcinoma	TUG1	miR-384	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Knockdown of long non-coding RNA TUG1 suppresses nasopharyngeal carcinoma progression by inhibiting epithelial-mesenchymal transition (EMT) via the promotion of miR-384.The results of luciferase reporter analysis verified that miR-384 was a direct target of TUG1 in NPC, and was down-regulated in NPC tissues, exhibiting suppressive role in cell proliferation, migration and invasion.	30581000	RID05693	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Colorectal cancer	CRCMSL	HMGB2	positively-F	RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000164104	NA	NA	3148	NA	HMG2	Long noncoding RNA CRCMSL suppresses tumor invasive and metastasis in colorectal carcinoma through nucleocytoplasmic shuttling of HMGB2.Mechanically, lnc-CRCMSL physically binds to HMGB2 and stabilizes the localization of HMGB2 in the cytoplasm. Our data highlight the anti-metastatic role of lnc-CRCMSL in stabilizing HMGB2 through lncRNA-protein interactions in the cytoplasm, and suggest that targeting lnc-CRCMSL may represent a therapeutic opportunity for managing metastatic CRC.	30575817	RID05694	interact with protein	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	SNHG16	miR-384	negatively-F	luciferase reporter assay;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93.SNHG16 levels were markedly downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated SNHG16 overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on SNHG16.	30573973	RID05695	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Hepatocellular carcinoma	FENDRR	GPC3	negatively-E	CHIRP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000147257	NA	400550	2719	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	DGSX|OCI-5|SDYS|SGB|SGBS|SGBS1	Long non-coding RNA FENDRR inhibits proliferation and invasion of hepatocellular carcinoma by down-regulating glypican-3 expression.Mechanistically, we demonstrated that FENDRR interacted directly with Glypican-3 (GPC3) promoter and methylated GPC3 promoter, which led to down-regulation of GPC3 expression. Ectopic expression of GPC3 ablated the inhibitory effects of FENDRR on HCC cell proliferation, migration and invasion.	30573358	RID05696	epigenetic regulation	NA		UP(LIHC);DATA(GSE117623)
Gastric cancer	LINC-PINT	miR-21	negatively-F	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000199004	NA	378805	NA	FLJ43663|LincRNA-Pint|MKLN1-AS1|PINT	NA	Long noncoding RNA LINC-PINT is inhibited in gastric cancer and predicts poor survival.The low expression level of LINC-PINT and high expression level of the miR-21 tumor were correlated with poor prognosis. LINC-PINT overexpression casued miR-21 inhibition in cells of human gastric cancer cell lines, while miR-21 overexpression did not alter LINC-PINT expression. LINC-PINT overexpression led to inhibited, while miR-21 overexpression led to promoted proliferation, migration, and invasion of gastric cancer cells.	30569513	RID05697	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Prostate cancer	PCA3	HMGB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-218-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000189403	NA	50652	3146	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	DKFZp686A04236|HMG1|HMG3|SBP-1	Long noncoding RNA PCA3 regulates prostate cancer through sponging miR-218-5p and modulating high mobility group box 1.PCA3 and HMGB1 were high-expressed in PCa, whereas miR-218-5p was low-expressed. PCA3 knockdown or miR-218-5p overexpression suppressed PCa cell proliferation, migration, and invasion, but promoted apoptosis. Besides, targeted relationships and interactions on the expression between miR-218-5p and PCA3 or HMGB1 were elucidated. PCA3 weakened cell viability and mobility whereas induced apoptosis through binding with miR-218-5p. Meanwhile, miR-218-5p also inhibited PCa tumorigenesis via downregulation of HMGB1. Knockdown of PCA3 impeded tumor growth by downregulating its downstream gene HMGB1	30569456	RID05698	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Nasopharynx carcinoma	CASC2	RBBP8	positively-E	luciferase reporter assay;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-18a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000101773	NA	255082	5932	C10orf5	COM1|CtIP|RIM|SCKL2	lncRNA CASC2/miR-18a-5p axis regulates the malignant potential of nasopharyngeal carcinoma by targeting RBBP8.We further confirmed that CASC2 could directly bind with miR-18a-5p and inhibit miR-18a-5p expression, using reporter gene and RNA immunoprecipitation assays. miR-18a-5p suppressed CASC2 upregulation-mediated decrease in proliferation and increase in apoptotic cell death. CASC2 regulates NPC malignancy through modulation of RBBP8 via sponging miR-18a-5p.	30569153	RID05699	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Osteosarcoma	LINC-ROR	miR-206	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	lincRNA-RoR|lincRNA-ST8SIA3|ROR	NA	The long non-coding RNA-ROR promotes osteosarcoma progression by targeting miR-206. In addition, miR-206 was verified to be a target miRNA of ROR using bioinformatics online program and luciferase report assay. miR-206 inhibition partially rescued the inhibitory effects on OS cells induced by ROR knockdown. In conclusion, these results suggested that ROR function as an oncogene in OS by sponging miR-206 and might be a potential therapeutic target for patients with OS.	30565392	RID05700	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Thyroid cancer	GREP1	CDC23	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-204-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000262152	GRCh38_16:2988256-3002016	ENSG00000094880	NA	283875	8697	LINC00514	ANAPC8|APC8|CUT23	Silencing of lncRNA LINC00514 inhibits the malignant behaviors of papillary thyroid cancer through miR-204-3p/CDC23 axis.Through bioinformatics prediction, we identified that LINC00514 served as the sponge for miR-204-3p, and miR-204-3p directly targeted CDC23. Thus, LINC00514 promoted CDC23 expression via restraining miR-204-3p activity, leading to PTC progression.	30553447	RID05701	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Coronary heart disease	RMRP	miR-206	negatively-F		downregulation		NA	NA	cell injury(+);PI3K/AKT/mTOR signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	NA	NA	6023	NA	CHH|NME1|RMRPR|RRP2	NA	Long noncoding RNA RMRP upregulation aggravates myocardial ischemia-reperfusion injury by sponging miR-206 to target ATG3 expression.The results showed that overexpression of RMRP aggravated hypoxia-induced injury in H9c2 cells. Moreover, miR-206 was negatively regulated by RMRP and overexpression of RMRP aggravated hypoxia injury by downregulation of miR-206. Furthermore, ATG3 was a target of miR-206, and he effects of miR-206 on hypoxia injury were through targeting ATG3. Besides, overexpression of RMRP activated PI3K/AKT/mTOR pathway in hypoxia-treated H9c2 cells, which were reversed by miR-206 overexpression at the same time.	30551524	RID05702	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Esophageal cancer	XIST	CDK6	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);JAK2/STAT3 signaling pathway(+)	ceRNA(miR-494)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000105810	NA	7503	1021	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	PLSTIRE	Long non-coding RNA XIST promotes the development of esophageal cancer by sponging miR-494 to regulate CDK6 expression.LncRNA XIST was overespressed in esophageal cancer tissues and cells. Suppression of XIST significantly inhibited the proliferation, migration and invasion, but induced apoptosis of two kinds of cells, TE-1 and SKGT-4. Moreover, miR-494 was down-regulated in esophageal cancer tissues and cells. XIST could sponge miR-494 and inhibition of miR-494 reversed the effects of XIST suppression on the malignant behaviors of TE-1 cells.	30551480	RID05703	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Non-small cell lung cancer	DLX6-AS1	PRR11	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-144)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000068489	NA	285987	55771	Evf-2|FLJ34048|NCRNA00212	FLJ11029	Knockdown of lncRNA DLX6-AS1 inhibits cell proliferation, migration and invasion while promotes apoptosis by downregulating PRR11 expression and upregulating miR-144 in non-small cell lung cancer.In addition, DLX6-AS1 and PRR11 were demonstrated to interact with microRNA-144 (miR-144) and DLX6-AS1 upregulated PRR11 expression by acting as a competing endogenous RNA (ceRNA) of miR-144 in NSCLC cells. Furthermore, DLX6-AS1 knockdown suppressed tumor growth in NSCLC in vivo by upregulating miR-144 and downregulating PRR11	30551440	RID05704	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE111842)
Acute myeloid leukemia	TUG1	miR-34a	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	epigenetic regulation	regulation	RNA-RNA	Adriamycin	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	TUG1 confers Adriamycin resistance in acute myeloid leukemia by epigenetically suppressing miR-34a expression via EZH2.	30551433	RID05705	epigenetic regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Hepatocellular carcinoma	KTN1-AS1	ERBIN	positively-E	luciferase reporter assay;RNA pull-down assay;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-23c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000186615	GRCh38_14:55496786-55580888	ENSG00000112851	NA	100129075	55914	C14orf33|MYCLo-3	ERBB2IP|LAP2	LncRNA KTN1-AS1 promotes tumor growth of hepatocellular carcinoma by targeting miR-23c/ERBB2IP axis.Mechanistically, KTN1-AS1 inversely regulated miR-23c abundance in HCC cells. Further evidence supported that KTN1-AS1 acted as a competing endogenous RNA (ceRNA) by directly sponging miR-23c in HCC cells. Interestingly, erbb2 interacting protein (ERBB2IP), a known target of miR-23c, was positively regulated by KTN1-AS1 and its restoration reversed KTN1-AS1 knockdown attenuated HCC cell growth.	30551364	RID05706	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Myocardial infarction	AZIN2-sv	TLN1	negatively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	angiogenesis(-);myocardial regeneration(-)	ubiquitination	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	NA	NA	ENSG00000137076	NA	NA	7094	NA	ILWEQ|TLN|talin-1	Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.Bach1-activated AZIN2-sv could participate in angiogenesis by promoting the PSMC5-mediated ubiquitination-dependent degradation of Tln1 and blocking the miR-214/PTEN/Akt pathway. Inhibition of AZIN2-sv induced angiogenesis and myocardial regeneration simultaneously, thus, AZIN2-sv could be an ideal therapeutic target for improving myocardial repair after MI.	30545799	RID05707	epigenetic regulation	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Myocardial infarction	MRPL36	AZIN2-sv	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	angiogenesis(-);myocardial regeneration(-)	enhancer	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	PCG	lncRNA	ENSG00000171421	NA	NA	NA	64979	NA	BRIP1|L36mt|MRP-L36|PRPL36|RPMJ	NA	Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.Bach1-activated AZIN2-sv could participate in angiogenesis by promoting the PSMC5-mediated ubiquitination-dependent degradation of Tln1 and blocking the miR-214/PTEN/Akt pathway.	30545799	RID05708	chromatin looping	prognosis	DOWN(LIHC,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)	
Myocardial infarction	AZIN2-sv	PTEN	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	AKT signaling pathway(-);angiogenesis(-)	ubiquitination	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	NA	NA	ENSG00000171862	NA	NA	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.Bach1-activated AZIN2-sv could participate in angiogenesis by promoting the PSMC5-mediated ubiquitination-dependent degradation of Tln1 and blocking the miR-214/PTEN/Akt pathway. Inhibition of AZIN2-sv induced angiogenesis and myocardial regeneration simultaneously, thus, AZIN2-sv could be an ideal therapeutic target for improving myocardial repair after MI.	30545799	RID05709	epigenetic regulation	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	H19	CDC42	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-15b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000070831	NA	283120	998	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CDC42Hs|G25K	LncRNA-H19 activates CDC42/PAK1 pathway to promote cell proliferation, migration and invasion by targeting miR-15b in hepatocellular carcinoma.	30543848	RID05710	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	CASC9	LIN7A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-758-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000111052	NA	101805492	8825	ESCCAL-1|linc-JPH1|LINC00981	LIN-7A|MALS-1|TIP-33|VELI1	Long noncoding RNA CASC9 promotes LIN7A expression via miR-758-3p to facilitate the malignancy of ovarian cancer.We showed that CASC9 works as a competing endogenous RNA (ceRNA) for miR-758-3p which targets LIN7A. CASC9 inhibits the level of miR-758-3p, and in turn stimulates LIN7A expression in ovarian cancer. Overexpression of LIN7A reverses the suppressive roles of CASC9 depletion on ovarian cancer. In sum, our findings reveal a novel undefined regulatory signaling pathway, namely CASC9/miR-758-3p/LIN7A axis, involved in ovarian cancer progression.	30537154	RID05711	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	DANCR	HMGA2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000149948	NA	57291	8091	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	BABL|HMGIC|LIPO	Long non-coding RNA DANCR promotes HMGA2-mediated invasion in lung adenocarcinoma cells.	30535487	RID05712	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colon cancer	B3GALT5-AS1	miR-203	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(+);cell migration(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000184809	GRCh38_21:39597147-39612910	ENSG00000207568	NA	114041	NA	C21orf88	NA	Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203	30530918	RID05713	transcriptional regulation	metastasis	UP(LIHC);DATA(GSE117623)	
Urinary bladder cancer	SNHG7	CTNNB1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell cycle(+);WNT/beta-catenin signaling pathway(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000168036	NA	84973	1499	NCRNA00061	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Knockdown of lncRNA SNHG7 inhibited cell proliferation and migration in bladder cancer through activating Wnt/beta-catenin pathway.	30527358	RID05714	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	TINCR	miR-107	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	GSE40967	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000198997	NA	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis.The expression levels of the TINCR and CD36 were down-regulated. Aberrantly-expressed lncRNAs and differential-expressed genes were identified by analyzing the dataset GSE40967.  We identified miR-107 as an inhibitory target of TINCR and CD36. Overexpression of TINCR could inhibit cell proliferation and promote apoptosis. MiR-107 overexpression in CRC cells induced proliferation and impeded apoptosis.	30521471	RID05715	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Malignant glioma	FOXD2-AS1	CCND2	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-185-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000118971	NA	84793	894	MGC12982	NA	Long noncoding RNA FOXD2-AS1 promotes glioma malignancy and tumorigenesis via targeting miR-185-5p/CCND2 axis.In glioma tissues, CCND2 expression was negatively associated with miR-185-5p, but positively correlated with FOXD2-AS1. FOXD2-AS1 knockdown and miR-185-5p mimics decreased CCND2 expression. Inhibition of miR-185-5p suppressed FOXD2-AS1 knockdown-induced decrease of CCND2 expression. Overexpression of CCND2 suppressed FOXD2-AS1 knockdown-induced inhibition of glioma malignancy	30520141	RID05716	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	HAND2-AS1	MIR21	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000199004	NA	79804	406991	DEIN|NBLA00301|UPH	MIRN21|hsa-mir-21|miR-21|miRNA21	Long noncoding RNA HAND2-AS1 inhibits cancer cell proliferation, migration, and invasion in esophagus squamous cell carcinoma by regulating microRNA-21.	30520131	RID05717	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Gastric cancer	SNHG20	ZFX	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-495-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000005889	NA	654434	7543	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	ZNF926	LncRNA SNHG20 contributes to cell proliferation and invasion by upregulating ZFX expression sponging miR-495-3p in gastric cancer.Moreover, we demonstrated that lncRNA SNHG20 inhibited zinc finger protein X-linked (ZFX) expression by negatively miR-495-3p expression in GC cells. In vivo, the current study also indicated that lncRNA SNHG20 knockdown reduced the tumor growth by downregulating ZFX expression.	30520073	RID05718	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807,GSE67939,GSE41245)
Malignant glioma	UCA1	NR2C2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-627-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000177463	NA	652995	7182	CUDR|LINC00178|onco-lncRNA-36|UCAT1	hTAK1|TAK1|TR2R1|TR4	NR2C2-uORF targeting UCA1-miR-627-5p-NR2C2 feedback loop to regulate the malignant behaviors of glioma cells.This study confirmed that lnc-UCA1 was up-regulated in glioma tissues and cells. UCA1 knockdown inhibited the malignancies of glioma cells by reducing proliferation, migration, and invasion, but inducing apoptosis. We found that lnc-UCA1 acted as miR-627-5p sponge in a sequence-specific manner.	30518750	RID05719	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Malignant glioma	LINC00320	CTNNB1	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);WNT/beta-catenin signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000224924	GRCh38_21:20651450-20803816	ENSG00000168036	NA	387486	1499	C21orf131|NCRNA00320|PRED14	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA Linc00320 inhibits glioma cell proliferation through restraining Wnt/beta-catenin signaling.In addition, we found that Linc00320 binds to beta-catenin and inhibits the activity of Wnt/beta-catenin signaling by disrupting beta-catenin binds to TCF4 in Glioma cells. Taken together, we firstly demonstrated the tumor suppressive lncRNA, Linc00320, is down-regulated in Glioma tissues and inhibits Glioma cell proliferation by restraining Wnt/beta-catenin signaling through segregating beta-catenin and TCF4 and revealed the novel HMGB1/Linc00320/beta-catenin axis in Glioma progression	30503496	RID05720	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	APC1	RAB5B	negatively-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);angiogenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000153107	GRCh38_2:111611639-111884690	ENSG00000111540	NA	NA	5869	NA	NA	APC-activated long noncoding RNA inhibits colorectal carcinoma pathogenesis through reduction of exosome production.Bioinformatics analysis and luciferase reporter assay unveiled that microRNA-150 (miR-150) could interact with ZFAS1, Myb 3' UTR and Sp1 3' UTR. Moreover, ZFAS1 acted as a molecular sponge of miR-150, giving rise to the downregulation of miR-150 level and upregulation of Myb and Sp1 levels. Moreover, miR-150 overexpression resulted in the reduction of AML cell proliferative ability and the increase of cell apoptotic rate.	30511962	RID05721	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	NORAD	JUNB	positively-E	StarbaseV2.0;shRNA;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)radiosensitvity(-)	ceRNA(miR-615-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000171223	NA	647979	3726	LINC00657	NA	LINC00657 played oncogenic roles in esophageal squamous cell carcinoma by targeting LINC00657 played oncogenic roles in esophageal squamous cell carcinoma by targeting miR-615-3p and JunB.LINC00657 was moderately increased in ESCC both in vivo and in vitro and up regulated by irradiation.The LINC00657 expression in ESCC tissues and cell lines were evaluated by quantitative real-time PCR.The expression of LINC00657 in ESCC cells was regulated by lentivirus transfection. Online bioinformaticsanalysis tools starbaseV2.0 were used to predict the potential targets of LINC00657 and miR-615-3p. Knockdown of LINC00657 could inhibit the invasion, migration and viability of ESCC cells. Moreover, LINC00657 could act as a ceRNA to increase the expression of JunB by binding to miR-615-3p. LINC00657 might be involved in regulating ESCC response to radiation; and it functioned as an oncogene in ESCC by targeting miR-615-3p and JunB, providing novel potential therapeutic targets.	30227324	RID05722	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	CCAT1	PKC	positively-E	TargetScan;luciferase reporter assay;siRNA	downregulation	RT-PCR	NA	NA	tumor growth(+);macrophage polarization(+)	ceRNA(miR-148a)	regulation	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1/miR-148a/PKCzeta prevents cell migration of prostate cancer by altering macrophage polarizationTAMs were obtained by culturing monocytes for 7 days in RPMI 1640 10% FBS with 50% of conditioned medium from PC-3 cells real-time PCR was performed to determine the expression of miR-148a, CCAT1, and PKCzeta. western blot was used to measure the level of PKCzeta.Luciferase reporter assay was used to determine the relationship between miR-148a and PKCzeta. The expression of miR-148a was highest in TAMs, while CCAT1 and PKCzeta were highest in M1 Macrophages. Overexpressed miR-148a promoted the level of IL-10 and cell migration. Down-regulated CCAT1 promoted the level of IL-10 and cell migration, while this effects were abolished by co-transfection of si-CCAT1 and miR-148a inhibitor.CCAT1 knockdown promoted M2 macrophages polarization by up-regulating miR-148a, while miR-148a up-regulation promoted M2 macrophages polarization by down-regulating the expression of PKCzeta.	30221381	RID05723	ceRNA or sponge	NA		
Osteosarcoma	OIP5-AS1	FN1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;siRNA	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-200b-3p)	regulation	RNA-protein	Doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000115414	NA	729082	2335	cyrano|linc-OIP5	CIG|FINC|GFND2|LETS|MSF	Fibronectin-1 modulated by the long noncoding RNA OIP5-AS1/miR-200b-3p axis contributes to doxorubicin resistance of osteosarcoma cells.fibronectin-1 (FN1), screened by microarray analysis in three paired chemo-resistant and chemo-sensitive OS cell lines, was significantly upregulated in the chemo-resistant OS cell lines and tissues and was related to unfavourable prognosis.mechanistic investigation demonstrated, by a series of assays that included luciferase reporter gene, RNA immunoprecipitation, RNA pull-down and rescue assays, that FN1 expression was regulated by the oncogenic long noncoding RNA (lncRNA) OIP5-AS1 through sponging miR-200b-3p. Thus, these results indicated the role and potential application of the lncRNA OIP5-AS1/miR-200b-3p/FN1 regulatory pathway as a promising target in treatment of OS chemo-resistance.	30204936	RID05724	ceRNA or sponge	chemoresistance,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteosarcoma	NEAT1	TGFB1	positively-E	shRNA;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+);	ceRNA(miR-339-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105329	NA	283131	7040	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CED|DPD1|TGFB|TGFbeta	NEAT1 induces osteosarcoma development by modulating the miR-339-5p/TGF-beta1 pathwaywe detected the NEAT1 expression in OS cell lines by performing quantitative reverse-transcription polymerase chain reaction.We observed that inhibition of NEAT1 restrained OS cell progression greatly.Here, we found that NEAT1 can modulate OS development via sponging miR-339-5p. MiR-339-5p was significantly decreased in OS cells, and its overexpression can remarkably repress the OS proliferation.Then, the following assays validated that transforming growth factor beta1 (TGF-beta1) can act as a functional target of miR-339-5p in OS cells.Finally, we indicated that NEAT1 could mediate TGF-beta1 expression by competitively sponging miR-339-5p. NEAT1 induced OS cell proliferation and cell mobility by binding to miR-339-5p and increasing TGF-beta1 in OS.Our findings implied that the novel identified NEAT1/miR-339-5p/TGF-beta1 axis might be a new molecular pathway or therapeutic target for OS diagnosis and treatment.	30203547	RID05725	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	CASC11	CDK1	positively-E	TargetScan;dual-luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE99416	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-340-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000170312	NA	100270680	983	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	CDC2|CDC28A	LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathwayExpressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCRThe relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual-luciferase reporter assay.qRT-PCR;ISHowed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.	30200804	RID05726	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Psoriasis	NFKB1	MIR31HG	positively-E	siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	TF	lncRNA	ENSG00000109320	NA	ENSG00000171889	GRCh38_9:21453802-21559900	4790	554202	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	hsa-lnc-31|LncHIFCAR|LOC554202	Knockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytesMIR31HG was significantly elevated in the lesional psoriatic skin compared with normal individuals'-skin. Knockdown of MIR31HG inhibited HaCaT keratinocytes proliferation.In addition, MIR31HG expression was found to be dependent on NF-kB activation.NF-kB activation mediated MIR31HG upregulation plays an important role in the regulation of HaCaT keratinocytes proliferation. It could be a potential diagnostic biomarker and therapeutic target for psoriasis.	30180891	RID05727	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cardiomyopathy	HOTAIR	AKT1	positively-F	overexpression	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell viability(+)	phosphorylation	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000142208	NA	100124700	207	HOXC-AS4|HOXC11-AS1|NCRNA00072	AKT|PKB|PRKBA|RAC|RAC-alpha	LncRNA HOTAIR improves diabetic cardiomyopathy by increasing viability of cardiomyocytes through activation of the PI3K/Akt pathway.HOTAIR expression was significantly downregulated in myocardial tissues and serum of patients with diabetic cardiomyopathy compared with patients with diabetes and healthy controls. Serum HOTAIR could be used to effectively distinguish patients with diabetic cardiomyopathy from healthy controls. High glucose treatment inhibited HOTAIR expression and Akt phosphorylation. HOTAIR overexpression promoted Akt phosphorylation. HOTAIR overexpression improved AC16 cell viability, while PI3K/Akt inhibitor treatment reduced this effect. LncRNA HOTAIR may improve diabetic cardiomyopathy by increasing the viability of cardiomyocytes through activation of the PI3K/Akt pathway.	30542437	RID05728	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	IATPR	SNAI1	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000124216	NA	101929447	6615	linc-ITGB1|TCONS_00018476	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05729	expression association	NA		UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	IATPR	SOX2	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000181449	NA	101929447	6657	linc-ITGB1|TCONS_00018476	NA	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05730	expression association	NA		UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	IATPR	NANOG	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000111704	NA	101929447	79923	linc-ITGB1|TCONS_00018476	FLJ12581|FLJ40451	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05731	expression association	NA		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Non-small cell lung cancer	IATPR	POU5F1	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000233911	NA	101929447	5460	TCONS_00018476|linc-ITGB1	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05732	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	IATPR	MYC	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000136997	NA	101929447	4609	linc-ITGB1|TCONS_00018476	bHLHe39|c-Myc|MYCC	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05733	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	IATPR	PROM1	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000007062	NA	101929447	8842	linc-ITGB1|TCONS_00018476	AC133|CD133|CORD12|MCDR2|PROML1|RP41|STGD4	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05734	expression association	NA		UP(BRCA);DATA(GSE109761)
Non-small cell lung cancer	IATPR	IRS1	negatively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000169047	NA	101929447	3667	TCONS_00018476|linc-ITGB1	HIRS-1	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05735	expression association	NA		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Non-small cell lung cancer	IATPR	vimentin	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33073486-33116781	NA	NA	101929447	NA	linc-ITGB1|TCONS_00018476	NA	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05736	expression association	NA		
Non-small cell lung cancer	IATPR	MIR211	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	association	RNA-RNA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000233387	GRCh38_10:33073486-33116781	ENSG00000207702	NA	101929447	406993	TCONS_00018476|linc-ITGB1	MIRN211|mir-211	Knockdown of long non-coding RNA linc-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer.Linc-ITGB1 was greatly upregulated in CSC spheres. Linc-ITGB1 knockdown markedly inhibited CSC formation and the expression of stemness-associated genes, such as Sox2, Nanog, Oct-4, c-Myc, and CD133. Depletion of linc-ITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that linc-ITGB1 knockdown increased the expression of the epithelial marker E-cadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMT-related transcription factor Snail mediated these effects of linc-ITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of linc-ITGB1 depletion.	30485693	RID05737	expression association	NA		
Osteoblast injury	MALAT1	PPM1E	negatively-E	overexpression;siRNA;shRNA;knockdown	downregulation	qPCR	NA	NA	cell injury(-);PPM1E/AMPK signaling pathway(+)	NA	association	RNA-protein	Dexamethasone	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000175175	NA	378938	22843	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CaMKP-N|KIAA1072|POPX1|PP2CH	Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1EAMPK Signaling.Lnc-MALAT1 expression was analyzed by quantitative real-time polymerase chain reaction assay.Lnc-MALAT1 expression was downregulated by Dex treatment in the established osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblastTsh. The level of LncM- ALAT1 was decreased in the necrotic femoral head tissues of Dex-administered patients .In osteoblastic cells and primary human osteoblasts, forced overexpression of Lnc-MALAT1 using a lentiviral vector (LV-MALAT1) inhibited Dex-induced cell viability reduction, cell death, and apoptosis. Conversely, transfection with Lnc- MALAT1 small interfering RNA aggravated Dex-induced cytotoxicity. Transfection with LV-MALAT1 downregulated Ppm1e (protein phosphatase, Mg 2+/Mn2+-dependent 1e) expression to activate AMPK signaling.Treatment of osteoblasts with AMPKalpha1 short hairpin RNA or dominant negative mutation (T172A) abolished LV-MALAT1-induced protection against Dex-induced cytotoxicity. Furthermore, LV-MALAT1 induced an increase in nicotinamide adenine dinucleotide phosphate activity and activation of Nrf2 signaling. Dex-induced reactive oxygen species production was significantly attenuated by LV-MALAT1 transfection in osteoblastic cells and primary osteoblasts.Lnc-MALAT1 protects human osteoblasts from Dex-induced injuries, possibly via activation of Ppm1e-AMPK signaling.	30439702	RID05738	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	LNCNEF	Wnt	negatively-E	overexpression	downregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000237396	GRCh38_20:22587522-22607517	NA	NA	101929685	NA	LINC01384|lncRNA-NEF	NA	LncRNA-NEF inhibits proliferation, migration and invasion of esophageal squamous-cell carcinoma cells by inactivating wnt/beta-catenin pathwayExpression of NEF was significantly downregulated in tumor tissues than in adjacent tissues in most patients.NEF overexpression decreased the expression levels of wnt/beta-catenin pathway-related proteins, while Wnt activator showed no significant effects on NEF. LncRNA NEF may inhibit the proliferation, migration and invasion of esophageal squamous-cell carcinoma cells by inactivating with wnt/beta-catenin pathway.	30402846	RID05739	expression association	NA		
Renal fibrosis	lnc-TSI	SMAD3	negatively-F	siRNA;shRNA;knockdown;ChIP;JASPAR;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-PCR	NA	NA	fibrotic(+)	phosphorylation	binding/interaction	NA	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	TF	NA	NA	ENSG00000166949	NA	NA	4088	NA	HSPC193|HsT17436|JV15-2|LDS1C|LDS3|MADH3|hMAD-3|hSMAD3|mad3	Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGFB1/Smad3 pathwayLnc-TSI is expressed in human TECs and is regulated by TGFB1 via a SMAD3-dependent mechanism.Lnc-TSI expression, as determined by in situ hybridization and RTPCR, was up-regulated in human fibrotic kidney but not in fibrotic liver or lung.Our ChIP analysis demonstrated the interaction between SMAD3 and promoter region of lnc-TSI (-1321 to -1330 bp), indicating that lnc-TSI is a transcriptional target of SMAD3.These data suggest that Smad3 binds with the promoter of lnc-TSI and up-regulates the expression of lnc-TSI. Furthermore, overexpression of lnc-TSI substantially decreased TGFB1-induced expression of SMAD3 target genes, including SNAIL1, COL1A1, and alphaSMA, whereas knocking down lnc-TSI enhanced their expression. We validated these effects of lnc-TSI on the phosphorylation of SMAD3 and downstream responses using CRISPR-Cas9. These data suggest that lnc-TSI negatively regulates the TGFB1/Smad3 pathway by specifically inhibiting the phosphorylation and subsequent nuclear translocation of SMAD3.We identified seven proteins that associated with lnc-TSI.These data suggest that lnc-TSI reduced renal fibrogenesis through negative regulation of the TGFB1/Smad pathway.	30305452	RID05740	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal fibrosis	lnc-TSI	SNAI1	negatively-E	siRNA;shRNA;knockdown;ChIP;JASPAR;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-PCR	NA	NA	fibrotic(+)	NA	regulation	NA	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	TF	NA	NA	ENSG00000124216	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGFB1/Smad3 pathwayLnc-TSI is expressed in human TECs and is regulated by TGFB1 via a SMAD3-dependent mechanism.Lnc-TSI expression, as determined by in situ hybridization and RTPCR, was up-regulated in human fibrotic kidney but not in fibrotic liver or lung.Our ChIP analysis demonstrated the interaction between SMAD3 and promoter region of lnc-TSI (-1321 to -1330 bp), indicating that lnc-TSI is a transcriptional target of SMAD3.These data suggest that Smad3 binds with the promoter of lnc-TSI and up-regulates the expression of lnc-TSI. Furthermore, overexpression of lnc-TSI substantially decreased TGFB1-induced expression of SMAD3 target genes, including SNAIL1, COL1A1, and alphaSMA, whereas knocking down lnc-TSI enhanced their expression. We validated these effects of lnc-TSI on the phosphorylation of SMAD3 and downstream responses using CRISPR-Cas9. These data suggest that lnc-TSI negatively regulates the TGFB1/Smad3 pathway by specifically inhibiting the phosphorylation and subsequent nuclear translocation of SMAD3.We identified seven proteins that associated with lnc-TSI.These data suggest that lnc-TSI reduced renal fibrogenesis through negative regulation of the TGFB1/Smad pathway.	30305452	RID05741	expression association	NA		UP(PAAD);DATA(GSE40174)
Renal fibrosis	lnc-TSI	COL1A1	negatively-E	siRNA;shRNA;knockdown;ChIP;JASPAR;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-PCR	NA	NA	fibrotic(+)	NA	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	PCG	NA	NA	ENSG00000108821	NA	NA	1277	NA	CAFYD|EDSARTH1|EDSC|OI1|OI2|OI3|OI4	Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGFB1/Smad3 pathwayLnc-TSI is expressed in human TECs and is regulated by TGFB1 via a SMAD3-dependent mechanism.Lnc-TSI expression, as determined by in situ hybridization and RTPCR, was up-regulated in human fibrotic kidney but not in fibrotic liver or lung.Our ChIP analysis demonstrated the interaction between SMAD3 and promoter region of lnc-TSI (-1321 to -1330 bp), indicating that lnc-TSI is a transcriptional target of SMAD3.These data suggest that Smad3 binds with the promoter of lnc-TSI and up-regulates the expression of lnc-TSI. Furthermore, overexpression of lnc-TSI substantially decreased TGFB1-induced expression of SMAD3 target genes, including SNAIL1, COL1A1, and alphaSMA, whereas knocking down lnc-TSI enhanced their expression. We validated these effects of lnc-TSI on the phosphorylation of SMAD3 and downstream responses using CRISPR-Cas9. These data suggest that lnc-TSI negatively regulates the TGFB1/Smad3 pathway by specifically inhibiting the phosphorylation and subsequent nuclear translocation of SMAD3.We identified seven proteins that associated with lnc-TSI.These data suggest that lnc-TSI reduced renal fibrogenesis through negative regulation of the TGFB1/Smad pathway.	30305452	RID05742	expression association	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Renal fibrosis	lnc-TSI	ACTA2	negatively-E	siRNA;shRNA;knockdown;ChIP;JASPAR;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-PCR	NA	NA	fibrotic(+)	NA	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Fibrosis	lncRNA	PCG	NA	NA	ENSG00000107796	NA	NA	59	NA	ACTSA	Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGFB1/Smad3 pathwayLnc-TSI is expressed in human TECs and is regulated by TGFB1 via a SMAD3-dependent mechanism.Lnc-TSI expression, as determined by in situ hybridization and RTPCR, was up-regulated in human fibrotic kidney but not in fibrotic liver or lung.Our ChIP analysis demonstrated the interaction between SMAD3 and promoter region of lnc-TSI (-1321 to -1330 bp), indicating that lnc-TSI is a transcriptional target of SMAD3.These data suggest that Smad3 binds with the promoter of lnc-TSI and up-regulates the expression of lnc-TSI. Furthermore, overexpression of lnc-TSI substantially decreased TGFB1-induced expression of SMAD3 target genes, including SNAIL1, COL1A1, and alphaSMA, whereas knocking down lnc-TSI enhanced their expression. We validated these effects of lnc-TSI on the phosphorylation of SMAD3 and downstream responses using CRISPR-Cas9. These data suggest that lnc-TSI negatively regulates the TGFB1/Smad3 pathway by specifically inhibiting the phosphorylation and subsequent nuclear translocation of SMAD3.We identified seven proteins that associated with lnc-TSI.These data suggest that lnc-TSI reduced renal fibrogenesis through negative regulation of the TGFB1/Smad pathway.	30305452	RID05743	expression association	NA		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE55807)
Thoracic aortic aneurysm	TP53COR1	TGFB1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Artery disease	lncRNA	PCG	NA	NA	ENSG00000105329	NA	102800311	7040	TRP53COR1|linc-p21|lincRNA-p21	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Upregulation of lincRNA-p21 in thoracic aortic aneurysms is involved in the regulation of proliferation and apoptosis of vascular smooth muscle cells by activating TGF-beta1 signaling pathwayExpression of lincRNA-p21 in those tissues was detected by reverse-transcription quantitative polymerase chain reaction (qRT-PCR.Expression of lincRNA-p21 in aortic media tissues and blood was significantly upregulated in TAA patients than in healthy controls.LincRNA-p21 overexpression inhibited proliferation and promoted apoptosis of VSMCs, while TGF-beta1 inhibitor reduced those effects.LincRNA-p21 overexpression significantly upregulated TGF-beta1 expression and promoted Smad2/3 phosphorylation , while treatment with TGF-beta1 showed no significant effects on lincRNA-P21 expression.LincRNA-p21 participates in TAA by regulating the proliferation and apoptosis of VSMCs through the activation of TGF-beta1 signaling pathway.	30302790	RID05744	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Focal segmental glomerulosclerosis	LOC105374325	BAX	positively-E	luciferase reporter assay;RNA pull-down assay;siRNA;	upregulation	RT-PCR;western blot	NA	NA	apoptosis process(+)	ceRNA(miR-34c;miR-196a/b)	regulation	RNA-protein	Adriamycin	NA	NA	Urinary system disease	Nephritis	lncRNA	PCG	NA	NA	ENSG00000087088	NA	105374325	581	NA	BCL2L4	The long noncoding RNA LOC105374325 causes podocyte injury in individuals with focal segmental glomerulosclerosisUsing an array of gene expression profiling, PCR and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC105374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax) and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein beta (C/EBPbeta) up-regulated LOC105374325 expression.Chromatin Immunoprecipitation (ChIP) analysis confirmed that C/EBPbeta bound to the promoter region of LOC105374325 in podocytes, which  was enhanced by ADR treatment. Overexpression of C/EBPbeta increased the expression of the luciferase reporter construct containing the binding sequence, and site-directed  mutations rescued the C/EBPbeta-mediated upregulation of the LOC105374325 promoter-luciferase reporter plasmid.P38 inhibition or C/EBPbeta silencing decreased LOC105374325 levels and inhibited apoptosis in Adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, the activation of the P38/C/EBPbeta pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.	30389788	RID05745	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Focal segmental glomerulosclerosis	LOC105374325	BAK1	positively-E	luciferase reporter assay;RNA pull-down assay;siRNA;	upregulation	RT-PCR;western blot	NA	NA	apoptosis process(+)	ceRNA(miR-34c;miR-196a/b)	regulation	RNA-protein	Adriamycin	NA	NA	Urinary system disease	Nephritis	lncRNA	PCG	NA	NA	ENSG00000030110	NA	105374325	578	NA	BAK|BCL2L7|CDN1	The long noncoding RNA LOC105374326 causes podocyte injury in individuals with focal segmental glomerulosclerosisUsing an array of gene expression profiling, PCR and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC5374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax) and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein beta (C/EBPbeta) up-regulated LOC105374325 expression.Chromatin Immunoprecipitation (ChIP) analysis confirmed that C/EBPbeta bound to the promoter region of LOC105374325 in podocytes, which  was enhanced by ADR treatment. Overexpression of C/EBPbeta increased the expression of the luciferase reporter construct containing the binding sequence, and site-directed  mutations rescued the C/EBPbeta-mediated upregulation of the LOC105374325 promoter-luciferase reporter plasmid.P38 inhibition or C/EBPbeta silencing decreased LOC105374325 levels and inhibited apoptosis in Adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, the activation of the P38/C/EBPbeta pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.	30389788	RID05746	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Focal segmental glomerulosclerosis	P38	LOC105374325	positively-E	luciferase reporter assay;RNA pull-down assay;siRNA;	upregulation	RT-PCR;western blot	NA	NA	apoptosis process(+)	NA	regulation	protein-RNA	Adriamycin	NA	NA	Urinary system disease	Nephritis	PCG	lncRNA	ENSG00000106305	NA	NA	NA	NA	105374325	NA	NA	The long noncoding RNA LOC105374327 causes podocyte injury in individuals with focal segmental glomerulosclerosisUsing an array of gene expression profiling, PCR and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax) and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein beta (C/EBPbeta) up-regulated LOC105374325 expression.Chromatin Immunoprecipitation (ChIP) analysis confirmed that C/EBPbeta bound to the promoter region of LOC105374325 in podocytes, which  was enhanced by ADR treatment. Overexpression of C/EBPbeta increased the expression of the luciferase reporter construct containing the binding sequence, and site-directed  mutations rescued the C/EBPbeta-mediated upregulation of the LOC105374325 promoter-luciferase reporter plasmid.P38 inhibition or C/EBPbeta silencing decreased LOC105374325 levels and inhibited apoptosis in Adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, the activation of the P38/C/EBPbeta pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.	30389788	RID05747	expression association	NA		
Focal segmental glomerulosclerosis	CEBPB	LOC105374325	positively-E	luciferase reporter assay;RNA pull-down assay;siRNA;	upregulation	RT-PCR;western blot	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	NA	Adriamycin	NA	NA	Urinary system disease	Nephritis	TF	lncRNA	ENSG00000172216	NA	NA	NA	1051	105374325	C/EBP-beta|IL6DBP|NF-IL6|TCF5	NA	The long noncoding RNA LOC105374328 causes podocyte injury in individuals with focal segmental glomerulosclerosisUsing an array of gene expression profiling, PCR and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC5374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax) and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein beta (C/EBPbeta) up-regulated LOC105374325 expression.Chromatin Immunoprecipitation (ChIP) analysis confirmed that C/EBPbeta bound to the promoter region of LOC105374325 in podocytes, which  was enhanced by ADR treatment. Overexpression of C/EBPbeta increased the expression of the luciferase reporter construct containing the binding sequence, and site-directed  mutations rescued the C/EBPbeta-mediated upregulation of the LOC105374325 promoter-luciferase reporter plasmid.P38 inhibition or C/EBPbeta silencing decreased LOC105374325 levels and inhibited apoptosis in Adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, the activation of the P38/C/EBPbeta pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.	30389788	RID05748	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Osteosarcoma	LINC00628	p-PI3K	positively-E	western blot	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000280924	GRCh38_1:204368431-204369719	NA	NA	127841	NA	NA	NA	LncRNA LINC00628 overexpression inhibits the growth and invasion through regulating PI3K/Akt signaling pathway in osteosarcoma.LINC00628 expression was decreased in osteosarcoma. The overexpression of LINC00628 inhibited the proliferation, invasion and migration and promoted cell apoptosis in osteosarcoma cells through the inactivation of PI3K/Akt signaling pathway.	30280767	RID05749	expression association	NA		
Osteosarcoma	LINC00628	p-Akt	positively-E	western blot	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000280924	GRCh38_1:204368431-204369719	NA	NA	127841	NA	NA	NA	LncRNA LINC00628 overexpression inhibits the growth and invasion through regulating PI3K/Akt signaling pathway in osteosarcoma.LINC00628 expression was decreased in osteosarcoma. The overexpression of LINC00628 inhibited the proliferation, invasion and migration and promoted cell apoptosis in osteosarcoma cells through the inactivation of PI3K/Akt signaling pathway.	30280767	RID05750	expression association	NA		
Osteosarcoma	LINC00628	BCL2	positively-E	western blot	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000280924	GRCh38_1:204368431-204369719	ENSG00000171791	NA	127841	596	NA	Bcl-2|PPP1R50	LncRNA LINC00628 overexpression inhibits the growth and invasion through regulating PI3K/Akt signaling pathway in osteosarcoma.LINC00628 expression was decreased in osteosarcoma. The overexpression of LINC00628 inhibited the proliferation, invasion and migration and promoted cell apoptosis in osteosarcoma cells through the inactivation of PI3K/Akt signaling pathway.	30280767	RID05751	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG14	MIR340	negatively-F	siRNA;PCR;shRNA;dual-luciferase reporter assay;knockdown;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000198995	NA	104472715	442908	115HG|IC-SNURF-SNRPN|LNCAT|NCRNA00214|U-UBE3A-ATS|UBE3A-AS|UBE3A-AS1|UBE3A-ATS|UBE3AATS	MIRN340|hsa-mir-340|mir-340	Long non-coding RNA SNHG14 exerts oncogenic functions in non-small cell lung cancer through acting as a miR-340 spongeIn the present study, we found that SNHG14 was aberrantly upregulated in NSCLC tissues from patients and cell lines compared to their normal counterparts.Increased SNHG14 expression was closely associated with aggressive tumor progression and poor clinical outcome of NSCLC patients.Further studies demonstrated that SNHG14 might serve as a competing endogenous RNA (ceRNA) by sponging miR-340 in NSCLC cells. Taken together, our study demonstrated that SNHG14/miR-340 axis might play a novel role in regulating the malignant behaviors of NSCLC, which provided a new potential diagnostic and therapeutic strategy for this malignant disease.	30254102	RID05752	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	
Spontaneous tumor regression	lncRNA-135528	CXCL10	positively-E	siRNA;western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(-);cell proliferation(+);cell cycle(+);JAK/STAT signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Other	Spontaneous tumor regression	lncRNA	PCG	NA	NA	ENSG00000169245	NA	NA	3627	NA	C7|crg-2|gIP-10|IFI10|INP10|IP-10|mob-1|SCYB10	LncRNA-135528 inhibits tumor progression by up-regulating CXCL10 through the JAK/STAT pathwaySpontaneous tumor regression can be observed in many tumors, however, studies related to the altered expression of lncRNA in spontaneous glioma regression are limited.We stably silenced or overexpressed lncRNA-135528 in G422 cells by transfecting with siRNA against lncRNA-135528 or lncRNA-135528 overexpression plasmid. Then, we examined lncRNA-135528 overexpressing and lncRNA-135528 silencing on glioma cells and its effects on CXCL10 and JAK/STAT pathways. The main findings indicated that lncRNA-135528 promoted glioma cell apoptosis, inhibited cell proliferation and arrested cell cycle progression; the up-regulation of lncRNA135528 led to significantly increased CXCL10 levels and the differential expression of mRNA associated with JAK/STAT pathway in glioma cells. lncRNA-135528 can inhibit tumor progression by up-regulating CXCL10 through the JAK/STAT pathway.	30232656	RID05753	expression association	NA		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE86978)
Gastric cancer	THORLNC	SOX9	positively-E	sequencing;qRT-PCR;western blot;RIP;luciferase reporter assay;overexpression;knockdown;siRNA;shRNA	upregulation	qRT-PCR	NA	NA	cell stemness(+)	NA	binding/interaction	NA	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000125398	NA	100506797	6662	THOR	CMD1|CMPD1|SRA1	LncRNA THOR increases the stemness of gastric cancer cells via enhancing SOX9 mRNA stabilityRNA-sequencing combined with quantitative real-time PCR (qRT-PCR indicated that lncRNA THOR level was significantly upregulated in gastric cancer tissues compared with that in normal adjacent tissues. Knockdown of THOR attenuated the stemnness of gastric cancer cells, evident by the decrease of stemness markers expression and capacity of cells spheroid formation. Further RNA-sequencing combined with qRT-PCRand western blotdemonstrated that expression of transcriptional factor SOX9 was remarkably decreased in gastric cancer cells with THOR stable knockdown. Additionally, RNA immunoprecipitation (RIP) combined with luciferase reporter assay revealed that THOR directly bound to SOX9 3'-untranslated region (3'UTR), but not its 5'UTR or coding area. Notably, overexpression of SOX9 rescued THOR knockdown-mediated inhibition on the stemness of gastric cancer cells. Thus, our results suggest that THOR could potentiate the stemness of gastric cancer cells via directly binding to SOX9 3'UTR.	30227327	RID05754	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Hepatitis C	lncRNA-IFI6	IFI6	negatively-F	luciferase reporter assay;ChIP;western blot;knockdown;siRNA;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);immune response(-)	histone modification	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	NA	NA	ENSG00000126709	NA	NA	2537	NA	6-16|FAM14C|G1P3|IFI-6-16|IFI616	A novel lncRNA regulates HCV infection through IFI6We found that lncRNAIFI6 gRNA significantly inhibited HCV infection compared to negative gRNA control. The expression of the antiviral ISG IFI6 was significantly increased following lncRNA-IFI6 gRNA editing compared to negative gRNA control in JFH1-infected Huh7.5.1 cells and PHHs. We observed that lncRNA-IFI6 regulation of HCV was independent of JAK-STAT signaling. lncRNA-IFI6 negatively regulated IFI6 promoter function through histone modification. Overexpression of the truncated spatial domain or full-length lncRNA-IFI6 inhibited IFI6 expression and increased HCV replication.A novel lncRNA, lncRNA-IFI6, regulates antiviral innate immunity in the JFH1 HCV infection model. lncRNA-IFI6 regulates HCV infection independently of the JAK-STAT pathway. lncRNA-IFI6 exerts its regulatory function via promoter activation and histone modification of IFI6 through its spatial domain.	30199576	RID05755	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842)
Endometrial cancer	HOTAIR	PRB	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);chemosensitivity(-)	histone modification	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding HOTAIR enhances the sensitivity to progesterone in endometrial cancer by epigenetic regulation of progesterone receptor isoform B.Inhibiting LSD1, a HOTAIR-associated protein that removed activating H3K4me2 chromatin marks, induced PRB expression and promoted apoptosis induced by MPA.Silencing HOTAIR strengthened the H3K4me2 occupation on the promotor of PRB.HOTAIR and LSD1 collaboratively repress PRB expression and thus mediate progesterone sensitivity in endometrial carcinoma cells.	30443761	RID05756	epigenetic regulation	chemoresistance		
Oral squamous cell carcinoma	EPIST	CYC1	negatively-E	western blot;RIP;siRNA	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000249082	GRCh38_5:135038831-135040047	ENSG00000179091	NA	101927953	1537	C5orf66-AS1|CTC-276P9.1|Epist	UQCR4	Long non-coding RNA C5orf66-AS1 prevents oral squamous cell carcinoma through inhibiting cell growth and metastasisThe levels of the lncRNA C5orf66 antisense RNA 1 (C5orf66-AS1) and of cytochrome c1 (CYC1) in OSCC tissues and cells were measured through reverse transcription-quantitative polymerase chain reaction. In addition, the levels of associated proteins were analyzed by western blot.The findings revealed that the expression of lncRNA C5orf66-AS1 in OSCC tissues and cells was significantly decreased.Overexpression of lncRNA C5orf66-AS1 significantly inhibited the proliferation, invasion and migration ability of OSCC cells, and promoted cell apoptosis, while lncRNA C5orf66-AS1 downregulation presented the opposite effects.In addition, it was observed that CYC1 was upregulated in OSCC tissues and cells, and was negatively regulated by lncRNA C5orf66-AS1. Notably, CYC1 silencing markedly eliminated the effects of lncRNA C5orf66-AS1 downregulation on OSCC cells. Taken together, these findings indicated that lncRNA C5orf66-AS1 may prevent OSCC progression by inhibiting OSCC cell growth and metastasis via the regulation of CYC1 expression.	30280186	RID05757	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Triple-negative breast cancer	PVT1	CDKN1A	negatively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell viability(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124762	NA	5820	1026	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	PVT1 affects EMT and cell proliferation and migration via regulating p21 in triple-negative breast cancer cells cultured with mature adipogenic mediumOur results demonstrated that the mature adipogenic medium promoted the epithelial-mesenchymal transition, enhanced the cell viability and migration potential of TNBC cells. In addition, we proved that mature adipogenic medium affected the PVT1 expression and inhibition of the PVT1 disturbed the role of mature adipogenic medium in TNBC cells. Finally, we illustrated that repression of p21 restored the phenotype caused by PVT1 knockdown in TNBC cells treated with mature adipogenic medium. Taken together, our results demonstrated that PVT1 affected the role of mature adipogenic medium in TNBC cells via modulating p21 expression.	30371726	RID05758	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	NEAT1	CTNNB1	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168036	NA	283131	1499	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	armadillo|beta-catenin|CTNNB	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT1 down-regulation decreased the CSC-like properties of A549/CDDP cells, while overexpression of NEAT1 increased the stemness of A549/CDDP cells. In addition, Wnt signaling pathway exerted a significant role in the CSC-like traits triggered by NEAT1 overexpression. To sum up, our progress in A549/CDDP suggested a deeper understanding about NSCLC chemo-resistance, recurrence and metastasis.In our present study, it was demonstrated that knockdown of NEAT1 greatly inhibited A549/CDDP cell survival and CSC-like traits. Reversely, overexpression of NEAT1 induced stemness of A549/CDDP cells through increasing tumor sphere volume, MMP-9, MMP-2, CD133, CD44, ABCG2, Sox2, Nanog and Oct4 protein levels and CD44 positive cell ratios.In our study, it was found that down-regulation of NEAT1 repressed Wnt/beta-catenin.signaling while overexpression of NEAT1 induced its activity. Taken these together, we indicated that stemness triggered by NEAT1 in A549/CDDP cells was dependent on Wnt signal pathway in vitro.In conclusion, our findings uncovered an oncogenic role for NEAT1 in stemness of A549/CDDP cells, which depended on Wnt signaling pathway. Our study suggested the possibility of developing NEAT1 as CSCs-target for NSCLC chemotherapy resistance and further studies are warranted.	30291867	RID05759	expression association	metastasis,recurrence,chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	NEAT1	MMP9	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100985	NA	283131	4318	LINC00084|NCRNA00084|TncRNA|VINC	CLG4B|GELB|MANDP2|MMP-9	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT2 down-regulat	30291867	RID05760	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	NEAT1	MMP2	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000087245	NA	283131	4313	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT3 down-regulat	30291867	RID05761	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	NEAT1	PROM1	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000007062	NA	283131	8842	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	AC133|CD133|CORD12|MCDR2|PROML1|RP41|STGD4	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT4 down-regulat	30291867	RID05762	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(BRCA);DATA(GSE109761)
Non-small cell lung cancer	NEAT1	CD44	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000026508	NA	283131	960	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CD44R|CSPG8|HCELL|IN|MC56|MDU2|MDU3|MIC4|Pgp1	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT5 down-regulat	30291867	RID05763	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	NEAT1	ABCG2	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000118777	NA	283131	9429	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ABCP|BCRP|CD338|EST157481|MXR	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT6 down-regulat	30291867	RID05764	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	NEAT1	SOX2	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000181449	NA	283131	6657	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT7 down-regulat	30291867	RID05765	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	NEAT1	NANOG	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000111704	NA	283131	79923	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	FLJ12581|FLJ40451	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT8 down-regulat	30291867	RID05766	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Non-small cell lung cancer	NEAT1	POU5F1	positively-E	siRNA;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+);biomarker(+);WNT signaling pathway(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000233911	NA	283131	5460	LINC00084|NCRNA00084|TncRNA|VINC	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	NEAT1 contributes to the CSC-like traits of A549/CDDP cells via activating Wnt signaling pathwayIn our present study, it was indicated that NEAT1 was up-regulated in A549/CDDP cells in which CSC-like properties were obviously enriched. NEAT8 down-regulat	30291867	RID05767	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	CXCL8	MALAT1	positively-E	shRNA;ChIP;luciferase reporter assay	upregulation	RT-qPCR	GSE3325;GSE6099	NA	cell proliferation(+);cell invasion(+)	NA	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000169429	NA	ENSG00000251562	GRCh38_11:65497688-65506516	3576	378938	3-10C|AMCF-I|b-ENAP|GCP-1|GCP1|IL-8|IL8|K60|LECT|LUCT|LYNAP|MDNCF|MONAP|NAF|NAP-1|NAP1|SCYB8|TSG-1	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	IL-8 Secreted from M2 Macrophages Promoted Prostate tumorigenesis via STAT3/MALAT1 PathwayHere we reported that, M2 macrophages (PMA/IL-4 treated THP1) induced MALAT1 expression in PCa cell lines. Knockdown MALAT1 expression level in PCa cell lines inhibited cellular proliferation, invasion, and tumor formation. Further mechanistic dissection revealed that M2 macrophages secreted IL-8 was sufficient to drive up MALAT1 expression level via activating STAT3 signaling pathway. Additional chromatin immunoprecipitation (ChIP) and luciferase reporter assays displayed that STAT3 could bind to the MALAT1 promoter region and transcriptionally stimulate the MALAT1 expression. In summary, our present study identified the IL-8/STAT3/MALAT1 axis as key regulators during prostate tumorigenesis and therefore demonstrated a new mechanism for the MALAT1 transcriptional regulation.	30591689	RID05768	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Neurocognitive disorder	AK006025	CXCL9	positively-E	RIP;ChIP;siRNA	upregulation	qPCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Other	Neurocognitive disorder	lncRNA	PCG	NA	NA	ENSG00000138755	NA	NA	4283	NA	CMK|crg-10|Humig|MIG|SCYB9	HIV-1 Nef-induced lncRNA AK006025 regulates CXCL9/10/11 cluster gene expression in astrocytes through interaction with CBP/P300We performed microarray analysis of lncRNAs from primary mouse astrocytes treated with Nef protein. Top ten lncRNAs were validated through real-time PCR analysis. Gene ontology (GO) and KEGG pathway analysis were applied to explore the potential functions of lncRNAs. RIP and ChIP assays were performed to demonstrate the mechanism of lncRNA regulating gene expression.Knockdown of lncRNA AK006025, not AK138360, inhibited significantly CXCL9, CXCL10 (IP-10), and CXCL11 expression in astrocytes treated with Nef protein. Mechanism study showed that AK006025 associated with CBP/P300 was enriched in the promoter of CXCL9, CXCL10, and CXCL11 genes.Our findings uncovered the expression profiles of lncRNAs and mRNAs in vitro, which might help to understand the pathways that regulate astrocyte activation during the process of HAND.	30382871	RID05769	transcriptional regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Neurocognitive disorder	AK006025	MIR675	positively-E	RIP;ChIP;siRNA	upregulation	qPCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	NA	Other	Neurocognitive disorder	lncRNA	miRNA	NA	NA	ENSG00000288367	NA	NA	100033819	NA	MIRN675|hsa-mir-675	HIV-1 Nef-induced lncRNA AK006025 regulates CXCL9/10/11 cluster gene expression in astrocytes through interaction with CBP/P300.Pro-inflammatory factors and neurotoxins from activated astrocytes by HIV-1 itself and its encoded proteins, including the negative factor (Nef), are involved in the pathogenesis of HAND. Knockdown of lncRNA AK006025, not AK138360, inhibited significantly CXCL9, CXCL10 (IP-10), and CXCL11 expression in astrocytes treated with Nef protein. Mechanism study showed that AK006025 associated with CBP/P300 was enriched in the promoter of CXCL9, CXCL10, and CXCL11 genes.	30382871	RID05770	transcriptional regulation	NA		
Neurocognitive disorder	AK006025	CXCL11	positively-E	RIP;ChIP;siRNA	upregulation	qPCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Other	Neurocognitive disorder	lncRNA	PCG	NA	NA	ENSG00000169248	NA	NA	6373	NA	b-R1|H174|I-TAC|IP-9|SCYB11|SCYB9B	HIV-1 Nef-induced lncRNA AK006025 regulates CXCL9/10/11 cluster gene expression in astrocytes through interaction with CBP/P300.Pro-inflammatory factors and neurotoxins from activated astrocytes by HIV-1 itself and its encoded proteins, including the negative factor (Nef), are involved in the pathogenesis of HAND. Knockdown of lncRNA AK006025, not AK138360, inhibited significantly CXCL9, CXCL10 (IP-10), and CXCL11 expression in astrocytes treated with Nef protein. Mechanism study showed that AK006025 associated with CBP/P300 was enriched in the promoter of CXCL9, CXCL10, and CXCL11 genes.	30382871	RID05771	transcriptional regulation	NA		UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	FEZF1-AS1	MIR4443	negatively-F	siRNA;dual-luciferase reporter assay;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000265483	NA	154860	100616407	NA	mir-4443	lncRNA FEZF1-AS1 contributes to cell proliferation, migration and invasion by sponging miR-4443 in hepatocellular carcinomaIn the present study, it was identified that FEZF1-AS1 was significantly upregulated in HCC cell lines and tissues, as determined by reverse transcription-quantitative polymerase chain reac- tion. Additionally, it was observed that higher expression of FEZF1-AS1 in patients with HCC indicated poorer prognosis. Furthermore, it was identified that knockdown of FEZF1-AS1 markedly inhibited the proliferation, colony formation, migra- tion and invasion of Hep3B and Huh7 cells, as determined by Cell Counting Kit-8, colony formation and Transwell assays. In terms of mechanism, it was observed that FEZF1-AS1 acted as a sponge for microRNA (miR)-4443. The results of a lucif- erase reporter assay revealed that overexpression of miR-4443 significantly inhibited the luciferase activity in Hep3B and Huh7 cells. Additionally, miR-4443 overexpression markedly inhibited the expression of FEZF1-AS1, and vice versa. It was additionally identified that miR-4443 was downregulated in HCC tissues. There was an inverse correlation between the expression of miR-4443 and FEZF1-AS1 in HCC tissues. Furthermore, through functional experiments, it was identi- fied that knockdown of FEZF1-AS1 significantly inhibited the proliferation, migration and invasion of HCC cells, whereas inhibition of miR-4443 reversed these effects.Collectively,the present results demonstrated that FEZF1-AS1 acts as an oncogene by acting as a sponge for miR-4443.	30365146	RID05772	ceRNA or sponge	prognosis		
Posterior capsule opacification	TGFB2	HOTAIR	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell viability(+);cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Other	Posterior capsule opacification	PCG	lncRNA	ENSG00000092969	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7042	100124700	G-TSF|LDS4|TGF-beta2	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	LncRNA HOTAIR mediates TGF-beta2-induced cell growth and epithelial-mesenchymal transition in human lens epithelial cellsIn this study, we confirmed that TGF-beta2 induces EMT in SRA01/04 cells via the up-regulation of the long non-coding RNA (lncRNA) HOTAIR. To study the effects of HOTAIR on the proliferation, migration and EMT of SRA01/04 cells as well as the underlying mechanism, we used small interfering RNA (siRNA) to specifically attenuate HOTAIR expression in SRA01/04 cells. CCK8 cell-counting kit was used to examine SRA01/04 cell viability; EdU cell proliferation kit was used to examine SRA01/04 cell proliferation; Transwell system and scratch assays were used to observe cell migration; and qPCR and western blotwere used to evaluate EMT progression. We found that inhibition of HOTAIR expression repressed SRA01/04 cell viability, proliferation, migration and prevented the TGF-beta2-induced changes in cellular processes via modulation of EMT. Ultimately, we found that HOTAIR affected the TGF-beta/Smad signaling pathway. In summary, we elucidated that HOTAIR affected the cell viability, proliferation, and migration in the TGF-beta2-induced EMT in SRA01/04 cells and suggested that modulation of HOTAIR may be helpful in PCO prevention and therapy.	30239553	RID05773	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Osteosarcoma	DUXAP9	Cyclin D1	positively-E	knockdown;overexpression;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	NA	NA	503638	NA	LINC01296|LNMAT1	NA	lncRNA LINC01296 regulates the proliferation, metastasis and cell cycle of osteosarcoma through cyclin D1The expression of LINC01296 in osteosarcoma tissues and adjacent healthy tissues of 30 patients was analyzed by quantitative real-time PCR (qRT-PCR. The relationship between LINC01296 expression and the survival of patients with osteosarcoma was also explored. The expression levels of LINC01296 in osteosarcoma cells and normal cells were compared. LINC01296 knockdown and overexpression were performed in MG63 and HOS8603 osteosarcoma cells by transfecting LINC01296 shRNA and an expression plasmid respectively, followed by investigation of the changes on cell proliferation, migration, apoptosis and cell cycle arrest. western blot was used to analyze the changes of cell cycle regulators. Cyclin D1 knockdown and overexpression were carried out to verify the interaction between LINC01296 and cyclin D1. LINC01296 overexpression was demonstrated as a biomarker of osteosarcoma, which was closely correlated with the poor survival of patients with osteosarcoma. A high expression of LINC01296 was observed in osteosarcoma cells, which was closely associated with enhanced proliferation, invasion, and migration of osteosarcoma cells. Cyclin D1 expression was positively correlated with the expression of LINC01296 in osteosarcoma cells. Cyclin D1 knockdown or overexpression played a deterministic role in mediating the effect of LINC01296 on osteosarcoma cells. LINC01296 is an oncogenic lncRNA in osteosarcoma. The proliferation, invasion and migration of osteosarcoma cells could be effectively retarded by inhibition of LINC01296. The cancer-promoting effect of LINC01296 on osteosarcoma was determined by cyclin D1.	30226542	RID05774	expression association	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Non-small cell lung cancer	GASAL1	TGFB1	positively-E	overexpression;siRNA;knockdown	downregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000105329	NA	401472	7040	GASL1	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA GASL1 inhibits tumor growth of non-small cell lung cancer by inactivating TGF-beta pathway.As  shown  in Figure 2a, serum levels of GASL1 were si-gnificantly higher in patients with NSCLC than in  healthy  controls  (p<0.05).Patients  were  divided  into  high expression group (n=49) and low expression group (n=49) according to the median serum level of  GASL1.  Survival  curves  of  those  two  groups  were plotted based on Kaplan-Meier method and compared by log-rank t-test. As shown in Figure 2c, survival of patients in high expression group was significantly better than that in low expres-sion group (p<0.001). Those data suggest that se-rum  GASL1  may  serve  as  a  potential  diagnostic  and prognostic biomarker for NSCLC.As showed in Figure 3, GASL1 overexpression  upregulated  (Figure  3a)  and GASL1  knockdown  (Figure  3b)  downregulated the expression of GASL1 in cells of NSCLC cell lines, but not in cells of the normal lung cell line.CCK-8 assay was performed to investigate the effects  of  LncRNA  GASL1  overexpression  and  knockdown  on  cell  proliferation  of  a  normal  hu-man lung tissue cell line WI-38, and two human NSCLC  cell  lines  NCI-H23  and  NCI-H299.  As  shown in Figure 4, GASL1 overexpression inhi-bited and knockdown promoted cell proliferation of NSCLC cell lines NCI-H23 and NCI-H299, but not normal human lung tissue cell line WI-38. In addition, TGF-beta1 (10 ng/ml) treatment reduced the  enhancing  effects  of  GASL1  knockdown  on  NSCLC cell proliferation.	30468472	RID05775	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	UCA1	MAPK1	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000100030	NA	652995	5594	CUDR|LINC00178|onco-lncRNA-36|UCAT1	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	LncRNA GASL1 inhibits tumor growth of non-small cell lung cancer by inactivating TGF-beta pathway.The results re-vealed that the transcripts of lncRNA UCA1 were significantly overexpressed (p  <  0.05)  in  all  the  lung cancer cell lines in comparison to the normal lung cell line (Figure 1).The results indicated that  the  suppression  of  lncRNA  UCA1  in  lung  NCI-H23 cancer cells significantly inhibited (p < 0.05) their proliferation time dependently (Figure 2B). These results further prompted us to exami-ne the effect of lncRNA UCA1 suppression on the cell  invasion  and  migration  of  lung  cancer  cells  by  Boyden  chamber  and  wound  healing  assays. The  results  showed  that  sup-pression of lncRNA UCA1 triggered apoptosis in lung  NCI-H23  cancer  cells  (Figure  3A).The results showed that suppression of UCA1 caused a significant de-crease  in  the  expression  of  MAPK1  (Figure  4A  and B), indicating that lncRNA UCA1 might exert its effects at least in part via MAPK1. Further, si-lencing of MAPK1 inhibited the proliferation, mi-gration, and invasion of the lung cancer NCI-H23 cells (Figure 4C-E).To  elucidate  if  MAPK1  and  lncRNA  UCA1  control the proliferation, invasion, and migration of  the  lung  cancer  cells  synergistically,  the  lung  cancer  cells  were  co-transfected  with  si-UCA1  and  si-MAPK1.  The  outcomes  of  this  research  showed  that  the  inhibition  of  MAPK1  and  lncR-NA UCA1 together had more profound effects on cell  proliferation,  invasion,  and  migration  than  lncRNA  UCA1  or  MAPK1  individually  (Figure  5A-C).  These  results  suggest  that  MAPK1  and  UCA1 exhibit synergistic effects on the prolifera-tion, migration, and invasion of lung cancer cells.	30468471	RID05776	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MRPL39	miR-130	negatively-F	luciferase reporter assay;	downregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	protein-RNA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000154719	GRCh38_21:25585656-25607517	NA	NA	54148	NA	C21orf92|FLJ20451|L39mt|MGC104174|MGC3400|MRP-L5|MSTP003|PRED22|PRED66|RPML5	NA	Long Noncoding RNA MRPL39 Inhibits Gastric Cancer Proliferation and Progression by Directly Targeting miR-130.We found that MRPL39 was significantly downregulated in GC tissues and cell lines and that its expression level was negatively associated with carcinoma size, tumor, lymph node, metastasis (TNM) stage, and lymphatic metastasis. Moreover, a luciferase assay demonstrated a direct binding between the miR-130 and MRPL39, and the reintroduction of miR-130 abrogated the anti-tumor effect of MRPL39 on GC cells.To  investigate  the  underlying  molecular  mechanism  ofMRPL39, LNCipedia.org database (https://lncipedia.org/db/search) was used to identify the potential target miRNA ofMRPL39.  Then,  we  analyzed  the  potential  binding  site  byLasergene  6.0  software  (DNASTAR,  Inc.,  Madison,  WI),referred by relevant literature on lncRNA studies, establish-ing  a  lot  of  luciferase  reporter  recombinant  plasmids  con-taining the full-length MRPL39 sequence. Luciferase reportassays were performed to determine the target gene. MiR-130was  found  to  be  the  potential  target  miRNA  of  MRPL39.Consequently,   an   inverse   correlation   was   observed   be-tween MRPL39 level and miR-130 expression in GC tissues(Fig. 3A). The expression of miR-130 also decreased aftertransfection   with   MRPL39   plasmid   in   GC   cell   lines(Fig.  3B).  Moreover,  qRT-PCRassay  displayed  that trans-forming growth factor beta receptor 2 (TGFbR2) expression(the target gene of miR-130) increased significantly with thepresence of MRPL39 (Fig. 3C).To  clarify  the  direct  relationship  between  MRPL39  andmiR-130 in GC cells, we cloned the wild-type MRPL39 se-quence  with the  potential  binding  site  of  miR-130  and  themutant  MRPL39  sequence  into  a  luciferase  reporter  genesystem  (Fig.  3D).  The  result  demonstrated  that  miR-130suppressed the luciferase activity of wild-type MRPL39 butnot the luciferase activity of mutant MRPL39 in GC cell lines(Fig. 3E)To elucidate whether MRPL39 serves its role by spongingmiR-130,  we  transfected  the  MRPL39  overexpressed  GCcells with miR-130/miR-con mimics (Fig. 4A). According tothe  CCK-8  assay,  cell  growth  was  significantly  promotedwith the restoration of miR-130 in the BGC823 and SGC-7901 cells (Fig. 4B). Moreover, IHC assay revealed that theoverexpression of miR-130 promoted Ki67-labeled nuclei inthe MRPL39 overexpressed GC cells (Fig. 4C). Similarly, theenhanced  migratory  distance  and  invasive  cells  were  alsopresented in the miR-130 overexpressing cells (Fig. 4D, E).CCK-8   assayshowed that the cell growth was suppressed significantly withoverexpression   of   MRPL39   compared   with   the   controlgroup (Fig. 2B).Moreover, IHC assay determined that the percentage of Ki67-labeled nuclei was lower in the MRPL39overexpression  group  than  that  of  corresponding  controlgroups in both cell lines (Fig. 2C). In addition, cell migratoryand  invasive  capacity  also  displayed  an  obvious  down-regulation  in  MRPL39  overexpressed  cells  compared  withthe control groups (Fig. 2D, E).	30452299	RID05777	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Oral submucous fibrosis	LINC00974	alpha-SMA	negatively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(+);TGF-beta/SMAD signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	NA	NA	147093	NA	NA	NA	LncRNA LINC00974 activates TGF-beta/Smad signaling to promote oral fibrogenesis.We found that the expression of LINC00974 in OSF tissues or myofibroblasts was aberrantly upregulated, and there was a positive correlation between LINC00974 and myofibroblast markers. We demonstrated that the expression levels of alpha-SMA, alpha-1 type I collagen, fibronectin were downregulated in the LINC00974-inhibited myofibroblasts. Additionally, the TGF-beta secretion and phosphorylated Smad2 expression were also repressed in the LINC00974-inhibited myofibroblasts. Hence,transwell migration and wound healing assays were applied to assessit, and our results suggested that silence of LINC00974 reduced themyofibroblast migration ability.Taken togeApart from behavioral phenotype, the expression ofalpha-SMA was alsoa distinct feature of myofibroblasts.15Consistent with the reducedactivities, we observed that the mRNA and protein expression levelsofalpha-SMA were downregulated in LINC00974-inhibited fBMFs(Figure 4A,B). Moreover, the expression of two main components inECM,alpha-1 type I collagen and fibronectin, were attenuated as well(Figure 4A,B).ther, these findings suggested that the expression of LINC00974determined the activation of myofibroblast.These resultsindicated that LINC00974 may involve in the TGF-beta1-associatedmyofibroblasts activation.	30447113	RID05778	expression association	NA	UP(LIHC);DATA(GSE117623)	
Oral submucous fibrosis	LINC00974	alpha-1 type I collagen	negatively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(+);TGF-beta/SMAD signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	NA	NA	147093	NA	NA	NA	LncRNA LINC00974 activates TGF-beta/Smad signaling to promote oral fibrogenesis.We found that the expression of LINC00974 in OSF tissues or myofibroblasts was aberrantly upregulated, and there was a positive correlation between LINC00974 and myofibroblast markers. We demonstrated that the expression levels of alpha-SMA, alpha-1 type I collagen, fibronectin were downregulated in the LINC00974-inhibited myofibroblasts. Additionally, the TGF-beta secretion and phosphorylated Smad2 expression were also repressed in the LINC00974-inhibited myofibroblasts. Hence,transwell migration and wound healing assays were applied to assessit, and our results suggested that silence of LINC00974 reduced themyofibroblast migration ability.Taken togeApart from behavioral phenotype, the expression ofalpha-SMA was alsoa distinct feature of myofibroblasts.15Consistent with the reducedactivities, we observed that the mRNA and protein expression levelsofalpha-SMA were downregulated in LINC00974-inhibited fBMFs(Figure 4A,B). Moreover, the expression of two main components inECM,alpha-1 type I collagen and fibronectin, were attenuated as well(Figure 4A,B).ther, these findings suggested that the expression of LINC00974determined the activation of myofibroblast.These resultsindicated that LINC00974 may involve in the TGF-beta1-associatedmyofibroblasts activation.	30447113	RID05779	expression association	NA	UP(LIHC);DATA(GSE117623)	
Oral submucous fibrosis	LINC00974	fibronectin	negatively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(+);TGF-beta/SMAD signaling pathway(+)	NA	regulation	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	NA	NA	147093	NA	NA	NA	LncRNA LINC00974 activates TGF-beta/Smad signaling to promote oral fibrogenesis.We found that the expression of LINC00974 in OSF tissues or myofibroblasts was aberrantly upregulated, and there was a positive correlation between LINC00974 and myofibroblast markers. We demonstrated that the expression levels of alpha-SMA, alpha-1 type I collagen, fibronectin were downregulated in the LINC00974-inhibited myofibroblasts. Additionally, the TGF-beta secretion and phosphorylated Smad2 expression were also repressed in the LINC00974-inhibited myofibroblasts. Hence,transwell migration and wound healing assays were applied to assessit, and our results suggested that silence of LINC00974 reduced themyofibroblast migration ability.Taken togeApart from behavioral phenotype, the expression ofalpha-SMA was alsoa distinct feature of myofibroblasts.15Consistent with the reducedactivities, we observed that the mRNA and protein expression levelsofalpha-SMA were downregulated in LINC00974-inhibited fBMFs(Figure 4A,B). Moreover, the expression of two main components inECM,alpha-1 type I collagen and fibronectin, were attenuated as well(Figure 4A,B).ther, these findings suggested that the expression of LINC00974determined the activation of myofibroblast.These resultsindicated that LINC00974 may involve in the TGF-beta1-associatedmyofibroblasts activation.	30447113	RID05780	expression association	NA	UP(LIHC);DATA(GSE117623)	
Oral submucous fibrosis	LINC00974	SMAD2	negatively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(+);TGF-beta/SMAD signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Mouth disease	lncRNA	TF	ENSG00000226629	GRCh38_17:41549606-41554495	ENSG00000175387	NA	147093	4087	NA	JV18-1|MADH2|MADR2	LncRNA LINC00974 activates TGF-beta/Smad signaling to promote oral fibrogenesis.We found that the expression of LINC00974 in OSF tissues or myofibroblasts was aberrantly upregulated, and there was a positive correlation between LINC00974 and myofibroblast markers. We demonstrated that the expression levels of alpha-SMA, alpha-1 type I collagen, fibronectin were downregulated in the LINC00974-inhibited myofibroblasts. Additionally, the TGF-beta secretion and phosphorylated Smad2 expression were also repressed in the LINC00974-inhibited myofibroblasts. Hence,transwell migration and wound healing assays were applied to assessit, and our results suggested that silence of LINC00974 reduced themyofibroblast migration ability.Taken togeApart from behavioral phenotype, the expression ofalpha-SMA was alsoa distinct feature of myofibroblasts.15Consistent with the reducedactivities, we observed that the mRNA and protein expression levelsofalpha-SMA were downregulated in LINC00974-inhibited fBMFs(Figure 4A,B). Moreover, the expression of two main components inECM,alpha-1 type I collagen and fibronectin, were attenuated as well(Figure 4A,B).ther, these findings suggested that the expression of LINC00974determined the activation of myofibroblast.These resultsindicated that LINC00974 may involve in the TGF-beta1-associatedmyofibroblasts activation.	30447113	RID05781	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	MAGI2-AS3	CFAP45	positively-E	dual-luciferase reporter assay;	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-15b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000213085	NA	100505881	25790	ENST00000414797	CCDC19|NESG1	Long noncoding RNA MAGI2-AS3 regulates CCDC19 expression by sponging miR-15b-5p and suppresses bladder cancer progression.In this present study, we screened out a novel lncRNA MAGI2-AS3 whose expression was downregulated in BCa tissues. Functionally, we showed that MAGI2-AS3 overexpression inhibits proliferation, migration and invasion of BCa cells.Bioinformatics analysis revealed that MAGI2-AS3 could serve as a competing endogenous RNA (ceRNA) for miR-15b-5p. In the meantime, miR-15b-5p directly targeted CCDC19, a tumor suppressor in BCa.Moreover, we analyzed the expressioncorrelations among MAGI2-AS3, miR-15b-5p and CCDC1 by qRT-PCR We found that miR-15b-5p expression was inversely corre-lated with that of MAGI2-AS3  and CCDC19 .Luciferase reporter assays were furthercarried out to evaluate the direct interaction between miR-15b-5pwith MAGI2-AS3 or CCDC19. Results illustrated that miR-15b-5pmimic transfection repressed the relative luciferase activity ofMAGI2-AS3-Wt reporter  or CCDC19-Wt reporter  inT24 cells, supporting a direct interaction between miR-15b-5p andMAGI2-AS3 or CCDC19. Thus, we guessed whether MAGI2-AS3 actsas a ceRNA for miR-15b-5p to regulate CCDC19 expression. Westernblotting analysis further revealed that CCDC19 expression wasrestored by miR-15b-5p inhibitors in MAGI2-AS3-silenced T24 andRT4 cells . Thus, above data demonstrate that MAGI2-AS3promotes CCDC19 expression by sponging miR-15b-5.Results showed that MAGI2-AS3 over-expression significantly suppressed the proliferation (Fig. 3A),colony formation (Fig. 3B), migration (Fig. 3C) and invasion (Fig. 3D)of BCa cells. Importantly, silencing of CCDC19 in MAGI2-AS3-overexpressing T24 and RT4 cells rescued the abilities of cell pro-liferation, colony formation, migration and invasion (Fig. 3AeD).Taken together, ourfindings demonstrate that MAGI2-AS3 sup-presses malignant behaviors of BCa cells through CCDC19.	30442369	RID05782	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Gastric cancer	CDKN2B-AS1	ZBTB16	negatively-E	knockdown;RIP	upregulation	qRT-PCR	NA	NA	tumor malignant transformation(+);epithelial to mesenchymal transition(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000109906	NA	100048912	7704	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	PLZF|ZNF145	Tumor suppressor PLZF regulated by lncRNA ANRIL suppresses proliferation and epithelial mesenchymal transformation of gastric cancer cells.In the present study, we found that PLZF was downregulated in the majority of GC cell lines and tumor tissues and that alteration of PLZF expression was closely correlated with a malignant phenotype, epithelial-mesenchymal transformation and overall survival. Furthermore, we assessed the expression levels of the lncRNA ANRIL in GC and found that it was negatively associated with the level of PLZF and that ANRIL indirectly methylated PLZF to suppress its expression via binding with polycomb repressive complex 2.In the wound healing assay, PLZF overexpression suppressed wound healing in both BGC823 and SGC7901 cells . Collectively, these find-ings indicated that increased PLZF expression in GC inhibited GC cell proliferation, migration and invasion.We screened a panel of lncRNAs to search for the associated lncRNA of PLZF expression and found that both ANRIL and HOTAIR knockdown recovered the expression of PLZF in BGC823 cells. Since ANRIL knockdown increased PLZF expression more than HOTAIR knockdown, we chose ANRIL to further study PLZF regulation. Furthermore, we confirmed the negative association between PLZF and ANRIL expression in BGC823 and SGC7901 cells; ANRIL knock-down increased the expression of PLZF in both BGC823 and SGC7901 cells.RIP experiment confirmed the interaction between ANRIL and PLZF in GC cells .Recent discoveries have marked lncRNAs as new important players in DNA methylation regu-lation . Therefore, we inferred that ANRIL may regulate PLZF methylation by binding to PRC2. MSP is a method for analyzing DNA methylation patterns in CpG islands, and it revealed that PLZF was methylated in BGC823 and SGC7901 cells, not in the normal cell lines GES1 . BGC823 and SGC7901 cells were treated with the methylation inhibitor 5-Aza, DNA methylation of PLZF was decreased, but PLZF expression was increased). In addition, the histone deacetylase (HDAC) inhibitor SAHA did not have the same effect, which suggested that PLZF was methylated, not acetylated.	30431129	RID05783	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Renal cell carcinoma	MALAT1	miR-22-3p	negatively-F	shRNA;overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);PI3K/AKT signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long non-coding RNA MALAT1 correlates with cell viability and mobility by targeting miR-22-3p in renal cell carcinoma via the PI3K/Akt pathway.The relationship between MALAT1 and miR-22-3p was examined by bioinformatic prediction analysis and luciferase reporter assay.MALAT1 was highly expressed and the expression of miR-22-3p was suppressed in RCC tissues and cell lines. In conclusion, lncR-MALAT1 affected the proliferation and migration of RCC cells by targeting miR-22-3p through the inactivation of the PI3K/Akt signaling pathway.The expression of MALAT1 and miR-22  -3p in RCC tissues and cell lines was detected through qRT-PCR As displayed in Fig. 1A, the expression level of MALAT1 in the RCC tumor tissue was significantly higher than that in adjacent normal tissues (P<0.01). Concurrently, the expression of MALAT1 in the RCC cell lines was signifi-cantly increased compared with the normal renal epithelial cells Ect1/E6E7 (P<0.05 and P<0.01). Transfection with MALAT1  shRNA  suppressed  cell  proliferation  compared  with MALTA1 scramble group ( P<0.05 and P<0).As  expected,  MALAT1  shRNA  significantly  inhibited  the  expression  of  matrix  metalloproteinase-3  (MMP-3)  and  promoted the expression of migration and invasion inhibitory protein (MIIP) (P<0.05). The above-mentioned results indicated that MALAT1 shRNA significantly inhibited the proliferation and migration of RCC cells.To investigate the related mechanism by which MALAT1 regulates the progression of RCC cells, we found  a  binding  site  for  MALAT1  on  miR-22-3p  through  bioinformatic analysis (TargetScan, http: //www.targetscan.org/)  (Fig.  3A).  Concurrently,  there  were  marked  negative  relevant  relations  between  the  expression  of  MALAT1  and  miR-22-3p in RCC tissues . As displayed in Fig. 3C, MALAT1  shRNA  significantly  elevated  the  expression  of  miR-22-3p  in  RCC  cells  (P<0.05),  but  then  this  effect  was  reversed through the co-transfection with miR-22-3p inhib-itor (P<0.05). Furthermore, the inhibiting effect of MALAT1 shRNA on the expression of MALAT1 was partially reversed by  the  co-transfection  of  miR-22-3p  inhibitor,  identifying  that  miR-22-3p  inhibitor  elevated  the  level  of  MALAT1  in  turn    (P<0.05 and P<0.05, respectively). Subsequently, we used the luciferase reporter assay to further examine the targeting  relationship  between  MALAT1  and  miR-22-3p.  The  results  demonstrated  that  the  luciferase  signal  in  the  lncR-MALAT1  MUT  and  the  lncR-MALAT1  WT  group remained at the same level, but the addition of miR-22  -3p mimic significantly  inhibited  the  luciferase  activity  by  binding  to  MALAT1 WT fragments. However, the regulatory relationship disappeared when binding to the MALAT1 MUT fragments, indicating that there existed a targeting relationship between MALAT1 and miR-22-3p (P<0.01). These results indicated that MALAT1 may promote the proliferation and migration of RCC cells by targeting miR-22  -3p.As displayed in Fig. 4A, MALAT1 shRNA significantly inhibited the expression of p-PI3K and p-Akt, but  the  addition  of  miR-22-3p  inhibitor  into  the  MALAT1  shRNA-treated Caki-1 cells significantly reversed the inhibi-tory effect of MALAT1 shRNA on the expression of p-PI3K and p-Akt (P<0.01, P<0.05). In addition, the expression of Akt in the MALAT1 shRNA group was much lower than that in the control group, indicating that MALAT1 shRNA inhibited the activation of Akt . Concurrently, miR-22-3p inhibitor reversed the inhibitory effect of MALAT1 shRNA on Akt accumulation on the cell membrane . All these results revealed that MALAT1 shRNA inhibited the activation of PI3K/Akt signaling pathway through the upregulation of the expression of miR-22  -3p.	30431104	RID05784	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	HAGLROS	ATG5	positively-F	dual-luciferase reporter assay;RIP;RNA pull-down assay;	upregulation	qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+);apoptosis process(-);cell autophagy(+)	ceRNA(miR-100)	regulation	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000057663	NA	102800310	9474	NA	APG5|APG5L|ASP|hAPG5	Long noncoding RNA HAGLROS regulates apoptosis and autophagy in colorectal cancer cells via sponging miR-100 to target ATG5 expression.The results showed that HAGLROS was highly expressed in CRC tissues and cells.Highly expression of HAGLROS correlated with a shorter survival time of CRC patients. Moreover, knockdown of HAGLROS in HCT-116 cells induced apoptosis by increasing the expression of Bax/Bcl-2 ratio, cleaved-caspase-3, and cleaved-caspase-9, and inhibited autophagy by decreasing the expression of LC3II/LC3I and Beclin-1 and increasing P62 expression. Furthermore, HAGLROS negatively regulated the expression of miR-100, and HAGLROS controlled HCT-116 cell apoptosis and autophagy through negatively regulation of miR-100. Autophagy related 5 (ATG5) was verified as a functional target of miR-100 and miR-100 regulated HCT-116 cell apoptosis and autophagy through targeting ATG5.The  results  showed  that  overexpression  ofHAGLROS alone significantly activated the PI3K/AKT/mTOR pathway .Furthermore, the results of MTT assay showed that theviability of HCT-116 cells in the pEX2-HAGLROS groupwas significantly increased compared with that of thepEX2 group (P< 0.05), and HCT-116 cell viability of sh-HAGLROS#2 group was markedly decreased relative tothat of sh-NC group (P< 0.05).The results showed that overexpression ofHAGLROS  significantly  increased  the  expression  ofLC3II/LC3I and Beclin-1 and decreased the expressionof P62, whereas knockdown of HAGLROS had oppositeeffects on the expression levels of these autophagymarkers (allP< 0.05).To verify it, the HCT-116cells were transfected with pEX2-HAGLROS-MS2 or pEX2-HAGLROS-mut-MS2 with miR-100 mimic or mimic control,and dual-luciferase reporter assay showed that HAGLROScould target miR-100 (P< 0.05; Figure 2B). To furtherconfirm that that HAGLROS and miR-100 were in the sameRISC, we performed a RIP assay using anti-Ago2. Theresults showed that anti-Ago2 precipitated the Ago2 proteinfrom the cell lysates , and higherHAGLROS and miR-100 were detected in the Ago2 pelletthan those in the input control .Furthermore, RNA pull-down assay was performed, and theresults of western blotshowed that Ago2 wasdetected after pull-down experiment with streptavidin beads,suggesting HAGLROS directly interacted with Ago2 . Moreover, a significant amount of miR-100 inthe HAGLROS pulled down pellet was revealed comparedwith control, while the amount of miR-100 in the loc285194pulled down pellet was only slightly increased . These data confirm the negative relationshipbetween HAGLROS and miR-100.The results showed that the effects of HAGLROS knockdown onHCT-116  cell  apoptosis  and  the  expression  levels  ofapoptosis-related  proteins   as  well  as  theexpression levels of autophagy markers  weresignificantly reversed by inhibition of miR-100 at the sametime, indicating that effects of HAGLROS downregulationon HCT-116 cell apoptosis and autophagy were achieved bynegative regulation of miR-100.As shown inFigure5A,HAGLROS overexpression alone resulted in a significant decrease in the expression levels ofPTEN and obvious increases in the expression of p-PI3K,p-AKT, and p-mTOR in HCT-116 cells. The expression changes of these proteins were significantly counteracted by overexpression of HAGLROS and miR-100 synchronously,but further enhanced after overexpression of HAGLROS,miR-100, and ATG5 concurrently . Notably,gefitinib-resistant HT-29 cells were established to confirmthe association between HAGLROS and PI3K/AKT/mTORpathway.  The  results  showed  that  overexpression  ofHAGLROS alone significantly activated the PI3K/AKT/mTOR pathway . Consistent results were alsoobtained after overexpression of HAGLROS, miR-100, andATG5 concurrently . These data indicated thatthe effects of HAGLROS in CRC cells were achievedpossible by regulating the activation of PI3K/AKT/mTORpathway.	30430634	RID05785	ceRNA or sponge	NA		UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	DANCR	KLF12	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-216a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000118922	NA	57291	11278	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	AP-2rep|AP2REP|HSPC122	DANCR contributed to hepatocellular carcinoma malignancy via sponging miR-216a-5p and modulating KLF12.As shown in Figure 1a, DANCR was dramatically elevated inHCC cells. In addition, we observed that miR-216a-5p was decreased inHCC cells compared with LO2 cells. This indicated that DANCR and miR-216a-5p might be involved in HCC progression.In Figure 2c,d, CCK-8 assay indicated that HCC cellproliferation was restrained by knockdown of DANCR. In addition, EdUassay was carried out and we found that HCC cell proliferation wassignificantly inhibited by LV-shDANCR (Figure 2e,f). These manifestedthat inhibition of DANCR could repress HCC cell proliferation.These data indicated that inhibition ofDANCR increased HCC cell apoptosis and blocked cell cycleprogression.As displayed in Figures 4a,c, LV-shDANCR dramaticallysuppressed HCC cell migration capacity. HCC cell invasion capacity was obviously inhibited by LV-shDANCR. These suggestedthat DANCR silence repressed HCC cell migration and invasion capacity.Cotransfection of the luciferase reporter plasmid contain-ing the wild type (WT) of DANCR with miR-216a-5p mimics decreasedthe reporter activity in HepG2 cells. Then, to test whetherDANCR can function as a sponge for miR-216a-5p, radioimmunopreci-pitation assay (RIPA) was used and DANCR and miR-216a-5p were moreabundant in Ago2 pellet than in immunoglobulin G pellet in HepG2 cells. These indicated that miR-216a-5p acted as a direct target of DANCR.Cotransfection of the luciferase reporter plasmid containing theWT-KLF12 with miR-216a-5p mimics decreased the reporter activityin HepG2 cells . In addition, KLF12 protein expression wasrepressed by miR-216a-5p mimics in HCC cells . Thesesuggested that KLF12 was a direct target of miR-216a-5p.Meanwhile, knockdown of DANCR inhibitedKLF12 expression via sponging miR-216a-5p in vivo.These data suggested that silencing DANCR inhibited HCC develop-ment through targeting miR-216a-5p and KLF12 in vivo.	30430564	RID05786	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Papillary thyroid carcinoma	GAS8-AS1	CCNG2	positively-E	luciferase reporter assay;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-135b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000138764	NA	750	901	C16orf3	NA	LncRNA GAS8-AS1 suppresses papillary thyroid carcinoma cell growth through the miR-135b-5p/CCND2 axis. Cell proliferation was detected by CCK-8 assay, si-GAS8-AS1 significantly promoted proliferation compared with the scramble group, and GAS8-AS1 overexpression prominently repressed proliferation compared with the control group in TPC1 and BCPAP cells. Our results showed that miR-135b-5p mimic significantly repressed luciferase activity when cotransfected with reporter containing WT GAS8-AS1 3'-UTR but not MT GAS8-AS1 3'-UTR. The synthetic si-GAS8-AS1 or pcDNA3.1-GAS8-AS1 was transfected into BCPAP cells. The result showed that GAS8-AS1 overexpression significantly suppressed mRNA expression of miR-135b-5p, while si-GAS8-AS1 promoted the expression of miR-135b-5pqRT-PCRanalysis exhibited that miR-135b-5p mimic significantly suppressed CCNG2 expression (fold change > 3) whereas miR-135b-5p inhibitor repressed CCNG2 expression in mRNA level (fold change > 3) (Figure 3D), CCNG2 protein expression was remarkably suppressed by the miR-135b-5p mimic but enhanced by the miR-135b-5p inhibitor when compared with the NC (Figure 3E). The above results indicated that GAS8-AS1 directly targets miR-135b-5p, which targets CCNG2. Our results showed that miR-135b-5p mimic significantly repressed luciferase activity when cotransfected with reporter containing WT GAS8-AS1 3'-UTR but not MT GAS8-AS1 3'-UTR (Figure 3A). The synthetic si-GAS8-AS1 or pcDNA3.1-GAS8-AS1 was transfected into BCPAP cells. The result showed that GAS8-AS1 overexpression significantly suppressed mRNA expression of miR-135b-5p, while si-GAS8-AS1 promoted the expression of miR-135b-5p (Figure 3B).Our results showed that the expressions of GAS8-AS1 and CCNG2 were markedly increased by 3.5-folds in tissues from mice transfected with LV-GAS8-AS1 compared with control and LV-ctrl group whereas miR-135b-5p expression was 3.5-folds higher than control or LV-ctrl group (Figure 5C,D). To conclude, these observations indicate that GAS8-AS1 repressed the development and progression of PTC through inhibition of miR-135b-5p and activation of CCNG2.	30429236	RID05787	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	HCG18	NOTCH1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-34c-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000148400	NA	414777	4851	Em:AB014087.1|FLJ25550|FLJ31598	TAN1	NOTCH1 regulates the proliferation and migration of bladder cancer cells by cooperating with long non-coding RNA HCG18 and microRNA-34c-5p. The resultof  Kaplan-Meier  analysis  revealed  that  the  overallsurvival rate of patients with low expression of NOTCH1was much lower than those with high expression of NOTCH1 (Figure 1C), indicating that NOTCH1 mayexert a crucial role in regulating BCa progression.According to the  experimental  result  of  luciferase  reporter  assay,miR-34c-5p mimics significantly impaired the luciferaseactivity  of  wild-type  NOTCH1  (NOTCH1-WT)  butnotthatofmutanttypeNOTCH1(NOTCH1-MUT)(Figure 2F). Moreover, inhibition of miR-34c-5p expres-sion strengthened the luciferase activity of NOTCH1-WT but not that of NOTCH1-MUT (Figure 2G). Toevaluate the regulatory relation between miR-34c-5p and NOTCH1, qRT-PCRand western blotwereconducted in J82 and T24 cell lines. The results showedthat both levels of NOTCH1 were decreased by miR-34c-5p  mimics  but  were  increased  by  miR-34c-5pinhibitors(Figure2Hand2I), indicating the negativeregulation of miR-34c-5p on NOTCH1.microarray  analysis  revealed  thatlncRNA HCG18 was significantly downregulated in BCatissues (Figure 3A).The  negative  correlation  between  theexpression of miR-34c-5p and that of HCG18 was analyzedby Spearman-s correlation analysis (Figure 3E, left).Simultaneously, the positive expression correlation be-tween HCG18 and NOTCH1 was analyzed (Figure 3E,right).  The result of luciferase reporteranalysis revealed that miR-34c-5p mimics observablyimpaired the luciferase activity of wild-type HCG18(HCG18-WT)  but  not  that  of  mutant  type  HCG18(HCG18-MUT) (Figure 3G). Whereas inhibition of miR-34c-5p expression strengthened the luciferase activity ofHCG18-WT but not that of HCG18-MUT (Figure 3H).Therefore, we confirmed the interaction between HCG18and miR-34c-5p in BCa cells. The regulatory effect ofHCG18 on miR-34c-5p was analyzed with qRT-PCR Theresults suggested that the expression level of miR-34c-5pwas increased by silenced HCG18 but was decreased byHCG18 overexpression (Figure 3I), indicating the negativeregulatory effect of HCG18 on miR-34c-5p. Furthermore,the mRNA levels and protein levels of NOTCH1 weretested in response to HCG18 knockdown or overexpres-sion. The results revealed the positive regulatory effect ofHCG18 on NOTCH1 (Figure 3J). Therefore, we confirmedthat HCG18 acted as a competing endogenous RNA(ceRNA) in BCa by regulating miR-34c-5p/NOTCH1 axis.Results of CCK-8 assay and colony formation assays demonstrated theeffects of HCG18-miR-34c-5p-NOTCH1 axis on cell pro-liferation. According to the data of Figure 4C-4E, cellproliferation and migration were promoted by the knock-down of NOTCH1 but were inhibited by the overexpres-sion of NOTCH1, indicating the tumor-suppressive role ofNOTCH1 in BCa progression. Whereas the proliferationand migration in cells transfected with sh-NOTCH1 wereinhibited by miR-34c-5p inhibitors or HCG18 overexpres-sion. In addition, the proliferation and migration in cellstransfected with pcDNA-NOTCH1 were promoted bymiR-34c-5p overexpression or HCG18 knockdown. Allthese findings suggested the oncogenic role of miR-34c-5pand the tumor-suppressive role of NOTCH1 in BCa as wellas the function of miR-34c-5p and HCG18 in NOTCH1-mediated BCa cell proliferation and migration.	30426533	RID05788	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	LSINCT5	APC	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	interact with protein	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000134982	NA	101234261	324	NA	DP2|DP2.5|DP3|PPP1R46	Long noncoding RNA LSINCT5 acts as an oncogene via increasing EZH2-induced inhibition of APC expression in osteosarcoma.In our study, we found that LSINCT5 was significantly upregulated in OS tissues than in adjacent normal tissues.LSINCT5 knockdown dramatically inhibited OS cell proliferation in vitro and tumor growth in vivo. Mechanistic exploration revealed that LSINCT5 interacted with EZH2 to suppress the expression of APC, a negative regulator of the Wnt/beta-catenin pathway. Moreover, rescue assays suggested that LSINCT5 exerted oncogenic roles by partially inhibiting APC expression in OS.Transwell migration andinvasion experiments indicated that LSINCT5 knockdown signifi-cantly reduced the number of OS cell migration and invasion(Fig. 2C and D).RIP and RNA pull-down assay indicated that EZH2 could precipitate LSINCT5in U2OS and Saos-2 cells and vice versa (Fig. 3B and C).In summary, these resultsdemonstrated that LSINCT5 interacted with EZH2 to inhibit APC expression, and the Wnt/b-catenin pathway in OS was activated.CCK8 assays indicated that the decreased proliferation induced by LSINCT5 knockdown was abolished by theintroduction of si-APC in U2OS and Saos-2 cells (Fig. 4B).Similarly,transwell assays showed that the suppressive effect of LSINCT5knockdown on migration and invasion was also reversed by APCsilencing in U2OS and Saos-2 cells (Fig. 4C and D). In conclusion, ourresults suggested that LSINCT5 performed oncogenic roles in OS bymodulating APC expression.	30420287	RID05789	interact with protein	NA	UP(PRAD);DATA(GSE104209)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Ovarian cancer	FEZF1-AS1	STAT3	positively-E	western blot;RNAi;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);JAK/STAT signaling pathway(+)	phosphorylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000168610	NA	154860	6774	NA	APRF	Long Noncoding RNA FEZF1-AS1 Promotes Proliferation and Inhibits Apoptosis in Ovarian Cancer by Activation of JAK-STAT3 Pathway.In order to identify the function of FEZF1-AS1 in ovarian cancer progression, we performed qRT-PCRassays to analyze FEZF1-AS1 expression in ovarian cancer tissues and adjacent normal tissues. We found that FEZF1-AS1 was highly expressed in cancer tissues (Figure 1A).Further FACS analysis showed that more cells were in G0/G1 stage after FEZF1-AS1 knockdown (Figure 2C). These data showed that FEZF1-AS1 promotes the proliferation of ES2 cells. Next, we analyzed the apoptotic status of ES2 cells after FEZF1-AS1 knockdown, results showed that FEZF1-AS1 knockdown significantly increased the percentage of apoptosis cells (Figure 2D). These results show that FEZF1-AS1 knockdown suppresses ovarian cancer cell proliferation and induces apoptosis.western blot results showed that FEZF1-AS1 knockdown in ES2 cells lead to the downregulation of STAT3 and a less active status of STAT3 (Figure 3A). Correlation analysis showed that FEZF1-AS1 expression was positively correlated with STAT3 expression (Figure 3B), and this was consistent with lower STAT3 expression in ovarian cancer cell line ES2. From these results, we know that FEZF1-AS1 promotes STAT3 expression.	30416194	RID05790	interact with protein	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	CA3-AS1	PTEN	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-93)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253549	GRCh38_8:85440596-85464915	ENSG00000171862	NA	100996348	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Overexpression of long non coding RNA CA3-AS1 suppresses proliferation, invasion and promotes apoptosis via miRNA-93/PTEN axis in colorectal cancer.To  determine  the  expression  of  CA3-AS1  in  CRC  tissues,  we  performed qRT-PCRexperiments to examine the expression of CA3-AS1 in 81 normal colorectal tissues and CRC tissues, and CA3-AS1 was significantly down-regulated in the CRC tissues compared with normal tissues (Fig. 1B)We used   CCK8   assay   to   evaluate   the   proliferation      and   our   results   showed   that overexpression of lncRNA CA3-AS1 inhibited the SW620 cell proliferation (Fig. 2B).We  also  detected  the   cell  apoptosis  using  flow  cytometry   and  we  found  that overexpression  of  lncRNA  CA3-AS1 promoted  the  cell  apoptosis  rates (Fig.  2C). LncRNA CA3-AS1  promoted  the  cells  apoptosis (Fig.  2E).  The luciferase activity of wild type CA3-AS1 was decreased in  miR-93  mimics  group,  while  transfection  of  miR-93  inhibitors  increased  the luciferase  activity  of  wild  type  CA3-AS1.  Besides,  miR-93  mimics  or  miR-93 inhibitors had no significant effect on the luciferase activity of mutant CA3-AS1 (Fig. 3B).  Moreover, overexpression of CA3-AS1 in SW620 cells inhibited the expression of  miR-93  compared  with  control  group;  the  expression  of  miR-93  was  increased  in down-regulation of CA3-AS1 in SW620 cells compared with control group (Fig. 3C). To  further  investigate  whether  the  effects  of  CA3-AS1  is  dependent  on  miR-93,  we found that co-transfection with lncRNA CA3-AS1 and miR-93 mimics decreased the cell  proliferation  compared  with  lncRNA  CA3-AS1  overexpression  group (Fig.  3D).   The number of invaded and migrated cells were also enhanced in co-transfection with lncRNA  CA3-AS1  and  miR-93  mimics  group (Fig.  3E).The  apoptosis  effect  was measured  via  western  blot  and  flow  cytometry,  and  we  found  that  miR-93  could decrease  the  cell  apoptosis (Fig.  3F,  Fig.  3G).  We  also  found  that  miR-93  was negatively regulated by CA3-AS1 (Fig. 3H).Our results demonstrated that the miR-93 was inversely correlated with lncRNA CA3-AS1. MiR-93  mimicsdecreased  the  luciferase  activity of  WT  3'UTR  of  PTEN,  while  the  luciferase  activity  of  WT  3'TUR  of  PTEN  was increased  in  miR-93  inhibitors  group;  whereas  miR-93  mimics  or  miR-93  inhibitors had  no  effect  on  the  luciferase  activity  of  mutant  3'UTR  of  PTEN (Fig.  4B). western blotwas also performed to measure the protein level of PTEN and  our  results  showed  that  overexpression  of  miR-93  decreased  the  expression  of PTEN,  suggesting  the  negative  regulation  between  miR-93  and  PTEN (Fig.  4D).Taken  together,  these  results  confirmed  that  the  CA3-AS1/miR-93/PTEN  axis  is important in colorectal cancer and lncRNA CA3-AS1 play an anti-tumor role in CRC via regulating the miR-93 and PTEN.	30415006	RID05791	ceRNA or sponge	NA	UP(PRAD);DATA(GSE104209)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Kidney disease	XIST	TLR4	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136869	NA	7503	7099	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ARMD10|CD284|hToll|TLR-4	Down-regulation of the long non-coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR-217-TLR4 pathway.The results indicated that XIST was clearly up-regulated in kidney tissues with membranous nephropathy compared with normal kidney tissues, while the expression of miR-217 was dramatically decreased (Figure 2a) and the level of TLR4 protein was increased (Figure 2b).The binging and interaction between XIST and miR-217 in AB8/13 cells were subsequently evaluated with RIP and RNA pull-down assay, respectively. AGO2 antibody was used in the RIP assay, and the level of XIST and miR-217 was examined. Compared with IgG, plenty of XIST and miR-217 were detected in the AGO2 antibody (Figure 4b). In the RNA pull-down assay, AGO2 in the pull-down complex of XIST was analysed by western blot (Figure 4c). The result demonstrated that miR-217 was deposited extensively in the pull-down complex of XIST, while it increased slightly in negative control (NC) (Figure 4d). These results proved that the miR-217 is a target of XIST.The results indicated that pcDNA-XIST inhibited miR-217 expression compared to its control pcDNA, which was restored by miR-127 mimic transfection (Figure 6a).Detection of miR-217 expression revealed that Ang II lowered the miR-217 level, and the level was elevated by siRNA-XIST, but was further reversed by miR-217 inhibitor (Figure 6c). The effect on the level of TLR4 protein was just the opposite (Figure 6d). These findings verified that XIST modulated TLR4 through miR-217.Finally, the impact of XIST expression on podocyte apoptosis induced by Ang II was investigated in AB8/13 cells. Figure 7a illustrated that the caspase-3 activity was decreased by Ang II but then rose with XIST interference, and was further inhibited by miR-217 inhibitor. The AB8/13 cell apoptosis condition was in accordance with the variation trend of caspase-3 activity (Figure 7b). We confirmed that inhibition of XIST reduced podocyte apoptosis induced by Ang II by regulating miR-217.	30414341	RID05792	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Urinary bladder cancer	HOXA-AS2	SMAD2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell stemness(+)	ceRNA(miR-125b)	regulation	NA	NA	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000175387	NA	285943	4087	HOXA3as	JV18-1|MADH2|MADR2	Long non-coding RNA HOXA-AS2 promotes the migration, invasion and stemness of bladder cancer via regulating miR-125b/Smad2 axis.As  shown  in  Figure  1A,  the  expression  of  HOXA-AS2  was  significantly up-regulated  in  clinical  bladder  cancer  samples  compared  with  the  normal  adjacent bladder  tissues.The  up-regulation  of HOXA-AS2   in   bladder   cancer   suggested   its   possible role   in promoting the development  and  progression  of  thiscancertype. Indeed,  as  shown  in  Table  1,  high expression of HOXA-AS2 was positively correlated with the advanced stage, invasion and lymph node metastasis of bladder cancer as well asthe expression of cancer stem cell marker OCT4 in patients. Moreover, expression of HOXA-AS2 was independent of  the  gender  and  age  ofbladder  cancer patients  and  the  size  of  the  tumor.Taken together,  these  findings  demonstrated  the  up-regulation  of  HOXA-AS2  in  bladder cancer and its positive correlation with the progression of bladder cancer.To  further  study  the  functional  role  of HOXA-AS2  in  the migration  and invasion of  bladder  cancer  cells,  knockdown  of  HOXA-AS2  was  performed  in  5637 and  T24  cells by siHOXA-AS2 transfection.  As  shown  in  Figure  2A  and  2B, significant down-regulation  of  HOXA-AS2 demonstratedthe  successful  knockdown by  siHOXA-AS2  in  both  5637  and  T24  cells.After  knockdown  of  HOXA-AS2,  the migratory ability  of  5637  and  T24  cells  was  significantly  reduced when compared with the siNC groupas determined by Transwell migration assay (Figure 2Cand 2D). In  addition,  the invasionof 5637  and  T24  cells  was also  suppressed  by ~50% after knockdown  of  HOXA-AS2when  compared  with  the  siNC  group,as  determined  by Transwell invasionassay  (Figure  2Eand  2F).  Therefore, knockdown of  HOXA-AS2 in bladder cancer suppressed the migration and invasion of cancer cells.he side population of 5637 and T24 cells was also  significantly  reducedafter  knockdown  of  HOXA-AS2  when  compared  with  the siNC   group as   determined   by   flow   cytometry   (Figure   3Cand   3D).   Hence, HOXA-AS2 knockdown was  able  to suppress the  stemness  of  bladder  cancer  cells.Importantly, dual-luciferase  reporterassay showedthat  the  luciferase  activity  of  thereporter containing HOXA-AS2-WT,   rather   than HOXA-AS2-MUT,   was   significantly decreased in T24cells transfected with the miR-125 mimic (Figure 4C),indicating the direct binding relationship between HOXA-AS2 and miR-125b.  As  shown  in  Figure 5Band  5C,  the  inhibitory  effect  of  siHOXA-AS2  on  the migration  and  invasion of bladder    cancer    cells    was    significantly    attenuated    by    miR-125b    inhibitor, demonstrating  the  involvement  of  miR-125b  down-regulation  in  the  HOXA-AS2 induced-migration  and  invasion of  bladder  cancer  cells. In  addition,  knockdown  of  HOXA-AS2  in  T24  cells  with  miR-125b knockdown  also  suppressed  cell  migration,  invasion  and  stemness  (Figure  5B-5F). Taken   together,   these   findings   demonstrated   the   involvement   of   miR-125b down-regulation in role of HOXA-AS2 inpromoting bladder cancer cells, particularly,in the migration, invasionand stemness of cancer cells.Figure 6A showed the putative binding sites between miR-125b and 3'UTR of Smad2. The dual-luciferase reporter assay showed that the luciferase activity of the reporter containing Smad2 3'UTR-WT,  rather  than Smad2 3'UTR-MUT,  was  significantly  decreased  in T24  cells  transfected  with  miR-125b  mimic(Figure  6B).	30412716	RID05793	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Multiple myeloma	LINC00461	BCL2	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-15a;miR-16)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000171791	NA	645323	596	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	Bcl-2|PPP1R50	Exosome-transmitted LINC00461 promotes multiple myeloma cell proliferation and suppresses apoptosis by modulating microRNA/BCL-2 expression.We found thatLINC00461 was expressed at a much higher level inthe plasma cells of patients with MM than in controlcells (Figure 1A). Furthermore, weanalyzed  the  correlation  between  LINC00461expression and the survival rate of patients withMM, and found that high expression of LINC00461was correlated with poor survival outcome (Figure1C).The result of MTT assays showed that knockdown ofLINC00461 significantly decreased cell viabilities of both U266 and OPM-2 cell lines (Figure 2B). More-over, we also tested the cell numbers of control cellsand LINC00461 knockdown cells at different days,and found that knockdown of LINC00461 dramati-cally suppressed MM cell proliferation (Figure 1C and1D).The above results indicatedthat knockdown of LINC00461 suppressed cell pro-liferation and colony formation capability of MM cell lines, which induced the cell apoptosis and G1cell cycle arrest.Significant inhibition was observedwhen miR-15a or miR-16 was co-transfected withthe  wild-type  LINC00461,  whereas  mutated LINC00461 luciferase activity was not obviously altered in comparison with the vector control (Figure3C and3D). Luciferase reporter assays demon-strated that miR-15a and miR-16 could significantly inhibit  luciferase  reporter  activity  of  wild-type LINC00461, which contains the potential bindingsites. These results indicated that LINC00461 is atarget of miR-15a and miR-16 in U266 and OPM-2 cell lines.The endogenous miRNAs associated with LINC00461were pulled down and detected via qPCR analysis. The results showed that both miR-15a and miR-16were significantly enriched by MS2-LINC00461compared with the empty vector (MS2) (Figure 4Dand4E), which suggested that miR-15a and miR-16could directly bind to LINC00461.Overexpression of miR-15a and miR-16 decreased the luciferase activity of psiCHECK2-BCL-2-WT in both U266 and OPM-2 cells (Figure5B and5C), whereas it had no significant effect onthe luciferase activity of psiCHECK2-BCL-2-MUTor control reporter (Figure 5B and5C). Consis-tently, ectopic expressions of miR-15a and miR-16also down-regulated the protein level of BCL-2(Figure 5D and5E). In addition, we measured the expression levels of BCL-2 in LINC00461 knock-down cells. As shown inFigure 5F, knockdown ofLINC00461 dramatically decreased the expressionof BCL-2. All these results suggested an importantrole of LINC00461 in regulating BCL-2 expressionvia miR-15a and miR-16.We isolatedMSCs from the paracarcinoma tissues of MM andnormal tissues, and then compared the expressionlevel of LINC00461 in MSCs.In this system, only exo-somes could move through the filter from the bottomchamber to the top chamber. We observed thatMSC-secreted exosomes significantly increased MMcell proliferation, which was completely abolished byLINC00461 knockdown (Figure 6E). Based onthese results, we concluded that MSC-secreted exo-somes could promote MM cell proliferation throughLINC00461 (Figure 6F).	30409700	RID05794	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	NEAT1	miR-193a-3p	negatively-F	luciferase reporter assay;RIP;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR-193a-3p. In addition, NEAT1 expression was elevated in CRC with T3+T4 stage (n = 318) as compared to those with T1+T2 stage (n = 74) or normal tissues (n = 27) (Figure -(Figure11B).We then drew the survival and recurrence curves, which showed that the CRC patients with NEAT1 high expression had shorter survival and higher tumour recurrence as compared to those with NEAT1 low expression (Figure -(Figure1D).1D). Moreover, the patients of early stage or late stage with NEAT1 high expression had the shorter survival (Figure -(Figure1E),1E), but had no difference in tumour recurrence as compared to those with NEAT low expression (Figure S1B).Then, knockdown of NEAT1 decreased cell viability in LOVO and HCT116 cell lines as compared to the sh-NC vector (Figure -(Figure2C),2C), but ectopic expression of NEAT1 displayed a proliferation promoting effect in SW480 cells (Figure -(Figure2D).2D). In addition, the number of colony formation in sh-NEAT1 transfected LOVO and HCT116 cell lines was significantly reduced as compared to empty vector (Figure -(Figure2E),2E), but NEAT1 overexpression increased the colony formation number in SW480 cell line (Figure -(Figure2F).2F). Interestingly, we also assessed the effects of NEAT1 on cell apoptosis in CRC cells by flow cytometry analysis, indicating that the index of cell apoptosis in sh-NEAT1 transfected LOVO and HCT116 cell lines was markedly increased as compared to sh-NC group (Figure S2A), but NEAT1 overexpression decreased the cell apoptosis in SW480 cell line (Figure S2B).To observe the effects of NEAT1 on CRC cell invasion, we conducted a transwell invasion assay, which showed that knockdown of NEAT1 weakened cell invasive potential in LOVO and HCT116 cell lines, but overexpression of NEAT1 promoted these effects in SW480 cell line (Figure -(Figure3A).3A).Thus, miR-107 and miR-193a-3p (miR-193a) were simultaneously identified to have the potential to bind with NEAT1 by starBase v2.0 and miRcode (Figure -(Figure4A).4A). Furthermore, miR-193a was downregulated but miR-107 was upregulated in CRC samples as compared to normal tissues (Figure -(Figure4B),4B), and NEAT1 had a negative correlation with miR-193a expression (Figure -(Figure4C1),4C1), but had no correlation with miR-107 expression (Figure -(Figure4C2)4C2) in CRC tissues. NEAT1 reduced the expression of miR-193a (Figure -(Figure4D),4D), but miR-193a had no effect on the expression of NEAT1 (Figure S3) in LOVO and HCT116 cell lines, indicated by qRT-PCRanalysis. The binding sites of miR-193a with wide type (WT) or mutant (Mut) NEAT1 are indicated in Figure -Figure4E.4E. To further confirm whether NEAT1 was a target of miR-193a, we co-transfected LOVO and HCT116 cells with WT or Mut NEAT1 reporter vector and the miR-193a mimic or miR-NC, indicating that miR-193a mimic decreased the luciferase activity of WT NEAT1 (Figure -(Figure44F).Then, we extracted the RNA and protein from the tumour tissues derived from the sh-NEAT1 and sh-NC groups, and detected the expression levels of NEAT1 and miR-193a by qRT-PCRand that of PCNA by western blot which indicated that NEAT1 expression was decreased (Figure -(Figure6E),6E), but miR-193a expression was increased (Figure -(Figure6F)6F) in sh-NEAT1 group as compared to sh-NC, and knockdown of NEAT1 downregulated the expression of PCNA in tumour tissues compared with the sh-NC group (Figure -(Figure6G).	30407674	RID05795	ceRNA or sponge	recurrence	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Pituitary cancer	H19	EIF4EBP1	negatively-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pituitary cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000187840	NA	283120	1978	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	4E-BP1|PHAS-I	Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours.We found that the H19 expression level was significantly downregulated in the prolactinomas and the other pituitary tumour subtypes compared with that in the normal pituitary glands (Figs. 1c, d). In addition, we found that there was a negative correlation between tumour volume and H19 level (Fig. 1e). These data suggest that H19 downregulation may be associated with the initiation or development of pituitary tumours.To test this idea, we stably expressed H19 in pituitary tumour GH3 cells (Fig. 2a) and found that H19 overexpression strongly inhibited GH3 cell proliferation (Fig. 2b). H19 overexpression also potently inhibited GH3 cell colony formation (Fig. 2c). However, we found that H19 overexpression in GH3 and HEK293 cells dramatically suppressed the phosphorylation of 4E-BP1, a well-characterized mTORC1 substrate, but had no effect on S6K1 phosphorylation, another well-characterized mTORC1 target (Fig. 3a, Supplementary Fig. 5).Together, these results strongly suggest that H19 can negatively regulate the mTORC1-mediated 4E-BP1 phosphorylation.Consistent with a role for 4E-BP1 in translation regulation, we found that H19 overexpression significantly inhibited protein synthesis in GH3 cells as determined by a 35S-Met uptake experiment (Fig. 3f). Taken together, these results indicate that 4E-BP1 might be the key target of H19 in regulating pituitary tumour growth by inhibiting 4E-BP1 phosphorylation and subsequent protein synthesis.To test this idea, we performed a co-immunoprecipitation assay to examine the interaction between Raptor and 4E-BP1 in GH3 and HEK293 cells. As shown in Fig. 5b, increased H19 expression attenuated Flag-4E-BP1 binding to HA-Raptor, whereas the interaction between HA-Raptor and Flag-S6K1 was not affected (Fig. 5c). Similar results were also obtained using HEK293 cells (Supplementary Fig. 10a, b). Consistently, H19 expression also affected the endogenous binding of Raptor with 4E-BP1 but not with S6K1 (Figs. 5d, e). These data suggest that the H19-mediated inhibition of 4E-BP1 phosphorylation is due to the inhibition of 4E-BP1 recruitment to mTORC1 by disrupting the Raptor and 4E-BP1 interaction. Indeed, we clearly detected exogenous H19 RNA in the immunoprecipitation of endogenous 4E-BP1 but not in S6K1, Raptor or AKT1 immunoprecipitations from GH3 cells (Fig. 5f, Supplementary Fig. 10d). In addition, H19 bound to 4E-BP1 in primary pituitary tumour cells (Supplementary Fig. 10e).Together, these data show that the TOS motif of 4E-BP1 is required for its interaction with H19 whereas the 3'-sequence between 2100 and 2200-nt of H19 is responsible for its interaction with 4E-BP1.Taken together, these results suggest that H19 effectively inhibits primary prolactinoma progression by inhibiting 4E-BP1 phosphorylation and that increasing H19 expression may serve as a potential therapeutic strategy for pituitary tumours.To compare the effect between CAB and H19 overexpression on pituitary tumour growth, we performed xenograft experiments and found that H19 overexpression was more potent in suppressing tumour growth than CAB (Figs. 7a-c). Interestingly, we found that H19 overexpression led to pronounced inhibition of 4E-BP1 phosphorylation as expected, but CAB treatment had less effect on 4E-BP phosphorylation in the xenograft tumours of GH3 cells (Fig. 7d). Simultaneously, in vitro experiments showed that H19 overexpression significantly suppressed GH3 cell proliferation compared with CAB treatment (Fig. 7e). Interestingly, CAB induced upregulation of H19 expression in a dose- and time-dependent manner (Figs. 7f, g).	30397197	RID05796	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Urinary bladder cancer	LNC-LBCS	HNRNPK	negaticely-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	self-renewal(+);chemoresistance(+);prognosis	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228412	GRCh38_6:19323428-19839080	ENSG00000165119	NA	100506885	3190	LBCS	CSBP|HNRPK|TUNP	Long Noncoding RNA LBCS Inhibits Self-Renewal and Chemoresistance of Bladder Cancer Stem Cells through Epigenetic Silencing of SOX2.Finally, we identified a novel lncRNA (ENSG00000228412), termed lnc-LBCS, that was significantly downregulated in BCSCs and affected sphere formation (Fig. 1E).Remarkably, lnc-LBCS was downregulated in bladder cancer tissues compared with normal tissues, and in high-grade compared with lower-grade tumors examined in a 120-case Cohort 1 (Fig. 1F and G).Multivariate analyses revealed that high lnc-LBCS expression was independent prognostic factor for OS and DFS in bladder cancer patients (Supplementary Tables S5 and S6). These data demonstrate that lnc-LBCS associates with cell differentiation of bladder cancer and may as a marker of good prognosis in bladder cancer.Serial sphere formation assays showed that lnc-LBCS overexpression inhibited long-term self-renewal over four generations of sphere formation (Supplementary Fig. S4B). Conversely, lnc-LBCS depletion significantly enhanced sphere formation in UM-UC-3 and 5637 cells (Fig. 2D; Supplementary Fig. S4C and S4D).To validate the results of lnc-LBCS knockdown, we also established lnc-LBCS KO cells using a CRISPR/Cas9 approach (Supplementary Fig. S6A and S6B). Lnc-LBCS KO cells displayed enhanced self-renewal capacity and tumor initiation of BCSCs in vitro and in vivo (Supplementary Fig. S6C-S6H), which agreed with the results of lnc-LBCS knockdown. Collectively, our results demonstrate that lnc-LBCS inhibits the self-renewal, tumor initiation, and propagation of BCSCs.Interestingly, after treated with GC chemotherapy, the relative tumor growth, the size, and weight in the lnc-LBCS overexpression group were significantly decreased compared with the control group (Fig. 3E-G; Supplementary Fig. S8A-S8C). Moreover, the tumors derived from the lnc-LBCS overexpression group exhibited a higher proportion of TUNEL-positive cells and lower Ki67 expression compared with the control group when treated with GC chemotherapy (Fig. 3H; Supplementary Fig. S7D and S7E; Supplementary Fig. S8G and S8I). Conversely, lnc-LBCS depletion significantly enhanced tumor growth and reduced apoptosis when treated with GC chemotherapy (Fig. 3I-L; Supplementary Fig. S7D and S7E; Supplementary Fig. S8D-S8F, S8H, and S8I). Consistent with the lnc-LBCS knockdown findings above, lnc-LBCS KO promoted the chemoresistance of BCSCs in vivo (Supplementary Fig. S9E-S9J). Overall, these data strongly indicate that lnc-LBCS suppresses chemoresistance of BCSCs in vitro and in vivo.To further identify the molecular mechanism and binding partners of lnc-LBCS in BCSCs, we performed RNA pull-down with biotin-labeled lnc-LBCS. Two overtly differential bands appeared by silver staining and were identified as hnRNPK and EZH2 by mass spectrometry (Fig. 4A; Supplementary Fig. S10A and S10B). We confirmed the special interaction of lnc-LBCS, hnRNPK, and EZH2 using western blot (Fig. 4B). We also verified this result using RIP assay and found that lnc-LBCS were enriched in both hnRNPK and EZH2 precipitates (Fig. 4C).Interestingly, hnRNPK and EZH2 interactions were observed significantly in lysates incubated with the lnc-LBCS RNA, but not the mock group. However, these interactions were abolished by treatment of lysates with ribonuclease (RNase; Fig. 4G), suggesting that lnc-LBCS RNA was essential to the formation of hnRNPK-EZH2 complex. Taken together, these results indicate that lnc-LBCS directly binds to hnRNPK and EZH2, and serves as a scaffold to induce the formation of this complex.To further verify the correlation between lnc-LBCS and SOX2, we detected the expression of SOX2 in two independent cohorts of bladder cancer specimens by qRT-PCRand IHC. Notably, the mRNA and the protein levels of SOX2 correlated negatively with the lnc-LBCS level (Fig. 5D-F, P < 0.001, P < 0.001, respectively). In summary, these data indicated that lnc-LBCS inhibited SOX2 expression.Fluorescence resonance energy transfer (FRET) was performed using in vitro synthesized predicted TFOs of lnc-LBCS and TTSs of the SOX2 promoter. Upon excitation at 460 nm, the emission at 580 nm increased, whereas the signal at 520 nm decreased in the lnc-LBCS (246-266 nt)/SOX2 TTS group compared with that of the control RNA/SOX2 TTS (Fig. 5I). However, lnc-LBCS (mut)/SOX2 TTS and lnc-LBCS (246-266 nt)/SOX2 TTS (mut) did not influence the signals at 520 and 580 nm (Fig. 5I; Supplementary Fig. S11G). Taken together, these data indicate that lnc-LBCS 246-266 nt fragment directly forms triplexes with the promoter sequences of SOX2. Similarly, lnc-LBCS overexpression attenuated the luciferase activity, but not when including the mutated region (Fig. 5L). Furthermore, knockdown of hnRNPK or EZH2 rescued the depression effect of lnc-LBCS on chemoresistance and SOX2 in bladder cancer cells (Fig. 5M and N; Supplementary Fig. S12). Overall, these data indicate that lnc-LBCS inhibits SOX2 transcription by directly guiding hnRNPK-EZH2 complex to mediate H3K27me3 of the SOX2 promoter.SOX2 upregulation significantly promoted BCSCs'-sphere formation and increased the population of ALDH+ cells in vitro, and enhanced tumor initiation in vivo. Moreover, SOX2 overexpression also rescued the inhibitory effects of lnc-LBCS on the self-renewal of BCSCs in vitro and in vivo (Fig. 6A-D; Supplementary Fig. S13C-S13E). Notably, SOX2 overexpression markedly enhanced the chemoresistance of BCSCs to gemcitabine and cisplatin in vitro and in vivo. In addition, SOX2 overexpression also rescued the repressive roles of lnc-LBCS on the chemoresistance of BCSCs (Fig. 6E-I; Supplementary Fig. S14A-S14G). In summary, these findings indicate that SOX2 is required for self-renewal and chemoresistance of BCSCs and rescues the suppressive effect of lnc-LBCS.Interestingly, high expression levels of SOX2 were found in bladder cancer samples and high-grade samples, indicating the potential role of SOX2 in bladder cancer initiation and stemness (Fig. 6J and K). Moreover, clinical correlation analysis revealed that SOX2 expression was strongly correlated with pathologic grade and stage (P = 0.001 and P < 0.001, respectively; Supplementary Table S7).Furthermore, the Kaplan-Meier survival analysis found that patients with high SOX2 expression had shorter OS and DFS in Cohort 1 and in the TCGA cohort (Fig. 6N-Q). Besides its role in stemness maintenance and development regulation, we revealed the critical role of SOX2 in bladder cancer initiation, progress, and prognosis prediction.	30397178	RID05797	interact with protein	chemoresistance,prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	LNC-LBCS	EZH2	negaticely-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	self-renewal(+);chemoresistance(+);prognosis	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228412	GRCh38_6:19323428-19839080	ENSG00000106462	NA	100506885	2146	LBCS	ENX-1|EZH1|KMT6|KMT6A	Long Noncoding RNA LBCS Inhibits Self-Renewal and Chemoresistance of Bladder Cancer Stem Cells through Epigenetic Silencing of SOX2.Finally, we identified a novel lncRNA (ENSG00000228412), termed lnc-LBCS, that was significantly downregulated in BCSCs and affected sphere formation (Fig. 1E).Remarkably, lnc-LBCS was downregulated in bladder cancer tissues compared with normal tissues, and in high-grade compared with lower-grade tumors examined in a 120-case Cohort 1 (Fig. 1F and G).Multivariate analyses revealed that high lnc-LBCS expression was independent prognostic factor for OS and DFS in bladder cancer patients (Supplementary Tables S5 and S6). These data demonstrate that lnc-LBCS associates with cell differentiation of bladder cancer and may as a marker of good prognosis in bladder cancer.Serial sphere formation assays showed that lnc-LBCS overexpression inhibited long-term self-renewal over four generations of sphere formation (Supplementary Fig. S4B). Conversely, lnc-LBCS depletion significantly enhanced sphere formation in UM-UC-3 and 5637 cells (Fig. 2D; Supplementary Fig. S4C and S4D).To validate the results of lnc-LBCS knockdown, we also established lnc-LBCS KO cells using a CRISPR/Cas9 approach (Supplementary Fig. S6A and S6B). Lnc-LBCS KO cells displayed enhanced self-renewal capacity and tumor initiation of BCSCs in vitro and in vivo (Supplementary Fig. S6C-S6H), which agreed with the results of lnc-LBCS knockdown. Collectively, our results demonstrate that lnc-LBCS inhibits the self-renewal, tumor initiation, and propagation of BCSCs.Interestingly, after treated with GC chemotherapy, the relative tumor growth, the size, and weight in the lnc-LBCS overexpression group were significantly decreased compared with the control group (Fig. 3E-G; Supplementary Fig. S8A-S8C). Moreover, the tumors derived from the lnc-LBCS overexpression group exhibited a higher proportion of TUNEL-positive cells and lower Ki67 expression compared with the control group when treated with GC chemotherapy (Fig. 3H; Supplementary Fig. S7D and S7E; Supplementary Fig. S8G and S8I). Conversely, lnc-LBCS depletion significantly enhanced tumor growth and reduced apoptosis when treated with GC chemotherapy (Fig. 3I-L; Supplementary Fig. S7D and S7E; Supplementary Fig. S8D-S8F, S8H, and S8I). Consistent with the lnc-LBCS knockdown findings above, lnc-LBCS KO promoted the chemoresistance of BCSCs in vivo (Supplementary Fig. S9E-S9J). Overall, these data strongly indicate that lnc-LBCS suppresses chemoresistance of BCSCs in vitro and in vivo.To further identify the molecular mechanism and binding partners of lnc-LBCS in BCSCs, we performed RNA pull-down with biotin-labeled lnc-LBCS. Two overtly differential bands appeared by silver staining and were identified as hnRNPK and EZH2 by mass spectrometry (Fig. 4A; Supplementary Fig. S10A and S10B). We confirmed the special interaction of lnc-LBCS, hnRNPK, and EZH2 using western blot (Fig. 4B). We also verified this result using RIP assay and found that lnc-LBCS were enriched in both hnRNPK and EZH2 precipitates (Fig. 4C).Interestingly, hnRNPK and EZH2 interactions were observed significantly in lysates incubated with the lnc-LBCS RNA, but not the mock group. However, these interactions were abolished by treatment of lysates with ribonuclease (RNase; Fig. 4G), suggesting that lnc-LBCS RNA was essential to the formation of hnRNPK-EZH2 complex. Taken together, these results indicate that lnc-LBCS directly binds to hnRNPK and EZH2, and serves as a scaffold to induce the formation of this complex.To further verify the correlation between lnc-LBCS and SOX2, we detected the expression of SOX2 in two independent cohorts of bladder cancer specimens by qRT-PCRand IHC. Notably, the mRNA and the protein levels of SOX2 correlated negatively with the lnc-LBCS level (Fig. 5D-F, P < 0.001, P < 0.001, respectively). In summary, these data indicated that lnc-LBCS inhibited SOX2 expression.Fluorescence resonance energy transfer (FRET) was performed using in vitro synthesized predicted TFOs of lnc-LBCS and TTSs of the SOX2 promoter. Upon excitation at 460 nm, the emission at 580 nm increased, whereas the signal at 520 nm decreased in the lnc-LBCS (246-266 nt)/SOX2 TTS group compared with that of the control RNA/SOX2 TTS (Fig. 5I). However, lnc-LBCS (mut)/SOX2 TTS and lnc-LBCS (246-266 nt)/SOX2 TTS (mut) did not influence the signals at 520 and 580 nm (Fig. 5I; Supplementary Fig. S11G). Taken together, these data indicate that lnc-LBCS 246-266 nt fragment directly forms triplexes with the promoter sequences of SOX2. Similarly, lnc-LBCS overexpression attenuated the luciferase activity, but not when including the mutated region (Fig. 5L). Furthermore, knockdown of hnRNPK or EZH2 rescued the depression effect of lnc-LBCS on chemoresistance and SOX2 in bladder cancer cells (Fig. 5M and N; Supplementary Fig. S12). Overall, these data indicate that lnc-LBCS inhibits SOX2 transcription by directly guiding hnRNPK-EZH2 complex to mediate H3K27me3 of the SOX2 promoter.SOX2 upregulation significantly promoted BCSCs'-sphere formation and increased the population of ALDH+ cells in vitro, and enhanced tumor initiation in vivo. Moreover, SOX2 overexpression also rescued the inhibitory effects of lnc-LBCS on the self-renewal of BCSCs in vitro and in vivo (Fig. 6A-D; Supplementary Fig. S13C-S13E). Notably, SOX2 overexpression markedly enhanced the chemoresistance of BCSCs to gemcitabine and cisplatin in vitro and in vivo. In addition, SOX2 overexpression also rescued the repressive roles of lnc-LBCS on the chemoresistance of BCSCs (Fig. 6E-I; Supplementary Fig. S14A-S14G). In summary, these findings indicate that SOX2 is required for self-renewal and chemoresistance of BCSCs and rescues the suppressive effect of lnc-LBCS.Interestingly, high expression levels of SOX2 were found in bladder cancer samples and high-grade samples, indicating the potential role of SOX2 in bladder cancer initiation and stemness (Fig. 6J and K). Moreover, clinical correlation analysis revealed that SOX2 expression was strongly correlated with pathologic grade and stage (P = 0.001 and P < 0.001, respectively; Supplementary Table S7).Furthermore, the Kaplan-Meier survival analysis found that patients with high SOX2 expression had shorter OS and DFS in Cohort 1 and in the TCGA cohort (Fig. 6N-Q). Besides its role in stemness maintenance and development regulation, we revealed the critical role of SOX2 in bladder cancer initiation, progress, and prognosis prediction.	30397178	RID05798	interact with protein	chemoresistance,prognosis		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Urinary bladder cancer	LNC-LBCS	SOX2	negaticely-E	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	self-renewal(+);chemoresistance(+);prognosis	DNA methylation	regulation	NA	Gemcitabine;Cisplatin	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000228412	GRCh38_6:19323428-19839080	ENSG00000181449	NA	100506885	6657	LBCS	NA	Long Noncoding RNA LBCS Inhibits Self-Renewal and Chemoresistance of Bladder Cancer Stem Cells through Epigenetic Silencing of SOX2.Finally, we identified a novel lncRNA (ENSG00000228412), termed lnc-LBCS, that was significantly downregulated in BCSCs and affected sphere formation (Fig. 1E).Remarkably, lnc-LBCS was downregulated in bladder cancer tissues compared with normal tissues, and in high-grade compared with lower-grade tumors examined in a 120-case Cohort 1 (Fig. 1F and G).Multivariate analyses revealed that high lnc-LBCS expression was independent prognostic factor for OS and DFS in bladder cancer patients (Supplementary Tables S5 and S6). These data demonstrate that lnc-LBCS associates with cell differentiation of bladder cancer and may as a marker of good prognosis in bladder cancer.Serial sphere formation assays showed that lnc-LBCS overexpression inhibited long-term self-renewal over four generations of sphere formation (Supplementary Fig. S4B). Conversely, lnc-LBCS depletion significantly enhanced sphere formation in UM-UC-3 and 5637 cells (Fig. 2D; Supplementary Fig. S4C and S4D).To validate the results of lnc-LBCS knockdown, we also established lnc-LBCS KO cells using a CRISPR/Cas9 approach (Supplementary Fig. S6A and S6B). Lnc-LBCS KO cells displayed enhanced self-renewal capacity and tumor initiation of BCSCs in vitro and in vivo (Supplementary Fig. S6C-S6H), which agreed with the results of lnc-LBCS knockdown. Collectively, our results demonstrate that lnc-LBCS inhibits the self-renewal, tumor initiation, and propagation of BCSCs.Interestingly, after treated with GC chemotherapy, the relative tumor growth, the size, and weight in the lnc-LBCS overexpression group were significantly decreased compared with the control group (Fig. 3E-G; Supplementary Fig. S8A-S8C). Moreover, the tumors derived from the lnc-LBCS overexpression group exhibited a higher proportion of TUNEL-positive cells and lower Ki67 expression compared with the control group when treated with GC chemotherapy (Fig. 3H; Supplementary Fig. S7D and S7E; Supplementary Fig. S8G and S8I). Conversely, lnc-LBCS depletion significantly enhanced tumor growth and reduced apoptosis when treated with GC chemotherapy (Fig. 3I-L; Supplementary Fig. S7D and S7E; Supplementary Fig. S8D-S8F, S8H, and S8I). Consistent with the lnc-LBCS knockdown findings above, lnc-LBCS KO promoted the chemoresistance of BCSCs in vivo (Supplementary Fig. S9E-S9J). Overall, these data strongly indicate that lnc-LBCS suppresses chemoresistance of BCSCs in vitro and in vivo.To further identify the molecular mechanism and binding partners of lnc-LBCS in BCSCs, we performed RNA pull-down with biotin-labeled lnc-LBCS. Two overtly differential bands appeared by silver staining and were identified as hnRNPK and EZH2 by mass spectrometry (Fig. 4A; Supplementary Fig. S10A and S10B). We confirmed the special interaction of lnc-LBCS, hnRNPK, and EZH2 using western blot (Fig. 4B). We also verified this result using RIP assay and found that lnc-LBCS were enriched in both hnRNPK and EZH2 precipitates (Fig. 4C).Interestingly, hnRNPK and EZH2 interactions were observed significantly in lysates incubated with the lnc-LBCS RNA, but not the mock group. However, these interactions were abolished by treatment of lysates with ribonuclease (RNase; Fig. 4G), suggesting that lnc-LBCS RNA was essential to the formation of hnRNPK-EZH2 complex. Taken together, these results indicate that lnc-LBCS directly binds to hnRNPK and EZH2, and serves as a scaffold to induce the formation of this complex.To further verify the correlation between lnc-LBCS and SOX2, we detected the expression of SOX2 in two independent cohorts of bladder cancer specimens by qRT-PCRand IHC. Notably, the mRNA and the protein levels of SOX2 correlated negatively with the lnc-LBCS level (Fig. 5D-F, P < 0.001, P < 0.001, respectively). In summary, these data indicated that lnc-LBCS inhibited SOX2 expression.Fluorescence resonance energy transfer (FRET) was performed using in vitro synthesized predicted TFOs of lnc-LBCS and TTSs of the SOX2 promoter. Upon excitation at 460 nm, the emission at 580 nm increased, whereas the signal at 520 nm decreased in the lnc-LBCS (246-266 nt)/SOX2 TTS group compared with that of the control RNA/SOX2 TTS (Fig. 5I). However, lnc-LBCS (mut)/SOX2 TTS and lnc-LBCS (246-266 nt)/SOX2 TTS (mut) did not influence the signals at 520 and 580 nm (Fig. 5I; Supplementary Fig. S11G). Taken together, these data indicate that lnc-LBCS 246-266 nt fragment directly forms triplexes with the promoter sequences of SOX2. Similarly, lnc-LBCS overexpression attenuated the luciferase activity, but not when including the mutated region (Fig. 5L). Furthermore, knockdown of hnRNPK or EZH2 rescued the depression effect of lnc-LBCS on chemoresistance and SOX2 in bladder cancer cells (Fig. 5M and N; Supplementary Fig. S12). Overall, these data indicate that lnc-LBCS inhibits SOX2 transcription by directly guiding hnRNPK-EZH2 complex to mediate H3K27me3 of the SOX2 promoter.SOX2 upregulation significantly promoted BCSCs'-sphere formation and increased the population of ALDH+ cells in vitro, and enhanced tumor initiation in vivo. Moreover, SOX2 overexpression also rescued the inhibitory effects of lnc-LBCS on the self-renewal of BCSCs in vitro and in vivo (Fig. 6A-D; Supplementary Fig. S13C-S13E). Notably, SOX2 overexpression markedly enhanced the chemoresistance of BCSCs to gemcitabine and cisplatin in vitro and in vivo. In addition, SOX2 overexpression also rescued the repressive roles of lnc-LBCS on the chemoresistance of BCSCs (Fig. 6E-I; Supplementary Fig. S14A-S14G). In summary, these findings indicate that SOX2 is required for self-renewal and chemoresistance of BCSCs and rescues the suppressive effect of lnc-LBCS.Interestingly, high expression levels of SOX2 were found in bladder cancer samples and high-grade samples, indicating the potential role of SOX2 in bladder cancer initiation and stemness (Fig. 6J and K). Moreover, clinical correlation analysis revealed that SOX2 expression was strongly correlated with pathologic grade and stage (P = 0.001 and P < 0.001, respectively; Supplementary Table S7).Furthermore, the Kaplan-Meier survival analysis found that patients with high SOX2 expression had shorter OS and DFS in Cohort 1 and in the TCGA cohort (Fig. 6N-Q). Besides its role in stemness maintenance and development regulation, we revealed the critical role of SOX2 in bladder cancer initiation, progress, and prognosis prediction.	30397178	RID05799	epigenetic regulation	chemoresistance,prognosis		UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	ARSR	STAT3	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000168610	NA	NA	6774	NA	APRF	lncARSR promotes liver cancer stem cells expansion via STAT3 pathway.To determine  the  expression  of  lncARSR  in liver  CSCs, we  enriched CSCs by  flow  cytometry  sorting  or  sphere formation. As  expected,lncARSR  levelswere upregulated in sorted EpCAM+ or CD133+ primary HCC cells(Fig. 1A&B).Considering the close association of liver CSCs with HCC chemoresistance, we  investigated the  expression  of lncARSRin  liver  CSCs.Cisplatin-resistant  HCC  xenografts were  established  as  described. In  comparison  with  control  tumors,  lncARSR  expressionwas markedly increased  in  the  cisplatin-resistantHCC  residual,  indicating  that  lncARSR  expression was associated  with  chemoresistance  (Fig.  1D).Flow-cytometric  analysis  revealed  adecreased proportion  of  liver  CSCs  in lncARSR siRNA transfected hepatoma  cells(Fig.  2B&C).Consistently, SMMC7721 si-lncARSRand  HCCLM3 si-lncARSR  cells formed small  and  fewer spheroids  than  controlcells  (Fig.  2D).Consistently, interfenrence lncARSR expression in HCC cells downregulated the expression of stemness-associated transcription factor (Fig. 3A&B)and liver CSC markers in hepatoma cells (Fig. 3C&D), which further supported that lncARSRcould promoteliver CSCs expansion.In  this  study,  our  data  demonstrated  that  the  phosphorylation  of  the  STAT3 molecule   was   evidently inactivated   in   both   the   SMMC7721   si-lncARSR   and   HCCLM3 si-lncARSR  cells(Fig. 4A). STAT3  reporter  assay  further  confirmed  the  effects  of  lncARSR  on   activation  (Fig. 4B).To further  confirm the  role  of STAT3 in lncARSR-mediated expansion  of liver  CSCs,the  special STAT3 inhibitor SI3-201 was  used(25).  As  expected,SI3-201diminished the  difference  inliver  CSC  proportion  between lncARSR knockdown hepatoma cells and control cells (Fig. 4C). Consistently,SI3-201 entirely depleted the discrepancy of self-renewal capacity between lncARSR knockdown hepatoma cells and control cells(Fig. 4D).Collectively, these data suggest distinct regulation of STAT3 by lncARSR in liver CSCs. As expected, we found that  lncARSR  expression  was upregulated  in  cisplatin-resistant  or  sorafenib-resistant  hepatoma cells (Fig. 5A&B);suggesting lncARSR was involved in drug resistance. Furthermore, lncARSR knockdown dramatically  increased  the  sensitivity  of  HCC  cells  to  the  same  dosages  of  sorafenib or  cisplatin  (Fig.5C&D). Taken  together,  these results  demonstrated  that  drug  sensitivity  of  HCC  to  sorafenib  and cisplatin  was  significantly increased  when  lncARSR  was interference,  suggesting  a  possible  role  of  lncARSR  in  the treatment of HCC drug resistance.	30391438	RID05800	expression association	chemoresistance		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Papillary thyroid carcinoma	H19	ER	positively-E	luciferase reporter assay;IHC;bioinformatics	upregulation	RT-qPCR	NA	NA	cell survival(+)	ceRNA(miR-3126-5p)	regulation	RNA-RNA	Aspirin	CSC	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Estrogen receptor beta upregulated by lncRNA-H19 to promote cancer stem-like properties in papillary thyroid carcinoma. Moreover, the effect of ERbeta on tumorigenesis was further examined in nude mice by injecting with control K-1 cells (NTC; non-targeting control), shERbeta-1 K-1 cells (shERbeta-1) and shERbeta-2 K-1 cells (shERbeta-2). As shown in Fig. 1h, the tumor volumes in shERbeta-1 and shERbeta-2 groups were apparently smaller than NTC group, indicating that ERbeta is critical for PTCSC maintenance.The results showed that H19 was the highest expressing lncRNA in spheroids as well as the highest differentially expressed lncRNA when compared with monolayer cells (Fig. 2a, b). Consistently, H19 expression was much higher in spheroid cells than in monolayer cells through FISH assay (Fig. 2c). Moreover, H19 expression level was significantly higher in PTC tissue specimens compared with the adjacent tissue specimens (Fig. 2d, e). Furthermore, the Kaplan-Meier survival analysis demonstrated that high H19 levels were a strong indicator for poor overall survival of thyroid cancers in TCGA database (Fig. 2f), suggesting a remarkably unfavorable prognosis and shorter lifespan. In summary, H19 is highly expressed in PTCSCs and PTC tissue specimens.Consistently, H19 RNA expression was also elevated by E2 treatment (50-nM) in a time-dependent manner in both TPC-1 cells and K-1 cells (Fig. 3b). Furthermore, E2 promoted H19 pre-RNA expression (Fig. 3c) and increased ESR2 but not ESR1 mRNA expression (Supplementary Figure 2d) in both TPC-1 and K-1 cells, which prompted that E2 regulates H19 transcription through ERbeta. Indeed, silencing of ERbeta significantly decreased both pre-H19 and H19 RNA levels (Fig. 3d).E2 treatment promoted H19-WT luciferase activity, while it had no effects on H19-Del and H19-Mut activities (Fig. 3e). Conversely, depletion of ERbeta dramatically attenuated H19-WT luciferase activity, whereas it caused no changes in H19-Del and H19-Mut activities (Supplementary Figure 2f and Fig. 3f). These data show that E2 promotes stem-like traits and increases H19 transcription in PTC cells.To confirm whether H19 acting as a competitive endogenous sponge interacts with miRNAs to release ERbeta expression, we searched for miRNAs that interact with H19 and also target 3'UTR region of ESR2 by bioinformatic tools. The mimics of six identified miRNAs (Supplementary Figure 3c), including miR-4268, miR-3198, miR-876-3p, miR-1976, miR-3126-5p and miR-127-5p, were transfected into K-1 cells. The results showed that the miR-3126-5p mimetic significantly decreased ERbeta protein expression (Supplementary Figure 3d), while miR-3126-5p inhibitor remarkably increased ERbeta protein level (Supplementary Figure 3e).To further examine the ERbeta expression in clinical samples, we performed immunohistochemistry (IHC) staining to measure ERbeta in PTC tissue specimens and the corresponding adjacent tissues. ERbeta exhibited higher expression in tumor tissue specimens compared to the corresponding adjacent tissues (Fig. 5a). Next, we assessed the expression of ERbeta using western blot assay in another six pairs of tumor tissue specimens, and similar ERbeta expression patterns were also observed (Fig. 5b). These results demonstrate that ERbeta is upregulated in PTC tissue specimens.Previous studies have demonstrated that aspirin (ASA) possesses antineoplastic actions against a wide range of solid tumors. Upon ASA treatment, H19 expression was dramatically decreased in both dose-dependent (Fig. 6a) and time-dependent (Fig. 6b) manners. ASA also resulted in a decrease in the protein expression level of ERbeta in a time-dependent manner (Fig. 6c). Moreover, H19-overexpressing plasmid in parallel with empty vector (EV) was transiently transfected into K-1 cells under ASA treatment. The expression of ERbeta was rescued by overexpression of H19 in the presence of ASA (Fig. 6d and Supplementary Figure 4a). Notably, E2-enhanced sphere formation abilities were substantially attenuated by ASA in K-1 cells (Fig. 6e). In conclusion, these results reveal that H19 mediates E2-induced stem-like properties through upregulating ERbeta expression in PTC cells, which can be inhibited by ASA (Fig. 6f).	30389909	RID05801	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	
Breast cancer	MEG3	miR-21	negatively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);glycolysis(+);apoptosis process(-);PI3K/AKT signaling pathway(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000199004	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	MEG3 overexpression inhibits the tumorigenesis of breast cancer by downregulating miR-21 through the PI3K/Akt pathway.The  expressions  of  MEG3  and  miR-21  in  20  paired  tissue  samples  including  breast  cancer  tissues  and  corresponding  adjacent  normal  tissues  were  initially  detected  by qRT-PCRGain-of-function  approaches  were  performed  in  MCF-7  and  MDA-MB-231  cells  by  introducing  with  MEG3  or  pcDNA.  qRT-PCR which  checked  the  transfection  efficiency  demonstrated  that  MEG3-transfected  MCF-7  and  MDA-MB-231  cells  showed a  marked  increase  of  MEG3  expression  when  compared  to  pcDNA-treated  cells  (Fig.  2A).  MTT  assay  uncovered  that  restoration  of  MEG3  expression  hindered  cell  proliferation  over  time  in  MCF-7  and  MDA-MB-231  cells  with  respect  to  pcDNA  group  (Fig.  2B). As shown in Fig. 2D and 2E,  forced  expression  of  MEG3  distinctly  reduced  the  glucose  consumption  and  lactate  production in both MCF-7 and MDA-MB-231 cells as compared with pcDNA group,  suggesting that MEG3 overexpression suppressed glycolysis in breast cancer cells. In  addition, flow cytometry analysis revealed that apoptosis was remarkably promoted in  MEG3-overexpressing MCF-7 and MDA-MB-231 cells with respect to pcDNA group  (Fig.  2F).  These  results  demonstrated  that  overexpression  of  MEG3  inhibited  the  tumorigenesis of breast cancer cells by blocking cell proliferation and glycolysis, and  inducing apoptosis.To confirm  the  interaction  between  MEG3  and  miR-21,  the  full-length  of  MEG3  harboring  the  wild-type  or  mutated  miR-21  binding  sites  was  cloned  into  pmirGlO  dual-luciferase  miRNA  Target  Expression  Vector,  as  shown  in  Fig.  3A.  Luciferase  reporter  assay  showed a significant reduction in luciferase activities after cotransfection with miR-21  mimics  with  MEG3  (WT)  in  MCF-7  cells,  but  not  the  MEG3  (MUT)  (Fig.  3B).RIP  assay  was  applied  in  MCF-7  cells  using  an  anti-Ago2  antibody and  we  found  that  MEG3  and  miR-21  were  both  enriched  in  Ago2  pellets  compared with  IgG  immunoprecipitates  (Fig.  3C).  Spearman  correlation  analysis  suggested a  negative  correlation  between  MEG3  and  miR-21  expression  in  breast  cancer  tissues  (Fig.  3D).Collectively, these results revealed that  MEG3 functioned as an endogenous sponge by directly binding to miR-21. qRT-PCR analysis  demonstrated  that  MEG3  expression  was  significantly  increased  in  MEG3-transfected  MCF-7  cells  while  miR-21  introduction  remarkably  attenuated  the  increase  of  MEG3  expression  (Fig.  4A).Together,  we  concluded  that  overexpression  of MEG3 inhibited  the tumorigenesis  of  breast cancer cells by sponging miR-21.Western   blot   analysis   exhibited   that   miR-21 overexpression   significantly  enhanced  the  protein  levels  of  p-Akt  and  PI3K  in  MCF-7  and  MDA-MB-231  cells,  while  ectopic  expression  of  MEG3  abolished  the  increase  of  protein  levels  of  p-Akt  and  PI3K  mediated  by  miR-21  overexpression  (Fig.  5).  Taken  together,  these  results  demonstrated that MEG3 overexpression reversed miR-21-mediated activation of the PI3K/Akt pathway in breast cancer cells.The results  showed  that  MEG3  overexpression  led  to  a  marked  decrease  of  tumor  size  (Fig.  6A)  and  tumor  growth  (Fig.  6B)  in  vivo compared  with  lenti-NC  group,  while  forced  expression  of  miR-21  significantly reverted the effects of MEG3 on tumor size and tumor growth.Therefore, these results demonstrated that overexpression of  MEG3 inhibited tumor growth in vivo in breast cancer by downregulating miR-21.	30389444	RID05802	ceRNA or sponge	NA		
Renal cell carcinoma	TUG1	miR-196a	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Long noncoding RNA TUG1 promotes renal cell carcinoma cell proliferation, migration and invasion by downregulating microRNA-196a.The results demonstrated that the expression level of lncRNA-TUG1 was significantly increased in RCC cells compared with HK-2 cells (Fig. 1).The results demonstrated that lncRNA-TUG1-overexpressing cells exhibited improved cell viability and a lower apoptosis rate, while lncRNA-TUG1-downregulated cells exhibited a poorer proliferative ability and a higher apoptosis rate, compared with the two control groups (Fig. 2B-D). Migration and invasion assays were performed to evaluate the impact of lncRNA-TUG1 on RCC migration and invasion. From these assays it was revealed that the migratory and invasive cell numbers were significantly increased in the lenti-lncRNA-TUG1 group, while significantly decreased in the lenti-shTUG1 group compared with the control (Fig. 2E-H). These results suggested that lncRNA-TUG1 may serve a tumor-promoting role in the development of RCC.To determine whether the low expression level of miR-196a was relevant to the overexpressed lncRNA-TUG1 in RCC cell lines, the present study determined the miR-196a expression level following transfection. The results demonstrated that the expression level of miR-196a significantly increased following transfection with miR-196a or lenti-shTUG1 compared with the controls, while it significantly decreased following transfection with miR-inhibitor or lenti-lncRNA-TUG1 (Fig. 3B). From these results, it was further hypothesized that miR-196a may be involved in the lncRNA-TUG1 tumor-promoting function in RCC via a binding interaction. Therefore, a luciferase reporter assay was performed to verify this hypothesis, which demonstrated that luciferase activity was significantly decreased following co-transfection of miR-196a mimics and wild-type lncRNA-TUG1 (Fig. 3C). The results of the present study indicated that there may be a binding site between lncRNA-TUG1 and miR-196a, through which miR-196a may serve an important role in the biological function of lncRNA-TUG1 in RCC.Cell viability was determined using an MTT assay following transfection of RCC 786-O cells with lncRNA-TUG1 or shTUG1, or co-transfection with lncRNA-TUG1 and miR-196a, shTUG1 and miR-inhibitor. Consistent with the above results, it was observed that cells transfected with lncRNA-TUG1 or shTUG1 had markedly better or poorer cell viability, respectively, compared with the controls. Furthermore, this decrease or increase in cell viability was able to be reversed by co-transfection with miR-inhibitor or miR-196a (Fig. 4). In general, these results confirmed the above findings, which revealed that lncRNA-TUG1 promoted RCC cell proliferation by suppressing miR-196a.In order to elucidate the molecular mechanisms underlying the tumor-promoting function of lncRNA-TUG1 in RCC, western blot was used to detect relevant protein expression levels, including JNK, p-ERK and p-AKT, in RCC 786-O cells. It was observed that the expression of p-AKT was upregulated when cells were transfected with lenti-lncRNA-TUG1, which was reversed following co-transfection with miR-196. By contrast, the expression of p-JNK and p-ERK exhibited a corresponding upregulation when RCC 786-O cells were transfected with lenti-shTUG1, which was reversed by co-transfection with miR-inhibitor (Fig. 5). These data indicated that lncRNA-TUG1 may regulate proliferation-associated proteins by suppressing miR-196a, thereby promoting tumorigenesis in RCC.	30387842	RID05803	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Renal cell carcinoma	TUG1	p-JNK	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Long noncoding RNA TUG1 promotes renal cell carcinoma cell proliferation, migration and invasion by downregulating microRNA-196a.The results demonstrated that the expression level of lncRNA-TUG1 was significantly increased in RCC cells compared with HK-2 cells (Fig. 1).The results demonstrated that lncRNA-TUG1-overexpressing cells exhibited improved cell viability and a lower apoptosis rate, while lncRNA-TUG1-downregulated cells exhibited a poorer proliferative ability and a higher apoptosis rate, compared with the two control groups (Fig. 2B-D). Migration and invasion assays were performed to evaluate the impact of lncRNA-TUG1 on RCC migration and invasion. From these assays it was revealed that the migratory and invasive cell numbers were significantly increased in the lenti-lncRNA-TUG1 group, while significantly decreased in the lenti-shTUG1 group compared with the control (Fig. 2E-H). These results suggested that lncRNA-TUG1 may serve a tumor-promoting role in the development of RCC.To determine whether the low expression level of miR-196a was relevant to the overexpressed lncRNA-TUG1 in RCC cell lines, the present study determined the miR-196a expression level following transfection. The results demonstrated that the expression level of miR-196a significantly increased following transfection with miR-196a or lenti-shTUG1 compared with the controls, while it significantly decreased following transfection with miR-inhibitor or lenti-lncRNA-TUG1 (Fig. 3B). From these results, it was further hypothesized that miR-196a may be involved in the lncRNA-TUG1 tumor-promoting function in RCC via a binding interaction. Therefore, a luciferase reporter assay was performed to verify this hypothesis, which demonstrated that luciferase activity was significantly decreased following co-transfection of miR-196a mimics and wild-type lncRNA-TUG1 (Fig. 3C). The results of the present study indicated that there may be a binding site between lncRNA-TUG1 and miR-196a, through which miR-196a may serve an important role in the biological function of lncRNA-TUG1 in RCC.Cell viability was determined using an MTT assay following transfection of RCC 786-O cells with lncRNA-TUG1 or shTUG1, or co-transfection with lncRNA-TUG1 and miR-196a, shTUG1 and miR-inhibitor. Consistent with the above results, it was observed that cells transfected with lncRNA-TUG1 or shTUG1 had markedly better or poorer cell viability, respectively, compared with the controls. Furthermore, this decrease or increase in cell viability was able to be reversed by co-transfection with miR-inhibitor or miR-196a (Fig. 4). In general, these results confirmed the above findings, which revealed that lncRNA-TUG1 promoted RCC cell proliferation by suppressing miR-196a.In order to elucidate the molecular mechanisms underlying the tumor-promoting function of lncRNA-TUG1 in RCC, western blot was used to detect relevant protein expression levels, including JNK, p-ERK and p-AKT, in RCC 786-O cells. It was observed that the expression of p-AKT was upregulated when cells were transfected with lenti-lncRNA-TUG1, which was reversed following co-transfection with miR-196. By contrast, the expression of p-JNK and p-ERK exhibited a corresponding upregulation when RCC 786-O cells were transfected with lenti-shTUG1, which was reversed by co-transfection with miR-inhibitor (Fig. 5). These data indicated that lncRNA-TUG1 may regulate proliferation-associated proteins by suppressing miR-196a, thereby promoting tumorigenesis in RCC.	30387842	RID05804	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Renal cell carcinoma	TUG1	p-ERK	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long noncoding RNA TUG1 promotes renal cell carcinoma cell proliferation, migration and invasion by downregulating microRNA-196a.The results demonstrated that the expression level of lncRNA-TUG1 was significantly increased in RCC cells compared with HK-2 cells (Fig. 1).The results demonstrated that lncRNA-TUG1-overexpressing cells exhibited improved cell viability and a lower apoptosis rate, while lncRNA-TUG1-downregulated cells exhibited a poorer proliferative ability and a higher apoptosis rate, compared with the two control groups (Fig. 2B-D). Migration and invasion assays were performed to evaluate the impact of lncRNA-TUG1 on RCC migration and invasion. From these assays it was revealed that the migratory and invasive cell numbers were significantly increased in the lenti-lncRNA-TUG1 group, while significantly decreased in the lenti-shTUG1 group compared with the control (Fig. 2E-H). These results suggested that lncRNA-TUG1 may serve a tumor-promoting role in the development of RCC.To determine whether the low expression level of miR-196a was relevant to the overexpressed lncRNA-TUG1 in RCC cell lines, the present study determined the miR-196a expression level following transfection. The results demonstrated that the expression level of miR-196a significantly increased following transfection with miR-196a or lenti-shTUG1 compared with the controls, while it significantly decreased following transfection with miR-inhibitor or lenti-lncRNA-TUG1 (Fig. 3B). From these results, it was further hypothesized that miR-196a may be involved in the lncRNA-TUG1 tumor-promoting function in RCC via a binding interaction. Therefore, a luciferase reporter assay was performed to verify this hypothesis, which demonstrated that luciferase activity was significantly decreased following co-transfection of miR-196a mimics and wild-type lncRNA-TUG1 (Fig. 3C). The results of the present study indicated that there may be a binding site between lncRNA-TUG1 and miR-196a, through which miR-196a may serve an important role in the biological function of lncRNA-TUG1 in RCC.Cell viability was determined using an MTT assay following transfection of RCC 786-O cells with lncRNA-TUG1 or shTUG1, or co-transfection with lncRNA-TUG1 and miR-196a, shTUG1 and miR-inhibitor. Consistent with the above results, it was observed that cells transfected with lncRNA-TUG1 or shTUG1 had markedly better or poorer cell viability, respectively, compared with the controls. Furthermore, this decrease or increase in cell viability was able to be reversed by co-transfection with miR-inhibitor or miR-196a (Fig. 4). In general, these results confirmed the above findings, which revealed that lncRNA-TUG1 promoted RCC cell proliferation by suppressing miR-196a.In order to elucidate the molecular mechanisms underlying the tumor-promoting function of lncRNA-TUG1 in RCC, western blot was used to detect relevant protein expression levels, including JNK, p-ERK and p-AKT, in RCC 786-O cells. It was observed that the expression of p-AKT was upregulated when cells were transfected with lenti-lncRNA-TUG1, which was reversed following co-transfection with miR-196. By contrast, the expression of p-JNK and p-ERK exhibited a corresponding upregulation when RCC 786-O cells were transfected with lenti-shTUG1, which was reversed by co-transfection with miR-inhibitor (Fig. 5). These data indicated that lncRNA-TUG1 may regulate proliferation-associated proteins by suppressing miR-196a, thereby promoting tumorigenesis in RCC.	30387842	RID05805	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Renal cell carcinoma	TUG1	p-AKT	positively-E	western blot	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Long noncoding RNA TUG1 promotes renal cell carcinoma cell proliferation, migration and invasion by downregulating microRNA-196a.The results demonstrated that the expression level of lncRNA-TUG1 was significantly increased in RCC cells compared with HK-2 cells (Fig. 1).The results demonstrated that lncRNA-TUG1-overexpressing cells exhibited improved cell viability and a lower apoptosis rate, while lncRNA-TUG1-downregulated cells exhibited a poorer proliferative ability and a higher apoptosis rate, compared with the two control groups (Fig. 2B-D). Migration and invasion assays were performed to evaluate the impact of lncRNA-TUG1 on RCC migration and invasion. From these assays it was revealed that the migratory and invasive cell numbers were significantly increased in the lenti-lncRNA-TUG1 group, while significantly decreased in the lenti-shTUG1 group compared with the control (Fig. 2E-H). These results suggested that lncRNA-TUG1 may serve a tumor-promoting role in the development of RCC.To determine whether the low expression level of miR-196a was relevant to the overexpressed lncRNA-TUG1 in RCC cell lines, the present study determined the miR-196a expression level following transfection. The results demonstrated that the expression level of miR-196a significantly increased following transfection with miR-196a or lenti-shTUG1 compared with the controls, while it significantly decreased following transfection with miR-inhibitor or lenti-lncRNA-TUG1 (Fig. 3B). From these results, it was further hypothesized that miR-196a may be involved in the lncRNA-TUG1 tumor-promoting function in RCC via a binding interaction. Therefore, a luciferase reporter assay was performed to verify this hypothesis, which demonstrated that luciferase activity was significantly decreased following co-transfection of miR-196a mimics and wild-type lncRNA-TUG1 (Fig. 3C). The results of the present study indicated that there may be a binding site between lncRNA-TUG1 and miR-196a, through which miR-196a may serve an important role in the biological function of lncRNA-TUG1 in RCC.Cell viability was determined using an MTT assay following transfection of RCC 786-O cells with lncRNA-TUG1 or shTUG1, or co-transfection with lncRNA-TUG1 and miR-196a, shTUG1 and miR-inhibitor. Consistent with the above results, it was observed that cells transfected with lncRNA-TUG1 or shTUG1 had markedly better or poorer cell viability, respectively, compared with the controls. Furthermore, this decrease or increase in cell viability was able to be reversed by co-transfection with miR-inhibitor or miR-196a (Fig. 4). In general, these results confirmed the above findings, which revealed that lncRNA-TUG1 promoted RCC cell proliferation by suppressing miR-196a.In order to elucidate the molecular mechanisms underlying the tumor-promoting function of lncRNA-TUG1 in RCC, western blot was used to detect relevant protein expression levels, including JNK, p-ERK and p-AKT, in RCC 786-O cells. It was observed that the expression of p-AKT was upregulated when cells were transfected with lenti-lncRNA-TUG1, which was reversed following co-transfection with miR-196. By contrast, the expression of p-JNK and p-ERK exhibited a corresponding upregulation when RCC 786-O cells were transfected with lenti-shTUG1, which was reversed by co-transfection with miR-inhibitor (Fig. 5). These data indicated that lncRNA-TUG1 may regulate proliferation-associated proteins by suppressing miR-196a, thereby promoting tumorigenesis in RCC.	30387842	RID05806	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Colorectal cancer	NEAT1	GDNF	positively-E	luciferase reporter assay;RNAi;overexpress;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-196a-5p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168621	NA	283131	2668	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ATF1|ATF2|HFB1-GDNF	LncRNA NEAT1 promotes colorectal cancer cell proliferation and migration via regulating glial cell-derived neurotrophic factor by sponging miR-196a-5p.The results of qPCR analysis showed that there was a lower expression of NEAT1 in NCM460 normal colonic epithelial cells, compared to the HCT116, HT29, SW480, and LoVo colorectal cancer cells (Fig. 1A).CCK8 assay demonstrated that suppression of NEAT1 significantly inhibited the cell proliferation of HCT116 cells (Fig. 1D), while up-regulation of NEAT1 effectively enhanced the cell proliferation of SW480 cells (Fig. 1E). Cell migration assay showed that the cell migration potential was strikingly inhibited in HCT116 cells after NEAT1 was knocked down, while the potential was promoted in SW480 cells after NEAT1 was overexpressed (Fig. 1F). Taken together, these results demonstrated that NEAT1 facilitated the cell proliferation and migration potential in CRCs.To dissect whether NEAT1 regulates the miR-196a-5p expression in CRCs, we employed qPCR assay to detect the miR-196a-5p expression in CRCs with NEAT1 knockdown or overexpression. The results demonstrated that miR-196a-5p expression was increased in HCT116 cells transfected with siNEAT1, but was decreased in SW480 cells transfected with pcDNA-NEAT1 (Fig. 2A).We further performed the luciferase reporter assay to detect the binding between NEAT1 and miR-196a-5p. luciferase reporter assay demonstrated an inhibition of luciferase activity in cells co-transfected with wild-type NEAT1 and miR-196a-5p mimics, while luciferase activity was restored in cells co-transfected with mutant NEAT1 and miR-196a-5p mimics (Fig. 2B). To further confirm the interaction between miR-196a-5p and NEAT1, RIP assay and RNA-pull down assay were then employed. The RIP analysis demonstrated that NEAT1 and miR-196a-5p were more abundant in Ago2 pellet than in the control IgG pellet (Fig. 2C). In addition, RNA pull-down assay using biotinylated miR-196a (miR-196a bio) probe demonstrated a greatly higher level of NEAT1 than control (NC-bio) or miR-196a bio Mut (Fig. 2D). These results demonstrated that NEAT1 directly regulated the miR-196a-5p expression in CRCs.Then, we found that miR-196a-5p inhibitor restored the inhibition of cell proliferation and migration potential caused by siNEAT1 in HCT116 cells, and miR-196a-5p mimics could repress NEAT1-induced cell proliferation and migration potential in SW480 cells (Fig. 3B,C). These results suggested that miR-196a-5p inhibits the role of NEAT1 in the cell proliferation and migration of CRCs.To determine whether miR-196a-5p regulates GDNF expression in CRCs, we used qPCR and western blotto examine GDNF expression in CRCs transfected with miR-196a-5p mimics or miR-196a-5p inhibitor. The results illustrated that miR-196a-5p mimics inhibited both the protein level and mRNA level of GDNF in HCT116 cells (Fig. 4A). Furthermore, the miR-196a-5p inhibitor promoted the GDNF expression in SW480 cells (Fig. 4B). We further employed the luciferase reporter assay to examine the binding between GDNF and miR-196a-5p. luciferase reporter assay demonstrated a suppression of luciferase activity in cells co-transfected with wild-type GDNF-3'-UTR and miR-196a-5p mimics, while luciferase activity was restored in cells co-transfected with mutant GDNF-3'UTR and miR-196a-5p mimics (Fig. 4C). These results illustrated that miR-196a-5p could directly modulate the GDNF expression in CRCs.To test this hypothesis, we applied qPCR and western blotto explore whether NEAT1 regulates the expression of GDNF. The results revealed that knockdown of NEAT1 inhibited the GDNF expression in HCT116 cells (Fig. 6A) and overexpression of NEAT1 increased the GDNF expression in SW480 cells (Fig. 6B). These results demonstrated that NEAT1 up-regulated the GDNF expression in CRCs. Then, we sought to determine the role of the NEAT1/miR-196a/GDNF pathway in CRCs. CCK8 and cell migration assays illustrated that the modulation of NEAT1/miR-196a/GDNF pathway affected the cell proliferation and migration potential of CSCs (Fig. 6C-F). These data revealed that NEAT1 played key roles by inhibiting the miR-196a-5p, and thereby up-regulated GDNF expression in CRCs.	30383193	RID05807	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	TPTE2P1	Caspase3	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253771	GRCh38_13:24924673-24968505	NA	NA	646405	NA	NA	NA	The long noncoding RNA TPTE2P1 promotes the viability of colorectal cancer cells.The expression level of the lncRNA TPTE2P1 wasmeasured  in  20  paired  human  samples  and  wassignificantly higher in cancer tissues than in adjacentnormal  tissues  (Figure  1A).After silencing byS3-shTPTE2P1, the apoptotic cells increased in bothHCT116  and  DLD-1  cells  (Figure  4A)  as  follows:10.53%   0.17% vs 1.84%   0.11% (P< 0.001) for earlyapoptosis   and   20.14%   0.22%   vs   3.45%   0.11%(P< 0.001) for late apoptosis in HCT116 cells, and7.50%   0.43%  vs  3.27%   0.55%  (P< 0.001)  for  earlyapoptosis in DLD-1 cells (Figure 4B).Consistent with the apoptosis analysis, western blotanalysis confirmed that activated caspase 3 and poly(ADP-ribose) polymerase 1 (PARP) were upregulated inHCT116 and DLD-1 cells after TPTE2P1 silencing (Figure5A). The proapoptotic protein BAD was upregulated andthe  antiapoptotic  proteins  BCL-2  and  BCL-xl  weredownregulated in both cell lines (Figure 5B). Cytochromec expression was also higher in DLD-1 cells in the S3group than in the shCon group. Furthermore, phos-phorylated p53 at Ser315 was decreased after knocking down TPTE2P1, while p53 in HCT116 and phosphory-lated p53 at Ser15 were increased (Figure 5C). These results indicated that TPTE2P1 could promote CRC cell viability by inhibiting apoptosis.To test whether TPTE2P1 could inhibit CRC tumor growthin vivo, we developed xenograft tumor models using BALB/cnudemice.S3-shTPTE2P1 inhibited tumor growth in vivo(Figure 6Aand6B). Tumors derived from S3-lentiviral-infected HCT116 cells had significantly smaller tumor volumes and lower tumor weights(Figure 6C and 6D).Furthermore, the BAD and p53 protein levels were higherin the S3-shTPTE2P1 group than in the shCon group(Figure6E).Thus,these results confirmed that TPTE2P1 could promote tumor growth in vivo.	30382596	RID05808	expression association	NA		
Colorectal cancer	TPTE2P1	PARP1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253771	GRCh38_13:24924673-24968505	ENSG00000143799	NA	646405	142	NA	ADPRT|ARTD1|PARP|PPOL	The long noncoding RNA TPTE2P1 promotes the viability of colorectal cancer cells.The expression level of the lncRNA TPTE2P1 wasmeasured  in  20  paired  human  samples  and  wassignificantly higher in cancer tissues than in adjacentnormal  tissues  (Figure  1A).After silencing byS3-shTPTE2P1, the apoptotic cells increased in bothHCT116  and  DLD-1  cells  (Figure  4A)  as  follows:10.53%   0.17% vs 1.84%   0.11% (P< 0.001) for earlyapoptosis   and   20.14%   0.22%   vs   3.45%   0.11%(P< 0.001) for late apoptosis in HCT116 cells, and7.50%   0.43%  vs  3.27%   0.55%  (P< 0.001)  for  earlyapoptosis in DLD-1 cells (Figure 4B).Consistent with the apoptosis analysis, western blotanalysis confirmed that activated caspase 3 and poly(ADP-ribose) polymerase 1 (PARP) were upregulated inHCT116 and DLD-1 cells after TPTE2P1 silencing (Figure5A). The proapoptotic protein BAD was upregulated andthe  antiapoptotic  proteins  BCL-2  and  BCL-xl  weredownregulated in both cell lines (Figure 5B). Cytochromec expression was also higher in DLD-1 cells in the S3group than in the shCon group. Furthermore, phos-phorylated p53 at Ser315 was decreased after knocking down TPTE2P1, while p53 in HCT116 and phosphory-lated p53 at Ser15 were increased (Figure 5C). These results indicated that TPTE2P1 could promote CRC cell viability by inhibiting apoptosis.To test whether TPTE2P1 could inhibit CRC tumor growthin vivo, we developed xenograft tumor models using BALB/cnudemice.S3-shTPTE2P1 inhibited tumor growth in vivo(Figure 6Aand6B). Tumors derived from S3-lentiviral-infected HCT116 cells had significantly smaller tumor volumes and lower tumor weights(Figure 6C and 6D).Furthermore, the BAD and p53 protein levels were higherin the S3-shTPTE2P1 group than in the shCon group(Figure6E).Thus,these results confirmed that TPTE2P1 could promote tumor growth in vivo.	30382596	RID05809	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Colorectal cancer	TPTE2P1	BAD	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253771	GRCh38_13:24924673-24968505	ENSG00000002330	NA	646405	572	NA	BBC2|BCL2L8	The long noncoding RNA TPTE2P1 promotes the viability of colorectal cancer cells.The expression level of the lncRNA TPTE2P1 wasmeasured  in  20  paired  human  samples  and  wassignificantly higher in cancer tissues than in adjacentnormal  tissues  (Figure  1A).After silencing byS3-shTPTE2P1, the apoptotic cells increased in bothHCT116  and  DLD-1  cells  (Figure  4A)  as  follows:10.53%   0.17% vs 1.84%   0.11% (P< 0.001) for earlyapoptosis   and   20.14%   0.22%   vs   3.45%   0.11%(P< 0.001) for late apoptosis in HCT116 cells, and7.50%   0.43%  vs  3.27%   0.55%  (P< 0.001)  for  earlyapoptosis in DLD-1 cells (Figure 4B).Consistent with the apoptosis analysis, western blotanalysis confirmed that activated caspase 3 and poly(ADP-ribose) polymerase 1 (PARP) were upregulated inHCT116 and DLD-1 cells after TPTE2P1 silencing (Figure5A). The proapoptotic protein BAD was upregulated andthe  antiapoptotic  proteins  BCL-2  and  BCL-xl  weredownregulated in both cell lines (Figure 5B). Cytochromec expression was also higher in DLD-1 cells in the S3group than in the shCon group. Furthermore, phos-phorylated p53 at Ser315 was decreased after knocking down TPTE2P1, while p53 in HCT116 and phosphory-lated p53 at Ser15 were increased (Figure 5C). These results indicated that TPTE2P1 could promote CRC cell viability by inhibiting apoptosis.To test whether TPTE2P1 could inhibit CRC tumor growthin vivo, we developed xenograft tumor models using BALB/cnudemice.S3-shTPTE2P1 inhibited tumor growth in vivo(Figure 6Aand6B). Tumors derived from S3-lentiviral-infected HCT116 cells had significantly smaller tumor volumes and lower tumor weights(Figure 6C and 6D).Furthermore, the BAD and p53 protein levels were higherin the S3-shTPTE2P1 group than in the shCon group(Figure6E).Thus,these results confirmed that TPTE2P1 could promote tumor growth in vivo.	30382596	RID05810	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	TPTE2P1	BCL2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253771	GRCh38_13:24924673-24968505	ENSG00000171791	NA	646405	596	NA	Bcl-2|PPP1R50	The long noncoding RNA TPTE2P1 promotes the viability of colorectal cancer cells.The expression level of the lncRNA TPTE2P1 wasmeasured  in  20  paired  human  samples  and  wassignificantly higher in cancer tissues than in adjacentnormal  tissues  (Figure  1A).After silencing byS3-shTPTE2P1, the apoptotic cells increased in bothHCT116  and  DLD-1  cells  (Figure  4A)  as  follows:10.53%   0.17% vs 1.84%   0.11% (P< 0.001) for earlyapoptosis   and   20.14%   0.22%   vs   3.45%   0.11%(P< 0.001) for late apoptosis in HCT116 cells, and7.50%   0.43%  vs  3.27%   0.55%  (P< 0.001)  for  earlyapoptosis in DLD-1 cells (Figure 4B).Consistent with the apoptosis analysis, western blotanalysis confirmed that activated caspase 3 and poly(ADP-ribose) polymerase 1 (PARP) were upregulated inHCT116 and DLD-1 cells after TPTE2P1 silencing (Figure5A). The proapoptotic protein BAD was upregulated andthe  antiapoptotic  proteins  BCL-2  and  BCL-xl  weredownregulated in both cell lines (Figure 5B). Cytochromec expression was also higher in DLD-1 cells in the S3group than in the shCon group. Furthermore, phos-phorylated p53 at Ser315 was decreased after knocking down TPTE2P1, while p53 in HCT116 and phosphory-lated p53 at Ser15 were increased (Figure 5C). These results indicated that TPTE2P1 could promote CRC cell viability by inhibiting apoptosis.To test whether TPTE2P1 could inhibit CRC tumor growthin vivo, we developed xenograft tumor models using BALB/cnudemice.S3-shTPTE2P1 inhibited tumor growth in vivo(Figure 6Aand6B). Tumors derived from S3-lentiviral-infected HCT116 cells had significantly smaller tumor volumes and lower tumor weights(Figure 6C and 6D).Furthermore, the BAD and p53 protein levels were higherin the S3-shTPTE2P1 group than in the shCon group(Figure6E).Thus,these results confirmed that TPTE2P1 could promote tumor growth in vivo.	30382596	RID05811	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Glioblastoma	HOTAIRM1	HOXA1	positively-E	RNAi;qRT-PCR;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000105991	NA	100506311	3198	HOXA-AS1|HOXA1-AS1|NCRNA00179	HOX1|HOX1F	Over-expressed lncRNA HOTAIRM1 promotes tumor growth and invasion through up-regulating HOXA1 and sequestering G9a/EZH2/Dnmts away from the HOXA1 gene in glioblastoma multiforme. First, we examined the expression levels of HOTAIRM1 in tumor tissues from 40 patients with glioma (WHO I and II, n-=-20; WHO III and IV, n-=-20) and 20 normal brain tissues. The CCK8 and BrdU cell proliferation assays indicated that cell growth and proliferation were reduced by the knockdown of HOTAIRM1 in GBM cells (Fig. -(Fig.2b2b and -andcc and Additional file 8: Figure S2B-C). A significant increase of cell apoptosis was observed in HOTAIRM1-inhibiting GBM cell lines (Fig. -(Fig.2d2d and Additional file 8: Figure S2D).The growth curves determined by CCK8 assays indicated that knockdown of HOTAIRM1 dramatically suppressed the growth of GBM cells (Fig. -(Fig.2f,2f, Additional file 8: Figure S2F and Additional file 9: Figure S3B). A significant decrease in cell proliferation and the increase of cell apoptosis were observed in shHOTAIRM1-transfected G0401 cells (Additional file 9: Figure S3C and D).GBM shows highly aggressive biological character. To investigate whether HOTAIRM1 affected GBM cell migration and invasion, wound healing and transwell invasion arrays were performed. The results showed HOTAIRM1 knockdown significantly inhibited migration and invasion capacity of GBM cells, compared with control group (Fig. 3 and Additional file 10: Figure S4). These results indicate that HOTAIRM1 promote GBM cells migration and invasion.To check whether the HOTAIRM1 plays a regulatory role in gene expression at the HOXA1 gene, we analyzed the changes in HOXA1 mRNAs levels, after silencing of HOTAIRM1. Introduction of shHOTAIRM1 resulted in decreasing in HOXA1 mRNA levels (Fig. -(Fig.4b4b and Additional file 11: Figure S5A, B). We also investigate the changes in mRNA levels for other genes in HOXA gene cluster after silencing of HOTAIRM1 by qRT-PCRmethod. The result indicates knockdown of HOTAIRM1 had no effect on other HOXA genes expression at the transcriptional level (Additional file 11: Figure S5C). These results indicate that the antisense lncRNA of HORAIRM1 regulates HOXA1 gene expression in cis.In our first ChIP assays, using antibodies against H3K9me2, and H3K27me3, we found H3K9me2 and H3K27me3 modifies in the HOXA1 TSS in GBM cell lines and primary GBM cells were significantly decreased compared with that in HA cells (Fig. 5a). We performed identical ChIP assays after knockdown of HOTAIRM1, H3K9me2 and H3k27me3 modifications were increased in the HOXA1 TSS regions in A172, U87, and G0401 cells (Fig. -(Fig.5c5c and Additional file 12: Figure S6A and B). Moreover, our ChIP assay results confirmed that G9a and EZH2 were also enriched in the TSS region of the HOXA1 gene in HOTAIRM1-inhibiting GBM cell (Fig. -(Fig.5d5d and Additional file 12: Figure S6C and D).HOXA2 is the closest gene to HOXA1 and HOXA11 is located downstream of the HOXA gene cluster. The H3K9me2/H3K27me3 and G9a/EZH2 enrichment increased in 3 regions (HOXA1-1, A1-2, A1-3) near to HOXA1 TSS, especially in predicted promoter region (HOXA1-2), whereas the change of enrichment was not detected in other 2 regions (HOXA1-4, 1-5) and in HOXA2, HOXA11 gene TSS regions (Additional file 12: Figure S6 F-I). So, we showed the result of the HOXA1-2 fragment in HOXA1 gene TSS regions in our ChIP experiment.These results indicated that silencing of HOTAIRM1 reduced gene-suppressive histone modification H3K9me2 and H3K27me3 in the TSS region of the HOXA1 gene, thereby decreasing HOXA1 mRNA expression level.We then performed ChIP assays to detect the potential interaction between DnmTs and the HOXA1 gene promoter after the HOTAIRM1-mediated knockdown. The results indicated that enrichments of DnmT1, DnmT3a, and DnmT3b in the promoter region of HOXA1 gene were increased by shHOTAIRM1 in A172 (Fig. -(Fig.6e)6e) and U87, G0401 cells (Additional file 13: Figure S7D-E). To examine whether knockdown of HOTAIRM1 affected DNA methyltransferases binding another locus, we analyzed DnmTs enrichments in the HOXA2 and HOXA11 gene TSS region. We found the loss of HOTAIRM1 had no effect on DnmT1, DnmT3a, and DnmT3b bonding to the HOXA2 and HOXA11 gene, suggesting that HOTAIRM1 specifically regulates the HOXA1 DNA methylation levels (Additional file 13: Figure S7F).To analyze the epigenetic regulation mechanism of HOTAIRM1 mediated, we first tested whether HOTAIRM1 interacts with G9a, EZH2, and Dnmts by performing RNA-ChIP assays. In GBM cells, HOTAIRM1 was pulled down by either antibody (Fig. 7a and -andb),b), suggesting that HOTAIRM1 formed a complex with G9a, EZH2, and Dnmts and prevented them from binding the TSS of the HOXA1 gene loci. This finding is consistent with the histone modifications of H3K9me2, H3K27me3 and DNA methylation levels in the HOXA1 gene domains.Given that hypomethylated DNA is associated with active genes, whereas hypermethylated genes are silent, we conclude that the transcriptional activation of the HOXA1 gene is regulated in part by HOTAIRM1-directed DNA demethylation.	30376874	RID05812	epigenetic regulation	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Cardiovascular system disease	CHRF	MYD88	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-489)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	NA	NA	ENSG00000172936	NA	NA	4615	NA	IMD68|MYD88D	The novel regulatory role of lncRNA-miRNA-mRNA axis in cardiovascular diseases.Ang-II-induced miR-489 downregulation in cardiomyocytes was confirmed by qRT-PCR To find out the target gene of miR-489, we screened some hypertro_x0002_phic associated genes (Cyclin T, GSK3beta, PKGI, Ras, MYL2, CSRP3, MCIP1, Foxo3a, Calcineurin, NFAT, Myocardin, Myd88) by luciferase assay.We performed real-time RT-PCRto detect lncRNA levels in response to Ang-II treatment. Among the lncRNAs, AK048451, which we named CHRF,.CHRF was also significantly increased in the heart of trans_x0002_verse aortic constriction mouse model (Online Figure XB) and human heart failure sample. Our results further reveal that Myd88 is a target of miR-489 in the hypertrophic pathway. Moreover, we demonstrated that CHRF acts as an endogenous sponge RNA and inhibits miR-489 expression and activity. The modulation of miR-489 and CHRF may pro_x0002_vide an intriguing approach for tackling cardiac hypertrophy.	30188595|24557880	RID05813	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiovascular system disease	GAS5	FOXO3	positively-E	MicroInspector	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-)	ceRNA(miR-23a)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000118689	NA	60674	2309	NCRNA00030|SNHG2	AF6q21|FKHRL1|FOXO2|FOXO3A	The novel regulatory role of lncRNA-miRNA-mRNA axis in cardiovascular diseases.the study showed that GAS5 contained a binding site for miR-23a and acted as a sponge of miR-23a. Up-regulated GAS5 expression inhibited cardiomyocyte hypertrophy through negatively regulating miR-23a and its target forkhead box O3 (Foxo3a)The lncRNA-GAS5/miR-23a/Foxo3a axis regulates cardiac hypertrophy by Wnt/beta-catenin signal pathway.We detected the expression levels of lncRNA GAS5 in the hypertrophic model cells induced by Ang-II and the control cells. The results showed that the expression of GAS5 was significantly decreased in Ang-II induced hypertrophic myocardium.We predicted lncRNA-targeted miRNAs using the online prediction software MicroInspector.lncRNA GAS5 Inhibits Wnt/beta-catenin Signal Pathway. In conclusion, we found in our study that lncRNA GAS5/miR-23a/Foxo3a plays an inhibitory role in the development of cardiac hypertrophy.	30188595|28899782	RID05814	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(BRCA);DATA(GSE51827,GSE86978)
Cardiovascular system disease	CARL	PHB2	positively-E	RNAi;luciferase reporter assay		qRT-PCR	NA	NA	apoptosis process(-)	ceRNA(miR-539)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	NA	NA	ENSG00000215021	NA	NA	11331	NA	Bap37|BCAP37|p22|REA	The novel regulatory role of lncRNA-miRNA-mRNA axis in cardiovascular diseases.we report that alncRNA, nam.ed cardiac apoptosis-related lncRNA (CARL), can suppress mitochondrial fissionand apoptosis by targeting miR-539 and PHB2. To understand whichlncRNA is involved in the regulation of miR-539, we separatelyknocked down the four lncRNAs by siRNA technology.To further test whether CARL mayact as a sponge for miR-539, we transfected the cells withmiR-539 sensor luciferase reporter	30188595|24710105	RID05815	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE67939)
Cardiovascular system disease	MDRL	MIR361	negatively-F	RNA pull-down assay;luciferase reporter assay;RNAhybrid	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponse	regulation	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	miRNA	NA	NA	ENSG00000199051	NA	NA	494323	NA	MIRN361|hsa-mir-361|mir-361	The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. We also employed inverse pull-down assay to test if MDRL could pull down miR-361, a biotin-labeled-specific MDRL probe was used. LncRNAs were chosen from the lncRNA array published online by Fantom company. Among 100 lncRNAs, AK009271 which we named mitochondrial dynamic related lncRNA (MDRL), was substantially reduced.these data suggest that MDRL targets miR-361/miR-484 in the cascades of mitochondrial fission and apoptosis	30188595|25057983	RID05816	ceRNA or sponge	NA		
Cardiovascular system disease	MDRL	MIR484	negatively-F	RNA pull-down assay;luciferase reporter assay;RNAhybrid	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponse	regulation	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	miRNA	NA	NA	ENSG00000272213	NA	NA	619553	NA	MIRN484|hsa-mir-484|mir-484	The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. We also employed inverse pull-down assay to test if MDRL could pull down miR-361, a biotin-labeled-specific MDRL probe was used. LncRNAs were chosen from the lncRNA array published online by Fantom company. Among 100 lncRNAs, AK009271 which we named mitochondrial dynamic related lncRNA (MDRL), was substantially reduced.these data suggest that MDRL targets miR-361/miR-484 in the cascades of mitochondrial fission and apoptosis	30188595|25057983	RID05817	ceRNA or sponge	NA		
Cardiovascular system disease	H19	SOX6	positively-E	starBase v2.0;luciferase reporter assay;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-19b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cardiovascular system disease	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000110693	NA	283120	55553	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Downregulation of long non-coding RNA H19 promotes P19CL6 cells proliferation and inhibits apoptosis during late-stage cardiac differentiation via miR-19b-modulated Sox6.Online software starBase v2.0 predicted H19 contains binding sequences complementary to miR-19b seed regions, as shown in Fig. 3a. Furtherly, the luciferase report assay indicated that miR-19b mimics inhibited luciferase activity of the wild type H19 reporter (H19-WT), but no change was observed for the luciferase activity in the mutant reporter (H19-Mut) .Downregulation of H19 promoted cell proliferation and inhibited cell apoptosis during late-stage cardiac differentiation by regulating the negative role of miR-19b in Sox6 expression, which suggested that the manipulation of H19 expression could serve as a potential strategy for heart disease.	30188595|27895893	RID05818	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Cardiovascular system disease	APF	ATG7	positively-E	RNA pull-down assay;luciferase reporter assay;RNAhybrid	upregulation	qRT-PCR	NA	NA	cell autophagy(-);apoptosis process(-)	ceRNA(miR-188)	regulation	RNA-protein	NA	CSC	Evading Apoptosis	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	NA	NA	ENSG00000197548	NA	NA	10533	NA	APG7L|DKFZp434N0735|GSA7	APF lncRNA regulates autophagy and myocardial infarction by targeting miR-188-3p.Our results showed thatknockdown of endogenous miR-188-3p by antagomir induced anincrease in ATG7 expression.We employed the luciferase assay system to test whether miR_x0002_188-3p could influence the translation of ATG7. Wecarried out qRT-PCRto detect lncRNAs levels on A/R treatment.Among those lncRNAs, only AK079427, which we named APF,was significantly upregulated on A/R treatment .we compared the sequences of APF withthat of miR-188-3p using the bioinformatics programmeRNAhybrid and noticed that APF contained a binding site ofmiR-188-3p.APF regulates autophagy and cell death through miR-188-3pand ATG7.	30188595|25858075	RID05819	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Cardiovascular system disease	NKRF	RIPK1	positively-E	RNAi;RNAhybrid	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-873)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000186416	GRCh38_X:119588337-119606443	ENSG00000137275	NA	55922	8737	ITBA4|NRF	AIEFL|IMD57|RIP|RIP-1|RIP1	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.We carried out quantitative reverse transcription polymerase chain reaction (qRT-PCR to detect lncRNAs levels in response to H2O2 treatment. To understand which lncRNA is involved in the regulation of miR-873, we separately knocked down the five lncRNAs by siRNA constructs. To understand the mechanism by which NRF regulates the levels of miR-873, we tested whether NRF could interact with miR-873. We compared the sequences of NRF with that of miR-873 using the bioinformatics program RNAhybrid and noticed that NRF contains a binding site of miR-873.In animal model, NRF levels were increased in response to I/R injury in the ischemic zone.Knockdown of NRF resulted in a decrease in the myocardial necrosis.aken together, these data suggest that NRF mediates necrotic cell death in cardiomyocytes through modulating miR-873-RIPK1/RIPK3 signaling pathway.	30188595|27258785	RID05820	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978,GSE41245)
Cardiovascular system disease	NKRF	RIPK3	positively-E	RNAi;RNAhybrid	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-873)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000186416	GRCh38_X:119588337-119606443	ENSG00000129465	NA	55922	11035	ITBA4|NRF	RIP3	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.We carried out quantitative reverse transcription polymerase chain reaction (qRT-PCR to detect lncRNAs levels in response to H2O2 treatment. To understand which lncRNA is involved in the regulation of miR-873, we separately knocked down the five lncRNAs by siRNA constructs. To understand the mechanism by which NRF regulates the levels of miR-873, we tested whether NRF could interact with miR-873. We compared the sequences of NRF with that of miR-873 using the bioinformatics program RNAhybrid and noticed that NRF contains a binding site of miR-873.In animal model, NRF levels were increased in response to I/R injury in the ischemic zone.Knockdown of NRF resulted in a decrease in the myocardial necrosis.aken together, these data suggest that NRF mediates necrotic cell death in cardiomyocytes through modulating miR-873-RIPK1/RIPK4 signaling pathway.	30188595|27258785	RID05821	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiovascular system disease	Ang262	miR\221	negatively-F	RT-qPCR	upregulation	sequencing	NA	NA	cell proliferation(+)	sponse	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Cardiovascular system disease	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Novel Long Non-Coding RNAs Are Regulated by Angiotensin II in Vascular Smooth Muscle Cells.To uncover the transcriptomic effects of Ang II, we treated rat VSMCs for three hours with Ang II and then performed RNA-seq of RNA isolated from control and Ang II-treated cells from two independently isolated biological replicates.we evaluated the functional consequences of this knockdown by assessing the rates of proliferation of VSMCs transfected with siRNAs targeting Lnc-Ang362. Results showed that these cells proliferate to a lesser extent than VSMCs transfected with control siRNAs (Fig. 7B, p< 0.05, N= 6), suggesting that the lncRNA plays a role in VSMC growth. Our RNA-seq analysis did not identify miR-221 or miR-222 because our method of RNA-sequencing does not assess small RNAs. To verify whether these miRNAs are upregulated in response to Ang II, we assessed the expression of mature miR-222 and miR-221 by RT-qPCR. We found that these miRNAs are indeed upregulated.	30188595|23697773	RID05822	ceRNA or sponge	NA		
Cardiovascular system disease	Ang262	miR\222	negatively-F	RT-qPCR	upregulation	sequencing	NA	NA	cell proliferation(+)	sponse	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Cardiovascular system disease	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Novel Long Non-Coding RNAs Are Regulated by Angiotensin II in Vascular Smooth Muscle Cells.To uncover the transcriptomic effects of Ang II, we treated rat VSMCs for three hours with Ang II and then performed RNA-seq of RNA isolated from control and Ang II-treated cells from two independently isolated biological replicates.we evaluated the functional consequences of this knockdown by assessing the rates of proliferation of VSMCs transfected with siRNAs targeting Lnc-Ang362. Results showed that these cells proliferate to a lesser extent than VSMCs transfected with control siRNAs (Fig. 7B, p< 0.05, N= 6), suggesting that the lncRNA plays a role in VSMC growth. Our RNA-seq analysis did not identify miR-221 or miR-222 because our method of RNA-sequencing does not assess small RNAs. To verify whether these miRNAs are upregulated in response to Ang II, we assessed the expression of mature miR-222 and miR-221 by RT-qPCR. We found that these miRNAs are indeed upregulated.	30188595|23697773	RID05823	ceRNA or sponge	NA		
Cardiovascular system disease	H19	CaMKII	positively-E	miRBase	upregulation	sequencing	NA	NA	cell growth(-)	ceRNA(miR-675)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The H19 long noncoding RNA is a novel negative regulator ofcardiomyocyte hypertrophy. H19 and its encoded miR-675 are upregulated in pathological cardiac hypertrophy.Consistent with the previously reported RNA-seq data,20-22 wefound H19 RNA level was significantly upregulated in hypertrophic hearts.Since H19 encodes miR-675-3p and miR-675-5p,17-19 and miR-675-3p is more abundant than miR-675-5p as seen from miRBase.we identified CaMKIIdelta as a downstream target of H19-miR-675 axis in inhibiting hypertrophic growth of cardiomyocytes.	30188595|27084844	RID05824	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Cardiovascular system disease	MALAT1	CXCR2	positively-E	starBase v2.0;TargetScan;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell survival(+);apoptosis process(-)	ceRNA(miR-22)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000180871	NA	378938	3579	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CD182|CMKAR2|IL8RB	Several publicly available bioinformatics web sites [Starbasev2.0 and TargetScan] showed that there were six poten_x0002_tial miRNAs with complementary base pairing with both MALAT1and CXCR2 : miR-1, miR-22-3p, miR-23a,miR-23b, miR-23c, and miR-376. The lncRNA MALAT1 shares a miRNA response element withmiR-22-3p.  luciferase assay and RIP experimentsshowed that direct binding existed between MALAT1 andmiR-22-3p.In summary, our study demonstrates the interactions amongthe lncRNA MALAT1, miR-22-3p and CXCR2 in ox-LDL-inducedendothelial dysfunction. MALAT1 protects the endothelial barrierfrom injury via inhibiting the expression of miR-22-3p and upreg_x0002_ulating the expression of CXCR2, which is associated with the AKTpathway.	30188595|26364720	RID05825	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cardiovascular system disease	MALAT1	AKT1	positively-E	starBase v2.1;TargetScan;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell survival(+);apoptosis process(-)	ceRNA(miR-22)	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cardiovascular system disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AKT|PKB|PRKBA|RAC|RAC-alpha	Several publicly available bioinformatics web sites [Starbasev2.0 and TargetScan] showed that there were six poten_x0002_tial miRNAs with complementary base pairing with both MALAT1and CXCR2 : miR-1, miR-22-3p, miR-23a,miR-23b, miR-23c, and miR-376. The lncRNA MALAT1 shares a miRNA response element withmiR-22-3p.  luciferase assay and RIP experimentsshowed that direct binding existed between MALAT1 andmiR-22-3p.In summary, our study demonstrates the interactions amongthe lncRNA MALAT1, miR-22-3p and CXCR2 in ox-LDL-inducedendothelial dysfunction. MALAT1 protects the endothelial barrierfrom injury via inhibiting the expression of miR-22-3p and upreg_x0002_ulating the expression of CXCR3, which is associated with the AKTpathway.	30188595|26364720	RID05826	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiovascular system disease	LINC-ROR	miR-133	negatively-F	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	sponse	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Cardiovascular system disease	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Non-Coding RNA-ROR Mediates the Reprogramming in Cardiac Hypertrophy. the expression of lncRNA-ROR is dramatically increased, downregulation of which attenuates the hypertrophic responses. lotting the expression levels of miR-208 or miR-133 over that of lncRNA-ROR revealed that a negative correlation existed between miR-133 and lncRNA-ROR, but no correlation between miR-208 and lncRNA-ROR .knocking down lncRNA-ROR dramatically increased the expression of miR-133.These results clearly demonstrate that lncRNA-ROR promotes the re-expression of fetal genes and growth of cardiomyocytes contributing to hypertrophic cardiomyopathy.	30188595|27082978	RID05827	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Epithelial ovarian cancer	LINC01116	BCL2	positively-E	RNAi	upregulation	qPT-PCR	NA	NA	apoptosis process(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000171791	NA	375295	596	TALNEC2	Bcl-2|PPP1R50	LINC01116 promotes the progression of epithelial ovarian cancer via regulating cell apoptosis. LINC01116 was overexpressed in EOC tissues than that of paracancerous tissues. Overexpressed LINC01116 resulted in upregulated Bcl-2, and downregulated cleaved Caspase-3 and cleaved Caspase-9 in EOC cells.In vitro experiments found that LINC01116 overexpression promoted proliferation and invasion of EOC cells. The above data elucidated that LINC01116 promotes  EOC  progression via  inhibiting  cell apoptosis.	30178832	RID05828	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	LINC01116	Caspase3	negatively-E	RNAi	upregulation	qPT-PCR	NA	NA	apoptosis process(+);cancer progression(+)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	NA	NA	375295	NA	TALNEC2	NA	LINC01116 promotes the progression of epithelial ovarian cancer via regulating cell apoptosis. LINC01116 was overexpressed in EOC tissues than that of paracancerous tissues. Overexpressed LINC01116 resulted in upregulated Bcl-2, and downregulated cleaved Caspase-3 and cleaved Caspase-9 in EOC cells.In vitro experiments found that LINC01116 overexpression promoted proliferation and invasion of EOC cells. The above data elucidated that LINC01116 promotes  EOC  progression via  inhibiting  cell apoptosis.	30178832	RID05829	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Epithelial ovarian cancer	LINC01116	Caspase9	negatively-E	RNAi	upregulation	qPT-PCR	NA	NA	apoptosis process(+);cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	NA	NA	375295	NA	TALNEC2	NA	LINC01116 promotes the progression of epithelial ovarian cancer via regulating cell apoptosis. LINC01116 was overexpressed in EOC tissues than that of paracancerous tissues. Overexpressed LINC01116 resulted in upregulated Bcl-2, and downregulated cleaved Caspase-3 and cleaved Caspase-9 in EOC cells.In vitro experiments found that LINC01116 overexpression promoted proliferation and invasion of EOC cells. The above data elucidated that LINC01116 promotes  EOC  progression via  inhibiting  cell apoptosis.	30178832	RID05830	expression association	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Acute myeloid leukemia	HOTAIR	p15	negatively-E	RNAi	upregulation	qPT-PCR	NA	NA	cell proliferation(+);self-renewal(+)	histone modification	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000086504	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long noncoding RNA HOTAIR promotes the self-renewal of leukemia stem cells through epigenetic silencing of p15. Here, we reported that the expression of HOTAIR was increased in LSC than in normal hematological stem and progenitor cells (HSPCs). HOTAIR inhibited p15 expression through zeste homolog 2 (EZH2)-enrolled tri-methylation of Lys 27 of histone H3 (H3K27me3) in p15 promoter.Long noncoding RNA HOTAIR promotes the self-renewal of leukemia stem cells through epigenetic silencing of p15.HOTAIR knockdown increases the expression of p15 via inhibiting EZH2-mediated H3K27me3.	30172749	RID05831	epigenetic regulation	NA		
Gastrointestinal system disease	MEG3	GDNF	positively-E	RIP;RNA pull-down assay	downregulation	qPT-PCR	NA	NA	apoptosis process(-);cell differentiation(+)	ceRNA(miR-211-5p)	regulation	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Gastrointestinal system disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168621	NA	55384	2668	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ATF1|ATF2|HFB1-GDNF	LncRNA-MEG3 protects against ganglion cell dysplasia in congenital intestinal atresia through directly regulating miR-211-5p/GDNF axis.The expression of MEG3 was detected to be declined in congenital intestinal atresia tissues at clinic and animal levels.MEG3 promoted the differentiation of BMSCs into intestinal ganglion cells and regulated GDNF expression in retinal ganglion cells (RGC-5 cells) via targeting miR-211-5p. MEG3 promoted the differentiation of BMSCs into intestinal ganglion cells and inhibited the apoptosis of intestinal ganglion cells under the exposure of hypoxia to protect against CIA injury via directly regulating miR-211-5p/GDNF axis.In our previous study, it was proved that miR-211could bind to the 3'-UTR of GDNF mRNAs to ganglion cell dysplasia in CIA.	30594782	RID05832	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Neuroblastoma	RMRP	TACR1	positively-E	TargetScan;miRcode;luciferase reporter assay;RNAi	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cancer progression(-);ERK1/2 signaling pathway(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000115353	NA	6023	6869	CHH|NME1|RMRPR|RRP2	NK1R|NKIR|SPR|TAC1R	LncRNA RMRP silence curbs neonatal neuroblastoma progression by regulating microRNA-206/tachykinin-1 receptor axis via inactivating extracellular signal-regulated kinases. RMRP was highly expressed in neuroblastoma tissues. TACR1 was a target of miR-206 and RMRP performed as a molecular sponge of miR-206 to sequester miR-206 from TACR1 in neuroblastoma cells.RMRP knockdown hindered the tumorigenesis and progression of neuroblastoma by regulating miR-206/TACR1 axis via inactivating ERK1/2 pathway, hinting a potential therapeutic target for neuroblastoma.	30582709	RID05833	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(PAAD);DATA(GSE40174)
Cervical cancer	DANCR	TGFBR1	positively-E	RegRNA 2.0;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+);ERK/SMAD signaling pathway()	ceRNA(miR-665)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000106799	NA	57291	7046	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	DANCR-mediated microRNA-665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway.We validated that transforming growth factor beta receptor 1 (TGFBR1) was a direct target of miR-665 and mediated the ERK/SMAD pathway. In addition, we identified miR-665 as the competing endogenous RNA for long noncoding (lnc)-DANCR. These observations suggested that lnc-DANCR-mediated miR-665 downregulation regulates the malignant phenotype of CC cells by targeting TGFBR1 through the ERK/SMAD pathway, which may present a pathway for novel therapeutic stratagems for CC therapy. We detected the level of DANCR in tissues and found that the level of DNACR in tumor tissues was upregulated compared with the adjacent normal tissues.	30582654	RID05834	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Pre-eclampsia	TUG1	miR-204-5p	negatively-F	bioinformatics	downregulation	RT-qPCR	NA	NA	cell invasion(+);cell metastasis(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cardiovascular system disease	Eclampsia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Long non-coding RNA TUG1 regulates the migration and invasion of trophoblast-like cells through sponging miR-204-5p.Our results demonstrate that TUG1 was downregulated in PE placental tissues compared with normal controls.Bioinformatics analysis and functional assays showed that TUG1 interacted with miR-204-5p and negatively regulated the expression and function of miR-204-5p in trophoblast cells.our results suggested that TUG1 regulates trophoblast migration and invasion partly through sponging miR-204-5p, and the TUG1/miR-204-5p axis could be a potential therapeutic target for the treatment of PE.	30575983	RID05835	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Gestational diabetes mellitus	MEG3	AFF1	positively-E	bioinformatics;luciferase reporter gene assay	upregulation	qPT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);angiogenesis(-);PI3K/AKT signaling pathway(-)	ceRNA(miR-370-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease of metabolism	Diabetes mellitus	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000172493	NA	55384	4299	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	AF-4|AF4|MLLT2|PBM1	MEG3 damages fetal endothelial function induced by gestational diabetes mellitus via AKT pathway.HUVEC cells extracted from GDM pregnancies presented increased apoptosis and decreased proliferation, migration and angiogenesis compared with those from healthy pregnancies. Meanwhile, MEG3 was overexpressed in HUVECs extracted from GDM pregnancies compared with that of healthy pregnancies. High dose of glucose treatment led to reduced angiogenesis and elevated MEG3 expression in HUVECs. MEG3 overexpression further promoted apoptosis, but inhibited proliferation, migration and angiogenesis of HUVECs. By bioinformatics and luciferase reporter gene assay, microRNA-370-3p was found to be the target gene of MEG3 and directly targeted on AFF1. Moreover, MEG3 overexpression led to downregulated microRNA-370-3p and upregulated AFF1 mainly through inhibiting PI3K/AKT pathway.                 CONCLUSIONS:MEG3 is overexpressed in HUVECs extracted from GDM pregnancies. MEG3 damages fetal endothelial function through targeting microRNA-370-3p and AFF1 via PI3K/AKT pathway.	30575893	RID05836	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807)
Hypertension	NR4A3	Giver	positively-E	RNAi;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	TF	lncRNA	ENSG00000119508	NA	NA	NA	8013	NA	CHN|CSMF|MINOR|NOR1	NA	A Novel Angiotensin II-Induced Long Noncoding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle Cells.Giver and its regulator Nr4a3 are important players in AngII-mediated VSMC dysfunction and could be novel targets for antihypertensive therapy.. H3K4me3 peaks depict start sites of these genes. To verify the regulation of Giver and nearby Nr4a3, RVSMC were treated with AngII for 1-6h and gene expression analyzed by RT-qPCR. ,these results demonstrate that Giver and its nearby gene Nr4a3 exhibit similar expression patterns in VSMC (suggesting co-regulation) in response to AngII and other stimuli implicated in the pathogenesis of CVD.GIVER and NR4a3 transcripts are increased in arteries collected from patients with hypertension.  To evaluate whether Nr4a3 is required for AngII-induced Giverexpression, we performed siRNA mediated knockdown or overexpression of Nr4a3. Transfection of RVSMC with siRNAs targeting Nr4a3 (siNr4a3) reduced Nr4a3 protein and RNA in both control and AngII treated cells relative to control siNTC oligonucleotides (Figure 3B-C, respectively). Notably, NR4a3 knockdown also significantly reduced AngII-induced Giver expression by ~30% (Figure 3D). Conversely, transfection of phNR4A3 vector expressing human NR4A3 (gift from Dr. Dennis Bruemmer, University of Pittsburgh) increased NR4A3 RNA and protein levels, and also enhanced Giver transcript expression (~1.5 fold) versus empty vector (Figure 3E-G). To further identify the specific NBRE binding sites involved (Figure 3A), we constructed luciferase reporter constructs driven by a series of Giver WT promoter fragments spanning from -3026, -1581, -1456, and -202 to +160 bp (Figure 3H).  these data demonstrate that Nr4a3 mediates AngII-induced Giver transcription via NBRE-related site located 1515 bp upstream of Giver  transcription start site (TSS). GIVER promotes inflammatory gene expression, oxidative stress, and proliferation in RVSMC.	30566058	RID05837	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Hypertension	Giver	NR4A3	negatively-E	RNAi	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	TF	NA	NA	ENSG00000119508	NA	NA	8013	NA	CHN|CSMF|MINOR|NOR1	A Novel Angiotensin II Induced Long Non-Coding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle Cells.We knocked down Giver with Dicer substrate siRNAs targeting Giverexon sequence (siGiver) in RVSMC. Compared to the non-targeting control siRNA (siNTC), Givertranscript was reduced by ~80% and ~50% in siGiver-transfected RVSMC with or without AngII treatment, respectively (Figure 4E). Surprisingly, Giver knock-down did not reduce Nr4a3 expression, but instead enhanced Nr4a3 expression in basal and AngII treated cells (Figure 4F), suggesting that AngII-induced Giver might suppress Nr4a3 expression, likely in a negative feedback regulatory loop.  These results, suggest that Giver negatively modulates Nr4a3 expression at the transcriptional level.GIVER promotes inflammatory gene expression, oxidative stress, and proliferation in RVSMC.	30566058	RID05838	transcriptional regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hypertension	Giver	CCL2	positively-E	RNA pull-down assay;RNAi	upregulation	RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000108691	NA	NA	6347	NA	GDCF-2|HC11|MCAF|MCP-1|MCP1|MGC9434|SCYA2|SMC-CF	A Novel Angiotensin II Induced Long Non-Coding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle CellsGiver knockdown differentially regulated (up- and downregulated) the expression of genes not only on chr5 on which it is located, but also those present on other chromosomes (Figure 5A). Using RT-qPCR we validated that Giver knockdown significantly reduced the expression of Ccl2, Il6, and Tnf-_x001f_ (Tnf) (Figure 5B-D), confirming that AngII inducible Giver can indeed upregulate inflammatory genes. Furthermore, Giver knockdown inhibited AngII-induced Nox1 expression at both RNA (Figure 5E) and protein levels (Figure 5F). Conversely, exogenously (Figure 5G-J) and endogenously (by CRISPR-on) (Figure 5K-N) overexpressing Giver markedly enhanced expression of Ccl2, Il6, Tnf, and Nox1. Together, these results indicate that AngII inducible Giver enhances the expression of distally located target genes (Online Table VIII) that are closely associated with inflammation (Ccl2, Il6, and Tnf) and oxidative stress (Nox1).	30566058	RID05839	expression association	NA		UP(PAAD);DATA(GSE40174)
Hypertension	Giver	IL6	positively-E	RNA pull-down assay;RNAi	upregulation	RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000136244	NA	NA	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	A Novel Angiotensin II Induced Long Non-Coding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle CellsGiver knockdown differentially regulated (up- and downregulated) the expression of genes not only on chr5 on which it is located, but also those present on other chromosomes (Figure 5A). Using RT-qPCR we validated that Giver knockdown significantly reduced the expression of Ccl2, Il6, and Tnf-_x001f_ (Tnf) (Figure 5B-D), confirming that AngII inducible Giver can indeed upregulate inflammatory genes. Furthermore, Giver knockdown inhibited AngII-induced Nox1 expression at both RNA (Figure 5E) and protein levels (Figure 5F). Conversely, exogenously (Figure 5G-J) and endogenously (by CRISPR-on) (Figure 5K-N) overexpressing Giver markedly enhanced expression of Ccl2, Il6, Tnf, and Nox1. Together, these results indicate that AngII inducible Giver enhances the expression of distally located target genes (Online Table VIII) that are closely associated with inflammation (Ccl2, Il6, and Tnf) and oxidative stress (Nox2).	30566058	RID05840	expression association	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Hypertension	Giver	TNF	positively-E	RNA pull-down assay;RNAi	upregulation	RT-qPCR	NA	NA	inflammatory response(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000228978	NA	NA	7124	NA	DIF|TNF-alpha|TNFA|TNFSF2	A Novel Angiotensin II Induced Long Non-Coding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle CellsGiver knockdown differentially regulated (up- and downregulated) the expression of genes not only on chr5 on which it is located, but also those present on other chromosomes (Figure 5A). Using RT-qPCR we validated that Giver knockdown significantly reduced the expression of Ccl2, Il6, and Tnf-_x001f_ (Tnf) (Figure 5B-D), confirming that AngII inducible Giver can indeed upregulate inflammatory genes. Furthermore, Giver knockdown inhibited AngII-induced Nox1 expression at both RNA (Figure 5E) and protein levels (Figure 5F). Conversely, exogenously (Figure 5G-J) and endogenously (by CRISPR-on) (Figure 5K-N) overexpressing Giver markedly enhanced expression of Ccl2, Il6, Tnf, and Nox1. Together, these results indicate that AngII inducible Giver enhances the expression of distally located target genes (Online Table VIII) that are closely associated with inflammation (Ccl2, Il6, and Tnf) and oxidative stress (Nox3).	30566058	RID05841	expression association	NA		DOWN(LIHC);DATA(GSE117623)
Hypertension	Giver	NONO	NA	RNA pull-down assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	interact with protein	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	NA	NA	ENSG00000147140	NA	NA	4841	NA	NMT55|NRB54|P54|P54NRB|PPP1R114	A Novel Angiotensin II Induced Long Non-Coding RNA Giver Regulates Oxidative Stress, Inflammation, and Proliferation in Vascular Smooth Muscle CellsResults confirmed specific interaction of Giver with NONO, but not with other two interacting partners, possibly due to unavailability of rat-specific antibodies for these two proteins (Figure 7C, Online Figure XII). NONO did not co-precipitate with control Ppia. Interaction with NONO was also confirmed by RNA_x0002_pull-down followed by western blot (Figure 7D). Together, these data confirm NONO interacts with Giverand may mediate some molecular functions of Giver.	30566058	RID05842	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Prostate cancer	MEG3	QKI-5	positively-E	luciferase reporter assay	downregulation	qPT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+);	ceRNA(miR-9-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 inhibits the progression of prostate cancer by modulating miR-9-5p/QKI-5 axis.LncRNA MEG3 was a down-regulated lncRNA in prostate cancer tissues and cells and could inhibit the expression of miR-9-5p, whereas miR-9-5p down-regulated QKI-5 expression. The qRT-PCRand western blot were employed to investigating the expression levels of lncRNA MEG3, miR-9-5p and QKI-5. The luciferase reporter assay was utilized to testifying the interactions relationship among these molecules. Overexpressed MEG3 and QKI-5 could decrease the abilities of proliferation, migration and invasion in prostate cancer cells effectively and increased the apoptosis rate.	30565858	RID05843	ceRNA or sponge	NA		
Ovarian cancer	LINC00161	MAPK1	positively-E	luciferase reporter assay;Targetscan	upregulation	qPT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-128)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000226935	GRCh38_21:28539318-28540355	ENSG00000100030	NA	118421	5594	C21orf100|NCRNA00161	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Linc00161 regulated the drug resistance of ovarian cancer by sponging microRNA-128 and modulating MAPK1.the expression of linc00161, miR-128 and MAPK1 in ovarian cancer-resistant tissues and cells was tested qRT-PCRThe targeted relationship between miR-128 and linc00161 as well as the relationship between miR-128 and MAPK1 were testified by Dual luciferase gene reporter assay.Linc00161 regulated the drug resistance of ovarian cancer via modulating microRNA-128/MAPK1.	30556928	RID05844	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TP53COR1	BBC3	negatively-E	microarray analysis;RNA pull-down assay	upregulation	qPT-PCR	NA	NA	apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000105327	NA	102800311	27113	TRP53COR1|linc-p21|lincRNA-p21	JFY-1|JFY1|PUMA	Long intergenic noncoding RNA-p21 inhibits apoptosis by decreasing PUMA expression in non-small cell lung cancer.LincRNA-p21 expression in NSCLC tissues and cell lines (A549, H1299, H1650, and NCI-H2087) was determined by quantitative real-time PCR.microarray analysis and RNA pull-down assay were used to predict the target genes of lincRNA-p21.LincRNA-p21 is aberrantly upregulated in NSCLC and inhibits cell apoptosis by decreasing PUMA expression.	30556447	RID05845	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Colorectal cancer	MIR4658	CCSlnc362	negatively-E	bioinformatics;RegRNA 2.0;luciferase activities assays	upregulation	qPT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	miRNA	lncRNA	ENSG00000266154	NA	NA	NA	100616439	NA	NA	NA	variant of rs1317082 at CCSlnc362 exon 1 created a binding site for miR-4658 to reduce the expression of CCSlnc362 and thus decreased the susceptibility to CRC.We found lncRNA CCSlnc362 expression was significantly increased in CRC samples.s. RT-PCRdata showed that CCSlnc362expression was increased in CRC cell lines, comparedwith normal colorectal epithelial cell line.Luciferase assay data showed that miR-4658 mimics significantly reduced the luciferase activitiesof the construct containing rs1317082 [C] allele in a dose_x0002_dependent manner but not in the construct containingrs1317082 [T] allele.CSlnc362 promotes cell proliferation and cell cycle in CRCcell lines.The T>C variant at rs1317082 created binding sites at CCSlnc362 for miR-4658 and diminished the tumor promoting role of CCSlnc362 in CRC and eventuallyprohibited cell proliferation and cell cycle in CRC.	30518759	RID05846	expression association	NA		
Nasopharynx carcinoma	THORLNC	IGF2BP1	positively-E	RNA pull-down assay;RIP	upregulation	qPT-PCR	NA	NA	cell proliferation(+);cell growth(-)	interact with protein	binding/interaction	RNA-protein	Triptonide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000159217	NA	100506797	10642	THOR	IMP-1	Triptonide inhibits human nasopharyngeal carcinoma cell growth via disrupting Lnc-RNA THOR-IGF2BP1 signaling.A LncRNA microarray analysis was performed to identify the differentially expressed LncRNAs after TN treatment in HONE-1 cells. Quantitative real-time 355 PCR (qRT-PCR was performed to quantify and validate the identified LncRNAs. Our results 356 show that expression of one particular LncRNA, THOR ('lnc-THOR'-, was significantly 357 decreased in TN-treated cells .Lnc-THOR silencing or knockout could efficiently inhibit human cancer cells 360 via disabling IGF2BP1.Significantly, expression of Lnc-THOR, IGF2BP1 and its mRNA targets (Myc, IGF2 and 489 Gli1) are significantly elevated in human NPC tissues and cells, but barely detectable in the 490 nasopharyngeal epithelial tissues and cells.To verify the direct association between Lnc-THOR and IGF2BP1 protein, a Lnc-THOR375 pull-down assay was performed. TN treatment in NPC cells disrupted LncRNA THOR -IGF2BP1 association, causing depletion of Lnc-THOR and downregulation of IGF2BP1 mRNA targets (Myc, IGF2 and Gli0).Lnc-THOR, IGF2BP1 and its mRNA targets are elevated in human NPC tissues and cells.	30503558	RID05847	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Nasopharynx carcinoma	THORLNC	MYC	positively-E	RNA pull-down assay;RIP	upregulation	qPT-PCR	NA	NA	cell proliferation(+);cell growth(-)	NA	association	NA	Triptonide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000136997	NA	100506797	4609	THOR	bHLHe39|c-Myc|MYCC	Triptonide inhibits human nasopharyngeal carcinoma cell growth via disrupting Lnc-RNA THOR-IGF2BP1 signaling.A LncRNA microarray analysis was performed to identify the differentially expressed LncRNAs after TN treatment in HONE-1 cells. Quantitative real-time 355 PCR (qRT-PCR was performed to quantify and validate the identified LncRNAs. Our results 356 show that expression of one particular LncRNA, THOR ('lnc-THOR'-, was significantly 357 decreased in TN-treated cells .Lnc-THOR silencing or knockout could efficiently inhibit human cancer cells 360 via disabling IGF2BP1.Significantly, expression of Lnc-THOR, IGF2BP1 and its mRNA targets (Myc, IGF2 and 489 Gli1) are significantly elevated in human NPC tissues and cells, but barely detectable in the 490 nasopharyngeal epithelial tissues and cells.To verify the direct association between Lnc-THOR and IGF2BP1 protein, a Lnc-THOR375 pull-down assay was performed. TN treatment in NPC cells disrupted LncRNA THOR -IGF2BP1 association, causing depletion of Lnc-THOR and downregulation of IGF2BP1 mRNA targets (Myc, IGF2 and Gli0).Lnc-THOR, IGF2BP2 and its mRNA targets are elevated in human NPC tissues and cells.	30503558	RID05848	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Nasopharynx carcinoma	THORLNC	IGF2	positively-E	RNA pull-down assay;RIP	upregulation	qPT-PCR	NA	NA	cell proliferation(+);cell growth(-)	NA	association	RNA-protein	Triptonide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000167244	NA	100506797	3481	THOR	C11orf43|FLJ44734|IGF-II	Triptonide inhibits human nasopharyngeal carcinoma cell growth via disrupting Lnc-RNA THOR-IGF2BP1 signaling.A LncRNA microarray analysis was performed to identify the differentially expressed LncRNAs after TN treatment in HONE-1 cells. Quantitative real-time 355 PCR (qRT-PCR was performed to quantify and validate the identified LncRNAs. Our results 356 show that expression of one particular LncRNA, THOR ('lnc-THOR'-, was significantly 357 decreased in TN-treated cells .Lnc-THOR silencing or knockout could efficiently inhibit human cancer cells 360 via disabling IGF2BP1.Significantly, expression of Lnc-THOR, IGF2BP1 and its mRNA targets (Myc, IGF2 and 489 Gli1) are significantly elevated in human NPC tissues and cells, but barely detectable in the 490 nasopharyngeal epithelial tissues and cells.To verify the direct association between Lnc-THOR and IGF2BP1 protein, a Lnc-THOR375 pull-down assay was performed. TN treatment in NPC cells disrupted LncRNA THOR -IGF2BP1 association, causing depletion of Lnc-THOR and downregulation of IGF2BP1 mRNA targets (Myc, IGF2 and Gli0).Lnc-THOR, IGF2BP3 and its mRNA targets are elevated in human NPC tissues and cells.	30503558	RID05849	expression association	NA		UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Nasopharynx carcinoma	THORLNC	GLI1	positively-E	RNA pull-down assay;RIP	upregulation	qPT-PCR	NA	NA	cell proliferation(+);cell growth(-)	NA	association	NA	Triptonide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000111087	NA	100506797	2735	THOR	GLI	Triptonide inhibits human nasopharyngeal carcinoma cell growth via disrupting Lnc-RNA THOR-IGF2BP1 signaling.A LncRNA microarray analysis was performed to identify the differentially expressed LncRNAs after TN treatment in HONE-1 cells. Quantitative real-time 355 PCR (qRT-PCR was performed to quantify and validate the identified LncRNAs. Our results 356 show that expression of one particular LncRNA, THOR ('lnc-THOR'-, was significantly 357 decreased in TN-treated cells .Lnc-THOR silencing or knockout could efficiently inhibit human cancer cells 360 via disabling IGF2BP1.Significantly, expression of Lnc-THOR, IGF2BP1 and its mRNA targets (Myc, IGF2 and 489 Gli1) are significantly elevated in human NPC tissues and cells, but barely detectable in the 490 nasopharyngeal epithelial tissues and cells.To verify the direct association between Lnc-THOR and IGF2BP1 protein, a Lnc-THOR375 pull-down assay was performed. TN treatment in NPC cells disrupted LncRNA THOR -IGF2BP1 association, causing depletion of Lnc-THOR and downregulation of IGF2BP1 mRNA targets (Myc, IGF2 and Gli0).Lnc-THOR, IGF2BP4 and its mRNA targets are elevated in human NPC tissues and cells.	30503558	RID05850	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	MALAT1	miR-429	negatively-F	luciferase reporter assays;RIP	upregulation	qPT-PCR	NA	NA	apoptosis process(-);cell invasion(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Overexpression of MALAT1 contributes to cervical cancer progression by acting as a sponge of miR-429.we indicated that MALAT1 inhibited cervical cancer progression via targeting miR-429. We observed that MALAT1 was significantly upregulated in human cervical cancer cell lines compared with the ectocervical epithelial cells. the targeting correlation between MALAT1 and miR-429 was confirmed by luciferase reporter assays and RIP experiments.	30515786	RID05851	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Malignant glioma	ZNF281	PROM1	negatively-E	luciferase reporter assay;immunofluorescent assays	downregulation	qPT-PCR	NA	NA	cell invasion(-);self-renewal(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000162702	GRCh38_1:200404940-200410056	ENSG00000007062	NA	23528	8842	ZBP-99	AC133|CD133|CORD12|MCDR2|PROML1|RP41|STGD4	Novel lncRNA-ZNF281 regulates cell growth, stemness and invasion of glioma stem-like U251s cells.he expression of lncRNA-ZNF281 was lower in glioma stem-like cells (U251s)Using immunofluorescent assays, we found thatlncRNA-ZNF281 could inhibit the expression of stem markers CD133, Nestin, OCT4 andNanog. Our data demonstrates that lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s). The underlying mechanisms may involve the regulation of stem cell markers (CD133, Nestin, OCT4 and Nanog) to reduce the self-renewal ability.	30509101	RID05852	expression association	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	UP(BRCA);DATA(GSE109761)
Malignant glioma	ZNF281	Nestin	negatively-E	luciferase reporter assay;immunofluorescent assays	downregulation	qPT-PCR	NA	NA	cell invasion(-);self-renewal(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000162702	GRCh38_1:200404940-200410056	NA	NA	23528	NA	ZBP-99	NA	Novel lncRNA-ZNF281 regulates cell growth, stemness and invasion of glioma stem-like U251s cells.he expression of lncRNA-ZNF281 was lower in glioma stem-like cells (U251s)Using immunofluorescent assays, we found thatlncRNA-ZNF281 could inhibit the expression of stem markers CD133, Nestin, OCT4 andNanog. Our data demonstrates that lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s). The underlying mechanisms may involve the regulation of stem cell markers (CD133, Nestin, OCT5 and Nanog) to reduce the self-renewal ability.	30509101	RID05853	expression association	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	
Malignant glioma	ZNF281	POU5F1	negatively-E	luciferase reporter assay;immunofluorescent assays	downregulation	qPT-PCR	NA	NA	cell invasion(-);self-renewal(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000162702	GRCh38_1:200404940-200410056	ENSG00000233911	NA	23528	5460	GZP1|ZBP-99|ZBP99|ZNP-99	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	Novel lncRNA-ZNF281 regulates cell growth, stemness and invasion of glioma stem-like U251s cells.he expression of lncRNA-ZNF281 was lower in glioma stem-like cells (U251s)Using immunofluorescent assays, we found thatlncRNA-ZNF281 could inhibit the expression of stem markers CD133, Nestin, OCT4 andNanog. Our data demonstrates that lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s). The underlying mechanisms may involve the regulation of stem cell markers (CD133, Nestin, OCT6 and Nanog) to reduce the self-renewal ability.	30509101	RID05854	expression association	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	ZNF281	NANOG	negatively-E	luciferase reporter assay;immunofluorescent assays	downregulation	qPT-PCR	NA	NA	cell invasion(-);self-renewal(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000162702	GRCh38_1:200404940-200410056	ENSG00000111704	NA	23528	79923	ZBP-99	FLJ12581|FLJ40451	Novel lncRNA-ZNF281 regulates cell growth, stemness and invasion of glioma stem-like U251s cells.he expression of lncRNA-ZNF281 was lower in glioma stem-like cells (U251s)Using immunofluorescent assays, we found thatlncRNA-ZNF281 could inhibit the expression of stem markers CD133, Nestin, OCT4 andNanog. Our data demonstrates that lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s). The underlying mechanisms may involve the regulation of stem cell markers (CD133, Nestin, OCT7 and Nanog) to reduce the self-renewal ability.	30509101	RID05855	expression association	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Esophagus squamous cell carcinoma	FALEC	DRP1	negatively-E	RNA pull-down assay	upregulation	qPT-PCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000035664	NA	100874054	NA	FAL1|LINC00568|ncRNA-a1	NA	Focally amplified lncRNA on chromosome 1 regulates apoptosis of esophageal cancer cells via DRP1 and mitochondrial dynamics.we compared. the expression patterns of lncRNA FAL1 viareal-time PCR analysis using 56 pairs of ESCC tissues and adja_x0002_cent normal tissues. The results in Fig. 3A show that the levelof FAL1 was remarkably higher in ESCC tissues than in adja_x0002_cent normal tissuesTo determine the effects of FAL1 on mitochondrial dynamicsproteins, the expression of FAL1 was knocked down by transfection with FAL1 siRNA in both KYSE450 and EC9706 cells.Successful knockdown of FAL1 in KYSE450 cells is shown inFig. 4A.  Interestingly, we found that the inhibition of FAL1 significantly increased the expression of DRP1 in KYSE450 cells.we identified a novel molecular mechanismfor FAL1 in the regulation of ESCC as it regulates the expres_x0002_sion of DRP1 and mitochondrial dynamics. Based on theseobservations, we speculate that a novel therapeutic strategythrough regulating the balance of the FAL1-DRP1 pathway andmitochondrial dynamics should be explored for the treatmentof ESCC.	30501006	RID05856	expression association	NA		
Breast cancer	HOTAIR	miR-218	negatively-F	RNA pull-down assay	upregulation	qPT-PCR	NA	NA	apoptosis process(-);DNA damage	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of lncRNA HOTAIR sensitizes breast cancer cells to ionizing radiation through activating miR-218.Our data showed that HOTAIR (HOX antisense intergenic RNA) was up-regulated in breast cancer cells and tissues, and the expression of HOTAIR increased following irradiation.we found that the radiosentizing effects of HOTAIR were related to the up-regulation of miR-218, a ceRNA of HOTAIR.HOTAIR inhibition sensitizes breast cancer cells to ionizing radiation, induced severe DNA damage and activated apoptosis pathways.	30429228	RID05857	ceRNA or sponge	NA		
Breast cancer	NLIPMT	GSK3	negatively-E	RNAi	downregulation	qPT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Overexpression of novel lncRNA NLIPMT inhibits metastasis by reducing phosphorylated glycogen synthase kinase 3beta  in breast cancer.glycogen synthase kinase 3beta (GSK3beta) was identified as an effector protein regulated by lnc-NLIPMT. Inhibition of GSK3beta activity restored NLIPMT-induced inhibition of proliferation and motility in breast cancer cells.Specific qRT-PCRprimers were designedfor these lncRNAs (Supporting Information Table 1). As a novellncRNA, lnc-NLIPMT was validated in BC cohort.Similar to our PCR results, lnc-NLIPMT wasdownregulated in tumor tissues than in normal tissues.To determine the potential target protein by NLIPMT, iTRAQcombined with nano LC-MS/MS analysis was used to identify thedifferentially expressed proteins in MDA-MB-231 and BT549 cellsafter transfection .Inhibition of GSK3beta activity restores thelnc-NLIPMT overexpression-mediated decrease in theproliferation and motility of BC cells.	30417392	RID05858	expression association	metastasis		
Lung cancer	XIC	MIR17	negatively-E		upregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	ENSG00000284536	NA	7502	406952	SXI1|XCE|XIST	MIR17-5p|MIR91|MIRN17|MIRN91|hsa-mir-17|miR-17|miR17-3p|miRNA17|miRNA91	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05859	ceRNA or sponge	chemoresistance		
Lung cancer	MALAT1	miR-101	negatively-E		upregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05860	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MEG3	miR-21-5p	negatively-E		downregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05861	ceRNA or sponge	chemoresistance		
Lung cancer	SNHG12	miR-181a	negatively-E		upregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05862	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Lung cancer	GAS5	miR-21	negatively-E		downregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05863	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Lung cancer	CCAT1	let-7c	negatively-E		upregulation		NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000247844	NA	ENSG00000199030	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05864	ceRNA or sponge	chemoresistance		
Lung cancer	AGER	miR-185	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000206320	GRCh38_CHR_HSCHR6_MHC_QBL_CTG1:32138576-32141932	ENSG00000208023	NA	177	NA	RAGE|SCARJ1|sRAGE	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05865	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Lung cancer	SNHG7	miR-193b	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05866	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Lung cancer	HATAIR	miR-613	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05867	ceRNA or sponge	metastasis		
Lung cancer	HOTTIP	miR-547-5p	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05868	ceRNA or sponge	metastasis		
Lung cancer	SNHG6	miR-146-a	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05869	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Lung cancer	CCAT1	miR-130a-3p	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05870	ceRNA or sponge	metastasis		
Lung cancer	HOXO-AS1	miR-147a	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05871	ceRNA or sponge	metastasis		
Lung cancer	BLACAT1	miR-144	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	linc-UBC1|LINC00912|onco-lncRNA-30	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05872	ceRNA or sponge	metastasis		
Lung cancer	LINC00319	MIR32	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000207698	NA	284836	407036	C21orf125|NCRNA00319|PRED49	MIRN32|hsa-mir-32|miR-32|miRNA32	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05873	ceRNA or sponge	metastasis		
Lung cancer	MIAT	miR-150	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05874	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Lung cancer	XLOC-00846	MIR874	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	ENSG00000216009	NA	NA	100126343	NA	MIRN874|hsa-mir-874|mir-874	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05875	ceRNA or sponge	metastasis		
Lung cancer	LINC00858	MIR422A	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000199156	NA	170425	494334	CRCAL-2	MIRN422A	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05876	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	
Lung cancer	GAS5	miR-23a	negatively-E		downregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05877	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Lung cancer	RMRP	miR-206	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	NA	NA	6023	NA	CHH|NME1|RMRPR|RRP2	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05878	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Lung cancer	UCA1	miR-193a-3p	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05879	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	
Lung cancer	NEAT1	MIR499B	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000283441	NA	283131	100616134	LINC00084|NCRNA00084|TncRNA|VINC	MIR499A|hsa-mir-499b	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05880	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	NEAT1	miR-377-3p	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05881	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	NEAT1	miR-181a-5p	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05882	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	NEAT1	miR-98-5p	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05883	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Lung cancer	MALAT1	miR-124	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05884	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	miR-204	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05885	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	HOXA11-AS	miR-200b	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05886	ceRNA or sponge	metastasis		
Lung cancer	HOXA11-AS	miR-124	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05887	ceRNA or sponge	metastasis		
Lung cancer	PVT1	miR-126	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05888	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Lung cancer	PVT1	miR-195	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05889	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Lung cancer	PVT1	miR-497	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05890	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Lung cancer	PVT1	miR-199a-5p	negatively-E				NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05891	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Lung cancer	H19	miR-484	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05892	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	
Lung cancer	H19	miR-107	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000198997	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05893	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	
Lung cancer	XIST	miR-449a	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05894	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Lung cancer	XIST	miR-140	negatively-E		upregulation		NA	NA	cell proliferation;cell invasion;cell metastasis;apoptosis process	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05895	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Lung cancer	H19	miR-484	negatively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05896	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Lung cancer	LINC00673	miR-150-5p	negatively-E				NA	NA	epithelial to mesenchymal transition(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72290091-72640472	NA	NA	100499467	NA	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05897	ceRNA or sponge	NA		
Lung cancer	MALAT1	miR-204	negatively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05898	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	XIC	MIR367	negatively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	ENSG00000199169	NA	7502	442912	SXI1|XCE|XIST	MIRN367|hsa-mir-367	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05899	ceRNA or sponge	NA		
Lung cancer	XIST	miR-141	negatively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Multidimensional communication of microRNAs and long non-coding RNAs in lung cancer.	30417217	RID05900	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Ischemic stroke	SNHG1	MIA3	positively-E	RNAi;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell injury(-)	ceRNA(miR-338)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000154305	NA	23642	375056	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ARNT|D320|ODCD2|TANGO|TANGO1|UNQ6077	LncRNA SNHG1 alleviates OGD induced injury in BMEC via miR-338/HIF-1beta  axis.The expression of SNHG1 and miR-338 after OGD were examined by qPCR.shRNA against SNHG1 was used to knockdown SNHG1 in BMEC. MiR-338-3p mimic and inhibitor were used to change the expression of miR-338 in BMEC. The relationship between SNHG1 and miR-338, and the relationship between miR-338 and HIF-1beta  were clarified using RNA pull-down and luciferase reporter gene assays, respectively.luciferase reporter assay showed that HIF-1beta was a direct target of miR-338.SNHG1 and miR-338 were upregulated in OGD induced BMEC.SNHG1 exerted protective effects against OGD induced injury via sponging miR-338.	30414401	RID05901	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939,GSE86978)
Ischemic stroke	SNHG1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000171791	NA	23642	596	LINC00057|lncRNA16|NCRNA00057|UHG	Bcl-2|PPP1R50	LncRNA SNHG1 alleviates OGD induced injury in BMEC via miR-338/HIF-1beta  axis.The expression of SNHG1 and miR-338 after OGD were examined by qPCR.SNHG1 and miR-338 were upregulated in OGD induced BMEC. SNHG1 silence aggravated OGD-induced cell apoptosis by down-regulating Bcl-2, HIF-1beta and VEGF-A, and upregulating caspase 3 activity and Bax.	30414401	RID05902	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ischemic stroke	SNHG1	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000112715	NA	23642	7422	LINC00057|lncRNA16|NCRNA00057|UHG	VEGF|VEGF-A|VPF	LncRNA SNHG1 alleviates OGD induced injury in BMEC via miR-338/HIF-1beta  axis.The expression of SNHG1 and miR-338 after OGD were examined by qPCR.SNHG1 and miR-338 were upregulated in OGD induced BMEC. SNHG1 silence aggravated OGD-induced cell apoptosis by down-regulating Bcl-2, HIF-1beta and VEGF-A, and upregulating caspase 4 activity and Bax.	30414401	RID05903	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Ischemic stroke	SNHG1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000087088	NA	23642	581	LINC00057|lncRNA16|NCRNA00057|UHG	BCL2L4	LncRNA SNHG1 alleviates OGD induced injury in BMEC via miR-338/HIF-1beta  axis.The expression of SNHG1 and miR-338 after OGD were examined by qPCR.SNHG1 and miR-338 were upregulated in OGD induced BMEC. SNHG1 silence aggravated OGD-induced cell apoptosis by down-regulating Bcl-2, HIF-1beta and VEGF-A, and upregulating caspase 5 activity and Bax.	30414401	RID05904	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ischemic stroke	SNHG1	Caspase3	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	LncRNA SNHG1 alleviates OGD induced injury in BMEC via miR-338/HIF-1beta  axis.The expression of SNHG1 and miR-338 after OGD were examined by qPCR.SNHG1 and miR-338 were upregulated in OGD induced BMEC. SNHG1 silence aggravated OGD-induced cell apoptosis by down-regulating Bcl-2, HIF-1beta and VEGF-A, and upregulating caspase 6 activity and Bax.	30414401	RID05905	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Colorectal cancer	SNHG5	CREB5	positively-E	RNA pull-down assay;luciferase reporter assays	upregulation	qPT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);apoptosis process(-)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000146592	NA	387066	9586	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	CRE-BPA|H_GS165L15.1	LncRNA SNHG5 promoted proliferation, migration and metastasis of CRC cells but inhibited apoptosis by modulating miR-132-3p/CERB5.25 pairs of samples containing CRC tissues and matched para-tumor tissues were obtained to examine SNHG5, miR-132-3p and CREB5 expression by qRT-PCRor western blot. The targeted relationship between miR-132-3p and SNHG5 or CREB5 was confirmed by dual luciferase report assay as well as RNA pull-down assay. SNHG5 or CREB5 was up-regulated in CRC tissues and cells, whereas miR-132-3p was down-regulated. Overexpression of SNHG5 and CREB5 resulted in the enhancement of proliferation, metastasis, migration and the inhibition of apoptosis in CRC cells, while miR-132-3p led to the opposite result. LncRNA SNHG5 promoted proliferation, migration and metastasis of CRC cells but inhibited apoptosis by modulating miR-132-3p/CERB5.	30395767	RID05906	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Urinary bladder cancer	MALAT1	CCND1	positively-E	RNA pull-down assay	upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000110092	NA	378938	595	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL1|D11S287E|PRAD1|U21B31	Knockdown of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 inhibits the proliferation and migration of bladder cancer cells by modulating the microRNA-34a/cyclin D1 axis.The present study revealed that MALAT1 was significantly upregulated in BC tissues and cell lines compared with the adjacent non-tumour tissues and the normal urinary tract epithelial cell line SV-HUC-1, respectively.knockdown of MALAT1 significantly inhibited BC cell proliferation and migration by targeting microRNA (miR)-34a. The expression levels of miR-34a were significantly decreased in BC tissues and cell lines compared with that of adjacent non-tumour tissues and SV-HUC-1 cells. In addition, the expression of miR-34a was inversely correlated with the expression of MALAT1 in BC tissues. The present study revealed that cyclin D1 (CCND1) was identified as a target gene of miR-34a, and its expression was negatively mediated by miR-34a in BC cells. In conclusion, the present findings demonstrated that the knockdown of lncRNA MALAT1 inhibits the proliferation and migration of BC cells by modulating the miR-34a/CCND1 axis, suggesting that the MALAT1/miR-34a/CCND1 axis may be a potential therapeutic target for BC treatment.	30387807	RID05907	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Pancreatic ductal adenocarcinoma	DLEU1	CXCR4	positively-E	bioinformatics;luciferase reporter assay	upregulation	qPT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-381)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000121966	NA	10301	7852	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	Long noncoding RNA DLEU1 aggravates pancreatic ductal adenocarcinoma carcinogenesis via the miR-381/CXCR4 axis.Our studies indicated that the DLEU1 expression level was upregulated in PDAC tissue samples compared with adjacent normal tissue. Bioinformatics analysis predicted that miR-381 potentially targeted the DLEU1 3'-untranslated region (UTR), suggesting an interaction between miR-381 and DLEU1. Furthermore, miR-381 also targeted the chemokine receptor-4 (CXCR4) messenger RNA 3'-UTR, which was validated by luciferase reporter assay.our study demonstrated the oncogenic role of DLEU1 in clinical PDAC specimens and cellular experiments, showing the potential involvement of DLEU1/miR-381/CXCR4 pathway. These results provide novel insight into PDAC tumorigenesis.	30382579	RID05908	ceRNA or sponge	chemoresistance	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Aplastic anemia	MEG3	TIGIT	positively-E	bioinformatics;miRcode;TargetScan	downregulation	qPT-PCR	NA	NA	cell viability(-)	ceRNA(miR-23a)	regulation	RNA-protein	NA	NA	NA	Immune system disease	Anemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000181847	NA	55384	201633	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DKFZp667A205|FLJ39873|VSIG9|VSTM3	MEG3 modulates TIGIT expression and CD4+T cell activation through absorbing miR-23a.MEG3 expression decreased in CD4+T cells of patients with AA.MEG3 expression was negatively correlated with miR-23a in CD4+T cells of patients with AA.Bioinformatics analysis by using miRcode (http://www.mircode.org) was used to clarify the underlying relation_x0002_ship between MEG3 and miR-23a. Data showed that MEG3 contained one conserved target site of miR-23a .we found that MEG3 expression was significantly downregulated in CD4T cells derived from AA patients. these results indicate that MEG3 inhibited CD4+T cell activity by negatively miR-23.	30382432	RID05909	ceRNA or sponge	NA		DOWN(PRAD,BRCA);DATA(GSE67980,GSE109761,GSE111065,GSE51827,GSE75367)
Intervertebral disc degeneration	LINC00641	ATG5	positively-E	luciferase reporter assays;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000258441	GRCh38_14:21200079-21206900	ENSG00000057663	NA	283624	9474	NA	APG5|APG5L|ASP|hAPG5	LINC00641 regulates autophagy and intervertebral disc degeneration by acting as a competitive endogenous RNA of miR-153-3p under nutrition deprivation stress.Quantitative reverse-transcription polymerase chain reaction (RT-qPCR) was used to analyze miR-153-3p and LINC00641 in response to nutrient deprivation.Pull-down assay and RNA fluorescent in situ hybridization were performed to validate LINC00641 target and the location.Upregulation of LINC00641 and downregulation of miR-153-3p are detected in NP cells under nutritional stress. LINC00641 can regulate autophagic cell death by targeting miR-153-3p and autophagy-related gene 5 (ATG5). MiR-153-3p inhibits autophagy and IDD by targeting ATG5.LINC00641 can regulate autophagic cell death by targeting miR-153-3p and autophagy-related gene 5 (ATG5).	30378116	RID05910	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Acute myocardial infarction	SLC8A1-AS1	SLC8A1	negatively-E	bioinformatics;luciferase reporter assay	downregulation	microarray	NA	NA	cGMP/PKG signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000227028	GRCh38_2:39786453-40255209	ENSG00000183023	NA	100128590	6546	NA	NCX1	LncRNA SLC8A1-AS1 protects against myocardial damage through activation of cGMP-PKG signaling pathway by inhibiting SLC8A1 in mice models of myocardial infarction.microarray data GSE66360 provided evidence indicating that SLC8A1-AS1 was poorly expressed in AMI. lncRNA SLC8A1-AS1, by downregulating SLC8A1 and activating the cGMP-PKG signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage.	30378115	RID05911	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	CASC2	miR-19a	negatively-F	miRcode;luciferase reporter gene assay	downregulation	qPT-PCR	NA	NA	chemoresistance(+)	sponse	binding/interaction	RNA-RNA	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000215417	NA	255082	NA	C10orf5	NA	Down-regulation of CASC2 contributes to cisplatin resistance in gastric cancer by sponging miR-19a.Results revealed that CASC2 was decreased in DDP-resistant gastric cancer tissues and cells.Gastric cancer patients with low CASC2 expression levels had a poor prognosis.CASC2 could function as a miR-19a sponge. miR-19a inhibition could overcome DDP resistance in BGC823/DDP and SGC7901/DDP cells, while miR-19a overexpression led to DDP resistance in BGC823 and SGC7901 cells.CASC2 overexpression overcame DDP resistance in gastric cancer by sponging miR-19a, providing a novel therapeutic target for gastric cancer chemoresistance.	30372881	RID05912	ceRNA or sponge	chemoresistance,prognosis	UP(LIHC);DATA(GSE117623)	
Hepatocellular carcinoma	DRHC	MYBBP1A	positively-F	RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(-);cell invasion(-);MEK/ERK signaling pathway(-)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000198265	GRCh38_17:67070444-67245989	ENSG00000132382	NA	NA	10514	NA	FLJ37886|P160|PAP2|Pol5	lncRNA DRHC inhibits proliferation and invasion in hepatocellular carcinoma via c-Myb-regulated MEK/ERK signaling.We initially profiled the expression of lncRNAs in 5 HCC tissues and their paired adjacent noncancerous tissues by lncRNA array. The 10 most significantly changed lncRNAs were then This article is protected by copyright. All rights reserved validated in 112 pairs of HCC and adjacent nontumor tissues by RT-PCRPatients with low lncRNA DRHC levels tended to have larger tumor .LncRNA DRHC bound with MYBBP1A and inhibited MEK/ERK signaling through lncRNA DRHC/MYBBP1A/c-Myb complex.Moreover, we found that lncRNA DRHC interacted with MYBBP1A and modulated MEK/ERK signaling via c-Myb	30362626	RID05913	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	DRHC	MYB	positively-F	RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(-);cell invasion(-);MEK/ERK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000198265	GRCh38_17:67070444-67245989	ENSG00000118513	NA	NA	4602	NA	c-myb	lncRNA DRHC inhibits proliferation and invasion in hepatocellular carcinoma via c-Myb-regulated MEK/ERK signaling.We initially profiled the expression of lncRNAs in 5 HCC tissues and their paired adjacent noncancerous tissues by lncRNA array. The 10 most significantly changed lncRNAs were then This article is protected by copyright. All rights reserved validated in 112 pairs of HCC and adjacent nontumor tissues by RT-PCRPatients with low lncRNA DRHC levels tended to have larger tumor .LncRNA DRHC bound with MYBBP1A and inhibited MEK/ERK signaling through lncRNA DRHC/MYBBP1A/c-Myb complex.Moreover, we found that lncRNA DRHC interacted with MYBBP1A and modulated MEK/ERK signaling via c-Myb	30362626	RID05914	expression association	NA		
Oral cavity cancer	HOTAIR	miR-126	negatively-F	RNA pull-down assay;RNAi	upregulation	qPT-PCR	NA	NA	PI3K/AKT/GSK3beta signaling pathway(-);apoptosis process(-);cell autophagy(+)	sponse	binding/interaction	RNA-RNA	Nimbolide	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Nimbolide, a neem limonoid inhibits cytoprotective autophagy to activate apoptosis via modulation of the PI3K/Akt/GSK-3beta signalling pathway in oral cancer.Downregulation of HOTAIR, a competing endogenous RNA that sponges miR-126 may be a major contributor to the inactivation of PI3K/Akt/GSK3beta signalling by nimbolide.we frst detected the infuence of HOTAIR on miR-126 expression in several OS cell lines. As shown in Fig. 4a and Figure s3, the miR-126 expression level was signifcantly increased after HOTAIR knockdown, indicat_x0002_ing that the depletion of HOTAIR led to the up-regulation of miR-126 expression.	30352996	RID05915	ceRNA or sponge	NA		
Oral cavity cancer	HOTAIR	GSK3	negatively-E	RNAi	upregulation	qPT-PCR	NA	NA	PI3K/AKT/GSK3beta signaling pathway(-);apoptosis process(-);cell autophagy(+)	NA	association	RNA-protein	Nimbolide	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Nimbolide, a neem limonoid inhibits cytoprotective autophagy to activate apoptosis via modulation of the PI3K/Akt/GSK-5beta signalling pathway in oral cancer.Overexpression of miR-126 upregulated the expression of GSK-3beta compared to control cells. Addition of nimbolide to miR-126 overexpressed cells enhanced this effect. Additionally, nimbolide downregulated the expression of Homeobox transcript antisense intergenic RNA (HOTAIR), a lncRNA that inhibits miR-126. Taken together, our results suggest that inhibition of HOTAIR by nimbolide could increase the expression of miR-126 leading to activation of GSK-3beta.	30352996	RID05916	expression association	NA		
Breast cancer	lnc-ATB	ZEB1	positively-E	luciferase reporter assay;RNAi	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.e found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression.we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects. Moreover, we proved that miR-141-3p directly bound to the 3' untranslated region (UTR) of ZEB1 and ZEB2 and negatively regulated ZEB1 and ZEB2 expression.our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-4p.Finally, we demonstrated that miR-141-3p could bind to the 3'-untranslated region (UTR) of ZEB1 and ZEB2 in 293T cells by luciferase reporter assay	30352165	RID05917	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	lnc-ATB	ZEB2	positively-E	luciferase reporter assay;RNAi	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-141-4p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000169554	NA	NA	9839	NA	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.e found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression.we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects. Moreover, we proved that miR-141-3p directly bound to the 3' untranslated region (UTR) of ZEB1 and ZEB2 and negatively regulated ZEB1 and ZEB2 expression.our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-4p.Finally, we demonstrated that miR-141-3p could bind to the 3'-untranslated region (UTR) of ZEB1 and ZEB2 in 294T cells by luciferase reporter assay	30352165	RID05918	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	lnc-ATB	N-cadherin	positively-E	RNAi	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.e found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression.we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects.our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-6p.	30352165	RID05919	expression association	NA		
Breast cancer	lnc-ATB	vimentin	positively-E	RNAi	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.e found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression.we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects.our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-7p.	30352165	RID05920	expression association	NA		
Breast cancer	lnc-ATB	E-cadherin	negatively-E	RNAi	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.e found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression.we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects.our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-8p.	30352165	RID05921	expression association	NA		
Gastric cancer	HOTAIR	PTEN	positively-E	luciferase reporter assay	upregulation	qPT-PCR	NA	NA	chemosensitivity(-);cell proliferation(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	Cisplatin;Adriamycin;Mitomycin;5-fluororacil	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXC-AS4|HOXC11-AS1|NCRNA00072	BZS|MHAM|MMAC1|PTEN1|TEP1	The contrary functions of lncRNA HOTAIR/miR-17-5p/PTEN axis and Shenqifuzheng injection on chemosensitivity of gastric cancer cells.The over-expressed HOTAIR and miR-17-5p, as well as under-expressed PTEN tended to significantly facilitate the viability, EMT process and proliferation of MKN28 cells that were subject to treatment of chemo-therapies .HOTAIR expression was positively correlated with miR-17-5p expression among the 317 gastriccancer patients investigated.The luciferase activity of pmirGLO-HOTAIR-Wt+miR-17-5p groupwas far below that of pmirGLO-HOTAIR-Wt+miR-NC group(P < 0.05), but pmirGLO-HOTAIR-Mut+miR-17-5p group possesseda luciferase enzyme activity that was no different from pmirGLO-HOTAIR-Wt+miR-NC group.MiR-17-5p inhibited PTEN to modify viability,proliferation, apoptosis, and EMT process of gastriccancer cells.	30338929	RID05922	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	H19	let-7c	negatively-F	RNAi	upregulation	qPT-PCR	NA	NA	WNT signaling pathway(-)	sponse	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000199030	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 regulation of oestrogen induction of symmetric division is achieved by antagonizing Let-7c in breast cancer stem-like cells.H19 inhibition was achieved by lentiviral infection, and the effi-ciency was about 70% by applying (qRT-PCR, which increased theasymmetric division ratio greatly, and Axitinib attenuated the H19stimulation of symmetric division.To identify the functional regulation of H19 on Let-7c, we con-structed the MS2-associated H19-Let-7c binding site to performthe RNA immunoprecipitation, which could pull down H19 andMS2, referring to Let-7c binding site. H19 inhibition did not restoreLet-7c level and failed to degrade Let-7c expression after connection.H19 overexpression and Wnt pathway stimulated the symmetric divisioneffectively, and Let-7c counteracting the promoting roles of Wntsignalling, we therefore hypothesized the signalling cascade of H19/Let-7c/ESR1/Wnt.	30338598	RID05923	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Oral squamous cell carcinoma	LINC01133	GDF15	negatively-E	RNAi;RT-qPCR	downregulation	RT-qPCR	NA	NA	cell metastasis(-);cell migration(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000130513	NA	100505633	9518	lncRNA-PAGBC	MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Long noncoding RNA LINC01133 inhibits oral squamous cell carcinoma metastasis through a feedback regulation loop with GDF15.The RNA levels of LINC01133 and growth and differentiation factor 15 (GDF15) in tissue samples from OSCC patients, and OSCC cell lines were tested by real-time quantitative polymerase chain reaction (RT-qPCR).Downstream genes of LINC01133 were screened using RNA-seq and validated by RT-qPCR.LINC01133 inhibited OSCC cell migration and invasion. RNA-seq data showed that Long noncoding RNA LINC01133 inhibits oral squamous cell carcinoma metastasis through a feedback regulation loop with GDF15.LINC01133 inhibited GDF15, and GDF15 could rescue inhibition of OSCC cell migration and invasion caused by LINC01133.	30332510	RID05924	expression association	metastasis	UP(BRCA);DATA(GSE111065)	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Oral squamous cell carcinoma	GDF15	LINC01133	negatively-F	RNAi;RT-qPCR	downregulation	RT-qPCR	NA	NA	cell metastasis(+);cell migration(+)	NA	regulation	protein-RNA	NA	NA	NA	Cancer	Oral cavity cancer	PCG	lncRNA	ENSG00000130513	NA	ENSG00000224259	GRCh38_1:159958035-159984750	9518	100505633	MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	lncRNA-PAGBC	Long noncoding RNA LINC01133 inhibits oral squamous cell carcinoma metastasis through a feedback regulation loop with GDF15.The RNA levels of LINC01133 and growth and differentiation factor 15 (GDF15) in tissue samples from OSCC patients, and OSCC cell lines were tested by real-time quantitative polymerase chain reaction (RT-qPCR).Downstream genes of LINC01133 were screened using RNA-seq and validated by RT-qPCR.LINC01133 inhibited OSCC cell migration and invasion. RNA-seq data showed that Long noncoding RNA LINC01133 inhibits oral squamous cell carcinoma metastasis through a feedback regulation loop with GDF15.LINC01133 inhibited GDF15, and GDF15 could rescue inhibition of OSCC cell migration and invasion caused by LINC01134.	30332510	RID05925	expression association	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(BRCA);DATA(GSE111065)
Non-small cell lung cancer	LINC00342	TP53	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000232931	GRCh38_2:95807052-95835003	ENSG00000141510	NA	150759	7157	NCRNA00342	LFS1|p53	Investigation of LINC00342 as a poor prognostic biomarker for human patients with non-small cell lung cancer.pathways, which were analyzed by western blot We found that LINC00342 was upregulated in the tissues, serum, and PBMC of patients with NSCLC.A multistage validation and risk score formula detection analysis was used. The effect of LINC00342 on proliferation was assessed by MTT, p53, and PTEN pathways, which were analyzed by western blotLINC00342 promoted proliferation by inhibiting the expression of p53 and PTEN proteins in NSCLC cell lines.	30320899	RID05926	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC00342	PTEN	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000232931	GRCh38_2:95807052-95835003	ENSG00000171862	NA	150759	5728	NCRNA00342	BZS|MHAM|MMAC1|PTEN1|TEP1	Investigation of LINC00342 as a poor prognostic biomarker for human patients with non-small cell lung cancer.pathways, which were analyzed by western blot We found that LINC00342 was upregulated in the tissues, serum, and PBMC of patients with NSCLC.A multistage validation and risk score formula detection analysis was used. The effect of LINC00342 on proliferation was assessed by MTT, p53, and PTEN pathways, which were analyzed by western blotLINC00342 promoted proliferation by inhibiting the expression of p54 and PTEN proteins in NSCLC cell lines.	30320899	RID05927	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Liver cancer	HULC	MIR186	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	sponse	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000251164	NA	ENSG00000207721	NA	728655	406962	HCCAT1|LINC00078|NCRNA00078	MIRN186|miR-186	Long non-coding RNA HULC affects downstream-related targets to regulate migration and invasion of hepatoma cells.The expression of highly upregulated in liver cancer (HULC) in hepatocellular carcinoma, and adjacent normal liver tissues and different hepatocellular carcinoma cells were detected by qPCR.Dual-luciferase reporter gene detected the interaction between HULC and miR-186.HULC plays an important role in the occurrence and development of hepatocellular carcinoma and can influence the biological behavior of hepatoma cells by regulating the expression of downstream-related targets.	30317774	RID05928	ceRNA or sponge	NA		
Urinary bladder cancer	PVT1	CDK1	positively-E	bioinformatics;Omnibus	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-31)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000170312	NA	5820	983	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CDC2|CDC28A	LncRNA PVT1 regulates growth, migration, and invasion of bladder cancer by miR-31/ CDK1.LncRNA PVT1 and mRNA CDK1 had a higher expression in bladder cancer cells than that in neighboring tissues.The Gene Expression Omnibus database was used for analyzing the differentially expressed lncRNA and messenger RNA (mRNA) in bladder cancer tissues, with the highly expressed lncRNA PVT1 and mRNA CDK1 screened out.LncRNA PVT1 was overexpressed in bladder cancer cells, and it was downregulated miR-31 to enhance CDK1 expression and facilitate bladder cancer cells proliferation, migration, and invasion.	30317572	RID05929	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Urinary bladder cancer	NBAT1	SOCS6	positively-E	bioinformatics;RNA pull-down assay;RIP;TargetScan	downregulation	qPCR	NA	NA	cell metastasis(-);cancer progression(-)	ceRNA(miR-21-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000170677	NA	729177	9306	CASC14|NBAT-1	CIS4|Cish4|HSPC060|SOCS4|SSI4|STAI4|STATI4	Long noncoding RNA neuroblastoma-associated transcript 1 gene inhibits malignant cellular phenotypes of bladder cancer through miR-21/SOCS6 axis.NBAT1 gene was low-expressed in BC tissues and cell lines and its low-expression was related with high pathological grade and metastasis of BC.SOCS6 gene was a target gene of miR-21-5p.low-expression of NBAT1 is associated with the progress and metastasis of BC, and NBAT1 inhibits malignant cellular phenotypes through miR-21-5p/SOCS6 axis in BC.	30310053	RID05930	ceRNA or sponge	metastasis		UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Lung cancer	CYTOR	CCND1	positively-E	bioinformatics;luciferase reporter assay	upregulation	microarray;qPCR	NA	NA	cell cycle(+)	ceRNA(miR-193b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000110092	NA	112597	595	C2orf59|LINC00152|MGC4677|NCRNA00152	BCL1|D11S287E|PRAD1|U21B31	The linc00152 Controls Cell Cycle Progression by Regulating CCND1 in 16HBE Cells Malignantly Transformed by Cigarette Smoke Extract.The linc00152 serum level in CSE-exposed individuals was increased in a dose-dependent manner and its high expression associated with metastasis and proliferation of lung cancer tissue.linc00152 promoted cyclin D1 expression and G1/S transition by functioning as an endogenous competitive RNA targeting miR-193b.	30289508	RID05931	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Cataract	H19	CRYAA	positively-E	bioinformatics;luciferase reporter assay	upregulation	sequencing;qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);apoptosis process(+)	ceRNA(miR-675)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000160202	NA	283120	1409	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CRYA1|HSPB4	Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function.LncRNA sequencing was performed to identify differentially expressed lncRNAs between the capsules of transparent and nuclear ARC lenses. Expression validation was confirmed by qRT-PCRBioinformatics and luciferase reporter assays were used to identify the binding target of miR-675. H19 is the precursor of miR-675, and a reduction of H19 inhibits miR-675 expression.Moreover, miR-676 increases the proliferation and migration while decreasing the apoptosis of HLECs upon oxidative stress.	30286462	RID05932	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Prostate cancer	TTTY15	let-7	negatively-F	CRISPR/Cas9	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000233864	NA	NA	NA	64595	NA	NCRNA00138	NA	The Long Noncoding RNA TTTY15, Which Is Located on the Y Chromosome, Promotes Prostate Cancer Progression by Sponging let-7;TTTY15 promoted PCa by sponging the microRNA let-7, consequently increasing CDK6 and FN1 expression;The Y-chromosomal lncRNA TTTY15 was upregulated in most PCa tissues and could promote PCa progression by sponging let-7.	30527798	RID05933	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Osteoarthritis	THRIL	miR-125b	negatively-F	RNAi	downregulation	qRT-PCR	NA	NA	JAK1/STAT3 signaling pathway(+);NF-kB signaling pathway(+)	sponge	regulation	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000280634	GRCh38_12:125025434-125027410	NA	NA	102659353	NA	BRI3BP-AS1|Linc1992|TCONS_00020260	NA	Long non-coding RNA THRIL promotes LPS-induced inflammatory injury by down-regulating microRNA-125b in ATDC5 cells;overexpression of THRIL enhanced the LPS-induced JAK1/STAT3 and NF-kB pathways activation by down-regulating miR-125b;Overexpression of THRIL promoted LPS-induced ATDC5 cell inflammatory injury by down-regulating miR-125b and then activating JAK1/STAT3 and NF-kB pathways.	30521964	RID05934	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	
Hepatocellular carcinoma	CASC11	PTEN	negatively-E	ChIP;luciferase reporter assay;RNAi;RIP;JASPAR	upregulation	qRT-PCR	TCGA;UCSC	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000171862	NA	100270680	5728	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	BZS|MHAM|MMAC1|PTEN1|TEP1	STAT3-induced upregulation of lncRNA CASC11 promotes the cell migration, invasion and epithelial-mesenchymal transition in hepatocellular carcinoma by epigenetically silencing PTEN and activating PI3K/AKT signaling pathway;Loss of CASC11 function efficiently suppressed cell migration, invasion and epithelial-mesenchymal transition (EMT). The mechanism which led to the upregulation of CASC11 was investigated;CASC11 epigenetically silenced PTEN by binding with EZH2. Finally, rescue assays were conducted to make confirmation. CASC11 was found to be activated by the transcription factor STAT3. Mechanically, the enhancer of zeste homolog 2 (EZH2) was found to be a binding partner of CASC11. Moreover, CASC11 epigenetically silenced PTEN by binding with EZH2.	30503497	RID05935	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	STAT3	CASC11	positively-F	ChIP;luciferase reporter assay;RNAi;RIP;JASPAR	upregulation	qRT-PCR	TCGA;UCSC	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	interact with protein	regulation	NA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000249375	GRCh38_8:127686343-127738987	6774	100270680	APRF	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	STAT3-induced upregulation of lncRNA CASC11 promotes the cell migration, invasion and epithelial-mesenchymal transition in hepatocellular carcinoma by epigenetically silencing PTEN and activating PI3K/AKT signaling pathway;Loss of CASC11 function efficiently suppressed cell migration, invasion and epithelial-mesenchymal transition (EMT). The mechanism which led to the upregulation of CASC11 was investigated;CASC11 epigenetically silenced PTEN by binding with EZH2. Finally, rescue assays were conducted to make confirmation. CASC11 was found to be activated by the transcription factor STAT3. Mechanically, the enhancer of zeste homolog 2 (EZH2) was found to be a binding partner of CASC11. Moreover, CASC11 epigenetically silenced PTEN by binding with EZH2.	30503497	RID05936	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Malignant glioma	NEAT1	CDK6	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR;microarray	GSE4290	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105810	NA	283131	1021	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	PLSTIRE	Long noncoding RNA nuclear enriched abundant transcript 1 impacts cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/ CDK6;There were target relationships and correlations on expressions between miR-139-5p and NEAT1/ CDK6. NEAT1 and CDK6 could promote cell proliferation and metastasis of glioma cells and impeded cell apoptosis, whereas miR-139-5p exerted suppressive effects on the biological functions of glioma cells. NEAT1 regulated CDK6 to affect glioma growth through sponging miR-139-5p	30515782	RID05937	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Osteosarcoma	NEAT1	HIF1A	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-186-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100644	NA	283131	3091	LINC00084|NCRNA00084|TncRNA|VINC	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	lncRNA nuclear-enriched abundant transcript 1 promotes cell proliferation and invasion by targeting miR-186-5p/HIF-1alpha in osteosarcoma;miR-186-5p was a downstream target of NEAT1 in OS;HIF-1alpha was a downstream target of miR-186-5p and that NEAT1 could exert its tumor oncogenic roles on OS cells via the miR-186-5p/HIF-1alpha axis.	30485482	RID05938	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Nasopharynx carcinoma	NPCCAT1	YY1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cancer progression(+)	interact with mRNA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	NA	NA	ENSG00000100811	NA	NA	7528	NA	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	Long noncoding RNA NPCCAT1 promotes nasopharyngeal carcinoma progression via upregulating YY1;NPCCAT1 directly binds YY1 mRNA 5'UTR, promotes YY1 mRNA translation, and upregulates YY1 protein level. Gain-of-function and loss-of-function assays revealed that YY1 promoted NPC cell proliferation and migration; rescue assays showed that depletion of YY1 attenuated the roles of NPCCAT1 overexpression in promoting NPC cell growth and migration in vitro and NPC tumor growth in<U+00A0>vivo.	30481541	RID05939	interact with mRNA	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Coronary artery disease	C2dat1	SIRT1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-34a-5p)	regulation	RNA-protein	PDGF-BB;TNF-	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	NA	NA	ENSG00000096717	NA	NA	23411	NA	SIR2L1	Long noncoding RNAs C2dat1 enhances vascular smooth muscle cell proliferation and migration by targeting MiR-34a-5p;elevated expression of C2dat1 suppressed microRNA-34a (miR-34a) expression and promoted sirtuin 1 (SIRT1) expression, which was a direct target gene of miR-34a;Restored expression of C2dat1 increased VSMC proliferation and migration through promoting SIRT1 expression	30474870	RID05940	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Respiratory failure	GAS5	ACE2	positively-E	RIP;RNA pull-down assay;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cancer progression(+)	ceRNA(miR-200c-3p)	regulation	RNA-protein	NA	NA	NA	Respiratory system disease	Respiratory failure	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000130234	NA	60674	59272	NCRNA00030|SNHG2	ACEH	Role of signaling pathway of long non-coding RNA growth arrest-specific transcript 5/microRNA-200c-3p/angiotensin converting enzyme 2 in the apoptosis of human lung epithelial cell A549 in acute respiratory distress syndrome;In ARDS, down-regulation of lncRNA GAS5 decreases ACE2 expression through increasing miR-200c-3p to promote the apoptosis of A549 cells, thus to promote the progression of ARDS;Quantitative real-time PCR (qRT-PCR was conducted to measure lncRNA GAS5, ACE2 and miR-200c-3p levels. RNA immunoprecipitation and RNA pull-down assay were used to detect the combination between GAS5 and miR-200c-3p. western blot was used to detect the protein level of ACE2	30440128	RID05941	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	ARAP1-AS1	NOTCH2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cancer progression(+)	ceRNA(miR-4735-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000256007	GRCh38_11:72685075-72693808	ENSG00000134250	NA	100874075	4853	NA	NA	Long non-coding RNA ARAP1-AS1 promotes the progression of bladder cancer by regulating miR-4735-3p/NOTCH2 axis;ARAP1-AS1 was enriched in the cytoplasm of BCa cells, suggesting that ARAP1-AS1 might act as a ceRNA to regulate gene expression and biological processes in bladder cancer. It was certified that ARAP1-AS1 can bind with miR-4735-3p in BCa cells;The results of all mechanism experiments indicated that ARAP1-AS1 regulated miR-4735-3p/NOTCH2 axis in BCa by acting as a ceRNA.	30404578	RID05942	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	EWSAT1	SNAI1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	histone modification	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000124216	NA	283673	6615	FLJ33768|LINC00277|NCRNA00277|TMEM84	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Increased EWSAT1 expression promotes cell proliferation, invasion and epithelial-mesenchymal transition in colorectal cancer;lncRNA EWSAT1 knockdown suppressed cell epithelial-mesenchymal transition (EMT) through reducing Snail1, Snail2, and N-cadherin expression, but increasing E-cadherin expression in CRC cells.	30402843	RID05943	epigenetic regulation	NA		UP(PAAD);DATA(GSE40174)
Colorectal cancer	EWSAT1	SNAI2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	histone modification	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000019549	NA	283673	6591	FLJ33768|LINC00277|NCRNA00277|TMEM84	SLUG|SLUGH|SLUGH1|SNAIL2	Increased EWSAT1 expression promotes cell proliferation, invasion and epithelial-mesenchymal transition in colorectal cancer;lncRNA EWSAT1 knockdown suppressed cell epithelial-mesenchymal transition (EMT) through reducing Snail1, Snail2, and N-cadherin expression, but increasing E-cadherin expression in CRC cells.	30402843	RID05944	epigenetic regulation	NA		
Colorectal cancer	EWSAT1	N-cadherin	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	histone modification	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000212766	GRCh38_15:69072926-69095820	NA	NA	283673	NA	FLJ33768|LINC00277|NCRNA00277|TMEM84	NA	Increased EWSAT1 expression promotes cell proliferation, invasion and epithelial-mesenchymal transition in colorectal cancer;lncRNA EWSAT1 knockdown suppressed cell epithelial-mesenchymal transition (EMT) through reducing Snail1, Snail2, and N-cadherin expression, but increasing E-cadherin expression in CRC cells.	30402843	RID05945	epigenetic regulation	NA		
Colorectal cancer	EWSAT1	E-cadherin	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	histone modification	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000212766	GRCh38_15:69072926-69095820	NA	NA	283673	NA	LINC00277|NCRNA00277|TMEM84	NA	Increased EWSAT1 expression promotes cell proliferation, invasion and epithelial-mesenchymal transition in colorectal cancer;lncRNA EWSAT1 knockdown suppressed cell epithelial-mesenchymal transition (EMT) through reducing Snail1, Snail2, and N-cadherin expression, but increasing E-cadherin expression in CRC cells.	30402843	RID05946	epigenetic regulation	NA		
Urinary bladder cancer	GAS6-DT	CDK9	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qRT-PCR	TANRIC	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-298)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000272695	GRCh38_13:113864112-113866834	ENSG00000136807	NA	100506394	1025	FLJ44054|GAS6-AS2	C-2k|CDC2L4|PITALRE|TAK	LncRNA GAS6-AS2 promotes bladder cancer proliferation and metastasis via GAS6-AS2/miR-298/CDK9 axis;In mechanism, GAS6-AS2 could function as a competitive endogenous RNA (ceRNA) via direct sponging miR-298, which further regulating the expression of CDK9.	30394665	RID05947	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Epithelial ovarian cancer	LINC00460	miR-338-3p	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	Long non-coding RNA LINC00460 promotes epithelial ovarian cancer progression by regulating microRNA-338-3p;A rescue experiment and luciferase reporter assay showed that LINC00460 exerted its oncogenic functions in EOC, at least in part, through binding miR-338-3p.	30372802	RID05948	ceRNA or sponge	NA		
Non-small cell lung cancer	PCAT6	LATS2	negatively-F	RNAi;RIP;ChIP	upregulation	qRT-PCR	TCGA;GSE19188; GSE18842	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000150457	NA	100506696	26524	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	NA	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer;PCAT6 additionally promoted NSCLC cell migration and invasion. Furthermore, mechanistic investigation demonstrated that the oncogenic activity of PCAT6 is partially attributable to its repression of LATS2 via association with the epigenetic repressor EZH2 (Enhancer of zeste homolog 2).	30314898	RID05949	expression association	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	PCAT6	EZH2	positively-F	RNAi;RIP;ChIP	upregulation	qRT-PCR	TCGA;GSE19188; GSE18842	NA	cell migration(+);cell invasion(+)	interact with protein	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000106462	NA	100506696	2146	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer;PCAT6 additionally promoted NSCLC cell migration and invasion. Furthermore, mechanistic investigation demonstrated that the oncogenic activity of PCAT6 is partially attributable to its repression of LATS2 via association with the epigenetic repressor EZH2 (Enhancer of zeste homolog 2).	30314898	RID05950	interact with protein	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	MEG3	PTEN	positively-E	RNAi	downregulation	qRT-PCR	GSE14001	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA MEG3 impacts proliferation, invasion, and migration of ovarian cancer cells through regulating PTEN;Compared with normal ovarian cells, expression levels of MEG3 and PTEN were relatively lower in ovarian cancer cells. There was a positive correlation between the expression of PTEN and the expression of MEG3. Enhanced expression level of PTEN suppressed SKOV3 cell proliferation, increased cell apoptosis rate, and decreased cell invasion and migration;LncRNA MEG3 and PTEN were down-regulated in ovarian cancer cells. LncRNA MEG3 regulated the downstream gene PTEN in ovarian cancer cells to prohibit cell proliferation, promote apoptosis and block cell cycle progression.	30310931	RID05951	expression association	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Gastric cancer	CYTOR	BCL2	positively-E	RNAi;HRP	upregulation	RT-qPCR	NA	NA	cell cycle(+);cell invasion(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171791	NA	112597	596	C2orf59|LINC00152|MGC4677|NCRNA00152	Bcl-2|PPP1R50	LINC00152 promotes the proliferation of gastric cancer cells by regulating B-cell lymphoma-2;The results revealed that LINC00152 was overexpressed in tissues, serum, and PBMCs of patients with gastric cancer. Moreover, LINC00152 could promote the migration and invasive abilities and suppress the apoptosis, of gastric cancer cells through regulating the Bcl-2 protein family. LINC00152 could bind with Bcl-2 directly to induce the activation of cell cycle signaling.	30304559	RID05952	interact with protein	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	LINC00662	YAP1	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	TCGA;GEO	NA	cell growth(+);Hippo/YAP1 signaling pathway(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000137693	NA	148189	10413	NA	YAP65	LINC00662 promotes gastric cancer cell growth by modulating the Hippo-YAP1 pathway;LINC00662 regulated YAP1-mediated GC cell proliferation by sponging miR-497-5p;Overall, our results revealed a critical role for the LINC00662-miR-497-5p-YAP1 axis in GC cell growth.	30297104	RID05953	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	Gm15290	miR-615-5p	negatively-F	RNAi;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressor miR-615-5p;The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P<0.0001). The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2, and SHMT2 Moreover, miR-615-5p mimic could antagonize the promoting effect of Gm15290 on cell proliferation and invasion.	30287504	RID05954	ceRNA or sponge	NA		
Colorectal cancer	FALEC	NUPR1	positively-E	RNAi;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-637)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000176046	NA	100874054	26471	FAL1|LINC00568|ncRNA-a1	COM1|p8	LncRNA FAL1 promotes carcinogenesis by regulation of miR-637/NUPR1 pathway in colorectal cancer;we demonstrate that lncRNA FAL1 acts as a sponge of miR-637, which functions as a suppressor via targeting and downregulation of NUPR1 expression;lncRNA FAL1 promotes carcinogenesis of CRC cells via regulation of the miR-637/NUPR1 pathway.	30267804	RID05955	ceRNA or sponge	NA		UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE55807,GSE75367)
Gastric cancer	CCAL	FOXM1	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	ceRNA(miR-149)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000111206	NA	NA	2305	NA	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Long non-coding RNA CCAL/miR-149/FOXM1 axis promotes metastasis in gastric cancer;Luciferase reporter assay indicated that CCAL directly bind to miR-149.We also showed that FOXM1 suppression by miR-149 could be partially rescued by CCAL overexpression;we observed a negative correlation between the expression of miR-149 and FOXM1 and a positive correlation between CCAL and FOXM1 levels. These results demonstrated that the CCAL/miR-149/FOXM1 axis functions as a key regulator in gastric cancer metastasis .	30250169	RID05956	ceRNA or sponge	metastasis		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Oral squamous cell carcinoma	GAS5	PTEN	positively-E	RNAi	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.	30576678	RID05957	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Oral squamous cell carcinoma	GAS5	PCNA	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000132646	NA	60674	5111	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05958	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Oral squamous cell carcinoma	GAS5	Cyclin D1	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05959	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral squamous cell carcinoma	GAS5	Ki-67	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05960	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral squamous cell carcinoma	GAS5	E-cadherin	negatively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05961	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral squamous cell carcinoma	GAS5	SNAI1	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000124216	NA	60674	6615	NCRNA00030|SNHG2	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05962	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Oral squamous cell carcinoma	GAS5	N-cadherin	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05963	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral squamous cell carcinoma	GAS5	vimentin	positively-E	RNAi;western blot	downregulation		NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in oral squamous cell carcinoma by regulating the miR-21/PTEN axis;overexpression of GAS5 showed the opposite effects. Furthermore, miR-21 overexpression reversed the effect of GAS5. western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation.western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC	30576678	RID05964	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Hepatocellular carcinoma	A1BG-AS1	SMAD7	positively-E	RNAi;luciferase reporter assay;RNA pull-down assay	downregulation	qRT-PCR	TCGA;HCC cohort	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-216a-5p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000268895	GRCh38_19:58347718-58355455	ENSG00000101665	NA	503538	4092	A1BG-AS|A1BGAS|FLJ23569|NCRNA00181	MADH7|MADH8	lncRNA A1BG-AS1 suppresses proliferation and invasion of hepatocellular carcinoma cells by targeting miR-216a-5p;miR-216a-5p restoration rescued A1BG-AS1 attenuated proliferation, migration and invasion of HCCLM3 cells. A1BG-AS1 positively regulated the levels of phosphatase and tensin homolog and SMAD family member 7, which were reduced by miR-216a-5p in HCC cells	30556161	RID05965	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Liver fibrosis	HOTTIP	SRF	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-150)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000112658	NA	100316868	6722	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	MCM1	Long noncoding RNA HOTTIP mediates SRF expression through sponging miR-150 in hepatic stellate cells. In this study, we reveal that BACE1-AS shares many miRNA-response elements with BACE1. The overexpression of BACE1-AS results in the repression of miRNAs that target BACE1, thus preventing BACE1 mRNA from being degraded. The knockdown of BACE1-AS increases the levels of these miRNAs, thereby reducing the expression of BACE1. Thus, BACE1-AS functions as a competing endogenous RNA (ceRNA). Our results also deepen the understanding of the regulation of BACE1 by BACE1-AS. In addition to increasing the stability of BACE1 mRNA through the formation of RNA duplexes, BACE1-AS can regulate BACE1 indirectly by acting as a ceRNA. Therefore, we propose that BACE1 functions as a ceRNA and forms a network through its associations with protein-coding genes, lncRNAs and miRNAs in the pathophysiology of AD. 	30548190	RID05966	ceRNA or sponge	NA		DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Thyroid cancer	XIST	MET	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell growth(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000105976	NA	7503	4233	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	DFNB97|HGFR|RCCP2	LncRNA XIST/miR-34a axis modulates the cell proliferation and tumor growth of thyroid cancer through MET-PI3K-AKT signaling.;Based on online database and online tool prediction results, miR-34a was underexpressed in thyroid cancer and might be a direct target of XIST. Herein, we confirmed the negative interaction between XIST and miR-34a;XIST serves as a ceRNA for miR-34a through sponging miR-34a, competing with MET for miR-34a binding, and finally modulating thyroid cancer cell proliferation and tumor growth.	30463570	RID05967	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Breast cancer	CASC15	KLF5	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-153-3p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000102554	NA	401237	688	LINC00340|lnc-SOX4-1	BTEB2|CKLF|IKLF	LncRNA cancer susceptibility candidate 15 accelerates the breast cancer cells progression via miR-153-3p/KLF5 positive feedback loop.This study uncovered that CASC15 expression level was aberrantly high-expressed in breast cancer tissue specimens and cells.Functionally, the loss-of-functional experiments showed that knockdown of CASC15 suppressed the malignant behaviors of breast cancer cells, such as proliferation, invasion and tumor growth in vitro and vivo.Mechanically, we confirmed that CASC15 functioned as a competing endogenous RNA (ceRNA) of miR-153-3p, besides, miR-153-3p targeted the 3'-UTR of KLF5 mRNA utilizing the bioinformatics online tools, luciferase reporter assay and RNA immunoprecipitation.Interestingly, we confirmed that the transcription factor KLF5 binds with the promoter region of CASC15 and activates the transcription.	30389133	RID05968	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Breast cancer	KLF5	CASC15	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000102554	NA	ENSG00000272168	GRCh38_6:21664184-22654455	688	401237	BTEB2|CKLF|IKLF	LINC00340|lnc-SOX4-1	LncRNA cancer susceptibility candidate 15 accelerates the breast cancer cells progression via miR-153-3p/KLF5 positive feedback loop.This study uncovered that CASC15 expression level was aberrantly high-expressed in breast cancer tissue specimens and cells.Functionally, the loss-of-functional experiments showed that knockdown of CASC15 suppressed the malignant behaviors of breast cancer cells, such as proliferation, invasion and tumor growth in vitro and vivo.Mechanically, we confirmed that CASC15 functioned as a competing endogenous RNA (ceRNA) of miR-153-3p, besides, miR-153-3p targeted the 3'-UTR of KLF5 mRNA utilizing the bioinformatics online tools, luciferase reporter assay and RNA immunoprecipitation.Interestingly, we confirmed that the transcription factor KLF5 binds with the promoter region of CASC15 and activates the transcription.	30389133	RID05969	interact with protein	NA	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Hepatocellular carcinoma	FER1L4	p-PI3K	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(-);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	bA563A22B.1|C20orf124|dJ309K20.1	NA	Upregulation of lncRNA FER1L4 suppresses the proliferation and migration of the hepatocellular carcinoma via regulating PI3K/AKT signal pathway.RESULTS:Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCRanalysis.Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis.Importantly, western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells.CONCLUSIONS:Our study suggested that FER1L4 might alleviate progression of hepatocellular carcinoma via blocking PI3K/AKT pathway, which encourages a better understanding of the pathogenesis of HCC and may provide a novel potential therapeutic target for clinical treatment.The results demonstrated that overexpression of FER1L4 inactivated the PI3K/AKT pathway, as evidenced by thedownregulations of p-PI3K and p-AKT.	30382631	RID05970	expression association	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	
Hepatocellular carcinoma	FER1L4	p-AKT	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(-);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	bA563A22B.1|C20orf124|dJ309K20.1	NA	Upregulation of lncRNA FER1L4 suppresses the proliferation and migration of the hepatocellular carcinoma via regulating PI3K/AKT signal pathway.RESULTS:Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCRanalysis.Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis.Importantly, western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells.CONCLUSIONS:Our study suggested that FER1L4 might alleviate progression of hepatocellular carcinoma via blocking PI3K/AKT pathway, which encourages a better understanding of the pathogenesis of HCC and may provide a novel potential therapeutic target for clinical treatment.The results demonstrated that overexpression of FER1L4 inactivated the PI3K/AKT pathway, as evidenced by thedownregulations of p-PI3K and p-AKT.	30382631	RID05971	expression association	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	
Colorectal cancer	MALAT1	SOX9	positively-E	miRCode;Targetscan;RNAi;luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE18105	NA	cell cycle(-);apoptosis process(-);cell viability(+);cell metastasis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000125398	NA	378938	6662	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CMD1|CMPD1|SRA1	The effects of lncRNA MALAT1 on proliferation, invasion and migration in colorectal cancer through regulating SOX9.By experimental verification, MALAT1 and SOX9 were expressed in a high percentage of colorectal cancer tumors and cells, while miR-145 was in a low expression.We also identified miR-145 as a target of MALAT1 and SOX9.MALAT1 played a role in regulating cancer process by functioning as a competing endogenous RNA.Silencing MALAT1 could effectively decrease the expression level of SOX9, thus suppress cell viability and metastasis.Down-regulated MALAT1 could induce resistance of G1 phase in cell cycle, and facilitation of colorectal cancer cell apoptosis.CONCLUSIONS:The regulatory function of lncRNA MALAT1 / miR-145 / SOX9 axis was revealed in colorectal cancer based on bioinformatics analysis.LncRNA MALAT1 could facilitate colorectal cancer cell proliferation, invasion and migration by down-regulating miR-145 and up-regulating SOX9.LncRNA MALAT1 could suppress cell cycle and apoptosis through MALAT1/miR-145/SOX9 axis.	30285605	RID05972	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Alzheimer's disease	LNCRNA-ATB	ZNF217	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-200)	regulation	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	TF	NA	NA	ENSG00000171940	NA	114004396	7764	NA	ZABC1	Suppression of lncRNA-ATB prevents amyloid-beta-induced neurotoxicity in PC12 cells via regulating miR-200/ZNF217 axis.RESULTS:The results showed that lncRNA-ATB was increased expressed in the CSF and serum of patients with AD.Abeta25-35-induced injury in PC12 cells and increased the expression of lncRNA-ATB.Suppression of lncRNA-ATB alleviated Abeta25-35-induced PC12 cell injury.Further studies showed that miR-200 was negatively regulated by lncRNA-ATB.Suppression of lncRNA-ATB alleviated Abeta25-35 injury by regulation of miR-200.Moreover, miR-200 negatively regulated ZNF217 expression and ZNF217 was a target of miR-200.CONCLUSIONS:Our findings indicate that lncRNA-ATB is highly expressed in AD patients.Suppression of lncRNA-ATB may protect PC12 cells against Abeta25-35-induced neurotoxicity via regulating miR-200/ZNF217 axis.	30248538	RID05973	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	NCK1-DT	MSH2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;RNAi	upregulation	microarray	GSE63514;GSE27678	NA	chemoresistance(+);apoptosis process(-)	ceRNA(miR-134-5p)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000095002	NA	101927597	4436	NCK1-AS1|SLC35G2-AS1	COCA1|HNPCC|HNPCC1	Suppression of long noncoding RNA NCK1-AS1 increases chemosensitivity to cisplatin in cervical cancer.Based on the microarray data of GSE63514 and GSE27678, NCK1-AS1 was upregulated in cervical cancer.Increased expression of NCK1-AS1, MSH2, and decreased expression of miR-134-5p were observed in cervical cancer tissues.In addition, NCK1-AS1 competitively bound to miR-134-5p to regulate MSH2.Therefore, si-NCK1-AS1 and miR-134-5p mimic both reduced MSH2 activity and increased cisplatin-induced apoptosis in cervical cancer cells.	30221354	RID05974	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842)
Triple-negative breast cancer	TP73-AS1	TWIST1	positively-E	RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	angiogenesis(+);tumorigenesis(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000122691	NA	57212	7291	KIAA0495|PDAM	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Knockdown of long non-coding RNA TP73-AS1 suppresses triple negative breast cancer cell vasculogenic mimicry by targeting miR-490-3p/TWIST1 axis.In this study, we found that long non-coding RNA TP73 antisense RNA 1 (TP73-AS1) was upregulated in VM positive TNBC tissues.Knockdown of TP73-AS1 suppressed TNBC cell line MDA-MB-231 cell VM formation in vitro.In addition, RNA immunoprecipitation assay and dual-luciferase reporter assay showed that TP73-AS1 bound to miR-490-3p in a sequence-specific manner.miR-490-3p was downregulated in VM positive tissues and was involved in TP73-AS1-mediated MDA-MB-Furthermore, TWIST1 was a target of miR-490-3p and participated in TP73-AS1/miR-490-3p-modulated MDA-MB-231 cell VM formation.	30193732	RID05975	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Pancreatic cancer	LINC01133	DKK1	negatively-E	luciferase reporter assay;RNA pull-down assay;ChIP;RNAi	upregulation	microarray;RT-qPCR	GSE32676;GSE16515	NA	tumorigenesis(-);WNT signaling pathway(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000107984	NA	100505633	22943	lncRNA-PAGBC	DKK-1|SK	Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.GSE32676 and GSE16515 revealed that LINC01133 was upregulated in pancreatic cancer, which was also associated with increased DKK1 methylation and higher expression of genes related to the Wnt signaling pathway, although the expression of DKK1 decreased in pancreatic cancer.In addition, LINC01133 bound to the promoter region of DKK1, resulting in the trimethylation of H3K27 and decreased DKK1 expression, while the expression of Wnt-5a, MMP-7, and beta-catenin increased upon LINC01133 binding.Finally, over-expressed LINC01133 enhanced the growth, proliferation, migration, metastasis, and invasion of pancreatic cancer cells.In summary, by inducing the methylation of DKK1 promoter, LINC01133 silencing suppresses the development of pancreatic cancer cells through the Wnt signaling pathway.LINC01133 activates wnt signaling pathway by inhibiting DKK1	30580676	RID05976	epigenetic regulation	metastasis	UP(BRCA);DATA(GSE111065)	UP(LIHC);DATA(GSE117623)
Pancreatic cancer	LINC01133	Wnt-5a	positively-E	luciferase reporter assay;RNA pull-down assay;ChIP;RNAi	upregulation	microarray;RT-qPCR	GSE32676;GSE16515	NA	tumorigenesis(-);WNT signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	NA	NA	100505633	NA	lncRNA-PAGBC	NA	Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.GSE32676 and GSE16515 revealed that LINC01133 was upregulated in pancreatic cancer, which was also associated with increased DKK1 methylation and higher expression of genes related to the Wnt signaling pathway, although the expression of DKK1 decreased in pancreatic cancer.In addition, LINC01133 bound to the promoter region of DKK1, resulting in the trimethylation of H3K27 and decreased DKK1 expression, while the expression of Wnt-5a, MMP-7, and beta-catenin increased upon LINC01133 binding.Finally, over-expressed LINC01133 enhanced the growth, proliferation, migration, metastasis, and invasion of pancreatic cancer cells.In summary, by inducing the methylation of DKK1 promoter, LINC01133 silencing suppresses the development of pancreatic cancer cells through the Wnt signaling pathway.LINC01133 activates wnt signaling pathway by inhibiting DKK1	30580676	RID05977	expression association	metastasis	UP(BRCA);DATA(GSE111065)	
Pancreatic cancer	LINC01133	MMP7	positively-E	luciferase reporter assay;RNA pull-down assay;ChIP;RNAi	upregulation	microarray;RT-qPCR	GSE32676;GSE16515	NA	tumorigenesis(-);WNT signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000137673	NA	100505633	4316	lncRNA-PAGBC	MMP-7|MPSL1|PUMP-1	Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.GSE32676 and GSE16515 revealed that LINC01133 was upregulated in pancreatic cancer, which was also associated with increased DKK1 methylation and higher expression of genes related to the Wnt signaling pathway, although the expression of DKK1 decreased in pancreatic cancer.In addition, LINC01133 bound to the promoter region of DKK1, resulting in the trimethylation of H3K27 and decreased DKK1 expression, while the expression of Wnt-5a, MMP-7, and beta-catenin increased upon LINC01133 binding.Finally, over-expressed LINC01133 enhanced the growth, proliferation, migration, metastasis, and invasion of pancreatic cancer cells.In summary, by inducing the methylation of DKK1 promoter, LINC01133 silencing suppresses the development of pancreatic cancer cells through the Wnt signaling pathway.LINC01133 activates wnt signaling pathway by inhibiting DKK1	30580676	RID05978	expression association	metastasis	UP(BRCA);DATA(GSE111065)	UP(LIHC);DATA(GSE117623)
Pancreatic cancer	LINC01133	CTNNB1	positively-E	luciferase reporter assay;RNA pull-down assay;ChIP;RNAi	upregulation	microarray;RT-qPCR	GSE32676;GSE16515	NA	tumorigenesis(-);WNT signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000168036	NA	100505633	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.GSE32676 and GSE16515 revealed that LINC01133 was upregulated in pancreatic cancer, which was also associated with increased DKK1 methylation and higher expression of genes related to the Wnt signaling pathway, although the expression of DKK1 decreased in pancreatic cancer.In addition, LINC01133 bound to the promoter region of DKK1, resulting in the trimethylation of H3K27 and decreased DKK1 expression, while the expression of Wnt-5a, MMP-7, and beta-catenin increased upon LINC01133 binding.Finally, over-expressed LINC01133 enhanced the growth, proliferation, migration, metastasis, and invasion of pancreatic cancer cells.In summary, by inducing the methylation of DKK1 promoter, LINC01133 silencing suppresses the development of pancreatic cancer cells through the Wnt signaling pathway.LINC01133 activates wnt signaling pathway by inhibiting DKK1	30580676	RID05979	expression association	metastasis	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	MALAT1	IL-21R	positively-E	luciferase reporter assay;Starbase v2.0	upregulation	RT-qPCR;western blot	TCGA	NA	tumorigenesis(+);IL-21R/JAK/STAT signaling pathway(+)	ceRNA(miR-152-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	IL-21R functions as an oncogenic factor and is regulated by the lncRNA MALAT1/miR-125a-3p axis in gastric cancer.As a result, the expression of IL-21R was found to be significantly increased in GC cell lines and tissues as compared with normal tissues, and was associated with tumor size and lymphatic metastasis, acting as an independent prognostic factor of poor survival and recurrence in patients with GC.The knockdown of IL-21R markedly suppressed GC cell proliferation and invasion, and IL-21R expression was further validated to be negatively regulated by miR-125a-3p (miR-125a).The overexpression of IL-21R reversed the tumor suppressive effects of miR-125a in<U+00A0>vitro and in<U+00A0>vivo.Moreover, lncRNA metastasis-associated lung adenocarcinoma transcript<U+00A0>1<U+00A0>(MALAT1) acted as a sponge of miR-125a to modulate the IL-21R signaling pathway in GC cells and represented a risk factor for survival and recurrence in patients with GC.Taken together, the findings of this study reveal an oncogenic role for IL-21R in gastric tumorigenesis and verify that its activation is partly due to the dysregulation of the lncRNA MALAT1/miR-125a axis.lncRNA MALAT1 functions as a sponge of miR-125a to regulate IL-21R/JAK/STAT signaling, thus leading to gastric tumorigenicity.	30387833	RID05980	ceRNA or sponge	metastasis,recurrence,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	HOTAIR	EZH2	positively-E	RIP;qRT-PCR	upregulation		NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|EZH1|KMT6|KMT6A	Hotair mediates tumorigenesis through recruiting EZH2 in colorectal cancer.In this study, Hotair was found to be upregulated in colorectal cancer (CRC) cells and clinical specimens.Further investigation showed that knockdown of Hotair dramatically suppressed cell proliferation and colony formation, suggesting that Hotair may stimulate tumorigenesis of CRC.The enhancer of zeste homolog 2 (EZH2), a regulator of epigenetic modification, was upregulated in CRC cells and clinical samples.And the silence of EZH2 significantly suppressed cell viability and colony formation.Furthermore, the RNA immunoprecipitation assay revealed that Hotair directly bound EZH2 in CRC cells.In conclusion, Hotair mediated tumorigenesis via recruiting EZH2, which might shed light on the development of a novel therapeutic approach for patients with CRC.Our study found that EZH2 was upregulated in CRC cells and clinical specimens, and its knockdown inhibited cell proliferation of CRC cells.	30362162	RID05981	interact with protein	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Intervertebral disc degeneration	MIR570HG	TXNIP	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-335-3P)	regulation	RNA-protein	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	NA	ENSG00000117289	NA	440993	10628	LINC00969	ARRDC6|EST01027|HHCPA78|THIF|VDUP1	LINC00969 promotes the degeneration of intervertebral disk by sponging miR-335-3p and regulating NLRP3 inflammasome activation.Long noncoding RNAs (LncRNAs) may serve as miRNA sponges to regulate the expressions of miRNA target genes.LncRNA LINC00969 has been indicated to be upregulated in intervertebral disk degeneration.Differently expressed LINC00969, miR-335-3p, and thioredoxin-interacting protein (TXNIP) were determined in nucleus pulposus (NP) tissues and cells isolated from patients with intervertebral disk degeneration.In this study, we demonstrated that LINC00969 was highly expressed, whereas miR-335-3p was aberrantly downregulated in NP tissues and cells of intervertebral disk degeneration patients.In addition, our results suggested that LINC00969 enhanced NP cell apoptosis.More importantly, LINC00969 was identified to function as a competitive endogenous RNA (ceRNA) for miR-335-3p to positively regulate TXNIP expression in vitro.	30592131	RID05982	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	ZNF205-AS1	EGR4	positively-E	ChIP;luciferase reporter assay;bioinformatics	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000263214	NA	ENSG00000135625	NA	81854	1961	NA	NGFI-C|PAT133	A positive feedback loop between ZNF205-AS1 and EGR4 promotes non-small cell lung cancer growth.ZNF205-AS1 was increased in NSCLC tissues and cell lines, and associated with poor prognosis of NSCLC patients.Bioinformatics prediction, combined with experimental verification revealed that early growth response 4 (EGR4) directly bound to ZNF205-AS1 promoter, increased the promoter activity of ZNF205-AS1, and activated ZNF205-AS1 transcription.Intriguingly, ZNF205-AS1 transcript directly interacted with EGR4 mRNA, increased EGR4 mRNA stability, and up-regulated EGR4 expression via RNA-RNA interaction.EGR4 was also increased in NSCLC and the expression of ZNF205-AS1 was significantly positively correlated with EGR4 in NSCLC tissues.Gain-of-function and loss-of-function assays demonstrated that both ZNF205-AS1 and EGR4 promoted NSCLC cell growth in vitro and NSCLC tumour growth in vivo.Concurrently depleting ZNF205-AS1 and EGR4 more significantly repressed NSCLC tumour growth in vivo.	30556283	RID05983	interact with protein	prognosis		
Non-small cell lung cancer	EGR4	ZNF205-AS1	positively-F	ChIP;luciferase reporter assay;bioinformatics	upregulation	qPCR	NA	NA	cell growth(+)	interact with mRNA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000135625	NA	ENSG00000263214	NA	1961	81854	NGFI-C|PAT133	NA	A positive feedback loop between ZNF205-AS1 and EGR4 promotes non-small cell lung cancer growth.ZNF205-AS1 was increased in NSCLC tissues and cell lines, and associated with poor prognosis of NSCLC patients.Bioinformatics prediction, combined with experimental verification revealed that early growth response 4 (EGR4) directly bound to ZNF205-AS1 promoter, increased the promoter activity of ZNF205-AS1, and activated ZNF205-AS1 transcription.Intriguingly, ZNF205-AS1 transcript directly interacted with EGR4 mRNA, increased EGR4 mRNA stability, and up-regulated EGR4 expression via RNA-RNA interaction.EGR4 was also increased in NSCLC and the expression of ZNF205-AS1 was significantly positively correlated with EGR4 in NSCLC tissues.Gain-of-function and loss-of-function assays demonstrated that both ZNF205-AS1 and EGR4 promoted NSCLC cell growth in vitro and NSCLC tumour growth in vivo.Concurrently depleting ZNF205-AS1 and EGR4 more significantly repressed NSCLC tumour growth in vivo.	30556283	RID05984	interact with mRNA	prognosis		
Colorectal cancer	DUXAP9	miR-26a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000225210	GRCh38_14:19062316-19131167	NA	NA	503638	NA	FLJ39632|LINC01296|lncRNA-CTD903|LNMAT1	NA	LINC01296/miR-26a/GALNT3 axis contributes to colorectal cancer progression by regulating O-glycosylated MUC1 via PI3K/AKT pathway.RESULTS:Differential expression of linc01296 is confirmed and closely correlated with the malignancy of CRC cell lines and poor clinical prognosis.Moreover, alteration of linc01296 affects CRC cell proliferation, metastasis and chemoresistance to 5-fluorouracil (5-FU) in vitro.Our investigation corroborates that linc01296 functions as an endogenous sponge of miR-26a to regulate mucin1 (MUC1) expression, catalyzed by GALNT3, which modulates the activity of PI3K/AKT pathway.CONCLUSION:These new findings indicate that linc01296/miR-26a/GALNT3 axis involves in the progression of CRC cells, illuminating the possible mechanism mediated by O-glycosylated MUC1 via PI3K/AKT pathway.	30547804	RID05985	ceRNA or sponge	metastasis,chemoresistance,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	
Colorectal cancer	DUXAP9	MUC1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000185499	NA	503638	4582	FLJ39632|LINC01296|lncRNA-CTD903|LNMAT1	ADMCKD|ADMCKD1|CD227|MCD|MCKD|MCKD1|PEM|PUM	LINC01296/miR-26a/GALNT3 axis contributes to colorectal cancer progression by regulating O-glycosylated MUC1 via PI3K/AKT pathway.RESULTS:Differential expression of linc01296 is confirmed and closely correlated with the malignancy of CRC cell lines and poor clinical prognosis.Moreover, alteration of linc01296 affects CRC cell proliferation, metastasis and chemoresistance to 5-fluorouracil (5-FU) in vitro.Our investigation corroborates that linc01296 functions as an endogenous sponge of miR-26a to regulate mucin1 (MUC1) expression, catalyzed by GALNT3, which modulates the activity of PI3K/AKT pathway.CONCLUSION:These new findings indicate that linc01296/miR-26a/GALNT3 axis involves in the progression of CRC cells, illuminating the possible mechanism mediated by O-glycosylated MUC1 via PI3K/AKT pathway.	30547804	RID05986	expression association	metastasis,chemoresistance,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	DOWN(LIHC);UP(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Pulmonary hypertension	H19	AT1R	positively-E	RNAi;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(let-7b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000144891	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	LncRNA H19 promotes the proliferation of pulmonary artery smooth muscle cells through AT 1 R via sponging let-7b in monocrotaline-induced pulmonary arterial hypertension.A dual-luciferase reporter assay was used to explore whether let-7b is a sponge miRNA of H19, and AT1R is a novel target of let-7b.RESULTS:The results showed that H19 was highly expressed in the serum and lungs of MCT-induced rats/mice, and H19 was upregulated by PDGF-BB in vitro.H19 upregulated AT1R expression via sponging miRNA let-7b following PDGF-BB stimulation.AT1R is a novel target of let-7b.Moreover, the overexpression of H19 and AT1R could facilitate PASMCs proliferation in vitro.CONCLUSION:Our study showed that H19 is highly expressed in MCT-induced rodent lungs and upregulated by PDGF-BB.The H19-let-7b-AT1R axis contributed to the pathogenesis of PAH by stimulating PASMCs proliferation.	30547791	RID05987	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Colorectal cancer	YAP1	MALAT1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	GSE 20916;GSE 92335;GSE 9348;GSE 14095	NA	epithelial to mesenchymal transition(+);angiogenesis(+)	interact with protein	regulation	protein-RNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10413	378938	YAP65	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	YAP1-induced MALAT1 promotes epithelial-mesenchymal transition and angiogenesis by sponging miR-126-5p in colorectal cancer.YAP1 was highly expressed in CRC tissues as assessed by GSE20916 and its expression was negatively correlated with overall survival in 83 CRC cases.Meanwhile, YAP1 promoted proliferation, invasion, and migration in colon cancer cells, in vitro and in vivo.MALAT1 was obviously expressed, with differential expression of 11 lncRNAs in HCT116 cells after transfection with siYAP1 or si-Ctl.Bioinformatics prediction, dual luciferase assay, RNA-IP, and RNA pull-down assay demonstrated that YAP1-induced MALAT1 promoted the expression of metastasis-associated molecules such as VEGFA, SLUG, and TWIST, by sponging miR-126-5p in CRC.These findings indicated that the YAP1-MALAT1-miR-126-5p axis could control angiogenesis and epithelial-mesenchymal transition in CRC, providing potential biomarkers and therapeutic targets for CRC.	30531836	RID05988	interact with protein	metastasis	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Colorectal cancer	MALAT1	miR-126-5p	negatively-F	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);angiogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	YAP1-induced MALAT1 promotes epithelial-mesenchymal transition and angiogenesis by sponging miR-126-5p in colorectal cancer.YAP1 was highly expressed in CRC tissues as assessed by GSE20916 and its expression was negatively correlated with overall survival in 83 CRC cases.Meanwhile, YAP1 promoted proliferation, invasion, and migration in colon cancer cells, in vitro and in vivo.MALAT1 was obviously expressed, with differential expression of 11 lncRNAs in HCT116 cells after transfection with siYAP1 or si-Ctl.Bioinformatics prediction, dual luciferase assay, RNA-IP, and RNA pull-down assay demonstrated that YAP1-induced MALAT1 promoted the expression of metastasis-associated molecules such as VEGFA, SLUG, and TWIST, by sponging miR-126-5p in CRC.These findings indicated that the YAP1-MALAT1-miR-126-5p axis could control angiogenesis and epithelial-mesenchymal transition in CRC, providing potential biomarkers and therapeutic targets for CRC.	30531836	RID05989	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Breast cancer	lncATB	TWIST1	positively-E	RNAi;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cancer progression(+);epithelial to mesenchymal transition(+);prognosis(-)	ceRNA(miR-200C)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000122691	NA	NA	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Long noncoding RNA ATB promotes the epithelial-mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer.Gain- and loss-of-function studies demonstrated that lncATB enhanced cell migration, invasion and clonogenicity in vitro and in vivo.LncATB promoted the EMT by acting as a sponge for the miR-200 family and restoring Twist1 expression.	30518916	RID05990	ceRNA or sponge	prognosis		UP(SKCM);DATA(GSE38495)
Lung non-small cell carcinoma	CYTOR	miR-195	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell radiosensitivity(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	NA	112597	NA	C2orf59|LINC00152|MGC4677|NCRNA00152	NA	Long noncoding RNA CYTOR sponges miR-195 to modulate proliferation, migration, invasion and radiosensitivity in nonsmall cell lung cancer cells.In the present study, we found that CYTOR promoted cell proliferation, migration and invasion ability, and induced radioresistance in NSCLC cells.Mechanistically, CYTOR could directly interact with miR-195 and increase its targets.Thus, CYTOR played an oncogenic role in NSCLC progression through sponging miR-195.	30487160	RID05991	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	
Hepatocellular carcinoma	WEE2-AS1	FERMT3	positively-E	luciferase reporter assay	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228775	GRCh38_7:141704003-141738346	ENSG00000149781	NA	285962	83706	NA	KIND3|MGC10966|MIG2B|UNC112C|URP2	Hepatitis B virus X protein related lncRNA WEE2-AS1 promotes hepatocellular carcinoma proliferation and invasion.WEE2-AS1 over-expressed in HCC and was positively correlated to hepatitis B virus (HBV) infection, hepatic vascular invasion, poor tumor differentiation and poor patient prognosis.WEE2-AS1 also accelerated the proliferation, migration, invasion and cell cycle progression of HCC cells.In conclusion, there is a preliminary HBx-WEE2-AS1- FERMT3 pathway which may serve as a therapeutic target for HBV-associated HCC.	30471857	RID05992	expression association	prognosis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Atherosclerosis	TUG1	PTEN	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171862	NA	55000	5728	FLJ20618|LINC00080|NCRNA00080	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA TUG1 promotes proliferation of vascular smooth muscle cell and atherosclerosis through regulating miRNA-21/PTEN axis.RESULTS:We found that the lncRNA TUG1 was highly expressed in serum samples from 38 patients with atherosclerosis, compared with 24 healthy volunteers.<U+00A0> LncRNA TUG1 was dramatically upregulated in atherosclerotic plaques of ApoE-/- mice.We also found that the expression of TUG1 was upregulated in vascular smooth muscle cell injury model.Through loss- and gain-of function approaches, we showed that TUG1 promotes cell proliferation and induces apoptosis in vitro.What's more, TUG1 expression level was reversely correlated with PTEN expression in patients with atherosclerosis.LncRNA TUG1 could compete with PTEN for miR-21 binding.	30468492	RID05993	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Clear cell renal cell carcinoma	LINC01138	SREBF1	positively-F		upregulation		NA	NA	cell proliferation(+)	DNA methylation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000215863	NA	ENSG00000072310	NA	388685	6720	FLJ39739|LINC00875	bHLHd1|SREBP-1c|SREBP1|SREBP1a	The LINC01138 interacts with PRMT5 to promote SREBP1-mediated lipid desaturation and cell growth in clear cell renal cell carcinoma.LINC01138 regulates ccRCC growth through sterol regulatory element-binding protein 1 (SREBP1)-mediated lipid desaturation.Mechanistically, we demonstrated that LINC01138 interacts with PRMT5 to increase arginine methylation and protein stability of SREBP1, promoting lipid desaturation and cell proliferation in ccRCC.Our study identified LINC01138 as a novel regulator of metabolic abnormalities in ccRCC, providing a potential therapeutic target for metabolic therapy.	30446222	RID05994	epigenetic regulation	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	LINC01138	PRMT5	NA		upregulation		NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000215863	NA	ENSG00000100462	NA	388685	10419	FLJ39739|LINC00875	HRMT1L5|SKB1|SKB1Hs	The LINC01138 interacts with PRMT5 to promote SREBP1-mediated lipid desaturation and cell growth in clear cell renal cell carcinoma.LINC01138 regulates ccRCC growth through sterol regulatory element-binding protein 1 (SREBP1)-mediated lipid desaturation.Mechanistically, we demonstrated that LINC01138 interacts with PRMT5 to increase arginine methylation and protein stability of SREBP1, promoting lipid desaturation and cell proliferation in ccRCC.Our study identified LINC01138 as a novel regulator of metabolic abnormalities in ccRCC, providing a potential therapeutic target for metabolic therapy.	30446222	RID05995	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Seminoma	H19	TDRG1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	microarray	NA	NA	cell survival(+);radioresistance(+)	ceRNA(miR-106b-5p)	binding/interaction	RNA-RNA	Cisplatin	NA	NA	Cancer	Seminoma	lncRNA	lncRNA	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000204091	GRCh38_6:40334775-40387590	283120	732253	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LINC00532|lincRNA-NR_024015	Long non-coding RNA H19 promotes TDRG1 expression and cisplatin resistance by sequestering miRNA-106b-5p in seminoma.The role of TDRG1 in tumorigenesis and the progression of seminoma, as well as its role in regulating chemosensitivity of seminoma to cisplatin through the PI3K/Akt/mTOR signaling pathway, has been previously defined.	30430771	RID05996	ceRNA or sponge	chemoresistance	UP(NSCLC);DATA(GSE74639)	
Colorectal cancer	ABHD11-AS1	SOX4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-133a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000124766	NA	171022	6659	LINC00035|NCRNA00035|WBSCR26	NA	Long non-coding RNA ABHD11-AS1 promotes colorectal cancer development through regulation of miR-133a/SOX4 axis.In the present study, qRT-PCRassay revealed that ABHD11-AS1 expression was markedly higher in colorectal cancer tissues and cell lines.In addition, patients who displayed overexpression of ABHD11-AS1 showed a significantly poorer progression free survival (PFS) and overall survival (OS) by Kaplan-Meier analysis.Loss-of-function experiments suggested that silencing of ABHD11-AS1 expression could significantly reduce the proliferation, colony formation, migration and invasion of colorectal cancer cells, and increase cell apoptosis.Moreover, bioinformatics analysis, biotin pull-down assay, luciferase reporter assay, and RIP assay disclosed that ABHD11-AS1 straightly interacted with miR-133a.Collectively, these findings manifested that the ABHD11-AS1/miR-133a/SOX4 axis may be a cogitable and promising therapeutic target for colorectal cancer.	30429229	RID05997	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Osteosarcoma	CCL18	UCA1	positively-E	microarray;RNAi;qRT-PCR	upregulation	microarray;RNAi;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	protein-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Bone cancer	PCG	lncRNA	ENSG00000006074	NA	ENSG00000214049	GRCh38_19:15828206-15836328	6362	652995	AMAC-1|CKb7|DC-CK1|DCCK1|MIP-4|PARC|SCYA18	CUDR|LINC00178|onco-lncRNA-36|UCAT1	Macrophage-derived CCL18 promotes osteosarcoma proliferation and migration by upregulating the expression of UCA1.KEY MESSAGES: CCL18 promotes proliferation and migration of osteosarcoma cells by EP300/ UCA1/ Wnt/beta-catenin pathway.We found that CCL18 enhanced the proliferation and migration of OS cells and upregulated UCA1 through transcription factor EP300.Subsequently, we explored the potential transcriptional factors that mediate CCL18-induced UCA1 expression. First, we searched for potential transcriptional factors that were identi- fied to bind the UCA1 promoter area by ChIP-seq using the UCSC website (Supplemental Fig. 1) and the transcriptional factors that were upregulated in the 143B cells following the CCL18 treatment using microarrays (Fig. 3a). TFAP2A, ATF3, STAT1, EP300, and TEAD4 were present in both lists, and their upregulation in the OS cells treated with CCL18 was validated by qRT-PCR(Fig. 3b). Among these transcriptional factors, EP300 was the most dramatically upregulated follow- ing the CCL18 treatment. The upregulation of EP300 in the 143B and MG63 cells following the CCL18 treatment was also validated by western blot (Fig. 3c). Thus, we focused on EP300 in our further studies and examined whether the silencing of EP300 influences UCA1 expression. The mixture of three siRNAs targeting EP300 efficiently reduced the EP300 level at both the mRNA and protein levels (Fig. 3d, e). The UCA1 level was dramatically downregulated in the 143B cells with knocked-down EP300 (Fig. 3f). Furthermore, CCL18 induced UCA1 expression in a dose-dependent man- ner. The silencing of EP300 could reverse the CCL18-induced upregulation of UCA1 expression (Fig. 3g). Altogether, these results suggest that CCL18 induces UCA1 expression through EP300. The authors found that the cytokine CCL18 was signifi- cantly overexpressed in aggressive human OS with lung metas- tasis.chose the eight most upregulated lncRNAs for further confirmation using qRT-PCR Among these lncRNAs, the long non-coding RNA urotheli carcinoma associated 1 (UCA1) was the most markedly increased lncRNA in the 143B cells treated with 20-ng/mlCCL18 (Fig. 2b). Thus, UCA1 was the most dramatically upregulated lncRNA in OS cells after CCL1	30426155	RID05998	expression association	NA		UP(PAAD);DATA(GSE40174)
Lung cancer	SNHG15	miR-211-3p	negatively-F	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983019-44986961	NA	NA	285958	NA	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	NA	LncRNA SNHG15 promotes proliferation and migration of lung cancer via targeting microRNA-211-3p.RESULTS:SNHG15 was highly expressed in LC tissues than that of normal lung tissues.Besides, LC patients with stage I-II presented lower expression of SNHG15 than those with stage III-IV.For in vitro studies, SNHG15 knockdown resulted in viability reduction, cell cycle arrest and reduced migration of LC cells, which were reversed by the microRNA-211-3p knockdown.CONCLUSIONS:SNHG15 is highly expressed in LC tissues, which promotes the occurrence and progression of LC via regulating proliferation and migration of LC cells by targeting microRNA-211-3p.The target microRNA of SNHG15 was predicted by bioinformatics and verified by dual-luciferase reporter gene assay.SNHG15 was highly expressed in LC tissues than that of normal lung tissues.For in vitro studies, SNHG15 knockdown resulted in viability reduction, cell cycle arrest and reduced migration of LC cells, which were reversed by the microRNA-211-3p knockdown.	30402848	RID05999	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	
Lung non-small cell carcinoma	MINCR	SLC7A5	positively-E	luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell growth(+);cell metastasis(+);prognosis(-)	ceRNA(miR-127)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280158-143281692	ENSG00000103257	NA	100507316	8140	LINC01604|TCONS_00015189	CD98|D16S469E|E16|LAT1|MPE16	Up-regulation of long noncoding RNA MINCR promotes non-small cell of lung cancer growth by negatively regulating miR-126/SLC7A5 axis.In the present study, results found that MINCR over expression in NSCLC tissue and cell lines was closely related to poor survival in NSCLC.Functional experiments found that decreased MINCR expression inhibits NSCLC cell proliferation and migration and promotes cells apoptosis.Results also found that MINCR functions as an oncogene in the metastasis of NSCLC, in part, by acting as a competing endogenous RNA to modulate the miR-126/SLC7A5 axis.Dysfunction of MINCR, miR-126 and SLC7A6 predicted poor prognosis of patients with NSCLC.	30528230	RID06000	ceRNA or sponge	metastasis,prognosis	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827)
Hepatocellular carcinoma	lncRNA-6195	ENO1	negatively-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000074800	NA	NA	2023	NA	ENO1L1|HEL-S-17|MPB1|NNE|PPH	A novel lncRNA, TCONS_00006195, represses hepatocellular carcinoma progression by inhibiting enzymatic activity of ENO1.Moreover, lncRNA-6195 could combine with alpha-enolase (ENO1) and repress its enzymatic activity, thus further inhibiting the energy metabolism in HCC cells.Our results suggest that lncRNA-6195 represses the growth of HCC by inhibiting the enzymatic activity of ENO1.Our results suggest that lncRNA-6195 represses the growth of HCC by inhibiting the enzymatic activity of ENO1.Stably transfected cell lines were selected using puromycin, and the expression level of lncRNA-6195 was confirmed by qRT-PCR	30518748	RID06001	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Endometriosis	AFAP1-AS1	ZEB1	positively-E	RNAi;luciferase reporter assay;qRT-PCR;immunohistochemistry;western blot	upregulation		NA	NA	cell growth(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000148516	NA	84740	6935	AFAP1-AS|AFAP1AS|MGC10981	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	AFAP1-AS1 levels were much higher in ectopic endometrial tissues than that in eutopic tissues.Long non-coding RNA AFAP1-AS1 promoting epithelial-mesenchymal transition of endometriosis is correlated with transcription factor ZEB1.The knockdown of AFAP1-AS1 significantly inhibited expression from promoter site pGL3-P886 of the EMT-related transcription factor ZEB1.Expression of epithelial-mesenchymal transition (EMT) markers was quantified using qRT-PCR immunohistochemistry, and western blot.	30506548	RID06002	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	miR-124	MALAT1	negatively-F	luciferase reporter assay;RNAi	upregulation		NA	NA	PI3K/AKT signaling pathway(+)	NA	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Interaction of lncRNA-MALAT1 and miR-124 regulates HBx-induced cancer stem cell properties in HepG2 through PI3K/Akt signaling.miR-124 interacts with lncRNA-MALAT1 by direct targeting.HBx upregulated lncRNA-MALAT1 expression while downregulating miR-124 expression in HepG2-X cells.Overexpression of miR-124 or silencing of lncRNA-MALAT1 both blocked HBx-induced CSC generation, stemness-related factor activation and tumorigenicity via PI3K/Akt signaling.Our results demonstrated that miR-124 interact with lncRNA-MALAT1 and involve in regulating HBx-induced CSC properties via PI3K/Akt signaling.	30500989	RID06003	expression association	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Endometriosis	MALAT1	miR-200s	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Reproductive system disease	Endometriosis	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Estradiol promotes EMT in endometriosis via MALAT1/miR200s sponge function.Notably, E2 could upregulate MALAT1 and downregulate miR200s expression levels and induce EMT in EECs and Ishikawa cells.In addition, a reciprocal inhibition was found between miR200s and MALAT1.Previous studies have reported that MALAT1 upregulation and miR200s downregulation are observed in endometriosis.All qRT-PCRreactions were performed in duplicate on a StepOnePlus RT-PCRsystem (Applied Biosystems). The relative mRNA and miRNA expression levels were calculated by 2-Ct method.	30500775	RID06004	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Malignant glioma	OIP5-AS1	Wnt-7b	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-410)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410.To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCRThe targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays.The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues.Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/beta-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells.	30498093	RID06005	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Breast cancer	NDRG1-ot1	NDRG1	negatively-F;positively-F	luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell invasion(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000104419	NA	NA	10397	NA	CAP43|CMT4D|DRG-1|DRG1|GC4|HMSNL|NDR1|NMSL|PROXY1|RIT42|RTP|TARG1|TDD5	the purpose of this study was to study how NDRG1-OT1 transcriptionally regulates its target gene NDRG1.Different effects of long noncoding RNA NDRG1-OT1 fragments on NDRG1 transcription in breast cancer cells under hypoxia.Luciferase reporter assays showed that NDRG1-OT1 decreased NDRG1 promoter activities.the second quarter fragment (150-263 nt) repressed NDRG1 by increasing the binding affinity of HNRNPA1the third quarter fragment (264-392 nt) improved NDRG1 promoter activity by recruiting HIF-1alpha;the fourth quarter fragment (393-508 nt) down-regulated NDRG1 promoter activity via down-regulation of KHSRP under hypoxia.Recently, long non-coding RNA (lncRNA) has been reported to promote or inhibit tumor aggressiveness by regulating gene expression.Therefore, the purpose of this study was to study how NDRG1-OT1 transcriptionally regulates its target gene NDRG1.	30497328	RID06006	transcriptional regulation	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Endometrial cancer	LOC134466	TAC1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	NA	NA	ENSG00000006128	NA	NA	6863	NA	NKNA|NPK|TAC2	LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis.We also found that TAC1 was the target gene of LOC134466 and miRNA, hsa-miR-196a-5p, might form a connection between LOC134466 and TAC1.The relationship was further proved by luciferase reporter assay.In vitro studies, DNA methylation and expression were determined by MSP and qRT-PCRrespectively.TAC1 transcription was regulated by LOC134466 via hsa-miR-196a-5p binding. the expression of TACR1, TACR2 and TACR3 was remarkably decreased through LOC134466 and TAC1 treatments.	30485833	RID06007	epigenetic regulation	NA		
Ovarian cancer	OVAAL	PSMD9	negatively-E	RIP;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(-);cell growth(-);senescence(+)	ceRNA(PTBP1)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000236719	GRCh38_1:180509380-180566523	ENSG00000110801	NA	148756	5715	LINC01131|OVAL|RMEL2	Rpn4|p27	Dual functions for OVAAL in initiation of RAF/MEK/ERK prosurvival signals and evasion of p27-mediated cellular senescence.This work identified a commonly up-regulated lncRNA, ovarian adenocarcinoma-amplified lncRNA (OVAAL), that conferred apoptotic resistance in multiple cancer types.Functional investigations showed that OVAAL depletion significantly inhibited cancer cell proliferation and retarded tumor xenograft growth.Mechanically, OVAAL physically interacted with serine/threonine-protein kinase 3 (STK3), which, in turn, enhanced the binding between STK3 and Raf-1.On the other hand, depletion of OVAAL triggered cellular senescence through polypyrimidine tract-binding protein 1 (PTBP1)-mediated p27 expression, which was regulated by competitive binding between OVAAL and p27 mRNA to PTBP1.	30478051	RID06008	ceRNA or sponge	NA		UP(PAAD,PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939)
Ovary adenocarcinoma	OVAAL	STK3	positively-F	RIP;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(-);cell growth(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000236719	GRCh38_1:180509380-180566523	ENSG00000104375	NA	148756	6788	LINC01131|OVAL	KRS1|MST2	Dual functions for OVAAL in initiation of RAF/MEK/ERK prosurvival signals and evasion of p27-mediated cellular senescence.This work identified a commonly up-regulated lncRNA, ovarian adenocarcinoma-amplified lncRNA (OVAAL), that conferred apoptotic resistance in multiple cancer types.Functional investigations showed that OVAAL depletion significantly inhibited cancer cell proliferation and retarded tumor xenograft growth.Mechanically, OVAAL physically interacted with serine/threonine-protein kinase 3 (STK3), which, in turn, enhanced the binding between STK3 and Raf-1.On the other hand, depletion of OVAAL triggered cellular senescence through polypyrimidine tract-binding protein 1 (PTBP1)-mediated p27 expression, which was regulated by competitive binding between OVAAL and p27 mRNA to PTBP1.	30478051	RID06009	interact with protein	NA		UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Osteosarcoma	UCA1	MIR182	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000207990	NA	652995	406958	CUDR|LINC00178|onco-lncRNA-36|UCAT1	hsa-mir-182|miR-182|MIRN182	Long Non-Coding RNA Urothelial Carcinoma Associated 1 Promotes Proliferation, Migration and Invasion of Osteosarcoma Cells by Regulating microRNA-182.UCA1 was highly expressed in osteosarcoma MG63 and OS-732 cells.miR-182 was up-regulated in OS-732 cells after UCA1 knockdown and participated in the effects of UCA1 on OS-732 cells.	30481751	RID06010	expression association	NA	UP(PAAD);DATA(GSE40174)	
Colorectal cancer	TP73-AS1	PTEN	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	microarray	NA	NA	cell proliferation(+);cell growth(-);apoptosis process(-)	ceRNA(miR-103)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000171862	NA	57212	5728	KIAA0495|PDAM	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA TP73-AS1 promotes colorectal cancer proliferation by acting as a ceRNA for miR-103 to regulate PTEN expression.We found that TP73-AS1 expression was significantly low in CRC tissues and cells,TP73-AS1 expression levels were positively associated with PTEN levels in clinical CRC samples.TP73-AS1 overexpression could increase PTEN expression through competitive binding to miR-103.Moreover, TP73-AS1 overexpression dramatically inhibited CRC cell growth, promoted apoptosis, downregulated Bcl-2 levels, and increased caspase-3 expression.we showed that TP73-AS1 inhibits CRC cell growth by functioning as a ceRNA (competing endogenous RNAs) to regulate PTEN levels.our data show that such TP73-AS1-induced PTEN expression through binding to miR-103 facilitated CRC cell proliferation.lncRNA TP73-AS1 expression was measured using in situ hybridization in tissue microarrays with BersinBio (Guangzhou, China).	30472379	RID06011	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Threatened abortion	TCL6	EGFR	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	EGFR signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	NA	Other	Threatened abortion	lncRNA	PCG	ENSG00000187621	GRCh38_14:95650498-95679833	ENSG00000146648	NA	27004	1956	TCL6e1|TNG1|TNG2	ERBB|ERBB1|ERRP	LncRNA-TCL6 promotes early abortion and inhibits placenta implantation via the EGFR pathway.The expression levels of lncRNA-TCL6 and epidermal growth factor receptor (EGFR) in placental tissues of normal pregnancy, threatened abortion pregnancy, spontaneous abortion pregnancy, and induced abortion pregnancy were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR.Rescue experiments were performed to investigate the relationship between EGFR and lncRNA-TCL6.The expression of lncRNA-TCL6 in placenta tissues of threatened abortion pregnancy was significantly higher than that of normal pregnancy.After knockdown of lncRNA-TCL6 in trophoblast cells, the protein expression levels of EGFR, ERK, and AKT were significantly increased when compared with those of the control group.	30468451	RID06012	expression association	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Prostate cancer	LINC00518	miR-216b-5p	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Paclitaxel	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000183674	GRCh38_6:10429255-10435015	NA	NA	221718	NA	C6orf218|MGC40222	NA	Long non-coding RNA Linc00518 promotes paclitaxel resistance of the human prostate cancer by sequestering miR-216b-5p.To characterise Linc00518 expression in prostate cancer and elucidate the potential mechanistic involvement in paclitaxel resistance, the relative expression of Linc00518 and miR-216b-5p was determined by real-time PCR.The regulatory effect of miR-216b-5p on either Linc00518 or GATA6 was interrogated with luciferase reporter assay.Linc00518 was highly expressed in prostate tumour both in vivo and in vitro.Linc00518 competitively inhibited miR-216b-5p through sponging mechanism.	30462844	RID06013	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	
Breast cancer	DSCAM-AS1	RRM2	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-204-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000171848	NA	100506492	6241	M41	C2orf48|FLJ25102	DSCAM-AS1 promotes tumor growth of breast cancer by reducing miR-204-5p and up-regulating RRM2.microarray analysis and quantitative Real Time fluorescence Polymerase Chain Reaction (qRT-PCR were employed to determine DSCAM-AS1 and miR-204-5p expression.Luciferase reporter assay was applied to examine the target relationship between DSCAM-AS1, miR-204-5p, and RRM2.DSCAM-AS1 directly targeted miR-204-5p.DSCAM-AS1 promoted the proliferation and invasion of BC cells by reducing miR-204-5p and inhibiting miR-204-5p expression.DSCAM-AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR-204-5p and enhancing RRM2 expression.RRM2 was up-regulated in BC cells, and miR-204-5p inhibited RRM2 expression by targeting RRM2.DSCAM-AS1 directly targeted miR-204-6p.	30457164	RID06014	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Non-small cell lung cancer	Lnc-SNHG1	MIR497	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	ENSG00000284027	NA	NA	574456	NA	MIRN497|hsa-mir-497|mir-497	Lnc-SNHG1 may promote the progression of non-small cell lung cancer by acting as a sponge of miR-497.The transcript level of lnc-SNHG1 was higher in lung adenocarcinoma specimens and NSCLC cell lines than in noncancer tissue and cells.we found that lnc-SNHG1 might modulate tumor growth by sponging miR-497.our study demonstrated that the lnc-SNHG1 regulated the expression of the insulin-like growth factor 1 receptor (IGF1-R) by acting as a sponge of miR-497 in NSCLC.In exploring the regulatory mechanism, we found that lnc-SNHG1 might modulate tumor growth by sponging miR-497.	30454699	RID06015	ceRNA or sponge	NA		
Gastric cancer	MIR4435-2HG	NTRK3	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	ceRNA(miR-497)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000140538	NA	541471	4916	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	TRKC	Long non-coding RNA LINC00978 promotes cell proliferation and tumorigenesis via regulating microRNA-497/NTRK3 axis in gastric cancer.LINC00978 was up-regulated in GC tissues and cell lines.LINC00978 functioned as competing endogenous RNA to inhibit miR-497 expression.	30452981	RID06016	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407)
Gastric cancer	STAT3	LINC00165	positively-E	luciferase reporter assay;ChIP;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000261706	GRCh38_21:44994362-44995185	6774	727701	APRF	C21orf135|NCRNA00165|NLC1-B	Long noncoding RNA LINC00165-induced by STAT3 exerts oncogenic properties via interaction with Polycomb Repressive Complex 2 to promote EMT in gastric cancer.our results showed that LINC00165 was upregulated in GC tissues and cell lines and high expression of LINC00165 was correlated with tumor-node-metastasis stage, invasion depth, and overall survival of GC patients.STAT3 could bind directly to the region between 547 bp to 537 bp (ATGTTGGGAAA) of LINC00165 promoter and activate its transcription.revealed that LINC00165 functioned as a scaffold for interaction with Polycomb Repressive Complex 2 to promote the epithelial-mesenchymal transition in GC cells.Online transcription factor binding site prediction analysis showed that there were STAT3 binding sites in the LINC00165 promoter region.	30448060	RID06017	transcriptional regulation	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Colorectal cancer	SCARNA2	EGFR	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000270066	GRCh38_1:109100193-109100619	ENSG00000146648	NA	677766	1956	HBII-382|mgU2-25/61	ERBB|ERBB1|ERRP	The lncRNA SCARNA2 mediates colorectal cancer chemoresistance through a conserved microRNA-342-3p target sequence.we found that lncRNA small Cajal body-specific RNA 2 (SCARNA2) is expressed higher in CRC tissues than in adjacent normal tissues, and a robust expression of SCARNA2 is correlated with a bad prognosis of CRC patients after surgery.SCARNA2 promotes chemotherapy resistance via competitively binding miR-342-3p to facilitate epidermal growth factor receptor (EGFR) and B-cell lymphoma 2 (BCL2) expression in CRC cells.Together, our results reveal a novel pathway that SCARNA2 regulates CRC chemoresistance through targeting miR-342-3p-EGFR/BCL2 pathway, providing a promising therapeutic target for CRC.	30443961	RID06018	ceRNA or sponge	chemoresistance,prognosis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	SCARNA2	BCL2	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000270066	GRCh38_1:109100193-109100619	ENSG00000171791	NA	677766	596	HBII-382|mgU2-25/61	Bcl-2|PPP1R50	The lncRNA SCARNA2 mediates colorectal cancer chemoresistance through a conserved microRNA-342-3p target sequence.we found that lncRNA small Cajal body-specific RNA 2 (SCARNA2) is expressed higher in CRC tissues than in adjacent normal tissues, and a robust expression of SCARNA2 is correlated with a bad prognosis of CRC patients after surgery.SCARNA2 promotes chemotherapy resistance via competitively binding miR-342-3p to facilitate epidermal growth factor receptor (EGFR) and B-cell lymphoma 2 (BCL2) expression in CRC cells.Together, our results reveal a novel pathway that SCARNA2 regulates CRC chemoresistance through targeting miR-342-3p-EGFR/BCL3 pathway, providing a promising therapeutic target for CRC.	30443961	RID06019	ceRNA or sponge	chemoresistance,prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	OIP5-AS1	SOX2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000181449	NA	729082	6657	cyrano|linc-OIP5	NA	Downregulation of long non-coding RNA Opa interacting protein 5-antisense RNA 1 inhibits breast cancer progression by targeting sex-determining region Y-box 2 by microRNA-129-5p upregulation.OIP5-AS1 was significantly upregulated in breast cancer tissues and in breast cancer cell lines, and OIP5-AS1 downregulation inhibited the malignant behavior of breast cancer in vitro and in vivo.For in-depth exploration of the mechanism of OIP5-AS1 in breast cancer, we found that expression of microRNA-129-5p(miR-129-5p), which was found to bind sites in the sequence of OIP5-AS1, in breast cancer tissues was negatively correlated with OIP5-AS1.Also, luciferase assays indicated that OIP5-AS1 acted as a miR-129-5p sponge, resulting in upregulated expression of the sex-determining region Y-box 2 (SOX2) transcription factor.	30443959	RID06020	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC);DATA(GSE117623)
Glioblastoma	AC003092.1	TFPI2	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	apoptosis process(+);chemosensitivity(+)	ceRNA(miR-195)	regulation	RNA-protein	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236453	GRCh38_7:94022833-94066661	ENSG00000105825	NA	NA	7980	NA	PP5|REF1|TFPI-2	Long noncoding RNA AC003092.1 promotes temozolomide chemosensitivity through miR-195/TFPI-2 signaling modulation in glioblastoma.we found that the expression of lncRNA AC003092.1 was markedly decreased in TMZ resistance (TR) of GB cells (U87TR and U251TR) compared with their parental cells (U87 and U251).Taken together, these data suggest that lncRNA AC003092.1 could inhibit the function of miR-195 by acting as an endogenous CeRNA, leading to increased expression of TFPI-2;this promotes TMZ-induced apoptosis, thereby making GB cells more sensitive to TMZ.Mechanistically, further investigation revealed that lncRNA AC003092.1 regulates TFPI-2 expression through miR-195 in GB.	30442884	RID06021	ceRNA or sponge	chemoresistance		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Ovarian cancer	LINC00319	miR-423-5p	negatively-F	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000188660	GRCh38_21:43446601-43453902	NA	NA	284836	NA	C21orf125|FLJ38036|NCRNA00319|PRED49	NA	LncRNA LINC00319 accelerates ovarian cancer progression through miR-423-5p/NACC1 pathway.LINC00319 expression was found to be upregulated in ovarian cancer tissues and cell lines.Bioinformatics analysis and luciferase reporter assay revealed that LINC00319 worked as the sponge for miR-423-5p.qRT-PCRand western blot results demonstrated that LINC00319 upregulates NACC1 expression through inhibiting miR-423-5p in ovarian cancer cells.we observed an inverse expression correlation between miR-423-5p and LINC00319 or between miR-423-5p and NACC1 in ovarian cancer tissues.our findings demonstrated that LINC00319 promotes ovarian cancer progression through upregulating NACC1 expression by restraining miR-423-5p.Furthermore, miR-423-5p directly targeted NACC1.Moreover, we observed an inverse expression correlation between miR-423-5p and LINC00319 or between miR-423-5p and NACC1 in ovarian cancer tissues.Finally, rescue assay showed that NACC1 restoration rescued the potentials of proliferation, migration and invasion in LINC00319-depleted ovarian cancer cells.In conclusion, our findings demonstrated that LINC00319 promotes ovarian cancer progression through upregulating NACC1 expression by restraining miR-423-5p.	30442370	RID06022	ceRNA or sponge	NA		
Ovarian cancer	LINC00319	NACC1	positively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-423-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000160877	NA	284836	112939	C21orf125|FLJ38036|NCRNA00319|PRED49	BEND8|BTBD14B|BTBD30|NAC-1|NAC1	LncRNA LINC00319 accelerates ovarian cancer progression through miR-423-5p/NACC1 pathway.LINC00319 expression was found to be upregulated in ovarian cancer tissues and cell lines.Bioinformatics analysis and luciferase reporter assay revealed that LINC00319 worked as the sponge for miR-423-5p.qRT-PCRand western blot results demonstrated that LINC00319 upregulates NACC1 expression through inhibiting miR-423-5p in ovarian cancer cells.we observed an inverse expression correlation between miR-423-5p and LINC00319 or between miR-423-5p and NACC1 in ovarian cancer tissues.our findings demonstrated that LINC00319 promotes ovarian cancer progression through upregulating NACC1 expression by restraining miR-423-5p.Furthermore, miR-423-5p directly targeted NACC1.Moreover, we observed an inverse expression correlation between miR-423-5p and LINC00319 or between miR-423-5p and NACC1 in ovarian cancer tissues.Finally, rescue assay showed that NACC1 restoration rescued the potentials of proliferation, migration and invasion in LINC00319-depleted ovarian cancer cells.In conclusion, our findings demonstrated that LINC00319 promotes ovarian cancer progression through upregulating NACC1 expression by restraining miR-423-6p.	30442370	RID06023	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HOTAIR	E-cadherin	negatively-E	RNAi;ChIP	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	histone modification	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOX transcript antisense intergenic RNA (HOTAIR), a well-known long non-coding RNA, plays an important role in the regulation of epithelial-to-mesenchymal transition (EMT).In this study, we propose a novel mechanism through which HOTAIR promotes EMT by switching histone H3 lysine 27 acetylation to methylation at the E-cadherin promoter, which induces the transcriptional inhibition of E-cadherin.In this study, HOTAIR knockdown significantly reversed EMT by increasing the expression of E-cadherin in GC cells.HOTAIR can promote the development of GC through the epigenetic regulation of E-cadherin, switching the state of the E-cadherin promoter from the transcriptionally active to the transcriptionally repressive state.	30431069	RID06024	epigenetic regulation	NA		
Urinary bladder cancer	DANCR	MSI2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor malignant transformation(-)	ceRNA(miR-149)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000153944	NA	57291	124540	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	Long non-coding RNA DANCR promotes malignant phenotypes of bladder cancer cells by modulating the miR-149/MSI2 axis as a ceRNA.The relative expression level of DANCR was determined by Real-Time qPCR in a total of 106 patients with urothelial bladder cancer and in different bladder cancer cell lines.Loss-of-function experiments were performed to investigate the biological roles of DANCR on bladder cancer cell proliferation, migration, invasion and tumorigenicity.we found that DANCR was significantly up-regulated in bladder cancer. we found that DANCR was distributed mostly in the cytoplasm and DANCR functioned as a miRNA sponge to positively regulate the expression of musashi RNA binding protein 2 (MSI2) through sponging miR-149 and subsequently promoted malignant phenotypes of bladder cancer cells, thus playing an oncogenic role in bladder cancer pathogenesis.	30419948	RID06025	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Gastric cancer	CYTOR	ETS1	positively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-193b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000134954	NA	112597	2113	C2orf59|LINC00152|MGC4677|NCRNA00152	ETS-1|EWSR2|FLJ10768	Knockdown of linc00152 inhibits the progression of gastric cancer by regulating microRNA-193b-3p/ETS1 axis.RT-qPCR assay was employed to detect the levels of linc00152, microRNA-193b-3p (miR-193b-3p) and ETS1 mRNA.Bioinformatics analyses and luciferase reporter assay were used to explore whether miR-193b-3p could interact with linc00152 or ETS1 3'UTR.Linc00152 expression was notably upregulated in GC tissues and cells.Linc00152 upregulation inhibited miR-193b-3p expression by direct interaction and abolished miR-193b-3p-mediated anti-proliferation, anti-migration and anti-invasion effects in GC cells.ETS1 was a target of miR-193b-3p and linc00152 could promote ETS1 expression by downregulating miR-193b-3p.	30404587	RID06026	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	HOXB-AS3	TP53	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cancer progression(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000141510	NA	404266	7157	NA	LFS1|p53	lncRNA HOXB-AS3 promotes hepatoma by inhibiting p53 expression.The expression of HOXB-AS3 in tumor tissues and adjacent tissues of hepatocellular carcinoma was detected by quantitative real time-polymerase chain reaction (qRT-PCR, and the relationship between the expression of HOXB-AS3 and tumor tissues was analyzed.The binding relationship between HOXB-AS3 and DNMT1 and the regulation mechanism of DNMT1 on p53 were tested by RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) experiments, respectively.The results of qRT-PCR;ISHowed that the expression of HOXB-AS3 was significantly higher in cancerous tissues of patients with hepatocellular carcinoma than in adjacent tissues.The results of RIP and ChIP experiments showed that HOXB-AS3 inhibited the expression of p53 by binding to DNMT1, and overexpression of p53 in Hep3B cells could partially reverse the changes in cell proliferation and apoptosis induced by HOXB-AS3.	30402841	RID06027	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	SNHG20	LIN28A	negatively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+) 	ceRNA(miR-197)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000131914	NA	654434	79727	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	CSDD1|FLJ12457|LIN-28|LIN28|ZCCHC1	Long non-coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR-197/LIN28 axis.In vitro and in vivo, loss-of-function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth.Bioinformatics and luciferase reporter assay revealed that miR-197 targeted the 3'-untranslated regions of SNHG20 and LIN28 by complementary binding.Validation experiments confirmed the associated functions of SNHG20/miR-197/LIN28 axis on OSCC proliferation and stemness.SNHG20 promoted LIN28 through sponging miR-197	30394668	RID06028	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC);DATA(GSE117623)
Hepatoblastoma	H19	PTK2	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell growth(-)	ceRNA(miR-138)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000169398	NA	283120	5747	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	FADK|FAK|FAK1|PPP1R71	H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2. Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR-138 and downregulated the expression of FADD via targeting miR-675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.	30367502	RID06029	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE75367)
Hepatoblastoma	H19	FADD	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell growth(-)	ceRNA(miR-675)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168040	NA	283120	8772	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	GIG3|MORT1	Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR-138 and downregulated the expression of FADD via targeting miR-675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.	30367502	RID06030	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Gastric cancer	MALAT1	ATG5	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-30b)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000057663	NA	378938	9474	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APG5|APG5L|ASP|hAPG5	LncRNA MALAT1 potentiates autophagy-associated cisplatin resistance by regulating the microRNA-30b/autophagy-related gene 5 axis in gastric cancer.Further investigations demonstrated that MALAT1 inhibited miR-30b expression by direct interaction. Moreover, miR-30b abolished MALAT1-induced CDDP resistance by inhibiting autophagy in AGS/CDDP and HGC-27/CDDP cells. Furthermore, ATG5 was found to be a target of miR-30b.Additionally, MALAT1 sequestered miR-30b from ATG5 to increase ATG5 expression in AGS/CDDP and HGC-27/CDDP cells.	30365113	RID06031	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	MALAT1	CCND1	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(+);cell viability(-);cell invasion(-);cell migration(-)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000110092	NA	378938	595	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	BCL1|D11S287E|PRAD1|U21B31	Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR-34a/cyclin D1 axis.In addition, MALAT1 promoted OS cell viability, invasion and migration, while MALAT1 silencing exhibited opposing effects. Moreover, MALAT1 functioned as a ceRNA to suppress miR-34a expression and in turn upregulate CCND1 in OS cells.	30365098	RID06032	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Sepsis	TFDP1	E-selectin	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	NA	NA	7027	NA	DILC|Dp-1|DP1|DRTF1	NA	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-0 siRNAs	30365067	RID06033	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Sepsis	TFDP1	CXCR1	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000163464	NA	7027	3577	DILC|Dp-1|DP1|DRTF1	CD181|CDw128a|CKR-1|CMKAR1|IL8RA	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-1 siRNAs	30365067	RID06034	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Sepsis	TFDP1	CCL5	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000161570	NA	7027	6352	DILC|Dp-1|DP1|DRTF1	D17S136E|MGC17164|RANTES|SCYA5|SISd|TCP228	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-2 siRNAs	30365067	RID06035	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Sepsis	TFDP1	TNF	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000228978	NA	7027	7124	DILC|DP1|DRTF1|Dp-1	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-3 siRNAs	30365067	RID06036	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC);DATA(GSE117623)
Sepsis	TFDP1	TLR4	negatively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000136869	NA	7027	7099	DILC|Dp-1|DP1|DRTF1	ARMD10|CD284|hToll|TLR-4	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-4 siRNAs	30365067	RID06037	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Sepsis	TFDP1	STAT3	negatively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	TF	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000168610	NA	7027	6774	DILC|Dp-1|DP1|DRTF1	APRF	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-5 siRNAs	30365067	RID06038	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Sepsis	TFDP1	IL6	negatively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);STAT3 signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000136244	NA	7027	3569	DILC|Dp-1|DP1|DRTF1	BSF2|HGF|HSF|IFNB2|IL-6	Long non-coding RNA DILC is involved in sepsis by modulating the signaling pathway of the interleukin-6/signal transducer and activator of transcription 3/Toll-like receptor 4 axis.On the other hand, compared with the scramble control, DILC and IL-6 small interfering (si)RNAs significantly suppressed the expression of IL-6, STAT3 and TLR4. In addition, DILC siRNA enhanced the expression of IL-6, STAT3 and TLR4, whereas the expression levels of TNF-alpha, CCL5, E-selectin and CXCR1 in LPS-treated THP-1 cells were downregulated following transfection with DILC and IL-6 siRNAs	30365067	RID06039	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Squamous cell carcinoma	UCA1	LC3-II	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA1 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID06040	expression association	NA	UP(PAAD);DATA(GSE40174)	
Squamous cell carcinoma	UCA1	p62	negatively-F	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000073792	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA2 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID06041	expression association	NA	UP(PAAD);DATA(GSE40174)	
Squamous cell carcinoma	UCA1	ATG5	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000057663	NA	652995	9474	CUDR|LINC00178|onco-lncRNA-36|UCAT1	APG5|APG5L|ASP|hAPG5	Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA3 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.	30362538	RID06042	expression association	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	H19	TWIST1	positively-E	RNA pull-down assay;RNAi;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	H19 downregulation can increase miR-326 expression in HCC cells. Meanwhile, miR-326 mimics can also inhibit HCC progression, whereas miR-326 inhibitors exhibited a reverse phenomenon by modulating H19 expression. In addition, a negative association between H19 and miR-326 was predicted and confirmed. Furthermore, the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression. Here, by performing bioinformatics analysis, TWIST1 was identified as a downstream target of miR-326. The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR-326 and modulate TWIST1 levels in HCC pathogenesis. Taken these together, these findings indicated that H19/miR-326/TWIST1 axis was involved in HCC development and can indicate a novel HCC target.	30362512	RID06043	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(SKCM);DATA(GSE38495)
Pancreatic ductal adenocarcinoma	NEAT1	RELA	positively-E	Chip;luciferase reporter assay;RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-302a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000173039	NA	283131	5970	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NFKB3|p65	RELA/NEAT1/miR-302a-3p/RELA feedback loop modulates pancreatic ductal adenocarcinoma cell proliferation and migration.RELA overexpression promoted PDAC cell proliferation and migration, which could be partially attenuated by the NEAT1 knockdown. By binding to RELA, miR-302a-3p inhibited RELA expression, as well as PDAC cell proliferation and migration. RELA downstream NEAT1 expression was negatively regulated by miR-302a-3p; the suppressive effect of NEAT1 knockdown on PDAC cell proliferation and migration was partially attenuated by miR-302a-3p inhibition. Moreover, through direct binding, the expression of miR-302a-3p was also negatively regulated by NEAT1. The expression of miR-302a-3p was downregulated and negatively correlated with RELA or NEAT1 in tissue samples, indicating that rescuing miR-302a-3p expression may inhibit PDAC cell proliferation and migration through RELA/NEAT1. In summary, RELA, NEAT1, and miR-302a-3p form a feedback loop in PDAC to modulate PDAC cell proliferation and migration.	30362505	RID06044	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteoarthritis	DANCR	JAK2	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);JAK2/STAT3 signaling pathway(+);inflammatory response(+)	ceRNA(miR-216a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000096968	NA	57291	3717	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	JTK10	The expression of DANCR in cartilage tissues from OA patients was detected using quantitative real-time PCR.Novel target of DANCR was then identified through bioinformatics analysis and confirmed by luciferase reporter assay and RNA immunoprecipitation assay.Additionally, DANCR regulated survival of OA chondrocytes through acting as a competitive endogenous RNA for miR-216a-5p.In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.	30361290	RID06045	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Pancreatic ductal adenocarcinoma	MALAT1	ZEB1	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-200c-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 upregulated SMAD3 expression to contribute to metastasis of cervical cancer by sponging miR-143-3p.Clinical data further indicated that MALAT-1 and ZEB1 expression was negatively correlated with miR-200c-3p transcript level of PDAC tissues. There was a positive correlation between MALAT-1 and ZEB1 level.Expressions of relative genes were assessed by quantitative real-time PCR and western blot, respectively.Moreover, RNA immunoprecipitation was performed to determine whether RNA-induced silencing complex contained MALAT-1 and its potential binding miRNA.Luciferase assays was used to confirm potential binding site.On the one hand, MALAT-1 functioned as a competing endogenous RNA to suppress miR-200c-3p expression, leading to upregulation of ZEB1 expression.	30352575	RID06046	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	OIP5-AS1	SMAD3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000166949	NA	729082	4088	cyrano|linc-OIP5	HsT17436|JV15-2|MADH3	Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 upregulated SMAD3 expression to contribute to metastasis of cervical cancer by sponging miR-143-3p.LncRNA OIP5-AS1 is demonstrated to mediate the physiological process of cervical cancer cells. Moreover, silencing SMAD3 via siRNA suppressed cell number, viability, migration and invasion, whereas overexpression of OIP5-AS1 promoted these abilities. Furthermore, lncRNA OIP5-AS1 exert its function via sponging miR-143-3p to regulate SMAD3 expression.	30341904	RID06047	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic carcinoma	PVT1	DGCR8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);chemosensitivity(-)	ceRNA(miR-1207-5p;miR-1207-3p)	regulation	RNA-protein	Gemcitabine	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000128191	NA	5820	54487	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	C22orf12|DGCRK6|Gy1|pasha	Gemcitabine exhibits a suppressive effect on pancreatic cancer cell growth by regulating processing of PVT1 to miR1207 .Pvt1 oncogene (non-protein coding) (PVT1) has been reported to be an oncogenic long non-coding RNA in tumorigenesis. In the present study, we show that the expression of PVT1 is correlated with gemcitabine efficacy in PC therapy. Inhibition of PVT1 led to decreased cell growth in PC cells treated with gemcitabine. We also demonstrate that gemcitabine treatment decreases PVT1 levels and increases its encoded miRNAs, such as the miR-1207 pair (miR-1207-5p/3p).Mechanistic studies revealed that miR-1207-5p and miR-1207-3p target the SRC proto-oncogene (non-receptor tyrosine kinase) and ras homolog family member A in PC cells, respectively. In particular, we observed that gemcitabine induced Drosha ribonuclease III (Drosha) and DGCR8 microprocessor complex subunit (DGCR8) upregulation and then triggered PVT1 processing.	30341811	RID06048	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic carcinoma	PVT1	DROSHA	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);chemosensitivity(-)	ceRNA(miR-1207-5p;miR-1207-3p)	regulation	RNA-protein	Gemcitabine	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000113360	NA	5820	29102	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Etohi2|HSA242976|RN3|RNASE3L|RNASEN	Gemcitabine exhibits a suppressive effect on pancreatic cancer cell growth by regulating processing of PVT1 to miR1207 .Pvt1 oncogene (non-protein coding) (PVT1) has been reported to be an oncogenic long non-coding RNA in tumorigenesis. In the present study, we show that the expression of PVT1 is correlated with gemcitabine efficacy in PC therapy. Inhibition of PVT1 led to decreased cell growth in PC cells treated with gemcitabine. We also demonstrate that gemcitabine treatment decreases PVT1 levels and increases its encoded miRNAs, such as the miR-1207 pair (miR-1207-5p/3p).Mechanistic studies revealed that miR-1207-5p and miR-1207-3p target the SRC proto-oncogene (non-receptor tyrosine kinase) and ras homolog family member A in PC cells, respectively. In particular, we observed that gemcitabine induced Drosha ribonuclease III (Drosha) and DGCR8 microprocessor complex subunit (DGCR8) upregulation and then triggered PVT1 processing.	30341811	RID06049	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827)
Multiple myeloma	NEAT1	SOX13	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000143842	NA	283131	9580	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ICA12|MGC117216|Sox-13	Overexpression of SOX13 was able to partially restore the inhibitory effect of NEAT1 on cell proliferation. Meanwhile, it was found that low expression of NEAT1 significantly inhibited tumor formation in vivo.NEAT1 and SOX13 were highly expressed in MM patients and MM cell lines, and the patient survival rate and platelet count were significantly decreased in the highly expressed NEAT1 group.Low expression of NEAT1 could inhibit the PI3K/AKT pathway to suppress cell proliferation, promote apoptosis, and inhibit cell cycle.Overexpression of SOX13 was able to partially restore the inhibitory effect of NEAT1 on cell proliferation. Highly expressed NEAT1 promoted cell proliferation through activation of PI3K/AKT pathway, thus participating in the development of MM.	30338809	RID06050	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Endometriosis	MALAT1	HIF1A	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell autophagy(+)	NA	association	NA	NA	NA	NA	Reproductive system disease	Endometriosis	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100644	NA	378938	3091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	In the present study, we found that both lncRNA-MALAT1 and autophagy level were up-regulated in ectopic endometrium from patients with endometriosis, and its expression level correlates positively with that of hypoxia-inducible factor-1alpha (HIF-1alpha).In cultured human endometrial stromal cells, both lncRNA-MALAT1 and autophagy were induced by hypoxia in a time-dependent manner and lncRNA-MALAT1 up-regulation was dependent on HIF-1alpha signalling.Our analyses also show that knockdown of lncRNA-MALAT1 suppressed hypoxia induced autophagy. Furthermore, inhibiting autophagy with specific inhibitor 3-Methyladenine (3-MA) and Beclin1 siRNA enhanced apoptosis of human endometrial stromal cells under hypoxia condition.	30324652	RID06051	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	NNT-AS1	MIR363	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell cycle(+);cell invasion(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000207572	NA	100652772	574031	NA	MIR-363|MIRN363|hsa-mir-363	We also showed that NNT-AS1 expression was upregulated in the GC cell lines.In addition, we showed that NNT-AS1 acted as a sponge competing endogenous RNA for microRNA-363 (miR-363), which was downregulated in the GC samples and cell lines. miR-363 expression was negatively related with NNT-AS1 expression in GC samples. Upregulated expression of miR-363 suppressed GC cell growth, cycle, and invasion.	30324628	RID06052	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Malignant glioma	GAS5	p62	positively-E	western blot;RNAi;siRNA	downregulation	qRT-PCR	NA	NA	chemoresistance(+);mTOR signaling pathway(+)	NA	association	RNA-protein	Cisplatin	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000073792	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA growth arrest-specific 5 facilitates glioma cell sensitivity to cisplatin by suppressing excessive autophagy in an mTOR-dependent manner.In the current study, the expression of GAS5 was decreased in glioma cell lines, and lower levels of GAS5 were observed in U138 and LN18 glioma cells that had low sensitivity to cisplatin.Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression.Cumulatively, these findings indicate that GAS5 may blunt the resistance of glioma cells to cisplatin by suppressing excessive autophagy through the activation of mTOR signaling, implying a promising therapeutic strategy against chemoresistance in glioma.	30317677	RID06053	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	GAS5	LC3II	negatively-E	western blot;RNAi;siRNA	downregulation	qRT-PCR	NA	NA	chemoresistance(+);mTOR signaling pathway(+)	NA	association	RNA-RNA	Cisplatin	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA growth arrest-specific 5 facilitates glioma cell sensitivity to cisplatin by suppressing excessive autophagy in an mTOR-dependent manner.In the current study, the expression of GAS5 was decreased in glioma cell lines, and lower levels of GAS5 were observed in U138 and LN18 glioma cells that had low sensitivity to cisplatin.Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression.Cumulatively, these findings indicate that GAS6 may blunt the resistance of glioma cells to cisplatin by suppressing excessive autophagy through the activation of mTOR signaling, implying a promising therapeutic strategy against chemoresistance in glioma.	30317677	RID06054	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	GACAT3	ELAVL1	positively-E	luciferase reporter assay;bioinformatics analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-330-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000066044	NA	104797537	1994	LINC01458|lncRNA-AC130710	Hua|HUR|MelG	Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines.Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)-3127-5p.Subsequently, ELAVL1 was identified as a direct target of miR-3127-5p by bioinformatics analysis and luciferase reporter assay.Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR-3127-5p, leading to glioma progression.Taken together, our study elucidated that GACAT3/miR-3127-5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.	30317610	RID06055	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Gastric cancer	HOTAIRM1	PTEN	positively-E	luciferase reporter assay;western blot;miRcode;TargetScan	downregulation	microarray;qRT-PCR	NA	NA	PI3K/AKT signaling pathway(-);cancer progression(-)	ceRNA(miR-17-5p);PI3K signaling pathway;AKT signaling pathway	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000171862	NA	100506311	5728	HOXA-AS1|HOXA1-AS1|NCRNA00179	BZS|MHAM|MMAC1|PTEN1|TEP1	HOTAIRM1 and phosphatase and tensin homolog (PTEN) were both downregulated in GC, whereas miR-17-5p was upregulated. Moreover, the PI3K/AKT pathway was found activated in GC. HOTAIRM1 targeted miR-17-5p, whereas PTEN was the downstream target gene of miR-17-5p. HOTAIRM1 suppressed proliferation and migration of GC cell line and induced their apoptosis, whereas miR-17-5p played the opposite role on GC cell line. HOTAIRM1 also postponed tumor growth in vivo and inhibited the PI3K/AKT pathway in GC.LncRNA HORAIRM1 suppressed the PI3K/AKT pathway in GC and inhibited the progression of GC by serving as a competing endogenous RNA of miR-17-5p, mediating the expression of PTEN. We used microarray analysis to identify differentially expressed lncRNAs and mRNAs, whereas the obviously changed pathways were found by gene set enrichment analysis.The coexpression network of lncRNA and mRNA was constructed by Cytoscape, and their target relationships with miRNAs were predicted by miRcode and TargetScan.qRT-PCRand western blot were performed to determine the expression levels of mRNAs and proteins in tissues and cell lines.dual-luciferase reporter assay was applied to achieve the determination of the specific target relationships.	30302796	RID06056	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	AFAP1-AS1	IGF1R	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	GSE16515;GSE32688	NA	cell growth(+);cell invasion(+)	ceRNA(miR-133a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000140443	NA	84740	3480	AFAP1-AS|AFAP1AS|MGC10981	CD221|IGFIR|IGFR|JTK13|MGC18216	The long coding RNA AFAP1-AS1 promotes tumor cell growth and invasion in pancreatic cancer through upregulating the IGF1R oncogene via sequestration of miR-133a.Screening of published microarray data (GEO accession Nos. GSE16515 and GSE32688), revealed lncRNA AFAP1-AS1 to be one of the most upregulated lncRNAs in PC tissues.In particular, it was hypothesized that AFAP1-AS1 may act as a competitive endogenous RNA (ceRNA), effectively becoming a sink for miR-133a whose expression was found to be downregulated in PC tissues and cell lines, and which was negatively correlated with the expression of AFAP1-AS1.We also found that the IGF1R oncogene which is an important regulator of MEK/ERK signaling pathway, was positively regulated by AFAP1-AS1 through ameliorating miR-133a-mediated IGF1R repression in PC tissues.Collectively, the findings provide new evidence that AFAP1-AS1 could regulate the progression of pancreatic cancer by acting as a ceRNA, and suggest it has potential for use as both a biomarker for the early detection PC and for the development of individualized therapies for PC.	30300116	RID06057	ceRNA or sponge	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Ovarian cancer	MALAT1	RBFOX2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100320	NA	378938	23543	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	FOX-2|HNRBP2|HRNBP2|RBM9	The long non-coding RNA MALAT1 promotes ovarian cancer progression by regulating RBFOX2-mediated alternative splicing.Gene expression profiling was performed on ovarian cancer cells grown in attached or forced suspension culture and confirmed by RT-qPCR.High MALAT1 is associated with increased stage, recurrence, and reduced survival in ovarian cancer, and in a small percentage of ovarian cancers MALAT1 is amplified.Suppression of MALAT1 also resulted in decreased expression of RBFOX2, and alternative processing of the pro-apoptotic tumor suppressor gene KIF1B.The lncRNA MALAT1 facilitates a pro-metastatic phenotype in ovarian cancer by promoting alternative RNA processing and differential expression of anti-apoptosis and epithelial to mesenchymal transition (EMT)-related genes.	30294913	RID06058	expression association	metastasis,recurrence	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)
Gallbladder cancer	MEG3	EZH2	negaticely-E	ChIP;RIP;western blot;RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000106462	NA	55384	2146	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA MEG3 regulates LATS2 by promoting the ubiquitination of EZH2 and inhibits proliferation and invasion in gallbladder cancer.We found that MEG3 was downregulated in GBC tissues and cells, and low expression of MEG3 was correlated with poor prognostic outcomes in patients.Moreover, we found that MEG3 was associated with EZH2 and attenuated EZH2 by promoting its ubiquitination.	30282996	RID06059	epigenetic regulation	prognosis		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gallbladder cancer	MEG3	LATS2	positively-E	ChIP;RIP;western blot;RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150457	NA	55384	26524	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Long noncoding RNA MEG3 regulates LATS2 by promoting the ubiquitination of EZH2 and inhibits proliferation and invasion in gallbladder cancer.We found that MEG3 was downregulated in GBC tissues and cells, and low expression of MEG3 was correlated with poor prognostic outcomes in patients.Moreover, we found that MEG3 was associated with EZH2 and attenuated EZH2 by promoting its ubiquitination.	30282996	RID06060	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	LOXL1-AS1	CCND1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-541-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000110092	NA	100287616	595	NA	BCL1|D11S287E|PRAD1|U21B31	LOXL1-AS1 down-regulation inhibits the expression of CCND1 and cell cycle progression, whereas these effects are abolished upon miR-541-3p suppression.RNA sequencing analysis revealed that it regulates the expression of cell cycle-related genes. LOXL1-AS1 is predominantly distributed in the cytoplasm, where it interacts with miR-541-3p. In addition, miR-541-3p targets the cell cycle regulator CCND1 in prostate cancer cells. LOXL1-AS1 down-regulation inhibits the expression of CCND1 and cell cycle progression, whereas these effects are abolished upon miR-541-3p suppression. In summary, our study revealed that LOXL1-AS1 regulates prostate cancer cell proliferation and cell cycle progression through miR-541-3p and CCND1. Modulation of their levels may be used to treat prostate cancer.	30278884	RID06061	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Osteoarthritis	TP53COR1	MIR451A	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	NA	ENSG00000284565	NA	102800311	574411	TRP53COR1|linc-p21|lincRNA-p21	MIR451|MIRN451|hsa-mir-451|hsa-mir-451a|mir-451a	LncRNA-p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR-451.LncRNA-p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR-451.Overexpression of lncRNA-p21 suppressed the expression of miR-451 while the silencing of lncRNA-p21 reversed this effect. MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. The increased cell viability and decreased apoptosis rate induced by lncRNA-p21 silencing was abolished by the miR-451 inhibitor. MiR-451 mimic effectively increased the downregulatory effect of pcDNA3.	30272288	RID06062	ceRNA or sponge	NA		
Gastric adenocarcinoma	CCAT1-L	MYC	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.Expressions of CCAT1-L and c-MYC mRNA and MYC protein in gastric adenocarcinoma tissue and adjacent normal tissues of 60 patients were analyzed using quantitative real-time polymerase chain reaction and western blot, respectively.CCAT1-L knockdown in MGC803 and MKN28 cells was performed using RNA interference, followed by evaluating cell proliferation, invasion, and migration with soft agar colony formation assay, scratch wound assay, and transwell assay.western blot was also used to analyze the expression of epithelial-mesenchymal transition-related proteins, including MYC, RAS, T-ERK, P-ERK, E-cadherin, and vimentin, in gastric adenocarcinoma MKN-28 cells.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001).CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01).Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.CCAT1-L knockdown inhibits epithelial-mesenchymal transition of gastric adenocarcinoma cells and thus suppresses the gastric adenocarcinoma metastasis.	30254457	RID06063	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric adenocarcinoma	CCAT1-L	RAS	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.Expressions of CCAT1-L and c-MYC mRNA and MYC protein in gastric adenocarcinoma tissue and adjacent normal tissues of 60 patients were analyzed using quantitative real-time polymerase chain reaction and western blot, respectively.CCAT1-L knockdown in MGC803 and MKN28 cells was performed using RNA interference, followed by evaluating cell proliferation, invasion, and migration with soft agar colony formation assay, scratch wound assay, and transwell assay.western blot was also used to analyze the expression of epithelial-mesenchymal transition-related proteins, including MYC, RAS, T-ERK, P-ERK, E-cadherin, and vimentin, in gastric adenocarcinoma MKN-28 cells.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001).CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01).Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.CCAT1-L knockdown inhibits epithelial-mesenchymal transition of gastric adenocarcinoma cells and thus suppresses the gastric adenocarcinoma metastasis.	30254457	RID06064	expression association	metastasis		
Gastric adenocarcinoma	CCAT1-L	ERK	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000133216	NA	NA	NA	NA	NA	Upregulation of long noncoding RNA CCAT1-L promotes epithelial-mesenchymal transition in gastric adenocarcinoma.Expressions of CCAT1-L and c-MYC mRNA and MYC protein in gastric adenocarcinoma tissue and adjacent normal tissues of 60 patients were analyzed using quantitative real-time polymerase chain reaction and western blot, respectively.CCAT1-L knockdown in MGC803 and MKN28 cells was performed using RNA interference, followed by evaluating cell proliferation, invasion, and migration with soft agar colony formation assay, scratch wound assay, and transwell assay.western blot was also used to analyze the expression of epithelial-mesenchymal transition-related proteins, including MYC, RAS, T-ERK, P-ERK, E-cadherin, and vimentin, in gastric adenocarcinoma MKN-28 cells.The expression of CCAT1-L and MYC in tumor tissue was significantly higher than that in adjacent normal tissues (P<0.001).CCAT1-L expression was also significantly higher in gastric adenocarcinoma cell lines than that in normal cell lines (P<0.01).Expressions of MYC, RAS, and vimentin, and the phosphorylation of ERK protein were dramatically decreased, while the expression of E-cadherin protein was increased by CCAT1-L knockdown in MKN-28 cell.CCAT1-L knockdown inhibits epithelial-mesenchymal transition of gastric adenocarcinoma cells and thus suppresses the gastric adenocarcinoma metastasis.	30254457	RID06065	expression association	metastasis		
Colorectal cancer	ZFAS1	VEGFA	positively-E	RNA pull-down assay;RNAi;dual-luciferase reporter assay;western blot;dual-luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000112715	NA	441951	7422	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	VEGF|VEGF-A|VPF	We found that ZFAS1 expression was higher in CRC tissues, where it was associated with poor overall survival (OS), we also showed that ZFAS1 upregulation was induced by nuclear transcription factor SP1. Moreover, ZFAS1 and VEGFA are both targets of miR-150-5p, while ZFAS1 binds to miR-150-5p in an AGO2-dependent manner. Additionally, ZFAS1 upregulation markedly promoted as well as ZFAS1 knockdown significantly suppressed CRC cell proliferation, migration, invasion and angiogenesis, and the inhibitory effect caused by ZFAS1 knockdown could be reversed by antagomiR-150-5p. Lastly, we demonstrated that ZFAS1 knockdown inhibited EMT process and inactivated VEGFA/VEGFR2 and downstream Akt/mTOR signaling pathway in CRC. Our data demonstrated that SP1-induced ZFAS1 contributed to CRC progression by upregulating VEGFA via competitively binding to miR-150-6p, which acts as a tumor suppressor by targeting VEGFA in CRC.	30250022	RID06066	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	CRNDE	MAPK1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000100030	NA	643911	5594	CRNDEP|LINC00180|LOC643911	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR-217/MAPK1 axis.CRNDE expression in HCC was verified by qRT-PCRThe overexpression of CRNDE was demonstrated by a microarray-based lncRNA profiling study.The dual-luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR-217 and MAPK1.MAPK1, the downstream target of miR-217, was predicted using bioinformatics and was further confirmed by qRT-PCRand western blot.CRNDE was up-regulated in HCC tissues and HCC cell lines.MiR-217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC.MAPK1, the possible target of miR-217, was negatively correlated with miR-217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE.MAPK1, the possible target of miR-217, was negatively correlated with miR-217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE.	30246921	RID06067	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	NEAT1	SMC1A	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-)	ceRNA(miR-23a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000072501	NA	283131	8243	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	DXS423E|KIAA0178|SB1.8|SMC1L1|Smcb	The qRT-PCRillustrated that NEAT1 and SMC1A expression was decreased but that miR-23a-3p expression was increased in primary AML cells and THP-1 cells compared with that in normal cells. The RIP assay and dual-luciferase assay revealed the targeting relationship between miR-23a-3p and NEAT1 or SMC1A. The CCK-8 assay showed that the overexpression of NEAT1 and SMC1A or repression of miR-23a-3p inhibited cell proliferation. Flow cytometry showed that the upregulation of NEAT1 and SMC1A or repression of miR-23a-3p promoted apoptosis and affected the cell cycle. NEAT1 repressed the expression of miR-23a-3p, and therefore promoted SMC1A, which in turn suppressed myeloid leukemia cell proliferation and enhanced apoptosis.	30246348	RID06068	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Pre-eclampsia	SNHG5	N-cadherin	positively-E	luciferase reporter assay;RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-26a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	NA	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	The lncRNA small nucleolar RNA host gene 5 regulates trophoblast cell proliferation, invasion, and migration via modulating miR-26a-5p/N-cadherin axis.Furthermore, miR-26a-5p was predicted to target the 3' untranslated region of N-cadherin, which was confirmed by luciferase reporter assay, and miR-26a-5p overexpression suppressed N-cadherin expression in HTR-8/SVneo cells. N-cadherin mRNA expression was downregulated in PE placental tissues and was positively correlated with SNHG5 expression. Both overexpression of miR-26a-5p and knockdown of N-cadherin suppressed HTR-8/SVneo cell invasion and migration, and also attenuated the effects of SNHG5 on the cellular functions of HTR-8/SVneo cells. In conclusion, our study suggested that SNHG5 promotes trophoblast cell proliferation, invasion, and migration at least partly via regulating the miR-26a-5p/N-cadherin axis.	30242892	RID06069	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Tongue squamous cell carcinoma	CRNDE	miR-384	negatively-F	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	CRNDE promotes cell tongue squamous cell carcinoma cell growth and invasion through suppressing miR-384.Overexpression of miR-384 suppressed TSCC cell proliferation, cell cycle, and invasion. Furthermore, we demonstrated that CRNDE promoted TSCC cell proliferation and invasion through inhibiting miR-384 expression. These results suggested that CRNDE acts as an oncogene in the development of TSCC, which partially occurs through inhibiting miR-384 expression.	30242873	RID06070	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Acute myeloid leukemia	HOXA-AS2	SOX4	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124766	NA	285943	6659	HOXA3as	NA	HOXA-AS2 predicts an adverse prognosis and promotes tumorigenesis via SOX4/PI3K/AKT pathway in acute myeloid leukemia,This study showed that HOXA-AS2 was overexpressed in AML patients.Moreover, it was suggested that the sex-determining region Y-box 4 (SOX4), which is closely involved in the PI3K/AKT pathway, might be one of the major downstream targets of HOXA-AS2. Silencing HOXA-AS2 decreased the expression of SOX4, whereas the upregulation of SOX4 partially abrogated the inhibitory effect of silencing HOXA-AS2 on leukemic cells. In conclusion, these findings suggest that HOXA-AS2 probably functions as an oncogene via SOX4/PI3K/AKT pathway and might be a useful biomarker for the prognostic prediction in AML patients, providing a potential therapeutic target for AML.	32369230	RID06071	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Acute myeloid leukemia	HOXA-AS2	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124762	NA	285943	1026	HOXA3as	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HOXA-AS2 predicts an adverse prognosis and promotes tumorigenesis via SOX4/PI3K/AKT pathway in acute myeloid leukemia,This study showed that HOXA-AS3 was overexpressed in AML patients. Further analysis demonstrated that silencing HOXA-AS2 suppressed the phosphorylation level of PI3K and AKT, which thereafter promoted the expression of P21 and P27.	32369230	RID06072	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Acute myeloid leukemia	HOXA-AS2	PSMD10	negatively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000101843	NA	285943	5716	HOXA3as	dJ889N15.2|p28|p28(GANK)	HOXA-AS2 predicts an adverse prognosis and promotes tumorigenesis via SOX4/PI3K/AKT pathway in acute myeloid leukemia,This study showed that HOXA-AS3 was overexpressed in AML patients. Further analysis demonstrated that silencing HOXA-AS2 suppressed the phosphorylation level of PI3K and AKT, which thereafter promoted the expression of P21 and P28.	32369230	RID06073	expression association	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Gastric cancer	PTCSC3	HOXA11-AS	negatively-E	overexpression	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-RNA	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	lncRNA	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000240990	GRCh38_7:27184507-27189298	100886964	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	LncRNA PTCSC3 Alleviates the Postoperative Distant Recurrence of Gastric Cancer by Suppression of lncRNA HOXA11-AS.we showed that PTCSC3 was downregulated in plasma of gastric cancer patients than in plasma of healthy controls.  PTCSC3 overexpression mediated the downregulation of HOXA11-AS in gastric cancer cells, while HOXA11-AS overexpression failed to significantly affect PTCSC3. PTCSC3 overexpression led to inhibited, while HOXA11-AS overexpression led to promoted migration and invasion of gastric cancer cells.HOXA11-AS overexpression reduced the effects of PTCSC3 overexpression.Therefore, lncRNA PTCSC3 alleviates in the postoperative distant recurrence of gastric cancer possible by suppression of HOXA11-AS.lncRNA PTCSC3 alleviates in the postoperative distant recurrence of gastric cancer possible by suppression of HOXA11-AS.	32368140	RID06074	expression association	recurrence	UP(SKCM);DATA(GSE38495)	
Pancreatic ductal adenocarcinoma	RELA	PICSAR	positively-E	overexpression;Chromatin immunoprecipitation assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000173039	NA	ENSG00000275874	GRCh38_21:44999208-45004727	5970	378825	NFKB3|p65	C21orf113|LINC00162|NCRNA00162|NLC1-C|PRED74	The overexpression of long intergenic ncRNA00162 induced by RelA/p65 promotes growth of pancreatic ductal adenocarcinoma.These data were validated in several PDAC cell lines, and significant upregulation of LINC00162 was found in all of them. Knock-down of LINC00162 significantly inhibited the proliferation, colony formation and migration of PATC cells in vitro and suppressed the growth of PATC xenografts in vivo.the result of Chromatin immunoprecipitation assay revealed that RelA/p65 directly bound to LINC00162, and the expression of LINC00162 in PDAC decreased after RelA/p65 knock-down, the proliferation ability of AsPc-1 also significantly inhibited after knocking down LINC00162 and RelA/p65 simultaneously, indicating that RelA/p65 directly involve in the transcriptional regulation of LINC00162.CONCLUSIONS: In sum, our results provide first evidence for the role of LINC00162 in promoting PDAC progression and the potential underlying mechanism of LINC00162 overexpression.	32364285	RID06075	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Gastric cancer	LINC00619	OPCML	positively-E	RNA22;DIANA;TargetScan	downregulation	RT-qPCR	NA	NA	cancer progression(-);cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+)	ceRNA(miR-224-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000204187	NA	ENSG00000183715	NA	414260	4978	C10orf136|bA168P8.1	IGLON1|OBCAM|OPCM	LINC00619 restricts gastric cancer progression by preventing microRNA-224-5p-mediated inhibition of OPCML.LINC00619 was identified among differentially expressed lncRNAs linked to gastric cancer based on microarray analysis and its relationships with miR-224-5p and opioid binding protein/cell adhesion molecule-like gene (OPCML) were investigated. LINC00619, miR-224-5p, and OPCML expression were measured in GC tissues and cells. Ectopic expression and depletion experiments were conducted to assess the effects of LINC00619, miR-224-5p and OPCML on cell proliferation, invasion, migration and apoptosis as well as their effects on the expression of apoptosis- and metastasis-related genes (Bcl-2, Bax, MMP-2 and MMP-9). Tumorigenicity in the nude mice was also examined. Gastric cancer was characterized by downregulation of LINC00619 and OPCML and upregulation of miR-224-5p. Additionally, we found that miR-224-5p could interact with both LINC00619 and OPCML. Upregulation of LINC00619, which binds to miR-224-5p, led to decreased miR-224-5p expression while increasing the expression of OPCML, a target gene of miR-224-5p. Overexpression of LINC00619 or OPCML or downregulation of miR-224-5p suppressed cell proliferation, invasion, migration and tumorigenicity while promoting apoptosis in GC. Our results indicated that LINC00619 functions as a tumor suppressor in GC by impairing miR-224-5p-mediated inhibition of OPCML.	32359894	RID06076	ceRNA or sponge	metastasis		UP(LIHC);DATA(GSE117623)
Cervical cancer	LINP1	KLF2	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000223784	GRCh38_10:6709530-6740532	ENSG00000127528	NA	108570035	10365	NA	LKLF	LINP1 promotes the progression of cervical cancer by scaffolding EZH2, LSD1, and DNMT1 to inhibit the expression of KLF2 and PRSS8.we found that the levels of LINP1 were significantly elevated in CC tissues by comparison with adjacent normal tissue.we found that downregulation of LINP1 significantly reduced the proliferation of CC cells and promoted apoptosis. Additionally, downregulation of LINP1 significantly decreased CC tumor growth in vivo. Further, we observed that LINP1 recruits EZH2, LSD1, and DNMT1, thereby reducing the expression of KLF2 and PRSS8. The results from our qRT-PCRanalyses showed that silencing LINP1 uprgulated the expression of KLF2 and PRSS8 in CC cells. The results from our loss-of-function assays showed that upregulation of KLF2 and PRSS8 inhibits cell proliferation and boosts cell apoptosis in CC. We also found that inhibition of KLF2 and PRSS8 reversed the inhibitory effect on cell proliferation associated with silencing LINP1. In short, LINP1 facilitates the progression of CC by suppressing KLF2 and PRSS8, and thus could provide a promising target for CC therapy.	32348690	RID06077	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LINP1	PRSS8	negatively-E	siRNA	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000223784	GRCh38_10:6709530-6740532	ENSG00000052344	NA	108570035	5652	NA	CAP1	LINP1 promotes the progression of cervical cancer by scaffolding EZH2, LSD1, and DNMT1 to inhibit the expression of KLF2 and PRSS8.we found that the levels of LINP1 were significantly elevated in CC tissues by comparison with adjacent normal tissue.we found that downregulation of LINP1 significantly reduced the proliferation of CC cells and promoted apoptosis. Additionally, downregulation of LINP1 significantly decreased CC tumor growth in vivo. Further, we observed that LINP1 recruits EZH2, LSD1, and DNMT1, thereby reducing the expression of KLF2 and PRSS8. The results from our qRT-PCRanalyses showed that silencing LINP1 uprgulated the expression of KLF2 and PRSS8 in CC cells. The results from our loss-of-function assays showed that upregulation of KLF2 and PRSS8 inhibits cell proliferation and boosts cell apoptosis in CC. We also found that inhibition of KLF2 and PRSS8 reversed the inhibitory effect on cell proliferation associated with silencing LINP1. In short, LINP1 facilitates the progression of CC by suppressing KLF2 and PRSS9, and thus could provide a promising target for CC therapy.	32348690	RID06078	expression association	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE55807,GSE75367)
Osteosarcoma	OR3A4P	G6PD	positively-E	miRDB;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+)	ceRNA(miR-1207-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000180068	GRCh38_17:3309986-3311446	ENSG00000160211	NA	390756	2539	OR3A4	G6PD1	LncRNA OR3A4 Regulated the Growth of Osteosarcoma Cells by Modulating the miR-1207-5p/G6PD Signaling.The expression level of OR3A4 in OS tissues and cell lines was detected by RT-qPCR.The targets of OR3A4 were predicted using the miRDB database. The binding between OR3A4 and miRNAs was confirmed by dual-luciferase reporter assay.OR3A4 was overexpressed in OS tissues and correlated with the advanced progression of OS patients.Down-regulation of OR3A4 significantly inhibited the proliferation and colony formation of OS cells. Mechanistically, OR3A4 acted as a sponge of miR-1207-5p. Glucose-6-phosphate dehydrogenase (G6PD) was identified as a target of miR-1207-5p.Knockdown of OR3A4 increased the expression of miR-1207-5p and consequently, suppressed the level of G6PD in OS cells.Our finding suggested the critical role of OR3A4 in the proliferation of OS cells via targeting the miR-1207-5p/G6PD axis.Our finding suggested the critical role of OR3A4 in the proliferation of OS cells via targeting the miR-1207-5p/G6PD axis.	32346295	RID06079	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung non-small cell carcinoma	MIAT	MMP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000087245	NA	440823	4313	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	CLG4|CLG4A|TBE-1	The long non-coding RNA MIAT/miR-139-5p/MMP2 axis regulates cell migration and invasion in non-small-cell lung cancer.In this study, MIAT, miR-139-5p and MMP2 expression were measured by quantitative reverse transcriptase PCR (qRT-PCR or western blot, respectively, and we found the expression of MIAT and MMP2 were elevated, while miR-139-5p was decreased in NSCLC tissues and cell lines. The relationship between miR-139-5p and MIAT or MMP2 was then confirmed by Luciferase reporter assay, and the results showed that MIAT directly interacted with miR-139-5p and miR-139- 5p targetedly suppressed MMP2 in NSCLC cells.expression analysis showed that MIAT indirectly regulated MMP2 by sponging miR-139-5p. Finally, rescue assay suggested that miR-139-5p restoration reversed MIAT-overexpression-induced promotion on the migration and invasion of NSCLC cells. In conclusion, our results demonstrated that lncRNA MIAT modulated the migration and invasion of NSCLC by regulating miR-139-5p and MMP2.	32345777	RID06080	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Clear cell renal cell carcinoma	PENG	PDZK1	positively-E	luciferase reporter assay;FISH;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-15b)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000174827	NA	NA	5174	NA	NHERF3|PDZD1	Long noncoding RNA PENG upregulates PDZK1 expression by sponging miR-15b to suppress clear cell renal cell carcinoma cell proliferation.To investigate the role and mechanism of ceRNAs in PDZK1 downregulation and the development of ccRCC, we searched databases for miRNAs and lncRNAs that regulate PDZK1 expression in ccRCC tissues and assessed their effects in ccRCC.We found that miR-15b was expressed at higher levels in ccRCC tissues, and its upregulation was clinically associated with lower PDZK1 level, larger tumor size and shorter survival time of ccRCC patients. Conversely, a novel lncRNA (lncPENG) was expressed at a lower level in ccRCC tissues, and its downregulation was associated with the same effects as upregulation of miR-15b.Downregulation of miR-15b and upregulation of lncPENG resulted in a significant increase in PDZK1 level and inhibition of proliferation in vitro and in vivo. Mechanistically, lncPENG directly bound to miR-15b and effectively functioned as a sponge for miR-15b to modulate the expression of PDZK1. Thus, lncPENG may function as a ceRNA to attenuate miR-15b-dependent PDZK1 downregulation and inhibit cell proliferation, suggesting that it may be clinically valuable as a therapeutic target and a prognostic biomarker of ccRCC.	32341409	RID06081	ceRNA or sponge	prognosis		UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Gastrointestinal stromal tumor	PCAT6	PRDX5	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell proliferation(+);cell stemness(+);apoptosis process(-)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastrointestinal stromal tumor	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000126432	NA	100506696	25824	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	ACR1|AOEB166|B166|MGC117264|MGC142283|MGC142285|PLP|PMP20|PRDX6|PRXV|SBBI10	PCAT6 mediates cellular biological functions in gastrointestinal stromal tumor via upregulation of PRDX5 and activation of Wnt pathway.miR-143-3p was identified as the downstream microRNA of PCAT6. Moreover, miR-143-3p itself served as a tumor suppressor in GIST. Subsequently, peroxiredoxin 5 (PRDX5) was verified as the target of miR-143-3p. PCAT6 promoted GIST cell proliferation and stemness via sponging miR-143-3p to upregulate PRDX5. In a word, PCAT6 promoted GIST cell proliferation and stemness but inhibited cell apoptosis via competing endogenous RNA pattern and activation of Wnt pathway, which might contribute to GIST treatment.	32339330	RID06082	ceRNA or sponge	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PAAD,BRCA);UP(PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Papillary thyroid carcinoma	HOTTIP	MYC	positively-E	starbase;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-744-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000136997	NA	100316868	4609	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	bHLHe39|c-Myc|MYCC	miR-744-5p mediates lncRNA HOTTIP to regulate the proliferation and apoptosis of papillary thyroid carcinoma cells.We observed that miR-744-5p expression was significantly declined in PTC tissues and cell lines.We also found that miR-744-5p down-regulated its downstream genes c-myc and attenuated cell proliferation induced by c-myc. Long non-coding RNA (lncRNA) HOTTIP was found to be up-regulated and to act as an oncogene in PTC.miR-744-5p bound to HOTTIP and was negatively regulated by HOTTIP. miR-744-5p acts as a tumor suppressor to inhibit proliferation and promotes the apoptosis of PTC cells via targeting c-myc. Moreover, miR-744-5p expression interferes with lncRNA HOTTIP ability to promote proliferation and downregulate apoptosis in papillary thyroid carcinoma.	32335029	RID06083	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LINC00691	LIN28A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);JAK/STAT signaling pathway	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000224074	GRCh38_3:24096269-24103238	ENSG00000131914	NA	152024	79727	NA	CSDD1|FLJ12457|LIN-28|LIN28|ZCCHC1	Overexpression of LINC00691 promotes the proliferation and invasion of gastric cancer cells via the Janus kinase/signal transducer and activator of transcription signalling pathway.Our data indicated that the expression of LINC00691 in GC was significantly higher than that in healthy controls and was associated with clinicopathological features and survival time.In the GC cell lines MKN-45 and HGC-27, the knockdown of LINC00691 suppressed proliferation, colony formation, migration, and invasion. Bioinformatics analysis and luciferase reporter gene experiments showed that LINC00691 activated Lin28 transcription. western blotindicated that the knockdown of LINC00691 contributed to the decreased expression of p-JAK2 and p-STAT3 in GC cells. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathway inhibitor ruxolitinib effectively suppressed the effects of LINC00691. In addition, both LINC00691 and Lin28 promoted the expression of epidermal growth factor (EGF). Therefore, our study clarified that LINC00691 is highly expressed in GC and is a potential biomarker for GC diagnosis and prognosis. LINC00691 promotes the proliferation and invasion of GC cells by activating Lin29 transcription and facilitating EGF expression through the JAK/STAT signalling pathway, which provides new ideas for targeted therapy of GC.	32330554	RID06084	transcriptional regulation	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	AOC4P	MMP2	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);WNT/beta-catenin signaling pathway(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000087245	NA	90586	4313	UPAT	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	AOC4P suppresses viability and invasion and induces apoptosis in NSCLC cells by inhibiting the Wnt/beta-catenin pathway.AOC4P expression in NSCLC cells was detected by qRT-PCRAOC4P was lowly expressed in NSCLC samples and cells.AOC4P overexpression suppressed tumor growth in a xenograft mouse model. Activation of the Wnt/beta-catenin pathway by BML-284 abolished the effects of AOC4P overexpression on cell viability, invasion and apoptosis in NSCLC cells. In conclusion, AOC4P overexpression suppresses viability and invasion and induces apoptosis in NSCLC cells via inhibition of the Wnt/beta-catenin pathway.Overexpression of AOC4P inhibited viability, the expression of MMP-2 and MMP-9, and invasion of NSCLC cells.	32325081	RID06085	expression association	NA		UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	AOC4P	MMP9	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);WNT/beta-catenin signaling pathway(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000100985	NA	90586	4318	AOC4|UPAT	CLG4B|GELB|MANDP2|MMP-9	AOC4P suppresses viability and invasion and induces apoptosis in NSCLC cells by inhibiting the Wnt/beta-catenin pathway.AOC4P expression in NSCLC cells was detected by qRT-PCRAOC4P was lowly expressed in NSCLC samples and cells.AOC4P overexpression suppressed tumor growth in a xenograft mouse model. Activation of the Wnt/beta-catenin pathway by BML-284 abolished the effects of AOC4P overexpression on cell viability, invasion and apoptosis in NSCLC cells. In conclusion, AOC4P overexpression suppresses viability and invasion and induces apoptosis in NSCLC cells via inhibition of the Wnt/beta-catenin pathway.Overexpression of AOC4P inhibited viability, the expression of MMP-2 and MMP-10, and invasion of NSCLC cells.	32325081	RID06086	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	CCAT1	COMMD3-BMI1	positively-E	MiRanda	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-218)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000269897	NA	100507056	100532731	CARLO5|CARLo-5|onco-lncRNA-40	BMI1|PCGF4|RNF51	Long non-coding RNA CCAT1 enhances human non-small cell lung cancer growth through downregulation of microRNA-218.in the present study, we showed that lncRNA-CCAT1 was upregulated in NSCLC tissues.In  vitro and in vivo results demonstrated that lncRNA-CCAT1 knockdown suppressed tumor proliferation and induced apoptosis. Furthermore, microRNA-218 (miR-218) was confirmed as an effective target of lncRNA-CCAT1 in NSCLC. B  lymphoma Mo-MLV insertion region  1 homolog (BMI-1), which served as a downstream target of miR-218, was also inhibited by lncRNA-CCAT1 knockdown. In conclusion, the present study indicated that upregulation of lncRNA-CCAT1 in NSCLC is associated with tumor malignant potential. lncRNA-CCAT1 enhances tumor growth in NSCLC by directly inhibiting miR-218 and indirectly increasing BMI-1 expression.	32323859	RID06087	ceRNA or sponge	NA		DOWN(PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Colorectal cancer	LINC00858	SMAD7	positively-E	Starbase v2.0;TargetScan	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-25-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000101665	NA	170425	4092	CRCAL-2	MADH7|MADH8	Long non-coding RNA LINC00858 promotes TP53-wild-type colorectal cancer progression by regulating the microRNA-25-3p/SMAD7 axis.LINC00858 was increased in CRC tumor tissues.Subsequently, using Starbase v2.0 database, miR-25-3p was confirmed to interact with LINC00858 and was downregulated by LINC00858. Reduction of miR-25-3p expression with an inhibitor significantly attenuated the biological effects of LINC00858 knockdown in CRC cells. Furthermore, using TargetScan, SMAD7 was validated to interact with miR-25-3p and was downregulated by miR-25-3p. Lastly, the ectopic overexpression of SMAD7 rescued the suppressive effects of LINC00858 knockdown in CRC cells. Collectively, the results from the present study, to the best of our knowledge, firstly demonstrated a novel LINC00858/miR-25-3p/SMAD7 regulatory axis that promoted CRC progression, indicating LINC00858 as a promising therapeutic target for CRC.	32323793	RID06088	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colon cancer	OIP5-AS1	MIR137	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	RNA-RNA	Oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000284202	NA	729082	406928	cyrano|linc-OIP5	hsa-mir-137|miR-137|MIRN137	Effects of long non-coding RNA Opa-interacting protein 5 antisense RNA 1 on colon cancer cell resistance to oxaliplatin and its regulation of microRNA-137.A total of 114 CC patients admitted to China-Japan Union Hospital of Jilin University were enrolled, and the expression of miR-137 and OIP5-AS1 in tumor tissues and corresponding normal tumor-adjacent tissues was determined.dual-luciferase reporter assay combined with RNA-binding protein immunoprecipitation to analyze the relationship between OIP5-AS1 and miR-137.Highly expressed in CC, OIP5-AS1 can affect the biological behavior of CC cells, and can also regulate the resistance of CC cells to L-OHP by mediating miR-137 expression.OIP5-AS1 targetedly inhibited miR-137 expression, and silencing OIP5-AS1 reversed the resistance of CC cells to L-OHP by promoting the expression of miR-137.	32308348	RID06089	expression association	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Triple-negative breast cancer	WEE2-AS1	TOB1	positively-E	FISH;starbase;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	ceRNA(miR-32-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228775	GRCh38_7:141704003-141738346	ENSG00000141232	NA	285962	10140	NA	APRO5|TOB|TROB|TROB1	LncRNA WEE2-AS1 promotes proliferation and inhibits apoptosis in triple negative breast cancer cells via regulating miR-32-5p/TOB1 axis.Our results showed that WEE2-AS1 was up-regulated in TNBC cell lines.WEE2-AS1 knockdown could inhibit TNBC cell proliferation, promote apoptosis, and suppress migration and invasion. Further, we found that miR-32-5p was down-regulated in TNBC cells and could be sponged by WEE2-AS1. Moreover, miR-32-5p could target its downstream gene transducer of ERBB2, 1 (TOB1), which was highly expressed and could play the oncogenic role in TNBC cells. Through rescue assays, we proved that WEE2-AS1/miR-32-5p/TOB1 axis could modulate cancer progression in TNBC cells. In conclusion, our results demonstrated the oncogenic function of lncRNA WEE2-AS1 in TNBC cells, providing a novel insight into TNBC therapy.	32307083	RID06090	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Ovarian cancer	CDKN2B-AS1	SMAD3	positively-E	luciferase reporter;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000166949	NA	100048912	4088	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	HsT17436|JV15-2|MADH3	LncRNA CDKN2B-AS1 promotes the progression of ovarian cancer by miR-143-3p/SMAD3 axis and predicts a poor prognosis.The abundances of CDKN2B-AS1, miR-143-3p, and SMAD3 mRNA were determined by quantitative real-time polymerase chain reaction (qRT-PCR.The interaction between CDKN2B-AS1 and miR-143-3p, or miR-143-3p and SMAD3 was demonstrated by bioinformatic, luciferase reporter, qRT-PCRand western blot.CDKN2B-AS1 was upregulated in OC and correlated with clinicopathologic features.The knockdown of CDKN2B-AS1 hampered the development of OC, as reflected by the suppression of cell proliferation, migration, and invasion, and the enhancement of cell apoptosis, whereas the effects could be rescued by the overexpression of SMAD3. The absence of CDKN2B-AS1 blocked tumor growth in vivo. CDKN2B-AS1 served as a molecular sponge for miR-143-3p, leading to the derepression of miR-143-3p target SMAD3, which eventually triggered the progression of OC. In conclusion, CDKN2B-AS1 promoted tumor growth, invasion, and migration of OC by regulation of miR-143-3p/SMAD3 axis, hinting that CDKN2B-AS1 might be a potential biomarker for OC diagnosis and treatment.	32305052	RID06091	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	ANKRD40CL	MAPK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000100030	NA	55018	5594	C17orf73|FLJ20694|LINC00483	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	LncRNA LINC00483 promotes gastric cancer development through regulating MAPK1 expression by sponging miR-490-3p.The expression levels of LINC00483, miR-490-3p and MAPK1 were detected by quantitative real-time polymerase chain reaction or western blot.The target association between miR-490-3p and LINC00483 or MAPK1 was confirmed by luciferase reporter assay.LINC00483 and MAPK1 levels were increased in gastric cancer tissues and cells.Knockdown of LINC00483 or MAPK1 inhibited cells viability, migration and invasion but promoted apoptosis in gastric cancer cells. Moreover, MAPK1 overexpression attenuated the effect of LINC00483 knockdown on gastric cancer development. LINC00483 could increase MAPK1 expression by competitively sponging miR-490-3p. miR-490-3p overexpression suppressed gastric cancer development, which was abated by introduction of LINC00483. Besides, inhibition of LINC00483 decreased xenograft tumor growth by regulating miR-490-3p/MAPK1 axis.CONCLUSION: Knockdown of LINC00483 inhibited gastric cancer development in vitro and in vivo by increasing miR-490-3p and decreasing MAPK1, elucidating a novel mechanism for understanding the development of gastric cancer.	32293550	RID06092	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SLC25A15	AKAP12	positively-E	miRDB;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000102743	GRCh38_13:40789412-40812460	ENSG00000131016	NA	10166	9590	D13S327|HHH|LNC-HC|ORC1|ORNT1	AKAP250|SSeCKS	The Human Novel Gene LNC-HC Inhibits Hepatocellular Carcinoma Cell Proliferation by Sequestering hsa-miR-183-5p.In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC. Mechanistically, LNC-HC inhibited the proliferation of HCC cells by directly interacting with hsa-miR-183-5p. LNC-HC rescued the expression of five tumor suppressors, including AKAP12, DYRK2, FOXN3, FOXO1, and LATS2, that were verified as target genes of hsa-miR-183-5p. Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in  vitro and suppress tumor growth in  vivo by competitively binding hsa-miR-183-5p as a competing endogenous RNA (ceRNA). These findings suggest that LNC-HC could be a biomarker of HCC and provide a novel therapeutic target for HCC treatment.	32278306	RID06093	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Hepatocellular carcinoma	SLC25A15	DYRK2	positively-E	miRDB;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000102743	GRCh38_13:40789412-40812460	ENSG00000127334	NA	10166	8445	D13S327|HHH|LNC-HC|ORC1|ORNT1	NA	The Human Novel Gene LNC-HC Inhibits Hepatocellular Carcinoma Cell Proliferation by Sequestering hsa-miR-183-5p.In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC. Mechanistically, LNC-HC inhibited the proliferation of HCC cells by directly interacting with hsa-miR-183-5p. LNC-HC rescued the expression of five tumor suppressors, including AKAP12, DYRK2, FOXN3, FOXO1, and LATS2, that were verified as target genes of hsa-miR-183-5p. Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in  vitro and suppress tumor growth in  vivo by competitively binding hsa-miR-183-6p as a competing endogenous RNA (ceRNA). These findings suggest that LNC-HC could be a biomarker of HCC and provide a novel therapeutic target for HCC treatment.	32278306	RID06094	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	SLC25A15	FOXN3	positively-E	miRDB;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000102743	GRCh38_13:40789412-40812460	ENSG00000053254	NA	10166	1112	D13S327|HHH|LNC-HC|ORC1|ORNT1	C14orf116|CHES1|PRO1635	The Human Novel Gene LNC-HC Inhibits Hepatocellular Carcinoma Cell Proliferation by Sequestering hsa-miR-183-5p.In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC. Mechanistically, LNC-HC inhibited the proliferation of HCC cells by directly interacting with hsa-miR-183-5p. LNC-HC rescued the expression of five tumor suppressors, including AKAP12, DYRK2, FOXN3, FOXO1, and LATS2, that were verified as target genes of hsa-miR-183-5p. Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in  vitro and suppress tumor growth in  vivo by competitively binding hsa-miR-183-7p as a competing endogenous RNA (ceRNA). These findings suggest that LNC-HC could be a biomarker of HCC and provide a novel therapeutic target for HCC treatment.	32278306	RID06095	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)
Hepatocellular carcinoma	SLC25A15	FOXO1	positively-E	miRDB;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000102743	GRCh38_13:40789412-40812460	ENSG00000150907	NA	10166	2308	D13S327|HHH|LNC-HC|ORC1|ORNT1	FKH1|FKHR|FOXO1A	The Human Novel Gene LNC-HC Inhibits Hepatocellular Carcinoma Cell Proliferation by Sequestering hsa-miR-183-5p.In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC. Mechanistically, LNC-HC inhibited the proliferation of HCC cells by directly interacting with hsa-miR-183-5p. LNC-HC rescued the expression of five tumor suppressors, including AKAP12, DYRK2, FOXN3, FOXO1, and LATS2, that were verified as target genes of hsa-miR-183-5p. Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in  vitro and suppress tumor growth in  vivo by competitively binding hsa-miR-183-8p as a competing endogenous RNA (ceRNA). These findings suggest that LNC-HC could be a biomarker of HCC and provide a novel therapeutic target for HCC treatment.	32278306	RID06096	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	SLC25A15	LATS2	positively-E	miRDB;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-183-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000102743	GRCh38_13:40789412-40812460	ENSG00000150457	NA	10166	26524	D13S327|HHH|LNC-HC|ORC1|ORNT1	KPM	The Human Novel Gene LNC-HC Inhibits Hepatocellular Carcinoma Cell Proliferation by Sequestering hsa-miR-183-5p.In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC. Mechanistically, LNC-HC inhibited the proliferation of HCC cells by directly interacting with hsa-miR-183-5p. LNC-HC rescued the expression of five tumor suppressors, including AKAP12, DYRK2, FOXN3, FOXO1, and LATS2, that were verified as target genes of hsa-miR-183-5p. Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in  vitro and suppress tumor growth in  vivo by competitively binding hsa-miR-183-9p as a competing endogenous RNA (ceRNA). These findings suggest that LNC-HC could be a biomarker of HCC and provide a novel therapeutic target for HCC treatment.	32278306	RID06097	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Colorectal cancer	PVT1	miR-16-5p	negaticely-E	luciferase reporter assay;RNA pull-down assay;starBase;miRTarBase	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	RNA stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	lncRNA PVT1 Promotes tumorigenesis of Colorectal Cancer by Stabilizing miR-16-5p and Interacting with the VEGFA/VEGFR1/AKT Axis. In this study, we observe that upregulated PVT1 is associated with poor prognosis and bad clinicopathological features of CRC patients.dual-luciferase reporter and RNA pull-down assays indicated that PVT1 binds to miR-16-5p, which has been shown to play strong tumor suppressive roles in CRC.Vascular endothelial growth factor A (VEGFA), a direct downstream target of miR-16-5p, was suppressed by PVT1 knockdown in CRC cells.Overexpression of VEGFA is known to modulate the AKT signaling cascade by activating vascular endothelial growth factor receptor 1 (VEGFR1). We, therefore, show that PVT1 loss combined with miR-16-5p overexpression reduces tumor volume maximally when propagated within a mouse xenograft model. We conclude that the PVT1-miR-16-5p/VEGFA/VEGFR1/AKT axis directly coordinates the response in CRC pathogenesis and suggest PVT1 as a novel target for potential CRC therapy.	32276209	RID06098	interact with mRNA	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Colorectal cancer	PVT1	VEGFA	negaticely-E	luciferase reporter assay;RNA pull-down assay;starBase;miRTarBase	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000112715	NA	5820	7422	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	VEGF|VEGF-A|VPF	lncRNA PVT1 Promotes tumorigenesis of Colorectal Cancer by Stabilizing miR-16-5p and Interacting with the VEGFA/VEGFR1/AKT Axis. In this study, we observe that upregulated PVT1 is associated with poor prognosis and bad clinicopathological features of CRC patients.dual-luciferase reporter and RNA pull-down assays indicated that PVT1 binds to miR-16-5p, which has been shown to play strong tumor suppressive roles in CRC.Vascular endothelial growth factor A (VEGFA), a direct downstream target of miR-16-5p, was suppressed by PVT1 knockdown in CRC cells.Overexpression of VEGFA is known to modulate the AKT signaling cascade by activating vascular endothelial growth factor receptor 1 (VEGFR1). We, therefore, show that PVT1 loss combined with miR-16-5p overexpression reduces tumor volume maximally when propagated within a mouse xenograft model. We conclude that the PVT1-miR-16-5p/VEGFA/VEGFR1/AKT axis directly coordinates the response in CRC pathogenesis and suggest PVT1 as a novel target for potential CRC therapy.	32276209	RID06099	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Lung adenocarcinoma	WDFY3-AS2	ZNF703	positively-E	luciferase reporter assay;RNA pull-down assay;chromatin immunoprecipitation assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-491-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000180769	GRCh38_4:84965534-85011277	ENSG00000183779	NA	404201	80139	C4orf12|FBI4|NCRNA00247	FLJ14299|NLZ1|ZEPPO1|ZNF503L|Zpo1	USF1-induced overexpression of long noncoding RNA WDFY3-AS2 promotes lung adenocarcinoma progression via targeting miR-491-5p/ZNF703 axis.The relative messenger RNA and protein levels were assessed by quantitative reverse transcription-polymerase chain reaction and western blot, respectively.Luciferase reporter assay, chromatin immunoprecipitation, RNA pull down, and RNA immunoprecipitation assays were conducted to probe into the interactions between relevant genes.WDFY3-AS2 expression was elevated in LUAD and WDFY3-AS2 transcription was activated by transcription factor USF1.Molecular mechanism assays revealed that WDFY3-AS2 could bind to miR-491-5p and miR-491-5p inhibition could reverse the inhibitory effect of WDFY3-AS2 silence on LUAD progression.USF1-acitvated WDFY3-AS2 promotes LUAD progression via targeting miR-491-5p/ZNF703 axis, suggesting the potential value of WDFY3-AS2 as a novel target for LUAD treatment.	32275336	RID06100	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC);DATA(GSE117623)
Ovarian cancer	EMX2OS	AKT3	positively-E	luciferase reporter assay; immunoprecipitation assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-654-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229847	GRCh38_10:117473215-117545068	ENSG00000117020	NA	196047	10000	EMX2-AS1|NCRNA00045	PKBG|PRKBG|RAC-gamma	LncRNA EMX2OS Induces Proliferation, Invasion and Sphere Formation of Ovarian Cancer Cells via Regulating the miR-654-3p/AKT3/PD-L1 Axis.The levels of EMX2OS in OC tissues and cell lines were determined by quantitative real-time PCR, and the function of EMX2OS was then analyzed both in vitro and in vivo. Luciferase assays and immunoprecipitation assays were performed to analyze the association between EMX2OS and miR-654 expression in OC cells.EMX2OS is overexpressed in human ovarian cancer tissues. Knockdown of EMX2OS reduced, while overexpression of EMX2OS enhanced the proliferation, invasion and sphere formation of OC cells. In addition, EMX2OS enhanced tumor growth in an in vivo xenograft model of human OC. We discovered that EMX2OS directly binds to miR-654 and suppresses its expression, thus leading to the upregulation of AKT3, which served as a direct target of miR-654. Moreover, miR-654 inhibited cell proliferation, invasion and sphere formation, and restoration of AKT3 reversed the effects of EMX2OS silencing or miR-654 overexpression. Furthermore, PD-L1 was identified as the key oncogenic component acting downstream of AKT3 in OC cells. Ectopic expression of PD-L1 reversed the anti-cancer functions by EMX2OS knockdown, AKT3 silencing or miR-654 upregulation in OC cells.These results demonstrated that the EMX2OS/miR-654/AKT3/PD-L1 axis confers aggressiveness in ovarian cancer and may represent a therapeutic target for OC metastasis.	32273754	RID06101	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Laryngeal carcinoma	HCG11	APOM	positively-E	mechanism assays	downregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-4469)	regulation	RNA-protein	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000235754	NA	493812	55937	bK14H9.3|FLJ14049|FLJ30357	G3a|NG20	LncRNA HCG11 suppresses laryngeal carcinoma cells progression via sponging miR-4469/APOM axis.The expression of HCG11, miR-4469, and apolipoprotein M (APOM) was detected by quantitative Real Time-PCR (qRT-PCR in tissues and cells.the mechanism assays were conducted to observe the interaction between miR-449 and HCG11 or APOM.low expression of HCG11 was discovered in laryngeal carcinoma tissues and cells. Overexpression of HCG11 retarded cell proliferation and enhanced cell apoptosis.Later, we found that APOM was also downregulated in laryngeal carcinoma tissues and cell lines, and inhibited laryngeal carcinoma progression. HCG11 positively regulated APOM at the post-transcriptional level. MiR-4469 was predicted to have the binding sites of HCG11 and APOM.Finally, it was indicated that the repression of APOM rescued the effects of HCG11 overexpression on cell proliferation and cell apoptosis.This study uncovered that HCG11 sponged miR-4469 to suppress laryngeal carcinoma progression by upregulating APOM expression.	32271435	RID06102	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE75367)
Papillary thyroid carcinoma	HOTAIRM1	TDG	positively-E	dual-luciferase reporter gene assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-107)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000139372	NA	100506311	6996	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The HOTAIRM1/miR-107/TDG axis regulates papillary thyroid cancer cell proliferation and invasion.In this study, we used quantitative reverse transcription PCR (qRT-PCR to show that HOTAIRM1 was significantly downregulated in PTC tissues and low HOTAIRM1 expression levels were associated with lymph node metastasis and advanced TNM stage.Overexpression of HOTAIRM1 was found to inhibit PTC cell proliferation, invasion, and migration in vitro. Additionally, we identified miR-107 as a target of HOTAIRM1 using online bioinformatics tools. Dual-luciferase reporter gene and RNA immunoprecipitation assays were used to confirm that HOTAIRM1 acted as a competing endogenous RNA of miR-107. Furthermore, enhancement of miR-107 could potentially reverse the effects of HOTAIRM1 overexpression in vitro. Inhibition of miR-107 suppressed PTC cell proliferation, invasion, and migration in vitro. HOTAIRM1 overexpression and miR-107 inhibition impaired tumorigenesis in vivo in mouse xenografts. Bioinformatics prediction and a dual-luciferase reporter gene assay demonstrated the binding between miR-107 and the 3'-untranslated region of TDG. The results of qRT-PCRand western blot assays suggested that HOTAIRM1 could regulate the expression of TDG in an miR-107-meditated manner. In conclusion, we validated HOTAIRM1 as a novel tumor-suppressor lncRNA in PTC and proposed that the HOTAIRM1/miR-107/TDG axis may serve as a therapeutic target for PTC.	32269214	RID06103	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Thyroid cancer	OTUD6B-AS1	miR-183-5p	negatively-E	OncomiR;StarBase 3.0;LncBase Predicted v.2;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000253738	GRCh38_8:91059318-91070583	NA	NA	100506365	NA	GS1-251I9.4	NA	OTUD6B-AS1 Inhibits Viability, Migration, and Invasion of Thyroid Carcinoma by Targeting miR-183-5p and miR-21.The potential targets of OTUD6B-AS1 were screened using the online programs OncomiR and StarBase 3.0, and the LncBase Predicted v.2. Luciferase reporter assay was used to confirm the interactions between OTUD6B-AS1 and its potential targets.OTUD6B-AS1 was downregulated in thyroid carcinoma tissue samples. The expression of OTUD6B-AS1 correlated with tumor size, clinical stage, and lymphatic metastasis of thyroid carcinoma. Overexpression of OTUD6B-AS1 significantly decreased the viability, migration, and invasion of thyroid carcinoma cells. Online programs predicted miR-183-5p and miR-21 as potential targets of OTUD6B-AS1. Luciferase reporter assays showed miR-183-5p and miR-21 bound to OTUD6B-AS1. Moreover, overexpression of miR-183-5p and miR-21 compromised the inhibitory effects of OTUD6B-AS1 on viability, migration, and invasion of thyroid carcinoma cells.Taken together, our findings present in vitro evidence of lncRNA OTUD6B-AS1 as a tumor suppressor in thyroid carcinomas. OTUD6B-AS1 inhibits viability, migration, and invasion of thyroid carcinoma by targeting miR-183-5p and miR-21.	32256450	RID06104	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Thyroid cancer	OTUD6B-AS1	miR-21	negatively-E	OncomiR;StarBase 3.0;LncBase Predicted v.3;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000253738	GRCh38_8:91059318-91070583	ENSG00000199004	NA	100506365	NA	GS1-251I9.4	NA	OTUD6B-AS1 Inhibits Viability, Migration, and Invasion of Thyroid Carcinoma by Targeting miR-183-5p and miR-21.The potential targets of OTUD6B-AS1 were screened using the online programs OncomiR and StarBase 3.0, and the LncBase Predicted v.2. Luciferase reporter assay was used to confirm the interactions between OTUD6B-AS1 and its potential targets.OTUD6B-AS1 was downregulated in thyroid carcinoma tissue samples. The expression of OTUD6B-AS1 correlated with tumor size, clinical stage, and lymphatic metastasis of thyroid carcinoma. Overexpression of OTUD6B-AS1 significantly decreased the viability, migration, and invasion of thyroid carcinoma cells. Online programs predicted miR-183-5p and miR-21 as potential targets of OTUD6B-AS1. Luciferase reporter assays showed miR-183-5p and miR-21 bound to OTUD6B-AS1. Moreover, overexpression of miR-183-5p and miR-21 compromised the inhibitory effects of OTUD6B-AS1 on viability, migration, and invasion of thyroid carcinoma cells.Taken together, our findings present in vitro evidence of lncRNA OTUD6B-AS1 as a tumor suppressor in thyroid carcinomas. OTUD6B-AS1 inhibits viability, migration, and invasion of thyroid carcinoma by targeting miR-183-5p and miR-22.	32256450	RID06105	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Non-small cell lung cancer	HOTAIR	miR-34a-5p	negatively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	sponge	binding/interaction	RNA-RNA	Berberine;Gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Novel regulation of miR-34a-5p and HOTAIR by the combination of berberine and gefitinib   leading to inhibition of EMT in human lung cancer.Herein, we performed series of in vitro experiments, including viability, migration, invasion, apoptosis and in vivo xenograft model, and identified that HOTAIR was remarkably elevated in NSCLC cells.We also observed that miR-34a-5p was dramatically inhibited in NSCLC cells and the binding correlation between HOTAIR and miR-34a-5p was confirmed by dual-luciferase reporter and RNA immunoprecipitation assays.We also showed that induction of miR-34a-5p and reduction of HOTAIR, and the interaction between miR-34a-5p and HOTAIR resulted in the suppression of epithelial-mesenchymal transition (EMT) as illustrated by induction of key epithelial markers E-cadherin expression, reduction of vimentin and EMT-inducing transcription factor snail.Excessive expression of snail resisted miR-34a-5p-inhibited cell growth. Snail binds to E-cadherin promoter and regulates E-cadherin expression. There was a synergy in combination of berberine and gefinitib in this process. Similar findings were also observed in a tumour xenograft model. Collectively, this is the first report demonstrating reciprocal interaction of miR-34a-5p- and HOTAIR-mediated regulation of snail resulting in inhibition of EMT process by the combination of berberine and gefitinib  suggesting that regulation of miR-34a-5p- and HOTAIR-mediated inhibition of EMT may provide novel treatment paradigms for lung cancer.	32248643	RID06106	ceRNA or sponge	NA		
Gastric cancer	DLX6-AS1	PDK1	positively-E	shRNA;miRDB;luciferase reporter assay;TargetScan;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-4290)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000152256	NA	285987	5163	Evf-2|FLJ34048|NCRNA00212	NA	DLX6 Antisense RNA 1 Modulates Glucose Metabolism and Cell Growth in Gastric Cancer by Targeting microRNA-4290.DLX6-AS1 was overexpressed in GC tissues and cell lines. DLX6-AS1 knockdown by short hairpin RNA (shRNA) significantly inhibited  cell viability  and  colony formation, and induced apoptosis. DLX6-AS1 silencing impaired aerobic glycolysis but stimulated mitochondrial respiration in GC cells. miR-4290 was confirmed as a downstream target of DLX6-AS1, and their expression levels were inversely correlated. GC cells expressing sh-DLX6-AS1 showed significantly lower level of 3-phosphoinositide-dependent protein kinase 1 (PDK1), a target of miR-4290, compared to cells expressing control shRNA.n addition, the suppressed GC cell malignancy  upon DLX6-AS1 knockdown could be prominently reversed by PDK1 overexpression. Meanwhile, PDK1 overexpression enhanced aerobic glycolysis but repressed mitochondrial respiration under sh-DLX6-AS1 treatment. Furthermore, DLX6-AS1 knockdown significantly delayed the tumor growth in a mouse xenograft model inoculated with GC cells. LncRNA DLX6-AS1 regulated tumor growth and aerobic glycolysis in GC by targeting miR-4290 and PDK1, suggesting DLX6-AS1 might serve as a novel potential therapeutic target for GC treatment from bench to clinic.	32239379	RID06107	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Hepatocellular carcinoma	HAND2-AS1	SOCS5	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-300)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000171150	NA	79804	9655	DEIN|FLJ11539|NBLA00301	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis.The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The interactions between HAND2-AS1 and miR-300, miR-300 and SOCS5 were validated using luciferase reporter assay.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.We also validated that HAND2-AS1 acted as a sponge of miR-300, and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues. Furthermore, we found that SOCS5 was a downstream target of miR-300. In addition, miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation. miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.CONCLUSION: lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS5 axis.	32224127	RID06108	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	HAND2-AS1	BAX	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000087088	NA	79804	581	DEIN|FLJ11539|NBLA00301	BCL2L4	Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis.The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The interactions between HAND2-AS1 and miR-300, miR-300 and SOCS5 were validated using luciferase reporter assay.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.We also validated that HAND2-AS1 acted as a sponge of miR-300, and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues. Furthermore, we found that SOCS5 was a downstream target of miR-300. In addition, miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation. miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.CONCLUSION: lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS6 axis.	32224127	RID06109	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	HAND2-AS1	Caspase3	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	NA	NA	79804	NA	DEIN|NBLA00301|UPH	NA	Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis.The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The interactions between HAND2-AS1 and miR-300, miR-300 and SOCS5 were validated using luciferase reporter assay.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.We also validated that HAND2-AS1 acted as a sponge of miR-300, and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues. Furthermore, we found that SOCS5 was a downstream target of miR-300. In addition, miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation. miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.CONCLUSION: lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS7 axis.	32224127	RID06110	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Hepatocellular carcinoma	HAND2-AS1	BCL2	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000171791	NA	79804	596	DEIN|FLJ11539|NBLA00301	Bcl-2|PPP1R50	Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis.The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The interactions between HAND2-AS1 and miR-300, miR-300 and SOCS5 were validated using luciferase reporter assay.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.We also validated that HAND2-AS1 acted as a sponge of miR-300, and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues. Furthermore, we found that SOCS5 was a downstream target of miR-300. In addition, miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation. miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.CONCLUSION: lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS8 axis.	32224127	RID06111	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	PVT1	ITGB8	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);MEK/ERK signaling pathway(+);apoptosis process(-)	ceRNA(miR-145-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000105855	NA	5820	3696	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	The long non-coding RNA PVT1/miR-145-5p/ITGB8 axis regulates cell proliferation, apoptosis, migration and invasion in non-small cell lung cancer cells.The expressions of PVT1, ITGB8, and miR-145-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR.The protein levels of ITGB8, MEK, p-MEK, ERK, and p-ERK were measured by western blotThe potential binding sites between miR-145-5p and PVT1 or ITGB8 were predicted by online software and verified by luciferase reporter assay.We found out that the expression levels of PVT1 and ITGB8 were upregulated in NSCLC tissues and cells.Knockdown of PVT1 or ITGB8 suppressed cell proliferation, migration, invasion and promoted apoptosis in NSCLC cells, which could be reversed by ITGB8 overexpression in NSCLC cells. Moreover, PVT1 could regulate ITGB8 expression via direct binding to miR-145-5p. Furthermore, PVT1 regulated the MEK/ERK pathway by affecting ITGB8 expression. In addition, knockdown of PVT1 inhibited tumor growth, ITGB8 expression, MEK/ERK signaling pathway, and increased miR-145-5p expression in vivo. In conclusion, the knockdown of PVT1 inhibited proliferation, migration, and invasion but induced apoptosis of NSCLC cells by regulating miR-145-5p/ITGB8 axis and inhibiting MEK/ERK signaling pathway, providing a novel avenue for the treatment of NSCLC.	32202906	RID06112	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Prostate cancer	BRD4	MANCR	positively-E	CHIP	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000141867	NA	ENSG00000231298	GRCh38_10:4650158-4678185	23476	100216001	CAP|HUNK1|HUNKI|MCAP	CR749391|LINC00704	Long non-coding RNA MANCR is a target of BET bromodomain protein BRD4 and plays a critical role in cellular migration and invasion abilities of prostate cancer.Androgen receptor (AR)-negative castration-resistant prostate cancer (CRPC) is highly aggressive and is resistant to most of the current therapies. Bromodomain and extra terminal domain (BET) protein BRD4 binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers. A BET inhibitor, JQ1, has been found to suppress the malignant phenotypes of prostate cancer cells, however, the target genes of JQ1 remain largely unknown. Here we show that SE-associated genes specific for AR-negative CRPC PC3 cells include genes involved in migration and invasion, and that JQ1 impairs migration and invasion of PC3 cells. We identified a long non-coding RNA, MANCR, which was markedly down-regulated by JQ1, and found that BRD4 binds to the MANCR locus. MANCR knockdown led to a significant decrease in migration and invasion of PC3 cells. Furthermore, RNA sequencing analysis revealed that expression of the genes involved in migration and invasion was altered by MANCR knockdown. In summary, our data demonstrate that MANCR plays a critical role in migration and invasion of PC3 cells.	32199616	RID06113	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Malignant glioma	MALAT1	GOLM1	positively-E	starBase;RIP;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell autophagy(+)	ceRNA(miR-384)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135052	NA	378938	51280	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	bA379P1.3|C9orf155|FLJ23608|GOLPH2|GP73	LncRNA MALAT1 knockdown inhibits cell migration and invasion by suppressing autophagy through miR-384/GOLM1 axis in glioma.The expression of MALAT1, microRNA-384 (miR-384) and Golgi membrane protein 1 (GOLM1) was detected by quantitative Real-time polymerase chain reaction (qRT-PCR.The protein levels of GOLM1, light chain3 (LC3-II/LC3-I), p62, Vimentin and E-cadherin were proved by western blot.Bioinformatics tool starBase was used to predict target genes and associated binding sites. RNA immunoprecipitation assay (RIP) and dual-luciferase reporter assay were utilized to verify the relationship between miR-384 and MALAT1 or GOLM1. Tumor formation analysis in nude mice was conducted to ascertain the role of MALAT1 in vivo.MALAT1 was highly expressed in glioma tissues and cells. MALAT1 knockdown inhibited autophagy, migration and invasion of glioma cells. MiR-384 was a target of MALAT1, and miR-384 inhibition reversed the effects of MALAT1 knockdown in glioma cells. GOLM1 was a target of miR-384, and miR-384 inhibition eliminated the function of GOLM1 downregulation in glioma cells. In addition, GOLM1 was regulated by MALAT1 through miR-384. Moreover, MALAT1 knockdown blocked tumor growth and development in vivo.MALAT1 knockdown depleted migration and invasion by inhibiting autophagy through MALAT1/miR-384/GOLM1 axis in glioma in vitro and in vivo. The MALAT1/miR-384/GOLM1 axis was first proposed in our report, enriching the action mechanism of MALAT1 in glioma.	32196610	RID06114	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)
Nasopharynx carcinoma	LINC00114	miR-203	negatively-E	microRNA.org;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	ERK/JNK signaling pathway(+);cell growth(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000223806	GRCh38_21:38733890-38747460	ENSG00000207568	NA	400866	NA	C21orf24|NCRNA00114	NA	LINC00114 promoted nasopharyngeal carcinoma progression and radioresistance in vitro and in vivo through regulating ERK/JNK signaling pathway via targeting miR-203.The expression of LINC00114 and microRNA-203 (miR-203) was measured by quantitative real-time polymerase chain reaction (qRT-PCR.The interaction between miR-203 and LINC00114 was predicted by bioinformatics tool microRNA.org and verified by dual-luciferase reporter assay.LINC00114 was upregulated in serums from NPC patients, tissues and cell lines of NPC. LINC00114 knockdown inhibited proliferation, migration, and radioresistance of NPC cells. MiR-203 was a target of LINC00114, and miR-203 inhibition eliminated the effects of LINC00114 knockdown. Besides, the extracellular signal-regulated kinases (ERK)/c-Jun N-terminal kinases (JNK) pathway was inactivated by LINC00114 knockdown but recovered by miR-203 inhibition. Moreover, LINC00114 knockdown suppressed tumor growth and radioresistance in vivo.LINC00114 contributed to NPC development and radioresistance through the regulation of ERK/JNK signaling pathway and the mediation of miR-203, suggesting that LINC00114 was a promising biomarker to defense NPC progression and radioresistance.	32196600	RID06115	expression association	NA		
Colorectal cancer	LINC-ROR	NF2	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-223-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000186575	NA	100885779	4771	lincRNA-RoR|lincRNA-ST8SIA3|ROR	ACN|BANF|merlin|merlin-1|SCH	Long noncoding RNA ROR promotes proliferation and invasion of colorectal cancer by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.The expression level of ROR in colorectal cancer cells was detected using qRT-PCRThen, transfection of ROR, ROR inhibitor, miRNA-223-3p-mimics and miRNA-223-3p-inhibitor, qRT-PCR and luciferase reporter assay were used to explore the molecular mechanisms.Lnc-ROR was highly expressed in colorectal cancers compared with adjacent non-cancerous normal tissues.The luciferase reporter assay showed ROR acted as sponge and directly competed with miRNA-223-3p, then decreasing the expression of tumor suppressor gene NF2.The findings of this study first revealed that ROR was upregulated in colorectal cancer cells and can promote cell proliferation and invasion by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.	32196591	RID06116	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE86978)
Osteosarcoma	MT1JP	MIR646	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000207802	NA	4498	693231	MT1|MT1J|MT1NP|MTB	MIRN646|hsa-mir-646	Long Noncoding MT1JP Enhanced the Inhibitory Effects of miR-646 on FGF2 in Osteosarcoma.Plasma levels of MT1JP in both OS patients (n = 42) and healthy controls (n = 42) were also measured by RT-qPCR.Overexpression experiments were performed to analyze the interaction among MT1JP, miR-646, and FGF2.The authors found that MT1JP was significantly downregulated in OS tissues than in adjacent noncancer tissues.In addition, plasma MT1JP was also downregulated in OS patients than in healthy controls. The lower plasma levels of MT1JP in OS patients distinguished early stage OS patients from healthy controls. miR-646 was positive, but FGF2 was negatively correlated with MT1JP across OS tissues. The MT1JP overexpression upregulated miR-646 and downregulated FGF2, while the miR-646 overexpression downregulated FGF2, but showed no significant effects on the MT1JP expression. MT1JP and miR-646 overexpression inhibited the migration and invasion of OS cells. The FGF2 overexpression played the opposite role and attenuated the effects of MT1JP and miR-646 overexpression. Conclusions: In conclusion, MT1JP might downregulate FGF2 through miR-646 to inhibit OS cell migration and invasion. The downregulation of plasma circulating MT1JP may serve as an early diagnostic biomarker for OS.	32196384	RID06117	expression association	circulating		
Osteosarcoma	MT1JP	FGF2	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000138685	NA	4498	2247	MT1|MT1J|MT1NP|MTB	FGFB	Long Noncoding MT1JP Enhanced the Inhibitory Effects of miR-646 on FGF2 in Osteosarcoma.Plasma levels of MT1JP in both OS patients (n = 42) and healthy controls (n = 42) were also measured by RT-qPCR.Overexpression experiments were performed to analyze the interaction among MT1JP, miR-646, and FGF2.The authors found that MT1JP was significantly downregulated in OS tissues than in adjacent noncancer tissues.In addition, plasma MT1JP was also downregulated in OS patients than in healthy controls. The lower plasma levels of MT1JP in OS patients distinguished early stage OS patients from healthy controls. miR-646 was positive, but FGF2 was negatively correlated with MT1JP across OS tissues. The MT1JP overexpression upregulated miR-646 and downregulated FGF2, while the miR-646 overexpression downregulated FGF2, but showed no significant effects on the MT1JP expression. MT1JP and miR-646 overexpression inhibited the migration and invasion of OS cells. The FGF2 overexpression played the opposite role and attenuated the effects of MT1JP and miR-646 overexpression. Conclusions: In conclusion, MT1JP might downregulate FGF2 through miR-646 to inhibit OS cell migration and invasion. The downregulation of plasma circulating MT1JP may serve as an early diagnostic biomarker for OS.	32196384	RID06118	expression association	circulating		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Urinary bladder cancer	LINC00319	RAP2A	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+);cell growth(+)	ceRNA(miR-3127)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000125249	NA	284836	5911	C21orf125|FLJ38036|NCRNA00319|PRED49	K-REV|RAP2	LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A.The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines.Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3'-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.	32194636	RID06119	ceRNA or sponge	NA		UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	FOXD3-AS1	RICTOR	positively-E	miRDB;TargetScan;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);AKT signaling pathway(+)	ceRNA(miR-335)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000164327	NA	100996301	253260	pasFOXD3	AVO3|KIAA1999|MGC39830|PIA	LncRNA FOXD3-AS1 Mediates AKT Pathway to Promote Growth and Invasion in Hepatocellular Carcinoma Through Regulating RICTOR.Quantitative real time-polymerase chain reaction was applied to evaluate the expression of FOXD3-AS1 in HCC tissues and cell lines.miRDB and TargetScan websites were utilized to predict the interaction network of FOXD3-AS1 as a competing endogenous RNA. The interaction was confirmed by luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay.FOXD3-AS1 was overexpressed in HCC, and HCC patients with the high level of FOXD3-AS1 had a poor prognosis. In addition, FOXD3-AS1 knockdown considerably inhibited the proliferation, migration, and invasion of Huh6 cells. Besides, FOXD3-AS1 functioned as a sponge of miR-335, and RICTOR was a direct target gene of miR-335. Furthermore, FOXD3-AS1 could enhance the level of RICTOR through sponging miR-335. Moreover, the knockdown of FOXD3-AS1 could competitively bind with miR-335 to suppress RICTOR expression, thereby inhibiting the growth of Huh6 cells through the deactivation of AKT signaling pathway. Conclusions: FOXD3-AS1 is crucial for the tumorigenesis and progression of HCC. The interaction among FOXD3-AS1, miR-335, and RICTOR provides a novel insight for understanding the molecular mechanism of HCC, and FOXD3-AS1, miR-335, and RICTOR can be regarded as the potential targets for HCC treatment.	32191537	RID06120	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nonalcoholic fatty liver disease	LNCARSR	YAP1	positively-E	RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	IRS2/AKT signaling pathway(+);cell proliferation(+);cell invasion(+)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Fatty liver disease	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000137693	NA	102723932	10413	lnc-TALC	YAP65	Long noncoding RNA lncARSR promotes nonalcoholic fatty liver disease and hepatocellular carcinoma by promoting YAP1 and activating the IRS2/AKT pathway.LncARSR was highly expressed in high fatty diet (HFD)-fed mice and high fatty acid-treated HepG2 cells. LncARSR was observed to bind to YAP1, which inhibited phosphorylation nuclear translocation. LncARSR activated the IRS2/AKT pathway by reducing YAP1 phosphorylation, and further increased lipid accumulation, cell proliferation, invasion and cell cycle. Silencing lncARSR in HFD-fed mice alleviated NAFLD by regulating YAP1/IRS2/AKT axis.Silencing lncARSR suppressed the IRS2/AKT pathway, consequently reducing HCC cell proliferation and invasion and inhibiting lipid accumulation in NAFLD mice by downregulating YAP1, which suggests a clinical application in treating NAFLD.	32169080	RID06121	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Papillary thyroid carcinoma	CTC	KIT	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cancer progression(-);chemoresistance(-)	ceRNA(miR-146)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000157404	NA	NA	3815	NA	C-Kit|CD117|PBT|SCFR	Long Noncoding RNA CTC Inhibits Proliferation and Invasion by Targeting miR-146 to Regulate KIT in Papillary Thyroid Carcinoma.The analysis of hundreds of clinical specimens revealed that CTC and KIT levels were downregulated, whereas miR-146 levels were greater in PTC tissues than in normal thyroid.Their expression levels correlated with one another. In conclusion, CTC functions as a competing endogenous RNA to inhibit the progression and chemoresistance of PTC cells, and identifies CTC serve as a potential therapeutic agent to suppress PTC progression.We demonstrated that CTC was a negative regulator of PTC cell migration and invasion in vitro and in vivo. We found that microRNA-146 (miR-146) is an inhibitory target of CTC. We then demonstrated that CTC functioned as a miR-146 decoy to de-repress expression of KIT. Further study demonstrated that CTC modulated the progression and chemoresistance of PTC cells via miR-146 and KIT.	32165673	RID06122	ceRNA or sponge	chemoresistance		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Esophagus squamous cell carcinoma	SNHG1	HOXC8	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-204)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000037965	NA	23642	3224	LINC00057|lncRNA16|NCRNA00057|UHG	HOX3|HOX3A	LncRNA SNHG1 Regulates the Progression of Esophageal Squamous Cell Cancer by the miR-204/HOXC8 Axis. The expression levels of SNHG1, microRNA (miR)-204 and homeobox c8 (HOXC8) were detected by quantitative real-time polymerase chain reaction and western blot. The target interaction among SNHG1, miR-204 and HOXC8 was validated by luciferase reporter assay and RNA immunoprecipitation. Xenograft model was established to investigate the role of SNHG1 in vivo.High expression of SNHG1 was exhibited in esophageal squamous cell cancer and indicated poor outcomes of patients. miR-204 was validated to sponge by SNHG1 and target HOXC8 in esophageal squamous cell cancer cells. miR-204 knockdown or HOXC8 restoration reversed the inhibitive role of SNHG1 silence in the progression of esophageal squamous cell cancer cells. Furthermore, inhibiting SNHG1 decreased xenograft tumor growth by regulating miR-204 and HOXC8.	32158227	RID06123	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Pancreatic cancer	OIP5-AS1	AGR2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);AKT/ERK signaling pathway(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000106541	NA	729082	10551	cyrano|linc-OIP5	AG2|HAG-2|PDIA17|XAG-2	Long non-coding RNA OIP5-AS1 promotes pancreatic cancer cell growth through sponging miR-342-3p via AKT/ERK signaling pathway.Quantitative real-time PCR analysis revealed that OIP5-AS1 is highly expressed in pancreatic cancer tissues versus adjacent non-tumor tissues.In vitro functional assays showed that downregulation of OIP5-AS1 or overexpression of miR-342-3p inhibited the proliferation, decreased Ki67 expression, and induced cell cycle arrest in pancreatic cancer cells.Dual-luciferase assay confirmed the interaction of OIP5-AS1 and miR-342-3p and verified anterior gradient 2 (AGR2) as a direct target of miR-342-3p.Results showed that depletion of miR-342-3p abolished the inhibitory effects of OIP5-AS1 knockdown on pancreatic cancer cell growth. The expression of Ki67, AGR2, cyclinD1, CDK4, CDK6, p-AKT, and p-ERK1/2 was reversed by silencing of miR-342-3p in pancreatic cancer cells with OIP5-AS1 knockdown. Further, knockdown of OIP5-AS1 suppressed tumor growth in a xenograft mouse model of pancreatic cancer. OIP5-AS1 induced pancreatic cancer progression via activation of AKT and ERK signaling pathways. Therefore, we demonstrate that OIP5-AS1 functions as oncogene in pancreatic cancer and its downregulation inhibits pancreatic cancer growth by sponging miR-342-3p via targeting AGR2 through inhibiting AKT/ERK signaling pathway.	32157498	RID06124	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE51827,GSE55807)
Hepatocellular carcinoma	LINC01352	APC	positively-E	RegRNA 2.0;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-135b)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000238078	GRCh38_1:220829255-220832429	ENSG00000134982	NA	101929730	324	NA	DP2|DP2.5|DP3|PPP1R46	HBx/ERalpha complex-mediated LINC01352 downregulation promotes HBV-related hepatocellular carcinoma via the miR-135b-APC axis.Here, we report that the long non-coding RNA LINC01352 is markedly downregulated by HBV/HBx (HBV X protein) in HCC cells and clinical samples. Further investigation revealed that the downregulation of LINC01352, which acts as an endogenous sponge, increases the expression of miR-135b, leading to the reduced production of adenomatous polyposis coli (APC), consequently activating Wnt/beta-catenin signalling to facilitate tumour progression.These findings strongly suggest that the LINC01352-miR-135b-APC axis regulated by the HBx/ERalpha complex acts as an important pathogenic factor for tumour progression, which may help provide a theoretical basis for the identification of new therapeutic targets for HBV-related HCC.	32157216	RID06125	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Liver cancer	HAND2-AS1	SOCS5	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);JAK/STAT signaling pathway(-)	ceRNA(miR-3118)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000171150	NA	79804	9655	DEIN|FLJ11539|NBLA00301	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	lncRNA HAND2-AS1 Inhibits Liver Cancer Cell Proliferation and Migration by Upregulating SOCS5 to Inactivate the JAK-STAT Pathway.qRT-PCRanalysis and TCGA database discovered the expression in liver cancer.Bioinformatic analysis and luciferase reporter assay were utilized to monitor the binding between HAND2-AS1 or SOCS5 mRNA and miR-3118.The authors discovered the downregulated HAND2-AS1 in liver cancer cells. HAND2-AS1 augmentation apparently impaired the capacity of liver cancer viability, proliferation, and migration. Cytoplasmic HAND2-AS1 directly bound to miR-3118 and released SOCS5, leading to upregulation of SOCS5. Next, the negative regulator role of SOCS5 in the adjusting JAK-STAT pathway was reconfirmed in this study. Conclusions: HAND2-AS1 enhanced inactivation of the JAK-STAT pathway through sponging miR-3118 and facilitating SOCS5 to retard cell proliferation and migration in liver cancer.	32155348	RID06126	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cervical cancer	MALAT1	NFKB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(-)	ceRNA(miR-625-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	MicroRNA-625-5p Sponges lncRNA MALAT1 to Inhibit Cervical Carcinoma Cell Growth by Suppressing NF-kB Signaling.The relative expression levels of miR-625-5p and NF-kB transcript were determined by real-time polymerase chain reaction.The regulatory effects of miR-625-5p on NF-kB and MALAT1 were interrogated by luciferase reporter assay.We demonstrated that miR-625-5p was downregulated and predicted better survival in cervical carcinoma. Ectopic over-expression of miR-625-5p inhibited cell growth via targeting NF-kB. We further identified MALAT1 as the competitive endogenous long non-coding RNA for miR-625-5p, and over-expression of MALAT1 attenuated the inhibitory effect of miR-625-5p on NF-kB signaling in cervical carcinoma. Our study characterized the suppressive expression of miR-625-5p in cervical carcinoma and unraveled the importance of MALAT1/miR-625-5p/NF-kB signaling in this disease.	32152961	RID06127	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	miR-509-3-5p	NONHSAT112228.2	negatively-E	luciferase reporter assay	upregulation		NA	NA	cell proliferation(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	MiR-509-3-5p-NONHSAT112228.2 Axis Regulates p21 and Suppresses Proliferation and Migration of Lung Cancer Cells.To gain an insight into the role of miR-509-3-5p in the regulation of p21 expression, we performed in silico prediction and showed that miR-509-3-5p might target the NONHSAT112228.2, a sense-overlapping lncRNA transcribed by a non-code gene overlapping with p21 gene. Mutation and luciferase report analysis suggested that miR-509-3-5p could target NONHSAT112228.2, thereby blocking its expression.Consistently, NONHSAT112228.2 expression was inversely correlated with both miR-509-3-5p and p21 expression in cancer cells. Ectopic expression of miR-509-3-5p and knockdown of NONHSAT112228.2 both promoted proliferation and migration of cancer cells.Interestingly, high-expression of NONHSAT112228.2 accompanied by low-expression of p21 was observed in lung cancer tissues and associated with lower overall survival.Taken together, our study found a new regulatory pathway of p21, in which MiR-509-3-5p functionally interacts with NONHSAT112228.2 to release p21 expression. MiR-509-3-5p- NONHSAT112228.2 regulatory axis can inhibit the proliferation and migration of lung cancer cells.	32141418	RID06128	ceRNA or sponge	NA		
Esophagus squamous cell carcinoma	TUG1	CDC42	positively-E	LncBase Predicted v.2;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-498)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000070831	NA	55000	998	FLJ20618|LINC00080|NCRNA00080	CDC42Hs|G25K	Long Non-Coding RNA Taurine Upregulated Gene 1 (TUG1) Downregulation Constrains Cell Proliferation and Invasion through Regulating Cell Division Cycle 42 (CDC42) Expression Via MiR-498 in Esophageal Squamous Cell Carcinoma Cells.Expression patterns of TUG1, microRNA-498 (miR-498), and cell division cycle 42 (CDC42) mRNA were assessed using quantitative real time polymerase chain reaction (qRT-PCR.The relationship between miR-498 and TUG1 or CDC42 was predicted by online bioinformatics database LncBase Predicted v.2 or microT-CDS and confirmed through dual-luciferase reporter system or RNA immunoprecipitation assay (RIP).TUG1 and CDC42 were upregulated while miR-498 was strikingly decreased in ESCC tissues and cells.Importantly, TUG1 decrease restrained CDC42 expression via binding to miR-498 in ESCC cells.Also, the suppressive impacts of TUG1 silencing on the proliferation and invasion of ESCC cells were mitigated by miR-498 reduction. Meanwhile, the repression of proliferation and invasion induced by miR-498 elevation was weakened by CDC42 overexpression. CONCLUSIONS Inhibition of TUG1 hampered cell proliferation and invasion by downregulating CDC42 via upregulating miR-498 in ESCC cells. Thus, TUG1 might be an underlying therapeutic target for ESCC.	32139664	RID06129	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	FEZF1-AS1	SOX4	positively-E	overexpression;luciferase reporter assays	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell proliferation(+);cell invasion(-);apoptosis process(-)	ceRNA(miR-130a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000124766	NA	154860	6659	NA	NA	Long non-coding RNA FEZF1-AS1 induced progression of ovarian cancer via regulating miR-130a-5p/SOX4 axis.Interactions of FEZF1-AS1 and its target genes were identified by luciferase reporter assays.Our data showed overexpression of FEZF1-AS1 in OC cell lines and tissues. Cell migration, proliferation, invasion, wound healing and colony formation were suppressed by silencing of FEZF1-AS1.In contrast, cell apoptosis was promoted by FEZF1-AS1 knock-down in vitro.Furthermore, online bioinformatics analysis and tools suggested that FEZF1-AS1 directly bound to miR-130a-5p and suppressed its expression. Moreover, the inhibitory effects of miR-130a-5p on the OC cell growth were reversed by FEZF1-AS1 overexpression, which was associated with the increase in SOX4 expression. In conclusion, our results revealed that FEZF1-AS1 promoted the metastasis and proliferation of OC cells by targeting miR-130a-5p and its downstream SOX4 expression.	32135030	RID06130	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Esophageal cancer	LINC01234	CCNE1	positively-E	luciferase reporter gene assay;RIP;RNA pull-down assay	upregulation	RT-qPCR;microarray	NA	NA	cancer progression(+)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000105173	NA	100506465	898	onco-lncRNA-32	CCNE	Long noncoding RNA LINC01234 silencing exerts an anti-oncogenic effect in esophageal cancer cells through microRNA-193a-5p-mediated CCNE1 downregulation.The Gene Expression Omnibus (GEO) database was used for microarray-based EC expression profiling.Expression analyses of miR-193a-5p, LINC01234, CCNE1, caspase-3, p21, Bax, cyclinD1 and Bcl-2 were performed using RT-qPCR and western blot.microarray-based analyses revealed that LINC01234 expression was increased in primary EC samples, whereas that of miR-193a-5p was decreased. We found that CCNE1 was a target of miR-193a-5p and that LINC01234, in turn, sponges miR-193a-5p.After treatment with si-LINC01234 or miR-193a-5p mimic, EC cells (Eca-109 and EC9706) exhibited cyclinD1 and Bcl-2 downregulation, and caspase-3, p21, Bax and cleaved caspase-3 upregulation. LINC01234 silencing or miR-193a-5p upregulation resulted in decreased proliferation and colony formation, and increased apoptosis of EC cells. In addition, LINC01234 silencing or miR-193a-5p upregulation resulted in reduced in vivo EC tumor growth and CCNE1 expression in nude mice.We found that silencing of LINC01234 suppresses EC development by inhibiting CCNE1 through competitively binding to miR-193a-5p, which suggests that LINC01234 may represent a novel target for EC therapy.	32130660	RID06131	ceRNA or sponge	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Gastric cancer	PCAT18	CLDN11	positively-E	luciferase reporter gene assay;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-135b)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265369	GRCh38_18:26687621-26703638	ENSG00000013297	NA	728606	5010	LINC01092	OSP|OTM	lncRNA PCAT18 inhibits proliferation, migration and invasion of gastric cancer cells through miR-135b suppression to promote CLDN11 expression.Transfection was conducted to build over-expression and down-expression models. Moreover, RT-qPCR and western blot were used to detect the transcriptional and translational levels.The potential binding of miR-135b and its downstream and upstream molecules was validated by dual luciferase reporter gene assay or RIP.PCAT18 down-expression promoted proliferation, migration and invasion of gastric cancer cells.we found that PCAT18 could bind miR-135b which also was bound with CLDN11. We found that miR-135b is negatively correlated with CLDN11; PCAT18 and CLDN11 are positively correlated. Moreover, miR-135b mimics could down-regulate protein level of CLDN11, whereas CLDN11 could reverse this effect. In in-vivo experiment, PCAT18 over-expression restrained tumor growth and metastasis.CONCLUSIONS: Over-expressed lncRNA PCAT18 inhibits proliferation, migration and invasion of gastric cancer cells through regulation of miR-135b/CLDN11.	32119960	RID06132	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)
Pancreatic ductal adenocarcinoma	NORAD	PAK4	positively-E	starBase 3.0;TargetScan;miRDB;RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-433)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000130669	NA	647979	10298	LINC00657	NA	Long noncoding RNA LINC00657 enhances the malignancy of pancreatic ductal adenocarcinoma by acting as a competing endogenous RNA on microRNA-433 to increase PAK4 expression.The expression profile of LINC00657 in PDAC was estimated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR).The results revealed that LINC00657 was evidently upregulated in the PDAC tumors and cell lines.High LINC00657 expression significantly correlated with the pathological T stage, lymph node metastasis, and shorter overall survival. Functional analysis demonstrated that LINC00657 knockdown inhibited the proliferation, migration, and invasion while promoted the apoptosis of PDAC cells. In addition, LINC00657 knockdown markedly suppressed tumor growth of these cells in vivo. In terms of the mechanism, LINC00657 could directly interact with microRNA-433 (miR-433) and effectively worked as an miR-433 sponge, thus decreasing the competitive binding of miR-433 to PAK4 mRNA and ultimately increasing PAK4 expression. The actions of LINC00657 knockdown on malignant phenotype of PDAC cells were strongly attenuated by miR-433 inhibition and PAK4 restoration. These results indicate that LINC00657 promotes PDAC progression by increasing the output of the miR-433-PAK4 regulatory loop, thus highlighting the importance of the LINC00657-miR-433-PAK4 network in PDAC pathogenesis.	32116086	RID06133	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE75367)
Cervical cancer	GAS5	Cyclin B1	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long non-coding RNA GAS5 regulates the growth and metastasis of human cervical cancer cells via induction of apoptosis and cell cycle arrest.The results showed that GAS5 was significantly downregulated in human cervical cancer tissues.The results also showed that cervical cancer progresses with the suppression of GAS5 expression levels. Additionally, the expression of GAS5 was also significantly (p  <  0.05) downregulated in human cervical cancer cell lines. Nonetheless, overexpression of GAS5 caused a remarkable decrease in the proliferation of C33A and HeLa cervical cancer cells. The decrease in the proliferation rate was attributed to the induction of apoptosis of C33A and HeLa cells which was accompanied with upregulation of Bax and suppression of Bcl-2. Additionally, GAS5 overexpression also promoted the arrest of C33A and HeLa cells at the G2/M check point of cell cycle via suppression of cyclin B1 and CDK1 expression. The transwell assays showed that GAS5 overexpression significantly (p  <  0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. The bioinformatics analysis as well as the dual luciferase assay showed GAS5 acts as a target of miR-135a. Interestingly, the expression of miR-135a was upregulated in the human cervical cancer cells and its suppression exerted growth inhibitory effects on the C33A and HeLa cells. However, silencing of GAS5 could nullify the effects of miR-135a suppression on the proliferation of C33A and HeLa cells. Taken together, the results of this study point towards the therapeutic implications of GAS5 in the treatment of cervical cancer.	32105659	RID06134	expression association	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Cervical cancer	GAS5	CDK1	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000170312	NA	60674	983	NCRNA00030|SNHG2	CDC2|CDC28A	Long non-coding RNA GAS5 regulates the growth and metastasis of human cervical cancer cells via induction of apoptosis and cell cycle arrest.The results showed that GAS5 was significantly downregulated in human cervical cancer tissues.The results also showed that cervical cancer progresses with the suppression of GAS5 expression levels. Additionally, the expression of GAS5 was also significantly (p  <  0.05) downregulated in human cervical cancer cell lines. Nonetheless, overexpression of GAS5 caused a remarkable decrease in the proliferation of C33A and HeLa cervical cancer cells. The decrease in the proliferation rate was attributed to the induction of apoptosis of C33A and HeLa cells which was accompanied with upregulation of Bax and suppression of Bcl-2. Additionally, GAS5 overexpression also promoted the arrest of C33A and HeLa cells at the G2/M check point of cell cycle via suppression of cyclin B1 and CDK1 expression. The transwell assays showed that GAS5 overexpression significantly (p  <  0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. The bioinformatics analysis as well as the dual luciferase assay showed GAS5 acts as a target of miR-135a. Interestingly, the expression of miR-135a was upregulated in the human cervical cancer cells and its suppression exerted growth inhibitory effects on the C33A and HeLa cells. However, silencing of GAS5 could nullify the effects of miR-135a suppression on the proliferation of C33A and HeLa cells. Taken together, the results of this study point towards the therapeutic implications of GAS6 in the treatment of cervical cancer.	32105659	RID06135	expression association	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Cervical cancer	miR-135a	GAS5	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	miRNA	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Long non-coding RNA GAS5 regulates the growth and metastasis of human cervical cancer cells via induction of apoptosis and cell cycle arrest.The results showed that GAS5 was significantly downregulated in human cervical cancer tissues.The results also showed that cervical cancer progresses with the suppression of GAS5 expression levels. Additionally, the expression of GAS5 was also significantly (p  <  0.05) downregulated in human cervical cancer cell lines. Nonetheless, overexpression of GAS5 caused a remarkable decrease in the proliferation of C33A and HeLa cervical cancer cells. The decrease in the proliferation rate was attributed to the induction of apoptosis of C33A and HeLa cells which was accompanied with upregulation of Bax and suppression of Bcl-2. Additionally, GAS5 overexpression also promoted the arrest of C33A and HeLa cells at the G2/M check point of cell cycle via suppression of cyclin B1 and CDK1 expression. The transwell assays showed that GAS5 overexpression significantly (p  <  0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. The bioinformatics analysis as well as the dual luciferase assay showed GAS5 acts as a target of miR-135a. Interestingly, the expression of miR-135a was upregulated in the human cervical cancer cells and its suppression exerted growth inhibitory effects on the C33A and HeLa cells. However, silencing of GAS5 could nullify the effects of miR-135a suppression on the proliferation of C33A and HeLa cells. Taken together, the results of this study point towards the therapeutic implications of GAS7 in the treatment of cervical cancer.	32105659	RID06136	expression association	metastasis		DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Pancreatic cancer	CASC2	PTEN	positively-E	overexpression;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	NA	association	RNA-protein	Ginsenoside Rg3;Gemcitabine	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	BZS|MHAM|MMAC1|PTEN1|TEP1	Ginsenoside Rg3 suppresses the growth of gemcitabine-resistant pancreatic cancer cells by upregulating lncRNA-CASC2 and activating PTEN signaling.The level of long noncoding RNA cancer susceptibility candidate 2 (CASC2) and PTEN expression was upregulated by the ginsenoside Rg3 treatment, and CASC2/PTEN signaling was involved in the ginsenoside Rg3-induced cell growth suppression and apoptosis in GEM-resistant pancreatic cancer cells.	32104955	RID06137	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Malignant glioma	BCYRN1	TAZ	positively-E	LncBase Predicted V.2;overexpression;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-125a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000102125	NA	618	6901	BC200|BC200a|LINC00004|NCRNA00004	BTHS|CMD3A|EFE|EFE2|G4.5|LVNCX|Taz1	The lncRNA BCYRN1 Functions as an Oncogene in Human Glioma by Downregulating miR-125a-5p in vitro.The correlation between the expression of BCYRN1 and miR-125a-5p was verified by quantitative real-time PCR.The upregulation of BCYRN1 promoted the proliferation, migration and invasion of glioma cells. Meanwhile, the knockdown of BCYRN1 had the opposite effects. BCYRN1 was negatively correlated with miR-125a-5p. Additionally, TAZ, the endogenous target of miR-125a-5p, could be regulated by BCYRN1 in RNA and protein levels. Mechanistically, upregulated expression of BCYRN1 in glioma acts as a sponge to sequester the endogenous tumor suppressor miR-125a-5p and to further increase the expression TAZ. Our findings suggest that BCYRN1 is a novel oncogene and a new therapeutic target for glioma.	32104095	RID06138	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	XIC	MIR454	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	ENSG00000211514	NA	7502	768216	SXI1|XCE|XIST	MIRN454|hsa-mir-454|mir-454	LncRNA XIST interacts with miR-454 to inhibit cells proliferation, epithelial mesenchymal transition and induces apoptosis in triple-negative breast cancer.XIST was down-regulated in TNBC tissues and cell lines. Overexpressed XIST inhibited cell proliferation, epithelial mesenchymal transition (EMT) and induced apoptosis in vitro as well as suppressed TNBC tumor growth in vivo. MicroRNA (miR)- 454 was up-regulated in TNBC tissues and cell lines. Knockdown of miR-454 inhibited TNBC progression by suppressing cell proliferation, EMT and inducing cell apoptosis. Moreover, miR-454 was predicted and confirmed to be a target of XIST, and rescue assay indicated that overexpressed miR-454 could reverse XIST restoration mediated-anti-tumor effects on TNBC cells. In conclusion, XIST interacts with miR-454 to inhibit cells proliferation, EMT and induce apoptosis in TNBC, indicating a promising treatment strategy for TNBC patients.	32098924	RID06139	ceRNA or sponge	NA		
Ovarian cancer	BLACAT1	miR-519d-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	linc-UBC1|LINC00912|onco-lncRNA-30	NA	Down-regulation of lncRNA BLACAT1 inhibits ovarian cancer progression by suppressing the Wnt/beta-catenin signaling pathway via regulating miR-519d-3p.Quantitative RT-PCRshowed that BLACAT1 was aberrantly up-regulated in ovarian cancer tissues compared with normal tissues.Luciferase assay verified the binding relationship between microRNA-519d-3p and lncRNA BLACAT1, and BLACAT1 negatively regulated the expression of miR-519d-3p. We also found that miR-519d-3p overexpression could inhibit ovarian cancer cells proliferation, migration and invasion.Inhibition of BLACAT1 was sufficient to down-regulate the expression of RPS15A and nuclear beta-catenin but did not cause an obvious change in cytoplasmic beta-catenin expression. Taken together, BLACAT1 knockdown inhibited the progression of ovarian cancer by suppressing the Wnt/beta-catenin signaling pathway via regulating miR-519d-3p. Our work provided a proper understanding of the critical roles of BLACAT1 in ovarian cancer.	32095930	RID06140	ceRNA or sponge	NA		
Non-small cell lung cancer	miR-141-3p	ATB	negatively-E	Starbase;dual-luciferase reporter assay; RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA ATB promotes human non-small cell lung cancer proliferation and metastasis by suppressing miR-141-3p.In this study, lncRNA-ATB was significantly up-regulated in NSCLC tissues and cell lines, and high lncRNA-ATB expression indicated poor prognosis. Knockdown of lncRNA-ATB suppressed NSCLC cell growth, colony formation, migration, invasion and reversed epithelial-mesenchymal transition. In vivo study showed that silencing lncRNA-ATB inhibited tumor growth. Further mechanism studies demonstrated that lncRNA-ATB was a target of miR-141-3p. MiR-141-3p expression was negatively related to lncRNA-ATB expression in NSCLC tissues. These results suggested that inhibiting lncRNA-ATB might be an approach for NSCLC treatment.	32092085	RID06141	expression association	metastasis,prognosis		
Esophagus squamous cell carcinoma	SNHG12	BCL9	positively-E	starBase 3.0	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-);cell growth(-);apoptosis process(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000116128	NA	85028	607	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	Long noncoding RNA SNHG12 suppresses esophageal squamous cell carcinoma progression through competing endogenous RNA networks.Real-time quantitative polymerase chain reaction (qRT-PCR was used to verify the expression levels of SNHG12 in ESCC tissues and cell lines.SNHG12 was downregulated in human ESCA tissues compared to control tissues.knockdown of SNHG12 not only promoted proliferation, colony formation, migration, and invasion and inhibited apoptosis in ESCC cells in vitro, but also increased tumor growth in vivo.This is the first study to reveal that SNHG12 is downregulated in ESCC tissues and could be used as a prognostic tool. SNHG12 suppressed tumor progression in ESCC cells, serving as a potential biomarker. The SNHG12/miRNA-195-5p/BCL9 network is proposed to be the mechanism leading to ESCC progression.	32086782	RID06142	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	PLACT1	IkBalpha	negatively-E	RIP	upregulation	qRT-PCR	GSE61166	NA	cell proliferation(+);cell invasion(+);NF-kB signaling pathway(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lncRNA-PLACT1-sustains activation of NF-kB pathway through a positive feedback loop with IkBalpha/E2F1 axis in pancreatic cancer.The expression and clinical features of PLACT1 were analyzed in a 166-case cohort of PDAC by qRT-PCRand in situ hybridization.Chromatin isolation by RNA purification assays were utilized to examine the interaction of PLACT1 with IkBalpha promoter. We identified a novel lncRNA-PLACT1, which was significantly upregulated in tumor tissues and correlated with progression and poor survival in PDAC patients. Moreover, PLACT1 promoted the proliferation and invasion of PDAC cells in vitro.PLACT1 suppressed IkBalpha expression by recruiting hnRNPA1 to IkBalpha promoter, which led to increased H3K27me3 that decreased the transcriptional level of IkBalpha.E2F1-mediated overexpression of PLACT1 modulated the progression of PDAC by sustained activation of NF-kB signaling pathway through forming a positive feedback loop with IkBalpha. Importantly, administration of the NF-kB signaling pathway inhibitor significantly suppressed PLACT1-induced sustained activation of NF-kB signaling pathway, leading to reduced tumorigenesis in vivo.Our findings suggest that PLACT1 provides a novel epigenetic mechanism involved in constitutive activation of NF-kB signaling pathway and may represent a new therapeutic target of PDAC.	32085715	RID06143	transcriptional regulation	NA		
Triple-negative breast cancer	IQANK1	MTDH	positively-E	LncBase Predicted v.2;overexpression;RIP	upregulation	microarray	GSE76250	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000147649	NA	642574	92140	FAM83H-AS1|onco-lncRNA-3	3D3|AEG-1|LYRIC	LncRNA FAM83H-AS1 promotes triple-negative breast cancer progression by regulating the miR-136-5p/metadherin axis.Our data show that the FAM83H-AS1 levels are increased in human TNBC cells and tissues.Bioinformatics analysis revealed that miR-136-5p is a potential target of FAM83H-AS1. MiR-136-5p expression is decreased in TNBC tissues, and its overexpression suppresses TNBC cell proliferation, migration, and invasion.MiR-136-5p suppression reverses the FAM83H-AS1 silencing-mediated inhibition of TNBC cell proliferation, migration, and invasion, suggesting that FAM83H-AS1 exerts its oncogenic effect by inhibiting miR-136-5p. Our data identify metadherin (MTDH) as the target gene of miR-136-5p, and demonstrate that the MTDH expression is increased in human TNBC tissues, which induces proliferation, migration, and invasion of TNBC cells. Importantly, our in vivo data show that FAM83H-AS1 also promotes tumor growth in TNBC mouse xenografts. Together, our results demonstrate that FAM83H-AS1 functions as an oncogenic lncRNA that regulates miR-136-5p and MTDH expression during TNBC progression, and suggest that targeting the FAM83H-AS1/miR-136-5p/MTDH axis may serve as a novel therapeutic target in TNBC.In addition, we analyzed online data using the Gene Expression Profiling Interactive Analysis 2 (GEPIA2) (http://gepia2.cancer-pku.cn/#index) [50] and cBioPortal (https://www.cbioportal.org/) databases.	32074085	RID06144	ceRNA or sponge	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Malignant glioma	GAS5-AS1	TUSC2	positively-E	dual-luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-106b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000270084	GRCh38_1:173862473-173863941	ENSG00000262485	NA	100506046	11334	NA	C3orf11|FUS1|PAP|PDAP2	LncRNA GAS5-AS1 inhibits glioma proliferation, migration, and invasion via miR-106b-5p/TUSC2 axis.Expression of GAS5-AS1 and microRNA-106b-5p (miR-106b-5p) in glioma tissues and cells was detected by quantitative reverse transcription PCR, northern blotting, or fluorescent in situ hybridization.BALB/c nude mice were used to establish a glioma xenograft animal model by subcutaneous injection of U251 cells transfected with small interfering RNA targeting GAS5-AS1.A dual-luciferase reporter assay was conducted to confirm the targeting relationship between GAS5-AS1 and miR-106b-5p. GAS5-AS1 expression was downregulated in glioma tissues and cells, and upregulation of GAS5-AS1 expression inhibited glioma cell proliferation, migration, and invasion.GAS5-AS1 expression was correlated with the glioma tumor grade. In nude mice, upregulation of  GAS5-AS1  markedly suppressed glioma  tumor  growth. GAS5-AS1 overexpression significantly increased the miR-106b-5p level in glioma cells, and GAS5-AS1 expression was negatively related to miR-106b-5p expression in glioma tissues. Overexpression of miR-106b-5p reversed the inhibitory effects of GAS5-AS1 upregulation on glioma cell proliferation and metastasis, while restoration of TUSC2 rescued the proliferation and invasion of glioma cells transfected with miR-106b-5p mimics. In summary, lncRNA  GAS5-AS1  inhibited glioma proliferation, migration, and invasion by sponging miR-106b-5p and regulating the expression of TUSC2. Our results suggest GAS5-AS1 as a novel target for the treatment and prognosis prediction of gliomas.	32072565	RID06145	ceRNA or sponge	metastasis,prognosis	DOWN(PAAD,SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	LINC00160	PIK3R3	positively-E	dual-luciferase reporter assay;starBase;miRcode;mirDIP	upregulation	RT-qPCR	NA	NA	cell autophagy(+);cell viability(+);chemoresistance(+)	ceRNA(miR-132)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230978	GRCh38_21:34723807-34737204	ENSG00000117461	NA	54064	8503	C21orf52|NCRNA00160	p55	Long non-coding RNA LINC00160 functions as a decoy of microRNA-132 to mediate autophagy and drug resistance in hepatocellular carcinoma via inhibition of PIK3R3. Interaction among LINC00160, miR-132 and PIK3R3 was verified by dual luciferase reporter gene assay.LINC00160 and PIK3R3 were up-regulated but miR-132 was down-regulated in HCC tissues and cells. LINC00160 may regulate miR-132 and PIK3R3 was the target gene of miR-132. LINC00160 increased the expression of LC3I/LC3II and Atg5 but decreased the p62 expression, while silencing of LINC00160 or over-expression of miR-132 suppressed HCC cell viability, autophagy, drug-resistance and tumorigenicity in nude mice but promoted HCC cell apoptosis by inhibiting the PIK3R3 expression. Taken together, silencing of LINC00160 suppresses autophagy and drug resistance in HCC by regulating miR-132-targeted PIK3R3.	32067991	RID06146	ceRNA or sponge	chemoresistance		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Gastric cancer	RGMB-AS1	NFIB	positively-E		upregulation		NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-)	ceRNA(miR-22-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000147862	NA	503569	4781	NA	NFI-RED|NFIB2|NFIB3	RGMB-AS1/miR-22-3p/NFIB axis contributes to the progression of gastric cancer.In this study, our results demonstrated that RGMB-AS1 was upregulated in GC cells and knockdown of RGMB-AS1 suppressed cell proliferation, migration, invasion, EMT process and promoted cell apoptosis.Molecular mechanism experiments indicated that RGMB-AS1 could bind with miR-22-3p and NFIB was a downstream target gene of miR-22-3p. Additionally, RGMB-AS1 suppression upregulated the expression of miR-22-3p and miR-22-3p inhibitor could reverse the inhibitive role of sh-RGMB-AS1-1 in NFIB expression. Rescues assays showed that NFIB overexpression partially recovered the inhibitory function on cell proliferation, migration, invasion, EMT process and the promotive function on cell apoptosis caused by RGMB-AS1 depletion. Taken together, RGMB-AS1 contributes to the progression of GC by regulating miR-22-3p/NFIB axis, indicating a new ther	32064882	RID06147	ceRNA or sponge	NA		UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Hepatocellular carcinoma	HOTAIR	HIF1A	positively-E	starBase;luciferase assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100644	NA	100124700	3091	HOXC-AS4|HOXC11-AS1|NCRNA00072	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	LncRNA HOTAIR knockdown inhibits glycolysis by regulating miR-130a-3p/HIF1A in hepatocellular carcinoma under hypoxia.The expression levels of HOTAIR, microRNA-130a-3p (miR-130a-3p) and hypoxia inducible factor 1 alpha (HIF1A) were measured by quantitative real-time polymerase chain reaction and western blot, respectively.The target interaction between miR-130a-3p and HOTIR or HIF1A was analyzed by bioinformatics analysis, luciferase assay, RNA pull-down and RNA immunoprecipitation. We found that HOTAIR expression was enhanced in HCC tissues and cells.Under hypoxia condition, HOTAIR expression was increased and its knockdown inhibited glycolysis in HCC cells. HOTAIR was validated as a decoy of miR-130a-3p and miR-130a-3p deficiency reversed the suppressive effect of HOTAIR silence on glycolysis under hypoxia. HIF1A was indicated as a target of miR-130a-3p and miR-130a-3p overexpression repressed glycolysis under hypoxia by targeting HIF1A. Moreover, HIF1A expression was regulated by HOTAIR and miR-130a-3p. In conclusion, knockdown of HOTAIR suppressed glycolysis by regulating miR-130a-3p and HIF1A in HCC cells treated by hypoxia, elucidating a novel mechanism in HCC glycolysis.	32062551	RID06148	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Lung adenocarcinoma	miR-383-5p	TMPO-AS1	negatively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000257167	GRCh38_12:98512973-98516422	NA	100128191	NA	NA	Long noncoding RNA TMPO-AS1 promotes lung adenocarcinoma progression and is negatively regulated by miR-383-5p.Herein, in our study, we identified that lncRNA TMPO-AS1 is significantly upregulated in LUAD tissues and cell lines. Knockdown of TMPO-AS1 remarkably suppressed LUAD cell growth, induced apoptosis as well as G1/S arrest, and inhibited LUAD cell invasion, whereas overexpression of TMPO-AS1 exerts the opposite effects.Next, we implemented online database analysis tools to find that mir-383-5p could target TMPO-AS1, and our data showed that TMPO-AS1 was negatively correlated with mir-383-5p in LUAD specimens. We found that inhibiting miR-383-5p expression led to a marked upregulation of TMPO-AS1 level, while overexpression of miR-383-5p markedly suppressed TMPO-AS1's expression and function, suggesting that TMPO-AS1 is negatively regulated by miR-383-5p. In addition, we confirmed that miR-383-5p directly targeted TMPO-AS1 by binding to microRNA binding sites in the TMPO-AS1 sequence with a luciferase reporter and RIP assays. Besides, the inhibition of TMPO-AS1 significantly suppressed the tumorigenesis ability of LUAD cells in vivo. Together, these results demonstrate that TMPO-AS1 could be considered as a potential therapeutic target for LUAD patients.	32062549	RID06149	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Gastric cancer	LINC00460	CCNG2	negatively-E	ChIP;RIP;RNA pull-down assay	upregulation	qRT-PCR	GSE54129;GSE64951	NA	cell proliferation(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000138764	NA	728192	901	NA	NA	Upregulation of lncRNA LINC00460 Facilitates GC Progression through Epigenetically Silencing CCNG2 by EZH2/LSD1 and Indicates Poor Outcomes.In this research, we discovered that LINC00460 is remarkably upregulated in GC tissues compared to the non-tumor tissues.What's more, the biological function of LINC00460 was mediated, to certain extent, by the direct interaction with enhancer of zeste homolog 2 (EZH2) and lysine (K)-specific demethylase 1A (LSD1) proteins.Further analyses indicated that LINC00460 promoted GC proliferation at least partly through the downregulation of tumor suppressor-gene Cyclin G2 (CCNG2), which is mediated by EZH2 and LSD1. In conclusion, our results suggested that LINC00460 acted as an oncogene in GC to inhibit the expression of CCNG2 at least partly by binding with EZH2 and LSD1. Our study could provide additional insights into the development of novel target therapeutic methods for GC.	32059342	RID06150	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Triple-negative breast cancer	LINC00173	miR-490-3p	negatively-E	ENCORI;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000196668	GRCh38_12:116533422-116536518	NA	NA	100287569	NA	FLJ42957|NCRNA00173	NA	LncRNA LINC00173 enhances triple-negative breast cancer progression by suppressing miR-490-3p expression.Quantitative PCR analysis was performed to determine the expression of LINC00173 in TNBC and adjacent breast tissues.TNBC patients with high tumoral LINC00173 levels had a lower recurrence-free survival and overall survival rate than those with low LINC00173 expression.Mechanistic investigation revealed that LINC00173 suppressed miR-490-3p to promote aggressive phenotype in TNBC cells. There was an inverse correlation between miR-490-3p and LINC00173 in TNBC.Altogether, LINC00173 functions as an oncogene in TNBC through antagonization of miR-490-3p. Upregulation of LINC00173 is associated with poor prognosis in TNBC. Targeting LINC00173 provides a potential therapeutic strategy for TNBC.	32058222	RID06151	ceRNA or sponge	recurrence,prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	
Ovarian cancer	LOXL1-AS1	VMA21	positively-E	luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-18b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000160131	NA	100287616	203547	NA	MEAX|XMEA	Non-coding RNA LOXL1-AS1 exhibits oncogenic activity in ovarian cancer via regulation of miR-18b-5p/VMA21 axis.LOXL1-AS1 is significantly overexpressed in ovarian carcinoma tissue compared with adjacent non-cancerous sample.The luciferase reporter gene assay reveals the relationship between LOXL1-AS1 and miR-18b-5p, miR-18b-5p and its target gene, Vacuolar ATPase Assembly Factor VMA21 (VMA21). Transfection of LOXL1-AS1 siRNA or miR-18b-5p mimics inhibits the growth and aggressive phenotypes of SKOV3 and OVCAR3 cell. Furthermore, miR-18b-5p suppresses ovarian carcinoma cell proliferation and metastasis by targeting VMA21 and LOXL1-AS1 regulates ovarian carcinoma cell growth and metastasis through sponging miR-18b-5p. These findings suggest that lncRNA LOXL1-AS1 promotes ovarian cancer cell growth, migratory and invasiveness via modulating miR-18b-5p/VMA21 axis.	32058209	RID06152	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827)
Urinary bladder cancer	MST1P2	SIRT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	Sirt1/p53 signaling pathway(+);chemoresistance(+)	ceRNA(miR-133b)	regulation	NA	Cisplatin	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000186301	GRCh38_1:16645622-16650289	ENSG00000096717	NA	11209	23411	MSPL-2|MSPL2|MSTP2	SIR2L1	LncRNA MST1P2/miR-133b axis affects the chemoresistance of bladder cancer to cisplatin-based therapy via Sirt1/p53 signaling.We demonstrated that lncRNA MST1P2 (lnc-MST1P2) expression was dramatically upregulated, whereas miR-133b expression was downregulated in DDP-resistant bladder cancer cell lines, SW 780/DDP and RT4/DDP.Lnc-MST1P2 and miR-133b negatively regulated each other via targeting miR-133b. Both lnc-MST1P2 silence and miR-133b overexpression could resensitize DDP-resistant bladder cancer cells to DDP treatment. More important, miR-133b could directly target the Sirt1 3'-untranslated region to inhibit its expression. Inc-MST1P2/miR-133b axis affected the resistance of bladder cancer cells to DDP via Sirt1/p53 signaling. In conclusion, MST1P2 serves as a competing endogenous RNA for miR-133b to counteract miR-133b-induced suppression on Sirt1, therefore enhancing the resistance of bladder cancer cells to DDP. MST1P2/miR-133b axis affects the resistance of bladder cancer cells to DDP via downstream Sirt1/p53 signaling.	32052927	RID06153	ceRNA or sponge	chemoresistance		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical squamous cell carcinoma	BLACAT1	miR-424	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell migration(+);cell invasion(+)	NA	association	RNA-RNA	NA	CSC	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	linc-UBC1|LINC00912|onco-lncRNA-30	NA	LncRNA BLACAT1 Is Upregulated in Cervical Squamous Cell Carcinoma (CSCC) and Predicts Poor Survival.The function of oncogenic lncRNA BLACAT1 has been studied in several types of cancer, while its role in cervical squamous cell carcinoma (CSCC) is unknown. We showed that BLACAT1 was upregulated in CSCC tissue comparing to adjacent non-cancer tissue of CSCC patients. BLACAT1 expression in CSCC tissues was not affected by HPV infection. Patients with higher BLACAT1 level in CSCC tissues showed a significantly lower overall 5-year survival rate. BLACAT1 expression was inversely correlated with several tumor-suppressive miRNAs, such as miR-424 and miR-143. miR-424 and miR-143 overexpression did not significantly affect BLACAT1, while BLACAT1 overexpression caused downregulated miR-424 and miR-143. Overexpression of miR-424 and miR-143 led to inhibited migration and invasion, while BLACAT1 overexpression led to promoted migration and invasion of CSCC cells. In addition, overexpression of miR-424 and miR-143 attenuated the effects of BLACAT1 overexpression. Therefore, BLACAT1 overexpression may promote CSCC by downregulating miR-424 and miR-143.	32046460	RID06154	expression association	NA		
Cervical squamous cell carcinoma	BLACAT1	miR-143	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell migration(+);cell invasion(+)	NA	association	RNA-RNA	NA	CSC	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	linc-UBC1|LINC00912|onco-lncRNA-30	NA	LncRNA BLACAT1 Is Upregulated in Cervical Squamous Cell Carcinoma (CSCC) and Predicts Poor Survival.The function of oncogenic lncRNA BLACAT1 has been studied in several types of cancer, while its role in cervical squamous cell carcinoma (CSCC) is unknown. We showed that BLACAT1 was upregulated in CSCC tissue comparing to adjacent non-cancer tissue of CSCC patients. BLACAT1 expression in CSCC tissues was not affected by HPV infection. Patients with higher BLACAT1 level in CSCC tissues showed a significantly lower overall 5-year survival rate. BLACAT1 expression was inversely correlated with several tumor-suppressive miRNAs, such as miR-424 and miR-143. miR-424 and miR-143 overexpression did not significantly affect BLACAT1, while BLACAT1 overexpression caused downregulated miR-424 and miR-143. Overexpression of miR-424 and miR-143 led to inhibited migration and invasion, while BLACAT1 overexpression led to promoted migration and invasion of CSCC cells. In addition, overexpression of miR-424 and miR-143 attenuated the effects of BLACAT1 overexpression. Therefore, BLACAT1 overexpression may promote CSCC by downregulating miR-424 and miR-144.	32046460	RID06155	expression association	NA		
Ovarian cancer	ITCH	HULC	negatively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	PCG	lncRNA	ENSG00000078747	NA	ENSG00000251164	NA	83737	728655	AIP4	HCCAT1|LINC00078|NCRNA00078	Circular RNA-ITCH Inhibits the Proliferation of Ovarian Carcinoma by Downregulating lncRNA HULC.In this study, we observed that circular RNA-ITCH was downregulated, while lncRNA HULC was upregulated in ovarian carcinoma. Circular RNA-ITCH and HULC were inversely and significantly correlated. Overexpression of circular RNA-ITCH resulted in inhibited, while overexpression of HULC promoted the proliferation of cells of ovarian cancer cell lines. Overexpression of circular RNA-ITCH led to inhibited HULC in cells of ovarian cancer cell lines, while overexpression of HULC failed to significantly affect the expression of circular RNA-ITCH but attenuated the inhibitory effects of circular RNA-ITCH overexpression. However, overexpression of circular RNA-ITCH failed to affect cancer cell behaviors. Therefore, circular RNA-ITCH may inhibit the proliferation of ovarian carcinoma by downregulating HULC.	32046413	RID06156	expression association	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)	
Breast cancer	SNHG17	miR-124-3p	negatively-E	Starbase2.0;luciferase reporter activity assays;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000196756	GRCh38_20:38419638-38435409	NA	NA	388796	NA	NA	NA	Long non-coding RNASNHG17 promotes the progression of breast cancer by sponging miR-124-3p.58 pairs of BC tissues and adjacent non-cancerous tissues were harvested to measure SNHG17 expression levels. SNHG17 was knockdown to study its biological behavior in BC cells. The microRNAs (miRNAs) that can bind to SNHG17 were predicated using Starbase2.0 and were tested using luciferase reporter activity and RIP assays.An increased SNHG17 was observed in BC samples and cell lines compared with corresponding control.Increased SNHG17 was closely associated with poor prognosis.SNHG17 depletion suppressed cell proliferation, migration and invasion in vitro, as well as inhibited tumor growth in xenograft tumor models. Mechanistically, SNHG17 could function as an endogenous sponge of miR-124-3p in BC cells. Moreover, the repression of cell proliferation, migration and invasion induced by SNHG17 knockdown would reversed by miR-124-3p inhibitor.The present study demonstrated that the lncRNASNHG17 could regulate the progression of BC by sponging miR-124-3p.	32042267	RID06157	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Hepatocellular carcinoma	OIP5-AS1	SOX4	positively-E	RIP;RNA pull-down assay;TargetScan;Starbase;miRanda;miRDB;ChipBase;LncRNAdb	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000124766	NA	729082	6659	cyrano|linc-OIP5	NA	LncRNA OIP5-AS1 interacts with miR-363-3p to contribute to hepatocellular carcinoma progression through up-regulation of SOX4. we found OIP5-AS1 expression was upregulated in HCC cells compared with normal human liver cells. Knockdown of OIP5-AS1 suppressed HCC cell proliferation, induced cells cycle arrest and cells apoptosis.Bioinformatics analysis revealed OIP5-AS1 could interact with miR-363-3p, thereby repressing HCC development. We also observed miR-363-3p was significantly decreased in HCC cells and overexpression of miR-363-3p repressed HCC progression. The correlation between OIP5-AS1 and miR-363-3p was confirmed by performing RIP assay and RNA pull-down assay. Subsequently, SOX4 was predicted as a target of miR-363-3p and miR-363-3p modulated SOX4 levels negatively in vitro.Apart from these, in vivo experiments established that OIP5-AS1 can suppress HCC development through regulating miR-363-3p and SOX4. Collectively, these demonstrated that OIP5-AS1 was involved in HCC progression via targeting miR-363-3p and SOX4. OIP5-AS1 can act as a novel candidate for HCC diagnosis, prognosis, and therapy.	32042127	RID06158	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Breast cancer	TUSC8	MYLIP	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-190b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237361	GRCh38_13:44400173-44405984	ENSG00000007944	NA	400128	29116	LINC01071|XLOC_010588	IDOL|MIR	Long non-coding RNA TUSC8 inhibits breast cancer growth and metastasis via miR-190b-5p/MYLIP axis.Here, we found that TUSC8 was significantly down-regulated in breast cancer tissues and its high expression predicted better prognosis of breast cancer patients.Functionally, knock-down of TUSC8 drastically promoted the proliferation, migration and invasion of breast cancer cells in vitro and facilitated tumorigenicity and metastasis in vivo. Mechanistically, the results of luciferase reporter, RIP and RNA pull-down assays proved that TUSC8 functioned as molecular sponge for miR-190b-5p. Furthermore, we showed that TUSC8 served as a competing endogenous RNA (ceRNA) of myosin regulatory light chain interacting protein (MYLIP) through competitively binding with miR-190b-5p and suppressed breast cancer metastasis through regulating the expression of epithelial-mesenchymal transition (EMT) related markers. Clinically, the receiver operating characteristic curve (ROC) analyses revealed that the combination usage of TUSC8 and MYLIP might become novel promising diagnostic biomarkers for breast cancer. Taken together, these results suggested that TUSC8 inhibited breast cancer growth and metastasis via miR-190b-5p/MYLIP axis, providing us new insights into developing potential therapeutic targets for breast cancer patients.	32039833	RID06159	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827)
Sinonasal squamous cell carcinoma	AC091729.7	SRSF2	NA	RIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Squamous cell carcinoma	lncRNA	PCG	ENSG00000224079	GRCh38_7:1074450-1078036	ENSG00000161547	NA	NA	6427	NA	PR264|SC-35|SC35|SFRS2|SFRS2A|SRp30b	A Novel LncRNA, AC091729.7 Promotes Sinonasal Squamous Cell Carcinomas Proliferation and Invasion Through Binding SRSF2.In the current study, lncRNA AC091729.7 expression was examined in SNSCC samples by using microarray, RNA in situ hybridization (ISH) and real-time fluorescence quantitative PCR (qRT-PCR. Human protein microarray (HuprotTM Protoarray) and RNA immunoprecipitation (RIP) were used for identifying AC091729.7 binding proteins in SNSCC. Results showed AC091729.7 was upregulated and closely connected with the survival of the SNSCC patients. Knockdown of AC091729.7 suppressed SNSCC cell migration, proliferation, invasion in vitro. Furthermore, downregulation of AC091729.7 could inhibit the growth of SNSCC in vivo. Moreover, Human protein microarray and RIP suggested that AC091729.7 directly combine with the serine/arginine rich splicing factor 2 (SRSF2). Our results suggest that in the cell progression of SNSCC, lncRNA AC091729.7 plays a carcinogenic role and serves as a novel biomarker and latent curative target in SNSCC patients.	32039035	RID06160	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE75367)
Colorectal cancer	AGER-1	AGER	positively-E	mirbase;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-182)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000206320	NA	NA	177	NA	RAGE|SCARJ1|sRAGE	Long non-coding RNA AGER-1 inhibits colorectal cancer progression through sponging miR-182.A total of 159 paired colorectal cancer specimens and adjacent tissues was applied to detect the expression of lnc-AGER-1 by the quantitative Real-time PCR (qRT-PCR, and a series of functional assays was executed to uncover the role of this lncRNA on colorectal cancer.We found that the expression of lnc-AGER-1 in the tumor tissues was significantly down-regulated, while compared with adjacent normal tissues . Also, lnc-AGER-1 was observably associated with clinical T status . Patients with advanced T status exerted a significantly lower level of lnc-AGER-1 than those with early T status . Over-expression of lnc-AGER-1 inhibited cell proliferation and migration efficiency, and induced cell cycle arrest at the G0/G1 phase, and promoted cell apoptosis. Further research proved that lnc-AGER-1 altered the expression of its neighbor gene, AGER, through acting as a competing endogenous RNA for miR-182 in colorectal cancer.lnc-AGER-1 has a suppressive role in colorectal cancer development via modulating AGER, which may serve as a target for colorectal cancer diagnosis and treatment.	32031046	RID06161	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Multiple myeloma	SNHG16	Foxa3a	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG19 as a novel therapeutic target for MM.	32025219	RID06162	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Multiple myeloma	SNHG16	BAX	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000087088	NA	100507246	581	Nbla10727|Nbla12061|ncRAN	BCL2L4	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG20 as a novel therapeutic target for MM.	32025219	RID06163	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Multiple myeloma	SNHG16	CCND1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000110092	NA	100507246	595	Nbla10727|Nbla12061|ncRAN	BCL1|D11S287E|PRAD1|U21B31	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG21 as a novel therapeutic target for MM.	32025219	RID06164	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Multiple myeloma	SNHG16	BCL2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000171791	NA	100507246	596	Nbla10727|Nbla12061|ncRAN	Bcl-2|PPP1R50	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG22 as a novel therapeutic target for MM.	32025219	RID06165	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Multiple myeloma	SNHG16	Cyclin D1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG23 as a novel therapeutic target for MM.	32025219	RID06166	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Multiple myeloma	SNHG16	PIK3CA	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000121879	NA	100507246	5290	Nbla10727|Nbla12061|ncRAN	PI3K	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG24 as a novel therapeutic target for MM.	32025219	RID06167	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Multiple myeloma	SNHG16	p-AKT	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-342-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p.In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.SNHG16 expression was up-regulated in MM tissues.Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG25 as a novel therapeutic target for MM.	32025219	RID06168	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Hepatocellular carcinoma	NKILA	NFKB1	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	NKILA, a prognostic indicator, inhibits tumor metastasis by suppressing NF-kB/Slug mediated epithelial-mesenchymal transition in hepatocellular carcinoma.we demonstrated that NKILA was down-regulated in HCC tissues and cell lines, and decreased NKILA expression was significantly associated with larger tumor size and positive vascular invasion in HCC patients. Moreover, NKILA inhibits migration and invasion of HCC cells both in vitro and in vivo. Mechanistically, NKILA prevents Slug/epithelial to mesenchymal transition (EMT) pathway via suppressing phosphorylation of IkBalpha, p65 nuclear translocation and NF-kB activation. In conclusion, these results indicate that NKILA might serve as an effective prognostic biomarker and a promising therapeutic target against HCC metastasis.	32015685	RID06169	expression association	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	NKILA	IkBalpha	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	phosphorylation	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	NKILA, a prognostic indicator, inhibits tumor metastasis by suppressing NF-kB/Slug mediated epithelial-mesenchymal transition in hepatocellular carcinoma.we demonstrated that NKILA was down-regulated in HCC tissues and cell lines, and decreased NKILA expression was significantly associated with larger tumor size and positive vascular invasion in HCC patients. Moreover, NKILA inhibits migration and invasion of HCC cells both in vitro and in vivo. Mechanistically, NKILA prevents Slug/epithelial to mesenchymal transition (EMT) pathway via suppressing phosphorylation of IkBalpha, p66 nuclear translocation and NF-kB activation. In conclusion, these results indicate that NKILA might serve as an effective prognostic biomarker and a promising therapeutic target against HCC metastasis.	32015685	RID06170	interact with protein	metastasis,prognosis		
Glioblastoma	PABPC1	BDNF-AS	positively-E	overexpression	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	RNA stability	binding/interaction	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000070756	NA	ENSG00000245573	GRCh38_11:27506830-27698231	26986	497258	PAB1|PABP1|PABPC2|PABPL1	BDNF-AS1|BDNFAS|BDNFOS|BT2A|BT2B|BT2C|BT2D|NCRNA00049	PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay.In this study, we confirmed that lncRNA brain-derived neurotrophic factor antisense (BDNF-AS) was downregulated in glioblastoma tissues and cells, interacted and stabilized by polyadenylate-binding protein cytoplasmic 1 (PABPC1).Overexpression of BDNF-AS inhibited the proliferation, migration, and invasion, as well as induced the apoptosis of glioblastoma cells. In the in vivo study, PABPC1 overexpression combined with BDNF-AS overexpression produced the smallest tumor and the longest survival. Moreover, BDNF-AS could elicit retina and anterior neural fold homeobox 2 (RAX2) mRNA decay through STAU1-mediated decay (SMD), and thereby regulated the malignant behaviors glioblastoma cells. Knockdown of RAX2 produced tumor-suppressive function in glioblastoma cells and increased the expression of discs large homolog 5 (DLG5), leading to the activation of the Hippo pathway. In general, this study elucidated that the PABPC1-BDNF-AS-RAX2-DLG5 mechanism may contribute to the anticancer potential of glioma cells and may provide potential therapeutic targets for human glioma.	32015336	RID06171	interact with mRNA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Glioblastoma	BDNF-AS	RAX2	negatively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000173976	NA	497258	84839	BDNF-AS1|BDNFAS|BDNFOS|BT2A|BT2B|BT2C|BT2D|NCRNA00049	ARMD6|CORD11|MGC15631|RAXL1	PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay.In this study, we confirmed that lncRNA brain-derived neurotrophic factor antisense (BDNF-AS) was downregulated in glioblastoma tissues and cells, interacted and stabilized by polyadenylate-binding protein cytoplasmic 1 (PABPC1).Overexpression of BDNF-AS inhibited the proliferation, migration, and invasion, as well as induced the apoptosis of glioblastoma cells. In the in vivo study, PABPC1 overexpression combined with BDNF-AS overexpression produced the smallest tumor and the longest survival. Moreover, BDNF-AS could elicit retina and anterior neural fold homeobox 2 (RAX2) mRNA decay through STAU1-mediated decay (SMD), and thereby regulated the malignant behaviors glioblastoma cells. Knockdown of RAX2 produced tumor-suppressive function in glioblastoma cells and increased the expression of discs large homolog 5 (DLG5), leading to the activation of the Hippo pathway. In general, this study elucidated that the PABPC1-BDNF-AS-RAX2-DLG6 mechanism may contribute to the anticancer potential of glioma cells and may provide potential therapeutic targets for human glioma.	32015336	RID06172	expression association	NA	UP(LIHC);DATA(GSE117623)	
Oral squamous cell carcinoma	CCAT1	DDR2	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);ERK/AKT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000162733	NA	100507056	4921	CARLO5|CARLo-5|onco-lncRNA-40	NTRKR3|TKT|TYRO10	Knockdown of Long Non-Coding RNA (lncRNA) Colon Cancer-Associated Transcript-1 (CCAT1) Suppresses Oral Squamous Cell Carcinoma Proliferation, Invasion, and Migration by Inhibiting the Discoidin Domain Receptor 2 (DDR2)/ERK/AKT Axis.CCAT1 and DDR2 expression was measured by qRT-PCRRNA immunoprecipitation (RIP) assay were employed to identify the interaction between DDR2 and CCAT1. Protein levels involved in DDR2/ERK/AKT pathway were estimated by western blot assay. The findings revealed that CCAT1expression was upregulated in OSCC cell lines.  Moreover, DDR2 expression in OSCC cell lines was downregulated and CCAT1 silencing repressed the expression of DDR2.RIP assays validated the binding of CCAT1 and DDR2 protein. Moreover, CCAT1 silencing suppressed the ERK/AKT signaling through DDR2 in TCA-8113 cells.Downregulation of CCAT1 suppressed TCA-8113 cell proliferation, invasion, and migration by inactivation of the ERK/AKT pathway via inhibition of DDR2, suggesting the value of CCAT1 in diagnosis and treatment of patients with OSCC.	32009633	RID06173	interact with protein	NA		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Ovarian cancer	TTN-AS1	ROCK2	positively-E	starBase2.0;dual-luciferase reporter activity assays	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-139-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000134318	NA	100506866	9475	NA	NA	Long non-coding RNA TTN-AS1 promotes tumorigenesis of ovarian cancer through modulating the miR-139-5p/ROCK2 axis.Quantitative reverse transcriptase-polymerase chain reaction assay (qRT-PCR was used to detect the expression of TTN-AS1 in OC tissues and cell lines.A high level of TTN-AS1 was found in OC tissues and cell lines.Functionally, knockdown of TTN-AS1 inhibited cell proliferation, colony formation, invasion and migration of OC cells in vitro, and suppressed tumor formation in vivo. Mechanistically, TTN-AS1 functioned as a competing endogenous RNA by sponging microRNA-139-5p (miR-139-5p) to elevate Rho-associated coiled-coil containing protein kinase 2 (ROCK2). Downregulation of miR-139-5p or upregulation of ROCK2 partially rescued the inhibitory impact of TTN-AS1 knockdown on OC cells. These results obtained in the present study suggested that TTN-AS1 promoted the progression of OC by regulating the miR-139-5p/ROCK2 axis.	32006899	RID06174	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Endometrial cancer	LOXL1-AS1	RAP1B	positively-E	siRNA	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-28-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000127314	NA	100287616	5908	NA	DKFZp586H0723|K-REV|RAL1B	LncRNA LOXL1-AS1 promotes endometrial cancer progression by sponging miR-28-5p to upregulate RAP1B expression.Si-LOXL1-AS1 and miR-28-5p inhibitor were transfected to downregulate the expressions of LOXL1-AS1 and miR-28-5p, while miR-28-5p mimics were used to upregulate the miR-28-5p expression.Informatics analysis was used to explore the relationship among LOXL1-AS1, miR-28-5p and RAP1B.LOXL1-AS1 was found markedly up-regulated in EC tissues and cell lines. LOXL1-AS1 knockdown displayed evident suppression in cell proliferation, migration and invasion, as well as promotion in cell apoptosis. Moreover, the LOXL1-AS1 induced regulatory effects on EC cells were partially reversed by miR-28-5p inhibitor. Mechanistically, LOXL1-AS1 competitively bond to miR-28-5p, resulting in upregulation of RAP1B. Additionally, in vivo study confirmed the findings discovered in vitro.CONCLUSIONS: In summary, LOXL1-AS1 exerted oncogenic roles in EC progression by sponging miR-28-5p and thereby upregulating RAP1B. This finding might provide potential targets for EC therapy.	32006897	RID06175	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(NSCLC,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE38495,GSE55807)
Osteosarcoma	LINC02245	MIR29C	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000237638	GRCh38_2:64901840-65056226	ENSG00000284214	NA	400958	407026	NA	MIRN29C|miRNA29C|mir-29c	Long Noncoding RNA SERTAD2-3 Inhibits Osteosarcoma Proliferation and Migration by Competitively Binding miR-29c.Quantitative real-time PCR (qPCR) was used to measure gene expression levels.The binding site between the lnc-SERTAD2-3 and miR-29c RNAs was evaluated using a luciferase reporter assay.The expression of the lnc-SERTAD2-3 was significantly downregulated in OS samples and three OS cell lines (MG-63, U2OS, and Saos-2) compared to normal tissue.Overexpression of lnc-SERTAD2-3 inhibited proliferation and migration, and promoted apoptosis in OS cells. Moreover, we found that lnc-SERTAD2-3 could suppress miR-29c by direct binding. Moreover, reexpression of miR-29c reversed the effect of lnc-SERTAD2-3 on OS cells. Conclusion: Overall, lnc-SERTAD2-3, an OS suppressor, is involved in the inhibition of OS proliferation and migration by targeting miR-29c.	31999493	RID06176	ceRNA or sponge	NA		
Hepatocellular carcinoma	TINCR	DDX5	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000263077	NA	257000	1655	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	G17P1|HLR1|p68	Knockdown of terminal differentiation induced ncRNA (TINCR) suppresses proliferation and invasion in hepatocellular carcinoma by targeting the miR-218-5p/DEAD-box helicase 5 (DDX5) axis.we confirmed that TINCR expression was upregulated in HCC tumors and cell lines, and high TINCR expression was associated with larger tumor size, advanced tumor node metastasis stage, and poor prognosis. Mechanically, TINCR functioned as competing endogenous RNA (ceRNA) to regulate DEAD-box helicase 5 (DDX5) expression through sponging miR-218-5p. Moreover, the miR-218-5p expression was downregulated and DDX5 expression was upregulated in HCC tumors. The silencing of miR-218-5p or ectopic expression of DDX5 abated the tumor-suppressive effect of TINCR knockdown in vitro. Furthermore, si-TINCR-induced inactivation of AKT signaling was rescued by suppression of miR-218-5p or overexpression of DDX5. Also, the silencing of TINCR resulted in tumor growth inhibition in vivo. In summary, knockdown of TINCR suppressed HCC progression presumably by inactivation of AKT signaling through targeting the miR-218-5p/DDX5 axis, suggesting a novel TINCR/miR-218-5p/DDX5 pathway and therapy target for HCC.	31994189	RID06177	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hypopharyngeal squamous cell carcinoma	HOXA11-AS	miR-155	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Squamous cell carcinoma	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	lncRNA HOXA11-AS Promotes Proliferation and Migration via Sponging miR-155 in Hypopharyngeal Squamous Cell Carcinoma.Our previous study and others have demonstrated that HOXA11-AS is one of the most upregulated lncRNAs in HSCC.The current study demonstrated that the expression of HOXA11-AS was significantly upregulated in HSCC tumors and was positively associated with lymph node metastasis.functional experiments revealed that HOXA11-AS knockdown suppressed the proliferation and migration potential in FaDu cells. Furthermore, luciferase reporter gene assay combined with cellular functional experiments demonstrated that HOXA11-AS functioned as a molecular sponge for miR-155, and inhibition of miR-155 attenuated the suppressive effect of HOXA11-AS knockdown on the aggressive phenotype in HSCC. This study identifies a tumor-promoting role of HOXA11-AS in HSCC and suggests HOXA11-AS might be a potential diagnostic and therapeutic target for HSCC.	31987067	RID06178	ceRNA or sponge	metastasis		
Non-small cell lung cancer	MIR503HG	miR-489-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223749	GRCh38_X:134543119-134546642	NA	NA	84848	NA	H19X|MGC16121	NA	Knockdown of lncRNA MIR503HG suppresses proliferation and promotes apoptosis of non-small cell lung cancer cells by regulating miR-489-3p and miR-625-5p.Results showed that the expression of MIR503HG was significantly upregulated in NSCLC tissues compared with adjacent tissues.We found that downregulation of MIR503HG could clearly suppressed cell proliferation and cell cycle progression. We predicted and verified miR-489-3p and miR-625-5p as the direct targets of MIR503HG by bioinformatics analysis and luciferase reporter assay. Mechanically, MIR503HG negatively regulated miR-489-3p and miR-625-5p expressions in NSCLC cells. Moreover, downregulation of miR-489-3p and miR-625-5p weaken the decreased cell proliferation and increased apoptosis of A549 cells after MIR503HG knocking down. In conclusion, knockdown of MIR503HG suppressed proliferation and promoted apoptosis of NSCLC cells through regulating miR-489-3p and miR-625-5p. Our findings of this study suggested that MIR503HG could be a potential therapeutic target for NSCLC development.	31983569	RID06179	expression association	NA		
Non-small cell lung cancer	MIR503HG	miR-625-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223749	GRCh38_X:134543119-134546642	NA	NA	84848	NA	H19X|MGC16121	NA	Knockdown of lncRNA MIR503HG suppresses proliferation and promotes apoptosis of non-small cell lung cancer cells by regulating miR-489-3p and miR-625-5p.Results showed that the expression of MIR503HG was significantly upregulated in NSCLC tissues compared with adjacent tissues.We found that downregulation of MIR503HG could clearly suppressed cell proliferation and cell cycle progression. We predicted and verified miR-489-3p and miR-625-5p as the direct targets of MIR503HG by bioinformatics analysis and luciferase reporter assay. Mechanically, MIR503HG negatively regulated miR-489-3p and miR-625-5p expressions in NSCLC cells. Moreover, downregulation of miR-489-3p and miR-625-5p weaken the decreased cell proliferation and increased apoptosis of A549 cells after MIR503HG knocking down. In conclusion, knockdown of MIR503HG suppressed proliferation and promoted apoptosis of NSCLC cells through regulating miR-489-3p and miR-625-5p. Our findings of this study suggested that MIR504HG could be a potential therapeutic target for NSCLC development.	31983569	RID06180	expression association	NA		
Malignant glioma	SOX21-AS1	PAK5	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);cell proliferation(+);cell invasion(+)	ceRNA(miR-144-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000101349	NA	100507533	57144	NA	KIAA1264|PAK7	Long non-coding RNA SOX21-AS1 promotes cell proliferation and invasion through upregulating PAK7 expression by sponging miR-144-3p in glioma cells.RNA and protein levels were measured via quantitative reverse transcription-PCR (qRT-PCR and western blotIn addition, we examined cell proliferation, apoptosis, migration and invasion. The interaction between SOX21-AS1 (PAK7) and miR-144-3p was determined via RNA immunoprecipitation (RIP) assay and Luciferase reporter assay. SOX21-AS1 was upregulated in glioma tissues and cells. in vitro, SOX21-AS1 knockdown repressed proliferation, migration, invasion and enhanced apoptosis in glioma cells. In vivo, SOX21-AS1 knockdown suppressed tumor growth in mice. In addition, SOX21-AS1 could sponge miR-144-3p, which was determined to bind to PAK7. miR-144-3p knockdown promoted proliferation, migration, invasion and inhibited cell apoptosis. Importantly, the effects of SOX21-AS1 knockdown-induced proliferation, migration, invasion, and apoptosis were alleviated in glioma cells co-transfected with SOX21-AS1 and miR-144-3p knockdown. Furthermore, miR-144-3p knockdown also attenuated Wnt/beta-catenin pathway-associated protein levels induced by SOX21-AS1 knockdown. These results indicated that SOX21-AS1/miR-144-3p/PAK7 axis played an oncogenic role in glioma cells by regulating Wnt/beta-catenin pathway, which suggests a rational therapeutic strategy for glioma.	31973536	RID06181	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Colon cancer	ZNF667-AS1	TGFB1	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000166770	GRCh38_19:56477250-56504362	ENSG00000105329	NA	100128252	7040	MORT	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Long non-coding RNA mortal obligate RNA transcript inhibits the migration and invasion of colon cancer cells by inactivating transforming growth factor beta1. The present study demonstrated downregulation of lncRNA MORT in the tumor tissues of patients with colon cancer.Low MORT expression was associated with low overall survival rate. Moreover, the overexpression of MORT resulted in decreased, whereas treatment with transforming growth factor beta1 (TGF-beta1) resulted in increased, invasion and migration rates of colon cancer cells. In addition, TGF-beta1 treatment attenuated the inhibitory effect of MORT overexpression on the invasion and migration rates of colon cancer cells. The overexpression of MORT inhibited TGF-beta1 expression in colon cancer cells, whereas treatment with TGF-beta1 failed to affect the expression of the lncRNA. Therefore, it is postulated that MORT inhibits invasion and migration colon cancer cells by inactivating TGF-beta1.	31966041	RID06182	expression association	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	SNHG8	RECK	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000122707	NA	100093630	8434	LINC00060|NCRNA00060	hRECK|ST15	LncRNA SNHG8 accelerates proliferation and inhibits apoptosis in HPV-induced cervical cancer through recruiting EZH2 to epigenetically silence RECK expression.As a result, a notable increase of SNHG8 in HPV-induced CC cells was found compared with HPV-negative CC cells.Functionally, it identified that SNHG8 aggravated the cell proliferation and migration in Cell Counting Kit-8 and transwell assays.As detected by fluorescence in situ hybridization analysis and subcellular fractionation assay, SNHG8 was primarily expressed in the nucleus and exerted suppressive role on reversion inducing cysteine-rich protein with kazal motifs (RECK) expression, which implied a potential transcriptional regulation of SNHG8 on RECK level.Mechanically, SNHG8 was disclosed to interact with enhancer of zeste homolog 2 (EZH2) based on RNA immunoprecipitation assay. ChIP assay further unveiled the occupancy of EZH2 in the promoter region of RECK. An additional chromatin immunoprecipitation assay highlighted that SNHG8 intensified the enrichment of EZH2 and H3K27me3 in RECK promoter region. Altogether, it reflected that SNHG8 recruited EZH2 to downregulate RECK expression, leading to HPV-induced CC aggravation.	31961005	RID06183	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	FALEC	PTEN	negatively-E	RNA pull-down assay	upregulation		NA	NA	cell metastasis(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000171862	NA	100874054	5728	FAL1|LINC00568|ncRNA-a1	BZS|MHAM|MMAC1|PTEN1|TEP1	Exosomes transferring long non-coding RNA FAL1 to regulate ovarian cancer metastasis through the PTEN/AKT signaling pathway.When lncRNA FAL1 was knocked out, the promoting effects of SKOV3 cells-secreted exosomes on OC cell metastasis were weakened, along with increased PTEN level and decreased AKT phosphorylation level. SKOV3-secreted exosomes inhibited the PTEN/AKT signaling pathway by transferring lncRNA FAL1, thus inhibiting OC cell metastasis in vitro and in vivo.	31957817	RID06184	expression association	metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Ovarian cancer	FALEC	AKT1	negatively-E	RNA pull-down assay	upregulation		NA	NA	cell metastasis(-)	phosphorylation	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000142208	NA	100874054	207	FAL1|LINC00568|ncRNA-a1	AKT|PKB|PRKBA|RAC|RAC-alpha	Exosomes transferring long non-coding RNA FAL1 to regulate ovarian cancer metastasis through the PTEN/AKT signaling pathway.When lncRNA FAL1 was knocked out, the promoting effects of SKOV3 cells-secreted exosomes on OC cell metastasis were weakened, along with increased PTEN level and decreased AKT phosphorylation level. SKOV3-secreted exosomes inhibited the PTEN/AKT signaling pathway by transferring lncRNA FAL2, thus inhibiting OC cell metastasis in vitro and in vivo.	31957817	RID06185	interact with protein	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	SNHG3	PKM	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-330-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000067225	NA	8420	5315	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	OIP3|PK3|PKM2|THBP1	SNHG3 Functions as miRNA Sponge to Promote Breast Cancer Cells Growth Through the Metabolic Reprogramming.The expression of SNHG3, miR-330-5p, and PKM (Pyruvate Kinase M1/M2) was examined by real-time QPCR and immunoblot.The function of SNHG3 on the growth and metabolism of tumor cells was used by CCK8 and mitochondrial oxygen consumption assays. The binding between SNHG3, miR-330-5p, and PKM was examined by dual-luciferase reporter assays. Orthotopical xenograft of breast tumor experiments was performed to determine the function of SNHG3 in vivo. We demonstrated that exosomes secreted from CAFs reprogram the metabolic pathways after tumor cells uptake the exosomes. CAF-secreted exosomal lncRNA SNHG3 served as a molecular sponge for miR-330-5p in breast cancer cells. Moreover, PKM could be targeted by miR-330-5p and was controlled by SNHG3 in breast cancer cells. Mechanistically, SNHG3 knockdown in CAF-secreted exosomes suppressed glycolysis metabolism and cell proliferation by the increase of miR-330-5p and decrease of PKM expression in tumor cells. SNHG3 functions as a miR-330-5p sponge to positively regulate PKM expression, inhibit mitochondrial oxidative phosphorylation, increase glycolysis carboxylation, and enhance breast tumor cell proliferation. Overall, SNHG3 could play a major role in the development and progression of breast cancer and support the therapeutic potential of targeting communication between cancer cells and tumor microenvironment.	31956955	RID06186	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Colorectal cancer	UCA1	MYO6	positively-E	luciferase reporter assay;miRcode;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-143)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000196586	NA	652995	4646	CUDR|LINC00178|onco-lncRNA-36|UCAT1	DFNA22|DFNB37|KIAA0389	Circulating lncRNA UCA1 Promotes Malignancy of Colorectal Cancer via the miR-143/MYO6 Axis.In this study, we systematically analyzed the expression profiles of exosomal lncRNAs in CRC patients using a high-throughput microarray assay.we evaluated the UCA1 expression levels in a series of CRC tissues and the serum exosomes of CRC patients using quantitative real-time PCR.The miRNA binding sites of UCA1 were predicted using the miRcode online database, and miR-143 was validated to target UCA1 by dual-luciferase activity assay and AGO2 RNA immunoprecipitation.This study showed that UCA1 was upregulated in CRC tissues and functioned as an oncogene in CRC.Mechanistically, UCA1 was identified as a miR-143 sponge. We also found that MYO6 was a direct target of miR-1205, which functioned as an oncogene in CRC. Moreover, UCA was also upregulated in the serum exosomes of CRC patients and could transfer UCA1 to CRC cells to increase their abilities of cell proliferation and migration. In conclusion, these data suggest that UCA1 could be an oncogene for CRC and may serve as a candidate target for new therapies in human CRC.	31955010	RID06187	ceRNA or sponge	circulating	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807,GSE75367)
Abdominal aortic aneurysm	LINC00473	BASP1	positively-E	RIP;starBase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell viability(-)	ceRNA(miR-212-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000223414	NA	ENSG00000176788	NA	90632	10409	C6orf176|LNC473|bA142J11.1	CAP-23|CAP23|NAP-22|NAP22	LINC00473 inhibits vascular smooth muscle cell viability to promote aneurysm formation via miR-212-5p/BASP1 axis.LINC00473 was up-regulated in VSMCs after H2O2 treatment.Overexpression of LINC00473 inhibited VSMC cell proliferation and promoted cell apoptosis and its silence mitigated H2O2-induced injuries to VSMCs. Additionally, we uncovered that LINC00473 sponged miR-212-5p to regulate brain acid soluble protein 1 (BASP1) expression. Finally, rescue assays uncovered that overexpression of miR-212-5p or suppression of BASP1 reversed the effects of LINC00473 up-regulation on cell proliferation and cell apoptosis. And the positive correlation between LINC00473 and BASP1 as well as the negative relation of miR-212-5p to both LINC00473 and BASP1 were confirmed in AAA tissues. All finding illuminated that LINC00473 participated in AAA development by regulating miR-212-5p/BASP1 pathway, suggesting LINC00473 as a promising target for AAA therapy.	31954705	RID06188	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Multiple myeloma	MALAT1	SOX13	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell invasion(+)	ceRNA(miR-1271-5p)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143842	NA	378938	9580	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ICA12|MGC117216|Sox-13	Long non-coding RNA MALAT1 facilitates the tumorigenesis, invasion and glycolysis of multiple myeloma via miR-1271-5p/SOX13 axis.MALAT1, microRNA-1271-5p (miR-1271-5p), and SRY-Box 13 (SOX13) levels were examined by quantitative real-time polymerase chain reaction (qRT-PCR.Target relation was verified via dual-luciferase reporter assay.The up-regulation of MALAT1 and the down-regulation of miR-1271-5p were found in MM serums and cells.MALAT1 directly targeted miR-1271-5p and miR-1271-5p depression reverted the effects of MALAT1 knockdown on MM cells. SOX13 was a target of miR-1271-5p and SOX13 overexpression weakened the effects of miR-1271-5p on MM. MALAT1 indirectly modulated SOX13 expression through targeting miR-1271-5p. MALAT1 down-regulation inhibited MM growth by miR-1271-5p/SOX13 axis in vivo.CONCLUSION: LncRNA MALAT1 expedited MM tumorigenesis, invasion, and glycolysis via miR-1271-5p/SOX13 axis. MALAT1 might contribute to the therapy of MM as a promising indicator.	31953613	RID06189	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Papillary thyroid carcinoma	ASMTL-AS1	FOXO1	positively-E	lncRNASNP2;miRanda;RNA pull-down assay;overexpression	downregulation	qRT-PCR	NA	NA	cell growth(-)	ceRNA(miR-93-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000236017	GRCh38_X:1401769-1414028	ENSG00000150907	NA	80161	2308	ASMTL-AS|ASMTLAS|CXYorf2|FLJ13330|NCRNA00105	FKH1|FKHR|FOXO1A	Long non-coding RNA ASMTL-AS1 inhibits tumor growth and glycolysis by regulating the miR-93-3p/miR-660/FOXO1 axis in papillary thyroid carcinoma.In the current study, we found that a novel lncRNA, ASMTL antisense RNA 1 (ASMTL-AS1), was significantly downregulated in PTC.Regarding the mechanism, ASMTL-AS1 was capable of sponging miR-93-3p and miR-660 to elevate FOXO1 expression, leading to repressing glycolysis and tumorigenesis.FOXO1 could also increase ASMTL-AS1 expression via directly binding to ASMTL-AS1 promoter, which formed a positive feedback regulation loop. Importantly, the regulatory axis of ASMTL-AS1/miR-93-3p/miR-660/FOXO1 was also identified in vivo. Collectively, our data clearly indicate that ASMTL-AS1 functions as a novel tumor suppressor in PTC through regulation of miR-93-3p/miR-660/FOXO1 pathway. Targeting ASMTL-AS1 and its downstream pathway may be an effective therapeutic approach for patients with PTC.	31953163	RID06190	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Papillary thyroid carcinoma	ASMTL-AS1	FOXO1	positively-E	lncRNASNP2;miRanda;RNA pull-down assay;overexpression	downregulation	qRT-PCR	NA	NA	cell growth(-)	ceRNA(miR-660)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000236017	GRCh38_X:1401769-1414028	ENSG00000150907	NA	80161	2308	ASMTL-AS|ASMTLAS|CXYorf2|FLJ13330|NCRNA00105	FKH1|FKHR|FOXO1A	Long non-coding RNA ASMTL-AS1 inhibits tumor growth and glycolysis by regulating the miR-93-3p/miR-660/FOXO1 axis in papillary thyroid carcinoma.In the current study, we found that a novel lncRNA, ASMTL antisense RNA 1 (ASMTL-AS1), was significantly downregulated in PTC.Regarding the mechanism, ASMTL-AS1 was capable of sponging miR-93-3p and miR-660 to elevate FOXO1 expression, leading to repressing glycolysis and tumorigenesis.FOXO1 could also increase ASMTL-AS1 expression via directly binding to ASMTL-AS1 promoter, which formed a positive feedback regulation loop. Importantly, the regulatory axis of ASMTL-AS1/miR-93-3p/miR-660/FOXO1 was also identified in vivo. Collectively, our data clearly indicate that ASMTL-AS1 functions as a novel tumor suppressor in PTC through regulation of miR-93-3p/miR-660/FOXO1 pathway. Targeting ASMTL-AS2 and its downstream pathway may be an effective therapeutic approach for patients with PTC.	31953163	RID06191	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	BAN	BCAM	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000187244	NA	NA	4059	NA	CD239|LU	Upregulation of BCAM and its sense lncRNA BAN are associated with gastric cancer metastasis and poor prognosis.Here, we employed bioinformatics to systematically screen the metastasis-associated genes and found that the levels of basal cell adhesion molecule (BCAM) were significantly increased in GC tissues from patients with metastasis, as compared to those without metastasis. The upregulation of BCAM was also significantly associated with a shorter survival time. Depletion of BCAM inhibited GC cell migration and invasion. Knockout (KO) of BCAM by the CRISPR/Cas9 system reduced the invasion and metastasis of GC cells. To explore the mechanism of BCAM upregulation, we identified a previously uncharacterized BCAM sense lncRNA that spanned from exon 6 to intron 6 of BCAM, and named it as BCAM-associated long noncoding RNA (BAN). Knockdown of BAN inhibited BCAM expression at both mRNA and protein levels. Knockdown of BAN suppressed GC cell migration and invasion, which was effectively rescued by ectopic expression of BCAM. Further clinical data showed that BAN upregulation was associated with GC metastasis and poor prognosis. Importantly, BAN expression was also significantly associated with that of BCAM in GC tissues. Taken together, these results indicate that increased expression of BCAM and its sense lncRNA BAN promote GC cell invasion and metastasis, and are associated with poor prognosis of GC patients.	31951095	RID06192	expression association	metastasis,prognosis		UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE55807)
Nasopharynx carcinoma	SNHG7	GLI3	positively-E	Precomputed;TargetScan;dual-luciferase reporter gene assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000106571	NA	84973	2737	MGC16037|NCRNA00061	ACLS|GCPS|PAP-A|PAPA|PAPA1|PAPB|PHS|PPDIV	Downregulated long non-coding RNA SNHG7 restricts proliferation and boosts apoptosis of nasopharyngeal carcinoma cells by elevating microRNA-140-5p to suppress GLI3 expression.Overexpressed SNHG7 and GLI3, and underexpressed miR-140-5p were found in NPC tissues and cells.SNHG7 silencing and miR-140-5p elevation declined the drug resistance of drug-resistant NPC cells and their parent cells, restrained NPC cell colony formation ability and proliferation, and boosted cell apoptosis. SNHG7 specially bound to miR-140-5p, and SNHG7 silencing elevated miR-140-5p expression. GLI3 was a direct target gene of miR-140-5p and miR-140-5p elevation diminished GLI3 expression. MiR-140-5p inhibition reversed the impacts of SNHG7 silencing on NPC cells. In summary, our study reveals that downregulated SNHG7 restricts GLI3 expression by upregulating miR-140-5p, which further suppresses cell proliferation, and promotes apoptosis of NPC.	31944163	RID06193	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)
Gastric cancer	IGFL2-AS1	ARPP19	positively-E	RegRNA 2.0;DIANA-microT; miRDB;TargetScan;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-802)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268621	GRCh38_19:46189029-46203160	ENSG00000128989	NA	645553	10776	AC006262.5	ARPP-16|ARPP-19|ARPP16|ENSAL	LncRNA IGFL2-AS1 functions as a ceRNA in regulating ARPP19 through competitive binding to miR-802 in gastric cancer.We found that IGFL2-AS1 was highly expressed in GC tissues and cell lines. Knockdown of IGFL2-AS1 suppressed GC cell proliferation, migration, and invasion in vitro.Furthermore, we identified that IGFL2-AS1 exerted its function as a molecular sponge of miR-802. MiR-802 was demonstrated to be a tumor suppressor, and overexpression of miR-802 suppressed GC cell growth, migration, and invasion. Mechanistically, we revealed that the cAMP-regulated phosphoprotein 19 (ARPP19) was a direct target of miR-802 and could reverse the inhibitory function of miR-802. Moreover, our results confirmed that knockdown of IGFL2-AS1 inhibited GC tumor development in an in vivo GC tumor xenograft model. In summary, our data suggest that the IGFL2-AS1/miR-802/ARPP19 axis plays a critical role in the progression and metastasis of GC. Therapies targeting the IGFL2-AS1/miR-802/ARPP19 axis can potentially improve GC treatment.	31943339	RID06194	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Melanoma	MEG3	E-cadherin	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 promotes melanoma growth, metastasis and formation through modulating miR-21/E-cadherin axis.RT-PCRwas used to examine the expressions of lncRNA MEG3 and E-cadherin in melanoma patients and cell lines. Additionally, the target interactions among lncRNA MEG3, miR-21 and E-cadherin were determined by dual-luciferase reporter assay. The clinical data showed that lncRNA MEG3 and E-cadherin expressions were both declined in carcinoma tissues as compared with their para-carcinoma tissues.Our findings indicated that lncRNA MEG3 might inhibit the tumor growth, tumor metastasis and formation of melanoma by modulating miR-21/E-cadherin axis.	31938020	RID06195	ceRNA or sponge	metastasis		
Cervical cancer	CCAT1	RUNX2	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000247844	NA	ENSG00000124813	NA	100507056	860	CARLO5|CARLo-5|onco-lncRNA-40	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Knockdown of long non-coding RNA CCAT1 suppresses proliferation and EMT of human cervical cancer cell lines by down-regulating Runx2.The expression level of CCAT1 in CC tissues was examined by using qRT-PCRThe expression of Runx2 and other relative factors was examined via qRT-PCRand western blotOur findings indicated that CCAT1 was highly expressed in CC tissues contrasted with adjacent tissues. The proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) were suppressed, while the apoptosis was promoted by CCAT1 knockdown. Moreover, knockdown of CCAT1 could negatively regulate Runx2 to play anti-tumor roles in HeLa and SiHa cells. Further, CCAT1 knockdown could suppress PI3K/AKT signal pathway.Knockdown of CCAT1 suppressed proliferation, EMT, migration and invasion in HeLa and SiHa cells through down-regulating Runx2, which provided theoretical support for its application in CC treatment.	31935379	RID06196	expression association	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	RHOA	negaticely-E	luciferase gene reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-429)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067560	NA	378938	387	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ARH12|ARHA|Rho12|RHOH12	Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-429.	31933847	RID06197	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Lung adenocarcinoma	MALAT1	Cyclin D1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-430.	31933847	RID06198	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung adenocarcinoma	MALAT1	MMP9	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-431.	31933847	RID06199	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	MALAT1	vimentin	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-432.	31933847	RID06200	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung adenocarcinoma	MALAT1	E-cadherin	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-433.	31933847	RID06201	expression association	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Ovarian cancer	TUG1	MDM2	positively-E	StarBase;miRanda;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000135679	NA	55000	4193	FLJ20618|LINC00080|NCRNA00080	HDM2|MGC5370	Long noncoding RNA TUG1 facilitates cell ovarian cancer progression through targeting MiR-29b-3p/MDM2 axis.The expression of turine up-regulated gene 1 (TUG1) in human OC tissues and cell lines was measured by qRT-PCR The relationship between TUG1 and miR-29b-3p, as well as miR-29b-3p and MDM2 were identified using the luciferase reporter assays. We showed that the expression of TUG1 and MDM2 were significantly increased, but the expression of miR-29b-3p was remarkably decreased in OC tissues and cell lines.The relationship between TUG1 and miR-29b-3p, or miR-29b-3p and MDM2 were predicted by StarBase and miRanda online software. Besides, miR-29b-3p reversed the positive effect of TUG1 on the OC cell proliferation, migration, and invasion through inhibiting MDM2 expression and increasing p53 phosphorylation level. Moreover, knockdown of TUG1 suppressed tumor growth in vivo. Taken all together, this study shows that TUG1 plays a crucial oncogenic role and facilitates cell proliferation, migration, and invasion in OC through regulating miR-29b-3p/MDM2 axis.	31930662	RID06202	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	SBF2-AS1	MBNL3	positively-E	Precomputed;TargetScan;dual-luciferase reporter gene assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-302a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000076770	NA	283104	55796	NA	CHCR|FLJ11316|MBLX39|MBXL	LncRNA SBF2-AS1 affects the radiosensitivity of non-small cell lung cancer via modulating microRNA-302a/MBNL3 axis.Up-regulated SBF2-AS1 and MBNL3 and down-regulated miR-302a in NSCLC tissues of the radiotherapy resistant group.Down-regulated SBF2-AS1 or up-regulated miR-302a suppressed the proliferation while boosted the apoptosis of NCI-H1299 cells and decreased the radioresistance of the NCI-H1299R cells. Silencing SBF2-AS1 or up-regulating miR-302a restrained tumor growth in vivo.Our study presents that high expression of miR-302a or inhibition of SBF2-AS1 can enhance the radiosensitivity and apoptosis of NSCLC cells through downregulation of MBNL3, which is a therapeutic target for NSCLC.	31928130	RID06203	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	UP(PRAD);DOWN(BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	MALAT1	ATG5	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell autophagy(-);chemosensitivity(+)	ceRNA(miR-30e)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000057663	NA	378938	9474	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APG5|APG5L|ASP|hAPG5	Propofol facilitates cisplatin sensitivity via lncRNA MALAT1/miR-30e/ATG5 axis through suppressing autophagy in gastric cancer.The expression pattern of MALAT1 in GC cells was detected by qRT-PCR dual-luciferase reporter assay was subjected to verify the binding relationship between MALAT1 and miR-30e.Chemoresistant GC cells presented higher IC50 of cisplatin, increased autophagy activity and stronger expression of MALAT1.Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 overexpression promoted autophagy in GC cells. Mechanistic researches demonstrated that MALAT1 could bind with miR-30e to regulate ATG5 expression, thus causing the suppression of autophagy.Altogether, our study revealed a novel mechanism of propofol of lncRNA MALAT1/miR-30e/ATG5 mediated autophagy-related chemoresistance in GC, casting new lights on the understanding of propofol.	31926239	RID06204	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Gastric cancer	MNX1-AS1	BTG2	negatively-E	FISH;RIP;ChIP;luciferase reporter assay	upregulation	qRT-PCR	GSE62254	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000159388	NA	645249	7832	CCAT5|LOC645249|MAYA	APRO1|MGC126063|MGC126064|PC3|TIS21	TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2. LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR assays.The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays.the mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays.It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC.Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects.Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions.Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL2 axes, implicating it as a novel and potent target for the treatment of GC.	31924214	RID06205	transcriptional regulation	prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	MNX1-AS1	BCL2	positively-E	FISH;RIP;ChIP;luciferase reporter assay	upregulation	qRT-PCR	GSE62254	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-6785-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000171791	NA	645249	596	CCAT5|LOC645249|MAYA	Bcl-2|PPP1R50	TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2. LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR assays.The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays.the mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays.It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC.Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects.Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions.Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL3 axes, implicating it as a novel and potent target for the treatment of GC.	31924214	RID06206	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	TEAD4	MNX1-AS1	positively-E	FISH;RIP;ChIP;luciferase reporter assay	upregulation	qRT-PCR	GSE62254	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000197905	NA	ENSG00000243479	GRCh38_7:157010805-157016426	7004	645249	EFTR-2|RTEF-1|TCF13L1|TEF-3|TEFR-1	CCAT5|LOC645249|MAYA	TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2. LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR assays.The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays.the mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays.It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC.Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects.Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions.Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL4 axes, implicating it as a novel and potent target for the treatment of GC.	31924214	RID06207	transcriptional regulation	prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	UP(BRCA);DATA(GSE55807)
Neuroblastoma	SNHG16	HOXA7	positively-E	starBase;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000122592	NA	100507246	3204	Nbla10727|Nbla12061|ncRAN	HOX1|HOX1A	SNHG16 Silencing Inhibits Neuroblastoma Progression by Downregulating HOXA7 via Sponging miR-128-3p.The expression level of SNHG16 was measured by quantitative real time polymerase chain reaction (qRT-PCR.The starBase was employed to predict the interaction of miR-128-3p and SNHG16 or HOXA7, which was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The levels of SNHG16 and HOXA7 were conspicuously increased in NB tissues and cells, while the expression of miR-128-3p was obviously declined, compared with corresponding normal tissues and cells.SNHG16 silencing inhibited proliferation, migration and invasion and induced apoptosis of NB cells. We identified that SNHG16 directly interacted with miR-128-3p, and miR-128-3p could target the 3'UTR of HOXA7 in NB cells. Simultaneously, miR-128-3p expression was negatively associated with SNHG16 or HOXA7.Further studies indicated that SNHG16 overexpression rescued the effects of miR-128-3p-mediated on inhibiting proliferation, migration, invasion and promoting apoptosis of NB cells. Moreover, SNHG16 could modulate HOXA7 by sponging miR-128-3p in NB cells. Besides, SNHG16 silencing suppressed tumor growth in vivo. Knockdown of SNHG16 impeded proliferation, migration, invasion and induced apoptosis through the SNHG16/miR-128-3p/HOXA7 axis in NB cells.	31919621	RID06208	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Prostate cancer	VPS9D1-AS1	MEF2D	positively-E	starBase;RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-4739)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000261373	GRCh38_16:89711856-89718165	ENSG00000116604	NA	100128881	4209	MYU	NA	ZEB1 activated-VPS9D1-AS1 promotes the tumorigenesis and progression of prostate cancer by sponging miR-4739 to upregulate MEF2D.The expression of VPS9D1-AS1 was conspicuously upregulated in PCa tissues and cells. And absence of VPS9D1-AS1 inhibited cell proliferation, migration and invasion, and promoted cell apoptosis in PCa.Furthermore, VPS9D1-AS1/MEF2D could sponge with miR-4739. VPS9D1-AS1/MEF2D and miR-4739 were inversely correlated in tumor cells. And the expression of miR-4739 is markedly downregulated in PCa, meanwhile, that of MEF2D exhibited the opposite tendency. However, MEF2D was positively regulated by VPS9D1-AS1. Moreover, MEF2D upregulation offset the suppressive effects of VPS9D1-AS1 deficiency on cell proliferation, migration and invasion in PCa. Additionally, ZEB1 contained the binding sites of VPS9D1-AS1 promoter, and there existed positive relation between them. Taken together, above results illustrated that ZEB1 activated-VPS9D1-AS1 promotes the tumorigenesis and progression of PCa by sponging miR-4739 to upregulate MEF2D, which offering a new useful reference for studying the development process of PCa.	31918265	RID06209	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Acute myeloid leukemia	UCA1	SIRT1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000096717	NA	652995	23411	CUDR|LINC00178|onco-lncRNA-36|UCAT1	SIR2L1	Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR-204 in pediatric AML.Herein, we found an escalation of UCA1 expression and suppression of miR-204 expression in pediatric AML patients and cells. UCA1 silencing suppressed cell proliferative abilities, promoted apoptotic rates, decreased Ki67, and increased cleaved caspase-3 in AML cells. UCA1 sponged miR-204 and suppressed its expression.UCA1 overexpression inversed the miR-204 suppressed proliferation and promoted apoptosis. UCA1 also boosted the expression of SIRT1, a miR-204 target, via the sponging interaction. Furthermore, miR-204 inhibited inducible nitric oxide synthase and cyclooxygenase-2 expression, while UCA1 overexpression inversed the inhibitory effects in AML cells. Our findings concluded that UCA1 downregulation repressed cell proliferation and promoted apoptosis through inactivating SIRT1 signals by upregulating miR-204 in pediatric AML.	31916649	RID06210	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	KCNQ1OT1	LMX1A	positively-E	LncBase (Predicted v.2);StarBase;miRbase	downregulation	qPCR	NA	NA	cancer progression(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000162761	NA	10984	4009	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	LMX1|LMX1.1	LncRNA KCNQ1OT1 regulates microRNA-9-LMX1A expression and inhibits gastric cancer cell progression.Our previous study has shown that microRNA-9 ("miR-9"), being upregulated in human gastric cancer (GC), targets LMX1A to promote GC cell progression. Through searching long non-coding RNA (LncRNA) database, we identified that LncRNA KCNQ1OT1 is the competing endogenous RNA (ceRNA) of miR-9.KCNQ1OT1 putatively targets miR-9. Its level is downregulated in human GC tissues. In AGS cells and primary human GC cells, forced overexpression of KCNQ1OT1, by a lentiviral construct, induced miR-9 downregulation and LMX1A upregulation. Furthermore, KCNQ1OT1 overexpression inhibited GC cell survival, proliferation, migration and invasion, but inducing apoptosis activation. Contrarily, KCNQ1OT1 silencing, by targeted siRNAs, induced miR-9 accumulation and LMX1A downregulation. Consequently, GC cell proliferation, migration and invasion were enhanced. Importantly, KCNQ1OT1 overexpression or silencing was ineffective in LMX1A knockout AGC cells. Taken together, KCNQ1OT1 inhibits GC cell progression via regulating miR-9 and LMX1A expression.	31915311	RID06211	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(PAAD);DATA(GSE40174)
Oral tongue squamous cell carcinoma	HOTTIP	HMGA2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000149948	NA	100316868	8091	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	BABL|HMGIC|LIPO	Downregulation of lncRNA HOTTIP Suppresses the Proliferation, Migration, and Invasion of Oral Tongue Squamous Cell Carcinoma by Regulation of HMGA2-Mediated Wnt/beta-Catenin Pathway.The expression of HOTTIP, miR-124-3p, and high-mobility group AT-hook 2 (HMGA2) was detected by quantitative real-time polymerase chain reaction.Furthermore, dual-luciferase reporter assay was performed to confirm the combination between HOTTIP and miR-124-3p, miR-124-3p, and HMGA2.HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients.Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p. Besides, miR-124-3p targeted HMGA2 to block proliferation, migration, and invasion. HMGA2 could rescue the inhibitory effects of HOTTIP interference on proliferation, migration, and invasion. In addition, HMGA2 overexpression reversed the downregulation of beta-catenin and c-Myc protein levels and upregulation of E-cadherin level affected by HOTTIP silencing. Finally, HOTTIP silencing repressed tumor growth and resulted in a great rise on miR-124-3p and E-cadherin expression and a distinct fall on HMGA2, beta-catenin, and c-Myc protein levels. HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA2 axis through Wnt/beta-catenin pathway.	31910357	RID06212	ceRNA or sponge	metastasis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Oral tongue squamous cell carcinoma	HOTTIP	E-cadherin	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell growth(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Downregulation of lncRNA HOTTIP Suppresses the Proliferation, Migration, and Invasion of Oral Tongue Squamous Cell Carcinoma by Regulation of HMGA2-Mediated Wnt/beta-Catenin Pathway.The expression of HOTTIP, miR-124-3p, and high-mobility group AT-hook 2 (HMGA2) was detected by quantitative real-time polymerase chain reaction.Furthermore, dual-luciferase reporter assay was performed to confirm the combination between HOTTIP and miR-124-3p, miR-124-3p, and HMGA2.HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients.Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p. Besides, miR-124-3p targeted HMGA2 to block proliferation, migration, and invasion. HMGA2 could rescue the inhibitory effects of HOTTIP interference on proliferation, migration, and invasion. In addition, HMGA2 overexpression reversed the downregulation of beta-catenin and c-Myc protein levels and upregulation of E-cadherin level affected by HOTTIP silencing. Finally, HOTTIP silencing repressed tumor growth and resulted in a great rise on miR-124-3p and E-cadherin expression and a distinct fall on HMGA2, beta-catenin, and c-Myc protein levels. HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA3 axis through Wnt/beta-catenin pathway.	31910357	RID06213	expression association	metastasis		
Oral tongue squamous cell carcinoma	HOTTIP	MYC	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000136997	NA	100316868	4609	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	bHLHe39|c-Myc|MYCC	Downregulation of lncRNA HOTTIP Suppresses the Proliferation, Migration, and Invasion of Oral Tongue Squamous Cell Carcinoma by Regulation of HMGA2-Mediated Wnt/beta-Catenin Pathway.The expression of HOTTIP, miR-124-3p, and high-mobility group AT-hook 2 (HMGA2) was detected by quantitative real-time polymerase chain reaction.Furthermore, dual-luciferase reporter assay was performed to confirm the combination between HOTTIP and miR-124-3p, miR-124-3p, and HMGA2.HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients.Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p. Besides, miR-124-3p targeted HMGA2 to block proliferation, migration, and invasion. HMGA2 could rescue the inhibitory effects of HOTTIP interference on proliferation, migration, and invasion. In addition, HMGA2 overexpression reversed the downregulation of beta-catenin and c-Myc protein levels and upregulation of E-cadherin level affected by HOTTIP silencing. Finally, HOTTIP silencing repressed tumor growth and resulted in a great rise on miR-124-3p and E-cadherin expression and a distinct fall on HMGA2, beta-catenin, and c-Myc protein levels. HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA4 axis through Wnt/beta-catenin pathway.	31910357	RID06214	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Oral tongue squamous cell carcinoma	HOTTIP	CTNNB1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell growth(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Downregulation of lncRNA HOTTIP Suppresses the Proliferation, Migration, and Invasion of Oral Tongue Squamous Cell Carcinoma by Regulation of HMGA2-Mediated Wnt/beta-Catenin Pathway.The expression of HOTTIP, miR-124-3p, and high-mobility group AT-hook 2 (HMGA2) was detected by quantitative real-time polymerase chain reaction.Furthermore, dual-luciferase reporter assay was performed to confirm the combination between HOTTIP and miR-124-3p, miR-124-3p, and HMGA2.HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients.Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p. Besides, miR-124-3p targeted HMGA2 to block proliferation, migration, and invasion. HMGA2 could rescue the inhibitory effects of HOTTIP interference on proliferation, migration, and invasion. In addition, HMGA2 overexpression reversed the downregulation of beta-catenin and c-Myc protein levels and upregulation of E-cadherin level affected by HOTTIP silencing. Finally, HOTTIP silencing repressed tumor growth and resulted in a great rise on miR-124-3p and E-cadherin expression and a distinct fall on HMGA2, beta-catenin, and c-Myc protein levels. HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA5 axis through Wnt/beta-catenin pathway.	31910357	RID06215	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	MAGI2-AS3	SOCS1	positively-E	IntaRNA	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-155)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000185338	NA	100505881	8651	ENST00000414797	Cish1|JAB|SOCS-1|SSI-1|TIP3	LncRNA MAGI2-AS3 Upregulates Cytokine Signaling 1 by Sponging miR-155 in Non-Small Cell Lung Cancer.The authors found that MAGI2-AS3 and suppressor of cytokine signaling 1 (SOCS-1) were both downregulated in NSCLC.In NSCLC cells, MAGI2-AS3 overexpression mediated the upregulated, while miR-155 expression mediated the downregulated SOCS-1 overexpression.RNA binding analysis showed that MAGI2-AS3 may be a sponge of miR-155. Cell proliferation revealed decreased cell proliferation rate of NSCLC cells after MAGI2-AS3 and SOCS-1 overexpression. MiR-155 played an opposite role and reduced the effects of MAGI2-AS3 overexpression.Therefore, MAGI2-AS3 upregulates cytokine signaling 1 by sponging miR-155 to inhibit NSCLC cell proliferation.	31910343	RID06216	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	TP73-AS1	TGFB1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000105329	NA	57212	7040	KIAA0495|PDAM	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA TP73-AS1 Activates TGF-beta1 to Promote the Migration and Invasion of Colorectal Cancer Cell.All CRC patients (n=70, 40 males and 30 females, 38 to 66 years' old, 52.1   5.3 years' old) in this study were enrolled in the Affiliated Hospital of Southwest Medical University from July 2012 to January 2014. Cells, vectors, and transient transfections, RT-qPCR;western blotting, as well as measurements of cell migration and invasion abilities were carried out during the research.In the present study, we found that TP73-AS1 was upregulated in CRC tissues compared with adjacent non-CRC tissues in CRC patients. Upregulation of TP73-AS1 was closely correlated with poor prognosis. TGF-beta1 was also upregulated in CRC tissues and positive correlated with TP73-AS1. TP73-AS1 overexpression caused upregulated TGF-beta1 in CRC cells, while TGF-beta1 overexpression showed no significant effect on TP73-AS1. TP73-AS1 and TGF-beta1 overexpressions caused enhanced migration and invasion of CRC cells. TGF-beta inhibitor treatment caused suppressed migration and invasion of CRC cells and attenuated effects of TP73-AS1 and TGF-beta1 overexpression.Therefore, TP73-AS1 may inactivate TGF-beta1 to inhibit the migration and invasion of CRC cells.	31908524	RID06217	expression association	prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LOXL1-AS1	PIK3CA	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-142-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000121879	NA	100287616	5290	NA	PI3K	LOXL1-AS1 Drives The Progression Of Gastric Cancer Via Regulating miR-142-5p/PIK3CA Axis.RT-PCRwas done to measure the expression levels of LOXL1-AS1 and miR-142-5p in GC tissues.Furthermore, luciferase reporter assay was carried out to confirm the relationship of miR-142-5p with LOXL1-AS1. Additionally, western blot was done to detect the regulatory function of LOXL1-AS1 on PIK3CA, a target of miR-142-5p.LOXL1-AS1 expression in GC samples was significantly increased, which was correlated with unfavorable pathological indexes.Additionally, overexpressed LOXL1-AS1 notably reduced the expression of miR-142-5p, but enhanced the expression level of PIK3CA. In vivo experiments further validated that knockdown of LOXL1-AS1 inhibited the growth and metastasis of GC cells via regulating miR-142-5p and PIK3CA.LOXL1-AS1 was a sponge of tumor suppressor miR-142-5p in GC, enhanced the expression of PIK3CA indirectly and functioned as an oncogenic lncRNA.	31908498	RID06218	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Osteosarcoma	NCK-AS1	MIR137	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);chemosensitivity(-)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	NA	NA	ENSG00000284202	NA	NA	406928	NA	hsa-mir-137|miR-137|MIRN137	Knockdown Of lncRNA NCK-AS1 Regulates Cisplatin Resistance Through Modulating miR-137 In Osteosarcoma Cells.The expression of NCK1-AS1 and miR-137 in osteosarcoma cells was detected by qRT-PCRThe interaction between NCK1-AS1 and miR-137 was identified using a dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay.The results revealed that NCK1-AS1 was significantly upregulated in osteosarcoma cells, as well as in DDP-resistant osteosarcoma cells. NCK1-AS1 silence inhibited the proliferation, migration and invasion of osteosarcoma cells, whereas enhanced the sensitivity of osteosarcoma cells to DDP. Furthermore, NCK1-AS1 directly interacted with miR-137 and overexpression of miR-137 suppressed the proliferation, migration and invasion of osteosarcoma cells. Most importantly, miR-137 overexpression enhanced the sensitivity of osteosarcoma cells to DDP, and high expression of NCK1-AS1 reversed the influences of miR-137 overexpression on DDP-resistant cells.In short, NCK1-AS1 knockdown enhanced DDP sensitivity of osteosarcoma cells by regulating miR-137, which may be a novel potential target for anti-DDP resistance in human osteosarcoma.	31908475	RID06219	ceRNA or sponge	chemoresistance		
Head and neck squamous cell carcinoma	MX1	CD274	negatively-E	ChIP;dual-luciferase reporter assay	upregulation	qRT-PCR	GSE138147	NA	cell proliferation(-);cell metastasis(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000157601	GRCh38_21:41420020-41470071	ENSG00000120217	NA	4599	29126	IFI-78K|lncMX1-215|MxA	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	A novel IFNalpha-induced long noncoding RNA negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma.Differentially expressed lncRNAs were screened under IFNalpha stimulation using lncRNA sequencing. The role and mechanism of lncRNA in immunosuppression were investigated in HNSCC in vitro and in vivo.We identified a novel IFNalpha-induced upregulated lncRNA, lncMX1-215, in HNSCC.Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. Binding sites for H3K27 acetylation were found on PD-L1 and galectin-9 promoters. Mechanistically, we found that lncMX1-215 directly interacted with GCN5, a known H3K27 acetylase, to interrupt its binding to H3K27 acetylation. Clinically, negative correlations between lncMX1-215 and PD-L1 and galectin-9 expression were observed. Finally, overexpression of lncMX1-215 suppressed HNSCC proliferation and metastasis capacity in vitro and in vivo.ur results suggest that lncMX1-215 negatively regulates immunosuppression by interrupting GCN5/H3K27ac binding in HNSCC, thus providing novel insights into immune checkpoint blockade treatment.	31907020	RID06220	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Head and neck squamous cell carcinoma	MX1	galectin-9	negatively-E	ChIP;dual-luciferase reporter assay	upregulation	qRT-PCR	GSE138147	NA	cell proliferation(-);cell metastasis(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000157601	GRCh38_21:41420020-41470071	NA	NA	4599	NA	IFI-78K|lncMX1-215|MxA	NA	A novel IFNalpha-induced long noncoding RNA negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma.Differentially expressed lncRNAs were screened under IFNalpha stimulation using lncRNA sequencing. The role and mechanism of lncRNA in immunosuppression were investigated in HNSCC in vitro and in vivo.We identified a novel IFNalpha-induced upregulated lncRNA, lncMX1-215, in HNSCC.Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. Binding sites for H3K27 acetylation were found on PD-L1 and galectin-9 promoters. Mechanistically, we found that lncMX1-215 directly interacted with GCN5, a known H3K27 acetylase, to interrupt its binding to H3K27 acetylation. Clinically, negative correlations between lncMX1-215 and PD-L1 and galectin-9 expression were observed. Finally, overexpression of lncMX1-215 suppressed HNSCC proliferation and metastasis capacity in vitro and in vivo.ur results suggest that lncMX1-215 negatively regulates immunosuppression by interrupting GCN5/H3K28ac binding in HNSCC, thus providing novel insights into immune checkpoint blockade treatment.	31907020	RID06221	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367)	
Head and neck squamous cell carcinoma	MX1	GCN5	negatively-E	RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	GSE138147	NA	cell proliferation(-);cell metastasis(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000157601	GRCh38_21:41420020-41470071	ENSG00000259958	NA	4599	NA	IFI-78K|lncMX1-215|MxA	NA	A novel IFNalpha-induced long noncoding RNA negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma.Differentially expressed lncRNAs were screened under IFNalpha stimulation using lncRNA sequencing. The role and mechanism of lncRNA in immunosuppression were investigated in HNSCC in vitro and in vivo.We identified a novel IFNalpha-induced upregulated lncRNA, lncMX1-215, in HNSCC.Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. Binding sites for H3K27 acetylation were found on PD-L1 and galectin-9 promoters. Mechanistically, we found that lncMX1-215 directly interacted with GCN5, a known H3K27 acetylase, to interrupt its binding to H3K27 acetylation. Clinically, negative correlations between lncMX1-215 and PD-L1 and galectin-9 expression were observed. Finally, overexpression of lncMX1-215 suppressed HNSCC proliferation and metastasis capacity in vitro and in vivo.ur results suggest that lncMX1-215 negatively regulates immunosuppression by interrupting GCN5/H3K29ac binding in HNSCC, thus providing novel insights into immune checkpoint blockade treatment.	31907020	RID06222	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367)	
Lung cancer	lnc-BMP1-1	CAV1	positively-E	bio-information and literature analysis	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000105974	NA	NA	857	NA	BSCL3|CGL3|LCCNS|MSTP085|PPH3|VIP21	Down expression of lnc-BMP1-1 decreases that of Caveolin-1 is associated with the lung cancer susceptibility and cigarette smoking history	31901898	RID06223	expression association	NA		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Prostate cancer	DRAIC	NFKB1	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000245750	GRCh38_15:69462921-69843120	ENSG00000109320	NA	145837	4790	NA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	Long Noncoding RNA DRAIC Inhibits Prostate Cancer Progression by Interacting with IKK to Inhibit NF-kB Activation.Here, we show that cancers with decreased DRAIC expression have increased NF-kB target gene expression. DRAIC downregulation increased cell invasion and soft agar colony formation; this was dependent on NF-kB activation. DRAIC interacted with subunits of the IkB kinase (IKK) complex to inhibit their interaction with each other, the phosphorylation of IkBalpha, and the activation of NF-kB. DRAIC lncRNA inhibits prostate cancer progression through suppression of NF-kB activation by interfering with IKK activity.A cytoplasmic tumor-suppressive lncRNA interacts with and inhibits a major kinase that activates an oncogenic transcription factor in prostate cancer.When we generated the constitutively active IKK by over-expressing the IKKbeta (S177E/S181E) in androgen dependent LNCaP cells, the NF-kB activity was still repressed by DRAIC overexpression (Fig. 3H, compare with Fig. 3E), suggesting that DRAIC represses the NF-kB pathway downstream of active IKK. Intersecting these results leads to the conclusion that DRAIC is likely to repress the NF-kB pathway by interfering with the function of IKK.	31900260	RID06224	expression association	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	DLGAP1-AS2	YAP1	positively-E	GEPIA	upregulation	RT-qPCR	NA	NA	cell growth(+);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000262001	GRCh38_18:3603000-3610103	ENSG00000137693	NA	84777	10413	MGC11082	YAP65	LncRNA DLGAP1-AS2 modulates glioma development by up-regulating YAP1 expression.Here, we demonstrated that LncRNA DLGAP1-AS2 was up-regulated in glioma and was quite correlated with poor prognosis of glioma patients. Depletion of DLGAP1-AS2 in glioma cells could inhibit cell proliferation and cell migration, and induce cell apoptosis, resulting in the suppression of the progression of glioma consequently. Furthermore, knockdown of DLGAP1-AS2 inhibited the growth of xenograft glioma tumour in vivo as well. Finally, we verified Yes Associated Protein 1 (YAP1) was the downstream target of DLGAP1-AS2 and DLGAP1-AS2 modulated glioma cell proliferation, migration and apoptosis via regulating YAP1. Our study revealed novel mechanism about how did lncRNA DLGAP1-AS2 execute function in glioma and thus provided potential therapeutic interventions for the treatment of glioma.	31899508	RID06225	expression association	prognosis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Laryngeal squamous cell carcinoma	XIST	IRS1	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-144)	regulation	RNA-protein	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169047	NA	7503	3667	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	HIRS-1	lncRNA XIST promotes the progression of laryngeal squamous cell carcinoma by sponging miR-144 to regulate IRS1 expression.It was revealed that the level of XIST was significantly higher in LSCC tissues that were associated with advanced Tumor-Node-Metastasis (TNM) stage and the presence of lymph node metastasis.Further investigation revealed that XIST knockdown increased the expression of microRNA-144 (miR-144) by acting as an endogenous sponge of miR-144. Inhibition of miR-144 caused a partial reversal of the inhibitory effects mediated following depletion of XIST in LSCC cells.Moreover, an miR-144 target called insulin receptor substrate  1  (IRS1) was significantly decreased by XIST depletion in LSCC cells. IRS1 expression was positively correlated with XIST expression in LSCC tissues. In addition, knockdown of XIST impaired tumor growth in  vivo by regulating the miR-144/IRS1 axis. The present study demonstrated that the progression of LSCC is promoted by XIST sponging miR-144 to regulate IRS1 expression, suggesting that XIST can serve as a putative target in the therapy of LSCC.	31894287	RID06226	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Gastric cancer	CRAL	CYLD	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+)	ceRNA(miR-506)	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000083799	NA	NA	1540	NA	CYLD1|KIAA0849|USPL2	The long noncoding RNA CRAL reverses cisplatin resistance via the miR-505/CYLD/AKT axis in human gastric cancer cells.In this study, we identified a novel lncRNA, cisplatin resistance-associated lncRNA (CRAL), that was downregulated in cisplatin-resistant GC cells, impaired cisplatin-induced DNA damage and cell apoptosis and thus contributed to cisplatin resistance in GC cells.Furthermore, the results indicated that CRAL mainly resided in the cytoplasm and could sponge endogenous miR-505 to upregulate cylindromatosis (CYLD) expression, which further suppressed AKT activation and led to an increase in the sensitivity of gastric cancer cells to cisplatin in vitro and in preclinical models.Moreover, a specific small molecule inhibitor of AKT activation, MK2206, effectively reversed the cisplatin resistance in GC caused by CRAL deficiency. In conclusion, we provide the first evidence that a novel lncRNA, CRAL, could function as a competing endogenous RNA (ceRNA) to reverse GC cisplatin resistance via the miR-506/CYLD/AKT axis, which suggests that CRAL could be considered a potential predictive biomarker and therapeutic target for cisplatin resistance in gastric cancer.	31885317	RID06227	ceRNA or sponge	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Malignant glioma	RAD21	IGSF9B	negatively-E	RNA pull-down assay;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000164754	GRCh38_8:116845934-116874776	ENSG00000080854	NA	5885	22997	hHR21|KIAA0078|SCC1	KIAA1030|LINC00947|LOC283174|MIR4697HG	RAD21 inhibited transcription of tumor suppressor MIR4697HG and led to glioma tumorigenesis.In this study, we tested the expression of MIR4697HG in glioma cells and detected the comparatively down-regulated expression.We profiled the expression of MIR4697HG in glioblastoma multiforme (GBM) tissues according to GEPIA database as well as in glioma cells by qPCR.We also carried out luciferase reporter assay, pull down assay and RIP assay to verify the location and interaction among the indicated RNA molecules.The expression of MIR4697HG is down-regulated significantly in glioma cells due to the up-regulated expression of RAD21.RAD21-induced down-regulated expression of MIR4697HG is correlated with aggravation of glioma. The MIR4697HG/miR-766-5p/PRR12 axis predicts poor results in glioma and MIR4697HG could be considered as a promising biomarker for diagnosis and treatment of glioma.	31884342	RID06228	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)
Malignant glioma	IGSF9B	PRR12	positively-E	starBase;RNA pull-down assay;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-766-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000080854	GRCh38_11:133896438-133956968	ENSG00000126464	NA	22997	57479	KIAA1030|LINC00947|LOC283174|MIR4697HG	KIAA1205	RAD21 inhibited transcription of tumor suppressor MIR4697HG and led to glioma tumorigenesis.In this study, we tested the expression of MIR4697HG in glioma cells and detected the comparatively down-regulated expression. RAD1 is an upstream regulator for MIR4697HG. This study aimed at exploring the regulatory mechanism and function of RAD1/MIR4697HG/PRR12 axis in glioma.METHODS: We profiled the expression of MIR4697HG in glioblastoma multiforme (GBM) tissues according to GEPIA database as well as in glioma cells by qPCR. Functional experiments confirmed relevant role of MIR4697HG in regulating glioma cell proliferation and migration. We also carried out luciferase reporter assay, pull down assay and RIP assay to verify the location and interaction among the indicated RNA molecules.RESULTS: The expression of MIR4697HG is down-regulated significantly in glioma cells due to the up-regulated expression of RAD21. MiR-766-5p was identified functioning as a sponge for MIR4697HG and is sequestered by MIR4697HG. We also found either miR-766-5p inhibitor or PRR12 knockdown rescued the function depletion caused by MIR4697HG overexpression. In all, the down-regulated expression of MIR4697HG inhibited PRR12 to suppress glioma and led to the deterioration of glioma.CONCLUSION: RAD21-induced down-regulated expression of MIR4697HG is correlated with aggravation of glioma. The MIR4697HG/miR-766-5p/PRR12 axis predicts poor results in glioma and MIR4698HG could be considered as a promising biomarker for diagnosis and treatment of glioma.	31884342	RID06229	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	LUNAR1	IGF1	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000278090	GRCh38_15:99014526-99031054	ENSG00000017427	NA	104564224	3479	NA	IGF|IGF-I|IGF1A|IGFI	The Novel Notch-induced Long Noncoding RNA LUNAR1 Determines the Proliferation and Prognosis of Colorectal Cancer.The downregulation of LUNAR1 in SW620 cells inhibited cell proliferation, migration, invasion and tumour growth while inducing apoptosis. Moreover, the inhibition of LUNAR1 can significantly suppress IGF1 signalling in CRC. These results indicated that LUNAR1 was increased in CRC and might promote tumour progression. Thus, LUNAR1 may constitute a promising prognostic marker for the clinical management of CRC.Significantly increased expression of LUNAR1 in clinical CRC specimens was detected compared with that in matching normal tissues.	31882986	RID06230	expression association	prognosis		UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	EFNA1	EIF4B	positively-E	FISH;catRAPID	upregulation	qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000169242	GRCh38_1:155127876-155134899	ENSG00000063046	NA	1942	1975	ECKLG|EPLG1|GMAN|LERK1|TNFAIP4	NA	Long noncoding RNA GMAN promotes hepatocellular carcinoma progression by interacting with eIF4B.We found that lncRNA-GMAN was significantly overexpressed in HCC tissues.Knockdown of GMAN induced apoptosis and suppressed invasive and migration potential in vitro and vivo, whereas ectopic GMAN expression produced the opposite effect.Mechanistic analyses indicated that GMAN directly combined with eukaryotic translation initiation factor 4B (eIF4B) and promoted its phosphorylation at serine-422 by preventing eIF4B binding and dephosphorization of the protein phosphatase 2A subunit B. The results demonstrated the stability of p-eIF4B and the elevation of mRNA translation and anti-apoptosis-related protein expression, which further induced proliferation and metastasis of HCC. The current study demonstrates that GMAN regulates the progression of HCC by inhibiting apoptosis and promoting the survival of cancer cells.	31875526	RID06231	interact with protein	metastasis	UP(NSCLC,BRCA);DATA(GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	AFAP1-AS1	AFAP1	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS|MGC10981	AFAP|AFAP-110	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS1 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06232	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Oral squamous cell carcinoma	AFAP1-AS1	RHOA	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000067560	NA	84740	387	AFAP1-AS|AFAP1AS|MGC10981	ARH12|ARHA|Rho12|RHOH12	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS2 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06233	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Oral squamous cell carcinoma	AFAP1-AS1	RAC2	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000128340	NA	84740	5880	AFAP1-AS|AFAP1AS|MGC10981	EN-7	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS3 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06234	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	AFAP1-AS1	RAB10	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000084733	NA	84740	10890	AFAP1-AS|AFAP1AS|MGC10981	NA	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS4 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06235	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Oral squamous cell carcinoma	AFAP1-AS1	ARHGDIA	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000141522	NA	84740	396	AFAP1-AS|AFAP1AS|MGC10981	GDIA1|RHOGDI	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS5 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06236	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	AFAP1-AS1	PFN1	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000108518	NA	84740	5216	AFAP1-AS|AFAP1AS|MGC10981	NA	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS6 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06237	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	AFAP1-AS1	RHOC	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000155366	NA	84740	389	AFAP1-AS|AFAP1AS|MGC10981	ARH9|ARHC	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06238	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	AFAP1-AS1	RHOC	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000155366	NA	84740	389	AFAP1-AS|AFAP1AS|MGC10981	ARH9|ARHC	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06239	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	AFAP1-AS1	AFAP1	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS|MGC10981	AFAP|AFAP-110	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06240	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Oral squamous cell carcinoma	AFAP1-AS1	RHOA	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000067560	NA	84740	387	AFAP1-AS|AFAP1AS|MGC10981	ARH12|ARHA|Rho12|RHOH12	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06241	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Oral squamous cell carcinoma	AFAP1-AS1	RAC2	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000128340	NA	84740	5880	AFAP1-AS|AFAP1AS|MGC10981	EN-7	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06242	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	AFAP1-AS1	RAB10	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000084733	NA	84740	10890	AFAP1-AS|AFAP1AS|MGC10981	NA	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06243	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Oral squamous cell carcinoma	AFAP1-AS1	RhoGD	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	NA	NA	84740	NA	AFAP1-AS|AFAP1AS|MGC10981	NA	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06244	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	
Oral squamous cell carcinoma	AFAP1-AS1	PFN1	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000108518	NA	84740	5216	AFAP1-AS|AFAP1AS|MGC10981	NA	Expression and functions of long non-coding RNA actin filament-associated protein 1-antisense RNA1 in oral squamous cell carcinoma.Quantitative real-time polymerase chain reaction (qRT-PCR was used to detect the expression of lncRNA AFAP1-AS1 in the tumor tissue and matching adjacent normal tissue of OSCC patients (n=55), SCC25 cells, and normal oral keratinocyte lines (NOK) cells. The correlation between AFAP1-AS1 expression and the clinicopathological characteristics of OSCC patients was analyzed. The relationship between AFAP1-AS1 and prognosis was also studied with the Kaplan-Meier method. AFAP1-AS1 siRNA was transfected into the SCC25 cells. Cell counting kit-8 (CCK-8) and Trans-well were used to detect cell proliferation, invasion, and migration. The expression of the invasion-associated protein, AFAP1, and Rho GTPase family members, was detected by western blot. In addition, the immunofluorescence of the cytoskeletal actin filament was observed.RESULTS: The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05). After transfected by AFAP1-AS1 siRNA, the expression of AFAP1-AS1 was downregulated. The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25. Moreover, AFAP1-AS1 siRNA upregulated the expression levels of AFAP1, RhoA, Rac2, Rab10, RhoGDI, and Pfn1 but downregulated the expression of RhoC. Immunofluorescence showed that AFAP1-AS1 also reduced the formation of stress filaments in the cytoskeleton and affected the integrity of the actin fila-ment.CONCLUSIONS: The expression of AFAP1-AS1 was high in the OSCC tissues and SCC25 cells and is associated with the development and prognosis of OSCC. The knockdown of AFAP1-AS7 might inhibit the proliferation and invasion of OSCC cells by regulating the integrity of the actin filament.	31875436	RID06245	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	CARMN	miR-21	negatively-E		downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	DNA methylation	regulation	RNA-RNA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000249669	GRCh38_5:149406689-149432835	ENSG00000199004	NA	728264	NA	CARMEN|MIR143HG	NA	LncRNA miR143HG suppresses miR-21 through methylation to inhibit cell invasion and migration.Quantitative polymerase chain reaction (PCR) and paired t test were used to measure and compare expression levels of miR143HG and miR-21 in LSCC and nontumor tissues.We found that miR143HG was downregulated in LSCC and inversely correlated with miR-21.In LSCC cells, miR143HG overexpression led to the downregulated expression of miR-21, whereas miR-21 overexpression failed to affect miR143HG. Methylation-specific PCR results showed that miR143HG overexpression led to increased methylation of miR-21. Low expression levels of miR143HG were correlated with poor survival. Overexpression of miR143HG led to decreased, whereas miR-21 overexpression resulted in increased rate of LSCC cell migration and invasion. In addition, miR-21 overexpression led to reduced effects of miR143HG on cell invasion and migration. Therefore, miR143HG suppresses miR-21 via methylation to regulate cell behaviors in LSCC.	31872875	RID06246	epigenetic regulation	NA	UP(PRAD);DATA(GSE104209)	
Hepatocellular carcinoma	GATA3-AS1	PTEN	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000171862	NA	399717	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Long Noncoding RNA GATA3-AS1 Promotes Cell Proliferation and Metastasis in Hepatocellular Carcinoma by Suppression of PTEN, CDKN1A, and TP53.Real-time quantitative PCR (RT-qPCR) assay was conducted to detect GATA3-AS1 expression levels in 80 cases of pairs HCC tissues and matched normal tissues. GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues.The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects. In addition, GATA3-AS1 knockdown resulted in upregulated expression levels of tumor-suppressive genes, PTEN, CDKN1A, and TP53, in Hep3B and HCCLM3 cells, while restoration of GATA3-AS1 decreased PTEN, CDKN1A, and TP53 expression levels.Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP53.	31871924	RID06247	expression association	metastasis	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	GATA3-AS1	CDKN1A	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000124762	NA	399717	1026	NA	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	Long Noncoding RNA GATA3-AS1 Promotes Cell Proliferation and Metastasis in Hepatocellular Carcinoma by Suppression of PTEN, CDKN1A, and TP53.Real-time quantitative PCR (RT-qPCR) assay was conducted to detect GATA3-AS1 expression levels in 80 cases of pairs HCC tissues and matched normal tissues. GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues.The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects. In addition, GATA3-AS1 knockdown resulted in upregulated expression levels of tumor-suppressive genes, PTEN, CDKN1A, and TP53, in Hep3B and HCCLM3 cells, while restoration of GATA3-AS1 decreased PTEN, CDKN1A, and TP53 expression levels.Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP54.	31871924	RID06248	expression association	metastasis	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	GATA3-AS1	TP53	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000197308	GRCh38_10:8050450-8053484	ENSG00000141510	NA	399717	7157	NA	LFS1|p53	Long Noncoding RNA GATA3-AS1 Promotes Cell Proliferation and Metastasis in Hepatocellular Carcinoma by Suppression of PTEN, CDKN1A, and TP53.Real-time quantitative PCR (RT-qPCR) assay was conducted to detect GATA3-AS1 expression levels in 80 cases of pairs HCC tissues and matched normal tissues. GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues.The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects. In addition, GATA3-AS1 knockdown resulted in upregulated expression levels of tumor-suppressive genes, PTEN, CDKN1A, and TP53, in Hep3B and HCCLM3 cells, while restoration of GATA3-AS1 decreased PTEN, CDKN1A, and TP53 expression levels.Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP55.	31871924	RID06249	expression association	metastasis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Ovarian cancer	C2orf92	MIR1972-1	negatively-F	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	chemosensitivity(+)	sponge	binding/interaction	protein-RNA	Cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000228486	GRCh38_2:97664217-97703066	ENSG00000238728	NA	728537	100302243	LINC01125	MIR1972|hsa-mir-1972|hsa-mir-1972-1	Long Noncoding RNA LINC01125 Enhances Cisplatin Sensitivity of Ovarian Cancer via miR-1972.LINC01125 and miR-1972 expressions were measured by qRT-PCRThe interaction between LINC01125 and miR-1972 was verified through dual-luciferase reporter and RNA immunoprecipitation (RIP) assays, and bioinformatics analysis was performed to predict the target genes of miR-1972.Our results indicated that LINC01125 expression was significantly downregulated in CDDP-resistant OC tissues and cell lines. Overexpression of LINC01125 inhibited OC cell proliferation and enhanced the cytotoxicity of CDDP in OC cells. Additionally, LINC01125 participated in the apoptosis pathway by directly binding to miR-1972 in OC cells. CONCLUSIONS Therefore, we suggest that LINC01125 might act as a tumor suppressor in OC and enhances the cisplatin sensitivity of OC cells by binding to miR-1972.	31865363	RID06250	ceRNA or sponge	chemoresistance		
Lung adenocarcinoma	GMDS-DT	CYLD	positively-E	luciferase reporter assay;western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-96-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000250903	GRCh38_6:2245718-2525976	ENSG00000083799	NA	100508120	1540	GMDS-AS1	CYLD1|KIAA0849|USPL2	LncRNA GMDS-AS1 inhibits lung adenocarcinoma development by regulating miR-96-5p/CYLD signaling.In this study, we found that the expression of lncRNA GMDS-AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells.pregulated GMDS-AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. The results indicate that GMDS-AS1 acts as a tumor suppressor gene to affect the development of LUAD. Further studies revealed that GMDS-AS1 is a target gene of miR-96-5p, and GMDS-AS1 regulates proliferation and apoptosis of LUAD cells in association with miR-96-5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR-96-5p. Through various validations, we confirmed that GMDS-AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR-96-5p. Moreover, the intervention of GMDS-AS1/miR-96-5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS-AS1/miR-96-5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.	31860169	RID06251	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Breast cancer	DANCR	SOCS3	negatively-E	ChIP;RIP;Western immunoblots	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000184557	NA	57291	9021	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CIS3|Cish3|SOCS-3|SSI-3	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription.Long non-coding RNA (lncRNA) is involved in the regulation of tumorigenesis and metastasis. In this study, we focused on the clinical relevance, biological effects, and molecular mechanisms of the lncRNA differentiation antagonizing non-protein coding RNA (DANCR) in breast cancer. We compared the expression of DANCR between breast cancer and normal tissues, and between breast cancer cell lines and normal breast epithelial cells using quantitative real-time PCR (qRT-PCR analysis. By knocking down and overexpressing DANCR, we assessed its significance in regulating viability (MTT assay), migration/invasion (Transwell assay), epithelial-mesenchymal transition (western blot), stemness (mammosphere formation assay and western blot), and production of inflammatory cytokines (qRT-PCRand ELISA) of breast cancer cells in  vitro, as well as xenograft growth in  vivo. Furthermore, using ChIP and RNA immunoprecipitation, we examined the reciprocal regulation between DANCR and suppressor of cytokine signaling 3 (SOCS3) in breast cancer. DANCR was significantly up-regulated in tissue samples from patients with breast cancer, as well as in breast cancer cell lines, as compared with normal tissues and breast epithelial cells, respectively. The highest DANCR expression levels were associated with advanced tumor grades or lymph node metastasis. DANCR was necessary and sufficient to control multiple malignant phenotypes of breast cancer cells in  vitro and xenograft growth in  vivo. Mechanistically, DANCR promoted the binding of enhancer of zeste homolog 2 (EZH2) to the promoter of SOCS3, thereby epigenetically inhibiting SOCS3 expression. Functionally, SOCS3 up-regulation or EZH2 inhibition could rescue multiple malignant phenotypes induced by DANCR. Our data indicate that DANCR is a pleiotropic oncogenic lncRNA in breast cancer. Boosting SOCS3 expression may reverse the oncogenic activities of DANCR and thus provide a therapeutic strategy for breast cancer treatment.	31860165	RID06252	interact with protein	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	MIR503HG	WNT1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000125084	NA	84848	7471	H19X|MGC16121	INT1	Long non-coding RNA MIR503HG serves as a tumor suppressor in non-small cell lung cancer mediated by wnt1.The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR assay was conducted to access the expression level of MIR503HG in NSCLC cell lines and tissues.MIR503HG was downregulated in NSCLC. MIR503HG downregulated Wnt1 expression in NSCLC.Lon non-coding RNA MIR503HG was downregulated in NSCLC. The over-expression of MIR503HG suppressed cell proliferation and promoted cell apoptosis in vitro and repressed tumorigenesis in vivo. MIR503HG suppressed NSCLC progression via negatively regulating Wnt1 expression.	31858550	RID06253	expression association	NA		
Colorectal cancer	LINC00324	miR-214-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000178977	GRCh38_17:8220624-8224043	NA	NA	284029	NA	C17orf44|FLJ34790|MGC104931|NCRNA00324	NA	Knockdown of long non-coding RNA LINC00324 inhibits proliferation, migration and invasion of colorectal cancer cell via targeting miR-214-3p.The expression level of LINC00324 and miR-214-3p was measured by quantitative real time polymerase chain reaction (qRT-PCR in CRC cells.The target of LINC00324 was predicted by online software and confirmed by luciferase reporter assay.We first detected the expression of LIN00324 was increased while miR-214-3p was decreased in CRC cells.Knockdown of LIN00324 suppressed proliferation, migration and invasion in SW620 and HCT15 cells. Moreover, overexpression of miR-214-3p also inhibited CRC cell proliferation, migration and invasion. Then, we identified miR-214-3p as directly target of LINC00324 and the expression of miR-214-3p was downregulated by LINC00324. In addition, inhibiting miR-214-3p reversed the effects of LINC00324 on CRC cell proliferation, migration and invasion.CONCLUSIONS: Our results proved that LINC00324 regulated CRC cell proliferation, migration and invasion by sponging miR-214-3p, suggesting that it might be a potential therapeutic target for CRC therapy.	31858541	RID06254	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Hepatocellular carcinoma	LINC02882	TNKS2	positively-E	LncBase v.2;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251138	GRCh38_12:73820315-74402600	ENSG00000107854	NA	100507377	80351	RP11-81H3.2	ARTD6|PARP-5b|PARP-5c|PARP5B|PARP5C|pART6|TANK2|TNKL	RP11-81H3.2 Acts as an Oncogene via microRNA-490-3p Inhibition and Consequential Tankyrase 2 Up-Regulation in Hepatocellular Carcinoma.Here, we have identified a long non-coding RNA, RP11-81H3.2, which is enriched in HCC and can promote its proliferation, migration, and invasion both in vitro and in vivo. In addition, our results showed that RP11-81H3.2 binds to and regulate miR-490-3p expression in the HCC cells. Moreover, we found that RP11-81H3.2 regulates the expression of TNKS2 via miR-490-3p. Further, we found that RP11-81H3.2 and miR-490-3p form a regulatory loop; the release of RP11-81H3.2 leads to the suppression of miR-490-3p expression, thus, further enhancing the expression of RP11-81H3.2.Our data have provided a novel target for the diagnosis and treatment of HCC, and sheds light on the lncRNA-miRNA regulatory nexus that can control the HCC related pathogenesis.	31858324	RID06255	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TSPOAP1-AS1	THBS1	negatively-F	RIP;RNA pull-down assay;ChIP;western blot	upregulation	microarray	NA	NA	cell proliferation(+);cell migration(+)	DNA methylation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000265148	GRCh38_17:58324472-58415766	ENSG00000137801	NA	100506779	7057	BZRAP1-AS1	THBS|THBS-1|TSP|TSP-1|TSP1	Long non-coding RNA BZRAP1-AS1 silencing suppresses tumor angiogenesis in hepatocellular carcinoma by mediating THBS1 methylation.microarray-based data analysis was initially employed to screen genes and lncRNAs that are differentially expressed in HCC and the candidate BZRAP1-AS1 was identified as a hit.The expression of BZRAP1-AS1 and thrombospondin-1 (THBS1) in HCC tissues and cells were then determined using RT-qPCR.The gene methylation level was measured by methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) assays. Next, the interactions between BZRAP1-AS1, DNA methyltransferase 3B (DNMT3b), and THBS1 were assessed by RIP, RNA pull-down and ChIP assays. Finally, the roles of BZRAP1-AS1, DNMT3b and THBS1 in angiogenesis in vitro as well as tumorigenesis in vivo were evaluated by a battery of the gain- and loss-of function experiments.BZRAP1-AS1 was identified as a highly expressed lncRNA in HCC tissues and cells. Down-regulation of BZRAP1-AS1 in HCC cells inhibited HUVEC proliferation, migration and angiogenesis. By interacting with DNMT3b, BZRAP1-AS1 induced methylation of the THBS1 promoter and inhibited the transcription of THBS1, resulting in promoted angiogenesis of HUVECs. Moreover, silencing of BZRAP1-AS1 repressed the angiogenesis as well as the tumor growth of HCC in vivo via up-regulating THBS1.This study provides evidence that angiogenesis in HCC is hindered by silencing of BZRAP1-AS1. Thus, BZRAP1-AS1 may be a promising marker for the treatment of HCC.	31847842	RID06256	epigenetic regulation	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE109761,GSE111065)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	TSPOAP1-AS1	DNMT3B	NA	RIP;RNA pull-down assay;ChIP;western blot	upregulation	microarray	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000265148	GRCh38_17:58324472-58415766	ENSG00000088305	NA	100506779	1789	BZRAP1-AS1	NA	Long non-coding RNA BZRAP1-AS1 silencing suppresses tumor angiogenesis in hepatocellular carcinoma by mediating THBS1 methylation.microarray-based data analysis was initially employed to screen genes and lncRNAs that are differentially expressed in HCC and the candidate BZRAP1-AS1 was identified as a hit.The expression of BZRAP1-AS1 and thrombospondin-1 (THBS1) in HCC tissues and cells were then determined using RT-qPCR.The gene methylation level was measured by methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) assays. Next, the interactions between BZRAP1-AS1, DNA methyltransferase 3B (DNMT3b), and THBS1 were assessed by RIP, RNA pull-down and ChIP assays. Finally, the roles of BZRAP1-AS1, DNMT3b and THBS1 in angiogenesis in vitro as well as tumorigenesis in vivo were evaluated by a battery of the gain- and loss-of function experiments.BZRAP1-AS1 was identified as a highly expressed lncRNA in HCC tissues and cells. Down-regulation of BZRAP1-AS1 in HCC cells inhibited HUVEC proliferation, migration and angiogenesis. By interacting with DNMT3b, BZRAP1-AS1 induced methylation of the THBS1 promoter and inhibited the transcription of THBS1, resulting in promoted angiogenesis of HUVECs. Moreover, silencing of BZRAP1-AS1 repressed the angiogenesis as well as the tumor growth of HCC in vivo via up-regulating THBS1.This study provides evidence that angiogenesis in HCC is hindered by silencing of BZRAP1-AS1. Thus, BZRAP1-AS2 may be a promising marker for the treatment of HCC.	31847842	RID06257	interact with protein	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE109761,GSE111065)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	MNX1-AS1	RAB1A	positively-E	starBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);cell growth(+);cell metastasis(+)	ceRNA(miR-218-5p	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000138069	NA	645249	5861	CCAT5|LOC645249|MAYA	RAB1|YPT1	Long Noncoding RNA MNX1 antisense RNA 1 Exerts Oncogenic Functions in Bladder Cancer by Regulating miR-218-5p/RAB1A Axis.LncRNA MNX1 antisense RNA 1 (MNX1-AS1) is significantly overexpressed in patients with bladder cancer, suggesting that it might be associated with bladder cancer.Mechanistic analysis demonstrated that miR-218-5p was a direct target of RAB1A. MNX1-AS1 could competitively bind to miR-218-5p to regulate RAB1A expression in bladder cancer cells.Taken together, MNX1-AS1 functions as a sponge to miR-218-5p to modulate RAB1A expression in bladder cancer, which suggests that MNX1-AS1 might serve as a novel therapeutic target and a novel biomarker for metastasis and prognosis in bladder cancer. Our study demonstrates that long noncoding RNA MNX1-AS1 promotes the initiation and progression of bladder cancer. MNX1-AS1 regulates RAB1A expression to promote proliferation, migration, invasion, and epithelial-mesenchymal transitions of bladder cancer cells via miR-218-5p, which contributes to the tumor growth and metastasis of bladder cancer. Collectively, these results suggest that MNX1-AS1 might serve as a potential biomarker for bladder cancer.	31843814	RID06258	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Nasopharynx carcinoma	HCG18	CCND1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000110092	NA	414777	595	Em:AB014087.1|FLJ25550|FLJ31598	BCL1|D11S287E|PRAD1|U21B31	LncRNA HCG18 contributes to nasopharyngeal carcinoma development by modulating miR-140/CCND1 and Hedgehog signaling pathway.Reverse Transcription-Polymerase Chain Reaction (RT-PCR was used to determine the levels of HCG18 in NPC tissue and cell lines.Insights of the mechanism of ceRNAs were gained from bioinformatic methods and Luciferase analysis. western blot was performed to determine the expression of tumor-related pathways.We found that HCG18 expression was upregulated in both NPC specimens and cell lines.Higher levels of HCG18 were associated with positive lymph node metastasis and poor prognosis of NPC patients. Importantly, the multivariate analysis confirmed that HCG18 was an independent risk factor for outcome. Functionally, the downregulation of HCG18 exhibited tumor-suppressive effects via the inhibition of cell proliferation and metastasis. Mechanistically, HCG18 may directly bind to miR-140 and effectively act as a ceRNA for miR-140 to increase the expression of cyclin D1 (CCND1). In addition, HCG18 may contribute to NPC progression via modulating Wnt/beta-catenin signaling and Hedgehog pathway.CONCLUSIONS: Our findings suggested that HCG18 served as an oncogenic lncRNA in NPC progression, which may provide a novel biomarker of an unfavorable outcome and a potential therapeutic target for NPC.	31841193	RID06259	ceRNA or sponge	metastasis,prognosis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	BLACAT1	miR-142-5p	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	linc-UBC1|LINC00912|onco-lncRNA-30	NA	LncRNA BLACAT1 regulates the viability, migration and invasion of oral squamous cell carcinoma cells by targeting miR-142-5p.The expressions of BLACAT1 and miR-142-5p in OSCC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR. Cell viability was evaluated by MTT assay. Cell migration and invasion were evaluated by transwell migration assay and transwell invasion assay, respectively. The protein levels of CyclinD1, p21, p27, MMP-2, MMP-9 and MMP-14 were detected by western blot The interaction of BLACAT1 and miR-142-5p was verified by luciferase reporter assay.RESULTS: The expression of BLACAT1 was increased and the expression of miR-142-5p was decreased in OSCC cells. The knockdown of BLACAT1 suppressed the viability, migration and invasion of OSCC cells. miR-142-5p was identified as a target of BLACAT1 and BLACAT1 overexpression suppressed miR-142-5p expression. Furthermore, overexpression of miR-142-5p showed similar effects on OSCC cells viability, migration and invasion with BLACAT1 knockdown, and inhibition of miR-142-5p restored the effects of BLACAT1 knockdown OSCC cells viability, migration and invasion.CONCLUSIONS: LncRNA BLACAT1 knockdown suppressed the viability, migration and invasion of OSCC cells by sponging miR-142-5p, indicating that BLACAT1 might be a novel target for the treatment of OSCC.	31841186	RID06260	ceRNA or sponge	NA		
Melanoma	CASC15	CTNNB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);wnt/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000168036	NA	401237	1499	CANT|LINC00340|lnc-SOX4-1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Non-Coding RNA-CASC15 Promotes Cell Proliferation, Migration, and Invasion by Activating Wnt/beta-Catenin Signaling Pathway in Melanoma.Quantitative real-time polymerase chain reaction was applied to explore CASC15 and beta-catenin expression in melanoma tissues and cells. western blot was carried out to investigate beta-catenin, glycogen synthase kinase-3beta, Survivin, Bax, Bcl-2, and epithelial-mesenchymal transition (EMT)-related protein expression level. Cell proliferation, apoptosis, migration, and invasion were observed by colony formation assay, flow cytometry, and transwell migration and invasion assays, respectively. The activity of Wnt/beta-catenin signaling pathway was measured by Topflash luciferase reporter assay.RESULTS: The expression of CASC15 and beta-catenin was upregulated in melanoma tissues and cells. Knockdown of CASC15 suppressed Wnt/beta-catenin signaling pathway and inhibited beta-catenin expression. Furthermore, inhibition of CASC15 decreased proliferation and increased apoptosis of melanoma cells by downregulating Survivin and Bcl-2 and upregulating Bax in A375 and SK-MEL-28 cells. Silencing of CASC15 inhibited migration and invasion of melanoma cells by repressing EMT process.CONCLUSION: Our study demonstrated that CASC15 promoted the proliferation, migration, and invasion of melanoma cells via activating Wnt/beta-catenin signaling pathway, implying that CASC15 might be a potential therapeutic target and prognostic biomarker for melanoma.	31838468	RID06261	expression association	prognosis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Melanoma	CASC15	BCL2	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);wnt/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000171791	NA	401237	596	LINC00340|lnc-SOX4-1	Bcl-2|PPP1R50	Long Non-Coding RNA-CASC15 Promotes Cell Proliferation, Migration, and Invasion by Activating Wnt/beta-Catenin Signaling Pathway in Melanoma.Quantitative real-time polymerase chain reaction was applied to explore CASC15 and beta-catenin expression in melanoma tissues and cells. western blot was carried out to investigate beta-catenin, glycogen synthase kinase-3beta, Survivin, Bax, Bcl-2, and epithelial-mesenchymal transition (EMT)-related protein expression level. Cell proliferation, apoptosis, migration, and invasion were observed by colony formation assay, flow cytometry, and transwell migration and invasion assays, respectively. The activity of Wnt/beta-catenin signaling pathway was measured by Topflash luciferase reporter assay.RESULTS: The expression of CASC15 and beta-catenin was upregulated in melanoma tissues and cells. Knockdown of CASC15 suppressed Wnt/beta-catenin signaling pathway and inhibited beta-catenin expression. Furthermore, inhibition of CASC15 decreased proliferation and increased apoptosis of melanoma cells by downregulating Survivin and Bcl-2 and upregulating Bax in A375 and SK-MEL-28 cells. Silencing of CASC15 inhibited migration and invasion of melanoma cells by repressing EMT process.CONCLUSION: Our study demonstrated that CASC15 promoted the proliferation, migration, and invasion of melanoma cells via activating Wnt/beta-catenin signaling pathway, implying that CASC16 might be a potential therapeutic target and prognostic biomarker for melanoma.	31838468	RID06262	expression association	prognosis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Melanoma	CASC15	BAX	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);wnt/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664184-22654455	ENSG00000087088	NA	401237	581	LINC00340|lnc-SOX4-1	BCL2L4	Long Non-Coding RNA-CASC15 Promotes Cell Proliferation, Migration, and Invasion by Activating Wnt/beta-Catenin Signaling Pathway in Melanoma.Quantitative real-time polymerase chain reaction was applied to explore CASC15 and beta-catenin expression in melanoma tissues and cells. western blot was carried out to investigate beta-catenin, glycogen synthase kinase-3beta, Survivin, Bax, Bcl-2, and epithelial-mesenchymal transition (EMT)-related protein expression level. Cell proliferation, apoptosis, migration, and invasion were observed by colony formation assay, flow cytometry, and transwell migration and invasion assays, respectively. The activity of Wnt/beta-catenin signaling pathway was measured by Topflash luciferase reporter assay.RESULTS: The expression of CASC15 and beta-catenin was upregulated in melanoma tissues and cells. Knockdown of CASC15 suppressed Wnt/beta-catenin signaling pathway and inhibited beta-catenin expression. Furthermore, inhibition of CASC15 decreased proliferation and increased apoptosis of melanoma cells by downregulating Survivin and Bcl-2 and upregulating Bax in A375 and SK-MEL-28 cells. Silencing of CASC15 inhibited migration and invasion of melanoma cells by repressing EMT process.CONCLUSION: Our study demonstrated that CASC15 promoted the proliferation, migration, and invasion of melanoma cells via activating Wnt/beta-catenin signaling pathway, implying that CASC17 might be a potential therapeutic target and prognostic biomarker for melanoma.	31838468	RID06263	expression association	prognosis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cutaneous squamous carcinoma	TP53	PRECSIT	negatively-E	western blot	upregulation	qRT-PCR	GSE138232	NA	cancer progression(+);STAT3 signaling pathway(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Skin carcinoma	TF	lncRNA	ENSG00000141510	NA	ENSG00000255874	GRCh38_13:110863987-110870330	7157	283487	BCC7|BMFS5|LFS1|P53|TRP53	C13orf29|LINC00346|NCRNA00346	p53-Regulated Long Noncoding RNA PRECSIT Promotes Progression of Cutaneous Squamous Cell Carcinoma via STAT3 Signaling.The expression of LINC00346 was up-regulated in cSCC cells compared with normal human epidermal keratinocytes. Elevated expression of LINC00346 was noted in tumor cells in cSCC tissue sections in  vivo, as compared with cSCC in situ, and actinic keratosis by RNA in situ hybridization; and the expression in seborrheic keratosis and normal skin was very low. Immunohistochemical analysis of cSCC tissue sections and functional assays of cSCC cells in culture showed that LINC00346 expression is down-regulated by p53. Knockdown of LINC00346 inhibited invasion of cSCC cells in culture and suppressed growth of human cSCC xenografts in  vivo. Knockdown of LINC00346 inhibited expression of activated STAT3 and resulted in down-regulation of the expression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13. Based on these observations LINC00346 was named p53 regulated carcinoma-associated STAT3-activating long intergenic non-protein coding transcript (PRECSIT). These results identify PRECSIT as a new p53-regulated lncRNA, which promotes progression of cSCC via STAT3 signaling.	31837949	RID06264	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Acute myeloid leukemia	KCNQ1OT1	TSPAN3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);chemoresistance(+)	ceRNA(miR-193a-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000140391	NA	10984	10099	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	TM4-A|TM4SF8|TSPAN-3	LncRNA KCNQ1OT1 contributes to the progression and chemoresistance in acute myeloid leukemia by modulating Tspan3 through suppressing miR-193a-3p.The expression of KCNQ1OT1, miR-193a-3p, and Tspan3 was measured by qRT-PCRThe relationship between miR-193a-3p and KCNQ1OT1 or Tspan3 was predicted by bioinformatics tool Diana and verified by dual-luciferase reporter assay, RIP assay or RNA pull-down assay.KCNQ1OT1 and Tspan3 were up-regulated, while miR-193a-3p was down-regulated in ADR resistant AML samples and cells.KCNQ1OT1 knockdown reduced ADR resistance, inhibited proliferation, migration and invasion but promoted apoptosis of ADR resistant AML cells, miR-193a-3p inhibition reversed these effects. MiR-193a-3p was a target of KCNQ1OT1 and combined with Tspan3 3' untranslated region (3' UTR). Enrichment of miR-193a-3p decreased ADR resistance, inhibited proliferation, migration and invasion and stimulated apoptosis in ADR resistant AML cells, but Tspan3 overexpression overturned these impacts.KCNQ1OT1 aggravates AML progression and chemoresistance to ADR by inducing Tspan3 expression via adsorbing miR-193a-3p in ADR resistant AML cells, providing a theoretical basis for the treatment of AML with chemoresistance.	31837329	RID06265	ceRNA or sponge	chemoresistance	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD);UP(NSCLC);DATA(GSE117623,GSE74639,GSE104209)
Cervical cancer	PCGEM1	FBXW11	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);beta-catenin/TCF signaling pathway(+);NF-kB signaling pathway(+)	ceRNA(miR-182)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000072803	NA	64002	23291	LINC00071|NCRNA00071|PCAT9	BTRC2|BTRCP2|Fbw11|Fbw1b|FBXW1B|Hos|KIAA0696	The long noncoding RNA PCGEM1 promotes cell proliferation, migration and invasion via targeting the miR-182/FBXW11 axis in cervical cancer.qRT-PCRwas performed to investigate PCGEM1 expression levels in CC tissues and cell lines.MS2-binding sequences-MS2-binding protein-based RIP assay (MS2-RIP), RNA pull-down and Luciferase reporter assays were performed to investigate the interaction between PCGEM1 and miR-182. The association between miR-182 and F-box and WD repeat domain containing 11 (FBXW11) was verified by luciferase reporter assay.Our present study showed that PCGEM1 was significantly upregulated in CC tissues and cell lines. Overexpression of PCGEM1 was correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node, distant metastasis and poor prognosis in CC patients. Functionally, PCGEM1 promoted cell proliferation, cell cycle progression, migration and invasion, while suppressed cell apoptosis in CC cells. Further mechanistic investigation revealed that PCGEM1 associated with miR-182 and suppressed its expression. PCGEM1 could act as a competing endogenous (ceRNA) of oncogene F-box and WD repeat domain containing 11 (FBXW11) for miR-182 in CC cells. Additionally, PCGEM1 was capable to activate the NF-kB and beta-catenin/TCF signaling pathways, which was reversed by inhibition of FBXW11.In conclusion, our findings demonstrated that PCGEM1-miR-182-FBXW11 axis play an important role in CC progression, and indicated a promising therapeutic target for CC patients.	31832017	RID06266	ceRNA or sponge	metastasis,prognosis	UP(PAAD);DATA(GSE60407)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE41245)
Acute myeloid leukemia	CDKN2B-AS1	TP53BP2	positively-E	luciferase reporter assay;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-34a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000143514	NA	100048912	7159	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	53BP2|ASPP2|PPP1R13A	LncRNA ANRIL promotes cell proliferation, migration and invasion during acute myeloid leukemia pathogenesis via negatively regulating miR-34a.Expression patterns of ANRIL and miR-34a in the bone marrow (BM) samples and cell lines were determined using qRT-PCR The dual-luciferase reporter assay was employed to validate the relationship between miR-34a and Histone deacetylase 1 (HDAC1).The binding of E2 F1 (E2 F transcription factor 1) with gene promoter was analyzed by ChIP. Furthermore, the tumorigenicity of AML was determined by xenograft transplantation in nude mice.ANRIL was up-regulated both in the BM samples from AML patients and cell lines (HL-60 and THP-1), of which expression was negatively correlated with miR-34a expression.ANRIL knockdown inhibited cell proliferation, migration and invasion but promoted apoptosis of AML cells, while overexpression of miR-34a exerted opposite effects. miR-34a was verified as a downstream gene targeted by ANRIL. Moreover, HDAC1 was a direct target of miR-34a, and HDAC1 overexpression impaired the recruitment of E2 F1 to ASPP2 (apoptosis stimulating proteins of p53) gene promoter. ANRIL knockdown significantly inhibited the tumorigenesis of AML.ANRIL promotes AML development through HDAC1-mediated epigenetic suppression of ASPP2 via negatively regulating miR-34a, which might serve as a therapeutic target for AML treatment.	31830533	RID06267	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939)
Colorectal cancer	LINC00265	EGFR	positively-E	western blot	upregulation	sequencing	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000188185	GRCh38_7:39733430-39793092	ENSG00000146648	NA	349114	1956	NCRNA00265|NCRNA00265-1	ERBB|ERBB1|ERRP	Long Noncoding RNA LINC00265 Targets EGFR and Promotes Deterioration of Colorectal Cancer: A Comprehensive Study Based on Data Mining and in vitro Validation.Comprehensive bioinformatics analysis were performed to investigate the expression, clinical significance and potential biologic functions of LINC00265 in CRC based on the data from the Cancer Genome Atlas (TCGA).To further investigate the potential role of LINC00265 in CRC, we knocked down the LINC00265 expression in HT29 cells. The cell proliferation, invasion, cycle distribution, and apoptosis were evaluated in control, NC and siRNA groups. Additionally, effect of LINC00265 on the expression of EGFR was also measured.The expression level of LINC00265 is increased in CRC tissues. Elevated level of LINC00265 is correlated with lymph node metastases and advanced pathological stage. We obtained 269 LINC00265 related genes; the results of functional analysis of these genes revealed that LINC00265 might involve in carcinogenesis of CRC. In addition, further experiments indicated that LINC00265 knockdown impaired cell proliferation and invasion, promoted cell cycle distribution and apoptosis in HT29 cells. Moreover, western blotrevealed that downregulation of LINC00265 suppressed the expression of EGFR.Our results indicate that LINC00265 induces cell proliferation, migration and inhibits CRC cells apoptosis by targeting EGFR. LINC00265 could be served as a diagnostic factor and therapeutic target for CRC patients.	31824175	RID06268	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Endometrial cancer	lncRNA-14327.1	KCNN4	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	protein stability	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	NA	NA	ENSG00000104783	NA	NA	3783	NA	DHS2|IK|IK1|IKCA1|KCA4|KCa3.1|SK4|hIKCa1|hKCa4|hSK4	The Long Non-Coding RNA-14327.1 Promotes Migration and Invasion Potential of Endometrial Carcinoma Cells by Stabilizing the Potassium Channel Kca3.1.The Kca3.1 binding candidate lncRNAs were screened using RNA immunoprecipitation sequencing assay in the endometrial carcinoma cell line.The overexpression efficiency of the lncRNAs was detected by qRT-PCRSeveral Kca3.1 binding lncRNAs were obtained from RNA immunoprecipitation sequencing assay. Stable expression of lncRNA-14327.1, one of the candidate lncRNAs, led to significant upregulation of Kca3.1 protein level, cell migration and invasion abilities, but suppressed cell proliferation and induced cell cycle arrest. Additionally, our data also demonstrated that Lenti-lncRNA-14327.1 could stabilize the protein of Kca3.1 and subsequently increase intracellular Ca2+ concentration.Taken together, our results demonstrated that the lncRNA-14327.1 promoted cell migration and invasion potential of endometrial carcinoma cells by stabilizing Kca3.1 protein, implying that the lncRNA-14327.1/Kca3.1 might be a promising therapeutic target in endometrial carcinoma, particularly the metastatic one.	31819513	RID06269	interact with protein	metastasis		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE51827,GSE67939,GSE86978)
Malignant glioma	HOXA-AS2	RND3	negatively-E	luciferase reporter assay;RIP;RNA-protein pull down assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000115963	NA	285943	390	HOXA3as	ARHE|Rho8|RhoE	Long Non-Coding RNA HOXA-AS2 Enhances The Malignant Biological Behaviors In Glioma By Epigenetically Regulating RND3 Expression.The expression of HOXA-AS2 and RND3 mRNA was determined using qRT-PCRanalysis. Dual-luciferase reporter, RIP, RNA-protein pull down and ChIP assays were performed to explore the molecular mechanism of HOXA-AS2 in glioma.HOXA-AS2 expression was increased in glioma tissues and cells. High HOXA-AS2 expression was associated with larger tumor size and advanced pathological stage. Functionally, knockdown of HOXA-AS2 suppressed cell proliferation and invasion, and promoted apoptosis. Mechanically, HOXA-AS2 epigenetically inhibited RND3 transcription by binding to EZH2. Moreover, overexpression of RND3 exerted similar tumor-suppressive effects to the depletion of HOXA-AS2. Furthermore, the anti-cancer effects induced by si-HOXA-AS2 were greatly reversed by silencing of RND3. Finally, knockdown of HOXA-AS2 impaired tumor growth in vivo possibly via increasing RND3 expression.Taken together, HOXA-AS2 recruits EZH2 to the promoter region of RND3 and inhibits its expression, thereby facilitating glioma progression. Our findings provide a prospective therapeutic strategy for glioma intervention.	31819475	RID06270	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065,GSE55807)
Colon adenocarcinoma	ELFN1-AS1	Erk	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236081	GRCh38_7:1738630-1742291	NA	NA	101927125	NA	MYCLo-2	NA	Extracellular vesicles from human umbilical cord mesenchymal stem cells treated with siRNA against ELFN1-AS1 suppress colon adenocarcinoma proliferation and migration. We found that ELFN1-AS1 levels were obviously increased in COAD patients and COAD tumor cells.Knockdown of ELFN1-AS1 expression by siRNA inhibited COAD cell proliferation and migration. Moreover, silencing ELFN1-AS1 significantly reduced the activation of extracellular signal-regulated protein kinase (Erk), up-regulated the protein expression of E-cadherin and down-regulated vimentin. In addition, we treated human umbilical cord mesenchymal stem cells (hUCMSCs) with siRNA-ELFN1-AS1 and found that EVs from siRNA-ELFN1-AS1-treated hUCMSCs could inhibit COAD cell proliferation and migration in vitro. These findings suggested that ELFN1-AS1 could promote the progression of COAD and that hUCMSC-EVs might be an attractive vehicle for the clinical administration of lncRNA-specific siRNAs in patients with COAD.	31814902	RID06271	expression association	NA	UP(SKCM);DATA(GSE38495)	
Colon adenocarcinoma	ELFN1-AS1	IRS1	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236081	GRCh38_7:1738630-1742291	ENSG00000169047	NA	101927125	3667	MYCLo-2	HIRS-1	Extracellular vesicles from human umbilical cord mesenchymal stem cells treated with siRNA against ELFN1-AS1 suppress colon adenocarcinoma proliferation and migration. We found that ELFN1-AS1 levels were obviously increased in COAD patients and COAD tumor cells.Knockdown of ELFN1-AS1 expression by siRNA inhibited COAD cell proliferation and migration. Moreover, silencing ELFN1-AS1 significantly reduced the activation of extracellular signal-regulated protein kinase (Erk), up-regulated the protein expression of E-cadherin and down-regulated vimentin. In addition, we treated human umbilical cord mesenchymal stem cells (hUCMSCs) with siRNA-ELFN1-AS1 and found that EVs from siRNA-ELFN1-AS1-treated hUCMSCs could inhibit COAD cell proliferation and migration in vitro. These findings suggested that ELFN1-AS2 could promote the progression of COAD and that hUCMSC-EVs might be an attractive vehicle for the clinical administration of lncRNA-specific siRNAs in patients with COAD.	31814902	RID06272	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Colon adenocarcinoma	ELFN1-AS1	vimentin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	NA	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236081	GRCh38_7:1738630-1742291	NA	NA	101927125	NA	MYCLo-2	NA	Extracellular vesicles from human umbilical cord mesenchymal stem cells treated with siRNA against ELFN1-AS1 suppress colon adenocarcinoma proliferation and migration. We found that ELFN1-AS1 levels were obviously increased in COAD patients and COAD tumor cells.Knockdown of ELFN1-AS1 expression by siRNA inhibited COAD cell proliferation and migration. Moreover, silencing ELFN1-AS1 significantly reduced the activation of extracellular signal-regulated protein kinase (Erk), up-regulated the protein expression of E-cadherin and down-regulated vimentin. In addition, we treated human umbilical cord mesenchymal stem cells (hUCMSCs) with siRNA-ELFN1-AS1 and found that EVs from siRNA-ELFN1-AS1-treated hUCMSCs could inhibit COAD cell proliferation and migration in vitro. These findings suggested that ELFN1-AS3 could promote the progression of COAD and that hUCMSC-EVs might be an attractive vehicle for the clinical administration of lncRNA-specific siRNAs in patients with COAD.	31814902	RID06273	expression association	NA	UP(SKCM);DATA(GSE38495)	
Malignant glioma	ZFAT-AS1	CDX2	negatively-E	RIP;RNA pull-down assay;western blot;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000248492	GRCh38_8:134598071-134600689	ENSG00000165556	NA	594840	1045	NCRNA00070|SAS-ZFAT|ZFAT-AS|ZFATAS	CDX3	DGCR8/ZFAT-AS1 Promotes CDX2 Transcription in a PRC2 Complex-Dependent Manner to Facilitate the Malignant Biological Behavior of Glioma Cells.In the present study, DGCR8 and CDX2 were highly expressed and ZFAT-AS1 was markedly downregulated in glioma tissues and cells. DGCR8 or CDX2 knockdown or ZFAT-AS1 overexpression suppressed glioma cell proliferation, migration, and invasion and facilitated apoptosis. DGCR8 might decrease ZFAT-AS1 expression by attenuating its stability in a manner of inducing its cleavage. Importantly, ZFAT-AS1 could inhibit CDX2 transcription by mediating the methylation of histone H3 on lysine 27 (H3K27me3) modification induced by PRC2 in the CDX2 promoter region. In addition, CDX2 transcriptionally activated DGCR8 expression by binding to its promoter regions, forming a positive feedback loop of DGCR8/ZFAT-AS1/CDX2. In conclusion, DGCR8/ZFAT-AS1 promotes CDX2 transcription in a PRC2 complex-dependent manner to facilitate the malignant biological behavior of glioma cells.	31813799	RID06274	transcriptional regulation	NA		
Malignant glioma	DGCR8	ZFAT-AS1	negatively-E	RIP;RNA pull-down assay;western blot;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	RNA stability	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000128191	NA	ENSG00000248492	GRCh38_8:134598071-134600689	54487	594840	C22orf12|DGCRK6|Gy1|pasha	NCRNA00070|SAS-ZFAT|ZFAT-AS|ZFATAS	DGCR8/ZFAT-AS1 Promotes CDX2 Transcription in a PRC2 Complex-Dependent Manner to Facilitate the Malignant Biological Behavior of Glioma Cells.In the present study, DGCR8 and CDX2 were highly expressed and ZFAT-AS1 was markedly downregulated in glioma tissues and cells. DGCR8 or CDX2 knockdown or ZFAT-AS1 overexpression suppressed glioma cell proliferation, migration, and invasion and facilitated apoptosis. DGCR8 might decrease ZFAT-AS1 expression by attenuating its stability in a manner of inducing its cleavage. Importantly, ZFAT-AS1 could inhibit CDX2 transcription by mediating the methylation of histone H3 on lysine 27 (H3K27me3) modification induced by PRC2 in the CDX2 promoter region. In addition, CDX2 transcriptionally activated DGCR8 expression by binding to its promoter regions, forming a positive feedback loop of DGCR8/ZFAT-AS1/CDX2. In conclusion, DGCR8/ZFAT-AS1 promotes CDX2 transcription in a PRC3 complex-dependent manner to facilitate the malignant biological behavior of glioma cells.To clarify the relationship between DGCR8 and ZFAT-AS1, using the bioinformatics database starBase v2.0, it was predicted that ZFAT-AS1 harbored a binding sequence of DGCR8 and FUS, but the influence of FUS on ZFAT-AS1 was not significant (Figures S1G and S1H). To validate this hypothesis, we performed an RNA immunoprecipitation (RIP) assay. Results of the RIP assay showed that the enrichment of ZFAT-AS1 was significantly increased in the anti-DGCR8 group compared with the negative control anti-normal immunoglobulin (Ig)G group and the negative RNA control GAPDH (Figures 2A and 2B).	31813799	RID06275	interact with mRNA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	
Non-small cell lung cancer	LINC01088	EZH2	positively-E	RIP;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249307	GRCh38_4:78939485-79309673	ENSG00000106462	NA	100505875	2146	NA	ENX-1|EZH1|KMT6|KMT6A	linc01088 promotes cell proliferation by scaffolding EZH2 and repressing p21 in human non-small cell lung cancer.The expression patterns of linc01088, p21 and EZH2 were examined both in NSCLC tissues and cell lines using RT-qPCR assay.RNA immunoprecipitation (RIP) assay was performed to determine the direct binding relationship between linc01088 and zeste homolog 2 (EZH2).western blot and RT-qPCR analysis were performed to assess p21 level within knockdown of either linc01088 or EZH2.linc01088 and EZH2 were highly expressed both in NSCLC tissues and cell lines. Knockdown of linc01088 suppressed the proliferation of NSCLC cells, and prolonged the G1 phase while shortened S and G2-M phases. RIP assay revealed the direct binding relationship between linc01088 and EZH2. Knockdown of either linc01088 or EZH2 induced up-regulation of p21 expression, which subsequently inhibited the tumor growth.We demonstrated that linc01088 could promote cell proliferation via binding with EZH2 to repress p21, which aggravates the tumorigenesis of NSCLC. Therefore, linc01088 might be a potential oncogene and target for novel anti-tumor therapies.	31811854	RID06276	interact with protein	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	LINC01088	CDKN1A	negatively-E	RIP;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249307	GRCh38_4:78939485-79309673	ENSG00000124762	NA	100505875	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	linc01088 promotes cell proliferation by scaffolding EZH2 and repressing p21 in human non-small cell lung cancer.The expression patterns of linc01088, p21 and EZH2 were examined both in NSCLC tissues and cell lines using RT-qPCR assay.RNA immunoprecipitation (RIP) assay was performed to determine the direct binding relationship between linc01088 and zeste homolog 2 (EZH2).western blot and RT-qPCR analysis were performed to assess p21 level within knockdown of either linc01088 or EZH2.linc01088 and EZH2 were highly expressed both in NSCLC tissues and cell lines. Knockdown of linc01088 suppressed the proliferation of NSCLC cells, and prolonged the G1 phase while shortened S and G2-M phases. RIP assay revealed the direct binding relationship between linc01088 and EZH2. Knockdown of either linc01088 or EZH2 induced up-regulation of p21 expression, which subsequently inhibited the tumor growth.We demonstrated that linc01088 could promote cell proliferation via binding with EZH2 to repress p21, which aggravates the tumorigenesis of NSCLC. Therefore, linc01089 might be a potential oncogene and target for novel anti-tumor therapies.	31811854	RID06277	expression association	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Oesophageal squamous cell carcinoma	LINC01518	PIK3CA	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);PIK3CA/AKT signaling pathway(+)	ceRNA(miR-1-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000233515	GRCh38_10:42644445-42691723	ENSG00000121879	NA	101929397	5290	NA	PI3K	LINC01518 knockdown inhibits tumorigenicity by suppression of PIK3CA/Akt pathway in oesophageal squamous cell carcinoma.LINC01518 and miR-1-3p expression levels in ESCC cells were detected by qRT-PCR Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. The relationships between LINC01518, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and miR-1-3p were explored by luciferase reporter assay. The alteration of the PIK3CA/protein kinase B (Akt) pathway was examined by western blot. We found that LINC01518 expression was upregulated and miR-1-3p expression was downregulated in ESCC cells. LINC01518 knockdown inhibited cell proliferation and promoted apoptosis in ESCC cells. In addition, LINC01518 functioned as a competing endogenous RNA (ceRNA) for miR-1-3p in ESCC cells and miR-1-3p downregulation blocked the effects of LINC01518 knockdown on cell proliferation and apoptosis in ESCC cells. Moreover, PIK3CA was identified as a target of miR-1-3p and LINC01518 knockdown inhibited the PIK3CA/Akt pathway by upregulating miR-1-3p in ESCC cells. In conclusion, LINC01518 knockdown inhibited tumorigenicity in ESCC cells by suppression of PIK3CA/Akt pathway through upregulating miR-1-3p.	31810385	RID06278	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Colorectal cancer	STARD13-AS	Cyclin E	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236581	GRCh38_13:33180401-33281584	NA	NA	100874241	NA	STARD13-AS2	NA	Long Non-Coding RNA STARD13-AS Suppresses Cell Proliferation And Metastasis In Colorectal Cancer.Bioinformatics prediction and qRT-PCRresults showed that STARD13-AS expression was decreased in CRC tissues. Patients with low STARD13-AS expression exhibited distant and lymphatic metastasis as well as enhancement in tumor size. STARD13-AS expression was downregulated in CRC cell lines compared to normal human colon mucosal epithelial cell line NCM460 and STARD13-AS expression in SW620 and LoVo cell lines was lowest. Moreover, we observed that while STARD13-AS overexpression suppressed the cell cycle, proliferation, migration, and invasion, while promoted apoptosis both in LoVo and SW620 cells. In addition, STARD13-AS overexpression inhibited Cyclin E, Cyclin D, N-cadherin and vimentin expression, and promoted E-cadherin expression both in LoVo and SW620 cells.Expression of STARD13-AS suppresses cell proliferation and metastasis in CRC, suggesting that STARD13-AS might act as a potential target for CRC treatment.	31807011	RID06279	expression association	metastasis		
Colorectal cancer	STARD13-AS	Cyclin D	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236581	GRCh38_13:33180401-33281584	NA	NA	100874241	NA	STARD13-AS2	NA	Long Non-Coding RNA STARD13-AS Suppresses Cell Proliferation And Metastasis In Colorectal Cancer.Bioinformatics prediction and qRT-PCRresults showed that STARD13-AS expression was decreased in CRC tissues. Patients with low STARD13-AS expression exhibited distant and lymphatic metastasis as well as enhancement in tumor size. STARD13-AS expression was downregulated in CRC cell lines compared to normal human colon mucosal epithelial cell line NCM460 and STARD13-AS expression in SW620 and LoVo cell lines was lowest. Moreover, we observed that while STARD13-AS overexpression suppressed the cell cycle, proliferation, migration, and invasion, while promoted apoptosis both in LoVo and SW620 cells. In addition, STARD13-AS overexpression inhibited Cyclin E, Cyclin D, N-cadherin and vimentin expression, and promoted E-cadherin expression both in LoVo and SW620 cells.Expression of STARD13-AS suppresses cell proliferation and metastasis in CRC, suggesting that STARD14-AS might act as a potential target for CRC treatment.	31807011	RID06280	expression association	metastasis		
Colorectal cancer	STARD13-AS	N-cadherin	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236581	GRCh38_13:33180401-33281584	NA	NA	100874241	NA	STARD13-AS2	NA	Long Non-Coding RNA STARD13-AS Suppresses Cell Proliferation And Metastasis In Colorectal Cancer.Bioinformatics prediction and qRT-PCRresults showed that STARD13-AS expression was decreased in CRC tissues. Patients with low STARD13-AS expression exhibited distant and lymphatic metastasis as well as enhancement in tumor size. STARD13-AS expression was downregulated in CRC cell lines compared to normal human colon mucosal epithelial cell line NCM460 and STARD13-AS expression in SW620 and LoVo cell lines was lowest. Moreover, we observed that while STARD13-AS overexpression suppressed the cell cycle, proliferation, migration, and invasion, while promoted apoptosis both in LoVo and SW620 cells. In addition, STARD13-AS overexpression inhibited Cyclin E, Cyclin D, N-cadherin and vimentin expression, and promoted E-cadherin expression both in LoVo and SW620 cells.Expression of STARD13-AS suppresses cell proliferation and metastasis in CRC, suggesting that STARD15-AS might act as a potential target for CRC treatment.	31807011	RID06281	expression association	metastasis		
Colorectal cancer	STARD13-AS	vimentin	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236581	GRCh38_13:33180401-33281584	NA	NA	100874241	NA	STARD13-AS2	NA	Long Non-Coding RNA STARD13-AS Suppresses Cell Proliferation And Metastasis In Colorectal Cancer.Bioinformatics prediction and qRT-PCRresults showed that STARD13-AS expression was decreased in CRC tissues. Patients with low STARD13-AS expression exhibited distant and lymphatic metastasis as well as enhancement in tumor size. STARD13-AS expression was downregulated in CRC cell lines compared to normal human colon mucosal epithelial cell line NCM460 and STARD13-AS expression in SW620 and LoVo cell lines was lowest. Moreover, we observed that while STARD13-AS overexpression suppressed the cell cycle, proliferation, migration, and invasion, while promoted apoptosis both in LoVo and SW620 cells. In addition, STARD13-AS overexpression inhibited Cyclin E, Cyclin D, N-cadherin and vimentin expression, and promoted E-cadherin expression both in LoVo and SW620 cells.Expression of STARD13-AS suppresses cell proliferation and metastasis in CRC, suggesting that STARD16-AS might act as a potential target for CRC treatment.	31807011	RID06282	expression association	metastasis		
Colorectal cancer	STARD13-AS	E-cadherin	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236581	GRCh38_13:33180401-33281584	NA	NA	100874241	NA	STARD13-AS2	NA	Long Non-Coding RNA STARD13-AS Suppresses Cell Proliferation And Metastasis In Colorectal Cancer.Bioinformatics prediction and qRT-PCRresults showed that STARD13-AS expression was decreased in CRC tissues. Patients with low STARD13-AS expression exhibited distant and lymphatic metastasis as well as enhancement in tumor size. STARD13-AS expression was downregulated in CRC cell lines compared to normal human colon mucosal epithelial cell line NCM460 and STARD13-AS expression in SW620 and LoVo cell lines was lowest. Moreover, we observed that while STARD13-AS overexpression suppressed the cell cycle, proliferation, migration, and invasion, while promoted apoptosis both in LoVo and SW620 cells. In addition, STARD13-AS overexpression inhibited Cyclin E, Cyclin D, N-cadherin and vimentin expression, and promoted E-cadherin expression both in LoVo and SW620 cells.Expression of STARD13-AS suppresses cell proliferation and metastasis in CRC, suggesting that STARD17-AS might act as a potential target for CRC treatment.	31807011	RID06283	expression association	metastasis		
Non-small cell lung cancer	CERNA2	SYF2	positively-E	Luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell cycle(+);cell proliferation(+)	ceRNA(miR-621)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000117614	NA	642934	25949	HOST2	CBPIN|DKFZp564O2082|fSAP29|NTC31|p29	LncRNA HOST2 enhances gefitinib-resistance in non-small cell lung cancer by down-regulating miRNA-621.The relative expression levels of HOST2, miRNA-621 and SYF2 in NSCLC cell lines were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR.Meanwhile, the binding relationship between miRNA-621 to HOST2 and SYF2 was verified by Dual-Luciferase reporter gene assay.HOST2 showed significantly greater abundance in gefitinib-resistant PC9 cells (PC9/GR) relative to parental cells.The up-regulation of HOST2 markedly enhanced gefitinib-resistance, the proliferative ability and cell cycle progression of PC9 cells. Subsequent Dual-Luciferase reporter gene assay showed the binding relationship between HOST2 and miRNA-621. Moreover, miRNA-621 was lowly expressed in PC9/GR cells compared with parental cells. Up-regulation of miRNA-621 significantly suppressed the proliferative ability and cell cycle progression, as well as reversed gefitinib-sensitivity of PC9 cells. More importantly, miRNA-621 up-regulation abolished the biological function of HOST2 in NSCLC. SYF2 was confirmed as the target gene of miRNA-621 in the same way. In addition, the overexpression of SYF2 remarkably enhanced gefitinib-resistance, while reversed the inhibitory effects of miRNA-621 on the proliferative ability and cell cycle of NSCLC cells.HOST2 elevates gefitinib-resistance in NSCLC by degrading miRNA-621 to upregulate SYF2.	31799663	RID06284	ceRNA or sponge	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	LINRIS	IGF2BP2	negatively-E	RNA pull-down assay;RIP;Dual-luciferase reporter gene assay	upregulation	sequencing	NA	NA	cancer progression(+)	protein stability	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000073792	NA	NA	10644	NA	IMP-2|p62	LncRNA LINRIS stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer.The proteins that interact with LINRIS (Long Intergenic Noncoding RNA for IGF2BP2 Stability) were confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assays.LINRIS was upregulated in CRC tissues from patients with poor overall survival (OS), and LINRIS inhibition led to the impaired CRC cell line growth.knockdown of LINRIS resulted in a decreased level of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), a newly found N6-methyladenosine (m6A) 'reader'.LINRIS is an independent prognostic biomarker for CRC. The LINRIS-IGF2BP2-MYC axis promotes the progression of CRC and is a promising therapeutic target.	31791342	RID06285	interact with protein	prognosis		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Prostate cancer	MEG3	EZH2	NA	RIP;western blot;ChIP	downregulation	qRT-PCR	GSE55909	NA	cell viability(-);cell migration(+);cell invasion(+);tumorigenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000106462	NA	55384	2146	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ENX-1|EZH1|KMT6|KMT6A	LncRNA MEG3 inhibits the progression of prostate cancer by facilitating H3K27 trimethylation of EN2 through binding to EZH2.Expressions of relative molecules were detected by Quantitative real time PCR (qRT-PCR and western blot. Chromatin immunoprecipitation and RNA immunoprecipitation (RIP) assays were used to evaluate the interaction between intra-nuclear MEG3, histone methyltransferase EZH2 and Engrailed-2 (EN2).EN2 expression was inversely proportional to MEG3 in the prostate cancer tissues and PC3 cells. RIP results showed that intra-nuclear MEG3 could bind to EZH2. Knockdown of MEG3 and/or EZH2 up-regulated EN2 expression and reduced the recruitment of EZH2 and H3K27me3 to EN2, while over-expressed MEG3 caused opposite effects. MEG3 over-expression suppressed cell viability, colony formation, cell invasion and migration of PC3 cells in vitro and inhibited tumourigenesis of PC3 cells in vivo, while EN2 over-expression diminished the effects. These findings indicated that MEG3 facilitated H3K27 trimethylation of EN2 via binding to EZH2, thus suppressed the development of prostate cancer.	31790140	RID06286	interact with protein	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Prostate cancer	MEG3	EN2	negatively-E	RIP;western blot	downregulation	qRT-PCR	GSE55909	NA	cell viability(-);cell migration(+);cell invasion(+);tumorigenesis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000164778	NA	55384	2020	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	LncRNA MEG3 inhibits the progression of prostate cancer by facilitating H3K27 trimethylation of EN2 through binding to EZH2.Expressions of relative molecules were detected by Quantitative real time PCR (qRT-PCR and western blot. Chromatin immunoprecipitation and RNA immunoprecipitation (RIP) assays were used to evaluate the interaction between intra-nuclear MEG3, histone methyltransferase EZH2 and Engrailed-2 (EN2).EN2 expression was inversely proportional to MEG3 in the prostate cancer tissues and PC3 cells. RIP results showed that intra-nuclear MEG3 could bind to EZH2. Knockdown of MEG3 and/or EZH2 up-regulated EN2 expression and reduced the recruitment of EZH2 and H3K27me3 to EN2, while over-expressed MEG3 caused opposite effects. MEG3 over-expression suppressed cell viability, colony formation, cell invasion and migration of PC3 cells in vitro and inhibited tumourigenesis of PC3 cells in vivo, while EN2 over-expression diminished the effects. These findings indicated that MEG3 facilitated H3K27 trimethylation of EN2 via binding to EZH3, thus suppressed the development of prostate cancer.	31790140	RID06287	expression association	NA		UP(LIHC);DATA(GSE117623)
Pancreatic ductal adenocarcinoma	LUCAT1	MIR539	negatively-F	RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000202560	NA	100505994	664612	SCAL1|SCAT5	MIRN539|hsa-mir-539|mir-539	LncRNA LUCAT1 contributes to cell proliferation and migration in human pancreatic ductal adenocarcinoma via sponging miR-539.Here we initially analyzed the expression patterns of lncRNA LUCAT1 and evaluated its clinical significance. The qRT-PCRanalysis and in situ hybridization staining showed that lncRNA LUCAT1 expression was significantly increased in tumorous tissues compared with adjacent normal tissues. Additionally, we found that increased lncRNA LUCAT1 expression was linked to larger tumor size and lymphatic invasion. Consistently, lncRNA LUCAT1 was remarkably up-regulated in PDAC cell lines. To better understand the biological role of lncRNA LUCAT1, we evaluated the effects of lncRNA LUCAT1 knockdown on PDAC cell proliferation, cell cycle progression, migration, and invasion using MTT assays, flow cytometry, Transwell migration, and invasion assays, respectively. Functional studies demonstrated that lncRNA LUCAT1 knockdown dramatically suppressed PDAC cell proliferation, induced cell cycle arrest and inhibited cell migration and invasion. Tumor xenograft in vivo assays displayed that lncRNA LUCAT1 inhibited tumorigenecity of PDAC cells. Mechanistic studies uncovered that lncRNA LUCAT1 acted as a molecular sponge of miR-539 and that miR-539 mediated the effects of lncRNA LUCAT1 on PDAC cell proliferation, cell cycle progression, and motility. Collectively, our findings may offer some novel insights into understanding lncRNA LUCAT1 in PDAC.	31789465	RID06288	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Urinary bladder cancer	NNT-AS1	PODXL	positively-E	starBase;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);WNT signaling pathway(+)	ceRNA(miR-1301-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000128567	NA	100652772	5420	RP11-159F24.1	gp135|Gp200|PC|PCLP|PDX|PODXL1	NNT-AS1 enhances bladder cancer cell growth by targeting miR-1301-3p/PODXL axis and activating Wnt pathway. Here, we found that NNT-AS1 was upregulated in BC cells.Later, miR-1301-3p, the downstream gene of NNT-AS1, was found at a low level in BC cells. In addition, we found that miR-1301-3p targeted to PODXL.PODXL expression downregulated in NNT-AS1-silenced cells was restored by miR-1301-3p inhibition. Importantly, NNT-AS1 was discovered to activate Wnt pathway, and the treatment of LiCl recovered the repressive role of NNT-AS1 silencing in BC cell growth. Through restoration assays, we observed that PODXL overexpressing countervailed NNT-AS1 depletion-mediated suppression on BC cell growth and Wnt pathway. These data suggested that NNT-AS1 enhances BC cell growth and activates Wnt pathway by targeting miR-1301-3p/PODXL axis.	31782983	RID06289	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	UP(PAAD);DOWN(PAAD);DATA(GSE40174,GSE60407)
Hepatocellular carcinoma	MYCNOS	PREX2	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-340)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233718	GRCh38_2:15918350-15942249	ENSG00000046889	NA	10408	80243	MYCN-AS1|N-CYM|NCYM	DEP.2|DEPDC2|FLJ12987|P-REX2|PPP1R129	LncRNA MYCNOS facilitates proliferation and invasion in hepatocellular carcinoma by regulating miR-340.In the present study, MYCNOS was up-regulated in both HCC tissues and cell lines, and elevated MYCNOS expression was correlated to shorter survival time of HCC patients.In addition, MYCNOS acted as a negative regulator of miR-340 in HCC cells, and all effects of MYCNOS knockdown were abrogated by further miR-340 inhibition. We also discovered that oncogene phosphatidylinositol-3, 4, 5-trisphosphate-dependent Rac exchange factor 2 (PREX2) was a downstream target of miR-340, and PREX2 expression was positively correlated to that of MYCNOS in HCC tissues. In conclusion, our findings demonstrated that MYCNOS knockdown inhibited HCC progression through regulating miR-340.MYCNOS knockdown significantly inhibited proliferation in HCC cells in vitro accompanied by exacerbated cell apoptosis; it also suppressed tumor growth in mouse model in vivo.	31776854	RID06290	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Esophagus squamous cell carcinoma	ZFAS1	STAT3	positively-E	RIP;luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000168610	NA	441951	6774	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	APRF	Exosomal lncRNA ZFAS1 regulates esophageal squamous cell carcinoma cell proliferation, invasion, migration and apoptosis via microRNA-124/STAT3 axis.LncRNA ZFAS1 was upregulated and miR-124 was down-regulated in ESCC tissues.Silencing of ZFAS1 contributed to suppressed proliferation, migration, invasion and tumor growth in vitro and induced apoptosis of ESCC cells. LncRNA ZFAS1 was considered to be a competing endogenous RNA to regulate miR-124, thereby elevating STAT3 expression. Exosomes shuttled ZFAS1 stimulated proliferation, migration and invasion of ESCC cells and restricted their apoptosis with increased STAT3 and declined miR-124. Furthermore, in vivo experiment suggested that elevated ZFAS1-exo promoted tumor growth in nude mice.This study highlights that exosomal ZFAS1 promotes the proliferation, migration and invasion of ESCC cells and inhibits their apoptosis by upregulating STAT3 and downregulating miR-124, thereby resulting in the development of tumorigenesis of ESCC.	31775815	RID06291	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical cancer	SNHG16	SPI1	NA	RIP;luciferase reporter assay;western blot;ChIP	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000066336	NA	100507246	6688	Nbla10727|Nbla12061|ncRAN	OF|PU.1|SFPI1|SPI-1|SPI-A	Long noncoding RNA SNHG16 promotes the tumorigenicity of cervical cancer cells by recruiting transcriptional factor SPI1 to upregulate PARP9.Using the dual-luciferase reporter gene assay, RNA immunoprecipitation, chromatin immunoprecipitation, we were able to determine that SNHG16 recruited SPI1 protein to promote transcription of PARP9 to upregulate its transcription in cervical cancer cells.it was observed that silencing SNHG16 inhibited PARP9 expression, proliferation, and invasion of cervical cancer cells, which was rescued by co-transfection of SNHG16 silencing and PARP9 overexpression.Moreover, in vivo experimental results showed that silencing SNHG16 reduced the expression of PARP9 and suppressed tumor growth. These data indicate that SNHG16 recruits SPI1 to upregulate PARP9, which promotes the tumorigenicity of cervical cancer cells. The regulation of their expression might provide a new direction for treating cervical cancer.	31774223	RID06292	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	SNHG16	PARP9	positively-E	RIP;luciferase reporter assay;western blot;ChIP	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000138496	NA	100507246	83666	Nbla10727|Nbla12061|ncRAN	ARTD9|BAL|BAL1	Long noncoding RNA SNHG16 promotes the tumorigenicity of cervical cancer cells by recruiting transcriptional factor SPI1 to upregulate PARP9.Using the dual-luciferase reporter gene assay, RNA immunoprecipitation, chromatin immunoprecipitation, we were able to determine that SNHG16 recruited SPI1 protein to promote transcription of PARP9 to upregulate its transcription in cervical cancer cells.it was observed that silencing SNHG16 inhibited PARP9 expression, proliferation, and invasion of cervical cancer cells, which was rescued by co-transfection of SNHG16 silencing and PARP9 overexpression.Moreover, in vivo experimental results showed that silencing SNHG16 reduced the expression of PARP9 and suppressed tumor growth. These data indicate that SNHG16 recruits SPI1 to upregulate PARP10, which promotes the tumorigenicity of cervical cancer cells. The regulation of their expression might provide a new direction for treating cervical cancer.	31774223	RID06293	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE75367)
Uveal melanoma	PVT1	MDM2	positively-E	RIP;luciferase reporter assay;western blot;ChIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);p53 signaling pathway(+)	ceRNA(miR-17-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000135679	NA	5820	4193	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HDM2|MGC5370	Long Noncoding RNA PVT1 Silencing Prevents the Development of Uveal Melanoma by Impairing MicroRNA-17-3p-Dependent MDM2 Upregulation.Highly expressed lncRNA PVT1 and MDM2, yet lowly expressed miR-17-3p, were identified in ocular uveal melanoma tissues versus normal adjacent tissues. Then, dual luciferase reporter gene assay, RNA binding protein immunoprecipitation, and RNA pull-down assays showed that lncRNA PVT1 specifically bound to miR-17-3p, and that MDM2 was a target gene of miR-17-3p. Gain- and loss-of-function studies elucidated that silencing of lncRNA PVT1 or overexpression of miR-17-3p resulted in decreased MDM2 expression and increased transcriptional activity of p53, in addition to inhibiting uveal melanoma cell proliferation, migration, and invasion, yet promoted cell apoptosis in vitro. In addition, lncRNA PVT1 silencing or miR-17-3p overexpression was noted to inhibit tumor growth in vivo.Downregulation of lncRNA PVT1 could potentially promote miR-17-3p expression to suppress tumorigenesis and development of uveal melanoma by activating the p53 signaling pathway through binding to MDM2.	31770435	RID06294	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	FOXD2-AS1	CPEB4	positively-E	RIP;luciferase reporter assay;western blot;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);chemoresistance(+)	ceRNA(miR-98-5p)	regulation	RNA-protein	Trimetazidine	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000113742	NA	84793	80315	MGC12982	KIAA1673	Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis.Highly expressed FOXD2-AS1 was found in glioma. There was more powerful chemotherapeutic resistance of TMZ resistant cell lines than that of the parent cell lines. Silence of FOXD2-AS1 suppressed proliferation and drug resistance and promoted apoptosis of drug-resistant glioma cells. Overexpressed FOXD2-AS1 presented an opposite trend. FOXD2-AS1 could be used as a competing endogenous RNA to adsorb miR-98-5p, thereby up-regulating CPEB4.Our study suggests that down-regulated FOXD2-AS1 repressed invasion, proliferation, migration and drug resistance of drug-resistant glioma cells while stimulating their apoptosis via increasing miR-98-5p and inhibiting CPEB4 expression.	31770107	RID06295	ceRNA or sponge	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	MBNL1-AS1	PHLPP2	positively-E	luciferase reporter assay;western blot	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-135a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000229619	GRCh38_3:152245262-152269565	ENSG00000040199	NA	401093	23035	LOC401093	KIAA0931|PHLPPL|PPM3B	LncRNA MBNL1-AS1 represses cell proliferation and enhances cell apoptosis via targeting miR-135a-5p/PHLPP2/FOXO1 axis in bladder cancer.The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO1 axis, providing a novel insight for BC diagnosis and treatment.	31769229	RID06296	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939)	UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MBNL1-AS1	FOXO1	positively-E	luciferase reporter assay;western blot	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-135a-6p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000229619	GRCh38_3:152245262-152269565	ENSG00000150907	NA	401093	2308	LOC401093	FKH1|FKHR|FOXO1A	LncRNA MBNL1-AS1 represses cell proliferation and enhances cell apoptosis via targeting miR-135a-5p/PHLPP2/FOXO1 axis in bladder cancer.The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO2 axis, providing a novel insight for BC diagnosis and treatment.	31769229	RID06297	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Pancreatic cancer	LINC01111	DUSP1	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	GSE61166;GSE89139;GSE86436;GSE100232;GSE101094;GSE57144;GSE71008	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	ceRNA(miR-3924)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000254300	GRCh38_8:76406654-76524356	ENSG00000120129	NA	101926978	1843	NA	CL100|HVH1|MKP-1|PTPN10	Long noncoding RNA LINC01111 suppresses pancreatic cancer aggressiveness by regulating DUSP1 expression via microRNA-3924.Here, we report a novel lncRNA, LINC01111, that is clearly downregulated in PC tissues and plasma of PC patients and acts as a tumor suppressor.The overexpression of LINC01111 significantly inhibited cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, the knockdown of LINC01111 enhanced cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo. Furthermore, we found that high expression levels of LINC01111 upregulated DUSP1 levels by sequestering miR-3924, resulting in the blockage of SAPK phosphorylation and the inactivation of the SAPK/JNK signaling pathway in PC cells and thus inhibiting PC aggressiveness. Overall, these data reveal that LINC01111 is a potential diagnostic biomarker for PC patients, and the newly identified LINC01111/miR-3924/DUSP1 axis can modulate PC initiation and development.	31767833	RID06298	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Gastric cancer	PRKCZ-AS1	CD209	negatively-E	western blot;TCGA	downregulation	qRT-PCR	NA	NA	JAK2/STAT3 signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000182873	GRCh38_1:2181794-2184389	ENSG00000090659	NA	100506504	30835	RP11-181G12.2	CDSIGN|CLEC4L|DC-SIGN|DC-SIGN1|hDC-SIGN	DC-SIGN mediates gastric cancer progression by regulating the JAK2/STAT3 signaling pathway and affecting LncRNA RP11-181G12.2 expression.Mechanistically, the relationship between DC-SIGN, RP11-181G12.2 and the JAK2/STAT3 signaling pathway was then investigated using qRT-PCRand western blot assays. Additionally, we analyzed DC-SIGN and RP11-181G12.2 expression levels in GC specimens based on the Cancer Genome Atlas database.In this study, the results showed that DC-SIGN was highly expressed in GC cells and significantly correlated with advanced clinical stage and lymphatic metastasis. Downregulation of DC-SIGN significantly inhibited the proliferation, cell cycle progression, migration and invasion of GC cells in vitro. The reverse results could partly be seen with the upregulation of DC-SIGN. Mechanistically, knockdown of DC-SIGN inactivated the JAK2/STAT3 signaling pathway, and overexpression of DC-SIGN activated the JAK2/STAT3 signaling pathway. In addition, through LncPath microarray analysis, we identified a lncRNA, RP11-181G12.2, that was significantly upregulated after knockdown of DC-SIGN; this was also confirmed by qRT-PCR Furthermore, RP11-181G12.2 knockdown enhanced DC-SIGN expression in GC cells, further activating the JAK2/STAT3 signaling pathway. In contrast, DC-SIGN overexpression suppressed RP11-181G12.2 expression.CONCLUSIONS: Our study suggests that DC-SIGN might be involved in the progression of GC by regulating the JAK2/STAT3 signaling pathway and affecting lncRNA RP11-181G12.2 expression.	31766099	RID06299	expression association	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Ovarian cancer	NCK1-DT	NCK1	positively-E	RIP;luciferase reporter assay;western blot	upregulation	sequencing	NA	NA	tumorigenesis(+);chemoresistance(+)	ceRNA(miR-137)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000158092	NA	101927597	4690	NCK1-AS1|SLC35G2-AS1	NCK|NCKalpha	NCK1-AS1 promotes NCK1 expression to facilitate tumorigenesis and chemo-resistance in ovarian cancer.As indicated by TCGA, NCK1-AS1 was markedly upregulated in OC tissues.Interestingly, silencing NCK1-AS1 confined cell proliferation, induced apoptosis and suppressed migration and invasion as well as enhanced DDP sensitivity in OC cells.As for mechanistic investigation, starBase suggested that NCK1-AS1 expression in OC tissues was significantly positively correlated with its adjacent gene, NCK adaptor protein 1 (NCK1).Furtherly, we demonstrated that the cytoplasmic NCK1-AS1 competed with NCK1 mRNA for miR-137 binding to boost NCK1 mRNA expression. Importantly, miR-137 inhibition could only offset the suppression of NCK1-AS1 depletion on NCK1 mRNA level but not the protein level. Moreover, NCK1-AS1 stabilized NCK1 protein by hindering c-Cbl-induced degradation via directly interacting with c-Cbl. Furthermore, NCK1 upregulation reversed the influences of NCK1-AS1 inhibition on the biological behaviors and DDP resistance of OC cells. This study disclosed a NCK1-AS1/NCK1 axis in regulating OC progression and chemo-resistance, opening a new path for treatment and chemo-resistance overcoming in OC.	31761329	RID06300	ceRNA or sponge	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	HAND2-AS1	PDCD4	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;western blot	downregulation	qRT-PCR	NA	NA	chemoresistance(-);cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-20a)	regulation	RNA-protein	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000150593	NA	79804	27250	DEIN|FLJ11539|NBLA00301	H731	LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer.Quantitative real-time polymerase chain reaction (qRT-PCR was performed to detect the expression of HAND2-AS1, miR-20a and programmed cell death factor 4 (PDCD4) mRNA.dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were utilized to verify the combination between miR-20a and HAND2-AS1. dual-luciferase reporter assay was used to analyze the association between miR-20a and PDCD4.HAND2-AS1 and PDCD4 were downregulated and miR-20a was upregulated in 5-FU-resistant CRC tissues and cells. HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. HAND2-AS1 acted as a sponge of miR-20a to regulate PDCD4 expression. Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Besides, HAND2-AS1 inhibited tumor growth in vivo.HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells.	31760170	RID06301	ceRNA or sponge	chemoresistance	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Hepatocellular carcinoma	HOXA11-AS	HOXA11	negatively-E	RNA pull-down assay;western blot	upregulation	sequencing	NA	NA	WNT signaling pathway(+)	DNA methylation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000005073	NA	221883	3207	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	HOX1|HOX1I	Silencing of long noncoding RNA HOXA11-AS inhibits the Wnt signaling pathway via the upregulation of HOXA11 and thereby inhibits the proliferation, invasion, and self-renewal of hepatocellular carcinoma stem cells.HCC stem cells showed high expression of HOXA11-AS and low expression of HOXA11. Both HOXA11-AS silencing and HOXA11 overexpression suppressed the self-renewal, proliferation, migration, and tumorigenicity of HCC stem cells in vivo, as evidenced by the decreased expression of cancer stem cell surface markers (CD133 and CD44) and stemness-related transcription factors (Nanog, Sox2, and Oct4). Moreover, silencing HOXA11-AS inactivated the Wnt signaling pathway by decreasing the methylation level of the HOXA11 promoter, thereby inhibiting HCC stem cell characteristics. Collectively, this study suggested that HOXA11-AS silencing exerts an antitumor effect, suppressing HCC development via Wnt signaling pathway inactivation by decreasing the methylation level of the HOXA11 promoter.	31757938	RID06302	epigenetic regulation	NA		
Oral squamous cell carcinoma	KCNQ1OT1	RAB14	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell migration(+);apoptosis process(-)	ceRNA(miR-185-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000119396	NA	10984	51552	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	FBP|RAB-14	KCNQ1OT1 promotes migration and inhibits apoptosis by modulating miR-185-5p/Rab14 axis in oral squamous cell carcinoma.KCNQ1OT1 expression in OSCC tissues and cells was examined by qRT-PCRThe binding region between KCNQ1OT1 and miR-185-5p was confirmed by luciferase assays. MiR-185-5p expression was measured by qRT-PCR Rab14 was confirmed as a downstream target gene of miR-185-5p by measuring luciferase activities.The protein level of Rab14 in OSCC cells transfected with miR-185-5p or si-KCNQ1OT1 was determined by western blot. The OSCC cell function and Rab14 expression after co-transfection of si-KCNQ1OT1 and miR-185-5p inhibitor were also examined. KCNQ1OT1 was upregulated in OSCC tissues and cells. KCNQ1OT1 silencing suppressed OSCC cell malignancy and downregulated miR-185-5p level, which showed upregulated expression in OSCC samples. Rab14 as a target gene of miR-185-5p was highly expressed in OSCC. KCNQ1OT1 knockdown impaired the invasion capability of OSCC cells, promoted apoptosis, and suppressed Rab14 expression. The inhibition of miR-185-5p in KCNQ1OT1 silencing cells reversed the suppression of Rab14 and restored the cancerous growth of OSCC cells. These results indicated that KCNQ1OT1 promoted OSCC tumorigenesis via the modulation of miR-185-5p/Rab14 axis, which may serve as a therapeutic target for the treatment of OSCC.	31755091	RID06303	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Laryngeal squamous cell carcinoma	CDKN2B-AS1	CDK6	positively-E	RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-497)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105810	NA	100048912	1021	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	PLSTIRE	Long Non-Coding RNA CDKN2B-AS1 Facilitates Laryngeal Squamous Cell Cancer Through Regulating miR-497/CDK6 Pathway.The expressions of CDKN2B-AS1, miR-497 and cyclin-dependent kinase 6 (CDK6) were detected in LSCC tissues and cell lines by real-time quantitative PCR (qRT-PCR.Bioinformatics analysis and luciferase activity assay were applied to analyze the interaction between CDKN2B-AS1 and miR-497.The expression of CDKN2B-AS1 was significantly higher in LSCC tissues than in adjacent normal tissues. Higher CDKN2B-AS1 was closely associated with lymph node metastasis and advanced clinical stage. Moreover, CDKN2B-AS1 knockdown by siRNA significantly inhibited the proliferation, induced cell apoptosis, and suppressed migration and invasion in LSCC cells. Mechanically, CDKN2B functions as an oncogenic lncRNA in LSCC via regulating miR-497/CDK6 axis.The observations in this study identify CDKN2B-AS1 an oncogenic role in the tumorigenesis of LSCC by regulating miR-497/CDK6 axis and indicate that it may serve as a potential target for LSCC treatment.	31754305	RID06304	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Medulloblastoma	CRNDE	miR-29c-3p	negatively-F	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	NA	Cancer	Medulloblastoma	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	643911	NA	CRNDEP|LINC00180|LOC643911	NA	Inhibition of Long Noncoding RNA CRNDE Increases Chemosensitivity of Medulloblastoma Cells by Targeting miR-29c-3p.RNA pull-down and RNA-binding protein immunoprecipitation (RIP) were performed to confirm the molecular interactions between CRNDE and miR-29c-3p involved in medulloblastoma cells. The in vivo role of CRNDE knockdown or miR-29c-3p overexpression on tumor growth and apoptosis was evaluated in a xenograft mouse model of human medulloblastoma. The transcript levels of lncRNA CRNDE were significantly higher in cisplatin-treated tumor cells with higher IC50 values.Depletion of CRNDE inhibited tumor cell proliferation and colony formation, induced cell apoptosis, and suppressed migration and invasion in medulloblastoma cells. Moreover, overexpression of miR-29c-3p inhibited tumor cell proliferation and colony formation, migration, and invasion, and enhanced apoptosis and chemosensitivity to cisplatin. In addition, CRNDE was found to act as a miR-29c-3p sponge. Furthermore, in vivo experiments showed the CRNDE/miR-29c-3p interactions involved in medulloblastoma. Our study demonstrates that CRNDE acts as a critical mediator of proliferation, apoptosis, migration, invasion, and resistance to chemotherapeutics via binding to and negatively regulating miR-29c-3p in medulloblastoma cells. These results provide novel molecular targets for treatment of medulloblastoma.	31753063	RID06305	ceRNA or sponge	chemoresistance	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	
Endometrial cancer	NEAT1	EZH2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-144-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ENX-1|EZH1|KMT6|KMT6A	LncRNA NEAT1 promotes endometrial cancer cell proliferation, migration and invasion by regulating the miR-144-3p/EZH2 axis.dual-luciferase reporter assay was used to verify the relationship among NEAT1, EZH2, and miR-144-3p. The expression level of EZH2 was measured by western blot and qPCR. Results NEAT1 was highly expressed in EC tissues and cells. Knockdown of NEAT1 inhibited the proliferation, migration and invasion of EC cells. Additionally, NEAT1 acted as a ceRNA of miR-144-3p, leading to EZH2 upregulation. Overexpression of miR-144-3p suppressed the proliferation and invasion of EC cells. Conclusions NEAT1 promotes EC cells proliferation and invasion by regulating the miR-144-3p/EZH2 axis.	31747378	RID06306	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Prostate cancer	HCP5	CEMIP	positively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-4656)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000103888	NA	10866	57214	D6S2650E|P5-1	HYBID|IR2155535|KIAA1199|TMEM2L	Long non-coding RNA HCP5 promotes prostate cancer cell proliferation by acting as the sponge of miR-4656 to modulate CEMIP expression.In the present study, we found the overexpressed expression of HCP5 in prostate cancer tissues and cell lines via RT-qPCR analysis.Functional experiments demonstrated that HCP5 acted as a competing endogenous RNA (ceRNA) to sponge miR-4656. Ectopic expression of HCP5 decreased the expression of miR-4656 in prostate cancer cells. MiR-4656 was found to be decreased in prostate cancer tissues and was negatively correlated with the expression of HCP5. Further luciferase reporter assay revealed that miR-4656 was able to bind the 3'-untranslated region (3'-UTR) of the cell migration inducing hyaluronidase 1 (CEMIP) and suppressed the expression of CEMIP.Consistent with the negative regulation of miR-4656 by HCP5, western blotuncovered that overexpression of HCP5 upregulated the abundance of CEMIP in prostate cancer cells. The CCK-8 assay showed that depletion of CEMIP significantly inhibited the HCP5-promoted proliferation of prostate cancer cells. Collectively, our data provide a novel mechanism by which HCP5 regulates the progression of prostate cancer.	31746434	RID06307	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	TP53	uc061hsf.1	positively-E	UCSC;PROMO;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000141510	NA	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	NA	P53-regulated lncRNA uc061hsf.1 inhibits cell proliferation and metastasis in human esophageal squamous cell cancer.The expression of lncRNA-uc061hsf.1 in ESCC tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR.The interaction between p53 and lncRNA uc061hsf.1 was analyzed using luciferase reporter gene and qRT-PCRThrough this approach, we identified the novel lncRNA uc061hsf.1, which was expressed in low level in ESCC and was correlated with lymph node metastasis and poor differentiation in ESCC patients. Knockdown or overexpression of lncRNA uc061hsf.1 in ESCC cells promoted or inhibited cell proliferation and metastasis, respectively. Mechanistically, lncRNA uc061hsf.1 was induced by p53, and luciferase reporter gene confirmed that lncRNA uc061hsf.1 was a direct transcriptional target of p53. We further found that uc061hsf.1 was able to regulate expression of the transcription factor FoxA1, thereby potentially influencing tumor cell migration. In conclusion, these results suggest that p53-regulated lncRNA uc061hsf.1 is a cancer suppressor gene which is associated with tumor progression in ESCC.	31743955	RID06308	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	uc061hsf.1	FOXA1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	NA	NA	ENSG00000129514	NA	NA	3169	NA	HNF3A|TCF3A	P53-regulated lncRNA uc061hsf.1 inhibits cell proliferation and metastasis in human esophageal squamous cell cancer.The expression of lncRNA-uc061hsf.1 in ESCC tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR.The interaction between p53 and lncRNA uc061hsf.1 was analyzed using luciferase reporter gene and qRT-PCRThrough this approach, we identified the novel lncRNA uc061hsf.1, which was expressed in low level in ESCC and was correlated with lymph node metastasis and poor differentiation in ESCC patients. Knockdown or overexpression of lncRNA uc061hsf.1 in ESCC cells promoted or inhibited cell proliferation and metastasis, respectively. Mechanistically, lncRNA uc061hsf.1 was induced by p53, and luciferase reporter gene confirmed that lncRNA uc061hsf.1 was a direct transcriptional target of p53. We further found that uc061hsf.1 was able to regulate expression of the transcription factor FoxA1, thereby potentially influencing tumor cell migration. In conclusion, these results suggest that p53-regulated lncRNA uc061hsf.2 is a cancer suppressor gene which is associated with tumor progression in ESCC.	31743955	RID06309	expression association	metastasis		UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Osteosarcoma	SNHG12	IGF1R	positively-E	luciferase reporter assay;;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell growth(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000140443	NA	85028	3480	ASLNC04080|C1orf79|LINC00100|PNAS-123	CD221|IGFIR|IGFR|JTK13|MGC18216	Downregulation of lncRNA SNHG12 reversed IGF1R-induced osteosarcoma metastasis and proliferation by targeting miR-195-5p.Therefore, the aim of the present study was to determine the function of lncSNHG12 in OS. A bioinformatics website was used to predict the downstream targets of lncSNHG12. In addition, qRT-PCRwas employed to assess lncSNHG12 expression in OS cells. Cell migration and proliferation in vitro were verified using the transwell migration, clone formation, and CCK8 assays. Tumor metastasis and xenograft formation were monitored in nude mice with or without downregulation of lncSNHG12. The results show that lncSNHG12 was upregulated in OS cell lines. Downregulation lncSNHG12 suppressed the metastasis and proliferation both in vitro and in vivo. Also, lncSNHG12 downregulation suppressed the expression of insulin growth factor 1 receptor (IGF1R) expression through sponging miR-195-5p, which was verified with the luciferase reporter assay and rescue experiments. These findings suggest that downregulation of lncSNHG12 may suppress aggressive OS phenotypes. Moreover, lncSNHG12 silencing inhibited OS metastasis and growth by targeting the miR-195-5p/IGF1R axis, which represents a candidate marker and target for OS treatment and management.	31743769	RID06310	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Breast cancer	LINC00899	DICER1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-425)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000231711	GRCh38_22:46039907-46044853	ENSG00000100697	NA	100271722	23405	NA	Dicer|HERNA|K12H4.8-LIKE|KIAA0928|MNG1	Long noncoding RNA LINC00899 suppresses breast cancer progression by inhibiting miR-425.Here, we found that LINC00899 is downregulated in breast cancer tissues and cell lines.Functional assays indicated that LINC00899 overexpression suppresses proliferation, migration and invasion of breast cancer cells in vitro. Moreover, LINC00899 was found to competitively bind miR-425, thereby functioning as a tumor suppressor by enhancing DICER1. Overexpression of miR-425 attenuated the LINC00899-induced inhibition of breast cancer cell proliferation and invasion. These findings highlight the important role of the LINC00899-miR-425-DICER1 axis in breast cancer cell proliferation and invasion, and could potentially lead to new lncRNA-based diagnostics or therapeutics for breast cancer.	31739288	RID06311	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	LOXL1-AS1	SEMA7A	positively-E	starBase;siRNA;RIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-28-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000138623	NA	100287616	8482	NA	CD108|H-Sema-L|SEMAL	LncRNA LOXL1-AS1/miR-28-5p/SEMA7A axis facilitates pancreatic cancer progression.In the present study, we first recognized miR-28-5p was downregulated in PC, and miR-28-5p overexpression inhibited cell proliferation and migration in PC. Then miR-28-5p was verified to act as a molecular sponge of LOXL1-AS1. Therefore, the function of LOXL1-AS1 was further explored in PC, presenting that LOXL1-AS1 suppression inhibited cell proliferation and migration. What is more, SEMA7A was found to be a target gene for miR-28-5p and was upregulated in PC. In addition, LOXL1-AS1 could positively regulate SEMA7A expression while miR-28-5p could negatively regulate SEMA7A expression. According to rescue experiments, SEMA7A overexpression partially neutralized LOXL1-AS1 silence-mediated inhibitory function on progression in PC. Taken together, all the data demonstrated that LOXL1-AS1/miR-28-5p/SEMA7A axis facilitated pancreatic cancer progression, which may be regarded as an innovative therapeutic target for PC treatment. SIGNIFICANCE OF THE STUDY: Our findings constitute the first report to delineate that lncRNA LOXL1-AS1/miR-28-5p/SEMA7A axis facilitates PC progression. According to our experimental results, we found the expression of miR-28-5p was downregulated in PC cells and miR-28-5p overexpression inhibited cell proliferation and migration in PC. LOXL1-AS1 could sponge miR-28-5p and then upregulate the expression of SEMA7A. Thus, LOXL1-AS1/miR-28-5p/SEMA7A axis facilitated PC progression. This initially proposed point might provide a novel molecular target for PC treatment.	31732974	RID06312	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	ID2-AS1	HDAC8	NA	siRNA;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000235092	GRCh38_2:8666636-8681864	ENSG00000147099	NA	100506299	55869	NA	HDACL1|KDAC8|MRXS6|RPD3|WTS	LncRNA ID2-AS1 suppresses tumor metastasis by activating the HDAC8/ID2 pathway in hepatocellular carcinoma.We found that ID2-AS1 expression decreased in metastatic HCC cell lines and HCC tissues, and lower ID2-AS1 expression predicted reduced overall survival in HCC patients.ID2-AS1 significantly suppressed the migration, invasion and metastasis of HCC cells in vitro and in vivo. Mechanistically, ID2-AS1 regulated the transcription of its adjacent gene inhibitor of DNA binding 2 (ID2) by blocking the binding of histone deacetylase 8 (HDAC8) on the ID2 enhancer. Furthermore, ID2-AS1 and ID2 suppressed the Twist-induced epithelial-mesenchymal transition (EMT) in HCC cells. In addition, ID2 expression was also significantly decreased in HCC tissues and was positively correlated with ID2-AS1 in HCC tissues and HCC cell lines. Taken together, our findings demonstrated that ID2-AS1 regulated adjacent ID2 transcription by manipulating chromatin modification and that the newly identified ID2-AS1/ID2 axis suppressed HCC metastasis by regulating EMT processes. Our findings provide insights into the molecular mechanisms underlying the metastasis of HCC cells.	31730902	RID06313	interact with protein	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Hepatocellular carcinoma	ID2-AS1	ID2	positively-E	shRNA;overexpression	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000235092	GRCh38_2:8666636-8681864	ENSG00000115738	NA	100506299	3398	NA	bHLHb26|GIG8	LncRNA ID2-AS1 suppresses tumor metastasis by activating the HDAC8/ID2 pathway in hepatocellular carcinoma.We found that ID2-AS1 expression decreased in metastatic HCC cell lines and HCC tissues, and lower ID2-AS1 expression predicted reduced overall survival in HCC patients.ID2-AS1 significantly suppressed the migration, invasion and metastasis of HCC cells in vitro and in vivo. Mechanistically, ID2-AS1 regulated the transcription of its adjacent gene inhibitor of DNA binding 2 (ID2) by blocking the binding of histone deacetylase 8 (HDAC8) on the ID2 enhancer. Furthermore, ID2-AS1 and ID2 suppressed the Twist-induced epithelial-mesenchymal transition (EMT) in HCC cells. In addition, ID2 expression was also significantly decreased in HCC tissues and was positively correlated with ID2-AS1 in HCC tissues and HCC cell lines. Taken together, our findings demonstrated that ID2-AS1 regulated adjacent ID2 transcription by manipulating chromatin modification and that the newly identified ID2-AS1/ID3 axis suppressed HCC metastasis by regulating EMT processes. Our findings provide insights into the molecular mechanisms underlying the metastasis of HCC cells.	31730902	RID06314	transcriptional regulation	metastasis		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE55807)
Osteosarcoma	CDKN2B-AS1	CDK4	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000135446	NA	100048912	1019	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	PSK-J3	CDKN2B-AS1 Exerts Oncogenic Role in Osteosarcoma by Promoting Cell Proliferation and Epithelial to Mesenchymal Transition.Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines.CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin).Taken together, our findings suggest that CDKN2B-AS1 represents a potential therapeutic target for OS.	31724892	RID06315	expression association	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Osteosarcoma	CDKN2B-AS1	Cyclin D1	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	CDKN2B-AS1 Exerts Oncogenic Role in Osteosarcoma by Promoting Cell Proliferation and Epithelial to Mesenchymal Transition.Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines.CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin).Taken together, our findings suggest that CDKN2B-AS2 represents a potential therapeutic target for OS.	31724892	RID06316	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Osteosarcoma	CDKN2B-AS1	E-cadherin	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	CDKN2B-AS1 Exerts Oncogenic Role in Osteosarcoma by Promoting Cell Proliferation and Epithelial to Mesenchymal Transition.Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines.CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin).Taken together, our findings suggest that CDKN2B-AS3 represents a potential therapeutic target for OS.	31724892	RID06317	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Osteosarcoma	CDKN2B-AS1	vimentin	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	CDKN2B-AS1 Exerts Oncogenic Role in Osteosarcoma by Promoting Cell Proliferation and Epithelial to Mesenchymal Transition.Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines.CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin).Taken together, our findings suggest that CDKN2B-AS4 represents a potential therapeutic target for OS.	31724892	RID06318	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Osteosarcoma	CDKN2B-AS1	N-cadherin	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	CDKN2B-AS1 Exerts Oncogenic Role in Osteosarcoma by Promoting Cell Proliferation and Epithelial to Mesenchymal Transition.Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines.CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin).Taken together, our findings suggest that CDKN2B-AS5 represents a potential therapeutic target for OS.	31724892	RID06319	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Colorectal cancer	RP11-468E2.5	STAT5A	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	phosphorylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000126561	NA	NA	6776	NA	MGF|STAT5	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT6, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06320	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Colorectal cancer	RP11-468E2.5	STAT6	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	phosphorylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000166888	NA	NA	6778	NA	D12S1644|IL-4-STAT|STAT6B|STAT6C	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT7, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06321	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Colorectal cancer	RP11-468E2.5	JAK2	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000096968	NA	NA	3717	NA	JTK10	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT8, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06322	expression association	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	RP11-468E2.5	STAT3	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	phosphorylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT9, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06323	interact with protein	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	RP11-468E2.5	CCND1	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT10, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06324	expression association	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	RP11-468E2.5	BCL2	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000171791	NA	NA	596	NA	Bcl-2|PPP1R50	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT11, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06325	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	RP11-468E2.5	CDKN1A	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT12, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06326	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	RP11-468E2.5	IFI27	negatively-E	RIP;western blot;siRNA	downregulation	microarray	NA	NA	cell proliferation(-);apoptosis process(+);JAK/STAT signaling pathway(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259321	GRCh38_14:24139445-24140444	ENSG00000165949	NA	NA	3429	NA	FAM14D|ISG12|ISG12A|P27	Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.The CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results. Altogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT13, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.	31718693	RID06327	expression association	NA		UP(PRAD,BRCA);DATA(GSE104209,GSE51827,GSE55807,GSE41245)
Pancreatic ductal adenocarcinoma	HULC	MIR133B	negatively-F	miRNA.org;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000251164	NA	ENSG00000199080	NA	728655	442890	HCCAT1|LINC00078|NCRNA00078	MIRN133B|miRNA133B|mir-133b	Circulating extracellular vesicle-encapsulated HULC is a potential biomarker for human pancreatic cancer.Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor-beta in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA-133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV-encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle-transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA-133b suppresses the EMT by targeting HULC. Extracellular vesicle-encapsulated HULC could be a potential circulating biomarker for human PDAC.	31715081	RID06328	ceRNA or sponge	circulating		
Pancreatic ductal adenocarcinoma	HULC	SNAI1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251164	NA	ENSG00000124216	NA	728655	6615	HCCAT1|LINC00078|NCRNA00078	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Circulating extracellular vesicle-encapsulated HULC is a potential biomarker for human pancreatic cancer.Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor-beta in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA-133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV-encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle-transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA-134b suppresses the EMT by targeting HULC. Extracellular vesicle-encapsulated HULC could be a potential circulating biomarker for human PDAC.An siRNA to HULC also decreased the N-cadherin and vimentin mRNA levels, whereas it increased that of E-cadherin, in Panc-1 and MiaPaCa-2 cells (Figure -(Figure2A2A and Figure S2). Consistent with these changes, the N-cadherin, vimentin, and Snail protein levels were decreased, and that of E-cadherin was increased, by HULC knockdown (Figure -(Figure2B).2B). Moreover, cells transfected with an siRNA to HULC showed significantly reduced proliferation, viability, invasion, and migration (Figure -(Figure2C-F).2C-F). Therefore, HULC is a TGF-beta-inducible lncRNA that is aberrantly expressed in tumor cells and can modulate PDAC cell phenotypes in part by regulating the EMT pathway.	31715081	RID06329	expression association	circulating		UP(PAAD);DATA(GSE40174)
Pancreatic ductal adenocarcinoma	HULC	N-cadherin	positively-E	siRNA;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Circulating extracellular vesicle-encapsulated HULC is a potential biomarker for human pancreatic cancer.Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor-beta in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA-133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV-encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle-transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA-134b suppresses the EMT by targeting HULC. Extracellular vesicle-encapsulated HULC could be a potential circulating biomarker for human PDAC.An siRNA to HULC also decreased the N-cadherin and vimentin mRNA levels, whereas it increased that of E-cadherin, in Panc-1 and MiaPaCa-2 cells (Figure -(Figure2A2A and Figure S2). Consistent with these changes, the N-cadherin, vimentin, and Snail protein levels were decreased, and that of E-cadherin was increased, by HULC knockdown (Figure -(Figure2B).2B). Moreover, cells transfected with an siRNA to HULC showed significantly reduced proliferation, viability, invasion, and migration (Figure -(Figure2C-F).3C-F). Therefore, HULC is a TGF-beta-inducible lncRNA that is aberrantly expressed in tumor cells and can modulate PDAC cell phenotypes in part by regulating the EMT pathway.	31715081	RID06330	expression association	circulating		
Pancreatic ductal adenocarcinoma	HULC	vimentin	positively-E	siRNA;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Circulating extracellular vesicle-encapsulated HULC is a potential biomarker for human pancreatic cancer.Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor-beta in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA-133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV-encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle-transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA-134b suppresses the EMT by targeting HULC. Extracellular vesicle-encapsulated HULC could be a potential circulating biomarker for human PDAC.An siRNA to HULC also decreased the N-cadherin and vimentin mRNA levels, whereas it increased that of E-cadherin, in Panc-1 and MiaPaCa-2 cells (Figure -(Figure2A2A and Figure S2). Consistent with these changes, the N-cadherin, vimentin, and Snail protein levels were decreased, and that of E-cadherin was increased, by HULC knockdown (Figure -(Figure2B).2B). Moreover, cells transfected with an siRNA to HULC showed significantly reduced proliferation, viability, invasion, and migration (Figure -(Figure2C-F).4C-F). Therefore, HULC is a TGF-beta-inducible lncRNA that is aberrantly expressed in tumor cells and can modulate PDAC cell phenotypes in part by regulating the EMT pathway.	31715081	RID06331	expression association	circulating		
Pancreatic ductal adenocarcinoma	HULC	E-cadherin	negatively-E	siRNA;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Circulating extracellular vesicle-encapsulated HULC is a potential biomarker for human pancreatic cancer.Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor-beta in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA-133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV-encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle-transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA-134b suppresses the EMT by targeting HULC. Extracellular vesicle-encapsulated HULC could be a potential circulating biomarker for human PDAC.An siRNA to HULC also decreased the N-cadherin and vimentin mRNA levels, whereas it increased that of E-cadherin, in Panc-1 and MiaPaCa-2 cells (Figure -(Figure2A2A and Figure S2). Consistent with these changes, the N-cadherin, vimentin, and Snail protein levels were decreased, and that of E-cadherin was increased, by HULC knockdown (Figure -(Figure2B).2B). Moreover, cells transfected with an siRNA to HULC showed significantly reduced proliferation, viability, invasion, and migration (Figure -(Figure2C-F).5C-F). Therefore, HULC is a TGF-beta-inducible lncRNA that is aberrantly expressed in tumor cells and can modulate PDAC cell phenotypes in part by regulating the EMT pathway.	31715081	RID06332	expression association	circulating		
Prostate cancer	RBMS3-AS3	VASH1	positively-E	RegRNA2.0;lncRNASNP2;miRDB;luciferase reporter gene assay;RIP;western blot;RNA pull-down assay	downregulation	microarray;RT-qPCR	GSE3325;GSE69223;GSE12348	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-4534)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000235904	GRCh38_3:29054570-29290726	ENSG00000071246	NA	100873979	22846	NA	KIAA1036	Long noncoding RNA RBMS3-AS3 acts as a microRNA-4534 sponge to inhibit the progression of prostate cancer by upregulating VASH1.Therefore, the present study set out to investigate the potential role of RBMS3-AS3/miR-4534/VASH1 axis in the development of prostate cancer. The biological functions of RBMS3-AS3, miR-4534, and VASH1 on cell proliferation, migration, invasion, and angiogenesis of prostate cancer were evaluated via gain- and loss-of-function experiments. Furthermore, tumor xenograft in nude mice was performed to examine tumorigenesis in vivo. The obtained results indicated that RBMS3-AS3 was poorly expressed in prostate cancer tissues and cells. Of note, overexpression of RBMS3-AS3 was found to suppress cell proliferation, migration, invasion, and angiogenesis as well as the tumorigenic ability of prostate cancer. VASH1 was verified as a target gene of miR-4534. VASH1 expression was found to be downregulated in prostate cancer tissues and cells. Interestingly, RBMS3-AS3 was observed to competitively bind to miR-4534 to upregulate VASH1 expression, resulting in a suppressive role in prostate cancer development. Also, in vitro findings were reproduced in vivo on tumor xenograft in nude mice. Taken together, the present study provides evidence suggesting that RBMS3-AS3 acts as a miR-4534 sponge to inhibit the development of prostate cancer by upregulating VASH1, highlighting a theoretical target for prostate cancer treatment.	31712637	RID06333	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Multiple myeloma	H19	BRD4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-152-3p	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141867	NA	283120	23476	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CAP|HUNK1|HUNKI|MCAP	Long Noncoding RNA H19 Promotes tumorigenesis of Multiple Myeloma by Activating BRD4 Signaling by Targeting MicroRNA 152-3p.In this study, the expression of H19, microRNA 152-3p (miR-152-3p), and BRD4 in MM patients was evaluated by quantitative real-time PCR (qRT-PCR and western blot.A luciferase reporter assay was conducted to confirm the interaction among H19, miR-152-3p, and BRD4.We found that levels of H19 and BRD4 were upregulated and the expression of miR-152-3p was downregulated in MM patients. dual-luciferase reporter assay showed H19 targeted miR-152-3p to promote BRD4 expression. Knockdown of H19 repressed proliferation and enhanced apoptosis and cell cycle G1 arrest by upregulating miR-152-3p in MM cells. Furthermore, H19 knockdown suppressed the growth of xenograft tumor, reduced Ki-67 and BRD4 levels, and increased cell apoptosis in xenograft tumor tissues. Taking these results together, H19 knockdown suppresses MM tumorigenesis via inhibiting BRD4-mediated cell proliferation through targeting miR-152-3p, implying that H19 is a promising biomarker and drug target for MM.	31712391	RID06334	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	DLX6-AS1	RUNX2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-505-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000124813	NA	285987	860	Evf-2|FLJ34048|NCRNA00212	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Long noncoding RNA DLX6-AS1 promotes breast cancer progression via miR-505-3p/RUNX2 axis. In the current study, the expression of DLX6-AS1 in the BC tissue samples was evaluated and the correlation between DLX6-AS1 expression and clinicopathological parameters were also analyzed. We found that DLX6-AS1 expression was much higher in tumor tissues than that in adjacent normal tissues and was positively associated with poor prognosis in BC patients. DLX6-AS1 knockdown significantly suppressed BC cell proliferation, invasion, migration, and promoted apoptosis. Moreover, luciferase reporter assay validated that DLX6-AS1 acted as an endogenous sponge to miR-505-3p and negatively regulated its expression. Additionally, miR-505-3p inhibited runt-related transcription factor 2 (RUNX2) expression by directly bind to its 3'- untranslated region (3'-UTR) and overexpression of RUNX2 partially reversed the effect of miR-505-3p mimics on BC cell proliferation and invasion. Furthermore, in BC tissues, miR-505-3p expression level was inversely associated with DLX6-AS1 and RUNX2, respectively. In conclusion, these findings demonstrated that DLX6-AS1 functioned as an oncogenic role that promoted BC proliferation and invasion through miR-505-3p/RUNX2 axis, which might serve as a potential therapeutic target for BC treatment.	31705901	RID06335	ceRNA or sponge	prognosis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	DLEU1	AKT1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000142208	NA	10301	207	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	AKT|PKB|PRKBA|RAC|RAC-alpha	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-2/Bax axis and caspase cascade in RCC cells.	31702026	RID06336	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	DLEU1	E-cadherin	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	NA	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-3/Bax axis and caspase cascade in RCC cells.	31702026	RID06337	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Renal cell carcinoma	DLEU1	N-cadherin	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-4/Bax axis and caspase cascade in RCC cells.	31702026	RID06338	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Renal cell carcinoma	DLEU1	vimentin	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-5/Bax axis and caspase cascade in RCC cells.	31702026	RID06339	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Renal cell carcinoma	DLEU1	BCL2	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000171791	NA	10301	596	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	Bcl-2|PPP1R50	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-6/Bax axis and caspase cascade in RCC cells.	31702026	RID06340	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	DLEU1	Caspase3	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	NA	NA	NA	10301	NA	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	NA	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-7/Bax axis and caspase cascade in RCC cells.	31702026	RID06341	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Renal cell carcinoma	DLEU1	Caspase9	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-8/Bax axis and caspase cascade in RCC cells.	31702026	RID06342	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Renal cell carcinoma	DLEU1	BAX	negatively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);apoptosis process(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000087088	NA	10301	581	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	BCL2L4	Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.DLEU1 knockdown also induced a significant downregulation in the expression of N-cadherin and vimentin, which are important mesenchymal markers, in KETR3 and 786-O cells (P<0.05; Fig. 4B). Collectively, these results suggested that DLEU1 knockdown interfered with the mesenchymal properties of RCC cells.DLEU1 knockdown suppresses the Akt pathway and disrupts EMT in RCC cellsThe phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway is an established pathway involved in the occurrence and development of cancer (26). To determine whether the Akt signaling pathway was involved in the function of DLEU1, the phosphorylation levels of Akt, and the expression of downstream proteins cyclin D1 and P70S6 kinase (P70S6K) were evaluated via western blot It was observed that silencing DLEU1 significantly reduced the phosphorylation levels of Akt in KETR3 and 786-O cells compared with the NC (P<0.05), but induced no notable effects on the expression of total Akt (Fig. 4A). Additionally, the expression levels of cyclin D1 and P70S6K, proteins involved in the cell cycle, were similarly downregulated in DLEU1 knockdown cells (P<0.05; Fig. 4A). From the results of western blot it was revealed that DLEU1 downregulation significantly inhibited the expression of Bcl-2, total caspase-3 and total caspase-9, and increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 in KETR3 and 786-O cells compared with in the NC group (P<0.05; Fig. 3B). Collectively, these findings suggested that the increase in apoptosis induced by DLEU1 knockdown may be dependent on its regulation of the Bcl-9/Bax axis and caspase cascade in RCC cells.	31702026	RID06343	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	PITPNA-AS1	WNT5A	positively-E	starBase;DIANA;PITA;miRmap;microT;PicTar;Targetscan;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-876-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236618	GRCh38_17:1516877-1518101	ENSG00000114251	NA	100306951	7474	NA	hWNT5A	PITPNA-AS1 abrogates the inhibition of miR-876-5p on WNT5A to facilitate hepatocellular carcinoma progression.Firstly, PITPNA-AS1 was observed to be heightened in HCC tissues. Then function assays proved that overexpressing or silencing PITPNA-AS1 could manipulate the proliferation and motility of HCC cells. Besides, PITPNA-AS1 was located in the cytoplasm. Among the candidate miRNAs of PITPNA-AS1, miR-876-5p was an obvious target. Moreover, mechanism experiments validated that PITPNA-AS1 modulated WNT5A expression by targeting miR-876-5p. Rescue experiments affirmed that WNT5A silencing rescued the miR-876-5p suppression-induced cellular processes in PITPNA-AS1-silenced Hep3B cells. And in vivo experiments determined that PITPNA-AS1 regulated HCC progression in vivo via miR-876-5p/WNT5A pathway. In conclusion, this work shed lights on the modulatory mechanism of PITPNA-AS1/miR-876-5p/WNT5A axis in HCC, which might be pivotal for exploring effective diagnostic biomarkers and treatment strategies for HCC patients.	31700026	RID06344	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)	UP(LIHC);DATA(GSE117623)
Acute myeloid leukemia	MIAT	miR-495	negatively-E	Starbase v3.0;LncBase Predicted v.2	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Long noncoding RNA MIAT promotes the progression of acute myeloid leukemia by negatively regulating miR-495.In this study, we find that MIAT is overexpressed in AML patient specimens and AML cell lines. Importantly, upregulation of MIAT is closely related with poor clinical outcome. Further investigations reveal that knockdown of MIAT inhibits the colony formation and proliferation, meanwhile, accelerates the apoptosis of AML cells in vitro. Consistently, MIAT knockdown slows AML progression in immunodeficient mice. Mechanistically, we confirm that MIAT can function as a sponge to inhibit microRNA-495 (miR-495), a tumor suppressor, in AML cells. Collectively, our results demonstrate that MIAT is involved in promoting the progression of AML, at least partly, through negative regulation of miR-495, and therefore provide a promising target for treatment of AML.	31698307	RID06345	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Neuroblastoma	SNHG1	PLK4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000142731	NA	23642	10733	LINC00057|lncRNA16|NCRNA00057|UHG	Sak|STK18	LncRNA SNHG1 contributes to tumorigenesis and mechanism by targeting miR-338-3p to regulate PLK4 in human neuroblastoma.The expression levels of SNHG1, miR-338-3p, and PLK4 were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR and western blot, respectively.The functional targets between miR-338-3p and SNHG1 or PLK4 were predicted by online software Diana tools and observed by Luciferase reporter assay and RIP assay.The expression levels of SNHG1 and PLK4 were increased in NB tissues and cells, and miR-338-3p expression was on the contrary. PLK4 was verified as a direct target of miR-338-3p and miR-338-3p could specially bind to SNHG1. The negative effect of SNHG1 down-regulation on cell proliferation, migration, and invasion could be rescued by miR-338-3p inhibition. The suppression of miR-338-3p mimics on cell proliferation, migration, and invasion could be reversed by PLK4 overexpression. In addition, SNHG1 knockdown weakened the volume and weight of tumor in vivo.SNHG1 conduced to tumorigenesis and mechanism by upregulating PLK4 and by acting as miR-338-3p sponge in neuroblastoma.	31696485	RID06346	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Hepatocellular carcinoma	FAM83A-AS1	NOP58	NA	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);apoptosis process(-)	interact with protein	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000204949	GRCh38_8:123193651-123202743	ENSG00000055044	NA	100131726	51602	HCCC11	HSPC120|NOP5	Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A.In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells.FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC. Moreover, FAM83A-AS1 could positively regulate FAM83A, and FAM83A could also promote the progression of HCC. In addition, FAM83A-AS1 and FAM83A were both verified to bind with NOP58, and FAM83A-AS1 enhanced the mRNA stability of FAM83A by binding with NOP58. In rescue assays, the suppressed influence of down-regulated FAM83A-AS1#1 on cell proliferation, migration as well as the accelerated influence of FAM83A-AS1#1 knockdown on cell apoptosis could be partially recovered by overexpression of FAM83A. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM83A. These findings offer a novel biological insight into HCC treatment.	31696213	RID06347	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	FAM83A-AS1	FAM83A	positively-E	qRT-PCR;pearman correlation analysis;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);apoptosis process(-)	mRNA stability	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000204949	GRCh38_8:123193651-123202743	ENSG00000147689	NA	100131726	84985	HCCC11	BJ-TSA-9|MGC14128	Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A.In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells.FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC. Moreover, FAM83A-AS1 could positively regulate FAM83A, and FAM83A could also promote the progression of HCC. In addition, FAM83A-AS1 and FAM83A were both verified to bind with NOP58, and FAM83A-AS1 enhanced the mRNA stability of FAM83A by binding with NOP58. In rescue assays, the suppressed influence of down-regulated FAM83A-AS1#1 on cell proliferation, migration as well as the accelerated influence of FAM83A-AS1#1 knockdown on cell apoptosis could be partially recovered by overexpression of FAM83A. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM84A. These findings offer a novel biological insight into HCC treatment.	31696213	RID06348	interact with mRNA	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE55807)
Cervical squamous cell carcinoma	WT1-AS	TP53	positively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000183242	GRCh38_11:32435518-32500632	ENSG00000141510	NA	51352	7157	WIT-1|WIT1|WT1-AS1|WT1AS	LFS1|p53	LncRNA WT1-AS up-regulates p53 to inhibit the proliferation of cervical squamous carcinoma cells.RT-qPCR, cell proliferation rate measurement, cell transfection, and western blot were carried out to analyze the samples. We found that HPV infection failed to affect WT1-AS expression in CSCC tissues, while WT1-AS was down-regulated in CSCC tissues compared with non-cancer tissues. P53 was also down-regulated in CSCC tissues and positively correlated with WT1-AS. Analysis of the survival of CSCC patients revealed that low levels of WT1-AS were accompanied by poor survival. Significantly up-regulated p53 was observed after WT1-AS over-expression in CSCC cells, while p53 over-expression failed to affect WT1-AS. P53 and WT1-AS over-expression resulted in the inhibited proliferation of CSCC cells.Therefore, WT1-AS is down-regulated in CSCC and it may inhibit CSCC cell proliferation at least partially by up-regulating p53.	31694597	RID06349	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MALAT1	VEGFA	positively-E	RNA pull-down assay;luciferase reporter assay;TargetScan	upregulation	qRT-PCR	NA	NA	angiogenesis(+);cell proliferation(+);cell migration(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	VEGF|VEGF-A|VPF	Long non-coding RNA MALAT1 promotes angiogenesis and immunosuppressive properties of HCC cells by sponging miR-140.Herein, we studied the interaction between MALAT1 and miR-140 on the regulation of angiogenesis and immunosuppressive properties. We revealed that the expression of MALAT1 and VEGF-A was significantly increased in HCC cells. Knockdown of MALAT1 in HCC cells suppressed the production of VEGF-A, impaired the angiogenesis of HUVECs, and facilitated the polarization of macrophage toward the M1 subset. Mechanistically, the interaction between MALAT1 and miR-140 or between miR-140 and VEGF-A was confirmed by multiple assays. Besides, a negative correlation between MALAT1 and miR-140 was found in HCC tissues. Furthermore, miR-140 inhibition significantly increased VEGF-A expression, promoted angiogenesis of HUVECs, and redirected the polarization of macrophages toward the M2 subset. In addition, in vivo studies also verified the regulatory network of the MALAT1/miR-140 axis on VEGF-A in HCC progression. In summary, this study revealed the mechanism that MALAT1 worked as a putative HCC promotor via inhibiting miR-140. Therefore, targeting MALAT1 or miR-140 might alleviate the progression of HCC in the future.In vivo verification of MALAT1 knockdown on macrophage polarization, angiogenesis and the 458 expression of miR-140 and VEGF-A.	31693399	RID06350	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	PRECSIT	WDR18	positively-E	starBase v3.0;luciferase reporter assay;TargetScan 7.1	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell viability(+);cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-542-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255874	GRCh38_13:110863987-110870330	ENSG00000065268	NA	283487	57418	C13orf29|LINC00346|NCRNA00346	Ipi3	A positive feedback loop involving the LINC00346/beta-catenin/MYC axis promotes hepatocellular carcinoma development.Interactions between LINC00346, miR-542-3p and WDR18 were assessed using luciferase reporter, RT-qPCR and western blot assays.We found that LINC00346 was upregulated in primary HCC tissues and HCC-derived cell lines and that LINC00346 may promote HCC cell viability, proliferation, migration and invasion. Furthermore, we found that LINC00346 may regulate WDR18 expression via competitively binding to miR-542-3p. This miRNA was found to be downregulated in primary HCC tissues and to act as a tumor suppressor that can inhibit HCC cell viability, proliferation, migration and invasion. In contrast, WDR18 was found to be upregulated in primary HCC tissues and to act as an oncogene. Additional functional studies indicated that WDR18 can activate the Wnt/beta-catenin signaling pathway and its downstream effectors in HCC cells. We also found that LINC00346, through competitive sponging of miR-542-3p, may enhance the expression of WDR18 and activate the Wnt/beta-catenin signaling pathway in HCC cells. Finally, a positive feedback loop involving LINC00346, beta-catenin and MYC in HCC cells was uncovered. Our results indicate an oncogenic role of LINC00346 in HCC cells via a positive feedback loop involving LINC00346, beta-catenin and MYC, and they may be instrumental for the design of novel HCC biomarkers and/or therapeutic strategies.	31691159	RID06351	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	CTNNB1	PRECSIT	positively-E	RNA pull-down assay	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell viability(+);cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000255874	GRCh38_13:110863987-110870330	1499	283487	CTNNB|EVR7|MRD19|NEDSDV|armadillo	C13orf29|LINC00346|NCRNA00346	A positive feedback loop involving the LINC00346/beta-catenin/MYC axis promotes hepatocellular carcinoma development.Interactions between LINC00346, miR-542-3p and WDR18 were assessed using luciferase reporter, RT-qPCR and western blot assays.We found that LINC00346 was upregulated in primary HCC tissues and HCC-derived cell lines and that LINC00346 may promote HCC cell viability, proliferation, migration and invasion. Furthermore, we found that LINC00346 may regulate WDR18 expression via competitively binding to miR-542-3p. This miRNA was found to be downregulated in primary HCC tissues and to act as a tumor suppressor that can inhibit HCC cell viability, proliferation, migration and invasion. In contrast, WDR18 was found to be upregulated in primary HCC tissues and to act as an oncogene. Additional functional studies indicated that WDR18 can activate the Wnt/beta-catenin signaling pathway and its downstream effectors in HCC cells. We also found that LINC00346, through competitive sponging of miR-542-3p, may enhance the expression of WDR18 and activate the Wnt/beta-catenin signaling pathway in HCC cells. Finally, a positive feedback loop involving LINC00346, beta-catenin and MYC in HCC cells was uncovered. Our results indicate an oncogenic role of LINC00346 in HCC cells via a positive feedback loop involving LINC00347, beta-catenin and MYC, and they may be instrumental for the design of novel HCC biomarkers and/or therapeutic strategies. To address this issue, we transfectedHCC cells with beta-catenin overexpression or knockdownplasmids and found that the transcript and protein levels ofLINC00346 and MYC were dramatically upregulated in beta_x0002_catenin overexpressing cells, whereas the opposite was ob_x0002_served in HCC cells after beta-catenin knockdown	31691159	RID06352	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Lung adenocarcinoma	LINC00355	CCNE1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-195)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227674	GRCh38_13:63851197-64076044	ENSG00000105173	NA	144766	898	NA	CCNE	A novel long non-coding RNA LINC00355 promotes proliferation of lung adenocarcinoma cells by down-regulating miR-195 and up-regulating the expression of CCNE1.Functionally, our findings demonstrated that LINC00355 silencing suppressed the proliferation in vitro and in vivo. In addition, we found that LINC00355 negatively regulated miR-195 in lung adenocarcinoma cells. Simultaneously, silencing LINC00355 by shRNA resulted in suppressed proliferation, colony formation and promoted cell cycle arrest and apoptosis via miR-195. Moreover, silencing LINC00355 by shRNA inhibited the cyclin E1 (CCNE1) gene expression via miR-195 in lung adenocarcinoma cells. Collectively, this study demonstrates the novel lncRNA LINC00355 in regulatory network of CCNE1 via miR-195 in lung adenocarcinoma, highlighting LINC00355 as a new target for the treatment of lung adenocarcinoma.	31689506	RID06353	ceRNA or sponge	NA	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Colorectal cancer	CASC2	BCL2	negatively-E	RIP;western blot;ChIP	downregulation	RT-qPCR	NA	NA	apoptosis process(+);cell viability(-)	NA	binding/interaction	RNA-protein	Berberine	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171791	NA	255082	596	C10orf5	Bcl-2|PPP1R50	To reveal the underlying mechanism of berberine-induced anti-tumor activity and cell apoptosis, RNA-sequencing followed by reverse-transcription quantitative PCR were performed. In addition, RNA immunoprecipitation, chromatin immunoprecipitation and western blotwere used to identify the functional regulation of CASC2/EZH2/BCL2 axis in berberine-induced CRC cell apoptosis. The data revealed that lncRNA CASC2 was upregulated by berberine treatment. Gain- or loss-of-function assays suggested that lncRNA CASC2 was required for the berberine-induced inhibition of cell viability and activation of cell apoptosis. Subsequently, the downstream antiapoptotic gene BCL2 was identified as a functional target of the berberine/CASC2 mechanism, as BCL2 reversed the berberine/CASC2-induced cell cytotoxicity. lncRNA CASC2 silenced BCL2 expression by binding to the promoter region of BCL2 in an EZH2-dependent manner. In summary, berberine may be a novel therapeutic agent for CRC and lncRNA CASC2 may serve as an important therapeutic target to improve the anticancer effect of berberine.	31173223	RID06354	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Head and neck squamous cell carcinoma	WWTR1-AS1	WWTR1	positively-E	western blot;TCGA;GO;KEGG	upregulation	qRT-PCR	NA	NA	cell viability(+);cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000241313	GRCh38_3:149656999-149661364	ENSG00000018408	NA	100128025	25937	NA	DKFZp586I1419|TAZ	To identify the potential signaling pathways involved in oncogenic roles of WWTR1-AS1, we picked up genes whose expression was significantly correlated with WWTR1-AS1 in TCGA- HNSCC data set via a bioinformatics approach. There were 544 genes negatively and 2482 genes positivelyassociated with WWTR1-AS1 expression in TCGA- HNSCC data set using the Pearson correlation coefficient (range from 0.4 to 1.0 or - 0.4 to - 1). These genes were pooled and analyzed by DAVID.22 As shown, GO and KEGG enrichment analyses revealed that these genes with high correlation were mainly involved in Hippo signaling and other cancer-related pathways such as pancreatic cancer, renal cell carcinoma, prostate cancer, glioma, non-small cell lung cancer, and chronic myeloid leukemia. Consistent with this, WWTR1-AS1 expression was positively associated with mRNA expression of WWTR1 in TCGA-HNSCC data set with the Pearson r correlation test.To further validate the significant correlation between WWTR1-AS1 and WWTR1 in HNSCC, we measured the expression of WWTR1 and determined its association with WWTR1-AS1 in HNSCC cell line as well as primary clinical samples. As data shown, mRNA level of WWTR1 was remarkably overexpressed and positively associated with WWTR1-AS1 expression in HNSCC cells. Moreover, the mRNA of WWTR1 expressed significantly higher in HNSCC samples when compared with their paired healthy mucosa. In accordance with the results of TCGA-HNSCC and HNSCC cells, WWTR1-AS1 expression in our clinical samples was positively associated with the mRNA expression of WWTR1.	31172583	RID06355	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Gastrointestinal stromal tumor	CCDC26	IGF1R	negatively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	Imatinib	NA	NA	Cancer	Gastrointestinal stromal tumor	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000140443	NA	137196	3480	RAM	CD221|IGFIR|IGFR|JTK13	Considering the opposing expression and role of CCDC26 and IGF-1R in GIST cells, we hypothesized that CCDC26 could interact with IGF-1R. To support this, we performed an RNA pull down experiment. Our results demonstrated that CCDC26 RNA could pull down IGF-1R protein (Figure 4A). Furthermore, we found that CCDC26 knockdown up-regulated IGF-1R (Figure 4B). To further investigate the relationship between CCDC26 and IGF-1R, we tested cell viability in GIST cells after transfection with CCDC26 siRNA or negative siRNA, which were pretreated with IGF-1R siRNA. The result revealed that IGF-1R knockdown abolished CCDC26 inhibition-mediated imatinib resistance (Figure 4C). These results indicated that CCDC26 knockdown induced imatinib resistance in GIST cells through IGF-1R interaction.	31166382	RID06356	expression association	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Ovarian cancer	MEG3	miR-219a-5p	positively-E	luciferase reporter gene assay;western blot	downregulation	PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	However, concurrent transfection of miR-219a-5p mimic and pMIR-MEG3-Mut failed to cause notable changes in luciferase activity, when compared with miR-NC+pMIR-MEG3-Wt group (P < .05). What  more, overexpression and underexpression of MEG3, respectively, triggered increase and decrease of miR-219a-5p expression (P < .05; Figure 5B), yet altering miR-219a-5p expression failed to generate any changes in MEG3 expression (P > .05; Figure 5C)	31161607	RID06357	expression association	NA		
Ovarian cancer	MEG3	EGFR	negatively-E	luciferase reporter gene assay;western blot	upregulation	PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	DNA methylation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000146648	NA	55384	1956	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ERBB|ERBB1|ERRP	This study was aimed to verify whether there existed any associations between long noncoding RNA MEG3/miR-219a-5p/EGFR axis and the development of ovarian cancer (OC).Ultimately, dual-luciferase reporter gene assay was performed to testify the targeted relationships among maternally expressed gene 3 (MEG3), miR-219a-5p, and estimated glomerular filtration rate (EGFR). It was indicated that underexpressed MEG3 and miR-219a-5p were significantly associated with unfavorable prognosis of patients with OC when compared with overexpressed MEG3 and miR-219a-5p (P < .05). In addition, the OC cells transfected with si-MEG3 or miR-219a-5p inhibitor exhibited stronger viability, proliferation, invasion, and migration than untreated cells (P < .05). Correspondingly, the apoptotic percentage of OC cells was reduced observably under treatments of si- MEG3 and miR-219a-5  inhibitor (P < .05).Moreover, MEG3 exerted mod_x005f_x0002_ulatory effects on the expression of miR-219a-5p (P < .05), and there was a sponging relationship between them (P < .05).	31161607	RID06358	epigenetic regulation	prognosis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	MEG3	ILF3	negatively-E	western blot	downregulation	PCR	NA	NA	cell autophagy(-)	NA	regulation	RNA-protein	Adenosine	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000129351	NA	55384	3609	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	Now that OE MEG3 increased the cytotoxicity of adenosine to HepG2 cells, we wonder whether autophagy is involved in the cytotoxicity regulation. Excitingly, OE MEG3 decreased the ratio of LC3-II/LC3-I, and reduced autophagosomes in HepG2 cells. The results indicated that OE MEG3 could also inhibit autophagy to some extent. Unexpectedly OE ILF3 was found to enhance the LC3-II/LC3-I and beclin-1, which indicated ILF3 in_x005f_x0002_creased autophagy via upregulated beclin-1, although beclin-1 was decreased after adding adenosine in the OE ILF3 treatment group, however, the autophagy was also promoted compared with control. Interestingly, ILF3 siRNA induced the autophagy inhibition, and synergized adenosine to inhibit autophagy in HepG2 cells (P < 0.01).	31144362	RID06359	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	SNHG7	miR-34a	negatively-F	luciferase reporter gene assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	Therefore, it was hypothesized that SNHG7 might also function as a sponge to negatively regulate certain miRNAs. The online software starBase v2.0 was applied to analyze the potential miRNA targets of SNHG7, and results showed that miR-34a could bind to complementary sequences in SNHG7. Furthermore, qRT-PCRresults showed that miR-34a expression was down-regulated in breast cancer tissues, and was negatively correlated with SNHG7 expression. In addition, the results showed that MCF-7 and T47D cells had a lower miR-34a level than MCF-10A cells. To study whether there was a direct interaction between SNHG7 and miR-34a, the luciferase assays were performed, and the results showed that miR-34a transfection significantly reduced the luciferase activity of the SNHG7-WT group compared with the miR-NC transfection, and had no influence on the luciferase activity of the SNHG7-MUT group. These results indicated a direct interaction between miR-34a and SNHG7. RIP assays were performed on the extracts of MCF-7-cells using an Ago2 antibody. The results showed that SNHG7 and miR-34a were preferentially enriched in the Ago2-containing miRNPs relative to the control IgG immunoprecipitates, which suggested that SNHG7 existed in Ago2-contained miRNA ribonucleoprotein complexes (miRNPs), probably via an association with miR-34a . Moreover, SNHG7 knockdown resulted in the increase of miR-34a level in MCF-7-cells, and SNHG7 overexpression significantly reduced miR-34a level in T47D cells ). These data indicated that SNHG7 could interact with miR-34a, and inhibit miR-34a expression in breast cancer cells.	31132353	RID06360	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Bile duct carcinoma	MIR122	UCA1	negatively-E	luciferase reporter gene assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);ERK/MAPK signaling pathway(+);cell invasion(+)	NA	NA	RNA-RNA	NA	NA	NA	Cancer	Bile duct cancer	miRNA	lncRNA	ENSG00000207778	NA	ENSG00000214049	GRCh38_19:15828206-15836328	406906	652995	hsa-mir-122|hsa-mir-122a|miR-122|MIRN122|MIRN122A	CUDR|LINC00178|onco-lncRNA-36|UCAT1	Luciferase reporter assay verified the putative binding position. The luciferase activity was decreased when cells were transfected with miR-122 mimics in the UCA1-wt group, but there were no differences in the UCA1-mut group, suggesting that miR-122 could directly bind to UCA1 and inhibit its expression (Figure 4E). The tendency was similar in the QBC939 and CCLP1 cell lines.	31106658	RID06361	expression association	NA		UP(PAAD);DATA(GSE40174)
Nasopharynx carcinoma	SOX2-OT	HNRNPA2B1	positively-E	Luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-146b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000122566	NA	347689	3181	DKFZp761J1324|NCRNA00043|SOX2OT	HNRPA2B1	Furthermore, we uncovered that miR-146b-5p and SOX2-OT were abundant in Ago2 groups in compar_x005f_x0002_ison with the immunoglobulin G (IgG) groups based on the RIP assay , which further verified that miR-146b-5p directly bound to SOX2-OT. Then, we utilized qRT-PCRassay to explore the mutual effects between miR-146b-5p and SOX2-OT. The findings elucidated that SOX2-OT inhibition led to an evident enhancement of miR-146b-5p expression, and miR-146b-5p overexpression observably declined the expression level of SOX2-OT. In addition, Pearson's correlation analysis validated that SOX2-OT expression was contrarily associated with miR-146b-5p in NPC tissues. In a word, SOX2-OT directly binds with the miR-146b-5p in NPC progression.	31099048	RID06362	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	RHPN1-AS1	TP53	positively-E	RNA pull-down assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000254389	GRCh38_8:143366631-143368548	ENSG00000141510	NA	78998	7157	C8orf51|MGC3113	LFS1|p53	To identify whether this long non-coding RNA  RHPN1-AS1 is involved in the regulation of c-Myc func_x005f_x0002_tion, we constructed the knockdown and overexpression  of c-Myc cell models using sh-c-Myc and pCDH-c-Myc.  As demonstrated in Fig. 5a, we observed significantly  lower expression level of RHPN1-AS1 in c-Myc KD cells  for both MCF7 and MDA-MB-231 cells. In contrary, we  saw significantly higher expression of RHPN1-AS1 in the both MCF7 and MDA-MB-231 cells with overexpressed  c-Myc. In silico analysis showed that there is  c-Myc-binding site in the RHPN1-AS1 gene promoter  domain. Using pGL3-based luciferase reporter  assay, we found that sh-c-Myc decreased the relative  luciferase activity in pGL3-RHPN1-AS1 transfected  cells, but not with cells transfected with pGL3-RHPN1-AS1-mut, indicating the direct binding between  c-Myc and RHPN1-AS1. As expected, overexpression of  c-Myc by pCDH-c-Myc significantly increased the rela_x0002_tive luciferase activity of cells transfected with pGL3- RHPN1-AS1, but not with cells transfected with pGL3- RHPN1-AS1-mut. The subsequent chromatin  immunoprecipitation (ChIP) assays verified the asso_x0002_ciation of c-Myc and the chromatin fragments within the RHPN1-AS1 gene.	31089812	RID06363	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	RHPN1-AS1	MIR4261	negatively-F	RNA pull-down assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000254389	GRCh38_8:143366631-143368548	ENSG00000265418	NA	78998	100422929	C8orf51	NA	To identify whether this long non-coding RNA  RHPN1-AS1 is involved in the regulation of c-Myc func_x005f_x0002_tion, we constructed the knockdown and overexpression  of c-Myc cell models using sh-c-Myc and pCDH-c-Myc.  As demonstrated in Fig. 5a, we observed significantly  lower expression level of RHPN1-AS1 in c-Myc KD cells  for both MCF7 and MDA-MB-231 cells. In contrary, we  saw significantly higher expression of RHPN1-AS1 in the both MCF7 and MDA-MB-231 cells with overexpressed  c-Myc. In silico analysis showed that there is  c-Myc-binding site in the RHPN1-AS1 gene promoter  domain. Using pGL3-based luciferase reporter  assay, we found that sh-c-Myc decreased the relative  luciferase activity in pGL3-RHPN1-AS1 transfected  cells, but not with cells transfected with pGL3-RHPN1-AS1-mut, indicating the direct binding between  c-Myc and RHPN1-AS1. As expected, overexpression of  c-Myc by pCDH-c-Myc significantly increased the rela_x0002_tive luciferase activity of cells transfected with pGL3- RHPN1-AS1, but not with cells transfected with pGL3- RHPN1-AS1-mut. The subsequent chromatin  immunoprecipitation (ChIP) assays verified the asso_x0002_ciation of c-Myc and the chromatin fragments within the RHPN1-AS1 gene.	31089812	RID06364	ceRNA or sponge	NA		
Breast cancer	MYC	RHPN1-AS1	negatively-F	RNA pull-down assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+)	sponge	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000254389	GRCh38_8:143366631-143368548	4609	78998	bHLHe39|c-Myc|MYCC	C8orf51|MGC3113	To identify whether this long non-coding RNA  RHPN1-AS1 is involved in the regulation of c-Myc func_x005f_x0002_tion, we constructed the knockdown and overexpression  of c-Myc cell models using sh-c-Myc and pCDH-c-Myc.  As demonstrated in Fig. 5a, we observed significantly  lower expression level of RHPN1-AS1 in c-Myc KD cells  for both MCF7 and MDA-MB-231 cells. In contrary, we  saw significantly higher expression of RHPN1-AS1 in the both MCF7 and MDA-MB-231 cells with overexpressed  c-Myc. In silico analysis showed that there is  c-Myc-binding site in the RHPN1-AS1 gene promoter  domain. Using pGL3-based luciferase reporter  assay, we found that sh-c-Myc decreased the relative  luciferase activity in pGL3-RHPN1-AS1 transfected  cells, but not with cells transfected with pGL3-RHPN1-AS1-mut, indicating the direct binding between  c-Myc and RHPN1-AS1. As expected, overexpression of  c-Myc by pCDH-c-Myc significantly increased the rela_x0002_tive luciferase activity of cells transfected with pGL3- RHPN1-AS1, but not with cells transfected with pGL3- RHPN1-AS1-mut. The subsequent chromatin  immunoprecipitation (ChIP) assays verified the asso_x0002_ciation of c-Myc and the chromatin fragments within the RHPN1-AS1 gene.	31089812	RID06365	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Breast cancer	RHPN1-AS1	TP53	negatively-E	western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000254389	GRCh38_8:143366631-143368548	ENSG00000141510	NA	78998	7157	C8orf51|MGC3113	LFS1|p53	In comparison with cells transfected with sh-ctrl, western blot assay showed that MCF7 cells and MDA-MB-231 cells  transfected with sh-RHPN1-AS-1 and sh-RHPN1-AS-2 showed lower expression of MDM2, higher expression of p53 and P21. Consistently, overexpression of RHPN1-AS1by plasmid pCDH-RHPN1-AS increased the expression of MDM2, but decreased the expression of P53 and P21. RT-PCRresults showed that the rela_x005f_x0002_tive RNA level of RHPN1-AS was signifcantly lower in the sh-RHPN1-AS-1 transfected cells, which showed lower expression level of MDM2, and higher level of P21 than the control cells (p<0.01, respectively). However, the relative RNA level of P53 was not signifcantly diferent in both cell groups. Furthermore, the RNA expression level of RHPN1-AS was signifcantly higher in the cells trans_x0002_fected with pCDH-RHPN1-AS, which had signifcantly higher expression of MDM2, and lower expression of P21 (p<0.01).	31089812	RID06366	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	miR-21	SNHG1	positively-E	siRNA;Luciferase reporter assay	upregulation	qRT-PCR	NA	NA	AKT signaling pathway(+)	NA	regulation	RNA-RNA	Sorafenib	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	ENSG00000199004	NA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	The Akt pathway was highly activated by overexpressed miR-21 in SR-HCC cells compared with parental HCC cells. Among ten screened candidates, SNHG1 showed the largest folds of alteration between SR-HCC and parental cells and between vehicle- and sorafenib-treated cells. Overexpressed SNHG1 contributes to sorafenib resistance by activating the Akt pathway via regulating SLC3A2. Depletion of SNHG1 enhanced the efficacy of sorafenib to induce apoptosis and autophagy of SR-HCC cells by inhibiting the activation of Akt pathway. Sorafenib induced translocation of miR-21 to the nucleus, where it promoted the expression of SNHG1, resulting in upregulation of SLC3A2, leading to the activation of Akt pathway. In contrast, SNHG1 was shown to have little effect on the expression of miR-21, which downregulated the expression of PTEN, leading to the activation of the Akt pathway independently of SNHG1.The present study has demonstrated that lncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and its nuclear expression is promoted by miR-21, whose nuclear translocation is induced by sorafenib. These results indicate that SNHG1 may represent a potentially valuable target for overcoming sorafenib resistance for HCC.	31053148	RID06367	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Cervical cancer	MIR205HG	FOXP2	positively-E	RIP;RNA pull-down;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor growth(+)	ceRNA(miR-122-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000128573	NA	642587	93986	LINC00510	CAGH44|SPCH1|TNRC10	qRT-PCRanalysis showed that the expression of MIR205HG was effectively down_x005f_x0002_regulated by shRNAs in C33A and HeLa cells, in which sh_x0002_MIR205HG#1 caused the maximum descent in the expression of MIR205HG (Fig. 1C). CCK-8 and EdU results suggested that the growth status of C33A and HeLa cells was dramatically inhibited on sh-MIR205HG transfection (Fig. 1D and E).	31023531	RID06368	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Melanoma	DSCAM-AS1	miR-136	negatively-F	luciferase reporter gene assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000235123	GRCh38_21:40383083-40385358	NA	NA	100506492	NA	M41	NA	In addition, the  expressing levels of miR-136 in melanoma tissue samples and paired normal tissue specimens were  measured by qRT-PCRassays, suggesting the lower expression of miR-136 in melanoma tissue  specimens. The qRT-PCRanalysis  also revealed that through enhancing the expres_x005f_x0002_sion of DSCAM-AS1 markedly depressed the  miR-136 levels in A375 and SK-MEL-2 cells,knockdown of DSCAM-AS1 notably promoted the expression of miR-136. Overall, these results detected that miR-136 was a direct target of DSCAM-AS1 in melanoma cells.	31002140	RID06369	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	
Head and neck cancer	PCAT1	MYC	positively-E	siRNA;TCGA;western blot	upregulation	qRT-PCR	NA	NA	cMYC/AKT1/p38/MAPK signaling pathway(-);apoptosis process(+)	NA	association	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000136997	NA	100750225	4609	PCA1|PCAT-1|PiHL	bHLHe39|c-Myc|MYCC	We next examined the status of c-Myc in HNSCC cell lines, and observed a significant downregulation of c-Myc at RNA and protein levels in PCAT-1 depleted JHU029 and Cal27 cell lines, in agreement with earlier observation. We examined c-Myc mRNA expression in HNSCC patient samples (n-=-14), and found a significant overexpression in tumors compared to adjacent non- tumor tissue. The c-Myc expression was positively and significantly correlated with PCAT-1 expression in the patient samples. Similarly, in the TCGA dataset, we found a significant positive correlation in expression between PCAT-1 and c-Myc in HNSCC.	30987615	RID06370	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Head and neck cancer	PCAT1	AKT1	positively-E	Transcriptome array;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000142208	NA	100750225	207	PCA1|PCAT-1|PiHL	AKT|PKB|PRKBA|RAC|RAC-alpha	Transcriptome array in PCAT-1 knockdown prostate cancer cells vs. control parental cells identified several PCAT-1 regulated genes. We chose to examine the proliferation associated genes AKT1 and STAT1, since we observed less proliferation in PCAT-1 depleted HNSCC cells. Downregulation of AKT1 mRNA and protein expression was observed in both PCAT-1 depleted HNSCC cell lines. A significantly higher expression of AKT1 mRNA was also observed in HNSCC patient samples (n-=-14), and a significant positive correlation was noted between AKT1 and PCAT-1. Similarly, in the TCGA dataset, we found a significant positive correlation in expression between PCAT-1 and AKT1 in HNSCC. However, we did not observe alteration of STAT1 expression in HNSCC cell lines upon PCAT-1 knockdown (data not shown). Our result indicates that PCAT-1 regulates c-Myc and AKT1 expression in regulation of HNSCC cell growth.	30987615	RID06371	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	FALEC	ECM1	positively-E	UALCAN;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	exert an enhancer-like function	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000143369	NA	100874054	1893	FAL1|LINC00568|ncRNA-a1	NA	Long non-coding RNAs (lncRNAs) have been shown to play important roles in many human diseases. However, their functions and mechanisms in tumorigenesis and development remain largely unknown. Here, we demonstrated that focally amplified lncRNA in epithelial cancer (FALEC) was upregulated and significantly correlated with lymph node metastasis, TNM stage in gastric cancer (GC). Further experiments revealed that FALEC knockdown significantly inhibited GC cells migration and invasion-in vitro.-Mechanistic investigations demonstrated that small interfering RNA-induced silencing of FALEC decreased expression of the nearby gene extracellular matrix protein 1 (ECM1) in-cis.-Additionally,-ECM1-and-FALEC-expression were positively correlated, and high levels of ECM1 predicted shorter survival time in GC patients. Our results suggest that the downregulation of-FALEC-significantly inhibited the migration and invasion of GC cells through impairing-ECM1-expression by exerting an enhancer-like function. Our work provides valuable information and a novel promising target for developing new therapeutic strategies in GC.	30984243	RID06372	chromatin looping	metastasis		UP(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE55807)
Ovarian cancer	SNHG12	SOX4	positively-E	luciferase reporter gene assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-129)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000124766	NA	85028	6659	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	SNHG12 was upregulated in OC tissues relative to adjacent normal ones. Patients with metastatic OC or those in stage III-IV had a higher level of SNHG12 compared with non-metastatic or stage I-II patients. The 5-year survival was markedly worse in OC patients with high-level SNHG12 than those in the low-level group. Similarly, SNHG12 was highly expressed in OC cell lines. Overexpression of SNHG12 accelerated A2780 and HO8910 cells to proliferate and migrate. We observed the binding between SNHG12 and miRNA-129, and the latter was lowly expressed in OC. The miRNA-129 overexpression partially reversed the promotive effects of SNHG12 on proliferative and migratory abilities of OC cells. Subsequently, SOX4 was proved to be the target gene of miRNA-129. The SOX4 overexpression was further confirmed to reverse the inhibitory effects of miRNA-129 on proliferative and migratory abilities of OC cells.	30964158	RID06373	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	HOXA-AS3	miR-29c	negatively-F	TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);MEK/ERK signaling pathway(+)	NA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000254369	GRCh38_7:27129977-27155928	NA	NA	100133311	NA	HOXA6as	NA	Then, the molecular mechanism of HOXA-AS3 in HCC was further studied. TargetScan data  validated that miR-29c was a potential binding target of HOXA-AS3. Overexpression of miR-29c by miR-29c mimic and knockdown of miR-29c by miR-29c inhibitor was confirmed in SMMC-7721 and HepG2 cells using RT-qPCR . To verify the interaction between HOXA-AS3 and miR-29c, luciferase reporter assay was carried out. Results showed that miR-29c overexpression considerably reduced the luciferase activity of the HOXA-AS3-WT, and miR-29c suppression increased the luciferase activity of the HOXA-AS3-WT, whereas neither miR-29c overexpression nor miR-29c suppression posed any impact on the luciferase activity of HOXA-AS3-Mut . RIP assay revealed that HOXA-AS3 and miR-29c expression were enriched in anti-Ago2 group compared with control group. We also found that the enrichment of HOXA-AS3 in anti-Ago2 group can be inhibited by miR-29c inhibitor and enhanced by miR-29c mimic . To investigate the correlation between HOXA-AS3 and miR-29c, RT-qPCR was performed, and results revealed that knockdown of HOXA-AS3 significantly increased miR-29c expression,  while HOXA-AS3 expression markedly increased in miR-29c inhibitor group . Meanwhile, miR-29c expression was significantly downregulated in HCC tissues compared with the adjacent non-tumor tissues. Pearson correlation analysis demonstrated that the expression of HOXA-AS3 and miR-29c were inversely correlated in HCC tissues. These data strongly suggest that HOXA-AS3 directly interacts with miR-29c to negatively regulate its expression in HCC.	30963785	RID06374	expression association	NA		
Hepatocellular carcinoma	HOXA-AS3	BMP1	positively-E	TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);MEK/ERK signaling pathway(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000254369	GRCh38_7:27129977-27155928	ENSG00000168487	NA	100133311	649	HOXA6as	BMP-1|PCOLC	BMP1 exhibited carcinogenic effect in various human cancers . Luciferase assay showed that luciferase activity of wild-type BMP1 was significantly reduced in miR-29c mimic-transfected cells, but rescued after co-transfection of miR-29c mimic+pcDNA3.1/HOXA-AS3 . However, there was no significant change in luciferase activity of mutant-type BMP1, indicating that BMP1 could interact with miR-29c. The conclusion that miR-29c could directly bind with BMP1 was further demonstrated in RNA pull-down assay . western blot assay manifested that BMP1 expression was reduced in miR-29c mimic transfected HCC cells, but rescued after co-transfection of miR-29c mimic+pcDNA3.1/HOXA-AS3, indicating that HOXA-AS3 could regulate BMP1 expression by targeting miR-29c. Moreover, BMP1 expression in HCC tissues was significantly upregulated compared to non-tumor tissues . Moreover, Spearman Rank correlation analysis demonstrated that there was a significantly negative correlation between BMP1 and miR-29c expression in tumor tissues, but a significantly positive correlation between HOXA-AS3 and BMP1 expression in tumor tissues (r = - 0.511, r = 0.555, P < 0.05). All these data suggested that BMP1 is a downstream target gene of miR-29c, and HOXA-AS3 can regulate BMP1 expression by targeting miR-29c.	30963785	RID06375	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Acute myeloid leukemia	H22954	BCL2	negatively-E	miRBase database;luciferase reporter gene assay;western blot	downregulation	RT-PCR	NA	NA	cell growth(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000171791	NA	NA	596	NA	Bcl-2|PPP1R50	Bioinformatic analysis and RNA antisense purification assay indicated that H22954 targeted the 3' untranslated region of the BCL2 gene. In luciferase assays, H22954 expression inhibited BCL2 expression. In transfected K562 cells and mouse xenograft tumors, H22954 overexpression reduced BCL-2 protein levels and promoted cell death. In AML patients, H22954 expression inversely correlated with BCL-2 protein levels in bone marrow cells, blast cell numbers and disease prognosis. These results indicate that H22954 is a novel regulator of BCL-2 and that reduced H22954 expression may play an important role in the pathogenesis of AML.	30959078	RID06376	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	TTN-AS1	miR-376b-3p	negatively-F	starBase;Luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	Using qRT-PCRexamination, we found that TTN-AS1 was expressed at a higher level in GC tissues and cell lines compared to the normal controls. Kaplan-Meier analysis of GC patients revealed the negative correlation between TTN-AS1 expression and the overall survival. To detect the biological function of TTN-AS1 in GC, we silenced TTN-AS1 to perform loss-of-function assays. The experimental results revealed that knockdown of TTN-AS1 obviously inhibited GC cell proliferation, induced cell apoptosis and impaired cell migration and invasion. In mechanism, TTN-AS1 was located in the cytoplasm of GC cells, indicating the post-transcriptional regulation of TTN-AS1 on gene expression. Bioinformatics analysis revealed the potential binding relation between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12. Mechanism experiments such as luciferase reporter assay and RNA pull-down assay demonstrated the interaction between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12 in GC cells.	30943745	RID06377	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Hepatocellular carcinoma	AK002107	TGFBR1	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);colony formation(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000106799	NA	NA	7046	NA	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	The site in miR-140-5p to which lncRNA AK002107 binds was identified . Furthermore, the luciferase reporter assay revealed that miR-140-5p significantly decreased the luciferase activity of the lncRNA-AK002107-WT vector compared with the lncRNA-AK002107-MUT vector (P < 0.05). Then, miR-140-5p expression in HCC cells was determined using real-time PCR assays . BEL-7402 and MHCC97H cell lines with stably silenced miR-140-5p expression were generated. We further investigated the regulatory relationship between lncRNA AK002107 and miR-140-5p. Knockdown of lncRNA AK002107 significantly increased miR-140-5p expression in the BEL-7402 and MHCC97H cells , suggesting that lncRNA AK002107 inhibits miR-140-5p expression.	30943320	RID06378	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	SNHG16	miR-98-5p	negatively-E	luciferase reporter;RIP	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	To confirm our hypothesis that miR-98-5p was targeted by SNHG16, luciferase reporter assay was performed. As a result, miR-98-5p over-expression markedly decreased the luciferase activities of pmirGLO-SNHG16-Wt, rather than pmirGLO-SNHG16-Mut, and miR-98-5p inhibition pre_x005f_x0002_sented opposite effects . RIP assay confirmed that SNHG16 and miR-98-5p were both immunoprecipitated by anti-Ago2, validating that SNHG16 could interact with miR_x0002_98-5p. Then we studied the correlation between SNHG16 and miR-98-5p. As a results, RT-qPCR assay demonstrated that knockdown of SNHG16 significantly increased the expression of miR-98-5p. Additionally, over_x0002_expression of miR-98-5p could obviously decrease SNHG16 expression in osteosarcoma cell lines and knockdown of miR-98-5p had opposite effects. We also found the downregulation of miR-98-5p in osteosarcoma tissues and a remarkably negative correlation between the expres_x0002_sion of SNHG16 and miR-98-5p in osteosarcoma tissues. Taken together, SNHG16 acts as a sponge for miR-98-5p and negatively regulates the expression of miR_x0002_98-5p in osteosarcoma.	30923843	RID06379	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Breast cancer	DANCR	miR-216a-5p	negatively-E	luciferase reporter gene assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);tumor growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	Figure 3B displayed that 216a-mimics could obviously reduce luciferase activity of DANCR-WT, while it had no distinct effects on DANCR-MUT. The results of qRT-PCR;ISHowed that breast cancer cells transfected with si-DANCR had higher level of miRNA-216a-5p, implying that inhibiting DANCR expression could lead to the increase of miRNA-216a-5p. In addition, Figure 3D demonstrated that 216a-inhibitor had abilities to increase DANCR expression, while 216a-mimics had opposite effects on DANCR expression. The above data proved that miRNA-216a-5p could regulate DANCR level in breast cancer cells by combining with DANCR.	30910842	RID06380	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Colorectal cancer	HCP5	miR-139-5p	negatively-E	qRT-PCR;luciferase reporter gene assay;western blot	downregulation	qRT-PCR;western blot	NA	NA	TNM stage(-);cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	Correlation analysis revealed that overexpression of HCP5 and down-regulation of miR-139-5p were significantly correlated with clinical stage, differentiation and distant metastasis in CRC patients (P < 0.05, Table 1). Furthermore, regression analysis showed that over-expressed HCP5 and down-regulated miR-139-5p predicted poor differentiation, higher TNM stage and distant metastasis in CRC patients (P < 0.05, Data not shown). As shown in Figure 1D, Kaplan-Meier survival analysis showed that the overall survival (OS) of patients with low HCP5 and high miR-139-5p expression was much higher than those with high HCP5 and low expression of miR-139-5p (P < 0.05).	30899394	RID06381	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Diffuse large b-cell lymphoma	SMAD5-AS1	miR-135b-5p	negatively-F	RNA pull-down assay;western blot;luciferase assay;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell viability(-);cell cycle(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	miRNA	ENSG00000164621	GRCh38_5:136129507-136134890	NA	NA	9597	NA	DAMS|SMAD5OS	NA	RIP assay was performed using anti-AGO2 in the TMD8 extract, and it was found that SMAD5 and miR-135b-5p were enriched preferentially in miRNPs containing AGO2 compared with anti-IgG immunoprecipitates. The results of RNA pull-down assay manifested that SMAD5-AS1 was more enriched in the wild-type miR-135b-5p compared with that in the mutant-type miR-135b-5p with broken SMAD5-AS1 binding site. The RT-qPCR results showed that the overexpression of SMAD5-AS1 in DLBCL cells could lead to the down-regulation of miR-135b-5p expression, while the down-regulation of SMAD5-AS1 could lead to the increase in miR-135b-5p expression (Fig. 5d). In the rescue experiment, the down-regulation of SMAD5-AS1 expression in TMD8 cells could reverse the increase in SMAD5-AS1 expression and inhibition on cell proliferation caused by the miR-135-5p inhibitor. Similarly, the overexpression of SMAD5-AS1 could reverse the loss of SMAD5-AS1 expression and enhancement of cell proliferation caused by the miR-135-5p mimic.	30874550	RID06382	ceRNA or sponge	NA		
Diffuse large b-cell lymphoma	SMAD5-AS1	APC	positively-E	RNA pull-down assay;western blot;luciferase assay;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell viability(-);cell cycle(-);apoptosis process(+)	ceRNA(miR-135b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000164621	GRCh38_5:136129507-136134890	ENSG00000134982	NA	9597	324	DAMS|SMAD5OS	DP2|DP2.5|DP3|PPP1R46	According to the prediction via bioinformatics (Targetscan 7.2 http://www.targetscan.org/vert_72/; miRDB http://www.mirdb.org/; miRTarBase http://mirtarbase.mbc.nctu.edu.tw/php/index.php), there might be a binding site in the APC 3'-UTR with miR-135-5p. Then, the luciferase assay confirmed that the 3'-UTR of wild-type APC could significantly lower the luciferase activity in miR-135b-5p group without significant influence on the luciferase activity in the miR-NC group. The 3'-UTR of mutant-type APC had no obvious influence on the luciferase activity in the miR-135b-5p group. Whether APC could be regulated by the expression of SMAD5-AS1 was verified then. According to the RT-qPCR results, the overexpression or down-regulation of SMAD5-AS1 could increase or decrease the mRNA expression in the APC gene. Moreover, the co-transfection of miR-135-5p mimic and APC-overexpressed plasmid or miR-135b-5p inhibitor and shAPC plasmid into TMD8 cells could restore the APC gene expression and cell proliferation.	30874550	RID06383	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Non-small cell lung cancer	MALAT1	TMX2-CTNND1	positively-E	luciferase assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell growth(+)	ceRNA(miR-197-3p)	regulation	RNA-protein	Cisplatin;Adriamycin;Gefitinib;Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000254462	NA	378938	100528016	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAS|CTNND1|p120(cas)|p120(ctn)	Our results indicated that MALAT1 and miR-197-3p were both over-expressed within NSCLC tissues and cells, when compared with normal tissues and cells (P < 0.05). The A549, H460, SPC-A-1 and SPC-A-1 displayed maximum resistances to cisplatin (IC50 = 15.70 ug/ml), adriamycin (IC50 = 5.58 ug/ml), gefitinib (96.82 umol/L) and paclitaxel (141.97 nmol/L). Over-expression of MALAT1 and miR-197-3p, or under-expression of p120-ctn were associated with promoted viability and growth of the cancer cells (P < 0.05), and they could significantly strengthen the chemo-resistance of cancer cells (P < 0.05). MALAT1 Wt or p120-ctn Wt co-transfected with miR-197-3p mimic was observed with significantly reduced luciferase activity within NSCLC cells (P < 0.05). Finally, the NSCLC mice models were observed with larger tumor size and weight under circumstances of over-expressed MALAT1 and miR-197-3p, or under-expressed p120-ctn (P < 0.05). In conclusion, MALAT1 could alter chemo-resistance of NSCLC cells by targeting miR-197-3p and regulating p120-ctn expression, which might assist in improvement of chemo-therapies for NSCLC.	30841025	RID06384	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(BRCA);DATA(GSE109761)
Breast cancer	ADAMTS9-AS2	miR-130a-5p	negatively-E	western blot;luciferase reporter gene assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);chemoresistance(-)	NA	regulation	RNA-RNA	Tamoxifen	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000241684	GRCh38_3:64684909-65053439	NA	NA	100507098	NA	NA	NA	MCF-7R cells were identified with TAM resistance. ADAMTS9-AS2 was lowly expressed in BC tissues and MCF-7R cells. Particularly, ADAMTS9-AS2 expression in BC tissues with grade III-IV or tumor size <<- cm was significantly lower than that of controls. Dual-luciferase reporter gene assay confirmed the binding condition between ADAMTS9-AS2 and microRNA-130a-5p, showing a negative correlation indicated by Pearson correlation analysis. PTEN was positively correlated with ADAMTS9-AS2. Overexpression of ADAMTS9-AS2 reversed the increased viability and decreased apoptosis induced by microRNA-130a-5p mimics transfection. In addition, PTEN knockdown reversed the decreased viability and accelerated apoptosis caused by ADAMTS9-AS2 overexpression.We found that ADAMTS9-AS2 is lowly expressed in BC tissues and drug-resistant BC cells. Low expression of ADAMTS9-AS2 inhibits PTEN expression and enhances tamoxifen resistance through targeting microRNA-130a-5p.	30840279	RID06385	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Breast cancer	ADAMTS9-AS2	PTEN	positively-E	western blot;dual-luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);chemoresistance(+)	ceRNA(miR-130a-5p)	regulation	RNA-protein	Tamoxifen	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000171862	NA	100507098	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	MCF-7R cells were identified with TAM resistance. ADAMTS9-AS2 was lowly expressed in BC tissues and MCF-7R cells. Particularly, ADAMTS9-AS2 expression in BC tissues with grade III-IV or tumor size <<- cm was significantly lower than that of controls. Dual-luciferase reporter gene assay confirmed the binding condition between ADAMTS9-AS2 and microRNA-130a-5p, showing a negative correlation indicated by Pearson correlation analysis. PTEN was positively correlated with ADAMTS9-AS2. Overexpression of ADAMTS9-AS2 reversed the increased viability and decreased apoptosis induced by microRNA-130a-5p mimics transfection. In addition, PTEN knockdown reversed the decreased viability and accelerated apoptosis caused by ADAMTS9-AS2 overexpression.We found that ADAMTS9-AS2 is lowly expressed in BC tissues and drug-resistant BC cells. Low expression of ADAMTS9-AS2 inhibits PTEN expression and enhances tamoxifen resistance through targeting microRNA-130a-5p.	30840279	RID06386	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Glioblastoma	NORAD	miR-190a-3p	negatively-F	western blot;luciferase reporter gene assay	downregulation	RT-qPCR	NA	NA	apoptosis process(+);cell proliferation(-);colony formation(-);cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	Overexpression of LINC00657 inhibited proliferation, colony formation, invasion and migration in glioma cells via inducing apoptosis. Dual luciferase report assay indicated LINC00657 was the target of miR-190a-3p. Overexpression of LINC00657 greatly inhibited the relative amount of miR-190a-3p. Besides, miR-190a-3p was found to be a negative regulator of PTEN. Additionally, active-caspase 3 was increased in cells transfected with pcDNA3.1-LINC00657. Finally, in vitro results were further confirmed by in vivo studies using nude mice bearing with glioblastoma tumors. In conclusion, LINC00657 was effective in inhibiting glioblastoma by acting as a molecular sponge of miR-190a-3p to regulate PTEN expression. Therefore, targeting LINC00657 may serve as a potential strategy for the treatment of patients with glioblastoma.	30837348	RID06387	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Glioblastoma	NORAD	PTEN	positively-E	western blot;luciferase reporter gene assay	downregulation	RT-qPCR	NA	NA	apoptosis process(-);cell proliferation(+);colony formation(+);cell invasion(+);cell migration(+)	ceRNA(miR-190a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000171862	NA	647979	5728	LINC00657	BZS|MHAM|MMAC1|PTEN1|TEP1	Overexpression of LINC00657 inhibited proliferation, colony formation, invasion and migration in glioma cells via inducing apoptosis. Dual luciferase report assay indicated LINC00657 was the target of miR-190a-3p. Overexpression of LINC00657 greatly inhibited the relative amount of miR-190a-3p. Besides, miR-190a-3p was found to be a negative regulator of PTEN. Additionally, active-caspase 3 was increased in cells transfected with pcDNA3.1-LINC00657. Finally, in vitro results were further confirmed by in vivo studies using nude mice bearing with glioblastoma tumors. In conclusion, LINC00657 was effective in inhibiting glioblastoma by acting as a molecular sponge of miR-190a-3p to regulate PTEN expression. Therefore, targeting LINC00657 may serve as a potential strategy for the treatment of patients with glioblastoma.	30837348	RID06388	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Papillary thyroid carcinoma	TTN-AS1	ZNRF2	positively-E	luciferase reporter assay;qRT-PCR;western blot assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000180233	NA	100506866	223082	NA	RNF202	Using the online bioinformatics anal_x005f_x0002_ysis tool StarBase (http://starbase.sysu.edu.cn), we predicted 16 miRNAs that potentially interacted with TTN-AS1. Then, we examined the expression changes of these miRNAs in response to TTN-AS1 knockdown. The results obtained showed that only miR-153-3p was significantly negatively regulated by TTN-AS1. Therefore, we selected miR-153-3p for further analysis. The putative binding sites between TTN-AS1 and miR-153-3p were obtained . To determine the interaction between TTN-AS1 and miR-153-3p, a luciferase reporter assay was carried out in BCPAP and K1 cells. Furthermore, the RIP assay further confirmed the interaction between TTN-AS1 and miR-153-3p. Subse_x005f_x0002_quently, the miR-153-3p expression was found to be lower in PTC tis_x0002_sues and cell lines . The expression of miR-153-3p was negatively regulated by TTN.	30811764	RID06389	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Cholangiocarcinoma	SNHG1	TLR4	positively-E	luciferase reporter;western blot;starBase v2.0	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000136869	NA	23642	7099	LINC00057|lncRNA16|NCRNA00057|UHG	ARMD10|CD284|hToll|TLR-4	To verify the direct binding between SNHG1 and miRNA-140, luciferase reporter constructs were generated. We observed that miR-140 significantly declined the luciferase activity of reporter vector comprising SNHG1-wt, while it had no significant effect on the luciferase activity of reporter vector containing SNHG1-mut . Additionally, our results exhibited that SNHG1 knockdown significantly enhanced miR-140 level, and SNHG1 overexpression markedly reduced miR-140 level . Collectively, these data indicated that SNHG1 targeted miR-140 and inhibited miR-140 expression in HCCC-9810 and RBE cells.	30764893	RID06390	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	LINC00994	RUNX2	positively-E	luciferase reporter;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell growth(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(+)	ceRNA(miR-765-3p)	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000189196	GRCh38_3:64078361-64087363	ENSG00000124813	NA	100287879	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	The levels of LINC00994, miR-765-3p and RUNX2 were further analyzed in 10 paired pancreatic samples with real-time qPCR and/or western blot. We found that the LINC00994 and RUNX2 were upregulated in tumor tissues, while miR-765-3p was downregulated . In addition, LINC00994 levels were negatively correlated with miR-765-3p levels in pancreatic cancers (r = -0.6362) .	30739523	RID06391	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	HAGLR	SOX4	positively-E	luciferase reporter;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-421)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000124766	NA	401022	6659	HOXD-AS1|Mdgt|MIR7704HG	NA	A previous study indicated that miR-421 is downregulated in BCa tissues, and in this study, we found that miR-421 expression was inversely correlated with HOXD-AS1 expression in BCa tissues. miRNAs often regulate downstream gene expres_x005f_x0002_sion via binding to the 3'-UTR of target mRNAs, and in this study, SOX4, a master regulator of EMT, was predicted as the direct target of miR-421 in BCa. These results suggested that HOXD-AS1 can diminish the miR-421-mediated inhibition of SOX4, thus leading toEMT in BCa.	30730081	RID06392	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	HOTAIR	DACH1	positively-E	luciferase reporter;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-217)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000165659	NA	100124700	1602	HOXC-AS4|HOXC11-AS1|NCRNA00072	DACH	HOTAIR was up-regulated and miR-217 was down-regulated in NSCLC cell lines. Silencing of HOTAIR significantly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells by facilitating miR-217 expression. Moreover, bioinformatics analysis and Luciferase reporter assay confirmed that DACH1 was a target of miR-217. Furthermore, the overexpression of miR-217 markedly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells. DACH1 reverses the effects of miR-217 overexpression in NSCLC cells.	30720199	RID06393	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	ANKRD40CL	HOXA10	positively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-144)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000253293	NA	55018	3206	C17orf73|FLJ20694|LINC00483	HOX1|HOX1H	LINC00483 and HOXA10 were found to be upregulated whereas miR-144 was downregulated in LAD. Silencing of LINC00483 could competitively bind to miR-144, thereby upregulating HOXA10. LINC00483 or HOXA10 silencing led to decreased HOXA10, MMP-2, MMP-9, vimentin, and N-cadherin but elevated miR-144 and E-cadherin. Moreover, after being transfected with silenced LINC00483, the cell proliferation, migration, and invasion were inhibited with enhanced . Consequently, the data of the study indicates that interference of LINC00483 weakens its competitive binding ability to miR-144, thus reducing HOXA10 expression, and enhancing radiosensitivity in LAD.	30714135	RID06394	ceRNA or sponge	NA		
Lung adenocarcinoma	ANKRD40CL	BAX	negatively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000087088	NA	55018	581	C17orf73|FLJ20694|LINC00483	BCL2L4	To demonstrate the relationship between lncRNA-SNHG7 and Bax protein, we used western blot to detect the expression level of Bax after knockdown of lncRNA-SNHG7. Compared to the negative control group, the cells transfected with lncRNA-SNHG7 siRNA showed up-regulation of Bax (Fig. -(Fig.6).6). p21 is a hallmark of cell cycle regulation and acts as an inhibitor of cell growth 17. western blot showed that expression of p21 was significantly increased when lncRNA-SNHG7 was suppressed by siRNA (Fig. -(Fig.6).6). As shown in a previous study, E-cadherin serves as a strong suppressor of cell migration 18. We also found that expression of E-cadherin was obviously increased after silencing lncRNA-SNHG7 (Fig. -(Fig.6).6). These data suggested that Bax, p21 and E-cadherin genes might serve as potential downstream targets of lncRNA-SNHG7, and that lncRNA-SNHG7 plays a role in regulating bladder cancer cell phenotypes by down-regulating expression of Bax, p21 and E-cadherin protein.	30714135	RID06395	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	ANKRD40CL	CDKN1A	negatively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000124762	NA	55018	1026	C17orf73|LINC00483	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	To demonstrate the relationship between lncRNA-SNHG7 and Bax protein, we used western blot to detect the expression level of Bax after knockdown of lncRNA-SNHG7. Compared to the negative control group, the cells transfected with lncRNA-SNHG7 siRNA showed up-regulation of Bax (Fig. -(Fig.6).6). p21 is a hallmark of cell cycle regulation and acts as an inhibitor of cell growth 17. western blot showed that expression of p21 was significantly increased when lncRNA-SNHG7 was suppressed by siRNA (Fig. -(Fig.6).6). As shown in a previous study, E-cadherin serves as a strong suppressor of cell migration 18. We also found that expression of E-cadherin was obviously increased after silencing lncRNA-SNHG7 (Fig. -(Fig.6).6). These data suggested that Bax, p21 and E-cadherin genes might serve as potential downstream targets of lncRNA-SNHG7, and that lncRNA-SNHG7 plays a role in regulating bladder cancer cell phenotypes by down-regulating expression of Bax, p21 and E-cadherin protein.	30714135	RID06396	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Lung adenocarcinoma	ANKRD40CL	E-cadherin	negatively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	NA	NA	55018	NA	C17orf73|LINC00483	NA	To demonstrate the relationship between lncRNA-SNHG7 and Bax protein, we used western blot to detect the expression level of Bax after knockdown of lncRNA-SNHG7. Compared to the negative control group, the cells transfected with lncRNA-SNHG7 siRNA showed up-regulation of Bax (Fig. -(Fig.6).6). p21 is a hallmark of cell cycle regulation and acts as an inhibitor of cell growth 17. western blot showed that expression of p21 was significantly increased when lncRNA-SNHG7 was suppressed by siRNA (Fig. -(Fig.6).6). As shown in a previous study, E-cadherin serves as a strong suppressor of cell migration 18. We also found that expression of E-cadherin was obviously increased after silencing lncRNA-SNHG7 (Fig. -(Fig.6).6). These data suggested that Bax, p21 and E-cadherin genes might serve as potential downstream targets of lncRNA-SNHG7, and that lncRNA-SNHG7 plays a role in regulating bladder cancer cell phenotypes by down-regulating expression of Bax, p21 and E-cadherin protein.	30714135	RID06397	expression association	NA		
Gastric cancer	LNCNEF	RUNX1	positively-E	western blot	downregulation		NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000237396	GRCh38_20:22587522-22607517	ENSG00000159216	NA	101929685	861	LINC01384|lncRNA-NEF	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	It was revealed that NEF was significantly downregulated in tumor tissues compared with in adjacent tissues. Levels of circulation NEF in serum were lower in patients with gastric carcinoma compared with in healthy controls, and were decreased with the increasing stages of primary tumor. Serum NEF is a sensitive diagnostic and prognostic marker for gastric carcinoma. NEF siRNA silencing promoted, and overexpression inhibited, gastric carcinoma proliferation. In addition, NEF overexpression promoted, and NEF siRNA silencing inhibited, Runx1 expression. Therefore, it was concluded that lncRNA NEF may participate in the regulation of cancer cell proliferation by regulating Runx1 expression.	30664208	RID06398	expression association	prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	LINC00958	PAX8	positively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	RT-qPCR	GSE27890	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000125618	NA	100506305	7849	NA	NA	The epithelial mesenchymal transition (EMT) process, cell invasion, and tumor growth were determined in vitro and in vivo. LINC00958 and PAX8 were up regulated, while miR-330-5p was down-regulated during PC. LINC00958 mainly expressed in the cytoplasm and LINC00958 competitively sponged miR-330-5p. Upregulated miR-330-5p or downregulated PAX8 inhibited the EMT process as well as theinvasion and metastasis ability of the PC cells. Moreover, the results indicated that miR-330-5p negatively targeted PAX8, and LINC00958 ultimately showcasing its ability to bind to miR-330-5p through its interaction with AGO2. Therefore, silencing of LINC00958 may bind to miR-330-5p to inhibit PAX8 in a competitive fashion, thereby preventing the progression of PC	30639194	RID06399	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Osteosarcoma	MIAT	VEGFC	positively-E	western blot;luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-128-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000150630	NA	440823	7424	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	VEGF-C|VRP	We found that the expression level of VEGFC was over-expressed in both OS tissues and cell lines when compared with the counterparts (P < 0.05), and that VEGFC expression was inversely associated with miR-128-3p expression in OS tissues (R2 = 0.1588, P = 0.040). Result of dual-luciferase reporter assay revealed that transfection of miR-128-3p mimics decreased the luciferase activity of VEGFC-WT but not VEGFC_x005f_x0002_Mut in MG63 cells (P < 0.05). In addition, we found that knockdown of MIAT decreased both mRNA and protein levels of VEGFC, but these effects were significantly reversed after inhibition of miR-128 3p (P < 0.05). These data suggested that MIAT promoted VEGFC expression by competi_x0002_tively binding to miR 128-3p in MG63 cells	30629798	RID06400	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	ZEB1-AS1	STAT3	positively-E	western blot;RIP	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);prognosis(-)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000168610	NA	220930	6774	NA	APRF	We selected STAT3 and SUZ12 to carry out the RNA immunoprecipitation assay and confirmed that ZEB1-AS1 directly bound to STAT3 in H1299 and A-427 cells (Fig. 5B). To identify the potential targets associated with cell proliferation of NSCLC, we detected the expression of ID1 in H1299 and A-427 cells with ZEB1-AS1 knockdown. ID1 protein was negatively correlated with ZEB1-AS1 knockdown in H1299 and A-427 cells (Fig. 5C). Inhibition of STAT3 increased the expression of ID1 mRNA and protein (Fig. 5D-F). The chromatin immunoprecipitation results showed that STAT3 bound to the ID1 promoter region, while ZEB1-AS1 knockdown reduced the binding between STAT3 and the ID1 promoter region (Fig. 5G). In addition, ZEB1-AS1 expression was negatively correlated with ID1 expression in 18 paired NSCLC and adjacent non-tumor lung tissues (P=0.021, Fig. 5H). These data suggest that ZEB1-AS1 might partially promote NSCLC cell proliferation by binding to STAT3 to silence ID1 transcription at the epigenetic level.	30626729	RID06401	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	ZEB1-AS1	ID1	negatively-E	western blot;RIP	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);prognosis(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000125968	NA	220930	3397	NA	bHLHb24|dJ857M17.1.2	We selected STAT3 and SUZ12 to carry out the RNA immunoprecipitation assay and confirmed that ZEB1-AS1 directly bound to STAT3 in H1299 and A-427 cells (Fig. 5B). To identify the potential targets associated with cell proliferation of NSCLC, we detected the expression of ID1 in H1299 and A-427 cells with ZEB1-AS1 knockdown. ID1 protein was negatively correlated with ZEB1-AS1 knockdown in H1299 and A-427 cells (Fig. 5C). Inhibition of STAT3 increased the expression of ID1 mRNA and protein (Fig. 5D-F). The chromatin immunoprecipitation results showed that STAT3 bound to the ID1 promoter region, while ZEB1-AS1 knockdown reduced the binding between STAT3 and the ID1 promoter region (Fig. 5G). In addition, ZEB1-AS1 expression was negatively correlated with ID1 expression in 18 paired NSCLC and adjacent non-tumor lung tissues (P=0.021, Fig. 5H). These data suggest that ZEB1-AS1 might partially promote NSCLC cell proliferation by binding to STAT3 to silence ID1 transcription at the epigenetic level.	30626729	RID06402	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	UP(NSCLC);DATA(GSE74639)
Neuroblastoma	SNHG7	STAT2	positively-E	western blot;luciferase assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-653-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000170581	NA	84973	6773	MGC16037|NCRNA00061	STAT113	Mechanically, the bioinformatics analysis predicted that miR-653-5p was the shared partner of SNHG7 and signal transducer and activator of transcription 2 (STAT2). Unsurprisingly, we further confirmed that SNHG7 could interact with miR-653-5p and therefore functioned as the ceRNA of STAT2 so as to regulate STAT2 expression in NB cells. Moreover, STAT2 expression was in inverse proportion to miR-653-5p level but in positive proportion to SNHG7 level in NB tissues. Importantly, the repressed NB progression induced by silenced SNHG7 was reversed by STAT2 overexpression or miR-653-5p inhibitors. Jointly, our findings elucidated SNHG7 facilitated NB progression through the miR-653-5p/STAT2 pathway, providing a novel therapeutic target and prognostic biomarker for this disease.	30623419	RID06403	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	DGCR5	MTOR	positively-E	western blot	downregulation	RT-qPCR	NA	NA	mTOR signaling pathway(-);cell proliferation(-);apoptosis process(+);cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000198793	NA	26220	2475	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	mTOR has been recognized as an atypical serine/threonine kinase that is involved in regulating significant cellular functions. In our present study, we observed that the mTOR signaling pathway was strongly activated in human cervical cancer cells. Meanwhile, upregulation of LINC00037 contributed to the inactivation of mTOR signaling whereas downregulation of LINC00037 activated the pathway. Subsequently, in vivo animal models using SiHa cells were established and we proved that LINC00037 repressed cervical cancer progression via targeting the mTOR signaling pathway. All these findings implied that LINC00037 could regulate cervical cancer pathogenesis via mTOR signaling. In conclusion, a novel role of LINC00037 was manifested in cervical cancer progression.	30613967	RID06404	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	ST3GAL6-AS1	FOXO1	negatively-E	western blot;RIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-);cell metastasis(-);cell proliferation(-);apoptosis process(+);TNM stage(-);PI3K/AKT signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000239445	GRCh38_3:98706236-98732757	ENSG00000150907	NA	100874207	2308	NA	FKH1|FKHR|FOXO1A	The correlation between ST3Gal6-AS1 and ST3Gal6 was further validated in several types of CRC cell lines. In addition, ST3Gal6 was dysregulated and positively correlated to ST3Gal6-AS1. ST3Gal6-AS1 recruited histone methyltransferase MLL1 to the promoter region of ST3Gal6, induced H3K4me3 modification and activated ST3Gal6 transcription. Furthermore, ST3Gal6-AS1/ST3Gal6 axis mediated alpha-2, 3 sialylation and inhibited the activation of PI3K/Akt signaling, thereby resulting in Foxo1 nuclear translocation in CRC cells. ST3Gal6-AS1 was a target of transcription factor Foxo1 and regulated by Foxo1. ST3Gal6-AS1 also inhibited CRC  in vitro. Overexpression of ST3Gal6-AS1 significantly decreased the tumorigenesis, lung and liver metastasis of SW620 cells in vivo. ST3Gal6-AS1 expression was negatively correlated with tumor size, lymphatic metastasis, distant metastasis and tumor stage in CRC patients. Collectively, these data indicated that ST3Gal6-AS1, ST3Gal6, PI3K/Akt, and Foxo1 formed a positive feedback loop, which might play a key role in CRC progression.	30613961	RID06405	expression association	metastasis		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	ST3GAL6-AS1	ST3GAL6	positively-E	western blot;RIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-);cell metastasis(-);cell proliferation(-);apoptosis process(+);TNM stage(-);PI3K/AKT signaling pathway(-)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000239445	GRCh38_3:98706236-98732757	ENSG00000064225	NA	100874207	10402	NA	SIAT10|ST3GALVI	The correlation between ST3Gal6-AS1 and ST3Gal6 was further validated in several types of CRC cell lines. In addition, ST3Gal6 was dysregulated and positively correlated to ST3Gal6-AS1. ST3Gal6-AS1 recruited histone methyltransferase MLL1 to the promoter region of ST3Gal6, induced H3K4me3 modification and activated ST3Gal6 transcription. Furthermore, ST3Gal6-AS1/ST3Gal6 axis mediated alpha-2, 3 sialylation and inhibited the activation of PI3K/Akt signaling, thereby resulting in Foxo1 nuclear translocation in CRC cells. ST3Gal6-AS1 was a target of transcription factor Foxo1 and regulated by Foxo1. ST3Gal6-AS1 also inhibited CRC  in vitro. Overexpression of ST3Gal6-AS1 significantly decreased the tumorigenesis, lung and liver metastasis of SW620 cells in vivo. ST3Gal6-AS1 expression was negatively correlated with tumor size, lymphatic metastasis, distant metastasis and tumor stage in CRC patients. Collectively, these data indicated that ST3Gal6-AS1, ST3Gal6, PI3K/Akt, and Foxo1 formed a positive feedback loop, which might play a key role in CRC progression.	30613961	RID06406	expression association	metastasis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827)
Colorectal cancer	FOXO1	ST3GAL6-AS1	negatively-E	western blot;RIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(-);cell metastasis(-);cell proliferation(-);apoptosis process(+);TNM stage(-);PI3K/AKT signaling pathway(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000150907	NA	ENSG00000239445	GRCh38_3:98706236-98732757	2308	100874207	FKH1|FKHR|FOXO1A	NA	The correlation between ST3Gal6-AS1 and ST3Gal6 was further validated in several types of CRC cell lines. In addition, ST3Gal6 was dysregulated and positively correlated to ST3Gal6-AS1. ST3Gal6-AS1 recruited histone methyltransferase MLL1 to the promoter region of ST3Gal6, induced H3K4me3 modification and activated ST3Gal6 transcription. Furthermore, ST3Gal6-AS1/ST3Gal6 axis mediated alpha-2, 3 sialylation and inhibited the activation of PI3K/Akt signaling, thereby resulting in Foxo1 nuclear translocation in CRC cells. ST3Gal6-AS1 was a target of transcription factor Foxo1 and regulated by Foxo1. ST3Gal6-AS1 also inhibited CRC  in vitro. Overexpression of ST3Gal6-AS1 significantly decreased the tumorigenesis, lung and liver metastasis of SW620 cells in vivo. ST3Gal6-AS1 expression was negatively correlated with tumor size, lymphatic metastasis, distant metastasis and tumor stage in CRC patients. Collectively, these data indicated that ST3Gal6-AS1, ST3Gal6, PI3K/Akt, and Foxo1 formed a positive feedback loop, which might play a key role in CRC progression.	30613961	RID06407	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Lung cancer	FBXL19-AS1	RAF1	positively-E	western blot;luciferase assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-431-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000132155	NA	283932	5894	MGC125469|MGC125470|MGC125472|NCRNA00095	c-Raf|CRAF|Raf-1	Pull-down assay further confirmed that miR-431-5p could directly bind with RAF1 (Figure 4C). Fatherly, we discovered that RAF1 expression was down-regulated in miR-431-5p mimic transfected lung cancer cells by western blot (Figure 4D). Moreover, the expression level of RAF1 was significantly up-regulated in lung cancer tissues compared with non-tumor tissues (Figure 4E). Moreover, Spearman Rank correlation analysis demonstrated that there was the negative correlation between expression of RAF1 and miR-431-5p in tumor tissues, and the positive correlation between expression of FBXL19-AS1 and RAF1 in tumor tissues (r = -0.231, r = 0.243, P<0.05, Figure 4F,G). The patients who had high levels of RAF1 came out with notably poorer prognosis than those who had low levels of RAF1 (Figure 4H). All these data suggested that RAF1 is a downstream target of miR-431-5p, and FBXL19-AS1 could regulate RAF1 expression by targeting miR-431-5p.	30610161	RID06408	ceRNA or sponge	prognosis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	MSC-AS1	miR-140-5p	negatively-F	RNA pull-down assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000235531	GRCh38_8:71828167-72118393	NA	NA	100132891	NA	NA	NA	Using the bioinformatics website (http://starbase.sysu.edu.cn/index.php), we found that both lncRNA MSC-AS1 and CDK6 were combined to miR-142 at some sites. The findings of dual-luciferase reporter gene assay showed decreased luciferase activity of WT lncRNA MSC-AS1 and miR-142, and that of WT CDK6 and miR-142 also significantly declined (both p<0.05) (Figure 4C). RNA pull-down assay provided another confirmation that there was a binding site between lncRNA MSC-AS1 and miR-142 (Figure 4D). With lncRNA MSC-AS1 knockdown, miR-142 was significantly elevated, while mRNA and protein expression in CDK6 was greatly decreased, and protein expression in p-PI3K/t-PI3K and p-AKT/t-AKT also steeply declined (all p<0.05), but all these results were the opposite with overexpressed lncRNA MSC-AS1 (Figure 4E, 4F).	32155139	RID06409	ceRNA or sponge	NA		
Osteosarcoma	MSC-AS1	CDK6	positively-E	RNA pull-down assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000235531	GRCh38_8:71828167-72118393	ENSG00000105810	NA	100132891	1021	NA	PLSTIRE	miRs are already regarded as a standard in assessment in cancer clinics by affecting different oncogenes and tumor suppressor genes expression [23]. Gain-of-function assays indicated that miR-142 overexpression reduced OS cell development by suppressing cell proliferation and invasion and arrested the cell cycle in the S phase [19]. In the present study, we assessed the mechanism of lncRNA MSC-AS1 in OS biological behaviors and cell sensitivity to DDP via binding to miR-142. Consequently, our data showed that downregulated MSC-AS1 could promote expression of miR-142 to decrease CDK6 expression and inhibit the activation of the PI3K/AKT signaling pathway to slow OS progression and make it more sensitive to DDP.	32155139	RID06410	ceRNA or sponge	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	LEF1-AS1	WNK1	positively-E	luciferase reporter gene assay system;RNA pull-down assay;mirDIP;starBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-136-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000060237	NA	641518	65125	NA	HSAN2|HSN2|PPP1R167|PRKWNK1	Besides, the prediction results regarding the expression pattern of miR-136-5p revealed that miR-136-5p was poorly expressed miR in HCC. The mirDIP and starBase databases were used to continue exploring the downstream regulatory genes of miR-136-5p with results showing 76 potential target genes of miR-136-5p, among which the implication of WNK1 was documented in the regulation of HCC. The correlation analysis between WNK1 expression and the survival rate of patients with HCC showed that an elevated WNK1 expression in HCC was linked to lower survival rate in patients with HCC. Altogether, it can be hypothesized that the lncRNA LEF1-AS1-miR-136-5p-WNK1 axis may exhibit a participatory role in the development of HCC.	32068261	RID06411	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical squamous cell carcinoma	TGFB1	loc285194	negatively-F	western blot	downregulation	qRT-PCR	NA	NA	cell migration(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Cervical cancer	PCG	lncRNA	ENSG00000105329	NA	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	NA	Enzyme-linked immunosorbent assay (ELISA) and western blot were used to measure levels of transforming growth factor--1 (TGF--1). A lncRNA loc285194 expression vector was constructed and transfected into SiHa and C33A cells that underwent a transwell assay for cell migration. RESULTS Expression of lncRNA loc285194 was downregulated in HPV-positive and HPV-negative tissue samples and plasma from patients with CSCC and distinguished between patients and healthy controls. Plasma levels of loc285194 and TGF--1 were significantly correlated with the presence of CSCC. In SiHa and C33A cells, TGF--1 expression was downregulated, and cell migration was inhibited following lncRNA loc285194 overexpression. Although lncRNA loc285194 expression was not affected by TGF--1 treatment, its effects on cell migration were reduced by TGF--1. CONCLUSIONS The expression of lncRNA loc285194 inhibited the migration of CSCC cells in vitro through the inactivation of TGF--1.	31774069	RID06412	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Non-small cell lung cancer	PVT1	miR181a-5p	negatively-E	western blot;Luciferase assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	NA	regulation	RNA-RNA	Xiaoji Decoction;Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	XJD decreased SP1 protein, which were overcame by overexpressed PVT1 and inhibitors of miR181a-5p. Overexpressed SP1 reversed the inhibitory effect of XJD on cell growth. Importantly, XJD and DDP exhibited synergy on regulation of PVT1, miR181a-5p, and SP1 expressions. The similar results were observed in one in vivo model. In conclusions, XJD inhibits NSCLC cell growth via reciprocal interaction of PVT1 and miR181a-5p followed by reducing SP1 expression. XJD and DDP exhibit synergy. This study provides a novel mechanism by which XJD enhances the anti-cancer effect of DDP in NSCLC cells.	31707347	RID06413	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Non-small cell lung cancer	miR181a-5p	PVT1	negatively-E	western blot;Luciferase assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	NA	regulation	RNA-RNA	Xiaoji Decoction;Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	XJD decreased SP1 protein, which were overcame by overexpressed PVT1 and inhibitors of miR181a-5p. Overexpressed SP1 reversed the inhibitory effect of XJD on cell growth. Importantly, XJD and DDP exhibited synergy on regulation of PVT1, miR181a-5p, and SP1 expressions. The similar results were observed in one in vivo model. In conclusions, XJD inhibits NSCLC cell growth via reciprocal interaction of PVT1 and miR181a-5p followed by reducing SP1 expression. XJD and DDP exhibit synergy. This study provides a novel mechanism by which XJD enhances the anti-cancer effect of DDP in NSCLC cells.	31707347	RID06414	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Non-small cell lung cancer	PVT1	SP1	negatively-E	western blot;Luciferase assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	NA	regulation	NA	Xiaoji Decoction;Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000185591	NA	5820	6667	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	XJD decreased SP1 protein, which were overcame by overexpressed PVT1 and inhibitors of miR181a-5p. Overexpressed SP1 reversed the inhibitory effect of XJD on cell growth. Importantly, XJD and DDP exhibited synergy on regulation of PVT1, miR181a-5p, and SP1 expressions. The similar results were observed in one in vivo model. In conclusions, XJD inhibits NSCLC cell growth via reciprocal interaction of PVT1 and miR181a-5p followed by reducing SP1 expression. XJD and DDP exhibit synergy. This study provides a novel mechanism by which XJD enhances the anti-cancer effect of DDP in NSCLC cells.	31707347	RID06415	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	LINC01638	TGFB1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000233521	GRCh38_22:27221349-27225134	ENSG00000105329	NA	105372978	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	By contrast, LINC01638 shRNA knockdown led to significantly downregulated expression of TGF-beta1 in cells in the PDAC cell line, PL45 (P<0.05; Fig. 4B); however, LINC01638 knockdown did not alter expression of TGF-beta1 in the hTERT-HPNE normal pancreas duct cell line. In addition, treatment with exogenous TGF-beta1 at concentrations of 10, 20 and 40 ng/ml did not significantly affect the expression of LINC01638 in the two cell lines (data not shown). Therefore, LINC01638 is likely to be an upstream activator of TGF-beta1 in PDAC.	31702018	RID06416	expression association	NA	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	EZR-AS1	TGFB1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-);TGF-beta signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000105329	NA	101409257	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Silencing of lncRNA EZR-AS1 significantly down-regulated the expression of TGF-beta, Smad2 (a signal transduction protein of TGF-beta), and alpha-SMA (a response protein of TGF-beta) in HCT116 and HT29 cells at the protein level (P<0.01). The protein levels of TGF-beta, Smad2, and alpha-SMA in HCT116 and HT29 cells were not significantly influenced by the transfection of NC-EZR-AS1 (Figure 5A,B).	31693738	RID06417	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	EZR-AS1	SMAD2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-);TGF-beta signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000175387	NA	101409257	4087	NA	JV18-1|MADH2|MADR2	Silencing of lncRNA EZR-AS1 significantly down-regulated the expression of TGF-beta, Smad2 (a signal transduction protein of TGF-beta), and alpha-SMA (a response protein of TGF-beta) in HCT116 and HT29 cells at the protein level (P<0.01). The protein levels of TGF-beta, Smad2, and alpha-SMA in HCT116 and HT29 cells were not significantly influenced by the transfection of NC-EZR-AS1 (Figure 5A,B).	31693738	RID06418	expression association	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	EZR-AS1	alpha-SMA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-);TGF-beta signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	NA	NA	101409257	NA	NA	NA	Silencing of lncRNA EZR-AS1 significantly down-regulated the expression of TGF-beta, Smad2 (a signal transduction protein of TGF-beta), and alpha-SMA (a response protein of TGF-beta) in HCT116 and HT29 cells at the protein level (P<0.01). The protein levels of TGF-beta, Smad2, and alpha-SMA in HCT116 and HT29 cells were not significantly influenced by the transfection of NC-EZR-AS1 (Figure 5A,B).	31693738	RID06419	expression association	NA		
Colorectal cancer	SMAD2	EZR-AS1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);epithelial to mesenchymal transition(-);apoptosis process(+);TGF-beta signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000175387	NA	ENSG00000233893	GRCh38_6:158817979-158822252	4087	101409257	JV18-1|MADH2|MADR2	NA	The intervention of SB431542 significantly inhibited TGF-beta-induced up-regulation of pSmad2 in HCT116 and HT29 cells at the protein level (P<0.01) (Figure 6A), and TGF-beta-induced up-regulation of lncRNA EZR-AS1 expression (P<0.05) (Figure 6B). In addition, Smad2 was further silenced to block TGF-beta signaling in HCT116 and HT29 cells by the transfection of sh-Smad2 (P<0.01) (Figure 6C,D). Silencing of Smad2 also significantly down-regulated lncRNA EZR-AS1 expression in HCT116 and HT29 cells (P<0.01) (Figure 6E).	31693738	RID06420	expression association	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Colorectal cancer	EZR-AS1	E-cadherin	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-);TGF-beta signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	NA	NA	101409257	NA	NA	NA	As shown in Figure 1C, silencing of lncRNA EZR-AS1 significantly up-regulated E-cadherin expression, and down-regulated Vimentin expression in HCT116 and HT29 cells at the protein level (P<0.05). The levels of E-cadherin and Vimentin in HCT116 and HT29 cells were not significantly influenced by silencing of lncRNA EZR-AS1 (Figure 1D).	31693738	RID06421	expression association	NA		
Colorectal cancer	EZR-AS1	Vimentin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-);TGF-beta signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	NA	NA	101409257	NA	NA	NA	As shown in Figure 1C, silencing of lncRNA EZR-AS1 significantly up-regulated E-cadherin expression, and down-regulated Vimentin expression in HCT116 and HT29 cells at the protein level (P<0.05). The levels of E-cadherin and Vimentin in HCT116 and HT29 cells were not significantly influenced by silencing of lncRNA EZR-AS1 (Figure 1D).	31693738	RID06422	expression association	NA		
Gastric cancer	COL1A1-014	miR-1273h-5p	negatively-F	miRanda;miRcode;Luciferase reporter assay;western blot	upregulation	RT-PCR;western blot	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cel invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	We found that COL1A1-014 was frequently upregulated in GC tissues as well as cells. COL1A1-014 increased cell proliferation, colony forming efficiency, migration ability, invasion ability, and weight and volume of grafted tumors, while reduced cell apoptosis. Overexpression of COL1A1-014 increased the mRNA expression of chemokine (CXCmotif) ligand (CXCL12) and high levels of CXCL12 and CXCR4 proteins in GC cells. The levels of miR-1273h-5p showed an inverse correlation with COL1A1-014 and CXCL12 in GC cells transfected with miR-1273h-5p. The mRNAs of wild-type COL1A1-014 and CXCL12 showed reduction in HEK293 cells transfected with miR-1273h-5p. This suggested that COL1A1-014 functions as an efficient miR-1273h-5p sponge and as a competing endogenous RNA (ceRNA) to regulate CXCL12. The proliferative activity of COL1A1-014 on GC cells was blocked by CXCL12-CXCR4 axis inhibitor AMD-3100.	31650323	RID06423	ceRNA or sponge	chemoresistance		
Colorectal cancer	MIR503HG	TGFB2	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000092969	NA	84848	7042	H19X|MIR503HG2	G-TSF|LDS4|TGF-beta2	CR4 and RKO cells were transfected with MIR503HG and TGF-beta2 expression vectors. Comparing to NC (empty vector transfection) and C (cells without transfections) groups, MIR503HG and TGF-beta2 mRNA expression levels were significantly increased at 24 h after transfections (Fig. 3A, p < 0.05). Moreover, MIR503HG overexpression was ac_x005f_x0002_companied by TGF-beta2 downregulation in cells of both cell lines (Fig. 3B, p < 0.05), while TGF-beta2 overexpression did not affect MIR503HG (Fig. 3C	31278965	RID06424	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	TINCR	TP53	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000141510	NA	257000	7157	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	LFS1|p53	Analysis of deep sequencing data (15 libraries) by linear regression showed that P53 mRNA and PLAC2 were significantly and positively correlated (Supplemental Fig. 1). To further confirm this correlation, P53 mRNA expression in two types of tissues was also detected by performing RT-qPCR. Expression data were compared between 2 types of tissues by performing paired t-test. It was observed that expression levels of p53 mRNA were also significantly lower in HCC tissues than in non-cancer tissues (Fig. 3A, p < 0.05). Correlations between p53 mRNA and PLAC2 were analyzed by performing linear regression. It was found that p53 mRNA and PLAC2 were positively and significantly correlated in HCC tissues (Fig. 3B), but not in adjacent normal tissues (Fig. 3C). Analysis of deep sequencing data by linear regression showed that P53 mRNA and PLAC2 were significantly and positively correlated.	31233763	RID06425	expression association	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	HOTAIR	HOXA5	negatively-E	RNA pull-down assay;western blot;luciferase assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106004	NA	100124700	3202	HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX1|HOX1C	LncRNA HOTAIR was found to be upregulated in AML cells and tissues. With silencing of HOTAIR and overexpression of HOXA5, AML cell proliferation was decreased while the apoptosis was induced. Furthermore, HOTAIR was observed to recruit Dnmt3b and to increase HOXA5 promoter methylation. Moreover, silencing HOTAIR and upregulating HOXA5 were found to induce apoptosis and reduce proliferation of AML cells in vivo.	31168296	RID06426	epigenetic regulation	NA		
Acute myeloid leukemia	HOTAIR	DNMT3B	positively-E	RNA pull-down assay;western blot;luciferase assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000088305	NA	100124700	1789	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	It was found that the HOTAIR-Wt group showed decreased degradation of Dnmt3b expression while the HOTAIR-Mut group showed no Dnmt3b. Furthermore, CHIP was performed to detect whether Dnmt3b could directly bind to HOXA5 promoter region and whether HOTAIR affected the binding of Dnmt3b with HOXA5 promoter. Compared with the oe-NC group, Dnmt3b was remarkably enriched in HOXA5 promoter region in the oe-HOTAIR group. Compared with the oe-HOTAIR-+-sh-NC group, the oe-HOTAIR-+-sh-Dnmt3b group showed reduced enrichment of Dnmt3b in HOXA5 promoter region (p-<-0.05). western blotshowed that compared with the oe-NC group, the expression of HOXA5 in the oe-HOTAIR group was significantly decreased. In contrast to the oe-HOTAIR-+-sh-NC group, the expression of HOXA5 in the oe-HOTAIR-+-sh-Dnmt3b group was notably increased (p-<-0.05). Taken together, HOTAIR, together with Dnmt3b, was able to promote the methylation of HOXA5 and then inhibited the expression of HOXA5.	31168296	RID06427	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	GAS8-AS1	AFAP1-AS1	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	lncRNA	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000272620	GRCh38_4:7754077-7778928	750	84740	C16orf3	AFAP1-AS|AFAP1AS|MGC10981	GAS8-AS1 overexpression mediated the downregulation of AFAP1-AS1 in colon cancer cells, while AFAP1-AS1 overexpression did not significantly affect GAS8-AS1 expression. Expression level of GAS8-AS1 decreased, while expression level of AFAP1-AS1 increased with the increase of primary tumor diameters. GAS8-AS1 overexpression led to inhibited, while AFAP1-AS1 overexpression led to promoted proliferation of CRC cells, and AFAP1-AS1 overexpression reduced the inhibitory effects of GAS8-AS1 overexpression on cancer cell proliferation. Therefore, GAS8-AS may inhibit CRC cell proliferation by downregulating AFAP1-AS1.	31132513	RID06428	expression association	NA		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Triple-negative breast cancer	NRON	snaR	negatively-E		upregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	lncRNA	ENSG00000253079	GRCh38_9:126408041-126408410	NA	NA	641373	NA	NCRNA00194	NA	Expression levels of snaR increased, while expression levels of NRON decreased along with the increase of clinical stages. The snaR overexpression resulted in promoted cancer cell proliferation but did not significantly affect NRON expression. NRON overexpression inhibited cancer cell proliferation and down-regulated snaR. The snaR overexpression reduced the effects of NRON overexpression. We therefore conclude that NRON may down-regulate lncRNA snaR to inhibit cancer cell proliferation in TNBC.	30996114	RID06429	expression association	NA		
Hepatocellular carcinoma	HBX	SNHG20	positively-E	RNA pull-down assay;western blot;luciferase assay;RIP	upregulation	western blot;qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);apoptosis process(-)	NA	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	PCG	lncRNA	NA	NA	ENSG00000234912	GRCh38_17:77086716-77099902	NA	654434	NA	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	Besides, SNHG20 was highly expressed in HBV(+) HCC cells than in HBV(-) HCC cells. SNHG20 expression level was positively associated with HBV x protein (HBx) in HCC cells, and HBx-SNHG20 involved in regulating the proliferation and apoptosis of HCC cells. Moreover, SNHG20 was confirmed to interact with PTEN, which negatively regulated PTEN protein level. Finally, we proved HBx-SNHG20-PTEN signalling pathway involved in the regulation of HCC cell proliferation and apoptosis. In vivo experiments showed SNHG20 knockdown inhibited tumour growth of HBV(+) HCC. HBx promoted the proliferation of HCC cell and reduced the apoptosis of HCC cells through the SNHG20/PTEN signalling pathway.	30690477	RID06430	expression association	NA		UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)
Hepatocellular carcinoma	SNHG20	PTEN	negatively-E	RNA pull-down;RIP	upregulation	qRT-PCR	NA	NA	cell growth(-);cell proliferation(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000171862	NA	654434	5728	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	BZS|MHAM|MMAC1|PTEN1|TEP1	SNHG20 expression level was positively associated with HBV x protein (HBx) in HCC cells, and HBx-SNHG20 involved in regulating the proliferation and apoptosis of HCC cells. Moreover, SNHG20 was confirmed to interact with PTEN, which negatively regulated PTEN protein level. Finally, we proved HBx-SNHG20-PTEN signalling pathway involved in the regulation of HCC cell proliferation and apoptosis. In vivo experiments showed SNHG20 knockdown inhibited tumour growth of HBV(+) HCC. HBx promoted the proliferation of HCC cell and reduced the apoptosis of HCC cells through the SNHG20/PTEN signalling pathway.	30690477	RID06431	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Oral squamous cell carcinoma	MYC	SNHG16	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000163597	GRCh38_17:76557733-76565357	4609	100507246	bHLHe39|c-Myc|MYCC	Nbla10727|Nbla12061|ncRAN	Depletion of SNHG16 in CAL-27 cells strikingly inhibited cell proliferation, migration and invasion, as indicated by downregulation of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, depletion of SNHG16 induced cell apoptosis and inhibited epithelial-to-mesenchymal transition as indicated by induction of cleaved caspase-3 and epithelial cadherin (E-cadherin) along with reduction of N-cadherin and Snail. Intriguingly, c-Myc knockdown led to the similar functional effects as that of SNHG16 knockdown in TSCCA cells. However, these changes caused by c-Myc knockdown were abrogated by SNHG16 overexpression. Knockdown of SNHG16 conspicuously repressed tumor growth in nude mice. Similarly, silencing of c-Myc markedly inhibited tumor growth and reduced SNHG16 expression in nude mice. Moreover, overexpression of SNHG16 blocked the inhibitory effect of c-Myc silencing on tumor growth in vivo. Thus, we conclude that c-Myc-induced upregulation of SNHG16 enhances progression and carcinogenesis in OSCC.	30607006	RID06432	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	TPTEP1	miR-328-5p	negatively-F	miRDB;luciferase reporter assay;western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);	sponge	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000100181	GRCh38_22:16601887-16698742	NA	NA	387590	NA	psiTPTE22	NA	Conversely, overexpression of TPTEP1 decreased miR-328-5p levels in A549 and NCI-H1299 cells (Fig. 3G and H). Transfection of miR-328-5p mimics was confirmed to increase miR-328-5p levels in A549 and NCI-H1299 cells (Fig. 3I and J). In the dual-luciferase reporter assay, overexpression of miR-328-5p was indicated to decrease the relative luciferase activity of pGL3-TPTEP1-wild-type (WT) plasmid but did not influence the relative luciferase activity of pGL3-TPTEP1-Mut in A549 cells (Fig. 3K). Similarly, miR-328-5p mimics also suppressed the relative luciferase activity of pGL3-TPTEP1-WT in NCI-H1299 cells (Fig. 3L). These results indicated that TPTEP1 directly interacts with miR-328-5p in NSCLC cells.	32323798	RID06433	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Non-small cell lung cancer	TPTEP1	SRCIN1	positively-E	miRDB;luciferase reporter assay;western blot	downregulation	RT-qPCR	NA	NA	Src signaling pathway(-);STAT3 signaling pathway(-)	ceRNA(miR-328-5p)	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000100181	GRCh38_22:16601887-16698742	ENSG00000017373	NA	387590	80725	psiTPTE22	KIAA1684|p140Cap|SNIP	Pearson correlation analysis revealed a significant positive correlation between TPTEP1 and SRCIN1 mRNA levels in NSCLC tumors. The present results provided insight into the roles of TPTEP1 in NSCLC and the underlying mechanisms.	32323798	RID06434	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Papillary thyroid carcinoma	PSTPIP1	HOTTIP	negatively-E		downregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	association	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	PCG	lncRNA	ENSG00000140368	NA	ENSG00000243766	GRCh38_7:27198575-27207259	9051	100316868	CD2BP1|CD2BP1L|CD2BP1S|H-PIP|PAPAS|PSTPIP	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	PAPAS was downregulated, while the lncRNA HOXA transcript at the distal tip (HOTTIP) was upregulated in patients with PTC. PAPAS and HOTTIP were inversely associated in PTC. PAPAS overexpression led to the downregulation of HOTTIP in PTC cells, while PAPAS expression was not significantly affected by HOTTIP overexpression, suggesting that PAPAS was upstream of HOTTIP. PAPAS expression level decreased, while HOTTIP expression level increased with the increase of clinical staging. PAPAS overexpression led to the inhibition of cell proliferation, while HOTTIP overexpression increased proliferation of PTC cells, and HOTTIP overexpression decreased the effects of PAPAS overexpression. lncRNA PAPAS overexpression may inhibit tumor growth in papillary thyroid carcinoma by downregulating lncRNA HOTTIP.	32194727	RID06435	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Clear cell renal cell carcinoma	NR2F2-AS1	RAC1	positively-E		upregulation	RT-qPCR	NA	NA	cell stemness(+)	NA	association	RNA-protein	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000247809	GRCh38_15:96110040-96327361	ENSG00000136238	NA	644192	5879	NA	p21-Rac1|Rac-1|TC-25	NR2F2-AS1 was upregulated in ccRCC, and high NR2F2-AS1 expression levels in ccRCC tissues were associated with poor survival. Rac1 was also upregulated in ccRCC and positively correlated with NR2F2-AS1. In ccRCC cells, NR2F2-AS1 overexpression mediated the upregulation of Rac1, whereas NR2F2-AS1 siRNA was accompanied by Rac1 downregulation. NR2F2-AS1 and Rac1 overexpression resulted in the increased ccRCC cell stemness, whereas NR2F2-AS1 and Rac1 siRNA silencing played an opposite role. Rac1 overexpression inhibited the role of NR2F2-AS1 siRNA silencing.	32109138	RID06436	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Prostate cancer	CCAT1	FSCN1	positively-E	luciferase activity;RNAi;RNA pull-down;western blot;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);chemosensitivity(+)	ceRNA(miR-24-3p)	regulation	RNA-protein	Paclitaxel	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000075618	NA	100507056	6624	CARLO5|CARLo-5|onco-lncRNA-40	FLJ38511|p55|SNL	The interaction among CCAT1, miR-24-3p and FSCN1 was explored by luciferase activity, RNA immunoprecipitation, RNA pull-down and western blot, respectively. Results showed that the expressions of CCAT1 were up-regulated and miR-24-3p was down-regulated in PCa and PTX-resistant PCa cells (PC3-TXR and DU145-TXR). Knockdown of CCAT1 or overexpression of miR-24-3p inhibited survival rate, half maximal inhibitory concentration (IC50) of PTX but increased apoptosis in PC3-TXR and DU145-TXR cells after treatment of PTX. miR-24-3p was bound to CCAT1 and its abrogation reversed knockdown of CCAT1-mediated increase of PTX sensitivity in PC3-TXR and DU145-TXR cells. Moreover, FSCN1 restoration attenuated miR-24-3p-mediated inhibition of PTX resistance. Besides, FSCN1 level was enhanced in PCa and PTX-resistant PCa cells and regulated by CCAT1 and miR-24-3p. Our data suggested interference of CCAT1 contributed to PTX sensitivity in PCa by regulating miR-24-3p and FSCN1, indicating a novel avenue for treatment of PCa through regulating chemoresistance.	32089062	RID06437	ceRNA or sponge	chemoresistance		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Papillary thyroid carcinoma	WT1-AS	miR-203	positively-E		downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000183242	GRCh38_11:32435518-32500632	ENSG00000207568	NA	51352	NA	WIT-1|WIT1|WT1-AS1|WT1AS	NA	We found that WT1-AS was significantly downregulated in PTC and associated with clinical stages. In PTC tissues, WT1-AS was negatively correlated with survivin but positively correlated with miR-203. In PTC cells, WT1-AS overexpression led to significantly upregulated miR-203 and downregulated survivin. MiR-203 overexpression failed to affect WT1-AS but downregulated survivin. Cell proliferation assay showed that overexpression of WT1-AS and miR-203 led to decreased, while survivin overexpression led to increased proliferation of PTC cells. In addition, survivin overexpression attenuated the effects of WT1-AS and miR-203 overexpression.	32021456	RID06438	expression association	NA	UP(SKCM);DATA(GSE38495)	
Osteosarcoma	DDX11-AS1	DDX11	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-873-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000013573	NA	100506660	1663	CONCR|SCAT4	CHL1|ChlR1|KRG-2|WABS	In this research, a dramatically upregulated expression of DDX11-AS1 was detected in osteosarcoma cells. Loss-of-function assays revealed that decreased expression of DDX11-AS1 impaired osteosarcoma cell proliferation, metastasis as well as epithelial-mesenchymal transition (EMT) process. Afterwards, molecular mechanism tests validated that DDX11-AS1 could sponge miR-873-5p to upregulate DDX11 expression in osteosarcoma. Additionally, functional tests delineated that upregulation of miR-873-5p inhibited cell proliferation, metastasis as well as EMT process in osteosarcoma progression. Further, DDX11-AS1 was verified to regulate the mRNA stability of DDX11 through binding with IGF2BP2 in osteosarcoma. Final rescue tests in vitro and in vivo further elucidated that DDX11 overexpression could reversed the DDX11-AS1 downregulation-mediated effect on osteosarcoma progression. To sum up, DDX11-AS1 contributes to osteosarcoma progression via stabilizing DDX11.	32014424	RID06439	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367)
Ovarian cancer	SNHG14	DGCR8	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000128191	NA	104472715	54487	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	C22orf12|DGCRK6|Gy1|pasha	SNHG14 level was dramatically higher in ovarian cancer specimens. Moreover, cell migration and invasion were significantly attenuated via the inhibition of SNHG14, while enhanced via the SNHG14 overexpression. Besides, the expression of DGCR8 mRNA and protein was markedly downregulated after the knockdown of SNHG14, while upregulated after SNHG14 overexpression. Furthermore, the expression level of DGCR8 was increased in cancer tissues and positively related to the expression of SNHG14 in ovarian cancer tissues.	31841176	RID06440	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Tongue squamous cell carcinoma	CASC15	miR-124	negatively-E	linear regression;shRNA	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	We found that CASC15 was upregulated, while miR-124 was downregulated in TSCC tissues than in non-cancer tissues of TSCC patients. CASC15 and miR-125 expression was not significantly different among patients with different clinical stages, and patients with high level of CASC15 and low level of miR-125 showed low overall survival rate. CASC15 and miR-124 were inversely correlated in TSCC tissues, and CASC15 overexpression in TSCC cells resulted in downregulation of miR-124. In contrast, overexpression of miR-124 showed no significant effect on CASC15 expression. CASC15 overexpression resulted in the increased, while miR-124 overexpression resulted in the decreased migration and invasion rates of TSCC cells.	31665008	RID06441	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Prostate cancer	IUR	miR-200	positively-E	western blot	downregulation	qPCR	NA	NA	cell invasion(-);cell migration(-)	NA	regulation	RNA-RNA	Imatinib	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	In PC tissues, microRNA (miR)-200 was positively, while ZEB1 was inversely correlated with IUR. In PC cells, IUR and miR-200 overexpression mediated the downregulated ZEB1. IUR overexpression mediated the upregulation of miR-200, while IUR expression was not significantly affected by miR-200 overexpression. Cell invasion and migration analysis showed that IUR and miR-200 overexpression resulted in decreased invasion and migration rates. ZEB1 overexpression played an opposite role and attenuated the effects of IUR and miR-200 overexpression. Therefore, IUR can downregulate ZEB1 by upregulating miR-200 to inhibit PC cell invasion and migration.	31545930	RID06442	expression association	NA		
Prostate cancer	IUR	ZEB1	negatively-E		downregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-200)	regulation	NA	Imatinib	NA	NA	Cancer	Prostate cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	In PC tissues, microRNA (miR)-200 was positively, while ZEB1 was inversely correlated with IUR. In PC cells, IUR and miR-200 overexpression mediated the downregulated ZEB1. IUR overexpression mediated the upregulation of miR-200, while IUR expression was not significantly affected by miR-200 overexpression. Cell invasion and migration analysis showed that IUR and miR-200 overexpression resulted in decreased invasion and migration rates. ZEB1 overexpression played an opposite role and attenuated the effects of IUR and miR-200 overexpression. Therefore, IUR can downregulate ZEB1 by upregulating miR-200 to inhibit PC cell invasion and migration.	31545930	RID06443	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LOC105372579	FOXP4	positively-E	luciferase reporter assay;miRDB;ChipBase;StarBase;TargetScan7;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-4316)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000137166	NA	105372579	116113	NA	FLJ40908	LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling.Materials and methods: The expression levels of lncRNA LOC105372579 in HCC tissues and cell lines were analyzed by qRT-PCR The effects of LOC105372579 silencing on proliferation, migration and invasion were determined by using cell counting kit-8, colony formation assay and Transwell assay. Moreover, the xenograft mouse model was used to detect how LOC105372579 regulates HCC growth in vivo.Results: LOC105372579 was highly expressed in HCC tissues and cell lines. Moreover, upregulated levels of LOC105372579 predicted poor prognosis. LOC105372579 silencing suppressed the proliferation of HCC cells in vitro. We also validated that LOC105372579 knockdown inhibited the migration, invasion, and epithelial-sesenchymal transition of HCC cells. Xenograft assay demonstrated that LOC105372579 promotes tumor growth in vivo. Mechanistically, we identified that LOC105372579 is a sponge for miR-4316 and that FOXP4 is a direct target of miR-4316.Conclusion: Thus, our findings supported that LOC105372579 contributes to HCC cell proliferation, migration, invasion, and EMT by activating miR-4316/FOXP4 signaling.	31114338	RID06444	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Glioma	LINC00515	PRMT5	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-16)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000260583	GRCh38_21:25582770-25583326	ENSG00000100462	NA	282566	10419	NA	HRMT1L5|SKB1|SKB1Hs	Long noncoding RNA LINC00515 promotes cell proliferation and inhibits apoptosis by sponging miR-16 and activating PRMT5 expression in human glioma.Introduction: In recent years, an increasing amount of literature has demonstrated the functional role of long non-coding RNA (lncRNA) in human diseases. LINC00515 is a newly defined lncRNA and is reported to act as an oncogene in multiple myeloma. However, the function of LINC00515 in glioma is still uncertain. Materials and methods: We examined the expression levels of LINC00515 in human glioma tissues and cell lines using real-time PCR analysis. In addition, we confirmed the distribution of LINC00515 in glioma cells and suppressed LINC00515 expression with siRNAs. CCK-8, colony formation assay and apoptosis analysis were used to study the function of LINC00515 in glioma progression. Then, we used bioinformatics prediction and subsequent experiments to reveal the underlying molecular mechanism. Results: We found that LINC00515 was up-regulated in glioma tissues and cell lines. LINC00515 was mainly located in the cytoplasm in glioma cells. Knockdown of LINC00515 led to decreased proliferation and increased apoptosis of glioma cells. Mechanistically, our data indicated that there was a LINC00515/miR-16/PRMT5 regulatory axis in glioma. LINC00515 could activate PRMT5 expression and promote glioma progression by acting as a sponge of miR-16. Conclusion: LINC00515 expression is elevated in human glioma and promotes growth and inhibits apoptosis of glioma cells. The regulatory cascade LINC00515/miR-16/PRMT5 plays a critical role in glioma progression.	31114220	RID06445	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	MBNL1-AS1	TGFBR2	positively-E	RNAi;RNA pull-down assay;western blot;luciferase assay	downregulation	microarray;RT-qPCR	GSE101929;GSE102286;GSE33532	NA	chemosensitivity(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-301b-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229619	GRCh38_3:152245262-152269565	ENSG00000163513	NA	401093	7048	LOC401093	MFS2|TBR-ii|TBRII	microRNA-301b-3p downregulation underlies a novel inhibitory role of long non-coding RNA MBNL1-AS1 in non-small cell lung cancer.Non-small cell lung cancer (NSCLC) is the second most prevalent cause of cancer-related fatality. Long non-coding RNAs (lncRNAs) have been observed to exercise functions in NSCLC. Here, the current study aimed to explore the potential mechanism of lncRNA MBNL1-AS1 in NSCLC.Methodsmicroarray analysis was performed to screen the differentially expressed lncRNA associated with NSCLC and its potential mechanism. The lncRNA MBNL1-AS1 expression was quantified in 56 paired NSCLC and adjacent normal tissue samples. In an attempt to outline the function of lncRNA MBNL1-AS1 in NSCLC and to identify the interaction among lncRNA MBNL1-AS1, microRNA-301b-3p (miR-301b-3p) and TGFBR2, ectopic expression, depletion, and reporter assay experiments were conducted to detect CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC.ResultsInitially, the intersection among lncRNA MBNL1-AS1, miR-301b-3p, and TGFBR2 was observed in NSCLC. While a poor expression of lncRNA MBNL1-AS1 and TGFBR2, along with a high expression of miR-301b-3p was observed in NSCLC tissues. A demonstration of lncRNA MBNL1-AS1 restoration significantly decreased CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC. LncRNA MBNL1-AS1 functioned as a sponge of miR-301b-3p, which inverted the inhibitory role of lncRNA MBNL1-AS1 in CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC. LncRNA MBNL1-AS1 positively regulated TGFBR2 which was a target gene of miR-301b-3p. At last, upregulated lncRNA MBNL1-AS1 or depleted miR-301b-3p suppressed the xenograft tumor formation in vivo.ConclusionCollectively, the present study suggests an inhibitory role of lncRNA MBNL1-AS1 in CSC drug resistance of NSCLC by upregulating miR-301b-3p-targeted TGFBR2.	31113460	RID06446	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	UCA1	CDK6	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(-);MAPK signaling pathway(-);Notch signaling pathway(-);cell survival(-);apoptosis process(+);cell migration(-);cell migration(-)	ceRNA(miR-193a)	regulation	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000105810	NA	652995	1021	CUDR|LINC00178|onco-lncRNA-36|UCAT1	PLSTIRE	Knockdown of lncRNA-UCA1 inhibits cell viability and migration of human glioma cells by miR-193a-mediated downregulation of CDK6.Background: Long noncoding RNA urothelial carcinoma-associated 1 (lncRNA-UCA1) is generally recognized as an oncogenic molecule in several human malignant tumors. However, the available evidence does not necessarily imply an unequivocal causal function of UCA1 in glioblastoma. The current study was aimed to probe the biological function of lncRNA-UCA1 in human glioblastoma cell lines. Besides, we further investigated the potential mechanisms.Methods: Cell viability, apoptosis, as well as migration and invasion were measured using a commercial cell counting kit-8, flow cytometry, and 24-Transwell assay, respectively. LncRNA-UCA1, microRNA-193a (miR-193a), and CDK6 at messenger RNA levels were evaluated by quantitative real-time polymerase chain reaction method. Protein level was examined by western blot RNA immunoprecipitation was utilized to validate lncRNA-UCA1 associated with miR-193a. Luciferase activity assay was used to identify the miR-193a-targeted CDK6 3'-untranslated region.Results: lncRNA-UCA1 knockdown weakened cell viability, augmented apoptosis progression, as well as suppressed migration and invasion behaviors in glioblastoma cells, whereas lncRNA-UCA1 silence exhibited the opposite functions. lncRNA-UCA1 functioned as an endogenous sponge of miR-193a. miR-193a silence reversed the biological function of lncRNA-UCA1 knockdown on U-118 MG cells. miR-193a negatively regulated the expression of CDK6, and it affected the U-118 MG cells through regulating CDK6 expression. CDK6 overexpression abrogated the blockage of PI3K/AKT, mitogen-activated protein kinase (MAPK), and Notch signaling pathways. Furthermore, lncRNA-UCA1 and miR-193a could affect these signaling cascades through regulating CDK6 expression. The regulatory mechanisms of lncRNA-UCA1 were further consolidated in clinical specimens.Conclusion: lncRNA-UCA1 silence reduced cell viability, promoted apoptosis progression, while impeding the migration and invasion of glioblastoma cells by miR-193a-mediated silence of CDK6, with blockage of PI3K/AKT, MAPK, and Notch pathways.	31111564	RID06447	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Osteosarcoma	LncRNA-SRA1	MIR208A	negatively-E	RIP	downregulation	microarray;qRT-PCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	NA	NA	ENSG00000199157	NA	NA	406990	NA	MIR208|MIRN208|MIRN208A|hsa-mir-208a|miRNA208	LncRNA-SRA1 Suppresses Osteosarcoma Cell Proliferation While Promoting Cell Apoptosis.Objective: Osteosarcoma is a common malignant bone tumor that is frequently found in the long bones of children and adolescents. The aim of this study is to examine long noncoding RNA-steroid receptor RNA activator 1 expression in osteosarcoma to explore the biological function of long noncoding RNA steroid receptor RNA activator 1 on proliferation, migration, and invasion along with apoptosis and its regulatory mechanism, which would facilitate the early diagnosis and targeted therapy of osteosarcoma.Methods: First, microarray analysis was applied to determine the expression of long noncoding RNAs in osteosarcoma tissues and paired normal tissues. Then, quantitative real-time polymerase chain reaction was utilized to validate microarray findings. Next, osteosarcoma cancerous cell lines SJSA-1 and U2OS were transfected with pcDNA3.1-SRA1 or pCMV-sh-SRA1 to increase or decrease steroid receptor RNA activator 1 expression levels, and microRNA-208a inhibitors, mimic to investigate the effects of microRNA-208a on osteosarcoma as well as the regulatory relation between long noncoding RNA steroid receptor RNA activator 1 and microRNA-208a. Cell proliferation was evaluated through Cell Counting Kit-8 and colony formation assays. Flow cytometry analysis was conducted to evaluate the apoptosis ratio. The migration and invasion abilities were measured using wound-healing and transwell assays.Results: Long noncoding RNA-steroid receptor RNA activator 1 expression was downregulated in osteosarcoma tissues and cells compared with that in corresponding normal tissues, whereas microRNA-208a expression was upregulated in osteosarcoma tissues. Moreover, the restoration of long noncoding RNA steroid receptor RNA activator 1 inhibited cell proliferation, and upregulation of long noncoding RNA steroid receptor RNA activator 1 restrained cell migration and invasion but boosted the apoptosis rate in osteosarcoma cells. In addition, long noncoding RNA steroid receptor RNA activator 1 targeting microRNA-208a was involved in the progression of osteosarcoma. Furthermore, upregulating microRNA-208a exerted similar roles of silencing long noncoding RNA steroid receptor RNA activator 1 in cell apoptosis, proliferation, migration, and invasion, which were reversed by enhancing the expression of long noncoding RNA steroid receptor RNA activator 1.Conclusions: In our study, long noncoding RNA steroid receptor RNA activator 1 played an antitumor role in osteosarcoma as it reduced cell migration, invasion, and proliferation, but facilitated cell apoptosis via sponging microRNA-208a, which could be regarded as a potential therapeutic target of osteosarcoma treatment.	31106680	RID06448	ceRNA or sponge	NA		
Non-small cell lung cancer	LINC01234	OTUB1	positively-E	RNA pull-down assay;western blot;luciferase assay;Starbase;ChIP	upregulation	RT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-140)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000167770	NA	100506465	55611	onco-lncRNA-32	FLJ20113|FLJ40710	SP1-mediated overexpression of lncRNA LINC01234 as a ceRNA facilitates non-small-cell lung cancer progression via regulating OTUB1.Long noncoding RNAs (lncRNAs) have been confirmed to be strongly associated with the progression of various types of cancer. LncRNA LINC01234 (LINC01234) is a newly identified tumor-related lncRNA whose upregulation has been confirmed in some tumors. However, its potential expressions and possible functions in non-small-cell lung cancer (NSCLC) have not been explored. In this study, we first found that LINC01234 expressions were distinctly upregulated in both NSCLC samples and cell lines using RT-PCR Our group also showed that LINC01234 upregulations were modulated by nuclear transcription factor SP1. The results form clinical investigations indicated that high LINC01234 expressions were associated with positively lymph node metastasis and advanced tumor-metastasis-node (TMN) stage. Kaplan-Meier assays indicated that patients with NSCLC having high LINC01234 expressions tend to have unfavorable clinical prognosis. Using multivariate assays, it was confirmed that LINC01234 was an independent prognostic factor for patients with NSCLC. In vitro assays showed that inhibition of LINC01234 suppressed NSCLC cell proliferation, cell colony formation and metastasis, and greatly promoted apoptosis. Mechanistic investigations revealed LINC01234 promotes the progression of NSCLC cells by the modulation of miR-140 to positively regulate OTUB1 expression. Taken together our findings, they provided an exhaustive assay of LINC01234 in NSCLC and imperative clues for insights into the potential effects of lncRNAs-miRNAs regulatory network in NSCLC.	31106421	RID06449	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE86978)
Non-small cell lung cancer	SP1	LINC01234	positively-E	JASPAR;ChIP;luciferase reporter assay	upregulation	RT-PCR;microarray	TCGA	NA	cancer progression(+);colony formation(+);cell metastasis(+);cell growth(+);apoptosis process(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000249550	GRCh38_12:113583886-113773726	6667	100506465	NA	onco-lncRNA-32	Our group also showed that LINC01234 upregulations were modulated by nuclear transcription factor SP1. The results form clinical investigations indicated that high LINC01234 expressions were associated with positively lymph node metastasis and advanced tumor-metastasis-node (TMN) stage. Kaplan-Meier assays indicated that patients with NSCLC having high LINC01234 expressions tend to have unfavorable clinical prognosis. Using multivariate assays, it was confirmed that LINC01234 was an independent prognostic factor for patients with NSCLC. In vitro assays showed that inhibition of LINC01234 suppressed NSCLC cell proliferation, cell colony formation and metastasis, and greatly promoted apoptosis. Mechanistic investigations revealed LINC01234 promotes the progression of NSCLC cells by the modulation of miR-140 to positively regulate OTUB1 expression. Taken together our findings, they provided an exhaustive assay of LINC01234 in NSCLC and imperative clues for insights into the potential effects of lncRNAs-miRNAs regulatory network in NSCLC;          Therefore, we searched the JASPAR database using LINC01234 promoter sequence. As the results shown in Figure 2a, several SP1 binding sites in LINC01234 promoter sequence were predicted. In addition, we next applied real time PCR analyses to determine the SP1 expressing levels in NSCLC cells after silencing or overexpressing SP1. The results indicated that siRNAs against SP1 were capable to reduce the SP1 mRNA levels, and pcDNA3.1 SP1 could effectively elevate the SP1 expression (Figure 2b). Furthermore, silence of SP1 in NSCLC cells by transfecting SP1 siRNAs remarkably increased the levels of LINC01234, whereas enhanced expression of SP1 caused significantly reduced levels of LINC01234 (Figure 2c). In addition, the data from ChIP analyses demonstrated that the binding activities of SP1 in the binding site 3 (BS3) of LINC01234 promoter were remarkably elevated in NSCLC cells (Figure 2d). Besides, the results of luciferase activity analyses validated that forced expression of SP1 resulted in dramatically increased luciferase activities in NSCLC cells treated with BS3 luciferase reporter plasmids but not BS1 or BS2 luciferase reporter plasmids. Overall, these data validated that SP1 activated LINC01234 aberrantly expression in human NSCLC cells.Knockdown of LINC01234 inhibited NSCLC cell growth and induced cell apoptosis.To determine the dysregulated lncRNAs in NSCLC, microarray profile data were downloaded from the TCGA datasets.	31106421	RID06450	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)
Gastric cancer	TRPM2-AS	HMGA1	positively-E	StarBase;luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	TCGA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-195)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000137309	NA	101928607	3159	TRPM2-AS1	HMG-R|HMGA1A|HMGIY	ELK1-induced upregulation of lncRNA TRPM2-AS promotes tumor progression in gastric cancer by regulating miR-195/ HMGA1 axis. However, the expression and role of TRPM2-AS in the development of gastric cancer (GC) have not been elucidated. In the current study, we provided evidence that the expression levels of TRPM2-AS were increased in both GC tissues and cell lines. We also showed that overexpression of TRPM2-AS was modulated by ELK1, a transcription factor. The results of clinical assays showed that higher expressions of TRPM2-AS were significantly related with invasion depth, TNM stage, lymphatic metastasis, and shorter overall survival. Further clinical assays using multivariate analysis suggested that TRPM2-AS expression was an independent prognostic factor in patients with GC. Functional experiments illustrated that depression of TRPM2-AS suppressed proliferation, migration, and invasion in GC cells. In terms of mechanism, we found that TRPM2-AS directly inhibited miR-195, which targeted the 3'-untranslated region of high-mobility group AT-hook 1 (HMGA1) messenger RNA. Overall, these findings revealed that ELK1-induced overexpression of TRPM2-AS promoted the development and progression of GC in part through miR-195/HMGA1 signaling axis, and established its candidacy as a new cancer biomarker for GC patients.In this study, we first analyzed RNA sequencing data of GC and normal gastric tissues downloaded from The Cancer Genome Atlas (TCGA) datasets using the R package DEseq.Hence, we next used the starbase algorithmto predict the potential target miRNAs of TRPM2 AS. RNA pull-down assays further confirmed that TRPM2 AS directly precipitated miR 195 in GC cells.	31104318	RID06451	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209)
Gastric cancer	ELK1	TRPM2-AS	positively-E	JASPAR;ChIP;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cancer progression(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000126767	NA	ENSG00000230061	GRCh38_21:44414588-44425272	2002	101928607	NA	TRPM2-AS1	ELK1-induced upregulation of lncRNA TRPM2-AS promotes tumor progression in gastric cancer by regulating miR-195/ HMGA1 axis. However, the expression and role of TRPM2-AS in the development of gastric cancer (GC) have not been elucidated. In the current study, we provided evidence that the expression levels of TRPM2-AS were increased in both GC tissues and cell lines. We also showed that overexpression of TRPM2-AS was modulated by ELK1, a transcription factor. The results of clinical assays showed that higher expressions of TRPM2-AS were significantly related with invasion depth, TNM stage, lymphatic metastasis, and shorter overall survival. Further clinical assays using multivariate analysis suggested that TRPM2-AS expression was an independent prognostic factor in patients with GC. Functional experiments illustrated that depression of TRPM2-AS suppressed proliferation, migration, and invasion in GC cells. In terms of mechanism, we found that TRPM2-AS directly inhibited miR-195, which targeted the 3'-untranslated region of high-mobility group AT-hook 1 (HMGA1) messenger RNA. Overall, these findings revealed that ELK1-induced overexpression of TRPM2-AS promoted the development and progression of GC in part through miR-195/HMGA1 signaling axis, and established its candidacy as a new cancer biomarker for GC patients.In this study, we first analyzed RNA sequencing data of GC and normal gastric tissues downloaded from The Cancer Genome Atlas (TCGA) datasets using the R package DEseq.	31104318	RID06452	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	UP(BRCA);DATA(GSE55807)
Anaplastic thyroid carcinoma	HCP5	miR-128-3p	negatively-F	luciferase reporter assay;RIP;StarBase v2.0	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	Knockdown of HCP5 exerts tumor-suppressive functions by up-regulating tumor suppressor miR-128-3p in anaplastic thyroid cancer.Anaplastic thyroid cancer (ATC) is a rare type of thyroid cancer with a high mortality rate. HLA complex P5 (HCP5), a long non-coding RNA (lncRNA), has been shown to be implicated in several types of cancer, such as follicular thyroid carcinoma (PTC), the main type of thyroid cancer. However, the role of HCP5 in ATC remains unclear. The present study aimed to investigate the expression of HCP5 in ATC and its potential roles. The expression levels of HCP5 and microRNA (miR)-128-3p were tested using qRT-PCR MTT assay was performed to detect cell viability. Cell apoptosis was evaluated by detecting apoptotic rate and caspase-3/7 activity. Luciferase reporter and RNA immunoprecipitation (RIP) assays were carried out to confirm the association between HCP5 and miR-128-3p. Compared with human thyroid follicular cell line Nthy-ori 3-1 cells, HCP5 expression level was significantly increased in ATC cell lines. Besides, HCP5 expression level was increased in ATC tissues when compared with adjacent normal tissues. Knockdown of HCP5 reduced cell viability, while elevated apoptotic rate and caspase-3/7 activity in ARO and SW1736 cells. MiR-128-3p was predicted to be a target gene of HCP5. The expression level of miR-128-3p was significantly decreased in ATC cells and tissues, as compared to Nthy-ori 3-1 cells and adjacent normal tissues, respectively. MiR-128-3p overexpression reduced ATC cell viability, and induced cell apoptosis. HCP5 directly bound to miR-128-3p and regulated the expression of miR-128-3p in ARO and SW1736 cells. Furthermore, the effects of HCP5 knockdown on ATC cell viability and apoptosis were attenuated by the inhibitor of miR-128-3p. These findings suggested that knockdown of HCP5 exerted anti-tumor effect via sponging miR-128-3p in ATC, which might provide a potential approach for the treatment of ATC.	31102936	RID06453	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cervical cancer	NOC2L-4.1	YAP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+)	ceRNA(miR-630)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	NA	NA	ENSG00000137693	NA	NA	10413	NA	COB1|YAP|YAP-1|YAP2|YAP65|YKI	LncRNA NOC2L-4.1 functions as a tumor oncogene in cervical cancer progression by regulating the miR-630/YAP1 pathway.Long noncoding RNA (lncRNA) is a new class of noncoding RNA playing an indispensable role in different diseases by regulating miRNA. Our previous studies have suggested that miR-630 was decreased in patients with cervical cancer. Recently, studies have shown that lncRNA NOC2L-4.1 was abnormally expressed in patients with cervical cancer and can target miR-630. Therefore, we wanted to identify the integrated relationship between lncRNA NOC2L-4.1 and miR-630 in the pathological processes regarding cervical cancer either in vitro or in vivo. Quantitative reverse transcription-polymerase chain reaction detection shows that compared with human normal cervical epithelial cell, the expression of lncRNA NOC2L-4.1 was significantly increased and the expression of miR-630 was decreased in cell lines of cervical cancer. Moreover, luciferase reporter assay showed that miR-630 was a target of lncRNA NOC2L-4.1. The in vitro study found that downregulation of lncRNA NOC2L-4.1 suppressed cervical cancer cell migration (transwell assays) and proliferation (cell counting kit-8 and cloning formation assays). miR-630 specific inhibitor treatment reversed the inhibitory effect of lncRNA NOC2L-4.1 on cell proliferation and migration. Further studies also found that yes-associated protein 1 (YAP1) was the target of miR-630. Overexpression YAP1 suppressed miR-630 overexpression induced cell proliferation and inhibition of migration. Tumors induced by implantation of lncRNA NOC2L-4.1-knockdown Hela cells in nude mice showed that lncRNA NOC2L-4.1 silencing decreased the growth of tumors in both volume and weight by regulation of miR-630/YAP1. Taken together, our study reveals the important role of lncRNA NOC2L-4.1/miR-630/YAP1 regulatory network in cervical cancer, which provides new insights concerning the pathogenesis of cervical cancer.	31099044	RID06454	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Thyroid cancer	LINC00313	ALX4	negatively-E	dual-luciferase reporter analysis	upregulation	microarray;RT-qPCR	TCGA	NA	AKT/mTOR signaling pathway(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);cell invasion(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000185186	GRCh38_21:43461960-43479534	ENSG00000052850	NA	114038	60529	C21orf84|NCRNA00313	FPP|KIAA1788|PFM|PFM2	Downregulated long noncoding RNA LINC00313 inhibits the epithelial-mesenchymal transition, invasion, and migration of thyroid cancer cells through inhibiting the methylation of ALX4.Thyroid cancer represents one of the prevalent endocrine cancer with relatively high incidence rate around the world, accompanied by unchanged fatality rate. We probe into the specific role of LINC00313 in mediation of cellular processes of thyroid cancer including proliferation, migration, and invasion through the methylation of aristaless-like homeobox 4 (ALX4). Thyroid cancer-related long noncoding RNAs (lncRNAs) and genes were analyzed by microarray-based analysis. The antitumor effect of LINC00313 was examined with the gain- and loss-of-function experiments. In addition, the binding of LINC00313 and the promoter region of ALX4, and the interaction of LINC00313 with methylation-related proteins were detected. Later, xenograft tumors in nude mice were induced expecting to dig out the modulatory function of LINC00313 in tumor growth of thyroid carcinoma. The microarray-based analysis manifested that LINC00313 was overexpressed, whereas ALX4 was downregulated in thyroid cancer, the results of which were also verified in thyroid cancer tissues. Besides, our results demonstrated that LINC00313 bound to the ALX4 promoter region, and LINC00313 recruited DNMT1 and DNMT3B proteins to promote the methylation of ALX4 promoter region, thus suppressing the ALX4 expression. Finally, the downregulation of LINC00313 and upregulation of ALX4 repressed the AKT/mTOR signaling axis, thus inhibiting proliferative, migratory, invasive abilities as well as epithelial-to-mesenchymal transition (EMT) of thyroid cancer cells. Collectively, downregulated LINC00313 suppresses cell proliferation, migration, as well as invasion of thyroid cancer by inhibiting the methylation of ALX4 and increasing its expression by inactivation of the AKT/mTOR signaling pathway.It is proven that LINC00313 recruited methylated proteins, including DNMT1 and DNMT3B to promote the methylation of ALX4 promoter.	31093972	RID06455	epigenetic regulation	NA		UP(PAAD);DATA(GSE40174)
Cervical cancer	SPRY4-IT1	ZEB1	positively-E	dual-luciferase reporter analysis	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	NA	NA	ENSG00000148516	NA	100642175	6935	SPRIGHTLY	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	SPRY4-IT1 was detected by quantitative PCR. Wound-healing assay and Transwell assay were performed to detect cell migration and invasion, respectively. western blot assays were used to analyze the protein expression of E-cadherin, N-cadherin and vimentin. Tumor xenografts experiments were performed to detect the effect of SPRY4-IT1 in vivo. dual-luciferase reporter assay was used to investigate potential molecular mechanism of SPRY4-IT1 in CC cells.SPRY4-IT1 was up-regulated in CC cell lines. Knockdown of SPRY4-IT1 significantly inhibited CC cells migration and invasion in vitro and in vivo Moreover, knockdown of SPRY4-IT1 significantly suppressed the epithelial-mesenchymal transition (EMT) of CC by increased E-cadherin expression and decreased the N-cadherin and vimentin expression. Mechanically, SPRY4-IT1 could directly bind to miR-101-3p and effectively act as a competing endogenous RNA (ceRNA) for miR-101-3p to regulate the expression of the target gene ZEB1Conclusions: Our findings indicate that the SPYR4-IT1/miR-101-3p/ZEB1 axis contributes to CC migration and invasion, which may provide novel insights into the function of lncRNA-driven tumorigenesis of CC.Knockdown of SPRY4-IT1 inhibits cell proliferation, cell migration, cell invasion and EMT of CC in vitro.	31092700	RID06456	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	AWPPH	FZD7	positively-E	luciferase reporter assay;miRDB;TargetScan7	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);cell invasion(+)	ceRNA(miR-93-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000155760	NA	NA	8324	NA	FzE3	LncRNA AWPPH promotes osteosarcoma progression via activation of Wnt/beta-catenin pathway through modulating miR-93-3p/FZD7 axis.Long noncoding RNAs (lncRNAs) have important regulatory roles in osteosarcoma (OS) progression. Recent researches have shown lncRNA AWPPH promotes lung cancer progression and bladder cancer development. Yet, the function of AWPPH in OS is unknown. In this research, results indicated AWPPH levels were increased in OS tissues in contrast to paracancerous controls. Up-regulated AWPPH was associated with advanced stage, tumor size and metastasis. Besides, AWPPH up-regulation indicated a low survival rate in OS patients. Silencing of AWPPH suppressed proliferation, migration and invasion of OS cells. Mechanistically, AWPPH was demonstrated to sponge miR-93-3p and promote FZD7 expression, causing activation of Wnt/beta-catenin. Inhibition of miR-93-3p effectively reversed the effects of AWPPH knockdown on OS cells. Collectively, our findings suggested AWPPH may be a prognostic biomarker and potential therapeutic target. AWPPH enhances FZD7-mediated activation of Wnt/beta-catenin by sponging miR-93-3p to promote OS progression.Bioinformatic analysis (miRDB  analysis) indicated miR-93-3p was a possible target.Bioinformatics analysis (TargetScan7 analysis) suggested FZD7 is a  potential target of miR-93-3p.To validate it, luciferase reporter  assay was conducted. MiR-93-3p mimics markedly reduced the  activity of wt-FZD7-reporter (Fig. 4A and B). Additionally, FZD7  expression was inversely correlated with miR-93-3p in OS tissues.	31092328	RID06457	ceRNA or sponge	metastasis,prognosis		
Hepatocellular carcinoma	HNRNPAB	lnc-ELF209	negatively-E	ChIP	downregulation	qRT-PCR;microarray	NA	NA	cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000197451	NA	NA	NA	3182	NA	ABBP1|HNRPAB	NA	HNRNPAB-regulated lncRNA-ELF209 inhibits the malignancy of hepatocellular carcinoma.Our previous study demonstrated that heterogeneous nuclear ribonucleoprotein AB (HNRNPAB) is a key gene that facilitates metastasis of hepatocellular carcinoma (HCC). However, the molecular mechanisms behind this relationship are not fully understood. In our study, we utilized long-noncoding RNA (lncRNA) microarrays to identify a HNRNPAB-regulated lncRNA named lnc-ELF209. Our findings from chromatin immunoprecipitation assays indicate that HNRNPAB represses lnc-ELF209 transcription by directly binding to its promoter region. We also analyzed clinical samples from HCC patients and cell lines with quantitative real-time polymerase chain reactions, RNA in situ hybridization and immunohistochemistry, and found that there is a negative relationship between HNRNPAB and lnc-ELF209 expression. Up/downregulation assays and rescue assays indicate that lnc-ELF209 inhibits cell migration, invasion and epithelial-mesenchymal transition regulated by HNRNPAB. This suggests a new regulatory mechanism for HNRNPAB-promoted HCC progression. RNA pull-down and LC-MS/MS were used to determine triosephosphate isomerase, heat shock protein 90-beta and vimentin may be involved in the tumor-suppressed function of lnc-ELF209. Furthermore, we found lnc-ELF209 could stabilize TPI protein expression. We also found that lnc-ELF209 overexpression in HCCLM3 cell resulted in a lower rate of lung metastatic, which suggested a less aggressive HCC phenotype. Collectively, these findings offer new insights into the regulatory mechanisms that underlie HNRNPAB cancer-promoting activities and demonstrate that lnc-ELF209 is a HNRNPAB-regulated lncRNA that may play an important role in the inhibition of HCC progression.	31090062	RID06458	interact with protein	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)	
Hepatocellular carcinoma	lnc-ELF209	TPI1	positively-E	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000111669	NA	NA	7167	NA	HEL-S-49|TIM|TPI|TPID	In our study, we utilized long-noncoding RNA (lncRNA) microarrays to identify a HNRNPAB-regulated lncRNA named lnc-ELF209. Our findings from chromatin immunoprecipitation assays indicate that HNRNPAB represses lnc-ELF209 transcription by directly binding to its promoter region. We also analyzed clinical samples from HCC patients and cell lines with quantitative real-time polymerase chain reactions, RNA in situ hybridization and immunohistochemistry, and found that there is a negative relationship between HNRNPAB and lnc-ELF209 expression. Up/downregulation assays and rescue assays indicate that lnc-ELF209 inhibits cell migration, invasion and epithelial-mesenchymal transition regulated by HNRNPAB. This suggests a new regulatory mechanism for HNRNPAB-promoted HCC progression. RNA pull-down and LC-MS/MS were used to determine triosephosphate isomerase, heat shock protein 90-beta and vimentin may be involved in the tumor-suppressed function of lnc-ELF209. Furthermore, we found lnc-ELF209 could stabilize TPI protein expression. We also found that lnc-ELF209 overexpression in HCCLM3 cell resulted in a lower rate of lung metastatic, which suggested a less aggressive HCC phenotype. Collectively, these findings offer new insights into the regulatory mechanisms that underlie HNRNPAB cancer-promoting activities and demonstrate that lnc-ELF209 is a HNRNPAB-regulated lncRNA that may play an important role in the inhibition of HCC progression.As TPI has the highest  score (201) in the RNA pull-down assays, we performed RIP-qPCR to confirm the interaction between lnc-ELF209  and TPI (Fig. 4d).Furthermore,  knockdown of TPI enhanced the ability of migration and  invasion of HCC (Supporting Information Fig. S4). These  results suggested that lnc-ELF209 might play its antitumor  role through binding and stabilizing TPI in HCC.	31090062	RID06459	interact with protein	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	PYCARD-AS1	PYCARD	negatively-F	knockdown;RNA pull-down assay	upregulation	qRT-PCR;microarray	GSE85032	NA	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000261359	GRCh38_16:31201885-31203452	ENSG00000103490	NA	100652740	29108	C16orf98|PYCARDOS	ASC|CARD5|TMS-1	A long noncoding RNA distributed in both nucleus and cytoplasm operates in the PYCARD-regulated apoptosis by coordinating the epigenetic and translational regulation.Long noncoding RNAs (lncRNAs) participate in various biological processes such as apoptosis. The function of lncRNAs is closely correlated with their localization within the cell. While regulatory potential of many lncRNAs has been revealed at specific subcellular location, the biological significance of discrete distribution of an lncRNA in different cellular compartments remains largely unexplored. Here, we identified an lncRNA antisense to the pro-apoptotic gene PYCARD, named PYCARD-AS1, which exhibits a dual nuclear and cytoplasmic distribution and is required for the PYCARD silencing in breast cancer cells. The PYCARD-regulated apoptosis is controlled by PYCARD-AS1; moreover, PYCARD-AS1 regulates apoptosis in a PYCARD-dependent manner, indicating that PYCARD is a critical downstream target of PYCARD-AS1. Mechanistically, PYCARD-AS1 can localize to the PYCARD promoter, where it facilitates DNA methylation and H3K9me2 modification by recruiting the chromatin-suppressor proteins DNMT1 and G9a. Moreover, PYCARD-AS1 and PYCARD mRNA can interact with each other via their 5' overlapping region, leading to inhibition of ribosome assembly in the cytoplasm for PYCARD translation. This study reveals a mechanism whereby an lncRNA works at different cellular compartments to regulate the pro-apoptotic gene PYCARD at both the epigenetic and translational levels, contributing to the PYCARD-regulated apoptosis, and also sheds new light on the role of discretely distributed lncRNAs in diverse biological processes.Mechanistically, PYCARD-AS1 can localize to the PYCARD promoter, where it facilitates DNA methylation and H3K9me2 modification by recruiting the chromatin-suppressor proteins DNMT1 and G9a.PYCARD-AS1 is a negative regulator of PYCARD.Knockdown of PYCARD-AS1 increased PYCARD expression (S2H Fig), and the PYCARD-AS1-knockdown SKBR3 cells showed increased sensitivity to paclitaxel treatment compared with the control cells (Fig 2I and S2I Fig).	31086376	RID06460	interact with protein	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	HAGLROS	ATG12	positively-E	dual-luciferase reporter analysis;RIP;TargetScan	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-5095)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000145782	NA	102800310	9140	NA	APG12|APG12L	In this research, we planned to dig the possible influences and mechanism of long noncoding (lnc) RNA HAGLROS in the development and progression of hepatocellular carcinoma (HCC). The levels of lncRNA HAGLROS in HCC tumor samples and their relationship with clinicopathological characteristics and prognosis of patients with HCC were studied. Subsequently, overexpression and silenced approaches were used in HCC cells for detecting the effects of lncRNA HAGLROS on cell viability, apoptosis, and autophagy. Furthermore, we investigated whether HAGLROS could function as a competing endogenous RNA (ceRNA) to regulate miR-5095 expression in HCC cells, and explored the correlation between miR-5095 and ATG12. Besides, the correlation of HAGLROS, the consequent PI3K/AKT/mTOR signaling pathway was further explored. The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation. In contrast to the lower level, a higher level of HAGLROS correlated with a shorter survival time of patients with HCC. The suppression of HAGLROS decreased cell viability, promoted apoptosis, and inhibited autophagy. Moreover, HAGLROS negatively regulated miR-5095 expression, which further regulated HCC cell viability, apoptosis, and autophagy. In addition, ATG12 was targeted by miR-5095 and was then involved in miR-5095-regulated HCC cell biological processes including viability, apoptosis, and autophagy. Furthermore, overexpression of HAGLROS activated PI3K/AKT/mTOR signals. Our results revealed that HAGLROS is highly expressed in HCC, and its high level may correlate with the progression and development of HCC involving the processes of cell viability, apoptosis, and autophagy through the miR-5095/ATG12 axis and PI3K/AKT/mTOR signals.Dual-luciferase reporter and RNA-binding protein immunoprecipitation (RIP) assays further presented that HAGLROS and miR-5095 were in the same RNAinduced silencing complex (P < 0.05, Fig. 2B and C), thus verifying their relationship.	31082725	RID06461	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	LINC00511	miR-424	negatively-F	dual-luciferase reporter analysis;RT-PCR;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);cell growth(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72290091-72640472	NA	NA	400619	NA	onco-lncRNA-12	NA	The expressions of LINC00511 in HCC tissues and cell lines were evaluated by qRT-PCR The correlations between LINC00511 expression and the clinicopathological parameters and prognosis of HCC patients were determined using several statistical methods. CCK-8 assay, colony formation assay, flow cytometry cell cycle, apoptosis assay, EdU assay, wound healing assay, and transwell assay were used to investigate the role of LINC00511 on the malignant phenotypes in vitro. Insights into the potential mechanisms of ceRNAs were determined by bioinformatics analysis, dual-luciferase reporter assays and RT-PCR LINC00511 expression was significantly up-regulated in HCC tissues and cell lines, and its high expression was distinctly associated with nodal metastasis, vascular invasion, and clinical stage. Furthermore, statistical assays revealed that HCC patients with higher LINC00511 expression levels had worse overall survival rates. Importantly, the multivariate analysis confirmed that LINC00511 expression was an independent prognostic factor of the overall survival in patients with HCC. Functionally, the inhibition of LINC00511 significantly suppressed the capability of proliferation, migration, and invasion in HCC cell lines. Bioinformatic tools predicted that miR-424 both targeted the 3'-UTR of LINC00511, which was confirmed using the luciferase reporter assay and RT-PCR LINC00511 plays an important role in the malignant progression of HCC via modulation of miR-424.Knockdown of LINC00511 Inhibited HCC Cell Growth and Promoted Cell Apoptosis.These data  validated that LINC00511 acted as a miR-424  sponge in HCC.	31081082	RID06462	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Prostate cancer	AFAP1-AS1	RBM5	negatively-E	knockdown;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000003756	NA	84740	10181	AFAP1-AS|AFAP1AS|MGC10981	H37|LUCA-15|LUCA15	LncRNA AFAP1-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR in both prostate cancer cells and tissue samples. In addition, to identify the function of AFAP1-AS1 on prostate cancer in vitro, cell proliferation, transwell assay, and Matrigel assay were conducted. Furthermore, by performing qRT-PCRand western blot assay, the underlying mechanism was explored.The expression level of AFAP1-AS1 was significantly higher in prostate cancer samples than that in corresponding ones. Additionally, the cell proliferation, migration, and invasion capacities were inhibited after AFAP1-AS1 was knocked down in prostate cancer cells. Moreover, the mRNA and protein expressions of RBM5 were upregulated after AFAP1-AS1 was knocked down. Furthermore, the RBM5 expression level was negatively related to AFAP1-AS1 expression level in prostate cancer samples. AFAP1-AS1 acts as an oncogene in prostate cancer by enhancing cell metastasis and proliferation via suppressing RBM5, which might be a novel therapeutic strategy in treatment for prostate cancer.western blot assay data showed that after AFAP1-AS1 was knocked down the protein expression of RBM5 was upregulated (Figure 4B).	31081081	RID06463	interact with protein	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Breast cancer	RP1	CDKN1B	negatively-E	luciferase reporter assay;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	transcriptional regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000104237	GRCh38_8:54509422-54871720	ENSG00000111276	NA	6101	1027	DCDC4A|ORP1	KIP1|P27KIP1	KLF5 regulated lncRNA RP1 promotes the growth and metastasis of breast cancer via repressing p27kip1 translation.Increasing evidence suggest that lncRNAs (long noncoding RNAs) play important roles in human cancer. Breast cancer is a heterogeneous disease and the potential involvement of lncRNAs in breast cancer remains unexplored. In this study, we characterized a novel lncRNA, RP1-5O6.5 (termed as RP1). We found that RP1 was highly expressed in breast cancer and predicted poor prognosis of breast cancer patients. Gain-of-function and loss-of-function assays showed that RP1 promoted the proliferation and metastasis of breast cancer cells in vitro and in vivo. Mechanistically, RP1 maintained the EMT and stemness states of breast cancer cells via repressing p27kip1 protein expression. RP1 combined with the complex p-4E-BP1/eIF4E to prevent eIF4E from interacting with eIF4G, therefore attenuating the translational efficiency of p27kip1 mRNA. Furthermore, we found that p27kip1 evidently downregulated Snail1 but not ZEB1 to inhibit invasion of breast cancer cells. Kruppel-like factor 5 (KLF5) was positively correlated with RP1 in breast cancer tissues. Moreover, we demonstrated that KLF5 recruited p300 to the RP1 promoter to enhance RP1 expression. Taken together, our findings demonstrated that KLF5-regulated RP1 plays an oncogenic role in breast cancer by suppressing p27kip1, providing support for the clinical investigation of therapeutic approaches focusing on RP1.RP1 promotes proliferation, invasion, and stemness of breast cancer cells via p27kip1.	31073122	RID06464	transcriptional regulation	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	KLF5	RP1	positively-E	JASPAR;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000102554	NA	ENSG00000104237	GRCh38_8:54509422-54871720	688	6101	BTEB2|CKLF|IKLF	DCDC4A|ORP1	KLF5 regulated lncRNA RP1 promotes the growth and metastasis of breast cancer via repressing p27kip1 translation.Increasing evidence suggest that lncRNAs (long noncoding RNAs) play important roles in human cancer. Breast cancer is a heterogeneous disease and the potential involvement of lncRNAs in breast cancer remains unexplored. In this study, we characterized a novel lncRNA, RP1-5O6.5 (termed as RP1). We found that RP1 was highly expressed in breast cancer and predicted poor prognosis of breast cancer patients. Gain-of-function and loss-of-function assays showed that RP1 promoted the proliferation and metastasis of breast cancer cells in vitro and in vivo. Mechanistically, RP1 maintained the EMT and stemness states of breast cancer cells via repressing p27kip1 protein expression. RP1 combined with the complex p-4E-BP1/eIF4E to prevent eIF4E from interacting with eIF4G, therefore attenuating the translational efficiency of p27kip1 mRNA. Furthermore, we found that p27kip1 evidently downregulated Snail1 but not ZEB1 to inhibit invasion of breast cancer cells. Kruppel-like factor 5 (KLF5) was positively correlated with RP1 in breast cancer tissues. Moreover, we demonstrated that KLF5 recruited p300 to the RP1 promoter to enhance RP1 expression. Taken together, our findings demonstrated that KLF5-regulated RP1 plays an oncogenic role in breast cancer by suppressing p27kip1, providing support for the clinical investigation of therapeutic approaches focusing on RP1.To explore the mechanism of RP1 upregulation in breast cancer, we searched for transcriptional factor binding sites in the RP1 promoter via the JASPAR online program.Importantly, there was a strong positive correlation between the expression levels of KLF5 and RP1 in breast cancer tissues (P = 0.0316) (Fig. 6b).For further confirmation, we performed a chromatin immunoprecipitation (ChIP) assay followed by a luciferase reporter assay to map the binding sites for KLF5 onto the promoter of RP1.RP1 promotes breast cancer progression and predicts poor prognosis of breast cancer.	31073122	RID06465	transcriptional regulation	metastasis,prognosis	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	TPTEP1	STAT3	negatively-E	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);tumorigenesis(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000100181	GRCh38_22:16601887-16698742	ENSG00000168610	NA	387590	6774	psiTPTE22	APRF	The differential expressions of LncRNAs in HCC cells treated with cisplatinum were determined by RNA-seq. The roles of TPTEP1 in HCC development by applying gene function gain and loss analysis in MHCC97H and QYG-7703 cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR, cell proliferation, colony formation, cell invasion and flow cytometry assays. The underlying mechanism of TPTEP1 sensitizing hepatocellular carcinoma cells to cisplatinum was examined by RNA-pull down, western blot, subcellular fractionation, RNA immunoprecipitation and dual-luciferase reporter assays. The effect of TPTEP1 on tumorigenesis in vivo was performed with a subcutaneous xenograft mouse model of HCC. In addition, TPTEP1 expression was detected in clinical tumor tissue samples by qRT-PCRLncRNA TPTEP1 was highly expressed in cisplatinum-treated HCC cells, which sensitizes hepatocellular carcinoma cell to cisplatinum-induced apoptosis. TPTEP1 overexpression inhibited, while TPTEP1 knockdown promoted HCC cell proliferation, tumorigenicity and invasion. Furthermore, TPTEP1 exerted its tumor suppressing activities by interacting with signal transducer and activator of transcription 3 (STAT3) to inhibit its phosphorylation, homodimerization, nuclear translocation and down-stream genes transcription. Moreover, TPTEP1 overexpression obviously inhibits tumor masses in vivo in a subcutaneous xenograft mouse model of HCC and TPTEP1 is frequently downregulated in HCC tissues, compared to its corresponding pre-tumor tissues.LncRNA TPTEP1 inhibits hepatocellular carcinoma cells progression by affecting IL-6/STAT3 signaling. Taken together, our findings suggest a tumor suppressing role of TPTEP1 in HCC progression  provide a novel understanding of TPTEP1 during the chemotherapy for HCC.Overall, these results demonstrated that TPTEP1 inhibits STAT3 transcriptional activity in HCC cells.To further explore the mechanism underlying TPTEP1 suppresses HCC cell proliferation and invasion, biotin-labeled RNA pull-down accompanied by mas  spectrometric assays were performed to investigate the TPTEP1-interacting proteins in HCC cells.Subsequently, the interaction between TPTEP1 and STAT3 was confirmed by RIP assays (Fig. 3b).	31072375	RID06466	transcriptional regulation	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Laryngeal squamous cell carcinoma	XIST	EZH2	positively-E	luciferase reporter assay;knockdown;Starbase;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	ceRNA(miR-124-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA XIST increases the aggressiveness of laryngeal squamous cell carcinoma by regulating miR-124-3p/EZH2.The long non-coding RNAs (lncRNAs) are an emerging class of cancer regulators. The objective of the study was to elucidate the roles and underlying mechanisms of XIST in laryngeal squamous cell carcinoma. Quantitative real-time PCR (qRT-PCR suggested that XIST was highly upregulated in laryngeal squamous cancerous (LSCC) tissues. Knockdown of XIST, mediated by lentiviral transfection of XIST-specific short-hairpin RNA (shRNA), led to the inhibition of proliferation, migration, and invasion of LSCC cells in vitro. In vivo, XIST knockdown also suppressed the growth of LSCC xenografts in mice. Upregulation of miR-124 and downregulation of EZH2 were concomitantly observed after XIST knockdown, and our data suggested that XIST served as the competitive endogenous RNA of miR-124 to modulate EZH2 expression. Moreover, ectopic overexpression of EZH2 prominently attenuated the anti-proliferation activity by XIST knockdown. Therefore, XIST plays an important role in progression of LSCC by modulating the miR-124-EZH2 axis.Altogether, our data indicated that XIST knockdown inhibits proliferation, migration, and invasion of LSCC cells.Using the Starbase bioinformatical tool, miRNAs containing complementary bases with XIST were searched and we focused on miR-124 (Fig. 4A). The wild type (pmirGLOXIST-WT) and mutated binding site (pmirGLO-XIST-Mut) of miR-124 in the XIST sequence were cloned into the reporter vector and we employed luciferase assays to confirm the interaction between miR-124 and XIST.Using targetscan (www.targetscan.org) and starbase (starbase.sysu.edu.cn), it was found that EZH2 is a potential target of miR-124, whereby XIST may serve as a regulator of miR-124.	31071316	RID06467	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteosarcoma	LINC-PINT	miRNA-21	negatively-E	RT-qPCR;bioinformatics	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000231721	GRCh38_7:130938963-131110176	NA	NA	378805	NA	LincRNA-Pint|MKLN1-AS1|PINT	NA	LncRNA LINC-PINT Inhibits Cancer Cell Proliferation, Invasion, and Migration in Osteosarcoma by Downregulating miRNA-21.Background: Downregulation of LncRNA LINC-PINT has been observed in different types of cancer cells, indicating its role as a tumor suppressor. Materials and Methods: Expression of LINC-PINT and miRNA-21 in tumor tissues and adjacent healthy tissues of 56 patients with osteosarcoma was detected by real-time quantitative PCR. Correlations between expression levels of LncRNA LINC-PINT and miRNA-21 were analyzed by Pearson's correlation coefficient. Results: In this study, we found that LncRNA LINC-PINT was inhibited, whereas miRNA-21 was promoted in tumor tissues than in adjacent healthy tissues of patients with osteosarcoma. Expression levels of LncRNA LINC-PINT were affected by both tumor size and tumor metastasis. LncRNA LINC-PINT and miRNA-21 were significantly and reversely correlated in both tumor cells and adjacent healthy tissues. LncRNA LINC-PINT overexpression led to downregulated miRNA-21 expression in cancer cells, whereas miRNA-21 overexpression did not significantly affect LINC-PINT expression. Overexpression of LncRNA LINC-PINT inhibited whereas miRNA-21 overexpression promoted cancer cell proliferation, migration, and invasion. In addition, miRNA-21 overexpression partially rescued the inhibited cell proliferation, migration, and invasion mediated by LncRNA LINC-PINT overexpression. Conclusion: Therefore, LncRNA LINC-PINT may inhibit cancer cell proliferation, invasion, and migration in osteosarcoma by downregulating miRNA-21.	31070482	RID06468	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Non-small cell lung cancer	AFAP1-AS1	HBP1	negatively-E	ChIP;RNAi;RIP	upregulation	qRT-PCR;microarray	GSE31210; GSE19804;GSE18842;GSE19188	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000105856	NA	84740	26959	AFAP1-AS|AFAP1AS|MGC10981	NA	Long noncoding RNA actin filament-associated protein 1 antisense RNA 1 promotes malignant phenotype through binding with lysine-specific demethylase 1 and repressing HMG box-containing protein 1 in non-small-cell lung cancer.The number of documented long noncoding RNAs (lncRNAs) has dramatically increased, and their biological functions and underlying mechanisms in pathological processes, especially cancer, remain to be elucidated. Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) is a 6810-nt lncRNA located on chromosome 4p16.1 that was first reported to be upregulated in esophageal adenocarcinoma tissues and cell lines. Here we reported that AFAP1-AS1, recruiting and binding to lysine-specific demethylase 1 (LSD1), was generally overexpressed in human non-small-cell lung cancer (NSCLC) tissues using quantitative real-time PCR. Higher AFAP1-AS1 expression was significantly correlated with larger tumor size (P = .008), lymph node metastasis (P = .025), higher TNM stage (P = .024), and worse overall survival in NSCLC patients. In vitro experiments revealed that AFAP1-AS1 downregulation inhibited cell migration and induced apoptosis; AFAP1-AS1 knockdown also hindered tumorigenesis in vivo. Moreover, mechanistic investigations including RNA immunoprecipitation and ChIP assays validated that AFAP1-AS1 repressed HMG box-containing protein 1 (HBP1) expression by recruiting LSD1 to the HBP1 promoter regions in PC-9 and H1975 cells. Furthermore, HBP1 functions as a tumor suppressor, and its ectopic expression hindered cell proliferation. Rescue assays determined that the oncogenic effect of AFAP1-AS1 is partially dependent on the epigenetic silencing of HBP1. In conclusion, our results indicate that AFAP1-AS1 is carcinogenic and that the AFAP1-AS1/LSD1/HBP1 axis could constitute a new therapeutic direction for NSCLC.Taken together, these data indicated that AFAP1 AS1 promoted the proliferation of lung cancer cells by inhibiting apoptosis and promoting cell cycle transition.	31069893	RID06469	expression association	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978,GSE41245)
Hepatocellular carcinoma	C1QTNF1-AS1	SOCS3	positively-E	dual-luciferase reporter analysis;TargetScan;miRcode	downregulation	RT-qPCR;sequencing	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-221-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000265096	GRCh38_17:79018131-79027673	ENSG00000184557	NA	100507410	9021	NA	CIS3|Cish3|SOCS-3|SSI-3	Differentially expressed lncRNAs and genes were examined via RNA-seq. GO analysis and KEGG pathway enrichment analysis were carried out based on the function of dys-regulated mRNAs. RT-qPCR was employed to detect the relative mRNA expression level of C1QTNF1-AS1, miR-221-3p, SOCS3 and key genes in the JAK/STAT signaling pathway in HCC tissues and cells, and western blotwas conducted to detect the relative protein expression levels of SOCS3 and key proteins in the JAK/STAT signaling pathway in HCC tissues and cells. MTT assay, transwell assay and flow cytometry were utilized to assess HCC cell proliferation, invasion, migration and apoptosis. Dual luciferase reporter gene assay was used to verify the targeted relationship between C1QTNF1-AS1 and miR-221-3p, as well as between miR-221-3p and SOCS3. A tumorigenicity assay in nude mice was conducted to investigate the effects of C1QTNF1-AS1 on HCC tumor growth in vivo. C1QTNF1-AS1 and SOCS3 were down-regulated, while miR-221-3p was up-regulated in HCC tissues and cells. In HepG2 and Huh7 cells, overexpression of C1QTNF1-AS1 or SOCS3, as well as silence of miR-221-3p inhibited HCC cell proliferation, migration, and invasion and promoted HCC cell apoptosis. The results of the dual luciferase reporter gene assay indicated that miR-221-3p could directly target both C1QTNF1-AS1 and SOCS3. In addition, up-regulation of C1QTNF1-AS1 suppressed HCC tumor growth in vivo.Overexpression of C1QTNF1-AS1 down-regulated miR-221-3p and subsequently up-regulated SOCS3, thereby inhibiting HCC cell proliferation, migration and invasion and promoting apoptosis through the JAK/STAT signaling pathway.The targeted relationships between miRNA and mRNA were analyzed using TargetScan 7.1 , while the binding sites between lncRNA and miRNA were predicted using miRcode . A co-expression network was built after the correlation coefcient between diferentially expressed lncRNAs and genes was calculated.	31069760	RID06470	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Malignant glioma	MT1JP	AKT1	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+);PTEN/AKT signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000142208	NA	4498	207	MT1|MT1J|MT1NP|MTB	AKT|PKB|PRKBA|RAC|RAC-alpha	Long noncoding RNA MT1JP inhibits proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of PTEN/Akt signaling pathway.This study is carried out to elucidate the role of long noncoding RNAs (lncRNAs) MT1JP in proliferation, invasion, migration, and apoptosis of glioma cells through the regulation of PTEN/Akt signaling pathway. The expression of MT1JP in 80 normal brain tissues and 138 glioma tissues, as well as glioma cell lines, was detected by quantitative reverse-transcription polymerase chain reaction. Besides, glioma cells with overexpression and low expression of MT1JP were constructed to confirm the role of MT1JP in proliferation, invasion, migration, and apoptosis of glioma cells and the growth of glioma cells in vivo through the regulation of PTEN/Akt signaling pathway. MT1JP expression was downregulated in glioma tissues and cells. The low expression of MT1JP was considered as an independent risk factor for predicting overall survival in gliomas. After transfection of MT1JP overexpression plasmid, glioma cells showed decreased proliferation, migration and invasion ability, increased apoptosis rate, and decreased the tumorigenic ability of nude mice. The trends were opposite in glioma cells transfected with MT1JP poor expression plasmid. Collectively, our study suggests that lncRNA MT1JP is responsible for inhibiting proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of PTEN/Akt signaling pathway.	31066040	RID06471	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	MT1JP	PTEN	positively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+);PTEN/AKT signaling pathway(+)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000171862	NA	4498	5728	MT1|MT1J|MT1NP|MTB	BZS|MHAM|MMAC1|PTEN1|TEP1	Long noncoding RNA MT1JP inhibits proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of PTEN/Akt signaling pathway.This study is carried out to elucidate the role of long noncoding RNAs (lncRNAs) MT1JP in proliferation, invasion, migration, and apoptosis of glioma cells through the regulation of PTEN/Akt signaling pathway. The expression of MT1JP in 80 normal brain tissues and 138 glioma tissues, as well as glioma cell lines, was detected by quantitative reverse-transcription polymerase chain reaction. Besides, glioma cells with overexpression and low expression of MT1JP were constructed to confirm the role of MT1JP in proliferation, invasion, migration, and apoptosis of glioma cells and the growth of glioma cells in vivo through the regulation of PTEN/Akt signaling pathway. MT1JP expression was downregulated in glioma tissues and cells. The low expression of MT1JP was considered as an independent risk factor for predicting overall survival in gliomas. After transfection of MT1JP overexpression plasmid, glioma cells showed decreased proliferation, migration and invasion ability, increased apoptosis rate, and decreased the tumorigenic ability of nude mice. The trends were opposite in glioma cells transfected with MT1JP poor expression plasmid. Collectively, our study suggests that lncRNA MT1JP is responsible for inhibiting proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of PTEN/Akt signaling pathway.	31066040	RID06472	expression association	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	HOXA-AS2	miR-520a-3p	negatively-F	StarBase 2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000253552	GRCh38_7:27107777-27134302	NA	NA	285943	NA	HOXA3as	NA	Long noncoding RNA HOXA-AS2 promotes non-small cell lung cancer progression by regulating miR-520a-3p.Background: The HOXA cluster antisense RNA 2 (HOXA-AS2) has recently been discovered to be involved in carcinogenesis in multiple cancers. However, the role and underlying mechanism of HOXA-AS2 in non-small cell lung cancer (NSCLC) yet need to be unraveled. Methods: HOXA-AS2 expression in NSCLC tissues and cell lines was detected using quantitative real-time PCR (qRT-PCR. Furthermore, the effects of HOXA-AS2 on NSCLC cell proliferation, apoptosis, migration, and invasion were assessed by MTS, flow cytometry, wound healing and transwell invasion assays, respectively. Starbase2.0 predicted and luciferase reporter and RNA immunoprecipitation (RIP) assays were used to validate the association of HOXA-AS2 and miR-520a-3p in NSCLC cells. Results: Our results revealed that HOXA-AS2 in NSCLC tissues were up-regulated and cell lines, and were associated with poor prognosis and overall survival. Further functional assays demonstrated that HOXA-AS2 knockdown significantly inhibited NSCLC cell proliferation, induced cell apoptosis and suppressed migration and invasion. Starbase2.0 predicted that HOXA-AS2 sponge miR-520a-3p at 3'-UTR, which was confirmed using luciferase reporter and RIP assays. miR-520a-3p expression was inversely correlated with HOXA-AS2 expression in NSCLC tissues. In addition, miR-520a-3p inhibitor attenuated the inhibitory effect of HOXD-AS2-depletion on cell proliferation, migration and invasion of NSCLC cells. Moreover, HOXA-AS2 could regulate HOXD8 and MAP3K2 expression, two known targets of miR-520a-3p in NSCLC. Conclusion: These findings implied that HOXA-AS2 promoted NSCLC progression by regulating miR-520a-3p, suggesting that HOXA-AS2 could serve as a therapeutic target for NSCLC.	31064819	RID06473	ceRNA or sponge	prognosis,metastasis	UP(NSCLC);DATA(GSE74639)	
Ovarian cancer	EGF	LINC01089	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	protein-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	PCG	lncRNA	ENSG00000138798	NA	ENSG00000212694	GRCh38_12:121795267-121803906	1950	338799	NA	AK096174|LIMT	M2-like tumor-associated macrophages-secreted EGF promotes epithelial ovarian cancer metastasis via activating EGFR-ERK signaling and suppressing lncRNA LIMT expression.Background: Ovarian cancer (OC) is the gynecologic malignant tumor with high mortality. Accumulating evidence indicates that M2-like tumor-associated macrophages (TAMs) can secret EGF to participate in ovarian cancer growth, migration, and metastasis. An EGF-downregulated lncRNA, LIMT (lncRNA inhibiting metastasis), was identified as a critical regulator of mammary cell migration and invasion. Nevertheless, whether EGF secreted from M2-like TAMs regulates LIMT expression in ovarian cancer progression remains largely unknown. Methods: The human OC cell lines OV90 and OVCA429 were recruited in this study. The differentiation of the human monocyte cell line THP-1 into M2-like TAMs was confirmed using flow cytometry within the application of phorbol 12-myristate 13-acetate (PMA). ELISA was performed to detect EGF concentration in co-culture system of M2-like TAMs and OC cell lines. Moreover, CCK-8, flow cytometry and immunofluorescence staining of Ki67 were performed to assess the capacity of cell proliferation. Besides, cell migration and invasion were determined by wound healing and transwell assays. Furthermore, the expression levels of epithelial-mesenchymal transition (EMT) markers and EGFR/ERK signals were analyzed by qRT-PCRand western blot. Female athymic nude mice (8-12 weeks of age; n = 8 for each group) were recruited for in vivo study. Results: In the present study, THP-1 cells exhibited the phenotype markers of M2-like TAMs with low proportion of CD14+ marker and high proportion of CD68+, CD204+, CD206+ markers within the application of PMA. After co-culturing with M2-like TAMs, EGF concentration in the supernatants was significantly increased in a time-dependent manner. Besides, OC cells presented better cell viability, higher cell proliferation, and stronger migration and invasion. The expression of EMT-related markers N-cadherin, Vimentin and EGFR/ERK signals were markedly up-regulated, while E-cadherin was significantly decreased. However, these effects induced by co-culture system were reversed by the application of AG1478 (an EGFR inhibitor) or LIMT overexpression. Furthermore, the endogenous expression of LIMT was decreased in OC cell lines compared with the control group. Also, the in vivo experiments verified that the inhibition of EGFR signaling by AG1478 or overexpression of LIMT effectively repressed the tumor growth. Conclusion: Taken together, we demonstrated that EGF secreted by M2-like TAMs might suppress LIMT expression via activating EGFR-ERK signaling pathway to promote the progression of OC.All these results indicated that EGF might be a key growth factor secreted by M2-like TAMs to repress LIMT expression via EGFR signal.	31062668	RID06474	expression association	metastasis	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Colorectal cancer	BDNF-AS	GSK-3beta	negatively-E	RNA pull-down assay;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	NA	NA	497258	NA	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	NA	LncRNA BDNF-AS suppresses colorectal cancer cell proliferation and migration by epigenetically repressing GSK-3beta expression.This study was designed to investigate the molecular mechanism and biological roles of long non-coding RNA (lncRNA) brain-derived neurotrophic factor antisense (BDNF-AS) in colorectal cancer (CRC). The quantitative real-time PCR (qRT-PCR and western blot were performed to detect the expressions of lncRNA BDNF-AS and glycogen synthase kinase-3beta (GSK-3beta) in human CRC tissues and cell lines. The cell proliferation, transwell migration, and invasion assays were carried out to evaluate the effect of lncRNA BDNF-AS on the growth of CRC cells. RNA pull-down and RNA immunoprecipitation (RIP) assays were conducted to confirm the interaction between lncRNA BDNF-AS and enhancer of Zeste Homologue 2 (EZH2). Chromatin immunoprecipitation (ChIP) assay was used to verify the enrichment of EZH2 and histone H3 lysine 27 trimethylation (H3K27me3) in the promoter region of GSK-3beta in CRC cells. LncRNA BDNF-AS expression was significantly decreased, while GSK-3beta was highly expressed in human CRC tissues and cell lines. Moreover, lncRNA BDNF-AS induced inhibition of proliferation, migration, and invasion of CRC cells via inhibiting GSK-3beta expression. Mechanistically, BDNF-AS led to GSK-3beta promoter silencing in CRC cells through recruitment of EZH2. In conclusion, lncRNA BDNF-AS functioned as an oncogene in CRC and shed new light on lncRNA-directed therapeutics in CRC. SIGNIFICANCE OF THE STUDY: LncRNA BDNF-AS is recently reported to be remarkably downregulated in a variety of tumours and served as a tumour suppressor. However, the functions and underlying mechanism of lncRNA BDNF-AS in CRC pathogenesis have not been reported yet. Our study is the first to demonstrate the effect of lncRNA BDNF-AS in CRC and revealed that lncRNA BDNF-AS expression is negatively correlated with the aggressive biological behaviour of CRC. Further investigation demonstrated that lncRNA BDNF-AS functioned as a tumour suppressor in CRC progression by suppressing GSK-3beta expression through binding to EZH2 and H3K27me3 with the GSK-3beta promoter, shedding light on the diagnosis and therapy for CRC.	31062382	RID06475	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	
Colorectal cancer	FOXD3-AS1	SIRT1	positively-E	luciferase reporter assay;knockdown;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-135a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000096717	NA	100996301	23411	pasFOXD3	SIR2L1	Long noncoding RNA FOXD3-AS1 promotes colon adenocarcinoma progression and functions as a competing endogenous RNA to regulate SIRT1 by sponging miR-135a-5p.More and more documents have proved that the abnormal expression of long noncoding RNAs (lncRNAs) are correlated with the initiation and progression of colorectal cancer (CRC). lncRNA FOXD3-AS1 has been reported in glioma for its oncogenic property. According to the survival analysis of The Cancer Genome Atlas database, FOXD3-AS1 upregulation implied lower survival rate of patients with CRC. Quantitative real-time polymerase chain reaction showed the overexpression of FOXD3-AS1 in both CRC tissues and cells. The Kaplan-Meier method demonstrated the prognostic value of FOXD3-AS1 for patients with CRC. To explore the effect of FOXD3-AS1 on CRC progression, loss-of-function experiments were carried out, whose results indicated that knockdown of FOXD3-AS1 suppressed cell proliferation, migration, and invasion, inhibited cell cycle and promoted cell apoptosis in vitro. In vivo experiments affirmed that FOXD3-AS1 affected tumor growth. FOXD3-AS1 expression was enriched in the cytoplasm of CRC cells. Mechanism experiments revealed that FOXD3-AS1 served as a competing endogenous RNA to upregulate SIRT1 by sponging miR-135a-5p. In addition, SIRT1 silencing also restrained cell proliferation and motility. Rescue assays revealed the biological function of FOXD3-AS1/miR-135a-5p/SIRT1 axis in CRC progression. In conclusion, FOXD3-AS1 promotes CRC progression by regulating miR-135a-5p/SIRT1 axis, shedding lights on the way to CRC treatments.Here, we continued to find the downstream target messenger RNA (mRNA). Through searching on four bioinformatics websites (targetScan, picTar, PITA, and miRanda), 89 mRNAs were distinguished.	31058315	RID06476	ceRNA or sponge	prognosis,metastasis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial cancer	Lnc-NA	NR4A1	positively-E	luciferase reporter assay;bioinformatics	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-);apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	TF	NA	NA	ENSG00000123358	NA	NA	3164	NA	GFRP1|HMR|N10|NAK-1|NGFIB|NUR77|TR3	Lnc-NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1.Endometrioid endometrial carcinoma (EEC) is the most common gynaecologic malignancy worldwide. Long non-coding RNAs have previously been demonstrated to play important roles in regulating human diseases, particularly cancer. However, the biological functions and molecular mechanisms of long non-coding RNAs in EEC have not been extensively studied. Here, we describe the discovery of Lnc-NA from the promoter of the transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) gene. The role and function of Lnc-NA in EEC remain unknown. In this study, we used quantitative real-time polymerase chain reactions to confirm that Lnc-NA expression was down-regulated in 30 EEC cases (90%) and in EEC cell lines compared with that in the paired adjacent tissues and normal endometrial cells. In vitro experiments further demonstrated that overexpressing Lnc-NA decreased EEC cell proliferation, migration and invasion and promoted apoptosis via inactivation of the apoptosis signalling pathway. Moreover, the results show that Lnc-NA expression was positively correlated with NR4A1. Furthermore, Lnc-NA regulated NR4A1 expression and activated the apoptosis signalling pathway to inhibit tumour progression. In summary, our results demonstrate that the Lnc-NA-NR4A1 axis could be a useful tumour suppressor and a promising therapeutic target for EEC.To verify the binding sites of Lnc NA and NR4A1, we first an alysed the reliability of Lnc NA through software and showed that the sequence of Lnc NA had a Fickett score of 0.367 34 with an incomplete putative open reading frame of 68 AA and a pI of 11.789 978 027 3, which, in total, classifies it as a non coding se quence with a coding probability of 0.179 828 9.22 Then, we used Lasergene software to predict the region of NR4A1 that is anti sense to Lnc NA. The combined area is approximately 383 bp (Table S3) and is located in the untranslated region of NR4A1 (Figure 1G). Subsequently, we confirmed their binding using luciferase reporter gene technology (Figure 1H). These results indicated that Lnc NA is positively correlated with NR4A1 expression in EECs.	31050196	RID06477	interact with protein	metastasis		DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)
Breast cancer	LINC00511	CDK6	positively-E	luciferase reporter assay;western blot;starBase	upregulation	RT-PCR	NA	NA	cytotoxicity(+)	ceRNA(miR-29c)	regulation	RNA-protein	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000105810	NA	400619	1021	onco-lncRNA-12	PLSTIRE	LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer via regulating miR-29c/CDK6 axis.Aims: Drug resistance is becoming a major clinical challenge to the success of breast cancer treatment. Compelling evidence has shown the association between the deregulated long non-coding RNAs (lncRNAs) and drug resistance in various malignancies. However, the effects of long intergenic noncoding RNA 00511 (LINC00511), a newly identified oncogenic lncRNA, on the drug resistance of breast cancer cells remain unknown.Main methods: RT-qPCR was performed to detect the expressions of LINC00511, miR-29c, and cyclin dependent kinase 6 (CDK6) in breast cancer tissues and cells. Pearson correlation analysis was used to analyze the correlation between miR-29c, CDK6 and LINC00511 expression in breast cancer tissues. The interactions between LINC00511, CDK6 and miR-29c were explored by luciferase reporter assay, RT-qPCR and western blot. MTT assay and flow cytometry analysis were applied to evaluate paclitaxel cytotoxicity.Key findings: LINC00511 and CDK6 were upregulated while miR-29c was downregulated in breast cancer tissues and cells. miR-29c was negatively correlated with LINC00511 and CDK6 expression while LINC00511 was positively correlated with CDK6 expression in breast cancer tissues. LINC0051 directly interacted with miR-29c to suppress its expression. LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells by upregulating miR-29c. CDK6 was identified as a target of miR-29c. CDK6 knockdown attenuated the effects of miR-29c inhibition on paclitaxel cytotoxicity in breast cancer cells. LINC00511 positively regulated CDK6 expression in breast cancer cells.Significance: LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells via regulating miR-29c/CDK6 axis.	31047896	RID06478	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Pancreatic ductal adenocarcinoma	FOXO1	LETR1	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cell proliferation(-);WNT/beta-catenin signaling pathway(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000150907	NA	ENSG00000248441	GRCh38_15:95186634-95327129	2308	400456	FKH1|FKHR|FOXO1A	LINC01197	FOXO1-regulated lncRNA LINC01197 inhibits pancreatic adenocarcinoma cell proliferation by restraining Wnt/beta-catenin signaling.Background: Recent studies have revealed that numerous oncogenic long non-coding RNAs (lncRNAs) play pivotal roles in pancreatic ductal adenocarcinoma (PDAC) progression, but little is known about tumor-suppressive lncRNAs in PDAC. This study was conducted to evaluate the function of tumor-suppressive LINC01197 in PDAC progression and investigate the detailed mechanisms.Methods: LncRNA microarray was used to identify differentially expressed lncRNAs in FOXO1-overexpressing PANC1 cells. LINC01197 expression was evaluated by quantitative PCR, Northern blotting, and fluorescence in situ hybridization. The Cancer Genome Atlas database was used to analyze the prognostic role of LNC01197 in PDAC. A luciferase reporter assay was performed to confirm the interaction between LNC01197 and FOXO1. The biological function of LINC01197 was evaluated by colony formation assay in vitro and in an animal subcutaneous tumorigenesis experiment and Ki67 staining in vivo. RNA-pull-down, western blot, RNA immunoprecipitation assay, and co-immunoprecipitation were further performed to determine the molecular mechanism of LNC01197 and beta-catenin in the Wnt pathway.Results: We found that a FOXO1-related lncRNA, LINC01197, was significantly decreased in PDAC malignant tissues and that its low expression predicted poor prognosis. Moreover, LINC01197 was mainly localized in the nucleus and inhibited PDAC cell proliferation both in vitro and in vivo. Mechanistically, LINC01197 was found to bind to beta-catenin and inhibit Wnt/beta-catenin signaling activity by disrupting beta-catenin binding to TCF4 in PDAC cells.Conclusions: The novel FOXO1/LINC01197/beta-catenin axis was dysregulated during PDAC progression. Our study provides insight into the mechanisms of LINC01197 in PDAC and reveal a potential target for PDAC clinical therapy and prognostic prediction.	31027497	RID06479	interact with protein	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Triple-negative breast cancer	PTCSC3	H19	negatively-E	RT-qPCR;bioinformatics	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	lncRNA	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000130600	GRCh38_11:1995171-2001470	100886964	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LncRNA PTCSC3 inhibits triple-negative breast cancer cell proliferation by downregulating lncRNA H19.Long noncoding RNA (lncRNA) PTCSC3 (hereafter PTCSC3 is used to represent lncRNA PTCSC3) inhibits glioma and thyroid cancer, indicating its potential tumor suppression function in other types of cancers. We explored the potential involvement of PTCSC3 in triple-negative breast cancer (TNBC). In the current study, we found that PTCSC3 was downregulated in tumor tissues of patients with TNBC. PTCSC3 expression was positively correlated with plasma levels of PTCSC3. LncRNA H19 was upregulated and was inversely correlated with PTCSC3 in tumor tissues. PTCSC3 overexpression led to downregulated H19 in TNBC cells, while H19 overexpression did not affect PTCSC3 expression. PTCSC3 inhibited and H19 promoted proliferation of TNBC cells. H19 overexpression attenuated the effects of PTCSC3 overexpression. Cancer cell migration and invasion were not significantly affected by PTCSC3 overexpression. Therefore, lncRNA PTCSC3 inhibits TNBC cell proliferation by downregulating lncRNA H19.RT-qPCR was also performed to investigate the differential expression of H19 in 69 TNBC patients. It was observed that H19 was upregulated in tumor (Figure 2A, P < 0.05). Linear regression was performed to analyze the correlation between expression levels of H19 and PTCSC3. The results showed that H19 was inversely correlated with PTCSC3 only tumor tissues (Figure 2B). In contrast, expression levels of PTCSC3 and H19 in tumor adjacent normal tissues were not significantly correlated (Figure 2C).	31026090	RID06480	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(NSCLC);DATA(GSE74639)
Intrahepatic cholangiocarcinoma	LNCNEF	RUNX1	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell metastasis(-);cell invasion(-)	NA	regulation	NA	NA	CSC	NA	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000237396	GRCh38_20:22587522-22607517	ENSG00000159216	NA	101929685	861	LINC01384|lncRNA-NEF	AML1|AMLCR1|CBFA2|PEBP2A2	Down-regulation of lncRNA-NEF indicates poor prognosis in intrahepatic cholangiocarcinoma.LncRNA-NEF is a tumor suppressor lncRNA in liver cancer. The present study aimed to investigate the role of lncRNA-NEF in intrahepatic cholangiocarcinoma (IHCC), which is second most common type of primary cancer of the hepatobiliary system that causes high mortality rate. In the present study we found that lncRNA-NEF was down-regulated, while Runt-related transcription factor 1 (RUNX1) was up-regulated in tumor tissues than in adjacent healthy tissues of IHCC patients. Expression levels of lncRNA-NEF and RUNX1 were significantly and reversely correlated in tumor tissues but not in adjacent healthy tissues. Plasma levels of lncRNA-NEF were significantly lower in IHCC patients than in healthy controls. Down-regulation of lncRNA-NEF effectively distinguished stage I and II IHCC patients from healthy controls. Patients were followed up for 5 years, patients with high plasma levels of lncRNA-NEF showed significantly better survival conditions compared with patients with low expression levels of lncRNA-NEF. LncRNA-NEF overexpression led to inhibited expression of RUNX1 in cells of IHCC cell lines and inhibited cancer cell migration and invasion. In contrast, RUNX1 overexpression showed no significant effects on lncRNA-NEF expression, but attenuated the effects of lncRNA-NEF overexpression on cancer cell migration and invasion. We therefore concluded that lncRNA-NEF participated in IHCC possibly by interacting with RUNX1.Compared with control group (C) and negative control group (NC), lncRNA-NEF overexpression led to significantly inhibited expression of RUNX1 in cells of both HuCCT1 and TFK-1 human IHCC cell lines (Figure 5A). In contrast, RUNX1 overexpression did not significantly alter the expression of lncRNA-NEF in those cells (Figure 5B).	31015363	RID06481	expression association	prognosis,metastasis		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	XIST	miR-34a	negatively-F	luciferase reporter assay;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Long noncoding RNA XIST regulates the EGF receptor to promote TGF-beta1-induced epithelial-mesenchymal transition in pancreatic cancer.Background: This study focuses on the lncRNA XIST (X inactive-specific transcript), an lncRNA involved in multiple human cancers, and investigates the functional significance of XIST and the molecular mechanisms underlying the epithelial-mesenchymal transition (EMT) in pancreatic cancer (PC).Methods: Clinical specimens from 25 patients as well as 5 human PC cell lines were analyzed for XIST, YAP, and microRNA(miR)-34a by quantitative real-time PCR (qRT-PCR and immunohistochemistry. To investigate how XIST influences cell proliferation, invasiveness, and apoptosis in PC, we performed the CCK-8 assays, Transwell assays, and flow cytometry. Luciferase reporter assays, qRT-PCR and western blot were applied to prove that miR-34a directly binds to XIST.Results: Up-regulation of XIST and Yes associated protein (YAP) and down-regulation of miR-34a were consistently observed in the clinical specimens and PC cell lines. Silencing XIST reduced the expression of YAP and suppressed transforming growth factor (TGF)-beta1-induced EMT, while over-expression of XIST increased the expression of YAP and promoted EMT. In addition, inhibition of epidermal growth factor receptor (EGFR) hampered the XIST-promoted EMT. The results from the luciferase reporter assays confirmed that miR-34a directly targets XIST and suggested that XIST regulates cell proliferation, invasiveness, and apoptosis in PC by sponging miR-34a.Conclusions: XIST promotes TGF-beta1-induced EMT by regulating the miR-34a-YAP-EGFR axis in PC.	31013436	RID06482	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Pancreatic cancer	XIST	YY1AP1	positively-E	western blot;shRNA	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000163374	NA	7503	55249	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	HCCA2|YAP|YY1AP	Clinical specimens from 25 patients as well as 5 human PC cell lines were analyzed for XIST, YAP, and microRNA(miR)-34a by quantitative real-time PCR (qRT-PCR and immunohistochemistry. To investigate how XIST influences cell proliferation, invasiveness, and apoptosis in PC, we performed the CCK-8 assays, Transwell assays, and flow cytometry. Luciferase reporter assays, qRT-PCR and western blot were applied to prove that miR-34a directly binds to XIST. Up-regulation of XIST and Yes associated protein (YAP) and down-regulation of miR-34a were consistently observed in the clinical specimens and PC cell lines. Silencing XIST reduced the expression of YAP and suppressed transforming growth factor (TGF)-beta1-induced EMT, while over-expression of XIST increased the expression of YAP and promoted EMT. In addition, inhibition of epidermal growth factor receptor (EGFR) hampered the XIST-promoted EMT. The results from the luciferase reporter assays confirmed that miR-34a directly targets XIST and suggested that XIST regulates cell proliferation, invasiveness, and apoptosis in PC by sponging miR-34a.Conclusions: XIST promotes TGF-beta1-induced EMT by regulating the miR-34a-YAP-EGFR axis in PC.To test this, we first used short hairpin RNA (sh-XIST) to knock down the lncRNA 268 XIST, while using a non-silencing shRNA as the negative control (sh-NC). Both of qRT-PCRand 269 western blot revealed that the expression levels of YAP and EGFR mRNA and proteins were 270 significantly reduced in XIST-silenced MIAPaCa-2 and PATU8988T (Fig. 3A and 3B).	31013436	RID06483	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Pancreatic cancer	XIST	EGFR	positively-E	western blot;shRNA	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000146648	NA	7503	1956	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ERBB|ERBB1|ERRP	Clinical specimens from 25 patients as well as 5 human PC cell lines were analyzed for XIST, YAP, and microRNA(miR)-34a by quantitative real-time PCR (qRT-PCR and immunohistochemistry. To investigate how XIST influences cell proliferation, invasiveness, and apoptosis in PC, we performed the CCK-8 assays, Transwell assays, and flow cytometry. Luciferase reporter assays, qRT-PCR and western blot were applied to prove that miR-34a directly binds to XIST. Up-regulation of XIST and Yes associated protein (YAP) and down-regulation of miR-34a were consistently observed in the clinical specimens and PC cell lines. Silencing XIST reduced the expression of YAP and suppressed transforming growth factor (TGF)-beta1-induced EMT, while over-expression of XIST increased the expression of YAP and promoted EMT. In addition, inhibition of epidermal growth factor receptor (EGFR) hampered the XIST-promoted EMT. The results from the luciferase reporter assays confirmed that miR-34a directly targets XIST and suggested that XIST regulates cell proliferation, invasiveness, and apoptosis in PC by sponging miR-34a.Conclusions: XIST promotes TGF-beta1-induced EMT by regulating the miR-34a-YAP-EGFR axis in PC.To test this, we first used short hairpin RNA (sh-XIST) to knock down the lncRNA 268 XIST, while using a non-silencing shRNA as the negative control (sh-NC). Both of qRT-PCRand 269 western blot revealed that the expression levels of YAP and EGFR mRNA and proteins were 270 significantly reduced in XIST-silenced MIAPaCa-2 and PATU8988T (Fig. 3A and 3B).	31013436	RID06484	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	HOXA11-AS	ABCC10	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(let-7i)	regulation	RNA-protein	Propofol	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124574	NA	221883	89845	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	EST182763|MRP7|SIMRP7	Propofol promotes apoptosis of colorectal cancer cells via alleviating the suppression of lncRNA HOXA11-AS on miRNA let-7i.To date, surgical resection is the mainstay for the treatment of colorectal cancer (CRC). Propofol (2,6-diisopropylphenol), one of the most commonly used intravenous anaesthetic agents, has been reported to be involved in modulating the malignancy of a variety of human cancers. However, the underlying mechanisms remain poorly understood. In this study, using a cell counting kit (CCK-8), flow cytometry, and caspase-3 cleavage assays, we found that propofol promoted cell apoptosis and inhibited cell proliferation in both Colo205 and SW620 cells, through the down-regulation of HOXA11-AS and up-regulation of let-7i. Moreover, gain-of-function studies of HOXA11-AS or loss-of-function studies of let-7i also revealed a negative correlation between HOXA11-AS and let-7i in propofol-mediated biological functions of CRC cells. Furthermore, our mechanistic experiments revealed that HOXA11-AS acts as a molecular sponge for let-7i, thereby regulating the expression of ABCC10. We investigate the theory that propofol suppresses colorectal cancer tumorigenesis by modulating the HOXA11-AS-let-7i-ABCC10 regulatory network, indicating the potential for propofol to control CRC development.	31013434	RID06485	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	TRERNA1	CDH1	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	DNA methylation	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000039068	NA	100887755	999	LINC00651|ncRNA-a7|treRNA	CD324|UVO|uvomorulin	LncRNA TRERNA1 facilitates hepatocellular carcinoma metastasis by dimethylating H3K9 in the CDH1 promoter region via the recruitment of the EHMT2/SNAI1 complex.Materials and methods: The lncRNA TRERNA1 expression levels were detected in HCC by quantitative real-time PCR (qPCR). The function of TRERNA1 was examined by wound-healing assays, transwell assays and tail vein injection experiments. The potential regulatory mechanisms of TRERNA1 on its target genes were explored by ChIP, RIP, IP and WB assays. Elevated TRERNA1 levels promoted HCC cell migration and invasion in vitro and in vivo. TRERNA1 recruited EHMT2 to dimethylate H3K9 in the CDH1 promoter region. Furthermore, EHMT2 bound to SNAI1 to suppress CDH1 expression in HCC cells. After inhibiting TRERNA1, the expression level of CDH1 was restored and was involved in the regulation of the EHMT2/SNAI1 complex. The level of TRERNA1 was positively correlated with tumour metastasis and was negatively correlated with the expression of CDH1 in HCC tissues.Conclusions: For the first time, the current study reveals that TRERNA1 promotes cell metastasis and the invasion of HCC via the recruitment of EHMT2 and/or the EHMT2/SNAI1 complex to suppress CDH1. These data identify a novel mechanism that regulates TRERNA1 in metastatic HCC and provides a potential targeted therapy for HCC patients.These results suggested that TRERNA1 epigenetically silenced CDH1 by altering its H3K9me2 lev els in trans, which depended on EHMT2.	31012192	RID06486	epigenetic regulation	metastasis		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Uveal melanoma	PVT1	EZH2	positively-E	knockdown;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|EZH1|KMT6|KMT6A	LncRNA PVT1 knockdown affects proliferation and apoptosis of uveal melanoma cells by inhibiting EZH2.Patients and methods: 40 cases of UM tissues and 40 cases of adjacent tissues surgically resected in our hospital from October 2015 to April 2018 were collected. The expression level of lncRNA PVT1 in these tissues was determined by Reverse Transcription-Polymerase Chain Reaction (RT-PCR. Stable knockdown of lncRNA PVT1 was constructed in human UM cell line OCM-1 using small interfering RNA (siRNA). The impact of lncRNA PVT1 on UM cell proliferation was detected by Cell Counting kit-8 (CCK-8) and colony formation assay. Flow cytometry was applied to measure the apoptotic level of UM cells in the blank control group and lncRNA PVT1 knockdown group. Meanwhile, the expression level of enhancer of zeste homologue 2 (EZH2) was determined by western blot.Results: The expression level of lncRNA PVT1 in UM tissues was remarkably higher than that in the adjacent tissues (p<0.05). UM cell proliferation was notably repressed after lncRNA PVT1 knockdown by siRNA. Flow cytometry results indicated that the number of apoptotic UM cells in lncRNA PVT1 knockdown group significantly increased compared with that in the blank control group (p<0.05). The protein expression of EZH2 was suppressed after lncRNA PVT1 knockdown (p<0.05).Conclusions: LncRNA PVT1 knockdown in UM cells can repress the proliferation of UM cells and promote their apoptosis by regulating EZH2 expression.	31002139	RID06487	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Retinoblastoma	NKILA	XIST	negatively-E	bioinformatics	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	lncRNA	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000229807	GRCh38_X:73820649-73852723	105416157	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	LncRNA NKILA Inhibits Retinoblastoma by Downregulating lncRNA XIST.Purpose: Although retinoblastoma is rare but can be deadly in some severe cases. To find novel therapeutic targets for retinoblastoma, we explored the potential role of lncRNA NKILA in retinoblastoma. Results: We found that, comparing to healthy controls, NKILA was downregulated, while lncRNA XIST was upregulated in plasma of retinoblastoma patients and they were inversely correlated. Downregulation of NKILA distinguished early-stage patients from healthy controls. Overexpression of lncRNA NKILA mediated the downregulation of XIST in retinoblastoma cells, while XIST overexpression failed to significantly affect NKILA. Overexpression of NKILA resulted in decreased, while XIST overexpression resulted in increased proliferation, migration and invasion rates of retinoblastoma cells. In addition, rescue experiment showed that XIST overexpression attenuated the effects of NKILA overexpression on cancer cell behaviors. Conclusions: Therefore, NKILA inhibits retinoblastoma possibly by downregulating XIST, but the causality has not been fully validated.	30995132	RID06488	expression association	metastasis		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Pancreatic cancer	SMIM31	AGR2	positively-E	western blot;RIP;RNA22;RNA pull-down assay	upregulation	qRT-PCR	GSE22780;GSE32676;GSE71989;GSE91035;GSE16515	NA	cell autophagy(-);apoptosis process(-)	ceRNA(miR-143-5p)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000248771	GRCh38_4:164754064-164803795	ENSG00000106541	NA	100505989	10551	LINC01207	AG2|HAG-2|PDIA17|XAG-2	Long non-coding RNA LINC01207 silencing suppresses AGR2 expression to facilitate autophagy and apoptosis of pancreatic cancer cells by sponging miR-143-5p.Pancreatic cancer is a serious malignancy accompanied by a well-documented poor prognosis. Accumulating studies have indicated the crucial roles played by long non-coding RNAs (lncRNAs) in proliferation, apoptosis and invasion of cancer cells. The aim of the current study was to investigate the role of lncRNA LINC01207 in autophagy and apoptosis of pancreatic cancer cells and its regulatory mechanism interacting with miR-143-5p. Initially, expression profiles of lncRNAs and genes associated with pancreatic cancer were identified. The expression patterns of LINC01207, miR-143-5p and AGR2 in both pancreatic cancer and adjacent tissues were then determined. The binding relationship of LINC01207 to miR-143-5p and targeting relationship of miR-143-5p to AGR2 were subsequently verified. Silencing of LINC01207, or up-regulation or down-regulation of miR-143-5p was introduced into the pancreatic cancer cells, so as to analyze their effects on the cell growth, apoptosis and autophagy. Besides, these regulatory effects were further explored with the determination of the autophagy- and apoptosis-related gene or proteins. LINC01207 and AGR2 were highly expressed while miR-143-5p was poorly expressed in pancreatic cancer. Functionally, LINC01207 can bind to miR-143-5p, and AGR2 was a target gene of miR-143-5p. Importantly, silencing of LINC01207 down-regulated the expression of AGR2 by up-regulating miR-143-5p. Moreover, silencing of LINC01207 and up-regulation of miR-143-5p promoted cell apoptosis and autophagy, corresponding to increased expression of autophagy- and apoptosis-related proteins, in addition to inhibited cell growth. Taken together, silencing of LINC01207 prevents the progression of pancreatic cancer by impairing miR-143-5p-targeted AGR2 expression, providing a potential target for pancreatic cancer treatment.High expression of AGR2 was identified in pancreatic cancer through the data analysis of GSE22780 (Fig. 2A), GSE32676 (Fig. 2B), GSE71989 (Fig. 2C) and GSE91035 (Fig. 2D). Data analysis of the microarray data GSE16515 further indicated that LINC01207 and AGR2 were highly expressed in pancreatic cancer (Fig. 2E) and were positively correlated.Further online website RNA22 prediction analysis showed that there were binding sites of LINC01207 to miR-143-5p and of miR-143-5p to AGR2.	30991076	RID06489	ceRNA or sponge	prognosis	UP(BRCA);DATA(GSE55807)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE51827,GSE55807)
Esophagus squamous cell carcinoma	MEG3	DKK2	positively-E	miRDB;luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-);WNT/beta-catenin signaling pathway(-);cancer progression(-)	ceRNA(miR-4261)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000155011	NA	55384	27123	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	Downregulated MEG3 contributes to tumour progression and poor prognosis in oesophagal squamous cell carcinoma by interacting with miR-4261, downregulating DKK2 and activating the Wnt/beta-catenin signalling.Long noncoding RNA (lncRNA) MEG3 has been widely reported to be decreased in a growing list of primary human tumours and play a key role in tumour suppression. However, there are few reports about MEG3 expression and function in oesophagal squamous cell carcinoma (ESCC). Here, we found that MEG3 expression was significantly downregulated in tumour tissues, and its low expression was associated with large tumour size, lymph node metastasis and advanced clinical stage in ESCC patients. Univariate and multivariate analyses revealed low expression of MEG3 as an independent predictor for disease-free survival and overall survival. Cell experiments showed that MEG3 inhibited ESCC cell proliferation, migration and invasion. Subsequently, miR-4261 was identified and confirmed to be the target of MEG3, and MEG3 functions, at least in part, by targeting miR-4261. Additionally, Dickkopf-2 (DKK2), a Wnt/beta-catenin signalling inhibitor, was identified to be a target of miR-4261. MEG3 interacted with miR-4261, derepressed DKK2 and blocked the Wnt/beta-catenin signalling, thereby inhibiting tumourigenesis and progression in ESCC. In vivo experiments also confirmed this conclusion. Our study for the first time elaborated the critical role of MEG3-miR-4261-DKK2-Wnt/beta-catenin signalling axis in ESCC, and MEG3 could represent a novel diagnostic and prognostic biomarker and therapeutic target in ESCC.Furthermore, we performed luciferase reporter assay and found that the luciferase activity of wild-type reporter was obviously suppressed when transfection with miR-4261 mimic compared to mimic control (Figure 4(F)). Collectively, these data indicated that miR-4261 is a target of MEG3, and MEG3 can directly regulate miR-4261 expression.	30990378	RID06490	ceRNA or sponge	metastasis,prognosis		UP(PAAD);DATA(GSE40174)
Melanoma	UCA1	HOXB3	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-28-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000120093	NA	652995	3213	CUDR|LINC00178|onco-lncRNA-36|UCAT1	HOX2|HOX2G	Knockdown of lncRNA-UCA1 inhibits the proliferation and migration of melanoma cells through modulating the miR-28-5p/HOXB3 axis.In the present study, reverse transcription quantitative polymerase chain reaction and western blot were used to examine the mRNA and protein expression levels, respectively. Cell Counting Kit-8 and wound healing assays were conducted to study cell proliferation and migration, respectively. A luciferase reporter assay was used to confirm the targeting relationship. It was demonstrated that UCA1 expression was increased in melanoma tissues and cell lines. In addition, UCA1 expression was higher in melanoma tissues at stage III-IV than in tissues at stage I-II. Inhibition of UCA1 expression markedly reduced melanoma cell proliferation and migration. Further investigation revealed that UCA1 functioned in melanoma cells through directly binding with microRNA (miR)-28-5p. The expression of miR-28-5p was significantly reduced in melanoma tissues and had an inverse correlation with UCA1 expression. In addition, miR-28-5p expression was higher in melanoma tissues at advanced stages than in stage I-II tissues. Furthermore, homeobox (HOX)B3 was identified as a target gene of miR-28-5p in melanoma cells, and HOXB3 overexpression reversed the suppressive effects of UCA1 downregulation on melanoma cell proliferation and migration. Finally, HOXB3 was upregulated in melanoma tissues compared with its expression in adjacent tissues, and HOXB3 expression was increased in melanoma tissues at advanced stages. Taken together, the regulatory network of the UCA1/miR-28-5p/HOXB3 axis in melanoma was demonstrated for the first time in the present study, expanding the understanding of the molecular mechanism underlying melanoma progression. Future studies may further confirm the function of this signaling pathway in vivo.	30988802	RID06491	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	DOWN(BRCA);DATA(GSE51827,GSE86978)
Ovarian cancer	GEHT1	HIF1A	positively-F	RNA pull-down assay;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);apoptosis process(-)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	NA	NA	ENSG00000100644	NA	NA	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA GEHT1 promoted the proliferation of ovarian cancer cells via modulating the protein stability of HIF1alpha.Cancer cells preferentially metabolize glucose via the aerobic glycolysis pathway, which is also named as Warburg effect. Increasing evidence has suggested that suppression of glycolysis inhibits the progression of cancers. In the present study, we found that the long non-coding RNA gastric carcinoma high expressed transcript 1 (GHET1) was overexpressed in ovarian cancer tissues and cell lines. Up-regulation of GHET1 was positively correlated with the tumor size and metastasis of the ovarian cancer patients. Overexpression of GEHT1 significantly promoted the proliferation and colony formation of ovarian cancer cells. Mechanistically, the candidate binding partners of GHET1 were explored by pull-down and mass spectrum. Of note, GHET1 was found to interact with the E3 ubiquitin ligase von Hippel-Lindau (VHL), which consequently blocked VHL-mediated degradation of hypoxia-inducible factor-1alpha (HIF1alpha) and enhanced the protein level of HIF1alpha in ovarian cancer cells. The up-regulated HIF1alpha promoted the glucose uptake and lactate generation of ovarian cancer cells. Collectively, our results suggested the oncogenic function of GHET1 via up-regulating the glycolysis in ovarian cancer and can be considered as a promising anti-cancer target.	30988076	RID06492	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Oral squamous cell carcinoma	LEF1-AS1	LATS1	interact	RIP;RPISeq;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell survival(+);cell proliferation(+);apoptosis process(-);Hippo signaling pathway(-);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000131023	NA	641518	9113	NA	WARTS	Knockdown of lncRNA LEF1-AS1 inhibited the progression of oral squamous cell carcinoma (OSCC) via Hippo signaling pathway.It is verified that long non-coding RNAs (lncRNAs) play crucial roles in various cancers. LncRNA LEF1-AS1 is a reported oncogene in colorectal cancer and glioblastoma. In this study, we unveiled that LEF1-AS1 markedly increased in oral squamous cell carcinoma (OSCC) tissues and cell lines. Besides, OSCC patients with high levels of LEF1-AS1 were apt to poor prognosis. Functionally, LEF1-AS1 knockdown inhibited cell survival, proliferation and migration, whereas enhanced cell apoptosis and induced G0/G1 cell cycle arrest in vitro. Consistently, LEF1-AS1 silence hindered tumor growth in vivo. Moreover, LEF1-AS1 inhibition stimulated the activation of Hippo signaling pathway through directly interacting with LATS1. Furtherly, we disclosed that LEF1-AS1 silence abolished the interaction of LEF1-AS1 with LATS1 while enhanced the binding of LATS1 to MOB, therefore promoting YAP phosphorylation but impairing YAP1 nuclear translocation. Additionally, we demonstrated that LEF1-AS1 regulated YAP1 translocation via a LATS1-dependent manner. Furthermore, we also uncovered that YAP1 overexpression abolished the suppressive impact of LEF1-AS1 repression on the biological processes of OSCC cells. In a word, we concluded that LEF1-AS1 served an oncogenic part in OSCC through suppressing Hippo signaling pathway by interacting with LATS1, suggesting the therapeutic and prognostic potential of LEF1-AS1 in OSCC.And the direct interactivity of LEF1-AS1 with LATS1 was further confirmed by using RIP assays conducted in both SCC4 and SCC15 cells (Figure 6c), whereas such interaction was markedly hampered upon LEF1-AS1 suppression (Figure 6d).Interestingly, depletion of LEF1-AS1 strikingly elevated the cytoplasmic YAP1 expression but reduced the nuclear YAP1 level both in SCC4 and SCC15 cells (Figure 6f). Altogether, these findings uncovered that LEF1-AS1 facilitated YAP1 translocation by inactivating Hippo signaling via directly interacting with LATS1.	30983488	RID06493	interact with protein	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	MALAT1	PNPO	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);colony formation(+);apoptosis process(-)	ceRNA(miR-216b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000108439	NA	378938	55163	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PDXPO	Pyridoxine 5'-phosphate oxidase is correlated with human breast invasive ductal carcinoma development.Pyridoxine 5'-phosphate oxidase (PNPO) is a converting enzyme for an active form of vitamin B6. This study aims to evaluate the biological function and the regulatory mechanism of PNPO in human breast invasive ductal carcinoma (IDC). We unveiled for the first time that PNPO was upregulated in patients with IDC and was correlated with the overall survival of patients with metastasis at the later stages. Suppression of PNPO inhibited breast cancer cell proliferation, migration, invasion and colony formation, arrested cell cycle at the G2/M phase and induced cell apoptosis. PNPO was positively correlated with lncRNA MALAT1 which was negatively correlated with miR-216b-5p. PNPO was down-regulated and up-regulated by miR-216b-5p mimics and inhibitors, respectively, in breast cancer cells. A microRNA response element was found in both PNPO and MALAT1 transcripts for miR-216b-5p and the dual-luciferase reporter assay confirmed the binding of these transcripts. Knockdown of MALAT1 resulted in an increase of miR-216b-5p and a decrease of PNPO mRNA, indicating a regulatory mechanism of competing endogenous RNAs. Taken together, these results reveal the biological function and a regulatory mechanism of PNPO, in which the MALAT1/miR-216b-5p/PNPO axis may be important in IDC development. Targeting this axis may have therapeutic potential for breast cancer.The expression of PNPO mRNA (Figure 9A), miR- 216b-5p (Figure 9B), and MALAT1 (Figure 9C) in breast tissues was detected by qRT-PCR	30982780	RID06494	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PRAD,BRCA);UP(SKCM);DATA(GSE104209,GSE38495,GSE111842)
Non-small cell lung cancer	CRNDE	CDK6	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-641)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000105810	NA	643911	1021	CRNDEP|LINC00180|LOC643911	PLSTIRE	lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) Promotes Proliferation and Inhibits Apoptosis in Non-Small Cell Lung Cancer Cells by Regulating the miR-641/CDK6 Axis.BACKGROUND The lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) gene has been reported as a potential oncogene in NSCLC. Nevertheless, the molecular mechanism of CRNDE in NSCLC progression remains largely unknown. MATERIAL AND METHODS qRT-PCRassay was performed to detect the expression levels of CRNDE, miR-641, and cyclin-dependent kinase 6 (CDK6) in NSCLC. western blot assay was employed to assess CDK6 protein level in treated NSCLC cells. si-CRNDE#1, si-CRNDE#2, miR-641 mimics, miR-641 inhibitors, or Vector-CDK6 were transfected into NSCLC cells to change the expression levels of CRNDE, miR-641, or CDK6. dual-luciferase reporter assay was performed to validate the direct interrelated miRNA of CRNDE and the potential target of miR-641. MTT and flow cytometry assays were performed to assess the capacities of cell proliferation and apoptosis, respectively. RESULTS CRNDE level was upregulated in NSCLC, and its knockdown suppressed NSCLC cells proliferation and enhanced apoptosis, whereas miR-641 antagonized the regulatory effect of CRNDE knockdown by directly binding to CRNDE. Moreover, CDK6 was a target of miR-641 and miR-641 exerted anti-proliferation and pro-apoptosis effects through CDK6. CONCLUSIONS CRNDE promoted proliferation and inhibited apoptosis of NSCLC cells at least in part by regulating the miR-641/CDK6 axis, suggesting that CRNDE is a potential therapeutic target for NSCLC treatment.	30982057	RID06495	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Prostate cancer	SNHG15	FKBP1A	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000088832	NA	285958	2280	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	FKBP-12|FKBP1|FKBP12|FKBP12C|PKC12|PPIASE	LncRNA SNHG15 acts as an oncogene in prostate cancer by regulating miR-338-3p/FKBP1A axis.Long non-coding RNAs (lncRNAs) are crucial regulators in the progression of various diseases. Although the role of lncRNAs in prostate cancer (PCa) has been studied in recent years, there are still numerous lncRNAs need to be elucidated. This study aims to detect the role of lncRNA small nucleolar RNA host gene 15 (SNHG15) in human prostate cancer. Using qRT-PCRanalysis, we identified the upregulation of SNHG15 in PCa cell lines. Loss-of function assays were conducted to determine the regulatory effect of SNHG15 on PCa cell proliferation, migration and epithelial-mesenchymal transition (EMT). According to the results of functional assays, we found that knockdown of SNHG15 impaired cell viability, suppressed cell proliferation, inhibited cell migration and invasion, reversed EMT progress. All these findings revealed the oncogenic function of SNHG15 in PCa. Mechanism investigation revealed that SNHG15 was located in the cytoplasm of PCa cells and acted as a molecular sponge of microRNA-338-3p (miR-338-3p). Moreover, FKBP prolyl isomerase 1A (FKBP1A) was a target of miR-338-3p. This investigation demonstrated that SNHG15 may serve as a competing endogenous RNA (ceRNA) to regulate miR-338-3p and FKBP1A. Finally, the involvement of miR-338-3p and FKBP1A in SNHG15-mediated biological function was demonstrated by performing rescue assays. In summary, our study revealed the function of a novel pathway in PCa.	30981837	RID06496	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)
Osteoarthritis	TNF	HULC	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	RT-qPCR	NA	NA	inflammatory response(-)	NA	association	protein-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	PCG	lncRNA	ENSG00000228978	NA	ENSG00000251164	NA	7124	728655	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	HCCAT1|LINC00078|NCRNA00078	Long non-coding RNA highly up-regulated in liver cancer protects tumor necrosis factor-alpha-induced inflammatory injury by down-regulation of microRNA-101 in ATDC5 cells.Methods: Relative expression levels of pro-inflammatory cytokines (IL-6, IL-8 and MCP-1) and HULC in OA cartilage tissues and normal cartilage tissues were determined by RT-qPCR. TNF-alpha induced inflammatory injury model in ATDC5 cells was constructed, and the biological functions of HULC overexpression or suppression in TNF-alpha-injured ATDC5 cells were assessed. The relevancy between miR-101 and HULC was investigated by utilizing bioinformatics prediction, luciferase reporter assay, RNA pull-down and immunoprecipitation. MiR-101 mimic and inhibitor were transfected into ATDC5 cells, and its regulatory effect on TNF-alpha-injured ATDC5 cells was examined. Further, NF-kB and MAPK signaling pathways were finally detected by western blot.Results: Enhancement of IL-6, IL-8 and MCP-1 were observated in OA cartilage tissues, but repression of HULC was discovered in OA cartilage tissues. HULC expression was decreased by TNF-alpha treatment, and overexpressed HULC significantly relieved TNF-alpha-induced ATDC5 cells injury. Additionally, miR-101 was mutual repressed with HULC, and overexpressed miR-101 reversed the protective effect of HULC in TNF-alpha-injured ATDC5 cells. Besides, HULC blocked NF-kB and MAPK pathways via repression of miR-101.Conclusions: The discoveries testified that HULC protected ATDC5 cells against TNF-alpha-induced inflammatory injury by repression of miR-101.	30981080	RID06497	expression association	NA	DOWN(LIHC);DATA(GSE117623)	
Osteoarthritis	HULC	miR-101-3p	negatively-E	bioinformatics;luciferase reporter assay;RNA pull-down assay;RIP	downregulation	RT-qPCR	NA	NA	inflammatory response(-);p38/MAPK signaling pathway(-);NF-kB signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long non-coding RNA highly up-regulated in liver cancer protects tumor necrosis factor-alpha-induced inflammatory injury by down-regulation of microRNA-101 in ATDC5 cells.Methods: Relative expression levels of pro-inflammatory cytokines (IL-6, IL-8 and MCP-1) and HULC in OA cartilage tissues and normal cartilage tissues were determined by RT-qPCR. TNF-alpha induced inflammatory injury model in ATDC5 cells was constructed, and the biological functions of HULC overexpression or suppression in TNF-alpha-injured ATDC5 cells were assessed. The relevancy between miR-101 and HULC was investigated by utilizing bioinformatics prediction, luciferase reporter assay, RNA pull-down and immunoprecipitation. MiR-101 mimic and inhibitor were transfected into ATDC5 cells, and its regulatory effect on TNF-alpha-injured ATDC5 cells was examined. Further, NF-kB and MAPK signaling pathways were finally detected by western blot.Enhancement of IL-6, IL-8 and MCP-1 were observated in OA cartilage tissues, but repression of HULC was discovered in OA cartilage tissues. HULC expression was decreased by TNF-alpha treatment, and overexpressed HULC significantly relieved TNF-alpha-induced ATDC5 cells injury. Additionally, miR-101 was mutual repressed with HULC, and overexpressed miR-101 reversed the protective effect of HULC in TNF-alpha-injured ATDC5 cells. Besides, HULC blocked NF-kB and MAPK pathways via repression of miR-101   Conclusions: The discoveries testified that HULC protected ATDC5 cells against TNF-alpha-induced inflammatory injury by repression of miR-101.Results showed that miR-101 expression level was obviously down-regulated by HULC overexpression compared with its control group (P < 0.05, Fig. 5). But, miR-101 expression level was significantly up-regulated by HULC suppression (P < 0.001, Fig. 5).HULC inhibited the activations of NF-kB and p38MAPK signaling pathways by down-regulation of miR-101.	30981080	RID06498	ceRNA or sponge	NA		
Laryngeal carcinoma	DGCR5	miR-506	negatively-E	RIP;western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	WNT signaling pathway(+);cell stemness(+);radiosensitivity(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000237517	GRCh38_22:18985836-18994501	NA	NA	26220	NA	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	NA	DGCR5 promotes cancer stem cell-like properties of radioresistant laryngeal carcinoma cells by sponging miR-506 via Wnt pathway.Cancer stem cells (CSCs) have been recognized as the significant cause of tumor recurrence. Long noncoding RNAs (lncRNAs) are involved in various cancers, including human laryngeal cancer. So far the correlation between lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) and CSC-like properties in human laryngeal cancer remains barely known. In our current study, two human larynx squamous carcinoma cell lines (Hep-2 and Hep-2R) with different radio sensitivities were cultured. Interestingly, CSC-like phenotypes were much more enriched in Hep-2R cells. We found that DGCR5 was upregulated and microRNA-506 (miR-506) was downregulated in Hep-2R cells. In addition, silence of DGCR5 could inhibit the stemness and enhance the radiosensitivity of Hep-2R cells. Meanwhile, overexpression of miR-506 also suppressed the CSC-like traits and the radiosensitivity was increased significantly. In addition, miR-506 was predicted as target of DGCR5 and the correlation between them was validated in our study. Finally, we observed that Wnt pathway exerted a significant role in human laryngeal CSCs and DGCR5 inhibition could repress Wnt signaling activity by sponging miR-506. In vivo assays were performed and we found that DCGR5 depressed stemness of human laryngeal cancer cells through modulating miR-506 and Wnt signaling pathway. Taken these together, we reported that DGCR5 induced CSC-like properties by sponging miR-506 through activating Wnt in human laryngeal carcinoma cells.Then, to detect whether DGCR5 can interact with miR 506 directly, RIP assay was carried out.	30980388	RID06499	ceRNA or sponge	recurrence		
Hepatocellular carcinoma	EPB41L4A-DT	FOXL1	positively-E	bioinformatics;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(-);tumorigenesis(-);cell metastasis(-)	ceRNA(miR-301a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000278921	GRCh38_5:112419583-112420978	ENSG00000176678	NA	54508	2300	EPB41L4A-AS2|FLJ11235	FKH6|FKHL11|FREAC7	Long noncoding RNA EPB41L4A-AS2 inhibits hepatocellular carcinoma development by sponging miR-301a-5p and targeting FOXL1.Methods: To figure out the specific role of lncRNA EPB41L4A-AS2 in HCC. Fluorescence in situ hybridization (FISH) was first used to determine the cellular sublocalization of EPB41L4A-AS2 to determine its primary mode of action. qRT-PCR western blot and hematoxylin-eosin staining were then used to measure the expression of genes in cells and tissues. Cell proliferation and invasion assays were performed to determine the effects of EPB41L4A-AS2, miR-301a-5p and FOXL1 on the malignant phenotype of tumor cells. With luciferase reporter assay, the direct interaction between target genes were further confirmed for research on molecular mechanism. Finally, the mice hepatocarcinoma model was also established to disclose the tumor suppressor effects of EPB41L4A-AS2 in vivo.Here, we have identified a novel lncRNA EPB41L4A-AS2, which is significantly downregulated both in HCC cells and tissues, and plays a negative regulatory role in HCC proliferation and invasion. Mechanistically, cytoplasmic lncRNA EPB41L4A-AS2 functions as an efficient miR-301a-5p sponge, thereby release the expression inhibition of forkhead box L1 (FOXL1). Indeed, lncRNA EPB41L4A-AS2 inhibits proliferation and migration by upregulating FOXL1 expression and FOXL1 was confirmed as a direct target of miR-301a-5p. MiR-301a-5p shows an inverse correlation with EPB41L4A-AS2 expression and was verified as a direct target of EPB41L4A-AS2 as well. Correspondingly, FOXL1 and miR-301a-5p show opposite biological effects in cell proliferation and migration. Moreover, miR-301a-5p overexpression rescued the EPB41L4A-AS2 upregulation induced depression in proliferation, migration and invasion of HCC cells, as well as promotion effect on FOXL1 expression. Also, in vivo experiments proved that EPB41L4A-AS2 suppress tumor growth and extrahepatic metastasis (lung) via the miR-301a-5p-FOXL1 axis.Conclusions: Taken together, this research revealed a concrete mechanism of lncRNA EPB41L4A-AS2 in HCC, which may serve as a potential biomarkers and novel therapeutic targets for further clinical application.We identified that EPB41L4A-AS2 might sponge with miR-301a-5p via bioinformatics analysis (Fig. 4f ).	30971290	RID06500	ceRNA or sponge	metastasis		UP(PAAD);DATA(GSE40174)
Lung cancer	YAP/TAZ-TEADcomplex	NORAD	negatively-E	ChIP	downregulation	RT-qPCR	TCGA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	protein-RNA	NA	CSC	NA	Cancer	Lung cancer	PCG	lncRNA	NA	NA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	647979	NA	LINC00657	Here, we show that lncRNA NORAD is downregulated in lung and breast cancers, and that NORAD low expression in these cancer types is associated with lymph node metastasis and poor prognosis.   NORAD is transcriptionally repressed by the Hippo pathway transducer YAP/TAZ-TEAD complex in conjunction with the action of NuRD complex. Functionally, NORAD elicits potent inhibitory effects on migration and invasion of multiple lung and breast cancer cell lines, and repression of NORAD expression participates in the migration- and invasion-stimulatory effects of the YAP pathway. Mechanistically, NORAD exploits its multiple repeated sequences to function as a multivalent platform for binding and sequestering S100P, thereby suppressing S100P-elicited pro-metastatic signaling network. Using cell and mouse models, we show that the S100P decoy function of NORAD suppresses lung and breast cancer migration, invasion, and metastasis. Together, our study identifies NORAD as a novel metastasis suppressor, elucidates its regulatory and functional mechanisms, and highlights its prognostic value.NORAD is repressed by YAP/TAZ-TEAD complex.These data support a role of YAP/TAZ-TEAD complex in repressing NORAD transcription.Through chromatin immunoprecipitation (ChIP) analysis with primers covering this region, we confirmed the recruitment of TEAD4 to NORAD promoter (Fig. 2j), consistent with data retrieved from the UCSC Genome Browser.Analysis of TCGA data sets observed inverse correla_x0002_tions of NORAD expression with TEAD3 and TEAD4 expression in breast invasive carcinoma and a weak but significant inverse correlation between NORAD and TEAD4 expression in lung adenocarcinoma (Fig. S3).NORAD expression also inversely correlated with the expression of NuRD complex components MTA1, MTA2, and HDAC2 in breast invasive carcinoma. Our findings support that TEAD binds to the NORAD promoter and recruits YAP/TAZ and NuRD complex to repress NORAD transcription.	30967631	RID06501	interact with protein	metastasis,prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)
Breast cancer	YAP/TAZ-TEADcomplex	NORAD	negatively-E	ChIP	downregulation	RT-qPCR	TCGA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	protein-RNA	NA	CSC	NA	Cancer	Breast cancer	PCG	lncRNA	NA	NA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	647979	NA	LINC00657	Here, we show that lncRNA NORAD is downregulated in lung and breast cancers, and that NORAD low expression in these cancer types is associated with lymph node metastasis and poor prognosis.   NORAD is transcriptionally repressed by the Hippo pathway transducer YAP/TAZ-TEAD complex in conjunction with the action of NuRD complex. Functionally, NORAD elicits potent inhibitory effects on migration and invasion of multiple lung and breast cancer cell lines, and repression of NORAD expression participates in the migration- and invasion-stimulatory effects of the YAP pathway. Mechanistically, NORAD exploits its multiple repeated sequences to function as a multivalent platform for binding and sequestering S100P, thereby suppressing S100P-elicited pro-metastatic signaling network. Using cell and mouse models, we show that the S100P decoy function of NORAD suppresses lung and breast cancer migration, invasion, and metastasis. Together, our study identifies NORAD as a novel metastasis suppressor, elucidates its regulatory and functional mechanisms, and highlights its prognostic value.NORAD is repressed by YAP/TAZ-TEAD complex.These data support a role of YAP/TAZ-TEAD complex in repressing NORAD transcription.Through chromatin immunoprecipitation (ChIP) analysis with primers covering this region, we confirmed the recruitment of TEAD4 to NORAD promoter (Fig. 2j), consistent with data retrieved from the UCSC Genome Browser.Analysis of TCGA data sets observed inverse correla_x0002_tions of NORAD expression with TEAD3 and TEAD4 expression in breast invasive carcinoma and a weak but significant inverse correlation between NORAD and TEAD4 expression in lung adenocarcinoma (Fig. S3).NORAD expression also inversely correlated with the expression of NuRD complex components MTA1, MTA2, and HDAC2 in breast invasive carcinoma. Our findings support that TEAD binds to the NORAD promoter and recruits YAP/TAZ and NuRD complex to repress NORAD transcription.	30967631	RID06502	interact with protein	metastasis,prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)
Lung cancer	NORAD	S100P	negatively-E	RNA pull-down assay;RIP	downregulation	RT-qPCR	TCGA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000163993	NA	647979	6286	LINC00657	NA	NORAD is transcriptionally repressed by the Hippo pathway transducer YAP/TAZ-TEAD complex in conjunction with the action of NuRD complex. Functionally, NORAD elicits potent inhibitory effects on migration and invasion of multiple lung and breast cancer cell lines, and repression of NORAD expression participates in the migration- and invasion-stimulatory effects of the YAP pathway. Mechanistically, NORAD exploits its multiple repeated sequences to function as a multivalent platform for binding and sequestering S100P, thereby suppressing S100P-elicited pro-metastatic signaling network. Using cell and mouse models, we show that the S100P decoy function of NORAD suppresses lung and breast cancer migration, invasion, and metastasis. Together, our study identifies NORAD as a novel metastasis suppressor, elucidates its regulatory and functional mechanisms, and highlights its prognostic value.NORAD binds S100P through its multiple repeated units.This finding indicates that a single repeat of NORAD can directly bind S100P.Importantly, addition of EGTA to the pull-down reaction abrogated the interaction between NORAD and S100P, whereas supplement of calcium increased binding (Fig. 4e). Finally, the interaction between endogenous NORAD and endogenous S100P was detected in H460 and ZR75 cells using RNA immunoprecipitation (RIP) (Fig. 4f, g). Our data indicate that NORAD serves as a multivalent binding platform for the active form of S100P.	30967631	RID06503	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC);UP(PAAD);DATA(GSE117623,GSE40174)
Breast cancer	NORAD	S100P	negatively-E	RNA pull-down assay;RIP	downregulation	RT-qPCR	TCGA	NA	cell migration(-);cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000163993	NA	647979	6286	LINC00657	NA	NORAD is transcriptionally repressed by the Hippo pathway transducer YAP/TAZ-TEAD complex in conjunction with the action of NuRD complex. Functionally, NORAD elicits potent inhibitory effects on migration and invasion of multiple lung and breast cancer cell lines, and repression of NORAD expression participates in the migration- and invasion-stimulatory effects of the YAP pathway. Mechanistically, NORAD exploits its multiple repeated sequences to function as a multivalent platform for binding and sequestering S100P, thereby suppressing S100P-elicited pro-metastatic signaling network. Using cell and mouse models, we show that the S100P decoy function of NORAD suppresses lung and breast cancer migration, invasion, and metastasis. Together, our study identifies NORAD as a novel metastasis suppressor, elucidates its regulatory and functional mechanisms, and highlights its prognostic value.NORAD binds S100P through its multiple repeated units.This finding indicates that a single repeat of NORAD can directly bind S100P.Importantly, addition of EGTA to the pull-down reaction abrogated the interaction between NORAD and S100P, whereas supplement of calcium increased binding (Fig. 4e). Finally, the interaction between endogenous NORAD and endogenous S100P was detected in H460 and ZR75 cells using RNA immunoprecipitation (RIP) (Fig. 4f, g). Our data indicate that NORAD serves as a multivalent binding platform for the active form of S100P.	30967631	RID06504	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC);UP(PAAD);DATA(GSE117623,GSE40174)
Osteosarcoma	HIF2PUT	HIF-2alpha	positively-E	western blot	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA HIF2PUT inhibited osteosarcoma stem cells proliferation, migration and invasion by regulating HIF2 expression.Purpose: The function of lncRNAs in cancer stem cells (CSCs) remains to be elucidated. The present study aimed to investigate the regulating role of a novel lncRNA, hypoxia-inducible factor-2alpha (HIF-2alpha) promoter upstream transcript (HIF2PUT), in osteosarcoma stem cells.The expression of lncRNA HIF2PUT and HIF-2alpha in osteosarcoma stem cell lines and tissues was monitored by real-time PCR and western blot. The proliferation ability was examined by MTT assay when HIF2PUT overexpression or knockdown. The self-renewing capabilities of the cells were assessed by spheroid formation assay. The migration and invasion of cells were monitored by wound-healing assay and transwell cell assay, respectively. The correlation of HIF2PUT and HIF-2alpha expression was determined in osteosarcoma cancer tissues.Results: LncRNA HIF2PUT and HIF-2alpha were downregulated in osteosarcoma cell lines. HIF2PUT exhibited a significant decline in proliferation capacity. Wound healing and transwell assays showed that lncRNA overexpression inhibited osteosarcoma stem cell migration and invasion. HIF2PUT inhibited sphere formation in osteosarcoma stem cells. Increased HIF2PUT expression inhibited the enrichment of CD133 in osteosarcoma stem cells. There was a strong positive correlation between relative HIF2PUT level and relative HIF-2alpha level in the 30 paired osteosarcoma cancer tissues.Conclusions: Overexpression of lncRNA HIF2PUT significantly attenuated the proliferation, migration and invasion of osteosarcoma stem cells. Furthermore, we demonstrated that lncRNA overexpression inhibited the sphere-formation of osteosarcoma stem cells by downregulating HIF-2alpha. These findings suggest that lncRNA HIF2PUT may act as a tumour suppressor in osteosarcoma. LncRNA HIF2PUT/HIF-2alpha may be a novel therapeutic target in the treatment of osteosarcoma.	30966832	RID06505	expression association	NA		
Clear cell renal cell carcinoma	URRCC	EGFL7	positively-E	ChIP;western blot;luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE46699;GSE53757	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000172889	NA	NA	51162	NA	ZNEU1	A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma.Methods: Candidate lncRNAs were selected using microarray analysis and quantitative real-time PCR (qRT-PCR was performed to detect lncRNAs expression in human ccRCC tissues. Overexpression and knocking down experiments in vivo and in vitro were performed to uncover the biological roles of lncRNA-URRCC on ccRCC cell proliferation and invasion. microarray, chromatin immunoprecipitation, Luciferase reporter assay and western blot were constructed to investigate the molecular mechanisms underlying the functions of lncRNA-URRCC.The microarray analysis and qRT-PCRidentified a new lncRNA, URRCC, whose expression is upregulated in RCC samples and associated with poor prognosis, leading to promote ccRCC cell proliferation and invasion. Mechanistically, URRCC enhances the expression of EGFL7 via mediating histone H3 acetylation of EGFL7 promoter, activation of P-AKT signaling, and suppressing P-AKT downstream gene, FOXO3. In return, FOXO3 could inhibit the transcription of URRCC via binding to the special region on the promoter of URRCC.Conclusions: Our data suggests that targeting this newly identified feed-back loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling may enhance the efficacy of existing therapy and potentially imparts a new avenue to develop more potent therapeutic approaches to suppress RCC progression.Taken together, all results above illustrated that URRCC enhanced EGFL7 expression by mediating histone H3 acetylation across EGFL7 promoter region.Moreover, ChIP assay showed that TSA could reverse the down-regulation of EGFL7 caused by sh-URRCC both on acetylation and expression of EGFL7.	30953521	RID06506	epigenetic regulation	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Clear cell renal cell carcinoma	FOXO3	URRCC	negatively-E	bioinformatics;luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE46699;GSE53757	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	TF	lncRNA	ENSG00000118689	NA	NA	NA	2309	NA	AF6q21|FKHRL1|FOXO2|FOXO3A	NA	A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma.Methods: Candidate lncRNAs were selected using microarray analysis and quantitative real-time PCR (qRT-PCR was performed to detect lncRNAs expression in human ccRCC tissues. Overexpression and knocking down experiments in vivo and in vitro were performed to uncover the biological roles of lncRNA-URRCC on ccRCC cell proliferation and invasion. microarray, chromatin immunoprecipitation, Luciferase reporter assay and western blot were constructed to investigate the molecular mechanisms underlying the functions of lncRNA-URRCC.The microarray analysis and qRT-PCRidentified a new lncRNA, URRCC, whose expression is upregulated in RCC samples and associated with poor prognosis, leading to promote ccRCC cell proliferation and invasion. Mechanistically, URRCC enhances the expression of EGFL7 via mediating histone H3 acetylation of EGFL7 promoter, activation of P-AKT signaling, and suppressing P-AKT downstream gene, FOXO3. In return, FOXO3 could inhibit the transcription of URRCC via binding to the special region on the promoter of URRCC.Conclusions: Our data suggests that targeting this newly identified feed-back loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling may enhance the efficacy of existing therapy and potentially imparts a new avenue to develop more potent therapeutic approaches to suppress RCC progression.Taken together, all results above illustrated that URRCC enhanced EGFL7 expression by mediating histone H3 acetylation across EGFL7 promoter region.Moreover, ChIP assay showed that TSA could reverse the down-regulation of EGFL7 caused by sh-URRCC both on acetylation and expression of EGFL7.Overall, these data suggested that FOXO3 silenced URRCC transcription by binding to its specific promoter in ccRCC.	30953521	RID06507	interact with protein	metastasis,prognosis	UP(BRCA);DATA(GSE51827,GSE86978)	
Renal cell carcinoma	SANT1	SLC47A2	positively-E	ChIP;western blot	downregulation	qPCR	NA	NA	prognosis	epigenetic regulation	regulation	RNA-protein	NA	CSC	NA	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000180638	NA	NA	146802	NA	FLJ31196|MATE2|MATE2-K	A novel human lncRNA SANT1 cis-regulates the expression of SLC47A2 by altering SFPQ/E2F1/HDAC1 binding to the promoter region in renal cell carcinoma.SLC47A2 encodes MATE 2-K in the kidney, which mediates the secretion of certain endogenous and exogenous compounds. SLC47A2 was dramatically repressed in patients with renal cell carcinoma (RCC), and a lower level of SLC47A2 might act as a negative prognostic marker, although the mechanism is not well understood. In this study, we aimed to investigate the mechanism via which SLC47A2 is downregulated in RCC. Based on the annotation information of the SLC47A2 locus available in the UCSC genome browser database, we identified a novel lncRNA, which is transcribed from the SLC47A2 locus and named it SANT1. Overexpression and knock-down assays were performed to investigate the effects of SANT1 on cis-regulation of SLC47A2. We verified the direct binding between SANT1 and SFPQ/E2F1/HDAC1 using the cross-linking and immunoprecipitation (CLIP) assay. Chromatin immunoprecipitation was performed to confirm the molecular mechanism via which SANT1 activates the transcription of the SLC47A2 coding region. We observed that SANT1 can cis-regulate its own genetic locus. In tumour-adjacent tissues, the SLC47A2 locus highly expresses SANT1, which can remove the regulatory SFPQ/E2F1/HDAC1 suppressor complex from the promoter region, thereby significantly increasing the levels of the H3K27ac modification and RNAPII binding. Owing to a low SANT1 level, the binding of this inhibitory complex in the promoter region is upregulated in RCC, which results in silencing of the SLC47A2 coding region. In conclusion, we identified a novel lncRNA and elucidated the mechanism via which it regulates SLC47A2 expression in RCC.SANT1 expression from site E of eight RCC tissues (RC) and paired adjacent tissues (RN) was detected using qPCR. Similar to the SLC47A2 mRNA level, SANT1 was downregulated in RCC (Fig. 1G).	30951404	RID06508	epigenetic regulation	prognosis		UP(LIHC);DATA(GSE117623)
Gastric cancer	ADPGK-AS1	KDM1B	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cancer progression(+)	ceRNA(miR-3196)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260898	GRCh38_15:72782835-72798199	ENSG00000165097	NA	100287559	221656	NA	AOF1|bA204B7.3|C6orf193|dJ298J15.2|FLJ33898|FLJ34109|FLJ43328|LSD2	Upregulation of the long noncoding RNA ADPGK-AS1 promotes carcinogenesis and predicts poor prognosis in gastric cancer.Background: Numerous previous studies have revealed that many long non-coding RNAs (lncRNAs) are upregulated in gastric cancer (GC) and are associated with tumor onset and progression in GC. ADPGK-AS1, a novel lncRNA, has been discovered as an oncogenic lncRNA in pancreatic cancer while its function in GC remains unclear.Materials and methods: The expression of ADPGK-AS1 and miR-3196 was determined by RT-qPCR. The expression of KDM1B was assessed by RT-qPCR and WB. The association between ADPGK-AS1 and overall survival of GC patients was explored using Kaplan-Meier curves. The function of ADPGK-AS1 in GC was examined through CCK-8, EdU, transwell as well as flow cytometry analysis. The interaction of miR-3196 and ADPGK-AS1 or KDM1B was confirmed by RIP, RNA pull down and luciferase reporter assay.Materials and Methods RESULTS: ADPGK-AS1 was increased in GC tissues and cell lines. GC patients with an increased expression of ADPGK-AS1 had a poor prognosis compared to those with a reduced expression. ADPGK-AS1 knockdown led to inhibition of GC cell proliferation and migration. The suppressive effect of ADPGK-AS1 silence on GC progression was abolished by KDM1B upregulation.Results CONCLUSIONS: We unveiled that ADPGK-AS1 could promote GC progression via sponging miR-3196 and therefore upregulating KDM1B, providing a novel prognostic biomarker and therapeutic target for GC patients.Keywords: ADPGK-AS1; Gastric cancer; KDM1B; miR-3196.	30944080	RID06509	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Prostate cancer	UCA1	CXCR4	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-);cancer progression(+)	ceRNA(miR-204)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000121966	NA	652995	7852	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	LncRNA UCA1 acts as a sponge of miR-204 to up-regulate CXCR4 expression and promote prostate cancer progression.Prostate cancer (PCa) is a devastating malignant disease with a poor prognosis. The aim of current study is to investigate the role of lncRNA-urothelial carcinoma associated 1 (UCA1) in the progression of PCa. We evaluated the expression levels of UCA1 in a total of 16 benign prostatic hyperplasia tissues (BPH) and 40 PCa tissues, as well as PCa cells. The functional regulatory effects of UCA1 were investigated using a series of cell function approaches. Our data showed that UCA1 is frequently overexpressed in PCa tissues compared with BPH tissues (P<0.01). Moreover, the higher expression of UCA1 was observed in patients with Gleason score <<- (P<0.05). In consistent, we found the expression levels of UCA1 was higher in the PCa cell lines PC-3, LnCaP, and DU-145 than in the normal prostate epithelial cell line RWPE-1 (P<0.01). Functionally, we found knockdown of UCA1 in PC-3 significantly suppressed cell growth and invasion of PC-3, while overexpression of UCA1 in DU-145 cells promote cell growth and invasion. Mechanistically, UCA1 overexpression permitted activation of CXCR4 oncogenes through inhibition of miR-204 activity, as evidenced by the positive association of these two genes with UCA1 levels and inverse correlation with miR-204 expression in PCa tissues. Luciferase activity assay further confirmed the targetting relationship between UCA1 and miR-204, CXCR4, and miR-204. The up-regulation of UCA1 in PC-3 cells significantly impaired the inhibitory effect of miR-204 on CXCR4 expression. Taken together, our research revealed that UCA1 works as an oncogene by targetting miR-204. The UCA1-miR-204-CXCR4 regulatory network regulated the growth and metastasis of PCa, providing new insight in the management of patients with such malignancy.UCA1 promotes proliferation and invasion of PCa cells.Therefore, to further confirm the physical interaction between UCA and miR-204, we performed RNA immunoprecipitation (RIP) assay. As shown in Figure 3E, both miR-204 and UCA1 are able to bind to Ago2 protein in PCa cells.	30940776	RID06510	ceRNA or sponge	metastasis,prognosis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Thyroid cancer	TNRC6C-AS1	STK4	negatively-E	luciferase reporter assay	upregulation	microarray;RT-qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000204282	NA	ENSG00000101109	NA	11322	6789	EVER1|EVIN1|LAK-4P|TNRC6C-AS1	KRS2|MST1|YSK3	Suppression of long non-coding RNA TNRC6C-AS1 protects against thyroid carcinoma through DNA demethylation of STK4 via the Hippo signalling pathway.Objectives: Thyroid carcinoma (TC) represents a malignant neoplasm affecting the thyroid. Current treatment strategies include the removal of part of the thyroid; however, this approach is associated with a significant risk of developing hypothyroidism. In order to adequately understand the expression profiles of TNRC6C-AS1 and STK4 and their potential functions in TC, an investigation into their involvement with Hippo signalling pathway and the mechanism by which they influence TC apoptosis and autophagy were conducted.Methods: A microarray analysis was performed to screen differentially expressed lncRNAs associated with TC. TC cells were employed to evaluate the role of TNRC6C-AS1 by over-expression or silencing means. The interaction of TNRC6C-AS1 with methylation of STK4 promoter was evaluated to elucidate its ability to elicit autophagy, proliferation and apoptosis.Results: TNRC6C-AS1 was up-regulated while STK4 was down-regulated, where methylation level was elevated. STK4 was verified as a target gene of TNRC6C-AS1, which was enriched by methyltransferase. Methyltransferase's binding to STK4 increased expression of its promoter. Over-expressed TNRC6C-AS1 inhibited STK4 by promoting STK4 methylation and reducing the total protein levels of MST1 and LATS1/2. The phosphorylation of YAP1 phosphorylation was decreased, which resulted in the promotion of SW579 cell proliferation and tumorigenicity.Conclusion: Based on our observations, we subsequently confirmed the anti-proliferative, pro-apoptotic and pro-autophagy capabilities of TNRC6C-AS1 through STK4 methylation via the Hippo signalling pathway in TC.RT-qPCR and western blotmethods were performed in order to determine the expression levels of lncRNA TNRC6C AS1 and STK4 in TC and adjacent normal tissues.	30938030	RID06511	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE86978)
Adrenocortical cancer	UCA1	CDK6	positively-E	luciferase reporter assay;miRDB	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(+)	ceRNA(miR-298)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Adrenal gland cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000105810	NA	652995	1021	CUDR|LINC00178|onco-lncRNA-36|UCAT1	PLSTIRE	Long non-coding RNA UCA1 promoted the growth of adrenocortical cancer cells via modulating the miR-298-CDK6 axis.Adrenocortical cancer (ACC) is an aggressive malignancy with no available effective treatments; therefore, exploring the molecular mechanisms involved in the initiation and progression of ACC is quite important. Here, we found that the long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was highly expressed in ACC tissues and closely associated with the TNM stage and metastasis of ACC patients. Overexpression of UCA1 significantly promoted the proliferation and suppressed the apoptosis of ACC cells. Mechanism study showed that UCA1 acted as sponge of miR-298 and decreased the expression abundance of miR-298 in ACC cells. Further investigation identified that miR-298 bound the 3'-UTR of the cyclin-dependent kinase 6 (CDK6) and inhibited the expression of CDK6. Consistently, ectopic expressed UCA1 suppressed miR-298 and up-regulated the expression of CDK6, which promoted the cell cycle progression of ACC cells. Taken together, our results identified the potential oncogenic function of UCA1 in ACC by regulating the miR-298-CDK6 axis.The results suggested that miR-298 was a can_x0002_didate-binding partner of UCA1. The predicted binding sites of miR-298 in UCA1 were shown in Fig. 3A.	30935924	RID06512	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	EGR1	FOXD2-AS1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+);apoptosis process(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000120738	NA	ENSG00000237424	GRCh38_1:47432133-47434641	1958	84793	225|AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268	MGC12982	Long non-coding RNAs (lncRNAs) are regarded as a group of biomarkers in the initiation and development of various cancers, including hepatocellular carcinoma (HCC). LncRNA FOXD2-AS1 has been studied in human colorectal cancer and glioma as an oncogene. However, the function and mechanism of lncRNA FOXD2-AS1 in hepatocellular carcinoma are marked. In this study, we found that high expression of FOXD2-AS1 predicted poor prognosis of HCC patients in the TCGA database. The dysregulation of FOXD2-AS1 was determined in HCC tissues and cell lines by qRT-PCR Functionally, silenced FOXD2-AS1 efficiently suppressed HCC progression by regulating cell proliferation, apoptosis, migration and epithelial-mesenchymal transition (EMT). Mechanistically, FOXD2-AS1 was found to be activated by the transcription factor EGR1. Furthermore, FOXD2-AS1 could activate the Wnt/beta-catenin signaling pathway. The mechanism contributed to the interaction between FOXD2-AS1 and Wnt/beta-catenin signaling pathway was analyzed. It was uncovered that FOXD2-AS1 enhanced the activity of Wnt/beta-catenin signaling pathway by epigenetically silencing the inhibitor of Wnt/beta-catenin signaling pathway (DKK1). Rescue assays demonstrated that DKK1 and Wnt/beta-catenin signaling pathway involved in FOXD2-AS1-mediated HCC progression. In conclusion, our study demonstrated that EGR1-induced upregulation of lncRNA FOXD2-AS1 promotes the progression of hepatocellular carcinoma via epigenetically silencing DKK1 and activating Wnt/beta-catenin signaling pathway.The binding motif of EGR1 obtained from JASPAR was illustrated (Figure 4C). We chose the top two binding sites between EGR1 and FOXD2-AS1 promoter to do further study. These two binding sequenced were defined as part 1 (P1) and part 2 (P2) of FOXD2-AS1 promoter. ChIP assay revealed the strong affinity of EGR1 in the P2 of FOXD2-AS1 promoter (Figure 4D). Luciferase reporter assay demonstrated the binding of EGR1 in part 2 of FOXD2- AS1 promoter (Figure 4E F). Furthermore, we found that EGR1 was highly expressed in HCC tissues (Figure 4G), which is consistent with the expression of FOXD2-AS1 (Figure 4H). All these experimental results suggested that EGR1 is the transcription activator of FOXD2-AS1 in HCC.	30929558	RID06513	transcriptional regulation	prognosis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)
Hepatocellular carcinoma	FOXD2-AS1	DKK1	negatively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+);apoptosis process(-)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000107984	NA	84793	22943	MGC12982	DKK-1|SK	According to the above data, FOXD2-AS1 negatively modulated the expression of DKK1.Long non-coding RNAs (lncRNAs) are regarded as a group of biomarkers in the initiation and development of various cancers, including hepatocellular carcinoma (HCC). LncRNA FOXD2-AS1 has been studied in human colorectal cancer and glioma as an oncogene. However, the function and mechanism of lncRNA FOXD2-AS1 in hepatocellular carcinoma are marked. In this study, we found that high expression of FOXD2-AS1 predicted poor prognosis of HCC patients in the TCGA database. The dysregulation of FOXD2-AS1 was determined in HCC tissues and cell lines by qRT-PCR Functionally, silenced FOXD2-AS1 efficiently suppressed HCC progression by regulating cell proliferation, apoptosis, migration and epithelial-mesenchymal transition (EMT). Mechanistically, FOXD2-AS1 was found to be activated by the transcription factor EGR1. Furthermore, FOXD2-AS1 could activate the Wnt/beta-catenin signaling pathway. The mechanism contributed to the interaction between FOXD2-AS1 and Wnt/beta-catenin signaling pathway was analyzed. It was uncovered that FOXD2-AS1 enhanced the activity of Wnt/beta-catenin signaling pathway by epigenetically silencing the inhibitor of Wnt/beta-catenin signaling pathway (DKK1). Rescue assays demonstrated that DKK1 and Wnt/beta-catenin signaling pathway involved in FOXD2-AS1-mediated HCC progression. In conclusion, our study demonstrated that EGR1-induced upregulation of lncRNA FOXD2-AS1 promotes the progression of hepatocellular carcinoma via epigenetically silencing DKK1 and activating Wnt/beta-catenin signaling pathway.Moreover, EZH2 can repress the expression of DKK1. Here, we hypothesized that FOXD2-AS1 activated Wnt/beta-catenin signaling pathway by epigenetically silencing DKK1. The results of the RIP assay showed that FOXD2-AS1 could bind with EZH2 in HCC cells (Figure 6A). Moreover, we found that knockdown of FOXD2- AS1 led to the increased mRNA level of DKK1 (Figure 6B), further indicating the negative regulatory effect of FOXD2- AS1 on DKK1. Then, we found that knockdown of EZH2 (Figure 6C) led to the increased mRNA and protein levels of DKK1 (Figure 6D E). Finally, ChIP assay revealed that EZH2 could directly bind to the DKK1 promoter and reconcile H3K4me2 demethylation. Nevertheless, FOXD2-AS1 knockdown partially attenuated the above phenomenon (Figure 6F). Therefore, we confirmed that FOXD2-AS1 activated Wnt/beta- catenin signaling pathway by epigenetically silencing DKK1.	30929558	RID06514	epigenetic regulation	prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC);DATA(GSE117623)
Hemangioma	NEAT1	VEGFA	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay;bioinformatics	upregulation	RT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-361-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112715	NA	283131	7422	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	VEGF|VEGF-A|VPF	Long non-coding RNA NEAT1 promotes the progression of hemangioma via the miR-361-5p/VEGFA pathway.Hemangioma (HA) is the most common benign vascular neoplasm of infancy that is resulted from abnormal proliferation of endothelial cells. Recent studies demonstrated that long non-coding RNAs (lncRNAs) were closely related to the pathogenesis of HA. LncRNA Nuclear enriched abundant transcript 1 (NEAT1) was involved in multiple tumor formation and biological behaviors of endothelial cells. However, the role and molecular mechanism of NEAT1 in HA are still unknown. The expression levels of NEAT1 and miR-361-5p were detected in proliferating phase HAs, involuting phase HAs, and normal skin tissues. The role and mechanism of NEAT1 on the proliferation, migration and apoptosis of hemangioma endothelial cells (HemECs) were analyzed by Cell Counting Kit (CCK)-8, transwell, flow cytometry, caspase-3 activity, dual-luciferase assay, RNA immunoprecipitation, Biotin-labeled miR-361-5p pull-down assay and western blot by gain- and loss-of-functions. We found that compared with normal skin tissues, NEAT1 expression was elevated, whereas miR-361-5p decreased in HA tissues especially in proliferating phase HAs. Downregulation of NEAT1 significantly suppressed the viability, PCNA expression and migration, but increased apoptotic cell numbers and caspase-3 activity of HemECs. NEAT1 functioned as a competing endogenous RNA to regulate VEGFA expression via sponging miR-361-5p. Taken together, these findings indicate that NEAT1 promotes the proliferation and migration, whereas inhibits the apoptosis of HemECs via regulating miR-361-5p/VEGFA axis.	30928097	RID06515	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Breast cancer	GATD3	SOX2	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000160221	GRCh38_21:44133610-44210114	ENSG00000181449	NA	8209	6657	C21orf33|D21S2048E|ES1|GATD3A|GT335|HES1|KNP-I|KNP-Ia|KNPH|KNPI	NA	Long non-coding RNA ES1 controls the proliferation of breast cancer cells by regulating the Oct4/Sox2/miR-302 axis.ES1 is a long non-coding RNA (lncRNA) that regulates pluripotency of human embryonic stem cells, which is known to be a downstream target of stemness factors Oct4 and Nanog, and serves as a modular scaffold for Sox2. However, the role of ES1 in cancer biology is not fully characterized. The results of our study show that ES1 transcript is upregulated in both high-grade and P53-mutated breast tumor tissues. Knockdown experiments show that ES1 suppression in breast cancer cells restricts cancer cell proliferation and cell cycle progression. Moreover, ES1 inhibition can also induce apoptosis and cellular senescence. Additionally, our data reveal that ES1 transcript promotes cell migration as well as the epithelial to mesenchymal transition of breast cancer cells. Furthermore, loss of ES1 expression downregulates the expression of Oct4/Sox2 and consequently leads to downregulation of their targets, miR-302 and miR-106b. Altogether, for the first time, our findings reveal that ES1 controls the proliferation and death of breast cancer cells by regulating the Oct4/Sox2/miR-302/miR-106b axis.Our findings showed that the expression of Oct4/Sox2 stemness factors was downregulated when ES1 was inhibited (Fig. 7A,B). We also investigated the expression of miR-302, miR-106b and let-7, which are the targets of Sox2/Oct4.In summary, our data showed that ES1 by interacting with Sox2 in a feedback loop regulates its own expression and the expression of Sox2 and Oct4.Additionally, Oct4 has binding sites in the vicinity of lncRNA ES1 and regulates its expression in hESCs.	30927330	RID06516	interact with protein	NA		UP(LIHC);DATA(GSE117623)
Breast cancer	GATD3	POU5F1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000160221	GRCh38_21:44133610-44210114	ENSG00000233911	NA	8209	5460	C21orf33|ES1|GATD3A|GT335|HES1|KNPH|KNPI	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4|Oct3/4	Long non-coding RNA ES1 controls the proliferation of breast cancer cells by regulating the Oct4/Sox2/miR-302 axis.ES1 is a long non-coding RNA (lncRNA) that regulates pluripotency of human embryonic stem cells, which is known to be a downstream target of stemness factors Oct4 and Nanog, and serves as a modular scaffold for Sox2. However, the role of ES1 in cancer biology is not fully characterized. The results of our study show that ES1 transcript is upregulated in both high-grade and P53-mutated breast tumor tissues. Knockdown experiments show that ES1 suppression in breast cancer cells restricts cancer cell proliferation and cell cycle progression. Moreover, ES1 inhibition can also induce apoptosis and cellular senescence. Additionally, our data reveal that ES1 transcript promotes cell migration as well as the epithelial to mesenchymal transition of breast cancer cells. Furthermore, loss of ES1 expression downregulates the expression of Oct4/Sox2 and consequently leads to downregulation of their targets, miR-302 and miR-106b. Altogether, for the first time, our findings reveal that ES1 controls the proliferation and death of breast cancer cells by regulating the Oct4/Sox2/miR-302/miR-106b axis.	30927330	RID06517	interact with protein	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	GAS5	PTEN	positively-E	western blot;luciferase reporter assay;RIP	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell growth(-);cell invasion(-)	ceRNA(miR-205)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	Upregulation of Long Noncoding RNA GAS5 Inhibits Lung Cancer Cell Proliferation and Metastasis via miR-205/PTEN Axis.BACKGROUND Long noncoding RNA (lncRNA) is a key part of noncoding RNA class and increasing evidences have manifested that it plays a significant role in the physiology and pathology. The growth arrest-specific transcript 5 (GAS5) is a vital tumor suppressor in some types of cancers. However, the function of GAS5 in lung cancer remains largely no clear. The purpose of the current study was to identify the biological role of GAS5 in non-small cell lung cancer (NSCLC). MATERIAL AND METHODS To study the role of GAS5 in the NSCLC, the RT-PCR western blot, Luciferase assay, and RNA immunoprecipitation assay was employed to determine the relationship of GAS5, miR-205, and PTEN. CCK8 assay, Cell migration and invasion assay was used for the role of GAS5 in lung cancer cell proliferation and metastasis. RESULTS The results indicated that GAS5 was drastically downregulated in lung cancer cell lines. Further functional analysis showed that down-expression of GAS5 remarkably induced NSCLC growth, migration, and invasion. The luciferase reporter assays determined that miR-205 was a direct target of GAS5 in lung cancer. Moreover, the Phosphatase and tensin homologue (PTEN) was known as a direct target of miR-205 and miR-205/PTEN rescued the effects of GAS5 in NSCLC cells. CONCLUSIONS To sum up, our results illustrate that upregulation of GAS5 in NSCLC suppresses its growth, migration, and invasion via the miR-205/PTEN axis.	30926767	RID06518	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Urinary bladder cancer	TUG1	CCND2	positively-E	luciferase reporter assay;western blot;StarBase	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-194-5p)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000118971	NA	55000	894	FLJ20618|LINC00080|NCRNA00080	NA	lncRNA TUG1 Promotes Cisplatin Resistance by Regulating CCND2 via Epigenetically Silencing miR-194-5p in Bladder Cancer.Taurine-upregulated gene 1 (TUG1) has been involved in tumorigenesis of several human cancers, but its precise biological role in bladder cancer remains largely elusive. In this study, we found that TUG1 was upregulated in bladder cancer and the expression of TUG1 was positively and negatively correlated with CCND2 and miR-194-5p, respectively. MiR-194-5p expression was frequently decreased through promoter hypermethylation, while it was epigenetically increased following cisplatin and 5-aza-2'-deoxycytidine (5-Aza-DC) treatment. Furthermore, knockdown of TUG1 attenuated the expression of epigenetic regulator Enhancer of zeste homolog 2 (EZH2), and it alleviated the promoter hypermethylation of miR-194-5p and induced its expression. Increased miR-194-5p expression or decreased TUG1 expression significantly sensitized bladder cancer cells to cisplatin, inhibited the proliferation, and induced apoptosis. Besides, CCND2 was a direct target of miR-194-5p, while miR-194-5p was regulated by TUG1. CCND2 could partially restore the tumor-suppressive effects on cell proliferation and cisplatin resistance following TUG1 silencing. Additionally, TUG1 expression was correlated with clinical stage, lymphatic metastasis, and patient prognosis. In conclusion, TUG1 promotes bladder cancer cell growth and chemoresistance by regulating CCND2 via EZH2-associated silencing of miR-194-5p. Our study may be conducive to elucidating the molecular mechanism of and providing novel therapeutic target and biomarker for bladder cancer.Besides, we detected the expression of TUG1 in bladder cancer cell lines (5637, HT1376, J82, and T24) and a noncancerous human uroepithelial cell SV-HUC-1 by qPCR. We found that all four of the bladder cancer cell lines exhibited a significantly higher expression of TUG1 over SV-HUC-1, and the strongest overexpression of TUG1 was detected in bladder cancer cells T24 and 5637 (Figure 1D).	30925453	RID06519	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Pancreatic cancer	MSC-AS1	CDK14	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-29b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000235531	GRCh38_8:71828167-72118393	ENSG00000058091	NA	100132891	5218	NA	PFTAIRE1|PFTK1	The role of lncRNA MSC-AS1/miR-29b-3p axis-mediated CDK14 modulation in pancreatic cancer proliferation and Gemcitabine-induced apoptosis.Pancreatic ductal adenocarcinoma (PDAC) remains a leading cause of cancer-related death due to the failure of traditional therapies. In the present study, we attempted to construct a lncRNA-miRNA-mRNA network which may modulate PDAC cell proliferation and Gemcitabine-induced cell apoptosis starting from CDK14, a new member of the CDK family and an oncogene in many cancers. Based on TCGA data, a significant positive correlation was observed between lncRNA MSC-AS1 and CDK14. Moreover, MSC-AS1 expression was upregulated in PDAC tissues. Higher MSC-AS1 expression was correlated with poorer prognosis in patients with PDAC. MSC-AS1 knockdown in Panc-1 and BxPC-3 cells significantly inhibited the cell proliferation. Moreover, miR-29b-3p, which has been reported to act as a tumor suppressor, was predicted to bind to both MSC-AS1 and CDK14. Contrary to MSC-AS1, higher miR-29b-3p expression was correlated to better prognosis in patients with PDAC. In both PDAC cell lines, miR-29b-3p negatively regulated MSC-AS1 and CDK14. As confirmed using luciferase reporter gene and RIP assays, MSC-AS1 served as a ceRNA for miR-29b-3p to counteract miR-29b-mediated CDK14 repression. MSC-AS1 knockdown inhibited CDK14 protein levels and PDAC proliferation and enhanced gemcitabine-induced cell death and apoptosis while miR-29b-3p inhibition exerted an opposing effect; the effect of MSC-AS1 knockdown was partially attenuated by miR-29b-3p inhibition. Taken together, we demonstrated that MSC-AS1/miR-29b-3p axis modulates the cell proliferation and GEM-induced cell apoptosis in PDAC cell lines through CDK14. We provided a novel experimental basis for PDAC treatment from the perspective of lncRNA-miRNA-mRNA network.As online tools predicted, miR-29b-3p can target both MSCAS1 and CDK14; next, as confirmed by real-time PCR, once miR-29b-3p mimics or inhibitor transfected, miR-29b-3p was expressed in Panc-1 cell and BxPC-3 cell (Figure 4(a)), taken that we could verify the predicted interaction and regulation.	30915884	RID06520	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Malignant glioma	LOC730100	FOXA1	positively-E	luciferase reporter assay;bioinformatics;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-760)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000231918	GRCh38_2:51032601-52407917	ENSG00000129514	NA	730100	3169	NA	HNF3A	Then, we validated its high expression in 53 glioma tissues by qRT-PCRLong non-coding RNA LOC730100 enhances proliferation and invasion of glioma cells through competitively sponging miR-760 from FOXA1 mRNA.Glioma is the most malignant cancer in central nervous system. And researchers have indicated that long noncoding RNAs (lncRNAs) are closely related with glioma progression. Nevertheless, LOC730100 function in glioma is ill studied. In the current research, we showed that LOC730100 expression was increased in glioma tissues and cell lines. Furthermore, LOC730100 upregulation is linked to a poor prognosis in glioma patients. Loss-of-function assays showed that LOC730100 knockdown inhibited proliferation, migration and invasion of glioma cells, but increasing apoptosis. Notably, we found that LOC730100 was mainly localized in the cytoplasm of glioma cells. We demonstrated that LOC730100 was a competing endogenous RNA (ceRNA) for miR-760 and promoted the expression of FOXA1. We proved that miR-760 suppresses glioma progression and FOXA1 overexpression reversed it. In conclusion, our findings revealed that LOC730100 promoted glioma progression through regulating miR-760/FOXA1 axis.Through bioinformatics analysis, we identified that LOC730100 might be a ceRNA for miR-760 while FOXA1 is a possible target ofTo validate it, luciferase reporter assay was conducted. Results showed that miR-760 mimics significantly suppressed the relative luciferase activity of wild-type reporter of LOC730100 or FOXA1 30 -UTR (Fig. 3B), suggesting their direct interaction. Moreover, we found that LOC730100 silencing promoted the level of miR-760 (Fig. 3C) while miR-760 mimics significantly suppressed the expression of FOXA1 in glioma cells (Fig. 3D), which was further validated by western blot (Fig. 3E). Notably, inhibition of miR-760 could abolish the effect of LOC730100 silencing on FOXA1 expression (Fig. 3E), indicating that LOC730100 promoted FOXA1 expression by suppressing miR-760. What s more, we observed that there was a reverse expression correlation between LOC730100 and miR-760 or between miR-760 and FOXA1 in glioma tissues.	30914197	RID06521	ceRNA or sponge	prognosis		UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Colorectal cancer	SBF2-AS1	HDAC3	positively-E	luciferase reporter assay;RNA pull-down assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-619-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000171720	NA	283104	8841	NA	HD3|KDAC3|RPD3|RPD3-2	Long noncoding RNA SBF2-AS1 promotes colorectal cancer proliferation and invasion by inhibiting miR-619-5p activity and facilitating HDAC3 expression.Evidence, demonstrating long noncoding RNAs (lncRNAs) as critical players in cancer, remains to increase. lncRNA SBF2-AS1 was reported to be involved in several cancers, such as hepatocellular carcinoma. However, the role of SBF2-AS1 in colorectal cancer (CRC) is unknown. We showed lncRNA SBF2-AS1 expression was growing in CRC samples, especially in advanced cases. Accordingly, SBF2-AS1 possesses higher expression in CRC cell lines than in normal cell line. Moreover, SBF2-AS1 high expression indicated a low survival rate. Functionally, SBF2-AS1 knockdown suppressed the proliferation, migration, and invasion of CRC cells. In terms of mechanism, SBF2-AS1 upregulation restrained the activity of miR-619-5p and led to overexpression of HDAC3. Importantly, downregulation of miR-619-5p or HDAC3 overexpression reversed SBF2-AS1-silencing-caused suppression on proliferation and metastasis. Summarily, our findings elucidated a crucial role of SBF2-AS1 as a miR-619-5p sponge, shedding novel light on lncRNA-related prognostics.Then, we wondered how SBF2 AS1 regulates CRC progression. According to bioinformatics analysis, we found that SBF2 AS1 might be a molecular sponge for miR 619 5p because it ranked top among all candidates and has been reported to serve as a tumor suppressor. We mutated the potential interacting site for generating a luciferase reporter (Figure 3a). Importantly, the miR 619 5p level was reduced in tumor tissues compared with adjacent normal tissues (Figure 3b). Luciferase intensity in SBF2 AS1 WT reporter expressing SW480 cells was inhibited by miR 619 5p mimics (Figure 3c), indicating their direct interaction. RNA pull-down assay also validated the interaction between SBF2 AS1 and miR 619 5p (Figure 3d). Furthermore, the miR 619 5p level was increased in SW480 and HCT 116 cells after SBF2 AS1 silencing (Figure 3e).	30912164	RID06522	ceRNA or sponge	metastasis,prognosis	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Colon cancer	B4GALT1-AS1	YY1AP1	positively-E	luciferase reporter assay;RIP	upregulation	sequencing	NA	NA	cell stemness(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233554	GRCh38_9:33166948-33182865	ENSG00000163374	NA	101929639	55249	NA	HCCA2|YAP|YY1AP	lncRNA B4GALT1-AS1 promotes colon cancer cell stemness and migration by recruiting YAP to the nucleus and enhancing YAP transcriptional activity.Here, an RNA-sequencing assay revealed long noncoding RNAs (lncRNAs) with an ectopic expression between colon cancer (CC) and normal colon epithelial cells, in which lncRNA B4GALT1-AS1 exhibited the highest change. A 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay indicated that B4GALT1-AS1 knockdown had no effect on CC cell viability, however, cell clone formation analysis showed that B4GALT1-AS1 knockdown attenuated the capacity of cell clone formation. Additionally, gene set enrichment analysis of this data set revealed that positive enrichment of stem cell-differentiated signatures and negative embryonic stem cell function and adult tissue stem module were observed in CC cells with B4GALT1-AS1 knockdown. Furthermore, B4GALT1-AS1 knockdown suppressed the stemness-marker expression, the ability of cell spheroid formation, and ALDH1 activity in CC cells. Mechanistically, RNA-sequencing data found that the Hippo pathway in cancer was shown on pathways mostly upregulated by B4GALT1-AS1 knockdown, and B4GALT1-AS1 directly bound to the yes-associated protein (YAP), a downstream executor of the Hippo pathway, and B4GALT1-AS1 knockdown promoted the nuclear cytoplasm translocation of YAP and decreased YAP transcriptional activity. Notably, YAP overexpression attenuated the inhibitory effects mediated by B4GALT1-AS1 knockdown. Our results identify the direct binding of lncRNA B4GALT1-AS1 to YAP, which is responsible for CC cell stemness.RIP analysis showed that YAP not TAZ could bind to B4GALT1 AS1 (Figure 5d).Furthermore,the luciferase reporter assay showed that B4GALT1 AS1 knockdown decreased YAP transcriptional activity, evident by the decrease of 8xGTIIC luciferase activity (Figure 5g).B4GALT1 AS1 knockdown decreases the capacity of cell migration, invasion, and epithelial mesenchymal transition (EMT) process of CC cells.	30912138	RID06523	interact with protein	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Cervical squamous cell carcinoma	LNCNEF	TGFB1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	RNA-protein	NA	CSC	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237396	GRCh38_20:22587522-22607517	ENSG00000105329	NA	101929685	7040	LINC01384|lncRNA-NEF	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA NEF inhibits migration and invasion of HPV-negative cervical squamous cell carcinoma by inhibiting TGF-beta pathway.LncRNA NEF was a recently identified tumor suppressor lncRNA in hepatocellular carcinoma. Our study aimed to explore the role of NEF in cervical squamous cell carcinoma (CSCC) patients. In the present study, expression of NEF in tumor tissue (cervical biopsies for healthy control) and serum of human papillomaviruses (HPV)-negative and HPV-positive CSCC patients as well as healthy controls was detected by qRT-PCR Diagnostic and prognostic values of NEF for CSCC were evaluated by ROC curve and survival curve analysis, respectively. NEF expression vector was transfected into CSCC cells and the effects on cell migration and invasion as well as TGF-beta1 expression were investigated by Transwell migration assay, Transwell invasion assay, and western blot, respectively. We found that expression of NEF in cervical tissues (tumor tissues for CSCC patients) and serum was significantly down-regulated in HPV-negative CSCC patients than in healthy controls and HPV positive patients, but no significant differences were found between healthy controls and HPV positive patients. Low serum levels of NEF distinguished HPV-negative CSCC patients from healthy controls and indicated poor survival. NEF overexpression inhibited the migration and invasion of HPV-negative but not HPV-positive CSCC cells. NEF overexpression down-regulated TGF-beta1 in HPV-negative CSCC cells but not in HPV-positive CSCC cells. TGF-beta1 treatment reduced the effects of NEF overexpression on cell migration and invasion. Therefore, we conclude that lncRNA NEF may inhibit the migration and invasion of HPV-negative cervical squamous cell carcinoma by inhibiting TGF-beta pathway. In the present study, expression of TGF-beta1 in cells of HPV-negative human cervical squamous cell carcinoma cell line, C33A, and HPV-positive human cervical squamous cell carcinoma cell line, SiHa, was detected by western blot after transfection of NEF expression vector. As shown in Figure 5, NEF overexpression significantly down-regulated, while NEF siRNA silencing significantly up-regulated the expression of TGF-beta1 in cells of human cervical squamous cell carcinoma cell line, C33A (P<0.05), but not in HPV-positive human cervical squamous cell carcinoma cell line, SiHa. In addition, TGF-beta1 (10 ng/ml, Sigma-Aldrich) treatment showed no significant effects on NEF expression (data not shown).	30910843	RID06524	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	AB073614	PTEN	positively-E	western blot	upregulation	qRT-PCR	NA	NA	PTEN/PI3K/AKT signaling pathway(+);cell proliferation(+);colony formation(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000171862	NA	NA	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Upregulation of lncRNA AB073614 functions as a predictor of epithelial ovarian cancer prognosis and promotes tumor growth in vitro and in vivo.Methods: We examined lncRNA AB073614 expression using quantitative real time polymerase chain reaction (qRT-PCR in 75 paired of EOC tissue samples and adjacent normal tissues. Association of lncRNA AB073614 expression with overall survival (OS) was evaluated using Kaplan-Meier analysis. Univariate and multivariate analysis of factors associated with OS were assessed in EOC patients. After lncRNA AB073614 knockdown using siRNAs, the cell viability and cell colony forming assays were performed. western blotwas used to assess relative protein expression.Results: In present study, we demonstrated that lncRNA AB073614 was significantly upregulated in ovarian cancer tissues compared to adjacent normal tissues in patients. Higher lncRNA AB073614 expression significantly associated with tumor size, lymph node invasion, FIGO stage, and shorter OS rate of EOC patients. Furthermore, multivariate Cox regression analysis results showed that higher lncRNA AB0736141 was identified as an independent risk factor of OS in EOC patients. Moreover, we demonstrated that lncRNA AB0736141 knockdown suppressed EOC cell proliferation ability and cell colony formation in vitro. In vivo, we showed that AB0736141 knockdown suppressed tumor growth. We also revealed that lncRNA AB0736141 knockdown inhibited the PTEN/PI3K/AKT signaling pathway in EOC.Conclusions: Thus, these results indicated that LncRNA AB073614 may serve as a prognostic biomarker and potential target of treatment for EOC.	30909184	RID06525	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Urinary bladder cancer	TP53COR1	GLS2	negatively-E	knockdown;overexpression	downregulation	qRT-PCR	NA	NA	cell growth(-);cell proliferation(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	NA	ENSG00000135423	NA	102800311	27165	TRP53COR1|linc-p21|lincRNA-p21	GA|GLS|LGA|hLGA	LincRNA-p21 suppresses glutamine catabolism and bladder cancer cell growth through inhibiting glutaminase expression.Long intergenic non-coding RNA p21 (lincRNA-p21) is down-regulated in some solid tumors. Glutamine catabolism plays an important role in cancer development. However, the role of lincRNA-p21 and its association with glutamine catabolism remain unknown in bladder cancer (BC). In the present study, we investigated the involvement of lincRNA-p21 and glutamine catabolism in BC cell growth and found that ectopic linRNA-p21 expression reduced the proliferation and growth of BIU87 and 5637 cells. Opposite results were observed in lincRNA-p21 silenced J82 and T24 cells. The expression of glutaminase (GLS), intracellular level of glutamate and alpha-Ketoglutarate (alpha-KG) were negatively regulated by lincRNA-p21. GLS overexpression reversed the suppressive function of lincRNA-p21 on BC cell growth and proliferation. In contrast, GLS reduction by siRNA blunted the viability of lincRNA-p21 lowly expressed BC cells. Furthermore, lincRNA-p21 and GLS abundance dictated the sensitivity of BC cells to bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) treatment. Importantly, reduced lincRNA-p21 expression and increased GLS mRNA level were observed in BC tissues compared with the normal tissues. Our results demonstrate that lincRNA-p21 suppresses the BC cell growth through inhibiting GLS and glutamine catabolism. Targeting this cascade may be a promising treatment strategy for BC patients.To determine the abundance of lincRNA-p21 in BC patients, we collected BC and normal tissues and analyzed the  mRNA expression of lincRNA-p21 using qRT-PCRassay.   The results showed that lincRNA-p21 was down-regulated  in BC tissues compared with normal tissues (Figure 6A).   Likewise, lincRNA-p21 expression was lower in BC tissues  than that in adjacent tissues (Figure 6B).   We then analyzed GLS mRNA expression in these tissues by qRT-PCRassay.    GLS was up-regulated in BC the same BC tissues as compared with the normal and their adjacent normal tissues  (Figure 6C,D).   These results suggest inverse correlation between lincRNA-p21 and GLS expression in BC patients.	30902882	RID06526	expression association	NA		DOWN(LIHC,NSCLC,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE60407,GSE38495,GSE111842)
Hemangioma	UCA1	miR-200c	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Hemangioma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Silence of long non-coding RNA UCA1 inhibits hemangioma cells growth, migration and invasion by up-regulation of miR-200c.Methods: qRT-PCRwas carried out to detect the expression of lncRNA UCA1 in human IH tissues. Two hemangioma cell lines (EOMA and HemECs) were transfected with shRNAs specific for lncRNA UCA1, or a plasmid for expression lncRNA UCA1. The expression of miR-200c in cell was suppressed or overexpressed by miRNA-mediated transfection. CCK-8 assay, flow cytometry, Transwell assay, and western blot were performed to detect cell survival, migration and invasion.Results: LncRNA UCA1 was up-regulated in proliferating-phase hemangioma samples, as compared to involuting-phase. Silence of lncRNA UCA1 significantly reduced EOMA cells viability, migration and invasion, and induced apoptosis. These observations were coupled with the down-regulations of CyclinD1, CDK6 and CDK4, the cleavage of caspase-3 and caspase-9, as well as the decreased expression levels of MMP-9 and Vimentin. miR-200c was highly expressed in lncRNA UCA1 silenced-cells. Besides, the anti-tumor effects of lncRNA UCA1 silence towards EOMA cells were reversed by miR-200c suppression. Same effects of lncRNA UCA1 and miR-200c on HemECs cells were observed. Furthermore, silence of lncRNA UCA1 repressed mTOR, AMPK and Wnt/beta-catenin signaling via a miR-200c-dependent fashion.Conclusion: This study evidences that silence of lncRNA UCA1 inhibits hemangioma cells growth, migration and invasion possibly via its regulation on miR-200c expression and the activation of mTOR, AMPK and Wnt/beta-catenin signaling pathways.	30898646	RID06527	transcriptional regulation	NA	UP(PAAD);DATA(GSE40174)	
Ovarian cancer	AWPPH	CTNNB1	positively-E	overexpression;western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA AWPPH promotes the proliferation, migration and invasion of ovarian carcinoma cells via activation of the Wnt/beta-catenin signaling pathway.The oncogenic role of the long noncoding RNA associated with poor prognosis of hepatocellular carcinoma (lncRNA AWPPH) was reported in various types of malignancies; however, its involvement in ovarian carcinoma (OC) remains unknown. Thus, the present study investigated the role of AWPPH in OC. The expression of AWPPH in tissues and serum acquired from patients with OC, and healthy controls, was determined via reverse transcription-quantitative polymerase chain reaction. The diagnostic value of serum AWPPH expression was evaluated by receiver operating characteristic curve analysis. Additionally, survival curve analysis was performed to determine the prognostic value of AWPPH for OC. An AWPPH overexpression vector was transfected into OC cell lines. Cell proliferation, migration and invasion were analyzed via Cell Counting Kit-8, Transwell migration and invasion assays, respectively. The expression of beta-catenin was investigated via western blot. It was revealed that the expression levels of AWPPH were significantly upregulated in OC tissues and serum compared with healthy controls. The serum levels of AWPPH were able to effectively diagnose and predict the prognosis of patients with OC. AWPPH overexpression promoted the proliferation, migration and invasion of OC cells, and upregulated beta-catenin expression. Treatment with a Wnt agonist markedly altered AWPPH expression; however, inhibition of Wnt suppressed the effects of AWPPH overexpression on proliferation, migration and invasion of OC cells. Therefore, it was revealed that AWPPH may promote OC via activation of the Wnt/beta-catenin signaling pathway.	30896797	RID06528	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	KB-1471A8.2	CDK4	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);chemosensitivity(-);apoptosis process(+)	NA	association	RNA-protein	Paclitaxel	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	NA	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	LncRNA KB-1471A8.2 Overexpression Suppresses Cell Proliferation and Migration and Antagonizes the Paclitaxel Resistance of Ovarian Cancer Cells.Objective: The aim was to investigate the lncRNA KB-1471A8.2 function in ovarian cancer progression and paclitaxel resistance. Methods: The expression and distribution of KB-1471A8.2 was detected by qRT-PCR The cell proliferation, apoptosis, invasion, migration and chemoresistance were analyzed by CCK8 assay, flow cytometry and transwell assay. The expression of DEPTOR, whose sequence is reverse overlapped with KB-1471A8.2 was analyzed by qRT-PCR western blot and immunofluorescence. The cell cycle and the cell cycle related gene expression were analyzed by flow cytometry and qRT-PCR respectively. Results: KB-1471A8.2 was significantly downregulated in both ovarian cancer tissues and chemoresistant ovarian cancer cells. Overexpression of KB-1471A8.2 significantly inhibited the proliferation, invasion, migration, and paclitaxel resistance, and increased the apoptosis of ovarian cancer cells. KB-1471A8.2 was mainly distributed in the nucleus of ovarian cancer cells. KB-1471A8.2 overexpression significantly decreased the S phase cell ratio, increased the G0/G1 phase cell ratio, but not affected the expression and distribution of DEPTOR. However, cyclin-dependent kinase 4 (CDK4), which is an important regulator of G1/S transition, was significantly decreased in KB-1471A8.2-overexpressed ovarian cancer cells. Conclusion: KB-1471A8.2 could significantly inhibit the development and paclitaxel resistance of ovarian cancer cells, at least partly, by suppressing CDK4 expression.	30892073	RID06529	expression association	chemoresistance		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Breast cancer	FBXL19-AS1	MIR718	negatively-E	dual-luciferase reporter assay;RIP;DIANA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+);tumor growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000211524	NA	283932	100313781	NCRNA00095	hsa-mir-718	LncRNA FBXL19-AS1 promotes breast cancer cells proliferation and invasion via acting as a molecular sponge to miR-718.Long non-coding RNAs (lncRNAs) have been suggested to serve vital roles in tumor initiation and progression. However, the expression and underlying mechanisms of lncRNA FBXL19-AS1 in breast cancer (BC) remain unclear. In the present study, we found that FBXL19-AS1 expression was significantly up-regulated and correlated with advanced clinical features and poor overall survival of BC patients. Functionally, FBXL19-AS1 inhibition suppressed BC cells proliferation, invasion, and epithelial-mesenchymal transition (EMT) processes in vitro and reduced tumor growth in vivo In addition, we found that FBXL19-AS1 might function as a ceRNA to sponge miR-718, and miR-718 could rescue the effects of FBXL19-AS1 on BC cells progression. Therefore, these findings suggested that FBXL19-AS1 might serve as an oncogenic lncRNA and promoted BC progression by sponging miR-718, indicating FBXL19-AS1 could serve as a potential therapeutic target for BC treatment.qRT-PCR;ISHowed that FBXL19-AS1 expression was significantly up-regulated in BC tissues compared with ANT (Figure 1A; P<0.05).Using the online software  program DIANA, miR-718 was found to potentially bind to FBXL19-AS1 (Figure 3A).   dual-luciferase reporter assay showed that miR-718 mimics significantly reduced the luciferase activity of FBXL19-AS1-Wt in BC cells (Figure 3B;  P<0.05).  qRT-PCR;ISHowed that FBXL19-AS1 knockdown remarkably increased miR-718 expression in BC cells (Figure 3C;  P<0.05).  Moreover, RIP assay showed that FBXL19-AS1 and miR-718 were co-immunoprecipitated by the anti-Ago2 antibody (Figure 3D;  P<0.05).  In addition, we showed that miR-718 expression was significantly de_x0002_creased in BC tissues and cell lines (Figure 3E,F;  P<0.05).  Correlation analysis revealed that FBXL19-AS1 expression was negatively correlated with miR-718 expression in BC tissues (Figure 3G;  P<0.05).  Those data indicated that FBXL19-AS1 might act as a molecular sponge for miR-718 in BC cells.	30886065	RID06530	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	
Cervical cancer	CDKN2B-AS1	TGFbetaI	positively-E	luciferase reporter assay;bioinformatics	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);cell senescence(-)	ceRNA(miR-181a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Interference of the long noncoding RNA CDKN2B-AS1 upregulates miR-181a-5p/TGFbetaI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells.Long noncoding RNA (lncRNA) CDKN2B-AS1 has been shown to play a crucial role in the development as well as in the prognosis of various human cancers, including cervical cancer. However, the underlying mechanisms need to be further explored between CDKN2B-AS1 and cervical cancer. In the present study, RT-PCRshowed that the mRNA level of CDKN2B-AS1 was significantly upregulated while the miR-181a-5p was downregulated in cervical cancer cell lines. In addition, the interference of CDKN2B-AS1 by shRNA resulted in the suppression of cell proliferation, invasion, migration and promotion of apoptosis and senescence, and either CDKN2B-AS1 overexpression or miR-181a-5p showed reversed results. Further studies demonstrated that CDKN2B-AS1 could directly interact with miR-181a-5p, and that there was an inverse correlation between miR-181a-5p and CDKN2B-AS1. In addition, we found that TGFbetaI was a target of miR-181a-5p and could be downregulated by CDKN2B-AS1 knockdown. Moreover, the in vivo experiments further demonstrated the contribution of CDKN2B-AS1 in cervical cancer including tumor growth, apoptosis inhibition and senescence inhibition, and CDKN2B-AS1 knockdown could inhibit the aforementioned activities. In summary, our study demonstrated that the CDKN2B-AS1/miR-181a-5p/TGFbetaI axis might play a vital role in cervical cancer development.	30884187	RID06531	ceRNA or sponge	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	
Breast cancer	TP53	C2orf92	positively-E	ChIP	downregulation	qRT-PCR;microarray	NA	NA	PTEN/AKT signaling pathway(+);apoptosis process(+);cell proliferation(-)	interact with protein	binding/interaction	NA	LXR-623	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000228486	GRCh38_2:97664217-97703066	7157	728537	LFS1|p53	LINC01125	Long non-coding RNAs (lncRNAs) serve as novel and crucial regulators that participate in cancer tumorigenesis and diverse biological processes. Here, we report a previously uncharacterized mechanism underlying lncRNA-mediated exocytosis of LXR-623 via the phosphatase and tensin homolog (PTEN)/protein kinase B (AKT)/p53 axis to suppress the proliferation of cancer cells in vitro. We found that LXR-623 significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at S phase in breast cancer cells in a concentration- and time-dependent manner. Experiments using a xenograft mouse model revealed the inhibitory effects of LXR-623 on tumor growth. We used lncRNA microarray to investigate the potential genes regulated by LXR-623. As a result, LINC01125 was found to be significantly upregulated in the cells treated with LXR-623. Gain- and loss-of-function assays were conducted to investigate the anti-proliferation role of LINC01125. LINC01125 knockdown resulted in the inhibition of the cytotoxic effect of LXR-623; in contrast, LINC01125 overexpression significantly enhanced the effect of LXR-623. LXR-623 and LINC01125-mediated anti-growth regulation is, at least in part, associated with the participation of the PTEN/AKT/mouse double minute 2 homolog (MDM2)/p53 pathway. In addition, SF1670, a specific PTEN inhibitor with prolonged intracellular retention, may strongly block the anti-proliferation effect induced by LXR-623 and LINC01125 overexpression. Chromatin immunoprecipitation (ChIP) assay results suggest that p53 binds to the promoter of LINC01125 to strengthen the expression of the PTEN/AKT pathway. Taken together, our findings suggest that LXR-623 possesses significant antitumor activity in breast cancer cells that is partly mediated through the upregulation in LINC01125 expression and enhancement in apoptosis via the PTEN/AKT/MDM2/p53 pathway.We  used The Cancer Genome Atlas (TCGA) database to  analyze the expression of LINC01125 (Fig. 3d) and found  that LINC01125 expression was downregulated in BC  tissues.qRT-PCRwas used to confirm the downregulation of LINC01125 expression in MDA-MB-231,  BT549, MCF-7, and MDA-MB-453 cells than in MCF-  10A cells.	30867411	RID06532	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Colorectal cancer	SATB2-AS1	SATB2	positively-E	RIP;ChIP	downregulation	qPCR;microarray	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225953	GRCh38_2:199457697-199476935	ENSG00000119042	NA	150538	23314	NA	FLJ21474|KIAA1034	However, the involvement of lncRNA in colorectal carcinoma progression remains largely unknown, especially in colorectal carcinoma metastasis. In this study, we investigated the changes in lncRNA expression in colorectal carcinoma and identified a new lncRNA, the antisense transcript of SATB2 (SATB2-AS1), as a key regulator of colorectal carcinoma progression. SATB2-AS1 was frequently downregulated in colorectal carcinoma cells and tissues, and patients whose tumors expressed SATB2-AS1 at low levels had a shorter overall survival and poorer prognosis. Downregulation of SATB2-AS1 significantly promoted cell proliferation, migration, and invasion in vitro and in vivo, demonstrating that it acts as a tumor suppressor in colorectal carcinoma. SATB2-AS1 suppressed colorectal carcinoma progression by serving as a scaffold to recruit p300, whose acetylation of H3K27 and H3K9 at the SATB2 promoter upregulated expression of SATB2, a suppressor of colorectal carcinoma growth and metastasis. SATB2 subsequently recruited HDAC1 to the Snail promoter, repressing Snail transcription and inhibiting epithelial-to-mesenchymal transition. Taken together, these data reveal SATB2-AS1 as a novel regulator of the SATB2-Snail axis whose loss facilitates progression of colorectal carcinoma. SIGNIFICANCE: These data show that the lncRNA SATB2-AS1 mediates epigenetic regulation of SATB2 and Snail expression to suppress colorectal cancer progression.See related commentary by Li, p. 3536.To identify novel functional lncRNAs in colorectal carcinoma  metastasis, we performed lncRNA microarray analysis to compare  lncRNA expression levels between colorectal carcinoma tissues  with and without metastasis.  Of interest, the expression of lncRNA SATB2-AS1  (AK056625) was downregulated in the colorectal carcinoma  tissues with metastasis.Similar to SATB2-AS1, SATB2  mRNA was significantly downregulated in the majority of colorectal carcinoma samples (P <  0.001, Supplementary Fig. S4),  and SATB2-AS1 and SATB2 RNA levels in these tissues were  positively correlated (R2   0.1698, P  shown in Fig. 3B (right), a signi 0.008, Fig. 3B left).	30858153	RID06533	epigenetic regulation	metastasis,prognosis		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Colorectal cancer	SATB2-AS1	SNAI1	negatively-E	RIP;ChIP;BLAST	downregulation	qPCR;microarray	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225953	GRCh38_2:199457697-199476935	ENSG00000124216	NA	150538	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	In this study, we investigated the changes in lncRNA expression in colorectal carcinoma and identified a new lncRNA, the antisense transcript of SATB2 (SATB2-AS1), as a key regulator of colorectal carcinoma progression. SATB2-AS1 was frequently downregulated in colorectal carcinoma cells and tissues, and patients whose tumors expressed SATB2-AS1 at low levels had a shorter overall survival and poorer prognosis. Downregulation of SATB2-AS1 significantly promoted cell proliferation, migration, and invasion in vitro and in vivo, demonstrating that it acts as a tumor suppressor in colorectal carcinoma. SATB2-AS1 suppressed colorectal carcinoma progression by serving as a scaffold to recruit p300, whose acetylation of H3K27 and H3K9 at the SATB2 promoter upregulated expression of SATB2, a suppressor of colorectal carcinoma growth and metastasis. SATB2 subsequently recruited HDAC1 to the Snail promoter, repressing Snail transcription and inhibiting epithelial-to-mesenchymal transition. Taken together, these data reveal SATB2-AS1 as a novel regulator of the SATB2-Snail axis whose loss facilitates progression of colorectal carcinoma. SIGNIFICANCE: These data show that the lncRNA SATB2-AS1 mediates epigenetic regulation of SATB2 and Snail expression to suppress colorectal cancer progression.See related commentary by Li, p. 3536.Interestingly, both SATB2-AS1- and SATB2-  overexpression resulted in significantly decreased mRNA and  protein levels of Snail, a central regulator of EMT (Fig. 6B and C).To further explore the underlying mechanism of how SATB2  regulates Snail expression, we searched Snail promoter sequence  with BLAST software and identified that three potential binding  regions with AT-rich sequence (42.5%, 29.3%, and 30.8%) were  predicted to be embedded in Snail gene promoter (Fig. 6D, top).ChIP assays revealed that endogenous SATB2 protein was bound  to the most AT-rich region (P1, 1069 to - 710 bp) of Snail  promoter (Fig. 6D).	30858153	RID06534	epigenetic regulation	metastasis,prognosis		UP(PAAD);DATA(GSE40174)
Head and neck squamous cell carcinoma	TP53	TP53COR1	positively-E	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	cancer progression(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Head and neck cancer	TF	lncRNA	ENSG00000141510	NA	NA	NA	7157	102800311	BCC7|BMFS5|LFS1|P53|TRP53	TRP53COR1|linc-p21|lincRNA-p21	The biological functions of lincRNA-p21 were investigated in vitro and in vivo. RNA immunoprecipitation and pull-down assays were used to detect the direct binding of lincRNA-p21.Results: Lower lincRNA-p21 expression was observed in HNSCC tissues and indicated worse prognosis. Both wild and mutant type p53 transcriptionally regulated lincRNA-p21, but nuclea factor Y subunit alpha (NF-YA) was essential for mutant p53 in the regulation of lincRNA-p21. Ectopic expression of lincRNA-p21 significantly inhibited cell proliferation capacity in vitro and in vivo and vice versa. Moreover, the overexpression of lincRNA-p21 induced G1 arrest and apoptosis. Knockdown NF-YA expression reversed tumor suppressor activation of lincRNA-p21 in mutant p53 cells, not wild-type p53 cells. A negative correlation was observed between lincRNA-p21 and the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in HNSCC tissues. High lincRNA-p21 expression inhibited Janus kinase 2 (JAK2)/STAT3 signal activation and vice versa. Further, we observed direct binding to STAT3 by lincRNA-p21 in HNSCC cells, which suppressed STAT3-induced oncogenic potential.Conclusions: Our results revealed the transcriptional regulation of lincRNA-p21 by the mutant p53/NF-YA complex in HNSCC. LincRNA-p21 acted as a tumor suppressor in HNSCC progression, which was attributed to direct binding to STAT3 and blocking of JAK2/STAT3 signaling.We next conducted qRT-PCRto examine lincRNA-p21 expression in HNSCC tissues and cell lines.We focused on possible transcriptional regulation of  lincRNA-p21 by p53 and investigated whether p53 was  able to bind the promoter of lincRNA-p21. Using a ChIP  assay, we observed that p53 bound to the promoter of  lincRNA-p21 under DOX stimulation in Detroit 562 and  HN30 cells (Fig. 2e).An EMSA was used to further determine whether p53 binds to the promoter of  lincRNA-p21. A database prediction indicated that the  lincRNA-p21 promoter presented a putative binding region for p53 (Fig. 2g).Together, these results revealed that lincRNA-p21 was a  direct transcriptional target of p53.Furthermore, we observed the positive correlation between lincRNA-p21  and TP53 mRNA in 70 HNSCC patients (Fig. 2j).	30857539	RID06535	interact with protein	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Head and neck squamous cell carcinoma	TP53COR1	STAT3	negatively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	JAK2/STAT3 signaling pathway(-);cancer progression(-)	epigenetic regulation	binding/interaction	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	NA	NA	ENSG00000168610	NA	102800311	6774	TRP53COR1|linc-p21|lincRNA-p21	ADMIO|ADMIO1|APRF|HIES	p53-targeted lincRNA-p21 acts as a tumor suppressor by inhibiting JAK2/STAT3 signaling pathways in head and neck squamous cell carcinoma.Background: Long intergenic noncoding RNA p21 (lincRNA-p21) is considered a target of wild-type p53, but little is known about its regulation by mutant p53 and its functions during the progression of head and neck squamous cell carcinoma (HNSCC).Methods: RNAscope was used to detect the expression and distribution of lincRNA-p21. Chromatin immunoprecipitation and electrophoretic mobility shift assays were performed to analyze the transcriptional regulation of lincRNA-p21 in HNSCC cells. The biological functions of lincRNA-p21 were investigated in vitro and in vivo. RNA immunoprecipitation and pull-down assays were used to detect the direct binding of lincRNA-p21.Results: Lower lincRNA-p21 expression was observed in HNSCC tissues and indicated worse prognosis. Both wild and mutant type p53 transcriptionally regulated lincRNA-p21, but nuclear transcription factor Y subunit alpha (NF-YA) was essential for mutant p53 in the regulation of lincRNA-p21. Ectopic expression of lincRNA-p21 significantly inhibited cell proliferation capacity in vitro and in vivo and vice versa. Moreover, the overexpression of lincRNA-p21 induced G1 arrest and apoptosis. Knockdown NF-YA expression reversed tumor suppressor activation of lincRNA-p21 in mutant p53 cells, not wild-type p53 cells. A negative correlation was observed between lincRNA-p21 and the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in HNSCC tissues. High lincRNA-p21 expression inhibited Janus kinase 2 (JAK2)/STAT3 signal activation and vice versa. Further, we observed direct binding to STAT3 by lincRNA-p21 in HNSCC cells, which suppressed STAT3-induced oncogenic potential.Conclusions: Our results revealed the transcriptional regulation of lincRNA-p21 by the mutant p53/NF-YA complex in HNSCC. LincRNA-p21 acted as a tumor suppressor in HNSCC progression, which was attributed to direct binding to STAT3 and blocking of JAK2/STAT3 signaling.As shown in  Fig. 6f, lincRNA-p21 level negatively correlated with  that of p-STAT3 in HNSCC tissues (P<0.001).	30857539	RID06536	epigenetic regulation	prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Cholangiocarcinoma	MIR22HG	CTNNB1	negatively-F		downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-)	transcriptional regulation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000168036	NA	84981	1499	C17orf91	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA MIR22HG inhibits cell proliferation and migration in cholangiocarcinoma by negatively regulating the Wnt/beta-catenin signaling pathway.Background: Cholangiocarcinoma (CCA) is one of the most common primary biliary malignant tumors with a high mortality. MIR22HG has been reported to act as a tumor-suppressor gene in several types of cancers. However, the role and molecular regulatory mechanism of MIR22HG in CCA still remains unclear. The present study aimed to investigate the role and underlying mechanism of MIR22HG in CCA.Methods: The expression of MIR22HG was detected by RT-qPCR assayin CCA tissues and cells. CCK-8, colony formation and transwell assays were performed to study the biological function of MIR22HG in CCA. western blot and immunofluorescence assays were performed to detect the expression ofWnt/beta-catenin signaling pathway markers. In vivo assays were conducted to explore the biological role of MIR22HG.Results: We first found that MIR22HG expression was significantly down-regulated in CCA tissues and cell lines. Moreover, MIR22HG expression was related to TNM stage and bore prognostic significance in CCA patients. Function experiments demonstrated that overexpression of MIR22HG inhibited cell proliferation, migration and invasion in CCA, whereas knockdown of MIR22HG caused the opposite result. It was found that MIR22HG negatively regulated mRNA and the expression levels of proteins in the Wnt/beta-catenin signaling pathway (beta-catenin, cyclin D1 and c-myc). The effect of MIR22HG overexpression on CCA progression could be partly rescued by activating the Wnt/beta-catenin signaling pathway. MIR22HG suppressed CCA tumorigenesis in vivo.Conclusions: In summary, the results of the present study show that MIR22HG repressed cell proliferation, migration and invasion in CCA by negatively regulating the Wnt/beta-catenin signaling pathway. MIR22HG may be a novel target for diagnosis and therapy in CCA.	30856284	RID06537	transcriptional regulation	prognosis	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	TINCR	miR-7-5P	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000223573	GRCh38_19:5558167-5578349	NA	NA	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	SP1-induced lncRNA TINCR overexpression contributes to colorectal cancer progression by sponging miR-7-5p.Mounting evidences have indicated that long noncoding RNAs (lncRNAs) play pivotal roles in human diseases, especially in cancers. Recently, TINCR was proposed to be involved in tumor progression. However, its role in colorectal cancer (CRC) remains elusive. In our study, we found that SP1-induced TINCR was significantly upregulated in CRC tissues and cell lines. Moreover, cox multivariate survival analysis revealed that high TINCR was an independent predictor of poor overall survival (OS). Functionally, knockdown of TINCR obviously suppressed CRC cells proliferation, migration and invasion in vitro, and inhibited CRC cells growth and metastasis in vivo. Mechanistically, we identified TINCR could act as a miR-7-5p sponge using RNA pull down, luciferase reporter and RIP assays. Furthermore, we showed that TINCR might promote CRC progression via miR-7-5p-mediated PI3K/Akt/mTOR signaling pathway. Lastly, we revealed that plasma TINCR expression was upregulated in CRC when compared to healthy controls and could be a promising diagnostic biomarker for CRC. Based on above results, our data indicated that TINCR might serve as a potential diagnostic and prognostic biomarker for CRC.	30853664	RID06538	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Colorectal cancer	SP1	TINCR	positively-E	JASPAR;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000223573	GRCh38_19:5558167-5578349	6667	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	Mounting evidences have indicated that long noncoding RNAs (lncRNAs) play pivotal roles in human diseases, especially in cancers. Recently, TINCR was proposed to be involved in tumor progression. However, its role in colorectal cancer (CRC) remains elusive. In our study, we found that SP1-induced TINCR was significantly upregulated in CRC tissues and cell lines. Moreover, cox multivariate survival analysis revealed that high TINCR was an independent predictor of poor overall survival (OS). Functionally, knockdown of TINCR obviously suppressed CRC cells proliferation, migration and invasion in vitro, and inhibited CRC cells growth and metastasis in vivo. Mechanistically, we identified TINCR could act as a miR-7-5p sponge using RNA pull down, luciferase reporter and RIP assays. Furthermore, we showed that TINCR might promote CRC progression via miR-7-5p-mediated PI3K/Akt/mTOR signaling pathway. Lastly, we revealed that plasma TINCR expression was upregulated in CRC when compared to healthy controls and could be a promising diagnostic biomarker for CRC. Based on above results, our data indicated that TINCR might serve as a potential diagnostic and prognostic biomarker for CRC.The ChIP data indicated that SP1   could bind to E1 sites (Fig. 2B).	30853664	RID06539	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)
Osteosarcoma	DBH-AS1	p-PI3K	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	NA	NA	138948	NA	BPR|NCRNA00118	NA	Downregulation of long non-coding RNA DBH-AS1 inhibits osteosarcoma progression by PI3K-AKT signaling pathways and indicates good prognosis.Objective: Long non-coding RNA DBH-AS1 (DBH-AS1) has emerged as a novel regulator in cancer initiation and progression of several tumors. However, the expression of DBH-AS1 in osteosarcoma and its effect on the tumorigenesis of osteosarcoma are unclear. The purpose of this study was to determine the role of DBH-AS1 in osteosarcoma progression.Patients and methods: The expression level of DBH-AS1 in 119 pairs of osteosarcoma tissues and five cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The association of DBH-AS1 expression with clinicopathological factors and prognosis was also analyzed. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8), EdU and cell colony formation assays and apoptosis in MG63 and U2OS cells was examined by flow cytometry. Following that, transwell invasion and wound-healing assays were used to explore cell migration and invasion, respectively. The expression of the PI3K/Akt pathway-related proteins was examined by western blotResults: We observed that DBH-AS1 was distinctly overexpressed in osteosarcoma tissue and cells, and associated with lymph node status and metastasis status. Osteosarcoma patients with a higher DBH-AS1 expression showed significantly poorer overall survival than those with lower DBH-AS1 expression. Multivariate analysis demonstrated that high DBH-AS1 expression was an independent poor prognostic factor for osteosarcoma patients. Functional assays revealed that knockdown of DBH-AS1 inhibited cell proliferation, migration and invasion, while promoted apoptosis in osteosarcoma. Moreover, suppression of DBH-AS1 could inhibit the activation of the PI3K/Akt pathway, which was demonstrated by examining the expression levels of p-PI3K and p-Akt.Conclusions: Our data first reported that DBH-AS1 may act as an oncogenic lncRNA by modulating the PI3K/Akt pathway in osteosarcoma, which may serve as a candidate prognostic biomarker and target for new therapies in osteosarcoma.	30840262	RID06540	expression association	metastasis,prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	
Osteosarcoma	DBH-AS1	p-Akt	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	NA	NA	138948	NA	BPR|NCRNA00118	NA	Downregulation of long non-coding RNA DBH-AS1 inhibits osteosarcoma progression by PI3K-AKT signaling pathways and indicates good prognosis.Objective: Long non-coding RNA DBH-AS1 (DBH-AS1) has emerged as a novel regulator in cancer initiation and progression of several tumors. However, the expression of DBH-AS1 in osteosarcoma and its effect on the tumorigenesis of osteosarcoma are unclear. The purpose of this study was to determine the role of DBH-AS1 in osteosarcoma progression.Patients and methods: The expression level of DBH-AS1 in 119 pairs of osteosarcoma tissues and five cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The association of DBH-AS1 expression with clinicopathological factors and prognosis was also analyzed. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8), EdU and cell colony formation assays and apoptosis in MG63 and U2OS cells was examined by flow cytometry. Following that, transwell invasion and wound-healing assays were used to explore cell migration and invasion, respectively. The expression of the PI3K/Akt pathway-related proteins was examined by western blotResults: We observed that DBH-AS1 was distinctly overexpressed in osteosarcoma tissue and cells, and associated with lymph node status and metastasis status. Osteosarcoma patients with a higher DBH-AS1 expression showed significantly poorer overall survival than those with lower DBH-AS1 expression. Multivariate analysis demonstrated that high DBH-AS1 expression was an independent poor prognostic factor for osteosarcoma patients. Functional assays revealed that knockdown of DBH-AS1 inhibited cell proliferation, migration and invasion, while promoted apoptosis in osteosarcoma. Moreover, suppression of DBH-AS1 could inhibit the activation of the PI3K/Akt pathway, which was demonstrated by examining the expression levels of p-PI3K and p-Akt.Conclusions: Our data first reported that DBH-AS1 may act as an oncogenic lncRNA by modulating the PI3K/Akt pathway in osteosarcoma, which may serve as a candidate prognostic biomarker and target for new therapies in osteosarcoma.	30840262	RID06541	expression association	metastasis,prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	
Triple-negative breast cancer	LNCNEF	miRNA-155	negatively-E	RT-qPCR	downregulation	RT-qPCR	NA	NA	prognosis(-);cell migration(+);cell invasion(-)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000237396	GRCh38_20:22587522-22607517	NA	NA	101929685	NA	LINC01384|lncRNA-NEF	NA	LncRNA NEF is downregulated in triple negative breast cancer and correlated with poor prognosis.LncRNA NEF has been proved to be a tumor suppressor in liver cancer. In the present study, we found that lncRNA NEF was downregulated and miRNA-155 was upregulated in plasma of triple-negative breast cancer (TNBC) patients compared with those in controls. These two factors were inversely correlated only in TNBC patients but not in controls. Altered expression of lncRNA NEF and miRNA-155 distinguished TNBC patients from healthy controls. Follow-up study showed that low level of lncRNA NEF and high level of miRNA-155 were correlated with poor survival. LncRNA NEF overexpression inhibited the migration and invasion of TNBC cells, while miRNA-155 overexpression promoted the migration and invasion of TNBC cells, but showed no significant effects on cancer cell proliferation. MiRNA-155 overexpression partially rescued the inhibited cell migration and invasion caused by lncRNA NEF overexpression. LncRNA NEF overexpression inhibited miRNA-155 expression, while miRNA-155 overexpression showed no significant effect on lncRNA NEF expression. Therefore, lncRNA NEF may participate in TNBC by negatively regulating miRNA-155.Plasma levels of lncRNA NEF and miRNA-155 in both 64 patients  with TNBC and 58 healthy females were measured by RT-qPCR.	30839051	RID06542	expression association	prognosis		
Prostate cancer	BRE-AS1	miR-145-5p	positively-E	bioinformatics	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA BRE-AS1 interacts with miR-145-5p to regulate cancer cell proliferation and apoptosis in prostate carcinoma and has early diagnostic values.Long non-coding RNA (LncRNA) BRE-AS1 has recently proven to be a tumor suppressor in lung cancer. The present study aimed to investigate the involvement of lncRNA BRE-AS1 in prostate carcinoma (PC). In the present study we found that plasma BRE-AS1 and miR-145-5p were both down-regulated in PC patients than in healthy controls. Down-regulation of BRE-AS1 and miR-145-5p effectively distinguished early-stage PC patients from healthy controls. A significant and positive correlation between BRE-AS1 and miR-145-5p was only found in PC patients. BRE-AS1 overexpression mediated miR-145-5p up-regulation in PC cells, while miR-145-5p overexpression did not significantly affect BRE-AS1. Overexpression of BRE-AS1 and miR-145-5p led to inhibited proliferation and promoted apoptosis of PC cells. miR-145-5p inhibitor attenuated the effects of BRE-AS1 overexpression on cancer cell behaviors. Therefore, lncRNA BRE-AS1 may regulate cancer cell proliferation and apoptosis in PC by interacting with miR-145-5p.Correlations between plasma levels of BRE-AS1 and miR-145-5p in both PC patients and healthy controls were analyzed by Pearson s correlation coefficient.	30833361	RID06543	ceRNA or sponge	NA		
Clear cell renal cell carcinoma	AFAP1-AS1	PTEN	negatively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000171862	NA	84740	5728	AFAP1-AS|AFAP1AS|MGC10981	BZS|MHAM|MMAC1|PTEN1|TEP1	Silencing of lncRNA AFAP1-AS1 Inhibits Cell Growth and Metastasis in Clear Cell Renal Cell Carcinoma.The lncRNA AFAP1-AS1, oriented from an antisense direction to the protein-coding gene AFAP1 in the opposite strand, was upregulated in a variety of tumors and associated with poor prognosis, including lung cancer, breast cancer, ovarian cancer, and so on. However, the biological role of AFAP1-AS1 in clear cell renal cell carcinoma (ccRCC) is still unknown. We observed that AFAP1-AS1 expression was significantly upregulated in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. Knockdown of AFAP1-AS1 markedly suppressed the progression of proliferation, invasion, migration, and EMT in ccRCC cells. Downregulation of AFAP1-AS1 resulted in an increase in E-cadherin and a decrease in vimentin. Noticeably, we found that PTEN has a negative correlation with the lncRNA AFAP1-AS1 expression. Further studies verified that PTEN deficiency effectively attenuated the ability of AFAP1-AS1 in promoting ccRCC cell proliferation, invasion, migration, and EMT. Moreover, the similar biological response of silencing AFAP1-AS1 was observed in our ccRCC mice model. Knockdown of AFAP1-AS1 evidently suppressed tumor growth. Taken together, our results provide the evidences that silencing of AFAP1-AS1 inhibits cell proliferation, EMT, and metastasis through PTEN-dependent signaling, and our findings elucidate a novel potential therapeutic target or biomarker for the treatment of ccRCC.First, the expression level of AFAP1-AS1 in ccRCC   cell panel, including 786-O, Caki-1, ACHN, and A498   cells was detected using qRT-PCRFurthermore, the correlation of PTEN and AFAP1-AS1   was analyzed by Pearson correlation test.	30832752	RID06544	expression association	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	ESR1	LINC00472	positively-E	luciferase reporter assay;ChIP	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);tumor growth(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000233237	GRCh38_6:71343427-71420745	2099	79940	ER|ESR|ESRA|ESTRR|Era|NR3A1	C6orf155|P53RRA	To study the mechanisms underlying the lncRNA's connection to breast cancer, we investigated the molecular targets and regulation of LINC00472 in breast cancer cells, and analyzed relevant molecular features in relation to patient survival. Gene expression profiles of breast cancer cells overexpressing LINC00472 were analyzed for its regulatory pathways and downstream targets. Effects of LINC00472 overexpression on cell behaviors were evaluated in vitro and in vivo. Meta-analysis was performed using online datasets and our own study.Results: Analysis of LINC00472 transcriptome revealed ERalpha upregulation of LINC00472 expression, and an ERalpha-binding site in the LINC00472 promoter was identified. Evaluation of LINC00472 overexpression also indicated a possible link between LINC00472 and NF-kB. Cell experiments confirmed that LINC00472 suppressed the phosphorylation of p65 and IkBalpha through binding to IKKbeta, inhibiting its phosphorylation. High LINC00472 expression inhibited tumor growth both in vitro and in vivo and suppressed aggressive tumor cell behaviors in vitro. Suppressing LINC00472 expression in ER-positive tumor cells increased cell aggressive behaviors. Tamoxifen treatment of ER-positive cells inhibited ERalpha and LINC00472 expression and increased p65 and IkBalpha phosphorylation. Meta-analysis showed that LINC00472 expression were higher in ER-positive than ER-negative tumors and that high expression was associated with better disease outcomes in ER-positive patients.Conclusions: The study demonstrates that ERalpha upregulates LINC00472 which suppresses the phosphorylation of NF-kB, and suggests that endocrine treatment may lower LINC00472 and increase NF-kB activities, leading to tumor progression and disease recurrence.Upregulated LINC00472 expression was expected in the cells transfected with a LINC00472  plasmid.  To validate the microarray findings, we performed qRT-PCRanalysis on three top transcripts, and the   PCR results were consistent with the microarray findings (Fig. 3b).We performed a luciferase   reporter assay to evaluate the interaction between ERalpha and   the LINC00472 promoter.  The assay results showed that after   overexpressing ESR1 in 293T (Fig. 4c), cells transfected   with an intact promoter of LINC00472 had elevated luciferase signals, whereas the cells with a mutant LINC00472  promoter that did not contain the ERalpha binding site had no   increase in luciferase activity (Fig. 4d).A ChIP assay further   demonstrated that ERalpha was able to bind to the LINC00472  promoter (Fig. 4e).	30830488	RID06545	interact with protein	recurrence	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Breast cancer	LINC00472	NFKB1	negatively-E	overexpression	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);tumor growth(-)	phosphorylation	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000109320	NA	79940	4790	C6orf155|P53RRA	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	To study the mechanisms underlying the lncRNA's connection to breast cancer, we investigated the molecular targets and regulation of LINC00472 in breast cancer cells, and analyzed relevant molecular features in relation to patient survival. Gene expression profiles of breast cancer cells overexpressing LINC00472 were analyzed for its regulatory pathways and downstream targets. Effects of LINC00472 overexpression on cell behaviors were evaluated in vitro and in vivo. Meta-analysis was performed using online datasets and our own study.Results: Analysis of LINC00472 transcriptome revealed ERalpha upregulation of LINC00472 expression, and an ERalpha-binding site in the LINC00472 promoter was identified. Evaluation of LINC00472 overexpression also indicated a possible link between LINC00472 and NF-kB. Cell experiments confirmed that LINC00472 suppressed the phosphorylation of p65 and IkBalpha through binding to IKKbeta, inhibiting its phosphorylation. High LINC00472 expression inhibited tumor growth both in vitro and in vivo and suppressed aggressive tumor cell behaviors in vitro. Suppressing LINC00472 expression in ER-positive tumor cells increased cell aggressive behaviors. Tamoxifen treatment of ER-positive cells inhibited ERalpha and LINC00472 expression and increased p65 and IkBalpha phosphorylation. Meta-analysis showed that LINC00472 expression were higher in ER-positive than ER-negative tumors and that high expression was associated with better disease outcomes in ER-positive patients.Conclusions: The study demonstrates that ERalpha upregulates LINC00472 which suppresses the phosphorylation of NF-kB, and suggests that endocrine treatment may lower LINC00472 and increase NF-kB activities, leading to tumor progression and disease recurrence.Our experiments showed no changes in LINC00472 expression in relation to TNF-alpha, but NF-kB phosphorylation, a   downstream target of TNF-alpha, was suppressed by LINC00472  overexpression.	30830488	RID06546	interact with protein	recurrence		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	LINC00460	miR-320a	negatively-F		upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	Long noncoding RNA 00460 (LINC00460) promotes glioma progression by negatively regulating miR-320a.Objective: Long noncoding RNA 00460 (LINC00460) has been reported to contribute to tumorigenesis in multiple types of human malignancies. However, the biological role and the underlying molecular mechanism of LINC00460 in glioma remain unclear. The aim of this study was to investigate the clinical value, the biological function, and the potential mechanism of LINC00460 in glioma.Methods: The expression level of LINC00460 in glioma tissues and cell lines was examined by quantitative real-time polymerase chain reaction (qRT-PCR. Cell Counting Kit-8, flow cemetery, wound healing, and transwell invasion assays were used to explore the effect of LINC00460 on glioma cell proliferation, apoptosis, migration, and invasion. qRT-PCRand reporter assays were used to further verify the regulatory mechanism of LINC00460 in glioma progression.Results: LINC00460 expression was upregulated in glioma tissues and cell lines compared with non-tumor brain samples and astrocyte cell line (NHA), respectively. Moreover, increased LINC00460 expression was closely associated with glioma tumor grade. Loss-of-function assays revealed that knockdown of LINC00460 significantly inhibited glioma cell proliferation, induced cell apoptosis, and suppressed migration and invasion. The mechanistic assays disclosed that LINC00460 binded to miR-320a in a sequence-specific manner and regulated its expression. Moreover, miR-320 inhibition partially attenuated LINC00460 knockdown-mediated suppressive effects on glioma cell proliferation, migration, and invasion.Conclusion: These findings suggested that LINC00460 might function as an oncogenic lncRNA in glioma development and could be explored as a potential therapeutic target for glioma.	30825219	RID06547	transcriptional regulation	NA		
Colorectal cancer	HAGLR	HOXD3	negatively-E	RIP;RNA pull-down assay;ChIP	downregulation	RT-PCR	GSE8671;GSE21510;GSE32323;GSE41328;GSE23878;GSE9348;TCGA	NA	MAPK/AKT signaling pathway(+);cell growth(-);cell metastasis(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000128652	NA	401022	3232	HOXD-AS1|Mdgt|MIR7704HG	HOX1D|HOX4|HOX4A	Real-time PCR and in situ hybridization were used to detect the expression of HOXD-AS1 in CRC tissue samples and cell lines. Gain- and loss-of-function experiments were performed to investigate the biological roles of HOXD-AS1 in CRC cell line. RNA pull down, RNA immunoprecipitation and chromatin immunoprecipitation assays were conducted to investigate the mechanisms underlying the functions of HOXD-AS1 in CRC.Results: We observed that HOXD-AS1 was located in the nucleus of CRC cells and that nuclear HOXD-AS1 was downregulated in most CRC specimens and cell lines. Lower levels of nuclear HOXD-AS1 expression were associated with poor outcomes of CRC patients. HOXD-AS1 downregulation enhanced proliferation and migration of CRC cells in vitro and facilitated CRC tumourigenesis and metastasis in vivo. Mechanistic investigations revealed that HOXD-AS1 could suppress HOXD3 transcription by recruiting PRC2 to induce the accumulation of the repressive marker H3K27me3 at the HOXD3 promoter. Subsequently, HOXD3, as a transcriptional activator, promoted Integrin beta3 transcription, thereby activating the MAPK/AKT signalling pathways.Conclusion: Our results reveal a previously unrecognized HOXD-AS1-HOXD3-Integrin beta3 regulatory axis involving in epigenetic and transcriptional regulation constitutes to CRC carcinogenesisd progression.An inverse correlation between HOXD-AS1 and HOXD3 expression was observed  in our tissue samples (R = 0.435, P = 0.009, Fig. 3c). These  results suggest that HOXD-AS1 can inversely regulate  HOXD3, but not HOXD1, at the transcriptional level.	30823921	RID06548	epigenetic regulation	metastasis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	
Pancreatic cancer	RREB1	AGAP2-AS1	positively-E	RIP;ChIP;Jaspar;siRNA	upregulation	qRT-PCR;microarray	GSE16515	NA	cell proliferation(+);cell migration(+);cell invasion(+);prognosis	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000124782	NA	ENSG00000255737	GRCh38_12:57726271-57728356	6239	100130776	HNT	LOC100130776|PUNISHER	To verify the expression  results from the microarray, we determined the expression levels of AGAP2-AS1 in 46 pairs of PC and normal  tissues by quantitative real-time polymerase chain reaction (qRT-PCR..Long noncoding RNAs (lncRNAs) have been reported to be involved in a variety of human diseases, including cancers. However, their mechanisms have not yet been fully elucidated. We investigated lncRNA changes that may be associated with pancreatic cancer (PC) by analyzing published microarray data, and identified AGAP2-AS1 as a relatively overexpressed lncRNA in PC tissues. qRT-PCRassays were performed to examine expression levels of AGAP2-AS1. MTT assays, colony formation assays, and EdU assays were used to determine the proliferative capacity of cells. Flow cytometry and TUNEL assays were used to study the regulation of AGAP2-AS1 in the cell cycle and apoptosis. Transwell experiments were used to study changes in cell invasion and metastasis, and a nude mouse model was established to assess the effects of AGAP2-AS1 on tumorigenesis in vivo. RNA sequencing was performed to probe AGAP2-AS1-related pathways. Subcellular fractionation and FISH assays were used to determine the distribution of AGAP2-AS1 in PC cells, and RIP and ChIP were used to determine the molecular mechanism of AGAP2-AS1-mediated regulation of potential target genes. Increased expression of AGAP2-AS1 was associated with tumor size and pathological stage progression in patients with PC. RREB1 was found to activate transcription of AGAP2-AS1 in PC cells. AGAP2-AS1 affected proliferation, apoptosis, cycle arrest, invasion, and metastasis of PC cells in vitro, and AGAP2-AS1 regulated PC proliferation in vivo. Furthermore, AGAP2-AS1 epigenetically inhibited the expression of ANKRD1 and ANGPTL4 by recruiting zeste homolog 2 (EZH2), thereby promoting PC proliferation and metastasis. In summary, our data show that RREB1-induced upregulation of AGAP2-AS1 regulates cell proliferation and migration in PC partly through suppressing ANKRD1 and ANGPTL4 by recruiting EZH2. AGAP2-AS1 represents a potential target for the diagnosis and treatment of PC in the future.As shown in Fig. 2g,  the expression level of AGAP2-AS1 was positively correlated with the level of RREB1 in PC tissues.The results of chromatin immunoprecipitation (ChIP)  experiments showed that RREB1 could bind to the promoter region of AGAP2-AS1.	30814490	RID06549	transcriptional regulation	metastasis,prognosis	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	AGAP2-AS1	ANKRD1	negatively-E	knockdown;RIP;ChIP	upregulation	qRT-PCR;microarray	GSE16515	NA	cell proliferation(+);cell migration(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000148677	NA	100130776	27063	LOC100130776|PUNISHER	ALRP|C-193|CARP|CVARP|MCARP	To verify the expression  results from the microarray, we determined the expression levels of AGAP2-AS1 in 46 pairs of PC and normal  tissues by quantitative real-time polymerase chain reaction (qRT-PCR..Long noncoding RNAs (lncRNAs) have been reported to be involved in a variety of human diseases, including cancers. However, their mechanisms have not yet been fully elucidated. We investigated lncRNA changes that may be associated with pancreatic cancer (PC) by analyzing published microarray data, and identified AGAP2-AS1 as a relatively overexpressed lncRNA in PC tissues. qRT-PCRassays were performed to examine expression levels of AGAP2-AS1. MTT assays, colony formation assays, and EdU assays were used to determine the proliferative capacity of cells. Flow cytometry and TUNEL assays were used to study the regulation of AGAP2-AS1 in the cell cycle and apoptosis. Transwell experiments were used to study changes in cell invasion and metastasis, and a nude mouse model was established to assess the effects of AGAP2-AS1 on tumorigenesis in vivo. RNA sequencing was performed to probe AGAP2-AS1-related pathways. Subcellular fractionation and FISH assays were used to determine the distribution of AGAP2-AS1 in PC cells, and RIP and ChIP were used to determine the molecular mechanism of AGAP2-AS1-mediated regulation of potential target genes. Increased expression of AGAP2-AS1 was associated with tumor size and pathological stage progression in patients with PC. RREB1 was found to activate transcription of AGAP2-AS1 in PC cells. AGAP2-AS1 affected proliferation, apoptosis, cycle arrest, invasion, and metastasis of PC cells in vitro, and AGAP2-AS1 regulated PC proliferation in vivo. Furthermore, AGAP2-AS1 epigenetically inhibited the expression of ANKRD1 and ANGPTL4 by recruiting zeste homolog 2 (EZH2), thereby promoting PC proliferation and metastasis. In summary, our data show that RREB1-induced upregulation of AGAP2-AS1 regulates cell proliferation and migration in PC partly through suppressing ANKRD1 and ANGPTL4 by recruiting EZH2. AGAP2-AS1 represents a potential target for the diagnosis and treatment of PC in the future.	30814490	RID06550	epigenetic regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Pancreatic cancer	AGAP2-AS1	ANGPTL4	negatively-E	knockdown;RIP;ChIP	upregulation	qRT-PCR;microarray	GSE16515	NA	cell proliferation(+);cell migration(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000167772	NA	100130776	51129	LOC100130776|PUNISHER	ARP4|FIAF|HFARP|NL2|PGAR|pp1158	To verify the expression  results from the microarray, we determined the expression levels of AGAP2-AS1 in 46 pairs of PC and normal  tissues by quantitative real-time polymerase chain reaction (qRT-PCR..Long noncoding RNAs (lncRNAs) have been reported to be involved in a variety of human diseases, including cancers. However, their mechanisms have not yet been fully elucidated. We investigated lncRNA changes that may be associated with pancreatic cancer (PC) by analyzing published microarray data, and identified AGAP2-AS1 as a relatively overexpressed lncRNA in PC tissues. qRT-PCRassays were performed to examine expression levels of AGAP2-AS1. MTT assays, colony formation assays, and EdU assays were used to determine the proliferative capacity of cells. Flow cytometry and TUNEL assays were used to study the regulation of AGAP2-AS1 in the cell cycle and apoptosis. Transwell experiments were used to study changes in cell invasion and metastasis, and a nude mouse model was established to assess the effects of AGAP2-AS1 on tumorigenesis in vivo. RNA sequencing was performed to probe AGAP2-AS1-related pathways. Subcellular fractionation and FISH assays were used to determine the distribution of AGAP2-AS1 in PC cells, and RIP and ChIP were used to determine the molecular mechanism of AGAP2-AS1-mediated regulation of potential target genes. Increased expression of AGAP2-AS1 was associated with tumor size and pathological stage progression in patients with PC. RREB1 was found to activate transcription of AGAP2-AS1 in PC cells. AGAP2-AS1 affected proliferation, apoptosis, cycle arrest, invasion, and metastasis of PC cells in vitro, and AGAP2-AS1 regulated PC proliferation in vivo. Furthermore, AGAP2-AS1 epigenetically inhibited the expression of ANKRD1 and ANGPTL4 by recruiting zeste homolog 2 (EZH2), thereby promoting PC proliferation and metastasis. In summary, our data show that RREB1-induced upregulation of AGAP2-AS1 regulates cell proliferation and migration in PC partly through suppressing ANKRD1 and ANGPTL4 by recruiting EZH2. AGAP2-AS1 represents a potential target for the diagnosis and treatment of PC in the future.	30814490	RID06551	epigenetic regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Laryngeal squamous cell carcinoma	SOX2-OT	PTEN	negatively-E	RNA pull-down assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	epigenetic regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000171862	NA	347689	5728	DKFZp761J1324|NCRNA00043|SOX2OT	BZS|MHAM|MMAC1|PTEN1|TEP1	Long noncoding RNA SOX2-OT facilitates laryngeal squamous cell carcinoma development by epigenetically inhibiting PTEN via methyltransferase EZH2.Long noncoding RNAs (lncRNAs) play important roles in the initiation and progression of various cancers, including laryngeal squamous cell carcinoma (LSCC). Recently, lncRNA Sox2 overlapping transcript (SOX2-OT) has been identified as an oncogene in various cancers. However, the functional role and the regulatory mechanism of SOX2-OT in LSCC remains unclear. In this study, we found that SOX2-OT expression was increased and negatively correlated with PTEN expression in LSCC tissues. Furthermore, SOX2-OT overexpression promoted LSCC cell proliferation, migration, invasion, and suppressed cell apoptosis in vitro, as well as facilitated the in vivo tumorigenicity. By contrast, SOX2-OT silencing exerted the opposite effect. Mechanically, SOX2-OT interacted with EZH2 and recruited EZH2 to induce H3K27me3 and epigenetically inhibited PTEN expression in LSCC cells. Additionally, EZH2 silencing and PTEN overexpression significantly abrogated the SOX2-OT overexpression-mediated promotion of LSCC cell malignant behavior. Collectively, our findings demonstrate that SOX2-OT inhibits PTEN expression to facilitate LSCC development through EZH2-mediated H3K27me3. - 2019 IUBMB Life, 71(9):1230-1239, 2019.	30811870	RID06552	epigenetic regulation	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Gastric cancer	HOTAIR	STAT3	positively-E	luciferase reporter assay	upregulation	ISH	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-454-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168610	NA	100124700	6774	HOXC-AS4|HOXC11-AS1|NCRNA00072	APRF	To evaluate HOTAIR and miR-454-3p expression, we used ISH   assay.Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1.BACKGROUND Gastric cancer is a common gastrointestinal tumor. The incidence and mortality of gastric cancer are very high. Therefore, it is important to study targeted drugs. Recent studies found long chain non-coding RNA (lncRNAs) and microRNAs (miRNAs) were abnormal in gastric cancer. MATERIAL AND METHODS We collected adjacent normal and cancer tissues of gastric cancer patients and measured HOTAIR, miR-454-3p, STAT3, and Cyclin D1 expression and analyzed the correlation with clinical status. We also measured AGS and SGC7901 cells proliferation rate of different groups by MTT assay, and we evaluated AGS and SGC7901 cell apoptosis and cell cycle by flow cytometry. In addition, we assessed the relative proteins expressions by WB assay. Finally, we explored the correlation between miR-454-3p and STAT3 by use of double luciferase reporter. RESULTS lncRNA HOTAIR was negatively correlated with miR-454-3p expression in gastric cancer tissues. lncRNA HOTAIR knockdown suppressed AGS and SGC7901, which are gastric cancer cell lines that promote cell proliferation by increasing cell apoptosis and keeping the cell cycle in G1 phase. In further mechanism research, we found that the STAT3 and Cyclin D1 proteins expressions were suppressed by lncRNA HOTAIR down-regulation in AGS and SGC7901 cells. CONCLUSIONS Our results suggest that lncRNA HOTAIR knockdown stimulates miR-454-3p expression to inhibit gastric cancer growth by depressing STAT3/Cyclin D1 activity.	30810117	RID06553	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	HOTAIR	Cyclin D1	positively-E	luciferase reporter assay	upregulation	ISH	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-454-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	To evaluate HOTAIR and miR-454-3p expression, we used ISH   assay.Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1.BACKGROUND Gastric cancer is a common gastrointestinal tumor. The incidence and mortality of gastric cancer are very high. Therefore, it is important to study targeted drugs. Recent studies found long chain non-coding RNA (lncRNAs) and microRNAs (miRNAs) were abnormal in gastric cancer. MATERIAL AND METHODS We collected adjacent normal and cancer tissues of gastric cancer patients and measured HOTAIR, miR-454-3p, STAT3, and Cyclin D1 expression and analyzed the correlation with clinical status. We also measured AGS and SGC7901 cells proliferation rate of different groups by MTT assay, and we evaluated AGS and SGC7901 cell apoptosis and cell cycle by flow cytometry. In addition, we assessed the relative proteins expressions by WB assay. Finally, we explored the correlation between miR-454-3p and STAT3 by use of double luciferase reporter. RESULTS lncRNA HOTAIR was negatively correlated with miR-454-3p expression in gastric cancer tissues. lncRNA HOTAIR knockdown suppressed AGS and SGC7901, which are gastric cancer cell lines that promote cell proliferation by increasing cell apoptosis and keeping the cell cycle in G1 phase. In further mechanism research, we found that the STAT3 and Cyclin D1 proteins expressions were suppressed by lncRNA HOTAIR down-regulation in AGS and SGC7901 cells. CONCLUSIONS Our results suggest that lncRNA HOTAIR knockdown stimulates miR-454-3p expression to inhibit gastric cancer growth by depressing STAT3/Cyclin D1 activity.	30810117	RID06554	ceRNA or sponge	NA		
Oral squamous cell carcinoma	MEG3	SOCS5	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(-);apoptosis process(+)	ceRNA(miR-548d-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171150	NA	55384	9655	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	LncRNA MEG3 suppresses migration and promotes apoptosis by sponging miR-548d-3p to modulate JAK-STAT pathway in oral squamous cell carcinoma.Oral squamous cell carcinoma (OSCC) is a lethal malignancy and its prognosis remains dismal. Thus, a deeper understanding of the mechanisms is needed to provide a new insight for new therapies. It has been reported that long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was downregulated in OSCC tissues, however, its functional mechanism remains uncertain. Here, we found that the overexpression of MEG3 suppressed migration and promoted apoptosis in OSCC cell lines, while inhibition of MEG3 exhibited opposite effect. We also found that MEG3 could effectively sponge miR-548d-3p and decrease its expression level. Moreover, miR-548d-3p repressed the expression of SOCS5 and SOCS6 through binding their 3'UTR, thereby modulating the JAK-STAT signaling pathway and functioning as an oncogene in OSCC cells. Importantly, overexpression of MEG3 enhanced the expression of SOCS5 and SOCS6 to regulate JAK-STAT pathway, whereas miR-548d-3p overexpression decreased the effects of MEG3 on levels of SOCS5/SOCS6. Furthermore, upregulated expression of miR-548d-3p could abrogate the effect of MEG3 overexpression on migration and apoptosis in OSCC cell lines. In addition, the overexpression of MEG3 inhibited tumor migration and facilitated apoptosis in vivo. Together, our results revealed that MEG3 could modulate JAK-STAT pathway via miR-548d-3p/SOCS5/SOCS6 to suppresses migration and promote apoptosis in OSCC. Our research indexed a new functional mechanism of MEG3 in OSCC, and this mechanism may be a potential prognostic factor and therapeutic target. - 2019 IUBMB Life, 2019.	30809930	RID06555	ceRNA or sponge	prognosis		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Oral squamous cell carcinoma	MEG3	SOCS6	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(-);apoptosis process(+)	ceRNA(miR-548d-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000170677	NA	55384	9306	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CIS4|Cish4|HSPC060|SOCS4|SSI4|STAI4|STATI4	LncRNA MEG3 suppresses migration and promotes apoptosis by sponging miR-548d-3p to modulate JAK-STAT pathway in oral squamous cell carcinoma.Oral squamous cell carcinoma (OSCC) is a lethal malignancy and its prognosis remains dismal. Thus, a deeper understanding of the mechanisms is needed to provide a new insight for new therapies. It has been reported that long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was downregulated in OSCC tissues, however, its functional mechanism remains uncertain. Here, we found that the overexpression of MEG3 suppressed migration and promoted apoptosis in OSCC cell lines, while inhibition of MEG3 exhibited opposite effect. We also found that MEG3 could effectively sponge miR-548d-3p and decrease its expression level. Moreover, miR-548d-3p repressed the expression of SOCS5 and SOCS6 through binding their 3'UTR, thereby modulating the JAK-STAT signaling pathway and functioning as an oncogene in OSCC cells. Importantly, overexpression of MEG3 enhanced the expression of SOCS5 and SOCS6 to regulate JAK-STAT pathway, whereas miR-548d-3p overexpression decreased the effects of MEG3 on levels of SOCS5/SOCS6. Furthermore, upregulated expression of miR-548d-3p could abrogate the effect of MEG3 overexpression on migration and apoptosis in OSCC cell lines. In addition, the overexpression of MEG3 inhibited tumor migration and facilitated apoptosis in vivo. Together, our results revealed that MEG3 could modulate JAK-STAT pathway via miR-548d-3p/SOCS5/SOCS6 to suppresses migration and promote apoptosis in OSCC. Our research indexed a new functional mechanism of MEG3 in OSCC, and this mechanism may be a potential prognostic factor and therapeutic target. - 2019 IUBMB Life, 2019.	30809930	RID06556	ceRNA or sponge	prognosis		UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Prostate cancer	HOTTIP	CTNNB1	positively-E		upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(-);cell cycle(-);cell proliferation(+);chemosensitivity(-)	transcriptional regulation	association	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Knockdown of the long noncoding RNA HOTTIP inhibits cell proliferation and enhances cell sensitivity to cisplatin by suppressing the Wnt/beta-catenin pathway in prostate cancer.Background: Prostate cancer (PCa) is a prevalent and deadly cancer worldwide. Considering the malignant progression and therapeutic resistance of PCa, further dissection of the underlying mechanisms and exploration of novel therapeutic targets for PCa are urgently needed. The long noncoding RNA HOTTIP has recently been revealed as an oncogenic regulator in different cancers; however, whether HOTTIP is involved in PCa remains poorly understood. Here, we examined the crucial roles of HOTTIP in the proliferation and chemoresistance of PCa.Methods: Quantitative real-time PCR (qRT-PCR was performed to detect the HOTTIP messenger RNA (mRNA) levels in PCa samples from patients and PCa cells. Then, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and cell cycle and flow cytometry assays were performed to investigate the proliferation and cisplatin-resistance of PCa cells with silenced HOTTIP compared with a negative control. We applied western blot, qRT-PCRand a TOP/FOP assay to explore the relevant mechanisms.Results: In this study, we found that the HOTTIP mRNA levels were increased in the PCa patient samples and PCa cell lines compared with the controls. The knockdown of HOTTIP not only inhibited the proliferation of PCa cells but also facilitated cell cycle arrest and chemosensitivity to cisplatin. Furthermore, the qRT-PCR western blot, TOP/FOP assays, MTT assay, and flow cytometry revealed that Wnt/beta-catenin signaling was related to the regulation of HOTTIP in cell proliferation, cell cycle arrest, and chemoresistance to cisplatin in PCa.Conclusion: Taken together, our findings suggest that HOTTIP may be a potent therapeutic target for PCa, and HOTTIP inhibitors might be regarded as effective strategies for PCa therapy.	30809864	RID06557	transcriptional regulation	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	LINC01554	PKM	negatively-E	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(-);tumorigenesis(-)	ubiquitination	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236882	GRCh38_5:95838245-95860133	ENSG00000067225	NA	202299	5315	C5orf27|FIS|FLJ38821	OIP3|PK3|PKM2|THBP1	LINC01554-Mediated Glucose Metabolism Reprogramming Suppresses Tumorigenicity in Hepatocellular Carcinoma via Downregulating PKM2 Expression and Inhibiting Akt/mTOR Signaling Pathway.Background and Aims: Cancer cells prefer aerobic glycolysis to maintain growth advantages, but the role of long non-coding RNAs (lncRNAs) in glycometabolism still remains unclear. Here we identified one cytoplasmic lncRNA LINC01554 as a significantly downregulated lncRNA in hepatocellular carcinoma (HCC) and aimed to investigate its role in cellular glucose metabolism in the development and progression of HCC. Methods: Quantitative real-time PCR was used to determine the expression level of LINC01554. Downregulation of LINC01554 by miR-365a at transcriptional level was assessed by luciferase reporter assay. Subcellular fractionation assay and RNA fluorescence in situ hybridization were performed to detect the subcellular localization of LINC01554. RNA pull-down assay, mass spectrometry, and RNA immunoprecipitation assay were used to identify the underlying molecular mechanisms. The tumor-suppressive function of LINC01554 was determined by both in vitro assay and nude mice xenograft model. Results: LINC01554 was frequently downregulated in HCC, which was significantly associated with tumor invasion (P = 0.005), tumor size (P = 0.041), tumor staging (P = 0.023) and shorter survival (P = 0.035) of HCC patients. Luciferase reporter assay unraveled that LINC01554 was negatively regulated by miR-365a. Subcellular fractionation assay and RNA FISH revealed the cytoplasmic predominance of LINC01554 in MIHA cells and HCC clinical samples. Ectopic expression of LINC01554 inhibited HCC cell growth, colony formation in soft agar, foci formation, and tumor formation in nude mice. LINC01554 promoted the ubiquitin-mediated degradation of PKM2 and inhibited Akt/mTOR signaling pathway to abolish aerobic glycolysis in HCC cells. Further study found that LINC01554-knockout could effectively reverse the tumor-suppressive effect of LINC01554. Conclusions: Our results identify LINC01554 as a novel tumor suppressor in HCC and unravel its underlying molecular mechanism in reprogramming cellular glucose metabolism. LINC01554 could possibly serve as a novel prognostic biomarker and provide the rationale for HCC therapy.To further validate the negative regulation   role of LINC01554 on PKM2, LINC01554 mRNA levels  and PKM2 protein levels were measured in 11 pairs of   HCC tissues and corresponding non-tumor tissues.	30809309	RID06558	epigenetic regulation	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MIR365A	LINC01554	negatively-E	TargetScan;miRanda;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	AKT/mTOR signaling pathway(-);tumorigenesis(-)	NA	association	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	ENSG00000199130	NA	ENSG00000236882	GRCh38_5:95838245-95860133	100126355	202299	MIR365-1|MIRN365-1|hsa-mir-365a|mir-365a	C5orf27|FIS	By exploring   two bioinformatic databases, TargetScanand miRanda, we found miR-365a-3p was a putative   miRNA targeting LINC01554 (Figure S3D).Cancer cells prefer aerobic glycolysis to maintain growth advantages, but the role of long non-coding RNAs (lncRNAs) in glycometabolism still remains unclear. Here we identified one cytoplasmic lncRNA LINC01554 as a significantly downregulated lncRNA in hepatocellular carcinoma (HCC) and aimed to investigate its role in cellular glucose metabolism in the development and progression of HCC. Methods: Quantitative real-time PCR was used to determine the expression level of LINC01554. Downregulation of LINC01554 by miR-365a at transcriptional level was assessed by luciferase reporter assay. Subcellular fractionation assay and RNA fluorescence in situ hybridization were performed to detect the subcellular localization of LINC01554. RNA pull-down assay, mass spectrometry, and RNA immunoprecipitation assay were used to identify the underlying molecular mechanisms. The tumor-suppressive function of LINC01554 was determined by both in vitro assay and nude mice xenograft model. Results: LINC01554 was frequently downregulated in HCC, which was significantly associated with tumor invasion (P = 0.005), tumor size (P = 0.041), tumor staging (P = 0.023) and shorter survival (P = 0.035) of HCC patients. Luciferase reporter assay unraveled that LINC01554 was negatively regulated by miR-365a. Subcellular fractionation assay and RNA FISH revealed the cytoplasmic predominance of LINC01554 in MIHA cells and HCC clinical samples. Ectopic expression of LINC01554 inhibited HCC cell growth, colony formation in soft agar, foci formation, and tumor formation in nude mice. LINC01554 promoted the ubiquitin-mediated degradation of PKM2 and inhibited Akt/mTOR signaling pathway to abolish aerobic glycolysis in HCC cells. Further study found that LINC01554-knockout could effectively reverse the tumor-suppressive effect of LINC01554. Conclusions: Our results identify LINC01554 as a novel tumor suppressor in HCC and unravel its underlying molecular mechanism in reprogramming cellular glucose metabolism. LINC01554 could possibly serve as a novel prognostic biomarker and provide the rationale for HCC therapy.	30809309	RID06559	expression association	prognosis		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Liver cancer	DLX6-AS1	WEE1	positively-E	dual-luciferase reporter analysis;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-424-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000166483	NA	285987	7465	Evf-2|FLJ34048|NCRNA00212	WEE1A	Long noncoding RNA DLX6-AS1 promotes liver cancer by increasing the expression of WEE1 via targeting miR-424-5p.Long noncoding RNAs (lncRNAs) played an important role in tumorigenesis and development of hepatocellular carcinoma (HCC). In this study, we first demonstrated that lncRNA DLX6 antisense RNA 1 (DLX6-AS1) was upregulated in cancer tissues and cells lines compared with normal adjacent and cell line. Knock-down DLX6-AS1 by transfection with small interfering RNA (siRNA) suppressed cell proliferation, migration, and invasion of HCC cells. Cell cycle analysis showed that cells transfected with siRNA were arrested in G0/G1 phase. Then, we performed dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay to show that DLX6-AS1 could bind with miR-424-5p. And cotransfection inhibitor of miR-424-5p with siRNA of DLX6-AS1 could abolish the inhibitory effect of siRNA of DLX6-AS1 on cell proliferation, migration, and invasion. Moreover, we further demonstrated that the oncogene WEE1 G2 checkpoint kinase (WEE1) was the target of miR-424-5p and expression levels of WEE1 were positive correlation with that of DLX6-AS1. Taken together, these results suggested that upregulated DLX6-AS1 promoted cell proliferation, migration, and invasion of HCC through increasing expression of WEE1 via targeting miR-424-5p.	30805988	RID06560	ceRNA or sponge	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Pancreatic cancer	LINC02041	Jagged-1	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-);chemoresistance(-)	NA	association	RNA-protein	Gemcitabine	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228952	GRCh38_3:187448845-187449450	NA	NA	105374261	NA	RP11-567G11.1	NA	Depletion of the lncRNA RP11-567G11.1 inhibits pancreatic cancer progression.Methods: We evaluated the expression of RP11-567G11.1 in pancreatic cancer tissues via in situ hybridization. We also constructed RP11-567G11.1 knockdown cell models and used CCK8 and flow cytometry to detect the function of this lncRNA. western blot and qPCR were used to detect the expression levels of factors related to RP11-567G11.1.Results: The results illustrated that RP11-567G11.1 was significantly up-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues. Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, suppressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. Also depletion of RP11-567G11.1 in pancreatic cancer cells inhibited factors downstream of the NOTCH signaling pathway.Conclusion: RP11-567G11.1 plays a crucial role in pancreatic cancer. Importantly, depletion of RP11-567G11.1 boosts the sensitivity of pancreatic cancer cells to gemcitabine, suggesting that this lncRNA is a promising target for pancreatic cancer treatment.	30802827	RID06561	expression association	chemoresistance		
Pancreatic cancer	LINC02041	HES1	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-);chemoresistance(-)	NA	association	NA	Gemcitabine	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000228952	GRCh38_3:187448845-187449450	ENSG00000114315	NA	105374261	3280	RP11-567G11.1	bHLHb39|FLJ20408|HES-1|HRY	Depletion of the lncRNA RP11-567G11.1 inhibits pancreatic cancer progression.Methods: We evaluated the expression of RP11-567G11.1 in pancreatic cancer tissues via in situ hybridization. We also constructed RP11-567G11.1 knockdown cell models and used CCK8 and flow cytometry to detect the function of this lncRNA. western blot and qPCR were used to detect the expression levels of factors related to RP11-567G11.1.Results: The results illustrated that RP11-567G11.1 was significantly up-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues. Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, suppressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. Also depletion of RP11-567G11.1 in pancreatic cancer cells inhibited factors downstream of the NOTCH signaling pathway.Conclusion: RP11-567G11.1 plays a crucial role in pancreatic cancer. Importantly, depletion of RP11-567G11.1 boosts the sensitivity of pancreatic cancer cells to gemcitabine, suggesting that this lncRNA is a promising target for pancreatic cancer treatment.	30802827	RID06562	expression association	chemoresistance		UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Pancreatic cancer	LINC02041	HES5	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-);chemoresistance(-)	NA	association	NA	Gemcitabine	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000228952	GRCh38_3:187448845-187449450	ENSG00000197921	NA	105374261	388585	RP11-567G11.1	bHLHb38	Depletion of the lncRNA RP11-567G11.1 inhibits pancreatic cancer progression.Methods: We evaluated the expression of RP11-567G11.1 in pancreatic cancer tissues via in situ hybridization. We also constructed RP11-567G11.1 knockdown cell models and used CCK8 and flow cytometry to detect the function of this lncRNA. western blot and qPCR were used to detect the expression levels of factors related to RP11-567G11.1.Results: The results illustrated that RP11-567G11.1 was significantly up-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues. Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, suppressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. Also depletion of RP11-567G11.1 in pancreatic cancer cells inhibited factors downstream of the NOTCH signaling pathway.Conclusion: RP11-567G11.1 plays a crucial role in pancreatic cancer. Importantly, depletion of RP11-567G11.1 boosts the sensitivity of pancreatic cancer cells to gemcitabine, suggesting that this lncRNA is a promising target for pancreatic cancer treatment.	30802827	RID06563	expression association	chemoresistance		
Pancreatic cancer	LINC02041	ATOH1	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-);chemoresistance(-)	NA	association	NA	Gemcitabine	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000228952	GRCh38_3:187448845-187449450	ENSG00000172238	NA	105374261	474	RP11-567G11.1	bHLHa14|HATH1|MATH-1|Math1	Depletion of the lncRNA RP11-567G11.1 inhibits pancreatic cancer progression.Methods: We evaluated the expression of RP11-567G11.1 in pancreatic cancer tissues via in situ hybridization. We also constructed RP11-567G11.1 knockdown cell models and used CCK8 and flow cytometry to detect the function of this lncRNA. western blot and qPCR were used to detect the expression levels of factors related to RP11-567G11.1.Results: The results illustrated that RP11-567G11.1 was significantly up-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues. Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, suppressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. Also depletion of RP11-567G11.1 in pancreatic cancer cells inhibited factors downstream of the NOTCH signaling pathway.Conclusion: RP11-567G11.1 plays a crucial role in pancreatic cancer. Importantly, depletion of RP11-567G11.1 boosts the sensitivity of pancreatic cancer cells to gemcitabine, suggesting that this lncRNA is a promising target for pancreatic cancer treatment.	30802827	RID06564	expression association	chemoresistance		
Colorectal cancer	SUMO1P3	CPEB3	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	epigenetic regulation	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000235082	GRCh38_1:160317403-160317706	ENSG00000107864	NA	474338	22849	NA	KIAA0940	LncRNA SUMO1P3 promotes proliferation and inhibits apoptosis in colorectal cancer by epigenetically silencing CPEB3.Colorectal cancer (CRC) is a prevalent malignancy characterized with high morbidity and death rate. Due to late diagnosis, most CRC patients missed the proper timing for radical operation, which led to the high mortality in CRC. Therefore, identifying new prognostic and therapeutic targets is important. Long non-coding RNAs are reported as essential regulators for tumor progression, including in CRC. LncRNA SUMO1P3 has been documented as an oncogene promoting proliferation, cell cycle, and metastasis in several cancers, but its role in CRC has never been unveiled. The purpose of our study is to interrogate the functions and mechanism of SUMO1P3 in colorectal cancer. We validated the upregulation and the prognostic significance of SUMO1P3 in CRC. The loss-of-function assays suggested that SUMO1P3 provoked CRC cell proliferative ability, and retarded apoptotic ability. Cytoplasmic polyadenylation element binding protein 3 (CPEB3) has been newly acknowledged as a tumor suppressive gene in several cancers, and has been revealed to present low expression in CRC. We predicted through UCSC database and validated by ChIP assay that EZH2, a crucial regulator of trimethylation of histone H3 at lysine 27 (H3K27me3), bound to CPEB3 promoter. Further, we validated that SUMO1P3 epigenetically repressed CPEB3 through EZH2. Finally, rescue assays indicated that SUMO1P3 provoked proliferation, cell cycle, and retarded apoptosis through CPEB3. Consequently, current study showed that lncRNA SUMO1P3 promoted cell proliferative ability and inhibited apoptotic ability in CRC by epigenetically silencing CPEB3, providing a novel prognostic marker for CRC patients.ChIP assay validated that CPEB3 promoter  was abundant in the precipitates of anti-EZH2, indicating the  binding of EZH2 to CPEB3 promoter (Fig. 3E).  Also, RIP assay further  validated the interaction between SUMO1P3 and EZH2 (Fig. 3F).	30799082	RID06565	epigenetic regulation	metastasis,prognosis	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)	
Gastric cancer	SLC25A5-AS1	PTEN	positively-E	dual-luciferase reporter analysis;Targetscan;miRanda	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	ceRNA(miR-19a-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000224281	GRCh38_X:119465986-119469128	ENSG00000171862	NA	100303728	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Down-regulated lncRNA SLC25A5-AS1 facilitates cell growth and inhibits apoptosis via miR-19a-3p/PTEN/PI3K/AKT signalling pathway in gastric cancer.Mounting evidence has illustrated the vital roles of long non-coding RNAs (lncRNAs in gastric cancer (GC). Nevertheless, the majority of their roles and mechanisms in GC are still largely unknown. In this study, we investigate the roles of lncRNA SLC25A5-AS1 on tumourigenesis and explore its potential mechanisms in GC. The results showed that the expressions of SLC25A5-AS1 in GC were significantly lower than that of adjacent normal tissues, which were significantly associated with tumour size, TNM stage and lymph node metastasis. Moreover, SLC25A5-AS1 could inhibit GC cell proliferation, induce G1/G1 cell cycle arrest and cell apoptosis in vitro, as well as GC growth in vivo. dual-luciferase reporter assay confirmed the direct interaction between SLC25A5-AS1 and miR-19a-3p, rescue experiment showed that co-transfection miR-19a-3p mimics and pcDNA-SLC25A5-AS1 could partially restore the ability of GC cell proliferation and the inhibition of cell apoptosis. The mechanism analyses further found that SLC25A5-AS1 might act as a competing endogenous RNAs (ceRNA), which was involved in the derepression of PTEN expression, a target gene of miR-19a-3p, and regulate malignant phenotype via PI3K/AKT signalling pathway in GC. Taken together, this study indicated that SLC25A5-AS1 was down-regulated in GC and functioned as a suppressor in the progression of GC. Moreover, it could act as a ceRNA to regulate cellular behaviours via miR-19a-3p/PTEN/PI3K/AKT signalling pathway. Thus, SLC25A5-AS1 might be served as a potential target for cancer therapeutics in GC.SLC25A5 AS1 inhibits cell growth and   promotes apoptosis via miR 19a 3p  PTEN/PI3K/AKT   signalling pathway.	30793479	RID06566	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Breast cancer	LINC00968	WNT2	negatively-E	luciferase reporter assay;RIP;western blot	downregulation	qPCR	GSE26910	NA	WNT2/beta-catenin signaling pathway(-);chemosensitivity(+);prognosis	transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000246430	GRCh38_8:56494923-56559823	ENSG00000105989	NA	100507632	7472	NA	INT1L1|IRP	Long non-coding RNA LINC00968 attenuates drug resistance of breast cancer cells through inhibiting the Wnt2/beta-catenin signaling pathway by regulating WNT2.Background: Breast cancer is one the most common cancers, making it the second leading cause of cancer-related death among women. Long non-coding RNAs (lncRNAs), with tightly regulated expression patterns, also serve as tumor suppressor during tumorigenesis. The present study aimed to elucidate the role of LINC00968 in breast cancer via WNT2-mediated Wnt2/beta-catenin signaling pathway.Methods: Breast cancer chip GSE26910 was utilized to identify differential expression in LINC00968 and WNT2. The possible relationship among LINC00968, transcriptional repressor HEY and WNT2 was analyzed and then verified. Effects of LINC00968 on activation of the Wnt2/beta-catenin signaling pathway was also tested. Drug resistance, colony formation, cell migration, invasion ability and cell apoptosis after transfection were also determined. Furthermore, tumor xenograft in nude mice was performed to test tumor growth and weight in vivo.Results: WNT2 expression exhibited at a high level, whereas LINC00968 at a low expression in breast cancer which was also associated with poor prognosis in patients. LINC00968 targeted and negatively regulated WNT2 potentially via HEY1. Either overexpressed LINC00968 or silenced inhibited activation of the Wnt2/beta-catenin signaling pathway, thereby reducing drug resistance, decreasing colony formation ability, as well as suppressing migration and invasion abilities of breast cancer cells in addition to inducing apoptosis. Lastly, in vivo experiment suggested that LINC00968 overexpression also suppressed transplanted tumor growth in nude mice.Conclusion: Collectively, overexpressed LINC00968 contributes to reduced drug resistance in breast cancer cells by inhibiting the activation of the Wnt2/beta-catenin signaling pathway through silencing WNT2. This study offers a new target for the development of breast cancer treatment.	30791958	RID06567	transcriptional regulation	prognosis,chemoresistance	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Breast cancer	MT1JP	miR-24-3p	negatively-F	dual-luciferase reporter analysis	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell growth(-);chemosensitivity(+);WNT/beta-catenin signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000255986	GRCh38_16:56635739-56637086	NA	NA	4498	NA	MT1|MT1J|MT1NP|MTB	NA	To investigate the role of MT1JP in breast   cancer, we first used qRT-PCRto examine   the relative expression of MT1JP in 56 paired   samples of breast cancer tissues and adjacent   non-tumor tissues.MT1JP inhibits tumorigenesis and enhances cisplatin sensitivity of breast cancer cells through competitively binding to miR-24-3p.Accumulating evidence indicates that long non-coding RNAs (lncRNAs) play a key role in the development of many human cancers. MT1JP is a lncRNA that is reportedly involved in gastric cancer development, but a biological role and mechanism for MT1JP in breast cancer is unknown. Here, we found that MT1JP expression was significantly down-regulated in breast cancer tissues and cell lines, and that decreased MT1JP expression was associated with breast cancer progression and poor survival of breast cancer patients. Additionally, we found that overexpression of MT1JP in breast cancer cells significantly inhibited cell proliferation and invasion, and also enhanced the cisplatin sensitivity of breast cancer cells. We then investigated a possible mechanism for these results, finding that MT1JP binds to and negatively regulates miR-24-3p, which is known to be an oncogene in some human cancers. Our rescue experiments showed that the tumor suppressive and cisplatin-sensitizing functions of MT1JP were mediated by negative regulation of miR-24-3p. Finally, western blot results showed that MT1JP inhibited the Wnt/beta-catenin signaling pathway. Collectively, our data indicate that MT1JP functions as an anti-tumor lncRNA, enhances cisplatin sensitivity in breast cancer, and may serve as a novel diagnostic and therapeutic marker of breast cancer.The dual-luciferase reporter assay   confirmed the relationship between MT1JP and   miR-24-3p.In addition,   we examined miR-24-3p expression in 56   paired samples of breast cancer tissue and   adjacent normal tissue by qRT-PCRand found   that miR-24-3p expression was significantly   higher in breast cancer tissues than in adjacent   normal tissues (Figure 5D). Furthermore, the   expression of miR-24-3p was negatively associated with MT1JP expression in breast cancer   tissues (Figure 5E). These data strongly suggest that MT1JP targets and negatively regulates miR-24-3p expression in breast cancer   tissues.	30787983	RID06568	ceRNA or sponge	chemoresistance		
Pancreatic cancer	TUG1	MT2A	negatively-E	RIP;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000125148	NA	55000	4502	FLJ20618|LINC00080|NCRNA00080	MT2	Overexpressed long noncoding RNA TUG1 affects the cell cycle, proliferation, and apoptosis of pancreatic cancer partly through suppressing RND3 and MT2A.Background: Long noncoding RNAs (lncRNAs) are involved in various human diseases, including cancers. However, their mechanisms remain undocumented. We investigated alterations in lncRNA that may be related to pancreatic cancer (PC) through analysis of microarray data.Methods: In the present study, quantitative real-time PCR analysis was used to examine the expression of taurine upregulated 1 (TUG1) in PC tissue samples and PC cell lines. In PC cell lines, MTT assays, colony formation assays, and flow cytometry were used to investigate the effects of TUG1 on proliferation, cell cycle regulation, and apoptosis. Moreover, we established a xenograft model to assess the effect of TUG1 on tumor growth in vivo. The molecular mechanism of potential target genes was detected through nuclear separation experiments, RNA immunoprecipitation (RIP), chromatin immunoprecipitation assays (ChIP), and other experimental methods.Results: The findings suggest that the abnormally high expression of TUG1 in PC tissues was associated with tumor size and pathological stage. Knockdown of TUG1 blocked the cell cycle and accelerated apoptosis, thereby inhibiting the proliferation of PC cells. In addition, RIP experiments showed that TUG1 can recruit enhancer of zeste homolog 2 (EZH2) to the promoter regions of Rho family GTPase 3 (RND3) and metallothionein 2A (MT2A) and inhibit their expression at the transcriptional level. Furthermore, ChIP experiments demonstrated that EZH2 could bind to the promoter regions of RND3 and MT2A. The knockdown of TUG1 reduced this binding capacity.Conclusion: In conclusion, our data suggest that TUG1 may regulate the expression of PC-associated tumor suppressor genes at the transcriptional level and these may become potential targets for the diagnosis and treatment of PC.	30787623	RID06569	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PAAD,BRCA);UP(PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE86978)
Pancreatic cancer	TUG1	RND3	negatively-E	RIP;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000115963	NA	55000	390	FLJ20618|LINC00080|NCRNA00080	ARHE|Rho8|RhoE	Overexpressed long noncoding RNA TUG1 affects the cell cycle, proliferation, and apoptosis of pancreatic cancer partly through suppressing RND3 and MT2A.Background: Long noncoding RNAs (lncRNAs) are involved in various human diseases, including cancers. However, their mechanisms remain undocumented. We investigated alterations in lncRNA that may be related to pancreatic cancer (PC) through analysis of microarray data.Methods: In the present study, quantitative real-time PCR analysis was used to examine the expression of taurine upregulated 1 (TUG1) in PC tissue samples and PC cell lines. In PC cell lines, MTT assays, colony formation assays, and flow cytometry were used to investigate the effects of TUG1 on proliferation, cell cycle regulation, and apoptosis. Moreover, we established a xenograft model to assess the effect of TUG1 on tumor growth in vivo. The molecular mechanism of potential target genes was detected through nuclear separation experiments, RNA immunoprecipitation (RIP), chromatin immunoprecipitation assays (ChIP), and other experimental methods.Results: The findings suggest that the abnormally high expression of TUG1 in PC tissues was associated with tumor size and pathological stage. Knockdown of TUG1 blocked the cell cycle and accelerated apoptosis, thereby inhibiting the proliferation of PC cells. In addition, RIP experiments showed that TUG1 can recruit enhancer of zeste homolog 2 (EZH2) to the promoter regions of Rho family GTPase 3 (RND3) and metallothionein 2A (MT2A) and inhibit their expression at the transcriptional level. Furthermore, ChIP experiments demonstrated that EZH2 could bind to the promoter regions of RND3 and MT2A. The knockdown of TUG1 reduced this binding capacity.Conclusion: In conclusion, our data suggest that TUG1 may regulate the expression of PC-associated tumor suppressor genes at the transcriptional level and these may become potential targets for the diagnosis and treatment of PC.	30787623	RID06570	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065,GSE55807)
Glioblastoma	HOXB-AS1	HOXB2	positively-E	bioinformatics;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-885-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000230148	GRCh38_17:48543551-48551250	ENSG00000173917	NA	100874362	3212	NA	HOX2|HOX2H	Long non-coding RNA HOXB-AS1 promotes proliferation, migration and invasion of glioblastoma cells via HOXB-AS1/miR-885-3p/HOXB2 axis.Long non-coding RNAs (lncRNAs) have been proved to play important roles in carcinogenesis and development of numerous cancers, but their biological functions in glioblastoma remain largely unknown. In this study, we found HOXB-AS1 was highly expressed in human glioblastoma tissues and cell lines, and was associated with survival time of patients. Our results showed HOXB-AS1 knockdown inhibited proliferation via inducing S phase cell cycle arrest, and suppressed migration ability of cells. In terms of mechanism, HOXB-AS1 were mainly located in cytoplasm and functioned as ceRNA via sponging of miR-885-3p. We proved inhibition of miR-885-3p antagonized the effects of HOXB-AS1 konckdown and promoted the proliferation and migration of glioblastoma. Finally, we found the sponging of miR-885-3p by HOXB-AS1 could further affecting the expression of HOXB2. Taken together, we demonstrated that HOXB-AS1/miR-885-3p/HOXB2 axis could regulate the proliferation and migration of glioblastoma, which could serve as a potential biomarker for glioblastoma patients.HOXB-AS1 was   one of the most significantly up-regulated lncRNAs.Further bioinformatic analysis found a potential binding site of miR-885-3p   on HOXB-AS1 sequence (Figure 4B).As shown in   Figure 4D, the luciferase reporter assay revealed the directly   target of miR-885-3p on HOXB-AS1, as the relative luciferase   activity was remarkably decreased by miR-885-3p in Wt   group and showed no obviously change in Mut group.	30784279	RID06571	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827)	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE111065)
Non-small cell lung cancer	SNHG20	ZEB2	positively-E	luciferase reporter assay;starBase v2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-154)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000169554	NA	654434	9839	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	KIAA0569|SIP-1|SIP1|ZFHX1B	SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge.Long noncoding RNAs (LncRNAs) play critical roles in the development and progression of cancers. However, little is known about the function and mechanism of lncRNAs in non-small cell lung cancer (NSCLC). In this study, we investigated the expression and functional role of lncRNA small nucleolar RNA host gene 20 (SNHG20) as well as its underlying mechanism in NSCLC. Our results showed that SNHG20 was significantly up-regulated in NSCLC tissues and cells. High SNHG20 expression was implicated with poor prognosis in NSCLC patients. Moreover, SNHG20 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NSCLC cells. Furthermore, SNHG20 could function as a competing endogenous RNA (ceRNA) to elevate ZEB2 and RUNX2 expression by sponging miR-154. Rescue assays revealed that miR-154 inhibition could reverse the inhibitory effect of SNHG20 silence on proliferation, migration and invasion in NSCLC cells. More importantly, SNHG20 knockdown suppressed tumor growth in NSCLC in vivo through suppressing miR-154 and elevating ZEB2 and RUNX2 expression. In summary, knockdown of lncRNA SNHG20 suppressed proliferation, migration and invasion, and promotes apoptosis through up-regulating ZEB2 and RUNX2 expression by sponging miR-154 in NSCLC, providing a promising therapeutic target for NSCLC patients.	30780105	RID06572	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	SNHG20	RUNX2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-154)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124813	NA	654434	860	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge.Long noncoding RNAs (LncRNAs) play critical roles in the development and progression of cancers. However, little is known about the function and mechanism of lncRNAs in non-small cell lung cancer (NSCLC). In this study, we investigated the expression and functional role of lncRNA small nucleolar RNA host gene 20 (SNHG20) as well as its underlying mechanism in NSCLC. Our results showed that SNHG20 was significantly up-regulated in NSCLC tissues and cells. High SNHG20 expression was implicated with poor prognosis in NSCLC patients. Moreover, SNHG20 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NSCLC cells. Furthermore, SNHG20 could function as a competing endogenous RNA (ceRNA) to elevate ZEB2 and RUNX2 expression by sponging miR-154. Rescue assays revealed that miR-154 inhibition could reverse the inhibitory effect of SNHG20 silence on proliferation, migration and invasion in NSCLC cells. More importantly, SNHG20 knockdown suppressed tumor growth in NSCLC in vivo through suppressing miR-154 and elevating ZEB2 and RUNX2 expression. In summary, knockdown of lncRNA SNHG20 suppressed proliferation, migration and invasion, and promotes apoptosis through up-regulating ZEB2 and RUNX2 expression by sponging miR-154 in NSCLC, providing a promising therapeutic target for NSCLC patients.	30780105	RID06573	ceRNA or sponge	prognosis	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	FGF13-AS1	IGF2BPs	interact	RIP;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	prognosis;cell proliferation(-);cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226031	GRCh38_X:138711452-138716617	NA	NA	100129662	NA	NA	NA	Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1/IGF2BPs/Myc feedback loop.LncRNAs have been proven to play crucial roles in various processes of breast cancer. LncRNA FGF13-AS1 has been identified as one of the 25 downregulated lncRNAs in breast cancer through analyzing data from two cohorts and TCGA by another group of our lab. In this study, we report that FGF13-AS1 expression is decreased in breast cancer tissue compared with corresponding normal tissue, and the downregulation of FGF13-AS1 is associated with poor prognosis. Functional studies show that FGF13-AS1 inhibits breast cancer cells proliferation, migration, and invasion by impairing glycolysis and stemness properties. Mechanistically, FGF13-AS1 reduces the half-life of c-Myc (Myc) mRNA by binding RNA-binding proteins, insulin-like growth factor 2 mRNA binding proteins (IGF2BPs) and disrupting the interaction between IGF2BPs and Myc mRNA. Furthermore, Myc transcriptionally inhibits FGF13-AS1, forming a feedback loop in this signaling pathway. These results reveal for the first time that FGF13-AS1 functions as a tumor suppressor by inhibiting glycolysis and stemness properties of breast cancer cells, and the FGF13-AS1/IGF2BPs/Myc feedback loop could be a novel therapeutic target for breast cancer patients.Therefore, we speculated that FGF13-  AS1 might bind IGF2BPs and disrupt the interaction between IGF2BPs  and Myc mRNA.  To test this idea, we performed RNA immunoprecipitation (RIP) assays using IGF2BP1 antibody in MDA-MB-  231 and MCF-7 cells.  We observed a marked enrichment of FGF13-AS1  pulled down by IGF2BP1 antibody compared with the IgG control antibody (Fig. 5b).  Of note, Myc mRNA was also observed, which was  consistent with previous studies.  We next performed RNA pull-down  assays to further confirm the interaction between IGF2BP1 and FGF13-  AS1.  As indicated in Fig. 5c, an enhancement of IGF2BP1 was found in  the presence of FGF13-AS1, but not the antisense RNA.  These results  indicate a specific interaction between FGF13-AS1 and IGF2BP proteins.	30771425	RID06574	interact with protein	prognosis	UP(LIHC);DATA(GSE117623)	
Breast cancer	MYC	FGF13-AS1	negatively-E	LASAGNA-Search 2.0;ChIP;RIP;dual-luciferase reporter analysis	downregulation	RT-qPCR	TCGA	NA	cell stemness(-);glycolysis(-)	transcriptional regulation	regulation	NA	NA	CSC	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000226031	GRCh38_X:138711452-138716617	4609	100129662	bHLHe39|c-Myc|MYCC	NA	LncRNAs have been proven to play crucial roles in various processes of breast cancer. LncRNA FGF13-AS1 has been identified as one of the 25 downregulated lncRNAs in breast cancer through analyzing data from two cohorts and TCGA by another group of our lab. In this study, we report that FGF13-AS1 expression is decreased in breast cancer tissue compared with corresponding normal tissue, and the downregulation of FGF13-AS1 is associated with poor prognosis. Functional studies show that FGF13-AS1 inhibits breast cancer cells proliferation, migration, and invasion by impairing glycolysis and stemness properties. Mechanistically, FGF13-AS1 reduces the half-life of c-Myc (Myc) mRNA by binding RNA-binding proteins, insulin-like growth factor 2 mRNA binding proteins (IGF2BPs) and disrupting the interaction between IGF2BPs and Myc mRNA. Furthermore, Myc transcriptionally inhibits FGF13-AS1, forming a feedback loop in this signaling pathway. These results reveal for the first time that FGF13-AS1 functions as a tumor suppressor by inhibiting glycolysis and stemness properties of breast cancer cells, and the FGF13-AS1/IGF2BPs/Myc feedback loop could be a novel therapeutic target for breast cancer patients.As indicated in Fig. 4a,  FGF13-AS1 overexpression significantly decreased the expression of  Myc, but not HIF-1alpha.In conclusion, FGF13-AS1 suppresses breast cancer glycolysis and  stemness properties by decreasing the stability of Myc mRNA.Since we found that FGF13-AS1 was downregulated in breast  cancer, we further explored the transcriptional regulation of FGF13-  AS1.  As a transcription factor, Myc was reported to function as a negative regulator in LncRNA biogenesis [27].  Thus, we next examined  the possibility that Myc transcriptionally regulated FGF13-AS1 using  bioinformatics software.  The LASAGNA-Search 2.0 software predicted a  potential binding site for Myc in the promoter region of FGF13-AS1  (Fig. 6a).Moreover, chromatin immunoprecipitation (ChIP) assays confirmed that this putative binding site in the FGF13-AS1 promoter effectively bound to Myc protein in breast cancer cells.Taken together, these  data support that Myc inhibits the transcription of FGF13-AS1, thus  exerting an autoregulatory feedback loop.	30771425	RID06575	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(LIHC);DATA(GSE117623)
Breast cancer	FGF13-AS1	MYC	negatively-E	RIP;dual-luciferase reporter analysis	downregulation	RT-qPCR	TCGA	NA	cell stemness(-);glycolysis(-)	NA	association	NA	NA	CSC	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	lncRNA	TF	ENSG00000226031	GRCh38_X:138711452-138716617	ENSG00000136997	NA	100129662	4609	NA	bHLHe39|c-Myc|MYCC	Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1/IGF2BPs/Myc feedback loop.LncRNAs have been proven to play crucial roles in various processes of breast cancer. LncRNA FGF13-AS1 has been identified as one of the 25 downregulated lncRNAs in breast cancer through analyzing data from two cohorts and TCGA by another group of our lab. In this study, we report that FGF13-AS1 expression is decreased in breast cancer tissue compared with corresponding normal tissue, and the downregulation of FGF13-AS1 is associated with poor prognosis. Functional studies show that FGF13-AS1 inhibits breast cancer cells proliferation, migration, and invasion by impairing glycolysis and stemness properties. Mechanistically, FGF13-AS1 reduces the half-life of c-Myc (Myc) mRNA by binding RNA-binding proteins, insulin-like growth factor 2 mRNA binding proteins (IGF2BPs) and disrupting the interaction between IGF2BPs and Myc mRNA. Furthermore, Myc transcriptionally inhibits FGF13-AS1, forming a feedback loop in this signaling pathway. These results reveal for the first time that FGF13-AS1 functions as a tumor suppressor by inhibiting glycolysis and stemness properties of breast cancer cells, and the FGF13-AS1/IGF2BPs/Myc feedback loop could be a novel therapeutic target for breast cancer patients.As indicated in Fig. 4a,  FGF13-AS1 overexpression significantly decreased the expression of  Myc, but not HIF-1alpha.In conclusion, FGF13-AS1 suppresses breast cancer glycolysis and  stemness properties by decreasing the stability of Myc mRNA.	30771425	RID06576	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	DNM3OS	SNAI1	positively-E	knockdown	upregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000230630	GRCh38_1:172138397-172144840	ENSG00000124216	NA	100628315	6615	DNM3-AS1|MIR199A2HG	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Long non-coding RNA DNM3OS promotes tumor progression and EMT in gastric cancer by associating with Snail.Long non-coding RNAs (lncRNAs) act as tumor suppressors or oncogenes in tumor development and progression. In the present study, we explored the expression and biological role of the lncRNA DNM3OS in gastric cancer (GC). We observed that DNM3OS was upregulated in GC tissues and cell lines, and high DNM3OS expression was correlated with malignant features and served as an indicator of a poor prognosis for GC patients. DNM3OS knockdown inhibited the proliferation of GC cells, and reduced DNM3OS suppressed tumor growth in vivo. Moreover, DNM3OS depletion inhibited the migration and invasion of GC cells through the suppression of the Snail-mediated epithelial-mesenchymal transition (EMT). In conclusion, we demonstrated that DNM3OS serves as an oncogenic lncRNA in GC, and we implicated DNM3OS as a promising prognostic factor and a potential therapeutic target for GC patients.	30770102	RID06577	expression association	prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Breast cancer	TFAP2A-AS1	SMAD2	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay;bioinformatics	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);tumorigenesis(-)	ceRNA(miR-933)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000229950	GRCh38_6:10409340-10416446	ENSG00000175387	NA	100130275	4087	NA	JV18-1|MADH2|MADR2	Long Non-Coding RNA TFAP2A-AS1 Inhibits Cell Proliferation and Invasion in Breast Cancer via miR-933/SMAD2.BACKGROUND It is well documented that long non-coding RNAs (lncRNAs) are involved in the progression of multiple human tumors by sponging microRNAs (miRNAs). However, whether lncRNA TFAP2A-AS1 plays a role in the tumorigenesis of breast cancer (BC) remains undetermined. MATERIAL AND METHODS Real-time PCR (qRT-PCR assay was performed to detect the relative mRNA expression of TFAP2A-AS1 and miR-933. Flow cytometry analysis, CCK-8 assay, and Transwell assay were applied to detect the effects of TFAP2A-AS1 overexpression on cell cycle, apoptosis, viability, and invasion of BC cells. In vivo proliferation assay was performed to evaluate the effects of TFAP2A-AS1 overexpression on tumor growth. Bioinformatics methods, dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were used to predict and validate the interaction between TFAP2A-AS1 and miR-933, as well as SMAD2 and miR-933. western blot assay was performed to examine the protein expression of SMAD2 in treated BC cells. RESULTS TFAP2A-AS1 expression was significantly lower in BC tissues and cell lines, and patients with high TFAP2A-AS1 expression exhibited a better prognosis than those with low TFAP2A-AS1 expression. Overexpression of TFAP2A-AS1 in BC cells caused cell cycle arrest, promoted cell apoptosis, suppressed cell ability, and attenuated cell invasion in vitro, and inhibited tumor growth in vivo. TFAP2A-AS1 was revealed to act as a miRNA sponge for miR-933 and then regulated the expression of Smad2. CONCLUSIONS Results from the present study suggest that TFAP2A-AS1 acts as a tumor suppressor in BC via the miR-933/SMAD2 axis.	30768589	RID06578	ceRNA or sponge	prognosis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	GAS5	RECK	positively-E	western blot;luciferase reporter assay;starBase v2.0	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-135b)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000122707	NA	60674	8434	NCRNA00030|SNHG2	hRECK|ST15	GAS5 Regulates RECK Expression and Inhibits Invasion Potential of HCC Cells by Sponging miR-135b.Objectives: Long noncoding RNA (LncRNA) growth arrest-specific 5 (GAS5) has been characterized as a tumor suppressor in numerous kinds of human cancers. Its anticancer function in hepatocellular carcinoma (HCC) includes repression of cell proliferation and metastasis, leaving the internal mechanisms unclear. In this study, we intended to examine the anti-invasion effects of GAS5 on HCC and explore the downstream regulatory mechanisms. Expression of GAS5 and microRNA-135b (miR-135b) was analyzed by qRT-PCRin paired HCC tissue samples. Their correlation with HCC patients' survival was determined. Transwell assays were done to evaluate in vitro invasion ability. Targeting of GAS5 and RECK by miR-135b was confirmed by qRT-PCR western blot, and luciferase reporter assays.Results: Decreased GAS5 and increased miR-135b in HCC inversely correlate with each other and both correlate with poor prognosis of HCC patients. Functionally, GAS5 suppresses while miR-135b promotes HCC cell invasion capacities in vitro. Mechanistically, GAS5 is a target of miR-135b. Furthermore, GAS5 positively regulates expression of RECK, also a target of miR-135b, which further inhibits MMP-2 expression and contributes to invasion repression.Conclusion: GAS5 acted as a tumor suppressor in HCC invasion in a competing endogenous RNA manner. Our findings indicate that GAS5 is a promising therapeutic target for HCC treatment.Numerous studies have demonstrated that lncRNA  GAS5 is downregulated in various types of human cancers,  including HCC.GAS5 Represses While miR-135b Promotes HCC Cell  Migration and Invasion In Vitro.Bioinformatics prediction by starBase v2.0 found about 20  miRNA binding sites within GAS5 sequence.Among these miRNAs, miR-135b attracted our attention since we had proved an inverse correlation between GAS5 and miR-135b expression levels in HCC tissues and cell lines.	30733959	RID06579	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	TMPOP2	E-cadherin	negatively-E	siRNA;luciferase report assay;ChIP	upregulation	RT-qPCR	NA	NA	cell cycle(+);cell proliferation(+);p53 signaling pathway(+)	NA	NA	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	NA	NA	100533619	NA	lncRNA-EBIC	NA	Human Papillomavirus E6/E7 and Long Noncoding RNA TMPOP2 Mutually Upregulated Gene Expression in Cervical Cancer Cells. in TMPOP2-depleted HeLa cells. Interestingly, expression of several cell cycle-related and p53 signaling genes was changed, such as that of p21, which was upregulated, and cyclin E and CDK2, which were downregulated, indicating that TMPOP2 might be involved in the regulation of the cell cycle and p53 pathway. Reciprocally, ectopic expression of TMPOP2 was demonstrated to sequester tumor repressor microRNAs (miRNAs) miR-375 and miR-139 which target HPV16/18 E6/E7 mRNA and resulted in an upregulation of HPV16/18 E6/E7 genes. Thereby, HPV16/18 E6/E7 and the long noncoding RNA (lncRNA) TMPOP2 form a positive feedback loop to mutually derepress gene expression in cervical cancer cells. Moreover, results of RNA sequencing and cell cycle analysis showed that knockdown of TMPOP2 impaired the expression of cell cycle genes, induced cell cycle arrest, and inhibited HeLa cell proliferation. 	30728257	RID06580	expression association	NA	UP(LIHC);DATA(GSE117623)	
Cervical cancer	E6	TMPOP2	positively-E	siRNA;luciferase report assay;ChIP	upregulation	RT-qPCR	NA	NA	cell cycle(+);cell proliferation(+);p53 signaling pathway(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	PCG	lncRNA	NA	NA	ENSG00000262904	GRCh38_16:74667506-74668706	NA	100533619	NA	lncRNA-EBIC	Human Papillomavirus E6/E7 and Long Noncoding RNA TMPOP2 Mutually Upregulated Gene Expression in Cervical Cancer Cells. in TMPOP2-depleted HeLa cells. Interestingly, expression of several cell cycle-related and p53 signaling genes was changed, such as that of p21, which was upregulated, and cyclin E and CDK2, which were downregulated, indicating that TMPOP2 might be involved in the regulation of the cell cycle and p53 pathway. Reciprocally, ectopic expression of TMPOP2 was demonstrated to sequester tumor repressor microRNAs (miRNAs) miR-375 and miR-139 which target HPV16/18 E6/E7 mRNA and resulted in an upregulation of HPV16/18 E6/E7 genes. Thereby, HPV16/18 E6/E7 and the long noncoding RNA (lncRNA) TMPOP2 form a positive feedback loop to mutually derepress gene expression in cervical cancer cells. Moreover, results of RNA sequencing and cell cycle analysis showed that knockdown of TMPOP2 impaired the expression of cell cycle genes, induced cell cycle arrest, and inhibited HeLa cell proliferation. 	30728257	RID06581	expression association	NA		UP(LIHC);DATA(GSE117623)
Cervical cancer	E7	TMPOP2	positively-E	siRNA;luciferase report assay;ChIP	upregulation	RT-qPCR	NA	NA	cell cycle(+);cell proliferation(+);p53 signaling pathway(+)	NA	association	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	NA	NA	ENSG00000262904	GRCh38_16:74667506-74668706	NA	100533619	NA	lncRNA-EBIC	Human Papillomavirus E6/E7 and Long Noncoding RNA TMPOP2 Mutually Upregulated Gene Expression in Cervical Cancer Cells. in TMPOP2-depleted HeLa cells. Interestingly, expression of several cell cycle-related and p53 signaling genes was changed, such as that of p21, which was upregulated, and cyclin E and CDK2, which were downregulated, indicating that TMPOP2 might be involved in the regulation of the cell cycle and p53 pathway. Reciprocally, ectopic expression of TMPOP2 was demonstrated to sequester tumor repressor microRNAs (miRNAs) miR-375 and miR-139 which target HPV16/18 E6/E7 mRNA and resulted in an upregulation of HPV16/18 E6/E7 genes. Thereby, HPV16/18 E6/E7 and the long noncoding RNA (lncRNA) TMPOP2 form a positive feedback loop to mutually derepress gene expression in cervical cancer cells. Moreover, results of RNA sequencing and cell cycle analysis showed that knockdown of TMPOP2 impaired the expression of cell cycle genes, induced cell cycle arrest, and inhibited HeLa cell proliferation. 	30728257	RID06582	expression association	NA		UP(LIHC);DATA(GSE117623)
Cervical cancer	TMPOP2	E6	negatively-E	siRNA;luciferase report assay;BLAST	upregulation	RT-qPCR;sequencing	NA	NA	cell cycle(+);cell proliferation(+);p53 signaling pathway(+)	ceRNA(miR-375)	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	NA	NA	100533619	NA	lncRNA-EBIC	NA	Human Papillomavirus E6/E7 and Long Noncoding RNA TMPOP2 Mutually Upregulated Gene Expression in Cervical Cancer Cells. in TMPOP2-depleted HeLa cells. Interestingly, expression of several cell cycle-related and p53 signaling genes was changed, such as that of p21, which was upregulated, and cyclin E and CDK2, which were downregulated, indicating that TMPOP2 might be involved in the regulation of the cell cycle and p53 pathway. Reciprocally, ectopic expression of TMPOP2 was demonstrated to sequester tumor repressor microRNAs (miRNAs) miR-375 and miR-139 which target HPV16/18 E6/E7 mRNA and resulted in an upregulation of HPV16/18 E6/E7 genes. Thereby, HPV16/18 E6/E7 and the long noncoding RNA (lncRNA) TMPOP2 form a positive feedback loop to mutually derepress gene expression in cervical cancer cells. Moreover, results of RNA sequencing and cell cycle analysis showed that knockdown of TMPOP2 impaired the expression of cell cycle genes, induced cell cycle arrest, and inhibited HeLa cell proliferation. 	30728257	RID06583	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Cervical cancer	TMPOP2	E7	negatively-E	siRNA;luciferase report assay;BLAST	upregulation	RT-qPCR;sequencing	NA	NA	cell cycle(+);cell proliferation(+);p53 signaling pathway(+)	ceRNA(miR-139)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000262904	GRCh38_16:74667506-74668706	NA	NA	100533619	NA	lncRNA-EBIC	NA	Human Papillomavirus E6/E7 and Long Noncoding RNA TMPOP2 Mutually Upregulated Gene Expression in Cervical Cancer Cells. in TMPOP2-depleted HeLa cells. Interestingly, expression of several cell cycle-related and p53 signaling genes was changed, such as that of p21, which was upregulated, and cyclin E and CDK2, which were downregulated, indicating that TMPOP2 might be involved in the regulation of the cell cycle and p53 pathway. Reciprocally, ectopic expression of TMPOP2 was demonstrated to sequester tumor repressor microRNAs (miRNAs) miR-375 and miR-139 which target HPV16/18 E6/E7 mRNA and resulted in an upregulation of HPV16/18 E6/E7 genes. Thereby, HPV16/18 E6/E7 and the long noncoding RNA (lncRNA) TMPOP2 form a positive feedback loop to mutually derepress gene expression in cervical cancer cells. Moreover, results of RNA sequencing and cell cycle analysis showed that knockdown of TMPOP2 impaired the expression of cell cycle genes, induced cell cycle arrest, and inhibited HeLa cell proliferation. 	30728257	RID06584	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pancreatic cancer	PRECSIT	BRD4	positively-E	luciferase reporter assay;RIP;bioinformatics	upregulation	RT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell growth(+);chemosensitivity(-)	ceRNA(miR-188-3p)	regulation	RNA-protein	Gemcitabine	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255874	GRCh38_13:110863987-110870330	ENSG00000141867	NA	283487	23476	C13orf29|LINC00346|NCRNA00346	CAP|HUNK1|HUNKI|MCAP	Long non-coding RNA LINC00346 promotes pancreatic cancer growth and gemcitabine resistance by sponging miR-188-3p to derepress BRD4 expression.Methods: The effects of overexpression and knockdown of LINC00346 on the proliferation, cell cycle progression, apoptosis, and gemcitabine resistance were investigated. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were performed to search for potential microRNAs (miRs) that can interact with LINC00346.Results: Overexpression of LINC00346 significantly enhanced the proliferation, colony formation, and tumorigenesis of pancreatic cancer cells. Conversely, knockdown of LINC00346 suppressed pancreatic cancer cell proliferation and caused a cell-cycle arrest at the G2/M-phase. Depletion of LINC00346 also enhanced gemcitabine sensitivity in pancreatic cancer cells both in vitro and in vivo. Mechanistic investigation revealed that LINC00346 acted as a sponge for miR-188-3p and blocked the repression of BRD4 by miR-188-3p in pancreatic cancer cells. Clinical evidence indicated a negative correlation between LINC00346 and miR-188-3p in pancreatic cancer specimens. Rescue experiments showed that LINC00346 attenuated the growth-suppressing and chemosensitizing effects of miR-188-3p on pancreatic cancer cells. In addition, silencing of BRD4 significantly inhibited LINC00346-induced pancreatic cancer cell proliferation and colony formation.Conclusions: LINC00346 shows the ability to promote pancreatic cancer growth and gemcitabine resistance, which is in part mediated by antagonization of miR-188-3p and induction of BRD4. Targeting LINC00346 may improve gemcitabine-based therapeutic efficacy.Real-time PCR analysis revealed that  LINC00346 was expressed at higher levels in pancreatic  cancer cells than in HPDE6c7 pancreatic epithelial cells  (Fig. 1a).We employed Reverse Transcription and quantitative Real Time-PCR in breast cancer tissues   and adjacent non-tumor tissues for examining the   expression of lncRNA TUBA4B.	30728036	RID06585	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	TUBA4B	miR-19	negatively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	sponge	binding/interaction	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000243910	GRCh38_2:219253243-219272197	NA	NA	80086	NA	FLJ13940|TUBA4	NA	Long non-coding RNA Tubulin Alpha 4B (TUBA4B) inhibited breast cancer proliferation and invasion by directly targeting miR-19.Objective: Long non-coding RNA (lncRNA) is a significant member of the non-coding RNA family. New evidence has shown that it plays a pivotal role in the processes of tumor genesis and development. According to previous verification, the lncRNA Tubulin Alpha 4B (TUBA4B) is a tumor-associated molecule, but how TUBA4B expresses and functions in breast cancer is still not clear.Patients and methods: We conducted this study to examine what expression and biological role TUBA4B plays in breast cancer. The expression of TUBA4B was measured in breast cancer samples and cell lines. CCK8 assays and transwell assays were used for evaluating the effects of TUBA4B on breast cancer cell proliferation and invasion. Luciferase reporter assays were used for identifying the direct target of TUBA4B.Results: According to the results, TUBA4B was largely downregulated in breast cancer samples and cell lines. The functional analysis demonstrated that breast cancer cells proliferation and invasion could be inhibited by overexpression of TUBA4B. The results of Luciferase reporter assays indicated that TUBA4B directly targeted miR-19, which could rescue the effects of TUBA4B on breast cancer cells.Conclusions: It is suggested that TUBA4B was downregulated in breast cancer and suppressed proliferation and invasion of breast cancer by targeting miR-19.Along with the high level of miR-19,   TUBA4B s expression decreased sharply (Figure   3D, E). These results indicated the interaction   between TUBA4B and miR-19.  With the help of   Luciferase reporter assays, we could verify the   interaction between TUBA4B and miR-19.	30720178	RID06586	ceRNA or sponge	NA	UP(BRCA);DATA(GSE86978)	
Gastric cancer	PICART1	ERK	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+);PI3K/AKT signaling pathway(-);ERK/MAPK signaling pathway(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000246640	GRCh38_17:50050349-50055746	ENSG00000133216	NA	284080	NA	NA	NA	Long non-coding RNA PICART1 inhibits cell proliferation by regulating the PI3K/AKT and MAPK/ERK signaling pathways in gastric cancer.Patients and methods: The relative expression level of lncRNA-PICART1 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Cell counting kit-8 (CCK-8) assay and colony formation assay were used to determine the ability of cell proliferation. Flow cytometric analysis was performed to detect cell cycle and cell apoptosis. The protein expressions of ERK, p-ERK, AKT and p-AKT were detected by western blot. Furthermore, the transfected cells were used to perform tumor xenograft formation assay.Results: LncRNA-PICART1 was lowly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay and flow cytometric analysis validated that up-regulated lncRNA-PICART1 significantly suppressed cell proliferation, whereas promoted cell apoptosis. Besides, the over-expression of lncRNA-PICART1 remarkably inhibited the PI3K/AKT and ERK/MAPK signaling pathways. Tumor xenograft formation assay indicated that lncRNA-PICART1 overexpression significantly inhibited tumor formation.Conclusions: Our research illustrated that lncRNA-PICART1 functioned as a tumor suppressor in GC. The regulation of the PI3K/AKT and ERK/MAPK signaling pathways might be the underlying mechanism of the tumor suppressor role of lncRNA-PICART1. In addition, our study might bring novel insights into biomarkers and therapeutic strategies for GC.All data indicated that lncRNA-PICART1 inhibited cell cycle progression and promoted cell apoptosis in GC cells.	30720166	RID06587	expression association	NA		
Gastric cancer	PICART1	AKT1	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+);PI3K/AKT signaling pathway(-);ERK/MAPK signaling pathway(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000246640	GRCh38_17:50050349-50055746	ENSG00000142208	NA	284080	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA PICART1 inhibits cell proliferation by regulating the PI3K/AKT and MAPK/ERK signaling pathways in gastric cancer.Patients and methods: The relative expression level of lncRNA-PICART1 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Cell counting kit-8 (CCK-8) assay and colony formation assay were used to determine the ability of cell proliferation. Flow cytometric analysis was performed to detect cell cycle and cell apoptosis. The protein expressions of ERK, p-ERK, AKT and p-AKT were detected by western blot. Furthermore, the transfected cells were used to perform tumor xenograft formation assay.Results: LncRNA-PICART1 was lowly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay and flow cytometric analysis validated that up-regulated lncRNA-PICART1 significantly suppressed cell proliferation, whereas promoted cell apoptosis. Besides, the over-expression of lncRNA-PICART1 remarkably inhibited the PI3K/AKT and ERK/MAPK signaling pathways. Tumor xenograft formation assay indicated that lncRNA-PICART1 overexpression significantly inhibited tumor formation.Conclusions: Our research illustrated that lncRNA-PICART1 functioned as a tumor suppressor in GC. The regulation of the PI3K/AKT and ERK/MAPK signaling pathways might be the underlying mechanism of the tumor suppressor role of lncRNA-PICART1. In addition, our study might bring novel insights into biomarkers and therapeutic strategies for GC.All data indicated that lncRNA-PICART1 inhibited cell cycle progression and promoted cell apoptosis in GC cells.	30720166	RID06588	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LINC00518	JAK	positively-E	western blot	upregulation	qRT-PCR	NA	NA	JAK/STAT3 signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000183674	GRCh38_6:10429255-10435015	NA	NA	221718	NA	C6orf218|MGC40222	NA	Knockdown of long non-coding RNA LINC00518 inhibits cervical cancer proliferation and metastasis by modulating JAK/STAT3 signaling.Patients and methods: The expression levels of LINC00518 in CC tissues and cell lines were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR, and its clinical significance was assessed by statistical analysis. Cell apoptosis was determined by flow cytometry. The cell proliferation was evaluated by MTT assay and colony forming assay, and the migration and invasion were evaluated by wound healing assays and transwell assay. western blot was used to detect the expression of relative proteins, including EMT markers and the JAK/STAT3 signaling markers.Results: We found that LINC00518 was upregulated in CC tissues and associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, lymph node metastasis, depth of cervical invasion and poor survival of CC patients. Univariate and multivariate Cox regression analysis showed that LINC00518 played a significant role of independent prognostic markers in overall survival rates. Furthermore, knocking down LINC00518 expression significantly suppressed CC cell proliferation, migration and invasion, and induced apoptosis in vitro. Mechanistically, the downregulation of LINC00518 suppressed JAK/STAT3 activation and subsequently decreased N-Cadherin and Vimentin.Conclusions: The present work first suggests that LINC00518 acts as an oncogene in CC via regulation of the JAK/STAT3 signaling pathway. In the future, LINC00518 may serve as a predictive biomarker and potential therapeutic target for CC patients.The results showed that   LINC00518 expression was up-regulated in CC   tissues compared to normal cervical tissues (Figure 1A and 1B).	30720156	RID06589	expression association	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	
Cervical cancer	WT1-AS	FOXN2	positively-E	luciferase reporter assay;RNA22;TargetScan	downregulation	qRT-PCR	TCGA	NA	cell growth(-);cell migration(-);cell invasion(-)	ceRNA(miR-203a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000183242	GRCh38_11:32435518-32500632	ENSG00000170802	NA	51352	3344	WIT-1|WIT1|WT1-AS1|WT1AS	HTLF	Long non-coding RNA WT1-AS inhibits cell aggressiveness via miR-203a-5p/FOXN2 axis and is associated with prognosis in cervical cancer.Patients and methods: The Cancer Genome Atlas (TCGA) was used to identify differentially expressed lncRNAs in cervical carcinoma. The level of lncRNA WT1-AS in cervical carcinoma tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The lentiviral vector encoding WT1-AS (LV-WT1-AS) or miR-203a-5p mimic was transfected into cervical carcinoma cells. Cell Counting Kit-8 (CCK-8), wound healing and transwell invasion assays were applied to assess the role of WT1-AS in cervical cancer cell growth and migration. WT1-AS directly bound to miR-203a-5p was confirmed using Luciferase reporter assay. The level of forkhead box N2 (FOXN2) was assessed by quantitative Real Time-Polymerase Chain Reaction analysis. A xenograft model was constructed to explore the role of WT1-AS in cervical cancer cell growth in vivo.Results: WT1-AS was down-regulated in both cervical cancer tissues and cell lines. Functional analyses indicated that the over-expression of WT1-AS remarkably inhibited cervical carcinoma cell growth, migration and invasion. The results of the Luciferase reporter assays verified that miR-203a-5p is a direct target of WT1-AS. Moreover, FOXN2 was identified as a direct target gene of miR-203a-5p, and the up-regulation of miR-203a-5p reversed the inhibitory effects of WT1-AS in cervical cancer cells.Conclusions: Our results demonstrated that WT1-AS was under-expressed in cervical carcinoma and suppresses cervical cancer cell growth and aggressiveness via a miR-203a-5p/FOXN2 axis.	30720155	RID06590	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	EZH2	TCAM1P-004	negatively-E	western blot;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	protein-RNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000106462	NA	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	NA	Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.The levels of TCAM1P-004 and RP11-  598D14.1 in 50 pairs of HCC tumors and corresponding adjacent  normal tissues were measured by qRT-PCR  Their expression  levels were reduced significantly in HCC tumor tissues.ChIP  assays showed that EZH2, EED, and SUZ12 were enriched in the  promoter regions of TCAM1P-004 and RP11-598D14.1 in Hep3B  cells, and the levels were higher than in MIHA cells.	30718359	RID06591	epigenetic regulation	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	
Hepatocellular carcinoma	EZH2	RP11-598D14.1	negatively-E	western blot;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	protein-RNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000249945	GRCh38_4:175457726-175473197	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	NA	Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.	30718359	RID06592	epigenetic regulation	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	
Hepatocellular carcinoma	TCAM1P-004	IGF2BP1	interact	western blot;RIP;RNA pull-down;mass spectrometry	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000159217	NA	NA	10642	NA	IMP-1	The levels of TCAM1P-004 and RP11-  598D14.1 in 50 pairs of HCC tumors and corresponding adjacent  normal tissues were measured by qRT-PCR  Their expression  levels were reduced significantly in HCC tumor tissues (P <   0.001;  Fig. 1D).Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.	30718359	RID06593	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	TCAM1P-004	H1-2	interact	western blot;RIP;RNA pull-down;mass spectrometry	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000187837	NA	NA	3006	NA	H1.2|H1c|H1F2|H1s-1|HIST1H1C	Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.	30718359	RID06594	interact with protein	NA		
Hepatocellular carcinoma	RP11-598D14.1	IGF2BP1	interact	western blot;RIP;RNA pull-down;mass spectrometry	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249945	GRCh38_4:175457726-175473197	ENSG00000159217	NA	NA	10642	NA	CRD-BP|CRDBP|IMP-1|IMP1|VICKZ1|ZBP1	Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.	30718359	RID06595	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	RP11-598D14.1	STAU1	interact	western blot;RIP;RNA pull-down;mass spectrometry	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249945	GRCh38_4:175457726-175473197	ENSG00000124214	NA	NA	6780	NA	PPP1R150|STAU	Genome-Wide Screening and Functional Analysis Identifies Tumor Suppressor Long Noncoding RNAs Epigenetically Silenced in Hepatocellular Carcinoma.Long noncoding RNAs (lncRNA) play critical roles in the development of cancer, including hepatocellular carcinoma (HCC). However, the mechanisms underlying their deregulation remain largely unexplored. In this study, we report that two lncRNAs frequently downregulated in HCC function as tumor suppressors and are epigenetically silenced by histone methyltransferase EZH2. lncRNAs TCAM1P-004 and RP11-598D14.1 were inhibited by EZH-mediated trimethylation of H3K27me3 at their promoters. Downregulation of TCAM1P-004 and RP11-598D14.1 was frequently observed in HCC tumors compared with adjacent normal tissues. Both lncRNAs inhibited cell growth, cell survival, and transformation in HCC cells in vitro as well as tumor formation in vivo. Using RNA pull-down and mass spectrometry, we demonstrated that TCAM1P-004 bound IGF2BP1 and HIST1H1C, whereas RP11-598D14.1 bound IGF2BP1 and STAU1. These lncRNA-protein interactions were critical in regulating p53, MAPK, and HIF1alpha pathways that promoted cell proliferation in HCC. Overexpression of EZH2 was critical in repressing TCAM1P-004 and RP11-598D14.1, and EZH2-TCAM1P-004/RP11-598D14.1-regulated pathways were prevalent in human HCC. Aberrant suppression of TCAM1P-004 and RP11-598D14.1 led to loss of their tumor-suppressive effects by disrupting the interaction with IGF2BP1, HIST1H1C, and STAU1, which in turn promoted HCC development and progression. Collectively, these findings demonstrate the role of TCAMP1P-004 and RP11-598D14.1 in suppressing tumor growth and suggest that EZH2 may serve as a therapeutic target in HCC. SIGNIFICANCE: EZH2-mediated loss of lncRNAs TCAM1P-004 and RP11-598D14.1 hinders the formation of tumor suppressor lncRNA-protein complexes and subsequently promotes HCC growth.	30718359	RID06596	interact with protein	NA		UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Renal cell carcinoma	XIC	CDKN1A	positively-E	knockdown;western blot;luciferase reporter assay;starbase v2.0;RNA pull-down	downregulation	RT-PCR	NA	NA	cell proliferation(-);tumor growth(-)	ceRNA(miR-106b-5p)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000124762	NA	7502	1026	SXI1|XCE|XIST	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA XIST regulates miR-106b-5p/P21 axis to suppress tumor progression in renal cell carcinoma.Long non-coding RNAs (lncRNAs) have been demonstrated to exert important roles in cancer development and progression. The biological function of lncRNA X-inactive specific transcript (XIST) in the development of renal cell carcinoma (RCC) and the underlying mechanisms are still largely unknown. In this study, we found that XIST was down-regulated in RCC tissues and cells. Overexpression of XIST significantly suppressed cell proliferation and induced cell G0/G1 arrest in vitro and inhibited tumor growth in vivo. We further found that XIST could directly interact with miR-106b-5p and increase the expression of P21. Thus, XIST positively regulated the expression of P21 through sponging miR-106b-5p, and played a tumor suppressor role in RCC. Moreover, we found that curcumin could regulate XIST/miR-106b-5p/P21 axis in RCC cells. Our study exhibits the role of XIST as a miRNA sponge in RCC and supports the potential application of XIST in RCC therapy.To assess whether lncRNA XIST is aberrantly expressed in RCC  tissues, a total of 50 paired RCC tissues and adjacent normal tissues  were collected and analyzed for XIST expression using RT-PCRand  subsequently normalized to GAPDH.Through searching in starbase v2.0 database, we observed  that miR-106b-5p had putative binding sites with XIST(Fig. 3G).  Subsequently, we used the biotin-labeled pull-down system to  further analyze the direct binding of miR-106b-5p and XIST.	30717973	RID06597	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	C3orf85	ACLY	negatively-E	western blot;siRNA	downregulation	microarray;qRT-PCR	NA	NA	prognosis;cell proliferation(-);cell migration(-);cell invasion(-);tumorigenesis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241224	GRCh38_3:109118252-109151401	ENSG00000260245	NA	401081	47	FLJ22763	ACL|ATPCL|CLATP	Long non-coding RNA FLJ22763 is involved in the progression and prognosis of gastric cancer.Long noncoding RNAs (lncRNAs) play important roles in carcinogenesis. It is necessary to uncover the detailed pattern of comprehensive lncRNA expression in the genome during the development of gastric cancer (GC). We implemented lncRNA microarray analysis in 5 paired GC tissues to detect the lncRNA expression profile. Moreover, we set out to explore the biological function, clinical application and molecular basis of the aberrant lncRNA in GC. In addition, we used the high-throughput microarray to identify the target gene of the aberrant lncRNA. We found that FLJ22763, a novel lncRNA, had significantly lower expression in GC tissues. Decreased expression of FLJ22763 was positively correlated with a lower-level histological grade and the depth of invasion. The ectopic expression of lncRNA FLJ22763 significantly suppressed the biological malignant behavior of GC cells and inhibited xenograft tumor growth (both P < 0.001). Notably, FLJ22763 displayed a considerable predictive effect in the prognosis of GC (log-rank, P = 0.003). Furthermore, we found that FLJ22763 was negatively associated with ACLY, regulating the mRNA and protein levels of ACLY. Our findings suggested that FLJ22763 may act as a suppressor gene to regulate the expression of ACLY, and its down-expression may be an independent prognostic factor in patients with GC.We further confirmed the expression of  FLJ22763 in GC tissue from 75 patients and normal control tissue by  PCR. In addition, the expression of lncRNA FLJ22763 was also low  across GC cell lines (Fig. 1A and B).The expression levels of  FLJ22763 and ACLY were tested by qRT-PCR	30716442	RID06598	expression association	prognosis	UP(PRAD);DATA(GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gallbladder cancer	TFDP1	CTNNB1	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	self-renewal(+);tumorigenesis(+);cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000168036	NA	7027	1499	DILC|DP1|DRTF1|Dp-1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA DILC promotes the progression of gallbladder carcinoma.Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) contribute to tumorigenesis, progression and recurrence of various malignancies including Gallbladder carcinoma (GBC). Lnc-DILC is reported to be the tumor suppressor gene to play an important role in liver cancer stem cells (CSCs). However, the role of lnc-DILC in GBC remains to be elucidated. Herein, we show that lnc-DILC is upregulated in gallbladder CSCs and GBC patients' tissues. Knockdown of lnc-DILC attenuates the self-renewal, tumorigenicity, proliferation and metastasis of gallbladder CSCs. Mechanistically, lnc-DILC promotes gallbladder CSCs expansion via Wnt/beta-catenin pathway. Special Wnt/beta-catenin inhibitor FH535 diminishes the discrepancy of self-renewal, growth and metastasis between lnc-DILC interference GBC cells and their control cells. In conclusion, lnc-DILC drives gallbladder CSCs self-renewal, tumorigenicity, proliferation and metastasis by activating Wnt/beta-catenin signaling, and may therefore prove to be a potential therapeutic target for GBC patients.The luciferase reporter of beta-catenin further confirmed the effect of lnc-DILC  on beta-catenin activation (Fig. 5B).	30716440	RID06599	expression association	metastasis,recurrence	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	MALAT1	ABC	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	NA	association	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115657	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. In addition, the metastasis and invasion of HCT-116 and HCT-116/5-FU cells were regulated via targeting miR-20b-5p. Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. The present study proposes a new direction to investigate the molecular mechanisms underlying the invasion and metastasis of CRC, whereby the interaction between MALAT1 and miR-20b-5p could be a novel therapeutic target for CRC.The expression levels of drug resistance-associated proteins MDR1, MRP1, BCRP,  and ABC in HCT-116 and HCT-116/5-FU cells were downregulated by  MALAT1 silencing, and the downregation in HCT-116/5FU cells was  higher than that in HCT-116 cells, indicating the suppression of 5-FU  resistance (Fig. 4B).	30716387	RID06600	expression association	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	MALAT1	ABCG2	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	NA	association	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000118777	NA	378938	9429	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	ABCP|BCRP|CD338|EST157481|MXR	Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. In addition, the metastasis and invasion of HCT-116 and HCT-116/5-FU cells were regulated via targeting miR-20b-5p. Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. The present study proposes a new direction to investigate the molecular mechanisms underlying the invasion and metastasis of CRC, whereby the interaction between MALAT1 and miR-20b-5p could be a novel therapeutic target for CRC.	30716387	RID06601	expression association	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	MALAT1	MDR1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	NA	association	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109436	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. In addition, the metastasis and invasion of HCT-116 and HCT-116/5-FU cells were regulated via targeting miR-20b-5p. Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. The present study proposes a new direction to investigate the molecular mechanisms underlying the invasion and metastasis of CRC, whereby the interaction between MALAT1 and miR-20b-5p could be a novel therapeutic target for CRC.	30716387	RID06602	expression association	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	MALAT1	MRP1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	NA	association	RNA-protein	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000113318	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. In addition, the metastasis and invasion of HCT-116 and HCT-116/5-FU cells were regulated via targeting miR-20b-5p. Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. The present study proposes a new direction to investigate the molecular mechanisms underlying the invasion and metastasis of CRC, whereby the interaction between MALAT1 and miR-20b-5p could be a novel therapeutic target for CRC.	30716387	RID06603	expression association	metastasis,chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Colorectal cancer	MALAT1	miR-20b-5p	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. Furthermore, MALAT1 silencing downregulated the expression of ATP-binding cassette transporters (ABC), breast cancer resistance protein (BCRP), and multi-drug resistance proteins including MDR1 and MRP1, resulting in decreased resistance of cancer cells to 5-FU. In addition, the metastasis and invasion of HCT-116 and HCT-116/5-FU cells were regulated via targeting miR-20b-5p. Based on these observations, we infer that inhibition of MALAT1 suppressed CRC progression and metastasis and improved the sensitivity of cancer cells to 5-FU. The present study proposes a new direction to investigate the molecular mechanisms underlying the invasion and metastasis of CRC, whereby the interaction between MALAT1 and miR-20b-5p could be a novel therapeutic target for CRC.The luciferase activity in cells cotransfected with miR-20b-5p and WT MALAT1 3 -UTR reporter was  markedly decreased (Fig. 5B), which verified that the MALAT1 targets  miR-20b-5p, and the binding site was shown in Fig. 5C.	30716387	RID06604	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Pancreatic cancer	TUSC7	miR-371a-5p	negatively-F	western blot;RIP;luciferase reporter assay;LncBase Predicted v.2	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-);cell stemness(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LOC285194|LSAMP-AS3|NCRNA00295	NA	LncRNA TUSC7 suppresses pancreatic carcinoma progression by modulating miR-371a-5p expression.Pancreatic carcinoma is one of the most common and lethal human malignancies worldwide. Long noncoding RNAs (lncRNAs) are a well-known type of nonprotein-coding transcripts implicated in cancer development and progression. Increasing evidence has indicated that lncRNA tumor suppressor candidate 7 (TUSC7) is a novel cancer suppressor gene in various cancers. Nevertheless, the function of TUSC7 in pancreatic carcinoma is urgent to be clarified. We found that TUSC7 was notably decreased in tissues and cell lines of pancreatic carcinoma. Moreover, the low expression of TUSC7 was correlated with advanced clinical grades and poorer overall survival. Our findings revealed that TUSC7 repressed cell proliferation, migration, invasion, epithelial-mesenchymal transition, and stemness whereas facilitated cell apoptosis of pancreatic carcinoma cells. Further investigations demonstrated that miR-371a-5p directly bound with TUSC7 and negatively regulated by TUSC7. MiR-371a-5p rescued the inhibitory effects of TUSC7 on the development of pancreatic carcinoma. We conclude that lncRNA TUSC7 suppresses pancreatic carcinoma progression by modulating miR-371a-5p expression, indicating an innovative therapeutic strategy for pancreatic carcinoma.We uncovered that miR 371a 5p was the predicted  target of TUSC7 by LncBase Predicted v.2 in DIANA tools (Figure 4a).   To further verify the correlation between miR 371a 5p and TUSC7,  we performed the luciferase reporter assay and RIP assay.	30714151	RID06605	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Osteosarcoma	EPIC1	MEF2D	negatively-E	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-)	ubiquitination	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000116604	NA	284930	4209	Lnc-EPIC1	NA	Long non-coding RNA EPIC1 inhibits viability and invasion of osteosarcoma cells by promoting MEF2D ubiquitylation.Background: Long non-coding RNAs (lncRNAs) can modulate gene expression through different mechanisms, but the fundamental molecular mechanism behind EPIC1 and osteosarcoma (OS) was poorly understood.Methods: Bone tumor tissues and the matched normal tissues were obtained from 36 OS patients who received tumor resection from 2014 to 2018. The expression of EPIC1 and MEF2D was determined by quantitative real-Time PCR and western blot. Cell viability and invasion were evaluated by MTT assay and transwell assay. The animal xenograft model was also established.Results: EPIC1 was down-regulated, but MEF2D was up-regulated in OS tissues and OS cell lines. Overexpression of EPIC1 inhibited cell viability and invasion of OS cells. Targeting relationship between EPIC1 and MEF2D was confirmed by RNA pull-down and RNA immunoprecipitation (RIP). The MEF2D protein binding to ubiquitin was significantly increased in OS cells overexpressing EPIC1. The co-transfection with pcDNA-EPIC1 and pcDNA-MEF2D rescued the inhibition of cell viability and invasion caused by the overexpression of EPIC1. Overexpression of EPIC1 suppressed tumor growth in the OS xenograft model.Conclusion: Our findings indicated that overexpression of EPIC1 inhibited cell viability and invasion of OS cells by promoting MEF2D ubiquitylation, which provided innovative lncRNA and protein targets for treating OS.	30703420	RID06606	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Cervical cancer	LINC01305	TNXB	positively-F	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	PI3K/AKT signaling pathway(+);epithelial to mesenchymal transition(+);cell invasion(+);cell migration(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000231453	GRCh38_2:174326027-174330643	ENSG00000233323	NA	285084	7148	NA	TNXB1|TNXB2|TNXBS|XB|XBS	LncRNA LINC01305 silencing inhibits cell epithelial-mesenchymal transition in cervical cancer by inhibiting TNXB-mediated PI3K/Akt signalling pathway.Cervical cancer (CC) remains one of the leading malignancies afflicting females worldwide, with its aetiology associated with long-term papillomavirus infection. Recent studies have shifted their focus and research attention to the relationship between long non-coding RNAs (lncRNAs) and CC therapeutic. Thus, the aim of the current study was to investigate the underlying mechanism of lncRNA LINC01305 on the cell invasion, migration and epithelial-mesenchymal transition (EMT) of CC cells via modulation of the PI3K/Akt signalling pathway by targeting tenascin-X B (TNXB). The expressions of LINC01305, TNXB, MMP2, MMP9, E-cadherin, vimentin, PI3K, Akt, p-PI3K, p-Akt and TNXB were detected in this study. After which, the cell invasion and migration abilities of the CC cells were determined respectively. Bioinformatics and the application of a dual luciferase reporter gene assay provided verification indicating that TNXB is the target gene of lncRNA LINC01305. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotmethods revealed that the expressions of MMP2, MMP9, vimentin, PI3K, Akt, p-PI3K and p-Akt were decreased following the down-regulation of LncRNA LINC01305 or overexpression of TNXB. LncRNA LINC01305 silencing or TNXB overexpression was noted to decrease the migration and invasion of SiHa cells. Taken together, the key findings of the current study present evidence suggesting that lncRNA LINC01305 silencing suppresses EMT, invasion and migration via repressing the PI3K/Akt signalling pathway by means of targeting TNXB in CC cells, which ultimately provides novel insight and identification of potential therapeutic targets for CC.	30697971	RID06607	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE55807)
Gastric cancer	LINC01939	EGR2	positively-E	luciferase reporter assay;western blot	downregulation	RT-PCR	NA	NA	cell metastasis(-);cell invasion(-);cell migration(-);epithelial to mesenchymal transition(-)	ceRNA(miR-17-5p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228799	GRCh38_2:899462-905539	ENSG00000122877	NA	101060385	1959	NA	KROX20	LINC01939 inhibits the metastasis of gastric cancer by acting as a molecular sponge of miR-17-5p to regulate EGR2 expression.Accumulating evidence have suggested that long noncoding RNAs (lncRNAs) are known to regulate diverse tumorigenic processes. Recently, a novel lncRNA LINC01939 was underexpressed and emerged as a tumor suppressive lncRNA in gastric cancer (GC). In this study, we aimed to investigate the biological function and molecular mechanism of LINC01939 in GC. We found that LINC01939 expression was significantly downregulated in GC tissues and cell lines. Low expression of LINC01939 was correlated with tumor metastasis and shorter survival in GC patients. Functionally, LINC01939 overexpression remarkably inhibited the invasion and migration of GC cells in vitro and in vivo. Mechanistically, LINC01939 regulated the expression of early growth response 2 (EGR2) protein by competitively binding to miR-17-5p. Upregulation of miR-17-5p reversed GC metastasis and EMT process caused by LINC01939 by rescue analysis. Taken together, these results suggested that LINC01939 repressed GC invasion and migration by functioning as a ceRNA for miR-17-5p to regulate EGR2 expression. Our findings provided a novel prognostic marker and therapeutic target for GC patients.To assess the correlation between LINC01939 and GC metastasis, we performed reverse transcription and quantitative PCR (RT-PCR to investigate the expression of LINC01939 in a larger cohort of GC tissues.Thus, our results suggest that LINC01939 may  suppress GC metastasis and EMT process by targeting  miR-17-5p to upregulate EGR2 expression.	30683847	RID06608	ceRNA or sponge	metastasis,prognosis		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE86978)
Colorectal cancer	CASC2	BCL2	negatively-E	RIP;western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	NA	regulation	RNA-protein	Berberine	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171791	NA	255082	596	C10orf5	Bcl-2|PPP1R50	Berberine Promotes Apoptosis of Colorectal Cancer via Regulation of the Long Non-Coding RNA (lncRNA) Cancer Susceptibility Candidate 2 (CASC2)/AU-Binding Factor 1 (AUF1)/B-Cell CLL/Lymphoma 2 (Bcl-2) Axis.BACKGROUND Berberine, a natural isoquinoline alkaloid derived from Berberis genus plants, has been reported to have anti-cancer effects. While cell behavior can be modulated by long non-coding RNAs (lncRNAs), the contributions of lncRNAs in progression and berberine effects on colorectal cancer are largely unknown. Therefore, the present study investigated the involvement and regulatory function of lncRNA cancer susceptibility candidate 2 (CASC2) during the treatment of human colorectal cancer using berberine. MATERIAL AND METHODS Reverse transcription-quantitative PCR (RT-qPCR) was performed to detect the expression levels of lncRNA CASC2 and Bcl-2 mRNA in colorectal cancer cells. MTT assay was performed to evaluate cell viability. Flow cytometry and TUNEL assay were used to analyze the apoptosis of cancer cells. RNA immunoprecipitation (RIP) assay was done to verify the interaction between lncRNA CASC2 and (AU-binding factor 1) AUF1, or AUF1 and B-cell CLL/lymphoma 2 (Bcl-2). RESULTS Treatment with berberine suppressed cell viability of colorectal cancer by promoting apoptosis level. LncRNA CASC2 was upregulated in cells treated with berberine, and knockdown of lncRNA CASC2 reversed the berberine-induced apoptosis. In addition, anti-apoptotic gene Bcl-2 was suppressed by berberine treatment and lncRNA CASC2, inducing the pro-apoptotic effects. Moreover, lncRNA CASC2 binds to AUF1, which sequestered AUF1 from binding to Bcl-2 mRNA, thus inducing the inactivation of Bcl-2 translation. CONCLUSIONS Our study reveals that lncRNA CASC2 mediates the berberine-induced pro-apoptotic effect via inhibition of Bcl-2 expression at the post-transcriptional level.	30681073	RID06609	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	CASC2	HNRNPD	negatively-E	RIP;western blot	downregulation	RT-qPCR	NA	NA	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	Berberine	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000138668	NA	255082	3184	C10orf5	AUF1|HNRPD	Berberine Promotes Apoptosis of Colorectal Cancer via Regulation of the Long Non-Coding RNA (lncRNA) Cancer Susceptibility Candidate 2 (CASC2)/AU-Binding Factor 1 (AUF1)/B-Cell CLL/Lymphoma 2 (Bcl-2) Axis.BACKGROUND Berberine, a natural isoquinoline alkaloid derived from Berberis genus plants, has been reported to have anti-cancer effects. While cell behavior can be modulated by long non-coding RNAs (lncRNAs), the contributions of lncRNAs in progression and berberine effects on colorectal cancer are largely unknown. Therefore, the present study investigated the involvement and regulatory function of lncRNA cancer susceptibility candidate 2 (CASC2) during the treatment of human colorectal cancer using berberine. MATERIAL AND METHODS Reverse transcription-quantitative PCR (RT-qPCR) was performed to detect the expression levels of lncRNA CASC2 and Bcl-2 mRNA in colorectal cancer cells. MTT assay was performed to evaluate cell viability. Flow cytometry and TUNEL assay were used to analyze the apoptosis of cancer cells. RNA immunoprecipitation (RIP) assay was done to verify the interaction between lncRNA CASC2 and (AU-binding factor 1) AUF1, or AUF1 and B-cell CLL/lymphoma 2 (Bcl-2). RESULTS Treatment with berberine suppressed cell viability of colorectal cancer by promoting apoptosis level. LncRNA CASC2 was upregulated in cells treated with berberine, and knockdown of lncRNA CASC2 reversed the berberine-induced apoptosis. In addition, anti-apoptotic gene Bcl-2 was suppressed by berberine treatment and lncRNA CASC2, inducing the pro-apoptotic effects. Moreover, lncRNA CASC2 binds to AUF1, which sequestered AUF1 from binding to Bcl-2 mRNA, thus inducing the inactivation of Bcl-2 translation. CONCLUSIONS Our study reveals that lncRNA CASC2 mediates the berberine-induced pro-apoptotic effect via inhibition of Bcl-2 expression at the post-transcriptional level.	30681073	RID06610	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	MIR22HG	NCOR2	positively-E	luciferase reporter assay;western blot;RIP;TargetScan;miRTarBase;miRbase;miRDB	downregulation	qRT-PCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-10a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000196498	NA	84981	9612	C17orf91|DKFZp686O06159|MGC14376	CTG26|SMRT|SMRTE|TNRC14|TRAC-1	LncRNA MIR22HG inhibits growth, migration and invasion through regulating the miR-10a-5p/NCOR2 axis in hepatocellular carcinoma cells.Despite the rapidly identified numbers of lncRNA in humans, exploration of the molecular mechanisms of lncRNA is lagging, because the molecular mechanisms of lncRNA can be various and complex in different conditions. In this study, we found a new molecular mechanism for a versatile molecule, MIR22HG. MIR22HG is an lncRNA that contributes to the initiation and progression of many human cancers, including hepatocellular carcinoma (HCC). We report that MIR22HG was downregulated in 120 HCC samples compared with adjacent nontumor liver tissues. More interestingly, decreased expression of MIR22HG in HCC could predict poor prognosis of HCC patients. Knockdown of MIR22HG promoted the growth, migration and invasion of HCC cells. In exploring the molecular mechanism of MIR22HG, we found that MIR22HG functioned as a tumor suppressor in hepatocellular carcinomas, in part through serving as a competing endogenous RNA to modulate the miRNA-10a-5p level. Moreover, NCOR2 was verified to act as the downstream target gene of MIR22HG/miR-10a-5p. In addition, the MIR22HG/miRNA-10a-5p/NCOR2 axis inhibited the activation of the Wnt/beta-catenin pathway. Together, our results demonstrated that MIR22HG inhibited HCC progression in part through the miR-10a-5p/NCOR2 signaling axis and might act as a new prognostic biomarker for HCC patients.We then detected MIR22HG expression  level in 8 HCC cell lines by performing qRT-PCRanalysis and  found that the expression of MIR22HG was decreased along  with ability of HCC cells to metastasize (Figure S1F).	30680848	RID06611	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	CASC2	PTEN	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA CASC2 upregulates PTEN to suppress pancreatic carcinoma cell metastasis by downregulating miR-21.Background: The mechanism of pancreatic cancer metastasis remains poorly understood. Recently, lncRNA CASC2 has been demonstrated to be a tumor suppressor in various types of cancer. This study aimed to explore the mechanism of CASC2 in the regulation of pancreatic cancer metastasis.Methods: The expression levels of CASC2 and miR-21 in pancreatic cells were detected by qRT-PCR Using specific expression vectors, including mimics or shRNA, the expression levels of CASC2, miR-21 and PTEN in pancreatic cells were altered. The association between CASC2, miR-21 and PTEN was detected. Then, cell migration and invasion were assessed using the transwell assay.Results: CASC2 expression was downregulated in the pancreatic cancer cell lines CAPAN-1, BxPC-3, JF305, PANC-1 and SW1990 compared with levels in normal human pancreatic HPDE6-C7 cells. CACS2 overexpression inhibited the migration and invasion of PANC-1 cells and significantly inhibited the expression of miR-21 and PTEN. MiR-21 was a direct target of CACS2. The overexpression of miR-21 significantly abolished the antimetastatic effects of CASC2 on PANC-1 cells. Moreover, the downregulation of PTEN significantly abolished the antimetastatic effects of CASC2.Conclusion: CASC2 functions as a tumor suppressor in pancreatic cancer cells to inhibit tumor cell migration and invasion. Our work revealed a novel regulatory mechanism of the CASC2/miR-21/PTEN axis that may be important in pancreatic cancer.	30675129	RID06612	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Oral squamous cell carcinoma	CASC9	AKT1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cancer progression(+);AKT/mTOR signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000142208	NA	101805492	207	ESCCAL-1|linc-JPH1|LINC00981	AKT|PKB|PRKBA|RAC|RAC-alpha	Increased expression of lncRNA CASC9 promotes tumor progression by suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway in oral squamous cell carcinoma.Recent studies showed that lncRNA CASC9 was upregulated and acted as an oncogene in a variety of tumors. However, the expression and biological functions of CASC9 in oral squamous cell carcinoma (OSCC) remain unknown. In this study, we found for the first time that CASC9 was remarkably upregulated in OSCC tissues and cell lines compared with paired noncancerous tissues and normal oral epithelial cells. Highly expressed CASC9 is strongly associated with tumor size, clinical stage, regional lymph node metastasis and overall survival time in OSCC patients. In vitro, CASC9 knockdown in OSCC cells SCC15 and CAL27 significantly promotes autophagy and apoptosis, while inhibiting proliferation. Moreover, the expression levels of p-AKT, p-mTOR, P62 and BCL-2 were significantly decreased, while the expression levels of BAX and the LC3BII/LC3BI ratio were increased in CASC9-knockdown SCC15 and CAL27 cells. After the addition of the AKT activator SC79 in CASC9-knockdown SCC15 and CAL27 cells, we found that the increased autophagy and apoptosis were remarkably rescued. Furthermore, the increased apoptosis was remarkably rescued in CASC9-knockdown OSCC cells treated with the autophagy inhibitor Autophinib. In addition, CASC9 depletion suppressed tumor growth in vivo. In conclusion, our findings demonstrate that lncRNA CASC9 promotes OSCC progression through enhancing cell proliferation and suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway. CASC9 could potentially be used as a valuable biomarker for OSCC diagnosis and prognosis.	30674868	RID06613	expression association	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MIR503HG	ZEB1	negatively-E	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-);cell metastasis(-);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000148516	NA	84848	6935	H19X|MGC16121	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.	30672010	RID06614	expression association	metastasis,recurrence		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MIR503HG	SNAI1	negatively-E	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-);cell metastasis(-);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000223749	GRCh38_X:134543119-134546642	ENSG00000124216	NA	84848	6615	H19X|MGC16121	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.	30672010	RID06615	expression association	metastasis,recurrence		UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	MIR503HG	N-cadherin	negatively-E	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-);cell metastasis(-);epithelial to mesenchymal transition(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000223749	GRCh38_X:134543119-134546642	NA	NA	84848	NA	H19X|MGC16121	NA	lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.	30672010	RID06616	expression association	metastasis,recurrence		
Urinary bladder cancer	MIR503HG	E-cadherin	positively-E	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-);cell metastasis(-);epithelial to mesenchymal transition(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000223749	GRCh38_X:134543119-134546642	NA	NA	84848	NA	H19X|MIR503HG2	NA	lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.	30672010	RID06617	expression association	metastasis,recurrence		
Gastric cancer	MIR22HG	NOTCH2	negatively-E	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-);NOTCH2 signaling pathway(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000134250	NA	84981	4853	C17orf91|DKFZp686O06159|MGC14376	NA	Long Noncoding RNA (lncRNA) MIR22HG Suppresses Gastric Cancer Progression through Attenuating NOTCH2 Signaling.BACKGROUND Long noncoding RNAs (lncRNAs) are important regulators in human disease, including cancers. LncRNA MIR22HG has been shown to inhibit the progression of endometrial carcinoma, lung cancer, and hepatocellular carcinoma. Its role in gastric cancer is unclear. This study investigated MIR22HG effects on gastric cancer. MATERIAL AND METHODS Gastric cancer tissues (n=43) and adjacent normal tissues (n=21) were collected. Patients' 5-year overall survival rate was analyzed. Human normal gastric mucosal cell line (GES-1) and gastric cancer cell lines (MKN-45, AGS, SGC-7901) were cultured. AGS and MKN-45 cells were transfected by pcDNA3 empty vector, pcDNA3-MIR22HG overexpression vector, MIR22HG siRNA and its negative control, NOTCH2 siRNA and its negative control, respectively. Proliferation was explored by CCK-8 assay. Migration and invasion were explored by Transwell. qRT-PCRand western blot were used to investigate mRNA and proteins expression, respectively. RESULTS MIR22HG expression was decreased in gastric cancer tissues and cells (P<0.05). Low MIR22HG expression indicated lower 5-year overall survival rate (P<0.05). Upregulation of MIR22HG inhibited AGS and MKN-45 cell proliferation, migration and invasion (all P<0.05). Downregulation of MIR22HG elevated AGS and MKN-45 cell proliferation, migration, and invasion (all P<0.05). MIR22HG negatively regulated NOTCH2 signaling. Silencing MIR22HG elevated HEY1 and nucleus NOTCH2 expression. Silencing of NOTCH2 suppressed AGS and MKN-45 cells proliferation, migration and invasion (all P<0.05). CONCLUSIONS LncRNA MIR22HG suppressed gastric cancer progression through attenuating NOTCH2 signaling.	30670679	RID06618	expression association	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	OTUD6B-AS1	E-cadherin	negatively-E	western blot;knockdown	downregulation	qRT-PCR	TCGA	NA	WNT/beta-catenin signaling pathway(-);epithelial to mesenchymal transition(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253738	GRCh38_8:91059318-91070583	NA	NA	100506365	NA	GS1-251I9.4	NA	Novel long noncoding RNA OTUD6B-AS1 indicates poor prognosis and inhibits clear cell renal cell carcinoma proliferation via the Wnt/beta-catenin signaling pathway.Methods: The expression level of OTUD6B-AS1 was measured in 75 paired human ccRCC tissue and corresponding adjacent normal renal tissue samples. The correlations between the OTUD6B-AS1 expression level and clinicopathological features were evaluated using the chi-square test. The effects of OTUD6B-AS1 on ccRCC cells were determined via MTT assay, clone formation assay, transwell assay, and flow cytometry. Furthermore, the impact of OTUD6B-AS1 overexpression on the activation of the Wnt/beta-catenin signaling pathway was investigated. Finally, ACHN cells with OTUD6B-AS1 overexpression were subcutaneously injected into nude mice to evaluate the influence of OTUD6B-AS1 on tumor growth in vivo.Results: In this study, we found that the expression of the lncRNA OTUD6B-AS1 was downregulated in ccRCC tissue samples and that patients with low OTUD6B-AS1 expression had shorter overall survival than patients with high OTUD6B-AS1 expression, which showed that the different expression level of OTUD6B-AS1 indirectly correlated with survival of patients. Lentivirus-mediated OTUD6B-AS1 overexpression significantly decreased the proliferation of ccRCC cells and promoted the apoptosis of the cells. Furthermore, OTUD6B-AS1 overexpression partly inhibited cell migration and invasion. The overexpression of OTUD6B-AS1 decreased the activity of the Wnt/beta-catenin pathway and suppressed the expression of epithelial-to-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin and Snail) in ccRCC cells. In addition, compared with the parental ACHN cells, OTUD6B-AS1-overexpressing ACHN cells injected into nude mice exhibited decreased tumor growth in vivo.Conclusions: Taken together, our findings present a road map for targeting the newly identified lncRNA OTUD6B-AS1 to suppress ccRCC progression in cell lines, and these results elucidate a novel potential therapeutic target for ccRCC treatment. To explore the role of the lncRNA OTUD6B-AS1 in  ccRCC, we analyzed the expression of OTUD6B-AS1 in  a cohort of 75 ccRCC tissue samples and matched nontumor samples using qRT-PCRanalysis,   with our results  showing that OTUD6B-AS1 expression was remarkably  decreased in the ccRCC tissue samples compared with  the paired adjacent normal tissue samples (Fig. 2a and  b).	30670025	RID06619	expression association	prognosis	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Colorectal cancer	SNHG6	E2F5	positively-E	luciferase reporter assay;DIANA lncBase v.2;TargetScan 7.1	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+);apoptosis process(-)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000133740	NA	641638	1875	HBII-276HG|NCRNA00058|U87HG	NA	Long noncoding RNA SNHG6 functions as a competing endogenous RNA by sponging miR-181a-5p to regulate E2F5 expression in colorectal cancer.Methods: The expression of SNHG6 was determined by quantitative real-time PCR in CRC tissues and cells. SNHG6 was downregulated by using RNAi technology. Cell proliferation was examined by MTT and clone formation assays. Cell migration and invasion were determined by wound healing and transwell assays. Fluorescence in situ hybridization assays were performed to examine subcellular localization of SNHG6 in CRC cells. Fluorescence reporter and western blot assays were used to explore the potential mechanisms of SNHG6 in CRC progression.Results: In this study, we found that SNHG6 was significantly upregulated in CRC tissues and cell lines, compared with normal tissues and normal colorectal epithelial cell line NCM460, respectively. High expression of SNHG6 was positively correlated with tumor size, advanced TNM stage, and distant metastasis. Survival analyses revealed that SHNG6 was significantly associated with poor clinical outcomes and could serve as an independent prognostic factor. Loss-of-function studies demonstrated that SNHG6 knockdown inhibited CRC cell proliferation, induced G0/G1 arrest, promoted apoptosis, suppressed CRC cell migration and invasion, and restrained tumor growth. Mechanistic investigations showed that SNHG6 acted as a competing endogenous RNA for miR-181a-5p and attenuated the inhibitory effect of miR-181a-5p on E2F5.Conclusion: Taken together, these results demonstrated that SNHG6 plays a crucial role in CRC progression via miR-181a-5p/E2F5 axis. Therefore, SNHG6 may serve as a prognostic and therapeutic biomarker in CRC.Recently, a growing number of lncRNAs have been reported   to act as ceRNAs by sponging miRNAs and preventing them   from binding functional mRNA targets.21  To investigate the   underlying mechanisms of SNHG6 in CRC tumorigenesis,   bioinformatics tool DIANA lncBase v.2  (22) was used to   predict potential lncRNA miRNA interaction for SNHG6.    We identified that SNHG6 held a potential binding site for   miR-181a-5p at the region of 173 197 amino acids (Figure   5A).  Then, luciferase reporter assay was performed to confirm   the bioinformatics prediction	30666158	RID06620	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Malignant glioma	AGO2	CTNNB1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	tumorigenesis(-);cancer progression(-);apoptosis process(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000168036	NA	27161	1499	CASC7|EIF2C2|LESKRES|LINC00980|PPD|Q10	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA CASC7 inhibits the progression of glioma via regulating Wnt/beta-catenin signaling pathway.Increasing evidence reveal the important role of long non-coding RNAs (lncRNAs) in the initiation and progression of glioma. However, the role of lncRNA cancer susceptibility candidate 7 (CASC7) in glioma is largely unknown. At first, the expression level of CASC7 was tested in glioma tissues and cell lines by using qRT-PCR We applied Kaplan-Meier method to analyze the correlation between the expression level between CASC7 expression and the overall survival rate of glioma patients. We found that CASC7 was downregulated in glioma tissues and cell liens and predicted poor prognosis for patients with glioma. To determine the involvement of CASC7 in the biological processes of glioma, we conducted gain or loss-of function assays in two glioma patients. We found that CASC7 suppressed glioma cell proliferation and induced glioma cell apoptosis. Mechanistically, the expression level of CASC7 was negatively correlated with the expression levels of core factors of Wnt/beta-catenin signaling pathway in glioma cells. Moreover, TOP flash luciferase activity further revealed the negative effect of CASC7 on the activity of Wnt/beta-catenin signaling pathway. Finally, rescue assays were carried out to determine that Wnt/beta-catenin signaling pathway involved in CASC7-mediated glioma progression. Taken together, all research findings suggested that CASC7 inhibited the progression of glioma via regulating Wnt/beta-catenin signaling pathway.	30661904	RID06621	expression association	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	MIR31HG	miR-214	negatively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21453802-21559900	NA	NA	554202	NA	hsa-lnc-31|LncHIFCAR|LOC554202	NA	Long noncoding RNA MIR31HG is activated by SP1 and promotes cell migration and invasion by sponging miR-214 in NSCLC.Long non-coding RNAs(lncRNAs) have been reported to play pivotal roles in various cancers. Recently, MIR31HG was proposed to be involved in tumor progression. However, its role in non small cell lung cancer(NSCLC) remains elusive. In this work, we found that SP1-induced MIR31HG was significantly upregulated in NSCLC tissues and cell lines. Moreover, Cox multivariate survival analysis revealed that high MIR31HG was an independent predictor of poor overall survival(OS). Functionally, knockdown of TINCR obviously suppressed NSCLC cells migration and invasion in vitro and inhibited NSCLC cells metastasis in vivo. Mechanistically, we identified MIR31HG could act as a miR-214 sponge using RNA pull down, luciferase reporter and RIP assays. Lastly, we verified that overexpression of MIR31HG effectively reverses miR-214-induced inhibition of NSCLC cells progression. Therefore, MIR31HG might serve as a promising prognostic marker and potential therapeutic target for NSCLC patients.Firstly, we used qRT-PCRto analyze MIR31HG expression in NSCLC  cell lines, as shown in Fig. 1B, the results revealed that MIR31HG in the  A549, H1299, H1975 and H460 was significantly upregulated compared with the normal human lung epithelial cell line (BEAS-2B).	30659947	RID06622	ceRNA or sponge	metastasis,prognosis		
Gastric cardia adenocarcinoma	SP1	SEMA3B-AS1	positively-E	ChIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000261891	NA	6667	101928931	NA	NA	MiR-6872 host gene SEMA3B and its antisense lncRNA SEMA3B-AS1 function synergistically to suppress gastric cardia adenocarcinoma progression.Methods: The expression levels of SEMA3B, SEMA3B-AS1, and miR-6872 were respectively detected by qRT-PCR western blot, or immunohistochemical staining assays. The methylation status was determined by BGS and BS-MSP methods. In vitro assays were preformed to explore the biological effects of SEMA3B, SEMA3B-AS1, and miR-6872-5p in gastric cancer cells. Chromatin immunoprecipitation assay was used to detect the binding of protein to DNA. The interaction of SEMA3B-AS1 with MLL4 was identified by RNA immunoprecipitation and RNA pull-down assays.Results: Frequent downregulation of SEMA3B, SEMA3B-AS1, and miR-6872 was detected in GCA tissues and gastric cancer cells. Aberrant hypermethylation of the promoter region was more tumor specific  was negatively correlated with the expression level of SEMA3B, SEMA3B-AS1, and miR-6872-5p. Transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and CpG sites hypermethylation within promoter region eliminated Sp1 binding ability. Overexpression of SEMA3B and SEMA3B-AS1 inhibited gastric cancer cell proliferation, migration, and invasion in vitro. SEMA3B-AS1 induced the expression of SEMA3B by interacting with MLL4. ZNF143 might be the target gene of miR-6872-5p and miR-6872-5p functioning synergistically with SEMA3B to suppress cell invasion. Furthermore, SEMA3B, SEMA3B-AS1, and miR-6872-5p expression levels were associated with GCA patients' survival.Conclusions: SEMA3B, SEMA3B-AS1, and miR-6872 may act as tumor suppressors and may serve as potential targets for antitumor therapy.ChIP assay confirmed   the binding of Sp1 to the four sites (Fig. 3m).	30656427	RID06623	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cardia adenocarcinoma	SEMA3B-AS1	SEMA3B	positively-E	knockdown;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	interact with protein	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000261891	NA	ENSG00000012171	NA	101928931	7869	NA	LUCA-1|SemA|sema5|SEMAA|semaV	MiR-6872 host gene SEMA3B and its antisense lncRNA SEMA3B-AS1 function synergistically to suppress gastric cardia adenocarcinoma progression.Methods: The expression levels of SEMA3B, SEMA3B-AS1, and miR-6872 were respectively detected by qRT-PCR western blot, or immunohistochemical staining assays. The methylation status was determined by BGS and BS-MSP methods. In vitro assays were preformed to explore the biological effects of SEMA3B, SEMA3B-AS1, and miR-6872-5p in gastric cancer cells. Chromatin immunoprecipitation assay was used to detect the binding of protein to DNA. The interaction of SEMA3B-AS1 with MLL4 was identified by RNA immunoprecipitation and RNA pull-down assays.Results: Frequent downregulation of SEMA3B, SEMA3B-AS1, and miR-6872 was detected in GCA tissues and gastric cancer cells. Aberrant hypermethylation of the promoter region was more tumor specific and was negatively correlated with the expression level of SEMA3B, SEMA3B-AS1, and miR-6872-5p. Transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and CpG sites hypermethylation within promoter region eliminated Sp1 binding ability. Overexpression of SEMA3B and SEMA3B-AS1 inhibited gastric cancer cell proliferation, migration, and invasion in vitro. SEMA3B-AS1 induced the expression of SEMA3B by interacting with MLL4. ZNF143 might be the target gene of miR-6872-5p and miR-6872-5p functioning synergistically with SEMA3B to suppress cell invasion. Furthermore, SEMA3B, SEMA3B-AS1, and miR-6872-5p expression levels were associated with GCA patients' survival.Conclusions: SEMA3B, SEMA3B-AS1, and miR-6872 may act as tumor suppressors and may serve as potential targets for antitumor therapy.	30656427	RID06624	interact with protein	NA		
Prostate cancer	MALAT1	AR	positively-E	luciferase reporter assay;western blot;StarBase 2.0	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-320b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169083	NA	378938	367	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AIS|DHTR|HUMARA|NR3C4|SBMA|SMAX1	Silencing of lncRNA MALAT1 inhibits cell cycle progression via androgen receptor signaling in prostate cancer cells.Prostate cancer is the second common cancer in men with high morbidity and mortality. Androgen receptor (AR) signaling plays a crucial role in occurrence and development of prostate cancer. In this study, we demonstrated that lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was increased in prostate cancer cells after androgen stimulation, as well as AR. The silencing of MALAT1 inhibited dihydrotestosterone (DHT) administration-induced acceleration of proliferation and cell cycle progression, and increase of AR expression in prostate cancer cells. MALAT1 bound to miR-320b and negatively regulated its expression, and vice versa. AR is a target of miR-320b. The phenotypic changes induced by silencing of MALAT1 were abolished by miR-320b inhibition or AR overexpression. Additionally, MALAT1 knockdown also suppressed the tumorigenesis of prostate cancer cells in nude mice. In summary, the silencing of MALAT1 inactivated AR signaling by sponging miR-320b, and inhibited proliferation and cell cycle progression in prostate cancer cells, suggesting that MALAT1 may be a new target in diagnosis and therapy of prostate cancer in clinic.	30642743	RID06625	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Prostate cancer	MALAT1	DHT	positively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Silencing of lncRNA MALAT1 inhibits cell cycle progression via androgen receptor signaling in prostate cancer cells.Prostate cancer is the second common cancer in men with high morbidity and mortality. Androgen receptor (AR) signaling plays a crucial role in occurrence and development of prostate cancer. In this study, we demonstrated that lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was increased in prostate cancer cells after androgen stimulation, as well as AR. The silencing of MALAT1 inhibited dihydrotestosterone (DHT) administration-induced acceleration of proliferation and cell cycle progression, and increase of AR expression in prostate cancer cells. MALAT1 bound to miR-320b and negatively regulated its expression, and vice versa. AR is a target of miR-320b. The phenotypic changes induced by silencing of MALAT1 were abolished by miR-320b inhibition or AR overexpression. Additionally, MALAT1 knockdown also suppressed the tumorigenesis of prostate cancer cells in nude mice. In summary, the silencing of MALAT1 inactivated AR signaling by sponging miR-320b, and inhibited proliferation and cell cycle progression in prostate cancer cells, suggesting that MALAT1 may be a new target in diagnosis and therapy of prostate cancer in clinic.	30642743	RID06626	transcriptional regulation	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Tongue cancer	MALAT1	JAG1	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell invasion(-);epithelial to mesenchymal transition(-)	ceRNA(miR-124)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000270408	NA	378938	182	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AGS|AHD|AWS|CD339|HJ1|JAGL1	LncRNA UCA1/miR-124 axis modulates TGFbeta1-induced epithelial-mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling.Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor beta1 (TGFbeta1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFbeta1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin. Regarding the molecular mechanism, UCA1 could directly bind to microRNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFbeta1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation.	30635938	RID06627	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE111842,GSE51827,GSE86978)
Tongue cancer	UCA1	JAG1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell invasion(-);epithelial to mesenchymal transition(-)	ceRNA(miR-124)	regulation	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000270408	NA	652995	182	CUDR|LINC00178|onco-lncRNA-36|UCAT1	AGS|AHD|AWS|CD339|HJ1|JAGL1	LncRNA UCA1/miR-124 axis modulates TGFbeta1-induced epithelial-mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling.Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor beta1 (TGFbeta1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFbeta1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin. Regarding the molecular mechanism, UCA1 could directly bind to microRNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFbeta1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation.	30635938	RID06628	ceRNA or sponge	metastasis,prognosis	UP(PAAD);DATA(GSE40174)	UP(LIHC);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE111842,GSE51827,GSE86978)
Tongue cancer	UCA1	TGFbeta1	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell invasion(-);epithelial to mesenchymal transition(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA UCA1/miR-124 axis modulates TGFbeta1-induced epithelial-mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling.Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor beta1 (TGFbeta1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFbeta1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin. Regarding the molecular mechanism, UCA1 could directly bind to microRNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFbeta1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation.	30635938	RID06629	expression association	metastasis,prognosis	UP(PAAD);DATA(GSE40174)	
Gastric cancer	ZEB2-AS1	ZEB2	positively-E	western blot	upregulation	RT-qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000169554	NA	100303491	9839	ZEB2-AS|ZEB2AS|ZEB2NAT	KIAA0569|SIP-1|SIP1|ZFHX1B	However, its role in the pathogenesis of gastric cancer remains unknown. The Wnt/beta-catenin pathway contributes to the development of gastric cancer. ZEB2-AS1 expression was firstly detected in the gastric carcinoma tissue samples as well as in gastric cancer cells. Knockdown of ZEB2-AS1 was performed by ZEB2-AS1-shRNA, and the viability, migration, invasion, and apoptosis of gastric cancer cells were determined by CCK-8, scratch assay, transwell, and flow cytometry, respectively. Furthermore, levels of Ki-67, PCNA, VEGF, MMP9, epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin and ZEB2), cleaved caspase 3/8/9 and PARP, active beta-catenin, c-Myc, cyclinD1, and AXIN2 were assayed by western blot or real-time PCR. Additionally, the role and mechanism of ZEB2-AS1 were confirmed in a xenograft nude mouse model. We found ZEB2-AS1 expression was increased in gastric carcinoma samples, and it was correlated with tumor progression. Also, its expression was elevated in gastric cancer cells. Knockdown of ZEB2-AS1 reduced the proliferation, migration, invasion, and EMT, but increased the apoptosis of gastric carcinoma cells. Furthermore, ZEB2-AS1 downregulation remarkably suppressed the expression of Ki-67, PCNA, VEGF and MMP9, and the activation of Wnt/beta-catenin signaling, whereas elevated the levels of cleaved caspase 3/8/9 and PARP in gastric cancer cells. And ZEB2 overexpression reversed the effects of ZEB2-AS1 downregulation on the proliferation, EMT and inactivation of Wnt/beta-catenin signaling. Additionally, ZEB2-AS1 knockdown inhibited tumor growth, Ki-67 staining, and the expression of VEGF, MMP9, active beta-catenin, c-Myc, cyclinD1, and AXIN2 in mice. In conclusion, ZEB2-AS1 promotes the tumorigenesis of gastric carcinoma that is related to the upregulation of ZEB2 and the activation of the Wnt/beta-catenin pathway. These data suggest that  ZEB2-AS1 functioned and activated the Wnt/beta-catenin signaling pathway via elevating ZEB2 expression	30635820	RID06630	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	Rg3	CCAT1	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	association	RNA-RNA	Ginsenoside Rg3	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	NA	NA	ENSG00000247844	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	Ginsenoside Rg3 inhibits cell growth, migration and invasion in Caco-2 cells by downregulation of lncRNA CCAT1.Background: Colorectal cancer (CRC) is a troublesome disease with high morbidity and mortality. Ginsenoside Rg3 possesses anti-cancer properties. Colon Cancer Associated Transcript 1 (CCAT1) participates in the genesis, development, invasion and metastasis of colorectal cancer. In our study, we explored the effects of Rg3 on CRC cell line Caco-2 by regulating CCAT1.Methods: CRC tissue was obtained from hospital and Caco-2 cells were purchased. Caco-2 cells were treated with Rg3 and/or transfected with pc- CCAT1 or pcDNA3.1. The group without Rg3 treatment was treated as control. Cell viability, cell apoptosis, cell migration and invasion were detected by Cell Counting Kit-8 assay, flow cytometry and Transwell chamber migration/invasion assay, respectively. The expression of CyclinD1, apoptosis related proteins (p53, Bcl-2, Bax, pro-/Cleaved-Caspase-3), migration and invasion related proteins (MMP-9 and vimentin), and phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT) related proteins (p/t-PI3K, p/t-AKT) were examined by western blot. The expression of CCAT1 was measured by quantitative real time RCR (qRT-PCR.Results: Rg3 significantly decreased cell viability, migration and invasion, and promoted apoptosis. Meanwhile, the expression of Cyclin D1, matrix metalloproteinase (MMP)-9 and vimentin was downregulated. The expression of apoptosis-related proteins p53, Bax, and Cleaved-Caspase-3 were upregulated while Bcl-2 was downregulated by the treatment of Rg3 compared with control. Furthermore, CCAT1 was upregulated in CRC tissue and Rg3 negatively regulated CCAT1 expression. Transfection with pc-CCAT1 led to the opposite results as compared with transfection with pcDNA3.1 in Rg3 treated cells. In addition, Rg3 decreased the phosphorylation of PI3K and AKT.Conclusion: Ginsenoside Rg3 inhibits migration and invasion, and promotes apoptosis of Caco-2 cells by suppression expression of LncRNA CCAT1.	30633886	RID06631	transcriptional regulation	metastasis		
Gastric cancer	LINC02465	PIK3CA	positively-E	western blot;knockdown	upregulation	qRT-PCR	TCGA	NA	cancer progression(+);PI3K/AKT signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249618	GRCh38_4:129771596-129975329	ENSG00000121879	NA	107986313	5290	NA	PI3K	Knockdown of LINC02465 Suppresses Gastric Cancer Cell Growth and Metastasis Via PI3K/AKT Pathway.Gastric cancer (GC) is the second primary cause of cancer-associated mortality around the world. Long noncoding RNAs (lncRNAs) are critical modulators of multiple cellular processes, and their abnormal expression and/or function are related to a variety of diseases, including cancer. Various lncRNAs have been shown to exert a functional role in GC, but more still remain to be identified, since the therapies for GC patients are limited. Here we discover LINC02465, a novel recognized lncRNA, is upregulated and correlated with tumor size, tumor stage, lymph node metastasis, and differentiation in gastric cancer. In addition, we found that high LINC02465 level in GC patients is closely related to poor prognosis. Moreover, our findings reveal that LINC02465 silence suppresses cell proliferation and migration, invasion, and epithelial-mesenchymal transition in vitro. Conversely, LINC02465 overexpression displays a completely opposite way. Meanwhile, LINC02465 inhibition also limits tumor growth in vivo. Mechanistically, LINC02465 inhibition inactivates PI3K/AKT signaling pathway, and the activation of this pathway by 740Y-P reverses the inhibition effect of LINC02465 suppression on biological behaviors of GC cells. Taken together, LINC02465 is an oncogenic lncRNA that facilitates the tumorigenesis and progression of GC via PI3K/AKT pathway, demonstrating a novel effective therapeutic target and prognostic biomarker for GC patients.	30632400	RID06632	expression association	metastasis,prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Breast cancer	UCA1	CDKN1A	negatively-E	RIP;ChIP	upregulation	RT-PCR	NA	NA	chemoresistance(+);cell cycle(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	interact with protein	association	RNA-protein	Tamoxifen	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway.Tamoxifen is the gold standard for breast cancer endocrinotherapy. However, drug resistance remains a major limiting factor of tamoxifen treatment. Long non-coding (lnc) RNA serves an important role in drug resistance; however, the molecular mechanisms of tamoxifen resistance in breast cancer endocrinotherapy are largely unclear. lncRNA urothelial cancer associated 1 (lncRNA UCA1, UCA1) has been proven to be dysregulated in human breast cancer and promotes cancer progression. In the present study, it was demonstrated that UCA1 was significantly upregulated in breast cancer tissues compared with healthy tissues. Furthermore, the expression level of UCA1 was significantly greater in tamoxifen-resistant breast cancer cells (LCC2 and LCC9) when compared with those in the tamoxifen-sensitive breast cancer cells (MCF-7 and T47D). UCA1 silencing in LLC2 and LLC9 cells increased tamoxifen drug sensitivity by promoting cell apoptosis and arresting the cell cycle at the G2/M phase. Notably, the induced overexpression of UCA1 in MCF-7 and T47D cells decreased the drug sensitivity of tamoxifen. The molecular mechanism involved in UCA1-induced tamoxifen-resistance was also investigated. It was identified that UCA1 was physically associated with the enhancer of zeste homolog 2 (EZH2), which suppressed the expression of p21 through histone methylation (H3K27me3) on the p21 promoter. In addition, it was demonstrated that UCA1 expression was paralleled to the phosphorylation of CAMP responsive element binding protein (CREB) and AKT. When LCC2 cells were treated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway inhibitor LY294002, the phosphorylation levels of CREB and AKT were significantly downregulated. Taken together, it was concluded that UCA1 regulates the EZH2/p21 axis and the PI3K/AKT signaling pathway in breast cancer, and may be a potential therapeutic target for solving tamoxifen resistance.UCA1 contributes to tamoxifen resistance in breast cancer cells through the PI3K/AKT signaling pathway.It was revealed that the level of UCA1   expression in LCC2 and LCC9 cells was >20-fold greater   when compared with that in MCF-7 and T47D cells (P<0.001),   suggesting a positive association between tamoxifen resistance   and UCA1 expression in breast cancer cells.	30628639	RID06633	interact with protein	chemoresistance	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Breast cancer	UCA1	CREB	positively-E	RIP;ChIP	upregulation	RT-PCR	NA	NA	chemoresistance(+);cell cycle(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	phosphorylated	regulation	RNA-protein	Tamoxifen	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118260	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	Long non-coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway.Tamoxifen is the gold standard for breast cancer endocrinotherapy. However, drug resistance remains a major limiting factor of tamoxifen treatment. Long non-coding (lnc) RNA serves an important role in drug resistance; however, the molecular mechanisms of tamoxifen resistance in breast cancer endocrinotherapy are largely unclear. lncRNA urothelial cancer associated 1 (lncRNA UCA1, UCA1) has been proven to be dysregulated in human breast cancer and promotes cancer progression. In the present study, it was demonstrated that UCA1 was significantly upregulated in breast cancer tissues compared with healthy tissues. Furthermore, the expression level of UCA1 was significantly greater in tamoxifen-resistant breast cancer cells (LCC2 and LCC9) when compared with those in the tamoxifen-sensitive breast cancer cells (MCF-7 and T47D). UCA1 silencing in LLC2 and LLC9 cells increased tamoxifen drug sensitivity by promoting cell apoptosis and arresting the cell cycle at the G2/M phase. Notably, the induced overexpression of UCA1 in MCF-7 and T47D cells decreased the drug sensitivity of tamoxifen. The molecular mechanism involved in UCA1-induced tamoxifen-resistance was also investigated. It was identified that UCA1 was physically associated with the enhancer of zeste homolog 2 (EZH2), which suppressed the expression of p21 through histone methylation (H3K27me3) on the p21 promoter. In addition, it was demonstrated that UCA1 expression was paralleled to the phosphorylation of CAMP responsive element binding protein (CREB) and AKT. When LCC2 cells were treated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway inhibitor LY294002, the phosphorylation levels of CREB and AKT were significantly downregulated. Taken together, it was concluded that UCA1 regulates the EZH2/p21 axis and the PI3K/AKT signaling pathway in breast cancer, and may be a potential therapeutic target for solving tamoxifen resistance. ). A previous study demonstrated that cell cycle  progression was greatly arrested in UCA1 knockdown cells,  and CREB expression levels were significantly downregulated  simultaneously (33).	30628639	RID06634	epigenetic regulation	chemoresistance	UP(PAAD);DATA(GSE40174)	
Breast cancer	UCA1	AKT1	positively-E	RIP;ChIP	upregulation	RT-PCR	NA	NA	chemoresistance(+);cell cycle(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	association	RNA-protein	Tamoxifen	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000142208	NA	652995	207	CUDR|LINC00178|onco-lncRNA-36|UCAT1	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway.Tamoxifen is the gold standard for breast cancer endocrinotherapy. However, drug resistance remains a major limiting factor of tamoxifen treatment. Long non-coding (lnc) RNA serves an important role in drug resistance; however, the molecular mechanisms of tamoxifen resistance in breast cancer endocrinotherapy are largely unclear. lncRNA urothelial cancer associated 1 (lncRNA UCA1, UCA1) has been proven to be dysregulated in human breast cancer and promotes cancer progression. In the present study, it was demonstrated that UCA1 was significantly upregulated in breast cancer tissues compared with healthy tissues. Furthermore, the expression level of UCA1 was significantly greater in tamoxifen-resistant breast cancer cells (LCC2 and LCC9) when compared with those in the tamoxifen-sensitive breast cancer cells (MCF-7 and T47D). UCA1 silencing in LLC2 and LLC9 cells increased tamoxifen drug sensitivity by promoting cell apoptosis and arresting the cell cycle at the G2/M phase. Notably, the induced overexpression of UCA1 in MCF-7 and T47D cells decreased the drug sensitivity of tamoxifen. The molecular mechanism involved in UCA1-induced tamoxifen-resistance was also investigated. It was identified that UCA1 was physically associated with the enhancer of zeste homolog 2 (EZH2), which suppressed the expression of p21 through histone methylation (H3K27me3) on the p21 promoter. In addition, it was demonstrated that UCA1 expression was paralleled to the phosphorylation of CAMP responsive element binding protein (CREB) and AKT. When LCC2 cells were treated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway inhibitor LY294002, the phosphorylation levels of CREB and AKT were significantly downregulated. Taken together, it was concluded that UCA1 regulates the EZH2/p21 axis and the PI3K/AKT signaling pathway in breast cancer, and may be a potential therapeutic target for solving tamoxifen resistance.	30628639	RID06635	expression association	chemoresistance	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	LINC00339	HOXC6	positively-E	dual-luciferase reporter analysis;RIP;Targetscan;lncBase v2.0	upregulation	microarray;qPCR	GSE27515	NA	cell cycle(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-377-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000197757	NA	29092	3223	HSPC157|NCRNA00339	HOX3|HOX3C	Long noncoding RNA Linc00339 promotes triple-negative breast cancer progression through miR-377-3p/HOXC6 signaling pathway.Recently, long noncoding RNAs (lncRNAs) have become the key gene regulators and prognostic biomarkers in various cancers. Through microarray data, Linc00339 was identified as a candidate oncogenic lncRNA. We compared the expression levels of Linc00339 in several breast cancer cell lines and normal mammary gland epithelial cell line. The effects of Linc00339 on tumor progression were examined both in vitro and in vivo. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were applied to evaluate the functions of Linc00339, miR-377-3p, and HOXC6 on cell proliferation. Flow cytometry analysis was used to detect apoptosis and cell cycle distribution. Overall survival (OS) was analyzed using data from The Cancer Genome Atlas and molecular taxonomy of breast cancer international consortium (METABRIC). Dual luciferase assay and RNA immunoprecipitation were performed to confirm the interaction between Linc003339 and miR-377-3p. Linc00339 was increased in breast cancer cell lines compared with the normal epithelial cell. Through in vitro and in vivo experiments, Linc00339 overexpression promoted triple-negative breast cancer (TNBC) proliferation, inhibited cell cycle arrest, and suppressed apoptosis. Silencing of Linc00339 obtained the opposite effects. Mechanistic investigations demonstrated that Linc00339 could sponge miR-377-3p and regulate its expression. Higher expression of miR-377-3p indicated longer OS in breast cancer patients, especially in TNBC patients. Overexpression of miR-377-3p retarded TNBC cell growth through regulating cell cycle distribution and apoptosis. And miR-377-3p was involved in Linc00339-mediated TNBC proliferation through regulating HOXC6 expression. Knockdown of HOXC6 inhibited TNBC progression. In conclusion, our results illuminated that the novel Linc00339/miR-377-3p/HOXC6 axis played a critical role in TNBC progression and might be a promising therapeutic target for TNBC treatment.Expression levels of Linc00339 in benign and malignant breast epithelial cell lines were determined by qPCR.	30618083	RID06636	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Breast cancer	LINC00518	CDX2	negatively-E	luciferase reporter assay;RIP;western blot;RIP	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	ENSG00000183674	GRCh38_6:10429255-10435015	ENSG00000165556	NA	221718	1045	C6orf218|MGC40222	CDX3	Down-regulated expression of LINC00518 prevents epithelial cell growth and metastasis in breast cancer through the inhibition of CDX2 methylation and the Wnt signaling pathway.Breast cancer (BC)-related mortality is associated with the potential metastatic properties of the primary breast tumors. The following study was conducted with the main focus on the effect of LINC00518 on the growth and metastasis of BC epithelial cells via the Wnt signaling pathway through regulation of the methylation of CDX2 gene. Initially, differentially expressed long intergenic non-protein coding RNAs (lincRNAs) related to BC were screened out in the Cancer Genome Atlas (TCGA) database, after which we detected the LINC00518 expression and localization in BC tissues and cells. Then the CDX2 positive expression and methylation level were identified. The targeting relationship of LINC00518 and CDX2, and binding methyltransferase in the promoter region were examined. BC epithelial cell proliferation, colony formation ability, invasion, migration and apoptosis were further evaluated. The lincRNA expression data related to BC downloaded from the TCGA database revealed that there was a high expression of LINC00518 in BC, and a negative correlation between LINC00518 and CDX2. In addition, LINC00518 promotes CDX2 methylation by recruiting DNA methyltransferase through activating the Wnt signaling pathway. The down-regulation of LINC00518 inhibited proliferation, invasion, migration, and EMT of BC epithelial cells while enhancing apoptosis. The inhibitory effects of LINC00518 down-regulation was reversed by CDX2 down-regulation. In conclusion, our findings revealed that down-regulation of LINC00518 might have the ability to suppress BC progression by up-regulating CDX2 expression through the reduction of methylation and blockade of the Wnt signaling pathway, resulting in the inhibition of proliferation and promotion of apoptosis of BC epithelial cells.The results of RT-qPCR  showed that there was a significantly higher LINC00518 expression in BC tissues than that in adjacent normal tissue (p < 0.05).	30611858	RID06637	epigenetic regulation	metastasis	UP(SKCM);DATA(GSE38495)	
Prostate cancer	GHET1	KLF2	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	HIF-1alpha/Notch-1 signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000127528	NA	102723099	10365	lncRNA-GHET1	LKLF	Knockdown of LncRNA GHET1 suppresses prostate cancer cell proliferation by inhibiting HIF-1alpha/Notch-1 signaling pathway via KLF2.Prostate cancer (PC) is one of the most common cancers in male groups worldwide. Long noncoding RNAs (LncRNAs) are reported to be dysregulated in a variety of cancers, including PC. This study aimed to explore the role of LncRNA GHET1 in the pathogenesis of PC. RT-qPCR was carried out to examine the relative expression level of GHET1 in PC patients. In vitro, GHET1 siRNA (si-GHET1) was used to investigate the biological role of GHET1 in PC cell lines. Cell proliferation was detected by CCK-8 and colony formation assay, while cell cycle and cell apoptosis were analyzed using flow cytometry. Moreover, western blot was carried out to measure the protein expression levels of KLF2 and HIF-1alpha/Notch-1 signal pathway. We found that GHET1 showed higher expression in PC tissues and had a negative correlation with KLF2 expression. Knockdown of GHET1 significantly suppressed the cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis. Additionally, si-GHET1 transfection induced KLF2 upregulation and HIF-1alpha/Notch-1 signal pathway suppression, which could be rescued by si-KLF2 transfection. These results suggest the key role of GHET1 in PC progression. Moreover, GHET1 might be explored to be a potential target for clinical treatment of PC. - 2019 BioFactors, 45(3):364-373, 2019.	30609158	RID06638	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	CASC2	AKT1	negatively-F	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000142208	NA	255082	207	C10orf5	AKT|PKB|PRKBA|RAC|RAC-alpha	Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway.Methods: The CASC2 expression was measured in PTC samples and normal tissues by using quantitative real-time polymerase chain reaction. The lentiviral vectors were used to establish CASC2 overexpression models in PTC cell lines to determine the effects of CASC2 on cell proliferation, apoptosis, migration, and invasion. A tumor xenograft animal model was used to examine the functions of overexpression CASC2.Results: CASC2 expression was significantly decreased in PTC tumor tissues than adjacent normal tissues. CASC2 downregulation in PTC tissues significantly correlated with the tumor size, the presence of multifocal lesions, and the advanced pathological stage. CASC2 overexpression suppressed the cell proliferation and promoted apoptosis in PTC cell lines and CASC2 overexpression resulted in the inactivation of protein kinase B (PKB/AKT) and extracellular signal-regulated kinases (ERK1/2). The regulatory effects of CASC2 on PTC cell biological behavior were further enhanced by mitogen-activated protein kinase kinase (MEK) inhibitor U0126 or AKT1/2/3 inhibitor MK-2206 2HCl. CASC2 overexpression suppressed tumor growth in PTC cells in xenograft mouse models.Conclusion: Our results indicated that CASC2 significantly suppressed tumorigenesis in PTC and CASC2 may serve as a novel prognostic marker or therapeutic target.	30609134	RID06639	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	CASC2	MAPK3	negatively-F	western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	association	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000102882	NA	255082	5595	C10orf5	ERK1|p44erk1|p44mapk|PRKM3	Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway.Methods: The CASC2 expression was measured in PTC samples and normal tissues by using quantitative real-time polymerase chain reaction. The lentiviral vectors were used to establish CASC2 overexpression models in PTC cell lines to determine the effects of CASC2 on cell proliferation, apoptosis, migration, and invasion. A tumor xenograft animal model was used to examine the functions of overexpression CASC2.Results: CASC2 expression was significantly decreased in PTC tumor tissues than adjacent normal tissues. CASC2 downregulation in PTC tissues significantly correlated with the tumor size, the presence of multifocal lesions, and the advanced pathological stage. CASC2 overexpression suppressed the cell proliferation and promoted apoptosis in PTC cell lines and CASC2 overexpression resulted in the inactivation of protein kinase B (PKB/AKT) and extracellular signal-regulated kinases (ERK1/2). The regulatory effects of CASC2 on PTC cell biological behavior were further enhanced by mitogen-activated protein kinase kinase (MEK) inhibitor U0126 or AKT1/2/3 inhibitor MK-2206 2HCl. CASC2 overexpression suppressed tumor growth in PTC cells in xenograft mouse models.Conclusion: Our results indicated that CASC2 significantly suppressed tumorigenesis in PTC and CASC2 may serve as a novel prognostic marker or therapeutic target.	30609134	RID06640	expression association	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	HIF1A-AS2	BAX	negatively-E	western blot;knockdown	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000087088	NA	100750247	581	3'aHIF-1A|aHIF	BCL2L4	Upregulated AHIF-mediated radioresistance in glioblastoma.Long non-coding RNAs (lncRNAs) play vital roles in the pathobiology of glioblastoma multiforme (GBM). Though radiotherapy remains the most effective component of multiple therapies for patients with GBM, lncRNAs conferring GBM radioresistance are less unknown. Here, the present study identified that the antisense transcript of hypoxia-inducible factor-1alpha (AHIF) was upregulated in GBM cells after radiotherapy. The deregulation of AHIF affected GBM cell clonogenic formation, DNA repair and apoptosis. Notably, knockdown of AHIF inhibited tumorigenesis after radiotherapy in vivo. Further biochemical analysis identified that AHIF regulated proteins associated with apoptosis after radiotherapy. Thus, the present data illustrate that suppression of AHIF increases radiosensitivity in GBM cells, which may be a potential diagnostic and therapeutic target for GBM patients.	30606477	RID06641	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	HIF1A-AS2	Caspase7	negatively-E	western blot;knockdown	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258667	GRCh38_14:61707564-61751099	NA	NA	100750247	NA	3'aHIF-1A|aHIF	NA	Upregulated AHIF-mediated radioresistance in glioblastoma.Long non-coding RNAs (lncRNAs) play vital roles in the pathobiology of glioblastoma multiforme (GBM). Though radiotherapy remains the most effective component of multiple therapies for patients with GBM, lncRNAs conferring GBM radioresistance are less unknown. Here, the present study identified that the antisense transcript of hypoxia-inducible factor-1alpha (AHIF) was upregulated in GBM cells after radiotherapy. The deregulation of AHIF affected GBM cell clonogenic formation, DNA repair and apoptosis. Notably, knockdown of AHIF inhibited tumorigenesis after radiotherapy in vivo. Further biochemical analysis identified that AHIF regulated proteins associated with apoptosis after radiotherapy. Thus, the present data illustrate that suppression of AHIF increases radiosensitivity in GBM cells, which may be a potential diagnostic and therapeutic target for GBM patients.	30606477	RID06642	expression association	NA		
Glioblastoma	HIF1A-AS2	BCL2	negatively-E	western blot;knockdown	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	NA	association	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258667	GRCh38_14:61707564-61751099	ENSG00000171791	NA	100750247	596	3'aHIF-1A|aHIF	Bcl-2|PPP1R50	Upregulated AHIF-mediated radioresistance in glioblastoma.Long non-coding RNAs (lncRNAs) play vital roles in the pathobiology of glioblastoma multiforme (GBM). Though radiotherapy remains the most effective component of multiple therapies for patients with GBM, lncRNAs conferring GBM radioresistance are less unknown. Here, the present study identified that the antisense transcript of hypoxia-inducible factor-1alpha (AHIF) was upregulated in GBM cells after radiotherapy. The deregulation of AHIF affected GBM cell clonogenic formation, DNA repair and apoptosis. Notably, knockdown of AHIF inhibited tumorigenesis after radiotherapy in vivo. Further biochemical analysis identified that AHIF regulated proteins associated with apoptosis after radiotherapy. Thus, the present data illustrate that suppression of AHIF increases radiosensitivity in GBM cells, which may be a potential diagnostic and therapeutic target for GBM patients.	30606477	RID06643	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Endometrial cancer	ATB	miR-126	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);PIK3R2/Sox2 signaling pathway(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Long Noncoding RNA-ATB Impairs the Function of Tumor Suppressor miR-126-Mediated Signals in Endometrial Cancer for Tumor Growth and Metastasis.Methods: Endometrial cancer tissues and normal tissues (n = 35) were collected to determine the expression and clinical significance of Lnc-ATB, and bioinformatics analysis was used to predict the miRNA target. siRNA was used to estimate the function of Lnc-ATB in EC cell lines and in vivo.Result: The expression of Lnc-ATB is up-regulated in tumor tissues and EC cell lines. Patients with high expressed Lnc-ATB have high FIGO stage and poor tumor differentiation. The tumor suppressor miR-126 interacted with Lnc-ATB. Down-regulated miR-126 negative correlated with FIGO stage and tumor differentiation. Knockdown of Lnc-ATB in RL95 and HEC1A cell lines increased the miR-126 level and impaired the cell vitality, induced caspase-3-related tumor apoptosis and G1/S arrest. However, abrogation of miR-126 by its inhibitors counteracted Lnc-ATB knockdown-induced tumor inhibition via regulation of miR-126 target gene PIK3R2 and Sox2-related apoptosis and cell cycle pathway. Meanwhile, Lnc-ATB knockdown also suppressed the migration and invasion and inhibited TGF-beta-induced epithelial-mesenchymal transition (EMT) phenotype via miR-126. Knockdown of Lnc-ATB in vivo remarkably induced tumor regression via restoration of tumor suppressor miR-126, leading to deceased tumor volume, reduced expression of PCNA and PIK3R2/Sox2 signals and EMT phenotype in tumor tissues.Conclusion: These data demonstrate the tumorigenic role of Lnc-ATBs in endometrial cancer via abrogation of tumor suppressor miR-126 signals.These results demonstrated that Lnc-ATB  could function as competitive endogenous RNA (ceRNA)  directly sponge to miR-126 and abrogate the availability of  miR-126 in EC cells.The results of quantitative real time polymerase chain  reaction (Q-PCR) indicated that the Lnc-ATB level was  significantly elevated in EC tissues when compared with  normal tissues (Fig. 1A).	30601064	RID06644	ceRNA or sponge	metastasis		
Papillary thyroid carcinoma	NEAT1	FN1	positively-E	luciferase reporter assay;western blot;bioinformatics	upregulation	qRT-PCR	NA	NA	PI3K/AKT signaling pathway(+);chemosensitivity(-)	ceRNA(miR-101-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000115414	NA	283131	2335	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CIG|FINC|GFND2|LETS|MSF	Downregulation of NEAT1 reverses the radioactive iodine resistance of papillary thyroid carcinoma cell via miR-101-3p/FN1/PI3K-AKT signaling pathway.Considering the resistance of papillary thyroid cancer (PTC) 131I therapy, this study was designed to find a solution at molecular respect. By probing into lncRNA-NEAT1/miR-101-3p/FN1 axis and PI3K/AKT signaling pathway, this study provided a potential target for PTC therapy. 131I-resistant cell lines were established by continuous treatment with median-lethal 131I. Bioinformatic analysis was applied to filtrate possible lncRNA/miRNA/mRNA and related signaling pathway. Luciferase reporter assay was employed in the verification of the targeting relationship between lncRNA and miRNA as well as miRNA and mRNA. MTT assay and flow cytometry assay were performed to observe the impact of NEAT1/miR-101-3p/FN1 on cell viability and apoptosis in radioactivity iodine (RAI)-resistant PTC cell lines, respectively. western blot and qRT-PCRwere conducted to measure the expression of proteins and mRNAs in RAI-resistant PTC tissues and cells. Meanwhile, endogenous PTC mice model were constructed, in order to verify the relation between NEAT1 and RAI-resistance in vivo. NEAT1 was over-expressed in RAI-resistant PTC tissues and cell lines and could resist RAI by accelerating proliferation accompanied by suppressing apoptosis. It indicated that overexpressed NEAT1 restrained the damage of RAI to tumor in both macroscopic and microcosmic. Besides, NEAT1/miR-101-3p exhibited a negative correlation by directly targeting each other. The expression of FN1, an overexpressed downstream protein in RAI-resistance PTC tissues, could be tuned down by miR-101-3p, while the decrease could be restored by NEAT1. In conclusion, both in vitro and in vivo, NEAT1 suppression could inhibit 131I resistance of PTC by upregulating miR-101-3p/FN1 expression and inactivated PI3K/AKT signaling pathway both in vitro and in vivo.	30596336	RID06645	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Pancreatic cancer	TUG1	ITGB1	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000150093	NA	55000	3688	FLJ20618|LINC00080|NCRNA00080	CD29|FNRB|GPIIA|MDF2|MSK12	Long Noncoding RNA TUG1/miR-29c Axis Affects Cell Proliferation, Invasion, and Migration in Human Pancreatic Cancer.Given the low resection rate and chemoresistance of patients with pancreatic cancer (PC), their survival rates are typically poor. Long noncoding RNAs (lncRNAs) have recently been shown to play an important role in tumourigenesis and human cancer progression, including in PC. In this study, we aimed to investigate the role of taurine-upregulated gene 1 (TUG1) in PC. A quantitative polymerase chain reaction was used to analyse TUG1 expression in PC tissues and peritumoural normal tissues. TUG1 was overexpressed in PC tissues compared with that in peritumoural normal tissues, and the high expression of TUG1 was associated with the poor prognosis of patients with PC. Furthermore, TUG1 knockdown significantly inhibited the proliferation and invasion of PC cells both in vitro and in vivo, while overexpression TUG1 promoted tumour cell proliferation, migration, and invasion. TUG1 directly targeted miR-29c, a tumour suppressor in several cancers. TUG1 knockdown significantly increased the expression of miR-29c and subsequently induced the downregulation of integrin subunit beta 1 (ITGB1), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9). The downregulation of miR-29c abolished the TUG1 knockdown-mediated inhibition of tumour growth in vitro and in vivo, whereas the upregulation of miR-29c enhanced the effects of TUG1 knockdown on PC cells. In conclusion, we demonstrate for the first time the oncogenic role of TUG1 in PC. The downregulation of TUG1 significantly inhibited the growth and migratory ability of PC cells in vitro and in vivo by targeting miR-29c. Our study provides a novel potential diagnostic biomarker and therapeutic target for PC.qRT-PCRperformed to analyse TUG1 expression in 72 PC samples and 20 peritumoural  normal tissues.	30595764	RID06646	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	TUG1	MMP2	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000087245	NA	55000	4313	FLJ20618|LINC00080|NCRNA00080	CLG4|CLG4A|TBE-1	Long Noncoding RNA TUG1/miR-29c Axis Affects Cell Proliferation, Invasion, and Migration in Human Pancreatic Cancer.Given the low resection rate and chemoresistance of patients with pancreatic cancer (PC), their survival rates are typically poor. Long noncoding RNAs (lncRNAs) have recently been shown to play an important role in tumourigenesis and human cancer progression, including in PC. In this study, we aimed to investigate the role of taurine-upregulated gene 1 (TUG1) in PC. A quantitative polymerase chain reaction was used to analyse TUG1 expression in PC tissues and peritumoural normal tissues. TUG1 was overexpressed in PC tissues compared with that in peritumoural normal tissues, and the high expression of TUG1 was associated with the poor prognosis of patients with PC. Furthermore, TUG1 knockdown significantly inhibited the proliferation and invasion of PC cells both in vitro and in vivo, while overexpression TUG1 promoted tumour cell proliferation, migration, and invasion. TUG1 directly targeted miR-29c, a tumour suppressor in several cancers. TUG1 knockdown significantly increased the expression of miR-29c and subsequently induced the downregulation of integrin subunit beta 1 (ITGB1), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9). The downregulation of miR-29c abolished the TUG1 knockdown-mediated inhibition of tumour growth in vitro and in vivo, whereas the upregulation of miR-29c enhanced the effects of TUG1 knockdown on PC cells. In conclusion, we demonstrate for the first time the oncogenic role of TUG1 in PC. The downregulation of TUG1 significantly inhibited the growth and migratory ability of PC cells in vitro and in vivo by targeting miR-29c. Our study provides a novel potential diagnostic biomarker and therapeutic target for PC.	30595764	RID06647	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Pancreatic cancer	TUG1	MMP9	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	ceRNA(miR-29c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000100985	NA	55000	4318	FLJ20618|LINC00080|NCRNA00080	CLG4B	Long Noncoding RNA TUG1/miR-29c Axis Affects Cell Proliferation, Invasion, and Migration in Human Pancreatic Cancer.Given the low resection rate and chemoresistance of patients with pancreatic cancer (PC), their survival rates are typically poor. Long noncoding RNAs (lncRNAs) have recently been shown to play an important role in tumourigenesis and human cancer progression, including in PC. In this study, we aimed to investigate the role of taurine-upregulated gene 1 (TUG1) in PC. A quantitative polymerase chain reaction was used to analyse TUG1 expression in PC tissues and peritumoural normal tissues. TUG1 was overexpressed in PC tissues compared with that in peritumoural normal tissues, and the high expression of TUG1 was associated with the poor prognosis of patients with PC. Furthermore, TUG1 knockdown significantly inhibited the proliferation and invasion of PC cells both in vitro and in vivo, while overexpression TUG1 promoted tumour cell proliferation, migration, and invasion. TUG1 directly targeted miR-29c, a tumour suppressor in several cancers. TUG1 knockdown significantly increased the expression of miR-29c and subsequently induced the downregulation of integrin subunit beta 1 (ITGB1), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9). The downregulation of miR-29c abolished the TUG1 knockdown-mediated inhibition of tumour growth in vitro and in vivo, whereas the upregulation of miR-29c enhanced the effects of TUG1 knockdown on PC cells. In conclusion, we demonstrate for the first time the oncogenic role of TUG1 in PC. The downregulation of TUG1 significantly inhibited the growth and migratory ability of PC cells in vitro and in vivo by targeting miR-29c. Our study provides a novel potential diagnostic biomarker and therapeutic target for PC.	30595764	RID06648	ceRNA or sponge	chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Melanoma	SNHG7	PI3KR3	positively-E	western blot;knockdown;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	ceRNA(miR-9)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	Long non-coding RNA SNHG7 promotes malignant melanoma progression through negative modulation of miR-9.Long non-coding small nucleolar RNA host gene 7 (lncRNA SNHG7) was verified to act as an onco-gene in human cancers. Nevertheless, the role of SNHG7 in malignant melanoma remains elusive. The present study showed an increase of SNHG7 expression in malignant melanoma tissues and cell lines. Besides, SNHG7 knockdown inhibited proliferation and migration in malignant melanoma cells. Bioinformatics analysis demonstrated that SNHG7 functions as a molecular sponge for miR-9 in biological behavior of melanoma cells. And miR-9 could inhibit the expression of PI3KR3 by binding with the 3'-UTR. Furthermore, PI3KR3, pAKT, cyclin D1 and Girdin expression was down-regulated after SNHG7 knockdown by siRNA. In addition, SNHG7 knockdown decreased xenograft growth in vivo. Taken together, this research demonstrated that SNHG7 was an oncogene in malignant melanoma, providing a novel insight for the pathogenesis and new potential therapeutic target for malignant melanoma.	32365219	RID06649	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Non-small cell lung cancer	E2F1	SBF2-AS1	positively-E	ChIP;luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000246273	GRCh38_11:9758268-9811335	1869	283104	RBBP3|RBP3	NA	E2F1-Induced Overexpression of Long Noncoding RNA SBF2-AS1 Promotes Non-Small-Cell Lung Cancer Metastasis Through Regulating miR-362-3p/GRB2 Axis.Long noncoding RNA SBF2 antisense RNA 1 (lncRNA SBF2-AS1) has been reported to be involved in non-small-cell lung cancer (NSCLC) tumorigenesis. However, the biological role and regulatory mechanism of lncRNA SBF2-AS1 on NSCLC metastasis remain largely unknown. In this study, the expression level and functional role of SBF2-AS1 were investigated in both NSCLC tissues and cell lines. We found that SBF2-AS1 was upregulated in both NSCLC tissues and cell lines. Patients with high levels of SBF2-AS1 have larger tumors, higher malignancy, and poor prognosis. Knockdown of SBF2-AS1 significantly inhibited tumor growth in vivo and cell proliferation, migration, and invasion in vitro. Moreover, bioinformatics analysis, chromatin immunoprecipitation assay, and luciferase reporter assay proved that the upregulation of SBF2-AS1 was mediated by transcription factor E2F1. Further experiments demonstrated that miR-362-3p had complementary binding site with 3'-UTR of SBF2-AS1. Besides, luciferase reporter assay validated that GRB2 was the target protein of miR-362-3p. Rescue experiments showed that SBF2-AS1 silencing inhibited cell invasion and migration, while cotransfection si-SBF2-AS1 and miR-362-3p inhibitor rescued the effect of si-SBF2-AS1. These results demonstrate that E2F1-induced overexpression of SBF2-AS1 promotes the expression of GRB2 by targeting miR-362-3p to facilitate the metastasis of NSCLC. Next, siE2F1 or si-NC was transfected into A549 and H1299 cells and qRT-PCRresults showed that downregulation of E2F1 significantly decreased the expression of SBF2-AS1.	32364763	RID06650	transcriptional regulation	metastasis,prognosis	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)
Non-small cell lung cancer	SBF2-AS1	GRB2	positively-E	dual-luciferase reporter assay;starBase v3.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+);cell metastasis(+)	ceRNA(miR-362-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000177885	NA	283104	2885	NA	NCKAP2	E2F1-Induced Overexpression of Long Noncoding RNA SBF2-AS1 Promotes Non-Small-Cell Lung Cancer Metastasis Through Regulating miR-362-3p/GRB2 Axis.Long noncoding RNA SBF2 antisense RNA 1 (lncRNA SBF2-AS1) has been reported to be involved in non-small-cell lung cancer (NSCLC) tumorigenesis. However, the biological role and regulatory mechanism of lncRNA SBF2-AS1 on NSCLC metastasis remain largely unknown. In this study, the expression level and functional role of SBF2-AS1 were investigated in both NSCLC tissues and cell lines. We found that SBF2-AS1 was upregulated in both NSCLC tissues and cell lines. Patients with high levels of SBF2-AS1 have larger tumors, higher malignancy, and poor prognosis. Knockdown of SBF2-AS1 significantly inhibited tumor growth in vivo and cell proliferation, migration, and invasion in vitro. Moreover, bioinformatics analysis, chromatin immunoprecipitation assay, and luciferase reporter assay proved that the upregulation of SBF2-AS1 was mediated by transcription factor E2F1. Further experiments demonstrated that miR-362-3p had complementary binding site with 3'-UTR of SBF2-AS1. Besides, luciferase reporter assay validated that GRB2 was the target protein of miR-362-3p. Rescue experiments showed that SBF2-AS1 silencing inhibited cell invasion and migration, while cotransfection si-SBF2-AS1 and miR-362-3p inhibitor rescued the effect of si-SBF2-AS1. These results demonstrate that E2F1-induced overexpression of SBF2-AS1 promotes the expression of GRB2 by targeting miR-362-3p to facilitate the metastasis of NSCLC.	32364763	RID06651	ceRNA or sponge	metastasis,prognosis	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	HCP5	miR-27b-3p	negatively-E	Starbase;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+)	NA	regulation	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.	32357145	RID06652	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	HCP5	Vimentin	positively-E	western blot	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.	32357145	RID06653	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	HCP5	N-cadherin	positively-E	western blot	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	NA	NA	10866	NA	D6S2650E|P5-1	NA	The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.	32357145	RID06654	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	CYCSP5	E-cadherin	negatively-E	western blot	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227735	GRCh38_1:244598391-244598687	NA	NA	360158	NA	HCP5	NA	The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.	32357145	RID06655	expression association	metastasis		
Esophageal cancer	RPPH1	BAX	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259001	GRCh38_14:20343048-20343685	ENSG00000087088	NA	85495	581	H1RNA|RPPH1-1	BCL2L4	Value of long non-coding RNA Rpph1 in esophageal cancer and its effect on cancer cell sensitivity to radiotherapy.Methods: Eighty-three patients with esophageal cancer admitted to Qilu Hospital of Shandong University and 90 healthy participants who received physical examinations were collected as research participants. The expression of Rpph1 was determined by qRT-PCR siRNA-NC and siRNA-Rpph1 were transfected into esophageal cancer cell lines, and cells without transfection were designated as the blank control group. Cell survival was tested by colony formation assays, and the levels of proteins related to apoptosis and epithelial-mesenchymal transitions were determined by western blot assays. Cell proliferation was assessed by MTT assays, cell apoptosis by flow cytometry, and cell migration by wound-healing assays. Changes in cell cycle distribution were monitored.Results: Rpph1 was highly expressed in esophageal carcinoma, making it a promising marker for the diagnosis of esophageal cancer. Rpph1 could also be used to distinguish different short-term responses, T stages, N stages, and clinical stages of esophageal cancer patients. The results of 3-year overall survival favored patients with lower Rpph1 expression over patients with higher Rpph1 expression (P < 0.05). In vitro and in vivo experiments showed that silencing Rpph1 expression led to higher sensitivity of esophageal cancer cells to radiotherapy, stronger apoptosis in esophageal cancer cells induced by radiotherapy, higher expression of Bax and caspase-3, and lower expression of Bcl-2 (Bax, caspase-3, and Bcl-2 are apoptosis-related proteins). Additionally, silencing Rpph1 attenuated radiation-induced G2/M phase arrest, and significantly inhibited the expression of proteins involved in cell proliferation, migration, and epithelial-mesenchymal transition regulation in esophageal cancer cells.Conclusion: Rpph1 is highly expressed in esophageal cancer. Silencing Rpph1 expression can promote cell apoptosis, inhibit cell proliferation and migration, and increase radio-sensitivity.	32351293	RID06656	expression association	chemoresistance	DOWN(BRCA);DATA(GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	RPPH1	Caspase3	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259001	GRCh38_14:20343048-20343685	NA	NA	85495	NA	H1RNA|RPPH1-1	NA	Value of long non-coding RNA Rpph1 in esophageal cancer and its effect on cancer cell sensitivity to radiotherapy.Methods: Eighty-three patients with esophageal cancer admitted to Qilu Hospital of Shandong University and 90 healthy participants who received physical examinations were collected as research participants. The expression of Rpph1 was determined by qRT-PCR siRNA-NC and siRNA-Rpph1 were transfected into esophageal cancer cell lines, and cells without transfection were designated as the blank control group. Cell survival was tested by colony formation assays, and the levels of proteins related to apoptosis and epithelial-mesenchymal transitions were determined by western blot assays. Cell proliferation was assessed by MTT assays, cell apoptosis by flow cytometry, and cell migration by wound-healing assays. Changes in cell cycle distribution were monitored.Results: Rpph1 was highly expressed in esophageal carcinoma, making it a promising marker for the diagnosis of esophageal cancer. Rpph1 could also be used to distinguish different short-term responses, T stages, N stages, and clinical stages of esophageal cancer patients. The results of 3-year overall survival favored patients with lower Rpph1 expression over patients with higher Rpph1 expression (P < 0.05). In vitro and in vivo experiments showed that silencing Rpph1 expression led to higher sensitivity of esophageal cancer cells to radiotherapy, stronger apoptosis in esophageal cancer cells induced by radiotherapy, higher expression of Bax and caspase-3, and lower expression of Bcl-2 (Bax, caspase-3, and Bcl-2 are apoptosis-related proteins). Additionally, silencing Rpph1 attenuated radiation-induced G2/M phase arrest, and significantly inhibited the expression of proteins involved in cell proliferation, migration, and epithelial-mesenchymal transition regulation in esophageal cancer cells.Conclusion: Rpph1 is highly expressed in esophageal cancer. Silencing Rpph1 expression can promote cell apoptosis, inhibit cell proliferation and migration, and increase radio-sensitivity.	32351293	RID06657	expression association	chemoresistance	DOWN(BRCA);DATA(GSE86978)	
Esophageal cancer	RPPH1	BCL2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259001	GRCh38_14:20343048-20343685	ENSG00000171791	NA	85495	596	H1RNA|RPPH1-1	Bcl-2|PPP1R50	Value of long non-coding RNA Rpph1 in esophageal cancer and its effect on cancer cell sensitivity to radiotherapy.Methods: Eighty-three patients with esophageal cancer admitted to Qilu Hospital of Shandong University and 90 healthy participants who received physical examinations were collected as research participants. The expression of Rpph1 was determined by qRT-PCR siRNA-NC and siRNA-Rpph1 were transfected into esophageal cancer cell lines, and cells without transfection were designated as the blank control group. Cell survival was tested by colony formation assays, and the levels of proteins related to apoptosis and epithelial-mesenchymal transitions were determined by western blot assays. Cell proliferation was assessed by MTT assays, cell apoptosis by flow cytometry, and cell migration by wound-healing assays. Changes in cell cycle distribution were monitored.Results: Rpph1 was highly expressed in esophageal carcinoma, making it a promising marker for the diagnosis of esophageal cancer. Rpph1 could also be used to distinguish different short-term responses, T stages, N stages, and clinical stages of esophageal cancer patients. The results of 3-year overall survival favored patients with lower Rpph1 expression over patients with higher Rpph1 expression (P < 0.05). In vitro and in vivo experiments showed that silencing Rpph1 expression led to higher sensitivity of esophageal cancer cells to radiotherapy, stronger apoptosis in esophageal cancer cells induced by radiotherapy, higher expression of Bax and caspase-3, and lower expression of Bcl-2 (Bax, caspase-3, and Bcl-2 are apoptosis-related proteins). Additionally, silencing Rpph1 attenuated radiation-induced G2/M phase arrest, and significantly inhibited the expression of proteins involved in cell proliferation, migration, and epithelial-mesenchymal transition regulation in esophageal cancer cells.Conclusion: Rpph1 is highly expressed in esophageal cancer. Silencing Rpph1 expression can promote cell apoptosis, inhibit cell proliferation and migration, and increase radio-sensitivity.	32351293	RID06658	expression association	chemoresistance	DOWN(BRCA);DATA(GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG5	RNF38	positively-E	StarBase;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cancer progression(+)	ceRNA(miR-363-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000137075	NA	387066	152006	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-363-3p/RNF38 axis.Patients and methods: The expression levels of SNHG5, miR-363-3p, and Ring Finger Protein 38 (RNF38) were measured by using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR or western blot assay, respectively. Cell proliferation was analyzed by MTT assay. Flow cytometry was used to investigate cell apoptosis. Cell migration and invasion abilities were detected by transwell assay. The relationship among SNHG5, miR-363-3p, and RNF38 was confirmed using bioinformatics analysis and Luciferase reporter assay.Results: The expression of SNHG5 and RNF38 was elevated in HCC tissues and cell lines, and highly expressed SNHG5 and RNF38 could induce apoptosis and repress proliferation, migration, as well as invasion in HCC cells. Further investigations showed that SNHG5 might act as a competing endogenous RNA of miR-26a-5p and thereby cause the derepression of the downstream target RNF38. Moreover, rescue experiments indicated that SNHG5 silence inhibited the progression of HCC cells by regulating miR-363-3p, and the facilitated effects of RNF38 in the progression of HCC cells were regulated by miR-363-3p.Conclusions: LncRNA SNHG5 may promote human HCC progression by regulating the miR-363-3p/RNF38 axis, providing a novel insight into the pathogenesis of HCC and therapeutic strategy for HCC treatment.	32329834	RID06659	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Glioblastoma	PCED1B-AS1	HIF1A	positively-E	western blot;qRT-PCR;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);glucose metabolic process(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000247774	GRCh38_12:47205896-47216460	ENSG00000100644	NA	100233209	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long Noncoding RNA PCED1B-AS1 Promotes the Warburg Effect and tumorigenesis by Upregulating HIF-1alpha in Glioblastoma.Accumulating evidence suggests that long noncoding RNA (lncRNA) functions as a critical regulator in cancer biology. Here, we characterized the role of lncRNA PCED1B antisense RNA 1 (PCED1B-AS1) in glioblastoma (GBM). PCED1B-AS1 was notably upregulated in GBM tissues and cell lines and closely associated with larger tumor size and higher grade. Patients with high PCED1B-AS1 had shorter survival time than those with low PCED1B-AS1. Functional experiments showed that depletion of PCED1B-AS1 significantly inhibited, while overexpression of PCED1B-AS1 promoted cell proliferation, glucose uptake, and lactate release. Mechanistically, PCED1B-AS1 was able to directly bind to the 5'-UTR of HIF-1alpha mRNA and potentiate HIF-1alpha translation, leading to increased HIF-1alpha protein level, thereby promoting the Warburg effect and tumorigenesis. Importantly, PCED1B-AS1 lost the carcinogenic properties in the absence of HIF-1alpha. In addition, we also confirmed the existence of the PCED1B-AS1/HIF-1alpha regulatory axis in vivo. Taken together, our findings demonstrate that PCED1B-AS1 is a novel oncogenic lncRNA in GBM and functions in a HIF-1alpha-dependent manner, which provides a promising prognostic biomarker and druggable target for GBM.	32326742	RID06660	transcriptional regulation	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colon cancer	HNF1A-AS1	OTX1	positively-E	western blot;RNA pull-down assay;RIP;ChIP;dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	angiogenesis(+);ERK/MAPK signaling pathway(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000115507	NA	283460	5013	C12orf27|FLJ38690|HAS1|NCRNA00262	NA	Long non-coding RNA HNF1A-AS1 upregulates OTX1 to enhance angiogenesis in colon cancer via the binding of transcription factor PBX3.Colon cancer shows characteristics of metastasis, which is associated with angiogenesis. Increasing evidence highlights long non-coding RNAs (lncRNAs) as important participants in angiogenesis of cancers, including colon cancer. Hence, this study investigated the role of HNF1A-AS1 in angiogenesis of colon cancer. RT-qPCR and western blotwere applied to detect HNF1A-AS1 and OTX1 expression in colon cancer tissues and cell lines. Then the interactions among HNF1A-AS1, PBX3, OTX1 and ERK/MAPK pathway were evaluated with RNA pull-down, RIP, ChIP and dual-luciferase reporter gene assays. Next, HCT116 and SW620 cells were treated with si-HNF1A-AS1 and/or oe-OTX1 plasmids to assess the effects of HNF1A-AS1 and OTX1 on angiogenesis, which was further evaluated in nude mice injected with SW620 cells transfected with sh-HNF1A-AS1 or sh-OTX1 lentivirus. HNF1A-AS1 and OTX1 were highly expressed in colon cancer. Silencing of HNF1A-AS1 inhibited angiogenesis of colon cancer in vivo and in vitro. HNF1A-AS1 increased the OTX1 expression by binding to transcription factor PBX3 to promote angiogenesis in colon cancer. Further, HNF1A-AS1 upregulated OTX1 to activate the ERK/MAPK pathway. Altogether, our findings identified HNF1A-AS1 as a tumor-promoting RNA in colon cancer, which could serve as a potential therapeutic target for colon cancer treatment.	32325080	RID06661	transcriptional regulation	metastasis	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	
Breast cancer	SNHG1	LMO4	positively-E	dual-luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell migration(+);cancer progression(+)	ceRNA(miR-573)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000143013	NA	23642	8543	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Long non-coding RNA SNHG1 promotes breast cancer progression by regulation of LMO4.Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) was reported to be a critical regulator of tumorigenesis and is frequently deregulated in several cancer types. However, the exact mechanism by which SNHG1 contributes to breast cancer progression has not been fully elucidated. The identification of the molecular mechanism of SNHG1 is important for understanding the development of breast cancer and for improving the prognosis of the patients with this disease. In the present study, increased expression levels of SNHG1 were noted in breast cancer tumors following analysis of differentially expressed lncRNAs between 1,063 tumor and 102 normal tissues derived from The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA) dataset. This finding was further validated using 50 pairs of normal and tumor tissues that were collected from patients with breast cancer. Notably, SNHG1 expression was significantly correlated with estrogen receptor (ER)/progesterone receptor (PR) negative status (ER-/PR-) and advanced clinical stage in breast cancer tissues. Knockdown of SNHG1 led to cell growth arrest, cell cycle redistribution and cell migration inhibition of breast cancer cells. The miRDB database predicted that miR-573 interacts with SNHG1. RT-PCR confirmed the negative regulation of miR-573 levels by SNHG1 in breast cancer cells and the dual-luciferase reporter assay confirmed their complementary binding. The repression of miR-573 by SNGH1 decreased LIM domain only 4 (LMO4) mRNA and protein expression levels in the breast cancer cell lines tested and induced the expression of cyclin D1 and cyclin E. In vitro experiments indicated that LMO4 overexpression could reverse siSNHG1-induced cell growth arrest, cell cycle redistribution and inhibition of cell migration in breast cancer cells. Moreover, the tumor xenograft model indicated that SNHG1 knockdown inhibited MDA-MB-231 growth in vivo and LMO4 overexpression reversed the tumor growth inhibition induced by SNHG1 knockdown. The present study demonstrated that SNHG1 acts as a novel oncogene in breast cancer via the SNHG/miR-573/LMO4 axis and that it could be a promising therapeutic target for patients with breast cancer.	32323846	RID06662	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE75367)
Osteosarcoma	GHET1	CTNNB1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-);cancer progression(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000168036	NA	102723099	1499	lncRNA-GHET1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA GHET1 promotes osteosarcoma development and progression via Wnt/beta-catenin signaling pathway.Osteosarcoma (OS) is known as a malignant tumor with a high mortality rate of children and adults worldwide. Long non-coding RNAs (lncRNAs) have been revealed as oncogenes or tumor suppressors that are involved in the tumorigenesis and metastasis of some types of cancer. However, the biological role of long non-coding RNA gastric carcinoma proliferation enhancing transcript 1 (lncGHET1) and its regulatory mechanism in OS progression have not been elucidated. The aim of the present study was to investigate the role of lncGHET1 in OS. The present study explored lncGHET1 expression using a reverse transcription-quantitative (RT-q)PCR assay. Furthermore, the Cell Counting Kit-8 assay, flow cytometry detection, wound healing and transwell invasion assays were performed to evaluate its biological role and the underlying mechanisms in vitro. Additionally, the effect of lncGHET1 was evaluated in vivo in a xenograft model. lncGHET1 expression was significantly upregulated in OS cell lines compared with in an osteoblastic cell line according to the RT-qPCR assay. The results of a knockdown functional experiment suggested that inhibition of lncGHET1 attenuated cell proliferation, migration, invasion and epithelial-to-mesenchymal transition, and promoted apoptosis, partly through regulating the Wnt/beta-catenin signaling pathway in OS. These findings indicated that lncGHET1 may serve an essential regulatory role in the biological processes of OS. The present study identified a novel therapeutic target for diagnosis and treatment of human OS.	32319657	RID06663	transcriptional regulation	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Endometrial cancer	LINC01410	CHD7	positively-E	qRT-PCR;western blot;dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-23c)	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000238113	GRCh38_9:62801461-62813486	ENSG00000171316	NA	103352539	55636	NA	CRG|FLJ20357|FLJ20361|KIAA1416	LINC01410/miR-23c/CHD7 functions as a ceRNA network to affect the prognosis of patients with endometrial cancer and strengthen the malignant properties of endometrial cancer cells.In previous studies, long non-coding RNA LINC01410 (LINC01410) has been found to promote cells proliferation and invasion in colon and gastric cancers. However, the function of LINC01410 in endometrial cancer (EC) is still elusive. The expression patterns of LINC01410/miR-23c/Chromodomain Helicase DNA-Binding Protein 7 (CHD7) in EC tissues and the prognosis of patients with different expression of LINC01410/miR-23c/CHD7 were determined by consulting TCGA database. EC patients with complete clinical data were applied for clinicopathological correlation analysis. The biological characteristics of EC cells were analyzed with the support of CCK-8 and transwell assays. CHD7 expression was assessed by qRT-PCRand western blot assays. Targeted associations between LINC01410 and miR-23c, as well as miR-23c and CHD7 were speculated by prediction website and verified by dual-luciferase assay. Rescue assays were performed to explore the interrelation among LINC01410, miR-23c and CHD7. Our data illustrated that LINC01410 high expression was presented in EC tissues and was positively related to the poor prognosis of patients in EC, as well as the malignant behaviors of EC cells. Through bioinformatics analysis, we surmised that LINC01410/miR-23c/CHD7 may play a role through the formation of competing endogenous RNA (ceRNA) mechanism. CHD7 expression was positively regulated by LINC01410, and inversely controlled by miR-23c. Furthermore, the promoting effects of miR-23c inhibitor or CHD7 upregulation on EC cell growth and aggressiveness were attenuated by LINC01410 silencing. Our results indicated that high expression of LINC01410 promoted EC cell progression through modulating miR-23c/CHD7 axis, providing a new direction for revealing the molecular mechanism of EC.	32314193	RID06664	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE75367)
Breast cancer	EZH2	PHACTR2-AS1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	transcriptional regulation	regulation	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000235740	GRCh38_6:143554325-143562031	2146	285740	ENX-1|EZH1|KMT6|KMT6A	lncIHS|NR027113	The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer.Aberrant activation of histone methyltransferase EZH2 and ribosome synthesis strongly associate with cancer development and progression. We previously found that EZH2 regulates RNA polymerase III-transcribed 5S ribosomal RNA gene transcription. However, whether EZH2 regulates ribosome synthesis is still unknown. Here, we report that EZH2 promotes ribosome synthesis by targeting and silencing a long noncoding RNA PHACTR2-AS1. PHACTR2-AS1 directly bound ribosome DNA genes and recruited histone methyltransferase SUV39H1, which in turn triggered H3K9 methylation of these genes. Depletion of PHACTR2-AS1 resulted in hyperactivation of ribosome synthesis and instability of ribosomal DNA, which promoted cancer cell proliferation and metastasis. Administration of PHACTR2-AS1-30nt-RNA, which binds to SUV39H1, effectively inhibited breast cancer growth and lung metastasis in mice. PHACTR2-AS1 was downregulated in breast cancer patients, where lower PHACTR2-AS1 expression promoted breast cancer development and correlated with poor patient outcome. Taken together, we demonstrate that PHACTR2-AS1 maintains a H3K9 methylation-marked silent state of ribosomal DNA genes, comprising a regulatory axis that controls breast cancer growth and metastasis. SIGNIFICANCE: These findings reveal that EZH2 mediates ribosomal DNA stability via silencing of PHACTR2-AS1, representing a potential therapeutic target to control breast cancer growth and metastasis.	32312833	RID06665	transcriptional regulation	metastasis	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	
Breast cancer	PHACTR2-AS1	SUV39H1	interact	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	histone modification	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000235740	GRCh38_6:143554325-143562031	ENSG00000101945	NA	285740	6839	lncIHS|NR027113	KMT1A|SUV39H	The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer.Aberrant activation of histone methyltransferase EZH2 and ribosome synthesis strongly associate with cancer development and progression. We previously found that EZH2 regulates RNA polymerase III-transcribed 5S ribosomal RNA gene transcription. However, whether EZH2 regulates ribosome synthesis is still unknown. Here, we report that EZH2 promotes ribosome synthesis by targeting and silencing a long noncoding RNA PHACTR2-AS1. PHACTR2-AS1 directly bound ribosome DNA genes and recruited histone methyltransferase SUV39H1, which in turn triggered H3K9 methylation of these genes. Depletion of PHACTR2-AS1 resulted in hyperactivation of ribosome synthesis and instability of ribosomal DNA, which promoted cancer cell proliferation and metastasis. Administration of PHACTR2-AS1-30nt-RNA, which binds to SUV39H1, effectively inhibited breast cancer growth and lung metastasis in mice. PHACTR2-AS1 was downregulated in breast cancer patients, where lower PHACTR2-AS1 expression promoted breast cancer development and correlated with poor patient outcome. Taken together, we demonstrate that PHACTR2-AS1 maintains a H3K9 methylation-marked silent state of ribosomal DNA genes, comprising a regulatory axis that controls breast cancer growth and metastasis. SIGNIFICANCE: These findings reveal that EZH2 mediates ribosomal DNA stability via silencing of PHACTR2-AS1, representing a potential therapeutic target to control breast cancer growth and metastasis.	32312833	RID06666	epigenetic regulation	metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)
Osteosarcoma	LINC00612	SOX4	positively-E	qRT-PCR;dual-luciferase reporter analysis;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-214-5p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214851	GRCh38_12:9055589-9065070	ENSG00000124766	NA	253128	6659	C12orf33|FLJ41814|MGC40170	NA	LINC00612 functions as a ceRNA for miR-214-5p to promote the proliferation and invasion of osteosarcoma in vitro and in vivo.Long noncoding RNAs (lncRNAs) are key regulators that participate in multiple biological processes, including cancer formation and progression. The biological function and molecular mechanism of LINC00612 in the progression of osteosarcoma has not been elucidated before. In this study, we evaluated the expression of LINC00612 in osteosarcoma by qRT-PCR ShRNA-induced LINC00612 downregulation and plasmid-transduced LINC00612 overexpression were conducted in U2OS and HOS cells. The in vitro functional effects of LINC00612 downregulation and overexpression on osteosarcoma cells were evaluated by CCK-8 assay, colony formation assay, scratch assay, transwell invasion assay and flow cytometry; in vivo tumor xenografts were conducted in nude mice. The effects of LINC00612 downregulation and overexpression on epithelial-mesenchymal transition (EMT) were assessed by scratch assay, transwell assay and qRT-PCR The possibility of LINC00612 acting as a competing endogenous RNA (ceRNA) to target microRNA miR-214-5p was examined by dual-luciferase reporter assay. Then, miR-214-5p was downregulated or overexpressed to examine its effect on invasion and SOX4 expression in osteosarcoma cells. LINC00612 was found to be significantly upregulated in osteosarcoma cells and metastatic osteosarcoma. LINC00612 overexpression promoted the proliferation, invasion and in vivo explant growth of osteosarcoma. In addition, LINC00612 overexpression regulated EMT by elevating the expression of ZEB1, Snail, and Fibronectin 1 and inhibiting E-cadherin. MiR-214-5p was confirmed to be a ceRNA of LINC00612. LINC00612 overexpression upregulated SOX4 by inhibiting miR-214-5p. Our study shows that LINC00612 plays an important role in regulating the proliferation and invasion of osteosarcoma by endogenously competing with miR-214-5p and mediating EMT.	32311343	RID06667	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Esophagus squamous cell carcinoma	TUG1	XBP1	positively-E	Starbase;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	ceRNA(miR-498)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000100219	NA	55000	7494	FLJ20618|LINC00080|NCRNA00080	XBP2	LncRNA TUG1 promotes tumor growth and metastasis of esophageal squamous cell carcinoma by regulating XBP1 via competitively binding to miR-498.Esophageal squamous cell carcinoma (ESCC) is a major subtype of esophageal cancer with high mortality. Previous reports suggested that lncRNA taurine upregulated gene 1 (TUG1) functioned as an oncogene in numerous cancers. The purpose of this study was to explore the potential mechanism of TUG1 carcinogenesis in ESCC. The expression of TUG1 and miR-498 was measured by a quantitative real-time polymerase chain reaction (qRT-PCR. Cell proliferation and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry. Cell migration and invasion were identified through the transwell assay. The interaction between miR-498 and TUG1 or X-box binding protein 1 (XBP1) was predicted by bioinformatics software starBase and verified by luciferase reporter assay. The expression of XBP1 was quantified by qRT-PCRand western blot Xenograft tumor mouse model was established to determine the function of TUG1 in vivo. TUG1 was upregulated in ESCC tissues and cells, and its high expression was associated with tumor lymph node metastasis and low cumulative survival. TUG1 knockdown inhibited proliferation, migration, and invasion but promoted apoptosis in ESCC cells. It was confirmed that miR-498 was a target of TUG1, and XBP1 was a target of miR-498. The expression of miR-498 was reduced in ESCC tissues while XBP1 expression was notably enhanced. Mechanism analysis manifested that TUG1 regulated proliferation, apoptosis, migration, and invasion by upregulating XBP1 via targeting miR-498 in vitro. Furthermore, knockdown of TUG1 attenuated tumor growth in vivo. TUG1 accelerated tumorigenesis and metastasis by inducing XBP1 expression through directly targeting miR-498 in ESCC.	32305055	RID06668	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Melanoma	MIAT	miR-150	negatively-E	StarBase 3.0;western blot;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Long non-coding RNA MIAT promotes the growth of melanoma via targeting miR-150.Melanoma is a common skin cancer and it can lead to high mortality probably by early invasion and metastasis. LncRNA MIAT is involved in tumor proliferation, invasion and epithelial-to-mesenchymal transition (EMT). However, the roles of MIAT in melanoma still require further investigation. Thus, the aim of the study is to investigate the roles of MIAT in melanoma, especially the effects of MIAT on EMT of melanoma cancer cells. The results showed that the expression of MIAT was significantly upregulated in melanoma tissue and cells compared with the normal skin and normal melanocytes; moreover, miR-150 was confirmed as a target of MIAT. Furthermore, knockdown of MIAT inhibited cell proliferation and invasion in melanoma cancer cells and transfection of miR-150 inhibitors partial abrogated the anti-tumor effects of MIAT siRNA. In addition, MIAT siRNA also inhibited the EMT of melanoma cells, while miR-150 inhibitors can reverse the effects of MIAT siRNA. Finally, knockdown of MIAT also inhibited the carcinogenic effects of melanoma in vivo by targeting miR-150. In conclusion, we reported that MIAT promotes the proliferation, invasion and EMT of melanoma cells via targeting miR-150, which suggested that MIAT might be a therapeutic target for the treatment of melanoma.	32300960	RID06669	transcriptional regulation	metastasis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Breast cancer	NONHSAT141924	p-CREB	positively-E	western blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);chemosensitivity(-)	transcriptional regulation	association	RNA-protein	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA NONHSAT141924 promotes paclitaxel chemotherapy resistance through p-CREB/Bcl-2 apoptosis signaling pathway in breast cancer.Breast cancer is the most prevalent malignant neoplasm among women worldwide. Despite continuous improvement of breast cancer individualized comprehensive therapy, local recurrence and distant metastasis still remain the challenges due to the development of acquired drug-resistance. Long non-coding RNAs (LncRNAs) is known to participated in the development of breast cancer. However, the mechanisms of LncRNAs involving in drug-resistance of breast cancer during chemotherapy remain to be further elucidated. Aiming to screen for candidate LncRNAs responsible for breast cancer mechanism, we first investigated the expression patterns of LncRNAs and mRNAs in paired breast cancer tissues and normal tissues using Agilent Human lncRNA array. The microarray results clearly demonstrated multiple differentially expressed mRNAs and LncRNAs including LncRNA NONHSAT141924. The remarkable up-regulation of LncRNA NONHSAT141924 in breast cancer MCF-7 was further confirmed by quantitative real-time PCR. GO and KEGG pathway analysis demonstrated that LncRNA NONHSAT141924 was most closely associated with paclitaxel (PTX)-resistant phenotype. To further explore the mechanism by which LncRNA NONHSAT141924 contributes to PTX-resistant characteristics, LncRNA NONHSAT141924 was transfected into MCF-7 breast cancer cell line. Overexpression of LncRNA NONHSAT141924 significantly reduced MCF-7 cell survivability through modulation of p-CREB/Bcl-2 apoptosis signaling pathway, one of the major pathways participated in LncRNAs-mediated chemotherapy resistance. Taken together, our study provides a new LncRNA-mediated regulatory mechanism for PTX-resistance of breast cancer and suggests that therapeutic inhibition of LncRNA NONHSAT141924 might be an efficient strategy for PTX-resistant breast cancer treatment.	32284761	RID06670	transcriptional regulation	metastasis,recurrence,chemoresistance		
Breast cancer	NONHSAT141924	BCL2	positively-E	western blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);chemosensitivity(-)	transcriptional regulation	association	RNA-protein	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000171791	NA	NA	596	NA	Bcl-2|PPP1R50	LncRNA NONHSAT141924 promotes paclitaxel chemotherapy resistance through p-CREB/Bcl-2 apoptosis signaling pathway in breast cancer.Breast cancer is the most prevalent malignant neoplasm among women worldwide. Despite continuous improvement of breast cancer individualized comprehensive therapy, local recurrence and distant metastasis still remain the challenges due to the development of acquired drug-resistance. Long non-coding RNAs (LncRNAs) is known to participated in the development of breast cancer. However, the mechanisms of LncRNAs involving in drug-resistance of breast cancer during chemotherapy remain to be further elucidated. Aiming to screen for candidate LncRNAs responsible for breast cancer mechanism, we first investigated the expression patterns of LncRNAs and mRNAs in paired breast cancer tissues and normal tissues using Agilent Human lncRNA array. The microarray results clearly demonstrated multiple differentially expressed mRNAs and LncRNAs including LncRNA NONHSAT141924. The remarkable up-regulation of LncRNA NONHSAT141924 in breast cancer MCF-7 was further confirmed by quantitative real-time PCR. GO and KEGG pathway analysis demonstrated that LncRNA NONHSAT141924 was most closely associated with paclitaxel (PTX)-resistant phenotype. To further explore the mechanism by which LncRNA NONHSAT141924 contributes to PTX-resistant characteristics, LncRNA NONHSAT141924 was transfected into MCF-7 breast cancer cell line. Overexpression of LncRNA NONHSAT141924 significantly reduced MCF-7 cell survivability through modulation of p-CREB/Bcl-2 apoptosis signaling pathway, one of the major pathways participated in LncRNAs-mediated chemotherapy resistance. Taken together, our study provides a new LncRNA-mediated regulatory mechanism for PTX-resistance of breast cancer and suggests that therapeutic inhibition of LncRNA NONHSAT141924 might be an efficient strategy for PTX-resistant breast cancer treatment.	32284761	RID06671	transcriptional regulation	metastasis,recurrence,chemoresistance		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	ZEB2-AS1	EZH2	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cancer progression(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000106462	NA	100303491	2146	ZEB2-AS|ZEB2AS|ZEB2NAT	ENX-1|EZH1|KMT6|KMT6A	Knockdown of ZEB2-AS1 inhibits cell invasion and induces apoptosis in colorectal cancer.Methods: Relative level of ZEB2-AS1 in CRC tissues and matched normal ones was determined by quantitative real-time polymerase chain reaction (qRT-PCR. Correlation between ZEB2-AS1 level and survival of CRC patients was analyzed by Kaplan-Meier method. Regulatory effects of ZEB2-AS1 on cellular behaviors of CRC cells were evaluated. The interactions between ZEB2-AS1 with LSD1 and EZH2 were explored by RNA immunoprecipitation (RIP) assay. 5-Ethynyl-2'- deoxyuridine (EdU) assay was performed to elucidate the roles of ZEB2-AS1, LSD1 and EZH2 on the proliferative ability of CRC cells. Finally, Spearman's correlation analysis was performed to analyze the relationship between ZEB2-AS1 level and expressions of proliferation- and invasion-related genes.Results: ZEB2-AS1 was upregulated in CRC tissues relative to matched controls. Its level remained higher in CRC patients with <<- cm in tumor size, nodal metastasis and stage III-IV. CRC patients with low-level ZEB2-AS1 presented worse survival compared with those with high-level ZEB2-AS1. qRT-PCRdata showed higher abundance of ZEB2-AS1 in CRC cell lines than colonic epithelial cell line. Knockdown of ZEB2-AS1 attenuated the proliferative, migratory and invasive abilities, but induced apoptosis of DLD1 and SW620 cells. RIP assay demonstrated the interaction between ZEB2-AS1 and LSD1, EZH2. Moreover, EdU assay revealed that transfection of sh-ZEB2-AS1 attenuated the proliferative ability, which was further reduced after co-transfection of sh-LSD1 or sh-EZH2. Finally, correlation analysis showed that mRNA level of ZEB2-AS1 was positively correlated to those of LSD1, EZH2, MMP9, MMP12 and KRAS, but negatively correlated to KLF2.Conclusions: LncRNA ZEB2-AS1 is upregulated in CRC. It accelerates CRC cells to proliferate via interacting with EZH2 and LSD1, thus promoting the progression of CRC.	32277632	RID06672	transcriptional regulation	metastasis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Urinary bladder cancer	BCAR4	TLX1	positively-E	knockdown;TargetScan7;Luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-644a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000107807	NA	400500	3195	NA	HOX11|TCL3	Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer.Methods: RT-PCRwas used to examine the expression of BCAR4 and miR-644a. CCK8 assay, colony formation assay, Transwell assay were used to detect the progression of bladder cancer cells after transfecting of indicated plasmids.Results: The expression of BCAR4 was higher in bladder cancer cell lines than normal urothelial cell line. Moreover, the expression of BCAR4 was associated with the advanced stage and metastasis of bladder cancer. Through knockdown of BCAR4, we discovered that knockdown of BCAR4 significantly decreased the proliferation, migration and invasive abilities of bladder cancer cells. Mechanically, we showed that BCAR4 can bind to miR-644a directly and targets TLX1. Moreover, we also showed that miR-644a was also highly expressed in bladder cancer cells and inhibition of miR-644a or overexpression of TLX1 can increased the migration abilities of bladder cancer caused by knockdown of BCAR4.Conclusion: We showed that BCAR4 sponged miR-644a to modulate the expression of TLX1 and promote bladder cancer development.	32273720	RID06673	ceRNA or sponge	metastasis		UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	YY1	LINC01134	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000236423	GRCh38_1:3900352-3917225	7528	100133612	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression.Materials and methods: qRT-PCRand western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes.Results: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop.Conclusion: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.	32272940	RID06674	transcriptional regulation	prognosis,metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	LINC01134	IGF2BP1	positively-E	starBase;knockdown;FISH;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236423	GRCh38_1:3900352-3917225	ENSG00000159217	NA	100133612	10642	NA	IMP-1	Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression.Materials and methods: qRT-PCRand western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes.Results: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop.Conclusion: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.	32272940	RID06675	ceRNA or sponge	prognosis,metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	FENDRR	NPR3	positively-E	dual-luciferase reporter analysis;TargetScan;Starbase	downregulation	qRT-PCR	NA	NA	p38/MAPK signaling pathway(-);cell viability(-);apoptosis process(+)	ceRNA(miR-362-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000113389	NA	400550	4883	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	ANPRC|C5orf23|FLJ14054|GUCY2B|NPRC	LncRNA FENDRR Upregulation Promotes Hepatic Carcinoma Cells Apoptosis by Targeting miR-362-5p Via NPR3 and p38-MAPK Pathway.Background: Abnormal long noncoding RNA FOXF1 adjacent noncoding developmental regulatory RNA (FENDRR) expression has been discovered in multiple human cancers pathogenesis, but its role in hepatocellular carcinoma (HCC) cells is rarely reported. Its effects on HCC cells are covered in this study. Materials and Methods: MiR-362-5p and NPR3 expressions in HCC tissues and cell were detected by quantitative real-time polymerase chain reaction and western blot as needed. Cell viability and apoptosis were detected by MTT assay and flow cytometry, respectively. Target gene and potential binding sites of FENDRR, miR-362-5p, and NPR3 were predicted and confirmed by TargetScan and Starbase, and dual-luciferase reporter assay. Results: FENDRR expression was downregulated while miR-362-5p expression was upregulated in HCC tissues and cells. FENDRR upregulation inhibited HCC cells viability yet induced apoptosis, which was reversed by miR-362-5p. In addition, miR-362-5p resulted in p38-mitogen-activated protein kinase (MAPK) pathway activation and NPR3 expression decrease in HCC cells, which was reversed by FENDRR. Conclusion: FENDRR inhibited HCC cells viability yet promoted apoptosis by targeting miR-362-5p by promoting NPR3 and deactivating p38-MAPK pathway, thus exerting its anticarcinogenic effects in HCC cells.	32251605	RID06676	ceRNA or sponge	NA		
Gastric cancer	miR-223-5p	TP73-AS1	negatively-E	dual-luciferase reporter analysis	downregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	association	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	57212	NA	KIAA0495|PDAM	MicroRNA-223-5p targets long non-coding RNA TP73 antisense RNA1 to promote the invasion of gastric cancer.Long non-coding RNA (lncRNA) TP73 antisense RNA 1 (TP73-AS1) has been characterized as an oncogenic lncRNA in GC. However, by analyzing The Cancer Genome Atlas (TCGA) dataset we observed the downregulation of TP73-AS1 in GC. In addition, TP73-AS1 is predicted to interact with microRNA-223-5p (miR-223-5p), which is also a critical player in cancer biology. This study was therefore carried out to investigate the roles of miR-223-5p and TP73-AS1 in gastric cancer (GC) and to explore the interactions between them. In this study, 68 GC patients were included as research subjects. Expression of miR-223-5p and TP73-AS1 was analyzed by RT-qPCR. Dual-luciferase assay and overexpression experiments were used to analyze gene interactions. Transwell assays were used to analyze cell invasion and migration. We found that miR-223-5p was upregulated and TP73-AS1 was downregulated in GC and they were inversely correlated. Altered miR-223-5p and TP73-AS1 expression predicted poor disease-specific survival. Dual-luciferase assay showed that miR-223-5p may bind TP73-AS1 and overexpression experiments showed that miR-223-5p overexpression downregulated TP73-AS1 in gastric cancer cells. Cell invasion and migration assays showed that miR-223-5p could promote the invasion and migration of gastric cancer cells, while TP73-AS1 could inhibit the invasion and migration of gastric cancer cells. In addition, miR-223-5p attenuated the effects of TP73-AS1 overexpression. Therefore, miR-223-5p may target TP73-AS1 to promote the invasion and migration of gastric cancer patients.	32248369	RID06677	transcriptional regulation	NA		UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	CCAT2	VEGFA	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	angiogenesis(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-424)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000112715	NA	101805488	7422	LINC00873|NCCP1	VEGF|VEGF-A|VPF	LncRNA CCAT2 promotes angiogenesis in glioma through activation of VEGFA signalling by sponging miR-424.Glioma is characterized by high morbidity, high mortality and poor prognosis. Recent studies exhibited that lncRNA CCAT2 is overexpressed in glioma and promotes glioma progression, but the specific molecular biological mechanism remains to be determined. We performed qRT-PCRto evaluate the expression of related genes, western blotto measure protein levels, colony formation assay to detect the proliferative ability of glioma cells, flow cytometry to measure cell apoptosis, bioinformatics analysis and dual luciferase assay to verify the binding sites and the targeted regulatory relationship in A172 and U251 cell lines and tube formation assay to determine endothelial angiogenesis. LncRNA CCAT2 and VEGFA were highly expressed, while miR-424 was expressed at low levels in NHA cells. Furthermore, knockdown of lncRNA CCAT2 decreased cell proliferation, increased cell apoptosis and inhibited endothelial angiogenesis in glioma. Moreover, lncRNA CCAT2 shared a complementary sequence with miR-424 which in turn directly bound to the 3'-UTR of VEGFA. Further investigation indicated that lncRNA CCAT2 promoted cell proliferation and endothelial angiogenesis by inducing the PI3K/AKT signalling pathway in glioma. The oncogenic lncRNA CCAT2 is highly associated with the development of glioma and exerts its function by upregulating VEGFA via miR-424.	32236863	RID06678	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Osteosarcoma	EWSR1	SOX2	positively-E	luciferase reporter assay;western blot;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000182944	GRCh38_22:29268009-29300525	ENSG00000181449	NA	2130	6657	EWS	NA	EWS promotes cell proliferation and inhibits cell apoptosis by regulating miR-199a-5p/Sox2 axis in osteosarcoma.Objective: Osteosarcoma is one of the most common malignant bone tumors which mainly occurs in children and adolescents. It is characterized by high malignancy and high metastasis rate, resulting in high mortality and disability. Accumulating studies have validated that long noncoding RNAs (lncRNAs) exerted vital roles in multiple cancer progression by regulating the expression of specific genes. This work aimed to explore the potential molecular mechanism of EWS in osteosarcoma.Results: In this study, we discovered that both EWS and Sox2 were highly expressed in osteosarcoma tissue samples. In addition, the expression of EWS was positively associated with Sox2 level. We conducted a series of functional assays and observed that Sox2 overexpression could significantly overturned the enhancement of cell proliferation and the decline of cell apoptosis induced by EWS knockdown in osteosarcoma. Moreover, we found a key upstream regulatory gene of Sox2: miR-199a-5p.Conclusions: Through molecular biology studies and rescue assays, we further demonstrated that EWS promotes tumor growth through the miR-199a-5p/Sox2 signaling axis in osteosarcoma. These findings may provide an important theoretical basis for the clinical diagnosis and treatment of osteosarcoma.To further explore the molecular mechanism by which EWS regulates Sox2 expression, we first detected the mRNA level of Sox2 in MG63 transfected cells by RT-qPCR.	32236759	RID06679	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978,GSE41245)	UP(LIHC);DATA(GSE117623)
Clear cell renal cell carcinoma	ZNF710-AS1-202	ZNF710	negatively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	transcriptional regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	NA	NA	ENSG00000140548	NA	NA	374655	NA	NA	Overexpression of antisense long non-coding RNA ZNF710-AS1-202 promotes cell proliferation and inhibits apoptosis of clear cell renal cell carcinoma via regulation of ZNF710 expression.Antisense long non-coding RNAs (AS lncRNAs) have been increasingly recognized as important regulators of gene expression and have been found to play crucial roles in the development and progression of tumors. The present study explored the roles of AS lncRNA ZNF710-AS1-202 in clear cell renal cell carcinoma (ccRCC). The expression levels of ZNF710-AS1-202 were detected in 46 human ccRCC tissues and 34 healthy adjacent renal tissues. The associations between the levels of ZNF710-AS1-202 expression and the clinicopathological features of the patients were evaluated by the Chi2 test. Gain- and loss-of-function experiments were performed to analyze the role of ZNF710-AS1-202 in ccRCC cell proliferation and survival in vitro. Reverse transcription-quantitative PCR and/or western blot were employed to detect ZNF710-AS1-202, zinc finger protein 710 (ZNF710) and cyclin B1 expression. The Cell Counting Kit-8 and colony formation assays, as well as flow cytometry, were used to detect cell proliferation or apoptosis. The subcellular localization of ZNF710-AS1-202 was analyzed by RNA fluorescence in situ hybridization. The results revealed that ZNF710-AS1-202 was downregulated in human ccRCC tissues and was associated with the pathological grade, tumor size, local invasion and TNM stage, but not with lymph node metastasis or distant metastasis. However, ZNF710-AS1-202 overexpression promoted the proliferation of RCC cells and inhibited apoptosis. Opposite results were observed when ZNF710-AS1-202 was knocked down by small interfering RNA. Furthermore, ZNF710-AS1-202, which was mainly expressed in the cytoplasm of RCC cells, regulated ZNF710 mRNA and protein expression in opposing manners. In conclusion, the present study revealed that ZNF710-AS1-202 and ZNF710 may serve as promising therapeutic targets for ccRCC.	32236626	RID06680	transcriptional regulation	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	XIST	SMAD2	negatively-E	RIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(-);chemosensitivity(+)	transcriptional regulation	association	NA	Cisplatin	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000175387	NA	7503	4087	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	JV18-1|MADH2|MADR2	Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin.Long noncoding RNAs (lncRNAs) play critical roles in tumour progression and metastasis. Emerging evidence indicates that the lncRNA X inactive-specific transcript (XIST) is dysregulated in several tumor types, including non-small cell lung cancer (NSCLC). However, in NSCLC and other cancers the oncogenic mechanism of XIST remains incompletely understood. Here, we confirmed that XIST is upregulated in human NSCLC specimens, and is especially overexpressed in tumors previously treated with cisplatin (cis-diamminedichloroplatinum(II); DDP). In vitro, XIST knockdown inhibited NSCLC cell growth and promoted DDP chemosensitivity by stimulating apoptosis and pyroptosis. Moreover, XIST's oncogenic effects and ability to promote DDP chemoresistance were largely related to its binding to the TGF-beta effector SMAD2, which inhibited its translocation to the nucleus and prevented the transcription of p53 and NLRP3, crucial regulators of apoptosis and pyroptosis, respectively. Using DDP-resistant NSCLC cells, mouse xenograft studies verified the oncogenic function of XIST and its ability to inhibit programmed cell death, thereby mediating DDP chemoresistance. These findings suggest that XIST expression may serve as a novel biomarker to predict DDP treatment efficacy, and may help in the design of new therapies to circumvent DDP chemoresistance in NSCLC and other tumor types.	32209729	RID06681	transcriptional regulation	metastasis,chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Diffuse large b-cell lymphoma	NEAT1	GLI1	positively-E	dual-luciferase reporter analysis;RIP;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);tumorigenesis(+)	ceRNA(miR-34b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000111087	NA	283131	2735	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	GLI	MYC-regulated lncRNA NEAT1 promotes B cell proliferation and lymphomagenesis via the miR-34b-5p-GLI1 pathway in diffuse large B-cell lymphoma.Methods: The expression levels of NEAT1, GLI1 and miR-34b-5p were detected by RT-qPCR and western blot in DLBCL tissues and cell lines. MTT and colony formation assays were performed to examine cell proliferation, while annexin-V staining and TUNEL assays were performed to measure cell apoptosis. The effect of NEAT1, GLI1 and miR-34b-5p on cell cycle-associated proteins was evaluated by western blot. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were employed to investigate the interaction between NEAT1 and miR-34b-5p or GLI1 and miR-34b-5p. Moreover, chromatin immunoprecipitation (ChIP) was performed to demonstrate the interaction between MYC and NEAT1.Results: NEAT1 and GLI1 were upregulated while miR-34b-5p was downregulated in DLBCL tissues and cell lines compared to normal controls. Knockdown of NEAT1 or overexpression of miR-34b-5p inhibited cell proliferation but promoted cell apoptosis. Overexpression of NEAT1 reversed GLI1-knockdown induced attenuation of cell proliferation. In other words, NEAT1 acted as a competing endogenous RNA (ceRNA), regulating the miR-34b-5p-GLI1 axis, further affecting the proliferation of DLBCL. Moreover, MYC modulated NEAT1 transcription by directly binding to the NEAT1 promoter.Conclusion: We revealed that MYC-regulated NEAT1 promoted DLBCL proliferation via the miR-34b-5p-GLI1 pathway, which could provide a novel therapeutic target for DLBCL.	32206038	RID06682	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Diffuse large b-cell lymphoma	MYC	NEAT1	negatively-E	RT-qPCR;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000245532	GRCh38_11:65422774-65445540	4609	283131	bHLHe39|c-Myc|MYCC	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	We detected NEAT1 expression modulated by MYC, and as expected, the mRNA level of NEAT1 was suppressed by MYC overexpression (Fig. -(Fig.6f).6f). JASPAR analysis predicted two MYC binding sites, BS1 and BS2, on the NEAT1 promoter (Fig. -(Fig.6g),6g), and ChIP assay results showed that MYC could bind to BS1 but not to BS2 (Fig. -(Fig.6h).6h). Finally, NEAT1 expression was measured after MYC knockdown, and a marked increase was observed in response to MYC knockdown (Fig. -(Fig.6i).6i). This evidence collectively suggested that MYC could directly bind to the NEAT1 promoter to regulate its expression, further affecting DLBCL proliferation.	32206038	RID06683	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Esophagus squamous cell carcinoma	ACTG1P25	PFKFB3	positively-E	RNA pull-down assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);glycolysis(+);cancer progression(-)	epigenetic regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234996	GRCh38_1:202861754-202875241	ENSG00000170525	NA	148709	5209	AGPG	NA	Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming.Tumor cells often reprogram their metabolism for rapid proliferation. The roles of long noncoding RNAs (lncRNAs) in metabolism remodeling and the underlying mechanisms remain elusive. Through screening, we found that the lncRNA Actin Gamma 1 Pseudogene (AGPG) is required for increased glycolysis activity and cell proliferation in esophageal squamous cell carcinoma (ESCC). Mechanistically, AGPG binds to and stabilizes 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). By preventing APC/C-mediated ubiquitination, AGPG protects PFKFB3 from proteasomal degradation, leading to the accumulation of PFKFB3 in cancer cells, which subsequently activates glycolytic flux and promotes cell cycle progression. AGPG is also a transcriptional target of p53; loss or mutation of TP53 triggers the marked upregulation of AGPG. Notably, inhibiting AGPG dramatically impaired tumor growth in patient-derived xenograft (PDX) models. Clinically, AGPG is highly expressed in many cancers, and high AGPG expression levels are correlated with poor prognosis, suggesting that AGPG is a potential biomarker and cancer therapeutic target.	32198345	RID06684	epigenetic regulation	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	TP53	ACTG1P25	negatively-E	RNAScope ISH assays	upregulation	qPCR	NA	NA	cell proliferation(+);glycolysis(+);cancer progression(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000234996	GRCh38_1:202861754-202875241	7157	148709	LFS1|p53	AGPG	Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming.Tumor cells often reprogram their metabolism for rapid proliferation. The roles of long noncoding RNAs (lncRNAs) in metabolism remodeling and the underlying mechanisms remain elusive. Through screening, we found that the lncRNA Actin Gamma 1 Pseudogene (AGPG) is required for increased glycolysis activity and cell proliferation in esophageal squamous cell carcinoma (ESCC). Mechanistically, AGPG binds to and stabilizes 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). By preventing APC/C-mediated ubiquitination, AGPG protects PFKFB3 from proteasomal degradation, leading to the accumulation of PFKFB3 in cancer cells, which subsequently activates glycolytic flux and promotes cell cycle progression. AGPG is also a transcriptional target of p53; loss or mutation of TP53 triggers the marked upregulation of AGPG. Notably, inhibiting AGPG dramatically impaired tumor growth in patient-derived xenograft (PDX) models. Clinically, AGPG is highly expressed in many cancers, and high AGPG expression levels are correlated with poor prognosis, suggesting that AGPG is a potential biomarker and cancer therapeutic target.	32198345	RID06685	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Melanoma	MIR4435-2HG	FLOT2	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-802)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000132589	NA	541471	2319	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	ECS-1|ECS1|ESA|ESA1|M17S1	Long non-coding RNA MIR4435-2HG recruits miR-802 from FLOT2 to promote melanoma progression.Objective: The regulatory mechanism of lncRNA MIR4435-2HG has been extensively investigated in human cancers other than melanoma. This study aims to elucidate the role of lncRNA MIR4435-2HG in melanoma.Material and methods: The mRNA expression was detected by RT-qPCR. MTT assay, Transwell assay and dual-luciferase reporter assay were used to investigate the regulatory mechanism of lncRNA MIR4435-2HG.Results: Upregulation of lncRNA MIR4435-2HG was identified in melanoma and promoted melanoma cell proliferation, migration and invasion. In addition, lncRNA MIR4435-2HG serves as the ceRNA of miR-802. MiR-802 inhibited melanoma progression by downregulating lncRNA MIR4435-2HG. Besides, miR-802 directly targets FLOT2. And knockdown of FLOT2 restrained the progression of melanoma by downregulating lncRNA MIR4435-2HG and upregulating miR-802.Conclusions: LncRNA MIR4435-2HG promotes cell proliferation, migration and invasion in melanoma by sponging miR-802 and upregulating FLOT2.	32196611	RID06686	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Renal cell carcinoma	SNHG5	TWIST1	positively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000122691	NA	387066	7291	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Long non-coding RNA SNHG5 affects the invasion and apoptosis of renal cell carcinoma by regulating the miR-363-3p-Twist1 interaction.Non-coding RNA dysregulation is associated with many human diseases, including cancer. This study explored the effects of lncRNA SNHG5 on clear cell renal cell carcinoma (ccRCC). We found that lncRNA SNHG5 is upregulated in human ccRCC tissues and that lncRNA SNHG5 inhibition reduced ccRCC cell invasion and promoted apoptosis in vitro. Bioinformatics database searching revealed that lncRNA SNHG5 is predicted to regulate the interaction between miR-363-3p and Twist1. We further verified a ccRCC biomarker panel, which consists of lncRNA SNHG5, miR-363-3p, and Twist1 in ccRCC tissue samples. The direct SNHG5-miR-363-3p and Twist1-miR-363-3p interactions were confirmed via dual-luciferase reporter assays. Additionally, functional assays demonstrated that SNHG5 promotes cell invasion and inhibits apoptosis, while miR-363-3p inhibits cell invasion and promotes apoptosis via an interaction with Twist1. Furthermore, we found that Twist1 promotes tumor metastasis by regulating matrix metalloproteinase (MMP)2 and MMP9 levels. Together, these results suggest that lncRNA SNHG5 may predict ccRCC patient clinical outcome and serve as a novel anti-ccRCC therapeutic target.	32194916	RID06687	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(SKCM);DATA(GSE38495)
Non-small cell lung cancer	PVT1	RAB34	positively-E	dual-luciferase reporter analysis;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-148)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000109113	NA	5820	83871	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NARR|RAB39|RAH	PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis.Methods: The quantitative real-time PCR (qRT-PCR and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull-down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro.Results: In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo.Conclusion: Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets.	32184617	RID06688	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE75367,GSE86978)
Acute myeloid leukemia	miR-194-5p	NEAT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(-)	DNA methylation	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	miRNA	lncRNA	NA	NA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	Down-regulation of lncRNA NEAT1 regulated by miR-194-5p/DNMT3A facilitates acute myeloid leukemia.Methods: Bone marrow samples were collected for monocyte separation. qRT-PCRassay was performed to investigate the expression patterns of NEAT1 and miR-194-5p in AML. CCK-8, soft agar colony formation, flow cytometry and transwell assays were employed to explore the biological functions of NEAT1 or miR-194-5p. Methylation PCR was performed to monitor the methylation of NEAT1. Luciferase reporter assay was subjected to verify the relationship between miR-194-5p and DNMT3A. Immunofluorescence and western blot were performed to detect the alterations of protein expression.Results: NEAT1 and miR-194-5p were both down-regulated in AML. Overexpression of either NEAT1 or miR-194-5p repressed proliferation, induced apoptosis and restrained migration and invasion of AML cells. There was a negative correlation between NEAT1 and DNMT3A in AML. Knockdown of DNMT3A dramatically decreased the methylation of NEAT1. Moreover, DNMT3A was identified as a downstream target of miR-194-5p. Furthermore, down-regulation of DNMT3A rescued the impacts on the malignant phenotypes of NEAT1 inhibition by miR-194-5p inhibitor.Conclusion: Altogether, down-regulation of NEAT1 mediated by miR-194-5p/DNMT3A axis promotes AML progression, which might provide therapeutic targets in AML treatment.	32179410	RID06689	epigenetic regulation	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Ovarian cancer	NORAD	miR-199a-3p	negatively-E	dual-luciferase reporter analysis	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	LncRNA NORAD was highly expressed and miR-199a-3p was lowly expressed in ovarian cancer, and the expression levels of LNCRNARAD and miR-199a-3p were negatively correlated. Cell experiments showed that inhibiting the expression of lncRNA NORAD or up-regulating the expression of miR-199a-3p could inhibit the proliferation, invasion, migration, and EMT of ovarian cancer cells, while up-regulating the expression of lncRNA NORAD or inhibiting the expression of miR-199a-3p could promote their proliferation, invasion, migration, and EMT. dual-luciferase reporter assay confirmed that there was a regulatory relationship between lncRNA NORAD and miR-199a-3p.LncRNA NORAD was highly expressed in ovarian cancer tissues, while silencing lncRNA NORAD expression could inhibit the proliferation, invasion, migration, and EMT of ovarian cancer cells by regulating miR-199a-3p, which might be a new target for the diagnosis and treatment of ovarian cancer.	32141533	RID06690	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Retinoblastoma	TMPO-AS1	HIF1A	positively-E	qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);cancer progression(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000100644	NA	100128191	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA TMPO-AS1 up-regulates the expression of HIF-1alpha and promotes the malignant phenotypes of retinoblastoma cells via sponging miR-199a-5p.Methods: Paired RB samples were collected, and the expression levels of TMPO-AS1, miR-199a-5p and HIF-1alpha were examined by quantitative real-time polymerase chain reaction (qRT-PCR; TMPO-AS1 overexpressing plasmids and TMPO-AS1 shRNA were transfected into HXO-RB44 and SO-Rb50 cell lines respectively, and then proliferation, migration and invasion of RB cells were detected by CCK-8 assay and Transwell method. qRT-PCRand western blot were used to analyze the regulatory function of TMPO-AS1 on miR-199a-5p and HIF-1alpha; luciferase reporter gene assay was used to determine the regulatory relationship between miR-199a-5p and TMPO-AS1.Results: TMPO-AS1 was significantly up-regulated in cancerous tissues of RB samples (relatively expression: 2.97 vs 3.93, p < 0.001), negatively correlated with miR-199a-5p (r=-0.4813, p < 0.01). There was one binding site on TMPO-AS1 for miR-199a-5p. After transfection of TMPO-AS1 shRNAs into RB cells, the proliferation, migration and invasion of cancer cells was significantly inhibited, while TMPO-AS1 had opposite effects; TMPO-AS1 was also demonstrated to regulate the expression of HIF-1alpha on both mRNA and protein levels via negatively regulating miR-199a-5p.Conclusion: TMPO-AS1 is abnormally up-regulated in RB tissues, and it can modulate the proliferation and migration of RB cells. It has the potential to be the "ceRNA" to regulate HIF-1alpha expression by sponging miR-199a-5p.	32139259	RID06691	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Oesophageal squamous cell carcinoma	LY6E-DT	TIMM50	positively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cancer progression(+)	histone modification	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000282681	GRCh38_CHR_HSCHR8_4_CTG7:143012485-143018437	ENSG00000105197	NA	100133669	92609	LOC100133669	TIM50|TIM50L	Long non-coding RNA LOC100133669 promotes cell proliferation in oesophageal squamous cell carcinoma.Materials and methods: ISH was used to detect LOC100133669 expression in ESCC tissues. The full-length LOC100133669 was identified by using RACE assay. Subcellular distribution of LOC100133669 was examined by nuclear/cytoplasmic RNA fractionation and qPCR. The role of LOC100133669 in ESCC cell growth was determined by colony formation, MTT and flow cytometry experiments in vitro, as well as xenograft tumour experiment in vivo. RNA pull-down assay was performed to find LOC100133669-interacted protein, which was further examined by RIP, IP, western blot and rescue experiments.Results: LOC100133669 was upregulated in ESCC tissues compared with adjacent non-tumour tissues. High LOC100133669 expression was associated with poor prognosis of patients with ESCC. We defined LOC100133669 to be 831 nt in length and mainly localized in the cytoplasm of ESCC cells. Knockdown of LOC100133669 inhibited ESCC cell proliferation and cell cycle progression, while overexpression of LOC100133669 showed the opposite effects. Furthermore, LOC100133669 could bind to Tim50 and upregulated its protein level through inhibiting ubiquitination. Overexpression of Tim50 in part abolished the LOC100133669 depletion-caused inhibitory effect on ESCC cell proliferation.Conclusions: LOC100133669 plays an oncogenic role in ESCC and may serve as a promising diagnostic marker and therapeutic target for ESCC patients.	32130753	RID06692	epigenetic regulation	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Breast cancer	H19	LIN28A	positively-E	western blot	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(let-7)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000131914	NA	283120	79727	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CSDD1|FLJ12457|LIN-28|LIN28|ZCCHC1	H19/let-7/Lin28 ceRNA network mediates autophagy inhibiting epithelial-mesenchymal transition in breast cancer.Long non-coding RNA (lncRNA) H19 and Lin28 protein have been shown to participate in various pathophysiological processes, including cellular proliferation, autophagy and epithelial-mesenchymal transition (EMT). A number of studies have investigated lncRNAs, microRNAs and mRNAs, and their roles in the initiation and progression of cancer, in doing so identifying competitive endogenous RNA (ceRNA) networks, including the H19/let-7/Lin28 network. However, whether the H19/let-7/Lin28 ceRNA network is involved in autophagy and EMT in breast cancer (BC) remains unclear. The present study demonstrated that the H19/let-7/Lin28 loop was required for the downregulation of autophagy in BC cells via western blot reverse transcription-quantitative PCR and autophagy flux monitoring. Using wound healing, migration and invasion assays, and morphological assays, the H19/let-7/Lin28 loop was revealed to promote EMT in BC cells. Moreover, the H19/let-7/Lin28 network was found to contribute to autophagy by inhibiting EMT in BC cells. To the best of our knowledge, the present study is the first to suggest the important roles of the H19/let-7/Lin28 ceRNA network in BC autophagy and EMT, thus providing insight for the use of these molecules as prognostic biomarkers and therapeutic targets in BC metastasis.	32124962	RID06693	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	UP(LIHC);DATA(GSE117623)
Breast cancer	SNHG16	RRM2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-30a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000171848	NA	100507246	6241	Nbla10727|Nbla12061|ncRAN	C2orf48|FLJ25102	The SNHG16/miR-30a axis promotes breast cancer cell proliferation and invasion by regulating RRM2.Recent studies have reported that the lncRNA small nucleolar RNA host gene 16 (SNHG16) is highly expressed in breast cancer tissue. In the present study, we demonstrated that SNHG16 is an oncogene involved in cell proliferation and invasion in breast cancer. First, we examined the functional role of SNHG16 in breast cancer cells by knocking down SNHG16 expression via siRNA. We found that SNHG16 inhibition reduced the proliferation and invasion of breast cancer cells in vitro. Then, based on bioinformatic prediction and functional assay validation, we demonstrated SNHG16 interaction with miR-30a and its role in breast cancer cells. Finally, we examined the functional role of RRM2 in breast cancer cells by knocking down RRM2 expression via siRNA. Our results indicated that the SNHG16/miR-30a axis regulated the expression of ribonucleotide reductase M2 (RRM2) in breast cancer cells. These results provide novel insight into breast cancer tumorigenesis and suggest that SNHG16 could serve as a therapeutic target in breast cancer.	32122142	RID06694	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Osteosarcoma	LINC01354	integrinbeta1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	association	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000231768	GRCh38_1:234527887-234531803	NA	NA	100506795	NA	NA	NA	LINC01354 Promotes Osteosarcoma Cell Invasion by Up-regulating Integrin beta1.Expression of LINC01354 in OS tissues, serum and cell lines was measured and the association between LINC01354 expression and clinicopathological factors was analyzed. The functional effects of LINC01354 were examined in vitro by using transwell assays, western blot, immunohistochemistry (IHC) and in vivo in a xenograft tumor mouse model.LINC01354 was overexpressed in OS tissues, serum and cells. LINC01354 overexpression promoted OS cells invasion, EMT and integrin beta1 expression, while knockdown of LINC01354 inhibited OS cell invasion, epithelial-mesenchymal transition (EMT) and integrin beta1 expression. In addition, integrin-beta1 blockage with MAB13 antibody abrogated the effects of LINC01354 overexpression on promoting OS cells invasion and EMT. In addition, LINC01354 promoted OS cell metastasis in vivo.LINC01354 promote OS cell EMT and invasion through up-regulating integrin beta1. Our study suggested that LINC01354 may be regarded as a potential target for the clinical treatment of OS.	32111497	RID06695	transcriptional regulation	metastasis	UP(LIHC);DATA(GSE117623)	
Gastric cancer	TMPO-AS1	SOX4	positively-E	dual-luciferase reporter analysis;StarBase;Targetscan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000124766	NA	100128191	6659	NA	NA	Long Non-Coding RNA TMPO-AS1 Promotes Cell Migration and Invasion by Sponging miR-140-5p and Inducing SOX4-Mediated EMT in Gastric Cancer.Methods: TMPO-AS1 and miR-140-5p expression levels were detected in GC tissues and cell lines by RT-qPCR analysis. Knockdown or overexpression of TMPO-AS1 was conducted to evaluate the effects of TMPO-AS1 on the malignant behaviors of GC cells. Bioinformatic prediction and dual-luciferase reporter assay were performed to investigate the direct interaction between TMPO-AS1 and miR-140-5p in GC.Results: We observed that TMPO-AS1 was up-regulated in GC tissues, and high TMPO-AS1 expression in GC patients was closely correlated with aggressive clinicopathologic characteristics and poor overall survival. Functionally, gain- and loss-of-function studies showed that TMPO-AS1 overexpression enhanced the proliferation, migration, invasion and EMT of GC cells in vitro, whereas knockdown of TMPO-AS1 inhibited these malignant traits. Importantly, we demonstrated that TMPO-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-140-5p in GC cells, thereby diminishing the inhibition on SOX4, an EMT regulator.Conclusion: Our findings indicated that TMPO-AS1 promotes GC progression partly by regulating miR-140-5p/SOX4 axis, and may serve as a novel therapeutic target for GC.	32110100	RID06696	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Cervical cancer	TDRG1	SOX4	positively-E	dual-luciferase reporter analysis;TargetScan;Starbase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-214-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000124766	NA	732253	6659	LINC00532|lincRNA-NR_024015	NA	LncRNA TDRG1 promotes the proliferation, migration, and invasion of cervical cancer cells by sponging miR-214-5p to target SOX4.The pathogenesis of cervical cancer (CC) at molecular level has attracted much research attention. The current study aimed to explore the effects of LncRNA TDRG1 on cellular process in CC cells and its molecular mechanism. Expressions of TDRG1 and miR-214-5p in CC and normal tissues and CC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR. The effects of TDRG1, miR-214-5p, and SOX4 on cell proliferation, migration, invasion, and EMT process of CC cells were detected by Cell Counting Kit-8 (CCK-8), colony formation, wound-healing, Transwell, and western blot assays, respectively. StarBase and Targetscan7.2 were used to predict the target genes of TDRG1 and miR-214-5p, and the predictions were verified by dual-luciferase reporter assay. The expression of SOX4 in CC and normal tissues, and CC cells transfected with siTDRG1 or miR-214-5p inhibitor was determined by qRT-PCR The results showed that expression of TDRG1 was up-regulated, while that of miR-214-5p was down-regulated in CC. The target genes of TDRG1 and miR-214-5p were verified to be miR-214-5p and SOX4, respectively. Knocking down TDRG1 expression could inhibit cell proliferation, colony, migration, and invasion abilities, and EMT process, whereas the inhibition of miR-214-5p expression partially reversed such results. Moreover, high SOX4 expression was observed in CC tissues, and down-regulating TDRG1 expression reduced the SOX4 expression while down-regulating miR-214-5p expression alleviated such an inhibition. In conclusion, TDRG1 acts as cancer promoter in CC through promoting cell proliferation, migration, invasion, and EMT process to modulate SOX4 expression through adsorbing miR-214-5p.	32106739	RID06697	ceRNA or sponge	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Retinoblastoma	NORAD	PBX3	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+);cancer progression(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000167081	NA	647979	5090	LINC00657	NA	Long noncoding RNA NORAD promotes the progression of retinoblastoma by sponging miR-136-5p/PBX3 axis.Expressions of TDRG1 and miR-214-5p in CC and normal tissues and CC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR. The effects of TDRG1, miR-214-5p, and SOX4 on cell proliferation, migration, invasion, and EMT process of CC cells were detected by Cell Counting Kit-8 (CCK-8), colony formation, wound-healing, Transwell, and western blot assays, respectively. StarBase and Targetscan7.2 were used to predict the target genes of TDRG1 and miR-214-5p, and the predictions were verified by dual-luciferase reporter assay. The expression of SOX4 in CC and normal tissues, and CC cells transfected with siTDRG1 or miR-214-5p inhibitor was determined by qRT-PCR The results showed that expression of TDRG1 was up-regulated, while that of miR-214-5p was down-regulated in CC. The target genes of TDRG1 and miR-214-5p were verified to be miR-214-5p and SOX4, respectively. Knocking down TDRG1 expression could inhibit cell proliferation, colony, migration, and invasion abilities, and EMT process, whereas the inhibition of miR-214-5p expression partially reversed such results. Moreover, high SOX4 expression was observed in CC tissues, and down-regulating TDRG1 expression reduced the SOX4 expression while down-regulating miR-214-5p expression alleviated such an inhibition. In conclusion, TDRG1 acts as cancer promoter in CC through promoting cell proliferation, migration, invasion, and EMT process to modulate SOX4 expression through adsorbing miR-214-5p.	32096159	RID06698	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE111842,GSE55807)
Hepatocellular carcinoma	MIR4435-2HG	MAPK	positively-E	RNAi;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell survival(+);MAPK/ERK signaling pathway(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	NA	NA	541471	NA	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	NA	LINC00978 expression was significantly up-regulated in human HCC tissue relative to adjacent normal tissue, and LINC00978 high expression was correlated with poor HCC overall survival. LINC00978 was up-regulated in HCC cell lines. ShRNA-mediated LINC00978 knockdown significantly decreased HCC cell proliferation, and induced HCC cell cycle arrest and apoptosis in vitro. LINC00978 knockdown led to significant decrease in tumor xenograft size in vivo. western blots revealed LINC00978 inhibition decreased ERK, p38, and c-Jun N-terminal kinase (JNK) phosphorylation in HCC cells.LINC00978 is highly expressed in human HCC tissue and correlates with poor HCC prognosis. LINC00978 promotes HCC cell proliferation, cell cycle progression, and survival, partially by activating the MAPK/ERK pathway. Our findings partially elucidated the roles of LINC00978 in HCC carcinogenesis, and identified a therapeutic target for HCC.	32077915	RID06699	transcriptional regulation	prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Hepatocellular carcinoma	MIR4435-2HG	ERK	positively-E	RNAi;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell survival(+);MAPK/ERK signaling pathway(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000133216	NA	541471	NA	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	NA	LINC00978 expression was significantly up-regulated in human HCC tissue relative to adjacent normal tissue, and LINC00978 high expression was correlated with poor HCC overall survival. LINC00978 was up-regulated in HCC cell lines. ShRNA-mediated LINC00978 knockdown significantly decreased HCC cell proliferation, and induced HCC cell cycle arrest and apoptosis in vitro. LINC00978 knockdown led to significant decrease in tumor xenograft size in vivo. western blots revealed LINC00978 inhibition decreased ERK, p38, and c-Jun N-terminal kinase (JNK) phosphorylation in HCC cells.LINC00978 is highly expressed in human HCC tissue and correlates with poor HCC prognosis. LINC00978 promotes HCC cell proliferation, cell cycle progression, and survival, partially by activating the MAPK/ERK pathway. Our findings partially elucidated the roles of LINC00978 in HCC carcinogenesis, and identified a therapeutic target for HCC.	32077915	RID06700	transcriptional regulation	prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Colorectal cancer	NEAT1	VEGFA	positively-E	dual-luciferase reporter analysis;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-205-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112715	NA	283131	7422	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	VEGF|VEGF-A|VPF	Long non-coding RNA NEAT1 promotes colorectal cancer progression by regulating miR-205-5p/VEGFA axis.In our study, the expression of NEAT1, miR-205-5p, and vascular endothelial growth factor A (VEGFA) in CRC cell lines were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were examined by wound healing and transwell assays, respectively. RNA-binding protein immunoprecipitation (RIP), and dual-luciferase and RNA pull-down assays were conducted to determine the correlation between miR-205-5p and NEAT1 or VEGFA. VEGFA, matrix metalloproteinase (MMP)2, and MMP9 protein and mRNA expression were measured by western blot and RT-qPCR analysis, respectively. Our results demonstrated high expression of NEAT1 and VEGFA and low expression of miR-205-5p in CRC cell lines. The RIP and dual-luciferase assays confirmed miR-205-5p as a target of NEAT1. In addition, VEGFA was identified as a direct target of miR-205-5p. Inhibition of NEAT1 or overexpression of miR-205-5p was able to repress VEGFA expression. Moreover, downregulation of NEAT1 and VEGFA inhibited cell proliferation, migration, and invasion. NEAT1 overexpression facilitated tumor growth by modulating miR-205-5p. Taken together, lncRNA NEAT1 was found to be upregulated in CRC cell lines, promoting CRC cell proliferation, migration, and invasion through regulating the miR-205-5p/VEGFA signaling pathway. These findings suggest that NEAT1 may be a promising biomarker in CRC diagnosis and treatment.	32065361	RID06701	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cholangiocarcinoma	MIAT	CCND1	positively-E	starBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-551b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000110092	NA	440823	595	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	BCL1|D11S287E|PRAD1|U21B31	In the present study, we found that the expression of MIAT in CCA tissues was prominently higher than that in normal bile duct tissues. Moreover, TCGA-CHOL data in the GEPIA platform further revealed the upregulated expression of MIAT in CCA tissues. Additionally, quantitative real-time PCR results showed that MIAT expression was increased in CCA cell lines compared to the human intrahepatic biliary epithelial cell line. Functionally, MIAT knockdown significantly inhibited cell proliferation and induced G0/G1 phase arrest as well as apoptosis in HuCCT-1 and QBC939 cells. Conversely, ectopic expression of MIAT obviously facilitated the proliferation, cell cycle progression and apoptosis resistance of RBE cells. Mechanistically, MIAT directly interacted with miR-551b-3p and inversely modulated miR-551-3p level in CCA cells. Furthermore, MIAT knockdown reduced the expression of cyclin D1 (CCND1), which was rescued by miR-551b-3p silencing in HuCCT-1 cells. Importantly, CCND1 restoration partially reversed MIAT knockdown-induced proliferation inhibition, G0/G1 phase arrest and apoptosis in HuCCT-1 cells. In conclusion, MIAT was frequently overexpressed in CCA. MIAT contributed to the growth of CCA cells by targeting miR-551b-3p/CCND1 axis.	32064660	RID06702	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	TP53COR1	MDM2	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+);NF-kB signaling pathway(+);STAT3 signaling pathway(+)	epigenetic regulation	association	RNA-protein	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000135679	NA	102800311	4193	TRP53COR1|linc-p21|lincRNA-p21	ACTFS|HDMX|LSKB|hdm2	LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development.Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-kB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.	32062693	RID06703	epigenetic regulation	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Prostate cancer	TUG1	Nrf2	positively-E	western blot;LncTar Web Server	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);NRF2 signaling pathway(+)	transcriptional regulation	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Long noncoding RNA TUG1 regulates prostate cancer cell proliferation, invasion and migration via the Nrf2 signaling axis.Methods: Reverse transcription-quantitative polymerase chain reaction (qRT-PCR and western blotwere used to assess the mRNA expression of TUG1 and protein expression levels of Nrf2 pathway members, respectively. The migration, invasion, and proliferation abilities of cells were assessed by the wound-healing, Transwell migration/invasion, and CCK8 assays, respectively.Results: TUG1 was strikingly upregulated in PCa cells compared with non-tumorigenic human prostate epithelial cells. The LncTar Web Server, which is a bioinformatics tool, was used to predict the target association between TUG1 and Nrf2. Moreover, the expression of TUG1 showed a strikingly positive correlation with that of Nrf2 in TCGA PCa RNA-Seq data (r = 0.26,P = 4.63E-09). Subsequently, inhibition of TUG1 using siRNA resulted in deceased proliferation, migration, and invasion of PCa cells; however, these effects were reversed by treatment with oltipraz (an activator of Nrf2). Finally, we evaluated the Nrf2 pathway to reveal the underlying mechanism of TUG1 in PCa cells, and found that TUG1 knockdown decreased the protein expression of Nrf2 downstream members (e.g., HO-1, FTH1, and NQO1).Conclusions: LncRNA TUG1 plays an oncogenic role in human PCa cells by promoting the cell proliferation and invasion in PCa cell lines, at least partly via the Nrf2 signaling pathway.	32057513	RID06704	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Gastric cancer	AFAP1-AS1	FGF7	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-155-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000140285	NA	84740	2252	AFAP1-AS|AFAP1AS|MGC10981	KGF	We used qRT-PCRto detect the relative expression of AFAP1-AS1 in GC tissues and cell lines.The loss-of-function assays were conducted to detect the effect of AFAP1-AS1 on GC development. Bioinformatics analysis, luciferase reporter gene analysis, and RIP analysis were used to identify and validate target genes of AFAP1-AS1. Finally, rescue tests were performed to confirm the influence of the AFAP1-AS1-miR-155-5p-FGF7 axis on GC development.AFAP1-AS1 was upregulated in GC tissues and cell lines and was closely correlated with poor prognosis of GC patients. AFAP1-AS1 knockdown inhibited proliferation, migration, and invasion of GC cells, indicating that AFAP1-AS1 acts as an oncogene in GC. Bioinformatics analysis, dual-luciferase reporter gene detection, and RIP assays validated that AFAP1-AS1 directly interacts to miR-155-5p and could positively affect cell proliferation, migration, and invasion by regulation of the expression of miR-155-5p and FGF7. Further rescue assays revealed that AFAP1-AS1 promotes cell proliferation and metastasis through the miR-155-5p/FGF7 axis in GC.AFAP1-AS1 might be an oncogenic lncRNA that promoted GC progression by acting as a competing endogenous RNA (ceRNA) that regulates the expression of FGF7 through sponging miR-155-5p, suggesting that AFAP1-AS1 may be a novel potential therapeutic target for GC.	32051698	RID06705	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Oral squamous cell carcinoma	LINC01234	PAK4	positively-E	dual-luciferase reporter analysis	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell proliferation(+)	ceRNA(miR-433)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000130669	NA	100506465	10298	onco-lncRNA-32	NA	We evaluated the expression profile and prognostic value of Linc01234 in OSCC tissues by RT-qPCR. Then, functional in vitro experiments were performed to investigate the effects of Linc01234 on tumor growth, migration and invasion in OSCC.Mechanistically, RT-qPCR, bioinformatic analysis and dual-luciferase reporter assays were performed to identify a competitive endogenous RNA (ceRNA) mechanism involving Linc01234, miR-433-3p and PAK4.We found that Linc01234 was clearly upregulated in OSCC tissues and cell lines, and its level was positively associated with T stage, lymph node metastasis, differentiation and poor prognosis of patients with OSCC.Our results shown that Linc01234 inhibited cell proliferation and metastatic abilities in CAL27 and SCC25 cells following its knockdown.Mechanistic analysis indicated that Linc01234 may act as a ceRNA (competing endogenous RNA) of miR-433-3p to relieve the repressive effect of miR-433-3p on its target PAK4.Our results indicated that Linc01234 promotes OSCC progression through the Linc01234/miR-433/PAK4 axis and might be a potential therapeutic target for OSCC.	32041570	RID06706	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE75367)
Triple-negative breast cancer	GPER1	lncRNA-Glu	negatively-E	western blot	downregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell metastasis(+)	interact with protein	association	protein-RNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000164850	NA	NA	NA	2852	NA	CEPR|CMKRL2|DRY12|FEG-1|GPCR-Br|GPER|GPR30|LERGU|LERGU2|LyGPR|mER	NA	GPER-regulated lncRNA-Glu promotes glutamate secretion to enhance cellular invasion and metastasis in triple-negative breast cancer.Triple-negative breast cancer (TNBC) is a group of breast cancer with heterogeneity and poor prognosis and effective therapeutic targets are not available currently. TNBC has been recognized as estrogen-independent breast cancer, while the novel estrogen receptor, namely G protein-coupled estrogen receptor (GPER), was claimed to mediate estrogenic actions in TNBC tissues and cell lines. Through mRNA microarrays, lncRNA microarrays, and bioinformatics analysis, we found that GPER is activated by 17beta-estradiol (E2) and GPER-specific agonist G1, which downregulates a novel lncRNA (termed as lncRNA-Glu). LncRNA-Glu can inhibit glutamate transport activity and transcriptional activity of its target gene VGLUT2 via specific binding. GPER-mediated reduction of lncRNA-Glu promotes glutamate transport activity and transcriptional activity of VGLUT2. Furthermore, GPER-mediated activation of cAMP-PKA signaling contributes to glutamate secretion. LncRNA-Glu-VGLUT2 signaling synergizes with cAMP-PKA signaling to increase autologous glutamate secretion in TNBC cells, which activates glutamate N-methyl-D-aspartate receptor (NMDAR) and its downstream CaMK and MEK-MAPK pathways, thus enhancing cellular invasion and metastasis in vitro and in vivo. Our data provide new insights into GPER-mediated glutamate secretion and its downstream signaling NMDAR-CaMK/MEK-MAPK during TNBC invasion. The mechanisms we discovered may provide new targets for clinical therapy of TNBC.	32030797	RID06707	interact with protein	metastasis,prognosis		
Cervical cancer	CAR10	PDPK1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);apoptosis process(-);cancer progression(+)	ceRNA(miR-125b-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000148848	GRCh38_10:126012381-126388477	ENSG00000140992	NA	NA	5170	NA	PDK1	LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p.Cervical cancer is one of the malignant tumors that seriously threaten women's health. The mechanism of development needs to be deeply studied. In recent years, lncRNA has been identified as one of the important factors affecting the malignant progression of tumors. In this study, we illustrated the important mechanism of lncRNA CAR10 in the development of cervical cancer. We found that CAR10 is significantly increased in4 cervical cancer tissues and cells, which can promote the proliferation of cervical cancer cells in vitro and in vivo, indicating that CAR10 is involved in the progression of cervical cancer as an oncogene. Further studies showed that CAR10 is a target gene of miR-125b-5p, and miR-125b-5p can inhibit the effect of CAR10 on the proliferation of cervical cancer cells. In addition, we also found that 3-phosphoinositide-dependent protein kinase 1 (PDPK1) is also a target gene of miR-125b-5p, and CAR10 can upregulate the expression level of PDPK1. The results showed that CAR10 acts as a ceRNA to upregulate the expression of PDPK1 by sponging miR-125b-5p. Knockdown of PDPK1 can inhibit the effect of CAR10 on cervical cancer cells. Our study demonstrates that, based on ceRNA mechanism, CAR10/miR-125b-5p/PDPK1 network can regulate the proliferation of cervical cancer cells and play an important role in the development of cervical cancer. In addition, our study also suggests that intervention of CAR10/miR-125b-5p/PDPK1 network may be a new strategy for targeted therapy of cervical cancer.	32025520	RID06708	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Ovarian cancer	FLVCR1-DT	YAP1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-513)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000198468	GRCh38_1:212852105-212858138	ENSG00000137693	NA	642946	10413	FLVCR1-AS1|LQK1|NCRNA00292	YAP65	FLVCR1-AS1 might regulate cell growth, migration and invasion via targeting YAP1 in OSC cells.	31412903	RID06709	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Colorectal cancer	MIR17HG	RELA	positively-E	qRT-PCR;siRNA;ChIP;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000215417	GRCh38_13:91347820-91354579	ENSG00000173039	NA	407975	5970	C13orf25|FLJ14178|LINC00048|MIHG1|miR-17-92|MIRH1|MIRHG1|NCRNA00048	NFKB3|p65	Mechanistically, MIR17HG increased the expression of nuclear  factor kappa B(NF-kB)/RELA by competitively sponging the microRNA miR-375.	31409641	RID06710	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	MIR17HG	BLNK	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000215417	GRCh38_13:91347820-91354579	ENSG00000262509	NA	407975	29760	C13orf25|FLJ14178|LINC00048|MIHG1|miR-17-92|MIRH1|MIRHG1|NCRNA00048	BASH|bca|BLNK-s|Ly57|SLP-65|SLP65	MIR17HG promotes CRC growth and metastasis through suppressing BLNK  expression binding with miR-17-5p.The overexpression of miR-17-5p resulted in  the blunting of the luciferase activity of wild type but not the mutated BLNK 3 UTR, which suggested that miR-17-5p directly regulated BLNK expression by binding the  BLNK 3 UTR.	31409641	RID06711	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE86978)
Glioblastoma	STAT1	HAS2-AS1	positively-E	ChIP	upregulation	qRT-PCR;ISH	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000115415	NA	ENSG00000248690	GRCh38_8:121639293-121994185	6772	594842	ISGF-3|STAT91	HAS2-AS|HAS2AS|HASNT|NCRNA00077	The transcription factor STAT1 could raise HAS2-AS1 by binding to its promoter region. Subsequently, STAT1 was knocked down or overexpressed in the corresponding GBM cells (Figure 3B), and HAS2-AS1 levels were measured by the qRT-PCR(Figure 3C).According to the results, the reduction of STAT1 reduced HAS2-AS1 in both LN229 and PG1. In the meantime,elevated STAT1 raised the HAS2-AS1 expression level in A172 cells. By scanning the promoter region of HAS2-AS1,two predicted STAT1 binding sites with highest scores were chosen (Figure 4D). Afterwards, ChIP was carried out to illuminate the binding between STAT1 and HAS2-AS1 promoter region. What-s interesting is that only Site 1 group had the PCR products in the STAT1 immunopre-cipitation, implying that STAT1 bound to HAS2-AS1 promoter at the -975 to -965 bp region (Figure 3E).	31385362	RID06712	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Glioblastoma	HAS2-AS1	PRPS1	positively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-608)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000248690	GRCh38_8:121639293-121994185	ENSG00000147224	NA	594842	5631	HAS2-AS|HAS2AS|HASNT|NCRNA00077	CMTX5|DFN2|DFNX1	To figure out whether miR 608 plays a role in the association between HAS2 AS1 and PRPS1, LN229 and PG1 were cotransfected with siHAS2 AS1 and miR 608 inhibitor. Indeed, miR 608 inhibitor effectively reversed the reduction of PRPS1 protein levels induced by siHAS2 AS1 (Figure 5F). Next, the qRT-PCRwas employed to assess the correlation between HAS2 AS1 and PRPS1 expressions in 15 glioma tissues. The results revealed that there HAS2 AS1 expression was positively correlated with PRPS1 expression, confirming the existence of a HAS2 AS1 miR 608 PRPS1 regulatory axis in GBM (Figure 5G). PRPS1 expression was over- expressed or lowered in glioma cells to analyze the oncogenic role of PRPS1 in glioma (Figure 5H and Figure S3B).Colony formation and EdU incorporation assays showed that PRPS1 could enhance the proliferation ability of glioma cells (Figure 5I and 5J and Figure S3C and S3D).	31385362	RID06713	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Breast cancer	SNHG7	MIR381	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000199020	NA	84973	494330	NCRNA00061	MIRN381|hsa-mir-381|mir-381	MiRNA-381 was newly confirmed as a direct target of SNHG7 and it mediated the suppressing effects of SNHG7 on breast cancer cells.The dual-luciferase reporter assays were performed, and the results demonstrated that miRNA-381 was a direct target of lncRNA SNHG7(Figure 3E). The expression of miRNA-381 was measured in the clinical samples. The expression of miRNA-381 and SNHG7 showed a significantly negative correlation, which further indicated the sponging effect between miRNA-381 and SNHG7 (Figure 3F).	31378900	RID06714	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Melanoma	SSATX	TCF	positively-E	luciferase reporter assay;western blot;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	TF	NA	NA	ENSG00000101076	NA	NA	NA	NA	NA	We then used qRT-PCRto analyze the expression of TCF4, cyclin D1, FOSL1, and FST, which are several well-known downstream target genes of the Wnt/beta-catenin pathway. The expression levels of TCF4, FOSL1, and FST were found to be elevated in A2058 shSSATX cells compared with A2058 scramble cells (Fig. 4E). These data show an important correlation between SSATX expression and Wnt/beta-catenin signaling pathway activity and suggest that SSATX affects the biological activity of melanoma cells through this pathway.	31352009	RID06715	expression association	NA		
Multiple myeloma	PTENP1	TSC1	negatively-E	RT-PCR;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-19b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000165699	NA	11191	7248	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	hamartin|KIAA0243|LAM|TSC	According to the results of real time-PCR, a negative correlation with a correlation coefficient of 0.05 was established between PTENP1 and miR-19b expression.Furthermore, luciferase assays were conducted to confirm the regulatory relationships among PTENP1, miR-19b, and TSC1. As shown in Figure 6B and Figure 6C, miR-19b evidently reduced the luciferase activity of OPM2 and KMS 11 cells transfected by wild type 3'UTR of PTENP1 or wild type 3'UTR of TSC1.	31338886	RID06716	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	RNA00887	miR-613	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA	regulation	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	The results indicated LINC00887 overexpression reduced the levels of miR-613, miR-206 and miR-1-2 (Fig. 5B).This suggested a linear association between the miRNAs and LINC00887.	31322230	RID06717	ceRNA or sponge	NA		
Non-small cell lung cancer	RNA00887	MIR206	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA	regulation	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	NA	NA	ENSG00000207604	NA	NA	406989	NA	MIRN206|miRNA206|mir-206	The results indicated LINC00887 overexpression reduced the levels of miR-613, miR-206 and miR-1-2 (Fig. 5B).This suggested a linear association between the miRNAs and LINC00887.	31322230	RID06718	ceRNA or sponge	NA		
Non-small cell lung cancer	LINC00887	MIR1-2	negatively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA	regulation	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214145	GRCh38_3:194296191-194322871	ENSG00000265142	NA	100131551	406905	NA	MIRN1-2|hsa-mir-1-2|miRNA1-2|mir-1-2	The results indicated LINC00887 overexpression reduced the levels of miR-613, miR-206 and miR-1-2 (Fig. 5B).This suggested a linear association between the miRNAs and LINC00887.	31322230	RID06719	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Thyroid cancer	NR2F1-AS1	CCND1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000110092	NA	441094	595	FLJ42709	BCL1|D11S287E|PRAD1|U21B31	NR2F1-AS1 sponged miRNA-338-3p to up-regulate CCND1 expression to promote TC progression.Relative expression of NR2F1-AS1, miRNA-338-3p and cyclin D1 (CCND1) was determined by quantitative real time polymerase chain reaction. In addition, western blotwas adopted for evaluation of protein expression of CCND1. Targeted relationships between NR2F1-AS1 and miRNA-338-3p, as well as miRNA-338-3p and CCND1 were predicted using bioinformatics analysis and validated by dual-luciferase reporter gene assay.NR2F1-AS1 and CCND1 were overexpressed, whereas miRNA-338-3p was down-regulated in TC tissues and cell lines.	31304680	RID06720	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Malignant glioma	SNHG20	MDM2	positively-E	TargetScan;luciferase reporter assay;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-4486)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000135679	NA	654434	4193	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	HDM2|MGC5370	Significantly negative correlation between the expression of SNHG20 and miR-4486 was observed in glioma tissues (Figure 3F).Overexpression of miR-4486 reversed the promotion effect of SNHG20 on the proliferation of U87 cells (Figure 3G). These data indicated that SNHG20 sponged miR-4486 and decreased the level of miR-4486 in glioma cells.Further study revealed that miR-4486 targeted the E3 ubiquitin ligase mouse double minute 2 (MDM2) and negatively regulated the expression of MDM2. Down-regulation of MDM2 by miR-4486 increased the abundance of p53 in glioma cells.	31298384	RID06721	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	SNHG7	RBM5	negatively-E	western blot;qRT-PCRhRNA	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000003756	NA	84973	10181	MGC16037|NCRNA00061	H37|LUCA-15|LUCA15	Our study suggests that SNHG7 could promote cell invasion and migration in HCC cells through downregulating RBM5, which may offer a new therapeutic intervention for HCC patients.	31298322	RID06722	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Cervical cancer	LINC01535	EZH2	positively-E	luciferase reporter assay;western blot;ChIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(+);cell growth(+);tumorigenesis(+)	ceRNA(miR-214)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000226686	GRCh38_19:37251867-37265547	ENSG00000106462	NA	101927667	2146	NA	ENX-1|EZH1|KMT6|KMT6A	In this study, we identified that lncRNA LINC01535 physically binds miR-214, relieves the repressive roles of miR-214 on its target EZH2, and therefore up regulates EZH2 protein expression.Intriguingly, we also found that EZH2 directly represses the expression of miR-214.The expression of LINC01535 is reversely as sociated with the expression of miR-214 and positively associated with the expression of EZH2 in cervical cancer tissues.	31273925	RID06723	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	ADPGK-AS1	OTX1	positively-E	luciferase reporter assay;RIP;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-3196)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000260898	GRCh38_15:72782835-72798199	ENSG00000115507	NA	100287559	5013	NA	NA	ADPGK-AS1 acted as a competing endogenous RNA (ceRNA) via modulating miR-3196/OTX1 axis in BC.Correlation analysis demonstrated that the expression of OTX1 was negatively correlated with miR-3196, but positively correlated with ADPGK-AS1 (Fig. 5H, I).	31264061	RID06724	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	
Non-small cell lung cancer	SNHG14	HMGB1	positively-E	qRT-PCR;western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);chemoresistance(-)	ceRNA(miR-34a)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000189403	NA	104472715	3146	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	DKFZp686A04236|HMG1|HMG3|SBP-1	SNHG14 silencing exerted its regulatory effect by miR-34a and HMGB1 mediated the regulatory effect of miR-34a on NSCLC cells.SNHG14 regulated HMGB1 expression by sponging miR-34a. Besides, our data revealed that SNHG14 and HMGB1 were upregulated and miR-34a was downregulated in clinical NSCLC samples compared with normal samples(Supplement Fig. 1A). Moreover, these data indicated a significant inverse correlation between miR-34a level and SNHG14 or HMGB1 expression, and a positive correlation between SNHG14 level and HMGB1 expression in NSCLC tissues (Supplement Fig. 1D ).	31252267	RID06725	ceRNA or sponge	chemoresistance	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Acute myeloid leukemia	HOXB-AS3	CDK1	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000170312	NA	404266	983	NA	CDC2|CDC28A	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06726	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Acute myeloid leukemia	HOXB-AS3	CCNB2	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000157456	NA	404266	9133	NA	HsT17299	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06727	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD,PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE55807)
Acute myeloid leukemia	HOXB-AS3	CDC25A	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000164045	NA	404266	993	NA	NA	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06728	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC);DATA(GSE117623)
Acute myeloid leukemia	HOXB-AS3	PCNA	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000132646	NA	404266	5111	NA	NA	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06729	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Acute myeloid leukemia	HOXB-AS3	CDC6	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000094804	NA	404266	990	NA	CDC18L	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06730	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Acute myeloid leukemia	HOXB-AS3	MCM4	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000104738	NA	404266	4173	NA	CDC21|CDC54|hCdc21|MGC33310|P1-Cdc21	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06731	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE86978)
Acute myeloid leukemia	HOXB-AS3	MCM6	positively-E	RT-qPCR;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000233101	GRCh38_17:48549630-48606414	ENSG00000076003	NA	404266	4175	NA	Mis5	We validated a set of HOXB-AS3 regulated genes by RT-qPCR and confirmed that several genes involved in the cell cycle progression (CDK1, CCNB2, and CDC25A), DNA replication (PCNA), and assembly of pre-replicative complex (CDC6, MCM4, MCM6) were indeed downregulated when HOXB-AS3 was knocked down (Fig. -(Fig.3d).3d). Conversely, these genes were upregulated when HOXB-AS3 was overexpressed (Additional file 1: Figure S9). These findings suggested that HOXB-AS3 induced the expression of a number of genes involving in cell cycle progression and DNA replication to contribute to myeloid cell proliferation.	31234830	RID06732	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	MNX1-AS1	CDKN1A	negatively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000124762	NA	645249	1026	CCAT5|LOC645249|MAYA	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	The underlying mechanism of MNX1-AS1 in GC was explored by performing RT-qPCR and western blot assay.The mRNA and protein expressions of CDKN1A were remarkably down-regulated after MNX1-AS1 overexpression. Furthermore, the expression level of CDKN1A was negatively correlated with the expression of MNX1-AS1 in GC tissues.	31210302	RID06733	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Glioblastoma	TRG-AS1	SUZ12	positively-E	RT-qPCR;RIP;luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-877-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000281103	GRCh38_7:38330978-38378804	ENSG00000178691	NA	100506776	23512	NA	CHET9|JJAZ1|KIAA0160	western blotalso proved a higher protein level of SUZ12 in GBM cells (Fig. 3E). In Fig. 3F, most of miR-877-5p expression was detected in wild type bio-SUZ12 group. Luciferase reporter assay showed that miR-877-5p mimics decreased the luciferase activity of wild type SUZ12 vectors (Fig. 3G).TRG-AS1 promotes glioblastoma cell proliferation by acting as a ceRNA of miR-877-5p to regulate SUZ12 expression.RT-qPCR revealed that knockdown of TRG-AS1 would downregulate the mRNA expression of SUZ12 (Fig. 3H). RIP assay was also performed to verify the ceRNA mechanism. The expressions of TRG-AS1, miR-877-5p and SUZ12 could all be detected from anti-AGO2 group, indicating that TRG-AS1 acted as ceRNA of miR-877-5p to regulate SUZ12 expression.The luciferase activity of wild type SUZ12 vector was significantly weakened by overexpression of miR-877-5p, but was later rescued by pcDNA3.1/TRG-AS1 (Fig. 3K). Based on these assays, TRG-AS1 acts as a ceRNA of miR-877-5p to regulate SUZ12 expression.	31196742	RID06734	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Malignant glioma	SNHG1	PHLDA1	positively-E	starBase;miRcode;TargetScan;miRDB;luciferase reporter assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);tumorigenesis(+)	ceRNA(miR-194)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000139289	NA	23642	22822	LINC00057|lncRNA16|NCRNA00057|UHG	DT1P1B11|PHRIP|TDAG51	Through online databases,a luciferase reporter assay and an RNA pull-down assay,we confirmed that SNHG1 functions as a sponge for miR-194, which acts as a suppressor in glioma.We also verified that pleckstrin homology like domain family A, member 1 (PHLDA1) is the functional target of miR-194.Moreover,rescue experiments demonstrated that SNHG1 regulates PHLDA1 expression in a miR-194-dependent manner.Taken together,our study shows that SNHG1 promotes glioma progression by competitively binding to miR- 194 to regulate PHLDA1 expression,which may provide a novel therapeutic strategy for glioma.	31189920	RID06735	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	IGF2-AS	SHOX2	positively-E	miRWalk;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);glycolysis(+);miR-338-3p/PKM2 signaling pathway(-)	ceRNA(miR-503)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Gastric cancer	lncRNA	TF	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000168779	NA	51214	6474	IGF2-AS1|IGF2AS|PEG8	OG12|OG12X|SHOT	SHOX2 is a target of miR-503,and IGF2-AS acted as a ceRNA for miR-503 to up-regulate SHOX2 and then affects the progression of GC.	31183590	RID06736	ceRNA or sponge	NA		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Malignant glioma	LINC00689	PKM	positively-E	starBase;knockdown;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);glycolysis(+)	ceRNA(miR-338-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Brain glioma	lncRNA	PCG	ENSG00000231419	GRCh38_7:159006522-159030195	ENSG00000067225	NA	154822	5315	NA	OIP3|PK3|PKM2|THBP1	LINC00689 functioned as a competing endogenous RNA (ceRNA) by directly interacting with miR-338-3p to promote pyruvate kinase M2 (PKM2) expression.We also revealed that restoration of PKM2 abolished the effects of LINC00689 silencing on glioma cell proliferation, migration, invasion and glycolysis.Intriguingly, LINC00689 silencing obviously reduced the level of PKM2 protein in both U251 and U87 cells (P < 0.05, Fig. 4E). And miR-338-3p knockdown reversed LINC00689 silencing-induced PKM2 repression in glioma cells (Fig. 4E).Taken together, our results revealed that LINC00689 acted as a ceRNA to interact with miR-338-3p and enhanced PKM2 expression in glioma.	31181442	RID06737	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Colorectal cancer	YY1	ARAP1-AS1	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000256007	GRCh38_11:72685075-72693808	7528	100874075	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NA	YY1 transcription factor (YY1) enhanced the transcription activity of ARAP1-AS1.To analyze whether YY1 regulated ARAP1-AS1 expression in CRC cells, the authors overexpressed or silenced YY1 in both SW480 and HT29 cells (Fig. 3F). The expression of ARAP1- AS1 was found to be positively regulated by YY1 in CRC cells (Fig. 3G).	31173500	RID06738	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE75367)
Nasopharynx carcinoma	PXN-AS1-L	SAPCD2	positively-E	TANRIC;RNA pull-down;RIP;luciferase reporter assay;qPCR;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	NA	ENSG00000186193	NA	NA	89958	NA	C9orf140|p42.3	Mechanistically,PXN-AS1-L directly interacts with SAPCD2 mRNA 3 untranslated region, prevents the binding of microRNAs AGO silencing complex to SAPCD2 mRNA, and upregulates the mRNA and protein level of SAPCD2.The expression of SAPCD2 is significantly positively associated with that of PXN AS1 L in NPC tissues.	31173488	RID06739	transcriptional regulation	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE55807)
Non-small cell lung cancer	OR3A4P	CDK1	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000180068	GRCh38_17:3309986-3311446	ENSG00000170312	NA	390756	983	OR3A4	CDC2|CDC28A	RT-qPCR results revealed that CDK1 of A549/ DDP cells was remarkably lower-expressed in the OR3A4/shRNA group compared with that in the control group (Figure 5A). western blotresults also revealed that CDK1 of A549/DDP cells was markedly downregulated in the OR3A4/shRNA group compared with that in the control group (Figure 5B).	31173293	RID06740	transcriptional regulation	chemoresistance		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Endometrial cancer	DANCR	MIR214	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000207949	NA	57291	406996	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	MIRN214|miRNA214|mir-214	miR-214 was found to be a target miRNA of DANCR and its expression was significantly decreased in EC tissues. Suppression of miR-214 abolished the effects of si-DANCR on cell proliferation and apoptosis in AN3CA and HEC-1B cells. DANCR played an important role in promoting tumorigenesis of EC via sponging miR-214.	31161373	RID06741	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Non-small cell lung cancer	LINC00668	KLF7	negatively-E	qRT-PCR;luciferase reporter assay;RIP;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-193a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000118263	NA	400643	8609	NA	UKLF	Mechanistic studies indicated that LINC00668 is a direct target of miR-193a, leading to down-regulation in the expression of its target gene KLF7. Our findings suggested that STAT3-induced LINC00668 contributed to NSCLC progression through upregulating KLF7 expression by sponging miR-193a, and may serve as a prognostic biomarker and a potential target for NSCLC.	31150989	RID06742	ceRNA or sponge	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	STAT3	LINC00668	positively-E	ChIP;luciferase reporter assays	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000265933	GRCh38_18:6919496-6929966	6774	400643	APRF	NA	We also showed that LINC00668 upregulation was induced by transcription factor STAT3.In addition, we also carried out ChIP assays for further verifying the enrichment of STAT3 at the promoter region of LINC00668. The results documented STAT3-binding activity round P2 site but not P1 site and P3 site of endogenous LINC00668 promoter region, which indicated that STAT3 directly bound with P2 sites of LINC00668 promoter (Fig. 2D). To further validate this result, we separately constructed the wild type P2 site or mutant P2 site of LINC00668 promoter into pGL3 luciferase reporter plasmids and subsequently conducted luciferase reporter assays in A549 cells. The results demonstrated that the luciferase activity in A549 cells was notably increased when transfecting wild type P2 site containing luciferase reporter plasmids, while the luciferase activity was not changed in A549 cells when they were transfected with mutant P2 site containing luciferase reporter plasmids (Fig. 2E). Therefore,these results confirmed that LINC00668 up-regulation in NSCLC was mediated by the STAT3 transcription factor.	31150989	RID06743	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Thyroid cancer	LINC00511	JAK2	negatively-E	luciferase reporter assay;ChIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	radioresistance(+);JAK2/STAT3 signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000096968	NA	400619	3717	onco-lncRNA-12	JTK10	TAF1 modulated JAK2 at transcriptional level. Moreover, LINC00511 bound to TAF1 and further promoted JAK2 expression.	31135274	RID06744	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Urinary bladder cancer	ZEB1-AS1	ZEB1	positively-F	western blot;RIP;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	The data from the present study demonstrated that ZEB1 AS1 induced BCa metastasis via an AUF1-mediated translation activation of ZEB1 mRNA mechanism.	31115480	RID06745	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	CRNDE	SIX1	positively-E	western blot;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-337-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000126778	NA	643911	6495	CRNDEP|LINC00180|LOC643911	DFNA23	Mechanistic investigations demonstrated that lncRNA CRNDE interacted with miR-337-3p and decreased its expression, thereby increasing the protein expression of miR-337-3p's target, SIX1. In addition, in vivo experiments using a xenograft tumor mouse model revealed that lncRNA CRNDE served as an oncogene, partly through sponging miR-337-3p and upregulating SIX1 in HCC.	31099050	RID06746	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)
Malignant glioma	BLACAT1	VASP	positively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell growth(+)	ceRNA(miR-605-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000125753	NA	101669762	7408	linc-UBC1|LINC00912|onco-lncRNA-30	NA	We also illustrated that BLACAT1 worked as the sponge for miR-605-3p and promoted VASP expression.This study highlights the important roles of BLACAT1/miR-605-3p/VASP axis in glioma progression.	31093978	RID06747	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Adrenocortical cancer	MALAT1	EIF4E	positively-E	luciferase reporter assay;DIANA-microT-CDS version 5.0;DIANA-miRPath version 6.0;miRanda;TargetScan	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-497)	regulation	RNA-protein	NA	NA	NA	Cancer	Adrenal gland cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000151247	NA	378938	1977	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	EIF4E1|EIF4EL1|EIF4F	We demonstrated miR-497 post-transcriptionally repressed MALAT1 while MALAT1 also competes for miR-497 binding to its molecular target, EIF4E (eukaryotic translation initiation factor 4E). These results further support the potential role of MALAT1 acting as miR-497 sponge whereby knockdown of MALAT1, relieving the competition for miR-497 binding to EIF4E, led to the reduction of EIF4E.	31085769	RID06748	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM,BRCA);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Adrenocortical cancer	MALAT1	SFPQ	negatively-E	RIP	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Adrenal gland cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116560	NA	378938	6421	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PPP1R140|PSF	This was further validated on an independent cohort of eight ACC and eight NAC in this study using RT-qPCR, demonstrating a significant reduction of four-fold in ACC compared to NAC (Fig. 4A). SFPQ was also underexpressed in ACC H295R cells compared to NAC tissues (Fig. 4A). We also found an upregulation of SFPQ mRNA transcript after MALAT1 knockdown (Fig. 4B) but no protein expression change was identified.	31085769	RID06749	transcriptional regulation	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Cervical cancer	CCAT1	MMP14	positively-E	qRT-PCR;StarBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-181a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000157227	NA	100507056	4323	CARLO5|CARLo-5|onco-lncRNA-40	MT1-MMP	Elevated CCAT1 suppressed miR-181a expression, which was accompanied by an increased expression of MMP14 and HB-EGF. Incontrast, knocking down CCAT1 resulted in increased expression ofmiR-181a,along with decreased expression of MMP14 and HB-EGF. Thus, CCAT1 is a key oncogenic lncRNA associated with cervical cancer and plays a role in promoting cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis.	31084453	RID06750	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Ovarian cancer	CREB1	HAS2-AS1	positively-E	ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000118260	NA	ENSG00000248690	GRCh38_8:121639293-121994185	1385	594842	NA	HAS2-AS|HAS2AS|HASNT|NCRNA00077	Transcription factor CREB1 could bind with the promoter of HAS2-AS1 and activate its transcriptional expression. Chromatin immunoprecipitation (ChIP) assay demonstrated the CREB1 occupancy at the HAS2-AS1 promoter region (-60 -53) (Fig. 2C). The enforced CREB1 expression could increase the HAS2-AS1 level in the SKOV3 cells (Fig. 2D). For the further identification of the binding, luciferase reporter vectors, wild type and mutant vectors, were constructed (Fig. 2E). Luciferase activity was measured using the co-transfection of reporter vectors, showing the increased activity of CREB1 and HAS2- AS1 promoter region (-60 -53) (Fig. 2F). Overall, data suggest that transcription factor CREB1 binds with the promoter of HAS2-AS1 and accelerates its transcriptional level.	31082772	RID06751	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Ovarian cancer	HAS2-AS1	RUNX2	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-466)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000248690	GRCh38_8:121639293-121994185	ENSG00000124813	NA	594842	860	HAS2-AS|HAS2AS|HASNT|NCRNA00077	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Mechanical investigation found that HAS2-AS1 could relive the RUNX2 protein expression via sponging the miR-466, acting as miRNA sponge.Luciferase reporter assay confirmed the molecular binding within miRNA-466 and the 3 -UTR of RUNX2 mRNA (Fig. 5B). In the SKOV3 cells transfected with miR-466 mimics, the RUNX2 mRNA was increased compared to the control (Fig. 5C). The siRNA for HAS2-AS1 transfection decreased the RUNX2 mRNA ex- pression in SKOV3 cells (Fig. 5D). western blot showed that the RUNX2 protein was decreased in the siRNA HAS2-AS1 transfection (Fig. 5E). KM-plotter showed that the patients with high RUNX2 expression had lower survival rate compared to those who with lower RUNX2 expression (Fig. 5F). The correlation analysis showed that HAS2-AS1 was positively correlated with the RUNX2 expression in EOC tissue (Fig. 5G).	31082772	RID06752	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hemangioma	OIP5-AS1	NOB1	positively-E	MiRBase;luciferase reporter assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Hemangioma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000141101	NA	729082	28987	cyrano|linc-OIP5	ART-4|MST158|NOB1P|PSMD8BP1	OIP5-AS1 knockdown suppressed the proliferation, migration, and invasion of HemECs cell, while overexpression of OIP5-AS1 had opposite effects LncRNA OIP5-AS1 acted as a ceRNA through binding with miR-195-5p to upregulate NOB1 in HemECs. qRT-PCRand western blotshowed that transfection with miR-195-5p mimic significantly reduced the mRNA and protein levels of NOB1, and the inhibition was reversed by overexpression of OIP5-AS1.In contrast, treatment with miR- 195-5p inhibitors increased the mRNA and protein level of NOB1, and the enhancement was restrained following silencing of OIP5-AS1 (Figures 4G,H).	31068824	RID06753	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Breast cancer	HOXC13-AS	PTEN	positively-E	luciferase reporter assay;Targetscan	upregulation	RT-qPCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000249641	GRCh38_12:53935328-53939643	ENSG00000171862	NA	100874366	5728	HOXC-AS5	BZS|MHAM|MMAC1|PTEN1|TEP1	We found that the miR-497-5p levels were downregulated in cancer tissues compared with the adjacent tissues and  miR-497-5p suppressed breast cancer cell proliferation. Further study showed that HOXC13 AS could function as a sponge for miR-497-5p then suppress miR-497-5p expression. Moreover, we next identified that Phosphatase and Tensin homolog (PTEN) is the target of miR-497-5p. Overexpression of miR-497-5p by chemical mimics decreased the expression of PTEN, while downregulation of miR-497-5p by HOXC13 AS rescued the expression of PTEN.	31066051	RID06754	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	NORAD	E2F1	positively-E	RT-qPCR;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);glycolysis(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000101412	NA	647979	1869	LINC00657	RBBP3|RBP3	The results of the present study also confirmed decreased E2F1 expression following transfection with mir-136-5p mimics, while upregulated expression was observed with the mir-136-5p inhibitor at the mrna (Fig. 3e) and protein level (Fig. 3F). it was further indicated that E2F1 was increased by norad wt, while norad mut failed to increase E2F1 at the mrna (Fig. 3G) and protein expression level (Fig. 3H).In addition, mir-136-5p was inversely correlated with E2F1, all of which were indicated to be statistically significant (Fig. 8C).	31059060	RID06755	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	LINC01018	FOXO1	positively-E	luciferase reporter assay;RIP;RT-qPCR;western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000250056	GRCh38_5:6582136-6600288	ENSG00000150907	NA	255167	2308	NA	FKH1|FKHR|FOXO1A	LINC01018 acted as a sponge of miR-182-5p, which targeted FOXO1.The results of dual-luciferase reporter assay dem- onstrated that the luciferase activity of LINC01018-WT was reduced in cells transfected with miR-182-5p mimic (P<0.05), whereas the luciferase activity of LINC01018-MUT exhibited no differences (P<0.05), indicating that LINC01018 could competitively bind to miR-182-5p (Fig. 3D). Moreover, to explore whether LINC01018 could regulate the expression of FOXO1 by competitively binding to miR-182-5p, RT-qPCR and western blotwere performed to measure FOXO1 and miR-182-5p expression when LINC01018 was overexpressed. As shown in Fig. 3, H I, Hep3B cells introduced with miR-182-5p inhibitor or pcDNA-LINC01018 showed elevated expression of FOXO1 and decreased expression of miR-182-5p (P<0.05). The afore- mentioned findings indicated that LINC01018 could in- crease the expression of FOXO1 by competitively binding to miR-182-5p.	31021172	RID06756	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	ZFAS1	WNT1	positively-E	dual-luciferase reporter assays ;qRT-PCR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);WNT/beta-catenin signaling pathway(+);cell cycle(+)	ceRNA(miR-200b-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000125084	NA	441951	7471	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	INT1	We identified miR-200b is a target of ZFAS1 and Wnt1 is a target of miR-200b. To confirm whether Wnt1 was a functional target of miR-200b, a dual- luciferase reporter assay was constructed. As shown in Figure 3(g), when wild type Wnt1 3 UTR and miR-200b mimics were co-transfected into the HEK 293 T cells, the luciferase activity was signifi- cantly decreased, while did not change the luciferase activity of Wnt1 mutant and miR-200b mimics co- transfection (Figure 3(h)).	30999814	RID06757	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Hepatocellular carcinoma	MNX1-AS1	COMMD8	positively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-218-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000169019	NA	645249	54951	CCAT5|LOC645249|MAYA	FLJ20502	We demonstrated that MNX1-AS1 promoted COMMD8 expression through sponging miR-218-5p, and then contributed to HCC progression. Restoration of COMMD8 significantly reversed the effects of MNX1-AS1 knockdown. In order to determine whether MNX1-AS1 could promote COMMD8 expression by sponging miR-218-5p, we performed luciferase reporter assay. We found that the luciferase re- porter activity of wt-COMMD8 was suppressed after MNX1-AS1 knockdown (Fig. 3K). Furthermore, MNX1-AS1 knockdown inhibited the expression of COMMD8 in HCC cells (Fig. 3L). Thus, COMMD8 expression was upregulated by MNX1-AS1 through sponging miR-218-5p in HCC.	30982576	RID06758	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	SNHG16	HMGB1	positively-E	Starbase;luciferase reporter assay;RNA pull-down assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-218-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000189403	NA	100507246	3146	Nbla10727|Nbla12061|ncRAN	DKFZp686A04236|HMG1|HMG3|SBP-1	SNHG16 might serve as a sponge competitive endogenous RNA (ceRNA) for miR-218-5p, thereby playing a role in regulating the expression of high mobility group box 1 (HMGB1) expression, a known direct miR-218-5p target in PC cells.The bioinformatics database (Starbase2.0) was utilized for predicting miRNAs that putatively bind SNHG16 based on the complementarity of bases. Among miRNAs, miR-218-5p was predicted as atarget of SNHG16 since a binding site for miR-218-5p was found in the SNHG16 transcript (Fig. 4A). To test this prediction, an assay for luciferase activity revealed miR-218-5p transfection caused a significant reduction in the activity of- Wt-SNHG16, but not of Mut-SNHG16 (Fig. 4B).Increased SNHG16 was found in the RNA pull-down assay for bio-WT-miR-218-5p in comparison to control (bio-NC) or bio-Mut- miR218-5p) probes (Fig. 4C). It was also observed that miR-218-5p increased conspicuously in the case of SNHG16-knockdown in AsPC1cells (P < 0.05, Fig. 4D). Conversely, overexpression of miR-218-5p caused a pronounced reduction of SNHG16 in AsPC-1cells (P < 0.05,Fig. 4E).	30981105	RID06759	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Prostate cancer	SNHG12	miR-195	negatively-E	luciferase reporter assay;qRT-PCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	SNHG12 acts as a molecular sponge for miR-195 in PCa cells.Moreover, miR-195 expression was increased in SNHG12 silenced DU145 cells but decreased in PC3 cells with SNHG12 overexpression (Figure 3C). The RT-qPCR analysis also suggested that miR-195 was downregulated in PCa tissues (Figure 3D), and miR-195 expression level was negatively associated with the expression of SNHG12 in PCa tissues (r= 0.253, P=0.017; Figure 3E).	30945357	RID06760	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Colorectal cancer	LINC00858	YWHAZ	positively-E	luciferase reporter assay;qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-22-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000164924	NA	170425	7534	CRCAL-2	14-3-3-zeta|KCIP-1|YWHAD	Mechanistically, bioinformatics analysis, dual-luciferase reporter assays, and western blot assays showed that LINC00858 functioned as competing endogenous RNA to repress miR-22-3p, which controlled its down-stream target YWHAZ.	30931636	RID06761	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Cervical cancer	PCAT6	CTNNB1	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	NA	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000168036	NA	100506696	1499	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Mechanistic investigation showed PCAT6 activates Wnt/beta-cat- enin signaling in CC cell lines by promoting the expression of beta-catenin, cyclin D1 and c-myc.	30915737	RID06762	expression association	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cervical cancer	PCAT6	Cyclin D1	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	NA	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	NA	NA	100506696	NA	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	NA	Mechanistic investigation showed PCAT6 activates Wnt/beta-cat- enin signaling in CC cell lines by promoting the expression of beta-catenin, cyclin D1 and c-myc.	30915737	RID06763	expression association	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	
Cervical cancer	PCAT6	MYC	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	NA	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000136997	NA	100506696	4609	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	bHLHe39|c-Myc|MYCC	Mechanistic investigation showed PCAT6 activates Wnt/beta-cat- enin signaling in CC cell lines by promoting the expression of beta-catenin, cyclin D1 and c-myc.	30915737	RID06764	expression association	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	LOC105369748	MBD2	positively-E	luciferase reporter assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-5095)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000134046	NA	NA	8932	NA	NA	In terms of mechanism, LOC105369748 was shown to promote MBD2 expression through competitively binding to microRNA(miR)-5095 in HCC.Then, qRT-PCRand western blotwere performed to test the relationship among LOC105369748, miR 5095, and MBD2. Results showed that MBD2 expression was significantly inhibited by LOC105369748 silencing or miR 5095 mimics (Figure 5f,g). Notably, LOC105369748 silencing induced downregulation of MBD2 was reversed by miR 5095 suppression in Huh7 and Hep3B cells (Figure 5f,g). Taken together results, our data suggested that LOC105369748 is a ceRNA for miR 5095 to promote MBD2 expression in HCC.	30912130	RID06765	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE75367)
Cervical cancer	SOX21-AS1	VDAC1	positively-E	luciferase reporter assay;qRT-PCR	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	ceRNA(miR-7)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000213585	NA	100507533	7416	NA	MGC111064|PORIN	Furthermore, our data showed that microRNA-7 (miR-7) interacted with SOX21-AS1 by directly targeting the miRNA-binding site in the SOX21-AS1 sequence, and quantitative real-time polymerase chain reaction results showed overexpression of SOX21-AS1 decreased the levels of miR-7 in CC cells. Moreover, we confirmed that miR-7 directly targeted the 3'-untranslated region of voltage dependent anion channel 1 (VDAC1).	30912129	RID06766	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Osteosarcoma	SNHG16	BCL9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1301)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000116128	NA	100507246	607	Nbla10727|Nbla12061|ncRAN	NA	SNHG16 promotes BCL9 expression by sponging miR-1301 to facilitate the proliferation, migration and invasion of OS cells.Notably, we found that enforced expression of miR-1301 markedly decreased the fluorescence intensity of vectors carrying wt SNHG16 (P < 0.05, Fig. 2C), whereas miR-1301 did not affect the luciferase activity of vectors carrying mt SNHG16 (Fig. 2C). Furthermore, RNA pull-down showed that SNHG16 directly bond to miR-1301, but mutagenesis of the binding sequences for SNHG16 in miR-1301 abrogated this interaction (P < 0.05, Fig. 2D). These evidences suggested that miR-1301 functioned as a ceRNA by sponging miR-1301 in OS cells.	30909141	RID06767	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00461	LRIG2	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-149-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000198799	NA	645323	9860	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	KIAA0806	Further investigation indicated that LINC00461 was a competing endogenous RNA (ceRNA) by directly sponging miR-149-5p in HCC cells. Moreover, LRIG2 was identified as the downstream target of miR-149-5p and its expression was regulated by LINC00461/miR-149-5p axis.	30879766	RID06768	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807,GSE75367,GSE86978)
Colorectal cancer	LINC02023	PTEN	positively-E	qRT-PCR;immunoblotting;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000239205	GRCh38_3:165150006-165158062	ENSG00000171862	NA	101928405	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Among these findings, a novel lncRNA named Linc02023 was differently expressed in CRC tumor tissues and corresponding adjacent normal tissues, with a significantly positive correlation with the expression of PTEN in both CRC and normal colorectal tissues (Supplementary Figs. 1A 1C). Then, the aberrant expression and association of closely correlated Linc02023 and PTEN were confirmed using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR.	30849479	RID06769	transcriptional regulation	NA	UP(PRAD);DATA(GSE104209)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Clear cell renal cell carcinoma	ZFAS1	SKA1	positively-E	western blot;qRT-PCR;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-10a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000154839	NA	441951	220134	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	C18orf24|MGC10200	Our studies validated that SKA1, as a key downstream target protein for miR-10a, is responsible for the biological role of ZFAS1. ZFAS1 positively regulated SKA1 expression via sponging miR-10a.	30841471	RID06770	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)
Malignant glioma	LINC01503	TOP-FLASH	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell growth(-);colony formation(-);cell invasion(-);cell migration(-);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	NA	NA	100506119	NA	lnc-PPP2R4-5|RP11-65J3.1	NA	Mechanistic investigation showed that LINC01503 can modulate Wnt/beta-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and beta-catenin, cyclin D1 and c-myc.	30840283	RID06771	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	
Malignant glioma	LINC01503	CTNNB1	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell growth(-);colony formation(-);cell invasion(-);cell migration(-);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000168036	NA	100506119	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Mechanistic investigation showed that LINC01503 can modulate Wnt/beta-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and beta-catenin, cyclin D1 and c-myc.	30840283	RID06772	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	LINC01503	Cyclin D1	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell growth(-);colony formation(-);cell invasion(-);cell migration(-);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	NA	NA	100506119	NA	NA	NA	Mechanistic investigation showed that LINC01503 can modulate Wnt/beta-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and beta-catenin, cyclin D1 and c-myc.	30840283	RID06773	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	
Malignant glioma	LINC01503	MYC	positively-E	qRT-PCR;western blot	upregulation	RT-PCR	NA	NA	cell growth(-);colony formation(-);cell invasion(-);cell migration(-);apoptosis process(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000136997	NA	100506119	4609	lnc-PPP2R4-5|RP11-65J3.1	bHLHe39|c-Myc|MYCC	Mechanistic investigation showed that LINC01503 can modulate Wnt/beta-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and beta-catenin, cyclin D1 and c-myc.	30840283	RID06774	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Cervical cancer	SP1	LUCAT1	positively-E	JASPAR;qRT-PCR;ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000248323	GRCh38_5:91054834-91314547	6667	100505994	NA	SCAL1|SCAT5	Furthermore, the results of qRT-PCRassays revealed that transfection of LUCAT1 siRNAs (si-SP1#1 and si-SP1#2) significantly reduced the expression of SP1, whereas transfecting pcDNA3.1-SP1 plasmid remarkably increased the expression levels of SP1 in HeLa and SiHa cells (Figure 2(b,c)). In addition, overexpression of SP1 dramatically enhanced the expression of LUCAT1 in HeLa and SiHa cells, whereas knockdown of SP1 led to a notably decreased expression of LUCAT1 (Figure 2(d)). Moreover, ChIP assays confirmed that there was a marked SP1-binding activity in the E2 site of LUCAT1 promoter (Figure 2(e)).	30831032	RID06775	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)
Cervical cancer	LUCAT1	miR-181a	negatively-E	starbase;luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	NA	NA	100505994	NA	SCAL1|SCAT5	NA	Mechanistically, Bioinformatic tools predicted that miR-181a may target LUCAT1, which was confirmed using luciferase reporter assay and RNA immunoprecipitation (RIP) assays.-	30831032	RID06776	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Triple-negative breast cancer	ZEB2-AS1	ZEB2	positively-E	JASPAR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000169554	NA	100303491	9839	ZEB2-AS|ZEB2AS|ZEB2NAT	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA-ZEB2-AS1 promotes the proliferation and metastasis of MDA231 cells in SCID mice.It is mainly endo-nuclear and situated near ZEB2, positively regulating ZEB2 expression and activating the epithelial mesenchymal transition via the PI3K/Akt/GSK3beta/Zeb2 signaling pathway.	30825262	RID06777	transcriptional regulation	metastasis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	ZEB1	LBX2-AS1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000148516	NA	ENSG00000257702	GRCh38_2:74502552-74505091	6935	151534	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	NA	Luciferase reporter assay performed in 293T cell demonstrated the fragment from 2000 to 1500 was responsible for the interaction between ZEB1 and LBX2-AS1 promoter (Fig. 4D). This interaction was further validated by ChIP assay (Fig. 4E). Thus, we confirmed that ZEB1 contributed to the transcriptional activation of LBX2-AS1 in ESCC. Finally, transwell assays revealed that overexpression of ZEB1 rescued the decreased cell migration induced by the knockdown of LBX2-AS1 or HNRNPC (Fig. 4F). Taken together, ZEB1 and LBX2-AS1 can form a positive feedback loop to regulate ESCC cell migration.	30824187	RID06778	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)
Cervical cancer	AFAP1-AS1	ARHGDIA	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000141522	NA	84740	396	AFAP1-AS|AFAP1AS	GDIA1|HEL-S-47e|NPHS8|RHOGDI|RHOGDI-1	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06779	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	AFAP1-AS1	PFN1	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000108518	NA	84740	5216	AFAP1-AS|AFAP1AS	ALS18	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06780	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	AFAP1-AS1	RAC2	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000128340	NA	84740	5880	AFAP1-AS|AFAP1AS	EN-7|Gx|HSPC022|IMD73A|IMD73B|IMD73C|p21-Rac2	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06781	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	AFAP1-AS1	RAB11A	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000103769	NA	84740	8766	AFAP1-AS|AFAP1AS	YL8	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06782	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(LIHC,PAAD,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Cervical cancer	AFAP1-AS1	RAB1B	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000174903	NA	84740	81876	AFAP1-AS|AFAP1AS	NA	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06783	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	AFAP1-AS1	LASP1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000002834	NA	84740	3927	AFAP1-AS|AFAP1AS	Lasp-1|MLN50	To investigate the potential mechanisms of AFAP1-AS1 regarding its promoting effect on the migration and invasion of cervical cancer cells, we examined the expression levels of several key molecules of the Rho/Rac signaling pathways by western blot The results suggested that the knockdown of AFAP1-AS1 increased the expression of RHOGDI, PFN1, RAB11A and RAC2, while it decreased the expression of RAB1B and LASP1 (Fig. 6).	30816545	RID06784	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	CASC9	CHEK1	positively-E	miRanda;luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-195/497)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000149554	NA	101805492	1111	ESCCAL-1|linc-JPH1|LINC00981	CHK1	Mechanical experiments demonstrated that lncRNA CASC9 positively regulated checkpoint kinase 1 (CHK1) by competitively binding to the miR 195/497 cluster in BC cells.Notably, Pearson's correlation analysis revealed that lncRNA CASC9 expression negatively correlated with miR-195 and miR-497 expression in the BC tissues; on the contrary, lncRNA CASC9 expression was found to positively correlate with CHK1 mRNA expression in the BC tissues (P<0.01; Fig. 6D). These results suggest that lncRNA positively regulates the expression of CHK1 through sponging the miR-195/497 cluster in BC cells.	30816435	RID06785	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE67939)
Esophagus squamous cell carcinoma	CYTOR	FYN	positively-E	miRcode;luciferase reporter assay;RIP;RNA pull-down assays;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);apoptosis process(-)	ceRNA(miR-153-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000010810	NA	112597	2534	C2orf59|LINC00152|MGC4677|NCRNA00152	MGC45350|SLK|SYN	Mechanically, LINC00152 functioned as a competing endogenous RNA (ceRNA) to sponge miR-153-3p, thereby facilitating its downstream target FYN.TRPC3 expression was negatively correlated with miR-153-3p expression (Fig. 5F), while positively correlated with LINC00152 expression (Fig. 5G). These data elucidated that LINC00152 could promote FYN expression through modulating miR-153-3p.	30784933	RID06786	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065)
Colon cancer	LINC01234	SHMT2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-642a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000182199	NA	100506465	6472	onco-lncRNA-32	SHMT	Mechanistic investigations have indicated that LINC01234 functions as a ceRNA for miR-642a-5p, thereby leading to the derepression of its endogenous target serine hydroxymethyltransferase 2 (SHMT2).We found that the SHMT2 mRNA and protein levels were significantly decreased or increased by miR-642a-5p overexpression or inhibition, respectively (Fig. 7g, h). Because LINC01234 can sponge miR-642a-5p, we next determined whether miR-642a-5p plays a role in the relationship between LINC01234 and SHMT2.	30755591	RID06787	ceRNA or sponge	NA	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)
Breast cancer	BLACAT1	CCR2	positively-E	qRT-PCR;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-193a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000121807	NA	101669762	729230	linc-UBC1|LINC00912|onco-lncRNA-30	CC-CKR-2|CD192|CKR2|CMKBR2|FLJ78302|MCP-1-R	Using luciferase assay, CCR2 was further confirmed as a target gene of miR-150-5p in SKBR3 cells, miR-150-5p inhibited the luciferase activity of reporter vector containing the wide-typed binding sites of CCR2 in SKBR3 cells, but not the mutated CCR2 3 -UTR (Fig. 4c). MiR-150-5p down-regulated CCR2 mRNA levels in SKBR3 and MDA-MB-231 cells by qRT-PCR(Fig. 4d).	30733855	RID06788	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Acute myeloid leukemia	CYTOR	CDK9	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-150-6p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000136807	NA	112597	1025	C2orf59|LINC00152|MGC4677|NCRNA00152	C-2k|CDC2L4|PITALRE|TAK	Luciferase reporter assay was carried out and validated the molecular binding within miR-193a and LINC00152, revealing the miRNA sponge functions (Fig. 3B). In the AML cells (THP-1, HL-60), miR-193a levels were profoundly decreased, showing the opposite phenotype (Fig. 3C). Interestingly, we again found that miR-193a targeted the 3 - UTR of CDK mRNA (Fig. 3D). So, LINC00152 positively regulates the CDK9 through sponging miR-193a.Then, the rescue experiments were conducted to validate the regulation within LINC00152 and CDK9.western blotstated that the si-LINC00152 transfection could decrease the CDK9 protein levels (Fig. 4A).	30707636	RID06789	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	SP1	LINC00665	positively-E	JASPAR;PROMO;qRT-PCR;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+);ERK signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000232677	GRCh38_19:36259540-36331770	6667	100506930	NA	CIP2A-BP	Mechanistically, transcription factor SP1 induced the transcription of linc00665 in LUAD cells, which exerted its oncogenic role by functioning as competing endogenous RNA (ceRNA) for miR-98 and subsequently activating downstream AKR1B10-ERK signaling pathway.Taken together, transcription factor SP1 binds to the promoter of linc00665 and partly upregulates the transcription of linc00665 in LUAD cells.	30692511	RID06790	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)
Lung adenocarcinoma	LINC00665	AKR1B10	positively-E	dual-luciferase assays;RNA pull-down assays;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+);ERK signaling pathway(+)	ceRNA(miR-98)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000232677	GRCh38_19:36259540-36331770	ENSG00000198074	NA	100506930	57016	CIP2A-BP	AKR1B11|AKR1B12|ALDRLn|ARL-1|ARL1|HIS|HSI	To further validate the binding of miR-98, dual-luciferase assays were conducted in 293T, A549, and H1299 cells. Luciferase vectors were constructed as described previously (Fig. 7d).  Similarly, miR-98 significantly reduced the luciferase activity of wild-type AKR1B10 3--UTR reporter, whereas no significant effect was observed when the putative binding site was mutated (Fig. 7f). Biotin-labeled RNA pull-down assays were performed to further confirm that linc00665 is physically associated with miR-98 in A549 and H1299 cells (Fig. 7g, h). A significant amount of linc00665 and miR-98 were observed in linc00665-probe pulled down pellets, compared with control groups (p-<-0.01, respectively). These data suggested that miR-98 could directly target linc00665 and AKR1B10.In addition, the regulatory relationships among linc00665, miR-98, and AKR1B10 were further analyzed by western blot (Fig. 7i). In brief, the results indicated that linc00665 functions as a ceRNA through binding miR-98, thereby de-repressing the expression of AKR1B10 in LUAD cells.	30692511	RID06791	ceRNA or sponge	metastasis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	LUCAT1	UBA52	negatively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(+);cell migration(+);cell invasion(+);chemoresistance(+);RPL40/MDM2/p53 signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	Oxaliplatin	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000221983	NA	100505994	7311	SCAL1|SCAT5	CEP52|HUBCEP52|L40|MGC126879|MGC126881|MGC57125|RPL40	The expression of UBA52, whereas LUCAT1 overexpression downregulated UBA52 levels (Figure 8C). However, LUCAT1 knockdown or overexpression did not significantly affect the mRNA levels of UBA52 (Figure 8C) indicating that LUCAT1 might affect UBA52 protein stability.	30690837	RID06792	transcriptional regulation	chemoresistance	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CXCR4	XIST	positively-E	luciferase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	RhoA signaling pathway(+);epithelial to mesenchymal transition(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000121966	NA	ENSG00000229807	GRCh38_X:73820649-73852723	7852	7503	CD184|D2S201E|fusin|HM89|HSY3RR|LESTR|NPY3R|NPYR|NPYY3R	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	To further confirm the direct binding between lncRNA XIST and miR-133a-3p, we constructed lncRNA XIST luciferase reporter plasmids with miR-133a-3p binding site (lncRNA XIST-WT) and its mutant type (lncRNA XIST-MUT). Cotransfection of lncRNA XIST-WT with miR-133a-3p significantly reduced the luciferase activity compared with miR-NC, whereas co-transfection of lncRNA XIST-MUT with miR-133a-3p did not show significant change in luciferase activity (Fig. 6f ).	30678736	RID06793	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Colorectal cancer	XIST	RHOA	positively-E	Targetscan;RT-qPCR;western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	RhoA signaling pathway(+);epithelial to mesenchymal transition(+);cell invasion(+)	ceRNA(miR-133a-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000067560	NA	7503	387	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	ARH12|ARHA|Rho12|RHOH12	To further confirm the direct binding between lncRNA XIST and miR-133a-3p, we constructed lncRNA XIST luciferase reporter plasmids with miR-133a-3p binding site (lncRNA XIST-WT) and its mutant type (lncRNA XIST-MUT). Cotransfection of lncRNA XIST-WT with miR-133a-3p significantly reduced the luciferase activity compared with miR-NC, whereas co-transfection of lncRNA XIST-MUT with miR-133a-3p did not show significant change in luciferase activity (Fig. 6f ).	30678736	RID06794	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065)
Lung cancer	LINC00163	TCF21	positively-E	qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000234880	GRCh38_21:44989864-44994086	ENSG00000118526	NA	727699	6943	C21orf134|NCRNA00163|NLC1-A|NLC1A	bHLHa23|POD1	qRT-PCRanalysis also indicated LINC00163 was reduced in lung cancer tissues (Figure 4H), suggesting TCF21 might also suppress lung cancer development. Finally, analysis based on TCGA database and Kaplan-Meier method revealed that TCF21 downregulation in lung cancer tissues correlates with a poor prognosis (Figure 4I and and4J).4J). These data demonstrated that LINC00163 promotes TCF21 expression and TCF21 might also suppress lung cancer progression.	30662806	RID06795	transcriptional regulation	prognosis		
Glioblastoma	GAPLINC	miR-331-3p	negatively-E	luciferase reporter assay;StarBase;RegRNA 2.0	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540	NA	In the mechanism, we found that GAPLINC acted as a competing endogenous RNA to sponge miR-331-3p and knockdown of GAPLINC promoted the expression of miR-331-3p.-	30657584	RID06796	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	
Malignant glioma	HOXA11-AS	HMGB2	positively-E	starBase;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-130a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000164104	NA	221883	3148	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	HMG2	We revealed that HOXA11-AS exerted its oncogenic effects by binding to miR-130a-5p, thereby neutralizing the suppressive effect of miR-130a-5p on HMGB2.	30657566	RID06797	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Breast cancer	LINC00461	ITGB3	positively-E	miRanda;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);AKT signaling pathway(+)	ceRNA(miR-30a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000259207	NA	645323	3690	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	CD61|GP3A|GPIIIa	Mechanical investigations revealed that LINC00461 positively modulated integrin beta3 (ITGB3) expression as miR-30a-5p sponge in BC cells. Taken together, LINC00461 exerts an oncogenic role in BC through miR-30a-5p/ITGB3 axis.	30623482	RID06798	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE75367)
Breast cancer	TINCR	SNAI1	positively-E	western blot;ChIP;RIP	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);chemoresistance(+)	ceRNA(miR-125b)	regulation	NA	Trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000124216	NA	257000	6615	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	TINCR was detected in the cytoplasm of breast cancer cells and could sponge miR-125b, thereby releasing HER-2 and inducing trastuzumab resistance.-In addition, Snail-1 was found to be the target gene of miR-125b and overexpression of Snail-1 could reverse the suppressed migration, invasion, and EMT caused by TINCR silencing.-	30621694	RID06799	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(PAAD);DATA(GSE40174)
Breast cancer	TINCR	ERBB2	positively-E	qPCR;RIP;miRcode;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);chemoresistance(+)	ceRNA(miR-125b)	regulation	RNA-protein	Trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000141736	NA	257000	2064	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	CD340|HER-2|HER2|NEU|NGL	Subsequently, we sought to identify the miRNA that is responsible for sponging TINCR and HER-2. Interestingly, the microRNA miR-125b was predicted to target both HER-2 and TINCR according to miRcode (http://mircode.org/) (Fig. -(Fig.5e).5e). TINCR knockdown increased miR-125b expression (Fig. -(Fig.5f).5f). Moreover, co-transfection of anti miR-125b abrogated the downregulated the expression of HER-2 that was induced by TINCR knockdown (Fig. -(Fig.5g).5g). Luciferase reporter assay showed that enhanced expression of miR-125b significantly suppressed the luciferase activity in both TINCR and HER-2 wild type reporters but was relatively unaffected in presence of mutant HER-2 reporter (Fig. -(Fig.5h-j).5h-j). RIP assay revealed that TINCR silencing promoted the enrichment of miR-125b bound to HER-2 (Fig. -(Fig.5k).5k). Collectively, our data indicates TINCR as a molecular sponge for miR-125b to modulate HER-2 expression.	30621694	RID06800	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Epithelial ovarian cancer	AOC4P	MMP9	positively-E	RT-PCR;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000100985	NA	90586	4318	UPAT	CLG4B	The anti-metastatic effect of AOC4P in EOC was partially mediated by the EMT process accompanied by the alterations in MMP9 and COL1A2 expression.	32334623	RID06801	transcriptional regulation	metastasis		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	AOC4P	COL1A2	positively-E	RT-PCR;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000164692	NA	90586	1278	UPAT	OI4	The anti-metastatic effect of AOC4P in EOC was partially mediated by the EMT process accompanied by the alterations in MMP9 and COL1A2 expression.	32334623	RID06802	transcriptional regulation	metastasis		UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Endometrial cancer	CTBP1-DT	PTEN	positively-E	IntaRNA;luciferase reporter assay;qPCR;western blot	downregulation	RT-qPCR	NA	NA	cell invasion(-);cell migration(-)	ceRNA(miR-216a)	regulation	RNA-protein	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000196810	GRCh38_4:1249300-1288291	ENSG00000171862	NA	92070	5728	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	BZS|MHAM|MMAC1|PTEN1|TEP1	Therefore, qPCR and western blot were performed to analyze the effects of CTBP1-AS2 and miR-216a overexpression on the expression of PTEN at mRNA (Fig.3c) and protein (Fig.3d) levels, respectively. It was observed that miR-216a overexpression led to downregulated PTEN (p < 0.05). CTBP1-AS2 overexpression led to upregulation of PTEN (p < 0.05).	32293505	RID06803	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Osteosarcoma	SP1	LMCD1-AS1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000227110	GRCh38_3:7951263-8611924	6667	100288428	NA	NA	We showed that SP1 can bind to the promoter region of LMCD1-AS1, resulting in its overexpression in osteosarcoma.Furthermore, we conducted ChIP assays by designing two primers covering d the SP1 binding sites, finding that SP1 could bind to both sites (Fig. 2K). Besides,three luciferase reporter plasmids were conducted (Fig. 2L).-dual-luciferase reporter assays suggested that SP1 can activate luciferase by binding to both the E1/2 and E3/4 elements (Fig. 2M). These data revealed that overexpression of LMCD1-AS1 in osteosarcoma cells may be induced by SP1.	32248969	RID06804	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Osteosarcoma	LMCD1-AS1	miR-106b-5p	negatively-E	Starbase 2.0;RT-PCR;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000227110	GRCh38_3:7951263-8611924	NA	NA	100288428	NA	NA	NA	Mechanistic studies revealed that LMCD1-AS1 was a sponge of miR-106b-5p activity.-LMCD1-AS1 modulated survival of osteosarcoma via targeting miR-106b-5p.	32248969	RID06805	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Lung adenocarcinoma	SNHG7	CBX7	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-181)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000100307	NA	84973	23492	MGC16037|NCRNA00061	NA	A xenograft mouse model was used to explore the effects of SNHG7 on tumor formation in vivo. Compared with the control group, SNHG7 knockdown and mir-181 overexpression significantly increased tumor volume and tumor weight (Figure 7D). Relative mRNA expression of cbx7, E-cadherin, and N-cadherin in the harvested tumor tissues was analyzed by qPCR (Figure 7E).	32201260	RID06806	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MIAT	miR-150-5p	negatively-E	starBase;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	MIAT acts as an oncogene in ovarian cancer cells through sponging miR-150-5p.  miR-150-5p was sponged and regulated by MIAT.	32186927	RID06807	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Gastric cancer	OIP5-AS1	ANO1	positively-E	starBase V2.0;qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);apoptosis process(-);cell growth(+)	ceRNA(miR-422a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000131620	NA	729082	55107	cyrano|linc-OIP5	DOG1|FLJ10261|ORAOV2|TAOS2|TMEM16A	OIP5-AS1 functions as an oncogenic competing endogenous RNA by binding to and sequestering miR-422a to elevate the expression of anoctamin-1.We used the online prediction software program starBase V2.0 (http://starbase.sysu.edu.cn/starbase2) to predict miRNA target sites and identified that OIP5-AS1 contains a binding site for miR-422a.To validate the targeting effect of miR-422a on OIP5-AS1, luciferase reporter plasmids containing the wild-type or mutant OIP5-AS1 were constructed and co-transfected with miR-422a or control mimics into BGC-823 and SGC-7901 cells.qRT-PCRdemonstrated that the expression of miR-422a was significantly higher in the sh-OIP5-AS1-transfected cells than in the control cells (Fig. 4E). In addition, the expression of miR-422a was significantly down-regulated in GC clinical samples,with a negative correlation with the OIP5-AS1 expression (Fig. 4F,G).Overall, these data indicated that OIP5-AS1 serves as a molecular sponge to directly interact with miR-422a	32147682	RID06808	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(BRCA);DATA(GSE109761,GSE55807)
Laryngeal carcinoma	LINC00886	VEGFA	positively-E	western blot; qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000240875	GRCh38_3:156747343-156817062	ENSG00000112715	NA	730091	7422	NA	VEGF|VEGF-A|VPF	Significant change in expression of VEGFA, PIK3R2, and DAPK2 over-expression of LINC00886 indicated that LINC00886 regulated biological function probablely by participating in the VEGFA/PI3K/AKT signaling pathway.	32111441	RID06809	epigenetic regulation	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Laryngeal carcinoma	LINC00886	PIK3R2	positively-E	western blot; qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000240875	GRCh38_3:156747343-156817062	ENSG00000105647	NA	730091	5296	NA	p85|P85B	Significant change in expression of VEGFA, PIK3R2, and DAPK2 over-expression of LINC00886 indicated that LINC00886 regulated biological function probablely by participating in the VEGFA/PI4K/AKT signaling pathway.	32111441	RID06810	epigenetic regulation	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Laryngeal carcinoma	LINC00886	DAPK2	positively-E	western blot; qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	DNA methylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000240875	GRCh38_3:156747343-156817062	ENSG00000035664	NA	730091	23604	NA	DRP-1|MGC119312	Significant change in expression of VEGFA, PIK3R2, and DAPK2 over-expression of LINC00886 indicated that LINC00886 regulated biological function probablely by participating in the VEGFA/PI5K/AKT signaling pathway.	32111441	RID06811	epigenetic regulation	NA		UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	METTL14	XIST	negatively-E	RNA-seq;RIP	downregulation	sequencing	NA	NA	cell proliferation(-);cell invasion(-);tumorigenesis(+)	methylated	regulation	protein-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000145388	NA	ENSG00000229807	GRCh38_X:73820649-73852723	57721	7503	KIAA1627	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	Mechanically, RNA-seq and Me-RIP identified lncRNA XIST as the downstream target of METTL14. Knockdown of METTL14 substantially abolished m6A level of XIST and augmented XIST expression.	32111213	RID06812	epigenetic regulation	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Acute myeloid leukemia	TUG1	RAB10	positively-E	LncBase Predicted v.2;DIANA TOOLS;qRT-PCR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-193a-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000084733	NA	55000	10890	FLJ20618|LINC00080|NCRNA00080	NA	TUG1 targeted miR-193a-5p and negatively regulated miR-193a-5p expression. Overexpressed miR-193a-5p resulted in the decrease of cell viability and the increase in the cell death in AML cells. Restoration experiments proved that TUG1 regulated the cell viability and death of AML cells through regulating the miR-193a-5p/Rab10 axis. Rab10 was a direct target of miR-193a-5p and was inversely regulated by miR-193a-5p. TUG1 regulated the cell viability and death of AML cells through upregulating Rab10.	32103996	RID06813	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	LOC646329	MIR29B1	negatively-E	RT-qPCR;luciferase reporter assay		RT-qPCR	NA	NA	cell cycle(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	NA	NA	ENSG00000265410	NA	NA	407024	NA	MIRN29B1|miR-29b|miRNA29B1|mir-29b-1	Assay result indicated 1.5-folds decreased luciferase activity when miR-29b-1 was overexpressed along with Luc::3 UTR sequence of SMAD3 construct, compared to the of-target (Luc::3 UTR sequence of SOX3.) construct (Fig. 4c).	32034483	RID06814	ceRNA or sponge	NA		
Hepatocellular carcinoma	DUXAP8	PDK2	positively-E	StarBase;dual-luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-422a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000005882	NA	503637	5164	NA	PDHK2	Overexpression of DUXAP8 significantly reduced the expression of miR-422a by sponging it, but enhanced the expression of PDK2.-	32022476	RID06815	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Cervical squamous cell carcinoma	NR2F1-AS1	SIK1	positively-E	qPCR;western blot	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	ceRNA(miR-17)	regulation	RNA-protein	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237187	GRCh38_5:93360779-93585649	ENSG00000142178	NA	441094	150094	FLJ42709	msk|SNF1LK	NR2F1-AS1 overexpression led to the upregulation of SIK1, a target of miR-17.-We analyzed the expression of SIK1, a target of miR-17, after transfection by performing qPCR (mRNA, Fig. 4b) and western blot (protein, Fig. 4b), respectively. It was observed that miR-17 overexpression led to the downregulation of SIK1 (p < 0.05). NR2F1-AS1 overexpression led to the upregulation of SIK1 and attenuated the inhibitory effects of miR-17 overexpression on SIK1 expression (p < 0.05).	31994002	RID06816	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	SNHG14	EZH2	positively-E	western blot;RIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);colony formation(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000106462	NA	104472715	2146	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	ENX-1|EZH1|KMT6|KMT6A	Upregulation of SNHG14 expression promoted cell invasion by affecting E-cadherin expression via interacting with EZH2. To explore their interaction in PDAC cells, we found  that E-cadherin mRNA expression is upregulated after SNHG14 knockdown in Panc1 and Panc28 cells (Fig. 4C).	31929143	RID06817	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cholangiocarcinoma	LINC01714	FOXO3	positively-E	qRT-PCRIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);chemoresistance(+)	Phosphorylation	binding/interaction	NA	Gemcitabine	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000227634	GRCh38_1:8201518-8215210	ENSG00000118689	NA	102724539	2309	NA	AF6q21|FKHRL1|FOXO2|FOXO3A	Furthermore, we found that LINC01714 physically interacted with Forkhead Box O3 (FOXO3) and increased the FOXO3 protein level. In addition, LINC01714 could decrease the phosphorylation level of FOXO3. Interestingly, LINC01714 was able to enhance the sensitivity to gemcitabine in CCA tumor cells through modulating phosphorylated FOXO3-Ser318.	31902744	RID06818	epigenetic regulation	chemoresistance		UP(BRCA);DATA(GSE51827,GSE86978)
Pancreatic cancer	CASC2	MUC6	positively-E	western blot;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-24)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000184956	NA	255082	4588	C10orf5	NA	CASC2 sponged miR 24 and activated its downstream target MUC6 to suppress pancreatic cancer growth and progression.	31894271	RID06819	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Melanoma	MITF-SOX10	DIRC3	negatively-E	RNA-seq;sirna	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	NA	NA	ENSG00000231672	NA	NA	729582	NA	FLJ14199	Changes in MITF and SOX10 protein levels are shown in S3 Fig. Reduction of MITF led to increased DIRC3 expression in both 501mel and SK-MEL-28, but not in A375 cells (Fig 2B), indicating that DIRC3 is transcriptionally repressed by MITF in at least a subset of melanoma cells, whilst SOX10 knockdown using two independent siRNAs increased DIRC3 expression in all three melanoma cell lines tested (Fig 2C).	31881017	RID06820	transcriptional regulation	metastasis		UP(LIHC);DATA(GSE117623)
Gastric cancer	SNHG7	miR-34a	negatively-E	starBase;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	The studies in vitro revealed that SNHG7 directly binds to miR-34a and negatively regulates miR-34a expression, and SNHG7 enhances gastric cancer cell migration and invasion through suppressing miR-34a-Snail-EMT axis.	31814518	RID06821	transcriptional regulation	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Nasopharynx carcinoma	XIST	ADAM17	positively-E	qPCR;western blot	upregulation	qPCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	ceRNA(miR -148a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000151694	NA	7503	6868	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	CD156B|cSVP|TACE	In addition, miR-148a-3p was validated as a target of XIST, and silencing of miR-148a-3p could reverse XIST knockdown-mediated functions in SUNE-1 and CNE2 cells. Furthermore, miR148a-3p was identified to target ADAM17, and ectopic expression of ADAM17 could abate miR-148a-3p-induced effects as well. Notably, ADAM17 was downregulated by XIST knockdown through upregulating miR-148a-3p.	31810117	RID06822	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Colorectal cancer	ZEB2-AS1	CRKL	positively-E	miRDB;TargetScan;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-1205)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000099942	NA	100303491	1399	ZEB2-AS|ZEB2AS|ZEB2NAT	NA	In addition, the correlation between CRKL and ZEB2-AS1, and CRKL and miR-1205, was analyzed, suggesting that the expression of CRKL positively correlated with ZEB2-AS1 level (r = 0.5721, p < 0.001), while negatively correlated with miR-1205 level (r = 0.4911, p < 0.001, Fig. 4F). Overall, these results revealed that CRKL was considered to be a target of miR-1205.	31755734	RID06823	ceRNA or sponge	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	RHPN1-AS1	IGF2BP2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-596)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000254389	GRCh38_8:143366631-143368548	ENSG00000073792	NA	78998	10644	C8orf51|MGC3113	IMP-2|p62	Furthermore, luciferase reporter assay was used to confirm targeting of miR-596 by RHPN1-AS1. Additionally, the regulatory function of RHPN1-AS1 on insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) was detected by western blot.RHPN1-AS1 knockdown suppressed the malignant phenotypes of HCC cells. RHPN1-AS1 overexpression significantly reduced miR-596 expression by sponging it, but enhanced IGF2BP2 expression.	31692433	RID06824	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE41245)
Lung adenocarcinoma	LINC00857	SPAG5	positively-E	starBase;TargetScan;qRT-PCR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);glycolysis(+);apoptosis process(-)	ceRNA(miR-1179)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237523	GRCh38_10:80207372-80219657	ENSG00000076382	NA	439990	10615	HUMT	DEEPEST|hMAP126|MAP126	We hypothesize that LINC00857 may regulate the SPAG5 expression via suppression of miR 1179. To confrm it, we evaluated the transcriptional and translational levels of SPAG5 after transfection in LUAD cell lines by qRT-PCRand western blot assays. LINC00857 knockdown led to an inhibition of the expression of SPAG5 both in mRNA and protein levels (Fig. 4f, g).	31667785	RID06825	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE55807)
Malignant glioma	TGFB1	lncRNA\ATB	positively-F	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	interact with protein	regulation	protein-RNA	NA	NA	NA	Cancer	Brain glioma	PCG	lncRNA	ENSG00000105329	NA	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	NA	LncRNA-ATB promotes TGF-beta-induced glioma cells invasion through NF-kB and P38/MAPK pathway.TGF-beta upregulated lncRNA-ATB expression in glioma LN-18 and U251 cells. Overexpression of lncRNA-ATB activated nuclear factor-kB (NF-kB) pathway and promoted P65 translocation into the nucleus, thus facilitated glioma cells invasion stimulated by TGF-beta. Similarly, lncRNA-ATB markedly enhanced TGF-beta-mediated invasion of glioma cells through activation P38 mitogen-activated protein kinase (P38/MAPK) pathway. Moreover, both the NF-kB selected inhibitor pyrrolidinedithiocarbamate ammonium and P38/MAPK specific inhibitor SB203580 partly reversed lncRNA-ATB induced glioma cells invasion mediated by TGF-beta	31140621	RID06826	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Lung cancer	MALAT1	miR-200a	positively-E	luciferase reporter assay;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemosensitivity(+)	sponge	binding/interaction	RNA-RNA	Gefitinib	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1 Promotes Lung Cancer Proliferation and Gefitinib Resistance by Acting as a miR-200a Sponge.The cell viability and proliferation of A549 cells transfected with MALAT1 shRNA were significantly lower than the control.The MALAT1 expression in gefitinib resistant A549 cells was upregulated. miR-200a significantly inhibited the fluorescence of pSi-Check 2 vector with MALAT1 gene, suggesting the direct binding between MALAT1 and miR-200a. In addition, LncRNA MALAT1 promotes ZEB1 expression in A549 cells.Our study showed that MALAT1 promoted the proliferation and gefitinib resistance of lung cancer cells by sponging miR-200a, which regulates expression of ZEB1 in the A549 cells.	31133357	RID06827	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Lung cancer	MALAT1	ZEB1	positively-E	RT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemosensitivity(+)	NA	NA	NA	Gefitinib	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	ZEB1 has been known as the down steam target of miR-200a,16 herein we confirmed that miR-200a downregulated the relative expression of ZEB1 in A549 cells at mRNA level (Fig. 5A, P < .01), and protein level (Fig. 5B). RT-PCRresults also showed that the overexpression of MALAT1 in A549 cells upregulated the relative ZEB1 expression at both mRNA level (Fig. 5C, P < .001), and protein level (Fig. 5D). Furthermore, a miR-200a inhibitor was used in the assay to inhibitthe expressionofmiR-200a (Fig. 5E).When we applied the same miR-200a inhibitor to A549 cells, we found the expression of ZEB1 was significantly upregulated (P < .001). In contrast,the application of miR-200a inhibitor did not present significant effects on the ZEB1 expression in the A549 cells with MALAT1 overexpression (Fig. 5F).	31133357	RID06828	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	ZNF407-AS1	MUC1-C	positively-E	TargetScan;miRanda;qRT-PCR;dual-luciferase reporter assay;FISH;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	ceRNA(miR-194)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000264247	GRCh38_18:74590317-74598885	NA	NA	400657	NA	LINC00909	NA	LINC00909 promotes tumor progression in human glioma through regulation of miR-194/MUC1-C axis.LINC00909 expression was significantly elevated in glioma tissues and cell lines. High LINC00909 expression was associated with advanced WHO grade, high Karnofsky Performance Score (KPS), and poor prognosis in patients with glioma. LINC00909 depletion inhibited glioma cells proliferation, invasion in vitro and reduced tumor growth in vivo.LINC00909 could act as a ceRNA to interact with miR-194 and thereby up-regulate the expression of MUC1-C, thus promoting the proliferation and invasion of glioma cells.	31132669	RID06829	ceRNA or sponge	prognosis		
Lung adenocarcinoma	HMMR-AS1	SIRT6	positively-E	TargetScan;miRanda;luciferase reporter assay;overexpression	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-138)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251018	GRCh38_5:163483065-163494058	ENSG00000077463	NA	101927813	51548	NA	NA	LncRNA HMMR-AS1 promotes proliferation and metastasis of lung adenocarcinoma by regulating MiR-138/sirt6 axis.HMMR-AS1 expression was significantly upregulated in LUAD tissues and was associated with larger tumor diameter, advanced TNM stage, lymph node metastasis, and shorter survival.Knockdown of HMMR-AS1 induced apoptosis and growth arrest in vitro and inhibited tumorigenesis in mouse xenografts.HMMR-AS1 functioned as a ceRNA of miR-138, thereby leading to repression of its endogenous target sirt6. Moreover, knockdown of HMMR-AS1 dramatically inhibited tumor growth and metastasis of LUAD in vivo.	31128573	RID06830	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	NBAT1	PTEN	positively-E	qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000171862	NA	729177	5728	CASC14|NBAT-1	BZS|MHAM|MMAC1|PTEN1|TEP1	Low expression of lncRNA NBAT-1 promotes gastric cancer development and is associated with poor prognosis.NBAT-1 and PTEN were lowly expressed in GC tissues compared with paracancerous tissues and normal gastric tissues.GC patients with stage -presented lower expression of NBAT-1 than those with stage -Besides, lower expression of NBAT-1 was found in GC patients with N2-N3 compared with those with N0-N1.NBAT-1 expression was not correlated with TNM stage and distant metastasis in GC patients.Upregulation of NBAT-1 in GC cells inhibited proliferation and arrested cell cycle.NBAT-1 was mainly localized in the cytoplasm of SGC-7901 and MGC-823 cells. NBAT-1 overexpression remarkably upregulated PTEN expression in GC cells.western blot further verified that the NBAT-1 overexpression upregulated the protein expression of PTEN (Figure 3D). It was indicated that the expression of NBAT-1 promoted GC development by upregulating the PTEN expression.	31128020	RID06831	expression association	metastasis,prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Epithelial ovarian cancer	MAGI1-IT1	ZEB1	positively-E	siRNA;FISH;western blot	downregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000272610	GRCh38_3:65872815-65954558	ENSG00000148516	NA	151877	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Long Noncoding RNA MAGI1-IT1 Promoted Invasion and Metastasis of Epithelial Ovarian Cancer via the miR-200a/ZEB Axis.MAGI1-IT1 expression was found to be significantly decreased in overexpressing miR-200a EOC cells.MAGI1-IT1 expression was remarkably increased in metastatic EOC tissues, and high MAGI1-IT1 was dramatically associated with EOC FIGO III-IV stage;  MAGI1-IT1 might be related to EOC dissemination via epithelial-mesenchymal transition (EMT).Upregulation of MAGI1-IT1 can remarkably facilitate EOC EMT phenotype, cells migration and invasion ability and intraperitoneal metastasis in nude mice, while downregulation of MAGI1-IT1 led to the opposite effect in vitro.MAGI1-IT1 was validated to promote EOC metastasis through upregulation of ZEB1 and ZEB2 by competitively binding miR-200a, and the restrictive effects of MAGI1-IT1 depletion on EOC metastasis could be reversed by inhibition of miR-200a and upregulation of ZEB1 and ZEB2.	31122127	RID06832	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Epithelial ovarian cancer	MAGI1-IT1	ZEB2	positively-E	siRNA;FISH;western blot	downregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000272610	GRCh38_3:65872815-65954558	ENSG00000169554	NA	151877	9839	NA	KIAA0569|SIP-1|SIP1|ZFHX1B	Long Noncoding RNA MAGI1-IT1 Promoted Invasion and Metastasis of Epithelial Ovarian Cancer via the miR-200a/ZEB Axis.MAGI1-IT1 expression was found to be significantly decreased in overexpressing miR-200a EOC cells.MAGI1-IT1 expression was remarkably increased in metastatic EOC tissues, and high MAGI1-IT1 was dramatically associated with EOC FIGO III-IV stage;  MAGI1-IT1 might be related to EOC dissemination via epithelial-mesenchymal transition (EMT).Upregulation of MAGI1-IT1 can remarkably facilitate EOC EMT phenotype, cells migration and invasion ability and intraperitoneal metastasis in nude mice, while downregulation of MAGI1-IT1 led to the opposite effect in vitro.MAGI1-IT1 was validated to promote EOC metastasis through upregulation of ZEB1 and ZEB2 by competitively binding miR-200a, and the restrictive effects of MAGI1-IT1 depletion on EOC metastasis could be reversed by inhibition of miR-200a and upregulation of ZEB1 and ZEB3.	31122127	RID06833	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Ovarian clear cell carcinoma	SNHG6	EZH2	positively-E	miRcode;starBase v2.0;TargetScan;luciferase reporter assay;siRNA;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-4465)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|EZH1|KMT6|KMT6A	Long Non-Coding RNA SNHG6 Promotes Cell Proliferation and Migration Through Sponging miR-4465 in Ovarian Clear Cell Carcinoma.SNHG6 expression was abnormally up-regulated in OCCC tissues relative to that in unpaired normal ovarian tissues.High SNHG6 expression was correlated with vascular invasion, distant metastasis and poor survival.Knockdown of SNHG6 in OCCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumour growth in vivo.Moreover, SNHG6 functioned as a competing endogenous RNA (ceRNA), effectively acting as a sponge for miR-4465 and thereby modulating the expression of enhancer of zeste homolog 2 (EZH2).	31119871	RID06834	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Pancreatic cancer	DLX6-AS1	miR-497-5p	positively-E	starBase v2.0;RNA pull-down assay;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+);cell growth(+);cell metastasis(+)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000231764	GRCh38_7:96955141-97014088	NA	NA	285987	NA	Evf-2|FLJ34048|NCRNA00212	NA	Long Noncoding RNA DLX6-AS1 Promotes tumorigenesis by Modulating miR-497-5p/FZD4/FZD6/Wnt/beta-catenin Pathway in Pancreatic Cancer.DLX6-AS1 was highly expressed in PC tissues and PC cell lines, and was negatively correlated with the survival of PC patients.Overexpression of DLX6-AS1 promoted proliferation, migration, and invasion of PC cells, inhibited apoptosis, increased Bcl-2, cyclin D1, and MMP-2 expression, and decreased cleaved caspase 3, p27, and E-cadherin expression in PC cells.In addition, overexpression of DLX6-AS1 promoted PC growth by increasing tumor volume and weight and increasing the number of liver and lung metastatic foci.Finally, the effect of DLX6-AS1 on proliferation, cell cycle, migration, invasion, and apoptosis of cells and expression of FZD4, FZD6, and beta-catenin was neutralized by overexpression of vectors of miR-497-5p, FZD4, or FZD6, totally or partially.	31118816	RID06835	transcriptional regulation	metastasis		
Colorectal cancer	LINC00707	miR-206	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000238266	GRCh38_10:6779549-6879450	NA	NA	100507127	NA	NA	NA	LINC00707 Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-206/FMNL2 Axis.LINC00707 was significantly over-expressed in CRC tissues and cell lines. Up-regulation of LINC00707 promoted cell proliferation, cell cycle progression, invasion, and migration of SW620 cells. Conversely, down-regulation of LINC00707 reduced cell growth and metastasis of HCT116 cells. MiR-206 was verified as a direct target of LINC00707, and its function was inhibited by LINC00707. FMNL2 was a target for miR-206 in CRC cells. Meanwhile, LINC00707 promoted tumor growth of CRC in vivo.	31115001	RID06836	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Colorectal cancer	LINC00707	FMNL2	positively-E	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000157827	NA	100507127	114793	NA	FHOD2|KIAA1902	LINC00707 Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-206/FMNL2 Axis.LINC00707 was significantly over-expressed in CRC tissues and cell lines. Up-regulation of LINC00707 promoted cell proliferation, cell cycle progression, invasion, and migration of SW620 cells. Conversely, down-regulation of LINC00707 reduced cell growth and metastasis of HCT116 cells. MiR-206 was verified as a direct target of LINC00707, and its function was inhibited by LINC00707. FMNL2 was a target for miR-206 in CRC cells. Meanwhile, LINC00708 promoted tumor growth of CRC in vivo.	31115001	RID06837	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE51827,GSE55807,GSE86978)
Cervical cancer	CYTOR	HOXA1	positively-E	dual-luciferase reporter assay;siRNA;TargetScan;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-216b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000105991	NA	112597	3198	C2orf59|LINC00152|MGC4677|NCRNA00152	HOX1|HOX1F	Long Non-Coding RNA 00152 Promotes Cell Proliferation in Cervical Cancer via Regulating miR-216b-5p/HOXA1 Axis.LINC00152 was up-regulated in CC tissues and cell lines. The high expression level of LINC00152 was positively correlated with poor prognosis and histologic grade in CC.The silence of LINC00152 could inhibit the proliferation of CC cells through inducing the cell cycle arrest at G0/G1 phase and promote apoptosis in vitro.Mechanically, we demonstrated that LINC00152 could modulate the proliferation of CC cells through elevating HOXA1 expression level via sponging miR-216b-5p.	31114990	RID06838	ceRNA or sponge	prognosis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Osteosarcoma	SNHG7	TP53	negatively-E;interact	RIP;ChIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000141510	NA	84973	7157	MGC16037|NCRNA00061	LFS1|p53	LncRNA SNHG7 Participates in Osteosarcoma Progression by Down-Regulating p53 via Binding to DNMT1.The expression of SNHG7 in osteosarcoma tissues was remarkably higher than that in paracancerous tissues. Moreover, SNHG7 expression in osteosarcoma with stage III and IV was higher than those in stage I and II. The inhibition of SNHG7 in osteosarcoma cells U2OS and HOS promoted cell proliferation, arrested cell cycle in the G0/G1 phase and induced apoptosis.SNHG7 inhibited the expression of p53 by binding to DNMT1. The overexpression of p53 in U2OS cells partially reversed the promoted cell proliferation and apoptosis caused by SNHG7.	31114984	RID06839	interact with protein	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	MIR100HG	miR-204-5p	negatively-E	miRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	LncRNA MIR100HG promotes cancer cell proliferation, migration and invasion in laryngeal squamous cell carcinoma through the downregulation of miR-204-5p.MIR100HG was upregulated, while miR-204-5p was downregulated in tumor tissues than in adjacent healthy tissues of laryngeal squamous cell carcinoma (LSCC) patients.Expression of MIR100HG was significantly affected by AJCC stage.MIR100HG promoted cancer cell proliferation, migration and invasion in LSCC possibly through the downregulation of miR-204-5p.	31114240	RID06840	expression association	NA	UP(PRAD,PAAD);DATA(GSE104209,GSE60407)	
Epithelial ovarian cancer	TP73-AS1	CDKN1A	interact	RT-PCR;luciferase reporter assay;chromatin immunoprecipitation	upregulation	RT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000124762	NA	57212	1026	KIAA0495|PDAM	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA TP73-AS1 accelerates the epithelial ovarian cancer via epigenetically repressing p21.In the EOC specimens and cell lines, TP73-AS1 was identified to be significantly up-regulated. EOC patients with high TP73-AS1 expression had poor survival rate. TP73-AS1 promoted the proliferation, invasion and reduced the apoptosis of EOC cells in vitro.And, the knockdown of TP73-AS1 inhibited the tumor growth in vivo. TP73-AS1 epigenetically repressed p21 via recruiting EZH2.	31105851	RID06841	interact with protein	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Papillary thyroid carcinoma	RP11-476D10.1	LRRK2	positively-E	RNA pull-down assay;RT-qPCR;siRNA;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(-);cell autophagy(-);apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260943	GRCh38_12:40140926-40142876	ENSG00000188906	NA	NA	120892	NA	AURA17|DARDARIN|PARK8|RIPK7|ROCO2	Silencing of Long Noncoding RNA RP11-476D10.1 Enhances Apoptosis and Autophagy While Inhibiting Proliferation of Papillary Thyroid Carcinoma Cells via microRNA-138-5p-dependent Inhibition of LRRK2.Initially, RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression.The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed.	31102261	RID06842	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	RP11-476D10.1	BCL2	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(-);cell autophagy(-);apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260943	GRCh38_12:40140926-40142876	ENSG00000171791	NA	NA	596	NA	Bcl-2|PPP1R50	Silencing of Long Noncoding RNA RP11-476D10.1 Enhances Apoptosis and Autophagy While Inhibiting Proliferation of Papillary Thyroid Carcinoma Cells via microRNA-138-5p-dependent Inhibition of LRRK2.Initially, RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression.The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed.	31102261	RID06843	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	RP11-476D10.1	BECN1	negatively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(-);cell autophagy(-);apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260943	GRCh38_12:40140926-40142876	ENSG00000126581	NA	NA	8678	NA	ATG6|VPS30|beclin1	Silencing of Long Noncoding RNA RP11-476D10.1 Enhances Apoptosis and Autophagy While Inhibiting Proliferation of Papillary Thyroid Carcinoma Cells via microRNA-138-5p-dependent Inhibition of LRRK2.Initially, RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression.The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed.	31102261	RID06844	ceRNA or sponge	NA		DOWN(NSCLC,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Papillary thyroid carcinoma	RP11-476D10.1	MAP1LC3B	negatively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(-);cell autophagy(-);apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260943	GRCh38_12:40140926-40142876	ENSG00000140941	NA	NA	81631	NA	ATG8F|LC3B|MAP1A/1BLC3|MAP1LC3B-a	Silencing of Long Noncoding RNA RP11-476D10.1 Enhances Apoptosis and Autophagy While Inhibiting Proliferation of Papillary Thyroid Carcinoma Cells via microRNA-138-5p-dependent Inhibition of LRRK2.Initially, RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression.The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed.	31102261	RID06845	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE55807)
Papillary thyroid carcinoma	RP11-476D10.1	BAX	negatively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(-);cell autophagy(-);apoptosis process(-)	ceRNA(miR-138-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000260943	GRCh38_12:40140926-40142876	ENSG00000087088	NA	NA	581	NA	BCL2L4	Silencing of Long Noncoding RNA RP11-476D10.1 Enhances Apoptosis and Autophagy While Inhibiting Proliferation of Papillary Thyroid Carcinoma Cells via microRNA-138-5p-dependent Inhibition of LRRK2.Initially, RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression.The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed.	31102261	RID06846	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	PSTPIP1	TGFB1	positively-E	overexpression;RT-qPCR	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000140368	GRCh38_15:76993359-77037475	ENSG00000105329	NA	9051	7040	CD2BP1|CD2BP1L|CD2BP1S|H-PIP|PAPAS|PSTPIP	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA PAPAS Promotes Oral Squamous Cell Carcinoma by Upregulating Transforming Growth factor-beta1.Plasma PAPAS and transforming growth factor beta1 (TGF-beta1) were both upregulated in patients with OSCC, and were positively correlated only in patients with OSCC.Plasma levels of PAPAS were not significantly affected by AJCC stages and upregulation of PAPAS distinguished stage I OSCC patients from healthy controls. High plasma levels of PAPAS were followed by low overall survival rate.PAPAS overexpression led to upregulation of TGF-beta1 in OSCC cells, while TGF-beta1 treatment failed to significantly affect PAPAS. PAPAS overexpression and exogenous TGF-beta1 treatment led to promoted invasion and migration of OSCC cells. In addition, TGF-beta inhibitor attenuated the effects of PAPAS overexpression.	31099126	RID06847	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	MIF-AS1	HOXB8	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-1249-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000281335	GRCh38_CHR_HSCHR22_1_CTG7:23894426-23898930	ENSG00000120068	NA	284889	3218	LOC284889|MIF-AS	HOX2|HOX2D	Long Non-Coding RNA MIF-AS1 Promotes Breast Cancer Cell Proliferation, Migration and EMT Process Through Regulating miR-1249-3p/HOXB8 Axis.MIF-AS1 was upregulated in BC tissues and cells.MIF-AS1 depletion inhibited BC cell proliferation, migration and epithelial-mesenchymal transition (EMT).MIF-AS1 regulated the level of Homeobox B8 (HOXB8) via binding to miR-1249-3p.Taken all together, our findings proved that MIF-AS1 acted as a ceRNA by modulating miR-1249-3p/HOXB8 axis in breast cancer.	31097355	RID06848	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	
Colorectal cancer	MELTF-AS1	MYCBP	positively-E	dual-luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-574-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228109	GRCh38_3:196999460-197004744	ENSG00000214114	NA	100507057	26292	AC068302.3|MFI2-AS1	AMY-1	Non-coding RNA MFI2-AS1 promotes colorectal cancer cell proliferation, migration and invasion through miR-574-5p/ MYCBP axis.LncRNA MFI2-AS1 and MYCBP were up-regulated in CRC tissues when compared with adjacent non-tumour tissues. The expression levels of MFI2-AS1 were significantly associated with tumour histological grade, lymph and distant metastasis, TNM stage and vascular invasion. Both MFI2-AS1 siRNA and miR-574-5p mimics inhibited proliferation, migration and invasion in LoVo and RKO cells. The transfection of miR-574-5p inhibitor showed MFI2-AS1 siRNA-induced changes in CRC cells. dual-luciferase reporter assay revealed target interactions between MFI2-AS1 and miR-574-5p, miR-574-5p and MYCBP.	31094023	RID06849	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MEG3	TGFB1	negatively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105329	NA	55384	7040	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Downregulation of Long Non-Coding RNA MEG3 Promotes Proliferation, Migration, and Invasion of Human Hepatocellular Carcinoma Cells by Upregulating TGF-beta1.Expression level of MEG3 was significantly lower in tumor tissues than in adjacent healthy tissues.Serum level of MEG3 was also significantly lower in hepatocellular carcinoma patients than in normal controls.Serum level of MEG3 was a diagnostic and prognostic marker for hepatocellular carcinoma.MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells , while TGF-beta inhibitor treatment reduced those enhancing effects.MEG3 siRNA silencing also increased the expression level of TGF-beta1.	31089680	RID06850	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	AGAP2-AS1	ANXA11	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	ceRNA(miR-16-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000122359	NA	100130776	311	LOC100130776|PUNISHER	ANX11	Long Non-Coding RNA AGAP2-AS1, Functioning as a Competitive Endogenous RNA, Upregulates ANXA11 Expression by Sponging miR-16-5p and Promotes Proliferation and Metastasis in Hepatocellular Carcinoma.AGAP2-AS1 expression was up-regulated in HCC tissues and cell lines, especially in metastatic and recurrent cases.AGAP2-AS1 promoted cell proliferation, migration, invasion, EMT progression and inhibited apoptosis of HCC cells in vitro and in vivo.AGAP2-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-16-5p in HCC cells.AGAP2-AS1 and miR-16-5p expression were markedly correlated with adverse clinical features and poor prognosis of HCC patients.We showed that hypoxia was responsible for the overexpression of AGAP2-AS1 in HCC. And the promoting effects of hypoxia on metastasis and EMT of HCC cells were reversed by AGAP2-AS1 knockdown.	31088485	RID06851	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Ovarian cancer	DLX6-AS1	NOTCH1	interact	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000148400	NA	285987	4851	Evf-2|FLJ34048|NCRNA00212	TAN1	Down-regulation of Long Noncoding RNA DLX6-AS1 Defines Good Prognosis and Inhibits Proliferation and Metastasis in Human Epithelial Ovarian Cancer Cells via Notch Signaling Pathway.We first verified the increased expression of DLX6-AS1 in EOC patient samples and cell lines.high DLX6-AS1 was significantly associated with FIGO stage, lymph node metastasis and poor prognosis.Furthermore, DLX6-AS1 as an independent prognostic factor in EOC patients.Functionally, the down-regulation of DLX6-AS1 decreased EOC cells proliferation, migration, invasion and induced cell cycle G1/S phase arrest and cell apoptosis.Knockdown of DLX6-AS1 down-regulated Notch1, p21, and Hes1, indicating that the activity of the Notch signaling pathway was inhibited.	31081076	RID06852	interact with protein	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	MIR155HG	SOX10	positively-E	TargetScan;miRwalk;RT-qPCR;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-155-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	ENSG00000234883	GRCh38_21:25561810-25575168	ENSG00000100146	NA	114614	6663	BIC|miPEP155|MIRHG2|NCRNA00172	DOM|WS2E|WS4	TGF-beta-induced Long Non-Coding RNA MIR155HG Promotes the Progression and EMT of Laryngeal Squamous Cell Carcinoma by Regulating the miR-155-5p/SOX10 Axis.MIR155HG and miR-155-5p were significantly upregulated in LSCC tissues, and were associated with the TNM stage, pathological differentiation and lymph node metastasis.Moreover, the knockdown of MIR155HG and miR-155-5p inhibited the proliferation, migration and invasion of LSCC cells, whereas their overexpression exerted the opposite effects in vitro and MIR155HG overexpression promoted tumorigenesis in vivo.MIR155HG in the TGF-beta-induced EMT of LSCC cells by regulating EMT markers through the miR-155/SOX10 axis.	31081043	RID06853	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Laryngeal squamous cell carcinoma	TGFB1	MIR155HG	interact	dual-luciferase reporter assay	upregulation	RT-PCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Larynx cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000234883	GRCh38_21:25561810-25575168	7040	114614	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	BIC|MIRHG2|NCRNA00172|miPEP155	TGF-beta-induced Long Non-Coding RNA MIR155HG Promotes the Progression and EMT of Laryngeal Squamous Cell Carcinoma by Regulating the miR-155-5p/SOX10 Axis.MIR155HG and miR-155-5p were significantly upregulated in LSCC tissues, and were associated with the TNM stage, pathological differentiation and lymph node metastasis.Moreover, the knockdown of MIR155HG and miR-155-5p inhibited the proliferation, migration and invasion of LSCC cells, whereas their overexpression exerted the opposite effects in vitro and MIR155HG overexpression promoted tumorigenesis in vivo.MIR155HG in the TGF-beta-induced EMT of LSCC cells by regulating EMT markers through the miR-155/SOX11 axis.	31081043	RID06854	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)
Liver cancer	PURPL	TP53	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000250337	GRCh38_5:27217714-27496994	ENSG00000141510	NA	643401	7157	LINC01021|LOC643401|RP11-46C20.1	LFS1|p53	Long noncoding RNA PURPL promotes cell proliferation in liver cancer by regulating p53.PURPL was significantly upregulated in liver cancer tissues compared with in paracancerous tissues, and was associated with tumor differentiation stage and tumor size.PURPL was also upregulated in various liver cancer cell lines. Silencing of PURPL inhibited liver cancer cells proliferation, blocked cell cycle progression, and promoted apoptosis.PURPL expression was negatively correlated with p53 mRNA expression.	31059022	RID06855	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	RMRP	ANXA2	positively-E	starbase;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-1-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000182718	NA	6023	302	CHH|NME1|RMRPR|RRP2	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	Long Noncoding RNA RMRP Promotes Proliferation and Invasion via Targeting miR-1-3p in Non-Small-Cell Lung Cancer.RMRP was elevated in NSCLC tissues and cell lines. High RMRP expression was closely associated with advanced stage for the clinical features and low overall survival in NSCLC patients.Loss of RMRP markedly inhibited cell proliferation, migration, and invasion.Moreover, the role of RMRP on NSCLC cell progression was modulated by the inhibition of miR-1-3p.	31050363	RID06856	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Malignant glioma	LINC01857	TRIM65	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-1281)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000224137	GRCh38_2:207662375-207679116	ENSG00000141569	NA	102724714	201292	AC079767.4	NA	LncRNA LINC01857 Promotes Growth, Migration, and Invasion of Glioma by Modulating miR-1281/TRIM65 Axis.LINC01857 levels were found to be upregulated in glioma.LINC01857 expression is negatively correlated with survival rate in glioma patients.LINC01857 downregulation impaired glioma proliferation and invasiveness. Furthermore, LINC01857 knockdown led to repressed growth of glioma in vivo.LINC01857 could be a sponge for miR-1281 and inhibits its level to upregulate TRIM65 expression.miR-1281 mimics also attenuated tumor cell proliferation, migration, and invasion.LINC01857 promotes glioma progression through modulating miR-1281/TRIM65 pathway.	31049960	RID06857	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	LINC00221	miR-519a	negatively-F	dual-luciferase reporter assay;miRcode;RNAhybrid	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);cell viability(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000187156	NA	NA	NA	338005	NA	C14orf98|NCRNA00221	NA	Linc00221 Modulates Cisplatin Resistance in Non-Small-Cell Lung Cancer via Sponging miR-519a.Linc00221 was highly expressed in cisplatin-resistant NSCLC tissues and cells and closely associated with poor prognosis. Linc00221 promoted the cisplatin resistance of NSCLC and miR-519a was a direct target of Linc00221. In addition, miR-519a could promote cisplatin sensitivity in NSCLC cells by targeting ZBTB5. Linc00221 could mediate the cisplatin sensitivity in NSCLC by adsorbing miR-519a to prevent its down-regulation of ZBTB5.To identify the specific binding miRNA and its corresponding binding site of Linc00221, miRcode (http://www.mircode.org/mircode/) and RNAhybrid (https://bibiserv.cebitec.uni-bielefeld.de/rnahybrid)were employed.  dual-luciferase reporter assays were used to detect the inhibitory effect of miR-519a on ZBTB5 and Linc00221, and pull down experiments were employed to determine the direct interaction between Linc00221 and miR-519a. The levels of Linc00221, miR-519a, and zinc finger and BTB domain-containing five (ZBTB5) in NSCLC tissues were detected by qRT-PCRand western blot. MTT assay showed that ZBTB5 knockdown in H1299/CR (Fig. 7c) and A549/CR (Fig. 7d) cells significantly suppressed the cell proliferation upon cisplatin treatment with various concentrations. Moreover, overexpression of Linc00221 in A549-cells significantly increased the cell viability compared with the control group, whereas co-transfection with si-ZBTB5-1 reversed this trend (Fig. 7i).	31029744	RID06858	ceRNA or sponge	prognosis,chemoresistance	UP(SKCM);DATA(GSE38495)	
Non-small cell lung cancer	LINC00221	ZBTB5	positively-E	dual-luciferase reporter assay;miRcode;RNAhybrid	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-519a)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000187156	NA	ENSG00000168795	NA	338005	9925	C14orf98|NCRNA00221	KIAA0354	Linc00221 Modulates Cisplatin Resistance in Non-Small-Cell Lung Cancer via Sponging miR-519a.Linc00221 was highly expressed in cisplatin-resistant NSCLC tissues and cells and closely associated with poor prognosis. Linc00221 promoted the cisplatin resistance of NSCLC and miR-519a was a direct target of Linc00221. In addition, miR-519a could promote cisplatin sensitivity in NSCLC cells by targeting ZBTB5. Linc00221 could mediate the cisplatin sensitivity in NSCLC by adsorbing miR-519a to prevent its down-regulation of ZBTB5.To identify the specific binding miRNA and its corresponding binding site of Linc00221, miRcode (http://www.mircode.org/mircode/) and RNAhybrid (https://bibiserv.cebitec.uni-bielefeld.de/rnahybrid)were employed.  dual-luciferase reporter assays were used to detect the inhibitory effect of miR-519a on ZBTB5 and Linc00221, and pull down experiments were employed to determine the direct interaction between Linc00221 and miR-519a. The levels of Linc00221, miR-519a, and zinc finger and BTB domain-containing five (ZBTB5) in NSCLC tissues were detected by qRT-PCRand western blot. MTT assay showed that ZBTB5 knockdown in H1299/CR (Fig. 7c) and A549/CR (Fig. 7d) cells significantly suppressed the cell proliferation upon cisplatin treatment with various concentrations. Moreover, overexpression of Linc00221 in A549-cells significantly increased the cell viability compared with the control group, whereas co-transfection with si-ZBTB5-1 reversed this trend (Fig. 8i).	31029744	RID06859	ceRNA or sponge	prognosis,chemoresistance	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Lung adenocarcinoma	TTN-AS1	PTEN	negatively-F	shRNA	upregulation	qRT-PCR	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(+)	RNA stability;interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000171862	NA	100506866	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA TTN-AS1 promotes the progression of lung adenocarcinoma by regulating PTEN/PI3K/AKT signaling pathway.We found a remarkable increase of TTN-AS1 expression in LAD cell lines in comparison with BEAS-2B cells. Functionally, silencing TTN-AS1 resulted in inhibited cell proliferation and migration in LAD cells. Mechanically, TTN-AS1 knockdown enhanced the level of PTEN protein while reduced p-AKT level. Meanwhile, PTEN inhibition observably recovered the repressive effect of TTN-AS1 silence on the biological behaviors of A549 cells. What's more, we demonstrated that TTN-AS1 modulated PTEN expression not at mRNA level but protein level. Intriguingly, TTN-AS1 was uncovered to reduce PTEN stability via inhibiting the interactivity of PTEN with MAGI2. qRT-PCRresult of TTN-AS1 expression in normal BEAS-2B cells and five LAD cell lines.	31027732	RID06860	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Lung adenocarcinoma	STAT1	LINC00467	positively-E	luciferase reporter assay;ChIP;bioinformatics	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000115415	NA	ENSG00000153363	GRCh38_1:211382736-211435570	6772	84791	ISGF-3|STAT91	C1orf97|MGC14801	STAT1-induced Upregulation of LINC00467 Promotes the Proliferation Migration of Lung Adenocarcinoma Cells by Epigenetically Silencing DKK1 to Activate Wnt/beta-catenin Signaling Pathway.lncRNA long intergenic non-protein coding RNA 467 (LINC00467) was expressed higher in TCGA LUAD samples and predicted poor prognosis in LUAD patients. High expression of LINC00467 was further detected in LUAD cell lines. Functionally, high expression level of LINC00467 promoted LUAD cell proliferation and migration, indicating that LINC00467 exerted oncogenic functions in LUAD progression. Considering the upregulation of LINC00467 in LUAD, we further detected the activator of LINC00467 promoter. Combining with bioinformatics analysis and mechanism experiments, we determined that LINC00467 was activated by STAT1 in LUAD. Moreover, high expression of LINC00467 was found to be associated with the activation of Wnt/beta-catenin signaling pathway. Rescue assays demonstrated that dickkopf WNT signaling pathway inhibitor 1 (DKK1; an inhibitor of Wnt/beta-catenin signaling pathway) and Wnt/beta-catenin signaling involved in DKK1-mediated LUAD cell proliferation and migration. Furthermore, LINC00467 was located in the nucleus of LUAD cell lines and negatively regulated DKK1 in LUAD cells. Mechanistically, we determined that LINC00467 epigenetically silenced DKK1 by recruiting enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) to DKK1 promoter. Based on TCGA data, LINC00467 was expressed higher in LUAD samples than that in normal samples. These experimental results suggested that STAT1 transcriptionally activated LINC00467 and increased its expression level in LUAD cells. Using bioinformatics prediction tool, we obtained DNA motif of STAT1 and predicted three binding sites of STAT1 in LINC00467 promoter. It was found that the effect of STAT1 on the luciferase activity was attenuated when site 3 (from -1584 to -1597 bp) was mutated, indicating that site 3 of LINC00467 promoter was responsible for the binding of STAT1 to LINC00467 promoter (Fig. 2F). Furthermore, ChIP assay verified that LINC00467 enrichment markedly increased the level of STAT1 antibody compared to IgG antibody (Fig. 2G). At first, we performed RIP assay to demonstrate the binding of EZH2 to LINC00467. Finally, ChIP assays revealed that knockdown of LINC00467 reduced the binding of EZH2 to DKK1 promoter and decreased H3K27me3 level.Finally, we performed luciferase activity analysis and found that LINC00467 negatively regulated the luciferase activity of DKK1 promoter.These results indicated that LINC00467 downregulated DKK1 by recruiting EZH2.	31027730	RID06861	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)
Lung adenocarcinoma	LINC00467	DKK1	negatively-E	luciferase reporter assay;RIP;ChIP;	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	histone modification	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000107984	NA	84791	22943	C1orf97|MGC14801	DKK-1|SK		31027730	RID06862	epigenetic regulation	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(LIHC);DATA(GSE117623)
Thyroid cancer	FOXD2-AS1	TERT	positively-E	luciferase reporter assay;RIP;TargetScan	upregulation	qRT-PCR	TCGA	NA	cancer progression(+)	ceRNA(miR-7-5p)	regulation	RNA-protein	NA	CSC	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000164362	NA	84793	7015	MGC12982	EST2|hEST2|TCS1|TP2|TRT	LncRNA FOXD2-AS1 Functions as a Competing Endogenous RNA to Regulate TERT Expression by Sponging miR-7-5p in Thyroid Cancer.FOXD2-AS1 was upregulated in thyroid carcinoma tissues and cells. High expression of FOXD2-AS1 significantly correlated with clinical stage, recurrence of thyroid carcinoma.Silencing FOXD2-AS1 inhibited cancer stem cell-like phenotypes and attenuates the anoikis resistance in vitro.Downregulating FOXD2-AS1 represses the tumorigenesis of thyroid carcinoma cells in vivo.FOXD2-AS1 acts as a competitive endogenous RNA (ceRNA) for miR-7-5p, up-regulating the expression of telomerase reverse transcriptase (TERT), which further promotes the cancer stem cells features and anoikis resistance in thyroid cancer cells. Using the publicly available algorithm TargetScan, we found that miR-7-5p that has been reported to act as a tumor-suppressive miRNA in thyroid cancer (42, 43) had 4 miRNA recognition sequences on FOXD2-AS1, suggesting that miR-7-5p was a potential target of FOXD2-AS1. Through analyzing RNA sequencing dataset of thyroid cancer from TCGA, we found that expression level of FOXD2-AS1 was increased in thyroid cancer tissues compared with the adjacent normal tissues (ANT). Real-time PCR analysis of FOXD2-AS1 expression in normal thyroid follicular epithelial cells PTFE and seven thyroid cancer cells, including four PTC cell lines, B-CPAP, BHT101, KTC-1 and K1, and two ATC cell lines, CAL-62, and 8305C, and one thyroid duct cell carcinoma cells, TT.	31024447	RID06863	ceRNA or sponge	recurrence	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(PAAD);DATA(GSE40174)
Prostate cancer	LINC00304	CCNA1	positively-E	overexpression	upregulation	qRT-PCR;microarray	GSE38241	NA	cell cycle(+);cell proliferation(+);apoptosis process(-)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000180422	GRCh38_16:89159146-89164245	ENSG00000133101	NA	283860	8900	C16orf81|FLJ36701|NCRNA00304	CT146	Androgen-responsive lncRNA LINC00304 Promotes Cell Cycle and Proliferation via Regulating CCNA1.We observed higher expression of LINC00304 in PCa cells and samples compared with normal prostate cells and tissues.Functional analysis of LINC00304 showed it was related to regulating cell cycle process, cellular developmental process, and focal adhesion.Further, we identified androgen-inhibited lncRNA, LINC00304 as a direct target of AR. overexpression of LINC00304 could significantly promote cell proliferation and cell cycle progression in PCa cells. We also find that LINC00304 can significantly promote CCNA1 expression in PCa cells.LINC00304 promoted PCa cell proliferation and cell cycle, and inhibited apoptosis in PCa cells by promoting CCNA1 expression. Differentially expressed lncRNA LINC00304 was identified using a publicly available gene expression data set (GSE38241) and quantitative polymerase chain reaction validation. To explore how LINC00304 promoted cell cycle progression, we overexpressed LINC00304 in LNCaP cells and detected the expression levels of cell cycle-related proteins, including DBF4, CDK1, CDK4, CKS2, CCNA1, CCNH, E2F8, and CCNE1.	31012142	RID06864	expression association	NA		UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	PKM	MEG3	negatively-E	shRNA	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	protein-RNA	Arsenic trioxide	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000067225	NA	ENSG00000214548	GRCh38_14:100779410-100861031	5315	55384	OIP3|PK3|PKM2|THBP1	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Arsenic Trioxide Inhibits EMT in Hepatocellular Carcinoma by Promoting lncRNA MEG3 via PKM2.PKM2 is upregulated, and MEG3 is downregulated in human hepatocellular carcinoma.Arsenic trioxide negatively regulated PKM2 and positively regulated MEG3.Arsenic trioxide inhibited the migration of HCC, but silencing MEG3 partially reversed this effect.On the other hand, the EMT-related biomarkers are alleviated under the treatment of arsenic trioxide, but this effect deteriorated when MEG3 is silenced.In conclusion, arsenic trioxide inhibits EMT in hepatocellular carcinoma by promoting lncRNA MEG3 and PKM2 negatively regulating MEG3.  Our results illustrated that MEG3 has a negative correlation with PKM2.	31003765	RID06865	expression association	NA	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)	
Acute myeloid leukemia	HOTTIP	DDA1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell cycle(+);cell proliferation(+)	ceRNA(miR-608)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000130311	NA	100316868	79016	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	C19orf58|MGC2594|PCIA1	LncRNA HOTTIP Promotes Proliferation and Cell Cycle Progression of Acute Myeloid Leukemia Cells.HOTTIP was highly expressed in AML-M5 patients than normal controls.HOTTIP expression was significantly up-regulated in AML cell lines U-937 and THP-1. Up-regulation of HOTTIP remarkably promoted the proliferative potential and cell cycle progression of AML cells.HOTTIP accelerated the proliferative ability and cell cycle of AML cells via up-regulating DDA1 expression by sponging microRNA-608. Relative expression levels of HOTTIP, microRNA-608 and DDA1 in AML patients were determined by quantitative Real-time polymerase chain reaction (qRT-PCR. Online prediction and analysis indicated that DDA1 was the target gene of microRNA-608 (Figure 4A). The binding condition between DDA1 and microRNA-608 was further confirmed by dual-luciferase reporter gene assay.	31002141	RID06866	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Liver cancer	SNHG1	TP53	negatively-E	RIP;CHIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000141510	NA	23642	7157	LINC00057|lncRNA16|NCRNA00057|UHG	LFS1|p53	LncRNA SNHG1 Promotes Liver Cancer Development Through Inhibiting p53 Expression via Binding to DNMT1.LC tissues and paracancerous tissues ,normal liver cell line (THLE-2) and LC cell lines (HepG, PLC, SMMC-7721, and SK-HEP-1) " up-regulated "SNHG1 expression was higher in LC tissues than that of paracancerous tissues.SNHG1 was highly expressed in LC cells than that of normal liver cells.SNHG1 knockdown inhibited the proliferative and invasive abilities, and arrested the cell cycle in the G0/G1 phase of SMMC-7721 and SK-HEP-1 cells.SNHG1 could bind to DNMT1 and inhibit p53 expression. Overexpression of p53 partially reversed the inhibitory effects of SNHG1 on proliferative and invasive abilities of LC cells. SNHG1 expression in LC tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The binding condition between SNHG1 and DNMT1 was determined by RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). The promoted cell cycle and in_x0002_vasive ability of LC cells by SNHG1 overexpres_x0002_sion were both reversed by p53 overexpression	31002127	RID06867	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Liver cancer	SNHG1	DNMT1	negatively-F	RIP;CHIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000130816	NA	23642	1786	LINC00057|lncRNA16|NCRNA00057|UHG	CXXC9|DNMT|MCMT	LncRNA SNHG1 Promotes Liver Cancer Development Through Inhibiting p53 Expression via Binding to DNMT1.LC tissues and paracancerous tissues ,normal liver cell line (THLE-2) and LC cell lines (HepG, PLC, SMMC-7721, and SK-HEP-1) " up-regulated "SNHG1 expression was higher in LC tissues than that of paracancerous tissues.SNHG1 was highly expressed in LC cells than that of normal liver cells.SNHG1 knockdown inhibited the proliferative and invasive abilities, and arrested the cell cycle in the G0/G1 phase of SMMC-7721 and SK-HEP-1 cells.SNHG1 could bind to DNMT1 and inhibit p53 expression. Overexpression of p53 partially reversed the inhibitory effects of SNHG1 on proliferative and invasive abilities of LC cells. SNHG1 expression in LC tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The binding condition between SNHG1 and DNMT1 was determined by RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). The promoted cell cycle and in_x0002_vasive ability of LC cells by SNHG1 overexpres_x0002_sion were both reversed by p53 overexpression	31002127	RID06868	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Endometrial cancer	CCAT1	c-MET	positively-E	siRNA;luciferase reporter assay;starBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-181a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	LncRNA CCAT1 Negatively Regulates miR-181a-5p to Promote Endometrial Carcinoma Cell Proliferation and Migration.The expression level of CCAT1 was significantly upregulated in EC tissue samples compared with matched adjacent healthy tissue samples from patients with endometrial cancer. Similarly, CCAT1 was significantly upregulated in several EC cell lines , compared with the normal human endometrial stromal cell line T-HESC.  CCAT1 knockdown significantly decreased EC cell proliferation and migration. In addition, CCAT1 was confirmed as a target gene of miR-181a-5p in EC. Overexpression of miR-181a-5p significantly decreased CCAT1 expression in EC cells, whilst knockdown of CCAT1 significantly increased miR-181a-5p expression in EC cells. Furthermore, miR-181a-5p expression was significantly downregulated in EC tissue samples compared with matched adjacent healthy tissue samples from patients with endometrial cancer. Similarly, miR-181a-5p expression was significantly downregulated in several EC cell lines , compared with normal human endometrial stromal cell line T-HESC. In addition, rescue experiments demonstrated that inhibition of miR-181a-5p significantly reversed the effect of CCAT1 knockdown on EC cell proliferation and migration. To investigate the correlation between CCAT1 and miR-181a-5p, bioinformatics analysis was performed using starBase (starbase.sysu.edu.cn) to identify potential targets of miR-181a-5p. Luciferase reporter gene assay was performed to confirm the potential association between CCAT1 and miR-181a-5p. Following transfection with siCCAT1, knockdown of CCAT1 expression was confirmed by RT-qPCR. western blot demonstrated that miR-181a-5p mimic transfection suppressed c-MET expression in KLE cells (Fig. 6A). Furthermore, CCAT1 knockdown led to decreased expression of c-MET (Fig. 6B), indicating that the CCAT1/miR-181a-5p axis may regulate c-MET to exert roles in EC progression.	30988798	RID06869	ceRNA or sponge	NA		
Tongue squamous cell carcinoma	ADAMTS9-AS2	EZH2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-600)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000106462	NA	100507098	2146	NA	ENX-1|EZH1|KMT6|KMT6A	LncRNA ADAMTS9-AS2 promotes tongue squamous cell carcinoma proliferation, migration and EMT via the miR-600/EZH2 axis.demonstrated that ADAMTS9-AS2 is the most upregulated lncRNA in lymph node metastatic TSCC tissues, indicating that it has an important effect on TSCC metastasis. Importantly, we show that ADAMTS9-AS2 perform its biological function via sponging miR-600 and enhancing the expression of enhancer of zeste homolog 2 (EZH2). In addition, we show that ADAMTS9-AS2 is a cytoplasmic lncRNA that shares the miRNA response elements (MREs) of miR-600 with EZH2, which is confirmed by a luciferase reporter assay and AGO2-dependent RNA immunoprecipitation (RIP). To confirm the role of ADAMTS9-AS2 on TSCC metastasis, we first transfected TSCC cells with siRNAs targeting ADAMTS9-AS2 or negative controls and verified ADAMTS9-AS2 expression via qRT-PCR	30970517	RID06870	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Small cell lung cancer	CASC11	TGFB1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell stemness(+)	NA	association	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000105329	NA	100270680	7040	CARLO7|CARLo-7|LINC00990|MYMLR|TCONS_00014535	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA CASC11 promotes TGF-beta1, increases cancer cell stemness and predicts postoperative survival in small cell lung cancer.Plasma lncRNA CASC11 and TGF-beta1 mRNA were upregulated in SCLC patients. Comparing to control (C) and negative control (NC) groups, lncRNA CASC11 overexpression led to upregulated TGF-beta1 expression in cells of SHP-77 and DMS 79 cell lines at both protein and mRNA levels	30965130	RID06871	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	CERNA2	let-7b	negatively-E	dual-luciferase reporter assay;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	transcriptional regulation	regulation	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000207875	NA	642934	NA	HOST2	NA	The expression and significance of lncRNA HOST2 and microRNA let-7b in HPV-positive cervical cancer tissues and cell lines.HOST2 was up-regulated but let-7b was down-regulated in HPV-positive CC tissues and cells. Dual-luciferase reporter gene assay confirmed the targeting relationship between HOST2 and let-7b. Over-expressed HOST2 reduced let-7b expression, promoted proliferation migration and invasion and inhibited the apoptosis of CaSki and HeLa cells; however, silencing HOST2 or overexpressing let-7b enhanced the expression of let-7b, inhibited proliferation migration and invasion, and promoted the apoptosis of CaSki and HeLa cells, and let-7b mimic could reverse the promoting effect of HOST2 on the growth of CC cells.	30964163	RID06872	transcriptional regulation	NA		
Urinary bladder cancer	PEG10	miR-134	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell survival(+);cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+);JAK/STAT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	23089	NA	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	lncRNA PEG10 promotes cell survival, invasion and migration by sponging miR-134 in human bladder cancer. lncRNA PEG10 functioned as an oncogene in bladder cancer by sponging miR-134 and thus preventing LRP6 from degradation by miR-134. LRP6 promoted bladder cancer progression probably through activating Wnt/beta-catenin and JAK/STAT signal pathways. LRP6 promoted viability, migration and invasion, and knockdown of LRP6 induced apoptosis of T24 cells. LRP6 activated JAK/STAT and Wnt/beta-catenin signal pathways	30953817	RID06873	ceRNA or sponge	NA		
Urinary bladder cancer	PEG10	LRP6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell survival(+);cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+);JAK/STAT signaling pathway(+)	ceRNA(miR-134)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000070018	NA	23089	4040	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	ADCAD2	lncRNA PEG10 promotes cell survival, invasion and migration by sponging miR-134 in human bladder cancer. lncRNA PEG10 functioned as an oncogene in bladder cancer by sponging miR-134 and thus preventing LRP6 from degradation by miR-134. LRP6 promoted bladder cancer progression probably through activating Wnt/beta-catenin and JAK/STAT signal pathways. LRP6 promoted viability, migration and invasion, and knockdown of LRP6 induced apoptosis of T24 cells. LRP6 activated JAK/STAT and Wnt/beta-catenin signal pathways	30953817	RID06874	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065)
Colorectal cancer	SNHG15	miR-338-3p	negatively-E	dual-luciferase reporter assay;LNCipedia;Linc2GO;lncRNAdb;Noncode	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983019-44986961	NA	NA	285958	NA	C7orf40|Linc-Myo1g|MYO1GUT	NA	LncRNA-SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR-338-3p.Researches showed that SNHG15 is overexpressed in gastric cancer (GC), nonsmall cell lung cancer(NSCLC) and breast cancer, and it could promote cell proliferation in these cancers.In this study, we proved that SNHG15 is up-regulated in CRC tissues than the matched noncancerous tissues(NCTs).The results of mechanism experiments showed that SNHG15 could bind to miR-338-3p and block its inhibition on the expression and activity of FOS or RAB14. In conclusion SNHG15 promotes cell proliferation through SNHG15/miR-338-3p/FOS-RAB14 axis in CRC. So we searched for miRNAs that might bind to SNHG15 using LNCipedia,Linc2GO,lncRNAdb and Noncode databases. Subsequently, we confirmed that miR-338-3p, miR-141-5p and miR-24-3p could all bind to SNHG15 through luciferase assays, whereas miR-338-3p has the strongest inhibitory effect on SNHG15. Next, we applied qRT-PCRto detect the expression of SNHG15 in CRC tissues and their matched NCTs.	30945457	RID06875	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	
Colorectal cancer	SNHG15	FOS	positively-E	dual-luciferase reporter assay;LNCipedia;Linc2GO;lncRNAdb;Noncode	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-388-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000170345	NA	285958	2353	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	AP-1|c-fos	LncRNA-SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR-338-3p.Researches showed that SNHG15 is overexpressed in gastric cancer (GC), nonsmall cell lung cancer(NSCLC) and breast cancer, and it could promote cell proliferation in these cancers.In this study, we proved that SNHG15 is up-regulated in CRC tissues than the matched noncancerous tissues(NCTs).The results of mechanism experiments showed that SNHG15 could bind to miR-338-3p and block its inhibition on the expression and activity of FOS or RAB14. In conclusion SNHG15 promotes cell proliferation through SNHG15/miR-338-3p/FOS-RAB14 axis in CRC. So we searched for miRNAs that might bind to SNHG15 using LNCipedia,Linc2GO,lncRNAdb and Noncode databases. Subsequently, we confirmed that miR-338-3p, miR-141-5p and miR-24-3p could all bind to SNHG15 through luciferase assays, whereas miR-338-3p has the strongest inhibitory effect on SNHG15. Next, we applied qRT-PCRto detect the expression of SNHG15 in CRC tissues and their matched NCTs.	30945457	RID06876	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	SNHG15	RAB14	positively-E	dual-luciferase reporter assay;LNCipedia;Linc2GO;lncRNAdb;Noncode	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-388-4p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000119396	NA	285958	51552	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	FBP|RAB-14	LncRNA-SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR-338-3p.Researches showed that SNHG15 is overexpressed in gastric cancer (GC), nonsmall cell lung cancer(NSCLC) and breast cancer, and it could promote cell proliferation in these cancers.In this study, we proved that SNHG15 is up-regulated in CRC tissues than the matched noncancerous tissues(NCTs).The results of mechanism experiments showed that SNHG15 could bind to miR-338-3p and block its inhibition on the expression and activity of FOS or RAB14. In conclusion SNHG15 promotes cell proliferation through SNHG15/miR-338-3p/FOS-RAB14 axis in CRC. So we searched for miRNAs that might bind to SNHG15 using LNCipedia,Linc2GO,lncRNAdb and Noncode databases. Subsequently, we confirmed that miR-338-3p, miR-141-5p and miR-24-3p could all bind to SNHG15 through luciferase assays, whereas miR-338-3p has the strongest inhibitory effect on SNHG15. Next, we applied qRT-PCRto detect the expression of SNHG15 in CRC tissues and their matched NCTs.	30945457	RID06877	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Breast cancer	MIR2052HG	LMTK3	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	histone modification;transcriptional regulation	regulation	RNA-protein	Aromatase inhibitor	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000254349	GRCh38_8:74599775-74823313	ENSG00000142235	NA	441355	114783	NA	KIAA1883|LMR3|PPP1R101|TYKLM3	The lncRNA MIR2052HG regulates ERalpha levels and aromatase inhibitor resistance through LMTK3 by recruiting EGR1.RNA-binding protein immunoprecipitation assays were performed to demonstrate that the transcription factor, early growth response protein 1 (EGR1), worked together with MIR2052HG to regulate that lemur tyrosine kinase-3 (LMTK3) transcription in MCF7/AC1 and CAMA-1 cells. The location of EGR1 on the LMTK3 gene locus was mapped using chromatin immunoprecipitation assays.Our findings support a model in which the MIR2052HG regulates LMTK3 via EGR1, and LMTK3 regulates ERalpha stability via the PKC/MEK/ERK/RSK1 axis.	30944027	RID06878	epigenetic regulation	NA		UP(PAAD);DATA(GSE40174)
Glioblastoma	p50	MALAT1	interact	luciferase reporter assay;siRNA	upregulation	qRT-PCR	TCGA;REMBRANDT	NA	cancer progression(+);chemoresistance(+)	interact with protein	binding/interaction	protein-RNA	Temozolomide	NA	NA	Cancer	Brain glioma	PCG	lncRNA	ENSG00000101017	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Temozolomide Treatment Induces lncRNA MALAT1 in an NF-kB and p53 Codependent Manner in Glioblastoma. luciferase reporter studies demonstrated that both kB and p53 cis-elements were required for efficient transactivation in response to temozolomide. Depletion of MALAT1 sensitized patient-derived GBM cells to temozolomide cytotoxicity, and in vivo delivery of nanoparticle-encapsulated anti-MALAT1 siRNA increased the efficacy of temozolomide in mice bearing intracranial GBM xenografts. These findings identify NF-kB and p53 as regulators of the lncRNA MALAT1 and suggest MALAT1 as a potential target for the chemosensitization of GBM. In this study, we used genome-wide expression analysis in U87 GBM to identify NF-kB-dependent factors altered in response to temozolomide and found the long noncoding RNA (lncRNA) MALAT1 as one of the most significantly upregulated. Raw gene expression and clinical data from the Repository for Molecular Brain Neoplasia Data (REMBRANDT) and TCGA datasets were accessed, analyzed, and downloaded from GlioVis data portal (gliovis.bioinfo.cnio.es) in October 2017. long noncoding RNA (lncRNA) MALAT1 as one of the most significantly upregulated. Knockdown of MALAT1 sensitizes GBM cells to TMZ. MALAT1 is induced by DNA damage in a p50/p53 dependent manner. qPCR analysis of MALAT1 expression.	30940658	RID06879	interact with protein	chemoresistance		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Glioblastoma	TP53	MALAT1	interact	luciferase reporter assay;siRNA	upregulation	qRT-PCR	TCGA;REMBRANDT	NA	cancer progression(+);chemoresistance(+)	interact with protein	binding/interaction	NA	Temozolomide	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000141510	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7157	378938	LFS1|p53	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Temozolomide Treatment Induces lncRNA MALAT1 in an NF-kB and p53 Codependent Manner in Glioblastoma. luciferase reporter studies demonstrated that both kB and p53 cis-elements were required for efficient transactivation in response to temozolomide. Depletion of MALAT1 sensitized patient-derived GBM cells to temozolomide cytotoxicity, and in vivo delivery of nanoparticle-encapsulated anti-MALAT1 siRNA increased the efficacy of temozolomide in mice bearing intracranial GBM xenografts. These findings identify NF-kB and p53 as regulators of the lncRNA MALAT1 and suggest MALAT1 as a potential target for the chemosensitization of GBM. In this study, we used genome-wide expression analysis in U87 GBM to identify NF-kB-dependent factors altered in response to temozolomide and found the long noncoding RNA (lncRNA) MALAT1 as one of the most significantly upregulated. Raw gene expression and clinical data from the Repository for Molecular Brain Neoplasia Data (REMBRANDT) and TCGA datasets were accessed, analyzed, and downloaded from GlioVis data portal (gliovis.bioinfo.cnio.es) in October 2017. long noncoding RNA (lncRNA) MALAT1 as one of the most significantly upregulated. Knockdown of MALAT1 sensitizes GBM cells to TMZ. MALAT1 is induced by DNA damage in a p50/p53 dependent manner. qPCR analysis of MALAT1 expression.	30940658	RID06880	interact with protein	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Urinary bladder cancer	LINC00612	PHF14	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;shRNA;FISH;RegRNA 2.0;Lncrnadb;miRcode;	upregulation	RT-qPCR;microarray	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-590)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214851	GRCh38_12:9055589-9065070	ENSG00000106443	NA	253128	9678	C12orf33|FLJ41814|MGC40170	KIAA0783	LINC00612 enhances the proliferation and invasion ability of bladder cancer cells as ceRNA by sponging miR-590 to elevate expression of PHF14.Bioinformatics analysis, dual-luciferase reporter assays, AGO2-RIP assays, RNA pull-down assays, real-time quantitative PCR (RT-qPCR) arrays, fluorescence in situ hybridization assays, and western blot assays were conducted to explore the underlying mechanisms of competitive endogenous RNAs (ceRNAs).miR-590 was shown to directly target the PHD finger protein 14 (PHF14) gene. LNIC00612 modulated the expression of E-cadherin and vimentin by competitively sponging miR-590 to elevate the expression of PHF14, thus affecting BC cellular epithelial-mesenchymal transition (EMT).Our results indicate that LINC00612 enhances the proliferation and invasion ability of BC cells by sponging miR-590 to upregulate PHF14 expression and promote BC cellular EMT. The target recognition sequence of LINC00612 miRNA was analyzed via bioinformatics (RegRNA 2.0 http://regrna2.mbc.nctu.edu.tw/detection.html; Lncrnadb http://www.lncrnadb.org; miRcode http://www.mircode.org/), and it was found that several miRNAss had a complementary sequence to LINC00612.	30940184	RID06881	ceRNA or sponge	NA		UP(LIHC,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Colorectal cancer	PCAT6	miR-204	negatively-F	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	chemoresistance(+);HMGA2/PI3K signaling pathway(+)	sponge	binding/interaction	RNA-RNA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228288	GRCh38_1:202810850-202812473	NA	NA	100506696	NA	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	NA	Long non-coding RNA PCAT6 targets miR-204 to modulate the chemoresistance of colorectal cancer cells to 5-fluorouracil-based treatment through HMGA2 signaling.we revealed that PCAT6 knockdown attenuated CRC chemoresistance to 5-FU through miR-204/HMGA2/PI3K; miR-204 inhibition could partially reverse the effect of PCAT6 knockdown. Taken together, we demonstrate that the abnormal PCAT6 overexpression inhibits miR-204 expression in CRC, thereby promoting HMGA2/PI3K signaling activity, ultimately enhancing the chemoresistance of CRC cells to 5-FU. The expression of miR-204 was determined in si-PCAT6 transfected HCT116 and SW480 cells by real-time PCR assays.  Furthermore, we performed luciferase reporter gene assay to validate the mechanism of PCAT6 interacting with miR-204. PCAT6 directly binds to miR-204 to inhibit its expression	30938104	RID06882	ceRNA or sponge	chemoresistance	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	
Skin squamous cell carcinoma	LINC01048	YAP1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;shRNA;FISH;CHIP	upregulation	qRT-PCR;microarray	TCGA	NA	cell proliferation(+);apoptosis process(+);Hippo signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000230390	GRCh38_13:37481467-37484769	ENSG00000137693	NA	103695431	10413	NA	YAP65	USF1-induced upregulation of LINC01048 promotes cell proliferation and apoptosis in cutaneous squamous cell carcinoma by binding to TAF15 to transcriptionally activate YAP1.Mechanistically, LINC01048 was proved to be transcriptionally activated by USF1. Pathway analysis and western blot assay showed that knockdown of LINC01048 led to the activation of Hippo pathway. Moreover, YAP1, a Hippo pathway factor, was positively regulated by LINC01048. Further mechanism investigation revealed that LINC01048 increased the binding of TAF15 to YAP1 promoter to transcriptionally activate YAP1 in CSCC cells. Finally, rescue assays demonstrated that YAP1 involved in LINC01048-mediated CSCC cell proliferation and apoptosis. In conclusion, USF1-induced upregulation of LINC01048 promoted CSCC by interacting with TAF15 to upregulate YAP1. LINC01048 interacted with TAF15 protein and increased its expression	30931936	RID06883	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Skin squamous cell carcinoma	USF1	LINC01048	positively-F	luciferase reporter assay;RNA pull-down assay;RIP;shRNA;FISH;CHIP	upregulation	qRT-PCR;microarray	TCGA	NA	cell proliferation(+);apoptosis process(+);Hippo signaling pathway(-)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	TF	lncRNA	ENSG00000158773	NA	ENSG00000230390	GRCh38_13:37481467-37484769	7391	103695431	bHLHb11|MLTFI|UEF	NA	USF1-induced upregulation of LINC01048 promotes cell proliferation and apoptosis in cutaneous squamous cell carcinoma by binding to TAF15 to transcriptionally activate YAP1.Mechanistically, LINC01048 was proved to be transcriptionally activated by USF1. Pathway analysis and western blot assay showed that knockdown of LINC01048 led to the activation of Hippo pathway. Moreover, YAP1, a Hippo pathway factor, was positively regulated by LINC01048. Further mechanism investigation revealed that LINC01048 increased the binding of TAF15 to YAP1 promoter to transcriptionally activate YAP1 in CSCC cells. Finally, rescue assays demonstrated that YAP1 involved in LINC01048-mediated CSCC cell proliferation and apoptosis. In conclusion, USF1-induced upregulation of LINC01048 promoted CSCC by interacting with TAF15 to upregulate YAP1.	30931936	RID06884	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Hepatocellular carcinoma	CCAT2	NDRG1	positively-E	dual-luciferase reporter assay;overexpression;	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	histone modification	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000104419	NA	101805488	10397	LINC00873|NCCP1	CAP43|DRG1|NDR1|RTP|TDD5	Long noncoding RNA CCAT2 promotes hepatocellular carcinoma proliferation and metastasis through up-regulation of NDRG1.we identified that NDRG1 was a downstream target of CCAT2. Meanwhile, depletion of CCAT2 inhibited cellular proliferation and metastasis behaviors induced by NDRG1- overexpression. Analysis of mechanism underlying these effects revealed that CCAT2 increased the expression of NDRG1 by enhancing its promoter activity. All these observations demonstrate that CCAT2 acts as an oncogene by up-regulating NDRG1, which may have the potential to be used as a promising prognostic biomarker and therapeutic target for HCC. Results showed that the expression of NDRG1 was significantly up-regulated after CCAT2 overexpressed in SMMC7721-cells. Therefore, we hypothesized that CCAT2 may function by enhancing NDRG1 promoter. So dual-luciferase gene reporter assays were carried out.	30922920	RID06885	epigenetic regulation	metastasis,prognosis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	PSTPIP1	miR-188-5p	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cancer progression(+)	NA	association	protein-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000140368	GRCh38_15:76993359-77037475	NA	NA	9051	NA	CD2BP1|CD2BP1L|CD2BP1S|H-PIP|PAPAS|PSTPIP	NA	LncRNA PAPAS promotes hepatocellular carcinoma by interacting with miR-188-5p.PAPAS and miR-188-5p downregulated each other. PAPAS overexpression promoted, while miR-188-5p overexpression inhibited the HCC cell proliferation. Rescue experiment showed that miR-34a overexpression attenuated the effects of PAPAS overexpression. However, PAPAS overexpression failed to affect significantly cancer cell migration and invasion. Therefore, lncRNA PAPAS promotes HCC by interacting with miR-188-5p. In the present study, we found that PAPAS was upregulated both in plasma from patients with HCC and tumors compared with plasma from healthy people and tumor-adjacent healthy tissues.	30920025	RID06886	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Urinary bladder cancer	CASC11	miRNA-150	negatively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000249375	GRCh38_8:127686343-127738987	NA	NA	100270680	NA	CARLO7|CARLo-7|LINC00990|MYMLR|TCONS_00014535	NA	lncRNA CASC11 promotes cancer cell proliferation in bladder cancer through miRNA-150. lncRNA CASC11 overexpression promoted, while miRNA-150 overexpression inhibited cancer cell proliferation. Therefore, lncRNA CASC11 may promote cancer cell proliferation in bladder cancer, and the actions of lncRNA CASC11 are likely through miRNA-150. n this study we showed that plasma lncRNA CASC11 was upregulated, while plasma miRNA-150 was downregulated in patients with early-stage bladder cancer than in healthy controls.	30916832	RID06887	expression association	NA	UP(LIHC);DATA(GSE117623)	
Chronic myeloid leukemia	HAND2-AS1	MIR1275	negatively-F	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000221697	NA	79804	100302123	DEIN|NBLA00301|UPH	MIRN1275|hsa-mir-1275|mir-1275	LncRNA HAND2-AS1 inhibits proliferation and promotes apoptosis of chronic myeloid leukemia cells by sponging with micRNA-1275.Luciferase reporter assay showed that HAND2-AS1 was a target gene of miR-1275. And after treating with miR-1275 inhibitor, HAND2-AS1 was significantly upregulated (p<0.01) and cell proliferation was inhibited (p<0.01). HAND2-AS1 was downregulated and miR-1275 was upregulated in CML, and HAND2-AS1 inhibited proliferation and promoted apoptosis of CML cells by sponging with microRNA-1275, which might be a novel therapeutic target for CML. Luciferase reporter assay was performed to explore the binding site of HAND2-AS1 and miR-1275.	30915755	RID06888	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Papillary thyroid carcinoma	LINC00673	TP53	negatively-E	ChIP;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000141510	NA	100499467	7157	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	LFS1|p53	LncRNA LINC00673 inhibits p53 expression by interacting with EZH2 and DNMT1 in papillary thyroid carcinoma. RIP and ChIP assay demonstrated that LINC00673 could bind to EZH2 and DNMT1. Besides, western blotshowed that LINC00673 negatively regulated p53 expression.High expression of LINC00673 in PTC predicts a poor prognosis. LINC00673 remarkably promotes the proliferation and invasion of PTC cells by inhibiting p53 expression by binding to EZH2 and DNMT1. LINC00673 expression in PTC tissues was significantly higher than that of the adjacent normal tissues.	30915752	RID06889	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	LINC00673	EZH2	interact	ChIP;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000106462	NA	100499467	2146	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	ENX-1|EZH1|KMT6|KMT6A	LncRNA LINC00673 inhibits p53 expression by interacting with EZH2 and DNMT1 in papillary thyroid carcinoma. RIP and ChIP assay demonstrated that LINC00673 could bind to EZH2 and DNMT1. Besides, western blotshowed that LINC00673 negatively regulated p53 expression.High expression of LINC00673 in PTC predicts a poor prognosis. LINC00673 remarkably promotes the proliferation and invasion of PTC cells by inhibiting p53 expression by binding to EZH2 and DNMT2.	30915752	RID06890	expression association	prognosis		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Papillary thyroid carcinoma	LINC00673	DNMT1	interact	ChIP;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000130816	NA	100499467	1786	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	CXXC9|DNMT|MCMT	LncRNA LINC00673 inhibits p53 expression by interacting with EZH2 and DNMT1 in papillary thyroid carcinoma. RIP and ChIP assay demonstrated that LINC00673 could bind to EZH2 and DNMT1. Besides, western blotshowed that LINC00673 negatively regulated p53 expression.High expression of LINC00673 in PTC predicts a poor prognosis. LINC00673 remarkably promotes the proliferation and invasion of PTC cells by inhibiting p53 expression by binding to EZH2 and DNMT3.	30915752	RID06891	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	CASC11	miR-188-5p	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	association	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000249375	GRCh38_8:127686343-127738987	NA	NA	100270680	NA	CARLO7|CARLo-7|LINC00990|MYMLR|TCONS_00014535	NA	LncRNA CASC11 promotes cancer cell proliferation in hepatocellular carcinoma by inhibiting miRNA-188-5p. Expression levels of CASC11 and miR-188-5p were inversely correlated in tumor tissues. CASC11 overexpression mediated the down-regulation of miR-188-5p, while miR-188-5p overexpression failed to affect CASC11 expression.LncRNA CASC11 promoted cancer cell proliferation in HCC possibly by inhibiting miR-188-5p. Expression of CASC11 and miR-188-5p in HCC and adjacent non-cancer tissues was analyzed by performing RT-qPCR experiments. CASC11-expression vectors and miR-188-5p mimics were transfected into cells of both SNU-398 and SNU-182 cell lines to further analyze the interactions between miR-188-5p and CSAS11.	30910841	RID06892	expression association	NA	UP(LIHC);DATA(GSE117623)	
Melanoma	ZFAS1	miR-150-5p	negatively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Melanoma	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 promotes tumorigenesis through regulation of miR-150-5p/RAB9A in melanoma.There was a direct binding between ZFAS1 and miR-150-5p. ZFAS1 negatively regulated miR-150-5p expression and upregulation of miR-150-5p was involved in ZFAS1 knockdown-induced effect on proliferation, apoptosis, migration, and invasion. In summary, we confirmed the tumor-promoting role of ZFAS1 in melanoma and provide evidence for the role and mechanism of the ZFAS1/miR-150-5p/RAB9A axis.	30889053	RID06893	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Melanoma	ZFAS1	RAB9A	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-150-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000123595	NA	441951	9367	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	RAB9	Long noncoding RNA ZFAS1 promotes tumorigenesis through regulation of miR-150-5p/RAB9A in melanoma.Using bioinformatics, we predicted the binding between RAB9A and miR-150-5p, and the direct interaction between RAB9A and miR-150-5p was confirmed by luciferase reporter and RNA immunoprecipitation assays. We also showed that RAB9A expression was regulated negatively by miR-150-5p, but was regulated positively by ZFAS1. Downregulation of RAB9A significantly inhibited the increase in proliferation, decrease in apoptosis, and increase in migration and invasion induced by miR-150-5p inhibitors. we confirmed the tumor-promoting role of ZFAS1 in melanoma and provide evidence for the role and mechanism of the ZFAS1/miR-150-5p/RAB9A axis. ZFAS1 was upregulated in melanoma tissues and cells	30889053	RID06894	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)
Malignant glioma	FOXD2-AS1	HMGA2	positively-E	luciferase reporter assay;RIP;TargetScan;miranda	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-185-5P)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000149948	NA	84793	8091	MGC12982	BABL|HMGIC|LIPO	FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway.MiR-185-5p was downregulated, whereas HMGA2 was upregulated in glioma tissues in comparison with para-carcinoma tissues. FOXD2-AS1 could regulate the expression of HMGA2 via miR-185-5p. Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2.lncRNA FOXD2-AS1 acted as a sponge of miR-185-5p and influenced the PI3K/Akt signaling pathway through regulating HMGA2. LncRNA FOXD2-AS1 modulated HMGA2 and PI3K/Akt downstream signaling through sponging miR-185-5p, thereby promoting tumorigenesis and progression of glioma. LncRNA FOXD2-AS1 was overexpressed in human glioma, and upregulated FOXD2-AS11 expression indicated higher WHO grade. A binding site of miR-185-5p on HMGA2 3'UTR was observed by two bioinformatics programs, including miranda and TargetScan. qRT-PCRand western blot results demonstrated that the mRNA and protein expression levels of PI3K and p-AKT were significantly down-regulated in the si-FOXD2-AS1 and miR-185-5p mimics groups, but dramatically up-regulated in the miR-185-5p inhibitor and p-HMGA2 groups.	30860979	RID06895	ceRNA or sponge	metastasis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Cervical cancer	SBF2-AS1	miR-361-5p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000246273	GRCh38_11:9758268-9811335	NA	NA	283104	NA	NA	NA	LncRNA SBF2-AS1 promotes the progression of cervical cancer by regulating miR-361-5p/FOXM1 axis.we showed that SBF2-AS1 upregulation restrained the activity of miR-361-5p and led to overexpression of FOXM1 in CC cells. Furthermore, we found that miR-361-5p inhibitors could rescue the effects of SBF2-AS1 inhibition on CC cells proliferation. Taken together, we demonstrated that the SBF2-AS1/miR-361-5p/FOXM1 axis might play an important role in CC progression.	30856345	RID06896	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	
Cervical cancer	SBF2-AS1	FOXM1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-361-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000111206	NA	283104	2305	NA	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	LncRNA SBF2-AS1 promotes the progression of cervical cancer by regulating miR-361-5p/FOXM1 axis.we showed that SBF2-AS1 upregulation restrained the activity of miR-361-5p and led to overexpression of FOXM1 in CC cells. Furthermore, we found that miR-361-5p inhibitors could rescue the effects of SBF2-AS1 inhibition on CC cells proliferation. Taken together, we demonstrated that the SBF2-AS1/miR-361-5p/FOXM2 axis might play an important role in CC progression. In the present study, our data showed that SBF2-AS1 expression was significantly increased in CC. LncRNA SBF2-AS1 acted as a sponge for miR-361-5p. Luciferase reporter assay revealed that miR-361-5p mimics significantly reduced the luciferase activity of SBF2-AS1-Wt reporter in CC cells. qRT-PCR;ISHowed that SBF2-AS1 expression was significantly increased in CC tissues and cell lines.	30856345	RID06897	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Malignant glioma	PVT1	miR-424	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell viability(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of lncRNA PVT1 Inhibits Glioma Progression by Regulating miR-424 Expression.the present study demonstrated that PVT1 knockdown could negatively regulate miR-424 to inhibit human glioma cell activity, migration, and invasiveness. PVT1 knockdown could negatively regulate miR-424 to inhibit cellular activity, migration, and invasiveness in human gliomas, which explained the oncogenic mechanism of PVT1 in human gliomas. Based on the negative correlation between PVT1 and miR-424, we then confirmed the direct interaction between PVT1 and miR-424 using RNA immunoprecipitation (RIP) and luciferase reporter assays. To investigate the relationship between PVT1 and miR-424 in human gliomas, we first studied their expression in primary human glioma tissues by qPCR. Compared with the adjacent normal tissues, the expression of PVT1 in human glioma tissues was visibly increased, and miR-424 was exceptionally decreased in human glioma tissues. These results indicated that PVT1 and miR-424 were in a common functional complex. Collectively, these data revealed that there was a direct crosstalk or interaction between PVT1 and miR-424.	30832754	RID06898	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Urinary bladder cancer	MEG3	PHLPP2	positively-E	RIP;overexpression	downregulation	qRT-PCR	NA	NA	cell invasion(-)	ceRNA(miR-27a)	regulation	RNA-protein	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000040199	NA	55384	23035	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	KIAA0931|PHLPPL|PPM3B	MEG3, as a Competing Endogenous RNA, Binds with miR-27a to Promote PHLPP2 Protein Translation and Impairs Bladder Cancer Invasion.Our mechanistic studies reveal that MEG3, as a ceRNA, inhibits the invasiveness of human bladder cancer cells via negative regulation of c-Myc by competing with PHLPP2 mRNA for miR-27a. In the current study, we demonstrated that maternally expressed gene 3 (MEG3) is significantly downregulated in human invasive bladder cancers in comparison to non-invasive bladder cancers, and that ectopic expression of MEG3 dramatically inhibits the invasiveness of human bladder cancer cells. We have discovered that MEG3 is downregulated in human highly invasive bladder cancers in comparison to non-invasive bladder cancers, whereas MEG3 overexpression attenuates c-Myc transcription through the inhibition of c-Jun phosphorylation in bladder cancer cells. This result shows that MEG3 can function as a ceRNA and competitively binds to miR-27a, therefore reducing the free form of miR-27a and in turn releasing miR-27a  inhibition of PHLPP2 translation	30826633	RID06899	ceRNA or sponge	NA		UP(LIHC);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	MEG3	MYC	negatively-E	RIP;overexpression	downregulation	qRT-PCR	NA	NA	cell invasion(-)	phosphorylation	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136997	NA	55384	4609	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	bHLHe39|c-Myc|MYCC	MEG3, as a Competing Endogenous RNA, Binds with miR-27a to Promote PHLPP2 Protein Translation and Impairs Bladder Cancer Invasion.Our mechanistic studies reveal that MEG3, as a ceRNA, inhibits the invasiveness of human bladder cancer cells via negative regulation of c-Myc by competing with PHLPP2 mRNA for miR-27a. In the current study, we demonstrated that maternally expressed gene 3 (MEG3) is significantly downregulated in human invasive bladder cancers in comparison to non-invasive bladder cancers, and that ectopic expression of MEG3 dramatically inhibits the invasiveness of human bladder cancer cells. We have discovered that MEG3 is downregulated in human highly invasive bladder cancers in comparison to non-invasive bladder cancers, whereas MEG3 overexpression attenuates c-Myc transcription through the inhibition of c-Jun phosphorylation in bladder cancer cells. This result shows that MEG3 can function as a ceRNA and competitively binds to miR-27a, therefore reducing the free form of miR-27a and in turn releasing miR-27a  inhibition of PHLPP2 translation	30826633	RID06900	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gallbladder cancer	PVT1	HK2	positively-E	dual-luciferase reporter assay;RIP;DIANA	upregulation	qRT-PCR	GSE76633;GSE104165	NA	cancer progression(+);glycolysis(+);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-143)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000159399	NA	5820	3099	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long non-coding RNA PVT1 promotes tumor progression by regulating the miR-143/HK2 axis in gallbladder cancer.The results of our study reveal a potential ceRNA regulatory pathway in which PVT1 modulates HK2 expression by competitively binding to endogenous miR-143 in GBC cells, which may provide new insights into novel molecular therapeutic targets for GBC. Analysis of the GSE76633 dataset from the GEO database revealed that the expression of PVT1 was significantly upregulated in GBC tissues. To identify the potential mechanisms by which PVT1 functioned in GBC cells, we used an online bioinformatics database (DIANA) to predict the potential targets for PVT1, the detailed results of which are displayed in Additional file 5: Table S3. Furthermore, we extracted and analyzed the GSE104165 cohort from the GEO database. Taken together, these results indicated that PVT1 could promote glycolysis by modulating the miR-143/HK2 axis in GBC cells. HK2 promotes cell proliferation, invasion and migration in vitro and tumor growth in vivo.	30825877	RID06901	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Tongue squamous cell carcinoma	RP5-916L7.2	MIR328	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	GSE84807	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000256276	NA	ENSG00000207948	NA	NA	442901	NA	MIRN328|hsa-mir-328|mir-328	lncRNA RP5-916L7.2 correlates with advanced tumor stage, and promotes cells proliferation while inhibits cells apoptosis through targeting miR-328 and miR-939 in tongue squamous cell carcinoma. lncRNA RP5-916L7.2 was up regulated in tumor tissue and positively correlated with tumor stage, and promoted cells proliferation while inhibited cells apoptosis by targeting miR-328-5p and miR-939-5p in TSCC. Five top DELs between oral squamous cell cancer tissue and normal oral mucosa tissue were selected as candidate lncRNAs in this study as shown in Table 1 by analyzing a published lncRNA profiles data with accession number GSE84807.  In addition, the luciferase assay displayed the miRNA binding site and the Mut site of miR-328-5p (Supplementary Fig. 2A) and miR-939-5p (Supplementary Fig. 2B), and the relative luciferase activity was lower in miR-328 group compared with miR-NC group (p-<-.01) (WT) (Supplementary Fig. 2C), and was also decreased in miR-939 group than that in miR-NC group (p-<-.01) (WT) (Supplementary Fig. 2D) in 293a cells. These data indicated that miR-328-5p and miR-939-5p were binding to lncRNA RP5-916L7.2.	30825424	RID06902	ceRNA or sponge	NA		
Tongue squamous cell carcinoma	RP5-916L7.2	MIR939	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	GSE84807	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000256276	NA	ENSG00000216133	NA	NA	100126351	NA	MIRN939|hsa-mir-939|mir-939	lncRNA RP5-916L7.2 correlates with advanced tumor stage, and promotes cells proliferation while inhibits cells apoptosis through targeting miR-328 and miR-939 in tongue squamous cell carcinoma. lncRNA RP5-916L7.2 was up regulated in tumor tissue and positively correlated with tumor stage, and promoted cells proliferation while inhibited cells apoptosis by targeting miR-328-5p and miR-939-5p in TSCC. Five top DELs between oral squamous cell cancer tissue and normal oral mucosa tissue were selected as candidate lncRNAs in this study as shown in Table 1 by analyzing a published lncRNA profiles data with accession number GSE84807.  In addition, the luciferase assay displayed the miRNA binding site and the Mut site of miR-328-5p (Supplementary Fig. 2A) and miR-939-5p (Supplementary Fig. 2B), and the relative luciferase activity was lower in miR-328 group compared with miR-NC group (p-<-.01) (WT) (Supplementary Fig. 2C), and was also decreased in miR-939 group than that in miR-NC group (p-<-.01) (WT) (Supplementary Fig. 2D) in 293a cells. These data indicated that miR-328-5p and miR-939-5p were binding to lncRNA RP5-916L7.2.	30825424	RID06903	ceRNA or sponge	NA		
Ovarian cancer	HAGLR	PIK3R3	positively-E	dual-luciferase reporter assay;siRNA;DIANA	upregulation	RT-qPCR;microarray	GSE119056;GSE53829	NA	epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+);	ceRNA(miR-186-5p)	regulation	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000117461	NA	401022	8503	HOXD-AS1|Mdgt|MIR7704HG	p55	HOXD-AS1 promotes the epithelial to mesenchymal transition of ovarian cancer cells by regulating miR-186-5p and PIK3R3.HOXD-AS1 was found to be significantly over-expressed in EOC tumors. SiRNA inhibition of HOXD-AS1 reduced cell migration, invasion, and epithelial-mesenchymal transition (EMT) in EOC cells in vitro by preventing HOXD-AS1 directly binding to miR-186-5p, and resulting in down-regulating of PIK3R3. The novel HOXD-AS1/miR-186-5p/PIK3R3 pathway was clinically relevant as we observed a significantly inverse correlation between HOXD-AS1/miR-186-5p and between miR-186-5p/PIK3R3 in an independent cohort of 200 EOC tissues. The lncRNA+mRNA arrays and miRNA arrays data have been deposited into GEO database under the accession number GSE119056. An additional set of miRNA expression microarray data, GSE53829, was retrieved from GEO database. The potential miRNAs that may bind to HOXD-AS1 were predicted by DIANA. We performed RT-qPCR to validate HOXD-AS1 up-regulation in an independent cohort comprising of 36 EOC tissues and 14 normal ovarian tissues and found HOXD-AS1 to be consistently and significantly up-regulated in EOC tissues.	30823895	RID06904	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Breast cancer	miR-140-3p	TRPM2-AS	negatively-E	dual-luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000230061	GRCh38_21:44414588-44425272	NA	101928607	NA	TRPM2-AS1	Identification of lncRNA TRPM2-AS/miR-140-3p/PYCR1 axis's proliferates and anti-apoptotic effect on breast cancer using co-expression network analysis.qRT-PCRdemonstrated that PYCR1 and TRPM2-AS were both overexpressed, while miR-140-3p was greatly down-regulated in BC cell. In addition, it was validated by dual luciferase assay that miR-140-3p directly targeted both TRPM2-AS and PYCR1. Furthermore, down-regulation of TRPM2-AS and PYCR1 inhibited proliferation yet promoted apoptosis of BC cell, and up-regulation of miR-140-3p in BC cell showed the same tendency. Taken together, TRPM2-AS could promote proliferation and inhibit apoptosis of BC cell through TRPM2-AS/miR-140-3p/PYCR1 axis. dual-luciferase reporter assay showed that luciferase activity of group with co-transfection of BC cells with miR-140-3p mimics and TNRC6CAS1-wt were lower than that of group with co-transfection of BC cells with miR-140-3p NC and TRPM2-AS-wt (Figure 6(a), P < 0.05), whereas TRPM2-AS-mut could not exert effects on it, indicating that miR-140-3p could directly bind to TRPM2-AS in BC.	30810442	RID06905	ceRNA or sponge	NA		UP(BRCA);DATA(GSE55807)
Breast cancer	TRPM2-AS	PYCR1	positively-E	dual-luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-140-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000183010	NA	101928607	5831	TRPM2-AS1	P5C	Identification of lncRNA TRPM2-AS/miR-140-3p/PYCR1 axis's proliferates and anti-apoptotic effect on breast cancer using co-expression network analysis.qRT-PCRdemonstrated that PYCR1 and TRPM2-AS were both overexpressed, while miR-140-3p was greatly down-regulated in BC cell. In addition, it was validated by dual luciferase assay that miR-140-3p directly targeted both TRPM2-AS and PYCR1. Furthermore, down-regulation of TRPM2-AS and PYCR1 inhibited proliferation yet promoted apoptosis of BC cell, and up-regulation of miR-140-3p in BC cell showed the same tendency. Taken together, TRPM2-AS could promote proliferation and inhibit apoptosis of BC cell through TRPM2-AS/miR-140-3p/PYCR1 axis.a	30810442	RID06906	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367)
Hepatocellular carcinoma	PVT1	ATG3	positively-E	luciferase reporter assay;StarBase v2.0;Targetscan v7.2	upregulation	qRT-PCR	NA	NA	cell autophagy(+)	ceRNA(miR-365)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000144848	NA	5820	64422	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	APG3L|DKFZp564M1178|FLJ22125|MGC15201|PC3-96	Long non-coding RNA PVT1 promotes autophagy as ceRNA to target ATG3 by sponging microRNA-365 in hepatocellular carcinoma.Further investigations revealed that PVT1 could upregulate autophagy-related gene 3 (ATG3) expression by acting as an endogenous sponge of miR-365, which was an inhibitor gene on ATG3 protein by targeting 3'UTR of ATG3 mRNA. Moreover, rescue assays indicated that the effect of PVT1 on autophagy of HCC cells were dependent on miR-365. In conclusion, our study demonstrated PVT1 might be a key regulator participating in autophagy in HCC cells. We proved that PVT1 could promote autophagy as ceRNA by targeting miR-365. The qRT-PCRresult showed that PVT1 expression in HCC tissues was significantly higher than the corresponding adjacent normal tissues. To demonstrate whether PVT1 function as ceRNA to regulate ATG3, we used bioinformatics analysis (StarBase v2.0 and Targetscan v7.2) to predict the potential miRNAs. PVT1 modulates ATG3 expression by sponging miR-365.	30794914	RID06907	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939,GSE86978)
Lung cancer	LINC00336	CBS	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;RNAfold webserve	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);ferroptosis(-)	ceRNA(miR-6852)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000197251	GRCh38_6:33586104-33593338	ENSG00000160200	NA	401253	875	C6orf227|FLJ43752|NCRNA00336	HIP4	Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA.LINC00336 served as an endogenous sponge of microRNA 6852 (MIR6852) to regulate the expression of cystathionine-beta-synthase (CBS), a surrogate marker of ferroptosis. Finally, we found that MIR6852 inhibited cell growth by promoting ferroptosis. These data show that the network of lncRNA and ceRNA has an important role in tumorigenesis and ferroptosis. RNA pull-downs identify ELAVL1 as an LINC00336-interacting protein. To determine which specific region(s) within LINC00336 contribute(s) to ELAVL1 binding, we predicted the secondary structure of LINC00336 using RNAfold Webserve. Given that ELAVL1 binds to many mRNAs, and that LINC00336 is highly expressed in lung cancer, we hypothesized that ELAVL1 may influence the posttranscriptional levels of interacting genes, including LINC00336. We used A549 cell line to overexpressed ELAVL1 by lentivirus and found that ELAVL1 promoted LINC00336 RNA expression by using qRT-PCR This result suggests that ELAVL1 directly promotes the RNA stability of LINC00336.	30787392	RID06908	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE41245)
Lung cancer	ELAVL1	LINC00336	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;RNAfold webserve	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);ferroptosis(-)	transcriptional regulation	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000066044	NA	ENSG00000197251	GRCh38_6:33586104-33593338	1994	401253	Hua|HUR|MelG	C6orf227|FLJ43752|NCRNA00336	Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA.LINC00336 served as an endogenous sponge of microRNA 6852 (MIR6852) to regulate the expression of cystathionine-beta-synthase (CBS), a surrogate marker of ferroptosis. Finally, we found that MIR6852 inhibited cell growth by promoting ferroptosis. These data show that the network of lncRNA and ceRNA has an important role in tumorigenesis and ferroptosis. RNA pull-downs identify ELAVL1 as an LINC00336-interacting protein. To determine which specific region(s) within LINC00336 contribute(s) to ELAVL1 binding, we predicted the secondary structure of LINC00336 using RNAfold Webserve. Given that ELAVL1 binds to many mRNAs, and that LINC00336 is highly expressed in lung cancer, we hypothesized that ELAVL1 may influence the posttranscriptional levels of interacting genes, including LINC00336. We used A549 cell line to overexpressed ELAVL1 by lentivirus and found that ELAVL1 promoted LINC00336 RNA expression by using qRT-PCR This result suggests that ELAVL1 directly promotes the RNA stability of LINC00336.	30787392	RID06909	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)	
Urinary bladder cancer	RMRP	miR-206	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	NA	NA	6023	NA	CHH|NME1|RMRPR|RRP2	NA	lncRNA-RMRP promotes proliferation, migration and invasion of bladder cancer via  miR-206.We found that the lncRNA RMRP was highly expressed in bladder cancer tissue.RMRP could promote the proliferation, migration and invasion of BC cell lines via regulating miR-206 as a sponge. We used qRT-PCRto detect the expression of lncRNA-RMRP in bladder cancer patients and tumor cells, and the clinical significance was also analyzed. To explore whether RMRP could bind with miR-206, we used luciferase reporter assay to work.	30779067	RID06910	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Renal cancer	EGFR-AS1	EGFR	positively-E	RIP;RNA pull-down assay	upregulation	RT-qPCR;	GSE40911;GSE61763;GSE76207;GSE82122;TCGA	NA	cell growth(+);cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000146648	NA	100507500	1956	NA	ERBB|ERBB1|ERRP	Long noncoding RNA EGFR-AS1 promotes cell growth and metastasis via affecting HuR mediated mRNA stability of EGFR in renal cancer.RNA pull-down and mass spectrometry analyses showed that EGFR-AS1 interacted with HuR, which was responsible for the mRNA stability of EGFR. EGFR-AS1 enhances the malignant phenotype of RCC cells by enhancing HuR-mediated mRNA stability of EGFR. First, we analyzed the differential lncRNA expression between RCC tissues and normal tissues in four GEO datasets (GSE40911, GSE61763, GSE76207, and GSE82122) and the TCGA database (577 tumor tissues and 126 normal tissues. After qRT-PCRanalysis of these lncRNAs in our own samples, we focused on three upregulated lncRNAs. EGFR-AS1 maintains EGFR mRNA stability by binding to HuR.	30770799	RID06911	interact with protein	metastasis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	ZFAS1	EZH2	positively-E	luciferase reporter assay;RIP;siRNA;shRNA	upregulation	RT-qPCR;microarray	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-144)	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000106462	NA	441951	2146	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	ENX-1|EZH1|KMT6|KMT6A	Long non-coding RNA ZNFX1-AS1 promotes the tumor progression and metastasis of colorectal cancer by acting as a competing endogenous RNA of miR-144 toregulate EZH2 expression.Further investigation demonstrated that lncRNA ZNFX1-AS1 functioned as a competing endogenous RNA (ceRNA) for miR-144, thereby leading to the depression of its endogenous target gene Polycomb group protein enhancer of zeste homolog 2 (EZH2). We found that lncRNA ZNFX1-AS1 is significantly upregulated in CRC, and the newly identified lncRNA ZNFX1-AS1-miR-144-EZH2 axis is involved in the regulation of CRC progression, which might be used as potential therapeutic targets for CRC patients. To further select the lncRNA that plays critical role in the progression of CRC, the expression of the above 6 lncRNAs was measured in another 106 paired CRC tissues and normal tissues using real-time PCR. lncRNA ZNFX1-AS1 functions as molecular sponge for miR-144 in gastric cancer cells.  Indeed, the RIP assay showed that lncRNA ZNFX1-AS1 could bind directly to Ago2, a component of the RNA-induced silencing complex (RISC) that involved in the miRNA-mediated repression of mRNA expression. Ectopic expression of miR-144 significantly decreased the mRNA and protein level of EZH2 in SW620 and LOVO cells (Fig. 6b, c), as lncRNA ZNFX1-AS1 could sponge to miR-144, we wondered whether lncNRA ZNFX1-AS1 can regulate the expression of EZH2, to our interest, knockdown of lncRNA ZNFX1-AS1 could significantly reduce the mRNA and protein level of EZH2 in SW620 and LOVO cells (Fig. 6b, c).	30770796	RID06912	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung cancer	H19	STAT3	positively-E	dual-luciferase reporter assay;siRNA;starbase 2.0	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell viability(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-29b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168610	NA	283120	6774	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	APRF	lncRNA H19 promotes viability and epithelial-mesenchymal transition of lung adenocarcinoma cells by targeting miR-29b-3p and modifying STAT3.si-H19 and miR-29b-3p mimic significantly increased the apoptosis of lung adenocarcinoma cells, and decreased the survival rate and viability of cells.Furthermore, miR-29b-3p was verified to be targeted and regulated by H19, and STAT3 was targeted and modified by miR-29b-3p. Ultimately, STAT3 was identified to decrease lung adenocarcinoma cell viability, survival, apoptosis and EMT imposed by miR-29b-3p. In conclusion, the results of the present study indicated that lncRNA H19/miR-29b-3p/STAT3 signaling was involved in the development of lung adenocarcinoma. The chip analysis results collected from The Cancer Genome Atlas starBase (version 2.0) data portal indicated that H19 expression in lung cancer tissues was significantly increased compared with in paracarcinoma tissues (P<0.05) and that there was a negative correlation between H19 expression and miR-29b-3p. By contrast, the miR-29b-3-p inhibitor group exhibited significantly increased proliferation and viability, as well as a significantly decreased percentage of apoptotic cells in comparison with the control group. It was predicted using starBase software that H19 could target miR-29b-3p at chr11: 2017218-2017240 and chr11: 2017218-2017320. STAT3 expression in lung adenocarcinoma cells was positively correlated with H19 expression (P<0.05), yet it appeared to be negatively correlated with miR-29b-3p expression (P<0.05).	30747209	RID06913	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	PCGEM1	SNAI1	positively-E	overexpression	upregulation	RT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000124216	NA	64002	6615	LINC00071|NCRNA00071|PCAT9	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	LncRNA PCGEM1 was overexpressed in GC cells and tissues, and was induced by hypoxia in GC cells. Additional experiments confirmed that the knockdown of PCGEM1 significantly repressed the invasion and metastasis of GC cells. SNAI1, a key transcription factor of EMT, was regulated by PCGEM1. Overexpression of SNAI1 rescued the inhibition of PCGEM1-knockdown during the invasion and metastasis of GC cells. In addition, PCGEM1 and SNAI1 jointly affected the biomarkers of EMT. CONCLUSION: Our findings indicated that PCGEM1 is a hypoxia-responsive lncRNA, and contributes to the invasion and metastasis of GC. The potential mechanism is attributed to the regulation of EMT by PCGEM1 and its influence on the expression of SNAI1. The RT-PCRresults showed that PCGEM1 was overexpressed in BGC-823 and SGC-7901 cells relative to their levels in control GES-1 cells (Fig. 1a, P-<-0.05) under 20% O2. o confirm the effect of PCGEM1 on the biological function of GC and to further verify that it is closely related to SNAI1, we stably suppressed PCGEM1 expression and overexpressed SNAI1.	30690667	RID06914	expression association	metastasis	UP(PAAD);DATA(GSE60407)	UP(PAAD);DATA(GSE40174)
Malignant glioma	AGAP2-AS1	HDGF	positively-E	luciferase reporter assay;DIANA;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-15a/b-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000143321	NA	100130776	3068	LOC100130776|PUNISHER	HMG1L2	Long non-coding RNA AGAP2-AS1 promotes the proliferation of glioma cells by sponging miR-15a/b-5p to upregulate the expression of HDGF and activating Wnt/beta-catenin signaling pathway.Higher expression of AGAP2-AS1was correlatedwith the lower overall survival of glioma patients. Functionally, AGAP2-AS1 knockdown inhibited glioma cell proliferation and accelerated glioma cell apoptosis. Mechanistically, AGAP2-AS1 upregulated HDGF by sponging miR-15a/b-5p. The function of AGAP2-AS1-miR-15a/b-5p-HDGF axis was confirmed by performing rescue assays. Experimental results suggested that miR-15a/b-5p and HDGF involved in AGAP2-AS1-mediated glioma cell proliferation. Moreover, AGAP2-AS1 and HDGFwere found to activate Wnt/beta-catenin signaling pathway in glioma cell lines. In summary, this study demonstrated that AGAP2-AS1 promoted glioma cell proliferation by sponging miR-15a/b-5p to upregulate the expression of HDGF. According to the TCGA data, we found that lncRNA AGAP2-AS1 was expressed higher in glioma tissue samples than that in normal samples. Furthermore, AGAP2-AS1 was subjected to qRT-PCRanalysis in paired glioma tissues and normal tissues which were resected from 91 patients with glioma. Next, we searched out 10 miRNAs from DIANA (http://carolina.imis.athenainnovation.gr/diana_tools/web/index.php-r=site%2Findex) and starBase (http://starbase.sysu.edu.cn/). We chose these ten miRNAs for further analysis due to their highest binding scores.  Luciferase reporter assay revealed that overexpression of miR-15a/b-5p decreased the luciferase activity of AGAP2-AS1 wild type reporter vector (AGAP2-AS1-WT).	30684575	RID06915	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Osteosarcoma	PVT1	c-MET	positively-E	bioinformatic;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-152)	regulation	RNA-protein	Gemcitabine	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	lncRNAPVT1 targets miR-152 to enhance chemoresistance of osteosarcoma to gemcitabine through activating c-MET/PI3K/AKT pathway.LncRNA PVT1 overexpression promoted cell proliferation and exhibited the anti-apoptotic property in LncRNA PVT1-overexpressing MG63 cells treated with gemcitabine. While, LncRNA PVT1-depleted MG63/ DOX cells treated with gemcitabine exhibited significant lower survival rate and high percentage of apoptosis. Next, we found that LncRNA PVT1 could target and downregulated the level of miR-152. Interestingly, miR-152 greatly rescued the biological outcomes of LncRNA PVT1 not only in MG63 but also in MG63/DOX cells. We observed that LncRNA PVT1 markedly induced PI3K/AKT pathway activation, which was abolished by miR-152 mimics overexpression. Finally, c-MET inhibitor was used to confirm the essential role of c-MET in LncRNA PVT1 and miR-152-regulated PI3K/AKT signaling.LncRNA PVT1 has been demonstrated to promote osteosarcoma development by regulating miR-195. dual-luciferase reporter assay and RIP were used to confirmed the interaction between LncRNA PVT1 and miR-152. To investigate whether lncRNA PVT1 played critical roles in chemoresistance of osteosarcoma to GEM, we detected the differential expression of PVT1 in OS drug-sensitive cells (MG63) and drug-resistant cell (MG63/DOX) by qRT-PCR The results showed that lncRNA PVT1 level was upregulated about 3.3 folds in MG63/DOX cells compared to MG63 cells.  First, the bioinformatic analyses revealed that lncRNA PVT1 exhibited sequence complementary to miR-152, suggesting lncRNA PVT1 was capable of recognizing and binding to miR-152. Then, we performed dual-luciferase reporter assay to confirm lncRNA PVT1 directly interacted with miR-152.  As Ago2 was a crucial component of RNA-induced silence complex (RISC), we carried out RIP to further determine lncRNA PVT1 associated with miR-152 within Ago2-containing complex.	30661902	RID06916	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Urinary bladder cancer	DANCR	CCND1	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR;microarray	GSE119639	NA	cell proliferation(+);cell metastasis(+);IL-11-STAT3 signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000110092	NA	57291	595	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	BCL1|D11S287E|PRAD1|U21B31	DANCR Promotes Metastasis and Proliferation in Bladder Cancer Cells by Enhancing IL-11-STAT3 Signaling and CCND1 Expression.Mechanistic investigations revealed that DANCR activated IL-11-STAT3 signaling and increased cyclin D1 and PLAU expression via guiding leucine-rich pentatricopeptide repeat containing (LRPPRC) to stabilize mRNA. Moreover, oncogenesis facilitated by DANCR was attenuated by anti-IL-11 antibody or a STAT3 inhibitor (BP-1-102). In conclusion, our findings indicate that DANCR induces BCa LN metastasis and proliferation via an LRPPRC-mediated mRNA stabilization mechanism. All primary data in the microarray analysis have been uploaded to GEO: GSE119639. To evaluate whether DANCR is involved in BCa progression, DANCR expression was investigated in a large 120-case cohort of BCas using qRT-PCR The results showed that DANCR was overexpressed in BCa tissues compared with normal adjacent tissues and in LN-positive bladder tumors compared with LN-negative tumors.To identify DANCR-interacting proteins in BCa cells, we performed RNA pull-down assays using in vitro-transcribed biotinylated DANCR.  We also verified this result using RNA immunoprecipitation (RIP), and we found that DANCR, but not U6, was enriched in LRPPRC precipitates. Taken together, these results suggest that DANCR upregulates the expression levels of IL-11, PLAU, MMP9, and CCND1, which contribute to cancer cell lymphatic metastasis and proliferation in BCa. First, we found that CCND1, PLAU, and IL-11, but not MMP9, mRNAs were enriched in LRPPRC precipitates using a RIP assay	30660488	RID06917	interact with protein	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	DANCR	IL11	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR;microarray	GSE119640	NA	cell proliferation(+);cell metastasis(+);IL-11-STAT3 signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000095752	NA	57291	3589	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	AGIF|IL-11	DANCR Promotes Metastasis and Proliferation in Bladder Cancer Cells by Enhancing IL-11-STAT3 Signaling and CCND1 Expression.Mechanistic investigations revealed that DANCR activated IL-11-STAT3 signaling and increased cyclin D1 and PLAU expression via guiding leucine-rich pentatricopeptide repeat containing (LRPPRC) to stabilize mRNA. Moreover, oncogenesis facilitated by DANCR was attenuated by anti-IL-11 antibody or a STAT3 inhibitor (BP-1-102). In conclusion, our findings indicate that DANCR induces BCa LN metastasis and proliferation via an LRPPRC-mediated mRNA stabilization mechanism. All primary data in the microarray analysis have been uploaded to GEO: GSE119639. To evaluate whether DANCR is involved in BCa progression, DANCR expression was investigated in a large 120-case cohort of BCas using qRT-PCR The results showed that DANCR was overexpressed in BCa tissues compared with normal adjacent tissues and in LN-positive bladder tumors compared with LN-negative tumors.To identify DANCR-interacting proteins in BCa cells, we performed RNA pull-down assays using in vitro-transcribed biotinylated DANCR.  We also verified this result using RNA immunoprecipitation (RIP), and we found that DANCR, but not U6, was enriched in LRPPRC precipitates. Taken together, these results suggest that DANCR upregulates the expression levels of IL-11, PLAU, MMP9, and CCND1, which contribute to cancer cell lymphatic metastasis and proliferation in BCa. First, we found that CCND1, PLAU, and IL-11, but not MMP9, mRNAs were enriched in LRPPRC precipitates using a RIP assay	30660488	RID06918	interact with protein	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD);DATA(GSE40174)
Urinary bladder cancer	DANCR	PLAU	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR;microarray	GSE119641	NA	cell proliferation(+);cell metastasis(+);IL-11-STAT3 signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000122861	NA	57291	5328	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	UPA|URK	DANCR Promotes Metastasis and Proliferation in Bladder Cancer Cells by Enhancing IL-11-STAT3 Signaling and CCND1 Expression.Mechanistic investigations revealed that DANCR activated IL-11-STAT3 signaling and increased cyclin D1 and PLAU expression via guiding leucine-rich pentatricopeptide repeat containing (LRPPRC) to stabilize mRNA. Moreover, oncogenesis facilitated by DANCR was attenuated by anti-IL-11 antibody or a STAT3 inhibitor (BP-1-102). In conclusion, our findings indicate that DANCR induces BCa LN metastasis and proliferation via an LRPPRC-mediated mRNA stabilization mechanism. All primary data in the microarray analysis have been uploaded to GEO: GSE119639. To evaluate whether DANCR is involved in BCa progression, DANCR expression was investigated in a large 120-case cohort of BCas using qRT-PCR The results showed that DANCR was overexpressed in BCa tissues compared with normal adjacent tissues and in LN-positive bladder tumors compared with LN-negative tumors.To identify DANCR-interacting proteins in BCa cells, we performed RNA pull-down assays using in vitro-transcribed biotinylated DANCR.  We also verified this result using RNA immunoprecipitation (RIP), and we found that DANCR, but not U6, was enriched in LRPPRC precipitates. Taken together, these results suggest that DANCR upregulates the expression levels of IL-11, PLAU, MMP9, and CCND1, which contribute to cancer cell lymphatic metastasis and proliferation in BCa. First, we found that CCND1, PLAU, and IL-11, but not MMP9, mRNAs were enriched in LRPPRC precipitates using a RIP assay	30660488	RID06919	interact with protein	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	DANCR	MMP9	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR;microarray	GSE119642	NA	cell proliferation(+);cell metastasis(+);IL-11-STAT3 signaling pathway(+)	NA	association	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000100985	NA	57291	4318	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CLG4B	DANCR Promotes Metastasis and Proliferation in Bladder Cancer Cells by Enhancing IL-11-STAT3 Signaling and CCND1 Expression.Mechanistic investigations revealed that DANCR activated IL-11-STAT3 signaling and increased cyclin D1 and PLAU expression via guiding leucine-rich pentatricopeptide repeat containing (LRPPRC) to stabilize mRNA. Moreover, oncogenesis facilitated by DANCR was attenuated by anti-IL-11 antibody or a STAT3 inhibitor (BP-1-102). In conclusion, our findings indicate that DANCR induces BCa LN metastasis and proliferation via an LRPPRC-mediated mRNA stabilization mechanism. All primary data in the microarray analysis have been uploaded to GEO: GSE119639. To evaluate whether DANCR is involved in BCa progression, DANCR expression was investigated in a large 120-case cohort of BCas using qRT-PCR The results showed that DANCR was overexpressed in BCa tissues compared with normal adjacent tissues and in LN-positive bladder tumors compared with LN-negative tumors.To identify DANCR-interacting proteins in BCa cells, we performed RNA pull-down assays using in vitro-transcribed biotinylated DANCR.  We also verified this result using RNA immunoprecipitation (RIP), and we found that DANCR, but not U6, was enriched in LRPPRC precipitates. Taken together, these results suggest that DANCR upregulates the expression levels of IL-11, PLAU, MMP9, and CCND1, which contribute to cancer cell lymphatic metastasis and proliferation in BCa. First, we found that CCND1, PLAU, and IL-11, but not MMP9, mRNAs were enriched in LRPPRC precipitates using a RIP assay	30660488	RID06920	expression association	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pancreatic cancer	TP73-AS1	BDH2	positively-E	dual-luciferase reporter assay;siRNA;StarBase V2.0	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-141)	regulation	RNA-protein	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000164039	NA	57212	56898	KIAA0495|PDAM	DHRS6|FLJ13261|PRO20933|SDR15C1|UCPA-OR|UNQ6308	LncRNA TP73-AS1 sponges miR-141-3p to promote the migration and invasion of pancreatic cancer cells through the up-regulation of BDH2.TP73-AS1 was up-regulated in pancreatic cancer tissue and cell lines. High levels of TP73-AS1 were correlated with poor clinicopathological characteristics and shorter overall survival. MiR-141 was a direct target for TP73-AS1, while BDH2 was a direct target for miR-141. The knockdown of TP73-AS1 significantly inhibited the migration and invasion of pancreatic cancer cells, while the miR-141 inhibitor significantly restored the migration and invasion. Therefore, TP73-AS1 positively regulated BDH2 expression by sponging miR-141. These findings suggest that TP73-AS1 serves as an oncogene and promotes the metastasis of pancreatic cancer.Moreover, TP73-AS1 could serve as a predictor and a potential drug biotarget for pancreatic cancer. To study the role of TP73-AS1 in pancreatic cancer metastasis, TP73-AS1 was silenced in both PANC-1 and BxPC-3 cell lines using TP73-AS1 siRNA. Using the Starbase V2.0 database, miR-141 was identified as a potential ceRNA target for TP73-AS1. dual-luciferase reporter assays showed that miR-141 mimics significantly reduced the luciferase activity of the TP73-AS1-wt luciferase reporter vector, while they did not affect the luciferase activity of the TP73-AS1-MUT luciferase reporter vector. In the present study, the levels of TP73-AS1 and its candidate target miR-141 in pancreatic cancer and adjacent normal tissue were detected using qRT-PCR	30643007	RID06921	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE55807)
Breast cancer	LINC01857	CREB1	positively-E	siRNA;RIP;CHIP	upregulation	qRT-PCR	GSE80266	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000224137	GRCh38_2:207662375-207679116	ENSG00000118260	NA	102724714	1385	AC079767.4	NA	LINC01857 as an oncogene regulates CREB1 activation by interacting with CREBBP in breast cancer.LINC01857 was highly expressed in breast cancer tissues and cells (p < 0.05). High LINC01857 expression predicted poor prognosis in breast cancer patients. Functionally, LINC01857 silencing impaired proliferation and enhanced apoptosis of breast cancer cells (p < 0.05). Decreased LINC01857 inhibited breast cancer cells migration and invasion ability (p < 0.05). In terms of mechanism, LINC01857 promoted H3K27Ac deposition on CREB1 promoter and initiated its transcription by recruiting CREBBP. Overexpression of CREB1 reversed the biological behavior of breast cancer cells induced by LINC01857 silencing (p < 0.05).  LINC01857 was highly expressed in breast cancer by screening of GEO database (GSE80266).	30628071	RID06922	interact with protein	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	DCST1-AS1	FAIM2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+)	ceRNA(miR-1254)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000232093	GRCh38_1:155045191-155046118	ENSG00000135472	NA	100505666	23017	RP11-307C12.11	KIAA0950|LFG|LFG2|LIFEGUARD|NMP35|TMBIM2	LncRNA DCST1-AS1 functions as a competing endogenous RNA to regulate FAIM2 expression by sponging miR-1254 in hepatocellular carcinoma.LncRNA DCST1-AS1 was highly expressed in HCC tissues, and the high expression of DCST1-AS1 was significantly correlated with larger tumours and shorter survival time. Moreover, DCST1-AS1 knockout significantly inhibited proliferation, promoted apoptosis and cycle arrest of HCC cells, and inhibited tumour growth in vivo. According to functional analysis, DCST1-AS1 competitively bound miR-1254, thus blocking the silencing effect of miR-1254 on the target gene Fas apoptosis inhibitor 2 (FAIM2). A novel lncRNA DCST1-AS1 that functions as an oncogene in HCC was discovered. DCST1-AS1 up-regulates the expression of FAIM2 by up-regulating the expression of miR-1254, ultimately promoting the proliferation of HCC cells. This research provides new therapeutic targets for HCC.	30617187	RID06923	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	LINC01436	EPAS1	positively-E	dual-luciferase reporter assay;RIP;CHIP	upregulation	qRT-PCR;microarray	NA	NA	prognosis(+);cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-30a-3p)	regulation	RNA-protein	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000231106	GRCh38_21:36005137-36007838	ENSG00000116016	NA	100996609	2034	AP000688.8	bHLHe73|HIF2A|HLF|MOP2|PASD2	Hypoxia-sensitive LINC01436 is regulated by E2F6 and acts as an oncogene by targeting miR-30a-3p in non-small cell lung cancer.identified a novel up-regulated lncRNA, LINC01436 (RefSeq: NR_110419.1), in non-small cell lung cancer (NSCLC). High expression of LINC01436 was significantly associated with poor overall survival. Notably, LINC01436 expression was transcriptionally repressed by E2F6 under normoxia, and the inhibitory effect was relieved in a hypoxic microenvironment. Gain- and loss-of-function studies revealed that LINC01436 acted as a proto-oncogene by promoting lung cancer cell growth, migration and invasion in vitro. Xenograft tumor assays in nude mice confirmed that LINC01436 promoted tumor growth and metastasis in vivo. Mechanistically, LINC01436 exerted biological functions by acting as a microRNA (miR)-30a-3p sponge to regulate the expression of its target gene EPAS1. We performed a microarray analysis to identify systematically genome-wide differential lncRNA expression in five paired NSCLC tumor and adjacent normal lung tissues. To validate this result, we investigated the LINC01436 expression levels in 100 paired NSCLC tumor and adjacent normal lung tissues using qRT-PCR Among the deregulated miRNA, miR-30a-3p, miR-196a-5p and miR-4417 were predicted to target LINC01436 using the miRanda algorithm.	30614188	RID06924	ceRNA or sponge	metastasis,prognosis		UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	E2F6	LINC01436	negatively-E	dual-luciferase reporter assay;CHIP;siRNA	upregulation	qRT-PCR;microarray	NA	NA	prognosis(+);cell growth(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000169016	NA	ENSG00000231106	GRCh38_21:36005137-36007838	1876	100996609	E2F-6	AP000688.8	Hypoxia-sensitive LINC01436 is regulated by E2F6 and acts as an oncogene by targeting miR-30a-3p in non-small cell lung cancer.identified a novel up-regulated lncRNA, LINC01436 (RefSeq: NR_110419.1), in non-small cell lung cancer (NSCLC). High expression of LINC01436 was significantly associated with poor overall survival. Notably, LINC01436 expression was transcriptionally repressed by E2F6 under normoxia, and the inhibitory effect was relieved in a hypoxic microenvironment. Gain- and loss-of-function studies revealed that LINC01436 acted as a proto-oncogene by promoting lung cancer cell growth, migration and invasion in vitro. Xenograft tumor assays in nude mice confirmed that LINC01436 promoted tumor growth and metastasis in vivo. Mechanistically, LINC01436 exerted biological functions by acting as a microRNA (miR)-30a-3p sponge to regulate the expression of its target gene EPAS1. We performed a microarray analysis to identify systematically genome-wide differential lncRNA expression in five paired NSCLC tumor and adjacent normal lung tissues. To validate this result, we investigated the LINC01436 expression levels in 100 paired NSCLC tumor and adjacent normal lung tissues using qRT-PCR To explore the potential mechanisms controlling the expression of LINC01436, we used the open regulatory annotation (ORegAnno) track in the UCSC genome browser and found an E2F6 binding site in the LINC01436 promoter region. Thus, we focused on the regulatory effect of E2F6 on LINC01436 expression. We predicted that E2F6 has two specific binding sites in LINC01436 promoter using jaspar. Using ChIP experiments, we confirmed the direct binding of E2F6 to LINC01436 promoter. We next performed luciferase reporter assays to validate promoter regulation. Co-transfection of the E2F6-overexpression vectors with LINC01436 promoter luciferase constructs significantly repressed the luciferase activity, whereas knockdown of E2F6 by siRNA enhanced the activity of LINC01436 promote.	30614188	RID06925	transcriptional regulation	metastasis,prognosis	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	
Cervical cancer	SNHG14	YWHAZ	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-206)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000164924	NA	104472715	7534	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	14-3-3-zeta|KCIP-1|YWHAD	LncRNA SNHG14 promotes the progression of cervical cancer by regulating miR-206/YWHAZ.Molecular mechanism explorations revealed that SNHG14 acted as a sponge of miR-206 and that YWHAZ was a downstream target gene of miR-206 in CC. Spearman's correlation analysis uncovered a significantly negative correlation between SNHG14 (or YWHAZ) and miR-206 expression, while a significantly positive correlation between SNHG14 and YWHAZ expression in CC tissues. We also found that the effect of SNHG14 knockdown on the CC progression could be partly rescued by overexpression of YWHAZ at the same time. Our findings revealed that SNHG14 acted as a sponge of miR-206 to regulate the expression of YWHAZ in CC, hinting the promising therapeutic target role of SNHG4 for CC patients. In this study, we discovered that the relative expression of SNHG14 was significantly upregulated in CC tissues and cells, and associated with the overall survival of CC patients. SNHG14 knockdown inhibits cell proliferation, migration, invasion, and promotes cell apoptosis in CC.  Firstly, starBase online website was used to predict the potential miRNAs which might be sponged by SNHG14.  To evaluate the interaction of miR-206 and SNHG14, luciferase assay was performed and the results displayed that the luciferase activity of mutant-type SNHG14 was significantly decreased in cells co-transfected with SNHG14-Wt and miR-206 mimic, while significantly increased in cells co-transfected of SNHG14-Wt and miR-206 inhibitor. RIP assay indicated that SNHG14 and miR-206 expression were strikingly abundant in Ago2 pellet in comparison to IgG control. RNA pull-down assay further validated that miR-206 could directly bind with SNHG14.	30611620	RID06926	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Urinary bladder cancer	OXCT1-AS1	JAK1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	GSE121738	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-455-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000248668	GRCh38_5:41869927-41872241	ENSG00000162434	NA	100874002	3716	SARRAH	JAK1A|JAK1B|JTK3	microarray expression profiles analysis revealed lncRNA OXCT1-AS1 promoted bladder cancer cell aggressiveness via miR-455-5p/JAK1 signaling. The dual-luciferase activity assay was performed to investigate the potential mechanism of competing endogenous RNA network. lncRNA OXCT1-AS1, which elevated in metastasis lymph node, was significantly upregulated in BCa cell lines compared with SVHUC-1. We demonstrated OXCT1-AS1 inhibited miR-455-5p to decrease its binding to the JAK1 3'-untranslated region, which could upregulate the expression of JAK1 at the protein level, thus promoting BCa proliferation and invasion. All the data have been submitted to NCBI Gene Expression Omnibus and are accessible (Series no. GSE121738).	30609030	RID06927	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	POU3F3	TGFB1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000198914	GRCh38_2:104853287-104858574	ENSG00000105329	NA	5455	7040	BRN1|OTF8|SNIBFIS|brain-1|oct-8	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA POU3F3 promotes cancer cell migration and invasion in nasopharyngeal carcinoma by up-regulating TGF-beta1.GF-beta1 inhibitor partially rescued the inhibited cancer cell migration and invasion caused by lncRNA POU3F3 overexpression. LncRNA POU3F3 overexpression led to down-regulated TGF-beta1 expression, while exogenous TGF-beta1 and TGF-beta1 inhibitor treatment did not significantly change the expression level of lncRNA POU3F3. Therefore, lncRNA POU3F3 may promote cancer cell migration and invasion in nasopharyngeal carcinoma by up-regulating TGF-beta1. Our study showed that plasma levels of lncRNA POU3F3 and TGF-beta1 (transforming growth factor-beta) were both increased in nasopharyngeal carcinoma patients than in healthy controls. RT-qPCR results showed that plasma levels of lncRNA POU3F3 were increased in nasopharyngeal carcinoma (NC) patients. Plasma levels of lncRNA POU3F3 and TGF-beta1 were positively correlated only in nasopharyngeal carcinoma patients. LncRNA POU3F3 overexpression led to up-regulated TGF-beta1 expression in cells nasopharyngeal carcinoma cell lines HTB-43 and C666-1. Our study failed to elucidate the mechanism of the regulatory role of lncRNA POU3F3 in the expression of TGF-beta1, which is a direction of our future studies.	30602452	RID06928	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Prostate cancer	SAP30L-AS1	SAP30L	negatively-E	CHIRP;overexpression	upregulation	qRT-PCR	NA	NA	cell growth(+)	histone modification	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000245275	GRCh38_5:154325568-154445850	ENSG00000164576	NA	386627	79685	FLJ38109|GALNT10-AS1	FLJ11526|NS4ATP2	Long non-coding RNA SAP30L-AS1 promotes prostate cancer growth through repressing SAP30L.Mechanistic investigation revealed that SAP30L-AS1 physically binds to the promoter of SAP30L and represses SAP30L expression. The expression of SAP30L is negatively associated with that of SAP30L-AS1 in prostate cancer tissues. Rescue assays demonstrated that overexpression of SAP30L attenuated the roles of SAP30L-AS1 in promoting prostate cancer proliferation and inhibiting prostate cancer apoptosis. In conclusion, SAP30L-AS1 is upregulated and has oncogenic roles in prostate cancer via repressing SAP30L. SAP30L-AS1 expression levels in 66 pairs of prostate cancer tissues and adjacent noncancerous tissues were detected by qRT-PCR As presented in Fig. 1A, SAP30L-AS1 was significantly overexpressed in prostate cancer (PCa) tissue specimens compared with adjacent noncancerous tissues. ChIRP assays presented that the promoter of SAP30L was specifically enriched by the probes against SAP30L-AS1 (Fig. 4C), suggesting that SAP30L-AS1 can specifically bind to the promoter of SAP30L. Next, the mRNA and protein expression levels of SAP30L in SAP30L-AS1 stably overexpressed and depleted prostate cancer cells were detected by qRT-PCRand western blot.	30599235	RID06929	epigenetic regulation	NA	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Retinoblastoma	MALAT1	STAT3	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;siRNA;RNAi	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-20b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168610	NA	378938	6774	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	APRF	Long non-coding RNA MALAT1 aggravates human retinoblastoma by sponging miR-20b-5p to upregulate STAT3.The interplay among MALAT1, miR-20b-5p and STAT3 were evaluated through dual luciferase reporter gene assay and RNA pull-down after RB cells treated with siRNA/pcDNA-MALAT1 or/and miR-20b-5p mimic/inhibitor. Both RB tissues and cells showed highly expressed MALAT1. When MALAT1 was downregulated, RB cell proliferation was hindered and apoptosis was accelerated. MALAT1 sponged miR-20b-5p and upregulated STAT3. Silencing MALAT1 or overexpressing miR-20b-5p inhibited proliferation and promoted apoptosis in RB cells. The tumor growth of nude mice treated with siRNA-MALAT1 was inhibited.CONCLUSION: MALAT1 could increase proliferation and reduce apoptosis by sponging miR-20b-5p to upregulate STAT3 in RB cells. We detected the expression of MALAT1 in 20 normal retinas and 40 RB tissue samples by RT-qPCR.	32336590	RID06930	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Neuroblastoma	DLX6-AS1	YAP1	positively-E	luciferase reporter assay;starBase v2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000137693	NA	285987	10413	Evf-2|FLJ34048|NCRNA00212	YAP65	Long non-coding RNA DLX6-AS1 regulates neuroblastoma progression by targeting YAP1 via miR-497-5p.Further analysis showed that DLX6-AS1 regulates the expression of YAP1 by sponging miR-497-5p. DLX6-AS1 directly interacts with miR-497-5p and reduces the binding of miR-497-5p to YAP1 3'UTR, thus inhibiting the degradation of YAP1 by miR-497-5p.SIGNIFICANCE: This work demonstrates that DLX6-AS1 partially enhances the proliferation, migration and invasion abilities of NB cells through the miR-497-5p/YAP1 pathway, DLX6-AS1 might act as a promising therapeutic target for NB. To investigate the role of DLX6-AS1 in NB, expression of DLX6-AS1 was measured using q-PCR. As shown in Fig. 1A, DLX6-AS1 was upre_x0002_gulated in NB tumor tissue compared with adjacent non-tumor tissue. Utilizing starBase v2.0 [25] (http://starbase.sysu.edu.cn/), we found DLX6-AS1 contains one conserved target site of miR-497-5p, a known tumor suppressor that suppresses cancer cell proliferation and invasion.  Luciferase reporter assays showed that miR-497-5p mimics significantly inhibited the luciferase activity in HEK293T cells co-transfected WT-DLX6-AS1 and miR-497-5p mimic, but had no effect when co-transfected with miR-497-5p mimic and MUT-DLX6-AS1	32289431	RID06931	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Neuroblastoma	DLX6-AS1	miR-497-5p	negatively-F	luciferase reporter assay;starBase v2.1	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	miRNA	ENSG00000231764	GRCh38_7:96955141-97014088	NA	NA	285987	NA	Evf-2|FLJ34048|NCRNA00212	NA	Long non-coding RNA DLX6-AS1 regulates neuroblastoma progression by targeting YAP1 via miR-497-5p.Further analysis showed that DLX6-AS1 regulates the expression of YAP1 by sponging miR-497-5p. DLX6-AS1 directly interacts with miR-497-5p and reduces the binding of miR-497-5p to YAP1 3'UTR, thus inhibiting the degradation of YAP1 by miR-497-5p.SIGNIFICANCE: This work demonstrates that DLX6-AS1 partially enhances the proliferation, migration and invasion abilities of NB cells through the miR-497-5p/YAP1 pathway, DLX6-AS1 might act as a promising therapeutic target for NB. To investigate the role of DLX6-AS1 in NB, expression of DLX6-AS1 was measured using q-PCR. As shown in Fig. 1A, DLX6-AS1 was upre_x0002_gulated in NB tumor tissue compared with adjacent non-tumor tissue. Utilizing starBase v2.0 [25] (http://starbase.sysu.edu.cn/), we found DLX6-AS1 contains one conserved target site of miR-497-5p, a known tumor suppressor that suppresses cancer cell proliferation and invasion.  Luciferase reporter assays showed that miR-497-5p mimics significantly inhibited the luciferase activity in HEK293T cells co-transfected WT-DLX6-AS1 and miR-497-5p mimic, but had no effect when co-transfected with miR-497-5p mimic and MUT-DLX6-AS1	32289431	RID06932	ceRNA or sponge	NA		
Breast cancer	NEAT1	CBX7	positively-E	StarBase v3.0	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100307	NA	283131	23492	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer.western blot revealed down-regulation of CBX7 and up-regulation of RTCB following NEAT1 inhibition. Based on the cytoplasmic and nuclear expression of NEAT1, we investigated the possible regulation of CBX7 and RTCB by NEAT1. Results showed that NEAT1 regulated the expression of CBX7 and RTCB, possibly by binding of NEAT1 to DNA in the nucleus, which facilitates cell proliferation, invasion and migration. Existing TCGA data for lncRNA NEAT1 expression in breast cancer tissues and clinicopathological data from the associated patients were downloaded from https://gdc.cancer.gov/. lncRNA NEAT1 Is Up-Regulated in Breast Cancer Tissues and Cell Lines. In the current study, StarBase 3.0 interaction target analyses revealed that CBX7 is positively co-expressed with NEAT1 in breast cancer while RTCB is negatively co-expressed with NEAT1 in breast cancer. Based on these findings, we considered that lncRNA NEAT1 may play a regulatory role in chromatin state, DNA binding, or the fate of newly-transcribed mRNA in the nucleus to regulate the expression of CBX7 and RTCB.	32273717	RID06933	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	NEAT1	RTCB	negatively-E	StarBase v3.0	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000100220	NA	283131	51493	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	C22orf28|FAAP|HSPC117	lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer.western blot revealed down-regulation of CBX7 and up-regulation of RTCB following NEAT1 inhibition. Based on the cytoplasmic and nuclear expression of NEAT1, we investigated the possible regulation of CBX7 and RTCB by NEAT1. Results showed that NEAT1 regulated the expression of CBX7 and RTCB, possibly by binding of NEAT1 to DNA in the nucleus, which facilitates cell proliferation, invasion and migration. Existing TCGA data for lncRNA NEAT1 expression in breast cancer tissues and clinicopathological data from the associated patients were downloaded from https://gdc.cancer.gov/. lncRNA NEAT1 Is Up-Regulated in Breast Cancer Tissues and Cell Lines. In the current study, StarBase 3.0 interaction target analyses revealed that CBX7 is positively co-expressed with NEAT1 in breast cancer while RTCB is negatively co-expressed with NEAT1 in breast cancer. Based on these findings, we considered that lncRNA NEAT1 may play a regulatory role in chromatin state, DNA binding, or the fate of newly-transcribed mRNA in the nucleus to regulate the expression of CBX8 and RTCB.	32273717	RID06934	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)
Non-small cell lung cancer	LINC00210	miR-328-5p	negatively-F	luciferase reporter assay;siRNA;bioinformatics	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000231814	GRCh38_1:217892900-217920804	NA	NA	100885798	NA	NCRNA00210	NA	LINC00210 plays oncogenic roles in non-small cell lung cancer by sponging microRNA-328-5p.A549 cells transfected with siLINC00210#1 and miR-328-5p inhibitor exhibited a significant increase in cell proliferation, and migratory and invasive ability compared with that in A549 cells transfected with siLINC00210#1. These findings suggest that LINC00210 may serve as an oncogenic role in NSCLC by sponging miR-328-5p. The results from the RT-qPCR revealed that LINC00210 expression level was significantly increased in NSCLC tissues compared with that in adjacent tissues. A luciferase reporter assay was performed following A549 cell transfection with miR-328-5p mimics and WT- or Mut-LINC00210 reporter plasmid. Through bioinformatics analysis, miR-328-5p was also identified as a potential target of LINC00210, therefore miR-328-5p was investigated in the present study.	32266029	RID06935	ceRNA or sponge	NA		
Esophagus squamous cell carcinoma	ICMT-DT	TPX2	positively-E	dual-luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell autophagy(+);chemoresistance(+)	interact with protein;transcriptional regulation	regulation	RNA-protein	Cisplatin	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000225077	GRCh38_1:6234692-6239444	ENSG00000088325	NA	148645	22974	C1orf211|LINC00337|MGC40168|NCRNA00337	C20orf1|C20orf2|DIL-2|p100	Long non-coding RNA LINC00337 induces autophagy and chemoresistance to cisplatin in esophageal squamous cell carcinoma cells via upregulation of TPX2 by recruiting E2F4.Next, the interactions among LINC00337, E2F4, and TPX2 were identified using chromatin immunoprecipitation, dual-luciferase reporter, and RNA-binding protein immunoprecipitation assays, suggesting that LINC00337 could recruit E2F4 to enhance the transcription of TPX2.The results demonstrated that LINC00337 upregulated TPX2, consequently leading to elevated levels of Beclin1 and LC3II/LC3I, promoted cell viability and autophagy, while inhibiting apoptosis and chemosensitivity to DDP in ESCC. In sum, the current study evidenced that the overexpression of LINC00337 could potentially enhance ESCC cell autophagy and chemoresistance to DDP via the upregulation of TPX2 by recruiting E2F4. Expression patterns of LINC00337 and targeting protein for Xenopus kinesin-like protein 2 (TPX2) in ESCC tissues and cells were detected using RT-qPCR and immunohistochemical staining.	32239565	RID06936	epigenetic regulation	chemoresistance		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE55807)
Non-small cell lung cancer	MIR17HG	miR-142-3p	positively-E	overexpression	downregulation	qRT-PCR	TCGA	NA	cell migration(-);cell invasion(-)	DNA methylation	regulation	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000215417	GRCh38_13:91347820-91354579	NA	NA	407975	NA	C13orf25|FLJ14178|LINC00048|MIHG1|miR-17-92|MIRH1|MIRHG1|NCRNA00048	NA	LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1.MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC.	32228546	RID06937	epigenetic regulation	NA	UP(LIHC);DATA(GSE117623)	
Non-small cell lung cancer	MIR17HG	BACH1	negatively-E	overexpression	downregulation	qRT-PCR	TCGA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000215417	GRCh38_13:91347820-91354579	ENSG00000156273	NA	407975	571	C13orf25|FLJ14178|LINC00048|MIHG1|miR-17-92|MIRH1|MIRHG1|NCRNA00048	BACH-1|BTBD24	LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1.MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC.	32228546	RID06938	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	LINC00520	HSPB1	positively-E	luciferase reporter assay;siRNA;RIP;starBase 3.0;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-577)	regulation	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000106211	NA	645687	3315	C14orf34|LASSIE	CMT2F|Hs.76067|Hsp25|HSP27|HSP28	Long noncoding RNA LINC00520 accelerates the progression of colorectal cancer by serving as a competing endogenous RNA of microRNA-577 to increase HSP27 expression.LINC00520 functioned as a competing endogenous RNA by sponging microRNA-577 (miR-577) and thereby increasing heat shock protein 27 (HSP27) expression. Rescue experiments revealed that inhibiting miR-577 or restoring HSP27 could abrogate the effects of LINC00520 silencing on malignant phenotypes of CRC. LINC00520 functioned as an oncogenic lncRNA in CRC, and it facilitated CRC progression by regulating the miR-577/HSP27 axis, suggesting that the LINC00520/miR-577/HSP27 axis is an effective target in anticancer management. In this study, high-LINC00520 expression was verified in CRC tissues and cell lines, and this high expression was associated with patients' unfavorable clinicopathological parameters and shorter overall survival and disease-free survival.  starBase 3.0 (https://starbase.sysu.edu.cn/) was used to predict the potential targets of LINC00520. To test the role of LINC00520 in CRC, we first analyzed its expression profile in 132 pairs of CRC tissues and surrounding adjacent normal tissues via RT-qPCR. To confirm this prediction, luciferase reporter assay was performed to assess the binding between miR-577 and LINC00520 in CRC cells. The interaction between miR-577 and LINC00520 was further determined using RIP assay, and the data revealed that LINC00520 and miR-577 were enriched in Ago2-containing immunoprecipitates compared to that observed in the IgG control.	32146708	RID06939	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	MAGI2-AS3	RECK	positively-E	IntaRNA	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-25)	regulation	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000122707	NA	100505881	8434	ENST00000414797	hRECK|ST15	LncRNA MAGI2-AS3 is downregulated in non-small cell lung cancer and may be a sponge of miR-25.In NSCLC cells, MAGI2-AS3 overexpression led to upregulated RECK. Bioinformatics analysis showed that MAGI2-AS3 may bind miR-25, which can directly target RECK. In NSCLC cells, miR-25 overexpression led to downregulated RECK and attenuated the effects of MAGI2-AS3 overexpression, while MAGI2-AS3 and miR-25 failed to affect each other. MAGI2-AS3 may sponge miR-25 to upregulate RECK, thereby inhibiting NSCLC cell invasion and migration. MAGI2-AS3 and RECK were both downregulated and they were correlated in NSCLC. Expression levels of MAGI2-AS3 and RECK mRNA in two types of tissues (non-tumor and NCSLC) were measured by qPCR. To predict the possible interaction between MAGI2-AS3 (NCBI Accession: NR_038343.2) and miR-25 (miRbase Accession: MI0000082), MAGI2-AS3 (long sequence) and miR-25 (short sequence) were inputted into IntaRNA (http://rna.informatik.uni-freiburg.de/IntaRNA/Input.jsp) RNA-RNA interaction online prediction program.	32138716	RID06940	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	MBNL1-AS1	miR-135a-5p	negatively-F	dual-luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229619	GRCh38_3:152245262-152269565	NA	NA	401093	NA	LOC401093	NA	Down-regulation of MBNL1-AS1 contributes to tumorigenesis of NSCLC via sponging miR-135a-5p.Then, we predicted that miR-135a-5p was a potential target of MBNL1-AS1 and its level was correlated with MBNL1-AS1 in NSCLC negatively. Our previous study indicated miR-135a-5p could induce lung cancer progression through regulating LOXL4. Here, we found that MBNL1-AS1 was able to regulate miR-135a-5p expression negatively. The direct binding association between MBNL1-AS1 and miR-135a-5p was proved using dual-luciferase reporter assay and RIP experiment. Subcutaneous xenotransplanted tumor model was set up and it was confirmed increased MBNL1-AS1 remarkably restrained tumorigenic ability of NSCLC through sponging miR-135a-5p in vivo. To sum up, our data revealed the significance of the MBNL1-AS1 and miR-135a-5p in NSCLC. Firstly, MBNL1-AS1 expression in NSCLC was assessed using qRT-PCR	32092823	RID06941	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939)	
Papillary thyroid carcinoma	LINC00520	SPHK2	positively-E	starBase 3.0;luciferase reporter assay;siRNA;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-577)	regulation	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000063176	NA	645687	56848	C14orf34|LASSIE	NA	Long noncoding RNA LINC00520 accelerates progression of papillary thyroid carcinoma by serving as a competing endogenous RNA of microRNA-577 to increase Sphk2 expression.LINC00520 functioned as a competing endogenous RNA by sponging microRNA-577 (miR-577) and thereby increasing sphingosine kinase 2 (Sphk2) expression. Rescue experiments revealed that inhibiting miR-577 or restoring Sphk2 could abrogate the effects of LINC00520 silencing on the malignant phenotypes of PTC. LINC00520 functioned as an oncogenic lncRNA in PTC, and it facilitated PTC progression by regulating the miR-577/Sphk2 axis, suggesting that the LINC00520/miR-577/Sphk2 axis is an effective target in anticancer management. starBase 3.0 (http://starbase.sysu.edu.cn/) was used to predict the potential targets of LINC00520. To examine the role of LINC00520 in PTC, we first analyzed its expression profile in 59 pairs of PTC tissues and adjacent normal tissues using RT-qPCR. To confirm this prediction, luciferase reporter assay was performed to assess the binding between miR-577 and LINC00520 in PTC cells. The interaction between miR-577 and LINC00520 was further determined using RIP assay.	32075502	RID06942	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	PCAT6	MIR15A	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000283785	NA	100506696	406948	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Silencing of long non-coding RNA PCAT6 restrains gastric cancer cell proliferation and epithelial-mesenchymal transition by targeting microRNA-15a.PCAT6 reversely regulated miR-15a and miR-15a inhibitor reversed the efficacy of sh-PCAT6 in cell proliferation and EMT. PCAT6 restrained the relate-proteins of RB/E2F and Wnt/beta-catenin pathways and miR-15a reverse this progress. Finally, PCAT6 was a target of miR-15a. Silencing of lncRNA PCAT6 restrained proliferation and EMT of GC cells by targeting miR-15a via RB/E2F and Wnt/beta-catenin pathways. Besides, the level of miR-15a and PCAT6 was tested by RT-qPCR. Besides, the target relation between miR-15a and PCAT6 were tested by luciferase assay. PCAT6 was highly expressed in GC cells and tissues. This implied PCAT6 was negatively regulated miR-15a.  It displayed PCAT6 level was declined in PCAT6-WT and basically no change in PCAT6-MUT, indicating miR-15a is a target of PCAT6 (p < 0.05, Fig. 8A). The targeting sequence was shown in Fig. 8B.	32039820	RID06943	ceRNA or sponge	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	
Prostate cancer	HOXA11-AS	ACTN4	positively-E	luciferase reporter assay;RIP;ChIP;starBase;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-518b)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000130402	NA	221883	81	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	FSGS1	CTCF-induced upregulation of HOXA11-AS facilitates cell proliferation and migration by targeting miR-518b/ACTN4 axis in prostate cancer. Subsequent molecular mechanism assays confirmed that HOXA11-AS bound with miR-518b and negatively regulates miR-518b expression. Besides, HOXA11-AS could regulate the expression of ACTN4 by sponging miR-518b. Moreover, rescued-function assays revealed that miR-518b inhibition or ACTN4 upregulation reversed the repressive effect of HOXA11-AS knockdown on PCa progression.  Through RT-qPCR analysis, we observed that HOXA11-AS was highly expressed in PCa tissues in contrast to adjacent normal tissues. Through searching starBase (http://starbase.sysu.edu.cn/index.php) under the screening condition (CLIP Data: strict stringency <<-2), five miRNAs predicted to bind with HOXA11-AS were demonstrated in Figure 2B. After miR-518b was overexpressed in PC3 and DU145 cells (Figure 2F), the luciferase activity of pmirGLO-HOXA11-AS-WT was notably reduced whereas no evident changes of the luciferase activity of pmirGLO-HOXA11-AS-Mut could be detected among different groups. Moreover, miR-518b expression was observably lower in PCa tissues than that in corresponding nontumor tissues (Figure S1B). After we applied RIP assay, HOXA11-AS and miR-518b were observed to be signally enriched in the anti-Ago2 group, suggesting that HOXA11-AS could bind with miR-518b in PC3 and DU145 cells.  ChIP assay was conducted to testify the binding capacity between CTCF and HOXA11-AS promoter in PC3 and DU145 cells.	31971633	RID06944	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	CDKN2B-AS1	ROCK1	positively-E	dual-luciferase reporter assay;overexpression;siRNA	upregulation	RT-qPCR	NA	NA	cell growth(+)	ceRNA(miR-324-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000067900	NA	100048912	6093	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	p160ROCK	Regulating of cell cycle progression by the lncRNA CDKN2B-AS1/miR-324-5p/ROCK1 axis in laryngeal squamous cell cancer.Results of dual-luciferase reporter assay showed that miR-324-5p could bind to CDKN2B-AS1 or Rho-associated coiled-coil containing protein kinase 1 (ROCK1). Finally, over-expression of ROCK1 in AMC-HN-8 cells revised the inhibitory effect of CDKN2B-AS1 siRNA on cell growth.The upregulation of CDKN2B-AS1 was correlated with overall survival, advanced clinical stage, and lymph node metastasis and promoted LSCC cell growth via miR-324-5p/ROCK1 axis. CDKN2B-AS1 was upregulated in LSCC tissues, and the upregulation of CDKN2B-AS1 was correlated with overall survival, advanced clinical stage, and lymph node metastasis. In AMC-HN-8 cells, the knockdown of CDKN2B-AS1 by siRNA inhibited cell viability, blocked cell cycle in G1 phase, and increased the expression levels of cyclin-dependent kinase inhibitor 1A (p21), cleaved caspase3, and cleaved PPoly (ADP-Ribose) polymerase 1. Finally, over-expression of ROCK1 in AMC-HN-8 cells revised the inhibitory effect of CDKN2B-AS1 siRNA on cell growth. To determine the function of CDKN2B-AS1 in LSCC, the expression level of CDKN2B-AS1 was firstly determined by RT-qPCR.	31960744	RID06945	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	NNT-AS1	E2F2	positively-E	dual-luciferase reporter assay;starBase v2.0	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-3666)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000007968	NA	100652772	1870	RP11-159F24.1	E2F-2	LncRNA NNT-AS1 Regulates the Progression of Lung Cancer Through the NNT-AS1/miR-3666/E2F2 Axis.NNT-AS1 and E2F2 were upregulated, but miR-3666 was downregulated in lung cancer tissues and cells. NNT-AS1 knockdown attenuated proliferation and invasion but enhanced apoptosis of lung cancer cells, while miR-3666 inhibition reversed these effects. It was confirmed that miR-3666 was a target of NNT-AS1 and it directly interacted with E2F2. The inhibitory proliferation and invasion, and acceleratory apoptosis of lung cancer cells, caused by miR-3666 enrichment, were overturned by E2F2 overexpression. Furthermore, E2F2 was regulated by NNT-AS1 through miR-3666. To monitor the expression levels of NNT-AS1 and miR-3666, qRT-PCRanalysis was performed. As shown in Figure 3A, the binding sites between NNT-AS1 and miR-3666 were analyzed by bioinformatics tool starBase v2.0. dual-luciferase reporter assay presented that the Luciferase activity was prominently declined in H1299 and A549 cells transfected with WT-NNT-AS1 and miR-3666, while the Luciferase activity had no difference in cells transfected with MUT-NNT-AS1 and miR-3666 or miR-NC. E2F transcription factor 2 (E2F2) is a member of the E2F protein family.	31957837	RID06946	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Esophagus squamous cell carcinoma	TUG1	c-MET	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	GSE61620;GSE61772	NA	radiosensitivity(+);cell proliferation(-);colony formation(-);apoptosis process(+)	ceRNA(miR-144-3p)	regulation	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	lncTUG1/miR-144-3p Affect the Radiosensitivity of Esophageal Squamous Cell Carcinoma by Competitively Regulating c-MET.lncTUG1 was upregulated in ESCC cells and tissues, and lncTUG1 expression was associated with an advanced pathological stage. The bioinformatics analysis revealed that lncTUG1 could specifically bind to miR-144-3p, which was downregulated in ESCC. There was a negative correlation between lncTUG1 and miR-144-3p. LncTUG1 inhibition retarded proliferation and colony formation and induced apoptosis in ESCC cells. Moreover, lncTUG1 knockdown dramatically improved the effect of radiotherapy on ESCC development both in vivo and in vitro.LncTUG1 promoted the progression of ESCC and elevated radiotherapy resistance in ESCC cells, accompanied by a high level of MET expression. Briefly, two data series consisting of two esophageal cancer cells and their derived radioresistant cell lines were obtained from the Gene Expression Omnibus (GEO) database (i.e., GSE61620, and GSE61772). lncTUG1, miR-144-3p and MET expression levels were detected in ESCC tissues and cells by qRT-PCR The dual-luciferase reporter system and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncTUG1 and miR-144-3p or miR-144-3p and MET.	31918742	RID06947	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Osteosarcoma	DANCR	SOX5	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;shRNA	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell autophagy(+)	ceRNA(miR-216a-5p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000134532	NA	57291	6660	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	L-SOX5|MGC35153	LncRNA DANCR Silence Inhibits SOX5-medicated Progression and Autophagy in Osteosarcoma via Regulating miR-216a-5p. The interaction among DANCR, miR-216a-5p and SOX5 was explored by luciferase reporter assay, RIP assay or Pull-down assay. Murine xenograft model was established using 143B cells transfected with sh-DANCR.  DANCR regulated SOX5 expression by sponging to miR-216a-5p. In conclusion, LncRNA DANCR silence inhibits SOX5-medicated progression and autophagy in osteosarcoma via regulating miR-216a-5p which indicating DANCR may act as a potential prognostic biomarker and therapeutic taarget for osteosarcoma. The expression of DANCR, microRNA-216a-5p (miR-216a-5p) and SOX5 was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR.  The interaction among DANCR, miR-216a-5p and SOX5 was explored by luciferase reporter assay, RIP assay or Pull-down assay. The expression of DANCR was measured and the results showed that DANCR was greatly up-regulated in all osteosarcoma tissues compared with that of the control tissues (Fig. 1A) and the level of DANCR in the high-grade osteosarcoma tissues (grade III-IV, n-=-25) was notably higher than that in the low-grade osteosarcoma tissues (grade I-II, n-=-20).	31918278	RID06948	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Acute myeloid leukemia	SNHG5	DNAJB9	positively-E	luciferase reporter assay;miRcode;starBase v2.0	upregulation	microarray;qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-32)	regulation	RNA-protein	NA	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000128590	NA	387066	4189	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	MDG1	Long non-coding RNA SNHG5 regulates chemotherapy resistance through the miR-32/DNAJB9 axis in acute myeloid leukemia.miR-32 was identified as the downstream target of SNHG5 and miR-32 inhibitor abrogated the inhibiting effects of downregulated SNHG5 on AML cell viability. Furthermore, inhibited SNHG5 decreased DNAJB9 expression levels by sponging miR-32. The SNHG5/miR-32/DNAJB9 axis targeted autophagy to regulate chemotherapy resistance. We carried out a genome-wide LncRNA expression study and found SNHG5 aberrantly overexpressed in AML comparing to the donors. To construct expression profiles of LncRNAs in AML, we used microarray (Arraystar Human LncRNAmicroarrayV4.0) to examine expression profiles of LncRNAs. To verify the reliability of the microarray, we used qRT-PCRanalysis to verify the microarray results in AML and healthy donors'-PBMCs samples. To further explore the underlying mechanisms involving SNGH5 in the development of AML, we examined a set of microRNAs that were predicted to bind SNHG5 by miRcode and starBase v2.0 program.  The dual-luciferase reporter gene system results showed that miR-32 mimic transfection successfully decreased relative luciferase activity in 293-T cells transfected with wild type SNHG5 instead of the mutated counterpart. Meanwhile, our study showed overexpression of DNAJB9 could reduce sensitivity, while shDNAJB9 promoted the sensitivity to ADM in HL60 cells.	31884339	RID06949	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE67939)
Gastric cancer	HOXC-AS1	MYC	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;DIANA	upregulation	qRT-PCR	GSE109476	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000250451	GRCh38_12:53999022-54000010	ENSG00000136997	NA	100874363	4609	NA	bHLHe39|c-Myc|MYCC	Our research illustrated a feedback loop of HOXC-AS1-MYC in aggravating GC cell growth and metastasis, highlighting HOXC-AS1 as a promising target for GC diagnosis and treatment.HOXC-AS1 was proved to be trans-activated by c-MYC in GC. In return, HOXC-AS1 positively regulated MYC expression in GC through targeting miR-590-3p/MYC axis in cytoplasm and modulating BRG1/beta-catenin complex-activated MYC transcription in nucleus. Furthermore, the rescue assays verified that MYC mediated HOXC-AS1-affected GC progression.Our research illustrated a feedback loop of HOXC-AS1-MYC in aggravating GC cell growth and metastasis, highlighting HOXC-AS1 as a promising target for GC diagnosis and treatment. Besides, data obtained from GSE109476 suggested the markedly enhanced expression level of HOXC-AS1 and HOXC-AS3 in GC tissues compared to adjacent non-tumor tissues. Fortunately, we unveiled that 2 miRNAs, miR-382-5p and miR-590-3p, were predicted by DIANA to interact with both HOXC-AS1 and MYC mRNA. Moreover, the competition between HOXC-AS1 and MYC mRNA in interacting with miR-590-3p was further validated by luciferase reporter assay. To sum up, HOXC-AS1 boosts MYC mRNA expression in the cytoplasm of GC cells via sponging miR-590-3p. The binding of HOXC-AS1 to MYC promoter was examined by DNA pull down assay. The interaction between HOXC-AS1 and BRG1 in GC cells was testified by RIP and RNA pull-down assays.	31870402	RID06950	ceRNA or sponge	metastasis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	MYC	HOXC-AS1	positively-E	UCSC;JASPAR;PROMO;ChIP;luciferase reporter assay	upregulation	qRT-PCR	GSE109476	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000250451	GRCh38_12:53999022-54000010	4609	100874363	bHLHe39|c-Myc|MYCC	NA	Our research illustrated a feedback loop of HOXC-AS1-MYC in aggravating GC cell growth and metastasis, highlighting HOXC-AS1 as a promising target for GC diagnosis and treatment.HOXC-AS1 was proved to be trans-activated by c-MYC in GC. In return, HOXC-AS1 positively regulated MYC expression in GC through targeting miR-590-3p/MYC axis in cytoplasm and modulating BRG1/beta-catenin complex-activated MYC transcription in nucleus. Furthermore, the rescue assays verified that MYC mediated HOXC-AS1-affected GC progression.Our research illustrated a feedback loop of HOXC-AS1-MYC in aggravating GC cell growth and metastasis, highlighting HOXC-AS1 as a promising target for GC diagnosis and treatment. Besides, data obtained from GSE109476 suggested the markedly enhanced expression level of HOXC-AS1 and HOXC-AS3 in GC tissues compared to adjacent non-tumor tissues. As predicted by three online tools including UCSC, JASPAR and PROMO, HOXC-AS1 seemed to be regulated by c-MYC, a well-recognized oncogene in diverse cancers including GC.  Moreover, the ChIP assay verified a predominant enrichment of HOXC-AS1 promoter in c-MYC-binding compounds. Of note, the luciferase activity of pGL3-HOXC-AS1 promoter was dampened by suppressing MYC but strengthened by overexpressing MYC.	31870402	RID06951	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(BRCA);DATA(GSE55807)
Thyroid cancer	DLX6-AS1	UPF1	negatively-E	starBase v2.0;shRNA	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000005007	NA	285987	5976	Evf-2|FLJ34048|NCRNA00212	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo.CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC. qRT-PCRwas first conducted to detect DLX6-AS1 expression in 60 patients'-tissues and 3 TC cell lines. As a result, DLX6-AS1 was signifi_x0002_cantly upregulated in TC tissues and cell line. DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. UPF1 was predicted as the target protein of DLX6-AS1 through Starbase v2.0. The results of qRT-PCR;ISHowed that, compared with the empty vector (control) group, the ex_x0002_pression level of UPF1 was significantly higher in TC cells of DLX6-AS1 shRNA (sh-DLX6-AS1) group. The Interaction Between UPF1 and DLX6-AS1.	31858555	RID06952	interact with protein	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	SNHG14	miR-613	negatively-F	luciferase reporter assay;RIP;DIANA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224078	GRCh38_15:24978583-25420336	NA	NA	104472715	NA	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	NA	Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613. Moreover, cell proliferation and invasion of lung adenocarcinoma were promoted via overexpression of SNHG14, while cell proliferation and invasion of lung adenocarcinoma were inhibited via silence of SNHG14. Moreover, RT-qPCR results revealed that miR-613 was downregulated via overexpression of SNHG14, while miR-613 was upregulated via knockdown of SNHG14. Further experiments showed that miR-613 was also a direct target of SNHG14 in lung adenocarcinoma.CONCLUSIONS: Our study suggests that SNHG14 enhances lung adenocarcinoma cell proliferation and invasion via targeting miR-613, which indicates that SNHG14 may be a potential therapeutic target in lung adenocarcinoma. DIANA LncBASE Predicted v.2 was used to find the miRNAs that contained complementary base with SNHG14. Furthermore, the luciferase assay revealed that co-transfection of SNHG14-WT and miR-613 largely decreased the luciferase activity, while the co-transfection of SNHG14-MUT and miR-613 had no effect on the luciferase activity either. Meanwhile, the RIP assay also identified that SNHG14 and miR-613 were significantly enriched in Ago2-containing beads compared to input group.	31858549	RID06953	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	
Breast cancer	LINC02273	AGR2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;CHIP;shRNA	upregulation	RT-qPCR;microarray	GSE6532;GSE9195;GSE19615;GSE17907;E-MTAB-365	NA	cell metastasis(+)	histone modification;transcriptional regulation	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245954	GRCh38_4:152090459-152110157	ENSG00000106541	NA	100996286	10551	NA	AG2|HAG-2|PDIA17|XAG-2	LINC02273 drives breast cancer metastasis by epigenetically increasing AGR2 transcription.Mechanistically, hnRNPL-LINC02273 formed a complex which activated AGR2 transcription and promoted cancer metastasis. The recruitment of hnRNPL-LINC02273 complex to AGR2 promoter region epigenetically upregulated AGR2 by augmenting local H3K4me3 and H3K27ac levels. Our findings uncover a key role of LINC02273-hnRNPL-AGR2 axis in breast cancer metastasis and provide potential novel therapeutic targets for metastatic breast cancer intervention. lncRNAs highly expressed in metastatic lymph nodes were identified by microarray. RNA pull-down and RIP assay were used to confirm the interaction of hnRNPL and LINC02273. Chromatin isolation by RNA purification followed by sequencing (ChIRP-seq), RNA-seq, ChIP-seq, and luciferase reporter assay reveal hnRNPL-LINC02273 regulates AGR2. We identified a novel long noncoding RNA LINC02273, whose expression was significantly elevated in metastatic lesions compared to the primary tumors, by genetic screen of matched tumor samples. Five GEO datasets were pooled (GSE6532, GSE9195, GSE19615, GSE17907, E_MTAB_365).	31856843	RID06954	epigenetic regulation	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE51827,GSE55807)
Breast cancer	HNRNPL	LINC02273	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;CHIP;shRNA	upregulation	RT-qPCR;microarray	GSE6532;GSE9195;GSE19615;GSE17907;E-MTAB-365	NA	cell metastasis(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000104824	NA	ENSG00000245954	GRCh38_4:152090459-152110157	3191	100996286	HNRPL	NA	LINC02273 drives breast cancer metastasis by epigenetically increasing AGR2 transcription.Mechanistically, hnRNPL-LINC02273 formed a complex which activated AGR2 transcription and promoted cancer metastasis. The recruitment of hnRNPL-LINC02273 complex to AGR2 promoter region epigenetically upregulated AGR2 by augmenting local H3K4me3 and H3K27ac levels. Our findings uncover a key role of LINC02273-hnRNPL-AGR2 axis in breast cancer metastasis and provide potential novel therapeutic targets for metastatic breast cancer intervention. lncRNAs highly expressed in metastatic lymph nodes were identified by microarray. RNA pull-down and RIP assay were used to confirm the interaction of hnRNPL and LINC02273. Chromatin isolation by RNA purification followed by sequencing (ChIRP-seq), RNA-seq, ChIP-seq, and luciferase reporter assay reveal hnRNPL-LINC02273 regulates AGR2. We identified a novel long noncoding RNA LINC02273, whose expression was significantly elevated in metastatic lesions compared to the primary tumors, by genetic screen of matched tumor samples. Five GEO datasets were pooled (GSE6532, GSE9195, GSE19615, GSE17907, E_MTAB_365). To explore how LINC02273 promotes breast cancer metastasis, RNA pull-down assays were performed to identify the protein partners binding to LINC02273. To further examine which motif of hnRNPL interacts with LINC02273, we made hnRNPL truncation mutants and determined their capacity to bind LINC02273 with RNA pull-down assay.	31856843	RID06955	interact with protein	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	HCP5	SOX4	positively-E	dual-luciferase reporter assay;starBase	upregulation	RT-qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell proliferation(+);cell migration(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000124766	NA	10866	6659	D6S2650E|P5-1	NA	Long Non-Coding RNA HCP5 Facilitates Cell Invasion And Epithelial-Mesenchymal Transition In Oral Squamous Cell Carcinoma By miR-140-5p/SOX4 Axis.HCP5 expression was significantly increased in OSCC tissues and cell lines. High HCP5 level was associated with the aggressive clinicopathological characteristics and poor prognosis of OSCC patients. In vitro gain- and loss-of-function experiments showed that HCP5 overexpression promoted, whereas HCP5 knockdown inhibited the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of OSCC cells. Mechanistically, we confirmed that HCP5 might serve as a competitive endogenous RNA (ceRNA) for miR-140-5p. Through RT-qPCR analysis, we observed that, compared with adjacent normal tissues, HCP5 expression was remarkably increased in OSCC tissues. Through the Starbase online software (http://starbase.sysu.edu.cn/index.php), we searched for the potential target miRNAs of HCP5, and found that miR-140-5p had putative HCP5 binding sites. Then, dual-luciferase reporter assay was carried out to further verify the bioinformatical prediction.	31849534	RID06956	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Melanoma	LINC00459	DKK3	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;miRcode	downregulation	RT-qPCR;microarray	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-218)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000229307	GRCh38_13:62323657-62328833	ENSG00000050165	NA	100874180	27122	NA	REIC|RIG	LINC00459 sponging miR-218 to elevate DKK3 inhibits proliferation and invasion in melanoma.Bioinformatics analyses suggested that miR-218 could be a direct target of LINC00459. In addition, miR-218 was proved to be able to directly target the dickkopf-related protein 3 (DKK3) gene. In conclusion, our analysis suggested that the LINC00459 could sponge miR-218 and increase the expression of DKK3 gene, thus inhibiting the invasion and proliferation of melanoma cells, which indicated that the LINC00459 could be an effective biomarker for melanoma and its potential as the therapeutic target. Significant decrease of lncRNALINC00459 in melanoma tissues. LINC00459 which on chromosome 13q21.31 with 2 exons was significantly decreased in melanoma tissues according to the result of microarray profiling. The RT-qPCR indicated that the LINC00459 expression in melanoma cell lines was significantly down-regulated comparing to that in human melanocytes cells. Based on the bioinformatics (miRcode http://www.mircode.org/), the reverse complementary recognition sequence of LINC00459 (target miRNA) was predicted, and the most relevant target miRNA has been screened out in the RNA pull-down analysis. Luciferase reporter assay of the pmirGLO-LINC00459-wt reporter vector indicated that the cells transfected with the reporter vector and miR-218 had significant lower luciferase activity compared to those transfected with miR-NC. Anti-AGO2 RIP assays showed that LINC00459 and miR-218 were more abundant in anti-AGO2 comparing with the anti-IgG immunoprecipitates.	31844121	RID06957	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	LOXL1-AS1	miR-143-3p	negatively-F	luciferase reporter assay;DIANA	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000261801	GRCh38_15:73908071-73928248	NA	NA	100287616	NA	NA	NA	LncRNA LOXL1-AS1 inhibited cell proliferation, migration and invasion as well as induced apoptosis in breast cancer via regulating miR-143-3p.Further investigation showed that silencing LOXL1-AS1 inhibited proliferation, promoted cell apoptosis and decreased the capacity of cell migrated and invasive in breast cancer cells. The analysis of luciferase reporter assay determined that LOXL1-AS1 directly targeted miR-143-3p in breast cancer cells. The rescue experiments further proved that miR-143-3p reversed the inhibited effects of si- LOXL1-AS1 on breast cancer cells.In this study, we verified that LncRNA LOXL1-AS1 inhibited cell proliferation, migration and invasion as well as induced apoptosis in breast cancer via regulating miR-143-3p, providing a novel therapeutic target and improving understanding of the regulatory mechanism of cell progression in breast cancer. The expression of LOXL1-AS1 and miR-143-3p was measured using qRT-PCR Luciferase reporter assay was applied to verify the relationship between LOXL1-AS1 and miR-143-3p.  In this study, we used Diana tool to predict the target miRNA of LOXL1-AS1 and the results showed that miR-143-3p has binding sites with LOXL1-AS1.	31841194	RID06958	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	
Breast cancer	GAS6-DT	FUT4	positively-E	luciferase reporter assay;starBase v3.0	upregulation	RT-qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-493)	regulation	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000272695	GRCh38_13:113864112-113866834	ENSG00000196371	NA	100506394	2526	FLJ44054|GAS6-AS2	CD15|ELFT|FCT3A|FUC-TIV	Long noncoding RNA GAS6-AS2 sponges microRNA-493, thereby enhancing the malignant characteristics of breast cancer cells via upregulation of FUT4.With regard to its mechanism, GAS6-AS2 acted as a competing endogenous RNA that sponged microRNA-493 (miR-493), thereby increasing the expression of fucosyltransferase IV (FUT4). Either miR-493 inhibition or FUT4 upregulation abrogated the consequences of GAS6-AS2 knockdown in BC cells. These results revealed that GAS6-AS2 sponges miR-493 to enhance the malignant characteristics of BC in vitro and in vivo by increasing FUT4 expression. GAS6-AS2 is overexpressed in BC tissues and cell lines. Total RNA was extracted from BC tissue samples and adjacent nontumorous tissues and used for the measurement of GAS6-AS2 expression by RT-qPCR. To test whether miR-493 can bind directly to GAS6-AS2, the luciferase reporter assay was performed on MCF-7 and MDA-MB-231 cells after cotransfection with either the miR-493 mimics or miR-NC and either GAS6-AS2-WT or GAS6-AS2-MUT. The RIP assay was conducted next to investigate the interaction between miR-493 and GAS6-AS2; the data showed that miR-493 and GAS6-AS2 were noticeably enriched on AGO2-bound beads compared with the IgG control (Fig. 3E, P < 0.05), suggesting that miR-493 could directly bind to GAS6-AS2 in BC cells. An miRNA that can bind to GAS6-AS2 was predicted using starBase v3.0	31839366	RID06959	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)
Gallbladder cancer	SSTR5-AS1	NONO	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE106671	NA	apoptosis process(-);chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	Gemcitabine	NA	Evading Apoptosis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000261713	GRCh38_16:1064087-1078731	ENSG00000147140	NA	146336	4841	NA	NMT55|NRB54|P54|P54NRB|PPP1R114	Long non-coding RNA SSTR5-AS1 facilitates gemcitabine resistance via stabilizing NONO in gallbladder carcinoma.Moreover, we found via streptavidin pull down assay that NONO specifically binds to sense sequence of SSTR5-AS1 and prevented proteasome mediated NONO degradation, which resulted in increased NONO protein level without affecting the transcription of NONO. NONO functions as the downstream effector of SSTR5-AS1 and is required for SSTR5-AS1 mediated gemcitabine resistance. SSTR5-AS1 is upregulated in GBC patients and gemcitabine-resistant GBC cells. SSTR5-AS1 directly interacts with NONO and prohibits proteasome mediated NONO degradation. To evaluate the role that lncRNAs plays in gemcitabine resistance in GBC, we first analyzed a Gene Expression Omnibus (GEO) dataset to identify differentially expressed lncRNAs in GBC (GSE106671).	31810606	RID06960	interact with protein	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Malignant glioma	PTENP1	PTEN	positively-E	luciferase reporter assay;TargetScan	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell growth(+)	ceRNA(miR-10a-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	psiPTEN|PTEN-rs|PTEN2|PTENpg1|PTH2	BZS|MHAM|MMAC1|PTEN1|TEP1	hUC-MSCs Secreted Exosomes Inhibit the Glioma Cell Progression Through PTENP1/miR-10a-5p/PTEN Pathway.Mechanistically, we identified that lncRNA PTENP1 could be packaged into exosome from hUC-MSCs, transferred to U87 cells, and then stabilized PTEN by binding miR-10a-5p competitively.Therefore, our data suggested that the exosomes from hUC-MSCs possess a higher anti-tumor capacity, at least partially, via regulating miR-10a-5p/PTEN signaling.  Thus, we first detected the expression of lncRNA PTENP1 in U87 cells af_x0002_ter treatment of hUC-MSCs derived exosomes by qRT-PCRassay.  Moreover, we found that the expression of lncRNA PTENP1 was apparently lower in tumor samples than that in normal tissues. We predicted by bioinformatic tools that miRNAs is a potential binding to lncBRM.  Among these miRNA candidates, we noticed five important miRNA, miR-10a-5p, miR-107, miR-let-7a-5p, miR-619-5p, and miR-6720-5p, which are predicted to directly target PTEN using TargetScan software. Then, the luciferase assays were performed to confirm whether miR-10a-5p interacts with lncRNA PTENP1 after co-transfecting these plasmids with miR-10a-5p mimics and miR-10a-5p inhibitor into U87 cells. LncRNA PTENP1/MiR-10a-5p/PTEN Cascades Contributed to the U87 Cell Growth.	31799671	RID06961	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Urinary bladder cancer	CASC15	miR-130b-3p	negatively-F	dual-luciferase reporter assay;DIANA	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	LncRNA CASC15 functions as an oncogene by sponging miR-130b-3p in bladder cancer. CASC15 expression was upregulated in BLCA tissue samples. Moreover, CASC15 downregulated the miR-130b-3p expression and promoted cell migration and invasion in BLCA in vitro. The rescue experiments also revealed that the inhibitory effects by the silence of CASC15 could be reversed through the inhibition of miR-130b-3p.CONCLUSIONS: Our study suggested a vital regulatory mechanism of CASC15 in BLCA, and the CASC15/miR-130b-3p axis might serve as a new therapeutic interventional target for BLCA patients. To determine the role of CASC15 in the tumorigenesis of BLCA, the RT-qPCR was performed to detect CASC15 expression in 56 patients'-tissues and 4 BLCA cell lines. Then, we used DIANA LncBASE Predicted v.2 (http://carolina.imis.athena-innovation.gr/diana_tools/web/index.php-r=lncbasev2%2Findex-pre_x0002_dicted) to predict the potential target microRNAs of CASC15. Furthermore, the results of the luciferase assay demonstrated that the luciferase activity was significantly reduced through the co-transfection of CASC15-WT and miR-130b-3p, while no significant changes of the luciferase activity were observed in the cells co-transfected CASC15-MUT and miR-130b-3p.	31799648	RID06962	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Osteosarcoma	TUG1	PFN2	positively-E	dual-luciferase reporter assay;starBase v2.0	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-140-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000070087	NA	55000	5217	FLJ20618|LINC00080|NCRNA00080	NA	Long non-coding RNA TUG1 regulates the progression and metastasis of osteosarcoma cells via miR-140-5p/PFN2 axis.Moreover, the dual-luciferase reporter assay was performed to verify the interrelation between miR-140-5p and TUG1 or PFN2.RESULTS: TUG1 and PFN2 levels were evidently upregulated in OS tissues and cell lines. The knockdown of either TUG1 or PFN2 could restrain cell proliferation, migration, and invasion in OS cells. In addition, miR-140-5p was a target of TUG1 to regulate PFN2. The functions of PFN2 knockdown in cell behaviors were rescued after co-transfection with either miR-140-5p inhibitor or overexpression vector of TUG1. Importantly, TUG1 silencing could impede tumor progression in vivo.CONCLUSIONS: TUG1 modulated cell proliferation, migration, and invasion via miR-140-5p/PFN2 axis in OS progression, which might trigger the development of therapeutic strategies for the treatment of OS. The levels of TUG1, microRNA-140-5p (miR-140-5p), and Profilin 2 (PFN2) were measured via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR, and the protein level of PNF2 was assessed using western blot. The prediction of starBase v2 indicated that miR-140-5p was a possible target of TUG1.	31799645	RID06963	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Lung cancer	LCAT1	RAC1	positively-E	dual-luciferase reporter assay;RIP;siRNA;miRanda;RegRNA2	upregulation	RT-qPCR	TCGA	NA	cancer progression(+);cell metastasis(+);cell proliferation(+)chemoresistance(+)	ceRNA(miR-4715-5p)	regulation	RNA-protein	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000136238	NA	NA	5879	NA	p21-Rac1|Rac-1|TC-25	Long noncoding RNA LCAT1 functions as a ceRNA to regulate RAC1 function by sponging miR-4715-5p in lung cancer.Mechanistically, LCAT1 functions as a competing endogenous RNA for miR-4715-5p, thereby leading to the upregulation of the activity of its endogenous target, Rac family small GTPase 1 (RAC1). To identify the role of lncRNAs in lung carcinogenesis, we first analyzed the RNA-seq data of 485 lung adenocarcinoma tissues and 56 adjacent normal tissues from TCGA. LCAT1 is upregulated in lung cancer and is associated with poor prognosis. To validate this observation, we quantified the expression level of LCAT1 in independent lung cancer samples using quantitative PCR (qPCR), which confirmed increased LCAT1 expression in lung cancer tissues compared to adjacent normal tissues. Furthermore, an immunoprecipitation assay for RNA binding protein in the A549 extracts revealed that LCAT1 binds to Ago2, a main component of the RNA-induced silencing complex that is involved in the miRNA-mediated repression of messenger RNA (mRNA). To test this hypothesis, we used two bioinformatics databases (miRanda and RegRNA2) to predict the potential interaction between miRNAs and LCAT1. We then prioritized these miRNAs according to their prediction score and free-energy, and chose the top four miRNAs (miR-23a-5p, miR-330-5p, miR-4715-5p and miR-4763-3p) for subsequent dual-luciferase reporter assays. LCAT1 promotes lung cancer cell proliferation and progression through sponging miR-4715-5p to regulate RAC1/PAK1 functions. Our data has demonstrated that genetic targeting of RAC1 by siRNA causes a significant reduction in cell proliferation and metastasis of lung cancer cells. The combination of EHop-016 and paclitaxel exhibited better efficacy than the respective monotherapy for treating lung cancer cells.	31779616	RID06964	ceRNA or sponge	metastasis,prognosis,chemoresistance		DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Esophagus squamous cell carcinoma	XLOC_001659	PIK3CA	positively-E	dual-luciferase reporter assay;bioinformatics	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-490-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	NA	NA	ENSG00000121879	NA	NA	5290	NA	PI3K	Knockdown of lncRNAXLOC_001659 inhibits proliferation and invasion of esophageal squamous cell carcinoma cells. Furthermore, lncRNAXLOC_001659 acts as an endogenous sponge by competitively binding to miR-490-5p to downregulate miR-490-5p. Further results confirmed that miR-490-5p targeted PIK3CA, and the recovery of PIK3CA rescued lncRNAXLOC_001659 knockdown or miR-490-5p overexpression-mediated inhibition of cell proliferation and invasion, which suggested the presence of an lncRNAXLOC_001659/miR-490-5p/PIK3CA regulatory axis.Knockdown of lncRNA XLOC_001659 inhibits proliferation and invasion of ESCC cells via regulation of miR-490-5p/PIK3CA, suggesting that it may play a role in ESCC tumorigenesis and progression. RT-qPCR assay was used to quantify the expression levels of lncRNAXLOC-001659 and miR-490-5p. dual-luciferase reporter assay was used to detect the target genes of lncRNAXLOC-001659 and miR-490-5p. The results of RT-qPCR showed that the expression of lncRNAXLOC_001659 was upregulated in ESCC cells. This study also performed extensive bioinformatics analysis on lncRNA XLOC_001659 to analyze miRNAs that may interact with lncRNA XLOC_001659.	31754291	RID06965	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Colorectal cancer	CASC21	YAP1	positively-E	dual-luciferase reporter assay;siRNA;LncBase v.2;starBase	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);epithelial to mesenchymal transition(+);cell viability(+);	ceRNA(miR-7-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000137693	NA	103021164	10413	CARLO2|CARLo-2|LINC01244	YAP65	Long noncoding RNA CASC21 exerts an oncogenic role in colorectal cancer through regulating miR-7-5p/YAP1 axis.Moreover, CASC21 knockdown displayed significant depression in cell viability, proliferation, migration, and invasion in colorectal cancer cells, as well as EMT process, while cell apoptosis was promoted by regulating the Bcl-2/Bax axis and Caspase cascade. Mechanistically, CASC21 could competently bind to miR-7-5p, resulting in increased YAP1 expression. Furthermore, up-regulation of YAP1 could rescue the inhibitory effects of CASC21 knockdown on EMT and cell invasion. Through the Gene Expression Profiling Interactive Analysis (GEPIA; http://gepia.cancer-pku.cn/), an online server derived from the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) dataset, we found that CASC21 expression was markedly higher in colorectal cancer tissues (n-=-275) than that in normal tissues (n-=-349), but compared with corresponding normal tissues, there was no significant difference in the expression of CASC21 in other tumor tissues, including hepatocellular carcinoma, non-small-cell lung cancer and gastric cancer. Expression of CASC21 in cells transfected with siRNAs was examined by RT-PCR In order to investigate the mechanism of CASC21, we predicted the potential miRNAs (miR-7-5p, miR-325, miR-449c-3p, miR-659-5p, and miR-922) that bind to CASC21 by bioinformatics analysis (LncBase Predicted v.2) [18]. As indicated in Fig. 4A, these miRNAs could both reduced the luciferase activity of CASC21, and the decrease caused by miR-7-5p was the most significant, indicating that miR-7-5p might bind to CASC21. The potential sites of miR-7-5p binding to CASC21 3'UTR predicted by Starbase were shown in the Fig. 4B.	31731190	RID06966	ceRNA or sponge	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Malignant glioma	FLVCR1-DT	E2F2	positively-E	dual-luciferase reporter assay;RIP;siRNA;miRDB	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+);colony formation(+)	ceRNA(miR-4731-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000198468	GRCh38_1:212852105-212858138	ENSG00000007968	NA	642946	1870	FLVCR1-AS1|LQK1|NCRNA00292	E2F-2	Long noncoding RNA FLVCR1-AS1 aggravates biological behaviors of glioma cells via targeting miR-4731-5p/E2F2 axis.Through bioinformatics analysis, we identified that FLVCR1-AS1 was a sponge for miR-4731-5p to upregulate E2F2 expression. Moreover, rescue assays indicated that FLVCR1-AS1 modulated E2F2 expression to participate in glioma progression. Altogether, our research demonstrates that the FLVCR1-AS1/miR-4731-5p/E2F2 axis is a novel signaling in glioma and may be a potential target for tumor therapy. We initially investigated the expression of FLVCR1-AS1 according to TCGA database. FLVCR1-AS1 was upregulated in glioma tissues. Then qRT-PCRwas conducted and confirmed that FLVCR1-AS1 was highly expressed in glioma tissues compared to normal tissues. Through bioinformatics analysis, we also found that FLVCR1-AS1 may be a potential sponge for miR-4731-5p. Luciferase reporter assay showed that FLVCR1-AS1-WT activity was inhibited by miR-4731-5p mimics in both U87 and U251-cells. RIP assay indicated that FLVCR1-AS1 and miR-4731-5p were enriched in anti-Ago2 group. Binding site of miR-4731-5p on FLVCR1-AS1 was analyzed using miRDB. We found that downregulation of FLVCR1-AS1 impeded proliferation, colony formation, migration and invasion of U87 and U251-cells (Fig. 4C ). However, restoration of E2F2 abrogated the effects mediated by FLVCR1-AS1 silencing.	31699367	RID06967	ceRNA or sponge	NA		UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Thyroid cancer	DUXAP9	MSI2	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;siRNA;RNAi;RNA22	upregulation	RT-qPCR;microarray	GSE66738; GSE97070	NA	cancer progression(+);cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-);AKT/STAT3 signaling pathway(+)	ceRNA(miR-143-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000153944	NA	503638	124540	FLJ39632|LINC01296|lncRNA-CTD903|LNMAT1	NA	Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer. LINC01296 was predicted to bind to miR-143-3p to modulate MSI2 expression, thus regulating the occurrence and development of TC. LINC01296 was up-regulated, while miR-143-3p was down-regulated in TC cells and tissues. LNC01296 specifically bound to miR-143-3p and MSI2 was a target of miR-143-3p. Besides, LINC01296 silencing or miR-143-3p overexpression inhibited migration, invasion, proliferation and advanced apoptosis of TC cells. Additionally, silenced LINC01296 or overexpressed miR-143-3p reduced phosphorylated STAT3/STAT3, phosphorylated AKT/AKT, B-cell lymphoma-2 (Bcl-2) and CyclinD1 levels but elevated BCL2-associated X (Bax), Cleaved Caspase3 and Caspase3 levels. Also, tumorigenesis of TC cells in nude mice was inhibited with the silencing of LINC01296. In summary, LINC01296/miR-143-3p/MSI2 axis regulated development of TC through the AKT/STAT3 signaling pathway. In order to determine whether LINC01296 played a role in TC, we predicted its binding site to miR-143-3p by using online prediction tool RNA22. Expression of LINC01296 and miR-143-3p in TC tissues and benign thyroid tumor tissues determined by RT-qPCR. LINC01296 silencing suppresses proliferation, invasion and migration and promotes apoptosis of TC cells. Silencing LINC01296 could impede the activation of the AKT/STAT3 signaling pathway via MSI2 through reducing its competitive binding to miR-143-3p. The expression box diagram of MSI2 in the GSE66738 microarray where the blue box on the left showed the expression of normal samples, and the red box on the right showed the expression of TC samples. The expression box diagram of miR-143-3p in the GSE97070 microarray where the blue box on the left showed the expression of normal samples, and the red box on the right showed the expression of TC samples.	31693087	RID06968	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE75367,GSE86978)
Gastric cancer	LINC00629	AQP4	positively-E	dual-luciferase reporter assay;RIP;RNA22;RNA pull-down	downregulation	RT-qPCR;microarray	GSE79973;GSE26595	NA	cancer progression(-);cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-196b-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227060	GRCh38_X:134549770-134560399	ENSG00000171885	NA	100506757	361	NA	MIWC	Long Noncoding RNA LINC00629 Restrains the Progression of Gastric Cancer by Upregulating AQP4 Through Competitively Binding to miR-196b-5p.In gastric cancer, expression of LINC00629 and AQP4 was downregulated, and expression of miR-196b-5p was upregulated. Proliferation, invasion, and migration of gastric cancer cells were reduced after overexpression of LINC00629. LINC00629 competitively bound to miR-196b-5p, while AQP4 was a target of miR-196b-5p. Either downregulating miR-196b-5p or upregulating AQP4 could restrain the development of gastric cancer in vitro. LINC00629 overexpression repressed the growth of transplanted tumors in vivo.  Initially, microarray-based gene expression profiling of gastric cancer was employed to identify differentially expressed genes. Through retrieval in GEO database, GSE79973 dataset was obtained and then underwent differential analysis, which showed a total of 1,767 differentially expressed genes were obtained. Moreover, the lower expression of LINC00629 in gastric cancer tissues relative to adjacent normal tissues was also confirmed by RT-qPCR. To further understand the potential mechanism of LINC00629 in gastric cancer, we retrieved GEO database and GSE26595 dataset, after which differential analysis was conducted and 41 differentially expressed miRNAs were harvested. Three miRNAs were found in the intersection between upregulated miRNAs in GSE26595 and putative miRNAs predicted by RNA22 database.  Further, dual-luciferase reporter gene assay, RIP assay along with RNA pull-down assay were carried out to verify the interaction between LINC00629 and miR-196b-5p.	31674022	RID06969	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	ARHGAP27P1	p15	positively-F	RIP	downregulation	RT-qPCR	NA	NA	cell cycle(-);cell proliferation(-);tumorigenesis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000086504	NA	146880	NA	NA	NA	Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16.We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. To explore the expression profile of ARHGAP27P1 in GC, we first detected ARHGAP27P1 expression levels in a cohort of 112 paired GC and adjacent noncancerous tissues by RT-qPCR. In addition, the expression of ARHGAP27P1 was downregulated in 64.3% (72/112) of GC tissues compared with that in the adjacent normal tissues. ARHGAP27P1 promoted expression of p15, p16 and p57. ARHGAP27P1 epigenetically activated p15, p16 and p57 transcription by binding to JMJD3. Therefore, we screened a panel of chromatin modifiers (JMJD3, EZH2, SMYD3, WDR5, KMT2C) that could potentially interact with lncRNAs by RIP experiments in SGC-7901 cells. Overexpression of ARHGAP27P1 inhibited GC tumorigenesis in vivo. We further found that the increase in association of ARHGAP27P1 with JMJD3 led to remarkable decrease in H3K27me3 levels, thereby promoting p15, p16 and p57 transcription.	31665700	RID06970	epigenetic regulation	NA		
Gastric cancer	ARHGAP27P1	p16	positively-F	RIP	downregulation	RT-qPCR	NA	NA	cell cycle(-);cell proliferation(-);tumorigenesis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000147889	NA	146880	NA	NA	NA	Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16.We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. To explore the expression profile of ARHGAP27P1 in GC, we first detected ARHGAP27P1 expression levels in a cohort of 112 paired GC and adjacent noncancerous tissues by RT-qPCR. In addition, the expression of ARHGAP27P1 was downregulated in 64.3% (72/112) of GC tissues compared with that in the adjacent normal tissues. ARHGAP27P1 promoted expression of p15, p16 and p57. ARHGAP27P1 epigenetically activated p15, p16 and p57 transcription by binding to JMJD3. Therefore, we screened a panel of chromatin modifiers (JMJD3, EZH2, SMYD3, WDR5, KMT2C) that could potentially interact with lncRNAs by RIP experiments in SGC-7901 cells. Overexpression of ARHGAP27P1 inhibited GC tumorigenesis in vivo. We further found that the increase in association of ARHGAP27P1 with JMJD3 led to remarkable decrease in H3K27me3 levels, thereby promoting p15, p16 and p57 transcription.	31665700	RID06971	epigenetic regulation	NA		
Gastric cancer	ARHGAP27P1	CDKN1C	positively-F	RIP	downregulation	RT-qPCR	NA	NA	cell cycle(-);cell proliferation(-);tumorigenesis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000129757	NA	146880	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16.We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. To explore the expression profile of ARHGAP27P1 in GC, we first detected ARHGAP27P1 expression levels in a cohort of 112 paired GC and adjacent noncancerous tissues by RT-qPCR. In addition, the expression of ARHGAP27P1 was downregulated in 64.3% (72/112) of GC tissues compared with that in the adjacent normal tissues. ARHGAP27P1 promoted expression of p15, p16 and p57. ARHGAP27P1 epigenetically activated p15, p16 and p57 transcription by binding to JMJD3. Therefore, we screened a panel of chromatin modifiers (JMJD3, EZH2, SMYD3, WDR5, KMT2C) that could potentially interact with lncRNAs by RIP experiments in SGC-7901 cells. Overexpression of ARHGAP27P1 inhibited GC tumorigenesis in vivo. We further found that the increase in association of ARHGAP27P1 with JMJD3 led to remarkable decrease in H3K27me3 levels, thereby promoting p15, p16 and p57 transcription.	31665700	RID06972	epigenetic regulation	NA		DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Cervical cancer	TP73-AS1	miR-329-3p	negatively-F	dual-luciferase reporter assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	NA	57212	NA	KIAA0495|PDAM	NA	Long Noncoding RNA TP73-AS1 Targets MicroRNA-329-3p to Regulate Expression of the SMAD2 Gene in Human Cervical Cancer Tissue and Cell Lines.LncRNA TP73-AS1 was overexpressed in cervical cancer tissues and cells and was associated with reduced expression of miR-329-3p. Down-regulation of lncRNA TP73-AS1 inhibited cell proliferation, migration and invasion and increased miR-329-3p expression. Expression of SMAD2 down-regulated miR-329-3p and was associated with increased expression of TP73-AS1. LncRNA TP73-AS1 knockdown resulted in miR-329-3p silencing. In tumor xenografts, expression of TP73-AS1 reduced the tumor volume and down-regulated the expression levels of the SMAD2 gene. Quantitative real-time polymerase chain reaction (qRT-PCR was used to determine the expression level of lncRNA TP73-AS1 in cervical cancer tissue and cells. In the study, data were included from the StarBase database, which showed that there was a binding site between lncRNA TP73-AS1 and miR-329-3p. The findings from the RNA immunoprecipitation assay (RIPA) showed that the expression of the Ago2-miR-329-3p complex in the Ago2 group was more than that in the IgG group, and that the relative expression of lncRNA TP73-AS1 in the Ago2 group was higher than that in the IgG group, indicating that lncRNA TP73-AS1 could target miR-329-3p. Figure 3C shows that luciferase activity of the miR-329-3p mimic and the TP73-AS1-WT co-transfection group was significantly reduced (p<0.001), and that of the TP73-AS1-MUT group was unchanged. LncRNA TP73-AS1 promoted cell proliferation by regulating miR-329-3p expression.	31663517	RID06973	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cervical cancer	TP73-AS1	SMAD2	positively-E	dual-luciferase reporter assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-329-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000175387	NA	57212	4087	KIAA0495|PDAM	JV18-1|MADH2|MADR2	Long Noncoding RNA TP73-AS1 Targets MicroRNA-329-3p to Regulate Expression of the SMAD2 Gene in Human Cervical Cancer Tissue and Cell Lines.LncRNA TP73-AS1 was overexpressed in cervical cancer tissues and cells and was associated with reduced expression of miR-329-3p. Down-regulation of lncRNA TP73-AS1 inhibited cell proliferation, migration and invasion and increased miR-329-3p expression. Expression of SMAD2 down-regulated miR-329-3p and was associated with increased expression of TP73-AS1. LncRNA TP73-AS1 knockdown resulted in miR-329-3p silencing. In tumor xenografts, expression of TP73-AS1 reduced the tumor volume and down-regulated the expression levels of the SMAD2 gene. Quantitative real-time polymerase chain reaction (qRT-PCR was used to determine the expression level of lncRNA TP73-AS1 in cervical cancer tissue and cells. In the study, data were included from the StarBase database, which showed that there was a binding site between lncRNA TP73-AS1 and miR-329-3p. The findings from the RNA immunoprecipitation assay (RIPA) showed that the expression of the Ago2-miR-329-3p complex in the Ago2 group was more than that in the IgG group, and that the relative expression of lncRNA TP73-AS1 in the Ago2 group was higher than that in the IgG group, indicating that lncRNA TP73-AS1 could target miR-329-3p. Figure 3C shows that luciferase activity of the miR-329-3p mimic and the TP73-AS1-WT co-transfection group was significantly reduced (p<0.001), and that of the TP73-AS1-MUT group was unchanged. LncRNA TP73-AS1 promoted cell proliferation by regulating miR-329-3p expression.	31663517	RID06974	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	BCYRN1	miR-204-5p	negatively-E	luciferase reporter assay;siRNA;LncBase v.2	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell cycle(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000236824	GRCh38_2:47335315-47335514	NA	NA	618	NA	BC200|BC200a|LINC00004|NCRNA00004	NA	BCYRN1 is correlated with progression and prognosis in gastric cancer.In lncRNA-microRNA interactome database, we found that there were putative binding sites between BCYRN1 and miR-204-5p. Furthermore, we confirmed that down-regulation of BCYRN1 inhibited GC cell proliferation, migration and invasion through directly up-regulated miR-204-5p expression. In conclusion, BCYRN1 acts as a promising prognostic predictor in GC patients and regulated GC cell proliferation, cell cycle, migration and invasion through targeting miR-204-5p. At first, we analyzed the The Cancer Genome Atlas (TCGA) database to determine whether BCYRN1 is dysregulated in GC. We observed that BCYRN1 expression was obviously higher in GC tissues than in the adjacent normal tissues in TCGA database. Furthermore, we performed qRT-PCRto confirm the expression of BCYRN1 between GC tissues and the adjacent normal tissues. In LncBase predicted v.2 of DIANA tools, we found miR-204-5p was the predicted target of BCYRN1. For exploring the relationship between miR-204-5p and BCYRN1, we conducted the luciferase reporter assay. In addition, we observed that there was a negative correlation between BCYRN1 and miR-204-5p in GC tissues. Our data showed transfection of miR-204-5p mimics obviously decreased the luciferase activity of wt-BCYRN1 (P<0.001, Figure 3C) whereas miR-204-5p inhibitor dramatically increases the luciferase activity of wt-BCYRN1 in GC cells (P<0.001, Figure 3C), which indicated that BCYRN1 was directly bound to miR-204-5p. Down-regulation of BCYRN1 inhibited GC cell proliferation, cell-cycle arrest, migration and invasion through directly up-regulated miR-204-5p expression.	31652309	RID06975	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	
Prostate cancer	SNHG4	ZIC5	positively-E	luciferase reporter assay;starBase	upregulation	qRT-PCR;microarray	TCGA;GSE21036	NA	cancer progression(+);cell metastasis(+);cell growth(+)	ceRNA(miR-377)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000139800	NA	724102	85416	NCRNA00059|U19H	NA	SP1-mediated upregulation of lncRNA SNHG4 functions as a ceRNA for miR-377 to facilitate prostate cancer progression through regulation of ZIC5.SNHG4 was highly expressed in PCa and its upregulation was induced by transcription factor SP1.SNHG4 knockdown inhibited the growth, migration, and invasion of PCa cells. In addition, miR-377 was a target of SNHG4 and ZIC5 was a target gene of miR-377 in PCa. SNHG4 promoted ZIC5-mediated growth and metastasis through modulating miR-377. Quantitative real-time polymerase chain reaction (qRT-PCR was utilized to detect SNHG4 expression in tissue samples and PCa cells. In order to screen dysregulated lncRNAs in PCa, we downloaded microarray data from The Cancer Genome Atlas (TCGA) datasets and R software was used for the analysis of above data. To demonstrate the above results, we performed RT-PCRfor the examination of SNHG4 levels in 113 pair surgical specimens of PCa tissues and their matched normal tissues. We thereby performed bioinformatics computation using public Gene Expression Omnibus datasets (GSE21036) to find the miRNAs, which were significantly downregulated in PCa specimens. Among these aberrantly downregulated miRNAs, we selected miR-377, which was reported as a tumor suppresser in multiple types of cancers, for further research, because we found that four of its predicted target lncRNAs (using "Starbase'-algorithm) including SNHG4, ZNF-252P-AS1, NEAT1, and VPS9D1-AS1, were also highly expressed in PCasamples using TCGA data set analyses. . Furthermore, we also conducted luciferase activity detection assays to further certify that miR-377 was a target of SNHG4.	31608997	RID06976	ceRNA or sponge	metastasis	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Prostate cancer	SP1	SNHG4	positively-E	JASPAP;ChIP;siRNA;luciferase reporter assay	upregulation	qRT-PCR;microarray	TCGA;GSE21037	NA	cancer progression(+);cell metastasis(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000281398	GRCh38_5:139274102-139284899	6667	724102	NA	NCRNA00059|U19H	SP1-mediated upregulation of lncRNA SNHG4 functions as a ceRNA for miR-377 to facilitate prostate cancer progression through regulation of ZIC5.SNHG4 was highly expressed in PCa and its upregulation was induced by transcription factor SP1.SNHG4 knockdown inhibited the growth, migration, and invasion of PCa cells. In addition, miR-377 was a target of SNHG4 and ZIC5 was a target gene of miR-377 in PCa. SNHG4 promoted ZIC5-mediated growth and metastasis through modulating miR-377. Quantitative real-time polymerase chain reaction (qRT-PCR was utilized to detect SNHG4 expression in tissue samples and PCa cells. In order to screen dysregulated lncRNAs in PCa, we downloaded microarray data from The Cancer Genome Atlas (TCGA) datasets and R software was used for the analysis of above data. To demonstrate the above results, we performed RT-PCRfor the examination of SNHG4 levels in 113 pair surgical specimens of PCa tissues and their matched normal tissues. Furthermore, we carried out ChIP analyses to certify which region in the SNHG4 promoter was the exact binding site of SP1. We thereby searched JASPAR algorithm and found that there were three high-score binding sites of SP1, which were involved in regulating diverse cellular processes, distributing in the promoter of SNHG4. To further certify that, we first synthesized SP1 siRNA (si-SP1) and cloned pcDNA3.1-SP1, which were capable to enhance SP1 expression.  For further clarifying that, we cloned wild-type or mutant type B1 site into luciferase reporter vector and subsequently detected the changes of luciferase activities.	31608997	RID06977	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)
Non-small cell lung cancer	GATA2-AS1	GATA1	positively-E	RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000244300	GRCh38_3:128489212-128502970	ENSG00000102145	NA	101927167	2623	NA	ERYF1|GATA-1|GF1|NF-E1|NFE1	A MYC target long non-coding RNA GATA2-AS1 regulates non-small cell lung cancer growth.GATA2-AS1 gene is located at antisense strand of GATA2 on chromosome while GATA2-AS1 RNA interacts with GATA1 protein at promoter region of GATA2 and then inhibits its transcription. Moreover, GATA2-AS1 is transcriptionally repressed by MYC in NSCLC cells. As GATA1 was reported to bind to GATA2 promoter and repress its transcription, we performed RNA immunoprecipitation (RIP) assays to demonstrate that ectopically expressed GATA1 was able to interact with GATA2-AS1. To further study the role of GATA2-AS1 after binding to GATA1 and FOG1, we carried out chromatin immunoprecipitation (ChIP) assay using GATA1 antibody. GATA2-AS1 inhibits NSCLC cells proliferation via GATA2. GATA2-AS1 is expressed at a lower level in cancer tissues. Total RNA of samples from cancer or adjacent normal tissues of NSCLC patients were extracted and analyzed by qPCR	31607132	RID06978	interact with protein	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE75367,GSE41245)
Non-small cell lung cancer	MYC	GATA2-AS1	negatively-E	ChIP	downregulation	qRT-PCR	NA	NA	cell growth(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000244300	GRCh38_3:128489212-128502970	4609	101927167	bHLHe39|c-Myc|MYCC	NA	A MYC target long non-coding RNA GATA2-AS1 regulates non-small cell lung cancer growth.GATA2-AS1 gene is located at antisense strand of GATA2 on chromosome while GATA2-AS1 RNA interacts with GATA1 protein at promoter region of GATA2 and then inhibits its transcription. Moreover, GATA2-AS1 is transcriptionally repressed by MYC in NSCLC cells. . To identify which region of the GATA2-AS1 promoter is bound and thus repressed by MYC, we employed an anti-MYC antibody and performed ChIP assay. GATA2-AS1 is expressed at a lower level in cancer tissues. Total RNA of samples from cancer or adjacent normal tissues of NSCLC patients were extracted and analyzed by qPCR	31607132	RID06979	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Cervical cancer	CRNDE	CCNB1	positively-E	dual-luciferase reporter assay;miRcode;starBase;DEmiRNA	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell growth(+);apoptosis process(-)	ceRNA(miR-183)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000134057	NA	643911	891	CRNDEP|LINC00180|LOC643911	CCNB	LncRNA CRNDE acts as an oncogene in cervical cancer through sponging miR-183 to regulate CCNB1 expression.Their expressions were up-regulated in CC tissues and cells. Silencing CRNDE-inhibited cell proliferation, migration and invasion, restricted solid tumor growth and promoted cell apoptosis. Moreover, our results suggested that miR-183 targeted the CCNB1 3'UTR and regulated its expression. Additionally, miR-183 mimic could inverse the antitumor function of CRNDE inhibition and partially eliminated the attenuated expression of CCNB1 induced by silencing CRNDE, indicating that CRNDE could positively regulate CCNB1 expression by sponging miR-183. Our study highlighted a role for the CRNDE/miR-183/CCNB1-axis in CC and offered a promising diagnostic strategy for CC treatment. TCGA database was used to download related information about CC. Combining miRode and starBase, we identified 231-paired lncRNA-siRNA interactions with CC specific. miRNA acts as a bridge communication between lncRNA and mRNA. Related data about miRNA-target genes were downloaded from miRcode (http://www.mircode.org/) and starBase v3.0 (http://starbase.sysu.edu.cn/agoClipRNA.php-source=lncRNA). Meanwhile, CC-specific DElncRNA EmiRNA interactions were selected. On the other hand, mRNA genes associated with DEmiRNA were downloaded from miRTarBase (http://mirtarbase.mbc.nctu.edu.tw/php/index.php).	31605132	RID06980	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE55807)
Oral squamous cell carcinoma	CCAT1	miR-181a	negatively-E	dual-luciferase reporter assay;RIP;shRMA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+);cell growth(+)	interact with miR;transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1 is a prognostic biomarker for the progression of oral squamous cell carcinoma via miR-181a-mediated Wnt/beta-catenin signaling pathway.Then dual luciferase reporter and RIP assays were utilized to study the interaction between CCAT1 and miR-181a. Cells transfected with sh-CCAT1 or treated with miR-181a inhibitor were subjected to western blot to investigate the role of Wnt/beta-catenin signaling in CCAT1-mediated proliferation and metastasis.  Knockdown of CCAT1 inhibited the proliferation, migration and invasion of OSCC cells, while the cell apoptosis was enhanced. Luciferase and RIP assays revealed that miR-181a was a direct target of CCAT1. Inhibition of miR-181a partially reversed the efficacy of sh-CCAT1. Moreover, sh-CCAT1 inhibited OSCC tissues growth through inhibiting Wnt signaling in a miR-181a-dependent manner in vivo. lncRNA CCAT1 activated Wnt/beta-catenin signaling via inhibiting miR-181a, resulting in the cell proliferation, migration and invasion of OSCC, suggesting that CCAT1 might serve as a potential target of OSCC treatment. CCAT1 was highly expressed in OSCC. The level of CCAT1 was assayed using qPCR in OSCC tissues and the paired normal tissues. Since we found CCAT1 directly binds to miR-181a, the regulation of CCAT1 in combination with miR-181a was investigated. CCAT1 promoted the tumor growth via miR-181a in vivo. Inhibiting miR-181a promoted the activation of Wnt signaling, resulting in enhanced tumor growth.	31599709	RID06981	transcriptional regulation	metastasis,prognosis		
Hepatocellular carcinoma	DUXAP10	GPR39	positively-E	luciferase reporter assay;TargetScan;miRDB;starBase v2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell cycle(+);PI3K/AKT signaling pathway(+);apoptosis process(-)	ceRNA(miR-1914)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257227	NA	ENSG00000183840	NA	503639	2863	NA	NA	microRNA-1914, which is regulated by lncRNA DUXAP10, inhibits cell proliferation by targeting the GPR39-mediated PI3K/AKT/mTOR pathway in HCC.Furthermore, the overexpression of lncRNA DUXAP10 negatively correlated with the expression of miR-1914 in HCC; thus, lncRNA DUXAP10 regulated miR-1914 expression and modulated the GPR39/PI3K/AKT-mediated cellular behaviours. In summary, the present study demonstrated for the first time that lncRNA DUXAP10-regulated miR-1914 plays a functional role in inhibiting HCC progression by targeting GPR39-mediated PI3K/AKT/mTOR pathway, and this miRNA represents a novel therapeutic target for patients with HCC. Target algorithms (TargetScan, miRDB and StarBase v2.0) were utilized to uncover potential targets of miR-1914. GPR39 was the predicted target. To verify this, we examined the mRNA and protein levels of GPR39 by qRT-PCRand WB assays and demonstrated that miR-1914 significantly inversely regulated GPR39 expression. Similarly, a dual-luciferase reporter assay showed that enhanced miR-1914 expression effectively suppressed the relative luciferase activity of wild-type (wt) GPR39 but not that of mutant (mt) GPR39. To better elucidate the underlying mechanism by which miR-1914 was depressed in HCC, we predicted the potential targets using Starbase v2.0 and discovered that lncRNA DUXAP10 is a molecular sponge that may regulate miR-1914. First, we used the GEO database to show that DUXAP10 was obviously higher in HCC samples than in normal liver tissues, and we confirmed that DUXAP10 was higher in HCC tissues than in neighbouring non-tumour tissue. Thus, the data showed that GPR39 was a functional target of miR-1914 in HCC. Conversely, DUXAP10 overexpression promoted cell proliferation, colony formation, cell cycle progression and PI3K/AKT signalling and inhibited apoptosis in Hep3B cells.	31576658	RID06982	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE55807)	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Malignant glioma	HOXC-AS2	ZEB1	positively-E	dual-luciferase reporter assay;RIP;CHIP;DIANA;Targetscan	upregulation	qRT-PCR	TCGA;CGGA	NA	epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+);	ceRNA(miR-876-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000250133	GRCh38_12:53993810-53996785	ENSG00000148516	NA	100874364	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Positive feedback loop of lncRNA HOXC-AS2/miR-876-5p/ZEB1 to regulate EMT in glioma.Depletion of HOXC-AS2 was associated with the inhibition of migration, invasion and EMT process in glioma cells. Mechanism, HOXC-AS2 can sponge miR-876-5p to affect ZEB1 expression. Meanwhile, ZEB1 can bind promoter region of HOXC-AS2 and regulate HOXC-AS2 at transcriptional level.Our results conclude that HOXC-AS2/miR-876-5p/ZEB1 constitutes a positive feedback loop to regulate EMT in GBM, providing a potential therapeutic target for glioma. LncRNA expression and survival data in glioma were downloaded from The Cancer Genome Atlas (TCGA) dataset (http://cancergenome.nih.gov). By using qRT-PCR we found that high-grade glioma (HGG) tissues had higher HOXC-AS2 level than low-grade glioma (LGG). HOXC-AS2 is upregulated in glioma tissues and cells. By using DIANA database (http://diana.imis.athena-innovation.gr/), we predicted potential target miRNA for HOXC-AS2 and we focus on a miR-876-5p which had been considered as a cancer suppressor gene in osteosarcoma18 and hepatocellular carcinoma. Then, we analyzed the expression of miR-876-5p in CGGA database and the result showed that miR-876-5p was downregulated in glioma (Figure S1C), consistent with previous reports. To confirm our prediction, we performed a dual-luciferase reporter assay to confirm that miR-876-5p binds directly to HOXC-AS2. We used RNA-binding protein immunoprecipitation (RIP) assay to better characterize the relation between HOXC-AS2 and miR-876-5p. Based on ceRNA hypothesis, we used bioinformatic website (Targetscan, http://www.targetscan.org/) and found that ZEB1 is a potential target of miR-876-5p. We performed chromatin immunoprecipitation assay (CHIP) to elucidate the binding of ZEB1 and HOXC-AS2 promoter region. Overexpressed ZEB1 then in turn up-regulates the expression of HOXC-AS2, which constitute a positive feedback loop and enhance migration, invasion and EMT program in glioma.	31571911	RID06983	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	FBXL19-AS1	miR-203a-3p	negatively-E	dual-luciferase reporter assay;miRcode;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000260852	GRCh38_16:30919319-30923269	NA	NA	283932	NA	MGC125469|MGC125470|MGC125472|NCRNA00095	NA	Long Noncoding RNA FBXL19-AS1 Induces Tumor Growth and Metastasis by Sponging miR-203a-3p in Lung Adenocarcinoma.FBXL19-AS1 was significantly upregulated in LUAD tissues and high FBXL19-AS1 expression in LUAD was associated with a poor prognosis.FBXL19-AS1 knockdown could arrest LUAD cells in G0/G1 phase and inhibit cell proliferation, migration and invasion in vitro and inhibited LUAD tumor progress in vivo. FBXL19-AS1 could act as a miR-203a-3p sponge. In addition,downregulation of miR-203a-3p reversed growth inhibition of LUAD cells caused by FBXL19-AS1 knockdown.FBXL19-AS1/miR-203a-3p axis was found to associate with baculoviral IAP repeat-containing protein 5.1-A-like (survivin), distal-less homeobox 5, E2F transcription factor 1, and zinc finger E-box binding homeobox 2 to regulate metastasis in LUAD cells. qRT-PCRwas performed to detect different expression levels of RNA transcripts. It  reasonable to speculate that FBXL19-AS1 could regulate proliferation and metastasis of LUAD cells by sponging miR-203a-3p to modulate expressions of several cancer-related genes.  Dual-luciferase assay was performed after cell transfection to determine the binding sites of miR-203a-3p and FBXL19-AS1. Furthermore, the metastasis-related targeting genes were preliminarily screened via miRanda algorithms (www.microrna.org) and TargetScan tool (www.targetscan.org).	31566718	RID06984	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	
Breast cancer	LINC01133	SOX4	negatively-E	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell metastasis(-)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124766	NA	100505633	6659	lncRNA-PAGBC	NA	LINC01133 inhibits breast cancer invasion and metastasis by negatively regulating SOX4 expression through EZH2.Mechanistic investigations revealed that LINC01133 repressed SOX4 expression by recruiting EZH2 to SOX4 promoter. Moreover, rescue experiments further confirmed that LINC01133 functional acted as an anti-oncogene, at least partly, via repressing SOX4 in breast cancer. The expression of LINC01133 was examined in 74 human breast cancer tissues and adjacent normal tissues using qRT-PCRwith normalization to GAPDH. LINC01133 expression is down-regulated in human breast tissues and correlated with lymph node metastasis and advanced TNM stage. In order to test this hypothesis, the antibody against EZH2 which was widely acknowledged as an important subunit of the PRC2 complex was adopted to perform RIP assay.  Furthermore, we performed RNA pull-down analysis to explore the interaction between EZH2 and LINC01133. And then, to further confirm whether LINC01133 inhibited SOX4 transcription by recruiting EZH2 to SOX4 promoter region, we designed SOX4 primers to the promoter region and conducted ChIP assays in LINC01133-overexpression MDA-MB-231 cells.	31557401	RID06985	ceRNA or sponge	metastasis	UP(BRCA);DATA(GSE111065)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Osteosarcoma	LINC-ROR	ABCB1	positively-E	StarBase v2.0;dual-luciferase reporter assay;miRcode	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-153-3p)	regulation	RNA-protein	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000085563	NA	100885779	5243	lincRNA-RoR|lincRNA-ST8SIA3|ROR	ABC20|CD243|CLCS|GP170|MDR1|p-170|P-gp|PGY1	Long non-coding RNA ROR regulated ABCB1 to induce cisplatin resistance in osteosarcoma by sponging miR-153-3p.MiRcode Tools and StarBase v2.0 predicted that miR-153-3p had complementary sequences with ROR and ABCB1 3'UTR, and following dual-luciferase reporter assay validated that miR-153-3p was a direct target of ROR and ABCB1. Moreover, ABCB1 overexpression alleviated the inhibitory effects on cell viability in different concentrations of DDP, cell proliferative capacity, migrated cells, and invaded cells in MG63/DDP and U2OS/DDP cells transfected with sh-ROR. ROR regulated ABCB1 expression in MG63/DDP and U2OS/DDP cells by sponging miR-153-3p.CONCLUSIONS: We found that ROR or ABCB1 knockdown can increase the cisplatin sensitivity of MG63/DDP and U2OS/DDP cells. ROR contributed to cisplatin resistance in OS via miR-153-3p/ABCB1 axis, unraveling a new regulatory network of chemoresistance in cisplatin-resistant OS cells and may provide a therapeutic target for OS patients. The levels of ROR and ABCB1 were both drastically increased, and miR-153-3p was apparently decreased in relapsed OS tissues, MG63/DDP, and U2OS/DDP cells. The levels of ROR, miR-153-3p, and ABCB1 in cisplatin-resistant OS tissues and cells were detected by qRT-PCRand/or western blot assay.	31539112	RID06986	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Gastric cancer	MYOSLID	MCL1	positively-E	RIP;shRNA;Cancer RNA-Seq Nexus;luciferase reporter assay	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-29c-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229647	GRCh38_2:207166120-207248668	ENSG00000143384	NA	105373853	4170	NA	BCL2L3|Mcl-1	Long non-coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-29c-3p in gastric cancer.we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR-29c-3p. We found for the first time that the expression of lncRNA MYOSLID was significantly up-regulated in GC tissues, and the up-regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. To investigate the expression of lncRNA MYOSLID in human GC, we searched the Cancer Genome Atlas (TCGA) database and found that the lncRNA MYOSLID gene copy number was significantly elevated in GC tissues compared with normal gastric tissue. Then, the expression of lncRNA MYOSLID in GC tissues was detected by real-time PCR and found that the expression of lncRNA MYOSLID was higher in GC tissues than in matched non-tumour tissues. To further confirm this hypothesis, we used an online bioinformatics database (Cancer RNA-Seq Nexus database) to analyse predicted miRNAs that bind to the lncRNA MYOSLID sequence. As expected, the luciferase reporter assay showed that miR-29c-3p directly targets the 3'UTR of lncRNA MYOSLID-WT to negatively regulate the luciferase activity of lncRNA MYOSLID-wt-3'UTR, rather than lncRNA MYOSLID-MUT's 3'UTR. RIP experiments were performed in SGC-7901 and BGC-823 cells, and coprecipitated RNA was subjected to qRT-PCRfor lncRNA MYOSLID. In conclusion, we report a novel gastric cancer-associated lncRNA MYOSLID and first discovered that lncRNA MYOSLID is a carcinogenic lncRNA that promotes cell proliferation and inhibits apoptosis in human GC via the miR-29c-3p-MCL-1 axis.	31497917	RID06987	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SATB2-AS1	SATB2	positively-E	RIP;RNA pull-down assay;	downregulation	qRT-PCR	TCGA;GSE9348;GSE8671;GSE39582;GSE17538;GSE14333;GSE2109;GSE13294;GSE21510;GSE37892;GSE4459	NA	cell metastasis(-)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225953	GRCh38_2:199457697-199476935	ENSG00000119042	NA	150538	23314	NA	FLJ21474|KIAA1034	LncRNA SATB2-AS1 inhibits tumor metastasis and affects the tumor immune cell microenvironment in colorectal cancer by regulating SATB2. RNA pull-down, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), chromatin isolation by RNA purification (ChIRP), Bisulfite Sequencing PCR (BSP) and bioinformatics analysis were utilized to explore the potential mechanisms of SATB2-AS1. Mechanistically, SATB2-AS1 directly binds to WDR5 and GADD45A, cis-activating SATB2 (Special AT-rich binding protein 2) transcription via mediating histone H3 lysine 4 tri-methylation (H3K4me3) deposition and DNA demethylation of the promoter region of SATB2. CRC gene expression data were obtained from the TCGA and GEO database. The independent datasets from GSE9348 (Hong Colorectal) [8], GSE8671 (Marra Colorectal) [9], GSE39582 (Marisa Colorectal) [10], GSE17538 (Smith Colorectal) [11], GSE14333 (Sieber Colorectal) [12], GSE2109 (EXPO Colorectal), GSE13294 (Jorissen Colorectal) [13], GSE21510 (Sugihara Colorectal) [14], GSE37892 (Olschwang Colorectal) [15] and GSE4459 (Watanabe Colorectal) [16] were analyzed in this study. Colorectal tissue-specific lncRNA SATB2-AS1 is downregulated in CRC tissues and predicts a good prognosis. This result was confirmed by qRT-PCRanalysis of our CRC cohort and data analysis of other independent cohorts. SATB2-AS1 directly binds to WDR5 and GADD45A. There were two specific bands in the SATB2-AS1 pull-down samples, which were excised and subjected to mass spectrometry analysis. In addition, RIP assays performed with an anti-WDR5 antibody also revealed the interaction between WDR5 and SATB2-AS1. Collectively, these data demonstrate that SATB2-AS1 promoted SATB2 expression by modulating DNA demethylation and H3K4me3 enrichment of the SATB2 promoter by recruiting WDR5 and GADD45A protein. However, further studies need to be performed to identify the precise molecular mechanism by which SATB2 mediates metastasis and the immune response in CRC.	31492160	RID06988	epigenetic regulation	metastasis,prognosis		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Gastric cancer	AWPPH	DKK2	positively-E	luciferase reporter assay;starBase v2.0	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-203a)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000155011	NA	NA	27123	NA	NA	Up-regulation of long non-coding RNA AWPPH inhibits proliferation and invasion of gastric cancer cells via miR-203a/DKK2 axis.Bioinformatics tool was employed to predict AWPPH's sponging miRNA, while luciferase reporter assays were used to verify the target. LncRNA AWPPH was remarkably downregulated in GC and associated with metastasis. MiR-203a was a predicted and further verified target of AWPPH. DKK2 was verified as a direct target of miR-203a. Upregulation of miR-203a attenuated the repressive effects of AWPPH on GC cell proliferation and invasion. AWPPH inhibited GC cell proliferation and invasion via miR-203a/DKK2 axis. To study the expression pattern of LncRNA-AWPPH in GC, qRT-PCRwas performed in 40 pairs of GC tissues and adjacent normal tissues. To further explore the underlining mechanism by which AWPPH regulates GC proliferation and invasion, the online bioinformatics tool StarBase v2.0 (http://starbase.sysu.edu.cn) was used to identify potential miRNAs that could bind to AWPPH.	31489578	RID06989	ceRNA or sponge	metastasis		UP(PAAD);DATA(GSE40174)
Cervical cancer	ANKRD40CL	RGS17	positively-E	dual-luciferase reporter assay;TargetScan;miRDB;miR TarBase	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);apoptosis process(-);epithelial to mesenchymal transition(+);cell invasion(+);cell migration(+)	ceRNA(miR-508-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000091844	NA	55018	26575	C17orf73|FLJ20694|LINC00483	RGS-17|RGSZ2	Long non-coding RNA Linc00483 accelerated tumorigenesis of cervical cancer by regulating miR-508-3p/RGS17 axis. miR-508-3p was identified as the downstream target of Linc00483, and miR-508-3p inhibitor abrogated the inhibiting effects of downregulated Linc00483 on cervical cancer cell viability. Furthermore, the expression levels of Linc00483 was positively correlated with RGS17 in the clinical samples and overexpressed Linc00483 increased RGS17 expression levels in cervical cancer cells by sponging miR-508-3p. The in vivo experiments showed that knock-down of Linc00483 inhibited cervical cancer cell tumorigenesis and lung metastasis in mice models.Knock-down of Linc00483 inhibited the development of cervical cancer by regulating miR-508-3p/RGS17 axis. Real-Time qPCR was used to determine the expression levels of Linc00483, miR-508-3p and RGS17 mRNA in cervical cancer tissues and cell lines. Linc00483 aberrantly overexpressed in both cervical cancer tissues and cell lines comparing to the Control groups. Online software (TargetScan, miRDB and miR TarBase) were used to predict the regulating mechanisms of Linc00483, miR-508-3p and RGS17, which were validated by dual-luciferase reporter gene system. The above results indicated that Linc00483 promoted cervical cancer cell proliferation and inhibited cell apoptosis. The above results indicated that Linc00483 promoted epithelial-mesenchymal transition (EMT) of cervical cancer cells, and promoted cell invasion and migration.	31454494	RID06990	ceRNA or sponge	metastasis		UP(LIHC);DATA(GSE117623)
Glioblastoma	UPF1	Linc-00313	positively-F	dual-luciferase reporter assay;RIP;CHIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+)	RNA stability	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000005007	NA	NA	NA	5976	NA	HUPF1|NORF1|RENT1|UTF|pNORF1|smg-2	NA	UPF1 regulates the malignant biological behaviors of glioblastoma cells via enhancing the stability of Linc-00313.UPF1 and Linc-00313 were both upregulated in glioma tissues and cells. Knockdown of UPF1 or Linc-00313 significantly inhibited malignant biological behaviors of glioma cells by regulating miR-342-3p and miR-485-5p, which are downregulated and functioned as tumor suppressors in glioma. Furthermore, Linc-00313 could acted as a competing endogenous RNA(ceRNA) to regulate the expression of Zic4 by binding to miR-342-3p and miR-485-5p. Interestingly, Zic4 could bind to the promoters of UPF1 and Linc-00313 respectively and upregulate the expression of them. These results indicated that a positive-feedback loop was formed in the regulation of the biological behaviors of glioma cells. The study is the first to prove that the UPF1-Linc-00313-miR-342-3p/miR-485-5p-Zic4-SHCBP1 pathway forms a positive-feedback loop and regulates the biological behaviors of U87 and U251 cells, which might provide a new therapeutic target for glioma.Here, we used qRT-PCRand western blot to measure the expression, cell Transfection to disrupt the expression of genes, cell viability analysis, quantization of apoptosis, cell migration, and invasion assays, Reporter vectors construction and luciferase assays to investigate the malignant biological behaviors of cells, human lncRNA microarrays, RNA-Immunoprecipitation, dual-luciferase gene reporter assay, half-life assay and chromatin immunoprecipitation to verify the binding sites, tumor xenograft implantation for in vivo experiment, SPSS 18.0 statistical software for data statistics. UPF1 promoted the stability of Linc-00313 and regulated the biological behaviors of glioma cells. Furthermore, the TCGA database was used to predict the expression of Zic4. In summary, this study showed that UPF1 could bind to Linc-00313 and enhance its stability. Linc-00313 inhibited the negative regulation of miR-342-3p and miR-485-5p on their common downstream target gene Zic4, which further regulated the transcription and expression levels of SHCBP1.  In addition, SHCBP1 could regulate the biological behaviors of glioma cells by activating the MEK/ERK signaling pathway. At the same time, Zic4 could positively regulate the transcriptional expression of UPF1 and Linc-00313, thus formed a positive-feedback loop that regulated the biological behaviors of glioma cells.	31427569	RID06991	interact with mRNA	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Glioblastoma	Linc-00313	ZIC4	positively-E	dual-luciferase reporter assay;RIP;CHIP;starBase	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-342-3p/miR-485-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	NA	NA	ENSG00000174963	NA	NA	84107	NA	NA	UPF1 regulates the malignant biological behaviors of glioblastoma cells via enhancing the stability of Linc-00313.UPF1 and Linc-00313 were both upregulated in glioma tissues and cells. Knockdown of UPF1 or Linc-00313 significantly inhibited malignant biological behaviors of glioma cells by regulating miR-342-3p and miR-485-5p, which are downregulated and functioned as tumor suppressors in glioma. Furthermore, Linc-00313 could acted as a competing endogenous RNA(ceRNA) to regulate the expression of Zic4 by binding to miR-342-3p and miR-485-5p. Interestingly, Zic4 could bind to the promoters of UPF1 and Linc-00313 respectively and upregulate the expression of them. These results indicated that a positive-feedback loop was formed in the regulation of the biological behaviors of glioma cells. The study is the first to prove that the UPF1-Linc-00313-miR-342-3p/miR-485-5p-Zic4-SHCBP1 pathway forms a positive-feedback loop and regulates the biological behaviors of U87 and U251 cells, which might provide a new therapeutic target for glioma.Here, we used qRT-PCRand western blot to measure the expression, cell Transfection to disrupt the expression of genes, cell viability analysis, quantization of apoptosis, cell migration, and invasion assays, Reporter vectors construction and luciferase assays to investigate the malignant biological behaviors of cells, human lncRNA microarrays, RNA-Immunoprecipitation, dual-luciferase gene reporter assay, half-life assay and chromatin immunoprecipitation to verify the binding sites, tumor xenograft implantation for in vivo experiment, SPSS 18.0 statistical software for data statistics. UPF1 promoted the stability of Linc-00313 and regulated the biological behaviors of glioma cells. Furthermore, the TCGA database was used to predict the expression of Zic4. In summary, this study showed that UPF1 could bind to Linc-00313 and enhance its stability. Linc-00313 inhibited the negative regulation of miR-342-3p and miR-485-5p on their common downstream target gene Zic4, which further regulated the transcription and expression levels of SHCBP1.  In addition, SHCBP1 could regulate the biological behaviors of glioma cells by activating the MEK/ERK signaling pathway. At the same time, Zic4 could positively regulate the transcriptional expression of UPF1 and Linc-00313, thus formed a positive-feedback loop that regulated the biological behaviors of glioma cells. The Starbase database was used to predict the binding sites of miR-342-3p, miR-485-5p with Linc-00313.	31427569	RID06992	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Glioblastoma	Linc-00313	SHCBP1	positively-E	JASPAP;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000171241	NA	NA	79801	NA	PAL	UPF1 regulates the malignant biological behaviors of glioblastoma cells via enhancing the stability of Linc-00313.UPF1 and Linc-00313 were both upregulated in glioma tissues and cells. Knockdown of UPF1 or Linc-00313 significantly inhibited malignant biological behaviors of glioma cells by regulating miR-342-3p and miR-485-5p, which are downregulated and functioned as tumor suppressors in glioma. Furthermore, Linc-00313 could acted as a competing endogenous RNA(ceRNA) to regulate the expression of Zic4 by binding to miR-342-3p and miR-485-5p. Interestingly, Zic4 could bind to the promoters of UPF1 and Linc-00313 respectively and upregulate the expression of them. These results indicated that a positive-feedback loop was formed in the regulation of the biological behaviors of glioma cells. The study is the first to prove that the UPF1-Linc-00313-miR-342-3p/miR-485-5p-Zic4-SHCBP1 pathway forms a positive-feedback loop and regulates the biological behaviors of U87 and U251 cells, which might provide a new therapeutic target for glioma.Here, we used qRT-PCRand western blot to measure the expression, cell Transfection to disrupt the expression of genes, cell viability analysis, quantization of apoptosis, cell migration, and invasion assays, Reporter vectors construction and luciferase assays to investigate the malignant biological behaviors of cells, human lncRNA microarrays, RNA-Immunoprecipitation, dual-luciferase gene reporter assay, half-life assay and chromatin immunoprecipitation to verify the binding sites, tumor xenograft implantation for in vivo experiment, SPSS 18.0 statistical software for data statistics. UPF1 promoted the stability of Linc-00313 and regulated the biological behaviors of glioma cells. Furthermore, the TCGA database was used to predict the expression of Zic4. In summary, this study showed that UPF1 could bind to Linc-00313 and enhance its stability. Linc-00313 inhibited the negative regulation of miR-342-3p and miR-485-5p on their common downstream target gene Zic4, which further regulated the transcription and expression levels of SHCBP1.  In addition, SHCBP1 could regulate the biological behaviors of glioma cells by activating the MEK/ERK signaling pathway. At the same time, Zic4 could positively regulate the transcriptional expression of UPF1 and Linc-00313, thus formed a positive-feedback loop that regulated the biological behaviors of glioma cells. The Starbase database was used to predict the binding sites of miR-342-3p, miR-485-5p with Linc-00313. The overexpression of SHCBP1 could promote the cell proliferation, migration, and invasion of U87 and U251 cells, and inhibit cell apoptosis. Silence of SHCBP1 had the opposite effect. The JASPAR CORE database was used to predict the Zic4 binding sites in the promoter region of SHCBP1. ChIP experiments were performed to demonstrate that Zic4 could bind to the SHCBP1 promoter region and regulate its transcription. It showed that Zic4 could regulate SHCBP1 at the transcriptional level. The simultaneous overexpression of Zic4 and miR-342-3p or miR-485-5p could mediate the effects on SHCBP1 expression caused by the overexpression of miR-342-3p, miR-485-5p, or Zic4 alone. These results suggested that the overexpression of miR-342-3p or miR-485-5p enhanced the negatively regulation of Zic4, which could reduce the transcription and expression of the Zic4 downstream target gene SHCBP1.	31427569	RID06993	transcriptional regulation	NA		UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842,GSE67939)
Clear cell renal cell carcinoma	ADAMTS9-AS2	FOXO1	positively-E	dual-luciferase reporter assay;RIP;LncBase v.2;BIBIServ2;RNA pull-down;DIANA;TargetScan	downregulation	qRT-PCR	NA	NA	cell proliferation(-);chemoresistance(-)	ceRNA(miR-27a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000150907	NA	100507098	2308	NA	FKH1|FKHR|FOXO1A	LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis.Both overexpressed ADAMTS9-AS2 and underexpressed miR-27a-3p in ccRCC cell lines led to the inhibition of cell proliferation and the reduction of chemoresistance. Additionally, Forkhead Box Protein O1 (FOXO1) was confirmed as the inhibitory target of miR-27a-3p. Induced by ADAMTS9-AS2 overexpression, cell proliferation and chemoresistance exhibited an obvious reduction, FOXO1 expression showed an evident increase, but all were reversed after miR-27a-3p was simultaneously overexpressed. ADAMTS9-AS2 was clearly downregulated in ccRCC clinical samples and cell lines. ADAMTS9-AS2 showed lower levels of expression in ccRCC tissues than in normal adjacent tissues, as analyzed by quantitative real-time polymerase chain reaction (qRT-PCR. Next, miR-27a-3p was identified as an inhibitory target of ADAMTS9-AS2 by dual-luciferase reporter and RNA immunoprecipitation assays. To assess whether ADAMTS9-AS2 was associated with RISC, a RNA immunoprecipitation (RIP) assay was performed using antibodies against human Ago2. In addition, we identified miR-27a-3p as a potential target of ADAMTS9-AS2, according to LncBase Predicted v.2 and BiBiServ2. The pull-down assay was carried out to further investigate whether ADAMTS9-AS2 and miR-27a-3p were binding partners. Two publicly available algorithms (DIANA TOOLS and TargetScan) were used to identify the potential targets of miR-27a-3p.	31400752	RID06994	ceRNA or sponge	chemoresistance	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Oesophageal cancer	HOTAIR	MIR204	negatively-F	dual-luciferase reporter assay;RNA pull-down assay;RIP;siRNA;miRcode;miRTarBase	upregulation	RT-qPCR	TCGA	NA	cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oesophageal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000207935	NA	100124700	406987	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MIRN204|RDICC|miRNA204|mir-204	Down-regulation of long non-coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up-regulation of microRNA-204.miR-204 was down-regulated, while HOTAIR and HOXC8 were up-regulated in the oesophageal cancer tissues. HOTAIR could competitively bind to miR-204 and miR-204 could further target HOXC8. The oesophageal cancer cells treated with si-HOTAIR or miR-204 mimic exhibited decreased expression levels of HOXC8, Vimentin and MMP-9, but increased E-cadherin level. Silenced HOTAIR or elevated miR-204 inhibited proliferation, migration and invasion, along with stimulated apoptosis of oesophageal cancer cells. In summary, our results show that lncRNA HOTAIR could specifically bind to miR-204 as a competing endogenous RNA and regulate miR-204 and HOXC8. The TCGA database revealed that the expression of HOTAIR and HOXC8 were up-regulated in the oesophageal cancer tissues while the expression of miR-204 was down-regulated. Analysis of the miRcode and miRTarBae websites revealed that HOTAIR could potentially interact with miR-204 and consequently regulate the expression of HOXC8 and interleukin-11 (IL-11). Luciferase activity determination further verified the interaction between miR-204 and HOTAIR or HOXC8. RNA pull-down as well as RIP assays was performed in an attempt to further verify the interaction among HOTAIR, miR-204 and HOXC8.	31389660	RID06995	ceRNA or sponge	NA		
Oesophageal cancer	HOTAIR	HOXC8	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;siRNA;miRcode;miRTarBase	upregulation	RT-qPCR	TCGA	NA	cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oesophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000037965	NA	100124700	3224	HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX3|HOX3A	Down-regulation of long non-coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up-regulation of microRNA-204.miR-204 was down-regulated, while HOTAIR and HOXC8 were up-regulated in the oesophageal cancer tissues. HOTAIR could competitively bind to miR-204 and miR-204 could further target HOXC8. The oesophageal cancer cells treated with si-HOTAIR or miR-204 mimic exhibited decreased expression levels of HOXC8, Vimentin and MMP-9, but increased E-cadherin level. Silenced HOTAIR or elevated miR-204 inhibited proliferation, migration and invasion, along with stimulated apoptosis of oesophageal cancer cells. In summary, our results show that lncRNA HOTAIR could specifically bind to miR-204 as a competing endogenous RNA and regulate miR-204 and HOXC8. The TCGA database revealed that the expression of HOTAIR and HOXC8 were up-regulated in the oesophageal cancer tissues while the expression of miR-204 was down-regulated. Analysis of the miRcode and miRTarBae websites revealed that HOTAIR could potentially interact with miR-204 and consequently regulate the expression of HOXC8 and interleukin-11 (IL-11). Luciferase activity determination further verified the interaction between miR-204 and HOTAIR or HOXC8. RNA pull-down as well as RIP assays was performed in an attempt to further verify the interaction among HOTAIR, miR-204 and HOXC8.	31389660	RID06996	ceRNA or sponge	NA		
Osteosarcoma	DLEU1	DDX5	positively-E	dual-luciferase reporter assay;starBase;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-671-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000263077	NA	10301	1655	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	G17P1|HLR1|p68	Further mechanistic analysis and functional assays demonstrated that DLEU1 exerted its role by sponging microRNA (miR)-671-5p in osteosarcoma cells. Moreover, DEAD-box helicase 5 (DDX5) was confirmed as the target of miR-671-5p. Furthermore, rescue assays indicated that miR-671-5p inhibitor significantly reversed the effects of DLEU1 knockdown on osteosarcoma cell proliferation and invasion while restoration of DDX5 rescued the proliferation and invasion of osteosarcoma cells transfected with miR-671-5p mimics. In conclusion, DLEU1 acted as an oncogene in osteosarcoma by directly sponging miR-671-5p and regulating the expression of DDX5. The target miRNA of DLEU1 and the target gene of miR-671-5p were predicted using bioinformatics online softwares starBase (http://starbase.sysu.edu.cn/index.php) and TargetScan (http://www.targetscan.org/vert_71/). The qRT-PCRanalysis was performed to examine the expression levels of DLEU1 in 50 paired osteosarcoma tissues and adjacent non-tumour tissues. The results showed that DLEU1 was frequently up-regulated in osteosarcoma tissues as compared to the adjacent non-tumour tissues. dual-luciferase reporter assay was performed to explore the relation between DLEU1 and miR-671-5p.	31379208	RID06997	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	ZFAS1	miR-193a-3p	negatively-F	luciferase reporter assay;DIANA	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 acts as an oncogene by targeting miR-193a-3p in human non-small cell lung cancer.ZFAS1 expression was significantly higher in NSCLC samples relative to adjacent tissues. The proliferation of NSCLC cells was inhibited by silence of ZFAS1, and conversely, ZFAS2 overexpression promoted the proliferative ability. Further experiments showed that miR-193a-3p was directly targeted by ZFAS1.CONCLUSIONS: ZFAS1 could enhance cell growth ability of NSCLC by targeting miR-193a-3p, suggesting that ZFAS1 may be a potential therapeutic target in NSCLC. ZFAS1 expression in NSCLC patients was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. DIANA LncBASE Predicted v.2 (http://carolina.imis.athena-innovation.gr/diana_tools/web/index.php-r=lncbasev2%2Findex-predicted) was used to search for the miRNAs which contained complementary base with ZFAS1.  Furthermore, the dual-luciferase reporter gene assay revealed that co-transfection of ZFAS1-WT and miR-193a_x0002_3p mimics largely decreased the luciferase activity, while the co-transfection of ZFAS1-MUT and miR-193a-3p had no effect on the luciferase activity. Meanwhile, correlation analysis demonstrated that miR-193a-3p expression level was negatively correlated to ZFAS1 expression in NSCLC tissues.	31378891	RID06998	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Gastric cancer	PCAT1	ZEB1	positively-E	luciferase reporter assay;siRNA;starBase v3.0	upregulation	qRT-PCR	TCGA	NA	chemoresistance(+)	ceRNA(miR-128)	regulation	NA	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000148516	NA	100750225	6935	PCA1|PCAT-1|PiHL	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	PCAT-1 contributes to cisplatin resistance in gastric cancer through miR-128/ZEB1 axis.Knockdown of PCAT-1 facilitated the sensitivity of DDP-resistant GC cells to DDP. Additionally, PCAT-1 functioned as a sponge of miR-128 in GC cells. Moreover, inhibition of miR-128 reversed the inductive effect of PCAT-1 knockdown on DDP sensitivity of GC cells. In addition, ZEB1 was identified as a target of miR-128, and overexpression of ZEB1 could block the inductive effect of PCAT-1 knockdown on DDP sensitivity of GC cells. Besides, PCAT-1 knockdown enhanced DDP sensitivity in tumors in vivo. In summary, PCAT-1 confers DDP resistance in GC cells through miR-128/ZEB1 axis, providing a promising therapeutic strategy for GC. To analyze the different lncRNA expression in GC tumor and normal tissues, we downloaded the normalized RNA-seq data of Stomach Adenocarcinoma (STAD) from TCGA data portal. To verify the result from the databases, qRT-PCRanalysis was conducted to measure PCAT-1 expression in 38 pair tumor and adjacent normal tissues. Starbase3.0 predicts that the sequence of PCAT-1 harbors a binding site of miR-128. To identify whether PCAT-1 acts as a sponge of miR-128 in GC cells, luciferase reporter assay was performed in BGC823/DDP and SGC7901/DDP cells.	31352238	RID06999	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	PTTG3P	CCND1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;miRCODE	upregulation	qPCR	GSE76427;GSE84402	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);tumor growth(+);OI3K/AKT signaling pathway(+)	ceRNA(miR-383)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000213005	GRCh38_8:66767400-66768005	ENSG00000110092	NA	26255	595	PTTG3	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA PTTG3P functions as an oncogene by sponging miR-383 and up-regulating CCND1 and PARP2 in hepatocellular carcinoma.In this study, we found that PTTG3P was up-regulated in HCC tissues and cells. Functional experiments demonstrated that knockdown of PTTG3P inhibited cell proliferation, migration and invasion, and promoted cell apoptosis, acting as an oncogene. Mechanistically, PTTG3P upregulated the expression of miR-383 targets Cyclin D1 (CCND1) and poly ADP-ribose polymerase 2 (PARP2) by sponging miR-383, acting as a competing endogenous RNA (ceRNA). The PTTG3P-miR-383-CCND1/PARP2 axis modulated HCC phenotypes. Moreover, PTTG3P also affected the PI3K/Akt signaling pathway. Firstly, we analyzed the profiles of HCC patients from the Gene Expression Omnibus (GEO) (GSE 76427 and GSE 84402 dataset), and found that PTTG3P was up-regulated in HCC tissues compared to adjacent non-tumor tissues. A total of 50 paired HCC tissues were evaluated for PTTG3P expression using qPCR. Knockdown of PTTG3P inhibits HCC tumor growth in vivo. Using the bioinformatics algorithms miRCODE (http://mircode.org/), we found that there existed potential interactions between PTTG3P and miR-383. Luciferase reporter assay was performed to determine the interaction between PTTG3P and miR-383. RNA pull-down assay demonstrated that PTTG3P was more enriched in miR-383 compared to that in mutant miR-383 with broken PTTG3P binding site. In addition, RIP assay indicated that both PTTG3P and miR-383 were enriched in Ago2-containg miRNA ribonucleoprotein complexes compared to IgG immunoprecipitates. In line with the findings in the above stidues, our data showed that knockdown of CCND1 and PARP2 suppressed the phophorylation of PI3K and Akt, similar to that of PTTG3P knockdown, while miR-383 inhibition can restore the inhibitory effects of PTTG3P knockdown on OI3K/Akt pathway. PTTG3P acted as an oncogenic lncRNA to promote HCC development through upregulating CCND1 and PARP2 as well as PI3K/Akt pathway via sponging miR-383.	31340767	RID07000	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	PTTG3P	PARP2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;miRCODE	upregulation	qPCR	GSE76427;GSE84402	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);tumor growth(+);OI3K/AKT signaling pathway(+)	ceRNA(miR-383)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000213005	GRCh38_8:66767400-66768005	ENSG00000129484	NA	26255	10038	PTTG3	ADPRTL2|ARTD2	Long non-coding RNA PTTG3P functions as an oncogene by sponging miR-383 and up-regulating CCND1 and PARP2 in hepatocellular carcinoma.In this study, we found that PTTG3P was up-regulated in HCC tissues and cells. Functional experiments demonstrated that knockdown of PTTG3P inhibited cell proliferation, migration and invasion, and promoted cell apoptosis, acting as an oncogene. Mechanistically, PTTG3P upregulated the expression of miR-383 targets Cyclin D1 (CCND1) and poly ADP-ribose polymerase 2 (PARP2) by sponging miR-383, acting as a competing endogenous RNA (ceRNA). The PTTG3P-miR-383-CCND1/PARP2 axis modulated HCC phenotypes. Moreover, PTTG3P also affected the PI3K/Akt signaling pathway. Firstly, we analyzed the profiles of HCC patients from the Gene Expression Omnibus (GEO) (GSE 76427 and GSE 84402 dataset), and found that PTTG3P was up-regulated in HCC tissues compared to adjacent non-tumor tissues. A total of 50 paired HCC tissues were evaluated for PTTG3P expression using qPCR. Knockdown of PTTG3P inhibits HCC tumor growth in vivo. Using the bioinformatics algorithms miRCODE (http://mircode.org/), we found that there existed potential interactions between PTTG3P and miR-383. Luciferase reporter assay was performed to determine the interaction between PTTG3P and miR-383. RNA pull-down assay demonstrated that PTTG3P was more enriched in miR-383 compared to that in mutant miR-383 with broken PTTG3P binding site. In addition, RIP assay indicated that both PTTG3P and miR-383 were enriched in Ago2-containg miRNA ribonucleoprotein complexes compared to IgG immunoprecipitates. In line with the findings in the above stidues, our data showed that knockdown of CCND1 and PARP2 suppressed the phophorylation of PI3K and Akt, similar to that of PTTG3P knockdown, while miR-383 inhibition can restore the inhibitory effects of PTTG3P knockdown on OI3K/Akt pathway. PTTG3P acted as an oncogenic lncRNA to promote HCC development through upregulating CCND1 and PARP2 as well as PI3K/Akt pathway via sponging miR-383.	31340767	RID07001	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Hepatocellular carcinoma	SNHG1	PDCD4	positively-E	dual-luciferase reporter assay;RIP;RegRNA;starBase;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000150593	NA	23642	27250	LINC00057|lncRNA16|NCRNA00057|UHG	H731	Long non-coding RNA SNHG1 functions as a competitive endogenous RNA to regulate PDCD4 expression by sponging miR-195-5p in hepatocellular carcinoma.We identified the potential target of SNHG1 through bioinformatics and dual-luciferase reporter gene. Furthermore, western blot and RIP assay was used for clarifying their interaction and functions in regulating the development of hepatocellular carcinoma. Our results indicated a high expression of SNHG1 in hepatocellular carcinoma cells. Downregulation of SNHG1 inhibited proliferative and migratory potentials of hepatocellular carcinoma cells in vitro and in vivo. Moreover, the expression of programmed cell death 4 (PDCD4) was positively regulated by SNHG1 through competing with miR-195-5p. These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression. qRT-PCRwas used for detecting the SNHG1 expression in hepatocellular carcinoma cells (Li-7, HuH7, HHCC, H-97, Hep3b, SMMC-7721) and human normal liver cells HL-7702. RegRNA and Starbase prediction showed that sequences in miR-195-5p were highly matched to SNHG1 3'UTR.  Luciferase activity was obviously downregulated in H-97 and HuH7 cells co-transfected with SNHG1 WT and miR-195-5p mimics, while it remained unchanged after transfection with SNHG1 MUT (Fig. 2D). RIP analysis was carried out to elucidate whether SNHG1 was involved in RNA-containing ribonucleoprotein complex. To investigate the potential role of miR-195-5p in the development of hepatocellular carcinoma, the target genes of miR-195-5p were screened out by bioinformatics prediction (TargetScan, Starbase, RegRNA).	31330233	RID07002	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Renal cell carcinoma	TUG1	VEGFA	positively-E	dual-luciferase reporter assay;shRNA;siRNA;overexpression;miRDB	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);tumorigenesis(+)	ceRNA(miR-299-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Knockdown of TUG1 by shRNA inhibited renal cell carcinoma formation by miR-299-3p/VEGF axis in vitro and in vivo.TUG1 overexpression (LV-TUG1) significantly inhibited the expression of miR-299-3p, whereas sh-TUG1 showed the opposite effect. dual-luciferase reporter assay further confirmed the targeting relationship between TUG1 and miR-299-3p. In addition, vascular endothelial growth factor (VEGFA) is a target of miR-299-3p. Knockdown of VEGFA (si-VEGFA) significantly inhibited the proliferation and motility of ACHN cells, and induced apoptosis. RT-qPCR results showed that sh-TUG1 similarly inhibited VEGFA expression. Further functional analysis indicated that sh-TUG1 inhibited tumorigenesis by down-regulating VEGFA levels. However, LV-TUG1 showed the opposite effects. These results indicate that sh-TUG1 inhibited renal cell carcinoma formation by miR-299-3p/VEGF axis in vitro and in vivo. RT-qPCR results showed that sh-TUG1 similarly inhibited VEGFA expression. The regulation of miR-299 by TUG1 was investigated by RT-qPCR and dual-luciferase reporter assay. miRDB analysis indicated that miR-299 is the target of TUG1, and knockdown of TUG1 significantly increased miR-299 levels, whereas miR-299 inhibitor had the opposite effect. However, overexpression of TUG1 significantly reduced the level of miR-299, while miR-299 showed the opposite effect. The targeting relationship of TUG1 and miR-299 was further confirmed by luciferase reporter assay. sh-TUG1 inhibited proliferation and induced apoptosis of ACHN cells and OS-RC-2-cells. sh-TUG1 suppressed invasion, migration and epithelial-mesenchymal transition (EMT) of ACHN cells and OS-RC-2-cells. sh-TUG1 restrained cell growth and motility by sponging miR-299 to downregulate VEGF level in ACHN cells. sh-TUG1 inhibited tumor formation by miR-299/VEGFA axis in vivo.	31310753	RID07003	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Acute myeloid leukemia	LINC00662	miR-340-5p	negatively-F	luciferase reporter assay;RNA pull-down assay;bioinformatics	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	High expression of long intergenic non-coding RNA LINC00662 contributes to malignant growth of acute myeloid leukemia cells by upregulating ROCK1 via sponging microRNA-340-5p.LINC00662 was significantly increased in AML tissues and cell lines. Knockdown of LINC00662 significantly reduced the growth of AML cells and upregulated AML cell apoptosis. In contrast, overexpression of LINC00662 promoted AML cell growth. MicroRNA-340-5p (miR-340-5p) was predicted as a target of LINC00662. Luciferase reporter assays and RNA pull-down assays confirmed that LINC00662 directly interacted with miR-340-5p. Expression of miR-340-5p was downregulated in AML and silencing of LINC00662 upregulated miR-340-5p expression in AML cells. Moreover, overexpression of miR-340-5p inhibited cell growth and increased apoptosis in AML cells. Inhibition of miR-340-5p significantly reversed the inhibitory effect of LINC00662 silencing on AML cell growth. In addition, Rho-associated protein kinase 1 (ROCK1) was verified as a target gene of miR-340-5p in AML cells. Restoration of ROCK1 expression partially reversed LINC00662 silencing or miR-340-5p overexpression-mediated inhibitory effect on AML cell growth. The RT-qPCR results demonstrate that LINC00662 expression was significantly upregulated in BM tissues from AML patients than that from normal controls. We therefore predicted the potential targeting miRNAs of LINC00662 by bioinformatics analysis. The RT-qPCR results demonstrate that LINC00662 expression was significantly upregulated in BM tissues from AML patients than that from normal controls.	31306637	RID07004	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Acute myeloid leukemia	LINC00662	ROCK1	positively-E	luciferase reporter assay;RNA pull-down assay;bioinformatics	upregulation	RT-qPCR	NA	NA	apoptosis process(-);cell growth(+)	ceRNA(miR-340-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000067900	NA	148189	6093	NA	p160ROCK	High expression of long intergenic non-coding RNA LINC00662 contributes to malignant growth of acute myeloid leukemia cells by upregulating ROCK1 via sponging microRNA-340-5p.LINC00662 was significantly increased in AML tissues and cell lines. Knockdown of LINC00662 significantly reduced the growth of AML cells and upregulated AML cell apoptosis. In contrast, overexpression of LINC00662 promoted AML cell growth. MicroRNA-340-5p (miR-340-5p) was predicted as a target of LINC00662. Luciferase reporter assays and RNA pull-down assays confirmed that LINC00662 directly interacted with miR-340-5p. Expression of miR-340-5p was downregulated in AML and silencing of LINC00662 upregulated miR-340-5p expression in AML cells. Moreover, overexpression of miR-340-5p inhibited cell growth and increased apoptosis in AML cells. Inhibition of miR-340-5p significantly reversed the inhibitory effect of LINC00662 silencing on AML cell growth. In addition, Rho-associated protein kinase 1 (ROCK1) was verified as a target gene of miR-340-5p in AML cells. Restoration of ROCK1 expression partially reversed LINC00662 silencing or miR-340-5p overexpression-mediated inhibitory effect on AML cell growth. The RT-qPCR results demonstrate that LINC00662 expression was significantly upregulated in BM tissues from AML patients than that from normal controls. We therefore predicted the potential targeting miRNAs of LINC00662 by bioinformatics analysis. The RT-qPCR results demonstrate that LINC00662 expression was significantly upregulated in BM tissues from AML patients than that from normal controls.	31306637	RID07005	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	LUCAT1	TCF7L2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;mirDB;RNA hybrid;DIANA;TargetScan	upregulation	microarray;qRT-PCR	TCGA	NA	cell growth(+);WNT/beta-catenin signaling pathway(+);cell stemness(+)	ceRNA(miR-5582-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000148737	NA	100505994	6934	SCAL1|SCAT5	TCF-4|TCF4	Long non-coding RNA LUCAT1/miR-5582-3p/TCF7L2 axis regulates breast cancer stemness via Wnt/beta-catenin pathway. LUCAT1 up-regulation promoted proliferation of BCCs, while LUCAT1 down-regulation inhibited self-renewal of BCSCs. MiR-5582-3p was directly bound to LUCAT1 and TCF7L2 and negatively regulated their expression. LUCAT1 affected Wnt/beta-catenin pathway.LUCAT1 might be a significant biomarker to evaluate prognosis in breast cancer. LUCAT1 increased stem-like properties of BCCs and stemness of BCSCs by competitively binding miR-5582-3p with TCF7L2 and enhancing the Wnt/beta-catenin pathway. Gene expression was downloaded from TCGA-BRCA. LUCAT1 is over-expressed in the BCSCs than BCCs and related to breast cancer stemness. To investigate differentially expressed lncRNAs between BCCs and BCSCs, we performed lncRNA microarray chips. To elucidate whether LUCAT1 functioned as a ceRNA in regulating BC stemness, we used mirDB (http://www.mirdb.org/) and RNA hybrid (https://bibiserv.cebitec.uni-bielefeld.de/rnahybrid/) to predict potential target microRNA of LUCAT1. To confirm the binding function of genes, we performed dual luciferase gene reporter assay. Moreover, RNA pull-down assay manifested that miR-5582-3p was more enriched in the wild-type LUCAT1 compared with that in the mutant-type LUCAT1. To predict the target mRNA of miR-5582-3p, we used RNAhybrid, DIANA (http://diana.imis.athena-innovation.gr/DianaTools/index.php) and Targetscan (http://www.targetscan.org/vert_72/). In the present study, LUCAT1 had a possible role in promoting BCCs stem-like properties and BCSCs stemness in vitro and in vivo.	31300015	RID07006	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)
Colorectal cancer	ZFAS1	miR-7-5p	negatively-F	luciferase reporter assay;bioinformatics	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cancer progression(+);cel invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long Non-coding RNA Zinc Finger Antisense 1 (ZFAS1) Regulates Proliferation, Migration, Invasion, and Apoptosis by Targeting MiR-7-5p in Colorectal Cancer.the relationship between ZFAS1 and miR-7-5p was verified by luciferase reporter assay.  It was verified that miR-7-5p was a direct target of ZFAS1 by bioinformatics analysis and luciferase reporter assay. In addition, knockdown of miR-7-5p inhibited proliferation, migration, and invasion, and promoted apoptosis in CRC cell lines, which could be rescue by miR-7-5p inhibitor.Our study indicated that ZFAS1 directly targeted miR-7-5p, and knockdown of it could inhibit tumor growth, migration, invasion, and induce apoptosis in CRC. Firstly, we analyzed ZFAS1 expression in 40 CRC tissues and adjacent tissues by RT-PCR Our results showed that ZFAS1 was upregulated in CRC tissues. Inhibition of ZFAS1 suppressed proliferation, invasion, and migration, and promoted apoptosis of CRC in vitro	31295229	RID07007	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Colorectal cancer	SNHG14	EPHA7	negatively-E	luciferase reporter assay;RNA pull-down assay;RIP;CHIP;starBase 2.0	upregulation	qRT-PCR	NA	NA	cell migration(+);cell growth(+)	ceRNA(miR-186-5p);transcriptional regulation;methylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000135333	NA	104472715	2045	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	Hek11	Long noncoding RNA SNHG14 facilitates colorectal cancer metastasis through targeting EZH2-regulated EPHA7. the mechanistic investigations confirmed that SNHG14-promoted CRC progression was mediated by EPHA7, which was negatively regulated by SNHG14 in CRC via an EZH2-dependent way. Importantly, EZH2 was proved as a transcription factor of EPHA7 and functioned as a repressor in EPHA7 transcription by enhancing methylation on EPHA7 promoter. Meanwhile, SNHG14 increased EZH2 expression in CRC via stabilizing its mRNA by interacting with FUS, and via freeing its mRNA from miR-186-5p-induced silence. All in all, our observations demonstrated that SNHG14 serves as a facilitator in CRC through targeting EZH2-repressed EPHA7 by enhancing EZH2 via recruiting FUS and absorbing miR-186-5p, indicating a promising new road for CRC diagnosis and treatment. SNHG14 is highly expressed and facilitates malignant phenotypes in CRC cells. Importantly, the expression level of EPHA7 was pronouncedly enhanced by SNHG14 silence but sharply diminished under SNHG14 overexpression (Fig. -(Fig.3d),3d), implying a negative regulation of SNHG14 on EPHA7 in CRC. Altogether, these results explained that EZH2 negatively modulates EPHA7 transcription by promoting methylation on EPHA7 promoter. SNHG14 stabilizes EZH2 mRNA through recruiting FUS. The starBase 2.0 (http://starbase.sysu.edu.cn/starbase2/index.php) predicted that FUS was the shared RBP that interacted with both SNHG14 and EZH2 mRNA. First of all, the RIP assays confirmed that both SNHG14 and EZH2 were dramatically harvested by FUS in LoVo and HT-29 cells.	31273190	RID07008	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	UP(LIHC);DATA(GSE117623)
Malignant glioma	ZFAS1	miR-432-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell viability(+);chemoresistance(+)	sponge	binding/interaction	RNA-RNA	Cisplatin	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	ZFAS1 knockdown inhibits viability and enhances cisplatin cytotoxicity by up-regulating miR-432-5p in glioma cells.The association between ZFAS1 and miR-432-5p was confirmed using luciferase reporter and RNA pull-down assays.Zinc finger antisense 1 expression was up-regulated, while miR-432-5p expression was down-regulated in both glioma tissues and cells. Knockdown of ZFAS1 and miR-432-5p overexpression inhibited cell viability and enhanced the chemosensitivity of glioma cells to cisplatin. MiR-432-5p was a direct target of ZFAS1 in glioma cells. Inhibition of miR-432-5p blocked the effects of ZFAS1 knockdown on cell viability and cisplatin sensitivity.Knockdown of ZFAS1 inhibited the viability and enhanced cisplatin sensitivity via targeting miR-432-5p in glioma cells. Firstly, we evaluated the expression level of ZFAS1 in glioma tissues and adjacent normal tissues using RT-qPCR.	31246330	RID07009	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Colorectal cancer	ATB	CDK2	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell viability(+)	ceRNA(miR-200c)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000123374	NA	NA	1017	NA	NA	Regulatory effects of lncRNA ATB targeting miR-200c on proliferation and apoptosis of colorectal cancer cells.The results of Cox regression analyses suggested that overexpressed lncRNA ATB, underexpressed miR-200c, poor tumor differentiation, lymph-vascular invasion, and perineural invasion were symbolic of shortened survival of the patients with CRC (all P < .05). Besides, transfection of pcDNA3.1-ATB and miR-200c inhibitor could boost the viability and proliferation of Lovo and SW620 cell lines (all P < .05). Meanwhile, the expressions of p53 and p21 were also reduced under treatments of pcDNA3.1-ATB and miR-200c inhibitor (P < .05). In addition, CDK2 seemed to reverse the contribution of miR-200c to intensifying viability and proliferation of Lovo and SW420 cell lines (P < .05). Furthermore, ATB might downregulate miR-200c expression by targeting it (P < .05), and CDK2 was subjected to dual regulation of both ATB and miR-200c (P < .05).  Eventually, the Luciferase reporter gene assay was carried out to judge if there existed a targeted relationship between ATB and miR-200c. Among the recruited patients with CRC, their CRC tissues exhibited higher ATB expression and lower miR-200c expression than adjacent nontumor tissues. Summing up the above, this investigation was advantageous in constructing a molecular axis, namely, lncRNA ATB/miR-200c/CDK2 signaling, that could partly explain the intensified proliferation and prohib_x0002_ited apoptosis of CRC cells, which potentially contributed to poor prognosis of patients with CRC.	31222825	RID07010	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	HAND2-AS1	BCL2L11	positively-E	dual-luciferase reporter assay;RNA pull down;overexpression	downregulation	qRT-PCR	GSE38666;TCGA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+)	ceRNA(miR-340-5p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000153094	NA	79804	10018	DEIN|FLJ11539|NBLA00301	BIM|BimEL|BimL|BimS|BOD	LncRNA HAND2-AS1 exerts anti-oncogenic effects on ovarian cancer via restoration of BCL2L11 as a sponge of microRNA-340-5p.HAND2-AS1 specifically sponged with miR-340-5p which was found to directly target BCL2L11. Importantly, HAND2-AS1 or BCL2L11 overexpression or miR-340-5p downregulation resulted in reduction of cell invasion and migration, together with decrease of cell proliferation and increase of cell apoptosis in OC. Besides, high-expressed HAND2-AS1 inhibited the tumorigenesis in nude mice. To sum up, these data suggests HAND2-AS1 as an anti-oncogene in OC through upregulation of BCL2L11 by competitively binding to miR-340-5p, which demonstrates that there are potential diagnosis and therapy values of HAND2-AS1 in OC. In silico analysis displayed poor expression of HAND2-AS1 in OC. HAND2-AS1 specifically sponged with miR-340-5p which was found to directly target BCL2L11. Through the analysis for microarray data GSE38666, lower expres_x0002_sion of HAND2-AS1 was identified in OC in the GSE38666 chip relative to normal controls. The expression of HAND2-AS1 in OC tissues compared with the normal ovarian tissues in the TCGA database from the GEPIA website.  Dual luciferase reporter gene assay also testified the binding relationship between HAND2-AS1 and miR-340-5p. The results of RNA-pull down assay (Figure 5e) suggested a significant increase of miR-340-5p enrichment in Bio-HAND2-AS1-WT relative to Bio-probe NC (p < .05), but the treatment of bio-HAND2-AS1-MUT and the treatment of Bio-probe NC shared no obvious difference (p > .05). To further explore the association between HAND2-AS1 and miR-340-5p, HAND2-AS1-specific siRNA (si-HAND2-AS1) and overexpression (oe-HAND2-AS1) methods were used.	31222748	RID07011	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	C1QTNF1-AS1	SOCS3	positively-E	dual-luciferase reporter assay;TargetScan 7.1	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);apoptosis process(+);JAK/STAT signaling pathway(-)	ceRNA(miR-221-3p)	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000265096	GRCh38_17:79018131-79027673	ENSG00000184557	NA	100507410	9021	NA	CIS3|Cish3|SOCS-3|SSI-3	Potential of C1QTNF1-AS1 regulation in human hepatocellular carcinoma. C1QTNF1-AS1 and SOCS3 was downregulated and miR-221-3p was upregulated in HCC tissues and cells. In HepG2 and Huh-7 cells, the overexpression of C1QTNF1-AS1 or SOCS3, and silencing of miR-221-3p inhibited proliferation, migration, invasion and JAK/STAT signaling pathway, while promoted cell apoptosis. The results of dual-luciferase assay indicated that C1QTNF1-AS1 regulated miR-221-3p and miR-221-3p targeted SOCS3 by directly binding. And the growth of HCC in vivo was impeded when C1QTNF1-AS1 was upregulated. Overexpression of C1QTNF1-AS1 could downregulate miR-221-3p thereby inhibited the proliferation, migration and invasion of HCC cells. The target miRNAs binding with C1QTNF1-AS1 and SOCS3, respectively, were predicted based on the analysis by TargetScan 7.1, the results were made into a intersection which includes miR-221-3p. The expression of C1QTNF1-AS1 was detected by RT-qPCR.	31222560	RID07012	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	LINC00473	CD274	positively-E	luciferase reporter assay;RIP;RNA pull-down;bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-);cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-195-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000223414	NA	ENSG00000120217	NA	90632	29126	C6orf176|LNC473|bA142J11.1	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	Long noncoding RNA LINC00473 drives the progression of pancreatic cancer via upregulating programmed death-ligand 1 by sponging microRNA-195-5p.Increased LINC00473 and PD-L1 but declined miR-195-5p were determined in PC tissues and cell lines, and it was found that LINC00473 mainly situated in the cytoplasm. Also, miR-195-5p was verified to bind with both LINC00473 and PD-L1. Next, with the aim to examine the ability of LINC00473, miR-195-5p, and PD-L1 on the PC progression, the expression of LINC00473, miR-195- 5p and PD-L1 were altered with mimics, inhibitors, overexpression vectors or siRNAs in PC cells and cocultured CD8+ T cells. It was demonstrated that LINC00473 sponged miR-195-5p to upregulate PD-L1 expression. More important, the obtained results revealed that LINC00473 silencing or miR-195-5p upregulation elevated the expression of Bcl-2 associated X protein (Bax), interferon (IFN)--Gamma, and interleukin (IL)-4 but reduced the expression of B-cell lymphoma-2 (Bcl-2), matrix metalloproteinase (MMP)-2, MMP-9, and IL-10, thus inducing the enhancement of the apoptosis as along with the inhibition of proliferation, invasion, and migration of the PC cells. LINC00473 silencing or miR-195-5p elevation activated the CD8+ T cells. As shown in Figure 4a, there was a binding site between miR-195-5p and PD-L1 via the online target prediction. The luciferase activity detection manifested that miR-195-5p mimic reduced the luciferase activity of PD-L1-WT. . RNA pull-down was utilized to seek for the interaction between LINC00473 and miR-159-5p and RIP assay analyzed the interaction between LINC00473 and AGO2.  the relative expression of miR-195-5p and PD-L1 in SW-1990 cells in response to the treatment of miR-195-5p mimic, miR-195-5p inhibitor or Atezolizumab (PD-L1 inhibitor), as determined by RT-qPCR	31206665	RID07013	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Glioblastoma	SNHG15	CDK6	positively-E	siRNA	upregulation	qRT-PCR	GSE4290;GSE16581;GSE108476	NA	tumorigenesis(+);chemoresistance(+)	NA	association	RNA-protein	Palbociclib;Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000105810	NA	285958	1021	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	PLSTIRE	SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. Here, we first compared the level of lncSNHG15 between normal brain tissue and GBM (database GSE4290) and found that lncSNHG15 was significantly higher in the GBM samples as compared to that in the normal brain. In addition, analysis performed on another database (GSE16581) showed that a higher expression of lncSNHG15 is associated with a high risk for GBM. Moreover, we examined a larger cohort of patients with glioma (GSE108476, N-=-524), a similar observation was made where patients with a higher lncSNHG15 was predicted to have a significantly shorter survival time. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6. SNHG15 silencing led to decreased GBM tumorigenesis and increased TMZ sensitivity. Palbociclib treatment suppressed GBM tumorigenesis was associated with downregulation of lncSNHG15. To further explore the connection between CDK6 and lncSNHG15, we showed that treating TMZ-R cells with CDK6 inhibitor, palbociclib also led to the decreased level of lncSNHG15; palbociclib-treated TMZ-R cells showed a significantly decreased ability to generate M2 GAM. Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15, coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Moreover, we showed a positive correlation between the level of lncSNHG15 and oncogenic/stemness markers such as EGFR, CDK6, SOX-2 and beta-catenin. In support, we observed a strong negative correlation between CDK6 mRNA level and miR-627-5p in the clinical TMZ-R samples. To further explore the regulatory signaling pathway(s) associated with CDK6, we employed 3 different algorithms (miRmap, PITA and microT) for predicting the microRNAs with the potential to target CDK6. Real-time PCR analysis showed that a significantly higher level of lncSNGH15 in samples from patients who are non-responsive towards TMZ as compared to ones with responsiveness.	31462285	RID07014	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Glioblastoma	SNHG15	SOX2	positively-E	siRNA	upregulation	qRT-PCR	GSE4290;GSE16581;GSE108476	NA	tumorigenesis(+);chemoresistance(+)	NA	association	NA	Palbociclib;Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000181449	NA	285958	6657	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	NA	SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. Here, we first compared the level of lncSNHG15 between normal brain tissue and GBM (database GSE4290) and found that lncSNHG15 was significantly higher in the GBM samples as compared to that in the normal brain. In addition, analysis performed on another database (GSE16581) showed that a higher expression of lncSNHG15 is associated with a high risk for GBM. Moreover, we examined a larger cohort of patients with glioma (GSE108476, N-=-524), a similar observation was made where patients with a higher lncSNHG15 was predicted to have a significantly shorter survival time. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6. SNHG15 silencing led to decreased GBM tumorigenesis and increased TMZ sensitivity. Palbociclib treatment suppressed GBM tumorigenesis was associated with downregulation of lncSNHG15. To further explore the connection between CDK6 and lncSNHG15, we showed that treating TMZ-R cells with CDK6 inhibitor, palbociclib also led to the decreased level of lncSNHG15; palbociclib-treated TMZ-R cells showed a significantly decreased ability to generate M2 GAM. Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15, coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Moreover, we showed a positive correlation between the level of lncSNHG15 and oncogenic/stemness markers such as EGFR, CDK6, SOX-2 and beta-catenin. In support, we observed a strong negative correlation between CDK6 mRNA level and miR-627-5p in the clinical TMZ-R samples. To further explore the regulatory signaling pathway(s) associated with CDK6, we employed 3 different algorithms (miRmap, PITA and microT) for predicting the microRNAs with the potential to target CDK6. Real-time PCR analysis showed that a significantly higher level of lncSNGH15 in samples from patients who are non-responsive towards TMZ as compared to ones with responsiveness.	31462285	RID07015	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(LIHC);DATA(GSE117623)
Glioblastoma	SNHG15	EGFR	positively-E	siRNA	upregulation	qRT-PCR	GSE4290;GSE16581;GSE108476	NA	tumorigenesis(+);chemoresistance(+)	NA	association	RNA-protein	Palbociclib;Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000146648	NA	285958	1956	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	ERBB|ERBB1|ERRP	SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. Here, we first compared the level of lncSNHG15 between normal brain tissue and GBM (database GSE4290) and found that lncSNHG15 was significantly higher in the GBM samples as compared to that in the normal brain. In addition, analysis performed on another database (GSE16581) showed that a higher expression of lncSNHG15 is associated with a high risk for GBM. Moreover, we examined a larger cohort of patients with glioma (GSE108476, N-=-524), a similar observation was made where patients with a higher lncSNHG15 was predicted to have a significantly shorter survival time. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6. SNHG15 silencing led to decreased GBM tumorigenesis and increased TMZ sensitivity. Palbociclib treatment suppressed GBM tumorigenesis was associated with downregulation of lncSNHG15. To further explore the connection between CDK6 and lncSNHG15, we showed that treating TMZ-R cells with CDK6 inhibitor, palbociclib also led to the decreased level of lncSNHG15; palbociclib-treated TMZ-R cells showed a significantly decreased ability to generate M2 GAM. Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15, coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Moreover, we showed a positive correlation between the level of lncSNHG15 and oncogenic/stemness markers such as EGFR, CDK6, SOX-2 and beta-catenin. In support, we observed a strong negative correlation between CDK6 mRNA level and miR-627-5p in the clinical TMZ-R samples. To further explore the regulatory signaling pathway(s) associated with CDK6, we employed 3 different algorithms (miRmap, PITA and microT) for predicting the microRNAs with the potential to target CDK6. Real-time PCR analysis showed that a significantly higher level of lncSNGH15 in samples from patients who are non-responsive towards TMZ as compared to ones with responsiveness.	31462285	RID07016	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Glioblastoma	SNHG15	CTNNB1	positively-E	siRNA	upregulation	qRT-PCR	GSE4290;GSE16581;GSE108476	NA	tumorigenesis(+);chemoresistance(+)	NA	association	RNA-protein	Palbociclib;Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000168036	NA	285958	1499	C7orf40|Linc-Myo1g|MYO1GUT	CTNNB|EVR7|MRD19|NEDSDV|armadillo	SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. Here, we first compared the level of lncSNHG15 between normal brain tissue and GBM (database GSE4290) and found that lncSNHG15 was significantly higher in the GBM samples as compared to that in the normal brain. In addition, analysis performed on another database (GSE16581) showed that a higher expression of lncSNHG15 is associated with a high risk for GBM. Moreover, we examined a larger cohort of patients with glioma (GSE108476, N-=-524), a similar observation was made where patients with a higher lncSNHG15 was predicted to have a significantly shorter survival time. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6. SNHG15 silencing led to decreased GBM tumorigenesis and increased TMZ sensitivity. Palbociclib treatment suppressed GBM tumorigenesis was associated with downregulation of lncSNHG15. To further explore the connection between CDK6 and lncSNHG15, we showed that treating TMZ-R cells with CDK6 inhibitor, palbociclib also led to the decreased level of lncSNHG15; palbociclib-treated TMZ-R cells showed a significantly decreased ability to generate M2 GAM. Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15, coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Moreover, we showed a positive correlation between the level of lncSNHG15 and oncogenic/stemness markers such as EGFR, CDK6, SOX-2 and beta-catenin. In support, we observed a strong negative correlation between CDK6 mRNA level and miR-627-5p in the clinical TMZ-R samples. To further explore the regulatory signaling pathway(s) associated with CDK6, we employed 3 different algorithms (miRmap, PITA and microT) for predicting the microRNAs with the potential to target CDK6. Real-time PCR analysis showed that a significantly higher level of lncSNGH15 in samples from patients who are non-responsive towards TMZ as compared to ones with responsiveness.	31462285	RID07017	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Glioblastoma	SNHG15	MIR627	negatively-E	siRNA;miRmap;PITA;microT	upregulation	qRT-PCR	GSE4290;GSE16581;GSE108476	NA	tumorigenesis(+);chemoresistance(+)	NA	association	RNA-RNA	Palbociclib;Temozolomide	CSC	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000207712	NA	285958	693212	C7orf40|Linc-Myo1g|MYO1GUT	MIRN627|hsa-mir-627|mir-627	SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. Here, we first compared the level of lncSNHG15 between normal brain tissue and GBM (database GSE4290) and found that lncSNHG15 was significantly higher in the GBM samples as compared to that in the normal brain. In addition, analysis performed on another database (GSE16581) showed that a higher expression of lncSNHG15 is associated with a high risk for GBM. Moreover, we examined a larger cohort of patients with glioma (GSE108476, N-=-524), a similar observation was made where patients with a higher lncSNHG15 was predicted to have a significantly shorter survival time. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6. SNHG15 silencing led to decreased GBM tumorigenesis and increased TMZ sensitivity. Palbociclib treatment suppressed GBM tumorigenesis was associated with downregulation of lncSNHG15. To further explore the connection between CDK6 and lncSNHG15, we showed that treating TMZ-R cells with CDK6 inhibitor, palbociclib also led to the decreased level of lncSNHG15; palbociclib-treated TMZ-R cells showed a significantly decreased ability to generate M2 GAM. Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15, coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Moreover, we showed a positive correlation between the level of lncSNHG15 and oncogenic/stemness markers such as EGFR, CDK6, SOX-2 and beta-catenin. In support, we observed a strong negative correlation between CDK6 mRNA level and miR-627-5p in the clinical TMZ-R samples. To further explore the regulatory signaling pathway(s) associated with CDK6, we employed 3 different algorithms (miRmap, PITA and microT) for predicting the microRNAs with the potential to target CDK6. Real-time PCR analysis showed that a significantly higher level of lncSNGH15 in samples from patients who are non-responsive towards TMZ as compared to ones with responsiveness.	31462285	RID07018	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	
Hepatocellular carcinoma	SNHG15	ZEB2	positively-E	knockdown;starBase2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+).	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000169554	NA	285958	9839	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	KIAA0569|SIP-1|SIP1|ZFHX1B	SNHG15 expression was markedly increased, whereas miR-141-3p expression was substantially reduced in HCC cells and tissue samples relative to normal controls.When SNHG15 was knocked down, this resulted in a significant disruption to the proliferation, as well as the invasive and migratory ability of these HCC cells. miR-141-3p was also found to be an SNHG15 target in HCC cells. LncRNA SNHG15 promotes hepatocellular carcinoma progression by sponging miR-141-3p. We first used qRT-PCRto assess SNHG15 expression in HCC cells and tissues. Next, starbase2.0 was employed for prediction of SNHG15 targeting miRNAs, with miR-141-3p being identified as a target of relevance on the basis of its biological function in tumor progression. Luciferase reporters confirmed miR-141-3p mimic binding to SNHG15 in SMMC-7721 cells. we conducted RIP, revealing SNHG15 and miR-141-3p to be preferentially enriched among Ago2-containing microribonucleoproteins. SNHG15 knockdown significantly increased SMMC-7721cell miR-141-3p expression, whereas overexpressing miR-141-3p declined SNHG15 expression.  These results suggested that SNHG15 modulated the expression ZEB2 and E2F3 through sponging  miR-141-3p in human HCC cells.	31310393	RID07019	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	SNHG15	E2F2	positively-E	knockdown;starBase2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+).	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000007968	NA	285958	1870	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	E2F-2	SNHG15 expression was markedly increased, whereas miR-141-3p expression was substantially reduced in HCC cells and tissue samples relative to normal controls.When SNHG15 was knocked down, this resulted in a significant disruption to the proliferation, as well as the invasive and migratory ability of these HCC cells. miR-141-3p was also found to be an SNHG15 target in HCC cells. LncRNA SNHG15 promotes hepatocellular carcinoma progression by sponging miR-141-3p. We first used qRT-PCRto assess SNHG15 expression in HCC cells and tissues. Next, starbase2.0 was employed for prediction of SNHG15 targeting miRNAs, with miR-141-3p being identified as a target of relevance on the basis of its biological function in tumor progression. Luciferase reporters confirmed miR-141-3p mimic binding to SNHG15 in SMMC-7721 cells. we conducted RIP, revealing SNHG15 and miR-141-3p to be preferentially enriched among Ago2-containing microribonucleoproteins. SNHG15 knockdown significantly increased SMMC-7721cell miR-141-3p expression, whereas overexpressing miR-141-3p declined SNHG15 expression.  These results suggested that SNHG15 modulated the expression ZEB2 and E2F3 through sponging  miR-141-3p in human HCC cells.	31310393	RID07020	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Hepatocellular carcinoma	SNHG16	HDAC2	positively-E	Luciferase reporter assay;statBase v2.0;	upregulation	RT-qPCR	NA	NA	cancer progression(+);	ceRNA(miR-490-3p)	regulation	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000196591	NA	100507246	3066	Nbla10727|Nbla12061|ncRAN	KDAC2|RPD3|YAF1	SNHG15 served as a molecular sponge for miR-490-3p. Further, miR-490-3p directly targets HDAC2. HDAC2 was involved in HCC progression by interacting with the SNHG15/miR-490-3p axis. Our research showed that up-regulation of SNHG15 was found in HCC and was related to aggressive behaviors in HCC patients. RT-qPCR and western blotwere applied to detect SNHG15, miR-490-3p and histone deacetylase 2 (HDAC2) expression. To explore the regulatory mechanism of SNHG15, its target miRNA was searched in starBASEv2.0 database.  Luciferase reporter assay showed that miR-490-3p mimics decreased SNHG15-wt luciferase activity, but not SNHG15-mut. lncRNA-SNHG15 accelerates the development of hepatocellular carcinoma by targeting miR-490-3p/ histone deacetylase 2 axis	31636472	RID07021	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Breast cancer	SNHG16	RRM2	positively-E	starBase;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-30a)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000171848	NA	100507246	6241	Nbla10727|Nbla12061|ncRAN	C2orf48|FLJ25102	SNHG16 inhibition reduced the proliferation and invasion of breast cancer cells in vitro.the SNHG16/miR-30a axis regulated the expression of ribonucleotide reductase M2 (RRM2) in breast cancer cells. Recent studies have reported that the lncRNA small nucleolar RNA host gene 16 (SNHG16) is highly expressed in breast cancer tissue. The SNHG16/miR-30a axis promotes breast cancer cell proliferation and invasion by regulating RRM2. To investigate whether SNHG16 interacts with miRNAs, we examined whether SNHG16 possesses a potential binding site for miR-30a using the starBase web tool. To verify whether SNHG16 binds with miR-30a in breast  cancer cells, a dual-luciferase reporter assay was conducted  and showed that the miR-30a mimic significantly reduced  the luciferase activity of WT-SNHG16 in breast cancer cells. Moreover, a RIP assay showed that SNHG16 and miR-30a expression was significantly enriched in the Ago2 pellet compared to the IgG control pellet.	32122142	RID07022	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Multiple myeloma	SNHG16	miR-342-3p	negatively-F	starBase v3.0;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Myeloma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p. SNHG16 expression was up-regulated in MM tissues. SNHG16 expression levels was measured by qRT-PCR  Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16. Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p. To further investigate the molecular mechanism of SNHG16 on MM cell proliferation and apoptosis, potential target miRNAs were predicted using StarBase 3.0 online bioinformatics software.	32025219	RID07023	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Cervical cancer	SNHG16	PARP9	positively-E	Luciferase reporter assay;RIP;LncMAP	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000138496	NA	100507246	83666	Nbla10727|Nbla12061|ncRAN	ARTD9|BAL|BAL1	SNHG16 recruited SPI1 protein to promote transcription of PARP9 to upregulate its transcription in cervical cancer cells. Long noncoding RNA SNHG16 promotes the tumorigenicity of cervical cancer cells by recruiting transcriptional factor SPI1 to upregulate PARP9. To identify SNHG16 expression in cervical cancer, RT-qPCR was conducted. Highly expressed SNHG16 in cervical cancer. Using the dual-luciferase reporter gene assay, RNA immunoprecipitation, chromatin immunoprecipitation, we were able to determine that SNHG16 recruited SPI1 protein to promote transcription of PARP9 to upregulate its transcription in cervical cancer cells. The SNHG16/SPI1/PARP9 axis regulates cervical cancer cell proliferation and invasion. The LncMAP database (http://bio-bigdata.hrbmu.edu.cn/LncMAP) suggested that SNHG16 may regulate PARP9 via transcriptional factor SPI1 in cervical cancer. SNHG16 recruits SPI1 to promote PARP9 expression in cervical cancer cells.	31774223	RID07024	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE75367)
Pancreatic cancer	SNHG16	HMGB1	positively-E	starBase v2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-218-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000189403	NA	100507246	3146	Nbla10727|Nbla12061|ncRAN	DKFZp686A04236|HMG1|HMG3|SBP-1	LncRNA SNHG16 promotes tumor growth of pancreatic cancer by targeting miR-218-5p,SNHG16 is up-regulated in human PC and is associated with poor survival. The expression of SNHG16 in the 46 tissue samples was assessed through qRT-PCRto check the role of SNHG16 in PC.  In comparison to normal tissues, the PC samples showed an upregulation of SNHG16. The bioinformatics database (Starbase2.0) was utilized for predicting miRNAs that putatively bind SNHG16 based on the complementarity of bases. To test this prediction, an assay for luciferase activity revealed miR-218-5p transfection caused a significant reduction in the activity of- Wt-SNHG16, but not of Mut-SNHG16. Increased SNHG16 was found in the RNA pull-down assay for bio-WT-miR-218-5p in comparison to control (bio-NC) or bio-Mut- miR-218-5p) probes. SNHG16 mediate HMGB1 expression through sponging miR-218-5p.  Importantly, downregulation of the miR-218-5p caused a partial reversal of the inhibition caused by SNHG16 depletion on cell proliferation, migration and invasion of AsPC-1 cells.	30981105	RID07025	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Colorectal cancer	SNHG16	miR-218-5p	negatively-E	Luciferase reporter assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long non-coding RNA SNHG16 affects cell proliferation and predicts a poor prognosis in patients with colorectal cancer via sponging miR-200a-3p. The expression level of SNHG16 in 56 pairs of CRC tissues and adjacent non-tumor tissues was explored using qRT-PCR SNHG16 expression is up-regulated in CRC tissues and associated with disease progression. We used the online software starBase to predict and select miRNAs interacted with SNHG16. We performed the luciferase reporter assay to confirm such interaction. The RNA binding protein immunoprecipitation (RIP) experiments on LoVo cell extracts were further performed. Finally, the Spearman Rank correlation analysis showed that the level of miR-200a-3p was negatively correlated with the level of SNHG16.  Interestingly, we found that miR-200a-3p could form complementary base pairing with SNHG16 and induce translational repression of a SNHG16 reporter gene. SNHG16 promotes cell proliferation of CRC cells. SNHG16 promotes migration and invasion of CRC cells. SNHG16 promotes tumor growth in vivo.	30962265	RID07026	transcriptional regulation	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Osteosarcoma	SNHG16	miR-98-5p	negatively-F	Luciferase reporter assay;RIP;starBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	LncRNA SNHG16 sponges miR-98-5p to regulate cellular processes in osteosarcoma. The expression of SNHG16 in HNSCC tissues and cells was detected by RT-qPCR assay. The interaction between SNHG16 and miR-98-5p was studied by luciferase reporter and RIP assays. SNHG16 is upregulated in osteosarcoma tissues and cell lines, and associated with the poor overall survival of patients. Through the Starbase online software, we searched for the potential target miRNAs of SNHG16, and observed that miR-98-5p had a putative binding site with SNHG16. To confirm our hypothesis that miR-98-5p was targeted by SNHG16, luciferase reporter assay was performed.  RIP assay confirmed that SNHG16 and miR-98-5p were both immunoprecipitated by anti-Ago2, validating that SNHG16 could interact with miR-98-5p. Rescue experiments implied that miR-98-5p suppression could reverse the effects brought by SNHG16 inhibition on cell proliferation, migration, invasion, cell cycle and apoptosis in osteosarcoma. declined cell proliferation in sh-SNHG16#1+NC inhibitor group was apparently rescued in sh-SNHG16+miR-98-5p inhibitor group. In addition, miR-98-5p inhibitor also rescued the inhibitory influences of downregulating SNHG16 on cell cycle. Moreover, SNHG16 knockdown (or miR-98-5p suppression) promoted (or impeded) cell apoptosis in U2OS, whereas inhibition of miR-98-5p countervailed the facilitative effect of SNHG16 knockdown on cell apoptosis. Transwell assay revealed that suppression of miR-98-5p reversed the hampered migration and invasion upon the knockdown of SNHG16 in U2OS cells. Results showed that the expression of ZEB1, E2F5 and STAT3 were reduced by SNHG16 knockdown and enhanced by miR-98-5p suppression, whereas inhibition of miR-98-5p attenuated the effects of SNHG16 knockdown on reducing ZEB1, E2F5 and STAT3 expression.	30923843	RID07027	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Osteosarcoma	SNHG16	BCL9	positively-E	starBase v3.0;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1301)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000116128	NA	100507246	607	Nbla10727|Nbla12061|ncRAN	NA	SNHG16 acted as a competing endogenous RNA (ceRNA) by directly interacting with miR-1301 and inversely regulated its abundance in OS cells.LncRNA SNHG16 promotes proliferation, migration and invasion of osteosarcoma cells by targeting miR-1301/BCL9 axis. SNHG16 expression was confirmed by qRT-PCRin OS and matched paracancerous tissues. Notably, SNHG16 expression was prominently up-regulated in OS as compared with that in paracancerous tissues. Next, miR-1301 was predicted as a candidate target of SNHG16 using starBase V3.0 online platform.  Notably, we found that enforced expression of miR-1301 markedly decreased the fluorescence intensity of vectors carrying wt SNHG16 (P-<-0.05, Fig. 2C), whereas miR-1301 did not affect the luciferase activity of vectors carrying mt SNHG16. Furthermore, RNA pull-down showed that SNHG16 directly bond to miR-1301, but mutagenesis of the binding sequences for SNHG16 in miR-1301 abrogated this interaction.	30909141	RID07028	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG16	FGF19	positively-E	starBase;dual-luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-302a-3p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000162344	NA	100507246	9965	Nbla10727|Nbla12061|ncRAN	NA	SNHG16 interacted with miR-302a-3p and depressed its expression.LncRNA SNHG16 promotes cell proliferation through miR-302a-3p/FGF19 axis in hepatocellular carcinoma.  Here, we showed that SNG16 was up-regulated and associated with poor prognosis in HCC. RT-qPCR analysis of SNHG16 expression level in indicated cell lines. To investigate whether SNHG16 interacted with miRNA, we found that SNHG16 possessed a potential binding site of miR-302a-3p using Starbase web tool. To confirm the interaction between miR-302a-3p and SNHG16, we performed dual-luciferase reporter assay. Moreover, biotin pull down assay indicated that the miR-302a-3p obtained a great enrichment in the SNHG16 pulled down pellets compared with negative control in both HepG2 and Huh7 cells.	30784284	RID07029	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Gastric cancer	SNHG16	DKK3	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000050165	NA	100507246	27122	Nbla10727|Nbla12061|ncRAN	REIC|RIG	LncRNA SNHG16 promotes epithelial- mesenchymal transition via down-regulation of DKK3 in gastric cancer. SNHG16 was found to be upregulated whereas DKK3 was downregulated in tumor tissues compared with adjacent normal tissues. All these results suggested that SNHG16 promotes GC progression via regulation of DKK3 directly or indirectly. To evaluate the role of SNHG16 on EMT in GC, si-SNHG16 or si-NC were transfected into HGC-27 and AGS cells. The interference efficiency of SNHG16 was over 70%, as detected by qRT-PCRassay. To further explore the target of SNHG16 in GC, Genechip assay was performed following SNHG16 knockdown, which displayed 7 upregulated genes and 21 downregulated genes in HGC-27  cells.  These results suggested that SNHG16 may activate the Wnt/beta-catenin pathway by regulation of beta-catenin protein to some extent.	31561329	RID07030	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Neuroblastoma	SNHG16	HOXA7	positively-E	Luciferase Reporter Assay;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000122592	NA	100507246	3204	Nbla10727|Nbla12061|ncRAN	HOX1|HOX1A	SNHG16 silencing inhibited proliferation, migration and invasion and induced apoptosis of NB cells. We identified that SNHG16 directly interacted with miR-128-3p, and miR-128-3p could target the 3'UTR of HOXA7 in NB cells. To investigate the function of SNHG16 and miR-128-3p in NB, we detected their expression levels in NB tissues using qRT-PCR The data showed that SNHG16 was obviously upregulated in NB tissues compared with the normal tissues. MiR-128-3p Targeted HOXA7, Negatively Regulated HOXA7 Expression and HOXA7-Mediated Cell Proliferation, Migration, Invasion and Apoptosis. To figure out the hidden mechanism of miR-128-3p in NB, starBase was hired to find the possible target genes. The output showed that miR-128-3p could bind to the 3'UTR of HOXA7, and luciferase reporter plasmids (HOXA7-WT and HOXA7-MUT) were constructed to corroborate the forecast. Meanwhile, the RIP assay also confirmed the interaction between miR-128-3p and HOXA7.	31919621	RID07031	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Pancreatic cancer	SNHG16	SREBF2	positively-E	dual-luciferase reporter assay;bioinformatics	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);hepatic lipid homeostasis(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000198911	NA	100507246	6721	Nbla10727|Nbla12061|ncRAN	bHLHd2|SREBP2	Both the knock down of lncRNA SNHG16 and SREBP2 and overexpression of miR-195 suppressed the proliferation, migration, invasion and lipogenesis in pancreatic cancer cells. LncRNA SNHG16 directly sponged miR-195 to modulate the lipogenesis via regulating the expression of SREBP2. The interactions among lncRNA SNHG16, miR-195 and SREBP2 were analyzed by dual-luciferase reporter assays. To study the roles of lncRNA SNHG16 in pancreatic cancer, the expression of lncRNA SNHG16 was analyzed in normal pancreatic cell HPDE6-C7 and pancreatic cancer cells PANC-1, BxPC-3, SW1990 and AsPC-1 using reverse transcription-PCR (RT-qPCR) assay. Compared with the HPDE6-C7 cells, all these four types of cancer cells showed increased expression of lncRNA SNHG16. To further investigate whether lncRNA SNHG16 directly targets miR-195, and miR-195 directly binds to SREBP2, we predicted the competitive binding sites for miR-195 by bioinformatics. Our results showed that the luciferase activity was obviously decreased by co-transfection with miR-195 mimics and wild-type lncRNA SNHG16 constructs (SNHG16-WT), but unaffected with mutated lncRNA SNHG16 constructs (SNHG16-MUT), suggesting that miR-195 was the functional direct target of lncRNA SNHG16.	31664866	RID07032	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	MYC	SNHG16	positively-E	shRNA	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000163597	GRCh38_17:76557733-76565357	4609	100507246	bHLHe39|c-Myc|MYCC	Nbla10727|Nbla12061|ncRAN	c-Myc induced upregulation of long non-coding RNA SNHG16 enhances progression and carcinogenesis in oral squamous cell carcinoma. In this paper, we found that c-Myc and SNHG16 were overexpressed in OSCC tissues and cell lines compared with normal tissues and normal human oral keratinocytes cells. There was a notable positive correlation between SNHG16 and c-Myc expression in OSCC tissues. c-Myc silencing by either shRNA c-Myc or by 10058-F4 (c-Myc inhibitor) resulted in a dose-dependent reduction in SNHG16 levels in CAL-27 and TSCCA cells; conversely, upregulation of c-Myc by pcDNA c-Myc markedly increased SNHG16 expression. Depletion of SNHG16 in CAL-27 cells strikingly inhibited cell proliferation, migration and invasion, as indicated by downregulation of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, depletion of SNHG16 induced cell apoptosis and inhibited epithelial-to-mesenchymal transition as indicated by induction of cleaved caspase-3 and epithelial cadherin (E-cadherin) along with reduction of N-cadherin and Snail. Intriguingly, c-Myc knockdown led to the similar functional effects as that of SNHG16 knockdown in TSCCA cells. However, these changes caused by c-Myc knockdown were abrogated by SNHG16 overexpression. In order to determine the biological functions of SNHG16 in OSCC, we analyzed the expression levels of SNHG16 in OSCC tissues and cell lines (SCC-25, CAL-27, Tca8113 and TSCCA) using qRT-PCR c-Myc positively regulates the expression of SNHG16 in OSCC cells. To inquiry the effect of c-Myc on SNHG16 expression, we altered the expression of c-Myc in CAL-27 and TSCCA cells using shRNA c-Myc, 10058-F4 and pcDNA c-Myc.	30607006	RID07033	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Diffuse large b-cell lymphoma	SNHG16	PIM1	positively-E	Luciferase reporter assay;starBase v3.0;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+);tumor growth(+)	ceRNA(miR-497-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000137193	NA	100507246	5292	Nbla10727|Nbla12061|ncRAN	PIM	Long non-coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B-cell lymphoma cells by targeting miR-497-5p/PIM1 axis. SNHG16 is overexpressed in DLBCL. We detected the expression of SNHG16 in DLBCL tissues and RLH tissues using qRT-PCR Taken together, SNHG16 knockdown inhibited cell proliferation and cell cycle progression, and it induced apoptosis of DLBCL cells. Knockdown of SNHG16 suppresses in vivo growth of DLBCL cells. According to the starBase V3.0 online platform,31, 32 more than a dozen candidate target miRNAs for SNHG16 were predicted. As shown in Figure -Figure4D,4D, miR-497-5p overexpression decreased the luciferase activity of vectors containing wt SNHG16 (P < .05), whereas the fluorescence intensity of vectors containing mt SNHG16 was not changed after miR-497-5p overexpression. Moreover, SNHG16 was obviously pulled down by biotinylated wt miR-497-5p.	31483572	RID07034	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Hepatocellular carcinoma	SNHG16	miR-195	negatively-F	RIP;luciferase reporter assays;starBase;miRanda	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	SNHG16 acted as an endogenous sponge by directly binding to miR-195 and downregulated its expression.Long intergenic noncoding RNA SNHG16 interacts with miR-195 to promote proliferation, invasion and tumorigenesis in hepatocellular carcinoma. To explore the biological effects of SNHG16 on HCC, the level of SNHG16 was assessed by qRT-PCRin HCC tissues and cell lines. Our results revealed that the expression level of SNHG16 in HCC was obviously increased compared with the adjacent non-tumor liver tissues. To elucidate the potential molecular mechanism of SNHG16, the potential target genes of SNHG16 were first predicted by the online softwares starBase and miRanda. To assess the relationship between SNHG16 and miR-195, luciferase assays were carried out. Additionally, results from RIP showed that both SNHG16 and miR-195 were more abundant in Ago2-containing beads than those in IgG immunoprecipitates in SMMC7721- cells.	31306653	RID07035	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Hepatocellular carcinoma	SNHG16	p62	positively-E	luciferase reporter assay;RIP;starBase;miRPath;miRanda	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cancer progression(+);cell cycle(+);PI3K/AKT/mTOR signaling pathway(+);NF-kB signaling pathway(+)	ceRNA(miR-17-5p)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000073792	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	The lncRNA SNHG16 affects prognosis in hepatocellular carcinoma by regulating p62 expression. SNHG16 is overexpression in patient HCC tissues and HCC cell lines.  To evaluate differentially expressed lncRNAs in human HCC, we performed microarray analysis on tissue samples from three patients with HCC and three control patients with hepatic hemangioma. We used quantitative RT-PCRto validate the microarray differences observed for the three most strongly upregulated and three most strongly downregulated lncRNAs. SNHG16 overexpression increases cell proliferation and migration in HCC cell lines. SNHG16 overexpression increases cell cycling and decreases apoptosis in HCC cell lines.  SNHG16 overexpression accelerates HCC tumor development in vivo. To begin to identify mechanism(s) by which SNHG16 may promote cancer development, we used Starbase, miRPath, and miRanda online prediction software to predict target genes of SNHG16. To determine whether miR-17-5p can affect p62 expression, we transfected Huh-7 and HepG2 cells with plasmids containing a luciferase reporter with the wild-type miR-17-5p binding site (SNHG16-wt) or mutated binding site (SNHG16-mut). RNA coimmunoprecipitation assays confirmed direct interaction between lncSNHG16 and miR-17-5p.  Together these results suggest that lncSNHG16 may act as an endogenous sponge of miR-17-5p to upregulate its target p62.  SNHG16 activates the mTOR pathway. SNHG16 activates the NF-kB pathway.Our study shows that SNGH16 can affect the prognosis of patients with HCC by regulating p62, which in turn increases PI3K/Akt/mTOR and NF-kB signaling.	31256427	RID07036	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Retinoblastoma	SNHG16	miR-140-5p	negatively-F	luciferase reporter assay;RIP;starBase v2.0	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);colony formation(+);apoptosis process(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long noncoding RNA SNHG16 promotes human retinoblastoma progression via sponging miR-140-5p.Clinical evidence revealed a negative correlation between SNHG16 and miR-140-5p in RB specimens. Rescue experiments showed that inhibition of miR-140-5p partially attenuated the growth-suppressing effects of SNHG16-depletion on RB cells.  SNHG16 is upregulated in RB tissues and cell lines. To elucidate the function of SNHG16 on RB progression, qRT-PCRwas performed to examine the expression of SNHG16 in RB tissues and cell line.  SNHG16 knockdown inhibits RB cell proliferation and colony formation.  SNHG16 knockdown induced RB apoptosis. To explore the molecular mechanism by which SNHG16 influences RB progression, we used Starbase2.0 to search miRNAs that interact with SNHG16.  Furthermore, luciferase reporter assay revealed that overexpression of miR-140-5p reduced the luciferase activity of WT-SNHG16, but it did not affect the luciferase activity of MT-SNHG16 in both SO-RB-50 and Y79 cells. ) RIP assay further confirmed that SNHG16 and miR-140-5p to be preferentially enriched among Ago2-containing micro-ribonucleoproteins in both SO-RB-50 and Y79 cells. D).These results implied that SNHG16 knockdown suppressed RB tumorigenesis in vivo.	31234025	RID07037	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Malignant glioma	SNHG16	EGFR	positively-E	luciferase reporter assay;bioinformatics;qRT-PCR;knockdown;overexpression	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);PI3K/AKT signaling pathway(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-373)	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000146648	NA	100507246	1956	Nbla10727|Nbla12061|ncRAN	ERBB|ERBB1|ERRP	lncRNA SNHG16 promotes glioma tumorigenicity through miR-373/EGFR axis by activating PI3K/AKT pathway, lncRNA SNHG16 was highly expressed in glioma and may exert oncogenic function as a competing endogenous RNA (ceRNA) to regulate EGFR by sponging of miR-373-3p through activating PI3K/AKT pathway. Firstly, we investigate the expression of SNHG16 and miR-373 in normal brain tissues (NBTs), low-grade gliomas (LGGs) and high-grade gliomas (HGGs) using qRT-PCRassay. To further investigate the molecular mechanism of SNHG16 on cell proliferation and invasion of glioma cells, we predicted its potential target miRNAs by bioinformatics analysis. Then, luciferase reporter assay was carried out to verify the bioinformatical prediction.To confirm the regulation between SNHG16 and miR-373, qRT-PCRassay was applied to assess the expression of miR-373 and SNHG16 in both LN229 and U251 cells. Furthermore, to investigate whether SNHG16 regulate EGFR through binding with miR-373, the expression of EGFR after inhibition or over-expression of miR-373 was assessed by western blot. SNHG16 regulates proliferation and invasion of glioma cells by miR-373/EGFR axis. the cell reproductive capacity was inhibited by over-expressing miR-373 while inhibition of miR-373 resulted in the promotion of cell proliferation. while down-regulation of miR-373 promoted the capacity of cell migration and invasion.	31226483	RID07038	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Breast cancer	SNHG17	miR-124-3p	negatively-F	starBase v2.0;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000196756	GRCh38_20:38419638-38435409	NA	NA	388796	NA	NA	NA	lncRNA SNHG17 could regulate the progression of BC by sponging miR-124-3p. Long non-coding RNASNHG17 promotes the progression of breast cancer by sponging miR-124-3p. Moreover, the repression of cell proliferation, migration and invasion induced by SNHG17 knockdown would reversed by miR-124-3p inhibitor. The expression of SNHG17 was upregulated in BC tissues compared with non-tumor breast tissues. The expression of SNHG17 in nuclear and cytoplasmic of MCF-7 and MDA-MB-231 cells by qRT-PCR The microRNAs (miRNAs) that can bind to SNHG17 were predicated using Starbase2.0 and were tested using luciferase reporter activity and RIP assays.	32042267	RID07039	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	
Melanoma	STAT3	SNHG17	positively-E	luciferase reporter assay;ChIP;JASPAR	upregulation	qRT-PCR;microarray	GSE3189	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);PI3K/AKT signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	TF	lncRNA	ENSG00000168610	NA	ENSG00000196756	GRCh38_20:38419638-38435409	6774	388796	APRF	NA	STAT3-induced Upregulation of lncRNA SNHG17 Predicts a Poor Prognosis of Melanoma and Promotes Cell Proliferation and Metastasis Through Regulating PI3K-AKT Pathway. High expressions of SNHG17 were observed in both melanoma tissues and cells. The levels of SNHG17 in melanoma tissues and cells were determined using RT-PCR The biological mechanism underlying up-regulation of SNHG17 was explored using ChIP analysis and luciferase reporter assays. qPCR analysis of SNHG17 expressions in melanoma tissues and matched normal tissues. Functional studies confirmed that the proliferation, migration, and invasion of melanoma cells were noticeably reduced by the down-regulation of SNHG17. We also found that knockdown of SNHG17 resulted in the remarkable diminution in the phosphorylation levels of PI3K and AKT, suggesting that the activity of the PI3K-AKT pathway was suppressed. Using JASPAR software, two binding sites of STAT3 to the SNHG17 promoter were primarily predicted. Moreover, the results of ChIP assays also directly revealed that STAT3 could directly bind to the promoter region of SNHG17 in A375 cells.	31599425	RID07040	transcriptional regulation	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	SNHG20	ZEB2	positively-E	starBase v2.0;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	TCGA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-154)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000169554	NA	654434	9839	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	KIAA0569|SIP-1|SIP1|ZFHX1B	SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge. To explore the role of SNHG20 in NSCLC, we firstly analyzed the expression level of SNHG20 in NSCLC tissues from TCGA-LUAD dataset. SNHG20 was upregulated in NSCLC tissues and cell lines. To confirm the result, we performed qRT-PCRanalysis to detect SNHG20 expression in 42 paired NSCLC tumor and adjacent normal tissues. To further investigate the molecular mechanism of SNHG20 in NSCLC, starBase v2.0 was used to predict the potential target miRNAs of SNHG20. To confirm this prediction, luciferase reporter assay was performed in A549 and H1299 cells. The effect of SNHG20 on miR-154 expression in NSCLC cells was further explored by qRT-PCRanalysis. miR-154 overexpression suppressed proliferation, migration and invasion and enhanced apoptosis in NSCLC cells. miR-154 inhibition reversed the effects of SNHG20 knockdown on proliferation, migration and invasion and apoptosis in NSCLC cells. SNHG20 elevated ZEB2 expression by sponging miR-154 in NSCLC cells. To confirm whether SNHG20 competitively binding to miR-154 to de-repress the miRNA targets ZEB2 and RUNX2, luciferase reporter assay was performed in A549 and H1299 cells. qRT-PCRanalysis indicated that miR-154 overexpression or SNHG20 knockdown remarkably reduced ZEB2 and RUNX2 expression, however, miR-154 inhibition eliminated the inhibitory effect of si-SNHG20 on ZEB2 and RUNX2 expression in A549 and H1299 cells. SNHG20 knockdown suppressed tumor growth in NSCLC in vivo. In conclusion, our studies revealed that SNHG20 promoted proliferation, migration and invasion, and suppressed apoptosis in NSCLC cells through increasing ZEB2 and RUNX2 expression by sponging miR-154.	30780105	RID07041	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	SNHG20	RUNX2	positively-E	starBase v2.0;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	TCGA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-155)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124813	NA	654434	860	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge. To explore the role of SNHG20 in NSCLC, we firstly analyzed the expression level of SNHG20 in NSCLC tissues from TCGA-LUAD dataset. SNHG20 was upregulated in NSCLC tissues and cell lines. To confirm the result, we performed qRT-PCRanalysis to detect SNHG20 expression in 42 paired NSCLC tumor and adjacent normal tissues. To further investigate the molecular mechanism of SNHG20 in NSCLC, starBase v2.0 was used to predict the potential target miRNAs of SNHG20. To confirm this prediction, luciferase reporter assay was performed in A549 and H1299 cells. The effect of SNHG20 on miR-154 expression in NSCLC cells was further explored by qRT-PCRanalysis. miR-154 overexpression suppressed proliferation, migration and invasion and enhanced apoptosis in NSCLC cells. miR-154 inhibition reversed the effects of SNHG20 knockdown on proliferation, migration and invasion and apoptosis in NSCLC cells. SNHG20 elevated ZEB2 expression by sponging miR-154 in NSCLC cells. To confirm whether SNHG20 competitively binding to miR-154 to de-repress the miRNA targets ZEB2 and RUNX2, luciferase reporter assay was performed in A549 and H1299 cells. qRT-PCRanalysis indicated that miR-154 overexpression or SNHG20 knockdown remarkably reduced ZEB2 and RUNX2 expression, however, miR-154 inhibition eliminated the inhibitory effect of si-SNHG20 on ZEB2 and RUNX2 expression in A549 and H1299 cells. SNHG20 knockdown suppressed tumor growth in NSCLC in vivo. In conclusion, our studies revealed that SNHG20 promoted proliferation, migration and invasion, and suppressed apoptosis in NSCLC cells through increasing ZEB2 and RUNX2 expression by sponging miR-154.	30780105	RID07042	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SNHG20	FOXK1	negatively-E	IntaRNA;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Vasculogenic mimicry(+)	mRNA decay	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000164916	NA	654434	221937	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	IMAGE:5164497	SNHG20 was up-regulated in glioma tissues and cells, and knockdown of SNHG20 inhibited VM formation. The expression of SNHG20 in glioma tissues as well as glioma cell lines U87 and U251 was detected by qRT-PCR SNHG20 promoted degradation of FOXK1 through SMD pathway and enhanced VM formation in glioma cells. Using the bioinformatics database (IntaRNA), we found FOXK1 mRNA might be a putative target of SNHG20 in a sequence-specific manner. To verify our hypothesis, we used dual-luciferase gene reporter assays to confirm the predicted binding site. In addition, transfection with FOXK1(-) could rescue the inhibitory effect of SNHG20(-) on proliferation, migration, invasion and VM of glioma cells, while FOXK1(+) could rescue the promoting effect of SNHG20 (+) similarly. ZRANB2 bound to SNHG20, and SNHG20 acted on FOXK1 via SMD pathway.	30744670	RID07043	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	ZRANB2	SNHG20	positively-F	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Vasculogenic mimicry(+)	RNA stability	binding/interaction	protein-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000132485	NA	ENSG00000234912	GRCh38_17:77086716-77099902	9406	654434	ZIS|ZIS1|ZIS2|ZNF265	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	SNHG20 was up-regulated in glioma tissues and cells, and knockdown of SNHG20 inhibited VM formation. The expression of SNHG20 in glioma tissues as well as glioma cell lines U87 and U251 was detected by qRT-PCR ZRANB2 promoted VM formation in glioma cells by increasing the stability of SNHG20. To explore the correlation between ZRANB2 and SNHG20, we further used RNA-IP assay to detect whether ZRANB2 directly bound with SNHG20. In addition, transfection with SNHG20(+) could rescued the inhibitory effect of ZRANB2(-) on proliferation, migration, invasion and VM of glioma cells, while SNHG20(-) could rescued the promoting effect of ZRANB2(+) similarly. ZRANB2 bound to SNHG20, and SNHG20 acted on FOXK1 via SMD pathway.	30744670	RID07044	interact with mRNA	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)
Malignant glioma	SNHG20	MMP1	positively-E	IntaRNA;dual-luciferase reporter assay;JASPAR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Vasculogenic mimicry(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000196611	NA	654434	4312	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	CLG	SNHG20 was up-regulated in glioma tissues and cells, and knockdown of SNHG20 inhibited VM formation. The expression of SNHG20 in glioma tissues as well as glioma cell lines U87 and U251 was detected by qRT-PCR SNHG20 promoted degradation of FOXK1 through SMD pathway and enhanced VM formation in glioma cells. Using the bioinformatics database (IntaRNA), we found FOXK1 mRNA might be a putative target of SNHG20 in a sequence-specific manner. To verify our hypothesis, we used dual-luciferase gene reporter assays to confirm the predicted binding site. In addition, transfection with FOXK1(-) could rescue the inhibitory effect of SNHG20(-) on proliferation, migration, invasion and VM of glioma cells, while FOXK1(+) could rescue the promoting effect of SNHG20 (+) similarly. ZRANB2 bound to SNHG20, and SNHG20 acted on FOXK1 via SMD pathway. FOXK1 bound to the promoters of MMP1, MMP9 and VE-cadherin and inhibited transcription. By quiring the bioinformatics database (JASPAR), we identified MMP1, MMP9, VE-Cadherin might be probable downstream molecules of FOXK1.	30744670	RID07045	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Malignant glioma	SNHG20	MMP9	positively-E	IntaRNA;dual-luciferase reporter assay;JASPAR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Vasculogenic mimicry(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000100985	NA	654434	4318	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	CLG4B	SNHG20 was up-regulated in glioma tissues and cells, and knockdown of SNHG20 inhibited VM formation. The expression of SNHG20 in glioma tissues as well as glioma cell lines U87 and U251 was detected by qRT-PCR SNHG20 promoted degradation of FOXK1 through SMD pathway and enhanced VM formation in glioma cells. Using the bioinformatics database (IntaRNA), we found FOXK1 mRNA might be a putative target of SNHG20 in a sequence-specific manner. To verify our hypothesis, we used dual-luciferase gene reporter assays to confirm the predicted binding site. In addition, transfection with FOXK1(-) could rescue the inhibitory effect of SNHG20(-) on proliferation, migration, invasion and VM of glioma cells, while FOXK1(+) could rescue the promoting effect of SNHG20 (+) similarly. ZRANB2 bound to SNHG20, and SNHG20 acted on FOXK1 via SMD pathway. FOXK1 bound to the promoters of MMP1, MMP9 and VE-cadherin and inhibited transcription. By quiring the bioinformatics database (JASPAR), we identified MMP1, MMP9, VE-Cadherin might be probable downstream molecules of FOXK1.	30744670	RID07046	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	SNHG20	VE-Cadherin	positively-E	IntaRNA;dual-luciferase reporter assay;JASPAR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Vasculogenic mimicry(+)	transcriptional regulation	regulation	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	NA	NA	654434	NA	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	NA	SNHG20 was up-regulated in glioma tissues and cells, and knockdown of SNHG20 inhibited VM formation. The expression of SNHG20 in glioma tissues as well as glioma cell lines U87 and U251 was detected by qRT-PCR SNHG20 promoted degradation of FOXK1 through SMD pathway and enhanced VM formation in glioma cells. Using the bioinformatics database (IntaRNA), we found FOXK1 mRNA might be a putative target of SNHG20 in a sequence-specific manner. To verify our hypothesis, we used dual-luciferase gene reporter assays to confirm the predicted binding site. In addition, transfection with FOXK1(-) could rescue the inhibitory effect of SNHG20(-) on proliferation, migration, invasion and VM of glioma cells, while FOXK1(+) could rescue the promoting effect of SNHG20 (+) similarly. ZRANB2 bound to SNHG20, and SNHG20 acted on FOXK1 via SMD pathway. FOXK1 bound to the promoters of MMP1, MMP9 and VE-cadherin and inhibited transcription. By quiring the bioinformatics database (JASPAR), we identified MMP1, MMP9, VE-Cadherin might be probable downstream molecules of FOXK1.	30744670	RID07047	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	
Non-small cell lung cancer	SNHG20	MIR197	negatively-F	luciferase reporter assay;bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);WNT/beta-catenin signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000207709	NA	654434	406974	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	MIRN197|miR-197|miRNA197	LncRNA SNHG20 was highly expressed in the cancer tissues and serum of patients with NSCLC. LncRNA SNHG20 could bind to micro RNA (miR)-197 in a targeted manner.  LncRNA SNHG20 could promote the proliferation and inhibit the apoptosis of NSCLC cells. After the down-regulation of miR-197 by small interfering RNA (siRNA), the key molecules TCF and LEF1 of the Wnt/beta-catenin pathway were significantly down-regulated. The expression of lncRNA SNHG20 in the tissues of 116 NSCLC patients was detected via qRT-PCR The targets of lncRNA SNHG20 were pre_x0002_dicted using the bioinformatics method. The results of luciferase reporter gene assay showed that the luorescence intensity markedly declined only after the interaction between wild-type lncRNA SNHG20 and miR-197, demonstrating that lncRNA SNHG20 binds to miR-197 in a targeted manner. SNHG20 may promote the proliferation and migration of NSCLC cells by silencing the expression of miR-197	31957836	RID07048	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	
Laryngeal squamous cell carcinoma	SNHG20	miR-140	negatively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000234912	GRCh38_17:77086716-77099902	NA	NA	654434	NA	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	NA	There was a mutual regulation between SNHG20 and miR-140, which could together affect the malignant progression of LSCC.MiR-140 was negatively correlated with SNHG20 in LSCC tissues and cells. Expression levels of SNHG20 in 56 pairs of LSCC tissues and adjacent normal tissues were measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Finally, the dual-luciferase reporter gene assay was performed to explore the potentials of SNHG20 and miR-140 in LSCC. SNHG20 Was Highly Expressed in LSCC Tissues and Cell Lines. Knockdown of SNHG20 Inhibited Cell Proliferation, and Overexpression of SNHG20 Promoted Cell Proliferation. Direct Targeting Effect of SNHG20 and Mir-140 was Displayed by Dual-Luciferase Reporter Gene Assay. Besides, in order to further understand the interaction between SNHG20 and miR-140 in LSCC cells, we co-overexpressed or co-silenced miR-140 and SNHG20 in LSCC cells, and the miR-140 expression in co-transfected cells was examined by qRT-PCR Evidence suggested that the transcriptional activ_x0002_ity of SNHG20 may be regulated by miRNA-140. Dual-luciferase reporter gene assay demonstrated that SNHG20 could regulate the reporter gene activity of the miRNA-140 promoter. The above findings suggested that SNHG20 could inhibit the expression of miRNA-140 and promote the proliferation of LSCC cells.	31081112	RID07049	transcriptional regulation	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	
Hepatocellular carcinoma	SNHG20	PTEN	negatively-F	RIP;RNA pull-down;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	protein degradation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000171862	NA	654434	5728	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	BZS|MHAM|MMAC1|PTEN1|TEP1	SNHG20 was confirmed to interact with PTEN, which negatively regulated PTEN protein level. Finally, we proved HBxSNHG20PTEN signalling pathway involved in the regulation of HCC cell proliferationHBx promoted the proliferation of HCC cell and reduced the apoptosis of HCC cells through the SNHG20/PTEN signalling pathway. Besides, SNHG20 was highly expressed in HBV(+) HCC cells than in HBV(-) HCC cells. LncRNA SNHG20 and PTEN expression levels were detected by quantitative real-time polymerase chain reaction and western blot. RNA pull-down and RIP assays were used to detect the interaction between SNHG20 and PTEN.  PTEN protein in HepG2.2.15 cells was degraded in siRNA_x0002_control group, whereas siRNA_x0002_SNHG20 suppressed the degradation of PTEN protein in HepG2.2.15 cells under CHX treatment. These findings indicated that SNHG20 interacted with PTEN, and PTEN pro_x0002_tein level was negatively regulated by SNHG20. SNHG20 overexpression promoted the degradation of PTEN protein in HepG2 cells under CHX treatment	30690477	RID07050	interact with protein	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	HBX	SNHG20	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	protein-RNA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	PCG	lncRNA	NA	NA	ENSG00000234912	GRCh38_17:77086716-77099902	NA	654434	NA	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	SNHG20 was confirmed to interact with PTEN, which negatively regulated PTEN protein level. Finally, we proved HBxSNHG20PTEN signalling pathway involved in the regulation of HCC cell proliferationHBx promoted the proliferation of HCC cell and reduced the apoptosis of HCC cells through the SNHG20/PTEN signalling pathway. HBx overexpression upregulated lnc-SNHG20 expression level in HepG2 cells, and HBx knockdown suppressed lncSNHG20 expression level in HepG2.2.15 cells. Luciferase reporter assay showed that HBx significantly increased the luciferase activity of SNHG20 promoter region, whereas siRNA_x0002_HBx significantly decreased the luciferase activity of SNHG20 promoter region. Besides, HBx overexpression promoted the proliferation of HepG2 cells, and HBx knockdown inhibited the proliferation of HepG2.2.15 cells.	30690477	RID07051	expression association	NA		UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)
Malignant glioma	SNHG20	MIR4486	negatively-F	luciferase reporter assay;TargetScan;miRDB;RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(+);MDM2/p53 signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000265210	NA	654434	100616118	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	NA	SNHG20 acted as a competing endogenous RNA (ceRNA) to sponge the expression of miR-4486. LncRNA SNHG20 promoted the proliferation of glioma cells via sponging miR-4486 to regulate the MDM2-p53 pathway. Differential expression of SNHG20 in glioma tissues and cell lines was analyzed by RT-qPCR. The targets prediction was analyzed with the TargetScan database. SNHG20 was overexpressed in glioma tissues and cell lines. To further understand the role of SNHG20 in regulating the growth of glioma cells, the possible miRNA binding sites of SNHG20 were predicted with the miRDB database. To investigate whether the binding of SNHG20 with miR-4486 affect_x0002_ed the stability of miR-4486, the expression of miR-4486 in U87 cells expressing control vector or SNHG20 was detected by RT-qPCR. These data indicated the SNHG20 was an upstream regulator of the miR-4486/MDM2/p53 axis. Molecular mechanism studies revealed that SNGH20 sponged miR-4486 and modulated the MDM2-p53 pathway. MiR-4486 Targeted MDM2 and Up-Regulated the Expressionof p53 in Glioma Cells.	31298384	RID07052	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	
Epithelial ovarian cancer	SNHG22	Gal-1	positively-E	starBase v3.0;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-2467)	regulation	NA	Cisplatin;Paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000267322	GRCh38_18:49813961-49851059	NA	NA	103091864	NA	SCARNA17HG	NA	SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma. Here, we found that SNHG22 was significantly increased in EOC tissues and was significantly associated with a low level of differentiation. Forced SNHG22 expression promoted chemotherapy resistance in EOC cells. Knockdown of SNHG22 expression increased the sensitivity of EOC cells to cisplatin and paclitaxel. To assess SNHG22 expression in EOC, we first analyzed SNHG22 expression in 90 cases of EOC tissues and 20 cases of normal ovarian tissues by qRT-PCR SNHG22 functions as a ceRNA to regulate Gal-1 expression in EOC. To explore potential target miRNAs of SNHG22, Starbase3.0 was used, and the results revealed 27 predicted target miRNAs.  We carried out an RNA immunoprecipitation (RIP) assay with an antibody against argonaute 2 (AGO2) in SKOV3 and OAW28 cells. Luciferase reporter vectors containing a wt or mu SNHG22/Gal-1 3'-UTR were cotransfected with miR-2467 mimics or a negative control into SKOV3 and OAW28 cells.	31581131	RID07053	ceRNA or sponge	chemoresistance,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)	
Papillary thyroid carcinoma	SNHG3	PSMD10	positively-E	qRT-PCRIP;starBase v2.0;dual-luciferase reporter assay;	upregulation	qRT-PCR	NA	NA	cancer progression(+);colony formation(+);cell proliferation(+);cell migration(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000101843	NA	8420	5716	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	p28	SNHG3 could bind to miR-214-3p as a competing endogenous RNA (ceRNA) for this miRNA, thereby regulating proteasome 26S subunit non-ATPase 10 (PSMD10) expression, a miR-214-3p target.SNHG3 is an oncogenic lncRNA in PTC, acting at least in part via the miR-214-3p/PSMD10 axis.lncRNA SNHG3 accelerates papillary thyroid carcinoma progression via the miR-214-3p/PSMD10 axis. In an effort to assess the importance of SNHG3 in PTC, we initially assessed the SNHG3 levels in 42 pairs of PTC tumor and adjacent normal tissues using qRT-PCR which revealed a marked increase in SNHG3 expression in PTC samples. . We queried a lncRNA-siRNA interaction database (StarBase v2.0), which predicted that SNHG3 may serve as a sponge for miR-214-3p. We then used dual-luciferase reporter assays to confirm this hypothesis, revealing that miR-214-3p overexpression obviously reduced luciferase activity associated with the WT but not mutated version of SNHG3. A RIP assay further confirmed the ability of SNHG3 to act as a miR-214-3p sponge. qRT-PCRfurther demonstrated that miR-214-3p expression was significantly increased in sh-SNHG3-transfected TPC-1 cells relative to controls. SNHG3 knockdown impairs PTC colony formation and proliferation. SNHG3 knockdown impairs PTC cell migration.	32048306	RID07054	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Colorectal cancer	SNHG3	RUNX2	positively-E	dual-luciferase reporter assay;RIP;starBase v2.0	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-539)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000124813	NA	8420	860	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	SNHG3 could bind to miR-539, thereby up-regulating the expression of its target gene runt-related transcription factor 2 (RUNX2), and play an oncogenic role in CRC progression. To verify SNHG3 expression in CRC, we extracted the RNA from 58 pairs CRC tissues and adjacent normal tissue specimens, and quantitatively analyzed the SNHG3 expression level using real time quantitative PCR(qRT-PCR. SNHG3 is upregulated and associated with poor prognosis in CRC. We used a prediction software programs (Starbse2.0) to screen of candidate miRNAs that could potentially bind with SNHG3. To determine this predication, dual-luciferase reporter assays were performed. In addition, RIP assay revealed that SNHG3 and miR-539 were significantly enriched in Ago2-containing microribonucleoprotein complexes, suggesting that the Ago2 protein could bind to SNHG3 and miR-539 directly in CRC cells. These findings suggested that SNHG3 promotes CRC cell proliferation, migration and invasion through regulating the miR-539/RUNX2 axis.	32187965	RID07055	ceRNA or sponge	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SNHG3	HOXC8	positively-E	luciferase reporter assay;qRT-PCRtarBase v2.0;TargetScan	upregulation	qRT-PCR	TCGA	NA	cell growth(+);cell proliferation(+);cell viability(+);colony formation(+)	ceRNA(miR-196a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000037965	NA	8420	3224	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	HOX3|HOX3A	LncRNA SNHG3 promotes cell growth by sponging miR-196a-5p and indicates the poor survival in osteosarcoma. Clinical data from 127 cases of OS patients as well as the relative expression levels of SNHG3 and miR-196a-5p were downloaded from The Cancer Genome Atlas (TCGA) database. The expression level of SNHG3 was examined in different OS cell lines by qRT-PCRanalysis, indicating that SNHG3 exhibited a higher expression in U-2OS cells but a lower expression in MG-63 cells, as compared with normal tissues. To reveal the molecular mechanism by which SNHG3 contributes to OS, we used the starBasev2.0 to identify three miRNAs that might bind to SNHG3, of which miR-196a-5p had the strongest binding ability with SNHG3. The binding sites of miR-196a-5p with WT or Mut SNHG3 were indicated in Figure 3(b). The transfection efficiency of miR-196a-5p inhibitor or mimic in U2-OS or MG-63 cell line was determined by qRT-PCRanalysis.  To confirm whether SNHG3 can bind to miR-196a-5p, we co-transfected U-2OS and MG-63 cells with WT or Mut SNHG3 and miR-196a-5p inhibitor or mimic, indicating that miR-196a-5p inhibitor increased the luciferase activity of WT SNHG3 in U-2OS cells, and its mimic had an opposite effect in MG-63 cells, but miR-196a-5p inhibitor or mimic had no effects on the luciferase activity of Mut SNHG3 as compared with the control group. Restoration of miR-196a-5p expression repressed cell proliferation and reversed SNHG3-induced tumor-promoting effects. We further identified HOXC8 as a target of miR-196a-5p, which downregulated the expression of HOXC8 and reversed SNHG3-caused HOXC8 upregulation. These results suggested that SNHG3 contributed to OS growth by sponging miR-196a-5p/HOXC8 axis.  the target genes of miR-196a-5p were identified using the TargetScanHuman7.1. Knockdown of SNHG3 inhibited cell viability and colony formation, but its overexpression reversed these effects.	30791797	RID07056	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Gastric cancer	SNHG3	MED18	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell viability(+)cell migration(+);cell invasion(+)	DNA methylation;transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000130772	NA	8420	54797	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	FLJ20045|p28b|SRB5	Long non-coding RNA SNHG3 promotes progression of gastric cancer by regulating neighboring MED18 gene methylation. To understand the mechanistic involvement of long non-coding RNA (lncRNA) SNHG3 in gastric cancer (GC), the relative abundance of SNHG3 was determined by real-time PCR. Mechanistically, we uncovered SNHG3 associated with EZH2 and negatively regulated MED18 expression through methylation modulation. SNHG3-deficiency significantly suppressed cell proliferation and cell viability in vitro and xenograft progression in vivo. Our results characterized the aberrant up-regulation of SNHG3 in GC and suggested a potential oncogenic role in this disease. SNHG3 epigenetically regulated neighboring gene MED18 transcription by binding to EZH2. MED18 suppressed proliferation, migration and invasion of GC cells. SNHG3 promoted GC progression partly by regulating MED18 expression. Next, we examined the potential interaction between SNHG3 and EZH2 using RIP assay and our results showed obvious enrichment of SNHG3 transcripts in the EZH2 immunoprecipitated complex compared with IgG control in both cell lines. The ChIP result further confirmed the direct binding of EZH2 on the MED18 promoter region, which indicated the epigenetic regulation on MED18 expression.	31534128	RID07057	epigenetic regulation	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	SNHG3	PKM	positively-E	qRT-PCR;dual-luciferase reporter assay;western blot;miRBase;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);glycolysis metabolic process(+);TGF-beta signaling pathway(+);IL-6/JAK2/STAT3 signaling pathway(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000067225	NA	8420	5315	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	OIP3|PK3|PKM2|THBP1	SNHG3 Regulates the miR-330 Expression in Breast Tumor Cells.Knockdown of CAF-Secreted Exosomal SNHG3 Inhibited Breast Cancer Cell Proliferation Through Increasing miR-330 and Decreasing PKM Expression. CAF-secreted exosomal lncRNA SNHG3 served as a molecular sponge for miR-330-5p in breast cancer cells. Moreover, PKM could be targeted by miR-330-5p and was controlled by SNHG3 in breast cancer cells. Mechanistically, SNHG3 knockdown in CAF-secreted exosomes suppressed glycolysis metabolism and cell proliferation by the increase of miR-330-5p and decrease of PKM expression in tumor cells. Pyruvate kinase (PKM) functions as a key glycolytic enzyme which converts phosphoenolpyruvate to pyruvate. Breast cancer derived CAFs secreted significantly increased SNHG3 than that of normal breast cells MCF10A. Analyzed for SNHG3 by real-time quantitative PCR. To illuminate the specific mechanism by which SNHG3 exhibit oncogenic function in tumor cells, we analyzed the potential targets of SNHG3 using bioinformatics databases (miRBase and starBase). Bioinformatics analysis indicated that SNHG3 consisted of the binding sequences against the region of miR-330-5p. However, suppression of miR-330 significantly enhanced the luciferase signals of SNHG3-wildtype in MD-MBA-453 cells, while no positive luciferase signals were observed on SNHG3-mutation. Moreover, real-time quantitative PCR showed that SNHG3 expression was significantly decreased via overexpression of SNHG3, while no significant alteration was observed in the SNHG3-mutant treatment in MD-MBA-453 cells.  western blot showed that increasing of miR-330 and SNHG3 knockdown significantly decreased the protein expression of PKM in breast tumor cells, while silencing of miR-330 and overexpression of SNHG3 markedly increased the PKM level in MD-MBA-453 cells. Knockdown of CAF-Secreted Exosomal SNHG3 Inhibited Breast Cancer Cell Proliferation Through Increasing miR-330 and Decreasing PKM Expression.SNHG3 Knockdown in CAF-Derived Exosomes Inhibited Breast Cancer by the Upregulation of miR-330 and the Downregulation of PKM.	31956955	RID07058	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	E2F1	SNHG3	positively-E	luciferase reporter assay;western blot;CHIP;JASPAR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000242125	GRCh38_1:28505980-28510892	1869	8420	RBBP3|RBP3	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	SNHG3 could be induced by E2F1.LncRNA SNHG3 Is Activated by E2F1 and Promotes Proliferation and Migration of Non-Small-Cell Lung Cancer Cells Through Activating TGF-|- Pathway and IL-6/JAK2/STAT3 Pathway.  In this study, we detected the upregulated expression of SNHG3 in NSCLC tissues as well as cells through quantitative reverse-transcription polymerase chain reaction (qRT-PCR analysis. Mechanistic investigations revealed that SNHG3 was a predicted direct transcriptional target of E2F1. We observed that the transcriptional activation of SNHG3 could be induced by E2F1. To explore the mechanism, rescue experiments were carried out, which revealed that the cotreatment with SB-431542, JSI-124, or JSI-124 + SB-431542 rescued the effects brought by the overexpression of SNHG3 on NSCLC cell proliferation, migration, and epithelial-mesenchymal transition process. Our results suggested that E2F1 activated SNHG3 and promoted cell proliferation and migration in NSCLC via transforming growth factor-beta pathway and interleukin-6/janus-activated kinase 2/signal transducer and activator of transcription 3 pathway, which implied that SNHG3 may be a biomarker for the treatment of patients with NSCLC. E2F1 activates SNHG3 transcription. SNHG3 promotes proliferation and migration of NSCLC cells via TGF-beta pathway and IL-6/JAK2/STAT3 pathway. In the present study, SNHG3-knockdown decreased the expression of IL-6, P-JAK2, and P-STAT3, suggesting that SNHG3 activated TGF-beta signaling path_x0002_way and IL-6/JAK2/STAT3 pathway in NSCLC cells. With the use of JASPAR online prediction tool, we found that the transcription factor E2F1 is predicted to have binding sites that bind to SNHG3 promoter. . To verify the interaction of E2F1 and SNHG3, we performed ChIP assay and the results revealed that endogenous E2F1 could bind to the SNHG3 promoter. Thus, this sequence was mutated for luciferase reporter assay. Luciferase reporter assays indicated that E2F1 could bind to the SNHG3 promoter and increase the luciferase activity of pGL3-SNHG3-Wt, but had no effect on the luciferase activity of pGL3-SNHG3-Mut.	31602642	RID07059	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)
Breast cancer	SNHG3	HDGF	positively-E	qRT-PCR;dual-luciferase reporter assay;western blot;RIP;starBase v2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000143321	NA	8420	3068	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	HMG1L2	SNHG3 upregulation inhibited miR-384 activity and led to hepatoma-derived growth factor (HDGF) overexpression in breast cancer cells.LncRNA SNHG3 Promotes Cell Proliferation and Invasion Through the miR-384/hepatoma-derived Growth Factor Axis in Breast Cancer. The findings of this study show that SNHG3 functions as an oncogene in breast cancer and promotes breast cancer cell proliferation and invasion by regulating the miR-384/HDGF axis. qRT-PCR;ISHowed that SNHG3 expression was significantly higher in breast cancer tissues than in adjacent normal tissues. Bioinformatics analysis showed that SNHG3 might interact with miR-384. A dual-luciferase reporter assay showed that miR-384 mimic significantly reduced the luciferase activity of WT-SNHG3 in breast cancer cells. qRT-PCR;ISHowed that SNHG3 knockdown remarkably increased miR-384 expression in breast cancer cells. Through starBase v2.0 Program prediction, 16 miRNAs were predicted as possible targets of SNHG3. RIP assays showed that SNHG3 and miR-384 (not miR-758-3p) expression was significantly enriched in the Ago2 pellet compared to that in the IgG control pellet. These data indicate that SNHG3 interacts with miR-384 and decreases its expression in breast cancer.	31586299	RID07060	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Clear cell renal cell carcinoma	SNHG3	TOP2A	positively-E	qPCR;western blot;luciferase reporter assay;starBase;miRcode;LncRNASNP2	upregulation	microarray;qRT-PCR	TCGA;GSE53757	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000131747	NA	8420	7153	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	TOP2|TOP2alpha|TOPIIA	SNHG3 could bind to miR-139-5p, thereby up-regulating the expression of its target gene TOP2A, and play a role in promoting tumor progression in ccRCC. The expression level of TOP2A in ccRCC tissues compared with in adjacent normal tissues in GEO cohort GSE53757 and TCGA database. According to the microarray results of 72 pairs of RCC specimens, the expression of SNHG3 were also upregulated in RCC. qRT-PCRresult demonstrated a significant increase in the SNHG3 expression in RCC cell lines compared with in the HK-2-cell, and the ACHN and Caki-1-cell lines exhibited the higher expression. In order to investigate the potential mechanism of SNHG3 in ccRCC, we used three prediction software programs (starBase, miRcode and LncRNASNP2 tools) to screen of candidate miRNAs molecules that could potentially target SNHG3. Then, we constructed a luciferase reporter vectors (psi-SNHG3) of wild-type SNHG3 to psicheck2 vector, and also designed a miR-139-5p mutant that wouldn't bound with SNHG3. To further explore whether the functions of SNHG3 were relied on sponging miR-139-5p in ccRCC, ACHN cells stably transfected with sh-SNHG3 or sh-Lacz were transfected with miR-139-5p inhibitor or a NC of the inhibitor. These results indicate that SNHG3 promotes ccRCC proliferation and metastation by sponging miR-139-5p. The qPCR and western blot results showed that SNHG3 knockdown could inhibit the expression of TOP2A, whereas miR-139-5p inhibitor could relieve the inhibition of TOP2A by SNHG3 knockdown.	31505165	RID07061	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Laryngeal carcinoma	SNHG3	WEE1	positively-E	qRT-PCR;luciferase reporter assay;starBase v2.0;TargetScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000166483	NA	8420	7465	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	WEE1A	SNHG3 could sponge miR-384 at the 3---UTR with complementary binding sites, which was validated by a dual-luciferase reporter assay.LncRNA SNHG3 regulates laryngeal carcinoma proliferation and migration by modulating the miR-384/WEE1 axis. Real time-PCR (RT-PCR was used to estimate the expression of SNHG3 in LC tissues and cell lines TU212, TU686, and Hep-2. SNHG3 was upregulated in laryngeal carcinoma tissues and cell lines. he bioinformatics Starbase v2.0 (http://starbase.sysu.edu.cn/starbase2/index.php) database revealed that miR-384 had a complementary sequence to SNHG3. The luciferase reporter assay confirmed the binding interaction between miR-384 and SNHG3 in 293T cells. Also, a qRT-PCRanalysis demonstrated that deletion of SNHG3 prominently enhanced expression of miR-384. A bioinformatic analysis by TargetScan (http://www.targetscan.org/) predicted WEE1 as a target of miR-384. In this work, our data indicated that the facilitation roles of the miR-384 inhibitor in cell migration and invasion were partly reversed by silencing WEE1.	31238052	RID07062	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Prostate cancer	SNHG4	ZIC5	positively-E	qRT-PCR;luciferase reporter assay;western blot;starBase	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell growth(+);cell invasion(+)	ceRNA(miR-377)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000139800	NA	724102	85416	NCRNA00059|U19H	NA	In addition, miR-377 was a target of SNHG4 and ZIC5 was a target gene of miR-377 in PCa. SNHG4 promoted ZIC5-mediated growth and metastasis through modulating miR-377. Quantitative real-time polymerase chain reaction (qRT-PCR was utilized to detect SNHG4 expression in tissue samples and PCa cells. Luciferase reporter assay, qRT-PCR and western blotwere carried out to explore and confirm the interaction among SNHG4, miR-377, and ZIC5. NHG4 was highly expressed in PCa and its upregulation was induced by transcription factor SP1. SNHG4 knockdown inhibited the growth, migration, and invasion of PCa cells.  Relative miR-377 expression by bioinformatics analyses using GSE21036 data set. Interestingly, bioinformatics analyses using TCGA data set (using "Starbase'-algorithm) suggested that the levels of miR-377 were relatively lower than that of SNHG4.	31608997	RID07063	ceRNA or sponge	metastasis	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	UP(LIHC);DATA(GSE117623)
Prostate cancer	SP1	SNHG4	positively-E	ChIP;JASPAR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell migration(+);cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000281398	GRCh38_5:139274102-139284899	6667	724102	NA	NCRNA00059|U19H	In addition, miR-377 was a target of SNHG4 and ZIC5 was a target gene of miR-377 in PCa. SNHG4 promoted ZIC5-mediated growth and metastasis through modulating miR-377. Quantitative real-time polymerase chain reaction (qRT-PCR was utilized to detect SNHG4 expression in tissue samples and PCa cells. Chromatin immunoprecipitation assays were conducted to determine the binding between SP1 and SNHG4 promoter. NHG4 was highly expressed in PCa and its upregulation was induced by transcription factor SP1. SNHG4 knockdown inhibited the growth, migration, and invasion of PCa cells. Relative miR-377 expression by bioinformatics analyses using GSE21036 data set. We thereby searched JASPAR algorithm and found that there were three high-score binding sites of SP1, which were involved in regulating diverse cellular processes, distributing in the promoter of SNHG4. Thedata confirmed that SP1 was able to bind to B1 site of SNHG4 promoter. For further clarifying that, we cloned wild-type or mutant type B1 site into luciferase reporter vector and subsequently detected the changes of luciferase activities.	31608997	RID07064	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)
Cervical cancer	SNHG4	c-Met	positively-E	luciferase reporter assay;RIP;miRcode	upregulation	qRT-PCR	NA	NA	cell growth(+);cancer progression(+)	ceRNA(miR-148a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000105976	NA	724102	NA	NCRNA00059|U19H	NA	SNHG4 could up-regulate the expression of c-Met by targeting and interacting with miR-148a-3p. Finally, silence SNHG4 down-regulated the expression of c-Met by promoting miR-148a-3p, and ultimately suppressed the growth of CC tumor in vivo. In the present study, qRT-PCRwas used to detect the expressions of SNHG4 and miR-148a-3p in CC tissues and cell lines. As exhibited in Figure 1(a), the SNHG4 expression in CC tissues was remarkably up-regulated, compared with the adjacent normal tissue. Long non-coding RNA SNHG4 promotes cervical cancer progression through regulating c-Met via targeting miR-148a-3p. Effects of silencing SNHG4 on the growth of CC cells. Firstly, the miRcode software for biological information predicted that there were potential binding sites of SNHG4 in miR-148a-3p. Besides, the dual-luciferase reporter gene results found that after co-transfection with miR-148a-3p, luciferase activity in SNHG4 WT groups were remarkably reduced (P < 0.05), while luciferase activity in SNHG4 MUT groups was not observably changed (Figure 3(c), P > 0.05). Moreover, RIP results showed that miR-148a-3p and SNHG4 in HeLa and SiHa cells were markedly enriched by Ago2 antibody. In our study, SNHG4 was identified as a sponge of miR-98-5p by dual-luciferase assay.	31590627	RID07065	ceRNA or sponge	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	
Lung cancer	SNHG4	miR-98-5p	negatively-F	luciferase reporter assay;TargerScan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000281398	GRCh38_5:139274102-139284899	NA	NA	724102	NA	NCRNA00059|U19H	NA	LncRNA SNHG4 promotes proliferation, migration, invasion and 2 epithelial-mesenchymal transition of lung cancer cells by regulating 3 miR-98-5p. In addition, we found that SNHG4 silencing induced up-regulation of miR-98-5p. MiR-98-5p inhibition abrogated the effect of SNHG4 silencing on proliferation and invasion of lung cancer cells. SNHG4 probably exerts its pro-survival and pro-metastatic effects by sponging anti-tumor miR-98-5p. SNHG4 acts as a sponge of miR-98-5p, which could directly target CDK6 and SALL4. Dual-luciferase assay was carried out to validate the interaction between SNHG4 and miR-98-5p. CDK6 and SALL4 are downstream targets of miR-98-5p through prediction on TargetScan database, and they were detected in the subsequent investigations. The expression of lncRNA SNHG4 was detected using real time-PCR in six lung cancer cell lines.	31220419	RID07066	ceRNA or sponge	metastasis	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	
Nasopharynx carcinoma	SNHG5	HMGB3	positively-E	RT-qPCR;starBase;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1179)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000029993	NA	387066	3149	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	HMG2A|HMG4|MGC90319	lncRNA-SNHG5 acted as a molecular sponge of miR-1179 in NPC.LncRNA SNHG5 promotes nasopharyngeal carcinoma progression by regulating miR-1179/HMGB3 axis. First, LncRNA-SNHG5 expression was increased in NPC tissues compared to normal tissues. Next, miR-1179 was predicted to have binding sites with LncRNA-SNHG5 in starBase version 2.0. Dual luciferase reporter was then performed to verify the above prediction. RT-qPCR showed that upregulation of SNHG5 decreased miR-1179 expression, while knockdown of SNHG5 increased miR-1179 expression. RT-qPCR and western blotwere employed to detect mRNA and protein expressions.  Functionally, upregulation of lncRNA-SNHG5 and downregulation of miR-1179 accelerated NPC cell proliferation, migration and invasion.	32131767	RID07067	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE109761,GSE111065,GSE55807,GSE67939)
Hepatocellular carcinoma	SNHG5	RNF38	positively-E	luciferase reporter assay;starBase;TargetScan	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000137075	NA	387066	152006	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-363-3p/RNF38 axis. The expression levels of SNHG5, miR-363-3p, and Ring Finger Protein 38 (RNF38) were measured by using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR or western blot assay, respectively. The relationship among SNHG5, miR-363-3p, and RNF38 was confirmed using bioinformatics analysis and Luciferase reporter assay. The expression of SNHG5 and RNF38 was elevated in HCC tissues and cell lines, and highly expressed SNHG5 and RNF38 could induce apoptosis and repress proliferation, migration, as well as invasion in HCC cells. Further investigations showed that SNHG5 might act as a competing endogenous RNA of miR-26a-5p and thereby cause the derepression of the downstream target RNF38. Moreover, rescue experiments indicated that SNHG5 silence inhibited the progression of HCC cells by regulating miR-363-3p, and the facilitated effects of RNF38 in the progression of HCC cells were regulated by miR-363-3p. SNHG5 is Upregulated in HCC Tissues and Cell Lines. RNF38 is Elevated in HCC Tissues and Cell Lines and Downregulated RNF38 Inhibits the Progression of HCC Cells. SNHG5 Silence Inhibits the Proliferation, Migration, and Invasion but Induces Apoptosis in HCC Cells. To further explore the underlying molecular mechanism of SNHG5 in HCC progression, the potential targets of SNHG5 were predicated using StarBase prediction program and SNHG5 con_x0002_tained the wild-type binding sequence of miR-363-3p. According to the prediction of the TargetScan software, RNF38 was predicted to be a target of miR-363-3p with putative binding sites.	32329834	RID07068	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	SNHG5	ZEB1	positively-E	qRT-PCR;luciferase reporter assay;RIP;siRNA;starBase	upregulation	qRT-PCR	TCGA	NA	cancer progression(+);cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-205-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000148516	NA	387066	6935	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	lncRNA SNHG5-mediated miR-205-5p downregulation contributes to the progression of clear cell renal cell carcinoma by targeting ZEB1. In our study, substantially higher abundance of SNHG5 was observed in ccRCC specimens and cell lines. SNHG5 knockdown obviously suppressed the proliferative, migratory, and invasive capabilities of ccRCC cells, whereas SNHG5 overexpression induced the opposite effects. Mechanistically, SNHG5 activated the transcription of ZEB1, which exerts a pivotal role in modulation of epithelia-mesenchymal transition (EMT) and tumor metastasis. SNHG5 was then shown to act as an endogenous sponge for miR-205-5p, which targets ZEB1 in ccRCC. Moreover rescue experiments revealed that SNHG5 promotes ccRCC cell proliferation, migration, and invasion in a miR-205-5p-dependent manner. Additionally, in vivo assays further indicated that overexpression or silencing of SNHG5 in ccRCC cells promoted or suppressed the tumorigenesis and metastasis, respectively. To determine whether SNHG5 is differentially expressed in ccRCC tissues, RNA sequencing data from ccRCC and nontumor kidney tissues downloaded from TCGA were analyzed. The results of qRT-PCRanalysis of 52 paired ccRCC specimens and matched nontumor kidney specimens were consistent, and as described in Figure 1C, SNHG5 abundance was obviously enhanced in the ccRCC samples examined in our study.  SNHG5 regulates tumorigenicity and metastasis in vivo. To investigate whether SNHG5 possesses similar mechanism in ccRCC, we used StarBase 18 and DIANA-LncBase 19 to predict the potential miRNAs regulated by SNHG5. A qRT-PCRassay was applied to validate the expression levels of candidate miRNAs in ccRCC cells transfected with si-SNHG5, si-NC, pcDNA3.1/SNHG5, or pcDNA3.1/Con. To determine the functional associations among SNHG5, miR-205-5p, and ZEB1 in ccRCC cells, we conducted a luciferase assay. As described in Figure 4C, a strong immunoprecipitation signal for the Ago2 protein was observed in extracts of ACHN cells.	32281285	RID07069	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Clear cell renal cell carcinoma	SNHG5	TWIST1	positively-E	qPCR;western blot;Luciferase reporter assay;RIP;TargetScan;PicTar;miRanda	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(+);cell migration(+)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000122691	NA	387066	7291	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Long Non-Coding RNA SNHG5 Affects the Invasion and Apoptosis of Renal Cell Carcinoma by Regulating the miR-363-3p-Twist1 Interaction. We found that lncRNA SNHG5 is upregulated in human ccRCC tissues and that lncRNA SNHG5 inhibition reduced ccRCC cell invasion and promoted apoptosis in vitro. Bioinformatics database searching revealed that lncRNA SNHG5 is predicted to regulate the interaction between miR-363-3p and Twist1. The direct SNHG5-miR-363-3p and Twist1-miR-363-3p interactions were confirmed via dual-luciferase reporter assays. Additionally, functional assays demonstrated that SNHG5 promotes cell invasion and inhibits apoptosis, while miR-363-3p inhibits cell invasion and promotes apoptosis via an interaction with Twist1.  Furthermore, we found that Twist1 promotes tumor metastasis by regulating matrix metalloproteinase (MMP)2 and MMP9 levels. The miRNAs that may target Twist1 were predicted using TargetScan (http://genes.mit.edu/targetscan/), PicTar (http://pictar.mdc-berlin.de/), and miRanda (http://cbio.mskcc.org/cgi-bin/mirnaviewer/mirnaviewer.pl). The qRT-PCRanalysis revealed that SNHG5 expression levels were significantly increased in ccRCC tissues compared to those in non-tumor tissues. Knockdown of lncRNA SNHG5 inhibited RCC cell invasion and promoted cell apoptosis by targeting miR-363-3p. Twist1 is a direct target of miR-363-3p. lncRNA SNHG5 is involved in metastasis of ccRCC in vitro and in vivo via regulation of the miR-363-3p-Twist1 interaction.	32194916	RID07070	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(SKCM);DATA(GSE38495)
Acute myeloid leukemia	SNHG5	DNAJB9	positively-E	qRT-PCR;luciferase reporter assay;shRNA;miRcode;starBase;miRdb;TargetScan	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);cell autophagy(+)	ceRNA(miR-32)	regulation	NA	NA	CSC	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000128590	NA	387066	4189	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	MDG1	miR-32 was identified as the downstream target of SNHG5 and miR-32 inhibitor abrogated the inhibiting effects of downregulated SNHG5 on AML cell viability. Expression profiles of LncRNAs and SNHG5 was obviously increased in AML. To construct expression profiles of LncRNAs in AML, we used microarray (Arraystar Human LncRNAmicroarrayV4.0) to examine expression profiles of LncRNAs. To verify the reliability of the microarray, we used qRT-PCRanalysis to verify the microarray results in AML and healthy donors'-PBMCs samples. Long non-coding RNA SNHG5 regulates chemotherapy resistance through the miR-32/DNAJB9 axis in acute myeloid leukemia. Therefore, these data proved SNHG5 promoted ADM resistance in AML cells. To further explore the underlying mechanisms involving SNGH5 in the development of AML, we examined a set of microRNAs that were predicted to bind SNHG5 by miRcode and starBase v2.0 program. These findings revealed SHNG5 may regulate chemotherapy sensitivity in AML cells through targeting of miR-32. The expression profiles of these miRNAs in HL60 cells transfected with SNHG5 overexpression vector or SNHG5 shRNA were examined by qRT-PCR The dual-luciferase reporter gene system results showed that miR-32 mimic transfection successfully decreased relative luciferase activity in 293-T cells transfected with wild type SNHG5 instead of the mutated counterpart. Based on these results, we explored the mechanisms underlying the activity of miR-32 in AML, the online software (miRdb, TargetScan and miRcode) showed seven overlapping potential downstream targets of miR-32, including DNAJB9, CD69, TOB1, TOB2, MAP2K4, MOAP1, and FBXW7. Therefore, SNHG5 regulates chemotherapy resistance in AML cells through the miR-32/DNAJB9 axis. The SNHG5/miR-32/DNAJB9 axis targets autophagy. However, there are no reports on DNAJB9 in leukemia. We found that DNAJB9 expression were negatively correlated with miR-32, and positively correlated with SNHG5 in AML cells. Our previous studies have found that leukemia cells regulate chemotherapy resistance through autophagy	31884339	RID07071	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE51827,GSE67939)
Glioblastoma	YY1	SNHG5	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);p38/MAPK signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	TF	lncRNA	ENSG00000100811	NA	ENSG00000203875	GRCh38_6:85650491-85678932	7528	387066	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	YY1-Activated Long Noncoding RNA SNHG5 Promotes Glioblastoma Cell Proliferation Through p38/MAPK Signaling Pathway. Gene expression was determined by qRT-PCRor western blot, as appropriate. SNHG5 was highly expressed in GBM. The relationship between YY1 and SNHG5 was assessed via ChIP and luciferase reporter assays. Loss- and gain-of-function assays revealed that SNHG5 promoted GBM cell proliferation and inhibited cell apoptosis in GBM. Mechanism experiments proved Yin Yang 1 (YY1) as transcriptional activator of SNHG5 in GBM. More importantly, we found that SNHG5 played the oncogenic role in GBM by activating p38/MAPK signaling pathway.  Therefore, these results indicated that YY1 could bind with SNHG5 promoter to accelerate its transcription.	31657621	RID07072	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)
Chronic myelogenous leukemia	SNHG5	TNFRSF10A	positively-E	Methylation-specific PCR;shRNA	upregulation	qPCR	NA	NA	cell proliferation(+);cell differentiation(-);apoptosis process(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Chronic myeloid leukemia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000104689	NA	387066	8797	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	Apo2|CD261|DR4|TRAILR-1|TRAILR1	Inhibition of SNHG5 suppressed K562 cell proliferation through inducing the differentiation and apoptosis by inhibiting methylation of DR4. Therefore, downregulated SNHG5 could play a key role in CML progression. lncRNA SNHG5 has been reported to be upregulated in CML. Additionally, MSP analysis provided evidence that inhibition of SNHG5 suppressed the methylation of DR4 CpG islands. Inhibition of SNHG5 suppressed K562 cell proliferation through inducing the differentiation and apoptosis by inhibiting methylation of DR4. The qPCR results showed that both SNHG5-shRNA1 and SNHG5-shRNA2 obviously decreased SNHG5 expression in K562 cells.	31506418	RID07073	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	SNHG5	E2F3	positively-E	qRT-PCR;luciferase reporter assay;RIP;starBase;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-205)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000112242	NA	387066	1871	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	SNHG5 acts as a sponge for miR-205, which inhibits tumour growth in glioma by targeting E2F transcription factor 3 (E2F3). Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis. First, we found that SNHG5 expression was higher in glioma. First, we confirmed the transfection efficiency in these cell lines by qRT-PCR SNHG5 promotes glioma cell glucose uptake, migration and invasion. SNHG5 sponges miR-205 which suppresses glioma glucose uptake, migration and invasion. Through the online database starBase v3.0 (http://starbase.sysu.edu.cn/), we found that miR-205 may be a target of SNHG5. Second, through qRT-PCR we determined that miR-205 expression levels were up-regulated after down-regulating SNHG5 in glioma cells and that miR-205 mimics could also down-regulate SNHG5 expression levels in glioma cells. In addition, SNHG5 luciferase reporter plasmids with wild-type and predicted mutant sites for miR-205 were constructed. We found that miR-205 mimics decreased the luciferase activity of the wild-type plasmid but did not reduce the luciferase activity of the mutant plasmid. In addition, SNHG5 luciferase reporter plasmids with wild-type and predicted mutant sites for miR-205 were constructed. We found that miR-205 mimics decreased the luciferase activity of the wild-type plasmid but did not reduce the luciferase activity of the mutant plasmid. In addition, we carried out an RNA pull-down assay, and the results illustrated that SNHG5 was pulled down by the target oligos.	31292168	RID07074	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	SNHG6	ETS1	positively-E	Luciferase reporter assay;RIP	upregulation	qRT-PCR;western blot	NA	NA	tumorigenesis(+)	ceRNA(miR-944;miR-181d-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000134954	NA	641638	2113	HBII-276HG|NCRNA00058|U87HG	ETS-1|EWSR2|FLJ10768	We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR-944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9.	32099396	RID07075	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Cholangiocarcinoma	SNHG6	miR-101-3p	negatively-E	Starbase;DIANA-LncBasev2;dual-luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);angiogenesis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	Further mechanistic studies revealed that SNHG6 could compete with the transcription factor E2F8 to bind with miR-101-3p, thus affecting E2F8 expression. Taken together, these results provided a comprehensive analysis of the role of SNHG6 in CCA cells and offered important clues to understand the key roles of competing endogenous RNA (ceRNA) mechanisms in human cholangiocarcinoma.	32226515	RID07076	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Cholangiocarcinoma	SNHG6	E2F8	positively-F	qPCR;western blot	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);angiogenesis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000129173	NA	641638	79733	HBII-276HG|NCRNA00058|U87HG	FLJ23311	Further mechanistic studies revealed that SNHG6 could compete with the transcription factor E2F8 to bind with miR-101-3p, thus affecting E2F8 expression. Taken together, these results provided a comprehensive analysis of the role of SNHG6 in CCA cells and offered important clues to understand the key roles of competing endogenous RNA (ceRNA) mechanisms in human cholangiocarcinoma.	32226515	RID07077	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	SNHG6	MYC	positively-E	GSEA;correlation analysis	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(let-7c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000136997	NA	641638	4609	HBII-276HG|NCRNA00058|U87HG	bHLHe39|c-Myc|MYCC	Mechanistic assays revealed that SNHG6 acted as a competing endogenous RNA (ceRNA) to sponge let-7c-5p and thereby modulating the depression of c-Myc by let-7c-5p. Taken together, SNHG6 promotes HCC cell proliferation via competitively binding let-7c-5p in hepatocellular carcinoma.	31563323	RID07078	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Esophagus squamous cell carcinoma	SNHG6	miR-186-5p	negatively-E	Luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	lncRNA SNHG6 was identified as a decoy for miR-186-5p, thereby promoting the expression of miR-186-5p target HIF1alpha.restoration of SNHG6 or HIF1alpha could reverse the inhibitory effect of miR-186-5p on ESCC cell proliferation, migration, and invasion.	31853782	RID07079	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Esophagus squamous cell carcinoma	SNHG6	HIF1A	positively-E	Luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-186-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100644	NA	641638	3091	HBII-276HG|NCRNA00058|U87HG	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	lncRNA SNHG6 was identified as a decoy for miR-186-5p, thereby promoting the expression of miR-186-5p target HIF1alpha.restoration of SNHG6 or HIF1alpha could reverse the inhibitory effect of miR-186-5p on ESCC cell proliferation, migration, and invasion.	31853782	RID07080	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Ovarian clear cell carcinoma	SNHG6	MIR4465	negatively-E	miRcode;starBase v2.0;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000264390	NA	641638	100616180	HBII-276HG|NCRNA00058|U87HG	NA	Further functional experiments demonstrated that knockdown of SNHG6 in OCCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumour growth in vivo. Moreover, SNHG6 functioned as a competing endogenous RNA (ceRNA), effectively acting as a sponge for miR-4465 and thereby modulating the expression of enhancer of zeste homolog 2 (EZH2). Taken together, our data suggest that SNHG6 is a novel molecule involved in OCCC progression and that targeting the ceRNA network involving SNHG6 may be a treatment strategy in OCCC.	31119871	RID07081	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Colorectal cancer	SNHG6	miR-181a-5p	negatively-E	DIANA lncBase v.2;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	NA	NA	641638	NA	HBII-276HG|NCRNA00058|U87HG	NA	In this study, we found that SNHG6 was significantly upregulated in CRC tissues and cell lines, compared with normal tissues and normal colorectal epithelial cell line NCM460, respectively. High expression of SNHG6 was positively correlated with tumor size, advanced TNM stage, and distant metastasis. Survival analyses revealed that SHNG6 was significantly associated with poor clinical outcomes and could serve as an independent prognostic factor. Loss-of-function studies demonstrated that SNHG6 knockdown inhibited CRC cell proliferation, induced G0/G1 arrest, promoted apoptosis, suppressed CRC cell migration and invasion, and restrained tumor growth. Mechanistic investigations showed that SNHG6 acted as a competing endogenous RNA for miR-181a-5p and attenuated the inhibitory effect of miR-181a-5p on E2F5.	30666158	RID07082	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Colorectal cancer	SNHG6	E2F5	positively-E	TargetScan 7.1;luciferase reporter	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000133740	NA	641638	1875	HBII-276HG|NCRNA00058|U87HG	NA	In this study, we found that SNHG6 was significantly upregulated in CRC tissues and cell lines, compared with normal tissues and normal colorectal epithelial cell line NCM460, respectively. High expression of SNHG6 was positively correlated with tumor size, advanced TNM stage, and distant metastasis. Survival analyses revealed that SHNG6 was significantly associated with poor clinical outcomes and could serve as an independent prognostic factor. Loss-of-function studies demonstrated that SNHG6 knockdown inhibited CRC cell proliferation, induced G0/G1 arrest, promoted apoptosis, suppressed CRC cell migration and invasion, and restrained tumor growth. Mechanistic investigations showed that SNHG6 acted as a competing endogenous RNA for miR-181a-5p and attenuated the inhibitory effect of miR-181a-5p on E2F5.	30666158	RID07083	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	SNHG6	UPF1	negatively-E	bioinformatics target gene prediction;qRT-PCR;western blot.	upregulation	qRT-PCR	NA	NA	TGF-beta/SMAD signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000005007	NA	641638	5976	HBII-276HG|NCRNA00058|U87HG	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	SNHG6 may play an oncogenic role in CRC cells by activating TGF-beta/Smad signaling pathway via targeting of UPF1 and inducing EMT via regulating ZEB1. This could be a prognostic biomarker and therapeutic target for CRC.	30662328	RID07084	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SNHG6	ZEB1	positively-E	bioinformatics target gene prediction;qRT-PCR;western blot.	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000148516	NA	641638	6935	HBII-276HG|NCRNA00058|U87HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	SNHG6 may play an oncogenic role in CRC cells by activating TGF-beta/Smad signaling pathway via targeting of UPF1 and inducing EMT via regulating ZEB1. This could be a prognostic biomarker and therapeutic target for CRC.	30662328	RID07085	expression association	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	SNHG6	VASP	positively-E		upregulation	sequencing	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000125753	NA	641638	7408	HBII-276HG|NCRNA00058|U87HG	NA	More importantly, SNHG6 and VASP both can bind directly to miR-26a, suggesting that SNHG6 could act as a ceRNA to sponge miR-26a, thereby promoting the expression of VASP, which leading to activated proliferation, migration and invasion of breast cancer cells. Taken together, this study revealed the important role of the SNHG6/miR-26a/VASP regulatory network in the development of breast cancer, and provided a reference for exploring new pathogenesis and biomarkers of breast cancer.	31387807	RID07086	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SNHG6	ETS1	negatively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell viability(-);cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000134954	NA	641638	2113	HBII-276HG|NCRNA00058|U87HG	ETS-1|EWSR2|FLJ10768	The overexpression of SNHG6 inhibited colon cell viability and proliferation by targeting ETS1 through the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. These results suggested that SNHG6 may directly suppress ETS1, which may be one of potential mechanisms through which it inhibits the viability and proliferation of colorectal cancer cells, and it provides novel insight into the carcinogenesis of colorectal cancer. In addition, it may assist in the development of a treatment approach for ETS1-activated colorectal cancer.	31322251	RID07087	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG6	SERPINH1	positively-E	Dual-luciferase reporter gene assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-139-5p)	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000149257	NA	641638	871	HBII-276HG|NCRNA00058|U87HG	CBP1|CBP2|HSP47|SERPINH2	In contrast, miR-139-5p was significantly down-regulated in HCC cells, the inhibition of miR-139-5p promotes the proliferation of HCC cells, and accelerated the cell cycle of HCC cells. Our study demonstrated the co-expression of SNHG6 and SERPINH1 in HCC cells for the first time, which revealed that SNHG6 could serve as a novel oncogene for the HCC therapy by its regulation.	31258024	RID07088	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Wilms' tumor	SNHG6	MIR15A	negatively-E	qPCR;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Wilms' tumor	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000283785	NA	641638	406948	HBII-276HG|NCRNA00058|U87HG	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Further study found that the knockdown of SNHG6 elevated the expression of miR-15a. Then, the combination of miR-15a inhibitor abolished the inhibiting effect of si-SNHG6 on WT progression. We also found that the TAK1/JNK and Wnt/beta-catenin signal pathways were inactivated by the knockdown of SNHG6 through elevating the expression of miR-15a. In summary, SNHG6 is an oncogene of WT development by targeting miR-15a.	31257923	RID07089	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Cervical cancer	SNHG7	DKK1	negatively-F	chromatin immunoprecipitation assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetically silence	binding/interaction	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000107984	NA	84973	22943	MGC16037|NCRNA00061	DKK-1|SK	SNHG7 was conspicuously higher expressed in CC cells. Knockdown of SNHG7 was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution of SNHG7 to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed that SNHG7 silencing weakened the binding of EZH2 to DKK1 promoter as well as the occupancy of H3K27me3 in DKK1 promoter.	32275170	RID07090	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	SNHG7	miR-181	negatively-E	bioinformatics analysis;luciferase assays	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	NA	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	Mechanistically, it was found that SNHG7 interacted with microRNA mir-181 and sequentially up-regulated cbx7. cbx7, which suppresses the Wnt/beta-catenin pathway in LUAD, was found to be a direct target of mir-181. Taken together, loss of SNHG7 in LUAD up-regulated mir-181 and then down-regulated the tumor suppressor cbx7.	32201260	RID07091	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Hepatocellular carcinoma	SNHG7	miR-122-5p	negatively-E	Luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	Luciferase reporter assay revealed the direct interaction between SNHG7 and miR-122-5p. Moreover, SNHG7 knockdown decreased the levels of ribosomal protein L4 (RPL4) mRNA and protein in HCC cells. Accordingly, the stability of RPL4 mRNA was reduced by SNHG7 silencing. More importantly, either miR-122-5p knockdown or RPL4 restoration partially reversed SNHG7 silencing-induced tumor suppressive effects on HCC cells. In conclusion, we demonstrated that SNHG7 expression was up-regulated in HCC. SNHG7 contributed to HCC progression by regulating miR-122-5p and RPL4. Therefore, SNHG7 might be a potential biomarker and therapeutic target for HCC.	31545291	RID07092	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Hepatocellular carcinoma	SNHG7	RPL4	positively-E	starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000174444	NA	84973	6124	MGC16037|NCRNA00061	L4	Luciferase reporter assay revealed the direct interaction between SNHG7 and miR-122-5p. Moreover, SNHG7 knockdown decreased the levels of ribosomal protein L4 (RPL4) mRNA and protein in HCC cells. Accordingly, the stability of RPL4 mRNA was reduced by SNHG7 silencing. More importantly, either miR-122-5p knockdown or RPL4 restoration partially reversed SNHG7 silencing-induced tumor suppressive effects on HCC cells. In conclusion, we demonstrated that SNHG7 expression was up-regulated in HCC. SNHG7 contributed to HCC progression by regulating miR-122-5p and RPL4. Therefore, SNHG7 might be a potential biomarker and therapeutic target for HCC.	31545291	RID07093	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	SNHG7	miR-34a-5p	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	glycolysis(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	LncRNA-SNHG7 was up-regulated in both breast cancer tissues and breast cancer cell lines. Knocking down lncRNA-SNHG7 inhibited breast cancer cell proliferation while overexpressing lncRNA-SNHG7 enhanced cell proliferation. Knocking down lncRNA-SNHG7 resulted in decreased expression of lactate dehydrogenase A (LDHA) and decreased glycolysis. LncRNA-SNHG7 targeted miR-34a-5p to regulate LDHA expression and glycolysis. c-Myc bound to promoter of lncRNA-SNHG7 and positively regulated lncRNA-SNHG7 expression.	31897328	RID07094	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Breast cancer	MYC	SNHG7	positively-E	ChIP;Luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glycolysis(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Breast cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000233016	GRCh38_9:136721366-136728184	4609	84973	bHLHe39|c-Myc|MYCC	MGC16037|NCRNA00061	LncRNA-SNHG7 was up-regulated in both breast cancer tissues and breast cancer cell lines. Knocking down lncRNA-SNHG7 inhibited breast cancer cell proliferation while overexpressing lncRNA-SNHG7 enhanced cell proliferation. Knocking down lncRNA-SNHG7 resulted in decreased expression of lactate dehydrogenase A (LDHA) and decreased glycolysis. LncRNA-SNHG7 targeted miR-34a-5p to regulate LDHA expression and glycolysis. c-Myc bound to promoter of lncRNA-SNHG7 and positively regulated lncRNA-SNHG7 expression.	31897328	RID07095	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)
Gastric cancer	SNHG7	miR-34a	negatively-E	starBase;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	The studies in vitro revealed that SNHG7 directly binds to miR-34a and negatively regulates miR-34a expression, and SNHG7 enhances gastric cancer cell migration and invasion through suppressing miR-34a-Snail-EMT axis. In conclusion, SNHG7 functions as oncogenic lncRNA in gastric cancer and may be a potential therapeutic target for gastric cancer patients.	31814518	RID07096	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Breast cancer	SNHG7	miR-34a	negatively-E	starBase v2.0;qRT-PCR;luciferase assays	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	In terms of mechanism, miR-34a was confirmed to be the target of SNHG7, and SNHG7 could sponge miR-34a to inhibit the expression of miR-34a. In vivo and in vitro experiments both showed that SNHG7 targeted miR-34a and promoted epithelial-to-mesenchymal transition (EMT) initiation and the Notch-1 pathway in breast cancer. In conclusion, SNHG7 promoted breast cancer tumorigenesis and progression by sponging miR-34a through EMT initiation and the Notch-1 pathway. These findings contribute to a better understanding of breast cancer pathogenesis and further provide the theoretical fundamental basis for treatment	31132353	RID07097	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Osteosarcoma	SNHG7	TP53	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	DNMT1	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000141510	NA	84973	7157	MGC16037|NCRNA00061	LFS1|p53	qRT-PCRresults demonstrated that the expression of SNHG7 in osteosarcoma tissues was remarkably higher than that in paracancerous tissues. Moreover, SNHG7 expression in osteosarcoma with stage III and IV was higher than those in stage I and II. The inhibition of SNHG7 in osteosarcoma cells U2OS and HOS promoted cell proliferation, arrested cell cycle in the G0/G1 phase and induced apoptosis. RIP and ChIP experiments illustrated that SNHG7 inhibited the expression of p53 by binding to DNMT1. The overexpression of p53 in U2OS cells partially reversed the promoted cell proliferation and apoptosis caused by SNHG7.	31114984	RID07098	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Neuroblastoma	SNHG7	STAT2	positively-E	bioinformatics analysis;luciferase reporter;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-653-5p)	regulation	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000170581	NA	84973	6773	MGC16037|NCRNA00061	STAT113	Unsurprisingly, we further confirmed that SNHG7 could interact with miR-653-5p and therefore functioned as the ceRNA of STAT2 so as to regulate STAT2 expression in NB cells. Moreover, STAT2 expression was in inverse proportion to miR-653-5p level but in positive proportion to SNHG7 level in NB tissues. Importantly, the repressed NB progression induced by silenced SNHG7 was reversed by STAT2 overexpression or miR-653-5p inhibitors. Jointly, our findings elucidated SNHG7 facilitated NB progression through the miR-653-5p/STAT2 pathway, providing a novel therapeutic target and prognostic biomarker for this disease.	30623419	RID07099	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG7	RBM19	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000122965	NA	84973	9904	MGC16037|NCRNA00061	DKFZp586F1023|KIAA0682|Mrd1	SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.	31486493	RID07100	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG7	ABCG2	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000118777	NA	84973	9429	MGC16037|NCRNA00061	ABCP|BCRP|CD338|EST157481|MXR	SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.	31486493	RID07101	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	SNHG7	MIR425	negatively-E	TargetScanHuman Release 7.2;Starbase v3.0;miRcode;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000199032	NA	84973	494337	NCRNA00061	MIRN425|hsa-mir-425|mir-425	SNHG7 could promote proliferation and metastasis of hepatic carcinoma cell in vitro and in vivo, suggesting that SNHG7 exerts tumorigenic role in hepatic carcinoma progression. Further mechanism research revealed that SNHG7 exhibited the tumorigenic role through Wnt/beta-catenin/EMT pathway as a miR-425 sponge. These findings provided new cues to understand the molecular signalling network in carcinogenesis of hepatic carcinoma, and it may provide new evidence for therapeutic application in hepatic carcinoma.	31478234	RID07102	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Breast cancer	SNHG7	MIR381	negatively-E	StarBase 2.0;Luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000199020	NA	84973	494330	NCRNA00061	MIRN381|hsa-mir-381|mir-381	miRNA-381 was newly confirmed as a direct target of SNHG7 and it mediated the suppressing effects of SNHG7 on breast cancer cells.Long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) promotes breast cancer progression by sponging miRNA-381	31378900	RID07103	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Prostate cancer	SNHG7	WNT2B	positively-E	Starbase v3.0; dual-luciferase activity assay	upregulation	sequencing	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-324-3p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000134245	NA	84973	7482	MGC16037|NCRNA00061	WNT13|XWNT2	Further study indicated that lncRNA SNHG7 acts as a sponge for miRNA-324-3p and positively regulates WNT2B by a sponge effect. Moreover, We confirmed that WNT2B, an important protein in the Wnt signal pathway, promotes the malignant phenotype of PCa cells and mediated the biological effects exerted by lncRNA SNHG7. Overall, our study suggested that lncRNA SNHG7 could promote PCa EMT via miR-324-3p and WNT2B in vitro. The lncRNA SNHG7/miR-324-3p /WNT2B axis regulatory network might provide a potential new therapeutic strategy for PCa treatment.	31324390	RID07104	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Prostate cancer	SNHG7	miR-324-3p	negatively-E	Starbase v3.0; dual-luciferase activity assay	upregulation	sequencing	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	NCRNA00061	NA	Further study indicated that lncRNA SNHG7 acts as a sponge for miRNA-324-3p and positively regulates WNT2B by a sponge effect. Moreover, We confirmed that WNT2B, an important protein in the Wnt signal pathway, promotes the malignant phenotype of PCa cells and mediated the biological effects exerted by lncRNA SNHG7. Overall, our study suggested that lncRNA SNHG7 could promote PCa EMT via miR-324-3p and WNT2B in vitro. The lncRNA SNHG7/miR-324-3p /WNT2B axis regulatory network might provide a potential new therapeutic strategy for PCa treatment.	31324390	RID07105	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Thyroid cancer	SNHG7	BDNF	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000176697	NA	84973	627	MGC16037|NCRNA00061	NA	SNHG7 expression level was higher in TC samples than that in corresponding ones. The SNHG7 expression was associated with tumor size and TNM stage. Moreover, TC cell proliferation was inhibited, and TC cell apoptosis was induced after SNHG7 was knocked down in vitro. Moreover, the mRNA and protein expressions of brain-derived neurotrophic factor (BDNF) were downregulated after knockdown of SNHG7. Furthermore, the expression level of BDNF was positively related to the expression of SNHG7 in TC tissues.	31210313	RID07106	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Cervical cancer	SNHG8	RECK	negatively-E	RIP;Bioinformatic analysis;ChIP	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);apoptosis process(-)	EZH2	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278705-118285316	ENSG00000122707	NA	100093630	8434	LINC00060|NCRNA00060	hRECK|ST15	As detected by fluorescence in situ hybridization analysis and subcellular fractionation assay, SNHG8 was primarily expressed in the nucleus and exerted suppressive role on reversion inducing cysteine-rich protein with kazal motifs (RECK) expression, which implied a potential transcriptional regulation of SNHG8 on RECK level. Mechanically, SNHG8 was disclosed to interact with enhancer of zeste homolog 2 (EZH2) based on RNA immunoprecipitation assay. ChIP assay further unveiled the occupancy of EZH2 in the promoter region of RECK. An additional chromatin immunoprecipitation assay highlighted that SNHG8 intensified the enrichment of EZH2 and H3K27me3 in RECK promoter region. Altogether, it reflected that SNHG8 recruited EZH2 to downregulate RECK expression, leading to HPV-induced CC aggravation.	31961005	RID07107	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	sONE	TP53	positively-E	qPCR;western blot	downregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c-Myc. Knocking down of sONE resulted in a marked decrease in TP53 and increase in c-Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a. In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOS-induced NO production, affecting TP53 and c-Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c-Myc proteins.	30968427	RID07108	expression association	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	sONE	MYC	negatively-E	qPCR;western blot	downregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c-Myc. Knocking down of sONE resulted in a marked decrease in TP53 and increase in c-Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a. In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOS-induced NO production, affecting TP53 and c-Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c-Myc proteins.	30968427	RID07109	expression association	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Peripheral primitive neuroectodermal tumor	SOX2-OT	MIR363	negatively-E	bioinformatics analysis;luciferase assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Sarcoma	lncRNA	miRNA	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000207572	NA	347689	574031	DKFZp761J1324|NCRNA00043|SOX2OT	hsa-mir-363|MIR-363|MIRN363	With the help of bioinformatics analysis and luciferase assay, SOX2OT was validated to harbor miR-363, acting as miRNA sponge or competing endogenous RNA (ceRNA). Furthermore, FOXP4 was validated to be the target protein of miR-363. western blot and RT-PCRconfirmed that SOX2OT was positively correlated with FOXP4 protein via sponging miR-363, forming a negative cascade regulation. In conclusion, our study realizes that SOX2OT acted as oncogene in the tumorigenesis of Ewing's sarcoma, suggesting the SOX2OT/miR-363/FOXP4 pathway in Ewing's sarcoma.	31312393	RID07110	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Peripheral primitive neuroectodermal tumor	SOX2-OT	FOXP4	positively-E	bioinformatics analysis;luciferase assay;western blot;RT-PCR	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-363)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Sarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000137166	NA	347689	116113	DKFZp761J1324|NCRNA00043|SOX2OT	FLJ40908	With the help of bioinformatics analysis and luciferase assay, SOX2OT was validated to harbor miR-363, acting as miRNA sponge or competing endogenous RNA (ceRNA). Furthermore, FOXP4 was validated to be the target protein of miR-363. western blot and RT-PCRconfirmed that SOX2OT was positively correlated with FOXP4 protein via sponging miR-363, forming a negative cascade regulation. In conclusion, our study realizes that SOX2OT acted as oncogene in the tumorigenesis of Ewing's sarcoma, suggesting the SOX2OT/miR-363/FOXP4 pathway in Ewing's sarcoma.	31312393	RID07111	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Malignant glioma	SOX21-AS1	PAK5	positively-E	RIP;Luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000101349	NA	100507533	57144	NA	KIAA1264|PAK7	In addition, SOX21-AS1 could sponge miR-144-3p, which was determined to bind to PAK7. miR-144-3p knockdown promoted proliferation, migration, invasion and inhibited cell apoptosis. Importantly, the effects of SOX21-AS1 knockdown-induced proliferation, migration, invasion, and apoptosis were alleviated in glioma cells co-transfected with SOX21-AS1 and miR-144-3p knockdown. Furthermore, miR-144-3p knockdown also attenuated Wnt/beta-catenin pathway-associated protein levels induced by SOX21-AS1 knockdown. These results indicated that SOX21-AS1/miR-144-3p/PAK7 axis played an oncogenic role in glioma cells by regulating Wnt/beta-catenin pathway, which suggests a rational therapeutic strategy for glioma.	31973536	RID07112	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Malignant glioma	SOX21-AS1	miR-144-3p	negatively-E	RIP;Luciferase reporter assay	upregulation	qRT-PCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000227640	GRCh38_13:94703454-94803430	NA	NA	100507533	NA	NA	NA	In addition, SOX21-AS1 could sponge miR-144-3p, which was determined to bind to PAK7. miR-144-3p knockdown promoted proliferation, migration, invasion and inhibited cell apoptosis. Importantly, the effects of SOX21-AS1 knockdown-induced proliferation, migration, invasion, and apoptosis were alleviated in glioma cells co-transfected with SOX21-AS1 and miR-144-3p knockdown. Furthermore, miR-144-3p knockdown also attenuated Wnt/beta-catenin pathway-associated protein levels induced by SOX21-AS1 knockdown. These results indicated that SOX21-AS1/miR-144-3p/PAK7 axis played an oncogenic role in glioma cells by regulating Wnt/beta-catenin pathway, which suggests a rational therapeutic strategy for glioma.	31973536	RID07113	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Cervical cancer	SOX21-AS1	miR-7	negatively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000227640	GRCh38_13:94703454-94803430	NA	NA	100507533	NA	NA	NA	Functional investigation showed that knockdown of SOX21-AS1 suppressed CC cells proliferation, migration, and invasion, as well as epithelial to mesenchymal transition progress. Furthermore, our data showed that microRNA-7 (miR-7) interacted with SOX21-AS1 by directly targeting the miRNA-binding site in the SOX21-AS1 sequence, and quantitative real-time polymerase chain reaction results showed overexpression of SOX21-AS1 decreased the levels of miR-7 in CC cells. Moreover, we confirmed that miR-7 directly targeted the 3'-untranslated region of voltage dependent anion channel 1 (VDAC1). Final in vitro assay suggested that in CC cells with SOX21-AS1, VDAC1 overexpression resulted in an increase of cell proliferation, migration, and invasion. Overall, our findings illuminate how SOX21-AS1 formed a regulatory network to confer an oncogenic function in CC and SOX21-AS1 could be regarded as an efficient therapeutic target and potential biomarker for CC patients.	30912129	RID07114	expression association	NA	UP(LIHC);DATA(GSE117623)	
Urinary bladder cancer	SOX2-OT	SOX2	positively-E	transcriptional analysis;RNA FISH;dual-luciferase reporter assays;western blots	upregulation	RT-qPCR	NA	NA	cell stemness(+)	ceRNA(miR-200c)	regulation	NA	NA	CSC	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	DKFZp761J1324|NCRNA00043|SOX2OT	NA	SOX2OT was highly expressed in bladder cancer, and increased SOX2OT expression was positively correlated with a high histological grade, advanced TNM stage and poor prognosis. Further experiments demonstrated that knockdown of SOX2OT inhibited the stemness phenotype of BCSCs. Moreover, inhibition of SOX2OT delayed xenograft tumour growth and decreased metastases in vivo. Mechanistically, we found that SOX2OT was mainly distributed in the cytoplasm and positively regulated SOX2 expression by sponging miR-200c. Furthermore, SOX2 overexpression reversed the SOX2OT silencing-induced inhibition of the BCSC stemness phenotype.	32019566	RID07115	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DATA(GSE117623)
Laryngeal squamous cell carcinoma	SOX2-OT	EZH2	positively-E	RNA pull-down assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000106462	NA	347689	2146	DKFZp761J1324|NCRNA00043|SOX2OT	ENX-1|EZH1|KMT6|KMT6A	Mechanically, SOX2-OT interacted with EZH2 and recruited EZH2 to induce H3K27me3 and epigenetically inhibited PTEN expression in LSCC cells. Additionally, EZH2 silencing and PTEN overexpression significantly abrogated the SOX2-OT overexpression-mediated promotion of LSCC cell malignant behavior. Collectively, our findings demonstrate that SOX2-OT inhibits PTEN expression to facilitate LSCC development through EZH2-mediated H3K27me3.	30811870	RID07116	epigenetic regulation	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Laryngeal squamous cell carcinoma	SOX2-OT	H3K27me3	positively-E	RNA pull-down assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	NA	NA	347689	NA	DKFZp761J1324|NCRNA00043|SOX2OT	NA	Mechanically, SOX2-OT interacted with EZH2 and recruited EZH2 to induce H3K27me3 and epigenetically inhibited PTEN expression in LSCC cells. Additionally, EZH2 silencing and PTEN overexpression significantly abrogated the SOX2-OT overexpression-mediated promotion of LSCC cell malignant behavior. Collectively, our findings demonstrate that SOX2-OT inhibits PTEN expression to facilitate LSCC development through EZH2-mediated H3K27me3.	30811870	RID07117	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Laryngeal squamous cell carcinoma	SOX2-OT	PTEN	negatively-E	RNA pull-down assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000171862	NA	347689	5728	DKFZp761J1324|NCRNA00043|SOX2OT	BZS|MHAM|MMAC1|PTEN1|TEP1	Mechanically, SOX2-OT interacted with EZH2 and recruited EZH2 to induce H3K27me3 and epigenetically inhibited PTEN expression in LSCC cells. Additionally, EZH2 silencing and PTEN overexpression significantly abrogated the SOX2-OT overexpression-mediated promotion of LSCC cell malignant behavior. Collectively, our findings demonstrate that SOX2-OT inhibits PTEN expression to facilitate LSCC development through EZH2-mediated H3K27me3.	30811870	RID07118	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Papillary thyroid carcinoma	ABHD11-AS1	SLC1A5	negatively-E	RegRNA 2.0;lncRNASNP2;luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	TCGA;GSE66783	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000105281	NA	171022	6510	LINC00035|NCRNA00035|WBSCR26	AAAT|ASCT2|M7V1|RDRC	With the increasing incidence of papillary thyroid cancer (PTC), more attention has been paid to exploring the mechanism of PTC initiation and progression. Based on these findings, we examined lncRNA ABHD11 antisense RNA 1 (ABHD11-AS1) expression and its clinical significance, biological function and mechanism in PTC. First, we analyzed thyroid ABHD11-AS1 expression in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Then, qRT-PCRwas applied to detect the expression in paired PTC tissues and adjacent normal tissues, as well as in PTC cell lines (TPC-1 and K-1) and a normal thyroid follicular epithelium cell line (Nthy-ori3-1). We found that ABHD11-AS1 was remarkably overexpressed in PTC, and high expression was related to tumor size, lymph node metastasis, extrathyroidal extension and advanced TNM stage. Moreover, ABHD11-AS1 enhanced the abilities of cell proliferation, migration, and invasion, inhibited apoptosis in vitro, promoted tumorigenesis in vivo via sponging miR-199a-5p and then induced SLC1A5 activation. Taken together, the data show that ABHD11-AS1 acts as a competing endogenous RNA (ceRNA) to exert malignant properties in PTC through the miR-199a-5p/SLC1A5 axis. The results indicated that SLC1A5 expression was increased by miR-199a-5p inhibition at both the mRNA and protein levels compared with that in the negative control conditions in TPC-1 and K-1 cells.	31409775	RID07119	ceRNA or sponge	metastasis	UP(BRCA);DATA(GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE41245)
Epithelial ovarian cancer	GAS5	PARP1	negatively-E	western blot;RNA pull-down assay;RIP;CHIP;luciferase reporter assay	downregulation	RT-qPCR;microarray	NA	NA	chemoresistance(-);cell cycle(-);	transcriptional regulation	regulation	NA	Cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000143799	NA	60674	142	NCRNA00030|SNHG2	ADPRT|ARTD1|PARP|PPOL	By microarray (3 EOC tissues vs. 3 normal ovary tissues) and RT- qPCR (53 EOC tissues vs. 10 normal ovary tissues) we identified lncRNA GAS5 to be dramatically low expressed in EOC samples and correlated with prognosis. Compared with sensitive cell lines, GAS5 was also low expressed in DDP resistant OC cell lines, and over-expression of GAS5 significantly enhanced the sensitivity of OC cells to DDP in vivo and in vitro. Meanwhile the over-expression of GAS5 also caused OC cells G0/G1 arrest and apoptosis increase. Mechanistically, GAS5 might regulate PARP1 expression by recruiting the transcription factor E2F4 to its promoter, and then affect the MAPK pathway activity. Due to the 5'TOP structure, GAS5 could be regulated by transcription inhibitor rapamycin in OC cells.	31391118	RID07120	transcriptional regulation	prognosis,chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827)
Glioma	MIR377	MEG3	positively-E	western blot	downregulation	RT-qPCR	NA	NA	cell migration(-);cell invasion(-);apoptosis process(+)	NA	association	NA	NA	CSC	NA	Cancer	Brain glioma	miRNA	lncRNA	ENSG00000199015	NA	ENSG00000214548	GRCh38_14:100779410-100861031	494326	55384	MIRN377|hsa-mir-377|mir-377	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Glioma is a common and fatal intracranial tumor. Both miR-377 and lncRNA MEG3 are tumor suppressors. MiR-377 mimics increased MEG3 expression and decreased the number of migrated and invaded U118 and U251 cells, without influence on apoptosis in both cell lines.  PTEN was increased by miR-377 mimics and si-MEG3 and decreased by pc-MEG3 in glioma cells.In summary, our present study investigated the tumor suppressive effect of both miR-377 and MEG3 in glioma cells. The expression of both miR-377 and MEG3 promoted cell apoptosis and inhibited glioma cell invasion and migration via regulating cell cycle distribution (G2/M arrest). MiR-377 mimics and si-MEG3 promoted PTEN mRNA expression, suggesting the link between miR-377, MEG3 and PTEN. However, the cross talk between miR-377 and MEG3 as well as underlying mechanism of the mediated glioma cell migration and invasion should be validated.Applied Biosystems (ABI) 7900 Fast Real-time PCR instrument (Applied Biosystems, Foster City, CA, USA) was used for PCR amplification.	31378455	RID07121	expression association	NA		
Pituitary adenoma	H19	EIF4EBP1	negatively-F	western blot	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-)	phosphorylation	binding/interaction	NA	Cabergoline	NA	Insensitivity to Antigrowth Signals	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000187840	NA	283120	1978	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	4E-BP1|PHAS-I	Our previous study demonstrated that the expression of long noncoding RNA (lncRNA) H19 was frequently downregulated in human primary pituitary adenomas and negatively correlated with tumor progression.Our previous study demonstrated that the expression of long noncoding RNA (lncRNA) H19 was frequently downregulated in human primary pituitary adenomas and negatively correlated with tumor progression. Our previous study demonstrated that the expression of long noncoding RNA (lncRNA) H19 was frequently downregulated in human primary pituitary adenomas and negatively correlated with tumor progression;H19 overexpression inhibits contralateral GH3 tumor growth in vivo;H19 overexpression cell medium inhibits in vitro proliferation of GH3 cells	31369093	RID07122	interact with protein	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807)
Nasopharynx carcinoma	ZFAS1	miR-135a	negatively-F	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Nasopharyngeal carcinoma (NPC) is one common head and neck malignancy with leading cause of cancer-related death. The expressions of ZFAS1 and microRNA-135a (miR-135a) were measured in NPC tissues or cells by quantitative real-time polymerase chain reaction (qRT-PCR. The interaction between ZFAS1 and miR-135a was explored by luciferase reporter assay and RNA immunoprecipitation (RIP). miR-135a was bound to ZFAS1 in NPC cells.Moreover, knockdown of ZFAS1 or addition of miR-135a inhibited cell proliferation, migration and invasion but promoted apoptosis in NPC cells.Our data suggested Inhibition of ZFAS1 protected against proliferation, migration and invasion but contributed to apoptosis by sponging miR-135a in NPC cells, providing a novel avenue for NPC treatment.	31307201	RID07123	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Hepatocellular carcinoma	H19	Beclin-1	positively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07124	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	H19	Caspase3	positively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07125	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	H19	Caspase9	positively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07126	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	H19	BCL2	negatively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000171791	NA	283120	596	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	Bcl-2|PPP1R50	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07127	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	H19	GTF2H1	negatively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000110768	NA	283120	2965	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	BTF2|P62|TFIIH	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07128	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	H19	PIK3CA	negatively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000121879	NA	283120	5290	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	PI3K	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07129	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Hepatocellular carcinoma	H19	AKT1	negatively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000142208	NA	283120	207	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	AKT|PKB|PRKBA|RAC|RAC-alpha	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07130	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	H19	MTOR	negatively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell injury(+);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	Chloroquine;Rapamycin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8-h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome-c-(Cyt-c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-akt-mTOR pathway in the hepatoma carcinoma cells.	31196153	RID07131	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Nasopharynx carcinoma	LINC01133	YBX1	negatively-F	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-);	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000065978	NA	100505633	4904	lncRNA-PAGBC	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	In this work, we demonstrated that LINC01133 was significantly downregulated in NPC tissues and cell lines. Loss and gain of function experiments provided evidence that LINC01133 inhibited NPC cell proliferation, invasion and migration both in vitro and in vivo.Importantly, RNA pull-down and RIP assays showed that LINC01133 directly combined with YBX1, and YBX1 can partly reverse the repression of NPC cell proliferation, migration, and invasion caused by LINC01133.These results confirmed that LINC01133 mediated NPC tumorigenesis by inhibiting YBX1.RNA extraction and quantitative real-time PCR (qRT-PCR.These results suggested that LINC01133 can bind to YBX1 but cannot change the protein expression of YBX1.	31106003	RID07132	interact with protein	NA	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Triple-negative breast cancer	HCP5	PTEN	negatively-E	western blot;siRNA	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);cell proliferation(-)	NA	regulation	NA	Cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000171862	NA	10866	5728	D6S2650E|P5-1	BZS|MHAM|MMAC1|PTEN1|TEP1	However, the molecular mechanism by which lncRNA regulates cisplatin (DDP) in triple-negative breast cancer (TNBC) remains unclear.Abnormal expression of lncRNA between MDA-MB-231 and MDA-MB-231/DDP was evaluated with microarray.western blot assay was used to detect the protein expression.HCP5 were significantly upregulated in MDA-MB-231/DDP cells compared with MDA-MB-231 cells.Overexpression of HCP5 promoted DDP resistance in MDA-MB-231 cells by inhibiting PTEN expression. In contrast, inhibition of HCP5 reversed DDP resistance in MDA-MB-231/ DDP cells by upregulating PTEN.	31028999	RID07133	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Glioma	ENST00000413528	miR-593-5p	negatively-F	luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA ENST00000413528 was detected in glioma tissues by lncRNA microarray. Then, we performed real-time PCR, CCK-8, colony formation assay, flow cytometry, caspase-3/7 assay and animal experiment to detect the function of ENST00000413528 in glioma after ENST00000413528 knockdown. Subsequent bioinformatics analysis, luciferase reporter assays and RNA immunoprecipitation (RIP) assay western blot indicated possible downstream regulatory molecules.Expression of ENST00000413528 was significantly increased in glioma tissues and LN229 and U251 cells. Knockdown of ENST00000413528 inhibited cell proliferation and induced apoptosis and cell cycle arrest in glioma cells.LncRNA ENST00000413528 regulated miR-593-5p by direct targeting.Long noncoding RNA ENST00000413528 sponges microRNA-593-5p to modulate human glioma growth via polo-like kinase 1.	30924320	RID07134	ceRNA or sponge	NA		
Glioma	SNHG20	BAX	negatively-E	siRNA;western blot	upregulation	RT-PCR	NA	NA	apoptosis process(-);PTEN/PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000087088	NA	654434	581	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	BCL2L4	A total of 80 cases of glioma specimens and 80 cases of para-carcinoma specimens were collected, and the expression level of SNHG20 was detected via reverse transcription-polymerase chain reaction (RT-PCR. The human glioma U118 and U251 cell lines with the stable knockout of SNHG20 were constructed using the small-interfering RNA (siRNA). The influence of SNHG20 on proliferation of human glioma cells was detected via cell counting kit-8 (CCK-8), and the protein expression levels of apoptosis-related genes, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax), were also detected. After SNHG20 knockout, the level of pro-apop totic gene Bax was significantly increased in the two kinds of glioma cell lines (p<0.05), while the level of anti-apoptotic gene B-cell lymphoma-2 (Bcl-2) was obviously inhibited (p<0.05) (Figure 5), suggesting that SNHG20 knockout may pro mote apoptosis of cancer cells.The expression level of SNHG20 messenger RNA (mRNA) in glioma tissues was significantly higher than that in para-carcinoma tissues (p<0.05). After the inhibition of siRNA on SNHG20, the proliferation of U118 and U251 cells was significantly inhibited, and the expression of Bax was significantly up-regulated, while that of Bcl-2 was down-regulated. The TUNEL results showed that the number of apoptotic cells in SNHG20 siRNA group was about 12 times that in control group (p<0.05). After SNHG20 knockout, the protein expressions in the PTEN/PI3K/AKT signaling pathway were inhibited (p<0.05).	30657567	RID07135	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioma	SNHG20	BCL2	positively-E	siRNA;western blot	upregulation	RT-PCR	NA	NA	apoptosis process(-);PTEN/PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000171791	NA	654434	596	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	Bcl-2|PPP1R50	A total of 80 cases of glioma specimens and 80 cases of para-carcinoma specimens were collected, and the expression level of SNHG20 was detected via reverse transcription-polymerase chain reaction (RT-PCR. The human glioma U118 and U251 cell lines with the stable knockout of SNHG20 were constructed using the small-interfering RNA (siRNA). The influence of SNHG20 on proliferation of human glioma cells was detected via cell counting kit-8 (CCK-8), and the protein expression levels of apoptosis-related genes, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax), were also detected. After SNHG20 knockout, the level of pro-apop totic gene Bax was significantly increased in the two kinds of glioma cell lines (p<0.05), while the level of anti-apoptotic gene B-cell lymphoma-2 (Bcl-2) was obviously inhibited (p<0.05) (Figure 5), suggesting that SNHG20 knockout may pro mote apoptosis of cancer cells.The expression level of SNHG20 messenger RNA (mRNA) in glioma tissues was significantly higher than that in para-carcinoma tissues (p<0.05). After the inhibition of siRNA on SNHG20, the proliferation of U118 and U251 cells was significantly inhibited, and the expression of Bax was significantly up-regulated, while that of Bcl-2 was down-regulated. The TUNEL results showed that the number of apoptotic cells in SNHG20 siRNA group was about 12 times that in control group (p<0.05). After SNHG20 knockout, the protein expressions in the PTEN/PI3K/AKT signaling pathway were inhibited (p<0.06).	30657567	RID07136	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	EPEL	RUNX2	positively-E	western blot;siRNA	upregulation	qRT-PCR;western blot	NA	NA	cell migration(+);cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	NA	NA	ENSG00000124813	NA	NA	860	NA	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	In conclusion, lncRNA EPEL and RUNX2 were upregu lated in gastric cancer patients. Patients with high expression level of lncRNA EPEL showed poor survival. LncRNA EPEL and RUNX2 overexpression promoted, while lncRNA EPEL siRNA silencing inhibited the migration, proliferation, and invasion of gastric cancers. In addition, RUNX2 overexpression completely rescued the inhibited cancer cell migration, proliferation, and invasion caused by lncRNA EPEL siRNA silencing. Interestingly, we observed a signifcant and positive cor relation between expression levels of lncRNA EPEL and RUNX2 in tumor tissues of gastric cancer. Therefore, lncRNA EPEL may achieve its regulatory role in the expression of RUNX2 through cancer-related factors.In conclusion, lncRNA EPEL and RUNX2 were upregu lated in gastric cancer patients.	31584135	RID07137	expression association	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SLNCR1	sPLA2	positively-E	RT-qPCR;western blot;siRNA	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);cell stemness(+);	NA	regulation	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000188257	NA	NA	NA	NA	NA	The development and progression of NSCLC are associated with pathological factors, which may mediate the interaction between lncRNA SLNCR1 and sPLA2. However, the present study failed to identify these pathological mediators. Future studies are needed to identify the mediators involved in this process.Reverse transcription-quantitative PCR (RT-qPCR) and ELISA were performed to measure the levels of lncRNA SLNCR1 and secretory phospholipase A2 (sPLA2) in lung biopsies, respectively.In conclusion, lncRNA SLNCR1 and secretory sPLA2 were both upregulated in NSCLC. lncRNA SLNCR1 may regulate cancer cell migration, invasion and stemness in NSCLC through interactions with secretory sPLA2.	31524254	RID07138	expression association	NA		
Thoracic aortic aneurysm	LOXL1-AS	Giver	positively-E	western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Aortic disease	lncRNA	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	Our data suggest that LOXL1-AS is an upstream activator of Giver in HAOSMC, and this interaction between two lncRNAs is involved in the regulation of the proliferation and apoptosis of HAOSMC. Our study may provide new insights to the pathogenesis of the TAA. However, the molecular mechanism underlying this interaction is unclear. It is likely that the interaction between LOXL1-AS and Giver is mediated by certain pathways activated in TAA due to the fact that LOXL1-AS and Giver are only significantly correlated in TAA patients but not in healthy controls.In conclusion, LOXL1-AS was overexpressed in TAA and may up-regulate Giver to promote TAA.LOXL1-AS regulated the proliferation and apoptosis of HAOSMC through Giver. LncRNA Giver was also up-regulated in TAA patients than in healthy controls in aortic media specimens, and was positively correlated with LOXL1-AS.	31471532	RID07139	expression association	NA		
Prostate cancer	miR-145	GAS5	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-);	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	miRNA	lncRNA	ENSG00000269936	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	The present study failed to elucidate the molecular mechanism of the regulation of lncRNA GAS5 by miR-145 in prostate carcinoma cells.Overexpression of miR-145 inhibits cell proliferation and promotes apoptosis through lncRNA GAS5.Overexpression of miR-145 results in upregulated lncRNA GAS5.lncRNA GAS5 and miR-145 expression levels are positively correlated in tumor tissues.lncRNA GAS5 and miR-145 expression levels are downregulated in tumor tissues compared with adjacent healthy tissues in patients with prostate carcinoma.	31423164	RID07140	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Breast cancer	EZH2	NKILA	negatively-E	western blot	downregulation	RT-qPCR;semi-quantitative RT-PCR	NA	NA	cell migration(+);cell invasion(+);	NA	regulation	NA	UNC1999;Tazemetostat	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000278709	GRCh38_20:57710156-57712780	2146	105416157	ENX-1|EZH1|KMT6|KMT6A	NA	Homeostatic expression of EZH2 and NF-kB is inversely associated with NKILA transcription and correlates with metastatic potential. Subsequent fluctuations in NKILA transcript levels were measured by both quantitative RT-qPCR using commercially available primers and semi-quantitative RT-PCRusing alternative NKILA primers.EZH2 specific inhibition significantly increased NKILA in MDA MB 231 cells, suggesting a role for EZH2 as a negative regulator of NKILA transcription.Inhibition of EZH2/1 significantly blunted MDA-MB-231 cell migration and invasion but had no observed effect on the motility of HMECs and MCF-7 cells.	31282094	RID07141	expression association	metastasis	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	
Breast cancer	NFKB1	NKILA	negatively-E	western blot	downregulation	RT-qPCR;semi-quantitative RT-PCR	NA	NA	cell migration(+);cell invasion(+);	NA	regulation	NA	UNC2000;Tazemetostat	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000109320	NA	ENSG00000278709	GRCh38_20:57710156-57712780	4790	105416157	CVID12|EBP-1|KBF1|NF-kB|NF-kB1|NF-kappa-B1|NF-kappaB|NF-kappabeta|NFKB-p105|NFKB-p50|NFkappaB	NA	As we previously observed an increase in NKILA transcript in HMECs following NF-kB inhibition, we anticipated a robust RTK response in these cells compared to MCF-7 and MDA-MB-231 cells.	31282094	RID07142	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Osteosarcoma	CCEPR	PCNA	positively-E	western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	NA	ENSG00000132646	NA	105682749	5111	CCHE1|lncRNA-CCHE1	NA	In our study, we found CCEPR positively regulated PCNA expression in osteo_x0002_sarcoma cells, and silencing of CCEPR inhibits steosar_x0002_coma cell proliferation through decreasing PCNA expression.High-expression of CCEPR in osteosarcoma tissues and cells.	30861164	RID07143	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Colorectal cancer	LINC01354	CTNNB1	positively-E	western blot;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000231768	GRCh38_1:234527887-234531803	ENSG00000168036	NA	100506795	1499	NA	armadillo|beta-catenin|CTNNB	LINC01354 mediated the stabilization of CTNNB1 through interacting with RNA-binding protein hnRNP-D.LINC01354 promoted proliferation, migration, invasion and EMT of CRC in vitro.LINC01354 was upregulated in the clinical CRC specimens and cell lines.	30987669	RID07144	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Prostate cancer	BLACAT1	MIR361	negatively-F	luciferase reporter assay;RIP;western blot;ChIP	downregulation	RT-PCR	NA	NA	cell proliferation(-)	sponge	binding/interaction	NA	5-azacytidine;Chidamide	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000199051	NA	101669762	494323	LINC00912|linc-UBC1|onco-lncRNA-30	MIRN361|hsa-mir-361|mir-361	Long non-coding RNA BLACAT1 inhibits prostate cancer cell proliferation through sponging miR-361.Real-time PCR was used to detect the expression of BLACAT1 and miR-361 in prostate cancer tissues and adjacent normal tissues (n=25). The function of BLACAT1 was detected through proliferation assay and apoptosis assay. The interaction between BLACAT1 and miR-361 in prostate cancer was studied by luciferase assay, RNA immunoprecipitation assay and chromatin immunoprecipitation analysis were performed to detect the BLACAT1 binding proteins. The xenograft mice experiment was performed to further confirm the functional significance of lncRNA BLACAT1 in vivo.	31957820	RID07145	ceRNA or sponge	NA		
Breast cancer	GSTP1P1	HSP90AA1	positively-E	RNA pull-down;siRNA;western blot;RT-qPCR	upregulation	microarray	GSE81971	NA	cell proliferation(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000257569	GRCh38_12:55900300-55900618	ENSG00000080824	NA	2951	3320	GST3L|GSTP1P|GSTPL|GSTPP|Lnc712	FLJ31884|Hsp89|Hsp90|HSP90N|HSPC1|HSPCA	Interestingly, we found that Lnc712 expression was decreased in cells with HSP90-knockdown (Fig.--(Fig.2d),2d), suggesting that HSP90 is required for Lnc712 function and stabilization. On the contrary, knockdown of Lnc712 did not affect HSP90 expression (Fig.--(Fig.2e2e and-Supplementary Fig. 2d). Together, these results indicated that Lnc712 and HSP90 form a functional ribonucleoprotein complex.However, our research may provide new strategy for inhibiting cancerous HSP90 by targeting Lnc712, which is specifically highly expressed in breast cancer cells but not in surrounding healthy tissues.	31892853	RID07146	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Prostate cancer	FOXA1	PCSEAT	positively-E	western blot;ChIP;dual-luciferase reporter assay	upregulation	qRT-PCR	GSM353634;GSM353626;GSM1902615;GSM353631;GSM353620;GSM2827606;GSE83860;GSE84432	NA	cell growth(+);cell migration(+);	enhancer	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	TF	lncRNA	ENSG00000129514	NA	ENSG00000286027	GRCh38_21:41580475-41582887	3169	105372808	HNF3A	PRCAT38	The knockout of enhancer E1 or E2 simultaneously impaired the transcription of PRCAT38 and TMPRSS2 and inhibited cell growth and migration. Moreover, the loop formation and enhancer activity were mediated by AR/FOXA1 binding and the activity of acetyltransferase p300.  FOXA1 is Required for Enhancer Activity and Chromatin Looping between Enhancers and Promoters of TMPRSS2 and PRCAT38. In our study, eRNA transcription from enhancer E2 is regulated by AR and FOXA1. Whether it functions in the regulation of TMPRSS2 and PRCAT38 requires further study.This suggested that it was FOXA1 binding, not the total amount of FOXA1, that regulates the transcription of the two genes.	31405024	RID07147	chromatin looping	NA	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)	
Estrogen-receptor negative breast cancer	TFAP2A	LINC00511	positively-E	RNA pull-down assay;ChIP;RIP	upregulation	qRT-PCR	TCGA;CCLE;	NA	cell proliferation(+);apoptosis process(-);cell growth(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	TF	lncRNA	ENSG00000137203	NA	ENSG00000227036	GRCh38_17:72290091-72640472	7020	400619	AP-2|AP-2alpha|AP2TF|BOFS|TFAP2	LCAL5|onco-lncRNA-12	At the transcriptional level, ER deficiency directly affected the expression of LINC00511 activated by transcription factor AP-2 (TFAP-2) in breast cancer cells.Taken together, these results indicated that LINC00511 promoted ER-negative breast cancer cell growth by affecting cell proliferation and apoptosis.	31395854	RID07148	transcriptional regulation	NA	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065,GSE55807)	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Estrogen-receptor negative breast cancer	LINC00511	CDKN1B	negatively-E	RNA pull-down assay;ChIP;RIP	upregulation	qRT-PCR	TCGA;CCLE;	NA	cell proliferation(+);apoptosis process(-);cell growth(+);	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000111276	NA	400619	1027	onco-lncRNA-12	KIP1|P27KIP1	So far, we hypothesized that LINC00511 regulated CDKN1B expression through EZH2-mediated H3K27me3 trimethylation at the promoter region of CDKN1B.The results revealed a negative correlation between LINC00511 and CDKN1B.	31395854	RID07149	interact with protein	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	MALAT1	TCF7L2	positively-E	siRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glycolysis metabolic process(+);gluconeogenesis(-)	interact with protein	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148737	NA	378938	6934	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	TCF-4|TCF4	We next sought to determine whether in an in vivo mouse model of HCC (Mdr2-/- mice), which is known to upregulate MALAT1 (8), TCF7L2 is upregulated and if its expression correlates with expression of genes controlling glycolysis and gluconeogenesis. Both western blotand immunohistochemistry show that the protein expression of TCF7L2 was elevated in the tumor samples compared with the non-tumor liver samples, with nuclear localization in HCC tumors compared with adjacent parenchyma. In previously performed RNA-seq analysis on PHM-1 cells overexpressing MALAT1, we detected increased expression of several glycolytic genes. Long Noncoding RNA MALAT1 Regulates Cancer Glucose Metabolism by Enhancing mTOR-Mediated Translation of TCF7L2. MALAT1 negatively affects gluconeogenesis. These results suggest that SRSF1 regulates the expression of TCF7L2 post-transcriptionally by regulating its translation in hepatocellular carcinoma cells, a phenomenon seen for other proteins.	30914432	RID07150	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)
Clear cell renal cell carcinoma	SNHG5	ZEB1	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+);cell metastasis(+);	ceRNA(miR-205-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000148516	NA	387066	6935	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	Pearson's correlation analyses showed that the level of ZEB1 mRNA was inversely correlated with miR-205-5p expression and positively correlated with SNHG5 expression in ccRCC tissues. Altogether, the results showed that SNHG5 may serve as a ceRNA to sponge miR-205-5p and thus regulates ZEB1 expression.SNHG5 expression is enhanced in ccRCC and is correlated with disease progression. SNHG5 is required for the proliferation, migration, and invasion of ccRCC cells.  SNHG5 regulates tumorigenicity and metastasis in vivo.SNHG5 enhances ccRCC cell proliferation, migration, and invasion by inhibiting the miR-205-5p/ZEB1 axis.	32281285	RID07151	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	CERNA2	STAT3	positively-E	RIP;dual-luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);	ceRNA(let-7b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000168610	NA	642934	6774	HOST2	APRF	HOST2 acted as a sponge of let-7b and miR-1266 in TNBC cells. Let-7b, rather than miR-1266, inhibited TNBC cell proliferation and invasion by binding to STAT3. HOST2, a cytoplasmic lncRNA, was up-regulated in TNBC tissues and cell lines and was correlated with poor prognosis in TNBC patients. HOST2 promoted proliferation and invasion of TNBC cells.	32248842	RID07152	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	CCAT1	miR-152	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	CCAT1 binds with miR-152, and the effect of si-CCAT1 in NSCLC cell proliferation, cell invasion and epithelial-mesenchymal transition was partially reversed by anti-miR-152.	32227563	RID07153	ceRNA or sponge	NA		
Osteosarcoma	DLEU2	miR-337-3p	negatively-E	RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);cell migration(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000231607	GRCh38_13:49956670-50125720	NA	NA	8847	NA	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	NA	LncRNA DLEU2 promotes tumour growth by sponging miR-337-3p in human osteosarcoma. DLEU2 exhibits a high expression in osteosarcoma. Up-regulation of DLEU2 ccelerates the migration and proliferation of osteosarcoma cells	32196715	RID07154	ceRNA or sponge	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	
Glioma	HOTAIRM1	HOXA	positively-E	CRISPR-cas9;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);	interact with protein	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The HOTAIRM1 gene body functions as an enhancer that interacts with chromatin harboring HOXA cluster genes. HOTAIRM1 maintains chromatin interactions between the HOTAIRM1 locus and HOXA cluster genes. High levels of HOTAIRM1 transcripts in glioma are correlated with decreased patient survival. qRT-PCRdata showed downregulation of all HOXA cluster genes following abrogation of HOTAIRM1 expression by polyA knock-in, in agreement with our expression analysis of HOTAIRM1 and HOXA cluster genes in glioma and normal brain tissue.	32180085	RID07155	interact with protein	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	FOXP4-AS1	FOXP4	positively-E	western blot;RIP;luciferase reporter assay;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(+)	ceRNA(miR-3184-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000234753	GRCh38_6:41452889-41548621	ENSG00000137166	NA	101060264	116113	NA	FLJ40908	FOXP4-AS1 acted as a sponge of miR-3184-5p to upregulate FOXP4. On the basis of GEPIA data, lncRNA FOXP4-AS1 and its nearby gene FOXP4 were both upregulated in esophageal carcinoma samples. Upregulation of FOXP4-AS1 and FOXP4 promoted ESCC cell proliferation and induced cell apoptosis.	32159250	RID07156	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Hepatocellular carcinoma	LINC00324	FASLG	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	microarray;RT-qPCR	GSE49515;TCGA	NA	cell viability(+);cell proliferation(+);cell migration(+);cell invasion(+);self-renewal(+);tumorigenesis(+)	interact with protein	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000178977	GRCh38_17:8220624-8224043	ENSG00000117560	NA	284029	356	C17orf44|FLJ34790|MGC104931|NCRNA00324	APT1LG1|CD178|FasL|TNFSF6	LINC00324 involved in the maintenance of the biological properties of LCSCs by upregulating the expression of FasL by recruitment of PU.1 to the FasL promoter region. Altogether, these findings suggested that overexpressed LINC00324 significantly increased the expression of stemness-related genes, and the cell viability, proliferation, migration, invasion, self-renewal, and tumorigenesis in HuH-7 stem cells, and the co-treatment with oe-LINC00324 and si-PU.1 reversed the effects induced by the overexpression of LINC00324.	32128906	RID07157	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00174	S100A10	negatively-E	RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-);	ceRNA(miR-320)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000179406	GRCh38_7:66376044-66493566	ENSG00000197747	NA	285908	6281	NCRNA00174	42C|ANX2LG|CAL1L|CLP11|P11	Overexpression of LINC00174 significantly reduced the expression of miR-320 by sponging it, in turn enhanced the expression of S100A10. LINC00174 can promote the proliferation, migration, and invasion of HCC cells.	32128852	RID07158	ceRNA or sponge	metastasis	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE55807,GSE67939)
Gastric cancer	ILF3-DT	PTBP3	positively-E	siRNA	upregulation	RT-qPCR	cBioPortal	NA	cell proliferation(+);cell migration(+);	ceRNA(miR-29a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000119314	NA	147727	9991	ILF3-AS1	DKFZp781I1117|ROD1	The results indicate that ILF3-AS1 could enhance PTBP3 expression as a miR-29a sponge, thereby promoting the proliferation and metastasis of GC cells.-The TCGA analysis showed that ILF3-AS1 was remarkably upregulated in GC tissues. ILF3-AS1 Promotes Proliferation and Migration of GC Cells. Very interestingly, we found that knockdown of ILF3-AS1 or overexpression of miR-29a significantly down-regulated the expression levels of PTBP3.	32117452	RID07159	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC01139	MYBL2	positively-E	luciferase assays;rescue experiment	upregulation	qRT-PCR	TCGA;GSE36736;GSE55092;GSE76427	NA	cell proliferation(-);colony formation(-);cell metastasis(-);	ceRNA(miR-30)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000101057	NA	339535	4605	LINK-A|TCONS_00000027	B-MYB|BMYB	Long noncoding RNA LINC01139 promotes the progression of hepatocellular carcinoma by upregulating MYBL2 via competitively binding to miR-30 family. Up-regulation of LINC01139 in HCC was correlated with poor prognosis.	32115147	RID07160	ceRNA or sponge	prognosis,metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	MELTF-AS1	FOXM1	positively-E	miRanda;Targetscan;luciferase reporter;RIP;qRT-PCR	upregulation	qRT-PCREPIA	TCGA;	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-134)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000228109	GRCh38_3:196999460-197004744	ENSG00000111206	NA	100507057	2305	AC068302.3|MFI2-AS1	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	The post-transcriptional regulation of FOXM1 by MFI2-AS1 occured mechanistically, playing a role of competing with endogenous RNA (ceRNA) in HCC to sponge miR-134. In present study, with high expression level in The Cancer Genome Atlas (TCGA) HCC samples, lncRNA MFI2 Antisense RNA 1 (MFI2-AS1) was closely related to poor prognosis and advanced stage among patients with HCC. Ectopic expression of MFI2-AS1 stimulated the proliferation and metastasis of HCC cells, but knockdown MFI2-AS1 suppressed HCC cell proliferation and metastasis, indicating that MFI2-AS1 exerted oncogenic functions in the tumorigenesis of HCC.	32106369	RID07161	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Diffuse large b-cell lymphoma	DBH-AS1	FN1	positively-E	western blot;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000115414	NA	138948	2335	BPR|NCRNA00118	CIG|FINC|GFND2|LETS|MSF	Long non-coding RNA DBH-AS1 promotes cancer progression in diffuse large B-cell lymphoma by targeting FN1 via RNA-binding protein BUD13. DBH-AS1 promotes cell proliferation, migration, andinvasion in DLBC.	32091157	RID07162	interact with protein	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Cervical cancer	FOXD2-AS1	HDGF	positively-E	lucifierase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-760)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000143321	NA	84793	3068	MGC12982	HMG1L2	FOXD2-AS1-possesses significant oncogenic activity in cervical cancer progression; this activity is mediated by sponging of miR-760 with consequent upregulation of HDGF.	32082174	RID07163	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Cervical cancer	FOXD2-AS1	MIR760	negatively-E	lucifierase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000211575	NA	84793	100126348	NA	MIRN760|hsa-mir-760|mir-760	FOXD2-AS1-possesses significant oncogenic activity in cervical cancer progression; this activity is mediated by sponging of miR-760 with consequent upregulation of HDGF.	32082174	RID07164	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Colorectal cancer	SYNE3	HMGB2	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;microarray	GSE113296	NA	epithelial to mesenchymal transition(+);apoptosis process(-);	NA	binding/interaction	NA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000176438	GRCh38_14:95407266-95516650	ENSG00000164104	NA	161176	3148	C14orf139|C14orf49|FLJ25605|LINC00341|NCRNA00341|Nesp3|Nesprin-3|NET53	HMG2	RNA-pull-down assay identifies LINC00341 physically binds to HMGB2 and stabilizes the localization of HMGB2 in the cytoplasm. Notably, LINC00341 knockdown leads to the shift of HMGB2 into nuclear, in which it triggers epithelial to mesenchymal transition (EMT) programming. Moreover, LINC00341 can also promote apoptosis. SIGNIFICANCE OF THE STUDY: LncRNAs are ubiquitous transcripts that play key roles in regulating gene expression at the levels of transcription, RNA processing, and translation. Aberrant expression and mutations of lncRNAs represent a driving force behind oncogenesis and development of tumours. However, the function of lncRNA still needs further exploration. Our study has revealed a new noncoding RNA-mediated regulatory network that highly likely protects colorectal carcinoma by preventing migration and apoptosis. The results will help further explore the molecular details about the progression of colorectal carcinoma and stimulate efforts to develop effective therapies.	32067238	RID07165	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Retinoblastoma	MIR7-3HG	PEG10	positively-E	dual luciferase assay;mircode	upregulation	qRT-PCR	GSE110811	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-27a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000176840	GRCh38_19:4769031-4785077	ENSG00000242265	NA	284424	23089	C19orf30|Huh7|LINC00306|NCRNA00306|PGSF1|PGSF1a|PGSF1b|uc002mbe.2	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	High expression of MIR7-3HG was presented in Rb tissues and cells. All data revealed that MIR7-3HG promoted Rb cells proliferation and suppressed the apoptosis of Rb cells through sponging miR-27a-3p and up-regulating PEG10. All data revealed that PEG10 expression was positively related to MIR7-3HG expression, but negatively linked to miR-27a-3p expression.	32035086	RID07166	ceRNA or sponge	NA		
Medulloblastoma	HOTAIR	YY1	positively-E	RNA pull-down;Luciferase assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell growth(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(-)	ceRNA(miR-1/miR-206)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Medulloblastoma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100811	NA	100124700	7528	HOXC-AS4|HOXC11-AS1|NCRNA00072	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	In this study, we found that HOTAIR and YY1 were up-regulated in medulloblastoma tissues and cell lines, and HOTAIR increased YY1 expression. The molecular mechanism demonstrated that HOTAIR negatively regulated miR-1 and miR-206 expression, which can directly target YY1 in medulloblastoma cells. Moreover, HOTAIR increased YY1 expression through binding to miR-1 and miR-206. The functional experiments showed that HOTAIR knockdown suppressed medulloblastoma cell proliferation, tumor growth, migration and invasion, and promoted cell apoptosis via the modulation of the miR-1/miR-206-YY1 axis, as well as epithelial to mesenchymal transition (EMT).	31986414	RID07167	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Oral squamous cell carcinoma	CCHE1	PAK2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-922)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	NA	NA	ENSG00000180370	NA	NA	5062	NA	PAK65|PAKgamma	qRT-PCRanalysis identified the upregulation of CCHE1 in OSCC cells. Knockdown of CCHE1 curbed the proliferation, migration, and invasion and hastened the apoptosis in OSCC cell lines. Moreover, it was found that miR-922 could interact with CCHE1. Besides, PAK2 was identified as the target gene of miR-922 and its expression was negatively modulated by miR-922 and positively regulated by CCHE1. Restoration assay manifested that the suppressing influence of CCHE1 depletion on OSCC progression was rescued by amplified PAK2.	31981240	RID07168	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	CDKN2B-AS1	MAP3K3	positively-E	RT-qPCR;RIP;luciferase reporter assay;starBase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);	ceRNA(miR-4458)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000198909	NA	100048912	4215	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	MAPKKK3|MEKK3	Our results suggested that CDKN2B-AS1 facilitated OS progression by sponging miR-4458 to enhance MAP3K3 expression, which provides a novel insight into improving diagnostic and therapeutic strategies for patients with OS.	31950433	RID07169	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Papillary thyroid carcinoma	CASC9	ADAM9	positively-E	luciferase teporter assay;western blot;Starbase	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+);	ceRNA(miR-488-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000168615	NA	101805492	8754	ESCCAL-1|linc-JPH1|LINC00981	CORD9|KIAA0021|MCMP|MDC9|Mltng	Downregulation of CASC9 significantly attenuated the proliferative, migrative, and invasive abilities of PTC cells, and suppressed tumorigenesis in vivo. While overexpression of CASC9 elevated the proliferation, migration, and invasion of PTC cells. miR-488-3p expression was decreased, and ADAM9 level was increased in PTC tissues and cells. CASC9 expression was negatively related to miR-488-3p, but positively associated with ADAM9 expression in PTC tissues. Molecular mechanism analysis revealed that CASC9 functioned via sponging miR-488-3p to regulate ADAM9 expression, followed by activation of EGFR-Akt signaling. In conclusion, lncRNA CASC9 promoted the malignant phenotypes of PTC via modulating miR-488-3p/ADAM9 pathway. This study may provide a novel therapeutic target for the treatment of PTC.	31943867	RID07170	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	UP(LIHC,PAAD,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical squamous cell carcinoma	MYC	SNHG12	positively-E	western blot;rescue experiment;qRT-PCR	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);apoptosis process(-);tumor growth(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000197989	GRCh38_1:28578538-28583132	4609	85028	bHLHe39|c-Myc|MYCC	ASLNC04080|C1orf79|LINC00100|PNAS-123	To the best of our knowledge, it is the first report to indicate that increased SNHG12 expression may be driven by the HPV16 E6 and E7 oncogene, through a mechanism that is dependent on c-Myc activation.	31943193	RID07171	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Cervical squamous cell carcinoma	SNHG12	SNAI2	positively-E	western blot;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);tumor growth(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000019549	NA	85028	6591	ASLNC04080|C1orf79|LINC00100|PNAS-123	SLUG|SLUGH|SLUGH1|SNAIL2	western blot demonstrated that knockdown of SNHG12 decreased the protein levels of p-ERK1/2 and Slug.	31943193	RID07172	transcriptional regulation	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Esophagus squamous cell carcinoma	MIAT	INCENP	positively-E	dual-luciferase reporter assay;LncBase v2.0;starBase v3.0;qRT-PCR	upregulation		NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);	ceRNA(miR-1301-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000149503	NA	440823	3619	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	FLJ31633	In this study, we found that MIAT was significantly increased in ESCC tissues, as well as cell lines. Downregulation of MIAT suppressed ESCC cell proliferation, cell cycle, migration, and invasion. Mechanical studies revealed that MIAT promoted ESCC cell proliferation and cell cycle by acting as a competitively endogenous RNA (ceRNA) to upregulate the inner centromere protein (INCENP) expression through sponging miR-1301-3p. Furthermore, we uncovered that MIAT-SOX2 formed a positive feedback loop to facilitate cell proliferation, migration, and invasion of ESCC. Our findings indicated that MIAT promoted ESCC progression via targeting INCENP/miR-1301-3p axis and interacting with SOX2, suggesting novel potential therapeutic targets for ESCC.	31943174	RID07173	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SOX2	MIAT	positively-E	dual-luciferase reporter assay;LncBase v2.0;starBase v3.0;qRT-PCR	upregulation		NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000181449	NA	ENSG00000225783	GRCh38_22:26646411-26676475	6657	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	In this study, we found that MIAT was significantly increased in ESCC tissues, as well as cell lines. Downregulation of MIAT suppressed ESCC cell proliferation, cell cycle, migration, and invasion. Mechanical studies revealed that MIAT promoted ESCC cell proliferation and cell cycle by acting as a competitively endogenous RNA (ceRNA) to upregulate the inner centromere protein (INCENP) expression through sponging miR-1301-3p. Furthermore, we uncovered that MIAT-SOX2 formed a positive feedback loop to facilitate cell proliferation, migration, and invasion of ESCC. Our findings indicated that MIAT promoted ESCC progression via targeting INCENP/miR-1301-3p axis and interacting with SOX2, suggesting novel potential therapeutic targets for ESCC.	31943174	RID07174	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	SNHG1	Cyclin D1	positively-E	dual-luciferase reporter assay;starBase v2.0	upregulation	RT-qPCR	NA	NA	cell proliferation(+);tumor growth(+);cell cycle(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	We further confirmed that, in PCa cells, SNHG1 can negatively regulate miR-195 expression by acting as a ceRNA, and Cyclin D1 is a direct target of miR-195. Overexpression of miR-195 abrogated the oncogenic role of SNHG1 in PCa cells. Collectively, our results identified SNHG1 as a novel oncogenic lncRNA in PCa, and indicated that SNHG1/miR-195/Cyclin D1 axis might be a potential therapeutic target for PCa patients.	31933880	RID07175	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Papillary thyroid carcinoma	LINC00311	TLR4	negatively-E	shRNA;dual-luciferase reporter assay;RIP;miRDB;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-330-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000179219	GRCh38_16:85282958-85285963	ENSG00000136869	NA	197196	7099	MGC22001|NCRNA00311|TMEM148	ARMD10|CD284|hToll|TLR-4	Mechanistic investigations revealed that LINC00311 was negatively correlated with the expression of miR-330-5p, meanwhile, TLR4 was a direct target of miR-330-5p. In addition, rescue assays further determined that LINC00311 contributed to the progression of PTC through regulating TLR4 expression. Taken together, these findings indicated that LINC00311 could promote cancer stem-like properties by targeting miR-330-5p/TLR4 pathway in PTC.	31894666	RID07176	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Urinary bladder cancer	LNCARSR	SOX4	positively-E	RNA pull-down;dual-luciferase reporter assay;miRDB	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);epithelial to mesenchymal transition(+);	ceRNA(miR-129-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000124766	NA	102723932	6659	lnc-TALC	NA	Mechanistically, lncARSR was mainly located in the cytoplasm and acted as a miRNA sponge to positively modulate the expression of Sex-determining region Y-related high-mobility-group box transcription factor 4 (SOX4) via sponging miR-129-5p and subsequently promoted the proliferation and metastasis of Bca cells, thus playing an oncogenic role in Bca pathogenesis. In conclusion, our study indicated that lncARSR plays a critical regulatory role in Bca cells and lncARSR may serve as a potential diagnostic biomarker and therapeutic target for bladder cancer.	31892841	RID07177	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Papillary thyroid carcinoma	LINC00400	RAF1	positively-E	western blot assay;luciferase reporter assay;LncBase Predicted v.2;StarBase v2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);tumor growth(+);	ceRNA(miR-485-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000229928	GRCh38_13:43158631-43159466	ENSG00000132155	NA	100874159	5894	NA	c-Raf|CRAF|Raf-1	LINC00460 was upregulated in PTC tissues and cells. Raf1 was upregulated in PTC tissues, but miR-485-5p was down-regulated. High LINC00460 expression was associated with poor prognosis. LINC00460 knockdown suppressed proliferation, migration, invation and EMT of PTC cells. Bioinformatics prediction revealed that LINC00460 had binding sites with miR-485-5p, which was validated by luciferase reporter assay. Moreover, LINC00460 promoted PTC progression by sponging miR-485-5p to elevate the expression of Raf1. Knockdown of LINC00460 restrained tumor growth in vivo.	31870440	RID07178	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	HIF1A-AS2	miR-129-5p	negatively-F	dual-luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000258667	GRCh38_14:61707564-61751099	NA	NA	100750247	NA	3'aHIF-1A|aHIF	NA	We found that overexpression of miR-129-5p decreased the luciferase activity of wild-type (WT) HIF1A-AS2 but not mutant HIF1A-AS2. Ectopic expression of HIF1A-AS2 suppressed miR-129-5p expression in MG-63 cells. We demonstrated that miR-129-5p was downregulated in osteosarcoma and was negatively associated with HIF1A-AS2 expression. Furthermore, ectopic expression of miR-129-5p suppressed osteosarcoma cell proliferation, cell cycle progression and invasion. In addition, overexpression of HIF1A-AS2 promoted cell proliferation, cell cycle progression and invasion of osteosarcoma cells through the modulation of miR-129-5p. These results indicated that HIF1A-AS2 might be a potential therapeutic target for osteosarcoma.	31866584	RID07179	ceRNA or sponge	NA		
Gastric cancer	OIP5-AS1	MIR641	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000207631	NA	729082	693226	cyrano|linc-OIP5	MIRN641|hsa-mir-641|mir-641	OPI5-AS1 was significantly upregulated, while miR-641 was downregulated in GC tissues and cells. OPI5-AS1 expression was remarkably inversely correlated with miR-641 in GC. Moreover, OPI5-AS1 could sponge miR-641 and regulate its expression in GC cells. Functional experiments showed that OPI5-AS1 overexpression remarkably accelerated GC cell proliferation and cell cycle.	31858545	RID07180	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Small cell lung cancer	LUADT1	TWIST1	positively-E	western blot;qPCR	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+);	ceRNA(miR-15a-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000122691	NA	106182249	7291	NA	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	We found that LUADT1 and Twist1 were upregulated in SCLC, while miR-15a-3p was downregulated in SCLC. However, LUADT1 was posively correlated with Twist1 but was not significnatly correlated with miR-15a-3p. Overexpression experiments showed that and LUADT1 and miR-15a-3p did not significantly affect the expression of each other. Moreover, LUADT1 overexpression mediated the upregualtion of Twist1, and miR-15a-3p overexpression played an oppsoite role. Transwell assays showed that LUADT1 and Twist1 overexpression mediated the increased rate of cell invasion and migration, while miR-15a-3p overexpression mediated the decreased rate of cell invasion and migration. In addition, miR-15a-3p overexpression played an oppsoite role and attenuated the effects of LUADT1 overexpression. Therefore, LUADT1 may sponge miR-15a-3p to upregulate Twist1 in SCLC, thereby promoting cancer cell invasion and migration.	31842825	RID07181	ceRNA or sponge	NA	UP(NSCLC,PRAD,SKCM);DATA(GSE74639,GSE104209,GSE38495)	UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	FOXD2-AS1	AKT1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);	ceRNA(miR-185)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000142208	NA	84793	207	MGC12982	AKT|PKB|PRKBA|RAC|RAC-alpha	FOXD2-AS1 was significantly upregulation in hepatocellular carcinoma tissues. FOXD2-AS1 knockdown suppressed Bel-7401 cell biological activities (proliferation, invasion, and migration) with miR-185 overexpression and AKT depressing in cell expression.	31841454	RID07182	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	LINC02418	SEC61G	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell invasion(-);	ceRNA(miR-4677-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214039	GRCh38_12:130032928-130045057	ENSG00000132432	NA	100190940	23480	NA	SSS1	LINC02418 was found as upregulated expression in both NSCLC tissues and cells. Functional assays showed that LINC02418 knockdown suppressed NSCLC cell proliferation and invasion but promoted cell apoptosis, while the overexpression of LINC02418 exerts opposite effects. Mechanistically, we showed LINC02418 could interact with microRNA-4677-3p (miR-4677-3p) to regulate Sec61 gamma subunit (SEC61G) expression.	31841189	RID07183	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111065,GSE55807,GSE86978)
Ovarian cancer	LINC-ROR	FLNB	negatively-E	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136068	NA	100885779	2317	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ABP-278|ABP-280|AOI|FH1|FLN-B|FLN1L|LRS1|SCT|TABP|TAP	In our study, we demonstrated that LncRNA-ROR was high expression in ovarian cancer tissues than in normal ovarian tissues, and LncRNA-ROR level was positively associated with clinical stages and the differentiation grades of malignant cells. Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB. Moreover, the binding site for miR-145 within LncRNA-ROR contributed to the reciprocal negative regulation of LncRNA-ROR and miR-145. Taken together, LncRNA-ROR promoted EMT by the miR-145/FLNB regulatory axis in ovarian cancer, providing a potential therapeutic target for ovarian cancer.	31829305	RID07184	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Nasopharynx carcinoma	LINC00958	NUAK1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-625)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000074590	NA	100506305	9891	NA	ARK5|KIAA0537	Our results demonstrated that LINC00958 works as an oncogene in NPC and plays a key role in the malignant phenotype of NPC cells by sponging miR-625 and increasing NUAK1 expression. The LINC00958-miR-625-NUAK1 pathway might be a target for anticancer therapy in patients with NPC.	31819474	RID07185	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatoblastoma	ZFAS1	RALY	positively-E	dual-luciferase reporter assay;RIP;Starbase v3.0	upregulation	qRT-PCR	GSE75271;GSE75283	NA	cell proliferation(+);cell invasion(+);cancer progression(+);HGF/c-MET signaling pathway(+)	ceRNA(miR-193a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000125970	NA	441951	22913	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	HNRPCL2|P542	High ZFAS1 expression was significantly associated with aggressive tumor phenotypes and poorer overall survival in HB. In vitro and in vivo function assays indicated that silencing of ZFAS1 significantly suppressed HB cell proliferation and invasion. Furthermore, miR-193a-3p was identified to be the target of ZFAS1. Subsequently, RALY was confirmed to be regulated by miR-193a-3p/ZFAS1 axis. Mechanistically, our results indicated that the ZFAS1 participated to the progression of HB via regulating the HGF/c-Met signaling. Collectively, these data demonstrated that ZFAS1 acted as an oncogene to promote initiation and progression of HB by regulating miR-193a-3p/RALY (RALY Heterogeneous Nuclear Ribonucleoprotein) axis via HGF/c-Met Pathway, which provides an efficient marker and new therapeutic target for HB.	31781561	RID07186	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colorectal cancer	LEF-AS1	KIF3B	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);apoptosis process(-);	ceRNA(miR-505)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000101350	NA	NA	9371	NA	FLA8|KIAA0359|KLP-11	The expression of LEF-AS1 in CRC tissue specimens was found to be markedly higher than that in normal colon tissues. After transfection with LEF-AS1 siRNA, the cell viability, as well as cell migration and invasion capacities, were both attenuated. However, the cell apoptosis rate was conversely elevated. dual-luciferase reporter assay revealed that LEF-AS1 could combine with miR-505, which was capable of targeted binding to KIF3B. In addition, LEF-AS1 siRNA transfection attenuated cell proliferation, migration, and invasion capacities, which could be partially reversed by the overexpression of KIF3B.	31773695	RID07187	ceRNA or sponge	NA		UP(LIHC,PAAD,BRCA);DOWN(PRAD,PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Pancreatic cancer	LINC00976	OTUD7B	positively-E	ITRAQ;bioinformatic analysis;rescue assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);EGFR/MAPK signaling pathway(+)	ceRNA(miR-137)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000163113	NA	106144608	56957	NA	CEZANNE|ZA20D1	linc00976 expression was overexpressed in PC tissues and cell lines and was positively associated with poorer survival in patients with PC. Function studies revealed that linc00976 knockdown significantly suppressed cell proliferation, migration and invasion in vivo and in vitro, whereas its overexpression reversed these effects. Based on Itraq results and online database prediction, Ovarian tumor proteases OTUD7B was found as a downstream gene of linc00976, which deubiquitinated EGFR mediates MAPK signaling activation. Furthermore, Bioinformatics analysis and luciferase assays and rescue experiments revealed that linc00976/miR137/OTUD7B established the ceRNA network modulating PC cell proliferation and tumor growth.	31747939	RID07188	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Hepatocellular carcinoma	RAB5IF	CTNNB1	positively-E	western blot;siRNA	upregulation	RT-qPCR	ATCC;TCGA	NA	cell proliferation(+);colony formation(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000101084	GRCh38_20:36605779-36612557	ENSG00000168036	NA	55969	1499	C20orf24|PNAS-11|RCAF1|RIP5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA RAB5IF is Overexpressed in HCCs and Patient Tissues. Depletion of LncRNA RAB5IF Inhibits Proliferation and Colony Formation of HCCs. Depletion of LncRNA RAB5IF Attenuates the Expression of LGR5, beta-Catenin and c-Myc in HCCs; Taken together, these findings for the first time demonstrate novel evidence that LncRNA RAB5IF promotes the growth hepatocellular carcinoma cells via upregulation of LGR6 mediated beta-catenin and c-Myc signaling axis as a potent oncogenic target.	31717443	RID07189	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	RAB5IF	MYC	positively-E	western blot;siRNA	upregulation	RT-qPCR	ATCC;TCGA	NA	cell proliferation(+);colony formation(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000101084	GRCh38_20:36605779-36612557	ENSG00000136997	NA	55969	4609	C20orf24|PNAS-11|RCAF1|RIP5	bHLHe39|c-Myc|MYCC	LncRNA RAB5IF is Overexpressed in HCCs and Patient Tissues. Depletion of LncRNA RAB5IF Inhibits Proliferation and Colony Formation of HCCs. Depletion of LncRNA RAB5IF Attenuates the Expression of LGR5, beta-Catenin and c-Myc in HCCs; Taken together, these findings for the first time demonstrate novel evidence that LncRNA RAB5IF promotes the growth hepatocellular carcinoma cells via upregulation of LGR7 mediated beta-catenin and c-Myc signaling axis as a potent oncogenic target.	31717443	RID07190	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Glioma	LINC00174	SOX9	positively-E	shRNA;luciferase reporter assay;RIP;miRDB	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);chemoresistance(-);tumor growth(-);	ceRNA(miR-138-5p)	regulation	NA	Temozolomide	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	TF	ENSG00000179406	GRCh38_7:66376044-66493566	ENSG00000125398	NA	285908	6662	NCRNA00174	CMD1|CMPD1|SRA1	Our results demonstrated that the expression level of LINC00174 was higher in glioma tissues, and LINC00174 down-regulation could remarkably prevent cell proliferation and promote cell apoptosis in both glioma cells and TMZ-resistant glioma cells. Mechanistic studies revealed that LINC00174 can sponge microRNA-138-5p (miR-138-5p) and down-regulate its expression, thereby up-regulating the protein level of miR-138-5p's target, sex-determining region Y (SRY)-box9 protein (SOX9). Additionally, in vivo experiments revealed that LINC00174 shRNA can serve as a tumor suppressor through down-regulating SOX9 in glioma. In this study, a novel established regulatory way of LINC00174/miR-138-5p/SOX9 axis was systematically studied, which may provide a new manner for glioma therapy.	31713817	RID07191	ceRNA or sponge	chemoresistance	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE86978)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Gastric cancer	LINC00470	PTEN	negatively-E	RIP;RNA pull-down;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000132204	GRCh38_18:1254383-1408344	ENSG00000171862	NA	56651	5728	C18orf2	BZS|MHAM|MMAC1|PTEN1|TEP1	In this study, our findings showed that LINC00470 was significantly upregulated in GC tissues and cell lines, and correlated with distant metastasis, TNM stage and poor prognosis. Overexpression and knockdown experiments revealed its oncogenic functions on GC cell proliferation, migration and invasion. Mechanistically, LINC00470 associated with PTEN mRNA and suppressed its stability through interaction with the N6-methyladenosine (m6A) writer METTL3. We also showed that LINC00470-METTL3-mediated PTEN mRNA degradation relied on the m6A reader protein YTHDF2-dependent pathway. Taken together, LINC00470 might serve as a therapeutic target for GC patients.	31711642	RID07192	interact with protein	metastasis,prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	GAS5	PTEN	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumor growth(+);chemoresistance(+);	ceRNA(miR-21)	regulation	NA	Doxorubicin	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	We found that GAS5 was downregulated in HCC cell lines and tumor tissues. Knockdown of GAS5 enhanced HCC cell proliferation in vitro and in vivo and increased HCC cell resistance to doxorubicin. GAS5 acted as a sponge for miR-21 silencing and consequently led to the elevation of PTEN expression. Our data demonstrated that GAS5 functioned as a tumor suppressor role in HCC through regulation of miR-21-PTEN singling pathways, suggesting a potential application of GAS5 in HCC therapy.	31705194	RID07193	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Triple-negative breast cancer	ROCR	SOX9	positively-E	ChIP;shRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000228639	GRCh38_17:72021851-72058073	ENSG00000125398	NA	102723505	6662	LINC02095	CMD1|CMPD1|SRA1	Linc02095-is up-regulated in TNBC BC cells and patient samples. Our results indicated that both linc02095 and SOX9 positively regulate the expression of each other in BC cells.SOX9 and linc02095 promote cell proliferation in TNBC cells. We conclude that linc02095 modulates SOX9 transcription, potentially by altering the loading or elongation of RNA polymerase II, without having an impact on the chromatin structure. we demonstrated significant enrichment of SOX9 at the promoter of linc02095, coregulated expression of linc02095 and SOX9 in BC cells, and reduced expression of linc02095 in SOX9-depleted cells. Based on these results, we conclude that SOX9 is a bona fide transcription activator of linc02095.	31690584	RID07194	interact with protein	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Breast cancer	HAND2-AS1	SOX7	positively-E	CCK-8;Transwell;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);	ceRNA(miR-1275)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000171056	NA	79804	83595	DEIN|FLJ11539|NBLA00301	NA	Downregulation of HAND2-AS1 was detected in breast cancer and was associated with adverse clinical features and prognosis. Furthermore, overexpression of HAND2-AS1 restrained cell viability, migration and invasion in breast cancer. In addition, reciprocal suppression between HAND2-AS1 and miR-1275 was identified in breast cancer cells. Further, SOX7, a target of miR-1275, strengthened the effect of HAND2-AS1 in breast cancer.	31683462	RID07195	ceRNA or sponge	prognosis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	CDKN2B-AS1	PBX3	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT signaling pathway(+);JAK/STAT signaling pathway(+)	ceRNA(miR-144)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000167081	NA	100048912	5090	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	NA	ANRIL was highly expressed in MHCC97 and Li-7 cells when compared to THLE-3 cells. ANRIL overexpression promoted cell viability, migration, invasion and suppressed apoptosis of MHCC97 and Li-7 cells. ANRIL negatively regulated miR-144, and oncogenic effects of ANRIL were attenuated when miR-144 was overexpressed. PBX3 was a direct target of miR-144. miR-144 overexpression blocked PI3K/AKT and JAK/STAT signalling pathways via targeting PBX3. Our data documented that ANRIL promoted hepatocellular carcinoma cells growth, migration and invasion. One of the possible mechanisms responsible for the tumour-promoting actions is that ANRIL sponging miR-144 to derepress PBX3.	31609763	RID07196	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE111842,GSE55807)
Urinary bladder cancer	LINC00319	ROMO1	positively-E	luciferase reporter assay;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	ceRNA(miR-4492)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000125995	NA	284836	140823	C21orf125|FLJ38036|NCRNA00319|PRED49	bA353C18.2|C20orf52|MTGMP	In addition, the data indicated LINC00319 was a sponge for miR-4492 and miR-4492 suppressed ROMO1 expression in BCa. Furthermore, our results illustrated miR-4492/ROMO1 axis regulates proliferation, migration, and invasion and LINC00319 exerts oncogenic roles through modulating miR-4492/ROMO1 axis. Similarly, miR-4492 mimics inhibited migration and invasion of T24 and J82 cellswhereas overexpression of ROMO1 reversed it.	31608995	RID07197	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	HHIP-AS1	HHIP	positively-E	western blot;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);cell migration(-);cell invasion(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000248890	GRCh38_4:144642919-144661357	ENSG00000164161	NA	646576	64399	NA	FLJ20992|HIP	The expression levels of HHIP-AS1 were significantly decreased in HCC tissues. Further investigation showed that HHIP-AS1 interacted with and positively regulated the stability of HHIP mRNA in a HuR-dependent manner.  HHIP-AS1 inhibits proliferation and enhances apoptosis in HCC cells. HHIP-AS1 represses HCC cell migration and invasion.HHIP-AS1 increases the stability of HHIP mRNA.HHIP-AS1 stabilizes HHIP mRNA through HuR. HHIP-AS1 exerts suppressive effects via HHIP.	31604528	RID07198	interact with protein	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Melanoma	STAT3	SNHG17	positively-E	luciferase reporter assay;ChIP;western blot	upregulation	RT-qPCR	GSE3189	NA	cell proliferation(-);apoptosis process(+);cell migration(-);cell invasion(-);PI3K/AKT signaling pathway(+);	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	TF	lncRNA	ENSG00000168610	NA	ENSG00000196756	GRCh38_20:38419638-38435409	6774	388796	APRF	NA	High expressions of SNHG17 were observed in both melanoma tissues and cells. Up-regulation of SNHG17 in melanoma patients was associated with lymph node metastasis and tumor stage. Survival assays revealed that those patients with high SNHG17 expression had significantly shorter survival time. SNHG17 was also confirmed to be independently associated with overall survival of melanoma patients. Functional studies confirmed that the proliferation, migration, and invasion of melanoma cells were noticeably reduced by the down-regulation of SNHG17. Mechanistically, the up-regulation of SNHG17 was induced by STAT3. We also found that knockdown of SNHG17 resulted in the remarkable diminution in the phosphorylation levels of PI3K and AKT, suggesting that the activity of the PI3K-AKT pathway was suppressed.	31599425	RID07199	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Glioma	LINC00473	CDK6	positively-E	luciferase reporter assay;RIP;DIANA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)tumor growth(+);	ceRNA(miR-637)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000223414	NA	ENSG00000105810	NA	90632	1021	C6orf176|LNC473|bA142J11.1	PLSTIRE	LINC00473 is upregulated in glioma. Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes in vitro, and reduced tumor growth in vivo. Correlation analysis showed that LINC00473 expression was positively correlated with CDK6 expression in glioma tissues. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.	31561732	RID07200	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Glioma	LINC00645	ZEB1	positively-E	western blot;luciferase reporter assay;RIP;miRDB;LncBase V2	upregulation	qRT-PCR	TCGA;CGGA;GSE4290	NA	cell proliferation(+);cell stemness(+);cell migration(+);cell invasion(+);ce	ceRNA(miR-205-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000258548	GRCh38_14:27612577-27639636	ENSG00000148516	NA	100505967	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	In the present study, linc00645 expression was significantly upregulated in GBM tissues and cell lines. Knockdown of linc00645 suppressed the proliferation, stemness, migration, invasion, and reversed transforming growth factor (TGF)-beta-induced motility of glioma cell lines. Furthermore, linc00645 directly interacted with miR-205-3p and upregulated of miR-205-3p impeded efficiently the increase of ZEB1 induced by linc00645 overexpression.	31558707	RID07201	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	H3K27	lnc-SLC4A1-1	positively-E	ChIP;RIP;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+);	acetylation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	PCG	lncRNA	NA	NA	NA	NA	NA	NA	NA	NA	Lnc-SLC4A1-1 was significantly up-regulated in BC tissue, serum samples and cell lines. In BC cells, lnc-SLC4A1-1 knockdown promoted cell apoptosis and suppressed cell proliferation, migration and invasion. Furthermore, lnc-SLC4A1-1 is transcriptionally activated by H3K27 acetylation, and lnc-SLC4A1-1 interacted with transcription factor (NF)-kB p65, thereby regulating CXCL8 expression. Meanwhile, CXCL8 overexpression partly reversed the effects of lnc-SLC4A1-1 knockdown on cell viability, apoptosis, migration and invasion in BC cells. Lnc-SLC4A1-1 could promote the development of BC by regulating NF-kB/CXCL8. the further experiments revealed that lnc-SLC4A1-1 overexpression remarkably promoted the expression of NF-kB p65 and CXCL8, while the opposite effects were found after lnc-SLC4A1-1 knockdown.Compared with cells with sh-lnc-SLC4A1-1, the number of apoptotic cells was obviously inhibited (p-<-.01, Figure 5(C)), meanwhile, cell viability (p-<-.01, Figure 5(B)), cell migration (p-<-.01, Figure 5(D)), and cell invasion (p-<-.01, Figure 5(E)) were all conspicuously increased in cells with sh-lnc-SLC4A1-1-+-pEX-CXCL8. These results suggested that CXCL8 overexpression partly reversed the effects of lnc-SLC4A1-1 knockdown on cell viability, apoptosis, migration and invasion.	31556319	RID07202	epigenetic regulation	NA		
Breast cancer	lnc-SLC4A1-1	CXCL8	positively-E	ChIP;RIP;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000169429	NA	NA	3576	NA	GCP-1|GCP1|IL8|LECT|LUCT|LYNAP|MDNCF|MONAP|NAF|NAP-1|NAP1|SCYB8	Lnc-SLC4A1-1 was significantly up-regulated in BC tissue, serum samples and cell lines. In BC cells, lnc-SLC4A1-1 knockdown promoted cell apoptosis and suppressed cell proliferation, migration and invasion. Furthermore, lnc-SLC4A1-1 is transcriptionally activated by H3K27 acetylation, and lnc-SLC4A1-1 interacted with transcription factor (NF)-kB p65, thereby regulating CXCL8 expression. Meanwhile, CXCL8 overexpression partly reversed the effects of lnc-SLC4A1-1 knockdown on cell viability, apoptosis, migration and invasion in BC cells. Lnc-SLC4A1-1 could promote the development of BC by regulating NF-kB/CXCL8. the further experiments revealed that lnc-SLC4A1-1 overexpression remarkably promoted the expression of NF-kB p65 and CXCL8, while the opposite effects were found after lnc-SLC4A1-1 knockdown.Compared with cells with sh-lnc-SLC4A1-1, the number of apoptotic cells was obviously inhibited (p-<-.01, Figure 5(C)), meanwhile, cell viability (p-<-.01, Figure 5(B)), cell migration (p-<-.01, Figure 5(D)), and cell invasion (p-<-.01, Figure 5(E)) were all conspicuously increased in cells with sh-lnc-SLC4A1-1-+-pEX-CXCL8. These results suggested that CXCL8 overexpression partly reversed the effects of lnc-SLC4A1-2 knockdown on cell viability, apoptosis, migration and invasion.	31556319	RID07203	interact with protein	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Glioblastoma	EGFR-AS1	RACK1	positively-E	western blot;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-133b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000204628	NA	100507500	10399	NA	Gnb2-rs1|GNB2L1|H12.3	The results indicated that lnc-EGFR-AS1 expression was increased in glioma cells and tissues. EGFR-AS1 knockdown suppressed proliferation, migration and invasion of glioma cells, but induced apoptosis. Additionally, lnc-EGFR-AS1 functioned as a sponge for miR-133b. Promoting lnc-EGFR-AS1 expression significantly reduced miR-133b expression. Furthermore, miR-133b could target the 3'-untranslated region (3'-UTR) of RACK1 and reduced its expression levels.  These findings elucidated that EGFR-AS1 accelerated cell proliferation, migration, invasion and prevented apoptosis in glioma cells by regulating miR-133b/RACK1, providing new insights for the diagnosis and molecular therapy of GBM.	31545240	RID07204	ceRNA or sponge	NA		DOWN(PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE75367)
Gastric cancer	SNHG3	MED18	negatively-E	western blot;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);	DNA methylation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000130772	NA	8420	54797	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	FLJ20045|p28b|SRB5	We first observed significant overexpression of SNHG3 in cancer cell lines were observed in our cell panel including MGC-803, AGS, BGC-823, SGC-7901, MKN-45, N87 and HGC-27.SNHG3 promoted cell proliferation both in vitro and in vivo.Knockdown of SNHG3 inhibited metastasis of GC cells both in vitro and in vivo.SNHG3 epigenetically regulated neighboring gene MED18 transcription by binding to EZH2.MED18 suppressed proliferation, migration and invasion of GC cells.Mechanistically, we uncovered SNHG3 associated with EZH2 and negatively regulated MED18 expression through methylation modulation.SNHG3 promoted GC progression partly by regulating MED18 expression.	31534128	RID07205	epigenetic regulation	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Esophagus squamous cell carcinoma	PANDAR	E2F1	positively-E	western blot;shRNA;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000101412	NA	101154753	1869	PANDA	RBBP3|RBP3	LncRNA PANDA is up-regulated in of ESCC tissues. Silence of PANDA promoted cell apoptosis and inhibited cell proliferation in vitro. PANDA knockdown attenuated xenograft growth and inhibited cell proliferation in vivo. PANDA regulated E2F1 to depress apoptosis in ESCC through dissociating from NF-YA. PANDA interacted with SAFA to promote ESCC cell proliferation.  PANDA binding SAFA to switch on the tumor proliferation programme though CyclinD1/2-Cyclin E1 and Bcl-2 pathways.PANDA regulated E2F1 to depress apoptosis in ESCC through dissociating from NF-YA. Further analysis revealed that PANDA expression was positively correlated with E2F1 mRNA expression in ESCC. Same as E2F1, the expression of SAFA was up-regulated in 24 paired primary cancerous and adjacent noncancerous in which PANDA expression had been measured.It was consistent with our study that PANDA regulated E2F1 expression by competitive combination with NF-YA in ESCC cells. Our study demonstrated that aberrant over-expression of PANDA in ESCC tissues and consequent up-regulation of E2F1 could 'drive'-tumorigenesis in progression of ESCC by promoting cell proliferation and suppressing cell apoptosis.	31495606	RID07206	interact with protein	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	PANDAR	HNRNPU	positively-E	western blot;shRNA;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000153187	NA	101154753	3192	PANDA	DEE54|EIEE54|GRIP120|HNRNPU-AS1|HNRPU|SAF-A|SAFA|U21.1|hnRNP U|pp120	LncRNA PANDA is up-regulated in of ESCC tissues. Silence of PANDA promoted cell apoptosis and inhibited cell proliferation in vitro. PANDA knockdown attenuated xenograft growth and inhibited cell proliferation in vivo. PANDA regulated E2F1 to depress apoptosis in ESCC through dissociating from NF-YA. PANDA interacted with SAFA to promote ESCC cell proliferation.  PANDA binding SAFA to switch on the tumor proliferation programme though CyclinD1/2-Cyclin E1 and Bcl-2 pathways.PANDA regulated E2F1 to depress apoptosis in ESCC through dissociating from NF-YA. Further analysis revealed that PANDA expression was positively correlated with E2F1 mRNA expression in ESCC. Same as E2F1, the expression of SAFA was up-regulated in 25 paired primary cancerous and adjacent noncancerous in which PANDA expression had been measured.	31495606	RID07207	interact with protein	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	PXN-AS1	PIP4K2B	positively-E	luciferase reporter assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell sphere formation(+)	ceRNA(miR-3064)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255857	GRCh38_12:120201274-120213231	ENSG00000141720	NA	100506649	8396	EyeLinc4	PIP5K2B|PIP5KIIB|PIP5KIIbeta	We showed that miR-3064 was significantly overexpressed in PC tissues compared to normal tissues. High miR-3064 was associated with worse prognosis in patients with PC. Functionally, ectopic expression of miR-3064 promoted the proliferation, invasion, clone formation and sphere formation of PC cells in vitro and stimulated PC growth in vivo, while specific knockdown of miR-3064 or CRISPR/Cas9-mediated knockout of miR-3064 resulted in opposite phenotypes. Further investigation revealed that miR-3064 directly targeted PIP4K2B, which was reduced in PC tissues and attenuated PC cell proliferation, invasion and sphere formation induced by miR-3064. Importantly, lncRNA PXN-AS1 expression was downregulated in PC samples, and it directly interacted with miR-3064 and suppressed its levels in PC cells. Enforced expression of PXN-AS1 remarkably decreased cell proliferation, invasion and sphere formation, while re-expression of miR-3064 abrogated these effects of PXN-AS1.	31488171	RID07208	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TP53	LINC01419	negatively-E	western blot;luciferase reporter assay;ChIP;RNA pull-down;RIP	upregulation	qRT-PCR	TCGA	NA	HR repair(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000253898	GRCh38_8:83403758-83408900	7157	103352670	LFS1|p53	PRLH1|TCONS_00014497	Importantly, we further showed an eightfold upregulation of PRLH1 expression in p53-mutated HCC samples compared to that in wild-type ones (Fig 1D), strongly suggesting a p53-repressed mechanism of PRLH1 expression. Among these candidates, lncRNA PRLH1, which was annotated as LINC01419 in the RefSeq gene sets, showed the largest upregulation in HCC tumors relative to that in normal tissues.The NF-Y transcription factor is required for the expression and p53-mediated repression of PRLH1.All these results confirm that PRLH1 can promote cell proliferation of mutated p53 HCC cells but not wild-type p53 HCC cells, indicating that the function of PRLH1 may be tightly related to the p53 or p53-regulated network.Furthermore, we identified a new p53/PRLH1 pathway to repress HR repair, demonstrating a transcription-dependent regulation of HR repair by p53. Thus, we suppose that p53 prevents the binding of NF-Y to the PRLH1 promoter in an indirect way rather than directly interacting with NF-Y.	31486214	RID07209	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	UP(SKCM);DATA(GSE38495)
Breast cancer	NONHSAT101069	TWIST1	positively-E	western blot;luciferase reporter assay;RIP;western blot;RNA pull-down	upregulation	microarray;qRT-PCR	NA	NA	chemoresistance(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-129-5p)	regulation	NA	Epirubicin	NA	NA	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000122691	NA	NA	7291	NA	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	The knockdown of NONHSAT101069 significantly repressed, whereas overexpression of NONHSAT101069 promoted the epirubicin resistance, migration, invasion and EMT process of BC cells both in vitro and in vivo.  Further mechanism-related researches uncovered that NONHSAT101069 functioned as a ceRNA (competing endogenous RNA) via sponging miR-129-5p. Twist1 was a direct downstream protein of NONHSAT101069/miR-129-5p axis in BC cells. To conclude, NONHSAT101069 was upregulated in BC tissues and promoted epirubicin resistance, migration and invasion of BC cells via regulation of NONHSAT101069/miR-129-5p/Twist1 axis, highlighting its potential as an oncogene and a therapeutic biomarker for BC. . NONHSAT01069 expression was positively correlated with Twist1 expression in BC specimens, as confirmed from TCGA.	31444414	RID07210	ceRNA or sponge	chemoresistance		UP(SKCM);DATA(GSE38495)
Osteosarcoma	LINC00460	FADS1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);	ceRNA(miR-1224-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000149485	NA	728192	3992	NA	D5D|FADS6|FADSD5|LLCDL1|TU12	In this study, we found high linc00460 expression predicted poor prognosis of pan-cancer patients. Linc00460 was up-regulated in OS tissues and cells. High linc00460 expression was positively correlated with distant metastasis and poor overall survival of OS patients. Knockdown of linc00460 suppressed OS cells proliferation and metastasis in vitro. In addition, an inverse correlation between linc00460/miR-1224-5p and miR-1224-5p/FADS1 was observed in OS. Mechanistically, linc00460 functioned as a competitively endogenous RNA (ceRNA) to up-regulate FADS1 expression via sponging miR-1224-5p in OS, thereby promoting OS progression.	31419446	RID07211	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	UFC1	CXCL10	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);apoptosis process(-)	ceRNA(miR-34a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000143222	GRCh38_1:161152776-161158856	ENSG00000169245	NA	51506	3627	HSPC155	C7|crg-2|gIP-10|IFI10|INP10|IP-10|mob-1|SCYB10	In present study, we found that UFC1 was highly expressed in breast tissue and cells lines compared with normal tissues and cell lines. Silenced UFC1 suppressed multiple biological activities of breast cancer cells, which also functioned as a miR-34a sponge in breast cancer. Furthermore, over-expressing miR-34a could prominently suppress cell growth, invasion, migration and inducing apoptosis in breast cancer cells. In addition, we verified that miR-34a was a target of CXCL10 by bioinformatics analysis and luciferase reporter assay .To sum up, silenced UFC1 might be capable of repress the proliferation, invasion, migration, EMT process and induce apoptosis of breast cancer in vitro.	31544897	RID07212	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE55807,GSE67939)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE86978)
Hemangioma	CYTOR	TPD52	positively-E	luciferase reporter assay;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	NA	Cancer	Hemangioma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000076554	NA	112597	7163	C2orf59|LINC00152|MGC4677|NCRNA00152	D52|hD52|N8L	Linc00152 was overexpressed in the proliferating-phase hemangioma tissues when compared with that in involuting-phase. Downregulation of linc00152 strikingly suppressed the cell viability, migration and invasion of hemangioma cells. Furthermore, silence of linc00152 repressed the growth and lung metastasis of hemangioma cell in vivo. Subsequent analysis revealed that linc00152 bound with miR-139-5p and linc00152 expression was inversely correlated with the level of miR-139-5p in IH. Same effects of miR-139-5p transfection on HemECs cells were observed as downregulation of linc00152. Moreover, tumor protein D52 (TPD52) was confirmed to be the target of miR-139-5p. Besides, the anti-tumor effect of linc00152 silence on hemangioma cell was reversed by rexpression of TPD52. This study demonstrates that downregulatuon of linc00152 restrains the aggressiveness of hemangioma cell in vitro and in vivo via interacting with miR-139-5p and further modulates the level of TPD52.	31542613	RID07213	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC);UP(BRCA);DATA(GSE117623,GSE55807)
Non-small cell lung cancer	LINC00342	miR-203a-3p	negatively-F	luciferase reporter assay;DIANA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000232931	GRCh38_2:95807052-95835003	NA	NA	150759	NA	NCRNA00342	NA	The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion. LINC00342 regulated the expression of miR-203a-3p by targeting it directly. MiR-203a-3p was down-regulated in NSCLC tissues and cells compared with normal tissues and cells. Furthermore, LINC00342 promoted NSCLC cells proliferation, colony formation, migration, and invasion by depleting the expression of miR-203a-3p.	31539128	RID07214	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)	
Pancreatic cancer	SNHG14	ANXA2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-613)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000182718	NA	104472715	302	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	ANX2|ANX2L4|CAL1H|LIP2|LPC2D	SNHG14 overexpression enhanced cell proliferative, growth and invasive abilities, and suppressed apoptotic rates and caspase-3 activity in pancreatic cancer cells, while SNHG14 knockdown exerted opposite effects.Collectively, our results suggest that SNHG14 potentiates pancreatic cancer progression through modulation of annexin A2 expression via acting as a competing endogenous RNA for miR-613.	31513352	RID07215	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	LINC00467	PPARA	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000186951	NA	84791	5465	C1orf97|MGC14801	hPPAR|NR1C1|PPAR	The ectopic expression of LINC00467 significantly suppressed cell viability,proliferation, migration and invasion. LINC00467 functioned as a sponge formiR-9-5a and negatively regulated miR-9-5p expression. We also identified PPARA as the direct target of miR-9-5p.	31480990	RID07216	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	LINC00460	RAP1A	positively-E	luciferase reporter assay;western blot;RNA pull-down assay;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-30a-3p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000116473	NA	728192	5906	NA	KREV-1|SMGP21	In NPC cell lines named C666-1 and 5-8F, LINC00460 overexpression promoted cancer cell migration, invasion and epithelial-mesenchymal transition (EMT), while depletion of LINC00460 exhibited opposite effects. We further demonstrated that LINC00460 regulated Rap1A expression through competitively binding to miR-30a-3p. LINC00460 knockdown suppressed NPC metastasis in a xenograft mouse model. Taken together, our findings suggested LINC00460 functioned as an oncogene in NPC which promoted invasion and metastasis, shedding lights on LINC00460 as a potential therapeutic target for NPC therapeutics from bench to clinic.	31414345	RID07217	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367)
Osteosarcoma	KCNQ1OT1	CCND2	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-4458)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000118971	NA	10984	894	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	Our work demonstrated the upregulation of KCNQ1OT1 in osteosarcoma through qRT-PCR Besides, loss of function assay (CCK-8, transwell migration) indicated KCNQ1OT1 promoted cell proliferation, migration in osteosarcoma. Mechanically, KCNQ1OT1 acting as sponge for miR-4458 antagonized its tumor-suppressive impact on CCND2 expression. The anti-apoptotic nature of KCNQ1OT1 was also unveiled via caspase-3 activity assay. Overexpressed KCNQ1OT1 acted as competing endogenous RNA (ceRNA) for miR-4458 and subsequently reinforced target gene CCND2.	31392505	RID07218	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Ovarian cancer	NORAD	STAT3	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell viability(+);cell invasion(+);cell migration(+);apoptosis process(-)	ceRNA(miR-608)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000168610	NA	647979	6774	LINC00657	APRF	NORAD was upregulated in ovarian cancer tissues and cells. Silencing of NORAD lessened cell viability, migration and invasion, but induced apoptosis of SKOV3 cells, whereas overex_x0002_pression of NORAD had opposite effects. Moreover, PG decreased the expression of NORAD.Overexpression of NORAD reversed the effects of PG treatment on the cell biological performances of SKOV3 cells, which were further reversed after overexpression of miR-608 simultaneously. Furthermore,STAT3 was tested as a target gene of miR-608, and the impact of NORAD in PG-treated SKOV3 cells were through the miR-608-mediated STAT3.	31299866	RID07219	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	DDX11-AS1	CLDN7	positively-E	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-873)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000181885	NA	100506660	1366	CONCR|SCAT4	CEPTRL2|CPETRL2|Hs.84359	We identified DDX11-AS1 as a new CRC-related lncRNA whose levels were distinctly up-regulated in CRC specimens and cell lines, partly induced by YY1. Clinical explorations suggested that increased expressions of DDX11- AS1 in CRC were positively associated with lymph nodes metastasis and TNM stage and had a distinct influence on the overall survival. Further multivariate assays indicated that DDX11-AS1 was an independent prognostic parameter implying a poorer clinical outcome for patients with CRC. Functional assays revealed that the knockdown of DDX11-AS1 suppressed the proliferation, migration, and invasion of CRC cells, and stimulate apoptosis. Mechanistic studies showed that the up-regulation of DDX11-AS1 competitively bound to miR-873 prevented CLDN7 from miRNAs-mediated degradations, thus facilitated the CRC progress. Further rescue assays were carried out to achieve confirmation.	31298324	RID07220	ceRNA or sponge	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	LINC81507	CAV1	positively-E	dual-luciferase assay;RIP;western blot	downregulation	RT-qPCR	NA	NA	cell growth(-);cell proliferation(-);cell migration(-);epithelial to mesenchymal transition(-);STAT3 signaling pathway(-)	ceRNA(miR-199b-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000105974	NA	NA	857	NA	CAV	Reduced expression of LINC81507 resulted in cell growth, proliferation, migration and epithelial-mesenchymal transition (EMT) in NSCLC cells, whereas ectopic overexpression of LINC81507 resulted in the opposite effects both in vitro and in vivo. Nuclear and Cytoplasmic fractionation assays showed LINC81507 mainly resided in cytoplasm. Bioinformatics analysis and dual-luciferase assays revealed that miR-199b-5p was a direct target of LINC81507 through binding Ago2. Mechanistic analysis demonstrated that miR-199b-5p specifically targeted the Caveolin1 (CAV1) gene, and LINC81507 inactivated the STAT3 pathway in a CAV1-dependent manner	31296840	RID07221	ceRNA or sponge	NA		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Colorectal cancer	NR4A1AS	NR4A1	positively-E	RIP;ChIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	TCGA;ONCOMINE	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000259884	GRCh38_12:52058459-52059503	ENSG00000123358	NA	115409980	3164	NR4A1-AS1	GFRP1|HMR|N10|NAK-1|NGFIB|NUR77|TR3	Previous studies have indicated that NR4A1 is an oncogene in CRC. Moreover, our results were consistent with other reports. Knocking down NR4A1 suppressed cell proliferation, migration, invasion, and increased the propor_x0002_tion of apoptotic cells by approximately 2.37-fold (15.70 +- 0.80 vs. 6.61 +- 0.49, P<0.01; Figure 6A). Meanwhile,NR4A1 depletion induced G0/G1 phase arrest, with an approximate 25.8% increase in G0/G1-phase cells and a 53.3% decrease in S-phase cells after si-NR4A1 treatment (Figure 6I). Similarly, NR4A1AS depletion also decreased the number of proliferating, migrating, and invading cells, and promoted cell cycle arrest and apoptosis (Figure 6).	31253658	RID07222	transcriptional regulation	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)
Non-small cell lung cancer	DGCR5	EPHB6	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-)	ceRNA(miR-211-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18985836-18994501	ENSG00000260195	NA	26220	2051	DGCR10|DGCR9|DGS-A|DGS-B|LINC00037|NCRNA00037|POM121L5P|X91348	HEP	RT-qPCR revealed that DGCR5 expression in NSCLC cells was significantly lower than in nor_x0002_mal cell. DGCR5 overexpression suppresses NSCLC cell growth, migration, and inva_x0002_sion. Online algorithms found EPH receptor B6 (EPHB6) and DGCR5 contains same miR-211-5p binding region. The predicted connections were further validated by lucif_x0002_erase activity reporter assay. Recue experiments showed DGCR5 regulates NSCLC cell behaviors via targeting miR-211-5p/EPHB6. These findings collectively identified DGCR5/miR-211-5p/EPHB6 triple axis in NSCLC, which may novel understanding regarding the tumorigenesis of NSCLC.	31241800	RID07223	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Breast cancer	LINC02862	DOCK4	positively-E	dual-luciferase reporter gene assay	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);epithelial to mesenchymal transition(-)	ceRNA(miR-18b-5p)	regulation	NA	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237571	GRCh38_2:215274992-215277947	ENSG00000128512	NA	115409987	9732	AC073284.4	FLJ34238|KIAA0716	Furthermore, the underlying functional experiments demonstrated that AC073284.4 might sponge miR-18b-5p to attenuate the invasion, metastasis, and EMT of BC cell through upregulating DOCK4 expression. In summary, AC073284.4 might serve as a competing endogenous RNA (ceRNA) in BC progression via modulating miR-18b-5p/DOCK4 axis, which weakens EMT and migration of BC. These results suggesting that AC073284.4 might function as a potential novel diagnostic biomarker in theprogression of BC.	31215650	RID07224	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)
Colon cancer	FENDRR	SOX4	negatively-E	western blot;immunohistochemistry;RAID v2.0	downregulation	qRT-PCR	NA	NA	cell viability(-);cell invasion(-);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000124766	NA	400550	6659	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	NA	We determined that attenuation of FENDRR was a frequent event in colon cancer tissues and colon cancer cell lines, in contrast to their normal counterparts. Low levels of FENDRR were associated with the clinical stages and poor prognosis. Moreover, ectopic expression of FENDRR repressed colon cancer cell viability, invasion and epithelial'-mesenchymal transition. Furthermore, through a series of in vitro and in vivo assays, we reported the discovery of FENDRR modulating the expression of SOX4 protein, and hence in the progression of colon cancer.;Thus, our data suggested a crucial role of FENDRR in regulating SOX4 protein level without much affecting its transcription.	31213846	RID07225	interact with protein	prognosis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Cervical cancer	STXBP5-AS1	PTEN	positively-E	luciferase reporter assay;RIP;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-96-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233452	GRCh38_6:146824539-147204614	ENSG00000171862	NA	729178	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	In our study, we showed that the expression of STXBP5-AS1 and PTEN was reduced while miR-96-5p expression was upregulated in CC. STXBP5-AS1 overexpression significantly reduced CC cells proliferation and invasion ability by suppressing miR-96-5p expression. MiR-96-5p promoted CC cells progression via regulating PTEN expression. Furthermore, STXBP5-AS1 was identified as a ceRNA to upregulate PTEN via sponging miR-96-5p in CC. Taken together, our findings revealed that STXBP5-AS1 might function as a ceRNA to drive CC cells proliferation and invasion via regulating miR-96-5p/PTEN axis.	31212131	RID07226	ceRNA or sponge	NA	UP(LIHC,PRAD);DOWN(PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Lung adenocarcinoma	MAFG-DT	MAFG	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-744-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000265688	GRCh38_17:81927829-81930753	ENSG00000197063	NA	92659	4097	MAFG-AS1	MGC13090|MGC20149	Silencing of MAFG-AS1 suppressed cell proliferation but induced cell apoptosis. RNA FISH staining showing the cytoplasmic localization of MAFG-AS1 in LUAD cells. Mechanism detection revealed that MAFG-AS1 served as a molecular sponge of miR-744-5p to upregulate its nearby gene MAF bZIP transcription factor G (MAFG) in LUAD cells. Functionally, MAFG overexpression attenuated the cellular processes mediated by MAFG-AS1 knockdown.	31211984	RID07227	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Hepatocellular carcinoma	F11-AS1	PTEN	positively-E	luciferase reporter assay;western blot;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-3146)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251165	GRCh38_4:186286094-186500997	ENSG00000171862	NA	285441	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	F11-AS1 is underexpressed in LIHC and suppresses LIHC progression in return.F11-AS1 can bind with and negatively regulate miR-3146, while miR-3146 can bind with and negatively regulate PTEN.Moreover, F11-AS1 positively regulates the messenger RNA and protein level of PTEN.F11-AS1 mediates PTEN expression by acting as competing endogenous RNA of miR-3146. In the meantime, overexpression of F11 AS1 induced reduction of LIHC cell migration ability and miR 3146 overexpression partly rescued the decline, which was later counteracted by overexpression of PTEN (Figure 4 D). To sum up, F11 AS1 regulates LIHC progression via the miR 3146/PTEN axis.	31168823	RID07228	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Colorectal cancer	PVT1	IRS1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000169047	NA	5820	3667	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HIRS-1	The interaction between lncRNA PVT1 and microRNA-214-3p (miR- 214-3p) and IRS1 was predicted using the RNA22 website. Next the dual luciferase reporter gene assay, RNA pull-down, and RNA immunoprecipitation assays verified lncRNA PVT1 to be a competitive endogenous RNA (ceRNA) against miR-214-3p, and IRS1 was found to be a target of miR-214-3p. The expression pattern of lncRNA PVT1, miR-214-3p, IRS1, phosphoinositide 3-kinase (PI3K), and Akt was characterized in response to lncRNA PVT1 silencing or miR- 214-3p upregulation. Meanwhile, their regulatory effects on cell proliferation, invasion, and apoptosis were detected in CRC cells. With increased levels of miR-214-3p and decreased levels of lncRNA PVT1 in CRC cells, the expression of phosphatidylinositol 3-kinase, putative (PI3K) and Akt was reduced, and consequently, the cell apoptosis was stimulated and cell proliferation and invasion were suppressed. All in all, lncRNA PVT1 competitively binds to miR- 214-3p to upregulate the expression of IRS1 thus activating the PI3K/Akt signaling pathway, thus accelerating CRC progression. This study suggests that lncRNA PVT1 might be a potential target of therapeutic strategies for CRC treatment.	31125260	RID07229	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842)
Gastric cancer	H19	SNAI1	positively-E	luciferase reporter assay;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-22-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000124216	NA	283120	6615	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	H19 was found to be upregulated in GC tissues and cells compared with the para cancerous tissues, and an elevated expression of H19 was associated with lymph node metastasis and TNM stage.-Furthermore, the downregulation of H19 suppressed the proliferation, invasion, migration and epithelial mesenchymal transition of GC cells in vitro and suppressed tumor growth in vivo.-H19 was also found to be able to bind with miR 22 3p, and H19 induced cell growth and metastasis were shown to be reversed by the upregulation of miR 22 3p;--the miR 22 3p level was found to inversely correlate with H19 expression in GC tissues.	31081061	RID07230	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	CASC19	CEMIP	positively-E	luciferase reporter assay;western blot;RIP;immunohistochemistry	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell proliferation(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000254166	GRCh38_8:127072694-127227541	ENSG00000103888	NA	103021165	57214	CARLo-6|LINC01245	HYBID|IR2155535|KIAA1199|TMEM2L	CASC19 expression was markedly upregulated in CRC tissues and CRC cell lines (P < 0.05). qRT-PCRrevealed that CASC19 expression was higher in 25 tissue samples from patients with aggressive CRC compared with the 27 tissue samples from patients with nonaggressive CRC (P < 0.05). Higher CASC19 expression was associated with poorer patient prognoses. Furthermore, in vitro experiments demonstrated that CASC19 overexpression enhanced CRC cell invasion, migration, and proliferation. CASC19 overexpression enhanced the expression of cell migration inducing hyaluronidase 1 (CEMIP) and epithelial-mesenchymal transition markers.	31011255	RID07231	ceRNA or sponge	prognosis	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	
Colorectal cancer	KCNQ1OT1	PPP1R1B	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR;microarray	GSE16066	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-760)	regulation	NA	Methotrexate	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000131771	NA	10984	84152	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	DARPP-32|FLJ20940	The expression level of RNA and proteins was, respectively, detected using qRT-PCRand western blot assays, whereas the dual luciferase reporter gene assay was implemented to verify the targeted relationship. The influence of the lncRNA/miRNA/mRNA axis on biological functions of MTX resistant cells and on the growth of tumours determined through both vitro and vivo experiments. LncRNA KCNQ1OT1 and PPP1R1B mRNA were overexpressed in MTX resistant CRC tumour cells. KCNQ1OT1 functioned as a sponge of miR 760, which targeted PPP1R1B. Knockdown of KCNQ1OT1 enhanced chemosensitivity towards MTX through the sponging of miR 760. MiR 760 expressed at low levels targeted PPP1R1B in the activated cAMP signalling pathway under MTX treatment. Knockdown of KCNQ1OT1 dampened the proliferation of MTX resistant (HT29/MTX) cells by regulating the miR 760/PPP1R1B axis, which also induced cell cycle arrest together with apoptosis.	30997746	RID07232	ceRNA or sponge	chemoresistance	UP(BRCA);DATA(GSE111842)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE55807)
Nasopharynx carcinoma	PTPRG-AS1	PRC1	positively-E	luciferase reporter assay	upregulation	RT-qPCR;microarray	GSE12452;GSE13597;GSE64634	NA	cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-194-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000241472	GRCh38_3:62221249-62369406	ENSG00000198901	NA	100506994	9055	NA	ASE1	Protein regulator of cytokinesis 1 (PRC1) has been reported in correlation with various malignancies. Functionality of PRC1 in nasopharyngeal carcinoma (NPC) was investigated, in perspective of long noncoding RNA (lncRNA) regulatory circuitry. Aberrant expressed messenger RNA and lncRNA were screened out from the Gene Expression Omnibus microarray database. NPC cell line CNE 2 was adopted for in vitro study and transfected with mimic or short hairpin RNA of miR 194 3p and PTPRG AS1. The radioactive sensitivity, cell viability, migration, invasion, and apoptosis were detected. PTPRG AS1 and PRC1 were upregulated in NPC, whereas miR 194 3p was downregulated. PTPRG AS1 was found to specifically bind to miR 194 3p as a competing endogenous RNA and miR 194 3p targets and negatively regulates PRC1. Overexpressed miR 194 3p or silenced PTPRG AS1 resulted in enhanced sensitivity to radiotherapy and cell apoptosis along with suppressed cell migration, invasion and proliferation in NPC.	30993702	RID07233	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD,SKCM);DOWN(PAAD,BRCA);DATA(GSE40174,GSE60407,GSE38495,GSE111842)
Cholangiocarcinoma	LINC01061	SEMA4D	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-612)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cholangiocarcinoma	lncRNA	PCG	NA	NA	ENSG00000187764	NA	401149	10507	NA	C9orf164|CD100|coll-4|FLJ39737|SEMAJ	Cholangiocarcinoma (CCA) is the most usual malignancy of biliary tract, possessing a relatively low overall survival rate due to limited treatment options. Recently, long non-coding RNAs (lncRNAs) have been testified to have marked regulatory impacts on human cancers. The purpose of this paper is to explore the potent regulation mechanism of LINC01061 involved in CCA. Firstly, it was observed that LINC01061 expression was heightened in CCA cell lines, whose knockdown suppressed cell proliferation, induced cell apoptosis and restrained cell migration.	30967271	RID07234	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	SP1	SEMA3B-AS1	positively-E	ChIP;western blot;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell viability(-);cell invasion(-)	DNA methylation	binding/interaction	NA	NA	NA	NA	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000261891	NA	6667	101928931	NA	NA	Frequent downregulation of SEMA3B and SEMA3B-AS1 was detected in esophageal cancer cells and ESCC tissues, and the expression level of SEMA3B and SEMA3B-AS1 in ESCC tissues was correlated with TNM stage and lymph node metastasis. SEMA3B and SEMA3B-AS1 shared the same CpG island in the promoter region and the expression of both genes might be regulated by the promoter methylation status. Furthermore, transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and the promoter hypermethylation of SEMA3B and SEMA3BAS1 influenced Sp1 binding ability. Moreover, over-expression of SEMA3B and SEMA3B-AS1 suppressed the viability and invasion of esophageal cancer cells in vitro. SEMA3B-AS1 influenced the protein expression of SEMA3B.	30915595	RID07235	epigenetic regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	SEMA3B-AS1	SEMA3B	positively-E	ChIP;western blot;luciferase reporter assay	downregulation	RT-PCR	TCGA;GSE89102	NA	cell viability(-);cell invasion(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000261891	NA	ENSG00000012171	NA	101928931	7869	NA	LUCA-1|SemA|sema5|SEMAA|semaV	Frequent downregulation of SEMA3B and SEMA3B-AS1 was detected in esophageal cancer cells and ESCC tissues, and the expression level of SEMA3B and SEMA3B-AS1 in ESCC tissues was correlated with TNM stage and lymph node metastasis. SEMA3B and SEMA3B-AS1 shared the same CpG island in the promoter region and the expression of both genes might be regulated by the promoter methylation status. Furthermore, transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and the promoter hypermethylation of SEMA3B and SEMA3BAS1 influenced Sp1 binding ability. Moreover, over-expression of SEMA3B and SEMA3B-AS1 suppressed the viability and invasion of esophageal cancer cells in vitro. SEMA3B-AS1 influenced the protein expression of SEMA3B.	30915595	RID07236	expression association	metastasis		
Nasopharynx carcinoma	NEAT1	miR-34a-5p	negatively-F	luciferase reporter assay;western blot;RIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Our data revealed that NEAT1 is upregulated, while miR-34a-5p is downregulated in NPC tissues and cell lines. NEAT1 knockdown repressed tumor growth in vitro and in vivo. Additionally, we discovered that NEAT1 directly binds to miR-34a-5p and suppresses miR-34a-5p expression. Moreover, NEAT1 knockdown exerted suppression effects on cell proliferation, migration, invasion, and EMT by miR-34a-5p. NEAT1 knockdown blocked Wnt/beta-catenin signaling via miR-34a-5p.;All these data hinted that NEAT1 might act as a ceRNA of miR-34a-5p.	30900419	RID07237	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Glioblastoma	AC016405.3	TET2	positively-E	luciferase reporter assay;western blot assay;CCK-8	downregulation	qRT-PCR;microarray	GSE104267;GSE103228	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-19a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000168769	NA	NA	54790	NA	IMD75|KIAA1546|MDS	It showed that AC016405.3 was downregulated in GBM tissue specimens and cell lines, and it also illustrated that the downregulated AC016405.3 was closely correlated with several aggressive features of patients with GBM. Functionally, we found that overexpression of AC016405.3 suppressed GBM cells proliferation and metastasis using a gain of function experiment. We further showed that microRNA (miR)-19a-5p, a carcinogenic miRNA, was a downstream miRNA of AC016405.3. AC016405.3 was revealed as a target of miR-19a-5p, and overexpression of miR- 19a-5p reversed the inhibitive effect of AC016405.3 on GBM cell proliferation and metastasis. Furthermore, a novel downstream gene of miR-19a-5p, TET2, was identified through a constructed microarray analysis. We showed that TET2 was downregulated in GBM and was involved in miR-19a-5p-mediated proliferation and metastasis by directly being targeted. Finally, through a western blot assay and a series of functional CCK-8 and metastatic assays, we showed that AC016405.3 suppressed proliferation and metastasis through modulation of TET2 by sponging of miR-19a-5p in GBM cells.	30888082	RID07238	ceRNA or sponge	metastasis		UP(LIHC);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	LMCD1-AS1	COL6A3	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-345-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000227110	GRCh38_3:7951263-8611924	ENSG00000163359	NA	100288428	1293	NA	NA	In our study, we confirmed that LMCD1-AS1 expression was significantly higher in CCA tissues and cell lines than in normal tissues and HIBEC, respectively. E2F1 could bind directly to the promoter region of LMCD1-AS1 and activate its transcription. Function study showed depletion of LMCD1-AS1 suppressed cell proliferation, clone formation and invasion, and induced apoptosis of CCA cells. Whereas, ectopic expressed LMCD1-AS1 facilitated CCA cell progression. In addition, LMCD1-AS1 could sponge miR-345e5p in CCA cells. Moreover, collagenVI-alpha3 chain (COL6A3) was found as a downstream target of miR-345e5p by bioinformatic prediction and dual-luciferase reporter assay.	30876691	RID07239	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE38495,GSE55807)
Cholangiocarcinoma	E2F1	LMCD1-AS1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cholangiocarcinoma	TF	lncRNA	ENSG00000101412	NA	ENSG00000227110	GRCh38_3:7951263-8611924	1869	100288428	RBBP3|RBP3	NA	In our study, we confirmed that LMCD1-AS1 expression was significantly higher in CCA tissues and cell lines than in normal tissues and HIBEC, respectively. E2F1 could bind directly to the promoter region of LMCD1-AS1 and activate its transcription. Function study showed depletion of LMCD1-AS1 suppressed cell proliferation, clone formation and invasion, and induced apoptosis of CCA cells. Whereas, ectopic expressed LMCD1-AS1 facilitated CCA cell progression. In addition, LMCD1-AS1 could sponge miR-345e5p in CCA cells. Moreover, collagenVI-alpha3 chain (COL6A3) was found as a downstream target of miR-345e5p by bioinformatic prediction and dual-luciferase reporter assay.	30876691	RID07240	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	LINC00702	PTEN	positively-E	luciferase reporter assay;western blot;RNA pull-down assay	downregulation	sequencing;qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(-);cell migration(-)	ceRNA(miR-510)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233117	GRCh38_10:4201141-4243912	ENSG00000171862	NA	100652988	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis in vitro and in vivo. Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.	30840927	RID07241	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Pancreatic cancer	DLEU2	SMAD2	positively-E	luciferase reporter assay;RIP;western blot;StarBase V2.0	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-455)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000175387	NA	8847	4087	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	JV18-1|MADH2|MADR2	We found that the DLEU2 level was substantially upregulated in PC tissues and PC cell lines, and significantly associated with poor clinical outcomes in PC patients. Overexpression of DLEU2 significantly induced PC cell proliferation and invasion, whereas knockdown of DLEU2 impaired cell proliferation and invasion in vitro. Furthermore, bioinformatics analysis, luciferase reporter assay, and RNA immunoprecipitation assay revealed that DLEU2 directly bond to microRNA-455 (miR-455) and functioned as an endogenous sponge for miR-455, which could remarkably suppress cell growth and invasion. We also determined that SMAD2 was a direct target of miR-455, and the restoration of SMAD2 rescued cell growth and invasion that were reduced by DLEU2 knockdown or miR-455 overexpression.	30838724	RID07242	ceRNA or sponge	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	IQANK1	ELAVL1	positively-E	RNA pull-down assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);radiosensitivity(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000066044	NA	642574	1994	FAM83H-AS1|onco-lncRNA-3	Hua|HUR|MelG	This study aimed to investigate the role of FAM83H-AS1 in ovarian cancer metastasis and radioresistance. We identified the upregulation of FAM83H-AS1 in OC and disclosed its association with cell radioresistance. Functionally, FAM83H-AS1 promoted cell migration, invasion, EMT, and retarded cell sensitivity to irradiation in OC. Mechanistically, FAM83H-AS1 interacted with HuR and stabilized its protein. Together, present study revealed that FAM83H-AS1 contributed to the radioresistance and cell metastasis in ovarian cancer through stabilizing HuR protein.	30831080	RID07243	interact with protein	metastasis	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807)
Osteosarcoma	ILF3-DT	SOX5	positively-E	luciferase reporter assay;western blot;RT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-212)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000134532	NA	147727	6660	ILF3-AS1	L-SOX5|MGC35153	In this study, we showed that ILF3-AS1 expression was significantly up-regulated in both osteosarcoma tissues and cell lines. We first reported that ILF3-AS1 upregulation was induced by nuclear transcription factor SP1. Clinical assays revealed that higher expression of ILF3-AS1 was associated with advanced clinical stage, distant metastasis and shorter overall survival. in multivariate analysis, ILF3-AS1 expression level was found to be an independent prognostic factor for osteosarcoma patients. Functional investigations showed that knockdown of ILF3-AS1 suppressed the proliferation, migration and invasion of osteosarcoma cells, and promoted apoptosis. Bioinformatic software predicted that miR-212 both targeted the 30- UTR of ILF3-AS1 and SOX5, which was confirmed using luciferase reporter assay, RT-PCRand western blot.	30819403	RID07244	ceRNA or sponge	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Osteosarcoma	SP1	ILF3-DT	positively-E	luciferase reporter assay;western blot;RT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000267100	GRCh38_19:10651862-10653844	6667	147727	NA	ILF3-AS1	In this study, we showed that ILF3-AS1 expression was significantly up-regulated in both osteosarcoma tissues and cell lines. We first reported that ILF3-AS1 upregulation was induced by nuclear transcription factor SP1. Clinical assays revealed that higher expression of ILF3-AS1 was associated with advanced clinical stage, distant metastasis and shorter overall survival. in multivariate analysis, ILF3-AS1 expression level was found to be an independent prognostic factor for osteosarcoma patients. Functional investigations showed that knockdown of ILF3-AS1 suppressed the proliferation, migration and invasion of osteosarcoma cells, and promoted apoptosis. Bioinformatic software predicted that miR-212 both targeted the 30- UTR of ILF3-AS1 and SOX5, which was confirmed using luciferase reporter assay, RT-PCRand western blot.	30819403	RID07245	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Prostate cancer	PCAT1	FKBP5	NA	catRAPID;RNA pull-down assay	upregulation	qRT-PCR;sequencing	GSE124519;GSE124291	NA	AKT signaling pathway(+);NF-kB signaling pathway(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000096060	NA	100750225	2289	PCA1|PCAT-1|PiHL	FKBP51|FKBP54|P54|PPIase|Ptg-10	LncRNA PCAT1 activates AKT and NF-kB signaling in castration-resistant prostate cancer by regulating the PHLPP/FKBP51/IKKalpha complex.lncRNA PCAT1 interacts with FKBP51 that mediates AKT and NF-kB signaling.Interestingly, among the 245 upregulated lncRNAs (Fold change > 2.0-fold, P < 0.01) in our lncRNA array data (Supplementary Table S5), only two lncRNAs, one of which was PCAT1, were predicted by the catRAPID omics module to interact with FKBP51.PCAT1 binds directly to FKBP51, displacing PHLPP from the PHLPP/FKBP51/IKKalpha complex, leading to activation of AKT and NF-kB signaling.	30773595	RID07246	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Hepatocellular carcinoma	NEAT1	HAVCR2	negatively-E	RNA pull-down assay;RIP;DIANA	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-155)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000135077	NA	283131	84868	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CD366|FLJ14428|Tim-3|TIM3|TIMD3	Repression of lncRNA NEAT1 enhances the antitumor activity of CD8 T cells against hepatocellular carcinoma via regulating miR-155/Tim-3 +.	30710754	RID07247	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE51827,GSE75367,GSE86978)
Malignant glioma	HCG11	MTA3	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell growth(-)	ceRNA(miR-4425)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000057935	NA	493812	57504	bK14H9.3|FLJ14049|FLJ30357	KIAA1266	HCG11 was downregulated in 84 pairs of glioma tissues and cell lines. Moreover, a low level of HCG11 indicted the lower overall survival rate of glioma patients. Regarding the mechanism, HCG11 was abundant in the cytoplasm of glioma cells and interacted with miR 4425 to release the expression of MTA3. miR 4425 and MTA3 participated in HCG11 mediated glioma growth.  LncRNA HCG11 suppresses the growth of glioma by cooperating with the miR 4425/MTA3 axis.	30706982	RID07248	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Cervical cancer	MALAT1	POSTN	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);AKT/mTOR signaling pathway(+)	ceRNA(miR-202-3p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000133110	NA	378938	10631	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	OSF-2|periostin|PN	Here we found that the expression of periostin was overexpressed in CC tissues and CC cell lines (HeLa and SiHa). Knockdown of periostin in HeLa or SiHa cells significantly decreased cell viability, cell migration and invasion, and reduced epithelial-sesenchymal transition (EMT). Moreover, periostin knockdown suppressed the activation of Akt/the mammalian target of rapamycin (mTOR) signaling pathway, which is crucial for periostin to regulate the above biological activities in CC cells. Furthermore, we found that the periostin expression was positively correlated with the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and negatively correlated with the expression of microRNA (miR)-202-3p in CC tissues. We confirmed that MALAT1 positively regulated the expression of periostin by negatively modulating miR-202-3p.	30633360	RID07249	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(PAAD);DATA(GSE40174)
Anaplastic thyroid carcinoma	PWAR5	EZH2	negatively-F	RIP;luciferase reporter assay;western blot;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000279192	GRCh38_15:24985053-24988232	ENSG00000106462	NA	8123	2146	PAR-5|PAR5	ENX-1|EZH1|KMT6|KMT6A	Here, we evaluated the long non-coding RNA (lncRNA) expression profile of nine ATC in comparison with five normal thyroid tissues by a lncRNA microarray. By this analysis, we identified 19 upregulated and 28 downregulated lncRNAs with a fold change >1.1 or < 1.1 and p-value < 0.05, in ATC samples. Some of them were subsequently validated by qRT-PCR Then, we investigated the role of the lncRNA Prader Willi/Angelman region RNA5 (PAR5), drastically and specifically downregulated in ATC. The restoration of PAR5 reduces proliferation and migration rates of ATC-derived cell lines indicating that its downregulation contributes to thyroid cancer progression. Our results suggest that PAR5 exerts its anti-oncogenic role by impairing Enhancer of Zeste Homolog 2 (EZH2) oncogenic activity since we demonstrated that PAR5 interacts with it in thyroid cancer cell lines, reducing EZH2 protein levels and its binding on the E-cadherin promoter, relieving E-cadherin from the negative regulation by EZH2. Consistently, EZH2 is overexpressed in ATC, but not in dierentiated thyroid carcinomas. The results reported here define a tumor suppressor role for PAR5 in undierentiated thyroid neoplasias, further highlighting the pivotal role of lncRNAs in thyroid carcinogenesis.	31963578	RID07250	interact with protein	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	ZEB2-AS1	PTEN	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000171862	NA	100303491	5728	ZEB2-AS|ZEB2AS|ZEB2NAT	BZS|MHAM|MMAC1|PTEN1|TEP1	ZEB2-AS1 was upregulated in NSCLC tissues and cell lines. Its level was higher in NSCLC patients with T3 T4 or accompanied with lymphatic metastasis relative to those with T1 T2 or without metastatic loci. Knockdown of ZEB2-AS1 suppressed proliferative, migratory, and invasive properties of NCI-H1650 and HCC827 cells. PTEN level was elevated after knockdown of ZEB2-AS1 or EZH2 in HCC827 cells. Subsequently, RIP assay proved the interaction between ZEB2-AS1 and EZH2. Knockdown of ZEB2-AS1 markedly reduced the binding of EZH2 on the PTEN promoter region. Notably, knockdown of PTEN reversed the effects of EZB2-AS1 on regulating proliferative, migratory, and invasive properties of NSCLC cells. lncRNA ZEB2-AS1 is upregulated in NSCLC, which elevates the viability and malignant degree of NSCLC cells by downregulating PTEN, thus aggravating the progression of NSCLC .	31695021	RID07251	interact with protein	metastasis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	EZH2	UGP2	negatively-E	ChIP	downregulation	RT-qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);WNT/beta-catenin signaling pathway(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000169764	GRCh38_2:63840952-63891562	2146	7360	ENX-1|EZH1|KMT6|KMT6A	SVUGP2|UGP1|UGPP1	lncRNA-SVUGP2 was depressed in NSCLC tissues and cells. Overexpression of lncRNA-SVUGP2 depressed proliferation, induced apoptosis, and suppressed migration and invasion of A549 and H1975 cells. In addition, lncRNA-SVUGP2 was repressed by EZH2 and was inversely correlated with EZH2 levels in H1975 cells. Repression of lncRNA-SVUGP2 potentially participated in the oncogenic function of EZH2. Besides, overexpression of lncRNA-SVUGP2 depressed the briskness of Wnt/b-catenin signal in H1975 cells. Our data reveal that lncRNA-SVUGP2 is under-expressed in NSCLC cells and the reduced expression of lncRNA-SVUGP2 may enhance the development and process of NSCLC by interacting with EZH2 and activating Wnt/b-catenin pathway.	31401873	RID07252	expression association	NA	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807)
Papillary thyroid carcinoma	PRDM16-DT	PIK3CA	negatively-E	western blot	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000177133	GRCh38_1:3059611-3069088	ENSG00000121879	NA	440556	5290	FLJ42875|LINC00982|lnc-dPrdm16	PI3K	Overexpression of long non-coding RNA LINC00982 suppresses cell proliferation and tumor growth of papillary thyroid carcinoma through PI3K-ATK signaling pathway.Long non-coding RNAs (lncRNAs) have been widely reported that involved in human cancers, including papillary thyroid carcinoma (PTC). The present study aims to investigate the biological role of LINC00982 in PTC. The mRNA expression of LINC00982 in human PTC tissues was detected using qPCR. Moreover, Kaplan-Meier method was performed to analyze the internal relevance between LINC00982 expression and overall survival (OS) rate of patients with PTC. In addition, gain- and loss-of-functions assays were performed to detect the effects of LINC00982 on the cell proliferation and migration in PTC cells. Furthermore, western blot assay was used to measure the alteration expression levels of apoptosis relative proteins and the relative protein involved phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. Finally, a xenograft model was used to analyze the antitumor role of LINC00982 in vivo Here, we found that LINC00982 was decreased in human PTC tissues. Patients with decreased LINC00982 expression levels had a reduced OS (P=0.0019) compared with those with high LINC00982 expression levels. Overexpression of LINC00982 suppressed the proliferation and migration of BHT101 and B-CPAP cells and promoted cell apoptosis. Knockdown of LINC00982 promoted the proliferation and migration of BHT101 and B-CPAP cells and induced cell apoptosis. Moreover, in vivo assay showed that overexpression of LINC00982 could suppress the growth of PTC. Finally, LINC00982 could regulate the activity of PI3K/AKT signaling pathway in vitro and in vivo Taken together, our findings demonstrated that overexpression of LINC00982 could suppress cell proliferation and induce cell apoptosis by regulating PI3K/AKT signaling pathway in PTC.	31262968	RID07253	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Hepatocellular carcinoma	SEMA3B-AS1	PTEN	positively-E	western blot	downregulation	RT-qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-718)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261891	NA	ENSG00000171862	NA	101928931	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In addition, SEMA3B-AS1 expression was not affect by cancer development, and low SEMA3B-AS1 levels were closely correlated with poor survival. SEMA3B-AS1 in HCC tissues was inversely correlated with microRNA (miR)-718 and positively correlated with PTEN. In HCC cells, SEMA3B-AS1 overexpression resulted in upregulated, while miR-718 overexpression resulted in downregulated phosphatase and tensin homolog (PTEN) expression. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells, while miR-718 overexpression resulted in an increased rate. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.	31251699	RID07254	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Cervical cancer	GHET1	PTEN	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000171862	NA	102723099	5728	lncRNA-GHET1	BZS|MHAM|MMAC1|PTEN1|TEP1	ISH and RT-PCRanalyses revealed that GHET1 expression was significantly up-regulated in cervical cancer tissue compared with that in adjacent normal tissue .To evaluate the effects of GHET1 knockdown in cervical cancer cells, CCK-8 assay was used to measure the proliferation rates of HeLa and SiHa cells transfected with either si-GHET1 or non-specific siRNA (Fig. 2A and B).The expression levels of lncRNA GHET1 and PTEN protein differed significantly between cancer and adjacent normal tissues (P < 0.05) and were negatively correlated in the clinical data. In vitro, proliferation rateswere significantly downregulated in SiHa and HeLa cells. The GHET1 knockdown (si-GHET1) groups showed significantly higher G1 phase and apoptosis rates and significantly suppressed invasion and migration abilities compared with the normal control (NC) group (P < 0.05 for all).	32176622	RID07255	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Colorectal cancer	LINC02381	PTEN	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell viability(-);cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000250742	GRCh38_12:54126053-54147485	ENSG00000171862	NA	400043	5728	LOC400043	BZS|MHAM|MMAC1|PTEN1|TEP1	Consistently, RT-qPCR results showed that LINC02381 was down regulated in CRC tissues and also in different cancerous cell lines. CRC cells treatment with de-methylating and chemotherapy agents indicated that DNA methylation of LINC02381 may be responsible for the transcriptional silencing of LINC02381 in colorectal cancer cells. Then, the functional changes of the cells in response to LINC02381 alteration were assessed and the data indicated that LINC02381 up-regulation suppressed cell viability and proliferation while increasing the apoptosis in CRC-originated cell lines. Mechanistically, LINC02381 overexpression was increased PTEN protein levels but decreased phospho-Akt levels. Finally, we proposed a hypothesized model for PI3K signaling regulation by LINC02381. Altogether, the result of this study suggests that LINC02381 might have suppressive effects on human colorectal cancer tumorigenesis partly by regulating PI3K signaling pathway.	32092325	RID07256	expression association	chemoresistance	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Retinoblastoma	LEF1-AS1	LEF1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000138795	NA	641518	51176	NA	TCF10|TCF1ALPHA|TCF7L3	In our study, LEF1-AS1 expression was increased in retinoblastoma tissues and cell lines compared with paired adjacent normal tissues and the retinal pigment epithelial cell line, respectively. Meanwhile, we found that patients with retinoblastoma with IIRC D-E or undifferentiated type had notably higher levels of LEF1-AS1 expression than those with IIRC A-C or differentiated type. High LEF1-AS1 expression predicted poor disease-free survival in patients with retinoblastoma. The in vitro assays suggested that silencing of LEF1-AS1 suppressed retinoblastoma cell proliferation, migration, and invasion through regulating the Wnt/beta-catenin pathway. In conclusion, LEF1-AS1 functions as an oncogenic lncRNA in retinoblastoma. LEF1-AS1 has been suggested to interact with LEF1 to regulate tumour cell proliferation and mobility, and LEF1 is a key regulatory factor of the Wnt signalling pathway.	31990064	RID07257	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Retinoblastoma	LEF1-AS1	CTNNB1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000168036	NA	641518	1499	LEF1NAT	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Silencing LEF1-AS1 expression negatively regulates beta-catenin and LEF1 expressionThe beta-catenin and LEF1 have been confirmed to function as key downstream effectors in the Wnt signalling pathway.24-26 To ex_x0002_plore the molecular mechanism of LEF1-AS1 in retinoblastoma, we conducted western blots to determine the effect of LEF1-AS1 on beta-catenin and LEF1 expression. We found that silencing LEF1-AS1 expression dramatically impaired beta-catenin and LEF1 expression in SO-Rb50 and HXO-RB44 cells (Figure 5)	31990064	RID07258	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	HAGLR	PDCD4	negatively-F	luciferase reporter assay;western blot;RIP;ChIP;RNA pull-down assay	upregulation	qRT-PCR	TCGA;GSE50710;GSE53137;GSE109467	NA	chemoresistance(+)	epigenetic regulation	regulation	NA	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000150593	NA	401022	27250	HOXD-AS1|Mdgt|MIR7704HG	H731	Our results revealed that HOXD-AS1 was upregulated in DDP-resistant gastric cancer tissues and cells. Patients with gastric cancer with high HOXD-AS1 expression levels had a poor prognosis. Knockdown of HOXD-AS1 facilitated the sensitivity of DDP-resistant gastric cancer cells to DDP. Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing counteracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells. In summary, HOXD-AS1 led to DDP resistance in gastric cancer by epigenetically suppressing PDCD4 expression,  providing a novel therapeutic strategy for patients with gastric cancer with chemoresistance.	31551012	RID07259	epigenetic regulation	chemoresistance,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE86978)
Hepatocellular carcinoma	MEG3	ERP29	positively-E	luciferase reporter assay;western blot;immunohistochemistry	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-483-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000089248	NA	55384	10961	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	C12orf8|ERp28|ERp31|PDI-DB|PDIA9	Bioinformatics found a competing endogenous RNAs (ceRNAs) regulatory network between microRNA-483-3p (miR-483-3p) and Long noncoding RNA (LncRNA MEG3), the above methods also were used to identify their expression, biological effects and their roles of HG on regulation of REp29 in HCC cells, dual-luciferase reporter assay was carried out to study the interaction of ERp29 with miR- 483-3p and miR-483-3p with MEG3. HG upregulated miR-483-3p expression in HCC cells and miR-483-3p overexpression suppressed ERp29 expression and also increased HCC cell proliferation and migration. Furthermore, we found that MEG3 was decreased in HCC cells incubated in medium with high glucose and knockdown of MEG3 downregulated ERp29 expression. Bioinformatics analysis found that MEG3 mediated its protective effects via binding to miR- 483-3p. Overall, our study established a novel regulatory network of LncRNA MEG3/miR483-3p/ERp29 in HCC which may be helpful in better understanding the effect of high glucose on poor prognosis of HCC and in exploring new diagnostic and therapeutic tools for managing HCC in patients with diabetes.	31251997	RID07260	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung adenocarcinoma	HAGLR	E2F1	negatively-E	overexpression;RNA pull-down assay	downregulation	microarray;qRT-PCR	GSE28582;GSE37745;TCGA	NA	cell growth(-);cell proliferation(-);apoptosis process(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000101412	NA	401022	1869	HOXD-AS1|Mdgt|MIR7704HG	RBBP3|RBP3	HAGLR suppresses LUAD cell growth in vitro To determine the effect of HAGLR on LUAD cell growth, we first conducted cell proliferation and colony formation analysis. As shown in Fig. 4A, overexpression of HAGLR significantly suppressed A549 cell proliferation over a course of 4 days by CCK-8 assay . The increase of HAGLR also significantly decreased A549 cell clonality . Concordantly, knockdown of HAGLR promoted the proliferation and colony formation of SPC-A1 cells. Cell apoptosis rate, as determined by FACS analysis, revealed that overexpression of HAGLR promoted apoptosis rate of A549 cells while knockdown of HAGLR reduced the apoptosis rate of SPC-A1 cells;The result of western blot showed overexpression of HAGLR decreased E2F1 level while knockdown of HAGLR promoted E2F1 level;	31194977	RID07261	epigenetic regulation	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Triple-negative breast cancer	sONE	miR-34a	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c Myc proteins.	30968427	RID07262	expression association	NA		
Triple-negative breast cancer	sONE	MIR15A	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	ENSG00000283785	NA	NA	406948	NA	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c Myc proteins.	30968427	RID07263	expression association	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367)	
Triple-negative breast cancer	sONE	miR-16	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c Myc proteins.	30968427	RID07264	expression association	NA	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE75367)	
Triple-negative breast cancer	sONE	let-7a	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP53/c Myc proteins.	30968427	RID07265	expression association	NA		
Triple-negative breast cancer	sONE	TP53	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP54/c Myc proteins.	30968427	RID07266	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	sONE	MYC	negatively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell viability(-);cell proliferation(-);colony formation(-);cell migration(-);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	Results showed that sONE is restrictedly expressed in TNBC patients;-its expression level is inversely correlated with the aggressiveness of the disease.-sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.-Mechanistically, sONE is a potential tumor suppressor lncRNA in TNBC cells;-repressing cellular viability, proliferation, colony forming ability, migration, and invasion capacities of MDA-MB-231.-Furthermore, sONE effects were found to be extended to affect the maestro tumor suppressor TP53 and the oncogenic transcription factor c Myc.-Knocking down of sONE resulted in a marked decrease in TP53 and increase in c Myc and consequently altering the expression status of their downstream tumor suppressor microRNAs (miRNAs) such as miR-34a, miR-15, miR-16, and let-7a.-In conclusion, this study highlights sONE as a downregulated tumor suppressor lncRNA in TNBC cells acting through repressing eNOSinduced NO production, affecting TP53 and c Myc proteins levels and finally altering the levels of a panel of tumor suppressor miRNAs downstream TP55/c Myc proteins.	30968427	RID07267	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Renal cell carcinoma	HNF1A	NR_023387	positively-E	JASPAR;overexpression;ChIP;luciferase reporter assayethylation assay	downregulation	microarray;RT-PCR	TCGA	NA	cell proliferation(-);cell migration(-);cell invasion(-);cell metastasis(-);tumor growth(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	PCG	lncRNA	ENSG00000135100	NA	NA	NA	6927	NA	HNF-1-alpha|HNF-1A|HNF1|HNF1alpha|HNF4A|IDDM20|LFB1|MODY3|TCF-1|TCF1	NA	Quantitative real time polymerase chain reaction (RT PCR) implied that NR_023387 was significantly downregulated in RCC tissues and cell lines, and lower expression of NR_023387 was correlated with shorter overall survival. Methylation specific PCR, MassARRAY, and demethylation drug treatment indicated that hypermethylation in the NR_023387 promoter contributed to its silencing in RCC. Besides, HNF4A regulated the expression of NR_023387 via transcriptional activation. Functional experiments demonstrated NR_023387 exerted tumor suppressive roles in RCC via suppressing the proliferation, migration, invasion, tumor growth, and metastasis of RCC. Furthermore, we identified MGP as a putative downstream molecule of NR_023387, which promoted the epithelial mesenchymal transition of RCC cells.	31432508	RID07268	transcriptional regulation	metastasis	UP(LIHC);DATA(GSE117623)	
Renal cell carcinoma	NR_023387	MGP	negatively-E	overexpression	downregulation	microarray;RT-PCR	TCGA	NA	cell proliferation(-);cell migration(-);cell invasion(-);cell metastasis(-);tumor growth(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	NA	NA	ENSG00000111341	NA	NA	4256	NA	GIG36|MGLAP|NTI	Quantitative real time polymerase chain reaction (RT PCR) implied that NR_023387 was significantly downregulated in RCC tissues and cell lines, and lower expression of NR_023387 was correlated with shorter overall survival. Methylation specific PCR, MassARRAY, and demethylation drug treatment indicated that hypermethylation in the NR_023387 promoter contributed to its silencing in RCC. Besides, HNF4A regulated the expression of NR_023387 via transcriptional activation. Functional experiments demonstrated NR_023387 exerted tumor suppressive roles in RCC via suppressing the proliferation, migration, invasion, tumor growth, and metastasis of RCC. Furthermore, we identified MGP as a putative downstream molecule of NR_023387, which promoted the epithelial mesenchymal transition of RCC cells.	31432508	RID07269	expression association	metastasis		UP(PAAD,SKCM,BRCA);DATA(GSE60407,GSE38495,GSE41245)
Prostate cancer	ADAMTS9-AS1	PRDM16	positively-E	luciferase reporter assay;miRcode	downregulation	qRT-PCR	TCGA	NA	cell proliferation(-)	ceRNA(miR-96)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000241158	GRCh38_3:64561322-64592757	ENSG00000142611	NA	101929335	63976	NA	KIAA1675|KMT8F|MEL1|MGC166915|PFM13	ADAMTS9-AS1 expression was significantly downregulated (P < 0.001) in the si-ADAMTS9-AS1 transfected cells compared to control cells. siRNA1 exhibited the largest downregulation and was thus selected for subsequent experiments (Figure 5B). Growth curves from CCK8 proliferation assays showed that ADAMTS9-AS1 knockdown significantly promoted DU145 cell proliferation.We found that knockdown of ADAMTS9-AS1 also significantly reduced PRDM16 mRNA levels; however, hsa-mir-96 expression was increased in DU145 cells (Figures 5D, E).These results suggest that ADAMTS9-AS1 functions as a ceRNA for hsa-mir-96, thereby leading to the regulation of its endogenous target PRDM16.	32153626	RID07270	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Triple-negative breast cancer	LUCAT1	MIR5702	negatively-F	RNA pull-down assay;RIP;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);epithelial to mesenchymal transition(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000263363	NA	100505994	100847053	SCAL1|SCAT5	NA	In our study, we identified that LUCAT1 expression was dramatically enhanced in TNBC samples and cells. High LUCAT1 expression was strongly associated with advanced stages and poor prognosis of TNBC. LUCAT1 contributed to TNBC development through accelerating cell proliferation, cell cycle progression and metastasis as well as attenuating cell apoptosis. Moreover, miR-5702 was proved to directly bind to LUCAT1 and be negatively modulated by LUCAT1. Knockdown of miR-5702 reversed the suppressing influences of LUCAT1 depletion on TNBC progression. In conclusion, it was the first investigation to shed light on the significant function and underlying regulatory mechanism of LUCAT1 in TNBC tumorigenesis. We validated that LUCAT1 induced tumorigenesis and metastasis.;In summary, our data reveal that LUCAT1 knockdown is a suppressing regulator of cellmigration, invasion, and EMT in TNBC.	31399501	RID07271	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Lung adenocarcinoma	CASC11	MYC	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	microarray;qRT-PCR	TCGA;GSE103085	NA	cell proliferation(+);colony formation(+)	interact with protein;enhancer	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000136997	NA	100270680	4609	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	bHLHe39|c-Myc|MYCC	Colorimetric assay results also showed a significant reduction in cell proliferation of A549 and ACC-LC-319 cells knocked down for either MYMLR or MYC . We then performed a colony formation assay and found that MYMLR knockdown markedly reduced the number of A549 cell colonies.	31361039	RID07272	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	LINC01436	FBOX11	positively-E	luciferase reporter assay;RIP;western blot;immunohistochemistry	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-585)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231106	GRCh38_21:36005137-36007838	NA	NA	100996609	NA	AP000688.8	NA	We demonstrated that LINC01436 was significantly up regulated in cancerous tissues of GC samples, and its overexpression was correlated with a worse prognosis for the patients. In the GC cell line BGC823 cells, LINC01436 knockdown repressed the proliferation and metastasis of cancer cells; conversely, in GC cell line AGS cells, overexpression of LINC01436 showed the opposite effects. We then demonstrated that miR 585, a tumor suppressor, could bind to both LINC01436 and the 3 UTR of F box protein 11 (FBOX11), and LINC01436 was proved to sponge miR 585 and repress it, and indirectly promoted the expression of FBOX11. Collectively, these results suggested that LINC01436 was an oncogenic lncRNA in GC and promoted proliferation and metastasis of GC cell via regulating miR 585 and FBOX11.	31829474	RID07273	ceRNA or sponge	metastasis,prognosis		
Breast cancer	FGF14-AS2	miR-205-5p	negatively-F	luciferase reporter assay;DIANA-LncBase v2	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	sponge	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000272143	GRCh38_13:102394630-102395703	NA	NA	283481	NA	NA	NA	FGF14-AS2 was down-regulated while miR-205-5p was up-regulated in breast cancer tissues and cells and correlated with tumor stage and size. Functionally, the overexpression of FGF14-AS2 or miR-205-5p knockdown suppressed proliferation, migration, and invasion, and induced apoptosis of breast cancer cells. Moreover, FGF14-AS2 could directly bind to miR-205-5p, and the overexpression of FGF14-AS2 undermined the miR-205-5p induced effects on proliferation, migration, invasion, and apoptosis in breast cancer cells.	31486497	RID07274	ceRNA or sponge	NA		
Hepatocellular carcinoma	LINC00488	TLN1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;Targetscan;RNA22	upregulation	microarray;RT-qPCR	TCGA	NA	cell proliferation(+);angiogenesis(+);apoptosis process(-)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214381	GRCh38_3:109178143-109216965	ENSG00000137076	NA	677779	7094	C3orf66|FLJ41232	ILWEQ|TLN	microarray-based analysis revealed a possible regulatory mechanism involving LINC00488, microRNA-330-5p (miR-330-5p) and talin-1 (TLN1) in HCC. Targetscan and RNA22 online tools predicted the relationship among LINC00488, miR-330-5p and TLN1, which were further validated by dual luciferase reporter gene assay, RNA pull-down and RIP. To evaluate the effects of LINC00488 and miR-330-5p on the cellular process of HCC, we performed a series of in vitro and in vivo experiments, with the expression of LINC00488, miR-330-5p, and TLN1 altered by delivering plasmids into Hep3B cell line. The obtained results demonstrated that cells with siRNA-mediated depletion of LINC00488 or restoration of miR-330-5p displayed suppressed abilities of in vitro proliferation as well as of in vivo tumor growth and angiogenesis, while in vitro apoptosis was notably induced. The fundamental findings of the present study collectively propose that lncRNA LINC00488 can competitively sponge miR-330-5p to regulate TLN1 in relation to the cell growth and angiogenesis in HCC.	31005556	RID07275	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Chondrosarcoma	RAMP2-AS1	KDR	positively-E	luciferase reporter assay;starBase;siRNA;TargetScan;miRTarBase;miRDB;miRWalk	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	ceRNA(miR-2355-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000197291	GRCh38_17:42753914-42761257	ENSG00000128052	NA	100190938	3791	NA	CD309|FLK1|VEGFR|VEGFR2	The exosomes secreted by chondrosarcoma cells could enhance HUVECs proliferation, migration and tube formation. LncRNA microarray analysis revealed that exosomes carried lncRNA RAMP2-AS1, and further verification showed that the level of RAMP2-AS1 was increased in the serum of chondrosarcoma patients and was closely related to local invasiveness, distant metastasis and poor prognosis. Subsequent experiments demonstrated that RAMP2-AS1 knockdown could partly abrogate the promoting effects on angiogenesis induced by exosomes derived from chondrosarcoma cells. Moreover, dual-luciferase reporter assay and rescue experiments suggested that the RAMP2-AS1/miR-2355-5p/VEGFR2 axis was responsible for exosome-induced angiogenesis of HUVECs.	32368088	RID07276	ceRNA or sponge	metastasis,prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colorectal cancer	RAMS11	TOP2A	positively-E	RNA pull-down assay;RIP;qPCR;western blot;ChIP	upregulation	sequencing;qRT-PCR	dbGaP(phs001722);GSE50760;TCGA	NA	chemoresistance(+);cell growth(+);cell migration(+)	transcriptional regulation	regulation	NA	Topoisomerase inhibitors	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000131747	NA	NA	7153	NA	TOP2|TOP2alpha|TOPIIA|TP2A	We prioritize RAMS11 due to its association with poor diseasefree survival and promotion of aggressive phenotypes in vitro and in vivo. A FDA-approved drug high-throughput viability assay shows that elevated RAMS11 expression increases resistance to topoisomerase inhibitors. Subsequent experiments demonstrate RAMS11-dependent recruitment of Chromobox protein 4 (CBX4) transcriptionally activates Topoisomerase II alpha (TOP2alpha). Overall, recent clinical trials using topoisomerase inhibitors coupled with our findings of RAMS11-dependent regulation of TOP2alpha supports the potential use of RAMS11 as a biomarker and therapeutic target for mCRC;RAMS11 promotes tumor growth and metastasis in vivo.	32358485	RID07277	transcriptional regulation	metastasis,chemoresistance		UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Breast cancer	A2M-AS1	CD2	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE45827;GSE65216;GSE102484;GSE65194;GSE65212;GSE65194;GSE102484	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245105	GRCh38_12:9065163-9068689	ENSG00000116824	NA	144571	914	NA	SRBC	Importantly, A2M-AS1 upregulation was significantly associated with ERnegative,HER2-positive, and basal-like breast cancer and with poor recurrence-free survival and metastasis-free survival in breast cancer patients. After validating these results in 96 collected human breast cancer tissues and 64 paired adjacent noncancerous tissues, we further investigated the roles of A2M-AS1 in human ER-negative and basal-like breast cancer cells. /e results revealed that A2M-AS1 significantly promotes human breast cancer cell proliferation, invasion, and migration. Additionally, bioinformatics analysis of genes coexpressed with A2M-AS1 in the context of human breast cancer combined with qRT-PCRand western blot assays revealed that A2M-AS1 exerts regulatory effects on downstream factors in the cell adhesion molecule pathway, including CD2 and SELL. /ese results imply that A2M-AS1 might be a promising candidate prognostic factor and therapeutic target for breast cancer.	32352014	RID07278	expression association	metastasis,recurrence,prognosis	DOWN(BRCA);DATA(GSE67939)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Breast cancer	A2M-AS1	SELL	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE45827;GSE65216;GSE102484	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245105	GRCh38_12:9065163-9068689	ENSG00000188404	NA	144571	6402	NA	CD62L|hLHRc|LAM-1|LAM1|Leu-8|LNHR|LSEL|Lyam-1|LYAM1|PLNHR	Importantly, A2M-AS1 upregulation was significantly associated with ERnegative,HER2-positive, and basal-like breast cancer and with poor recurrence-free survival and metastasis-free survival in breast cancer patients. After validating these results in 96 collected human breast cancer tissues and 64 paired adjacent noncancerous tissues, we further investigated the roles of A2M-AS1 in human ER-negative and basal-like breast cancer cells. /e results revealed that A2M-AS1 significantly promotes human breast cancer cell proliferation, invasion, and migration. Additionally, bioinformatics analysis of genes coexpressed with A2M-AS1 in the context of human breast cancer combined with qRT-PCRand western blot assays revealed that A2M-AS1 exerts regulatory effects on downstream factors in the cell adhesion molecule pathway, including CD2 and SELL. /ese results imply that A2M-AS1 might be a promising candidate prognostic factor and therapeutic target for breast cancer.	32352014	RID07279	expression association	metastasis,recurrence,prognosis	DOWN(BRCA);DATA(GSE67939)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung squamous cell carcinoma	LINC00519	YAP1	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);apoptosis process(-)	ceRNA(miR-450b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000258955	GRCh38_14:51304108-51331918	ENSG00000137693	NA	161342	10413	C14orf30	YAP65	Elevated level of LINC00519 was identified in LUSC tissues and cell lines.-High LINC00519 level predicted unsatisfactory prognosis.-Then, loss-of-function assays suggested the inhibitive role of silenced LINC00519 in cell proliferation, migration, invasion and tumour growth and promoting effect on cell apoptosis in LUSC.-Mechanically, LINC00519 was activated by H3K27 acetylation (H3K27ac).-Moreover, LINC00519 sponged miR-450b-5p and miR-515-5p to up-regulate Yes1 associated transcriptional regulator (YAP1).-Additionally, miR-450b-5p and miR-515-5p elicited anti-carcinogenic effects in LUSC.-Finally, rescue assays validated the effect of LINC00519-miR-450b-5p-miR-515-5p-YAP1 axis in LUSC.	32297697	RID07280	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Lung squamous cell carcinoma	LINC00520	YAP2	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);apoptosis process(-)	ceRNA(miR-515-6p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000137693	NA	645687	NA	C14orf34|LASSIE	NA	Elevated level of LINC00519 was identified in LUSC tissues and cell lines.-High LINC00519 level predicted unsatisfactory prognosis.-Then, loss-of-function assays suggested the inhibitive role of silenced LINC00519 in cell proliferation, migration, invasion and tumour growth and promoting effect on cell apoptosis in LUSC.-Mechanically, LINC00519 was activated by H3K27 acetylation (H3K27ac).-Moreover, LINC00519 sponged miR-450b-5p and miR-515-5p to up-regulate Yes1 associated transcriptional regulator (YAP1).-Additionally, miR-450b-5p and miR-515-5p elicited anti-carcinogenic effects in LUSC.-Finally, rescue assays validated the effect of LINC00519-miR-450b-5p-miR-515-5p-YAP2 axis in LUSC.	32297698	RID07281	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Ovarian cancer	TLR8-AS1	TLR8	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	TCGA;GSE82059	NA	chemoresistance(+);cell migration(+);NF-kB signaling pathway(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000233338	GRCh38_X:12902817-12908333	ENSG00000101916	NA	349408	51311	NA	CD288|hTLR8	Firstly, bioinformatics analyses identified TLR8-AS1 as a cancer-associated fibroblasts regulated lncRNA in ovarian cancer.-Further experiments revealed that TLR8-AS1 augmented cell metastasis and chemoresistance of ovarian cancer in vitro and in vivo.-Moreover, TLR8-AS1 upregulates TLR8 by stabilizing TLR8 mRNA, thus activating NF-kB signaling and promoting ovarian cancer metastasis and chemoresistance.-Besides, TCGA data analysis suggested that TLR8-AS1 is elevated in ovarian cancer in comparison to adjacent non-cancerous tissues.-High TLR8-AS1 expression levels were measured in metastatic ovarian cancer and correlated with poor patient prognosis.-The clinical data supported the mechanism and biological significance of TLR8-AS1 dysregulation in ovarian cancer development.	32278547	RID07282	transcriptional regulation	metastasis,chemoresistance,prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Gastric cancer	FTX	SIVA1	positively-E	luciferase reporter assay;TargetScan	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-215-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000184990	NA	100302692	10572	FLJ33139|LINC00182|MIR374AHG|NCRNA00182	CD27BP|SIVA|Siva-1|Siva-2	We found that the expression of FTX in tumor tissues of 71 GC patients was higher than that in paracancerous tissues, and the prognosis of patients with high FTX was poor. The expression of FTX in gastric cancer cells was higher than that in normal human gastric epithelial cells (GES-1). Transferring overexpression plasmid of FTX into gastric cancer cells (MGC-803 and SGC-7901) promoted cell proliferation and the ratio of cells in G0-G1 phase was decreased. Transferring si-FTX to MGC- 803 and SGC-7901 led to opposite results. There was a negative correlation between the expression of mi215-3p and FTX in MGC-803 and SGC- 7901 gastric cancer cells, and luciferase results showed that mi215-3p could directly bind to FTX and regulate cell growth and cell cycle changes. In addition, luciferase results showed that mi215-3p could bind directly to SIVA1. What s more, RT-qPCR and WB results showed that mi215 mimic could promote the expression of MGC-803, SGC-7901 SIVA1mRNA and protein.	32271421	RID07283	ceRNA or sponge	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE86978)
Colorectal cancer	NRIR	MYC	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE113296	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225964	GRCh38_2:6819463-6840464	ENSG00000136997	NA	104326052	4609	lncCMPK2|lncRNA-CMPK2	bHLHe39|c-Myc|MYCC	In the present study, the expression of lncCMPK2 was upregulated in CRC tissues and positively correlated with clinical stages and lymphatic metastasis. The overexpression of lncCMPK2 promoted the proliferation and cell cycle transition of CRC cells. Conversely, the silencing of lncCMPK2 restricted cell proliferation both in vitro and in vivo. lncCMPK2 was localized to the nucleus of CRC cells, bound to far upstream element binding protein 3 (FUBP3), and guided FUBP3 to the far upstream element (FUSE) of the c-Myc gene to activate transcription. lncCMPK2 also stabilized FUBP3. These results provide novel insights into the functional mechanism of lncCMPK2 in CRC progression and highlight its potential as a biomarker of advanced CRC and therapeutic target.	32203166	RID07284	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	NRIR	FUBP3	positively-E	RNA pull-down assay	upregulation	qRT-PCR	GSE113296	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225964	GRCh38_2:6819463-6840464	ENSG00000107164	NA	104326052	8939	lncCMPK2|lncRNA-CMPK2	FBP3	In the present study, the expression of lncCMPK2 was upregulated in CRC tissues and positively correlated with clinical stages and lymphatic metastasis. The overexpression of lncCMPK2 promoted the proliferation and cell cycle transition of CRC cells. Conversely, the silencing of lncCMPK2 restricted cell proliferation both in vitro and in vivo. lncCMPK2 was localized to the nucleus of CRC cells, bound to far upstream element binding protein 3 (FUBP3), and guided FUBP3 to the far upstream element (FUSE) of the c-Myc gene to activate transcription. lncCMPK2 also stabilized FUBP3. These results provide novel insights into the functional mechanism of lncCMPK2 in CRC progression and highlight its potential as a biomarker of advanced CRC and therapeutic target.	32203166	RID07285	interact with protein	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	SNHG3	RUNX2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-539)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000124813	NA	8420	860	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	AML3|CBFA1|CCD|CCD1|PEBP2A1|PEBP2aA1	Moreover, knockdown of SNHG3 markedly suppressed SW480 cell proliferation, as demonstrated by the CCK8 assay (P<0.050). Next, the effects of SNHG3 on CRC metastasis were explored. The wound-healing assays revealed that SW480 cells transfected with si-SNHG3 obviously suppress the scratch wound closure capacity compared to cells transfected with si-SNHG3 . Similarly, transwell assays demonstrated that SNHG3 depletion significantly decreased the invasion ability of SW480 cells;In addition, we found that RUNX2 expression was negative correlated with miR-539 expression, and positive correlated with SNHG3 expression in CRC tissues. What s more, the inhibitory effect on CRC cell proliferation, migration and invasion by SNHG3 knockdown could be restored by overexpression of RUNX2 or inhibition of miR- 539.	32187965	RID07286	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00460	AGR2	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000106541	NA	728192	10551	NA	AG2|HAG-2|PDIA17|XAG-2	We firstly detected LINC00460 expression was significantly upregulated in both HCC tumor tissues and cell lines. The upregulation of LINC00460 was positively associated with HCC progression. Functionally, LINC00460 facilitated HCC cell proliferation, migration, and invasion capacities, which due to that LINC00460 could physically bind to and repress miR-342-3p to elevate the expression of AGR2.	32184630	RID07287	ceRNA or sponge	NA		UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE51827,GSE55807)
Laryngeal squamous cell carcinoma	XIST	TRIB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-125b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000071575	NA	7503	28951	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	GS3955|TRB2	XIST was notably up-regulated in LSCC tissues and cells, and the high level of XIST was associated with the low survival rate of LSCC patients. XIST knockdown markedly repressed cell proliferation, migration and invasion and promoted the apoptosis of LSCC cells and the effects were antagonized by loss of miR-125b-5p. MiR-125b-5p was a target of XIST in LSCC cells, and it could bind to TRIB2 as well. Moreover, XIST-loss-induced down-regulation of TRIB2 could be significantly reversed by miR-125b-5p knockdown. XIST promoted the growth of LSCC tumor in vivo.	32149330	RID07288	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Ovarian cancer	LUCAT1	miR-199a-5p	negatively-E	luciferase reporter assay;miRcode	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	NA	NA	100505994	NA	SCAL1|SCAT5	NA	To sum up, we first observed that lncRNA LUCAT1 is highly expressed in ovarian cancer cells. Knockdown of lncRNA LUCAT1 inhibits the proliferation of ovarian cancer cells and promotes their apoptosis. LncRNA LUCAT1 may target miR-199a-5p to exert its effects.	32141534	RID07289	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Triple-negative breast cancer	LINC00857	FOXK1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR;ISH	TCGA;GSE58812	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000237523	GRCh38_10:80207372-80219657	ENSG00000164916	NA	439990	221937	HUMT	IMAGE:5164497	CCK8 assay showed that cell proliferation was significantly suppressed in HUMT-KO cells than controls. This was further validated in colony formation assay as the colonyforming capacity was significantly inhibited in the HUMTKO group . Wound healing assay, Transwell migration, and invasion assay indicated that HUMT silencing significantly suppressed the migration ability of cancer cells. Furthermore, a 3D invasion assay was conducted and showed a consistent result for invasion ability .	32138762	RID07290	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	SNHG5	HMGB3	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-1179)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000029993	NA	387066	3149	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	HMG2A|HMG4|MGC90319	Upregulation of lncRNA-SNHG5 and downregulation of miR-1179 were identified in NPC, which were associated with adverse clinical outcomes. Functionally, upregulation of lncRNA-SNHG5 and downregulation of miR- 1179 accelerated NPC cell proliferation, migration and invasion. Furthermore, lncRNA-SNHG5 acted as a molecular sponge of miR-1179 in NPC. Besides that, upregulation of HMGB3 was found in NPC, and knockdown of HMGB3 restrained NPC progression. Moreover, HMGB3, a target of miR-1179, regulated NPC progression by mediating LncRNA-SNHG5/miR-1179 axis.	32131767	RID07291	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE109761,GSE111065,GSE55807,GSE67939)
Non-small cell lung cancer	SNHG6	ETS1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);	ceRNA(miR-944)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000134954	NA	641638	2113	HBII-276HG|NCRNA00058|U87HG	ETS-1|EWSR2|FLJ10768	We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR- 944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9.	32099396	RID07292	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG6	ETS1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);	ceRNA(miR-181d-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000134954	NA	641638	2113	HBII-276HG|NCRNA00058|U87HG	ETS-1|EWSR2|FLJ10768	We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR- 944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9.	32099396	RID07293	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG6	WIPF1	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000115935	NA	641638	7456	HBII-276HG|NCRNA00058|U87HG	WASPIP|WIP	Therefore, we concluded that ETS1 enhanced the expression of WIPF1 via binding to its promoter. What  more, both mRNA and protein level of ETS1 target genes including WIPF1,  MMP2 and MMP9 could be restrained by SNHG6 silence .	32099396	RID07294	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG6	MMP2	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000087245	NA	641638	4313	HBII-276HG|NCRNA00058|U87HG	CLG4|CLG4A|TBE-1	Therefore, we concluded that ETS1 enhanced the expression of WIPF1 via binding to its promoter. What  more, both mRNA and protein level of ETS1 target genes including WIPF1,  MMP2 and MMP9 could be restrained by SNHG6 silence .	32099396	RID07295	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	SNHG6	MMP9	positively-E	luciferase reporter assay;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100985	NA	641638	4318	HBII-276HG|NCRNA00058|U87HG	CLG4B	Therefore, we concluded that ETS1 enhanced the expression of WIPF1 via binding to its promoter. What  more, both mRNA and protein level of ETS1 target genes including WIPF1,  MMP2 and MMP9 could be restrained by SNHG6 silence .	32099396	RID07296	expression association	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Salivary gland adenoid cystic carcinoma	EREG	MRPL23-AS1	positively-E	RNA pull-down assay;RIP;ChIP	upregulation	RT-PCR;microarray	GSE136698	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	NA	Cancer	Salivary gland carcinoma	PCG	lncRNA	ENSG00000124882	NA	ENSG00000226416	GRCh38_11:1983237-1989964	2069	100133545	ER	NA	Expression of lncRNA MRPL23-AS1 is upregulated in SACC and positively associated with EREG.-When stimulated with recombinant EREG protein, MRPL23-AS1 expression increased significantly.Overexpressing MRPL23-AS1 reversed the EREG knockdownnduced reductions in migration and invasion.	32098781	RID07297	expression association	NA	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE86978)	
Salivary gland adenoid cystic carcinoma	MRPL23-AS0	EZH2	positively-E	RNA pull-down assay;RIP;ChIP	upregulation	RT-PCR;microarray	GSE136699	NA	epithelial to mesenchymal transition(+)	enhancer	regulation	NA	NA	NA	NA	Cancer	Salivary gland carcinoma	lncRNA	PCG	NA	NA	ENSG00000106462	NA	NA	2146	NA	ENX-1|EZH1|KMT6|KMT6A	MRPL23-AS1 positively regulated epithelial-mesenchymal transition by forming an RNA-protein complex with enhancer of zeste homolog 2 (EZH2). MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin promoter region.	32098781	RID07298	chromatin looping	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Salivary gland adenoid cystic carcinoma	MRPL23-AS1	E-cadherin	negatively-E	RNA pull-down assay;RIP;ChIP	upregulation	RT-PCR;microarray	GSE136698	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Salivary gland carcinoma	lncRNA	PCG	ENSG00000226416	GRCh38_11:1983237-1989964	NA	NA	100133545	NA	NA	NA	MRPL23-AS1 significantly promoted cell migration and invasion.-This study identifies a novel metastasis_x0002_promoting lncRNA MRPL23-AS1, which mediates the transcrip_x0002_tional silencing of E-cadherin through forming an RNA protein complex with EZH2.-In addition, a significantly negative -correlation between E-cadherin and MRPL23-AS1 expression was found in SACC tissues .	32098781	RID07299	interact with protein	metastasis		
Urinary bladder cancer	TMPO-AS1	EBF1	positively-E	luciferase reporter assay;RIP;ChIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-98-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000164330	NA	100128191	1879	NA	COE1|EBF|OLF1	In this study, high expression of TMPO-AS1 was revealed in BCa tissues and cell lines, and TMPO-AS1- predicted poor prognosis. Moreover, TMPO-AS1 facilitated cell growth. Additionally, TMPO-AS1 also boosted the migration and invasion of BCa cells. Mechanistically, overexpressed EBF transcription factor 1 (EBF1) in BCa cell was verified to promote the transcription of TMPO-AS1. Later, we found that TMPO-AS1 was a cytoplasmic RNA and could sponge miR-98-5p. Besides, it was validated that EBF1 is a target gene of miR-98-5p and negatively correlated with miR-98-5p in terms of expression level.	32087328	RID07300	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	ASB16-AS1	WNT2	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR;microarray	GSE39001	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-1305)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000267080	GRCh38_17:44175968-44186723	ENSG00000105989	NA	339201	7472	C17orf65|DKFZp762C2414	INT1L1|IRP	In our study, we showed that the expression of ASB16-AS1 was increased while miR-1305 reduced was re in CC. Clinically, ASB16-AS1 and miR-1305 were correlated with poor-associated clinicopathological features of CC patients. Knockdown of ASB16-AS1 reduced CC cells proliferation, migration and invasion abilities by regulating miR-1305 in vitro and in vivo. Moreover, miR-1305 was directly bound to ASB16-AS1 and Wnt2, regulated their expression negatively. western blot assays showed that ASB16-AS1 functioned as an oncogene by Wnt/beta-catenin pathway.	32058219	RID07301	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	
Papillary thyroid carcinoma	SNHG3	PSMD10	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000101843	NA	8420	5716	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	p28	We then used a tumor xenograft model to assess the relevance of SNHG3 in vivo. We determined SNHG3 expression to be elevated in PTC tissues relative to controls, with advanced tumor node metastasis stage and lymph node metastasis being associated with this expression. Knocking down SNHG3 significantly reduced in vitro PTC cell migration, invasion, proliferation, and colony formation, and it further slowed the growth of tumors in vivo. We found that SNHG3 could bind to miR 214 3p as a competing endogenous RNA (ceRNA) for this miRNA, thereby regulating proteasome 26S subunit non ATPase 10 (PSMD10) expression, a miR 214 3p target. These results thus indicate that SNHG3 is an oncogenic lncRNA in PTC, acting at least in part via the miR 214 3p/PSMD10 axis.	32048306	RID07302	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Gastric cancer	LINC00511	miR-515-5p	negatively-F	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);MAPK signaling pathway(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72290091-72640472	NA	NA	400619	NA	LCAL5|onco-lncRNA-12	NA	LINC00511 levels were significantly higher in gastric cancer tissues and cell lines than in normal samples. The high expression of LINC00511 in gastric cancer patient samples positively correlated with advanced clinical characters and poor prognosis. Depleting LINC00511 reduced tumor cell proliferation, migration and invasion, slowed tumor growth, and accelerated cell apoptosis. Our mechanistic study results indicated that LINC00511 promotes gastric cancer progression in a miR- 515-5p-dependent manner.	32042282	RID07303	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Glioblastoma	SP1	SNHG12	positively-E	luciferase reporter assay;RIP;ChIP;immunofluorescence	upregulation	qRT-PCR	CGGA;GSE4290;GSE7696;GSE15824;GSE50161;GSE59612;GSE104267	NA	chemoresistance(+)	transcriptional regulation	regulation	NA	Temozolomide	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000185591	NA	ENSG00000197989	GRCh38_1:28578538-28583132	6667	85028	NA	ASLNC04080|C1orf79|LINC00100|PNAS-123	SNHG12 was upregulated in TMZ-resistant cells and tissues.-Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity.-An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1);this indicated that methylation and SP1 work together to regulate SNHG12 expression.-In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance.-Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition.-Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment.	32039732	RID07304	transcriptional regulation	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Glioblastoma	DNMTs	SNHG12	negatively-E	luciferase reporter assay;RIP;ChIP;immunofluorescence	upregulation	qRT-PCR	CGGA;GSE4290;GSE7696;GSE15824;GSE50161;GSE59612;GSE104267	NA	chemoresistance(+)	DNA methylation	regulation	NA	Temozolomide	NA	NA	Cancer	Brain glioma	PCG	lncRNA	NA	NA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|PNAS-123	SNHG12 was upregulated in TMZ-resistant cells and tissues.-Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity.-An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1);this indicated that methylation and SP1 work together to regulate SNHG12 expression.-In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance.-Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition.-Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment.	32039732	RID07305	epigenetic regulation	chemoresistance		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Glioblastoma	SNHG12	MAPK1	positively-E	luciferase reporter assay;RIP;ChIP;immunofluorescence	upregulation	qRT-PCR	CGGA;GSE4290;GSE7696;GSE15824;GSE50161;GSE59612;GSE104267	NA	chemoresistance(+)	ceRNA(miR-129-5p)	regulation	NA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000100030	NA	85028	5594	ASLNC04080|C1orf79|LINC00100|PNAS-123	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	SNHG12 was upregulated in TMZ-resistant cells and tissues.-Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity.-An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1);this indicated that methylation and SP1 work together to regulate SNHG12 expression.-In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance.-Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition.-Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment.	32039732	RID07306	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	SNHG12	E2F7	positively-E	luciferase reporter assay;RIP;ChIP;immunofluorescence	upregulation	qRT-PCR	CGGA;GSE4290;GSE7696;GSE15824;GSE50161;GSE59612;GSE104267	NA	chemoresistance(+)	ceRNA(miR-129-5p)	regulation	NA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000165891	NA	85028	144455	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	SNHG12 was upregulated in TMZ-resistant cells and tissues.-Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity.-An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1);this indicated that methylation and SP1 work together to regulate SNHG12 expression.-In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance.-Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition.-Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment.	32039732	RID07307	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC);DATA(GSE117623)
Cervical cancer	LINC01783	GBP1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-199b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233421	GRCh38_1:16533886-16535649	ENSG00000117228	NA	100132147	2633	NA	NA	Our results revealed LINC01783 is overexpressed in cervical cancer cells. Overexpressed LINC01783 considerably accelerated the cell proliferation, migration and invasion of cervical cancer cells while restrained cell apoptosis of them. Moreover, LINC01783 positively regulated the GBP1 expression via competitively binding to miR-199b-5p.	32021449	RID07308	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939,GSE86978)
Cholangiocarcinoma	NNT-AS1	miR-203	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);PI3K/AKT signaling pathway(+);epithelial to mesenchymal transition(+);ERK1/2 signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000207568	NA	100652772	NA	RP11-159F24.1	NA	NNT-AS1 overexpression was appeared in CCA tissues and cell lines. Proliferation was promoted by NNT-AS1 overexpression in CCLP1 and TFK1 cells. Besides, NNT-AS1 overexpression reduced E-cadherin level and raised levels of N-cadherin, vimentin, Snail and Slug. However, the opposite trend was occurred by NNT-AS1 knockdown. Further, NNT-AS1 overexpression promoted phosphatidylinositol 3 kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK)1/2 pathways. MiR-203 was sponged by NNT-AS1 and miR-203 mimic reversed the above promoting effects of NNT-AS1. Additionally, insulin-like growth factor type 1 receptor (IGF1R) and zinc finger E-box binding homeobox 1 (ZEB1) were two potential targets of miR-203.NNT-AS1 promoted proliferation, EMT and PI3K/AKT and ERK1/2 pathways in CCLP1 and TFK1 cells through down-regulating miR-203.	32019904	RID07309	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	
Gastric cancer	LINC-ROR	MRP1	positively-E	immunoblot	upregulation	RT-PCR	NA	NA	chemoresistance(+)	NA	regulation	NA	Adriamycin;Vincristine	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000113318	NA	100885779	NA	lincRNA-RoR|lincRNA-ST8SIA3|ROR	NA	We found that ROR expression levels are positively associated with increased MDR and poor prognosis of patients with gastric cancer. Regulator of reprogramming expression is increased in gastric cancer cells resistant to adriamycin (ADR) and vincristine (VCR). Depletion of ROR reduced MRP1 expression and increased apoptosis of drug-resistant gastric cancer cells in response to ADR and VCR treatment.	32019330	RID07310	expression association	prognosis,chemoresistance	UP(LIHC);DATA(GSE117623)	
Pancreatic cancer	HMGA2-AS1	HMGA2	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000197301	GRCh38_12:65851340-65882167	ENSG00000149948	NA	100129940	8091	RP11-366L20.2	BABL|HMGIC|LIPO	HMGA2-AS1 transcripts positively modulate HMGA2 expression and migration properties of PANC1 cells through HMGA2. HMGA2-AS1 is involved in the regulation of its own sense gene expression, mediating tumorigenesis.	32010621	RID07311	expression association	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric cancer	HOXA11-AS	miR-148a	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	HOXA11-AS and WNT1 expression levels were upregulated, while miR-148a level was downregulated in GC tissues and cell lines relative to matched controls.HOXA11-AS increased  -catenin pathway activity, which was abolished by miR-148a overexpression in GC cells.	32009419	RID07312	ceRNA or sponge	NA		
Esophageal cancer	PSMA3-AS1	EZH2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000257621	GRCh38_14:58265365-58298134	ENSG00000106462	NA	379025	2146	FLJ31306	ENX-1|EZH1|KMT6|KMT6A	PSMA3-AS1 is significantly up-regulated in ESCC tissues, and the PSMA3-AS1/miR-101/EZH2 axis plays a critical role in ESCC progression.	32005028	RID07313	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Oral squamous cell carcinoma	HOTAIR	miR-326	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR acted as a competitive endogenous RNA effectively sponging miR-326, thereby regulating the derepression of  HOTAIR over-expression promoted the progression of OSCC.metastasis-associated gene 2 (MTA2).	31995261	RID07314	ceRNA or sponge	metastasis		
Gastric cancer	AC093818.1	PDPK1	positively-E	overexpression;siRNA	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225205	GRCh38_2:172480840-172556596	ENSG00000140992	NA	NA	5170	NA	PDK1|PDPK2|PDPK2P|PRO0461	LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC.	31988283	RID07315	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Gastric cancer	STAT3	AC093818.1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000225205	GRCh38_2:172480840-172556596	6774	NA	ADMIO|ADMIO1|APRF|HIES	NA	RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells.AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression.	31988283	RID07316	transcriptional regulation	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Gastric cancer	SP1	AC093818.1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000225205	GRCh38_2:172480840-172556596	6667	NA	NA	NA	RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells.AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.2 overexpression.	31988283	RID07317	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Breast cancer	GACAT3	miR-497	negatively-E	overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	The expression of LncRNA GACAT3 was increased in breast cancer tissues and cell lines compared to paracancer tissues and normal cells. LncRNA GAC AT3 is associated with poor prognosis of breast cancer, preoperative MRI perfusion-related diffusion (D) reduction, and elevated perfusion fraction (f). After targeting CIR-497, LncRNA GACAT3 promotes the progression of breast cancer by down-regulating Caspase 9 and up-regulating Bcl-2.	31983109	RID07318	expression association	prognosis		
Breast cancer	GACAT3	Capsase9	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	Association of LncRNA-GACAT3 with MRI features of breast cancer and its molecular mechanism.The expression of LncRNA GACAT3 was increased in breast cancer tissues and cell lines compared to paracancer tissues and normal cells. Compared with the low expression group, patients with high expression had poorer MRI diffusionweighted imaging and lower overall survival. Down-regulation of LncRNA GACAT3 increased the expression of miR-497, and miR-497 mimics reduced the luciferase of LncRNA GACAT3. Increased LrcRNA GACAT3 in breast cancer cells could downregulate the expression of miR-497, down-regulate Capsase 9 and up-regulate Bcl-2 to promote proliferation and anti-apoptosis of breast cancer cells. In addition, knockdown of LncRNA GACAT3 promoted the enzymatic ac_x0002_tivity of caspase 9 and decreased the expression of Bcl-2	31983109	RID07319	expression association	NA		
Breast cancer	GACAT3	BCL2	positively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000171791	NA	104797537	596	LINC01458|lncRNA-AC130710	Bcl-2|PPP1R50	Association of LncRNA-GACAT3 with MRI features of breast cancer and its molecular mechanism.The expression of LncRNA GACAT3 was increased in breast cancer tissues and cell lines compared to paracancer tissues and normal cells. Compared with the low expression group, patients with high expression had poorer MRI diffusionweighted imaging and lower overall survival. Down-regulation of LncRNA GACAT3 increased the expression of miR-497, and miR-497 mimics reduced the luciferase of LncRNA GACAT3. Increased LrcRNA GACAT3 in breast cancer cells could downregulate the expression of miR-497, down-regulate Capsase 9 and up-regulate Bcl-2 to promote proliferation and anti-apoptosis of breast cancer cells. In addition, knockdown of LncRNA GACAT3 promoted the enzymatic ac_x0002_tivity of caspase 9 and decreased the expression of Bcl-3	31983109	RID07320	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	CP	IGF2	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000047457	GRCh38_3:149162410-149221829	ENSG00000167244	NA	1356	3481	AB073614|CP-2	C11orf43|GRDF|IGF-II|PP9974|SRS3	AB073614 expression level in GC samples was significantly higher than that of adjacent ones. Besides, the migration and invasion of GC cells were obviously repressed after AB073614 was knocked down. After AB073614 was knocked down in vitro, the mRNA and protein expressions of insulin-like growth factor 2 (IGF-2) was remarkably down-regulated.	31957827	RID07321	expression association	NA	UP(LIHC,PAAD,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE60407,GSE38495)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Cervical cancer	LINC00319	RPP25	positively-E	luciferase reporter assays;RIP; starBase; RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-3127-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000178718	NA	284836	54913	C21orf125|FLJ38036|NCRNA00319|PRED49	FLJ20374	LINC00319 was highly expressed in tissues and cell lines in cervical cancer. Further, overexpression of LINC00319 accelerates cell migration, invasion and EMT in cervical cancer. Moreover, LINC00319 could bind with miR-3127-5p and negatively regulated its expression.	31942724	RID07322	ceRNA or sponge	NA		UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Malignant glioma	LINC01116	radixin	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-31)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163364	GRCh38_2:176611464-176637931	NA	NA	375295	NA	TALNEC2	NA	Linc01116 is highly expressed in glioma tissue and cells, along with low expression of miR-31, and there was a negative correlation between the expression of linc01116 and miR-31 in glioma tissue. In addition, the expression of linc01116 in glioma patients with metastasis was significantly higher than that in patients without metastasis, while miR-31 was significantly lower. In vitro and in vivo studies shown that linc01116 promoted invasion and migration of glioma cells.	31933922	RID07323	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Prostate cancer	PCAT7	TGFBR1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	ceRNA(miR-324-5p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000231806	GRCh38_9:94555054-94603990	ENSG00000106799	NA	101928099	7046	PCAN-R2	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	PCAT7 was found to be elevated in primary PCa tissues with bone metastasis and associated with bone metastasis status and poor prognosis of patients with PCa.PCAT7 overexpression promotes PCa bone metastasis in vivo, as well as migration, invasion, and EMT of PCa cells in vitro; on the contrary, PCAT7 knockdown has an inverse effect. Mechanistically, PCAT7 activates TGF-beta/SMAD signaling by upregulating TGFBR1 expression via sponging miR-324-5p. In turn, TGF-beta signaling forms a positive feedback loop with PCAT7 via SMAD3/SP1 complex-induced PCAT7 upregulation.	31925912	RID07324	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	TINCR	ROCK1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-214-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000067900	NA	257000	6093	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	p160ROCK	TINCR and ROCK1 were upregulated, while miR-214-5p was downregulated in HCC.TINCR and ROCK1 overexpression led to increased rate of cancer cell proliferation, while miR-214-5p played an opposite role and reduced the effects of TINCR overexpression. Therefore, TINCR sponges miR-214-5p to upregulate ROCK1 in HCC, thereby promoting cancer cell invasion and migration.	31900116	RID07325	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatitis B	PVT1	EZH2	NA	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|EZH1|KMT6|KMT6A	Upregulation of PVT1 was detected in hepatitis B virus-positive HCC tissues compared with that noted in the HBV-negative samples. lncRNA PVT1 enhanced cell proliferation, migration, and invasion in the hepatitis B virus-positive Hep3B cells rather than the hepatitis B virus-negative HepG2 cells. PVT1 was able to bind EZH2 and obstruct the recruitment of EZH2 to the promoter of MYC therefore promoting MYC expression by altering H3K37me3 status in Hep3B liver cancer cells, and EZH2 protein was negatively correlated with lncRNA-PVT1 expression.	31894346	RID07326	interact with protein	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatitis B	PVT1	MYC	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Gastrointestinal system disease	Hepatitis	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	bHLHe39|c-Myc|MYCC	RNA pull-down assay was employed to examine the connection between PVT1 and the PRC2 complex. Chromatin immunoprecipitation was employed to test the combination with EZH2 protein and H3K27me3 level on the MYC promoter. The results revealed that upregulation of PVT1 was detected in hepatitis B virus-positive HCC tissues compared with that noted in the HBV-negative samples. lncRNA PVT1 enhanced cell proliferation, migration, and invasion in the hepatitis B virus-positive Hep3B cells rather than the hepatitis B virus-negative HepG2 cells. PVT1 was able to bind EZH2 and obstruct the recruitment of EZH2 to the promoter of MYC therefore promoting MYC expression by altering H3K37me3 status in Hep3B liver cancer cells, and EZH2 protein was negatively correlated with lncRNA-PVT1 expression. In conclusion, our results indicate that lncRNA PVT1 promotes hepatitis B virus-positive liver cancer progression by disturbing histone methylation on the MYC promoter, suggesting that lncRNA PVT1 may be a potential target for developing diagnostic and therapeutic strategies of hepatitis B virus-positive liver cancer at the early stages.	31894346	RID07327	epigenetic regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colon cancer	LINC00858	HNF1A	NA	RIP;luciferase reporter assay;lncMAP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);tumor growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000135100	NA	170425	6927	CRCAL-2	HNF-1-alpha|HNF-1A|HNF1|HNF1alpha|HNF4A|IDDM20|LFB1|MODY3|TCF-1|TCF1	LINC00858 was highly expressed in primary colon cancer tissues and colon cancer cell lines, and was mainly located in the nucleus. High LINC00858 expression was found to correlate with a poor differentiation, advanced TNM stages and lymph node metastasis. Exogenous overexpression of LINC00858 promoted cell proliferation, invasion and migration of colon cancer cells, and facilitated angiogenesis and tumor growth. In addition, we found that LINC00858 can bind to and upregulate the nuclear transcription factor HNF4alpha, leading to WNK2 expression downregulation.	31884577	RID07328	interact with protein	metastasis	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Colon cancer	LINC00858	WNK2	negatively-E	RIP;luciferase reporter assay;lncMAP;DisgeNET;ChIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);angiogenesis(+);tumor growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000165238	NA	170425	65268	CRCAL-2	KIAA1760|NY-CO-43|PRKWNK2|SDCCAG43	LINC00858 was highly expressed in primary colon cancer tissues and colon cancer cell lines, and was mainly located in the nucleus. High LINC00858 expression was found to correlate with a poor differentiation, advanced TNM stages and lymph node metastasis. Exogenous overexpression of LINC00858 promoted cell proliferation, invasion and migration of colon cancer cells, and facilitated angiogenesis and tumor growth. In addition, we found that LINC00858 can bind to and upregulate the nuclear transcription factor HNF4alpha, leading to WNK2 expression downregulation.	31884577	RID07329	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	LINC02835	p120-catenin	positively-E	RIP;RNA pull-down assay	upregulation	sequencing	GSE101432.	NA	cell invasion(+);cell migration(+)	interact with protein;protein stability	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285711	GRCh38_4:65225867-65241814	NA	NA	105377256	NA	lncMER52A	NA	HCC patients with higher lncMER52A had advanced TNM stage, less differentiated tumors, and shorter overall survival. LncMER52A promoted invasion and metastasis of HCC cells in vitro and in vivo. Mechanistically, lncMER52A stabilized p120-catenin and triggered the activation of Rho GTPase downstream of p120-catenin.lncMER52A, which promoted the progression of HCC cells via stabilizing p120-catenin and activating p120-ctn/Rac1/Cdc42 axis.	31874857	RID07330	interact with protein	metastasis		
Hepatocellular carcinoma	YY1	LINC02835	positively-E	ChIP;RNA pull-down assay	upregulation	sequencing	GSE101433.	NA	cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000285711	GRCh38_4:65225867-65241814	7528	105377256	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	lncMER52A		31874857	RID07331	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	
Oral squamous cell carcinoma	RBM5-AS1	YAP1	positively-E	luciferase reporter assay;RegRNA 2.0;overexpression;siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-1285-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000281691	GRCh38_3:50099603-50100988	ENSG00000137693	NA	100775107	10413	LUST	YAP65	LncRNA RBM5-AS1 to be highly expressed in OSCC tumor tissues and cancer cell lines. RBM5-AS1 promotes the proliferation, migration, and invasion of OSCC cells in vitro. We also found that RBM5-AS1 regulates the level of miR-1285-3p as a competitive endogenous RNA (ceRNA), therefore regulate the expression level of an oncogene-YAP1, a target of miR-1285-3p.	31869662	RID07332	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Oral squamous cell carcinoma	YY1	RBM5-AS1	positively-E	luciferase reporter assay;Consite;overexpression;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000281691	GRCh38_3:50099603-50100988	7528	100775107	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	LUST		31869662	RID07333	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colorectal cancer	HLA-F-AS1	PFN1	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell injury(-)	ceRNA(miR-330-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214922	GRCh38_6:29726601-29749049	ENSG00000108518	NA	285830	5216	NA	NA	Expressions of HLA-F-AS1 and PFN1 were significantly up-regulated while miR-330-3p was significantly down-regulated in CRC tissues and cell lines. Over-expressions of HLA-F-AS1 or transfection of miR-330-3p inhibitors could promote the proliferation, migration and invasion and block apoptosis of CRC cells, whereas knockdown of HLA-F-AS1 or transfection of miR-330-3p mimics led to the opposite effects. Additionally, HLA-F-AS1 could down-regulate miR-330-3p via sponging it. HLA-F-AS1 also enhanced the expressions of PFN1, which was validated as a target gene of miR-330-3p.	31863778	RID07334	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SLCO4A1-AS1	EGFR	positively-E	RNA pull-down assay;western blot	upregulation	RT-PCR	GSE32323;GES39582;GSE104836	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000146648	NA	100127888	1956	NA	ERBB|ERBB1|ERRP	We then collected CRC tissue samples and verified that SLCO4A1-AS1 is highly expressed in CRC tissues. Furthermore, SLCO4A1-AS1 was also upregulated in the CRC cell line. In situ hybridization results showed that high expression of SLCO4A1-AS1 was associated with poor prognosis in patients with CRC. Next, we found that SLCO4A1-AS1 promoted CRC cell proliferation, migration, and invasion.	31853225	RID07335	expression association	prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	SLCO4A1-AS1	MAPK	positively-E	RNA pull-down assay;western blot	upregulation	RT-PCR	GSE32323;GES39582;GSE104837	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	NA	NA	100127888	NA	NA	NA	We then collected CRC tissue samples and verified that SLCO4A1-AS1 is highly expressed in CRC tissues. Furthermore, SLCO4A1-AS1 was also upregulated in the CRC cell line. In situ hybridization results showed that high expression of SLCO4A1-AS1 was associated with poor prognosis in patients with CRC. Next, we found that SLCO4A1-AS1 promoted CRC cell proliferation, migration, and invasion.	31853225	RID07336	expression association	prognosis	UP(SKCM);DATA(GSE38495)	
Gastric cancer	MAGI2-AS3	ZEB1	positively-E	RNA pull-down assay;IntaRNA;miRcode;Annolnc;RNA22	upregulation	qRT-PCR	TCGA;GSE62254;GSE15457	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-141)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000148516	NA	100505881	6935	ENST00000414797	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA MAGI2-AS3 was overexpressed in gastric cancer tissues.lncRNA MAGI2-AS3 was an independent prognostic factor for both overall survival and disease-free survival of gastric cancer patients.MAGI2-AS3 was identified to be an epithelial-mesenchymal transition (EMT)-related lncRNA and was highly co-expressed with ZEB1/2 in both gastric cancer tissues and normal stomach tissues.lncRNA MAGI2-AS3 could positively regulate ZEB1 expression and the process of cell migration and invasion in gastric cancer.	31837602	RID07337	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	MAGI2-AS3	ZEB1	positively-E	RNA pull-down assay;IntaRNA;miRcode;Annolnc;RNA23	upregulation	qRT-PCR	TCGA;GSE62254;GSE15458	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000148516	NA	100505881	6935	ENST00000414797	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA MAGI2-AS3 was overexpressed in gastric cancer tissues.lncRNA MAGI2-AS3 was an independent prognostic factor for both overall survival and disease-free survival of gastric cancer patients.MAGI2-AS3 was identified to be an epithelial-mesenchymal transition (EMT)-related lncRNA and was highly co-expressed with ZEB1/2 in both gastric cancer tissues and normal stomach tissues.lncRNA MAGI2-AS3 could positively regulate ZEB1 expression and the process of cell migration and invasion in gastric cancer.	31837602	RID07338	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	BRD4	MAGI2-AS3	positively-E	RNA pull-down assay;siRNA	upregulation	qRT-PCR	TCGA;GSE62254;GSE15459	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000141867	NA	ENSG00000234456	GRCh38_7:79452877-79471208	23476	100505881	CAP|HUNK1|HUNKI|MCAP	ENST00000414797	LncRNA MAGI2-AS3 was overexpressed in gastric cancer tissues.lncRNA MAGI2-AS3 was an independent prognostic factor for both overall survival and disease-free survival of gastric cancer patients.MAGI2-AS3 was identified to be an epithelial-mesenchymal transition (EMT)-related lncRNA and was highly co-expressed with ZEB1/2 in both gastric cancer tissues and normal stomach tissues.lncRNA MAGI2-AS3 could positively regulate ZEB1 expression and the process of cell migration and invasion in gastric cancer.	31837602	RID07339	transcriptional regulation	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)
Colon adenocarcinoma	ZEB1-AS1	PAK2	positively-E	luciferase reporter assay;starBase;TargetScan;miRDIP;miRDB;miRPathDB	upregulation	qRT-PCR	NA	NA	cell migration(+);cell growth(+)	ceRNA(miR-455-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000180370	NA	220930	5062	NA	PAK65|PAKgamma	ZEB1-AS1 expression was significantly up-regulated in COAD tissues, and high ZEB1-AS1 level was correlated with the poor prognosis of COAD patients.ZEB1-AS1 promotes PAK2 expression by sponging miR-455-3p, thus facilitating COAD cell growth and metastasis.	31828845	RID07340	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	HOXC-AS3	PPP1R1A	positively-E	RNAhybrid;RNA pull-down assay;TargetScan;miRDB;luciferase reporter assay	upregulation	RT-PCR	TCGA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-3922-5p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251151	GRCh38_12:53981509-53985519	ENSG00000135447	NA	100874365	5502	NA	NA	HOXC-AS3 is aberrantly overexpressed in breast cancers especially the HER2+ type. Moreover, high expression of HOXC-AS3 has a relationship with poor clinical outcomes of breast cancer. In addition, HOXC-AS3 regulates cell Invasion and migration both in vitro and in vivo. Our results demonstrated that miR-3922-5p was a direct target of HOXC-AS3, and PPP1R1A was a target of miR-3922-5p in breast cance.	31797701	RID07341	ceRNA or sponge	NA		
Papillary thyroid carcinoma	SNHG1	SP1	positively-E	starBase;luciferase reporter assay	upregulation	microarray;qPCR	NA	NA	cell growth(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000185591	NA	23642	6667	LINC00057|lncRNA16|NCRNA00057|UHG	NA	SNHG1 was identified to be up-regulated in both PTC tissue and cells. Functionally, knockdown of SNHG1 repressed the proliferation, invasion and tumor growth in vitro and in vivo. Mechanistically, SNHG1 sponged miR-199a-5p by complementary binding with specificity protein 1 (SP1) 3'-UTR.	31791587	RID07342	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	SP1	SNHG1	positively-E	JASPSR;TRANSFAC;ChIP	upregulation	microarray;qPCR	NA	NA	cell growth(+);cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000255717	GRCh38_11:62851978-62855953	6667	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	SNHG1 was identified to be up-regulated in both PTC tissue and cells. Functionally, knockdown of SNHG1 repressed the proliferation, invasion and tumor growth in vitro and in vivo. Mechanistically, SNHG1 sponged miR-199a-5p by complementary binding with specificity protein 1 (SP1) 3'-UTR.	31791587	RID07343	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00662	WNT0A	negatively-E	ENCOPI;miRanda;luciferase reporter assay;RNA pull-down assay;RIP;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-15a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	LINC00662 was found to be upregulated in HCC, and high LINC00662 levels correlated with poor survival of HCC patients. LINC00662 upregulated WNT3A expression and secretion via competitively binding miR-15a, miR-16, and miR-107. Through inducing WNT3A secretion, LINC00662 activated Wnt/beta-catenin signaling in HCC cells in an autocrine manner and further promoted HCC cell proliferation, cell cycle, and tumor cell invasion, while repressing HCC cell apoptosis.	31785055	RID07344	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Hepatocellular carcinoma	LINC00662	WNT1A	negatively-E	ENCOPI;miRanda;luciferase reporter assay;RNA pull-down assay;RIP;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-16)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	LINC00662 was found to be upregulated in HCC, and high LINC00662 levels correlated with poor survival of HCC patients. LINC00662 upregulated WNT3A expression and secretion via competitively binding miR-15a, miR-16, and miR-107. Through inducing WNT3A secretion, LINC00662 activated Wnt/beta-catenin signaling in HCC cells in an autocrine manner and further promoted HCC cell proliferation, cell cycle, and tumor cell invasion, while repressing HCC cell apoptosis.	31785055	RID07345	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Hepatocellular carcinoma	LINC00662	WNT2A	negatively-E	ENCOPI;miRanda;luciferase reporter assay;RNA pull-down assay;RIP;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-107)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	LINC00662 was found to be upregulated in HCC, and high LINC00662 levels correlated with poor survival of HCC patients. LINC00662 upregulated WNT3A expression and secretion via competitively binding miR-15a, miR-16, and miR-107. Through inducing WNT3A secretion, LINC00662 activated Wnt/beta-catenin signaling in HCC cells in an autocrine manner and further promoted HCC cell proliferation, cell cycle, and tumor cell invasion, while repressing HCC cell apoptosis.	31785055	RID07346	ceRNA or sponge	NA	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Cervical cancer	DSCAM-AS1	ATXN7L3	positively-E	starBase;RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumorigenesis(+)	ceRNA(miR-877-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000235123	GRCh38_21:40383083-40385358	ENSG00000087152	NA	100506492	56970	M41	DKFZp761G2113	DSCAM-AS1 expression was up-regulated in CC cells.DSCAM-AS1 played as an oncogenic lncRNA by targeting miR-877-5p/ATXN7L3 axis to promote CC progression, which may provide insights into the prevention of CC.	31737900	RID07347	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	XLOC_006390	GDH1	positively-E	shRNA	upregulation	RT-PCR	NA	NA	metabolic process(+)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27193503-27200091	ENSG00000148672	NA	NA	NA	NA	NA	XLOC_006390/c-Myc may be a potential target for PC, and its abnormal activation also indicates the progression of PC.	31734356	RID07348	expression association	NA		
Pancreatic cancer	MYC	XLOC_006390	positively-E	PROMO;shRNA;overexpression	upregulation	RT-PCR	NA	NA	metabolic process(+)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000106031	GRCh38_7:27193503-27200091	4609	NA	bHLHe39|c-Myc|MYCC	NA	XLOC_006390/c-Myc may be a potential target for PC, and its abnormal activation also indicates the progression of PC.	31734356	RID07349	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	
Gastric cancer	TDRG1	HDGF	positively-E	starBase;luciferase reporter assay;TargetScan;RNA22;PITA;miRanda;PicTar	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-873-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000143321	NA	732253	3068	LINC00532|lincRNA-NR_024015	HMG1L2	LncRNA testis development-related gene 1 (TDRG1) is markedly upregulated in clinical GC tissues and GC cells.Overexpression of lncRNA TDRG1 promotes GC growth and metastatic-related traits in vitro and in vivo, and silencing TDRG1 causes opposite results.	31726370	RID07350	ceRNA or sponge	metastasis		UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Urinary bladder cancer	AC114812.8	FUT4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-371b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000224814	GRCh38_2:233693434-233708699	ENSG00000196371	NA	NA	2526	NA	CD15|ELFT|FCT3A|FUC-TIV|FUTIV|LeX|SSEA-1	AC114812.8 was significantly upregulated in BC and could markedly facilitate the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo.	31706102	RID07351	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367)
Breast cancer	LncCCAT1	TCF7L2	positively-E	starBase;AnnoLnc;RNA pull-down assay;luciferase reporter assay	upregulation	microarray	GSE125677;GSE125678	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell stemness(+)	ceRNA(miR-211)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000148737	NA	NA	6934	NA	TCF-4|TCF4	LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. Mechanistic investigation suggests that LncCCAT1 can interact with miR-204/211, miR-148a/152 and Annexin A2(ANXA2), then upregulate T-cell factor 4 (TCF4) or promote translocation of beta-catenin to the nucleus where it activates TCF4, leading to the activation of wingless/integrated (Wnt) signaling.	31695775	RID07352	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)
Breast cancer	LncCCAT1	TCF7L2	positively-E	starBase;AnnoLnc;RNA pull-down assay;luciferase reporter assay	upregulation	microarray	GSE125677;GSE125678	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell stemness(+)	ceRNA(miR-204)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	NA	NA	ENSG00000148737	NA	NA	6934	NA	TCF-4|TCF4	LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. Mechanistic investigation suggests that LncCCAT1 can interact with miR-204/211, miR-148a/152 and Annexin A2(ANXA2), then upregulate T-cell factor 4 (TCF4) or promote translocation of beta-catenin to the nucleus where it activates TCF4, leading to the activation of wingless/integrated (Wnt) signaling.	31695775	RID07353	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)
Breast cancer	TCF7L2	LncCCAT1	positively-E	overexpression;RNA pull-down assay;ChIP	upregulation	microarray	GSE125677;GSE125678	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell stemness(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000148737	NA	NA	NA	6934	NA	TCF-4|TCF4	NA	TCF4 activates the transcription of LncCCAT1Given that TCF4 is a transcription factor and studies have shown that many regulatory feed-forward loops are involved in tumor progression 14, we tested whether TCF4 could regulate the expression of LncCCAT1. As shown in Figure -Figure3L,3L, the expression of LncCCAT1 was upregulated by TCF4 overexpression but decreased by TCF4 knockdown. Subsequently, we predicted three DNA binding elements (DBEs) for TCF4 in the promoter region of LncCCAT1 by bioinformatics analysis (Figure -(Figure3M,3M, a). A chromatin immunoprecipitation (ChIP) assay showed that TCF4 was enriched in the promoter region of LncCCAT1, which was significantly enriched in the spheroid cells (Figure -(Figure3M,3M, b & c). Furthermore, TCF4 overexpression or knockdown could increase or decrease the enrichment of TCF4 in the LncCCAT1 promoter region, respectively (Figure -(Figure3N).3N). Taken together, these data indicated that TCF4 could promote LncCCAT1 transcription, thus forming a positive feedback circuit in BCSCs.	31695775	RID07354	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367)	
Breast cancer	LncCCAT1	DNMT1	positively-E	luciferase reporter assay;RIP;overexpression	upregulation	microarray	GSE125677;GSE125678	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell stemness(+)	ceRNA(miR-148a)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000130816	NA	NA	1786	NA	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	As LncCCAT1 shares a miR-148a/152 response element with DNA methyltransferase 1 (DNMT1), a known target of miR-148a/152 15, and participates in tumor progression by methylating and silencing tumor suppressor genes, we investigated whether LncCCAT1 could upregulate DNMT1 through sequestration of miR-148a/152. The predicted target sites interactions among LncCCAT1, miR-148a/152 and DNMT1 3'-UTR are illustrated in Figure -Figure4G.4G. miR-148a/152 overexpression reduced DNMT1 protein levels, while miR-148a/152 knockdown increased DNMT1 protein levels in two breast cancer cell lines, in contrast to the effect of LncCCAT1 overexpression or knockdown on DNMT1 protein (Figure S3D, Figure -Figure44H).	31695775	RID07355	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	LncCCAT1	TRDMT1	positively-E	luciferase reporter assay;RIP;overexpression	upregulation	microarray	GSE125677;GSE125678	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell stemness(+)	ceRNA(miR-152)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000107614	NA	NA	1787	NA	DMNT2|DNMT2|MHSAIIP|PUMET|RNMT1	As LncCCAT1 shares a miR-148a/152 response element with DNA methyltransferase 1 (DNMT1), a known target of miR-148a/152 15, and participates in tumor progression by methylating and silencing tumor suppressor genes, we investigated whether LncCCAT1 could upregulate DNMT1 through sequestration of miR-148a/152. The predicted target sites interactions among LncCCAT1, miR-148a/152 and DNMT1 3'-UTR are illustrated in Figure -Figure4G.4G. miR-148a/152 overexpression reduced DNMT1 protein levels, while miR-148a/152 knockdown increased DNMT1 protein levels in two breast cancer cell lines, in contrast to the effect of LncCCAT1 overexpression or knockdown on DNMT1 protein (Figure S3D, Figure -Figure45H).	31695775	RID07356	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	UCA1	CDKN1A	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	qRT-PCR	GSE118897	NA	cell proliferation(+);cell migration(+);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulated UCA1 is associated with poor prognosis in gastric cancer patients. UCA1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.  RNA sequencing (RNA-seq) analysis revealed that UCA1 knockdown preferentially affected genes that are linked to cell proliferation, cell cycle, and cell migration.UCA1 promotes cell proliferation progression through repressing p21 and Sprouty RTK signaling antagonist 1 (SPRY1) expression by binding to EZH2.UCA1 could mediate the trimethylation of H3K27 in promoters of p21 and SPRY1.	31689615	RID07357	expression association	prognosis	UP(PAAD);DATA(GSE40174)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	UCA1	SPRY1	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	qRT-PCR	GSE118897	NA	cell proliferation(+);cell migration(+);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000164056	NA	652995	10252	CUDR|LINC00178|onco-lncRNA-36|UCAT1	hSPRY1	Upregulated UCA1 is associated with poor prognosis in gastric cancer patients. UCA1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.  RNA sequencing (RNA-seq) analysis revealed that UCA1 knockdown preferentially affected genes that are linked to cell proliferation, cell cycle, and cell migration.UCA1 promotes cell proliferation progression through repressing p21 and Sprouty RTK signaling antagonist 1 (SPRY1) expression by binding to EZH2.UCA1 could mediate the trimethylation of H3K27 in promoters of p21 and SPRY1.	31689615	RID07358	expression association	prognosis	UP(PAAD);DATA(GSE40174)	UP(PAAD);DATA(GSE40174)
Lung adenocarcinoma	LINC00467	CCND1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-20b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000110092	NA	84791	595	C1orf97|MGC14801	BCL1|D11S287E|PRAD1|U21B31	Linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells. Furthermore, we elucidated that linc00467 promoted CCND1 expression in lung cancer cells via functioning as a molecular sponge for miR-20b-5p.	31686834	RID07359	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	RPPH1	TUBB3	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell proliferation(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259001	GRCh38_14:20343048-20343685	ENSG00000198211	NA	85495	10381	H1RNA|RPPH1-1	beta-4|CFEOM3|CFEOM3A|FEOM3	LncRNA RPPH1 was significantly upregulated in CRC tissues, and the RPPH1 overexpression was associated with advanced TNM stages and poor prognosis. RPPH1 was found to promote CRC metastasis in vitro and in vivo. Mechanistically, RPPH1 induced epithelial-mesenchymal transition (EMT) of CRC cells via interacting with beta-III tubulin (TUBB3) to prevent its ubiquitination.	31685807	RID07360	interact with protein	metastasis,prognosis	DOWN(BRCA);DATA(GSE86978)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Hepatocellular carcinoma	CDKN2B-AS1	ARL2	positively-E	overexpression;miRNA.org;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	mitochondrial function(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000213465	NA	100048912	402	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	ARFL2	LncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells.overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects.lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP-ribosylationfactor-like 2) expression via sponging miR-199a-5p.	31670868	RID07361	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE38495,GSE111842,GSE51827)
Prostate cancer	AFAP1-AS1	miR-512-3p	negatively-E	RIP;luciferase reporter gene assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000272620	GRCh38_4:7754077-7778928	NA	NA	84740	NA	AFAP1-AS|AFAP1AS|MGC10981	NA	Normal myofibroblast stromal cell lines and human PCA cell lines,tumor specimens" up-regulated "AFAP1-AS1 is highly expressed in prostate cancer tissues and cell lines. The expression level of AFAP1-AS1 is correlated with histological grade and distant metastasis. The overall level of patients with high expression of AFAP1-AS1 is low, and their survival rate is relatively low. Silencing AFAP1-AS1 can significantly increase the proliferation and migration of prostate cancer cells. AFAP1-AS1 silencing induces cell cycle arrest at G0/G1 phase.	31669642	RID07362	ceRNA or sponge	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	
Head and neck squamous cell carcinoma	LINC00052	EGFR	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-608)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000146648	NA	145978	1956	FLJ31461|NCRNA00052|TMEM83	ERBB|ERBB1|ERRP	LINC00052 was upregulated in HNSCC tumors. High expression of LINC00052 was associated with poor prognosis. Gain and loss of function studies revealed that LINC00052 promoted HNSCC cell proliferation, migration and invasion. MiR -608 was predicted as an interacting microRNA of LINC00052 via bioinformatics analysis and was further validated through luciferase reporter assay and RNA -binding protein immunoprecipitation assay. Moreover, we demonstrated that LINC00052 sponged miR -608 to regulate the expression of epidermal growth factor receptor (EGFR ), thereby promoting HNSCC progression in vitro and in vivo.	31639333	RID07363	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	SNHG15	HDAC2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000196591	NA	285958	3066	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	KDAC2|RPD3|YAF1	Our research showed that up-regulation of SNHG15 was found in HCC and was related to aggressive behaviors in HCC patients. Moreover, knockdown of SNHG15 restrained HCC cell proliferation, migration and invasion. In addition, SNHG15 served as a molecular sponge for miR-490-3p. Further, miR-490-3p directly targets HDAC2. HDAC2 was involved in HCC progression by interacting with the SNHG15/miR-490-3p axis.	31636472	RID07364	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Breast cancer	LUCAT1	SOX2	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-7-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000181449	NA	100505994	6657	SCAL1|SCAT5	NA	Highly up-regulated in breast cancer tissues and cell lines. Over-expression of lnc-LUCAT1 enhanced cell proliferation, migration and invasion in breast cancer cell lines. Moreover, lnc-LUCAT1 was found to be a target of miR-7-5p. There was a negative correlation between lnc-LUCAT1 and miR-7-5p. The reduction of miR-7-5p was required in the augmentation of breast cancer development induced by lnc-LUCAT1 over-expression. In addition, SOX2 acted as a target of miR-7-5p. SOX2 was an oncogene in breast cancer through promoting cell proliferation, migration and invasion. The in vivo study confirmed the role of lnc-LUCAT1 in promoting tumor growth, accompanied with down-regulated SOX2 expression, whereas up-regulated miR-7-5p.	31635802	RID07365	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	E2F1	SNHG3	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000242125	GRCh38_1:28505980-28510892	1869	8420	RBBP3|RBP3	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	We detected the upregulated expression of SNHG3 in NSCLC tissues as well as cells.high-level of SNHG3 was associated with a low overall survival rate of patients with NSCLC.SNHG3 had a significantly positive effect on NSCLC cell proliferation and migration.SNHG3 was a predicted direct transcriptional target of E2F1. We observed that the transcriptional activation of SNHG3 could be induced by E2F1.The cotreatment with SB-431542, JSI-124, or JSI-124 + SB-431542 rescued the effects brought by the overexpression of SNHG3 on NSCLC cell proliferation, migration, and epithelial-mesenchymal transition process.	31602642	RID07366	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)
Urinary bladder cancer	LNMAT2	PROX1	positively-E	overexpression;RNA pull-down assay	upregulation	qRT-PCR	GSE106534;TCGA	NA	cell proliferation(+);cell metastasis(+);cell growth(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000265251	GRCh38_8:28505116-28505182	ENSG00000117707	NA	100422903	5629	hsa-mir-4288	NA	LNMAT2 overexpression correlated with BCa LN metastasis.BCa cell-secreted exosome-mediated lymphangiogenesis promoted LN metastasis in BCa in a VEGF-C-independent manner.LNMAT2 stimulated human lymphatic endothelial cell (HLEC) tube formation and migration in vitro and enhanced tumor lymphangiogenesis and LN metastasis in vivo.LNMAT2 was loaded to BCa cell-secreted exosomes by directly interacting with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1).Subsequently, exosomal LNMAT2 was internalized by HLECs and epigenetically upregulated prospero homeobox 1 (PROX1) expression by recruitment of hnRNPA2B1 and increasing the H3K4 trimethylation level in the PROX1 promoter, ultimately resulting in lymphangiogenesis and lymphatic metastasis.	31593555	RID07367	epigenetic regulation	metastasis		UP(LIHC);DOWN(PAAD);DATA(GSE117623,GSE40174)
Epithelial ovarian cancer	ERLNC1	KISS1	negatively-E	UCSC;RNA pull-down assay;IHC	upregulation	qRT-PCR;microarray	NA	NA	cell metastasis(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000170498	NA	101929441	3814	ElncRNA1|TC0101441	NA	TC0101441 levels were elevated in EOC tissues compared with those in normal controls and significantly correlated with an advanced clinical stage and lymph node metastasis. TC0101441 was determined to be an independent prognostic predictor of overall survival (OS) and disease-free survival (DFS). Furthermore, loss-of-function assays showed that TC0101441 promoted the invasive and metastatic capacities of EOC cells both in vitro and in vivo. Mechanistically, the prometastatic effects of TC0101441 were linked to the induction of epithelial-mesenchymal transition (EMT). Importantly, KiSS1 was identified as a downstream target gene of TC0101441 and was downregulated by TC0101441 in EOC cells. After TC0101441 was silenced, the corresponding phenotypes of EOC cell invasion and EMT were reversed by the overexpression of KiSS1.	31577838	RID07368	expression association	metastasis,prognosis		
Hepatocellular carcinoma	SNHG6	MYC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(let-7c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000136997	NA	641638	4609	HBII-276HG|NCRNA00058|U87HG	bHLHe39|c-Myc|MYCC	In the present study, we globally investigated the expression of SNHG6 in 31 cancer type, and we found that SNHG6 was highly expressed in various cancers, especially in HCC.	31563323	RID07369	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Ovarian cancer	LINC00339	ROCK1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-148a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000067900	NA	29092	6093	HSPC157|NCRNA00339	p160ROCK	LINC00339 was overexpressed in ovarian cancer tissues, showed a poor prognosis in patients with ovarian cancer, and correlated with tumor size and advanced clinical stages.	31550677	RID07370	ceRNA or sponge	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	ZFAS1	PLP2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);chemoresistance(+)	ceRNA(miR-150-5p)	regulation	NA	Temozolomide	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000102007	NA	441951	5355	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	A4|A4-LSB|MGC126187	The expression of ZFAS1 was upregulated in both glioma tissues and cell lines. Functional experiments revealed that ZFAS1 promoted glioma proliferation, migration and invasion, and increased resistance to temozolomide in vitro.	31535380	RID07371	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Cervical cancer	lncRNA-CTS	ZEB2	positively-E	western blot;luciferase reporter assay;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-505)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	NA	NA	ENSG00000169554	NA	NA	9839	NA	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	In vitro and in vivo experiments, along with gain- and loss-of-function studies, showed that lncRNA-CTS enhanced cell migration, invasion, and the transforming growth factor (TGF)-beta1-induced-EMT process. Data also showed that lncRNA-CTS could function as a competing endogenous RNA for miR-505 in CC cells. Further investigations disclosed that ZEB2 was demonstrated as a downstream target of miR-505, and subsequently exerted its metastatic effects via the lncRNA-CTS/miR-505/ZEB2 axis in CC cells. Finally, lncRNACTS activated the SMAD/TGF pathway via miR-505 in CC cells.	31499118	RID07372	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Non-small cell lung cancer	LINC01123	MYC	positively-E	luciferase reporter assay;ChIP;RIP	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+)	ceRNA(miR-199a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000204588	GRCh38_2:109987063-109996140	ENSG00000136997	NA	440894	4609	NA	bHLHe39|c-Myc|MYCC	Three hundred sixty-four differentially expressed genes were identified in RNA-seq assay, and LINC01123 was one of the most overexpressed lncRNAs. Further validation in expanded NSCLC cohorts confirmed that LINC01123 was upregulated in 92 paired NSCLC tissues and associated with poor survival. Functional assays showed that LINC01123 promoted NSCLC cell proliferation and aerobic glycolysis. Mechanistic investigations revealed that LINC01123 was a direct transcriptional target of c-Myc. Meanwhile, LINC01123 increased c-Myc mRNA expression by sponging miR-199a-5p. In addition, rescue experiments showed that LINC01123 functioned as an oncogene depending on miR-199a-5p and c-Myc.	31488218	RID07373	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Endometrial cancer	LINP1	PIK3CA	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000223784	GRCh38_10:6709530-6740532	ENSG00000121879	NA	108570035	5290	NA	PI3K	LINP1 was proved to be up-regulated in EC cell lines and tissues by qRT-PCRassay. CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that up-regulated LINP1 can facilitate cell migration and invasion. The results of western blot validated that LINP1 can activate PI3K/AKT signaling. Besides, the tumor formation assay verified that LINP1 can promote tumor formation in vivo. CONCLUSIONS: Our research validated that LINP1 served as an oncogenic role in EC progression. The PI3K/AKT signaling pathway might be the underlying mechanism of EC progression.	31486482	RID07374	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Endometrial cancer	LINP1	AKT1	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000223784	GRCh38_10:6709530-6740532	ENSG00000142208	NA	108570035	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	LINP1 was proved to be up-regulated in EC cell lines and tissues by qRT-PCRassay. CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that up-regulated LINP1 can facilitate cell migration and invasion. The results of western blot validated that LINP1 can activate PI3K/AKT signaling. Besides, the tumor formation assay verified that LINP1 can promote tumor formation in vivo. CONCLUSIONS: Our research validated that LINP1 served as an oncogenic role in EC progression. The PI4K/AKT signaling pathway might be the underlying mechanism of EC progression.	31486482	RID07375	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	LINC00958	YWHAZ	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000164924	NA	100506305	7534	NA	14-3-3-zeta|KCIP-1|YWHAD	Clinical investigation showed that LINC00958 overexpression was associated with poor prognosis, acting as an independent prognostic factor for OSCC. Loss- and gain-of-function assays indicated that LINC00958 promoted the proliferation, invasion and reduced the apoptosis of OSCC cells in vitro. In vivo, knockdown of LINC00958 repressed the tumor growth. Mechanistically, bioinformatic tools and luciferase reporter assay indicated that miR-185-5p both targeted the 3'-UTR of LINC00958 and YWHAZ, constructing the LINC00958/miR-185-5p/YWHAZ regulatory axis.	31442551	RID07376	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Pancreatic ductal adenocarcinoma	PRECSIT	CTCF	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000255874	GRCh38_13:110863987-110870330	ENSG00000102974	NA	283487	10664	C13orf29|LINC00346|NCRNA00346	CFAP108|FAP108	We first show that LINC00346 is highly expressed in pancreatic tumor specimens as compared to normal pancreatic tissue based on interrogation of The Cancer Genome Atlas (TCGA) pancreatic adenocarcinoma dataset. Of significance, this upregulation of LINC00346 is associated with overall survival (OS) and disease-free survival (DFS), respectively. We further show that knockout (KO) of LINC00346 impairs pancreatic cancer cell proliferation, tumorigenesis, migration, and invasion ability. Importantly, these phenotypes can be restored by LINC00346 re-expression in KO cells (i.e., rescue experiment). RNA precipitation assays combined with mass spectrometry analysis indicate that LINC00346 interacts with CCCTC-binding factor (CTCF), a known transcriptional repressor of c-Myc. This interaction between LINC00346 and CTCF prevents the binding of CTCF to c-Myc promoter, relieving the CTCF-mediated repression of c-Myc.	31391552	RID07377	transcriptional regulation	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Pancreatic ductal adenocarcinoma	PRECSIT	MYC	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000255874	GRCh38_13:110863987-110870330	ENSG00000136997	NA	283487	4609	C13orf29|LINC00346|NCRNA00346	bHLHe39|c-Myc|MYCC		31391552	RID07378	transcriptional regulation	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Cervical cancer	LINC01133	AHDC1	positively-E	starBase;luciferase reporter assay;RIP;RNA22;microT;PicTar;miRmap	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-4784)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000126705	NA	100505633	27245	lncRNA-PAGBC	DJ159A19.3|RP1-159A19.1	A considerably up-regulated expression of LINC01133 was unveiled. The results of CCK-8, trypan blue exclusion, EdU and transwell migration assays manifested the facilitating property of LINC01133 in cervical cancer. The epithelial-mesenchymal transition (EMT) was also exacerbated by LINCO1133. Apoptotic rate of cervical cancer cells was promoted after silencing LINCO1133. Mechanically, LINC01133 functioning as a ceRNA targeted miR-4784 to augment AHDC1 expression. Finally, LINCO1133/miR-4784 aggravated the malignant growth and aggressiveness and EMT of cervical cancer in an AHDC1-dependant way.	31390932	RID07379	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111065)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	CASC19	ZEB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-130b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000254166	GRCh38_8:127072694-127227541	ENSG00000169554	NA	103021165	9839	CARLo-6|LINC01245	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA CASC19 was upregulated in NSCLC tissues and cell lines. NSCLC patients with high expression of CASC19 presented a worse survival. Knockdown of CASC19 attenuated proliferative, migratory, and invasive capacities of A549 and PC9 cells. CASC19 sponged miRNA-130b-3p and negatively regulated its level. ZEB2 was the direct target of miRNA-130b-3p. The knockdown of miRNA-130b-3p reversed the regulatory effects of CASC19 on A549 and PC9 cells.	31389608	RID07380	ceRNA or sponge	NA	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Oral squamous cell carcinoma	FEZF1-AS1	miR-196a	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000230316	GRCh38_7:122303658-122310119	NA	NA	154860	NA	NA	NA	The results of qRT-PCRproved that the expression level of FEZF1-AS1 in OSCC tissues was significantly higher than that of para-carcinoma tissues, and the difference was statistically significant. The pathological stage was significantly higher in patients with highexpression FEZF1-AS1 than those with low-expression FEZF1-AS1, while the overall survival rate was remarkably lower. The proliferation ability of cells in FEZF1-AS1 silencing group declined significantly when compared with the NC group. Similarly, qRT-PCRresults verified that the expression of miR-196a in OSCC cell lines and tissues was significantly reduced as well. Meanwhile, the miR-196a expression was negatively correlated with FEZF1-AS1. Subsequent Luciferase reporter gene assay confirmed that overexpression of miR-196a could markedly reduce the activity of Luciferase containing wildtype FEZF1-AS1 vector rather than decrease the activity of Luciferase containing mutant-type vector or empty vector.	31378890	RID07381	ceRNA or sponge	NA		
Colorectal cancer	GLCC1	MYC	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+)	interact with protein;RNA stability	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	bHLHe39|c-Myc|MYCC	we identify a lncRNA, GLCC1, which is significantly upregulated under glucose starvation in CRC cells, supporting cell survival and proliferation by enhancing glycolysis. Mechanistically, GLCC1 stabilizes c-Myc transcriptional factor from ubiquitination by direct interaction with HSP90 chaperon and further specifies the transcriptional modification pattern on c-Myc target genes, such as LDHA, consequently reprogram glycolytic metabolism for CRC proliferation. Clinically, GLCC1 is associated with tumorigenesis, tumor size and predicts poor prognosis.	31375671	RID07382	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	PDPK2P	PDK1	positively-E	RNA pull-down assay	upregulation	microarray	NA	NA	cancer progression(+);PDK1/AKT/caspase 3 signaling pathway(+)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000205918	GRCh38_16:2616121-2643296	ENSG00000152256	NA	653650	5163	NA	NA	LncRNA-PDPK2P was highly expressed in HCC tissues with a distinct positive correlation between PDPK2P and PDK1, and the upregulation was clinically associated with a larger tumor embolus, low differentiation and poor survival. Mechanistically, lncRNA-PDPK2P interacted with PDK1, and promoted HCC progression through the PDK1/AKT/caspase 3 signaling pathway. lncRNA-PDPK2P can promote HCC progression, suggesting it may be a clinically valuable biomarker and serve as a molecular target for the diagnosis, prognosis and therapy of hepatocellular carcinoma.	31368655	RID07383	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Breast cancer	CASC2	CDK19	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-18a-5p)	regulation	NA	Paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000155111	NA	255082	23097	C10orf5	bA346C16.3|CDC2L6|CDK11|KIAA1028	CASC2 expression was increased in PTX-resistant clinical samples and cell lines. PTX induced CASC2 expression in a concentration-dependent manner. Downregulation of CASC2 increased PTX toxicity and decreased IC50 value, while upregulation of CASC2 decreased PTX toxicity and increased IC50 value in MCF-7/PTX and MDA-MB-231/PTX cells. Moreover, downregulation of CASC2 decreased tumor growth in xenograft mice implanted with MCF-7/PTX cells. miR-18a-5p possessed a putative binding site in 3'-UTR of CASC2 and cyclin-dependent kinase 19 (CDK19). In PTX-resistant breast cancer cells, miR-18a-5p expression was decreased. CASC2 and miR-18a-5p could negatively regulate the expression of each other. CDK19 expression could be negatively regulated by miR-18a-5p, but positively regulated by CASC2. miR-18a-5p mimics or downregulation of CDK19 decreased tumor growth in xenograft mice implanted with MCF-7/PTX cells.	31352515	RID07384	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	FAM225A	miR-590-3p	negatively-E	microarray;qPCR;western blot;luciferase reporter assay;knockdown;RIP	upregulation	microarray;qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000231528	GRCh38_9:113113042-113119928	NA	NA	286333	NA	C9orf109|DKFZp686A0127|LINC00256A|NCRNA00256A	NA	We identified 384 dysregulated lncRNAs, of which FAM225A was one of the most up-regulated lncRNAs in NPC. FAM225A significantly associated with poor survival in NPC. N(6)-methyladenosine (m6A) was highly enriched within FAM225A and enhanced its RNA stability. FAM225A functioned as an oncogenic lncRNA that promoted NPC cell proliferation, migration, invasion, tumor growth and metastasis. Mechanistically, FAM225A functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target integrin beta3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote NPC cell proliferation and invasion.	31331909	RID07385	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	
Nasopharynx carcinoma	FAM225A	MIR1275	negatively-E	microarray;qPCR;western blot;luciferase reporter assay;knockdown;RIP	upregulation	microarray;qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000231528	GRCh38_9:113113042-113119928	ENSG00000221697	NA	286333	100302123	C9orf109|LINC00256A|NCRNA00256A	MIRN1275|hsa-mir-1275|mir-1275	We identified 384 dysregulated lncRNAs, of which FAM225A was one of the most up-regulated lncRNAs in NPC. FAM225A significantly associated with poor survival in NPC. N(6)-methyladenosine (m6A) was highly enriched within FAM225A and enhanced its RNA stability. FAM225A functioned as an oncogenic lncRNA that promoted NPC cell proliferation, migration, invasion, tumor growth and metastasis. Mechanistically, FAM225A functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target integrin beta3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote NPC cell proliferation and invasion.	31331909	RID07386	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	
Nasopharynx carcinoma	FAM225A	ITGB3	positively-E	microarray;qPCR;western blot;luciferase reporter assay;knockdown;RIP	upregulation	microarray;qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);tumor growth(+);cell metastasis(+)	ceRNA(miR-590-3p/miR-1275)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000231528	GRCh38_9:113113042-113119928	ENSG00000259207	NA	286333	3690	C9orf109|DKFZp686A0127|LINC00256A|NCRNA00256A	CD61|GP3A|GPIIIa	We identified 384 dysregulated lncRNAs, of which FAM225A was one of the most up-regulated lncRNAs in NPC. FAM225A significantly associated with poor survival in NPC. N(6)-methyladenosine (m6A) was highly enriched within FAM225A and enhanced its RNA stability. FAM225A functioned as an oncogenic lncRNA that promoted NPC cell proliferation, migration, invasion, tumor growth and metastasis. Mechanistically, FAM225A functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target integrin beta3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote NPC cell proliferation and invasion.	31331909	RID07387	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE75367)
Laryngeal carcinoma	HOTTIP	miR-128-3p	negatively-E	qPCR;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	NA	HOTTIP was capable of positively modulating HOXA13 expression via the competitive binding to miR-128-3p.</AbstractText>: The research results manifested that the expression of HOTTIP in testicular tissues from Hypo patients was prominently reduced in comparison with that in control testicular tissues.	31328440	RID07388	ceRNA or sponge	NA		
Laryngeal carcinoma	HOTTIP	HOXA13	positively-E	qPCR;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	HOX1|HOX1J	HOTTIP was capable of positively modulating HOXA13 expression via the competitive binding to miR-128-3p.</AbstractText>: The research results manifested that the expression of HOTTIP in testicular tissues from Hypo patients was prominently reduced in comparison with that in control testicular tissues.	31328440	RID07389	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Malignant glioma	LINC00319	TAF1	negatively-E	qPCR;western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000147133	NA	284836	6872	C21orf125|FLJ38036|NCRNA00319|PRED49	BA2R|CCG1|CCGS|DYT3|DYT3/TAF1|KAT4|NSCL2|TAF2A|TAFII250	LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma. In addition, high expression of high mobility group AT-hook 2 (HMGA2) was found in glioma which was also in positive relation to LINC00319 expression. Moreover, LINC00319 directly bound to TATA-box binding protein associated factor 1 (TAF1) and further regulated HMGA2. Finally, rescue assays verified that LIN00319 modulated the tumorigenesis of glioma by regulating HMGA2.	31325436	RID07390	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	LINC00319	HMGA2	positively-E	qPCR;western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000149948	NA	284836	8091	C21orf125|FLJ38036|NCRNA00319|PRED49	BABL|HMGIC|LIPO	LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma. In addition, high expression of high mobility group AT-hook 2 (HMGA2) was found in glioma which was also in positive relation to LINC00319 expression. Moreover, LINC00319 directly bound to TATA-box binding protein associated factor 1 (TAF1) and further regulated HMGA2. Finally, rescue assays verified that LIN00319 modulated the tumorigenesis of glioma by regulating HMGA2.	31325436	RID07391	expression association	prognosis		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	LINC00205	miR-122-5p	negatively-E	qPCR;luciferase reporter assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000223768	GRCh38_21:45288035-45297806	NA	NA	642852	NA	NCRNA00205	NA	The expression of LINC00205 was dramatically up-regulated in HCC tissues compared to adjacent nontumor tissues. Furthermore, the level of LINC00205 in both Hep3B and Huh7 cells was prominently higher than that in normal hepatic cell line LO2. Notably, the high expression of LINC00205 was strongly correlated with tumor size <<- cm, venous infiltration and advanced tumor stages. Functionally, LINC00205 knockdown obviously repressed the proliferation, migration and invasion of Hep3B and Huh7 cells in vitro. An inverse correlation between LINC00205 and miR-122-5p was detected in HCC tissues. Interestingly, LINC00205 knockdown increased the level of miR-122-5p in both Hep3B and Huh7 cells. Mechanistically, luciferase reporter assay demonstrated LINC00205 acted as a competing endogenous RNA (ceRNA) by directly interacting with miR-122-5p. More importantly, miR-122-5p overexpression significantly restrained the proliferation, migration and invasion of HCC cells.	31272761	RID07392	interact with protein	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)	
Hepatocellular carcinoma	LINC01551	miR-122-5p	negatively-E	qPCR;western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);cell viability(+);cell cycle(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000186960	GRCh38_14:28765640-28823817	NA	NA	387978	NA	C14orf23	NA	High expression of LINC01551 and ADAM10 yet low-expression of miR-122-5p were revealed in HCC tissues and cells. Overexpression of miR-122-5p could downregulate ADAM10. Biological prediction websites and fluorescence in situ hybridization assay verified that LINC01551 was mainly expressed in the cytoplasm. Silencing LINC01551 reduced HCC cell viability, proliferation, migration, invasion, and cell cycle entry yet induce cell apoptosis. Upregulation of LINC01551 increased its ability of competitively binding to miR-122-5p, thus reducing miR-122-5p and upregulating ADAM10 expression, as well as promoting the proliferative, migrative, and invasive ability.	31270840	RID07393	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842)	
Hepatocellular carcinoma	LINC01551	ADAM10	positively-E	qPCR;western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);cell viability(+);cell cycle(+)	ceRNA(miR-122-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000186960	GRCh38_14:28765640-28823817	ENSG00000137845	NA	387978	102	C14orf23	CD156C|HsT18717|kuz|MADM	High expression of LINC01551 and ADAM10 yet low-expression of miR-122-5p were revealed in HCC tissues and cells. Overexpression of miR-122-5p could downregulate ADAM10. Biological prediction websites and fluorescence in situ hybridization assay verified that LINC01551 was mainly expressed in the cytoplasm. Silencing LINC01551 reduced HCC cell viability, proliferation, migration, invasion, and cell cycle entry yet induce cell apoptosis. Upregulation of LINC01551 increased its ability of competitively binding to miR-122-5p, thus reducing miR-122-5p and upregulating ADAM10 expression, as well as promoting the proliferative, migrative, and invasive ability.	31270840	RID07394	ceRNA or sponge	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Intrahepatic cholangiocarcinoma	UCA1	MIR122	negatively-E	qPCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000207778	NA	652995	406906	CUDR|LINC00178|onco-lncRNA-36|UCAT1	hsa-mir-122|hsa-mir-122a|miR-122|MIRN122|MIRN122A	UCA1 expression was significantly upregulated in ICC tissues and cell lines compared with that in the adjacent non-tumour tissues and a human intrahepatic biliary epithelial cell line, respectively. The increased expression of UCA1 was significantly associated with lymph node metastasis and clinical T-stage in ICC. Furthermore, the ICC patients with high expression of UCA1 had a shorter survival time when compared with that of patients with low UCA1 expression. Knockdown of UCA1 caused a significant decrease in ICC cell proliferation and invasion, while ectopic overexpression of UCA1 significantly promoted the proliferation and invasion of ICC cells. Furthermore, it was revealed that UCA1 directly binds to microRNA (miR)-122 to negatively regulate its expression in ICC cells. In addition, miR-122 mimics abrogated the promoting effects of UCA1 on ICC cell proliferation and invasion. In addition, an inverse correlation between miR-122 and UCA1 expression in ICC tissues was observed.	31258634	RID07395	interact with protein	metastasis	UP(PAAD);DATA(GSE40174)	
Glioblastoma	DLEU1	TRAF4	positively-E	RNAi;qPCR;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+);angiogenesis(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000076604	NA	10301	9618	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	CART1|MLN62|RNF83	Significant upregulation of lncRNA deleted in lymphocytic leukemia 1 (DLEU1) was revealed in GBM and a number of other types of cancer. DLEU1 interacted with 315 miRNAs and 105 DEmRNAs. The DEmRNAs were mainly enriched in tumorigenesis-associated GO terms (angiogenesis, positive regulation of cell proliferation, positive regulation of fibroblast apoptotic processes and regulation of neutrophil migration) and pathways (Hippo signaling pathway, cancer pathways, and Wnt signaling pathway). Correlation analysis revealed that mRNA TNF receptor associated factor 4 (TRAF4) was associated with DLEU1 expression. RT-PCRdemonstrated that the expression levels of DLEU1 and TRAF4 were increased in GBM tissues. Small interfering RNA demonstrated that silencing DLEU1 downregulated TRAF4. The viability of GBM cells was significantly decreased following RNA interference with DLEU1 and TRAF4 production.	31257517	RID07396	expression association	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE75367)
Gastric cancer	HOXA11-AS	SRSF1	positively-E	qPCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000136450	NA	221883	6426	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	Up-regulation of HOXA11-AS was found in GC tissues, cell lines, and serum samples. In GC patients, decreased serum HOXA11-AS levels were negatively related with tumor size, TNM stage, and lymph node metastasis. The area under the receiver operating characteristic curve of serum HOXA11-AS in the diagnosis of GC was 0.924 (95%CI: 0.881-0.967; sensitivity, 0.787; specificity 0.978). Results of the Kaplan-Meier survival curves suggested the GC patients with a lower HOXA11-AS level having a better overall survival rate. HOXA11-AS promoted GC cell proliferation and invasion. SRSF1 may be the target regulated by HOXA11-AS in GC cells.	31235999	RID07397	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	LINC00324	CFAP251	positively-E	qPCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000178977	GRCh38_17:8220624-8224043	ENSG00000158023	NA	284029	144406	C17orf44|FLJ34790|MGC104931|NCRNA00324	CaM-IP4|MGC33630|WDR66	The upregulation of LINC00324 in OS tissues and cell lines and established its correlation with OS tumor progression and metastasis. Importantly, the prognostic significance of LINC00324 was identified in patients with OS. Gain- and loss-of-function assays revealed that LINC00324 accelerated cell proliferation and migration in OS. Mechanistically, we revealed that LINC00324 stabilized WD repeat-containing protein 66 (WDR66) messenger RNA through interacting with Hu antigen R. Rescue assays verified that WDR66 was required for the regulation of LINC00324 in promoting proliferation and migration of OS cells.	31225659	RID07398	interact with protein	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Ovarian cancer	PVT1	miR-140	negatively-E	qPCR;luciferase reporter assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);metabolic process(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	PVT1 was the most amplifed gene in ovarian cancer patients, and it was highly correlated with poor survival outcomes. Knockdown of PVT1 caused decreased cell viability, metabolic activity, and smaller proportion of S-phase cells. PVT1 directly bound to miR-140 and acted as a microRNA sponge, while transcription of PVT1 was regulated by the transcription factor FOXO4.	31222482	RID07399	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Ovarian cancer	FOXO4	PVT1	positively-E	qPCR;luciferase reporter assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);metabolic process(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000184481	NA	ENSG00000249859	GRCh38_8:127794526-128187101	4303	5820	AFX1|MLLT7	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	PVT1 was the most amplifed gene in ovarian cancer patients, and it was highly correlated with poor survival outcomes. Knockdown of PVT1 caused decreased cell viability, metabolic activity, and smaller proportion of S-phase cells. PVT1 directly bound to miR-140 and acted as a microRNA sponge, while transcription of PVT1 was regulated by the transcription factor FOXO4.	31222482	RID07400	transcriptional regulation	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Tongue squamous cell carcinoma	THORLNC	IGF2BP1	positively-E	qPCR;western blot;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000159217	NA	100506797	10642	THOR	IMP-1	THOR and IGF2BP1 were dramatically upregulated in TSCC tissues. The expression of THOR is positively correlated with IGF2BP1 mRNA level. THOR mediated IGF2 expression via interacting with IGF2BP1, and affected the downstream MEK-ERK signaling pathway to regulate TSCC cells proliferation. THOR/IGF2BP1/IGF2-MEK-ERK axis regulated the proliferation of TSCC cells, implying that THOR would be a promising therapeutic target for TSCC patients.	31220513	RID07401	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	TP73-AS1	miR-103	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	NA	57212	NA	KIAA0495|PDAM	NA	TP73-AS1 expression in HCC samples was conspicuously enhanced compared with paracancerous tissues, and patients with a relatively high level of TP73-AS1 had a higher tumor stage and a lower overall survival rate. Meanwhile, the proliferation ability of cells in the sh-TP73- AS1 group was strikingly lower than that in the control group, while cell apoptosis showed the opposite trend. Besides, qRT-PCRresults indicated a negative correlation between microRNA-103 and TP73-AS1 in HCC tissue specimens. The results of the luciferase reporting assay revealed that TP73-AS1 could be targeted by microRNA-103 through binding site. In addition, the cell recovery experiment demonstrated that TP73-AS1 and microRNA-103 might have a mutual regulation, and the two of which could together affect the malignant progression of HCC."	31210297	RID07402	interact with protein	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Prostate cancer	PANDAR	ROCK1	positively-E	RT-qPCR;western blot	upregulation	RT-qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000067900	NA	101154753	6093	PANDA	p160ROCK	By comparison with PANDAR expression in adjacent tissues, PANDAR expression level was significantly higher in prostate cancer samples, which was closely associated with patients' disease-free survival time. Moreover, after PANDAR was upregulated, cell migration and cell invasion capacities of prostate cancer cells were enhanced in vitro. In addition, after overexpression of PANDAR, the mRNA and protein expression of ROCK1 was upregulated, respectively. Furthermore, it was found that ROCK1 expression was positively correlated to PANDAR expression in prostate cancer tissues.	31210296	RID07403	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	TTN-AS1	miR-4677-3p	negatively-E	qRT-PCR;luciferase reporter assay;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	TTN-AS1 was upregulated in tissues and cells of lung adenocarcinoma and associated with poor overall survival.TTN-AS1 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition in lung cancer.TTN-AS1 directly bound with miR-4677-3p and negatively regulated miR-4677-3p. MiR-4677-3p rescued the inhibitive impacts of TTN-AS1 knockdown on lung adenocarcinoma.TTN-AS1 drove the invasion and migration of lung adenocarcinoma cells by targeting the miR-4677-3p/ZEB1 axis.	31173403	RID07404	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Lung adenocarcinoma	TTN-AS1	ZEB1	positively-E	qRT-PCR;luciferase reporter assay;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-4677-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000148516	NA	100506866	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	TTN-AS1 was upregulated in tissues and cells of lung adenocarcinoma and associated with poor overall survival.TTN-AS1 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition in lung cancer.TTN-AS1 directly bound with miR-4677-3p and negatively regulated miR-4677-3p. MiR-4677-3p rescued the inhibitive impacts of TTN-AS1 knockdown on lung adenocarcinoma.TTN-AS1 drove the invasion and migration of lung adenocarcinoma cells by targeting the miR-4677-3p/ZEB1 axis.	31173403	RID07405	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00858	MIR3182	negatively-E	RT-PCR;luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000263785	NA	170425	100422853	CRCAL-2	mir-3182	Over-expression of linc00858 significantly promoted cell proliferation, invasion.linc00858 facilitated the EMT process.linc00858 can bind with miR-3182 directly. Linc00858 can negatively regulate the expression of miR-3182.MMP2 was the direct target of miR-3182.linc00858 functioned through miR-3182/MMP2 axis.	31131637	RID07406	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Lung cancer	LINC00858	MMP2	positively-E	RT-PCR;luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-3182)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000087245	NA	170425	4313	CRCAL-2	CLG4|CLG4A|TBE-1	Over-expression of linc00858 significantly promoted cell proliferation, invasion.linc00858 facilitated the EMT process.linc00858 can bind with miR-3182 directly. Linc00858 can negatively regulate the expression of miR-3182.MMP2 was the direct target of miR-3182.linc00858 functioned through miR-3182/MMP2 axis.	31131637	RID07407	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Lung adenocarcinoma	HCP5	miR-203	negatively-E	qRT-PCR;knockdown;western blot;Chromatin immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000207568	NA	10866	NA	D6S2650E|P5-1	NA	HCP5 is induced by TGFbeta and transcriptionally regulated by SMAD3, which promotes LUAD tumor growth and metastasis. Moreover, HCP5 is overexpressed in tumor tissues of patients with LUAD, specifically in patients with EGFR and KRAS mutations and current smoker. HCP5 high expression level is positively correlated with poor prognosis of patients with LUAD. Finally, upregulation of HCP5 increases the expression of Snail and Slug by sponging the microRNA-203 (miR-203) and promoting epithelial-mesenchymal transition (EMT) in LUAD cells.	31131047	RID07408	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Lung adenocarcinoma	SMAD3	HCP5	positively-E	qRT-PCR;knockdown;western blot;Chromatin immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000166949	NA	ENSG00000206337	GRCh38_6:31463170-31478936	4088	10866	HsT17436|JV15-2|MADH3	D6S2650E|P5-1	HCP5 is induced by TGFbeta and transcriptionally regulated by SMAD3, which promotes LUAD tumor growth and metastasis. Moreover, HCP5 is overexpressed in tumor tissues of patients with LUAD, specifically in patients with EGFR and KRAS mutations and current smoker. HCP5 high expression level is positively correlated with poor prognosis of patients with LUAD. Finally, upregulation of HCP5 increases the expression of Snail and Slug by sponging the microRNA-203 (miR-203) and promoting epithelial-mesenchymal transition (EMT) in LUAD cells.	31131047	RID07409	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic neuroendocrine tumor	H19	VGF	positively-E	qRT-PCR;RNA-seq;western blot;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+);	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000128564	NA	283120	7425	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	SCG7|SgVII	H19 was significantly upregulated in pNEN tissues with malignant behaviors, and the upregulation predicted poor prognosis in pNENs.H19 overexpression promoted tumor growth and metastasis, whereas H19 knockdown led to the opposite phenotypes.H19 interacted with VGF, which was significantly upregulated in pNENs, and higher VGF expression was markedly related to poor differentiation and advanced stage.Furthermore, VGF was downregulated when H19 was knocked down, and VGF promoted cell proliferation, migration and invasion.H19 activated PI3K/AKT/CREB signaling and promoted pNEN progression by interacting with VGF.	31117050	RID07410	expression association	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	
Prostate cancer	lncAPP	miR-218	negatively-E	qRT-PCR;luciferase reporter assay;western blot;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	lncAPP enhanced cell proliferation and promoted migration and invasion.Upregulation of lncAPP promoted cell migration and invasion via competitively binding miR218 to facilitate ZEB2/CDH2 expression.lncAPP/miR218 axis plays a critical role in PCa progression.	31107971	RID07411	ceRNA or sponge	NA		
Prostate cancer	lncAPP	ZEB2/CDH2	positively-E	qRT-PCR;luciferase reporter assay;western blot;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	lncAPP enhanced cell proliferation and promoted migration and invasion.Upregulation of lncAPP promoted cell migration and invasion via competitively binding miR218 to facilitate ZEB2/CDH2 expression.lncAPP/miR218 axis plays a critical role in PCa progression.	31107971	RID07412	ceRNA or sponge	NA		
Uterine fibroid	H19	MED12/HMGA2	positively-E	qRT-PCR;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	DNA methylation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Uterine fibroid	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Expression levels of GASL1 in prostate tissues and sera from patients with PC and from healthy subjects were detected.GASL1 was significantly downregulated in the tissue and serum of patients with PC compared to those of healthy subjects. In addition, GASL1 was used to distinguish patients with PC from healthy controls, and low expression levels of GASL1 were associated with short survival time. Expression levels of GASL1 were significantly associated with tumor size. GASL1 overexpression inhibited PC cell growth. Overexpression of GASL1 upregulated Bcl-2 expression and downregulated GLUT-1 expression.	31089260	RID07413	epigenetic regulation	NA	UP(NSCLC);DATA(GSE74639)	
Malignant glioma	BLACAT1	Wnt/beta-catenin	positively-E	RT-qPCR;western blot;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	LINC00912|linc-UBC1|onco-lncRNA-30	NA	BLACAT1 was overexpressed in glioma tissues and cell lines. High BLACAT1 expression was correlated with high tumor grade in glioma patients. Functional assays determined that BLACAT1 promoted glioma cell proliferation, migration, invasion and epithelial-mesenchymal transition in vitro. In addition, it was demonstrated that BLACAT1 activated the Wnt/beta-catenin signaling pathway.	31086604	RID07414	expression association	NA		
Laryngeal squamous cell carcinoma	miR-140	SNHG20	negatively-E	qPCR;luciferase reporter assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	miRNA	lncRNA	NA	NA	ENSG00000234912	GRCh38_17:77086716-77099902	NA	654434	NA	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	The SNHG20 expression in LSCC tissues or cells remarkably increased than controls, and the difference was statistically significant.The LSCC patients with the high expression level of SNHG20 were more likely to develop advanced tumor compared with patients with low expression of SNHG20. Moreover, the LSCC patients with the high expression level of SNHG20 had a shorter overall survival than those with low level.The cell proliferation ability significantly decreased in the SNHG20 knockdown group, while notably increased in SNHG20 overexpression group.MiR-140 was negatively correlated with SNHG20 in LSCC tissues and cells. SNHG20 could be targeted by miR-140 through a certain binding site. There was a mutual regulation between SNHG20 and miR-140, which could together affect the malignant progression of LSCC.	31081112	RID07415	interact with protein	NA		UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)
Lung cancer	MSTO2P	EZH2	positively-E	qRT-PCR;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell autophagy(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203761	GRCh38_1:155745829-155750137	ENSG00000106462	NA	100129405	2146	MSTO2	ENX-1|EZH1|KMT6|KMT6A	MSTO2P expression in LCa tissues was remarkably higher than that in adjacent tissues.Meanwhile, compared with human bronchial epithelial cells, the level of MSTO2P was remarkably up-regulated in LCa cells. After down-regulating MSTO2P, the cell proliferation ability was weakened, and the protein levels of autophagy-related genes including Agt5, LC-3I, and LC-3II were remarkably down-regulated.MSTO2P promotes LCa cell proliferation and autophagy by up-regulating EZH2.	31081092	RID07416	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Osteosarcoma	ZFAS1	MIR646	negatively-E	qRT-PCR;luciferase reporter assay;western blot;knockdown	upregulation	qRT-PCR	NA	NA	colony formation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000207802	NA	441951	693231	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	MIRN646|hsa-mir-646	ZFAS1 was up-regulated in OS cells and promoted the colony formation, migration, and invasion of OS cells via activating the MAPK signaling pathway.Furthermore, miR-646 was a target of ZFAS1 and there was a negative relationship between ZFAS1 and miR-646 expression.ZFAS1 in OS cells up-regulated the expression of NOB1 through sponging miR-646, finally facilitating the growth of the OS cells.	31081072	RID07417	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Osteosarcoma	ZFAS1	NOB1	positively-E	qRT-PCR;luciferase reporter assay;western blot;knockdown	upregulation	qRT-PCR	NA	NA	colony formation(+);cell migration(+);cell invasion(+)	ceRNA(miR-646)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000141101	NA	441951	28987	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	ART-4|MST158|NOB1P|PSMD8BP1	ZFAS1 was up-regulated in OS cells and promoted the colony formation, migration, and invasion of OS cells via activating the MAPK signaling pathway.Furthermore, miR-646 was a target of ZFAS1 and there was a negative relationship between ZFAS1 and miR-646 expression.ZFAS1 in OS cells up-regulated the expression of NOB1 through sponging miR-646, finally facilitating the growth of the OS cells.	31081072	RID07418	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE75367,GSE86978)
Pituitary adenoma	RPSAP52	miR-15a/15b/16	negatively-E	qRT-PCR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Endocrine system disease	Pituitary adenoma	lncRNA	miRNA	ENSG00000241749	GRCh38_12:65758020-65826997	NA	NA	204010	NA	NA	NA	RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues.RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2.RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle.	31076808	RID07419	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Pituitary adenoma	RPSAP52	HMGA2	positively-E	qRT-PCR;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-15a/15b/16)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Endocrine system disease	Pituitary adenoma	lncRNA	TF	ENSG00000241749	GRCh38_12:65758020-65826997	ENSG00000149948	NA	204010	8091	NA	BABL|HMGIC|LIPO	RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues.RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2.RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle.	31076808	RID07420	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Head and neck squamous cell carcinoma	LINC00460	miR-206	negatively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell autophagy(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	LINC00460 and STC2 were highly expressed while miR-206 was poorly expressed in HNSCC. Besides, miR-206 was found to bind to both LINC00460 and STC2. After the transfection of HNSCC cells with miR-206 mimic or si-LINC00460, the expression of STC2, AKT, ERK, as well as the extent of AKT, ERK phosphorylation all decreased, which facilitated the apoptosis and autophagy of HNSCC cells.	31075234	RID07421	interact with protein	NA		
Head and neck squamous cell carcinoma	LINC00460	STC2	positively-E	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell autophagy(+)	NA	association	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000113739	NA	728192	8614	NA	STC-2	LINC00460 and STC2 were highly expressed while miR-206 was poorly expressed in HNSCC. Besides, miR-206 was found to bind to both LINC00460 and STC2. After the transfection of HNSCC cells with miR-206 mimic or si-LINC00460, the expression of STC2, AKT, ERK, as well as the extent of AKT, ERK phosphorylation all decreased, which facilitated the apoptosis and autophagy of HNSCC cells.	31075234	RID07422	expression association	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Glioblastoma	HOXB13	HOXC-AS3	positively-E	qRT-PCR;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000159184	NA	ENSG00000251151	GRCh38_12:53981509-53985519	10481	100874365	NA	NA	HOXB13 was highly expressed in GBM tissues. Furthermore, we showed that high-level expression of HOXB13 in GBM was associated with worse survival, suggesting that HOXB13 could be a prognostic marker for patients with GBM. GBM cells U87 and U251 overexpressing HOXB13 showed enhanced proliferation, migration, and invasion relative to the control cells, while knockdown of HOXB13 led to decreased cell proliferation, migration, and invasion abilities. In addition, dual-luciferase report assay, chromatin immunoprecipitation assay, and quantitative real-time polymerase chain reaction data showed that HOXB13 directly bound to HOXC-AS3 promoter. HOXC-AS3 was involved in HOXB13-induced proliferation, migration, and invasion of GBM cells.	31062400	RID07423	transcriptional regulation	prognosis	UP(PAAD);DATA(GSE40174)	
Glioblastoma	LNCARSR	miR-20b-3p	negatively-E	qRT-PCR;luciferase reporter assay;western blot;RIP;knockdown	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000233086	GRCh38_9:79505804-79567802	NA	NA	102723932	NA	lnc-TALC	NA	lnc-TALC correlated with TMZ resistance via competitively binding miR-20b-3p to facilitate c-Met expression.A phosphorylated AKT/FOXO3 axis regulated lnc-TALC expression in TMZ-resistant GBM cells.Furthermore, lnc-TALC increased MGMT expression by mediating the acetylation of H3K9, H3K27 and H3K36 in MGMT promoter regions through the c-Met/Stat3/p300 axis.lnc-TALC is required for TMZ resistance and GBM recurrence.Transfection of constitutively active FOXO3 significantly downregulated lnc-TALC levels in TMZ-resistant cells, whereas DNA-binding domain-truncated mutants (FOXO3-Mut) had no effect on lnc-TALC levels.	31053733	RID07424	ceRNA or sponge	recurrence,chemoresistance		
Glioblastoma	LNCARSR	c-Met	positively-E	qRT-PCR;luciferase reporter assay;western blot;RIP;knockdown	downregulation	qRT-PCR	TCGA	NA	chemoresistance(+)	ceRNA(miR-20b-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000105976	NA	102723932	NA	lnc-TALC	NA	lnc-TALC correlated with TMZ resistance via competitively binding miR-20b-3p to facilitate c-Met expression.A phosphorylated AKT/FOXO3 axis regulated lnc-TALC expression in TMZ-resistant GBM cells.Furthermore, lnc-TALC increased MGMT expression by mediating the acetylation of H3K9, H3K27 and H3K36 in MGMT promoter regions through the c-Met/Stat3/p300 axis.lnc-TALC is required for TMZ resistance and GBM recurrence.Transfection of constitutively active FOXO3 significantly downregulated lnc-TALC levels in TMZ-resistant cells, whereas DNA-binding domain-truncated mutants (FOXO3-Mut) had no effect on lnc-TALC levels.	31053733	RID07425	ceRNA or sponge	recurrence,chemoresistance		
Papillary thyroid carcinoma	MCM3AP-AS1	miR-211-5p	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000215424	GRCh38_21:46229196-46259390	NA	NA	114044	NA	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	NA	In papillary thyroid cancer, MCM3AP-AS1 was upregulated, while miR-211 was downregulated. MCM3AP-AS1 overexpression promoted papillary thyroid cancer proliferation, migration, and invasion. Further, MCM3AP-AS1 was shown to be negatively correlated with miR-211-5p. We next validated that miR-211-5p overexpression could reverse the promoting role of MCM3AP-AS1 in papillary thyroid cancer, whereby SPARC plays an important regulating role. In vivo, we confirmed the anti-tumor role of MCM3AP-AS1 silencing and the close relation among MCM3AP-AS1, miR-211-5p, and SPARC.	31030335	RID07426	interact with protein	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	
Papillary thyroid carcinoma	MCM3AP-AS1	SPARC	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-211-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000113140	NA	114044	6678	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	BM-40|ON|ONT	In papillary thyroid cancer, MCM3AP-AS1 was upregulated, while miR-211 was downregulated. MCM3AP-AS1 overexpression promoted papillary thyroid cancer proliferation, migration, and invasion. Further, MCM3AP-AS1 was shown to be negatively correlated with miR-211-5p. We next validated that miR-211-5p overexpression could reverse the promoting role of MCM3AP-AS1 in papillary thyroid cancer, whereby SPARC plays an important regulating role. In vivo, we confirmed the anti-tumor role of MCM3AP-AS1 silencing and the close relation among MCM3AP-AS1, miR-211-5p, and SPARC.	31030335	RID07427	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	UP(LIHC,PRAD,PAAD,SKCM,BRCA);DOWN(PRAD);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE86978)
Breast cancer	MAFG-DT	miR-339-5p	negatively-F	qRT-PCR;luciferase reporter assay;weatern blot	upregulation	qRT-PCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000265688	GRCh38_17:81927829-81930753	NA	NA	92659	NA	MAFG-AS1	NA	The level of lncRNA MAFG-AS1 is higher in breast carcinoma, and the aggressive phenotypes of breast carcinoma cell are enhanced by MAFG-AS1 transfection.MAFG-AS1 overexpression reduces the expression of miR-339-5p and miR-339-5p is the target of MAFG-AS1 in breast carcinoma.MMP15 is the functional regulated gene of miR-339-5p in breast carcinoma. The aggressiveness of breast carcinoma induced by lncRNA MAFG-AS1 is weakened by the miR-339-5p.Finally, the development of breast carcinoma cell is enhanced by MAFG-AS1 in vivo.	31002134	RID07428	interact with protein	NA		
Breast cancer	MAFG-DT	MMP15	positively-E	qRT-PCR;luciferase reporter assay;weatern blot	upregulation	qRT-PCR	NA	NA	cell invasion(+)	ceRNA(miR-339-5p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000265688	GRCh38_17:81927829-81930753	ENSG00000102996	NA	92659	4324	MAFG-AS1	MT2-MMP|MTMMP2|SMCP-2	The level of lncRNA MAFG-AS1 is higher in breast carcinoma, and the aggressive phenotypes of breast carcinoma cell are enhanced by MAFG-AS1 transfection.MAFG-AS1 overexpression reduces the expression of miR-339-5p and miR-339-5p is the target of MAFG-AS1 in breast carcinoma.MMP15 is the functional regulated gene of miR-339-5p in breast carcinoma. The aggressiveness of breast carcinoma induced by lncRNA MAFG-AS1 is weakened by the miR-339-5p.Finally, the development of breast carcinoma cell is enhanced by MAFG-AS1 in vivo.	31002134	RID07429	ceRNA or sponge	NA		UP(PAAD);DATA(GSE40174)
Colon cancer	LINC00504	MYC	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell migration(+);cell viability(+);	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000248360	GRCh38_4:14470465-14888169	ENSG00000136997	NA	201853	4609	NA	bHLHe39|c-Myc|MYCC	The lncRNA LINC00504 was markedly upregulated in colon cancer cell lines and specimens. LINC00504 increases viability and migration of colon cells in vitro. Furthermore, LINC00504 also enhances colon cancer xenograft tumors in vivo. We noted that LINC00504 regulates metabolism at a transcriptional level which influences multiple metabolic pathways, such as glucose metabolism, pentose phosphate pathway, and tricarboxylic acid cycle. Mechanistic study showed that LINC00504 could interact with c-Myc to promote chromatin recruitment of c-Myc and enhance its transactivation activity.	30998289	RID07430	expression association	NA	DOWN(LIHC);UP(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Pituitary adenoma	HULC	miR-130b	negatively-E	qRT-PCR;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);PI3K/AKT/mTOR signaling pathway(+);JAK1/STAT3 signaling pathway(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Evading Apoptosis	Endocrine system disease	Pituitary adenoma	lncRNA	miRNA	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	HULC was highly expressed in GH3 cells. Overexpression of HULC promoted GH3 cell viability, migration, invasion, PRL and GH secretion, as well as activated PI3K/AKT/mTOR and JAK1/STAT3 pathways. Knockdown of HULC had opposite effects and induced cell apoptosis. HULC negatively regulated the expression of miR-130b, and miR-130b participated in the effects of HULC on GH3 cells. FOXM1 was a target gene of miR-130b, which was involved in the regulation of GH3 cell viability, migration, invasion, and apoptosis, as well as PI3K/AKT/mTOR and JAK1/STAT3 pathways.	30994730	RID07431	interact with protein	NA		
Pituitary adenoma	HULC	FOXM1	positively-E	qRT-PCR;western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);PI3K/AKT/mTOR signaling pathway(+);JAK1/STAT3 signaling pathway(+);apoptosis process(-)	ceRNA(miR-130b)	regulation	NA	NA	NA	Evading Apoptosis	Endocrine system disease	Pituitary adenoma	lncRNA	TF	ENSG00000251164	NA	ENSG00000111206	NA	728655	2305	HCCAT1|LINC00078|NCRNA00078	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	HULC was highly expressed in GH3 cells. Overexpression of HULC promoted GH3 cell viability, migration, invasion, PRL and GH secretion, as well as activated PI3K/AKT/mTOR and JAK1/STAT3 pathways. Knockdown of HULC had opposite effects and induced cell apoptosis. HULC negatively regulated the expression of miR-130b, and miR-130b participated in the effects of HULC on GH3 cells. FOXM1 was a target gene of miR-130b, which was involved in the regulation of GH3 cell viability, migration, invasion, and apoptosis, as well as PI3K/AKT/mTOR and JAK1/STAT3 pathways.	30994730	RID07432	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Colorectal cancer	SNHG16	miR-200a-3p	negatively-E	qRT-PCR;luciferase reporter assay;RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	In the present study, SNHG16 was significantly up-regulated in CRC tissues and cell lines. Gain- and loss-of-function of SNHG16 further presented that SNHG16 promoted the progression of CRC cells, including proliferation, migration, and invasion. Further, in vivo study also revealed that overexpression of SNHG16 could promote tumor growth. Bioinformatics analysis and luciferase reporter assay showed that SNHG16 was a direct target of miR-200a-3p. MiR-200a-3p was inversely correlated with SNHG16 expression in CRC tissues. In brief, the above results elucidate the important role of SNHG16 in CRC tumorigenesis, suggesting that SNHG16 might be quite vital for the diagnosis and development of CRC.	30962265	RID07433	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Epithelial ovarian cancer	TPT1-AS1	miR-324-5p	negatively-E	qPCR;luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000170919	GRCh38_13:45341345-45417975	NA	NA	100190939	NA	NA	NA	TPT1-AS1 expression in metastatic EOC tissue was significantly higher than that in paired primary EOC tissue and nonmalignant ovarian tissue (P < 0.05). For instance, the expression of the lncRNA human ovarian cancer-specific transcript 2 (HOST2) was found to be upregulated in EOC tissue, promoting cell proliferation and metastasis by sponging miRNA let-7b.	30941821	RID07434	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	
Epithelial ovarian cancer	TPT1-AS1	CERNA2	positively-E	qPCR;luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-324-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000170919	GRCh38_13:45341345-45417975	ENSG00000285972	NA	100190939	642934	NA	HOST2	TPT1-AS1 expression in metastatic EOC tissue was significantly higher than that in paired primary EOC tissue and nonmalignant ovarian tissue (P < 0.05). For instance, the expression of the lncRNA human ovarian cancer-specific transcript 2 (HOST2) was found to be upregulated in EOC tissue, promoting cell proliferation and metastasis by sponging miRNA let-7b.	30941821	RID07435	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	LINC01980	GADD45A	positively-E	qPCR;microarray;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell cycle(+);apoptosis process(-);	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000225548	GRCh38_3:27797552-27931579	ENSG00000116717	NA	105377007	1647	NA	DDIT1|GADD45	In this study, we identified a novel lncRNA LINC01980, located in both the cytoplasm and nucleus, which was significantly upregulated in esophageal squamous cell carcinoma (ESCC) tissues through microarray profiling. Further analysis revealed that LINC01980 overexpression was positively correlated with deeper invasion of cancer, positive lymph node metastasis, and advanced TNM stage. Additionally, high LINC01980 expression in ESCC tissues was associated with poor prognosis. In vitro and in vivo experiments demonstrated that LINC01980 promoted ESCC growth. EdU incorporation assay implied that LINC01980 accelerated ESCC proliferation. Flow cytometry analysis showed that knockdown of LINC01980 induced cell cycle arrest and increased apoptosis. microarray analysis indicated that LINC01980 upregulated the expression of growth arrest and DNA damage inducible 45 alpha (GADD45A). Further experiments demonstrated that GADD45A promoted ESCC cell growth, indicating that GADD45A may be a downstream target of LINC01980. In conclusion, this study identified LINC01980 as a novel potential oncogene in ESCC, which can be a promising biomarker for prognosis and therapeutic targeting in ESCC.	30935686	RID07436	expression association	metastasis,prognosis	UP(PRAD);DATA(GSE104209)	UP(LIHC,PAAD,PRAD);DOWN(SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Nasopharynx carcinoma	LINC01116	MYC	positively-F	RNA pull-down assay;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell viability(+);cell proliferation(+);cell migration(+);	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000136997	NA	375295	4609	TALNEC2	bHLHe39|c-Myc|MYCC	LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity.Here, we found that LINC01116 was highly expressed in NPC cell lines, and inhibition of LINC01116 notably restrained cell viability, proliferation, and migration in NPC cells.Surprisingly, the cytoplasmic LINC01116 could directly interact with the 5'UTR of MYC mRNA, whereas such interaction had no influence on MYC mRNA expression, but facilitated MYC mRNA translation so as to enhance MYC protein level in NPC cells.Moreover, LINC01116 per se had no impact on the transcription of MYC targets but affected their expression through MYC-dependent manner.	31703161	RID07437	transcriptional regulation	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Breast cancer	CERS6-AS1	CERS6	positively-E	RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	interact with protein	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000227617	GRCh38_2:168771951-168786961	ENSG00000172292	NA	100861402	253782	NA	LASS6	Long noncoding RNA CERS6-AS1 functions as a malignancy promoter in breast cancer by binding to IGF2BP3 to enhance the stability of CERS6 mRNA.In this study, it was discovered that CERS6-AS1 was overexpressed in BC tissues and cells.Moreover, molecular mechanism exploration uncovered that there was a positive association between CERS6 and CERS6-AS1 (or IGF2BP3) expression in BC.Furthermore, IGF2BP3 serves as a RNA-binding protein for CERS6-AS1 and CERS6-AS1 promoted CERS6 mRNA stability by binding to IGF2BP3.Taken together, these evidences suggested that CERS6-AS1 promoted the progression of BC by binding to IGF2BP3 and thus enhancing the stability of CERS6 mRNA, providing a new underlying therapeutic target for BC to improve prognosis.	31701672	RID07438	interact with protein	prognosis	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842)	DOWN(PRAD,PAAD,SKCM);DATA(GSE104209,GSE60407,GSE38495)
Lung cancer	HOTAIR	PDPK1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-214-3p)	regulation	NA	Solamargine	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000140992	NA	100124700	5170	HOXC-AS4|HOXC11-AS1|NCRNA00072	PDK1	Novel reciprocal interaction of lncRNA HOTAIR and miR-214-3p contribute to the solamargine-inhibited PDPK1 gene expression in human lung cancer.Solamargine (SM) has been shown to have anti-cancer properties.We showed that SM inhibited the growth of non-small cell lung cancer (NSCLC) cells, which was enhanced in cells with silencing of long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), while it overcame by overexpression of HOTAIR.Intriguingly, HOTAIR could directly bind to miR-214-3p and sequestered miR-214-3p from the target gene PDPK1.HOTAIR effectively acted as a competing endogenous RNA (ceRNA) to stimulate the expression of target gene PDPK1.	31475459	RID07439	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Malignant melanoma	PEG10	Cyclin D1	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	23089	NA	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	Declination of long noncoding RNA paternally expressed gene 10 inhibits A375 cells proliferation, migration, and invasion via mediating microRNA-33a.We found that the enhancement of PEG10 was discovered in melanoma tissues compared to related nonmelanoma tissues.Declination of PEG10 frustrated cell viability, repressed cyclinD1 and CDK4 expression, and triggered apoptosis, as well as suppressed migration and invasion in A375 cells.A negative correction between PEG10 and miR-33a was confirmed, and repressed miR-33a inverted the functions of PEG10 repression in A375 cells.In addition, PEG10 repression discouraged the activation of PI3K/AKT and mTOR pathways via elevation of miR-33a.	31318088	RID07440	expression association	NA		
Malignant melanoma	PEG10	CDK4	positively-E	western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000242265	GRCh38_7:94656325-94669695	ENSG00000135446	NA	23089	1019	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	PSK-J3	Declination of long noncoding RNA paternally expressed gene 10 inhibits A375 cells proliferation, migration, and invasion via mediating microRNA-33a.We found that the enhancement of PEG10 was discovered in melanoma tissues compared to related nonmelanoma tissues.Declination of PEG10 frustrated cell viability, repressed cyclinD1 and CDK4 expression, and triggered apoptosis, as well as suppressed migration and invasion in A375 cells.A negative correction between PEG10 and miR-33a was confirmed, and repressed miR-33a inverted the functions of PEG10 repression in A375 cells.In addition, PEG10 repression discouraged the activation of PI3K/AKT and mTOR pathways via elevation of miR-33a.	31318088	RID07441	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Malignant melanoma	PEG10	miR-33a	negatively-E	western blot	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+);mTOR signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	23089	NA	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	Declination of long noncoding RNA paternally expressed gene 10 inhibits A375 cells proliferation, migration, and invasion via mediating microRNA-33a.We found that the enhancement of PEG10 was discovered in melanoma tissues compared to related nonmelanoma tissues.Declination of PEG10 frustrated cell viability, repressed cyclinD1 and CDK4 expression, and triggered apoptosis, as well as suppressed migration and invasion in A375 cells.A negative correction between PEG10 and miR-33a was confirmed, and repressed miR-33a inverted the functions of PEG10 repression in A375 cells.In addition, PEG10 repression discouraged the activation of PI3K/AKT and mTOR pathways via elevation of miR-33a.	31318088	RID07442	ceRNA or sponge	NA		
Breast cancer	PANDAR	MMP2	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000087245	NA	101154753	4313	PANDA	CLG4|CLG4A|TBE-1	Inhibition of lncRNA PANDAR reduces cell proliferation, cell invasion and suppresses EMT pathway in breast cancer.The expression of lncRNA PANDAR in 65 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR assay.The western blotwas also performed to detected the EMT related makers expression of E-cadherin, Vimentin, MMP2 and MMP9.Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP9 expression, but upregulating E-cadherin expression in breast cancer.Our results proved that PANDAR may serve as potential target of breast cancer treatment.	31104011	RID07443	expression association	NA	UP(SKCM);DATA(GSE38495)	UP(PAAD);DATA(GSE40174)
Breast cancer	PANDAR	MMP9	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000100985	NA	101154753	4318	PANDA	CLG4B	Inhibition of lncRNA PANDAR reduces cell proliferation, cell invasion and suppresses EMT pathway in breast cancer.The expression of lncRNA PANDAR in 65 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR assay.The western blotwas also performed to detected the EMT related makers expression of E-cadherin, Vimentin, MMP2 and MMP9.Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP10 expression, but upregulating E-cadherin expression in breast cancer.Our results proved that PANDAR may serve as potential target of breast cancer treatment.	31104011	RID07444	expression association	NA	UP(SKCM);DATA(GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	PANDAR	Vimentin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	NA	NA	101154753	NA	PANDA	NA	Inhibition of lncRNA PANDAR reduces cell proliferation, cell invasion and suppresses EMT pathway in breast cancer.The expression of lncRNA PANDAR in 65 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR assay.The western blotwas also performed to detected the EMT related makers expression of E-cadherin, Vimentin, MMP2 and MMP9.Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP11 expression, but upregulating E-cadherin expression in breast cancer.Our results proved that PANDAR may serve as potential target of breast cancer treatment.	31104011	RID07445	expression association	NA	UP(SKCM);DATA(GSE38495)	
Breast cancer	PANDAR	E-cadherin	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	NA	NA	101154753	NA	PANDA	NA	Inhibition of lncRNA PANDAR reduces cell proliferation, cell invasion and suppresses EMT pathway in breast cancer.The expression of lncRNA PANDAR in 65 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR assay.The western blotwas also performed to detected the EMT related makers expression of E-cadherin, Vimentin, MMP2 and MMP9.Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP12 expression, but upregulating E-cadherin expression in breast cancer.Our results proved that PANDAR may serve as potential target of breast cancer treatment.	31104011	RID07446	expression association	NA	UP(SKCM);DATA(GSE38495)	
Hepatocellular carcinoma	DDX11-AS1	LATS2	negatively-E	RIP;CHIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245614	GRCh38_12:31019434-31073847	ENSG00000150457	NA	100506660	26524	CONCR|SCAT4	NA	In this study, we found that DDX11-AS1 expression was dramatically higher in HCC tissues and cell lines. Higher DDX11-AS1 expression predicted poor overall survival of patients. Functionally, the proliferation, cell cycle progression, migration, and invasion of HCC cells were inhibited by DDX11-AS1 silencing, while promoted by ectopic expression of DDX11-AS1. RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays validated that DDX11-AS1 suppressed LATS2 expression by interacting with EZH2 and DNMT1 in HCC cells. Knockdown of DDX11-AS1 increased the mRNA and protein levels of LATS2. Overexpression of LATS2 abolished the promotive effect of DDX11-AS1 on cell growth and invasion. Besides, DDX11-AS1 promoted tumor formation in vivo. The mRNA levels of LATS2 were markedly decreased in tumor tissues and negatively correlated with DDX11-AS1 expression. Taken together, our data indicated that DDX11-AS1 may be a novel oncogene in hepatocarcinogenesis by repressing LATS2, providing a potential therapeutic target for HCC treatment.	31097223	RID07447	epigenetic regulation	NA	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Thyroid cancer	UCA1	MIR15A	negatively-E	siRNA	upregulation	qRT-PCR	NA	NA	cell growth(+);cell proliferation(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000283785	NA	652995	406948	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Long non-coding RNA UCA1 exerts growth modulation by miR-15a in human thyroid cancer TPC-1 cells.This study attempted to validate UCA1 possessed modulatory function on cell proliferation and epithelial mesenchymal transition (EMT) in human thyroid cancer cell line TPC-1.We found that overexpressed UCA1 strongly promoted cell proliferation.Further study revealed that miR-15a level in TPC-1 cells was suppressed by overexpressed UCA1.Simultaneous overexpression of UCA1 and miR-15a partly alleviated UCA1-induced growth, identifying that miR-15a was a possible target of UCA1.our study revealed UCA1/miR-15a axis implicated in thyroid cancer cells EMT, exposing a novel mechanism of thyroid cancer progression.	31062608	RID07448	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Cervical cancer	TUSC8	PTEN	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	ceRNA(miR-641)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237361	GRCh38_13:44400173-44405984	ENSG00000171862	NA	400128	5728	LINC01071|XLOC_010588	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA TUSC8 inhibits the invasion and migration of cervical cancer cells via miR-641/PTEN axis.We found that the expressions of TUSC8 and PTEN were decreased in CC tissues, whereas miR-641 expression was increased.In addition, TUSC8 and PTEN were upstream and downstream target molecule of miR-641, respectively.Overexpression of TUSC8 promoted PTEN expression, and suppressed the invasion and migration of Hela cells, whereas miR-641 mimic treatment changed the effects.These results demonstrated that overexpression of TUSC8 could inhibit the invasion and migration of CC cells by upregulating PTEN via miR-641.	31033083	RID07449	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	FOXD2-AS1	CDKN1B	negatively-E	RNA pull-down assay;RIP;CHIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000111276	NA	84793	1027	MGC12982	KIP1|P27KIP1	LncRNA FOXD2-AS1 plays an oncogenic role in hepatocellular carcinoma through epigenetically silencing CDKN1B(p27) via EZH2.The data indicated that FOXD2-AS1 expression was increased in HCC specimens and cell lines.Silencing FOXD2-AS1 arrest cell cycle in the G0/G1 phase, inhibited colony formation, cell proliferation and suppressed the in vivo growth of subcutaneous tumors.Our results revealed that FOXD2-AS1 could epigenetically silence CDKN1B by recruiting EZH2 to CDKN1B promoter region.	31004581	RID07450	epigenetic regulation	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Tongue squamous cell carcinoma	MALAT1	MMP9	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	LncRNA MALAT1 expression inhibition suppresses tongue squamous cell carcinoma proliferation, migration and invasion by inactivating PI3K/Akt pathway and downregulating MMP-9 expression.The expression of MALAT1 in tumor tissues and adjacent healthy tissues of tongue cancer patients, and the serum from tongue cancer patients as well as healthy controls, were detected by quantitative Real Time-PCR (qRT-PCR.The effects of MALAT1 overexpression on the PI3K/Akt pathway and MMP-9 expression were detected by western blot.The expression level of MALAT1 was remarkably higher in tumor tissues than that in adjacent healthy tissues.MALAT1 knockdown also reduced the phosphorylation level of Akt as well as the expression level of MMP-9.LncRNA MALAT1 expression inhibition can inhibit the proliferation, migration and invasion of tongue cancer cells by inactivating the PI3K/Akt pathway and downregulating MMP-9.	30657561	RID07451	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	LOC101927746	SSRP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-584-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000149136	NA	NA	6749	NA	FACT80	A novel lncRNA LOC101927746 accelerates progression of colorectal cancer via inhibiting miR-584-3p and activating SSRP1.We found that LOC101927746 expression was significantly increased in CRC tissues according to the GEO dataset.In terms of its mechanism, LOC101927746 could serve as a competing endogenous RNA to inhibit miR-584-3p and activate its target gene SSRP1.The expression of miR-584-3p was inversely correlated with either LOC101927746 or SSRP1 in CRC tissues.The expression of miR-584-3p was inversely correlated with either LOC101927746 or SSRP1 in CRC tissues.	30616889	RID07452	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE67939,GSE75367,GSE86978)
Colon cancer	MIR570MG	SMAD3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell growth(+);cell cycle(+);	ceRNA(miR-145)	regulation	NA	Regorafenib	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000166949	NA	NA	4088	NA	HsT17436|JV15-2|MADH3	Long Non-coding RNA MIR570MG Causes Regorafenib Resistance in Colon Cancer by Repressing miR-145/SMAD3 Signaling.Our research revealed the lncRNA MIR570MG increased in regorafenib-resistant colon cancer cells compared to the regorafenib-sensitive cells.dual-luciferase reporter assay confirmed that miR-145 bound to 3'-UTR of SMAD3, a transcriptional modulator activated by TGFbeta- resulting in blockage of TGFbeta-/SMAD3-mediated cell growth and cycle progression.In summary, our findings suggested that MIR570MG promoted regorafenib resistance via releasing SMAD3 from miR-145, leading to activation of SMAD3-mediated signaling pathways.	32195190	RID07453	ceRNA or sponge	chemoresistance		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	SNHG7	E-cadherin	negatively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	NCRNA00061	NA	LncRNA SNHG7 contributes to cell proliferation, invasion and prognosis of cervical cancer. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to detect the expression of lncRNA SNHG7 in 60 cervical cancer tissues and adjacent normal tissues.Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.LncRNA SNHG7 expression increased significantly in cervical cancer tissues.Meanwhile, the inhibition of lncRNA SNHG7 resulted in the increased protein expression level of E-cadherin, and decreased protein expressions of N-cadherin and Vimentin.	31773679	RID07454	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Cervical cancer	SNHG7	N-cadherin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	LncRNA SNHG7 contributes to cell proliferation, invasion and prognosis of cervical cancer. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to detect the expression of lncRNA SNHG7 in 60 cervical cancer tissues and adjacent normal tissues.Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.LncRNA SNHG7 expression increased significantly in cervical cancer tissues.Meanwhile, the inhibition of lncRNA SNHG7 resulted in the increased protein expression level of E-cadherin, and decreased protein expressions of N-cadherin and Vimentin.	31773679	RID07455	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Cervical cancer	SNHG7	Vimentin	positively-E	western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	MGC16037|NCRNA00061	NA	LncRNA SNHG7 contributes to cell proliferation, invasion and prognosis of cervical cancer. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to detect the expression of lncRNA SNHG7 in 60 cervical cancer tissues and adjacent normal tissues.Furthermore, western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.LncRNA SNHG7 expression increased significantly in cervical cancer tissues.Meanwhile, the inhibition of lncRNA SNHG7 resulted in the increased protein expression level of E-cadherin, and decreased protein expressions of N-cadherin and Vimentin.	31773679	RID07456	expression association	prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Malignant glioma	NCK1-DT	TRIM24	positively-E	RNA pull-down assay;luciferase activity assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-137)	regulation	NA	Temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000122779	NA	101927597	8805	NCK1-AS1|SLC35G2-AS1	hTIF1|RNF82|TIF1|Tif1a	NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/ TRIM24.The expression levels of NCK1-AS1, miR-137, or TRIM24 were detected by quantitative real-time polymerase chain reaction (qRT-PCR, western blot, in situ hybridization (ISH), or RNA pull-down assay.In addition, the relationship between NCK1-AS1 and miR-137 or TRIM24 and miR-137 was confirmed by dual luciferase activity assay.NCK1-AS1 expression was increased in regular and recurrent glioma tissues and TMZ-resistant cells.Moreover, suppression of NCK1-AS1 increased miR-137 expression, whereas overexpression of miR-137 decreased TRIM24 expression.NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway.	31750728	RID07457	ceRNA or sponge	chemoresistance		UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)
Hepatocellular carcinoma	NR4A1	WFDC21P	positively-E	ChIP	downregulation		NA	NA	cancer progression(-);cell proliferation(-);tumor growth(-);cell metastasis(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000123358	NA	ENSG00000261040	GRCh38_17:60083562-60091885	3164	645638	GFRP1|HMR|N10|NAK-1|NGFIB|NUR77|TR3	lnc-DC|LNCDC|LOC645638	Nur77-activated lncRNA WFDC21P attenuates hepatocarcinogenesis via modulating glycolysis.Orphan nuclear receptor Nur77, which is low expressed in HCC, functions as a tumor suppressor to suppress HCC.Here, we demonstrate that Nur77 could inhibit HCC development via transcriptional activation of the lncRNA WAP four-disulfide core domain 21 pseudogene (WFDC21P).Nur77 binds to its response elements on the WFDC21P promoter to directly induce WFDC21P transcription, which inhibits HCC cell proliferation, tumor growth, and tumor metastasis both in vitro and in vivo.In clinical HCC samples, WFDC21P expression positively correlated with that of Nur77, and the loss of WFDC21P is associated with worse prognosis.Mechanistically, WFDC21P could inhibit glycolysis by simultaneously interacting with PFKP and PKM2, two key enzymes in glycolysis.These interactions not only abrogate the tetramer formation of PFKP to impede its catalytic activity but also prevent the nuclear translocation of PKM2 to suppress its function as a transcriptional coactivator.	31959898	RID07458	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE86978)	DOWN(BRCA);DATA(GSE86978)
Hepatocellular carcinoma	WFDC21P	PFKP	negatively-F	ChIP	downregulation		NA	NA	cancer progression(-);cell proliferation(-);tumor growth(-);cell metastasis(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261040	GRCh38_17:60083562-60091885	ENSG00000067057	NA	645638	5214	lnc-DC|LNCDC|LOC645638	PFK-C|PFKF	Nur77-activated lncRNA WFDC21P attenuates hepatocarcinogenesis via modulating glycolysis.Orphan nuclear receptor Nur77, which is low expressed in HCC, functions as a tumor suppressor to suppress HCC.Here, we demonstrate that Nur77 could inhibit HCC development via transcriptional activation of the lncRNA WAP four-disulfide core domain 21 pseudogene (WFDC21P).Nur77 binds to its response elements on the WFDC21P promoter to directly induce WFDC21P transcription, which inhibits HCC cell proliferation, tumor growth, and tumor metastasis both in vitro and in vivo.In clinical HCC samples, WFDC21P expression positively correlated with that of Nur77, and the loss of WFDC21P is associated with worse prognosis.Mechanistically, WFDC21P could inhibit glycolysis by simultaneously interacting with PFKP and PKM2, two key enzymes in glycolysis.These interactions not only abrogate the tetramer formation of PFKP to impede its catalytic activity but also prevent the nuclear translocation of PKM2 to suppress its function as a transcriptional coactivator.	31959898	RID07459	interact with protein	metastasis,prognosis	DOWN(BRCA);DATA(GSE86978)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	WFDC21P	PKM	negatively-F	ChIP	downregulation		NA	NA	cancer progression(-);cell proliferation(-);tumor growth(-);cell metastasis(-)	interact with protein	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000261040	GRCh38_17:60083562-60091885	ENSG00000067225	NA	645638	5315	lnc-DC|LNCDC|LOC645638	OIP3|PK3|PKM2|THBP1	Nur77-activated lncRNA WFDC21P attenuates hepatocarcinogenesis via modulating glycolysis.Orphan nuclear receptor Nur77, which is low expressed in HCC, functions as a tumor suppressor to suppress HCC.Here, we demonstrate that Nur77 could inhibit HCC development via transcriptional activation of the lncRNA WAP four-disulfide core domain 21 pseudogene (WFDC21P).Nur77 binds to its response elements on the WFDC21P promoter to directly induce WFDC21P transcription, which inhibits HCC cell proliferation, tumor growth, and tumor metastasis both in vitro and in vivo.In clinical HCC samples, WFDC21P expression positively correlated with that of Nur77, and the loss of WFDC21P is associated with worse prognosis.Mechanistically, WFDC21P could inhibit glycolysis by simultaneously interacting with PFKP and PKM2, two key enzymes in glycolysis.These interactions not only abrogate the tetramer formation of PFKP to impede its catalytic activity but also prevent the nuclear translocation of PKM2 to suppress its function as a transcriptional coactivator.	31959898	RID07460	interact with protein	metastasis,prognosis	DOWN(BRCA);DATA(GSE86978)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Lung cancer	LCAL1	PRKAA2	negatively-F	RNA pull-down assay;shRNA	upregulation	qRT-PCR	NA	NA	tumor growth(-)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000286042	GRCh38_6:79307669-79313384	ENSG00000162409	NA	80078	5563	onco-lncRNA-27	AMPK|AMPKa2|PRKAA	LCAL1 enhances lung cancer survival via inhibiting AMPK-related antitumor functions.Recently, lung cancer-associated lncRNA 1 (LCAL1) has been identified to be overexpressed in lung cancer tissues, while inhibiting LCAL1 expression has shown potential to inhibiting lung cancer growth.In the present study, we provided the first evidence that LCAL1 may support lung cancer survival via inhibiting the activity of AMP-activated protein kinase (AMPK).According to our results, LCAL1 may physically interact with the catalytic subunit of tumor suppressor AMPK, prevent AMPK activation by upstream kinase (liver kinase B1), and thus inhibit the downstream AMPK signaling network.	30741368	RID07461	interact with protein	NA		UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	LINC00261	SNAI1	positively-E	siRNA	downregulation	qRT-PCR	NA	NA	cell growth(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000124216	NA	140828	6615	ALIEN|bA216C10.1|C20orf56|DEANR1|FALCOR|HCCDR1|NCRNA00261|onco-lncRNA-17|TCONS_00027846	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Linc00261 suppresses growth and metastasis of non-small cell lung cancer via repressing epithelial-mesenchymal transition.The expression level of linc00261 in 71 paired of NSCLC tissues and matched normal tissues, was detected using quantitative Real-time polymerase chain reaction (qRT-PCR.NSCLC cells were transfected with pcDNA3.1 or siRNA linc00261 to upregulate or downregulate linc00261 expression, respectively. Linc00261 expressed significantly lower in NSCLC tissues and cell lines than that in the adjacent normal tissues or control cell line.Furthermore, linc00261 inhibited the epithelial-mesenchymal transition of NSCLC via downregulating Snail.	31115010	RID07462	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	TSLD8	WWOX	positively-F	PuPGEA/gene nanocomplexes	downregulation	qRT-PCR	NA	NA	cancer progression(-)	protien stability	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000186153	NA	NA	51741	NA	FOR|SDR41C1|WOX1	A long non-coding RNA TSLD8 inhibits hepatocellular carcinoma by stabilizing WWOX.TSLD8 expression is significantly lowered in HCC tissues and cell lines.Furthermore, TSLD8 can interact with WWOX and protect WWOX from proteasome-mediated degradation.Collectively, our current study has identified a novel tumor suppressive lncRNA TSLD8 which exerts its tumor suppressive function by stabilizing WWOX.	31230746	RID07463	interact with protein	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842)
Osteosarcoma	PBB12	hsa-miR-204-5p	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Mechanisms underlying the promotion of osteosarcoma cell proliferation and invasion by lncRNA PBB12.Mechanistic research demonstrated that PBB12 can competitively bind to hsa-miR-204-5p by acting as a microRNA sponge.According to our research data, it was found that osteosarcoma patients with a high PBB12 level frequently showed increased metastasis.According to our research data, it was found that osteosarcoma patients with a high PBB12 level frequently showed increased metastasis.In vitro functional experimental data showed that in the osteosarcoma cell lines MG63 and SAOS-2, PBB12 silencing and overexpression significantly increases or reversed the inhibitory effect of KLF4 on the proliferation and invasion of tumor cells, respectively.The involvement of the interaction between PBB12 and the KLF4/hsa-miR-204-5p/ATF2 pathway in osteosarcoma progression was reported for the first time, and these data provide important theoretical support for gene therapy targeting KLF4 and hsa-miR-204-5p.	31894336	RID07464	ceRNA or sponge	metastasis		
Osteosarcoma	PBB12	KLF4	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(has-miR-204-5p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	NA	NA	ENSG00000136826	NA	NA	9314	NA	EZF|GKLF	Mechanisms underlying the promotion of osteosarcoma cell proliferation and invasion by lncRNA PBB12.Mechanistic research demonstrated that PBB12 can competitively bind to hsa-miR-204-5p by acting as a microRNA sponge.According to our research data, it was found that osteosarcoma patients with a high PBB12 level frequently showed increased metastasis.According to our research data, it was found that osteosarcoma patients with a high PBB12 level frequently showed increased metastasis.In vitro functional experimental data showed that in the osteosarcoma cell lines MG63 and SAOS-2, PBB12 silencing and overexpression significantly increases or reversed the inhibitory effect of KLF4 on the proliferation and invasion of tumor cells, respectively.The involvement of the interaction between PBB12 and the KLF4/hsa-miR-204-5p/ATF2 pathway in osteosarcoma progression was reported for the first time, and these data provide important theoretical support for gene therapy targeting KLF4 and hsa-miR-204-6p.	31894336	RID07465	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	XIST	miR-200b-3p	negatively-F	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Long non-coding RNA XIST promotes hepatocellular carcinoma progression by sponging miR-200b-3p.Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect XIST expression in HCC patients.By comparing with XIST expression in adjacent tissues, the XIST expression level was significantly higher in HCC samples.Further experiments showed that miR-200b-3p was directly targeted by XIST.Above results suggest that XIST could enhance the cell growth ability of HCC by targeting miR-200b-3p, which suggest that XIST may be a potential therapeutic target in HCC.	31799653	RID07466	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Colorectal cancer	ROR1-AS1	miR-375	negatively-F	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell metastasis(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000223949	GRCh38_1:64094379-64171342	NA	NA	101927034	NA	NA	NA	Long non-coding RNA ROR1-AS1 enhances colorectal cancer metastasis by targeting miR-375.Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to measure ROR1-AS1 expression of CRC tissues.Furthermore, Luciferase assays and RNA immunoprecipitation assay (RIP) were used to explore the underlying mechanism. By comparison with ROR1-AS1 expression in adjacent tissues, the ROR1-AS1 expression level was significantly higher in CRC samples. By comparison with ROR1-AS1 expression in adjacent tissues, the ROR1-AS1 expression level was significantly higher in CRC samples.The present study suggests that ROR1-AS1 could promote cell migration and invasion of CRC by sponging miR-375, which may offer a potential therapeutic target in CRC.	31486489	RID07467	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Cervical cancer	PVT1	miR<U+2011>16	negatively-F	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell cycle(+);cancer progression(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long non-coding RNA plasmacytoma variant translocation 1 gene promotes the development of cervical cancer via the NF-kB pathway.A LncRNA PVT1 overexpression vector or small interfering RNAs targeting LncRNA PVT1 were transfected into cervical cancer cells to generate LncRNA PVT1 overexpression and silencing in these cells.In summary, LncRNA PVT1 inhibits the effect of miR-16, promoting the cell cycle and inhibiting cellular apoptosis of cervical cancer cells, potentially via the NF-kB pathway.miR-16 mimics and inhibitor had opposite effects to those of NF-kB activity, and miR-16 was demonstrated to directly interact with the NF-kB gene as measured using the dual-luciferase assay.LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;	31322217	RID07468	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Cervical cancer	PVT1	CCND1	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell cycle(+);cancer progression(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000110092	NA	5820	595	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA plasmacytoma variant translocation 1 gene promotes the development of cervical cancer via the NF-kB pathway.A LncRNA PVT1 overexpression vector or small interfering RNAs targeting LncRNA PVT1 were transfected into cervical cancer cells to generate LncRNA PVT1 overexpression and silencing in these cells.In summary, LncRNA PVT1 inhibits the effect of miR-16, promoting the cell cycle and inhibiting cellular apoptosis of cervical cancer cells, potentially via the NF-kB pathway.miR-16 mimics and inhibitor had opposite effects to those of NF-kB activity, and miR-16 was demonstrated to directly interact with the NF-kB gene as measured using the dual-luciferase assay.LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;	31322217	RID07469	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Cervical cancer	PVT1	BCL2	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell cycle(+);cancer progression(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	Long non-coding RNA plasmacytoma variant translocation 1 gene promotes the development of cervical cancer via the NF-kB pathway.A LncRNA PVT1 overexpression vector or small interfering RNAs targeting LncRNA PVT1 were transfected into cervical cancer cells to generate LncRNA PVT1 overexpression and silencing in these cells.In summary, LncRNA PVT1 inhibits the effect of miR-16, promoting the cell cycle and inhibiting cellular apoptosis of cervical cancer cells, potentially via the NF-kB pathway.miR-16 mimics and inhibitor had opposite effects to those of NF-kB activity, and miR-16 was demonstrated to directly interact with the NF-kB gene as measured using the dual-luciferase assay.LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis;	31322217	RID07470	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	ZFPM2-AS1	MIR137	negatively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000284202	NA	102723356	406928	SCAT3	hsa-mir-137|miR-137|MIRN137	Long noncoding RNA ZFPM2-AS1 promotes the tumorigenesis of renal cell cancer via targeting miR-137.Expression levels of ZFPM2-AS1 in both RCC cells and 50 paired tissue samples were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR).In addition, western blot assay, Luciferase reporter gene assay and RNA immunoprecipitation assay were used to explore the possible underlying mechanism.The expression level of ZFPM2-AS1 in tumor tissues was significantly higher than that of corresponding normal tissues.The expression level of ZFPM2-AS1 in tumor tissues was significantly higher than that of corresponding normal tissues.In addition, miR-137 expression in tumor tissues was negatively correlated with ZFPM2-AS1 expression.Our findings indicated that ZFPM2-AS1 could promote metastasis and proliferation, whereas inhibiting the apoptosis of RCC via targeting miR-137.	31298319	RID07471	expression association	metastasis	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	
Non-small cell lung cancer	GNAS-AS1	NECAB3	positively-E	luciferase report assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-4319)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000235590	GRCh38_20:58818918-58850903	ENSG00000125967	NA	149775	63941	GNAS-AS|GNAS1AS|GNASAS|NCRNA00075|NESP-AS|NESPAS|SANG	APBA2BP|dJ63M2.4|dJ63M2.5|EFCBP3|NIP1|SYTIP2|XB51	GNAS-AS1/miR-4319/NECAB3 axis promotes migration and invasion of non-small cell lung cancer cells by altering macrophage polarization.Relative mRNA levels were determined by qRT-PCRInteraction between molecules was detected by luciferase report assay.GNAS-AS1 expression was dramatically enhanced in TAM, NSCLC cell lines, and clinical tumor tissues, and negatively correlated with overall survival of NSCLC patients.GNAS-AS1 promoted macrophage M2 polarization and NSCLC cell progression via directly inhibiting miR-4319, which could target N-terminal EF-hand calcium binding protein 3 (NECAB3) to inhibit its expression.GNAS-AS1/miR-4319/NECAB3 axis promotes tumor progression of NSCLC by altering macrophage polarization.	31267263	RID07472	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842)
Non-small cell lung cancer	NORAD	AKT1	positively-E	luciferase report assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-656-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000142208	NA	647979	207	LINC00657	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA NORAD promotes the occurrence and development of non-small cell lung cancer by adsorbing MiR-656-3p.Quantitative real-time polymerase chain reaction was adopted for the detection of the expression levels of NORAD, micro RNA (miR)-656-3p, and AKT serine/threonine kinase 1 (AKT1).Subsequently, the binding relationships between miR-656-3p and AKT1 and between miR-656-3p and NORAD were verified by dual-luciferase reporter gene assay. The lncRNA NORAD expression level in NSCLC patients was notably higher than that in people in control group, that in patients with metastasis was higher than that in patients without metastasis, and that in patients with NSCLC in stage III-IV was significantly higher than that in patients with NSCLC in stage I-II.According to the reporter gene assay, NORAD could bind to miR-656-3p.Besides, miR-656-3p was significantly under-expressed in cancer tissues of patients with NSCLC, and overexpression of miR-656-3p could block the proliferation and migration of A549/H460 cells and reversed promotion on cell proliferation and migration by NORAD.LncRNA NORAD is capable of promoting the proliferation and migration of NSCLC cells, and its mechanism may be that it increases the AKT1 expression by adsorbing miR-656-3p.	31207175	RID07473	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	GAS5	PTEN	positively-E	siRNA;luciferase report assay	downregulation	qRT-PCR	NA	NA	angiogenesis(-)	ceRNA(miR-29-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	BZS|MHAM|MMAC1|PTEN1|TEP1	Low Long Noncoding RNA Growth Arrest-Specific Transcript 5 Expression in the Exosomes of Lung Cancer Cells Promotes Tumor Angiogenesis.we found that growth arrest specific 5 (GAS5) was lowly expressed in the serum exosomes and lung cancer tissues of mice with lung cancer.In addition, we found that GAS5 competitively bound miRNA-29-3p with phosphatase and tensin homolog (PTEN), upregulating PTEN mRNA and protein expression, and inhibited level of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PI3K) and serine/threonine kinase 1 (AKT) phosphorylation in HUVECs.Overall, our results suggest that exosomal GAS5 could be a new therapeutic target for lung cancer which inhibits angiogenesis.	31186629	RID07474	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Melanoma	GAS6-DT	GAS6	positively-E	shRNA	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Melanoma	lncRNA	PCG	ENSG00000272695	GRCh38_13:113864112-113866834	ENSG00000183087	NA	100506394	2621	GAS6-AS2	AXLLG|AXSF	Increased expression of long noncoding RNA GAS6-AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression.In this study, we found that lncRNA GAS6-AS2 is significantly elevated in melanoma tissues and cells.Mechanistically, we found that GAS6-AS2 upregulates GAS6 expression, promotes GAS6 secretion, and activates AXL/AKT/ERK signals.Mechanistically, we found that GAS6-AS2 upregulates GAS6 expression, promotes GAS6 secretion, and activates AXL/AKT/ERK signals.	31162889	RID07475	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Head and neck squamous cell carcinoma	ZEB2-AS1	ZEB2	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	protien stability	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000169554	NA	100303491	9839	ZEB2-AS|ZEB2AS|ZEB2NAT	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Overexpression of ZEB2-AS1 promotes epithelial-to-mesenchymal transition and metastasis by stabilizing ZEB2 mRNA in head neck squamous cell carcinoma.ZEB2-AS1 was aberrantly overexpressed in a fraction of HNSCC samples.Antisense oligonucleotides (ASO)-mediated ZEB2-AS1 depletion markedly inhibited cell proliferation, migration and invasion while triggered apoptosis in HNSCC cells in part via modulating ZEB2 mRNA stability.	30950191	RID07476	interact with protein	metastasis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Urinary bladder cancer	LINC00536	WNT3A	positively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000249917	GRCh38_8:115950511-116325062	ENSG00000154342	NA	100859921	89780	NA	NA	High LINC00536 expression promotes tumor progression and poor prognosis in bladder cancer.In the present study, we found LINC00536 expression was highly expressed in BC tissues compared with controls and negatively associated with survival rate in BC patients.Mechanistically, Wnt3a was identified as the target of LINC00536.LINC00536 promoted malignant phenotypes via activating the Wnt3a/beta-Catenin signaling.	30851243	RID07477	expression association	prognosis		UP(PAAD);DATA(GSE40174)
Prostate cancer	HORAS5	AR	positively-E	siRNA	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	NA	NA	ENSG00000169083	NA	NA	367	NA	AIS|DHTR|HUMARA|NR3C4|SBMA|SMAX1	The long noncoding RNA HORAS5 mediates castration-resistant prostate cancer survival by activating the androgen receptor transcriptional program.We demonstrated that HORAS5 is a stable, cytoplasmic lncRNA that promotes CRPC proliferation and survival by maintaining AR activity under androgen-depleted conditions.Most strikingly, knockdown of HORAS5 causes a significant reduction in the expression of AR itself and oncogenic AR targets such as KIAA0101.Thus, we posit that HORAS5 is a novel, targetable mediator of CRPC through its essential role in the maintenance of oncogenic AR activity.	30776192	RID07478	expression association	NA		UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Colorectal cancer	XIC	NELL2	positively-E	luciferase report assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-486-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000184613	NA	7502	4753	SXI1|XCE|XIST	NRP2	LncRNA XIST facilitates proliferation and epithelial-mesenchymal transition of colorectal cancer cells through targeting miR-486-5p and promoting neuropilin-2.And the dual-luciferase reporter gene assay managed to verify the targeted relationships among XIST, miR-486-5p, and NRP-2.Our study results demonstrated that CRC tissues and cells were detected with significantly elevated XIST and NRP-2 expressions as well as markedly reduced miR-486-5p expression when compared with normal tissues and cells.Moreover, XIST was found to directly target miR-486-5p, and NRP-2 was directly targeted and modulated by miR-486-5p.Moreover, XIST was found to directly target miR-486-5p, and NRP-2 was directly targeted and modulated by miR-486-5p.	30656681	RID07479	ceRNA or sponge	NA		DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	LNCRNA-ATB	CTNNB1	positively-E	siRNA	upregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000168036	NA	114004396	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA-ATB promotes apoptosis of non-small cell lung cancer cells through MiR-200a/beta-Catenin.Compared with normal lung epithelial cells BEAS-2B, NCI-H838 cells had a significantly increased level of lncRNA-ATB (p<0.01), a significantly decreased level of miR-200a (p<0.01) and also a significantly increased level of beta-catenin (p<0.01).This study suggests that lncRNA-ATB promotes the apoptosis of NSCLC cells through inhibiting the expression of miR-200a and reversely promoting the expression of beta-catenin.	31983095	RID07480	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	LINC01555	NMU	positively-E	siRNA	upregulation	qRT-PCR	TCGA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000180869	GRCh38_1:84628230-84635020	ENSG00000109255	NA	439927	10874	C1orf180|FLJ35487	NA	The Long Noncoding RNA, LINC01555, Promotes Invasion and Metastasis of Colorectal Cancer by Activating the Neuropeptide, Neuromedin U.LINC01555 expression in SW620 and HCT116 CRC cells, and NCM460 normal colorectal cells, and 48 resection specimens containing CRC and adjacent normal tissue, was detected by quantitative real-time polymerase chain reaction (qRT-PCR.The Cancer Genome Atlas (TCGA) dataset showed that LINC01555 was highly expressed in CRC tissue when compared with adjacent normal colorectal tisIncreased expression of LINC01555 was found in CRC tissues and promoted the invasion of CRC cells by upregulating the expression of NmU.sue.Functional studies showed that knockdown of NmU reduced cell migration and invasion of CRC cells that overexpressed LINC01555.	31144675	RID07481	expression association	metastasis		
Breast cancer	NKILA	IL6	negatively-E	pcDNA3.1	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);angiogenesis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000136244	NA	105416157	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	Long non-coding RNA NKILA inhibited angiogenesis of breast cancer through NF-kB/IL-6 signaling pathway.The expression levels of NKILA, IL-6, VEGFA, VEGFR, apoptosis and epithelial-mesenchymal transition (EMT) and NF-kB/IL-6 signaling-related markers were determined using qRT-PCRor western blot.Cell viability and migration of MDA-MB-231 cells were significantly inhibited, while cell apoptosis was obviously promoted by overexpression of NKILA.Overexpression of NKILA significantly inhibited the protein levels of IL-6 and VEGFA in supernatant, as well as VEGFR in HUVEC, thus inhibited the angiogenesis of HUVEC.Overexpression of NKILA could inhibit cell proliferation, migration and promote apoptosis of breast cancer cells.It could also inhibit cell proliferation, migration and angiogenesis of HUVEC through inhibiting IL-6 secretion via NF-kB signaling pathway.	31862380	RID07482	expression association	NA		DOWN(BRCA);DATA(GSE75367,GSE86978)
Breast cancer	NKILA	VEGFA	negatively-E	pcDNA3.1	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);angiogenesis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000112715	NA	105416157	7422	NA	VEGF|VEGF-A|VPF	Long non-coding RNA NKILA inhibited angiogenesis of breast cancer through NF-kB/IL-6 signaling pathway.The expression levels of NKILA, IL-6, VEGFA, VEGFR, apoptosis and epithelial-mesenchymal transition (EMT) and NF-kB/IL-6 signaling-related markers were determined using qRT-PCRor western blot.Cell viability and migration of MDA-MB-231 cells were significantly inhibited, while cell apoptosis was obviously promoted by overexpression of NKILA.Overexpression of NKILA significantly inhibited the protein levels of IL-6 and VEGFA in supernatant, as well as VEGFR in HUVEC, thus inhibited the angiogenesis of HUVEC.Overexpression of NKILA could inhibit cell proliferation, migration and promote apoptosis of breast cancer cells.It could also inhibit cell proliferation, migration and angiogenesis of HUVEC through inhibiting IL-6 secretion via NF-kB signaling pathway.	31862380	RID07483	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Liver cancer	snaR	TGFB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	Long non-coding RNA snaR is involved in the metastasis of liver cancer possibly through TGF-beta1.To investigate the potential involvement of lncRNA snaR in hepatocellular carcinoma (HCC), expression of snaR in liver biopsies and plasma of patients with HCC and healthy controls was detected by reverse transcription-quantitative polymerase chain reaction.A snaR expression vector was transfected into HCC cells, and the effects on cell migration and invasion were analyzed by Transwell migration and Matrigel invasion assays, respectively.The expression of snaR and TGF-beta1 was significantly increased in the patients with HCC compared with the healthy controls.The plasma expression levels of snaR and TGF-beta1 were positively correlated in patients with HCC;snaR may promote the metastasis of liver cancer through TGF-beta1.	31186778	RID07484	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SNHG3	miR-196a-5p	negatively-F	luciferase reporter assay;starBasev2.0	upregulation	qRT-PCR	TCGA	NA	cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000242125	GRCh38_1:28505980-28510892	NA	NA	8420	NA	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	NA	LncRNA SNHG3 promotes cell growth by sponging miR-196a-5p and indicates the poor survival in osteosarcoma.The association between SNHG3 expression and the clinicopathological characteristics in OS patients was analyzed using the TCGA (The Cancer Genome Atlas) dataset.MiR-196a-5p-specific binding with SNHG3 or HOXC8 was confirmed by the luciferase report assay.As a result, the expression of SNHG3 was dramatically increased in OS tissue as compared with the adjacent normal tissues.SNHG3 was further identified to act as a sponge of miR-196a-5p, which counteracted the tumor-promoting effects caused by SNHG3 in OS cells.In conclusion, lncRNA SNHG3 promoted cell growth by sponging miR-196a-5p and indicated a poor prognosis in OS patients.	30791797	RID07485	ceRNA or sponge	prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Endometrial cancer	LINC01170	AKT1	positively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cancer progression(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000253807	GRCh38_5:124059794-124438625	ENSG00000142208	NA	103724389	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	LINC01170 promotes the progression of endometrial carcinoma by activating the AKT pathway.	30610803	RID07486	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LUCAT1	miR-199b-5p	negatively-E	RNA pull-down assay;luciferase activity assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000248323	GRCh38_5:91054834-91314547	NA	NA	100505994	NA	SCAL1|SCAT5	NA	Study of the biological function of LncRNA LUCAT1 on cervical cancer cells by targeting miR-199b-5p.LUCAT1 was highly expressed in SG and cancer tissues (P<0.050), and it had good diagnostic value for the development of CC (P<0.001).However, after transfecting miR-199b-5p into CC cells, it was found that the proliferation, invasion ability and anti-apoptosis protein of CC cells were significantly increased, while the apoptosis rate and apoptosis protein were significantly decreased by inhibiting LUCAT1 expression (P<0.050).LUCAT1 was highly expressed in CC. It was involved in the tumor development of CC by targeting miR-199b-5p, which was of great significance for the diagnosis and treatment of CC in the future.	32207530	RID07487	expression association	NA	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Breast cancer	PSMG3-AS1	miR-143-3p	negatively-F	bioinformatics	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000230487	GRCh38_7:1570073-1589626	NA	NA	114796	NA	NA	NA	Novel lncRNA PSMG3-AS1 functions as a miR-143-3p sponge to increase the proliferation and migration of breast cancer cells.The relative expression levels of lncRNA PSMG3-AS1 and microRNA (miR)-143-3p were determined using reverse-transcription quantitative PCR.Bioinformatics analysis was used to identify the relationship between PSMG3-AS1, miR-143-3p and COL1A1.The results of the present study demonstrated that PSMG3-AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR-143-3p was decreased.In conclusion, the results of the present study identified a novel lncRNA PSMG3-AS1, which serves as a sponge for miR-143-3p in the pathogenesis of breast cancer.	31661146	RID07488	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE51827)	
Hepatocellular carcinoma	UPF1	UCA1	negatively-E	RIP;siRNA	upregulation	qRT-PCR	NA	NA	cancer progression(-)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000005007	NA	ENSG00000214049	GRCh38_19:15828206-15836328	5976	652995	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	CUDR|LINC00178|onco-lncRNA-36|UCAT1	UPF1 inhibits the hepatocellular carcinoma progression by targeting long non-coding RNA UCA1.In this study, we demonstrated that UPF1 expression was significantly reduced in hepatocellular carcinoma (HCC) tissues compared with the adjacent normal tissues.Furthermore, we found that UPF1 could bind to long non-coding RNA urothelial cancer associated 1 (UCA1) and was negatively correlated with UCA1.	31040354	RID07489	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Clear cell renal cell carcinoma	MIR155HG	miR-155-5p	positively-E	TargetScan;miRDB	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000234883	GRCh38_21:25561810-25575168	NA	NA	114614	NA	BIC|miPEP155|MIRHG2|NCRNA00172	NA	Blocking lncRNA MIR155HG/miR-155-5p/-3p inhibits proliferation, invasion and migration of clear cell renal cell carcinoma.RT-qPCR was used to detect the expression of MIR155HG, miR-155-5p, miR-155-3p in clear cell renal cell carcinoma cell lines.Furthermore, TargetScan and miRDB were used to predict the co-target gene of miR-155-3p and miR-155-5p, and the functional analysis of co-target genes was performed using the DAVID.Interference of MIR155HG inhibited the cellular functions of ccRCC cells, which was reversed by overexpression of miR-155-3p and miR-155-5p.In addition, MIR155HG interference repressed the expression of miR-155-5p and miR-155-3p in ccRCCs, while inhibition of miR-155-5p and miR-155-3p restrained the proliferation, invasion and migration of ccRCCs.	31889587	RID07490	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Clear cell renal cell carcinoma	MIR155HG	miR-155-3p	positively-E	TargetScan;miRDB	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000234883	GRCh38_21:25561810-25575168	NA	NA	114614	NA	BIC|miPEP155|MIRHG2|NCRNA00172	NA	Blocking lncRNA MIR155HG/miR-155-5p/-3p inhibits proliferation, invasion and migration of clear cell renal cell carcinoma.RT-qPCR was used to detect the expression of MIR155HG, miR-155-5p, miR-155-3p in clear cell renal cell carcinoma cell lines.Furthermore, TargetScan and miRDB were used to predict the co-target gene of miR-155-3p and miR-155-5p, and the functional analysis of co-target genes was performed using the DAVID.Interference of MIR155HG inhibited the cellular functions of ccRCC cells, which was reversed by overexpression of miR-155-3p and miR-155-5p.In addition, MIR155HG interference repressed the expression of miR-155-5p and miR-155-3p in ccRCCs, while inhibition of miR-155-5p and miR-155-3p restrained the proliferation, invasion and migration of ccRCCs.	31889587	RID07491	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Lung adenocarcinoma	LINC00460	IL6	positively-E	bioinformatics;RIP;luciferase reporter assay;siRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-149-5p)	regulation	NA	Gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000136244	NA	728192	3569	NA	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Clinical importance of long non-coding RNA LINC00460 expression in EGFR-mutant lung adenocarcinoma.In lung cancer cells, LINC00460 promoted EGFR-TKI resistance as a competitive decoy for miR-149-5p, thereby facilitating interleukin (IL)-6 expression and inducing EMT-like phenotypes.The knockdown or knockout of LINC00460 in gefitinib-resistant non-small cell lung cancer cells restored the response to EGFR-TKI.In addition, as compared with patients with a low LINC00460 expression in tumors, those with a high LINC00460 expression had a significantly shorter progression-free survival following gefitinib therapy, and a shorter overall survival.	31789388	RID07492	ceRNA or sponge	chemoresistance		DOWN(BRCA);DATA(GSE75367,GSE86978)
Lung adenocarcinoma	LINC00460	EGFR	positively-E	bioinformatics;RIP;luciferase reporter assay;siRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-149-5p)	regulation	NA	Gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000146648	NA	728192	1956	NA	ERBB|ERBB1|ERRP	Clinical importance of long non-coding RNA LINC00460 expression in EGFR-mutant lung adenocarcinoma.In lung cancer cells, LINC00460 promoted EGFR-TKI resistance as a competitive decoy for miR-149-5p, thereby facilitating interleukin (IL)-6 expression and inducing EMT-like phenotypes.The knockdown or knockout of LINC00460 in gefitinib-resistant non-small cell lung cancer cells restored the response to EGFR-TKI.In addition, as compared with patients with a low LINC00460 expression in tumors, those with a high LINC00460 expression had a significantly shorter progression-free survival following gefitinib therapy, and a shorter overall survival.	31789388	RID07493	ceRNA or sponge	chemoresistance		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Colorectal cancer	MALAT1	miR-194-5p	negatively-F	RNA pull-down assay;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell growth(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	MALAT1 rs664589 Polymorphism Inhibits Binding to miR-194-5p, Contributing to Colorectal Cancer Risk, Growth, and Metastasis.Mechanistically, the miRNA miR-194-5p targeted MALAT1 for degradation in the nucleus in an Ago2-dependent manner;the rs664589 G allele altered the binding of MALAT1 to miR-194-5p, resulting in increased expression of MALAT1.	31311811	RID07494	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Non-small cell lung cancer	HOXA-AS2	miR-145-3p	positively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000253552	GRCh38_7:27107777-27134302	NA	NA	285943	NA	HOXA3as	NA	Long noncoding RNA HOXA-AS2 acts as an oncogene by targeting miR-145-3p in human non-small cell lung cancer.Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was utilized to detect HOXA-AS2 expression in NSCLC patients.HOXA-AS2 expression level in NSCLC tissues was significantly higher than adjacent tissues.Furthermore, the luciferase reporter gene assay also revealed that miR-145-3p was a direct target of HOXA-AS2 in NSCLC.Our results indicated that HOXA-AS2 could enhance the migration and invasion abilities of NSCLC by targeting miR-145-3p.	32096154	RID07495	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Esophagus adenocarcinoma	MIR22HG	STAT3	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000168610	NA	84981	6774	C17orf91|DKFZp686O06159|MGC14376	APRF	LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling.qRT-PCRand western blot were used to evaluate the mRNA and protein expression of related genes.In this study, abrogation of MIR22HG inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1).Mechanistically, MIR22HG silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines.	31291201	RID07496	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophagus adenocarcinoma	MIR22HG	MYC	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000136997	NA	84981	4609	C17orf91|DKFZp686O06159|MGC14376	bHLHe39|c-Myc|MYCC	LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling.qRT-PCRand western blot were used to evaluate the mRNA and protein expression of related genes.In this study, abrogation of MIR22HG inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1).Mechanistically, MIR22HG silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines.	31291201	RID07497	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Esophagus adenocarcinoma	MIR22HG	PTK2	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711447-1717174	ENSG00000169398	NA	84981	5747	C17orf91|DKFZp686O06159|MGC14376	FADK|FAK|FAK1|PPP1R71	LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling.qRT-PCRand western blot were used to evaluate the mRNA and protein expression of related genes.In this study, abrogation of MIR22HG inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1).Mechanistically, MIR22HG silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines.	31291201	RID07498	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE75367)
Cervical cancer	lncOGFRP1	SNAI1	positively-E	siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	NA	NA	ENSG00000124216	NA	NA	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Silencing long noncoding RNA OGFRP1 inhibits the proliferation and migration of cervical carcinoma cells.We found that the expression of lncOGFRP1 in cervical cancer tissues was significantly higher than that in normal cervical tissues .And the depletion of lncOGFRP1 inhibited the expression of beta-catenin, Vimentin, N-cadherin, and SNAIL and promoted the expression of E-cadherin.In summary, we first discovered the high expression of lncOGFRP1 in cervical cancer and revealed that silencing lncOGFRP1 inhibits the proliferation and migration of cervical carcinoma cells.	31512281	RID07499	expression association	NA		UP(PAAD);DATA(GSE40174)
Ovarian cancer	MEG3	PDGFRA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);angiogenesis(+)	ceRNA(miR-421)	regulation	NA	Anisomycin	CSC	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000134853	NA	55384	5156	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CD140a|GAS9|PDGFR2	Anisomycin inhibits angiogenesis in ovarian cancer by attenuating the molecular sponge effect of the lncRNA-Meg3/miR-421/PDGFRA axis.Further experiments demonstrated that the expression levels of endogenous long non-coding RNA (lncRNA) maternally expressed 3 (Meg3) were significantly decreased in anisomycin-treated HuOCSCs, whereas the expression levels of microRNA (miR)-421 were significantly increased.The results of luciferase reporter assays indicated that, when miR-421 was overexpressed in cells, the luciferase activities of wild-type platelet derived growth factor receptor alpha (PDGFRA) 3' untranslated region and Meg3 reporter plasmids were significantly decreased.Taken together, the present results demonstrated that anisomycin inhibited the activation downstream of the Notch1 pathway by attenuating the molecular sponge effect of the lncRNA-Meg3/miR-421/PDGFRA axis, ultimately inhibiting angiogenesis, proliferation and invasion in ovarian cancer cells.	31638182	RID07500	ceRNA or sponge	NA		UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Hepatocellular carcinoma	GAS5	miR-126-3p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	NA	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Differential expression profiling of long non-coding RNA GAS5 and miR-126-3p in human cancer cells in response to sorafenib.To better understand the molecular mechanism of the oral antitumor multikinase inhibitor sorafenib, we profiled the expression of a panel of lncRNAs and miRNAs by qPCR array in a sorafenib-treated hepatocellular carcinoma (HCC) cell line.By luciferase gene reporter assay, we discovered that GAS5 may act as a sponge for miR-126-3p in HCC cells.miR-126-3p expression in HCC tissues was decreased respect to their correspondent peritumoral tissues.The levels of plasmatic circulating miR-126-3p and GAS5 were significantly higher and lower in HCC patients compared to healthy subjects, respectively.This study highlighted the capability of sorafenib to modulate the expression of a wide range of ncRNAs and specifically, GAS5 and miR-126-3p were involved in the response to sorafenib of different cancer cell types.	31235746	RID07501	ceRNA or sponge	circulating,chemoresistance	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Pancreatic cancer	MCM3AP-AS1	FOXK1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-138-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000164916	NA	114044	221937	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	IMAGE:5164497	Long non-coding RNA MCM3AP-AS1 promotes growth and migration through modulating FOXK1 by sponging miR-138-5p in pancreatic cancer.MCM3AP-AS1, microRNA miR-138-5p (miR-138-5p) and FOXK1 levels were detected using quantitative real time PCR.dual-luciferase reporter assay was used to confirm the relationship between MCM3AP-AS1 and miR-138-5p, between miR-138-5p and FOXK1.dual-luciferase reporter assay demonstrated MCM3AP-AS1 could sponge microRNA-138-5p (miR-138-5p), and FOXK1 could bind with miR-138-5p.Positive correlation between MCM3AP-AS1 and FOXK1 was testified, as well as negative correlation between miR-138-5p and FOXK1.MCM3AP-AS1 promoted growth and migration through modulating miR-138-5p/FOXK1 axis in PC, providing insights into MCM3AP-AS1/miR-138-5p/FOXK1 axis as novel candidates for PC therapy from bench to clinic.	31830901	RID07502	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Glioblastoma	SCHLAP1	ACTN4	positively-E	RNA pull-down assay;luciferase activity assay	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000281131	GRCh38_2:180692104-180916939	ENSG00000130402	NA	101669767	81	LINC00913|PCAT11	FSGS1	Long Noncoding RNA SChLAP1 Forms a Growth-Promoting Complex with HNRNPL in Human Glioblastoma through Stabilization of ACTN4 and Activation of NF-kB Signaling .RNA-ISH and IHC were performed on a tissue microarray to assess expression of SChLAP1 and associated proteins in human gliomas.Proteins complexed with SChLAP1 were identified using RNA pull-down and mass spectrometry.SChLAP1 was increased in primary GBM samples and cell lines, and knockdown of the lncRNA suppressed growth.SChLAP1 was found to bind heterogeneous nuclear ribonucleoprotein L (HNRNPL), which stabilized the lncRNA and led to an enhanced interaction with the protein actinin alpha 4 (ACTN4).ACTN4 was also highly expressed in primary GBM samples and was associated with poorer overall survival in glioma patients.	31492748	RID07503	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CCAL	CTNNB1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	interact with protein	association	NA	Oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA CCAL transferred from fibroblasts by exosomes promotes chemoresistance of colorectal cancer cells.Mechanistically, CCAL interacts directly with mRNA stabilizing protein HuR (human antigen R) to increase beta-catenin mRNA and protein levels.RNA-ISH shows higher CCAL expressed in the tumor stroma compared to cancer nests of CRC tissues.Here, we show that lncRNA CCAL (colorectal cancer-associated lncRNA) promotes oxaliplatin (Oxa) resistance of CRC cells.	31381140	RID07504	interact with protein	chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Liver cancer	HAND2-AS1	BMPR1A	positively-E	RNA pull-down assay	upregulation	microarray	NA	NA	tumorigenesis(+);self-renewal(+);BMP signaling pathway(+)	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000107779	NA	79804	657	DEIN|FLJ11539|NBLA00301	ACVRLK3|ALK3|CD292	LncRNA HAND2-AS1 promotes liver cancer stem cell self-renewal via BMP signaling.Here, we identified a long noncoding RNA (lncRNA) termed HAND2-AS1 that is highly expressed in liver CSCs.Mechanistically, HAND2-AS1 recruits the INO80 chromatin-remodeling complex to the promoter of BMPR1A, thereby inducing its expression and leading to the activation of BMP signaling.Our findings reveal that HAND2-AS1 promotes the self-renewal of liver CSCs and drives liver oncogenesis, offering a potential new target for HCC therapy.	31334575	RID07505	transcriptional regulation	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761)
Prostate cancer	SNHG12	MIR133B	negatively-F	bioinformatics	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000199080	NA	85028	442890	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	MIRN133B|miRNA133B|mir-133b	Long noncoding RNA SNHG12 indicates the prognosis of prostate cancer and accelerates tumorigenesis via sponging miR-133b.Bioinformatic analysis revealed that SNHG12 was closely related to the progression of PCa and could target candidate microRNA (miR-133b).Direct interactions between miR-133b and SNHG12 have been found and SNHG12 acts as an oncogene to promote tumorigenesis of PCa by sponging tumor suppressor gene miR-133b.	31267540	RID07506	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Osteosarcoma	FER1L4	AKT1	positively-E	shRNA	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);apoptosis process(+)	NA	association	NA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000142208	NA	80307	207	bA563A22B.1|C20orf124|dJ309K20.1	AKT|PKB|PRKBA|RAC|RAC-alpha	Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells.Results showed that FER1L4 was observed to be lowly expressed in osteosarcoma cell lines (US-O2, MG-63 and SaOS-2 cells), especially MG63 cells.Furthermore, the protein levels of p-AKT and p-PI3K were remarkably suppressed when FER1L4 was knocked down.	31000382	RID07507	expression association	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	FER1L4	PIK3CA	positively-E	shRNA	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);apoptosis process(+)	NA	association	NA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000121879	NA	80307	5290	bA563A22B.1|C20orf124|dJ309K20.1	PI3K	Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells.Results showed that FER1L4 was observed to be lowly expressed in osteosarcoma cell lines (US-O2, MG-63 and SaOS-2 cells), especially MG63 cells.Furthermore, the protein levels of p-AKT and p-PI3K were remarkably suppressed when FER1L5 was knocked down.	31000382	RID07508	expression association	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Osteosarcoma	LINC00963	FN1	positively-E	luciferase reporter assay	upregulation	PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-204-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000115414	NA	100506190	2335	MetaLnc9	CIG|FINC|GFND2|LETS|MSF	The LncRNA LINC00963 facilitates osteosarcoma proliferation and invasion by suppressing miR-204-3p/FN1 axis. LINC00963 and miR-204-3p RNA expression levels were quantified by PCR in OS tissues and cells.Luciferase reporter assays were performed to verify direct interaction between LINC00963 and miR-204-3p and miR-204-3p and Fibronectin-1.LINC00963 was verified to be highly expressed in OS samples and cells.The luciferase reporter assay showed that LINC00963 can suppress miR-204-3p by directly binding miR-204-3p.Besides, we initially explored Fibronectin-1 (FN1) as the target of LINC00963/miR-204-3p axis in osteosarcoma.Our findings implied that LINC00963/miR-204-3p/FN1 can play an important role in proliferation and progression in osteosarcoma.	30975024	RID07509	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Laryngeal squamous cell carcinoma	ST7-AS1	CARM1	positively-F	luciferase reporter assay	upregulation	sequencing	NA	NA	cancer progression(+)	protien stability	binding/interaction	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000227199	GRCh38_7:116952446-116954334	ENSG00000142453	NA	93653	10498	ST7AS1|ST7OT1	PRMT4	The long noncoding RNA ST7-AS1 promotes laryngeal squamous cell carcinoma by stabilizing CARM1.ST7-AS1 is frequently overexpressed in LSCC tissues and cell lines.Mechanistically, ST7-AS1 could interact with CARM1, a well characterized protein arginine methyltransferase and protect CARM1 from ubiquitin-dependent degradation.CARM1 can methylate Sox-2, a pluripotent transcription factor.	30853182	RID07510	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Endometrial cancer	FRMD6-AS2	FRMD6	positively-E	ChIP;bioinformatics	downregulation	microarray	NA	NA	cancer progression(-)	chromatin looping	binding/interaction	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000258537	GRCh38_14:51454512-51599952	ENSG00000139926	NA	100874185	122786	NA	C14orf31|EX1|MGC17921|willin	The tumor suppressive effect of long non-coding RNA FRMD6-AS2 in uteri corpus endometrial carcinoma.Here, we reported that the expression of a novel long non-coding RNA (lncRNA) FRMD6-AS2 was reduced in UCEC compared to noncancerous endometrium tissues using the data from The Cancer Genome Atlas (TCGA) Project database.By over-expressing FRMD6-AS2 in UCEC cell lines, we observed that FRMD6-AS2 played a suppressive role in tumor growth, migration and invasion via activation of Hippo signaling pathway including FRMD6.Moreover, we also demonstrated that FRMD6-AS2 could interact with the 30kb upstream beyond FRMD6 and facilitate the chromatin looping towards the promoter region of FRMD6 to enhance the expression of FRMD6.We concluded that lncRNA FRMD6-AS2 repressed UCEC, at least in part, by increasing FRMD6.	31917993	RID07511	chromatin looping	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Liver cancer	PCNAP1	PCNA	positively-E	luciferase reporter assay	upregulation	qPCR;microarray;sequencing	NA	NA	cell growth(+)	ceRNA(miR-154)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249065	GRCh38_4:99160514-99161645	ENSG00000132646	NA	359806	5111	p1PCNA	NA	LncRNA PCNAP1 modulates hepatitis B virus replication and enhances tumor growth of liver cancer.Interestingly, the expression levels of PCNAP1 and PCNA were significantly elevated in the liver of HBV-infectious human liver-chimeric mice.PCNAP1 enhanced PCNA through sponging miR-154 targeting PCNA mRNA 3'UTR.Functionally, PCNAP1 or PCNA remarkably enhanced HBV replication and accelerated the growth of HCC in vitro and in vivo.	31410212	RID07512	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Renal cell carcinoma	MALAT1	BIRC5	positively-E	luciferase reporter assay;miRanda;starBase	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-203)	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000089685	NA	378938	332	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	API4|EPR-1|survivin	MALAT1 accelerates the development and progression of renal cell carcinoma by decreasing the expression of miR-203 and promoting the expression of BIRC5. qRT-PCRwas used for the assessment of BIRC5, miRNA-203 and MALAT1 expression.Furthermore, the targeted relationships between miR-203 and BIRC5, as well as MALAT1 and miR-203, were predicted by the miRanda/starBase database and verified by dual-luciferase reporter gene assay.The expression levels of BIRC5 and MALAT1 were higher in RCC tissues and cell lines than in adjacent normal tissues and a normal renal cortex proximal tubule epithelial cell line.Our study demonstrated that MALAT1 functions as a miR-203 decoy to increase BIRC5 expression in RCC.	31250518	RID07513	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Esophagus squamous cell carcinoma	MALAT1	YY1AP1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell stemness(+)	interact with protein	binding/interaction	NA	NA	CSC	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163374	NA	378938	55249	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HCCA2|YAP|YY1AP	Long noncoding RNA MALAT1 promotes the stemness of esophageal squamous cell carcinoma by enhancing YAP transcriptional activity.In this study, we found that MALAT1 expression was remarkably increased in ESCC cells compared to normal human esophageal epithelial cells.We also established that MALAT1 binds directly to Yes-associated protein (YAP), thereby enhancing YAP protein expression and increasing YAP transcriptional activity.Overall, this study has identified that a novel MALAT1-YAP axis promotes the stemness of ESCC cells, and thus could be a potential target for treatment of ESCC.	31116509	RID07514	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Gastric cancer	MALAT1	SOX2	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell stemness(+)	protien stability	binding/interaction	NA	NA	CSC	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000181449	NA	378938	6657	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1 increases the stemness of gastric cancer cells via enhancing SOX2 mRNA stability.We report that MALAT1 directly binds to sox2 mRNA (which encodes a critical master pluripotency factor), enhances the mRNA stability and increases its expression;Importantly, expression of MALAT1 and sox2 exhibited a positive correlation in clinical samples.Therefore, our results indicate the existence of a novel MALAT1-sox2 axis which promotes the stemness of gastric cancer cells and may be a potential target for gastric cancer.	31037832	RID07515	interact with protein	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC);DATA(GSE117623)
Cervical cancer	DLX6-AS1	ARPP19	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+)	ceRNA(miR-16-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000128989	NA	285987	10776	Evf-2|FLJ34048|NCRNA00212	ARPP-16|ARPP-19|ARPP16|ENSAL	Long Noncoding RNA DLX6-AS1 Promotes the Progression in Cervical Cancer by Targeting miR-16-5p/ARPP19 Axis.LncRNA DLX6-AS1 has been proven vital in various cancers, whereas its exact function is still largely unestablished in CC. Materials and Methods: The expression pattern of DLX6-AS1 and miR-16-5p in CC cells was determined by real-time quantitative polymerase chain reaction (RT-qPCR).RNA immunoprecipitation (RIP) and luciferase reporter assays were employed to certify the combination between miR-16-5p and DLX6-AS1 (or ARPP19).Elevated DLX6-AS1 expression was disclosed in CC cells.DLX6-AS1 was uncovered to sponge and negatively modulate miR-16-5p in CC. Besides, ARPP19 was uncovered as a downstream target gene of miR-16-5p in CC. Rescue experiments indicated that DLX6-AS1 enhanced the cellular process of CC cells through upregulating ARPP19.DLX6-AS1 accelerates the progression of CC through sponging miR-16-5p and upregulates ARPP19, which offers a novel insight into prognosis and remedy of CC.	32077747	RID07516	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Gastric cancer	ALKBH5	NEAT1	positively-E	bioinformatics;RIP	upregulation	RT-PCR	NA	NA	cell invasion(+);cell migration(+)	DNA methylation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000091542	NA	ENSG00000245532	GRCh38_11:65422774-65445540	54890	283131	FLJ20308|OFOXD1	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ALKBH5 promotes invasion and metastasis of gastric cancer by decreasing methylation of the lncRNA NEAT1.Bioinformatics predicted interactions of ALKBH5 with lncRNAs.Five methods were employed to assess the function of nuclear paraspeckle assembly transcript 1 (NEAT1), including gene silencing, RT-PCR separation of nuclear and cytoplasmic fractions, scrape motility assays, and transwell migration assays.Then, m6A RNA immunoprecipitation and immunofluorescence were used to detect methylated NEAT1 in GC cells.NEAT1 is a potential binding lncRNA of ALKBH5.NEAT1 was overexpressed in GC cells and tissue.The binding of ALKBH5 and NEAT1 influences the expression of EZH2 (a subunit of the polycomb repressive complex) and thus affects GC invasion and metastasis.	31290116	RID07517	epigenetic regulation	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)
Malignant glioma	PDIA3P1	RELA	positively-E	RNA pull-down assay;luciferase reporter assay;ChIP	upregulation	microarray;qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);angiogenesis(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000180867	GRCh38_1:147172744-147179622	ENSG00000173039	NA	171423	5970	GRP58P|PDIA3P	NFKB3|p65	Hypoxia-induced lncRNA PDIA3P1 promotes mesenchymal transition via sponging of miR-124-3p in glioma.Further studies revealed that PDIA3P1 functions as a ceRNA, sponging miR-124-3p to modulate RELA expression and activate the downstream NF-kb pathway, thus promoting the MES transition of glioma cells.In conclusion, PDIA3P1 is a crucial link between hypoxia and glioma MES transition through the PDIA3P1-miR-124-3p-RELA axis, which may serve as a prognostic indicator and potential therapeutic target for glioma treatment.In vitro study revealed that overexpression of PDIA3P1 enhanced the migration and invasion capacity of glioma cells, while knockdown of PDIA3P1 induced the opposite effect.	32127518	RID07518	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophagus squamous cell carcinoma	ZNF750	DANCR	negatively-E	luciferase reporter assay;RIP;CHIP	upregulation	qRT-PCR;sequencing	NA	NA	angiogenesis(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	PCG	lncRNA	ENSG00000141579	NA	ENSG00000226950	GRCh38_4:52712325-52723623	79755	57291	FLJ13841|Zfp750	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	Decreased ZNF750 promotes angiogenesis in a paracrine manner via activating DANCR/miR-4707-3p/FOXC2 axis in esophageal squamous cell carcinoma.RNA-seq and ChIP shows lncRNA DANCR is a direct downstream target of ZNF750.Furtherly, knockdown ZNF750 evokes DANCR expression, which prevents miR-4707-3p to interact with FOXC2 as a microRNA sponge in a ceRNA manner, leading to enhanced FOXC2 signaling and angiogenesis.In contrast, ZNF750 expression reverses the effect.Our study reveals a novel mechanism of ZNF750, highlights a significance of ZNF750 as a metastatic and prognostic biomarker, and offers potential therapeutic targets for ESCC patients harboring ZNF750 mutations.	32341351	RID07519	transcriptional regulation	metastasis,prognosis	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)
Esophagus squamous cell carcinoma	DANCR	FOXC2	positively-E	luciferase reporter assay;RIP;CHIP	upregulation	qRT-PCR;sequencing	NA	NA	angiogenesis(+)	ceRNA(miR-4707-3p)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000176692	NA	57291	2303	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	FKHL14|MFH-1	Decreased ZNF750 promotes angiogenesis in a paracrine manner via activating DANCR/miR-4707-3p/FOXC2 axis in esophageal squamous cell carcinoma.RNA-seq and ChIP shows lncRNA DANCR is a direct downstream target of ZNF750.Furtherly, knockdown ZNF750 evokes DANCR expression, which prevents miR-4707-3p to interact with FOXC2 as a microRNA sponge in a ceRNA manner, leading to enhanced FOXC2 signaling and angiogenesis.In contrast, ZNF750 expression reverses the effect.Our study reveals a novel mechanism of ZNF750, highlights a significance of ZNF750 as a metastatic and prognostic biomarker, and offers potential therapeutic targets for ESCC patients harboring ZNF750 mutations.	32341351	RID07520	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Hepatocellular carcinoma	DANCR	PSMD10	positively-F	RNA pull-down assay;luciferase activity assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);IL-6/STAT3 signaling pathway(+)	protien stability	regulation	NA	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000101843	NA	57291	5716	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	p28	LncRNA DANCR Promotes Sorafenib Resistance via Activation of IL-6/STAT3 Signaling in Hepatocellular Carcinoma Cells.The expression levels of DANCR in HCC tissues were detected by qRT-PCRThe MS2-binding sequences-MS2-binding protein-based RNA immunoprecipitation assay, RNA pull-down and luciferase reporter assay was used to detect the association between DANCR and PSMD10 mRNA.We found that DANCR was significantly overexpressed in HCC tissues and associated with prognosis of HCC patients.Mechanistically, the role of DANCR relied largely on the association with PSMD10.DANCR stabilized PSMD10 mRNA through blocking the repressing effect of several microRNAs on PSMD10.Besides, DANCR activated IL-6/STAT3 signaling via PSMD10.	32103983	RID07521	interact with protein	prognosis,chemoresistance	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807,GSE86978)
Urinary bladder cancer	SOD2	LIN28B	positively-E		upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000112096	GRCh38_6:159669069-159762529	ENSG00000187772	NA	6648	389421	GClnc1	CSDD2|FLJ16517	LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC.In this study, we identified an lncRNA, gastric cancer-associated lncRNA1 (GClnc1), which was in high abundance in bladder cancer tissues and its expression was related to poor survival rates in patients with bladder cancer.Mechanistically, we first found that GClnc1 bound to LIN28B and promoted the expression of myelocytomatosis proto-oncogene (MYC) through the LIN28B/let-7a/MYC pathway.LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC.	31298933	RID07522	transcriptional regulation	NA	DOWN(BRCA);DATA(GSE111065,GSE75367,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Urinary bladder cancer	LIN28B	MYC	positively-E	RNA pull-down assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(let-7a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000187772	GRCh38_6:104936616-105083332	ENSG00000136997	NA	389421	4609	CSDD2|FLJ16517	bHLHe39|c-Myc|MYCC	LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC.In this study, we identified an lncRNA, gastric cancer-associated lncRNA1 (GClnc1), which was in high abundance in bladder cancer tissues and its expression was related to poor survival rates in patients with bladder cancer.Mechanistically, we first found that GClnc1 bound to LIN28B and promoted the expression of myelocytomatosis proto-oncogene (MYC) through the LIN28B/let-7a/MYC pathway.LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC.	31298933	RID07523	ceRNA or sponge	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Nasopharynx carcinoma	DANCR	STAT3	positively-E	RNA pull-down assay;luciferase reporter assay;ChIP;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000168610	NA	57291	6774	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	APRF	Long noncoding RNA DANCR promotes nasopharyngeal carcinoma progression by interacting with STAT3, enhancing IL-6/JAK1/STAT3 signaling.In the current study, we investigated the expression and biological functions of DANCR in NPC cells and found that DANCR is highly expressed in NPC cells and IL-6 stimulation upregulates DANCR expression through an STAT3-dependent manner.Furthermore, DANCR specifically interacts with STAT3 to promote STAT3 activation in NPC cells.Taken together, the present study for the first time demonstrates that DANCR, acting as an oncogene in NPC, promotes NPC progression by interacting with STAT3 and enhancing JAK1 binding to STAT3 to strengthen IL-6/JAK1/STAT3 signaling, suggesting that it may be a potential target to be used as a novel strategy to develop NPC therapeutics.	30849642	RID07524	interact with protein	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Head and neck squamous cell carcinoma	LINC00460	PRDX1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with mRNA	binding/interaction	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000117450	NA	728192	5052	NA	NKEFA|PAGA	LncRNA LINC00460 promotes EMT in head and neck squamous cell carcinoma by facilitating peroxiredoxin-1 into the nucleus.RNA pull-down assays, LS-MS/MS analysis, and RNA and chromatin immunoprecipitation assays were performed to identify the molecular mechanism by which LINC00460 promotes HNSCC progression.LINC00460 enhanced HNSCC cell proliferation and metastasis in vitro and in vivo and induced epithelial-mesenchymal transition (EMT).LINC00460 primarily localized within the cytoplasm of HNSCC cells, physically interacted with PRDX1 and facilitated PRDX1 entry into the nucleus.High levels of LINC00460 and PRDX1 expression were positively associated with lymph metastasis, pathological differentiation and tumor size in HNSCC patients.	31429766	RID07525	interact with mRNA	metastasis		DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Ovarian cancer	KCNQ1OT1	CTNNB1	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000168036	NA	10984	1499	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Effects of LncRNA KCNQ1OT1 on proliferation and migration of ovarian cancer cells by Wnt/beta-catenin.The proliferation rate of cells was overtly decreased in KCNQ1OT1 knockdown group but significantly increased in KCNQ1OT1 overexpression group.The results of western blot and fluorescence immunoassay revealed that compared with that in control group, the expression level of beta-catenin protein evidently declined in KCNQ1OT1 knockdown group, but it was notably elevated in KCNQ1OT1 overexpression group.Increased lncRNA KCNQ1OT1 in ovarian cancer cells promotes the expression of beta-catenin, thereby facilitating the proliferation and migration of ovarian cancer cells.	31696465	RID07526	expression association	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	lncRNA-AC078883.3	PTEN	positively-E	luciferase reporter assay;bioinformatic	downregulation	RT-PCR	NA	NA	chemoresistance(-)	ceRNA(miR-19a)	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000171862	NA	NA	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Deregulation of lncRNA-AC078883.3 and microRNA-19a is involved in the development of chemoresistance to cisplatin via modulating signaling pathway of PTEN/AKT.Non-small cell lung cancer (NSCLC) remains the leading cause of cancer death worldwide.Real-time PCR, western blot Immunohistochemistry (IHC) assay, bioinformatic analysis, and luciferase assay were collaboratively used to establish the lncRNA-AC078883.3/miR-19a/PTEN/AKT pathway.Compared with the Cisplatin-Sensitive group, the Cisplatin-Resistance group exhibited lower levels of lncRNA-AC078883.3 and PTEN and higher levels of miR-19a and p-Akt.miR-19a contains a putative binding site of lncRNA-AC078883.3, which enabled the luciferase activity of wild-type lncRNA-AC078883.3 to be reduced by miR-19a.In addition, by directly targeting PTEN 3'-untranslated region (UTR), miR-19a repressed the luciferase activity of wild-type PTEN 3'-UTR.	31111480	RID07527	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Neuroblastoma	NHEG1	DDX5	positively-E	RNA pull-down assay;luciferase activity assay	upregulation	microarray;qRT-PCR	GSE80393	NA	cancer progression(+)	protien stability	binding/interaction	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000225391	GRCh38_6:136982165-136993234	ENSG00000263077	NA	100294720	1655	NA	G17P1|HLR1|p68	Long Noncoding RNA NHEG1 Drives beta-Catenin Transactivation and Neuroblastoma Progression through Interacting with DDX5.Herein, through integrating analysis of a public RNA sequencing dataset, neuroblastoma highly expressed 1 (NHEG1) was identified as a risk-associated lncRNA, contributing to an unfavorable outcome of NB.Mechanistically, NHEG1 bound to and stabilized DEAD-box helicase 5 (DDX5) protein through repressing proteasome-mediated degradation, resulting in beta-catenin transactivation that altered target gene expression associated with NB progression.We further determined a lymphoid enhancer binding factor 1 (LEF1)/transcription factor 7-like 2 (TCF7L2)/NHEG1/DDX5/beta-catenin axis with a positive feedback loop and demonstrated that NHEG1 harbored oncogenic properties via its interplay with DDX5.High NHEG1 or DDX5 expression was associated with poor survival of NB patients.	31982037	RID07528	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TGLC15	SOX4	positively-E	bioinformatics;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	protien stability	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000124766	NA	NA	6659	NA	NA	Long non-coding RNA TGLC15 advances hepatocellular carcinoma by stabilizing Sox4.We screened for novel lncRNAs using lncRNA profiling.TGLC15 expression was quantified by qRT-PCRCombined RNA immunoprecipitation (RIP) and mass spectrometry (MS) were utilized to uncover Sox4 as TGLC15 binding protein.TGLC15 is significantly overexpressed in tumor tissues and HCC cell lines.Mechanistic studies showed that TGLC15 interacted with Sox4 and interaction between TGLC15 and Sox4 could stabilize Sox4 via reduction in proteasome-mediated degradation.	31495979	RID07529	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Gastric cancer	VPS13B-DT	IL11	positively-E	bioinformatics	upregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with mRNA	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253948	GRCh38_8:98957575-99013743	ENSG00000095752	NA	105375666	3589	OLC8	AGIF|IL-11	The long non-coding RNA OLC8 enhances gastric cancer by interaction with IL-11.The lncRNA profiling was used to identify novel lncRNAs associated with GC.The expression of OLC8 was quantified using qRT-PCRIn current study, we have identified a novel lncRNA termed OLC8.OLC8 was significantly overexpressed in gastric cancer specimens and cell lines.Mechanistic study indicated that OLC8 associated with IL-11 transcripts.	31273847	RID07530	interact with mRNA	NA		UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	DLGAP1-AS1	CDK8	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell growth(+);cell metastasis(+)	ceRNA(miR-26b-5p)	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000132964	NA	649446	1024	FLJ35776|HsT914	K35	Long non-coding RNA DLGAP1-AS1 facilitates tumorigenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via the feedback loop of miR-26a/b-5p/IL-6/JAK2/STAT3 and Wnt/beta-catenin pathway.First of all, according to UCSC Genome Browser online database, DLGAP1-AS1 expression level was relatively low in normal human liver tissues (Fig. -(Fig.1a).1a). Comparatively, the significantly elevated DLGAP1-AS1 expression in liver hepatocellular carcinoma (LIHC) dataset in comparison with normal dataset was presented using GEPIA online database (Fig. -(Fig.1b).1b). First, opposite with DLGAP1-AS1, miR-26a-5p and miR-26b-5p were downregulated in HCC cell lines in comparison with normal cells (Fig. -(Fig.2b).2b). Besides, DLGAP1-AS1 knockdown led to elevated levels of miR-26a/b-5p in Hep G2 cells, whereas DLGAP1-AS1 overexpression resulted in miR-26a/b-5p downregulation in SNU-387 cells, implying that miR-26a/b-5p were negatively regulated by DLGAP1-AS1 (Fig. -(Fig.2c).2c). In order to determine the molecular interaction, we conducted RIP assay using antibodies against Ago2, and the enrichment of DLGAP1-AS1 and miR-26a/b-5p with Ago2 antibodies was observed, indicating that they were recruited to RNA-induced silencing complexes (RISCs) and might have functional interactions (Fig. -(Fig.2d).2d). Besides, RNA pull-down assay illustrated the direct bond between DLGAP1-AS1 and miR-26a/b-5p at the correct binding sites, because only wild-type probes for miR-26a/b-5p could significantly pull-down DLGAP1-AS1 (Fig. -(Fig.2e).2e). Moreover, DLGAP1-AS1 luciferase reporters containing wild-type and mutant binding sites were constructed and transfected into HEK-293T cells. Wild-type reporters displayed a significantly repressed luciferase activity with miR-26a/b-5p overexpression, while luciferase activity of mutant reporters could barely be lowered (Fig. -(Fig.2f).2f). In conclusion, DLGAP1-AS1 was proven to act as a molecular sponge to sequester miR-26a-5p and miR-26b-5p.Based on our preceding study on the interaction between DLGAP1-AS1 and miR-26a/b-5p, we proceeded to search for potential genes targeted by miR-26a/b-5p. Using three online bioinformatics tools, we found that there were 380 mRNAs that can be regulated by both miR-26a-5p and miR-26b-5p (Fig. S1b). Next, these candidate mRNAs were subjected to qRT-PCRanalysis in response to the upregulation of miR-26a-5p or miR-26b-5p. Top five downregulated mRNAs were shown in Fig. S1c, among which IL6 was expressed lowest in cells transfected with miR-26a-5p mimics or miR-26b-5p mimics. With the aid of starBase that the mRNA of IL-6, a characteristic inflammatory cytokine closely involved in cancers, was an appropriate target for them (Fig. -(Fig.3a).3a). IL-6 is noteworthy owing that it has been broadly characterized as a major cancerogenic factor contributing to malignancy, EMT and metastasis of multifarious cancers, including HCC19. Hence IL-6 was selected as our following study object. First, IL-6 mRNA expression was detected in HCC cell lines and normal cells, confirming its upregulation in HCC cells (Fig. -(Fig.3b).3b). Additionally, IL-6 protein level was quantified using ELISA, showing the same tendency (Fig. -(Fig.3c).3c). The influence of DLGAP1-AS1 knockdown or overexpression on IL-6 was assessed on levels of mRNA and protein, indicating IL-6 was positively related with DLGAP1-AS1, which could sponge miR-26a/b-5p and deregulate IL-6 expression (Fig. 3d, e). As for the molecular mechanism, RIP assay illustrated that DLGAP1-AS1, miR-26a/b-5p, and IL-6 mRNA were enriched in anti-Ago2 groups (Fig. -(Fig.3f).3f). RNA pull-down assay verified the binding capacity of IL-6 mRNA with wild-type biotinylated probes for miR-26a/b-5p (Fig. -(Fig.3g).3g). To determine the molecular regulation between miR-26a/b-5p and IL-6 mRNA, luciferase activity of wild-type IL-6-3'-UTR reporters was initially lowered by miR-26a/b-5p, and then partially recovered with DLGAP1-AS1. Meanwhile, the luciferase activity of mutant reporters was barely affected (Fig. -(Fig.3h).3h). In conclusion, DLGAP1-AS1 could function as a ceRNA in HCC cells to competitively bind to miR-26a-5p and miR-26b-5p, thus upregulating the downstream gene IL-6.Considering the partial rescue of IL6 for DLGAP1-AS1 in HCC cells, we further investigated whether some other downstream targets exerted functions in DLGAP1-AS1-induced HCC cell activities. Our research continued to pursue potential downstream genes that could participate in hepatocarcinogenesis via activating Wnt/beta-catenin pathway. Then, we analyzed whether DLGAP1-AS1 and miR-26a/b-5p could regulate the activity of Wnt/beta-catenin pathway by directly regulating CTNNB1. Through luciferase reporter assays, we determined that DLGAP1-AS1 and miR-26a/b-5p could not directly regulate CTNNB1 (Fig. S3a-c), thus to activating Wnt/beta-catenin pathway. With the help of starBase, we discovered the binding sequences between miR-26a/b-5p and the 3'-UTR regions of cyclin-dependent kinase 8 (CDK8) and low density lipoprotein receptor-related protein 6 (LRP6) (Fig. -(Fig.6a).6a). CDK8 has been identified to be a hallmark regulator to activate Wnt/beta-catenin signaling through beta-catenin stabilization23. LRP6 has been recognized as a co-receptor to facilitate Wnt/beta-catenin signaling via promoting beta-catenin nuclear translocation24. Besides, both CDK8 and LRP6 have been reported to act as oncogenes in HCC25. As a consequence, these two genes were chosen as our study objects. The expression levels of CDK8 and LRP6 were evaluated likewise using qRT-PCRfor mRNAs and WB for proteins, illustrating their increase in HCC cells compared with normal cells (Fig. 6b, c). Besides, CDK8 and LRP6 were positively regulated by DLGAP1-AS1 on mRNA and protein levels (Fig. 6d, e). To demonstrate the molecular mechanism, the enrichment of DLGAP1-AS1, miR-26a/b-5p and mRNAs of CDK8 and LRP6 in anti-Ago2 groups was exhibited by RIP assay, indicating the recruitment of these molecules in RISCs (Fig. -(Fig.6f).6f). RNA pull-down assay showed that wild-type miR-26a/b-5p probes could significantly pull-down mRNAs of CDK8 or LRP6, illustrating their binding capacity (Fig. -(Fig.6g).6g). Moreover, luciferase activity of wild-type CDK8 or LRP6-3'-UTR reporters, not of mutant reporters, was reduced by miR-26a/b-5p, and partially enhanced by addition of pcDNA3.1/DLGAP1-AS1 (Fig. -(Fig.6h).6h). In conclusion, DLGAP1-AS1 could also act as a ceRNA to sponge miR-26a/b-5p and regulate CDK8 and LRP6.We further investigated the contribution of DLGAP1-AS1 to promoting HCC growth and metastasis by adopting an in vivo tumor model. After the xenograft tumor model had been established, compared with sh-NC group, tumors with significantly smaller size and lighter weight were developed in sh-DLGAP1-AS1 group, while miR-26a/b-5p suppression or IL6 overexpression rescued the inhibitory effect of DLGAP1-AS1 knockdown on tumorigenicity in vivo (Fig. S4a and Fig. 8a, b). Furthermore, the expression levels of genes involved in our study were measured using qRT-PCR ELISA and WB from xenograft tumor tissues, showing that the expression tendencies of these genes were in consistence with those in vitro (Fig. 8c-e). Eventually, we evaluated the capacity of tumor metastasis through observing and measuring the metastatic nodules transferring to lung tissues, illustrating that HCC lung metastasis was prominently inhibited by DLGAP1-AS1 knockdown, and the inhibitory effect could be reversed by knockdown of miR-26a/b-5p or the upregulation of IL6 (Fig. -(Fig.8f).8f).	31949128	RID07531	ceRNA or sponge	metastasis	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	DLGAP1-AS1	LRP6	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell growth(+);cell metastasis(+)	ceRNA(miR-26b-5p)	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000070018	NA	649446	4040	FLJ35776|HsT914	ADCAD2	Long non-coding RNA DLGAP1-AS1 facilitates tumorigenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via the feedback loop of miR-26a/b-5p/IL-6/JAK2/STAT3 and Wnt/beta-catenin pathway.First of all, according to UCSC Genome Browser online database, DLGAP1-AS1 expression level was relatively low in normal human liver tissues (Fig. -(Fig.1a).1a). Comparatively, the significantly elevated DLGAP1-AS1 expression in liver hepatocellular carcinoma (LIHC) dataset in comparison with normal dataset was presented using GEPIA online database (Fig. -(Fig.1b).1b). First, opposite with DLGAP1-AS1, miR-26a-5p and miR-26b-5p were downregulated in HCC cell lines in comparison with normal cells (Fig. -(Fig.2b).2b). Besides, DLGAP1-AS1 knockdown led to elevated levels of miR-26a/b-5p in Hep G2 cells, whereas DLGAP1-AS1 overexpression resulted in miR-26a/b-5p downregulation in SNU-387 cells, implying that miR-26a/b-5p were negatively regulated by DLGAP1-AS1 (Fig. -(Fig.2c).2c). In order to determine the molecular interaction, we conducted RIP assay using antibodies against Ago2, and the enrichment of DLGAP1-AS1 and miR-26a/b-5p with Ago2 antibodies was observed, indicating that they were recruited to RNA-induced silencing complexes (RISCs) and might have functional interactions (Fig. -(Fig.2d).2d). Besides, RNA pull-down assay illustrated the direct bond between DLGAP1-AS1 and miR-26a/b-5p at the correct binding sites, because only wild-type probes for miR-26a/b-5p could significantly pull-down DLGAP1-AS1 (Fig. -(Fig.2e).2e). Moreover, DLGAP1-AS1 luciferase reporters containing wild-type and mutant binding sites were constructed and transfected into HEK-293T cells. Wild-type reporters displayed a significantly repressed luciferase activity with miR-26a/b-5p overexpression, while luciferase activity of mutant reporters could barely be lowered (Fig. -(Fig.2f).2f). In conclusion, DLGAP1-AS1 was proven to act as a molecular sponge to sequester miR-26a-5p and miR-26b-5p.Based on our preceding study on the interaction between DLGAP1-AS1 and miR-26a/b-5p, we proceeded to search for potential genes targeted by miR-26a/b-5p. Using three online bioinformatics tools, we found that there were 380 mRNAs that can be regulated by both miR-26a-5p and miR-26b-5p (Fig. S1b). Next, these candidate mRNAs were subjected to qRT-PCRanalysis in response to the upregulation of miR-26a-5p or miR-26b-5p. Top five downregulated mRNAs were shown in Fig. S1c, among which IL6 was expressed lowest in cells transfected with miR-26a-5p mimics or miR-26b-5p mimics. With the aid of starBase that the mRNA of IL-6, a characteristic inflammatory cytokine closely involved in cancers, was an appropriate target for them (Fig. -(Fig.3a).3a). IL-6 is noteworthy owing that it has been broadly characterized as a major cancerogenic factor contributing to malignancy, EMT and metastasis of multifarious cancers, including HCC19. Hence IL-6 was selected as our following study object. First, IL-6 mRNA expression was detected in HCC cell lines and normal cells, confirming its upregulation in HCC cells (Fig. -(Fig.3b).3b). Additionally, IL-6 protein level was quantified using ELISA, showing the same tendency (Fig. -(Fig.3c).3c). The influence of DLGAP1-AS1 knockdown or overexpression on IL-6 was assessed on levels of mRNA and protein, indicating IL-6 was positively related with DLGAP1-AS1, which could sponge miR-26a/b-5p and deregulate IL-6 expression (Fig. 3d, e). As for the molecular mechanism, RIP assay illustrated that DLGAP1-AS1, miR-26a/b-5p, and IL-6 mRNA were enriched in anti-Ago2 groups (Fig. -(Fig.3f).3f). RNA pull-down assay verified the binding capacity of IL-6 mRNA with wild-type biotinylated probes for miR-26a/b-5p (Fig. -(Fig.3g).3g). To determine the molecular regulation between miR-26a/b-5p and IL-6 mRNA, luciferase activity of wild-type IL-6-3'-UTR reporters was initially lowered by miR-26a/b-5p, and then partially recovered with DLGAP1-AS1. Meanwhile, the luciferase activity of mutant reporters was barely affected (Fig. -(Fig.3h).3h). In conclusion, DLGAP1-AS1 could function as a ceRNA in HCC cells to competitively bind to miR-26a-5p and miR-26b-5p, thus upregulating the downstream gene IL-6.Considering the partial rescue of IL6 for DLGAP1-AS1 in HCC cells, we further investigated whether some other downstream targets exerted functions in DLGAP1-AS1-induced HCC cell activities. Our research continued to pursue potential downstream genes that could participate in hepatocarcinogenesis via activating Wnt/beta-catenin pathway. Then, we analyzed whether DLGAP1-AS1 and miR-26a/b-5p could regulate the activity of Wnt/beta-catenin pathway by directly regulating CTNNB1. Through luciferase reporter assays, we determined that DLGAP1-AS1 and miR-26a/b-5p could not directly regulate CTNNB1 (Fig. S3a-c), thus to activating Wnt/beta-catenin pathway. With the help of starBase, we discovered the binding sequences between miR-26a/b-5p and the 3'-UTR regions of cyclin-dependent kinase 8 (CDK8) and low density lipoprotein receptor-related protein 6 (LRP6) (Fig. -(Fig.6a).6a). CDK8 has been identified to be a hallmark regulator to activate Wnt/beta-catenin signaling through beta-catenin stabilization23. LRP6 has been recognized as a co-receptor to facilitate Wnt/beta-catenin signaling via promoting beta-catenin nuclear translocation24. Besides, both CDK8 and LRP6 have been reported to act as oncogenes in HCC25. As a consequence, these two genes were chosen as our study objects. The expression levels of CDK8 and LRP6 were evaluated likewise using qRT-PCRfor mRNAs and WB for proteins, illustrating their increase in HCC cells compared with normal cells (Fig. 6b, c). Besides, CDK8 and LRP6 were positively regulated by DLGAP1-AS1 on mRNA and protein levels (Fig. 6d, e). To demonstrate the molecular mechanism, the enrichment of DLGAP1-AS1, miR-26a/b-5p and mRNAs of CDK8 and LRP6 in anti-Ago2 groups was exhibited by RIP assay, indicating the recruitment of these molecules in RISCs (Fig. -(Fig.6f).6f). RNA pull-down assay showed that wild-type miR-26a/b-5p probes could significantly pull-down mRNAs of CDK8 or LRP6, illustrating their binding capacity (Fig. -(Fig.6g).6g). Moreover, luciferase activity of wild-type CDK8 or LRP6-3'-UTR reporters, not of mutant reporters, was reduced by miR-26a/b-5p, and partially enhanced by addition of pcDNA3.1/DLGAP1-AS1 (Fig. -(Fig.6h).6h). In conclusion, DLGAP1-AS1 could also act as a ceRNA to sponge miR-26a/b-5p and regulate CDK8 and LRP6.We further investigated the contribution of DLGAP1-AS1 to promoting HCC growth and metastasis by adopting an in vivo tumor model. After the xenograft tumor model had been established, compared with sh-NC group, tumors with significantly smaller size and lighter weight were developed in sh-DLGAP1-AS1 group, while miR-26a/b-5p suppression or IL6 overexpression rescued the inhibitory effect of DLGAP1-AS1 knockdown on tumorigenicity in vivo (Fig. S4a and Fig. 8a, b). Furthermore, the expression levels of genes involved in our study were measured using qRT-PCR ELISA and WB from xenograft tumor tissues, showing that the expression tendencies of these genes were in consistence with those in vitro (Fig. 8c-e). Eventually, we evaluated the capacity of tumor metastasis through observing and measuring the metastatic nodules transferring to lung tissues, illustrating that HCC lung metastasis was prominently inhibited by DLGAP1-AS1 knockdown, and the inhibitory effect could be reversed by knockdown of miR-26a/b-5p or the upregulation of IL6 (Fig. -(Fig.8f).8f).	31949128	RID07532	ceRNA or sponge	metastasis	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065)
Cervical cancer	OIP5-AS1	ROCK1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000067900	NA	729082	6093	cyrano|linc-OIP5	p160ROCK	lncRNA OIP5-AS1 targets ROCK1 to promote cell proliferation and inhibit cell apoptosis through a mechanism involving miR-143-3p in cervical cancer.To assess the molecular function of OIP5-AS1 in human CC, we analyzed OIP5-AS1 expression in CC tissues according to GEPIA (Gene Expression Profiling Interactive Analysis, http://gepia.cancer-pku.cn) database by bioinformatics analysis. It was found that OIP5-AS1 expression in CC tissues (n=306, Table 1) was significantly higher than in adjacent normal controls (P<0.05) (Figure 1A). In addition, we examined the overall survival of these patients in terms of OIP5-AS1 expression pattern using the Kaplan-Meier plotter survival analysis. The data showed that the OIP5-AS1 expression level was highly correlated with the outcome (Figure 1B). We then applied hematoxylin-eosin (HE) staining analysis in tumor tissues as well as adjacent normal tissues. As shown in Figure 1C, the cell population in CC tissues was enhanced compared to adjacent normal controls.To further investigate the regulation mechanism of OIP5-AS1 on CC, we studied its function by loss-of-function analysis in C-33 cells, because of the highest expression of OIP5-AS1 in this cell line (Figure 1E). We knocked down OIP5-AS1 expression using its specific short hairpin RNA (shRNA), which was verified by qRT-PCR(Table 2) results (Figure 2A). A further CCK-8 proliferation assay demonstrated that OIP5-AS1 depletion dramatically attenuated the cell proliferation potential of C33A cells (P<0.05) (Figure 2B). Consistent with this, western blotof cell cycle markers cyclin A and cyclin B1 also showed their significantly decreased expression in OIP5-AS1-depleted C33A cells compared with normal controls (Figure 2C and D). Moreover, OIP5-AS1 depletion caused cell apoptosis in C33A cells as measured by Annexin V-FITC-PI staining (Figure 2E and F). Besides, we performed western blot assay to check the apoptosis markers Bax and cleaved Caspase-3 expression in these cell population and the results showed their significantly enhanced expression in OIP5-AS1-depleted C33A cells, which was consistent with Annexin V-FITC-PI apoptosis analysis (Figure 2G and H). Together, these data demonstrated that down-regulation of OIP5-AS1 could inhibit cell proliferation and promote cell apoptosis in cervical cancer cells.We then sought to identify the downstream effectors of lncRNA OIP5-AS1 in the regulation of CC. Our bioinformatics analysis according to GEPIA database showed that Rho Associated Coiled-Coil Containing Protein Kinase 1 (ROCK1) expression was positively correlated with OIP5-AS1 (R=0.55; Figure 3A). In addition, as a consequence, high ROCK1 levels were associated with poor survival rates of patients (Figure 3A). qRT-PCR(Table 2) assay verified that OIP5-AS1 overexpression could upregulate ROCK1 expression, while OIP5-AS1 depletion downregulated ROCK1 expression in C33A cells (Figure 3B). Furthermore, western blot assay demonstrated that OIP5-AS1 positively regulated ROCK1 protein expression as well (Figure 3C). Next, as shown in Figure 3D by qRT-PCR ROCK1 expression was much higher in CC tissues compared with adjacent normal controls (P<0.05).lncRNA OIP5-AS1 has been reported to function as a ceRNA and interact with some microRNAs (miRNAs) in multiple cancer cells (27). To determine whether OIP5-AS1 acted as a ceRNA to bind some miRNAs in the regulation of CC, we first checked the localization of OIP5-AS1 in the C33A cells using cytoplasmic and nuclear fractionation assay. It was found that OIP5-AS1 was mostly localized in cytoplasm of C33A cells (Figure 4A). Then, we used TargetScan (http://www.targetscan.org/vert_72/) to predict potential OIP5-AS1-miRNAs interactions, and miR-143-3p was identified. qRT-PCRanalysis showed negative correlation between OIP5-AS1 and miR-143-3p (Figure 4B). In OIP5-AS1-depletion C33A cells, the expression of miR-143-3p was enhanced, and vice versa (Figure 4B). In addition, miR-143-3p expression was much lower in cancer tissues compared with adjacent normal controls (P<0.05), as measured by qRT-PCRanalysis (Figure 4C) (Table 2). Overexpression of miR-143-3p significantly attenuated C33A cell proliferation by CCK-8 assay (Figure 4D and E). On the other hand, miR-143-3p overexpression promoted cell apoptosis (Figure 4F and G). The expression tendency of cell cycle markers (cyclin A and cyclin B1) and cell apoptosis markers (Bax and cleaved Caspase-3) in miR-143-3p overexpression cells was consistent with the cell phenotypes indicated above (Figure 4H). These data about miR-143-3p molecular function showed negative correlation with that of OIP5-AS1, indicating that OIP5-AS1 acts as a molecular sponge of miR-143-3p in the regulation of CC.We identified OIP5-AS1 as a molecular sponge of miR-143-3p in CC cells, then we sought to test the binding sites of miR-143-3p in OIP5-AS1. Luciferase reporter assay performed in C33A cells showed that the activity of luciferase reporters containing the theoretical binding sites in lncRNA OIP5-AS1 was inhibited by miR-143-3p overexpression in OIP5-AS1-WT constructs, while miR-143-3p depletion by its inhibitor promoted this reporter activity (Figure 5A). Besides, there was no effect in OIP5-AS1-Mut constructs by miR-143-3p (Figure 5A). Furthermore, overexpression of miR-143-3p binding deficiency mutant form (miR-143-3p Mut), which abolishes its binding with OIP5-AS1, on OIP5-AS1-WT luciferase reporter showed no effect either (Figure 5B). These results demonstrated the binding sites between OIP5-AS1 and miR-143-3p.	31939597	RID07533	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung squamous cell carcinoma	LNCRNA-ATB	ILF3	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-590-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000129351	NA	114004396	3609	NA	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	LncRNA-ATB Promotes Lung Squamous Carcinoma Cell Proliferation, Migration, and Invasion by Targeting microRNA-590-5p/NF90 Axis.As illustrated by Figure 1A, compared to adjacent normal tissues, lncRNA-ATB level was strikingly increased in LSC tissues (p<0.01).We found that the proliferative activity of lncRNA-ATB overexpressing NCI-H226 cells was markedly suppressed in comparison to the control by colony formation assay and CCK-8 assay (Fig. 2B, C, and F,p<0.05). Immunofluorescence revealed that lncRNA-ATB overexpression greatly elevated the proportion of Ki-67 positive rate in NCI-H226 cells (Fig. 2D, E,p<0.05). In contrast, lncRNAATB silencing led to the opposite phenotypes in NCI-H226 cells. In addition, in squamous cell lung carcinoma cell line EBC-1, the significant upregulation or downregulation of lncRNA-ATB levels was identified by RT-qPCR in EBC1-lncRNA-ATB-OE (overexpressing lncRNA-ATB) or EBC-1-sh lncRNA-ATB cells (silencing lncRNA-ATB), respectively (Fig. 2G). Consistent with what wasobservedin NCI-H226 cells, lncRNA-ATB overexpression strikingly increased the proliferative ability of EBC-1 cells, whereas lncRNA-ATB silencing greatly inhibited the proliferative capacity of EBC-1 (Fig. 2H).Results showed that the expression levels of epithelial phenotype-related genesEcadherinandcytokeratinwere dramatically upregulated in lncRNA-ATB silenced NCI-H226 cells, while the expression of mesenchymal property-related genesN-cadherin andvimentinwas remarkably downregulated in the level of mRNA and protein, compared to the control (Fig. 4AC, p<0.05).Luciferase reporter assay validated that lncRNA-ATB has a direct effect on microRNA-590-5p (Fig. 6N), and microRNA-590-5p has direct interaction with the 3'UTR of NF-90 (Fig. 6O). Similar to the results mentioned above, when treating lncRNA-ATB overexpressing NCI-H226 cells with microRNA590-5p mimics, NF-90 expression was greatly increased compared with untreated NCI-H226 cells overexpressing lncRNA-ATB (Fig. 7A,p<0.05). In addition, after treating lncRNA-ATB silenced NCI-H226 cells with microRNA-5905p antagomir, NF-90 expression was markedly decreased compared to untreated lncRNA-ATB silenced NCI-H226 cells (Fig. 7D ,p<0.05). Moreover, cell proliferative assay and Transwell assay (with or without Matrigel) revealed that compared to untreated cells, the proliferative activity and migratory and invasive abilities were remarkably elevated in lncRNA-ATB overexpressing NCI-H226 cells after treating with microRNA-590-5p mimics (Fig. 7G , p<0.05).	31934791	RID07534	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Urinary bladder cancer	ROR1-AS1	MIR504	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000223949	GRCh38_1:64094379-64171342	ENSG00000207800	NA	101927034	574507	NA	MIRN504|hsa-mir-504|mir-504	Upregulation of long non-coding RNA ROR1-AS1 promotes cell growth and migration in bladder cancer by regulation of miR-504.The relative expression levels of ROR1-AS1 was determined by RT-qPCR in a total of 65 cases of bladder cancer patients. Compared with adjacent matched normal bladder tissues, the ROR1-AS1 levels were notably upregulated in bladder cancer tissues (Fig 1A, p<0.05). Subsequently, we analyzed the expression levels of ROR1-AS1 in multiple bladder cancer cell lines (T24, 5637, J82, 253J and RT4). ROR1-AS1 expression was also increased significantly in the five bladder cancer cells compared with the normal bladder epithelial cell (SV-HUC-1) (Fig 1B, p<0.05).To examine the potential roles of ROR1-AS1 in the proliferation and migration of bladder cancer, T24 and 5637 cells were chose and treated with shRNA-ROR1-AS1 or shRNA-NC using MTT and wound scratch assays. As presented in Fig 3A, ROR1-AS1 siRNA transfected T24 cells significantly decreased ROR1-AS1 expression levels, and knockdown of ROR1-AS1 inhibited T24 cell growth and migration (p<0.05). Meanwhile, shRNA-ROR1-AS1 treated cells downregulated ROR1-AS1 expression in 5637 cells, and arrested 5637 cell proliferation and migration (Fig 3B, p<0.05). These data demonstrated that ROR1-AS1 contributes to cell proliferation and migration in bladder cancer. Pearson correlation analysis showed that miR-504 expression was negatively correlated with ROR1-AS1 expression in bladder cancer samples (Fig 4B, p<0.05). The potential binding sites for miR-504, ROR1-AS1-WT and ROR1-AS1-MUT were constructed in luciferase reporter gene vectors (Fig 4C). Results showed that transfection of miR-504 inhibitor in T24 and 5637 cells significantly suppressed miR-504 expression (Fig 4D, p<0.05). Knockdown of miR-504 increased the luciferase activity of ROR1-AS1-WT vector, but not ROR1-AS1-MUT vector in T24 and 5637 cells (Fig 4E, p<0.05). Transfection of shRNA-ROR1-AS1 into bladder cancer cells showed upregulation of miR-504 expression, but co-transfection with shRNA-ROR1-AS1 and miR-504 inhibitor reversed these effects (Fig 4F, p<0.05). These findings indicated that ROR1-AS1 bind with miR-504 and acts as a molecular sponge to decrease miR-504 expression.Due to the negatively regulation of ROR1-AS1 on miR-504 in bladder cancer cells, we speculated that the role of ROR1-AS1 in regulating bladder cancer cell proliferation and migration was mediated by sponging miR-504 expression. We transfected miR-504 inhibitor or inhibitor NC into the shRNA-ROR1-AS1 treated T24 and 5637 cells, and functional rescue experiments were performed. Interesting, we found that ROR1-AS1 knockdown mediated inhibitory effects on bladder cancer cell proliferation and migration were partially reversed by co-transfection with shRNA-ROR1-AS1 and miR-504 inhibitor (Fig 5A and 5B, p<0.05).	31929567	RID07535	ceRNA or sponge	NA	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Endometrial cancer	PCAT1	E-cadherin	negatively-E	knockdown;siRNA	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	LncRNA PCAT1 promotes metastasis of endometrial carcinoma through epigenetical downregulation of E-cadherin associated with methyltransferase EZH2.We applied quantitative RT-PCRanalysis on total RNAs extracted from one hundred pairs of endometrial carcinoma (EC, n = 100) and paracancerous tissue (PCT, n = 100). In comparison between these two groups, the expression of lncRNA PCAT1 is strongly significant different withp< 0.001 (Fig. 1A).The comparative study exhibited that the colony numbers from sh-PCAT1#1 and sh-PCAT1#2 treated KLE cells grew much less than that from sh-NC treated KLE cells (p< 0.001;Fig. 3D), and the colony numbers from sh-PCAT1#1 and sh-PCAT1#2 treated AN3CA cells grew much less than that from sh-NC treated AN3CA cells (p< 0.001;Fig. 3E) as well.We first transfected sh-NC, sh-PCAT1#1 and sh-PCAT1#2 constructs into KLE and AN3CA and then measured the mRNA level of Ecadherin, N-cadherin and Vimentin at transcription level after 48-hour culture. Our quantitative RT-PCRexhibits that E-cadherin but not Ncadherin and Vimentin strongly significantly increased, when lncRNA CAT1 was knocked-down in two groups of the cultured KLE cells treated with sh-PCAT1#1 and sh-PCAT1#2 constructs and controlled by sh-NC constructs (Fig. 5A left). The experiments with AN3CA cell lines displayed the similar results when lncRNA PCAT1 was knockeddown with sh-PCAT1#1 and sh-PCAT1#2 constructs compared with shNC constructs. In two lncRNA PCAT1 knocked-down groups, only expression of E-cadherin exhibited strongly significant increase on its mRNA transcription but there were no significant changes on the mRNA transcription of N-cadherin and Vimentin (Fig. 5A right).Under the condition of lncRNA PCAT1 knockdown in both KLE and AN3CA cell lines, the translation level of E-cadherin, N-cadherin and Vimentin exhibited the similar upregulation on protein expression. In KLE cells, only E-cadherin protein was significantly upregulated on western blotwhen expression of lncRNA PCAT1 was silenced down with sh-PCAT1#1 and sh-PCAT1#2 constructs compared with the sh-NC group. But the translation levels of N-cadherin and Vimentin were remained the same among three groups (Fig. 5B, left). In AN3CA cells with lncRNA PCAT1 knockdown caused by sh-PCAT1#1 and sh-PCAT1#2 constructs, only E-cadherin protein but not N-cadherin and Vimentin proteins exhibited upregulation controlled by the sh-NC constructs (Fig. 5B, right).Subsequently, under the conditions of EZH2 overexpression or knocking-down, we analyzed the E-cadherin translation in both KLE and AN3CA cells. Quantitative Western analysis on E-cadherin protein demonstrated that, when EZH2 was over-expressed in the EC cells, the protein expressions of E-cadherin were down-regulated significantly in both cell lines (Fig. 7D left and middle). Again, when expression of EZH2 was knocked-down, the protein expression of E-cadherin was dramatically increased. The EZH2 knockdown was performed with siEZH2 construct and controlled with si-EZH2 constructs as well (Fig. 7D left and right).In order to identify if the histone methyltransferation directly effects on the lncRNA PCAT1viaEZH2, we performed immunoprecipitation within KLE and AN3CA cell lines. After applied biotin conjugated probe specific against PCAT1, the biotin- lncRNA PCAT1 pulled down significant more EZH2 than that of the bio-NC in both KLE and AN3CA cells (Fig. 8A left). The biotin conjugate-pulled down-complex showed much more EZH2 protein enrichment in the biotin- lncRNA PCAT1 group than that of the complex from the bio-NC group (Fig. 8A middle and right). Reversely, we also carried out the immunoprecipitation by using antibody specific against EZH2 as the pull-down antibody and then employed the PCAT1 antibody to perform qRT-PCRanalysis to examine the expression level of the lncRNA PCAT1 in both within KLE and AN3CA cells. The qRT-PCRanalysis unveiled that the PCAT1 mRNA could be amplified much more from the pull-down complex with EZH2 antibody than that from the IgG pull-down (allp< 0.001; Fig. 8B).	31927050	RID07536	epigenetic regulation	metastasis	UP(LIHC);DATA(GSE117623)	
Esophagus squamous cell carcinoma	PCAT1	ANXA10	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-508-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000109511	NA	100750225	11199	PCA1|PCAT-1|PiHL	ANX14	LncRNA PCAT-1 Promoted ESCC Progression via Regulating ANXA10 Expression by Sponging miR-508-3p.As shown in Figure 1A, all three ESCC cells lines exhibited significantly higher PCAT-1 expression when compared with the normal esophageal squamous epithelial cells. Knockdown of PCAT-1 in KYSE150 and KYSE450 cells was carried out using RNA interference. Figure 1B and -andCC demonstrated the successful knockdown of PCAT-1 in KYSE150 and KYSE450 cells by two different PCAT-1 siRNAs (si-1 and si-2). As si-2 was more effective to down-regulated PCAT-1 expression, si-2 was selected for further in vitro functional assays and was named as si-PCAT1. As shown in Figure 1D and -andE,E, after PCAT-1 knockdown, the proliferative rates of these two cells lines were significantly decreased when compared with the siRNA control cells. In addition, transwell invasion assay and wound healing assay showed that both invasion and migration of KYSE150 and KYSE450 cells were inhibited after PCAT-1 knockdown (Figure 1F ).Using StarBase online analysis tool, miR-508-3p was found to potentially bind to PCAT-1 with putative binding sites indicated in Figure 2A. To study the interactions between miR-508-3p and PCAT-1, miR-508-3p mimics and inhibitors were used to manipulate its expression in ESCC cells. In KYSE150 cells, as shown in Figure 2B, miR-508-3p mimics and inhibitors successfully increased and decreased the relative expression level of miR-508-3p, respectively. dual-luciferase reporter assay demonstrated that the luciferase activity of the reporter containing PCAT-1-WT, rather than PCAT-1-MUT, was negatively correlated with the expression of miR-508-3p in KYSE150 cells (Figure 2C and -andD).D). Accordingly, the relative PCAT-1 expression in KYSE150 cells was also found to be negatively correlated with the expression of miR-508-3p (Figure 2E). On the other hand, the relative expression levels of miR-508-3p was down-regulated and up-regulated by overexpression and knockdown of PCAT-1, respectively (Figure 2F). Moreover, as shown in Figure 2I, overexpression of PCAT-1 also led to an increase in the proliferation of KYSE150 cells. In the presence of miR-508-3p mimics, the increase in KYSE150 cell proliferation was decreased. Similarly, both invasion and migration of KYSE150 cells were increased by overexpression of PCAT-1, such increases were reversed by miR-508-3p mimics (Figure 2J and -andKK).Furthermore, using StarBase online analysis tool, miR-508-3p was also found to potentially bind to ANXA10 3-UTR with putative binding sites indicated in Figure 3A. As shown in Figure 3B and -andC,C, dual-luciferase reporter assay indicated that the luciferase activity of the reporter containing ANXA10 3-UTR-WT, rather than ANXA10 3-UTR-MUT, was negatively correlated with the expression of miR-508-3p in KYSE150 cells. Besides, both mRNA and protein expression of ANXA10 were down-regulated and up-regulated by miR-508-3p mimics and inhibitor in KYSE150 cells, respectively (Figure 3D and -andE).E). Given the direct relationship between lncRNA PCAT-1 and miR-508-3p, the regulation of ANXA10 by PCAT-1 was also explored. As shown in Figure 3F and -andG,G, after knockdown of PCAT-1 in KYSE150 cells, both mRNA and protein expression of ANXA10 were down-regulated. Moreover, overexpression of PCAT-1 led to an increase in the mRNA and protein expression of ANXA10, such increase was also reversed in the presence of miR-508-3p mimics (Figure 3 3H and -andII).	31920393	RID07537	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC);DATA(GSE117623)
Triple-negative breast cancer	CCAT2	NOTCH2	positively-E	siRNA	upregulation	RT-PCR	NA	NA	cell stemness(+);tumorigenesis(+)	ceRNA(miR-205)	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000134250	NA	101805488	4853	LINC00873|NCCP1	NA	Long non-coding RNA CCAT2 promotes oncogenesis in triple-negative breast cancer by regulating stemness of cancer cells.Additional analyses were carried out in the metastatic breast cancer cells as well as BCSCs. Much higher levels of CCAT2 were demonstrated in 4173 and 4175 cells, two lungmetastatic sublines with high degree of malignancy derived from MDAMB-231 cells (Fig. 1C), and in ALDH + BCSCs compared to ALDH- nonstem breast cancer cells (Fig. 1D).Wound healing assay demonstrated the induction of cell migration by CCAT2 in both MDA-MB-231 (Fig. 2F, G) and MCF-10ASrc (Supplemental Fig. S3D-S3E) cells. In order to further validate the observations, shRNAs were applied to TNBC cells to knockdown CCAT2, followed by cell proliferation and cell invasion assays. As shown inFig. 2H, effects of two shRNA sequences were tested in MDAMB-231 cells, demonstrating 65'-0 % knockdown of endogenous CCAT2 by sh-CCAT2, much better than sh-CCAT2-2. As such sh-CCAT2 was used for all knockdown assays thereafter. As expected, decreased cell proliferation and invasion were observed in sh-CCAT2-treated MDA-MB-231 cells (Fig. 2I ).OCT4-PG1 is one of the OCT4 pseudogenes. A significant positive correlation between CCAT2 and OCT4-PG1 in expression was observed in human breast cancer (Fig. 4B). Upregulation of OCT4-PG1 was associated with the overexpression of CCAT2 in MDA-MB-231 cells at both mRNA and protein levels (Fig. 4C, D), and in MCF-10A-Src cells as well (Supplemental Fig. S5A, S5B). In consistence, knockdown of CCAT2 decreased the expression of OCT4-PG1 (Fig. 4E). To determine whether OCT4-PG1 regulates cancer stem cells in TNBC cells, OCT4-PG1 was knocked down in MDA-MB-231 cells by a shRNA, followed by ALDH analysis. As shown inFig. 5F and G, knockdown of OCT4-PG1 decreased stemness in TNBC cells. Moreover, we demonstrated the positive regulation of OCT4 expression by OCT4-PG1 (Supplemental Fig. S6), suggesting both OCT4 and OCT4-PG1 may mediate the stem cell regulation by CCAT2 in TNBC.Sequence analysis between CCAT2 and miRNAs predicted CCAT2miR-205 sponge interaction. A potential binding site to miR-205 was found within CCAT2 mRNA sequence (Fig. 6A). In order to confirm the interaction between CCAT2 and miR-205, gene expression vectors carrying either wild type (WT) or miR-205 binding site-mutated (MU) CCAT2 (Fig. 6A) were transfected into TNBC cells, followed by miR-205 expression analysis. WT CCAT2 decreased the miR-205 level by sponge interaction, while MU CCAT2 did not, in both MDA-MB-231 (Fig. 6B) and MCF-10A-Src (Supplemental Fig. S7) cells. Upregulation of miR205 was observed in CCAT2- knockdown cells (Fig. 6C).Notch2, as a well-demonstrated target gene of miR-205, was further analyzed. Inhibition of Notch2 by miR-205 was conformed in TNBC cells (Fig. 6K and Supplemental Fig. S9B). In consistence with the miR205 sponge by CCAT2, positive regulation of Notch2 by CCAT2 was demonstrated in both CCAT2 overexpressing or knocking down cells (Fig. 6L, M and Supplemental Fig. S9C). A positive correlation between CCAT2 and Notch2 in expression in human breast cancer patients (Fig. 6N) further supported the results above. In consideration of the important roles Notch signaling plays in regulating stem cell, out findings strongly suggested that CCAT2-miR-205-Notch is another signal pathway, along with CCAT2-OCT4-PG1, mediating the stemness regulation in TNBC by CCAT2 (Fig. 7).	31904506	RID07538	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Triple-negative breast cancer	CCAT2	OCT4-PG1	positively-E	siRNA	upregulation	RT-PCR	NA	NA	cell stemness(+);tumorigenesis(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000212993	NA	101805488	NA	LINC00873|NCCP1	NA	Long non-coding RNA CCAT2 promotes oncogenesis in triple-negative breast cancer by regulating stemness of cancer cells.Additional analyses were carried out in the metastatic breast cancer cells as well as BCSCs. Much higher levels of CCAT2 were demonstrated in 4173 and 4175 cells, two lungmetastatic sublines with high degree of malignancy derived from MDAMB-231 cells (Fig. 1C), and in ALDH + BCSCs compared to ALDH- nonstem breast cancer cells (Fig. 1D).Wound healing assay demonstrated the induction of cell migration by CCAT2 in both MDA-MB-231 (Fig. 2F, G) and MCF-10ASrc (Supplemental Fig. S3D-S3E) cells. In order to further validate the observations, shRNAs were applied to TNBC cells to knockdown CCAT2, followed by cell proliferation and cell invasion assays. As shown inFig. 2H, effects of two shRNA sequences were tested in MDAMB-231 cells, demonstrating 65'-0 % knockdown of endogenous CCAT2 by sh-CCAT2, much better than sh-CCAT2-2. As such sh-CCAT2 was used for all knockdown assays thereafter. As expected, decreased cell proliferation and invasion were observed in sh-CCAT2-treated MDA-MB-231 cells (Fig. 2I ).OCT4-PG1 is one of the OCT4 pseudogenes. A significant positive correlation between CCAT2 and OCT4-PG1 in expression was observed in human breast cancer (Fig. 4B). Upregulation of OCT4-PG1 was associated with the overexpression of CCAT2 in MDA-MB-231 cells at both mRNA and protein levels (Fig. 4C, D), and in MCF-10A-Src cells as well (Supplemental Fig. S5A, S5B). In consistence, knockdown of CCAT2 decreased the expression of OCT4-PG1 (Fig. 4E). To determine whether OCT4-PG1 regulates cancer stem cells in TNBC cells, OCT4-PG1 was knocked down in MDA-MB-231 cells by a shRNA, followed by ALDH analysis. As shown inFig. 5F and G, knockdown of OCT4-PG1 decreased stemness in TNBC cells. Moreover, we demonstrated the positive regulation of OCT4 expression by OCT4-PG1 (Supplemental Fig. S6), suggesting both OCT4 and OCT4-PG1 may mediate the stem cell regulation by CCAT2 in TNBC.Sequence analysis between CCAT2 and miRNAs predicted CCAT2miR-205 sponge interaction. A potential binding site to miR-205 was found within CCAT2 mRNA sequence (Fig. 6A). In order to confirm the interaction between CCAT2 and miR-205, gene expression vectors carrying either wild type (WT) or miR-205 binding site-mutated (MU) CCAT2 (Fig. 6A) were transfected into TNBC cells, followed by miR-205 expression analysis. WT CCAT2 decreased the miR-205 level by sponge interaction, while MU CCAT2 did not, in both MDA-MB-231 (Fig. 6B) and MCF-10A-Src (Supplemental Fig. S7) cells. Upregulation of miR205 was observed in CCAT2- knockdown cells (Fig. 6C).Notch2, as a well-demonstrated target gene of miR-205, was further analyzed. Inhibition of Notch2 by miR-205 was conformed in TNBC cells (Fig. 6K and Supplemental Fig. S9B). In consistence with the miR205 sponge by CCAT2, positive regulation of Notch2 by CCAT2 was demonstrated in both CCAT2 overexpressing or knocking down cells (Fig. 6L, M and Supplemental Fig. S9C). A positive correlation between CCAT2 and Notch2 in expression in human breast cancer patients (Fig. 6N) further supported the results above. In consideration of the important roles Notch signaling plays in regulating stem cell, out findings strongly suggested that CCAT2-miR-205-Notch is another signal pathway, along with CCAT2-OCT4-PG1, mediating the stemness regulation in TNBC by CCAT2 (Fig. 7).	31904506	RID07539	expression association	metastasis		
Osteosarcoma	RP11-361F15.2	CPEB4	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);M2-Like polarization(+);cell growth(+);tumorigenesis(+)	ceRNA(miR-30c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000225135	NA	ENSG00000113742	NA	NA	80315	NA	CPE-BP4|hCPEB-4	LncRNA RP11-361F15.2 promotes osteosarcoma tumorigenesis by inhibiting M2-Like polarization of tumor-associated macrophages of CPEB4.In our previous study, lncRNA microarray was conducted on osteosarcoma tissues (n= 3) with respective controls, and we identified a 24-fold upregulation of lncRNA RP11-361F15.2 in OS tissues when compared with control tissues (Fig. S1A). To understand the role of RP11-361F15.2 in OS tissues, relative RP11-361F15.2 expression levels were obtained compared with non-tumor tissues (Fig. 1A,n= 40 pairs, p= 0.0003). We observed that expression levels of RP11-361F15.2 were highly upregulated in OS tissues when compared with the nontumorous tissues. It was also evident that RP11-361F15.2 was highly expressed in metastatic tissues (Fig. 1B,n= 17/23,p< 0.001). It was clear that the MG63 cells with lncRNA knockdown RP11-361F15.2 (RP11-361F15.2 shRNA) showed decreased proliferation, when compared with its control (p= 0.0021).We observed that knockdown of RP11-361F15.2 (shRNA RP11-361F15.2) caused a significant decrease in the number of colonies formed by the MG-63 cell line (p= 0.0042), whereas U2OS cells with overexpression of RP11-361F15.2 (pcDNA RP11-361F15.2) caused an opposite effect (p= 0.0042) (Fig. 2C).Additionally, Pearson's correlation analysis indicated a strong negative correlation between RP11-361F15.2 and miR-30c-5p (Fig. 3C, p= 0.0958). Further, we performed luciferase assay, where in we used a luciferase reporter in the 3'UTR end of the RP11-361F15.2 and we observed in the presence of miR-30c-5p mimics, the luciferase activity was highly downregulated. But, when we tried the same experiment with a mutated RP11-361F15.2, it was clear that there was no change in the luciferase activity in the presence of miR-30c-5p. This indicated that miR-30c-5p can strongly inhibit RP11-361F15.2 (Fig. 3D,p= 0.0461). To identify if miR30c-5p and RP11-361F15.2 co-expressed or interacted with each other, we performedfluorescence in situ hybridization (FISH) and RNA immunoprecipitation (RIP) studies. Using FISH, we identified that miR30c-5p could co-localize with RP11-361F15.2 (Fig. 3J). We also performed RIP studies where in a miR-30c-5p overexpression model, IP with an anti-AGO2 antibody indicated that there is a strong interaction between miR-30c-5p and RP11-361F15.2 (Fig. 3K).To understand the interconnections between RP11-361F15.2, miR30c-5p, and CPEB4, we performed luciferase assay with the reporter attached to the CPEB4. Initially, in the presence of RP11-361F15.2, it was clear that CPEB4 was highly expressed. This confirmed our hypothesis that indeed RP11-361F15.2 positively regulated CPEB4 levels. However, in the presence of miR-30c-5p and RP11-361F15.2, the CPEB4 signal was downregulated. This indicated the strong role of miR30c-5p in regulating the expression of both lncRNA and CPEB4 (Fig. 7A) which was also confirmed using RT-PCRbased experiments (Fig. 7B and C). Similarly, we overexpressed RP11-361F15.2 and found a significant increase in CPEB4 levels. We also observed similar results when performing western blot experiments (Fig. 7D). Additionally, when we overexpressed RP11-361F15.2 and miR-30c-5p together it was clear that the CPEB4 expression levels were highly downregulated in U2OS cells (Fig. 7E,p= 0.0086). However, when we silenced RP11361F15.2 and miR-30c-5p, CPEB4 was highly upregulated in MG63 cells (Fig. 7F,p= 0.0006). This indicated that miR-30c-5p is a very strong regulator of CPEB4. Additionally, we performed migration and invasion studies on MG-63 and U2OS cell lines. Here also we observed silencing of RP11-361F15.2 along with inhibition of miR-30c-5p increases the migration/invasion of MG-63 cells (Fig. 7G,p= 0.0074/ 0.0086). But, overexpression of RP11-361F15.2 along with miR-30c-5p mimics highly decreased the migration/invasion of U2OS cells (Fig. 7H, p= 0.0065/0.0031). This further ascertained the strong effect of miR30c-5p on tumorigenesis through regulation RP11-361F15.2 and CPEB4.To understand the roles of RP11-361F15.2 and CPEB4 in anin vivo model, we developed a BALB/c nude mice model and subcutaneously transplanted MG-63 or U2OS cells. Firstly, we overexpressed RP11361F15.2 in U2OS cells and transplanted into the nude mice. Every week, we checked the developing weight and volume of the tumors. It was evident that, the tumor size kept increasing significantly when compared to its corresponding controls (Fig. 8A,p= 0.00018). On the contrary, we performed the same experiments on MG-63 cells which had RP11-361F15.2 silenced. When we transplanted these cells and observed the tumor growth, it was clear that the tumor volume and the weight decreased significantly, when compared to its corresponding controls (Fig. 8B,p= 0.0086). Further, we also transplanted cells with overexpression of CPEB4, CPEB4 with miR-3c-5p, and CPEB4 with RP11-361F15.2 and transplanted onto the nude mice model (Fig. 8C). It was clear, post 4 weeks that the tumors which had CPEB4 overexpressed cells had a bigger tumor size formed. Nevertheless, in the presence of miR-30c-5p, the tumor size decreased significantly. Additionally, another group of mice were transplanted with cells overexpressing both CPEB4 and RP11-361F15.2, and this produced the largest tumors. Post 4 weeks, we isolated the mRNA of the tumor samples and performed RT-PCRexperiments. We observed that when we silenced RP11-361F15.2, the tumors had less CPEB4 expression (p= 0.0054), whereas overexpression of RP11-361F15.2 showed increased CPEB4 expression (p= 0.00018,Fig. 8D). We also performed western blotfor all these tumors and confirmed that silencing of RP11-361F15.2 downregulated the expression of CPEB4 and overexpression of miR-30c-5p decreased CPEB4 expression (Fig. 8E). This above-mentioned data indeed clearly indicated that RP11361F15.2 has a key role in tumorigenesis through CPEB4 activation and miR-30c-5p acts as an important regulator of the pathway.	31904478	RID07540	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Colon cancer	LINC00662	CLDN8	positively-E	luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);ERK signaling pathway(+)	ceRNA(miR-340-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000156284	NA	148189	9073	NA	NA	LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.LINC00662 was markedly high expression in tumor tissues from 72 patients with colon cancer (Fig. 1a). The survival rate of colon cancer  patients with LINC00662 high expression was higher than that of colon cancer  patients with LINC00662 low expression, whereas, there was no statistically significant difference in survival rate between LINC00662 high expression and LINC00662 low expression (the relative expression of LINC00662->-4 as high expression; Fig. -Fig.1b).1b).CCK8 and clone formation assays were utilized for confirming the proliferation of LINC00662 overexpression or LINC00662 inhibition transfected colon cancer cells. High expression of LINC00662 observably facilitated the viability of HCT29 and LS174T cells (Fig. -(Fig.1f1f and g), in opposite terms, low expression of LINC00662 observably suppressed the viability of LOVO and CT26 cells (Fig. -(Fig.1h1h and i). High expression of LINC00662 endowed HCT29 and LS174T cells with strong colony forming ability to increase cell proliferation (Fig. 2a), conversely, low expression of LINC00662 prominently depressed colony forming ability of LOVO and CT26 cells to reduce cell proliferation (Fig. -(Fig.2b).2b). Flow cytometry results had displayed that high expression of LINC00662 signally declined HCT29 and LS174T cells'-apoptosis (Fig. -(Fig.2)2) and low expression of LINC00662 signally expedited LOVO and CT26'-apoptosis (Fig. -(Fig.2d).2d). By means of transwell assay, we found that the invasion ability of vector expressing LINC00662 transfected HCT29 and LS174T cells were markedly increased (Fig. -(Fig.2e)2e) and the invasion ability of siRNA-LINC00662 transfected LOVO and CT26 cells were markedly lowered (Fig. -(Fig.2f).2f). Next, the results of scratch-wound assay manifested that the migration ability of HCT29 and LS174T cells was observably inhibited by LINC00662 overexpression (Fig. -(Fig.2g),2g), otherwise, the migration ability of LOVO and CT26 cells was observably raised by LINC00662 inhibition (Fig. -(Fig.2h).2h). The apoptosis-related proteins including CASP3, Bax, Bcl-2 and XIAP, and the proliferation and metastasis-related proteins including VEGF and MMP-2 in protein level of colon cancer cells (HCT29, LS174T, LOVO and CT26 cells) transfected with LINC00662 overexpression or LINC00662 inhibition were detected by means of western blot (Fig. 3a). The results uncovered that high expression of LINC00662 signally descended cleaved CASP3 expression and Bax expression of HCT29 and LS174T cells, and low expression of LINC00662 signally motivated cleaved CASP3 expression and Bax expression of LOVO and CT26 cells in protein level (Fig. -(Fig.3b3b and c). Simultaneously, high expression of LINC00662 memorably facilitated the expressions of Bcl-2, XIAP, VEGF and MMP-2 in protein level of HCT29 and LS174T cells, and low expression of LINC00662 memorably descended the expressions of Bcl-2, XIAP, VEGF and MMP-2 in protein level of LOVO and CT26 cells (Fig. -(Fig.3d,3d, e, f and g).Starbase v2.0 database displayed that miR-340-5p had the putative binding site of LINC00662 (Fig. 5a). Luciferase reporter assay demonstrated that LINC00662-WT and miR-340-5p mimics co-transfection memorably depressed luciferase activity, however LINC00662-MUT and miR-370-3p mimics co-transfection failed to impact luciferase activity (Fig. -(Fig.5b).5b). Likewise, LINC00662-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity, however LINC00662-MUT and miR-370-3p inhibitors co-transfection failed to impact luciferase activity. Furthermore, LINC00662 antisense probe pull down not only LINC00662 RNA but also miR-340-5p (Fig. -(Fig.5c).5c). In addition, full-length LIN00662 RNA was able to enrich miR-340-5p from HCT29, LS174T, LOVO, and CT26 cells lysate (Fig. -(Fig.5d).5d). By means of RT-PCRassay, for HCT29 and LS174T cells, miR-340-5p expression in mRNA level was notably up-regulated by high expression of LINC00662, and for LOVO and CT26 cells, miR-340-5p expression in mRNA level was notably down-regulated by inhibition of LINC00662 (Fig. -(Fig.5e).5e). miR-340-5p expression in mRNA level was distinctly decreased in colon cancer tissues and cell lines (Fig. -(Fig.5f5f and g). In mRNA level, miR-340-5p expression had a negative correlation with LINC00662 expression, however, p-value was more than 0.05 (Fig. -(Fig.5h).5h). By virtue of RT-PCRassay, miR-340-5p mimics/inhibitors/negative controls were favorably transfected into colon cancer cells including HCT29, LS174T, LOVO and CT26 cells (Fig. -(Fig.5i).5i). The results of CCK8 assay uncovered that miR-340-5p inhibitors visibly inhibited HCT29 and LS174T cells'-viability (Fig. -(Fig.5j5j and k), and miR-340-5p mimics overtly facilitated LOVO and CT26 cells'-viability (Fig. -(Fig.5l5l and m). We determined cell proliferation, apoptosis, invasion and migration with the method of colony formation, flow cytometry, transwell and scratch-wound. miR-340-5p inhibitors visibly motivated HCT29 and LS174T cells'-colony forming ability and miR-340-5p mimics distinctly inhibited LOVO and CT26 cells'-colony forming ability (Fig. 6a). Cell apoptosis was obviously reduced in miR-340-5p inhibitors transfected HCT29 and LS174T cells and was overtly expedited in miR-340-5p mimics transfected LOVO and CT26 cells (Fig. -(Fig.6b).6b). High expression of miR-340-5p was distinctly promoted the invasion and migration of HCT29 and LS174T cells and inhibition of miR-340-5p was visibly inhibited the invasion and migration of LOVO and CT26 cells (Fig. -(Fig.6c6c and d).IL22 and CLDN8, as the target genes of miR-340-5p, were identified by TargetScan and miRDB database. IL22 and CLDN8 had the putative binding site of miR-340-5p (Fig. 8a). Luciferase reporter assay demonstrated that CLDN8-WT and miR-340-5p mimics co-transfection memorably depressed luciferase activity, however CLDN8-MUT and miR-340-5p mimics co-transfection failed to impact luciferase activity (Fig. -(Fig.8b).8b). Likewise, IL22-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity, however IL22-MUT and miR-370-3p inhibitors co-transfection failed to impact luciferase activity (Fig. -(Fig.8b).8b). In HCT29 and LS174T, miR-340-5p inhibitors overtly elevated the expressions of CLDN8, IL22 and phosphorylation (phosph)-ERK in protein level by virtue of western blot. In LOVO and CT29 cells, miR-340-5p mimics distinctly declined the expressions of CLDN8, IL22 and phosph-ERK in protein level by virtue of western blot (Fig. -(Fig.8c,8c, d, e and f).With the means of western blot, the expression of CLDN8, IL22, phosph-ERK, Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin in protein level of siRNA-LINC00662 and CLDN8/or IL22 overexpression co-transfected HCT29 and CT26 cells. The functions of LINC00662 knockdown declining the expression of CLDN8, IL22 and phosph-ERK in protein level of HCT29 and CT26 cells were reversed by CLDN8 or IL22 overexpression (Fig. 10a and b). The expression of Bax and E-cadherin in protein level of HCT29 and CT26 cells were distinctly increased by siRNA-LINC00662 and the expression of Bcl-2, XIAP, VEGF, MMP-2 and N-cadherin in protein level of HCT29 and CT26 cells were distinctly decreased by siRNA-LINC00662. Next, the functions of LINC00662 knockdown regulating Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin in protein level of HCT29 and CT26 cells were reversed by CLDN8 or IL22 overexpression (Fig. 10c and d).	31900207	RID07541	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DATA(GSE40174)
Colon cancer	LINC00662	IL22	positively-E	luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-);ERK signaling pathway(+)	ceRNA(miR-340-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000127318	NA	148189	50616	NA	IL-21|IL-22|IL-D110|IL-TIF|ILTIF|MGC79382|MGC79384|TIFa|TIFIL-23|zcyto18	LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.LINC00662 was markedly high expression in tumor tissues from 72 patients with colon cancer (Fig. 1a). The survival rate of colon cancer  patients with LINC00662 high expression was higher than that of colon cancer  patients with LINC00662 low expression, whereas, there was no statistically significant difference in survival rate between LINC00662 high expression and LINC00662 low expression (the relative expression of LINC00662->-4 as high expression; Fig. -Fig.1b).1b).CCK8 and clone formation assays were utilized for confirming the proliferation of LINC00662 overexpression or LINC00662 inhibition transfected colon cancer cells. High expression of LINC00662 observably facilitated the viability of HCT29 and LS174T cells (Fig. -(Fig.1f1f and g), in opposite terms, low expression of LINC00662 observably suppressed the viability of LOVO and CT26 cells (Fig. -(Fig.1h1h and i). High expression of LINC00662 endowed HCT29 and LS174T cells with strong colony forming ability to increase cell proliferation (Fig. 2a), conversely, low expression of LINC00662 prominently depressed colony forming ability of LOVO and CT26 cells to reduce cell proliferation (Fig. -(Fig.2b).2b). Flow cytometry results had displayed that high expression of LINC00662 signally declined HCT29 and LS174T cells'-apoptosis (Fig. -(Fig.2)2) and low expression of LINC00662 signally expedited LOVO and CT26'-apoptosis (Fig. -(Fig.2d).2d). By means of transwell assay, we found that the invasion ability of vector expressing LINC00662 transfected HCT29 and LS174T cells were markedly increased (Fig. -(Fig.2e)2e) and the invasion ability of siRNA-LINC00662 transfected LOVO and CT26 cells were markedly lowered (Fig. -(Fig.2f).2f). Next, the results of scratch-wound assay manifested that the migration ability of HCT29 and LS174T cells was observably inhibited by LINC00662 overexpression (Fig. -(Fig.2g),2g), otherwise, the migration ability of LOVO and CT26 cells was observably raised by LINC00662 inhibition (Fig. -(Fig.2h).2h). The apoptosis-related proteins including CASP3, Bax, Bcl-2 and XIAP, and the proliferation and metastasis-related proteins including VEGF and MMP-2 in protein level of colon cancer cells (HCT29, LS174T, LOVO and CT26 cells) transfected with LINC00662 overexpression or LINC00662 inhibition were detected by means of western blot (Fig. 3a). The results uncovered that high expression of LINC00662 signally descended cleaved CASP3 expression and Bax expression of HCT29 and LS174T cells, and low expression of LINC00662 signally motivated cleaved CASP3 expression and Bax expression of LOVO and CT26 cells in protein level (Fig. -(Fig.3b3b and c). Simultaneously, high expression of LINC00662 memorably facilitated the expressions of Bcl-2, XIAP, VEGF and MMP-2 in protein level of HCT29 and LS174T cells, and low expression of LINC00662 memorably descended the expressions of Bcl-2, XIAP, VEGF and MMP-2 in protein level of LOVO and CT26 cells (Fig. -(Fig.3d,3d, e, f and g).Starbase v2.0 database displayed that miR-340-5p had the putative binding site of LINC00662 (Fig. 5a). Luciferase reporter assay demonstrated that LINC00662-WT and miR-340-5p mimics co-transfection memorably depressed luciferase activity, however LINC00662-MUT and miR-370-3p mimics co-transfection failed to impact luciferase activity (Fig. -(Fig.5b).5b). Likewise, LINC00662-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity, however LINC00662-MUT and miR-370-3p inhibitors co-transfection failed to impact luciferase activity. Furthermore, LINC00662 antisense probe pull down not only LINC00662 RNA but also miR-340-5p (Fig. -(Fig.5c).5c). In addition, full-length LIN00662 RNA was able to enrich miR-340-5p from HCT29, LS174T, LOVO, and CT26 cells lysate (Fig. -(Fig.5d).5d). By means of RT-PCRassay, for HCT29 and LS174T cells, miR-340-5p expression in mRNA level was notably up-regulated by high expression of LINC00662, and for LOVO and CT26 cells, miR-340-5p expression in mRNA level was notably down-regulated by inhibition of LINC00662 (Fig. -(Fig.5e).5e). miR-340-5p expression in mRNA level was distinctly decreased in colon cancer tissues and cell lines (Fig. -(Fig.5f5f and g). In mRNA level, miR-340-5p expression had a negative correlation with LINC00662 expression, however, p-value was more than 0.05 (Fig. -(Fig.5h).5h). By virtue of RT-PCRassay, miR-340-5p mimics/inhibitors/negative controls were favorably transfected into colon cancer cells including HCT29, LS174T, LOVO and CT26 cells (Fig. -(Fig.5i).5i). The results of CCK8 assay uncovered that miR-340-5p inhibitors visibly inhibited HCT29 and LS174T cells'-viability (Fig. -(Fig.5j5j and k), and miR-340-5p mimics overtly facilitated LOVO and CT26 cells'-viability (Fig. -(Fig.5l5l and m). We determined cell proliferation, apoptosis, invasion and migration with the method of colony formation, flow cytometry, transwell and scratch-wound. miR-340-5p inhibitors visibly motivated HCT29 and LS174T cells'-colony forming ability and miR-340-5p mimics distinctly inhibited LOVO and CT26 cells'-colony forming ability (Fig. 6a). Cell apoptosis was obviously reduced in miR-340-5p inhibitors transfected HCT29 and LS174T cells and was overtly expedited in miR-340-5p mimics transfected LOVO and CT26 cells (Fig. -(Fig.6b).6b). High expression of miR-340-5p was distinctly promoted the invasion and migration of HCT29 and LS174T cells and inhibition of miR-340-5p was visibly inhibited the invasion and migration of LOVO and CT26 cells (Fig. -(Fig.6c6c and d).IL22 and CLDN8, as the target genes of miR-340-5p, were identified by TargetScan and miRDB database. IL22 and CLDN8 had the putative binding site of miR-340-5p (Fig. 8a). Luciferase reporter assay demonstrated that CLDN8-WT and miR-340-5p mimics co-transfection memorably depressed luciferase activity, however CLDN8-MUT and miR-340-5p mimics co-transfection failed to impact luciferase activity (Fig. -(Fig.8b).8b). Likewise, IL22-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity, however IL22-MUT and miR-370-3p inhibitors co-transfection failed to impact luciferase activity (Fig. -(Fig.8b).8b). In HCT29 and LS174T, miR-340-5p inhibitors overtly elevated the expressions of CLDN8, IL22 and phosphorylation (phosph)-ERK in protein level by virtue of western blot. In LOVO and CT29 cells, miR-340-5p mimics distinctly declined the expressions of CLDN8, IL22 and phosph-ERK in protein level by virtue of western blot (Fig. -(Fig.8c,8c, d, e and f).With the means of western blot, the expression of CLDN8, IL22, phosph-ERK, Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin in protein level of siRNA-LINC00662 and CLDN8/or IL22 overexpression co-transfected HCT29 and CT26 cells. The functions of LINC00662 knockdown declining the expression of CLDN8, IL22 and phosph-ERK in protein level of HCT29 and CT26 cells were reversed by CLDN8 or IL22 overexpression (Fig. 10a and b). The expression of Bax and E-cadherin in protein level of HCT29 and CT26 cells were distinctly increased by siRNA-LINC00662 and the expression of Bcl-2, XIAP, VEGF, MMP-2 and N-cadherin in protein level of HCT29 and CT26 cells were distinctly decreased by siRNA-LINC00662. Next, the functions of LINC00662 knockdown regulating Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin in protein level of HCT29 and CT26 cells were reversed by CLDN8 or IL22 overexpression (Fig. 10c and d).	31900207	RID07542	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DATA(GSE40174)
Gastric cancer	DANCR	FOXO1	negatively-E	RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);metastasis process(+)	ubiquitination degradation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000150907	NA	57291	2308	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	FKH1|FKHR|FOXO1A	LncRNA ANCR Promotes Invasion and Migration of Gastric Cancer by Regulating FoxO1 Expression to Inhibit Macrophage M1 Polarization.RNAs were extracted from TAMs (patients with GC (n = 30) and peripheral blood mononuclear cells (PBMCs) (healthy controls) (n = 30) and reversed transcribed into cDNA. qRTPCR results showed that compared with the control group, the expressions of LncRNA SNHG7, LncRNA DANCR, LncRNA ZFAS1, and LncRNA ANCR were up-regulated and LncRNA MEG3 was down-regulated. Among them, LncRNA ANCR had the highest expression level relative to the control group (Fig. 1a). Based on the above results, we speculated that LncRNA ANCR was involved in the occurrence of gastric cancer.Moreover, the expression of LncRNA ANCR in M1 type macrophage was examined by qRT-PCR and the results showed that the expression of LncRNA ANCR in the Induced group was down-regulated compared to the control group (Fig. 2b). Briefly, the expression of LncRNA ANCR was down-regulated after induction of M1 macrophage polarization.Moreover, in order to fully illustrate the role of LncRNA ANCR in modulating FoxO1 ubiquitination, we also explored the effect of LncRNA ANCR on the ubiquitination level of FoxO1 mutant FoxO1S256A, which could not be ubiquitinated and degraded. The results showed that overexpression of LncRNA ANCR had no significant effect on the ubiquitination level of the FoxO1 mutant (Fig. 4e). The above experimental results indicated that LncRNA ANCR could inhibit intracellular FoxO1 protein levels via promoting the ubiquitination and degradation of FoxO1 protein.After the coculture of transfected THP-1 cells with human GC cell HGC-27, we examined the invasion and migration ability of GC cells. Compared with the control group, the invasion and migration ability of GC cells was increased after the overexpression of LncRNA ANCR, while this increase was reversed after the transfection of pcDNAFoxO1 (Fig. 5c, d). These results further confirmed that FoxO1 was a downstream target molecule of LncRNA ANCR, and LncRNA ANCR could promote the invasion and migration of GC mainly via down-regulating FoxO1 protein expression.As expected, the results of tumor volume measurements indicated that the knockdown of LncRNA ANCR could significantly repress GC growth (Supplemental-Fig. 1). From the results of qRT-PCR it could be seen that the expression of LncRNA ANCR was significantly up-regulated after overexpression of LncRNA ANCR (Fig. 6c). In addition, western blotindicated that the expression of FoxO1 protein was down-regulated after overexpression of LncRNA ANCR (Fig. 6d). The above results demonstrated that LncRNA ANCR promoted the invasion and migration of GC by targeting the downregulation of FoxO1 protein expression.	31894487	RID07543	epigenetic regulation	metastasis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Urinary bladder cancer	BCAR4	WNT7A	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-370-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000154764	NA	400500	7476	NA	Wnt-7a	lncRNA BCAR4 sponges miR-370-3p to promote bladder cancer progression via Wnt signaling.Previous lncRNA expression profiling identified that lncRNA-BCAR4 was one of several significantly upregulated lncRNAs in bladder tumors, when compared with normal tissues (10). To confirm this observation, StarBase V3 was used to compare the expression of BCAR4 in bladder tumors and normal tissues using data derived from The Cancer Genome Atlas. The result suggested that BCAR4 was overexpressed in 411 bladder tumors compared with 19 healthy tissues (Fig. 1A). For validation, 30 pairs of tumors and matched normal tissues from patients with BC were collected. RT-qPCR data showed that BCAR4 was increased in the majority of patients with BC (Fig. 1B). In addition, in a panel of BC cell lines (T24, 5637 and SW780), the expression of BCAR4 was significantly increased compared to the immortalized bladder cell line SV-HUV1 (Fig. 1C). These data indicated that BCAR4 was highly expressed in BC.BCAR4 siRNA was transfected into BC cell lines to investigate the activity of BCAR4 in BC cells. Transfection of BCAR4 siRNA decreased BCAR4 expression in both T24 and 5637 cells (Fig. 2A and B). Knockdown of BCAR4 resulted in a reduction in cell viability in T24 cells (Fig. 2C). Similarly, the cell viability of 5637 cells was also greatly inhibited after BCAR4 knockdown (Fig. 2D). To clarify whether the reduction in cell viability caused by BCAR4 knockdown was associated with cell death, flow cytometric analysis was used to determine the cell apoptotic rate in T24 cells transfected with BCAR4 siRNA. A significant elevation of the percentage of cells in early [PI (propidium iodide)+/ AnnexinV-FITC-] and late (PI+/AnnexinV-FITC+) apoptosis was observed in BCAR4-silenced T24 cells (Fig. 2E). Similar to T24 cells, BCAR4 knockdown also induced cell apoptosis in 5637 cells (Fig. 2F). The data suggested that BCAR4 may promote BC cell proliferation and survival.western blotrevealed that p-beta-catenin levels were increased and p-GSK3beta levels were decreased in T24 cells after BCAR4 silencing (Fig. 3A and B). The ratio of p-beta-catenin to total beta-catenin was increased, while the ratio of p-GSK3beta to GSK3beta was decreased, suggesting the shutdown of Wnt/beta-catenin signaling (Fig. 3C). As in T24 cells, the level of p-beta-catenin was increased and the p-GSK3beta level was decreased in 5637 cells after BCAR4 silencing (Fig. 3D and E). Wnt/beta-catenin signaling was inactivated after BCAR4 silencing, as the ratio of p-beta-catenin to total beta-catenin was increased and the ratio of p-GSK3beta to GSK3beta was decreased (Fig. 3F). BCAR4 positively regulated Wnt7a expression via the repression of miR-370-3p in BC cells.To determine whether BCAR4 directly regulates miR-370-3p expression, luciferase plasmids containing BCAR4-WT BCAR4-Mut were constructed with a mutation at the putative binding sites of miR-370-3p (Fig. 5A). miR-370-3p mimic was transfected into T24 and 5637 cells to overexpress miR-370-3p (Fig. 5B). Overexpression of miR-370-3p reduced relative luciferase activity of T24 cells with BCAR4-WT, but not BCAR4-Mut (Fig. 5C). Similarly, miR-370-3p mimic also reduced relative luciferase activity of 5637 cells with BCAR4-WT, but not BCAR4-Mut (Fig. 5D). Collectively, the data demonstrated that BCAR4 directly repressed miR-370-3p expression via the prevention of miR-370-3p binding in BC cells.The clinical association between BCAR4, miR-370-3p and Wnt7a was then examined. RT-qPCR results showed that miR-370-3p was reduced in bladder tumors compared with matched healthy tissues (Fig. 7A). By contrast, Wnt7a mRNA expression was significantly increased in bladder tumors (Fig. 7B). Pearson's correlation analysis suggested that BCAR4 expression negatively correlated with miR-370-3p expression (Fig. 7C) and positively correlated with Wnt7a mRNA expression (Fig. 7D).	31894304	RID07544	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Endometrial cancer	LncRNA-SRA1	EIF4E-BP1	positively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA steroid receptor activator promotes the progression of endometrial cancer via Wnt/ beta-catenin signaling pathway.Expression levels of SRA in 146 EC patient tissues and 57 corresponding normal endometrial tissues were determined by real time-PCR and normalized to beta-actin. SRA expression in EC tissue was more than 2.9-fold higher than that in non-cancerous tissue (p < 0.05) (Figure -(Figure1A).1A). Lentiviral-mediated overexpression of SRA was performed to determine the functional role of this lncRNA in ECC-1 cells. qRT-PCRanalysis showed that SRA was successfully overexpressed in ECC-1 cells compared to that in control cells (p < 0.001) (Figure -(Figure3A).3A). We next examined the impact of SRA overexpression on cell proliferation. Results of CCK-8 assays showed that overexpression SRA in ECC-1 cells increased cell proliferation (Figure -(Figure3B),3B), suggesting that SRA was involved in the proliferation of EC cells. Thereafter, Colony formation assays confirmed that SRA overexpression promoted cell colony formation (Figure -(Figure3C).3C). Effects of SRA on invasive and migratory behaviors of cells were assessed by wound healing assays and Matrigel invasion, respectively. Overexpression of SRA resulted in increased migration of ECC-1 cells relative to empty vector-expressing controls (Figure -(Figure3D).3D). There was a significant difference between scratch width percentages of each cell line at 24 and 48 h after scratching. Empty vector and SRA overexpression groups of ECC-1 cells were significantly different in scratch width (Figure -(Figure3E).3E). Furthermore, SRA overexpression in ECC-1 cells significantly increased invasion relative to that in empty vector-expressing cells. Relative percentages of invaded cells of ECC-1 at 48h after incubation in empty vector and SRA overexpression groups were significantly different (Figure -(Figure3F).3F). Taken together, these results indicate that overexpression of SRA can promote invasion and migration of ECC-1 cells in vitro.To validate the interaction between SRA and EIF4E-BP1, luciferase assays were carried out. We constructed luciferase reporter plasmids for EIF4E-BP1 containing predicted wild-type and mutant-binding sites for EIF4E-BP1 (Figure -(Figure5A).5A). We found that downregulation of SRA reduced the luciferase activity of the wild-type plasmid but not that of the mutant plasmid. Co-transfection of the plasmid containing the wild-type UTR plus an EIF4E-BP1, but not a negative control, resulted in a significant increase in relative luciferase activity (Figure -(Figure5B).5B). In contrast, co-transfection of the plasmid with the mutated UTR plus either mimic completely transfected siSRA repression, demonstrating the specificity of these siSRA for EIF4E-BP1 suppression. In addition, p-EIF4E-BP1, EIF4E-BP1, and VEGF expression levels were analyzed by western blot. In ECC-1 cells, SRA knockdown and SRA overexpression regulated EIF4E-BP1 expression typical of tumor progression. The same results were obtained for cells transfected with EIF4E-BP1 (Figure -(Figure5C).5C). Expression levels of phospho-EIF4E-BP1 and EIF4E-BP1 were increased in SRA-overexpressed cells but decreased in SRA knocked-down cells. Expression levels of phosphor-EIF4E-BP1 and EIF4E-BP1 were also decreased in cells transfected with shEIF4E-BP1. There was no significant difference in the expression of VEGF.	31892849	RID07545	interact with protein	NA		
Colorectal cancer	TRPM2-AS	TAF15	interact	RNA pull-down assays;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000172660	NA	101928607	8148	TRPM2-AS1	hTAFII68|Npl3|RBP56|TAF2N	TRPM2-AS promotes cancer cell proliferation through control of TAF15.The knockdown efficacy was determined by RT-qPCR (Fig. 1C). Since sh-TRPM2-AS-1 and sh-TRPM2-AS-2 exhibited better knockdown efficacy, they were implemented in the subsequent loss-of-function assays. Knockdown of TRPM2-AS strikingly led to suppression on cell proliferation, as determined by CCK-8, colony formation and EdU assays (Fig. 1D ). Taken together, the aforementioned data indicate that TRPM2-AS positively regulates CRC cell proliferation.The knockdown efficacy was determined by RT-qPCR (Fig. 1C). Since sh-TRPM2-AS-1 and sh-TRPM2-AS-2 exhibited better knockdown efficacy, they were implemented in the subsequent loss-of-function assays. Knockdown of TRPM2-AS strikingly led to suppression on cell proliferation, as determined by CCK-8, colony formation and EdU assays (Fig. 1D ). Taken together, the aforementioned data indicate that TRPM2-AS positively regulates CRC cell proliferation.Rescue assays were conducted to further determine the role of TRPM2-AS/TRPM2 axis in CRC cell proliferation. The mRNA and protein levels of TRPM2 were upregulated in LoVo cells stably transfected with sh-TRPM-AS via transfection of pcDNA3.1/TRPM2 (Fig. 4A and B). The protein level of TRPM2 reduced by TRPM2-AS silencing was recovered again by introducing into TRPM2 expression vector (Figure S2A). The declined cell viability induced by TRPM2-AS silence was notably revived by TRPM2 overexpression (Fig. 4C). Consistently, the decreased colonies caused by TRPM2-AS knockdown was rescued by TRPM2 overexpression (Fig. 4D). The EdU assay also indicated that the suppressive effect of TRPM2-AS silence on cell proliferation was abrogated by TRPM2 upregulation. Additionally, we also assessed the role of TRPM2-AS/TRPM2 in regulating CRC cell migration and EMT process. The results shown in Figure S2B-C indicated that the inhibitory effect of TRPM2-AS downregulation on cell migration and EMT process was rescued by the overexpression of TRPM2. To sum up, TRPM2-AS regulates cell proliferation in CRC via a TRPM2-mediated manner.	31887411	RID07546	interact with protein	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	DLEU2	E2F7	positively-E	dual-luciferase reporter assay	upregulation	RT-PCR	NA	NA	prognosis;cell migration(+);cell invasion(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-30e-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000165891	NA	8847	144455	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	NA	Long non-coding RNA DLEU2 promotes the progression of esophageal cancer through miR-30e-5p/E2F7 axis.From the Gene Expression Profiling Interactive Analysis (GEPIA) [16], we observed that the expression of lncRNA DLEU2 was significantly up-regulated in EC tissues compared to normal tissues (P < 0.05,Fig. 1A).Obviously, up-regulation of lncRNA DLEU2 promoted the viability of TE-1 cells (P < 0.05,Fig. 1G). It was further confirmed by colony formation assay that silencing lncRNA DLEU2 inhibited the proliferation in Eca-109 and KYSE-150 cells, while up-regulation of lncRNA DLEU2 showed a promotive effect in TE-1 cells (P < 0.05, Fig. 1H and I).The wound-healing assay revealed that silencing lncRNA DLEU2 significantly diminished the migration ability of Eca-109 and KYSE-150 cells compared to the NC group (P < 0.05,Fig. 3A and B). Correspondingly, lncRNA DLEU2 overexpression significantly promoted the migration ability of TE-1 cells (P < 0.05,Fig. 3A and C). The results from transwell assay also showed that silencing lncRNA DLEU2 significantly decreased the invasion ability of Eca-109 and KYSE-150 cells (P < 0.05,Fig. 3D and E), lncRNA DLEU2 overexpression significantly promoted the invasion ability of TE-1 cells (P < 0.05,Fig. 3D and F).dual-luciferase reporter assay showed that the luciferase activity of lncRNA DLEU2 (wt) was obviously diminished by miR-30e-5p in both Eca-109 and KYSE-150 cells, but the luciferase activity of lncRNA DLEU2 (mut) was not changed (Fig. 4B). These data suggests that miR-30e-5p could bind with lncRNA DLEU2 in EC cells.The bioinformatics online database (TargetScan) was utilized to predict the potential target genes of miR-30e-5p. According to the prediction data, given their binding affinity for miR-30e-5p, eight candidate target genes were selected (SupplementaryFig. 1A). RT-PCRanalysis showed that miR-30e-5p could significantly inhibited their mRNA expression, expect for RORA, especially the expression of E2F7 mRNA was most obviously down-regulated (SupplementaryFig. 1B). Therefore, E2F7 was a target gene of miR-30e-5p, which possessed binding sites with miR-30e-5p (Fig. 4C). For further proof, cells were co-transfected with the pmirGLO-E2F7 (wild type, wt) or pmirGLOE2F7 (mutant type, mut) vectors and pCMV-miR-30e-5p. As suggested from the dual-luciferase reporter assay, we observed that miR-30e-5p significantly blocked the luciferase activity of the wild type E2F7, while it had no effect on the mutant type of E2F7 (Fig. 4D). Moreover, western blot assay was performed to further confirm the correlation between miR-30e-5p and E2F7 in EC cells. As shown inFig. 4E and F, in comparison with control cells, miR-30e-5p significantly inhibited the protein level of E2F7 in Eca-109 and KYSE-150 cells, while this tendency was significantly reversed when lncRNA DLEU2 was up-regulated. Taken together, these data indicate that E2F7 might be involved in the function of lncRNA DLEU2 in EC.To validate the effect of lncRNA DLEU2/miR-30e-5p/E2F7 axis on the growth and invasion of EC cells, the rescue assays were performed in EC cells. Eca-109 and KYSE-150 cells were transfected with control and siRNA-DLEU2, respectively; two group of cells were co-transfected with siRNA-DLEU2 and miR-30e-5p inhibitor or E2F7 expressed vector pcDNA3.1-E2F7. After being transfected for 48 h, we found that the decrease in expression of E2F7 protein caused by si-DLEU2 was reversed by miR-30e-5p inhibitor (Fig. 7A). Moreover, CCK8 assay showed that the inhibitory effect of si-DLEU2 on cell viability was significantly reversed by miR-30e-5p inhibitor or up-regulation of E2F7 in both Eca-109 and KYSE-150 cells (Fig. 7B and C). We also observed that the suppression in proliferation ability caused by si-DLEU2 was significantly restored by miR-30e-5p inhibitor or up-regulation of E2F7 (Fig. 7D). Furthermore, the depression in migration and invasion caused by silencing DLEU2 was strengthened by miR-30e-5p inhibitor or up-regulation of E2F7 (Fig. 8A, B). Taken together, our data suggest that lncRNA DLEU2 acts as a ceRNA to promote the growth, migration and invasion of EC cells via miR-30e-5p/E2F7 axis.	31884338	RID07547	ceRNA or sponge	prognosis	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	MIR4435-2HG	TGFB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+)	ceRNA(miR-202)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000105329	NA	541471	7040	AGD2|LINC00978|MIR4435-1HG|MORRBID|lncRNA-AWPPH	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA MIR4435-2HG-mediated upregulation of TGF-beta1 promotes migration and proliferation of nonsmall cell lung cancer cells.Plasma levels of TGF-beta1 and MIR4435-2HG in both lung cancer patients and healthy controls were measured by RT-qPCR and ELISA, respectively. Plasma levels of lncRNA MIR4435-2HG (Figure 1A) and TGF-beta1 (Figure 1B) were significantly higher in SCLC and NSCLC patients (P< .05) compared with healthy controls, and their levels were higher in NSCLC patients than in SCLC patients. As shown in Figure 2A,B, knockdown of MIR4435-2HG or TGF-beta1 inhibitor significantly reduced the viability of NSCLC cells. Additionally, the migration ability of NSCLC cells was remarkably inhibited by MIR4435-2HG knockdown and TGF-beta1 inhibitor (Figure 2C-F). The knockdown efficiency of MIR4435-2HG KD was confirmed via RT-qPCR assay (Figure 2G), and the inhibitory efficiency of TGF-beta1 inhibitor was proved by examining the expression of p/Smad2/3 (the downstream effectors of TGF-beta1; Figure 2H).Furthermore, luciferase reporter assay showed that MIR4435-2HG knockdown decreased the activity of Luc-TGFbeta1-30UTR, but had no effects on Luc-TGF-beta1-50UTR or Luc-TGFbeta1-CDS, this effect was reversed by Dicer knockdown (Figure 4E). These effects indicate that lncRNA MIR4435-2HG promotes TGF-beta1 expression in an miRNA- and 30UTR-dependent manner. Notably, Ago2-RNA immunoprecipitation (RIP) analysis disclosed that MIR4435-2HG knockdown substantially increased TGF-beta1 recruitment to Ago2 (Figure 4F). MiR-528 inhibitor (miR-528-I) or miR-202 inhibitor (miR-202-I) attenuated MIR4435-2HG-knockdown-mediated downregulation of TGF-beta1 expression (Figure 4G,H) Collectively, these results suggest that lncRNA MIR4435-2HG acts as an miRNA sponge for TGF-beta1 in NSCLC cells, at least through sponging miR-528 and miR-202.Finally, we tried to confirm whether lncRNA MIR4435-2HG exerts its effects on NSCLC cell progression through TGF-beta1. NSCLC cells with MIR4435-2HG knockdown were treated with exogenous TGF-beta1 (5 ng/mL, Sigma-Aldrich) and subjected to cell proliferation and migration analysis. As shown in Figure 5A,B, treatment of exogenous TGFbeta1 attenuated the decreased cell viability which was mediated by MIR4435-2HG knockdown. Additionally, the inhibitory effects of MIR4435-2HG knockdown on NSCLC cell migration ability were partially reversed by exogenous TGF-beta1 treatment (Figure 5C-F). Therefore, these results reveal that lncRNA MIR4435-2HG promotes the progression of NSCLC cells at least through TGF-beta1.	31875359	RID07548	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	MIR4435-2HG	TGFB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell proliferation(+)	ceRNA(miR-528)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000105329	NA	541471	7040	AGD2|LINC00978|MIR4435-1HG|MORRBID|lncRNA-AWPPH	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	LncRNA MIR4435-2HG-mediated upregulation of TGF-beta1 promotes migration and proliferation of nonsmall cell lung cancer cells.Plasma levels of TGF-beta1 and MIR4435-2HG in both lung cancer patients and healthy controls were measured by RT-qPCR and ELISA, respectively. Plasma levels of lncRNA MIR4435-2HG (Figure 1A) and TGF-beta1 (Figure 1B) were significantly higher in SCLC and NSCLC patients (P< .05) compared with healthy controls, and their levels were higher in NSCLC patients than in SCLC patients. As shown in Figure 2A,B, knockdown of MIR4435-2HG or TGF-beta1 inhibitor significantly reduced the viability of NSCLC cells. Additionally, the migration ability of NSCLC cells was remarkably inhibited by MIR4435-2HG knockdown and TGF-beta1 inhibitor (Figure 2C-F). The knockdown efficiency of MIR4435-2HG KD was confirmed via RT-qPCR assay (Figure 2G), and the inhibitory efficiency of TGF-beta1 inhibitor was proved by examining the expression of p/Smad2/3 (the downstream effectors of TGF-beta1; Figure 2H).Furthermore, luciferase reporter assay showed that MIR4435-2HG knockdown decreased the activity of Luc-TGFbeta1-30UTR, but had no effects on Luc-TGF-beta1-50UTR or Luc-TGFbeta1-CDS, this effect was reversed by Dicer knockdown (Figure 4E). These effects indicate that lncRNA MIR4435-2HG promotes TGF-beta1 expression in an miRNA- and 30UTR-dependent manner. Notably, Ago2-RNA immunoprecipitation (RIP) analysis disclosed that MIR4435-2HG knockdown substantially increased TGF-beta1 recruitment to Ago2 (Figure 4F). MiR-528 inhibitor (miR-528-I) or miR-202 inhibitor (miR-202-I) attenuated MIR4435-2HG-knockdown-mediated downregulation of TGF-beta1 expression (Figure 4G,H) Collectively, these results suggest that lncRNA MIR4435-2HG acts as an miRNA sponge for TGF-beta1 in NSCLC cells, at least through sponging miR-528 and miR-202.Finally, we tried to confirm whether lncRNA MIR4435-2HG exerts its effects on NSCLC cell progression through TGF-beta1. NSCLC cells with MIR4435-2HG knockdown were treated with exogenous TGF-beta1 (5 ng/mL, Sigma-Aldrich) and subjected to cell proliferation and migration analysis. As shown in Figure 5A,B, treatment of exogenous TGFbeta1 attenuated the decreased cell viability which was mediated by MIR4435-2HG knockdown. Additionally, the inhibitory effects of MIR4435-2HG knockdown on NSCLC cell migration ability were partially reversed by exogenous TGF-beta1 treatment (Figure 5C-F). Therefore, these results reveal that lncRNA MIR4435-2HG promotes the progression of NSCLC cells at least through TGF-beta1.	31875359	RID07549	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	GIHCG	MIR1281	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000262349	GRCh38_CHR_HSCHR12_1_CTG2_1:57935074-57936175	ENSG00000221160	NA	100506844	100302237	NA	MIRN1281|hsa-mir-1281	LncRNA GIHCG regulates microRNA-1281 and promotes malignant progression of breast cancer.To determine the role of GIHCG in BCa, we collected a total of 53 pairs of BCa tumor tissue specimens and adjacent ones. The expression of GIHCG in the above tissues was examined using qRT-PCR The results revealed that GIHCG expression was higher in BCa tumor tissues than in adjacent ones (Figure 1A). To explore the influence of GIHCG on the proliferation of BCa cells, we successfully constructed the sh-GIHCG model and the transfection efficiency was verified using qRT-PCR(Figure 2A). Subsequently, CCK8, cell clones, and EdU assays were performed to analyze cell proliferation in NC and sh-GIHCG groups. As a result, we found that the proliferation rate of BCa cells in the latter group was remarkably decreased (Figure 2B-2D).To further explore the interaction between GIHCG and microRNA-1281, microRNA-1281 was silenced in BCa cell lines knocked down GIHCG to investigate their role in BCa (Figure 4A). Subsequently, CCK-8, plate cloning, and EdU experiments confirmed that microRNA-1281 could counteract the proliferative effect of GIHCG on BCa cells (Figure 4B-4D), suggesting that GIHCG could modulate microRNA-1281 expression in BCa.TargetScan, miRbase, and MiRcode databases were applied to assess the potential relation between lncRNAs and miRNAs. Bioinformatics analysis suggested four miRNAs as potential targets of GIHCG (Figure 3A). Subsequently, qRTPCR was used to detect the difference in expression of the four potential miRNAs in sh-NC group and sh-GIHCG group. The difference in microRNA-1281 expression was found to be the most significant. Therefore, it was suggested that there might be an association between GIHCG and microRNA-1281(Figure 3B).	31858553	RID07550	expression association	NA		
Colorectal cancer	HCG18	MTDH	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-1271)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000147649	NA	414777	92140	Em:AB014087.1|FLJ25550|FLJ31598	3D3|AEG-1|LYRIC	The long non-coding RNA HCG18 promotes the growth and invasion of colorectal cancer cells through sponging miR-1271 and upregulating MTDH/Wnt/beta-catenin.To verify the high expression of HCG18 in colorectal cancer, we detected the expression of HCG18 in clinical tumour tissues of colorectal cancer by using RT-qPCR analysis. The results demonstrated that HCG18 was highly expressed in colorectal cancer tissues compared with adjacent normal tissues (Figure 1B). Moreover, high expression of HCG18 was also detected in colorectal cancer cell lines compared with the normal colonic epithelial cell line NCM-460 (Figure 1C). Overall, these results indicate that HCG18 is highly expressed in colorectal cancer.The CCK-8 assay revealed that HCG18 silencing significantly reduced the growth of colorectal cancer cells (Figure 2B). Moreover, the colony-forming capability of colorectal cancer cells was also markedly decreased by HCG18 knockdown (Figure 2C,D). In addition, HCG18 knockdown also suppressed the invasive potential of colorectal cancer cells (Figure 2E,F). To verify the inhibitory effect of HCG18 silencing on colorectal cancer cell growth and invasion, we further investigated the effect of HCG18 overexpression on colorectal cancer cell growth and invasion. The results demonstrated that HCG18 overexpression significantly increased the growth and invasion of colorectal cancer cells (Figure 3A-D). These results confirm that HCG18 contributes to the regulation of colorectal cancer cell growth and invasion.To validate whether miR-1271 directly targets HCG18, we performed a dual-luciferase reporter assay. The results revealed that miR-1271 overexpression markedly decreased the luciferase activity of the luciferase reporter vector containing wild-type HCG18, while it had no obvious effect on the luciferase reporter vector containing mutant HCG18 (Figure 4B). Moreover, an RNA pull-down assay revealed that HCG18 was enriched in the bound fractions precipitated by biotinylated miR-1271 mimics (Figure 4C). In addition, knockdown of HCG18 significantly increased miR-1271 expression, while HCG18 overexpression decreased miR-1271 expression (Figure 4D,E). Correlation analysis demonstrated that HCG18 expression was inversely correlated with miR-1271 expression in clinical specimens of colorectal cancer tissues (Figure 4F). Collectively, these results suggest that HCG18 functions as a sponge of miR-1271.The results showed that HCG18 silencing significantly decreased MTDH expression and suppressed Wnt/beta-catenin signalling in colorectal cancer cells (Figure 5A,B). Moreover, miR-1271 inhibition significantly reversed the inhibitory effect of HCG18 silencing on MTDH/Wnt/ beta-catenin signalling (Figure 5C,D). Notably, the inhibitory effect on colorectal cancer cell proliferation and invasion mediated by HCG18 silencing was also significantly reversed by miR-1271 inhibition (Figure 5E,F). Overall, our results suggest that HCG18 silencing represses MTDH/Wnt/beta-catenin signalling via regulation of miR-1271.To verify the miR-1271/MTDH axis as a downstream target of HCG18 in regulating colorectal cancer cell proliferation and invasion, we performed rescue experiments. We found that transfection with the MTDH expression vector significantly restored MTDH expression in HCG18 shRNA-transfected cells (Figure 6A). As expected, the inhibitory effect of HCG18 silencing on proliferation, invasion, and Wnt/beta-catenin signalling was partially reversed by MTDH overexpression (Figure 6B-D). These findings suggest that MTDH is a functional target of HCG18 in colorectal cancer cells.	31854468	RID07551	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Esophagus squamous cell carcinoma	SNHG6	HIF1A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-186-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000100644	NA	641638	3091	HBII-276HG|NCRNA00058|U87HG	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Silencing of Long Noncoding RNA SNHG6 Inhibits Esophageal Squamous Cell Carcinoma Progression via miR-186-5p/HIF1alpha Axis.To determine whether the expression of lncRNA SNHG6 was altered in ESCC tissues, 30 pairs of ESCC tissues and adjacent normal tissues were collected and the expression of lncRNA SNHG6 was determined using qRT-PCR The results revealed that the expression level of lncRNA SNHG6 was increased in ESCC tissues compared with that in their adjacent normal tissues (Fig. 1a). When lncRNA SNHG6 was knocked down by si-SNHG6 in EC109 and KYSE150 cells, the expression level of lncRNA SNHG6 was markedly reduced as expected (Fig. 2a). Under these conditions, a marked decrease in the viability of EC109 and KYSE150 cells was also found (Fig. 2b). Similarly, knockdown of lncRNA SNHG6 inhibited the colony formation ability of EC109 and KYSE150 cells (Fig. 2c). In parallel, the results of transwell migration and invasion assays showed that knockdown of lncRNA SNHG6 led to decreased cell migration and invasion in EC109 and KYSE150 cells (Fig. 2d, e).To confirm this prediction, luciferase reporter assay was performed in EC109 and KYSE150 cells. As expected, overexpression of miR-186-5p reduced the luciferase activity of reporter plasmids containing WT-lncRNA SNHG6. However, no changes were found when mutations were introduced into the miR-186-5p-binding sites of lncRNA SNHG6 sequence (Fig. 3d, e). The results of RNA pull-down assay showed that the expression level of lncRNA SNHG6 was higher in the Bio-miR-186-5p group than that in the Bio-NC group (Fig. 3f, g). Meanwhile, miR-186-5p was underexpressed in ESCC tissues compared with that in their adjacent normal tissues (Fig. 3h). In line with this, data from GEO database revealed that miR-186-5p was downregulated in ESCC tissues relative to normal tissues (Fig. 3i). Spearman correlation coefficient analysis suggested a negative correlation between lncRNA SNHG6 and miR-186-5p expression in ESCC specimens (Fig. 3j).We also performed luciferase reporter assay to validate whether HIF1alpha was a direct target of miR-186-5p (Fig. 4a). We found the reduction in luciferase activity of reporter plasmids containing WT-HIF1alpha upon overexpression of miR-186-5p in EC109 and KYSE150 cells. Notably, the luciferase activity of reporter plasmids containing MUT-HIF1alpha was not altered following miR-186-5p or miR-NC transfection (Fig. 4b, c). qRT-PCRanalysis showed that overexpression of miR-186-5p strikingly inhibited the expression of HIF1alpha in EC109 and KYSE150 cells, which is consistent with the results of western blot (Fig. 4d, e).In both EC109 and KYSE150 cells, a marked reduction in cell viability was observed in cells transfected with miR-186-5p. However, this effect was blocked by overexpression of SNHG6 or HIF1alpha (Fig. 5a, b). Likewise, a colony formation assay showed that miR-186-5p inhibited the colony formation ability of EC109 and KYSE150 cells, and this action was also blocked by overexpression of SNHG6 or HIF1alpha (Fig. 5c). Meanwhile, miR-186-5p led to a marked inhibition of cell migration and invasion, which was overturned by upregulation of SNHG6 or HIF1alpha (Fig. 5d, e).	31853782	RID07552	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Breast cancer	DLEU1	RAB22A	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-300)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000124209	NA	10301	57403	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	LncRNA DLEU1/microRNA-300/RAB22A axis regulates migration and invasion of breast cancer cells.DLEU1 expression in 60 breast cancer tissues and adjacent tissues was determined by qRT-PCR The results showed that DLEU1 was highly expressed in breast cancer (Figure 1A).To test whether DLEU1 can participate in the development of breast cancer through targeting RAB22A, the expression level of RAB22A in breast cancer cells was first detected. qRT-PCR;ISHowed highly expressed RAB22A in breast cancer cells compared to controls (Figure 3A). Transfection of RAB22A overexpression plasmid in BT549 cells successfully upregulated RAB22A expression, and transfection of RAB22A siRNA markedly downregulated its expression in MCF-7 cells at both mRNA and protein levels (Figures 3B-3D).qRT-PCRand western blot both showed that DLUE1 could positively regulate RAB22A expression in breast cancer cells (Figures 3E and 3F).Protein levels of E-cadherin and cytokeratin decreased, and vimentin expression increased in BT549 cells overexpressing RAB22A. For comparison, upregulated E-cadherin and cytokeratin, as well as downregulated vimentin were seen in MCF-7 cells with RAB22A knockdown (Figure 4B).Transfection efficacy of microRNA-300 mimics and inhibitor was verified (Figure 5B). By searching for the binding sequences of microRNA-300 to DLUE1 and RAB22A, we constructed wild-type and mutant-type plasmids of DLUE1 and RAB22A (Figure 5C). Luciferase activity decreased in DLEU1 WT and RAB22A WT group; however, we did not observe changes in luciferase activity of DLEU1 MUT and RAB22A MUT group (Figure 5D). qRT-PCRverified the negative correlation between mRNA expressions of microRNA-300 and RAB22A, which was the same at protein levels (Figures 5E and 5F). These results discovered that DLEU1 and RAB22A could bind to microRNA-300.Notably, co-overexpression of microRNA-300 and DLUE1 reversed the increased migratory and invasive potentials of BT549 cells overexpressing microRNA-300 (Figure 6C). Compared to those overexpressing microRNA-300, BT549 cells co-overexpressing microRNA-300 and DLUE1 presented lower levels of E-cadherin and cytokeratin, but a higher level of vimentin (Figure 6D). The enhanced migratory and invasive potentials of MCF-7 cells with microRNA-300 knockdown were reversed by the knockdown of both microRNA-300 and DLUE1 (Figure 6E). western blot results revealed that decreases in E-cadherin and cytokeratin, as well as an increase in vimentin in MCF-7 cells with microRNA-300 knockdown were reversed by DLUE1 knockdown (Figure 6F).	31841195	RID07553	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	UP(LIHC,PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE55807)
Lung squamous cell carcinoma	FAM201A	ABCE1	positively-E	knockdown	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000204860	GRCh38_9:38620474-38624990	ENSG00000164163	NA	158228	6059	C9orf122	OABP|RLI|RLI1|RNASEL1|RNASELI|RNS4I	Long noncoding RNA FAM201A mediates the metastasis of lung squamous cell cancer via regulating ABCE1 expression.Firstly, lncRNA FAM201A expression in 107 patients'-tissues (tumor and adjacent normal ones) was quantified using quantitative Reverse Transcription-Polymerase Chain Reaction. FAM201A expression in NSCLC tissues was higher than that in adjacent normal tissues (Figure 1A, p<0.01).Quantitative PCR showed the knockdown efficiency 48 h after transfection (Figures 2A and 2B, p<0.01). Cell proliferation in LSCC was limited, resulting from FAM201A silencing (Figures 2C and 2D, p<0.05). In addition, not only migration, but invasion of LSCC cells were weakened after the FAM201A level was restrained (Figures 3A and 3B, p<0.05). Therefore, these data suggest that lncRNA FAM201A can mediate the malignant abilities of LSCC cells in vitro, including proliferation, migration, and invasion.Based on bioinformatics analysis using TargetScan, we predicted that ATP-binding cassette transporter E1 (ABCE1), which exhibits increased expression in lung cancer, may be a downstream target for lncRNA FAM201A. This regulatory relation was verified based on a western blot assay (Figures 5A and 5B, p<0.01). ABCE1 expression was declined in cancer cells transfected with sh-FAM201A, compared to that in the vector controls (Figure 5B). Moreover, ABCE1 expression in NSCLC tissues was higher than that in adjacent normal tissues (Figure 5C, p<0.01).A positive correlation between ABCE1 and FAM201A expression in human cancer tissues was verified (Figure 5D; r=0.4250, p<0.0001). Altogether, our data suggest that ABCE1 is an effector protein targeted by FAM201A in LSCC.	31841188	RID07554	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Nephroblastoma	MIAT	DGCR8	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000128191	NA	440823	54487	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	C22orf12|DGCRK6|Gy1|pasha	Long noncoding RNA MIAT acts as an oncogene in Wilms' tumor through regulation of DGCR8.Firstly, the MIAT expression was detected via RT-qPCR in 50 Wilms'-tumor patients'-tissues. The results showed that MIAT was significantly upregulated in tumor tissue samples (Figure 1A). We divided 50 patients into two groups, according to the median expression of MIAT. Patients with high MIAT expression level had poorer overall survival than those with low MIAT expression level (Figure 1B).To detect the function of MIAT in Wilms'-tumor metastasis, the transwell assay was performed. The results showed that the cell migration ability of Wilms'-tumor cells was inhibited due to the loss of MIAT (Figure 3A). The outcome of the transwell assay also revealed that the cell invaded ability of Wilms'-tumor cells was remarkably decreased due to the loss of MIAT (Figure 3B).DGCR8 was predicted as the target proteins of MIAT through StarBase v2.0 (http://starbase.sysu. edu.cn/starbase2/rbpLncRNA.php). RT-qPCR results showed that the expression level of DGCR8 in Wilms'-tumor cells was remarkably lower in the sh-MIAT group compared with that in the NC group (Figure 4A). The western blot assay results showed that the expression level of DGCR8 in Wilms'-tumor cells was remarkably lower in the sh-MIAT group compared with that in the NC group (Figure 4B). Besides, the DGCR8 expression in Wilms'-tumor tissues was remarkably higher when compared with that of the adjacent tissues (Figure 4C). The correlation analysis demonstrated that the DGCR8 expression level positively correlated to MIAT expression in cancer tissues (Figure 4D).	31841180	RID07555	expression association	metastasis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic ductal adenocarcinoma	THAP9-AS1	YY1AP1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-484)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251022	GRCh38_4:82893009-82900960	ENSG00000163374	NA	100499177	55249	NA	HCCA2|YAP|YY1AP	lncRNA THAP9-AS1 Promotes Pancreatic Ductal Adenocarcinoma Growth and Leads to a Poor Clinical Outcome via Sponging miR-484 and Interacting with YAP.To explore lncRNAs involved in pancreatic ductal adenocarcinoma (PDAC), a publicly accessible microarray dataset from PDAC patients was analyzed between PDAC tissues and normal pancreatic tissues (GEO: GSE16515). Among the annotated potential lncRNAs, THAP9-AS1 levels were found to be increased in PDAC tissues compared with those in normal pancreatic tissues (Fig.1A).Additionally, to confirm the role of THAP9-AS1 in PDAC cells, THAP9-AS1 was overexpressed in PANC-1 cells that exhibit relatively low level of endogenous THAP9-AS1 expression (Fig.2D). THAP9-AS1 overexpression markedly promoted cell proliferation and colony formation capacity (Fig.2D and Fig.S2C). Moreover, THAP9-AS1 knockdown inhibited tumor sphere formation of PDAC cells represented in sphere number and sphere diameter (Fig.2E and FigS2D), whereas, ectopic overexpression of THAP9-AS1 enhanced tumor sphere forming ability (Fig.2F and Fig.S2E). These data show that lncRNA THAP9-AS1 drives PDAC cells proliferation and growth.Immunofluorescence staining revealed that THAP9-AS1 knockdown markedly alleviated protein level and nuclear translocation of Y AP (Fig.3D and Fig.S3D). On the other hand, ectopic overexpression of THAP9-AS1 positively regulated Y AP expression at both protein (Fig.3A) and mRNA levels (Fig.3C), but negatively regulated Y AP serine 127 phosphorylation (Fig.3A). Immunofluorescence staining further confirmed that THAP9-AS1 overexpression enhanced Y AP protein level and nuclear translocation (Fig.3E).We next determined whether THAP9-AS1 potentially interacted with miR-484 and whether miR-484 potentially targeted Y AP via the predicted binding motif (Fig.4A). To validate the direct binding between THAP9-AS1 and miR-484, the THAP9-AS1 with or without deletion mutations in miR-484 targeting site were cloned into MS2b plasmid to transcribe RNA combined with MS2-binding sequences and then co-transfected with the MS2bp-GFP expression plasmid and miR-484 mimics into HEK-293T cells. Subsequently, we performed RNA immunoprecipitation (RIP) assays to pull down miRNAs associated with THAP9-AS1 via GFP antibody and demonstrated via qRT-PCRanalysis that miR-484 associated with THAP9-AS1 via targeting site, while the non-targeting miR-191-5p used as negative control, was not associated with THAP9-AS1 (Fig.4C). RIP assays also indicated that miR-484 also associated with Y AP 3'-UTR specifically (Fig.4D). To further confirm the association of THAP9-AS1 with miR-484, based on pMir-reporter plasmid we constructed luciferase reporters containing the 5'-500nt of THAP9-AS1, which contains wild-type or deletion mutated miR-484 targeting site. These reporters were co-transfected with miR-484 mimics into HEK-293T cells. We found that miR-484 mimics reduced the reporter activity of the construct with wild-type THAP9-AS1 (Fig.4E).	31831555	RID07556	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Pancreatic ductal adenocarcinoma	THAP9-AS1	YY1AP1	positively-F	RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	phosphorylation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251022	GRCh38_4:82893009-82900960	ENSG00000163374	NA	100499177	55249	NA	HCCA2|YAP|YY1AP	lncRNA THAP9-AS1 Promotes Pancreatic Ductal Adenocarcinoma Growth and Leads to a Poor Clinical Outcome via Sponging miR-484 and Interacting with YAP.To explore lncRNAs involved in pancreatic ductal adenocarcinoma (PDAC), a publicly accessible microarray dataset from PDAC patients was analyzed between PDAC tissues and normal pancreatic tissues (GEO: GSE16515). Among the annotated potential lncRNAs, THAP9-AS1 levels were found to be increased in PDAC tissues compared with those in normal pancreatic tissues (Fig.1A).Additionally, to confirm the role of THAP9-AS1 in PDAC cells, THAP9-AS1 was overexpressed in PANC-1 cells that exhibit relatively low level of endogenous THAP9-AS1 expression (Fig.2D). THAP9-AS1 overexpression markedly promoted cell proliferation and colony formation capacity (Fig.2D and Fig.S2C). Moreover, THAP9-AS1 knockdown inhibited tumor sphere formation of PDAC cells represented in sphere number and sphere diameter (Fig.2E and FigS2D), whereas, ectopic overexpression of THAP9-AS1 enhanced tumor sphere forming ability (Fig.2F and Fig.S2E). These data show that lncRNA THAP9-AS1 drives PDAC cells proliferation and growth.Immunofluorescence staining revealed that THAP9-AS1 knockdown markedly alleviated protein level and nuclear translocation of Y AP (Fig.3D and Fig.S3D). On the other hand, ectopic overexpression of THAP9-AS1 positively regulated Y AP expression at both protein (Fig.3A) and mRNA levels (Fig.3C), but negatively regulated Y AP serine 127 phosphorylation (Fig.3A). Immunofluorescence staining further confirmed that THAP9-AS1 overexpression enhanced Y AP protein level and nuclear translocation (Fig.3E).We next determined whether THAP9-AS1 potentially interacted with miR-484 and whether miR-484 potentially targeted Y AP via the predicted binding motif (Fig.4A). To validate the direct binding between THAP9-AS1 and miR-484, the THAP9-AS1 with or without deletion mutations in miR-484 targeting site were cloned into MS2b plasmid to transcribe RNA combined with MS2-binding sequences and then co-transfected with the MS2bp-GFP expression plasmid and miR-484 mimics into HEK-293T cells. Subsequently, we performed RNA immunoprecipitation (RIP) assays to pull down miRNAs associated with THAP9-AS1 via GFP antibody and demonstrated via qRT-PCRanalysis that miR-484 associated with THAP9-AS1 via targeting site, while the non-targeting miR-191-5p used as negative control, was not associated with THAP9-AS1 (Fig.4C). RIP assays also indicated that miR-484 also associated with Y AP 3'-UTR specifically (Fig.4D). To further confirm the association of THAP9-AS1 with miR-484, based on pMir-reporter plasmid we constructed luciferase reporters containing the 5'-500nt of THAP9-AS1, which contains wild-type or deletion mutated miR-484 targeting site. These reporters were co-transfected with miR-484 mimics into HEK-293T cells. We found that miR-484 mimics reduced the reporter activity of the construct with wild-type THAP9-AS1 (Fig.4E).	31831555	RID07557	interact with protein	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Gastric cancer	LINC00682	LMX1A	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-9)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245870	GRCh38_4:41872741-41882955	ENSG00000162761	NA	101927074	4009	NA	LMX1|LMX1.1	LINC00682 inhibits gastric cancer cell progression via targeting microRNA-9-LMX1A signaling axis.In order to study the potential effect of LINC00682 on miR-9-LMX1A axis, the lentivirus encoding LINC00682-expressing construct ("LV-LINC00682") was added to AGS cells. Following selection by the puromycin-containing complete medium, two stable cell lines, "sLi-1" and "sLi-2", were established. qPCR results confirmed that LINC00682 levels increased over ten folds (versus control cells) in the LV-LINC00682-expressing stable cells (Figure 1A). Importantly, LINC00682 overexpression in AGS cells induced significant downregulation of miR-9 (Figure 1B), but a significant increase in LMX1A UTR luciferase activity (Figure 1C). Consequently, LMX1A mRNA levels increased over five-six folds by LV-LINC00682 (Figure 1D). Western blotting results confirmed that forced overexpression of LINC00682 induced LMX1A protein upregulation as well (Figure 1E). LMX1B mRNA and protein expression was however not significantly affected by LV-LINC00682 (Figure 1E and ?and1F1F).Our previous study has demonstrated that LMX1A functions as a tumor suppressor, inhibiting GC cell survival and proliferation [9]. By counting cell number, we show that forced overexpression of LINC00682 by LV-LINC00682 significantly inhibited AGS cell growth (Figure 1G). Furthermore, AGS cells with LV-LINC00682 presented with decreased cell viability (CCK-8 OD, Figure 1H) and inhibited EdU ratio (Figure 1I), suggesting proliferation inhibition. Testing cell migration, by the "Transwell" assays, show that LV-LINC00682-induced LINC00682 overexpression significantly inhibited AGS cell migration in vitro (Figure 1J). Furthermore, the "Matrigel Transwell" assay results demonstrated that AGS cell invasion was also suppressed by ectopic LINC00682 overexpression (Figure 1K).Importantly, significant apoptosis activation was detected in LINC00682-overexpressed AGS cells, evidenced by cleavages of caspase-3, caspase-9 and poly (ADP-ribose) polymerase (PARP) (Figure 1L), as well as increased caspase-3 activation (Figure 1M) and nuclear TUNEL ratio (Figure 1N). Additionally, LINC00682-overexpressed AGS cells presented with increased Annexin V staining (Figure 1O). The control lentivirus with empty vector ("LV-c") had no significant effect on LINC00682-miR-9-LMX1A/B expression (Figure 1AC1F) nor AGS cell functions (Figure 1GC1O). These results show that ectopic overexpression of LINC00682 induces miR-9 downregulation but LMX1A upregulation, inhibiting AGS cell survival, proliferation, migration and invasion.Since exogenous LINC00682 overexpression inhibited AGS cell progression in vitro (Figure 1), we hypothesized that LINC00682 silencing might promote cell progression. To test this hypothesis, two different siRNAs, targeting non-overlapping sequences ("Seq1/Seq2") of LINC00682 were transfected individually to AGS cells. Results from the qPCR confirmed that each siRNA resulted in over 90% reduction of LINC00682 expression in AGS cells (Figure 2A). miR-9 levels were significantly increased in LINC00682-silenced cells (Figure 2B), where LMX1A 3'-UTR luciferase activity was largely decreased (Figure 2C). In AGS cells LMX1A mRNA (Figure 2D) and protein (Figure 2E) levels were significantly downregulated by LINC00682 siRNAs. While the two had no effect on LMX1B expression (Figure 2E and ?2F).If miR-9 is the primary target of LINC00682, restoring miR-9 expression should abolish LINC00682-induced actions in GC cells. Thus, in the stable AGS cells with LV-LINC00682 ("sLi-1", see Figure 1), the miR-9-expressing lentivirus ("lv-miR-9", see our previous study [9]) was added. Two stable cell lines were established, "sL1/sL2". As shown, in LV-LINC00682 AGS cells, lv-miR-9 did not affect LINC00682 expression (Figure 4A). Yet it restored miR-9 expression, four-five times higher to the control level (Figure 4B). Further, LV-LINC00682-induced LMX1A mRNA (Figure 4C) and protein (Figure 4D) upregulation was completely blocked by lv-miR-9. LMX1B mRNA was again unchanged (Figure 4E). Importantly, LV-LINC00682-induced viability (CCK-8 OD) reduction (Figure 4F) and apoptosis activation (the increase in TUNEL staining) (Figure 4G) were abolished by lv-miR-9 in AGS cells. These results showed that ectopic miR-9 expression reversed LINC00682-induced inhibition on GC cells, suggesting that miR-9 is the target of LINC00682.Our study has previously shown that LMX1A is the direct and primary target of miR-9 in GC cells, therefore LINC00682 should be ineffective in LMX1A-depleted cells. To test this hypothesis, the CRISPR/Cas9 method by using non-overlapping sgRNA sequences ("S1/S2") [9] was utilized to knockout LMX1A in AGS cells. Two stable LMX1A knockout ("Cas9-LMX1A-ko") cell lines were established. Testing LMX1A protein expression by Western blotting confirmed complete LMX1A KO in the stable cells (Figure 4H). LV-LINC00682 (see Figure 1) or LINC00682 siRNA ("Seq1", see Figure 2) were transfected to LMX1A KO AGS cells, which significantly altered LINC00682 expression (Figure 4I). Yet, neither LV-LINC00682 nor LINC00682 siRNA affected viability (CCK-8 OD, Figure 4J) and proliferation (EdU ratio, Figure 4K) in the LMX1A KO cells. Therefore, LINC00682 was completely ineffective in LMX1A KO AGS cells, confirming LMX1A is the target protein of LINC00682.Expression of LINC00682 in human GC tissues was tested. Total RNA was extracted from fresh GC tissues and paired adjacent normal epithelial tissues from twelve (12) primary GC patients [9]. LINC00682 expression was examined by qPCR. Results show that LINC00682 levels are significantly downregulated in cancer tissues ("Can") (Figure 4L), when compared to those in the adjacent epithelial ("Epi") tissues (Figure 4L). Therefore, LINC00682 downregulation correlates with miR-9 upregulation and LMX1A downregulation in GC tissues (see the results from same set of tissue samples [9]).	31822638	RID07558	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Malignant glioma	PSMB8-AS1	RAB10	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-574-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000233140	GRCh38_CHR_HSCHR6_MHC_SSTO_CTG1:32934803-32937212	ENSG00000084733	NA	100507463	10890	TAP1-AS1|TAPSAR1|XXbac-BPG246D15.8	NA	PSMB8-AS1 activated by ELK1 promotes cell proliferation in glioma via regulating miR-574-5p/RAB10.For purpose of comprehending the role of PSMB8-AS1 in glioma, by utilizing GEPIA and TCGA databases, the expression of PSMB8-AS1 was upregulated in glioma tissues (Fig. 1A and 1B). Then through RT-qPCR, it measured that PSMB8-AS1 was observably highly expressed in glioma cells (U251, U87, SHG44 and A172) in comparison with that in normal human astrocyte cell (NHA) (Fig. 1C). For that PSMB8-AS1 expressed the highest and lowest in U251 and A172 cells separately among these glioma cells, U251 cell was transfected with sh-PSMB8-AS1#1/#2, and A172 cell with pcDNA3.1/PSMB8-AS1 to detect the knockdown and overexpression efficiency respectively (Fig. 1D). Subsequently, CCK-8 and colony formation assays measured that PSMB8-AS1#1/#2 depletion suppressed the proliferation of U251 cell, and upregulation of PSMB8-AS1 made opposite results in A172 cell (Fig. 1E and 1-F). With regard to cell apoptosis in glioma, TUNEL and flow cytometry elucidated that PSMB8-AS1#1/#2 knocking down inspired an increasing tendency in U251 cell apoptosis, similarly, PSMB8-AS1 overexpression repressed A172 cell apoptosis (Fig. 1G and 1-H). To sum up, the expression of PSMB8-AS1 is upregulated in glioma tissues and cells, and PSMB8-AS1 upregulation/downregulation exerted suppressive/promotive function on glioma cell proliferation.To enrich our knowledge about the regulation mechanism of PSMB8-AS1 in glioma, the miRNAs capable of binding with PSMB8-AS1 needed to be finding out. First of all, subcellular fractionation confirmed that PSMB8-AS1 had main portion in cytoplasm of U251 and A172 cells (Fig. 2A). And through starbase, three eligible miRNAs, including miR-574-5p, miR-22-3p and miR-382-3p, were selected out. To move forward, RT-qPCR indicated that miR-574-5p was the most obviously regulated by PSMB8-AS1 in U251 and A172 cells (Fig. 2B). RNA pull-down assay revealed that only miR-574-5p was significantly pulled down by bio-PSMB8A-AS1 (Figure S1A). Thus, we chose it for subsequent analyses. Then the binding sites of PSMB8-AS1 and miR-574-5p were predicted by starbase (Fig. 2C). RIP assay measured the relative enrichment of PSMB8-AS1 and miR-574-5p in U251 and A172 cells, which indirectly proved the binding relation between PSMB8-AS1 and miR-574-5p (Fig. 2D). Therefore, luciferase reporter assay confirmed the binding relationship existed between PSMB8-AS1 and miR-574-5p, as that miR-574-5p mimics lowered down the luciferase activity of PSMB8-AS1-WT in U251 and A172 cells (Fig. 2E). What'-more, the expression of miR-574-5p was detected by RT-qPCR in glioma cells and normal human astrocyte cell, and data displayed that miR-574-5p was low expressed in glioma cells, but high expressed in astrocyte cell (Fig. 2F). Overall, PSMB8-AS1 could bind with miR-574-5p, which negatively expressed in glioma cells.To perfect the molecular mechanism of PSMB8-AS1 in glioma progression, we made a plan to find the target gene of miR-574-5p. As shown in Fig. 3A, 4 qualified mRNAs (CALCOCO1, HOXC8, GALNT3 and RAB10) were collected by searching the information in PITA, microT, PicTar and RNA22 databases. Then according to GEPIA database, only the expression of RAB10 exhibited significant difference in glioma tissues and non-tumor tissues (Fig. 3B). RT-qPCR and western blot also verified the expression of RAB10 was much higher in glioma cells than that in astrocyte (Fig. 3C and Figure S1B). In hence, the conjectured binding sites of RAB10 3-UTR-WT/Mut and miR-574-5p were showed in Fig. 3D. Besides, miR-574-5p expression was downregulated and upregulated by transfecting miR-574-5p inhibitor and miR-574-5p mimics into U251 and A172 cells severally (Fig. 3E). Moreover, the expression of RAB10 was decreased/increased by knocking down PSMB8-AS1#1/overexpressing PSMB8-AS1, and this prohibitive/promotive effect was offset by miR-574-5p inhibitor/mimics (Fig. 3F and Figure S1C). The expression of RAB10 was further determined to be negatively regulated by miR-574-5p in two glioma cells by qRT-PCR(Figure S1D). Final luciferase reporter assay determined that pcDNA3.1/PSMB8-AS1 partly neutralized the depressant influence of miR-574-5p mimics in luciferase activity of RAB10 3'UTR-WT in U251 and A172 cells (Fig. 3G). In a summary, RAB10 is targeted by miR-574-5p, and PSMB8-AS1 could regulate RAB10 via modulating miR-574-5p in glioma.To confirm whether PSMB8-AS1 could promote glioma proliferation via regulating miR-574-5p/RAB10, several rescuing experiments were carried out. Before that, the knocking down and overexpressing efficiency of RAB10 were evaluated in U251 and A172 cells (Fig. 4 A). Through CCK-8 and colony formation assays, downregulating/upregulating miR-574-5p expression reversed the impedimental/promoted effects caused by knocking down/overexpressing PSMB8-AS1#1 on the proliferation of U251/A172 cell, meanwhile, this positively/negatively rescuing role of miR-574-5p inhibitor/mimics was counteracted by sh-RAB10#1/pcDNA3.1/RAB10 (Fig. 4B and 4C). Then TUNEL and flow cytometry illustrated that the inhibitory/encouraging role of PSMB8-AS1#1 insufficiency/addition in U251/A172 cell apoptosis was rescued by miR-574-5p inhibitor/mimics, in the same way, knocking down RAB10#1/overexpressing RAB10 made compensation to the stimulative/prohibitive influence in apoptosis of sh-PSMB8-AS1#1 + miR-574-5p inhibitor or pcDNA3.1/PSMB8-AS1 +miR-574-5p mimics transfected U251/A172 cell (Fig. 4D and 4E). Moreover, we confirmed that there were no significant changes in the proliferation and apoptosis of cells transfected with plasmids alone and the plasmids-+-negative control (Figure S2A-B). In general, PSMB8-AS1 promotes glioma proliferation via regulating miR-574-5p/RAB10.	31812014	RID07559	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	ELK1	PSMB8-AS1	positively-E		upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000126767	NA	ENSG00000233140	GRCh38_CHR_HSCHR6_MHC_SSTO_CTG1:32934803-32937212	2002	100507463	NA	TAP1-AS1|TAPSAR1|XXbac-BPG246D15.8	PSMB8-AS1 activated by ELK1 promotes cell proliferation in glioma via regulating miR-574-5p/RAB10.For purpose of comprehending the role of PSMB8-AS1 in glioma, by utilizing GEPIA and TCGA databases, the expression of PSMB8-AS1 was upregulated in glioma tissues (Fig. 1A and 1B). Then through RT-qPCR, it measured that PSMB8-AS1 was observably highly expressed in glioma cells (U251, U87, SHG44 and A172) in comparison with that in normal human astrocyte cell (NHA) (Fig. 1C). For that PSMB8-AS1 expressed the highest and lowest in U251 and A172 cells separately among these glioma cells, U251 cell was transfected with sh-PSMB8-AS1#1/#2, and A172 cell with pcDNA3.1/PSMB8-AS1 to detect the knockdown and overexpression efficiency respectively (Fig. 1D). Subsequently, CCK-8 and colony formation assays measured that PSMB8-AS1#1/#2 depletion suppressed the proliferation of U251 cell, and upregulation of PSMB8-AS1 made opposite results in A172 cell (Fig. 1E and 1-F). With regard to cell apoptosis in glioma, TUNEL and flow cytometry elucidated that PSMB8-AS1#1/#2 knocking down inspired an increasing tendency in U251 cell apoptosis, similarly, PSMB8-AS1 overexpression repressed A172 cell apoptosis (Fig. 1G and 1-H). To sum up, the expression of PSMB8-AS1 is upregulated in glioma tissues and cells, and PSMB8-AS1 upregulation/downregulation exerted suppressive/promotive function on glioma cell proliferation.To enrich our knowledge about the regulation mechanism of PSMB8-AS1 in glioma, the miRNAs capable of binding with PSMB8-AS1 needed to be finding out. First of all, subcellular fractionation confirmed that PSMB8-AS1 had main portion in cytoplasm of U251 and A172 cells (Fig. 2A). And through starbase, three eligible miRNAs, including miR-574-5p, miR-22-3p and miR-382-3p, were selected out. To move forward, RT-qPCR indicated that miR-574-5p was the most obviously regulated by PSMB8-AS1 in U251 and A172 cells (Fig. 2B). RNA pull-down assay revealed that only miR-574-5p was significantly pulled down by bio-PSMB8A-AS1 (Figure S1A). Thus, we chose it for subsequent analyses. Then the binding sites of PSMB8-AS1 and miR-574-5p were predicted by starbase (Fig. 2C). RIP assay measured the relative enrichment of PSMB8-AS1 and miR-574-5p in U251 and A172 cells, which indirectly proved the binding relation between PSMB8-AS1 and miR-574-5p (Fig. 2D). Therefore, luciferase reporter assay confirmed the binding relationship existed between PSMB8-AS1 and miR-574-5p, as that miR-574-5p mimics lowered down the luciferase activity of PSMB8-AS1-WT in U251 and A172 cells (Fig. 2E). What'-more, the expression of miR-574-5p was detected by RT-qPCR in glioma cells and normal human astrocyte cell, and data displayed that miR-574-5p was low expressed in glioma cells, but high expressed in astrocyte cell (Fig. 2F). Overall, PSMB8-AS1 could bind with miR-574-5p, which negatively expressed in glioma cells.To perfect the molecular mechanism of PSMB8-AS1 in glioma progression, we made a plan to find the target gene of miR-574-5p. As shown in Fig. 3A, 4 qualified mRNAs (CALCOCO1, HOXC8, GALNT3 and RAB10) were collected by searching the information in PITA, microT, PicTar and RNA22 databases. Then according to GEPIA database, only the expression of RAB10 exhibited significant difference in glioma tissues and non-tumor tissues (Fig. 3B). RT-qPCR and western blot also verified the expression of RAB10 was much higher in glioma cells than that in astrocyte (Fig. 3C and Figure S1B). In hence, the conjectured binding sites of RAB10 3-UTR-WT/Mut and miR-574-5p were showed in Fig. 3D. Besides, miR-574-5p expression was downregulated and upregulated by transfecting miR-574-5p inhibitor and miR-574-5p mimics into U251 and A172 cells severally (Fig. 3E). Moreover, the expression of RAB10 was decreased/increased by knocking down PSMB8-AS1#1/overexpressing PSMB8-AS1, and this prohibitive/promotive effect was offset by miR-574-5p inhibitor/mimics (Fig. 3F and Figure S1C). The expression of RAB10 was further determined to be negatively regulated by miR-574-5p in two glioma cells by qRT-PCR(Figure S1D). Final luciferase reporter assay determined that pcDNA3.1/PSMB8-AS1 partly neutralized the depressant influence of miR-574-5p mimics in luciferase activity of RAB10 3'UTR-WT in U251 and A172 cells (Fig. 3G). In a summary, RAB10 is targeted by miR-574-5p, and PSMB8-AS1 could regulate RAB10 via modulating miR-574-5p in glioma.To confirm whether PSMB8-AS1 could promote glioma proliferation via regulating miR-574-5p/RAB10, several rescuing experiments were carried out. Before that, the knocking down and overexpressing efficiency of RAB10 were evaluated in U251 and A172 cells (Fig. 4 A). Through CCK-8 and colony formation assays, downregulating/upregulating miR-574-5p expression reversed the impedimental/promoted effects caused by knocking down/overexpressing PSMB8-AS1#1 on the proliferation of U251/A172 cell, meanwhile, this positively/negatively rescuing role of miR-574-5p inhibitor/mimics was counteracted by sh-RAB10#1/pcDNA3.1/RAB10 (Fig. 4B and 4C). Then TUNEL and flow cytometry illustrated that the inhibitory/encouraging role of PSMB8-AS1#1 insufficiency/addition in U251/A172 cell apoptosis was rescued by miR-574-5p inhibitor/mimics, in the same way, knocking down RAB10#1/overexpressing RAB10 made compensation to the stimulative/prohibitive influence in apoptosis of sh-PSMB8-AS1#1 + miR-574-5p inhibitor or pcDNA3.1/PSMB8-AS1 +miR-574-5p mimics transfected U251/A172 cell (Fig. 4D and 4E). Moreover, we confirmed that there were no significant changes in the proliferation and apoptosis of cells transfected with plasmids alone and the plasmids-+-negative control (Figure S2A-B). In general, PSMB8-AS1 promotes glioma proliferation via regulating miR-574-5p/RAB10.	31812014	RID07560	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	EPIC1	YAP1	interact	RIP	upregulation	qRT-PCR	NA	NA	cell cycle(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000137693	NA	284930	10413	Lnc-EPIC1	YAP65	Long noncoding RNA EPIC1 interacts with YAP1 to regulate the cell cycle and promote the growth of pancreatic cancer cells.As a key transcriptional cofactor in the Hippo pathway, YAP1 is a key factor upstream of MYC that plays an important role in the development of PC [15]. We found a strong correlation between YAP1 and Lnc-EPIC1 by the catRAPID algorithm (Fig. 1A), and the possible binding sites of YAP1 and Lnc-EPIC1 are located at 600 bp and 1300 bp (Fig. 1B). The Gene Expression Profiling Interactive Analysis (GEPIA) tool was used to analyze TCCA-LIHC data, which showed that the expression of YAP1 was relatively high in PC (Fig. 1C). The patients with high expression of YAP1 had poor overall survival and a high tumor stage (Fig. 1B andD).First, we examined the expression of Lnc-EPIC1 in PC cells (SW1990 and HPAFII) and normal pancreatic cells (HPDE). qRT-PCRresults showed that Lnc-EPIC1 expression was significantly increased in the SW1990 cells and HPAFII cells compared to the HPDE cells (Fig. 1F). western blot results showed that YAP1 was highly expressed in the SW1990 cells and HPAFII cells (Fig. 1G).Nest, we examined the expression of Lnc-EPIC1 in PC tissue. qRT-PCRresults showed that Lnc-EPIC1 was highly expressed in human PC tissue samples. In addition, we analyzed the correlations between case data and Lnc-EPIC1, and the results showed that LncEPIC1 expression was significantly associated with tumor grade, TNM staging and lymph node metastasis status (Table 2). In addition, western blot results showed that the protein expression of YAP1 was significantly increased in the PC tissue samples (Fig. 1H).We used three siRNAs to specifically knock down Lnc-EPIC1 expression and transfected the siRNAs into SW1990 and HPAFII cells. As shown, siRNA1 and siRNA2 significantly reduced the expression of Lnc-EPIC1 (Fig. 2A,Fig. 2B). CCK-8 assay results showed that reduced Lnc-EPIC1 expression significantly inhibited PC cell activity (Fig. 2C andD). Colony formation results showed that reduced Lnc-EPIC1 expression significantly inhibited the colony formation ability of PC cells (Fig. 2E andF). Apoptosis assay results showed a significant increase in the apoptosis rate of LncEPIC1-downregulated PC cells (Fig. 2G andH). These results indicate that Lnc-EPIC1 promotes PC progression by promoting cell growth and inhibiting apoptosis. 3.5. YAP1 is a target of Lnc-EPIC1 According to the literature, MYC is the main target of Lnc-EPIC1, and this interaction has been proven in lung cancer and cholangiocarcinoma [11e13]. MYC is also a downstream target of YPA1 in PC [15,16]. Cell cycle experiments showed that knocking down Lnc-EPIC1 expression increased the percentage of G0/G1 PC cells and induced G1/S cell cycle arrest (Fig. 3A). Therefore, we verified the expression of several cyclin mRNAs in PC cells. qRT-PCR;ISHowed that Lnc-EPIC1 siRNA treatment significantly inhibited CDC20, CDK4 and Cyclin A1 (Fig. 3B). To verify whether Lnc-EPIC1 and YPA1 are directly linked in PC, we performed a RIP assay and showed the direct interaction of YPA1 and Lnc-EPIC1 in SW1990 cells (Fig. 3C). Next, we used the CRISPR-Cas9 system to establish YAP1-KO SW1990 cells, and qRT-PCRresults confirmed a significant decrease in YAP1 mRNA expression (Fig. 3D). Importantly, the YAP1-KO cells exhibited decreased cell growth (Fig. 3E) and colony formation ability (Fig. 3F) and an increased apoptosis rate (Fig. 3G). However, transfection of Lnc-EPIC1-specific siRNAs into YAP1-KO cells did not enhance these changes. Thesefindings indicate that YAP1 is a target of Lnc-EPIC1 in PC.To revalidate the functions of Lnc-EPIC1, we constructed LncEPIC1-overexpressing SW1990 cells and YAP1-KO cells using two lentiviral expression constructs (Lv-EPIC1-1 and Lv-EPIC1-2). qRTPCR results verified that Lnc-EPIC1 expression was significantly increased (Fig. 4A,Fig. 4B). Lv-EPIC1-1 promoted SW1990 cell growth (Fig. 4C) and colony formation ability (Fig. 4E). However, it did not affect the growth (Fig. 4D) or colony formation ability of YAP1-KO cells (Fig. 4F). These results fully demonstrate that LncEPIC1 interacts directly with YPA1 to promote tumor cell growth. Notably, overexpression of Lnc-EPIC1 did not further inhibit apoptosis in either SW1990 cells or YAP1-KO cells (Fig. 4G andH).	31810603	RID07561	interact with protein	metastasis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Malignant glioma	GATA6-AS	TUG1	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	lncRNA	NA	NA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	LncRNA GATA6-AS Promotes Cancer Cell Proliferation and Inhibits Apoptosis in Glioma by Downregulating lncRNA TUG1.RT-quantitative PCR (RT-qPCR) was performed to detect the differential expression of GATA6-AS in glioma and adjacent normal tissues of 58 glioma patients. Compared with normal tissues, significantly upregulated expression of GATA6-AS was observed in glioma tissues, indicating the involvement of this lncRNA in glioma. Univariate analysis found that age (> or <<-0 years), gender, and tumor stages have no significant effects on GATA6-AS expression. Risk ratios were 0.812, 1.428, and 1.232, respectively; 95% confidence intervals were 0.555'-.768, 0.711'-.020, and 0.508'-.545, respectively; p-values were 0.343, 0.888, and 0.596, respectively.RT-qPCR was also performed to detect GATA6-AS in plasma. Linear regression was performed to investigate the correlations between plasma levels of GATA6-AS and its expression in glioma or normal tissues. It was observed that plasma levels of GATA6-AS were significantly and positively correlated with its expression levels in glioma tissues (Fig. 2A), but not in adjacent normal tissues (Fig. 2B).Differential expression of TUG1 in glioma and adjacent normal tissues of 58 glioma patients was detected by RT-qPCR. Compared with normal tissues, TUG1 was significantly downregulated in glioma tissues (Fig. 3A, p-<-0.05). Linear regression was performed to investigate the correlations between expression levels of GATA6-AS and TUG1. It was observed that expression levels of TUG1 were inversely correlated with expression levels of GATA6-AS only in glioma tissues (Fig. 3B), but not in adjacent healthy tissues (Fig. 3C).Cells of Hs 683 and CCD-25Lu cell lines were transfected with GATA6-AS and TUG1 expression vectors to explore the possible interactions between GATA6-AS and TUG1. Overexpression of GATA6-AS and TUG1 was reached in cells of both cell lines at 24-h after transfection (Fig. 4A, p-<-0.05). Compared with untransfection (control [C]) cells and cell transfected with empty vectors (negative control [NC]), GATA6-AS overexpression led to the downregulation of TUG1 (Fig. 4B, p-<-0.05), whereas TUG1 overexpression failed to significantly affect GATA6-AS (Fig. 4C).Results of in vitro cell proliferation and apoptosis assay showed that, compared with control (C) and negative control (NC) groups, GATA6-AS overexpression led to promoted proliferation (Fig. 5A) and inhibited apoptosis (Fig. 5B) of cells of both Hs 683 and CCD-25Lu cell lines (p-<-0.05), TUG1 overexpression played an opposite role, and attenuated the effects of GATA6-AS overexpression.	31809214	RID07562	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Gastric cancer	NORAD	miR-214	negatively-F	luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);AKT/mTOR signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	LncRNA NORAD Promotes Proliferation And Inhibits Apoptosis Of Gastric Cancer By Regulating miR-214/Akt/mTOR Axis.First, the mRNA expressions of lncRNA NORAD and miR-214 in GC tissues (n = 36) and adjacent non-tumor tissues (n = 36) were determined by qRT-PCR The mRNA expression of lncRNA NORAD in GC tissues was significantly higher than that in adjacent tissues (Figure 1A, P < 0.05). Meanwhile, the results of correlation analysis showed that the mRNA expression of lncRNA NORAD in GC tissues was negatively correlated with the mRNA expression of miR-214 (Figure 1B). In addition, the mRNA expressions of lncRNA NORAD and miR-214 in GC cell lines were determined by qRT-PCR The results showed that mRNA expression of lncRNA NORAD in GC cell lines (BSG823, MKN28, BGC803, BGC823) were significantly higher than that in GSE1 cells (Figure 1C, P < 0.05), while the mRNA expression of miR-214 in GC cell lines were significantly lower than that in GSE1 cells (Figure 1D, P < 0.05). These results suggested that NORAD was highly expressed in GC tissues and cells, while miR-214 was down-regulated.First, we transfected pc-NORAD or sh-NORAD into BGC823 and BGC803 cells to determine the mRNA expressions of lncRNA NORAD and miR214 in the cells. The results showed that transfected pc-NORAD significantly up-regulated the expression of lncRNA NORAD in GC cells (Figure 2A, P < 0.05, P < 0.01) and significantly inhibited the expression of miR214 (Figure 2C, P < 0.05). Meanwhile, we transfected miR-214 mimic or its control into BGC823 and BGC803 cells and found that the transfected with miR-214 mimic significantly up-regulated the expression of miR-214 in cells (Figure 2B, P < 0.05, P < 0.01), indicating the successful transfection of miR-214 mimic. In addition, we through the biological analysis (http://starbase.sysu.edu.cn) to predict miR-214 might exist the lncRNA NORAD binding sites (Figure 2D). Furthermore, wild-type NORAD (NORAD-WT) or mutant NORAD (NORAD-MUT) was transfected with miR-214 mimic or its control into BGC823 and BGC803 cells, and luciferase activity was measured. The results showed that, compared with the control group, the luciferase activity in BGC823 and BGC803 cells co-transfected by NORAD-WT and miR-214 mimic were significantly decreased (Figure 2E, P <0.01), which indicated that miR-214 was a direct target of lncRNA NORAD. Moreover, the RNA pull-down results found that, compared with the control group, the mRNA expression of lncRNA NORAD in the bio-miR-214 group was remarkably up-regulated (Figure 2F, P <0.01), which further confirmed that miR-214 was a direct target of lncRNA NORAD.First, the protein expression of caspase-3 in pc-NORAD or sh-NORAD transfected BGC823 and BGC803 cells were detected by western blot. It was found that protein expression of caspase-3 in sh-NORAD group was significantly higher than that in control group (P < 0.05), while there was no significant difference in caspase-3 expression between pc-NORAD group and control group (Figure 4A, P > 0.05), which indicated that NORAD silencing significantly promoted the expression of caspase-3 in GC cells. Meanwhile, flow cytometry showed that the apoptosis rate of GC cells in the sh-NORAD group was significantly higher than that in the control group (P < 0.05), while the apoptosis rate of GC cells in the pcNORAD group was not significantly different from that in the control group (Figure 4B and -andC,C, P > 0.05). It suggested that NORAD silencing significantly promoted the apoptosis of GC cells. In addition, colony formation and EDU assay were used to detect the proliferation of BGC823 and BGC803 cells transfected with pc-NORAD or sh-NORAD. The results showed that the number of clones and EDU positive cells in pc-NORAD group were markedly more than those in control group (P < 0.05), while the number of clones and EDU positive cells in shNORAD group were significantly lower than those in control group (Figure 4D and -andE,E, P < 0.05), indicating that NORAD overexpression significantly promoted the cell proliferation.western blot was used to determine whether the Akt/mTOR pathway in mouse GC tissues and GC cells were related to the proliferation and apoptosis of GC cells mediated by NORAD/miR-214. The results showed that p-Akt and p-mTOR were significantly up-regulated in pc-NORAD-transfected tumor tissues (P < 0.05), while p-Akt and p-mTOR were significantly inhibited in sh-NORAD transfected tumor tissues (Figure 6A, P < 0.05). In addition, pc-NORAD or/and miR-214 mimic were transfected into BGC823 and BGC803 cells and the expressions of p-Akt and p-mTOR in the cells were detected. It was found that the expressions of p-Akt and p-mTOR were significantly up-regulated in GC cells transfected with pc- NORAD (P < 0.05), while miR-214 mimic significantly inhibited this promotion (Figure 6B, P < 0.05, P < 0.01). These results suggested that NORAD/miR-214-mediated GC cell proliferation and apoptosis were related to the activation of Akt/mTOR signaling pathway.	31802897	RID07563	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Oral squamous cell carcinoma	CACS15	MEG3	negatively-E	overexpression	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	Up-regulation of plasma lncRNA CACS15 distinguished early-stage oral squamous cell carcinoma patient.It was found that plasma CASC15 was up-regulated in oral squamous cell carcinoma patients comparing to oral ulcer patients, and the fold change is 1.87 (Figure 1, p < .05).MEG3 in plasma of oral squamous cell carcinoma patients was also detected by performing RT-qPCR experiments. Correlation between levels of CASC15 and MEG3 across plasma samples from oral squamous cell carcinoma patients was analyzed by linear regression. It was observed that CASC15 and MEG3 were significantly and inversely correlated across oral squamous cell carcinoma patients (R square = 0.6910, p < .0001, Figure 3). The significantly inverse correlation between CASC15 and MEG3 indicates the possible interaction between them.Aforementioned data indicate the possible interaction between CASC15 and MEG3, to further investigate the relationship between CASC15 and MEG3 and explore possible interactions between them, CASC15 and MEG3 expression vectors were transfected into SCC090 cells. At 24 hr after transfection, RT-qPCR experiments were performed to measure the expression levels of CASC15 and MEG3 in different transfection groups. It was observed that CASC15 and MEG3 expression levels were significantly increased in SCC090 cells transfected with CASC15 and MEG3 expression vectors comparing to control (C) and negative control (NC) (p < .05, Figure 4a,b). Therefore, over-expression of CASC15 and MEG3 was successfully achieved in SCC090 cells. In addition, comparing to C and NC two controls, cells transfected with CASC15 expression vector showed significantly reduced expression levels of MEG3 (Figure 4a, p < .05), indicating that CASC15 can downregulate MEG3 in SCC090 cells. In contrast, cells transfected with MEG3 expression vector showed no significantly altered CASC15 expression (Figure 4b), indicating that MEG3 is unable to regulate the expression of CASC15. Therefore, CASC15 is likely an upstream inhibitor of MEG3 in oral squamous cell carcinoma cells. The interaction between CASC15 and MEG3 may affect the behaviors of cancer cells. To test this hypothesis, the effects of the overexpression of CASC15 and MEG3 on the proliferation of SCC090 cells were analyzed by CCK-8 assay at 24 hr post-transfection. Analysis of cell proliferation data showed that MEG3 over-expression decreased, while CASC15 over-expression increased the proliferation rate of oral squamous cell carcinoma cells (Figure 4c). In addition, comparing to CASC15 over-expression group, cells with both MEG3 and CASC15 over-expression showed significantly reduced proliferation rate. Therefore, MEG3 over-expression attenuated the effects of CASC15 over-expression. Moreover, CASC15 over-expression failed to significantly affect the migration and invasion of SCC090 cells (data not shown, revealed by Transwell migration and invasion assay).	31793142	RID07564	expression association	NA		
Cervical cancer	FTH1P3	miR-145	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);metastasis process(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000269936	NA	2498	NA	FTHL3	NA	The long noncoding RNA FTH1P3 promotes the proliferation and metastasis of cervical cancer through microRNA-145.Next, the expression of FTH1P3 in cervical cancer cell lines was further investigated. As revealed in Fig. 1B, it was determined that FTH1P3 expression was significantly increased in cervical cancer cell lines (HeLa, SiHa, Caski, and C4-1) compared to cervical normal epithelial cells (ECT1/E6E7). Notably, higher expression of FTH1P3 was observed in the HeLa and SiHa cell lines. Therefore, HeLa and SiHa cells were selected for further studies.Bioinformatics analysis with miRcode software was performed and it was revealed that human miR-145 (hsa-miR-145) was a potential binding candidate of FTH1P3 (Fig. 4A). As revealed in Fig. 4B, FTH1P3 overexpression plasmid significantly increased the expression of FTH1P3 in both HeLa and SiHa cells compared with the negative control (P<0.01). After transfection of human miR-145 mimic, a significant increase of miR-145 expression in HeLa and SiHa cells was observed (Fig. 4C; P<0.01). The overexpression of FTH1P3 by plasmid transfection could significantly reduce the expression of miR-145, while miR-145 expression was inversely increased due to the downregulation of FTH1P3 (Fig. 4C and D; P<0.05). In addition, a luciferase reporter assay revealed that miR-145 mimic significantly suppressed the luciferase activities of FTH1P3-WT reporter vector. Conversely, after transfection with FTH1P3-MUT and the miRNA-145 mimic, the luciferase activities between these two cells were nearly comparable with that in the control cells (Fig. 4E; P<0.01). These data indicated that FTH1P3 was a potential target of miR-145.To investigate the role of miR-145 in cervical cancer progression, miR-145 expression in cervical cancer tissues and non-malignant tissues was detected by qRT-PCR As revealed in Fig. 5A, miR-145 expression in cervical cancer tissues was significantly downregulated compared with the non-malignant tissues (P<0.01). Consistently, the expression of miR-145 in five assessed cervical cancer cell lines were all significantly lower than that in normal cervical epithelial cells (Ect1/E6E7) (P<0.01; Fig. 5B). Moreover, the downregulated expression of miR-145 demonstrated a significant association with tumor size (P=0.035), lymph node metastasis (P=0.011) and FIGO stage (P=0.017). Spearman's correlation analysis revealed that miR-145 expression was inversely associated with FTH1P3 expression in cervical cancer tissues (Table II, r=-0.265, P=0.002), indicating that upregulated FTH1P3 expression in cervical cancer was correlated with downregulated miR-145 expression.As illustrated in Fig. 6A, the transfection of miR-145 inhibitor caused a significant reduction of miR-145 in cervical cancer cells (P<0.01). Moreover, downregulation of FTH1P3 significantly inhibited the proliferation, invasion and migration abilities and promoted apoptosis in HeLa and SiHa cells (Figs. 6 and -and7).7). Notably, the miRNA-145 inhibitor could enhance the cell proliferation, invasion and migration in cervical cancer cells compared to the RNA scramble group, while FTH1P3 siRNA revealed a significant bucking effect for miRNA-145 inhibitor in HeLa and SiHa cells compared to cells transfected with FTH1P3 siRNA+ RNA scramble group (Figs. 6 and -and77).	31789421	RID07565	ceRNA or sponge	metastasis	UP(NSCLC,BRCA);DOWN(BRCA);DATA(GSE74639,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Glioblastoma	Unigene56159	miR-194-5p	negatively-F	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Long non-coding RNA Unigene56159 promotes glioblastoma multiforme cell proliferation and invasion through negatively regulating microRNA-194-5p.A log2-fold change (FC) of >2 and a false discovery rate (P<0.05) were selected as the cut-off values based on the Benjamini-Hochberg method (27). The expression of Unigene56159 was obtained and 151 cases of valid data collected. The top 20 differentially expressed lncRNAs meeting this criteria were collected, and these lncRNAs were identified according to the level of log2FC (Fig. 1A). Among the differentially expressed lncRNAs, Unigene56159 expression levels were the highest in GBM, demonstrating markedly upregulated expression levels compared with normal brain tissue (Fig. 1A and B).It was noted that the Unigene56159 level were higher in U251 and T98G than in other cell lines. To identify the effect of Unigene56159 on the proliferative and invasive ability of GBM, U251 and T98G cells were selected and transfected with either si-Unigene56159 to knockdown Unigene56159 gene expression or with the si-NC. The transfection efficiency of si-Unigene56159 was high, exhibiting significantly decreased expression levels in the si-Unigene56159-transfected cells compared with the si-NC in both U251 and T98G cell lines (Fig. 2B). In both GBM cell lines, the knockdown of Unigene56159 resulted in a significant decrease compared with si-NC group at the similar time points in their proliferative capacity following 24'-2 h (Fig. 2C). Furthermore, Unigene56159 silencing significantly reduced the number of colonies (>50 cells) (Fig. 2D), in addition to the invasive capacity in both U251 and T98G cell lines compared with respective si-NC transfected cells (Fig. 2E). These data demonstrated a suppressive function of both proliferative and invasive processes following Unigene56159 silencing in GBM cells in vitro.The complementary sequence between Unigene56159 and miR-194-5p was identified using both the TargetScan database and starBase database. A dual-luciferase reporter assay was subsequently used to identify the putative miR-194-5p target site (Fig. 4A). Transfection efficiency was evaluated by increasing or decreasing miR-194-5p expression levels in U251 and T98G cell lines (Fig. 4B). Notably, miR-194-5p significantly decreased the luciferase activity of the Unigene56159-3'UTR-WT U251 cells, but not the Unigene56159-3'UTR-MUT U251 cells (Fig. 4C). To determine the role of Unigene56159 on the expression of miR-194-5p, U251 and T98G cells were transfected with siRNA-Unigene56159. The expression of miR-194-5p significantly increased in both U251 and T98G cell lines upon Unigene56159 knockdown compared with si-NC transfected cells (Fig. 4D). To further explore this, miR-194-5p expression levels in the 50 GBM samples were compared with normal brain samples and it was found that the expression was significantly decreased in GBM compared with normal tissue (P<0.001; Fig. 4E). In addition, the level of Unigene56159 expression was significantly negatively correlated with miR-194-5p in GBM patient samples (r=-0.4046; P=0.0036; Fig. 4F). These data confirmed that miR194-5p represses Unigene56159 in glioma cells.	31789416	RID07566	ceRNA or sponge	NA		
Malignant glioma	AWPPH	TGFB1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	NA	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	lncRNA AWPPH promotes the migration and invasion of glioma cells by activating the TGF-beta pathway.The current data suggest that AWPPH is likely involved in the regulation of tumor metastasis but not tumor growth in glioma. TGF-beta signaling serves pivotal roles in the metastasis of different types of cancer, including glioma (14). Therefore, the correlation between the plasma levels of AWPPH and TGF-beta1 was analyzed using all plasma samples. As presented in Fig. 3, the plasma levels of AWPPH were positively correlated with the plasma levels of TGF-beta1 in patients with glioma (P<0.0001; Fig. 3A) but not in healthy controls (P=0.5927; Fig. 3B).To further investigate the association between AWPPH and TGF-beta1 in glioma, an AWPPH expression vector was transfected into the human glioma cell lines CCD-25Lu and Hs 683 (P<0.05; Fig. 4A), and the expression of TGF-beta1 was detected by western blot(P<0.05; Fig. 4B). The results revealed that compared with control group and negative control group, AWPPH overexpression significantly promoted the expression of TGF-beta1 in CCD-25Lu and Hs 683 cells (P<0.05; Fig. 4B). By contrast, treatment with 5 or 10 ng/ml TGF-beta1 (Sigma-Aldrich; Merck KGaA) demonstrated no significant effects on AWPPH expression in CCD-25Lu and Hs 683 cells (P>0.05; Fig. 4C).The present data suggest that AWPPH is likely involved in the metastasis of glioma. Therefore, Transwell migration and invasion assays were performed to investigate the effects of AWPPH on the migration and invasion of in vitro cultured cells. As presented in Fig. 5, compared with the control (C) group, AWPPH overexpression significantly enhanced the migration (Fig. 5A) and invasion (Fig. 5B) of the human glioma cell lines CCD-25Lu and Hs 683. In addition, treatment with 100 nM TGF-beta inhibitor LY2109761 (Sigma-Aldrich; Merck KGaA) significantly inhibited cell migration and invasion compared with the control, and significantly attenuated the effects of AWPPH overexpression on the migration (Fig. 5A) and invasion (Fig. 5B) of glioma cells.	31788066	RID07567	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	BANCR	miR-195-5p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000278910	GRCh38_9:69296678-69311111	NA	NA	100885775	NA	LINC00586	NA	LncRNA BANCR Promotes Pancreatic Cancer tumorigenesis via Modulating MiR-195-5p/Wnt/beta-Catenin Signaling Pathway.The expression levels of BANCR in the tumors and adjacent healthy tissues of 45 patients with PC were measured by qRT-PCR Detailed information for these 45 patients is listed in Table 1. Data show that BANCR level was higher in PC tissues than that in the corresponding healthy tissues (Figure 1A). As shown in Figure 1B, -,aa statistical difference in BANCR level was present between the nonmetastatic (n = 18) and metastatic tissue samples (n = 27). Meanwhile, tumor-node-metastasis (TNM) stage (stage I, II, III, and  was positively associated with elevated BANCR expression (Figure 1C).To determine the effects of BANCR on PC cells, special siRNAs were used to knockdown BANCR expression in PC cells (including PANC-1 and SW1990 cell lines). The transfection efficiency was determined by qRT-PCR finding that si-BANCR1 and si-BANCR2 effectively downregulated BANCR levels both in PANC-1 and SW1990 cell lines (Figure 2A). By performing MTT assays, we found that BANCR downregulation could significantly decrease the viability of PANC-1 and SW1990 cells compared to parallel cell lines transfected with scramble siRNA (si-NC cells; Figure 2B and C). The colony formation assay results showed that the colony numbers in si-BANCR1 and si-BANCR2 group cells were obviously lower than those in NC groups (Figure 2D). Transwell assay was used to quantitatively assess PC cell invasion and migration. Compared to the si-NC groups, the number of invading PANC-1 and SW1990 cells in the si-BANCR1 and si-BANCR2 groups were largely reduced (Figure 2E). As expected, si-BANCR1 and si-BANCR2 groups show less migratory cells than that in si-NC groups (Figure 2F). These findings collectively suggested that knockdown of BANCR inhibited PC cell proliferation and metastasis.To investigate the effects of BANCR on miR-195-5p expression, 293T cells were transfected with the luciferase reporter plasmid pGL3.0-BANCR and miR-195-5p. Results showed that miR-195-5p could decrease the luciferase activity of BANCR, but it shows nonsignificant effect on the mutated form of BANCR (Figure 3E). Furthermore, we performed RIP assays using Ago2 antibody in PANC-1 and SW1990 cells. As expected, the endogenous levels of BANCR and miR-195-5p pull-down by Ago2 were much higher in miR-195-5p mimics groups than those in NC mimics groups (Figure 3F and G). In addition, the miR-195-5p expression level was decreased in the PANC-1 and SW1990 cells treated with si-BANCR1 and si-BANCR2 (Figure 3H and I). These results indicated that BANCR may interact with miR-195-5p by this putative binding site.The Wnt inhibitor XAV939 suppressed Wnt/beta-catenin signaling and relieved the roles of miR-195-5p inhibitor and decreased the levels of beta-catenin, c-Myc, and cyclinD1(Figure 5C and D). The western blot assay showed that BANCR overexpression led to the increase in protein levels of beta-catenin, c-Myc, and cyclinD1, and XAV939 alleviated the effects of BANCR overexpression on Wnt/beta-catenin signaling pathway (Figure 6A and B). These findings suggested that BANCR/miR-195-5p modulates PC cell proliferation and metastasis possibly through Wnt/beta-catenin signaling.	31769353	RID07568	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	
Clear cell renal cell carcinoma	LINC01094	CHSY1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell growth(+);metastasis process(+)	ceRNA(miR-224-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251442	GRCh38_4:78638780-78683185	ENSG00000131873	NA	100505702	22856	CTEPHA1	CSS1|KIAA0990	FOXM1-Activated LINC01094 Promotes Clear Cell Renal Cell Carcinoma Development via MicroRNA 224-5p/CHSY1.First, with the assistance of TCGA database, it was exposed that LINC01094 level was elevated in ccRCC tissues in comparison to nontumor samples (Fig. 1A). To validate the level of LINC01094 in ccRCC, we detected its expression pattern in cancerous cells. In contrast to normal renal tubular epithelial cells, upregulation of LINC01094 in ccRCC cells was demonstrated (Fig. 1B).This was followed by several functional experiments, and a CCK-8 assay illustrated that suppression of LINC01094 inhibited the viability of ACHN and 769-P cells (Fig. 1D). An EdU (5-ethynyl-2'-deoxyuridine) incorporation assay ascertained that depletion of LINC01094 led to the decreased percentage of EdU-positive cells, further suggesting the suppressed role of LINC01094 depletion in cell proliferation (Fig. 1E). Moreover, the results of a transwell assay showed that cell migratory capacity was restrained when LINC01094 was silenced (Fig. 1F). Consistently, knockdown of LINC01094 increased the E-cadherin level and decreased the N-cadherin level (Fig. 1G); in addition, LINC01094 insufficiency decreased the protein levels of Snail, fibronectin, MMP2, and MMP7 (Fig. 1H). To sum up, we concluded that LINC01094 downregulation hampered ccRCC progression by hindering cell proliferation, migration, and EMT process.In order to unveil the regulatory mechanism of LINC01094 in ccRCC, we utilized bioinformatics tool DIANA database to find out the putative miRNAs that could bind with LINC01094. Among the top six miRNAs with the highest predicted binding ability, only the expression of miR-224-5p was increased, owing to silencing of LINC01094, and no significant alterations occurred in the levels of other miRNAs (Fig. 3A). Previous investigations justified the tumor repressor role of miR-224-5p in several malignancies (23). In addition, miR-224-5p level was weakly expressed in ccRCC cells compared to control cells (Fig. 3B). Thus, we chose miR-224-5p as the object of subsequent researches. An RT-qPCR assay showed that miR-224-5p was overexpressed in ACHN and 769-P cells using a miR-224-5p mimic (Fig. 3C). Then, a luciferase reporter experiment showed that ectopic miR-224-5p only impaired the luciferase activity of LINC01094-WT, which unraveled the interaction of miR-224-5p to LINC01094. Meanwhile, the schematic exhibited the main components of luciferase reporter assay (Fig. 3D). Concordantly, an RNA immunoprecipitation (RIP) experiment validated that miR-224-5p and LINC01094 were enriched by Ago2 antibody in contrast to IgG antibody (Fig. 3E). Chondroitin sulfate synthase 1 (CHSY1) was proven to work as an oncogene in colorectal cancer (26) and hepatocellular carcinoma (25), and our findings showed that the CHSY1 level in ccRCC cells was higher than in normal cells (Fig. 4A). By using the starBase database, we discovered that there were putative binding sites between CHSY1 and miR-224-5p (Fig. 4B). Hence, CHSY1 was selected for the in-depth study. A luciferase reporter experiment showed that only the CHSY1-WT luciferase activity was weakened by overexpression of miR-224-5p and that of CHSY1-Mut had no variation under miR-224-5p improvement. In addition, corresponding schematic explained the major constituents of this luciferase reporter assay (Fig. 4C). Likewise, RT-qPCR analysis and western blot confirmed that the CHSY1 mRNA and protein levels were diminished via upregulation of miR-224-5p (Fig. 4D and -andE).E).Finally, rescue assays were carried out to investigate the role of LINC01094, miR-224-5p, and CHSY1 in ccRCC progression. Overexpression of CHSY1 was certified through RT-qPCR and western blot assays after transfection in 769-P cells (Fig. 5A). The CCK-8 experiment and EdU incorporation assay demonstrated that the inhibiting influence on cell proliferation caused by LINC01094 depletion was abrogated by miR-224-5p silencing or CHSY1 overexpression (Fig. 5B and -andC).C). The transwell assay showed that cell migration hampered by LINC01094 suppression was recovered by miR-224-5p knockdown or CHSY1 augmentation (Fig. 5D). In addition, western blot showed that miR-224-5p inhibitor or upregulation of CHSY1 abolished the impact of LINC01094 silencing on the protein levels of E-cadherin, N-cadherin, Snail, fibronectin, MMP2, and MMP7 (Fig. 5E and -andF).F). These results suggested that LINC01094 executed its carcinogenic function in ccRCC through regulation of miR-224-5p/CHSY1.To further research the effects of LINC01094 on ccRCC progression, we constructed an animal model to show that knockdown of LINC01094 obstructed tumor growth and metastasis in vivo (Fig. 6). These data also demonstrated that LINC01094 promoted ccRCC tumor growth and metastasis both in vitro and in vivo.	31767633	RID07569	ceRNA or sponge	metastasis	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Oral squamous cell carcinoma	AC007271.3	CTNNB1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000226925	GRCh38_2:102172621-102182108	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA AC007271.3 promotes cell proliferation, invasion, migration and inhibits cell apoptosis of OSCC via the Wnt/beta-catenin signaling pathway.To further confirm the role of AC007271.3 in OSCC, we detected the AC007271.3 levels in OSCC and MNT tissues of 97 patients. Based on the average AC007271.3 expression level, we divided the 97 patients into two groups, 36 patients with low expression and 61 with high expression. The results of qPCR showed that the relative expression level of AC007271.3 was higher in OSCC tissues compared with the MNT (Fig. 1A).The effects of AC007271.3 on the migration and invasion of OSCC cells were evaluated by the wound-healing and Matrigel invasion assay. Results showed that AC007271.3 knockdown significantly decreased the migrating distance and had markedly weaker invading capacity as compared with negative controls (Fig. 2D-E), suggesting that AC007271.3 silencing attenuate the migration and invasion of OSCC cells. Flow cytometry showed that the rates of OSCC cell apoptosis were notably enhanced in si-AC007271.3 transfected cells and the percentage of prominent apoptotic cells was distinctly increased (Fig. 2F). In total, these results indicated that AC007271.3 induced proliferation, migration, invasion, and suppressed OSCC cell apoptosis in vitro.Accumulating evidences have confirmed that lncRNAs may functionin malignant tumors by cooperating with signaling transduction pathways. Wnt/beta-catenin pathway is closely related with cell proliferation,invasion, migration, apoptosis, and involved in the occurrence anddevelopment of OSCC [12,13], thus it was assessed whetherAC007271.3 could activate the Wnt/beta-catenin pathway in OSCC cells.The results showed that the activity of luciferase was increased by thetransfection of AC007271.3 overexpression vector compared with thecontrol group, while the activity of luciferase was decreased aftertransfecting with AC007271.3 interference vector (*P < .05,**P < .01) (Fig. 3B). The immunofluorescence assay demonstratedthat the position of beta-catenin protein moved from the nucleus to cytoplasm in cells and decreased in cytoplasm when AC007271.3 wassilenced, while it translocated from cytoplasm to nucleus whenAC007271.3 was over expressed (Fig. 3C). Results showed that theexpression level of total beta-catenin protein was increased compared withthe control group when AC007271.3 was overexpressed. Moreover, weextracted nuclear protein and cytoprotein respectively. We found thatthe trend of nucleus beta-catenin expression level was consistent with thatof total beta-catenin protein, while opposite results were observed in OSCCcells when AC007271.3 was silenced (Fig. 3D-E). The increased expression level of total and nuclear beta-catenin indicated that AC007271.3could regulate the translocation of beta-catenin and thus activate the Wnt/beta-catenin signaling pathway.To further confirm that AC007271.3 promoted carcinogenesis inOSCC via Wnt/beta-catenin pathway, rescued experiments was performed.SCC9 and SCC15 cells cotransfected with AC007271.3 lentiviral vectorswere constructed and treated with xav939 (Selleck Chemicals, China),an inhibitor of Wnt/beta-catenin signaling pathway at the concentration of50 uM. As shown in Fig. 4A-D, the capacity of cell proliferation, migration and invasion ascended by AC007271.3 overexpression was restored when treated with xav939. Our results showed that overexpression of AC007271.3 increased the expression of the core proteinbeta-catenin and its downstream target genes (CyclinD1, c-myc and Bcl-2)compared with the control group, while opposite results were observedin OSCC cells when silencing AC007271.3 (Fig. 3D). Nevertheless, theseresults were abolished when treated with xav939 (Fig. 4E). Thus, itindicated that AC007271.3 might promote OSCC proliferation, invasion, migration and suppress apoptosis via Wnt/beta-catenin signalingpathway.beta-Catenin and its downstream target genes including CyclinD1, cmyc and Bcl-2 play crucial roles in Wnt/beta-catenin pathway. Westernblot results showed up regulation of AC007271.3 promoted the expression of beta-catenin compared with the control group (Fig. 5D).Therefore, these data suggested that AC007271.3 could promote thetumorigenesis of OSCC in vitro and in vivo via the Wnt/beta-catenin signaling pathway.	31759044	RID07570	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Oral squamous cell carcinoma	IL1R1-AS1	Cyclin D1	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000226925	GRCh38_2:102172621-102182108	NA	NA	112577460	NA	AC007271.3	NA	LncRNA AC007271.3 promotes cell proliferation, invasion, migration and inhibits cell apoptosis of OSCC via the Wnt/beta-catenin signaling pathway.To further confirm the role of AC007271.3 in OSCC, we detected the AC007271.3 levels in OSCC and MNT tissues of 97 patients. Based on the average AC007271.3 expression level, we divided the 97 patients into two groups, 36 patients with low expression and 61 with high expression. The results of qPCR showed that the relative expression level of AC007271.3 was higher in OSCC tissues compared with the MNT (Fig. 1A).The effects of AC007271.3 on the migration and invasion of OSCC cells were evaluated by the wound-healing and Matrigel invasion assay. Results showed that AC007271.3 knockdown significantly decreased the migrating distance and had markedly weaker invading capacity as compared with negative controls (Fig. 2D-E), suggesting that AC007271.3 silencing attenuate the migration and invasion of OSCC cells. Flow cytometry showed that the rates of OSCC cell apoptosis were notably enhanced in si-AC007271.3 transfected cells and the percentage of prominent apoptotic cells was distinctly increased (Fig. 2F). In total, these results indicated that AC007271.3 induced proliferation, migration, invasion, and suppressed OSCC cell apoptosis in vitro.Accumulating evidences have confirmed that lncRNAs may functionin malignant tumors by cooperating with signaling transduction pathways. Wnt/beta-catenin pathway is closely related with cell proliferation,invasion, migration, apoptosis, and involved in the occurrence anddevelopment of OSCC [12,13], thus it was assessed whetherAC007271.3 could activate the Wnt/beta-catenin pathway in OSCC cells.The results showed that the activity of luciferase was increased by thetransfection of AC007271.3 overexpression vector compared with thecontrol group, while the activity of luciferase was decreased aftertransfecting with AC007271.3 interference vector (*P < .05,**P < .01) (Fig. 3B). The immunofluorescence assay demonstratedthat the position of beta-catenin protein moved from the nucleus to cytoplasm in cells and decreased in cytoplasm when AC007271.3 wassilenced, while it translocated from cytoplasm to nucleus whenAC007271.3 was over expressed (Fig. 3C). Results showed that theexpression level of total beta-catenin protein was increased compared withthe control group when AC007271.3 was overexpressed. Moreover, weextracted nuclear protein and cytoprotein respectively. We found thatthe trend of nucleus beta-catenin expression level was consistent with thatof total beta-catenin protein, while opposite results were observed in OSCCcells when AC007271.3 was silenced (Fig. 3D-E). The increased expression level of total and nuclear beta-catenin indicated that AC007271.3could regulate the translocation of beta-catenin and thus activate the Wnt/beta-catenin signaling pathway.To further confirm that AC007271.3 promoted carcinogenesis inOSCC via Wnt/beta-catenin pathway, rescued experiments was performed.SCC9 and SCC15 cells cotransfected with AC007271.3 lentiviral vectorswere constructed and treated with xav939 (Selleck Chemicals, China),an inhibitor of Wnt/beta-catenin signaling pathway at the concentration of50 uM. As shown in Fig. 4A-D, the capacity of cell proliferation, migration and invasion ascended by AC007271.3 overexpression was restored when treated with xav939. Our results showed that overexpression of AC007271.3 increased the expression of the core proteinbeta-catenin and its downstream target genes (CyclinD1, c-myc and Bcl-2)compared with the control group, while opposite results were observedin OSCC cells when silencing AC007271.3 (Fig. 3D). Nevertheless, theseresults were abolished when treated with xav939 (Fig. 4E). Thus, itindicated that AC007271.3 might promote OSCC proliferation, invasion, migration and suppress apoptosis via Wnt/beta-catenin signalingpathway.beta-Catenin and its downstream target genes including CyclinD1, cmyc and Bcl-2 play crucial roles in Wnt/beta-catenin pathway. Westernblot results showed up regulation of AC007271.3 promoted the expression of beta-catenin compared with the control group (Fig. 5D).Therefore, these data suggested that AC007271.3 could promote thetumorigenesis of OSCC in vitro and in vivo via the Wnt/beta-catenin signaling pathway.	31759044	RID07571	expression association	NA		
Oral squamous cell carcinoma	IL1R1-AS1	MYC	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000226925	GRCh38_2:102172621-102182108	ENSG00000136997	NA	112577460	4609	AC007271.3	bHLHe39|c-Myc|MYCC	LncRNA AC007271.3 promotes cell proliferation, invasion, migration and inhibits cell apoptosis of OSCC via the Wnt/beta-catenin signaling pathway.To further confirm the role of AC007271.3 in OSCC, we detected the AC007271.3 levels in OSCC and MNT tissues of 97 patients. Based on the average AC007271.3 expression level, we divided the 97 patients into two groups, 36 patients with low expression and 61 with high expression. The results of qPCR showed that the relative expression level of AC007271.3 was higher in OSCC tissues compared with the MNT (Fig. 1A).The effects of AC007271.3 on the migration and invasion of OSCC cells were evaluated by the wound-healing and Matrigel invasion assay. Results showed that AC007271.3 knockdown significantly decreased the migrating distance and had markedly weaker invading capacity as compared with negative controls (Fig. 2D-E), suggesting that AC007271.3 silencing attenuate the migration and invasion of OSCC cells. Flow cytometry showed that the rates of OSCC cell apoptosis were notably enhanced in si-AC007271.3 transfected cells and the percentage of prominent apoptotic cells was distinctly increased (Fig. 2F). In total, these results indicated that AC007271.3 induced proliferation, migration, invasion, and suppressed OSCC cell apoptosis in vitro.Accumulating evidences have confirmed that lncRNAs may functionin malignant tumors by cooperating with signaling transduction pathways. Wnt/beta-catenin pathway is closely related with cell proliferation,invasion, migration, apoptosis, and involved in the occurrence anddevelopment of OSCC [12,13], thus it was assessed whetherAC007271.3 could activate the Wnt/beta-catenin pathway in OSCC cells.The results showed that the activity of luciferase was increased by thetransfection of AC007271.3 overexpression vector compared with thecontrol group, while the activity of luciferase was decreased aftertransfecting with AC007271.3 interference vector (*P < .05,**P < .01) (Fig. 3B). The immunofluorescence assay demonstratedthat the position of beta-catenin protein moved from the nucleus to cytoplasm in cells and decreased in cytoplasm when AC007271.3 wassilenced, while it translocated from cytoplasm to nucleus whenAC007271.3 was over expressed (Fig. 3C). Results showed that theexpression level of total beta-catenin protein was increased compared withthe control group when AC007271.3 was overexpressed. Moreover, weextracted nuclear protein and cytoprotein respectively. We found thatthe trend of nucleus beta-catenin expression level was consistent with thatof total beta-catenin protein, while opposite results were observed in OSCCcells when AC007271.3 was silenced (Fig. 3D-E). The increased expression level of total and nuclear beta-catenin indicated that AC007271.3could regulate the translocation of beta-catenin and thus activate the Wnt/beta-catenin signaling pathway.To further confirm that AC007271.3 promoted carcinogenesis inOSCC via Wnt/beta-catenin pathway, rescued experiments was performed.SCC9 and SCC15 cells cotransfected with AC007271.3 lentiviral vectorswere constructed and treated with xav939 (Selleck Chemicals, China),an inhibitor of Wnt/beta-catenin signaling pathway at the concentration of50 uM. As shown in Fig. 4A-D, the capacity of cell proliferation, migration and invasion ascended by AC007271.3 overexpression was restored when treated with xav939. Our results showed that overexpression of AC007271.3 increased the expression of the core proteinbeta-catenin and its downstream target genes (CyclinD1, c-myc and Bcl-2)compared with the control group, while opposite results were observedin OSCC cells when silencing AC007271.3 (Fig. 3D). Nevertheless, theseresults were abolished when treated with xav939 (Fig. 4E). Thus, itindicated that AC007271.3 might promote OSCC proliferation, invasion, migration and suppress apoptosis via Wnt/beta-catenin signalingpathway.beta-Catenin and its downstream target genes including CyclinD1, cmyc and Bcl-2 play crucial roles in Wnt/beta-catenin pathway. Westernblot results showed up regulation of AC007271.3 promoted the expression of beta-catenin compared with the control group (Fig. 5D).Therefore, these data suggested that AC007271.3 could promote thetumorigenesis of OSCC in vitro and in vivo via the Wnt/beta-catenin signaling pathway.	31759044	RID07572	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Oral squamous cell carcinoma	IL1R1-AS1	BCL2	positively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000226925	GRCh38_2:102172621-102182108	ENSG00000171791	NA	112577460	596	AC007271.3	Bcl-2|PPP1R50	LncRNA AC007271.3 promotes cell proliferation, invasion, migration and inhibits cell apoptosis of OSCC via the Wnt/beta-catenin signaling pathway.To further confirm the role of AC007271.3 in OSCC, we detected the AC007271.3 levels in OSCC and MNT tissues of 97 patients. Based on the average AC007271.3 expression level, we divided the 97 patients into two groups, 36 patients with low expression and 61 with high expression. The results of qPCR showed that the relative expression level of AC007271.3 was higher in OSCC tissues compared with the MNT (Fig. 1A).The effects of AC007271.3 on the migration and invasion of OSCC cells were evaluated by the wound-healing and Matrigel invasion assay. Results showed that AC007271.3 knockdown significantly decreased the migrating distance and had markedly weaker invading capacity as compared with negative controls (Fig. 2D-E), suggesting that AC007271.3 silencing attenuate the migration and invasion of OSCC cells. Flow cytometry showed that the rates of OSCC cell apoptosis were notably enhanced in si-AC007271.3 transfected cells and the percentage of prominent apoptotic cells was distinctly increased (Fig. 2F). In total, these results indicated that AC007271.3 induced proliferation, migration, invasion, and suppressed OSCC cell apoptosis in vitro.Accumulating evidences have confirmed that lncRNAs may functionin malignant tumors by cooperating with signaling transduction pathways. Wnt/beta-catenin pathway is closely related with cell proliferation,invasion, migration, apoptosis, and involved in the occurrence anddevelopment of OSCC [12,13], thus it was assessed whetherAC007271.3 could activate the Wnt/beta-catenin pathway in OSCC cells.The results showed that the activity of luciferase was increased by thetransfection of AC007271.3 overexpression vector compared with thecontrol group, while the activity of luciferase was decreased aftertransfecting with AC007271.3 interference vector (*P < .05,**P < .01) (Fig. 3B). The immunofluorescence assay demonstratedthat the position of beta-catenin protein moved from the nucleus to cytoplasm in cells and decreased in cytoplasm when AC007271.3 wassilenced, while it translocated from cytoplasm to nucleus whenAC007271.3 was over expressed (Fig. 3C). Results showed that theexpression level of total beta-catenin protein was increased compared withthe control group when AC007271.3 was overexpressed. Moreover, weextracted nuclear protein and cytoprotein respectively. We found thatthe trend of nucleus beta-catenin expression level was consistent with thatof total beta-catenin protein, while opposite results were observed in OSCCcells when AC007271.3 was silenced (Fig. 3D-E). The increased expression level of total and nuclear beta-catenin indicated that AC007271.3could regulate the translocation of beta-catenin and thus activate the Wnt/beta-catenin signaling pathway.To further confirm that AC007271.3 promoted carcinogenesis inOSCC via Wnt/beta-catenin pathway, rescued experiments was performed.SCC9 and SCC15 cells cotransfected with AC007271.3 lentiviral vectorswere constructed and treated with xav939 (Selleck Chemicals, China),an inhibitor of Wnt/beta-catenin signaling pathway at the concentration of50 uM. As shown in Fig. 4A-D, the capacity of cell proliferation, migration and invasion ascended by AC007271.3 overexpression was restored when treated with xav939. Our results showed that overexpression of AC007271.3 increased the expression of the core proteinbeta-catenin and its downstream target genes (CyclinD1, c-myc and Bcl-2)compared with the control group, while opposite results were observedin OSCC cells when silencing AC007271.3 (Fig. 3D). Nevertheless, theseresults were abolished when treated with xav939 (Fig. 4E). Thus, itindicated that AC007271.3 might promote OSCC proliferation, invasion, migration and suppress apoptosis via Wnt/beta-catenin signalingpathway.beta-Catenin and its downstream target genes including CyclinD1, cmyc and Bcl-2 play crucial roles in Wnt/beta-catenin pathway. Westernblot results showed up regulation of AC007271.3 promoted the expression of beta-catenin compared with the control group (Fig. 5D).Therefore, these data suggested that AC007271.3 could promote thetumorigenesis of OSCC in vitro and in vivo via the Wnt/beta-catenin signaling pathway.	31759044	RID07573	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gallbladder cancer	LncRNA-HGBC	SET	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-502-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	NA	NA	ENSG00000119335	NA	NA	6418	NA	2PP2A|I2PP2A|IGAAD|IPP2A2|MRD58|PHAPII|TAF-I|TAF-IBETA	LncRNA-HGBC stabilized by HuR promotes gallbladder cancer progression by regulating miR-502-3p/SET/AKT axis. To further validate the increased level of lncRNA-HGBC in GBC, we examined lncRNA-HGBC expression in another set of 43 cases containing both cancer and adjacent non-tumor tissues, and found that lncRNA-HGBC level was significantly higher in GBC tissues than in benign tissues (P-=-0.0074; Fig. 1a). Next, to determine if lncRNA-HGBC expression level is related to GBC progression, we analyzed the association between lncRNA-HGBC levels and clinicopathological characteristics in those GBC patients. Using the median expression level of lncRNA-HGBC as a cutoff, 43 GBC patients were stratified into two groups with low and high lncRNA-HGBC expression. As shown in Table 1, statistical analyses showed that high lncRNA-HGBC level was positively correlated with TNM stage (P-=-0.0096) and lymph node metastasis (P-=-0.0191). Accordingly, Kaplan-Meier and log-rank tests indicated that high lncRNA-HGBC expression levels were significantly correlated with reduced overall survival (OS) (P-<-0.001, Fig. -Fig.1b),1b), implicating an active role in cancer metastasis.Given that the lncRNA-HGBC RNA level was positively related to the existence of lymph node metastasis, we reasonably postulate that lncRNA-HGBC augments GBC cell invasive behavior. To test the hypothesis, we exploited cell transwell migration and matrigel invasion assays, and found that knocking down endogenous lncRNA-HGBC by specific shRNAs dramatically reduced the cell migration and invasion by around 30'-0% of controls in NOZ and SGC-996 cells (Fig. 3a, b and Additional file 3: Figure S3A, B). Conversely, overexpression of lncRNA-HGBC in GBC-SD and EH-GB1 cells increased the migration and invasion by 20'-0% (Fig. -(Fig.3c,3c, d and Additional file 3: Figure S3C, D). It is well established that increased metastatic capability of GBC is intimately associated with tumor cell phenotypic transformation, an event termed epithelial-mesenchymal transition (EMT) [26]. To evaluate the possibility of EMT involved in the invasiveness of GBC, we monitored EMT-specific markers such as vimentin and N-cadherin. lncRNA-HGBC knockdown in NOZ and SGC-996 cells decreased expression of vimentin and N-cadherin (Fig. -(Fig.3e).3e).Emerging lines of evidence have reported that cytoplasm lncRNAs can function as competing endogenous RNAs (ceRNAs) by binding to and sequestering specific miRNAs that block target gene expression [19, 20]. Given that lncRNA-HGBC is mainly located in the cytoplasm, we hypothesized that lncRNA-HGBC may function as miRNA sponge to restore gene expression targeted by miRNA in GBC progression. In a set of miRNAs that are putatively bound to lncRNA-HGBC in the Segal Lab program (Eran Segal; http://132.77.150.113/pubs/mir07/mir07_prediction.html) [24] (Additional file 1: Table S6), we were particularly interested in six tumor suppressor-associated miRNAs including miR-1, miR-26a, miR-630, miR-122, miR-502-3p and miR-618. To obtain the bona fide lncRNA-miRNA interaction, we subcloned full-length lncRNA-HGBC into the pmirGLO dual luciferase reporter vector. Dual luciferase assay showed that miR-502-3p and miR-618 could suppress the luciferase activity of lncRNA-HGBC, but not other four miRNAs (Fig. 5a), indicating a possible interaction between lncRNA-HGBC and miR-502-3p or miR-618.Therefore, we were primarily focused on the interaction between lncRNA-HGBC and miR-502-3p. Once miR-502-3p binding motif of GGTGCAT between 1176 and 1183-nt of lncRNA-HGBC was deleted as mutant HGBC-MUT, luciferase activity was not suppressed, as compared with decreased activity in the presence of wild type of miR-502-3p binding motif (Fig. -(Fig.5b).5b). A large body of mechanistic studies focusing on the interaction between miRNA and targeted mRNA have established the notion that miRNAs bind to their mRNA targets and cause translational suppression and/or RNA degradation by forming a complex with Argonaute2 (AGO2) [34]. To test this action model, RNA immunoprecipitation (RIP) experiments were employed in NOZ cell extracts using an AGO2 antibody. As shown in Fig. -Fig.5c,5c, both lncRNA-HGBC and miR-502-3p were specifically enriched in AGO2 antibody-associated complex, but not in the control IgG, suggesting that miR-502-3p is a bona fide lncRNA-HGBC-targeting miRNA. To further identify whether lncRNA-HGBC directly binds to endogenous miR-502-3p, we performed MS2-RIP to pull-down endogenous miRNAs associated with lncRNA-HGBC (Fig. -(Fig.5d,5d, above). The results demonstrated that lncRNA-HGBC in NOZ cells was significantly associated with miR-502-3p, but not with irrelevant microRNA (miR-122). However, mutation of miR-502-3p binding site in lncRNA-HGBC abolished their association (Fig. -(Fig.5d,5d, below), supporting the direct interaction between lncRNA-HGBC and miR-502-3p.miR-502-3p is appreciated to target multiple protein-coding genes including SET [35] that plays an important role in the development of various carcinomas [36, 37]. More importantly, SET was also upregulated in GBC tissues in our previous microarray data [23] (data not shown, GEO accession number: GSE76633). To decipher the regulatory mechanisms of miR-502-3p on SET, we transfected a luciferase reporter vector harboring 3'-UTR of SET into 293-T cellsand luciferase activity was then evaluated in the transfection of miR-502-3p mimics. As compared to the control vector, miR-502-3p mimics significantly reduced the luciferase activity of the SET reporter vector (Additional file 3: Figure S6A). Furthermore, after overexpression or knockdown of miR-502-3p in GBC cells (Additional file 3: Figure S6B), the expression of SET was decreased by miR-502-3p or increased by anti-miR-502-3p, respectively, at both mRNA and protein levels (Additional file 3: Figure S6C, S6D). These data indicate that SET is a direct target of miR-502-3p.	31752906	RID07574	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	TP73-AS1	miR-141-3p	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	NA	57212	NA	KIAA0495|PDAM	NA	LncRNA TP73-AS1 interacted with miR-141-3p to promote the proliferation of non-small cell lung cancer.Initially the expression levels of TP73-AS1 in 55 paired samples (NSCLC specimens and corresponding adjacent non-tumour tissues) were examined using real-time PCR. Results indicated that TP73-AS1 expression was significantly unregulated in tumour tissues compared that of paired normal tissues (Figure 1 A). Then TP73-AS1 expressions in two human NSCLC cell lines A459 and SPC-A1 and immortalised normal human bronchial epithelial cell line (16HBE) as control were determined using real-time PCR. Results suggested that the levels of TP73-AS1 expression were also at higher levels in A459 and SPC-A1 cell lines, compared to the control group (Figure 1 B). These data provide potential evidence that TP73-AS1 was more expressed in NSCLC tissues and cell lines and may be related to poorer prognosis; however, the detailed mechanism underlying the action of TP73-AS1 on NSCLC remains unclear.Higher lncRNA TP73-AS1 levels in both NSCLC tissues and cell lines as compared to non-cancer controls suggested that lncRNA TP73-AS1 might play a key role in NSCLC tumourigenesis. To investigate the detailed functions of TP73-AS1 in NSCLC, we generated a series of functional assays. We designed lncRNATP73-AS1 siRNA1, which we transfected into A459 and SPC-A1 cells to achieve TP73-AS1 knockdown, as verified using real-time PCR assays (Figure 2 A). After TP73-AS1 was knocked down, the cell proliferation was monitored with use of BrdU. As shown in Figure 2 B, the proliferation of A459 and SPC-A1 cells was significantly down-regulated by TP73-AS1 knockdown compared to the si-NC (negative control) group.Recently, it has been reported that lncRNAs can act as miRNA sponges, reducing their regulatory effect on mRNAs. This function introduces an extra layer of layer of complexity in the miRNA-target interaction network. Dysfunction of non-coding RNAs, mainly lncRNAs and miRNAs, can affect processes, including cancer cell proliferation, apoptosis, invasion, and the metastatic process in cancer  complexity in the miRNA-target interaction network. Among well-established miRNAs in cancers, miR-141 plays an essential role in the regulation of cancer cell proliferation. Furthermore, we employed luciferase assays to confirm the miR-141 regulation of TP73-AS1. A wild-type and mutated TP73-AS1 (wt-TP73-AS1and mut-TP73-AS1 containing an 8 bp mutation in the predicted binding sites of miR-142) luciferase reporter gene vector was constructed (Figure 3 A). These indicated vectors were co-transfected into HEK293 cells with miR-142 mimics or miR-142 NC; the luciferase activity was then monitored. Results showed that the luciferase activity of wt-TP73-AS1 vector could be significantly suppressed by miR-141 mimics; after mutation in the predicted binding sites of miR-141 in TP73-AS1, the effect of miR-141 mimics or miR-141 NC on luciferase activity was abolished (Figure 3 B), indicating that TP73-AS1 could directly bind to miR-141. We revealed that TP73-AS1 might act as a competing endogenous RNA (ceRNA) to promote NSCLC cell proliferation by sponging miR-141. Finally, we evaluated the expression levels of TP73-AS1 and miR-142 in tumour tissues. As exhibited by real-time PCR assays, miR-141 expression was significantly down-regulated in NSCLC tissues (Figure 3 C).	31749884	RID07575	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Osteosarcoma	SPRY4-IT1	ZEB1	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	NA	NA	ENSG00000148516	NA	100642175	6935	SPRIGHTLY	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA SPRY4-IT1 promotes progression of osteosarcoma by regulating ZEB1 and ZEB2 expression through sponging of miR-101 activity.The expression of SPRY4-IT1 and miR-101 was detected in three OS cell lines, Saos-2, MG-63 and U2OS, as well as the normal osteoblast cell line hFOB 1.19. Compared with the hFOB 1.19 cells, SPRY4-IT1 was significantly upregulated in all three OS cell lines (Fig. 1A). In contrast, a reduction in miR-101 was observed in the three tumour cell lines (Fig. 1B), highlighting a potential functional interaction between SPRY4-IT1 and miR-101. To examine this potential interaction, SPRY4-IT1 was knocked down in MG-63 and U2OS cells. As shown in Fig. 1C, shSPRY4-IT1 transfection significantly decreased the expression of SPRY4-IT1 compared with the control and shNC groups. This was accompanied by a significant increase in miR-101 expression (Fig. 1D). However, SPRY4-IT1 expression were not altered in cells transfected with miR-101 (Fig. 1E and F). These results suggest a unidirectional crosstalk between SPRY4-IT1 and miR-101, such that SPRY4-IT1 may function as an upstream modulator of miR-101 in OS cells.shSPRY4-IT1 or miR-101 mimic transfection was used to study the molecular functions of SPRY4-IT1 and miR-101, respectively. MTT and colony formation assays were first performed to investigate the effects of SPRY4-IT1 and miR-101 on cell growth. When compared with the scrambled control group, knockdown of SPRY4-IT1 or overexpression of miR-101 significantly reduced the growth of both MG-63 and U2OS cells in a time-dependent manner (Fig. 2A). Consistent with these results, colony formation assays revealed that SPRY4-IT1 knockdown or miR-101 overexpression both significantly reduced the number of colonies in MG-63 and U2OS cells (Fig. 2B and C).Together, these results demonstrate that SPRY4-IT1 and miR-101 are involved in the growth of OS cells at least partially by modulating proliferation, apoptosis and cell cycle progression.Increased cell migration and invasion have been identified as features of cancer metastasis, which is one of the hallmarks of cancer (23). The oncogenic function of SPRY4-IT1 and tumour suppressor function of miR-101 on cell migration and invasion were further explored. After 24 h, SPRY4-IT1 downregulation or miR-101 induction significantly inhibited wound closure in both MG-63 and U2OS cells, suggesting that the migratory ability was reduced (Fig. 3A and B). A Transwell assay was also performed to evaluate the effect of SPRY4-IT1 and miR-101 on the migratory and invasive capacities of OS cells. shSPRY4-IT1 transfection significantly reduced the number of migrated or invaded MG-63 and U2OS cells (Fig. 3C-F). Similarly, overexpression of miR-101 also significantly reduced the migration or invasion of MG-63 and U2OS cells (Fig. 3C-F). Taken together, our results suggested that SPRY4-IT1 promoted cell migration and invasion, whereas miR-101 functioned as a negative regulator of these properties in OS cells.Previously, it was reported that miR-101 may regulate the expression of both ZEB1 and ZEB2, both of which have been demonstrated to serve important roles in invasion and metastasis of lung and ovarian carcinoma (20,24). Therefore, the effects of SPRY4-IT1 and miR-101 on regulation of ZEB1 and ZEB2 expression were determined. qPCR analysis showed that transfection of shSPRY4-IT1 or miR-101 mimics was sufficient to significantly reduce the mRNA expression levels of ZEB1 and ZEB2 in both MG-63 and U2OS cells (Fig. 4A-D). western blot also showed that SPRY4-IT1 knockdown and miR-101 overexpression significantly decreased the protein expression levels of ZEB1 and ZEB2 (Fig. 4E-H). These findings suggest that SPRY4-IT1 and miR-101 may modulate OS tumorigenesis by regulating the expression of ZEB1 and ZEB2.An increasing number of studies have revealed that lncRNAs may sponge miRNAs and thus disinhibit the target genes of these miRNAs (25). To investigate the possibility of a SPRY4-IT1/miR-101/ZEB axis, the functional interactions between SPRY4-IT1 and miR-101, as well as miR-101 and ZEBs, were explored. RNAInter identified a putative miR-101 binding sequence located in SPRY4-IT1 (Fig. 5A). Compared with the scrambled control, miR-101 mimics significantly reduced SPRY4-IT1-WT-mediated relative luciferase activity, whereas transfection with miR-101 inhibitor increased luciferase activity (Fig. 5B). Mutagenesis of the SPRY4-IT1 fragment (SPRY4-IT1-MUT) completely abolished the effects of the miR-101 mimics and inhibitor. These results suggest that SPRY4-IT1 may directly interact with miR-101 in OS cells.	31746422	RID07576	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	SPRY4-IT1	ZEB2	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	NA	NA	ENSG00000169554	NA	100642175	9839	SPRIGHTLY	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA SPRY4-IT1 promotes progression of osteosarcoma by regulating ZEB1 and ZEB2 expression through sponging of miR-101 activity.The expression of SPRY4-IT1 and miR-101 was detected in three OS cell lines, Saos-2, MG-63 and U2OS, as well as the normal osteoblast cell line hFOB 1.19. Compared with the hFOB 1.19 cells, SPRY4-IT1 was significantly upregulated in all three OS cell lines (Fig. 1A). In contrast, a reduction in miR-101 was observed in the three tumour cell lines (Fig. 1B), highlighting a potential functional interaction between SPRY4-IT1 and miR-101. To examine this potential interaction, SPRY4-IT1 was knocked down in MG-63 and U2OS cells. As shown in Fig. 1C, shSPRY4-IT1 transfection significantly decreased the expression of SPRY4-IT1 compared with the control and shNC groups. This was accompanied by a significant increase in miR-101 expression (Fig. 1D). However, SPRY4-IT1 expression were not altered in cells transfected with miR-101 (Fig. 1E and F). These results suggest a unidirectional crosstalk between SPRY4-IT1 and miR-101, such that SPRY4-IT1 may function as an upstream modulator of miR-101 in OS cells.shSPRY4-IT1 or miR-101 mimic transfection was used to study the molecular functions of SPRY4-IT1 and miR-101, respectively. MTT and colony formation assays were first performed to investigate the effects of SPRY4-IT1 and miR-101 on cell growth. When compared with the scrambled control group, knockdown of SPRY4-IT1 or overexpression of miR-101 significantly reduced the growth of both MG-63 and U2OS cells in a time-dependent manner (Fig. 2A). Consistent with these results, colony formation assays revealed that SPRY4-IT1 knockdown or miR-101 overexpression both significantly reduced the number of colonies in MG-63 and U2OS cells (Fig. 2B and C).Together, these results demonstrate that SPRY4-IT1 and miR-101 are involved in the growth of OS cells at least partially by modulating proliferation, apoptosis and cell cycle progression.Increased cell migration and invasion have been identified as features of cancer metastasis, which is one of the hallmarks of cancer (23). The oncogenic function of SPRY4-IT1 and tumour suppressor function of miR-101 on cell migration and invasion were further explored. After 24 h, SPRY4-IT1 downregulation or miR-101 induction significantly inhibited wound closure in both MG-63 and U2OS cells, suggesting that the migratory ability was reduced (Fig. 3A and B). A Transwell assay was also performed to evaluate the effect of SPRY4-IT1 and miR-101 on the migratory and invasive capacities of OS cells. shSPRY4-IT1 transfection significantly reduced the number of migrated or invaded MG-63 and U2OS cells (Fig. 3C-F). Similarly, overexpression of miR-101 also significantly reduced the migration or invasion of MG-63 and U2OS cells (Fig. 3C-F). Taken together, our results suggested that SPRY4-IT1 promoted cell migration and invasion, whereas miR-101 functioned as a negative regulator of these properties in OS cells.Previously, it was reported that miR-101 may regulate the expression of both ZEB1 and ZEB2, both of which have been demonstrated to serve important roles in invasion and metastasis of lung and ovarian carcinoma (20,24). Therefore, the effects of SPRY4-IT1 and miR-101 on regulation of ZEB1 and ZEB2 expression were determined. qPCR analysis showed that transfection of shSPRY4-IT1 or miR-101 mimics was sufficient to significantly reduce the mRNA expression levels of ZEB1 and ZEB2 in both MG-63 and U2OS cells (Fig. 4A-D). western blot also showed that SPRY4-IT1 knockdown and miR-101 overexpression significantly decreased the protein expression levels of ZEB1 and ZEB2 (Fig. 4E-H). These findings suggest that SPRY4-IT1 and miR-101 may modulate OS tumorigenesis by regulating the expression of ZEB1 and ZEB2.An increasing number of studies have revealed that lncRNAs may sponge miRNAs and thus disinhibit the target genes of these miRNAs (25). To investigate the possibility of a SPRY4-IT1/miR-101/ZEB axis, the functional interactions between SPRY4-IT1 and miR-101, as well as miR-101 and ZEBs, were explored. RNAInter identified a putative miR-101 binding sequence located in SPRY4-IT1 (Fig. 5A). Compared with the scrambled control, miR-101 mimics significantly reduced SPRY4-IT1-WT-mediated relative luciferase activity, whereas transfection with miR-101 inhibitor increased luciferase activity (Fig. 5B). Mutagenesis of the SPRY4-IT1 fragment (SPRY4-IT1-MUT) completely abolished the effects of the miR-101 mimics and inhibitor. These results suggest that SPRY4-IT1 may directly interact with miR-101 in OS cells.	31746422	RID07577	ceRNA or sponge	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Malignant glioma	HOXA11-AS	miR-125a	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Silencing of lncRNA HOXA11-AS inhibits cell migration, invasion, proliferation, and promotes apoptosis in human glioma cells via upregulating microRNA-125a: in vitro and in vivo studies.First of all, we measured the expression of lncRNA HOXA11-AS and miR-125a in glioma cells and tissues using qRT-PCR lncRNA HOXA11-AS expression was significantly up-regulated in U251 cells compared to the normal nerve cells (Figure 1A), while miR-125a expression significantly down-regulated (Figure 1B). In glioma tissues, we found that lncRNA HOXA11-AS expression was increased significantly (Figure 1C) and miR-125a expression was decreased significantly (Figure 1D) with WHO tumor grade increase.In the current study, U251 cells were divided into five group: control; si-control; si-HOXA11-AS, si-HOXA11-AS+miR-125a inhibitor NC, and si-HOXA11-AS+miR-125a inhibitor. 48 hours after transfection, wound heal assay and transwell assay were used to compare the migration and invasion ability of each group, MTT assay was used to compare the proliferation of cells in each group, and flow cytometry analysis was used to detect the apoptosis of each group. As we expected, lncRNA HOXA11-AS silencing inhibited U251 cell migration, invasion and proliferation, while promoted cell apoptosis (Figure 3A-D). Besides, inhibition of miR-125a expression at least partially eliminated the effects of lncRNA HOXA11-AS silencing on U251 cells. Taken together, lncRNA HOXA11-AS silencing inhibited human glioma cellular functions via improving the expression of miR-125a.We performed a bioinformatics analysis using Starbase 2.0 (http://starbase.sysu.edu.cn) to predict the relationship between lncRNA HOXA11-AS and miR-125a, and the results showed that lncRNA HOXA11-AS and miR-125a indeed contain complementary base pairs (Figure 6A). To further verity this observation, we performed dual-luciferase activity assay. miR-125a mimics significantly decreases the luciferase activity of U251 cells co-transfected with lncRNA HOXA11-AS-WT (Figure 6B), but this decrease did not show in lncRNA HOXA11-AS-MUT co-transfection group. Both results indicated that miR-125a directly bint to HOXA11-AS.We further validated the effect of lncRNA HOXA11-AS and miR-125a on glioma growth in vivo. Figure 7A showed the picture of the representative transplanted tumor mice. Figure 7B showed the representative pictures of tumors from each group of mice. As shown in Figure 7B and -and7C,7C, lncRNA HOXA11-AS silencing largely inhibited the tumor weight (Figure 7C) and tumor volume (Figure 7D), and this inhibition was rescued by the miR-125a inhibitor. Thus, both in vitro and in vivo assays indicated that lncRNA HOXA11-AS mediated the proliferation of human glioma cells via regulating miR-125a expression.	31737190	RID07578	ceRNA or sponge	NA		
Hepatocellular carcinoma	LINC00511	EYA1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000104313	NA	400619	2138	onco-lncRNA-12	BOR	LINC00511 as a ceRNA promotes cell malignant behaviors and correlates with prognosis of hepatocellular carcinoma patients by modulating miR-195/EYA1 axis.To observe the expression level of LINC00511 in HCC tissue samples, we harvested clinical samples data from TCGA dataset and found that LINC00511 expression was higher in HCC patients than that of in normal human (Fig. 1A, P-<-0.001). The analysis of GSE101728 validated the high-regulated expression pattern of LINC00511 in HCC (Fig. 1B, P-=-0.0023). In accordance with the median value of LINC00511 expression, the patients specimens were divided into two groups, high LINC00511 expression group (> median value) and low LINC00511 expression group (< median value). As seen in Fig. 1C, a remarkable association between the OS of HCC patients and the different expression level of LINC00511 was confirmed, which proposed a hypothesis that LINC00511 maybe a biomarker to predict prognosis of HCC patients (P-=-0.026). For further exploration of LINC00511  clinical significance, we examined the correlation between high/low LINC00511 expression and clinical pathological parameters using 424 patients with complete clinical data (Table 1, P-<-0.05). Notably, LINC00511 was closely associated with pathological stage of HCC patients (P-=-0.045). Moreover, the mRNA expression level of LINC00511 in HCC cell lines was also increased compared with L-02 cell line (Fig. 1D, P-<-0.01). On the basis of qRT-PCRanalysis, we selected HepG2 with highest LINC00511 expression and Huh7 with lowest LINC00511 expression as materials in subsequent experiments.Next, functional experiments in vitro were implemented to detect the biological role of LINC00511 in HCC cells. Before that, si-con/si-LINC00511#1/si-LINC00511#2 and pcDNA3.1/pcDNA3.1-LINC00511 were respectively transfected into HepG2 or Huh7 cells to knockdown or overexpress LINC00511. On one hand, in Fig. 2A and B, LINC00511 expression was significantly decreased in HepG2 cells (P-<-0.01). According to CCK-8 analysis and colony formation trials, we discovered that the reduction of LINC00511 inhibited the cell proliferation and colony formation in HepG2 cells (Fig. 2C , P-<-0.01). Furthermore, the invasive ability of HepG2 cells was suppressed after LINC00511 knockdown and mean number of invaded cells validated this point (Fig. 2G and H, P-<-0.01). On the other hand, as can be seen from Fig. 3A, LINC00511 expression was successfully high-regulated by pcDNA3.1-LINC00511 in Huh7 cells (P-<-0.01). CCK-8 and colony formation assays indicated that the proliferation and colony formation of Huh7 cells were significantly promoted by high-regulated LINC00511 compared with the blank control group (Fig. 3B and C, P-<-0.01). Besides, transwell assay disclosed the same tendency as results of CCK-8 and colony formation assays, which suggested that overexpression of LINC00511 facilitated cell invasion (Fig. 3D, P-<-0.01). To sum up, these interesting results illustrated that LINC00511 could contribute to the cell behaviors of HCC cells.It is now well established that long noncoding RNA connected with mRNA and transcriptional pseudogenes by competing the capability of microRNA binding [17]. The intersection of LncBase v2.0, starbase v2.0 and TCGA database showed that miR-195 was a downstream target of LINC00511 in HCC (Fig. 4A). Moreover, based on the prediction of bioinformatics analysis, we ensured that LINC00511 can target miR-195 and the EYA1 can be targeted by miR-195. As Fig. 4B and C shown, the sequences of putative binding sites between miR-195 and LINC00511 or EYA1 were exhibited. Luciferase activity was obviously decreased in cells co-transfected with WT-LINC00511 or WT-EYA1 and agomiR-195, while they remained unchanged after transfection with MUT-LINC00511 or MUT-EYA1 (Fig. 4B and C, P-<-0.01). Moreover, as validated through qRT-PCRexamination, miR-195 expression was enhanced/attenuated due to the transfection with si-LINC00511/pcDNA3.1-LINC00511 in HepG2 cell or Huh7 cell (Fig. 4D and E, P-<-0.01).To further explore whether miR-195 could affect the role of LINC00511 in cell bahaviors in HCC cells, rescue experiments in vitro were conducted. Down-regulation of miR-195 significantly promoted the proliferation, colony formation, and invasion of HepG2 cells (Fig. 6A, C and E, P-<-0.01), while high-regulation of miR-195 obviously inhibited the proliferation, colony formation, and invasion of Huh7 cells (Fig. 6B, D and F, P-<-0.01). Additionally, EYA1 facilitated cell aggressiveness to a large extent, which was consistent with the role of LINC00511. More interestingly, on the basis of LINC00511 knockdown, the intervention of antamiR-195 or up-regulated EYA1 restored cell behaviors to normal level vice versa. Therefore, we concluded that LINC00511/miR-195 pair regulates malignant aggressiveness of HCC cells via regulating EYA1.	31731191	RID07579	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Gastric cancer	HULC	MYH9	positively-E	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000100345	NA	728655	4627	HCCAT1|LINC00078|NCRNA00078	DFNA17|EPSTS|FTNS|MHA|NMHC-II-A|NMMHCA	LncRNA HULC promotes the progression of gastric cancer by regulating miR-9-5p/MYH9 axis.Firstly, qRT-PCRwas used to determine the expression levels of HULC and miR-9-5p in 116 pairs of GC tissues and adjacent non-cancer gastric tissues. These data revealed that HULC expression was significantly increased and miR-9-5p expression was highly decreased in GC tissues compared with normal control (Fig. 1A and B). More interestingly, miR-9-5p level was inversely correlated with HULC expression in GC tissues (Fig. 1C). Subsequently, we detected the expression levels of HULC and miR-9-5p in GC cells. In contrast to negative control, qRT-PCRassay showed a significant upregulation of HULC expression and a dramatical downregulation of miR-9-5p level in GC cells (Fig. 1D and E).Then, to understand the role of HULC in GC, we carried out a detailed analysis of its targeted miRNAs using the online software miRcode (http://www.mircode.org). Previous researches reported that miR-9-5p was downregulated in GC and it hampered GC cell proliferation, invasion and metastasis in vitro [12,13]. As expected, the predicted data revealed that HULC harbored a putative targeted sequence for miR-9-5p (Fig. 2A). To confirm this, we performed the dual-luciferase reporter assays with HULC wild-type reporter vector (HULC-Wt) harboring the targeted sequence for miR-9-5p and the mutation of seeded sequence (HULC-Mut). As shown in Fig. 2B, in contrast to negative control, transient introduction of miR-9-5p mimics resulted in a 4.8-fold increase of miR-9-5p expression in SGC-7901 cells, and a 3.8-fold increase in AGS cells. Subsequent luciferase assays revealed that the luciferase activity of HULC-Wt was decreased by 59% in SGC-7901 cells and 54% in AGS cells after miR-9-5p overexpression (Fig. 2C and D). However, the mutation of the targeted sequence evidently abolished the effect of miR-9-5p overexpression on reporter gene expression (Fig. 2C and D). Additionally, RNA pull-down assay was performed to verify the endogenous interaction between HULC and miR-9-5p in GC cells. qRT-PCRresults showed that HULC enrichment in Bio-miR-9-5p group was higher than that in Bio-miR-NC group in SGC-7901 and AGS cells (Fig. 2E). In parallel, in comparison to negative control, miR-9-5p enrichment was substantially increased by transfection of Bio-HULC (Fig. 2F). Nevertheless, these effects were significantly abolished by the mutation of seeded sequence in both SGC-7901 and AGS cells (Fig. 2E and F).Then, online software TargetScan (http://www.targetscan.org/vert_72/) was performed to search for the targets of miR-9-5p. The predicted data revealed that MYH9 contained a putative binding site for miR-9-5p in its 3'-UTR (Fig. 5A). To verify whether MYH9 was a target of miR-9-5p, we performed the luciferase reporter assays by MYH9 3'-UTR reporter vector (MYH9-Wt) containing the putative miR-9-5p-binding site or the mutation of seeded sequence (MYH9-Mut). These results revealed that cotransfection of MYH9-Wt and miR-9-5p mimics into SGC-7901 and AGS cells induced lower luciferase activity than in cells cotransfected with miR-NC mimics (Fig. 5B and C). However, site-directed mutation of miR-9-5p-binding sequence significantly abrogated the effect of miR-9-5p on luciferase gene expression (Fig. 5B and C). Subsequently, we observed whether miR-9-5p regulated MYH9 expression in GC cells. In contrast to negative control, transient introduction of miR-9-5p mimics strikingly suppressed the expression levels of MYH9 mRNA and protein in SGC-7901 and AGS cells (Fig. 5D-F). Moreover, transwell assay and western blot results showed that miR-9-5p overexpression resulted in a repression in cell migration, invasion, and an increase in E-cadherin expression, as well as a decrease in N-cadherin, Vimentin, Snail, Slug and MMP-9 levels in SGC-7901 cells (Supplement Fig. 1A-C). Conversely, highly expressed MYH strikingly enhanced cell migration, invasion and EMT (Supplement Fig. 1A-C). Besides, miR-9-5p-mediated anti-migration, anti-invasion and anti-EMT effects were prominently abolished by cotransfection of Vector-MYH9 in SGC-7901 cells (Supplement Fig. 1A-C). All these data suggested that MYH9 was a functional target of miR-9-5p in GC cells.	31726371	RID07580	ceRNA or sponge	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	DLEU1	miR-4429	negatively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	SP1-DLEU1-miR-4429 feedback loop promotes cell proliferative and anti-apoptotic abilities in human glioblastoma.herefore, sh-DLEU1#1 and sh-DLEU1#3 were utilized to conduct subsequent functional assays. CCK-8 assay revealed that cell viability in U251 (P<0.01) and LN229 cells (P<0.01) was obviously inhibited following DLEU1 depletion (Figure 1D). The number of EdU-positive cells showed that DLEU1 knockdown repressed cell proliferative ability of U251 (P<0.05) and LN229 cells (P<0.05) (Figure 1E). As validated previously, activation of caspase-3 predicted cell apoptosis promotion. Therefore, we conducted caspase-3 activity assay to examine GBM cell apoptosis following DLEU1 depletion. As shown in Figure 1F, caspase-3 activity was enhanced via the transfection with sh-DLEU1#1 and sh-DLEU1#3 plasmids in U251 (P<0.01) and LN229 cells (P<0.01), indicating that declined DLEU1 expression induced more GBM cell apoptosis. It was well elucidated that the apoptotic process of cells was under the modulation of Bcl-2/Bax family protein [28,29]. Therefore, we assessed the apoptosis-related protein levels (Bcl-2, Bax) by western blot. We observed that the level of pro-apoptotic protein Bax was notably increased responding to DLEU1 knockdown in U251 and LN229 cells, whereas the level of anti-apoptotic protein Bcl-2 was distinctly decreased after silencing DLEU1 expression in in U251 and LN229 cells (Figure 1G). Overall, our findings pointed that DLEU1 as a positive regulator of GBM cell growth and negative regulator of cell apoptosis.qRT-PCRanalysis showed that SP1 overexpression promoted DLEU1 expression in U251 and LN229 cells (P<0.01; Figure 2D). Hence, the expression level of DLEU1 was positively related to SP1 expression. Mechanically, as illustrated in Figure 2E, only three binding sites of SP1 in DLEU1 promoter region were predicted by JASPAR. The putative binding sites 1 (-29 to -39 bp: CCTCGGCCCCA) and sites 2 (-137 to -127 bp: GGCTCTCCCTT) were included in fragment P1 (0 to -400 bp). The fragment P2 (-300 to -700 bp) contained the potential binding sites 3 (-484 to -475 bp: GGAGCTGGGA). ChIP assay demonstrated that the fragment P2 was responsible for the binding of SP1 to the DLEU1 promoter region in U251 and LN229 cells (P<0.001; Figure 2F). Luciferase reporter assay suggested that the relative luciferase activity of binding sites 3 wild-type (SITE 3-WT) was enhanced upon pcDNA-SP1 transfection in U251 and LN229 cells (P<0.01), but when the binding sites 3 was mutated, the promotion of luciferase activity disappeared (SITE 3-MUT) (Figure 2G). Taken together, DLEU1 was transcriptionally up-regulated by SP1.Influenced by the ceRNA notion, we further explored whether the DLEU1-mediated ceRNA mechanism was involved in the GBM development. Owing to the fact that cytoplasmic lncRNA could function as ceRNA, subcellular fractionation assay was implemented to unveil DLEU1 localization. It indicated that DLEU1 expression was more abundant in cytoplasmic fraction than that in nuclear fraction of GBM cells (Figure 3A), supporting that DLEU1 could affect gene expression post-transcriptionally. Afterward, we found six putative miRNAs (miR-6509-3p, miR-4429, miR-320a, miR-320b, miR-320c and miR-320d) which could be targeted by DLEU1 in Starbase dataset. qRT-PCRsuggested that only miR-4429 expression was obviously strengthened following DLEU1 depletion in U251 cells (P<0.01; Figure 3B). Additionally, it was presented that miR-4429 was lowly expressed in GBM cells (P<0.05) (Figure 3C). Based on the predicted binding sites between DLEU1 and miR-4429 acquired from Starbase (Figure 3D), luciferase reporter assay was performed and disclosed that miR-4429 mimics significantly reduced the luciferase activity of DLEU1-WT in U251 and LN229 (P<0.05) cells, rather than that of DLEU1-MUT (Figure 3E). To confirm that DLEU1 and miR-4429 were associated with the RNA-induced silencing complex (RISC), of which the key component was Ago2, therefore, RIP assay was carried out using specific antibodies against Ago2 and IgG proteins. Result from RIP assay exhibited that Ago2 complex were enriched with DLEU1 and miR-4429 in in U251 and LN229 cells (P<0.01; Figure 3F). Collectively, DLEU1 interacted with miR-4429 by acting as its sponge.Considering that SP1 was up-regulated and related positively to DLEU1 expression in GBM, we intended to probe whether SP1 acted as a target gene of miR-4429, forming a DLEU1/miR-4429/SP1 ceRNA mechanism. As expected, we found the potential binding sites of miR-4429 in SP1 3'UTR using TargetScan (Figure 4A). Luciferase reporter assay revealed that luciferase activity of SP1-WT was weakened in response to miR-4429 mimics, no distinct alteration was found in luciferase reporter of SP1-MUT in U251 and LN229 cells (P<0.05; Figure 4B). Using biotinylated miR-4429 probes in RNA pull-down assay, we observed that SP1 mRNA was greatly pulled down by bio-miR-4429-wt in U251 and LN229 cells (P<0.01), further confirming the interaction between miR-4429 and SP1 (Figure 4C). More importantly, the mRNA level and protein level of SP1 were decreased by miR-4429 mimics, but restored by pcDNA-DLEU1 in U251 and LN229 cells (P<0.05, P<0.01; Figure 4D,E). These data indicated that DLEU1 sponged miR-4429 to promote SP1 expression.We designed and carried out rescue assays in U251 cell line to evaluate the impact of SP1 LEU1-siR-4429 axis on GBM cell proliferation and apoptosis. CCK-8 assay suggested that GBM cell viability was significantly reduced through sh-DLEU1#3 transfection (P<0.01), but pcDNA-SP1 (P<0.05) or miR-4429 inhibitor (P<0.05) countervailed the reduction (Figure 5A). EdU assay proved that DLEU1 deficiency-induced proliferation decline (P<0.01) could be reversed by pcDNA-SP1 (P<0.05) or miR-4429 inhibitor (P<0.05) (Figure 5B). The decrease in GBM cell apoptosis induced by DLEU1 knockdown (P<0.01) was abolished through overexpressing SP1 (P<0.05) or down-regulating miR-4429 (P<0.05) (Figure 5C). In addition, Bax protein level strengthened by silencing DLEU1 was abrogated after enhancing SP1 or lessening miR-4429 expression. The opposite effect was observed in Bcl-2 protein level. Bcl-2 reduction caused by sh-DLEU1#3 could be counteracted via either SP1 overexpression or miR-4429 suppression (Figure 5D). Furthermore, we also detected the impacts of miR-4429 inhibitor or pcDNA-SP1 alone on GBM cell growth. CCK-8 assay suggested that miR-4429 inhibitor or pcDNA-SP1 alone could promote cell viability and decreased the activity of caspase-3 (Supplementary Figure S1A ). Above results demonstrated that DLEU1 functioned as a positive regulator of GBM growth via miR-4429/SP1.	31713587	RID07581	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Hepatocellular carcinoma	H19	MAPK1	positively-E	overexpression	upregulation	RT-PCR	NA	NA	cell invasion(+);prognosis;epithelial to mesenchymal transition(+);cell stemness(+)	ceRNA(miR-193b)	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000100030	NA	283120	5594	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	Macrophages-induced long noncoding RNA H19 up-regulation triggers and activates the miR-193b/MAPK1 axis and promotes cell aggressiveness in hepatocellular carcinoma.The expression level of H19 in 2 HCC cell lines were analyzed. We found that Hep-G2 cells 20 expressed relatively higher H19 level than Hep 3B2.1-7 cells (Figure S7).Furthermore, compared with pHBLV cells, the 6 transcription of EMT-related biomarkers changed dramatically, as E-cadherin decreased while both 7 N-cadherin and beta-catenin increased significantly in pHBLV-H19 Hep-G2 cells (Figure 2C-a). The 8 transcription of stemness genes, including Lin28, Sox2, Notch1, NANOG, and OCT-4, were 9 up-regulated in pHBL V-H19cells (Figure 2D-a). Consistent results were obtained in Hep 3B2.1-7 cells, 10 in which H19-overexpressing Hep 3B2.1-7 cells were more aggressive than the wide type ones, and 11 H19 up-regulation induced EMT and enhanced stemness genes transcription in Hep 3B2.1-7 cells 12 (Figure S2).To further investigate if the H19/miR-193b/MAPK1 regulatory axis participated in the 19 aggressiveness of HCC cells, we blocked the MAPK signaling pathway using either p38 inhibitor 20 SB203580 (SB), JNK inhibitor SP600125 (SP) or ERK inhibitor PD98059 (PD) in pHBLV-H19 cells. 21 After blocking the MAPK signaling pathway, less Hep-G2 cells migrated across the Matrigel layer compared with untreated (SB-treated: 72.33   6.74 vs. 190.30   11.14, P  -0.001; SP-treated: 128.70 1   9.26 vs. 190.30   11.14, P = 0.013; PD-treated: 100.70   2.90 vs. 190.30   11.14, P = 0.002, Figure 2 4D-a,b). Simultaneously, the transcription level of E-cadherin increased whereas the transcription 3 levels of N-cadherin, beta-catenin, snail and slug decreased (Figure 4D-c). Furthermore, the mRNA levels 4 of stemness related genes, such as Lin28, Notch1 and SOX2 decreased significantly (Figure 4D-d). 5 These results implied that LncRNA H19 overexpression dramatically accelerated the aggressiveness of 6 HCC cells via acting as a sponge to hijack miR-193b and reduce its inhibitory efficacy on MAPK1 7 gene.	31705929	RID07582	ceRNA or sponge	prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	PVT1	ERG	positively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	interact with protein	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000157554	NA	5820	2078	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	erg-3|p55	Long non-coding RNA PVT1 encapsulated in bone marrow mesenchymal stem cell-derived exosomes promotes osteosarcoma growth and metastasis by stabilizing ERG and sponging miR-183-5p.Ubiquitination plays a critical role in promoting protein degradation. Since the previous study has reported that the degradation and ubiquitination of ERG could be promoted by SPOP, an E3 ubiquitin ligase [18, 19], we further explored whether PVT1 regulates ubiquitination of ERG. The RNA pull-down assay confirmed the binding of SPOP and ERG proteins with PVT1 (Figure 2C), and the RIP assay revealed the existence of PVT1 in ERG-RNA binding complex (Figure 2D). These data suggested the direct interaction between PVT1 and ERG protein. We then overexpressed PVT1 in three osteosarcoma cell lines, and immunoblotted Ub-ERG using ubiquitination assay. The result indicated that overexpressing PVT1 markedly reduced ubiquitin-modified ERG protein (Figure 2E). The ubiquitination assay was also performed in PVT1-interfering osteosarcoma cells after being co-cultured with BMSC-EXO, and the result demonstrated that PVT1 in exosomes inhibited ubiquitination of ERG protein in osteosarcoma cells (Figure 2F).As reported, lncRNAs can act as competing endogenous RNAs (ceRNAs) to promote protein expressing by sponging microRNAs [20]. The online database (http://www.targetscan.org/) predicted the potential binding between PVT1 and miR-183-5p (Figure 3A). The luciferase reporter assay showed that the co-transfection with miR-183-5p mimic and pGL3-PVT1-wt vector significantly lowered the luciferase activity, while the co-transfection with miR-183-5p mimic and pGL3-PVT1-mut vector did not affect the luciferase activity (Figure 3B). Meanwhile, the interference of PVT1 in osteosarcoma cells dramatically increased miR-183-5p expression (Figure 3C). These data indicated that miR-183-5p was negatively regulated by PVT1. The online database also predicted the interaction between miR-183-5p and ERG 3'-UTR. The luciferase assay showed that the miR-183-5p mimic reduced the activity of ERG 3'-UTR and the protein expression of ERG (Figure 3D), suggesting that miR-183-5p promoted the down-regulation of ERG by targeting the 3'-UTR of ERG mRNA. Meanwhile, the co-transfection of si-PVT1 and miR-183-5p inhibitor restored the ERG protein expression which was reduced by interfering PVT1 in three osteosarcoma cell lines (Figure 3E).To elucidate the effect of PVT1/ERG on tumor growth in vivo, the mouse xenograft and pulmonary metastatic model were established. Compared with the control group, the BMSC-EXO injection markedly increased tumor growth, while the injection of BMSC-EXOsi-PVT1 negated such response (Figure 5A). The expression of PVT1 and ERG in tumor tissues was enhanced by BMSC-EXO injection, while it was reduced by BMSC-EXOsi-PVT1 injection (Figure 5B). In the pulmonary metastatic model, the number of lung metastatic nodules was dramatically increased after BMSC-EXO injection in comparison to the control group, while it was negated by BMSC-EXOsi-PVT1 injection (Figure 5C). Taken together, these data indicated that PVT1 in BMSC-EXO promotes osteosarcoma growth and metastasis via increasing ERG.	31699956	RID07583	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Osteosarcoma	PVT1	ERG	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	ceRNA(miR-183-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000157554	NA	5820	2078	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	erg-3|p55	Long non-coding RNA PVT1 encapsulated in bone marrow mesenchymal stem cell-derived exosomes promotes osteosarcoma growth and metastasis by stabilizing ERG and sponging miR-183-5p.Ubiquitination plays a critical role in promoting protein degradation. Since the previous study has reported that the degradation and ubiquitination of ERG could be promoted by SPOP, an E3 ubiquitin ligase [18, 19], we further explored whether PVT1 regulates ubiquitination of ERG. The RNA pull-down assay confirmed the binding of SPOP and ERG proteins with PVT1 (Figure 2C), and the RIP assay revealed the existence of PVT1 in ERG-RNA binding complex (Figure 2D). These data suggested the direct interaction between PVT1 and ERG protein. We then overexpressed PVT1 in three osteosarcoma cell lines, and immunoblotted Ub-ERG using ubiquitination assay. The result indicated that overexpressing PVT1 markedly reduced ubiquitin-modified ERG protein (Figure 2E). The ubiquitination assay was also performed in PVT1-interfering osteosarcoma cells after being co-cultured with BMSC-EXO, and the result demonstrated that PVT1 in exosomes inhibited ubiquitination of ERG protein in osteosarcoma cells (Figure 2F).As reported, lncRNAs can act as competing endogenous RNAs (ceRNAs) to promote protein expressing by sponging microRNAs [20]. The online database (http://www.targetscan.org/) predicted the potential binding between PVT1 and miR-183-5p (Figure 3A). The luciferase reporter assay showed that the co-transfection with miR-183-5p mimic and pGL3-PVT1-wt vector significantly lowered the luciferase activity, while the co-transfection with miR-183-5p mimic and pGL3-PVT1-mut vector did not affect the luciferase activity (Figure 3B). Meanwhile, the interference of PVT1 in osteosarcoma cells dramatically increased miR-183-5p expression (Figure 3C). These data indicated that miR-183-5p was negatively regulated by PVT1. The online database also predicted the interaction between miR-183-5p and ERG 3'-UTR. The luciferase assay showed that the miR-183-5p mimic reduced the activity of ERG 3'-UTR and the protein expression of ERG (Figure 3D), suggesting that miR-183-5p promoted the down-regulation of ERG by targeting the 3'-UTR of ERG mRNA. Meanwhile, the co-transfection of si-PVT1 and miR-183-5p inhibitor restored the ERG protein expression which was reduced by interfering PVT1 in three osteosarcoma cell lines (Figure 3E).To elucidate the effect of PVT1/ERG on tumor growth in vivo, the mouse xenograft and pulmonary metastatic model were established. Compared with the control group, the BMSC-EXO injection markedly increased tumor growth, while the injection of BMSC-EXOsi-PVT1 negated such response (Figure 5A). The expression of PVT1 and ERG in tumor tissues was enhanced by BMSC-EXO injection, while it was reduced by BMSC-EXOsi-PVT1 injection (Figure 5B). In the pulmonary metastatic model, the number of lung metastatic nodules was dramatically increased after BMSC-EXO injection in comparison to the control group, while it was negated by BMSC-EXOsi-PVT1 injection (Figure 5C). Taken together, these data indicated that PVT1 in BMSC-EXO promotes osteosarcoma growth and metastasis via increasing ERG.	31699956	RID07584	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colon cancer	ZEB2-AS1	CTNNB1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000168036	NA	100303491	1499	ZEB2-AS|ZEB2AS|ZEB2NAT	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Effect and mechanism of long non-coding RNA ZEB2-AS1 in the occurrence and development of colon cancer.To understand the role of ZEB2-AS1 in CC, we analyzed its expression pattern. We examined the expression levels of ZEB2-AS1 mRNA in 20 pairs of tumor tissues and adjacent normal tissues by RT-qPCR and found that the expression of ZEB2-AS1 was significantly upregulated in tumor tissues (p < 0.05) (Figure 1A). We then located ZEB2-AS1 expression using in-situ RNA hybridization and found that ZEB2-AS1 was expressed mainly in CC cell nucleus (Figure 1B).Compared with normal colonic epithelial cell CCD 841 CoN, ZEB2-AS1 expression was significantly upregulated in CC cell lines, such as HCT8, SW480 and HCT116 cells (Figure 2, p < 0.05), especially in HCT8 cells (p < 0.01), which was used in subsequent experiments.To determine the mechanism of ZEB2-AS1 regulating CC cells, we constructed ZEB2-AS1 overexpression plasmid by cloning the full length of ZEB2-AS1 into a PCDNA3 vector. We first confirmed that ZEB2-AS1 was overexpressed in HCT8 cells (Figure 3A). Then we compared changes in cell proliferation, apoptosis and migration of cell strains in overexpressed ZEB2-AS1 with those in control group. The cell growth curve detected by CCK-8 showed that the overexpression of ZEB2-AS1 in HCT8 cells promoted the cell growth (Figure 3B). Meanwhile, the results of flow cytometry showed that overexpression of ZEB2-AS1 resulted in significantly decreased apoptosis rate (p < 0.05) (Figure 3C). In addition, enhanced ZEB2-AS1 expression promoted the migration of HCT8 cells, as shown in the results of Transwell assay (Figure 3D). In conclusion, ZEB2-AS1 overexpression promotes proliferation and migration of CC cells.In order to explore the mechanism of ZEB2-AS1 regulating CC cells, we analyzed the expression of beta-catenin protein, c-myc and Cyclin D1 when ZEB2-AS1 was overexpressed or silenced in CC cell HCT8. Then we found that the expressions of all these three kinds of proteins were significantly decreased in HCT8 cell in the si-ZEB2-AS1 group (p < 0.05) (Figure 5), which indicated that ZEB2-AS1 could prevent degradation of beta-catenin proteins in CC cell samples, activate the transcription of downstream target genes (c-myc, CyclinD1) and promote cell proliferation. The results showed that ZEB2-AS1 could promote proliferation and migration of cancer cells by activating Wnt/beta-catenin signaling pathway.	31698657	RID07585	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colon cancer	TUG1	MMP14	negatively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000157227	NA	55000	4323	FLJ20618|LINC00080|NCRNA00080	MT1-MMP	Taurine up-regulated 1 accelerates tumorigenesis of colon cancer by regulating miR-26a-5p/MMP14/p38 MAPK/Hsp27 axis in vitro and in vivo.We firstly detected the levels of TUG1 and miR-26a-5p in three colon cancer cell lines 231 (SW620 ,HT-29 and CaCo-2) and normal human colon fibroblast (CCD-18Co) by RT-qPCR. 232 As shown in Figure 1A, TUG1 level in SW620 ,HT-29, CaCo-2 was significantly increased 233 and miR-26a-5p level was significantly decreased compared to CCD-18Co (Figure 1B).As shown in Figure 2B, the mRNA level of miR-26a-5p was 243 markedly increased in the sh-TUG1 group (Figure 2B). However, opverexpression of TUG1 244 significantly decreased miR-26a-5p level (Figure 2C). dual-luciferase reporter assay showed 245 that luciferase activity was significantly reduced in SW620 cells co-transfected with TUG wt 246 and miR-26a-5p mimic, whereas no significant changes were detected in SW620 cells transfected with TUG wt alone or TUG mut or/and miR-26a-5p mimic (Figure 2D). In short, 248 these results indicated that miR-26a-5p was a target of TUG1 in SW620 cells.The target relationship between miR-26a-5p and MMP-14 3'UTR (wt and mut) was 254 predicted by Targetscan7.0 (http://www.targetscan.org) (Figure 3A). The expression level of 255 MMP-14 was monitored by western blot. As shown in Figure 3B, the level of MMP-14 in the 256 sh-TUG1 group was noticeably decreased, indicating that TUG1 and MMP-14 had a positive 257 regulatory relationship. BrdU staining was applied to investigate the proliferative ability, 258 while transwell assay was utilized to determine the invasive capacity. As shown in Figure 3C, 259 BrdU-positive cells in the sh-TUG1 group were significantly less than the control group. 260 Meanwhile, transwell assay showed that the number of invading cells in the sh-TUG1 group 261 was also significantly reduced. Notably, the miR-26a-3p inhibitor reversed the inhibitory 262 effects of sh-TUG1 on cell proliferation and invasion (Figure 3D). Taken together, our results 263 indicated that TUG1 promoted proliferation and invasion of SW620 cells by regulating 264 miR-26a-5p/MMP-14 axis.western blot and immunofluorescent assay were applied to investigate the EMT 268 process of SW620 cells. As shown in Figure 4A, the downregulation of TUG1 significantly 269 inhibited the expression of mesenchymal marker proteins (Vimentin and N-cadherin) in 270 SW620 cells and promoted the expression of epithelial marker protein (E-cadherin). Contrary 271 results were observed in the miR-26a inhibitor group. In addition, immunofluorescent assay 272 showed that sh-TUG1 significantly reduced the number of Vimentin + punctum per cell. 273 However, this effect was counteracted by miR-22-3p inhibitor (Figure 4B). Therefore, the 274 present study suggested that TUG1 accelerated the EMT process in SW620 cells.	31697952	RID07586	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Colon cancer	TUG1	VEGFA	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Taurine up-regulated 1 accelerates tumorigenesis of colon cancer by regulating miR-26a-5p/MMP14/p38 MAPK/Hsp27 axis in vitro and in vivo.We firstly detected the levels of TUG1 and miR-26a-5p in three colon cancer cell lines 231 (SW620 ,HT-29 and CaCo-2) and normal human colon fibroblast (CCD-18Co) by RT-qPCR. 232 As shown in Figure 1A, TUG1 level in SW620 ,HT-29, CaCo-2 was significantly increased 233 and miR-26a-5p level was significantly decreased compared to CCD-18Co (Figure 1B).As shown in Figure 2B, the mRNA level of miR-26a-5p was 243 markedly increased in the sh-TUG1 group (Figure 2B). However, opverexpression of TUG1 244 significantly decreased miR-26a-5p level (Figure 2C). dual-luciferase reporter assay showed 245 that luciferase activity was significantly reduced in SW620 cells co-transfected with TUG wt 246 and miR-26a-5p mimic, whereas no significant changes were detected in SW620 cells transfected with TUG wt alone or TUG mut or/and miR-26a-5p mimic (Figure 2D). In short, 248 these results indicated that miR-26a-5p was a target of TUG1 in SW620 cells.The target relationship between miR-26a-5p and MMP-14 3'UTR (wt and mut) was 254 predicted by Targetscan7.0 (http://www.targetscan.org) (Figure 3A). The expression level of 255 MMP-14 was monitored by western blot. As shown in Figure 3B, the level of MMP-14 in the 256 sh-TUG1 group was noticeably decreased, indicating that TUG1 and MMP-14 had a positive 257 regulatory relationship. BrdU staining was applied to investigate the proliferative ability, 258 while transwell assay was utilized to determine the invasive capacity. As shown in Figure 3C, 259 BrdU-positive cells in the sh-TUG1 group were significantly less than the control group. 260 Meanwhile, transwell assay showed that the number of invading cells in the sh-TUG1 group 261 was also significantly reduced. Notably, the miR-26a-3p inhibitor reversed the inhibitory 262 effects of sh-TUG1 on cell proliferation and invasion (Figure 3D). Taken together, our results 263 indicated that TUG1 promoted proliferation and invasion of SW620 cells by regulating 264 miR-26a-5p/MMP-14 axis.western blot and immunofluorescent assay were applied to investigate the EMT 268 process of SW620 cells. As shown in Figure 4A, the downregulation of TUG1 significantly 269 inhibited the expression of mesenchymal marker proteins (Vimentin and N-cadherin) in 270 SW620 cells and promoted the expression of epithelial marker protein (E-cadherin). Contrary 271 results were observed in the miR-26a inhibitor group. In addition, immunofluorescent assay 272 showed that sh-TUG1 significantly reduced the number of Vimentin + punctum per cell. 273 However, this effect was counteracted by miR-22-3p inhibitor (Figure 4B). Therefore, the 274 present study suggested that TUG1 accelerated the EMT process in SW620 cells.	31697952	RID07587	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Colon cancer	TUG1	p38	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000100591	NA	55000	NA	FLJ20618|LINC00080|NCRNA00080	NA	Taurine up-regulated 1 accelerates tumorigenesis of colon cancer by regulating miR-26a-5p/MMP14/p38 MAPK/Hsp27 axis in vitro and in vivo.We firstly detected the levels of TUG1 and miR-26a-5p in three colon cancer cell lines 231 (SW620 ,HT-29 and CaCo-2) and normal human colon fibroblast (CCD-18Co) by RT-qPCR. 232 As shown in Figure 1A, TUG1 level in SW620 ,HT-29, CaCo-2 was significantly increased 233 and miR-26a-5p level was significantly decreased compared to CCD-18Co (Figure 1B).As shown in Figure 2B, the mRNA level of miR-26a-5p was 243 markedly increased in the sh-TUG1 group (Figure 2B). However, opverexpression of TUG1 244 significantly decreased miR-26a-5p level (Figure 2C). dual-luciferase reporter assay showed 245 that luciferase activity was significantly reduced in SW620 cells co-transfected with TUG wt 246 and miR-26a-5p mimic, whereas no significant changes were detected in SW620 cells transfected with TUG wt alone or TUG mut or/and miR-26a-5p mimic (Figure 2D). In short, 248 these results indicated that miR-26a-5p was a target of TUG1 in SW620 cells.The target relationship between miR-26a-5p and MMP-14 3'UTR (wt and mut) was 254 predicted by Targetscan7.0 (http://www.targetscan.org) (Figure 3A). The expression level of 255 MMP-14 was monitored by western blot. As shown in Figure 3B, the level of MMP-14 in the 256 sh-TUG1 group was noticeably decreased, indicating that TUG1 and MMP-14 had a positive 257 regulatory relationship. BrdU staining was applied to investigate the proliferative ability, 258 while transwell assay was utilized to determine the invasive capacity. As shown in Figure 3C, 259 BrdU-positive cells in the sh-TUG1 group were significantly less than the control group. 260 Meanwhile, transwell assay showed that the number of invading cells in the sh-TUG1 group 261 was also significantly reduced. Notably, the miR-26a-3p inhibitor reversed the inhibitory 262 effects of sh-TUG1 on cell proliferation and invasion (Figure 3D). Taken together, our results 263 indicated that TUG1 promoted proliferation and invasion of SW620 cells by regulating 264 miR-26a-5p/MMP-14 axis.western blot and immunofluorescent assay were applied to investigate the EMT 268 process of SW620 cells. As shown in Figure 4A, the downregulation of TUG1 significantly 269 inhibited the expression of mesenchymal marker proteins (Vimentin and N-cadherin) in 270 SW620 cells and promoted the expression of epithelial marker protein (E-cadherin). Contrary 271 results were observed in the miR-26a inhibitor group. In addition, immunofluorescent assay 272 showed that sh-TUG1 significantly reduced the number of Vimentin + punctum per cell. 273 However, this effect was counteracted by miR-22-3p inhibitor (Figure 4B). Therefore, the 274 present study suggested that TUG1 accelerated the EMT process in SW620 cells.	31697952	RID07588	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Colon cancer	TUG1	HSPB1	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106211	NA	55000	3315	FLJ20618|LINC00080|NCRNA00080	CMT2F|Hs.76067|Hsp25|HSP27|HSP28	Taurine up-regulated 1 accelerates tumorigenesis of colon cancer by regulating miR-26a-5p/MMP14/p38 MAPK/Hsp27 axis in vitro and in vivo.We firstly detected the levels of TUG1 and miR-26a-5p in three colon cancer cell lines 231 (SW620 ,HT-29 and CaCo-2) and normal human colon fibroblast (CCD-18Co) by RT-qPCR. 232 As shown in Figure 1A, TUG1 level in SW620 ,HT-29, CaCo-2 was significantly increased 233 and miR-26a-5p level was significantly decreased compared to CCD-18Co (Figure 1B).As shown in Figure 2B, the mRNA level of miR-26a-5p was 243 markedly increased in the sh-TUG1 group (Figure 2B). However, opverexpression of TUG1 244 significantly decreased miR-26a-5p level (Figure 2C). dual-luciferase reporter assay showed 245 that luciferase activity was significantly reduced in SW620 cells co-transfected with TUG wt 246 and miR-26a-5p mimic, whereas no significant changes were detected in SW620 cells transfected with TUG wt alone or TUG mut or/and miR-26a-5p mimic (Figure 2D). In short, 248 these results indicated that miR-26a-5p was a target of TUG1 in SW620 cells.The target relationship between miR-26a-5p and MMP-14 3'UTR (wt and mut) was 254 predicted by Targetscan7.0 (http://www.targetscan.org) (Figure 3A). The expression level of 255 MMP-14 was monitored by western blot. As shown in Figure 3B, the level of MMP-14 in the 256 sh-TUG1 group was noticeably decreased, indicating that TUG1 and MMP-14 had a positive 257 regulatory relationship. BrdU staining was applied to investigate the proliferative ability, 258 while transwell assay was utilized to determine the invasive capacity. As shown in Figure 3C, 259 BrdU-positive cells in the sh-TUG1 group were significantly less than the control group. 260 Meanwhile, transwell assay showed that the number of invading cells in the sh-TUG1 group 261 was also significantly reduced. Notably, the miR-26a-3p inhibitor reversed the inhibitory 262 effects of sh-TUG1 on cell proliferation and invasion (Figure 3D). Taken together, our results 263 indicated that TUG1 promoted proliferation and invasion of SW620 cells by regulating 264 miR-26a-5p/MMP-14 axis.western blot and immunofluorescent assay were applied to investigate the EMT 268 process of SW620 cells. As shown in Figure 4A, the downregulation of TUG1 significantly 269 inhibited the expression of mesenchymal marker proteins (Vimentin and N-cadherin) in 270 SW620 cells and promoted the expression of epithelial marker protein (E-cadherin). Contrary 271 results were observed in the miR-26a inhibitor group. In addition, immunofluorescent assay 272 showed that sh-TUG1 significantly reduced the number of Vimentin + punctum per cell. 273 However, this effect was counteracted by miR-22-3p inhibitor (Figure 4B). Therefore, the 274 present study suggested that TUG1 accelerated the EMT process in SW620 cells.	31697952	RID07589	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Nasopharynx carcinoma	CASC15	miR-101-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell growth(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	Long non-coding RNA CASC15 promotes nasopharyngeal carcinoma cell proliferation and metastasis by downregulating miR-101-3p.RT-qPCR was first conducted to detect CASC15 expression in 54 patients'-tissues and 4 NPC cell lines. The results demonstrated that CASC15 was significantly up-regulated in tumor tissues than that of the adjacent normal tissues (Figure 1A). Compared with NP69 cells, CASC15 expression was markedly higher in NPC cells (Figure 1B).In our study, CNE1 cell line was chosen for knockdown of CASC15 in vitro. RT-qPCR was utilized to detect CASC15 expression (Figure 2A). CCK-8 assay showed that the growth ability of CNE1 cells was significantly repressed after CASC15 knockdown (Figure 2B). Scratch wound assay showed that the migrated length of CNE1 cells decreased markedly after CASC15 was knocked down (Figure 2C). Furthermore, transwell assay showed that the number of invaded cells was significantly reduced after knock-down of CASC15 (Figure 2D).The Luciferase reporter gene assay revealed that co-transfection of CASC15-WT and miR-101-3p remarkably decreased Luciferase activity. However, no significant differences were observed in the Luciferase activity after co-transfection of CASC15-MUT and miR101-3p (Figure 3C). In addition, the results of the linear correlation analysis showed that the expression of miR-101-3p was negatively correlated with CASC15 expression in NPC tissues (Figure 3D).The ability of CASC15 in tumor formation and metastasis was detected in vivo. The results indicated that tumor size in the sh-CASC15 group was significantly smaller when compared with negative control shRNA group (Figure 4A). The weight of dissected tumors in sh-CASC15 group was remarkably smaller than that of negative control shRNA group (Figure 4B). Meanwhile, the number of metastatic nodules in lung tissues of the sh-CASC15 group was significantly reduced when compared with the negative control shRNA group (Figure 4C). Subsequently, the expression levels of CASC15 and miR-101-3p in dissected tumor tissues were detected by RT-qPCR. The results showed that CASC15 was lowly expressed in the sh-CASC15 group compared with the negative control shRNA group (Figure 4D). Howev er, miR-101-3p was highly expressed in the shCASC15 group when compared with the negative control shRNA group (Figure 4E).	31696476	RID07590	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Gastric cancer	AOC4P	MAPK3	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000102882	NA	90586	5595	UPAT	ERK1|p44erk1|p44mapk|PRKM3	LncRNA AOC4P affects biological behavior of gastric cancer cells through MAPK signaling pathway.To explore the expression level of lncRNA AOC4P in gastric cancer, the expression of lncRNA AOC4P in gastric cancer tissues and adjacent normal tissues was detected by RT-PCR As shown in Figure 1A, the expression level of lncRNA AOC4P was observed to be elevated in tumor tissues compared to normal tissues. Figure 3A, 3B showed that downregulated lncRNA AOC4P can inhibit the proliferation of gastric cancer cells to some extent. Figure 3C, 3D showed that downregulated lncRNA AOC4P can promote the apoptosis of gastric cancer cells to some extent. At the same time, as shown in Figure 3E, the cell migration ability of the lncRNA AOC4P-siRNA group was inhibited to some extent compared with the NC group.The effect of lncRNA AOC4P on the expression of MAPK pathway protein in gastric cancer cells was detected by western blot. The results of the experiment showed that after transfection of lncRNA AOC4P-siRNA, the expression levels of ERK1, JNK and p38 proteins were significantly lower than those in the NC group (Figure 4A, 4B). It was shown that inhibition of lncRNA AOC4P can affect the expression of downstream ERK1, JNK and p38 protein levels to regulate the function of the corresponding MAPK signaling pathway.	31696472	RID07591	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	AOC4P	MAPK8	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000107643	NA	90586	5599	UPAT	JNK|JNK1|PRKM8|SAPK1	LncRNA AOC4P affects biological behavior of gastric cancer cells through MAPK signaling pathway.To explore the expression level of lncRNA AOC4P in gastric cancer, the expression of lncRNA AOC4P in gastric cancer tissues and adjacent normal tissues was detected by RT-PCR As shown in Figure 1A, the expression level of lncRNA AOC4P was observed to be elevated in tumor tissues compared to normal tissues. Figure 3A, 3B showed that downregulated lncRNA AOC4P can inhibit the proliferation of gastric cancer cells to some extent. Figure 3C, 3D showed that downregulated lncRNA AOC4P can promote the apoptosis of gastric cancer cells to some extent. At the same time, as shown in Figure 3E, the cell migration ability of the lncRNA AOC4P-siRNA group was inhibited to some extent compared with the NC group.The effect of lncRNA AOC4P on the expression of MAPK pathway protein in gastric cancer cells was detected by western blot. The results of the experiment showed that after transfection of lncRNA AOC4P-siRNA, the expression levels of ERK1, JNK and p38 proteins were significantly lower than those in the NC group (Figure 4A, 4B). It was shown that inhibition of lncRNA AOC4P can affect the expression of downstream ERK1, JNK and p38 protein levels to regulate the function of the corresponding MAPK signaling pathway.	31696472	RID07592	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	AOC4P	p38	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000100591	NA	90586	NA	UPAT	NA	LncRNA AOC4P affects biological behavior of gastric cancer cells through MAPK signaling pathway.To explore the expression level of lncRNA AOC4P in gastric cancer, the expression of lncRNA AOC4P in gastric cancer tissues and adjacent normal tissues was detected by RT-PCR As shown in Figure 1A, the expression level of lncRNA AOC4P was observed to be elevated in tumor tissues compared to normal tissues. Figure 3A, 3B showed that downregulated lncRNA AOC4P can inhibit the proliferation of gastric cancer cells to some extent. Figure 3C, 3D showed that downregulated lncRNA AOC4P can promote the apoptosis of gastric cancer cells to some extent. At the same time, as shown in Figure 3E, the cell migration ability of the lncRNA AOC4P-siRNA group was inhibited to some extent compared with the NC group.The effect of lncRNA AOC4P on the expression of MAPK pathway protein in gastric cancer cells was detected by western blot. The results of the experiment showed that after transfection of lncRNA AOC4P-siRNA, the expression levels of ERK1, JNK and p38 proteins were significantly lower than those in the NC group (Figure 4A, 4B). It was shown that inhibition of lncRNA AOC4P can affect the expression of downstream ERK1, JNK and p38 protein levels to regulate the function of the corresponding MAPK signaling pathway.	31696472	RID07593	expression association	NA		
Breast cancer	FBXL19-AS1	FOXM1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(+)	ceRNA(miR-876-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000260852	GRCh38_16:30919319-30923269	ENSG00000111206	NA	283932	2305	MGC125469|MGC125470|MGC125472|NCRNA00095	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	FBXL19-AS1 promotes cell proliferation and inhibits cell apoptosis via miR-876-5p/FOXM1 axis in breast cancer.To evaluate the impact of FBXL19-AS1 on breast cancer tumor growth, FBXL19-AS1 levels were measured in both breast cancer cells (MCF-7, BT-549, MDA-MB-231, and SKBR3) and in non-tumorigenic epithelial cells (MCF-10A). The qRT-PCRresults demonstrated that FBXL19-AS1 expression was dramatically elevated in tumor cells, particularly in SKBR3 and MDA-MB-231 cells (Fig. 1A). Following this, shFBXL19-AS1#1/2/3 was transfected into SKBR3 and MDA-MB-231 cells. Higher transfection efficiency was found in shFBXL19-AS1#1/2 transfection than in shFBXL19-AS1#3 transfection (Fig. 1B). In shFBXL19-AS1#1/2-transfected cells, cell viability was inhibited compared with that of shNC-transfected cells (Fig. 1C). EdU assay also confirmed that cell proliferation was significantly inhibited by transfection with shFBXL19-AS1#2 (Fig. 1D). Caspase-3 activity assay showed that silencing of FBXL19-AS1 overtly stimulated cell apoptosis (Fig. 1E). In addition, the depletion of FBXL19-AS1 increased protein levels of cleaved caspase-3 and cleaved PARP, but not the level of total caspase-3 or total PARP in the two breast cancer cells (Supplementary Fig. S1A). These results suggested that FBXL19-AS1 inhibition suppressed cell proliferation but induced cell apoptosis in breast cancer cells.Then, miR-876-5p was overexpressed in MDA-MB-231 and SKBR3 cells (Fig. 2D) for the luciferase reporter assay. Luciferase reporter assay results showed that only the luciferase activity of FBXL19-AS1-WT was decreased by miR-876-5p mimics (Fig. 2E). In the RIP assay, both FBXL19-AS1 and miR-876-5p were enriched in the mixture, which was immunoprecipitated by the anti-Ago2 antibody (Fig. 2F). These two assays confirmed the binding between FBXL19-AS1 and miR-876-5p. qRT-PCRresults demonstrated that miR-876-5p expression was significantly increased when FBXL19-AS1 was silenced (Fig. 2G). Collectively, these data demonstrated that FBXL19-AS1 interacted with miR-876-5p.Based on the above data, the entire regulation mechanism underlying FBXL19-AS1 was further explored. The interplay between miR-876-5p and FOXM1 was sought by scanning starBase. The predicted and mutated binding sites are presented in Fig. 3A. The expression of FOXM1 was markedly high in cancer cells, consistent with the trend of FBXL19-AS1 (Fig. 3B). Additionally, miR-876-5p mimics reduced the luciferase reporter activity of FOXM1-WT, while the abundance of miR-876-5p and FOXM1 was observed in the Ago2 group, as examined by luciferase report and RIP experiments (Fig. 3C,D). Furthermore, FOXM1 expression was decreased by introducing miR-876-5p mimics into cells (Fig. 3E). Finally, to evaluate the influence of FBXL19-AS1 and miR-876-5p on FOXM1, cells were co-transfected with the shNC-+-NC inhibitor, shFBXL19-AS1#2-+-NC inhibitor, or shFBXL19-AS1#2-+-miR-876-5p inhibitor. It was found that miR-876-5p expression was significantly decreased after transfection with miR-876-5p inhibitor (Fig. 3F). qRT-PCRresults suggested that FOXM1 levels were reduced by shFBXL19-AS1#2, but partially recovered by miR-876-5p inhibitor (Fig. 3G). These data suggested that FBXL19-AS1 modulated FOXM1 via sponging miR-876-5p.Rescue experiments were carried out in SKBR3 cells to validate the FBXL19-AS1/miR-876-5p/FOXM1 pathway in breast cancer. In order to prepare for the rescue assays, FOXM1 was upregulated by introducing pcDNA3.1-FOXM1 into the SKBR3 cells (Fig. 4A). CCK-8 and EdU assays showed that the inhibitory effect of dFBXL19-AS1 silencing on cell proliferation was reversed by transfection with either miR-876-5p inhibitor or pcDNA3.1-FOXM1 (Fig. 4B,C). Moreover, the low caspase-3 activity in FBXL19-AS1-downregulated SKBR3 cell was increased by the inhibition of miR-876-5p as well as by overexpression of FOXM1 (Fig. 4D). These data indicated that both miR-876-5p and FOXM1 were involved in FBXL19-AS1-mediated cell growth. We also explored whether miR-876-5p/FOXM1 plays a role in regulating the growth of breast cancer cells. As expected, upregulation of miR-876-5p impaired cell proliferation but induced cell apoptosis, although these tendencies were recovered after the introduction of pcDNA3.1-FOXM1 (Fig. 4E and Supplementary Fig. S1B; see online supplementary material for a color version of this figure). These data suggested that FBXL19-AS1 modulated breast cancer tumor growth via sponging miR-876-5p to upregulate FOXM1.	31696201	RID07594	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Ovarian cancer	LINC00504	MIR1244-1	negatively-F	dual-luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000248360	GRCh38_4:14470465-14888169	ENSG00000284378	NA	201853	100302285	NA	MIR1244|MIRN1244|hsa-mir-1244|hsa-mir-1244-1	Long non-coding RNA LINC00504 regulates the Warburg effect in ovarian cancer through inhibition of miR-1244.The expression levels of LINC00504 in 45 paired OC tissues and matched adjacent noncancerous normal tissues were determined by qRT-PCR We found that 33 out of 45 samples showed significant upregulation of the levels of LINC00504 in OC tissues compared with that in normal tissues (Fig. 1a).To experimentally validate this finding, we constructed two luciferase reporter plasmids containing the widetype (WT) or mutated (Mut) binding site of LINC00504. Overexpression of miR-1244 significantly decreased the wild-type LINC00504 luciferase activity, whereas the mutant LINC00504 reporter luciferase activity was not affected in OVCAR-3 and SKOV-3 cell lines (Fig. 4b, c).To further verify our hypothesis, SKOV-3 cells were co-transfected with Vector + miR-NC, LINC00504(overexpression) OE + miR-NC, or LINC00504-OE + miR1244. Forced expression of LINC00504 evidently reduced miR-1244 expression, and this inhibition effect can be rescued by overexpression of miR-1244 in SKOV-3 (Fig. 6a). We found that upregulation of LINC00504 promoted SKOV-3 cell proliferation (Fig. 6b), colony formation (Fig. 6c), potential survival ability (Fig. 6d) and glucose consumption, lactate, and ATP production (Fig. 6g-h) as well as decreased O2 consumption (Fig. 6i). LINC00504 overexpression also led to upregulation of both mRNA and protein levels of PKM2, HK2, and PDK1 in and SKOV-3 cell lines (Fig. 6j, k). Importantly, LINC00504-mediated promotion effects on SKOV-3 cell growth and metabolism can be abolished via restored expression of miR-1244.	31691157	RID07595	ceRNA or sponge	NA	DOWN(LIHC);UP(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)	UP(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	LINC00504	PKM	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000248360	GRCh38_4:14470465-14888169	ENSG00000067225	NA	201853	5315	NA	OIP3|PK3|PKM2|THBP1	Long non-coding RNA LINC00504 regulates the Warburg effect in ovarian cancer through inhibition of miR-1244.The expression levels of LINC00504 in 45 paired OC tissues and matched adjacent noncancerous normal tissues were determined by qRT-PCR We found that 33 out of 45 samples showed significant upregulation of the levels of LINC00504 in OC tissues compared with that in normal tissues (Fig. 1a).To experimentally validate this finding, we constructed two luciferase reporter plasmids containing the widetype (WT) or mutated (Mut) binding site of LINC00504. Overexpression of miR-1244 significantly decreased the wild-type LINC00504 luciferase activity, whereas the mutant LINC00504 reporter luciferase activity was not affected in OVCAR-3 and SKOV-3 cell lines (Fig. 4b, c).To further verify our hypothesis, SKOV-3 cells were co-transfected with Vector + miR-NC, LINC00504(overexpression) OE + miR-NC, or LINC00504-OE + miR1244. Forced expression of LINC00504 evidently reduced miR-1244 expression, and this inhibition effect can be rescued by overexpression of miR-1244 in SKOV-3 (Fig. 6a). We found that upregulation of LINC00504 promoted SKOV-3 cell proliferation (Fig. 6b), colony formation (Fig. 6c), potential survival ability (Fig. 6d) and glucose consumption, lactate, and ATP production (Fig. 6g-h) as well as decreased O2 consumption (Fig. 6i). LINC00504 overexpression also led to upregulation of both mRNA and protein levels of PKM2, HK2, and PDK1 in and SKOV-3 cell lines (Fig. 6j, k). Importantly, LINC00504-mediated promotion effects on SKOV-3 cell growth and metabolism can be abolished via restored expression of miR-1244.	31691157	RID07596	expression association	NA	DOWN(LIHC);UP(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)	UP(NSCLC);DOWN(PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842)
Ovarian cancer	LINC00504	HK2	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000248360	GRCh38_4:14470465-14888169	ENSG00000159399	NA	201853	3099	NA	NA	Long non-coding RNA LINC00504 regulates the Warburg effect in ovarian cancer through inhibition of miR-1244.The expression levels of LINC00504 in 45 paired OC tissues and matched adjacent noncancerous normal tissues were determined by qRT-PCR We found that 33 out of 45 samples showed significant upregulation of the levels of LINC00504 in OC tissues compared with that in normal tissues (Fig. 1a).To experimentally validate this finding, we constructed two luciferase reporter plasmids containing the widetype (WT) or mutated (Mut) binding site of LINC00504. Overexpression of miR-1244 significantly decreased the wild-type LINC00504 luciferase activity, whereas the mutant LINC00504 reporter luciferase activity was not affected in OVCAR-3 and SKOV-3 cell lines (Fig. 4b, c).To further verify our hypothesis, SKOV-3 cells were co-transfected with Vector + miR-NC, LINC00504(overexpression) OE + miR-NC, or LINC00504-OE + miR1244. Forced expression of LINC00504 evidently reduced miR-1244 expression, and this inhibition effect can be rescued by overexpression of miR-1244 in SKOV-3 (Fig. 6a). We found that upregulation of LINC00504 promoted SKOV-3 cell proliferation (Fig. 6b), colony formation (Fig. 6c), potential survival ability (Fig. 6d) and glucose consumption, lactate, and ATP production (Fig. 6g-h) as well as decreased O2 consumption (Fig. 6i). LINC00504 overexpression also led to upregulation of both mRNA and protein levels of PKM2, HK2, and PDK1 in and SKOV-3 cell lines (Fig. 6j, k). Importantly, LINC00504-mediated promotion effects on SKOV-3 cell growth and metabolism can be abolished via restored expression of miR-1244.	31691157	RID07597	expression association	NA	DOWN(LIHC);UP(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Ovarian cancer	LINC00504	PDK1	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000248360	GRCh38_4:14470465-14888169	ENSG00000152256	NA	201853	5163	NA	NA	Long non-coding RNA LINC00504 regulates the Warburg effect in ovarian cancer through inhibition of miR-1244.The expression levels of LINC00504 in 45 paired OC tissues and matched adjacent noncancerous normal tissues were determined by qRT-PCR We found that 33 out of 45 samples showed significant upregulation of the levels of LINC00504 in OC tissues compared with that in normal tissues (Fig. 1a).To experimentally validate this finding, we constructed two luciferase reporter plasmids containing the widetype (WT) or mutated (Mut) binding site of LINC00504. Overexpression of miR-1244 significantly decreased the wild-type LINC00504 luciferase activity, whereas the mutant LINC00504 reporter luciferase activity was not affected in OVCAR-3 and SKOV-3 cell lines (Fig. 4b, c).To further verify our hypothesis, SKOV-3 cells were co-transfected with Vector + miR-NC, LINC00504(overexpression) OE + miR-NC, or LINC00504-OE + miR1244. Forced expression of LINC00504 evidently reduced miR-1244 expression, and this inhibition effect can be rescued by overexpression of miR-1244 in SKOV-3 (Fig. 6a). We found that upregulation of LINC00504 promoted SKOV-3 cell proliferation (Fig. 6b), colony formation (Fig. 6c), potential survival ability (Fig. 6d) and glucose consumption, lactate, and ATP production (Fig. 6g-h) as well as decreased O2 consumption (Fig. 6i). LINC00504 overexpression also led to upregulation of both mRNA and protein levels of PKM2, HK2, and PDK1 in and SKOV-3 cell lines (Fig. 6j, k). Importantly, LINC00504-mediated promotion effects on SKOV-3 cell growth and metabolism can be abolished via restored expression of miR-1244.	31691157	RID07598	expression association	NA	DOWN(LIHC);UP(PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Osteosarcoma	PCAT6	TGFBR1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000106799	NA	100506696	7046	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	LncRNA PCAT6 promotes tumor progression in osteosarcoma via activation of TGF-beta pathway by sponging miR-185-5p.To investigate the clinical importance of PCAT6 in OS, we determined the expression pattern of PCAT6 in OS tissues and their adjacent normal tissues (ANTs). qRT-PCRassays indicated that PCAT6 level was upregulated in OS tissues compared with ANT (Fig. 1a). Interestingly, the upregulation of PCAT6 was positively correlated with metastasis status and advanced stage of OS (Fig. 1bed andTable 1). Further analysis indicated that PCAT6 level was upregulated in OS cell lines (Fig. 1e). Survival analysis demonstrated that the upregulation of PCAT6 contributed to shorter overall survival and progression-free survival (Fig. 1f and g). Collectively, PCAT6 expression was increased in OS tissues and cell lines and correlated with poor prognosis in OS patients.To further determine the biological role of PCAT6 in OS, we silenced PCAT6 in U2OS and 143B cells (Fig. 2a). EdU, CCK8 and colony formation assays demonstrated that silencing PCAT6 inhibited proliferation of U2OS and 143B cells (Fig. 2bee). In order to investigate the impact of PCAT6 on metastasis of OS cells, transwell assay was performed. The results indicated that silencing PCAT6 significantly reduced the migrated and invaded OS cells (Fig. 2f). Taken together, PCAT6 enhances OS cell proliferation, migration, and invasion.The interaction between miR-185-5p and PCAT6 was examined by luciferase reporter assay and the results demonstrated that miR-185-5p decreased PCAT6-wt reporter  luciferase activity, but didn't have significant effect on PCAT6-mut reporter  luciferase activity (Fig. 3f and g). RIP assays indicated that miR-185-5p increased the enrichment of PCAT6 on Ago2 protein (Fig. 3h). Above results indicated that PCAT6 could act as a miR185-5p sponge. Functionally, miR-185-5p reversed the proproliferation and -metastasis effect of PCAT6 on OS cells (Fig. 3il). Collectively, PCAT6 promotes osteosarcoma progression via sponging miR-185-5p.Previous studies have reported that lncRNAs and miRNAs exert their functions by activating cancer-related pathways [8,18,19]. Therefore, Signal Finder 10 Pathway Reporter Arrays were utilized to investigate signaling pathways that were responsible for PCAT6 and miR-185-3p regulation. As shown inFig. 4a, the activity of TGFbpathway was significantly reduced by knockdown of PCAT6 and miR-185-5p mimics. Subsequently, western blot assays showed that silencing PCAT6 and miR-185-5p mimics decreased the protein expression of p-SMAD (Fig. 4b). To further elucidate the mechanism leading to the activation of TGF-bpathway by PCAT6, we predicted the target genes of miR-185-5p through Starbase. Among the targets predicted by StarBase, TGFBR1 and TGFBR2, which have been reported as the core components of TGF-bsignaling, were selected for further investigation. To examine that miR-185-5p directly targets TGFBR1/2, results of luciferase reporter assay indicated that miR-185-5p inhibited TGFBR1/2-wt reporter  luciferase activity, but had no effect on the luciferase activity of TGFBR1/2-mut reporter in U2OS and 143B cells (Fig. 4cee). qRT-PCRassays showed that miR-185-5p mimics decreased the expression of TGFBR1/2 compared with the vector group (Fig. 4f). Since PCAT6 acts as ceRNA, PCAT6 may regulate TGFBR1/2 expression by sponging miR185-5p. qRT-PCRand western blotindicated that knockdown of PCAT6 decreased the expression of TGFBR1/2 and miR185-5p inhibitor reversed the downregulation of TGFBR1/2 induced by PCAT6 knockdown at both mRNA and protein level (Fig. 4gei). In summary, PCAT6 activates TGF-bpathway by sponging miR-185-5p to upregulate TGFBR1/2.	31676070	RID07599	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Osteosarcoma	PCAT6	TGFBR2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000163513	NA	100506696	7048	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	MFS2|TBR-ii|TBRII	LncRNA PCAT6 promotes tumor progression in osteosarcoma via activation of TGF-beta pathway by sponging miR-185-5p.To investigate the clinical importance of PCAT6 in OS, we determined the expression pattern of PCAT6 in OS tissues and their adjacent normal tissues (ANTs). qRT-PCRassays indicated that PCAT6 level was upregulated in OS tissues compared with ANT (Fig. 1a). Interestingly, the upregulation of PCAT6 was positively correlated with metastasis status and advanced stage of OS (Fig. 1bed andTable 1). Further analysis indicated that PCAT6 level was upregulated in OS cell lines (Fig. 1e). Survival analysis demonstrated that the upregulation of PCAT6 contributed to shorter overall survival and progression-free survival (Fig. 1f and g). Collectively, PCAT6 expression was increased in OS tissues and cell lines and correlated with poor prognosis in OS patients.To further determine the biological role of PCAT6 in OS, we silenced PCAT6 in U2OS and 143B cells (Fig. 2a). EdU, CCK8 and colony formation assays demonstrated that silencing PCAT6 inhibited proliferation of U2OS and 143B cells (Fig. 2bee). In order to investigate the impact of PCAT6 on metastasis of OS cells, transwell assay was performed. The results indicated that silencing PCAT6 significantly reduced the migrated and invaded OS cells (Fig. 2f). Taken together, PCAT6 enhances OS cell proliferation, migration, and invasion.The interaction between miR-185-5p and PCAT6 was examined by luciferase reporter assay and the results demonstrated that miR-185-5p decreased PCAT6-wt reporter  luciferase activity, but didn't have significant effect on PCAT6-mut reporter  luciferase activity (Fig. 3f and g). RIP assays indicated that miR-185-5p increased the enrichment of PCAT6 on Ago2 protein (Fig. 3h). Above results indicated that PCAT6 could act as a miR185-5p sponge. Functionally, miR-185-5p reversed the proproliferation and -metastasis effect of PCAT6 on OS cells (Fig. 3il). Collectively, PCAT6 promotes osteosarcoma progression via sponging miR-185-5p.Previous studies have reported that lncRNAs and miRNAs exert their functions by activating cancer-related pathways [8,18,19]. Therefore, Signal Finder 10 Pathway Reporter Arrays were utilized to investigate signaling pathways that were responsible for PCAT6 and miR-185-3p regulation. As shown inFig. 4a, the activity of TGFbpathway was significantly reduced by knockdown of PCAT6 and miR-185-5p mimics. Subsequently, western blot assays showed that silencing PCAT6 and miR-185-5p mimics decreased the protein expression of p-SMAD (Fig. 4b). To further elucidate the mechanism leading to the activation of TGF-bpathway by PCAT6, we predicted the target genes of miR-185-5p through Starbase. Among the targets predicted by StarBase, TGFBR1 and TGFBR2, which have been reported as the core components of TGF-bsignaling, were selected for further investigation. To examine that miR-185-5p directly targets TGFBR1/2, results of luciferase reporter assay indicated that miR-185-5p inhibited TGFBR1/2-wt reporter  luciferase activity, but had no effect on the luciferase activity of TGFBR1/2-mut reporter in U2OS and 143B cells (Fig. 4cee). qRT-PCRassays showed that miR-185-5p mimics decreased the expression of TGFBR1/2 compared with the vector group (Fig. 4f). Since PCAT6 acts as ceRNA, PCAT6 may regulate TGFBR1/2 expression by sponging miR185-5p. qRT-PCRand western blotindicated that knockdown of PCAT6 decreased the expression of TGFBR1/2 and miR185-5p inhibitor reversed the downregulation of TGFBR1/2 induced by PCAT6 knockdown at both mRNA and protein level (Fig. 4gei). In summary, PCAT6 activates TGF-bpathway by sponging miR-185-5p to upregulate TGFBR1/2.	31676070	RID07600	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	PART1	CTNNB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-520h)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000168036	NA	25859	1499	DKFZP586D0823|NCRNA00206	armadillo|beta-catenin|CTNNB	LncRNA PART1 regulates colorectal cancer via targeting miR-150-5p/miR-520h/CTNNB1 and activating Wnt/beta-catenin pathway.To investigate the expression profile of PART1, 38 paired CRC and adjacent non-cancerous tissues were collected. qRT-PCRresults revealed that PART1 expression was significantly higher in tumor tissues compared with adjacent non-cancerous tissues (Fig. 1A).To investigate the underlying molecular mechanism of PART1 in CRC associated pathways including PI3K/AKT, Wnt and NF-kB, western blot was applied to evaluate relevant protein levels after knockdown of PART1. We observed that only beta-catenin was significantly down-regulated after PART1 knockdown, which indicated that PART1 was associated with Wnt/beta-catenin pathway instead of PI3K/AKT (p-AKT) or NF-kB (p-p65) pathway (Fig. 2A, S1B).Next, we investigated the interplay between PART1 and miR-150-5p/miR-520h after knockdown or up-regulation of PART1. According to the qRT-PCRresult, upregulation of PART1 inhibited expression of miR-150-5p and miR-520h, while knockdown of PART1 lead to up-regulated expression of miR-150-5p and miR-520h (Fig. 2G).Thus, we supposed that PART1 bound with miR-150-5p as well as miR-520h as a sponge. Next, we searched from StarBase V2.0 (http://starbase.sysu.edu.cn/) and demonstrated seed sequence of miR-150-5p and miR-520h and3'UTR of PART1 respectively in Fig. 2H. Dual luciferase reports were implemented to verify the binding relationship between miR-150-5p and PART1, as well as that of miR-520h and PART1.The results disclosed that miR-150-5p/miR-520h mimics significantly weakened the fluorescence of wild type PART1, while no noticeable change was observed in mutant type PART1 (Fig. 2I). RNA pull-down assay further validated that biotinylated PART1 of wild type could significantly pull down miR-150-5p and miR-520h (Fig. 2J).The results disclosed that PART1 knockdown could decrease the expression of CTNNB1, whereas PART1 overexpression had the opposite influence (Fig. 3C). Further, potential binding sites of CTNNB1 and miR-150-5p/miR-520h were obtained and we mutated the binding sites of CTNNB1 for following mechanism assays (Fig. 3D). After verification via dual luciferase assays and RIP assay, we confirmed that CTNNB1 bound with miR-150-5p/miR-520h at the predicted sites (Fig. 3E-F).	31669140	RID07601	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Colorectal cancer	PART1	CTNNB1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000168036	NA	25859	1499	DKFZP586D0823|NCRNA00206	armadillo|beta-catenin|CTNNB	LncRNA PART1 regulates colorectal cancer via targeting miR-150-5p/miR-520h/CTNNB1 and activating Wnt/beta-catenin pathway.To investigate the expression profile of PART1, 38 paired CRC and adjacent non-cancerous tissues were collected. qRT-PCRresults revealed that PART1 expression was significantly higher in tumor tissues compared with adjacent non-cancerous tissues (Fig. 1A).To investigate the underlying molecular mechanism of PART1 in CRC associated pathways including PI3K/AKT, Wnt and NF-kB, western blot was applied to evaluate relevant protein levels after knockdown of PART1. We observed that only beta-catenin was significantly down-regulated after PART1 knockdown, which indicated that PART1 was associated with Wnt/beta-catenin pathway instead of PI3K/AKT (p-AKT) or NF-kB (p-p65) pathway (Fig. 2A, S1B).Next, we investigated the interplay between PART1 and miR-150-5p/miR-520h after knockdown or up-regulation of PART1. According to the qRT-PCRresult, upregulation of PART1 inhibited expression of miR-150-5p and miR-520h, while knockdown of PART1 lead to up-regulated expression of miR-150-5p and miR-520h (Fig. 2G).Thus, we supposed that PART1 bound with miR-150-5p as well as miR-520h as a sponge. Next, we searched from StarBase V2.0 (http://starbase.sysu.edu.cn/) and demonstrated seed sequence of miR-150-5p and miR-520h and3'UTR of PART1 respectively in Fig. 2H. Dual luciferase reports were implemented to verify the binding relationship between miR-150-5p and PART1, as well as that of miR-520h and PART1.The results disclosed that miR-150-5p/miR-520h mimics significantly weakened the fluorescence of wild type PART1, while no noticeable change was observed in mutant type PART1 (Fig. 2I). RNA pull-down assay further validated that biotinylated PART1 of wild type could significantly pull down miR-150-5p and miR-520h (Fig. 2J).The results disclosed that PART1 knockdown could decrease the expression of CTNNB1, whereas PART1 overexpression had the opposite influence (Fig. 3C). Further, potential binding sites of CTNNB1 and miR-150-5p/miR-520h were obtained and we mutated the binding sites of CTNNB1 for following mechanism assays (Fig. 3D). After verification via dual luciferase assays and RIP assay, we confirmed that CTNNB1 bound with miR-150-5p/miR-520h at the predicted sites (Fig. 3E-F).	31669140	RID07602	ceRNA or sponge	NA	UP(PAAD,BRCA);DATA(GSE40174,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Malignant glioma	MATN1-AS1	CHD1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);apoptosis process(-)	ceRNA(miR-200b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000186056	GRCh38_1:30718504-30726827	ENSG00000153922	NA	100129196	1105	NA	NA	MATN1-AS1 promotes glioma progression by functioning as ceRNA of miR-200b/c/429 to regulate CHD1 expression.Thereby, we tested the expression levels of MATN1-AS1 in 80 pairs of glioma tissues and adjacent non-tumour tissues by RT-qPCR. The results showed that MATN1-AS1 was markedly highly expressed in glioma tissues in comparison with corresponding non-tumour tissues (Figure -(Figure1B).1B). Also, MATN1-AS1 expression in glioma cell lines (T98G, LN229, U87 and U251) and normal human astrocytes (NHAs) were detected. Consistently, MATN1-AS1 was revealed to be obviously upregulated in glioma cell lines compared with NHAs (Figure -(Figure1C).1C). In the light of these results, we put a preliminary hypothesis that MATN1-AS1 might act as a carcinogenic lncRNA in glioma.To study the biological role of MATN1-AS1 in glioma, MATN1-AS1 was silenced in U251 and U87 cells by transfecting with three different shRNAs (Figure -(Figure2A).2A). Then, MTT assay demonstrated that cell viability in either U87 or U251 cells is markedly inhibited by all of the shRNAs targeting MATN1-AS1, among which the sh-MATN1-AS1#2 elicited the highest inhibitory effect (Figure -(Figure2B).2B). According to these two results (Figure -(Figure2A,B),2A,B), the sh-MATN1-AS1#2 was chosen for following experiments and described just as sh-MATN1-AS1 subsequently. Seen from Figure -Figure2C,2C, knockdown of MATN1-AS1 caused a large reduction in the number of colonies in U87 and U251 cells. Additionally, the proportion of cells arrested in G0/G1 phase were increased after silencing MATN1-AS1 in U87 and U251 cells (Figure -(Figure2D).2D). Moreover, MATN1-AS1 knockdown distinctly increased the rate of cell apoptosis in both of two cells (Figure -(Figure2E).2E). At last, western blotaccordantly confirmed that the expression of cell cycle-associated proteins (CDK4 and Cyclin D1) and anti-apoptotic Bcl-2 were downregulated, whereas pro-apoptotic Bax was upregulated in U87 and U251 cells under MATN1-AS1 silence (Figure -(Figure2F).2F). These results revealed that silencing MATN1-AS1 repressed cell proliferation and stimulated cell apoptosis in vitro.And we constructed the wild-type MATN1-AS1 (MATN1-AS1-Wt) which contained the binding sites with miR-200b/c/429 and mutant MATN1-AS1 (MATN1-AS1-Mut) without binding sites (Figure -(Figure4B).4B). Then, the luciferase reporter assay indicated that only the luciferase activity of MATN1-AS1-WT but not that of MATN1-AS1-Mut is cut down by miR-200b/c/429 mimics in either U87 or U251 cells (Figure -(Figure4C).4C).As displayed in Figure -Figure5B,5B, CHD1 was only remarkably harvested in pellets pulled down by Bio-miR-200b/c/429-WT both in U87 and U251 cells. Subsequently, we observed that the luciferase activity of wild-type CHD1 was decreased by miR-200b/c/429 mimics and regained again under MATN1-AS1 overexpression, whereas that of CHD1-Mut changes little all the time in U251 cells (Figure -(Figure5C).5C). HEK-293T cells, which had been widely utilized in cell biology research due to their reliable growth and propensity for transfection, were also used here to further validate the interactions among MATN1-AS1, miR-200b/c/429 and CHD1. And the luciferase reporter assays conducted in HEK-293T cells confirm the competitive association between CHD1 and MATN1-AS1 in binding to miR-200b/c/429 (Figure -(Figure5C).5C). Furthermore, the luciferase activity of CHD1-WT was increased in U87 and U251 cells only under miR-200b/c/429 inhibition (Figure -(Figure5D).5D). Additionally, pull-down assay followed by western blotwas performed to determine the interaction between MATN1-AS1 and CHD1. As a result, no direct interaction between MATN1-AS1 and CHD1 was analysed (Figure S1D). To explore the relationship between the expression level of MATN1-AS1, miR-200b/c/429 and CHD1, we detected their expression in glioma tissues and cell lines, and the downregulation of miR-200b/c/429 and the upregulation of CHD1 were observed in glioma tissues and cell lines (Figure S2A,B). Then, Spearman's correlation analysis revealed that CHD1 expression was negatively correlated with miR-200b/c/429 expression but positively related to MATN1-AS1 level in glioma tissues (Figure -(Figure5E).5E).In order to understand the exact impact of MATN1-AS1-miR-200b/c/429-CHD1 axis on glioma cell activities, rescue assays were projected and conducted in U251 cells. The results of MTT assay and colony formation assay indicated that the suppressed proliferation in MATN1-AS1-downregulated U251 cells was elevated under CHD1 upregulation or miR-200b/c/429 inhibition (Figure -(Figure7A,B).7A,B). In addition, the increased proportion of U251 cells arrested in G0/G1 phase after MATN1-AS1 downregulation was reversed upon the co-transfection of either pcDNA3.1/CHD1 or miR-200b/c/429 inhibitors (Figure -(Figure7C).7C). As displayed in Figure -Figure7D,7D, enhanced cell apoptosis triggered by MATN1-AS1 silence was rescued after CHD1 overexpression or miR-200b/c/429 suppression. In the end, the results of western blot were in accordance with those of flow cytometry analysis (Figure -(Figure7E).7E). Taken together, MATN1-AS1 elicited oncogenic functions in glioma via regulating miR-200b/c/429-CHD1 axis.	31667976	RID07603	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	MATN1-AS1	CHD1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);apoptosis process(-)	ceRNA(miR-200c)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000186056	GRCh38_1:30718504-30726827	ENSG00000153922	NA	100129196	1105	NA	NA	MATN1-AS1 promotes glioma progression by functioning as ceRNA of miR-200b/c/429 to regulate CHD1 expression.Thereby, we tested the expression levels of MATN1-AS1 in 80 pairs of glioma tissues and adjacent non-tumour tissues by RT-qPCR. The results showed that MATN1-AS1 was markedly highly expressed in glioma tissues in comparison with corresponding non-tumour tissues (Figure -(Figure1B).1B). Also, MATN1-AS1 expression in glioma cell lines (T98G, LN229, U87 and U251) and normal human astrocytes (NHAs) were detected. Consistently, MATN1-AS1 was revealed to be obviously upregulated in glioma cell lines compared with NHAs (Figure -(Figure1C).1C). In the light of these results, we put a preliminary hypothesis that MATN1-AS1 might act as a carcinogenic lncRNA in glioma.To study the biological role of MATN1-AS1 in glioma, MATN1-AS1 was silenced in U251 and U87 cells by transfecting with three different shRNAs (Figure -(Figure2A).2A). Then, MTT assay demonstrated that cell viability in either U87 or U251 cells is markedly inhibited by all of the shRNAs targeting MATN1-AS1, among which the sh-MATN1-AS1#2 elicited the highest inhibitory effect (Figure -(Figure2B).2B). According to these two results (Figure -(Figure2A,B),2A,B), the sh-MATN1-AS1#2 was chosen for following experiments and described just as sh-MATN1-AS1 subsequently. Seen from Figure -Figure2C,2C, knockdown of MATN1-AS1 caused a large reduction in the number of colonies in U87 and U251 cells. Additionally, the proportion of cells arrested in G0/G1 phase were increased after silencing MATN1-AS1 in U87 and U251 cells (Figure -(Figure2D).2D). Moreover, MATN1-AS1 knockdown distinctly increased the rate of cell apoptosis in both of two cells (Figure -(Figure2E).2E). At last, western blotaccordantly confirmed that the expression of cell cycle-associated proteins (CDK4 and Cyclin D1) and anti-apoptotic Bcl-2 were downregulated, whereas pro-apoptotic Bax was upregulated in U87 and U251 cells under MATN1-AS1 silence (Figure -(Figure2F).2F). These results revealed that silencing MATN1-AS1 repressed cell proliferation and stimulated cell apoptosis in vitro.And we constructed the wild-type MATN1-AS1 (MATN1-AS1-Wt) which contained the binding sites with miR-200b/c/429 and mutant MATN1-AS1 (MATN1-AS1-Mut) without binding sites (Figure -(Figure4B).4B). Then, the luciferase reporter assay indicated that only the luciferase activity of MATN1-AS1-WT but not that of MATN1-AS1-Mut is cut down by miR-200b/c/429 mimics in either U87 or U251 cells (Figure -(Figure4C).4C).As displayed in Figure -Figure5B,5B, CHD1 was only remarkably harvested in pellets pulled down by Bio-miR-200b/c/429-WT both in U87 and U251 cells. Subsequently, we observed that the luciferase activity of wild-type CHD1 was decreased by miR-200b/c/429 mimics and regained again under MATN1-AS1 overexpression, whereas that of CHD1-Mut changes little all the time in U251 cells (Figure -(Figure5C).5C). HEK-293T cells, which had been widely utilized in cell biology research due to their reliable growth and propensity for transfection, were also used here to further validate the interactions among MATN1-AS1, miR-200b/c/429 and CHD1. And the luciferase reporter assays conducted in HEK-293T cells confirm the competitive association between CHD1 and MATN1-AS1 in binding to miR-200b/c/429 (Figure -(Figure5C).5C). Furthermore, the luciferase activity of CHD1-WT was increased in U87 and U251 cells only under miR-200b/c/429 inhibition (Figure -(Figure5D).5D). Additionally, pull-down assay followed by western blotwas performed to determine the interaction between MATN1-AS1 and CHD1. As a result, no direct interaction between MATN1-AS1 and CHD1 was analysed (Figure S1D). To explore the relationship between the expression level of MATN1-AS1, miR-200b/c/429 and CHD1, we detected their expression in glioma tissues and cell lines, and the downregulation of miR-200b/c/429 and the upregulation of CHD1 were observed in glioma tissues and cell lines (Figure S2A,B). Then, Spearman's correlation analysis revealed that CHD1 expression was negatively correlated with miR-200b/c/429 expression but positively related to MATN1-AS1 level in glioma tissues (Figure -(Figure5E).5E).In order to understand the exact impact of MATN1-AS1-miR-200b/c/429-CHD1 axis on glioma cell activities, rescue assays were projected and conducted in U251 cells. The results of MTT assay and colony formation assay indicated that the suppressed proliferation in MATN1-AS1-downregulated U251 cells was elevated under CHD1 upregulation or miR-200b/c/429 inhibition (Figure -(Figure7A,B).7A,B). In addition, the increased proportion of U251 cells arrested in G0/G1 phase after MATN1-AS1 downregulation was reversed upon the co-transfection of either pcDNA3.1/CHD1 or miR-200b/c/429 inhibitors (Figure -(Figure7C).7C). As displayed in Figure -Figure7D,7D, enhanced cell apoptosis triggered by MATN1-AS1 silence was rescued after CHD1 overexpression or miR-200b/c/429 suppression. In the end, the results of western blot were in accordance with those of flow cytometry analysis (Figure -(Figure7E).7E). Taken together, MATN1-AS1 elicited oncogenic functions in glioma via regulating miR-200b/c/429-CHD1 axis.	31667976	RID07604	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	MATN1-AS1	CHD1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);apoptosis process(-)	ceRNA(miR-429)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000186056	GRCh38_1:30718504-30726827	ENSG00000153922	NA	100129196	1105	NA	NA	MATN1-AS1 promotes glioma progression by functioning as ceRNA of miR-200b/c/429 to regulate CHD1 expression.Thereby, we tested the expression levels of MATN1-AS1 in 80 pairs of glioma tissues and adjacent non-tumour tissues by RT-qPCR. The results showed that MATN1-AS1 was markedly highly expressed in glioma tissues in comparison with corresponding non-tumour tissues (Figure -(Figure1B).1B). Also, MATN1-AS1 expression in glioma cell lines (T98G, LN229, U87 and U251) and normal human astrocytes (NHAs) were detected. Consistently, MATN1-AS1 was revealed to be obviously upregulated in glioma cell lines compared with NHAs (Figure -(Figure1C).1C). In the light of these results, we put a preliminary hypothesis that MATN1-AS1 might act as a carcinogenic lncRNA in glioma.To study the biological role of MATN1-AS1 in glioma, MATN1-AS1 was silenced in U251 and U87 cells by transfecting with three different shRNAs (Figure -(Figure2A).2A). Then, MTT assay demonstrated that cell viability in either U87 or U251 cells is markedly inhibited by all of the shRNAs targeting MATN1-AS1, among which the sh-MATN1-AS1#2 elicited the highest inhibitory effect (Figure -(Figure2B).2B). According to these two results (Figure -(Figure2A,B),2A,B), the sh-MATN1-AS1#2 was chosen for following experiments and described just as sh-MATN1-AS1 subsequently. Seen from Figure -Figure2C,2C, knockdown of MATN1-AS1 caused a large reduction in the number of colonies in U87 and U251 cells. Additionally, the proportion of cells arrested in G0/G1 phase were increased after silencing MATN1-AS1 in U87 and U251 cells (Figure -(Figure2D).2D). Moreover, MATN1-AS1 knockdown distinctly increased the rate of cell apoptosis in both of two cells (Figure -(Figure2E).2E). At last, western blotaccordantly confirmed that the expression of cell cycle-associated proteins (CDK4 and Cyclin D1) and anti-apoptotic Bcl-2 were downregulated, whereas pro-apoptotic Bax was upregulated in U87 and U251 cells under MATN1-AS1 silence (Figure -(Figure2F).2F). These results revealed that silencing MATN1-AS1 repressed cell proliferation and stimulated cell apoptosis in vitro.And we constructed the wild-type MATN1-AS1 (MATN1-AS1-Wt) which contained the binding sites with miR-200b/c/429 and mutant MATN1-AS1 (MATN1-AS1-Mut) without binding sites (Figure -(Figure4B).4B). Then, the luciferase reporter assay indicated that only the luciferase activity of MATN1-AS1-WT but not that of MATN1-AS1-Mut is cut down by miR-200b/c/429 mimics in either U87 or U251 cells (Figure -(Figure4C).4C).As displayed in Figure -Figure5B,5B, CHD1 was only remarkably harvested in pellets pulled down by Bio-miR-200b/c/429-WT both in U87 and U251 cells. Subsequently, we observed that the luciferase activity of wild-type CHD1 was decreased by miR-200b/c/429 mimics and regained again under MATN1-AS1 overexpression, whereas that of CHD1-Mut changes little all the time in U251 cells (Figure -(Figure5C).5C). HEK-293T cells, which had been widely utilized in cell biology research due to their reliable growth and propensity for transfection, were also used here to further validate the interactions among MATN1-AS1, miR-200b/c/429 and CHD1. And the luciferase reporter assays conducted in HEK-293T cells confirm the competitive association between CHD1 and MATN1-AS1 in binding to miR-200b/c/429 (Figure -(Figure5C).5C). Furthermore, the luciferase activity of CHD1-WT was increased in U87 and U251 cells only under miR-200b/c/429 inhibition (Figure -(Figure5D).5D). Additionally, pull-down assay followed by western blotwas performed to determine the interaction between MATN1-AS1 and CHD1. As a result, no direct interaction between MATN1-AS1 and CHD1 was analysed (Figure S1D). To explore the relationship between the expression level of MATN1-AS1, miR-200b/c/429 and CHD1, we detected their expression in glioma tissues and cell lines, and the downregulation of miR-200b/c/429 and the upregulation of CHD1 were observed in glioma tissues and cell lines (Figure S2A,B). Then, Spearman's correlation analysis revealed that CHD1 expression was negatively correlated with miR-200b/c/429 expression but positively related to MATN1-AS1 level in glioma tissues (Figure -(Figure5E).5E).In order to understand the exact impact of MATN1-AS1-miR-200b/c/429-CHD1 axis on glioma cell activities, rescue assays were projected and conducted in U251 cells. The results of MTT assay and colony formation assay indicated that the suppressed proliferation in MATN1-AS1-downregulated U251 cells was elevated under CHD1 upregulation or miR-200b/c/429 inhibition (Figure -(Figure7A,B).7A,B). In addition, the increased proportion of U251 cells arrested in G0/G1 phase after MATN1-AS1 downregulation was reversed upon the co-transfection of either pcDNA3.1/CHD1 or miR-200b/c/429 inhibitors (Figure -(Figure7C).7C). As displayed in Figure -Figure7D,7D, enhanced cell apoptosis triggered by MATN1-AS1 silence was rescued after CHD1 overexpression or miR-200b/c/429 suppression. In the end, the results of western blot were in accordance with those of flow cytometry analysis (Figure -(Figure7E).7E). Taken together, MATN1-AS1 elicited oncogenic functions in glioma via regulating miR-200b/c/429-CHD1 axis.	31667976	RID07605	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LNCOG	ADGRD1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-4455)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000257219	GRCh38_12:76259836-76305969	ENSG00000111452	NA	105369848	283383	LINC02407|lncRNA-OG|RP11-54A9.1	DKFZp434B1272|GPR133|PGR25	Differentially expressed long noncoding RNAs and regulatory mechanism of LINC02407 in human gastric adenocarcinoma.The expression levels of LINC02407 in 20 pairs of GC tissues and adjacent normal tissues were measured by qRT-PCR The results showed that LINC02407 expression was upregulated in GC samples relative to adjacent normal mucosal tissues (Figure -(Figure4A).4A). In addition, the expression levels of LINC02407 in a gastric mucosal normal cell line, GES-1, and five GC cell lines (HaCaT, MGC-803, MKN45, SGC-7901, and HGC-27) were analyzed. The results showed that LINC01354 expression was the highest in HGC-27 cells and the lowest in HaCaT cells (Figure -(Figure4B4B).Specially designed primers were applied to detect LINC02407 expression in transfected HGC-27 cells by qRT-PCR Chemically synthetic si-LINC02407 and si-NC were successfully transfected into HGC-27 cells, and si-LINC02407 successfully downregulated the LINC02407 expression level (Figure -(Figure5A).5A). LINC02407-overexpressing lentivirus was successfully transfected into HGC-27 cells, and LINC02407 was upregulated. Cell viability was strengthened by the LINC02407-overexpressing lentivirus relative to the overexpression-control lentivirus as shown in Figure -Figure5B.5B. Apoptosis analysis was performed as previously mentioned, and the results revealed that the LINC02407-overexpressing lentivirus could inhibit apoptosis by 67% in HGC-27 cells, while on the contrary, si-LINC02407 could increase apoptosis by 83% in HGC-27 cells (Figure -(Figure5C5C and Figure -Figure5D).5D). A wound healing assay indicated that the LINC02407-overexpressing lentivirus could enhance the migration and invasion rate by 48% in HGC-27 cells relative to the overexpression-control lentivirus, and si-LINC02407 could decrease the migration and invasion rate by 15% in HGC-27 cells compared with si-NC.The predicted results of miRanda software were considered to be miRNAs corresponding to mRNA. LncRNA and its candidate miRNAs are shown in Supplemental Table 2. We selected 5 of the 37 miRNAs reported to be closely related to the progression of GC, including hsa-miR-331-3p, hsa-miR-6845-5p, hsa-miR-4455, hsa-miR-4316, and hsa-miR-1258. A luciferase reporter assay was used to verify that LINC02407 could directly target hsa-miR-6845-5p and hsa-miR-4455. The results showed that luciferase activity was reduced in wild-type LINC02407 3'-UTR- and hsa-miR-6845-5p mimic co-transfected 293T cells in comparison to that in wild-type LINC02407 3'-UTR- and hsa-miR-6845-5p mimic NC co-transfected 293T cells (P < 0.05); the same result was found with hsa-miR-4455. Next, the effect of hsa-miR-6845-5p and hsa-miR-4455 on a GC cell line was evaluated. The hsa-miR-6845-5p-mimic could inhibit cell viability in hsa-miR-6845-5p-mimic and LINC02407-overexpressing vector-transfected HGC-27 cells (Figure -(Figure6B).6B). Additionally, the hsa-miR-6845-5p-mimic and hsa-miR-4455-mimic had negative effects on the apoptosis in hsa-miR-6845-5p-mimic- and LINC02407-Overexpressing vector-transfected HGC-27 cells (Figure -(Figure6C).6C). The hsa-miR-6845-5p-mimic and hsa-miR-4455-mimic could negatively impact the transwell invasion of HGC-27 cells (Figure -(Figure6D6D).The potential target mRNAs of hsa-miR-6845-5p were analyzed using miRanda software, and the results are showed in Supplemental Table 3. Figure -Figure7A7A shows the number of studies linking the potential target mRNAs of miR-6845-5p and the number of studies of potential target mRNAs linked to miR-4455 under the regulation of LINC02407, resulting in a Sankey diagram generated with R-3.5.2. Five mRNAs with high scores (ADGRD1, cholinergic receptor nicotinic delta, IgLON family member 5, KRI1, and troponin I1) were identified in a LINC02407 regulated pathway. A western blot assay revealed that ADGRD1 was regulated by the LINC02407-miR-6845-5p and miR-4455- ADGRD1 pathways (Figure -(Figure7B7B).	31660034	RID07606	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	LNCOG	ADGRD1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-6845-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000257219	GRCh38_12:76259836-76305969	ENSG00000111452	NA	105369848	283383	LINC02407|lncRNA-OG|RP11-54A9.1	DKFZp434B1272|GPR133|PGR25	Differentially expressed long noncoding RNAs and regulatory mechanism of LINC02407 in human gastric adenocarcinoma.The expression levels of LINC02407 in 20 pairs of GC tissues and adjacent normal tissues were measured by qRT-PCR The results showed that LINC02407 expression was upregulated in GC samples relative to adjacent normal mucosal tissues (Figure -(Figure4A).4A). In addition, the expression levels of LINC02407 in a gastric mucosal normal cell line, GES-1, and five GC cell lines (HaCaT, MGC-803, MKN45, SGC-7901, and HGC-27) were analyzed. The results showed that LINC01354 expression was the highest in HGC-27 cells and the lowest in HaCaT cells (Figure -(Figure4B4B).Specially designed primers were applied to detect LINC02407 expression in transfected HGC-27 cells by qRT-PCR Chemically synthetic si-LINC02407 and si-NC were successfully transfected into HGC-27 cells, and si-LINC02407 successfully downregulated the LINC02407 expression level (Figure -(Figure5A).5A). LINC02407-overexpressing lentivirus was successfully transfected into HGC-27 cells, and LINC02407 was upregulated. Cell viability was strengthened by the LINC02407-overexpressing lentivirus relative to the overexpression-control lentivirus as shown in Figure -Figure5B.5B. Apoptosis analysis was performed as previously mentioned, and the results revealed that the LINC02407-overexpressing lentivirus could inhibit apoptosis by 67% in HGC-27 cells, while on the contrary, si-LINC02407 could increase apoptosis by 83% in HGC-27 cells (Figure -(Figure5C5C and Figure -Figure5D).5D). A wound healing assay indicated that the LINC02407-overexpressing lentivirus could enhance the migration and invasion rate by 48% in HGC-27 cells relative to the overexpression-control lentivirus, and si-LINC02407 could decrease the migration and invasion rate by 15% in HGC-27 cells compared with si-NC.The predicted results of miRanda software were considered to be miRNAs corresponding to mRNA. LncRNA and its candidate miRNAs are shown in Supplemental Table 2. We selected 5 of the 37 miRNAs reported to be closely related to the progression of GC, including hsa-miR-331-3p, hsa-miR-6845-5p, hsa-miR-4455, hsa-miR-4316, and hsa-miR-1258. A luciferase reporter assay was used to verify that LINC02407 could directly target hsa-miR-6845-5p and hsa-miR-4455. The results showed that luciferase activity was reduced in wild-type LINC02407 3'-UTR- and hsa-miR-6845-5p mimic co-transfected 293T cells in comparison to that in wild-type LINC02407 3'-UTR- and hsa-miR-6845-5p mimic NC co-transfected 293T cells (P < 0.05); the same result was found with hsa-miR-4455. Next, the effect of hsa-miR-6845-5p and hsa-miR-4455 on a GC cell line was evaluated. The hsa-miR-6845-5p-mimic could inhibit cell viability in hsa-miR-6845-5p-mimic and LINC02407-overexpressing vector-transfected HGC-27 cells (Figure -(Figure6B).6B). Additionally, the hsa-miR-6845-5p-mimic and hsa-miR-4455-mimic had negative effects on the apoptosis in hsa-miR-6845-5p-mimic- and LINC02407-Overexpressing vector-transfected HGC-27 cells (Figure -(Figure6C).6C). The hsa-miR-6845-5p-mimic and hsa-miR-4455-mimic could negatively impact the transwell invasion of HGC-27 cells (Figure -(Figure6D6D).The potential target mRNAs of hsa-miR-6845-5p were analyzed using miRanda software, and the results are showed in Supplemental Table 3. Figure -Figure7A7A shows the number of studies linking the potential target mRNAs of miR-6845-5p and the number of studies of potential target mRNAs linked to miR-4455 under the regulation of LINC02407, resulting in a Sankey diagram generated with R-3.5.2. Five mRNAs with high scores (ADGRD1, cholinergic receptor nicotinic delta, IgLON family member 5, KRI1, and troponin I1) were identified in a LINC02407 regulated pathway. A western blot assay revealed that ADGRD1 was regulated by the LINC02407-miR-6845-5p and miR-4455- ADGRD1 pathways (Figure -(Figure7B7B).	31660034	RID07607	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Lung cancer	NEAT1	KLF3	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-1224)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000109787	NA	283131	51274	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BKLF	LncRNA NEAT1/miR-1224/KLF3 contributes to cell proliferation, apoptosis and invasion in lung cancer.StarBase showed that lncRNA NEAT1 significantly increased in lung cancer tissues (Figure 1A). In this study, we first detected the expression of lncRNA NEAT1 in lung cancer tissues and adjacent normal tissues by qRTPCR. The results showed that the expression level of lncRNA NEAT1 in lung cancer tissues was significantly higher than that of adjacent tissues (Figure 1B), suggesting the abnormal expression of lncRNA NEAT1 in lung cancer.To clarify the expression of miRNAs associated with lncRNA NEAT1 in lung cancer cells, the bioinformatics prediction tools were first used to search for miRNAs. The results indicated that lncRNA NEAT1 might have a direct effect on miR-1224 due to a similar binding sequence (Figure A). To verify whether lncRNA NEAT1 could bind to miR-1224 3'UTR, the Dual-Luciferase Reporter Gene Assay showed that the luciferase activity of lncRNA NEAT1-wild cells with miR1224 mimics was significantly reduced. However, no evident changes were observed in the luciferase activity of lncRNA NEAT1-mutant cells with miR-1224 mimics (Figure 2B). Furthermore, the qRT-PCRassay showed that miR-1224 was highly expressed in the cells transfected with lncRNA NEAT1-siRNA (Figure 2C). The results showed that lncRNA NEAT1-siRNA could specifically bind to the 3'UTR of miR-1224 and downregulate its expression level.The effect of miR-1224 on cell proliferation and apoptosis was then evaluated. MTT assay showed that miR-1224 significantly up-regulated and suppressed the proliferation of lung cancer cells (Figure 3D). As shown in Figure 3E, the flow cytometry assay demonstrated that the number of apoptotic cells in miR-1224 mimics group was significantly higher than that of the control group. In conclusion, these experiments indicated that the proliferative ability of A549 cells was inhibited, and the apoptosis rate of the cells was enhanced after miR-1224 up-regulation.The online software predicted that miR-1224 might be bound to the 3'UTR of KLF3 (Figure 4A). The Luciferase reporter gene assay was then used to verify this prediction. The result showed that the luciferase activity of the cells transfected with miR-1224 mimics and pMIR-KLF3-3'UTR wild was significantly inhibited. However, no evident changes were observed in the luciferase activity in the cells transfected with miR-1224 mimics and pMIR-KLF3-3'UTR mutant (Figure 4B). To detect the regulation of abnormal miR-1224 expression on KLF3, we performed the qRT-PCRassay. The results pointed out that the mRNA expression level of KLF3 was remarkably down-regulated in miR1224 over-expression group when compared with the control group (Figure 4C). These data demonstrated that miR-1224 could down-regulate KLF3 by directly binding to its 3'UTR.	31646570	RID07608	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807)
Lung cancer	LINC00511	KDM1A	interact	dual-luciferase reporter assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000004487	NA	400619	23028	onco-lncRNA-12	AOF2|BHC110|KDM1|KIAA0601|LSD1	LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.Further, we determined LINC00511 expression in NSCLC tissues collected from our hospital. Identically, LINC00511 was highly expressed in NSCLC tissues than non-tumoral tissues (Figure 2A).By conducting CCK-8 assay and flow cytometry, LINC00511 knockdown in A549 cells was found to inhibit cell viability (Figure 3D) but accelerated cell apoptosis (Figure 3E). On the contrary, LINC00511 overexpression in PC9 cells increased viability (Figure 3F), but inhibited apoptosis (Figure 3G). Transwell assay was then performed for determining invasive and migratory abilities of NSCLC cells influenced by LINC00511. LINC00511 knockdown greatly inhibited invasive and migratory abilities of A549 cells (Figure 4A). Contrarily, LINC00511 overexpression in PC9 cells promoted invasive and migratory abilities (Figure 4B).In this experiment, RIP assay showed that LINC00511 in A549 and PC9 cells could directly bind to LSD1 and EZH2, and had no binding relationship with CoREST (Figure 5B). LINC00511 knockdown remarkably upregulated mRNA levels of LATS2 and KLF2 in A549 and PC9 cells, while mRNA levels of p21, LATS1, and PTEN did not obviously change (Figure 5C). western blot indicated the upregulated LACT2 and KLF2 in A549 and PC9 cells after LINC00511 knockdown (Figure 5D). The above data suggested that LINC00511 could bind to EZH2 and LSD1 and regulate expressions of LATS2 and KLF2. We then explored the regulatory effects of EZH2 and LSD1 on LATS2 and KLF2. The mRNA levels of LATS2 and KLF2 in A549 and PC9 cells markedly increased after knockdown of LSD1 and EZH2 (Figure 6A), suggesting that LSD1 and EZH2 can regulate the transcriptional levels of LATS2 and KLF2. ChIP assay elucidated that EZH2, LSD1, H3K27me3 and H3K4me2 could bind to the promoter regions of LATS2 and KLF2 in A549 and PC9 cells (Figure 6B). After knockdown of LINC00511, levels of EZH2, LSD1, H3K27me3 and H3K4me2 that bound to LATS2 and KLF2 in A549 and PC9 cells were downregulated (Figure 6C and 6D). These results indicated that LINC00511 could inhibit expressions of LATS2 and KLF2 by promoting the binding of EZH2 and LSD1 to the promoter regions of LATS2 and KLF2.Gain-of-function experiment was carried out to verify the involvement of LATS2 in LINC00511-mediated NSCLC progression. Co-transfection of si-LINC00511 and si-LATS2 could partially reverse the decreased viability (Figure 8A), accelerated apoptosis (Figure 8B) and inhibited migratory abilities (Figure 8C) induced by LINC00511 knockdown.	31646568	RID07609	interact with protein	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00511	EZH2	interact	dual-luciferase reporter assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000106462	NA	400619	2146	onco-lncRNA-12	ENX-1|EZH1|KMT6|KMT6A	LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.Further, we determined LINC00511 expression in NSCLC tissues collected from our hospital. Identically, LINC00511 was highly expressed in NSCLC tissues than non-tumoral tissues (Figure 2A).By conducting CCK-8 assay and flow cytometry, LINC00511 knockdown in A549 cells was found to inhibit cell viability (Figure 3D) but accelerated cell apoptosis (Figure 3E). On the contrary, LINC00511 overexpression in PC9 cells increased viability (Figure 3F), but inhibited apoptosis (Figure 3G). Transwell assay was then performed for determining invasive and migratory abilities of NSCLC cells influenced by LINC00511. LINC00511 knockdown greatly inhibited invasive and migratory abilities of A549 cells (Figure 4A). Contrarily, LINC00511 overexpression in PC9 cells promoted invasive and migratory abilities (Figure 4B).In this experiment, RIP assay showed that LINC00511 in A549 and PC9 cells could directly bind to LSD1 and EZH2, and had no binding relationship with CoREST (Figure 5B). LINC00511 knockdown remarkably upregulated mRNA levels of LATS2 and KLF2 in A549 and PC9 cells, while mRNA levels of p21, LATS1, and PTEN did not obviously change (Figure 5C). western blot indicated the upregulated LACT2 and KLF2 in A549 and PC9 cells after LINC00511 knockdown (Figure 5D). The above data suggested that LINC00511 could bind to EZH2 and LSD1 and regulate expressions of LATS2 and KLF2. We then explored the regulatory effects of EZH2 and LSD1 on LATS2 and KLF2. The mRNA levels of LATS2 and KLF2 in A549 and PC9 cells markedly increased after knockdown of LSD1 and EZH2 (Figure 6A), suggesting that LSD1 and EZH2 can regulate the transcriptional levels of LATS2 and KLF2. ChIP assay elucidated that EZH2, LSD1, H3K27me3 and H3K4me2 could bind to the promoter regions of LATS2 and KLF2 in A549 and PC9 cells (Figure 6B). After knockdown of LINC00511, levels of EZH2, LSD1, H3K27me3 and H3K4me2 that bound to LATS2 and KLF2 in A549 and PC9 cells were downregulated (Figure 6C and 6D). These results indicated that LINC00511 could inhibit expressions of LATS2 and KLF2 by promoting the binding of EZH2 and LSD1 to the promoter regions of LATS2 and KLF2.Gain-of-function experiment was carried out to verify the involvement of LATS2 in LINC00511-mediated NSCLC progression. Co-transfection of si-LINC00511 and si-LATS2 could partially reverse the decreased viability (Figure 8A), accelerated apoptosis (Figure 8B) and inhibited migratory abilities (Figure 8C) induced by LINC00511 knockdown.	31646568	RID07610	interact with protein	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung cancer	LINC00511	LATS2	negatively-E	dual-luciferase reporter assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000150457	NA	400619	26524	onco-lncRNA-12	NA	LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.Further, we determined LINC00511 expression in NSCLC tissues collected from our hospital. Identically, LINC00511 was highly expressed in NSCLC tissues than non-tumoral tissues (Figure 2A).By conducting CCK-8 assay and flow cytometry, LINC00511 knockdown in A549 cells was found to inhibit cell viability (Figure 3D) but accelerated cell apoptosis (Figure 3E). On the contrary, LINC00511 overexpression in PC9 cells increased viability (Figure 3F), but inhibited apoptosis (Figure 3G). Transwell assay was then performed for determining invasive and migratory abilities of NSCLC cells influenced by LINC00511. LINC00511 knockdown greatly inhibited invasive and migratory abilities of A549 cells (Figure 4A). Contrarily, LINC00511 overexpression in PC9 cells promoted invasive and migratory abilities (Figure 4B).In this experiment, RIP assay showed that LINC00511 in A549 and PC9 cells could directly bind to LSD1 and EZH2, and had no binding relationship with CoREST (Figure 5B). LINC00511 knockdown remarkably upregulated mRNA levels of LATS2 and KLF2 in A549 and PC9 cells, while mRNA levels of p21, LATS1, and PTEN did not obviously change (Figure 5C). western blot indicated the upregulated LACT2 and KLF2 in A549 and PC9 cells after LINC00511 knockdown (Figure 5D). The above data suggested that LINC00511 could bind to EZH2 and LSD1 and regulate expressions of LATS2 and KLF2. We then explored the regulatory effects of EZH2 and LSD1 on LATS2 and KLF2. The mRNA levels of LATS2 and KLF2 in A549 and PC9 cells markedly increased after knockdown of LSD1 and EZH2 (Figure 6A), suggesting that LSD1 and EZH2 can regulate the transcriptional levels of LATS2 and KLF2. ChIP assay elucidated that EZH2, LSD1, H3K27me3 and H3K4me2 could bind to the promoter regions of LATS2 and KLF2 in A549 and PC9 cells (Figure 6B). After knockdown of LINC00511, levels of EZH2, LSD1, H3K27me3 and H3K4me2 that bound to LATS2 and KLF2 in A549 and PC9 cells were downregulated (Figure 6C and 6D). These results indicated that LINC00511 could inhibit expressions of LATS2 and KLF2 by promoting the binding of EZH2 and LSD1 to the promoter regions of LATS2 and KLF2.Gain-of-function experiment was carried out to verify the involvement of LATS2 in LINC00511-mediated NSCLC progression. Co-transfection of si-LINC00511 and si-LATS2 could partially reverse the decreased viability (Figure 8A), accelerated apoptosis (Figure 8B) and inhibited migratory abilities (Figure 8C) induced by LINC00511 knockdown.	31646568	RID07611	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC00511	KLF2	negatively-E	dual-luciferase reporter assay;RIP;CHIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000127528	NA	400619	10365	onco-lncRNA-12	LKLF	LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.Further, we determined LINC00511 expression in NSCLC tissues collected from our hospital. Identically, LINC00511 was highly expressed in NSCLC tissues than non-tumoral tissues (Figure 2A).By conducting CCK-8 assay and flow cytometry, LINC00511 knockdown in A549 cells was found to inhibit cell viability (Figure 3D) but accelerated cell apoptosis (Figure 3E). On the contrary, LINC00511 overexpression in PC9 cells increased viability (Figure 3F), but inhibited apoptosis (Figure 3G). Transwell assay was then performed for determining invasive and migratory abilities of NSCLC cells influenced by LINC00511. LINC00511 knockdown greatly inhibited invasive and migratory abilities of A549 cells (Figure 4A). Contrarily, LINC00511 overexpression in PC9 cells promoted invasive and migratory abilities (Figure 4B).In this experiment, RIP assay showed that LINC00511 in A549 and PC9 cells could directly bind to LSD1 and EZH2, and had no binding relationship with CoREST (Figure 5B). LINC00511 knockdown remarkably upregulated mRNA levels of LATS2 and KLF2 in A549 and PC9 cells, while mRNA levels of p21, LATS1, and PTEN did not obviously change (Figure 5C). western blot indicated the upregulated LACT2 and KLF2 in A549 and PC9 cells after LINC00511 knockdown (Figure 5D). The above data suggested that LINC00511 could bind to EZH2 and LSD1 and regulate expressions of LATS2 and KLF2. We then explored the regulatory effects of EZH2 and LSD1 on LATS2 and KLF2. The mRNA levels of LATS2 and KLF2 in A549 and PC9 cells markedly increased after knockdown of LSD1 and EZH2 (Figure 6A), suggesting that LSD1 and EZH2 can regulate the transcriptional levels of LATS2 and KLF2. ChIP assay elucidated that EZH2, LSD1, H3K27me3 and H3K4me2 could bind to the promoter regions of LATS2 and KLF2 in A549 and PC9 cells (Figure 6B). After knockdown of LINC00511, levels of EZH2, LSD1, H3K27me3 and H3K4me2 that bound to LATS2 and KLF2 in A549 and PC9 cells were downregulated (Figure 6C and 6D). These results indicated that LINC00511 could inhibit expressions of LATS2 and KLF2 by promoting the binding of EZH2 and LSD1 to the promoter regions of LATS2 and KLF2.Gain-of-function experiment was carried out to verify the involvement of LATS2 in LINC00511-mediated NSCLC progression. Co-transfection of si-LINC00511 and si-LATS2 could partially reverse the decreased viability (Figure 8A), accelerated apoptosis (Figure 8B) and inhibited migratory abilities (Figure 8C) induced by LINC00511 knockdown.	31646568	RID07612	expression association	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	PCAT6	PTEN	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228288	GRCh38_1:202810850-202812473	ENSG00000171862	NA	100506696	5728	KDM5B-AS1|KDM5BAS1|ncRNA-a2|onco-lncRNA-96|PCAN-R1	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA PCAT6 promotes occurrence and development of ovarian cancer by inhibiting PTEN.We used qRT-PCRassay to explore PCAT6 expression in 42 pairs of ovarian cancer tissues and paracancerous tissues or cancer cell lines. The results of qRT-PCRdemonstrated that PCAT6 expression in ovarian cancer tissues was higher than that in the paracancerous tissues, and the difference was statistically significant (Figure 1A). Meanwhile, PCAT6 was also highly expressed in ovarian cancer cells, compared to HOSEPiCs cells (Figure 1B).According to the results of qRT-PCR ovarian cancer tissues were divided into PCAT6 high expression group and PCAT6 low expression group. The number of each group was analyzed and the relationship between PCAT6 expression and age, clinical stage, distant metastasis and lymph node metastasis of ovarian cancer patients was analyzed, respectively. The results demonstrated that high expression of PCAT6 was positively related to lymph node metastasis and distant metastasis of ovarian cancer (Table I).To explore the effects of PCAT6 on the proliferation, invasion and migration ability of ovarian cancer cells, we first successfully constructed a PCAT6 knockdown model and validated it using qRT-PCRassay (Figure 2A). Subsequently, we used the CCK-8 test to explore the proliferation rate of those cells. The results of CCK-8 showed that the cell proliferation rate in the si-PCAT6 group was lower than that in the NC group (Figure 2B).The expression of PTEN was explored by qRT-PCRand western blot. We found that the knockdown of PTEN restored the role of knockdown of PCAT6 in ovarian cancer (Figure 4A and 4B). Subsequently, we revealed that the knockdown of PTEN counteracted the effect of the decreased PCAT6 on the metastasis by transwell experiment and wound healing assay (Figure 4C and 4D).	31646553	RID07613	expression association	metastasis	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	HULC	MET	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-2052)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000105976	NA	728655	4233	HCCAT1|LINC00078|NCRNA00078	DFNB97|HGFR|RCCP2	Long noncoding RNA HULC promotes hepatocellular carcinoma progression.Next, we measured HULC levels in HCC cell lines (HepG2, Huh7, Hep3B, HLF, Sk-hep1, 97H, and LM3) and normal human hepatocyte (7702). HULC was overexpressed in HCC cell lines (Figure 1E). Taken together, these findings indicate that HULC is upregulated in HCC. To determine the prognostic potential of HULC in HCC patients, we generated Kaplan-Meier survival curves for the TCGA cohort. Our results showed that high levels of HULC correlated with poor overall survival (OS) of HCC patients (Figure 1F). These data suggested that HULC might promote tumorigenesis in HCC.HULC expression was silenced or overexpressed in HLF and 97H cells to investigate the biological function of HULC in HCC cells (Supplementary Figure 1A, 1B). CCK-8 assays indicated that downregulation of HULC led to decreased cell viability (Figure 2A, -,2B),2B), whereas overexpression of HULC efficiently enhanced cell viability (Figure 2C, -,2D).2D). Additionally, trans-well assays showed that HULC knockdown significantly reduced migration and invasion (Figure 2E, -,2F2F and Supplementary Figure 1C), and overexpression of HULC contributed to migration and invasion of HLF and 97H cells (Figure 2G, -,2H2H and Supplementary Figure 1D). The results above demonstrated that HULC promotes the proliferation, migration, and invasion of HCC cells.By using bioinformatics predictions (DIANA Tools- LncBase Predicted v.2) [20], we found that HULC might be a ceRNA for miR-2052 (Figure 3A). We overexpressed miR-2052 through miR-2052 mimic transfection (Figure 3B) and silenced miR-2052 through miR-2052 inhibitor transfection (Figure 3C) in HLF and 97H cells. Luciferase reporter plasmid carrying the WT or MUT HULC sequence was cotransfected to measure luciferase activities. Our results showed that miR-2052 mimic transfection decreased the luciferase activity of HULC-WT reporter in HLF and 97H cells; however, mutation of the binding site abrogated this effect (Figure 3D, -,3E).3E). Moreover, HULC silencing increased miR-2052 levels (Figure 3F) while HULC overexpression decreased them (Figure 3G), indicating that HULC and miR-2052 inhibit each other  expression. Additionally, to test whether HULC and miR-2052 engage in direct physical interactions, we performed RNA pull down followed by qPCR analysis. Our results showed that HULC interacted with miR-2052 directly (Figure 3H, -,3I),3I), indicating that HULC acts as a sponge for miR-2052 in HCC cells.To determine the target genes of miR-2052, we searched four online bioinformatics tools (MicroT, miRDB, miRWalk, and TargetScan) and jointly predicted that four genes may be biological targets of miR-2052 (Supplementary Figure 3A). We tested the regulation of these genes by miR-2052 through qPCR, and chose MET in the end as the focus of subsequent experiments (Supplementary Figure 3B'-C). To further clarify the relationship between miR-2052 and MET, we identified the potential binding sites between miR- 2052 and MET (Figure 5A). Luciferase reporter assay results showed that miR-2052 mimic suppressed the luciferase activity of the MET wild type (WT) reporter, but not that of mutant (MUT) reporter in HLF and 97H cells. Moreover, qPCR and western blot (WB) showed that miR-2052 mimic suppressed, and miR-2052 inhibitor promoted, the expression of MET, respectively (Figure 5C, -,5D).5D). These results suggested that MET is a target of miR-2052. Consistently, we found that knockdown of HULC reduced, whereas overexpression of HULC increased MET expression (Figure 5E). Furthermore, inhibition of miR-2052 rescued HULC silencing-mediated downregulation of MET (Figure 5F), indicating that HULC promotes MET expression through sponging miR-2052 in HCC. In addition, WB of 42 pairs of HCC and control tissues revealed that MET was upregulated in HCC tissues (Figure 5G and Supplementary Figure 3D, -,3E).3E). Taken together, these results demonstrated that MET is a direct target of miR-2052 in HCC cells.To further analyze the effect of HULC on HCC growth in vivo, we exploited the xenograft mouse model. HLF cells overexpressing HULC have a remarkably increased tumor volume and weight (Figure 7A'-C). In addition, HULC, miR-2052, and MET levels were measured by qPCR in xenograft tumors. The results showed that HULC and MET expression was increased, whereas miR-2052 expression was decreased (Figure 7D'-F). Then, IHC results showed that xenograft tumors overexpressing HULC displayed high Ki67 and MET expression (Figure 7G). Moreover, we also measured MET expression in xenograft tumors by WB and the results showed that MET was increased in cells overexpressing HULC (Figure 7H). Taken together, these results indicated that HULC promotes HCC growth through the miR-2052/MET axis in vivo.	31645479	RID07614	ceRNA or sponge	prognosis		UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Ewing's sarcoma	HULC	TWIST1	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-186)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Ewing sarcomas	lncRNA	TF	ENSG00000251164	NA	ENSG00000122691	NA	728655	7291	HCCAT1|LINC00078|NCRNA00078	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	Small molecule inhibition of Ewing sarcoma cell growth via targeting the long non coding RNA HULC.Taken together, these results point to a potential role of the HULC lncRNA in ES tumorigenicity and suggest that its downregulation might be involved in the antitumorigenic activity of the small molecule YK-4-279.To investigate the ability of HULC as a sponge toward miR-186 and miR-218, we first evaluated their binding by generating a reporter construct with the HULC sequence harboring miR-186 and miR-218 binding sites downstream of the Renilla luciferase in psicheck II vector. This construct was co-transfected in TC-71 cells with either miR-186 or miR-218 oligonucleotide mimics, or scrambled mimic miRNA (scr miR). A significant reduction of the Renilla/Ffly ratio was observed in miR-186 and miR-218 transfected cells, confirming the ability of these miRNAs to bind HULC sequence (Fig.3B). Notably, the unrelated miR-663a mimic was not able to affect Renilla/Ffly activity (Fig.3B).Interestingly, co-transfection of the miR-sensors with the mimics (miR-186 or miR-218) exhibited a significant repression of Ren/Ffly activity compared to control cells, confirming the efficiency of the reporter system in the detection of variation of miR-186 and miR-218 levels (Supplementary Fig.S2B).Next, to evaluate the relevance of miR-186 to Ewing sarcoma prognosis, we scanned array dataset of ES patients by using R2 online tool (https://hgserver1.amc.nl/cgibin/r2/main.cg) Interestingly, Kaplan Meier analyses of event-free and overall survival from 64 ES patients [25] showed a positive correlation between miR-186 expression and patient prognosis (Fig.3E), suggesting a tumor suppressive function. In line with this, the overexpression of a specific miR-186 mimic was able to reduce the clonogenicity of TC-71 cells (Fig.3F). Furthermore, co-treatment of ES cells with YK-4-279 and mimic miR-186 enhanced the effect of the drug by sensitizing ES cells to the treatment (Fig.3G and H). Collectively, these experiments highlight a role for miR-186 as a potential tumor suppressor in ES pathogenesis.To functionally test this hypothesis, we ectopically modulated TWIST1 levels in TC-71 cells and evaluated their clonogenicity upon YK-4-279 treatment. Remarkably, overexpression of TWIST1 oncogene (Fig.5A) enhanced the clonogenic potential of TC-71 cells in the presence of YK-4-279 (Fig.5B). Particularly, clones generated by TWIST1overexpressing cells were still detectable at the highest YK-4-279 treatment (1 uM) and their number even overlapped those of the control pcDNA3.1 cultured with a YK-4-279 lower concentration (0.75 uM). Conversely, downregulation of TWIST1 expression by siRNA (Fig. 5C), increased ES cells sensitivity toward YK-4-279 treatment (Fig.5D).To further confirm our hypothesis, we measured the expression levels of HULC and TWIST1 in a pool of TC-71 cells which exhibit an increased resistance to YK-4-279 as shown by the significant rise of their IC 50 value and clonogenicity (Fig.5E and F). Importantly, YK-4279-resistant cells express high levels of both HULC lncRNA and TWIST1 protein, supporting the role of these two molecules in the YK-4-279-mediated chemoresistance (Fig.5G). According to their oncogenic role, most of the YK-4-279-sensitive lncRNAs identified by our initial array, were found to be upregulated in YK-resistant cells (Supplementary Fig. S3). In addition, the sensitivity of these cells to anti-cancer drugs currently used in ES therapy, such as vincristine and doxorubicin, was similar to that observed for parental control cells (Fig.5H). Remarkably, YK-resistant cells showed higher sensitivity to etoposide treatment, suggesting potential combination therapies to counteract YK-4-279 resistance (Fig. 5H).	31639426	RID07615	ceRNA or sponge	chemoresistance,prognosis		UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	LINC00470	ILF2	interact	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000132204	GRCh38_18:1254383-1408344	ENSG00000143621	NA	56651	3608	C18orf2	NF45	LncRNA LINC00470 promotes proliferation through association with NF45/NF90 complex in hepatocellular carcinoma.To understand the functional roles of LINC00470 in HCC progression, we first determined the LINC00470 expression in the immortalized normal liver cell line LO2 and six different HCC cell lines (Hep3B, SK-Hep-1, SMMC-7721, Huh7, PLC/PRF/5 and HepG2) via qRT-PCR The results demonstrated that the LINC00470 expression was much higher in all HCC cell lines than that in LO2 cells (Fig. 1a).To gain insight into the mechanism of LINC00470mediated proliferation promotion, we performed the flow cytometry to determine the effect of LINC00470 on cell apoptosis and cell cycle distribution. Neither overexpression nor knockdown of LINC00470 affected HCC cell apoptosis (data not shown). Depletion of LINC00470 resulted in an increase in the G1 population, and a decrease in S-phase population in Hep3B cells (Fig. 2g). In contrast, overexpression of LINC00470 significantly triggered G1/S-transition in SMMC-7721 cells (Fig. 2h). These results indicate that LINC00470 positively regulate HCC cell proliferation via promoting cell cycle progression.Recent studies have demonstrated that lncRNAs interact with specific proteins to exert their function [14]. To reveal the regulatory mechanism of LINC00470, a biotin RNA pull-down assay followed by mass spectrometry analysis was conducted to identify LINC00470-binding proteins (Supplemental Fig. 1). We found that NF45 and NF90 was the most enriched LINC00470-interacting partner. RNA pull-down assay validated that both NF45 and NF90 were enriched in Hep3B cell lysates pulled down by LINC00470 (Fig. 3a). For further confirmation, we performed an RIP assay using NF45 and NF90 antibodies. The results showed that LINC00470 was significantly pulled down by NF45 and NF90 antibodies compared to negative control IgG (Fig. 3b). Additionally, depletion of LINC00470 significantly attenuated the interaction of LINC00470 with NF45 and NF90 in Hep3B cells (Fig. 3c), while ectopic expression of LINC00470 significantly enhanced this interaction in SMMC-7721 cells (Fig. 3d). However, knockdown or overexpression of LINC00470 did not affect the protein expression of NF45 and NF90 (Fig. 3e), and neither NF45 nor NF90 silence influenced the LINC00470 expression (Fig. 3f).To validate whether LINC00470-mediated cyclin E1 upregulation contributed to its promotion on HCC cell proliferation, rescue experiments were performed. We silenced cyclin E1 expression in LINC00470-overexpressed SMMC-7721 cells (Fig. 5a). Strikingly, the results revealed that depletion of cyclin E1 partially abolished the LINC00470-induced cell proliferation and cell cycle progression (Fig. 5b, c). These results indicate that cyclin E1 is a bona fide functional target of LINC00470 in HCC.	31612313	RID07616	expression association	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Hepatocellular carcinoma	LINC00470	ILF3	interact	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000132204	GRCh38_18:1254383-1408344	ENSG00000129351	NA	56651	3609	C18orf2	DRBP76|MPHOSPH4|MPP4|MPP4110|NF110|NF110b|NF90|NF90a|NF90c|NF90ctv|NFAR-1|NFAR-2|NFAR110|NFAR90|TCP110	LncRNA LINC00470 promotes proliferation through association with NF45/NF90 complex in hepatocellular carcinoma.To understand the functional roles of LINC00470 in HCC progression, we first determined the LINC00470 expression in the immortalized normal liver cell line LO2 and six different HCC cell lines (Hep3B, SK-Hep-1, SMMC-7721, Huh7, PLC/PRF/5 and HepG2) via qRT-PCR The results demonstrated that the LINC00470 expression was much higher in all HCC cell lines than that in LO2 cells (Fig. 1a).To gain insight into the mechanism of LINC00470mediated proliferation promotion, we performed the flow cytometry to determine the effect of LINC00470 on cell apoptosis and cell cycle distribution. Neither overexpression nor knockdown of LINC00470 affected HCC cell apoptosis (data not shown). Depletion of LINC00470 resulted in an increase in the G1 population, and a decrease in S-phase population in Hep3B cells (Fig. 2g). In contrast, overexpression of LINC00470 significantly triggered G1/S-transition in SMMC-7721 cells (Fig. 2h). These results indicate that LINC00470 positively regulate HCC cell proliferation via promoting cell cycle progression.Recent studies have demonstrated that lncRNAs interact with specific proteins to exert their function [14]. To reveal the regulatory mechanism of LINC00470, a biotin RNA pull-down assay followed by mass spectrometry analysis was conducted to identify LINC00470-binding proteins (Supplemental Fig. 1). We found that NF45 and NF90 was the most enriched LINC00470-interacting partner. RNA pull-down assay validated that both NF45 and NF90 were enriched in Hep3B cell lysates pulled down by LINC00470 (Fig. 3a). For further confirmation, we performed an RIP assay using NF45 and NF90 antibodies. The results showed that LINC00470 was significantly pulled down by NF45 and NF90 antibodies compared to negative control IgG (Fig. 3b). Additionally, depletion of LINC00470 significantly attenuated the interaction of LINC00470 with NF45 and NF90 in Hep3B cells (Fig. 3c), while ectopic expression of LINC00470 significantly enhanced this interaction in SMMC-7721 cells (Fig. 3d). However, knockdown or overexpression of LINC00470 did not affect the protein expression of NF45 and NF90 (Fig. 3e), and neither NF45 nor NF90 silence influenced the LINC00470 expression (Fig. 3f).To validate whether LINC00470-mediated cyclin E1 upregulation contributed to its promotion on HCC cell proliferation, rescue experiments were performed. We silenced cyclin E1 expression in LINC00470-overexpressed SMMC-7721 cells (Fig. 5a). Strikingly, the results revealed that depletion of cyclin E1 partially abolished the LINC00470-induced cell proliferation and cell cycle progression (Fig. 5b, c). These results indicate that cyclin E1 is a bona fide functional target of LINC00470 in HCC.	31612313	RID07617	expression association	NA	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	TTN-AS1	KLF15	positively-E	luciferase reporter assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-376a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000163884	NA	100506866	28999	NA	KKLF	LncRNA TTN-AS1 sponges miR-376a-3p to promote colorectal cancer progression via upregulating KLF15.For the purpose of investigating the role of TTN-AS1 in CRC, we detected the expression levels of TTN-AS1 in colorectal tumor tissues and adjacent normal ones from 40 patients. As evident from Fig. 1A, a significant increased expression level of TTN-AS1 was observed in tumor tissues, compared with matched normal ones.In order to explore the function of TTN-AS1 in CRC progression, we knockdowned the expression of TTN-AS1 in SW480 and Lovo cell lines (Fig. 2A). Thereafter, cell proliferation, apoptosis and invasion ability were detected. As shown in Fig 2B-C, TTN-AS1 knockdown inhibited CRC cell viability and colony ability. Consistent result was found in the analysis of cell apoptosis. The apoptotic rate of CRC cells was increased upon TTN-AS1 knockdown (Fig 2D). Additionally, a significant decreased number of invasion cells was observed with si-TTN-AS1 transfection (Fig. 2E).Increase evidence revealed that lncRNAs act as ceRNAs for corresponding miRNAs. Thus, we predicted miR-376a-3p as the target of TTM-AS1 by informatics tools (Fig. 3A), which was verified by dual-luciferase reporter assay (Fig. 3B). Subsequently, qPCR analysis showed that knockdown of TTN-AS1 upregulated miR-376a-3p in CRC cell lines (Fig. 3C). Furthermore, the expression profile of miR -376a -3p in vivo was also determined. As shown in Fig. 3D, lowly expression level was observed in CRC tumor tissues, in comparison with that in normal tissues. Pearson correlation analysis revealed that there was a negative correlation between TTN-AS1 and miR - 376a -3p (Fig. 3E).MicroRNAs are known to function by base-pairing with 3 '-UTR of targeted mRNAs. We predicted the target gene using TargetScan software, and the predicted binding sites between miR -376a -3p and target mRNA KLF15 were shown in Fig. 5A. Subsequently, luciferase reporter assay confirmed the prediction (Fig. 5B). western blot was also performed and the result showed that the protein expression level of KLF15 was downregulated with the transfection of miR 376a 3p mimics (Fig. 5C). - - Furthermore, the expression profile of KLF15 in vivo was detected. As demonstrated in Fig. 5D, KLF15 expression was markedly upregulated in CRC tissues, in comparison with that in normal ones (Fig. 5D). Additionally, Pearson correlation analysis showed that miR-376a-3p and KLF15 exhibited a negative correlation (Fig. 5E).To further investigate the underlying mechanism, we wanted to detect whether TTN-AS1 regulated KLF15 via miR-376a-3p. QPCR and western blot assays demonstrated that knockdown of TTN-AS1 inhibited the expression of KLF15 both in mRNA and protein levels, and miR-376a-3p inhibitor mitigated the alterations (Fig. 6A-C). Moreover, Pearson correlation analysis revealed that TTN-AS1 expression had a positive correlation with KLF15 (Fig. 6D).For the purpose to verify the oncogenic role of TTN-AS1 on CRC tumor growth, Lovo cells transfected with sh-TTN-AS1 or sh-NC were injected into mice. Results showed that tumors originated from sh-TTN-AS1 mice were smaller (Fig. 7A) and lighter (Fig. 7B) than those from sh-NC group. Additionally, the proliferation marker, Ki-67, was downregulated in the tumors with sh-TTN-AS1 transfection (Fig. 7C).	31610194	RID07618	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Breast cancer	LINC02582	CHEK1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	ceRNA(miR-200c)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000261780	GRCh38_18:73324941-73349879	ENSG00000149554	NA	100505817	1111	CTD-2354A18.1	CHK1	Long noncoding RNA LINC02582 acts downstream of miR-200c to promote radioresistance through CHK1 in breast cancer cells.To investigate whether miR-200c regulates the expression of LINC02582, we suppressed miR-200c expression in MCF-7 and BT474 cells, which led to a significant increase in LINC02582 expression (Fig. -(Fig.2c).2c). Conversely, ectopic expression of miR-200c resulted in a significant reduction in LINC02582 in MDA-MB-231 and BT549 cells (Fig. -(Fig.2d).2d). However, we found no significant difference in miR-200c expression between LINC02582 knockdown or overexpression cells (Supplementary Fig. 2a). Subsequently, TargetScan and miRBase predicted the existence of interactions between miR-200c and LINC02582 (Fig. -(Fig.2e).2e). To confirm the binding between LINC02582 and miR-200c, we performed dual-luciferase assays, which showed that miR-200c decreased the luciferase activity of the wild-type LINC02582 vector, but not that of the mutant LINC02582 vector (Fig. -(Fig.2f).2f). MiRNAs are known to bind their targets and cause translational repression or RNA degradation in an AGO2-dependent manner. To test whether miR-200c regulates LINC02582 in such a manner, we conducted an RNA immunoprecipitation (RIP) experiment in MDA-MB-231 cells using anti-AGO2 antibodies. The results showed that LINC02582 and miR-200c were enriched in AGO2 immunoprecipitates relative to IgG immunoprecipitates, which confirmed direct binding between miR-200c and LINC02582 (Fig. 2g, h). Moreover, ectopic expression of miR-200c shortened the half-life of LINC02582 (Fig. -(Fig.2i).2i). Finally, qRT-PCRrevealed a negative correlation between miR-200c and LINC02582 expression in 42-paired samples of breast cancer tissue (Fig. -(Fig.2j).2j). These results indicated that LINC02582 is a target of miR-200c.To confirm the association between miR-200c, LINC02582, and CHK1 in breast cancer specimens, we performed ISH or IHC to examine the expression of these molecules in 136 breast cancer tissue samples from patients with breast cancer who had received radiotherapy (Fig. -(Fig.6g).6g). Decreased expression of miR-200c was associated with elevated CHK1 expression. However, a positive correlation between the expression of LINC02582 and CHK1 was observed in these breast cancer specimens. Briefly, 72.6% (53/73) of the tumors with low miR-200c expression exhibited high CHK1 expression, and 77.4% (55/71) of the tumors with high LINC02582 expression showed high CHK1 expression (Fig. -(Fig.6h).6h). Neither clinical or pathological characteristics were correlated with the expression of LINC02582 (Supplementary Table 4). Kaplan-Meier analysis showed that patients with low miR-200c expression had significantly worse recurrence-free survival and patients with high LINC02582 expression exhibited worse recurrence-free survival (Fig. 6i, j).To evaluate the biological functions of LINC02582, we inhibited its expression in MDA-MB-231 and BT549 cells (Fig. -(Fig.3a),3a), which had no effect on the viability of the breast cancer cells (Supplementary Fig. 2b). Interestingly, inhibition of LINC02582 expression reduced the surviving fraction of MDA-MB-231 and BT549 cells after irradiation (Fig. -(Fig.3b).3b). Conversely, overexpression of LINC02582 increased the surviving fraction of MCF-7 and BT474 cells after irradiation (Fig. 3c, d). Furthermore, LINC02582 silencing led to persistence of -Gamma-H2AX foci in MDA-MB-231 cells and BT549 cells at 24-h after irradiation (Fig. 3e, f, Supplementary Fig. 2c, d). LINC02582 silencing also markedly increased -Gamma-H2AX expression after irradiation. (Fig. -(Fig.3g,3g, Supplementary Fig. 2e). These results indicated that silencing of LINC02582 enhanced the radiosensitivity of breast cancer cells. To further investigate the effects of LINC02582 in vivo, MDA-MB-231 cells with LINC02582 knockdown were used to create a xenograft model (Supplementary Fig. 2f). When the tumor volume reached 150-mm3, local tumor irradiation was performed using a 2-Gy fractionated dose every other day for 10 days (Fig. -(Fig.3i).3i). Knockdown of LINC02582 had no effect on the growth of non-irradiated tumors, but caused tumor growth inhibition after irradiation (Fig. 3j, k). Taken together, these results demonstrated that silencing of LINC02582 enhanced the radiosensitivity of breast cancer cells both in vitro and in vivo.	31601781	RID07619	ceRNA or sponge	recurrence		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE67939)
Osteosarcoma	TTN-AS1	MBTD1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell growth(+);chemoresistance(+);	ceRNA(miR-134-5p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000011258	NA	100506866	54799	NA	FLJ20055|SA49P01	LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis.Bioinformatics analysis revealed that lncRNA TTN-AS1 was upregulated in osteosarcoma (Figure 1A). Clinical sample test results also showed that lncRNA TTN-AS1 was highly expressed in tumour tissues (2.08   2.45 vs. 1.00   0.02) (Figure 1B). Overexpression of lncRNA TTN-AS1 was also present in osteosarcoma cell lines (5.09   0.94 and 3.47   1.04 vs. 1.00   0.14) (Figure 1C). The predicted results from the bioinformatics analysis showed that lncRNA TTN-AS1 targeted miR-134-5p (Figure 3A). Clinical sample test results showed that miR-134-5p was expressed at low levels in osteosarcoma (0.52   0.41) (Figure 3B). Further experimental results showed that upregulation of lncRNA TTN-AS1 inhibited the expression of miR-134-5p, and downregulation of lncRNA TTN-AS1 gave the opposite results (Figure 3C'-D). Promotion or inhibition of miR-134-5p expression had no significant effects on lncRNA TTN-AS1 (Figure 3E'-F). Furthermore, the mutated lncRNA TTN-AS1 did not cause changes in the level of miR-134-5p (Figure 3G'-H). This indicated that lncRNA TTN-AS1 could be a target to regulate the level of miR-134-5p.The TargetScan website was used to predict the target gene of miR-134-5p (Figure 4A). The luciferase assay demonstrated that miR-134-5p targeted the 3'-UTR region of MBTD1 (Figure 4B, -,4C).4C). Further studies also showed that compared with the inhibitor-NC group, inhibition of miR-134-5p levels could upregulate MBTD1 mRNA and protein levels (Saos-2: 3.14   0.67 and 1.98   0.55; U-2OS: 2.21   0.13 and 2.07   0.57) (Figure 4D'-H). This indicated that miR-134-5p can directly target MBTD1.The cell viability of the osteosarcoma cell lines Saos-2 and U2OS treated with different concentrations of cisplatin was examined. The cell viability decreased by approximately 50% when the concentration of cisplatin was 10 uM (Figure 7A'-B). The relative cell viability of the sh-TTN-AS1 group (Saos-2: 0.27   0.02; U-2OS: 0.15   0.01) was significantly lower than that of the sh-NC group (Saos-2: 0.46   0.04; U-2OS: 0.45   0.05) in the presence of 10 uM cisplatin (Figure 7C'-D). The relative cell viability of the vector-TTN-AS1 group (Saos-2: 0.96   0.47; U-2OS: 0.78   0.30) was significantly higher than that of the sh-NC group (Saos-2: 0.75   0.02; U-2OS: 0.51   0.03) in the presence of 10 uM cisplatin (Figure 7E'-F). Upregulation of lncRNA TTN-AS1 partially reverses the inhibitory effect of cisplatin on cells.	31600142	RID07620	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	CASC15	miR-130b-3p	negatively-F	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p.RT-qPCR was conducted for detecting CASC15 expression in 55 patients'-tissues and four NSCLC cell lines. CASC15 was significantly upregulated in tumor tissue samples than that in adjacent tissues (Figure 1A). In addition, CASC15 level was significantly higher in NSCLC cells than that in 16HBE (Figure 1B). Results of CCK8 assay suggested that the cell growth ability of NSCLC cells was inhibited after CASC15 was knocked down (Figure 2B). Then, the results of wound healing assay showed that the migrated length of NSCLC cell was inhibited by knockdown of CASC15 (Figure 2C). In addition, the results of the transwell assay showed that the number of invaded NSCLC cells was reduced after CASC15 was knocked down (Figure 2D).We used DIANA LncBASE Predicted v.2 to predict potential target microRNAs of CASC15. MiR-130b-3p was one of those predicted microRNAs which was reported to suppress tumorigenesis in many tumors. The binding area of CASC15 by miR-130b-3p was shown in Figure 3A. Moreover, miR-130b-3p was upregulated in CASC15/ shRNA group compared with NC group (Figure 3B). Furthermore, the results of luciferase assay showed that luciferase activity was significantly reduced through co-transfection of CASC15-WT and miR-130b-3p, while no significant changes of luciferase activity were observed through co-transfection of CASC15-MUT and miR-130b3p (Figure 3C).The ability of CASC15 in tumor formation and metastasis was detected in vivo. The tumor size in CASC15/shRNA group was smaller compared with NC group (Figure 4A). The number of metastatic nodules in the lung of the CASC15/shRNA group was significantly reduced compared with NC group (Figure 4B). Moreover, the expression level of CASC15 and miR-130b-3p in dissected tumor tissues was detected by RT-qPCR. The results showed that CASC15 was lower-expressed in CASC15/shRNA group compared with NC group (Figure 4C), while miR-130b-3p was higher-expressed in CASC15/shRNA group compared with NC group (Figure 4D).	31599419	RID07621	ceRNA or sponge	metastasis	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Prostate cancer	TTN-AS1	miR-193a-5p	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000237298	GRCh38_2:178521183-178779963	NA	NA	100506866	NA	NA	NA	Long non-coding RNA TTN-AS1 promotes cell proliferation and inhibits cell apoptosis in prostatic cancer by sponging miR-193a-5p.To explore the roles of TTN-AS1 and miR193a-5p in PCa, the relative expression of TTNAS1 and miR-193a-5p was measured by qRTPCR. The results showed that TTN-AS1 was notably increased in prostatic cancer cells DU145, PC3, 22RV1, C4-2B, and LNCaP cells related to that in prostate epithelial cells RWPE-1 cells (Figure 1A). While the level of miR-193a-5p exhibited the opposite trends in PCa cells (Figure 1B). These results indicated that lncRNA TTN-AS1 was remarkably elevated and miR-193a-5p was conspicuously reduced in PCa cells.Since CyclinD117 was proliferation-related protein and p2118, p2719 were cell-cycle-arrest-related proteins, we further detect the protein levels of CyclinD1, p21, and p27 in si-TTN-AS1-transfected DU145 and PC3 cells. western blot results exhibited that the protein level of CyclinD1 was decreased and the protein levels of p21, p27 were increased in DU145 and PC3 cells transfected with si-TTN-AS1 (Figure 2D-F). Taken together, these data implicated that TTN-AS1 knockdown suppressed cell proliferation in DU145 and PC3 cells.To illustrate the biological mechanism of TTNAS1 in PCa, the putative target of TTN-AS1 was predicted by starBase v2.0 online database. The results presented that miR-193a-5p had complementary sequences with TTN-AS1 (Figure 5A). Meanwhile, the qRT-PCRresults showed that the level of miR-193a-5p was distinctly down-regulated in pcDNA-TTN-AS1-transfected DU145 and PC3 cells, while exhibited the opposite trend in siTTN-AS1 group (Figure 5B). Following dual-luciferase reporter assay indicated that the transfection of miR-193a-5p strikingly down-regulated the luciferase activity of WT-TTN-AS1 reporter, while the luciferase activity of MUT-TNN-AS1 had no significant change in any group (Figure 5C and D). These results implied that miR-193a5p was negatively interacted with TTN-AS1.However, the cell apoptosis rate showed the opposite trend compared with the results of cell viability (Figure 6H). In addition, the western blot results exhibited that anti-miR-193a-5p alleviated the repressive effect on the protein levels of CyclinD1, Bcl-2, and the promotion effects on the protein levels of p21, Bax induced by si-TTNAS1 in DU145 and PC3 cells (Figure 6D-G and I-L). Taken together, these data revealed that miR193a-5p inhibitor counteracted the inhibitory effect on cell proliferation and the promotion effect on cell apoptosis in DU145 and PC3 cells induced by si-TTN-AS1.	31599406	RID07622	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	LINC00974	CDK6	positively-E	overexpression;knockdown;siRNA	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	ENSG00000105810	NA	147093	1021	NA	PLSTIRE	LncRNA LINC00974 Upregulates CDK6 to Promote Cell Cycle Progression in Gastric Carcinoma.Expression levels of LINC00974 and CDK6 mRNA in both nontumor and GC tissues were measured by qPCR and compared by pairedt-test. Comparing with nontumor group, expression levels of LINC00974 (Fig. 1A) and CDK6 mRNA (Fig. 1B) were significantly higher in GC group (p<0.05). AGS cells were transfected with LINC00974 and CDK6 expression vectors as well as LINC00974 siRNA. Expression levels of LINC00974 and CDK6 mRNA were measured by qPCR. Comparing with two controls (C and NC), expression levels of LINC00974 and CDK6 mRNA were significantly altered at 24h post-transfection (Fig. 3A, p<0.05). Moreover, LINC00974 overexpression led to upregulated, whereas LINC00974 siRNA silencing led to downregulated CDK6 at both mRNA and protein levels (Fig. 3B,p<0.05). However, CDK6 overexpression failed to affect LINC00974 expression.The effects of LINC00974 and CDK6 overexpression as well as LINC00974 siRNA silencing on AGS cell progression and proliferation were analyzed by cell cycle assay and cell proliferation assay, respectively. Comparing with NC and C groups, LINC00974 overexpression promoted and siRNA silencing inhibited G1-S transition (Fig. 4A, p<0.05; reflected by the percentage of cells at G1 and G2 phases) and cell proliferation (Fig. 4B,p<0.05). In addition, CDK6 overexpression attenuated the effects of LINC00974 overexpression (p<0.05).	31596614	RID07623	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Non-small cell lung cancer	LINC00243	PDK4	positively-E	luciferase reporter assay;RNA pull-down assay;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);glycolysis(+)	ceRNA(miR-507)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229170	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30843303-30875311	ENSG00000004799	NA	401247	5166	bQB10J12.2|bQB230F21.2|C6orf214|FLJ40693|NCRNA00243	NA	Long non-coding RNA LINC00243 promotes proliferation and glycolysis in non-small cell lung cancer cells by positively regulating PDK4 through sponging miR-507.To explore the potential role of LINC00243 in NSCLC, we first analyzed LINC00243 expression in normal lung tissues (Normal) and lung cancer tissues (Tumor) in the TCGA database. As shown in Fig. 1a, LINC00243 expression level was about two-fold in Tumor group when compared to Normal group. Similarly, LINC00243 expression level significantly elevated to 3 to 15 folds in NSCLC cell lines (NCI-H1650, SK-MES-1, A549, SPC-A-1, H460 and H1299) compared with normal bronchial epithelial cell line BEAS-2B (Fig. 1b).The cell proliferation detected by CCK8 assay decreased to around 75% of sh-CTR in both A549 and H1299 cells after LINC00243 down-regulation (Fig. 2b, c). Colony formation assays showed in Fig. 2d indicated that LINC00243 downregulation dramatically inhibited NSCLC cell proliferation to 30'-0% of sh-CTR. Consistently, apoptosis levels of A549 and H1299 cells that assessed by relative caspase-3 activity significantly enhanced two to threefolds in LINC00243 shRNAs stably transfected NSCLC cells compared with sh-CTR (Fig. 2e).To explore the mechanism of how LINC00243 plays important roles in NSCLC cells, we first predicted miR-507 as the potential miRNA associated with LINC00243 function through miRcode (http://www.mirco de.org/mirco de/). In addition, the binding sites between LINC00243 and miR507 (LINC00243 wt) were predicted by RNAhybrid (https ://bibis erv.cebit ec.uni-biele feld.de/rnahy brid). Furthermore, the mutated binding sites between LINC00243 and miR-507 (LINC00243 mt) were established (Fig. 3a). The relative luciferase activity in A549 cells that co-transfected with miR-507 and LINC00243 wt is deceased more than two-fold compared to that co-transfected with miR-NC and LINC00243 wt. However, no difference of luciferase activity was observed when the cell was transfected with LINC00243 mt (Fig. 3b). Similar results were certified in another H1299 cell line (Fig. 3c), indicating the interaction between LINC00243 and miR-507. Next, the correlation between LINC00243 and miR-507 were further determined. In LINC00243 knockdown A549 and H1299 cells, miR-507 expression levels enhanced three to sixfolds compared with sh-CTR (Fig. 3d). Consistently, LINC00243 overexpression (pSin-LINC00243) suppressed miR-507 expression around two-fold in both cell lines (Fig. 3e). RNA pull-down assay showed that antisense DNA probe against LINC00243 could enrich LINC00243 and miR-507 mRNA expression three to sixfolds in A549 and six to eightfolds in H1299 cell lines (Fig. 3f and g), suggesting the interaction between LINC00243 and miR-507. The expression level of miR-507 in the 70 collected Tumor group is almost half compared to the matched Normal group (Fig. 3h). As expected, in 70 NSCLC tissues, LINC00243 expression is negatively correlated with miR507 expression (Fig. 3i). All the data demonstrated that LINC00243 acted as a molecular sponge for miR-507.We next verified the potential target of miR-507 through targetscan (http://www.targe tscan .org/vert_71/). As shown in Fig. 5a, pyruvate dehydrogenase kinase 4 (PDK4) was the predicted target of miR-507, and the binding sites (PDK4 3'UTR(WT)) and mutated binding sites (PDK4 3'UTR(MT)) between miR-507 and PDK4 were illustrated. In the A549 cell line, co-transfected with miR507 and PDK4 3'UTR(WT) inhibited relative luciferase activity to 30% when compared with that co-transfected with miR-NC and PDK4 3'UTR(WT) (Fig. 5b).Similarly, on protein level, miR-507 mimics inhibited, while miR-507 inhibitor enhanced PDK4 expression level (Fig. 5f). More importantly, in A549 and H1299 cells lines, the enhanced mRNA and protein levels of PDK4 after LINC00243 overexpression was dramatically inhibited by miR-507 mimics administration (Fig. 5g, h). These data indicated that LINC00243 regulated endogenous miR-507-targeted PDK4 expression.	31595421	RID07624	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE86978)
Papillary thyroid carcinoma	RPL34-DT	RGS4	positively-E	luciferase reporter assay;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-3663-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000234492	GRCh38_4:108538190-108620460	ENSG00000117152	NA	285456	5999	FLJ37673|RP11-462C24.1|RPL34-AS1	SCZD9	lncRNA RPL34-AS1 inhibits cell proliferation and invasion while promoting apoptosis by competitively binding miR-3663-3p/RGS4 in papillary thyroid cancer.In our study, we found that RPL34-AS1 expression is obviously higher in thyroid tissues than in other organ tissues (such as the heart, liver, spleen, lung, kidney, and brain; Figure 2a). We used qRT-PCRanalysis to examine the RPL34-AS1 expression in 77 PTC and adjacent normal tissues, and RPL34-AS1 expression was significantly downregulated in the PTC tissues compared with that in normal tissues (Figure 2b). To investigate the functional effects of RPL34-AS1 in PTC, we conducted the following in vitro assays, including a proliferation assay, Transwell invasion assays, and western blot. The overexpression of RPL34-AS1 was carried out by transfecting cells with a RPL34-AS1 overexpressing vector (pcDNA3.1-RPL34-AS1; Figure 3a). Our results showed that RPL34-AS1 overexpression significantly suppressed K1 and KTC-1 cell proliferation (Figure 3b), reduced the invaded cells number (Figure 3c), and promoted apoptosis of the K1 and KTC-1 cells (Figure 3d) compared with the transfection of empty vector groups.As lncRNAs have been found to interact with microRNAs, the miRNAs interacted with RPL34-AS1 were predicted using starBase software, and we revealed that miR-3663-3p was a potential binding site of RPL34-AS1. As shown in Figure 4a,RPL34-AS1 has a potential miR-3663-3p binding sequence. To further confirm that RPL34-AS1 binds miR-3663-3p, a dual-luciferase reporter assay was conducted using HEK 293 cells. The effect of miR-3663-3p overexpression by mimics is shown in Figure 4b. In the RPL34-AS1 transfection group, after transfection with the miR-3663-3p mimic, the relative luciferase activity was significantly decreased compared with the mimic NC siRNA groups (RPL34-AS1 + NC siRNA group), while the luciferase activity significantly elevated after transfection with the miR-3663-3p inhibitor (Figure 4c). After the RPL34-AS1'-'-UTR-mut group was treated with the miR-3663-3p mimic or miR-3663-3p inhibitor, the results indicated that there was no significant difference in relative luciferase activity between the RPL34-3'-UTR- mut and RPL34-AS1'-'-UTR-mut + mimic NC or control inhibitor groups. To further confirm this result, we conducted qRT-PCRto detect miR-3663-3p mRNA levels. As shown in Figure 4d, overexpression of RPL34-AS1 reduced the mRNA levels of miR-3663-3p, whereas knockdown of RPL34-AS1 upregulated the mRNA levels of miR-3663-3p. In addition, miR-3663-3P expression was significant higher in PTC tissues than that in normal tissues (Figure 4e), the correlation analysis indicates that RPL34-AS1 is negatively correlated with miR-3663-3p in K1 cells (Figure 4f).The results showed that the mRNA transcribed by RLuc-RGS4-3'-UTR-WT existed the miR-3663-3p binding sites with RGS4 while the mRNA transcribed by RLuc-RGS4-3'-UTR-MT was short of the predicted binding site (Figure 6b). To further confirm that miR-3663-3p indeed interacted with RGS4, we incubated miR-3663-3p and an control RNA with K1 and KTC cells cell lysates, and then conducted pull-down experiment to confirm. As shown in Figure 6c,d RGS4 interacted with miR-3663-3p, not with control RNA or beads alone. Next, we conducted RIP using a RGS4 antibody. The anti-RGS4 antibody, rather than the control antibody, successfully pulled down miR-3663- 3P detected by PCR. Further, we also found that miR-3663-3p can negatively regulate RGS4 expression via qPCR and western blot (Figure 6e).To further investigated the mechanism of RPL34-AS1 in PTC cells, Transwell and proliferation assay and apoptosis analysis were performed to confirm whether miR-3663-3p and RGS4 involved the role of RPL34-AS1. Transwell and CCK-8 assay results showed that overexpression of miR-3663-3p could block the inhibitory effect of RPL34-AS1 on K1 and KTC-1 cell invasion and proliferation, while the effect of miR-3663-3p could be reversed by overexpression of RGS4 (Figure 7a,b).Consistent with the above results, western blotdemonstrated that the enhancing apoptosis effect of RPL34- AS1 in K1 and KTC-1 cells was partially reversed by overexpressing miR-3663-3p, besides, overexpression of RGS4 could inhibit the effect of miR-3663-3p and restore the antiapoptotic effect of RPL34-AS1 (Figure 7c).	31587286	RID07625	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Breast cancer	SNHG3	HDGF	positively-E	luciferase reporter assay;RIP;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000143321	NA	8420	3068	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	HMG1L2	LncRNA SNHG3 promotes cell proliferation and invasion through the miR-384/hepatoma-derived growth factor axis in breast cancer.First, we examined SNHG3 expression in 60 pairs of breast cancer tissues. qRT-PCR;ISHowed that SNHG3 expression was significantly higher in breast cancer tissues than in adjacent normal tissues (Fig. 1a).To explore the roles of SNHG3 in breast cancer tumourigenesis, MDA-MB-231 and MCF-7 cells were transfected with siSNHG3 and si-NC (Fig. 2a). The CCK-8 and colony formation assay results indicated that SNHG3 inhibition significantly reduced breast cancer cell proliferation and colony formation abilities (Fig. 2b, c). Transwell assays revealed that SNHG3 suppression significantly reduced breast cancer cell migration and invasion abilities (Fig. 2d). Furthermore, a tail vein injection experiment was adopted to explore the effect of SNHG3 knockdown on breast cancer cell metastasis in vivo. The results revealed that si-SNHG3 significantly reduced the number of lung metastatic nodules compared with si-NC (Fig. 2g). These results indicate that SNHG3 might play critical roles in breast cancer progression.To further explore the underlying molecular mechanism by which SNHG3 regulates breast cancer, we performed a bioinformatics prediction analysis and found that miR-384 was a potential candidate. Bioinformatics analysis showed that SNHG3 might interact with miR-384 (Fig. 3a). A dual-luciferase reporter assay showed that miR-384 mimic significantly reduced the luciferase activity of WT-SNHG3 in breast cancer cells (Fig. 3b). qRT-PCR;ISHowed that SNHG3 knockdown remarkably increased miR-384 expression in breast cancer cells (Fig. 3c). In addition, miR-384 expression was significantly decreased in breast cancer tissues and cell lines (Fig. 3d, e). A correlation analysis revealed that SNHG3 expression was negatively correlated with miR-384 expression in breast cancer tissues (Fig. 3f). Through starBase v2.0 Program prediction, 16 miRNAs were predicted as possible targets of SNHG3 (Supplementary Table S2). Among the 16 candidate miRNAs predicted by starBase, we screened and analysed miR-758-3p and miR-384, whose effects on breast cancer have been rarely reported. Next, we identified functional miRNAs that may interact with SNHG3 in breast cancer cells. RIP assays showed that SNHG3 and miR-384 (not miR-758-3p) expression was significantly enriched in the Ago2 pellet compared to that in the IgG control pellet (Fig. 3g). These data indicate that SNHG3 interacts with miR-384 and decreases its expression in breast cancer.To confirm the function of miR-384, we transfected miR384 mimic or NC mimic sequences into breast cancer cells. The CCK-8 and colony formation assay results indicated that miR-384 significantly reduced breast cancer cell proliferation and colony formation abilities (Fig. 4a, b). Transwell assays revealed that miR-384 significantly reduced breast cancer cell migration and invasion abilities (Fig. 4c). Bioinformatics analyses (TargetScan) revealed that HDGF is a potential target of miR-384 (Fig. 4d). To confirm HDGF as a direct target of miR-384, we engineered luciferase reporter constructs containing the WT or MUT 3'-UTR of the HDGF gene. The luciferase reporter assay showed that miR-384 significantly decreased the luciferase activity of the WTHDGF 3'-UTR but not that of the MUT-HDGF 3'-UTR in MDA-MB-231 and MCF-7 cells (Fig. 4e). Furthermore, qRT-PCRand western blotrevealed that miR-384 mimic transfection in MDA-MB-231 and MCF-7 cells led to a considerable reduction in both the mRNA and protein levels of HDGF (Fig. 4f, g).Next, a correlation analysis revealed that HDGF expression was positively correlated with SNHG3 expression in breast cancer tissues (Fig. 5b). Furthermore, CCK-8, colony formation and transwell assays showed that the miR-384 inhibitor significantly rescued the proliferation, colony formation, migration and invasion abilities induced by si-SNHG3 in breast cancer cells (Fig. 5c-e). In addition, we knocked down HDGF expression in breast cancer cells using shRNA (Fig. 5f). The results show that HDGF knockdown cancelled the effect of miR-384 downregulation with a miR-384 inhibitor. Compared to those in cells cotransfected with miR-384 inhibitor and sh-NC, cell proliferation, colony formation, migration, and invasion were significantly suppressed in cells cotransfected with miR-384 inhibitor and sh-HDGF (Fig. 5g). These results indicate that SNHG3 promotes breast cancer progression by regulating the miR-384/HDGF axis (Fig. 5j).	31586299	RID07626	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Gastric cancer	MEG3	ATP4B	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell growth(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000186009	NA	55384	496	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	ATP6B	Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer.Heat map analysis showed that MEG3 was downregulated among the top 20 differentially expressed lncRNAs in GC and adjacent normal tissues (Figure 1A). Additionally, ATP4B expression was reduced among the top 20 differentially expressed mRNAs between these tissues (Figure 1B). Expression values are represented in shades of red and green, which indicate high expression levels and low expression levels, respectively. All the results suggested that MEG3 and ATP4B were downregulated in GC patients.The luciferase reporter assay showed that the luciferase activity in the MEG3-wt group mimics + miR was lower than that in the NC group (Figure 3C, P<0.01). RNA pull-down experiments showed that MEG3 enrichment levels in the bio-miR-181a-5p, DMSO + bio-miR-181a-5p and 5-Aza groups were higher than those in the bio-NC group (Figure 3A, P<0.01). In Figure 3B, linear regression analysis showed that the expression of MEG3 was negatively correlated with the expression of miR-181a-5p. As shown in Figure 3G, the expression of miR-181a-5p in the MEG3 overexpression group was significantly lower than that in the NC group (P<0.01). In addition, the enrichment level of ATP4B in the inhibitor - miR group was higher than that that in the mimics - miR group (Figure 3E, P<0.05). Linear regression analysis by qRT-PCR;ISHowed that the expression of ATP4B was negatively correlated with miR-181a-5p (Figure 3F), and the expression level of ATP4B in the miR-181a-5p overexpression group was significantly lower than that in the NC group (Figure 3D). All the results showed that ATP4B and miR-181a-5p were negatively regulated.To investigate the effect of MEG3 on tumor growth, we transfected MGC-803 cells with MEG3 to observe tumor size and volume. The results showed that tumor weight and volume in the MEG3 group were lower than those in the Con group (Figure 5A'-C, P<0.01). Next, we studied the expression of ATP4B and miR-181a-5p after MEG3 transfection. The results showed that the expression of ATP4B was increased in the MEG3 group, while the expression of miR-181a-5p was decreased (Figure 5D'-E, P<0.01). Therefore, we demonstrated a negative correlation between MEG3 and miR-181a-5p and found that upregulation of MEG3 in vivo can inhibit tumor growth.	31584879	RID07627	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Oral squamous cell carcinoma	GAS5	GSK3	positively-E	dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell growth(-)	ceRNA(miR-1297)	regulation	NA	Propofol	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Mouth disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	GAS5, a FoxO1-actived long noncoding RNA, promotes propofol-induced oral squamous cell carcinoma apoptosis by regulating the miR-1297-GSK3beta axis.To explore the underlying mechanism of the suppressive effects of propofol on OSCC cells, UM-SCC6 cells were treated with 20-ug/ml propofol for the indicated times, and lncRNA expression profiles were then obtained by RNA sequencing analysis. The sequencing results revealed more than 51 upregulated and 83 downregulated genes in UM-SCC6 cells upon propofol treatment compared with control cells (Figure 2(A,B)). Among the altered lncRNAs, we found that GAS5 was significantly increased in response to propofol treatment (Figure 2(C)). To confirm this, UM-SCC6 and SCC090 cells were treated with propofol at different doses and times. Consistent with the RNA sequencing analysis, GAS5 was dramatically upregulated upon propofol treatment in OSCC cells (Figure 2(D)).GAS5 can act as a competing endogenous RNA (ceRNA) to regulate tumourigenesis [14]. A recent study indicated that GAS5 sponges miR-205 and suppresses miR-205 expression [18]. Thus, we asked whether GAS5 promotes propofol-induced OSCC cell apoptosis by binding microRNAs. Based on the RNA sequencing data, we found that miR-1297 was dramatically decreased in response to propofol treatment (Figure 3(A)). The bioinformatics analysis also suggested that GAS5 contains a potential binding region of miR-1297 (Figure 3(B)). To confirm this, we first examined the expression of miR-1297 in response to propofol treatment and found that propofol significantly reduced miR-1297 expression in OSCC cells (Figure 3(C)). However, the propofol-induced downregulation of miR-1297 was recovered by GAS5 knockdown in OSCC cells (Figure 3(D,E)). Then, RIP was performed on UM-SCC6 cell extracts using an antibody against Ago2 to test whether GAS5 could function as a miR-1297 sponge. The q-RT-PCRresults showed that GAS5 and miR-1297 were preferentially enriched in the anti-Ago2 immunoprecipitates compared with the IgG immunoprecipitates (Figure 3(F,G)). We next inserted the wild-type GAS5 or the mutated version downstream of the luciferase gene in the reporter plasmid for the luciferase assay (Figure 3(H)). Compared with the control group, the luciferase activity of the vector with wild-type GAS5 was notably inhibited by miR-1297, and the reduction was abolished when the binding site was mutated (Figure 3(I)). In contrast, the luciferase activity of the vector with GAS5 was notably increased in response to propofol treatment; however, the increase disappeared when miR-1297 was overexpressed (Figure 3(J)). Thus, these results indicate that GAS5 can act as a ceRNA of miR-1297 and inhibits its expression.Having identified that GAS5 promotes propofol-induced apoptosis via binding miR-1297, we next sought to investigate the downstream targets of miR-1297. Previous studies have indicated that propofol induces cell apoptosis by downregulating Bcl2 expression [19]. Thus, we asked whether the Bcl2 is also involved in propofol-induced OSCC cell apoptosis. To this end, we first detected the expression levels of Bcl2 family proteins Bcl2 and Mcl1 in response to propofol treatment. Interestingly, we found that Mcl1, but not Bcl2, was significantly decreased in UM-SCC6 cells upon propofol treatment. Additionally, phosphorylation of Mcl1 at ser 159 was increased in response to propofol treatment (Figure 4(A)). Increasing evidence has indicated that phosphorylation of Mcl1 at ser 159 plays an important role in Mcl1 stability [20,21]. To further validate that propofol affects Mcl1 protein stability, we treated the indicated cells with the protein synthesis inhibitor cycloheximide (CHX) together with or without propofol treatment. Notably, propofol decreased Mcl1 stability (Figure 4(B,C)).	31583913	RID07628	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Oral squamous cell carcinoma	FOXO1	GAS5	positively-E		downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell growth(-)	transcriptional regulation	binding/interaction	NA	Propofol	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Mouth disease	TF	lncRNA	ENSG00000150907	NA	ENSG00000234741	GRCh38_1:173858559-173868882	2308	60674	FKH1|FKHR|FOXO1A	NCRNA00030|SNHG2	GAS5, a FoxO1-actived long noncoding RNA, promotes propofol-induced oral squamous cell carcinoma apoptosis by regulating the miR-1297-GSK3beta axis.To explore the underlying mechanism of the suppressive effects of propofol on OSCC cells, UM-SCC6 cells were treated with 20-ug/ml propofol for the indicated times, and lncRNA expression profiles were then obtained by RNA sequencing analysis. The sequencing results revealed more than 51 upregulated and 83 downregulated genes in UM-SCC6 cells upon propofol treatment compared with control cells (Figure 2(A,B)). Among the altered lncRNAs, we found that GAS5 was significantly increased in response to propofol treatment (Figure 2(C)). To confirm this, UM-SCC6 and SCC090 cells were treated with propofol at different doses and times. Consistent with the RNA sequencing analysis, GAS5 was dramatically upregulated upon propofol treatment in OSCC cells (Figure 2(D)).GAS5 can act as a competing endogenous RNA (ceRNA) to regulate tumourigenesis [14]. A recent study indicated that GAS5 sponges miR-205 and suppresses miR-205 expression [18]. Thus, we asked whether GAS5 promotes propofol-induced OSCC cell apoptosis by binding microRNAs. Based on the RNA sequencing data, we found that miR-1297 was dramatically decreased in response to propofol treatment (Figure 3(A)). The bioinformatics analysis also suggested that GAS5 contains a potential binding region of miR-1297 (Figure 3(B)). To confirm this, we first examined the expression of miR-1297 in response to propofol treatment and found that propofol significantly reduced miR-1297 expression in OSCC cells (Figure 3(C)). However, the propofol-induced downregulation of miR-1297 was recovered by GAS5 knockdown in OSCC cells (Figure 3(D,E)). Then, RIP was performed on UM-SCC6 cell extracts using an antibody against Ago2 to test whether GAS5 could function as a miR-1297 sponge. The q-RT-PCRresults showed that GAS5 and miR-1297 were preferentially enriched in the anti-Ago2 immunoprecipitates compared with the IgG immunoprecipitates (Figure 3(F,G)). We next inserted the wild-type GAS5 or the mutated version downstream of the luciferase gene in the reporter plasmid for the luciferase assay (Figure 3(H)). Compared with the control group, the luciferase activity of the vector with wild-type GAS5 was notably inhibited by miR-1297, and the reduction was abolished when the binding site was mutated (Figure 3(I)). In contrast, the luciferase activity of the vector with GAS5 was notably increased in response to propofol treatment; however, the increase disappeared when miR-1297 was overexpressed (Figure 3(J)). Thus, these results indicate that GAS5 can act as a ceRNA of miR-1297 and inhibits its expression.Having identified that GAS5 promotes propofol-induced apoptosis via binding miR-1297, we next sought to investigate the downstream targets of miR-1297. Previous studies have indicated that propofol induces cell apoptosis by downregulating Bcl2 expression [19]. Thus, we asked whether the Bcl2 is also involved in propofol-induced OSCC cell apoptosis. To this end, we first detected the expression levels of Bcl2 family proteins Bcl2 and Mcl1 in response to propofol treatment. Interestingly, we found that Mcl1, but not Bcl2, was significantly decreased in UM-SCC6 cells upon propofol treatment. Additionally, phosphorylation of Mcl1 at ser 159 was increased in response to propofol treatment (Figure 4(A)). Increasing evidence has indicated that phosphorylation of Mcl1 at ser 159 plays an important role in Mcl1 stability [20,21]. To further validate that propofol affects Mcl1 protein stability, we treated the indicated cells with the protein synthesis inhibitor cycloheximide (CHX) together with or without propofol treatment. Notably, propofol decreased Mcl1 stability (Figure 4(B,C)).	31583913	RID07629	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)
Hepatocellular carcinoma	MIR4435-2HG	EZH2	interact	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000106462	NA	541471	2146	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	ENX-1|EZH1|KMT6|KMT6A	LINC00978 promotes the progression of hepatocellular carcinoma by regulating EZH2-mediated silencing of p21 and E-cadherin expression.We first analyzed the expression levels of LINC00978 in human HCC tissues using the microarray data downloaded from GEO (GSE64041). The results showed that LINC00978 expression level was upregulated in HCC tissues compared with the parenchymal normal tissues (Fig. -(Fig.1a).1a). To validate the findings of GEO data analysis, we examined LINC00978 expression in a cohort of 33 paired HCC and adjacent non-cancerous tissues by using qRT-PCR Consistently, the expression level of LINC00978 was also significantly upregulated in HCC issues compared with the paired non-cancerous tissues (P-<-0.001, Fig. -Fig.1b).1b). Moreover, five cell lines including one normal liver epithelial cell line 7702 and 4 HCC cell lines (7721, 7402, HepG2, LM3) were detected for LINC00978 expression. The expression levels of LINC00978 in 7721, 7402, HepG2, and LM3 cells were significantly higher than that in 7702 cells (Fig. -(Fig.1c).1c).The increased expression of LINC00978 in HCC led us to hypothesize that LINC00978 might function as an oncogene in HCC. To this end, we knocked down LINC00978 expression in HCC cells by using shRNA. The knockdown efficiency was verified by using qRT-PCR(Fig. -(Fig.2a).2a). The results of cell counting assay showed that LINC00978 knockdown inhibited HCC cell proliferation (Fig. -(Fig.2b),2b), which was further confirmed by the results of colony formation assays (Fig. -(Fig.2c).2c). In addition, HCC cells transfected with LINC00978 shRNA had decreased S phase and increased apoptosis (Fig. 2d, e). Moreover, the expression levels of Bcl-2 and Cyclin D1 genes and proteins were decreased in LINC00978 shRNA transfected HCC cells (Fig. 2f, g). The number of migrated and invaded cells was decreased in sh-LINC00978 group compared with that in control group (Fig. 2h, i). The expression of epithelial marker E-cadherin was increased while that of mesenchymal markers N-cadherin and Vimentin was decreased in LINC00978 knockdown cells. In addition, the expression of EMT transcription factors including slug, snail, and twist was significantly downregulated in sh-LINC00978 transfected cells (Fig. 2j, k).We next wanted to know the importance of EZH2 to the oncogenic roles of LINC00978 in HCC. We overexpressed LINC00978 and knocked down EZH2 in HCC cells simultaneously (Fig. -(Fig.5a).5a). The results of cell counting and colony formation assays showed that the proliferation of HepG2 cells with LINC00978 overexpression and EZH2 knockdown was decreased compared with that of HepG2 cells with LINC00978 overexpression alone (Fig. 5b, c). The number of migrated and invaded cells was decreased in co-transfection group compared with LINC00978 overexpression alone group (Fig. 5d, e). In addition, the inhibition of p21 and E-cadherin expression levels by LINC00978 overexpression was reversed by EZH2 knockdown (Fig. 5f, g). Moreover, the increased expression of Cyclin D1, Bcl-2, N-cadherin, slug, and snail by LINC00978 overexpression was reversed by EZH2 knockdown. Collectively, these data indicate that EZH2 is critically involved in the promotion of HCC cell proliferation, migration and invasion by LINC00978.To demonstrate the importance of p21 and E-cadherin inhibition in the roles of LINC00978 in HCC, we co-transfected HepG2 cells with LINC00978 shRNAs and p21 siRNAs (or E-cadherin siRNAs). qRT-PCRresults showed that co-transfection reduced upregulation of p21 and E-cadherin by LINC00978 depletion (Fig. -(Fig.6a).6a). In addition, the results of cell counting and colony formation assays indicated that the proliferation of HepG2 cells co-transfected with sh-LINC00978 and si-p21 (or E-cadherin siRNAs) was increased compared with HepG2 cells transfected with sh-LINC00978 alone (Fig. 6b, c). The number of migrated and invaded cells was also increased in co-transfection group compared with sh-LINC00978 alone group (Fig. 6d, e). The expression levels of proliferation and metastasis related genes were also partially reversed in co-transfection group compared with sh-LINC00978 alone group (Fig. -(Fig.6f).6f). Collectively, these data indicate that LINC00978 promotes HCC cell proliferation, migration and invasion through the downregulation of p21 and E-cadherin.	31582742	RID07630	expression association	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	MIR4435-2HG	CDKN1A	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000124762	NA	541471	1026	AGD2|LINC00978|MIR4435-1HG|MORRBID|lncRNA-AWPPH	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LINC00978 promotes the progression of hepatocellular carcinoma by regulating EZH2-mediated silencing of p21 and E-cadherin expression.We first analyzed the expression levels of LINC00978 in human HCC tissues using the microarray data downloaded from GEO (GSE64041). The results showed that LINC00978 expression level was upregulated in HCC tissues compared with the parenchymal normal tissues (Fig. -(Fig.1a).1a). To validate the findings of GEO data analysis, we examined LINC00978 expression in a cohort of 33 paired HCC and adjacent non-cancerous tissues by using qRT-PCR Consistently, the expression level of LINC00978 was also significantly upregulated in HCC issues compared with the paired non-cancerous tissues (P-<-0.001, Fig. -Fig.1b).1b). Moreover, five cell lines including one normal liver epithelial cell line 7702 and 4 HCC cell lines (7721, 7402, HepG2, LM3) were detected for LINC00978 expression. The expression levels of LINC00978 in 7721, 7402, HepG2, and LM3 cells were significantly higher than that in 7702 cells (Fig. -(Fig.1c).1c).The increased expression of LINC00978 in HCC led us to hypothesize that LINC00978 might function as an oncogene in HCC. To this end, we knocked down LINC00978 expression in HCC cells by using shRNA. The knockdown efficiency was verified by using qRT-PCR(Fig. -(Fig.2a).2a). The results of cell counting assay showed that LINC00978 knockdown inhibited HCC cell proliferation (Fig. -(Fig.2b),2b), which was further confirmed by the results of colony formation assays (Fig. -(Fig.2c).2c). In addition, HCC cells transfected with LINC00978 shRNA had decreased S phase and increased apoptosis (Fig. 2d, e). Moreover, the expression levels of Bcl-2 and Cyclin D1 genes and proteins were decreased in LINC00978 shRNA transfected HCC cells (Fig. 2f, g). The number of migrated and invaded cells was decreased in sh-LINC00978 group compared with that in control group (Fig. 2h, i). The expression of epithelial marker E-cadherin was increased while that of mesenchymal markers N-cadherin and Vimentin was decreased in LINC00978 knockdown cells. In addition, the expression of EMT transcription factors including slug, snail, and twist was significantly downregulated in sh-LINC00978 transfected cells (Fig. 2j, k).We next wanted to know the importance of EZH2 to the oncogenic roles of LINC00978 in HCC. We overexpressed LINC00978 and knocked down EZH2 in HCC cells simultaneously (Fig. -(Fig.5a).5a). The results of cell counting and colony formation assays showed that the proliferation of HepG2 cells with LINC00978 overexpression and EZH2 knockdown was decreased compared with that of HepG2 cells with LINC00978 overexpression alone (Fig. 5b, c). The number of migrated and invaded cells was decreased in co-transfection group compared with LINC00978 overexpression alone group (Fig. 5d, e). In addition, the inhibition of p21 and E-cadherin expression levels by LINC00978 overexpression was reversed by EZH2 knockdown (Fig. 5f, g). Moreover, the increased expression of Cyclin D1, Bcl-2, N-cadherin, slug, and snail by LINC00978 overexpression was reversed by EZH2 knockdown. Collectively, these data indicate that EZH2 is critically involved in the promotion of HCC cell proliferation, migration and invasion by LINC00978.To demonstrate the importance of p21 and E-cadherin inhibition in the roles of LINC00978 in HCC, we co-transfected HepG2 cells with LINC00978 shRNAs and p21 siRNAs (or E-cadherin siRNAs). qRT-PCRresults showed that co-transfection reduced upregulation of p21 and E-cadherin by LINC00978 depletion (Fig. -(Fig.6a).6a). In addition, the results of cell counting and colony formation assays indicated that the proliferation of HepG2 cells co-transfected with sh-LINC00978 and si-p21 (or E-cadherin siRNAs) was increased compared with HepG2 cells transfected with sh-LINC00978 alone (Fig. 6b, c). The number of migrated and invaded cells was also increased in co-transfection group compared with sh-LINC00978 alone group (Fig. 6d, e). The expression levels of proliferation and metastasis related genes were also partially reversed in co-transfection group compared with sh-LINC00978 alone group (Fig. -(Fig.6f).6f). Collectively, these data indicate that LINC00978 promotes HCC cell proliferation, migration and invasion through the downregulation of p21 and E-cadherin.	31582742	RID07631	epigenetic regulation	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Hepatocellular carcinoma	MIR4435-2HG	E-cadherin	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	NA	NA	541471	NA	AGD2|LINC00978|MIR4435-1HG|MORRBID|lncRNA-AWPPH	NA	LINC00978 promotes the progression of hepatocellular carcinoma by regulating EZH2-mediated silencing of p21 and E-cadherin expression.We first analyzed the expression levels of LINC00978 in human HCC tissues using the microarray data downloaded from GEO (GSE64041). The results showed that LINC00978 expression level was upregulated in HCC tissues compared with the parenchymal normal tissues (Fig. -(Fig.1a).1a). To validate the findings of GEO data analysis, we examined LINC00978 expression in a cohort of 33 paired HCC and adjacent non-cancerous tissues by using qRT-PCR Consistently, the expression level of LINC00978 was also significantly upregulated in HCC issues compared with the paired non-cancerous tissues (P-<-0.001, Fig. -Fig.1b).1b). Moreover, five cell lines including one normal liver epithelial cell line 7702 and 4 HCC cell lines (7721, 7402, HepG2, LM3) were detected for LINC00978 expression. The expression levels of LINC00978 in 7721, 7402, HepG2, and LM3 cells were significantly higher than that in 7702 cells (Fig. -(Fig.1c).1c).The increased expression of LINC00978 in HCC led us to hypothesize that LINC00978 might function as an oncogene in HCC. To this end, we knocked down LINC00978 expression in HCC cells by using shRNA. The knockdown efficiency was verified by using qRT-PCR(Fig. -(Fig.2a).2a). The results of cell counting assay showed that LINC00978 knockdown inhibited HCC cell proliferation (Fig. -(Fig.2b),2b), which was further confirmed by the results of colony formation assays (Fig. -(Fig.2c).2c). In addition, HCC cells transfected with LINC00978 shRNA had decreased S phase and increased apoptosis (Fig. 2d, e). Moreover, the expression levels of Bcl-2 and Cyclin D1 genes and proteins were decreased in LINC00978 shRNA transfected HCC cells (Fig. 2f, g). The number of migrated and invaded cells was decreased in sh-LINC00978 group compared with that in control group (Fig. 2h, i). The expression of epithelial marker E-cadherin was increased while that of mesenchymal markers N-cadherin and Vimentin was decreased in LINC00978 knockdown cells. In addition, the expression of EMT transcription factors including slug, snail, and twist was significantly downregulated in sh-LINC00978 transfected cells (Fig. 2j, k).We next wanted to know the importance of EZH2 to the oncogenic roles of LINC00978 in HCC. We overexpressed LINC00978 and knocked down EZH2 in HCC cells simultaneously (Fig. -(Fig.5a).5a). The results of cell counting and colony formation assays showed that the proliferation of HepG2 cells with LINC00978 overexpression and EZH2 knockdown was decreased compared with that of HepG2 cells with LINC00978 overexpression alone (Fig. 5b, c). The number of migrated and invaded cells was decreased in co-transfection group compared with LINC00978 overexpression alone group (Fig. 5d, e). In addition, the inhibition of p21 and E-cadherin expression levels by LINC00978 overexpression was reversed by EZH2 knockdown (Fig. 5f, g). Moreover, the increased expression of Cyclin D1, Bcl-2, N-cadherin, slug, and snail by LINC00978 overexpression was reversed by EZH2 knockdown. Collectively, these data indicate that EZH2 is critically involved in the promotion of HCC cell proliferation, migration and invasion by LINC00978.To demonstrate the importance of p21 and E-cadherin inhibition in the roles of LINC00978 in HCC, we co-transfected HepG2 cells with LINC00978 shRNAs and p21 siRNAs (or E-cadherin siRNAs). qRT-PCRresults showed that co-transfection reduced upregulation of p21 and E-cadherin by LINC00978 depletion (Fig. -(Fig.6a).6a). In addition, the results of cell counting and colony formation assays indicated that the proliferation of HepG2 cells co-transfected with sh-LINC00978 and si-p21 (or E-cadherin siRNAs) was increased compared with HepG2 cells transfected with sh-LINC00978 alone (Fig. 6b, c). The number of migrated and invaded cells was also increased in co-transfection group compared with sh-LINC00978 alone group (Fig. 6d, e). The expression levels of proliferation and metastasis related genes were also partially reversed in co-transfection group compared with sh-LINC00978 alone group (Fig. -(Fig.6f).6f). Collectively, these data indicate that LINC00978 promotes HCC cell proliferation, migration and invasion through the downregulation of p21 and E-cadherin.	31582742	RID07632	epigenetic regulation	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Prostate cancer	IDH1-AS1	ATG5	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-216b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000231908	GRCh38_2:208255214-208256181	ENSG00000057663	NA	100507475	9474	NA	APG5|APG5L|ASP|hAPG5	PAX5-induced upregulation of IDH1-AS1 promotes tumor growth in prostate cancer by regulating ATG5-mediated autophagy.To determine the regulatory pattern of IDH1-AS1 in PCa cells, we analyzed its cellular localization. The results shows in Supplementary Fig. 1e indicated that IDH1-AS1 was predominantly located in cytoplasm of PCa cells. Results of pGL3 luciferase reporter assay revealed that there was no significant effect of IDH1-AS1 on the luciferase activity of ATG5 promoter (Supplementary Fig. 1f), which eliminated the transcriptional regulation of IDH1-AS1 on ATG5. Through RNA pull-down and mass-spectrometry analysis, we found that PTBP3 is a RBP which could interact with IDH1-AS1 (Fig. -(Fig.5a).5a). The interaction between PTBP3 and IDH1-AS1 or ATG5 was further proved by RIP assay (Fig. -(Fig.5b).5b). Then, we overexpressed PTBP3 in LNCaP and VCaP cell and found that ATG5 expression was observably increased (Fig. 5c, d). Subsequently, ATG5 mRNA stability was assessed in PCa cells treated with Actinomycin D after overexpression of PTBP3. It was found that PTBP3 overexpression enhanced the stability of ATG5 (Fig. -(Fig.5e).5e). Furthermore, we analyzed whether IDH1-AS1 affected the interaction between PTBP3 and ATG5. As a result, silencing of IDH1-AS1 attenuated the interaction between PTBP3 and ATG5 (Fig. -(Fig.5f).5f). Accordingly, knockdown of IDH1-AS1 impeded the mRNA stability of ATG5, which tendency was attenuated after co-transfection with PTBP3 expression vector (Fig. -(Fig.5g).5g). Taken together, IDH1-AS1 regulated ATG5 mRNA stability via interacting with PTBP3.CeRNA regulatory network is an important posttranscriptional regulatory mechanism of lncRNAs. Here, we also explored whether IDH1-AS1 and ATG5 could form a ceRNA pathway. Bioinformatics analysis suggested that miR-216b-5p had complementary base pairing with both IDH1-AS1 and ATG5. To validate their interaction, IDH1-AS1 or ATG5 3'UTR containing the binding sequences with miR-216b-5p was cloned into luciferase reporter vectors. It was uncovered that the luciferase activity of wild type reporters was decreased by miR-216b-5p mimics, whereas no obvious changes in mutant reporters (Fig. 6a, b). Then, we examined the mRNA and protein level of ATG5 in cells transfected with miR-NC or miR-216b-5p mimics. The levels of ATG5 were significantly impaired by the upregulation of miR-216b-5p (Fig. -(Fig.6c).6c). Ago2-RIP assay was used to prove the enrichment of IDH1-AS1, miR-216b-5p, and ATG5 in RISC complex (Fig. -(Fig.6d).6d). Afterwards, miR-216b-5p expression was found to be lower in PCa tissues than that in normal controls (Fig. -(Fig.6e).6e). Pearson correlation analysis revealed that miR-216b-5p had negative expression correlation with IDH1-AS1 and ATG5 (Fig. -(Fig.6f).6f). All these experimental results indicated that IDH1-AS1 functioned as a ceRNA to regulate ATG5 expression via sponging miR-216b-5p.	31570703	RID07633	ceRNA or sponge	NA		UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Prostate cancer	PAX5	IDH1-AS1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	TF	lncRNA	ENSG00000196092	NA	ENSG00000231908	GRCh38_2:208255214-208256181	5079	100507475	BSAP	NA	PAX5-induced upregulation of IDH1-AS1 promotes tumor growth in prostate cancer by regulating ATG5-mediated autophagy.To determine the regulatory pattern of IDH1-AS1 in PCa cells, we analyzed its cellular localization. The results shows in Supplementary Fig. 1e indicated that IDH1-AS1 was predominantly located in cytoplasm of PCa cells. Results of pGL3 luciferase reporter assay revealed that there was no significant effect of IDH1-AS1 on the luciferase activity of ATG5 promoter (Supplementary Fig. 1f), which eliminated the transcriptional regulation of IDH1-AS1 on ATG5. Through RNA pull-down and mass-spectrometry analysis, we found that PTBP3 is a RBP which could interact with IDH1-AS1 (Fig. -(Fig.5a).5a). The interaction between PTBP3 and IDH1-AS1 or ATG5 was further proved by RIP assay (Fig. -(Fig.5b).5b). Then, we overexpressed PTBP3 in LNCaP and VCaP cell and found that ATG5 expression was observably increased (Fig. 5c, d). Subsequently, ATG5 mRNA stability was assessed in PCa cells treated with Actinomycin D after overexpression of PTBP3. It was found that PTBP3 overexpression enhanced the stability of ATG5 (Fig. -(Fig.5e).5e). Furthermore, we analyzed whether IDH1-AS1 affected the interaction between PTBP3 and ATG5. As a result, silencing of IDH1-AS1 attenuated the interaction between PTBP3 and ATG5 (Fig. -(Fig.5f).5f). Accordingly, knockdown of IDH1-AS1 impeded the mRNA stability of ATG5, which tendency was attenuated after co-transfection with PTBP3 expression vector (Fig. -(Fig.5g).5g). Taken together, IDH1-AS1 regulated ATG5 mRNA stability via interacting with PTBP3.CeRNA regulatory network is an important posttranscriptional regulatory mechanism of lncRNAs. Here, we also explored whether IDH1-AS1 and ATG5 could form a ceRNA pathway. Bioinformatics analysis suggested that miR-216b-5p had complementary base pairing with both IDH1-AS1 and ATG5. To validate their interaction, IDH1-AS1 or ATG5 3'UTR containing the binding sequences with miR-216b-5p was cloned into luciferase reporter vectors. It was uncovered that the luciferase activity of wild type reporters was decreased by miR-216b-5p mimics, whereas no obvious changes in mutant reporters (Fig. 6a, b). Then, we examined the mRNA and protein level of ATG5 in cells transfected with miR-NC or miR-216b-5p mimics. The levels of ATG5 were significantly impaired by the upregulation of miR-216b-5p (Fig. -(Fig.6c).6c). Ago2-RIP assay was used to prove the enrichment of IDH1-AS1, miR-216b-5p, and ATG5 in RISC complex (Fig. -(Fig.6d).6d). Afterwards, miR-216b-5p expression was found to be lower in PCa tissues than that in normal controls (Fig. -(Fig.6e).6e). Pearson correlation analysis revealed that miR-216b-5p had negative expression correlation with IDH1-AS1 and ATG5 (Fig. -(Fig.6f).6f). All these experimental results indicated that IDH1-AS1 functioned as a ceRNA to regulate ATG5 expression via sponging miR-216b-5p.	31570703	RID07634	transcriptional regulation	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Prostate cancer	IDH1-AS1	PTBP3	interact	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000231908	GRCh38_2:208255214-208256181	ENSG00000119314	NA	100507475	9991	NA	DKFZp781I1117|ROD1	PAX5-induced upregulation of IDH1-AS1 promotes tumor growth in prostate cancer by regulating ATG5-mediated autophagy.To determine the regulatory pattern of IDH1-AS1 in PCa cells, we analyzed its cellular localization. The results shows in Supplementary Fig. 1e indicated that IDH1-AS1 was predominantly located in cytoplasm of PCa cells. Results of pGL3 luciferase reporter assay revealed that there was no significant effect of IDH1-AS1 on the luciferase activity of ATG5 promoter (Supplementary Fig. 1f), which eliminated the transcriptional regulation of IDH1-AS1 on ATG5. Through RNA pull-down and mass-spectrometry analysis, we found that PTBP3 is a RBP which could interact with IDH1-AS1 (Fig. -(Fig.5a).5a). The interaction between PTBP3 and IDH1-AS1 or ATG5 was further proved by RIP assay (Fig. -(Fig.5b).5b). Then, we overexpressed PTBP3 in LNCaP and VCaP cell and found that ATG5 expression was observably increased (Fig. 5c, d). Subsequently, ATG5 mRNA stability was assessed in PCa cells treated with Actinomycin D after overexpression of PTBP3. It was found that PTBP3 overexpression enhanced the stability of ATG5 (Fig. -(Fig.5e).5e). Furthermore, we analyzed whether IDH1-AS1 affected the interaction between PTBP3 and ATG5. As a result, silencing of IDH1-AS1 attenuated the interaction between PTBP3 and ATG5 (Fig. -(Fig.5f).5f). Accordingly, knockdown of IDH1-AS1 impeded the mRNA stability of ATG5, which tendency was attenuated after co-transfection with PTBP3 expression vector (Fig. -(Fig.5g).5g). Taken together, IDH1-AS1 regulated ATG5 mRNA stability via interacting with PTBP3.CeRNA regulatory network is an important posttranscriptional regulatory mechanism of lncRNAs. Here, we also explored whether IDH1-AS1 and ATG5 could form a ceRNA pathway. Bioinformatics analysis suggested that miR-216b-5p had complementary base pairing with both IDH1-AS1 and ATG5. To validate their interaction, IDH1-AS1 or ATG5 3'UTR containing the binding sequences with miR-216b-5p was cloned into luciferase reporter vectors. It was uncovered that the luciferase activity of wild type reporters was decreased by miR-216b-5p mimics, whereas no obvious changes in mutant reporters (Fig. 6a, b). Then, we examined the mRNA and protein level of ATG5 in cells transfected with miR-NC or miR-216b-5p mimics. The levels of ATG5 were significantly impaired by the upregulation of miR-216b-5p (Fig. -(Fig.6c).6c). Ago2-RIP assay was used to prove the enrichment of IDH1-AS1, miR-216b-5p, and ATG5 in RISC complex (Fig. -(Fig.6d).6d). Afterwards, miR-216b-5p expression was found to be lower in PCa tissues than that in normal controls (Fig. -(Fig.6e).6e). Pearson correlation analysis revealed that miR-216b-5p had negative expression correlation with IDH1-AS1 and ATG5 (Fig. -(Fig.6f).6f). All these experimental results indicated that IDH1-AS1 functioned as a ceRNA to regulate ATG5 expression via sponging miR-216b-5p.	31570703	RID07635	interact with protein	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807,GSE75367,GSE86978)
Diffuse large b-cell lymphoma	SNHG14	ZEB1	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);immune evasion(+)	ceRNA(miR-5590-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	TF	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000148516	NA	104472715	6935	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA SNHG14/miR-5590-3p/ZEB1 positive feedback loop promoted diffuse large B cell lymphoma progression and immune evasion through regulating PD-1/PD-L1 checkpoint.First, we applied microarray analysis to detect the differentially expressed lncRNAs in DLBCL in 3 pairs of DLBCL specimens and the matched adjacent non-tumor specimens. Consequently, we picked 5 lncRNAs that presented the most significant upregulation in DLBCL samples, which were SNHG14, DUXAP8, LINC00473, SOX21-AS1, and MIR503HG (Fig. -(Fig.1a).1a). By analyzing TCGA data through GEPIA (http://gepia.cancer-pku.cn/), we found that among the 5 lncRNAs, only SNHG14 exhibited significant high expression in DLBCL samples (Fig. -(Fig.1b),1b), further indicating the association of SNHG14 with DLBCL. Accordingly, high expression of SNHG14 was confirmed in DLBCL cell lines versus the normal B cell lymphocytes (Fig. -(Fig.1c1c).Later on, biological effect of SNHG14 in DLBCL was detected through in vitro loss-of-function assays. Two DLBCL cell lines, FARAGE and U2932, were applied in the experiments because they were verified to express the highest SNHG14 level among 4 DLBCL cell lines. RT-qPCR analysis confirmed the pronounced downregulation of SNHG14 in both DLBCL cell lines after the transfection of 3 SNHG14 specific shRNAs, and sh-SNHG14#1/2 silenced SNHG14 expression more significantly (Fig. -(Fig.1d).1d). Therefore, sh-SNHG14#1/2 were used for subsequent experiments. Depletion of SNHG14 impaired the viability and colony generation of two DLBCL cell lines (Fig. 1e, f). Invasive ability of DLBCL cells was weakened by SNHG14 knockdown (Fig. -(Fig.1g).1g). In addition, we tried to examine the EMT progression of DLBCL cells under SNHG14 silence. western blot and IF staining results depicted that E-cadherin was increased, whereas N-cadherin was decreased by the knockdown of SNHG14 in DLBCL cells (Fig. 1h, i). Together, it was suggested that SNHG14 was upregulated in DLBCL and served as an oncogene by promoting cell proliferation, invasion, and EMT. Luciferase reporter assay showed that among the 5 abovementioned miRNAs, miR-5590-3p overexpression led to the most significant reduction of luciferase activity of SNHG14 reporter (Fig. -(Fig.2b),2b), which suggested that miR-5590-3p presented the strongest association with SNHG14. Thus, we focused on exploring the interaction between SNHG14 and miR-5590-3p. Low expression of miR-5590-3p was validated by RT-qPCR analysis (Fig. -(Fig.2c).2c).To study the detailed interaction between miR-5590-3p and SNHG14, we mutated the predicted miR-5590-3p site on SNHG14 for luciferase reporter assay (Fig. -(Fig.2e).2e). The overexpression of miR-5590-3p decreased the luciferase activity of SNHG14 WT, but failed to affect the luciferase activity of SNHG14 Mut, confirming that miR-5590-3p interacted with SNHG14 at the predicted binding site (Fig. -(Fig.2e).2e).It was shown that miR-5590-3p was significantly related to 58 pathways, among which T cell receptor signaling pathway caught our attention (Fig. -(Fig.3a).3a). As reported, tumor cells interacted with and disturbed the cytotoxic functions of CD8+ T cells in tumor microenvironment6'-. Therefore, we deduced that SNHG14/miR-5590-3p could alter CD8+T cells in DLBCL. To mimic the tumor microenvironment, the DLBCL cells were co-cultured with CD8+ T cells. Flow cytometry analysis revealed that percentage of CD8+ T cells increased and apoptosis of CD8+ T cells decreased under the knockdown of SNHG14 or overexpression of miR-5590-3p in FARAGE and U2932 cells (Fig. 3b, c). Furthermore, since PD-1/PD-L1 interaction could inhibit the activity of CD8+ T cells and enhance the immune evasion in tumors11'-3, we deduced that SNHG14/miR-5590-3p could regulate the alteration of CD8+ T cells through PD-1/PD-L1 checkpoint. To confirm our hypothesis, we applied antibodies against PD-1 and PD-L1 to block PD-1/PD-L1 in the co-culture system. As a result, overexpression of SNHG14 or knockdown of miR-5590-3p in OCI-Ly7 and DB cells reduced the ratio of CD8+ T cells and induced the apoptosis of CD8+ T cells, and such phenomenon could be reversed by the treatment of anti-PD-1 or anti-PD-L1 (Fig. 3d, e). Together, SNHG14/miR-5590-3p induced interaction of DLBCL cells with CD8+ T cells and triggered apoptosis of CD8+ T cells through PD-1/PD-L1 immune checkpoint.	31570691	RID07636	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	TP73-AS1	PTEN	negatively-E	knockdown;siRNA	upregulation	RT-qPCR	NA	NA	radioresistance(+);apoptosis process(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000171862	NA	57212	5728	KIAA0495|PDAM	BZS|MHAM|MMAC1|PTEN1|TEP1	Down-regulated lncRNA TP73-AS1 reduces radioresistance in hepatocellular carcinoma via the PTEN/Akt signaling pathway.TP73-AS1 expression of HCC tissues and the adjacent normal tissues was detected by RT-qPCR, and the outcomes unraveled that (Figure 1a) the expression of lncRNA TP73-AS1 in HCC tissues was apparently higher than that in the adjacent normal tissues (P < 0.05). Expression of lncRNA TP73-AS1 of human normal liver cells and human HCC cell lines was also evaluated using RT-qPCR, and the outcomes implied that (Figure 1b) lncRNA TP73-AS1 expressed in the four cell lines, while when compared with HL-7702 human normal liver cell line, lncRNA TP73-AS1 expression was observable increased in HepG2 cell line, Hep3B cell line and SMCC-7721 cell line (all P < 0.05). Meanwhile, in contrast to Hep3B cell line, lncRNA TP73-AS1 expression was reduced in HepG2 cell line and SMCC-7721 cell line (both P < 0.05).After different doses (0, 2, 4, 6, 8 Gy) of irradiation of non-transfected Hep3B cells, TP73-AS1 expression was gradually heightened. Particularly, compared with 0 Gy, lncRNA TP73-AS1 expression in Hep3B cells was evidently elevated at doses of 2, 4, 6, and 8 Gy (all P < 0.05, Figure 3a). After treated with different doses (0, 2, 4, 6, 8 Gy), the expression of PTEN gradually lowered; relative to 0 Gy, PTEN expression in Hep3B cells was markedly restrained in 2, 4, 6, and 8 Gy (all P < 0.05, Figure 3b).To further investigate the effect of TP73-AS1 on the protein expression of PTEN/Akt signaling pathway, the expression of PTEN and pAkt/Akt in cells that have been transfected with overexpressed TP73-AS1 plasmids of each group was measured, and the outcomes reflected that at 0 Gy, TP73-AS1 and pAkt/Akt expression was heightened, while both mRNA and protein expression of PTEN was noticeably repressed in the oe-TP73-AS1 group, which was relative to the oe-NC group (all P < 0.05); in comparison to 0 Gy, TP73-AS1 and pAkt/Akt expression was advanced, but mRNA and protein expression of PTEN was lowered at 4 Gy in both the oe-TP73-AS1 group and the oe-NC group (all P < 0.05, Figure 3F-h).The outcomes of western blotindicated that (Figure 3e) when the dose was 0 Gy, there was no obvious difference in protein expression of PTEN and pAkt/Akt between the blank group and the si-NC group (P > 0.05), while protein expression of PTEN in the TP73-AS1-siRNA group was noticeably increased (P < 0.05), and that of pAkt/Akt was broadly reduced (P < 0.05); when the dose was 4 Gy, the protein expression of PTEN was markedly restricted in the blank group, the si-NC group and the TP73-AS1-siRNA group, and the levels of pAkt/Akt were all amplified, which was relative to the dose of 0 Gy (all P < 0.05).The cell proliferation was detected by MTT assay, OD value of the blank group at 0 Gy was taken as the control to calculate the relative proliferation ability in each group, the results illustrated that (Figure 4a) contrasted to 0 Gy of irradiation, the relative proliferation ability was declined in the blank group, the si-NC group and the TP73-AS1-siRNA group after 4 Gy of irradiation (all P < 0.05), there was no broad difference in relative proliferation ability between the blank group and the si-NC group at the same dose of irradiation (P > 0.05), while the relative proliferation ability in the TP73-AS1-siRNA group was significantly declined (P < 0.05).The outcomes of western blotsuggested that (Figure 6c-e) the protein expression of PTEN was evidently suppressed and expression of pAkt/Akt was apparently heightened in the blank group, the si-NC group and the TP73-AS1-siRNA group at 4 Gy of irradiation, which was in contrast to the dose of 0 Gy (all P < 0.05). At the same dose (4 Gy) of irradiation, no broad difference could be found in the protein expression of PTEN and pAkt/Akt in the blank group and the si-NC group (all P > 0.05), while protein expression of PTEN was elevated and expression of pAkt/Akt was reduced in the TP73-AS1-siRNA group (both P < 0.05).	31564201	RID07637	expression association	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	TP73-AS1	AKT1	positively-E	knockdown;siRNA	upregulation	RT-qPCR	NA	NA	radioresistance(+);apoptosis process(-);cell proliferation(+)	phosphorylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000142208	NA	57212	207	KIAA0495|PDAM	AKT|PKB|PRKBA|RAC|RAC-alpha	Down-regulated lncRNA TP73-AS1 reduces radioresistance in hepatocellular carcinoma via the PTEN/Akt signaling pathway.TP73-AS1 expression of HCC tissues and the adjacent normal tissues was detected by RT-qPCR, and the outcomes unraveled that (Figure 1a) the expression of lncRNA TP73-AS1 in HCC tissues was apparently higher than that in the adjacent normal tissues (P < 0.05). Expression of lncRNA TP73-AS1 of human normal liver cells and human HCC cell lines was also evaluated using RT-qPCR, and the outcomes implied that (Figure 1b) lncRNA TP73-AS1 expressed in the four cell lines, while when compared with HL-7702 human normal liver cell line, lncRNA TP73-AS1 expression was observable increased in HepG2 cell line, Hep3B cell line and SMCC-7721 cell line (all P < 0.05). Meanwhile, in contrast to Hep3B cell line, lncRNA TP73-AS1 expression was reduced in HepG2 cell line and SMCC-7721 cell line (both P < 0.05).After different doses (0, 2, 4, 6, 8 Gy) of irradiation of non-transfected Hep3B cells, TP73-AS1 expression was gradually heightened. Particularly, compared with 0 Gy, lncRNA TP73-AS1 expression in Hep3B cells was evidently elevated at doses of 2, 4, 6, and 8 Gy (all P < 0.05, Figure 3a). After treated with different doses (0, 2, 4, 6, 8 Gy), the expression of PTEN gradually lowered; relative to 0 Gy, PTEN expression in Hep3B cells was markedly restrained in 2, 4, 6, and 8 Gy (all P < 0.05, Figure 3b).To further investigate the effect of TP73-AS1 on the protein expression of PTEN/Akt signaling pathway, the expression of PTEN and pAkt/Akt in cells that have been transfected with overexpressed TP73-AS1 plasmids of each group was measured, and the outcomes reflected that at 0 Gy, TP73-AS1 and pAkt/Akt expression was heightened, while both mRNA and protein expression of PTEN was noticeably repressed in the oe-TP73-AS1 group, which was relative to the oe-NC group (all P < 0.05); in comparison to 0 Gy, TP73-AS1 and pAkt/Akt expression was advanced, but mRNA and protein expression of PTEN was lowered at 4 Gy in both the oe-TP73-AS1 group and the oe-NC group (all P < 0.05, Figure 3F-h).The outcomes of western blotindicated that (Figure 3e) when the dose was 0 Gy, there was no obvious difference in protein expression of PTEN and pAkt/Akt between the blank group and the si-NC group (P > 0.05), while protein expression of PTEN in the TP73-AS1-siRNA group was noticeably increased (P < 0.05), and that of pAkt/Akt was broadly reduced (P < 0.05); when the dose was 4 Gy, the protein expression of PTEN was markedly restricted in the blank group, the si-NC group and the TP73-AS1-siRNA group, and the levels of pAkt/Akt were all amplified, which was relative to the dose of 0 Gy (all P < 0.05).The cell proliferation was detected by MTT assay, OD value of the blank group at 0 Gy was taken as the control to calculate the relative proliferation ability in each group, the results illustrated that (Figure 4a) contrasted to 0 Gy of irradiation, the relative proliferation ability was declined in the blank group, the si-NC group and the TP73-AS1-siRNA group after 4 Gy of irradiation (all P < 0.05), there was no broad difference in relative proliferation ability between the blank group and the si-NC group at the same dose of irradiation (P > 0.05), while the relative proliferation ability in the TP73-AS1-siRNA group was significantly declined (P < 0.05).The outcomes of western blotsuggested that (Figure 6c-e) the protein expression of PTEN was evidently suppressed and expression of pAkt/Akt was apparently heightened in the blank group, the si-NC group and the TP73-AS1-siRNA group at 4 Gy of irradiation, which was in contrast to the dose of 0 Gy (all P < 0.05). At the same dose (4 Gy) of irradiation, no broad difference could be found in the protein expression of PTEN and pAkt/Akt in the blank group and the si-NC group (all P > 0.05), while protein expression of PTEN was elevated and expression of pAkt/Akt was reduced in the TP73-AS1-siRNA group (both P < 0.05).	31564201	RID07638	interact with protein	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG16	DKK3	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000050165	NA	100507246	27122	Nbla10727|Nbla12061|ncRAN	REIC|RIG	LncRNA SNHG16 promotes epithelial- mesenchymal transition via down-regulation of DKK3 in gastric cancer.It is well known that EMT is involved in metastaticevents in tumors. To evaluate the role of SNHG16on EMT in GC, si-SNHG16 or si-NC were transfected into HGC-27 and AGS cells. The interference efficiency of SNHG16 was over 70%, as detected by qRT-PCRassay (Fig. 1A). Next, we detected EMT- associated proteins using western blot assay. At pro- tein (Fig. 1B ) levels, SNHG16 knockdown upregu- lated the expressions of epithelial markers E-cadherin and Claudin-1, reduced the expressions of mesenchy- mal markers, such as N-cadherin, Vimentin. In addi- tion, it could reduce the level of transcription factors Zeb1 protein, but there were no obvious differences in Slug and Snail proteins.To further explore the target of SNHG16 in GC,Genechip assay was performed following SNHG16 knockdown (Fig. 3A), which displayed 7 upregulated genes and 21 downregulated genes in HGC-27 cells. Among them, a remarkable 3.26-fold increase of DKK3 gene expression was detected. qRT-PCRand western blot assays were performed to verify the au193 thenticity of Genechip results. Unexpectedly, the transcription level of DKK3 was only slightly increased by SNHG16 knockdown in both HGC-27 and AGS cells, as detected by qRT-PCRassay (Fig. 3B), but the DKK3 protein abundance was significantly increased (Fig. 3C and D). The discrepancy may be caused by the methodological differences between Genechip and qRT-PCRor the involvement of other regulatory mechanisms. To explore the correlation between SNHG16 and DKK3 clinically, the RNA expressions of SNHG16 and DKK3 in 20 pairs of GC tissues and their adjacent normal tissues were examined by qRT-PCRassay. It indicated an inverse correlation between the enhanced SNHG16 (Fig. 3E) and the declined DKK3 expressions (Fig. 3F), with r = -0.566 (Fig. 3G and H).To verify whether SNHG16 was engaged in EMT via the regulation of DKK3, a rescue experiment was performed to explore the correlation between SNHG16 and DKK3 in EMT. HGC-27 and AGS cells were transfected with sh-SNHG16 to gain stable cell lines by lentivirus-mediated SNHG16 knockdown. An inter218 ference efficiency above 65% was achieved in HGC-27 and AGS stable cells (Fig. 4A). The DKK3-transcript levels, as detected by qRT-PCR were not obvious  changed by SNHG16 knockdown in HGC-27 and AGS stable cells (Fig. 4B). Meanwhile, DKK3 gene was silenced by RNAi technology. Shown by qRT224 PCR and western blot results, the si3-DKK3 was the most optimal among the three siRNAs and was cho226 sen for the next experiment (Fig. 4C and D). The SNHG16 knockdown-induced inhibition of EMT was reversed by co-transfection of sh-SNHG16 and si3-DKK3 into HGC-27 and AGS cells (Fig. 4E), imply230 ing that SNHG16 promoted EMT via down-regulation of DKK3 protein in GC cells. Next, whether SNHG16 was associated with translo- cation of beta-catenin, which is involved in Wnt/beta-catenin signaling pathway, was then investigated. beta-catenin protein abundance in proteins from nucleus, cytoplasm and whole cell lysates of AGS cells were determined after SNHG16 knockdown. The results displayed decreased levels of beta-catenin protein in the nucleus, cytoplasm and whole cells (Fig. 4F), suggesting that SNHG16 does not participate in the beta-catenin translocation between cytoplasm and nucleus.	31561329	RID07639	expression association	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Esophagus squamous cell carcinoma	FOXD2-AS1	miR-195	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	cisplatin	NA	cell invasion(+);cell growth(+);chemoresistance(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	Overexpression of the Long Noncoding RNA FOXD2-AS1 Promotes Cisplatin Resistance in Esophageal Squamous Cell Carcinoma Through the miR-195/Akt/mTOR Axis.FOXD2-AS1 expression was examined in ESCC cells and tissues. FOXD2-AS1 transcription was assessed through qRT-PCRin 20 pairs of matched ESCC specimens and surrounding normal tissues. The results showed that FOXD2-AS1 transcription was remarkably higher in the ESCC specimens than in the corresponding control tissues (Fig. 1A). In addition, FOXD2-AS1 expression was also compared in normal esophageal cells, ESCC cells, and cisplatin-resistant ESCC cells (TE-1/DDP). FOXD2-AS1 expression was upregulated in TE-1/DDP cells compared to the parent TE-1 cells (Fig. 1C). In addition, qRT-PCRanalysis showed that miR-195 expression was repressed in ESCC cells, regardless of cisplatin resistance (Fig. 1B and D). The above findings demonstrate that the expression of the lncRNA FOXD2-AS1 was increased in ESCC cells regardless of cisplatin resistance, indicating that FOXD2-AS1 expression is conversely related to miR-195 expression.Previous research has shown that lncRNAs can function as ceRNAs, promoting transcription by binding to microRNAs (miRNAs)24. Bioinformatics method prediction showed that miR-195 was able to bind to FOXD2-AS1 (Fig. 2A), and qRT-PCR;ISHowed that repression of FOXD2-AS1 expression remarkably upregulated miR-195, while an increase in FOXD2-AS1 expression noticeably downregulated miR-195 (Fig. 2B and C), suggesting that FOXD2-AS1 represses miR-195 expression. Luciferase assays were performed in TE-1/DDP cells to verify the association between miR-195 and FOXD2-AS1. Transfection with a miR-195 mimic remarkably repressed FOXD2-AS1 luciferase activity, while transfection with a miR-195 inhibitor noticeably increased FOXD2-AS1 luciferase activity (Fig. 2D and E), suggesting that FOXD2-AS1 functions as a molecular sponge for miR-195.Our previous assays showed that FOXD2-AS1 was highly expressed in TE-1/DDP cells. Therefore, gain-of-function and loss-of-function assays were performed to investigate the complicated etiology of cisplatin resistance. Knockdown (KD) of FOXD2-AS1 markedly inhibited colony formation in TE-1/DDP cells (Fig. 3A and B). In contrast, overexpression of FOXD2-AS1 remarkably increased colony formation by TE-1/DDP cells (Fig. 3C and D). A CCK-8 survival assay showed that cell proliferation was dose-dependently inhibited by DDP. FOXD2-AS1 KD markedly inhibited the growth of DDP-supplemented cells when compared with control siRNA-transfected DDP-supplemented cells. Cells that overexpressed FOXD2-AS1 showed better survival (Fig. 3E and F). The above findings indicated that FOXD2-AS1 aggravated cisplatin resistance in ESCC cells.Cells were transfected with a FOXD2-AS1 expression vector to overexpress FOXD2-AS1 or a FOXD2-AS1-siRNA vector to KD FOXD2-AS1 expression to explore the contribution of FOXD2-AS1 to cisplatin resistance. The results showed that cell death was obviously altered after transfection of the FOXD2-AS1 expression vector or FOXD2-AS1-siRNA. Overexpression of FOXD2-AS1 inhibited cell death, while FOXD2-AS1 KD increased cell death, both in the early and late stage (Fig. 4).We examined whether KD of FOXD2-AS1 increases cisplatin sensitivity in vivo. Nude mice were administered a subcutaneous injection of TE-1 cells with either high expression of FOXD2-AS1 (transfected with the FOXD2-AS1-vector) or KD of FOXD2-AS1 expression (transfected with FOXD2-AS1-siRNA), and the resulting xenograft tumors were examined. Mice were then administered intraperitoneal injections of cisplatin (2 mg/kg) twice weekly for 4 weeks after the 10-day inoculation. The malignancy-counteracting impact was assessed by examining the tumor volume and weight after treatment. Tumor growth markedly decreased in the FOXD2-AS1-siRNA group treated with cisplatin (Fig. 7A), which was similar to the in vitro findings. In contrast, overexpression of FOXD2-AS1 increased the tumor volume and weight.	31558183	RID07640	ceRNA or sponge	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Papillary thyroid carcinoma	SLC26A4-AS1	E-cadherin	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233705	GRCh38_7:107650260-107662204	NA	NA	286002	NA	NA	NA	Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma.Simultaneously, SLC26A4-AS1 expression was measured in PTC cell lines (TPC-1, IHH4, and KTC-1) and human normal thyroid cell Nthy-ori 3-1 cells using RT-qPCR (Figure 1f). It was found that SLC26A4-AS1 expression was lower in TPC-1, IHH4, and KTC-1 cells than in Nthy-ori 3-1 cells, with the lowest SLC26A4-AS1 expression in TPC-1 cells. Hence, TPC-1 c e l l w a s selected for the following experiment.Subsequently, the effect of SLC26A4-AS1 on TPC-1 c e l l m i g r a t i o n was clarified. The silence of SLC26A4-AS1 increased TPC-1 c e l l migration, and SLC26A4-AS1 overexpression vector or SP600125 markedly reduced cell migration, which was further decreased by cotreatment of SP600125 and upregulated SLC26A4-AS1 (Figure 4a,b). Collectively, SLC26A4-AS1 inhibited cell migration of TPC-1 cells.The cell invasion ability was identified, which displayed that cell invasive ability in the presence of si-SLC26A4-AS1 was significantly increased; cell invasive ability decreased in response to SLC26A4-AS1 upregulation or SP600125, which was further lowered by treatment of SLC26A4-AS1 upregulation and SP600125 at the same time (Figure 5). Therefore, these findings demonstrated that SLC26A4-AS1 suppressed cell invasion ability in TPC-1 cell.TPC-1 cell apoptosis was elucidated with the process of flow cytometry. The apoptosis rate of TPC-1 cell treated with SLC26A4- AS1 silencing was obviously decreased, which was opposite in TPC-1 cells treated with vector overexpressing SLC26A4-AS1 or SP600125. Moreover, these effects of vector overexpressing SLC26A4-AS1 or SP600125 alone were further promoted by treatment in combination (Figure 7a,b). Therefore, these findings signified that SLC26A4-AS1 enhanced cell apoptosis of TPC-1 cell.	31556116	RID07641	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Papillary thyroid carcinoma	SLC26A4-AS1	ERK	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233705	GRCh38_7:107650260-107662204	ENSG00000133216	NA	286002	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|NS13|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma.Simultaneously, SLC26A4-AS1 expression was measured in PTC cell lines (TPC-1, IHH4, and KTC-1) and human normal thyroid cell Nthy-ori 3-1 cells using RT-qPCR (Figure 1f). It was found that SLC26A4-AS1 expression was lower in TPC-1, IHH4, and KTC-1 cells than in Nthy-ori 3-1 cells, with the lowest SLC26A4-AS1 expression in TPC-1 cells. Hence, TPC-1 c e l l w a s selected for the following experiment.Subsequently, the effect of SLC26A4-AS1 on TPC-1 c e l l m i g r a t i o n was clarified. The silence of SLC26A4-AS1 increased TPC-1 c e l l migration, and SLC26A4-AS1 overexpression vector or SP600125 markedly reduced cell migration, which was further decreased by cotreatment of SP600125 and upregulated SLC26A4-AS1 (Figure 4a,b). Collectively, SLC26A4-AS1 inhibited cell migration of TPC-1 cells.The cell invasion ability was identified, which displayed that cell invasive ability in the presence of si-SLC26A4-AS1 was significantly increased; cell invasive ability decreased in response to SLC26A4-AS1 upregulation or SP600125, which was further lowered by treatment of SLC26A4-AS1 upregulation and SP600125 at the same time (Figure 5). Therefore, these findings demonstrated that SLC26A4-AS1 suppressed cell invasion ability in TPC-1 cell.TPC-1 cell apoptosis was elucidated with the process of flow cytometry. The apoptosis rate of TPC-1 cell treated with SLC26A4- AS1 silencing was obviously decreased, which was opposite in TPC-1 cells treated with vector overexpressing SLC26A4-AS1 or SP600125. Moreover, these effects of vector overexpressing SLC26A4-AS1 or SP600125 alone were further promoted by treatment in combination (Figure 7a,b). Therefore, these findings signified that SLC26A4-AS1 enhanced cell apoptosis of TPC-1 cell.	31556116	RID07642	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Papillary thyroid carcinoma	SLC26A4-AS1	Vimentin	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233705	GRCh38_7:107650260-107662204	NA	NA	286002	NA	NA	NA	Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma.Simultaneously, SLC26A4-AS1 expression was measured in PTC cell lines (TPC-1, IHH4, and KTC-1) and human normal thyroid cell Nthy-ori 3-1 cells using RT-qPCR (Figure 1f). It was found that SLC26A4-AS1 expression was lower in TPC-1, IHH4, and KTC-1 cells than in Nthy-ori 3-1 cells, with the lowest SLC26A4-AS1 expression in TPC-1 cells. Hence, TPC-1 c e l l w a s selected for the following experiment.Subsequently, the effect of SLC26A4-AS1 on TPC-1 c e l l m i g r a t i o n was clarified. The silence of SLC26A4-AS1 increased TPC-1 c e l l migration, and SLC26A4-AS1 overexpression vector or SP600125 markedly reduced cell migration, which was further decreased by cotreatment of SP600125 and upregulated SLC26A4-AS1 (Figure 4a,b). Collectively, SLC26A4-AS1 inhibited cell migration of TPC-1 cells.The cell invasion ability was identified, which displayed that cell invasive ability in the presence of si-SLC26A4-AS1 was significantly increased; cell invasive ability decreased in response to SLC26A4-AS1 upregulation or SP600125, which was further lowered by treatment of SLC26A4-AS1 upregulation and SP600125 at the same time (Figure 5). Therefore, these findings demonstrated that SLC26A4-AS1 suppressed cell invasion ability in TPC-1 cell.TPC-1 cell apoptosis was elucidated with the process of flow cytometry. The apoptosis rate of TPC-1 cell treated with SLC26A4- AS1 silencing was obviously decreased, which was opposite in TPC-1 cells treated with vector overexpressing SLC26A4-AS1 or SP600125. Moreover, these effects of vector overexpressing SLC26A4-AS1 or SP600125 alone were further promoted by treatment in combination (Figure 7a,b). Therefore, these findings signified that SLC26A4-AS1 enhanced cell apoptosis of TPC-1 cell.	31556116	RID07643	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Papillary thyroid carcinoma	SLC26A4-AS1	TP53	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000233705	GRCh38_7:107650260-107662204	ENSG00000141510	NA	286002	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma.Simultaneously, SLC26A4-AS1 expression was measured in PTC cell lines (TPC-1, IHH4, and KTC-1) and human normal thyroid cell Nthy-ori 3-1 cells using RT-qPCR (Figure 1f). It was found that SLC26A4-AS1 expression was lower in TPC-1, IHH4, and KTC-1 cells than in Nthy-ori 3-1 cells, with the lowest SLC26A4-AS1 expression in TPC-1 cells. Hence, TPC-1 c e l l w a s selected for the following experiment.Subsequently, the effect of SLC26A4-AS1 on TPC-1 c e l l m i g r a t i o n was clarified. The silence of SLC26A4-AS1 increased TPC-1 c e l l migration, and SLC26A4-AS1 overexpression vector or SP600125 markedly reduced cell migration, which was further decreased by cotreatment of SP600125 and upregulated SLC26A4-AS1 (Figure 4a,b). Collectively, SLC26A4-AS1 inhibited cell migration of TPC-1 cells.The cell invasion ability was identified, which displayed that cell invasive ability in the presence of si-SLC26A4-AS1 was significantly increased; cell invasive ability decreased in response to SLC26A4-AS1 upregulation or SP600125, which was further lowered by treatment of SLC26A4-AS1 upregulation and SP600125 at the same time (Figure 5). Therefore, these findings demonstrated that SLC26A4-AS1 suppressed cell invasion ability in TPC-1 cell.TPC-1 cell apoptosis was elucidated with the process of flow cytometry. The apoptosis rate of TPC-1 cell treated with SLC26A4- AS1 silencing was obviously decreased, which was opposite in TPC-1 cells treated with vector overexpressing SLC26A4-AS1 or SP600125. Moreover, these effects of vector overexpressing SLC26A4-AS1 or SP600125 alone were further promoted by treatment in combination (Figure 7a,b). Therefore, these findings signified that SLC26A4-AS1 enhanced cell apoptosis of TPC-1 cell.	31556116	RID07644	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	SCAMP1	ZEB1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-429)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000085365	GRCh38_5:78360611-78480739	ENSG00000148516	NA	9522	6935	SCAMP37	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA SCAMP1 regulates ZEB1/JUN and autophagy to promote pediatric renal cell carcinoma under oxidative stress via miR-429.In order to mimick the oxidative stress in RCC, H2O2was used to treat the cells (ACHN and Caki-1). Cell viabilities were reduced in the presence of H2O2(Fig. 1A). Moreover, H2O2remarkably induced apoptosis rate of cells (Fig. 1B and C). Besides, we examined SCAMP1 level in RCC cells under H2O2treatment by RT-qPCR. SCAMP1 was downregulated in H2O2group compared to mock (Fig. 1D). These data suggest SCAMP1 may promote RCC tumorigenesis and suppress H2O2inhibited cell viability and -induced apoptosis.Under the condition of H2O2treatment, SCAMP1 knockdown led to slower growth rate of ACHN and Caki-1 cells (Fig. 2B). On the opposite side, we transfected empty vector or pcDNA3.1-SCAMP1 into the cells and then measured apoptosis by TUNEL experiment (Fig. 2C). In this assay, the results revealed SCAMP1 significantly decreased apoptotic cell number with positive TUNEL signal (Fig. 2D and E). Taken together, these data imply that SCAMP1 contributes to tumorigenesis of RCC cells under oxidative stress.To seek the potential effector (such as microRNA) of SCAMP1 in oxidative stress-mediated RCC phenotype, we used online tool starbase and luciferase reporter assay to show miR-429 bound to SCAMP1 and negatively modulated the luciferase activity in wildtype SCAMP1-containing Caki-1 cells (Fig. 3A and B). miR-429 mimic transfection resulted in downregulation of SCAMP1 (Fig. 3C). Moreover, we observed upregulation of miR-429 by H2O2treatment in RCC cells (Fig. 3D). These data suggest that miR-429 acts as key mediator for SCAMP1-induced biological roles.Then, we attempted to identify the underlying targets of miR-429 by TargetScan (Fig. 5A). ZEB1 and JUN were the two well-studied effectors for cancer tumorigenesis and progression. Luciferase reporter assay and RT-qPCR conclusively showed miR-429 directly affected ZEB1 and JUN expression (Fig. 5B and C). To validate this result, westernblot exhibited same expression pattern of proteins as RT-qPCR result and phosphorylated form of c-Jun was downregulated in miR-429 mimic cells (Fig. 5D). To examine the effect of H2O2on expression of ZEB1 and JUN, we conducted RT-qPCR and observed lower levels of both ZEB1 and JUN in RCC cells under H2O2treatment compared to mock group cells (Fig. 5E). Based on these findings, we believe ZEB1 and JUN may be key for miR-429-mediated functions.At molecular level, ZEB1 and JUN were the downstream targets of miR-429. Whether they function for miR-429-regulated cell viability and apoptosis was unclear. We transfected ZEB1 and JUN cDNAs into miR-429 mimic Caki-1 cells (Fig. 6A). Expectedly, ZEB1 and JUN overexpressions led to obvious enhancement of cell viability regulated by miR-429 mimic in the presence of H2O2(Fig. 6B). For apoptosis, ZEB1 and JUN could rescue miR-429 mimic-induced cell death rate of Caki-1 cells under H2O2treatment (Fig. 6C and D). Besides, miR-429 decreased activated caspase-3 level, which was enhanced by ZEB1 and JUN overexpression (Fig. 6E). To conclude, we suggest both ZEB1 and JUN can reverse the role of miR-429 in cell viability and apoptosis.	31550675	RID07645	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	SCAMP1	JUN	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-429)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000085365	GRCh38_5:78360611-78480739	ENSG00000177606	NA	9522	3725	SCAMP37	AP-1|c-Jun	LncRNA SCAMP1 regulates ZEB1/JUN and autophagy to promote pediatric renal cell carcinoma under oxidative stress via miR-429.In order to mimick the oxidative stress in RCC, H2O2was used to treat the cells (ACHN and Caki-1). Cell viabilities were reduced in the presence of H2O2(Fig. 1A). Moreover, H2O2remarkably induced apoptosis rate of cells (Fig. 1B and C). Besides, we examined SCAMP1 level in RCC cells under H2O2treatment by RT-qPCR. SCAMP1 was downregulated in H2O2group compared to mock (Fig. 1D). These data suggest SCAMP1 may promote RCC tumorigenesis and suppress H2O2inhibited cell viability and -induced apoptosis.Under the condition of H2O2treatment, SCAMP1 knockdown led to slower growth rate of ACHN and Caki-1 cells (Fig. 2B). On the opposite side, we transfected empty vector or pcDNA3.1-SCAMP1 into the cells and then measured apoptosis by TUNEL experiment (Fig. 2C). In this assay, the results revealed SCAMP1 significantly decreased apoptotic cell number with positive TUNEL signal (Fig. 2D and E). Taken together, these data imply that SCAMP1 contributes to tumorigenesis of RCC cells under oxidative stress.To seek the potential effector (such as microRNA) of SCAMP1 in oxidative stress-mediated RCC phenotype, we used online tool starbase and luciferase reporter assay to show miR-429 bound to SCAMP1 and negatively modulated the luciferase activity in wildtype SCAMP1-containing Caki-1 cells (Fig. 3A and B). miR-429 mimic transfection resulted in downregulation of SCAMP1 (Fig. 3C). Moreover, we observed upregulation of miR-429 by H2O2treatment in RCC cells (Fig. 3D). These data suggest that miR-429 acts as key mediator for SCAMP1-induced biological roles.Then, we attempted to identify the underlying targets of miR-429 by TargetScan (Fig. 5A). ZEB1 and JUN were the two well-studied effectors for cancer tumorigenesis and progression. Luciferase reporter assay and RT-qPCR conclusively showed miR-429 directly affected ZEB1 and JUN expression (Fig. 5B and C). To validate this result, westernblot exhibited same expression pattern of proteins as RT-qPCR result and phosphorylated form of c-Jun was downregulated in miR-429 mimic cells (Fig. 5D). To examine the effect of H2O2on expression of ZEB1 and JUN, we conducted RT-qPCR and observed lower levels of both ZEB1 and JUN in RCC cells under H2O2treatment compared to mock group cells (Fig. 5E). Based on these findings, we believe ZEB1 and JUN may be key for miR-429-mediated functions.At molecular level, ZEB1 and JUN were the downstream targets of miR-429. Whether they function for miR-429-regulated cell viability and apoptosis was unclear. We transfected ZEB1 and JUN cDNAs into miR-429 mimic Caki-1 cells (Fig. 6A). Expectedly, ZEB1 and JUN overexpressions led to obvious enhancement of cell viability regulated by miR-429 mimic in the presence of H2O2(Fig. 6B). For apoptosis, ZEB1 and JUN could rescue miR-429 mimic-induced cell death rate of Caki-1 cells under H2O2treatment (Fig. 6C and D). Besides, miR-429 decreased activated caspase-3 level, which was enhanced by ZEB1 and JUN overexpression (Fig. 6E). To conclude, we suggest both ZEB1 and JUN can reverse the role of miR-429 in cell viability and apoptosis.	31550675	RID07646	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE86978)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	NEAT1	ATG3	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	RT-qPCR	NA	NA	cell autophagy(+);chemoresistance(+)	ceRNA(miR-204)	regulation	NA	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000144848	NA	283131	64422	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APG3L|DKFZp564M1178|FLJ22125|MGC15201|PC3-96	LncRNA NEAT1 promotes autophagy via regulating miR-204/ATG3 and enhanced cell resistance to sorafenib in hepatocellular carcinoma.The NEAT1 will be involved in the process of drug resistance and autophagy of various cells. We verified the role of NEAT1 in liver cancer, through the database (http://ualcan.path.uab.edu/index.html) (based on the TCGA), we evaluated the expression of NEAT1, we found NEAT1 high expression in a variety of cancers (Figure 1a-c; p< .01), NEAT1 has a high expression in cell lines of HCC by using PCR (Figure 1d;p< .05); and high expression often associated with poor outcome (Figure 1f;p< .01).To further determine the occurrence of autophagy, the fluorescence quantification of LC3 was performed by immunofluorescence assay (Figure 3c), and we found that the fluorescence of LC3 increased (p< .05). On the contrary, to more intuitively observe the status of autophagy inside cells, we conducted electron microscopy (Figure 3d), and the results showed that autophagosome increased (p< .05). The NEAT1 will promote the autophagy of liver cancer cells, and the NEAT1 will be protective.The function of lncRNA is widespread, one of the most important role is regulate the expression of mRNA by acting as a ceRNA of miRNAs, and to further explore the mechanism of NEAT1, we analyzed the data from TCGA by the bioinformatics websites (http://www.linkedomics.org and http://ualcan.path.uab.edu/index. html). NEAT1 expression is positively related to the expression of ATG3, and drawing the heatmap (Figure 7a). Then we selected the most clearly associated factors with ATG3, we used the website (https://bibiserv.cebitec.uni-bielefeld.de/rnahybrid) to analyze the free energy between ATG3 and miRNA (Figure 7b), the results showed the minimum free energy (MFE) value of ATG3 and miR- 204 is maximum, it shows that the combination between them is most significant. At the same time, we conducted target prediction for ATG3 through miRanda website (http://www.microrna.org), and we found that only miR-204 showed the most difference among all miRNAs (Figure 7d). The survival rate of the miR-204 high-expression group was higher (Figure 7c;p< . 0 5 ) . T o v e r i f y t h e above conclusions, we constructed miR-204 overexpressed cell lines and determined the transfection efficiency (Figure 7e).Meanwhile, protein quantification showed that the expression of ATG3 was significantly reduced after overexpression of miR-204. The above results fully demonstrated that miR-204 can regulate the expression of ATG3.To further verify whether NEAT1 can regulate the expression of ATG3 through miR-204 and thus regulate autophagy. The NEAT1 cell line will be constructed, and the NEAT1 cell line will be saved via miR-204 transfection, and the tansfectional efficiency of NEAT1 was measured (Figure 8a,b) (p< .05). We conducted luciferase assay (Figure 8c,d), it proved the relationship between miR-204 and NEAT1 (p< .05). In addition, RIP assay indicated NEAT1 and miR-204 were highly enriched in Ago2 pellet (Figure 8e,f;p< . 0 5 ) . R N A p u l l-down assay displayed a higher level of NEAT1 than control or miR-495-3p probes in vitro (Figure 8g,h; P< .05). Finally, we detected the expression of ATG3 in cell lines by western blot under different factors. The results show that the overexpression of miR-204 will inhibit the upregulation of ATG3 which caused by NEAT1 (Figure 8i,j). It shows that NEAT1 can regulate the occurrence of autophagy through the regulation of ATG3 by miR-204.	31549407	RID07647	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE104209,GSE111842,GSE55807,GSE67939,GSE86978)
Gastric cancer	LUCAT1	YWHAZ	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-134-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000164924	NA	100505994	7534	SCAL1|SCAT5	14-3-3-zeta|KCIP-1|YWHAD	Long non-coding RNA LUCAT1 promotes proliferation and invasion in gastric cancer by regulating miR-134-5p/YWHAZ axis.The expression of lncRNA LUCAT1 in gastric cancer and adjacent tissue was detected by qRT-PCR As shown in Fig. 1A, the expression of lncRNA LUCAT1 in gastric cancer tissue was significant higher than that in adjacent tissues. Interestingly, with the development of gastric cancer, the expression of lncRNA LUCAT1 was increased, which was highest in stage IV (Fig. 1B). Moreover, there were higher lncRNA LUCAT1 levels in lymph node metastasis and distant metastasis tissues (Fig. 1C and D). Importantly, patients with high lncRNA LUCAT1 levels were always with short overall survival and disease-free survival periods (Fig. 1E and F).MiRDB tool was used to predict the binding site between lncRNA LUCAT1 and miR-134-5p. The predicted binding site was shown in Fig. 3A. After shRNA-1 or shRNA-2 transfection, the expression of miR-134-5p was significantly up-regulated (Fig. 3B). After transfected by miR-134-5p mimic, the expression of miR-134-5p was significantly up-regulated and vice versa, which confirmed the transfection was successful (Fig. 3C). Up-regulated miR-134-5p could decreased the expression of lncRNA LUCAT1 and vice versa (Fig. 3D). Compared to lncRNA LUCAT1-Mut group, the relative luciferase activity of LUCAT1-WT was significantly lower (Fig. 3E). In gastric cancer tissues, lncRNA LUCAT1 is negatively correlated with miR-134-5p expression (Fig. 3F).Targetscan online tool was used to predict the binding site between MiR-134-5p and YWHAZ, and the binding site was shown in Fig. 4A. Luciferase reporter assay showed that miR-134-5p significantly inhibited the luciferase activity of YWHAZ-WT reporter (Fig. 4B). After miR-134-5p mimic transfection, the gene level of YWHAZ was down-regulated and vice versa (Fig. 4C). Additionally, YWHAZ expression was negatively correlated with miR-134-5p in tumor tissues (Fig. 4D). Based on TCGA database, the YWHAZ transcript per million was higher in gastric cancer tissues than normal (Fig. 4E). Similarly, the level of YWHAZ was also higher in gastric cancer tissues of this study (Fig. 4F). Interestingly, shLUCAT1 decreased the expression of YWHAZ, while miR-134-5p inhibitor reversed the inhibition of shLUCAT1 (Fig. 4G).For rescue assay, 5 groups were set, including NC, shRNA, shRNA-+-miR-inhibitor, miR-134-5p, and miR-134-5p-+-oeYWHAZ groups. As shown in Fig. 5A , shRNA and miR-134-5p decreased the proliferation, colony formation, cell migration and invasion of SGC7901 cell line. However, the miR-inhibitor and oeYWHAZ could rescue the inhibition. The mechanism of miR-134-5p, YWHAZ and LUCAT1 in gastric cancer was shown in Fig. 5E.	31545227	RID07648	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Ovarian cancer	DANCR	miR-145	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);angiogenesis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000269936	NA	57291	NA	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	LncRNA DANCR promotes tumor growth and angiogenesis in ovarian cancer through direct targeting of miR-145.To determine the expression of DANCR in ovarian tissues, 20 pairs of ovarian normal and malignant tissues from patients were collected. The results showed that DANCR expression was significantly upregulated in ovarian malignant tissues, compared with normal ovarian tissues.To further confirm the inhibitory role of shDANCR on tumor angiogenesis in ovarian cancer, the A2780 cancer cell-based matrigel plug assay was performed. Our results showed that knockdown of DANCR inhibited tumor angiogenesis in A2780 matrigel plug tissues (Figure 2C). To further confirm the inhibition role of DANCR knockdown on ovarian tumor angiogenesis, the cell culture supernatants of A2780 and HO8910 cells were collected for HUVEC- related tube formation assay and invasion assay. Less branch points were observed in the group with A2780-shDANCR and HO8910- shDANCR medium treatment, compared with the shNC group (Figure 3A a n d 3B). Furthermore, the invasion of HUVEC cells was also inhibited in A2780-shDANCR and HO8910-shDANCR medium groups (Figure 3C and 3D). These results demonstrated that knockdown of DANCR inhibits tumor angiogenesis in ovarian cancer.Bioinformatics analysis by Target Scan (http://www.targetscan.org/) indicated that miR-145 was a potential direct target of DANCR. Luciferase assay demonstrated that miR-145 inhibited DANCR-mediated translation activity of luciferase (Figure 5A), but had no significant effect on the translation activity of luciferase with mutant DANCR (Figure 5A). Further results indicated that the knockdown of DANCR promoted miR- 145 expression not only in A2780 and HO8910 cells (Figure 5B), but also in A2780 and HO8910 tumors (Figure 5C). There was an inverse correlation between DANCR and miR-145 in ovarian cancer tissues (Figure 5D). These results indicated that DANCR directly targeted miR- 145 and inhibited miR-145 expression in ovarian cancer cells.To further investigate the role of miR-145 during DANCR regulation of angiogenesis, miR-145 was employed to transfect A2780 and HO8910 cells. Real-time PCR results indicated the significant upregulation of miR- 145 in miR-145-transfected A2780 cells (Figure 6A). Both western blot and ELISA results confirmed the downregulation of VEGF in miR- 145-transfected A2780 and HO8910 cells (Figure 6B and 6C). There was also an inverse correlation between miR-145 and VEGF expression in ovarian cancer tissues (Figure 6D). Transfection of miR-145 inhibitor efficiently blocked the upregulation of miR-145 mediated by DANCR knockdown DANCR (Figure 6E). The VEGF downregulation by DANCR knockdown in A2780 cells was also attenuated by miR-145 inhibitor transfection (Figure 6F). Knockdown of DANCR-mediated downregulation of HUVEC tube formation and invasion was also blocked in miR-145 inhibitor transfection (Figure 6G and 6H). Collectively, miR-145 played a crucial role during DANCR promoting angiogenesis in ovarian cancer.	31545000	RID07649	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Acute myeloid leukemia	LINC00641	ZBTB20	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-378a)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	TF	ENSG00000258441	GRCh38_14:21200079-21206900	ENSG00000181722	NA	283624	26137	NA	DKFZp566F123|DPZF|ODA-8S|ZNF288	Long non-coding RNA LINC00641 promotes cell growth and migration through modulating miR-378a/ZBTB20 axis in acute myeloid leukemia.To characterize the roles of LINC00641 in AML, we analyzed the RNA-Seq data (from TCGA) using a novel tool (GEPIA). As shown in Figure 1A, we found that the levels of LINC00641 were significantly increased in the AML specimens. To demonstrate the analysis results, we carried out qRT-PCRexperiments to examine the LINC00641 levels in AML patients. The results showed that the LINC00641 levels were distinctly increased in AML specimens compared with normal blood samples (Figure 1B).To uncover the influences of LINC00641 on cellular growth and apoptosis of AML cells, we conducted loss of function studies using LINC00641 siRNAs. Real Time-PCR analyses demonstrated that LINC00641 siRNAs (si-lnc#1 and si-lnc#2) successfully silenced the levels of LINC00641 in AML cells (Figure 2A). Subsequently, the data from CCK-8 assays revealed that the proliferation abilities of AML cells were remarkably impeded by depressing LINC00641 expression (Figure 2B). Moreover, the cell cycles of AML cells treated with LINC00641 siRNAs were examined by flow cytometry analyses. The data confirmed that G0/G1 cell cycle arrest was induced when LINC00641 in AML cells was knocked down (Figures 2C and D). Besides, flow cytometry analyses were also utilized for the determination of cell apoptosis. The results suggested that inducing apoptosis happened in AML cells when their LINC00641 expression was repressed (Figure 2E). Accordingly, the levels of cellular apoptosis relevant molecules such as caspase-3 and caspase-9 were determined by western blot. The results elucidated that the protein levels of caspase-3 and caspase-9 were markedly elevated in AML cells when their LINC00641 expression was silenced (Figure 2F).Vice versa, the forced expression of miR-378a notably reduced LINC00641 levels, while repressing miR-378a levels remarkably increased LINC00641 expression (Figure 3F). Therefore, these data further demonstrated that LINC00641 expression was inversely associated with miR-378a levels, indicating that miR-378a might directly interact with LINC00641. For further directly confirming that, we next performed Luciferase activity detection analyses. The results certified that co-transfection with miR-378a mimics and LINC00641 wt but not LINC00641 mut significantly depressed the Luciferase activities in AML cells, which validated that miR378a directly interacted with LINC00641 (Figure 3G). For further clarifying that, RNA-pull down analyses were conducted and the results proved that LINC00641 could predominantly precipitate miR-378a in HL-60 and THP-1 cells (Figure 3H). Hence, these above data demonstrated that miR378a was a target of LINC00641. Next, we aimed to investigate whether LINC00641 was able to restore the inhibitory impact of miR-378a on malignant phenotypes. To achieve that, CCK-8 assays were carried out in AML cells after various treatments. As the results presented in Figure 3I, LINC00641 could accelerate AML cells growth, and enhancing miR-378a expression led to significant inhibition of AML cell proliferation, while re-introduction of LINC00641 was capable to reverse the impeding influences of miR-378a on cellular proliferation. In summary, these results displayed that LINC00641 modulated AML malignant phenotypes via sponging miR-378a.Moreover, we next investigated the functions of ZBTB20 on AML cells through loss-of-function studies. For that purpose, siRNAs targeting ZBTB20 were synthesized and the knockdown efficiency was determined by qPCR analyses (Figure 4E). Then, CCK-8 assays were conducted and the data indicated that the depression of ZBTB20 resulted in dramatically inhibition of AML cell growth (Figure 4F). Thereafter, the transwell invasion assays were also performed and we discovered that ZBTB20 knockdown remarkably reduced the invasive AML cells (Figure 4G). These data suggested that ZBTB20 could modulate the malignancies of AML. Therefore, we next sought to clarify whether ZBTB20 was a target of miR-378a. The predicted binding position between miR-378a and ZBTB20 was shown in Figure 4H. We, then, constructed Luciferase reporters, respectively containing predicted Wild-type binding position (wt ZBTB20) or mutated-type binding position (mut ZBTB20). Subsequently, the Luciferase reporters were separately co-transfected with miR-378a mimics into AML cells. The data from the Luciferase activity detection assays revealed that the Luciferase activities were significantly decreased in AML cells co-transfected with wt ZBTB20 and miR-378a mimics, which validated that miR-378a directly interacted with ZBTB20 mRNA 3'UTR. Taken together, these data demonstrated that ZBTB20 was a target gene of miR-378a in AML cells.	31539138	RID07650	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE55807)
Pancreatic cancer	PCAT1	RBM5	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000003756	NA	100750225	10181	PCA1|PCAT-1|PiHL	H37|LUCA-15|LUCA15	Long noncoding RNA PCAT-1 accelerates the metastasis of pancreatic cancer by repressing RBM5.Moreover, we next investigated the functions of ZBTB20 on AML cells through loss-of-function studies. For that purpose, siRNAs targeting ZBTB20 were synthesized and the knockdown efficiency was determined by qPCR analyses (Figure 4E). Then, CCK-8 assays were conducted and the data indicated that the depression of ZBTB20 resulted in dramatically inhibition of AML cell growth (Figure 4F). Thereafter, the transwell invasion assays were also performed and we discovered that ZBTB20 knockdown remarkably reduced the invasive AML cells (Figure 4G). These data suggested that ZBTB20 could modulate the malignancies of AML. Therefore, we next sought to clarify whether ZBTB20 was a target of miR-378a. The predicted binding position between miR-378a and ZBTB20 was shown in Figure 4H. We, then, constructed Luciferase reporters, respectively containing predicted Wild-type binding position (wt ZBTB20) or mutated-type binding position (mut ZBTB20). Subsequently, the Luciferase reporters were separately co-transfected with miR-378a mimics into AML cells. The data from the Luciferase activity detection assays revealed that the Luciferase activities were significantly decreased in AML cells co-transfected with wt ZBTB20 and miR-378a mimics, which validated that miR-378a directly interacted with ZBTB20 mRNA 3'UTR. Taken together, these data demonstrated that ZBTB20 was a target gene of miR-378a in AML cells.The results of wound healing assay revealed that knockdown of PCAT-1 reduced the migrated distance of CFPAC-1 pancreatic cancer cells (Figure 3A). Besides, the knockdown of PCAT-1 reduced the migrated distance of Panc-1 pancreatic cancer cells (Figure 3B).The outcome of the transwell assay also revealed that PCAT-1 was knocked down in pancreatic cancer cells, the number of invaded cells was remarkably decreased in CFPAC-1 pancreatic cancer cells (Figure 4A). Moreover, the number of invaded cells was remarkably decreased via knockdown of PCAT-1 in Panc-1 pancreatic cancer cells (Figure 4B).Our further experiments revealed that RBM5 was remarkably lower-expressed in pancreatic cancer tissues compared with adjacent tissues (Figure 5A). The correlation analysis revealed that the negative association was seen between RBM5 and PCAT-1 expression in pancreatic cancer tissues (Figure 5B). Then, the RT-qPCR results showed that RBM5 was upregulated in PCAT-1 shRNA group compared with the empty vector group in vitro (Figure 5C). western blot assay showed that the protein level of RBM5 could be upregulated by knocking down PCAT-1 (Figure 5D).	31539121	RID07651	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Cervical cancer	TDRG1	ELK1	positively-E	dual-luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000126767	NA	732253	2002	LINC00532|lincRNA-NR_024015	NA	LncRNA TDRG1 functions as an oncogene in cervical cancer through sponging miR-330-5p to modulate ELK1 expression.To investigate the function of lncRNA TDRG1 in cervical cancer, we down-regulated lncRNA TDRG1 in HeLa and SIHA cells using the siRNA transfection. qRT-PCRresults showed that lncRNA TDRG1 was effectively knocked down by si-TDRG1 (Figure 2A). siTDRG1#3 for HeLa and siTDRG1#1 for SIHA were selected for the following experiments due to the higher interference efficiency. Cell proliferation analysis results indicated that the cell viability of HeLa and SIHA cells was significantly inhibited by the lncRNA TDRG1 silencing (Figure 2B and C). Scratch assay and transwell assay results also demonstrated that the migration and invasion rates were significantly decreased in lncRNA TDRG1 silenced cells compared with siNC groups (Figure 2D and E). Moreover, cells were also arrested in the G1 phase of the cell cycle by TDRG1 knockdown (Figure 2F), indicating by flow cytometry analysis. Cell apoptosis analysis by flow cytometry showed that the percentage of apoptotic cells was increased from (12.80 2.85)% in siNC group to (36.8 2.08)% in the siTDRG1 group in HeLa cells and (33.5 1.05)% to (53 2.15)% in SIHA cells (Figure 2G).We used Starbase v2.0 and TargetScan to predict the possible target miRNA of lncRNA TDRG1. As shown in Figure 3A, miR-330-5p could potentially interact with lncRNA TDRG1. To verify the binding relation between miR-330-5p and lncRNA TDRG1, we conducted dual-luciferase reporter assays in HeLa cells. The results suggested that lncRNA TDRG1 was effectively up-regulated by lncRNA TDRG1 reporter vector (Figure 3B left). MiR-330-5p mimic reduced the luciferase activity of the lncRNA TDRG1 re porter vector compared with NC group, and this reduction disappeared when the target site on lncRNA TDRG1 was mutated (Figure 3B right). MiRNAs usually exert their function by forming RNA-induced silencing complex (RISC), of which Ago2 is a core component32. To determine whether lncRNA TDRG1 formed a RISC with miR-330-5p, we performed a RIP assay by using an Ago2 antibody. As shown in Figure 3C, the result showed that miR-330-5p was enriched by Ago2 antibody in lncRNA TDRG1 overexpressing cells.In addition, miRNA pull-down assays indicated that lncRNA TDRG1 could be pulled down by miR-330-5p (Figure 3D). Since lncRNAs could down-regulate the expression of their target miRNAs via sponge effect, we performed a correlation analysis of the expression levels of miR-330-5p and TDRG1 in cervical cancer samples by using qRT-PCR The results showed that lncRNA TDRG1 transcript level was negatively correlated with miR-330-5p transcript level (Figure 3E).We further used the bioinformatics algorithms TargetScan to predict the downstream target of miR-330-5p. As shown in Figure 4A, miR-330-5p could potentially bind to the 3'-untranslated region (3'-UTR) of ELK1. Luciferase reporter assays indicated that miR-330-5p mimic significantly reduced the luciferase activity of the wildtype 3'-UTR of ELK1 (ELK1-wt), but had no effect on the mutant 3'-UTR of ELK1 (ELK1-mut), which suggested a direct interaction between miR-330-5p and ELK1 (Figure 4A). To investigate the effect of miR-330-5p and lncRNA TDRG1 on ELK1 protein expression, we performed overexpression and knockdown assays. As shown in Figure 4B, the miR-330-5p mimic down-regulated ELK1 protein expression while miR-330-5p inhibitor up-regulates ELK1 in human cervical cancer HeLa and SIHA cells. In addition, ELK1 expression was increased by lncRNA TDRG1 (Figure 4C). The result in Figure 4D showed that the expression of ELK1 was positively correlated with lncRNA TDRG1 whereas negatively with miR-330-5p.Since lncRNA TDRG1 functions as a CeRNA of miR-330-5p, we performed rescue experiments to investigate whether miR-330-5p was involved in lncRNA TDRG1-mediated cell activity change. To determine the function of miR-330-5p in human cervical cancer cells, we transfected miR-330-5p-inhibitor into HeLa and SIHA cells to down-regulation of miR-330-5p. For rescue experiments, miR-330-5p-inhibitor and si-TDRG1 were co-transfected into HeLa and SIHA cells. Intriguingly, miR-330-5p-inhibitor promoted cell proliferation, migration, invasion, and cell cycle arrest, as well as decreased cell apoptosis in both HeLa and SIHA cells (Figures 5 and 6).	31539116	RID07652	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	HOTTIP	JUN	interact	dual-luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	immune evasion(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000177606	NA	100316868	3725	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	AP-1|c-Jun	Long non-coding RNA HOTTIP enhances IL-6 expression to potentiate immune escape of ovarian cancer cells by upregulating the expression of PD-L1 in neutrophils.Next, the mechanism of IL-6 overexpression in OC was studied. The bioinformatics prediction website indicated that HOTTIP may promote IL-6 transcription by binding to c-jun (Fig. 3a). Fractionation of nuclear/cytoplasmic RNA displayed that HOTTIP was predominantly localized in nucleus (Additional file 1: Figure S1). Dual luciferase reporter gene assay revealed that both c-jun and HOTTIP could increase the activity of IL-6 promoter (Fig. 3b, p <-0.05). Moreover, two binding sites between c-jun and IL-6 promoter with the highest score were predicted, which were further conformed by the ChIP assay. In addition, the effect of HOTTIP on the binding of c-jun and IL-6 promoter was evaluated. The results noted that HOTTIP enhanced the binding of c-jun and IL-6 promoter (Fig. 3c, p <-0.05). Moreover, the interaction between c-jun and HOTTIP was verified in SKOV3 cells by RIP assay (Fig. 3d, p <-0.05). When HOTTIP was overexpressed in SKOV3 cells, the expression and secretion levels of IL-6 were enhanced; however, the expression and secretion levels of IL-6 were reduced following HOTTIP silencing (Fig. 3e & f, p <-0.05), suggesting HOTTIP can promote expression of IL-6. Altogether, HOTTIP could augment transcription of IL-6 via transcription factor c-jun.The effect of HOTTIP on T cell immunity was evaluated in vivo. At the 10th d of tumorigenesis, the neutrophils treated with the medium from the normal SKOV3 cells or SKOV3 cells overexpressing HOTTIP were intraperitoneally injected with PBS and intraperitoneally injected with CD3+ T cells into the established NOD/SCID mice with or without PD-L1 antibody. Subsequently, the body weight of the mice and the tumor volume were recorded. As revealed in Fig. 5a, no significant difference was visible in body weight upon different treatments (p->-0.05). However, the tumor volume of mice injected with neutrophils treated with SKOV3 cells overexpressing HOTTIP was much heavier than that in neutrophils treated with normal SKOV3 cells (Fig. 5b, p <-0.05). Then all the tumors were excised and the percentage of CD3+ T cells was measured by immunohistochemical staining. A decline of the infiltrated CD3+ T cells was observed in mice injected with neutrophils added with SKOV3 cells overexpressing HOTTIP while CD3+ T cells increased following the addition of PD-L1 antibody (Fig. 5c, p <-0.05). Meanwhile, the IFN--Gamma expression in CD3+ T cells was detected through flow cytometry to determine the immune activity of T cells. The results showed that the expression of IFN--Gamma+ in CD3+ T cells was relatively lower in neutrophils added with SKOV3 cells overexpressing HOTTIP, while the results was restored by adding PD-L1 antibody (Fig. 5d, p <-0.05). These results indicated that HOTTIP could promote the expression of PD-L1 in neutrophils, while suppressing T cell immunity in vivo.To confirm the HOTTIP expression in OC tissues as well as the association with prognosis of OC patients, initially, the expression of HOTTIP was evaluated in OC tissues and normal fallopian tube fimbriae tissues using RT-qPCR. The results found that HOTTIP expression was elevated in OC tissue relative to that in normal fallopian tube fimbriae tissues (Fig. 6a, p <-0.05). Next, we conducted clinical follow-up to analyze the association of HOTTIP expression with prognosis of OC. It was revealed that the OS of patients with higher expression of HOTTIP (cut off value was 3.22) was far shorter than that of OC patients with lower HOTTIP expression (Fig. 6b, p <-0.05).Subsequent correlation analysis revealed a positive correlation between expression of IL-6 and expression of HOTTIP (Fig. 6c, p <-0.05). Moreover, HOTTIP could also positively associate with the PD-L1 expression in neutrophils (Fig. 6d, p <-0.05). The aforementioned data supported a strong and positive correlation between HOTTIP expression and PD-L1 expression in neutrophils.	31533774	RID07653	interact with protein	prognosis		DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE51827,GSE75367,GSE86978)
Ovarian cancer	HOTTIP	IL6	positively-E	overexpression	upregulation	qPCR	NA	NA	immune evasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000136244	NA	100316868	3569	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	BSF2|HGF|HSF|IFNB2|IL-6	Long non-coding RNA HOTTIP enhances IL-6 expression to potentiate immune escape of ovarian cancer cells by upregulating the expression of PD-L1 in neutrophils.Next, the mechanism of IL-6 overexpression in OC was studied. The bioinformatics prediction website indicated that HOTTIP may promote IL-6 transcription by binding to c-jun (Fig. 3a). Fractionation of nuclear/cytoplasmic RNA displayed that HOTTIP was predominantly localized in nucleus (Additional file 1: Figure S1). Dual luciferase reporter gene assay revealed that both c-jun and HOTTIP could increase the activity of IL-6 promoter (Fig. 3b, p <-0.05). Moreover, two binding sites between c-jun and IL-6 promoter with the highest score were predicted, which were further conformed by the ChIP assay. In addition, the effect of HOTTIP on the binding of c-jun and IL-6 promoter was evaluated. The results noted that HOTTIP enhanced the binding of c-jun and IL-6 promoter (Fig. 3c, p <-0.05). Moreover, the interaction between c-jun and HOTTIP was verified in SKOV3 cells by RIP assay (Fig. 3d, p <-0.05). When HOTTIP was overexpressed in SKOV3 cells, the expression and secretion levels of IL-6 were enhanced; however, the expression and secretion levels of IL-6 were reduced following HOTTIP silencing (Fig. 3e & f, p <-0.05), suggesting HOTTIP can promote expression of IL-6. Altogether, HOTTIP could augment transcription of IL-6 via transcription factor c-jun.The effect of HOTTIP on T cell immunity was evaluated in vivo. At the 10th d of tumorigenesis, the neutrophils treated with the medium from the normal SKOV3 cells or SKOV3 cells overexpressing HOTTIP were intraperitoneally injected with PBS and intraperitoneally injected with CD3+ T cells into the established NOD/SCID mice with or without PD-L1 antibody. Subsequently, the body weight of the mice and the tumor volume were recorded. As revealed in Fig. 5a, no significant difference was visible in body weight upon different treatments (p->-0.05). However, the tumor volume of mice injected with neutrophils treated with SKOV3 cells overexpressing HOTTIP was much heavier than that in neutrophils treated with normal SKOV3 cells (Fig. 5b, p <-0.05). Then all the tumors were excised and the percentage of CD3+ T cells was measured by immunohistochemical staining. A decline of the infiltrated CD3+ T cells was observed in mice injected with neutrophils added with SKOV3 cells overexpressing HOTTIP while CD3+ T cells increased following the addition of PD-L1 antibody (Fig. 5c, p <-0.05). Meanwhile, the IFN--Gamma expression in CD3+ T cells was detected through flow cytometry to determine the immune activity of T cells. The results showed that the expression of IFN--Gamma+ in CD3+ T cells was relatively lower in neutrophils added with SKOV3 cells overexpressing HOTTIP, while the results was restored by adding PD-L1 antibody (Fig. 5d, p <-0.05). These results indicated that HOTTIP could promote the expression of PD-L1 in neutrophils, while suppressing T cell immunity in vivo.To confirm the HOTTIP expression in OC tissues as well as the association with prognosis of OC patients, initially, the expression of HOTTIP was evaluated in OC tissues and normal fallopian tube fimbriae tissues using RT-qPCR. The results found that HOTTIP expression was elevated in OC tissue relative to that in normal fallopian tube fimbriae tissues (Fig. 6a, p <-0.05). Next, we conducted clinical follow-up to analyze the association of HOTTIP expression with prognosis of OC. It was revealed that the OS of patients with higher expression of HOTTIP (cut off value was 3.22) was far shorter than that of OC patients with lower HOTTIP expression (Fig. 6b, p <-0.05).Subsequent correlation analysis revealed a positive correlation between expression of IL-6 and expression of HOTTIP (Fig. 6c, p <-0.05). Moreover, HOTTIP could also positively associate with the PD-L1 expression in neutrophils (Fig. 6d, p <-0.05). The aforementioned data supported a strong and positive correlation between HOTTIP expression and PD-L1 expression in neutrophils.	31533774	RID07654	expression association	prognosis		DOWN(BRCA);DATA(GSE75367,GSE86978)
Ovarian cancer	HOTTIP	CD274	positively-E	overexpression	upregulation	qPCR	NA	NA	immune evasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000120217	NA	100316868	29126	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	Long non-coding RNA HOTTIP enhances IL-6 expression to potentiate immune escape of ovarian cancer cells by upregulating the expression of PD-L1 in neutrophils.Next, the mechanism of IL-6 overexpression in OC was studied. The bioinformatics prediction website indicated that HOTTIP may promote IL-6 transcription by binding to c-jun (Fig. 3a). Fractionation of nuclear/cytoplasmic RNA displayed that HOTTIP was predominantly localized in nucleus (Additional file 1: Figure S1). Dual luciferase reporter gene assay revealed that both c-jun and HOTTIP could increase the activity of IL-6 promoter (Fig. 3b, p <-0.05). Moreover, two binding sites between c-jun and IL-6 promoter with the highest score were predicted, which were further conformed by the ChIP assay. In addition, the effect of HOTTIP on the binding of c-jun and IL-6 promoter was evaluated. The results noted that HOTTIP enhanced the binding of c-jun and IL-6 promoter (Fig. 3c, p <-0.05). Moreover, the interaction between c-jun and HOTTIP was verified in SKOV3 cells by RIP assay (Fig. 3d, p <-0.05). When HOTTIP was overexpressed in SKOV3 cells, the expression and secretion levels of IL-6 were enhanced; however, the expression and secretion levels of IL-6 were reduced following HOTTIP silencing (Fig. 3e & f, p <-0.05), suggesting HOTTIP can promote expression of IL-6. Altogether, HOTTIP could augment transcription of IL-6 via transcription factor c-jun.The effect of HOTTIP on T cell immunity was evaluated in vivo. At the 10th d of tumorigenesis, the neutrophils treated with the medium from the normal SKOV3 cells or SKOV3 cells overexpressing HOTTIP were intraperitoneally injected with PBS and intraperitoneally injected with CD3+ T cells into the established NOD/SCID mice with or without PD-L1 antibody. Subsequently, the body weight of the mice and the tumor volume were recorded. As revealed in Fig. 5a, no significant difference was visible in body weight upon different treatments (p->-0.05). However, the tumor volume of mice injected with neutrophils treated with SKOV3 cells overexpressing HOTTIP was much heavier than that in neutrophils treated with normal SKOV3 cells (Fig. 5b, p <-0.05). Then all the tumors were excised and the percentage of CD3+ T cells was measured by immunohistochemical staining. A decline of the infiltrated CD3+ T cells was observed in mice injected with neutrophils added with SKOV3 cells overexpressing HOTTIP while CD3+ T cells increased following the addition of PD-L1 antibody (Fig. 5c, p <-0.05). Meanwhile, the IFN--Gamma expression in CD3+ T cells was detected through flow cytometry to determine the immune activity of T cells. The results showed that the expression of IFN--Gamma+ in CD3+ T cells was relatively lower in neutrophils added with SKOV3 cells overexpressing HOTTIP, while the results was restored by adding PD-L1 antibody (Fig. 5d, p <-0.05). These results indicated that HOTTIP could promote the expression of PD-L1 in neutrophils, while suppressing T cell immunity in vivo.To confirm the HOTTIP expression in OC tissues as well as the association with prognosis of OC patients, initially, the expression of HOTTIP was evaluated in OC tissues and normal fallopian tube fimbriae tissues using RT-qPCR. The results found that HOTTIP expression was elevated in OC tissue relative to that in normal fallopian tube fimbriae tissues (Fig. 6a, p <-0.05). Next, we conducted clinical follow-up to analyze the association of HOTTIP expression with prognosis of OC. It was revealed that the OS of patients with higher expression of HOTTIP (cut off value was 3.22) was far shorter than that of OC patients with lower HOTTIP expression (Fig. 6b, p <-0.05).Subsequent correlation analysis revealed a positive correlation between expression of IL-6 and expression of HOTTIP (Fig. 6c, p <-0.05). Moreover, HOTTIP could also positively associate with the PD-L1 expression in neutrophils (Fig. 6d, p <-0.05). The aforementioned data supported a strong and positive correlation between HOTTIP expression and PD-L1 expression in neutrophils.	31533774	RID07655	expression association	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Clear cell renal cell carcinoma	SNHG3	TOP2A	positively-E	luciferase reporter assay;knockdown	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000131747	NA	8420	7153	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	TOP2|TOP2alpha|TOPIIA	LncRNA SNHG3 promotes clear cell renal cell carcinoma proliferation and migration by upregulating TOP2A.The analysis of RNA-sequence data of 72 normal tissue and 524 ccRCC specimens in TCGA database indicated that the expression of SNHG3 was elevated in ccRCC tissues compared with in the normal tissues (Fig. 1A).Then, CCK-8 assays revealed that knockdown SNHG3 inhibited ACHN and Caki-1 cell growth (Fig. 2D), and the Ethynyl deoxy Uridine (EdU) dye assays exhibited a reduced proliferation rate in the SNHG3 silenced RCC cells (Fig. 2E). Similarly, colony formation assays demonstrated that silencing SNHG3 decreased the clone forming ability of RCC cells (Fig. 2F). Additionally, GSEA results also indicated that high SNHG3 expression exhibited significant relations with the expression of DNA repair and apoptosis-related genes in ccRCC (Fig. 2G). We then adopted flow cytometry cell apoptosis analysis to assess the apoptotic rates of SNHG3 knockdown cells. As speculated, SNHG3 knockdown significantly increased the proportion of apoptotic cells (Fig. 2H). Moreover, western blot results indicated that the expression levels of proliferation related protein CDK6 was decreased and the apoptosisrelated proteins Bax was increased, while Bcl-2 decreased in SNHG3 silenced RCC cells (Fig. 2I). Overall, the above results demonstrate that SNHG3 can influence ccRCC cell growth in vitro.To further explore whether SNHG3 affects tumorigenesis and metastasis in vivo, ACHN cells stably transfected with sh-Lacz/sh-SNHG3 were injected into nude mice subcutaneously or intravenously. We identified that there was a dramatic decrease in tumor weight and volume in the sh-SNHG3 group compared with sh-Lacz group (Fig. 4A, B and 4C). And after the mice were sacrificed at the end of the experiment, the SNHG3 expression measured in the sh-Lacz group was higher than that in the SNHG3 knockdown group (Fig. 4D). What's more, IHC analysis revealed that the tumors developed from sh-SNHG3 cells showed less Ki-67 expression than tumors formed from sh-Lacz cells (Fig. 4E). Besides, the number of liver metastatic nodules formed from sh-SNHG3 group was smaller compared with that in the sh-Lacz group (Fig. 4F). Thesefindings suggest that knockdown SNHG3 expression inhibits tumor growth and metastasis in vivo, which is consistent with its biological functions in vitro.dual-luciferase reporter assays in HEK293T and ACHN cells indicated that co-transfection of psi-SNHG3 together with miR139-5p mimics, but not the mutant significantly decreased the luciferase activities, while miR-139-5p inhibitor promoted luciferase activities compared with the control group (Fig. 5D). After that we examined the expression of miR-139-5p in TCGA and found that miR139-5p existed lower expression in ccRCC tissues (Tumor vs Normal, 506 vs 71) (Fig. 5I) and the paired tissues (paired tumor vs paired normal, 71 vs 71) (Fig. 5J). The Kaplan-Meier survival analysis indicated that the OS and DFS time of ccRCC patients with lower miR139-5p expression were significantly shorter than those with higher miR-139-5p expression (Fig. 5K, L). These results indicate that SNHG3 promotes ccRCC proliferation and metastation by sponging miR-1395p.The functions of microRNAs mostly depend on their downstream target genes. Using the online software including starbase and mirDB, we found that miR-139-5p could bind to the 3'UTR region of TOP2A by bioinformatics analysis (Fig. 6A). In addition, as previously reported, TOP2A was the target gene of miR-139-5p in pancreatic cancer [17]. Thus we transfected ACHN cells with miR-139-5p mimics or inhibitor and its negative control, respectively, the expression of TOP2A decreased or increased accordingly (Fig. 6B). And then, luciferase reporter vector psi-TOP2A containing the 3'UTR of TOP2A was constructed. dual-luciferase reporter assays in HEK-293T and ACHN cells showed that miR-139-5p decreased while its inhibitor increased the luciferase activities. We also noticed that mutations brought into the binding sequence of miR-139-5p with TOP2A (Fig. 6A) abolished its suppressive effects (Fig. 6C).As TOP2A is a factor of poor prognosis for many tumors, we have made a comparison between levels of TOP2A in tumors with high level of miR-139-5p and tumors with low levels of miR-139-5p. The results showed that the expression level of TOP2A increased when SNHG3 was high, and decreased when SNHG3 was low (Fig. 8A). On the contrary, the expression level of TOP2A decreased when miR-139-5p was high and increased when miR-139-5p was low (Fig. 8B). And whether in the high or low group of TOP2A expression, the higher of SNHG3 level, the worse the survival outcome (Fig. 8C and D); similarly, the higher the expression level of TOP2A and the lower of miR-139-5p, the worse the survival outcome (Fig. 8E). However, when TOP2A was low, the expression level of miR-139-5p had no significant effect on survival (Fig. 8F).	31505165	RID07656	ceRNA or sponge	metastasis,prognosis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE55807)
Gastric cancer	LINC01303	EZH2	positively-E	luciferase reporter assay;knockdown;RIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);prognosis	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000250548	GRCh38_14:61556273-61570653	ENSG00000106462	NA	101927780	2146	NA	ENX-1|EZH1|KMT6|KMT6A	LINC01303 functions as a competing endogenous RNA to regulate EZH2 expression by sponging miR-101-3p in gastric cancer.We also analysed the mRNA expression levels of LINC01303 in 30 pairs of GC tissues and adjacent non-tumour tissues by real-time PCR assay. The results showed that the expression of LINC01303 in GC tissues was significantly higher than that in non-tumour tissues (Figure -(Figure1B,1B, P < .05).To elucidate the effect of LINC01303 on GC cell proliferation, we overexpressed or knocked out LINC01303 to construct SGC7901-LINC01303 cells stably transfected with BGC823-shLINC01303 cells for further study (Figure -(Figure2A).2A). In order to analyse the effect of knockout or overexpression on the proliferation of gastric cancer cells, we showed that the overexpression of LINC01303 significantly increased the cell proliferation of GC cells by CCK8 and colony formation experiments, while the down-regulation of LINC01303 significantly inhibited the proliferation of GC cells (Figure -(Figure2B,C).2B,C). At the same time, in order to prove that LINC01303 can also affect the proliferation of gastric cancer in vivo, we further confirmed that LINC01303 significantly promoted the tumorigenicity of GC by subcutaneous xenograft nude mouse model (Figure -(Figure2D-F).2D-F). Taken together, these data indicate that LINC01303 contributes to the proliferation of GC cells.To clarify whether LINC01303 is capable of modulating GC cell migration and invasion. We performed wound healing and transwell experiments. The results showed that overexpression of LINC01303 significantly promoted the migration and invasion of GC cells (Figure -(Figure3B).3B). Conversely, knockdown of LINC01303 significantly inhibited the migration and invasion of GC cells (Figure -(Figure3A).3A). Similarly, wound healing experiments further demonstrated that a more efficient wound closure rate was observed in cells overexpressing LINC01303, while a lower wound closure rate was detected in LINC01303 knockdown cells (Figure -(Figure3C,D).3C,D). To demonstrate, in addition, the lung metastasis nude mouse model further confirmed that LINC01303 significantly promoted GC metastasis in vivo. (Figure -(Figure3E,F),3E,F), indicating that LINC01303 promotes GC progression by modulating cell migration and invasion in vitro and in vivo.Then, we found that LINC01303 may act as a sponge to adsorb miR-101-3p. Further predictions suggest that miR-101-3p may target the 3'UTR of EZH2. Next, we designed the luciferase reporter gene experiment, as shown in Figure -Figure4A.4A. The results showed that the miR-101-3p simulation significantly inhibited the reporter gene activation ability of LINC01303-WT and EZH2-WT (Figure -(Figure44B,-B,4).4). However, the miR-101-3p mimic has no inhibitory ability to the mutated luciferase reporter gene of the binding site (Figure -(Figure44B,-B,4).4). These results suggest that miR-101-3p may interact with LINC01303 and EZH2. RT-PCRresults also showed that LINC01303 knockdown increased the expression level of miR-101-3p (Figure -(Figure4D),4D), while miR-101-3p mimic significantly inhibited the expression level of EZH2. (Figure -(Figure4E).4E). western blot confirmed that miR-101-3p inhibited EZH2 expression in SGC7901 and BGC823 cells (Figure -(Figure4F).4F). At the same time, we have been suggested that LINC01303 may regulate the expression level of EZH2 by competitively adsorbing miR-101-3p. To clarify this hypothesis, we knockdown LINC01303 and found that EZH2 expression levels were reduced, while miR-101-3p expression levels were up-regulated (Figure -(Figure4G,H).4G,H). Importantly, we found for the first time that miR-101-3p expression levels were negatively correlated with LINC01303 or EZH2 expression levels in GC tissues (Figure -(Figure4I,J).4I,J). In summary, our results demonstrate that LINC01303 regulates the miR-101-3p/EZH2 axis in GC.	31497936	RID07657	ceRNA or sponge	metastasis,prognosis		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Ovarian cancer	MALAT1	miR-503-5p	negatively-F	luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA-MALAT1 regulates proliferation and apoptosis of ovarian cancer cells by targeting miR-503-5p.First of all, qRT-PCRwas performed to determine MALAT1 expression in OC cell lines and HOSE cells. The expression of MALAT1 was increased in OC cell lines (CaOV3, SKOV3, OVCAR3, and OV90) in comparison to that in normal HOSE cells (all P<0.05; Figure 1A). To investigate the mechanism by which MALAT1 regulates OC cell proliferation and apoptosis, a lot of studies have reported the correlation between lncRNAs and microRNAs.23,24 In our study, miR-503-5p expression was upregulated after MALAT1 was suppressed by si-MALAT1, while down-regulated when SKOV3 and OVCAR3 cells were transfected with pcDNA3.1-MALAT1 plasmids (Figure 3A). Then, mimics NC/miR-503-5p mimics or inhibitor NC/miR-503-5p inhibitor was transfected into SKOV3 and OVCAR3 cells to achieve miR-503-5p inhibition or overexpression, and RT-PCRwas used to verify the efficiency of transfection (Figure 3B). MALAT1 expression was downregulated by miR-503-5p overexpression, whereas upregulated by miR-503-5p inhibition (Figure 3C). Noncoding RNAs have been shown to target mRNAs via direct or indirect RNA-RNA interaction, and so we suspected that there may be a direct interaction between MALAT1 and miR-503-5p. To clarify the interaction between miR-503-5p and MALAT1, at first, starBase and RegRNA 2.0 analyses were used in our study to predict the interaction between MALAT1 and miR-503-5p. To clarify the relationship between miR-503-5p and MALAT1, a wild-type MALAT1 luciferase reporter vector (named WT-MALAT1) and a mutant-type MALAT1 luciferase reporter vector (named MT-MALAT1) containing a 10-bp mutation in the predicted miR-503-5p binding site was constructed (Figure 3D). After that, we co-transfected indicated vector with miR-503-5p mimics or miR-503-5p inhibitor in OVCAR3 cells, respectively. After co-transfection, the luciferase activity was examined using Dual Luciferase assays. A decreased reporter activity was shown in WT-MALAT1 and miR-503-5p mimics co-transfection, and increased reporter activity was exhibited when WT-MALAT1 and miR-503-5p inhibitors were transfected together into OVCAR3 cells (Figure 3E). However, after the mutation in the predicted binding site of miR-503-5p, the changes of the luciferase activity were totally abolished (Figure 3E). The binding of lncRNA-MALAT1 and miR-503-5p was further verified by RNA pull-down assay. The results showed that substantial miR-503-5p can be pulled down by MALAT1 probe (Figure 3F). MALAT1 enrichment by miR-503-5p probe was also found by Northern blot (Figure 3G). Taken together, miR-503-5p can directly bind with MALAT1.Cell proliferation and apoptosis were monitored in response to co-effect of MALAT1 and miR-503-5p. Cell proliferation by MTT assay showed that proliferation rate was inhibited after MALAT1 was knockdown and this inhibition was reversed by transfection of miR-503-5p inhibitor (Figure 4A and -andB).B). EdU staining on SKOV3 and OVCAR3 cells demonstrated that cells transfection with si-MALAT1 had significantly deceased positive cells. Transfection of miR-503-5p inhibitor could increase the number of positive cells and even partially reverse the inhibition of si-MALAT1 on positive cells. Moreover, flow cytometry assay demonstrated that apoptotic rate was increased in SKOV3 and OVCAR3 cells after transfection of MALAT1 knockdown, but transfection of miR-503-5p inhibition can suppress the cell apoptotic rate in tumor cells (Figure 4E). Furthermore, the co-effect of MALAT1 and miR-503-5p on apoptotic-related proteins was evaluated. The differential p53, Bax, Bcl-2, and Survivin protein levels were examined using western blot assays. Co-transfected si-MALAT1 and inhibitor NC markedly increased the levels of p53 and Bax proteins, and on the contrary, the levels of Bcl-2 and Survivin proteins were significantly decreased. Expressions of proapoptotic proteins (p53 and Bax) were elevated after cells were transfected with MALAT1 knockdown plasmid, while cells transfected with miR-503-5p inhibition had decreased apoptotic rate. miR-503-5p inhibition can partially reverse the inhibitory effect of si-MALAT1 on expressions of anti-apoptotic proteins (Bcl-2 and Survivin) (Figure 4F). Taken together, MALAT1 regulates OC cell growth through interaction with miR-503-5p.	31496733	RID07658	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Hepatocellular carcinoma	HOXA11-AS	EZH2	interact	RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|EZH1|KMT6|KMT6A	HOXA11-AS promotes the migration and invasion of hepatocellular carcinoma cells by inhibiting miR-124 expression by binding to EZH2.The relative expression of HOXA11-AS was evaluated in 66 tumor and surrounding normal tissues. The HCC samples showed higher levels of HOXA11-AS in comparison with the corresponding normal tissues (Fig. 1a). Additionally, the relative expression of HOXA11-AS in the healthy liver cells (HL-7702) and the HCC lines (HepG2, Hep3B, MHCC-97H and BEL7402) was also measured. The relative expression of HOXA11-AS in the HepG2 and Hep3B cells within the si-HOXA11-AS group was dramatically reduced (Fig. 2a) along with a remarkably decreased invasion and migration capacity (Fig. 2b, c) when compared to the si-NC group. The pCDNA-HOXA11-AS vector and empty vector were also used to transfect the MHCC-97H and BEL7402 cells. The HOXA11-AS relative expression was significantly increased in the MHCC-97H and BEL7402 cells transfected with the pCDNA-HOXA11-AS (Fig. 3a). At the same time, the MHCC-97H and BEL7402 cells in the pCDNA-HOXA11-AS group displayed a significant increase in HCC cell invasion and migration (Fig. 3b, c).qRT-PCRwas performed to detect the expression of miR124 in the normal and HCC tissues, and it was much lower in the HCC tissues compared to the normal surrounding tissues (Fig. 4a). A Pearson correlation analysis revealed a negative correlation between miR-124 and HOXA11AS (Fig. 4b). After transfection with the HOXA11-AS-1 siRNA, the expression of miR-124 was significantly increased in the HepG2 and Hep3B cell lines (Fig. 4c), while the overexpression of HOXA11-AS-1 in MHCC97H and BEL7402 cells leads to a significant decrease of miR-124 (Fig. 4d). Besides, CHIP assay indicated that after transfection with the HOXA11-AS-1 siRNA, the activity of EZH2 binding to the promoter of miR-124 showed a significant decrease in the HepG2 and Hep3B cell lines (Fig. 4e, f). In addition, an RIP assay was conducted to assess the enrichment level of HOXA11-AS with EZH2 in the HepG2 and Hep3B cells. Compared with the IgG group, the HOXA11-AS enrichment was much more in the EZH2 overexpressed group, suggesting that HOXA11-AS binds to EZH2 in HepG2 and Hep3B cells (Fig. 4g).	31493246	RID07659	interact with protein	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Hepatocellular carcinoma	HOXA11-AS	miR-124	negatively-F	RIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	HOXA11-AS promotes the migration and invasion of hepatocellular carcinoma cells by inhibiting miR-124 expression by binding to EZH2.The relative expression of HOXA11-AS was evaluated in 66 tumor and surrounding normal tissues. The HCC samples showed higher levels of HOXA11-AS in comparison with the corresponding normal tissues (Fig. 1a). Additionally, the relative expression of HOXA11-AS in the healthy liver cells (HL-7702) and the HCC lines (HepG2, Hep3B, MHCC-97H and BEL7402) was also measured. The relative expression of HOXA11-AS in the HepG2 and Hep3B cells within the si-HOXA11-AS group was dramatically reduced (Fig. 2a) along with a remarkably decreased invasion and migration capacity (Fig. 2b, c) when compared to the si-NC group. The pCDNA-HOXA11-AS vector and empty vector were also used to transfect the MHCC-97H and BEL7402 cells. The HOXA11-AS relative expression was significantly increased in the MHCC-97H and BEL7402 cells transfected with the pCDNA-HOXA11-AS (Fig. 3a). At the same time, the MHCC-97H and BEL7402 cells in the pCDNA-HOXA11-AS group displayed a significant increase in HCC cell invasion and migration (Fig. 3b, c).qRT-PCRwas performed to detect the expression of miR124 in the normal and HCC tissues, and it was much lower in the HCC tissues compared to the normal surrounding tissues (Fig. 4a). A Pearson correlation analysis revealed a negative correlation between miR-124 and HOXA11AS (Fig. 4b). After transfection with the HOXA11-AS-1 siRNA, the expression of miR-124 was significantly increased in the HepG2 and Hep3B cell lines (Fig. 4c), while the overexpression of HOXA11-AS-1 in MHCC97H and BEL7402 cells leads to a significant decrease of miR-124 (Fig. 4d). Besides, CHIP assay indicated that after transfection with the HOXA11-AS-1 siRNA, the activity of EZH2 binding to the promoter of miR-124 showed a significant decrease in the HepG2 and Hep3B cell lines (Fig. 4e, f). In addition, an RIP assay was conducted to assess the enrichment level of HOXA11-AS with EZH2 in the HepG2 and Hep3B cells. Compared with the IgG group, the HOXA11-AS enrichment was much more in the EZH2 overexpressed group, suggesting that HOXA11-AS binds to EZH2 in HepG2 and Hep3B cells (Fig. 4g).	31493246	RID07660	ceRNA or sponge	NA		
Malignant glioma	LINC00174	SLC2A1	positively-E	dual-luciferase reporter assay;RNA pull-down assays;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);glycolysis(+)	ceRNA(miR-152-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Brain glioma	lncRNA	PCG	ENSG00000179406	GRCh38_7:66376044-66493566	ENSG00000117394	NA	285908	6513	NCRNA00174	CSE|DYT18|DYT9|GLUT|GLUT1|HTLVR	Long non-coding RNA LINC00174 promotes glycolysis and tumor progression by regulating miR-152-3p/SLC2A1 axis in glioma.We first identified the expression of LINC00174 in glioma tissues and normal tissues in 45 paired samples by RT-qPCR. The results showed that LINC00174 expression was increased significantly in glioma tissues compared with that in PTBE (Fig. 1a, P <-0.001). Cell proliferation and apoptosis were then identified by CCK8 and Tunel, respectively. As shown in Fig. 2c-d, cell proliferation of U251 and LN229 cells with pcDNA3.1-LINC00174 transfection was promoted compared with that of pcDNA3.1 transfected cells (P-<-0.001), and pcDNA3.1-LINC00174 also decreased cell apoptosis of glioma cells (P-<-0.001). On the contrary, pLKO.1-LINC00174 transefection significantly inhibited cell proliferation and facilitated cell apoptosis of U251 and LN229 cells compared with that of pLKO.1 transfected cells (Fig. 2c-d, P <-0.001). Moreover, the effect of LINC00174 knockdown on tumor growth was also examined by a nude-mouse transplanted tumor model. The results exhibited that shLINC00174 obviously delayed tumor growth, decreased tumor volume, and reduced tumor weight compared with the shNC group (Fig. 2e, P <-0.001). The LINC0074 knockdown also effectively inhibited the expression of Ki67 in tumor tissues in comparison with that in tumor tissues of shNC group (Fig. 2f, P <-0.001).To further explore the underlying mechanism by which LINC00174 facilitated cell proliferation, migration, invasion and glycolysis of U251 and LN229 cells, the targeted miRNAs of LINC00174 were predicted. By FISH analysis in Fig. 4a, the expression of LINC00174 mainly located in the cytoplasm. From the analysis of Starbase (http://starbase.sysu.edu.cn), miR-152-3p was predicted to combine with LINC00174, which was verified by luciferase reporter assay (Fig. 4b-c). Furthermore, immunoprecipitation was carried out to verify the bioinformatical prediction. Also, RIP assay was performed to unveil whether LINC00174 interact miR-152-3p directly. As shown in Fig. 4d, the enrichment levels of LINC00174 and miR-152-3p in Ant-Ago2 group were higher than that in Ant-IgG group, the results suggested that miR-152-3p could directly target LINC00174 (P-<-0.001, Fig. 4d). By RNA pull down analysis, the LINC00174 enrichment in Bio-miR-152-3p-MUT showed no significance compared with the Bio-NC, while the LINC00174 enrichment in Bio-miR-152-3p-WT was significantly increased compared with the the Bio-NC (P-<-0.001, Fig. 4e).	31492194	RID07661	ceRNA or sponge	NA	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE86978)	UP(PAAD,PRAD);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE67939)
Gastric cancer	NEAT1	PIK3R1	positively-E	dual-luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);apoptosis process(-)	ceRNA(miR-497-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000145675	NA	283131	5295	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	GRB1|p85|p85-ALPHA	Long noncoding RNA NEAT1 promotes the growth of gastric cancer cells by regulating miR-497-5p/PIK3R1 axis.To explore the role of NEAT1 in GC, NEAT1 expression levels was first quantified in GC tissues. qRT-PCRresults showed NEAT1 expression was significantly upregulated in GC tissues compared with adjacent normal tissues (Figure 1 A).The miR-497-5p level was significantly decreased in GC tissues compared with adjacent normal tissues (Figure 2 A). The chemosynthetic miR-497-5p mimics was employed and transfected into SGC-7901 and HGC-27 cells, whose transfection efficiency was verified (Figure 2 B). MTT assay and flow cytometry illustrated miR497-5p overexpression inhibited proliferation and promoted apoptosis in SGC-7901 and HGC-27 cells compared to scramble control (NC, miR mimics; Figure 2 C and D). Moreover, miR497-5p overexpression dramatically enhanced expression levels of CDKN1A, Bax and cleaved caspase-3, as well as decreased levels of cyclin D1 and Bcl-2 (Figure 2 E). Taken together, our data demonstrated miR-497-5p upregulation inhibited proliferation and promoted apoptosis in GC cells.The correlations between NEAT1 and miR497-5p expression in GC tissues were determined by qRT-PCR suggesting miR-497-5p expression was negatively correlated with NEAT1 level (Figure 3 A). The binding sites of miR-497-5p on NEAT1 were predicted through miRDB (http:// www.mirdb.org/, Figure 3 B). Therefore, we speculated that NEAT1 might negatively regulate expression of miR-497-5p by directly binding to it. To verify our hypothesis, NEAT1 overexpression plasmid was constructed and transfected into SGC-7901 and HGC-27 cells (Figure 3 C). RNA pull-down assay showed miR-497-5p expression was highly enriched by overexpression of NEAT1 (Figure 3 D). Besides, NEAT1 overexpression significantly decreased miR-497-5p level and NEAT1 knockdown could enhance miR-4975p expression (Figure 3 E). Collectively, these results suggested NEAT1 negatively regulated miR-497-5p expression level as sponges.PIK3R1 was predicted to be one of the potential targets of miR-497-5p using TargetScan (http://www.targetscan.org/vert_71/). Therefore, we constructed dual-luciferase reporter plasmids containing WT or mutants of PIK3R1 3'UTR (Figure 4 A). Plasmids containing PIK3R1 3'UTR were co-transfected into 293T cells with miR-497-5p or NC (miR mimics). Then, the relative luciferase activities were measured. Our results showed mutations on the 3'UTR of PIK3R1 abolished the suppressive ability of miR-497-5p compared with wild type (Figure 4 B left). We also co-transfected luciferase reporter plasmids with NEAT1 overexpression plasmids or NC, further confirming that decrease of miR-497-5p by NEAT1 overexpression could enhance the relative luciferase activities under the condition of WT 3'UTR of PIK3R1 (Figure 4 B right). Furthermore, cells expressing miR-497-5p possessed remarkably decreased PIK3R1 protein level, and cells expressing NEAT1 showed the contrary results (Figure 4 C-D). PIK3R1 was a target of miR-497-5p and NEAT1 could regulate PIK3R1 expression through regulating miR-497-5p.We established GC xenograft model using BALB/c nude mice. Tumors expressing siNEAT1 (siNEAT1 group) were smaller than those expressing NC (Vector, NC group; Figure 6 A). Immuno-histochemical results of Ki67 showed that Ki67 expression in siNEAT1 group was much less than that in NC group (Figure 6 B). Apoptosis in siNEAT1 group was promoted than that in the NC group detected by TUNEL assay (Figure 6 C). The miR-497-5p level was increased upon siNEAT1 treatment (Figure 6 D), and PIK3R1 protein level was decreased (Figure 6 E). Our in vivo results indicated NEAT1 knockdown could inhibit tumor growth by upregulating miR-4975p, which in turn decreasing PIK3R1 expression.	31486491	RID07662	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE51827,GSE55807,GSE86978)
Urinary bladder cancer	ITGB1	miR-10a	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000150093	GRCh38_10:32887273-33005792	NA	NA	3688	NA	CD29|FNRB|GPIIA|MDF2|MSK12	NA	LncRNA ITGB1 promotes the development of bladder cancer through regulating microRNA-10a expression.The expression of ITGB1 in 36 BCa tissue specimens and adjacent normal ones was detected by qRT-PCR The results indicated that ITGB1 expression was remarkably upregulated in BCa tissues (Figure 1A). In addition, ITGB1 expression was found remarkably higher in bladder tumor cell lines, especially EGB and 253j cell lines, than that in epithelial immortalized cells (SV-HUC-1) (Figure 1B).To investigate the function of ITGB1 in BCa, a knockdown model of ITGB1 was constructed. After transfection of the ITGB1 lentiviral vector in the EJ and 253j cell lines, qRT-PCRwas performed to verify the interference efficiency, and the difference was statistically significant (Figure 2A). After knockdown of ITGB1 in EJ and 253j cell lines, CCK-8 and colony formation assay were performed to detect the proliferation of BCa cells. The results showed that compared with those transfected with shNC, the proliferation of BCa cells transfected with sh-ITGB1 was remarkably reduced (Figure 2B-2D).Therefore, it is considered that there could be an interaction between ITGB1 and microRNA-10a. In this study, the expression of microRNA-10a in 36 BCa tissue specimens and adjacent normal ones was detected by qRT-PCR The results indicated that microRNA-10a was remarkably down-regulated in BCa tissues compared with the normal ones (Figure 3C). Similarly, ITGB1 level was found remarkably lower in BCa cells than in normal bladder epithelial immortalized cells (SV-HUC-1), and the difference was statistically significant (Figure 3D). Subsequently, the expressions of ITGB1 and microRNA-10a were both detected by qRT-PCRand found they were negatively correlated in BCa tissues (Figure 3E). To investigate the function of microRNA-10a in BCa, microRNA-10a mimics was constructed. After transfection of microRNA-10a mimics in EJ and 253j cell lines, the qRT-PCRexperiment was performed to verify the interference efficiency (Figure 4A). After overexpression of microRNA-10a in EJ and 253j cell lines, CCK-8 and colony formation assays showed that compared with those transfected with miR-NC, cell proliferation ability was remarkably attenuated after overexpression of microRNA-10a (Figure 4B-4D).To further explore the interaction between ITGB1 and microRNA-10a in BCa cells, rescue experiments were conducted by co-transfection of microRNA-10a inhibitor and si-ITGB1 in BCa cells. qRT-PCRassay detected ITGB1 level after cell co-transfection (Figure 5A). Subsequently, our results showed that microRNA-10a could abolish the regulatory effect of ITGB1 on the proliferative ability in BCa (Figure 5B and 5C).	31486485	RID07663	expression association	NA	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	
Prostate cancer	DANCR	miR-135a	negatively-F	luciferase reporter assay;knockdown;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712325-52723623	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	NA	DANCR sponges miR-135a to regulate paclitaxel sensitivity in prostate cancer.To explore the role of DANCR in prostate cancer, its expression was measured in 36 patients'-tissues and prostate cancer cells. As shown in Figure 1A, the expression of DANCR was significantly enhanced in tumor tissues compared with that in normal samples.In order to clarify the role of DANCR in paclitaxel sensitivity to prostate cancer, DANCR siRNA and siRNA control were transfected into DU145 cells and then treated with paclitaxel or not. The results of qRT-PCR;ISHowed that the expression of DANCR was decreased in cells transfected with DANCR siRNA (Figure 2A). Moreover, MTT assay showed that down-regulation of DANCR could reduce cell proliferation and aggravated paclitaxel-induced proliferation inhibition in DU145 cells (Figure 2B). To further clarify the effect of down-regulation of DANCR and paclitaxel on cell proliferation, we also used western blot to detect the expression changes of Ki-67 and PCNA. The results showed that knockdown of DANCR could reduce the levels of Ki-67 and PCNA in cells with or without treatment of paclitaxel (Figure 2C). In addition, the analysis of flow cytometry revealed that silence of DANCR or paclitaxel could induce apoptosis, and silencing DANCR enhanced the apoptotic rate induced by paclitaxel (Figure 2D). Besides, DANCR knockdown promoted the expression levels of C-Caspase-3 and Bax protein in cells with or without treatment of paclitaxel (Figure 2E). These results suggested that down-regulation of DANCR can improve paclitaxel-induced proliferation inhibition and apoptosis promotion in prostate cancer cells.We used bioinformatics software starBase to predict that DANCR and miR-135a have complementary targeting sites (Figure 3A). To validate this prediction, luciferase reporter assay was performed by transfecting WT or MUT DANCR luciferase reporter vectors into DU145 cells.As described in Figure 3B, overexpression of miR-135a led to a 50% reduction of luciferase activity in WT group, while it showed little effect in MUT group. Moreover, the expression level of miR-135a was markedly decreased in prostate cancer tissues and cells compared with that in corresponding controls (Figure 3C and 3D). Additionally, the data of qRTPCR showed that miR-135a mimics or DANCR siRNA caused greatly increase of miR-135a abundance in DU145 cells (Figure 3E and 3F). These results suggested that DANCR can target and negatively regulate the expression of miR-135a.In order to verify whether miR-135a was involved in knockdown of DANCR-mediated paclitaxel sensitivity to prostate cancer cells, we co-transfected DANCR siRNA and inhibitor control, DANCR siRNA and miR-135a inhibitor in DU145 cells, respectively, and cultured them with 30 nM paclitaxel. Firstly, qRT-PCRassay showed that the expression level of miR-135a in cells was significantly decreased by the introduction of inhibitor of miR-135a (Figure 5A). Moreover, miRNA-135a inhibitor could reverse the down-regulation of DANCR-induced anti-proliferation role in prostate cancer cells stimulated with paclitaxel (Figure 5B). In addition, the levels of Ki-67 and PCNA protein inhibited by DANCR knockdown were restored by miR-135a deficiency in paclitaxel-treated cells (Figure 5C and 5D). Furthermore, inhibition of miR-135a weakened silencing DANCR-induced apoptosis production in paclitaxel-treated cells (Figure 5E). Meanwhile, western blot results showed that the expression levels of C-Caspase-3 and Bax protein in cells transfected with DANCR siRNA and miR-135a inhibitor were decreased (Figure 5F). These results suggested that down-regulation of miR-135a reversed silence of DANCR-mediated promoting effect on paclitaxel sensitivity to prostate cancer cells.	31486484	RID07664	ceRNA or sponge	chemoresistance	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Gastric cancer	MIR4435-2HG	DSP	negatively-F	luciferase reporter assay;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000096696	NA	541471	1832	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	DPI|DPII|KPPS2|PPKS2	LncRNA MIR4435-2HG targets desmoplakin and promotes growth and metastasis of gastric cancer by activating Wnt/beta-catenin signaling.The expression of the above lncRNAs was validated in all samples by RT-qPCR (Figure 1C and Supplementary Figure 1A). Furthermore, we found that MIR4435-2HG expression was considerably up-regulated in 57 additional GC specimens, compared to matched samples of normal gastric mucosa (Figure 1D and -and1E).1E). To assess the clinical significance of MIR4435-2HG, a high-expression group (n = 30) and a low-expression group (n = 27) were defined based on median MIR4435-2HG expression levels. Correlation analysis revealed that MIR4435-2HG expression was positively associated with TNM stage (Table 1).In addition, MIR4435-2HG expression was examined in GC cell lines and normal gastric epithelial cells by RT-qPCR. Compared to normal gastric epithelial GES-1 cells, up-regulation of MIR4435-2HG was observed in the HGC-27, SNU-5, and SGC7901 GC cell lines (Figure 1F). These data suggested that up-regulation of MIR4435-2HG might contribute to GC pathogenesis.To evaluate whether down-regulation of MIR4435-2HG would affect the migration and invasion of SNU5 and HGC-27 cells, we conducted transwell assays. Results showed that MIR4435-2HG suppression attenuated migration and invasion in both cell lines (Figure 2E and -and2F).2F). To investigate the molecular bases of this inhibition, the expression of EMT-related proteins was examined by western blot (WB). Markedly decreased expression of N-cadherin, VEGF, and alpha-SMA was observed in sh-MIR4435-2HG-transfected SNU5 (Figure 2G). Meanwhile, significantly decreased expression of MMP9, VEGF, and alpha-SMA was observed in sh-MIR4435-2HG-transfected HGC27 (Figure 2G). These findings suggest that MIR4435-2HG promotes migration and invasion of GC cells by inducing EMT.Research showed that lncRNAs may regulate intracellular signaling through their interaction with RNA-binding proteins [15, 16]. Therefore, RNA-pull-down experiments were performed to search for MIR4435-2HG-interacting proteins. A specific band associated with biotinylated sense MIR4435-2HG was identified by silver staining after the pull-down assay (Figure 4A, red box). This band was cut out, digested, and subjected to mass spectrometry, which identified DSP, DCD, DSC1, HEL-S-270, HRNR, and JUP as MIR4435-2HG-interacting proteins (Figure 4B, Supplementary Figure 1D). Next, we examined the effect of MIR4435-2HG silencing on the expression of the above proteins by RT-qPCR. Results showed that DSP and HRNR were up-regulated in HGC-27 cells transfected with shMIR4435-2HG (Figure 4C). Furthermore, we verified the interaction of DSP with MIR4435-2HG or HRNR with MIR4435-2HG by RNA pull-down assay; DSP was detected in sense, but not antisense, MIR4435-2HG pull-down protein complexes (Figure 4D). In contrast, HRNR could not interact with MIR4435-2HG. Finally, we studied the interaction between MIR4435-2HG and DSP in HGC-27/shMIR4435-2HG and HGC-27/shNC xenografts by WB and IHC assays. Results demonstrated that the expression of DSP was inversely related to that of MIR4435-2HG (Figure 4E). These data suggest that MIR4435-2HG interacts with DSP, reducing its expression.To test the hypothesis that MIR4435-2HG regulates the Wnt/beta-catenin signaling through DSP to promote GC tumorigenesis and progression, we conducted rescue assays by co-transfecting shMIR4435-2HG and si-DSP into HGC-27 cells. As expected, CCK8 assays showed that DSP silencing partly rescued growth inhibition induced by shMIR4435-2HG (Figure 6A). In turn, apoptosis was reduced in cells co-transfected with shMIR44352HG and si-DSP, compared to cells transfected with shMIR4435-2HG or scrambled NC shRNA alone (Figure 6B and Supplementary Figure 1E). Similarly, partial restoration of migratory and invasive capacity was seen in MIR4435-2HG knockdown cells after si-DSP transfection. Under this condition, the number of migrating and invading cells was also lower in co-transfected with shMIR44352HG and si-DSP group than that transfected with shMIR4435-2HG (Figure 6C, -,6D6D and Supplementary Figure 2C).	31484163	RID07665	interact with protein	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Prostate cancer	NEAT1	HMGA2	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell invasion(+)	ceRNA(miR-98-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000149948	NA	283131	8091	LINC00084|NCRNA00084|TncRNA|VINC	BABL|HMGI-C|HMGIC|LIPO|SRS5|STQTL9	Long non-coding RNA-NEAT1, a sponge for miR-98-5p, promotes expression of oncogene HMGA2 in prostate cancer.To investigate the role of NEAT1 in PCa, we first measured NEAT1 expression in BPH, PCa and matched adjacent HC tissues. Although NEAT1 level exhibits no obvious difference in BPH and HC tissues (P>0.05, Figure 1A), it is clearly showed that the expression level of NEAT1 is significantly up-regulated in PCa tissues, compared with BPH (P<0.0001) and HC tissues (P<0.0001, with average 6.42-fold increase compared with matched healthy tissues, Figure 1B). Consistently, the overexpression of NEAT1 in PCa is also validated in cell lines, as shown that NEAT1 is up-regulated in DU145, PC3 and LNCaP PCa cell lines compared with normal prostate epithelial cell line RWPE- 1 (-(FigureFigure 1C). Then cell proliferation ability was determined by CCK8 assay in RWPE-1, PC3 and DU145 cell lines. It showed that the proliferation ability of PC3 and DU145, which have high NEAT1 expression level, was much stronger that normal prostate epithelial cell line RWPE-1 (Figure 1D). Taken together, these finding suggest that NEAT1 may play a key role in the progression of PCa.By using CCK-8 assay, we observed that the cell viability of NEAT1-knockdown cells was significantly inhibited compared with control cells (Figure 1F). Likewise, PC3 and DU145 cells with reduced NEAT1 expression showed impaired colony formation capability (Figure 1G), suggesting that high-expression level of NEAT1 is required for cell growth in PCa cells. Furthermore, we evaluated the invasion ability of control cell or NEAT1-knockdown PCa cells by using Transwell-Matrigel invasion assay. In line with our hypothesis, NEAT1 siRNA treatment significantly inhibited cell invasion in PC3 and DU145 cells (P<0.001, Figure 1H). Collectively, our data clearly showed NEAT1 contributes to cell growth and invasion in PCa cells.To support the hypothesis that HMGA2 is a novel target of miR-98-5p, PC3 and DU145, cells were subjected to miR-98-5p mimics and negative control treatment. As expected, HMGA2 mRNA level was significantly reduced by miR-98-5p overexpression (Figure 2C). Furthermore, to confirm the direct interaction between miR-98-5p and HMGA2 in vitro, we cloned miR-98-5p-binding sites of HMGA2 into luciferase report plasmid to establish WT of HMGA2 3'-UTR report plasmids. Besides, we mutated miR-98-5p-binding region and constructed mutant 3'-UTR regions of HMGA2. PC-3 and DU-145 cells were transiently transfected with these constructs along with miR-98-5p mimics or NC. In line with our hypothesis, miR-98-5p overexpression remarkably inhibited luciferase activity of the reporter genes containing WT 3'-UTR regions of HMGA2, but no inhibitory effects were observed in mutated cell lines, suggesting that HMGA2 is a direct target of miR-98-5p in PCa cells (Figure 2C). And we also showed that the expression level of HMGA2 and miR-98-5p were negatively correlated in PCa tissues (Supplementary Figure S2C).Together, we for the first time showed that NEAT1 functions as a miR-98-5p sponge to activate oncogene HMGA2 in PCa cells.Since NEAT1 is able to regulate HMGA2 expression in PCa cells, we then questioned whether HMGA2 in fact has oncogenic role in the development of PCa cells. We subsequently treated PC3 cells by using HMGA2 siRNA or NC. As shown in Figure 3A, the cell viability was remarkably suppressed by HMGA2 knockdown. In addition, HMGA2 inhibition led to the reduced colony formation (Figure 3B) and invasion ability (Figure 3C). Collectively, these findings confirmed that HMGA2 functions as oncogene in PCa cells.	31481527	RID07666	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Gastric adenocarcinoma	MALAT1	AKT3	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117020	NA	378938	10000	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	PKBG|PRKBG|RAC-gamma	MALAT1 promotes gastric adenocarcinoma through the MALAT1/miR-181a-5p/AKT3 axis.In order to identify the function of MALAT1 in gastric adenocarcinoma, we first examined the serum levels of MALAT1 in 70 patients with gastric adenocarcinoma and 70 healthy controls by quantitative reverse transcription polymerase chain reaction (qRT-PCR. The clinical parameters between the two groups of samples including age and gender are shown in electronic supplementary material, figure S1. Statistical analysis indicated that the serum levels of MALAT1 were not affected by these parameters (electronic supplementary material, figure S1A). Next, our qRT-PCRresults showed that MALAT1 was highly expressed in the serum of patients with gastric adenocarcinoma (figure 1a). In addition, patients were divided into two groups according to pathological stage. As shown in figure 1b, the expression of MALAT1 in the blood samples of patients with higher malignancy (high-grade group) was significantly higher than that in patients with low malignancy (low-grade group). Therefore, we conclude that MALAT1 is highly expressed in patients with gastric adenocarcinoma and correlates with higher malignancy.To further explore the biological effects of MALAT1 on cell viability, we then examined the proliferation and apoptosis of MGC-803 cells after knocking down MALAT1. The results showed that, after MALAT1 knockdown, the proliferation ability of MGC-803 cells was significantly reduced (figure 3a). A clonogenic survival assay was used to assess cell apoptosis in MGC-803 cells exposed to radiation at 8 Gy with an average dose rate of 100 cGy min-1. Cells were then cultured to allow colony formation and the number of colonies was counted. The results showed that knockdown of MALAT1 remarkably reduced the colony number compared with the control group (figure 3b), indicating that cell apoptosis was increased by MALAT1 depletion.To further clarify the mechanism of MALAT1, we predicted the possible binding targets of MALAT1 by bioinformatics. Several miRNAs were found, such as miR-6807-3p, miR-217, miR-181a-5p, miR-3690 and miR-942-5p. We examined the expression of the miRNAs above in MGC-803 cells after knocking down MALAT1. Our results revealed that the expression of miR-181a-5p was significantly upregulated in MALAT1 knockdown MGC-803 cells (figure 4a), whereas no significant differences were observed in other miRNAs. The predicted binding sequence is shown in figure 4b. The sequences of miR-181a-5p including the binding sites of MALAT1 and the mutated binding sites were subsequently subcloned into a pMIR reporter vector to determine if miR-181a-5p was a direct functional target of MALAT1. In MGC-803 cells, the luciferase reporter assay showed a remarkable decrease in luciferase activity when MALAT1 was co-transfected with miR-181a-5p-WT. However, no significant differences were observed when cells were co-transfected with miR-181a-5p-mut and MALAT1 (electronic supplementary material, figure S3A). We further identified that miR-181a-5p and AKT3 could interact in three positions through bioinformatics prediction (figure 5a). The sequences of AKT3 including the binding sites of miR-181a-5p and the mutated binding sites were subsequently subcloned into a pMIR reporter vector to determine if AKT3 was a direct functional target of miR-181a-5p. In MGC-803 cells, the luciferase reporter assay showed a remarkable decrease in luciferase activity when miR-181a-5p was co-transfected with AKT3-WT. However, no significant differences were observed when cells were co-transfected with AKT3-mut and miR-181a-5p (electronic supplementary material, figure S3B). Next, we examined the protein levels of AKT3 under various conditions. Our results showed that MGC-803 cells expressed higher levels of AKT3 than GES-1 cells (figure 5b,c). In addition, knockdown of MALAT1 by siMALAT1-1 or siMALAT1-2 reduced the expression of AKT3, consistent with the result that overexpression of miR-181a-5p decreased the protein level of AKT3 (figure 5b,c). Therefore, our results suggest that MALAT1 upregulates the expression of AKT3 through targeting miR-181a-5p.To confirm whether the inhibitory role of MALAT1 relies on the interaction with miR-181a-5p and the AKT3 pathway, we overexpressed miR-181a-5p or directly inhibited the AKT pathway with the inhibitor ipatasertib in MGC-803 cells. Our results showed that both miR-181a-5p and ipatasertib inhibited cell proliferation (figure 6a) and increased cell apoptosis (figure 6b) in MGC-803 cells, which is consistent with the effects of MALAT1 knockdown. Our data further indicate that MALAT1 competitively binds to miR-181a-5p, making miR-181a-5p unable to bind to AKT3 mRNA, thereby upregulating AKT3 protein levels and ultimately promoting tumour growth.	31480991	RID07667	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Papillary thyroid carcinoma	SP1	SAMMSON	positively-E	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+);tumorigenesis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000240405	GRCh38_3:69999550-70518064	6667	101927152	NA	LINC01212	Long noncoding RNA SAMMSON promotes papillary thyroid carcinoma progression through p300/Sp1 axis and serves as a novel diagnostic and prognostic biomarker.First, we evaluated SAMMSON expression in 70 pairs of PTC and adjacent normal tissues. As shown in Figure 1a, SAMMSON was notably overexpressed in PTC tissues in comparison to paracancerous tissues. Similarly, the SAMMSON expression in PTC cell lines was significantly higher than that in normal follicular epithelial Nthy-ori 3'- cells (Figure 1b).To explore the mechanism by which SAMMSON functions in PTC, we performed RNA pull-down assay, followed by mass spectrometry. The results showed that SAMMSON could bind to many proteins (Figure 4a, Table S1), among which p300 attracted our attention because it was an important histone acetyltransferase involved in multiple cellular processes.14 Next, we confirmed the interaction between SAMMSON and p300 by RNA pull-down assay and subsequent western blotin TPC-1 and BCPAP cells (Figure 4b). Consistently, SAMMSON was considerably enriched by p300 antibody compared to nonspecific IgG antibody, as illustrated by RIP assay (Figure 4c). However, ablation of SAMMSON did not alter the expression level of p300 mRNA or protein (Figure 4d). Through analyzing the ENCODE ChIP-seq database, we found that a large amount of H3K27ac and H3K9ac were enriched within the promoter region of Sp1 (Figure 4e), suggesting that Sp1 may be regulated by p300. As expected, ChIP-qPCR results showed that p300 as well as H3K27ac and H3K9ac directly bound to the Sp1 promoter, and these occupations were dramatically decreased after SAMMSON knockdown both in TPC-1 and BCPAP cells (Figure 4f), implying that SAMMSON acts as a scaffold to recruit p300 to the Sp1 promoter. Further, exogenous expression of SAMMSON significantly increased Sp1 mRNA and protein expression, while these upregulation effects were obviously abrogated by silencing of p300 (Figure 4g), suggesting that p300 is required for SAMMSON-mediated regulation of Sp1. Moreover, knockdown of p300 or Sp1 could evidently block the enhanced proliferative and invasive capabilities of TPC-1 and BCPAP cells caused by SAMMSON overexpression (Figure 4h). Collectively, these data demonstrate that SAMMSON upregulates Sp1 expression via recruiting p300 to Sp1 promoter and accelerating histone H3 acetylation.	31478331	RID07668	expression association	prognosis,metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)
Papillary thyroid carcinoma	SAMMSON	EP300	interact	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);metastasis process(+);cell invasion(+);tumorigenesis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000100393	NA	101927152	2033	LINC01212	KAT3B|p300	Long noncoding RNA SAMMSON promotes papillary thyroid carcinoma progression through p300/Sp1 axis and serves as a novel diagnostic and prognostic biomarker.First, we evaluated SAMMSON expression in 70 pairs of PTC and adjacent normal tissues. As shown in Figure 1a, SAMMSON was notably overexpressed in PTC tissues in comparison to paracancerous tissues. Similarly, the SAMMSON expression in PTC cell lines was significantly higher than that in normal follicular epithelial Nthy-ori 3'- cells (Figure 1b).To explore the mechanism by which SAMMSON functions in PTC, we performed RNA pull-down assay, followed by mass spectrometry. The results showed that SAMMSON could bind to many proteins (Figure 4a, Table S1), among which p300 attracted our attention because it was an important histone acetyltransferase involved in multiple cellular processes.14 Next, we confirmed the interaction between SAMMSON and p300 by RNA pull-down assay and subsequent western blotin TPC-1 and BCPAP cells (Figure 4b). Consistently, SAMMSON was considerably enriched by p300 antibody compared to nonspecific IgG antibody, as illustrated by RIP assay (Figure 4c). However, ablation of SAMMSON did not alter the expression level of p300 mRNA or protein (Figure 4d). Through analyzing the ENCODE ChIP-seq database, we found that a large amount of H3K27ac and H3K9ac were enriched within the promoter region of Sp1 (Figure 4e), suggesting that Sp1 may be regulated by p300. As expected, ChIP-qPCR results showed that p300 as well as H3K27ac and H3K9ac directly bound to the Sp1 promoter, and these occupations were dramatically decreased after SAMMSON knockdown both in TPC-1 and BCPAP cells (Figure 4f), implying that SAMMSON acts as a scaffold to recruit p300 to the Sp1 promoter. Further, exogenous expression of SAMMSON significantly increased Sp1 mRNA and protein expression, while these upregulation effects were obviously abrogated by silencing of p300 (Figure 4g), suggesting that p300 is required for SAMMSON-mediated regulation of Sp1. Moreover, knockdown of p300 or Sp1 could evidently block the enhanced proliferative and invasive capabilities of TPC-1 and BCPAP cells caused by SAMMSON overexpression (Figure 4h). Collectively, these data demonstrate that SAMMSON upregulates Sp1 expression via recruiting p300 to Sp1 promoter and accelerating histone H3 acetylation.	31478331	RID07669	interact with protein	prognosis,metastasis	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	SNHG7	MIR425	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000199032	NA	84973	494337	NCRNA00061	MIRN425|hsa-mir-425|mir-425	lncRNA SNHG7 sponges miR-425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/beta-catenin/EMT signalling pathway.To determine whether there was a difference of SNHG7 expressional profile in hepatic carcinoma and adjacent histologically normal hepatic tissues, 40 pairs of specimens were analysed with qRT-PCR The result suggested that SNHG7 was significantly overexpressed in hepatic carcinoma tissue compared with adjacent normal tissue (Figure 1A). Moreover, the SNHG7 expression level may be associated with the metastasis of hepatic carcinoma (Figure 1B). Further, Kaplan-Meier survival analysis also showed that up-regulated SNHG7 was positive correlation with poor OS of patients with hepatic carcinoma (Figure 1C). Furthermore, statistical analysis revealed that there is a significant association between overexpressed SNHG7 and bad clinical stage (Figure 1D). Overall, these findings elucidated that the overexpressed SNHG7 may be associated with progression, metastasis, and poor prognosis of patients with hepatic carcinoma.RNA interference was performed to explore the biologic function of SNHG7 in hepatic carcinoma. siRNA targeting the coding region of SNHG7 (SNHG7-inhi) was transfected into HepG2 and HCC-LM3 cells, respectively. The knockdown efficiency of SNHG7-siRNA was confirmed by RT-PCRassay, and result showed that the expression level of SNHG7 in SNHG7-siRNA-transfected HepG2 and HCC-LM3 cells was drastically decreased by 70% (Figure 2A). MTT and colony formation assay suggested that knockdown of SNHG7 significantly suppressed the proliferation of HepG2 and HCC-LM3 cells (Figure 2B-E). In addition, transfection of SNHG7-siRNA induced significantly increased percentage of apoptotic cells in HepG2 and HCC-LM3 cells (Figure 2F,G), suggesting that knockdown of SNHG7 could promote apoptosis of hepatic carcinoma. Subsequently, cell invasion and migration assays illustrated that overexpressed SNHG7 was positive correlated with migration ability of HepG2 and HCC-LM3 cells (Figure 2H-K). Meanwhile, wound-healing assay suggested that knockdown of SNHG7 retarded the closing of scratch wound (Figure 2I,M). Furthermore, silence of SNHG7 led to decreased level of metastasis related protein MMP-9 (matrix metallopeptidase 9), N-cadherin, and increased level of cell adhesion protein E-cadherin (Figure 2N). Above result suggested that knockdown of SNHG7 could impede hepatic carcinoma cell proliferation and metastasis.To determine whether SNHG7 could interact with the miRNA as ceRNAs or natural miRNA sponge as previous report, targetscan was conducted with bioinformatic database (TargetScanHuman Release 7.2, Starbase v3.0 and miRcode). Bioinformatics analysis indicated that there are putative binding sites between SNHG7 and miR-425 (Figure 3A). Then dual-luciferase reporter assay was conducted to validate the interaction between miR-425-5p and SNHG7 in HepG2 cells. Result revealed that luciferase activity of SNHG7-Wt was dramatically reduced by miR-425 mimic. In contrast, the luciferase activity of SNHG7-Mut experienced no statistical changes (Figure 3B). These results indicated that SNHG7 could sponge miR-425 as a ceRNA.miR-425 rescue experiments were performed to explore how SNHG7 exerted its biological role through sponging miR-425. A significant increased miR-425 expression was observed while SNHG7 was knockdown both in HepG2 and HCC-LM3 cells (Figure 3C). The result further confirmed SNHG7 sponging miR-425 as a ceRNA. Then, miR-425-mimic was transfected into HepG2 and HCC-LM3 cells to elucidate the function of miR-425 in hepatic carcinoma proliferation and metastasis. Wound healing and transwell assays suggested that migratory and invasive ability were significant reduced in cells transfected with miR-425-mimic (Figure 3D-I). Meanwhile, the EMT related proteins (beta-catenin, MMP-9, E-cadherin, and N-cadherin) were examined. While transfected with miR-425-mimic, the protein levels of beta-catenin, MMP-9, and N-cadherin were decreased markedly. In contrast, E-cadherin expression was increased notably both in miR-425-mimic transfected HepG2 and HCC-LM3 cells (Figure 3J). Moreover, downregulation of miR-425 could significantly block the antimigration effect, which is induced by SNHG7-inhi treatment in HepG2 cells (Figure 3K-L). Above results suggested that SNHG7 promotes metastasis of hepatic carcinoma cell via Wnt/beta-catenin/EMT signalling pathway as a miR-425 sponge.	31478234	RID07670	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	
Hepatocellular carcinoma	MALAT1	SNAI2	positively-E	dual-luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);metastasis process(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000019549	NA	378938	6591	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	SLUG|SLUGH|SLUGH1|SNAIL2	miR-124-3p availability is antagonized by LncRNA-MALAT1 for Slug-induced tumor metastasis in hepatocellular carcinoma.Expression levels of MALAT1 in six common solid malignant cell lines (stomach carcinoma: SGC-7901 and NCL-N87; hepatocarcinoma: HepG2 and Huh-7; prostate cancer: DU145 and LNCaP) were detected. As shown in Figure -Figure1F,1F, after normalization to GAPDH expression, MALAT1 expression levels were highest in HepG2 and Huh-7 cells (P < .001). We then examined MALAT1 expression in human liver cell lines and HCC cell lines; the MALAT1 levels were significantly increased in the HCC cell lines (Figure -(Figure1G).1G). Next, we altered the expression of MALAT1 in HepG2 and Huh-7 cells to investigate the biological role of MALAT1 in liver cancer. Three separate MALAT1 siRNAs were synthesized and transfected into HepG2 cell lines, either separately or in combination. MALAT1 expression was significantly lower in si-MALAT1 transfected cells than in control cells (P < .001). siRNA1 decreased MALAT1 expression to the greatest extent, so siRNA1 was used for subsequent experiments (Figure -(Figure1H).1H). Transwell assays and scratch wound assays showed significantly reduced invasion and migration abilities of cells with downregulated MALAT1 expression compared to those of the control cells (Figure -(Figure1I,J).1I,J). These results indicate that MALAT1 promotes the migration and invasion of HCC cells.Many previous studies have shown that lncRNAs can function as ceRNAs in carcinogenesis. The ceRNA theory suggests that certain lncRNAs can bind to specific miRNAs by partial hybridization, rendering the miRNA to be unable to bind to its target gene, thereby causing the target mRNA to lose the inhibition of the miRNA.17, 18 Therefore, we considered whether MALAT1 had the same effect in HCC cell lines. As expected, RNA immunoprecipitation (RIP) testing of HCC cell extracts confirmed our hypothesis. MALAT1 and Ago2 can bind directly (Figure -(Figure2A).2A). Ago2 is involved in miRNA-mediated mRNA suppression and is a component of the RNA-induced silencing complex. This means that MALAT1 can act as a ceRNA for specific miRNAs. To further validate this hypothesis, we used the online bioinformatics database Starbase 2.019 and observed that the MALAT1 sequence contains potential miR-124-3p-binding sites (Figure -(Figure2B).2B). Next, luciferase reporter plasmids containing a mutant MALAT1 sequence (the site of the mutation was the miR-124-3p binding site in the MALAT1 molecular sequence predicted by bioinformatics) or the wild-type MALAT1 sequence were constructed. The luciferase activity of MALAT1-WT was shown to be decreased in the dual-luciferase reporter assay results, and there was no change in the luciferase activity of MALAT1-MUT in HEK293 cells (Figure -(Figure2C).2C). Additionally, RNA-binding protein immunoprecipitation experiments showed that miR-124-3p and MALAT1 were significantly enriched in the immunoprecipitates of Ago2 relative to those of the control IgG immunoprecipitates (Figure -(Figure2D).2D). Notably, real-time PCR analysis of 30 HCC tissues demonstrated a significant negative correlation between miR-124-3p and MALAT1 levels (Figure -(Figure2E).2E). Real-time PCR showed that MALAT1 knockdown caused a significant increase in miR-124-3p expression levels (Figure -(Figure2F),2F), and MALAT1 expression was decreased in cells transfected with miR-124-3p mimics. (Figure -(Figure2G).2G). These results indicate that MALAT1 and miR-124-3p have a negative regulatory relationship in HCC cells. Functional miR-124-3p experiments were performed using HepG2 and Huh7 cells. The results showed that migration and invasion abilities were upregulated in the si-MALAT1 + miR-124-3p inhibitor groups (Figure -(Figure2H,I).2H,I). In HCC cells, these properties were attenuated by si-MALAT1. As expected, these data indicate that MALAT1  function depends partially on miR-124-3p.As shown in an online database, Slug may be an alternative downstream target for miR-124-3p (Figure -(Figure44A).19 We constructed a mutated Slug3'-UTR, and luciferase activity was demonstrated using a dual-luciferase reporter assay. The results showed that the luciferase activity was decreased by only wild-type Slug and not by mutant Slug (P < .001, Figure -Figure4B).4B). Notably, real-time PCR analysis of 30 HCC tissues revealed a significant negative correlation between miR-124-3p and Slug levels (Figure -(Figure4C).4C). In vitro, we demonstrated that the upregulation of miR-124-3p inhibited Slug mRNA and protein expression in HCC cells (Figure -(Figure4D-G).4D-G). As previously stated, miR-124-3p reduces HCC cell invasion and metastasis. However, does miR-124-3p's function depend on its target gene, Slug- We overexpressed Slug in HCC cells overexpressing miR-124-3p and found that Slug restored the altered invasion and metastatic potential caused by the miR-124-3p mimic. This suggests that the biological function of miR-124-3p is partially dependent on its target gene, Slug.To investigate whether Slug correlated with MALAT1 in HCC cells, we performed an expression analysis. As expected, a positive correlation was found between MALAT1 and Slug expression in HCC using the TCGA database (Figure -(Figure66A).16 We obtained similar results for 30 HCC tissues (Figure -(Figure6B).6B). Similarly, MALAT1 knockdown caused the downregulation of Slug expression, and this dynamics was reversed by transfection with a miR-124-3p inhibitor (Figure -(Figure6C).6C). This result further confirmed that MALAT1 positively regulates Slug expression via miR-124-3p. Further results indicated that increased Slug levels reversed the invasion and metastasis attenuation in HCC cells induced by MALAT1 knockdown (Figure -(Figure6D,E)6D,E) and confirmed that MALAT1 promoted HCC metastasis dependent on Slug.	31466138	RID07671	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Gastric cancer	DLX6-AS1	POU2F1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-204-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000143190	NA	285987	5451	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	OCT1|OTF1|Oct1Z|oct-1B	DLX6-AS1/miR-204-5p/OCT1 positive feedback loop promotes tumor progression and epithelial-mesenchymal transition in gastric cancer.We collected and analyzed the RNA-seq data of 375 GCs and 32 normal samples from TCGA database. The results showed that DLX6-AS1 was overexpressed in GC tissues (P-=-0.0004, Fig. 1a). After excluding samples that lacked data regarding survival time and status, a total of 372 GC patients were divided into two groups for Kaplan-Meier curve analysis according to the median value of DLX6-AS1 expression. The result indicated that high expression of DLX6-AS1 was significantly associated with poor prognosis of GC patients (P-=-0.042, Fig. 1b). Furthermore, we performed qRT-PCRto analyze the expression level of DLX6-AS1 in 56 GC and corresponding noncancerous tissues. The results of qRT-PCRwere consistent with the data in TCGA database (P-<-0.01, Fig. 1c).To elucidate the function of DLX6-AS1, DLX6-AS1 was knocked down by transfecting three different siRNAs into cells. At 48 h after transfection, we performed qRT-PCRto verify that DLX6-AS1 was effectively suppressed by siRNA #2 and #3 (P-<-0.01, Fig. 2a). The results of CCK-8 assay revealed that DLX6-AS1 downregulation reduced cell growth ability (P-<-0.01, Fig. 2b). Similarly, the number of visible colonies was decreased in cells transfected with DLX6-AS1 knockdown compared to transfection with si-NC (P-<-0.01, Supplementary Fig. 2a). The influence of DLX6-AS1 on invasion and migration was investigated by Transwell assay. We observed that siRNA transfection significantly inhibited the migration and invasion capacity of GC cells (P-<-0.01, Fig. 2c). Furthermore, we obtained similar results at different concentrations of chemoattractant (P-<-0.01, Supplementary Figs. 3, 4).To explore the possible molecular mechanism of DLX6-AS1 in GC, we performed bioinformatics prediction to identify the target of DLX6-AS1 by intersecting the predicted results between miRcode, DIANA-LncBase and downregulated miRNAs in TCGA. As shown in Fig. 3a, we identified four miRNAs (miR-100-3p, miR-145-5p, miR-195-3p, and miR-204-5p) that showed the possibility of interacting with DLX6-AS1. Then, we performed qRT-PCRto detect expression of the corresponding miRNAs. The results showed that only miR-204-5p was upregulated in si-DLX6-AS1-transfected cell lines (P-<-0.01, Fig. 3b). Consequently, we selected miR-204-5p for further study. The potential base pair binding sites between miR-204-5p and DLX6-AS1 are shown in Fig. 3c. To further verify our hypothesis, we co-transfected luciferase reporter vectors and miR-204-5p mimic or miR-NC into the HEK293T, SGC-7901 and AGS cell lines. As shown in Fig. 3d, luciferase activity was significantly reduced in the DLX6-AS1-WT together with miR-204-5p mimic reaction system (P-<-0.05). This indicated that miR-204-5p interacted with DLX6-AS1 through sequence matching.To further clarify the oncogenic mechanism of the DLX6-AS1/miR-204-5p axis, we identified mRNAs that were positively co-expressed with DLX6-AS1 based on expression data from TCGA. As a result, we found a significant positive correlation between OCT1 and DLX6-AS1 in 375 GC samples (P-=-3.22E-10, r-=-0.659, Fig. 5a). According to the prediction of miRTarBase, the 3'-UTR region of OCT1 contains potential binding sites for miR-204-5p (Fig. 5b). We performed a luciferase reporter assay by co-transfecting with OCT1-WT or OCT1-MUT constructed plasmids and miR-204-5p mimic or miR-NC into the HEK293T, SGC-7901 and AGS cell lines. As shown in Fig. 5c, luciferase activity was significantly reduced in the OCT1-WT together with miR-204-5p mimics reaction system (P-<-0.05). The results of qRT-PCRand western blot showed that the expression of OCT1 could be promoted by miR-204-5p inhibitor (P-<-0.01), but the effects could be weakened by co-transfection with si-DLX6-AS1 and miR-204-5p inhibitor (P-<-0.01, Fig. 5d, e). As shown in Fig. 5f, there was a negative relationship between miR-204-5p and OCT1 expression from 56 GC tissues (P-=-1.87E-4, r-=---0.472). Collectively, our results indicated that DLX6-AS1 positively regulates OCT1 expression by binding miR-204-5p in GC.To further explore the regulatory mechanism of DLX6-AS1 in GC, we matched the promoter sequences of DLX6-AS1 with potential transcription factors using JASPAR. Interestingly, we found that the transcription factor OCT1 contained binding sites that could interact with the DLX6-AS1 promoter, and we chose the top five of them for further investigation (Fig. 7a, b). As shown in Fig. 7c, d, the P2 region (from - 750 to - 1350 bp) of the DLX6-AS1 promoter showed strong affinity to OCT1 by ChIP assays (P-<-0.01). Moreover, we performed a luciferase assay to further investigate the specific binding sites between OCT1 and the DLX6-AS1 promoter. As shown in Fig. 7e, luciferase activity was elevated in WT and MUT2 of the P2 region group which was co-transfected with the OCT1 overexpression vector (P-<-0.01). The results indicated that the sequence between - 928 and - 939 bp in the promoter is the validated binding site of OCT1. Furthermore, overexpression of OCT1 upregulated DLX6-AS1 in GC cell lines as shown in Fig. 7f (P-<-0.01). According to qRT-PCRassays in 56 GC tissues, there was a positive correlation between OCT1 and DLX6-AS1 (P-=-2.31E-8, r-=-0.671, Fig. 7g). Hence, the results from our study revealed that DLX6-AS1/miR-204-5p/OCT1 formed a positive feedback loop in GC (Fig. 7h).	31463827	RID07672	ceRNA or sponge	chemoresistance,prognosis		UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807)
Gastric cancer	POU2F1	DLX6-AS1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000143190	NA	ENSG00000231764	GRCh38_7:96955141-97014088	5451	285987	OCT1|OTF1|Oct1Z|oct-1B	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	DLX6-AS1/miR-204-5p/OCT1 positive feedback loop promotes tumor progression and epithelial-mesenchymal transition in gastric cancer.We collected and analyzed the RNA-seq data of 375 GCs and 32 normal samples from TCGA database. The results showed that DLX6-AS1 was overexpressed in GC tissues (P-=-0.0004, Fig. 1a). After excluding samples that lacked data regarding survival time and status, a total of 372 GC patients were divided into two groups for Kaplan-Meier curve analysis according to the median value of DLX6-AS1 expression. The result indicated that high expression of DLX6-AS1 was significantly associated with poor prognosis of GC patients (P-=-0.042, Fig. 1b). Furthermore, we performed qRT-PCRto analyze the expression level of DLX6-AS1 in 56 GC and corresponding noncancerous tissues. The results of qRT-PCRwere consistent with the data in TCGA database (P-<-0.01, Fig. 1c).To elucidate the function of DLX6-AS1, DLX6-AS1 was knocked down by transfecting three different siRNAs into cells. At 48 h after transfection, we performed qRT-PCRto verify that DLX6-AS1 was effectively suppressed by siRNA #2 and #3 (P-<-0.01, Fig. 2a). The results of CCK-8 assay revealed that DLX6-AS1 downregulation reduced cell growth ability (P-<-0.01, Fig. 2b). Similarly, the number of visible colonies was decreased in cells transfected with DLX6-AS1 knockdown compared to transfection with si-NC (P-<-0.01, Supplementary Fig. 2a). The influence of DLX6-AS1 on invasion and migration was investigated by Transwell assay. We observed that siRNA transfection significantly inhibited the migration and invasion capacity of GC cells (P-<-0.01, Fig. 2c). Furthermore, we obtained similar results at different concentrations of chemoattractant (P-<-0.01, Supplementary Figs. 3, 4).To explore the possible molecular mechanism of DLX6-AS1 in GC, we performed bioinformatics prediction to identify the target of DLX6-AS1 by intersecting the predicted results between miRcode, DIANA-LncBase and downregulated miRNAs in TCGA. As shown in Fig. 3a, we identified four miRNAs (miR-100-3p, miR-145-5p, miR-195-3p, and miR-204-5p) that showed the possibility of interacting with DLX6-AS1. Then, we performed qRT-PCRto detect expression of the corresponding miRNAs. The results showed that only miR-204-5p was upregulated in si-DLX6-AS1-transfected cell lines (P-<-0.01, Fig. 3b). Consequently, we selected miR-204-5p for further study. The potential base pair binding sites between miR-204-5p and DLX6-AS1 are shown in Fig. 3c. To further verify our hypothesis, we co-transfected luciferase reporter vectors and miR-204-5p mimic or miR-NC into the HEK293T, SGC-7901 and AGS cell lines. As shown in Fig. 3d, luciferase activity was significantly reduced in the DLX6-AS1-WT together with miR-204-5p mimic reaction system (P-<-0.05). This indicated that miR-204-5p interacted with DLX6-AS1 through sequence matching.To further clarify the oncogenic mechanism of the DLX6-AS1/miR-204-5p axis, we identified mRNAs that were positively co-expressed with DLX6-AS1 based on expression data from TCGA. As a result, we found a significant positive correlation between OCT1 and DLX6-AS1 in 375 GC samples (P-=-3.22E-10, r-=-0.659, Fig. 5a). According to the prediction of miRTarBase, the 3'-UTR region of OCT1 contains potential binding sites for miR-204-5p (Fig. 5b). We performed a luciferase reporter assay by co-transfecting with OCT1-WT or OCT1-MUT constructed plasmids and miR-204-5p mimic or miR-NC into the HEK293T, SGC-7901 and AGS cell lines. As shown in Fig. 5c, luciferase activity was significantly reduced in the OCT1-WT together with miR-204-5p mimics reaction system (P-<-0.05). The results of qRT-PCRand western blot showed that the expression of OCT1 could be promoted by miR-204-5p inhibitor (P-<-0.01), but the effects could be weakened by co-transfection with si-DLX6-AS1 and miR-204-5p inhibitor (P-<-0.01, Fig. 5d, e). As shown in Fig. 5f, there was a negative relationship between miR-204-5p and OCT1 expression from 56 GC tissues (P-=-1.87E-4, r-=---0.472). Collectively, our results indicated that DLX6-AS1 positively regulates OCT1 expression by binding miR-204-5p in GC.To further explore the regulatory mechanism of DLX6-AS1 in GC, we matched the promoter sequences of DLX6-AS1 with potential transcription factors using JASPAR. Interestingly, we found that the transcription factor OCT1 contained binding sites that could interact with the DLX6-AS1 promoter, and we chose the top five of them for further investigation (Fig. 7a, b). As shown in Fig. 7c, d, the P2 region (from - 750 to - 1350 bp) of the DLX6-AS1 promoter showed strong affinity to OCT1 by ChIP assays (P-<-0.01). Moreover, we performed a luciferase assay to further investigate the specific binding sites between OCT1 and the DLX6-AS1 promoter. As shown in Fig. 7e, luciferase activity was elevated in WT and MUT2 of the P2 region group which was co-transfected with the OCT1 overexpression vector (P-<-0.01). The results indicated that the sequence between - 928 and - 939 bp in the promoter is the validated binding site of OCT1. Furthermore, overexpression of OCT1 upregulated DLX6-AS1 in GC cell lines as shown in Fig. 7f (P-<-0.01). According to qRT-PCRassays in 56 GC tissues, there was a positive correlation between OCT1 and DLX6-AS1 (P-=-2.31E-8, r-=-0.671, Fig. 7g). Hence, the results from our study revealed that DLX6-AS1/miR-204-5p/OCT1 formed a positive feedback loop in GC (Fig. 7h).	31463827	RID07673	expression association	chemoresistance,prognosis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE55807)	
Gastric cancer	CTC-497E21.4	NET1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);RhoA signaling pathway(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000173848	NA	NA	10276	NA	ARHGEF8|NET1A	LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway.RTFQ-PCR was used to detect the expression of CTC-497E21.4 in 60 GC tissues and paired adjacent normal tissues, and the result showed that the expression of CTC-497E21.4 was significantly upregulated in 60 GC tissues compared with adjacent normal tissues (P-=-0.0012, Fig. 1a).Because the expression of CTC-497E21.4 was relatively higher in SGC-7901 and MKN-45 cell lines, we transfected shRNA vector in these two cell lines and an overexpression plasmid was transfected in the AGS cell line (Figure S1). The results showed that sh-CTC-497E21.4 (2#, 3#) had higher knockdown efficiency, so we chose sh2 and sh3 for further study. CCK-8 assay and colony formation assay indicated that CTC-497E21.4 silencing inhibited the proliferation of SGC-7901 and MKN-45 cells (Fig. 2a ), while CTC-497E21.4 overexpression promoted the proliferation of AGS cells (Fig. S2). The transwell invasion assay analysis and wound healing assay found that knockdown of CTC-497E21.4 reduced the number of invaded SGC-7901 and MKN-45 cells and the migration speed was decreased (Fig. 3a ). Conversely, enhancing CTC-497E21.4 produced the opposite effect (Figure S4). These findings inferred that CTC-497E21.4 was involved in cell invasion and migration in GC.FISH and subcellular fractionation analysis were used to detect the distribution of CTC-497E21.4 and the results showed that CTC-497E21.4 was more abundant in the cytoplasm (Fig. 5a, b). To identify the potential miRNA targets of CTC-497E21.4, Starbase, and miRcode, DIANA Tools were used to predict 4 miRNAs (miR-185, miR-761, miR-22, miR-490) which may act as biological targets of CTC-497E21.4 (Fig. 5c). RTFQ-PCR was conducted to validate the binding of candidate miRNAs with CTC-497E21.4 and selected miR-22 for further study. We also detected the expression of CTC-497E21.4 in GC cells transfected with miR-22 inhibitor to determine the direct interaction between CTC-497E21.4 and miR-22 (Figs. 5d, S5). And luciferase reporter assay confirmed this strong relationship between miR-22 and CTC-497E21.4 (Fig. 5e). Similarly, we predicted target genes of miR-22 by TargetScan and NET1 was selected to be the target of miR-22 (Figure S6). Luciferase reporter assay also validated the relationship between miR-22 and NET1 (Fig. 5f).Since NET1 is a RhoA-specific guanine exchange factor (GEF) and RhoA is one of the most extensively investigated members of the Rho GTPase family of proteins, the RhoA signaling pathway has been associated with cell proliferation as well as tumor invasion and metastasis [23, 24]. We tested whether expression of NET1 stimulated RhoA signaling pathway. We transfected sh-CTC-497E21.4, si-NET1 and miR-22 inhibitor vectors into SGC-7901 cell lines and detected the changes in RhoA relative genes. As presented in Fig. 7a, there was a change trend that knockdown of sh-CTC-497E21.4 or si-NET1 could affect NET1, RhoA, CDC42 and Rac1 in mRNA level. In addition, the result of western blot showed that sh-CTC-497E21.4, miR-22 inhibitor, and si-NET1 not only regulated the expression of RhoA, CDC42, and Rac1 at the total protein level, but also showed corresponding changes in phosphorylated proteins (Fig. 7b). Therefore, we speculated that NET1 may work as a RhoGEF and participated in the activation of RhoA signaling pathway which was mediated by CTC-497E21.4/miR-22/NET1 axis. Taken together, our data indicated that CTC-497E21.4 modulated GC cell proliferation, cell cycle, invasion and metastasis via RhoA pathway (Fig. 7c).	31451992	RID07674	ceRNA or sponge	metastasis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Kidney clear cell carcinoma	LINC00997	S100A11	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000281332	GRCh38_7:32760279-32762924	ENSG00000163191	NA	401321	6282	NA	S100C	LINC00997, a novel long noncoding RNA, contributes to metastasis via regulation of S100A11 in kidney renal clear cell carcinoma.LINC00997 expression in KIRC metastases was higher than in nonmetastatic tumors (Fig. 1A). We collected 18 cases of KIRC at our hospital and found that LINC00997 was detected at higher expression levels in tumors compared to adjacent normal tissues (P < 0.05). Meanwhile, LINC00997 was also associated with metastasis (P < 0.05) (Fig. 1B). As LINC00997 and S100A11 were both highly expressed in KIRC and predicted a poor prognosis, we next examined their biological effects. 786-O cells were transfected with si-LINC00997, si-S100A11 or negative controls. Transfected cells were cultured for subsequent arrays. A wound healing assay was performed to evaluate migration ability of 786-O cells. Our results showed that inhibiting LINC00997 or S100A11 decreased migration in 786-O cells (Fig. 3A). Transwell assays were also performed, demonstrating that interfering with LINC00997 or S100A11 expression inhibits migration of 786-O cells (both P < 0.05) (Fig. 3B). western blot was performed and revealed that interfering with LINC00997 or S100A11 expression inhibits metastasis-associated molecular expression of VIM, MMP2 and MMP7 (all P < 0.05) (Fig. 3C). Taken together, thesefindings indicate that LINC00997 and S100A11 regulate cancer cell migration in KIRC.Finally, we assessed the relationship between LINC00997 and S100A11. Our bioinformatics prediction demonstrated that LINC00997 might combine with the S100A11 promoter (Li et al., 2015). The S100A11 promoter has two potential binding sites for the STAT3 protein suggested by analysis of the JASPAR database (Mathelier et al., 2016). LINC00997 also has the potential of combining with STAT3 protein, as suggested by analyzing the LNCPRO database (Lu et al., 2013). Therefore, we hypothesized that LINC00997 combines with the STAT3 transcription factor to regulate S100A11 expression, promoting KIRC metastasis. To test our hypothesis, we constructed luciferase plasmids of the S100A11 promoter, S100A11-pro-luc (S100A11-pro wt), S100A11-pro-1 mut (1264-1274: CTTTTTAGAAT to GCAAAGTC TGC) and S100A11-pro-2 mut (335-345: TTTACAGAAAA to GCCTGC ATTCG) for the following assays. To confirm that LINC00997 combines with the S100A11 promoter, the plasmid and vector, along with siLINC00997 and negative control, were transfected into HEK293 cells. Results from dual-luciferase reporter gene assays showed that silencing LINC00997 significantly decreases luciferase values of S100A11-pro transfected cells compared to negative control cells (Fig. 4A). To identify combined activity of STAT3 with the S100A11 promoter, we transfected these luciferase plasmids, si-STAT3 and their controls into HEK293 cells. Dual-luciferase reporter gene assays were performed, and results demonstrated that si-STAT3 significantly inhibits luciferase values in both S100A11-pro wt and S100A11-pro-2 mut cells (both P < 0.05) but not in S100A11-pro-1 mut cells (P > 0.05, not significant) (Fig. 4B). Lastly, the interaction between LINC00997 and STAT3 was assessed through RIP assays in 786-O cells, which demonstrated that LINC00997 combines with the STAT3 protein (Fig. 4C). Importantly, to confirm the gene regulating expression ability of LINC00997 and STAT3, si-LINC00997, si-STAT3 and their controls were transfected into 786-O cells. western blot results revealed that interfering with LINC00997 or STAT3 expression inhibited S100A11 expression compared to controls in 786-O cells (both P < 0.05)(Fig. 4D). These results suggest that the LINC00997-STAT3-S100A11 axis regulates metastasis in KIRC (Fig. 4E).	31442606	RID07675	expression association	metastasis,prognosis		DOWN(LIHC,BRCA);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE111842,GSE55807)
Kidney clear cell carcinoma	LINC00997	STAT3	interact	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000281332	GRCh38_7:32760279-32762924	ENSG00000168610	NA	401321	6774	NA	APRF	LINC00997, a novel long noncoding RNA, contributes to metastasis via regulation of S100A11 in kidney renal clear cell carcinoma.LINC00997 expression in KIRC metastases was higher than in nonmetastatic tumors (Fig. 1A). We collected 18 cases of KIRC at our hospital and found that LINC00997 was detected at higher expression levels in tumors compared to adjacent normal tissues (P < 0.05). Meanwhile, LINC00997 was also associated with metastasis (P < 0.05) (Fig. 1B). As LINC00997 and S100A11 were both highly expressed in KIRC and predicted a poor prognosis, we next examined their biological effects. 786-O cells were transfected with si-LINC00997, si-S100A11 or negative controls. Transfected cells were cultured for subsequent arrays. A wound healing assay was performed to evaluate migration ability of 786-O cells. Our results showed that inhibiting LINC00997 or S100A11 decreased migration in 786-O cells (Fig. 3A). Transwell assays were also performed, demonstrating that interfering with LINC00997 or S100A11 expression inhibits migration of 786-O cells (both P < 0.05) (Fig. 3B). western blot was performed and revealed that interfering with LINC00997 or S100A11 expression inhibits metastasis-associated molecular expression of VIM, MMP2 and MMP7 (all P < 0.05) (Fig. 3C). Taken together, thesefindings indicate that LINC00997 and S100A11 regulate cancer cell migration in KIRC.Finally, we assessed the relationship between LINC00997 and S100A11. Our bioinformatics prediction demonstrated that LINC00997 might combine with the S100A11 promoter (Li et al., 2015). The S100A11 promoter has two potential binding sites for the STAT3 protein suggested by analysis of the JASPAR database (Mathelier et al., 2016). LINC00997 also has the potential of combining with STAT3 protein, as suggested by analyzing the LNCPRO database (Lu et al., 2013). Therefore, we hypothesized that LINC00997 combines with the STAT3 transcription factor to regulate S100A11 expression, promoting KIRC metastasis. To test our hypothesis, we constructed luciferase plasmids of the S100A11 promoter, S100A11-pro-luc (S100A11-pro wt), S100A11-pro-1 mut (1264-1274: CTTTTTAGAAT to GCAAAGTC TGC) and S100A11-pro-2 mut (335-345: TTTACAGAAAA to GCCTGC ATTCG) for the following assays. To confirm that LINC00997 combines with the S100A11 promoter, the plasmid and vector, along with siLINC00997 and negative control, were transfected into HEK293 cells. Results from dual-luciferase reporter gene assays showed that silencing LINC00997 significantly decreases luciferase values of S100A11-pro transfected cells compared to negative control cells (Fig. 4A). To identify combined activity of STAT3 with the S100A11 promoter, we transfected these luciferase plasmids, si-STAT3 and their controls into HEK293 cells. Dual-luciferase reporter gene assays were performed, and results demonstrated that si-STAT3 significantly inhibits luciferase values in both S100A11-pro wt and S100A11-pro-2 mut cells (both P < 0.05) but not in S100A11-pro-1 mut cells (P > 0.05, not significant) (Fig. 4B). Lastly, the interaction between LINC00997 and STAT3 was assessed through RIP assays in 786-O cells, which demonstrated that LINC00997 combines with the STAT3 protein (Fig. 4C). Importantly, to confirm the gene regulating expression ability of LINC00997 and STAT3, si-LINC00997, si-STAT3 and their controls were transfected into 786-O cells. western blot results revealed that interfering with LINC00997 or STAT3 expression inhibited S100A11 expression compared to controls in 786-O cells (both P < 0.05)(Fig. 4D). These results suggest that the LINC00997-STAT3-S100A11 axis regulates metastasis in KIRC (Fig. 4E).	31442606	RID07676	interact with protein	metastasis,prognosis		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophageal cancer	CCAT2	BAX	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000087088	NA	101805488	581	LINC00873|NCCP1	BCL2L4	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07677	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	CCAT2	APC	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000134982	NA	101805488	324	LINC00873|NCCP1	DP2|DP2.5|DP3|PPP1R46	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07678	expression association	metastasis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Esophageal cancer	CCAT2	CTNNB1	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000168036	NA	101805488	1499	LINC00873|NCCP1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07679	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Esophageal cancer	CCAT2	PCNA	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000132646	NA	101805488	5111	LINC00873|NCCP1	NA	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07680	expression association	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Esophageal cancer	CCAT2	Cyclin D1	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07681	expression association	metastasis		
Esophageal cancer	CCAT2	MYC	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000136997	NA	101805488	4609	LINC00873|NCCP1	bHLHe39|c-Myc|MYCC	Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.The expression of lncRNA CCAT2 in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and one normal esophageal epithelial cell (HEEC) was examined by RT-qPCR. The expression was significantly higher in all esophageal cancer cell lines compared with that in HEEC (P<0.05; Fig. 1A). Subsequently, siRNA was used to silence lncRNA CCAT2 in Eca-109 cells. The RT-qPCR data showed no off-target effect occurring, and the knockdown of lncRNA CCAT2 was successfully performed (Fig. 1B).Flow cytometry was used to analyze apoptosis in esophageal cancer cells, following annexin V staining. The number of apoptotic cells in the si-CCAT2 group was significantly higher compared with the control and si-NC groups (P<0.05; Fig. 4). Similarly, the immunohistochemistry staining showed significantly decreased expression of beta-catenin and PCNA in the si-CCAT2 group (P<0.05; Fig. 5). Protein expression, determined by western blot, showed significant upregulation of Bax and APC in the si-CCAT2 group compared with the control and si-NC groups, whereas cyclin D1 and c-Myc proteins were significantly downregulated (P<0.05; Fig. 6).To further analyze how lncRNA CCAT2 functions in esophageal cancer cells, the effect of the Wnt signaling pathway on the cell proliferation, invasion and metastasis was investigated, using a Wnt signaling inhibitor (FH535). No differences in the effects on apoptosis, proliferation, migration and invasion of Eca-109 cells were observed between the si-CCAT2 + FH535 group and the si-CCAT2 or FH535 groups (Figs. 7'-). Expression of beta-catenin, PCNA, Bax, APC, cyclin D1 and c-Myc were also similar among these groups (Figs. 10 and 11).	31423241	RID07682	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	HOTTIP	HMGB3	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	glycolysis(+)	ceRNA(miR-615-3p)	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000029993	NA	100316868	3149	HOXA-AS6|HOXA13-AS1|NCRNA00213|RP1-170O19.3	HMG2A|HMG4|MGC90319	Long non-coding RNA HOTTIP promotes hypoxia-induced glycolysis through targeting miR-615-3p/HMGB3 axis in non-small cell lung cancer cells.Firstly, we determined the expression of HOTTIP in NSCLC tissues and cell lines by qRT-PCR In contrast to their counterparts, HOTTIP expression was significantly elevated in NSCLC tissues and cell lines (Fig. 1A and B). In order to observe whether hypoxia affected HOTTIP expression in NSCLC, A549 and H1299 cells were exposed at different times (0, 3, 6, 12, 24 and 48 h) in a hypoxic incubator with 1% O2. As demonstrated by qRT-PCR hypoxia resulted in a increase of HOTTIP expression in a time-dependent manner (Fig. 1C and D). Together, these results suggested that hypoxia increased HOTTIP expression in NSCLC cells.To explore whether HOTTIP was involved in the metabolic response to hypoxia in NSCLC cells, we manipulated HOTTIP expression by transfection of si-HOTTIP prior to hypoxic exposure. qRT-PCRresults revealed that transfection of si-HOTTIP, but not a scrambled control sequence, significantly reduced the expression of HOTTIP in both A549 and H1299 cells under hypoxic conditions (Fig. 2A and B). Subsequent experimental data revealed that HOTTIP deficiency substantially abrogated the promotional effect of hypoxic stress on glucose consumption, lactate production and HK2 expression in both A549 and H1299 cells (Fig. 2C). Taken together, these results hinted that hypoxia promoted glycolysis through upregulating HOTTIP expression in NSCLC cells.To further explore the molecular mechanism by which HOTTIP deficiency repressed hypoxia-induced glycolysis, we carried out a detailed analysis of its target miRNAs by starBase v2.0 software. These predicted data showed that HOTTIP harbored a complementary sequence for miR-615-3p (Fig. 3A). To determine whether HOTTIP might act as a sponge to sequester miR-615-3p, we used the HOTTIP reporter plasmids (HOTTIP-WT or HOTTIP-MUT) in dual-luciferase reporter assays. Transfection of HOTTIP-WT in the presence of miR-615-3p mimics induced about a 68% decrease of luciferase activity in A549 cells and a 72% decrease in H1299 cells (Fig. 3B and C). Whereas, site-directed mutation of the target sequence for miR-615-3p abrogated the effect of miR-615-3p mimics on luciferase activity under the same conditions (Fig. 3B and C). Ago2, a key component of RNA-induced silencing complex (RISC), play an important role in the mature process of miRNAs (Iwakawa and Tomari, 2015). To verify the endogenous interaction between HOTTIP and miR-615-3p, RIP assays were performed with anti-Ago2 antibody. In comparison to negative control, the enrichment of HOTTIP was highly elevated by transfection of miR-6153p mimics in RISC in both A549 and H1299 cells (Fig. 3D and E).Subsequently, we determined whether HOTTIP affected miR-615-3p expression in NSCLC cells. qRT-PCRresults revealed that in contrast to corresponding control, miR-615-3p expression was strikingly decreased by transfection of pcDNA-HOTTIP, while it was highly increased in the presence of si-HOTTIP in both A549 and H1299 cells (Fig. 4F and G), indicating that HOTTIP negatively modulated miR-615-3p expression in NSCLC cells. All these results strongly pointed to a role of HOTTIP as a molecular sponge for miR-615-3p in NSCLC cells.MiRNAs have been postulated to exert biological function by regulating their molecular targets (Hammond, 2015). Thus, to predict target genes of miR-615-3p, online software starBase was used. The predicted data reveraled that HMGB3 contained a putative target sequence for miR-615-3p in its 3'-UTR (Fig. 7A). To determine whether HMGB3 was a target of miR-615-3p, we performed 3'-UTR luciferase reporter assays. When we used HMGB3 3'-UTR reporter construct (HMGB3-WT) harboring the putative miR-615-3p target sequence, cotransfection of HMGB3-WT and miR-615-3p mimics into A549 and H1299 cells produced lower luciferase activity than in cells cotransfected with miR-NC mimics (Fig. 7B and C). Moreover, a mutant reporter (HMGB3-MUT), in which all predicted miR-615-3p binding sites were mutated, completely abrogated the inhibitory effect of miR 615-3p (Fig. 7B and C). More interestingly, in contrast to a scrambled control sequence, HMGB3 mRNA was substantially enriched in the presence of miR-615-3p mimics in both A549 and H1299 cells (Fig. 7D and E). These results together indicated that HMGB3 was a direct target of miR-615-3p in NSCLC cells.Next, HMGB3 expression was assessed by qRT-PCRin NSCLC tissues and cells. As expected, the data revealed a significant upregulation of HMGB3 mRNA expression in NSCLC tissues and cells compared with their counterparts (Fig. 8A and B). Moreover, HMGB3 expression was inversely correlated with miR-615-3p level (Fig. 8C), and it was positively correlated with HOTTIP level in NSCLC tissues (Fig. 8D). More intriguingly, hypoxia markedly promoted HMGB3 expression in a timedependent manner (Fig. 8E and F).	31422060	RID07683	ceRNA or sponge	NA		UP(SKCM,BRCA);DOWN(BRCA);DATA(GSE38495,GSE109761,GSE111065,GSE55807,GSE67939)
Pancreatic cancer	MTA2TR	MTA2	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);	NA	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	NA	NA	ENSG00000149480	NA	NA	9219	NA	MTA1L1|PID	LncRNA-MTA2TR functions as a promoter in pancreatic cancer via driving deacetylation-dependent accumulation of HIF-1alpha. MTA2TR expression was further confirmed in 40-paired PC and NP tissues, revealing it to be more highly expressed in PC relative to NP samples (Figure -(Figure1C).1C). Since MTA2TR is overexpressed in PC cells and tissues, we used 2 kinds of siRNAs to knockdown endogenous MTA2TR expression to evaluate its roles in BxPC-3 cells as well as in SW1990 cells (Figure -(Figure2A).2A). MTA2TR knockdown significantly disrupted BxPC-3/SW1990 cells cell proliferation and colony formation as determined via MTT and colony formation assay (Figure -(Figure2B,2B, C). Similarly, invasion and migration of these cells were disrupted upon MTA2TR knockdown as determined based on Transwell and wound healing analyses (Figure -(Figure2D,2D, E).We next wanted to determine which MTA2TR targets were resulting in the observed PC cell phenotypes. lncRNAs are well known to be able to mediate regulation of gene expression both near their own transcriptional site (in-cis) and at distinct independent loci (in-trans) 25. Since MTA2TR is adjacent to MTA2 gene, which is an oncogenic driver in numerous cancers, we wonder whether MTA2TR exerts cis-acting effect on MTA2 expression (Figure -(Figure4A).4A). Coincidently, we revealed that MTA2TR knockdown decreased, while MTA2TR overexpression increased both mRNA and protein levels of MTA2 in PC cells (Figure -(Figure4B,4B, C). Meanwhile, MTA2 pre-mRNA was also decreased by MTA2TR knockdown but increased after MTA2TR overexpression (Figure -(Figure4D,4D, E). Meanwhile, stability of MTA2 mRNA had no significant changes in MTA2TR knockdown and overexpression BxPC-3 cells, which indicated MTA2 is regulated by MTA2TR but not in post-transcriptional level (Figure -(Figure4F,4F, G). To further verify MTA2TR regulate MTA2 transcription, BxPC-3 cells were transfected using a MTA2 promoter-containing luciferase reporter vector. MTA2TR overexpression was associated with a marked increase in activity at the MTA2 promoter, while knockdown of MTA2TR impaired this promoter activity (Figure -(Figure4H).4H). These results thus indicated that MTA2TR regulates MTA2 transcription.Next, we investigated the mechanism controlling MTA2TR expression in PC cells. Since we had previously demonstrated that hypoxia induces lncRNA-NUTF2P3 overexpression 27, we wonder whether the aberrant expression of MTA2TR was also attributed to the hypoxia condition of PC. MTA2TR was upregulated in PC cells upon hypoxia in a time-dependent fashion (Figure -(Figure7A).7A). In addition, the RT-PCRresults showed that HIF-1alpha knockdown dramatically inhibited the hypoxia-induced MTA2TR overexpression (Figure -(Figure7B),7B), which was further validated by RNA-FISH assay (Figure -(Figure7C).7C). Meanwhile, the Jaspar database displayed three potential hypoxia responsive elements (HREs) on the MTA2TR promoter area (Figure -(Figure7D).7D). ChIP assay determined only the P2 region, but not P1 and P3 in the MTA2TR promoter mediates HIF-1alpha-binding to the MTA2TR promoter (Figure -(Figure7E).7E). Furthermore, HIF-1alpha binding to the MTA2TR promoter was obviously enhanced under hypoxia (Figure -(Figure7F).7F). To confirm functional binding of HIF-1alpha to the MTA2TR promoter, BxPC-3 cells were transfected with luciferase reporter vectors bearing wild-type (WT) or mutated HRE (MUT). The results showed that MTA2TR promoter activity was enhanced by hypoxia, but impaired by HIF-1alpha knockdown (Figure -(Figure7G).7G). Besides, RIP assay indicated that the binding of MTA2TR and ATF3 increased under hypoxia (Figure S8A), which was further verified via a combination of ATF3 protein immunofluorescence analyses and RNA-FISH assessment of MTA2TR in BxPC-3 cells under normoxic and hypoxic conditions (Figure S8B). In addition, ChIP assay verified that the combination of ATF3 on the MTA2 promoter region was also increased (Figure S8C). Therefore, these results suggest that MTA2TR is regulated by hypoxia-induced HIF-1alpha at the transcriptional level.We further explored the link between MTA2TR expression and clinical characteristics of PC patients. The univariate analyses revealed that overexpression of MTA2TR was correlated with tumor sizes, poor tumor differentiation, lymphatic invasion, distant metastasis and advanced TNM stage (Table S3). Furthermore, the Kaplan-Meier analysis displayed a relationship between higher MTA2TR mRNA levels and decreased overall survival (OS) (Figure -(Figure10A).10A). Moreover, there was a positive correlation between MTA2TR and MTA2 expression (Figure -(Figure10B).10B). Coincidently, survival data of TCGA from OncoLnc showed that PC patients with high MTA2 expression had a shorter survival time (Figure -(Figure10C).10C). In agreement, the co-staining fluorescence assay further showed an increased MTA2TR accompanied with increased HIF-1alpha protein expression in PC tissue compared with NP tissue (Figure -(Figure10D).10D). TCGA data from ChIPBase revealed HIF-1alpha expression to be positively correlated with that of MTA2 in PC (Figure -(Figure10E).10E). Taken together, these results intensively imply the hypoxia-induced HIF-1alpha/MTA2TR/MTA2 axis promotes PC development. Thereafter, we depicted a schematic diagram to depict MTA2TR played a vital role in regulation of HIF-1alpha/MTA2 feedback during hypoxia stress (Figure -(Figure1010F).	31410216	RID07684	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	HIF1A	MTA2TR	positively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);	NA	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000100644	NA	NA	NA	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	NA	LncRNA-MTA2TR functions as a promoter in pancreatic cancer via driving deacetylation-dependent accumulation of HIF-1alpha. MTA2TR expression was further confirmed in 40-paired PC and NP tissues, revealing it to be more highly expressed in PC relative to NP samples (Figure -(Figure1C).1C). Since MTA2TR is overexpressed in PC cells and tissues, we used 2 kinds of siRNAs to knockdown endogenous MTA2TR expression to evaluate its roles in BxPC-3 cells as well as in SW1990 cells (Figure -(Figure2A).2A). MTA2TR knockdown significantly disrupted BxPC-3/SW1990 cells cell proliferation and colony formation as determined via MTT and colony formation assay (Figure -(Figure2B,2B, C). Similarly, invasion and migration of these cells were disrupted upon MTA2TR knockdown as determined based on Transwell and wound healing analyses (Figure -(Figure2D,2D, E).We next wanted to determine which MTA2TR targets were resulting in the observed PC cell phenotypes. lncRNAs are well known to be able to mediate regulation of gene expression both near their own transcriptional site (in-cis) and at distinct independent loci (in-trans) 25. Since MTA2TR is adjacent to MTA2 gene, which is an oncogenic driver in numerous cancers, we wonder whether MTA2TR exerts cis-acting effect on MTA2 expression (Figure -(Figure4A).4A). Coincidently, we revealed that MTA2TR knockdown decreased, while MTA2TR overexpression increased both mRNA and protein levels of MTA2 in PC cells (Figure -(Figure4B,4B, C). Meanwhile, MTA2 pre-mRNA was also decreased by MTA2TR knockdown but increased after MTA2TR overexpression (Figure -(Figure4D,4D, E). Meanwhile, stability of MTA2 mRNA had no significant changes in MTA2TR knockdown and overexpression BxPC-3 cells, which indicated MTA2 is regulated by MTA2TR but not in post-transcriptional level (Figure -(Figure4F,4F, G). To further verify MTA2TR regulate MTA2 transcription, BxPC-3 cells were transfected using a MTA2 promoter-containing luciferase reporter vector. MTA2TR overexpression was associated with a marked increase in activity at the MTA2 promoter, while knockdown of MTA2TR impaired this promoter activity (Figure -(Figure4H).4H). These results thus indicated that MTA2TR regulates MTA2 transcription.Next, we investigated the mechanism controlling MTA2TR expression in PC cells. Since we had previously demonstrated that hypoxia induces lncRNA-NUTF2P3 overexpression 27, we wonder whether the aberrant expression of MTA2TR was also attributed to the hypoxia condition of PC. MTA2TR was upregulated in PC cells upon hypoxia in a time-dependent fashion (Figure -(Figure7A).7A). In addition, the RT-PCRresults showed that HIF-1alpha knockdown dramatically inhibited the hypoxia-induced MTA2TR overexpression (Figure -(Figure7B),7B), which was further validated by RNA-FISH assay (Figure -(Figure7C).7C). Meanwhile, the Jaspar database displayed three potential hypoxia responsive elements (HREs) on the MTA2TR promoter area (Figure -(Figure7D).7D). ChIP assay determined only the P2 region, but not P1 and P3 in the MTA2TR promoter mediates HIF-1alpha-binding to the MTA2TR promoter (Figure -(Figure7E).7E). Furthermore, HIF-1alpha binding to the MTA2TR promoter was obviously enhanced under hypoxia (Figure -(Figure7F).7F). To confirm functional binding of HIF-1alpha to the MTA2TR promoter, BxPC-3 cells were transfected with luciferase reporter vectors bearing wild-type (WT) or mutated HRE (MUT). The results showed that MTA2TR promoter activity was enhanced by hypoxia, but impaired by HIF-1alpha knockdown (Figure -(Figure7G).7G). Besides, RIP assay indicated that the binding of MTA2TR and ATF3 increased under hypoxia (Figure S8A), which was further verified via a combination of ATF3 protein immunofluorescence analyses and RNA-FISH assessment of MTA2TR in BxPC-3 cells under normoxic and hypoxic conditions (Figure S8B). In addition, ChIP assay verified that the combination of ATF3 on the MTA2 promoter region was also increased (Figure S8C). Therefore, these results suggest that MTA2TR is regulated by hypoxia-induced HIF-1alpha at the transcriptional level.We further explored the link between MTA2TR expression and clinical characteristics of PC patients. The univariate analyses revealed that overexpression of MTA2TR was correlated with tumor sizes, poor tumor differentiation, lymphatic invasion, distant metastasis and advanced TNM stage (Table S3). Furthermore, the Kaplan-Meier analysis displayed a relationship between higher MTA2TR mRNA levels and decreased overall survival (OS) (Figure -(Figure10A).10A). Moreover, there was a positive correlation between MTA2TR and MTA2 expression (Figure -(Figure10B).10B). Coincidently, survival data of TCGA from OncoLnc showed that PC patients with high MTA2 expression had a shorter survival time (Figure -(Figure10C).10C). In agreement, the co-staining fluorescence assay further showed an increased MTA2TR accompanied with increased HIF-1alpha protein expression in PC tissue compared with NP tissue (Figure -(Figure10D).10D). TCGA data from ChIPBase revealed HIF-1alpha expression to be positively correlated with that of MTA2 in PC (Figure -(Figure10E).10E). Taken together, these results intensively imply the hypoxia-induced HIF-1alpha/MTA2TR/MTA2 axis promotes PC development. Thereafter, we depicted a schematic diagram to depict MTA2TR played a vital role in regulation of HIF-1alpha/MTA2 feedback during hypoxia stress (Figure -(Figure1010F).	31410216	RID07685	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	
Papillary thyroid carcinoma	MIAT	miR-212	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	NA	Myocardial infarction associated transcript (MIAT) promotes papillary thyroid cancer progression via sponging miR-212.To identify the roles of MIAT in the progression of PTC, the expression level of MIAT was measured in PTC tissues and adjacent normal tissues by qRT-PCR As shown in Fig. 1A, the expression of MIAT was significantly higher in PTC tissues than in normal tissues. We also evaluated the expression levels of MIAT in PTC cell lines (TPC-1, BCPAP, and IHH-4) and human thyroid follicular epithelial cell line Nthy-ori 3-1. The results demonstrated that MIAT was significantly up-regulated in the three PTC cell lines compared with Nthy-ori 3-1 cells (Fig. 1B, P-<- 0.01).To investigate the function of MIAT in PTC progression, we transfected sh-MIAT or sh-NC into TPC-1 cells to knockdown MIAT (Fig. 2A). We detected the cell proliferation by CCK8 assay at 24-h, 48-h and 72-h time point and found that knockdown of MIAT significantly inhibited proliferation of TPC-1 cells at 48-h and 72-h time point (Fig. 2B). Consistent with this result, knockdown of MIAT significantly inhibited cell colony formation of TPC-1 cells (Fig. 2C).Next, we investigated the effect of MIAT on migration and invasion in TPC-1 cells. Wound healing assay demonstrated that knockdown of MIAT impaired the migratory speed of TPC-1 cells compared with sh-NC group (Fig. 3A). Transwell invasion assay revealed that knockdown of MIAT suppressed the invasive activity of TPC-1 cells (P-<-0.01; Fig. 3B).To explore the regulatory mechanism of MIAT in PTC cells, a potential binding site of MIAT and miR-212 was predicted using tools miRcode (Fig. 4A). To confirm the potential MIAT-miR-212 interaction, luciferase assay was performed. The results demonstrated that miR-212 overexpression was significantly decreased luciferase activity of Wt- MIAT-3'UTR, but not of Mut-MIAT-3'UTR (P-<-0.05; Fig. 4B). Further, miR-212 mimics significantly decreased MIAT expression in TPC-1 cells, while miR-212 inhibitor increased MIAT expression in TPC-1 cells (P-<-0.01, Fig. 4C). We also shown that knockdown of MIAT significantly increased miR-212 expression in TPC-1 cells (Fig. 4D). Finally, we found that miR-212 expression was downregulated in PTC tissues (Fig. 4E) and negatively correlated with MIAT expression (r=-0.611, P-<-0.001; Fig. 4F). These results implied that miR-212 might be a direct target of MIAT in PTC cells.To investigate whether the interaction with miR-212 contributes to the biological roles of MIAT in PTC, sh-NC, sh-MIAT, or sh-MIAT-+-miR-212 inhibitor were transfected into TPC-1 cells, then cell proliferation, migration and invasion were determined. qRT-PCRanalysis revealed that knockdown of MIAT obviously increased miR-212 expression, while miR-212 inhibitor reversed this trend (P-<-0.01; Fig. 5A). Moreover, we also revealed that MIAT knockdown significantly inhibited proliferation, migration and invasion, and these inhibition effects were partly abolished by miR-212 inhibitor in TPC-1 cells (Fig. 5B ). These results suggested that repression of miR-212 partially reversed the MIAT depleted-induced inhibitory effects on PTC cells. In other words, MIAT exerts oncogenic activity in PTC via sponging miR-212.	31404776	RID07686	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	
Multiple myeloma	MALAT1	miR-181a-5p	negatively-F	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA MALAT1/miR-181a-5p affects the proliferation and adhesion of myeloma cells via regulation of Hippo-YAP signaling pathway.The LncRNA MALAT1 expression in myeloma cells was detected by RT-qPCR analysis. As shown in Figure 1, LncRNA MALAT1 expression in U266, MM.1S, and RPMI8226 were increased compared with HS-5 and LncRNA MALAT1 expression was highest in U266. Therefore, U266 was chosen for the subsequent experiment.The RT-qPCR analysis and western blotwere used to verify the transfection effects. As shown in Figure 2(a,b), compared with control group and sh-RNA group, mRNA expression level and protein expression level of LncRNA MALAT1 were all decreased and sh-MALAT1-1 transfected cells expressed lower LncRNA MALAT1 than sh-MALAT1-2 transfected cells. Therefore, sh-MALAT1-1 transfected cells were chosen for the subsequent experiment. Compared with control group and sh-RNA group, CCK-8 assay displayed that cell proliferation was suppressed in sh-MALAT1-1 group (Figure 2(c)) and western blotdisplayed that expression of CDK2 and cyclinE1 was increased while P21 expression was decreased in sh-MALAT1-1 group (Figure 2(d)).ELISA assay was used to detect the expression of inflammatory factors and adhesion factors. As shown in Figure 3, compared with control group and sh-RNA group, the expression levels of IL-1, TNFalpha, IFN-Gamma and Muc-1, ICAM-1, VCAM-1 were all decreased in sh-MALAT1-1 group. These data reveal that LncRNA MALAT1 interference inhibits adhesion of myeloma cells.Bioinformatics analysis predicted the potential target gene of LncRNA MALAT1 and results demonstrated that miR-181a-5p is a downstream target gene of LncRNA MALAT1 (Figure 5(a)). dual-luciferase reporter assay was used to improve the prediction. As shown in Figure 5(b), transfection of MALAT1 wild-type and miR-181a-5p mimics reduced the fluorescence activity, indicating that MALAT1 and miR-181a-5p have binding sites. In addition, compared with control group and sh-RNA group, miR-181a-5p was overexpressed in sh-MALAT1-1 group (Figure 5(c)).	31397203	RID07687	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Osteosarcoma	BC050642	MYC	negatively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	NA	NA	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	The potential value of lncRNA-BC050642 in osteosarcoma origination and outcomes.In this study, we detected BC050642 levels in osteosarcoma, adjacent and healthy tissues as well as in tumor cell lines U2OS and normal osteoblastic cell line hFOB1.19 through qRT-PCR All the continuous data obtained in our study conformed to the normality and homogeneity of variance. Student  t-test results showed that BC050642 expression was significantly higher in osteosarcoma tissues than in adjacent and healthy controls (Figure 1(A), p-<-.001). Compared with normal osteoblastic cell line hFOB1.19, BC050642 expression was significantly up-regulated in osteosarcoma cell lines U2OS (Figure 1(B), p-<-.001). Taken together, these results confirmed that BC050642 expression showed increased tendency in osteosarcoma.C-myc was considered to be related to the expression of BC050642 and to the prognosis of osteosarcoma, we measured its expression using ELISA analysis. The outcome proved that c-myc expression was decreased in cancer tissues compared to adjacent and healthy ones (Figure 2(A), p-<-.05). As for in cell lines, c-myc expression was also lower in U2OS than in hFOB1.19 (Figure 2(B), p-<-.05). These findings suggested that the expressions of C-myc were decreased in osteosarcoma.To determine whether BC050642 functioned as an oncogene in osteosarcoma, we conducted MTT assay, colony formation assay and FACS assay. MTT assay showed that the proliferation of cells transfected with si-BC050642 was significantly decreased than those transfected with si-NC (Figure 3(A)). The clone number of cells transfected with si-BC050642 was reduced when compared with those transfected with si-NC (Figure 3(B,C), p-<-.05). Besides, apoptosis percentage of U2OS cells was significantly increased in si-BC050642 group compared to si-NC group (Figure 3(D,E), p-<-.05). These findings suggested that the knockdown of BC050642 resulted in inhibition on cell proliferation and colony formation, and promoting effects on cell apoptosis of osteosarcoma cell lines U2OS, revealing the oncogenic potential of BC050642 in osteosarcoma.To examine the effect of c-myc on osteosarcoma, pcDNA 3.1-c-myc was designed to enhance the expression of c-myc in osteosarcoma cell lines. The efficiency of the transfection was detected through qRT-PCR As displayed in Figure 4, the transfection of pcDNA 3.1-c-myc obviously promote the expression of c-myc in osteosarcoma cells. Following, the cell experiments were designed to explore the function of c-myc in osteosarcoma. The restored expression of c-myc inhibited cell proliferation (Figure 5(A)) and suppressed colony formation number (Figure 5(B,C)). In addition, cell apoptosis assay showed that the over-expression of c-myc promoted cell apoptosis (Figure 5(D,E)). These results demonstrated that the anti-tumor of c-myc on cell proliferation, colony formation and apoptosis.To investigate whether the expression of BC050642 was related to the progression of osteosarcoma, we estimated its relationship with clinicopathologic characteristics. According to the expression of BC050642, osteosarcoma cases were sorted into high and low BC050642 expression groups, based on a median expression of 3.958- -0.504. As displayed in Table 1, Ennking (p-=-.000) and histological type (p=.022) were significantly related to the expression of BC050642. Whereas, BC050642 had no relationship with age, gender, tumor site, therapies, distant metastasis or recurrence.	31397185	RID07688	expression association	metastasis,recurrence,prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Laryngeal carcinoma	SNHG1	NOTCH1	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000148400	NA	23642	4851	LINC00057|lncRNA16|NCRNA00057|UHG	TAN1	LncRNA SNHG1 promotes cell proliferation in laryngeal cancer via Notch1 signaling pathway.Compared to paracancerous tissues, SNHG1 was highly expressed in LC as qRT-PCRdata revealed (Figure 1A). Besides, SNHG1 expression remained higher in LC with T3-T4 relative to those with T1-T2 (Figure 1B). In comparison to non-metastatic LC patients, those with lymph node metastasis presented a higher level of SNHG1 (Figure 1C). The Kaplan-Meier analysis indicated that LC patients with high-level SNHG1 had worse survival than those with a low level (Figure 1D). The above data indicated the involvement of SNHG1 in LC, which may be related to poor prognosis of LC.SNHG1 has been identified to promote the proliferative, migratory and invasive abilities of pituitary tumor cells by activating TGFBR2/ SMAD3 and RAB11A/Wnt/beta-catenin pathway24. Here, we found that SNHG1 knockdown suppressed the mRNA levels of Notch1 and Hes1 in TU212 and Hep2 cells (Figure 3A, 3C). western blot also showed the downregulated protein levels of Notch1 and Hes1 due to SNHG1 knockdown (Figure 3B, 3D). We believed that SNHG1 negatively regulated expressions of Notch1 and Hes1 in LC cells.We speculated the involvement of Notch1 pathway in SNHG1-regulated progression of LC. Firstly, we found the downregulated mRNA levels of Notch1 and Hes, due to SNHG1 knockdown that were partially reversed after co-transfection of si-SNHG1 and pcDNA-Notch1 (Figure 4A, 4C). Similar trends were yielded at the protein levels of Notch1 and Hes1 as well (Figure 4B, 4D). CCK-8 assay showed that Notch1 overexpression reversed the inhibited viability in LC cells with SNHG1 knockdown (Figure 4E). The above results demonstrated that SNHG1 promoted LC cells to proliferate by mediating Notch1 and Hes1.	31378897	RID07689	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Laryngeal carcinoma	SNHG1	HES1	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000114315	NA	23642	3280	LINC00057|lncRNA16|NCRNA00057|UHG	bHLHb39|FLJ20408|HES-1|HRY	LncRNA SNHG1 promotes cell proliferation in laryngeal cancer via Notch1 signaling pathway.Compared to paracancerous tissues, SNHG1 was highly expressed in LC as qRT-PCRdata revealed (Figure 1A). Besides, SNHG1 expression remained higher in LC with T3-T4 relative to those with T1-T2 (Figure 1B). In comparison to non-metastatic LC patients, those with lymph node metastasis presented a higher level of SNHG1 (Figure 1C). The Kaplan-Meier analysis indicated that LC patients with high-level SNHG1 had worse survival than those with a low level (Figure 1D). The above data indicated the involvement of SNHG1 in LC, which may be related to poor prognosis of LC.SNHG1 has been identified to promote the proliferative, migratory and invasive abilities of pituitary tumor cells by activating TGFBR2/ SMAD3 and RAB11A/Wnt/beta-catenin pathway24. Here, we found that SNHG1 knockdown suppressed the mRNA levels of Notch1 and Hes1 in TU212 and Hep2 cells (Figure 3A, 3C). western blot also showed the downregulated protein levels of Notch1 and Hes1 due to SNHG1 knockdown (Figure 3B, 3D). We believed that SNHG1 negatively regulated expressions of Notch1 and Hes1 in LC cells.We speculated the involvement of Notch1 pathway in SNHG1-regulated progression of LC. Firstly, we found the downregulated mRNA levels of Notch1 and Hes, due to SNHG1 knockdown that were partially reversed after co-transfection of si-SNHG1 and pcDNA-Notch1 (Figure 4A, 4C). Similar trends were yielded at the protein levels of Notch1 and Hes1 as well (Figure 4B, 4D). CCK-8 assay showed that Notch1 overexpression reversed the inhibited viability in LC cells with SNHG1 knockdown (Figure 4E). The above results demonstrated that SNHG1 promoted LC cells to proliferate by mediating Notch1 and Hes1.	31378897	RID07690	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Lung cancer	CASC11	CDK1	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-302)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000170312	NA	100270680	983	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	CDC2|CDC28A	LncRNA CASC11 promotes the development of lung cancer through targeting microRNA-302/CDK1 axis.Expression level of CASC11 in 30 pairs of lung cancer tissues and paracancerous tissues was determined by qRT-PCR CASC11 was highly expressed in lung cancer tissues compared with that of paracancerous tissues (Figure 1A). We predicted potential binding targets for CASC11 and microRNA-302 through bioinformatics (Figure 2A). Based on the binding sites, wt CASC11 3'UTR and mut CASC11 3'UTR were first constructed. As dual-luciferase reporter gene data showed, luciferase activity markedly decreased in lung cancer cells co-transfected with microRNA-302 mimic and wt CASC11 3'UTR. We did not observe a significant change of luciferase activity in mut CASC11 3'UTR group, demonstrating the binding between microRNA-302 and CASC11 (Figure 2B). Furthermore, microRNA-302 was upregulated by transfection of si-CASC11 in A549 and H157 cells (Figure 2C). On the contrary, microRNA-302 expression was downregulated, whereas CASC11 expression was upregulated by transfection of microRNA-302 inhibitor (Figure 2D and 2E).qRT-PCRwas conducted to determine microRNA-302 expression in 30 pairs of lung cancer and paracancerous tissues. MicroRNA-302 expression was lower in lung cancer tissues compared to that of paracancerous tissues (Figure 3A). We found that microRNA-302 was negatively correlated with CASC11 (Figure 3B). MicroRNA-302 inhibitor was then transfected into A549 and H157 cells. Colony formation assay revealed that microRNA-302 knockdown could markedly enhance the proliferative potential, but was further reversed by CASC11 knockdown (Figure 3C). CCK-8 assay yielded the identical results (Figure 3D).Expression level of CDK1 in 30 pairs of lung cancer tissues and paracancerous tissues was determined by qRT-PCR Higher level of CDK1 was observed in lung cancer tissues than that of paracancerous tissues (Figure 4A). Besides, CDK1 expression was positively correlated to CASC11 expression (Figure 4B). The potential binding sites between CDK1 and microRNA-302 were predicted by bioinformatics, followed by construction of wt CDK1 3'UTR and mut CDK1 3'UTR. Lower luciferase activity was seen in cells co-transfected with microRNA-302 mimic and wt CDK1 3'UTR, whereas no significant difference was found in mut CDK1 3'UTR group (Figure 4D). We therefore confirmed the binding between microRNA-302 and CDK1. CDK1 expression was downregulated in A549 and H157 cells transfected with si-CASC11, but were markedly upregulated after transfection of microRNA-302 inhibitor as qRT-PCRrevealed.	31378894	RID07691	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Oral squamous cell carcinoma	OIP5-AS1	NRP1	positively-E	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-338-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000099250	NA	729082	8829	cyrano|linc-OIP5	CD304|NRP|VEGF165R	Long noncoding RNA OIP5-AS1 promotes the progression of oral squamous cell carcinoma via regulating miR-338-3p/NRP1 axis.qRT-PCRanalysis was used to investigate the OIP5-AS1 expression in OSCC cells. Result revealed that OIP5-AS1 expressions were obviously increased in four OSCC cell lines (SCC9, SCC15, Ca9-22 and HSU3) compared with that in NHOK cells (Fig. 1A). Moreover, the expression levels of OIP5-AS1 were remarkably upregulated in OSCC tissues compared with their adjacent normal tissues (Fig. 1B).To assess whether OIP5-AS1 affects OSCC migration and invasion, the wound healing and transwell invasion assays were performed. Wound-healing assay revealed that silencing of OIP5-AS1 in SCC9 cells underwent a slower closing of scratch wounds compared with sh-NC group (Fig. 3A). Transwell invasion assay demonstrated that knockdown of OIP5-AS1 obviously decreased invasion capabilities (Fig. 3B). These results suggested that OIP5-AS1 depletion inhibited OSCC metastasis in vitro.To investigate the potential mechanism of OIP5-AS1 in OSCC cells, we examined the potential miRNAs that interacts with OIP5-AS1, since lncRNA exerted it biological role by functioning as miRNA sponges [18]. We used starbse2.0 software to predict miRNAs associated with OIP5-AS1.Among miRNAs, miR-338-3p turned out to be the possible target of OIP5-AS1 (Fig. 4A). dual-luciferase reporter assay was performed to confirm whether OIP5-AS1 was a functional target of miR-338-3p. As shown in Fig. 4B, overexpression of miR-338-3p significantly decreased luciferase activity of WT-OIP5-AS1, which had no effect on the MT-OIP5-AS1 repoter vector. RIP assays further demonstrated that the interaction between miR-338-3p and OIP5-AS1 in SCC9 cells (Fig. 4C). In addition, OIP5-AS1 depletion obviously increased miR-338-3p expression in SCC9 cells (Fig. 4D), while miR-338-3p mimics transfection significantly decreased OIP5-AS1 expression in SCC9 cells (Fig. 4E). We also found that miR-338-3p expression was decreased in OSCC tissues (Fig. 4F), and its expression was negative correlated with OIP5-AS1 in OSCC tissues (Fig. 4G). Importantly, knockdown of OIP5-AS1 could significantly decrease the expression of neuropilin1 (NRP1), a directed target of miR-338-3p in OSCC cells (Fig. 4H), suggesting OIP5-AS1 can regulate NRP1 expression by sponging miR-338-3p in OSCC cells.Our existing results had suggested that OIP5-AS1 promoted NRP1 through sponging miR-338-3p in OSCC cells. Thus, we performed rescue experiments to confirm the association with OIP5-AS1, miR-338-3p and NRP1 in OSCC cells. We found that knockdown of OIP5-AS1 significantly increased miR-338-3p expression, and decreased NRP1 expression in SCC9 cells, while miR-338-3p inhibitor or overexpression NRP1 plasmid (pCDNA-NRP1) partially reversed these trends (Fig. 5A and B).CCK8 and colony formation assays revealed that transfection of miR-338-3p inhibitor or pCDNA3.1-NRP1 plasmid could largely promoted proliferation ability of OIP5-AS1 knockdown SCC9 cells (Fig. 5C and D).The same tendencies were observed in SCC9 cell migration and invasion after the same transfections (Fig. 5E and F).These results suggested that OIP5-AS1/miR-338-3p/NRP1 axis could regulate OSCC progression.	31369989	RID07692	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761)
Colorectal cancer	DUXAP8	RAB14	positively-E	luciferase reporter assay;ChIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-577)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000119396	NA	503637	51552	NA	FBP|RAB-14	STAT3-induced upregulation of lncRNA DUXAP8 functions as ceRNA for miR-577 to promote the migration and invasion in colorectal cancer through the regulation of RAB14.For demonstrating the above results, we carried out qPCR to measure DUXAP8 expression in 127 pair of CRC tissues and matched normal colorectal tissues. We discovered that DUXAP8 levels were markedly upregulated in CRC samples than that in the corresponding adjacent normal specimens (Figure 1D). In addition, the expression of DUXAP8 showed a higher level in CRC cell lines than that in normal colorectal cells (Figure 1E). All the above results indicated that DUXAP8 was frequently down-regulated in CRC.In addition, Real Time-PCR was carried out to measure the levels of DUXAP8 in CRC cells when their STAT3 was silenced or elevated. The data suggested that knockdown of STAT3 resulted in remarkably decreased DUXAP8 levels, while enhancing STAT3 expression dramatically promoted the levels of DUXAP8 (Figures 2D, 2E). Moreover, the ChIP assays revealed that STAT3 was capable of directly binding to the P3 site of DUXAP8 promoter (Figure 2F). Therefore, we respectively cloned wild-type or mutant-type P3 site into pGL3 vector (P3 wild-type or P3 mutant), and sequentially performed dual-luciferase reporter assays for further demonstrating that STAT3 was capable of interacting with DUXAP8 promoter. The results indicated that forced STAT3 expression increased the Luciferase activities in cells after treatment with P3 wild-type reporters, whereas the activities of Luciferase were not altered in HCT116 cells after co-transfection with pcDNA3.1-STAT3 and P3 mutant vectors (Figure 2G). Our findings clarified that STAT3 induced the aberrant expression of DUXAP8 in CRC.Afterward, the effects of DUXAP8 on cellular growth were explored using CCK-8 assays. The results indicated that silence of DUXAP8 in HCT116 and LOVO cells remarkably depressed the cell proliferation at 48, 72, and 96 h post-transfection (Figure 3B). Moreover, depletion of DUXAP8 led to a markedly decreased colony number of HCT116 and LOVO cells (Figure 3C). In addition, EdU assay was carried out to evaluate the impact of DUXAP8 depletion on cellular proliferation. As the results presented in Figures 4D and 4E, knockdown of DUXAP8 by DUXAP8 siRNAs transfection dramatically attenuated the cell proliferation of HCT116 and LOVO cells. To assess whether the effects of DUXAP8 on colorectal cellular proliferation were dependent on the modulation of cell apoptosis, we next performed flow cytometry. The data suggested that transfection of DUXAP8 siRNAs induced remarkable cell apoptosis of HCT116 and LOVO cells (Figure 3F). western blotwas performed and we found that repressing the expression of DUXAP8 notably elevated the protein levels of caspase 3/9 (Figure 3G). Our results validated that DUXAP8 could affect CRC development.To investigate whether silencing the expression of DUXAP8 had an impact on the oncogenic behavior of CRC cells, the HCT116 and LOVO cell metastasis was further evaluated using wound-healing and transwell assays. Wound-healing detection revealed that the scratching gaps in DUXAP8 silenced-cells were significantly wider than that of the controls, suggesting that knockdown of DUXAP8 markedly reduced the migration of CRC cells (Figures 4A and B). Meanwhile, transwell invasion assays certified that depression of DUXAP8 resulted in a marked reduction of cellular invasion of HCT116 and LOVO cells (Figures 4C and D). Overall, all the observations demonstrated that suppression of DUXAP8 was capable of impeding the cellular migration and invasion of CRC cells.Next, we attempted to uncover the mechanisms by which DUXAP8 orchestrated CRC development. Since lncRNAs might serve as miRNA sponges to affect cellular phenotypes, we first utilized qRT-PCRanalysis to determine the subcellular location of DUXAP8. As the data shown in Figure 5A, DUXAP8 was mainly expressed in the cytoplasm, indicating that DUXAP8 might act as a miRNA sponge. Hence, we next applied an online bioinformatics tool 'StarBase'-to predict the possible DUXAP8 targeting miRNAs. Among those predicted miRNAs, miR-577, which acted as tumor suppressor in cancer, was found to be a DUXAP8 possible target (Figure 5B). Bioinformatics analyses using TCGA dataset by 'StarBase'-discovered that miR-577 expression was negatively correlated with DUXAP8 expression in CRC tissues (Figure 5C). We next employed Luciferase activity detection assays to examine whether miR-577 was the exact target of DUXAP8. The results manifested that forcing miR-577 expression remarkably depressed the Luciferase activities of DUXAP8 wt reporter-transfected HCT116 and LOVO cells, while had no impact on that of DUXAP8 mut reporter-transfected cells (Figure 5D). In addition, RNA pull-down analysis certified that there was a substantial enrichment of miR-577 in the DUXAP8-pulled down pellets compared with the control group, which indicated that DUXAP8 could precipitate miR-577 in CRC cells (Figure 5E).	31364111	RID07693	ceRNA or sponge	metastasis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE86978)
Colorectal cancer	STAT3	DUXAP8	positively-E	luciferase reporter assay;ChIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000271672	GRCh38_22:15826566-15827187	6774	503637	APRF	NA	STAT3-induced upregulation of lncRNA DUXAP8 functions as ceRNA for miR-577 to promote the migration and invasion in colorectal cancer through the regulation of RAB14.For demonstrating the above results, we carried out qPCR to measure DUXAP8 expression in 127 pair of CRC tissues and matched normal colorectal tissues. We discovered that DUXAP8 levels were markedly upregulated in CRC samples than that in the corresponding adjacent normal specimens (Figure 1D). In addition, the expression of DUXAP8 showed a higher level in CRC cell lines than that in normal colorectal cells (Figure 1E). All the above results indicated that DUXAP8 was frequently down-regulated in CRC.In addition, Real Time-PCR was carried out to measure the levels of DUXAP8 in CRC cells when their STAT3 was silenced or elevated. The data suggested that knockdown of STAT3 resulted in remarkably decreased DUXAP8 levels, while enhancing STAT3 expression dramatically promoted the levels of DUXAP8 (Figures 2D, 2E). Moreover, the ChIP assays revealed that STAT3 was capable of directly binding to the P3 site of DUXAP8 promoter (Figure 2F). Therefore, we respectively cloned wild-type or mutant-type P3 site into pGL3 vector (P3 wild-type or P3 mutant), and sequentially performed dual-luciferase reporter assays for further demonstrating that STAT3 was capable of interacting with DUXAP8 promoter. The results indicated that forced STAT3 expression increased the Luciferase activities in cells after treatment with P3 wild-type reporters, whereas the activities of Luciferase were not altered in HCT116 cells after co-transfection with pcDNA3.1-STAT3 and P3 mutant vectors (Figure 2G). Our findings clarified that STAT3 induced the aberrant expression of DUXAP8 in CRC.Afterward, the effects of DUXAP8 on cellular growth were explored using CCK-8 assays. The results indicated that silence of DUXAP8 in HCT116 and LOVO cells remarkably depressed the cell proliferation at 48, 72, and 96 h post-transfection (Figure 3B). Moreover, depletion of DUXAP8 led to a markedly decreased colony number of HCT116 and LOVO cells (Figure 3C). In addition, EdU assay was carried out to evaluate the impact of DUXAP8 depletion on cellular proliferation. As the results presented in Figures 4D and 4E, knockdown of DUXAP8 by DUXAP8 siRNAs transfection dramatically attenuated the cell proliferation of HCT116 and LOVO cells. To assess whether the effects of DUXAP8 on colorectal cellular proliferation were dependent on the modulation of cell apoptosis, we next performed flow cytometry. The data suggested that transfection of DUXAP8 siRNAs induced remarkable cell apoptosis of HCT116 and LOVO cells (Figure 3F). western blotwas performed and we found that repressing the expression of DUXAP8 notably elevated the protein levels of caspase 3/9 (Figure 3G). Our results validated that DUXAP8 could affect CRC development.To investigate whether silencing the expression of DUXAP8 had an impact on the oncogenic behavior of CRC cells, the HCT116 and LOVO cell metastasis was further evaluated using wound-healing and transwell assays. Wound-healing detection revealed that the scratching gaps in DUXAP8 silenced-cells were significantly wider than that of the controls, suggesting that knockdown of DUXAP8 markedly reduced the migration of CRC cells (Figures 4A and B). Meanwhile, transwell invasion assays certified that depression of DUXAP8 resulted in a marked reduction of cellular invasion of HCT116 and LOVO cells (Figures 4C and D). Overall, all the observations demonstrated that suppression of DUXAP8 was capable of impeding the cellular migration and invasion of CRC cells.Next, we attempted to uncover the mechanisms by which DUXAP8 orchestrated CRC development. Since lncRNAs might serve as miRNA sponges to affect cellular phenotypes, we first utilized qRT-PCRanalysis to determine the subcellular location of DUXAP8. As the data shown in Figure 5A, DUXAP8 was mainly expressed in the cytoplasm, indicating that DUXAP8 might act as a miRNA sponge. Hence, we next applied an online bioinformatics tool 'StarBase'-to predict the possible DUXAP8 targeting miRNAs. Among those predicted miRNAs, miR-577, which acted as tumor suppressor in cancer, was found to be a DUXAP8 possible target (Figure 5B). Bioinformatics analyses using TCGA dataset by 'StarBase'-discovered that miR-577 expression was negatively correlated with DUXAP8 expression in CRC tissues (Figure 5C). We next employed Luciferase activity detection assays to examine whether miR-577 was the exact target of DUXAP8. The results manifested that forcing miR-577 expression remarkably depressed the Luciferase activities of DUXAP8 wt reporter-transfected HCT116 and LOVO cells, while had no impact on that of DUXAP8 mut reporter-transfected cells (Figure 5D). In addition, RNA pull-down analysis certified that there was a substantial enrichment of miR-577 in the DUXAP8-pulled down pellets compared with the control group, which indicated that DUXAP8 could precipitate miR-577 in CRC cells (Figure 5E).	31364111	RID07694	expression association	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Non-small cell lung cancer	SDPR-AS	CAVIN2	negatively-E	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000168497	NA	NA	8436	NA	cavin-2|PS-p68|SDPR|SDR	Long non-coding RNA SDPR-AS affects the development of non-small cell lung cancer by regulating SDPR through p38 MAPK/ERK signals.To grab the potential impact of lncRNA SDPR-AS in lung cancer, we evaluated the level of SDPR-AS in different subtypes of lung cancer tissues and cells. The levels of SDPR-AS in AC, SCC and LCC tissues and cells were dramatically lower relative to those in non-rumor tissues and in BEAS-2B cells (p-<-.05, Figure 1). However, there was no apparent difference in SDPR-AS expression between SCLC and adjacent non-rumor tissues, as well as SCLC NCI-H446 and BEAS-2B cells.To further grab the impact of SDPR-AS in NSCLC cells, H522, H661 and H520 cells were transfected with the following plenty of vectors including pcDNA-SDPR-AS, sh-SDPR-AS or their corresponding controls. SDPR-AS was confirmed to be successfully overexpressed and knocked down in H522, H661 and H520 cells, respectively (Figure 2(A)). The highly expressed SDPR-AS significantly inhibited H522 cell viability and colony forming ability and promoted cell apoptosis (p-<-.05), whereas depression of SDPR-AS exhibited opposite effects (Figure 2(B)). Consistent results about the effects of SDPR-AS dysregulation on cell viability, colony forming ability and apoptosis were obtained in H661 and H520 cells (Figure 2(C,D)).The effects of SDPR-AS dysregulation on NSCLC cell migration and invasion were also observed. The results uncovered that high level of SDPR-AS significantly depressed the migration and invasion of H522 (Figure 3(A)), H661 (Figure 3(B)) and H520 (Figure 3(C)) cells (p-<-.05), whereas depression of SDPR-AS exhibited opposite effects in these cells.It is reported that SDPR-AS and SDPR are positively associated with cell process of renal cell carcinoma cells [12]. We thus detected the expression levels of SDPR in different subtypes of lung cancer tissues and cells. The results showed that, compared with adjacent non-rumor tissues and normal lung epithelial of BEAS-2B cells, the SDPR expressions were also significantly down-regulated in AC, SCC and LCC tissues and cells (p-<-.05), but not exhibited significant changes in SCLC tissues and cells (Figure 4(A,B)). Moreover, SDPR expression was also significantly up-regulated in pcDNA-SDPR-AS transfected H522, H661 and H520 cells and markedly down-regulated in sh-SDPR-AS transfected (p-<-.05, Figure 4(C)). We thereby deducted that SDPR expression was positively correlated with SDPR-AS expression in NSCLC cells.To further investigated whether effects of SDPR-AS on the cell biological processes of NSCLC cells were through regulation of SDPR, SDPR was suppression in H522 cells by cell transfection. The transfection efficiency of SDPR knockdown was confirmed by qRT-PCR(p-<-.001, Figure 5A). H522 cells were then cotransfection with si-SDPR and pcDNA-SDPR-AS. The results uncovered that depression of SDPR could significantly reverse the effects of SDPR-AS overexpression on H522 cell viability, colony forming ability, apoptosis, migration and invasion (Figure 5(B )). These findings implying that impacts of SDPR-AS on the malignant behaviors of NSCLC cells may be through regulation of SDPR.	31352804	RID07695	expression association	NA		UP(PRAD);DATA(GSE104209)
Malignant glioma	FOXD2-AS1	CDK1	positively-E	dual-luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);	ceRNA(miR-31)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000170312	NA	84793	983	MGC12982	CDC2|CDC28A	Long noncoding RNA FOXD2-AS1 promotes glioma cell cycle progression and proliferation through the FOXD2-AS1/miR-31/CDK1 pathway.We analyzed the RNA-Seq data for lncRNAs in brain cancers available from The Cancer Genome Atlas (TCGA) database. FOXD2-AS1 was upregulated in glioma. FOXD2-AS1 level was positively correlated to malignant degree according to the analysis of 511 cases of low-grade glioma (LGG) and 156 cases of glioblastoma (GBM) (Figure 1A). Moreover, FOXD2-AS1 levels in normal tissues (n = 7), grade I-II (n = 13) and grade III-IV (n = 18) glioma tissues were determined. The data confirmed that FOXD2-AS1 level increased with the worsen of glioma (Figure 1B). Based on the TCGA data, Kaplan-Meier curves revealed worse overall survival (OS) LGG and GBM patients expressing high level of FOXD2-AS1 (Figure 1C). Identically, FOXD2-AS1 was upregulated in glioma cells U87 and U251 relative to normal astrocytes SVG p12 (Figure 1D). Collectively, high-level FOXD2-AS1 indicated poor prognosis in glioma patients.Silence of FOXD2-AS1 reduced viability in glioma cells as CCK-8 results revealed (Figure 2B). In addition, colony formation assay showed a strike decline in clonogenic growth following FOXD2-AS1 knockdown (Figure 2C). EdU assay yielded the same conclusion that silence of FOXD2-AS1 attenuated proliferative ability in glioma (Figure 2D). As shown by flow cytometry, downregulation of FOXD2-AS1 in glioma cells elevated cell ratio in G1 phase (Figure 2E). Silence of FOXD2-AS1 induced G1 phase arrest and proliferative suppression in glioma cells.The microRNA.org program was utilized for searching the possible targets of FOXD2-AS1, and miR-31 was finally selected (Figure 4A). Our results showed downregulation of miR-31 in glioma tissues relative to normal brain tissues (Figure 4B). miR-31 level increased by transfection of si- FOXD2-AS1 in glioma cells (Figure 4C). Subsequently, biological function of miR-31 in glioma was mainly discussed. CCK-8 assay demonstrated the reduced viability in glioma cells overexpressing miR-31 (Figure 4D). Transfection of miR-31 mimics markedly arrested cells in G1 phase (Figure 4E). Moreover, luciferase activity declined by cotransfection of miR-31 mimics and FOXD2- AS1-WT (Figure 4F). These data indicated that FOXD2- AS1 sponged miR-31 to regulate glioma cell growth.To explore the mechanisms of miR-31 in regulating glioma cells, target genes of miR-31 were predicted by miRTarBase and miRanda. CDK1 was observed as a potential target of miR-31 (Figure 5A and 5B). In a same way, the binding relationship between CDK1 and miR-31 in glioma cells was verified (Figure 5B). These results indicated that miR-31 repressed CDK1 transcription. CCK-8 assay revealed that silence of FOXD2-AS1 in glioma cells inhibited glioma cell proliferation (Figure 5C). Moreover, transfection of miR-31 inhibitor counteracted viability reduction owing to FOXD2- AS1 knockdown, indicating that FOXD2-AS1 was a miR-31 sponge (Figure 5C). After cotransfection of si-FOXD2-AS1 and miR-31 inhibitor, downregulated CDK1 protein in glioma cells with FOXD2-AS1 knockdown was partially reversed (Figure 5D). Therefore, FOXD2-AS1 was confirmed to enhance CDK1 expression by inhibiting miR-31 in glioma cells. In brief, FOXD2-AS1/miR-31/CDK1 regulatory loop was identified in gliomas. The schematic diagram of the mechanism was showed in Figure 5F.	31347720	RID07696	ceRNA or sponge	prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Breast cancer	NEAT1	TIMM17A	positively-E	luciferase reporter assay;RIP	upregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-133b)	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000134375	NA	283131	10440	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	TIM17|TIM17A	LncRNA NEAT1 Silenced miR-133b Promotes Migration and Invasion of Breast Cancer Cells.We then investigated the mechanism by which miR-133b expression is down-regulated in breast cancer cells and tissues. LncRNAs usually act as competing endogenous RNAs (ceRNA) by binding miRNAs and could even repress their expression [10]. Ago crosslinking-immunoprecipitation and high-throughput sequencing (CLIP-seq) data in the StarBase indicated that lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) might interact with miR-133b, and the predicted potential binding site between NEAT1 and miR-133b was illustrated in Figure 2A.To validate whether NEAT1 is associated with the down-regulation of miR-133b in breast cancer cells, we first identified specific interactions between NEAT1 and miR-133b by luciferase reporter assay. Figure 2A showed that miR-133b overexpression reduced the luciferase activities of the NEAT1-WT reporter vector but not the NEAT1-MUT reporter. RIP assays performed on MCF-7 and MDA-MB-231 cell extracts using antibodies against Ago2 further demonstrated that NEAT1 and miR-133b were all enriched in Ago2-immunoprecipitation (Ago2-IP) relative to the control (IgG-IP; Figure 2B). Moreover, NEAT1 overexpression decreased the levels of miR-133b while NEAT1 knockdown increased the levels of miR-133b in MCF-7 and MDA-MB-231 cells (Figure S1A and Figure 2C). These results suggested that NEAT1 might repress the expression of miR-133b via direct binding at the specific site.To identify the role of miR-133b in breast cancer progression, we introduced the inhibitor or mimics of miR-133b into MCF-7 and MDA-MB-231 cells. (Figure S1B). The wound healing assays (Figure 3A,B) and transwell assays (Figure 3C,D) showed that the migration and invasion capacities of MCF-7 and MDA-MB-231 cells were significantly reduced by the overexpression of miR-133b, but strongly enhanced by depleting miR-133b. Our data demonstrated that down-regulation of miR-133b was involved in breast cancer metastasis.To investigate the underlying molecular mechanism by which miR-133b promotes breast cancer cell migration, invasion, proliferation and stemness, we performed the Venn diagram analysis of predicted miR-133b targets from four independent databases: TargetScan, miRanda, miRDB and PicTar. 111 mRNAs were found in the intersection part (Figure 4A). TIMM17A was selected for further experimental verification based on the following conditions (Table S5): related to breast cancer, related to cancer migration or invasion, has not been reported as a miR-133b target, high expression in breast tumor (StarBase database), and correlated with poor survival of breast cancer patients (Kaplan Meier Plotter). TIMM17A was found to promote breast cancer tumorigenesis and metastasis [21], and its high expression is associated with adverse pathological and clinical outcomes in human breast cancer [22]. However, it has not been reported as the target of miR-133b. The predicted interaction between miR-133b and the target sites in the TIMM17A 3'-UTR was illustrated in Figure 4B. Perfect base-pairings between the seed region and the cognate target have been observed, and the free energy value of the hybrid was well within the range of genuine miRNA-target pairs (-19.5 kcal/mol). Subsequently, we confirmed that miR-133b directly targeted the predicted binding sites in the TIMM17A 3'-UTR by a luciferase reporter assay (Figure 4C). Moreover, we observed that TIMM17A mRNA and protein levels were significantly decreased in the cells transfected with the miR-133b mimics, while remarkably increased by suppression of the endogenous miR-133b (Figure 4E). The above results suggested that miR-133b down-regulated TIMM17A protein levels through directly binding to its 3'-UTR and degrading TIMM17A mRNA.	31344855	RID07697	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Prostate cancer	SNHG7	WNT2B	positively-E	luciferase reporter assay;knockdown	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-324-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000134245	NA	84973	7482	MGC16037|NCRNA00061	WNT13|XWNT2	Knockdown of LncRNA SNHG7 inhibited epithelial-mesenchymal transition in prostate cancer though miR-324-3p/WNT2B axis in vitro.Firstly, LncRNA SNHG7 expression was measured in 499 patients with PCa tissues and paired normal tissues according to the data of TCGA. Compared with adjacent normal tissues, lncRNA SNHG7 expression was significantly upregulated in PCa tissues (*P < 0.05, Fig. 1A). Secondly, the expression of lncRNA SNHG7 was measured in PCa cell lines, compared with the normal prostate epithelial cell line RWPE, lncRNA SNHG7 was significantly upregulated in PCa cell lines, and the expression levels of lncRNA SNHG7 in PC-3 and Du-145 were higher than those in LNCaP (Fig. 1B). Therefore, LncRNA SNHG7 is upregulated in prostate cancer tissues and cells.To explore the function of lncRNA SNHG7 on prostate cancer cells, We use siRNA to inhibit the expression of lncRNA SNHG7. qRT-PCRanalysis displayed that transfection with siRNA led to significantly expression repression of lncRNA SNHG7 in PC-3 and Du-145 cells (Fig. 2A). Then we carried out MTT assay, the results indicated that lncRNA SNHG7 depletion decreased the proliferation rate of PC-3 and Du-145 cells (Fig. 2B). Additionally, colony formation assay also showed that knockdown lncRNA SNHG7 could reduce the colony numbers (Fig. 2C), suggesting lncRNA SNHG7 exerts a positive effect on the proliferation of PCa cells. To further investigating the role of lncRNA SNHG7 on metastasis, transwell assay was performed. LncRNA SNHG7 inhibition suppressed cell migration and invasion dramatically (Fig. 2D and E). These data suggested that silencing SNHG7 inhibited cell proliferation, migration and invasion in PCa cells.One critical step of tumor metastasis is EMT, therefore we explored whether lncRNA SNHG7 could modulate EMT in PCa cells. We can see fromFig. 3, we knocked down lncRNA SNHG7 in prostate cancer cell lines. Successful LncRNA SNHG7 knockdown resulted in downregulated N-cadherin and upregulated E-cadherin in Du-145 and PC-3 cells as demonstrated by western blot (Fig. 3A and C). Moreover, real-time PCR analysis also confirmed that knockdown of lncRNA SNHG7 significantly reduced the expression of mesenchymal markers (N-cadherin, Vimentin, Snail, Slug, Mmp-2, Mmp-9, and Twist-1) but increased the expression of epithelial markers (E-cadherin) (*P < 0.05,Fig. 3B and D). These data indicated that lncRNA SNHG7 could promote EMT in prostate cancer cells.To confirm the direct binding relationship between lncRNA SNHG7 and miR-324-3p, a dual-luciferase activity assay was performed. We discovered that miR-324-3p significantly reduced the luciferase activities of pGL3-SNHG7-wt, but there was no obvious reduction found in cells transfected with miR-324-3p and pGL3-SNHG7-mut (Fig. 4C). In addition, an inverse correlation was found between the expression of miR-324-3p and lncRNA SNHG7 in PCa tissues (Fig. 4D). We then explored the genes that were potentially regulated by miR-324-3p. As shown inFig. 5A, Bioinformatics tools confirmed miR-324-3p targeted with the 5'-UTR of WNT2B mRNA (Fig. 5A). Luciferase reporter assay confirmed the binding within WNT2B mRNA and miR-324-3p. The ectopic expression of miR-324- 3p could significantly decrease the luciferase activity of the wt WNT2B 5'UTR, but not of the mut WNT2B 5'-UTR (Fig. 5B); In addition, RT-PCRvalidated that lncRNA SNHG7 knockdown significantly reduced the mRNA level of WNT2B in Du-145 and PC-3 cells, the reduced mRNA expression caused by lncRNA SNHG7 knockdown could be restored by inhibition of miR-324-3p (Fig. 5C and D). Moreover, western blotshows results consistent with qRT-PCR(Fig. 5E and F). Overall, the above data indicated that lncRNA SNHG7 positively regulated WNT2B through sponging miR-324-3p, constituting the lncRNA SNHG7/miR-324-3p/WNT2B pathway.To directly test whether lncRNA SNHG7 promotes prostate cancer progression through miR-324-3p/WNT2B axis, we conducted proliferation, migration and invasion assays in the PC-3 and Du-145 cells. The results showed that knockdown lncRNA SNHG7 could inhibit PCa cell proliferation, migration and invasion, whereas suppression of miR324-3p or WNT2B restoration in the meantime could reverse the effects of lncRNA SNHG7 silencing (Fig. 7A ). Taken together, our results proved that lncRNA SNHG7 contributes to PCa progression through regulating miR-324-3p/WNT2B axis expression.	31324390	RID07698	ceRNA or sponge	metastasis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	TTTY15	TBX4	positively-E	knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000233864	NA	ENSG00000121075	NA	64595	9496	NCRNA00138	NA	Male-Specific Long Noncoding RNA TTTY15 Inhibits Non-Small Cell Lung Cancer Proliferation and Metastasis via TBX4.To determine whether TTTY15 plays a role in NSCLC, we tested the expression of TTTY15 in 37 pairs of NSCLC tissue samples and their paired nontumor tissue samples. The data suggested that TTTY15 expression in tumor tissue was significantly lower than that in the matching nontumor tissue (mean delta cycle threshold (dCT) of tumors vs. normal tissue samples: 0.65 vs. 1.26, p < 0.0001; Figure 1A).To investigate the effects of TTTY15 on the migration of A549 and H441 cells, we performed a wound healing scratch assay. The data revealed that the proportion of the recovered region increased for the TTTY15 knockdown A549 and H441 cells as compared to the scramble cells (Figure 3A). Furthermore, we performed a Transwell invasion assay to evaluate the influence of TTTY15 on the invasiveness of NSCLC cells. The results indicated that the knockdown of TTTY15 significantly increased cell invasion as compared to the scramble cells (Figure 3B). These data meant that the knockdown of TTTY15 may promote cell migration and the invasive motility of NSCLC cells.The data suggested that the knockdown of TTTY15 decreased the expression levels of LINC00674 but not CCDC3 (Figure 4B), indicating that TTTY15 may target and regulate LINC00674 expression. LINC00674, located in chromosomal region 17q23, is a long noncoding RNA gene, however, the function of LINC00674 is still unknown. Since lncRNA may regulate expression of genes on a large scale, we investigated whether TTTY15 could interact with this chromatin region and regulate the transcription of protein-coding genes located near LINC00674, including TBX4, KPNA2, and TIMP2 (Figure 4C). The results revealed that the knockdown of TTTY15 dramatically decreased the expression of TBX4 in A549 and H441 cells (Figure 4D). The spatial proximity of TTTY15 and LINC00674 chromatin segments was revealed through TTTY15 4C-sequencing and bioinformatic analysis. Moreover, TTTY15 was found to regulate the expression of TBX4 located near LINC00674.To investigate the potential mechanism by which TTTY15 regulates TBX4 expression in NSCLC, we analyzed the distribution of TTTY15 in cells. The cell fractional data indicated that TTTY15 was mainly localized in the nucleus (Figure 6A). Since other studies suggest that TBX4 is downregulated and hypermethylated in lung cancer-associated fibroblasts [19] and cancers, we speculated that TTTY15 may participate in the methylation status of the TBX4 promoter. We performed an RNA immunoprecipitation assay to determine whether there is a physical interaction between the DNA methyltransferases (DNMTs) and TTTY15. The results revealed that TTTY15 interacts with DNMT3A but not DNMT1 (Figure 6B). Therefore, we evaluated the expression level of DNMT3A in NSCLC. The results showed that the expression of DNMT3A in tumor tissue was higher than that in the nontumor tissue (mean dCT of tumors vs. normal tissues: 1.37 vs. 0.43, p < 0.0001; Figure 6C). We also investigated the correlation between DNMT3A expression and the clinical features of the patients. We found that the expression of DNMT3A correlated TNM stage but not age or tumor size (Table S2). To test whether DNMT3A regulates the expression of TBX4 in NSCLC, DNMT3A was knocked down in A549 and H441 cells. The data revealed that the knockdown of DNMT3A increased the expression of TBX4 (Figure 6D). To elucidate the mechanisms of regulatory action of TTTY15, DNMT3A, and TBX4 in NSCLC, we performed western blot and chromatin immunoprecipitation (ChIP) on A549 and H441 cell lysates. The results indicated that the knockdown of TTTY15 did not affect DNMT3A protein expression (Figure 6E) but increased the binding ability of DNMT3A to the TBX4 promoter (Figure 6F). We then performed methylation-specific PCR to verify the CpG methylation status. The results revealed that knockdown of TTTY15 increased the methylated status in CpG islands (Figure 6G). Next, to determine whether the TTTY15 NMT3A-TBX4 axis is involved in NSCLC, we knocked down DNMT3A and checked whether the cell migration and invasion abilities increased by shTTTY15 would be attenuated. The findings showed that the knockdown of DNMT3A indeed inhibited the cell migration and invasion in A549/shTTTY15 and H441/shTTTY15 cells (Figure S1).	31311130	RID07699	epigenetic regulation	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	TTTY15	DNMT3A	interact	RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233864	NA	ENSG00000119772	NA	64595	1788	NCRNA00138	NA	Male-Specific Long Noncoding RNA TTTY15 Inhibits Non-Small Cell Lung Cancer Proliferation and Metastasis via TBX4.To determine whether TTTY15 plays a role in NSCLC, we tested the expression of TTTY15 in 37 pairs of NSCLC tissue samples and their paired nontumor tissue samples. The data suggested that TTTY15 expression in tumor tissue was significantly lower than that in the matching nontumor tissue (mean delta cycle threshold (dCT) of tumors vs. normal tissue samples: 0.65 vs. 1.26, p < 0.0001; Figure 1A).To investigate the effects of TTTY15 on the migration of A549 and H441 cells, we performed a wound healing scratch assay. The data revealed that the proportion of the recovered region increased for the TTTY15 knockdown A549 and H441 cells as compared to the scramble cells (Figure 3A). Furthermore, we performed a Transwell invasion assay to evaluate the influence of TTTY15 on the invasiveness of NSCLC cells. The results indicated that the knockdown of TTTY15 significantly increased cell invasion as compared to the scramble cells (Figure 3B). These data meant that the knockdown of TTTY15 may promote cell migration and the invasive motility of NSCLC cells.The data suggested that the knockdown of TTTY15 decreased the expression levels of LINC00674 but not CCDC3 (Figure 4B), indicating that TTTY15 may target and regulate LINC00674 expression. LINC00674, located in chromosomal region 17q23, is a long noncoding RNA gene, however, the function of LINC00674 is still unknown. Since lncRNA may regulate expression of genes on a large scale, we investigated whether TTTY15 could interact with this chromatin region and regulate the transcription of protein-coding genes located near LINC00674, including TBX4, KPNA2, and TIMP2 (Figure 4C). The results revealed that the knockdown of TTTY15 dramatically decreased the expression of TBX4 in A549 and H441 cells (Figure 4D). The spatial proximity of TTTY15 and LINC00674 chromatin segments was revealed through TTTY15 4C-sequencing and bioinformatic analysis. Moreover, TTTY15 was found to regulate the expression of TBX4 located near LINC00674.To investigate the potential mechanism by which TTTY15 regulates TBX4 expression in NSCLC, we analyzed the distribution of TTTY15 in cells. The cell fractional data indicated that TTTY15 was mainly localized in the nucleus (Figure 6A). Since other studies suggest that TBX4 is downregulated and hypermethylated in lung cancer-associated fibroblasts [19] and cancers, we speculated that TTTY15 may participate in the methylation status of the TBX4 promoter. We performed an RNA immunoprecipitation assay to determine whether there is a physical interaction between the DNA methyltransferases (DNMTs) and TTTY15. The results revealed that TTTY15 interacts with DNMT3A but not DNMT1 (Figure 6B). Therefore, we evaluated the expression level of DNMT3A in NSCLC. The results showed that the expression of DNMT3A in tumor tissue was higher than that in the nontumor tissue (mean dCT of tumors vs. normal tissues: 1.37 vs. 0.43, p < 0.0001; Figure 6C). We also investigated the correlation between DNMT3A expression and the clinical features of the patients. We found that the expression of DNMT3A correlated TNM stage but not age or tumor size (Table S2). To test whether DNMT3A regulates the expression of TBX4 in NSCLC, DNMT3A was knocked down in A549 and H441 cells. The data revealed that the knockdown of DNMT3A increased the expression of TBX4 (Figure 6D). To elucidate the mechanisms of regulatory action of TTTY15, DNMT3A, and TBX4 in NSCLC, we performed western blot and chromatin immunoprecipitation (ChIP) on A549 and H441 cell lysates. The results indicated that the knockdown of TTTY15 did not affect DNMT3A protein expression (Figure 6E) but increased the binding ability of DNMT3A to the TBX4 promoter (Figure 6F). We then performed methylation-specific PCR to verify the CpG methylation status. The results revealed that knockdown of TTTY15 increased the methylated status in CpG islands (Figure 6G). Next, to determine whether the TTTY15 NMT3A-TBX4 axis is involved in NSCLC, we knocked down DNMT3A and checked whether the cell migration and invasion abilities increased by shTTTY15 would be attenuated. The findings showed that the knockdown of DNMT3A indeed inhibited the cell migration and invasion in A549/shTTTY15 and H441/shTTTY15 cells (Figure S1).	31311130	RID07700	interact with protein	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065)
Hepatocellular carcinoma	SNHG17	ZEB2	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000169554	NA	388796	9839	NA	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA SNHG15 promotes hepatocellular carcinoma progression by sponging miR-141-3p.We first used qRT-PCRto assess SNHG15 expression in HCC cells and tissues. As expected, SNHG15 was upregulated in HCC tissues relative to healthy controls (Figure 1A). Consistent with this result, HCC cell lines also exhibited increased SNHG15 expression compared with the LO2 control liver cells (Figure 1B). This suggested that SNHG15 might be important in the context of HCC.We further assessed how SNHG15 affected HCC cell migratory/invasive potential abilities using respective wound healing and transwell-based invasive assays. We found knocking down SNHG15 to significantly decrease both migratory and invasive capabilities in SMMC-7721 cells (Figure 3A,B).A hypothesis identifying lncRNAs as competing endogenous RNAs (ceRNAs) has proposed that they can regulate miRNA expression via binding them in a competitive fashion.20 Thus, we measure the expression of SNHG15 in SMMC-7721 cell nuclear and cytoplasmic fractions via qRT-PCR We found SNHG15 to be mainly located in the cytoplasm, suggesting that SNHG15 might exert the functions of ceRNA in HCC cells (Figure 4A). Next, starbase2.0 was employed for prediction of SNHG15 targeting miRNAs, with miR-141-3p being identified as a target of relevance on the basis of its biological function in tumor progression (Figure 4B). Luciferase reporters confirmed miR-141-3p mimic binding to SNHG15 in SMMC-7721 cells (Figure 4C). To assess if SNHG15 and mIR-141-3p interact in a manner that is dependent upon Ago2, we conducted RIP, revealing SNHG15 and miR-141-3p to be preferentially enriched among Ago2-containing microribonucleoproteins (Figure 4D). SNHG15 knockdown significantly increased SMMC-7721cell miR-141-3p expression (Figure 4E), whereas overexpressing miR-141-3p declined SNHG15 expression (Figure 4F). Relative miR-141-3p expression in the HCC cell lines and tissues was also measured, revealing it to be markedly decreased in HCC tissues and cell lines relative to corresponding controls (Figure 4G and H). SNHG15 was also found to negatively correlate with miR-141-3p (Figure 4I). On the basis of all the above results, we concluded that SNHG15 targets miR-141-3p in HCC cells.We next sought to determine whether SNHG15-mediated phenotypes pertaining to HCC proliferation and invasion were miR-141-3p-dependent via conducting rescue assays by transfecting miR-141-3p into SNHG15-depletion- SMMC-7721 cells. We found miR-141-3p inhibitors to reverse the SNHG15 knockdown-mediated increase in miR-141-3p levels (Figure 5A). Furthermore, SNHG15 knockdown-mediated inhibitory effects on cell proliferation, cycle arrest, migration/invasion were partially rescued using miR-141-3p inhibitors in SMMC-7721 cells (Figure 5B-E). These results suggested that SNHG15 promoted HCC cells progression via modulating miR-141-3p.miR-141-3p is known to suppress HCC by regulating multiple genes, including E2F3 and ZEB2.21, 22 Thus, we explored the relationship between ZEB2/E2F3 and SNHG15 in HCC. The correlation analysis detected SNHG15 expression to be positively correlated with ZEB2 and E2F3 expression in HCC tissues (Figure 6A,B). Rescue assays showed that downregulation of SNHG15 expression notably decreased ZEB2 and E2F3 expression in SMMC-7721 cells, whereas miR-141-3p could partially reverse this trend (Figure 6C,D). These results suggested that SNHG15 modulated the expression ZEB2 and E2F3 through sponging miR-141-3p in human HCC cells.	31310946	RID07701	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	SNHG17	E2F3	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000112242	NA	388796	1871	NA	NA	LncRNA SNHG15 promotes hepatocellular carcinoma progression by sponging miR-141-3p.We first used qRT-PCRto assess SNHG15 expression in HCC cells and tissues. As expected, SNHG15 was upregulated in HCC tissues relative to healthy controls (Figure 1A). Consistent with this result, HCC cell lines also exhibited increased SNHG15 expression compared with the LO2 control liver cells (Figure 1B). This suggested that SNHG15 might be important in the context of HCC.We further assessed how SNHG15 affected HCC cell migratory/invasive potential abilities using respective wound healing and transwell-based invasive assays. We found knocking down SNHG15 to significantly decrease both migratory and invasive capabilities in SMMC-7721 cells (Figure 3A,B).A hypothesis identifying lncRNAs as competing endogenous RNAs (ceRNAs) has proposed that they can regulate miRNA expression via binding them in a competitive fashion.20 Thus, we measure the expression of SNHG15 in SMMC-7721 cell nuclear and cytoplasmic fractions via qRT-PCR We found SNHG15 to be mainly located in the cytoplasm, suggesting that SNHG15 might exert the functions of ceRNA in HCC cells (Figure 4A). Next, starbase2.0 was employed for prediction of SNHG15 targeting miRNAs, with miR-141-3p being identified as a target of relevance on the basis of its biological function in tumor progression (Figure 4B). Luciferase reporters confirmed miR-141-3p mimic binding to SNHG15 in SMMC-7721 cells (Figure 4C). To assess if SNHG15 and mIR-141-3p interact in a manner that is dependent upon Ago2, we conducted RIP, revealing SNHG15 and miR-141-3p to be preferentially enriched among Ago2-containing microribonucleoproteins (Figure 4D). SNHG15 knockdown significantly increased SMMC-7721cell miR-141-3p expression (Figure 4E), whereas overexpressing miR-141-3p declined SNHG15 expression (Figure 4F). Relative miR-141-3p expression in the HCC cell lines and tissues was also measured, revealing it to be markedly decreased in HCC tissues and cell lines relative to corresponding controls (Figure 4G and H). SNHG15 was also found to negatively correlate with miR-141-3p (Figure 4I). On the basis of all the above results, we concluded that SNHG15 targets miR-141-3p in HCC cells.We next sought to determine whether SNHG15-mediated phenotypes pertaining to HCC proliferation and invasion were miR-141-3p-dependent via conducting rescue assays by transfecting miR-141-3p into SNHG15-depletion- SMMC-7721 cells. We found miR-141-3p inhibitors to reverse the SNHG15 knockdown-mediated increase in miR-141-3p levels (Figure 5A). Furthermore, SNHG15 knockdown-mediated inhibitory effects on cell proliferation, cycle arrest, migration/invasion were partially rescued using miR-141-3p inhibitors in SMMC-7721 cells (Figure 5B-E). These results suggested that SNHG15 promoted HCC cells progression via modulating miR-141-3p.miR-141-3p is known to suppress HCC by regulating multiple genes, including E2F3 and ZEB2.21, 22 Thus, we explored the relationship between ZEB2/E2F3 and SNHG15 in HCC. The correlation analysis detected SNHG15 expression to be positively correlated with ZEB2 and E2F3 expression in HCC tissues (Figure 6A,B). Rescue assays showed that downregulation of SNHG15 expression notably decreased ZEB2 and E2F3 expression in SMMC-7721 cells, whereas miR-141-3p could partially reverse this trend (Figure 6C,D). These results suggested that SNHG15 modulated the expression ZEB2 and E2F3 through sponging miR-141-3p in human HCC cells.	31310946	RID07702	ceRNA or sponge	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Colorectal cancer	SLCO4A1-AS1	PARD3	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell autophagy(+)	ceRNA(miR-508-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000148498	NA	100127888	56288	NA	ASIP|Baz|Bazooka|PAR3|PARD3A|PPP1R118	LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis.As shown in Figure 1A'-B, PARD3 protein was overexpressed in most CRC tissues (19 cases out of 23) compared with adjacent control tissues. In addition, the expression of SLCO4A1-AS1 was significantly up-regulated in 23 CRC tissues compared with the control tissues (Figure 1C). ISH analysis illustrated that SLCO4A1-AS1 levels were elevated in higher clinical stage of CRC (P<0.001, Figure 1D). Furthermore, EdU positive cells at mitosis S-stage increased with the overexpression of SLCO4A1-AS1 in LOVO cells, and the number of EdU-positive cells was decreased after 3-MA treatment (Figure 4C). On the contrary, SLCO4A1-AS1 knockdown decreased the number of EdU-positive cells, which was restored by treatment with rapamycin (Figure 4C). Flow cytometry assay showed that cell cycle distribution was consistent with that result from EdU staining (Figure 4D). Moreover, SLCO4A1-AS1 overexpression repressed cell apoptosis, whereas this effect was blocked by autophagy inhibition (Figure 4E). In conclusion, the data suggested that SLCO4A1-AS1 may induce protective autophagy in CRC cells.To determine whether SLCO4A1-AS1 serves as a ceRNA, we use online bioinformatics analysis (miRanda, PicTar and TargetScan) to predict the potential miRNA binding sites. Then, RNA pull-down tests determined the involved miRNAs interacted with SLCO4A1-AS1, and miR-508-3p, miR-26a and miR-486-5p were identified to interact with SLCO4A1-AS1 (Figure 7B). We then detected the expression of PARD3 in SW620 cells after up- or down-regulating miRNA expression. Interestingly, among these miRNAs, the expression of endogenous PARD3 was significantly down-regulated by miRNA-508-3p (Figure 7C). Besides, the specific interaction of SLCO4A1-AS1 and miR-508-3p in SW620 cells was confirmed by RIP assay (Figure 7D).As shown in Figure 7E'-F, luciferase reporter gene assay showed that the expression of WT 3'UTR of PARD3 was decreased with the presence of miR-508-3p, whilePARD33'UTR Mut did not respond much to miR-508-3p. MTS and colony formation assays showed that overexpression of miR-508-3p in LOVO cells inhibited cell proliferation, which was restored by the up-regulation of SLCO4A1-AS1. Luciferase activity assay demonstrated that ectopic expression of SLCO4A1-AS1 restrained the inhibitory effect of miR-508-3p on cell proliferation and apoptosis, indicating that SLCO4A1-AS1 bound directly to miR-508-3p (Figure 7G). However, no significant change in the miR-508-3p level was observed after overexpression or knockdown of SLCO4A1-AS1 (Figure 7H'-I). Taken together, our data indicated that SLCO4A1-AS1 regulates PARD3 expression via acting as a sponge molecule of miR-508-3p.	31308265	RID07703	ceRNA or sponge	NA	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	RP5-1120P11.3	WIPF2	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-196b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231881	GRCh38_6:44058792-44089288	ENSG00000171475	NA	NA	147179	NA	WICH|WIRE	RP5-1120P11.3 promotes hepatocellular carcinoma development via the miR-196b-5p-WIPF2 axis.To evaluate the role of the lncRNA in HCC, we examined 6 lncRNAs we preciously focused on in our lab and found in HCC that only RP5-1120P11.3 was significantly increased in HCC cell line HepG-2 compared to human immortalized liver cell line HL-7702 (Fig.1 A). Next, we assessed the expression level of RP5-1120P11.3 in 12 pairs of HCC patients and our resulted showed that RP5-1120P11.3 was dramatically increased in tumor tissues in comparison with adjacent normal tissues (Fig.1 B).Interestingly, we found that overall cell viabilities of both HepG2 and Smmc-7721 cells were significantly decreased when treated with siRNA targeting RP5-1120P11.3 (Fig.2 B), suggesting that RP5-1120P11.3 was required for cell growth of HCC. To further dissect the reason for decreased cell viability, we utilized EdUlabeling experiments to monitor the proliferation of HCC cells transfected with control or RP5-1120P11.3 siRNA. Our data illustrated a significant reduction of numbers of proliferating cells in cells treated with RP5-1120P11.3 siRNA in comparison with cells treated with control siRNA (Fig.2C), indicating that RP5-1120P11.3 was required for proliferation of HCC in vitro. Besides, we analyzed the number of apoptotic cells and found that inhibition of RP5-1120P11.3 caused significant up-regulation of apoptosis in HCC cells (Fig. 2D), suggesting that RP5-1120P11.3 contributed to inhibition of cell apoptosis.Thus, we designed mutations in the binding sites of RP5-1120P11.3 and installed the wildtype and mutated sequences in luciferase reporter plasmids. We co-transfected the luciferase reporter plasmids with miRNA mimics of control miRNA and miR-196b-5p into 293T cells and analyzed the luciferase signals. Importantly, our data showed that overexpression of miR-196b-5p reduced luciferase signals of wildtype RP5-1120P11.3 but not binding sites mutated RP5-1120P11.3 (Fig.2 B), suggesting an interaction between miR-196b-5p and RP5-1120P11.3. To validate if RP5-1120P11.3 functions as a competing endogenous RNA for miR-196b-5p, we examined the expression level of miR-196b-5p in cells transfected with siRNA targeting RP5-1120P11.3. Interestingly, our data showed that miR-196b-5p was up-regulated in HCC cells treated with RP5-1120P11.3 siRNA (Fig.3 C), suggesting that miR-196b-5p was inhibited by RP5-1120P11.3. Furthermore, we analyzed the expression level of miR-196b-5p in HCC clinical samples and cell lines, our data showed significant decreases of miR-196b-5p levels in both clinical HCC samples (Fig.3 D) and HCC cell lines (Fig.3 E) compared to the control group respectively, indicating that RP5-1120P11.3 inhibits miR-196b-5p in HCC.Since RP5-1120P11.3 functions through inhibition of miR-196b-5p in HCC and no targets of miR-196b-5p in HCC has been identified yet, we next set out to identify genes that targeted by miR-196b-5p in HCC. We predicted targets of miR-196b-5p with online prediction (PicTar, http://www.pictar.org/). Interestingly, the prediction returned that miR-196b-5p shared a complementary sequence in the 3'-untranslated region of WIPF2 (Fig.5 A). Thus, we generated luciferase report plasmids containing wildtype 3'-UTR of WIPF2 and binding sites mutated 3'-UTR of WIPF2 and tested the effects miR-196b-5p on expression of WIPF2. Our data showed that overexpression of miR-196b-5p resulted in decreased luciferase activities of constructs containing wildtype 3'-UTR of WIPF2 but not binding sites mutated 3'-UTR of WIPF2 (Fig. 5A), suggesting that miR-196b-5p regulates mRNA level of WIPF2 via directly binding with WIPF2. Hence, miR-196b-5p mimics were transfected into HepG2 and Smmc-7721 cells to introduce overexpression of miR-196b-5p. Overexpression of miR-196b-5p resulted in decreases of both protein level (Fig.5B) and mRNA level (Fig.5C) of WIPF2, suggesting that miR-196b-5p regulates WIPF2 post-transcriptionally in HCC. Additionally, we tested the mRNA expression level of WIPF2 in the HCC clinical samples and found that WIPF2 was elevated in clinical HCC tissues in comparison with adjacent control tissues (Fig.5D) which further indicated that WIPF2 is a target of miR-196b-5p in HCC. Thus, our results proposed a model that RP5-1120P11.3 inhibits miR-196b-5p and in turn facilitates the expression of WIPF2 in HCC.To further address the oncogenic role of RP5-1120P11.3 in HCC, we inoculated nude mice with HepG2 cells transfected with control siRNA or siRNA targeting RP5-1120P11.3. Importantly, we found that inhibition of RP5-1120P11.3 significantly depressed the volumes of xenografts generated in vivo (Fig.7 A). Moreover, the sizes and weights of xenografts generated from HepG2 cells transfected with siRNA targeting RP5-1120P11.3 were significantly smaller than the xenografts generated from HepG2 cells transfected with control siRNA (Fig.7 B), indicating that RP5-1120P11.3 contributes to tumorigenesis of HCC in vivo. Besides, we  extracted  RNA  and  protein  from  the  xenografts  and  found  that  xenografts generated  from  HepG2  cells  transfected  with  siRNA  targeting  RP5-1120P11.3 displayed  significantly  overexpressed  miR-196b-5p  (Fig.7  C).  Moreover,  WIPF2 were downregulated at both mRNA level and protein level (Fig.7 D) in the xenografts generated from HepG2 cells transfected with siRNA targeting RP5-1120P11.3.Take together, our data illustrated that RP5-1120P11.3 contributes to tumorigenesis of HCC in vivo via miR-196b-5p/WIPF2 axis.	31299165	RID07704	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Breast cancer	TATDN1	miR-140-3p	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000147687	GRCh38_8:124488485-124539458	NA	NA	83940	NA	CDA11	NA	TATDN1 promotes the development and progression of breast cancer by targeting microRNA-140-3p.We examined TATDN1 expression in BCa tissues and paracancerous tissues by qRT-PCR Results showed that TATDN1 was highly expressed in tumor tissues compared with those of controls (Figure 1A). Moreover, TATDN1 expression was higher in BCa tissues with stage III-IV relative to those with stage I-II (Figure 1B).Since TATDN1 was highly expressed in BCa, we next explored its underlying mechanism. Firstly, TATDN1 expression in BCa cell lines was determined by qRT-PCR Identically, TATDN1 was highly expressed in BCa cells than that of breast cells (Figure 2A). The transfection of constructed pcDNA-TATDN1 in MCF-7 and MDA-MB-231 cells remarkably upregulated the TATDN1 expression (Figure 2B). BCa cells overexpressing TATDN1 showed higher viability than controls as CCK-8 assay indicated (Figure 2C, 2D). Besides, TATDN1 overexpression markedly accelerated cell cycle progression in MCF-7 and MDA-MB-231 cells (Figure 2E, 2F).Potential binding sites between TATDN1 and microRNA-140-3p were found through online prediction (Figure 3A). Further studies revealed that microRNA-140-3p was lowly expressed in BCa tissues (Figure 3B). Transfection of microRNA-140-3p mimics greatly upregulated microRNA-140-3p expression in MCF-7 and MDA-MB-231 cells, indicating a sufficient transfection efficacy (Figure 3C). Through dual-luciferase reporter gene assay, we confirmed the binding of microRNA-140-3p to TATDN1 (Figure 3D, 3E). To verify whether TATDN1 exerted its functions by sponging microRNA-140-3p, BCa cells were co-overexpressed with microRNA-140-3p and TATDN1. MicroRNA-140-3p overexpression partially reversed the promotive effect of TATDN1 on viability of MCF-7 and MDA-MB-2319 cells (Figure 3F, 3G). Similarly, microRNA-140-3p overexpression also partially reversed the promoted cell cycle progression due to overexpressed TATDN1 (Figure 3H, 3I). Taken together, we confirmed that TATDN1 regulated cellular behaviors of BCa cells by sponging microR NA-140-3p.MicroRNAs degrade their target genes to exert biological functions. We subsequently predicted that NOV A1 was the potential target for microRNA-140-3p (Figure 4A). The NOV A1 expression in BCa tissues was examined, and we found that was highly expressed in BCa than controls (Figure 4B). The transfection of pcDNA-NOV A1 sufficiently upregulated the NOV A1 expression in BCa cells (Figure 4C). Moreover, the dual-luciferase reporter gene assay verified the binding of NOV A1 to microRNA-140-3p (Figure 4D, 4E). Rescue experiments were carried out by co-transfection of pcDNA-NOV A1 and microRNA-140-3p mimics in BCa cells. In co-overexpressed MCF-7 and MDA-MB-231 cells, the upregulated NOV A1 partially reversed the inhibitory effect of microRNA-140-3p on cell proliferation (Figure 4F, 4G). In addition, the upregulated NOV A1 reversed the inhibited cell cycle progression in BCa cells overexpressing microRNA-140-3p (Figure 4H, 4I). It is demonstrated that TATDN1 may exert its function by adsorbing microRNA-140-3p to degrade the downstream NOV A1.	31298381	RID07705	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)	
Acute myeloid leukemia	SNHG1	miR-488-5p	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	sponge	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	LncRNA SNHG1 overexpression regulates the proliferation of acute myeloid leukemia cells through miR-488-5p/NUP205 axis.qRT-PCRwas used to detect the expressions of SNHG1 and miR-488-5p in pAML and THP1 cells. The results indicated that SNHG1 was highly expressed in pAML and THP-1 cells (Figure 1A), while miR-488-5p was lowly expressed (Figure 1B).The potential binding site for SNHG1 and miR488-5p was predicted through bioinformatics (Figure 2A). MiR-488-5p mimic and miR-488-5p inhibitor were constructed, and their transfection efficacies in pRML and THP-1 cells were verified (Figure 2B and 2C). After knockdown of SNHG1, the expression of miR-488-5p increased in pAML and THP-1 cells, suggesting a negative correlation between them (Figure 2D and 2E). Subsequently, RIP results suggested a potential binding relationship between SNHG1 and miR-488-5p (Figure 2F). Dual-luciferase reporter gene assay showed that overexpression of miR-488-5p markedly reduced the fluorescence intensity of SNHG1-WT group, whereas SNHG1-MUT group was not affected (Figure 2G and 2H). These results confirmed that SNHG1 downregulated the miR-488-5p expression by sponging it in pAML and THP-1 cells.The potential binding site for NUP205 and miR-488-5p was predicted through bioinformatics as well (Figure 3A). Both qRT-PCRand western blot data revealed an increased expression of NUP205 in pAML and THP-1 cells (Figure 3B and 3C). Subsequently, dual-luciferase reporter gene assay showed that the overexpression of miR-488-5p markedly reduced the fluorescence intensity of NUP205-WT group, whereas NUP205-MUT group was not affected (Figure 3D and 3E). The above indicated that NUP205 was the potential target gene of miR-488-5p.To verify whether SNHG1 regulated the biological behaviors of leukemia cells through miR-488-5p/NUP205 axis, gain-of-function experiments were conducted by co-transfection of si-SNHG1 and NUP205 overexpression plasmid. The inhibitory effect of SNHG1 knockdown on viabilities of pAML and THP-1 cells was reversed by NUP205 overexpression (Figure 4A and 4B). Similarly, leukemia cells co-transfected with si-SNHG1 and NUP205 overexpression plasmid showed higher cell proportion in S phase and lower proportion in G0/G1 phase than those only transfected with si-SNHG1 (Figure 4C and 4D). We may conclude that SNHG1 regulated cellular behaviors of AML through NUP205.	31298340	RID07706	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Oral squamous cell carcinoma	FALEC	CRKL	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-761)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000099942	NA	100874054	1399	FAL1|LINC00568|ncRNA-a1	NA	LncRNA FAL1 promotes the development of oral squamous cell carcinoma through regulating the microRNA-761/CRKL pathway.To study the role of lncRNA FAL1 in OSCC, its expression in 20 pairs of OSCC tissues and adjacent normal tissues was detected by qRTPCR. The results showed that lncRNA FAL1 was highly expressed in OSCC tissues (Figure 1A).Studies19 have shown that lncRNA can competitively interact with MREs to abolish the inhibitory effect of microRNA on target RNAs. To elucidate the possible mechanism of lncRNA FAL1 in regulating the biological performances of OSCC, we first predicted the binding sites of lncRNA FAL1 by bioinformatics (Figure 2A). The results indicated that lncRNA FAL1 could bind to microRNA-761. In addition, we found that the expression level of microRNA-761 in OSCC tissues was significantly lower than that of adjacent normal oral tissues (Figure 2B). MicroRNA-761 was lowly expressed in OSCC cell lines as well (Figure 2C). To further elucidate the regulatory effect of lncRNA FAL1 on microRNA-761, we determined microRNA-761 expression in OSCC cells transfected with si-FAL1. As the data showed, the mRNA level of microRNA-761 in OSCC cells was markedly upregulated after lncRNA FAL1 knockdown (Figure 2D and 2E). Next, we constructed wild-type (lncRNA FAL1-WT) and mutant-type vectors containing lncRNA FAL1 (lncRNA FAL-MUT), and co-transfected them with microRNA-761 mimics in OSCC cells. Decreased Luciferase activity was observed in the lncRNA FAL1-WT group, whereas the lncRNA FAL-MUT group showed no significant change in Luciferase activity (Figure 2F and 2G). Dual-Luciferase reporter gene assay confirmed that lncRNA FAL1 could directly sponge microRNA-761, thereafter participating in the development of OSCC.To further explore the specific regulatory mechanism of microRNA-761 in OSCC, we predicted the target gene CRKL of microRNA-761 by bioinformatics (Figure 3A). CRKL expression was significantly higher in OSCC tissues at both mRNA and protein levels (Figure 3B and 3C). Consistently, CRKL was also highly expressed in OSCC cell lines (Figure 3D). To verify the regulatory effect of microRNA-761 on CRKL, we constructed a wild-type (CRKL-WT) and mutant-type sequence of CRKL (CRKL-MUT). OSCC cells were co-transfected with CRKL-WT or CRKL-MUT and microRNA-761 mimics. The results demonstrated that the Luciferase activity of the CRKLWT group was remarkably decreased, which was not significantly altered in the CRKL-MUT group (Figure 3E and 3F). These results suggested that CRKL was a target gene of microRNA-761. Meanwhile, microRNA-761 could inhibit CRKL expression by binding to the 3'UTR of CRKL.To verify whether microRNA-761 could regulate CRKL in OSCC cells, we determined the protein level of CRKL after transfection with microRNA-761 inhibitor in OSCC cells. western blot showed that the protein expression of CRKL was remarkably upregulated (Figure 4A). To further validate the role of microRNA-761/CRKL axis in the development of OSCC regulated by lncRNA FAL1, OSCC cells were co-transfected with si-FAL1 and microRNA-761 inhibitor. The CCK-8 assay demonstrated that the inhibitory effect of lncRNA FAL1 knockdown on the proliferation of OSCC cells was reversed by microRNA-761 knockdown (Figure 4B and 4C). Subsequently, CRKL was observed to be significantly downregulated after transfection of si-FAL1 (Figure 4D). Gain-of-function experiments revealed that inhibited proliferation of OSCC cells by lncRNA FAL1 knockdown was reversed by CRKL overexpression (Figure 4E and 4F). The above data illustrated that lncRNA FAL1 promoted the development of OSCC by regulating the microRNA-761/CRKL pathway.	31298329	RID07707	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Gastric cancer	AK027294	PCNA	positively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000132646	NA	NA	5111	NA	NA	Long non-coding RNA AK027294 promotes tumor growth by upregulating PCNA in gastric cancer.Firstly, AK027294 expression was monitored by RT-qPCR in 58 GC patients'-tissues and 4 GC cell lines. AK027294 was remarkably higher-expressed in tumor tissue samples compared with adjacent tissues (Figure 1A). AK027294 expression level was higher in GC cells than that in GES (Figure 1B).MKN-45 GC cell lines were chosen for the overexpression of AK027294. Then, AK027294 expression was detected by RT-qPCR (Figure 2D). MTT assay showed that cell growth ability of MKN-45 cells was promoted via overexpression of AK027294 (Figure 2E). Moreover, colony formation assay revealed that the number of colonies was significantly increased via overexpression of AK027294 in MKN-45 cells (Figure 2F). Furthermore, EdU incorporation assay showed that EdU positive cells were increased after overexpression of AK027294 in MKN-45 cells (Figure 3B).We conducted RT-qPCR and western blot assay to explore the association between PCNA and AK027294. The expression level of PCNA in HGC-27 cells in the sh-AK027294 group was remarkably lower than that in control group (Figure 4A). The expression level of PCNA in MKN-45 cells in AK027294 lentivirus group was remarkably higher than that in control group (Figure 4B). Besides, PCNA expression was remarkably higher in GC tissues compared with that in adjacent tissues (Figure 4C). Furthermore, PCNA expression was significantly higher in GC cells compared with GES cell (Figure 4D).We further found the positive correlation between PCNA and AK027294 expression level in GC tissues (Figure 4E).	31298327	RID07708	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Colorectal cancer	SOD2-OT1	CDKN1A	negatively-E	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000285427	GRCh38_6:159760258-159762332	ENSG00000124762	NA	100129518	1026	SOD2	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA GClnc1 promotes progression of colorectal cancer by inhibiting p53 signaling pathway.To clarify the relationship between the expression of GClnc1 and the development of CRC, we first detected the expression level of GClnc1 in CRC tissues and normal colon tissues by qRTPCR. The results showed that the level of GClnc1 in CRC tissues was conspicuously higher than that of normal colon tissue (Figure 1A). After paired analysis of tissue samples, we found that the majority of patients with CRC had high expression of GClnc1 (Figure 1B).To further explore how GClnc1 affected the proliferation of colon cancer cells, we performed cell localization of GClnc1. The results found that GClnc1 was mainly expressed in the cytoplasm (Figure 3A). Subsequently, RNA pull-down assay and western blot were performed to determine the specific interaction between GClnc1 and p53 (Figure 3B, 3C). RIP experiment found that the level of GClnc1 in the p53 antibody precipitation complex was significantly higher than that of the IgG control group (Figure 3D). Next, to investigate whether GClnc1 could inhibit the expression of p53, we over-expressed GClnc1 in HCT116 cells. The results indicated the mRNA and protein expressions of p53 were not significantly changed. However, the expression of p21, as well as BAX, was remarkably reduced (Figure 3E, 3F). Additionally, the Luciferase reporter gene assay revealed that over-expression of GClnc1 could inhibit the Luciferase activity of p53 (Figure 3G). Moreover, ChIP and qRT-PCRassay confirmed that GClnc1 over-expression markedly inhibited the binding condition of p53 to p21. The above results indicated that GClnc1 could affect the levels of p21 and BAX by inhibiting the activity of p53.To confirm that GClnc1 promoted the proliferation of CRC cells by affecting p53 activity, we silenced GClnc1 in HCT116 cells. western blot results found that the protein level of p53 was not affected. At the same time, we simultaneously knocked down p53 in cells as well (Figure 4A). qRT-PCRresults indicated that the expressions of BAX and p21 were significantly increased after knockdown of GClnc1 in HCT116 cells. However, they markedly decreased after knocking down GClnc1 and p53 (Figure 4B). Furthermore, CCK8 experiments showed that knockdown of p53 remarkably reversed the decrease in cell viability caused by knockdown of GClnc1 (Figure 4C).The above results demonstrated that GClnc1 could inhibit the expressions of BAX and p21 by p53 and promote the proliferation of CRC cells.	31298323	RID07709	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Colorectal cancer	SOD2	BAX	negatively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000112096	GRCh38_6:159669069-159762529	ENSG00000087088	NA	6648	581	GClnc1	BCL2L4	Long non-coding RNA GClnc1 promotes progression of colorectal cancer by inhibiting p53 signaling pathway.To clarify the relationship between the expression of GClnc1 and the development of CRC, we first detected the expression level of GClnc1 in CRC tissues and normal colon tissues by qRTPCR. The results showed that the level of GClnc1 in CRC tissues was conspicuously higher than that of normal colon tissue (Figure 1A). After paired analysis of tissue samples, we found that the majority of patients with CRC had high expression of GClnc1 (Figure 1B).To further explore how GClnc1 affected the proliferation of colon cancer cells, we performed cell localization of GClnc1. The results found that GClnc1 was mainly expressed in the cytoplasm (Figure 3A). Subsequently, RNA pull-down assay and western blot were performed to determine the specific interaction between GClnc1 and p53 (Figure 3B, 3C). RIP experiment found that the level of GClnc1 in the p53 antibody precipitation complex was significantly higher than that of the IgG control group (Figure 3D). Next, to investigate whether GClnc1 could inhibit the expression of p53, we over-expressed GClnc1 in HCT116 cells. The results indicated the mRNA and protein expressions of p53 were not significantly changed. However, the expression of p21, as well as BAX, was remarkably reduced (Figure 3E, 3F). Additionally, the Luciferase reporter gene assay revealed that over-expression of GClnc1 could inhibit the Luciferase activity of p53 (Figure 3G). Moreover, ChIP and qRT-PCRassay confirmed that GClnc1 over-expression markedly inhibited the binding condition of p53 to p21. The above results indicated that GClnc1 could affect the levels of p21 and BAX by inhibiting the activity of p53.To confirm that GClnc1 promoted the proliferation of CRC cells by affecting p53 activity, we silenced GClnc1 in HCT116 cells. western blot results found that the protein level of p53 was not affected. At the same time, we simultaneously knocked down p53 in cells as well (Figure 4A). qRT-PCRresults indicated that the expressions of BAX and p21 were significantly increased after knockdown of GClnc1 in HCT116 cells. However, they markedly decreased after knocking down GClnc1 and p53 (Figure 4B). Furthermore, CCK8 experiments showed that knockdown of p53 remarkably reversed the decrease in cell viability caused by knockdown of GClnc1 (Figure 4C).The above results demonstrated that GClnc1 could inhibit the expressions of BAX and p21 by p53 and promote the proliferation of CRC cells.	31298323	RID07710	expression association	NA	DOWN(BRCA);DATA(GSE111065,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	SOD2	TP53	interact	luciferase reporter assay;RNA pull-down assays;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000112096	GRCh38_6:159669069-159762529	ENSG00000141510	NA	6648	7157	GClnc1	LFS1|p53	Long non-coding RNA GClnc1 promotes progression of colorectal cancer by inhibiting p53 signaling pathway.To clarify the relationship between the expression of GClnc1 and the development of CRC, we first detected the expression level of GClnc1 in CRC tissues and normal colon tissues by qRTPCR. The results showed that the level of GClnc1 in CRC tissues was conspicuously higher than that of normal colon tissue (Figure 1A). After paired analysis of tissue samples, we found that the majority of patients with CRC had high expression of GClnc1 (Figure 1B).To further explore how GClnc1 affected the proliferation of colon cancer cells, we performed cell localization of GClnc1. The results found that GClnc1 was mainly expressed in the cytoplasm (Figure 3A). Subsequently, RNA pull-down assay and western blot were performed to determine the specific interaction between GClnc1 and p53 (Figure 3B, 3C). RIP experiment found that the level of GClnc1 in the p53 antibody precipitation complex was significantly higher than that of the IgG control group (Figure 3D). Next, to investigate whether GClnc1 could inhibit the expression of p53, we over-expressed GClnc1 in HCT116 cells. The results indicated the mRNA and protein expressions of p53 were not significantly changed. However, the expression of p21, as well as BAX, was remarkably reduced (Figure 3E, 3F). Additionally, the Luciferase reporter gene assay revealed that over-expression of GClnc1 could inhibit the Luciferase activity of p53 (Figure 3G). Moreover, ChIP and qRT-PCRassay confirmed that GClnc1 over-expression markedly inhibited the binding condition of p53 to p21. The above results indicated that GClnc1 could affect the levels of p21 and BAX by inhibiting the activity of p53.To confirm that GClnc1 promoted the proliferation of CRC cells by affecting p53 activity, we silenced GClnc1 in HCT116 cells. western blot results found that the protein level of p53 was not affected. At the same time, we simultaneously knocked down p53 in cells as well (Figure 4A). qRT-PCRresults indicated that the expressions of BAX and p21 were significantly increased after knockdown of GClnc1 in HCT116 cells. However, they markedly decreased after knocking down GClnc1 and p53 (Figure 4B). Furthermore, CCK8 experiments showed that knockdown of p53 remarkably reversed the decrease in cell viability caused by knockdown of GClnc1 (Figure 4C).The above results demonstrated that GClnc1 could inhibit the expressions of BAX and p21 by p53 and promote the proliferation of CRC cells.	31298323	RID07711	interact with protein	NA	DOWN(BRCA);DATA(GSE111065,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Malignant glioma	SNHG5	E2F3	positively-E	luciferase reporter assay;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-205)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000112242	NA	387066	1871	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis.First, we analysed the expression profiles of SNHG5 in the TCGA database and found that the expression level of SNHG5 in glioma tissues was significantly higher than that in non-malignant tissues (Figure 1A). Next, we detected the expression of SNHG5 in glioma tissues (n=20) and normal brain tissues (n=20). The results indicated that compared with normal tissues, the expression level of SNHG5 is significantly increased in gliomas (Figure 1B). Additionally, we detected a significant increase in SNHG5 expression in glioma cell lines (U87 and U251) compared with that in NHAs (Figure 1C). These data illustrate that SNHG5 may play a pivotal role in promoting the malignant evolution of glioma.To investigate the effect of SNHG5 on glioma cells, the expression of SNHG5 was decreased by si-SNHG5 in U87 and U251 cells. First, we confirmed the transfection efficiency in these cell lines by qRT-PCR(Figure 2A). Studies have shown that glucose metabolism has drawn a significant amount of attention in cancer research. We wondered whether SNHG5 could affect glucose metabolism in glioma [20]. Thus, we performed a glucose uptake assay, and the results manifested that compared with the NC, the down-regulation of SNHG5 significantly decreased the ability of cell lines to uptake glucose (Figure 2B,C). Moreover, compared with the NC group, the migration ability of si-SNHG5 U87 and U251 cells was impaired as well (Figure 2D,E). A similar result was obtained in the transwell assay (Figure. 2F,G). These results suggest that SNHG5 promotes glucose uptake, migration and invasion in glioma cell lines.Accumulating evidence has shown that lncRNAs can act as competing endogenous RNA (ceRNAs) during tumourigenesis. CeRNAs can interact with functional miRNAs to regulate gene expression. Through the online database starBase v3.0 (http://starbase.sysu.edu.cn/), we found that miR-205 may be a target of SNHG5 (Figure 3A). To determine whether SNHG5 can interact with miR-205 in glioma, we performed the following experiments. First, we explored the expression of miR-205 in glioma tissues and cell lines. The results showed that miR-205 was down-regulated in glioma tissues and cell lines compared with that in normal brain tissues and NHAs (Figure 3B,C). Second, through qRT-PCR we determined that miR-205 expression levels were up-regulated after down-regulating SNHG5 in glioma cells and that miR-205 mimics could also down-regulate SNHG5 expression levels in glioma cells (Figure 3D,E). In addition, SNHG5 luciferase reporter plasmids with wild-type and predicted mutant sites for miR-205 were constructed. We found that miR-205 mimics decreased the luciferase activity of the wild-type plasmid but did not reduce the luciferase activity of the mutant plasmid (Figure 3F). Furthermore, MS2-RIP was conducted to verify the binding interaction between miR-205 and SNHG5. The results showed that, compared with the empty vector and MS2-tagged mutant-type SNHG5, MS2-tagged wild-type SNHG5 was enriched for miR-205 (Figure 3G). In addition, we carried out an RNA pull-down assay, and the results illustrated that SNHG5 was pulled down by the target oligos (Figure 3H,I). These findings clarify that SNHG5 is a sponge for miR-205.To explore the mechanism of miR-205 in glioma cell lines, we used starBase v3.0 to identify the potential targets of miR-205. Fortunately, we found that E2F3 may be a target of miR-205. Figure 5A shows miR-205 binding to the predicted sites of the 3'-UTR of E2F3. Next, we analysed the expression of E2F3 in glioma tissues and cell lines. The results showed that E2F3 was up-regulated in glioma tissues and cell lines compared with that in normal brain tissues and NHAs (Figure 5B ). Then, luciferase reporter plasmids that contained wild-type and mutated E2F3 3'-UTR were constructed. Our data showed that the luciferase activity of the wild-type E2F3 3'-UTR vector was significantly decreased, while that of the mutant vector was not (Figure 5E,F). qRT-PCR western blot and immunofluorescence demonstrated that the expression levels of endogenous E2F3 were down-regulated when miR-205 was increased and that the inhibitory effect of miR-205 on E2F3 could be restored by an E2F3 plasmid (Figure 5G ). In addition, we also found that E2F3 restored the effects of miR-205 on glucose uptake, migration and invasion (Figure 5J ). In summary, these results confirm that miR-205 plays a role through E2F3 in glioma cells.	31292168	RID07712	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Posterior capsule opacification	FEZF1-AS1	FEZF1	positively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Other	Posterior capsule opacification	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000128610	NA	154860	389549	NA	ZNF312B	LncRNA FEZF1-AS1 Promotes TGF- beta 2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.Using real-time RT-PCR we first detected FEZF1-AS1 levels and found that FEZF1-AS1 was upregulated in TGF-beta2-treated SRA01/04-cells compared to its expression in the blank control group (Figure 1(a)). Meanwhile, the viability and proliferation of TGF-beta2-treated SRA01/04-cells, which were detected by CCK-8 and EdU assays, respectively, increased compared to that observed in control cells (Figures 1(b)'-(d)). Previous studies found that FEZF1-AS1 knockdown repressed the proliferation of gastric cancer and lung adenocarcinoma cells, inhibited cell cycle progression by causing G1/S arrest, and decreased the levels of cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 4 (CDK4), cyclin-dependent kinase 6 (CDK6), and cyclin D1 [10, 11]. Interestingly, western blot demonstrated that CDK2, CDK4, CDK6, and cyclin D1 protein levels were upregulated in the TGF-beta2-treated cells compared to their expression in the blank control cells (Figures 1(e) and 1(f)). Additionally, the wound healing assay showed that cell migration was increased in the TGF-beta2-treated cells compared to that in the control cells (Figures 1(g) and 1(h)). These data suggested that FEZF1-AS1 was upregulated and accompanied by the increased proliferation and migration of TGF-beta2-treated SRA01/04-cells, implying that FEZF1-AS1 was associated with the proliferation and migration of SRA01/04-cells after TGF-beta2 stimulation.We next used wound healing (Figures 2(a)'-(c)) and Transwell assays (Figures 2(c)'-(e)) following FEZF1-AS1 knockdown or overexpression to explore the role of FEZF1-AS1 in TGF-beta2-induced SRA01/04-cell migration, which showed that FEZF1-AS1 promoted TGF-beta2-induced SRA01/04-cell migration.Previous studies found that FEZF1-AS1 increased FEZF1 protein levels [6, 12]. Thus, we speculated that FEZF1-AS1 plays a positive role in TGF-beta2-induced SRA01/04-cell proliferation and migration via upregulating FEZF1 protein levels. FEZF1-AS1 knockdown inhibited (Figure 4(a)) FEZF1 protein levels, and its overexpression increased FEZF1 protein levels (Figures 4(a) and 4(b)). Moreover, FEZF1 siRNAs were also used to downregulate the FEZF1 mRNA level (Figure 2(c), FEZF1 siRNA2 showed the best efficiency and was used in subsequent experiments) without affecting the FEZF1-AS1 level (Figure 4(d)). In SRA01/04-cells, FEZF1 siRNA2 inhibited TGF-beta2- and FEZF1-AS1-induced proliferation (Figures 4(e) and 4(g)) and migration (Figures 4(f) and 4(h)). These results suggested that FEZF1-AS1 promoted the proliferation and migration of TGF-beta2-induced SRA01/04-cells via upregulating FEZF1 protein levels.	31281667	RID07713	expression association	NA		UP(LIHC);DATA(GSE117623)
Gastric cancer	MHRT	ROCK2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-4529-5p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	NA	NA	ENSG00000134318	NA	104564225	9475	NA	NA	Myosin Heavy Chain-Associated RNA Transcripts Promotes Gastric Cancer Progression Through the miR-4529-5p/ROCK2 Axis.To study the role of MHRT in gastric cancer, we first analyzed the expression level of MHRT in clinical gastric cancer samples and gastric cancer cell lines. Interestingly, we observed that the RNA level of MHRT was significantly higher in gastric cancer samples in comparison with adjacent tissues (Fig. 1a).To explore the role of MHRT upregulation in cancer cells, we first downregulated MHRT in SGC-7901 and BGC823 cells with small interfering RNA (siRNA). Our data showed that MHRT was significantly downregulated in cells transfected with MHRT siRNA (Fig. 2a). We then analyzed the growth of cells transfected with control or MHRT siRNA. Interestingly, our data revealed that downregulation of MHRT resulted in significant inhibition of cell growth in both SGC-7901 and BGC-823 cells (Fig. 2b). In addition, EdU assay showed that reduced MHRT levels inhibited cell proliferation in gastric cancer cells (Fig. 2c), suggesting that MHRT is required for the proliferation of gastric cancer cells.It has been reported that lncRNAs frequently function as competing endogenous RNAs for miRNAs, thereby regulating the expression of certain coding genes. In this way, lncRNAs regulate a wide variety of biological processes. Therefore, we predicted potential miRNAs with high binding affinity for MHRT using online algorithms (http://spong escan .rc.ufl.edu/). The prediction algorithms yielded a miRNA, miR-4529-5p, with sequences complementary to MHRT (Fig. 3a). Thus, we cloned wildtype MHRT and binding site-mutated MHRT sequences in luciferase reporter plasmids. miR-4529-5p was overexpressed in 293T cells by transfecting miR-4529-5p mimics. Ectopically expressed miR-4529-5p suppressed the luciferase signal of constructs containing wild-type MHRT but not binding site-mutated MHRT (Fig. 3b), indicating that MHRT binds to and is negatively regulated by miR-4529-5p. Interestingly, downregulation of MHRT resulted in a significant increase in miR-4529-5p (Fig. 3c) in both SGC-7901 and BGC-823 cells, suggesting that MHRT functions as a competing endogenous RNA for miR-4529-5p to dilute the cellular level of miR4529-5p in gastric cancer cells. Hence, we suspected that miR-4529-5p is downregulated in gastric cancer. To test this hypothesis, the expression level of miR-4529-5p was analyzed in both clinical gastric cancer samples as well as in gastric cancer cell lines. As expected, we found that miR-4529-5p was significantly downregulated in clinical gastric cancer tissues (Fig. 3d) and gastric cancer cell lines (Fig. 3e) compared to adjacent normal tissues. Hence, our data illustrated that MHRT binds to and inhibits miR4529-5p expression in gastric cancer.To dissect the role of MHRT in miR-4529-5p-mediated progression of gastric cancer, we abolished the expression of miR-4529-5p with microRNA inhibitor. Our results showed that miR-4529-5p was successfully downregulated with miRNA inhibitors (Fig. 4a). Next, we inhibited miR4529-5p in gastric cancer cells previously transfected with MHRT siRNA. Our results showed that cell growth inhibition achieved by transfection with MHRT siRNA was overcome in both SGC-7901 and BGC-823 cells by additional inhibition of miR-4529-5p (Fig. 4b), suggesting that MHRT knockdown resulted in miR-4529-5p-dependent cell growth inhibition. Moreover, our data showed that the percentage of EdU-positive cells were increasing significantly when both MHRT and miR-4529-5p were inhibited compared to MHRT inhibition alone in gastric cancer cells (Fig. 4c), suggesting that elevated miR4529-5p inhibits proliferation. Additionally, our data showed that co-inhibition of MHRT and miR-4529-5p attenuated the induction of apoptosis by inhibition of MHRT alone (Fig. 4d), indicating that MHRT regulates apoptosis via miR-4529-5p. Besides, we analyzed the invasion of gastric cancer cells transfected with MHRT siRNA or MHRT siRNA together with miR-4529-5p inhibitor. Our data illustrated that additional knockdown of miR4529-5p restored the invasion capability of gastric cancer cells that was inhibited by MHRT inhibition alone (Fig. S2). Taken together, our data demonstrated that MHRT regulates gastric cancer cells through miR-4529-5p.Next, we set out to identify mRNAs that are targeted by miR-4529-5p in gastric cancer using online software (TargetScan, http://www.targe tscan .org/ and miRanda, www. micro rna.org/). Among the predicted targets, we found that ROCK2 showed a sequence complementary to miR-4529-5p in the 3'-untranslated region. Hence, we constructed luciferase reporter plasmids containing wild-type and mutated 3'-untranslated region (3'UTR) of ROCK2. 293T cells were co-transfected with the luciferase reporter plasmids and control miRNA mimics or miR-4529-5p mimics. The luciferase reporter assay revealed that miR-4529-5p inhibited the expression of the reporter with wild-type 3'UTR of ROCK2 but not the mutated 3'UTR (Fig. 5a), indicating that miR4529-5p binds to 3'UTR of ROCK2 and regulates the mRNA degradation of ROCK2. Moreover, we examined the protein and mRNA levels of ROCK2 in SGC-7901 and BGC-823 cells transfected with miR-4529-5p mimics. It was observed that both protein levels (Fig. 5b) and mRNA levels (Fig. 5c) of ROCK2 were significantly reduced when miR-4529-5p was upregulated, suggesting that ROCK2 is a downstream target of miR-4529-5p in gastric cancer. As miR-4529-5p was inhibited in gastric cancer by MHRT, we hypothesized that ROCK2 was elevated in gastric cancers. As expected, our data revealed that ROCK2 was significantly upregulated in gastric tumor tissues in comparison with adjacent normal tissues (Fig. 5d). Thus, our data illustrated that ROCK2 is a downstream target of miR-4529-5p in gastric cancer and it is elevated in gastric cancer.In summary, our data illustrated that in addition to its oncogenic role in cardiomyocytes, MHRT exhibited an oncogenic role in gastric cancer by inhibiting miR-4529-5p, a novel miRNA identified in gastric cancer. Moreover, our data illustrated that miR-4529-5p binds to and degrades ROCK2 mRNA to maintain a low level of ROCK2 in normal cells. Once the inhibition of ROCK2 in normal cells is overcome, ectopically expressed ROCK2 promotes tumorigenesis of gastric cancer.	31273599	RID07714	ceRNA or sponge	NA		UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	UCA1	miR-26a	negatively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs.UCA1 is a lncRNA whose expression is found to related to the initiation and progression of many kinds of cancers. To explore its function in GC, we first analyzed the expression of UCA1 in GC tissues and noncancerous control tissues by using two published microarray datasets, GSE54129 (111 GC patients and 21 control) and GSE65801 (32 paired GC and noncancerous tissues). We found a significantly overexpressed UCA1 in patients with GC (Fig. 1a). We also collected 40 paired GC and noncancerous tissue samples (21 intestinal, 13 diffused and 7 mixed) and examined the UCA1 level by qRT-PCR We found UCA1 level only up-regulated in the intestinal GC subtype tissues significantly (Fig. -(Fig.1b).1b).To further explore the biological function of UCA1 in the GC cells, we first constructed UCA1 overexpression vector and established UCA1 overexpression GC cell lines (Fig. 2a). As shown in Fig. -Fig.2b,2b, GC cells with overexpressed UCA1 have significantly increased cell viability. Meanwhile, we constructed UCA1 knockdown vector which expresses two guide RNAs targeting the promoter region of UCA1 and then established UCA1 knockdown cell lines (Fig. -(Fig.2c,2c, d). The UCA1 promoter region knockout was confirmed by genotyping and sequencing(Additional file 1: Figure S1). As shown in Additional file 1: Figure S1A, The wildtype PCR product is 1705-bp which between bands of 1500-bp and 2000-bp of the marker lane. Meanwhile, the expected UCA1 knockdown PCR products are around 1103-bp which located between bands of 1000-bp and 1500-bp of the marker lane.Accumulating evidence indicates that lncRNAs can exert "Sponge-like'-effects on various miRNAs, which subsequently inhibits miRNA-mediated functions [19]. So, we firstly analyzed the potential of interaction between UCA1 and miRNAs. We found miR-26a and -b may bind with UCA1 directly, and this binding was subsequently confirmed by dual-luciferase assay (Fig. 3a, b), RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B). Meanwhile, when UCA1 was overexpressed in the GC cells, the expression of endogenous miR-26a and -b was significantly downregulated Fig. -Fig.3c3c and d. We also detected the protein level of two miR-26 targets EZH2 and CDK6 that were confirmed by other researchers [20, 21]. As shown in the right panel of Fig. -Fig.3c3c and d, the level of EZH2 and CDK6 was significantly increased in the UCA1 overexpression cells, suggesting the function of miR-26 was repressed. To further determine miR-26a and -b level in vivo, we detected miR-26a and -b expression using qRT-PCR We found decreased miR-26a in all the GC tissues and decreased miR-26b in intestinal GC tissues (Fig. -(Fig.3e).3e). We also found a significant strong negative correlation between UCA1 and miR-26b (Fig. -(Fig.33e).In addition, we also found miR-214 and -193 have the potential to be 'sponged'-by UCA1 (Fig. 4a), and both were reported function as tumor suppressors [22, 23]. Dual luciferase assay was processed to confirm the interaction between miRNAs and UCA1. As shown in Fig. -Fig.4b,4b, luciferase activities were repressed by miR-193a and---214 mimics, and up-regulated by miR-193a and---214 inhibitors, meanwhile, the level of miR-193a and---214 was reduced in UCA1 overexpression cells (Fig. -(Fig.4c).4c). In the GC tissues, both of miR-193 and miR-214 were reduced and negatively correlated with UCA1 level (Additional file 4: Figure S4A), indicating the direct interaction between miRNAs and UCA1. The direct interaction between UCA1 and miR-193 or miR-214 was confirmed by RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B) in GC cells.	31272462	RID07715	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Gastric cancer	UCA1	miR-26b	negatively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000199121	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs.UCA1 is a lncRNA whose expression is found to related to the initiation and progression of many kinds of cancers. To explore its function in GC, we first analyzed the expression of UCA1 in GC tissues and noncancerous control tissues by using two published microarray datasets, GSE54129 (111 GC patients and 21 control) and GSE65801 (32 paired GC and noncancerous tissues). We found a significantly overexpressed UCA1 in patients with GC (Fig. 1a). We also collected 40 paired GC and noncancerous tissue samples (21 intestinal, 13 diffused and 7 mixed) and examined the UCA1 level by qRT-PCR We found UCA1 level only up-regulated in the intestinal GC subtype tissues significantly (Fig. -(Fig.1b).1b).To further explore the biological function of UCA1 in the GC cells, we first constructed UCA1 overexpression vector and established UCA1 overexpression GC cell lines (Fig. 2a). As shown in Fig. -Fig.2b,2b, GC cells with overexpressed UCA1 have significantly increased cell viability. Meanwhile, we constructed UCA1 knockdown vector which expresses two guide RNAs targeting the promoter region of UCA1 and then established UCA1 knockdown cell lines (Fig. -(Fig.2c,2c, d). The UCA1 promoter region knockout was confirmed by genotyping and sequencing(Additional file 1: Figure S1). As shown in Additional file 1: Figure S1A, The wildtype PCR product is 1705-bp which between bands of 1500-bp and 2000-bp of the marker lane. Meanwhile, the expected UCA1 knockdown PCR products are around 1103-bp which located between bands of 1000-bp and 1500-bp of the marker lane.Accumulating evidence indicates that lncRNAs can exert "Sponge-like'-effects on various miRNAs, which subsequently inhibits miRNA-mediated functions [19]. So, we firstly analyzed the potential of interaction between UCA1 and miRNAs. We found miR-26a and -b may bind with UCA1 directly, and this binding was subsequently confirmed by dual-luciferase assay (Fig. 3a, b), RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B). Meanwhile, when UCA1 was overexpressed in the GC cells, the expression of endogenous miR-26a and -b was significantly downregulated Fig. -Fig.3c3c and d. We also detected the protein level of two miR-26 targets EZH2 and CDK6 that were confirmed by other researchers [20, 21]. As shown in the right panel of Fig. -Fig.3c3c and d, the level of EZH2 and CDK6 was significantly increased in the UCA1 overexpression cells, suggesting the function of miR-26 was repressed. To further determine miR-26a and -b level in vivo, we detected miR-26a and -b expression using qRT-PCR We found decreased miR-26a in all the GC tissues and decreased miR-26b in intestinal GC tissues (Fig. -(Fig.3e).3e). We also found a significant strong negative correlation between UCA1 and miR-26b (Fig. -(Fig.33e).In addition, we also found miR-214 and -193 have the potential to be 'sponged'-by UCA1 (Fig. 4a), and both were reported function as tumor suppressors [22, 23]. Dual luciferase assay was processed to confirm the interaction between miRNAs and UCA1. As shown in Fig. -Fig.4b,4b, luciferase activities were repressed by miR-193a and---214 mimics, and up-regulated by miR-193a and---214 inhibitors, meanwhile, the level of miR-193a and---214 was reduced in UCA1 overexpression cells (Fig. -(Fig.4c).4c). In the GC tissues, both of miR-193 and miR-214 were reduced and negatively correlated with UCA1 level (Additional file 4: Figure S4A), indicating the direct interaction between miRNAs and UCA1. The direct interaction between UCA1 and miR-193 or miR-214 was confirmed by RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B) in GC cells.	31272462	RID07716	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Gastric cancer	UCA1	miR-193a	negatively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs.UCA1 is a lncRNA whose expression is found to related to the initiation and progression of many kinds of cancers. To explore its function in GC, we first analyzed the expression of UCA1 in GC tissues and noncancerous control tissues by using two published microarray datasets, GSE54129 (111 GC patients and 21 control) and GSE65801 (32 paired GC and noncancerous tissues). We found a significantly overexpressed UCA1 in patients with GC (Fig. 1a). We also collected 40 paired GC and noncancerous tissue samples (21 intestinal, 13 diffused and 7 mixed) and examined the UCA1 level by qRT-PCR We found UCA1 level only up-regulated in the intestinal GC subtype tissues significantly (Fig. -(Fig.1b).1b).To further explore the biological function of UCA1 in the GC cells, we first constructed UCA1 overexpression vector and established UCA1 overexpression GC cell lines (Fig. 2a). As shown in Fig. -Fig.2b,2b, GC cells with overexpressed UCA1 have significantly increased cell viability. Meanwhile, we constructed UCA1 knockdown vector which expresses two guide RNAs targeting the promoter region of UCA1 and then established UCA1 knockdown cell lines (Fig. -(Fig.2c,2c, d). The UCA1 promoter region knockout was confirmed by genotyping and sequencing(Additional file 1: Figure S1). As shown in Additional file 1: Figure S1A, The wildtype PCR product is 1705-bp which between bands of 1500-bp and 2000-bp of the marker lane. Meanwhile, the expected UCA1 knockdown PCR products are around 1103-bp which located between bands of 1000-bp and 1500-bp of the marker lane.Accumulating evidence indicates that lncRNAs can exert "Sponge-like'-effects on various miRNAs, which subsequently inhibits miRNA-mediated functions [19]. So, we firstly analyzed the potential of interaction between UCA1 and miRNAs. We found miR-26a and -b may bind with UCA1 directly, and this binding was subsequently confirmed by dual-luciferase assay (Fig. 3a, b), RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B). Meanwhile, when UCA1 was overexpressed in the GC cells, the expression of endogenous miR-26a and -b was significantly downregulated Fig. -Fig.3c3c and d. We also detected the protein level of two miR-26 targets EZH2 and CDK6 that were confirmed by other researchers [20, 21]. As shown in the right panel of Fig. -Fig.3c3c and d, the level of EZH2 and CDK6 was significantly increased in the UCA1 overexpression cells, suggesting the function of miR-26 was repressed. To further determine miR-26a and -b level in vivo, we detected miR-26a and -b expression using qRT-PCR We found decreased miR-26a in all the GC tissues and decreased miR-26b in intestinal GC tissues (Fig. -(Fig.3e).3e). We also found a significant strong negative correlation between UCA1 and miR-26b (Fig. -(Fig.33e).In addition, we also found miR-214 and -193 have the potential to be 'sponged'-by UCA1 (Fig. 4a), and both were reported function as tumor suppressors [22, 23]. Dual luciferase assay was processed to confirm the interaction between miRNAs and UCA1. As shown in Fig. -Fig.4b,4b, luciferase activities were repressed by miR-193a and---214 mimics, and up-regulated by miR-193a and---214 inhibitors, meanwhile, the level of miR-193a and---214 was reduced in UCA1 overexpression cells (Fig. -(Fig.4c).4c). In the GC tissues, both of miR-193 and miR-214 were reduced and negatively correlated with UCA1 level (Additional file 4: Figure S4A), indicating the direct interaction between miRNAs and UCA1. The direct interaction between UCA1 and miR-193 or miR-214 was confirmed by RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B) in GC cells.	31272462	RID07717	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Gastric cancer	UCA1	miR-214	negatively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|onco-lncRNA-36|UCAT1	NA	The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs.UCA1 is a lncRNA whose expression is found to related to the initiation and progression of many kinds of cancers. To explore its function in GC, we first analyzed the expression of UCA1 in GC tissues and noncancerous control tissues by using two published microarray datasets, GSE54129 (111 GC patients and 21 control) and GSE65801 (32 paired GC and noncancerous tissues). We found a significantly overexpressed UCA1 in patients with GC (Fig. 1a). We also collected 40 paired GC and noncancerous tissue samples (21 intestinal, 13 diffused and 7 mixed) and examined the UCA1 level by qRT-PCR We found UCA1 level only up-regulated in the intestinal GC subtype tissues significantly (Fig. -(Fig.1b).1b).To further explore the biological function of UCA1 in the GC cells, we first constructed UCA1 overexpression vector and established UCA1 overexpression GC cell lines (Fig. 2a). As shown in Fig. -Fig.2b,2b, GC cells with overexpressed UCA1 have significantly increased cell viability. Meanwhile, we constructed UCA1 knockdown vector which expresses two guide RNAs targeting the promoter region of UCA1 and then established UCA1 knockdown cell lines (Fig. -(Fig.2c,2c, d). The UCA1 promoter region knockout was confirmed by genotyping and sequencing(Additional file 1: Figure S1). As shown in Additional file 1: Figure S1A, The wildtype PCR product is 1705-bp which between bands of 1500-bp and 2000-bp of the marker lane. Meanwhile, the expected UCA1 knockdown PCR products are around 1103-bp which located between bands of 1000-bp and 1500-bp of the marker lane.Accumulating evidence indicates that lncRNAs can exert "Sponge-like'-effects on various miRNAs, which subsequently inhibits miRNA-mediated functions [19]. So, we firstly analyzed the potential of interaction between UCA1 and miRNAs. We found miR-26a and -b may bind with UCA1 directly, and this binding was subsequently confirmed by dual-luciferase assay (Fig. 3a, b), RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B). Meanwhile, when UCA1 was overexpressed in the GC cells, the expression of endogenous miR-26a and -b was significantly downregulated Fig. -Fig.3c3c and d. We also detected the protein level of two miR-26 targets EZH2 and CDK6 that were confirmed by other researchers [20, 21]. As shown in the right panel of Fig. -Fig.3c3c and d, the level of EZH2 and CDK6 was significantly increased in the UCA1 overexpression cells, suggesting the function of miR-26 was repressed. To further determine miR-26a and -b level in vivo, we detected miR-26a and -b expression using qRT-PCR We found decreased miR-26a in all the GC tissues and decreased miR-26b in intestinal GC tissues (Fig. -(Fig.3e).3e). We also found a significant strong negative correlation between UCA1 and miR-26b (Fig. -(Fig.33e).In addition, we also found miR-214 and -193 have the potential to be 'sponged'-by UCA1 (Fig. 4a), and both were reported function as tumor suppressors [22, 23]. Dual luciferase assay was processed to confirm the interaction between miRNAs and UCA1. As shown in Fig. -Fig.4b,4b, luciferase activities were repressed by miR-193a and---214 mimics, and up-regulated by miR-193a and---214 inhibitors, meanwhile, the level of miR-193a and---214 was reduced in UCA1 overexpression cells (Fig. -(Fig.4c).4c). In the GC tissues, both of miR-193 and miR-214 were reduced and negatively correlated with UCA1 level (Additional file 4: Figure S4A), indicating the direct interaction between miRNAs and UCA1. The direct interaction between UCA1 and miR-193 or miR-214 was confirmed by RAP assay (Additional file 3: Figure S3A) and FISH (Additional file 3: Figure S3B) in GC cells.	31272462	RID07718	ceRNA or sponge	NA	UP(PAAD);DATA(GSE40174)	
Hepatocellular carcinoma	SNAI3-AS1	UPF1	interact	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260630	GRCh38_16:88663298-88687282	ENSG00000005007	NA	197187	5976	MGC23284	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	Long non-coding RNA SNAI3-AS1 promotes the proliferation and metastasis of hepatocellular carcinoma by regulating the UPF1/Smad7 signalling pathway.To investigate the roles of SNAI3-AS1 in HCC, SNAI3-AS1 expression was examined in HCC tissues and cell lines. qRT-PCRrevealed that expression of SNAI3-AS1 was significantly elevated in 69.5% (32/46) of HCC tissues when compared with matched adjacent normal tissues (Figure -(Figure1A).1A). In vitro experiments were performed to determine the effect of SNAI3-AS1 on HCC cells proliferation and metastasis. Firstly, we reduced SNAI3-AS1 expression with lentiviral shRNA-SNAI3-AS1 in HepG2 and Hep3B cells (Figure -(Figure2A).2A). MTT and plate colony formation assays showed that knockdown of SNAI3-AS1 impaired HepG2 and Hep3B cells proliferation (Figure -(Figure2B,C).2B,C). To further examine the effects of SNAI3-AS1 on HCC metastasis, transwell and wound healing assays were used to detected cell invasion and migration. Transwell assay with Matrigel indicated that down-regulation of SNAI3-AS1 inhibited the invasive activity of HepG2 and Hep3B cells (Figure -(Figure2D).2D). The wound healing assay showed that suppression of SNAI3-AS1 expression in HepG2 and Hep3B cells resulted in slower wound closure than that in negative control cells (Figure -(Figure2E,F).2E,F). In addition, SNAI3-AS1 knockdown inhibited the expression of CDK4, CDK6, c-myc and two cell cycle associated protein cyclin B1 and cyclin D1 (Figure -(Figure2G).2G). Taken together, SNAI3-AS1 knockdown inhibited proliferation and metastasis of HCC cells in vitro.Recently, several studies have found that many lncRNAs are involved in multiple regulation pathways through their interaction with RNA-binding proteins (RBPs). To test this hypothesis, we sought to identify proteins that are associated with SNAI3-AS1, and starBase and DIANA LncBase software were used for biological information prediction. The result showed that SNAI3-AS1 contains a potential binding site for UPF1. UPF1 is known to interact with many RNA substrates and promote mRNA stability.17 Next, we constructed luciferase reporter vectors of SNAI3-AS1, and luciferase reporter assay result showed cotransfection cells with pCMV-SNAI3-AS1-WT and UPF1 vector significantly inhibited luciferase reporter activity, however, pCMV-SNAI3-AS1-Mut in UPF1 putative targeting sites did not resulted in these effects (Figure -(Figure4A).4A). To further validate the interaction between SNAI3-AS1 and UPF1, we performed RNA immunoprecipitation (RIP) with an antibody against UPF1 using cell extracts from HepG2 and Hep3B HCC cell lines. We observed an enrichment of SNAI3-AS1 with UPF1 antibody as compared to the non-specific antibody (IgG control; Figure -Figure4B).4B). Meanwhile, Pearson's correlation analysis suggested that UPF1 expression was inversely correlated with SNAI3-AS1 in HCC tissues (Figure -(Figure4C),4C), and knockdown of SNAI3-AS1 could increase UPF1RNA and protein levels in HepG2 and Hep3B cells (Figure -(Figure4D,E).4D,E). We further studied the roles of SNAI3-AS1 and UPF1 in HCC cell invasion using transwell invasion assay. The results showed that UPF1 suppressed HepG2 and Hep3B cells invasion, whereas SNAI3-AS1 promoted invasion. However, the inhibitory effect of SNAI3-AS1-shRNA on HCC cell invasion could be partially restored by UPF1 inhibition (Figure -(Figure4F,G).4F,G). These observations suggest that SNAI3-AS1 knockdown could suppress HCC cell invasion by regulating UPF1 expression.Since increasing evidence identified that tumour migration and invasion is tightly involved in EMT, so we speculated that SNAI3-AS1 induces EMT in HCC cells. Firstly, we examined the effect of SNAI3-AS1 on cell phenotype. Knockdown of SNAI3-AS1 induced the reversion of mesenchymal-like morphological feature into an epithelial phenotype in HepG2 cells (Figure -(Figure5A).5A). western blot and qRT-PCRanalysis indicated that epithelial marker E-cadherin showed increased expression, whereas mesenchymal markers (N-cadherin and vimentin) and some EMT relative protein markers showed decreased expression in SNAI3-AS1-knockdown HepG2 and Hep3B cells (Figure -(Figure5B,D).5B,D). To further explore the effect of targeting SNAI3-AS1 on EMT, IF was employed to analyse the expression of EMT markers in HepG2 and Hep3B cells. As shown in Figure -Figure5C,5C, SNAI3-AS1-shRNA increased expression of E-cadherin but decreased expression of N-cadherin and vimentin compared with negative control cells. In addition, knockdown of SNAI3-AS1 significantly reduced the expression of two matrix metalloproteinases MMP-2 and MMP-9 that are closely correlated with metastasis (Figure -(Figure5E).5E). Overall, these data indicated that SNAI3-AS1 induced EMT in HCC cells.Study had shown that UPF1 could promote TGF-beta signalling and inhibits neural differentiation by targeting Smad7 mRNA,16 thus, we hypothesize that SNAI3-AS1 promotes HCC cell invasion by regulating the ability of UPF1 to mediate the TGF-beta/Smad pathway. To further study the relationship between UPF1 and Smad7, two specific siRNAs ( siRNA #1,#2) against UPF1 gene transcript were introduced into HepG2 and Hep3B cells, and produced the greatest reduction in endogenous UPF1 expression (Figure -(Figure6A).6A). western blot confirmed that Smad7 expression level was up-regulated when UPF1 was silenced in HCC cells (Figure -(Figure6B).6B). While the Smad7 expression level was down-regulated when UPF1 was overexpressed in HCC cells (Figure -(Figure6C).6C). Pearson's correlation analysis showed that Smad7 mRNA expression was significantly negatively correlated with UPF1 in HCC tissues (Figure -(Figure6D).6D). Previous studies had demonstrated the key role of Smad7 in the TGF-beta pathway. As shown in our study, UPF1 could affect the expression of Smad7 in HCC. Therefore, we speculated that SNAI3-AS1 could affect the TGF-beta pathway by regulating UPF1. As shown in Figure -Figure6E,6E, SNAI3-AS1 knockdown significantly decreased phosphorylation of Smad2/3, whereas total Smad2/3 expression level was similar between groups. In addition, the rescue experiments were conducted to prove that SNAI3-AS1 promotes tumour EMT by regulating UPF1. As shown before, knockdown of SNAI3-AS1 increased epithelial marker E-cadherin and decreased mesenchymal markers N-cadherin and vimentin, however, these effects could be partially restored by UPF1 inhibition (Figure -(Figure6F).6F). All these results demonstrated that SNAI3-AS1 promotes HCC tumorigenesis by binding UPF1, regulating Smad7 expression, and inducing activation of the TGF-beta/Smad pathway (Figure -(Figure77).	31264769	RID07719	interact with protein	metastasis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	UCA1	CDC42	positively-E	knockdown	upregulation	RT-PCR	NA	NA	chemosensitivity(+)	ceRNA(miR-18a)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000070831	NA	652995	998	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CDC42Hs|G25K	Long noncoding RNA UCA1 enhances sensitivity to oncolytic vaccinia virus by sponging miR-18a/miR-182 and modulating the Cdc42/filopodia axis in colorectal cancer.Our previous study demonstrated that UCA1 is a potential biomarker for OVV therapy in ovarian cancer. To determine whether it regulates OVV spread in other cancer types, qRT-PCRassays was performed to determine relative expression levels in various colorectal cancer cell lines. CaCo2, COLO205, and HCT116-cells expressed relatively higher levels of UCA1, whereas LoVo, HT29, SW480, and T84-cells expressed lower levels (Fig. 1A). Cell lines were then infected with OVV-LG at an MOI of 0.01 (Fig. 1B ). As expected, high viral EGFP expression and virus yields were observed in CaCo2 and HCT116-cells. Conversely, these were low in LoVo, HT-29, and T84-cells. However, a correlation between UCA1 expression and OVV spread was not observed for SW480 and COLO205-cells. As shown in Fig. 1E and F, we used siRNA to analyze the effects of UCA1 suppression on OVV-LG spread with CaCo2 and HCT116, in which UCA1 expression correlated with OVV-LG spread. As expected, UCA1 knockdown inhibited OVV-LG spread in CaCo2 and HCT116-cells (Fig. 1G and H). These results illustrate that UCA1 expression is responsible for OVV-LG spread in some colorectal cancer cell lines.Having shown that UCA1 upregulation in colorectal cancer cells is important for OVV spread, the underlying mechanism was then investigated. First, binding and entry assays using OVV-LG were performed to monitor viral entry and early gene expression based on viral luciferase activity shortly after OVV-LG infection. Results showed that the production of viral progeny by cell-attached viruses was higher in LoVo, HT29, and SW480-cells than in other colorectal cancer cells (Fig. 2A). Moreover, entry efficacy, as determined by measuring luciferase activity after OVV-LG absorption to colorectal cancer cells (Fig. 2B), was relatively high in SW480 and HCT116-cells compared to that in other colorectal cancer cells. Next, we measured the production of early (M1L), intermediate (G8R), and late (A5L) viral transcripts by real-time PCR. No viral transcripts were changed in colorectal cancer cell lines (Fig. 2C,E). To investigate plaque sizes, colorectal cancer cell monolayers were infected with OVV-LG and plaque size was quantified under methylcellulose treatment (Fig. 2F). In CaCo2, SW480, and HCT116-cells, plaque sizes were larger and this result was consistent with viral EGFP expression and virus yield. In cells treated with inhibitors of cell-to-cell-spread (cytochalasin D), there was a substantial increase in plaque size, as compared to that in cells treated with an inhibitor of intracellular transport (nocodazole). Collectively, OVV cell-to-cell spread, not but binding, entry, and replication, is enhanced by UCA1 expression in colorectal cancer cell lines.Moreover, previous research demonstrated that activated Cdc42 occurs in ovarian cancer, which is associated with metastasis and filopodia formation and enhanced OVV-LG cell-to-cell spread. Therefore, the expression of active Cdc42 was tested in colorectal cancer cell lines (Fig. 3A). We observed a correlation among UCA1 expression, OVV spread, and activated Cdc42 expression in CaCo2, HCT116, LoVo, and T84-cells. In SW480-cells, results suggested that activated Cdc42 expression increased OVV spread despite low UCA1 expression. In COLO205-cells, although high UCA1 expression was observed, OVV spread was suppressed because activated Cdc42 expression was low. Moreover, Cdc42 depletion promoted a significant decrease in viral EGFP expression and virus yield (Fig. 3B ). In contrast, activated Cdc42 expression did not induce efficient OVV spread in HT29-cells (Fig. 3A). Next, we tested the lengths of filopodia, which are actin-rich structures regulated by Cdc42, in colorectal cancer cell lines. CaCo2, SW480, and HCT116-cells, in which activated Cdc42 expression was upregulated, exhibited an increase in filopodia compared to that in HT29 and T84-cells (Fig. 3E). These results suggested that a UCA1/Cdc42/filopodia formation pathway is important for OVV cell-to-cell spread in colorectal cancer cell lines.A recent study indicated that UCA1 regulates multiple miRNAs (miR-18a, miR-204, miR-182, miR-185, miR-195, miR-124, miR-206, and miR-145) and downstream pathways. Furthermore, other studies revealed that these miRNAs downregulate Cdc42 expression or filopodia formation. To validate the miRNAs involved in UCA1-regulated OVV spread, we investigated the expression of miRNAs in CaCo2 and HCT116-cells, in which UCA1 expression promotes OVV spread via Cdc42 activation. UCA1 knockdown affected the expression of several miRNAs (Fig. 4A and B). In both cell lines, the expression of only miR-18a and miR-182 was upregulated by UCA1 knockdown. These results suggested that miR-18a and miR-182 are regulated by UCA1 and important for OVV spread in colorectal cancer.	31262449	RID07720	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	UCA1	CDC42	positively-E	knockdown	upregulation	RT-PCR	NA	NA	chemosensitivity(+)	ceRNA(miR-182)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000070831	NA	652995	998	CUDR|LINC00178|onco-lncRNA-36|UCAT1	CDC42Hs|G25K	Long noncoding RNA UCA1 enhances sensitivity to oncolytic vaccinia virus by sponging miR-18a/miR-182 and modulating the Cdc42/filopodia axis in colorectal cancer.Our previous study demonstrated that UCA1 is a potential biomarker for OVV therapy in ovarian cancer. To determine whether it regulates OVV spread in other cancer types, qRT-PCRassays was performed to determine relative expression levels in various colorectal cancer cell lines. CaCo2, COLO205, and HCT116-cells expressed relatively higher levels of UCA1, whereas LoVo, HT29, SW480, and T84-cells expressed lower levels (Fig. 1A). Cell lines were then infected with OVV-LG at an MOI of 0.01 (Fig. 1B ). As expected, high viral EGFP expression and virus yields were observed in CaCo2 and HCT116-cells. Conversely, these were low in LoVo, HT-29, and T84-cells. However, a correlation between UCA1 expression and OVV spread was not observed for SW480 and COLO205-cells. As shown in Fig. 1E and F, we used siRNA to analyze the effects of UCA1 suppression on OVV-LG spread with CaCo2 and HCT116, in which UCA1 expression correlated with OVV-LG spread. As expected, UCA1 knockdown inhibited OVV-LG spread in CaCo2 and HCT116-cells (Fig. 1G and H). These results illustrate that UCA1 expression is responsible for OVV-LG spread in some colorectal cancer cell lines.Having shown that UCA1 upregulation in colorectal cancer cells is important for OVV spread, the underlying mechanism was then investigated. First, binding and entry assays using OVV-LG were performed to monitor viral entry and early gene expression based on viral luciferase activity shortly after OVV-LG infection. Results showed that the production of viral progeny by cell-attached viruses was higher in LoVo, HT29, and SW480-cells than in other colorectal cancer cells (Fig. 2A). Moreover, entry efficacy, as determined by measuring luciferase activity after OVV-LG absorption to colorectal cancer cells (Fig. 2B), was relatively high in SW480 and HCT116-cells compared to that in other colorectal cancer cells. Next, we measured the production of early (M1L), intermediate (G8R), and late (A5L) viral transcripts by real-time PCR. No viral transcripts were changed in colorectal cancer cell lines (Fig. 2C). To investigate plaque sizes, colorectal cancer cell monolayers were infected with OVV-LG and plaque size was quantified under methylcellulose treatment (Fig. 2F). In CaCo2, SW480, and HCT116-cells, plaque sizes were larger and this result was consistent with viral EGFP expression and virus yield. In cells treated with inhibitors of cell-to-cell-spread (cytochalasin D), there was a substantial increase in plaque size, as compared to that in cells treated with an inhibitor of intracellular transport (nocodazole). Collectively, OVV cell-to-cell spread, not but binding, entry, and replication, is enhanced by UCA1 expression in colorectal cancer cell lines.Moreover, previous research demonstrated that activated Cdc42 occurs in ovarian cancer, which is associated with metastasis and filopodia formation and enhanced OVV-LG cell-to-cell spread. Therefore, the expression of active Cdc42 was tested in colorectal cancer cell lines (Fig. 3A). We observed a correlation among UCA1 expression, OVV spread, and activated Cdc42 expression in CaCo2, HCT116, LoVo, and T84-cells. In SW480-cells, results suggested that activated Cdc42 expression increased OVV spread despite low UCA1 expression. In COLO205-cells, although high UCA1 expression was observed, OVV spread was suppressed because activated Cdc42 expression was low. Moreover, Cdc42 depletion promoted a significant decrease in viral EGFP expression and virus yield (Fig. 3B ). In contrast, activated Cdc42 expression did not induce efficient OVV spread in HT29-cells (Fig. 3A). Next, we tested the lengths of filopodia, which are actin-rich structures regulated by Cdc42, in colorectal cancer cell lines. CaCo2, SW480, and HCT116-cells, in which activated Cdc42 expression was upregulated, exhibited an increase in filopodia compared to that in HT29 and T84-cells (Fig. 3E). These results suggested that a UCA1/Cdc42/filopodia formation pathway is important for OVV cell-to-cell spread in colorectal cancer cell lines.A recent study indicated that UCA1 regulates multiple miRNAs (miR-18a, miR-204, miR-182, miR-185, miR-195, miR-124, miR-206, and miR-145) and downstream pathways. Furthermore, other studies revealed that these miRNAs downregulate Cdc42 expression or filopodia formation. To validate the miRNAs involved in UCA1-regulated OVV spread, we investigated the expression of miRNAs in CaCo2 and HCT116-cells, in which UCA1 expression promotes OVV spread via Cdc42 activation. UCA1 knockdown affected the expression of several miRNAs (Fig. 4A and B). In both cell lines, the expression of only miR-18a and miR-182 was upregulated by UCA1 knockdown. These results suggested that miR-18a and miR-182 are regulated by UCA1 and important for OVV spread in colorectal cancer.	31262449	RID07721	ceRNA or sponge	metastasis	UP(PAAD);DATA(GSE40174)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG6	SERPINH1	positively-E	dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000149257	NA	641638	871	HBII-276HG|NCRNA00058|U87HG	CBP1|CBP2|HSP47|SERPINH2	Up-regulation of SNHG6 activates SERPINH1 expression by competitive binding to miR-139-5p to promote hepatocellular carcinoma progression.The expression level of SNHG6 in HCC samples was significantly higher than in the control group (**P = 0.0038, Figure 4a). In addition, SNHG6 expression level in five cultured cell lines, including the normal liver cell line, HL-7702, and four HCC cell lines (HepG2, Hep3b, HLE, Huh7) was compared. Based on the results of qRT-PCR the SNHG6 expression level was up-regulated in all four HCC cell lines, especially in HepG2 HCC cell line compared with HL-7702 cell line (**PHepG2 = 0.0093, *PHep3b = 0.018, *PHLE = 0.030, *PHuh-7 = 0.044, Figure 4b).Based on the observation results in the si-SNHG6 group, colony number in HepG2 and Hep3b cells was significantly decreased compared with si-NC group (**P = 0.0049, **P = 0.0026, Figure 5a). Up-regulation of SNHG6 in HCC cell lines encouraged us to study whether the inhibition of SNHG6 would suppress HCC migration and invasion. HepG2 and Hep3b cell lines were also selected because they possessed the highest expression level of SNHG6 expression among the four HCC cell lines. In cell migration assay, inhibition of SNHG6 significantly suppressed the numbers of migrating cells in both HepG2 and Hep3b cell lines (*P = 0.047, *P = 0.025; *P = 0.040, *P = 0.033, Figure 5b). Cell invasion assay showed the similar results with cell migration assay. MiR-139-5p was screened out previously by using a Venn diagram. We performed luciferase reporter assay to determine the targeted relationship between miR-139-5p and SNHG6, the binding sites were shown in Figure 7a. After binding to the miR-139-5p by SNHG6, the luciferase activity in SNHG6-wt group was significantly decreased compared with the SNHG6-mut group (**P = 0.0028, Figure 7b). In Figure 7c, as expected, RNAs were significantly more enriched in the Ago-IP fractions of HepG2 cells compared with IgG-IP group (***P< 0.001). Besides, miR-139-5p expression levels in HCC tissues and normal tissues were detected by qRT-PCR the results showed that miR-139-5p expression was significantly decreased in tumor group compared with normal group (**P = 0.0049, Figure 7d). We also indicated that the miR-139-5p expression levels in five cell lines (HepG2, Hep3b, HLE, Huh-7 and the normal cell line HL-7702). It showed that miR-139-5p expression was obviously down-regulated in all four HCC cell lines compared with HL-7702 cell line (**P = 0.0062, **P = 0.0032, *P = 0.020, **P = 0.0048, Figure 7e).In addition, our further studies showed that the 3-UTR of SERPINH1 contains a conserved binding site for miR-139-5p, and the binding sites were shown in Figure 9a. The results of luciferase reporter assay showed that miR-139-5p obviously suppressed the luciferase activity of SERPINH1-wt 3-UTR reporter gene (**P = 0.0076, Figure 9b). Therefore, these results suggested that SERPINH1 was the direct target of miR-139-5p in HCC. Both mRNA and protein level of SERPINH1 were down-regulated by miR-139-5p mimics or instead up-regulated by miR-139-5p inhibitor, and the results were shown in Figure 9c (*P = 0.044, *P = 0.013). Besides, the results of qRT-PCRand western blot showed that SERPINH1 was significantly up-regulated in HCC tissues and cells (**P = 0.0029; **P= 0.0087, *P = 0.023, *P = 0.050, *P = 0.046, Figure 9d,e). Similar with the results of SNHG6, overexpression of SERPINH1 can promote the cell viability dramatically, while the inhibition of SERPINH1 can suppress the cell viability dramatically (*P = 0.038, *P = 0.024; *P = 0.045, *P = 0.041, Figure 10a,b). However, the addition of miR-139-5p can inhibit SERPIN1 expression. Cell viability of SERPINH1+ miR-139-5p group was similar to the NC group. Additionally, the number of colonies in the SERPINH1 group was almost two times than the number of colonies in the NC group (*P = 0.045, *P = 0.026, Figure 10c). The results of migration and invasion assay were shown in Figure 10d, the overexpression of SERPINH1 can induce the migration and invasion of HCC cells significantly (*P = 0.024, *P = 0.019, *P = 0.033, *P = 0.010), while the results showed in SERPINH1+ miR-139-5p group were similar with the NC group. In cell cycle assay, we found the HCC cells in the si-SERPINH1 group were detained in G0/G1 stage, while the overexpression of SERPINH1 can accelerate the cell cycle of HCC cells (*P = 0.042, *P = 0.031, Figure 10e).	31258024	RID07722	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	UP(PAAD,BRCA);DOWN(PRAD);DATA(GSE40174,GSE104209,GSE109761,GSE111065)
Hepatocellular carcinoma	SNHG16	p62	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-17-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000073792	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	The lncRNA SNHG16 affects prognosis in hepatocellular carcinoma by regulating p62 expression.We used quantitative RT-PCRto validate the microarray differences observed for the three most strongly upregulated and three most strongly downregulated lncRNAs (Figure 1b). Hierarchical clustering showed that HCC tissues clustered together separately from control tissues. The cancer-specific genes SNHG16, TDO2, and NNMT were upregulated in HCC tissues, while as expected, the cancer-specific genesRP11'-96E2.4,SLC5A9, and RP11'-02E16.3were downregulated.The most strongly upregulated lncRNA in our data set was SNHG16, encoded by a 7571-bp region at chromosome 17q25.1, which are all overexpression in tumor tissues and tumor cell lines; expression is low in normal liver tissue (Li, Xu, Song, Wu, & Wang, 2019; Ye, Zhang, Du, Chai, & Zhou, 2019). Previous studies have also reported that SNHG16 may act as an oncogene to promote cervical cancer and bladder cancer progression (Cao et al., 2018; Zhu et al., 2018). Therefore, we chose to focus on SNHG16 in our study.To determine whether SNHG16 expression affects patient prognosis, we used quantitative RT-PCRto measure SNHG16 expression in a larger cohort of 108 HCC patient tissues, which included the 30 patients with HCC analyzed above. The median expression across all patients was used to divide them into a group showing high SNHG16 expression (57 patients, 52.8%) or low expression (51, 47.2%; Table 1). Patients with high SNHG16 expression showed higher incidence of multiple tumors (p= .047) and macrovascular invasion (p= .044). There were no significant differences in other clinicopathological features between the two arms.We observed that patients expressing high SNHG16 showed higher rates of multiple tumors and macrovascular invasion than patients expressing low SNHG16 (Table 1). This suggests that tumors expressing high SNHG16 grow faster.To begin to identify mechanism(s) by which SNHG16 may promote cancer development, we used Starbase, miRPath, and miRanda online prediction software to predict target genes of SNHG16. We found hsa-miR-17-5p as a potential miRNA target, of which one downstream target gene is p62 (Figure 4a,b). Fluorescence in situ RNA hybridization of HepG2 and Huh-7 cells showed that hsa-miR-17-5p is located in the cytoplasm, which may indicate involvement in posttranscriptional regulation of genes (Fatica & Bozzoni, 2014; Figure 4c).To determine whether miR-17-5p can affect p62 expression, we transfected Huh-7 and HepG2 cells with plasmids containing a luciferase reporter with the wild-type miR-17-5p binding site (SNHG16-wt) or mutated binding site (SNHG16-mut). Negative control cells were transfected with a miRNA-17b-5p mimic (miR- NC). In parallel, we cotransfected certain cultures with plasmids expressing the p62 gene whose 3'-UTR contained either the wild- type (p62-wt) or mutant (p62-mut) binding site for miRNA-17b-5p. While miR-17-5p repressed SNHG16-wt luciferase activity, miR-NC did not (Figure 4d,e). Neither miR-17-5p nor miR-NC affected SNHG16-mut luciferase activity. Similarly, miR-17-5p significantly repressed the luciferase activity of p62-wt, while miR-NC did not (Figure 4d,e). Neither miR-NC nor miR-17-5p affected the luciferase activity of p62-mut.RNA coimmunoprecipitation assays confirmed direct interaction between lncSNHG16 and miR-17-5p (Figure 5a). We measured miR- 17-5p and p62 expression in the same cohort of 30 HCC tissues using quantitative RT-PCR Levels of lncSNHG16 correlated negatively with levels of miR-17-5p (Figure 5b) and positively with levels of p62 (Figure 5c). Together these results suggest that lncSNHG16 may act as an endogenous sponge of miR-17-5p to upregulate its target p62.The p62 protein regulates the mTOR pathway (Zhang et al., 2018) and accumulates in most cases of chronic liver disease that progress to HCC (Denk et al., 2006). We therefore investigated whether silencing or overexpression of SNHG16 could affect the expression of the mTOR pathway and its downstream target p70S6K by western blot. Levels of mTOR, phospho-mTOR (p-mTOR), p70S6K, and p62 were higher in SNHG16-overexpressing cells than in NC cells (Figure 6a). In contrast, levels of mTOR, p-mTOR, p70S6K, and p62 were lower in sh-SNHG16 cells than in sh-NC cells (Figure 6a). Similar results were observed at the mRNA level, based on quantitative RT-PCR(Figure 6b).The p62 protein, like p100 and p52, regulates the NF-kB pathway (Zhang et al., 2017). To determine whether SNHG16 affects NF-kB signaling, we measured levels of p62, p100, p52, NF-kB, and phospho-NF-kB ( p-NF-kB) protein in HCC cells in which SNHG16 was overexpressed or knocked down. SNHG16 overexpression increased the expression of all these proteins, while sh-SNHG16 reduced their expression (Figure 7a). Similar results were observed at the mRNA level, based on quantitative RT-PCR(Figure 7b). To verify the axis connecting SNHG16, p62, and the NF-kB pathway, we examined expression of the proteins after incubating Huh-7 and HepG2 cells with the NF-kB inhibitor SC75741. Treating cells with the NF-kB inhibitor reduced levels of p62 protein (Figure 7c) as well as levels of SNHG16 and p62 mRNAs (Figure 7d).	31256427	RID07723	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Colon cancer	MBNL1-AS1	MYL9	positively-E	luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-412-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229619	GRCh38_3:152245262-152269565	ENSG00000101335	NA	401093	10398	LOC401093	LC20|MLC2|MRLC1|MYRL2	Long non-coding RNA MBNL1-AS1 regulates proliferation, migration, and invasion of cancer stem cells in colon cancer by interacting with MYL9 via sponging microRNA-412-3p.The first step in calculating our results in our experiment, the objective of understanding whether MBNL1-AS1 and MYL9 may affect colon cancer , began with screening DEGs and lncRNAs from colon cancer-related microarray datasets GSE41328 and GSE75970, based on the GEO and TCGA database. The MBNL1-AS1 was downregulated in colon cancer (Fig. 1A and B). Moreover , through analysis of GSE75970, MYL9 was also downregulated in colon cancer (Fig. 1C), which suggested that MYL9 expression was related to the prognosis of colon cancer based on the TCGA database (Fig. 1D).As shown in Fig. 4C, bioinformatics analysis showed that there were specific binding regions between MBNL1-AS1 and miR-412-3p, and between MYL9 and miR-412-3p. miR412-3p could negatively regulates MYL9, and competitively bind to MBNL1-AS1. MBNL1-AS1 and MYL9 were targets of miR-412-3p, which were verified by dual-luciferase reporter gene assay (Fig. 4E). Moreover , the luciferase activity was reduced after co-transfection of miR-412-3p mimic with wtmiR-412-3p/MBNL1-AS1 or wt-miR-412-3p/MYL9 (p < 0.05), while the luciferase activity of mut-3'UTR showed no significant difference (P > 0.05), suggesting that miR-412-3p specifically bound to MBNL1-AS1 and MYL9.Next, the results of RNA-pull down (Fig. 4F) revealed that after treatment with bio-miR-412-3p-wt, CSCs showed evidently increased MBNL1-AS1 expression (P < 0.05), while no obvious difference was found in cells probed with bio-miR-412-3p-mut (P > 0.05), which implied that bio-miR412-3p-wt could promote the enrichment of MBNL1-AS1 around it. It could be concluded that MBNL1-AS1 could competitively bind to miR-412-3p and reduce miR-412-3p expression.Moreover , the findings of RIP (Fig. 4G) showed that in contrast to CSCs transfected with NC inhibitor , the amount of MBNL1-AS1 coprecipitated with Ago2 antibody in cells transfected with miR-412-3p inhibitor markedly elevated, while that of miR-412-3p co-precipitated with Ago2 antibody significantly decreased (both P < 0.05). Furthermore, the amount of MBNL1-AS1 and miR-412-3p precipitated by Ago2 antibody in cells treated with IgG showed obvious reduction (both P < 0.05). These results revealed that MBNL1-AS1 acted as a ceRNA of miR-412-3p. Finally , RT-qPCR (Fig. 4H) displayed that CSCs transfected with MBNL1-AS1 overexpression plasmid or miR-412-3p inhibitor showed elevated expression of MBNL1-AS1 and MYL9 and decreased miR-412-3p expression, while CSCs transfected with miR-412-3p mimic presented the opposite results (all P < 0.05). However , MBNL1-AS1 overexpression reversed the miR-412-3p-caused reduction of MYL9 (P < 0.05), suggesting that elevated MBNL1-AS1 repressed miR-412-3p so as to upregulate MYL9.With the data that verified role of miR-412-3p in CSC viability in colon cancer in hand, the focus of the experiment further studied the mechanisms of miR-412-3p in CSC invasion and migration in colon cancer . T ranswell assay (Fig. 6AD) displayed elevated cell migration and invasion in CSCs after upregulation of miR-412-3p, but inhibited cell migration and invasion in CSCs after inhibition of miR-412-3p (both P < 0.05). However , overexpressed MBNL1-AS1 reversed the elevated cell migration and invasion induced by upregulated miR-412-3p expression.With the findings of MBNL1-AS1 and miR-412-3p regulating molecular mechanisms of colon CSCs, our last objective of observing whether depleted miR-412-3p affected xenograft tumor formation in nude mice was evaluated. The findings of xenografts in nude mice (Fig. 8) revealed that after upregulating miR-412-3p, mice showed suppressed tumor formation, but promoted tumor formation after inhibiting miR-412-3p (P < 0.05), Besides, overexpressed MBNL1-AS1 resulted in suppressed tumor formation which was induced by miR-412-3p, which indicated that upregulated MBNL1AS1 repressed tumor formation of CSCs in colon cancer by downregulating miR-412-3p.	31255531	RID07724	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Colorectal cancer	LNRRIL6	IL6	positively-E	RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);IL-6/STAT3 signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000136244	NA	NA	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	LNRRIL6, a novel long noncoding RNA, protects colorectal cancer cells by activating the IL-6-STAT3 pathway.The findings of this study demonstrated that patients with higher expression of LNRRIL6 might present with larger tumor sizes, poor differentiation, and increased potential for lymph node metastasis (P < 0.05; Table 1). The Kaplan-Meier survival analysis revealed that lower expression of LNRRIL6 resulted in better outcomes (mean: 49 months vs. 36 months; P < 0.01; Fig. 1A). Clinically, our data suggest that the expression of LNRRIL6 is closely related to clinical outcome, whereby upregulation of LNRRIL6 is associated with worse outcomes. Similar results were obtained from the analysis of tissues from pathological specimens. Thus, LNRRIL6 is significantly upregulated in tumor tissues (P < 0.01; Fig. 1B).To validate the effects of LNRRIL6 in vivo, we observed LNRRIL6 overexpressing and knockdown cells after injection into nude mice. Our findings revealed that tumor volume (Fig. 4A) and mass (Fig. 4B) of mice inoculated with LNRRIL6 overexpressing cells were significantly higher than those of mice with LNRRIL6 normal-expressing cells. Analogously, the LNRRIL6+ group exhibited greater numbers of Ki-67-positive cells, suggesting higher rates of proliferation (Fig. 4C). In addition, the LNRRIL6+ group exhibited fewer cleaved caspase-3-positive cells, indicating less death of CRC cells in the LNRRIL6+ group (Fig. 4D). Similar findings were observed using NCM460 cells. Although NCM460 cells displayed limited tumorigenicity, the volume and mass of the tumors containing LNRRIL6+ cells were significantly higher than those obtained from LNRRIL N cells (Fig. S3H,I).Figure 6A confirms that LNRRIL6 was primarily localized in the nucleus. Results from the ChIRP assay demonstrated that the LNRRIL6 antisense probe pull-down group exhibited significant enrichment only in the IL-6 promoter region (LacZ; P < 0.01). We observed no enrichment effect in the beta-actin promoter region. Moreover, the LNRRIL6 antisense probe pull-down group did not exhibit enrichment effects in the STAT3 promoter region (Fig. S4A). These findings suggest that LNRRIL6 directly binds to the IL-6 promoter region (Fig. 6B).	31246342	RID07725	expression association	metastasis		DOWN(BRCA);DATA(GSE75367,GSE86978)
Head and neck squamous cell carcinoma	MYOSLID	SNAI2	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000229647	GRCh38_2:207166120-207248668	ENSG00000019549	NA	105373853	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2	Long noncoding RNA MYOSLID promotes invasion and metastasis by modulating the partial epithelial-mesenchymal transition program in head and neck squamous cell carcinoma.We detected MYOSLID expression in 15 paired fresh OSCC cancer tissues and adjacent normal tissues by RT-qPCR. The results showed that MYOSLID expression in the cancer group (0.01127- -0.01655) was higher than that in the adjacent cancer normal tissues (0.00299- -0.00608) (p-=-0.037) (Fig. 3a). Meanwhile, we detected the MYOSLID expression levels in a normal oral epithelium cell line, HIOEC, and 4 OSCC cell lines, Cal27, Tca8113, SCC4, and SCC9. The results showed that the Cal27 cell line had a higher MYOSLID expression level (0.49254- -0.07004) compared with that in Tca8113 (0.20549- -0.01073), SCC4 (0.02700- -0.00008), and SCC9 (0.03700- -0.00009) (p-<-0.05). Unexpectedly, we found that the human normal oral epithelium cell line HIOEC had the highest MYOSLID expression levels of all of the cell lines that were examined (Fig.3c).Pearson correlation analysis revealed that the expression level of MYOSLID was correlated with Slug (r-=-0.2723, p-=-0.0094), PDPN (r-=-0.3455, p-=-0.0009) and LAMB3 (r-=-0.5644, p-=-0.0001) expression, as shown in Fig. -Fig.44c.The expression level of MYOSLID was the highest in Cal27 cell line, and Cal27 cell line had a co-expression of p-EMT makers (PDPN, LAMB3) and classical EMT markers (E-cadherin, Vimentin) (Fig. -(Fig.3c,3c, f, g). This indicates that the state of the Cal27 cell line is the closest to a p-EMT. The two siRNA sequences MYOSLID-homo-96 and MYOSLID-homo-232 were selected to knockdown MYOSLID in Cal27 cell lines, as they were validated to have a higher knockout efficiency compared with that of MYOSLID-homo-696 (Fig. -(Fig.3d).3d). Wound healing assays showed that the knockdown of MYOSLID expression significantly reduced the 48-h healing rate (p-<-0.05, Fig. -Fig.4a).4a). Moreover, the transwell assay showed that the number of cells passed through the filter that was coated with Matrigel of the siRNA groups was much lower than that of the negative control group (p-<-0.05, Fig. -Fig.44b).To further verify the molecular mechanicals of aberrant MYOSLID expression affects the ability of invasion and metastasis of OSCC cells was by regulating the p-EMT program. Expression levels of p-EMT markers Slug, PDPN, LAMB3 and EMT markers E-cadherin, Vimentin were detected after knockdown MYOSLID in OSCC cell line. The results showed that knockdown MYOSLID expression significantly inhibited Slug, PDPN and LAMB3 mRNA and protein expression levels compared to those in the controls (p-<-0.05, Fig. -Fig.3e,3e, Fig. 5c). Interestingly, the expression levels of the classical EMT biomarkers E-cadherin and Vimentin remained unchanged after silencing MYOSLID (Fig. -(Fig.55c).	31238980	RID07726	expression association	metastasis		
Head and neck squamous cell carcinoma	MYOSLID	PDPN	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000229647	GRCh38_2:207166120-207248668	ENSG00000162493	NA	105373853	10630	NA	aggrus|Gp38|GP40|PA2.26|T1A-2	Long noncoding RNA MYOSLID promotes invasion and metastasis by modulating the partial epithelial-mesenchymal transition program in head and neck squamous cell carcinoma.We detected MYOSLID expression in 15 paired fresh OSCC cancer tissues and adjacent normal tissues by RT-qPCR. The results showed that MYOSLID expression in the cancer group (0.01127- -0.01655) was higher than that in the adjacent cancer normal tissues (0.00299- -0.00608) (p-=-0.037) (Fig. 3a). Meanwhile, we detected the MYOSLID expression levels in a normal oral epithelium cell line, HIOEC, and 4 OSCC cell lines, Cal27, Tca8113, SCC4, and SCC9. The results showed that the Cal27 cell line had a higher MYOSLID expression level (0.49254- -0.07004) compared with that in Tca8113 (0.20549- -0.01073), SCC4 (0.02700- -0.00008), and SCC9 (0.03700- -0.00009) (p-<-0.05). Unexpectedly, we found that the human normal oral epithelium cell line HIOEC had the highest MYOSLID expression levels of all of the cell lines that were examined (Fig.3c).Pearson correlation analysis revealed that the expression level of MYOSLID was correlated with Slug (r-=-0.2723, p-=-0.0094), PDPN (r-=-0.3455, p-=-0.0009) and LAMB3 (r-=-0.5644, p-=-0.0001) expression, as shown in Fig. -Fig.44c.The expression level of MYOSLID was the highest in Cal27 cell line, and Cal27 cell line had a co-expression of p-EMT makers (PDPN, LAMB3) and classical EMT markers (E-cadherin, Vimentin) (Fig. -(Fig.3c,3c, f, g). This indicates that the state of the Cal27 cell line is the closest to a p-EMT. The two siRNA sequences MYOSLID-homo-96 and MYOSLID-homo-232 were selected to knockdown MYOSLID in Cal27 cell lines, as they were validated to have a higher knockout efficiency compared with that of MYOSLID-homo-696 (Fig. -(Fig.3d).3d). Wound healing assays showed that the knockdown of MYOSLID expression significantly reduced the 48-h healing rate (p-<-0.05, Fig. -Fig.4a).4a). Moreover, the transwell assay showed that the number of cells passed through the filter that was coated with Matrigel of the siRNA groups was much lower than that of the negative control group (p-<-0.05, Fig. -Fig.44b).To further verify the molecular mechanicals of aberrant MYOSLID expression affects the ability of invasion and metastasis of OSCC cells was by regulating the p-EMT program. Expression levels of p-EMT markers Slug, PDPN, LAMB3 and EMT markers E-cadherin, Vimentin were detected after knockdown MYOSLID in OSCC cell line. The results showed that knockdown MYOSLID expression significantly inhibited Slug, PDPN and LAMB3 mRNA and protein expression levels compared to those in the controls (p-<-0.05, Fig. -Fig.3e,3e, Fig. 5c). Interestingly, the expression levels of the classical EMT biomarkers E-cadherin and Vimentin remained unchanged after silencing MYOSLID (Fig. -(Fig.55c).	31238980	RID07727	expression association	metastasis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Head and neck squamous cell carcinoma	MYOSLID	LAMB3	negatively-E	knockdown	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000229647	GRCh38_2:207166120-207248668	ENSG00000196878	NA	105373853	3914	NA	BM600-125kDa|kalinin-140kDa|LAMNB1|nicein-125kDa	Long noncoding RNA MYOSLID promotes invasion and metastasis by modulating the partial epithelial-mesenchymal transition program in head and neck squamous cell carcinoma.We detected MYOSLID expression in 15 paired fresh OSCC cancer tissues and adjacent normal tissues by RT-qPCR. The results showed that MYOSLID expression in the cancer group (0.01127- -0.01655) was higher than that in the adjacent cancer normal tissues (0.00299- -0.00608) (p-=-0.037) (Fig. 3a). Meanwhile, we detected the MYOSLID expression levels in a normal oral epithelium cell line, HIOEC, and 4 OSCC cell lines, Cal27, Tca8113, SCC4, and SCC9. The results showed that the Cal27 cell line had a higher MYOSLID expression level (0.49254- -0.07004) compared with that in Tca8113 (0.20549- -0.01073), SCC4 (0.02700- -0.00008), and SCC9 (0.03700- -0.00009) (p-<-0.05). Unexpectedly, we found that the human normal oral epithelium cell line HIOEC had the highest MYOSLID expression levels of all of the cell lines that were examined (Fig.3c).Pearson correlation analysis revealed that the expression level of MYOSLID was correlated with Slug (r-=-0.2723, p-=-0.0094), PDPN (r-=-0.3455, p-=-0.0009) and LAMB3 (r-=-0.5644, p-=-0.0001) expression, as shown in Fig. -Fig.44c.The expression level of MYOSLID was the highest in Cal27 cell line, and Cal27 cell line had a co-expression of p-EMT makers (PDPN, LAMB3) and classical EMT markers (E-cadherin, Vimentin) (Fig. -(Fig.3c,3c, f, g). This indicates that the state of the Cal27 cell line is the closest to a p-EMT. The two siRNA sequences MYOSLID-homo-96 and MYOSLID-homo-232 were selected to knockdown MYOSLID in Cal27 cell lines, as they were validated to have a higher knockout efficiency compared with that of MYOSLID-homo-696 (Fig. -(Fig.3d).3d). Wound healing assays showed that the knockdown of MYOSLID expression significantly reduced the 48-h healing rate (p-<-0.05, Fig. -Fig.4a).4a). Moreover, the transwell assay showed that the number of cells passed through the filter that was coated with Matrigel of the siRNA groups was much lower than that of the negative control group (p-<-0.05, Fig. -Fig.44b).To further verify the molecular mechanicals of aberrant MYOSLID expression affects the ability of invasion and metastasis of OSCC cells was by regulating the p-EMT program. Expression levels of p-EMT markers Slug, PDPN, LAMB3 and EMT markers E-cadherin, Vimentin were detected after knockdown MYOSLID in OSCC cell line. The results showed that knockdown MYOSLID expression significantly inhibited Slug, PDPN and LAMB3 mRNA and protein expression levels compared to those in the controls (p-<-0.05, Fig. -Fig.3e,3e, Fig. 5c). Interestingly, the expression levels of the classical EMT biomarkers E-cadherin and Vimentin remained unchanged after silencing MYOSLID (Fig. -(Fig.55c).	31238980	RID07728	expression association	metastasis		
Hepatocellular carcinoma	MCM3AP-AS1	MIR455	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000207726	NA	114044	619556	C21orf85|MCM3AP-AS|MCM3APAS|MCM3APASB|NCRNA00031	MIRN455|hsa-mir-455|mir-455	LncRNA MCM3AP-AS1 Regulates Epidermal Growth Factor Receptor and Autophagy to Promote Hepatocellular Carcinoma Metastasis by Interacting with miR-455.To determine the specific effects of MCM3AP-AS1 on HCC metastasis, we generated MCM3AP-AS1 knockdown HepG2 and Huh-7 cells by siRNA. Significantly reduced MCM3AP-AS1 expression levels were observed in the cells (Fig. 1A). Then, we examined whether MCM3AP-AS1 affected invasion and lymphangiogenesis of HepG2 and Huh7 cells. The transwell assay showed that MCM3AP-AS1 knockdown in HepG2 and Huh-7 cells reduced the number of invaded cells (Fig. 1B, C). Moreover, lymphatic vessel assay demonstrated that MCM3AP-AS1 depletion in HCC cells strikingly attenuated lymphatic vessel formation of HDLECs cultured with CM of HepG2 and Huh-7 cells (Fig. 1D). Taken together, MCM3AP-AS1 knockdown suppressed metastasis of HCC cells.To clarify how MCM3AP-AS1 played a role in metastasis of HCC cells, online bioinformatic tool was utilized to identify downstream targets. miR-455 was one of the putative targets and bound MCM3AP-AS1 by complementary sequences (Fig. 2A). To validate, luciferase reporter assay also indicated that miR-455 mimic or inhibitor reduced or elevated luciferase activity in 293T cells transfected with wild type MCM3AP-AS1 fused with luciferase gene, meanwhile, mutant MCM3AP-AS1 does not result in substantial changes in luciferase activity (Fig. 2B). In HepG2 cells, miR-455 mimic strikingly impaired (decreased by*70'-0%) MCM3AP-AS1 expression, whereas miR-455 inhibitor increased (*25'-0-folds) MCM3AP-AS1 level (Fig. 2C). Likewise, MCM3AP-AS1 knockdown caused elevation (*4'--folds) of miR-455, and MCM3AP-AS1 resulted in reduction (decreased by*65'-0%) of miR-455 (Fig. 2D). More importantly, Reverse Transcription-quantitative PCR showed decreased level of miR-455 in clinical HCCs compared with adjacent normal tissues (Fig. 2E). In summary, our result suggests that miR-455 can directly mutually target MCM3AP-AS1 and may play a suppressive role in HCC.It has been verified that autophagy is involved in cancer metastasis (Huanget al., 2018). Based on this information, we proposed that autophagy might be important for miR455-regulated metastasis. As shown in the western blot results, miR-455 mimic upregulated Beclin1 protein level and LC3 II/I ratio and dropped ATG7 level. In contrast, miR-455 inhibitor caused reduced Beclin1 level and LC3 II/I ratio and elevated ATG7 level (Fig. 5A). To test whether autophagy affects invasion and lymphangiogenesis of HCC cells, the number of invaded miR-455 mimic plus ATG7 HepG2 cells was increased compared with miR-455 mimic alone cells (Fig. 5B, C). Besides, ATG7 largely rescued lymphatic vessel formation of HDLECs incubated with CM of miR-455 mimic HepG2 cells (Fig. 5D). To sum up, our data suggest that autophagy is critical for reverting miR455-inhibited metastasis of HCC cells.To examine whether MCM3AP-AS1 and EGFR were dysregulated in human HCC tissues, we analyzed their expression levels in published The Cancer Genome Atlas data sets of human liverHCC. As shown in the results, MCM3APAS1 and EGFR were significantly upregulated in HCC tissues (n=306) compared with normal tissues (n=13) (Fig. 6A, B). MCM3AP-AS1 positively correlated with EGFR levels in HCCs (p=0.01095,R=0.39) (Fig. 6C). In addition, we found that low MCM3AP-AS1 and EGFR levels were associated with higher overall survival rate of HCC patients (Fig. 6D, E). Taken together, our results suggest that MCM3AP-AS1 and EGFR clinically play a critical role in HCCs.	31237446	RID07729	ceRNA or sponge	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	
Ovarian cancer	AGAP2-AS1	MEG3	negatively-E	overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	PCG	lncRNA	ENSG00000255737	NA	ENSG00000214548	GRCh38_14:100779410-100861031	100130776	55384	LOC100130776|PUNISHER	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	The Long Non-Coding RNA (lncRNA) AGAP2-AS1 is Upregulated in Ovarian Carcinoma and Negatively Regulates lncRNA MEG3.Expression of MEG3 was also detected by RT-qPCR. Compared with adjacent healthy tissues, expression levels of MEG3 were significantly decreased in tumor tissues (Figure 2A, p<0.05). Linear regression analysis showed that expression levels of AGAP2-AS1 and MEG3 were inversely and significantly correlated in tumor tissues (Figure 2B), but no significant correlation between expression levels of AGAP2-AS1 and MEG3 was observed in adjacent healthy tissues (Figure 2B).The inverse correlation between AGAP2-AS1 and MEG3 in tumor tissues of OC patients indicated the possible interaction between AGAP2-AS1 and MEG3 in OC. To further investigate the interaction between AGAP2-AS1 and MEG3 in OC, AGAP2-AS1 and MEG3 expression vectors were transfected into cells of OVCAR3 and A2780 cell lines. As shown in Figure 3A, overexpression of AGAP2-AS1 and MEG3 was reached at 36 h after transfection (p<0.05). Compared with the control (C) and negative control (NC) groups, AGAP2-AS1 overexpression led to downregulation of MEG3 in cells of OVCAR3 and A2780 cell lines (Figure 3B, p<0.05), while MEG3 overexpression failed to significantly affect AGAP2-AS1 expression (Figure 3C, p<0.05).Results of in vitro cell proliferation assay showed that, compared with control (C) and negative control (NC) groups, AGAP2-AS1 overexpression promoted, but MEG3 inhibited, proliferation of cells of OVCAR3 (Figure 4A) and A2780 (Figure 4B) cell lines (p<0.05). In addition, MEG3 overexpression reduced the effects of AGAP2-AS1 overexpression on proliferation of cancer cell (p<0.05).	31233485	RID07730	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Non-small cell lung cancer	TMPO-AS1	TMPO	positively-E	knockdown	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000257167	GRCh38_12:98512973-98516422	ENSG00000120802	NA	100128191	7112	NA	LAP2|LEMD4|TP	Long noncoding RNA TMPO-AS1 promotes progression of non-small cell lung cancer through regulating its natural antisense transcript TMPO.Firstly, we examined the expression of TMPO-AS1 and TMPO mRNA levels in NSCLC cells by qRT-PCRassay. As shown inFig. 1A and B, compared to normal control BEAS-2B cells, the expression of both TMPO-AS1 and TMPO mRNA were significantly upregulated in NSCLC cells (P<0.01). Thus, we intend to verify whether TMPO-AS1 regulates TMPO mRNA stability and expression in NSCLC cells. The results of RPA assay showed that overlapping region of TMPO mRNA was protected from RNase digestion, but non-overlapping region of TMPO mRNA was digested (Fig. 2B). Two specific shRNAs were used to knockdown of TMPO-AS1 in NSCLC cells (Fig. 2C). Cells were treated witha-amanitin to stop new transcripts produce and the degradation of TMPO mRNA was measured by qRT-PCR The results showed that knockdown of TMPO-AS1 shortened the half-life of TMPO mRNA (Fig. 2D). These data suggested that TMPO-AS1 associated with TMPO mRNA and increased TMPO mRNA stability.The function of TMPO-AS1 on tumor biological processes was determined after knockdown of TMPO-AS1 in NSCLC cells by shRNA transfection. The growth curves determined by CCK-8 assays showed that cell growth was dramatically inhibited by knockdown of endogenous TMPO-AS1 expression in H460 and H1299 cells (Fig. 3A). Colony formation assay indicated that down-regulation of TMPO-AS1 could significantly repress the colony formation ability of NSCLC cells (Fig. 3B). We also examined the effect of TMPO-AS1 knockdown on cell migration and invasion. Our results showed that a significant increase of wound width was observed in TMPO-AS1 silencing cells compared to negative control cells (Fig. 3C). Likewise, invasion of NSCLC cells was decreased by TMPO-AS1 silencing (Fig. 3D). These data revealed that TMPO-AS1 played oncogenic role on cell growth and invasion.To examine the effect of TMPO-AS1 on tumorigenesis in vivo, H460 depleted TMPO-AS1 cells were subcutaneously injected into nude mice. The results showed that tumor volumes and weights were markedly lower in sh-TMPO-AS1 treated group than that in control group (Fig. 4F and G). Moreover, the qRT-PCRanalysis validated that TMPO-AS1 expression levels remained significantly decreased (Fig. 4H), and the mRNA and protein levels of TMPO simultaneously reduced in the sh-TMPO-AS1 transfected group (Fig. 4I and J).	31230752	RID07731	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Osteosarcoma	FOXD2-AS1	CDKN1A	negatively-E	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000124762	NA	84793	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HIF-1alpha induced long noncoding RNA FOXD2-AS1 promotes the osteosarcoma through repressing p21.The expression and abundance of lncRNA FOXD2-AS1 in the clinical individuals were tested using the RT-PCR showing the remarked up-regulation of LncRNA FOXD2-AS1 in OS specimens compared to the normal controls (Fig. 1A, Table 1).The significant high-expression of FOXD2-AS1 was inspected from the point of upstream transcriptional level. There were two potential binding sites for the transcription factor HIF-1alpha at the promoter region of FOXD2-AS1 (Fig. 2A). The luciferase reporter vectors for the potential binding sites were respectively constructed (Fig. 2B). Luciferase gene reporter assay was performed using these vectors, suggesting that there was significant binding within HIF-1alpha and E2 region (-252--241, cctacgtgtccg) (Fig. 2C). Chromatin immunoprecipitation (ChIP) revealed that HIF-1alpha antibody could precipitate the DNA fragments at the E2 region (Fig. 2D). The overexpression plasmid of HIF-1alpha was transfected into the MG63 cells and then the FOXD2-AS1 level was up-regulated (Fig. 2E). The data from the TCGA indicated that HIF-1alpha expression was increased in the OS patients compared to the controls (Fig. 2F). The correlation analysis of FOXD2-AS1 and HIF-1alpha was analyzed using the GEPIA database (http://gepia.cancer-pku.cn/index.html) (Fig. 2G). Therefore, we confirmed that HIF-1alpha could mediate the over-expression of lncRNA FOXD2-AS1 in OS cells.To determine the biological roles of FOXD2-AS1 for the OS cells, the oligonucleotides targeting the FOXD2-AS1 was analyzed to silence the FOXD2-AS1 (Fig. 3A). CCK-8 assay indicated that FOXD2-AS1 knockdown remarkedly repressed the proliferative activity of OS (MG63, Saos-2) cells (Fig. 3B and C). The invasive ability for the OS (MG63, Saos-2) cells was inspected using the transwell assay, indicating the repressed invasion induced by the FOXD2-AS1 knockdown (Fig. 3D and E). Apoptosis of the OS (MG63, Saos-2) cells was inspected using flow cytometry showed that FOXD2-AS1 knockdown increased the apoptotic rate of OS cells (Fig. 3F and G). In vivo mice assay, we also found that stable FOXD2-AS1 knockdown could inhibit the tumor growth of MG63 cells compared to the control transfection (Fig. 3H and I). Overall, these data suggests that FOXD2-AS1 knockdown inhibits the malignant biological properties of OS cells.The mechanism mediated by the FOXD2-AS1 for the OS was investigated. We found that FOXD2-AS1 was located in the nucleus more than cytoplasm (Fig. 4A). RNA immunoprecipitation (RIP) suggested that FOXD2-AS1 could interact with EZH2 at the molecular level (Fig. 4B). After FOXD2-AS1 was repressed, RT-PCRindicated that p21 expression was increased compared with the controls (Fig. 4C). What  more, the knockdown of EZH2 was constructed using the shRNA transfection (Fig. 4D), which in return up-regulate the p21 mRNA (Fig. 4E). western blotillustrated that the knockdown of EZH2 and FOXD2-AS1 could both up-regulate the p21 protein level (Fig. 4F). Chromatin immunoprecipitation (ChIP) showed that the knockdown of FOXD2-AS1 reduce the molecular binding within the EZH2 and H3K27me3 with p21 promoter region (Fig. 4G). The public database of TCGA indicated that the lower expression of p21 protein predicted the poor prognosis of OS patients (Fig. 4H). Therefore, FOXD2-AS1 epigenetically represses the p21 via recruiting EZH2.	31228799	RID07732	expression association	prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	FOXD2-AS1	EZH2	interact	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000106462	NA	84793	2146	MGC12982	ENX-1|EZH1|KMT6|KMT6A	HIF-1alpha induced long noncoding RNA FOXD2-AS1 promotes the osteosarcoma through repressing p21.The expression and abundance of lncRNA FOXD2-AS1 in the clinical individuals were tested using the RT-PCR showing the remarked up-regulation of LncRNA FOXD2-AS1 in OS specimens compared to the normal controls (Fig. 1A, Table 1).The significant high-expression of FOXD2-AS1 was inspected from the point of upstream transcriptional level. There were two potential binding sites for the transcription factor HIF-1alpha at the promoter region of FOXD2-AS1 (Fig. 2A). The luciferase reporter vectors for the potential binding sites were respectively constructed (Fig. 2B). Luciferase gene reporter assay was performed using these vectors, suggesting that there was significant binding within HIF-1alpha and E2 region (-252--241, cctacgtgtccg) (Fig. 2C). Chromatin immunoprecipitation (ChIP) revealed that HIF-1alpha antibody could precipitate the DNA fragments at the E2 region (Fig. 2D). The overexpression plasmid of HIF-1alpha was transfected into the MG63 cells and then the FOXD2-AS1 level was up-regulated (Fig. 2E). The data from the TCGA indicated that HIF-1alpha expression was increased in the OS patients compared to the controls (Fig. 2F). The correlation analysis of FOXD2-AS1 and HIF-1alpha was analyzed using the GEPIA database (http://gepia.cancer-pku.cn/index.html) (Fig. 2G). Therefore, we confirmed that HIF-1alpha could mediate the over-expression of lncRNA FOXD2-AS1 in OS cells.To determine the biological roles of FOXD2-AS1 for the OS cells, the oligonucleotides targeting the FOXD2-AS1 was analyzed to silence the FOXD2-AS1 (Fig. 3A). CCK-8 assay indicated that FOXD2-AS1 knockdown remarkedly repressed the proliferative activity of OS (MG63, Saos-2) cells (Fig. 3B and C). The invasive ability for the OS (MG63, Saos-2) cells was inspected using the transwell assay, indicating the repressed invasion induced by the FOXD2-AS1 knockdown (Fig. 3D and E). Apoptosis of the OS (MG63, Saos-2) cells was inspected using flow cytometry showed that FOXD2-AS1 knockdown increased the apoptotic rate of OS cells (Fig. 3F and G). In vivo mice assay, we also found that stable FOXD2-AS1 knockdown could inhibit the tumor growth of MG63 cells compared to the control transfection (Fig. 3H and I). Overall, these data suggests that FOXD2-AS1 knockdown inhibits the malignant biological properties of OS cells.The mechanism mediated by the FOXD2-AS1 for the OS was investigated. We found that FOXD2-AS1 was located in the nucleus more than cytoplasm (Fig. 4A). RNA immunoprecipitation (RIP) suggested that FOXD2-AS1 could interact with EZH2 at the molecular level (Fig. 4B). After FOXD2-AS1 was repressed, RT-PCRindicated that p21 expression was increased compared with the controls (Fig. 4C). What  more, the knockdown of EZH2 was constructed using the shRNA transfection (Fig. 4D), which in return up-regulate the p21 mRNA (Fig. 4E). western blotillustrated that the knockdown of EZH2 and FOXD2-AS1 could both up-regulate the p21 protein level (Fig. 4F). Chromatin immunoprecipitation (ChIP) showed that the knockdown of FOXD2-AS1 reduce the molecular binding within the EZH2 and H3K27me3 with p21 promoter region (Fig. 4G). The public database of TCGA indicated that the lower expression of p21 protein predicted the poor prognosis of OS patients (Fig. 4H). Therefore, FOXD2-AS1 epigenetically represses the p21 via recruiting EZH2.	31228799	RID07733	interact with protein	prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Gastric cancer	ICMT-DT	CDKN1A	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225077	GRCh38_1:6234692-6239444	ENSG00000124762	NA	148645	1026	C1orf211|LINC00337|NCRNA00337	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA LINC00337 promote gastric cancer proliferation through repressing p21 mediated by EZH2.In the gastric cancer tissue samples, LINC00337 expression was found to be highly increased (Figure 1A). Moreover, the LINC00337 level was higher than the adjacent normal tissue (Figure 1B). In the GEPIA database (http://gepia.cancer-pku.cn/) based on the TCGA, LINC00337 level was markedly higher in the gastric cancer tissue compared with the normal controls (Figure 1C). Then, the Kaplan-Meier plotter analysis (http://kmplot.com/analysis/) revealed that the higher LINC00337 expression indicates the poor clinical outcome for gastric cancer patients (Figure 1D). Overall, this data concludes that ectopic LINC00337 overexpression indicates the poor clinical outcome.In the gastric cancer cells, LINC00337 levels were proudly up-regulated (Figure 2A). In order to investigate the role of LINC00337 in the gastric cancer cells'-tumor phenotype, silencing expression oligonucleotides were synthesized in SGC-7901 and BGC-823 cells (Figure 2B). The proliferative ability of gastric cancer cells measured by CCK-8 showed that LINC00337 silencing impaired the proliferation (Figure 2C, -,2D).2D). Transwell invasion assay indicated that LINC00337 silencing impaired the invasive ability of SGC-7901 and BGC-823 cells (Figure 2E). In vivo xenograft mice assay showed that LINC00337 silencing reduced the tumor growth, volume and weight, comparing the controls (Figure 2F, -,2G).2G). Overall, this data suggests that LINC00337 silencing represses the proliferation, invasion and tumor growth of gastric cancer cells in vitro and in vivo.The subcellular location analysis showed that LINC00337 was mainly located in the nuclear, instead of the cytoplasm (Figure 3A). In the screening of cycle-related proteins, we found that p21 was increased when the LINC00337 silenced in the SGC-7901 cells (Figure 3B). In the SGC-7901 cells, the LINC00337 silencing transfection and EZH2 silencing transfection both up-regulated the p21 protein levels (Figure 3C, -,3D).3D). RNA binding protein immunoprecipitation (RIP) assay showed that LINC00337 could closely bind with the EZH2 (Figure 3E). EZH2 acts as the core of subunit of PRC2. It was assumed that LINC00337 could recruit EZH2 to p521 promoter region to silence p21 protein levels. Then, the chromatin immunoprecipitation (ChIP) was performed and showed that EZH2 directly targeted p21 promoter region (Figure 3F). Overall, results show that LINC00337 directly bind with EZH2 to represses the p21 via EZH2-mediated inhibition.In the above findings, we recognized that LINC00337 epigenetically represses the p21 via EZH2-mediated inhibition. However, whether p21 could recover the oncogenic role of LINC00337 on gastric cancer tumorigenesis is still indeterminate (Figure 4A). CCK-8 assay showed that co-transfection of LINC00337 and p21 siRNAs recovered the inhibition of gastric cancer cells induced by LINC00337 knockdown (Figure 4B). Transwell invasion assay indicated that co-transfection of LINC00337 and p21 siRNAs recovered invasive ability of gastric cancer cells (Figure 4C). The Kaplan-Meier analysis from the TCGA database showed that the lower p21 expression and higher EZH2 expression was closely correlated with the poor prognosis of gastric cancer patients (Figure 4D, -,4E).4E). Therefore, data suggests that p21 could recover the oncogenic role of LINC00337 on gastric cancer tumorigenesis.	31217892	RID07734	expression association	prognosis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Gastric cancer	ICMT-DT	EZH2	interact	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225077	GRCh38_1:6234692-6239444	ENSG00000106462	NA	148645	2146	C1orf211|LINC00337|MGC40168|NCRNA00337	ENX-1|EZH1|KMT6|KMT6A	Long noncoding RNA LINC00337 promote gastric cancer proliferation through repressing p21 mediated by EZH2.In the gastric cancer tissue samples, LINC00337 expression was found to be highly increased (Figure 1A). Moreover, the LINC00337 level was higher than the adjacent normal tissue (Figure 1B). In the GEPIA database (http://gepia.cancer-pku.cn/) based on the TCGA, LINC00337 level was markedly higher in the gastric cancer tissue compared with the normal controls (Figure 1C). Then, the Kaplan-Meier plotter analysis (http://kmplot.com/analysis/) revealed that the higher LINC00337 expression indicates the poor clinical outcome for gastric cancer patients (Figure 1D). Overall, this data concludes that ectopic LINC00337 overexpression indicates the poor clinical outcome.In the gastric cancer cells, LINC00337 levels were proudly up-regulated (Figure 2A). In order to investigate the role of LINC00337 in the gastric cancer cells'-tumor phenotype, silencing expression oligonucleotides were synthesized in SGC-7901 and BGC-823 cells (Figure 2B). The proliferative ability of gastric cancer cells measured by CCK-8 showed that LINC00337 silencing impaired the proliferation (Figure 2C, -,2D).2D). Transwell invasion assay indicated that LINC00337 silencing impaired the invasive ability of SGC-7901 and BGC-823 cells (Figure 2E). In vivo xenograft mice assay showed that LINC00337 silencing reduced the tumor growth, volume and weight, comparing the controls (Figure 2F, -,2G).2G). Overall, this data suggests that LINC00337 silencing represses the proliferation, invasion and tumor growth of gastric cancer cells in vitro and in vivo.The subcellular location analysis showed that LINC00337 was mainly located in the nuclear, instead of the cytoplasm (Figure 3A). In the screening of cycle-related proteins, we found that p21 was increased when the LINC00337 silenced in the SGC-7901 cells (Figure 3B). In the SGC-7901 cells, the LINC00337 silencing transfection and EZH2 silencing transfection both up-regulated the p21 protein levels (Figure 3C, -,3D).3D). RNA binding protein immunoprecipitation (RIP) assay showed that LINC00337 could closely bind with the EZH2 (Figure 3E). EZH2 acts as the core of subunit of PRC2. It was assumed that LINC00337 could recruit EZH2 to p521 promoter region to silence p21 protein levels. Then, the chromatin immunoprecipitation (ChIP) was performed and showed that EZH2 directly targeted p21 promoter region (Figure 3F). Overall, results show that LINC00337 directly bind with EZH2 to represses the p21 via EZH2-mediated inhibition.In the above findings, we recognized that LINC00337 epigenetically represses the p21 via EZH2-mediated inhibition. However, whether p21 could recover the oncogenic role of LINC00337 on gastric cancer tumorigenesis is still indeterminate (Figure 4A). CCK-8 assay showed that co-transfection of LINC00337 and p21 siRNAs recovered the inhibition of gastric cancer cells induced by LINC00337 knockdown (Figure 4B). Transwell invasion assay indicated that co-transfection of LINC00337 and p21 siRNAs recovered invasive ability of gastric cancer cells (Figure 4C). The Kaplan-Meier analysis from the TCGA database showed that the lower p21 expression and higher EZH2 expression was closely correlated with the poor prognosis of gastric cancer patients (Figure 4D, -,4E).4E). Therefore, data suggests that p21 could recover the oncogenic role of LINC00337 on gastric cancer tumorigenesis.	31217892	RID07735	interact with protein	prognosis		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Breast cancer	HCP5	BIRC3	positively-E	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell growth(+)	ceRNA(miR-219a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000206337	GRCh38_6:31463170-31478936	ENSG00000023445	NA	10866	330	D6S2650E|P5-1	API2|c-IAP2|cIAP2|hiap-1|MALT2|MIHC|RNF49	LncRNA HCP5 promotes triple negative breast cancer progression as a ceRNA to regulate BIRC3 by sponging miR-219a-5p.To assess the expression of HCP5 in TNBC, we first detected the mRNA level in the human normal breast epithelial cell line MCF-10A and breast cancer cell lines by qPCR. We found that HCP5 expression was higher in TNBC cell lines MDA-MB-231 and MDA-MB-468 than in MCF-10A and other cell lines (Figure -(Figure1A).1A). Then we assessed the expression of HCP5 in human breast cancer tissues, we detected HCP5 mRNA by RNA Scope- 2.0 technology in 30 paired case-control TMA. We found that HCP5 was higher in TNBC tissues than in normal breast tissues and other molecular subtypes (Figure -(Figure1B1B and Table S1, P = 0.007). The association between HCP5 expression and clinicopathologic parameters was also tested by the chi-squared tests. The results suggested that HCP5 expression was higher in breast cancer patients with TNM III stage (Table S2, P < 0.001). Furthermore, we found that there were more HCP5-positive specimens in TNBC than in other subtypes (Table S3, P = 0.006), which indicated that HCP5 expression was positively associated with TNBC. Our above results suggested that HCP5 upregulation may be associated with the occurrence and progression of TNBC.In order to test the biological functions of HCP5, we knocked down HCP5 by siRNA in MDA-MB-231 and MDA-MB-468 cells. By performing CCK-8 assays, we found that endogenous HCP5 knockdown could significantly slower the proliferative capacity of MDA-MB-231 and MDA-MB-468 cells compared with NC cells (Figure -(Figure2A).2A). The LIVE/DEAD- assay results indicated that compared with NC group, the MDA-MB-231 and MDA-MB-468 cells transfected with HCP5 siRNA showed an apoptosis enhancement (Figure -(Figure22B).Then, we investigated the in vivo activity of HCP5 in nude mice. To confirm whether HCP5 affects tumorigenesis, we examined TNBC cell lines MDA-MB-231 and MDA-MB-468 transfected with lentiviral LV10-sh-HCP5 sense sequence or control scramble sequence LV10-sh-NC. Tumors were grown for 30 days and the mice were sacrificed and tumors excised (n = 6 for each group). We found that HCP5 knockdown significantly reduced the tumor volume and weight of TNBC cell lines compared with control groups (Figure -(Figure3A,B).3A,B). These data revealed that HCP5 was involved in tumorigenesis and downregulation of HCP5 inhibited TNBC cell growth both in vitro and in vivo.To further study the ceRNA mechanism of HCP5, a dual-luciferase reporter assay was used to test whether HCP5 and BIRC3 are targets of miR-219a-5p. The luciferase assay showed that the luciferase activity was reduced in HEK293T cells that were cotransfected with miR-219a-5p and BIRC3-wt or HCP5-wt but was no change in HEK293T cells containing HCP5-mut or BIRC3-mut (Figure -(Figure5D).5D). The results confirmed that miR-219a-5p targeting both BIRC3 and HCP5.Then, we performed RNA immunoprecipitation (RIP) experiments to further investigate the potential direct binding between lncRNA HCP5 and the miRNAs. As shown in Figure -Figure5E,5E, HCP5 was pulled down by miR-219a-5p, but the miR-219a-5p mutation group was unable to pull down HCP5, meaning that recognition between HCP5 and miR-219a-5p was specific both in MDA-MB-231 and in MDA-MB-468 cells. We also used an inverse pull-down assay to investigate whether HCP5 could pull down miR-219a-5p using a biotin-labeled specific HCP5 probe. The qPCR results suggested that miR-219a-5p could recognize the HCP5 probe not the NC probe.We detected BIRC3 mRNA and protein level in breast cancer cell lines by qPCR and western blot. The results suggested that BIRC3 expression was upregulated in MDA-MB-231 and MDA-MB-468 than in MCF-10A and other breast cancer cell lines (Figure -(Figure6A).6A). Then we assessed the expression of BIRC3 in human breast cancer tissues by immunohistochemical staining (IHC) in TMA. We found that BIRC3 was higher in TNBC tissues than in normal breast tissues and other molecular subtypes (Figure -(Figure6B6B and Table S4). The association between BIRC3 expression and clinicopathologic parameters was also tested by the chi-squared tests. We found there were more BIRC3-positive specimens in TNBC than in other subtypes (Table S5). And further we found that there were 10 samples with BIRC3 high expression in 12 HCP5-positive samples and seven samples with BIRC3 high expression in 18 HCP5 negative samples (Table S6), which suggested the expression of HCP5 and BIRC3 was positive association. Correspondingly, an immunostaining analysis of xenografted tumor tissues revealed that BIRC3 expression was also decreased in the HCP5 knockdown group (Figure -(Figure66C).	31215169	RID07736	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Pancreatic cancer	DANCR	E2F2	positively-E	luciferase reporter assay;knockdown;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);prognosis	ceRNA(miR-214-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000007968	NA	57291	1870	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	E2F-2	Long Non-Coding RNA Differentiation Antagonizing Nonprotein Coding RNA (DANCR) Promotes Proliferation and Invasion of Pancreatic Cancer by Sponging miR-214-5p to Regulate E2F2 Expression.DANCR expression in 50 paired PC and adjacent normal tissues were measured by qRT-PCRassay. Significant upregulation of DANCR was observed in PC tissues in comparison to normal tissues (Figure 1A). We also examined DANCR expression in different PC cell lines. DANCR expression in PC cells (PANC-1, SW1990, CAPAN-1, BxPC-3, and AsPC-1) appeared to be higher than that in HPDE6-C7 cells (Figure 1B).To explore effects of lncRNA DANCR on cell proliferation, migration, and invasion of PC, we silenced DANCR expression in PANC-1 and SW1990 cells through si-DANCR (Figure 2A). CCK-8 assay demonstrated that cell viability of PC was obviously inhibited in the si-DANCR group in comparison to the si-NC group (Figure 2B). Next, flow cytometry was performed to detect the cell cycle distribution and cell apoptosis. We found that DANCR knockdown led to cell cycle arrest at G0/G1 phase (Figure 2C) and promoted cell apoptosis (Figure 2D) in PANC-1 and SW1990 cells. In addition, DANCR knockdown markedly decreased the number of PC cell colonies using colony formation assay (Figure 2E). Furthermore, si-DANCR suppressed cell migration and invasion of PC, as shown by the results from Transwell assays (Figure 2F, 2G).By using bioinformatics software (Starbase v3.0), miR-214-5p was found to be a potential target of DANCR (Figure 3A). miR-214-5p mimics dramatically reduced the relative luciferase activity of DANCR-wt by luciferase reporter assay, but did not affect the DANCR-mut reporter (Figure 3B). Moreover, miR-214-5p expression was markedly upregulated in PANC-1 and SW1990 cells transfected with si-DANCR compared with si-NC (Figure 3C).To further study whether DANCR exerts biological effects in PC by targeting miR-214-5p, we reduced miR-214-5p expression with miRNA inhibitor in PANC-1 and SW1990 cells (Figure 4A). CCK-8 and colony formation assay revealed DANCR inhibition dramatically suppressed cell growth of PC, and miR-214-5p inhibitor greatly restored the effects (Figure 4B, 4C). In addition, the repression of cell migration and invasion induced by DANCR knockdown was reversed by miR-214-5p inhibitor, as determined using Transwell assays (Figure 4D, 4E). In brief, knockdown of DANCR suppressed PC cell proliferation, migration, and invasion by miR-214-5p.miRNAs can function as negative regulators of target genes at the post-transcriptional level. E2F2, an important regulator of cell proliferation and invasion in tumor progression, was identified as a potential target of miR-214-5p using bioinformatics software (TargetScan, Figure 5A). Luciferase reporter assay showed that miR-214-5p overexpression caused a remarkable decline in luciferase activity of E2F2-wt (Figure 5B). Expression of E2F2 mRNA in clinical tissues was measured with qRT-PCRassay. As shown in Figure 5C, E2F2 was obviously overexpressed in tumor tissues of PC patients in comparison to normal tissues. In addition, miR-214-5p expression exhibited a negative correlation with E2F2 expression (Figure 5D).Next, we investigated whether E2F2 expression was regulated by lncRNA DANCR in PC cells. We found that DANCR knockdown significantly inhibited E2F2 expression in PANC-1 and SW1990 cells, while this repression was restored by treatment with miR-214-5p inhibitor (Figure 5E, 5F). Furthermore, DANCR expression had a positive correlation with E2F2 expression in PC tissues (Figure 5G). These results show that DANCR upregulates E2F2 expression via sponging miR-214-5p in PC.	31213582	RID07737	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PAAD,PRAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842,GSE55807,GSE41245)
Pancreatic cancer	XIC	TGFB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-141-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	NA	NA	ENSG00000092969	NA	7502	7042	SXI1|XCE|XIST	G-TSF|LDS4|TGF-beta2	LncRNA XIST enhanced TGF-beta2 expression by targeting miR-141-3p to promote pancreatic cancer cells invasion.The expression of miR-141-3p and lncRNA XIST in PC and the adjacent normal tissues was detected by qRT-PCR As shown in Figure 1A,B, it indicated that miR-141-3p is down-regulated in tumor tissues, while XIST is highly expressed in PC. The correlation analysis of miR-141-3p and lncRNA XIST showed they were negatively correlated (Figure 1C, r2 = 0.645, P<0.01). Therefore, the level expression of LncRNA XIST is up-regulated in PC and negatively correlated with miR-141-5p.To excavate the function of XIST in PC cell lines, we transfected cells with siXIST, siControl or Mock. We found siXIST could significantly decrease the expression of XIST (Figure 2A), and siXIST inhibited cell proliferation (Figure 2B). The migration and invasion was significantly inhibited after siXIST transfection (Figure 2C,D). Therefore, XIST is also a pro-cancerous factor in PC cells, and silencing its expression can inhibit tumor cellular processes, such as the activities of proliferation and invasion.The aforementioned studies suggested that there might be interactions between miR-141-3p and XIST. Therefore, we further excavate the influence of up-regulated miR-141-3p expression on high-level expression of XIST. The intracellular miR-141-3p levels were increased when cells transfected with miR-141-3p mimics (Figure 4A) while XIST expression was down-regulated (Figure 4B). Meanwhile, when cells transfected with miR-141-3p inhibitor, intracellular miR-141-3p levels were reduced (Figure 4C) and XIST expression was up-regulated (Figure 4D), these data further validated the negative interaction of miR-141-3p and XIST.The previous studies have shown that XIST might accelerate the process of TGF-beta-induced EMT by regulating the miR-367/141-ZEB2 axis in NSCLC. However, whether XIST has a regulatory effect on the function of TGF-beta in PC remains unknown. To address this issue, we used software to predict that miR-141-3p and TGF-beta2 might interact (Figure 5A). The dual fluorescence reporter system was used to validate the interaction between miR-141-3p and TGF-beta2. The results indicate miR-141-3p mimic could cause the fluorescence decrease by matching directly with sequence of wild-type TGF-beta2 (Figure 5B), but not affect the mutant one (Figure 5B). Similarly, the miR-141-3p inhibitor enhanced the fluorescence of the wild-type TGF-beta2 (Figure 5C) whereas it did not exert an influence on the mutant one (Figure 5C).After co-transfection of cells with miR-141-3p mimic and pcDNA3.1-XIST, we found that the TGF-beta2 protein expression was inhibited by miR-141-3p, while overexpression of XIST reversed down-regulation on TGF- beta2 by miR-141-3p (Figure 6). These results indicate XIST and miR-141-3p interactions affect the TGF-beta2 expression in PC cell lines.	31213574	RID07738	ceRNA or sponge	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	LINC00968	PROX1	positively-E	dual-luciferase reporter assay;RNA pull-down assays;RIP	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);angiogenesis(+)	ceRNA(miR-423-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000246430	GRCh38_8:56494923-56559823	ENSG00000117707	NA	100507632	5629	NA	NA	Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p.Data analysis of the microarray GSE26910 and GEPIA database revealed that the LINC00968 was significantly lower in BC samples compared to that of the normal samples (Figure 1(a,b)). Next, RT-qPCR was conducted to determine the transcription level of LINC00968 in BC tissues and cell lines. It was found that the expression of LINC00968 in BC tissues was about threefold lower than that in matched adjacent normal tissues (p < 0.05; Figure 1(c)). The potential effects of LINC00968 on the proliferation, migration and tube formation of MDA-MB-231 and MCF-7 cells transduced with lentivirus vector expressing LINC00968 (Lenti-LINC00968) or Lenti-NC were examined. Initially, CCK-8 results suggested that the viability of MDA-MB-231 cells was reduced by transduction of Lenti-LINC00968, and gradually reduced with the prolongation of culture time (p < 0.05) (Figure 2(a)). As shown by Transwell and angiogenesis assays, migration ability of MDA-MB-231 cells and angiogenesis of HUVECs was further inhibited following the transduction of Lenti-LINC00968 (p < 0.05) (Figure 2(b,c)). Consistent reductions were observed in viability, migration ability and angiogenesis when MCF-7 cells transduced with Lenti-LINC00968 (Figure 2(d,f)). Those data suggested that overexpression of LINC00968 inhibited viability, migration, and angiogenesis of BC cells.LncRNA subcellular localization website revealed that LINC00968 was localized in the cytoplasm, which was also shown by FISH (Figure 4(a)). In addition, complementary sequence of LINC00968 that bound to hsa-miR-423-5p was found by RNA22 website (Figure 4(b)). dual-luciferase reporter assay was carried out for the verification of this result. It was found that the co-transfection of LINC00968-wt and hsa-miR-423-5p mimic in MDA-MB-231 cells resulted in a significant decrease in luciferase activity as compared to co-transfection of LINC00968-wt and NC mimic (Figure 4(c)). RT-qPCR assay revealed that inhibition of hsa-miR-423-5p led to an increase in LINC00968 expression (Figure 4(d)). These results indicated that LINC00968 could bind to hsa-miR-423-5p.The bioinformatics prediction on RNA22 website (https://cm.jefferson.edu/rna22/) was used to determine the binding site of hsa-miR-423-5p to PROX1 3-UTR (Figure 6(a)). The lower expression of PROX1 was shown in BC cells than that in normal cells in TCGA obtained from GEPIA database (Figure 6(b)). The relationship between hsa-miR-423-5p and PROX1 was determined with the application of the dual luciferase reporter gene assay and the findings showed that the luciferase activity of the PROX1-wt containing putative binding site was remarkably reduced following the transfection of the cells with hsa-miR-423-5p mimic (p < 0.05) (Figure 6(c)). These results indicated that PROX1 is a target gene of hsa-miR-423-5p. Subsequently, hsa-miR-423-5p was found to be overexpressed in MDA-MB-231 and MCF-7 cells by transfection with hsa-miR-423-5p mimic, and mRNA expression of PROX1 in the MDA-MB-231 and MCF-7 cells was not affected by transfection with hsa-miR-423-5p mimic (Figure 6(d)). The PROX1 protein expression was down-regulated by transfection with hsa-miR-423-5p mimic (Figure 6(e)). Next, MDA-MB-231 and MCF-7 cells that stably expressed hsa-miR-423-5p and PROX1 were established using hsa-miR-423-5p mimic and pcDNA-PROX1. The proliferation (Figure 6(f,i)) and migration (Figure 6(g,j)) of MDA-MB-231 and MCF-7 cells and angiogenesis (Figure 6(h,k)) that were inhibited by hsa-miR-423-5p mimic transfection were restored by transfection with both hsa-miR-423-5p mimic and pcDNA-PROX1. Therefore, these results provided evidence that hsa-miR-423-5p might be involved in the progression of BC through post-transcriptional regulation of PROX1.	31213129	RID07739	ceRNA or sponge	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC);DOWN(PAAD);DATA(GSE117623,GSE40174)
Thyroid cancer	SNHG7	BDNF	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000176697	NA	84973	627	MGC16037|NCRNA00061	NA	Knockdown of long noncoding RNA SNHG7 inhibits the proliferation and promotes apoptosis of thyroid cancer cells by downregulating BDNF.First, qRT-PCRwas conducted for detecting SNHG7 expression in 64 patients'-tissues and 3 TC cell lines. As a result, SNHG7 was significantly upregulated in tumor tissue samples (Figure 1).The outcome of cell apoptosis assay revealed that after SNHG7 was knocked down in TC cells, cell apoptosis rate of SW579 TC cell was remarkably increased (Figure 3).qRT-PCRresults showed that compared with the BDNF level in empty vector (control) group, expression level of BDNF in TC cells was lower in SNHG7 lentiviruses (sh-SNHG7) group (Figure 4A). western blot assay found out that after SNHG7 was knocked down, BDNF could be downregulated at protein level (Figure 4B). We further found that BDNF expression of TC tissues was significantly higher compared with that of corresponding tissues (Figure 4C). Correlation analysis demonstrated that BDNF expression level positively correlated to SNHG7 expression in cancer tissues (Figure 4D).	31210313	RID07740	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	HOXA-AS2	IGF2	negatively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000167244	NA	285943	3481	HOXA3as	C11orf43|GRDF|IGF-II|PP9974|SRS3	Long noncoding RNA HOXA-AS2 promotes cell migration and invasion via upregulating IGF-2 in non-small cell lung cancer as an oncogene.First, the expression level of HOXA-AS2 was detected by performing qRT-PCRin NSCLC samples and cell lines. The result revealed that HOXA-AS2 was significantly upregulated in tumor tissue samples (Figure 1A). HOXA-AS2 expression in NSCLC cells was remarkably higher when compared with that in normal human bronchial epithelial cells (16HBE; Figure 1B).SPCA1 and A549 cell lines were used for the overexpression and knockdown of HOXA-AS2 in this study. HOXA-AS2 expression was detected by qRT-PCRfor verifying the transfection efficacy (Figure 2A and 2B). Wound healing assay revealed that the knockdown of HOXA-AS2 inhibited migration of SPCA1 cells (Figure 2C). Conversely, the overexpression of HOXA-AS2 promoted the migratory ability of A549 cells (Figure 2D).Transwell assay revealed that knockdown of HOXA-AS2 suppressed the invasive ability of SPCA1 cells (Figure 3A). Furthermore, transwell assay revealed that after HOXA-AS2 was overexpressed, the invasive ability of A549 cells was promoted (Figure 3B and 3C).IGF2 expression was significantly lower in HOXA-AS2 shRNA (sh-HOXA-AS2) group when compared with that in empty vector (control) group as qRT-PCRdata revealed (Figure 4A). Besides, the expression level of IGF2 was markedly higher in HOXA-AS2 lentiviruses (HOXAAS2) group compared with that in empty vector (control) group (Figure 4B). western blot identically revealed that knockdown of HOXA-AS2 inhibited the protein level of IGF2 in NSCLC cells (Figure 4C). Moreover, after HOXA-AS2 was overexpressed, IGF2 was upregulated at the protein level (Figure 4D).Furthermore, we found out that the expression of IGF2 in NSCLC tissues was remarkably higher when compared with that of adjacent tissues (Figure 5A). Correlation analysis demonstrated that the IGF2 expression level was positively correlated to HOXA-AS2 expression in NSCLC tissues (Figure 5B).	31210310	RID07741	expression association	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Epithelial ovarian cancer	KCNMA1-AS1	Caspase3	positively-E	knockdown	upregulation	qRT-PCR	GEO	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000236467	GRCh38_10:76888044-76980624	NA	NA	101929328	NA	NA	NA	KCNMA1-AS1 attenuates apoptosis of epithelial ovarian cancer cells and serves as a risk factor for poor prognosis of epithelial ovarian cancer.KCNMA1-AS1 expression in 60 ovarian cancer tissues and 30 normal ovarian tissues was detected by qRT-PCR The results indicated a higher expression of KCNMA1-AS1 in ovarian cancer than that of normal ovarian tissues (p<0.001, Figure 7A).Transfection efficacy was validated by qRT-PCR(Figure 8B-8C). We then carried out CCK-8 and transwell assay for evaluating the regulatory effects of KCNMA1-AS1 on proliferation and migration of ovarian cancer cells, respectively. Cell proliferation was detected after transfection for 6, 24, 48, 72 and 96 h, respectively. The results showed a remarkable decrease in the proliferative ability after transfection with si-KCNMA1-AS1 2 in ovarian cancer cells (Figure 8D-8F). The transwell assay obtained similar results (Figure 8G), indicating that overexpressed KCNMA1-AS1 promoted proliferation and migration of ovarian cancer cells.Apoptosis was remarkably induced after transfection with si-KCNMA1-AS1 in ovarian cancer cells (Figure 9A and 9B). Moreover, the expressions of activated Caspase-3 and Caspase-9 were elevated after KCNMA1-AS1 knockdown (Figure 9C and 9D). Bcl-xL has a significant anti-apoptotic effect. The data also elucidated that Bcl-xL expression remarkably decreased after transfection with si-KCNMA1AS1 (Figure 9C and 9D), suggesting that KCNMA1-AS1 participated in the development of EOC by regulating cell apoptosis.	31210304	RID07742	expression association	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Epithelial ovarian cancer	KCNMA1-AS1	Caspase9	positively-E	knockdown	upregulation	qRT-PCR	GEO	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000236467	GRCh38_10:76888044-76980624	NA	NA	101929328	NA	NA	NA	KCNMA1-AS1 attenuates apoptosis of epithelial ovarian cancer cells and serves as a risk factor for poor prognosis of epithelial ovarian cancer.KCNMA1-AS1 expression in 60 ovarian cancer tissues and 30 normal ovarian tissues was detected by qRT-PCR The results indicated a higher expression of KCNMA1-AS1 in ovarian cancer than that of normal ovarian tissues (p<0.001, Figure 7A).Transfection efficacy was validated by qRT-PCR(Figure 8B-8C). We then carried out CCK-8 and transwell assay for evaluating the regulatory effects of KCNMA1-AS1 on proliferation and migration of ovarian cancer cells, respectively. Cell proliferation was detected after transfection for 6, 24, 48, 72 and 96 h, respectively. The results showed a remarkable decrease in the proliferative ability after transfection with si-KCNMA1-AS1 2 in ovarian cancer cells (Figure 8D-8F). The transwell assay obtained similar results (Figure 8G), indicating that overexpressed KCNMA1-AS1 promoted proliferation and migration of ovarian cancer cells.Apoptosis was remarkably induced after transfection with si-KCNMA1-AS1 in ovarian cancer cells (Figure 9A and 9B). Moreover, the expressions of activated Caspase-3 and Caspase-9 were elevated after KCNMA1-AS1 knockdown (Figure 9C and 9D). Bcl-xL has a significant anti-apoptotic effect. The data also elucidated that Bcl-xL expression remarkably decreased after transfection with si-KCNMA1AS1 (Figure 9C and 9D), suggesting that KCNMA1-AS1 participated in the development of EOC by regulating cell apoptosis.	31210304	RID07743	expression association	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	
Epithelial ovarian cancer	KCNMA1-AS1	BCL2L1	negatively-E	knockdown	upregulation	qRT-PCR	GEO	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000236467	GRCh38_10:76888044-76980624	ENSG00000171552	NA	101929328	598	NA	Bcl-X|bcl-xL|bcl-xS|BCL2L|BCLX|PPP1R52	KCNMA1-AS1 attenuates apoptosis of epithelial ovarian cancer cells and serves as a risk factor for poor prognosis of epithelial ovarian cancer.KCNMA1-AS1 expression in 60 ovarian cancer tissues and 30 normal ovarian tissues was detected by qRT-PCR The results indicated a higher expression of KCNMA1-AS1 in ovarian cancer than that of normal ovarian tissues (p<0.001, Figure 7A).Transfection efficacy was validated by qRT-PCR(Figure 8B-8C). We then carried out CCK-8 and transwell assay for evaluating the regulatory effects of KCNMA1-AS1 on proliferation and migration of ovarian cancer cells, respectively. Cell proliferation was detected after transfection for 6, 24, 48, 72 and 96 h, respectively. The results showed a remarkable decrease in the proliferative ability after transfection with si-KCNMA1-AS1 2 in ovarian cancer cells (Figure 8D-8F). The transwell assay obtained similar results (Figure 8G), indicating that overexpressed KCNMA1-AS1 promoted proliferation and migration of ovarian cancer cells.Apoptosis was remarkably induced after transfection with si-KCNMA1-AS1 in ovarian cancer cells (Figure 9A and 9B). Moreover, the expressions of activated Caspase-3 and Caspase-9 were elevated after KCNMA1-AS1 knockdown (Figure 9C and 9D). Bcl-xL has a significant anti-apoptotic effect. The data also elucidated that Bcl-xL expression remarkably decreased after transfection with si-KCNMA1AS1 (Figure 9C and 9D), suggesting that KCNMA1-AS1 participated in the development of EOC by regulating cell apoptosis.	31210304	RID07744	expression association	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(PRAD,BRCA);DOWN(SKCM);DATA(GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Cervical cancer	MELTF	p-AKT	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);metastasis process(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000163975	GRCh38_3:196980590-197029835	NA	NA	4241	NA	CD228|FLJ38863|MAP97|MFI2|MGC4856|MTf|MTF1	NA	Up-regulation of long non-coding RNA MFI2 functions as an oncogenic role in cervical cancer progression.To determine the relative expression level of MFI2 in cervical cancer, we used the qRTPCR assay. As shown in Figure 1A, MFI2 was over-expressed in cervical cancer tissues. Consistently, the expression level of MFI2 was up-regulated in cervical cancer cell lines (Figure 1B).The CCK8 assay was recruited to examine the ability of MFI2 on cell proliferation. As shown in Figure 2A, MFI2 up-regulation group promoted cell proliferation in comparison with control group. To figure out the effect of MFI2 on cell apoptosis, flow cytometric analysis was involved in this study. As shown in Figure 2B, apoptotic cells were significantly decreased in MFI2 over-expression group while increased in MFI2 down-expression group. Besides, we employed transwell assay and Matrigel assay to detect the ability of cell migration and invasion. As shown in Figures 3A and 3B, over-expressed MFI2 significantly accelerated cell migration and invasion. Taken together, the results showed that MFI2 functioned as an oncogenic role in cervical cancer.To explore the underlying mechanism of LNC00961 on the progression of OSCC, we used western blot assay to determine if there were alternations on some markers in the PI3K/AKT pathway. As shown in Figure 5, in MFI2 over-expression group, the expression level of phosphorylation-AKT was significantly decreased. Besides, the alternation of BCL2 and Bax indicated that MFI2 over-expression can induce cell apoptosis. Therefore, MFI2 functioned as an oncogenic role in cervical cancer by activating the PI3K/AKT signaling pathway.	31210294	RID07745	expression association	metastasis		
Cervical cancer	MELTF	BCL2	positively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);metastasis process(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000163975	GRCh38_3:196980590-197029835	ENSG00000171791	NA	4241	596	CD228|FLJ38863|MAP97|MFI2|MGC4856|MTf|MTF1	Bcl-2|PPP1R50	Up-regulation of long non-coding RNA MFI2 functions as an oncogenic role in cervical cancer progression.To determine the relative expression level of MFI2 in cervical cancer, we used the qRTPCR assay. As shown in Figure 1A, MFI2 was over-expressed in cervical cancer tissues. Consistently, the expression level of MFI2 was up-regulated in cervical cancer cell lines (Figure 1B).The CCK8 assay was recruited to examine the ability of MFI2 on cell proliferation. As shown in Figure 2A, MFI2 up-regulation group promoted cell proliferation in comparison with control group. To figure out the effect of MFI2 on cell apoptosis, flow cytometric analysis was involved in this study. As shown in Figure 2B, apoptotic cells were significantly decreased in MFI2 over-expression group while increased in MFI2 down-expression group. Besides, we employed transwell assay and Matrigel assay to detect the ability of cell migration and invasion. As shown in Figures 3A and 3B, over-expressed MFI2 significantly accelerated cell migration and invasion. Taken together, the results showed that MFI2 functioned as an oncogenic role in cervical cancer.To explore the underlying mechanism of LNC00961 on the progression of OSCC, we used western blot assay to determine if there were alternations on some markers in the PI3K/AKT pathway. As shown in Figure 5, in MFI2 over-expression group, the expression level of phosphorylation-AKT was significantly decreased. Besides, the alternation of BCL2 and Bax indicated that MFI2 over-expression can induce cell apoptosis. Therefore, MFI2 functioned as an oncogenic role in cervical cancer by activating the PI3K/AKT signaling pathway.	31210294	RID07746	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	MELTF	BAX	negatively-E	overexpression;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);metastasis process(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000163975	GRCh38_3:196980590-197029835	ENSG00000087088	NA	4241	581	CD228|FLJ38863|MAP97|MFI2|MGC4856|MTf|MTF1	BCL2L4	Up-regulation of long non-coding RNA MFI2 functions as an oncogenic role in cervical cancer progression.To determine the relative expression level of MFI2 in cervical cancer, we used the qRTPCR assay. As shown in Figure 1A, MFI2 was over-expressed in cervical cancer tissues. Consistently, the expression level of MFI2 was up-regulated in cervical cancer cell lines (Figure 1B).The CCK8 assay was recruited to examine the ability of MFI2 on cell proliferation. As shown in Figure 2A, MFI2 up-regulation group promoted cell proliferation in comparison with control group. To figure out the effect of MFI2 on cell apoptosis, flow cytometric analysis was involved in this study. As shown in Figure 2B, apoptotic cells were significantly decreased in MFI2 over-expression group while increased in MFI2 down-expression group. Besides, we employed transwell assay and Matrigel assay to detect the ability of cell migration and invasion. As shown in Figures 3A and 3B, over-expressed MFI2 significantly accelerated cell migration and invasion. Taken together, the results showed that MFI2 functioned as an oncogenic role in cervical cancer.To explore the underlying mechanism of LNC00961 on the progression of OSCC, we used western blot assay to determine if there were alternations on some markers in the PI3K/AKT pathway. As shown in Figure 5, in MFI2 over-expression group, the expression level of phosphorylation-AKT was significantly decreased. Besides, the alternation of BCL2 and Bax indicated that MFI2 over-expression can induce cell apoptosis. Therefore, MFI2 functioned as an oncogenic role in cervical cancer by activating the PI3K/AKT signaling pathway.	31210294	RID07747	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	HOTAIR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);	ceRNA(miR-130a-5p)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148516	NA	100124700	6935	HOXC-AS4|HOXC11-AS1|NCRNA00072	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	CCL18-induced HOTAIR upregulation promotes malignant progression in esophageal squamous cell carcinoma through the miR-130a-5p-ZEB1 axis.To evaluate the expression status of CCL18 in ESCC tissues, we detected CCL18 mRNA in 25 pairs of ESCC tissues and adjacent benign esophageal tissues. The statistical analysis showed that the expression levels of CCL18 mRNA in ESCC tissues were significantly higher than those in non-cancerous esophageal tissues (P< 0.001,Fig. 1A).Kaplan-Meier survival analysis also demonstrated that patients with low CCL18 expression had a significantly longer survival time than those with high CCL18 expression (Fig. 1D,P= 0.022), which was associated with poor survival prognosis in patients with esophageal cancer. To further confirm the increased expression of CCL18 in ESCC, we detected the expression of CCL18 in the five ESCC cell lines (ECA109, KYSE30, KYSE140 KYSE510, and TE-1) and HEECs by qRT-PCRand ELISA. Compared with HEECs, the expression of CCL18 mRNA (Fig. 1E) and protein (Fig. 1F) in all the types of ESCC cells increased. Transwell chambers were used to examine the invasiveness of esophageal cancer cells treated with recombinant CCL18. Compared to the case for the PBS-treated cancer cells, treatment with recombinant CCL18 (rCCL18, 5'-0 ng/mL) enhanced the invasiveness of ECA109 cells in a dose-dependent manner (Fig. 1G and H). To further determine whether CCL18 contributes to the invasiveness of the cancer cells, two CCL18-siRNAs were transfected into TE-1 cells to interfere with the function of CCL18 (Supplementary Fig. S1,P< 0.01). Transfection of TE-1 cells with either of the two CCL18-siRNAs also reduced the number of invasive cancer cells (Fig. 1I). Collectively, these data suggest that CCL18 promotes the process of malignant progression in ESCC.HOTAIR expression was markedly higher in ESCC tissues than in noncancerous esophageal tissues (P< 0.001,Fig. 2A).To further validate whether these miRNAs were regulated by HOTAIR in esophageal cancer cells, we performed qRT-PCRto determine their levels in TE-1 cells transfected with sh-Vector or sh-HOTAIR. Compared with the cancer cells transfected with sh-Vector, the expression levels of all 18 miRNAs in the TE1 cells transfected with sh-HOTAIR, miR-130a-5p showed the greatest fold change in response to HOTAIR knockdown (Fig. 3A). In addition, a bioinformatics prediction tool indicated that there were complementary sequences with miR-130a-5p seed regions in HOTAIR (Fig. 3B). Therefore, we chose miRNA-130a-5p for the subsequent experiments. In order to verify whether HOTAIR regulated the miR-130a-5p expression through the potential interaction at the putative miR-130a-5p binding sites, the wild type of HOTAIR or mutant HOTAIR fragment containing the putative miR-130a-5p binding sites was cloned into a dual-luciferase reporter. The luciferase activity was analyzed after the co-transfection of TE-1 cells with a miR-130a-5p mimic or scramble and the HOTAIR-Wt or HOTAIR-Mut plasmids. The results showed that the relative luciferase activity of the HOTAIR-Wt plasmid was significantly suppressed after co-transfection with the miR-130a-5p mimic. In contrast, this effect was not detected in the plasmid carrying the HOTAIRMut (Fig. 3C). This result demonstrates that the putative binding sites are vital for the reciprocal repression of HOTAIR and mir-130a-5p. To investigate the role of miR-130a-5p in ESCC, the expression of miR130a-5p in 25 ESCC tissue samples and 25 adjacent benign esophageal tissue samples was detected by qRT-PCR The results demonstrated that the miR-130a-5p expression in ESCC tissues was significantly lower than that in the adjacent paired tissue samples (Fig. 3D). To assess whether HOTAIR functions as a molecular sponge for miR-130a-5p, we analyzed the expression of HOTAIR and miR-130a-5p in 25 ESCC tissue samples. We observed a negative correlation between the HOTAIR and miR-130a-5p expression (Fig. 3E; r = 0.52,P= 0.008). These results suggest that HOTAIR may promote CCL18 signaling by acting as a ceRNA for miR-130a-5p.To verify that ZEB1 was a direct target of miR-130a-5p, the 3--UTR of ZEB1 with wild-type or mutant seed sequence recognition sites was cloned into a luciferase reporter. The luciferase activity was analyzed after the cotransfection of TE-1 cells with a miR-130a-5p mimic or scramble and the ZEB1 3-UTR-Wt or ZEB1 3-UTR-Mut plasmids. The results showed that the overexpression of miR-130a-5p led to a marked decrease in the luciferase activity of the plasmid carrying ZEB1 3-UTR-Wt, while no significant changes in luciferase activity were observed in TE-1 cells transfected with the ZEB1 3-UTR-Mut plasmid (Fig. 4B). To confirm that miR-130a-5p regulates the expression of ZEB1, we examined the expression of ZEB1 mRNA in ECA109 and TE-1 cells transfected with miR-130a-5p mimics or a miR-130a-5p inhibitor (Supplementary Fig. S4). We found that miR-130a-5p overexpression markedly decreased the expression of ZEB1 in ECA109 and TE-1 cells, while the downregulation of miR-130a-5p increased the expression of ZEB1, compared with the control group (Fig. 4C). To further explore the effects of HOTAIR on ZEB1 function, we performed western blot to detect the expression of EMT markers. We found that the Ecadherin expression decreased and Vimentin expression increased in ESCC cells transfected with pcDNA3.1-ZEB1 (Supplementary Fig. S6). Furthermore, HOTAIR knockdown markedly increased the expression of E-cadherin and decreased the expression of Vimentin. However, the inhibition of EMT induced by shHOTAIR was reversed by co-transfection with shHOTAIR + si-ZEB1 (Fig. 5E). These data suggest that HOTAIR may act as an miR-130a-5p sponge to upregulate the expression of its target ZEB1, thereby promoting the progression of EMT in ESCC.In order to investigate the biological roles of HOTAIR and miR130a-5p in ESCC, we employed gain-of-function and loss-of-function approaches. Compared with the control group, the proliferation of ECA109 and TE-1 cells transfected with miR-130a-5p mimics decreased, while the cell proliferation increased following the transfection with miR-130a-5p inhibitor. Furthermore, ECA109 and TE-1 cells transfected with shHOTAIR showed reduced cell proliferation compared with the control group. However, co-transfection with shHOTAIR and miR-130a-5p inhibitor rescued the inhibitory effect induced by HOTAIR knockdown. These results imply that the oncogenic activity of HOTAIR may occur partly through the negative regulation of miR-130a5p (Fig. 6A and B). We verified these findings in vitro using an in vivo xenograft model. TE-1 cells stably infected with Lv-shHOTAIR, Lv-miR-130a-5p inhibitor, or shHOTAIR + Lv-miR-130a-5p were subcutaneously injected into the dorsal flank of nude mice. After 6 weeks, the nude mice were sacrificed, and the tumor tissues were removed and weighed. Compared with the control group, the volume and size of tumors from mice in the shHOTAIR group and the shHOTAIR + Lv-miR-130a-5p group decreased significantly, while the shHOTAIR + Lv-miR-130a-5p group had a stronger anti-cancer effect. In contrast, the volume and size of tumors from mice in the Lv-miR-130a-5p inhibitor group markedly increased (Fig. 6C and D).	31207321	RID07748	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	PVT1	BCL2	positively-E	knockdown	upregulation	qRT-PCR	5-fluorouracil	NA	cell growth(+);chemoresistance(+);apoptosis process(-)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	LncRNA PVT1 Mediates Antiapoptosis and 5-Fluorouracil Resistance via Increasing Bcl2 Expression in Gastric Cancer.First, we explored the expression of PVT1 in different stages of GC using the Cancer RNA-Seq Nexus (CRN; http://syslab4.nchu.edu.tw) so that we could access PVT1 gene expression data of GC patients from the TCGA stomach carcinoma RNA-Seq dataset [14]. As shown in Figure 1(a), the expression of PVT1 increased with cancer progression, compared to that of adjacent normal tissues. To explore the effects of PVT1 on GC, we stably overexpressed and stably silenced PVT1 expression in SGC-7901 cells (Figure 1(b)) and observed the influence of PVT1 on the tumorigenicity of gastric cancer cells in a mouse model. We noticed that the subcutaneous xenografts formed from PVT1-overexpressed GC cells had larger volume than xenografts formed from vector-control cells (Figures 1(c) left panel and 1(d)). Conversely, the subcutaneous xenografts formed from PVT1-silenced GC cells had smaller volume than vector-control tumors (Figures 1(c) right panel and 1(e)). An orthotopic mouse model was also established. As shown in Figure 1(f), the orthotopic xenograft formed from PVT1-overexpressed SGC-7901 cells also exhibited larger volume. Based on these results, we believe that PVT1 can regulate the growth of GC, and PVT1 may play a crucial role in the progression of GC.Next, we investigated the functions of PVT1 on GC cell behaviors. The clone formation assay showed that the count of clones formed by PVT1-overexpressed cells was significantly increased (Figure 2(a)), but significantly decreased by PVT1-silenced cells (Figure 2(b)). In the apoptosis analysis, upregulating PVT1 decreased the apoptosis of SGC-7901 cells; downregulating PVT1 increased the apoptosis of SGC-7901 cells (Figures 2(c) and 2(d)). To confirm the effects of PVT1 on apoptosis, TUNEL staining was conducted to investigate the apoptosis in the xenografts. Compared to the control xenograft, decreasing DNA fragmentation was observed in the subcutaneous xenograft formed by PVT1-overexpressed GC cells and increasing DNA fragmentation was observed from PVT1-silenced GC cells, respectively (Figures 2(e) and 2(f)). Similar results were also observed in the orthotopic xenograft (Figures 2(g) and 2(h)). Taken together, these results indicated that PVT1 can regulate the apoptosis of GC cells.To elucidate the underlying mechanism of PVT1 inducing apoptosis, we screened the common factors that may be related to this apoptosis process using the RT-PCR The results showed that the Bcl2 mRNA was significantly increased when PVT1 was upregulated (Figure 3(a)) and significantly decreased when PVT1 was silenced (Figure 3(b)). Consistently, the following western blot indicated that the PVT1 can regulate the expression of Bcl2 protein but has no effect on the Bax protein. Beyond that, we noticed that the downstream apoptosis executor of Bcl2, cleaved caspase-3, was decreased when the PVT1 was overexpressed and increased when PVT1 was silenced (Figure 3(c)). To further verify the regulation of PVT1 on Bcl2, we evaluated the expression of Bcl2 protein in xenografts through the IHC assay. The IHC assay showed that the Bcl2 staining was evidently strengthened in subcutaneous xenografts formed from PVT1-overexpressed SGC-7901 cells but weakened in that from PVT1-silenced SGC-7901 cells (Figure 4(d)). Consistently, IHC showed Bcl2 staining was also strengthened when PVT1 was overexpressed in the orthotopic GC tumor (Figure 4(e)). In addition, Kaplan-Meier survival analysis in GEO datasets revealed that GC patients with both high level of PVT1 and Bcl2 suffered shortest first progression survival (FPS) (Figure 4(f)) and overall survival (OS) (Figure 4(g)). Collectively, those results demonstrated that the effects of PVT1 on apoptosis were achieved by regulating Bcl2. High levels of PVT1 combined with Bcl2 can predict poor prognosis in GC.It was reported that Bcl2 can determine the resistance of 5-Fu in carcinoma [15, 16]; hence, we supposed PVT1 may possibly enhance 5-fu resistance in GC via its promotion to Bcl2. To confirm this supposition, the IC50 values were estimated from growth inhibition curves. The results showed that, compared with their matched control group, the IC50 of 5-Fu was significantly increased when PVT1 was overexpressed (Figure 4(a)), but significantly decreased when PVT1 was silenced (Figure 4(b)). The following RT-PCRand western blot assay showed that the 5-Fu treatment can decrease Bcl2 mRNA and protein of GC cells. Although 5-Fu had an inhibitory effect on Bcl2 in PVT1-overexpressed SGC-7901 cells, the same dose of 5-Fu treatment could not offset the promoting effect of PVT1 on Bcl2 and the level of Bcl2 after 5-Fu treatment was still significantly high compared to the norm (Figures 4(c) and 4(d)).	31205469	RID07749	expression association	prognosis,chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Malignant glioma	RP11-732M18.3	14-3-3beta	interact	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell cycle(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236537	NA	NA	NA	NA	NA	NA	NA	The binding of lncRNA RP11-732M18.3 with 14-3-3 beta/alpha accelerates p21 degradation and promotes glioma growth.To further study lncRNA RP11-732M18.3 expression in human glioma tissues, we examined a panel of paired tumor and normal tissue specimens that were collected from patients with glioma (n-=-60) and normal brain tissues (n-=-30). lncRNA RP11-732M18.3 transcripts were expressed at higher levels in the tumor tissues, as compared to the normal tissues, after normalizing to U6 transcript expression by qRT-PCRanalyses (Figs. 1a, Student's t-test). The expression levels of lncRNA RP11-732-M18.3 in glioma cell lines were higher than the normal cells (Figs. S1e, Student's t-test).As shown in Fig. 2b, decreased expression of lncRNA RP11-732M18.3 weakened tumor growth in vivo, as compared with the controls. The same results were observed with the U251 cell line group, indicating that the position of cell injected did not affect tumor growth (Fig. 2c, Student's t-test). The tumor weight of the knockout group was less than that of the control group (Fig. 2d, Student's t-test). The expression levels of RP11-732M18.3 in allograft tumors was lower than in controls (Fig. S1f, Student's t-test). In these xenograft tissues, lncRNA RP11-732M18.3 knockdown effectively reduced Ki67 expression (Fig. 2e and f, Student's t-test). In addition, a nude mouse model of orthotopic tumors showed that lncRNA RP11-732M18.3 knockdown decreased tumor volume (Fig. 2g). Thus, lncRNA RP11-732M18.3 has a certain impact on the proliferation of glioma cells.Given the impact of lncRNA RP11-732M18.3 depletion on the proliferation of glioma cells in vivo, several assays were conducted with the three stable knockdown or overexpression cell lines to study this phenotype in vitro (Fig. S2a and S2b, Student's t-test). The results of the cell counting kit-8 and colony formation assays in vitro showed that knockdown of lncRNA RP11-732M18.3 decreased the proliferative capacity of U87MG, U251, and A172 cells, compared with that of parallel stable cell lines containing empty vectors (Fig. 3a, c, and S3a, Student's t-test). In contrast, overexpression of endogenous lncRNA RP11-732M18.3 dramatically increased the proliferative capacity of glioma cells (Fig. 3b, c, and S3a, Student's t-test).Cdk2 phosphorylates Rb as cells progress through G1 [25]. Previous studies have suggested that the p21 CDK-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases [[27], [28], [29]]. In addition, the cyclin E-Cdk2 complex is necessary for the G1/S transition and the expression levels of CDK2 and CCNE1 are closely related to G1/S transition [29,30]. Hence, the expression levels of p21, CDK2, and CCNE1 were examined after overexpression/depletion of lncRNA RP11-732-M18.3. The results showed that knockdown of lncRNA RP11-732M18.3 increased the expression level of p21, while that of CDK2 and CCNE1 was decreased (Fig. 4a, Student's t-test). In contrast, overexpression of lncRNA RP11-732-M18.3 had the opposite effect (Fig. 4b, Student's t-test). To confirm this finding, A172 cells were subjected to western blot which showed that lncRNA RP11-732-M18.3 regulates the expression of p21 (Figs. S3d, Student's t-test). In addition, inhibition of RP11-732-M18.3 increased the expression of p21 in allograft tumor cells (Figs. S4, Student's t-test).To investigate the molecular mechanism by which lncRNA RP11-732M18.3 is associated with p21 expression, p21 mRNA expression was determined by qRT-PCR The results showed that lncRNA RP11-732M18.3 had no effect on p21 mRNA levels (Fig. 5a, Student's t-test). However, degradation assay results revealed that lncRNA RP11-732M18.3 promoted p21 degradation (Fig. 5b, Student's t-test). In addition, MG132 decreased the degradation of p21 and knockdown lncRNA RP11-732M18.3 inhibition the ubiquitination of p21 (Fig. 5c). Collectively, these data indicate that lncRNA RP11-732M18.3 promoted glioma cell proliferation by promoting p21 degradation.	31202814	RID07750	interact with protein	NA		
Malignant glioma	RP11-732M18.3	14-3-3alpha	interact	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell cycle(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236537	NA	NA	NA	NA	NA	NA	NA	The binding of lncRNA RP11-732M18.3 with 14-3-3 beta/alpha accelerates p21 degradation and promotes glioma growth.To further study lncRNA RP11-732M18.3 expression in human glioma tissues, we examined a panel of paired tumor and normal tissue specimens that were collected from patients with glioma (n-=-60) and normal brain tissues (n-=-30). lncRNA RP11-732M18.3 transcripts were expressed at higher levels in the tumor tissues, as compared to the normal tissues, after normalizing to U6 transcript expression by qRT-PCRanalyses (Figs. 1a, Student's t-test). The expression levels of lncRNA RP11-732-M18.3 in glioma cell lines were higher than the normal cells (Figs. S1e, Student's t-test).As shown in Fig. 2b, decreased expression of lncRNA RP11-732M18.3 weakened tumor growth in vivo, as compared with the controls. The same results were observed with the U251 cell line group, indicating that the position of cell injected did not affect tumor growth (Fig. 2c, Student's t-test). The tumor weight of the knockout group was less than that of the control group (Fig. 2d, Student's t-test). The expression levels of RP11-732M18.3 in allograft tumors was lower than in controls (Fig. S1f, Student's t-test). In these xenograft tissues, lncRNA RP11-732M18.3 knockdown effectively reduced Ki67 expression (Fig. 2e and f, Student's t-test). In addition, a nude mouse model of orthotopic tumors showed that lncRNA RP11-732M18.3 knockdown decreased tumor volume (Fig. 2g). Thus, lncRNA RP11-732M18.3 has a certain impact on the proliferation of glioma cells.Given the impact of lncRNA RP11-732M18.3 depletion on the proliferation of glioma cells in vivo, several assays were conducted with the three stable knockdown or overexpression cell lines to study this phenotype in vitro (Fig. S2a and S2b, Student's t-test). The results of the cell counting kit-8 and colony formation assays in vitro showed that knockdown of lncRNA RP11-732M18.3 decreased the proliferative capacity of U87MG, U251, and A172 cells, compared with that of parallel stable cell lines containing empty vectors (Fig. 3a, c, and S3a, Student's t-test). In contrast, overexpression of endogenous lncRNA RP11-732M18.3 dramatically increased the proliferative capacity of glioma cells (Fig. 3b, c, and S3a, Student's t-test).Cdk2 phosphorylates Rb as cells progress through G1 [25]. Previous studies have suggested that the p21 CDK-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases [[27], [28], [29]]. In addition, the cyclin E-Cdk2 complex is necessary for the G1/S transition and the expression levels of CDK2 and CCNE1 are closely related to G1/S transition [29,30]. Hence, the expression levels of p21, CDK2, and CCNE1 were examined after overexpression/depletion of lncRNA RP11-732-M18.3. The results showed that knockdown of lncRNA RP11-732M18.3 increased the expression level of p21, while that of CDK2 and CCNE1 was decreased (Fig. 4a, Student's t-test). In contrast, overexpression of lncRNA RP11-732-M18.3 had the opposite effect (Fig. 4b, Student's t-test). To confirm this finding, A172 cells were subjected to western blot which showed that lncRNA RP11-732-M18.3 regulates the expression of p21 (Figs. S3d, Student's t-test). In addition, inhibition of RP11-732-M18.3 increased the expression of p21 in allograft tumor cells (Figs. S4, Student's t-test).To investigate the molecular mechanism by which lncRNA RP11-732M18.3 is associated with p21 expression, p21 mRNA expression was determined by qRT-PCR The results showed that lncRNA RP11-732M18.3 had no effect on p21 mRNA levels (Fig. 5a, Student's t-test). However, degradation assay results revealed that lncRNA RP11-732M18.3 promoted p21 degradation (Fig. 5b, Student's t-test). In addition, MG132 decreased the degradation of p21 and knockdown lncRNA RP11-732M18.3 inhibition the ubiquitination of p21 (Fig. 5c). Collectively, these data indicate that lncRNA RP11-732M18.3 promoted glioma cell proliferation by promoting p21 degradation.	31202814	RID07751	interact with protein	NA		
Malignant glioma	RP11-732M18.3	CDKN1A	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+);cell cycle(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236537	NA	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	The binding of lncRNA RP11-732M18.3 with 14-3-3 beta/alpha accelerates p21 degradation and promotes glioma growth.To further study lncRNA RP11-732M18.3 expression in human glioma tissues, we examined a panel of paired tumor and normal tissue specimens that were collected from patients with glioma (n-=-60) and normal brain tissues (n-=-30). lncRNA RP11-732M18.3 transcripts were expressed at higher levels in the tumor tissues, as compared to the normal tissues, after normalizing to U6 transcript expression by qRT-PCRanalyses (Figs. 1a, Student's t-test). The expression levels of lncRNA RP11-732-M18.3 in glioma cell lines were higher than the normal cells (Figs. S1e, Student's t-test).As shown in Fig. 2b, decreased expression of lncRNA RP11-732M18.3 weakened tumor growth in vivo, as compared with the controls. The same results were observed with the U251 cell line group, indicating that the position of cell injected did not affect tumor growth (Fig. 2c, Student's t-test). The tumor weight of the knockout group was less than that of the control group (Fig. 2d, Student's t-test). The expression levels of RP11-732M18.3 in allograft tumors was lower than in controls (Fig. S1f, Student's t-test). In these xenograft tissues, lncRNA RP11-732M18.3 knockdown effectively reduced Ki67 expression (Fig. 2e and f, Student's t-test). In addition, a nude mouse model of orthotopic tumors showed that lncRNA RP11-732M18.3 knockdown decreased tumor volume (Fig. 2g). Thus, lncRNA RP11-732M18.3 has a certain impact on the proliferation of glioma cells.Given the impact of lncRNA RP11-732M18.3 depletion on the proliferation of glioma cells in vivo, several assays were conducted with the three stable knockdown or overexpression cell lines to study this phenotype in vitro (Fig. S2a and S2b, Student's t-test). The results of the cell counting kit-8 and colony formation assays in vitro showed that knockdown of lncRNA RP11-732M18.3 decreased the proliferative capacity of U87MG, U251, and A172 cells, compared with that of parallel stable cell lines containing empty vectors (Fig. 3a, c, and S3a, Student's t-test). In contrast, overexpression of endogenous lncRNA RP11-732M18.3 dramatically increased the proliferative capacity of glioma cells (Fig. 3b, c, and S3a, Student's t-test).Cdk2 phosphorylates Rb as cells progress through G1 [25]. Previous studies have suggested that the p21 CDK-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases [[27], [28], [29]]. In addition, the cyclin E-Cdk2 complex is necessary for the G1/S transition and the expression levels of CDK2 and CCNE1 are closely related to G1/S transition [29,30]. Hence, the expression levels of p21, CDK2, and CCNE1 were examined after overexpression/depletion of lncRNA RP11-732-M18.3. The results showed that knockdown of lncRNA RP11-732M18.3 increased the expression level of p21, while that of CDK2 and CCNE1 was decreased (Fig. 4a, Student's t-test). In contrast, overexpression of lncRNA RP11-732-M18.3 had the opposite effect (Fig. 4b, Student's t-test). To confirm this finding, A172 cells were subjected to western blot which showed that lncRNA RP11-732-M18.3 regulates the expression of p21 (Figs. S3d, Student's t-test). In addition, inhibition of RP11-732-M18.3 increased the expression of p21 in allograft tumor cells (Figs. S4, Student's t-test).To investigate the molecular mechanism by which lncRNA RP11-732M18.3 is associated with p21 expression, p21 mRNA expression was determined by qRT-PCR The results showed that lncRNA RP11-732M18.3 had no effect on p21 mRNA levels (Fig. 5a, Student's t-test). However, degradation assay results revealed that lncRNA RP11-732M18.3 promoted p21 degradation (Fig. 5b, Student's t-test). In addition, MG132 decreased the degradation of p21 and knockdown lncRNA RP11-732M18.3 inhibition the ubiquitination of p21 (Fig. 5c). Collectively, these data indicate that lncRNA RP11-732M18.3 promoted glioma cell proliferation by promoting p21 degradation.	31202814	RID07752	expression association	NA		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Osteosarcoma	HOXA11-AS	RAB3D	positively-E	dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-125a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000105514	NA	221883	9545	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	D2-2|GOV|RAB16|RAD3D	The lncRNA HOXA11-AS regulates Rab3D expression by sponging miR-125a-5p promoting metastasis of osteosarcoma.The expression levels of lncRNA HOXA11-AS in 61 OS patients'-resected tumors and para-tumor tissues were detected by fluorescence quantitative PCR method. The results showed that the expression level of HOXA11-AS in tumor tissues was significantly higher than that in para-tumor tissues (P<0.01, Figure 1A), and its expression level in OS cell lines was significantly higher than that in normal human osteoblasts (P<0.01, Figure 1B).In vitro experiments showed that down-regulation of HOXA11-AS expression in MG-63 and KHOS cells could inhibit cell proliferation, while up-regulation of HOXA11-AS expression could promote cell proliferation (Figure 2A and -andB).B). In vivo experiments showed that down-regulation of HOXA11-AS expression in MG-63 and KHOS cells could inhibit the growth of subcutaneous solid tumors in nude mice, while up-regulation of HOXA11-AS expression could promote the growth of subcutaneous solid tumors in nude mice (Figure 2C ).The invasion and migration ability by up-regulating and down-regulating HOXA11-AS gene in both MG-63 and KHOS cell lines were detected, respectively. The results showed that the migration and invasion ability of MG-63 and KHOS cells decreased significantly after HOXA11-AS siRNA inhibited HOXA11-AS expression, the migration and invasion of MG-63, and KHOS cells increased significantly after overexpressed HOXA11-AS (P<0.01, Figure 3). These results suggested that HOXA11-AS could promote the migration and invasion of OS cells.RT-PCRresults showed that the expression level of miR-125a-5p in OS tissues was significantly lower than that in their adjacent tissues (P<0.01, Figure 4B). Luciferase reporter gene test also confirmed that HOXA11-AS could directly regulate the expression of miR-125a-5p (P<0.01, Figure 4A). Inhibiting the expression of HOXA11-AS in MG-63 and KHOS cells could significantly increase the expression level of miR-125a-5p (P<0.01, Figure 4C). Overexpression of HOXA11-AS in MG-63 and KHOS cells could significantly inhibit the expression of miR-125a-5p (P<0.01, Figure 4D).Compared with the control group, it was found that miR-125a-5p mimic could inhibit the migration and invasion of OS, while miR-125a-5p inhibitors could promote the migration and invasion of OS (P<0.05, Figure 5). When HOXA11-AS- siRNAs and miR-125a-5p inhibitors were transfected into MG-63 cells at the same time, and the ability of HOXA11-AS- siRNAs to inhibit cell migration and invasion was counteracted. When pcDNA-HOXA11-AS and miR-125a-5p mimic were transfected into KHOS cells at the same time, it could inhibit the ability of pcDNA-HOXA11-AS to promote cell migration and invasion (Figure 5).Immunohistochemical and RT-PCRresults showed that the expression level of Rab3D in tumor tissues was significantly higher than that in their adjacent tissues (Figure 6A). The online software TargetScan analysis showed that miR-125a-5p may be combined with 3 'UTR of Rab3D. Luciferase reporter gene analysis showed that miR-125a-5 could target the 3'UTR of Rab3D (Figure 6D and -andE).E). miR-125a-5p could inhibit the expression of Rab3D (Figure 6D and -andE),E), while HOXA11-AS could promote the expression of Rab3D by inhibiting the expression of miR-125a-5p (Figure 6H and -andII).	31191012	RID07753	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE51827,GSE75367,GSE86978)
Ovarian cancer	CDKN2B-AS1	HMGA2	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	cisplatin	NA	chemosensitivity(-);apoptosis process(-);cell growth(+)	ceRNA(let-7a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149948	NA	100048912	8091	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	BABL|HMGIC|LIPO	LncRNA ANRIL affects the sensitivity of ovarian cancer to cisplatin via regulation of let-7a/HMGA2 axis.As for ovarian tissues shown in Figure 1, the ovarian cancer tissues had apparently higher ANRIL expression and lower let-7a expression than its adjacent normal tissues (all P<0.05). Additionally, compared with normal HOSEPiCs, the cisplatin-sensitive and cisplatin-resistant cell lines (SKOV3 and SKOV3/DDP cells) had significantly increased ANRIL expression and decreased in let-7a expression (all P<0.05).In SKOV3 and SKOV3/DDP cells (Figure 3), the NC siRNA group had no significant difference from the Blank group in the cell apoptosis rate (P>0.05); however, the ANRIL siRNA and let-7a mimic groups had apparently increased apoptosis rate (all P<0.05). In addition, the cell apoptosis rate in the ANRIL siRNA + let-7a-inhibitor group was remarkably lower than the ANRIL siRNA group (P<0.05).By using the website http://starbase.sysu.edu.cn/index.php (Figure 4A), we found that ANRIL can specifically regulate let-7a, and the binding site of let-7a to HMGA2 was also predicted with the software Target Scan (Figure 4B). According to the results of dual-luciferase reporter gene assay, let-7a mimic had no obvious effect on the luciferase activity of ANRIL-MUT and HMGA2-MUT (all P>0.05), but it can effectively reduce the luciferase activity of ANRIL-WT and HMGA2-WT (P<0.05, Figure 4C,D). All those results indicated that there was reciprocal repression between ANRIL and let-7a, and between let-7a and HMGA2.As shown in Figure 5, ANRIL and HMGA2 were down-regulated and let-7a was up-regulated in SKOV3 and SKOV3/DDP cells in the ANRIL siRNA and let-7a mimic groups (all P<0.05), as compared with the Blank group. No alterations were found between Blank group and NC siRNA in these molecules (all P>0.05). Moreover, with ANRIL siRNA group as the baseline, ANRIL siRNA+ let-7a-inhibitor group presented obvious increases of ANRIL and HMGA2, and remarkable decrease of let-7a (all P<0.05).	31189742	RID07754	ceRNA or sponge	chemoresistance	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Lung cancer	H19	miR-200a	positively-E	dual-luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);metastasis process(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	LncRNA H19 promotes lung cancer proliferation and metastasis by inhibiting miR-200a function.To understand the potential function of lncRNA H19 in lung cancer, we first evaluated the expression levels of H19 mRNA in lung cancer tissues and cell lines. Comparing with the paired adjacent normal tissues, the lung cancer tissues expressed significantly more H19 mRNA (Fig. 1a). Similarly, the expression level of H19 mRNA was higher in the lung cancer cell lines, A549, H1299, H23 and SPC-A1, than it in the primary lung cell line, 16HBE (Fig. 1b). These data suggest that lncRNA H19 may be involved in development of lung cancer.Since H19 expression was increased in lung cancer tissues and cells, we further explored the biological function of H19 in lung cancer. H19 was overexpressed in A549 cells through H19 expression plasmid transfection, and as shown in Fig. 2a, H19 expression was increased over 20 folds. As a consequence, cell growth was stimulated by more than 50% (Fig. 2b) and the cell viability was significantly elevated (Fig. 2c). In contrast, H19 knockdown in A549 by shRNA (Fig. 2d) remarkably inhibited cell growth (Fig. 2e) and cell viability (Fig. 2f). These data indicate that lncRNA H19 plays a role in promoting lung cancer cell growth.EMT is related to cancer metastasis, and enhances cell migration and invasion [4]. OCLN and FN1 is a representative epithelial and mesenchymal marker, respectively, and EZH2 and TWIST1 play important roles in EMT [5]. H19 overexpression repressed OCLN expression (Fig. 3c), and heightened expression of EZH2, FN1 and TWIST1 (Fig. 3d ). These results indicated that H19 enhances EMT to stimulate lung cancer cell migration and invasion.To investigate the mechanism underlying that H19 promotes lung cancer cell migration and invasion, we predicted potential H19-binding miRNAs with an online software RNAhybird (https ://bibis erv2.cebit ec.uni-biele feld.de/rnahy brid). miR-200a (Fig. 4a) and other miRNAs (Table S1) were predicted to bind to H19, and miR-200a was reported to bind to H19 [17]. To verify the interaction between H19 and miR200a, biotin-labeled miR-200a was transfected into A549 cells to perform RNA pull-down assay. Compared to nonspecific miRNA control, miR-200a enriched H19 mRNA at 14 folds or so (Fig. 4b), indicating interaction between H19 and miR-200a. H19 overexpression in A549 cells suppressed miR-200a expression more than 50% (Fig. 4c). Moreover, miR-200a dramatically reduced the activity of the H19-fused luciferase (Fig. 4d). These data suggest that H19 interacts with miR-200a to inhibit miR-200a function. Consistent with the results that H19 upregulation in lung tumors (Fig. 1a), the expression of miR-200a was significantly decreased in the lung cancer tissues (Fig. 4e). In addition, the miR200a levels were associated with the stage of lung cancers (Fig. 4f). These results indicate that miR-200a has an important role in the lung cancer development.ZEB1 and ZEB2 are two important regulators of EMT, and furthermore, are targets of miR-200a [18]. Based on these reported results, we investigated if H19-affected expression of ZEB1 and ZEB2 to promote EMT. In agreement with the reported results, miR-200a transfection in A549 cells significantly declined both mRNA and protein levels of ZEB1 and ZEB2 (Fig. 5a, b). As we hypothesized, H19 overexpression boosted the expression levels of ZEB1 and ZEB2 by about 2 and 3-folds, respectively (Fig. 5c). These data hint that H19 manipulates expression of ZEB1 and ZEB2 via suppressing miR-200a. Consistently, H19 overexpression-enhanced cell viability was abolished by miR-200a transfection (Fig. 5d). Considering the importance of ZEB1 and ZEB2 in EMT, it suggests that H19 captures and inhibits miR-200a, and therefore upregulates expression of miR-200a targeted genes, ZEB1 and ZEB2, to promote EMT.	31187349	RID07755	ceRNA or sponge	metastasis	UP(NSCLC);DATA(GSE74639)	
Laryngeal squamous cell carcinoma	LNCNEF	CTNNB1	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);WNT/beta-catenin signaling pathway(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000237396	GRCh38_20:22587522-22607517	ENSG00000168036	NA	101929685	1499	LINC01384|lncRNA-NEF	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA NEF inhibits proliferation and promotes apoptosis of laryngeal squamous cell carcinoma cells by inhibiting Wnt/beta-catenin signaling.Differential expression in tumor tissues and adjacent healthy tissues usually indicates the involvement of a certain gene in cancer. As shown in Fig. 5A, NEF overexpression significantly inhibited the proliferation of UM-SCC-17A cells (P<0.05). In addition, NEF overexpression significantly promoted apoptosis of UM-SCC-17A cells (P<0.05; Fig. 5B and C). However, Wnt agonist treatment at a dose of 10 ng/ml significantly reduced the effects of NEF overexpression on proliferation and apoptosis of UM-SCC-17A cells (P<0.05; Fig. 5A-C). The percentages of apoptotic cells in the control, negative control, NEF and NEF + Wnt agonist groups were 20.6, 20.66, 38.29 and 29.64% of the total number of cells, respectively.	31186702	RID07756	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung adenocarcinoma	LINC00467	EZH2	interact	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000106462	NA	84791	2146	C1orf97|MGC14801	ENX-1|EZH1|KMT6|KMT6A	Long intergenic non-coding RNA 00467 promotes lung adenocarcinoma proliferation, migration and invasion by binding with EZH2 and repressing HTRA3 expression.To validate the GEO and TCGA results, RT-qPCR assays were used to measure linc00467 expression in 35 paired LAD and adjacent normal lung tissues. The relative expression of lncRNA was calculated using the Cq value  method. The expression level of linc00467 in LAD tissues was increased compared with that in adjacent normal lung tissues (P<0.001; Fig. 2A). Then, the association between linc00467 expression and patients' clinical characteristics were evaluated (Table I). The linc00467 expression levels were significantly increased in patients with larger tumours compared with smaller tumours (P=0.013; Fig. 2B), and in those with more advanced TNM stages (P=0.021; Fig. 2C). However, there were no significant associations between linc00467 expression and other clinical parameters, including age, sex, differentiation, lymph node metastasis and smoking history.As linc00467 was confirmed to promote LAD cell proliferation in vitro, its effects on LAD cell migration and invasion was additionally investigated. A Transwell assay was used to evaluate the biological effect of linc00467 on the LAD cell metastasis. linc00467 knockdown significantly suppressed the migratory and invasive abilities of A549 and H1299 cells (Fig. 6A and B), while linc00467 overexpression increased the migratory and invasive abilities of PC9 cells (Fig. 6C). These results suggested that linc00467 promoted the migration and invasion of LAD cells.lncRNAs are able to bind RNA-binding proteins (RBPs) to regulate the expression of downstream genes. Therefore, the present study investigated whether linc00467 regulated HTRA3 expression by binding to RBPs. The probability of an interaction between linc00467 and RBPs was first determined using an lncRNA prediction website (http://annolnc.cbi.pku.edu.cn/index.jsp). The sequence of linc00467 was input into the AnnoLnc database, and entered into the protein interaction page; subsequently, the interaction score between lncRNA and protein could be predicted. The interaction score for linc00467 and EZH2 was 96.0705, close to the maximum value of 100. Whether linc00467 repressed HTRA3 transcription was next investigated by recruiting EZH2 to the HTRA3 promoter. EZH2 expression was first knocked down in A549 and H1299 cells using transfection with siRNA (Fig. 10A and B). In addition, western blotwas performed to measure HTRA3 protein expression levels when EZH2 was downregulated. The results indicated that HTRA3 protein expression levels were increased in the EZH2-downregulated group compared with in the control group (Fig. 10C and D). Then, an RIP assay was performed to directly address whether linc00467 and EZH2 are binding partners. The RIP assay suggested that linc00467 was able to directly bind EZH2 in A549 and H1299 cells (Fig. 10E and 10F). In addition, a ChIP assay was used to verify that EZH2 bound to the promoter of HTRA3 (Fig. 10G). The results demonstrated that linc00467 repressed HTRA3 expression by binding with EZH2.	31180543	RID07757	interact with protein	metastasis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Lung adenocarcinoma	LINC00467	HTRA3	negatively-E	RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000170801	NA	84791	94031	C1orf97|MGC14801	Prsp|Tasp	Long intergenic non-coding RNA 00467 promotes lung adenocarcinoma proliferation, migration and invasion by binding with EZH2 and repressing HTRA3 expression.To validate the GEO and TCGA results, RT-qPCR assays were used to measure linc00467 expression in 35 paired LAD and adjacent normal lung tissues. The relative expression of lncRNA was calculated using the Cq value  method. The expression level of linc00467 in LAD tissues was increased compared with that in adjacent normal lung tissues (P<0.001; Fig. 2A). Then, the association between linc00467 expression and patients' clinical characteristics were evaluated (Table I). The linc00467 expression levels were significantly increased in patients with larger tumours compared with smaller tumours (P=0.013; Fig. 2B), and in those with more advanced TNM stages (P=0.021; Fig. 2C). However, there were no significant associations between linc00467 expression and other clinical parameters, including age, sex, differentiation, lymph node metastasis and smoking history.As linc00467 was confirmed to promote LAD cell proliferation in vitro, its effects on LAD cell migration and invasion was additionally investigated. A Transwell assay was used to evaluate the biological effect of linc00467 on the LAD cell metastasis. linc00467 knockdown significantly suppressed the migratory and invasive abilities of A549 and H1299 cells (Fig. 6A and B), while linc00467 overexpression increased the migratory and invasive abilities of PC9 cells (Fig. 6C). These results suggested that linc00467 promoted the migration and invasion of LAD cells.lncRNAs are able to bind RNA-binding proteins (RBPs) to regulate the expression of downstream genes. Therefore, the present study investigated whether linc00467 regulated HTRA3 expression by binding to RBPs. The probability of an interaction between linc00467 and RBPs was first determined using an lncRNA prediction website (http://annolnc.cbi.pku.edu.cn/index.jsp). The sequence of linc00467 was input into the AnnoLnc database, and entered into the protein interaction page; subsequently, the interaction score between lncRNA and protein could be predicted. The interaction score for linc00467 and EZH2 was 96.0705, close to the maximum value of 100. Whether linc00467 repressed HTRA3 transcription was next investigated by recruiting EZH2 to the HTRA3 promoter. EZH2 expression was first knocked down in A549 and H1299 cells using transfection with siRNA (Fig. 10A and B). In addition, western blotwas performed to measure HTRA3 protein expression levels when EZH2 was downregulated. The results indicated that HTRA3 protein expression levels were increased in the EZH2-downregulated group compared with in the control group (Fig. 10C and D). Then, an RIP assay was performed to directly address whether linc00467 and EZH2 are binding partners. The RIP assay suggested that linc00467 was able to directly bind EZH2 in A549 and H1299 cells (Fig. 10E and 10F). In addition, a ChIP assay was used to verify that EZH2 bound to the promoter of HTRA3 (Fig. 10G). The results demonstrated that linc00467 repressed HTRA3 expression by binding with EZH2.	31180543	RID07758	expression association	metastasis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(PAAD);DATA(GSE40174)
Oesophageal squamous cell carcinoma	IRF1-AS	ILF3	interact	luciferase reporter assay;RIP;RNA pull-down assays	downregulation	qRT-PCR	NA	NA	immunotherapies(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Oesophageal cancer	lncRNA	PCG	NA	NA	ENSG00000129351	NA	NA	3609	NA	CBTF|DRBF|DRBP76|MMP4|MPHOSPH4|MPP4|MPP4110|NF-AT-90|NF110|NF110b|NF90|NF90a|NF90b|NF90c|NF90ctv|NFAR|NFAR-1|NFAR-2|NFAR110|NFAR2|NFAR90|TCP110|TCP80	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response.The analysis of the expression changes in the lncRNAs indicated that 499 lncRNAs were upregulated and 495 lncRNAs were downregulated among the three IFN-beta-treated cell lines (Fig. 1A). To the best of our knowledge, the biological function of these IFN-regulated lncRNAs remains largely unknown (Fig. 1B). Among the upregulated lncRNAs (Fig. 1B), GAS5 has been previously reported to be regulated by the IFN pathway and play an antitumor role in ESCC [15]. Then, we confirmed the IFN-beta-mediated upregulation of the 6 top-ranked lncRNAs using RT-qPCR (Supplementary Fig. S3).To further confirm the tumor suppressive role of IRF1-AS, we stably overexpressed IRF1-AS in KYSE30 and KYSE180-cells (Fig. 3A). The CCK8 and colony formation assays showed that the overexpression of IRF1-AS impaired ESCC cell proliferation (Fig. 3B) and colony formation (Fig. 3C). The apoptosis analysis indicated that the overexpression of IRF1-AS promoted cisplatin-induced cell apoptosis in vitro (Fig. 3D). Further in vivo xenograft results showed that the IRF1-AS overexpression tumors exhibited decreased tumor volumes (Fig. 3E and F) and tumor weights (Fig. 3G). Furthermore, the IHC staining and TUNEL assays of the xenografts confirmed that the overexpression of IRF1-AS inhibited tumor growth and promoted tumor apoptosis (Fig. 3H). Altogether, these results demonstrate that IRF1-AS may inhibit tumor growth in vitro and in vivo by functioning as a tumor suppressive lncRNA.To further investigate the possible mechanism by which IRF1-AS upregulates IRF1, we performed RNA pull-down and mass spectrometry assays to detect IRF1-AS interacting proteins. According to the mass spectrometry results, we found that ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9) were enriched exclusively in the IRF1-AS group and ranked at the top (Fig. 4C). ILF3 and DHX9 are both located in the nucleus and have RNA-binding motifs [21,22]. Moreover, ILF3 and DHX9 are associated with each other and function as transcriptional co-activators [23]. Therefore, we hypothesized that IRF1-AS interacts with ILF3 and DHX9 to transcriptionally activate IRF1. Then, we immunoprecipitated endogenous ILF3 and DHX9 to determine whether ILF3 and DHX9 interact with IRF1-AS in vivo. IRF1-AS was detected in the complexes immunoprecipitated using both anti-ILF3 and anti-DHX9 antibodies (Fig. 4D).Subsequently, we analyzed the promoter sequence of IRF1-AS and identified several previously reported IRF1 binding core sequences (GAAAs) in this region (Supplementary Fig. S10A) [27]. Moreover, we used the Jaspar online database to predict the BSs of IRF1 in the IRF1-AS promoter. We found five predicted BSs in the IRF1-AS promoter region, all of which contain the IRF1 binding core sequence (Supplementary Fig. S10B). Then, we retrieved the ChIP-seq results using an anti-IRF1 antibody from the ENCODE project and found that IRF1 has binding peaks around the IRF1-AS promoter region in K562-cells following different stimulations (Fig. 5C). Then, we performed a ChIP-qPCR assay and found that IRF1 could indeed bind the IRF1-AS promoter (Fig. 5D). To further confirm that IRF1 could activate the transcription of IRF1-AS and determine the possible BSs, we constructed and inserted a wild-type and mutant IRF1-AS promoter sequence into a pGL4.10 vector containing luciferase genes. The mutant construction of the IRF1-AS promoter is shown in Fig. 5E. Predicted BSs 1 to 4 had overlapping regions; thus, we constructed a deletion mutation of these four BSs simultaneously. The results of the dual luciferase reporter gene assays showed that IRF1 remarkably increased the luciferase activity, and the deletion of the predicted BSs significantly decreased the luciferase activities (Fig. 5F). Taken together, these results indicate that IRF1 directly binds the IRF1-AS promoter and activates the transcription of IRF1-AS.	31173852	RID07759	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oesophageal squamous cell carcinoma	IRF1-AS	DHX9	interact	luciferase reporter assay;RIP;RNA pull-down assays	downregulation	qRT-PCR	NA	NA	immunotherapies(+);cell growth(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Oesophageal cancer	lncRNA	PCG	NA	NA	ENSG00000135829	NA	NA	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response.The analysis of the expression changes in the lncRNAs indicated that 499 lncRNAs were upregulated and 495 lncRNAs were downregulated among the three IFN-beta-treated cell lines (Fig. 1A). To the best of our knowledge, the biological function of these IFN-regulated lncRNAs remains largely unknown (Fig. 1B). Among the upregulated lncRNAs (Fig. 1B), GAS5 has been previously reported to be regulated by the IFN pathway and play an antitumor role in ESCC [15]. Then, we confirmed the IFN-beta-mediated upregulation of the 6 top-ranked lncRNAs using RT-qPCR (Supplementary Fig. S3).To further confirm the tumor suppressive role of IRF1-AS, we stably overexpressed IRF1-AS in KYSE30 and KYSE180-cells (Fig. 3A). The CCK8 and colony formation assays showed that the overexpression of IRF1-AS impaired ESCC cell proliferation (Fig. 3B) and colony formation (Fig. 3C). The apoptosis analysis indicated that the overexpression of IRF1-AS promoted cisplatin-induced cell apoptosis in vitro (Fig. 3D). Further in vivo xenograft results showed that the IRF1-AS overexpression tumors exhibited decreased tumor volumes (Fig. 3E and F) and tumor weights (Fig. 3G). Furthermore, the IHC staining and TUNEL assays of the xenografts confirmed that the overexpression of IRF1-AS inhibited tumor growth and promoted tumor apoptosis (Fig. 3H). Altogether, these results demonstrate that IRF1-AS may inhibit tumor growth in vitro and in vivo by functioning as a tumor suppressive lncRNA.To further investigate the possible mechanism by which IRF1-AS upregulates IRF1, we performed RNA pull-down and mass spectrometry assays to detect IRF1-AS interacting proteins. According to the mass spectrometry results, we found that ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9) were enriched exclusively in the IRF1-AS group and ranked at the top (Fig. 4C). ILF3 and DHX9 are both located in the nucleus and have RNA-binding motifs [21,22]. Moreover, ILF3 and DHX9 are associated with each other and function as transcriptional co-activators [23]. Therefore, we hypothesized that IRF1-AS interacts with ILF3 and DHX9 to transcriptionally activate IRF1. Then, we immunoprecipitated endogenous ILF3 and DHX9 to determine whether ILF3 and DHX9 interact with IRF1-AS in vivo. IRF1-AS was detected in the complexes immunoprecipitated using both anti-ILF3 and anti-DHX9 antibodies (Fig. 4D).Subsequently, we analyzed the promoter sequence of IRF1-AS and identified several previously reported IRF1 binding core sequences (GAAAs) in this region (Supplementary Fig. S10A) [27]. Moreover, we used the Jaspar online database to predict the BSs of IRF1 in the IRF1-AS promoter. We found five predicted BSs in the IRF1-AS promoter region, all of which contain the IRF1 binding core sequence (Supplementary Fig. S10B). Then, we retrieved the ChIP-seq results using an anti-IRF1 antibody from the ENCODE project and found that IRF1 has binding peaks around the IRF1-AS promoter region in K562-cells following different stimulations (Fig. 5C). Then, we performed a ChIP-qPCR assay and found that IRF1 could indeed bind the IRF1-AS promoter (Fig. 5D). To further confirm that IRF1 could activate the transcription of IRF1-AS and determine the possible BSs, we constructed and inserted a wild-type and mutant IRF1-AS promoter sequence into a pGL4.10 vector containing luciferase genes. The mutant construction of the IRF1-AS promoter is shown in Fig. 5E. Predicted BSs 1 to 4 had overlapping regions; thus, we constructed a deletion mutation of these four BSs simultaneously. The results of the dual luciferase reporter gene assays showed that IRF1 remarkably increased the luciferase activity, and the deletion of the predicted BSs significantly decreased the luciferase activities (Fig. 5F). Taken together, these results indicate that IRF1 directly binds the IRF1-AS promoter and activates the transcription of IRF1-AS.	31173852	RID07760	interact with protein	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Oesophageal squamous cell carcinoma	IRF1-AS	IRF1	positively-E	luciferase reporter assay;RIP;RNA pull-down assays	downregulation	qRT-PCR	NA	NA	immunotherapies(+);cell growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Oesophageal cancer	lncRNA	TF	NA	NA	ENSG00000125347	NA	NA	3659	NA	IRF-1|MAR	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response.The analysis of the expression changes in the lncRNAs indicated that 499 lncRNAs were upregulated and 495 lncRNAs were downregulated among the three IFN-beta-treated cell lines (Fig. 1A). To the best of our knowledge, the biological function of these IFN-regulated lncRNAs remains largely unknown (Fig. 1B). Among the upregulated lncRNAs (Fig. 1B), GAS5 has been previously reported to be regulated by the IFN pathway and play an antitumor role in ESCC [15]. Then, we confirmed the IFN-beta-mediated upregulation of the 6 top-ranked lncRNAs using RT-qPCR (Supplementary Fig. S3).To further confirm the tumor suppressive role of IRF1-AS, we stably overexpressed IRF1-AS in KYSE30 and KYSE180-cells (Fig. 3A). The CCK8 and colony formation assays showed that the overexpression of IRF1-AS impaired ESCC cell proliferation (Fig. 3B) and colony formation (Fig. 3C). The apoptosis analysis indicated that the overexpression of IRF1-AS promoted cisplatin-induced cell apoptosis in vitro (Fig. 3D). Further in vivo xenograft results showed that the IRF1-AS overexpression tumors exhibited decreased tumor volumes (Fig. 3E and F) and tumor weights (Fig. 3G). Furthermore, the IHC staining and TUNEL assays of the xenografts confirmed that the overexpression of IRF1-AS inhibited tumor growth and promoted tumor apoptosis (Fig. 3H). Altogether, these results demonstrate that IRF1-AS may inhibit tumor growth in vitro and in vivo by functioning as a tumor suppressive lncRNA.To further investigate the possible mechanism by which IRF1-AS upregulates IRF1, we performed RNA pull-down and mass spectrometry assays to detect IRF1-AS interacting proteins. According to the mass spectrometry results, we found that ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9) were enriched exclusively in the IRF1-AS group and ranked at the top (Fig. 4C). ILF3 and DHX9 are both located in the nucleus and have RNA-binding motifs [21,22]. Moreover, ILF3 and DHX9 are associated with each other and function as transcriptional co-activators [23]. Therefore, we hypothesized that IRF1-AS interacts with ILF3 and DHX9 to transcriptionally activate IRF1. Then, we immunoprecipitated endogenous ILF3 and DHX9 to determine whether ILF3 and DHX9 interact with IRF1-AS in vivo. IRF1-AS was detected in the complexes immunoprecipitated using both anti-ILF3 and anti-DHX9 antibodies (Fig. 4D).Subsequently, we analyzed the promoter sequence of IRF1-AS and identified several previously reported IRF1 binding core sequences (GAAAs) in this region (Supplementary Fig. S10A) [27]. Moreover, we used the Jaspar online database to predict the BSs of IRF1 in the IRF1-AS promoter. We found five predicted BSs in the IRF1-AS promoter region, all of which contain the IRF1 binding core sequence (Supplementary Fig. S10B). Then, we retrieved the ChIP-seq results using an anti-IRF1 antibody from the ENCODE project and found that IRF1 has binding peaks around the IRF1-AS promoter region in K562-cells following different stimulations (Fig. 5C). Then, we performed a ChIP-qPCR assay and found that IRF1 could indeed bind the IRF1-AS promoter (Fig. 5D). To further confirm that IRF1 could activate the transcription of IRF1-AS and determine the possible BSs, we constructed and inserted a wild-type and mutant IRF1-AS promoter sequence into a pGL4.10 vector containing luciferase genes. The mutant construction of the IRF1-AS promoter is shown in Fig. 5E. Predicted BSs 1 to 4 had overlapping regions; thus, we constructed a deletion mutation of these four BSs simultaneously. The results of the dual luciferase reporter gene assays showed that IRF1 remarkably increased the luciferase activity, and the deletion of the predicted BSs significantly decreased the luciferase activities (Fig. 5F). Taken together, these results indicate that IRF1 directly binds the IRF1-AS promoter and activates the transcription of IRF1-AS.	31173852	RID07761	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oesophageal squamous cell carcinoma	IRF1	IRF1-AS	positively-E	luciferase reporter assay;RIP;RNA pull-down assays	downregulation	qRT-PCR	NA	NA	immunotherapies(+);cell growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Oesophageal cancer	TF	lncRNA	ENSG00000125347	NA	NA	NA	3659	NA	IRF-1|MAR	NA	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response.The analysis of the expression changes in the lncRNAs indicated that 499 lncRNAs were upregulated and 495 lncRNAs were downregulated among the three IFN-beta-treated cell lines (Fig. 1A). To the best of our knowledge, the biological function of these IFN-regulated lncRNAs remains largely unknown (Fig. 1B). Among the upregulated lncRNAs (Fig. 1B), GAS5 has been previously reported to be regulated by the IFN pathway and play an antitumor role in ESCC [15]. Then, we confirmed the IFN-beta-mediated upregulation of the 6 top-ranked lncRNAs using RT-qPCR (Supplementary Fig. S3).To further confirm the tumor suppressive role of IRF1-AS, we stably overexpressed IRF1-AS in KYSE30 and KYSE180-cells (Fig. 3A). The CCK8 and colony formation assays showed that the overexpression of IRF1-AS impaired ESCC cell proliferation (Fig. 3B) and colony formation (Fig. 3C). The apoptosis analysis indicated that the overexpression of IRF1-AS promoted cisplatin-induced cell apoptosis in vitro (Fig. 3D). Further in vivo xenograft results showed that the IRF1-AS overexpression tumors exhibited decreased tumor volumes (Fig. 3E and F) and tumor weights (Fig. 3G). Furthermore, the IHC staining and TUNEL assays of the xenografts confirmed that the overexpression of IRF1-AS inhibited tumor growth and promoted tumor apoptosis (Fig. 3H). Altogether, these results demonstrate that IRF1-AS may inhibit tumor growth in vitro and in vivo by functioning as a tumor suppressive lncRNA.To further investigate the possible mechanism by which IRF1-AS upregulates IRF1, we performed RNA pull-down and mass spectrometry assays to detect IRF1-AS interacting proteins. According to the mass spectrometry results, we found that ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9) were enriched exclusively in the IRF1-AS group and ranked at the top (Fig. 4C). ILF3 and DHX9 are both located in the nucleus and have RNA-binding motifs [21,22]. Moreover, ILF3 and DHX9 are associated with each other and function as transcriptional co-activators [23]. Therefore, we hypothesized that IRF1-AS interacts with ILF3 and DHX9 to transcriptionally activate IRF1. Then, we immunoprecipitated endogenous ILF3 and DHX9 to determine whether ILF3 and DHX9 interact with IRF1-AS in vivo. IRF1-AS was detected in the complexes immunoprecipitated using both anti-ILF3 and anti-DHX9 antibodies (Fig. 4D).Subsequently, we analyzed the promoter sequence of IRF1-AS and identified several previously reported IRF1 binding core sequences (GAAAs) in this region (Supplementary Fig. S10A) [27]. Moreover, we used the Jaspar online database to predict the BSs of IRF1 in the IRF1-AS promoter. We found five predicted BSs in the IRF1-AS promoter region, all of which contain the IRF1 binding core sequence (Supplementary Fig. S10B). Then, we retrieved the ChIP-seq results using an anti-IRF1 antibody from the ENCODE project and found that IRF1 has binding peaks around the IRF1-AS promoter region in K562-cells following different stimulations (Fig. 5C). Then, we performed a ChIP-qPCR assay and found that IRF1 could indeed bind the IRF1-AS promoter (Fig. 5D). To further confirm that IRF1 could activate the transcription of IRF1-AS and determine the possible BSs, we constructed and inserted a wild-type and mutant IRF1-AS promoter sequence into a pGL4.10 vector containing luciferase genes. The mutant construction of the IRF1-AS promoter is shown in Fig. 5E. Predicted BSs 1 to 4 had overlapping regions; thus, we constructed a deletion mutation of these four BSs simultaneously. The results of the dual luciferase reporter gene assays showed that IRF1 remarkably increased the luciferase activity, and the deletion of the predicted BSs significantly decreased the luciferase activities (Fig. 5F). Taken together, these results indicate that IRF1 directly binds the IRF1-AS promoter and activates the transcription of IRF1-AS.	31173852	RID07762	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Gastric cancer	SNHG5	BAX	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000087088	NA	387066	581	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	BCL2L4	LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.SNHG5 expression in cisplatin-sensitive and cisplatin-resistant GC patients was determined. Patients with cisplatin-resistant GC had a higher level of SNHG5 relative to cisplatin-sensitive ones (Figure 1A). Identically, the cellular expression of SNHG5 was higher in cisplatin-resistant GC cells (BGC823/DDP and SGC7901/DDP) compared with that of parental GC cells (BGC823 and SGC7901) (Figure 1B).To clarify the role of SNHG5 in cisplatin-resistant GC, we examined cisplatin sensitivity in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. First of all, the transfection efficacy of si-SNHG5 was determined (Figure 2A). OD450 and IC50 markedly decreased in cisplatin-resistant GC cells transfected with si-SNHG5 (Figure 2B, C). Higher apoptotic rate was observed in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown (Figure 2D). It is indicated that SNHG5 silence enhanced cisplatin sensitivity in drug-resistant GC.Subsequently, we detected the regulatory effect of SNHG5 on parental GC cells. Transfection of pcDNA-SNHG5 sufficiently upregulated SNHG5 expression in GC cells (Figure 3A). Higher OD450 and IC50 were observed in cisplatin-induced GC cells overexpressing SNHG5 (Figure 3B, 3C). Moreover, SNHG5 overexpression greatly decreased cisplatin-induced GC cell apoptosis (Figure 3D). It is suggested that SNHG5 overexpression attenuated cisplatin sensitivity of GC cells.western blot and RT-PCRwere conducted to observe changes in apoptosis-specific and drug resistance-specific genes in GC cells. SNHG5 overexpression downregulated the mRNA level of Bax (Figure 4A) and upregulated Bcl-2 (Figure 4B) in GC cells. The mRNA levels of MDR1 and MRP1 increased by SNHG5 overexpression (Figure 4C, 4D). Identically, expression changes were similar at their protein levels (Figure 4E).	31173289	RID07763	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG5	MDR1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000109436	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.SNHG5 expression in cisplatin-sensitive and cisplatin-resistant GC patients was determined. Patients with cisplatin-resistant GC had a higher level of SNHG5 relative to cisplatin-sensitive ones (Figure 1A). Identically, the cellular expression of SNHG5 was higher in cisplatin-resistant GC cells (BGC823/DDP and SGC7901/DDP) compared with that of parental GC cells (BGC823 and SGC7901) (Figure 1B).To clarify the role of SNHG5 in cisplatin-resistant GC, we examined cisplatin sensitivity in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. First of all, the transfection efficacy of si-SNHG5 was determined (Figure 2A). OD450 and IC50 markedly decreased in cisplatin-resistant GC cells transfected with si-SNHG5 (Figure 2B, C). Higher apoptotic rate was observed in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown (Figure 2D). It is indicated that SNHG5 silence enhanced cisplatin sensitivity in drug-resistant GC.Subsequently, we detected the regulatory effect of SNHG5 on parental GC cells. Transfection of pcDNA-SNHG5 sufficiently upregulated SNHG5 expression in GC cells (Figure 3A). Higher OD450 and IC50 were observed in cisplatin-induced GC cells overexpressing SNHG5 (Figure 3B, 3C). Moreover, SNHG5 overexpression greatly decreased cisplatin-induced GC cell apoptosis (Figure 3D). It is suggested that SNHG5 overexpression attenuated cisplatin sensitivity of GC cells.western blot and RT-PCRwere conducted to observe changes in apoptosis-specific and drug resistance-specific genes in GC cells. SNHG5 overexpression downregulated the mRNA level of Bax (Figure 4A) and upregulated Bcl-2 (Figure 4B) in GC cells. The mRNA levels of MDR1 and MRP1 increased by SNHG5 overexpression (Figure 4C, 4D). Identically, expression changes were similar at their protein levels (Figure 4E).	31173289	RID07764	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Gastric cancer	SNHG5	MRP1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000113318	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.SNHG5 expression in cisplatin-sensitive and cisplatin-resistant GC patients was determined. Patients with cisplatin-resistant GC had a higher level of SNHG5 relative to cisplatin-sensitive ones (Figure 1A). Identically, the cellular expression of SNHG5 was higher in cisplatin-resistant GC cells (BGC823/DDP and SGC7901/DDP) compared with that of parental GC cells (BGC823 and SGC7901) (Figure 1B).To clarify the role of SNHG5 in cisplatin-resistant GC, we examined cisplatin sensitivity in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. First of all, the transfection efficacy of si-SNHG5 was determined (Figure 2A). OD450 and IC50 markedly decreased in cisplatin-resistant GC cells transfected with si-SNHG5 (Figure 2B, C). Higher apoptotic rate was observed in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown (Figure 2D). It is indicated that SNHG5 silence enhanced cisplatin sensitivity in drug-resistant GC.Subsequently, we detected the regulatory effect of SNHG5 on parental GC cells. Transfection of pcDNA-SNHG5 sufficiently upregulated SNHG5 expression in GC cells (Figure 3A). Higher OD450 and IC50 were observed in cisplatin-induced GC cells overexpressing SNHG5 (Figure 3B, 3C). Moreover, SNHG5 overexpression greatly decreased cisplatin-induced GC cell apoptosis (Figure 3D). It is suggested that SNHG5 overexpression attenuated cisplatin sensitivity of GC cells.western blot and RT-PCRwere conducted to observe changes in apoptosis-specific and drug resistance-specific genes in GC cells. SNHG5 overexpression downregulated the mRNA level of Bax (Figure 4A) and upregulated Bcl-2 (Figure 4B) in GC cells. The mRNA levels of MDR1 and MRP1 increased by SNHG5 overexpression (Figure 4C, 4D). Identically, expression changes were similar at their protein levels (Figure 4E).	31173289	RID07765	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Gastric cancer	SNHG5	BCL2	negatively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000171791	NA	387066	596	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	Bcl-2|PPP1R50	LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.SNHG5 expression in cisplatin-sensitive and cisplatin-resistant GC patients was determined. Patients with cisplatin-resistant GC had a higher level of SNHG5 relative to cisplatin-sensitive ones (Figure 1A). Identically, the cellular expression of SNHG5 was higher in cisplatin-resistant GC cells (BGC823/DDP and SGC7901/DDP) compared with that of parental GC cells (BGC823 and SGC7901) (Figure 1B).To clarify the role of SNHG5 in cisplatin-resistant GC, we examined cisplatin sensitivity in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. First of all, the transfection efficacy of si-SNHG5 was determined (Figure 2A). OD450 and IC50 markedly decreased in cisplatin-resistant GC cells transfected with si-SNHG5 (Figure 2B, C). Higher apoptotic rate was observed in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown (Figure 2D). It is indicated that SNHG5 silence enhanced cisplatin sensitivity in drug-resistant GC.Subsequently, we detected the regulatory effect of SNHG5 on parental GC cells. Transfection of pcDNA-SNHG5 sufficiently upregulated SNHG5 expression in GC cells (Figure 3A). Higher OD450 and IC50 were observed in cisplatin-induced GC cells overexpressing SNHG5 (Figure 3B, 3C). Moreover, SNHG5 overexpression greatly decreased cisplatin-induced GC cell apoptosis (Figure 3D). It is suggested that SNHG5 overexpression attenuated cisplatin sensitivity of GC cells.western blot and RT-PCRwere conducted to observe changes in apoptosis-specific and drug resistance-specific genes in GC cells. SNHG5 overexpression downregulated the mRNA level of Bax (Figure 4A) and upregulated Bcl-2 (Figure 4B) in GC cells. The mRNA levels of MDR1 and MRP1 increased by SNHG5 overexpression (Figure 4C, 4D). Identically, expression changes were similar at their protein levels (Figure 4E).	31173289	RID07766	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	ATXN8OS	miR-204	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);cell invasion(+)	sponge	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000230223	GRCh38_13:70107213-70171738	NA	NA	6315	NA	KLHL1AS|NCRNA00003|SCA8	NA	lncRNA ATXN8OS promotes breast cancer by sequestering miR-204.The expression of ATXN8OS in BC tissues and matched non-tumour tissues was analysed using RT-qPCR. The expression of ATXN8OS was found to be significantly higher in the human MDA-MB-231 and MCF-7 BC cell lines than in the MCF-10A normal breast cell line (Fig. 1A).To investigate the function of ATXN8OS in BC cells, MDA-MB-231 and MCF7 BC cells were transfected with si-ATXN8OS. RT-qPCR showed an efficient knockdown of ATXN8OS in the cell lines (Fig. 2A). The CCK-8 assay was used to measure the effect of ATXN8OS on the proliferation of human BC cells. Cell viability was reduced significantly in ATXN8OS-knockdown BC cells compared with the control knockdown cells (Fig. 2B and C). Flow cytometry analysis showed that transfection with si-ATXN8OS induced G0/G1 arrest and decreased the S phase population compared with the control knockdown (Fig. 2D and E). A Transwell assay was performed to determine whether ATXN8OS regulated BC cell invasion. Knockdown of ATXN8OS in cells reduced the number of invasive cells compared with the control knockdown (Fig. 2F and G).To explore the molecular mechanism of ATXN8OS in BC, StarBase V3.0 was used to predict the potential targets of ATXN8OS. The analysis revealed that ATXN8OS contains complementary binding sites to the 3'UTR of miR-204. RT-qPCR showed that the expression level of miR-204 was negatively correlated with the expression of ATXN8OS (P=0.0017; Fig. 3A). To identify the relationship between ATXN8OS and miR-204, the expression levels of miR-204 and its downstream genes in si-ATXN8OS BC cells were determined. The results demonstrated that the expression of miR-204 was significantly upregulated after knockdown of ATXN8OS in human MDA-MB-231 and MCF-7 BC cells (Fig. 3B). The expression of downstream targets of miR-204, including JAK2, FOXA1, ANGPT1 and TGFbetaR2, was significantly decreased after the inhibition of ATXN8OS in both of the human BC cell lines tested (Fig. 3C-E). To determine whether ATXN8OS suppresses miR-204 by directly binding miR-204 in BC cells, Wt ATXN8OS and Mut ATXN8OS sequences containing the target sites of miR-204 were cloned into a luciferase reporter system (Fig. 3F). The luciferase activity of Wt ATXN8OS was reduced in the BC cells containing the miR-204 mimic; however, the luciferase activity of Wt ATXN8OS was increased in the BC cells containing the miR-204 inhibitor (Fig. 3G).	31173245	RID07767	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Malignant glioma	GAS5	GSTM3	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000134202	NA	60674	2947	NCRNA00030|SNHG2	GST5	LncRNA GAS5 regulates the proliferation, migration, invasion and apoptosis of brain glioma cells through targeting GSTM3 expression. The effect of LncRNA GAS5 on glioma cells.The expression of GAS5 in normal brain tissue, primary glioma tissues (grade I, II, III and IV), normal HEB cells and glioma cells (U251 and U87) was detected by RT-qPCR. The results showed that the relative expression of GAS5 was significantly reduced in primary glioma tissues (grade I, II, III and IV) and compared to the normal brain tissue (p < 0.01, Fig. 1a). Furthermore, we observed lower CAS5 expression in glioma cells (U251 and U87) compared with the normal HEB cells (p < 0.01, Fig. 1b). There was no significant difference between both types of glioma cells (p > 0.05) (Fig. 1b). These results suggested lncRNA GAS5 was down-regulated in primary glioma tissue (grade I, II, III and IV) and glioma cells, suggesting that GAS5 may be involved in glioma pathogenesis.The cell migration (Fig. 2d) and invasion (Fig. 2e) was also determined after the transfection in both U251 and U87 cells. The result demonstrated a decreased cell migration and invasion rates in glioma cells overexpressing GAS5. In U251 cells, the migration and invasion rates were declined from 100% to around 70% and 75%, respectively (p < 0.01). Meanwhile, the migration and invasion rates were both dropped from 100% to around 73% in U87 cells following GAS5 overexpression (p < 0.01). Moreover, the effect of GAS5 overexpression on ROS production in glioma cells (U251 and U87) was detected using flow cytometry. Compared with the control group, GAS5 overexpression significantly enhanced ROS production (p < 0.01, Fig. 2f). These results indicated that overexpression of GAS5 inhibited the proliferation, migration and invasion and induced apoptosis and ROS production of glioma cells.Bioinformatics was used to predict the target site of GAS5, and the results indicated that GSTM3 possess a binding site structure for GAS5 (Fig. 3a). RT-qPCR and western blot were used to detect the expression of GSTM3 in primary glioma tissues (grade I, II, III and IV) and glioma cells (U251 cells and U87 cells), respectively. The results showed that the expression of GSTM3 was significantly up-regulated in primary glioma tissues (grade I, II, III and IV) compared to the normal brain tissue (p < 0.01, Fig. 3b). Additionally, we observed that GSTM3 in glioma cells (U251 cells and U87 cells) were higher than the normal HEB cells (p < 0.01, Fig. 3c, d). Luciferase reporter analysis was used to detect whether GSTM3 was the direct target for GAS5. The results indicated that GAS5 overexpression significantly reduced luciferase activity in wild -type GSTM3 transfected cells (p < 0.01), but had no effect on luciferase activity in mutated GSTM3 cell lines (p > 0.05) (Fig. 3e). Furthermore, the results of western blot indicated that GAS5 overexpression down-regulated the expression of GSTM3 in glioma cells (U251 cells and U87 cells) (p < 0.01, Fig. 3f).We further investigated the effects of GAS5 and GSTM3 on the growth of in vivo glioblastoma xenograft. Control vector, pcDNA-GAS5 vector, siNC, or GSTM3 siRNA were transfected into U251 cells. Subsequently, cells were subcutaneously injected into nude mice (n = 8) and the tumor sizes and volume were measured after 4 weeks. The results showed that pcDNA-GAS5 vector and GSTM3 siRNA significantly reduced the tumor volumes and weights compared to the control groups (p < 0.05, Fig. 5a-c). Therefore, similar to the in vitro results, we suggested that GAS5 inhibits the progression of glioma through repressing GSTM3 expression in vivo.	31172354	RID07768	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Laryngeal squamous cell carcinoma	PTCSC3	HOTAIR	negatively-E	siRNA;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	lncRNA	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000228630	GRCh38_12:53962308-53974956	100886964	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	LncRNA PTCSC3 inhibits cell proliferation in laryngeal squamous cell carcinoma by down-regulating lncRNA HOTAIR.Plasma levels of PTCSC3 in 66 LSCC patients and 52 healthy volunteers were measured by RT-qPCR. It was observed that plasma levels of PTCSC3 were significantly lower in LSCC patients compared with control group (Figure 1A, P<0.05). Diagnostic values of plasma PTCSC3 for LSCC were evaluated by ROC curve analysis. As shown in Figure 1B, area under the curve was 0.91, with standard error of 0.026 and 95% confidence interval of 0.85'-.96 (Figure 1B).PTCSC3 and HOTAIR overexpression were performed in cells of UM-SCC-17A cell line (Figure 3A, P<0.05). Comparing with control cells (C) and NC cells (NC), overexpression of PTCSC3 led to significantly inhibited expression of HOTAIR in cells of UM-SCC-17A (Figure 3B, P<0.05). In addition, PTCSC3 was not significantly affected by HOTAIR overexpression (Figure 3C, P<0.05).Comparing with NC and C two controls, groups, PTCSC3 overexpression mediated the inhibited, while HOTAIR overexpression mediated the promoted proliferation of LSCC cells (Figure 4, P<0.05). In addition, HOTAIR overexpression attenuated the inhibitory effects of PTCSC3 overexpression on cancer cell proliferation (P<0.05). However, cancer cell invasion and migration were not significantly affected by PTCSC3 overexpression (data not shown).	31171714	RID07769	expression association	NA	UP(SKCM);DATA(GSE38495)	
Cervical cancer	LINC00958	RRM2	positively-E	luciferase reporter assay;RIP;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	radioresistance(+);cell proliferation(+);cell growth(+)	ceRNA(miR-5095)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000171848	NA	100506305	6241	NA	C2orf48|FLJ25102	Long noncoding RNA LINC00958 regulates cell sensitivity to radiotherapy through RRM2 by binding to microRNA-5095 in cervical cancer.The expression of LINC00958 in cervical cancer tissue of the radiation-resistant group and the radiation-sensitive group were determined by RT-qPCR. As shown in Figure 1e, LINC00958 concentration was higher in the radiation- resistant group than that in the radiation-sensitive group.In comparison to the cells transfected with scramble siRNA, the cell proliferation was evidently decreased in those transfected with sh-LINC00958, which was even decreased in those transfected with sh-LINC00958 and exposed to 6 Gy X-ray irradiation. Then flow cytometry was applied to determination Hela cell apoptosis (Figure 2d,e). The apoptosis rate was increased after sh-LINC00958 treatment than after scramble siRNA treatment, and the apoptosis rate of cells following both of sh-LINC00958 transfection and 6 Gy X-ray irradiation was much higher than that of cells following sh- LINC00958 transfection alone. western blotwas performed to analyze the expression of apoptosis-related proteins (caspase-3 a n d c a s p a s e-8; Figure 2f). The expression levels of caspase-3 a n d c a s p a s e-8 were highest in the cells following combined treatment of sh-LINC00958 and 6 Gy X-ray irradiation and lowest in the cell regarded as NC. These results provided strong evidence that cell proliferation could be suppressed and apoptosis could be elevated by combining radiotherapy with LINC00958 silencing in cervical cancer cells.The subcellular localization and expression of LINC00958 in Hela cells were analyzed by FISH assay and RT-qPCR respectively (Figure 3a,b). The results showed that LINC00958 was mainly distributed in the cytoplasm of Hela cells. The targeting relationship between LINC00958 and miR-5095 as well as miR-5095 and RRM2 were determined by a dual-luciferase reporter assay (Figure 3c,d). Results from the assays showed that LINC00958 could regulate miR-5095 and in turn, miR-5095 could regulate RRM2 by possibly binding to its 3'-UTR, suggesting that miR- 5095 and RRM2 might be implicated in regulating cervical cancer cell sensitivity to radiotherapy by LINC00598. In addition, RIP and RNA pull-down analysis (Figure 3e,f) also indicated that LINC00958 could specifically bind to the AGO2 protein. To further confirm that LINC00598 could regulate the expression of miR-5095 and RRM2, the levels of miR-5095 and RRM2 in Hela cells transfected with sh-LINC00958 were determined by RT- qPCR (Figure 3g). The cells treated with sh-LINC00958 exhibited obviously reduced LINC00958 expression and elevated miR-5095 expression versus those. These results provided evidence that the LINC00958/miR-5095/RRM2 axis was associated with cervical cancer cell sensitivity to radiotherapy.The SF of Hela cells was then assessed by plate clone formation assay (Figure 5f), which showed that under the same condition of 6 Gy X-ray irradiation, upregulation of miR- 5095 decreased SF, which was elevated after miR-5095 downregulation. Next, flow cytometry (Figure 5d,e) and western blot(Figure 5g) were used to evaluate apoptosis of Hela cells after different treatments. The apoptosis rate was found to be higher in the cells following miR-5095 mimic transduction combined 6 Gy X-ray irradiation with elevated levels of caspase-3 a n d c a s p a s e-8 and to be lower in those following miR-5095 inhibitor transduction combined 6 Gy X-ray irradiation with reduced levels of caspase-3 a n d c a s p a s e-8, than that of the cells following scramble siRNA transduction combined 6 Gy X-ray irradiation These results provided sufficient evidence that repressed cell proliferation and induced cell apoptosis could be achieved through upregulation of miR- 5095, which could, in turn, downregulate RRM2, thereby promoting cervical cancer cell sensitivity to radiotherapy.We performed a tumorigenicity assay to examine the effect of LINC00958 on the tumor formation ability of Hela cells in nude mice. The image of the xenograft tumor is shown in Figure 6a. As shown in Figure 6b,c, in relation to the mice served as NC, the tumor volume and tumor weight were lower in those treated with scramble siRNA and 6 Gy X-ray irradiation, and were, even more, lower in those treated with sh- LINC00958 and 6 Gy X-ray irradiation. These results provided evidence that the tumorigenic ability of cervical cancer cells was weakened by LINC00958 silencing in combination with radiotherapy.	31169309	RID07770	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Papillary thyroid carcinoma	n384546	AKT3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	NA	NA	ENSG00000117020	NA	NA	10000	NA	PKBG|PRKBG|RAC-gamma	A novel lncRNA n384546 promotes thyroid papillary cancer progression and metastasis by acting as a competing endogenous RNA of miR-145-5p to regulate AKT3.For further select the lncRNA which plays critical roles in the initiation and progression of PTC, the expression of seven lncRNAs which have significant difference in previous validation experience was analyzed in tissues of another 53 PTC patients using qRT-PCR Results showed that n384546 was the most significantly dysregulated lncRNA in PTC tissues compared with adjacent normal thyroid tissue (Fig. 1c, d). The noncode v5.0 database shows that n384546 is a 3513-bp transcript with two exons and is localized on the reverse strand of chromosome 4: 172987196'-72995762, and its expression in thyroid is the highest of all human tissues in the Human Body Map (Fig. S1). In addition, transwell assays and wound healing assays were implemented to determine migration and invasion ability of PTC cells. As shown in Fig. 3a-c, after transfection of Gapmer-n384546, the migration and invasion abilities were both significantly inhibited in B-CPAP and KTC-1 cells compared with Scrambled Gapmer transfection. Moreover, western blotshowed that the protein level of E-cadherin was remarkably increased while N-cadherin was decreased in Gapmer-n384546 transfected cells compared with Scrambled Gapmer transfected cells. This indicated that EMT ability was inhibited after knockdown of n384546, which was consistent with the previous results (Fig. -(Fig.3d3d).To characterize whether n384546 exerted its function through miR-145-5p in PTC cell lines, we co-transfected Gapmer-n384546 and anti-miR-145 or mimic-miR-145 into the B-CPAP and KTC-1 cells. As shown in Fig. -Fig.5,5, the proliferation, migration, and invasion abilities of Gapmer-n384546 or mimic-miR-145 transfected cells were decreased compared with Scrambled Gapmer transfected cells. Also, the percentage of apoptotic cells in Gapmer-n384546 or mimic-miR-145 transfected cells increased. These results revealed that mimic-miR-145 had the similar effect on proliferation, apoptosis, migration, and invasion of PTC cells as Gapmer-n384546. The inhibition of cell proliferation and viability induced by Gapmer-n384546 was partially reversed by anti-miR-145 co-transfection in both B-CPAP and KTC-1 cells (Fig. 5a, b, Fig. S3), and the effect of Gapmer-n384546 on cell apoptosis could also be reversed by anti-miR-145 (Fig. -(Fig.5c).5c). Transwell and wound healing assays showed suppression of migration and invasion abilities in PTC cells induced by Gapmer-n384546 were partially reversed by anti-miR-145 (Fig. 5d , Fig. S4). western blotshowed that effect of Gapmer-n384546 on apoptosis-related proteins and EMT-related proteins could be reversed by anti-miR-145 (Fig. -(Fig.5g).5g). These results suggested that the function of n384546 in PTC partially rely on miR-145-5p.In view of these results, we tried to predicted possible target genes of miR-145-5p. A previous study showed Akt signaling was inhibited after miR-145 overexpression in thyroid cancer cells, while AKT3 is a target of miR-14521. Another study reported that overexpression of miR-145 could inhibit cell proliferation by targeting DUSP6 in thyroid cancer20. By using the Targetscan database and miRanda algorithms, we found that 3'UTR regions of AKT3 and DUSP6 both have the predicted binding sites of miR-145-5p (Fig. -(Fig.6a).6a). This result is consistent with previous reports that AKT3 and DUSP6 are target genes of miR-145-5p21,24. We further examined the expression levels of AKT3 and DUSP6 in Scrambled Gapmer and Gapmer-n384546 transfected cells. Transfection of Gapmer-n384546 significantly decreased AKT3 expression in both mRNA and protein levels compared with Scrambled Gapmer (Fig. 6b, c). But the expression of DUSP6 did not change after Gapmer-n384546 transfection (Fig. S5). Furthermore, qRT-PCRanalysis showed that AKT3 was significantly upregulated in the PTC specimens compared with normal specimens in PTC patients (Fig. -(Fig.6d).6d). In addition, AKT3 expression was higher in PTC cells compared with Nthy-ori 3-1 cells (Fig. -(Fig.6e6e).Then, we used a dual-luciferase reporter assay to verify that n384546 regulates AKT3 expression by sponging miR-145-5p. As shown in Fig. -Fig.6h,6h, transfection of Gapmer-n384546 could significantly reduce the luciferase activity of AKT3 3'UTR compared with Scrambled Gapmer. The Gapmer-n384546 induced loss of AKT3 could efficiently be reversed by co-transfection of anti-miR-145. However, the upregulation of AKT3 3'UTR luciferase activity induced by anti-miR-145 could not be reversed by co-transfection of Gapmer-n384546. These results indicated that knockdown of n384546 could not decrease the AKT3 activity after inhibition of miR-145-5p, which confirmed that n384546 regulated the expression and activity of AKT3 by sponging miR-145-5p.	31160577	RID07771	ceRNA or sponge	metastasis		DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Cervical cancer	GHET1	E2F6	positively-F	knockdown;siRNA;overexpression;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);epithelial to mesenchymal transition(+);AKT/mTOR signaling pathway(+);WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000169016	NA	102723099	1876	lncRNA-GHET1	E2F-6	LncRNA GHET1 promotes cervical cancer progression through regulating AKT/mTOR and Wnt/beta-catenin signaling pathways.We proposed to examine the biological role of GHET1 in Cervical cancer (CC) and the underlying mechanism and validated the up-regulated expression of GHET1 in CC cell lines. Loss-of-function assays demonstrated that down-regulation of GHET1 inhibited cell growth, migration and epithelial-to-mesenchymal transition (EMT) in CC. Furthermore, we validated that GHET1 down-regulation could inactivate AKT/mTOR and Wnt/beta-catenin pathways, and that respective activation of these two pathways abrogated the inhibitive effect of GHET1 knockdown on CC cell growth, migration and EMT . Moreover, we unfolded a preliminary investigation on the modulation of GHET1 on AKT/mTOR and Wnt/beta-catenin pathways. We found that GHET1 stabilized E2F6 mRNA through interacting with IGF2BP2, so as to regulate the activity of AKT/mTOR and Wnt/beta-catenin pathways. Rescue assays also proved that GHET1 regulated these two pathways and CC cell growth, migration and EMT through E2F6. In conclusion, we revealed that down-regulation of GHET1 suppresses cervical cancer progression through regulating AKT/mTOR and Wnt/beta-catenin signaling pathways, indicating GHET1 as a promising molecular biomarker for CC treatment improvement.	31682716	RID07772	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Retinoblastoma	TCL6	PTEN	positively-E	siRNA;overexpression;luciferase reporter assay	downregulation	qPCR	GSE53757;GSE46699	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000187621	GRCh38_14:95650498-95679833	ENSG00000171862	NA	27004	5728	TCL6e1|TNG1|TNG2	BZS|MHAM|MMAC1|PTEN1|TEP1	Long non-coding RNA T-cell leukemia/lymphoma 6 serves as a sponge for miR-21 modulating the cell proliferation of retinoblastoma through PTENwe found the expression of lncRNA T-cell leukemia/lymphoma 6 (TCL6) was significantly downregulated in Rb tissues and cell lines. Knockdown of lncRNA TCL6 promoted cell proliferation while reduced cell apoptosis in Rb cells. Moreover, lncRNA TCL6 serves as a sponge for miR-21, a previously-reported oncogenic miRNA in Rb, by direct targeting to negatively regulated miR-21 expression, therefore modulating Rb proliferation through miR-21. TCL6 overexpression inhibited Rb cell proliferation while miR-21 overexpression exerted an opposing effect; the effect of TCL6 overexpression was partially attenuated by miR-21 overexpression. PTEN/PI3K/AKT signaling pathway was involved in lncRNA TCL6/miR-21 axis modulating Rb cell proliferation. Taken together, lncRNA TCL6 serves as a tumor suppressor by acting as a sponge for miR-21 to counteract miR-21-mediated PTEN repression.	31680766	RID07773	ceRNA or sponge	NA	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Thyroid cancer	FOXD3-AS1	PCNA	negatively-E	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000132646	NA	100996301	5111	pasFOXD3	NA	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayThe expression of FOXD3-AS1 and miR-296-5p in thyroid cancer tissues and cells was detected through qRT-PCRThe expression of FOXD3-AS1 in thyroid cancer tissues was much higher than that in normal tissues.Specific shRNA targeting FOXD3-AS1 was transfected into FTC-133 cells and transfection efficiency was detected through qRT-PCRThe knockdown of FOXD3-AS1 largely suppressed clone formation compared with the control.The western blotin Fig.2D-2F showed that the expression of PCNA,cyclinD1,CDK4 was increased and the level of p27 was decreased compared with the control.Thus, we revealed that inhibition of LncRNA FOXD3-AS1 suppressed cell proliferation in thyroid cancer cells.	31678422	RID07774	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Thyroid cancer	FOXD3-AS1	CCND1	negatively-E	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000110092	NA	100996301	595	pasFOXD3	BCL1|D11S287E|PRAD1|U21B31	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayThe expression of FOXD3-AS1 and miR-296-5p in thyroid cancer tissues and cells was detected through qRT-PCRThe expression of FOXD3-AS1 in thyroid cancer tissues was much higher than that in normal tissues.Specific shRNA targeting FOXD3-AS1 was transfected into FTC-133 cells and transfection efficiency was detected through qRT-PCRThe knockdown of FOXD3-AS1 largely suppressed clone formation compared with the control.The western blotin Fig.2D-2F showed that the expression of PCNA,cyclinD1,CDK4 was increased and the level of p27 was decreased compared with the control.Thus, we revealed that inhibition of LncRNA FOXD3-AS1 suppressed cell proliferation in thyroid cancer cells.	31678422	RID07775	expression association	NA		UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Thyroid cancer	FOXD3-AS1	DCTN6	positively-E	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000104671	NA	100996301	10671	pasFOXD3	WS-3	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayThe expression of FOXD3-AS1 and miR-296-5p in thyroid cancer tissues and cells was detected through qRT-PCRThe expression of FOXD3-AS1 in thyroid cancer tissues was much higher than that in normal tissues.Specific shRNA targeting FOXD3-AS1 was transfected into FTC-133 cells and transfection efficiency was detected through qRT-PCRThe knockdown of FOXD3-AS1 largely suppressed clone formation compared with the control.The western blotin Fig.2D-2F showed that the expression of PCNA,cyclinD1,CDK4 was increased and the level of p27 was decreased compared with the control.Thus, we revealed that inhibition of LncRNA FOXD3-AS1 suppressed cell proliferation in thyroid cancer cells.	31678422	RID07776	expression association	NA		DOWN(LIHC,PRAD);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Thyroid cancer	FOXD3-AS1	MMP2	positively-E	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000087245	NA	100996301	4313	pasFOXD3	CLG4|CLG4A|TBE-1	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayThe expression of FOXD3-AS1 and miR-296-5p in thyroid cancer tissues and cells was detected through qRT-PCRThe expression of FOXD3-AS1 in thyroid cancer tissues was much higher than that in normal tissues.western blot showed that the expression of MMP-2 and MMP-9 was decreased and the level of TIMP-1 was increased compared with the control. Thus, the above results showed that inhibition of LncRNA FOXD3-AS1 suppressed cell invasion and migration in thyroid cancer cells.	31678422	RID07777	expression association	NA		UP(PAAD);DATA(GSE40174)
Thyroid cancer	FOXD3-AS1	MMP9	negatively-E	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000230798	GRCh38_1:63320878-63324441	ENSG00000100985	NA	100996301	4318	pasFOXD3	CLG4B	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayThe expression of FOXD3-AS1 and miR-296-5p in thyroid cancer tissues and cells was detected through qRT-PCRThe expression of FOXD3-AS1 in thyroid cancer tissues was much higher than that in normal tissues.western blot showed that the expression of MMP-2 and MMP-9 was decreased and the level of TIMP-1 was increased compared with the control. Thus, the above results showed that inhibition of LncRNA FOXD3-AS1 suppressed cell invasion and migration in thyroid cancer cells.	31678422	RID07778	expression association	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Thyroid cancer	FOXD3-AS1	miR-296-5p	negatively-F	luciferase reporter assay;shRNA;siRNA;miRanda;Targetscan;MicrocosmTargets	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+);TGF-beta/SMAD signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000230798	GRCh38_1:63320878-63324441	NA	NA	100996301	NA	FAST|pasFOXD3	NA	Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathwayWe found that the expression of lncRNA FOXD3-AS1was upregulated and it had negative correlation with the level of miR-296-5p in thyroid cancer tissues and cells. LncRNA FOXD3-AS1 knockdown effectively suppressed cell proliferation and cell invasion in vitro.Further study revealed that miR-296-5p was a target of lncRNA FOXD3-AS1 and FOXD3-AS1 exerted anti-tumor effect through up-regulating miR-296-5p. Moreover, we found that FOXD3-AS1 knockdown suppressed the aggressive biological behaviors of thyroid cancer through inactivating the TGF-beta1/Smads signaling pathway. Subsequently, the in vivo experiments further verified that the FOXD3-AS1/miR-296-5p axis exerted obvious anti-tumor effect through inhibiting tumor growth and metastasis and the TGF-beta1/Smads signaling pathway was also inactivated in vivo by the inhibition of FOXD3-AS1.Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathway.	31678422	RID07779	ceRNA or sponge	metastasis		
Prostate cancer	NEAT1	ACSL4	positively-E	RIP;dual-luciferase reporter assay;shRNA;starBase;miRcode;Targetscan;miRDB;overexpression	upregulation	qRT-PCR	Oncomine	NA	cell proliferation(+);cell invasion(+);chemoresistance(+)	ceRNA(miR-34a-5p,miR-204-5p)	association	NA	Docetaxel	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000068366	NA	283131	2182	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ACS4|FACL4|LACS4|MRX63|MRX68	LncRNA NEAT1 promotes docetaxel resistance in prostate cancer by regulating ACSL4 via sponging miR-34a-5p and miR-204-5p.NEAT1 was expressed at high levels in docetaxel-resistant prostate cancer (PCa) clinical samples and related cell lines. When knockdown NEAT1, cell proliferation and invasion in docetaxel-resistant PCa cells in vitro and in vivo were downregulated.we identified miR-34a-5p and miR-204-5p were co-expressed miRNAs formed complementary base pairing with NEAT1.The possible target of miR-34a-5p and miR-204-5p were predicted using two online prediction tools:Targetscan and miRDB.Only 18 target-genes were found in above two databases after Venn analysis.Finally, ACSL4 were found significantly increased in PC3-DR and DU145-DR cells, compared to non-resistant cell lines.Innovatively, we concluded that NEAT1 contributes to the docetaxel resistance by increasing ACSL4 via sponging miR-34a-5p and miR-204-5p in PCa cells.	31672604	RID07780	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Pancreatic cancer	SNHG16	SREBF2	positively-E	shRNA;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-195)	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000198911	NA	100507246	6721	Nbla10727|Nbla12061|ncRAN	bHLHd2|SREBP2	LncRNA SNHG16 induces the SREBP2 to promote lipogenesis and enhance the progression of pancreatic cancer. The proliferation, migration, invasion and lipogenesis were determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, transwell and Oil Red O staining assays, respectively. The interactions among lncRNA SNHG16, miR-195 and SREBP2 were analyzed by dual-luciferase reporter assays.Both the knock down of lncRNA SNHG16 and SREBP2 and overexpression of miR-195 suppressed the proliferation, migration, invasion and lipogenesis in pancreatic cancer cells. LncRNA SNHG16 directly spongedmiR-195 to modulate the lipogenesis via regulating the expression of SREBP2.LncRNA SNHG16 accelerated the development of pancreatic cancer and promoted lipogenesis via directly regulating miR-195/SREBP2 axis.	31664866	RID07781	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	XIST	MDR1	positively-E	shRNA;miRcode;dual-luciferase reporter assay;RIP;RNA pull-down assay;overexpression	upregulation	RT-qPCR	NA	NA	chemoresistance(+);chemosensitivity(-);cell survival(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-144-3p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000109436	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Upregulation of Long Noncoding RNA (lncRNA) X-Inactive Specific Transcript (XIST) is Associated with Cisplatin Resistance in Non-Small Cell Lung Cancer (NSCLC) by Downregulating MicroRNA-144-3pThis study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.Tissue samples were from patients with NSCLC who responded cisplatin (DDP-sensitive) (n=24), patients with NSCLC unresponsive to cisplatin (DDP-resistant) (n=30), and normal lung tissue (n=25). In H460/DDP and A549/DDP cells, expression of XIST, microRNA (miR)-144-3p, MDR1, and multidrug resistance-associated protein 1 (MRP1) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot. The MTT assay measured cell survival and proliferation, a transwell assay evaluated cell migration, and flow cytometry measured apoptosis. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays examined the relationship between XIST and miR-144-3p. Tumor xenografts from A549/DDP cells were studied in BALB/c nude mice.In tissue from patients with DDP-resistant NSCLC and the mouse A549/DDP tumor xenograft, lncRNA-XIST expression was upregulated and miR-144-3p expression was inhibited. In A549/DDP and H460/DDP cells, downregulation of lncRNA-XIST and upregulation of miR-144-3p reduced cell survival, proliferation, migration, induced apoptosis and suppressed MDR1 and MRP1 expression.Upregulation of lncRNA-XIST was associated with cisplatin resistance in NSCLC by downregulating miRNA-144-3p in H460/DDP and A549/DDP cells, a murine A549/DDP tumor xenograft, and human tumor tissues from patients with cisplatin-resistant NSCLC.	31659146	RID07782	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Non-small cell lung cancer	XIST	MRP1	positively-E	shRNA;miRcode;dual-luciferase reporter assay;RIP;RNA pull-down assay;overexpression	upregulation	RT-qPCR	NA	NA	chemoresistance(+);chemosensitivity(-);cell survival(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-144-3p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000113318	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	Upregulation of Long Noncoding RNA (lncRNA) X-Inactive Specific Transcript (XIST) is Associated with Cisplatin Resistance in Non-Small Cell Lung Cancer (NSCLC) by Downregulating MicroRNA-144-3pThis study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.Tissue samples were from patients with NSCLC who responded cisplatin (DDP-sensitive) (n=24), patients with NSCLC unresponsive to cisplatin (DDP-resistant) (n=30), and normal lung tissue (n=25). In H460/DDP and A549/DDP cells, expression of XIST, microRNA (miR)-144-3p, MDR1, and multidrug resistance-associated protein 1 (MRP1) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot. The MTT assay measured cell survival and proliferation, a transwell assay evaluated cell migration, and flow cytometry measured apoptosis. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays examined the relationship between XIST and miR-144-3p. Tumor xenografts from A549/DDP cells were studied in BALB/c nude mice.In tissue from patients with DDP-resistant NSCLC and the mouse A549/DDP tumor xenograft, lncRNA-XIST expression was upregulated and miR-144-3p expression was inhibited. In A549/DDP and H460/DDP cells, downregulation of lncRNA-XIST and upregulation of miR-144-3p reduced cell survival, proliferation, migration, induced apoptosis and suppressed MDR1 and MRP1 expression.Upregulation of lncRNA-XIST was associated with cisplatin resistance in NSCLC by downregulating miRNA-144-3p in H460/DDP and A549/DDP cells, a murine A549/DDP tumor xenograft, and human tumor tissues from patients with cisplatin-resistant NSCLC.	31659146	RID07783	ceRNA or sponge	chemoresistance	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	
Hepatocellular carcinoma	LINC00467	TRAF5	positively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-);cancer progression(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000082512	NA	84791	7188	C1orf97|MGC14801	RNF84	LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinomaLINC00467 expression was examined by a quantitative reverse transcriptase-polymerase chain reaction. CCK-8, EdU, transwell, western blot and caspase-3 activity analyses were utilized to testify the role of LINC00467 in Hepatocellular carcinoma (HCC). The interaction between IGF2BP3 and LINC00467 (or TRAF5) was investigated by luciferase reporter, RIP and RNA pull-down assays.LINC00467 upregulation in HCC tissues and cells was observed. LINC00467 silencing suppressed cell proliferation and metastasis, whereas it facilitated cell apoptosis in HCC. The gene for tumor necrosis factor receptor-associated factor 5 (TRAF5) was a neighboring gene of that for LINC00467 and its expression was positively modulated by LINC00467 in HCC. TRAF5 knockdown inhibited HCC progression. LINC00467 deficiency could decrease the mRNA stability of TRAF5 in HCC. Insulin-like growth factor-2 messenger RNA-binding protein 3 (IGF2BP3) could bind with LINC00467 and its depletion could lower TRAF5 mRNA stability in HCC. Final rescue assays further indicated that downregulation of IGF2BP3 or TRAF5 acted against LINC00467 upregulation-mediated function on HCC progression.LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in HCC.	31656043	RID07784	expression association	metastasis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC00467	IGF2BP3	positively-F	shRNA;starBase;overexpression;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-);cancer progression(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000136231	NA	84791	10643	C1orf97|MGC14801	CT98|IMP-3|IMP3	LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinomaLINC00467 expression was examined by a quantitative reverse transcriptase-polymerase chain reaction. CCK-8, EdU, transwell, western blot and caspase-3 activity analyses were utilized to testify the role of LINC00467 in Hepatocellular carcinoma (HCC). The interaction between IGF2BP3 and LINC00467 (or TRAF5) was investigated by luciferase reporter, RIP and RNA pull-down assays.LINC00467 upregulation in HCC tissues and cells was observed. LINC00467 silencing suppressed cell proliferation and metastasis, whereas it facilitated cell apoptosis in HCC. The gene for tumor necrosis factor receptor-associated factor 5 (TRAF5) was a neighboring gene of that for LINC00467 and its expression was positively modulated by LINC00467 in HCC. TRAF5 knockdown inhibited HCC progression. LINC00467 deficiency could decrease the mRNA stability of TRAF5 in HCC. Insulin-like growth factor-2 messenger RNA-binding protein 3 (IGF2BP3) could bind with LINC00467 and its depletion could lower TRAF5 mRNA stability in HCC. Final rescue assays further indicated that downregulation of IGF2BP3 or TRAF5 acted against LINC00467 upregulation-mediated function on HCC progression.LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in HCC.	31656043	RID07785	expression association	metastasis	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495)
Osteosarcoma	TUSC7	MIR211	negatively-F	siRNA;overexpression;dual-luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+);colony formation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000207702	NA	285194	406993	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	MIRN211|mir-211	Long non-coding RNA TUSC7 suppresses osteosarcoma by targeting miR-211After normalization to paired non-tumor tissues, miR-211 was shown to be significantly up-regulated in osteosarcoma tissues and TUSC7 was significantly down-regulated in osteosarcoma tissue.The suppressive role of TUSC7 was also revealed by invasion and colony formation assay, whereby TUSC7 overexpression inhibited cell invasion and colony formation. Meanwhile, overexpression and down-regulation of TUSC7 induced and reduced apoptosis, respectively, in both MG63 and HOS cell lines .The dual-luciferase reporter assay indicated that the relative luciferase activity was decreased in HEK293T transfection with wild-type vector via enhanced miR-211 expression, and the foregoing inhibition was recovered by Mut vector. These results suggested that TUSC7 is a specific target gene of miR-211.In sum, we reported that miR-211 is up-regulated in osteosarcoma and it demonstrates negative correlation with TUSC7 levels. TUSC7 acts as a tumor suppressor in osteosarcoma. miR-211 and TUSC7 are likely to be promising new therapeutic targets in osteosarcoma.	31652435	RID07786	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Colorectal cancer	LINC01234	KLF6	negatively-E	siRNA;overexpression;knockdown;immunohistochemistry	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell viability(+);colony formation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249550	GRCh38_12:113583886-113773726	ENSG00000067082	NA	100506465	1316	onco-lncRNA-32	BCD1|COPEB|CPBP|GBF|PAC1|ST12|Zf9	Upregulated Long Noncoding RNA LINC01234 Predicts Unfavorable Prognosis for Colorectal Cancer and Negatively Correlates With KLF6 ExpressionWe tested mRNA levels using quantitative reverse transcription PCR (qRT-PCR. Tissue samples from patients with CRC, inflammatory bowel disease (IBD), hyperplastic polyp, and adenoma were included. Correlations between clinicopathological parameters, overall survival (OS) rate, and LINC01234 were analyzed using Kruskal-Wallis H test. Additionally, cell proliferation, apoptosis, and tumor formation in nude mice were tested to investigate the mechanism of LINC01234. western blot was used to determine protein levels.LINC01234 expression was significantly upregulated in CRC tissues and CRC cell lines than in non-tumor tissues and normal epithelial cells, respectively. LINC01234 was associated with high tumor stage, larger tumor size, and metastasis. Patients with higher LINC01234 expression showed reduced OS. Cell proliferation was inhibited by LINC01234 knockdown, whereas apoptosis was enhanced. Mice injected with SW480 cells with LINC01234 knockdown displayed decreased tumor volume, weight, and Ki-67 levels compared with those injected with control cells. KLF6 was negatively regulated by LINC01234. Overexpression of KLF6 showed effects similar to those observed following LINC01234 knockdown on cell proliferation and apoptosis.LINC01234 could be a prognostic biomarker in CRC patients. Upregulation of LINC01234 in CRC promotes tumor development through negative regulation of KLF6.	31650732	RID07787	expression association	metastasis,prognosis	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE60407,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE67939)
Gastric adenocarcinoma	MEG3	SOCS3	positively-E	starBase;overexpression;western blot	downregulation	qPCR	NA	NA	Fak/Src signaling pathway(+);tumor growth(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-665)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000184557	NA	55384	9021	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	CIS3|Cish3|SOCS-3|SSI-3	miR-665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by lncRNA MEG3MiR-665 was upregulated and suppressor of cytokine signaling 3 (SOCS3) was downregulated in gastric adenocarcinoma tissues and cells. Elevated miR-665 was positively correlated with tumor size, lymph node metastasis, invasion depth, TNM stage, and poor differentiation in gastric adenocarcinoma patients. Overexpression of miR-665 promoted, whereas knockdown of miR-665 suppressed the proliferation,migration, and EMT of gastric adenocarcinoma cells.Furthermore, we demonstrated that miR-665 functioned through targeting SOCS3, followed by activation of the FAK/Src signaling pathway in gastric adenocarcinoma cells. miR-665 antagomir inhibited tumor growth as well as the activation of the FAK/Src pathway but increased SOCS3 expression in nude mice. In addition, miR-665 expression was negatively regulated by long noncoding RNA maternally expressed gene 3 (MEG3). In conclusion, miR-665 acted as an oncogene in gastric adenocarcinoma by inhibiting SOCS3 followed by activation of the FAK/Src pathway and it was negatively modulated by MEG3. miR-665 may be a promising therapeutic target for the treatment of gastric adenocarcinoma.	31650535	RID07788	ceRNA or sponge	metastasis		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE51827,GSE86978)
Urinary bladder cancer	MALAT1	VEGE-C	positively-E	siRNA;dual-luciferase reporter assay;Targetscan;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);chemosensitivity(-)	ceRNA(miR-101-3p)	regulation	NA	Cisplatin	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	LncRNA-MALAT1 mediates cisplatin resistance via miR-101-3p/VEGF-C pathway in bladder cancerqRT-PCRanalysis showed that MALAT1 expression was upregulated in the cancer tissues compared to that in the adjacent normal tissues.Bioinformatics analysis revealed that miR-101-3p is a candidate target of MALAT1. Then, dual-luciferase reporter assay was introduced to further confirm the intermolecular binding between MALAT1 and miR-101-3p.We performed bioinformatics analysis and TargetScan analysis and found that VEGF-C is a candidate target of miR-101-3p.We firstly designed the siRNAs specific to VEGF-C and transfected them into EJ-M3 and 5637 cells. qPCR and western blotrevealed that all the three VEGF-C siRNAs (siVEGFCs) inhibited the VEGF-C expression effectively, and the siVEGF-C-2 was chosen for further research.Collectively, these results demonstrated that MALAT1 played its roles via the MALAT1/miR-101-3p/VEGF-C regulatory pathway in cisplatin resistance of BCs.	31650173	RID07789	ceRNA or sponge	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Breast cancer	LINC00589	FOXP2	positively-E	RegRNA 2.0;luciferase reporter assay;overexpression;knockdown	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+);cell cycle(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000128573	NA	619351	93986	C8orf75|TSLNC8	CAGH44|SPCH1|TNRC10	LncRNA TSLNC8 inhibits proliferation of breast cancer cell through the miR-214-3p/FOXP2 axisqRT-PCRassays were carried out to evaluate the level of TSLNC8 in breast cancer tissues and cell lines. MTT, colony formation, and anchorage-independent growth assays were performed to investigate the effect of TSLNC8 on cell proliferation, and flow cytometry assays were conducted to detect cell percent of different phases. Luciferase reporter assays were used to confirm the interaction of different molecules.TSLNC8 is significantly increased in breast cancer tissues and cell lines. Up-regulation of TSLNC8 reduces the proliferation capacity of breast cancer cells and the transition from G1 to S phase of the cell cycle. Further analysis indicated that TSLNC8 could directly bind to miR-214-3p. Up-regulation of miR-214-3p may attenuate the suppressive role of TSLNC8 on the proliferation capacity of breast cancer cells. Moreover, miR-214-3p was found to directly interact with the 3'-untranslated region (UTR) of Forkhead box P2 (FOXP2) in luciferase assays,suggesting that FOXP2 may be one of the downstream targets of miR-412-3p.TSLNC8 was found to inhibit the proliferation and G1/S phase transition of breast cancer cells, an effect mediated by miR-214-3p/FOXP2 axis. Our study provides evidence that TSLNC8 may act as a suppressive lncRNA and represent a novel therapeutic target for breast cancer therapy.	31646574	RID07790	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,PRAD);DATA(GSE117623,GSE40174,GSE104209)
Non-small cell lung cancer	XIST	CBLL1	positively-E	dual-luciferase reporter assay;RIP;western blot;knockdown;siRNA;shRNA;DIANA;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);tumor growth(+);	ceRNA(miR-212-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000105879	NA	7503	79872	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	FLJ23109|HAKAI|RNF188	Downregulation of long non-coding RNA XIST inhibits cell proliferation, migration,invasion and EMT by regulating miR-212-3p/CBLL1 axis in non-small cell lung cancer cells.Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR was performed to detect the expression of XIST,miR-212-3p and Casitas B-lineage proto-oncogene like 1 (CBLL1). dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to analyze the relationship among XIST, miR-212-3p and CBLL1. Cell Counting Kit-8 (CCK-8) assay and transwell invasion assay were carried out to evaluate cell proliferation, migration and invasion, respectively. western blotwas conducted to examine the protein expression of CBLL1, E-cadherin, N-cadherin and Vimentin.Murine xenograft assay was conducted to explore the role of XIST in vivo.Expression levels of XIST and CBLL1 were markedly upregulated, while the miR-212-3p level was markedly downregulated in NSCLC tissues and cells. MiR-212-3p was identified as a direct target of XIST, and miR-212-3p was predicted to target CBLL1. XIST knockdown repressed NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro, and suppressed tumor growth in vivo, while miR-212-3p inhibition restored the effects. Furthermore,CBLL1 overexpression could abolish the effects of miR-212-3p overexpression on NSCLC cell proliferation,migration, invasion and EMT in vitro.XIST was significantly decreased in NSCLC tissues and cells, and XIST knockdown suppressed the proliferation, migration,invasion and EMT of NSCLC cells by miR-212-3p/CBLL1 axis. These findings facilitated our understanding of lncRNA regulation in NSCLC.	31646569	RID07791	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE55807)
Colorectal cancer	DLX6-AS1	PIK3CA	positively-E	siRNA;western blot;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000121879	NA	285987	5290	Evf-2|FLJ34048|NCRNA00212	PI3K	The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation,invasion and migration via modulating PI3K/AKT/mTOR pathwayQuantitative real-time PCR was performed to detect gene expression;cell counting kit-8, colony formation,cell invasion, and migration assays were performed to determine cell proliferation, invasion,and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity;in vivo tumor growth was evaluated in a nude mice xenograft model.DLX6-AS1 was up-regulated in 60 Colorectal cancer (CRC) tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion,and migration, but inhibited cell apoptosis;while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition,DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation,invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.	31646562	RID07792	expression association	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Colorectal cancer	DLX6-AS1	AKT1	positively-E	siRNA;western blot;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000142208	NA	285987	207	Evf-2|FLJ34048|NCRNA00212	AKT|PKB|PRKBA|RAC|RAC-alpha	The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation,invasion and migration via modulating PI3K/AKT/mTOR pathwayQuantitative real-time PCR was performed to detect gene expression;cell counting kit-8, colony formation,cell invasion, and migration assays were performed to determine cell proliferation, invasion,and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity;in vivo tumor growth was evaluated in a nude mice xenograft model.DLX6-AS1 was up-regulated in 60 Colorectal cancer (CRC) tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion,and migration, but inhibited cell apoptosis;while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition,DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation,invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.	31646562	RID07793	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	DLX6-AS1	MTOR	positively-E	siRNA;western blot;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000198793	NA	285987	2475	Evf-2|FLJ34048|NCRNA00212	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation,invasion and migration via modulating PI3K/AKT/mTOR pathwayQuantitative real-time PCR was performed to detect gene expression;cell counting kit-8, colony formation,cell invasion, and migration assays were performed to determine cell proliferation, invasion,and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity;in vivo tumor growth was evaluated in a nude mice xenograft model.DLX6-AS1 was up-regulated in 60 Colorectal cancer (CRC) tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion,and migration, but inhibited cell apoptosis;while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition,DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation,invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.	31646562	RID07794	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Colorectal cancer	PCAT1	miR-149-5p	negatively-F	siRNA;DIANA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	LncRNA PCAT-1 regulated cell proliferation,invasion, migration and apoptosis in colorectal cancer through targeting miR-149-5p.The qRT-PCRassay was used to carry out the expression of prostate cancer-associated ncRNA transcripts1 (PCAT-1) and miR-149-5p. The western blots were used to measure the protein expression of CDK4, Cyclin D1, MMP-2, MMP-9, Bcl-2, Bax and beta-actin. Additionally, flow cytometry and MTT assay were used to assess cell apoptosis and cell proliferation, respectively. Moreover, transwell assay was applied to measure the ability of cells migrated and invasion in Colorectal cancer (CRC). Luciferase reporter assay was performed to detect luciferase activities.In this study, lncRNA PCAT-1 expression was significantly upregulated in CRC cells and tissues. More than that, knockdown of lncRNA PCAT-1 inhibited cell proliferation, migration and invasion while promoted cell apoptosis in CRC cells. Of note, lncRNA PCAT-1 directly targeted miR-149-5p and miR-149-5p expression was significantly downregulated in CRC cells and tissues. Moreover, miR-149-3p reversed the suppressive effects of PCAT-1 on the cell growth of CRC cells.Our study demonstrated that LncRNA PCAT-1 regulated cell proliferation,invasion,migration and apoptosis in colorectal cancer through targeting miR-149-5p and provided a new regulatory mechanism of CRC.	31646561	RID07795	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Gastric cancer	CASC9	BMI1	positively-E	RNA pull-down assay;RIP;siRNA;shRNA	upregulation	qRT-PCR	NA	NA	apoptosis process(-);tumor growth(+)	histone modification	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75120409-75352327	ENSG00000168283	NA	101805492	648	ESCCAL-1|linc-JPH1|LINC00981	PCGF4|RNF51	LncRNA CASC9 Suppressed the Apoptosis of Gastric Cancer Cells through Regulating BMI1.The expressions of lncRNA and protein in GC tissues and cell lines were detected by qRT-PCRand western blot. GC cell apoptosis was detected by flow cytometry analysis. RNA pull-down and RNA immunoprecipitation (RIP) assays were conducted to verify the interaction between CASC9 and BMI1. LncRNA CASC9 was upregulated in GC tissue and GC cells, and high CASC9 expression was positively correlated with TNM stage and lymph node metastasis. Silencing CASC9 promoted the apoptosis of GC cells. LncRNA CASC9 could interact with BMI1 and positively regulate BMI1 expression. Silencing CASC9 promoted the ubiquitination of BMI1. In addition, lncRNA CASC9 regulated the apoptosis of GC cells through BMI1. Furthermore, interfering CASC9 inhibited the tumor growth of GC. LncRNA CASC9 could interact with BMI1 to regulate the degradation of BMI1,thus to affect the apoptosis of GC cells and suppressed tumor growth.	31642035	RID07796	epigenetic regulation	metastasis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Oesophageal squamous cell carcinoma	ZEB1-AS1	ZEB1	positively-E	siRNA;shRNA;starBase;overexpression;	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA ZEB1-AS1 down-regulation suppresses the proliferation and invasion by inhibiting ZEB1 expression in oesophageal squamous cell carcinoma.Here, we discovered that ZEB1-AS1 and ZEB1 were markedly up-regulated in oesophageal squamous cell carcinoma (ESCC) tissues and cells relative to their corresponding normal control. ZEB1-AS1 and ZEB1 overexpressions were both related to TNM staging and lymph node metastasis as well as poor prognosis in ESCC. The hypomethylation of ZEB1-AS1 promoter triggered ZEB1-AS1 overexpression in ESCC tissues and cells. In addition, ZEB1-AS1 knockdown mediated by siRNA markedly suppressed the proliferation and invasion in vitro in EC9706 and TE1 cells, which was similar with ZEB1 siRNA treatment, coupled with EMT alterations including the up-regulation of E-cadherin level as well as the down-regulation of N-cadherin and vimentin levels. Notably,ZEB1-AS1 depletion dramatically down-regulated ZEB1 expression in EC9706 and TE1 cells, and ZEB1 overexpression obviously reversed the inhibitory effects of proliferation and invasion triggered by ZEB1-AS1 siRNA. ZEB1-AS1 shRNA evidently inhibited tumour growth and weight, whereas ZEB1 elevation partly recovered the tumour growth in ESCC EC9706 and TE1 xenografted nude mice. In conclusion,ZEB1-AS1 overexpression is tightly involved in the development and progression of ESCC, and it exerts the antitumour efficacy by regulating ZEB1 level in ESCC.	31638344	RID07797	expression association	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	OSER1-DT	RAB23	positively-E	dual-luciferase reporter assay;fluorescent immunohistochemistry;western blot;immunofluorescence assay;shRNA;	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+);IKK/NF-kB signaling pathway(+);tumor growth(+)	ceRNA(miR-372-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223891	GRCh38_20:44210907-44226027	ENSG00000112210	NA	100505783	51715	OSER1-AS1	NA	lncRNA OSER1-AS1 acts as a ceRNA to promote tumorigenesis in hepatocellular carcinoma by regulating miR-372-3p/Rab23 axis.The results of database and qRT-PCRanalysis demonstrated that OSER1-AS1 was highly expressed in hepatocellular carcinoma (HCC) tissues and the high expression of OSER1-AS1 was closely associated with larger tumor size, advanced tumor stages, lower disease free survival and overall survival of HCC patients. OSER1-AS1 knockdown significantly inhibited the proliferation, invasion and migration of HCC cells, and induced the apoptosis. In addition, the dual-luciferase reporter assay directly demonstrated that OSER1-AS1 functioned as a molecular sponge for miR-372-3p to promote Rab23 expression. Moreover, the results of immunohistochemistry and western blotshowed that Rab23 was highly expressed in HCC tissues,and the high expression of Rab23 was closely associated with the poor overall survival of HCC patients. Immunofluorescence assay also found the subcellular localization of Rab23 in HCC cells. Rab23 was obviously downregulated in cells that were transfected with miR-372-3p mimics. MiR-372-3p mimics significantly inhibited the proliferation and invasion of HCC cells). Rab23 restoration partially reversed miR-372-3p-induced tumor suppressive effects on HCC cells. In conclusion, we found that OSER1-AS1 acted as a ceRNA to sponge miR-372-3p, thereby positively regulating the Rab23 expression and ultimately acting as a tumor suppressor gene in HCC progression.	31635804	RID07798	ceRNA or sponge	NA		UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Infantile hemangioma	MALAT1	MAP3K3	positively-E	shRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	ceRNA(miR-424)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Hemangioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198909	NA	378938	4215	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	MAPKKK3|MEKK3	LncRNA-MALAT1 promotes tumorogenesis of infantile hemangioma by competitively binding miR-424 to stimulate MEKK3/NF-kB pathway qRT-PCRwas used to quantify the expressions of MALAT1, miR-424, and MEKK3 in IH tissues . The cell proliferation, apoptosis, migration, invasion, and tube formation ability were assessed by MTT assay, colony formation assay, flow cytometric analysis, transwell assay and tube formation assay, respectively. The interaction among MALAT1, miR-424 and MEKK3 was evaluated by luciferase reporter assay. Immunohistochemistry (IHC) and western blot were utilized to evaluate the expression levels of MEKK3, Ki-67 and NF-kB pathwayrelated proteins both in vitro and in vivo.In IH tissues, MALAT1 and MEKK3 were overexpressed while miR-424 was downregulated. Silencing MALAT1 or overexpression of miR-424 significantly inhibited the IH cell proliferation, migration and tube formation, but promoted the cell apoptosis. Knockdown of MALAT1 suppressed the expression of MEKK3 and inactivated the IKK/NF-kB pathway by sponging miR-424. Overexpression of MEKK3 in HemEcs reversed the impact of knockdown of MALAT1 and overexpression of miR-424 on the cell proliferation, apoptosis, migration, invasion and tube formation rate. The tumor xenografts experiments demonstrated that silencing MALAT1 significantly inhibited the tumor growth in vivo and Ki-67 in the tumor tissues was also significantly suppressed.MALAT1 promoted the IH progression through inhibiting miR-424 to activate MEKK3-mediated IKK/NF-kB pathway, suggesting that MALAT1, miR-424 and MEKK3 could be used as potential targets to improve IH treatment efficiency.	31610202	RID07799	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	LINC00589	IL6	negatively-E	western blot;overexpression;immunofluorescence assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);IL-6/STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000136244	NA	619351	3569	C8orf75|TSLNC8	BSF2|HGF|HSF|IFNB2|IL-6	Long Non-Coding RNAs (lncRNAs) Tumor-Suppressive Role of lncRNA on Chromosome 8p12 (TSLNC8) Inhibits Tumor Metastasis and Promotes Apoptosis by Regulating Interleukin 6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Hypoxia-Inducible Factor 1-alpha (HIF-1a) Signaling Pathway in Non-Small Cell Lung Cancer.qRT-PCRwas carried out to evaluate the expression of TSLNC8 in lung cancer cell lines. The effects of TSLNC8 on A549 cells proliferation, migration, and invasion were analyzed using CCK-8 assay, wound healing assay,Transwell assay, and western blot We used flow cytometry to assess cell apoptosis, and cell autophagy was assessed by western blotand immunofluorescence staining. Levels of proteins in the IL-6/STAT3/HIF-1a pathway were measured by western blotThe results revealed that TSLNC8 was significantly downregulated in lung cancer cells compared to normal bronchial epithelial cells. Further experiments showed that overexpression of TSLNC8 in A549 cells significantly inhibited proliferation in a time-dependent manner and promoted cell apoptosis. We found that TSLNC8 overexpression suppressed cell migration and invasion, and upregulation of TSLNC8 regulated the protein levels of Beclin-1, p62, ATG14, and LC3-II and inhibited the IL-6/STAT3/HIF-1a signaling pathway.lncRNA TSLNC8 remarkably inhibited the proliferation and migration and accelerated apoptosis of lung cancer cells by targeting the IL-6/STAT3/HIF-1a signaling pathway. TSLNC8 may be a potential therapeutic target for the diagnosis and treatment of NSCLC.	31601776	RID07800	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Non-small cell lung cancer	LINC00589	STAT3	negatively-E	western blot;overexpression;immunofluorescence assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);IL-6/STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000168610	NA	619351	6774	C8orf75|TSLNC8	APRF	Long Non-Coding RNAs (lncRNAs) Tumor-Suppressive Role of lncRNA on Chromosome 8p12 (TSLNC8) Inhibits Tumor Metastasis and Promotes Apoptosis by Regulating Interleukin 6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Hypoxia-Inducible Factor 1-alpha (HIF-1a) Signaling Pathway in Non-Small Cell Lung Cancer.qRT-PCRwas carried out to evaluate the expression of TSLNC8 in lung cancer cell lines. The effects of TSLNC8 on A549 cells proliferation, migration, and invasion were analyzed using CCK-8 assay, wound healing assay,Transwell assay, and western blot We used flow cytometry to assess cell apoptosis, and cell autophagy was assessed by western blotand immunofluorescence staining. Levels of proteins in the IL-6/STAT3/HIF-1a pathway were measured by western blotThe results revealed that TSLNC8 was significantly downregulated in lung cancer cells compared to normal bronchial epithelial cells. Further experiments showed that overexpression of TSLNC8 in A549 cells significantly inhibited proliferation in a time-dependent manner and promoted cell apoptosis. We found that TSLNC8 overexpression suppressed cell migration and invasion, and upregulation of TSLNC8 regulated the protein levels of Beclin-1, p62, ATG14, and LC3-II and inhibited the IL-6/STAT3/HIF-1a signaling pathway.lncRNA TSLNC8 remarkably inhibited the proliferation and migration and accelerated apoptosis of lung cancer cells by targeting the IL-6/STAT3/HIF-1a signaling pathway. TSLNC8 may be a potential therapeutic target for the diagnosis and treatment of NSCLC.	31601776	RID07801	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	LINC00589	HIF1A	negatively-E	western blot;overexpression;immunofluorescence assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);IL-6/STAT3 signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000100644	NA	619351	3091	C8orf75|TSLNC8	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	Long Non-Coding RNAs (lncRNAs) Tumor-Suppressive Role of lncRNA on Chromosome 8p12 (TSLNC8) Inhibits Tumor Metastasis and Promotes Apoptosis by Regulating Interleukin 6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Hypoxia-Inducible Factor 1-alpha (HIF-1a) Signaling Pathway in Non-Small Cell Lung Cancer.qRT-PCRwas carried out to evaluate the expression of TSLNC8 in lung cancer cell lines. The effects of TSLNC8 on A549 cells proliferation, migration, and invasion were analyzed using CCK-8 assay, wound healing assay,Transwell assay, and western blot We used flow cytometry to assess cell apoptosis, and cell autophagy was assessed by western blotand immunofluorescence staining. Levels of proteins in the IL-6/STAT3/HIF-1a pathway were measured by western blotThe results revealed that TSLNC8 was significantly downregulated in lung cancer cells compared to normal bronchial epithelial cells. Further experiments showed that overexpression of TSLNC8 in A549 cells significantly inhibited proliferation in a time-dependent manner and promoted cell apoptosis. We found that TSLNC8 overexpression suppressed cell migration and invasion, and upregulation of TSLNC8 regulated the protein levels of Beclin-1, p62, ATG14, and LC3-II and inhibited the IL-6/STAT3/HIF-1a signaling pathway.lncRNA TSLNC8 remarkably inhibited the proliferation and migration and accelerated apoptosis of lung cancer cells by targeting the IL-6/STAT3/HIF-1a signaling pathway. TSLNC8 may be a potential therapeutic target for the diagnosis and treatment of NSCLC.	31601776	RID07802	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Oesophageal adenocarcinoma	PVT1	YAP1	positively-E	RIP;immunofluorescence assay;CRISPR-Cas9	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell invasion(+);colony formation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000137693	NA	5820	10413	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	YAP65	LncRNA PVT1 up-regulation is a poor prognosticator and serves as a therapeutic target in esophageal adenocarcinoma.PVT1 expression was assessed by qPCR in normal, Barrett  esophagus (BE), and esophageal adenocarcinoma (EAC) tissues and statistical analysis was performed to determine the association of PVT1 expression and EAC (stage, metastases, and survival). PVT1 antisense oligonucleotides (ASOs) were tested for their antitumor activity in vitro and in vivo.PVT1 expression was up-regulated in EACs compared with paired BEs, and normal esophageal tissues. High expression of PVT1 was associated with poor differentiation, lymph node metastases, and shorter survival. Effective knockdown of PVT1 in EAC cells using PVT1 ASOs resulted in decreased cell proliferation, invasion,colony formation, tumor sphere formation, and reduced proportion of ALDH1A1+ cells. Mechanistically, we discovered mutual regulation of PVT1 and YAP1 in EAC cells. Inhibition of PVT1 by PVT1 ASOs suppressed YAP1 expression through increased phosphor-LATS1and phosphor-YAP1 while knockout of YAP1 in EAC cells significantly suppressed PVT1 levels indicating a positive regulation of PVT1 by YAP1. Most importantly, we found that targeting both PVT1 and YAP1 using their specific ASOs led to better antitumor activity in vitro and in vivo.Our results provide strong evidence that PVT1 confers an aggressive phenotype to EAC and is a poor prognosticator. Combined targeting of PVT1 and YAP1 provided the highest therapeutic index and represents a novel therapeutic strategy.	31601234	RID07803	expression association	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Malignant glioma	TGFB1	LINC00115	positively-E		upregulation	qRT-PCR	REMBRANDT;TCGA	NA	tumorigenesis(+);self-renewal(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000225880	GRCh38_1:826206-827522	7040	79854	CED|DPD1|TGFB|TGFbeta	FLJ22639|NCRNA00115	TGF-b-activated lncRNA LINC00115 is a critical regulator of glioma stem-like cell tumorigenicity.We found TGF-b1-induced higher levels of SMAD2 phosphorylation (p-SMAD2) and a TGF-b1 signaling downstream effector, inhibitor of DNA-binding protein 1 (ID1) protein expression at 3 h compared with those at 0-, 0.5-, or 8-h time points. Thus, we performed RNA-Seq transcriptome analysis to compare lncRNA expression levels treated with or without TGF-b1 for 3 h in GSCs.Among lncRNAs, LINC00115 is one of the top differentially expressed TGF-b1-induced genes. To validate the RNA-Seq results, we performed qRT-PCR analysis of LINC00115 expression. The median patient survival times of these patients were 15.9 and 20.2 months in REMBRANDT, and 13.0 and 19.4 months in GSE83300 dataset, respectively. In the TCGA RNASeq (WHO grade III and GBM tumors) dataset, patients with high LINC00115 expression (upper quartile) also had a statistically significant poor prognosis. These data suggested that LINC00115 is highly expressed in GBM and its expression is putatively correlated with glioma patient survival.	31599491	RID07804	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE51827,GSE86978)
Malignant glioma	LINC00115	ZEB1	positively-E	shRNA;DIANA;RNAhybrid;RIP;qPCR;RNA pull-down assay	upregulation	qRT-PCR	REMBRANDT;TCGA	NA	cell proliferation(+);tumorigenesis(+);tumor growth(+);self-renewal(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000225880	GRCh38_1:826206-827522	ENSG00000148516	NA	79854	6935	FLJ22639|NCRNA00115	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	TGF-b-activated lncRNA LINC00115 is a critical regulator of glioma stem-like cell tumorigenicity.LINC00115 is upregulated by TGF-b,acts as a miRNA sponge, and upregulates ZEB1 by competitively binding of miR-200s, thereby enhancing ZEB1 signaling and GSC self-renewal. LINC00115 also promotes ZNF596 transcription by preventing binding of miR-200s to the 50-UTR of ZNF596, resulting in augmented ZNF596/EZH2/STAT3 signaling and GBM tumor growth. Inhibition of EZH2 by genetic approaches or a small molecular inhibitor markedly suppresses LINC00115-driven GSC self-renewal and tumorigenicity. Moreover, LINC00115 is highly expressed in GBM,and LINC00115 expression or correlated co-expression with ZEB1 or ZNF596 is prognostic for clinical GBM survival. Our work defines a critical role of LINC00115 in GSC self-renewal and tumorigenicity,and suggests LINC00115 as a potential target for GBM treatment.	31599491	RID07805	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	LINC00115	ZNF596	positively-E	overexpression;shRNA;RIP;luciferase reporter assay	upregulation	qRT-PCR	REMBRANDT;TCGA	NA	cell proliferation(+);cell viability(+);cell migration(+)	ceRNA(miR-200s)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000225880	GRCh38_1:826206-827522	ENSG00000172748	NA	79854	169270	FLJ22639|NCRNA00115	NA	TGF-b-activated lncRNA LINC00115 is a critical regulator of glioma stem-like cell tumorigenicity.LINC00115 is upregulated by TGF-b,acts as a miRNA sponge, and upregulates ZEB1 by competitively binding of miR-200s, thereby enhancing ZEB1 signaling and GSC self-renewal. LINC00115 also promotes ZNF596 transcription by preventing binding of miR-200s to the 50-UTR of ZNF596, resulting in augmented ZNF596/EZH2/STAT3 signaling and GBM tumor growth. Inhibition of EZH2 by genetic approaches or a small molecular inhibitor markedly suppresses LINC00115-driven GSC self-renewal and tumorigenicity. Moreover, LINC00115 is highly expressed in GBM,and LINC00115 expression or correlated co-expression with ZEB1 or ZNF596 is prognostic for clinical GBM survival. Our work defines a critical role of LINC00115 in GSC self-renewal and tumorigenicity,and suggests LINC00115 as a potential target for GBM treatment.	31599491	RID07806	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827,GSE86978)
Non-small cell lung cancer	NBR2	HEY1	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+);tumor growth(+);EZH2/STAT4 signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000164683	NA	10230	23462	NCRNA00192	bHLHb31|CHF-2|CHF2|HERP2|HESR-1|HESR1|HRT-1	LncRNA NBR2 inhibits EMT progression by regulating Notch1 pathway in NSCLC.The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. qRT-PCRand western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin,E-cadherin, HEY1, HEY2, and HEYL.The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells.LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.	31599420	RID07807	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE51827,GSE86978)
Non-small cell lung cancer	NBR2	HEY2	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+);tumor growth(+);EZH2/STAT4 signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000135547	NA	10230	23493	NCRNA00192	bHLHb32|HERP1|HESR2	LncRNA NBR2 inhibits EMT progression by regulating Notch1 pathway in NSCLC.The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. qRT-PCRand western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin,E-cadherin, HEY1, HEY2, and HEYL.The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells.LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.	31599420	RID07808	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	UP(SKCM);DATA(GSE38495)
Non-small cell lung cancer	NBR2	HEYL	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+);tumor growth(+);EZH2/STAT4 signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000163909	NA	10230	26508	NCRNA00192	bHLHb33|HESR3|HEY3	LncRNA NBR2 inhibits EMT progression by regulating Notch1 pathway in NSCLC.The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. qRT-PCRand western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin,E-cadherin, HEY1, HEY2, and HEYL.The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells.LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.	31599420	RID07809	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	
Non-small cell lung cancer	NBR2	NOTCH1	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+);tumor growth(+);EZH2/STAT4 signaling pathway(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000148400	NA	10230	4851	NCRNA00192	TAN1	LncRNA NBR2 inhibits EMT progression by regulating Notch1 pathway in NSCLC.The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. qRT-PCRand western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin,E-cadherin, HEY1, HEY2, and HEYL.The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells.LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.	31599420	RID07810	expression association	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	MNX1-AS1	STAT3	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000168610	NA	645249	6774	CCAT5|LOC645249|MAYA	APRF	Downregulating long non-coding RNA CCAT5 inhibits tumor growth, invasion and metastasis in colorectal cancer through suppressing STAT3.Real time-quantitative polymerase chain reaction (RT-qPCR) was utilized to measure CCAT5 expression of CRC tissues. Besides, function assays including wound healing assay and transwell assay were conducted. Furthermore, RT-qPCR and western blot assay were used to explore the underlying mechanism.By comparison with CCAT5 expression in adjacent tissues, the CCAT5 expresion level was significantly higher in CRC samples. Moreover, after CCAT5 was downregulated,cell migration and cell invasion of CRC cells were suppressed. Besides, after knockdown of CCAT5, the mRNA and protein expression of STAT3 was repressed. Furthermore, it was found that STAT3 expression was positively correlated to CCAT5 expression in CRC tissues.Results suggest that CCAT5 could promote cell migration and invasion of CRC by upregulating STAT3, which may offer a potential therapeutic target in CRC.	31599415	RID07811	expression association	metastasis	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Clear cell renal cell carcinoma	lnc-DILC	PTEN	positively-E	Co-immunoprecipitation;RNA pull-down assay;western blot;siRNA;RIP;overexpression;	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PTEN/AKT signaling pathway(+)	histone modification	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641473	ENSG00000171862	NA	NA	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	Long noncoding RNA lnc-DILC stabilizes PTEN and suppresses clear cell renal cell carcinoma progression.lnc-DILC expression in human clear cell renal cell carcinoma (ccRCC) tissues was detected by qRT-PCR Overexpression and knockdown experiments were carried out to determine the effects of lnc-DILC on ccRCC cell proliferation, migration and invasion. To reveal the underlying mechanisms of lnc-DILC functions in ccRCC cells. RNA immunoprecipitation, RNA pull-down,in vivo ubiquitination, co-immunoprecipitation and western blot assays were performed.Here, we identified that lnc-DILC levels were dramatically downregulated in ccRCC tissues. Loss of lnc-DILC expression was correlated with larger tumor size, advanced tumor grade and lymph node metastasis, and also predicted worse prognosis in patients with ccRCC. Functionally, knockdown and overexpression experiments demonstrated that lnc-DILC inhibited cell proliferation, migration and invasion in ccRCC cells. Mechanistic investigation revealed that lnc-DILC bound to tumor suppressor PTEN and suppressed its degradation. lnc-DILC repressed the PTEN ubiquitination through blocking the interaction between PTEN and E3 ubiquitin ligase WWP2 and recruiting the deubiquitinase USP11 to PTEN. Moreover, we demonstrated that PTEN-AKT signaling was crucial for lnc-DILC-mediated suppressive effects.In summary, our research revealed a novel mechanism by which lnc-DILC regulates PTEN stability via WWP2 and USP11, and shed light on potential therapeutic strategies by the restoration of lnc-DILC expression in patients with ccRCC.	31592114	RID07812	epigenetic regulation	metastasis,prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Papillary thyroid carcinoma	SOX2	COMETT	positively-E	ChIP;dual-luciferase reporter assay	upregulation	qPCR	TCGA	NA	cell invasion(+);cell growth(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000181449	NA	ENSG00000231210	GRCh38_7:116563594-116663829	6657	100996266	NA	COMET|LINC01510	SOX2-induced upregulation of lncRNA LINC01510 promotes papillary thyroid carcinoma progression by modulating miR-335/SHH and activating Hedgehog pathway.In this study, we firstly reported that LINC01510 was highly expressed in both PTC tissues and cell lines. Additionally,we used dual-luciferase reporter assay and confirmed that SOX2 could bind directly to the LINC01510 promoter region, activating its transcription. Functional assays with a series of cell experiments indicated that knockdown of LINC01510 suppressed the proliferation, migration and invasion of SW1736 and TPC-1 cells. Moreover, down-regulation of LINC01510 resulted in accelerated apoptosis by promoting the expression of Caspase3/9. In particular, LINC01510 acted as an endogenous sponge by directly binding miR-335, resulting in the suppression of miR-335 expressions. Besides, we confirmed that SHH was a target of miR-335 and miR-335 over-expression distinctly reduced SHH expression in PTC cells. Finally, in the cytoplasm, we provided evidenced that LINC01510 acted as a sponge for miR-335, reducing its ability to promote SHH expression. In addition, the results of western blot indicated that knockdown of LINC01510 inhibited the expression of SHH and GLI1, suggesting that Hedgehog pathway was suppressed. Taken together, our findings revealed that the newly identified LINC01510/miR-335/SHH axis could be a therapeutic target for PTC.	31590919	RID07813	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	
Papillary thyroid carcinoma	COMETT	SHH	positively-E	Targetscan;starBase;miRDB;dual-luciferase reporter assay;siRNA	upregulation	qPCR	TCGA	NA	cell invasion(+);cell growth(+);apoptosis process(-)	ceRNA(miR-355)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000164690	NA	100996266	6469	COMET|LINC01510	HHG1|HLP3|HPE3|MCOPCB5|SMMCI|TPT|TPTPS	SOX2-induced upregulation of lncRNA LINC01510 promotes papillary thyroid carcinoma progression by modulating miR-335/SHH and activating Hedgehog pathway.In this study, we firstly reported that LINC01510 was highly expressed in both PTC tissues and cell lines. Additionally,we used dual-luciferase reporter assay and confirmed that SOX2 could bind directly to the LINC01510 promoter region, activating its transcription. Functional assays with a series of cell experiments indicated that knockdown of LINC01510 suppressed the proliferation, migration and invasion of SW1736 and TPC-1 cells. Moreover, down-regulation of LINC01510 resulted in accelerated apoptosis by promoting the expression of Caspase3/9. In particular, LINC01510 acted as an endogenous sponge by directly binding miR-335, resulting in the suppression of miR-335 expressions. Besides, we confirmed that SHH was a target of miR-335 and miR-335 over-expression distinctly reduced SHH expression in PTC cells. Finally, in the cytoplasm, we provided evidenced that LINC01510 acted as a sponge for miR-335, reducing its ability to promote SHH expression. In addition, the results of western blot indicated that knockdown of LINC01510 inhibited the expression of SHH and GLI1, suggesting that Hedgehog pathway was suppressed. Taken together, our findings revealed that the newly identified LINC01510/miR-335/SHH axis could be a therapeutic target for PTC.	31590919	RID07814	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Cervical cancer	SNHG4	MET	positively-E	siRNA;dual-luciferase reporter assay;RIP;miRcode;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-148a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000281398	GRCh38_5:139274102-139284899	ENSG00000105976	NA	724102	4233	NCRNA00059|U19H	DFNB97|HGFR|RCCP2	Long non-coding RNA SNHG4 promotes cervical cancer progression through regulating c-Met via targeting miR-148a-3p.The purpose of this study was to investigate the effect of SNHG4 on cervical cancer (CC) and the corresponding mechanism. The qRT-PCRwas used to determine the expressions of SNHG4 and miR-148a-3p in CC cell lines and tissues. Cell apoptosis and proliferation were measured by flow cytometry and MTT assay, respectively. The interaction between SNHG4, miR-148a-3p and c-Met was verified by bioinformatics, dual-luciferase reporter gene and RNA immunoprecipitation (RIP), and the effect of SNHG4 on the growth of CC tumor in vivo was explored. The expression of SNHG4 was increased in both CC cell lines and tissues, while the expression of miR-148a-3p was down-regulated. Meanwhile, silencing SNHG4 remarkably inhibited CC cell proliferation and promoted apoptosis. In addition, miR-148a-3p was a direct target gene of SNHG4, and down-regulation of miR-148a-3p could observably reverse the effect of silencing SNHG4 on the proliferation and apoptosis of CC cells. More importantly, SNHG4 could up-regulate the expression of c-Met by targeting and interacting with miR-148a-3p. Finally, in vivo experiments confirmed that silence SNHG4 down-regulated the expression of c-Met by promoting miR-148a-3p, and ultimately suppressed the growth of CC tumor in vivo. In conclusion, SNHG4 could be used as a competitive endogenous RNA to bind to miR-148a-3p,thereby up-regulating the expression of c-Met and ultimately promoting the progression of CC,which provided a potential therapeutic target for the targeted treatment of CC.	31590627	RID07815	ceRNA or sponge	NA	DOWN(LIHC,BRCA);UP(SKCM);DATA(GSE117623,GSE38495,GSE111842)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Nasopharynx carcinoma	AK027294	EZH1	negatively-E	siRNA;RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	Glycyrrhiza glabra	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	NA	ENSG00000108799	NA	NA	2145	NA	KIAA0388|KMT6B	Glycyrrhiza glabra suppresses nasopharyngeal carcinoma cell proliferation through inhibiting the expression of lncRNA, AK027294.Glycyrrhiza glabra is considered as potential drug for nasopharyngeal carcinoma (NPC).In present study, we analyzed the differential expression of lncRNA between G. glabra-treated and untreated C666-1 cells. Out of those tumor-related lncRNAs, AK027294 had a strongest down-regulation upon G. glabra treatment. Knockdown of AK027294 suppresses the proliferation of C666-1 cells by inducing the apoptosis. Moreover, either G. glabra treatment or knockdown of AK027294 significantly increases the production of EZH1 (Enhancer of zeste 1 polycomb repressive complex 2 subunit). Collectively, we have identified a potential mechanism that the down-regulation of AK027294 contributes to the anti-cancer function of G. glabra and also provide the potential inter-relationship between AK027294 and EZH1.	31589096	RID07816	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	MEG3	SLC34A2	positively-E	siRNA;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-650)	regulation	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000157765	NA	55384	10568	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NAPI-3B	Long non-coding RNA MEG3 regulates migration and invasion of lung cancer stem cells via miR-650/SLC34A2 axis.Long non-coding RNA maternally expressed gene 3 (MEG3) is related to the occurrence and development of nonsmall cell lung cancer (NSCLC).qRT-PCRand western blot were performed to examine the expressions of MEG3,miR-650, solute carrier family 34 member 2 (SLC34A2), octamer-binding transcription factor 4 (Oct4), and CD133. Sphere assay was employed to evaluate sphere-forming ability. Cell migration and invasion were analyzed by Transwell assay. The relationships among MEG3, miR-650, and SLC34A2 were validated by luciferase reporter, RIP, and RNA pull-down assays. We found MEG3 was downregulated in LCSCs. MEG3 depletion strengthened stem cell-like characteristics and sphere-forming ability in LCCs. Upregulation of MEG3 suppressed migration and invasion in LCCs and LCSCs. miR-650 was bound to MEG3 and upregulated in LCSCs. miR-650 inhibitor alleviated si-MEG3-induced promotion of stem cell-like characteristics in lung cancer cells (LCCs) H1299. Furthermore, miR-650 mimic attenuated the MEG3 upregulation-mediated inhibition of migration and invasion. In addition, SLC34A2 was a target of miR-650 and downregulated in LCSCs. miR-650 mimic induced stem cell-like characteristics in LCCs, which was weakened by overexpression of SLC34A2. In contrast, the repression of SLC34A2 mitigated the miR-650 silencing-induced inhibition of migration and invasion in LCCs and LCSCs. Besides, MEG3 regulated SLC34A2 expression by sponging miR-650. Importantly, SLC34A2 weakened MEG3-mediated stem cell-like state and cell metastasis. Our data suggested MEG3 was involved in stem cell-like state of LCCs and curbed migration and invasion through miR-650/SLC34A2 axis in NSCLC.	31585300	RID07817	ceRNA or sponge	metastasis		UP(LIHC);DATA(GSE117623)
Lung adenocarcinoma	LINC01419	RCCD1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay;shRNA;starBase;RNA22;miRmap;microT;western blot	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-519b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253898	GRCh38_8:83403758-83408900	ENSG00000166965	NA	103352670	91433	PRLH1|TCONS_00014497	MGC14386	LINC01419 promotes cell proliferation and metastasis in lung adenocarcinoma via sponging miR-519b-3p to up-regulate RCCD1.Our findings showed that LINC01419 level was high in LUAD cells, and LINC01419 knockdown inhibited carcinogenesis via suppressing cell proliferation, migration as well as invasion. Moreover, bioinformatics prediction, luciferase reporter experiments and RIP assay were used to confirm miR-519-3p was sequestered and negatively regulated by LINC01419. Subsequently, RCCD1 was identified as a miR-519b-3p target and had inverse relationship with miR-519b-3p. LINC01419 was positively related to RCCD1. Furthermore, rescue assays confirmed that miR-519b-3p inhibitor or RCCD1 overexpression could neutralize the effect of LINC01419 silenced in cell proliferation, migration and invasion. Taken together,all the results indicated that LINC01419 exhibited oncogenic behaviors LUAD via binding to miR-519b-3p to enhance the expression of RCCD1, manifesting the underlying therapy values of LINC01419 in LUAD.	31582214	RID07818	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842)
Esophageal cancer	RPL34-DT	RPL34	negatively-E	overexpression;knockdown	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234492	GRCh38_4:108538190-108620460	ENSG00000109475	NA	285456	6164	FLJ37673|RP11-462C24.1|RPL34-AS1	L34	RPL34-AS1 functions as tumor suppressive lncRNA in esophageal cancer.In our study, we found RPL34-AS1 expression levels in esophageal cancer tissue and specimens and cell lines were lower than in adjacent normal tissue specimens and normal esophageal cell line, respectively. In addition, esophageal cancer patients with T3-T4 or positive lymph node metastasis had lower RPL34-AS1expression levels than esophageal cancer patients with  T1-T2 or negative lymph node metastasis, respectively. In survival analysis suggested esophageal cancer patients with low RPL34-AS1 expression had short overall survival than those with high RPL34-AS1 expression. Our in vitro experiments suggested RPL34-AS1 inhibits esophageal cancer cell proliferation, migration and invasion through down-regulating RPL34 expression. In conclusion,RPL34-AS1 functions as tumor suppressor in esophageal cancer.	31574377	RID07819	expression association	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	GAS5	miR-21	negatively-F	overexpression;knockdown;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Acts As A Tumor Suppressor In Laryngeal Squamous Cell Carcinoma Via miR-21This study is to investigate the critical roles and biological function of lncRNA growth arrest-specific 5 (GAS5) in tumorigenesis of laryngeal squamous cell carcinoma (LSCC).GAS5 expression in both LSCC tissues and human SUN1076 and SNU899 cell lines were analyzed by Real-time quantitative RT-PCRmethod. Ectopic expression of GAS5 by vector transfection in LSCC cell lines and followed by in vitro experiments was to investigate the critical roles and function of GAS5 in LSCC. Cell Counting Kit 8 (CCK8) assay and PE/7AAD Annexin V Apoptosis analysis was to evaluate cell proliferation ability and cell apoptosis. Co-transfection of GAS5 and miR-21 was to explore the interaction between GAS5 and miR-21 in LSCC. BAX and CDK6 protein level were analyzed by western blot method.This study demonstrated that GAS5 was significantly downregulated in LSCC tissue and human LSCC cell lines. GAS5 levels were correlated with the clinicopathological features of LSCC patients. In addition, the ectopic expression of GAS5 significantly inhibited cell proliferation and promoted apoptosis. Co-expression analyses indicated that GAS5 is negatively correlated with miR-21 in LSCC tissues. Overexpression of miR-21 eliminated GAS5-mediated cell apoptosis and proliferation suppression. Furthermore, GAS5, which upregulated BAX mRNA expression and downregulated CDK6 mRNA expression, was reversed by ectopic expression of miR-21.GAS5 suppresses LSCC progression through the negative regulation of miR-21 and its targets involved in cell proliferation and apoptosis, indicating that GAS5 may serve as a biomarker and potential target for LSCC therapy.	31572003	RID07820	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Hepatocellular carcinoma	DUXAP8	KLF2	negatively-E	siRNA;ChIP;RIP	upregulation	qRT-PCR	GSE70880;GSE113850;GSE124535;TCGA	NA	cell growth(+);cell proliferation(+);colony formation(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000127528	NA	503637	10365	NA	LKLF	We identified hundreds of lncRNAs which were dysregulated in HCC tissues through performing integrative analyses using the RNA sequencing data and independent gene microarray data from Gene Expression Omnibus and the Cancer Genome Atlas.Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes. Further experimental validation revealed that down-regulation of lncRNA DUXAP8 inhibited HCC cells proliferation and colony formation ability. Mechanistically, DUXAP8 repressed tumor suppressor KLF2 transcription through interacting with histone-lysine N-methyltransferase enzyme enhancer of zeste homolog 2.Taken together, our findings can provide a valuable resource of HCC-associated lncRNAs and new insights into the biological functions of lncRNAs in HCC development.	31571902	RID07821	transcriptional regulation	NA	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	NBR2	miRNA-21	negatively-E	dual-luciferase reporter assay;overexpression	downregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000198496	GRCh38_17:43125551-43153671	NA	NA	10230	NA	NCRNA00192	NA	LncRNA NBR2 suppresses migration and invasion of colorectal cancer cells by downregulating miRNA-21We found that NBR2 was downregulated in colorectal cancer tissues than in adjacent healthy tissues. Decreased expression levels of NBR2 in tumor tissues were observed with the increase of clinical stages. MiRNA-21 was upregulated in colorectal cancer tissues than in adjacent healthy tissues, and was significantly and inversely correlated with NBR2. NBR2 overexpression downregulated miRNA-21 in colorectal cancer cells, while miRNA-21 overexpression failed to significantly affect NBR2 expression. NBR2 overexpression suppressed migration and invasion of colorectal cancer cells. MiRNA-21 overexpression played an opposite role and attenuated the effects of NBR2 overexpression. NBR2 overexpression did not significantly alter cancer cell proliferation. Therefore, lncRNA NBR2 inhibited colorectal cancer cell migration and invasion possibly by downregulating miRNA-21.	31571148	RID07822	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939)	
Epithelial ovarian cancer	STAT3	ABHD11-AS1	positively-E	Immunofluorescence	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000225969	GRCh38_7:73735038-73736158	6774	171022	ADMIO|ADMIO1|APRF|HIES	LINC00035|NCRNA00035|WBSCR26	lncRNA ABHD11-AS1, regulated by the EGFR pathway,contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2Immunohistochemistry, western blot, and qRT-PCRanalysis were used to determine the expression pattern of ABHD11-AS1 and epidermal growth factor receptor (EGFR) in both Epithelial ovarian cancer (EOC) tissues and cell lines, respectively. Colony formation,transwell and wound healing assays were performed to evaluate the roles of EGFR and ABHD11-AS1 on the capacity of cell proliferation, migration, and invasion. western blotwas performed to measure the regulation of EGFR pathway on STAT3. Moreover, chromatin immunoprecipitation was employed to demonstrate the interaction between ABHD11-AS1 and STAT3. RNA immunoprecipitation was subjected to prove the direct binding between ABHD11-AS1 and EZH2. Immunofluorescence staining was performed to measure the expression and localization of TIMP2. EOC mouse model was conducted for validating the role of ABHD11-AS1 in vivo.	31568657	RID07823	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(BRCA);DATA(GSE55807)
Epithelial ovarian cancer	ABHD11-AS1	TIMP2	negatively-E	shRNA;siRNA;RIP	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000035862	NA	171022	7077	LINC00035|NCRNA00035|WBSCR26	CSC-21K|DDC8	lncRNA ABHD11-AS1, regulated by the EGFR pathway,contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2Immunohistochemistry, western blot, and qRT-PCRanalysis were used to determine the expression pattern of ABHD11-AS1 and epidermal growth factor receptor (EGFR) in both Epithelial ovarian cancer (EOC) tissues and cell lines, respectively. Colony formation,transwell and wound healing assays were performed to evaluate the roles of EGFR and ABHD11-AS1 on the capacity of cell proliferation, migration, and invasion. western blotwas performed to measure the regulation of EGFR pathway on STAT3. Moreover, chromatin immunoprecipitation was employed to demonstrate the interaction between ABHD11-AS1 and STAT3. RNA immunoprecipitation was subjected to prove the direct binding between ABHD11-AS1 and EZH2. Immunofluorescence staining was performed to measure the expression and localization of TIMP2. EOC mouse model was conducted for validating the role of ABHD11-AS1 in vivo.	31568657	RID07824	transcriptional regulation	NA	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	TINCR	TCF4	positively-E	starBase;siRNA;BiBiserv2;dual-luciferase reporter assay	upregulation	sequencing;qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	ceRNA(miR-137)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000196628	NA	257000	6925	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	bHLHb19|E2-2|ITF2|SEF2-1B	Knockdown of long non-coding RNA TINCR decreases radioresistance in colorectal cancer cells.Firstly, TINCR was selected using sequencing analyses and the starBase database. Cell Counting Kit-8, scratch wound healing, and transwell assays revealed that TINCR inhibited proliferation and migration in SW620 and HTC116 cells. Intriguingly, TINCR expression was up-regulated in a radioresistant colorectal cancer (CRC) cell line (SW620R). Although TINCR had no significant effects on SW620R cell proliferation or migration, knockdown of TINCR reduced the radioresistance, and its overexpression had opposite effects. We then focused on transcription factor 4 (TCF4) as it is downregulated in CRC and associated with increased stemness in tumors. We found that TINCR and TCF4 levels were positively related in SW620R cells. TINCR knockdown reduced sphere formation ability in SW620R cells. TINCR also suppressed the OCT4 and SOX2 stemness genes, despite having no effect on NANOG. The expression levels of these genes were substantially higher in SW620R than in SW620 cells. To further explore the mechanism of TINCR and radioresistance, miR-137 was analyzed as it targets TCF4. We firstly confirmed that TCF4 is a target of miR-137. We then identified that TINCR knockdown enhanced miR-137 expression in SW620R cells. Collectively, these findings suggest that TINCR knockdown inhibits TCF4 by regulating miR-137 expression.	31540772	RID07825	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE51827)
Nasopharynx carcinoma	SMAD5-AS1	SMAD5	positively-E	siRNA;dual-luciferase reporter assay;FISH;RNA pull-down assay;immunoprecipitation;western blot	upregulation	qRT-PCR	GSE64634	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);tumorigenesis(+)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000164621	GRCh38_5:136129507-136134890	ENSG00000113658	NA	9597	4090	DAMS|SMAD5OS	Dwfc|JV5-1|MADH5	Long noncoding RNA SMAD5-AS1 acts as a microRNA-106a-5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma.microarray-based analysis identified highly expressed lncRNAmothers against decapentaplegic homolog 5 (SMAD5)-antisense RNA 1 (AS1) related to Nasopharyngeal carcinoma (NPC). Interestingly, it is found that SMAD5-AS1 competitively bound to microRNA (miR)-106a-5p to regulate SMAD5. Herein, the study aimed to clarify the role of SMAD5-AS1/miR-106a-5p/SMAD5 axis in the process of epithelialmesenchymal transition (EMT) in NPC. SMAD5-AS1 was highly expressed and miR-106a-5p was poorly expressed in NPC tissues and cell lines. The NPC cells were treated with a series of small interfering RNAs, mimics, or inhibitors to explore the effects of SMAD5-AS1, SMAD5, and miR-106a-5p on EMT, cell proliferation,migration, and invasion inNPC.Of note, SMAD5-AS1 silencing ormiR-106a-5p overexpression reduced expression of N-cadherin, matrix metallopeptidase 9, Snail, and Vimentin while elevating E-cadherin expression,thus inhibitingEMT, cell proliferation, migration, and invasion inNPC by down-regulation of SMAD5.Moreover,SMAD5 silencing could reduce the ability of EMT induced by SMAD5-AS1 up-regulation. SMAD5-AS1 silencing or miR-106a-5p elevation inhibited tumorigenesis in nudemice.Taken together, SMAD5-AS1 silencing suppressed EMT, cell proliferation, migration, and invasion inNPCby elevatingmiR-106a-5p to down-regulate SMAD5,which provided a novel therapeutic target for NPC treatment.	31557058	RID07826	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE51827)
Triple-negative breast cancer	LINC01096	miR-3130-3p	negatively-E	luciferase reporter assay;siRNA;overexpression	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);apoptosis process(-);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000246095	GRCh38_4:13546075-13547801	NA	NA	285548	NA	NA	NA	LINC01096 knockdown inhibits progression of triple-negative breast cancer by increasing miR-3130-3p.Sixty Triple-negative breast cancer (TNBC) patients were recruited. T47-D and BT-549 cells were cultured for experiments in vitro. The expression levels of LINC01096 and miR-3130-3p were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Cell viability, apoptosis, migration, and invasion were determined by MTT,flow cytometry, and trans-well assays. The target association between LINC01096 and miR-3130-3p was confirmed by the luciferase reporter assay.The expression of LINC01096 was enhanced in TNBC tissues and cells. High expression of LINC01096 predicted poor outcomes of patients with TNBC. Silence of LINC01096 led to the suppression of cell viability, migration,and invasion, as well as the promotion of apoptosis in TNBC cells. MiR-3130-3p was targeted by LINC01096 and lowly expressed in TNBC. Overexpression of miR-3130-3p repressed cell viability, migration, and invasion, while it induced apoptosis. However, the knockdown of miR-3130-3p induced the opposite effect. This was weakened by inhibiting LINC01096.Knockdown of LINC01096 inhibited cell viability, migration, and invasion;however, it promoted apoptosis in TNBC by up-regulating miR-3130-3p, indicating a novel target for the treatment of TNBC.	31539132	RID07827	expression association	NA		
Esophageal cancer	CCAT1	PLK1	positively-E	shRNA;immunohistochemistry;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+);tumor growth(+);chemosensitivity(-)	ceRNA(miR-143)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000166851	NA	100507056	5347	CARLO5|CARLo-5|onco-lncRNA-40	PLK	lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR-143/PLK1/BUBR1 axis.The correlation between CCAT1 expression and drug resistance to cisplatin (CDDP) in esophageal squamous cell carcinoma (ESCC) cells was analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and quantitative real-time polymerase chain reaction (qRT-PCR assays. CCAT1 knockdown and miR-143 overexpression or inhibition were used to verify the effects on proliferation and drug resistance via MTT, western blot, flow cytometry, and immunofluorescence assays. qRT-PCRand western blot were applied to detect the potential regulatory relationship among CCAT1, miR-143, PLK1, and BUBR1. A xenograft tumor assay was performed to validate the role of CCAT1 in vivo. The expression of CCAT1 was positively correlated with drug resistance in several ESCC cell lines. CCAT1 knockdown and miR-143 overexpression inhibited cell proliferation and CDDP drug resistance. Moreover, the downstream target of CCAT1 was found to be miR-143, which can regulate the expression of PLK1 and BUBR1. In vivo assays showed that CCAT1 knockdown suppressed tumor growth and enhanced the sensitivity of tumors to CDDP in nude mice. Taken together, we discovered a novel mechanism by which CCAT1 promotes cell proliferation and enhances drug resistance by regulating the miR-143/PLK1/BUBR1 signaling axis both in vitro and in vivo. Our findings further suggest that lncRNA CCAT1 may be a potential therapeutic target for overcoming chemoresistance in esophageal cancer.	31544294	RID07828	ceRNA or sponge	chemoresistance		UP(PAAD,SKCM);DOWN(BRCA);DATA(GSE40174,GSE38495,GSE111842)
Esophageal cancer	CCAT1	BUB1B	positively-E	shRNA;immunohistochemistry;overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+);tumor growth(+);chemosensitivity(-)	ceRNA(miR-143)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000247844	NA	ENSG00000156970	NA	100507056	701	CARLO5|CARLo-5|onco-lncRNA-40	Bub1A|BUBR1|MAD3L|SSK1	lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR-143/PLK1/BUBR1 axis.The correlation between CCAT1 expression and drug resistance to cisplatin (CDDP) in esophageal squamous cell carcinoma (ESCC) cells was analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and quantitative real-time polymerase chain reaction (qRT-PCR assays. CCAT1 knockdown and miR-143 overexpression or inhibition were used to verify the effects on proliferation and drug resistance via MTT, western blot, flow cytometry, and immunofluorescence assays. qRT-PCRand western blot were applied to detect the potential regulatory relationship among CCAT1, miR-143, PLK1, and BUBR1. A xenograft tumor assay was performed to validate the role of CCAT1 in vivo. The expression of CCAT1 was positively correlated with drug resistance in several ESCC cell lines. CCAT1 knockdown and miR-143 overexpression inhibited cell proliferation and CDDP drug resistance. Moreover, the downstream target of CCAT1 was found to be miR-143, which can regulate the expression of PLK1 and BUBR1. In vivo assays showed that CCAT1 knockdown suppressed tumor growth and enhanced the sensitivity of tumors to CDDP in nude mice. Taken together, we discovered a novel mechanism by which CCAT1 promotes cell proliferation and enhances drug resistance by regulating the miR-143/PLK1/BUBR1 signaling axis both in vitro and in vivo. Our findings further suggest that lncRNA CCAT1 may be a potential therapeutic target for overcoming chemoresistance in esophageal cancer.	31544294	RID07829	ceRNA or sponge	chemoresistance		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Non-small cell lung cancer	DLEU2	SOX9	positively-E	shRNA;dual-luciferase reporter assay;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+);cell metastasis(+)	ceRNA(miR-30c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000125398	NA	8847	6662	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	CMD1|CMPD1|SRA1	lncRNA DLEU2 modulates cell proliferation and invasion of non-small cell lung cancer by regulating miR-30c-5p/SOX9 axis.Our studies confirmed that lncRNA DLEU2 was highly expressed in NSCLC tissues and cell lines, which was correlated with shorter overall survival in NSCLC patients. In vitro, knockdown of lncRNA DLEU2 inhibited proliferation, invasion, migration and induced apoptosis of both A549 and LLC cells; In vivo, it suppressed tumor growth and metastasis. lncRNA DLEU2 directly interacted with miR-30c-5p, which further targeted SOX9 and exerted oncogenic functions in NSCLC. Mechanistically, overexpression of lncRNA DLEU2 exhibits tumorigenic effects through downregulating the inhibitory effect of miR-30c-5p on SOX9 expression. In conclusion, Our finding confirmed that lncRNA DLEU2 as a novel oncogenic in NSCLC, which provide a potential novel diagnostic and therapeutic target for NSCLC.	31541993	RID07830	ceRNA or sponge	metastasis	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Papillary thyroid carcinoma	RMRP	MAPK1	positively-E	dual-luciferase reporter assay;LncBasePredictedV2.0;Targetscan;miRanda;western blot;siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+);cell metastasis(+)	ceRNA(miR-675)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000100030	NA	6023	5594	CHH|NME1|RMRPR|RRP2	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	MicroRNA-675 directly targets MAPK1 to suppress the oncogenicity of papillary thyroid cancer and is sponged by long non-coding RNA RMRP.The expression profile of miR-675 in papillary thyroid cancer (PTC) tissues and cell lines was determined using RT-qPCR. CCK-8, transwell migration and invasion assays, and xenograft tumors in nude mice were employed to analyze proliferation, in vitro migration and invasion, and in vivo tumor growth of PTC cells, respectively. The putative target of miR-675 was predicted using bioinformatic algorithms and was confirmed using luciferase reporter assays,RT-qPCR, and western blot.miR-675 expression was decreased in PTC tissues and cell lines. A low level of miR-675 expression was significantly correlated with lymphatic metastasis and TNM stage in PTC patients. Ectopic miR-675 expression suppressed PTC cell proliferation, migration, and invasion in vitro and hindered tumor growth in vivo. Mitogen-activated protein kinase 1 (MAPK1) was found to be the direct target gene of miR-675 in PTC cells. MAPK1 reintroduction negated the tumor-suppressing effect of miR-675 overexpression in PTC cells. Furthermore, the lncRNA mitochondrial RNA processing endoribonuclease (RMRP) functioned as a ceRNA of miR-675 in PTC cells. Silencing RMRP expression inhibited the growth and metastasis of PTC cells by sponging miR-675 and regulating MAPK1.These findings revealed that miR-675 directly targets MAPK1 and is sponged by lncRNA RMRP to inhibit the oncogenicity of PTC, suggesting the RMRP-miR-675-MAPK1 pathway is an effective target for the treatment of PTC patients.	31564913	RID07831	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical squamous cell carcinoma	HAND2-AS1	ROCK1	negatively-E	western blot;overexpression	downregulation	qPCR;RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000067900	NA	79804	6093	DEIN|NBLA00301|UPH	P160ROCK|ROCK-I	lncRNA HAND2-AS1 inhibits cancer cell proliferation, migration and invasion by downregulating ROCK1 in HPV-positive and negative cervical squamous cell carcinoma.The current study revealed that lncRNA HAND2-AS1 was downregulated, while Rho-associated protein kinase 1 (ROCK1) was upregulated in serum of human papillomavirus (HPV)-positive and -negative patients with CSCC compared with healthy controls. Correlation analysis revealed that the expression levels of lncRNA HAND2-AS1 were negatively correlated with the expression levels of ROCK1 in HPV-positive and -negative patients with CSCC but not in healthy controls. Downregulation of lncRNA HAND2-AS1 distinguished patients with CSCC from healthy controls. Additionally, lncRNA HAND2-AS1 overexpression led to reduced expression levels of ROCK1 in HPV-positive and -negative human CSCC cell lines but not in normal cervical cell lines. ROCK1 overexpression did not significantly affect the expression of lncRNA HAND2-AS1 in all the cell lines investigated. lncRNA HAND2-AS1 overexpression inhibited, while ROCK1 overexpression promoted the proliferation, migration and invasion of HPV-positive and -negative human CSCC cell lines but not normal cervical cell lines. ROCK1 overexpression attenuated the effects of lncRNA HAND2-AS1 overexpression on cancer cell proliferation, migration and invasion. lncRNA HAND2-AS1 may inhibit cancer cell proliferation, migration and invasion by downregulating ROCK1 in HPV-positive and -negative CSCC.	31555362	RID07832	expression association	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	MEG3	MTSS1	positively-E	shRNA;dual-luciferase reporter assay;Targetscan;miRanda;LncBasePredictedV2.0;northern blot	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+);cell metastasis(+)	ceRNA(miR-96-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000170873	NA	55384	9788	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	KIAA0429|MIM|MIMA|MIMB	Long non-coding RNA MEG3 suppresses the growth of glioma cells by regulating the miR-96-5p/MTSS1 signaling pathway.Previous studies have revealed that lncRNA maternally expressed gene 3 (MEG3) is involved in the initiation and progression of cancer; however, the underlying mechanisms remain unclear.In the present study, MEG3 was downregulated in glioma tissue. In addition, downregulation of MEG3 was observed in human glioma cell lines compared with normal astrocyte cells. Furthermore, overexpressed MEG3 inhibited the proliferation,migration and invasion of glioma cells. Additionally,microRNA- 96-5p (miR- 96-5p) was a promising target of MEG3, and the promoting effects of miR- 96-5p on cell growth and metastasis could be reversed by upregulated MEG3. Metastasis suppressor 1 (MTSS1) was predicted as the putative target of miR- 96-5p, and its expression was restored by MEG3.In summary, the present data provided novel insight into the roles of MEG3 in glioma, and MEG3/miR- 96-5p/MTSS1 signaling could be a promising therapeutic target for the treatment of patients with glioma.	31545491	RID07833	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE111065)
Laryngeal squamous cell carcinoma	loc285194	HK2	negatively-E	western blot;overexpression	upregulation	RT-qPCR	NA	NA	tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	NA	NA	ENSG00000159399	NA	NA	3099	NA	HKII|HXK2	LncRNA loc285194 inhibits tumor growth of laryngeal squamous cell carcinoma cells by downregulating hexokinase 2.The expression of loc285194 and hexokinase 2 (HK-2) mRNA in laryngeal biopsies of patients with laryngeal squamous cell carcinoma (LSCC). or healthy controls was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The diagnostic value of loc285194 and HK-2 mRNA for LSCC was evaluated using receiver operating characteristic curve analysis. The correlation between expression of loc285194 and HK-2 mRNA was analyzed using the Pearson correlation coefficient. The association between loc285194 and clinicopathological data of patients with LSCC was analyzed using the Chi-square test. LncRNA loc285194 and HK-2 expression vectors were transfected into human LSCC cell lines and the effects on HK-2 expression, lncRNA loc285194 expression and cell proliferation was detected by western blot, RT-qPCR and CCK-8 assays, respectively. It was observed that loc285194 was upregulated, while HK-2 mRNA was downregulated in patients with LSCC compared with healthy controls. The results demonstrated that the downregulation of loc285194 may be a sensitive diagnostic marker for LSCC. The expression levels of loc285194 and HK-2 mRNA were inversely correlated in patients with LSCC, but not in healthy controls. loc285194 expression was significantly associated with tumor size, but not distant tumor metastasis. Loc285194 overexpression significantly inhibited HK-2 expression and LSCC cell proliferation. HK-2 overexpression did not significantly affect Loc285194 expression, but promoted LSCC proliferation and attenuated the inhibitory effects of loc285194 overexpression on LSCC cell proliferation. lncRNA loc285194 may inhibit tumor growth of LSCC cells by downregulating HK-2.	31555348	RID07834	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Epithelial ovarian cancer	TINCR	FGF2	positively-E	overexpression;siRNA;RIP;starBase;Targetscan;microRNA.org;dual-luciferase reporter assay;RIPA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cancer progression(+)	ceRNA(miR-335)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000138685	NA	257000	2247	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	FGFB	Silencing the long noncoding RNA, TINCR, a molecular sponge of miR-335, inhibits the malignant phenotype of epithelial ovarian cancer via FGF2 suppression.Here, TINCR expression levels in epithelial ovarian cancer (EOC) tissues and cell lines were determined by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 assays, flow cytometric analysis, Transwell migration and invasion assays, and in vivo xenograft experiments were performed to determine the influence of TINCR on the malignant phenotype of EOC cells in vitro and in vivo. The molecular mechanisms associated with the tumor-promoting roles of TINCR during EOC progression were elucidated using a series of experiments. TINCR expression was higher in EOC tissues and cell lines compared with normal cells. An analysis of the association between TINCR expression and clinicopathological characteristics showed that increased TINCR expression was closely related to tumor size, FIGO stage, and lymphatic metastasis. In addition, the overall survival rates of EOC patients with high TINCR expression levels were lower than in those with low TINCR expression levels. Functional experiments showed that TINCR deficiency attenuated the proliferation, migration, and invasion of EOC cells in vitro and hindered EOC tumor growth in vivo. In addition, EOC cell apoptosis increased after TINCR knockdown. Mechanistically, TINCR was shown to function as a sponge of microRNA-335 (miR-335) in EOC cells, thereby regulating fibroblast growth factor 2 (FGF2) expression. miR-335 inhibition partially counteracted the effect of TINCR knockdown on the aggressive behavior of EOC cells. This study showed, for the first time to the best of our knowledge, that silencing TINCR, which interacts with miR-335, inhibited EOC progression in vitro and in vivo by decreasing FGF2 expression. Hence, this lncRNA could be a potential prognostic biomarker and effective target for therapeutic intervention in EOC.	31545411	RID07835	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Non-small cell lung cancer	FENDRR	TIMP2	positively-E	siRNA;immunofluorescence assay;immunoblot;starBase;miRDB;Targetscan;miRTarBase	downregulation	qRT-PCR	TCGA	NA	cell migration(+);cell invasion(+);cell growth(+);colony formation(+)	ceRNA(miR-761)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000035862	NA	400550	7077	FOXF1-AS1|lincFOXF1|onco-lncRNA-21	CSC-21K	LncRNA FENDRR suppresses the progression of NSCLC via regulating miR-761/TIMP2 axis.The levels of FENDRR in non-small cell lung cancer (NSCLC) cells and tissues were analyzed using qRT-PCRassay. The growth and colony formation abilities of NSCLC cell were analyzed by the MTT and colony formation tests. The mobility and invasiveness of NSCLC cell were analyzed using the wound closure and Transwell invasion assay. The impact of FENDRR on the tumor growth of NSCLC cells in vivo was detected using xenograft model. Bioinformatics analysis and luciferase reporter gene bioassay were selected to identify the bindings sites between miR-761 and FENDRR. Additional, the results of Transwell invasion and colony formation experiments indicated that FENDRR inhibited the aggressiveness of NSCLC depend on miR-761. Tissue inhibitor of metalloproteinase 2 (TIMP2) was identified as the downstream target of miR-761 and its level was positively regulated by FENDRR. Cotransfection assays using A549 and H1975 cells future implied that downexpression of TIMP2 rescued the aggressiveness phenotypes of NSCLC cell inhibited by FENDRR. Altogether, we demonstrated that lncRNA FENDRR suppressed the progression of NSCLC via binding to miR-761 and regulating TIMP2 expression.	31545237	RID07836	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG7	RPL4	positively-E	shRNA;starBase	upregulation	qRT-PCR	TCGA;GSE45436	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-122-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000174444	NA	84973	6124	MGC16037|NCRNA00061	L4	LncRNA SNHG7 accelerates the proliferation, migration and invasion of hepatocellular carcinoma cells via regulating miR-122-5p and RPL4.The recent study finds a strong correlation between lncRNA small nucleolar RNA host gene 7 (SNHG7) and hepatocellular carcinoma (HCC) metastasis. However, the molecular mechanism by which SNHG7 regulates HCC progression has not been investigated. In this study, we found that SNHG7 was highly expressed in HCC tissues compared to non-tumor tissues. Data from public databases consistently indicated the up-regulated expression of SNHG7 in HCC. Furthermore, the levels of SNHG7 were up-regulated in four HCC cell lines (Huh7, Hep3B, HCCLM3,MHCC97 H) compared with LO2 cells. Interestingly, the elevated expression of SNHG7 was closely correlated with advanced tumor stages, high tumor grades, vascular invasion and poor prognosis of HCC. Knockdown of SNHG7 markedly inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97H cells, and prominently suppressed the growth and metastasis of HCCLM3 cells in vivo. Mechanistically, SNHG7 silencing increased the level of miR-122-5p in HCC cells. Luciferase reporter assay revealed the direct interaction between SNHG7 and miR-122-5p. Moreover, SNHG7 knockdown decreased the levels of ribosomal protein L4 (RPL4) mRNA and protein in HCC cells. Accordingly, the stability of RPL4 mRNA was reduced by SNHG7 silencing. More importantly, either miR-122-5p knockdown or RPL4 restoration partially reversed SNHG7 silencing-induced tumor suppressive effects on HCC cells. In conclusion, we demonstrated that SNHG7 expression was upregulated in HCC. SNHG7 contributed to HCC progression by regulating miR-122-5p and RPL4. Therefore,SNHG7 might be a potential biomarker and therapeutic target for HCC.	31545291	RID07837	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nasopharynx carcinoma	H19	HRAS	positively-E	luciferase reporter assay;western blot;shRNA;RNAhybrid	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);cell viability(+);cancer progression(+);cell growth(+)	ceRNA(let-7)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000174775	NA	283120	3265	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	HRAS1	Upregulation of lncRNA H19 promotes nasopharyngeal carcinoma proliferation and metastasis in let-7 dependent manner.The aim of this study is to analyse the expression status of long non-coding RNA (lncRNA) H19 in nasopharyngeal carcinoma and to unravel its oncogenic properties at molecular level. The  abundance of H19, let-7a, b, g, i and HRAS was quantified by real-time PCR. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. Cell proliferation was evaluated by the cell counting. Cell migration and cell invasion were determined using transwell chamber and scattering colony formation. Tumour progression was monitored in xenograft tumour model and tail vein injection was adopted for lung metastasis assessment. Luciferase reporter assay was employed to interrogate the potential regulatory action of let-7 genes on H19 expression. The endogenous HRAS protein was quantified by western blot. H19 was aberrantly over-expression in nasopharyngeal carcinoma, which intimately associated with poorer prognosis. H19-deficency significantly inhibited cell viability and suppressed cell proliferation. Furthermore, both migrative and invasive capacity were compromised by H19 knockdown. H19-silencing remarkably delayed xenograft tumour progression and lung metastasis. Mechanistically, H19 competitively sponged let-7 genes and therefore up-regulated HRAS, which consequently contributed to its oncogenic activity in nasopharyngeal carcinomas. Our study uncovered the oncogenic properties of H19 in nasopharyngeal carcinoma and highlighted the H19-let-7-HRAS signalling axis underlying the incidence and metastasis of this disease.	31556327	RID07838	ceRNA or sponge	metastasis,prognosis	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE67939)
Hepatocellular carcinoma	CASC2	MIR183	negatively-F	luciferase reporter assay;miRcode	downregulation	RT-qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+);colony formation(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000207691	NA	255082	406959	C10orf5	MIRN183|miR-183|miRNA183	The Long Non-Coding RNA CASC2 Suppresses Cell Viability, Migration, and Invasion in Hepatocellular Carcinoma Cells by Directly Downregulating miR-183.Researchers have reported that cancer susceptibility candidate 2 (CASC2), a long non-coding RNA, is down-regulated in various cancers, including HCC. Our study aimed to investigate the molecular mechanism(s) of CASC2 in HCC.Real-time quantitative PCR (RT-qPCR) was used to analyze the expression of CASC2 and miR-183 in HCC tissues and cells. The viability of HCC SMMC-7721 and Huh-7 cells was detected through MTT assay. Colony formation assay was performed to assess the colony formation ability of HCC cells. The migration and invasion abilities of HCC cells were evaluated by Transwell assay. western blot was conducted to examine levels of key Wnt/beta-catenin signaling pathway factors, C-myc, cyclinD,survivin, and beta-catenin. The interaction between CASC2 and miR-183 was affirmed by bioinformatics analysis and luciferase reporter assay.CASC2 was down-regulated in HCC tissues and cell lines, while miR-183 was up-regulated. The expression of miR-183 was negatively correlated with CASC2 expression in HCC tissues. Overexpression of CASC2 inhibited cell viability, colony formation,migration, and invasion in HCC cells, as well as Wnt/beta-catenin signaling pathway activity. miR-183 was a downstream target of CASC2 and negatively regulated by CASC2. Introduction of miR-183 rescued CASC2-induced suppressive effects on HCC cell viability, colony formation, migration, and invasion and Wnt/beta-catenin signaling.CASC2 inhibited cell viability and the colony formation, migration, and invasion abilities of HCC cells by directly downregulating miR-183 through inactivation of the Wnt/beta-catenin signaling pathway.	31538425	RID07839	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Non-small cell lung cancer	MAGI2-AS3	PTEN	positively-E	dual-luciferase reporter assay;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell viability(+)	ceRNA(miR-23a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000171862	NA	100505881	5728	ENST00000414797	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA MAGI2-AS3 suppresses the proliferation and invasion of non-small cell lung carcinoma through miRNA-23a-3p/PTEN axis.To uncover the biological role of long non-coding RNA (lncRNA) MAGI2-AS3 in the progression of non-small cell lung carcinoma (NSCLC) and its molecular mechanism.LncRNA MAGI2-AS3 level in NSCLC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. Chi-square test was conducted to analyze the correlation between MAGI2-AS3 level and pathological characteristics of NSCLC patients. Survival analysis was performed in NSCLC patients with high expression or low expression of MAGI2-AS3. In vitro influences of MAGI2-AS3 on viability and invasive ability of A549 and PC9 cells were evaluated. MicroRNA-23a-3p (miRNA-23a-3p), the target gene of MAGI2-AS3 was determined through the dual-luciferase reporter gene assay. In a similar way, the target gene of miRNA-23a-3p was identified. Finally, the regulatory effect of MAGI2-AS3/miRNA-23a-3p/PTEN (gene of phosphate and tension homology deleted on chromosome ten) axis on cellular behaviors of NSCLC cells was assessed.LncRNA MAGI2-AS3 was downregulated in NSCLC tissues and cell lines. Its level was closely related to tumor size, Tumor Node Metastasis (TNM) stage and distant metastasis of NSCLC patients. The worse prognosis was identified in NSCLC patients with low expression of MAGI2-AS3 relative to those with a high expression. Overexpression of MAGI2-AS3 markedly attenuated viability and invasive ability of A549 and PC9 cells. MiRNA-23a-3p was verified to be the target gene of MAGI2-AS3, and furthermore, PTEN was the target of miRNA- 23a-3p. Overexpression of miRNA-23a-3p could reverse the inhibited viability and invasion in NSCLC cells overexpressing MAGI2-AS3.MAGI2-AS3 is downregulated in NSCLC. Overexpression of MAGI2-AS3 suppresses the proliferative and invasive abilities of NSCLC via miRNA-23a-3p/PTEN axis.	31539127	RID07840	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Non-small cell lung cancer	LBX2-AS1	NOTCH1	positively-E	siRNA;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000257702	GRCh38_2:74502552-74505091	ENSG00000148400	NA	151534	4851	NA	TAN1	Novel long non-coding RNA LBX2-AS1 indicates poor prognosis and promotes cell proliferation and metastasis through Notch signaling in non-small cell lung cancer.Recent reports have suggested that long non-coding RNA LBX2 antisense RNA 1 (LBX2-AS1) acts as an important regulator in cancer progression. This study aimed to investigate the clinical significance of LBX2-AS1 in non-small cell lung cancer (NSCLC) patients and its biological functions.The expressions of LBX2-AS1 were examined in 165 paired NSCLC tissues and adjacent normal tissues from NSCLC patients by qRT-PCR The clinical significance of LBX2-AS1 was determined using a series of statistical methods. The effects of LBX2-AS1 knockdown on NSCLC cell proliferation, migration,and invasion were investigated by CCK-8 assays, colony formation assays, EdU proliferation assays, Wound healing assays, and transwell assays. The promotive roles of LBX2-AS1 on Notch1 signal were determined using RTPCR and western blot.We found that LBX2-AS1 was highly expressed in NSCLC tissues and cell lines.The increased levels of LBX2-AS1 were observed to be positively correlated with TNM stage, histological grade, and lymph node metastasis. Furthermore, the Kaplan-Meier survival curves indicated that patients with higher expressions of LBX2-AS1 had unfavorable overall survival. Lost-of-functions assays revealed that the knockdown of LBX2-AS1 in H1299 and A549 cells inhibited cell proliferation, migration,and invasion. Mechanistic studies revealed that the suppression of LBX2-AS1 resulted in the reduced expressions of Notch1, p21, and Hes1,suggesting that LBX2-AS1 might promote the activation of the Notch pathway.Our study identified a novel NSCLC-related lncRNA LBX2-AS1, which may represent a novel prognostic biomarker and a potential therapeutic target for NSCLC.	31539129	RID07841	expression association	metastasis,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	LBX2-AS1	CDKN1A	positively-E	siRNA;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000257702	GRCh38_2:74502552-74505091	ENSG00000124762	NA	151534	1026	NA	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	Novel long non-coding RNA LBX2-AS1 indicates poor prognosis and promotes cell proliferation and metastasis through Notch signaling in non-small cell lung cancer.Recent reports have suggested that long non-coding RNA LBX2 antisense RNA 1 (LBX2-AS1) acts as an important regulator in cancer progression. This study aimed to investigate the clinical significance of LBX2-AS1 in non-small cell lung cancer (NSCLC) patients and its biological functions.The expressions of LBX2-AS1 were examined in 165 paired NSCLC tissues and adjacent normal tissues from NSCLC patients by qRT-PCR The clinical significance of LBX2-AS1 was determined using a series of statistical methods. The effects of LBX2-AS1 knockdown on NSCLC cell proliferation, migration,and invasion were investigated by CCK-8 assays, colony formation assays, EdU proliferation assays, Wound healing assays, and transwell assays. The promotive roles of LBX2-AS1 on Notch1 signal were determined using RTPCR and western blot.We found that LBX2-AS1 was highly expressed in NSCLC tissues and cell lines.The increased levels of LBX2-AS1 were observed to be positively correlated with TNM stage, histological grade, and lymph node metastasis. Furthermore, the Kaplan-Meier survival curves indicated that patients with higher expressions of LBX2-AS1 had unfavorable overall survival. Lost-of-functions assays revealed that the knockdown of LBX2-AS1 in H1299 and A549 cells inhibited cell proliferation, migration,and invasion. Mechanistic studies revealed that the suppression of LBX2-AS1 resulted in the reduced expressions of Notch1, p21, and Hes1,suggesting that LBX2-AS1 might promote the activation of the Notch pathway.Our study identified a novel NSCLC-related lncRNA LBX2-AS1, which may represent a novel prognostic biomarker and a potential therapeutic target for NSCLC.	31539129	RID07842	expression association	metastasis,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Non-small cell lung cancer	LBX2-AS1	HES1	positively-E	siRNA;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000257702	GRCh38_2:74502552-74505091	ENSG00000114315	NA	151534	3280	NA	bHLHb39|FLJ20408|HES-1|HRY	Novel long non-coding RNA LBX2-AS1 indicates poor prognosis and promotes cell proliferation and metastasis through Notch signaling in non-small cell lung cancer.Recent reports have suggested that long non-coding RNA LBX2 antisense RNA 1 (LBX2-AS1) acts as an important regulator in cancer progression. This study aimed to investigate the clinical significance of LBX2-AS1 in non-small cell lung cancer (NSCLC) patients and its biological functions.The expressions of LBX2-AS1 were examined in 165 paired NSCLC tissues and adjacent normal tissues from NSCLC patients by qRT-PCR The clinical significance of LBX2-AS1 was determined using a series of statistical methods. The effects of LBX2-AS1 knockdown on NSCLC cell proliferation, migration,and invasion were investigated by CCK-8 assays, colony formation assays, EdU proliferation assays, Wound healing assays, and transwell assays. The promotive roles of LBX2-AS1 on Notch1 signal were determined using RTPCR and western blot.We found that LBX2-AS1 was highly expressed in NSCLC tissues and cell lines.The increased levels of LBX2-AS1 were observed to be positively correlated with TNM stage, histological grade, and lymph node metastasis. Furthermore, the Kaplan-Meier survival curves indicated that patients with higher expressions of LBX2-AS1 had unfavorable overall survival. Lost-of-functions assays revealed that the knockdown of LBX2-AS1 in H1299 and A549 cells inhibited cell proliferation, migration,and invasion. Mechanistic studies revealed that the suppression of LBX2-AS1 resulted in the reduced expressions of Notch1, p21, and Hes1,suggesting that LBX2-AS1 might promote the activation of the Notch pathway.Our study identified a novel NSCLC-related lncRNA LBX2-AS1, which may represent a novel prognostic biomarker and a potential therapeutic target for NSCLC.	31539129	RID07843	expression association	metastasis,prognosis	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	MEG3	SOX11	positively-E	RNA pull-down assay;luciferase reporter assay;siRNA;starBase;mirBase;western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell growth(+);cell viability(+);apoptosis process(-)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000176887	NA	55384	6664	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	NA	lncRNA MEG3 inhibits the growth of hepatocellular carcinoma cells by sponging miR-9-5p to upregulate SOX11.This study used western blot and qRT-PCRto evaluate the expression of MEG3, miR-9-5p, and Sex determining Region Y-related HMG-box 11 (SOX11) in HCC tissues and cell lines. RNA pull-down and luciferase reporter assay were used to evaluate these molecular interactions.3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry detected the viability and apoptosis of HCC cells, respectively. The results showed that MEG3 and SOX11 were poorly expressed but miR-9-5p was highly expressed in HCC. The expression levels of these molecules suggested a negative correlation between MEG3 and miR-9-5p and a positive correlation with SOX11, confirmed by Pearson correlation analysis and biology experiments. Furthermore, MEG3 could combine with miR-9-5p, and SOX11 was a direct target of miR-9-5p. Moreover, MEG3 over-expression promoted cell apoptosis and growth inhibition in HCC cells through sponging miR-9-5p to upregulate SOX11. Therefore, the interactions among MEG3, miR-9-5p, and SOX11 might offer a novel insight for understanding HCC pathogeny and provide potential diagnostic markers and therapeutic targets for HCC.	31531526	RID07844	ceRNA or sponge	NA		UP(LIHC,BRCA);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Gastric cancer	GAS5	TP53	positively-F	RNA pull-down assay;RIP;siRNA	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	LFS1|p53	Long non-coding RNA GAS5 inhibits migration and invasion in gastriccancer via interacting with p53 protein.In this study, we planned to investigate the role of GAS5 in gastric cancer (GC) metastasis.Gene expressions were detected by qRT-PCR ISH staining was applied to assess GAS5 level inclinical tissues. Gain-of-function assays were conducted to evaluate the function of GAS5 in GC metastasis.RNA pull down, RIP and cycloheximide assays were performed to confirm the relationship between GAS5and p53 protein.GAS5 expression was markedly decreased in GC tissues and cell lines, and its low expression wasstrongly related to GC metastasis and unsatisfactory prognosis. GAS5 overexpression repressed GC cellmigration and invasion by targeting p53. Intriguingly, GAS5 relied on the exon 12 to interact with andstabilize p53 protein.Our data implied that GAS5 is a suppressor in GC metastasis via modulating p53 signaling,suggesting GAS5 as a potential therapeutic target for GC, especially for patients with metastasis.	31530437	RID07845	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	PDIA3P1	TRAF6	positively-E	siRNA;RNA pull-down assay;RIP;Targetscan	upregulation	qRT-PCR	GSE43541;GSE58074;GSE32301;GSE42531;GSE63351	NA	NF-kB signaling pathway(+);chemosensitivity(-)	ceRNA(miR-125/124)	regulation	NA	Doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180867	GRCh38_1:147172744-147179622	ENSG00000175104	NA	171423	7189	GRP58P|PDIA3P	RNF85	A hMTR4-PDIA3P1-miR-125/124-TRAF6 Regulatory Axis and Its Function in NF kappa B Signaling and Chemoresistance.We found that lncRNA PDIA3P1 (protein disulfide isomerase family A member 3 pseudogene 1) was up-regulated in multiple cancer types and following treatment with DNA-damaging chemotherapeutic agents, like doxorubicin (Dox). Higher PDIA3P1 level was associated with poorer recurrence-free survival of human hepatocellular carcinoma (HCC). Both gain-of-function and loss-of-function studies revealed that PDIA3P1 protected cancer cells from Dox-induced apoptosis and allowed tumor xenografts to grow faster and to be more resistant to Dox treatment. Mechanistically, miR-125a/b and miR-124 suppressed the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6), but PDIA3P1 bound to miR-125a/b/miR-124 and relieved their repression on TRAF6, leading to activation of the nuclear factor kappa B (NF-kB) pathway. Consistently, the effect of PDIA3P1 inhibition in promoting Dox-triggered apoptosis was antagonized by silencing the inhibitor of kBalpha (IkBalpha) or overexpressing TRAF6. Administration of BAY 11-7085, an NF-kB inhibitor attenuated PDIA3P1-induced resistance to Dox treatment in mouse xenografts. Moreover, up-regulation of PDIA3P1 was significantly correlated with elevation of TRAF6, phosphorylated p65, or NF-kB downstream antiapoptosis genes in human HCC tissues. These data indicate that enhanced PDIA3P1 expression may confer chemoresistance by acting as a microRNA sponge to increase TRAF6 expression and augment NF-kB signaling. Subsequent investigations into the mechanisms of PDIA3P1 up-regulation revealed that human homologue of mRNA transport mutant 4 (hMTR4), which promotes RNA degradation, could bind to PDIA3P1, and this interaction was disrupted by Dox treatment. Overexpression of hMTR4 attenuated Dox-induced elevation of PDIA3P1, whereas silencing hMTR4 increased PDIA3P1 level, suggesting that Dox may up-regulate PDIA3P1 by abrogating the hMTR4-mediated PDIA3P1 degradation.There exists a hMTR4-PDIA3P1-miR-125/124-TRAF6 regulatory axis that regulates NF-kB signaling and chemoresistance, which may be exploited for anticancer therapy.	31509261	RID07846	ceRNA or sponge	recurrence,chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Chronic myelogenous leukemia	SNHG5	TNFRSF10A	negatively-E	shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell differentiation(-);apoptosis process(-)	transcriptional regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Chronic myeloid leukemia	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000104689	NA	387066	8797	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	Apo2|CD261|DR4|TRAILR-1|TRAILR1	Long Noncoding RNA (lncRNA) Small Nucleolar RNA Host Gene 5 (SNHG5) Regulates Proliferation, Differentiation, and Apoptosis of K562 Cells in Chronic Myeliod Leukemia.Human chronic myelogenous leukemia (CML) is a hematopoietic stem cell disorder with high malignant and invasive activity. lncRNA SNHG5 has been reported to be upregulated in CML.K562 cells were transfected with shRNA, and the expression level of SNHG5 was assessd by quantitative RTPCR. The proliferation ability was determined by CCK-8 assay. western blotwas performed to detect protein expressions related to cell proliferation, differentiation, and apoptosis. Cell apoptosis rate was analyzed by flow cytometry. The DNA methylation level was determined by methylation-specific PCR (MSP).Our results show that inhibition of SNHG5 induced by RNA interference significantly inhibits K562 cells proliferation and induces cell differentiation with the increased expression of CD42b, CD11b, CD14, GATA-1, and b-globin. Flow cytometry analysis indicated that inhibition of SNHG5 significantly induced cell apoptosis with decreased expression of Bcl-2 and increased expression of Bax and cleaved capase-3. Additionally, western blot and MSP analyses confirmed that inhibition of SNHG5 increased the expression of DR4 gene through suppressing its methylation.Inhibition of SNHG5 suppressed K562 cell proliferation through inducing the differentiation and apoptosis by inhibiting methylation of DR4. Therefore, downregulated SNHG5 could play a key role in CML progression, and might provide a new strategy for the treatment of CML.	31506418	RID07847	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	MIAT	SIRT1	positively-E	shRNA;miRWalk;LncBasePredictedV2.0;luciferase reporter assay;Targetscan	upregulation	RT-PCR	TCGA	NA	cancer progression(+);tumorigenesis(+);cell proliferation(+);cell migration(+);colony formation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-22-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000096717	NA	440823	23411	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	SIR2L1	lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senesc.The long noncoding RNA (lncRNA) myocardial infarction-associated transcript (miat) was first identified as an HCC specific SALncRNA. Knockdown of miat significantly promoted cellular senescence and inhibited HCC progression. Mechanistic study revealed that SAL-miat acted as a competitive endogenous RNA (ceRNA) that upregulated the expression of sirt1 by sponging miR-22-3p. Moreover, miat downregulation activated the tumor suppressor pathway (p53/p21 and p16/pRb) and stimulated senescent cancer cells to secrete senescence-associated secretory phenotype (SASP), which contributed to inhibition of tumor cell proliferation, and resulted in the suppression of HCC tumorigenesis. Together, our study provided mechanistic insights into a critical role of miat as a miRNA sponge in HCC cellular senescence, which might offer a potential therapeutic strategy for HCC treatment.	31503007	RID07848	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	TINCR	miR-21	negatively-E		downregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000199004	NA	257000	NA	FLJ90734|LINC00036|NCRNA00036|onco-lncRNA-16|PLAC2	NA	LncRNA PLAC 2 downregulated miR-21 in non-small cell lung cancer and predicted survival.A total of 187 NSCLC patients were admitted by The First Hospital of Jilin University from December 2010 to December 2014. All the patients were diagnosed by histopathological approaches. Transient cell transfections, RT-qPCR, invasion, and migration ability measurement, were applied for the experiments.PLAC2 was down-regulated, while miR-21 was up-regulated in NSCLC tissues compared to non-cancer tissues. Low PLAC2 levels in NSCLC tissues were associated with poor survival of NSCLC patients. PLAC2 and miR-21 were inversely correlated, and PLAC 2 over-expression in NSCLC cells resulted in the down-regulation of miR-21. However, miR-21 over-expression did not significantly affect PLAC2 expression. In addition, PLAC2 over-expression resulted in decreased migration and invasion rates of NSCLC cells. MiR-21 over-expression played the opposite role and attenuated the effects of PLAC2 over-expression.In conclusion, lncRNA PLAC2 down-regulated miR-21 in NSCLC and inhibited cancer cell migration and invasion.	31500623	RID07849	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	
Anaplastic thyroid carcinoma	MALAT1	FOXA1	positively-E	siRNA;Targetscan;luciferase reporter assay;RIP;RNA pull-down assay;shRNA;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+);cell autophagy(-)	ceRNA(miR-200a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000129514	NA	378938	3169	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HNF3A	Long noncoding RNA MALAT1 knockdown inhibits progression of anaplastic thyroid carcinoma by regulating miR-200a-3p/FOXA1.In this study, we focused on the effect of MALAT1 on cell proliferation, apoptosis, migration,invasion, and autophagy formation in anaplastic thyroid carcinoma (ATC) and explored the interaction between miR-200a-3p and MALAT1 or FOXA1. Moreover, murine xenograft model was established to investigate the roles and mechanism of MALAT1 in ATC progression in vivo. Results showed that MALAT1 expression was enhanced and miR-200a-3p was reduced in ATC tissues and cells. Knockdown of MALAT1 or overexpression of miR-200a-3p inhibited cell proliferation, migration and invasion but increased apoptosis and autophagy formation in ATC cells. Moreover, miR-200a-3p was directly bound to MALAT1 and its inhibition reversed the inhibitory effect of MALAT1 knockdown on progression of ATC. In addition,FOXA1 was indicated as a target of miR-200a-3p and its restoration attenuated the anti-cancer role of miR-200a-3p in ATC cells. Furthermore, MALAT1 functioned as a competing endogenous RNA (ceRNA) via sponging miR-200a-3p to derepress FOXA1 expression. Besides, interference of MALAT1 decreased tumor growth by upregulating miR-200a-3p and downregulating FOXA1. Collectively, MALAT1 knockdown suppressed ATC progression by regulating miR-200a-3p/FOXA1, providing a novel avenue for treatment of ATC.	31500506	RID07850	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Mantle cell lymphoma	HAGLROS	ATG5	positively-E	siRNA;shRNA;Targetscan	upregulation	qPCR	NA	NA	cell viability(+);apoptosis process(-);cell autophagy(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-100)	regulation	NA	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000057663	NA	102800310	9474	NA	APG5|APG5L|ASP|hAPG5	Long noncoding RNA HAGLROS promotes the process of mantle cell lymphoma by regulating miR-100/ATG5 axis and involving in PI3K/AKT/mTOR signal.HAGLROS level in mantle cell lymphoma cell lines was detected, followed by investigation of the influences of HAGLROS silencing on Mino cell biological performances. Afterwards, the express patterns of HAGLROS vs. miR-100, as well as miR-100 vs. ATG5, were investigated. Furthermore, whether HAGLROS could regulate the signals of PI3K/AKT/mTOR was analyzed. HAGLROS level was high in mantle cell lymphoma cell lines. Silencing of HAGLROS inhibited Mino cell viability, increased apoptosis and decreased autophagy by sponging miR-100. Moreover, miR-100 targeted ATG5 fixed. Furthermore, HAGLROS suppression resulted in inhibition on the briskness of PI3K/AKT/mTOR signals. Concurrently HAGLROS suppression and miR-100 inhibitor markedly changed the impacts of HAGLROS down-regulation alone on activating PI3K/AKT/mTOR signals, which could further change after co-transfection of si-HAGLROStmiR-100 inhibitortsiATG5. Our findings point out that expression of HAGLROS is increased in mantle cell lymphoma cells and may function as an oncogene in mantle cell lymphoma. HAGLROS may promote tumour development by regulating miR-100/ATG5/PI3K/AKT/mTOR axis.	31498006	RID07851	ceRNA or sponge	NA		UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Colon cancer	ZEB2-AS1	BCL2	positively-E	siRNA;luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-143)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000171791	NA	100303491	596	ZEB2-AS|ZEB2AS|ZEB2NAT	Bcl-2|PPP1R50	Long non-coding RNA ZEB2-AS1 promotes proliferation and inhibits apoptosis of colon cancer cells via miR-143/bcl-2 axis.Here, we firstly observed that ZEB2-AS1 was significantly upregulated in colon cancer and predicted a poor prognosis. Functional assays showed that silencing ZEB2-AS1 expression remarkably inhibited proliferation, suppressed cell cycle transition while induced apoptosis in CC cells. In addition, miR-143 was demonstrated to act as a tumor suppressor and predicted as a downstream target of ZEB2-AS1 in CC. Furthermore, bcl-2 was identified as a direct target of miR-143 and ZEB2-AS1 could regulate the expression of bcl-2 via miR-143 in CC. A rescue assay indicated that downregulation of miR-143 partly abolished the suppressive effect of ZEB2-AS1 silencing on CC cells proliferation. Collectively, our results revealed that ZEB2-AS1 was upregualted and functioned as an oncogene via regulating miR-143/bcl-2 axis in colon cancer. These findings suggest that ZEB2-AS1 may serve a novel biomarker in the diagnosis and a potential therapeutic target in the treatment of colon cancer.	31497237	RID07852	ceRNA or sponge	prognosis	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Gastric cancer	HULC	FOXM1	positively-E	RNA pull-down assay;RIP;RPISeq;siRNA;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(-);chemoresistance(-)	transcriptional regulation	binding/interaction	NA	Cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251164	NA	ENSG00000111206	NA	728655	2305	HCCAT1|LINC00078|NCRNA00078	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	METase/lncRNA HULC/FoxM1 reduced cisplatin resistance in gastric cancer by suppressing autophagy.Autophagy plays an important role in regulating cisplatin (CDDP) resistance in gastric cancer cells. However, the underlying mechanism of methioninase (METase) in the regulation of autophagy and CDDP resistance of gastric cancer cells is still not clear.western blot was used to detect the levels of autophagy-related proteins, multidrug-resistant 1 (MDR-1), and FoxM1 protein. LncRNA HULC was detected by qRT-PCR Cell viability was detected using CCK-8 assay. The interaction between lncRNA HULC and FoxM1 was confirmed by RNA pull-down and RIP assay.Lentiviral vector carrying METase (LV-METase) suppressed autophagy and CDDP resistance of drug-resistant gastric cancer cells. LncRNA HULC was significantly downregulated in drug-resistant gastric cancer cells transfected with LV-METase. Besides, we found that lncRNA HULC interacted with FoxM1. In addition, METase suppressed autophagy to reduce CDDP resistance of drug-resistant gastric cancer cells through regulating HULC/FoxM1, and interfering HULC suppressed autophagy to reduce CDDP resistance of drug-resistant gastric cancer cells through regulating FoxM1. Finally,interfering HULC inhibited tumor growth in vivo.METase suppressed autophagy to reduce CDDP resistance of drug-resistant gastric cancer cells through regulating HULC/FoxM1 pathway.	31485766	RID07853	transcriptional regulation	chemoresistance		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Renal cell carcinoma	LINC-ROR	VEGFA	positively-E	shRNA;Targetscan;miRanda;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR- 206)	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000112715	NA	100885779	7422	lincRNA-RoR|lincRNA-ST8SIA3|ROR	VEGF|VEGF-A|VPF	lncRNA regulator of reprogramming (ROR ) is promotes the progression of renal cell carcinoma (RCC) through the miR-206/VEGF axis.ROR was found to be upregulated and microRNA (miR)-206 was found to be downregulated in RCC tissues and cells. Furthermore, the knockdown of ROR inhibited the proliferation,migration and invasion of RCC cells. It was found that ROR binds to miR- 206, and that ROR- induced cell proliferation and metastasis were reversed by the overexpression of miR- 206. In addition, the levels of miR- 206 and ROR were negatively correlated in RCC tissues. Furthermore, the overexpression of miR- 206 notably suppressed the proliferation, migration and invasion of RCC cells, and these effects were enhanced by the knockdown of vascular endothelial growth factor (VEGF); cell growth and metastasis induced by miR- 206 inhibitors could be reversed by the knockdown of VEGF. In addition, the expression levels of miR- 206 and VEGF were inversely correlated in RCC samples. In summary, the results of the present study revealed that ROR was upregulated in RCC tissues, which promoted tumor progression by regulating the miR-206/VEGF axis. The present findings provided a novel insight into the potential functions of ROR in RCC , and the ROR /miR- 206/VEGF pathway may be a promising therapeutic target for the treatment of patients with RCC .	31485634	RID07854	ceRNA or sponge	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Anaplastic thyroid carcinoma	NEAT1	SPAG9	positively-E	dual-luciferase reporter assay;RIP;siRNA;starBase;Targetscan;RNA pull-down assay;shRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);apoptosis process(-);cell autophagy(-)	ceRNA(miR-9-5p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000008294	NA	283131	9043	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CT89|FLJ13450|FLJ14006|FLJ26141|FLJ34602|HLC4|HSS|JIP-4|JIP4|JLP|KIAA0516|MGC117291|MGC14967|MGC74461|PHET|PIG6|SYD1	LncRNA nuclear paraspeckle assembly transcript 1(NEAT1) enhances the resistance of anaplastic thyroid carcinoma cells to cisplatin by sponging miR-9-5p and regulating SPAG9 expression.Reverse transcription-quantitative PCR assays were performed to detect the expression levels of NEAT1, microRNA (miR)-9-5p and sperm-associated antigen 9 (SPAG9). western blotwas conducted to assess the protein expression levels of p62, microtubule-associated proteins 1A/1B light chain 3B and SPAG9. Cell proliferation was detected using the Cell Counting kit-8 assay, and cell apoptosis was determined by flow cytometry. Dual-luciferase reporter and RNA immunoprecipitation assays were performed to verify the interaction between NEAT1 and miR-9-5p, or miR-9-5p and SPAG9. Furthermore, an animal model was used to investigate the regulatory effects of NEAT1 on cisplatin (DDP)-resistance in tumors in vivo. The present results demonstrated that NEAT1 was upregulated in ATC tissues and cell lines, and NEAT1 silencing resulted in decreased DDP-resistance of ATC cells. In addition, NEAT1 suppressed miR-9-5p expression by binding to miR-9-5p and SPAG9 was a direct target of miR-9-5p. miR-9-5p overexpression sensitized ATC cells to DDP. Notably, NEAT1 silencing exerted its inhibitory effect on DDP-resistance of ATC via the miR-9-5p/SPAG9 axis in vitro and in vivo. In conclusion, the present study demonstrated that NEAT1 silencing ameliorated DDP-resistance of ATC, at least in part by reducing miR-9-5p sponging and regulating SPAG5 expression; therefore, NEAT1 may be considered a potential therapeutic target of ATC.	31485599	RID07855	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Diffuse large b-cell lymphoma	SNHG16	PIM1	positively-E	shRNA;luciferase reporter assay;RNA pull-down assay;starBase	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+);cell growth(+)	ceRNA(miR-497-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000137193	NA	100507246	5292	Nbla10727|Nbla12061|ncRAN	PIM	Long non-coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B-cell lymphoma cells by targeting miR-497-5p/PIM1 axis.Here we disclosed that small nucleolar RNA host gene 16(SNHG16) was overexpressed in DLBCL tissues and the derived cell lines. SNHG16 knockdown significantly suppressed cell proliferation and cell cycle progression, and it induced apoptosis of DLBCL cells in vitro. Furthermore, silencing of SNHG16 markedly repressed in vivo growth of OCI-LY7 cells. Mechanistically, SNHG16 directly interacted with miR-497-5p by acting as a competing endogenous RNA (ceRNA) and inversely regulated the abundance of miR-497-5p in DLBCL cells. Moreover, the proto-oncogene proviral integration site for Moloney murine leukaemia virus 1 (PIM1) was identified as a novel direct target of miR-497-5p. SNHG16 overexpression rescued miR-497-5p-induced down-regulation of PIM1 in DLBCL cells. Importantly, restoration of PIM1 expression reversed SNHG16 knockdown-induced inhibition of proliferation,G0/G1 phase arrest and apoptosis of OCI-LY7 cells. Our study suggests that the SNHG16/miR-497-5p/PIM1 axis may provide promising therapeutic targets for DLBCL progression.	31483572	RID07856	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Gastric cancer	CCAT1	miR-219-1	negatively-F	shRNA;Targetscan;miRBase;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+);cell growth(+);tumorigenesis(+)	sponge	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000247844	NA	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	lncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miR-219-1.The results exhibited the fact that colon cancer associated transcript-1 (CCAT1) was expressed higher in 57 GC tissue samples than in 57 paired adjacent normal tissue samples. The expression of CCAT1 was also increased in GC cell lines (MKN45, Hs746T, and SGC-7901) compared with the gastric epithelial cell line GES-1. Besides this, decreased cell proliferation with increased cell apoptosis was detected in SGC-7902 cells transfected with CCAT1 short hairpin RNA (shRNA). At the same time, a lower cell invasion ability was measured in SCG-7901 cells transfected with CCAT1 shRNA. In addition, miR-219-1 was predicted and convinced a direct target of CCAT1. The expression of miR-219-1 was decreased in GC tissues and GC cell lines. Further studies demonstrated that the roles of CCAT1 in cell proliferation, apoptosis, and invasion were inhibited by miR-219-1. Finally, in vivo experiment indicated that tumor growth of GC was suppressed through knockdown of CCAT1. In conclusion, these results suggested that CAT1 promotes the tumorigenesis and progression of GC by negatively regulating miR-219-1.	31478245	RID07857	ceRNA or sponge	NA		
Osteosarcoma	FER1L4	SOCS5	positively-E	siRNA;starBase;miRNA.org;miRanda;RNA pull-down assay;dual-luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(-);epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-18a-5p)	regulation	NA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171150	NA	80307	9655	bA563A22B.1|C20orf124|dJ309K20.1	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5.The levels of FER1L4 were decreased significantly in OS tissues and cell lines compared with non-tumorous tissues or hFOB1.19. Knockdown of FER1L4 in OS cells decreased the apoptosis rate, but increased the OS cell proliferation, upregulated the expression levels of CD133 and Nanog, as well as promoted Twist1 expression, increased the N-cadherin and Vimentin expression. In turn, the opposite trends were observed upon overexpression of FER1L4. In addition, the expression of PI3K, p-AKT (Ser470) and p-AKT (Thr308) was upregulated by siFER1L4, while decreased upon overexpression of FER1L4. MicroRNA (miRNA) -18a-5p, an osteosarcomapromoting miRNA which was suggested a target of FER1L4 in osteosarcoma, was identified to be a functional target of FER1L4 on the regulating of cell apoptosis and EMT, presently. The effects of FER1L4 overexpression on the markers of cell apoptosis, proliferation, EMT, and stemness and PI3K/AKT signaling were all reversed by miR-18a-5p upregulation. Furthermore, the suppressor of cytokine signaling 5 (SOCS5) was confirmed a target gene of miR-18a-5p by luciferase gene reporter assay and SOCS5 suppression by miR-18a-5p attenuated the effects of FER1L4 overexpression on the OS cells apoptosis and the expressed levels of PI3K, AKT, Twist1, Ncadherin and Vimentin. In conclusion, our data indicated thatthe overexpression of FER1L4 promoted apoptosis and inhibited the EMT markers expression and PI3K/AKT signaling pathway activation in OS cells via downregulating miR-18a-5p to promote SOCS5.	31473323	RID07858	ceRNA or sponge	NA	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Colorectal cancer	SNHG14	SKIL	positively-E	luciferase reporter assay;RIP;shRNA;starBase	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell metastasis(+);cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-32-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000136603	NA	104472715	6498	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	SNO|SnoA|SnoN	SNHG14 promotes the tumorigenesis and metastasis of colorectal cancer through miR-32-5p/SKIL axis.The expression of genes including SNHG14, miR-32-5p, and ski-oncogene-like (SKIL) was measured by RTqPCR assay. 5-Ethynyl-2'-deoxyuridine (EdU) assay was employed to measure cell proliferation. Cell migration and invasion were evaluated by transwell assay.western blot assay was performed to test the protein expression. The binding capacity between miR-32-5p and SNHG14 (or SKIL) was explored by luciferase reporter and RNA immunoprecipitation (RIP) assays. SNHG14 expression is upregulated in CRC cells. Moreover, SNHG14 suppression inhibited the proliferation, metastasis, and epithelialmesenchymal transition (EMT) process in CRC cells. miR-32-5p presented lower expression, which was negatively regulated by SNHG14. SKIL could combine with miR-32-5p. The mRNA and protein expression of SKIL was downregulated by SNHG14 knockdown or miR-32-5p overexpression. At last, the inhibitory effect of SNHG14 suppression on proliferation, metastasis, and EMT process was rescued by SKIL overexpression. SNHG14 regulates CRC progression via miR-32-5p/SKIL axis, providing a novel point in treatment of CRC patients.	31471872	RID07859	ceRNA or sponge	metastasis	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Glioblastoma	SNHG15	CDK6	positively-E	siRNA	upregulation	qRT-PCR	GSE16581	NA	chemoresistance(+);cell stemness(+);tumorigenesis(+);chemosensitivity(-)	ceRNA(miR-627-5p)	regulation	NA	Temozolomide;palbociclib	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000105810	NA	285958	1021	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	PLSTIRE	Modulating lncRNA SNHG15/CDK6/miR-627 circuit by palbociclib, overcomestemozolomide resistance and reduces M2-polarization of glioma associated microglia in glioblastoma multiforme.We showed that SNHG15 was upregulated in GBM cells and associated with a poor prognosis for the patients of GBM using public databases. Next, we collected temozolomide sensitive (TMZ-S) and resistant (TMZ-R) clinical samples and demonstrated that co-culturing TMZ-R cells with HMC3 (microglial) cells promoted M2-polarization of HMC3 and the secretion of pro-GBM cytokines TGF-beta and IL-6.Comparative qPCR analysis of TMZ-S and TMZ-R cells showed that a significantly higher level of SNHG15,coincidental with a higher level of Sox2, beta-catenin, EGFR, and CDK6 in TMZ-R cells. Subsequently, using bioinformatics tool, a potential mechanistic route for SNHG15 to promote GBM tumorigenesis was by inhibiting tumor suppressor, miR-627-5p which leads to activation of CDK6. Gene-silencing technique was employed to demonstrate that suppression of SNHG15 indeed led to the suppression of GBM tumorigenesis, accompanied by an increase miR-627-5p and decreased its two oncogenic targets, CDK6 and SOX-2. In addition, SNHG15-silenced TMZ-R cells became significantly sensitive towards TMZ treatment and less capable of promoting M2-phenotype in the HMC3 microglia cells. We then evaluated the potential anti-GBM activity of CDK6 inhibitor, palbociclib, using TMZ-R PDX mouse models. Palbociclib treatment significantly reduced tumorigenesis in TMZ-R/HMC3 bearing mice and SNHG15 and CDK6 expression was significantly reduced while miR-627-5p level was increased. Additionally, palbociclib treatment appeared to overcome TMZ resistance as well as reduced M2 markers in HMC3 cells.Together, we provided evidence supporting the usage of CDK6 inhibitor for TMZ-resistant GBM cases.Further investigation is warranted for the consideration of clinical trials.	31462285	RID07860	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Gastric cancer	LDC1P	WNT1	positively-E	siRNA;immunohistochemistry;shRNA;overexpression	upregulation	RT-qPCR	GSE54129;TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260386	GRCh38_1:31500085-31509648	ENSG00000125084	NA	149086	7471	LINC01225	INT1	Long non-coding RNA LINC01225 promotes proliferation,invasion and migration of gastric cancer via Wnt/beta-catenin signalling pathway.Here, we verified that LINC01225 was up-regulated in tumour tissues and plasma of gastric cancer (GC). Analysis with clinicopathological information suggested that up-regulation of LINC01225 was associated with advanced disease and poorer overall survival. Receiver operating characteristic (ROC) analysis showed that plasma LINC01225 had a moderate accuracy for diagnosis of GC. In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. Mechanistic investigations showed that LINC01225 silencing inhibited epithelial-mesenchymal transition (EMT) process and attenuated Wnt/beta-catenin signalling of GC. Furthermore, ectopic expression of Wnt1 or suppression of GSK-3beta abolished the si-LINC01225-mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC. In conclusion, LINC01225 promotes the progression of GC through Wnt/beta-catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.	31460694	RID07861	expression association	NA		
Gastric cancer	LDC1P	CTNNB1	positively-E	siRNA;immunohistochemistry;shRNA;overexpression	upregulation	RT-qPCR	GSE54129;TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000260386	GRCh38_1:31500085-31509648	ENSG00000168036	NA	149086	1499	LINC01225	armadillo|beta-catenin|CTNNB	Long non-coding RNA LINC01225 promotes proliferation,invasion and migration of gastric cancer via Wnt/beta-catenin signalling pathway.Here, we verified that LINC01225 was up-regulated in tumour tissues and plasma of gastric cancer (GC). Analysis with clinicopathological information suggested that up-regulation of LINC01225 was associated with advanced disease and poorer overall survival. Receiver operating characteristic (ROC) analysis showed that plasma LINC01225 had a moderate accuracy for diagnosis of GC. In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. Mechanistic investigations showed that LINC01225 silencing inhibited epithelial-mesenchymal transition (EMT) process and attenuated Wnt/beta-catenin signalling of GC. Furthermore, ectopic expression of Wnt1 or suppression of GSK-3beta abolished the si-LINC01225-mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC. In conclusion, LINC01225 promotes the progression of GC through Wnt/beta-catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.	31460694	RID07862	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	OECC	PIK3CA	positively-E	shRNA;overexpression	upregulation	RT-qPCR;sequencing	NA	NA	cell metastasis(+);cell proliferation(+);colony formation(+);cell viability(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000121879	NA	NA	5290	NA	PI3K	Long non-coding RNA OECC promotes cell proliferation and metastasis through the PI3K/Akt/mTOR signaling pathway in human lung cancer.It was initially revealed that the relative transcript level of OECC was highly upregulated in clinical human lung cancer tissues as well as in cultured lung cancer cells. Knockdown of OECC with specific short hairpin RNAs in lung cancer cell lines A549 and 95D inhibited colony formation and cell viability, as evidenced using colony formation assays and cell proliferation assays. Furthermore, depletion of OECC in A549 and 95D cells suppressed migration and invasion, which was verified using Transwell assays. RNA-sequence analysis suggested that the phosphoinositide 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin signaling pathway was positively regulated by OECC in lung cancer cells A549. In addition, overexpression of Akt in OECC-depleted A549 and 95D cells reversed the suppression of proliferation and migration caused by OECC depletion. The results of the present study identified lncRNA OECC as a novel regulator of lung cancer progression and provided new clues for the clinical treatment of lung cancer.	31452780	RID07863	expression association	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Lung cancer	OECC	AKT1	positively-E	shRNA;overexpression	upregulation	RT-qPCR;sequencing	NA	NA	cell metastasis(+);cell proliferation(+);colony formation(+);cell viability(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000142208	NA	NA	207	NA	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA OECC promotes cell proliferation and metastasis through the PI3K/Akt/mTOR signaling pathway in human lung cancer.It was initially revealed that the relative transcript level of OECC was highly upregulated in clinical human lung cancer tissues as well as in cultured lung cancer cells. Knockdown of OECC with specific short hairpin RNAs in lung cancer cell lines A549 and 95D inhibited colony formation and cell viability, as evidenced using colony formation assays and cell proliferation assays. Furthermore, depletion of OECC in A549 and 95D cells suppressed migration and invasion, which was verified using Transwell assays. RNA-sequence analysis suggested that the phosphoinositide 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin signaling pathway was positively regulated by OECC in lung cancer cells A549. In addition, overexpression of Akt in OECC-depleted A549 and 95D cells reversed the suppression of proliferation and migration caused by OECC depletion. The results of the present study identified lncRNA OECC as a novel regulator of lung cancer progression and provided new clues for the clinical treatment of lung cancer.	31452780	RID07864	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	OECC	MTOR	positively-E	shRNA;overexpression	upregulation	RT-qPCR;sequencing	NA	NA	cell metastasis(+);cell proliferation(+);colony formation(+);cell viability(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000198793	NA	NA	2475	NA	FLJ44809|FRAP|FRAP1|FRAP2|RAFT1|RAPT1	Long non-coding RNA OECC promotes cell proliferation and metastasis through the PI3K/Akt/mTOR signaling pathway in human lung cancer.It was initially revealed that the relative transcript level of OECC was highly upregulated in clinical human lung cancer tissues as well as in cultured lung cancer cells. Knockdown of OECC with specific short hairpin RNAs in lung cancer cell lines A549 and 95D inhibited colony formation and cell viability, as evidenced using colony formation assays and cell proliferation assays. Furthermore, depletion of OECC in A549 and 95D cells suppressed migration and invasion, which was verified using Transwell assays. RNA-sequence analysis suggested that the phosphoinositide 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin signaling pathway was positively regulated by OECC in lung cancer cells A549. In addition, overexpression of Akt in OECC-depleted A549 and 95D cells reversed the suppression of proliferation and migration caused by OECC depletion. The results of the present study identified lncRNA OECC as a novel regulator of lung cancer progression and provided new clues for the clinical treatment of lung cancer.	31452780	RID07865	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Osteosarcoma	AFAP1-AS1	TWIST1	positively-E	RIP;siRNA	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell cycle(+);cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000122691	NA	84740	7291	AFAP1-AS|AFAP1AS|MGC10981	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	LncRNA AFAP1-AS1 promotes tumorigenesis and epithelial-mesenchymal transition of osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway.LncRNA AFAP1-AS1 has been validated to be abnormally upregulated and play oncogenic roles in various malignant tumors.Quantitative reverse transcription PCR (qRT-PCR is applied to examine AFAP1-AS1 expression in OS tissues and OS cell lines. The function of AFAP1-AS1 in OS cells is investigated via in-vitro and in-vivo assays. western blot and rescue experiments are applied to detect the expression changes of key molecules including epithelial-mesenchymal transition markers and identify the underlying molecular mechanism. RNA immunoprecipitation is performed to reveal the interaction between AFAP1-AS1 and RhoC.AFAP1-AS1 expression is upregulated in human OS tissues and cell lines. AFAP1-AS1 knockdown induces OS cell apoptosis and cell cycle G0/G1 arrest, suppresses OS cells growth, migration, invasion, vasculogenic mimicry formation and epithelial-mesenchymal transition (EMT), and affects actin filament integrity. AFAP1-AS1 knockdown suppresses OS tumor formation and growth in nude mice. AFAP1-AS1 knockdown elicits a signaling inhibition including decreased levels of RhoC, ROCK1, p38MAPK and Twist1. Moreover, AFAP1-AS1 interacts with RhoC. Overexpression of RhoC can partly reverse AFAP1-AS1 downregulation-induced cell EMT inhibition.AFAP1-AS1 is overexpressed in osteosarcoma and plays an oncogenic role in osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway, in which RhoC acts as the interaction target of AFAP1-AS1. Our findings indicated a novel molecular mechanism underlying the tumorigenesis and progression of osteosarcoma. AFAP1-AS1 could serve as a promising therapeutic target in OS treatment.	31443665	RID07866	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	UP(SKCM);DATA(GSE38495)
Osteosarcoma	AFAP1-AS1	RHOC	positively-E	RIP;siRNA	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell cycle(+);cell growth(+);cell migration(+);cell invasion(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000155366	NA	84740	389	AFAP1-AS|AFAP1AS|MGC10981	ARH9|ARHC	LncRNA AFAP1-AS1 promotes tumorigenesis and epithelial-mesenchymal transition of osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway.LncRNA AFAP1-AS1 has been validated to be abnormally upregulated and play oncogenic roles in various malignant tumors.Quantitative reverse transcription PCR (qRT-PCR is applied to examine AFAP1-AS1 expression in OS tissues and OS cell lines. The function of AFAP1-AS1 in OS cells is investigated via in-vitro and in-vivo assays. western blot and rescue experiments are applied to detect the expression changes of key molecules including epithelial-mesenchymal transition markers and identify the underlying molecular mechanism. RNA immunoprecipitation is performed to reveal the interaction between AFAP1-AS1 and RhoC.AFAP1-AS1 expression is upregulated in human OS tissues and cell lines. AFAP1-AS1 knockdown induces OS cell apoptosis and cell cycle G0/G1 arrest, suppresses OS cells growth, migration, invasion, vasculogenic mimicry formation and epithelial-mesenchymal transition (EMT), and affects actin filament integrity. AFAP1-AS1 knockdown suppresses OS tumor formation and growth in nude mice. AFAP1-AS1 knockdown elicits a signaling inhibition including decreased levels of RhoC, ROCK1, p38MAPK and Twist1. Moreover, AFAP1-AS1 interacts with RhoC. Overexpression of RhoC can partly reverse AFAP1-AS1 downregulation-induced cell EMT inhibition.AFAP1-AS1 is overexpressed in osteosarcoma and plays an oncogenic role in osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway, in which RhoC acts as the interaction target of AFAP1-AS1. Our findings indicated a novel molecular mechanism underlying the tumorigenesis and progression of osteosarcoma. AFAP1-AS1 could serve as a promising therapeutic target in OS treatment.	31443665	RID07867	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Osteosarcoma	AFAP1-AS1	ROCK1	positively-E	RIP;siRNA	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell cycle(+);cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754077-7778928	ENSG00000067900	NA	84740	6093	AFAP1-AS|AFAP1AS|MGC10981	p160ROCK	LncRNA AFAP1-AS1 promotes tumorigenesis and epithelial-mesenchymal transition of osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway.LncRNA AFAP1-AS1 has been validated to be abnormally upregulated and play oncogenic roles in various malignant tumors.Quantitative reverse transcription PCR (qRT-PCR is applied to examine AFAP1-AS1 expression in OS tissues and OS cell lines. The function of AFAP1-AS1 in OS cells is investigated via in-vitro and in-vivo assays. western blot and rescue experiments are applied to detect the expression changes of key molecules including epithelial-mesenchymal transition markers and identify the underlying molecular mechanism. RNA immunoprecipitation is performed to reveal the interaction between AFAP1-AS1 and RhoC.AFAP1-AS1 expression is upregulated in human OS tissues and cell lines. AFAP1-AS1 knockdown induces OS cell apoptosis and cell cycle G0/G1 arrest, suppresses OS cells growth, migration, invasion, vasculogenic mimicry formation and epithelial-mesenchymal transition (EMT), and affects actin filament integrity. AFAP1-AS1 knockdown suppresses OS tumor formation and growth in nude mice. AFAP1-AS1 knockdown elicits a signaling inhibition including decreased levels of RhoC, ROCK1, p38MAPK and Twist1. Moreover, AFAP1-AS1 interacts with RhoC. Overexpression of RhoC can partly reverse AFAP1-AS1 downregulation-induced cell EMT inhibition.AFAP1-AS1 is overexpressed in osteosarcoma and plays an oncogenic role in osteosarcoma through RhoC/ROCK1/p38MAPK/Twist1 signaling pathway, in which RhoC acts as the interaction target of AFAP1-AS1. Our findings indicated a novel molecular mechanism underlying the tumorigenesis and progression of osteosarcoma. AFAP1-AS1 could serve as a promising therapeutic target in OS treatment.	31443665	RID07868	expression association	NA	UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MIR4435-2HG	TGFB1	positively-E	overexpression	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000105329	NA	541471	7040	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	CED|DPD1|TGFB|TGFbeta	LncRNA MIR4435-2HG is a potential early diagnostic marker for ovarian carcinoma.We found that both MIR4435-2HG and transforming growth factor beta 1 (TGF-beta1) were upregulated in ovarian carcinoma (OC). MIR4435-2HG is associated with tumor metastasis but not with tumor size. Upregulation of MIR4435-2HG distinguished early stage (Stage I and II) OC patients from healthy controls. Correlation analysis showed that plasma levels of MIR4435-2HG and TGF-beta1 were positively correlated only in OC patients. qPCR and western blotresults showed that MIR4435-2HG overexpression led to upregulation of TGF-beta1 in OC cells, while TGF-beta1 treatment did not significantly affect MIR4435-2HG expression. Transwell invasion and migration assays showed that MIR4435-2HG and TGF-beta1 promoted the invasion and migration of OC cells while TGF-beta inhibitor suppressed the invasion and migration of these cells. Further analysis of the Transwell invasion and migration assay results showed that TGF-beta inhibitor reduced the effects of MIR4435-2HG overexpression. Therefore, our results suggested that lncRNA MIR4435-2HG may promote OC by upregulating TGF-beta1. Further characterization of the functions of MIR4435-2HG in OC may provide novel targets for cancer therapies.	31435668	RID07869	expression association	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	EIF3J-DT	CTNND2	positively-E	dual-luciferase reporter assay;RNA pull-down assay;shRNA	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-122e5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000179523	GRCh38_15:44527257-44537046	ENSG00000169862	NA	645212	1501	EIF3J-AS1	GT24|NPRAP	Hypoxia-induced lncRNA EIF3J-AS1 accelerates hepatocellular carcinoma progression via targeting miR-122e5p/CTNND2 axis.LncRNA EIF3J-AS1 is recently reported to be highly expressed in HCC and correlates with recurrence-free survival.We demonstrated that EIF3J-AS1 expression was obviously upregulated in HCC tissues compared to adjacent noncancerous tissues. Moreover, the elevated levels of EIF3J-AS1 was detected in four HCC cell lines (HepG2, SMMC-7721, MHCC97H, HCCLM3) compared with the normal hepatic cell line LO2. Notably, the expression of EIF3J-AS1 was correlated with prognostic features including tumor size, vascular invasion and tumor stage. TCGA-LIHC data indicated that the upregulated expression of EIF3J-AS1 predicted poor prognosis of HCC. EIF3J-AS1 knockdown remarkably suppressed the proliferation, migration and invasion of HCC cells. Mechanistically, EIF3J-AS1 inversely regulated miR-122e5p expression via acting as a competing endogenous RNA (ceRNA) in HCC cells. Furthermore, catenin delta 2 (CTNND2) was recognized as a novel target of miR-122e5p. CTNND2 restoration partially reversed EIF3J-AS1 knockdown-induced inhibitory effects on HCC cell proliferation, migration and invasion. Importantly, we found that hypoxia induced EIF3J-AS1 and CTNND2 expression, and led to miR-122e5p downregulation in HCC cells. EIF3J-AS1 knockdown partially abolished hypoxiainduced HCC cell proliferation and mobility. In conclusion, our results provide a new insight into the molecular pathogenesis of HCC, and EIF3J-AS1 may be a potential therapeutic target for HCC	31421822	RID07870	ceRNA or sponge	recurrence,prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Non-small cell lung cancer	GIAT4RA	HELLS	negatively-E	RIP;shRNA	downregulation	qRT-PCR	NA	NA	cell growth(+);colony formation(+);cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000119969	NA	NA	3070	NA	ICF4|LSH|Nbla10143|PASG|SMARCA6	GIAT4RA functions as a tumor suppressor in non-small cell lung cancer by counteracting Uchl3-sediated deubiquitination of LSH.Here, we showed that GIAT4RA, a poorly characterized lncRNA LOC102723729, was significantly decreased in lung cancer cells and tissues; while no association was observed with clinical risk factors, expression was linked with clinical stage and lymphatic metastasis. Higher expression of GIAT4RA was linked with overall survival in NSCLC. GIAT4RA inhibited many characteristics of tumorigenesis including cell growth, clonal formation, migration and invasion, epithelial-sesenchymal transition, tumor sphere and tumor growth in vivo. Mechanistically, GIAT4RA was essential for the degradation of chromatin modifier lymphoid-specific helicase (LSH) by counteracting the deubiquintination in proteasome pathway by binding to 227-589 AA of LSH. GIAT4RA interfered with ubiquitin hydrolase Uchl3-mediated interaction and stabilization of LSH. LSH knockdown rescued GIAT4RA-promoted features, and LSH overexpression prevented GIAT4RA-induced phenotypes. Taken together, lncRNA GIAT4RA plays a critical role in NSCLC adenocarcinoma as a ubiquitination regulator and tumor suppressor.	31417184	RID07871	transcriptional regulation	metastasis		UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE111842)
Gastric cancer	KRT19P3	COPS7A	positively-E	RNA pull-down assay;RIP;siRNA;immunohistochemistry	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);tumorigenesis(+);cell growth(+);NF-kB signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249681	GRCh38_4:109879070-109879897	ENSG00000111652	NA	442114	50813	NA	CSN7A	Long non-coding RNA KRT19P3 suppresses proliferation and metastasis through COPS7A-mediated NF-kB pathway in gastric cancer.The present study confirmed the downregulation of KRT19P3 in GC tissues and cells. Decreased expression of KRT19P3 was correlated with larger tumor size, advanced TNM stage, Lauren  classification, positive lymph node metastasis, and poor prognosis. Enforced expression of KRT19P3 significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, KRT19P3 knockdown had opposite effects. Mechanistically, RNA pull-down and RNA immunoprecipitation assay revealed that KRT19P3 could directly bind COPS7A. KRT19P3 enhanced COPS7A protein stability in GC cells, and KRT19P3 suppressed GC cell proliferation and metastasis partly through regulation of COPS7A expression. COPS7A could promote deubiquitinylation of IkBalpha, which was executed by CSN-associated deubiquitinylase USP15, and then KRT19P3 inactivated nuclear factor kappa-B (NF-kB) signaling pathway in a COPS7A-dependent manner. For the first time, we revealed that KRT19P3 could suppress tumor growth and metastasis through COPS7A-mediated NF-kB pathway, which may serve as potential targets for treatment of GC in the future.	31409899	RID07872	transcriptional regulation	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Cholangiocarcinoma	FLVCR1-DT	miR-458-5p	negatively-F	shRNA;luciferase reporter assay;miRanda	upregulation	RT-qPCR	NA	NA	cell growth(+);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000198468	GRCh38_1:212852105-212858138	NA	NA	642946	NA	FLVCR1-AS1|LQK1|NCRNA00292	NA	lncRNA FLVCR1-AS1 regulates cell proliferation, migration and invasion by sponging miR-485-5p in human cholangiocarcinomav.The expression levels of FLVCR1-AS1 in CCA tumor tissues, adjacent normal tissues,CCA cell lines and a cholangiocyte cell line were determined by reverse transcription-quantitative polymerase chain reaction. A significantly higher expression level of FLVCR1-AS1 was identified in CCA tumor tissues and the CCA cell lines HuCCT1 and CCLP1 compared with the normal controls. Short hairpin RNA targeting FLVCR1-AS1 (shFLVCR1-AS1) and a control plasmid (shNC) were transfected into CCA cell lines. Cell proliferation, colony formation, migration and invasion of CCA cells transfected with shFLVCR1-AS1 were significantly suppressed compared with the shNC groups. The expression levels of migration and invasion-associated proteins, including Twist, matrix metalloproteinase (MMP)-2 and MMP-9, were also significantly suppressed by shFLVCR1-AS1-treatment. Furthermore, FLVCR1-AS1 knockdown inhibited tumor growth in a xenograft model. Mechanistically, FLVCR1-AS1 was demonstrated to sponge microRNA-485-5p (miR-485-5p) in human CCA. The expression of miR-458-5p was significantly decreased in CCA tissue compared with normal tissue, and Pearson's correlation analysis revealed that FLVCR1-AS1 expression was negatively correlated with miR-485-5p expression in CCA tissues. These results suggested that lncRNA FLVCR1-AS1 may be used as a novel therapeutic target and a potential diagnostic marker for CCA.	31404302	RID07873	ceRNA or sponge	NA		
Prostate cancer	LINC00662	miR-34a	negatively-F	dual-luciferase reporter assay;siRNA;RNA pull-down assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000261824	GRCh38_19:27681072-27794005	NA	NA	148189	NA	NA	NA	Long noncoding RNA LINC00662 functions as miRNA sponge to promote the prostate cancer tumorigenesis through targeting miR-34a. LINC00662 expression was first detected in PCa cell lines and tissue samples by qRT-PCR Based on follow-up data, correlations of LINC00662 expression and clinicopathological features, including overall survival, in PCa patients were evaluated. Cell proliferation, migration, invasion, and apoptosis were detected by CCK-8 assay, colony-forming assay, Wound-healing assay, transwell assay, and flow cytometry, respectively. Additionally, LINC00662-specific miRNA was further confirmed using the dual-luciferase reporter assay and RT-PCRLINC00662 was significantly upregulated in PCa tissues and cell lines compared with adjacent normal tissue and a normal prostate epithelial cell line. Higher expression of LINC00662 was positively associated with distant metastasis and shorter overall survival. In addition, multivariate analysis revealed that tissue LINC00662 expression was confirmed to be an independent prognostic factor for PCa. Furthermore, LINC00662 silencing inhibited the proliferation, migration, and invasion of PC-3 and LNCaP cells, and promoted apoptosis in vitro. Bioinformatics methods and luciferase reporter assay revealed the close link within miR-34a and 3'-untranslated region (UTR) of LINC00662 and further confirmed that LINC00662 could function as a sponge of miR-34a in PCa cells. Also, the results of RT-PCRshowed that knockdown of LINC00662 suppressed the expression levels of miR-34a.The current results further enhanced our understanding of the effects of LINC00662 in PCa and may help to provide a new potential target for PCa treatment.	31114993	RID07874	ceRNA or sponge	metastasis,prognosis	UP(LIHC,SKCM);DOWN(NSCLC,PRAD);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Lung cancer	FER1L4	PIK3CA	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);colony formation(+);cell metastasis(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000121879	NA	80307	5290	bA563A22B.1|C20orf124|dJ309K20.1	PI3K	Long non-coding RNA FER1L4 inhibits cell proliferation and metastasis through regulation of the PI3K/AKT signaling pathway in lung cancer cells.The present study aimed to investigate the role of a novel lncRNA , Fer-1-like family member 4 (FER 1L4), in lung tumorigenesis. In the present study, it was demonstrated that the expression level of FER 1L4 was significantly decreased in clinical lung cancer tissues and in cultured lung cancer cells, as evidenced by reverse transcription-quantitative polymerase chain reaction analysis. Overexpression of FER 1L4 in lung cancer cell lines A549 and 95D inhibited colony formation, cell proliferation and cell migration capacity, measured by colony formation assays, cell proliferation assays and Transwell assays, respectively. Overexpression of FER 1L4 led to a reduction in the expression levels of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) in A549 and 95D cells, whereas, activation of PI3K/Akt signaling using a small molecular inhibitor of phosphatase and tensin homolog, reversed the inhibitory effects of FER 1L4 on cell proliferation and metastasis. All of these results suggested that the lncRNA FER 1L4 suppressed cell proliferation and metastasis by inhibiting the PI3K/Akt signaling pathway in lung cancer.	31115514	RID07875	expression association	metastasis	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Lung cancer	FER1L4	AKT1	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);colony formation(+);cell metastasis(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000142208	NA	80307	207	bA563A22B.1|C20orf124|dJ309K20.1	AKT|PKB|PRKBA|RAC|RAC-alpha	Long non-coding RNA FER1L4 inhibits cell proliferation and metastasis through regulation of the PI3K/AKT signaling pathway in lung cancer cells.The present study aimed to investigate the role of a novel lncRNA , Fer-1-like family member 4 (FER 1L4), in lung tumorigenesis. In the present study, it was demonstrated that the expression level of FER 1L4 was significantly decreased in clinical lung cancer tissues and in cultured lung cancer cells, as evidenced by reverse transcription-quantitative polymerase chain reaction analysis. Overexpression of FER 1L4 in lung cancer cell lines A549 and 95D inhibited colony formation, cell proliferation and cell migration capacity, measured by colony formation assays, cell proliferation assays and Transwell assays, respectively. Overexpression of FER 1L4 led to a reduction in the expression levels of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) in A549 and 95D cells, whereas, activation of PI3K/Akt signaling using a small molecular inhibitor of phosphatase and tensin homolog, reversed the inhibitory effects of FER 1L4 on cell proliferation and metastasis. All of these results suggested that the lncRNA FER 1L4 suppressed cell proliferation and metastasis by inhibiting the PI3K/Akt signaling pathway in lung cancer.	31115514	RID07876	expression association	metastasis	UP(LIHC,NSCLC,PAAD);DATA(GSE117623,GSE74639,GSE60407)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cholangiocarcinoma	MEG3	BMI1	negatively-E	siRNA;starBase	downregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+);cell growth(+);cell migration(+);cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168283	NA	55384	648	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	PCGF4|RNF51	LncRNA-MEG3 inhibits cell proliferation and invasion by modulating Bmi1/RNF2 in cholangiocarcinomaMEG3 expression was significantly downregulated in both CCA tissues and cells in comparison with that in nontumor controls, respectively, and this downexpression was prominently associated with advanced TNM stage, lymph node invasion, and poor survival. Moreover, decreased MEG3 was an independent forecaster of poor prognosis for CCA patients. Functionally, MEG3 overexpression inhibited CCA growth in vitro and in vivo. Enhanced MEG3 also suppressed migration and invasion of CCLP-1 and QBC939 cells by reversing epithelial-mesenchymal transition (EMT) process. On the contrary, the proliferation, metastasis, and EMT were facilitated via knocking down MEG3. In addition, the expression of B lymphoma Mo-MLV insertion region 1 (Bmi1) and RING finger protein 2 was impacted by gain or loss of MEG3, furthermore, the malignant processes induced by MEG3 knockdown were rescued by means of silencing Bmi1. These data suggested that MEG3 caused tumor suppressive effects partly through mediating polycomb repressive complex 1. Our findings elucidate that MEG3 exerts critical functions in CCA development and likely acts as a promising tumor indicator or intervention target for CCA.	31119760	RID07877	expression association	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE86978)
Cholangiocarcinoma	MEG3	MIR211	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell viability(+);PI3K/AKT signaling pathway(+);AMPK signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000207702	NA	55384	406993	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MIRN211|mir-211	Long noncoding RNA MEG3 is a tumor suppressor in choriocarcinoma by upregulation of microRNA-211.lncRNA MEG3 was overexpressed, and the effects of lncRNA MEG3 on cell viability, proliferation, apoptosis, migration, and invasion were assessed by the cell counting kit-8 assay, western blot flow cytometry (plus western blot, and transwell assay (plus western blot, respectively. Then, the expression level of miR-211 was detected by realtime quantitative polymerase chain reaction. After that, the effects of dysregulated microRNA-211 (miR-211) with overexpressing lncRNA MEG3 on JEG-3 cells and BeWo cells were testified. western blotwas used to study the involvements of the signaling pathways in the lncRNA MEG3-associated modulation. We found that lncRNA MEG3 upregulation reduced cell viability, inhibited proliferation, migration and invasion, and promoted apoptosis. Expression of miR-211 was upregulated after lncRNA MEG3 overexpression. Effects of lncRNA MEG3 overexpression were augmented by miR-211 overexpression, while they were declined by miR-211 silencing. Phosphorylated levels of PI3K, AKT, and AMP-activated protein kinase (AMPK) were decreased by lncRNA MEG3 overexpression via regulation of miR-211. To sum up, lncRNA MEG3 could repress proliferation, migration and invasion, and promote apoptosis of JEG-3 and BeWo cells through upregulating miR-211. The PI3K/AKT and AMPK pathways were inhibited by lncRNA MEG3 overexpression via regulation of miR-211.	31124134	RID07878	expression association	NA		
Endometrial cancer	OGFRP1	SIRT1	positively-E	shRNA;siRNA;Targetscan;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);apoptosis process(-);cell viability(+);tumor growth(+);cell metastasis(+);PI3K/AKT/GSK3beta signaling pathway(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000182057	GRCh38_22:42269703-42279534	ENSG00000096717	NA	388906	23411	NA	SIR2L1	Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer by regulating miR-124-3p/SIRT1 axis and by activating PI3K/AKT/ GSK-3beta pathway.We measured the level of OGFRP1 in endometrial cancer tissues and evaluated the influences of OGFRP1 dysregulation on the tumour cell biological processes of endometrial cancer cells. Further, the regulatory relationships between OGFRP1 and miR-124-3p, between miR-124-3p and Sirtuin1 (SIRT1) were, respectively, investigated. The interaction between OGFRP1 dysregulation and activation of PI3K/AKT/ GSK-3b pathway was revealed by western blot. OGFRP1 was up-regulated in endometrial cancer tissues and cells. OGFRP1 suppression inhibited the malignant behaviour (inhibited cell viability, promoted cell apoptosis, and suppressed cell migration and invasion) of the Ishikawa cells via negatively regulating miR-124-3p. SIRT1 was a target gene of miR-124-3p, and miR-124-3p regulated tumour growth and metastasis by the down-stream signal of SIRT1. Moreover, suppression of OGFRP1 restrained the activation of PI3K/AKT/GSK-3b signals in the Ishikawa cells via miR-124-3p/SIRT1 axis. Our experiments revealed that upregulation of OGFRP1 may enhance the progression of endometrial cancer by regulating miR-124-3p/SIRT1 axis and by activating PI3K/AKT/GSK-3b pathway. OGFRP1 may be of significance in illustrating the biology of endometrial cancer.	31131636	RID07879	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	ECRG4	BCYRN1	negatively-E	ELISA	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);cell migration(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	PCG	lncRNA	ENSG00000119147	NA	ENSG00000236824	GRCh38_2:47335315-47335514	84417	618	augurin|C2orf40	BC200|BC200a|LINC00004|NCRNA00004	Esophageal cancer related gene-4 inhibits the migration and proliferation of oral squamous cell carcinoma through BC200 lncRNA/MMP-9 and -13 signaling pathway. Using the tongue carcinoma cell line, TCA8113 as a cell model, we showed that forced expression of ECRG4 down-regulated the expression of the BC200 long noncoding RNA (lncRNA) and matrix metalloproteinases (MMP-9 and MMP-13). Restoration of BC200 lncRNA rescued ECRG4-mediated down-regulation of MMP-9 and -13. Furthermore, over-expression of Ecrg4 inhibited cell proliferation and migration, which was abolished by forced expression of BC200 lncRNA in TCA8113 cells. Our results indicate that ECRG4 inhibits the malignant phenotype of TCA8113 cells most likely through suppression of BC200 lncRNA/MMPs signaling pathway, rationalizing that BC200 lncRNA may be a potential target for oral squamous cell carcinoma (OSCC) therapy.	31152845	RID07880	expression association	metastasis		UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Oral squamous cell carcinoma	ECRG4	MMP9	negatively-E	ELISA	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);cell migration(+);cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000119147	GRCh38_2:106063246-106078155	ENSG00000100985	NA	84417	4318	augurin|C2orf40	CLG4B	Esophageal cancer related gene-4 inhibits the migration and proliferation of oral squamous cell carcinoma through BC200 lncRNA/MMP-9 and -13 signaling pathway. Using the tongue carcinoma cell line, TCA8113 as a cell model, we showed that forced expression of ECRG4 down-regulated the expression of the BC200 long noncoding RNA (lncRNA) and matrix metalloproteinases (MMP-9 and MMP-13). Restoration of BC200 lncRNA rescued ECRG4-mediated down-regulation of MMP-9 and -13. Furthermore, over-expression of Ecrg4 inhibited cell proliferation and migration, which was abolished by forced expression of BC200 lncRNA in TCA8113 cells. Our results indicate that ECRG4 inhibits the malignant phenotype of TCA8113 cells most likely through suppression of BC200 lncRNA/MMPs signaling pathway, rationalizing that BC200 lncRNA may be a potential target for oral squamous cell carcinoma (OSCC) therapy.	31152845	RID07881	expression association	metastasis		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Oral squamous cell carcinoma	ECRG4	MMP13	negatively-E	ELISA	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);cell migration(+);cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000119147	GRCh38_2:106063246-106078155	ENSG00000137745	NA	84417	4322	augurin|C2orf40	CLG3	Esophageal cancer related gene-4 inhibits the migration and proliferation of oral squamous cell carcinoma through BC200 lncRNA/MMP-9 and -13 signaling pathway. Using the tongue carcinoma cell line, TCA8113 as a cell model, we showed that forced expression of ECRG4 down-regulated the expression of the BC200 long noncoding RNA (lncRNA) and matrix metalloproteinases (MMP-9 and MMP-13). Restoration of BC200 lncRNA rescued ECRG4-mediated down-regulation of MMP-9 and -13. Furthermore, over-expression of Ecrg4 inhibited cell proliferation and migration, which was abolished by forced expression of BC200 lncRNA in TCA8113 cells. Our results indicate that ECRG4 inhibits the malignant phenotype of TCA8113 cells most likely through suppression of BC200 lncRNA/MMPs signaling pathway, rationalizing that BC200 lncRNA may be a potential target for oral squamous cell carcinoma (OSCC) therapy.	31152845	RID07882	expression association	metastasis		UP(PAAD);DATA(GSE40174)
Esophagus squamous cell carcinoma	DANCR	ZEB1	positively-E	siRNA;overexpression;dual-luciferase reporter assay;starBase;miRWalk	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-33a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000148516	NA	57291	6935	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	MicroRNA-33a-5p suppresses esophageal squamous cell carcinoma progression via regulation of lncRNA DANCR and ZEB1Herein, we discovered that miR-33a-5p was down-regulated in both esophageal squamous cell carcinoma (ESCC) tissues and cell lines, compared with their normal counterparts, and decreased expression of miR-33a- 5p was found to be closely associated with poor patient prognosis of ESCC. Moreover, functional experiments revealed that up-regulation of miR-33a-5p inhibited cell proliferation and metastasis of ESCC cells. In addition, the expression level of miR-33a-5p was found to be negatively correlated with the long non-coding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR), in both ESCC tissues and cell lines. Furthermore, zinc-finger-enhancer binding protein 1 (ZEB1) was predicted and confirmed to be a direct target of miR-33a-5p in ESCC. Further mechanistic investigation indicated that DANCR may function as a competing endogenous RNA (ceRNA) to sponge miR-33a-5p, and thereby up-regulate ZEB1 expression in ESCC. This study highlights the functions of miR-33a-5p in the progression of ESCC and suggests that the DANCR/miR-33a-5p/ ZEB1 axis may be a potential prognostic and therapeutic target.	31401160	RID07883	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	KCNQ1OT1	MYC	positively-E	western blot;luciferase reporter assay;RNA pull-down assay;RIP;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell differentiation(-);apoptosis process(-)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000136997	NA	10984	4609	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	bHLHe39|c-Myc|MYCC	LncRNA KCNQ1OT1 controls cell proliferation, differentiation and apoptosis by sponging miR-326 to regulate c-Myc expression in acute myeloid leukemia.The expressions of KCNQ1OT1, microRNA-326 (miR-326) and c-Myc were measured by quantitative real-time polymerase chain reaction and western blot, respectively. Phorbol myristate acetate (PMA) was used for cell differentiation. Cell proliferation, apoptosis and differentiation were measured by MTT assay, flow cytometry and qRT-PCR respectively. The interaction between miR-326 and KCNQ1OT1 or c-Myc was explored by luciferase activity, RNA immunoprecipitation or RNA pull-down assay. We found the expression of KCNQ1OT1 was enhanced in treatment of acute myeloid leukemia (AML)samples compared with control. KCNQ1OT1 knockdown inhibited cell proliferation but promoted apoptosis and cell differentiation. KCNQ1OT1 was a decoy of miR-326 and c-Myc was a target of miR-326. KCNQ1OT1 regulated AML cell proliferation, apoptosis and differentiation by sponging miR-326. Moreover, overexpression of miR-326 suppressed proliferation but promoted apoptosis and PMA- induced differentiation by targeting c-Myc in AML cells. Besides, c-Myc protein level was suppressed by KCNQ1OT1 interference and rescued by miR-326 abrogation. Our data showed that KCNQ1OT1 regulates proliferation, differentiation and apoptosis in AML cells by acting as a competing endogenous RNA (ceRNA) for miR-326 to regulate c-Myc, providing a novel avenue for AML treatment.	31390869	RID07884	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Acute myeloid leukemia	H19	TCF	positively-E	dual-luciferase reporter assay;western blot	upregulation		NA	NA	apoptosis process(-);cell proliferation(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000101076	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	LncRNA-H19 inhibits apoptosis of acute myeloid leukemia cells via targeting miR-29a-3p.Blood samples were collected from 40 AML patients. The AML cells were cultured. Cell counting kit-8 (CCK-8) was used to detect cell proliferation and flow cytometry was applied to analyze cell cycle and determine the apoptosis rate. Moreover, the action target of lncRNA-H19 was detected through a dual-luciferase reporter assay and western blot was performed to detect the change in protein level.The expression of lncRNA-H19 in AML patients was markedly higher than that in normal controls and compared with human embryonic kidney (HEK)-293T cells, AML cell Kasumi-1 exhibited an increased lncRNA-H19 expression. LncRNA-H19 could promote cell proliferation, but suppress cell apoptosis. It is bound to micro RNA (miR)-29a-3p in a targeted manner. and the expression level of miR-29a-3p in AML patients was prominently lower than that in normal controls. After miR-29a-3p was inhibited, the expression of intranuclear beta-catenin was significantly increased and the Wnt/beta-catenin pathway critical molecules T-cell factor (TCF) and lymphoid enhancer factor 1 (LEF1) were evidently up-regulated after the down-regulation of miR-29a-3p.CONCLUSIONS: LncRNA-H19 targets miR-29a-3p to promote the proliferation of AML cells, but inhibit the apoptosis through the Wnt/ beta-catenin signaling pathway.	31389605	RID07885	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Acute myeloid leukemia	H19	LEF1	positively-E	dual-luciferase reporter assay;western blot	upregulation		NA	NA	apoptosis process(-);cell proliferation(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000138795	NA	283120	51176	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	TCF10|TCF1ALPHA|TCF7L3	LncRNA-H19 inhibits apoptosis of acute myeloid leukemia cells via targeting miR-29a-3p.Blood samples were collected from 40 AML patients. The AML cells were cultured. Cell counting kit-8 (CCK-8) was used to detect cell proliferation and flow cytometry was applied to analyze cell cycle and determine the apoptosis rate. Moreover, the action target of lncRNA-H19 was detected through a dual-luciferase reporter assay and western blot was performed to detect the change in protein level.The expression of lncRNA-H19 in AML patients was markedly higher than that in normal controls and compared with human embryonic kidney (HEK)-293T cells, AML cell Kasumi-1 exhibited an increased lncRNA-H19 expression. LncRNA-H19 could promote cell proliferation, but suppress cell apoptosis. It is bound to micro RNA (miR)-29a-3p in a targeted manner. and the expression level of miR-29a-3p in AML patients was prominently lower than that in normal controls. After miR-29a-3p was inhibited, the expression of intranuclear beta-catenin was significantly increased and the Wnt/beta-catenin pathway critical molecules T-cell factor (TCF) and lymphoid enhancer factor 1 (LEF1) were evidently up-regulated after the down-regulation of miR-29a-3p.CONCLUSIONS: LncRNA-H19 targets miR-29a-3p to promote the proliferation of AML cells, but inhibit the apoptosis through the Wnt/ beta-catenin signaling pathway.	31389605	RID07886	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	SNHG6	VASP	positively-E		upregulation		NA	NA	cell invasion(+);cell proliferation(+);cell migration(+)	ceRNA(miR-26a)	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000125753	NA	641638	7408	HBII-276HG|NCRNA00058|U87HG	NA	Silencing lncRNA SNHG6 suppresses proliferation and invasion of breast cancer cells through miR-26a/VASP axis.In the previous study, we found that the expression level of LncRNA SNHG6 in breast cancer tissues and cells was significantly increased. Our study found that knockdown of SNHG6 significantly inhibited the proliferation, migration and invasion of breast cancer cells MCF-7 and MDA-MB-231 cells. Further study showed that knockdown of SNHG6 significantly inhibited the expression level of VASP. More importantly, SNHG6 and VASP both can bind directly to miR-26a, suggesting that SNHG6 could act as a ceRNA to sponge miR-26a, thereby promoting the expression of VASP, which leading to activated proliferation, migration and invasion of breast cancer cells. Taken together, this study revealed the important role of the SNHG6/miR-26a/VASP regulatory network in the development of breast cancer, and provided a reference for exploring new pathogenesis and biomarkers of breast cancer.	31387807	RID07887	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	RUSC1-AS1	CDKN1A	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);colony formation(+);cell cycle(+);cancer progression(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000225855	GRCh38_1:155316863-155324176	ENSG00000124762	NA	284618	1026	C1orf104|FLJ35976	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	LncRNA RUSC1-AS1 promotes the PROLIFERATION of breast cancer cells by epigenetic silence of KLF2 and CDKN1A.RUSC1-AS1 level in BCa tissues and adjacent normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The correlation between RUSC1-AS1 expression with tumor size, clinical stage and overall survival of BCa patients was analyzed. Influences of RUSC1-AS1 knockdown on viability, clonality, cell cycle and apoptosis of BCa cell lines MCF-7 and BT549 were evaluated. Target genes of RUSC1-AS1 were predicted by bioinformatics, and their interaction was further confirmed by RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and rescue experiments.A higher abundance of RUSC1-AS1 was identified in BCa tissues relative to controls. The expression level of RUSC1-AS1 was positively correlated to tumor size and clinical grade, but negatively correlated to the overall survival of BCa patients. The silence of RUSC1-AS1 markedly inhibited viability, clonality, cell cycle progression, and induced apoptosis of MCF-7 and BT549 cells. Finally, CDKN1A and KLF2 were found to be the target genes of RUSC1-AS1, which were tumor-suppressor genes involved in RUSC1-AS1-mediated BCa progression.RUSC1-AS1 is highly expressed in BCa, which promotes the progression of BCa through mediating CDKN1A and KLF2. RUSC1-AS1 may serve as a potential hallmark for BCa.	31378902	RID07888	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Breast cancer	RUSC1-AS1	KLF2	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell viability(+);colony formation(+);cell cycle(+);cancer progression(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000225855	GRCh38_1:155316863-155324176	ENSG00000127528	NA	284618	10365	C1orf104|FLJ35976	LKLF	LncRNA RUSC1-AS1 promotes the PROLIFERATION of breast cancer cells by epigenetic silence of KLF2 and CDKN1A.RUSC1-AS1 level in BCa tissues and adjacent normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The correlation between RUSC1-AS1 expression with tumor size, clinical stage and overall survival of BCa patients was analyzed. Influences of RUSC1-AS1 knockdown on viability, clonality, cell cycle and apoptosis of BCa cell lines MCF-7 and BT549 were evaluated. Target genes of RUSC1-AS1 were predicted by bioinformatics, and their interaction was further confirmed by RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and rescue experiments.A higher abundance of RUSC1-AS1 was identified in BCa tissues relative to controls. The expression level of RUSC1-AS1 was positively correlated to tumor size and clinical grade, but negatively correlated to the overall survival of BCa patients. The silence of RUSC1-AS1 markedly inhibited viability, clonality, cell cycle progression, and induced apoptosis of MCF-7 and BT549 cells. Finally, CDKN1A and KLF2 were found to be the target genes of RUSC1-AS1, which were tumor-suppressor genes involved in RUSC1-AS1-mediated BCa progression.RUSC1-AS1 is highly expressed in BCa, which promotes the progression of BCa through mediating CDKN1A and KLF2. RUSC1-AS1 may serve as a potential hallmark for BCa.	31378902	RID07889	expression association	NA	DOWN(LIHC,PRAD,BRCA);UP(NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Non-small cell lung cancer	OR3A4P	SOX4	positively-E	western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000180068	GRCh38_17:3309986-3311446	ENSG00000124766	NA	390756	6659	OR3A4	NA	Long non-coding RNA OR3A4 is associated with poor prognosis of human non-small cell lung cancer and regulates cell proliferation via up-regulating SOX4.LncRNA OR3A4 expression in 52-paired NSCLC tissues and adjacent normal tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR. Cell proliferation assay and cell apoptosis assay were used to investigate the function of OR3A4 in NSCLC. Furthermore, the underlying mechanism was explored by qRT-PCRand western blot assay.RESULTS: OR3A4 expression was remarkably upregulated in NSCLC tissues when compared with adjacent normal tissues. The overall survival of NSCLC patients in high OR3A4 expression group was significantly worse than those in low OR3A4 expression group. After the silence of OR3A4, the proliferation of NSCLC cells was significantly inhibited. Besides, tHE APOPTOSIS OF NSCLC CELLS WAS REMARKABLY PROMOTED after the silence of OR3A4. Meanwhile, knockdown of OR3A4 significantly down-regulated the mRNA and protein levels of SOX4 in NSCLC cells. Furthermore, the expression of SOX4 was found upregulated in both NSCLC tissues and cells.These above results suggested that OR3A4 could promote cell proliferation and suppress cell apoptosis in NSCLC through up-regulating SOX4. Our findings demonstrated that OR3A4 might serve as a new therapeutic intervention for NSCLC patients.	31378892	RID07890	expression association	prognosis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	LINC00460	PAK1	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000149269	NA	728192	5058	NA	NA	LINC00460 promotes hepatocellular carcinoma development through sponging miR-485-5p to up-regulate PAK1. We observed that LINC00460 was significantly up-regulated in HCC cells, which implied that LINC00460 was involved in HCC development. Then, LINC00460 was silenced in Hep3B and Huh-7 cells and we found that knockdown of LINC00460 greatly inhibited HCC cell proliferation. In addition, HCC cell apoptosis was induced and meanwhile, cell cycle progression was blocked by down-regulation of LINC00460 in vitro. Furthermore, we proved that Hep3B and Huh-7 cell migration and invasion capacity was repressed by decrease of LINC00460. Recently, a growing number of studies have indicated the correlation between lncRNAs and microRNAs. Currently, we displayed that miR-485-5p was greatly decreased in HCC cells and LINC00460 could sponge miR-485-5p to regulate HCC progression. The binding association between LINC00460 and miR- 485-5p was confirmed using dual-luciferase reporter assay, RNA pulled down and RIP assay in our research. Subsequently, PAK1 was predicted as a downstream target of miR-485-5p and we demonstrated that miR-485-5p suppressed PAK1 levels in vitro. Finally, in vivo experiments were conducted to validate that knockdown of LINC00460 repressed HCC development through modulating miR-485-5p to increase PAK1. Taken these together, we indicated that LINC00460 promoted HCC progression through sponging miR-485-5p and up-regulating PAK1.	31376654	RID07891	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Esophageal cancer	PVT1	FSCN1	positively-E	starBase;Targetscan;miRcode;siRNA;dual-luciferase reporter assay;RNA pull-down assay;RIP;FISH	upregulation	microarray	GSE23400;GSE38129;GSE77861;GSE45168;TCGA	NA	cell migration(+);cell invasion(+);apoptosis process(-);cell viability(+);tumor growth(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000075618	NA	5820	6624	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FLJ38511|p55|SNL	Down-regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA-145-mediated inhibition of FSCN1.Initially, microarray-based gene expression profiling of EC was employed to identify differentially expressed genes. Moreover, the expression of lncRNA PVT1 was examined and the cell line presenting with the highest level of lncRNA PVT1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lncRNA PVT1, FSCN1, and miR-145. The effect of lncRNA PVT1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain-of-function and loss-of-function experiments. We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR-145 and regulate its expression, and FSCN1 is a target gene of miR-145. Overexpression of miR-145 or silencing of lncRNA PVT1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our in vivo results showed that overexpression of miR-145 or silencing of lncRNA PVT1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down-regulation of lncRNA PVT1 could potentially promote expression of miR-145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of FSCN1. This highlights the potential of lncRNA PVT1 as a therapeutic target for EC treatment.	31369196	RID07892	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE75367,GSE86978)
Lung adenocarcinoma	TTN-AS1	CDK5	positively-E	shRNA;lnCeDB;LncBase;miRanda;Targetscan;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);epithelial to mesenchymal transition(+)	ceRNA(miR-142-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000164885	NA	100506866	1020	NA	PSSALRE	LncRNA TTN-AS1 promotes migration, invasion, and epithelial mesenchymal transition of lung adenocarcinoma via sponging miR-142-5p to regulate CDK5.In the present study, we revealed that the expression of TTN-AS1 was upregulated in LUAD tissues and cell lines. High TTN-AS1 expression was associated with TNM stage and lymph node metastasis of LUAD patients. In addition, high expression of TTN-AS1 was correlated with poor postoperative prognosis of LUAD patients. Knockdown of TTN-AS1 significantly inhibited the growth, proliferation, migration, and invasion ability of LUAD cells in vitro. Then, by using bioinformation analysis and luciferase reporter experiment, we identified that TTN-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-142-5p to regulate the expression of cyclindependent kinase 5 (CDK5) in LUAD. Since CDK5 is a key regulator in the process of epithelial mesenchymal transition (EMT), we detected the expression of EMT-related proteins, consequently, EMT was suppressed by knockdown of TTNAS1 while this phenomenon was rescued by miR-142-5p inhibitor. Taken above, our study revealed that TTN-AS1 played an important role in LUAD progression. TTN-AS1/miR-142-5p/CDK5 regulatory axis may serve as a novel therapeutic target in the treatment of LUAD.	31363080	RID07893	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE55807)
Malignant glioma	DLEU1	MEF2D	positively-E	RIP;siRNA;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-421)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000116604	NA	10301	4209	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.The levels of DLEUI in glioma tissues and cell lines were examined using quantitative real-time PCR. The potential effects of DLEU1 on the proliferation, mobility, invasion and apoptosis of glioma cells were evaluated using corresponding in vitro experiments. The association between DLEU1 and microRNA (miR)-421 was also determined using luciferase reporter activity and RNA immunoprecipitation (RIP) assays.The results revealed that DLEU1 was significantly upregulated in glioma tissues and cell lines. Increased DLEU1 was positively associated with the high-grade carcinoma (III V). Functional studies revealed that knockdown of DLEU1 expression by siRNA led to decreased proliferation, migration and invasion and increased apoptosis in human glioma cells. Furthermore, luciferase reporter activity and RIP assays confirmed that DLEUI could act as a competing endogenous RNA (ceRNA) for miR-421 that functioned as a tumor suppressor in glioma. Moreover, inhibition miR-421 partially restored the effect of DLEU1 knockdown on the glioma cells. DLEU1 could regulate myocyte enhancer factor 2D (MEF2D) expression, a known target of miR-421 in glioma cells.Taken together, these findings suggested that DLEU1 regulated MEF2D expression to promote glioma progression by sponging miR-421 and that DLEU1 might be a potential therapeutic target for glioma.	31360066	RID07894	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Laryngeal squamous cell carcinoma	RGMB-AS1	NLRP3	positively-E	shRNA;immunohistochemistry;RIP;dual-luciferase reporter assay;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000162711	NA	503569	114548	NA	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCU|MWS|NALP3|PYPAF1	LncRNA RGMB-AS1 promotes laryngeal squamous cell carcinoma cells progression via sponging miR-22/NLRP3 axis.In our research, lncRNA RGMB-AS1 was shown to be upregulated in LSCC tissues. High RGMB-AS1 expression was closely associated with advanced clinical features and poor prognosis. Silencing of lncRNA RGMB-AS1 suppressed LSCC cells proliferation and invasion in vitro and inhibited tumor growth in vivo. In mechanism, lncRNA RGMB-AS1 could sponge miR-22 to upregulate the expression of NLRP3. Additionally, we verified that the suppression of LSCC progression induced by lncRNA RGMB-AS1 reduction required the activity of miR-22. Altogether, these findings elucidated that lncRNA RGMB-AS1 could exert as an oncogenic factor through modulating miR-22/NLRP3 pathway, suggesting a potential novel target for the treatment of LSCC.	31351424	RID07895	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Hepatocellular carcinoma	MALAT1	miR-200a	negatively-F	starBase;dual-luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long Noncoding RNA MALAT1 Regulates Hepatocellular Carcinoma Growth Under Hypoxia via Sponging MicroRNA-200a.Quantitative reverse transcription PCR (qRT-PCR assay was performed to detect the mRNA levels of MALAT1 and microRNA-200a (miR-200a) in HCC cells. Cell invasion and migration ability were evaluated by Transwell assay. Starbase v2.0 and luciferase reporter assay were employed to identify the association between MALAT1 and miR-200a. Cell proliferation and apoptosis were measured by MTT assay and flow cytometry, respectively.MALAT1 levels were significantly upregulated in HCC cells under hypoxia. Hypoxia promoted proliferation, migration, and invasion, and blocked apoptosis in Hep3B cells, which were weakened by knockdown of MALAT1. Starbase v2.0 showed that MALAT1 and miR-200a have a complementarity region, and luciferase reporter assay verified that MALAT1 interacted with miR- 200a in Hep3B cells. Moreover, MALAT1 negatively regulated the expression of miR-200a. miR-200a levels were dramatically downregulated in HCC cells under hypoxia. Upregulation of miR-200a inhibited proliferation, migration, and invasion, and induced apoptosis in Hep3B cells under hypoxia. Interestingly, downregulation of miR-200a partially reversed the tumor-suppressive effect of knockdown of MALAT1 on Hep3B cells in hypoxic condition.LncRNA MALAT1 was involved in proliferation, migration, invasion, and apoptosis by interacting with miR-200a in hypoxic Hep3B cells, revealing a new mechanism of MALAT1 involved in hypoxic HCC progression.	31347327	RID07896	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Diffuse large b-cell lymphoma	TUG1	MET	positively-E	siRNA;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);tumor growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000105976	NA	55000	4233	FLJ20618|LINC00080|NCRNA00080	DFNB97|HGFR|RCCP2	Downregulation of long non-coding RNA TUG1 suppresses tumor growth by promoting ubiquitination of MET in diffuse large B-cell lymphoma.The expression of lncRNA TUG1 and MET in DLBCL tissues and cell lines was determined by quantitative real-time PCR and western blot. Cell proliferation, invasion and apoptosis were determined by cell counting kit-8 assay, transwell assay and flow cytometer. The animal xenograft model was established by the injection of DLBCL cells carrying si-TUG1. The expression of TUG1 and MET was upregulated in DLBCL tissues and cells. We demonstrated that MET was altered in the TUG1 knockdown DLBCL cells, and confirmed the interaction between TUG1 and MET by RNA pull-down and RNA immunoprecipitation. Furthermore, knockdown of TUG1 reduced MET protein level by promoting ubiquitination, and suppressed tumor growth in vitro and in vivo. Our findings demonstrated that TUG1 exerted its oncogenic function in DLBCL by inhibiting the ubiquitination and the subsequent degradation of MET. Knockdown of TUG1 through MET downregulation suppressed DLBCL cell proliferation and tumor growth.	31338678	RID07897	transcriptional regulation	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC,PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE38495)
Papillary thyroid carcinoma	CAVIN2-AS1	CAVIN2	positively-E	siRNA	downregulation	RT-qPCR	TCGA	NA	AKT signaling pathway(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233766	GRCh38_2:191846534-192044525	ENSG00000168497	NA	105373813	8436	LOC105373813	cavin-2|PS-p68|SDPR|SDR	Serum deprivation response functions as a tumor suppressor gene in papillary thyroid cancerWe reanalyzed the RNA-Seq data of PTC from The Cancer Genome Atlas (TCGA) database and found that serum deprivation response (SDPR) was significantly downregulated in PTC. Quantitative reverse transcriptionpolymerase chain reaction (RT-qPCR) was performed to assess the expression of SDPR. Both loss- and gain-of-function experiments, and flow cytometry were performed to investigate the functions. SDPR was significantly downregulated in PTC.SDPR induction also initiated the mesenchymal-epithelial transition, alongside suppressing AKT signaling and cyclin family expression.LOC105373813 expression level was significantly downregulated in PTC tissues compared with paired adjacent normal tissues.We then investigated whether LOC105373813 could modulate the expression of SDPR by using siRNA targeting LOC105373813 based on the aforementioned findings. The efficiency of LOC105373813 siRNA was monitored through RT-qPCR. The results demonstrated that knockdown of LOC105373813 significantly decreased the expression of SDPR.Taken together, these data demonstrated that LOC105373813 could regulate the expression of SDPR.	31334828	RID07898	expression association	NA		UP(PRAD);DATA(GSE104209)
Colorectal cancer	FGD5-AS1	CDCA7	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;shRNA;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-302e)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225733	GRCh38_3:14920347-14948424	ENSG00000144354	NA	100505641	83879	NA	FLJ14736|JPO1	Long noncoding RNA FGD5-AS1 promotes colorectal cancer cell proliferation, migration, and invasion through upregulating CDCA7 via sponging miR-302e. The expression levels of long noncoding RNA FGD5-AS1, CDCA7 mRNA, and miR-302e were assessed by RT-qPCR. The protein levels of CDCA7 were assessed by western blot. The function of FGD5-AS1 was detected using cell viability assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, transwell, and caspase-3 activity assay. Additionally, the microRNAs (miRNAs) sponge potential of FGD5-AS1 was examined by RNA immunoprecipitation assay, RNA pull-down assay, and luciferase reporter assay. FGD5-AS1 was increased in colorectal cancer cell lines compared to normal cell lines. Inhibition of FGD5-AS1 suppressed cell proliferation, migration, invasion, and accelerated cell apoptosis in CRC. FGD5-AS1 competitively bound with miR-302e to modulate CDCA7. The inhibiting effects of FGD5-AS1 knockdown on CRC cell proliferation, migration, and invasion, and the promoting effects on CRC cell apoptosis could be revived by miR-302e suppression or CDCA7 upregulation. LncRNA FGD5-AS1 could promote CRC progression through sponging miR-302e and upregulating CDCA7. FGD5-AS1 might serve as a potential therapeutic target for CRC.	31332696	RID07899	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE51827,GSE86978)
Gastric cancer	TONSL-AS1	TONSL	positively-E	siRNA;dual-luciferase reporter assay;FISH	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232600	GRCh38_8:144437675-144439971	ENSG00000260716	NA	100287098	4796	NA	IKBR|NFKBIL2	A novel long non-coding RNA TONSL-AS1 regulates progression of gastric cancer via activating TONSL.We found a novel lncRNA, named TONSL-AS1, was downregulated in gastric cancer tissues and cell lines compared with the normal. TONSL-AS1 inhibited cell migration, invasion and proliferation in SGC-7901, MGC-803 cells. Furthermore, TONSL-AS1 could suppress cell tumorigenesis in vivo. Mechanistically, TONSL-AS1's genomic neighboring gene TONSL, which was reported as a tumor suppress gene, was upregulated by TONSL. Additionally, the TONSL-AS1 was positively associated with TONSL in cancer tissues. Our study revealed that the tumor-inhibiting effect of TONSL-AS1 in gastric cancer cells was associated with TONSL. In general, our results indicated that TONSL-AS1 works as a tumor suppressor lncRNA, which may be a new therapeutic target for gastric cancer.	31158361	RID07900	transcriptional regulation	NA		UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827)
Liposarcoma	LINC00423	NFATC3	positively-E	RNA pull-down assay;RIP;siRNA	downregulation	qRT-PCR;sequencing	TCGA	NA	cell growth(+);cell proliferation(+);MAPK signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lipomatous cancer	lncRNA	TF	ENSG00000226968	GRCh38_13:32877431-32911650	ENSG00000072736	NA	100874167	4775	NA	NFAT4|NFATX	Linc00423 as a tumor suppressor in retroperitoneal liposarcoma via activing MAPK signaling pathway through destabilizing of NFATC3. High-throughput sequencing with computational methods for assembling the transcriptome of five paired RLS patient  tissues. We found that long intergenic noncoding RNA 423 (linc00423) was downregulated in RLS tissues. Gain-of-function assays revealed that overexpressed linc00423 obviously inhibited RLS cell growth in vitro and in vivo. Additionally, RNA sequence, RNA-pull-down and RIP assays evidenced that linc00423 involved in MAPK signaling pathway via destabilizing of nuclear factor of activated T-cells 3 (NFATC3). Summing up, our findings demonstrated that linc00423 acted as the tumor suppressor in RLS cells through regulating the protein level of NFATC3 at a post-transcriptional level and negatively regulated the MAPK signaling pathway at a transcriptional level. Linc00423 might serve as a candidate prognostic biomarker and a target for novel therapies of RLS patients.	31160581	RID07901	transcriptional regulation	prognosis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Pancreatic cancer	MIR155HG	MIR802	negatively-F	shRNA;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000234883	GRCh38_21:25561810-25575168	ENSG00000211590	NA	114614	768219	BIC|MIRHG2|NCRNA00172|miPEP155	MIRN802|hsa-mir-802	Long noncoding RNA MIR155HG facilitates pancreatic cancer progression through negative regulation of miR-802.In this research, our group found that lncRNA MIR155HG expression was remarkably increased in PC tumor tissue and cells compared to that in the adjacent normal tissue and cells. In addition, higher MIR155HG expression was positively associated with the poor prognosis of patients. In addition, we exhibited that silence of MIR155HG by short hairpin RNA knockdown significantly inhibited cell growth and promoted cell apoptosis in PC cells. We performed bioinformatics analysis to search for the target of MIR155HG. As demonstrated by Luciferase reporter assay, we found that miR-802, a tumor suppressor in various cancer, is a direct target of MIR155HG. We demonstrated that the tumor-promoting effects of MIR155HG were contributed by negative regulation of miR-802 in PC cells. In summary, our results suggest that lncRNA MIR155HG might be applied as a novel diagnostic and therapeutic target for PC.	31161625	RID07902	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE111842,GSE51827,GSE86978)	
Pancreatic cancer	XIST	ZEB1	positively-E	shRNA;western blot;dual-luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-429)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA XIST promotes pancreatic cancer migration, invasion and EMT by sponging miR-429 to modulate ZEB1 expression.QPCR was applied to detect the expression levels of XIST and miR-429 in PC tissues and cell lines. The roles of XIST and miR-429 on PC cell migration, invasion and epithelial-mesenchymal transition (EMT) were assessed by wound healing, transwell, qPCR and western blot assays, respectively. The regulating relationship among XIST, miR-429 and zinc finger E-box binding homeobox 1 (ZEB1) was investigated in PC cells. XIST was frequently upregulated while miR-429 was commonly downregulated in PC tissues, especially in metastatic PC tissues. Knockdown of XIST in two PC cell lines caused inhibition of migration, invasion and EMT capacities. Forced expression of miR-429 exerted the similar tumor suppressing effects. XIST repressed miR-429 expression thus upregulated ZEB1, one of the targets of miR-429. ZEB1 mediated the tumor suppressing roles of XIST knockdown in PC cells. We identified the critical axis of XIST/miR-429/ZEB1 in PC cell migration, invasion and EMT, which may aid in developing new therapeutic strategies for PC.	31163263	RID07903	ceRNA or sponge	metastasis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	NORAD	miR-199a-3p	negatively-F	siRNA;dual-luciferase reporter assay;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	Long noncoding RNA NORAD regulates cancer cell proliferation and migration in human osteosarcoma by endogenously competing with miR-199a-3p. NORAD expressions were evaluated by qRT-PCRin in vitro osteosarcoma cell lines and in vivo clinical specimens. SiRNA-induced NORAD downregulation was conducted in Saos-2 and 143B cells, and the functional effects of NORAD downregulation on osteosarcoma cells were evaluated by CCK-8 proliferation assay, 24-well transwell invasion assay and in vivo tumor explant assay, respectively. The possibility of NORAD endogenously competing microRNA target, hsa-miR-199a-3p was examined by dual-luciferase reporter assay and qRT-PCR Then, hsa-miR-199a-3p was downregulated in NORAD-inhibited osteosarcoma cells to examine its role in regulating NORAD inhibition induced cancer suppression in osteosarcoma cells. NORAD was found to be significantly overexpressed in both osteosarcoma cells and osteosarcoma tumors. In Saos-2 and 143B cells transfected with NORAD-specific siRNA, their proliferation, invasion, and in vivo explant growth were all markedly suppressed. HsamiR- 199a-3p was confirmed to be the competing target of NORAD. Its downregulation in Saos-2 and 143B cells inversely augment proliferation and invasion that were initially suppressed by NORAD-downregulation. The results of our study show that NORAD plays an important role in regulating cancer cell functions of osteosarcoma, possibly through endogenously competing with hsa-miR-199a-3p.	31169973	RID07904	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Oesophageal squamous cell carcinoma	MNX1-AS1	SIRT1	positively-E	siRNA;Annolnc	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000096717	NA	645249	23411	CCAT5|LOC645249|MAYA	SIR2L1	LncRNA MNX1-AS1 promotes progression of esophageal squamous cell carcinoma by regulating miR-34a/SIRT1 axis.The expression levels of lncRNA MNX1-AS1 were examined in ESCC tissues by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR. The role of lncRNA MNX1-AS1 was performed by WST-1 proliferation assays, migration and invasion assays. Besides, the molecular mechanism of lncRNA MNX1-AS1 was verified by online bioinformatics, qRT-PCRand rescue assays.MNX1-AS1 was signifcantly upregulated in ESCC tissues. It was conformed that high MNX1-AS1 expression was associated with ESCC lymph node metastasis. Moreover, we found that knockdown of MNX1-AS1 apparently suppressed the cell proliferation, migration, and invasion capacity. Flow cytometry analysis showed MNX1-AS1 regulated ESCC cell cycle and apoptosis progression. Mechanism analysis revealed that miR-34a inhibitor could rescue the influence of inhibiting MNX1-AS1 on ESCC cells migration by serving as competing endogenous RNA (ceRNAs). Furthermore, we found that miR-34a specifically targeted SIRTI.Taken together, we demonstrated that lncRNA MNX1-AS1/miR-34a/SIRT1 regulatory axis could play an important role in ESCC progression, and MNX1-AS1 may act as a novel potential biomarker for esophageal squamous cell carcinoma.	31170665	RID07905	ceRNA or sponge	metastasis	UP(BRCA);DATA(GSE55807)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	DLX6-AS1	CADM1	negatively-E	dual-luciferase reporter assay;ChIP;FISH;shRNA;RIP	upregulation	microarray;RT-qPCR	TCGA	NA	STAT3 signaling pathway(+);self-renewal(+);cell proliferation(+);tumorigenesis(+);tumor growth(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000182985	NA	285987	23705	Evf-2|FLJ34048|NCRNA00212	BL2|IGSF4|IGSF4A|Necl-2|NECL2|RA175|ST17|SYNCAM|SYNCAM1|TSLC1	Down-regulated lncRNA DLX6-AS1 inhibits tumorigenesis through STAT3 signaling pathway by suppressing CADM1 promoter methylation in liver cancer stem cells.A microarray-based analysis was performed to initially screen differentially expressed lncRNAs associated with HCC. We then analyzed the lncRNA DLX6-AS1 levels as well as CADM1 promoter methylation. The mRNA and protein expression of CADM1, STAT3, CD133, CD13, OCT-4, SOX2, and Nanog were then detected. We quantified our results by evaluating the spheroid formation, proliferation, and tumor formation abilities, as well as the proportion of tumor stem cells, and the recruitment of DNA methyltransferase (DNMT) in LCSCs when lncRNA DLX6-AS1 was either overexpressed or silenced.LncRNA DLX6-AS1 was upregulated in HCC. The silencing of lncRNA DLX6-AS1 was shown to reduce and inhibit spheroid formation, colony formation, proliferation, and tumor formation abilities, as well as attenuate CD133, CD13, OCT-4, SOX2, and Nanog expression in LCSCs. Furthermore, downregulation of lncRNA DLX6-AS1 contributed to a reduction in CADM1 promoter methylation via suppression of DNMT1, DNMT3a, and DNMT3b in LCSCs and inactivating the STAT3 signaling pathway.This study demonstrated that down-regulated lncRNA DLX6-AS1 may inhibit the stem cell properties of LCSCs through upregulation of CADM1 by suppressing the methylation of the CADM1 promoter and inactivation of the STAT3 signaling pathway.	31171015	RID07906	transcriptional regulation	NA		UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)
Breast cancer	LINC01287	CCND1	positively-E	knockdown;western blot;siRNA	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234722	GRCh38_7:153355365-153413985	ENSG00000110092	NA	103724390	595	TCONS_l2_00027522	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA LINC01287 promotes breast cancer cells proliferation and metastasis by activating Wnt/<U+00DF>-catenin signaling.The relative expressions of LINC01287 in BC tissues and cells were determined using RT-PCR The associations between the LINC01287 expression, the clinicopathological factors, and the overall survival of BC patients were statistically examined. The apoptosis and proliferation abilities of MCF-7 and MDA-MB-468 cells were analyzed by MTT and flow cytometry assay after LINC01287 knockdown. The effects of LINC01287 in migration and invasion were determined using wound-healing and transwell assays. The protein expressions of the Wnt/beta-catenin pathway were determined using western blot.We showed that the levels of LINC01287 were significantly upregulated in BC tissues and BC cell lines, and the abnormal expressions of LINC01287 were correlated with TNM stage and lymph node metastasis. A distinct difference was observed and indicated that BC patients with higher LINC01287 expressions had significantly shorter overall survival than patients with lower LINC01287 expressions. The multivariate analysis demonstrated that LINC01287 expression was independently correlated with the overall survival. Si-LINC01287 transfection significantly inhibited the proliferation and metastasis of BC cells, and further promoted apoptosis. Besides, the knockdown of LINC01287 suppressed Wnt/beta-catenin activation and affected the expressions of beta-catenin, cyclin D1, and c-myc.CONCLUSIONS: Our findings indicated that the new lncRNA LINC01287 was correlated with poor clinical outcome and may function as a novel prognostic biomarker and therapeutic target in the development of antineoplastic therapies for BC.	31173295	RID07907	expression association	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Breast cancer	LINC01287	MYC	positively-E	knockdown;western blot;siRNA	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000234722	GRCh38_7:153355365-153413985	ENSG00000136997	NA	103724390	4609	TCONS_l2_00027522	bHLHe39|c-Myc|MYCC	Long non-coding RNA LINC01287 promotes breast cancer cells proliferation and metastasis by activating Wnt/<U+00DF>-catenin signaling.The relative expressions of LINC01287 in BC tissues and cells were determined using RT-PCR The associations between the LINC01287 expression, the clinicopathological factors, and the overall survival of BC patients were statistically examined. The apoptosis and proliferation abilities of MCF-7 and MDA-MB-468 cells were analyzed by MTT and flow cytometry assay after LINC01287 knockdown. The effects of LINC01287 in migration and invasion were determined using wound-healing and transwell assays. The protein expressions of the Wnt/beta-catenin pathway were determined using western blot.We showed that the levels of LINC01287 were significantly upregulated in BC tissues and BC cell lines, and the abnormal expressions of LINC01287 were correlated with TNM stage and lymph node metastasis. A distinct difference was observed and indicated that BC patients with higher LINC01287 expressions had significantly shorter overall survival than patients with lower LINC01287 expressions. The multivariate analysis demonstrated that LINC01287 expression was independently correlated with the overall survival. Si-LINC01287 transfection significantly inhibited the proliferation and metastasis of BC cells, and further promoted apoptosis. Besides, the knockdown of LINC01287 suppressed Wnt/beta-catenin activation and affected the expressions of beta-catenin, cyclin D1, and c-myc.CONCLUSIONS: Our findings indicated that the new lncRNA LINC01287 was correlated with poor clinical outcome and may function as a novel prognostic biomarker and therapeutic target in the development of antineoplastic therapies for BC.	31173295	RID07908	expression association	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Melanoma	NEAT1	E2F3	positively-E	starBase;Targetscan;shRNA;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cancer progression(+)	ceRNA(miR-495-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112242	NA	283131	1871	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	lncRNA NEAT1 facilitates melanoma cell proliferation, migration, and invasion via regulating miR-495-3p and E2F3In our present research, we displayed NEAT1 was overexpressed in melanoma cells. A series of functional assays showed that overexpression of NEAT1 promoted the proliferation, migration, and invasion of melanoma cells. By contrast, NEAT1 knockdown obviously restrained melanoma cell progression. Mechanistically, it was revealed that NEAT1 could directly bind with miR-495-3p, which led to a negative effect on miR-495-3p levels. In addition, miR-495-3p was significantly decreased in melanoma cells. Furthermore, E2F3 was postulated as the target of miR-495-3p and overexpression of this miR could suppress the levels of E2F3. Meanwhile, it was exhibited that melanoma cell proliferation, migration, and invasion induced by E2F3 silence was abrogated by miR-495-3p. Moreover, an in vivo xenograft nude mice model was established using A375 cells and it was indicated that NEAT1 promoted melanoma progression in vivo via regulating the miR-495-3p/E2F3 axis. In conclusion, we suggest that NEAT1 exerts an oncogenic effect on melanoma development via inhibition of miR-495-3p and induction of E2F3. NEAT1 might serve as a crucial prognostic biomarker of melanoma.	31173352	RID07909	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE55807)
Colon cancer	NEAT1	CDK6	positively-E	shRNA	upregulation		NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-495-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105810	NA	283131	1021	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	PLSTIRE	NEAT1 promotes colon cancer progression through sponging miR-495-3p and activating CDK6 in vitro and in vivo.In our study, the function of NEAT1 was studied in colon cancer. As we observed, NEAT1 level was obviously elevated in colon cancer cells. Then, HCT-116 and SW620 cells were stably infected with shRNA-NEAT1 for 48<U+2009>hr. As exhibited, silence of NEAT1 could greatly repress colon cancer cell progression. Apoptosis of colon cancer cells was triggered and the cell cycle progression was remarkably inhibited by downregulation of NEAT1. Interestingly, as exhibited, miR-495-3p was obviously decreased in colon cancer cells and it significantly suppressed colon cancer progression. Subsequently, miR-495-3p was predicted as a target of NEAT1. CDK6 was speculated as the target of miR-495-3p and miR-495-3p modulated its expression negatively. Finally, it was indicated that NEAT1 promoted colon cancer development through modulating miR-495-3p and CDK6 in vivo. Taken these together, we reported that NEAT1 could sponge miR-495-3p to contribute to colon cancer progression through activating CDK6.	31173354	RID07910	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	BLACAT1	has-miR-485-5p	negatively-F	dual-luciferase reporter assay;shRNA;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	LINC00912|linc-UBC1|onco-lncRNA-30	NA	Long noncoding RNA BLACAT1 is overexpressed in hepatocellular carcinoma and its downregulation suppressed cancer cell development through endogenously competing against hsa-miR-485-5p.BLACAT1 expression in bothin vitro HCC cell lines and in vivo human HCC clinical samples were assessed by qRT-PCR In HeG2 and MHCC97 L cells, BLACAT1 downregulation was induced by lentiviral infection to evaluate its functions in regulating HCC cancer cell proliferation and invasion in vitro, and xenograft in vivo. A BLACAT1 endogenously competing candidate, human microRNA-485-5p (has-miR-485-5p) was assessed in dualluciferase assay and qRT-PCRin HCC cells. Furthermore, has-miR-485-5p was inhibited in BLACAT1-downregulated HeG2 and MHCC97 L cells to evaluate the correlation of has-miR-485-5p in BLACAT1-associated functional regulation in HCC cells.BLACAT1was found to be overexpressed in both HCC cells and human HCC tumors. In HeG2 and MHCC97 L cells, lentivirus-induced BLACAT1 downregulation inhibited cancer cellin vitro proliferation and invasion, and in vivo xenograft growth. Has-miR-485-5p was confirmed to be bound by BLACAT1 and its expression in HCC cells inversely regulated by BLACAT1. Then, has-miR-485-5p downregulation reversed the inhibitory effects of BLACAT1 downregulation on HCC cancer cell in vitro functions.BLACAT1 is aberrantly upregulated in HCC and its inhibition had tumor suppressing effects in human HCC, possibly through endogenously competing against has-miR-485-5p. The BLACAT1/ has-miR-485- 5p regulatory axis may be a molecular target for future HCC therapy.	31174090	RID07911	ceRNA or sponge	NA		
Gallbladder cancer	MALAT1	ABI3BP	negatively-E	shRNA;FISH;RIP;RNA pull-down assay;ChIP	upregulation	microarray;RT-qPCR	NA	NA	cell growth(+);senescence(-);cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000154175	NA	378938	25890	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	DKFZP586L2024|NESHBP|TARSH	Long noncoding RNA MALAT1 potentiates growth and inhibits senescence by antagonizing ABI3BP in gallbladder cancer cells.microarray-based analysis initially provided data suggesting that the expression of MALAT1 was upregulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. Kaplan-Meier method was then adopted to analyze the relationship between the MALAT1 expression and overall survival and disease-free survival of patients with GBC. A set of in vitro and in vivo experiments were conducted by transducing ABI3BP-vector or sh-MALAT1 into GBC cells.The results confirmed that the cancer prevention effects triggered by restored ABI3BP and depleted MALAT1 as evidenced by suppressed cell growth and enhanced cell senescence. MALAT1 was observed to downregulate ABI3BP expression through recruitment of the enhancer of zeste homolog 2 (EZH2) to the ABI3BP promoter region while the silencing of MALAT1 or suppression of H3K27 methylation was observed to promote the expression of ABI3BP. Furthermore, GBC patients with high expression of MALAT1 indicated poor prognosis.The current study clarifies that MALAT1 silencing and ABI3BP elevation impede the GBC development through the H3K27 methylation suppression induced by EZH2, highlighting a promising competitive paradigm for therapeutic approaches of GBC.	31174563	RID07912	transcriptional regulation	prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Colon cancer	LINC00261	miR-324-3p	negatively-F	RNA pull-down assay;RIP;shRNA	downregulation	qRT-PCR	NA	NA	cell viability(+);cell proliferation(+);colony formation(+);apoptosis process(-);WNT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000259974	GRCh38_20:22547671-22578642	NA	NA	140828	NA	ALIEN|C20orf56|DEANR1|FALCOR|HCCDR1|LCAL62|NCRNA00261|TCONS_00027846|onco-lncRNA-17	NA	LINC00261 suppresses human colon cancer progression via sponging miR-324-3p and inactivating the Wnt/beta-catenin pathway. We found LINC00261 was reduced in colon cancer cells. Meanwhile, overexpressed LINC00261 repressed colon cancer cell viability and proliferation capacity. In addition, colony cancer cell colony formation was inhibited and apoptosis was enhanced by upregulation of LINC00261. Also, colon cancer cell migration and invasion both were restrained by LINC00261. miR-324-3p can exert important functions in several carcinomas, but its role in colon cancer is uninvestigated. In the current study, miR-324-3p was examined and miR-324-3p was greatly increased in colon cancer cells. Moreover, the association between miR-324-3p and LINC00261 was confirmed via performing RNA immunoprecipitation and RNA-pull-down experiments. In cancer biology, aberrant modulation of the Wnt signaling pathway remains a prevalent theme. Overexpression of LINC00261 obviously impaired colon cancer progression via inactivating the Wnt pathway. Furthermore, in the xenograft model assay, an increase of LINC00261 could suppress colon tumor growth via sponging miR-324-3p and inactivating the Wnt pathway. Overall, our results showed that LINC00261 repressed colon cancer progression via regulating miR-324-3p and the Wnt pathway. LINC00261 could be established as a novel therapeutic target for colon cancer.	31183860	RID07913	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Retinoblastoma	CDKN2B-AS1	MYC	positively-E	dual-luciferase reporter assay;shRNA;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-);cell viability(+);cell migration(+);cell invasion(+);apoptosis process(-);JAK/STAT signaling pathway(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000136997	NA	100048912	4609	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|p15AS|PCAT12|RP11-145E5.4	bHLHe39|c-Myc|MYCC	Silence of lncRNA ANRIL represses cell growth and promotes apoptosis in retinoblastoma cells through regulating miR-99a and c-Myc.Retinoblastoma is a rare cancer of the immature retina. This study designed to see the function of the lncRNA ANRIL in retinoblastoma Y79 cells. ANRIL, miR-99a and c-Myc expression in Y79 cells was altered by transfection and then trypan blue, transwell assay and flow cytometry were carried out to evaluate the changes of cell phenotype. The connection between ANRIL, miR-99a and c-Myc was measured by luciferase reporter assay and RNA immunoprecipitation analysis. As a result, ANRIL expression was highly expressed in human retinoblastoma tissue as relative to the adjacent noncancerous tissues. ANRIL suppression inhibited Y79 cells viability, migration, invasion, while promoted apoptosis. ANRIL negatively regulated miR-99a by binding to miR-99a. Silence of miR-99a reversed the ANRIL-knockdown effects on Y79 cells. miR-99a overexpression suppressed Y79 cell viability, migration, invasion, and enhanced apoptosis through downregulating c-Myc. Meanwhile, we found that miR-99a inhibited JAK/ STAT and PI3K/AKT pathways. To conclude, it seems that ANRIL suppression inhibits cell growth and metastasis in retinoblastoma Y79 cells by regulating miR-99a and c-Myc.	31184221	RID07914	expression association	metastasis	UP(SKCM);DATA(GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Oesophageal squamous cell carcinoma	TP53	PGM5-AS1	positively-E	siRNA;luciferase reporter assay;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000265923	NA	7157	572558	LFS1|p53	FAM233A|LOC572558	p53-induced long non-coding RNA PGM5-AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR-466/PTEN axis. In the present study, we found that PGM5-AS1 was frequently downregulated in ESCC tissues, plasma, and cell lines, and low PGM5-AS1 expression was positively correlated with poor differentiation, advanced tumor node metastasis (TNM) stage, and lymph node metastasis. Importantly, PGM5-AS1 was identified to be an effective diagnostic and prognostic biomarker for ESCC patients. Functional experiments revealed that exogenous expression of PGM5-AS1 significantly suppressed the proliferation, migration, and invasion of ESCC cells in vitro as well as tumor growth in vivo.Mechanistically, PGM5-AS1 was transcriptionally activated by p53 and it could directly interact with and sequester miR-466 to elevate PTEN expression, thereby inhibiting ESCC progression. Overall, our data indicate that PGM5-AS1 is a novel tumor suppressor in ESCC and restoration of PGM5-AS1 may be a promising avenue for treatment of ESCC patient.	31185143	RID07915	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)	
Oesophageal squamous cell carcinoma	PGM5-AS1	PTEN	positively-E	siRNA;luciferase reporter assay;ChIP;miRanda;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	ceRNA(miR-466)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	PCG	ENSG00000265923	NA	ENSG00000171862	NA	572558	5728	FAM233A|LOC572558	BZS|MHAM|MMAC1|PTEN1|TEP1	p53-induced long non-coding RNA PGM5-AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR-466/PTEN axis. In the present study, we found that PGM5-AS1 was frequently downregulated in ESCC tissues, plasma, and cell lines, and low PGM5-AS1 expression was positively correlated with poor differentiation, advanced tumor node metastasis (TNM) stage, and lymph node metastasis. Importantly, PGM5-AS1 was identified to be an effective diagnostic and prognostic biomarker for ESCC patients. Functional experiments revealed that exogenous expression of PGM5-AS1 significantly suppressed the proliferation, migration, and invasion of ESCC cells in vitro as well as tumor growth in vivo.Mechanistically, PGM5-AS1 was transcriptionally activated by p53 and it could directly interact with and sequester miR-466 to elevate PTEN expression, thereby inhibiting ESCC progression. Overall, our data indicate that PGM5-AS1 is a novel tumor suppressor in ESCC and restoration of PGM5-AS1 may be a promising avenue for treatment of ESCC patient.	31185143	RID07916	ceRNA or sponge	metastasis,prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Malignant glioma	A1CF	FAM224A	positively-F	dual-luciferase reporter assay;RIP;ChIP;shRNA;starBase;Targetscan	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000148584	NA	ENSG00000233522	GRCh38_Y:18326253-18353210	29974	401630	ACF|ACF64|ACF65|APOBEC1CF|ASP	LINC00230A|NCRNA00230A	Inhibition of the aberrant A1CF-FAM224AmiR- 590-3p-ZNF143 positive feedback loop attenuated malignant biological behaviors of glioma cells. Quantitative RT-PCRand western blotwere employed to detect the expression levels of A1CF, lncRNA family with sequence similarity 224 member A (FAM224A), miR-590-3p, zinc finger protein 143 (ZNF143) and ArfGAP with SH3 domain, ankyrin repeat and PH domain 3 (ASAP3) in glioma tissues and cell lines. The Cell Counting Kit-8 assay, migration and invasion assays, and flow cytometry analysis were conducted to evaluate the function of A1CF, FAM224A, miR-590-3p, ZNF143 and ASAP3 in the malignant biological behaviors of glioma cells. Moreover, luciferase reporter, RIP and ChIP assays were used to investigate the interactions among A1CF, FAM224A, miR-590-3p, ZNF143, ASAP3 and MYB. Finally, the xenograft tumor growth assay further ascertained the biological roles of A1CF, FAM224A and miR-590-3p in glioma cells.A1CF was upregulated and functioned as an oncogene via stabilizing and increasing FAM224A expression; moreover, high A1CF and FAM224A expression levels indicated a poorer prognosis for glioma patients. Conversely, miR-590-3p was downregulated and exerted a tumor-suppressive function in glioma cells. Inhibition of A1CF significantly restrained cell proliferation, migration and invasion, and promoted apoptosis by upregulating miR-590-3p in a FAM224Adependent manner. FAM224A was a molecular sponge of miR-590-3p and they were in an RNA-induced silencing complex. ZNF143 was upregulated in glioma tissues and cell lines. MiR-590-3p could negatively modulate the expression of ZNF143 via binding to the ZNF143 3'-UTR. Moreover, ZNF143 participated in miR-590-3p-induced tumor-suppressive activity on glioma cells. ASAP3 and MYB were transcriptionally activated by ZNF143, and importantly, ZNF143 could directly target the promoter of FAM224A and stimulate its expression, collectively forming a positive feedback loop.The present study clarifies that the A1CF-FAM224A-miR-590-3p-ZNF143 positive feedback loop conducts critical regulatory effects on the malignant progression of glioma cells, which provides a novel molecular target for glioma therapy.	31186064	RID07917	transcriptional regulation	prognosis	UP(LIHC);DATA(GSE117623)	
Malignant glioma	FAM224A	ZNF143	positively-E	dual-luciferase reporter assay;RIP;ChIP;shRNA;starBase;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000233522	GRCh38_Y:18326253-18353210	ENSG00000166478	NA	401630	7702	LINC00230A|NCRNA00230A	pHZ-1|SBF|STAF	Inhibition of the aberrant A1CF-FAM224AmiR- 590-3p-ZNF143 positive feedback loop attenuated malignant biological behaviors of glioma cells. Quantitative RT-PCRand western blotwere employed to detect the expression levels of A1CF, lncRNA family with sequence similarity 224 member A (FAM224A), miR-590-3p, zinc finger protein 143 (ZNF143) and ArfGAP with SH3 domain, ankyrin repeat and PH domain 3 (ASAP3) in glioma tissues and cell lines. The Cell Counting Kit-8 assay, migration and invasion assays, and flow cytometry analysis were conducted to evaluate the function of A1CF, FAM224A, miR-590-3p, ZNF143 and ASAP3 in the malignant biological behaviors of glioma cells. Moreover, luciferase reporter, RIP and ChIP assays were used to investigate the interactions among A1CF, FAM224A, miR-590-3p, ZNF143, ASAP3 and MYB. Finally, the xenograft tumor growth assay further ascertained the biological roles of A1CF, FAM224A and miR-590-3p in glioma cells.A1CF was upregulated and functioned as an oncogene via stabilizing and increasing FAM224A expression; moreover, high A1CF and FAM224A expression levels indicated a poorer prognosis for glioma patients. Conversely, miR-590-3p was downregulated and exerted a tumor-suppressive function in glioma cells. Inhibition of A1CF significantly restrained cell proliferation, migration and invasion, and promoted apoptosis by upregulating miR-590-3p in a FAM224Adependent manner. FAM224A was a molecular sponge of miR-590-3p and they were in an RNA-induced silencing complex. ZNF143 was upregulated in glioma tissues and cell lines. MiR-590-3p could negatively modulate the expression of ZNF143 via binding to the ZNF143 3'-UTR. Moreover, ZNF143 participated in miR-590-3p-induced tumor-suppressive activity on glioma cells. ASAP3 and MYB were transcriptionally activated by ZNF143, and importantly, ZNF143 could directly target the promoter of FAM224A and stimulate its expression, collectively forming a positive feedback loop.The present study clarifies that the A1CF-FAM224A-miR-590-3p-ZNF143 positive feedback loop conducts critical regulatory effects on the malignant progression of glioma cells, which provides a novel molecular target for glioma therapy.	31186064	RID07918	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842)
Prostate cancer	LOXL1-AS1	EGFR	positively-E	dual-luciferase reporter assay;Targetscan;siRNA	downregulation	qRT-PCR;microarray	GSE33455	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);chemoresistance(+);tumorigenesis(+)	NA	association	NA	Doxorubicin	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000146648	NA	100287616	1956	NA	ERBB|ERBB1|ERRP	LncRNA LOXL1-AS1/miR-let-7a-5p/EGFR-related pathway regulates the doxorubicin resistance of prostate cancer DU-145 cells.microarray analysis was conducted to determine differentially expressed lncRNAs and mRNAs. Gene Set Enrichment analysis was implemented for verification of dys-regulated signaling pathways between DU-145 cells and doxorubicin-resistant prostate cancer DU-145 cells. Relative expression of lncRNA LOXL1-AS1 in doxorubicin-resistant prostate cancer DU-145 cells was analyzed by qRT-PCR CCK-8 assay and flow cytometry analysis were employed to detect cell proliferation and apoptosis, respectively. Cell migration was performed by transwell assay. Furthermore, targeted relationships between lncRNA LOXL1-AS1 and miR-let-7a-5p, as well as miR-let-7a-5p and EGFR were predicted using bioinformatics analysis and validated by dual-luciferase reporter gene assay. Besides, tumor xenograft assay was utilized for verification of the roles of LOXL1-AS1 in PCa progression in vivo. microarray analysis showed that lncRNA LOXL1-AS1 and EGFR were both downregulated, while miR-let-7a-5p was upregulated in doxorubicin-resistant prostate cancer DU-145 cells. MiR-let-7a-5p could target both lncRNA LOXL1-AS1 and EGFR to affect PCa progression. Upregulation of lncRNA LOXL1-AS1 promoted cell proliferation and migration, while suppressed cell apoptosis. Besides, it was further confirmed that EGFR was downregulated in drug-resistant PCa cells and negatively correlated with miR-let-7a- 5p. Tumor xenograft assay verified that silence of lncRNA LOXL1-AS1 inhibited the tumor growth in vivo in DU-145 cells. Our results demonstrated that the lncRNALOXL1-AS1/miR-let-7a-5p/EGFR axis significantly affected proliferation, migration, and apoptosis of drug-resistant DU-145 Cells, which may provide us with a potential treatment strategy for drug-resistant PCa patients.	31188543	RID07919	expression association	chemoresistance	DOWN(BRCA);DATA(GSE111842)	UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Prostate cancer	TP53COR1	STAT3	negatively-E	RIP;shRNA;ChIP	upregulation	qPCR	NA	NA	chemosensitivity(-)	transcriptional regulation	binding/interaction	NA	Enzalutamide	NA	NA	Cancer	Prostate cancer	lncRNA	TF	NA	NA	ENSG00000168610	NA	102800311	6774	TRP53COR1|linc-p21|lincRNA-p21	ADMIO|ADMIO1|APRF|HIES	LncRNA-p21 alters the antiandrogen enzalutamideinduced prostate cancer neuroendocrine differentiation via modulating the EZH2/ STAT3 signaling. While the antiandrogen enzalutamide (Enz) extends the castration resistant prostate cancer (CRPC) patients'-survival an extra 4.8 months, it might also result in some adverse effects via inducing the neuroendocrine differentiation (NED). Here we found that lncRNA-p21 is highly expressed in the NEPC patients derived xenograft tissues (NEPC-PDX). Results from cell lines and human clinical sample surveys also revealed that lncRNA-p21 expression is up-regulated in NEPC and Enz treatment could increase the lncRNA-p21 to induce the NED. Mechanism dissection revealed that Enz could promote the lncRNA-p21 transcription via altering the androgen receptor (AR) binding to different androgen-response-elements, which switch the EZH2 function from histone-methyltransferase to non-histone methyltransferase, consequently methylating the STAT3 to promote the NED. Preclinical studies using the PDX mouse model proved that EZH2 inhibitor could block the Enz-induced NED. Together, these results suggest targeting the Enz/AR/lncRNA-p21/EZH2/STAT3 signaling may help urologists to develop a treatment for better suppression of the human CRPC progression.	31189930	RID07920	transcriptional regulation	chemoresistance		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Laryngeal squamous cell carcinoma	SSTR5-AS1	SSTR5	positively-E	RIP;overexpression	downregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000261713	GRCh38_16:1064087-1078731	ENSG00000162009	NA	146336	6755	NA	SS-5-R|SST5	Aberrant methylation-mediated downregulation of lncRNA SSTR5-AS1 promotes progression and metastasis of laryngeal squamous cell carcinoma.In the present study, we screen expression profiles of lncRNAs in advanced Laryngeal squamous cell carcinoma (LSCC) patients with paired tumor tissues and corresponding normal tissues by microarrays. We identify numerous differentially expressed transcripts, and after the necessary verification of the transcripts expression in expanded samples, we experimentally validate the expression patterns of the remarkable low expressed gene, SSTR5, and its antisense lncRNA, SSTR5-AS1. Downregulation of SSTR5 is detected in LSCC tissues and laryngeal carcinoma cells. Aberrant DNA hypermethylation of the CpG sites clustered in the exon 1 and accumulation of inactive histone modifications at SSTR5 promoter region may be epigenetic mechanisms for its inactivation in LSCC. SSTR5-AS1 may play antitumor role in LSCC and may be regulated by the hypermethylation of the same CpG sites with SSTR5. SSTR5-AS1 inhibits laryngeal carcinoma cells proliferation, migration, and invasion. SSTR5-AS1 increases the enrichment of MLL3 and H3K4me3 at the promoter region of SSTR5 by interacting with MLL3 and further induces the transcription of SSTR5. Furthermore, SSTR5-AS1 interacts with and recruits TET1 to its target gene E-cadherin to activate its expression.These findings suggest that the identified lncRNAs and mRNAs may be potential biomarkers in metastatic LSCC, and SSTR5-AS1 may act as a tumor suppressor as well as a potential biomarker for antitumor therapy.	31196171	RID07921	epigenetic regulation	metastasis		
Gastric cancer	TUBA4B	PTEN	positively-E	mRNA sequencing;RIPA;overexpression;FISH;miRCode	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);tumor growth(+);cell metastasis(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000243910	GRCh38_2:219253243-219272197	ENSG00000171862	NA	80086	5728	FLJ13940|TUBA4	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA TUBA4B functions as a competitive endogenous RNA to inhibit gastric cancer progression by elevating PTEN via sponging miR-214 and miR-216a/b.qRT-PCRwas employed to detect the expression of TUBA4B in GC tissues, cell lines and plasma. In vitro and in vivo experiments were carried out using colony formation/CCK-8/transwell invasion/cell apoptosis assay and xenograft tumor model, respectively. mRNA sequencing was used to identify the TUBA4B-related downstream genes.TUBA4B was significantly decreased in GC tissues, cells and plasma. Low TUBA4B was positively correlated with larger tumor size, lymph node metastasis and advanced TNM stage. Moreover, TUBA4B was identified as an effective biomarker for the diagnosis and prognosis of patients with GC. Functionally, ectopic expression of TUBA4B inhibited GC cell proliferation, invasion and induced apoptosis in vitro as well as dampened tumor growth and metastasis in vivo. Furthermore, TUBA4B was found to be a competitive endogenous RNA (ceRNA) that could physically bind to and sequester miR-214 and miR-216a/b to increase the expression of their common downstream target PTEN, resulting in inactivation of PI3K/AKT signaling pathway, thereby retarding GC progression.Our data highlight the compelling regulatory role of TUBA4B in GC, and reactivation of TUBA4B may be a promising therapeutic avenue for GC patients.	31198405	RID07922	expression association	metastasis,prognosis	UP(BRCA);DATA(GSE86978)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Endometrial cancer	TUSC7	SOCS5	positively-E	RNA pull-down assay;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000171150	NA	285194	9655	LINC00902|LOC285194|LSAMP-AS3|NCRNA00295	CIS6|Cish5|CISH6|KIAA0671|SOCS-5	Long noncoding RNA TUSC7 inhibits cell proliferation, migration and invasion by regulating SOCS4 (SOCS5) expression through targeting miR-616 in endometrial carcinoma.The expression levels of TUSC7 and microRNAs-616 (miR-616) were analyzed by real-time PCR and in situ hybridization. Cell cycle and cell metastasis associated protein expressions were determined by western blot. Cell proliferation, cycle and metastasis were determined by CCK-8 cell viability, colony formation, flow cytometer, wound scratch and transwell assays respectively in vitro. RNA pull-down, luciferase and western blot assays were used to examine the target relationship between TUSC7 and miR-616 or that between miR-616 and suppressors of cytokine signaling 4 (5) (SOCS4 (SOCS5)). The functional effects of TUSC7 through sponging miR-616 were further examined using a xenograft tumor mouse model in vivo.TUSC7 was downexpressed in EC tissues and cell lines, and TUSC7 upregulation could remarkably inhibit cell proliferation, cycle progression and metastasis in EC cells. Mechanistic investigations demonstrated that TUSC7 can interact with miR-616 and decrease its expression, thereby upregulating the expression of miR-616's targets SOCS4 (SOCS5). Additionally, in vivo experiments using a xenograft tumor mouse model revealed that TUSC7 can serve as a tumor suppressor through sponging miR-616, and upregulating SOCS4 (SOCS5) in EC.In this study, a newly identified regulatory mechanism of lncRNA TUSC7/miR-616/ SOCS4 (SOCS5) axis was systematically studied, which may hold promise as a promising target for EC treatment.	31200002	RID07923	expression association	metastasis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Cervical cancer	CRNDE	BBC3	positively-E	siRNA;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell growth(+);cancer progression(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000105327	NA	643911	27113	CRNDEP|LINC00180|LOC643911	JFY1|PUMA	Long non-coding RNA CRNDE enhances cervical cancer progression by suppressing PUMA expression.Our results indicated that CRNDE expression was increased in cervical cancer tissues and several cervical cancer cell lines. Through loss-of-function and gain-of-function approaches, we found that CRNDE knockdown markedly reduced cervical cancer cell proliferation, while CRNDE overexpression significantly promoted cervical cancer cell growth. Consistently, CRNDE decreasing obviously inhibited tumorigenicity of cervical cancer cells in vivo, whereas CRNDE increasing markedly promoted cervical cancer progression. Mechanistically, we verified that CRNDE bond to p53 upregulated modulator of apoptosis (PUMA), and PUMA was required for CRNDE to enhance cervical cancer cell growth. Our study demonstrated that CRNDE, combined with PUMA, could be utilized as factor for the clinical diagnosis and prognosis of cervical cancer, and might be potential target for developing effective therapeutic strategy to prevent cervical cancer progression.	31202167	RID07924	transcriptional regulation	prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111065,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	DLEU1	IGF1R	positively-E	luciferase reporter assay;RIP;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);colony formation(+);epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+);tumor growth(+);cancer progression(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000140443	NA	10301	3480	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	CD221|IGFIR|IGFR|JTK13|MGC18216	Long non-coding RNA deleted in lymphocytic leukaemia 1 promotes hepatocellular carcinoma progression by sponging miR-133a to regulate IGF-1R expression.In this study, real-time quantitative polymerase chain reaction (qRT-PCR in HCC tissues and cell lines revealed that DLEU1 expression was up-regulated, and the increased DLEU1 was closely associated with advanced tumour-node-metastasis stage, vascular metastasis and poor overall survival. Function experiments showed that knockdown of DLEU1 significantly inhibited HCC cell proliferation, colony formation, migration and invasion, and suppressed epithelial to mesenchymal transition (EMT) process via increasing the expression of E-cadherin and decreasing the expression of N-cadherin and Vimentin. Luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay demonstrated that DLEU1 could sponge miR-133a. Moreover, miR-133a inhibition significantly reversed the suppression effects of DLEU1 knockdown on HCC cells. Besides, we found that silenced DLEU1 significantly decreased insulin-like growth factor 1 receptor (IGF-1R) expression (a target of miR-133a) and its downstream signal PI3K/AKT pathway in HCC cells, while miR-133a inhibitor partially reversed this trend. Furthermore, DLEU1 knockdown impaired tumour growth in vivo by regulating miR-133a/IGF-1R axis. Collectively, these findings indicate that DLEU1 promoted HCC progression by sponging miR-133a to regulate IGF-1R expression. Deleted in lymphocytic leukaemia 1/miR-133a/IGF-1R axis may be a novel target for treatment of HCC.	31207081	RID07925	ceRNA or sponge	metastasis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Hepatocellular carcinoma	LINC01391	CTNNBIP1	positively-F	RNA pull-down assay;RIP;overexpression;shRNA;western blot	downregulation	qRT-PCR;microarray	NA	NA	tumor growth(+);WNT/beta-catenin signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	binding/interaction	NA	Piplartine	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000244578	GRCh38_3:138935189-138944020	ENSG00000178585	NA	103344930	56998	NA	ICAT|MGC15093	Piplartine suppresses proliferation and invasion of hepatocellular carcinoma by LINC01391-modulated Wnt/beta-catenin pathway inactivation through ICAT.We identified LINC01391 using microarray analysis and validated its expression by qRTPCR. Functional assays were applied to evaluate the biological effects of LINC01391 and inhibitory of beta-catenin and T-cell factor (ICAT) on HepG2 and SMMC-7721 cells. The binding relationship between LINC01391 and ICAT was determined by RNA pull-down and RNA immunoprecipitation (RIP). Results showed that piplartine attenuated cell proliferation and invasion but promoted cell apoptosis. Upregulation of LINC01391 induced by piplartine inhibited HCC cell proliferation, invasion in vitro, and tumor growth in vivo. LINC01391 interacted with ICAT and promoted its inhibitory effect on the Wnt/beta-catenin pathway, as enhanced interaction between beta- catenin and ICAT, and dampened interaction of beta-catenin and TCF/LEF were induced by overexpression of LINC01391. Knockdown of ICAT also promoted cell proliferation in vitro and tumor growth in vivo. Our study supported a role for piplartine and LINC01391 in HCC treatment. We found that LINC01391 inhibited the Wnt/ beta-catenin pathway and suppressed tumor growth via ICAT.	31207322	RID07926	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807)
Cervical cancer	LINC00052	STAT3	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000168610	NA	145978	6774	FLJ31461|NCRNA00052|TMEM83	APRF	LINC00052 inhibits tumor growth, invasion and metastasis by repressing STAT3 in cervical carcinoma.LINC00052 expression was detected by quantitative Real-time polymerase chain reaction (qRT-PCR in CERVICAL CANCer tissue samples and cell lines. Moreover, the correlation between LINC00052 expression level and disease-free survival rate of cervical cancer patients was analyzed. In vitro functions of LINC00052 in cervical cancer cells were evaluated by proliferation assay, wound healing assay and transwell assay. In addition, qRT-PCRand western blot were utilized to explore the underlying mechanism of LINC00052 in mediating the progression of cervical cancer. LINC00052 expression level was lower in cervical cancer samples than that in adjacent tissues, which was correlated with disease-free survival time. Moreover, cell proliferation, migration and invasion were inhibited through overexpression of LINC00052 in vitro. The mRNA and protein expression of signal transducers and activators of transcription 3 (STAT3) was downregulated after overexpressing LINC00052 in cervical cancer cells. The STAT3 expression level was negatively correlated with the expression of LINC00052 in cervical cancer tissues.LINC00052 could repress metastasis and invasion of cervical cancer cell via suppressing STAT3. LINC00052 might be a novel tumor suppressor in cervical cancer.	31210293	RID07927	expression association	metastasis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Oral squamous cell carcinoma	CASC2	CDK1	negatively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000170312	NA	255082	983	C10orf5	CDC2|CDC28A	Long noncoding RNA CASC2 alleviates the growth, migration and invasion of oral squamous cell carcinoma via downregulating CDK1.CASC2 expression in OSCC cell lines and 40 paired OSCC samples were detected by quantitative Real-time polymerase chain reaction (qRT-PCR. Moreover, in vitro functions of CASC2 in regulating the cellular behaviors of OSCC cells were identified by performing transwell assay, wound healing assay and proliferation assay. The underlying mechanism of CASC2 in mediating the progression of OSCC was explored by qRT-PCRand western blot.CASC2 expression was remarkably downregulated in OSCC tissues compared with that in adjacent normal samples. Moreover, proliferation, invasion and migration were inhibited in OSCC cells overexpressing CASC2. CASC2 overexpression in OSCC cells downregulated CDK1 at both mRNA and protein levels in vitro. Besides, the expression of CDK1 in OSCC tissues was negatively correlated to the expression of CASC2.CASC2 suppresses the migration, invasion and proliferation of OSCC cells through downregulating CDK1, which may offer a new therapeutic intervention for OSCC patients.	31210307	RID07928	expression association	NA	UP(LIHC);DATA(GSE117623)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Malignant glioma	LINC00052	KLF6	positively-E	western blot;overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000067082	NA	145978	1316	FLJ31461|NCRNA00052|TMEM83	BCD1|COPEB|CPBP|GBF|PAC1|ST12|Zf9	Long noncoding RNA LINC00052 suppressed the proliferation, migration and invasion of glioma cells by upregulating KLF6.Quantitative Real-time polymerase chain reaction (qRT-PCR was performed to detect LINC00052 expression in 40 glioma samples and 4 glioma cell lines. Besides, regulatory effects of LINC00052 on the in vitro behaviors of glioma cells were evaluated by the proliferation assay, transwell assay and wound healing assay. Furthermore, the interaction between LINC00052 and kruppel-like factor 6 (KLF6) in mediating the progression of glioma was studied by performing qRT-PCRand western blot.LINC00052 expression was remarkably downregulated in glioma samples compared with that in adjacent samples. Moreover, cell proliferation, invasion, and migration of glioma were inhibited after overexpression of LINC00052 in vitro. Besides, LINC00052 overexpression upregulated mRNA and protein level of KLF6. Besides, the expression of KLF6 in tumor tissues was positively correlated to the expression of LINC00052.These results suggested that LINC00052 could repress cell migration, invasion and proliferation in glioma through upregulating KLF6, which may offer a new therapeutic intervention for glioma patients.	31210314	RID07929	expression association	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE67939)
Non-small cell lung cancer	H19	miR-675	positively-E	luciferase reporter assay;siRNA	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Upregulation of miR-675-5p induced by lncRNA H19 was associated with tumor progression and development by targeting tumor suppressor p53 in non-small cell lung cancer.Luciferase assay and reverse transcription-polymerase chain reaction (RT-PCR were conducted to study the regulatory relationship between P53 and microRNA-675 (miR-675). Real-time PCR, western blot analysis, and MTT assay were performed to explore the impact of H19 and miR-675 in the signaling pathway involved in COPD induced NSCLC. In NSCLC patients with COPD, H19 and miR-675 levels were strikingly upregulated while P53 level was significantly downregulated. P53 was identified as a target gene of miR-675, and H19 remarkably upregulated miR-675, while H19 siRNA notably inhibited miR-675. In addition, miR- 675 and H19 dramatically suppressed the expression of P53 and Bax while inducing the expression of Bcl-2. Finally, H19 and miR-675 induced proliferation of A549 and MRC-5 cells. These finding indicated that COPD (hypoxia)-induced H19 promoted expression of miR-675 associated with NSCLC though target apoptosisrelated protein P53, BAX, and Bcl-2.	31219199	RID07930	expression association	NA	UP(NSCLC);DATA(GSE74639)	
Non-small cell lung cancer	H19	TP53	negatively-E	luciferase reporter assay;siRNA	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LFS1|p53	Upregulation of miR-675-5p induced by lncRNA H19 was associated with tumor progression and development by targeting tumor suppressor p53 in non-small cell lung cancer.Luciferase assay and reverse transcription-polymerase chain reaction (RT-PCR were conducted to study the regulatory relationship between P53 and microRNA-675 (miR-675). Real-time PCR, western blot analysis, and MTT assay were performed to explore the impact of H19 and miR-675 in the signaling pathway involved in COPD induced NSCLC. In NSCLC patients with COPD, H19 and miR-675 levels were strikingly upregulated while P53 level was significantly downregulated. P53 was identified as a target gene of miR-675, and H19 remarkably upregulated miR-675, while H19 siRNA notably inhibited miR-675. In addition, miR- 675 and H19 dramatically suppressed the expression of P53 and Bax while inducing the expression of Bcl-2. Finally, H19 and miR-675 induced proliferation of A549 and MRC-5 cells. These finding indicated that COPD (hypoxia)-induced H19 promoted expression of miR-675 associated with NSCLC though target apoptosisrelated protein P53, BAX, and Bcl-2.	31219199	RID07931	expression association	NA	UP(NSCLC);DATA(GSE74639)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Prostate cancer	LNC-LBCS	AR	negatively-F	shRNA;siRNA;RNA pull-down assay;RIP;ChIP;FISH	downregulation	qPCR	GSE93929;TCGA	NA	cell proliferation(+)	post-transcriptional level	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000228412	GRCh38_6:19323428-19839080	ENSG00000169083	NA	100506885	367	LBCS	AIS|DHTR|HUMARA|NR3C4|SBMA|SMAX1	A novel AR translational regulator lncRNA LBCS inhibits castration resistance of prostate cancer. We explore the CRPC associated lncRNAs by transcriptome microarray. The expression and clinical features of lnc-LBCS are analyzed in three independent large-scale cohorts. The functional role and mechanism of lnc-LBCS are further investigated by gain and loss of function assays in vitro.The expression of Lnc-LBCS was lower in CRPC cells lines and tissues. LBCS downregulation was correlated with higher Gleason Score, T stage and poor prognosis of PCa patients. LBCS overexpression decreases, whereas LBCS knockdown increases, the traits of castration resistance in prostate cancer cells under androgen ablated or AR blocked condition. Moreover, knockdown of LBCS was sufficient to activate AR signaling in the absence of androgen by elevating the translation of AR protein. Mechanistically, LBCS interacted directly with hnRNPK to suppress AR translation efficiency by forming complex with hnRNPK and AR mRNA.Lnc-LBCS functions as a novel AR translational regulator that suppresses castration resistance of prostate cancer by interacting with hnRNPK. This sheds a new insight into the regulation of CRPC by lncRNA mediated AR activation and LBCS-hnRNPK-AR axis provides a promising approach to the treatment of CRPC.	31221168	RID07932	transcriptional regulation	prognosis		UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111065,GSE55807)
Retinoblastoma	SNHG16	miR-140-5p	negatively-E	luciferase reporter assay;RIP;shRNA;starBase	upregulation	qRT-PCR	NA	NA	tumor growth(+);cell proliferation(+);apoptosis process(-);colony formation(+)	sponge	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Retinoblastoma	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long noncoding RNA SNHG16 promotes human retinoblastoma progression via sponging miR-140-5p.The expression levels of SNHG16 were measured in RB tissues and cell lines. The effects of SNHG16 knockdown on the proliferation, colony formation, cell cycle progression and apoptosis were investigated using corresponding experiments. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were applied to identify potential microRNAs (miRs) that could bind with SNHG16. A nude model was established to investigate the effect of SNHG16 knockdown on tumor growth in vivo. We found that SNHG16 expression was upregulated in RB tissues and cell lines compared with normal controls. Knockdown of SNHG16 in RB cells significantly inhibited the proliferation and colony formation, and promoted apoptosis in vitro, as well as retarded tumor growth in vivo. Mechanistic investigation illustrated that SNHG16 acted as a sponge for miR-140-5p and regulated its expression in RB cells. Clinical evidence revealed a negative correlation between SNHG16 and miR-140-5p in RB specimens. Rescue experiments showed that inhibition of miR-140-5p partially attenuated the growth-suppressing effects of SNHG16-depletion on RB cells.. Collectively, SNHG16 exerts oncogenic role in RB by sponging miR-140-5p, suggesting that SNHG16 might be a potential therapy target for RB.	31234025	RID07933	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Prolactinoma	FOXP1	CLRN1-AS1	negatively-E	shRNA;RIP;FISH;JASPAR	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);apoptosis process(-);cell autophagy(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Endocrine system disease	Functioning pituitary adenoma	TF	lncRNA	ENSG00000114861	NA	ENSG00000239265	GRCh38_3:150852484-151080726	27086	116933	12CC4|hFKH1B|HSPC215|QRF1	CLRN1OS|UCRP	FOXP1-induced lncRNA CLRN1-AS1 acts as a tumor suppressor in pituitary prolactinoma by repressing the autophagy via inactivating Wnt/beta-catenin signaling pathway.We explored an lncRNA that was differentially downregulated in prolactinoma samples. LncRNA clarin 1 antisense RNA 1 (CLRN1-AS1) was downregulated in 42 patient samples and inactivated the Wnt/beta-catenin signaling pathway. Functionally, CLRN1-AS1 suppressed cell proliferation, promoted apoptosis, and inhibited autophagy. Subcellular fractionation assay revealed that CLRN1-AS1 was located in the cytoplasm of prolactinoma cells. Based on bioinformatics analysis and mechanism experiments, we determined that CLRN1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-217 to upregulate the dickkopf WNT signaling pathway inhibitor 1 (DKK1). Furthermore, Forkhead box P1 (FOXP1) was verified to be a transcription suppressor of CLRN1-AS1. In summary, this study revealed that FOXP1-induced CLRN1- AS1 regulated cellular functions in pituitary prolactinoma by sponging miR-217 to release the DKK1/Wnt/beta-catenin signaling pathway.	31235696	RID07934	transcriptional regulation	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)	
Prolactinoma	CLRN1-AS1	DKK1	positively-E	shRNA;RIP;FISH;starBase;Ago2-RIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);apoptosis process(-);cell autophagy(+);cell growth(+)	ceRNA(miR-217)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Endocrine system disease	Functioning pituitary adenoma	lncRNA	PCG	ENSG00000239265	GRCh38_3:150852484-151080726	ENSG00000107984	NA	116933	22943	CLRN1OS|UCRP	DKK-1|SK	FOXP1-induced lncRNA CLRN1-AS1 acts as a tumor suppressor in pituitary prolactinoma by repressing the autophagy via inactivating Wnt/beta-catenin signaling pathway.We explored an lncRNA that was differentially downregulated in prolactinoma samples. LncRNA clarin 1 antisense RNA 1 (CLRN1-AS1) was downregulated in 42 patient samples and inactivated the Wnt/beta-catenin signaling pathway. Functionally, CLRN1-AS1 suppressed cell proliferation, promoted apoptosis, and inhibited autophagy. Subcellular fractionation assay revealed that CLRN1-AS1 was located in the cytoplasm of prolactinoma cells. Based on bioinformatics analysis and mechanism experiments, we determined that CLRN1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-217 to upregulate the dickkopf WNT signaling pathway inhibitor 1 (DKK1). Furthermore, Forkhead box P1 (FOXP1) was verified to be a transcription suppressor of CLRN1-AS1. In summary, this study revealed that FOXP1-induced CLRN1- AS1 regulated cellular functions in pituitary prolactinoma by sponging miR-217 to release the DKK1/Wnt/beta-catenin signaling pathway.	31235696	RID07935	ceRNA or sponge	NA		UP(LIHC);DATA(GSE117623)
Laryngeal carcinoma	SNHG3	WEE1	positively-E	dual-luciferase reporter assay;siRNA;starBase;Targetscan	upregulation	RT-PCR	NA	NA	cell migration(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-384)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000166483	NA	8420	7465	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	WEE1A	LncRNA SNHG3 regulates laryngeal carcinoma proliferation and migration by modulating the miR-384/WEE1 axis.Real time-PCR (RT-PCR was used to estimate the expression of SNHG3 in laryngeal carcinoma (LC) tissues and cell lines TU212, TU686, and Hep-2. Cell viability, migration, and invasion were evaluated. Our results showed increased SNHG3 in LC tissues and cell lines. Loss of function of SNHG3 reduced cell viability, migration, and invasion of TU212 and TU686 cells. western blot demonstrated that the protein levels of MMP2 and MMP9 decreased after SNHG3 silencing. Additionally, bioinformatics software predicted that SNHG3 could sponge miR-384 at the 3'-UTR with complementary binding sites, which was validated by a dual-luciferase reporter assay. RT-PCRanalysis revealed that knockdown of SNHG3 upregulated miR-384 expression and that overexpression of miR-384 decreased SNHG3. Furthermore, a dual-luciferase reporter assay showed that miR-384 could bind to the 3'-UTR of WEE1, and inhibition of miR-384 markedly increased WEE1 expression. The mRNA and protein levels of WEE1 were downregulated upon deletion of SNGH3. Suppression of WEE1 partly abolished the tumorigenic migration and invasion potential of the miR-384 inhibitor in migration and invasion. Inhibition of miR-384 partially reversed the biological activities of SNHG3 in TU212 and TU686 cells. Collectively, our results indicate that SNHG3 regulated LC cell migration and invasion via the miR-384/WEE1 axis.	31238052	RID07936	ceRNA or sponge	NA	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Colorectal cancer	YWHAE	miR-323a-3p	negatively-F	western blot;overexpression	upregulation	RT-qPCR	NA	NA	cell cycle(+);KRAS/ERK1/2 signaling pathway(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000108953	GRCh38_17:1344275-1400222	NA	NA	7531	NA	FLJ45465	NA	YWHAE long non-coding RNA competes with miR-323a-3p and miR-532-5p through activating K-Ras/Erk1/2 and PI3K/Akt signaling pathways in HCT116 cells.RNA-seq analysis showed that YWHAE gene is upregulated in colorectal cancer specimens. Additionally, bioinformatics analysis suggested that YWHAE lncRNA sponges miR-323a-3p and miR-532-5p that were predicted to target K-Ras 3'UTR sequence. Overexpression of YWHAE lncRNA resulted in upregulation of K-Ras gene expression, while overexpression of both miR-323a-3p and miR-532-5p had an inverse effect, detected by RT-qPCR. Consistently, western blotconfirmed that YWHAE lncRNA overexpression upregulated K-Ras/Erk1/2 and PI3K/Akt signaling pathways, while miR-323a-3p and miR-532-5p overexpression suppressed both pathways in HCT116 cells. Furthermore, dual luciferase assay validated the direct interaction of miR-323a-3p and miR-532-5p with K-Ras 3'UTR sequence and supported the sponging effect of YWHAE lncRNA over both miRNAs. These results suggested YWHAE lncRNA as an oncogene that exerts its effect through sponging miR-323a-3p and miR-532-5p and in turn, upregulates K-Ras/Erk1/2 and PI3K/Akt signaling pathways. Consistently, flow cytometry analysis, MTT assay and measuring cyclin D1 gene expression, confirmed the cell cycle stimulatory effect of YWHAE lncRNA, while miR-323a-3p and miR-532-5p showed an inhibitory effect on cell cycle progression. Finally, wound-healing assay supported the cell migratory effect of YWHAE lncRNA in HCT116 cells. This study identified a novel mechanism involving YWHAE-encoded lncRNA, miR-323a-3p and miR-532-5p in regulating HCT116 cell survival and suggested a potential therapeutic avenue for colorectal cancer.	31238337	RID07937	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761)	
Colorectal cancer	YWHAE	miR-532-5p	negatively-F	western blot;overexpression	upregulation	RT-qPCR	NA	NA	cell cycle(+);KRAS/ERK1/2 signaling pathway(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000108953	GRCh38_17:1344275-1400222	NA	NA	7531	NA	FLJ45465	NA	YWHAE long non-coding RNA competes with miR-323a-3p and miR-532-5p through activating K-Ras/Erk1/2 and PI3K/Akt signaling pathways in HCT116 cells.RNA-seq analysis showed that YWHAE gene is upregulated in colorectal cancer specimens. Additionally, bioinformatics analysis suggested that YWHAE lncRNA sponges miR-323a-3p and miR-532-5p that were predicted to target K-Ras 3'UTR sequence. Overexpression of YWHAE lncRNA resulted in upregulation of K-Ras gene expression, while overexpression of both miR-323a-3p and miR-532-5p had an inverse effect, detected by RT-qPCR. Consistently, western blotconfirmed that YWHAE lncRNA overexpression upregulated K-Ras/Erk1/2 and PI3K/Akt signaling pathways, while miR-323a-3p and miR-532-5p overexpression suppressed both pathways in HCT116 cells. Furthermore, dual luciferase assay validated the direct interaction of miR-323a-3p and miR-532-5p with K-Ras 3'UTR sequence and supported the sponging effect of YWHAE lncRNA over both miRNAs. These results suggested YWHAE lncRNA as an oncogene that exerts its effect through sponging miR-323a-3p and miR-532-5p and in turn, upregulates K-Ras/Erk1/2 and PI3K/Akt signaling pathways. Consistently, flow cytometry analysis, MTT assay and measuring cyclin D1 gene expression, confirmed the cell cycle stimulatory effect of YWHAE lncRNA, while miR-323a-3p and miR-532-5p showed an inhibitory effect on cell cycle progression. Finally, wound-healing assay supported the cell migratory effect of YWHAE lncRNA in HCT116 cells. This study identified a novel mechanism involving YWHAE-encoded lncRNA, miR-323a-3p and miR-532-5p in regulating HCT116 cell survival and suggested a potential therapeutic avenue for colorectal cancer.	31238337	RID07938	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761)	
Thyroid cancer	LINC00210	IGF1R	positively-E	RIP;dual-luciferase reporter assay;miRDB	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000231814	GRCh38_1:217892900-217920804	ENSG00000140443	NA	100885798	3480	NCRNA00210|RP11-72L13.1	CD221|IGFIR|IGFR|JTK13|MGC18216	Linc00210 enhances the malignancy of thyroid cancer cells by modulating miR-195-5p/IGF1R/Akt axis. We found that Linc00210 expression was upregulated in thyroid cancer (TC) tissues compared to the matched noncancerous tissues. Overexpression of Linc00210 augmented the proliferation, migration, and invasion of TC cells. Mechanistically, Linc00210 served as a sponge for miR-195-5p, thereby counteracting its ability in downregulating the expression of IGF1R and the activation of PI3K/Akt signaling. Moreover, inhibition of Linc00210 suppressed the growth of TC cells in nude mice. Our findings for the first time uncovered the oncogenic property of Linc00210 in TC.	31240707	RID07939	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Malignant glioma	LINC00526	AXL	negatively-E	siRNA;RIP;lncLocator;ChIP;shRNA;JASPAR	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+);PI3K/AKT/NF-kB signaling pathway(+)	transcriptional regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000264575	GRCh38_18:5236724-5238598	ENSG00000167601	NA	147525	558	C18orf18|HsT959|MGC17515	ARK|JTK11|Tyro7|UFO	Long non-coding RNA LINC00526 represses glioma progression via forming a double negative feedback loop with AXL. In this study, we identified a novel lncRNA LINC00526, which is significantly low expressed in glioma. Low expression of LINC00526 is correlated with aggravation and poor survival in glioma. Functional assays revealed that ectopic expression of LINC00526 inhibits glioma cell proliferation, migration, and invasion. LINC00526 silencing promotes glioma cell proliferation, migration and invasion. Mechanistically, we found that LINC00526 directly interacts with EZH2, represses the binding of EZH2 to AXL promoter, attenuates the transcriptional activating roles of EZH2 on AXL, and therefore represses AXL expression. Via repressing AXL, LINC00526 further represses PI3K/Akt/NF-kB signalling. Intriguingly, we identified that NFKB1 and NFKB2 directly binds LINC00526 promoter and represses LINC00526 transcription. We further found that via activating NF-kB signalling, AXL represses LINC00526 transcription. Therefore, LINC00526/EZH2/AXL/ PI3K/Akt/NF-kB form a feedback loop in glioma. Analysis of the TCGA data revealed that the expression of LINC00526 is inversely correlated with that of AXL in glioma tissues. In addition, functional rescue assays revealed that the tumour suppressive roles of LINC00526 are dependent on the negative regulation of AXL. Collectively, our data identified LINC00526 as a tumour suppressor in glioma via forming a double negative feedback loop with AXL. Our data also suggested LINC00526 as a potential prognostic biomarker and therapeutic candidate for glioma.	31240814	RID07940	transcriptional regulation	prognosis	DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)	UP(LIHC,SKCM);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE67939)
Malignant glioma	PEG10	miR-506	negatively-F	shRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell viability(+);RAF/MEK/ERK signaling pathway(+);JAK/STAT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	23089	NA	HB-1|KIAA1051|2-Mar|Mart2|MEF3L|RGAG3|RTL2|SIRH1	NA	Knockdown long non-coding RNA PEG10 inhibits proliferation, migration and invasion of glioma cell line U251 by regulating miR-506.We explored the effects of PEG10 on the human glioma cell line U251 cells. U251 cells were transfected with sh-PEG10 and/or miR-506 inhibitor. The expression of PEG10 and miR-506 was measured by qRT-PCR Cell viability, cell apoptosis, cell migration and invasion were detected by CCK-8 assay, flow cytometry and Transwell chamber assay, respectively. The cell proliferation and apoptosis related p16, p53, Bcl-2, Bax, and pro-/Cleaved-Caspase-3/9, migration and invasion related-protein: matrix metalloproteinases MMP-2, MMP-9 and vimentin, and Raf/MEK/ERK and JAK1/STAT3 pathways-related proteins were accessed by western blot. Transfection with sh-PEG10 inhibited cell viability, migration and invasion, and increased cell apoptosis. Meanwhile, PEG10 silence upregulated the expression of p16 and p53, Bax, cleaved-Caspase-3/9 expression, and downregulated Bcl-2 expression. PEG10 silence upregulated miR-506 expression. Co-transfection with sh-PEG10 and miR-506 inhibitor impaired the tumor suppressive effects. PEG10 knockdown decreased the phosphorylation of Raf/MEK/ERK and JAK1/STAT3-related proteins Raf, MEK, ERK, JAK1 and STAT3. PEG10 knockdown inhibited cell viability, migration and invasion, induced cell apoptosis through miR-506 upregulation, as well as inactivation of Raf/MEK/ERK and JAK1/STAT3 signal pathways.Knockdown long non-coding RNA PEG10 inhibits proliferation, migration and invasion of glioma cell line U251 by regulating miR-506.We explored the effects of PEG10 on the human glioma cell line U251 cells. U251 cells were transfected with sh-PEG10 and/or miR-506 inhibitor. The expression of PEG10 and miR-506 was measured by qRT-PCR Cell viability, cell apoptosis, cell migration and invasion were detected by CCK-8 assay, flow cytometry and Transwell chamber assay, respectively. The cell proliferation and apoptosis related p16, p53, Bcl-2, Bax, and pro-/Cleaved-Caspase-3/9, migration and invasion related-protein: matrix metalloproteinases MMP-2, MMP-9 and vimentin, and Raf/MEK/ERK and JAK1/STAT3 pathways-related proteins were accessed by western blot. Transfection with sh-PEG10 inhibited cell viability, migration and invasion, and increased cell apoptosis. Meanwhile, PEG10 silence upregulated the expression of p16 and p53, Bax, cleaved-Caspase-3/9 expression, and downregulated Bcl-2 expression. PEG10 silence upregulated miR-506 expression. Co-transfection with sh-PEG10 and miR-506 inhibitor impaired the tumor suppressive effects. PEG10 knockdown decreased the phosphorylation of Raf/MEK/ERK and JAK1/STAT3-related proteins Raf, MEK, ERK, JAK1 and STAT3. PEG10 knockdown inhibited cell viability, migration and invasion, induced cell apoptosis through miR-506 upregulation, as well as inactivation of Raf/MEK/ERK and JAK1/STAT3 signal pathways.	31241046	RID07941	ceRNA or sponge	NA		
Breast cancer	LINC01355	CCND1	negatively-E	siRNA;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);tumorigenesis(+);tumor growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000283124	GRCh38_CHR_HSCHR1_4_CTG3:23288771-23294952	ENSG00000110092	NA	100996511	595	HYPAL	BCL1|D11S287E|PRAD1|U21B31	LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1.In the present work, we focus on functional long non-coding RNAs (lncRNAs) embedded in this locus. Small interfering RNA was used to identify lncRNA candidates with growth-suppressive activities in breast cancer. The mechanism involved was also explored. LINC01355 were downregulated in breast cancer cells relative to non-malignant breast epithelial cells. Overexpression of LINC01355 significantly inhibited proliferation, colony formation, and tumorigenesis of breast cancer cells. LINC01355 arrested breast cancer cells at the G0/G1 phase by repressing CCND1. Moreover, LINC01355 interacted with and stabilized FOXO3 protein, leading to transcriptional repression of CCND1. Importantly, LINC01355-mediated suppression of breast cancer growth was reversed by knockdown of FOXO3 or overexpression of CCND1. Clinically, LINC01355 was downregulated in breast cancer specimens and correlated with more aggressive features. There was a negative correlation between LINC01355 and CCND1 expression in breast cancer samples. LINC01355 acts as a tumor suppressor in breast cancer, which is ascribed to enhancement of FOXO3-mediated transcriptional repression of CCND1. Re-expression of LINC01355 may provide a potential therapeutic strategy to block breast cancer growth and progression.	31243265	RID07942	transcriptional regulation	NA	UP(LIHC);DOWN(PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Non-small cell lung cancer	HNF1A-AS1	CDK6	positively-E	siRNA;dual-luciferase reporter assay;RNA pull-down assay;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumorigenesis(+);cell cycle(+)	ceRNA(miR-149-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000105810	NA	283460	1021	C12orf27|HAS1|NCRNA00262	MCPH12|PLSTIRE	lncRNA HNF1A-AS1 modulates non-small cell lung cancer progression by targeting miR-149-5p/Cdk6.We found that HNF1A-AS1 was relatively upregulated in both NSCLC patient tissues and cell lines. Functional studies established that overexpression of HNF1A-AS1 promoted cell proliferation, cell cycle, invasion, and migration of NSCLC cells in vitro. The promotion abilities of HNF1A-AS1 on NSCLC cell progression were suppressed via knockdown of HNF1A-AS1. miR-149-5p was then proved to be a novel target of HNF1A-AS1, whose expression was negatively correlated with HNF1A-AS1 in NSCLC patient tissues and cell lines. HNF1A-AS1 increased the expression of cyclin-dependent kinase 6 (Cdk6) via sponging with miR-149-5p. Gain- and loss-of-functional studies indicated that HNF1A-AS1 promoted NSCLC progression partially through inhibition of miR-363-3p and induction of Cdk6. Subcutaneous xenotransplanted tumor model confirmed that interference of HNF1A-AS1 suppressed the tumorigenic ability of NSCLC via upregulation of miR-149-5p and downregulation of Cdk6 in vivo. In conclusion, our findings clarified the biologic significance of the HNF1A-AS1/miR-149-5p/Cdk6 axis in NSCLC progression and provided novel evidence that HNF1A-AS1 may be a new potential therapeutic target for the treatment of NSCLC.	31243821	RID07943	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM);DATA(GSE117623,GSE104209,GSE60407,GSE38495)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Epithelial ovarian cancer	NORAD	miR-155-5p	negatively-F	shRNA;dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(+);cell cycle(+);tumor growth(+)	sponge	binding/interaction	NA	Bufalin	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR-155-5p.NORAD expression was evaluated by qRT-PCRin epithelial ovarian cancer (EOC) cell lines and in situ EOC clinical samples. Lentivirus-mediated NORAD downregulation was conducted in OVCAR-3 and ES-2 cells, and its effect on cancer cell proliferation, bufalin chemoresistance, cell-cycle transition in vitro, and xenotransplantation in vivo were examined, respectively. The likelihood of an lncRNA-microRNA (miRNA) signaling pathway was examined by probing the possible downstream competing target of NORAD, hsa-miR-155-5p. Moreover, hsa-miR-155-5p was knocked down in NORAD-downregulated EOC cells to functionally evaluate the correlation between NORAD and hsa-miR-155-5p in EOC.We found that NORAD was substantially upregulated in both EOC cell lines and human tumors. In OVCAR-3 and ES-2 cells, lentivirus-mediated NORAD downregulation had significant anticancer effects, as it suppressed cell proliferation, decreased bufalin chemoresistance, arrested cell-cycle transition, and inhibited xenograft growth. Also, hsa-miR-155-5p was confirmed to be the competing target of NORAD in EOC, and its knockdown in OVCAR-3 and ES-2 cells reversed the NORAD downregulation-induced anticancer functions.NORAD is upregulated in EOC. Inhibition of NORAD, possibly through endogenously competing against hsa-miR-155-5p, can be a new tumor-suppressing strategy in EOC.	31250987	RID07944	ceRNA or sponge	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Wilms' tumor	SNHG6	MIR15A	negatively-F	RIP;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+);JAK/STAT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000283785	NA	641638	406948	HBII-276HG|NCRNA00058|U87HG	MIRN15A|hsa-mir-15a|miRNA15A|mir-15a	Silencing long non-coding RNA SNHG6 restrains proliferation, migration and invasion of Wilms'-tumour cell lines by regulating miR-15a.CCK8 assays and bromodeoxyuridine were used to determine cell viability and cell proliferation, respectively. Flow cytometric analysis was performed to measure cell apoptosis rate. Cell mobility was tested through transwell and migration assays. western blot was employed to test the expression of proteins related to cell proliferation, cell apoptosis and signal pathways. In the results, overexpression of SNHG6 was found in Wilms'-tumour (WT) tissues. The knockdown of SNHG6 suppressed cell proliferation, migration and incursion, but promoted apoptosis. Further study found that the knockdown of SNHG6 elevated the expression of miR-15a. Then, the combination of miR-15a inhibitor abolished the inhibiting effect of si-SNHG6 on WT progression. We also found that the TAK1/JNK and Wnt/b-catenin signal pathways were inactivated by the knockdown of SNHG6 through elevating the expression of miR-15a. In summary, SNHG6 is an oncogene of WT development by targeting miR-15a.	31257923	RID07945	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	
Malignant glioma	LNCNEF	TGFB1	negatively-E	siRNA;western blot	downregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237396	GRCh38_20:22587522-22607517	ENSG00000105329	NA	101929685	7040	LINC01384|lncRNA-NEF	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	lncRNA NEF inhibits glioma by downregulating TGF-beta1.It was determined that NEF expression was downregulated in tumor tissues compared with adjacent heathy tissues. A low blood NEF level in patients with glioma effectively distinguished patients from healthy controls who had high blood NEF levels. Blood NEF levels were significantly correlation with distant tumor metastasis, but not tumor growth. Blood NEF levels were negatively correlated with blood transforming growth factor (TGF)-beta1 levels in patients with distant tumor metastasis, but not in patients with non-metastatic glioma and healthy controls. NEF overexpression inhibited cancer cell migration and invasion. In addition, NEF overexpression downregulated TGF-beta1 expression. The authors of the current study concluded that lncRNA NEF may inhibit glioma cell migration and invasion by downregulating TGF-beta1.	31258706	RID07946	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Oral squamous cell carcinoma	HOXA11-AS	PIM1	positively-E	siRNA;shRNA;starBase;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);tumor growth(+);apoptosis process(-);chemoresistance(+)	ceRNA(miR-214-3p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000137193	NA	221883	5292	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	PIM	LncRNA HOXA11-AS Promotes Proliferation and Cisplatin Resistance of Oral Squamous Cell Carcinoma by Suppression of miR-214-3p Expression.Drug resistance to platinum limited therapeutic options for oral squamous cell carcinoma (OSCC). In the current study, we investigated the role of lncRNA HOMEOBOX A11 (HOXA11) antisense RNA (HOXA11-AS) in OSCC resistance to cisplatin (CDDP). We used clinical tissues and OSCC cell lines and induced CDDP resistance in OSCC cells. Gain and loss of function were performed in OSCC-resistant cells. Xenograft mice were also established. HOXA11-AS expression was increased in OSCC clinical tissues and cell lines and upregulated in CDDP-resistant cells. Upregulation of HOXA11-AS promoted proliferation in CDDP-sensitive cells and inhibitedCDDP-induced cytotoxicity. In contrast, downregulation ofHOXA11-AS decreased proliferation in CDDP-resistant cells and increased CDDP-induced cytotoxicity. Knockdown of HOXA11-AS inhibited the tumor growth in xenograft mice injected by CDDP. Downregulation of HOXA11-AS increased apoptosis and caspase 3 activities in CDDP-resistant OSCC cells. Bioinformatics, reporter assay, and loss and gain of function assay indicated that HOXA11-AS and miR-214-3p could negatively regulate each other. miR-214-3p was decreased in OSCC clinical tissues and cell lines. We further revealed that protooncogene serine/threonine-protein kinase (PIM1) was the target of miR-214-3p. PIM1 expression could be negatively regulated by miR-214-3p and positively regulated by HOXA11-AS. Inhibition of PIM1 suppressed anti-miR-214-3p-induced increase of cell proliferation and decrease of apoptosis. In summary, HOXA11-AS was identified to facilitate CDDP-resistance in OSCC and miR- 214-3p/PIM1 was found to be the downstream target of HOXA11-AS. The findings highlight the importance of HOXA11-AS/miR- 214-3p/PIM1 axis in the drug resistance of OSCC and provide potential targets for improving chemotherapy of OSCC.	31275988	RID07947	ceRNA or sponge	chemoresistance		DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE41245)
Hepatocellular carcinoma	LMCD1-AS1	P4HA2	positively-E	luciferase reporter assay;siRNA;Immunofluorescence;ChIP;lncRNASNP	downregulation	qRT-PCR	TCGA;GSE76427	NA	tumor growth(+);chemoresistance(+)	ceRNA(let-7g)	regulation	NA	Aspirin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227110	GRCh38_3:7951263-8611924	ENSG00000072682	NA	100288428	8974	NA	C-P4Halpha(II)	Aspirin targets P4HA2 through inhibiting NF-kB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.western blot, qRT-PCRassay, immunofluorescence staining, luciferase reporter gene assay, and ChIP assay were applied to demonstrate the molecularmechanism of the regulation of P4HA2 expression by aspirin. Amouse xenograftmodel, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kB/P4HA2 axis and LMCD1-AS1/ let-7g/P4HA2 axis in vitro and in vivo. The TCGA databasewas used to evaluate the correlation among P4HA2, let- 7g, LMCD1-AS1 and overall survival of HCC patients.In xenograft mice, aspirin was capable of targeting P4HA2 to decrease collagen deposition, resulting in the inhibition of liver tumour growth. TCGA database analysis revealed the close association between a higher P4HA2 concentration in HCC patients and shorter overall survival or a higher cancer stage and the pathological grade. Mechanistically, NF-kB can bind to the promoter of P4HA2 to activate its transcription.Moreover, lncRNA LMCD1-AS1 functions as a molecular sponge of let-7g to post-transcriptionally induce the target gene of let-7g, namely, P4HA2.Our findings disclose the novel role and regulatorymechanismof aspirin in the suppression ofHCC by disrupting abnormal collagen deposition.	31278071	RID07948	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)
Endometrial cancer	NEAT1	MIR361	negatively-F	shRNA;RIP;StarBase	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);chemoresistance(+);STAT3 signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000199051	NA	283131	494323	LINC00084|NCRNA00084|TncRNA|VINC	MIRN361|hsa-mir-361|mir-361	Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironmentrelated genes. We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.We identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.NEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.	31287002	RID07949	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Endometrial cancer	NEAT1	MEF2D	positively-E	shRNA;RIP;StarBase;siRNA	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);chemoresistance(+);STAT3 signaling pathway(+)	ceRNA(miR-361)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000116604	NA	283131	4209	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironmentrelated genes. We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.We identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.NEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.	31287002	RID07950	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Endometrial cancer	NEAT1	ROCK1	positively-E	shRNA;RIP;StarBase;siRNA	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);chemoresistance(+);STAT3 signaling pathway(+)	ceRNA(miR-361)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	p160ROCK	Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironmentrelated genes. We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.We identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.NEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.	31287002	RID07951	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Endometrial cancer	NEAT1	WNT7A	positively-E	shRNA;RIP;StarBase;siRNA	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);chemoresistance(+);STAT3 signaling pathway(+)	ceRNA(miR-361)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000154764	NA	283131	7476	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	Wnt-7a	Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironmentrelated genes. We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.We identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.NEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.	31287002	RID07952	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Endometrial cancer	NEAT1	VEGFA	positively-E	shRNA;RIP;StarBase;siRNA	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);chemoresistance(+);STAT3 signaling pathway(+)	ceRNA(miR-361)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112715	NA	283131	7422	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	VEGF|VEGF-A|VPF	Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironmentrelated genes. We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.We identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.NEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.	31287002	RID07953	ceRNA or sponge	metastasis,chemoresistance,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Non-small cell lung cancer	SNHG1	miR-140-5p	negatively-F	luciferase reporter assay;RIP;shRNA;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);chemoresistance(+);tumor growth(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Long non-coding RNA SNHG1 contributes to cisplatin resistance in non-small cell lung cancer by regulating miR-140- -catenin pathway.qRT-PCRassay was performed to assess the expression levels of SNHG1 and miR-140-5p. western blotwas used to determine Wnt1, cyclinD1, c-Myc and -catenin levels. The direct correlation between SNHG1 and miR-140-5p was verified by dual- luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CCK-8 assay and Transwell assay were applied to determine cell proliferation ability, and cell migration and invasion capacities, respectively. Tumor xenograft was performed to confirm the effect of SNHG1 on DDP resistance of NSCLC in vivo. Our data showed SNHG1 was upregulated in DDP-resistant NSCLC tissues and cell lines. SNHG1 knockdown suppressed the proliferation, migration, invasion and DDP-resistance in DDP-resistance NSCLC cell lines in vitro and inhibited tumor growth in vivo. Moreover, SNHG1 repressed miR-140-5p expression by directly binding to miR-140-5p. SNHG1-knockdown-mediated regulatory effect was antagonized by miR-140-5p. Furthermore, -catenin signaling was involved in SNHG1/miR-140-5p-mediated regulation in DDP-resistance NSCLC cell lines. The results suggested that SNHG1 knockdown ameliorated DDP resistance of NSCLC by regulating miR-140-5p/W -catenin pathway, providing a new potential therapeutic target for DDP-resistance NSCLC treatment.	31288529	RID07954	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Head and neck squamous cell carcinoma	HOTAIR	STC2	positively-E	siRNA;dual-luciferase reporter assay;FISH;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+);tumor growth(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113739	NA	100124700	8614	HOXC-AS4|HOXC11-AS1|NCRNA00072	STC-2	Long non-coding RNA HOTAIR/microRNA-206 sponge regulates STC2 and further influences cell biological functions in head and neck squamous cell carcinoma.HNSCC-related differentially expressed genes and regulation network amongst HOTAIR, miR-206 and STC2 were identified. Next, effect of HOTAIR on cell biological functions of HNSCC was identified after transfection of cells with HOTAIR overexpressed plasmids or siRNA against HOTAIR. PI3K/AKT signalling pathway-related gene expression was measured after miR-206 and STC2 were suppressed. Cell invasion, migration and proliferation were assessed. Finally, tumour growth was assessed to determine the effects of HOTAIR/miR-206/STC2 axis in vivo.HOTAIR specifically bound to miR-206 and miR-206 targeted STC2. Downregulated HOTAIR or upregulated miR-206 suppressed HNSCC cell proliferation, invasion and migration. miR-206 inhibited PI3K/AKT signalling pathway by down-regulating STC2. Besides, silenced HOTAIR or overexpressed miR-206 repressed the tumour growth of nude mice with HNSCC.HOTAIR regulated HNSCC cell biological functions by binding to miR-206 through STC2.	31297902	RID07955	ceRNA or sponge	NA		UP(PAAD,BRCA);DATA(GSE40174,GSE55807)
Non-small cell lung cancer	FAM201A	EGFR	positively-E	shRNA;dual-luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+);apoptosis process(-)	ceRNA(miR-370)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000204860	GRCh38_9:38620474-38624990	ENSG00000146648	NA	158228	1956	C9orf122	ERBB|ERBB1|ERRP	Long noncoding RNA FAM201A involves in radioresistance of non-small-cell lung cancer by enhancing EGFR expression via miR-370.Quantitative Polymerase Chain Reaction (qPCR) was used to determine the expression of FAM201A in NSCLC tissues. The Chi-square tests explored the association between FAM201A level and the poor clinicopathological characteristics (including radioresistance) of NSCLC. Univariate and multivariate Cox proportional hazards regression analyses were used to evaluate various prognostic factors for overall survival (OS). The effect of FAM201A on OS was tested by the log-rank test. A549/SK-MES-1 cell lines transfected with short hairpin RNA (shRNA) were used to verify the promoting effects of FAM201A on radiotherapy resistance in vitro and in vivo. Cell apoptosis (analyzed by flow cytometry), cell proliferation (determined by Cell Counting Kit-8), and mice xenograft models were performed to confirm the results. The downstream targets of FAM201A were predicted by bioinformatics tools. Additionally, the dual-luciferase reporter assay, qPCR, and western blot were performed to confirm their interaction.FAM201A was significantly upregulated in tissues obtained from NSCLC patients resistant to radiotherapy. Increased FAM201A expression was strongly associated with radioresistance and inferior survival in NSCLC, as demonstrated by clinical data. The silence of FAM201A could inhibit cell proliferation and further cell apoptosis of NSCLC cells under X-ray irradiation both in vitro and in vivo. Moreover, by competitively targeting miR-370, FAM201A elevated the epidermal growth factor receptor (EGFR) and the hypoxia-inducible factor 1alpha (HIF-1beta- levels. After FAM201A knockdown, EGFR and HIF-1beta-were repressed with enhanced radiosensitivity.The interference of FAM201A impairs its suppression of miR-370, resulting in the upregulation of EGFR and HIF-1beta-and enhancement of radiosensitivity in NSCLC patients. Collectively, our results indicated that this regulatory axis might serve as a potential therapeutic target to increase the sensitivity of radiotherapy in NSCLC patients.	31298332	RID07956	ceRNA or sponge	prognosis,metastasis		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Malignant glioma	MELTF-AS1	MMP14	positively-E	western blot	upregulation	qPCR	NA	NA	tumor growth(+);apoptosis process(-);cell migration(+);cell invasion(+)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228109	GRCh38_3:196999460-197004744	ENSG00000157227	NA	100507057	4323	AC068302.3|MFI2-AS1	MT1-MMP	MFI2-AS1 regulates the aggressive phenotypes in glioma by modulating MMP14 via a positive feedback loop.The quantitative Real Time PCR (qPCR) assay was used to assess the level of MFI2-AS1, matrix metalloproteinase 14 (MMP14), and miR-485-5p in glioma tissues and cell lines. The growth of glioma cell was analyzed using the 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The migration and invasion of glioma cell were investigated using wound healing and transwell invasion analysis. The apoptosis of glioma cell was detected using flow cytometry. The expression of MMP14 was determined by western blot. The growth of glioma cell in vivo was assessed using the xenograft model.We showed that MFI2-AS1 was markedly overexpressed in glioma cells and clinical tissues. The higher level of MFI2-AS1 is related to the poor prognosis in patients with glioma. Furthermore, the downregulation of MFI2-AS1 suppresses the growth, aggressiveness, and induces apoptosis of glioma cells. Also, MMP14 is the target gene of miR-485-5p and its level is positively modulated by MFI2-AS1. The rescue experiments reveal that miR-485-5p inhibition reverses the suppressive impacts of MFI2-AS1 silencing on the growth, migration, and invasive abilities of glioma cells. Finally, we elaborate that MFI2-AS1 silencing represses glioma cell growth in vivo and suppress the expression of MMP14.In summary, the downregulation of MFI2-AS1 restrains the aggressive phenotypes of glioma cells via downregulating the expression of MMP14.	31298339	RID07957	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	NBAT1	GSK3B	positively-E	dual-luciferase reporter assay;RNA pull-down assay;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-346)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000082701	NA	729177	2932	CASC14|NBAT-1	NA	LncRNA NBAT1 suppresses cell proliferation and migration via miR-346/GSK-3beta axis in renal carcinoma.The expression of NBAT1 and glycogen synthase kinase-3beta (GSK-3beta)-mediated Wnt/beta- catenin-related proteins were measured by quantitative real-time PCR (qRT-PCR and western blot in RCC cell lines. Cell viability, migration, and invasion were estimated by CCK-8 and Transwell assay. The association of miR-346 with GSK-3beta expression was verified using luciferase assay. NBAT1 was significantly downregulated in RCC cells, and inhibited RCC cell proliferation, migration, and invasion. Furthermore, NBAT1 negatively regulated miR-346 expression. In addition, miR-346 overexpression and the knockdown of GSK-3beta, a direct target of miR-346 could overturn the inhibitory effect of NBAT1 on Wnt/beta-catenin signaling and cell proliferation, migration, and invasion. NBAT1 functioned as an endogenous sponge by competing for miR-346 binding to GSK-3beta and therefore alleviated RCC cells.	31298469	RID07958	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	E2F6	CASC2	negatively-F	shRNA;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);tumor growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000169016	NA	ENSG00000177640	GRCh38_10:118046279-118210158	1876	255082	E2F-6	C10orf5	E2F6-mediated lncRNA CASC2 down-regulation predicts poor prognosis and promotes progression in gastric carcinoma.The expressions of cancer susceptibility candidate 2 (CASC2), E2F6 and matrix metalloprotein-2 (MMP-2) were measured by quantitative real-time polymerase chain reaction and western blot. The inhibitory effect of E2F6 on CASC2 was evaluated using luciferase reporter assay. Cell growth was assessed by colony formation assay and cell counting kit-8. Cell invasion and apoptosis were measured by transwell assay and flow cytometry assay, respectively. In vivo tumorigenicity was assessed by tumor xenografts in nude mice.Our data revealed that CASC2 was downregulated while E2F6 was upregulated in GC tissues and cell lines. Remarkably, lower expression of CASC2 was associated with poor survival in GC patients. E2F6 inhibited the expression of CASC2. Subsequently, reliable data showed that downregulation of E2F6 suppressed the proliferation and invasion, and promoted the apoptosis of GC cells. Furthermore, downregulation of E2F6 decreased the expression of MMP-2 and increased the activity of caspase-3. However, these changes triggered by E2F6 knockdown could be reversed by inhibition of CASC2. Moreover, we also proved that downregulation of CASC2 reverses the effect of E2F6 knockdown on tumor growth in vivo.Our data demonstrated that E2F6 could regulate the proliferation, invasion and apoptosis of GC cells via inhibiting the expression of CASC2, suggesting that E2F6/CASC2 axis is another regulator of GC progression.	31301415	RID07959	expression association	prognosis	UP(PAAD,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	UP(LIHC);DATA(GSE117623)
Urinary bladder cancer	HCG22	PTBP1	negatively-E	RNA pull-down assay;RIP;shRNA;overexpression	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237894	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:31098369-31104804	ENSG00000011304	NA	285834	5725	PBMUCL2|FLJ37114	HNRNP-I|HNRPI|pPTB|PTB|PTB-1|PTB2|PTB3|PTB4	Long noncoding RNA HCG22 suppresses proliferation and metastasis of bladder cancer cells by regulation of PTBP1. Consistent with the data of The Cancer Genome Atlas database, it was validated that lncRNA HLA complex group 22 (HCG22) was weakly expressed in BCa samples and lowly expressed HCG22 was closely correlated with low overall survival of the BCa patient. To verify the role of HCG22 in BCa progression, functional experiments were carried out in two representative BCa cells (J82 and T24) and the negative effects of HCG22 expression on the cell proliferation, migration, and epithelial-sesenchymal transition were identified. Mechanistically, polypyrimidine tract-binding protein 1 (PTBP1), which was highly expressed in BCa tissues and cell lines, was negatively regulated by HCG22 and the PTBP1-mediated Warburg effect was also obstructed by HCG22. Furthermore, HCG22 modulated the expression of PTBP1 through destabilizing human antigen R (HuR). And functional rescue assays confirmed that HCG22 functioned in bladder cancer through downregulating PTBP1. In conclusion, the present study revealed that HCG22 inhibited BCa progression via the HuR/PTBP1 axis, opening new prospects for potent therapeutic regimens for BCa patients.	31304601	RID07960	transcriptional regulation	metastasis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	SNHG16	miR-195	negatively-E	dual-luciferase reporter assay;RIP;siRNA;starBase;miRanda	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557733-76565357	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long intergenic noncoding RNA SNHG16 interacts with miR-195 to promote proliferation, invasion and tumorigenesis in hepatocellular carcinoma.Our observations showed that the expression level of SNHG16 in HCC tissues and cell lines was upregulated compared with adjacent noncancerous tissues and normal cells. In vitro, loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation and weakened invasion of SMMC7721 and HepG2 cells. miR-195 expression was significantly decreased in HCC tissues and negatively correlated with SNHG16 expression. Furthermore, RIP and dual-luciferase reporter assays showed that SNHG16 acted as an endogenous sponge by directly binding to miR-195 and downregulated its expression. SNHG16 overexpression inverted the inhibitory effect of miR-195 on proliferation and invasion of SMMC7721 and HepG2 cells. Additionally, SNHG16 depletion resulted in lower tumor growth and weight loss, in vivo. In conclusion, our findings reported that the oncogenic role of SNHG16 in HCC tumorigenesis through a novel SNHG16-miR-195 axis, which provided a novel insight for HCC and helped to probe a potential therapeutic target for the deadly disease.	31306653	RID07961	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	
Malignant glioma	FOXP1	HCG11	negatively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;JASPAR	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000114861	NA	ENSG00000228223	GRCh38_6:26521709-26527404	27086	493812	12CC4|hFKH1B|HSPC215|QRF1	bK14H9.3|FLJ14049|FLJ30357	Long non-coding RNA HCG11 modulates glioma progression through cooperating with miR-496/CPEB3 axis.Based on The Cancer Genome Atlas (TCGA) data set and qRT-PCRanalysis, the expression pattern of HCG11 was identified in glioma samples. The mechanism associated with HCG11 downregulation was determined by mechanism experiments. Gain-of-function assays were conducted for the identification of HCG11 function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull-down assay was used to explore the downstream molecular mechanism of HCG11. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.HCG11 was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro-496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR-496 involved in HCG11-mediated glioma progression.HCG11 inhibited glioma progression by regulating miR-496/CPEB3 axis.	31310044	RID07962	transcriptional regulation	NA	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE55807)	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Malignant glioma	HCG11	CPEB3	positively-E	dual-luciferase reporter assay;RNA pull-down assay;RIP;siRNA;starBase	downregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-)	ceRNA(miR-496)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000107864	NA	493812	22849	bK14H9.3|FLJ14049|FLJ30357	KIAA0940	Long non-coding RNA HCG11 modulates glioma progression through cooperating with miR-496/CPEB3 axis.Based on The Cancer Genome Atlas (TCGA) data set and qRT-PCRanalysis, the expression pattern of HCG11 was identified in glioma samples. The mechanism associated with HCG11 downregulation was determined by mechanism experiments. Gain-of-function assays were conducted for the identification of HCG11 function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull-down assay was used to explore the downstream molecular mechanism of HCG11. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.HCG11 was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro-496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR-496 involved in HCG11-mediated glioma progression.HCG11 inhibited glioma progression by regulating miR-496/CPEB3 axis.	31310044	RID07963	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	
Ewing's sarcoma	SOX2-OT	FOXP4	positively-E	siRNA;luciferase reporter assay;Targetscan	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-363)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Sarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000137166	NA	347689	116113	DKFZp761J1324|NCRNA00043|SOX2OT	FLJ40908	LncRNA SOX2 overlapping transcript acts as a miRNA sponge to promote the proliferation and invasion of Ewing  sarcoma.SOX2OT was identified to be up-regulated in Ewing  sarcoma tissue and cells. In vitro, SOX2OT knockdown suppressed Ewing  sarcoma cells proliferation and invasion, and triggered apoptosis. In vivo xenograft assays, SOX2OT knockdown significantly inhibited Ewing  sarcoma growth. With the help of bioinformatics analysis and luciferase assay, SOX2OT was validated to harbor miR-363, acting as miRNA sponge or competing endogenous RNA (ceRNA). Furthermore, FOXP4 was validated to be the target protein of miR-363. western blot and RT-PCRconfirmed that SOX2OT was positively correlated with FOXP4 protein via sponging miR-363, forming a negative cascade regulation. In conclusion, our study realizes that SOX2OT acted as oncogene in the tumorigenesis of Ewing  sarcoma, suggesting the SOX2OT/miR-363/FOXP4 pathway in Ewing  sarcoma.	31312393	RID07964	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367)
Colorectal cancer	SNHG12	miR-16	negatively-E	Targetscan;siRNA	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-);cell growth(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long non-coding RNA SNHG12 promotes proliferation and invasion of colorectal cancer cells by acting as a molecular sponge of microRNA-16.Polymerase chain reaction analysis was performed to examine the expression of lncRNA and microRNA (miR). Cell Counting Kit-8 and Transwell assays were used to assess cell proliferation and invasion. A luciferase reporter assay was performed to confirm a predicted targeting association between lncRNA and miR. It was observed that SNHG12 was markedly upregulated in CRC tissues when compared with that in adjacent non-tumour tissues, and its high expression was associated with CRC progression, as well as poor prognosis of patients. In addition, the expression of SNHG12 was higher in CRC cell lines when compared with that in a normal intestinal epithelial cell line. Knockdown of SNHG12 significantly inhibited CRC cell proliferation and invasion, while ectopic overexpression of SNHG12 had the opposite effect. A Bioinformatics analysis predicted that SNHG12 and miR-16 have complementary binding sites, which was confirmed by a luciferase reporter gene assay. The expression levels of miR-16 were markedly decreased in CRC tissues and cell lines compared with those in normal tissues or cells, and were inversely correlated with the expression levels of SNHG12 in CRC tissues. Furthermore, silencing of miR-16 eliminated the suppressive effects of SNHG12 knockdown on CRC cell proliferation and invasion. In conclusion, the present study demonstrated that SNHG12 promotes CRC cell proliferation and invasion, at least in part, by acting as a molecular sponge of miR-16, suggesting that SNHG12 may be a promising therapeutic target for CRC.	31316616	RID07965	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Lung adenocarcinoma	H19	CDH1	negatively-E	siRNA;overexpression;shRNA;ChIP;FISH;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	CD324|UVO|uvomorulin	Long non-coding RNA H19 is responsible for the progression of lung adenocarcinoma by mediating methylation-dependent repression of CDH1 promoter.First, lung adenocarcinoma tissues were collected to detect CDH1 methylation. Then, the regulatory mechanisms of lncRNA H19 were detected mainly in concert with the treatment of overexpression of lncRNA H19, siRNA against lncRNA H19, overexpression of CDH1 and demethylating agent A-5az in lung adenocarcinoma A549 cell. The expression of lncRNA H19 and epithelial-mesenchymal transition (EMT)-related factors as well as cell proliferation, sphere-forming ability, apoptosis, migration and invasion were detected. Finally, we observed xenograft tumour in nude mice so as to ascertain tumorigenicity of lung adenocarcinoma cells. LncRNA H19 and methylation of CDH1 were highly expressed in lung adenocarcinoma tissues. A549 cells with silencing of lncRNA H19, overexpression of CDH1 or reduced CDH1 methylation by demethylating agent 5-Az had suppressed cell proliferation, sphere-forming ability, apoptosis, migration and invasion, in addition to inhibited EMT process. Silencing lncRNA H19 could reduce methylation level of CDH1. In vivo, A549 cells with silencing lncRNA H19, overexpression of CDH1 or reduced CDH1 methylation exhibited low tumorigenicity, reflected by the smaller tumour size and lighter tumour weight. Taken together, this study demonstrates that silencing of lncRNA H19 inhibits EMT and proliferation while promoting apoptosis of lung adenocarcinoma cells by inhibiting methylation of CDH1 promoter.	31317666	RID07966	transcriptional regulation	NA	UP(NSCLC);DATA(GSE74639)	UP(LIHC,NSCLC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807)
Colorectal cancer	SNHG6	ETS1	negatively-E	overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66920561-66926398	ENSG00000134954	NA	641638	2113	HBII-276HG|NCRNA00058|U87HG	ETS-1|EWSR2|FLJ10768	LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer.In the present study, it was demonstrated that SNHG6 expression was downregulated in colorectal cancer tissues by reverse transcription quantitative polymerase chain reaction assays; however, ETS1 expression levels were upregulated. Overexpression of SNHG6 not only inhibited the proliferation of colon cancer cells in vitro by inducing apoptosis, but also inhibited cell proliferation, invasion and migration. The overexpression of SNHG6 inhibited colon cell viability and proliferation by targeting ETS1 through the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. These results suggested that SNHG6 may directly suppress ETS1, which may be one of potential mechanisms through which it inhibits the viability and proliferation of colorectal cancer cells, and it provides novel insight into the carcinogenesis of colorectal cancer. In addition, it may assist in the development of a treatment approach for ETS1-activated colorectal cancer.	31322251	RID07967	expression association	metastasis	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE111065)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	LINC00641	PLSCR4	positively-E	siRNA;RIP;RNA pull-down assay;dual-luciferase reporter assay;starBase;overexpression;Targetscan	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000258441	GRCh38_14:21200079-21206900	ENSG00000114698	NA	283624	57088	NA	NA	Long non-coding RNA LINC00641 suppresses non-small-cell lung cancer by sponging miR-424-5p to upregulate PLSCR4.In this research, we launched an investigation into the biological functions and the underlying molecular mechanisms of LINC00641 in NSCLC. At first, downregulation of LINC00641 was identified in NSCLC cells. Functionally, LINC00641 suppressed cell proliferation and induced cell apoptosis in NSCLC, indicating that LINC00641 exerted tumor-suppressive role in NSCLC. Through mechanism investigation, we determined that LINC00641 acted as a competing endogenous RNA (ceRNA) in NSCLC by sponging miR-424-5p to upregulate phospholipid scramblase (PLSCR4) expression. Further rescue assays indicated that miR-424-5p and PLSCR4 could reverse LINC00641- mediated cellular processes. Taken together, it is demonstrated in our study that LINC00641 can function as a tumor suppressor in NSCLC via a ceRNA network.	31322545	RID07968	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Acute myeloid leukemia	LINP1	HNF4A	negatively-E	knockdown	upregulation	qRT-PCR	NA	NA	AMPK/WNT5A signaling pathway(+)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000223784	GRCh38_10:6709530-6740532	ENSG00000101076	NA	108570035	3172	NA	HNF4|MODY|MODY1|NR2A1|TCF14	LncRNA LINP1 regulates acute myeloid leukemia progression via HNF4beta-AMPK/WNT5A signaling pathway.LncRNAs play critical roles in various pathophysiological and biological processes, such as protein translation, RNA splicing, and epigenetic modification. Indeed, abundant evidences demonstrated that lncRNA act as competing endogenous RNAs (ceRNAs) to participate in tumorigenesis. However, little is known about the underlying function of lncRNA in nonhomologous end joining (NHEJ) pathway 1 (LINP1) in pediatric and adolescent acute myeloid leukemia (AML). The expression of LINP1 was examined in AML patient samples by qRT-PCR Cell proliferation was examined by CCK-8 and Edu assays. beta-Galactosidase senescence assay, mGlucose uptake assay, lactate production assay, and Gene Ontology (GO) analysis were performed for functional analysis. We found that LINP1 was significantly overexpressed in AML patients at diagnosis, whereas downregulated after complete remission (CR). Furthermore, knockdown of LINP1 expression remarkably suppressed glucose uptake and AML cell maintenance. Mechanistically, LINP1 was found to inhibit the glucose metabolism by suppressing the expression of HNF4a. Both LINP1 and HNF4a knockdown reduced the expression levels of AMPK phosphorylation and WNT5A, indicating for the first time that LINP1 strengthened the HNF4a-AMPK/WNT5A signaling pathway involved in cell glucose metabolism modulation and AML cell survival. Taken together, our results indicated that LINP1 promotes the malignant phenotype of AML cells and stimulates glucose metabolism, which can be regarded as a potential prognostic marker and therapeutic target for AML.	31325181	RID07969	expression association	prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Pancreatic ductal adenocarcinoma	TP53TG1	KRAS	positively-E	siRNA;dual-luciferase reporter assay;RIP;miRcode;DIANA-lncBase	upregulation	RT-qPCR	GSE16515;GSE15471	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-96)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000182165	GRCh38_7:87322943-87345552	ENSG00000133703	NA	11257	3845	H_RG012D21.9|LINC00096|TP53AP1	K-Ras4B|KRAS1|KRAS2	Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA-96.In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)-96 and effectively function as a sponge for miR-96, thus antagonizing the functions of miR-96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR-96 and regulate KRAS expression, which highlights the importance of the complicated miRNA-lncRNA network in modulating the progression of PDAC.	31325400	RID07970	ceRNA or sponge	NA	DOWN(PAAD,BRCA);UP(BRCA);DATA(GSE60407,GSE111842,GSE51827,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Esophageal cancer	H19	STAT3	negatively-E	western blot;dual-luciferase reporter assay;shRNA;overexpression;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000168610	NA	283120	6774	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	APRF	LncRNA H19 promotes epithelial mesenchymal transition and metastasis of esophageal cancer via STAT3/EZH2 axisLong non-coding RNA H19 (lncRNA H19) has been widely reported in esophageal cancer (EC), and previous study had found that lncRNAH19 was up-regulated in EC and promoted cell proliferation and metastasis. However, the mechanism still needs further studied.Levels of lncRNA H19 were analyzed by qRT-PCRin matched samples from 30 patients. Expression levels of lncRNA H19, let-7, STAT3 and EZH2 were additionally identified by qRT-PCRand western blot in five EC cell lines. The effects of lncRNA H19 on cell proliferation, migration, invasion and apoptosis in cell lines were performed by MTT assay, colony formation assay, Transwell assay and flow cytometry in vitro, and tumor formation was detected by xenograft nude mice model in vivo. The expression level of STAT3, EZH2, beta-catenin, and EMT and metastasis related molecules such as E-cadherin, N-cadherin, Snail-1 and MMP-9 was assessed by qRT-PCRand western blot. Finally, luciferase reporter assay and RIP assay were used to verify the interaction between lncRNA H19 and let-7c, and their subsequent regulation of STAT3. Results: Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion.Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion as well as EMT and metastasis via STAT3-EZH2-beta-catenin pathway, while lncRNA H19 regulated STAT3 negatively regulated let-7c in EC cell lines.lncRNA H19 facilitates EMT and metastasis of EC through let-7c/STAT3/EZH2/beta-catenin axis.	31102664	RID07971	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Esophageal cancer	H19	EZH2	negatively-E	western blot;dual-luciferase reporter assay;shRNA;overexpression;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	ENX-1|EZH1|KMT6|KMT6A	LncRNA H19 promotes epithelial mesenchymal transition and metastasis of esophageal cancer via STAT3/EZH2 axisLong non-coding RNA H19 (lncRNA H19) has been widely reported in esophageal cancer (EC), and previous study had found that lncRNAH19 was up-regulated in EC and promoted cell proliferation and metastasis. However, the mechanism still needs further studied.Levels of lncRNA H19 were analyzed by qRT-PCRin matched samples from 30 patients. Expression levels of lncRNA H19, let-7, STAT3 and EZH2 were additionally identified by qRT-PCRand western blot in five EC cell lines. The effects of lncRNA H19 on cell proliferation, migration, invasion and apoptosis in cell lines were performed by MTT assay, colony formation assay, Transwell assay and flow cytometry in vitro, and tumor formation was detected by xenograft nude mice model in vivo. The expression level of STAT3, EZH2, beta-catenin, and EMT and metastasis related molecules such as E-cadherin, N-cadherin, Snail-1 and MMP-9 was assessed by qRT-PCRand western blot. Finally, luciferase reporter assay and RIP assay were used to verify the interaction between lncRNA H19 and let-7c, and their subsequent regulation of STAT3. Results: Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion.Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion as well as EMT and metastasis via STAT3-EZH2-beta-catenin pathway, while lncRNA H19 regulated STAT3 negatively regulated let-7c in EC cell lines.lncRNA H19 facilitates EMT and metastasis of EC through let-7c/STAT3/EZH2/beta-catenin axis.	31102664	RID07972	expression association	metastasis	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Esophageal cancer	let-7c	H19	negatively-F	RIP;western blot;dual-luciferase reporter assay;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	miRNA	lncRNA	ENSG00000199030	NA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	LncRNA H19 promotes epithelial mesenchymal transition and metastasis of esophageal cancer via STAT3/EZH2 axisLong non-coding RNA H19 (lncRNA H19) has been widely reported in esophageal cancer (EC), and previous study had found that lncRNAH19 was up-regulated in EC and promoted cell proliferation and metastasis. However, the mechanism still needs further studied.Levels of lncRNA H19 were analyzed by qRT-PCRin matched samples from 30 patients. Expression levels of lncRNA H19, let-7, STAT3 and EZH2 were additionally identified by qRT-PCRand western blot in five EC cell lines. The effects of lncRNA H19 on cell proliferation, migration, invasion and apoptosis in cell lines were performed by MTT assay, colony formation assay, Transwell assay and flow cytometry in vitro, and tumor formation was detected by xenograft nude mice model in vivo. The expression level of STAT3, EZH2, beta-catenin, and EMT and metastasis related molecules such as E-cadherin, N-cadherin, Snail-1 and MMP-9 was assessed by qRT-PCRand western blot. Finally, luciferase reporter assay and RIP assay were used to verify the interaction between lncRNA H19 and let-7c, and their subsequent regulation of STAT3. Results: Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion.Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion as well as EMT and metastasis via STAT3-EZH2-beta-catenin pathway, while lncRNA H19 regulated STAT3 negatively regulated let-7c in EC cell lines.lncRNA H19 facilitates EMT and metastasis of EC through let-7c/STAT3/EZH2/beta-catenin axis.	31102664	RID07973	expression association	metastasis		UP(NSCLC);DATA(GSE74639)
Small cell lung cancer	LINC00173	Etk	positively-E	shRNA;luciferase reporter assay;FISH;siRNA;overexpression;RNA pull-down assay;RIP	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196668	GRCh38_12:116533422-116536518	NA	NA	100287569	NA	FLJ42957|NCRNA00173	NA	Linc00173 promotes chemoresistance and progression of small cell lung cancer by sponging miR-218 to regulate Etk expression. Long intergenic nonprotein coding RNA 173 (Linc00173) was first shown to be involved in chemoresistance and progression of small-cell lung cancer (SCLC). We found that Linc00173 was highly expressed in SCLC chemoresistant cell lines, and promoted SCLC cells chemoresistance, proliferation, and migrationinvasion. Animal studies validated that Linc00173 induced tumor chemoresistance and growth of SCLC in vivo. Moreover, Linc00173 upregulated Etk through functioning as a competitive endogenous RNA (ceRNA) by "Sponging'-miRNA-218 and led to the upregulation of GSKIP and NDRG1, resulting in the translocation of beta-catenin. Importantly, expression analysis revealed that both Linc00173 and Etk were upregulated in SCLC patient samples and exhibiting positive Linc00173/Etk correlation. High expression of Linc00173 closely correlated with chemoresistance, extensive stage, and shorter survival in SCLC patients. Collectively, our study illustrated a Linc00173-mediated process that facilitated chemoresistance and progression in SCLC, which might provide treatment strategy against SCLC.	31477834	RID07974	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	
Small cell lung cancer	LINC00173	GSKIP	positively-E	western blot;siRNA;immunohistochemical staining	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196668	GRCh38_12:116533422-116536518	ENSG00000100744	NA	100287569	51527	FLJ42957|NCRNA00173	C14orf129	Linc00173 promotes chemoresistance and progression of small cell lung cancer by sponging miR-218 to regulate Etk expression. Long intergenic nonprotein coding RNA 173 (Linc00173) was first shown to be involved in chemoresistance and progression of small-cell lung cancer (SCLC). We found that Linc00173 was highly expressed in SCLC chemoresistant cell lines, and promoted SCLC cells chemoresistance, proliferation, and migrationinvasion. Animal studies validated that Linc00173 induced tumor chemoresistance and growth of SCLC in vivo. Moreover, Linc00173 upregulated Etk through functioning as a competitive endogenous RNA (ceRNA) by "Sponging'-miRNA-218 and led to the upregulation of GSKIP and NDRG1, resulting in the translocation of beta-catenin. Importantly, expression analysis revealed that both Linc00173 and Etk were upregulated in SCLC patient samples and exhibiting positive Linc00173/Etk correlation. High expression of Linc00173 closely correlated with chemoresistance, extensive stage, and shorter survival in SCLC patients. Collectively, our study illustrated a Linc00173-mediated process that facilitated chemoresistance and progression in SCLC, which might provide treatment strategy against SCLC.	31477834	RID07975	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Small cell lung cancer	LINC00173	NDRG1	positively-E	western blot;siRNA;immunohistochemical staining	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);WNT/beta-catenin signaling pathway(+)cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196668	GRCh38_12:116533422-116536518	ENSG00000104419	NA	100287569	10397	FLJ42957|NCRNA00173	CAP43|DRG1|NDR1|RTP|TDD5	Linc00173 promotes chemoresistance and progression of small cell lung cancer by sponging miR-218 to regulate Etk expression. Long intergenic nonprotein coding RNA 173 (Linc00173) was first shown to be involved in chemoresistance and progression of small-cell lung cancer (SCLC). We found that Linc00173 was highly expressed in SCLC chemoresistant cell lines, and promoted SCLC cells chemoresistance, proliferation, and migrationinvasion. Animal studies validated that Linc00173 induced tumor chemoresistance and growth of SCLC in vivo. Moreover, Linc00173 upregulated Etk through functioning as a competitive endogenous RNA (ceRNA) by "Sponging'-miRNA-218 and led to the upregulation of GSKIP and NDRG1, resulting in the translocation of beta-catenin. Importantly, expression analysis revealed that both Linc00173 and Etk were upregulated in SCLC patient samples and exhibiting positive Linc00173/Etk correlation. High expression of Linc00173 closely correlated with chemoresistance, extensive stage, and shorter survival in SCLC patients. Collectively, our study illustrated a Linc00173-mediated process that facilitated chemoresistance and progression in SCLC, which might provide treatment strategy against SCLC.	31477834	RID07976	expression association	chemoresistance	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Colorectal cancer	HIF1A	LINC00511	positively-E	JASPAR;luciferase reporter assay;ChIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000100644	NA	ENSG00000227036	GRCh38_17:72290091-72640472	3091	400619	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	onco-lncRNA-12	HIF-1alpha induced lncRNA LINC00511 accelerates the colorectal cancer proliferation through positive feedback loop. Present research found that LINC00511 was significantly up-regulated in the CRC tissue samples and cell lines. Consistently, LINC00011 overexpression was correlated with larger tumor size and advanced tumor stage. Functionally, LINC00511 promoted the proliferation and reduced the apoptosis of CRC cells in vitro, and LINC00511 knockdown repressed tumor growth in vivo. Mechanistically, hypoxia-inducible factor 1alpha (HIF- 1alpha) bound the promoter region of LINC00511 to active tits transcription. Moreover, LINC00511 functioned as the miR-153-5p sponge in the cytoplasmic portion, and miR-153-5p also targeted the 3'-UTR of HIF-1alpha. In conclusion, this study identifies the roles of LINC00511 in CRC progression and uncovers the positive feedback loop of HIF-1alpha/LINC00511/miR-153-5p in CRC, providing a potential therapeutic target.	32092829	RID07977	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Colorectal cancer	LINC00511	HIF1A	positively-E	luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-153-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000100644	NA	400619	3091	onco-lncRNA-12	bHLHe78|HIF-1alpha|HIF1|MOP1|PASD8	HIF-1alpha induced lncRNA LINC00511 accelerates the colorectal cancer proliferation through positive feedback loop. Present research found that LINC00511 was significantly up-regulated in the CRC tissue samples and cell lines. Consistently, LINC00011 overexpression was correlated with larger tumor size and advanced tumor stage. Functionally, LINC00511 promoted the proliferation and reduced the apoptosis of CRC cells in vitro, and LINC00511 knockdown repressed tumor growth in vivo. Mechanistically, hypoxia-inducible factor 1alpha (HIF- 1alpha) bound the promoter region of LINC00511 to active tits transcription. Moreover, LINC00511 functioned as the miR-153-5p sponge in the cytoplasmic portion, and miR-153-5p also targeted the 3'-UTR of HIF-1alpha. In conclusion, this study identifies the roles of LINC00511 in CRC progression and uncovers the positive feedback loop of HIF-1alpha/LINC00511/miR-153-5p in CRC, providing a potential therapeutic target.	32092829	RID07978	ceRNA or sponge	NA	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Colorectal cancer	CACNA1G-AS1	TP53	negatively-E	shRNA;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000250107	GRCh38_17:50556207-50562108	ENSG00000141510	NA	253962	7157	CAS1	LFS1|p53	Upregulated lncRNA CACNA1G-AS1 aggravates the progression of colorectal cancer by downregulating p53. CACNA1G-AS1 level in CRC tissues and adjacent normal tissues was first determined. Its level in CRC patients with different tumor stages was detected as well. Changes in proliferative and invasive abilities of HCT116 and SW480 cells influenced by CACNA1G-AS1 were evaluated. Subcellular distribution of CACNA1G-AS1 was analyzed. Through western blot, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assay, the interaction between CACNA1G- AS1 and EZH2 was assessed. The biological function of the target gene of CACNA1G-AS1 was finally explored.CACNA1G-AS1 was upregulated in CRC tissues compared to adjacent normal ones. Its level remained higher in CRC patients with stage III-IV compared to those with stage I-II. Knockdown of CACNA1G-AS1 reduced proliferative and invasive abilities of HTC116 and SW480 cells. CACNA1G-AS1 was mainly distributed in the nucleus. Moreover, CACNA1G-AS1 was verified to interact with EZH2. Knockdown of CACNA1G-AS1 or EZH2 upregulated p53 level and decreased the recruitment ability of EZH2 on p53. Finally, p53 knockdown could partially reverse the regulatory effect of CACNA1G-AS1 on the proliferative ability of HCT116 cells.CACNA1G-AS1 downregulates p53 level by forming a carcinogenic complex with EZH2, thereby enhancing the proliferative and invasive abilities of CRC cells.	31957825	RID07979	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	CCAT1	MAPK1	positively-E	shRNA;knockdown;overexpression;starBase;dual-luciferase reporter assay;RIP;Targetscan;GEPIA	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000247844	NA	ENSG00000100030	NA	100507056	5594	CARLO5|CARLo-5|onco-lncRNA-40	ERK|ERK2|MAPK2|p41mapk|PRKM1|PRKM2	LncRNA CCAT1/miR-490-3p/MAPK1/c-Myc Positive Feedback Loop Drives Progression of Acute Myeloid Leukemia.In this study, we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects. CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.	31790145	RID07980	ceRNA or sponge	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Acute myeloid leukemia	CCAT1	MYC	positively-E	shRNA;knockdown;overexpression;starBase;dual-luciferase reporter assay;RIP;Targetscan;GEPIA	upregulation	qRT-PCR	TCGA	NA	cell viability(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000247844	NA	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	bHLHe39|c-Myc|MYCC	LncRNA CCAT1/miR-490-3p/MAPK1/c-Myc Positive Feedback Loop Drives Progression of Acute Myeloid Leukemia.In this study, we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects. CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.	31790145	RID07981	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Gastric cancer	FOXP4-AS1	KDM1A	positively-E	shRNA;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234753	GRCh38_6:41452889-41548621	ENSG00000004487	NA	101060264	23028	NA	AOF2|BHC110|KDM1|KIAA0601|LSD1	The carcinogenic complex lncRNA FOXP4-AS1/ EZH2/LSD1 accelerates proliferation, migration and invasion of gastric cancer.To clarify the role of lncRNA FOX4-AS1 in the progression of gastric cancer (GC) via interacting with EZH2/LSD1.Relative level of FOXP4-AS1 in GC tissues and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The potential influences of FOXP4-AS1 on cellular behaviors of GC cells were evaluated via a series of functional experiments. Bioinformatics prediction, RNA immunoprecipitation (RIP) assay, and western blot were conducted to verify the potential of EZH2/LSD1 as a target of FOXP4-AS1.FOXP4-AS1 was upregulated in GC tissues relative to controls. Its level was higher in GC patients with stage III-IV than those with stage I-II. The survival rate was lower in GC patients presenting the high expression of FOXP4-AS1 compared with those presenting low expression. Transfection of sh-FOXP4-AS1 1# or sh-FOXP4-AS1 2# attenuated proliferative, migratory, and invasive abilities of AGS and BGC7901 cells. FOXP4-AS1 could bind to LSD1 and EZH2, and positively regulated their expression levels. Transfection of sh-LSD1 or sh-EZH2 reduced the proliferative ability of GC cells.FOXP4-AS1 binds to EZH2/ LSD1 to form a carcinogenic complex, thus accelerating GC cells to proliferate, migrate and invade.	31646567	RID07982	expression association	NA		DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	FOXP4-AS1	EZH2	positively-E	shRNA;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234753	GRCh38_6:41452889-41548621	ENSG00000106462	NA	101060264	2146	NA	ENX-1|EZH1|KMT6|KMT6A	The carcinogenic complex lncRNA FOXP4-AS1/ EZH2/LSD1 accelerates proliferation, migration and invasion of gastric cancer.To clarify the role of lncRNA FOX4-AS1 in the progression of gastric cancer (GC) via interacting with EZH2/LSD1.Relative level of FOXP4-AS1 in GC tissues and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The potential influences of FOXP4-AS1 on cellular behaviors of GC cells were evaluated via a series of functional experiments. Bioinformatics prediction, RNA immunoprecipitation (RIP) assay, and western blot were conducted to verify the potential of EZH2/LSD1 as a target of FOXP4-AS1.FOXP4-AS1 was upregulated in GC tissues relative to controls. Its level was higher in GC patients with stage III-IV than those with stage I-II. The survival rate was lower in GC patients presenting the high expression of FOXP4-AS1 compared with those presenting low expression. Transfection of sh-FOXP4-AS1 1# or sh-FOXP4-AS1 2# attenuated proliferative, migratory, and invasive abilities of AGS and BGC7901 cells. FOXP4-AS1 could bind to LSD1 and EZH2, and positively regulated their expression levels. Transfection of sh-LSD1 or sh-EZH2 reduced the proliferative ability of GC cells.FOXP4-AS1 binds to EZH2/ LSD1 to form a carcinogenic complex, thus accelerating GC cells to proliferate, migrate and invade.	31646567	RID07983	expression association	NA		UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Papillary thyroid carcinoma	LUCAT1	CDKN1A	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000124762	NA	100505994	1026	SCAL1|SCAT5	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07984	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Papillary thyroid carcinoma	LUCAT1	CDKN1C	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000129757	NA	100505994	1028	SCAL1|SCAT5	BWCR|BWS|KIP2|P57	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07985	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Papillary thyroid carcinoma	LUCAT1	TP53	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000141510	NA	100505994	7157	SCAL1|SCAT5	LFS1|p53	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07986	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	LUCAT1	BAX	negatively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000087088	NA	100505994	581	SCAL1|SCAT5	BCL2L4	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07987	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Papillary thyroid carcinoma	LUCAT1	EZH2	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000106462	NA	100505994	2146	SCAL1|SCAT5	ENX-1|EZH1|KMT6|KMT6A	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07988	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Papillary thyroid carcinoma	LUCAT1	HDAC1	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000116478	NA	100505994	3065	SCAL1|SCAT5	GON-10|HD1|KDAC1|RPD3L1	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07989	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE86978)
Papillary thyroid carcinoma	LUCAT1	DNMT1	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000130816	NA	100505994	1786	SCAL1|SCAT5	CXXC9|DNMT|MCMT	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07990	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Papillary thyroid carcinoma	LUCAT1	NRF2	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000154727	NA	100505994	NA	SCAL1|SCAT5	NA	LncRNA LUCAT1 as a novel prognostic biomarker for patients with papillary thyroid cancer. This study has been focused on the determination of the role of a specific lncRNA in papillary thyroid cancer. Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. LUCAT1 was specifically located at the cell nucleus in tumoral regions of patient tissues. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. These facts were corroborated by an enhanced expression of P21, P57, P53 and BAX, and a reduced expression of EZH2 and HDAC1. In addition, a significant decrease was observed on DNMT1 and NRF2 genes, helping to clarify the role of LUCAT1 on PTC . Our study reveals the involvement of LUCAT1 in PTC development, through acting in cell-cycle regulation, proliferation, epigenetic modifications through LUCAT1/ CDK1/ EZH2/ P57/ P21/ HDAC1/ DNMT1/ P53/ BAX axis and apoptosis, via extrinsic pathway activating caspases. These findings indicate that LUCAT1 is maybe a potential therapeutic target and molecular biomarker for PTC .	31591432	RID07991	expression association	prognosis	DOWN(BRCA);DATA(GSE51827,GSE75367,GSE86978)	
Triple-negative breast cancer	NEAT1	CCNE1	positively-E	shRNA	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105173	NA	283131	898	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	CCNE	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07992	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Triple-negative breast cancer	NEAT1	CCND1	positively-E	shRNA	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000110092	NA	283131	595	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07993	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Triple-negative breast cancer	NEAT1	CASP3	negatively-E	shRNA;immunofluorescence;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000164305	NA	283131	836	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	apopain|CPP32|CPP32B|Yama	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07994	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Triple-negative breast cancer	NEAT1	ATP7A	positively-E	shRNA	upregulation	qRT-PCR;microarray	NA	NA	chemosensitivity(-)	NA	association	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000165240	NA	283131	538	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	MNK	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07995	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE75367,GSE86978)
Triple-negative breast cancer	NEAT1	ATP8B	positively-E	shRNA	upregulation	qRT-PCR;microarray	NA	NA	chemosensitivity(-)	NA	association	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07996	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Triple-negative breast cancer	NEAT1	SOX2	positively-E	shRNA	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000181449	NA	283131	6657	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness.Based on our microarray finding, we identified several dysregulated lncRNAs that are highly expressed in breast cancer patients.Further validation was performed in the circulation of 192 normal controls and 179 breast cancer patients by quantitative reverse transcription-PCR (qRT-PCR.Significant inhibition of cell proliferation and colony formation was observed in shNEAT1 in both MDA-MB-231 and cisR/taxR .Knockdown of NEAT1 reduced the expression of cyclin E1 and D1, indicating that NEAT1 is required in cell cycle progression.qRT-PCRresults identified that drug transporter genes, such as ATP7A and ATP7B, were downregulated in shNEAT1 cells. Interestingly, a stemness marker, SOX2, was also downregulated in shNEAT1 cells .These findings provide evidence that NEAT1 is a potential therapeutic target to overcome chemoresistance for treating TNBC.	30894512	RID07997	expression association	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(LIHC);DATA(GSE117623)
Colorectal cancer	CREB1	LEF1-AS1	positively-E	siRNA;overexpression;Jaspar;ChIP;luciferase reporter assay;qPCR	upregulation	RT-PCR;microarray	TCGA	NA	cell growth(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000118260	NA	ENSG00000232021	GRCh38_4:108167525-108258037	1385	641518	NA	NA	CREB1-induced lncRNA LEF1-AS1 contributes to colorectal cancer progression via the miR-489/DIAPH1 axis.This research aimed to investigate the roles and mechanisms of LEF1-AS1 in colorectal cancer (CRC). We firstly showed that LEF1-AS1 expression was upregulated in human CRC tissues and cell lines. LEF1-AS1 upregulation was demonstrated to be induced by CREB1. Clinical study revealed that high LEF1-AS1 expression was positively associated with histological grade, lymph nodes metastasis, and decreased survivals of CRC patients. Functionally, down-regulation of LEF1-AS1 using si-LEF1-AS1 decreased cell growth, migration and invasion, as well as increased apoptosis in CRC cells. Mechanically, LEF1-AS1 functioned as competing endogenous RNA (ceRNA) for miR-489 to positively recover DIAPH1, thus playing an oncogenic role in CRC pathogenesis. Overall, our observations identified a novel CRC-related lncRNA LEF1-AS1 and discovered a critical role for this lncRNA as a ceRNA in CRC pathogenesis, suggesting that it may serve as a novel biomarker for prognosis and act as a therapeutic target for CRC treatment.	32248974	RID07998	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Colorectal cancer	LEF1-AS1	DIAPH1	positively-E	miRDB;luciferase reporter assay;RIP;qPCR;GSCALite;GEPIA;UALCAN	upregulation	RT-PCR;microarray	TCGA	NA	tumorigenesis(+);apoptosis process(-);cell cycle(+);epithelial to mesenchymal transition(+)	ceRNA(miR-489)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232021	GRCh38_4:108167525-108258037	ENSG00000131504	NA	641518	1729	NA	DFNA1|hDIA1|LFHL1	CREB1-induced lncRNA LEF1-AS1 contributes to colorectal cancer progression via the miR-489/DIAPH1 axis.This research aimed to investigate the roles and mechanisms of LEF1-AS1 in colorectal cancer (CRC). We firstly showed that LEF1-AS1 expression was upregulated in human CRC tissues and cell lines. LEF1-AS1 upregulation was demonstrated to be induced by CREB1. Clinical study revealed that high LEF1-AS1 expression was positively associated with histological grade, lymph nodes metastasis, and decreased survivals of CRC patients. Functionally, down-regulation of LEF1-AS1 using si-LEF1-AS1 decreased cell growth, migration and invasion, as well as increased apoptosis in CRC cells. Mechanically, LEF1-AS1 functioned as competing endogenous RNA (ceRNA) for miR-489 to positively recover DIAPH1, thus playing an oncogenic role in CRC pathogenesis. Overall, our observations identified a novel CRC-related lncRNA LEF1-AS1 and discovered a critical role for this lncRNA as a ceRNA in CRC pathogenesis, suggesting that it may serve as a novel biomarker for prognosis and act as a therapeutic target for CRC treatment.	32248974	RID07999	ceRNA or sponge	metastasis,prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)
Lung adenocarcinoma	ACTA2-AS1	GRB2	positively-E	siRNA;miRDB;luciferase reporter assay;RIP;Targetscan;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	ceRNA(miR-634)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000177885	NA	100132116	2885	UC001kfo|uc001kfo.1|ZXF1	NCKAP2	Downregulation of long non-coding RNA ZXF1 restricts cell survival by targeting miR-634-GRB2 in lung adenocarcinoma.In our in vitro experiments, qRT-PCRrevealed that the expression level of ZXF1 in LA tissues and tumor cells were significantly higher than that in adjacent normal tissues and normal cells. Furthermore, bioinformatics analysis, luciferase reporter assay, western blot and RNA immunoprecipitation (RIP) assay showed that ZXF1 could directly interact with miR-634, which targets GRB2. Therefore, we propose that ZXF1 could function as an oncogene partly by sponging miR- 634 and therefore regulating GRB2 expression in LA. Overall, this study demonstrated, for the first time, that the lncRNA ZXF1/miR-634/GRB2 axis plays crucial roles in modulating LA progression. Moreover, lncRNA ZXF1 might potentially improve LA prognosis and serve as a therapeutic target for the treatment of LA.	32160453	RID08000	ceRNA or sponge	prognosis,metastasis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LAMTOR5	DLEU2	positively-E	ChIP;ddPCR;RIP	upregulation	qPCR;ddPCR	NA	NA	viral replication(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000134248	NA	ENSG00000231607	GRCh38_13:49956670-50125720	10542	8847	HBXIP|MGC71071|XIP	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	Hepatitis B protein HBx binds the DLEU2 lncRNA to sustain cccDNA and host cancer-related gene transcription.We explored, in relevant cellular models of HBV replication, the functional consequences of HBx interaction with DLEU2, a long non-coding RNA (lncRNA) expressed in the liver and increased in human hepatocellular carcinoma (HCC), in the regulation of host target genes and the HBV cccDNA.We show that HBx binds the promoter region, enhances the transcription and induces the accumulation of DLEU2 in infected hepatocytes. We found that nuclear DLEU2 directly binds HBx and the histone methyltransferase enhancer of zeste homolog 2 (EZH2), the catalytic active subunit of the polycomb repressor complex 2 (PRC2) complex. Computational modelling and biochemical evidence suggest that HBx and EZH2 share two preferential binding sites in DLEU2 intron 1. HBx and DLEU2 co-recruitment on the cccDNA displaces EZH2 from the viral chromatin to boost transcription and viral replication. DLEU2-H Bx association with target host promoters relieves EZH2 repression and leads to the transcriptional activation of a subset of EZH2/PRC2 target genes in HBV-infected cells and HBV-related HCCs.Our results highlight the ability of HBx to bind RNA to impact on the epigenetic control of both viral cccDNA and host genes and provide a new key to understand the role of DLEU2 and EZH2 overexpression in HBV-related HCCs and HBx contribution to hepatocytes transformation.	32114505	RID08001	transcriptional regulation	NA	UP(NSCLC,PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)
Hepatocellular carcinoma	DLEU2	EZH2	positively-E	RIP;RNA pull-down assay;immunoblot	upregulation	qPCR;ddPCR	NA	NA	viral replication(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000106462	NA	8847	2146	BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2OS|TRIM13OS	ENX-1|EZH1|KMT6|KMT6A	Hepatitis B protein HBx binds the DLEU2 lncRNA to sustain cccDNA and host cancer-related gene transcription.We explored, in relevant cellular models of HBV replication, the functional consequences of HBx interaction with DLEU2, a long non-coding RNA (lncRNA) expressed in the liver and increased in human hepatocellular carcinoma (HCC), in the regulation of host target genes and the HBV cccDNA.We show that HBx binds the promoter region, enhances the transcription and induces the accumulation of DLEU2 in infected hepatocytes. We found that nuclear DLEU2 directly binds HBx and the histone methyltransferase enhancer of zeste homolog 2 (EZH2), the catalytic active subunit of the polycomb repressor complex 2 (PRC2) complex. Computational modelling and biochemical evidence suggest that HBx and EZH2 share two preferential binding sites in DLEU2 intron 1. HBx and DLEU2 co-recruitment on the cccDNA displaces EZH2 from the viral chromatin to boost transcription and viral replication. DLEU2-H Bx association with target host promoters relieves EZH2 repression and leads to the transcriptional activation of a subset of EZH2/PRC2 target genes in HBV-infected cells and HBV-related HCCs.Our results highlight the ability of HBx to bind RNA to impact on the epigenetic control of both viral cccDNA and host genes and provide a new key to understand the role of DLEU2 and EZH2 overexpression in HBV-related HCCs and HBx contribution to hepatocytes transformation.	32114505	RID08002	expression association	NA	UP(PAAD,SKCM);DOWN(PRAD,BRCA);DATA(GSE40174,GSE67980,GSE38495,GSE67939,GSE41245)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Non-small cell lung cancer	CCAT1	HOXA1	positively-E	miRTarBase;Targetscan;mirDIP;dual-luciferase reporter assay;RIP;immunohistochemistry;siRNA	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);apoptosis process(-);chemosensitivity(-)	ceRNA(miR-218)	regulation	NA	Gefitinib	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000247844	NA	ENSG00000105991	NA	100507056	3198	CARLO5|CARLo-5|onco-lncRNA-40	HOX1|HOX1F	lncRNA CCAT1 Acts as a MicroRNA-218 Sponge to Increase Gefitinib Resistance in NSCLC by Targeting HOXA1.The aim of this study is to explore the roles of CCAT1 on gefitinib resistance in NSCLC and to explore the underlying mechanisms. The quantitative real-time PCR (qRT-PCR analysis was to investigate the expression pattern of CCAT1 in gefitinib-resistant NSCLC patient tissues and cell lines, and then the effects of CCAT1 on gefitinib resistance of NSCLC in vitro and in vivo. Furthermore, bioinformatics online program predictions and luciferase reporter assay were used to validate the association of CCAT1 and miR-218 in NSCLC cells. In this study, CCAT1 was observed to be upregulated in gefitinib-resistant patient tissues and cell lines. In vitro and in vivo experiments demonstrated that CCAT1 knockdown impaired cell proliferation and promoted the gefitinib-induced cell apoptosis. Furthermore, we demonstrated that CCAT1 acts as a sponge for miR-218, and verified that HOXA1 is a novel target of miR-218. These results suggest that CCAT1 may serve as a promising therapeutic target for the treatment of epidermal growth factor receptor (EGFR) plus NSCLC patients.	32084702	RID08003	ceRNA or sponge	chemoresistance		UP(PAAD,SKCM);DATA(GSE40174,GSE38495)
Serous ovarian carcinoma	NRAD1	SOX9	positively-E	miRBase;Targetscan;RNA22;miRmap;microT;miRanda;starBase;PicTar;JASPAR	upregulation	qRT-PCR	GSE18520;GSE36668;GSE119055;GSE83693;TCGA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000233725	GRCh38_13:43908669-44030461	ENSG00000125398	NA	121838	6662	LINC00284|NCRNA00284	CMD1|CMPD1|SRA1	Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma. Data on lncRNAs, mRNAs, and miRNAs with differential expression in SOC, compared to normal ovarian tissue, were obtained from the Gene Expression Omnibus (GEO) database. Data on lncRNA expression and clinical data in SOC were obtained from The Cancer Genome Atlas (TCGA). lncRNA-miRNA interactions were predicted by the miRBase database. Different online tools, i.e., TargetScan, RNA22, miRmap, microT, miRanda, StarBase, and PicTar, were cooperatively utilized to predict the mRNAs targeted by miRNAs. The plugin of BiNGO in Cytoscape and KOBAS 3.0 were used to conduct the functional and pathway enrichment analyses. The lncRNA, miRNAs, and mRNAs identified to be expressed at statistically significant and different levels between SOC and healthy fallopian tube tissues were further validated using qRT-PCR A total of 4 lncRNAs (LINC00284, HAGLR, HCAT158, and BLACAT1) and 111 mRNAs were found to be upregulated in SOC tissues compared to normal tissues, based on the GEO database. LINC00284 was found to be highly expressed in SOC, in association with the upregulation of the transcription factor SOX9. The high LINC00284 expression was associated with poor prognosis and proved to be an independent risk factor in patients with SOC, based on TCGA database. The qRT-PCRvalidation results closely recapitulated the expression profiles and prognostic scores of the aforementioned bioinformatic analyses. The LINC00284-related ceRNA network was found to be associated with SOC carcinogenesis by biofunctional analysis. In conclusion, the LINC00284-related ceRNA network may provide valuable information on the mechanisms of SOC initiation and progression. Importantly, LINC00284 proved to be a new potential prognostic biomarker for SOC.	32076467	RID08004	transcriptional regulation	prognosis		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Polycystic ovary syndrome	LNCSRLR	IL6	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000240032	GRCh38_3:146066344-146069185	ENSG00000136244	NA	109729161	3569	lncRNA-SRLR	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Upregulation of the lncRNA SRLR in polycystic ovary syndrome regulates cell apoptosis and IL-6 expression. Increased levels of interleukin-6 (IL-6) contribute to the development of polycystic ovary syndrome (PCOS); in renal cell carcinoma, the long non-coding RNA (lncRNA) SRLR upregulates IL-6. In this study, we demonstrated that the levels of the lncRNA SRLR were upregulated in PCOS patients with high expression of plasma IL-6 compared with heathy females. The levels of the lncRNA SRLR in the plasma had a positive correlation with expression of IL-6 in patients with PCOS but not in healthy females. Upregulation of the lncRNA SRLR in plasma could distinguish PCOS patients from healthy females. Overexpression of the lncRNA SRLR led to upregulation of IL- 6 and promoted apoptosis of human granulosa-like tumour cells (KGN). Therefore, the lncRNA SRLR participated in PCOS by regulating cell apoptosis and IL-6 expression. Significance of the Study: The lncRNA SRLR mediates its effects on apoptosis and IL-6 expression in PCOS and could be used to distinguish PCOS patients from healthy controls. Plasma circulating levels of the lncRNA SRLR may be a potential target for the treatment of PCOS.	31999854	RID08005	expression association	circulating		DOWN(BRCA);DATA(GSE75367,GSE86978)
Colorectal cancer	LINC00461	CCND1	positively-E	lncRNASNP2;DIANA;RNA pull-down assay;luciferase reporter assay;overexpression;miRWalk;miRTarBase;RIP;Targetscan	upregulation	RT-qPCR	NA	NA	cancer progression(+);chemosensitivity(-);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-593-5p)	regulation	NA	Cisplatin	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000110092	NA	645323	595	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA LINC00461 mediates cisplatin resistance of rectal cancer via miR-593-5p/CCND1 axis. This research was the first attempt to decipher the underlying function and mechanism of long intergenic non-protein coding RNA 461 (LINC00461) in rectal cancer and also its relation to cisplatin resistance of rectal cancer. Data from this study revealed that LINC00461 expression was upregulated in rectal cancer cells. LINC00461 depletion restrained rectal cancer progression and sensitized rectal cancer cells to cisplatin. Molecular mechanism assays testified that LINC00461 bound with miR-593-5p. Besides, miR-593-5p upregulation improved the sensitivity of rectal cancer cells to cisplatin. Additionally, cyclin D1 (CCND1) was manifested to be a downstream target of miR-593-5p. Furthermore, CCND1 upregulation could reverse the effect of LINC00461 downregulation on rectal cancer progression and cisplatin resistance of rectal cancer. To sum up, LINC00461 mediates cisplatin resistance of rectal cancer by targeting miR-593-5p/CCND1 axis, shedding new light on the treatment of rectal cancer.	31972361	RID08006	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065,GSE55807)
Colorectal cancer	ELFN1-AS1	TRIM44	positively-E	luciferase reporter assay;DIANA;starBase;RIP;shRNA	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-4644)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236081	GRCh38_7:1738630-1742291	ENSG00000166326	NA	101927125	54765	MYCLo-2	DIPB|MC7	ELFN1-AS1 accelerates the proliferation and migration of colorectal cancer via regulation of miR-4644/TRIM44 axis.Our study detected that ELFN1-AS1 expression was elevated in CRC tissues and cells, and ELFN1-AS1 upregulation was correlated with poor prognosis of CRC sufferers. Besides, it was viewed that ELFN1-AS1 knockdown impeded the proliferation and migration abilities as well as activated the apoptosis ability of CRC cells. In subsequence, mechanism assays also displayed that ELFN1-AS1 targeted miR-4644 to augment TRIM44 level. Finally, rescue experiments confirmed that TRIM44 took part in the ELFN1-AS1-medatied promotional influences on CRC cells proliferation and migration. In conclusion, ELFN1-AS1 exerted pro-proliferation, anti-apoptosis and pro-migration functions on CRC cells by acting as a sponge of miR-4644 to increase TRIM44 expression at mRNA and protein level, providing an additional molecule responsible for the carcinogenesis and progression for CRC.	31929141	RID08007	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE75367)
Hepatocellular carcinoma	LINC00958	HDGF	positively-E	luciferase reporter assay;RIP;siRNA;shRNA;overexpression;starBase;miRDB;RNA pull-down assay;	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-3619-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000143321	NA	100506305	3068	NA	HMG1L2	M6A-mediated upregulation of LINC00958 increases lipogenesis and acts as a nanotherapeutic target in hepatocellular carcinoma.Differentially expressed lncRNA profile in HCC was constructed using TCGA data. LINC00958 expression level was examined in HCC cell lines and tissues. Univariate and multivariate analyses were performed to demonstrate the prognostic value of LINC00958. Loss-of-function and gain-of-function experiments were used to assess the effects of LINC00958 on cell proliferation, motility, and lipogenesis. Patient-derived xenograft model was established for in vivo experiments. RNA immunoprecipitation, dual luciferase reporter, biotin-labeled miRNA pull-down, fluorescence in situ hybridization, and RNA sequencing assays were performed to elucidate the underlying molecular mechanisms. We developed a PLGA-based nanoplatform encapsulating LINC00958 siRNA and evaluated its superiority for systemic administration.We identified a lipogenesis-related lncRNA, LINC00958, whose expression was upregulated in HCC cell lines and tissues. High LINC00958 level independently predicted poor overall survival. Functional assays showed that LINC00958 aggravated HCC malignant phenotypes in vitro and in vivo. Mechanistically, LINC00958 sponged miR- 3619-5p to upregulate hepatoma-derived growth factor (HDGF) expression, thereby facilitating HCC lipogenesis and progression. METTL3-mediated N6-methyladenosine modification led to LINC00958 upregulation through stabilizing its RNA transcript. A PLGA-based nanoplatform loaded with si-LINC00958 was developed for HCC systemic administration. This novel drug delivery system was controlled release, tumor targeting, safe, and presented satisfactory antitumor efficacy.	31915027	RID08008	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE41245)
Head and neck squamous cell carcinoma	SCAT1	CAV1	positively-E	lncBase;miRWalk;miRTarBase	upregulation		TCGA	NA	cell stemness(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000267123	GRCh38_17:78605233-78632155	ENSG00000105974	NA	101928710	857	LINC02081|XLOC_012582	BSCL3|CGL3|LCCNS|MSTP085|PPH3|VIP21	LncRNA LOXL1\AS1 regulates the tumorigenesis and development of lung adenocarcinoma through sponging miR\423\5p and targeting MYBL2.&#10;Our present study suggested that LOXL1\AS1 expression was considerably increased in LUAD tissues and cells. Moreover, LOXL1\AS1 deficiency notably hampered cell proliferation and migration as well as dramatically facilitated cell apoptosis. Through molecular mechanism assays, LOXL1\AS1 was identified as a cytoplasmic RNA and acted as a sponge of miR\423\5p. Furthermore, MYBL2 was targeted and negatively modified by miR\423\5p. Rescue experiments revealed that MYBL2 knockdown could counteract miR\423\5p repression\mediated enhancement on the progression of LOXL1\AS1 downregulated LUAD cells. More importantly, MYBL2 was discovered to interact with LOXL1\AS1 promoter, indicating a positive feedback loop of LOXL1\AS1/miR\423\5p/MYBL2 in LUAD. These findings manifested the carcinogenic role of LOXL1\AS1 and LOXL1\AS1/miR\423\5p/MYBL2 feedback loop in LUAD, which could be helpful to explore effective therapeutic strategy for LUAD patients.	31807160	RID08009	expression association	NA		UP(LIHC,NSCLC,SKCM);DATA(GSE117623,GSE74639,GSE38495)
Lung adenocarcinoma	LOXL1-AS1	MYBL2	positively-E	starBase;RNA pull-down assay;luciferase reporter assay;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-423-5p),transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000101057	NA	100287616	4605	NA	B-MYB|BMYB	LncRNA LOXL1-AS1 regulates the tumorigenesis and development of lung adenocarcinoma through sponging miR-423-5p and targeting MYBL2.Our present study suggested that LOXL1-AS1 expression was considerably increased in LUAD tissues and cells. Moreover, LOXL1-AS1 deficiency notably hampered cell proliferation and migration as well as dramatically facilitated cell apoptosis. Through molecular mechanism assays, LOXL1-AS1 was identified as a cytoplasmic RNA and acted as a sponge of miR-423-5p. Furthermore, MYBL2 was targeted and negatively modified by miR-423-5p. Rescue experiments revealed that MYBL2 knockdown could counteract miR-423-5p repression-mediated enhancement on the progression of LOXL1-AS1 downregulated LUAD cells. More importantly, MYBL2 was discovered to interact with LOXL1-AS1 promoter, indicating a positive feedback loop of LOXL1-AS1/miR-423-5p/MYBL2 in LUAD. These findings manifested the carcinogenic role of LOXL1-AS1 and LOXL1-AS1/miR-423-5p/MYBL2 feedback loop in LUAD, which could be helpful to explore effective therapeutic strategy for LUAD patients.	31758653	RID08010	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	UP(PAAD);DATA(GSE40174)
Ewing's sarcoma	DLX6-AS1	CDK4	positively-E	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Sarcoma	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000135446	NA	285987	1019	Evf-2|FLJ34048|NCRNA00212	PSK-J3	Long noncoding RNA DLX6-AS1 targets miR-124-3p/CDK4 to accelerate Ewing  sarcoma. Results unveil that DLX6-AS1 expression was increased in the tissue sample and cells. Functionally, the silencing of DLX6-AS1 could repress the proliferation and accelerate the apoptosis of Ewing  sarcoma cells. Mechanically, DLX6-AS1 functioned as the sponge of miR-124-3p, and then miR-124-3p targeted the 3'-UTR of CDK4 mRNA, forming the DLX6-AS1/miR-124-3p/CDK4 regulatory pathway. In conclusion, the critical role of DLX6-AS1 might unveil a potential therapeutic target for Ewing  sarcoma.	31737208	RID08011	ceRNA or sponge	NA		DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Cervical cancer	MIR205HG	KRT17	positively-E	GEPIA;shRNA;starBase;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000128422	NA	642587	3872	LINC00510	PCHC1	Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1.Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1 and activated the apoptosis of cervical cancer cells. Based on the finding that MIR205HG could regulate KRT17 expression, we further probed the detailed mechanism between MIR205HG and KRT17. It was observed from mechanism experiments that MIR205HG depleted SRSF1 to increase KRT17 expression. The whole mechanism of MIR205HG/SRSF1/KRT17 axis affecting cell proliferation, apoptosis and migration in cervical cancer was validated using rescue assays. In conclusion, MIR205HG modulated the biological activities of cervical cancer cells via targeting SRSF1 and regulating KRT17, which better understood the pathogenesis of cervical carcinoma and excavated a novel therapeutic target.	31655037	RID08012	expression association	NA		UP(NSCLC,PAAD);DATA(GSE74639,GSE40174)
Cervical cancer	MIR205HG	SRSF1	negatively-F	GEPIA;shRNA;starBase;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000230937	GRCh38_1:209428817-209432848	ENSG00000136450	NA	642587	6426	LINC00510	ASF|MGC5228|SF2|SF2p33|SFRS1|SRp30a	Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1.Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1 and activated the apoptosis of cervical cancer cells. Based on the finding that MIR205HG could regulate KRT17 expression, we further probed the detailed mechanism between MIR205HG and KRT17. It was observed from mechanism experiments that MIR205HG depleted SRSF1 to increase KRT17 expression. The whole mechanism of MIR205HG/SRSF1/KRT17 axis affecting cell proliferation, apoptosis and migration in cervical cancer was validated using rescue assays. In conclusion, MIR205HG modulated the biological activities of cervical cancer cells via targeting SRSF1 and regulating KRT17, which better understood the pathogenesis of cervical carcinoma and excavated a novel therapeutic target.	31655037	RID08013	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Pancreatic cancer	LINC01559	YY1AP1	positively-E	lncBase;luciferase reporter assay;Targetscan;RPISeq;RIP	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);cell growth(+)	ceRNA(miR-607),transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000180861	GRCh38_12:13371089-13387167	ENSG00000163374	NA	283422	55249	C12orf36|FLJ33810	HCCA2|YAP|YY1AP	LINC01559 accelerates pancreatic cancer cell proliferation and migration through YAP-mediated pathway. Several online databases indicated that LINC01559 was at a low expression in normal pancreatic tissues but was obviously upregulated in PAAD tissues. Further, our results showed that LINC01559 was stimulated in PC cell lines relative to normal controls. Furthermore, we validated that LINC01559 facilitated PC cell proliferation and migration in vitro. Also, silencing LINC01559 obstructed PC cell growth in vivo. Besides, LINC01559 was revealed to be mainly in the cytoplasm of PC cells and therefore served as a ceRNA of Yes-associated protein (YAP) in PC cells via sponging miR-607. Surprisingly, we also proved that LINC01559 could interact with YAP protein, which might hinder YAP phosphorylation and enhance YAP transcriptional activity in PC cells. Furthermore, we demonstrated that YAP was the downstream effector in LINC01559-regulated PC development. Collectively, our findings unmasked that LINC01559 accelerates PC progression through relying on YAP, providing a new potential target for clinical treatment of patients with PC.	31608998	RID08014	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Epithelial ovarian cancer	SNHG22	LGALS1	positively-E	starBase;RIP;luciferase reporter assay;CRISPR-Cas9	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-2467)	regulation	NA	Cisplatin;Paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000267322	GRCh38_18:49813961-49851059	ENSG00000100097	NA	103091864	3956	SCARNA17HG	GBP	SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma.Here, we found that SNHG22 was significantly increased in EOC tissues and was significantly associated with a low level of differentiation. Forced SNHG22 expression promoted chemotherapy resistance in EOC cells. Knockdown of SNHG22 expression increased the sensitivity of EOC cells to cisplatin and paclitaxel. Importantly, we found that SNHG22 could directly interact with miR-2467 and lead to the release of miR-2467-targeted Gal-1 mRNA. Moreover, SNHG22 overexpression induced EOC cell resistance to chemotherapy agents via PI3K/AKT and ERK cascade activation. In summary, our findings demonstrate that SNHG22 plays a critical role in the chemotherapy resistance of EOC by mediating the miR-2467/Gal-1 regulatory axis.	31581131	RID08015	ceRNA or sponge	chemoresistance,prognosis	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE51827,GSE75367,GSE86978)
Renal cell carcinoma	LINC00461	SALL1	negatively-E	siRNA	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-942)	regulation	NA	Sunitinib	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000103449	NA	645323	6299	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	Hsal1|TBS|ZNF794	LINC00461 affects the survival of patients with renal cell carcinoma by acting as a competing endogenous RNA for microRNA-942.The expression levels of four miRNAs were determined by reverse transcription-quantitative (RT-q)PCR. miR-942 mimics were transfected into OS-RC-2 cells and RNA sequencing was performed on the miR-942- and negative control-transfected cells. Downregulated genes, including those of long non-coding RNAs (lncRNAs) and mRNAs, were identified. The target genes of miR-942 were predicted, followed by protein-protein interaction network construction and functional enrichment analyses of miR-942 target genes. In addition, RCC RNA-seq and miRNA-seq data were downloaded from The Cancer Genome Atlas (TCGA) database. The contributions of lncRNA and/or mRNAs to survival prediction were assessed and a competing endogenous RNA (ceRNA) network consisting of miR-942, lncRNA and mRNAs was constructed. The expression levels of LINC00461, miR-942, spalt-like transcription factor 1 (SALL1), methionyl aminopeptidase 1 (METAP1) and DDB1 and CUL4 associated factor 1 (DCAF11) were verified using RT-qPCR. The role of LINC00461 in cell viability was detected by MTT assay. The expression level of miR-942 was significantly increased in sunitinib-resistant cells. A total of seven lncRNAs and 155 mRNAs were predicted as target genes of miR-942 in the miR-942 mimic-treated samples, compared with the mimic control-treated group. These potential target genes were significantly associated with 'protein binding'- 'TNF-beta signaling pathway'- 'negative transcriptional regulation'-and 'RNA binding'- Through the integrated analysis of RNA-sequencing and TCGA data, an miR-942-related ceRNA network, which was predicted to significantly affect the survival of patients with RCC, was constructed. The expression levels of lncRNA LINC00461 and the genes SALL1, METAP1, and DCAF11 were further verified. The viability of OS-RC-2 cells was decreased following co-transfection with miR-942 mimics and LINC00641 siRNA, and was comparable to that of wild type OS-RC-2 cells (P>0.05). Therefore, lncRNA LINC00461 may act as an miR-942 ceRNA, and affect the survival of patients with RCC by regulating the expression of SALL1, METAP1 and DCAF11.	31545458	RID08016	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Renal cell carcinoma	LINC00461	METAP1	negatively-E	siRNA	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-942)	regulation	NA	Sunitinib	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000164024	NA	645323	23173	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	KIAA0094|MAP1A|MetAP1A	LINC00461 affects the survival of patients with renal cell carcinoma by acting as a competing endogenous RNA for microRNA-942.The expression levels of four miRNAs were determined by reverse transcription-quantitative (RT-q)PCR. miR-942 mimics were transfected into OS-RC-2 cells and RNA sequencing was performed on the miR-942- and negative control-transfected cells. Downregulated genes, including those of long non-coding RNAs (lncRNAs) and mRNAs, were identified. The target genes of miR-942 were predicted, followed by protein-protein interaction network construction and functional enrichment analyses of miR-942 target genes. In addition, RCC RNA-seq and miRNA-seq data were downloaded from The Cancer Genome Atlas (TCGA) database. The contributions of lncRNA and/or mRNAs to survival prediction were assessed and a competing endogenous RNA (ceRNA) network consisting of miR-942, lncRNA and mRNAs was constructed. The expression levels of LINC00461, miR-942, spalt-like transcription factor 1 (SALL1), methionyl aminopeptidase 1 (METAP1) and DDB1 and CUL4 associated factor 1 (DCAF11) were verified using RT-qPCR. The role of LINC00461 in cell viability was detected by MTT assay. The expression level of miR-942 was significantly increased in sunitinib-resistant cells. A total of seven lncRNAs and 155 mRNAs were predicted as target genes of miR-942 in the miR-942 mimic-treated samples, compared with the mimic control-treated group. These potential target genes were significantly associated with 'protein binding'- 'TNF-beta signaling pathway'- 'negative transcriptional regulation'-and 'RNA binding'- Through the integrated analysis of RNA-sequencing and TCGA data, an miR-942-related ceRNA network, which was predicted to significantly affect the survival of patients with RCC, was constructed. The expression levels of lncRNA LINC00461 and the genes SALL1, METAP1, and DCAF11 were further verified. The viability of OS-RC-2 cells was decreased following co-transfection with miR-942 mimics and LINC00641 siRNA, and was comparable to that of wild type OS-RC-2 cells (P>0.05). Therefore, lncRNA LINC00461 may act as an miR-942 ceRNA, and affect the survival of patients with RCC by regulating the expression of SALL1, METAP1 and DCAF11.	31545458	RID08017	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Renal cell carcinoma	LINC00461	DCAF11	negatively-E	siRNA	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-942)	regulation	NA	Sunitinib	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000100897	NA	645323	80344	ECONEXIN|EyeLinc1|LOC645323|NDIME|Visc-1a|Visc-1b|Visc-2	GL014|PRO2389|WDR23	LINC00461 affects the survival of patients with renal cell carcinoma by acting as a competing endogenous RNA for microRNA-942.The expression levels of four miRNAs were determined by reverse transcription-quantitative (RT-q)PCR. miR-942 mimics were transfected into OS-RC-2 cells and RNA sequencing was performed on the miR-942- and negative control-transfected cells. Downregulated genes, including those of long non-coding RNAs (lncRNAs) and mRNAs, were identified. The target genes of miR-942 were predicted, followed by protein-protein interaction network construction and functional enrichment analyses of miR-942 target genes. In addition, RCC RNA-seq and miRNA-seq data were downloaded from The Cancer Genome Atlas (TCGA) database. The contributions of lncRNA and/or mRNAs to survival prediction were assessed and a competing endogenous RNA (ceRNA) network consisting of miR-942, lncRNA and mRNAs was constructed. The expression levels of LINC00461, miR-942, spalt-like transcription factor 1 (SALL1), methionyl aminopeptidase 1 (METAP1) and DDB1 and CUL4 associated factor 1 (DCAF11) were verified using RT-qPCR. The role of LINC00461 in cell viability was detected by MTT assay. The expression level of miR-942 was significantly increased in sunitinib-resistant cells. A total of seven lncRNAs and 155 mRNAs were predicted as target genes of miR-942 in the miR-942 mimic-treated samples, compared with the mimic control-treated group. These potential target genes were significantly associated with 'protein binding'- 'TNF-beta signaling pathway'- 'negative transcriptional regulation'-and 'RNA binding'- Through the integrated analysis of RNA-sequencing and TCGA data, an miR-942-related ceRNA network, which was predicted to significantly affect the survival of patients with RCC, was constructed. The expression levels of lncRNA LINC00461 and the genes SALL1, METAP1, and DCAF11 were further verified. The viability of OS-RC-2 cells was decreased following co-transfection with miR-942 mimics and LINC00641 siRNA, and was comparable to that of wild type OS-RC-2 cells (P>0.05). Therefore, lncRNA LINC00461 may act as an miR-942 ceRNA, and affect the survival of patients with RCC by regulating the expression of SALL1, METAP1 and DCAF11.	31545458	RID08018	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939)
Nasopharynx carcinoma	DRAIC	SATB1	positively-E	starBase;Targetscan;RNA pull-down assay;RIP;dual-luciferase reporter assay;shRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-122)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000245750	GRCh38_15:69462921-69843120	ENSG00000182568	NA	145837	6304	NA	NA	Long noncoding RNA DRAIC acts as a microRNA-122 sponge to facilitate nasopharyngeal carcinoma cell proliferation, migration and invasion via regulating SATB1.In this study, we found that DRAIC was significantly increased in NPC tissues. Increased expression of DRAIC was positively correlated with advanced clinical stages of NPC patients. Functional assays revealed that ectopic expression of DRAIC enhances NPC cell growth, migration and invasion. DRAIC knockdown represses NPC cell growth, migration and invasion. Mechanistically, we identified two miR-122 binding sites on DRAIC. RNA pull-down, RNA immunoprecipitation, and dualluciferase reporter assays confirmed the binding of DRAIC to miR-122. Via binding of miR-122, DRAIC upregulated the expression of miR-122 target SATB1, which was abolished by the mutation of miR-122 binding sites on SATB1. Moreover, the oncogenic roles of DRAIC on NPC were reversed by the mutation of miR-122 binding sites on SATB1, simultaneous overexpression of miR-122, or depletion of SATB1. In addition, the expression of SATB1 was also increased and positively associated with that of DRAIC in NPC tissues. In conclusion, these findings revealed the important roles of DRAIC-miR-122- SATB1 axis in NPC and suggested that DRAIC may be a potential therapeutic target for NPC.	31497998	RID08019	ceRNA or sponge	NA	UP(BRCA);DATA(GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	EPAS1	NLUCAT1	positively-E	RNAi	upregulation	qPCR;sequencing;microarray	TCGA	NA	chemosensitivity(-);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000116016	NA	NA	NA	2034	NA	bHLHe73|HIF2A|HLF|MOP2|PASD2	NA	The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-kB and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.	31417181	RID08020	expression association	prognosis,chemoresistance	UP(LIHC,NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE109761,GSE111065,GSE55807)	
Lung adenocarcinoma	NFKB1	NLUCAT1	positively-E	RNAi	upregulation	qPCR;sequencing;microarray	TCGA	NA	chemosensitivity(-);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000109320	NA	NA	NA	4790	NA	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	NA	The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-kB and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.	31417181	RID08021	expression association	prognosis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Lung adenocarcinoma	NRF2	NLUCAT1	positively-E	siRNA;ChIP	upregulation	qPCR;sequencing;microarray	TCGA	NA	chemosensitivity(-);apoptosis process(-)	NA	regulation	NA	Cisplatin	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000154727	NA	NA	NA	NA	NA	NA	NA	The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-kB and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.	31417181	RID08022	expression association	prognosis,chemoresistance		
Hepatocellular carcinoma	FOXD2-AS1	TMEM9	positively-E	luciferase reporter assay;RIP;starBase;overexpression	downregulation	microarray;qRT-PCR	NA	NA	chemosensitivity(+);NRF2 signaling pathway(+)	ceRNA(miR-150-5p)	regulation	NA	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000116857	NA	84793	252839	NA	DERM4|TMEM9A	LncRNA FOXD2-AS1 as a competitive endogenous RNA against miR-150-5p reverses resistance to sorafenib in hepatocellular carcinoma.The current study elucidated the role of a long non-coding RNA (lncRNA), FOXD2- AS1, in the pathogenesis of hepatocellular carcinoma (HCC) and the regulatory mechanism underlying FOXD2-AS1/miR-150-5p/transmembrane protein 9 (TMEM9) signalling in HCC. microarray analysis was used for preliminary screening of candidate lncRNAs in HCC tissues. qRT-PCRand western blot were used to detect the expression of FOXD2-AS1. Cell proliferation assays, luciferase assay and RNA immunoprecipitation were performed to examine the mechanism by which FOXD2-AS1 mediates sorafenib resistance in HCC cells. FOXD2-AS1 and TMEM9 were significantly decreased and miR-150-5p was increased in SR-HepG2 and SRHUH7 cells compared with control parental cells. Overexpression of FOXD2-AS1 increased TMEM9 expression and overcame the resistance of SR-HepG2 and SRHUH7 cells. Conversely, knockdown of FOXD2-AS1 decreased TMEM9 expression and increased the sensitivity of HepG2 and Huh7 cells to sorafenib. Our data also demonstrated that FOXD2-AS1 functioned as a sponge for miR-150-5p to modulate TMEM9 expression. Taken together, our findings revealed that FOXD2-AS1 is an important regulator of TMEM9 and contributed to sorafenib resistance. Thus, FOXD2- AS1 may serve as a therapeutic target against sorafenib resistance in HCC.	31210410	RID08023	ceRNA or sponge	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE55807)
Laryngeal carcinoma	LINC-PINT	PTCH1	positively-E	DIANA;overexpression;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);chemoresistance(-);cell viability(+);apoptosis process(-);cell stemness(+)	ceRNA(miR-425-5p)	regulation	NA	Cisplatin	CSC	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000185920	NA	378805	5727	LincRNA-Pint|MKLN1-AS1|PINT	BCNS|NBCCS|PTC|PTC1|PTCH	Long noncoding RNA LINC-PINT regulates laryngeal carcinoma cell stemness and chemoresistance through miR-425-5p/PTCH1/SHH axis.In this study, LINC-PINT expression in normal and tumor tissues were studied. Using a bioinformatic approach, microRNA (miRNA) targets of LINC-PINT and gene targets of the miRNA were determined. The impact of LINC-PINT on cell proliferation and chemoresistance was determined. Further through a set of silencing and reexpression studies phenotype rescue was studied. LINC-PINT expression was downregulated in laryngeal tumors. LINC-PINT targeted miR-425-5p by three sites. miR-425-5p also targeted PTCH1 a protein of the Hedgehog pathway. Downregulation of LINC-PINT was associated with increased cancer stemness and chemoresistance to cisplatin. Our results indicate a probable role of LINC-PINT in the pathology of laryngeal tumors. LINC-PINT re-expression in laryngeal tumors may be explored for reversion of cancer cell stemness and also for rescue of drug resistance phenotype.	31131448	RID08024	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)	DOWN(BRCA);DATA(GSE51827,GSE86978)
Hepatocellular carcinoma	SNHG10	SCARNA13	positively-E	shRNA;overexpression;luciferase reporter assay	upregulation	qPCR;sequencing;microarray	TCGA;GSE120021;GSE119773;GSE120095	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	snoRNA	ENSG00000247092	GRCh38_14:95521943-95534889	ENSG00000252481	NA	283596	677768	C14orf62|FLJ40557|LINC00063|NCRNA00063	U93	LncRNA SNHG10 Facilitates Hepatocarcinogenesis and Metastasis by Modulating Its Homolog SCARNA13 via a Positive Feedback Loop.Here, we aimed to identify hepatocellular carcinoma (HCC)-specific ncRNA and to investigate their roles in hepatocarcinogenesis and metastasis. RNA-seq of xenografts generated by lung metastasis identified long noncoding RNA small nucleolar RNA host gene 10 (SNHG10) and its homolog SCARNA13 as novel drivers for the development and metastasis of HCC. SNHG10 expression positively correlated with SCARNA13 expression in 64 HCC cases, and high expression of SNHG10 or SCARNA13 was associated with poor overall survival. As SCARNA13 showed significant rise and decline after overexpression and knockdown of SNHG10, respectively, we hypothesized that SNHG10 might act as an upstream regulator of SCARNA13. SNHG10 and SCARNA13 coordinately contributed to the malignant phenotype of HCC cells, where SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression by regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. SCARNA13 mediated SNHG10-driven HCC cell proliferation, invasion, and migration and facilitated the cell cycle and epithelial-sesenchymal transition of HCC cells by regulating SOX9. Overall, we identified a complex circuitry underlying the concomitant upregulation of SNHG10 and its homolog SCARNA13 in HCC in the process of hepatocarcinogenesis and metastasis.	31101763	RID08025	expression association	metastasis	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)	DOWN(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE111842,GSE55807)
Hepatocellular carcinoma	SNHG10	MYB	positively-E	JASPAR;PROMO;LASAGNA;siRNA;miRcode;lncRNASNP2;LncBase;RIP;ChIRP;overexpression	upregulation	qPCR;sequencing;microarray	TCGA;GSE120021;GSE119773;GSE120095	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);epithelial to mesenchymal transition(+)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000247092	GRCh38_14:95521943-95534889	ENSG00000118513	NA	283596	4602	C14orf62|FLJ40557|LINC00063|NCRNA00063	c-myb	LncRNA SNHG10 Facilitates Hepatocarcinogenesis and Metastasis by Modulating Its Homolog SCARNA13 via a Positive Feedback Loop.Here, we aimed to identify hepatocellular carcinoma (HCC)-specific ncRNA and to investigate their roles in hepatocarcinogenesis and metastasis. RNA-seq of xenografts generated by lung metastasis identified long noncoding RNA small nucleolar RNA host gene 10 (SNHG10) and its homolog SCARNA13 as novel drivers for the development and metastasis of HCC. SNHG10 expression positively correlated with SCARNA13 expression in 64 HCC cases, and high expression of SNHG10 or SCARNA13 was associated with poor overall survival. As SCARNA13 showed significant rise and decline after overexpression and knockdown of SNHG10, respectively, we hypothesized that SNHG10 might act as an upstream regulator of SCARNA13. SNHG10 and SCARNA13 coordinately contributed to the malignant phenotype of HCC cells, where SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression by regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. SCARNA13 mediated SNHG10-driven HCC cell proliferation, invasion, and migration and facilitated the cell cycle and epithelial-sesenchymal transition of HCC cells by regulating SOX9. Overall, we identified a complex circuitry underlying the concomitant upregulation of SNHG10 and its homolog SCARNA13 in HCC in the process of hepatocarcinogenesis and metastasis.	31101763	RID08026	ceRNA or sponge	metastasis	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)	
Head and neck squamous cell carcinoma	ZFAS1	ZNFX1	negatively-E	starBase	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000124201	NA	441951	57169	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	FLJ11277|KIAA1404	Oncogenic Role of ZFAS1 lncRNA in Head and Neck Squamous Cell Carcinomas. The expression level of ZFAS1 in HNSCC cell lines was analyzed using qRT-PCR Based on the HNSCC TCGA data, the ZFAS1 expression profile, clinicopathological features, and expression of correlated genes were analyzed in patient tissue samples. The selected genes were classified according to their biological function using the PANTHER tool. The interaction between lncRNA:miRNA and miRNA:mRNA was tested using available online tools. All statistical analyses were accomplished using GraphPad Prism 5.The expression of ZFAS1 was up-regulated in the metastatic FaDu cell line relative to the less aggressive SCC-25 and SCC-040 and dysplastic DOK cell lines. The TCGA data indicated an up-regulation of ZFAS1 in HNSCCs compared to normal tissue samples. The ZFAS1 levels typically di ered depending on the cancer stage and T-stage. Patients with a lower expression of ZFAS1 presented a slightly longer disease-free survival and overall survival. The analysis of genes associated with ZFAS1, as well its targets, indicate that they are linked with crucial cellular processes. In the group of patients with low expression of ZFAS1, we detected the up-regulation of suppressors and down-regulation of genes associated with epithelial-to-mesenchymal transition (EMT) process, metastases, and cancer-initiating cells. Moreover, the negative correlation between ZFAS1 and its host gene, ZNFX1, was observed. The analysis of interactions indicated that ZFAS1 has a binding sequence for miR-150-5p. The expression of ZFAS1 and miR-150-5p is negatively correlated in HNSCC patients. miR-150-5p can regulate the 30UTR of EIF4E mRNA. In the group of patients with high expression of ZFAS1 and low expression of miR-150-5p, we detected an up-regulation of EIF4E.In HNSCC, ZFAS1 displays oncogenic properties, regulates important processes associated with EMT, cancer-initiating cells, and metastases, and might a ect patients'-clinical outcomes. ZFAS1 likely regulates the cell phenotype through miR-150-5p and its downstream targets. Following further validation, ZFAS1 might prove a new and valuable biomarker.	31010087	RID08027	expression association	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)
Head and neck squamous cell carcinoma	ZFAS1	miR-150-5p	negatively-F	TargetScanHuman;miRDB;TarBase	upregulation	qRT-PCR	TCGA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Oncogenic Role of ZFAS1 lncRNA in Head and Neck Squamous Cell Carcinomas. The expression level of ZFAS1 in HNSCC cell lines was analyzed using qRT-PCR Based on the HNSCC TCGA data, the ZFAS1 expression profile, clinicopathological features, and expression of correlated genes were analyzed in patient tissue samples. The selected genes were classified according to their biological function using the PANTHER tool. The interaction between lncRNA:miRNA and miRNA:mRNA was tested using available online tools. All statistical analyses were accomplished using GraphPad Prism 5.The expression of ZFAS1 was up-regulated in the metastatic FaDu cell line relative to the less aggressive SCC-25 and SCC-040 and dysplastic DOK cell lines. The TCGA data indicated an up-regulation of ZFAS1 in HNSCCs compared to normal tissue samples. The ZFAS1 levels typically di ered depending on the cancer stage and T-stage. Patients with a lower expression of ZFAS1 presented a slightly longer disease-free survival and overall survival. The analysis of genes associated with ZFAS1, as well its targets, indicate that they are linked with crucial cellular processes. In the group of patients with low expression of ZFAS1, we detected the up-regulation of suppressors and down-regulation of genes associated with epithelial-to-mesenchymal transition (EMT) process, metastases, and cancer-initiating cells. Moreover, the negative correlation between ZFAS1 and its host gene, ZNFX1, was observed. The analysis of interactions indicated that ZFAS1 has a binding sequence for miR-150-5p. The expression of ZFAS1 and miR-150-5p is negatively correlated in HNSCC patients. miR-150-5p can regulate the 30UTR of EIF4E mRNA. In the group of patients with high expression of ZFAS1 and low expression of miR-150-5p, we detected an up-regulation of EIF4E.In HNSCC, ZFAS1 displays oncogenic properties, regulates important processes associated with EMT, cancer-initiating cells, and metastases, and might a ect patients'-clinical outcomes. ZFAS1 likely regulates the cell phenotype through miR-150-5p and its downstream targets. Following further validation, ZFAS1 might prove a new and valuable biomarker.	31010087	RID08028	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	
Colorectal cancer	RP11	ZEB1	positively-E	siRNA;western blot;RIP;RNA pull-down assay	upregulation	microarray;qRT-PCR	GSE110715;TCGA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);cell metastasis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000105618	GRCh38_19:54115410-54131719	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	m6A-induced lncRNA RP11 triggers the dissemination of colorectal cancer cells via upregulation of Zeb1.lncRNA expression profiles in matched normal and CRC tissue were checked using microarray analysis. The biological roles of a novel lncRNA, namely RP11-138 J23.1 (RP11), in development of CRC were checked both in vitro and in vivo. Its association with clinical progression of CRC was further analyzed.RP11 was highly expressed in CRC tissues, and its expression increased with CRC stage in patients. RP11 positively regulated the migration, invasion and epithelial mesenchymal transition (EMT) of CRC cells in vitro and enhanced liver metastasis in vivo. Post-translational upregulation of Zeb1, an EMT-related transcription factor, was essential for RP11-induced cell dissemination. Mechanistically, the RP11/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, Siah1 and Fbxo45, and subsequently prevented the proteasomal degradation of Zeb1. m6A methylation was involved in the upregulation of RP11 by increasing its nuclear accumulation. Clinical analysis showed that m6A can regulate the expression of RP11, further, RP11 regulated Siah1-Fbxo45/Zeb1 was involved in the development of CRC.m6A-induced lncRNA RP11 can trigger the dissemination of CRC cells via post-translational upregulation of Zeb1. Considering the high and specific levels of RP11 in CRC tissues, our present study paves the way for further investigations of RP11 as a predictive biomarker or therapeutic target for CRC.	30979372	RID08029	expression association	metastasis		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LASP1-AS	LASP1	positively-E	siRNA;overexpression	upregulation	microarray;RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000002834	NA	NA	3927	NA	Lasp-1|MLN50	Increased long noncoding RNA LASP1-AS is critical for hepatocellular carcinoma tumorigenesis via upregulating LASP1.In this study, a lncRNAs and mRNAs microarray analysis was performed in three pairs of HCC patitents'-tumor. We found lncRNA LIM and SH3 protein 1 antisense (LASP1- AS) and its sense-cognate gene LIM and SH3 protein 1 (LASP1) were upregulated in HCC and both are correlated with poorer prognosis and lower survival of HCC patients. Meanwhile, the expression of LASP1-AS correlated positively with LASP1 expression in HCC tissues. LASP1-AS promoted the proliferation, migration, and invasion abilities of HCC in vitro and vivo by enhancing LASP1 expression. Our study explored lncRNA LASP1-AS as an oncogene in HCC and promoted proliferation and metastasis capabilities of HCC via increasing the expression of its sense-cognate gene LASP1. LncRNA LASP1-AS might be a potential valuable prognostic biomarker and potential therapeutic target of HCC.	30677131	RID08030	expression association	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	CACS15	ABCC1	positively-E	miRanda;luciferase reporter assay;RNA pull-down assay;siRNA	upregulation	qRT-PCR	TCGA	NA	chemoresistance(-)	ceRNA(miR-145)	regulation	NA	Oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000103222	NA	NA	4363	NA	GS-X|MRP|MRP1	LncRNA CACS15 contributes to oxaliplatin resistance in colorectal cancer by positively regulating ABCC1 through sponging miR-145. Our results discovered that CASC15 was up-regulated in OXA-resistant CRC tissues and cells. Patients with high CASC15 expression level had a poor prognosis. CASC15 knockdown re-sensitized HT29/OXA and HCT116/OXA cells to OXA. Moreover, CASC15 could act as a competing endogenous RNA (ceRNA) to de-repress ABCC1 expression through sponging miR-145. miR-145 overexpression or ABCC1 knockdown could mimic the functional role of down-regulated CACS15 in OXA resistance, which was counteracted by CASC15 overexpression. Furthermore, CASC15 knockdown facilitated OXA sensitivity of OXA-resistant CRC cells in vivo. In summary, CASC15 silencing overcame OXA resistance of CRC by regulating miR-145/ABCC1 axis, providing a potential therapeutic target for CRC chemoresistance.	30639170	RID08031	ceRNA or sponge	chemoresistance,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	PSTPIP1	miRNA-188-5p	negatively-F	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000140368	GRCh38_15:76993359-77037475	NA	NA	9051	NA	CD2BP1|CD2BP1L|CD2BP1S|H-PIP|PAPAS|PSTPIP	NA	LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p.The relative level of PAPAS was determined in GC tissues and cell lines by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR. The Kaplan- Meier method was introduced to assess the prognostic potential of PAPAS in the overall survival of GC patients. Regulatory effects of PAPAS on proliferative, migratory, and invasive abilities of HGC-27 and AGS cells were detected by cell counting kit-8 (CCK-8), transwell, and wound closure assay, respectively. Subsequently, the binding relation between PAPAS and miRNA-188-5p was verified by the Dual-Luciferase reporter gene assay. Correlation between expression levels of PAPAS and miRNA-188-5p in GC tissues was explored. Finally, rescue experiments were conducted to uncover the role of PAPAS/miRNA-188-5p axis in the progression of GC.PAPAS was upregulated in GC tissues and cell lines compared to controls. GC patients expressing a high level of PAPAS suffered worse prognosis relative to those with low level. The silence of PAPAS remarkably attenuated proliferative, migratory, and invasive abilities of HGC-27 cells. Overexpression of PAPAS in AGS cells obtained the opposite trends. MiRNA-188- 5p was the direct target of PAPAS, which was negatively regulated by PAPAS. MiRNA-188-5p was able to reverse the regulatory effects of PA-PAS on proliferative, migratory, and invasive abilities of GC cells.LncRNA PAPAS is upregulated in GC and closely related to lymphatic metastasis, distant metastasis, and poor prognosis of GC patients. PAPAS aggravate the malignant progression of GC by negatively regulating the miRNA-188-5p level.	31858543	RID08032	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Gastric cancer	TOB1-AS1	NEU1	positively-E	dual-luciferase reporter assay;starBase;siRNA	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-23a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229980	GRCh38_17:50866679-50910774	ENSG00000234846	NA	400604	4758	NA	NEU	Long non-coding RNA TOB1-AS1 modulates cell proliferation, apoptosis, migration and invasion through miR-23a/NEU1 axis via Wnt/beta-catenin pathway in gastric cancer.We collected 21-paired GC and para-carcinoma tissue specimens, and the levels of TOB1-AS1 and lysosomal sialidase (NEU1) were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR. The protein expression levels of NEU1, beta-catenin, c-Myc, Cyclin D1, N-cadherin were determined via western blot. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry was performed to evaluate cell proliferation. Besides, GC cell migration and invasion capacities were identified by transwell assay. dual-luciferase reporter assay was employed to examine the interrelation between miR-23a and TOB1-AS1 or NEU1. Finally, the role of TOB1-AS1 was verified in vivo.The levels of TOB1-AS1 were decreased in GC tissues and cell lines. Either TOB1-AS1 or NEU1 upregulation accelerated GC cell apoptosis, hampered proliferation, migration, and invasion. Further, the role of TOB1- AS1 silencing on cell behaviors was abrogated by NEU1 upregulation. TOB1-AS1 and NEU1 exerted their roles via Wnt/beta-catenin signaling pathway. Overexpression of TOB1-AS1 blocked GC development in vivo. Mechanically, miR-23a was targeted by TOB1-AS1, but directly targeted NEU1.TOB1-AS1/miR-23a/NEU1 axis regulated proliferation, apoptosis, migration, and invasion of GC cells via Wnt/beta-catenin pathway, providing the evidence for serving TOB1- AS1 as an underlying therapeutic target in human GC treatment.	31799657	RID08033	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Pancreatic cancer	NBDY	KRAS	positively-E	shRNA	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);tumor growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000204272	GRCh38_X:56729241-56819179	ENSG00000133703	NA	550643	3845	LINC01420|NoBody	K-Ras4B|KRAS1|KRAS2	Long Non-coding RNA LINC01420 Contributes to Pancreatic Cancer Progression Through Targeting KRAS Proto-oncogene.In this study, we probed the role and latent mechanism of LINC01420 in PC.Several online tools were applied. Gene expression was evaluated by qRT-PCRor western blot. Both in vitro and in vivo assays were conducted to probe LINC01420 function in PC. ChIP, RIP, and luciferase reporter assays were performed to determine relationships between genes.The bioinformatics analyses revealed LINC01420 was highly expressed in PC tissues. Besides, LINC01420 was pronouncedly upregulated in PC cell lines and its depletion controlled PC cell proliferation and EMT in vitro and hindered tumor growth in vivo. Importantly, KRAS was proved to mediate LINC01420-facilitated PC cell proliferation. Further, we explained that KRAS transcription was regulated by MYC, while LINC01420 enhanced the binding of MYC to KRAS promoter in the nucleus of PC cells. Intriguingly, LINC01420 boosted MYC expression in the cytoplasm of PC cells by sponging miR-494-3p.This study illustrated that LINC01420 accelerates PC progression through releasing miR-494-3p-silenced MYC in cytoplasm and upregulating MYC-activated KRAS in nucleus, unveiling LINC01420 as a latent therapeutic strategy for PC patients.	31562613	RID08034	expression association	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE55807)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)
Pancreatic cancer	NBDY	MYC	positively-E	RPISeq;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);tumor growth(+)	ceRNA(miR-494-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000204272	GRCh38_X:56729241-56819179	ENSG00000136997	NA	550643	4609	LINC01420|NoBody	bHLHe39|c-Myc|MYCC	Long Non-coding RNA LINC01420 Contributes to Pancreatic Cancer Progression Through Targeting KRAS Proto-oncogene.In this study, we probed the role and latent mechanism of LINC01420 in PC.Several online tools were applied. Gene expression was evaluated by qRT-PCRor western blot. Both in vitro and in vivo assays were conducted to probe LINC01420 function in PC. ChIP, RIP, and luciferase reporter assays were performed to determine relationships between genes.The bioinformatics analyses revealed LINC01420 was highly expressed in PC tissues. Besides, LINC01420 was pronouncedly upregulated in PC cell lines and its depletion controlled PC cell proliferation and EMT in vitro and hindered tumor growth in vivo. Importantly, KRAS was proved to mediate LINC01420-facilitated PC cell proliferation. Further, we explained that KRAS transcription was regulated by MYC, while LINC01420 enhanced the binding of MYC to KRAS promoter in the nucleus of PC cells. Intriguingly, LINC01420 boosted MYC expression in the cytoplasm of PC cells by sponging miR-494-3p.This study illustrated that LINC01420 accelerates PC progression through releasing miR-494-3p-silenced MYC in cytoplasm and upregulating MYC-activated KRAS in nucleus, unveiling LINC01420 as a latent therapeutic strategy for PC patients.	31562613	RID08035	ceRNA or sponge	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Pancreatic cancer	NBDY	MYC	positively-E	TRRUST;RPISeq	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);tumor growth(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000204272	GRCh38_X:56729241-56819179	ENSG00000136997	NA	550643	4609	LINC01420|NoBody	bHLHe39|c-Myc|MYCC	Long Non-coding RNA LINC01420 Contributes to Pancreatic Cancer Progression Through Targeting KRAS Proto-oncogene.In this study, we probed the role and latent mechanism of LINC01420 in PC.Several online tools were applied. Gene expression was evaluated by qRT-PCRor western blot. Both in vitro and in vivo assays were conducted to probe LINC01420 function in PC. ChIP, RIP, and luciferase reporter assays were performed to determine relationships between genes.The bioinformatics analyses revealed LINC01420 was highly expressed in PC tissues. Besides, LINC01420 was pronouncedly upregulated in PC cell lines and its depletion controlled PC cell proliferation and EMT in vitro and hindered tumor growth in vivo. Importantly, KRAS was proved to mediate LINC01420-facilitated PC cell proliferation. Further, we explained that KRAS transcription was regulated by MYC, while LINC01420 enhanced the binding of MYC to KRAS promoter in the nucleus of PC cells. Intriguingly, LINC01420 boosted MYC expression in the cytoplasm of PC cells by sponging miR-494-3p.This study illustrated that LINC01420 accelerates PC progression through releasing miR-494-3p-silenced MYC in cytoplasm and upregulating MYC-activated KRAS in nucleus, unveiling LINC01420 as a latent therapeutic strategy for PC patients.	31562613	RID08036	expression association	NA	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE109761,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Colorectal cancer	REST	ITIH4-AS1	negatively-E	JASPAR;RNAi;overexpression;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000084093	NA	ENSG00000239799	GRCh38_3:52823935-52825314	5978	100873993	DFNA27|NRSF|XBR	NA	Long non-coding RNA ITIH4-AS1 accelerates the proliferation and metastasis of colorectal cancer by activating JAK/STAT3 signaling. Interestingly, a significant overexpression of ITIH4-AS1 was observed in CRC cell lines relative to normal NCM460 cells. Besides, we testified the facilitating role of ITIH4-AS1 in CRC cell growth and metastasis both in vitro and in vivo. Additionally, we explained that ITIH4-AS1 upregulation in CRC was attributed to downregulation or even depletion of REST, a presently identified transcriptional repressor for ITIH4-AS1. Meanwhile, the contribution of ITIH4-AS1 to CRC development was validated to rely on the activation of JAK/STAT3 pathway. More importantly, we verified that FUS interacted with both ITIH4-AS1 and STAT3, and that ITIH4-AS1 evoked nuclear translocation of p-STAT3 in CRC through recruiting FUS. To sum up, our findings unveiled for the first time that REST downregulation-enhanced ITIH4-AS1 exerts pro-tumor functions in CRC through FUS-dependent activation of JAK/STAT3 pathway, implying that targeting ITIH4-AS1 may be a novel effective strategy for CRC therapy.	31557619	RID08037	transcriptional regulation	metastasis	UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE111842)	
Colorectal cancer	ITIH4-AS1	FUS	positively-E	starBase;RNA pull-down assay;RIP;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);cell growth(+)	NA	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000239799	GRCh38_3:52823935-52825314	ENSG00000089280	NA	100873993	2521	NA	ALS6|FUS1|hnRNP-P2|HNRNPP2|TLS	Long non-coding RNA ITIH4-AS1 accelerates the proliferation and metastasis of colorectal cancer by activating JAK/STAT3 signaling. Interestingly, a significant overexpression of ITIH4-AS1 was observed in CRC cell lines relative to normal NCM460 cells. Besides, we testified the facilitating role of ITIH4-AS1 in CRC cell growth and metastasis both in vitro and in vivo. Additionally, we explained that ITIH4-AS1 upregulation in CRC was attributed to downregulation or even depletion of REST, a presently identified transcriptional repressor for ITIH4-AS1. Meanwhile, the contribution of ITIH4-AS1 to CRC development was validated to rely on the activation of JAK/STAT3 pathway. More importantly, we verified that FUS interacted with both ITIH4-AS1 and STAT3, and that ITIH4-AS1 evoked nuclear translocation of p-STAT3 in CRC through recruiting FUS. To sum up, our findings unveiled for the first time that REST downregulation-enhanced ITIH4-AS1 exerts pro-tumor functions in CRC through FUS-dependent activation of JAK/STAT3 pathway, implying that targeting ITIH4-AS1 may be a novel effective strategy for CRC therapy.	31557619	RID08038	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	DNMT1	ADAMTS9-AS2	negatively-E	siRNA	upregulation	qRT-PCR;sequencing	TCGA	NA	cell invasion(+)	DNA methylation	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000130816	NA	ENSG00000241684	GRCh38_3:64684909-65053439	1786	100507098	CXXC9|DNMT|MCMT	NA	Identification of lncRNAs associated with early-stage breast cancer and their prognostic implications.In this study, we performed RNA sequencing to identify long noncoding RNA expression profiles associated with early-stage breast cancer. RNA sequencing was performed on six invasive ductal carcinoma (IDC) tissues along with paired normal tissue samples, seven ductal carcinoma in situ tissues, and five apparently normal breast tissues. We identified 375 differentially expressed lncRNAs (DElncRNAs) in IDC tissues compared to paired normal tissues. Antisense transcripts (~ 58%) were the largest subtype among DElncRNAs. About 20% of the 375 DElncRNAs were supported by typical split readings leveraging their detection confidence. Validation was performed in n = 52 IDC and paired normal tissue by qRT-PCRfor the identified targets (ADAMTS9-AS2, EPB41L4A-AS1, WDFY3-AS2, RP11-295M3.4, RP11-161M6.2, RP11-490M8.1, CTB-92J24.3, and FAM83H-AS1). We evaluated the prognostic significance of DElncRNAs based on TCGA datasets and report that overexpression of FAM83H-AS1 was associated with patient poor survival. We confirmed that the downregulation of ADAMTS9-AS2 in breast cancer was due to promoter hypermethylation through in vitro silencing experiments and pyrosequencing.	30959550	RID08039	epigenetic regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)
Acute myeloid leukemia	MEG3	ALG9	positively-E	dual-luciferase reporter assay;RIP;immunofluorescence staining;siRNA	downregulation	qRT-PCR	NA	NA	chemoresistance(-);cell proliferation(+);cell growth(+)	ceRNA(miR-155)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000086848	NA	55384	79796	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	DIBD1	LncRNA MEG3 contributes to drug resistance in acute myeloid leukemia by positively regulating ALG9 through sponging miR- 155.qRT-PCRand western blot were used for comparison analyses of ALG9, MEG3, and miR-155 levels. CCK-8 and colony formation assays were determined for drug sensitivity and proliferative capability of AML cells. Luciferase reporter assay was used to confirm the targets of miR-155.The mannosyltransferase ALG9 and MEG3 was downregulated in peripheral blood mononuclear cells (PBMCs) of M5/multidrug resistance (MDR) AML patients and adriamycin (ADR)-resistant AML cell lines, which determined a positive correlation in AML patients. Low expression of ALG9 and MEG3 predicted poor prognosis of AML patients. The altered level of ALG9 was found corresponding to the drugresistant phenotype and sphere formation of AML cells. MiR-155 was overexpressed in M5/MDR patients and ADR-resistant AML cells, as well as inversely correlated to ALG9 expression. MEG3 was a direct target of miR-155 and could sponge miR-155 in AML cells. MEG3 interacted with miR-155 to regulate ALG9 expression, which reversed the effects of ALG9 regulation on proliferation and drug resistance in AML cells.MEG3 sponged miR-155 by competing endogenous RNA (ceRNA) mechanism, which further modulated ALG9 expression and AML procession, providing a novel therapeutic target for AML chemoresistance.	32359033	RID08040	ceRNA or sponge	chemoresistance,prognosis		DOWN(LIHC,PRAD,PAAD,SKCM);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495)
Non-small cell lung cancer	PVT1	SOX9	positively-E	starBase;dual-luciferase reporter assay;shRNA;RIP	upregulation	RT-qPCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-361-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000125398	NA	5820	6662	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CMD1|CMPD1|SRA1	Long non-coding RNA PVT1 contributes to cell growth and metastasis in non-small-cell lung cancer by regulating miR-361-3p/SOX9 axis and activating Wnt/beta-catenin signaling pathway.The expression levels of PVT1, sex determining region Y (SRY)-related high mobility group (HMG)-box9 (SOX9), and microRNA (miR)-361-3p in NSCLC tissues and cells were detected by quantitative real-time polymerase chain reaction (RT-qPCR). The protein levels of SOX9, beta-catenin, and c-Myc were detected by western blot assay. Cell proliferation, apoptosis, migration and invasion were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, transwell assays, severally. The interaction between miR-361-3p and PVT1 or SOX9was predicted by starBase, and then verified by the dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. PVT1 and SOX9 was highly expressed in NSCLC tumor tissues and cells. PVT1 facilitated proliferation, migration, invasion and hindered apoptosis of NSCLC cells. MiR-361-3p was a target of PVT1 in NSCLC cells. SOX9 acted as a target of miR-361-3p. PVT1 worked as a miR-361-3p sponge to regulate SOX9 expression. PVT1 modulate the Wnt/beta-catenin Signaling Pathway by miR-361-3p/SOX9 axis. Our studies disclosed that PVT1 boosted proliferation, migration, invasion and curbed apoptosis by miR-361-3p/SOX9 axis, providing the possible therapeutic strategy for NSCLC.	32197208	RID08041	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Head and neck squamous cell carcinoma	BLACAT1	PSEN1	positively-E	siRNA;western blot;immunofluorescence staining	upregulation	qRT-PCR	NA	NA	radiosensitivity(+);cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000080815	NA	101669762	5663	linc-UBC1|LINC00912|onco-lncRNA-30	AD3|FAD|PS1|S182	Knockdown of lncRNA BLACAT1 enhances radiosensitivity of head and neck squamous cell carcinoma cells by regulating PSEN1.BLACAT1 and PSEN1 expression in HNSCC tissues and cells were measured by qRT-PCR Kaplan-Meier method and Spearman Rank correlation analysis determined the prognostic roles and association of BLCAT1 and PSEN1 in HNSCC. The impacts of BLACAT1 and PSEN1, alone and in combination, on radiosensitivity of HNSCC cells were separately assessed through CCK-8, colony formation, flow cytometry, western blot and -GammaH2AX foci staining assays.Our study disclosed that BLACAT1 and PSEN1 were both in association with poor prognosis and radioresistance of HNSCC cells. BLACAT1 knockdown improved the radiosensitivity of HNSCC cells by changing cellular activities containing repressed cell viability, accelerated cell apoptosis, induced cell cycle arrest, and stimulated DNA damage response. Further, we found that PSEN1 was positively correlated with BLACAT1. Rescue assays confirmed that BLACAT1 regulated the radiosensitivity of HNSCC cells by modulating PSEN1.	31944856	RID08042	expression association	prognosis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung adenocarcinoma	HOXC-AS3	FOXM1	positively-E	shRNA;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000251151	GRCh38_12:53981509-53985519	ENSG00000111206	NA	100874365	2305	NA	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Long noncoding RNA HOXC-AS3 facilitates the progression of invasive mucinous adenocarcinomas of the lung via modulating FUS/FOXM1.The purpose of present study is to manifest HOXC-AS3-regulated inner mechanism in IMA development. It revealed that HOXCAS3 was highly expressed in IMA cells. Additionally, it was identified that the significant down-regulation of HOXC-AS3 obstructed cell proliferation and migration in IMA. As far as mechanism is concerned, it found that HOXC-AS3 recruited FUS to stabilize FOXM1 mRNA, accelerating IMA progression. Taken together, these data suggested that HOXC-AS3 may be recognized as a novel therapeutic target for patients with IMA or at least offer new views for molecular therapy.	31925650	RID08043	expression association	NA		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Head and neck squamous cell carcinoma	LINC00958	MYC	positively-E	siRNA;JASPAR;ChIP;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell viability(+);colony formation(+);radiosensitivity(-);chemosensitivity(-)	transcriptional regulation	binding/interaction	NA	Cisplatin	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000136997	NA	100506305	4609	NA	bHLHe39|c-Myc|MYCC	LINC00958-MYC positive feedback loop modulates resistance of head and neck squamous cell carcinoma cells to chemo- and radiotherapy in vitro. A cohort of 48 HNSCC vs normal tissues was collected for qRTPCR analysis of LINC00958 and c-Myc expression and statistical analyses. HNSCC cell lines were subjected to transfection with LINC00958 and c-Myc siRNAs or cDNA and their negative control siRNA or empty vector for qRT-PCR western blot, cell viability, colony formation, luciferase reporter, chromatin immunoprecipitation, and RNA immunoprecipitation assays.The data showed that LINC00958 expression was upregulated in HNSCC tissues and cell lines, upregulation of which was associated with poor tumor differentiation, advanced tumor stage, and shorter overall survival of patients. In vitro, LINC00958 expression induced HNSCC cell viability and colony formation, whereas knockdown of LINC00958 expression enhanced HNSCC cell sensitivity to ionizing radiation and cisplatin treatment. Mechanistically, LINC00958 is a direct target of c-Myc and can enhance the transcriptional activity of c-Myc, thus to form a positive feedback gene network in HNSCC cells, and in turn to modulate HNSCC cell resistance to chemo- and radiotherapy.This study demonstrated the LINC00958 interplay with c-Myc as a feedback loop facilitated HNSCC development and resistance to chemo- and radiotherapy. Targeting of such a network could be further evaluated as a novel therapeutic strategy for HNSCC patients.	31413594	RID08044	transcriptional regulation	chemoresistance	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	HULC	APOBEC3B	negatively-E	siRNA;western blot;Targetscan;microRNA;miRwalk;luciferase reporter assay	upregulation	RT-qPCR	TCGA	NA	cell growth(+)	ceRNA(miR-539)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000179750	NA	728655	9582	HCCAT1|LINC00078|NCRNA00078	FLJ21201|PHRBNL	Long non-coding RNA HULC activates HBV by modulating HBx/STAT3/ miR-539/APOBEC3B signaling in HBV-related hepatocellular carcinoma. Long noncoding RNA HULC is identified and highly expressed in hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) is a key driver of liver cancer. In the present study, we found that HULC remarkably elevated the levels of HBeAg, HBsAg, HBcAg, pgRNA, HBx, HBV DNA and covalently closed circular DNA (cccDNA), which activated the HBV replication in HBV-expressing hepatoma cells or de novo HBV-infected cell lines (PHH, HepG2- NTCP and dHepaRG). Mechanistically, HULC enhanced HBV cccDNA stability by down-regulating the APOBEC3B in hepatoma cells. HULC significantly up-regulated microRNA-539, which targeted the 3'UTR of APOBEC3B mRNA. Luciferase reporter gene assays revealed a putative STAT3-binding site located in the upstream of miR-539 promoter. Moreover, we identified that HULC was able to elevate HBx, which co-activated the STAT3 to stimulate the miR-539 promoter. Then, miR-539 down-regulated APOBEC3B and promoted HBV replication. Functionally, HULC enhanced the growth of hepatoma cells by activating HBV in vitro and in vivo, which could be blocked by overexpressing APOBEC3B. In conclusion, HULC activates HBV by modulating HBx/ STAT3/miR-539/APOBEC3B signaling in HBV-related HCC.	30981758	RID08045	ceRNA or sponge	NA		DOWN(LIHC,PRAD);UP(PAAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Hepatocellular carcinoma	OR3A4P	AGGF1	positively-E	siRNA;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);angiogenesis(+);cell proliferation(+);cell migration(+);cell invasion(+);AKT/mTOR signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180068	GRCh38_17:3309986-3311446	ENSG00000164252	NA	390756	55109	OR3A4	FLJ10283|GPATC7|GPATCH7|HSU84971|VG5Q	LncRNA OR3A4 participates in the angiogenesis of hepatocellular carcinoma through modulating AGGF1/akt/mTOR pathway.The upregulation of OR3A4 in HCC tissues and cell lines and its prognostic significance were first identified. Loss-of-function assays, including CCK-8, transwell and tube formation assay, validated OR3A4 as a promoter for HCC progression and angiogenesis. The association of OR3A4 and AGGF1 with HCC and poor prognosis was identified by qRT-PCRand Kaplan-Meier analysis. western blot and spearman's correlation curve verified the effect of OR3A4 on AGGF1 level and their positive association. Rescue assays revealed that OR3A4 promoted cancer progression and angiogenesis in HCC via AGGF1/akt/mTOR. Together, present study revealed OR3A4 as a novel prognostic target for HCC, which regulated tumor progression and angiogenesis through AGGF1/akt/ mTOR pathway.	30710550	RID08046	expression association	prognosis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Lung cancer	JPX	TWIST1	positively-E	dual-luciferase reporter assay;siRNA	upregulation	microarray;RT-qPCR	NA	NA	cell proliferation(+);WNT/beta-catenin signaling pathway(+);tumor growth(+);tumorigenesis(+);cell metastasis(+)	ceRNA(miR-362-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000122691	NA	554203	7291	DCBALD06|ENOX|LINC00183|NCRNA00183	ACS3|bHLHa38|BPES2|BPES3|CRS|CRS1|H-twist|SCS|TWIST	lncRNA JPX/miR-33a-5p/Twist1 axis regulates tumorigenesis and metastasis of lung cancer by activating Wnt/beta-catenin signaling. RT-qPCR and western blot were conducted to detect the expression levels of lncRNA JPX and Twist1 in lung cancer cell lines and tissues. The impact of JPX on Twist1 expression, cell growth, invasion, apoptosis, and in vivo tumor growth were investigated in lung cancer cells by western blot, rescue experiments, colony formation assay, flow cytometry, and xenograft animal experiment.We observed that lncRNA JPX was upregulated in lung cancer metastatic tissues and was closely correlated with tumor size and an advanced stage. Functionally, JPX promoted lung cancer cell proliferation in vitro and facilitated lung tumor growth in vivo. Additionally, JPX upregulated Twist1 by competitively sponging miR-33a- 5p and subsequently induced EMT and lung cancer cell invasion. Interestingly, JPX and Twist1 were coordinately upregulated in lung cancer tissues and cells. Mechanically, the JPX/miR-33a-5p/Twist1 axis participated in EMT progression by activating Wnt/beta-catenin signaling.These findings suggest that lncRNA JPX, a mediator of Twist1 signaling, could predispose lung cancer cells to metastasis and may serve as a potential target for targeted therapy.	31941509	RID08047	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827)	UP(SKCM);DATA(GSE38495)
Glioma	PAXIP1-DT	KIF14	positively-E	LncMAP;overexpression;shRNA;western blot;dual-luciferase reporter assay;RIP;UCSC;JASPAR;ChIP	upregulation	RT-qPCR	GSE104291	NA	angiogenesis(+);cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000273344	GRCh38_7:155003448-155005703	ENSG00000118193	NA	202781	9928	PAXIP1-AS1	KIAA0042	Long non-coding RNA PAXIP1-AS1 facilitates cell invasion and angiogenesis of glioma by recruiting transcription factor ETS1 to upregulate KIF14 expression.Firstly, we identified differentially expressed lncRNA PAXIP1-AS1 as associated with glioma based on bioinformatic data. Then, validation experiments were conducted to confirm a high expression level of lncRNA PAXIP1-AS1 in glioma tissues and cells, accompanied by upregulated KIF14. We further examined the binding between lncRNA PAXIP1-AS1, KIF14 promoter activity, and transcription factor ETS1. Next, overexpression vectors and shRNAs were delivered to alter the expression of lncRNA PAXIP1-AS1, KIF14, and ETS1 to analyze their effects on glioma progression in vivo and in vitro.LncRNA PAXIP1-AS1 was mainly distributed in the nucleus of glioma cells. LncRNA PAXIP1-AS1 could upregulate the KIF14 promoter activity by recruiting transcription factor ETS1. Overexpression of lncRNA PAXIP1-AS1 enhanced migration, invasion, and angiogenesis of human umbilical vein endothelial cells in glioma by recruiting the transcription factor ETS1 to upregulate the expression of KIF14, which was further confirmed by accelerated tumor growth in nude mice. The key findings of this study highlighted the potential of the lncRNA PAXIP1-AS1/ETS1/KIF14 axis as a therapeutic target for glioma treatment, due to its role in controlling the migration and invasion of glioma cells and its angiogenesis.	31823805	RID08048	expression association	NA		UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Colorectal cancer	BFAL1	RHEB	positively-E	shRNA;luciferase reporter assay;Targetscan;RNAhybrid	upregulation	qPCR	GSE20916;GSE31737;GSE129950;GSE130152	NA	tumor growth(+);cell proliferation(+);mTOR signaling pathway(+)	ceRNA(miR-155-5p,miR-200a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000106615	NA	NA	6009	NA	RHEB2	Long noncoding RNA BFAL1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal cancer via the RHEB/ mTOR pathway. In the present study, we revealed the mechanism by which a lncRNA participates in gut bacteria-induced carcinogenesis: Bacteroides fragilis-associated lncRNA1 (BFAL1) in CRC tissues mediates ETBF carcinogenesis. BFAL1 was highly expressed in CRC tissues compared with that in adjacent normal tissues. In vitro, BFAL1 was upregulated in ETBF-treated CRC cells. Mechanistically, ETBF promoted tumor growth via BFAL1 by activating the Ras homolog, which is the MTORC1 binding/mammalian target of the rapamycin (RHEB/mTOR) pathway. Furthermore, BFAL1 regulated RHEB expression by competitively sponging microRNAs miR-155-5p and miR- 200a-3p. Clinically, both high expression of BFAL1 and high abundance of ETBF in CRC tissues predicted poor outcomes for patients with CRC. Thus, BFAL1 is a mediator of ETBF-induced carcinogenesis and may be a potential therapeutic target for ETBF-induced CRC.	31515468	RID08049	ceRNA or sponge	NA		UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Cervical cancer	SP1	POU3F3	positively-E	RegRNA;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	PCG	lncRNA	ENSG00000185591	NA	ENSG00000198914	GRCh38_2:104853287-104858574	6667	5455	NA	BRN1|OTF8	SP1-mediated long noncoding RNA POU3F3 accelerates the cervical cancer through miR-127-5p/FOXD1. POU3 F3 was validated to be up-regulated in the cervical cancer tissue specimens and cells comparing with normal controls. Moreover, the ectopic overexpression of POU3 F3 was closely correlated with poor prognosis. In vitro, POU3 F3 promoted the proliferation, invasion of cervical cancer cells. In vivo, POU3 F3 knockdown repressed the tumor growth of cervical cancer cells. The transcriptional expression of POU3 F3 was activated by the transcription factor SP1. Mechanically, POU3 F3 acted as the sponge to target miR-127-5p, while miR-127-5p bind with the 3'- UTR of FOXD1 gene. In conclusion, our data verifies that lncRNA POU3 F3, induced by transcription factor SP1, acts as an oncogene in the cervical cancer tumorigenesis via regulating miR-127-5p/FOXD1 axis, providing a possible therapeutic target for cervical cancer.	31252264	RID08050	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Cervical cancer	POU3F3	FOXD1	positively-E	Targetscan;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-127-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000198914	GRCh38_2:104853287-104858574	ENSG00000251493	NA	5455	2297	BRN1|OTF8	FKHL8|FREAC4	SP1-mediated long noncoding RNA POU3F3 accelerates the cervical cancer through miR-127-5p/FOXD1. POU3 F3 was validated to be up-regulated in the cervical cancer tissue specimens and cells comparing with normal controls. Moreover, the ectopic overexpression of POU3 F3 was closely correlated with poor prognosis. In vitro, POU3 F3 promoted the proliferation, invasion of cervical cancer cells. In vivo, POU3 F3 knockdown repressed the tumor growth of cervical cancer cells. The transcriptional expression of POU3 F3 was activated by the transcription factor SP1. Mechanically, POU3 F3 acted as the sponge to target miR-127-5p, while miR-127-5p bind with the 3'- UTR of FOXD1 gene. In conclusion, our data verifies that lncRNA POU3 F3, induced by transcription factor SP1, acts as an oncogene in the cervical cancer tumorigenesis via regulating miR-127-5p/FOXD1 axis, providing a possible therapeutic target for cervical cancer.	31252264	RID08051	ceRNA or sponge	prognosis		UP(BRCA);DATA(GSE55807)
Malignant glioma	SP1	CASC11	positively-E	JASPAR;RegRNA;ChIP;luciferase reporter assay	upregulation	RT-PCR	TCGA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000185591	NA	ENSG00000249375	GRCh38_8:127686343-127738987	6667	100270680	NA	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	SP1 induced lncRNA CASC11 accelerates the glioma tumorigenesis through targeting FOXK1 via sponging miR-498. In this work, we found that lncRNA CASC11 was significantly up-regulated in the glioma specimens and cells, and the ectopic overexpression indicated the poor prognosis of glioma patients. CASC11 expression could be activated by the transcription factor SP1. In vivo and vitro, the knockdown of CASC11 impaired the proliferation, migration and tumor growth of glioma cells. In mechanical experiments, the miR-498 was found to target the 3'-UTR of lncRNA CASC11 and FOXK1 mRNA. Taken together, the data suggest the regulation of SP1/ CASC11/miR-498/FOXK1 in the gliomagenesis, which might provide a potential therapeutic strategy for glioma.	31121483	RID08052	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC);DATA(GSE117623)
Malignant glioma	CASC11	FOXK1	positively-E	starBase;luciferase reporter assay;siRNA;western blot	upregulation	RT-PCR	TCGA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);cell growth(+)	ceRNA(miR-498)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000164916	NA	100270680	221937	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	IMAGE:5164497	SP1 induced lncRNA CASC11 accelerates the glioma tumorigenesis through targeting FOXK1 via sponging miR-498. In this work, we found that lncRNA CASC11 was significantly up-regulated in the glioma specimens and cells, and the ectopic overexpression indicated the poor prognosis of glioma patients. CASC11 expression could be activated by the transcription factor SP1. In vivo and vitro, the knockdown of CASC11 impaired the proliferation, migration and tumor growth of glioma cells. In mechanical experiments, the miR-498 was found to target the 3'-UTR of lncRNA CASC11 and FOXK1 mRNA. Taken together, the data suggest the regulation of SP1/ CASC11/miR-498/FOXK1 in the gliomagenesis, which might provide a potential therapeutic strategy for glioma.	31121483	RID08053	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Ovarian cancer	UNC5B-AS1	NDRG2	negatively-E	western blot;ChIP;RNA pull-down assay;shRNA	upregulation	RT-qPCR	TCGA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000237512	GRCh38_10:71217220-71218294	ENSG00000165795	NA	728978	57447	UASR1	SYLD	UNC5B-AS1 promoted ovarian cancer progression by regulating the H3K27me on NDRG2 via EZH2.This study is proposed to investigate the function and mechanism of UNC5B-AS1 in OC. UNC5B-AS1 expression in OC samples was obtained from gene expression profiling interactive analysis (GEPIA) based on The Cancer Genome Atlas data. Gene expressions were detected by quantitative real-time polymerase chain reaction (RT-qPCR) and western blot. Biological functions of UNC5B-AS1 were assessed by cell counting kit-8, colony formation, and caspase-3 analysis. GEPIA revealed the UNC5B-AS1 upregulation in OC samples. RT-qPCR assay confirmed the upregulation of UNC5B-AS1 in OC cells. Functionally, depletion of UCN5B-AS1 hindered proliferation and prompted apoptosis in OC cells. Mechanistically, we found that UNC5B-AS1 interacted with zeste 2 polycomb repressive complex 2 subunit (EZH2) to trigger trimethylation of histone H3 at lysine 27 (H3K27me3) on N-myc downstream regulated gene-2 (NDRG2) promoter and epigenetically repressed NDRG2. Rescue assay indicated the participation of NDRG2 in the regulation of UNC5B-AS1 on OC progression. Together, we first illustrated that UNC5B-AS1 promoted OC progression by regulating the H3K27me on NDRG2 via EZH2, indicating UNC5B-AS1 as a potential molecular target for OC treatment.	31903696	RID08054	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(NSCLC);DATA(GSE117623,GSE74639,GSE104209,GSE51827,GSE55807,GSE86978)
Renal cell carcinoma	NONHSAT113026	NFKB1	negatively-E	immunohistochemistry;IntaRNA;luciferase reporter assay	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);tumorigenesis(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000207587	GRCh38_14:101048658-101048748	ENSG00000109320	NA	664613	4790	hsa-mir-544|MIR544|MIRN544	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	LncRNA NONHSAT113026 represses renal cell carcinoma tumorigenesis through interacting with NF-kB/p50 and SLUG.The expression level of NOAT113026 was estimated by qPCR from 76 pairs of RCC and non-tumor (NT) samples. The correlation between NOAT113026 and clinical data of RCC patients was analyzed. NOAT113026 was overexpressed in 786-O and ACHN cell lines by lentivirusmediated technology and the oncological behavioral changes of RCC cells were observed along with tumorigenicity in experimental nude mice. Compared to the adjacent tissues, NOAT113026 was noticeably downregulated in RCC. Survival analysis showed that the lower the expression level of NOAT113026 was, the shorter the disease-free survival and overall survival in RCC would be. Overexpression of NOAT113026 can decrease the ability of cell migration, invasion, proliferation, and colony formation by regulating NF-kB/p50 and SLUG through a mechanism that involves lncRNA-mRNA interactions. In conclusion, our data suggest that NOAT113026 could be a carcinostatic RNA in RCC, which may serve as a potential prognostic factor and a promising therapeutic target for malignant RCC.	31545257	RID08055	transcriptional regulation	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Renal cell carcinoma	NONHSAT113026	SNAI2	negatively-E	immunohistochemistry;IntaRNA;luciferase reporter assay	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+);tumorigenesis(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000207587	GRCh38_14:101048658-101048748	ENSG00000019549	NA	664613	6591	hsa-mir-544|MIR544|MIRN544	SLUG|SLUGH|SLUGH1|SNAIL2	LncRNA NONHSAT113026 represses renal cell carcinoma tumorigenesis through interacting with NF-kB/p50 and SLUG.The expression level of NOAT113026 was estimated by qPCR from 76 pairs of RCC and non-tumor (NT) samples. The correlation between NOAT113026 and clinical data of RCC patients was analyzed. NOAT113026 was overexpressed in 786-O and ACHN cell lines by lentivirusmediated technology and the oncological behavioral changes of RCC cells were observed along with tumorigenicity in experimental nude mice. Compared to the adjacent tissues, NOAT113026 was noticeably downregulated in RCC. Survival analysis showed that the lower the expression level of NOAT113026 was, the shorter the disease-free survival and overall survival in RCC would be. Overexpression of NOAT113026 can decrease the ability of cell migration, invasion, proliferation, and colony formation by regulating NF-kB/p50 and SLUG through a mechanism that involves lncRNA-mRNA interactions. In conclusion, our data suggest that NOAT113026 could be a carcinostatic RNA in RCC, which may serve as a potential prognostic factor and a promising therapeutic target for malignant RCC.	31545257	RID08056	transcriptional regulation	prognosis		
Ovarian cancer	LINC00511	CDKN1A	negatively-E	RIP;ChIP	upregulation	sequencing;microarray;qRT-PCR	GTEx;TCGA;GSE10971; GSE29450; GSE54388	NA	cell proliferation(+);colony formation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000124762	NA	400619	1026	onco-lncRNA-12	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	An integrated analysis reveals the oncogenic function of lncRNA LINC00511 in human ovarian cancer. In this study, we found hundreds of dysregulated lncRNAs in ovarian cancer by performing genome-wide analysis using RNA sequencing data from Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) project, and three microarray datasets from Gene Expression Omnibus (GEO). Moreover, our results revealed that up- or down-regulation of some lncRNAs expression in ovarian cancer is accompanied by their genomic loci copy number amplification or deletion. Importantly, some lncRNAs expression levels are significantly associated with ovarian cancer patients'-poor prognosis. Further experimental validation and mechanistic investigation indicate that LINC00511 exerts oncogenic function in ovarian cancer cells through interacting with EZH2 and repressing P21 expression. Taken together, the findings in the current study may provide a useful resource of novel ovarian cancer associated lncRNAs and potential diagnostic biomarker and therapeutic targets for ovarian cancer.	31016892	RID08057	expression association	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Malignant glioma	SP1	LINC00511	positively-E	JASPAR;ChIP;luciferase reporter assay	upregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	TF	lncRNA	ENSG00000185591	NA	ENSG00000227036	GRCh38_17:72290091-72640472	6667	400619	NA	onco-lncRNA-12	Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR-124-3p/CCND2 axis. Results indicated that LINC00511 was up-regulated in glioma tissues and cell lines, moreover its overexpression positively correlated with the poor prognosis and advanced pathological stages. For the upstream regulation, LINC00511 was epigenetically up-regulated by transcription factor specificity protein 1 (SP1). Gain and loss of functional experiments demonstrated that LINC00511 promoted the proliferation and invasion of glioma cells in vitro. The knockdown of LINC00511 repressed the tumour growth in vivo. Mechanistically, LINC00511 positively regulated the CCND2 expression via competitively sponging with miR-124-3p. Overall, our finding illuminates that LINC00511 is induced by SP1 and accelerates the glioma progression through targeting miR-124-3p/CCND2 axis, constructing the SP1/LINC00511/miR-124-3p/CCND2 axis.	30973678	RID08058	transcriptional regulation	prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)
Malignant glioma	LINC00511	CCND2	positively-E	lncLocator;starBase;siRNA;luciferase reporter assay	upregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000118971	NA	400619	894	onco-lncRNA-12	NA	Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR-124-3p/CCND2 axis. Results indicated that LINC00511 was up-regulated in glioma tissues and cell lines, moreover its overexpression positively correlated with the poor prognosis and advanced pathological stages. For the upstream regulation, LINC00511 was epigenetically up-regulated by transcription factor specificity protein 1 (SP1). Gain and loss of functional experiments demonstrated that LINC00511 promoted the proliferation and invasion of glioma cells in vitro. The knockdown of LINC00511 repressed the tumour growth in vivo. Mechanistically, LINC00511 positively regulated the CCND2 expression via competitively sponging with miR-124-3p. Overall, our finding illuminates that LINC00511 is induced by SP1 and accelerates the glioma progression through targeting miR-124-3p/CCND2 axis, constructing the SP1/LINC00511/miR-124-3p/CCND2 axis.	30973678	RID08059	ceRNA or sponge	prognosis	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Breast cancer	TALAM1	MALAT1	positively-F	RIP	upregulation	ddPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	109136579	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	An antisense transcript mediates MALAT1 response in human breast cancer.Here using a collection of breast cancer cells and in vitro and in vivo migration assays we characterized the dynamics of expression and demonstrated that TALAM1 regulates and synergizes with MALAT1 during tumorigenesis.Down-regulation of TALAM1 was shown to greatly impact on the capacity of breast cancer cells to migrate in vitro or to populate the lungs of immunocompromised mice. Additionally, we demonstrated that TALAM1 cooperates with MALAT1 in the regulation of the properties guiding breast cancer aggressiveness and malignancy.By characterizing this sense/anti-sense pair we uncovered the complexity of MALAT1 locus regulation, describing new potential candidates for cancer targeting.	31382922	RID08060	expression association	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Oral squamous cell carcinoma	TUG1	DLX1	positively-E	dual-luciferase reporter assay;western blot;RIP;RegRNA;starBase;Targetscan;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-524-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000144355	NA	55000	1745	FLJ20618|LINC00080|NCRNA00080	NA	Long noncodingRNATUG1regulates the development of oral squamous cell carcinoma through sponging miR-524-5p to mediate DLX1 expression as a competitive endogenous RNA.LncRNA TUG1 expression remains high in oral squamous cell carcinoma (OSCC) tissues.In this study, TUG1 expression in OSCC cells was detected by quantitative real-time polymerase chain reaction. Proliferative and migratory potentials of OSCC cells were determined by Cell Counting Kit 8, 5-Ethynyl-2'- deoxyuridine (EdU), and Transwell assay, respectively. We identified the potential target of TUG1 through bioinformatics and dual-luciferase reporter gene assay. Furthermore, their interaction and functions in regulating the development of OSCC were clarified by western blot and RNA immunoprecipitation assay. Our results demonstrated a high expression of TUG1 in OSCC cells. Overexpression of TUG1 markedly accelerated proliferative and migratory potentials of OSCC cells. Besides, TUG1 could positively regulate the expression of distal-less homeobox 1 (DLX1) by competing with miR-524-5p. These results indicated that TUG1 participated in the development of OSCC as a competing endogenous RNA to competitively bind to miR-524-5p and thus mediate DLX1 expression.	30980391	RID08061	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	
Hepatocellular carcinoma	MACC1-AS1	TGFB1	positively-E	siRNA;IntaRNA	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-663)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228598	GRCh38_7:20141916-20153531	ENSG00000105329	NA	100874041	7040	NA	CED|DPD1|TGFB|TGFbeta	Long Non-Coding RNA MACC1-AS1 Is Involved in Distant Recurrence of Hepatocellular Carcinoma After Surgical Resection.Measurement of preoperative plasma levels of MACC1-AS1 was performed by qPCR, and the comparison between the HCC and Control group was performed by unpaired t test. The overexpression of TGF-b1 in SNU-182 and SNU-398 cells was confirmed by qPCR.MACC1-AS1 was overexpressed in HCC patients. In comparison to pretreatment level, distant recurrence (DR) was accompanied by increased levels of MACC1-AS1 in plasma, but this phenomenon was not observed in cases of local recurrence (LR) or non-recurrence (NR). In HCC cells, MACC1-AS1 positively regulated the expression of TGF-b1. MACC1-AS1 overexpression resulted in increased invasion and migration rates of HCC cells, while siRNA silencing resulted in reduced rates. Moreover, TGF-b1 overexpression reduced the effects of MACC1-AS1 siRNA silencing.MACC1-AS1 is involved in the distant recurrence of HCC, and its actions are possibly mediated by TGF-b1.	32267834	RID08062	ceRNA or sponge	recurrence		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	LINC01354	ATF1	positively-E	RNA pull-down assay;Targetscan;luciferase reporter assay	upregulation	qRT-PCR	TCGA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-340-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000231768	GRCh38_1:234527887-234531803	ENSG00000123268	NA	100506795	466	NA	TREB36	LINC01354 enhances the proliferation and invasion of lung cancer cells by regulating miR-340-5p/ATF1 signaling pathway.In the current study, our results showed that LINC01354 was significantly increased in NSCLC tissues and cell lines. High LINC01354 expression was associated with advanced TNM stage and poor prognosis in NSCLC patients. Loss-of-function assays revealed that knockdown of LINC01354 reduced lung cancer cells proliferation and invasive ability in vitro. Subsequently, mechanism studies showed that LINC01354 positively regulated the ATF1 expression via competitive binding to miR-340-5p. Therefore, our results illustrated that LINC01354 might act as an oncogenic role by modulating the miR-340-5p/ ATF1 axis, providing a novel therapeutic therapy for NSCLC treatment.	31538498	RID08063	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Nasopharynx carcinoma	LINC00520	USP39	positively-E	lncRNAtor;RNA pull-down assay;dual-luciferase reporter assay;Targetscan;shRNA	upregulation	qRT-PCR	TCGA	NA	cell growth(+)	ceRNA(miR-26b-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000258791	GRCh38_14:55781132-55796731	ENSG00000168883	NA	645687	10713	C14orf34|LASSIE	CGI-21|SAD1|SNRNP65	Long non-coding RNA 520 is a negative prognostic biomarker and exhibits pro-oncogenic function in nasopharyngeal carcinoma carcinogenesis through regulation of miR-26b-3p/USP39 axis.In present study, we aims to investigate the role and mechanism of LINC00520 in the NPC carcinogenesis. Results indicated that LINC00520 was significantly increasing in NPC tissues and cells in comparison to their corresponding controls. Moreover, the aberrant overexpression of LINC00520 indicated the poor prognosis of NPC patients. Silence of LINC00520 was able to repress NPC cell growth in vitro while overexpression of LINC00520 inversed this process. Moreover, in vivo tumor xenografts were establishing using CNE-1/SUNE-1 cells to investigate the function of LINC00520 in NPC tumorigenesis. Rescue assay was conducting to further confirm that LINC00520 contributed to NPC progression by regulating miR-26b-3p/ubiquitin-specific protease 39 (USP39) signal pathway. Taken together, our study discovered the oncogenic role of LINC00520 in clinical specimens and cellular experiments, showing the potential LINC00520/ miR-26b-3p/USP39 pathway. This results and findings provide a novel insight for NPC tumorigenesis.	30898716	RID08064	ceRNA or sponge	prognosis	UP(LIHC,PRAD,SKCM);DATA(GSE117623,GSE104209,GSE38495)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE111842)
Colorectal cancer	E2F1	AP002754.2	positively-E	Cistrome;JASPAR;ChIP;luciferase reporter assay	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell growth(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000101412	NA	NA	NA	1869	NA	E2F-1|RBAP1|RBBP3|RBP3	NA	Risk SNP-mediated enhancer-promoter interaction drives colorectal cancer through both FADS2 and AP002754.2. Here we first performed a comprehensive expression quantitative trait loci (eQTL) analysis in CRC tissues adjusted for multiple confounders to test the determinants of germline variants in established GWAS susceptibility loci on mRNA and long non-coding RNA (lncRNA) expression. Combining integrative functional genomic/epigenomic analyses and a large-scale population study consisting of 6,024 cases and 10,022 controls, we then prioritized rs174575 with a C>G change as a potential causal candidate for CRC at 11q12.2, as its G allele was associated with an increased risk of CRC (OR = 1.26, 95%CI = 1.17-1.36, P = 2.57X10-9). rs174575 acted as an allele-specific enhancer to distally facilitate expression of both FADS2 and lncRNA AP002754.2 via long-range enhancer-promoter interaction loops, which were mediated by E2F1. AP002754.2 further activated a transcriptional activator that upregulated FADS2 expression. FADS2, in turn, was overexpressed in CRC tumor tissues and functioned as a potential oncogene that facilitated CRC cell proliferation and xenograft growth in vitro and in vivo by increasing the metabolism of PGE2, an oncogenic molecule involved in CRC tumorigenesis. Our findings represent a novel mechanism by which a non-coding variant can facilitate long-range genome interactions to modulate the expression of multiple genes including not only mRNA, but also lncRNA, which provides new insights into the understanding of CRC etiology.	32127356	RID08065	transcriptional regulation	NA	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)	
Colorectal cancer	AP002754.2	RAPSN	positively-E	overexpression;knockdown	upregulation	qPCR	TCGA	NA	cell proliferation(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000165917	NA	NA	5913	NA	CMS11|CMS4C|FADS|FADS2|RAPSYN|RNF205	Risk SNP-mediated enhancer-promoter interaction drives colorectal cancer through both FADS2 and AP002754.2. Here we first performed a comprehensive expression quantitative trait loci (eQTL) analysis in CRC tissues adjusted for multiple confounders to test the determinants of germline variants in established GWAS susceptibility loci on mRNA and long non-coding RNA (lncRNA) expression. Combining integrative functional genomic/epigenomic analyses and a large-scale population study consisting of 6,024 cases and 10,022 controls, we then prioritized rs174575 with a C>G change as a potential causal candidate for CRC at 11q12.2, as its G allele was associated with an increased risk of CRC (OR = 1.26, 95%CI = 1.17-1.36, P = 2.57X10-9). rs174575 acted as an allele-specific enhancer to distally facilitate expression of both FADS2 and lncRNA AP002754.2 via long-range enhancer-promoter interaction loops, which were mediated by E2F1. AP002754.2 further activated a transcriptional activator that upregulated FADS2 expression. FADS2, in turn, was overexpressed in CRC tumor tissues and functioned as a potential oncogene that facilitated CRC cell proliferation and xenograft growth in vitro and in vivo by increasing the metabolism of PGE2, an oncogenic molecule involved in CRC tumorigenesis. Our findings represent a novel mechanism by which a non-coding variant can facilitate long-range genome interactions to modulate the expression of multiple genes including not only mRNA, but also lncRNA, which provides new insights into the understanding of CRC etiology.	32127356	RID08066	expression association	NA		UP(PAAD);DATA(GSE40174)
Gastric cancer	LOXL1-AS1	USF1	positively-E	starBase;RNA pull-down assay;luciferase reporter assay;RIP;shRNA	upregulation	RT-qPCR	NA	NA	tumorigenesis(+);cell stemness(+);cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+);cell growth(+)	ceRNA(miR-708-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000158773	NA	100287616	7391	NA	FCHL|FCHL1|HYPLIP1|MLTF|MLTFI|UEF|bHLHb11	LncRNA LOXL1-AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR-708-5p/USF1 pathway.RT-qPCR was performed to measure the expression pattern of LOXL1-AS1 in gastric cancer. To ascertain its definite role, CCK-8, EdU, western blot, transwell and sphere formation assays were adopted. RNA pull-down, RIP, ChIP and luciferase reporter assays were carried out to investigate the molecular mechanism of LOXL1-AS1 in gastric carcinoma.LOXL1-AS1 was highly expressed in tissues and cells of gastric cancer. The upregulation of LOXL1-AS1 predicted poor prognosis in gastric carcinoma. Our findings demonstrated that LOXL1-AS1 accelerated the deterioration of gastric cancer by inducing cell proliferation, migration, EMT and stemness. Moreover, the expression of USF1 in gastric cancer was higher than in normal control and LOXL1-AS1 negatively modulated USF1. Functionally, LOXL1-AS1 acted as a ceRNA to upregulate USF1 via sponging miR-708-5p. Besides, we confirmed USF1 promoted the transcription of stemness marker SOX2. Rescue experiments testified the stimulative role of LOXL1- AS1/miR-708-5p/USF1 pathway in gastric cancer progression. It was also validated that LOXL1-AS1 facilitated cell growth of gastric carcinoma in vivo.Our study unravelled that LOXL1-AS1/miR-708-5p/USF1 pathway contributed to the development of gastric cancer.	31468594	RID08067	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	MINCR	ZEB1	positively-E	dual-luciferase reporter assay;RNA pull-down assay;FISH;starBase	upregulation	RT-qPCR	NA	NA	radiosensitivity(-);PI3K/AKT signaling pathway(+)	ceRNA(miR-223)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000253716	GRCh38_8:143280158-143281692	ENSG00000148516	NA	100507316	6935	LINC01604|TCONS_00015189	AREB6|BZP|FECD6|NIL-2-A|PPCD3|TCF8|ZEB|Zfhep|Zfhx1a	LncRNA MINCR regulates irradiation resistance in nasopharyngeal carcinoma cells via the microRNA-223/ZEB1 axis. The interactions among MINCR, miR-223 and ZEB1 were verified via dual luciferase reporter gene assay, RNA pull-down and FISH assays. The gain- and loss-of-functions were performed to explore their effects on NPC cell viability, apoptosis and radiosensitivity. Levels of MINCR, miR-223, ZEB1, and AKT/PI3K-related proteins were detected after different treatments. An in vivo analysis was carried out in nude mice. Consequently, MINCR was upregulated in NPC, and linked with worse prognosis and radiotherapy efficacy. MINCR intervention weakened NPC cell radioresistance. MINCR sponged miR-223 to regulate ZEB1. Inactivating AKT eliminated the increased radioresistance of CNE2 cells induced by overexpressing MINCR. Briefly, MINCR diminished NPC cell radiosensitivity by sponging miR- 223, increasing ZEB1 and activating the AKT/PI3K axis. This study may offer novel insight for NPC treatment.	31760895	RID08068	ceRNA or sponge	prognosis	DOWN(PRAD,BRCA);UP(BRCA);DATA(GSE104209,GSE111842,GSE55807)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	SNHG7	DKK1	positively-E	western blot;shRNA;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000107984	NA	84973	22943	MGC16037|NCRNA00061	DKK-1|SK	Long Noncoding RNA SNHG7 Activates Wnt/b-Catenin Signaling Pathway in Cervical Cancer Cells by Epigenetically Silencing DKK1.The levels of SNHG7 in CC cells were reflected by quantitative real-time polymerase chain reaction. The functions of SNHG7 on CC tumorigenesis were explored by colony formation, CCK-8 (Cell Counting Kit-8), EdU (ethynyl deoxyuridine), and western blot assays. The influences of SNHG7 depletion on the binding of EZH2 to DKK1 promoter and H3K27me3 occupancy in DKK1 promoter were studied by chromatin immunoprecipitation assay.SNHG7 was conspicuously higher expressed in CC cells. Knockdown of SNHG7 was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution of SNHG7 to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed that SNHG7 silencing weakened the binding of EZH2 to DKK1 promoter as well as the occupancy of H3K27me3 in DKK1 promoter.SNHG7 epigenetically silences DKK1 to exacerbate the malignancy of CC via Wnt/b-catenin signaling pathway.	32275170	RID08069	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Cervical cancer	SNHG7	EZH2	negatively-F	shRNA;RIP;RNA pull-down assay;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	colony formation(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000106462	NA	84973	2146	MGC16037|NCRNA00061	ENX-1|EZH1|KMT6|KMT6A	Long Noncoding RNA SNHG7 Activates Wnt/b-Catenin Signaling Pathway in Cervical Cancer Cells by Epigenetically Silencing DKK1.The levels of SNHG7 in CC cells were reflected by quantitative real-time polymerase chain reaction. The functions of SNHG7 on CC tumorigenesis were explored by colony formation, CCK-8 (Cell Counting Kit-8), EdU (ethynyl deoxyuridine), and western blot assays. The influences of SNHG7 depletion on the binding of EZH2 to DKK1 promoter and H3K27me3 occupancy in DKK1 promoter were studied by chromatin immunoprecipitation assay.SNHG7 was conspicuously higher expressed in CC cells. Knockdown of SNHG7 was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution of SNHG7 to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed that SNHG7 silencing weakened the binding of EZH2 to DKK1 promoter as well as the occupancy of H3K27me3 in DKK1 promoter.SNHG7 epigenetically silences DKK1 to exacerbate the malignancy of CC via Wnt/b-catenin signaling pathway.	32275170	RID08070	expression association	NA	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Cervical cancer	MYC	PVT1	positively-E	immunohistochemistry;ISH	upregulation	qRT-PCR	TANRIC	NA	cell proliferation(+);cell viability(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000249859	GRCh38_8:127794526-128187101	4609	5820	bHLHe39|c-Myc|MYCC	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	C-Myc-activated long non-coding RNA PVT1 enhances the proliferation of cervical cancer cells by sponging miR-486-3p.Our study is designed to demonstrate the regulatory network involving c-Myc and lncRNA-PVT1 in cervical cancer. qRT-PCRand western blot assays were performed in our research to estimate the expression levels of RNA and proteins. CCK8 assays were applied to demonstrate the viability of HeLa and SiHa cells. Immunofluorescence assay was then used to investigate the colocalization of lncRNA-PVT1 and miR-486-3p. Binding of c-Myc to the promoter region of PVT1 was identified by CHIP-assay. Functionally, upregulation of lncRNAPVT1 enhanced the proliferation and viability of cervical cancer cells. Mechanistically, lncRNA-PVT1 sponged miR-486-3p and released its repression of ECM1. Besides, c- Myc functioned as an activator of lncRNA-PVT1 and upregulated its expression by binding to the promoter of PVT1 in cervical cancer cells. LncRNA-PVT1 was upregulated by c-Myc and thus enhanced the proliferation of cervical cancer cells by sponging miR-486-3p.	31943014	RID08071	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Cervical cancer	PVT1	ECM1	positively-E	western blot;miRcode;RNAhybrid;RNA pull-down assay;luciferase reporter assay;immunofluorescence;shRNA	upregulation	qRT-PCR	TANRIC	NA	cell proliferation(+);cell viability(+)	ceRNA(miR-486-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000143369	NA	5820	1893	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	C-Myc-activated long non-coding RNA PVT1 enhances the proliferation of cervical cancer cells by sponging miR-486-3p.Our study is designed to demonstrate the regulatory network involving c-Myc and lncRNA-PVT1 in cervical cancer. qRT-PCRand western blot assays were performed in our research to estimate the expression levels of RNA and proteins. CCK8 assays were applied to demonstrate the viability of HeLa and SiHa cells. Immunofluorescence assay was then used to investigate the colocalization of lncRNA-PVT1 and miR-486-3p. Binding of c-Myc to the promoter region of PVT1 was identified by CHIP-assay. Functionally, upregulation of lncRNAPVT1 enhanced the proliferation and viability of cervical cancer cells. Mechanistically, lncRNA-PVT1 sponged miR-486-3p and released its repression of ECM1. Besides, c- Myc functioned as an activator of lncRNA-PVT1 and upregulated its expression by binding to the promoter of PVT1 in cervical cancer cells. LncRNA-PVT1 was upregulated by c-Myc and thus enhanced the proliferation of cervical cancer cells by sponging miR-486-3p.	31943014	RID08072	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(NSCLC,SKCM,BRCA);DATA(GSE74639,GSE38495,GSE55807)
Non-small cell lung cancer	SNHG7	MMP2	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000087245	NA	84973	4313	MGC16037|NCRNA00061	CLG4|CLG4A|TBE-1	SNHG7 mediates cisplatin-resistance in non-small cell lung cancer by activating PI3K/AKT pathway.SNHG7 expression in NSCLC and para-cancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR. Meanwhile, the correlation between SNHG7 expression with clinical stage and cisplatin-resistance in NSCLC patients was analyzed. After transfection of si-SNHG7 or p-complementary deoxyribonucleic acid (pcDNA)-SNHG7, changes in cellular behaviors of A549/DDP cells were evaluated, including cell viability, apoptosis, migration, invasion and cell cycle. The regulatory effects of SNHG7 on the expressions of genes were determined by qRT-PCRas well. Furthermore, western blot was conducted to determine the protein expressions of drug-resistance genes minimal residual disease1 (MRD1), P-glycoprotein (P-gp), BCRP and relative genes in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway.Compared with adjacent normal tissues, SNHG7 was highly expressed in NSCLC tissues. Moreover, SNHG7 expression was significantly higher in advanced-stage NSCLC patients than those in early-stage. SNHG7 level remained significantly higher in DDP-resistant NSCLC tissues and cell lines as well. Knockdown of SNHG7 remarkably enhanced cisplatin-resistance in NSCLC cells, manifesting as decreased cell viability, migratory and invasive rates, DNA synthesis capacity, and promoted apoptosis. Meanwhile, SNHG7 knockdown down-regulated the mRNA levels of matrix metalloprotein2 (MMP2), MMP7 and MMP9 in vitro. After SNHG7 knockdown, the expressions of drug-resistant and relative genes in the PI3K/AKT pathway were notably down-regulated.SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.	31486493	RID08073	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD);DATA(GSE40174)
Non-small cell lung cancer	SNHG7	MMP7	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000137673	NA	84973	4316	MGC16037|NCRNA00061	MPSL1|PUMP-1	SNHG7 mediates cisplatin-resistance in non-small cell lung cancer by activating PI3K/AKT pathway.SNHG7 expression in NSCLC and para-cancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR. Meanwhile, the correlation between SNHG7 expression with clinical stage and cisplatin-resistance in NSCLC patients was analyzed. After transfection of si-SNHG7 or p-complementary deoxyribonucleic acid (pcDNA)-SNHG7, changes in cellular behaviors of A549/DDP cells were evaluated, including cell viability, apoptosis, migration, invasion and cell cycle. The regulatory effects of SNHG7 on the expressions of genes were determined by qRT-PCRas well. Furthermore, western blot was conducted to determine the protein expressions of drug-resistance genes minimal residual disease1 (MRD1), P-glycoprotein (P-gp), BCRP and relative genes in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway.Compared with adjacent normal tissues, SNHG7 was highly expressed in NSCLC tissues. Moreover, SNHG7 expression was significantly higher in advanced-stage NSCLC patients than those in early-stage. SNHG7 level remained significantly higher in DDP-resistant NSCLC tissues and cell lines as well. Knockdown of SNHG7 remarkably enhanced cisplatin-resistance in NSCLC cells, manifesting as decreased cell viability, migratory and invasive rates, DNA synthesis capacity, and promoted apoptosis. Meanwhile, SNHG7 knockdown down-regulated the mRNA levels of matrix metalloprotein2 (MMP2), MMP7 and MMP9 in vitro. After SNHG7 knockdown, the expressions of drug-resistant and relative genes in the PI3K/AKT pathway were notably down-regulated.SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.	31486493	RID08074	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(LIHC);DATA(GSE117623)
Non-small cell lung cancer	SNHG7	MMP9	positively-E	siRNA	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell migration(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	association	NA	Cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000100985	NA	84973	4318	MGC16037|NCRNA00061	CLG4B	SNHG7 mediates cisplatin-resistance in non-small cell lung cancer by activating PI3K/AKT pathway.SNHG7 expression in NSCLC and para-cancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR. Meanwhile, the correlation between SNHG7 expression with clinical stage and cisplatin-resistance in NSCLC patients was analyzed. After transfection of si-SNHG7 or p-complementary deoxyribonucleic acid (pcDNA)-SNHG7, changes in cellular behaviors of A549/DDP cells were evaluated, including cell viability, apoptosis, migration, invasion and cell cycle. The regulatory effects of SNHG7 on the expressions of genes were determined by qRT-PCRas well. Furthermore, western blot was conducted to determine the protein expressions of drug-resistance genes minimal residual disease1 (MRD1), P-glycoprotein (P-gp), BCRP and relative genes in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway.Compared with adjacent normal tissues, SNHG7 was highly expressed in NSCLC tissues. Moreover, SNHG7 expression was significantly higher in advanced-stage NSCLC patients than those in early-stage. SNHG7 level remained significantly higher in DDP-resistant NSCLC tissues and cell lines as well. Knockdown of SNHG7 remarkably enhanced cisplatin-resistance in NSCLC cells, manifesting as decreased cell viability, migratory and invasive rates, DNA synthesis capacity, and promoted apoptosis. Meanwhile, SNHG7 knockdown down-regulated the mRNA levels of matrix metalloprotein2 (MMP2), MMP7 and MMP9 in vitro. After SNHG7 knockdown, the expressions of drug-resistant and relative genes in the PI3K/AKT pathway were notably down-regulated.SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.	31486493	RID08075	expression association	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Glioblastoma	HOTAIR	HK2	positively-E	shRNA;RNA pull-down assay	upregulation	qRT-PCR	GSE2221;TCGA	NA	cell proliferation(+);chemoresistance(-);cell growth(+);apoptosis process(-)	ceRNA(miR-125)	regulation	NA	Temozolomide	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000159399	NA	100124700	3099	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR/miR-125 axis-mediated Hexokinase 2 expression promotes chemoresistance in human glioblastoma. Drug resistance is one of the major obstacles in glioblastoma (GBM) treatments using temozolomide (TMZ) based conventional chemotherapy.In our study, we found that HK2 expression is crucial for GBM proliferation and chemoresistance. In contrast to the healthy brain, HK2 expression is much higher in human GBM, especially in those patients with GBM recurrence.HK2 depletion in GBM cells suppressed the GBM cell proliferation and increased sensitivity to TMZ-induced apoptosis.Furthermore, we also revealed that the abnormal expression of HK2 was modulated by the expression of HOTAIR, a long non-coding RNA (lncRNA). The absence of HOTAIR in GBM cells suppressed the HK2 expression in protein and mRNA level and, therefore, inhibited the cell proliferation and enhanced the cytotoxicity of TMZ both in vivo and in vitro. HOTAIR promoted the expression of HK2 by targeting mir-125, which suppressed the GBM cell proliferation and increased the TMZ-induced apoptosis. These findings shed light on a new therapeutic strategy in modulating HOTAIR/miR-125, which may interfere with the expression of HK2, and enhance the therapeutic sensitivity of GBM to TMZ.	32279420	RID08076	ceRNA or sponge	recurrence,chemoresistance		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Gastric cancer	SNHG1	NOTCH1	positively-E	siRNA;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000148400	NA	23642	4851	LINC00057|lncRNA16|NCRNA00057|UHG	TAN1	lncRNA SNHG1 suppresses gastric cancer cell proliferation and promotes apoptosis via Notch1 pathway.SNHG1 was knocked down using small-interfering RNAs (siRNAs) in gastric cancer cell line MGC-803 and then the changes in the expression levels of SNHG1 and Notch1 in each group of cells were evaluated via quantitative reverse transcription polymerase chain reaction (qRT-PCR.After intervention of SNHG1 by siRNAs, compared with NC-siRNA group, SNHG1-siRNA group exhibited notably lowered RNA and messenger RNA (mRNA) levels of SNHG1 and Notch1 (p<0.05), a substantially lowered proliferation rate (p<0.05), a remarkably raised apoptosis rate (p<0.05) and markedly decreased protein expression levels of Notch1 and Bax (p<0.05). Additionally, the cells treated with Notch1 inhibitor had the proliferation substantially inhibited (p<0.05), while there was no notable change in the RNA expression of SNHG1 in the cells.LncRNA SNHG1 can depend on the Notch1 pathway to suppress the proliferation of gastric cancer cells and promote their apoptosis.	32277646	RID08077	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nasopharynx carcinoma	MACC1-AS1	SMAD2	positively-E	FISH;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell stemness(+)	ceRNA(miR-145)	regulation	NA	NA	CSC	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000228598	GRCh38_7:20141916-20153531	ENSG00000175387	NA	100874041	4087	NA	JV18-1|MADH2|MADR2	The long non-coding RNA MACC1-AS1 promotes nasopharyngeal carcinoma cell stemness via suppressing miR-145-mediated inhibition on SMAD2/ MACC1-AS1 axis.In this work, it was shown that lncRNA MACC1-AS1 was highly expressed in NPC tissues and cells relative to the adjacent tissues and nasal mucosa cells, respectively. Additionally, MACC1-AS1 expression was positively correlated with the high rate of lymph node metastasis and large tumor size. in vitro and in vivo experiments revealed that MACC1-AS1 knockdown reduced the stemness of NPC cells, which was indicated by the decrease of sphere-forming ability, ALDH1 activity, stemness marker expression and tumor-initiating capacity. Mechanistic research showed that MACC1-AS1 antagonized the activity of miR-145, which could target Smad2. In turn, smad2 directly bound to MACC1-AS1 promoter and thus increased MACC1-AS1 expression. Notably, knockdown of miR-145 or overexpression of Smad2 rescued the inhibition of MACC1-AS1 knockdown on the stemness of NPC cells. Therefore, these results demonstrate a novel MACC1-AS1/miR-145/Smad2 negative loop responsible for NPC cell stemness.	32058221	RID08078	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Nasopharynx carcinoma	SMAD2	MACC1-AS1	positively-E	JASPAR;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell stemness(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Nasopharynx carcinoma	TF	lncRNA	ENSG00000175387	NA	ENSG00000228598	GRCh38_7:20141916-20153531	4087	100874041	JV18-1|MADH2|MADR2	NA	The long non-coding RNA MACC1-AS1 promotes nasopharyngeal carcinoma cell stemness via suppressing miR-145-mediated inhibition on SMAD2/ MACC1-AS1 axis.In this work, it was shown that lncRNA MACC1-AS1 was highly expressed in NPC tissues and cells relative to the adjacent tissues and nasal mucosa cells, respectively. Additionally, MACC1-AS1 expression was positively correlated with the high rate of lymph node metastasis and large tumor size. in vitro and in vivo experiments revealed that MACC1-AS1 knockdown reduced the stemness of NPC cells, which was indicated by the decrease of sphere-forming ability, ALDH1 activity, stemness marker expression and tumor-initiating capacity. Mechanistic research showed that MACC1-AS1 antagonized the activity of miR-145, which could target Smad2. In turn, smad2 directly bound to MACC1-AS1 promoter and thus increased MACC1-AS1 expression. Notably, knockdown of miR-145 or overexpression of Smad2 rescued the inhibition of MACC1-AS1 knockdown on the stemness of NPC cells. Therefore, these results demonstrate a novel MACC1-AS1/miR-145/Smad2 negative loop responsible for NPC cell stemness.	32058221	RID08079	transcriptional regulation	metastasis	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Cervical squamous cell carcinoma	NKILA	miRNA-21	negatively-F	overexpression	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000278709	GRCh38_20:57710156-57712780	NA	NA	105416157	NA	NA	NA	LncRNA NKILA inhibits the proliferation and promotes the apoptosis of CSCC cells by downregulating miRNA-21.In our studies, we found that serum NKILA was at lower levels and serum microRNA-21 (miRNA-21) was at higher levels in patients with early stage CSCC than in the healthy female. Altered expression of NKILA and miRNA-21 can effectively separate patients with CSCC at an early stage from healthy controls. Serum levels of NKILA were significantly and negatively correlated with miRNA-21 in patients with CSCC but not in normal controls. Overexpression of NKILA mediated the inhibited expression of miRNA-21 in CSCC cells, but mimic transfection of miRNA-21 did not significantly change the expression level of NKILA. Overexpression of NKILA repressed the proliferation and promoted the apoptosis of CSCC cells, while miRNA-21 showed opposite functions. In addition, miRNA-21 mimic transfection reduced the effects of NKILA on CSCC cells. Collectively, lncRNA NKILA could repress the proliferation and promote the apoptosis of CSCC cells by downregulating miRNA-21.	31950510	RID08080	ceRNA or sponge	NA		
Gastric cancer	GAS5	miR-21	negatively-F	Targetscan;miRanda;miRDB;dual-luciferase reporter assay;overexpression	downregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	NA	NCRNA00030|SNHG2	NA	The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression.The expression of miR-21 and GAS5 mRNA was analyzed by quantitative real-time-PCR. Overexpression of GAS5 was used to investigate the biological functions of GAS5 in cells. The cell proliferation was detected by cell counting kit-8 assay and the cell migration and invasion were detected by Transwell. Cell apoptosis was evaluated by Annexin V-FITC/PI staining and apoptosis-related proteins were detected by western blot. The mechanism of GAS5 in vivo was evaluated by the tumorigenesis of nude mice, and dual luciferase reporter was used to determine if miR-21 is a GAS5 target. The inhibition of miR-21 and the simultaneous overexpression of GAS5 and miR-21 were further performed, and the above indicators were detected again.GAS5 was low expression and miR-21 was high expression in gastric cancer tissues and cells. GAS5 overexpression reduced the proliferation, migration, and invasion of gastric cancer cells and increased the apoptosis of gastric cancer cells. The growth rate of GAS5 group slowed down and the volume of tumor decreased. miR-21 is a GAS5 target and GAS5 inhibits the proliferation of gastric cancer cells by targeting miR-21.Our research shown that overexpression of GAS5 can significantly inhibit the proliferation, migration, invasion and tumor formation of gastric cancer cells, and promote the apoptosis of gastric cancer cells, which may be related to the targeting inhibition of miR-21 expression by GAS5.	31910411	RID08081	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Malignant glioma	LINC00473	YAP1	positively-E	shRNA;starBase;dual-luciferase reporter assay;RIP;Targetscan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000223414	NA	ENSG00000137693	NA	90632	10413	C6orf176|LNC473|bA142J11.1	YAP65	Long non-coding RNA LINC00473/miR-195-5p promotes glioma progression via YAP1-TEAD1-Hippo signaling.In the present study, LINC00473 was significantly increased in glioma tissues and in cell models, and predicted a poor prognosis in patients with glioma. Notably, LINC00473 knockdown not only suppressed cell proliferation, invasion and migration of glioma cells, but also blocked cell cycle progression and induced apoptosis. Subcutaneous xenotransplanted tumor model experiments revealed that reduced LINC00473 expression was able to suppress in vivo glioma growth. Mechanistically, LINC00473 functioned as a competing endogenous (ce)RNA to decrease microRNA (miR)-195-5p expression. Moreover, Yes-associated protein 1 (YAP1) and TEA domain family member 1 (TEAD1) were identified as downstream targets of miR-195-5p, whose expression levels were inhibited by miR-195-5p. LINC00473 knockdown suppressed glioma progression through the decrease of miR-195-5p and subsequent increase of YAP1 and TEAD1 expression levels. These results indicated LINC00473 might act as a ceRNA to sponge miR-195-5p, thus promoting YAP1 and TEAD1 expressions, and shedding light on the underlying mechanisms of LINC00473-induced glioma progression.	31894297	RID08082	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE111065,GSE55807)
Malignant glioma	LINC00473	TEAD1	positively-E	shRNA;starBase;dual-luciferase reporter assay;RIP;Targetscan	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+);apoptosis process(-);tumor growth(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000223414	NA	ENSG00000187079	NA	90632	7003	C6orf176|LNC473|bA142J11.1	AA|TCF13|TEF-1	Long non-coding RNA LINC00473/miR-195-5p promotes glioma progression via YAP1-TEAD1-Hippo signaling.In the present study, LINC00473 was significantly increased in glioma tissues and in cell models, and predicted a poor prognosis in patients with glioma. Notably, LINC00473 knockdown not only suppressed cell proliferation, invasion and migration of glioma cells, but also blocked cell cycle progression and induced apoptosis. Subcutaneous xenotransplanted tumor model experiments revealed that reduced LINC00473 expression was able to suppress in vivo glioma growth. Mechanistically, LINC00473 functioned as a competing endogenous (ce)RNA to decrease microRNA (miR)-195-5p expression. Moreover, Yes-associated protein 1 (YAP1) and TEA domain family member 1 (TEAD1) were identified as downstream targets of miR-195-5p, whose expression levels were inhibited by miR-195-5p. LINC00473 knockdown suppressed glioma progression through the decrease of miR-195-5p and subsequent increase of YAP1 and TEAD1 expression levels. These results indicated LINC00473 might act as a ceRNA to sponge miR-195-5p, thus promoting YAP1 and TEAD1 expressions, and shedding light on the underlying mechanisms of LINC00473-induced glioma progression.	31894297	RID08083	ceRNA or sponge	prognosis	UP(SKCM);DATA(GSE38495)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065)
Pancreatic cancer	DIO3OS	ALDOA	positively-E	starBase;dual-luciferase reporter assay;siRNA;Targetscan;western blot	upregulation	qRT-PCR;sequencing	TCGA	NA	cell proliferation(+);cell invasion(+);tumor growth(+)	ceRNA(miR-122)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000258498	GRCh38_14:101552221-101560438	ENSG00000149925	NA	64150	226	C14orf134|DIO3-AS1|NCRNA00041	NA	Long noncoding RNA DIO3OS interacts with miR-122 to promote proliferation and invasion of pancreatic cancer cells through upregulating ALDOA.We performed the meta-analysis on PC samples and non-tumor samples retrieved from the TCGA database, and measured the levels of DIO3OS in PC cell lines and a normal pancreatic duct epithelial cell line HPDE6-C7. Cell proliferation was evaluated via CCK-8 assay. Cell invasion in vitro was investigated by transwell assay. The RNA immunoprecipitation assay and luciferase reporter assay was utilized to confirm the putative miR-122-binding site in DIO3OS. The effects of DIO3OS on PC progression were tested using in vivo subcutaneous xenografts.Our results showed that DIO3OS was highly expressed in human PC tissues and PC cell lines. DIO3OS exhibited oncogenic properties in stimulating PC cell proliferation and invasion in vitro and promoting cancer growth in vivo. Through online predictive tools and functional experiments, we found that DIO3OS could bind directly to microRNA-122 (miR-122) and inhibited its expression, which functioned as a tumor suppressor in PC cells. We also verified that ALDOA was the direct target of miR-122, and the tumor suppressive effects caused by DIO3OS knockdown or miR-122 overexpression could be rescued by re-expression of ALDOA in PC cells.Overall, our study suggested that lncRNA DIO3OS promotes PC cell growth and invasion by competing for miR-122 to modulate the expression of ALDOA. These findings yield a better understanding of the potential mechanisms by which gain of DIO3OS expression accelerates PC progression.	31384177	RID08084	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Colorectal cancer	MALAT1	miR-101	negatively-F	dual-luciferase reporter assay;western blot;CRISPR-Cas9	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Long non-coding RNA Malat1 activated autophagy, hence promoting cell proliferation and inhibiting apoptosis by sponging miR-101 in colorectal cancer.First, the expression level of Malat1 in 96 pairs of colorectal cancer tissues and four cell lines was detected by qRT-PCR Subsequently, the autophagy activity in colorectal cancer tissues and cell lines was detected by western blot. Furthermore, the CCK-8 assay and flow cytometry (FCM) were performed to detect the role of autophagy activated by Malat1 in colorectal cancer cell lines.In this study, significantly increased Malat1 expression and autophagy activity were found in colorectal cancer tissues compared with the adjacent normal tissues. Also, the Malat1 level was positively correlated with the expression of LC3-II mRNA in vivo. Moreover, autophagy activation and cell proliferation were significantly facilitated by Malat1 in colorectal cancer cells, while apoptosis decreased. Above all, the inhibition of autophagy by 3-MA not only relieved the Malat1-induced cell proliferation but also promoted the Malat1-induced cell apoptosis. In addition, Malat1 was found to act as an endogenous sponge by directly binding to miR-101 to reduce miR-101. Furthermore, the suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of CRC were abolished by Malat1.Long non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.	31372165	RID08085	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Prostate cancer	FEZF1-AS1	NOTCH1	positively-E	siRNA;western blot	downregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000148400	NA	154860	4851	NA	TAN1	Highly expressed long non-coding RNA FEZF1- AS1 promotes cells proliferation and metastasis through Notch signaling in prostate cancer.We performed real-time PCR and western blot to evaluate the expressing changes of relevant signaling pathways. Among these signaling pathways involved in regulating multiple sides of malignant behaviors, we focused on Notch1 signaling, because it was closely related to cancerous development and progression. Real-time PCR analyses validated that the mRNA expressing levels of Notch1, p21 and Hes1 were significantly decreased in PC-3 and DU145 cells when their endogenous FEZF1- AS1 was knocked down (Figure 4A and B). Similar results that FEZF1-AS1 siRNAs remarkably recued the levels of Notch1, p21, and Hes1 in PCa cells were also observed when using western blot (Figure 4C). Hence, these data suggested that FEZF1-AS1 was capable to modulate the activity of Notch1 signaling in PCa cells.Functional investigations suggested that knockdown of FEZF1-AS1 could suppress cells proliferation, trigger late apoptosis, and inhibit cells invasion and migration. Mechanistic assays demonstrated that FEZF1-AS1 exhibited its tumor- promotive roles by activating the Notch signaling pathway.	31298365	RID08086	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Prostate cancer	FEZF1-AS1	CDKN1A	positively-E	siRNA;western blot	downregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000124762	NA	154860	1026	NA	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	Highly expressed long non-coding RNA FEZF1- AS1 promotes cells proliferation and metastasis through Notch signaling in prostate cancer.We performed real-time PCR and western blot to evaluate the expressing changes of relevant signaling pathways. Among these signaling pathways involved in regulating multiple sides of malignant behaviors, we focused on Notch1 signaling, because it was closely related to cancerous development and progression. Real-time PCR analyses validated that the mRNA expressing levels of Notch1, p21 and Hes1 were significantly decreased in PC-3 and DU145 cells when their endogenous FEZF1- AS1 was knocked down (Figure 4A and B). Similar results that FEZF1-AS1 siRNAs remarkably recued the levels of Notch1, p21, and Hes1 in PCa cells were also observed when using western blot (Figure 4C). Hence, these data suggested that FEZF1-AS1 was capable to modulate the activity of Notch1 signaling in PCa cells.Functional investigations suggested that knockdown of FEZF1-AS1 could suppress cells proliferation, trigger late apoptosis, and inhibit cells invasion and migration. Mechanistic assays demonstrated that FEZF1-AS1 exhibited its tumor- promotive roles by activating the Notch signaling pathway.	31298365	RID08087	expression association	metastasis		UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Prostate cancer	FEZF1-AS1	HES1	positively-E	siRNA;western blot	downregulation	RT-PCR	TCGA	NA	cell proliferation(+);cell metastasis(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000114315	NA	154860	3280	NA	bHLHb39|FLJ20408|HES-1|HRY	Highly expressed long non-coding RNA FEZF1- AS1 promotes cells proliferation and metastasis through Notch signaling in prostate cancer.We performed real-time PCR and western blot to evaluate the expressing changes of relevant signaling pathways. Among these signaling pathways involved in regulating multiple sides of malignant behaviors, we focused on Notch1 signaling, because it was closely related to cancerous development and progression. Real-time PCR analyses validated that the mRNA expressing levels of Notch1, p21 and Hes1 were significantly decreased in PC-3 and DU145 cells when their endogenous FEZF1- AS1 was knocked down (Figure 4A and B). Similar results that FEZF1-AS1 siRNAs remarkably recued the levels of Notch1, p21, and Hes1 in PCa cells were also observed when using western blot (Figure 4C). Hence, these data suggested that FEZF1-AS1 was capable to modulate the activity of Notch1 signaling in PCa cells.Functional investigations suggested that knockdown of FEZF1-AS1 could suppress cells proliferation, trigger late apoptosis, and inhibit cells invasion and migration. Mechanistic assays demonstrated that FEZF1-AS1 exhibited its tumor- promotive roles by activating the Notch signaling pathway.	31298365	RID08088	expression association	metastasis		UP(LIHC,NSCLC,SKCM,BRCA);DOWN(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Oesophageal squamous cell carcinoma	PCAT1	miR-326	negatively-F	RegRNA;dual-luciferase reporter assay	upregulation	RT-qPCR	TCGA	NA	cell growth(+);cell cycle(+);tumorigenesis(+);AKT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Oesophageal cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1|PiHL	NA	Long noncoding RNA PCAT1, a novel serum-based biomarker, enhances cell growth by sponging miR-326 in oesophageal squamous cell carcinoma.Here, we confirmed that PCAT1 was highly expressed in ESCC tissues and cell lines. Knockdown of PCAT1 inhibited the growth of ESCC cells, whereas overexpression of PCAT1 showed the opposite effect both in vitro and in vivo. Moreover, knockdown of PCAT1 arrested the cell cycle at G2/M phase, reduced the expression of cyclin B1 and CDC2, and caused cells to be more sensitive to paclitaxel. Furthermore, PCAT1 could bind to miR-326, a tumour suppressor in diverse human cancers. Rescue experiments revealed that enforced expression of miR-326 attenuated the promotive effect of PCAT1 on ESCC cell growth. In addition, we discovered that PCAT1 was present in ESCC cell-derived exosomes, was higher in the serum of ESCC patients than those of healthy volunteer donors, and promoted cell growth through exosomes. Thus, our data indicate that PCAT1 promotes ESCC cell proliferation by sponging miR-326 and may serve as a non-invasive biomarker for ESCC.	31273188	RID08089	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Cervical cancer	LINC00511	BCL2	positively-E	shRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000171791	NA	400619	596	onco-lncRNA-12	Bcl-2|PPP1R50	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08090	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	LINC00511	BAX	negatively-E	shRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000087088	NA	400619	581	onco-lncRNA-12	BCL2L4	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08091	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	LINC00511	CASP3	negatively-E	shRNA	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000164305	NA	400619	836	onco-lncRNA-12	apopain|CPP32|CPP32B|Yama	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08092	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE55807)
Cervical cancer	LINC00511	MMP2	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000087245	NA	400619	4313	onco-lncRNA-12	CLG4|CLG4A|TBE-1	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08093	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	UP(PAAD);DATA(GSE40174)
Cervical cancer	LINC00511	MMP9	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000100985	NA	400619	4318	onco-lncRNA-12	CLG4B	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08094	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Cervical cancer	LINC00511	MRP1	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000113318	NA	400619	NA	onco-lncRNA-12	NA	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08095	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	
Cervical cancer	LINC00511	ABCB1	positively-E	shRNA;western blot	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	Paclitaxel	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000085563	NA	400619	5243	onco-lncRNA-12	ABC20|CD243|CLCS|GP170|MDR1|p-170|P-gp|PGY1	LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel.The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.	31180057	RID08096	expression association	metastasis,chemoresistance	UP(LIHC,NSCLC,PRAD,SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE38495)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE111065,GSE51827,GSE86978)
Osteosarcoma	CASC11	SNAI1	positively-E	RIP;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);cell metastasis(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000124216	NA	100270680	6615	CARLo-7|ENST00000518376|LINC00990|MYMLR|TCONS_00014535	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	Long noncoding RNA CASC11 promotes osteosarcoma metastasis by suppressing degradation of snail mRNA.Osteosarcoma (OS) is the most common primary bone tumor in adolescents. Dysregulation of long noncoding RNAs (lncRNAs) is associated with the cancer progression, of which cancer susceptibility candidate 11 (CASC11) has been indicated as an oncogene in several human cancers. However, the underlying mechanisms by which CASC11 contributes to OS metastasis remain undetermined. Here, we found that CASC11 expression in OS tissues was markedly higher than that in noncancerous tissues. Clinical association analysis revealed that high CASC11 expression correlated with clinical stage, distant metastasis and poor prognosis of OS patients. Gain- and loss-of-function assays demonstrated that CASC11 promoted migration, invasion, epithelial-mesenchymal transition (EMT) and metastasis of OS cells in vitro and in vivo. CASC11 associated with the EMT inducer Snail mRNA and increased its stability. Association of CASC11 with Snail mRNA blocked the repressing effect of miR-122, miR-145, miR-211, miR-34a and miR-137 on Snail. Moreover, CASC11-specific siRNAs significantly inhibit tumor metastasis in vivo. Taken together, our findings suggest that CASC11 may be a candidate prognostic biomarker and a novel therapeutic target for OS.	30906630	RID08097	expression association	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Cervical cancer	RP11-552M11.4	ATF1	positively-E	lncLocator;FISH;LncBase;luciferase reporter assay;Targetscan;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-3941)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000243960	GRCh38_1:111438638-111441364	ENSG00000123268	NA	NA	466	NA	TREB36	Long non-coding RNA RP11-552M11.4 favors tumorigenesis and development of cervical cancer via modulating miR-3941/ATF1 signaling.Herein, we unveiled that the expression of lncRNA RP11-552M11.4 tested by qRT-PCRwas enhanced in tumor tissues compared with the para-carcinoma tissues and related to FIGO Stage, lymph node metastasis, vascular invasion and distant metastasis in CC. Additionally, CC patients with high lncRNA RP11- 552M11.4 level suffered from poor clinical outcomes. Moreover, silenced lncRNA RP11-552M11.4 restrained cell proliferation, migration and invasion in CC cells. Subsequently, the mechanistic studies revealed that lncRNA RP11-552M11.4 functioned as a ceRNA of ATF1 in CC by acting as the endogenous sponge for miR-3941, which was identified as a tumor suppressor in CC. Moreover, both miR-3941 inhibition and ATF1 overexpression restored the impacts of inhibited lncRNA RP11-552M11.4 on cellular processes in CC cells. Our observations elucidated the carcinogenic role of lncRNA RP11-552M11.4 in CCwas mediated throughmiR-3941/ATF1 axis, giving a new insight into the effective target for the treatment and prognosis of cervical cancer.	30790638	RID08098	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Hepatocellular carcinoma	MCM3AP-AS1	FOXA1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay;overexpression;knockdown;starBase;Targetscan;picTar;PITA;miRanada	upregulation	qRT-PCR	GSE65485;TCGA;GSE45436;GSE54236	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);colony formation(+);tumor growth(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000129514	NA	114044	3169	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	HNF3A	A novel lncRNA MCM3AP-AS1 promotes the growth of hepatocellular carcinoma by targeting miR-194-5p/FOXA1 axis.The expression of lncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) in HCC tissues and cell lines was detected by qRT-PCRand fluorescence in situ hybridization. Immunoblotting, CCK-8, EdU, colony formation and flow cytometry were performed to investigate the role of MCM3AP-AS1 in HCC cell proliferation, cell cycle and apoptosis in vitro. A subcutaneous tumor mouse model was constructed to analyze in vivo growth of HCC cells after MCM3AP-AS1 knockdown. The interactions among MCM3AP-AS1, miR-194-5p and FOXA1 were measured by RNA pull-down, RNA immunoprecipitation and luciferase reporter assay.We revealed a novel oncogenic lncRNA MCM3AP-AS1, which is overexpressed in HCC and positively correlated with large tumor size, high tumor grade, advanced tumor stage and poor prognosis of HCC patients. MCM3AP-AS1 knockdown suppressed HCC cell proliferation, colony formation and cell cycle progression, and induced apoptosis in vitro, and depletion of MCM3AP-AS1 inhibited tumor growth of HCC in vivo. Mechanistically, MCM3AP-AS1 directly bound to miR-194-5p and acted as competing endogenous RNA (ceRNA), and subsequently facilitated miR-194-5p  target gene forkhead box A1 (FOXA1) expression in HCC cells. Interestingly, FOXA1 restoration rescued MCM3AP-AS1 knockdown induced proliferation inhibition, G1 arrest and apoptosis of HCC cells.Our results recognized MCM3AP-AS1 as a novel oncogenic lncRNA, which indicated poor clinical outcomes in patients with HCC. MCM3AP-AS1 exerted an oncogenic role in HCC via targeting miR-194-5p and subsequently promoted FOXA1 expression. Our findings suggested that MCM3AP-AS1 could be a potential prognostic biomarker and therapeutic target for HCC.	30782188	RID08099	ceRNA or sponge	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Nasopharynx carcinoma	HOTTIP	miR-4301	negatively-F	miRDB;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Long Noncoding RNA HOTTIP Promotes Nasopharyngeal Cancer Cell Proliferation, Migration, and Invasion by Inhibiting miR-4301.HOTTIP levels in cancer specimens and cell lines were analyzed using qRT-PCR HOTTIP function in NPC was determined by Cell Counting Kit-8 (CCK8) and Transwell assay.HOTTIP expression was increased in NPC tissues. Higher levels of HOTTIP are correlated with lower survival in NPC patients. HOTTIP silencing suppressed the proliferation, cell cycle, migration, and invasion of NPC cells. HOTTIP served as a sponge for miR-4301. miR-4301 expression was significantly inhibited by HOTTIP in NPC cells. miR-4301 overexpression dramatically inhibited NPC cell proliferation, migration, and invasion.This study showed that HOTTIP acts as an oncogene in NPC by sponging miR-4301.	30685769	RID08100	ceRNA or sponge	NA		
Non-small cell lung cancer	DANCR	CDKN1A	negatively-E	RIP;siRNA	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+);cell cycle(+);cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712325-52723623	ENSG00000124762	NA	57291	1026	AGU2|ANCR|KIAA0114|lncRNA-ANCR|SNHG13	CAP20|CDKN1|CIP1|P21|p21CIP1|p21Cip1/Waf1|SDI1|WAF1	Long non-coding RNA DANCR promotes the progression of non-small-cell lung cancer by inhibiting p21 expression.We examined the expression of lncRNA DANCR in NSCLC by qRT-PCRand explored its biological roles in NSCLC progression by cell and molecular biology studies.DANCR expression level was increased in human NSCLC. The knockdown of DANCR inhibited NSCLC cell proliferation by inducing cell apoptosis and cell cycle arrest. In addition, DANCR knockdown suppressed NSCLC cell migration and invasion via inhibition of epithelial-sesenchymal transition (EMT). On the contrary, DANCR overexpression had the opposite effects. DANCR knockdown inhibited EZH-2-mediated epigenetic silencing of p21 promoter and increased p21 expression. Moreover, DANCR knockdown inhibited NSCLC cell proliferation, migration, and invasion in a p21-dependent manner.DANCR plays oncogenic roles in NSCLC and may provide a novel biomarker for NSCLC diagnosis and prognosis.	30613152	RID08101	expression association	prognosis	DOWN(LIHC,PRAD);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495)	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE109761,GSE75367,GSE86978)
Breast cancer	miR-7	XIST	negatively-E	Targetscan;miRcode;luciferase reporter assay;RIP;RNA pull-down assay;ChIP		RT-qPCR	NA	NA	tumor growth(+)	sponge	binding/interaction	NA	NA	CSC	NA	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	MiR-7 reduces the BCSC subset by inhibiting XIST to modulate the miR-92b/ Slug/ESA axis and inhibit tumor growth.We examined miR-7 expression in breast cancer and developed a BCSC-driven xenograft mouse model, to evaluate the effects of miR-7 overexpression on the decrease of the BCSC subset in vitro and in vivo. In addition, we determined how miR-7 decreased the BCSC subset by using the ALDEFLUOR, lentivirus infection, dual-luciferase reporter, and chromatin immunoprecipitation-PCR assays.MiR-7 was expressed at low levels in breast cancer tissues compared with normal tissues, and overexpression of miR-7 directly inhibited lncRNA XIST, which mediates the transcriptional silencing of genes on the X chromosome, and reduced epithelium-specific antigen (ESA) expression by increasing miR-92b and inhibiting slug.The findings from this study uncover the molecular mechanisms by which miR-7 inhibits XIST, modulates the miR-92b/Slug/ESA axis, and decreases the RELA and CD44 expression, resulting in a reduced BCSC subset and breast cancer growth inhibition. These findings suggest a potentially targeted treatment approach to breast cancer.	32143670	RID08102	ceRNA or sponge	NA		DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)
Lung adenocarcinoma	ROR1-AS1	miR-375	negatively-F	shRNA;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000223949	GRCh38_1:64094379-64171342	NA	NA	101927034	NA	NA	NA	Long noncoding RNA ROR1-AS1 enhances lung adenocarcinoma metastasis and induces epithelial-mesenchymal transition by sponging miR-375.Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to measure ROR1-AS1 expression of LAC tissues. Function assays including wound healing assay and transwell assay were conducted to detect the effect of knockdown of ROR1-AS1 on the metastasis of LAC, and luciferase assays and RNA immunoprecipitation assay (RIP) were also performed to explore the underlying mechanism.ROR1-AS1 expression level was significantly higher in LAC samples compared with that in adjacent tissues, which was associated with patients'-prognosis. Knockdown of ROR1-AS1 inhibited cell migration and cell invasion of LAC cells via suppressing epithelial-mesenchymal transition (EMT) process. Furthermore, it was discovered that ROR1- AS1 acted as a competing endogenous RNA via sponging miR-375 in LAC.These results suggested that ROR1-AS1 could act as a sponge for miR-375 and promo//e cell migration and invasion through suppressing the process of EMT in LAC, which may offer a potential therapeutic target in LAC.	31983094	RID08103	ceRNA or sponge	metastasis,prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Premature menopause	DLEU1	miR-146b-5p	negatively-F	IntaRNA;RNA pull-down assay;overexpression	upregulation	RT-qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	NA	NA	NA	NA	Reproductive system disease	Ovarian disease	lncRNA	miRNA	ENSG00000176124	GRCh38_13:50082169-50906856	NA	NA	10301	NA	BCMS|BCMS1|DLB1|LEU1|LINC00021|NCRNA00021|XTP6	NA	LncRNA DLEU1 is overexpressed in premature ovarian failure and sponges miR- 146b-5p to increase granulosa cell apoptosis. DLEU1 expression was increased (Fig. 1A, p < 0.01), and miR-146b-5p expression was decreased (Fig. 1B, p < 0.01) in POF.IntaRNA 2.0 and RNA pull-down assay were performed to predict and validate the direct interaction between DLEU1 and miR-146b-5p.We found direct interaction between DLEU1 and miR-146b-5p and subcellular location of DLEU1 in KGN cells.To further analyze their interactions, DLEU1 and miR-146b-5p were overexpressed in KGN cells. Their overexpression was confirmed by RT-qPCR every 24 h until 96 h.DLEU1 promoted cell apoptosis, while MiR-146b-5p decreased cell apoptosis.DLEU1 is overexpressed in POF and miR-146b-5p was downregulated in POF. DLEU1 may sponge miR-146b-5p in the cytoplasm to promote GC apoptosis, thereby promoting POF.	34740384	RID08104	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Gastric cancer	PVT1	BNIP3	negatively-E	siRNA;luciferase reporter assay;overexpression;RNA pull-down assay;ChIP	downregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000176171	NA	5820	664	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Nip3	Methionine deficiency promoted mitophagy via lncRNA PVT1-mediated promoter demethylation of BNIP3 in gastric cancer.The levels of lncRNA PVT1 in gastric cancer cells and human gastric cancer xenografts of nude mice were down-regulated under the condition of Met deficiency.The results of qPCR showed that Met-- induced significant down-regulation of lncRNA PVT1 level.Studies have shown that DNA methylation in the BNIP3 promoter region can significantly increase the resistance of gastric cancer patients to chemotherapy drugs and reduce the overall survival time of patients.MKN45 cells were divided into si-control, si-PVT1'-, si-PVT1'- group, pcDNA and pcDNA-PVT1.The results showed that down-regulation of lncRNA PVT1 could reduce the methylation level of BNIP3 promoter, while overexpression of lncRNA PVT1 increased the methylation level of BNIP3 promoter.Moreover, luciferase reporter assay showed that the activity of BNIP3 promoter increased significantly after interference with lncRNA PVT1, whereas the activity of BNIP3 promoter was decreased after overexpression of lncRNA PVT1.Next, we performed RNA pull-down assay to verify which DNMT lncRNA PVT1 could interact with. The results showed that lncRNA PVT1 could bind to DNMT1, but not to DNMT3a and DNMT3b.Furthermore, ChIP assay showed that DNMT1 bound to BNIP3 promoter, interfered with lncRNA PVT1 to inhibit the binding of DNMT1 to BNIP3 promoter, and overexpression of lncRNA PVT1 promoted the binding of DNMT1 to BNIP3 promoter.We found that up-regulation of lncRNA PVT1 significantly reduced the mRNA and protein expression levels of BNIP3, and this effect was reversed by 5-Aza.LncRNA PVT1 inhibits the proliferation of gastric cancer cells via mediating BNIP3.Our study suggested that Met deficiency could down-regulate the expression of lncRNA PVT1, further demethylated the promoter of BNIP3, thus inhibiting the proliferation of gastric cancer cells by activating mitophagy.	34678458	RID08105	epigenetic regulation	chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,BRCA);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Ovarian cancer	NRSN2-AS1	PRKX	positively-E	FISH;starBase;RIP;RNA pull-down assay;luciferase reporter assay;MSigDB;shRNA;overexpression	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	ceRNA(miR-744-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225377	GRCh38_20:316860-348490	ENSG00000183943	NA	100507459	5613	NA	PKX1	Long non-coding RNA NRSN2-AS1 facilitates tumorigenesis and progression of ovarian cancer via miR-744-5p/PRKX axis. According to the experimental outcomes of qRT-PCR among these lncRNAs, the expression levels of RP1-223E5.4, AC004540.5, NRSN2-AS1, and CTD-3065J16.9 in OV cells was higher than that of other lncRNAs.To find the potential miRNA binding with NRSN2-AS1, we made use of starBase (http://starbase.sysu.edu.cn/) and found 14 miRNA candidates.To test the binding affinity between NRSN2-AS1 and miR-744-5p, RIP assay was carried out in OV cells.Further, we applied starBase to predict the binding region between NRSN2-AS1 and miR-744-5p, and mutated their binding sites based on the rule of complementary base pairing.The data from RNA pull-down assay suggested that miR-744-5p was highly enriched in Bio-NRSN2-AS1-Wt, rather than in Bio-NRSN2-AS1-Mut.Furthermore, we utilized dual-luciferase reporter assay to further test the binding relationship between NRSN2-AS1 and miR-744-5p.We used starBase to predict all possible mRNAs that might combine with miR-744-5p.We also sorted out candidate mRNAs which were related to Wnt/beta-catenin signaling pathway by using MSigDB database.Through qRT-PCR we observed that among these candidate mRNAs, PRKX expression was the most significantly higher in OV cells comparing with normal ovarian epithelial cells.Subsequently, RIP assay was carried out and the experimental results illustrated that miR-744-5p and PRKX jointly existed in RISC complex precipitated by anti-Ago2 antibody.The binding sites between miR-744-5p and PRKX were projected with the use of starBase, and mutated binding sites were obtained. Moreover, the outcome of RNA pull-down assay indicated that miR-744-5p was greatly enriched in Bio-PRKX-Wt, rather than Bio-PRKX-Mut.In addition, the luciferase activity of PRKX 3'UTR-Wt was only overtly decreased when miR-744-5p was overexpressed in OV cells.NRSN2-AS1 activates Wnt/beta-catenin signaling pathway in OV cells via regulating miR-744-5p/PRKX.As shown in cell proliferation assays, the inhibited proliferation of OV cells transfected with sh-NRSN2-AS1#1 was improved by inhibiting miR-744-5p or overexpressing PRKX. Transwell assays illustrated that the migratory and invasive capabilities of OV cells hampered by sh-NRSN2-AS1#1 were also reversed by miR-744-5p silencing or PRKX overexpression.In conclusion, the foregoing assays suggest that NRSN2-AS1/miR-744-5p/PRKX axis regulates OV cell growth.This work might advance our understanding of OV and provide evidence for supporting NRSN2-AS1 as a potential biomarker for OV treatment.	34791059	RID08106	ceRNA or sponge	NA	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Parkinson's disease	ZFAS1	TXNIP	negatively-E	overexpression;knockout;Co-immunoprecipitation;western blot;knockdown	downregulation	qRT-PCR	NA	NA	cell pyroptosis(+);inflammatory response(+)	histone modification	regulation	NA	NA	CSC	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000117289	NA	441951	10628	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	ARRDC6|EST01027|HHCPA78|THIF|VDUP1	A Novel Long-Noncoding RNA LncZFAS1 Prevents MPP+ -Induced Neuroinflammation Through MIB1 Activation. LncZFAS1 overexpressing (oe-LncZFAS1) cells showed significantly lower cleavage of Gsdmd, pro-IL-1beta, and caspase-1 following MPP+ treatment compared to the empty vector transfected control cells (oe-vector), although there was no impact on the overall pre-cleaved peptide levels.Consequently, oe-LncZFAS1 SH-SY5Y cells were resistant to MPP+- induced pyroptosis.To confirm the role of lncZFAS on MMP+- induced pyroptosis, lncZFAS was stably knocked-out in SH-SY5Y cells (sgRNA-ZFAS1).LncZFAS1 Inhibited MPP+ -Induced Pyroptosis in SH-SY5Y Human Neuroblasts.LncZFAS1 overexpression significantly decreased intracellular oxidative stress compared to corresponding empty vector transfected control cells.LncZFAS1 knockout significantly increased TXNIP protein levels but did not impact the transcriptional levels.Moreover, sgRNA-ZFAS1 cells showed increased TXNIP expression and TXR1 association even after treatment with the MG132 proteasome inhibitor, which resulted in increased inflammasome activation.The levels of TXNIP ubiquitination in oe-LncZFAS1 SH-SY5Y cells were assessed by Co-IP and western blot.Moreover, Lnc- ZFAS1 overexpression significantly induced MIB1 transcriptional and protein levels in SH-SY5Y cells following MPP+ treatment.To verify that LncZFAS1- induced TXNIP ubiquitination depends on the MIB1 protein interaction, a MIB1 knockdown SH-SY5Y cell line was generated on the oe-ZFAS1 background.MIB1 knockdown was shown to rescue TXNIP protein levels in oe-ZFAS1 cells and reduced TXNIP ubiquitination following MPP+ treatment.A series of similar experiments was conducted with sgRNAZFAS1 cells, showing decreased TXNIP ubiquitination and MIB1 association.Lnc- ZFAS1 significantly downregulates miR590-3p, a putative regulator of MIB1.To determine whether miR590-3p regulates MIB1 expression, SH-SY5Y cells were treated with a miR590-3p or a miR590-3p inhibitor and respective negative controls, and MIB1 protein levels were assessed by western blot.To validate direct miR590-3p binding to the 3'UTR, a MIB1 luciferase reporter system was generated with the WT MIB1 3'UTR (WT-MIB1) or a miR590- 3p resistant 3'UTR (mut-MIB1).LncZFAS1 knockdown significantly increased miR590-3p expression.The intracellular localization of LncZFAS1 was assessed by FISH staining and confocal microscopy.sgRNA-ZFAS1 cells showed decreased MIB1 transcriptional and protein levels (Fig. 9I ) and increased miR590-3p expression.LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p, exposing a novel research idea regarding the mechanism of Parkinson  disease.	34775541	RID08107	epigenetic regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Parkinson's disease	ZFAS2	MIB1	positively-E	western blot;luciferase reporter assay;overexpression;knockdown;FISH	downregulation	qRT-PCR	NA	NA	cell pyroptosis(+);inflammatory response(+)	ceRNA(miR-[0-9]90-3p)	regulation	NA	NA	CSC	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	NA	NA	ENSG00000101752	NA	NA	57534	NA	DIP-1|KIAA1323|MIB|ZZANK2|ZZZ6	A Novel Long-Noncoding RNA LncZFAS1 Prevents MPP+ -Induced Neuroinflammation Through MIB1 Activation. LncZFAS1 overexpressing (oe-LncZFAS1) cells showed significantly lower cleavage of Gsdmd, pro-IL-1beta, and caspase-1 following MPP+ treatment compared to the empty vector transfected control cells (oe-vector), although there was no impact on the overall pre-cleaved peptide levels.Consequently, oe-LncZFAS1 SH-SY5Y cells were resistant to MPP+- induced pyroptosis.To confirm the role of lncZFAS on MMP+- induced pyroptosis, lncZFAS was stably knocked-out in SH-SY5Y cells (sgRNA-ZFAS1).LncZFAS1 Inhibited MPP+ -Induced Pyroptosis in SH-SY5Y Human Neuroblasts.LncZFAS1 overexpression significantly decreased intracellular oxidative stress compared to corresponding empty vector transfected control cells.LncZFAS1 knockout significantly increased TXNIP protein levels but did not impact the transcriptional levels.Moreover, sgRNA-ZFAS1 cells showed increased TXNIP expression and TXR1 association even after treatment with the MG132 proteasome inhibitor, which resulted in increased inflammasome activation.The levels of TXNIP ubiquitination in oe-LncZFAS1 SH-SY5Y cells were assessed by Co-IP and western blot.Moreover, Lnc- ZFAS1 overexpression significantly induced MIB1 transcriptional and protein levels in SH-SY5Y cells following MPP+ treatment.To verify that LncZFAS1- induced TXNIP ubiquitination depends on the MIB1 protein interaction, a MIB1 knockdown SH-SY5Y cell line was generated on the oe-ZFAS1 background.MIB1 knockdown was shown to rescue TXNIP protein levels in oe-ZFAS1 cells and reduced TXNIP ubiquitination following MPP+ treatment.A series of similar experiments was conducted with sgRNAZFAS1 cells, showing decreased TXNIP ubiquitination and MIB1 association.Lnc- ZFAS1 significantly downregulates miR590-3p, a putative regulator of MIB1.To determine whether miR590-3p regulates MIB1 expression, SH-SY5Y cells were treated with a miR590-3p or a miR590-3p inhibitor and respective negative controls, and MIB1 protein levels were assessed by western blot.To validate direct miR590-3p binding to the 3'UTR, a MIB1 luciferase reporter system was generated with the WT MIB1 3'UTR (WT-MIB1) or a miR590- 3p resistant 3'UTR (mut-MIB1).LncZFAS1 knockdown significantly increased miR590-3p expression.The intracellular localization of LncZFAS1 was assessed by FISH staining and confocal microscopy.sgRNA-ZFAS1 cells showed decreased MIB1 transcriptional and protein levels (Fig. 9I ) and increased miR590-3p expression.LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p, exposing a novel research idea regarding the mechanism of Parkinson  disease.	34775541	RID08108	ceRNA or sponge	NA		UP(PAAD);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Cervical cancer	E7	MALAT1	positively-E	siRNA;luciferase reporter assay;ChIP;RNA pull-down assay;overexpression;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	LncRNA MALAT1 was regulated by HPV16 E7 independently of pRB in cervical cancer cells.MALAT1 RNA levels were examined using qRT-PCRin clinical specimen.MALAT1 was upregulated in cervical tissues and cervical cancer cell lines infected with HPVs.Overexpressed HPV16 E7 enhanced MALAT1 expression significantly.HPV16 E7 was knocked down in Caski and SiHa cells by two different siRNAs against HPV16 E7.E7 was involved in the upregulation of MALAT1.Subsequently, in order to investigate the relationship between E7 and SP1 binding sites, C33A cells were transiently co-transfected SP1 luciferase reporter plasmid pGM-SP1-Luc with E7 or SP1 expressing plasmid.To further address whether E7 could bind directly to the MALAT1 promoter, ChIP analysis was performed.The PCR product of MALAT1 promoter was detected after pulling down E7 in E7-overexpressing C33A cells.Firstly, Co-IP assay was performed. C33A cells were co-transfected pCMV-flag-SP1 with pCMV-myc-E7FL . The co-IP result showed that wild type HPV16E7  interacted with SP1 in C33A cells.Wild-type HPV16 E7  can interact with SP1 and form a complex with MALAT1 promoter.E7 FL  promote cell proliferation, invasion, and migration, which can be reversed by siMALAT1.Finally, CCK-8 assays indicated that E7FL  both remarkably increased C33A cells growth, and all above promotion effect could be reversed by siMALAT1.To our knowledge, this was the first reported function model for E7 as transcription activator to directly bind to the target promoter.	34659524	RID08109	transcriptional regulation	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Cervical cancer	E7N	MALAT1	positively-E	siRNA;luciferase reporter assay;ChIP;RNA pull-down assay;overexpression;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	PCG	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	LncRNA MALAT1 was regulated by HPV16 E7 independently of pRB in cervical cancer cells.MALAT1 RNA levels were examined using qRT-PCRin clinical specimen.MALAT1 was upregulated in cervical tissues and cervical cancer cell lines infected with HPVs.Overexpressed HPV16 E7 enhanced MALAT1 expression significantly.HPV16 E7 was knocked down in Caski and SiHa cells by two different siRNAs against HPV16 E7.E7 was involved in the upregulation of MALAT1.Subsequently, in order to investigate the relationship between E7 and SP1 binding sites, C33A cells were transiently co-transfected SP1 luciferase reporter plasmid pGM-SP1-Luc with E7 or SP1 expressing plasmid.To further address whether E7 could bind directly to the MALAT1 promoter, ChIP analysis was performed.The PCR product of MALAT1 promoter was detected after pulling down E7 in E7-overexpressing C33A cells.Firstly, Co-IP assay was performed. C33A cells were co-transfected pCMV-flag-SP1 with pCMV-myc-E7FL . The co-IP result showed that wild type HPV16E7  interacted with SP1 in C33A cells.Wild-type HPV16 E7  can interact with SP1 and form a complex with MALAT1 promoter.E7 FL  promote cell proliferation, invasion, and migration, which can be reversed by siMALAT1.Finally, CCK-8 assays indicated that E7FL  both remarkably increased C33A cells growth, and all above promotion effect could be reversed by siMALAT1.To our knowledge, this was the first reported function model for E7 as transcription activator to directly bind to the target promoter.	34659524	RID08110	transcriptional regulation	NA		UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Cervical cancer	SP1	MALAT1	positively-E	Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell growth(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Cervical cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6667	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	LncRNA MALAT1 was regulated by HPV16 E7 independently of pRB in cervical cancer cells.MALAT1 RNA levels were examined using qRT-PCRin clinical specimen.MALAT1 was upregulated in cervical tissues and cervical cancer cell lines infected with HPVs.Overexpressed HPV16 E7 enhanced MALAT1 expression significantly.HPV16 E7 was knocked down in Caski and SiHa cells by two different siRNAs against HPV16 E7.E7 was involved in the upregulation of MALAT1.Subsequently, in order to investigate the relationship between E7 and SP1 binding sites, C33A cells were transiently co-transfected SP1 luciferase reporter plasmid pGM-SP1-Luc with E7 or SP1 expressing plasmid.To further address whether E7 could bind directly to the MALAT1 promoter, ChIP analysis was performed.The PCR product of MALAT1 promoter was detected after pulling down E7 in E7-overexpressing C33A cells.Firstly, Co-IP assay was performed. C33A cells were co-transfected pCMV-flag-SP1 with pCMV-myc-E7FL . The co-IP result showed that wild type HPV16E7  interacted with SP1 in C33A cells.Wild-type HPV16 E7  can interact with SP1 and form a complex with MALAT1 promoter.E7 FL  promote cell proliferation, invasion, and migration, which can be reversed by siMALAT1.Finally, CCK-8 assays indicated that E7FL  both remarkably increased C33A cells growth, and all above promotion effect could be reversed by siMALAT1.To our knowledge, this was the first reported function model for E7 as transcription activator to directly bind to the target promoter.	34659524	RID08111	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Colorectal cancer	E2F4	AGAP2-AS1	positively-E	UCSC;JASPAR;shRNA;ChIP;luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000205250	NA	ENSG00000255737	GRCh38_12:57726271-57728356	1874	100130776	E2F-4	LOC100130776|PUNISHER	E2F4-induced AGAP2-AS1 up-regulation accelerates the progression of colorectal cancer via miR-182-5p/CFL1 axis.We adopted RT-qPCR to detect AGAP2-AS1 expression in CRC and normal tissues.AGAP2-AS1 expresses highly in CRC cells and AGAP2-AS1 depletion represses proliferation and migration, whereas enhancing the apoptosis of CRC cells.Based on the speculation of UCSC ( http://genome.ucsc.edu/ ) and JASPAR ( http://jaspar.genereg. net/ ) databases, E2F4 was predicted to be the underlying transcrip- tion factor of AGAP2-AS1.Silencing the expression of E2F4 via specific shRNA against E2F4 (sh- E2F4) resulted in the evidently reduced AGAP2-AS1 expression in CRC cells.Sub- sequently, we conducted ChIP assay to explore the binding affinity between E2F4 and different AGAP2-AS1 promoter fragments.P FL and P D were also inserted into pGL3 luciferase reporter vector, and the results of lu- ciferase reporter assay which was performed in HEK-293T revealed that E2F4 overexpression can successfully increase the luciferase activity of P FL instead of PD.Subcellular fractionation detection and FISH assay were performed to estimate subcellular location of AGAP2-AS1 in CRC cells and it was demonstrated that AGAP2-AS1 was primarily distributed in the cytoplasm of CRC cells.We then looked for the miRNAs that might in- terplay with AGAP2-AS1 by starBase.Next, RT-qPCR assay was carried out and the results demonstrated that after silencing AGAP2-AS1, the miR-182-5p ex- pression was the most boosted.The result of luciferase reporter as- say unveiled that overexpressing miR-182-5p led to luciferase ac- tivity decreasing of AGAP2-AS1-WT, yet no noticeable change was surveyed in that of AGAP2-AS1-Mut group. Besides, RNA pull-down assay results unveiled that AGAP2-AS1 could be pulled down only by biotinylated miR-182-5p WT.Then, we noticed that inhibiting miR-182-5p could abolish the suppressing effects of AGAP2-AS1 knockdown on CRC cell proliferation.miR-182-5p re- straint could greatly recover the repressive function of AGAP2-AS1 suppression on the migration and invasion of LoVo and SW480 cells.Those data showed that AGAP2-AS1 could sponge miR-182-5p to exert oncogenic functions in CRC.By the use of starBase, we found four mRNAs (CFL1, ATP1B3, RARG and PKN2) exhibited potential interactions with miR-182-5p fol- lowing such thresholds.Furthermore, we unveiled that the expression of CFL1 was significantly diminished after the overexpression of miR-182- 5p, while no obvious change was observed in other three candi- date mRNAs (ATP1B3, RARG and PKN2).It elucidated that only the luciferase activity of CFL1-WT was sharply reduced un- der the co-transfection of miR-182-5p mimics into HEK-293T cells.Besides, cell proliferation inhibited by AGAP2-AS1 inhibition was counteracted again by overexpressing CFL1. The apoptosis boosted by AGAP2-AS1 silence was recovered by over- expressing CFL1.Transwell assay showed that the suppressive function of silencing AGAP2-AS1 on CRC cell migratory and invasive ability were abolished by CFL1 overexpres- sion . The above findings revealed that AGAP2-AS1 could mediate the development of CRC cells via regulating miR- 182-5p/CFL1 axis.AGAP2-AS1 relies on CFL1 to aggravate in vivo tumorigenesis and metastasis in CRC.E2F4-stimulated AGAP2-AS1 aggravated CRC development through regulating miR-182- 5p/CFL1 axis, implying that AGAP2-AS1 might become a potent new target for future therapies for CRC.	34838479	RID08112	transcriptional regulation	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Colorectal cancer	AGAP2-AS1	CFL1	positively-E	starBase;luciferase reporter assay;RNA pull-down assay;knockdown;overexpression	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumorigenesis(+);cell metastasis(-)	ceRNA(miR-182-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000172757	NA	100130776	1072	LOC100130776|PUNISHER	CFL	E2F4-induced AGAP2-AS1 up-regulation accelerates the progression of colorectal cancer via miR-182-5p/CFL1 axis.We adopted RT-qPCR to detect AGAP2-AS1 expression in CRC and normal tissues.AGAP2-AS1 expresses highly in CRC cells and AGAP2-AS1 depletion represses proliferation and migration, whereas enhancing the apoptosis of CRC cells.Based on the speculation of UCSC ( http://genome.ucsc.edu/ ) and JASPAR ( http://jaspar.genereg. net/ ) databases, E2F4 was predicted to be the underlying transcrip- tion factor of AGAP2-AS1.Silencing the expression of E2F4 via specific shRNA against E2F4 (sh- E2F4) resulted in the evidently reduced AGAP2-AS1 expression in CRC cells.Sub- sequently, we conducted ChIP assay to explore the binding affinity between E2F4 and different AGAP2-AS1 promoter fragments.P FL and P D were also inserted into pGL3 luciferase reporter vector, and the results of lu- ciferase reporter assay which was performed in HEK-293T revealed that E2F4 overexpression can successfully increase the luciferase activity of P FL instead of PD.Subcellular fractionation detection and FISH assay were performed to estimate subcellular location of AGAP2-AS1 in CRC cells and it was demonstrated that AGAP2-AS1 was primarily distributed in the cytoplasm of CRC cells.We then looked for the miRNAs that might in- terplay with AGAP2-AS1 by starBase.Next, RT-qPCR assay was carried out and the results demonstrated that after silencing AGAP2-AS1, the miR-182-5p ex- pression was the most boosted.The result of luciferase reporter as- say unveiled that overexpressing miR-182-5p led to luciferase ac- tivity decreasing of AGAP2-AS1-WT, yet no noticeable change was surveyed in that of AGAP2-AS1-Mut group. Besides, RNA pull-down assay results unveiled that AGAP2-AS1 could be pulled down only by biotinylated miR-182-5p WT.Then, we noticed that inhibiting miR-182-5p could abolish the suppressing effects of AGAP2-AS1 knockdown on CRC cell proliferation.miR-182-5p re- straint could greatly recover the repressive function of AGAP2-AS1 suppression on the migration and invasion of LoVo and SW480 cells.Those data showed that AGAP2-AS1 could sponge miR-182-5p to exert oncogenic functions in CRC.By the use of starBase, we found four mRNAs (CFL1, ATP1B3, RARG and PKN2) exhibited potential interactions with miR-182-5p fol- lowing such thresholds.Furthermore, we unveiled that the expression of CFL1 was significantly diminished after the overexpression of miR-182- 5p, while no obvious change was observed in other three candi- date mRNAs (ATP1B3, RARG and PKN2).It elucidated that only the luciferase activity of CFL1-WT was sharply reduced un- der the co-transfection of miR-182-5p mimics into HEK-293T cells.Besides, cell proliferation inhibited by AGAP2-AS1 inhibition was counteracted again by overexpressing CFL1. The apoptosis boosted by AGAP2-AS1 silence was recovered by over- expressing CFL1.Transwell assay showed that the suppressive function of silencing AGAP2-AS1 on CRC cell migratory and invasive ability were abolished by CFL1 overexpres- sion . The above findings revealed that AGAP2-AS1 could mediate the development of CRC cells via regulating miR- 182-5p/CFL1 axis.AGAP2-AS1 relies on CFL1 to aggravate in vivo tumorigenesis and metastasis in CRC.E2F4-stimulated AGAP2-AS1 aggravated CRC development through regulating miR-182- 5p/CFL1 axis, implying that AGAP2-AS1 might become a potent new target for future therapies for CRC.	34838479	RID08113	ceRNA or sponge	metastasis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Lung adenocarcinoma	ENST00000609697	RASL12	positively-E		downregulation	qRT-PCR;microarray	TCGA	NA	angiogenesis(+);cell proliferation(+)	ceRNA(miR-6791-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000103710	NA	NA	51285	NA	RIS	Identification of a novel prognosis-associated ceRNA network in lung adenocarcinoma via bioinformatics analysis.The Cancer Genome Atlas (TCGA) LUAD database, and Kaplan-Meier (KM) survival analysis tools were used to validate the microarray data and construct the lncRNA-siRNA'-mRNA ceRNA regulatory network. Then, quantitative real-time PCR (qRT-PCR was used to validate the DE lncRNAs in 7 LUAD cell lines.The GO and KEGG analysis results suggested that the DE genes were most enriched in angiogenesis and cell proliferation, and were closely related to human cancers. Moreover, the differential expression of ENST00000609697, ENST00000602992, and NR_024321 was consistent with the microarray data, as determined by qRT-PCRvalidation in 7 LUAD cell lines; however, only ENST00000609697 was associated with the overall survival of LUAD patients (log-rank P = 0.029). Finally, through analysis of ENST00000609697 target genes, we identified the ENST00000609697-hsa-miR-6791-5p-RASL12 ceRNA network, which may play a tumor-suppressive role in LUAD.ENST00000609697 was abnormally expressed in LUAD. Furthermore, downregulation of ENST00000609697 and its target gene RASL12 was associated with poor prognosis in LUAD. The ENST00000609697-hsa-miR-6791-5p-RASL12 axis may play a tumor-suppressive role. These results suggest new potential prognostic and therapeutic biomarkers for LUAD.	34819106	RID08114	ceRNA or sponge	prognosis		UP(LIHC);DATA(GSE117623)
Gastric cancer	HULC	MYH9	positively-E	RNAi	upregulation		NA	NA	cell metastasis(+);cancer progression(+)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000100345	NA	728655	4627	HCCAT1|LINC00078|NCRNA00078	DFNA17|EPSTS|FTNS|MHA|NMHC-II-A|NMMHCA	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08115	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	KCNQ1OT1	LMX1A	positively-E		downregulation		NA	NA	cancer progression(+);cell survival(+)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000162761	NA	10984	4009	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	LMX1|LMX1.1	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08116	ceRNA or sponge	metastasis,prognosis	UP(BRCA);DATA(GSE111842)	UP(PAAD);DATA(GSE40174)
Colorectal cancer	LINC01116	ATF1	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(+)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000123268	NA	375295	466	TALNEC2	TREB36	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08117	ceRNA or sponge	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE86978)
Nasopharynx carcinoma	circRNA_000543	PDGFRB	positively-E		upregulation		NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	NA	ENSG00000113721	NA	NA	5159	NA	CD140b|JTK12|PDGFR|PDGFR1	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08118	ceRNA or sponge	metastasis,prognosis		UP(LIHC);DATA(GSE117623)
Hepatocellular carcinoma	HULC	miR-9	negatively-E		upregulation		NA	NA	cholesterol homeostasis(-)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000251164	NA	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08119	transcriptional regulation	metastasis,prognosis		
Hepatocellular carcinoma	HULC	PPARA	positively-E		upregulation		NA	NA	cholesterol homeostasis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251164	NA	ENSG00000186951	NA	728655	5465	HCCAT1|LINC00078|NCRNA00078	hPPAR|NR1C1|PPAR	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08120	ceRNA or sponge	metastasis,prognosis		UP(LIHC,PAAD);DOWN(PRAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE38495,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	HULC	ACSL1	positively-E		upregulation		NA	NA	cholesterol homeostasis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000151726	NA	728655	2180	HCCAT1|LINC00078|NCRNA00078	ACS1|FACL1|FACL2|LACS|LACS1|LACS2	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08121	ceRNA or sponge	metastasis,prognosis		UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	DUXAP8	IGF1R	positively-E		upregulation		NA	NA	tumorigenesis(+)	ceRNA(miR-9-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000140443	NA	503637	3480	NA	CD221|IGFIR|IGFR|JTK13|MGC18216	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08122	ceRNA or sponge	metastasis,prognosis	UP(LIHC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE86978)
Hepatocellular carcinoma	MEG3	MDK	positively-E		downregulation		NA	NA	cell growth(+);cell survival(+);cell metastasis(+)	ceRNA(miR-9-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000110492	NA	55384	4192	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	FLJ27379|MK|NEGF2	The dual role of microRNA-9 in gastrointestinal cancers: oncomiR or tumor suppressor- LncRNA highly up-regulated in liver cancer (HULC) has been recently reported as an oncogene implicated in different human tumors. It has been shown that HULC was over-expressed and miR-9-5p was down-expressed in GC, and both were significantly correlated with clinic-pathologic characteristics of gastric cancer patients. Myosin heavy chain 9 (MYH9) was a direct target of miR-9-5p in GC cells. HULC can regulate MYH9 amplification by acting as a molecular sponge of miR-9-5p. Furthermore, MYH9 was over-expressed and its transcription was positively correlated with HULC value while negatively associated with miR-9-5p level in gastric cancer tissues. Regarding to the accelerating role of MYH9 on GC metastasis, it has been suggested that HULC silencing suppressed gastric cancer progression through modulating miR-9-5p/MYH9 axis.LncRNA KCNQ1OT1 inhibits the development of gastric cancer cells by regulating miR-9 and LIM homeobox transcription factor 1alpha (LMX1A) expression. LMX1A, act as a tumor suppressor protein, is downexpressed in gastric cancer. miR-9 up-regulation is related with decreased LMX1A 3'-UTR activity and induce gastric cancer cell progression and survival.LncRNAs also participate in CRC formation, development, metastasis, autophagy and drug resistance [86'-8]. Recently, Bi and co-researchers expressed that long intergenic non-protein coding RNA 1116 (LINC01116) was over-expressed in CRC tissues, while miR-9-5p was down regulated. Knockdown of LINC01116 mitigated development, dissemination and invasion of CRC cell. Furthermore, Zhao and co-workers showed that lncRNAs LINC00665 can elevate the proliferation, migration and invasion as well as prevented cellular death of CRC cells by regulating miR-9-5p/ATF1 axis. Activating transcription factor 1(ATF1) is a member of the ATF/CREB family which modulates the expression of genes involved in cell viability and controlling cell transformation.Chen et al. studied the function of circRNAs in NPC radio-resistance and demonstrated that circRNA_000543 expression was significantly up-regulated in cancerous tissues. CircRNA_000543 was also high-expressed but miR-9 was down-regulated in resistant samples compared to radiosensitive samples. Their investigation revealed that circRNA_000543 knockdown induced sensitivity to irradiation in nasopharyngeal cancerous cells through targeting miR-9/platelet-derived growth factor receptor B (PDGFRB) axis. miR-9 levels were significantly down-expressed in NPC tissue and reversely affected with circRNA_000543 amplification. PDGFRB is involved in vessels development, EMT and metastasis. PDGFRB stimulation increases the miR-9 expression and sequentially, miR-9 prevents PDGFRB activation by targeting this growth factor mRNA. In conclusion, miR-9 was negatively related with circRNA_000543 and PDFGRB expression.LncRNAs HULC participates in abnormal lipid metabolism in HCC via modulating miR-9/PPARA/ACSL1/cholesterol/RXRA pathway. Particularly, HULC induces the methylation of the promoter region of miR-9, leading to the inhibition of miR-9 expression.miR-9 can target the transcription factor, peroxisome proliferator activated receptor alpha (PPARA) which is frequently amplified in liver. Down-expression of miR-9 causes to up-regulation of PPARA and the consequently transactivation of ACSL1 which promotes lipogenesis and enhances triglycerides and cholesterol in hepatoma cells.LncRNA double homeobox A pseudogene 8 (DUXAP8) is an oncogene and a potential biomarker in different tumors. It has been reported that DUXAP8 and insulin-like growth factor 1 receptor (IGF1R) were over-expressed and miR-9-3p was down-expressed in HCC tissues and cells versus normal tissues and cell line. IGF1R has tyrosine kinase function and an antiapoptotic role via promoting cell survival in various tumors. DUXAP8 participated to HCC tumorigenesis possibly through the miR-9-3p/IGF1R pathway. Another lncRNA, maternally expressed gene 3 (MEG3) as a tumor suppressor affects HCC cell viability, apoptosis and metastasis via targeting of miR-9-5p/MDK pathway. MDK as a direct target of miR-9-5p is a pleiotropic factor accelerating tumor cell growth, survival, metastasis, dissemination and angiogenesis.Altogether, our results show the differentially expressive miR-9 in digestive tract tumors, which will provide valuable data for identification of diagnostic and prognostic biomarker and molecular targeted therapy based on miRs.	34781141	RID08123	ceRNA or sponge	metastasis,prognosis		UP(BRCA);DATA(GSE55807)
Malignant glioma	FAM87A	PPM1H	positively-E	miRcode;miRDB;Targetscan;mirDIP;luciferase reporter assay;RIP;shRNA;siRNA	downregulation	qRT-PCR	TCGA	NA	PI3K/AKT signaling pathway(+);tumor growth(+)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000182366	GRCh38_8:375931-384079	ENSG00000111110	NA	157693	57460	NA	ARHCL1|FLJ13253|KIAA1157|NERPP-2C	FAM87A as a Competing Endogenous RNA of miR-424-5p Suppresses Glioma Progression by Regulating PPM1H. RNA expression and clinical data on glioma were accessed from The Cancer Genome Atlas (TCGA) database.Dysregulated lncRNAs (DElncRNAs) and miRNAs (DEmiRNAs) with binding sites were screened by the miRcode database.miRDB, TargetScan, and mirDIP databases were applied to predict downstream genes of miR-424-5p.FAM87A Is Lowly Expressed in Glioma Tissue and Cells and Negatively Correlated with TNM Staging and Metastasis.Downstream modulatory miRNAs of FAM87A were predicted in the miRcode database and intersected with DEmiRNAs to obtain 5 miRNAs.Binding sites of FAM87A and miR-424-5p were predicted utilizing miRcode. Results of dual-luciferase reporter genes revealed that hastened miR- 424-5p restrained expression of cells with wild-type (WT) FAM87A but had no effect on the expression of cells with mutant (MUT) FAM87A. A binding relationship between miR-424-5p and FAM87A was displayed.Result was further confirmed by the RIP assay.Downstream regulatory target genes of miR-424-5p were predicted by the bioinformatic database, and then the predicted results were overlapped with the DEmRNAs and 9 DEmRNAs (PPM1H, ANKRD33B, PCDHAC2, RSPO3, SPTBN2, UNC13A, KIF5A, SYT4, and HTR2A) with binding sites that were acquired.PPM1H was selected as the study object. qRT-PCRresults expressed that PPM1H was notably repressed in the glioma tissue, positively relevant with FAM87A and negatively relevant with miR-424-5p.The binding sites of miR-424-5p and PPM1H were found by Targetscan. Dual-luciferase reporter gene assay results indicated that facilitated miR-424-5p decreased the luciferase activity of cells with PPM1H 3'-UTR WT, while luciferase activity of cells with PPM1H 3'-UTR MUT was not affected. RIP test on T98G cells showed that the overexpression of FAM87A could restrain binding of PPM1H and miR-424-5p, indicating that FAM87A was highly likely to competitively bind to miR-424-5p with PPM1H, thereby modulating the development of glioma.Furthermore, sh-PPM1H was used to construct cell line with si-PPM1H, and role of PPM1H in glioma was explored through a series of cell functions.PI3K/Akt Signaling Pathway Is Regulated by FAM87A/miR-424-5p/PPM1H Signaling axis.FAM87A Inhibits Tumor Growth In Vivo.Taken together, FAM87A as a tumor eliminator was downregulated in glioma. FAM87A could restrain progression of glioma through targeting PPM1H through sponge of miR- 424-5p, while the FAM87A/miR-424-5p/PPM1H signaling axis can modulate the PI3K/Akt signaling pathway. In a word, the FAM87A/miR-424-5p/PPM1H axis plays a crucial part in glioma and can be utilized as a key treatment target.	34712356	RID08124	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE86978)
Lung cancer	HOTAIR	miR-34a	negatively-E	overexpression;RNAi	upregulation		NA	NA	PI3K/AKT signaling pathway(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Differential expression of long non-coding RNAs as diagnostic markers for lung cancer and other malignant tumors.Over-expression of LncRNA HOTAIR promotes transformation of malignant tumors, leading to a poor prognosis. Furthermore, HOTAIR combines with EZH2 and SUZ12, and directly binds miR-34a promoter region, regulating expression level of miRNA. Suppressing miR-34a expression activates the PI3K/AKT signaling that enhances lung cancer development.lncRNA-PVTL5 can act as a competitive endogenous miR-126 RNA to accelerate cell proliferation by regulating the miR-126/SLC7A5 axis. LncRNA PVTL5 plays a significant role in lung cancer progression. Besides, the regulatory network could be one of the molecular mechanisms for the occurrence and malignant transformation of lung cancer.It has also been shown that inhibiting miR-101-3p and activating the Wnt/beta-catenin signaling pathway upregulates lncRNA SNHG1, promoting NSCLC progression.In addition, a surgeon found that lncRNA SNHG12 up-regulates the expression of miR-181a to silence the expressions of MAPK1 and MAP2K1, and inhibits the MAPK/Slug signaling pathway by suppressing the level of phosphorylation MAPK1 (p-MAPK1), MAP2K1 (p-MAP2K1), and Slug phosphorylation. SNHG12-miR-181a-MAPK/Slug axis has been established in their research, and the role of lncRNA SNHG12 in NSCLC multidrug resistance (MDR) was partially elucidated, providing a new therapeutic target for the treatment of NSCLC MDR.Liu et al.Reported that the lncRNA HULC overexpression can promote cell proliferation and inhibit cell apoptosis by up-regulating the expression of SPHK1 protein expression in NSCLC, which induces the activation of its downstream PI3K/AKT signaling pathway.This study aimed at systematically describing lncRNAs from five aspects based on recent studies: concepts, classification, structure, molecular mechanism, signal pathway, as well as review lncRNA implications in malignant tumor.	34670194	RID08125	transcriptional regulation	prognosis		
Lung cancer	PVTL5	SLC7A5	positively-E		upregulation		NA	NA	cell proliferation(+)	ceRNA(miR-126)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000103257	NA	NA	8140	NA	CD98|D16S469E|E16|LAT1|MPE16	Differential expression of long non-coding RNAs as diagnostic markers for lung cancer and other malignant tumors.Over-expression of LncRNA HOTAIR promotes transformation of malignant tumors, leading to a poor prognosis. Furthermore, HOTAIR combines with EZH2 and SUZ12, and directly binds miR-34a promoter region, regulating expression level of miRNA. Suppressing miR-34a expression activates the PI3K/AKT signaling that enhances lung cancer development.lncRNA-PVTL5 can act as a competitive endogenous miR-126 RNA to accelerate cell proliferation by regulating the miR-126/SLC7A5 axis. LncRNA PVTL5 plays a significant role in lung cancer progression. Besides, the regulatory network could be one of the molecular mechanisms for the occurrence and malignant transformation of lung cancer.It has also been shown that inhibiting miR-101-3p and activating the Wnt/beta-catenin signaling pathway upregulates lncRNA SNHG1, promoting NSCLC progression.In addition, a surgeon found that lncRNA SNHG12 up-regulates the expression of miR-181a to silence the expressions of MAPK1 and MAP2K1, and inhibits the MAPK/Slug signaling pathway by suppressing the level of phosphorylation MAPK1 (p-MAPK1), MAP2K1 (p-MAP2K1), and Slug phosphorylation. SNHG12-miR-181a-MAPK/Slug axis has been established in their research, and the role of lncRNA SNHG12 in NSCLC multidrug resistance (MDR) was partially elucidated, providing a new therapeutic target for the treatment of NSCLC MDR.Liu et al.Reported that the lncRNA HULC overexpression can promote cell proliferation and inhibit cell apoptosis by up-regulating the expression of SPHK1 protein expression in NSCLC, which induces the activation of its downstream PI3K/AKT signaling pathway.This study aimed at systematically describing lncRNAs from five aspects based on recent studies: concepts, classification, structure, molecular mechanism, signal pathway, as well as review lncRNA implications in malignant tumor.	34670194	RID08126	ceRNA or sponge	prognosis		UP(LIHC,PAAD,BRCA);DOWN(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827)
Non-small cell lung cancer	miR-101-3p	SNHG1	negatively-E		upregulation		NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	sponge	binding/interaction	NA	NA	CSC	NA	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	23642	NA	LINC00057|lncRNA16|NCRNA00057|UHG	Differential expression of long non-coding RNAs as diagnostic markers for lung cancer and other malignant tumors.Over-expression of LncRNA HOTAIR promotes transformation of malignant tumors, leading to a poor prognosis. Furthermore, HOTAIR combines with EZH2 and SUZ12, and directly binds miR-34a promoter region, regulating expression level of miRNA. Suppressing miR-34a expression activates the PI3K/AKT signaling that enhances lung cancer development.lncRNA-PVTL5 can act as a competitive endogenous miR-126 RNA to accelerate cell proliferation by regulating the miR-126/SLC7A5 axis. LncRNA PVTL5 plays a significant role in lung cancer progression. Besides, the regulatory network could be one of the molecular mechanisms for the occurrence and malignant transformation of lung cancer.It has also been shown that inhibiting miR-101-3p and activating the Wnt/beta-catenin signaling pathway upregulates lncRNA SNHG1, promoting NSCLC progression.In addition, a surgeon found that lncRNA SNHG12 up-regulates the expression of miR-181a to silence the expressions of MAPK1 and MAP2K1, and inhibits the MAPK/Slug signaling pathway by suppressing the level of phosphorylation MAPK1 (p-MAPK1), MAP2K1 (p-MAP2K1), and Slug phosphorylation. SNHG12-miR-181a-MAPK/Slug axis has been established in their research, and the role of lncRNA SNHG12 in NSCLC multidrug resistance (MDR) was partially elucidated, providing a new therapeutic target for the treatment of NSCLC MDR.Liu et al.Reported that the lncRNA HULC overexpression can promote cell proliferation and inhibit cell apoptosis by up-regulating the expression of SPHK1 protein expression in NSCLC, which induces the activation of its downstream PI3K/AKT signaling pathway.This study aimed at systematically describing lncRNAs from five aspects based on recent studies: concepts, classification, structure, molecular mechanism, signal pathway, as well as review lncRNA implications in malignant tumor.	34670194	RID08127	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Non-small cell lung cancer	SNHG12	miR-181a	positively-F		upregulation		NA	NA	MAPK/SLUG signaling pathway(-);chemoresistance(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|PNAS-123	NA	Differential expression of long non-coding RNAs as diagnostic markers for lung cancer and other malignant tumors.Over-expression of LncRNA HOTAIR promotes transformation of malignant tumors, leading to a poor prognosis. Furthermore, HOTAIR combines with EZH2 and SUZ12, and directly binds miR-34a promoter region, regulating expression level of miRNA. Suppressing miR-34a expression activates the PI3K/AKT signaling that enhances lung cancer development.lncRNA-PVTL5 can act as a competitive endogenous miR-126 RNA to accelerate cell proliferation by regulating the miR-126/SLC7A5 axis. LncRNA PVTL5 plays a significant role in lung cancer progression. Besides, the regulatory network could be one of the molecular mechanisms for the occurrence and malignant transformation of lung cancer.It has also been shown that inhibiting miR-101-3p and activating the Wnt/beta-catenin signaling pathway upregulates lncRNA SNHG1, promoting NSCLC progression.In addition, a surgeon found that lncRNA SNHG12 up-regulates the expression of miR-181a to silence the expressions of MAPK1 and MAP2K1, and inhibits the MAPK/Slug signaling pathway by suppressing the level of phosphorylation MAPK1 (p-MAPK1), MAP2K1 (p-MAP2K1), and Slug phosphorylation. SNHG12-miR-181a-MAPK/Slug axis has been established in their research, and the role of lncRNA SNHG12 in NSCLC multidrug resistance (MDR) was partially elucidated, providing a new therapeutic target for the treatment of NSCLC MDR.Liu et al.Reported that the lncRNA HULC overexpression can promote cell proliferation and inhibit cell apoptosis by up-regulating the expression of SPHK1 protein expression in NSCLC, which induces the activation of its downstream PI3K/AKT signaling pathway.This study aimed at systematically describing lncRNAs from five aspects based on recent studies: concepts, classification, structure, molecular mechanism, signal pathway, as well as review lncRNA implications in malignant tumor.	34670194	RID08128	expression association	prognosis,chemoresistance	DOWN(LIHC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)	
Non-small cell lung cancer	HULC	SPHK1	positively-E		upregulation		NA	NA	cell proliferation(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251164	NA	ENSG00000176170	NA	728655	8877	HCCAT1|LINC00078|NCRNA00078	SPHK	Differential expression of long non-coding RNAs as diagnostic markers for lung cancer and other malignant tumors.Over-expression of LncRNA HOTAIR promotes transformation of malignant tumors, leading to a poor prognosis. Furthermore, HOTAIR combines with EZH2 and SUZ12, and directly binds miR-34a promoter region, regulating expression level of miRNA. Suppressing miR-34a expression activates the PI3K/AKT signaling that enhances lung cancer development.lncRNA-PVTL5 can act as a competitive endogenous miR-126 RNA to accelerate cell proliferation by regulating the miR-126/SLC7A5 axis. LncRNA PVTL5 plays a significant role in lung cancer progression. Besides, the regulatory network could be one of the molecular mechanisms for the occurrence and malignant transformation of lung cancer.It has also been shown that inhibiting miR-101-3p and activating the Wnt/beta-catenin signaling pathway upregulates lncRNA SNHG1, promoting NSCLC progression.In addition, a surgeon found that lncRNA SNHG12 up-regulates the expression of miR-181a to silence the expressions of MAPK1 and MAP2K1, and inhibits the MAPK/Slug signaling pathway by suppressing the level of phosphorylation MAPK1 (p-MAPK1), MAP2K1 (p-MAP2K1), and Slug phosphorylation. SNHG12-miR-181a-MAPK/Slug axis has been established in their research, and the role of lncRNA SNHG12 in NSCLC multidrug resistance (MDR) was partially elucidated, providing a new therapeutic target for the treatment of NSCLC MDR.Liu et al.Reported that the lncRNA HULC overexpression can promote cell proliferation and inhibit cell apoptosis by up-regulating the expression of SPHK1 protein expression in NSCLC, which induces the activation of its downstream PI3K/AKT signaling pathway.This study aimed at systematically describing lncRNAs from five aspects based on recent studies: concepts, classification, structure, molecular mechanism, signal pathway, as well as review lncRNA implications in malignant tumor.	34670194	RID08129	expression association	prognosis		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Atherosclerosis	SCIRT	miR-146a	negatively-F	IntaRNA;RNA pull-down assay;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000237686	GRCh38_6:43931572-44074655	ENSG00000253522	NA	101929705	NA	NA	NA	LncRNA SCIRT is downregulated in atherosclerosis and suppresses the proliferation of human aortic smooth muscle cells (HAOSMCs) by sponging miR-146a in cytoplasm. RT-qPCRs were performed to detect the differential expression of SCIRT and miR-146a in plasma samples from both atherosclerosis patients (n = 56) and controls (n = 56). The results showed that SCIRT was significantly downregulated in atherosclerosis.IntaRNA 2.0 was applied to predict the interaction between SCIRT and miR-146a, and the prediction revealed multiple potential base pairings between them.RNA pull-down assay was performed to verify the direct interaction between SCIRT and miR-146a. The results showed that expression levels of SCIRT were significantly higher in Bio-miR-146a pull-down sample compared to that in Bio-NC group, suggesting the direct interaction between them.The overexpression of SCIRT or miR-146a was confirmed in HAOSMCs every 24 h until 96 h.Overexpression of SCIRT and miR-146a did not regulate the expression of each other.The results illustrated that SCIRT could suppress the proliferation of VSMCs, and miR-146a could promote cell proliferation. Moreover, SCIRT inhibited the role of miR-146a in cell proliferation.	34742341	RID08130	ceRNA or sponge	NA		
Gastric adenocarcinoma	TUG1	VEGFA	positively-E	shRNA;overexpression;starBase;luciferase reporter assay;RIP;RNA pull-down assay;ELISA	upregulation	RT-qPCR	GTEx;TCGA	NA	cell proliferation(+);cell migration(+);angiogenesis(+);tumor growth(+)	ceRNA(miR-29c-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	FLJ20618|LINC00080|NCRNA00080	VEGF|VEGF-A|VPF	Long noncoding RNA TUG1 upregulates VEGFA to enhance malignant behaviors in stomach adenocarcinoma by sponging miR-29c-3p.Integrative analysis of GTEx and TCGA revealed that TUG1 is highly expressed in STAD tissues when compared with normal tissues.miR-29c- 3p was significantly downregulated in STAD tissues compared with normal tissues.These results hinted that TUG1 upregulation and miR-29c- 3p downregulation might be involved in the progression of STAD.RT-qPCR analysis confirmed that each vector was successfully transfected into cells.The suppression efficiency for TUG1 expression of sh-TUG1- 1 was slightly higher than that of sh-TUG1- 2.The overexpression of TUG1 enhanced not only the migratory characteristic but also the expression of BMP4, ICAM1, and VCAM1 of STAD cells. The knockdown of TUG1 had the opposite effects.These results demonstrated that the expression of both TUG1 and miR-29c- 3p in STAD cells has a great impact on the tube formation of HUVECs, suggesting that TUG1 upregulation and miR-29c- 3p downregulation are involved in the angiogenesis of endothelial cells during STAD progression.The correlation analysis from the starbase platform revealed an inverse correlation between the expression of TUG1 and miR-29c- 3p in STAD.The level of miR-29c- 3p expression was decreased when TUG1 was overexpressed but elevated when TUG1 was knocked down.Then, dual-luciferase assay was performed and determined that the level of miR-29c- 3p is directly regulated by TUG1.Ago2-RIP assay was conducted and validated the physical interaction between miR-29c- 3p and its potential binding lncRNA TUG1 in AGS cells.Consistently, biotin-coupled RNA pull-down further confirmed that miR-29c- 3p directly interacted with TUG1 in AGS and MGC-803 cells.The abovementioned data demonstrated that TUG1 directly binds to miR-29c- 3p to serve as its molecular sponge, thereby playing a negative regulatory role for miR-29c- 3p expression in STAD cells.CCK-8 and clonogenic assays revealed that miR-29c- 3p is capable of reversing the effects of TUG1 on the cell proliferation of STAD.Based on starbase, we found that VEGFA expression in STAD is negatively related to miR-29c- 3p (r = -0.161, p < 0.001) but positive correlated with TUG1 (r = 0.237, p < 0.001). RT-qPCR and ELISA results demonstrated that TUG1 overexpression and miR-29c- 3p inhibitor significantly elevated VEGFA levels in MGC-803 cells, while the TUG1 depletion and miR-29c- 3p mimic obviously decreased the expression of VEGFA in AGS cells. Dual-luciferase assay demonstrated that miR-29c- 3p is directly bound to VEGFA. Consistently, Ago2-RIP and RNA pull-down assays further confirmed miR-29c- 3p directly interacts with VEGFA.The transfection efficiency of sh-VEFGA dectecting by RT-qPCR and WB was displayed in Figure 7A. In the CCK-8 assay, the increase of cell proliferation.cell migration ability was significantly strengthened by TUG1 overexpression, and this enhancement was partly reversed by VEFGA depletion in MGC-803.TUG1-induced promotion role in angiogenesis is dependent on VEFGA.Overexpressing TUG1 significantly promoted tumor growth compared with the control.WB analysis for Ki-67, BMP4, ICAM1, VCAM1, and CD31 was performed to verify that TUG1 drove STAD tumor growth, metastasis, and angiogenesis via VEFGA in vivo.This finding confirmed that lncRNA TUG1 acts as a ceRNA for miR-29c- 3p to promote tumor progression and angiogenesis by upregulating VEGFA, indicating TUG1 as a therapeutic target in STAD management.	34762771	RID08131	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Acute myeloid leukemia	HOTTIP	MIR196B	positively-F	ChIRP;ChIP;overexpression;western blot;miRTarBase	downregulation	sequencing;qPCR	TCGA;GSE182601	NA	apoptosis process(-)	transcriptional regulation	binding/interaction	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000207584	NA	100316868	442920	HOXA-AS6|HOXA13-AS1|NCRNA00213	MIRN196B|miR-196b|miRNA196B	A coordinated function of lncRNA HOTTIP and miRNA-196b underpinning leukemogenesis by targeting FAS signaling.To identify miRNAs that are directly targeted by HOTTIP, small RNA sequencing was performed in wild-type (WT) and HOTTIP-/- MOLM13 AML cells.We found that a strong elevation and positive correlation of expression of miR-196b with HOTTIP and a group of HOXA genes and their co-factors PBX3 and MESI1.TCGA Kaplan-Meier survival plots show that the expression patterns of HOXA9, HOXA10, PBX3, MEIS1, HOTTIP, miR-196b, and miR-10a correlate and exhibit prognostic significance, and OS was significantly longer in patients having AML with low expression (blue color line) than those having AML with higher expression (red color line).Our data analysis shows posterior HOXA genes are aberrantly overexpressed in MLL-associated MOLM13 cells compared to KASUMI-1/t (8;21) cells.We employed ChIRP-seq to identify HOTTIP binding genomewide.Next, we asked whether HOTTIP controls the chromatin signature at its targeted miRNA loci, using chromatin immunoprecipitation sequencing (ChIP-seq) for histone modifications (H3K4me3, H3K79me2; active; and H3K27me3; repressive) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) to compare chromatin signatures between WT and HOTTIP-/- MOLM13 cells.Surprisingly, miR-196b also targets HOXA9 and MEIS1, which play essential oncogenic roles.Both HOXA9 and MEIS1 were significantly elevated upon miR-196b inhibition.Repression of miR-196b manifested a higher rate of apoptosis compared to NTC-treated MOLM13 cells.Next, we carried out western blotusing WT, HOTTIP-/-, CBS7/9+/-, and the HOTTIP-activated CBS7/9+/- MOLM13 cells. Cleaved CASP3 protein level was markedly increased in HOTTIP-/-and CBS7/9+/- compared to WT cells, whereas the change in cleaved CASP3 protein level was undetectable upon HOTTIP reactivation, which closely resembles WT MOLM13 cells.Thus, HOTTIP remodels the chromatin architecture around miRNAs to promote their transcription and consequently represses tumor suppressors and promotes leukemogenesis.	34845377	RID08132	transcriptional regulation	prognosis		
Silicosis	SNHG1	SP1	positively-E	starBase;LncBase;NPInter;Targetscan;miRWalk;siRNA;overexpression;luciferase reporter assay;Immunofluorescence;western blot;immunohistochemical staining	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);fibrotic(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	TF	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000185591	NA	23642	6667	LINC00057|lncRNA16|NCRNA00057|UHG	NA	Long non-coding RNA SNHG1 promotes fibroblast-to-myofibroblast transition during the development of pulmonary fibrosis induced by silica particles exposure. The differential expression of lnc-SNHG1 and miR-326 in lung tissues and TGF-beta1-treated fibroblasts was detected by the qRT-PCRmethod.We found that lnc-SNHG1 was highly expressed in fibrotic lung tissues of mice and TGF-beta1-treated fibroblasts.LncRNA SNHG1 regulates fibroblasts migration, invasion and promotes the expression of fibrotic molecules.To explore the mechanism involved in lnc-SNHG1 mediated fibroblastic effects, three bioinformatics databases (starBase, LncBase, and NPInter) were used to predict the targeted miRNAs of lnc-SNHG1 and identified potential binding sites of miR-326.Thus, luciferase reporter plasmids containing wild-type (WT) or mutant (MUT) sequences of lnc-SNHG1 in the binding sites of miR-326 were generated.Additionally, we also observed that miR-326 levels were reduced by 70% after lnc-SNHG1 plasmids transfection, while miR-326 levels were increased by almost 3.5-fold after lnc-SNHG1 knockdown than the control cells.Given the roles of lnc-SNHG1 and miR-326 in fibrotic progression, we further studied the potential targets of miR-326 by bioinformatic analysis (TargetScan, miRWalk, and starBase) and found the conserved binding sites of miR-326 in the specificity protein 1 (SP1) 3'UTR region.Similar results were found in immunohistochemical staining, and it showed the increased expression of SP1 in the silica group, and the expression was decreased in the miR-326 group.Taken together, these results suggested that lnc-SNHG1 promoted the progression of silica particles exposure-induced pulmonary fibrosis by mediating fibroblast-tomyofibroblast transition through the miR-326/SP1 axis	34741930	RID08133	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Colorectal cancer	XIST	NLK	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-92b-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000087095	NA	7503	51701	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	NA	The expression of NLK is functionally associated with colorectal cancers (CRC). The mRNA levels of NLK were detected by qRT-PCRin tumor tissues and adjacent tissues.NLK was upregulated in CRC.NLK downregulation decreased the proliferation, colony forming, and migration abilities of RKO cells.NLK knockdown promoted the RKO cell apoptosis and G1 phase cell cycle arrest of RKO cells.Specially, XIST exhibited higher expression in the CRC tissues than in the adjacent tissues whereases the opposite pattern appeared with miR-92b-3p.We then explored the functional relevance of this pattern to CRC in RKO cells. In response to XIST downregulation via RNAi, the expression of miR-92b-3p was significantly upregulated while NLK expression was suppressed.We established a luciferase-based reporter system in which was to measure the influence of upstream stimulation on the transcription level of downstream target genes.Next, we focused on the relationship between NLK and miR-92b-3p. Similarly, miR-92b-3p suppressed the expression of NLK, and disturbing the potential binding between two disrupted this regulatory relationship.We demonstrated that XIST acts directly on the miR-92b-3p transcript and regulates its expression. In a similar way, miR-92b-3p regulates the expression of NLK. Overall data suggested a possible role ceRNA in CRC cells, in which the XIST/miR-92b-3p/NLK signaling axis could play critical roles, therefore possessing potential therapeutic values.	34729110	RID08134	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Gastric cancer	CYTOR	SIRT2	positively-E	miRcode;western blot;siRNA	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-138)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000068903	NA	112597	22933	C2orf59|LINC00152|MGC4677|NCRNA00152	SIR2L	The LINC00152/miR-138 Axis Facilitates Gastric Cancer Progression by Mediating SIRT2.We first used qRT-PCRanalysis to examine the level of LINC00152 in GC patients.LINC00152 expression was significantly elevated in GC tissues compared to that in adjacent nontumor tissues.Next, we aimed at identifying the main target genes of miR-138, which were predicted by using the miRcode website.SIRT2 was predicted to be a potential downstream target of miR-138, which has been confirmed to mediate the GC progression.In addition, we further confirmed that ectopic miR-138 mimic could markedly reduce the SIRT2 level in vitro using qRTPCR and western blot.We determined that the level of miR-138 was negatively correlated with SIRT2 level.To evaluate the possible effects of SIRT2 on GC cell proliferation and apoptosis, we silenced the SIRT2 in HGC27 and MKN45 cells by a specific siRNA (si-SIRT2).Finally, the flow cytometry results showed the elevated apoptosis in si- SIRT2 transfected cells than in si-NC transfected cells.LINC00152/miR-138/SIRT2 Axis Exerted Tumor-Promoting Function in GC by Inducing Cell Growth.LINC00152/miR-138/SIRT2 Axis Exerted Tumor-Promoting Function in GC by Suppressing Cell Apoptosis.Overall, this study elucidates the molecular mechanism of LINC00152 underlying the malignant phenotype of GC cells by mediating miR-138/SIRT2 axis, which provides a new understanding of the role and molecular mechanism of lncRNA in GC and also provides a new way for the treatment of gastric cancer.	34697541	RID08135	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(PAAD,BRCA);DATA(GSE104209,GSE60407,GSE38495,GSE111842,GSE111065,GSE55807,GSE75367)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)
Skin squamous cell carcinoma	HOTAIR	SP1	positively-E		upregulation	RT-qPCR	NA	NA	cell stemness(+);cancer progression(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Skin carcinoma	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000185591	NA	100124700	6667	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR/Sp1/miR-199a critically regulates cancer stemness and malignant progression of cutaneous squamous cell carcinoma.The long non-coding RNA (lncRNA), HOX antisense intergenic RNA (HOTAIR) is a well-characterized oncogene in multiple human cancers, but not in cutaneous squamous cell carcinoma (CSCC). By measuring its expression using RT-qPCR, we detected higher expression of HOTAIR in CSCC than in normal tissues,and in vivo models showed that HOTAIR was essential in maintaining multiple stem cell phenotypes of CSCSCs in vitro and in vivo xenograft growth as well as metastasis. Mechanistically, HOTAIR directly interacted with and up-regulated Sp1. Sp1 then induced DNMT1-mediated promoter methylation and direct transcriptional repression of miR-199a-5p. Targeting Sp1 or DNMT1 further boosted the in vivo anti-tumor and anti-metastasis activities of targeting HOTAIR. In conclusion, HOTAIR, by up-regulating Sp1 and targeting miR-199a, promotes stemness and progression of CSCC. Targeting HOTAIR, Sp1 or the underlying mechanisms may thus benefit CSCC treatment.	34697449	RID08136	expression association	metastasis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Skin squamous cell carcinoma	HOTAIR	miR-199a-5p	negatively-E		upregulation	RT-qPCR	NA	NA	cell stemness(+);cancer progression(+)	transcriptional regulation	regulation	NA	NA	CSC	NA	Cancer	Skin carcinoma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR/Sp1/miR-199a critically regulates cancer stemness and malignant progression of cutaneous squamous cell carcinoma.The long non-coding RNA (lncRNA), HOX antisense intergenic RNA (HOTAIR) is a well-characterized oncogene in multiple human cancers, but not in cutaneous squamous cell carcinoma (CSCC). By measuring its expression using RT-qPCR, we detected higher expression of HOTAIR in CSCC than in normal tissues,and in vivo models showed that HOTAIR was essential in maintaining multiple stem cell phenotypes of CSCSCs in vitro and in vivo xenograft growth as well as metastasis. Mechanistically, HOTAIR directly interacted with and up-regulated Sp1. Sp1 then induced DNMT1-mediated promoter methylation and direct transcriptional repression of miR-199a-5p. Targeting Sp1 or DNMT1 further boosted the in vivo anti-tumor and anti-metastasis activities of targeting HOTAIR. In conclusion, HOTAIR, by up-regulating Sp1 and targeting miR-199a, promotes stemness and progression of CSCC. Targeting HOTAIR, Sp1 or the underlying mechanisms may thus benefit CSCC treatment.	34697449	RID08137	transcriptional regulation	metastasis		
Oral squamous cell carcinoma	ZFAS1	CCL5	positively-E		upregulation		NA	NA	cancer progression(+)	ceRNA(miR-6499-3p)	regulation	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000161570	NA	441951	6352	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	D17S136E|MGC17164|RANTES|SCYA5|SISd|TCP228	Long Noncoding RNA ZFAS1 Promotes Progression of Oral Squamous Cell Carcinoma Through Targeting miR-6499-3p/CCL5 Axis.We identified the lncRNA ZFAS1 levels in OSCC cells and tissues and confirmed its relationship to tumor progression. Secondly, we identified a lncRNA-miRNA-mRNA network, which was closely associated with OSCC development using bioinformatics methods. Next, our hypothesis that lncRNA ZFAS1 modulates OSCC progression was verified with in vitro and in vivo experiments. Firstly, we found lncRNA ZFAS1 expression increased within OSCC cells and tissues and was positively associated with tumor progression. Secondly, its lncRNA-miRNA-mRNA network was determined, and the target of ZFAS1 was identified as miR-6499-3p/C-C motif chemokine ligand 5 (CCL5). Mechanistically, we found that ZFAS1 up-regulated CCL5 by competitively sponging miR-6499-3p. Further studies demonstrated that ZFAS1 promoted tumor progression in vivo and in vitro. Our results indicate that ZFAS1 serves as a crucial oncogenic factor in OSCC occurrence and development and may therefore serve as a possible therapeutic target for OSCC.	34697152	RID08138	ceRNA or sponge	chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	UP(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE86978)
Osteosarcoma	MALAT1	VEGFA	positively-E	western blot;ELISA;siRNA;luciferase reporter assay;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	VEGF|VEGF-A|VPF	LncRNA MALAT1 Promotes Tumor Angiogenesis by Regulating MicroRNA-150-5p/VEGFA Signaling in Osteosarcoma: In-Vitro and In-Vivo Analyses. real-time RT-PCRanalysis was used to detect MALAT1 expression in OS cell lines in order to assess its level.The MALAT1 expression level was elevated in the OS cell line.The angiogenesis-related gene, VEGFA level was analyzed in MG63 and SaOS2 cells and cell culture supernatants of MG63 and SaOS2 cells via western blot and ELISA.knocking down MALAT1 by si-MALAT1 transfection greatly reduced VEGFA expression and secretion level in MG63 and SaOS2 cells but had no impact on HGF or VEGFD/C.MALAT1 knockdown dramatically inhibited the expression of miR-150-5p in MG63 and SaOS2 cells.mutant MALAT1 3-UTR were used to measure relative luciferase activity. In MG63 cells cotransfected with miR-150-5p mimic and wild MALAT1 3'-UTR.The regulation and interaction between MALAT1 and miR-150-5p have been confirmed using various molecular techniques like RNA pull down, ribonucleoprotein immunoprecipitation analysis, and luciferase reporter assay and in various studies.MG63 cells were grown in coverslips and transfected with si-MALAT/si-control, miR- 150-5p mimic, or control miRNA for 24 h, then inversely kept on CAM bed at day 4.LncRNA MALAT1 Regulates VEGFA-Mediated Tumor Angiogenesis in OS by Targeting miR-150-5p.Overall, our findings suggest that MALAT1 promotes angiogenesis by regulating the miR-150-5p/VEGFA signaling in OS microenvironment. The findings of the molecular mechanisms of MALAT1 in tumor angiogenesis offer a new viewpoint on OS treatment.	34692524	RID08139	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Lung adenocarcinoma	ICMT-DT	YTHDF1	positively-E	RegRNA;RNA pull-down assay;miRDB;western blot;luciferase reporter assay;shRNA	upregulation	qRT-PCR	GTEx;TCGA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);tumor growth(+);cell metastasis(+)	ceRNA(miR-1285-3p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000225077	GRCh38_1:6234692-6239444	ENSG00000149658	NA	148645	54915	C1orf211|LINC00337|MGC40168|NCRNA00337	C20orf21|FLJ20391	LncRNA LINC00337 sponges mir-1285-3p to promote proliferation and metastasis of lung adenocarcinoma cells by upregulating YTHDF1. Through the analysis of TCGA and GTEx databases, we found that LINC00337 was significantly increased in lung adenocarcinoma tissues.By searching an online bioinformatics database (RegRNA 2.0, http:// regrn a2. mbc. nctu. edu. tw/), we observed that six miRNAs possessed putative binding sites for LINC00337.Later, we utilized a biotin pull-down system to continuously probe miRNAs that directly interplay with LINC00337. We unraveled a significant amount of miR- 1285-3p in the LINC00337 pull-down pellet relative to the control group, as examined by qRT-PCR but the proportions of miR-492, miR-1273a, miR-5095, miR- 1273 g-3p, and miR-1304-5p in the LINC00337 pull-down pellet displayed a clear elevation relative to the control group.By searching miRDB, we observed seven target genes of miR-1285-3p, with scores >95 (http:// mirdb. org/): AHI1, DAB2IP, BTRC, YTHDF1, TMEM41B, SIKE1, and FMO5.Results of qRT-PCR;ISHowed that the YTHDF1 levels in cancer tissues were significantly increased (Fig. 5B), and western blot showed that downregulation of LINC00337 decreased the protein level of YTHDF1.dual-luciferase reporter assays were implemented using a human YTHDF1 3'-UTR fragment with supposed binding sites of miR-1285-3p and the YTHDF1 promoter reporter vector for the notarizing effect of miR-1285-3p on YTHDF1. Cells transfected with stable sh-LINC00337 exhibited a dramatically decreased relative luciferase activity of YTHDF1-3'-UTR.Knockdown of miR-1285-3p and upregulation of YTHDF1 reversed the cell proliferation that was reduced by LINC00337 shRNA.Both knockdown of YTHDF1 and upregulation of miR-1285-3p reversed the effects caused by overexpression of LINC00337 on cell apoptosis, migration, and invasion.Inhibition of LINC00337 suppresses lung adenocarcinoma tumor growth and metastasize in vivo.These results suggest that LINC00337 acts as an oncogenic lncRNA, targeting miR-1285-3p and regulating YTHDF1 expression, to promote the progression of lung adenocarcinoma.	34663343	RID08140	ceRNA or sponge	metastasis		DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)
Rheumatoid arthritis	THRIL	MMP1	negatively-E	siRNA;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000196611	NA	102659353	4312	BRI3BP-AS1|Linc1992|TCONS_00020260	CLG	LncRNA THRIL is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.Small interfering RNA targeting  THRIL  or lentivirus overexpressing  THRIL  was used to knockdown or overexpress  THRIL . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. A significant decrease in  THRIL  expression was found in RA FLSs compared with cells from healthy control (HC)patients.  THRIL  is mainly localized in the nucleus. Knockdown of  THRIL  increased the proliferation, migration, and invasion of RA FLSs. In contrast,  THRIL  overexpression had the opposite effect.  THRIL  knockdown increased interleukin-1beta (IL-1beta)-triggered expression of matrix metalloproteinase ( MMP )-1,  MMP-3 , and  MMP-13 .  THRIL  overexpression led to a significant decrease in  MMP-13  expression in response to stimulation with IL-1beta. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 ( CDK1 ) and G2 and S phase-expressed-1 ( GTSE1 ), both of which are associated with cellular mobility and proliferation, were downregulated with  THRIL  overexpression. Reduced expression of lncRNA  THRIL  represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA  THRIL  might be a potential target for RA therapy.	34733920	RID08141	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Rheumatoid arthritis	THRIL	MMP3	negatively-E	siRNA;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000263313	NA	102659353	4314	BRI3BP-AS1|Linc1992|TCONS_00020260	STMY|STMY1	LncRNA THRIL is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.Small interfering RNA targeting  THRIL  or lentivirus overexpressing  THRIL  was used to knockdown or overexpress  THRIL . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. A significant decrease in  THRIL  expression was found in RA FLSs compared with cells from healthy control (HC)patients.  THRIL  is mainly localized in the nucleus. Knockdown of  THRIL  increased the proliferation, migration, and invasion of RA FLSs. In contrast,  THRIL  overexpression had the opposite effect.  THRIL  knockdown increased interleukin-1beta (IL-1beta)-triggered expression of matrix metalloproteinase ( MMP )-1,  MMP-3 , and  MMP-13 .  THRIL  overexpression led to a significant decrease in  MMP-13  expression in response to stimulation with IL-1beta. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 ( CDK1 ) and G2 and S phase-expressed-1 ( GTSE1 ), both of which are associated with cellular mobility and proliferation, were downregulated with  THRIL  overexpression. Reduced expression of lncRNA  THRIL  represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA  THRIL  might be a potential target for RA therapy.	34733920	RID08142	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Rheumatoid arthritis	THRIL	MMP13	negatively-E	siRNA;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000137745	NA	102659353	4322	BRI3BP-AS1|Linc1992|TCONS_00020260	CLG3	LncRNA THRIL is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.Small interfering RNA targeting  THRIL  or lentivirus overexpressing  THRIL  was used to knockdown or overexpress  THRIL . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. A significant decrease in  THRIL  expression was found in RA FLSs compared with cells from healthy control (HC)patients.  THRIL  is mainly localized in the nucleus. Knockdown of  THRIL  increased the proliferation, migration, and invasion of RA FLSs. In contrast,  THRIL  overexpression had the opposite effect.  THRIL  knockdown increased interleukin-1beta (IL-1beta)-triggered expression of matrix metalloproteinase ( MMP )-1,  MMP-3 , and  MMP-13 .  THRIL  overexpression led to a significant decrease in  MMP-13  expression in response to stimulation with IL-1beta. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 ( CDK1 ) and G2 and S phase-expressed-1 ( GTSE1 ), both of which are associated with cellular mobility and proliferation, were downregulated with  THRIL  overexpression. Reduced expression of lncRNA  THRIL  represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA  THRIL  might be a potential target for RA therapy.	34733920	RID08143	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(PAAD);DATA(GSE40174)
Rheumatoid arthritis	THRIL	CDK1	negatively-E	siRNA;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000170312	NA	102659353	983	BRI3BP-AS1|Linc1992|TCONS_00020260	CDC2|CDC28A	LncRNA THRIL is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.Small interfering RNA targeting  THRIL  or lentivirus overexpressing  THRIL  was used to knockdown or overexpress  THRIL . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. A significant decrease in  THRIL  expression was found in RA FLSs compared with cells from healthy control (HC)patients.  THRIL  is mainly localized in the nucleus. Knockdown of  THRIL  increased the proliferation, migration, and invasion of RA FLSs. In contrast,  THRIL  overexpression had the opposite effect.  THRIL  knockdown increased interleukin-1beta (IL-1beta)-triggered expression of matrix metalloproteinase ( MMP )-1,  MMP-3 , and  MMP-13 .  THRIL  overexpression led to a significant decrease in  MMP-13  expression in response to stimulation with IL-1beta. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 ( CDK1 ) and G2 and S phase-expressed-1 ( GTSE1 ), both of which are associated with cellular mobility and proliferation, were downregulated with  THRIL  overexpression. Reduced expression of lncRNA  THRIL  represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA  THRIL  might be a potential target for RA therapy.	34733920	RID08144	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE55807)
Rheumatoid arthritis	THRIL	GTSE1	negatively-E	siRNA;overexpression	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000075218	NA	102659353	51512	BRI3BP-AS1|Linc1992|TCONS_00020260	B99|GTSE-1|Lnc_bc060912	LncRNA THRIL is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.Small interfering RNA targeting  THRIL  or lentivirus overexpressing  THRIL  was used to knockdown or overexpress  THRIL . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. A significant decrease in  THRIL  expression was found in RA FLSs compared with cells from healthy control (HC)patients.  THRIL  is mainly localized in the nucleus. Knockdown of  THRIL  increased the proliferation, migration, and invasion of RA FLSs. In contrast,  THRIL  overexpression had the opposite effect.  THRIL  knockdown increased interleukin-1beta (IL-1beta)-triggered expression of matrix metalloproteinase ( MMP )-1,  MMP-3 , and  MMP-13 .  THRIL  overexpression led to a significant decrease in  MMP-13  expression in response to stimulation with IL-1beta. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 ( CDK1 ) and G2 and S phase-expressed-1 ( GTSE1 ), both of which are associated with cellular mobility and proliferation, were downregulated with  THRIL  overexpression. Reduced expression of lncRNA  THRIL  represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA  THRIL  might be a potential target for RA therapy.	34733920	RID08145	expression association	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367)	UP(LIHC,PAAD,SKCM);DATA(GSE117623,GSE40174,GSE38495)
Head and neck squamous cell carcinoma	LINC00460	miR-206	negatively-F	knockdown;overexpression	upregulation		NA	NA	AKT signaling pathway(+);cell cycle(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08146	ceRNA or sponge	metastasis,prognosis		
Head and neck squamous cell carcinoma	PRDX1	LINC00460	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Head and neck cancer	PCG	lncRNA	ENSG00000117450	NA	ENSG00000233532	GRCh38_13:106374477-106384315	5052	728192	NKEFA|PAGA	NA	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08147	transcriptional regulation	metastasis,prognosis	DOWN(LIHC,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	
Esophagus squamous cell carcinoma	LINC00460	miR-1224-5p	negatively-F	knockdown	upregulation		NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	NA	NA	728192	NA	NA	NA	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08148	ceRNA or sponge	metastasis,prognosis		
Non-small cell lung cancer	LINC00460	MIR539	negatively-F		upregulation		NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000202560	NA	728192	664612	NA	MIRN539|hsa-mir-539|mir-539	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08149	ceRNA or sponge	metastasis,prognosis		
Non-small cell lung cancer	LINC00460	EGFR	positively-E		upregulation		NA	NA	chemoresistance(+)	ceRNA(miR-769-5p)	regulation	NA	Gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000146648	NA	728192	1956	NA	ERBB|ERBB1|ERRP	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08150	ceRNA or sponge	metastasis,prognosis,chemoresistance		UP(LIHC,NSCLC,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE109761,GSE111065,GSE55807)
Papillary thyroid carcinoma	LINC00460	FOXA1	positively-E		upregulation		NA	NA	cell growth(+)	ceRNA(miR-302c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000129514	NA	728192	3169	NA	HNF3A	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08151	ceRNA or sponge	metastasis,prognosis		UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Papillary thyroid carcinoma	LINC00460	RAF1	positively-E		upregulation		NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000132155	NA	728192	5894	NA	c-Raf|CRAF|Raf-1	LncRNA LINC00460: Function and mechanism in human cancer.High expression of LINC00460 was detected in HNSCC tissues and was associated with poor survival.In some studies, LINC00460 promoted HNSCC progression by sponging miRNAs and inhibiting their expression.Xue et al.28 found that LINC00460 silencing affected cell cycle distribution and promoted cell apoptosis and autophagy.Jiang et al.18 found that PRDX1 is an RBP that binds with LINC00460 to affect cell proliferation, migration and EMT in HNSCC. Silencing PRDX1 decreased the expression of LINC00460, whereas PRDX1 overexpression increased the expression of LINC00460. PRDX1 facilitated the transcription of LINC00460 and EMT-related genes in the nucleus.Liang et al.32 found that LINC00460 was significantly elevated in most of tumor tissues and ESCC cell lines.Knockdown of LINC00460 suppressed the metastasis potential and EMT of EC cells by directly binding to miR- 1224-5p.Wang et al.34 indicated that LINC00460 is competitively bound with miR-539 sites to restrain the suppressive effect on NSCLC cell proliferation. In addition, Ma et al.35 found that LINC00460 is involved in gefitinib resistance in NSCLC cells by targeting epidermal growth factor receptor (EGFR) through sponging miR-769-5p.The upregulated expression of LINC00460 in LC tissues predicted poor prognosis, and silencing of LINC00460 inhibited cell growth in LC.71 Ye et al.22 found that LINC00460 promoted LC cell growth partially by upregulating FOXA1, the special target site for LINC00460 and miR-302c-5p, and the effects were partially regulated by the LINC00460/miR-302c-5p/FOXA1 axis.It was found that LINC00460 was upregulated in PTC tissues and was associated with poor prognosis,38 advanced TNM stage, and lymph node metastasis.39 Li et al.38 indicated that LINC00460 promoted cell migration, invasion, and EMT of PTC by sponging miR-485-5p to increase the expression of Raf1. Zou et al.23 also found that LINC00460 knockdown restrained PTC progression by downregulating MMP-9 expression by sponging miR-539.In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460.	34821482	RID08152	ceRNA or sponge	metastasis,prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Breast cancer	SNHG14	KLF7	positively-E	western blot;luciferase reporter assay;knockdown	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-543)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000118263	NA	104472715	8609	NCRNA00214|UBE3A-AS|UBE3A-AS1|UBE3A-ATS	UKLF	LncRNA SNHG14 accelerates breast cancer progression through sponging miR-543 and regulating KLF7 expression.The expression levels of SNHG14, miR-543, and KLF7 mRNA were determined by quantitative real-time PCR. western blotwas used to evaluate KLF7 protein level. The direct interactions between miR-543 and SNHG14 or KLF7 were confirmed using dual-luciferase reporter assays. Our data indicated that SNHG14 expression was increased in BC tissues and cells, and SNHG14 knockdown mitigated the proliferation, migration, and invasion and facilitated apoptosis of BC cells. SNHG14 directly interacted with miR-543. MiR-543 mediated the regulatory effects of SNHG14 silencing on BC cell behaviors. Moreover, KLF7 was a direct target of miR-543. Overexpressed miR-543-mediated anti-proliferation, anti-migration, anti-invasion, and pro-apoptosis effects were mediated by KLF7. Furthermore, SNHG14 modulated KFL7 expression through acting as a competing endogenous RNA (ceRNA) of miR-543 in BC cells. Our study suggested that SNHG14 knockdown hindered BC progression in vitro at least partly through acting as a ceRNA of miR-543 and modulating KLF7 expression, providing evidence for SNHG14 as a potential target for BC therapy.	34783894	RID08153	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE109761,GSE51827)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)
Cardiac fibrosis	TDRG1	TNFRSF21	positively-E	western blot;luciferase reporter assay;knockdown	upregulation	RT-qPCR	NA	NA	fibrotic(+);inflammatory response(+)	ceRNA(miR-605-3p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Fibrosis	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000146072	NA	732253	27242	LINC00532|lincRNA-NR_024015	CD358|DR6	LncRNA TDRG1 aggravates TGF-beta1-induced fibrogenesis and inflammatory response of cardiac fibroblasts via miR-605-3p/TNFRSF21 axis.This study aimed to explore the effects of lncRNA testis development related gene 1 (TDRG1) on the fibrogenesis and inflammatory response of transforming growth factor-beta1 (TGF-beta1)-stimulated human cardiac fibroblasts (HCFs). Levels of proinflammatory cytokines were evaluated by ELISA. RT-qPCR was applied to reveal the expression levels of TDRG1, miR-605-3p and TNFRSF21. western blotwas prepared to detect protein levels of TNFRSF21 and fibrosis related genes. Luciferase reporter assay was conducted for confirming the interaction between miR-605-3p and TDRG1/TNFRSF21. We found that TGF-beta1-stimulated HCFs showed high concentrations of proinflammatory cytokines, and increased protein levels of fibrosis related genes, suggesting the dysfunctions of TGF-beta1-stimulated HCFs. In addition, TDRG1 was upregulated in TGF-beta1-stimulated HCFs. We found that interfering with TDRG1 alleviated dysfunctions of TGF-beta1-stimulated HCFs. Moreover, TDRG1 bound with miR-605-3p. MiR-605-3p exerted the anti-fibrogenic and anti-inflammatory effects in TGF-beta1-treated HCFs. As a target gene of miR-605-3p, TNFRSF21, reversed the anti-fibrogenic and anti-inflammatory effects of TDRG1 knockdown in TGF-beta1-treated HCFs. Overall, our study confirmed that TDRG1 aggravates fibrogenesis and inflammatory response in TGF-beta1-treated HCFs via the miR-605-3p/TNFRSF21 axis.	34775426	RID08154	ceRNA or sponge	NA		UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Kidney disease	NNT-AS1	SMAD4	positively-E	LncBASE;luciferase reporter assay;RNA pull-down assay;RIP;siRNA;Targetscan;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);inflammatory response(+)	ceRNA(miR-214-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000141646	NA	100652772	4089	RP11-159F24.1	DPC4|MADH4	LncRNA NNT-AS1 regulates proliferation, ECM accumulation and inflammation of human mesangial cells induced by high glucose through miR-214-5p/smad4.qRT-PCRanalysis of HGMC showed considerably higher (about 3.2 times) expression of NNTAS1 in 25 mmol/L high glucose (HG) group.Potential binding elements of miR-214-5p in NNTAS1 were identified through LncBASE online database.Following this, relative luciferase assay confirmed reduced miR-214-5p expression almost 73% in HGMC lines inoculated with NNT-ASI wild-type (WT) than miR-NC and NNT-AS1 mutant showed relatively same expression as miR-NC.RNA pull-down experiment using biotin-labelled NNT-AS1 probe confirmed that NNT-AS1 interacted with miR- 214-5p in HGMC cells.Finally, the results from RNA immunoprecipitation demonstrated more enrichment of NNT-AS1 (26 times) and miR-214-5p (18 times) by Ago2 in comparison to IgG group.The results suggested the decreased expression of miR-214-5p (80%) in the si-NC group containing active NNT-AS1. Whereas, the expression of miR-214-5p was considerably higher (about 3 times) (P < 0.01) in the HGMC groups transfected with si-NNT-AS1#1 and si-NNT-AS1#2 in which the NNTAS1 was silenced.TargetScan software predicted the 3'-UTR site of smad4 which might be the possible target of miR-214-5p and luciferase reporter assay was performed for verification.Furthermore, the expression levels of smad4 were analyzed through western blotin HGMCs transfected with miR-NC, NC-inhibitor, miR-214-5p and miR-214-5p inhibitor.NNT-AS1 is a regulator of Hg-induced proliferation and causes accumulation of ECM and inflammation in mesangial cells through miR-214-5p/smad4 axis.The data suggests that NNT-AS1 can be positively used as a potential biomarker and indicator of DN and causes extracellular matrix (ECM) accumulation and inflammation of human mesangial cells.	34742256	RID08155	ceRNA or sponge	NA	DOWN(NSCLC,PAAD);UP(SKCM);DATA(GSE74639,GSE60407,GSE38495)	DOWN(LIHC,NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Leukemia	Hmrhl	PDGFRB	negatively-E	siRNA;ChIRP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	PCG	NA	NA	ENSG00000113721	NA	NA	5159	NA	CD140b|JTK12|PDGFR|PDGFR1	LncRNA Hmrhl regulates expression of cancer related genes in chronic myelogenous leukemia through chromatin association.In our recently published study on Hmrhl, we had observed that most significant upregulation in the expression of Hmrhl was in lymphocyte tumor samples among all the other cancers.Hmrhl RNA silencing because of physical association of Hmrhl RNA at the chromatin level, we overlapped the high throughput sequencing data from both RNA-seq and ChIRP-seq study.We further analysed the subset of common genes based on their role in signaling pathways in cancer as well as role in the developmental process and subsequently identified PDGFRbeta, TP53 and ZIC1 as our top hits among the genes that were physically occupied with Hmrhl and also significantly dysregulated upon Hmrhl silencing.These results therefore suggested that Hmrhl might function as a potential regulator of PDGFRB, TP53 and ZIC1.In order to gain a further insight into the possible role of Hmrhl RNA in cancer associated cellular phenotypes, we selected PDGRF-beta, which is known to have essential role in activation of the intracellular signaling pathway that leads to cell migration, invasion, and proliferation, for our further experiments.In case of cellular proliferation, we observed that overexpression of PDGRF-beta was able to restore the decline in cell-proliferation after Hmrhl downregulation at time points 72 h.These results further confirm PDGRF-beta to be an important target of Hmrhl in leukemia.Integrating whole transcriptome analysis and genome-wide chromatin association of Hmrhl, we systematically identified three genes (ZIC1, PDGRFbeta and TP53) as potential regulatory targets of Hmrhl RNA. Promoters of all of the three genes show high affinity for Hmrhl binding and a significant downregulated expression after Hmrhl depletion.ZIC1, which was one of the dominating TFs in our TF matrix analysis (Figure 4C, Supplementary Table S2), has been reported for its oncogenic as well as tumor suppressive behavior in various cancers.Dysregulation of ZIC1 expression may be thus associated with the outcome of our cancer phenotype study indicating Hmrhl as probable promoter of leukemogenesis with a role in cell proliferation, migration and invasion.Stimulation of the PDGRF  leads to the activation of the intracellular signaling pathway that further promotes cell migration, invasion, and proliferation.In order to determine the actual physical occupancy of various TFs, particularly inK562 cell lines, we took a look at the promoter region of Hmrhl from ENCODE project consortium, and interestingly, we came up with certain transcription factors like TAL1 andGATA2 that are highly enriched within the upstream of Hmrhl (Figure 8C). Among them, TAL1, is a primary regulator of erythroid differentiation with an established role in genesis of hemopoietic malignancies.We also took advantage of the TAL1 ChIP-seq dataset for K562 available from ENCODE.To further experimentally validate this, we performed TAL1 Chromatin Immunoprecipitation study (ChIP) to pull-down TAL1 associated chromatin and scored for the promoter region of Hmrhl.To address this, we silenced Tal1 using siRNA in K562 cell line.In summation, our study provides abundant evidence to elucidate significance of lncRNA Hmrhl as an oncogene in erythroleukemia and its regulation by TAL1. Mechanistically, our data suggests its role in elevation of cell growth and migration in vitro possibly by involvement of signalling pathway genes and target gene regulation via triplex formation by binding at chromatin level. Of course, more indepth research is required to fully comprehend the under lying mechanisms of Hmrhl RNA not only in leukemia but in other cancers which might reveal some potential therapeutic targets. Also, as indicated from the current study, involvement of Hmrhl in development and differentiation especially in neurogenesis and haematopoiesis needs further exploration to understand the complexity behind these processes.	34734184	RID08156	expression association	NA		UP(LIHC);DATA(GSE117623)
Leukemia	Hmrhl	TP53	negatively-E	siRNA;ChIRP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    	34734184	RID08157	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Leukemia	Hmrhl	ZIC1	negatively-E	siRNA;ChIRP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	lncRNA	TF	NA	NA	ENSG00000152977	NA	NA	7545	NA	ZIC|ZNF201	                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    	34734184	RID08158	expression association	NA		UP(LIHC);DATA(GSE117623)
Leukemia	TAL1	Hmrhl	positively-E	ChIP;RNA pull-down assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Leukemia	TF	lncRNA	ENSG00000162367	NA	NA	NA	6886	NA	bHLHa17|SCL|TCL5	NA	                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    	34734184	RID08159	transcriptional regulation	NA	UP(LIHC,PAAD,PRAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE75367,GSE86978)	
Esophagus squamous cell carcinoma	TUG1	CDC42	positively-E		upregulation		NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-498)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000070831	NA	55000	998	FLJ20618|LINC00080|NCRNA00080	CDC42Hs|G25K	                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 	34771549	RID08160	ceRNA or sponge	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophageal cancer	SNHG1	CDC42	positively-E	siRNA	upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-195)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000070831	NA	23642	998	LINC00057|lncRNA16|NCRNA00057|UHG	CDC42Hs|G25K	                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 	34771549	RID08161	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Malignant glioma	SNHG15	VEGFA	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-153)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000112715	NA	285958	7422	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	VEGF|VEGF-A|VPF	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08162	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Malignant glioma	SNHG15	CDC42	positively-E	knockdown	upregulation		NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-153)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000070831	NA	285958	998	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	CDC42Hs|G25K	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08163	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	LINC00958	NET1	positively-E		upregulation		NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-22)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000173848	NA	100506305	10276	NA	ARHGEF8|NET1A	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08164	ceRNA or sponge	metastasis,prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065,GSE55807)
Osteosarcoma	MALAT1	ROCK1	positively-E		upregulation		NA	NA	cell invasion(+)	ceRNA(miR-144-3p)	regulation	NA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067900	NA	378938	6093	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	p160ROCK	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08165	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Osteosarcoma	MALAT1	ROCK2	positively-E		upregulation		NA	NA	cell invasion(+)	ceRNA(miR-144-3p)	regulation	NA	NA	CSC	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000134318	NA	378938	9475	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08166	ceRNA or sponge	metastasis,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD,BRCA);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE75367)
Cancer	TUG1	RND3	negatively-E		upregulation		NA	NA	tumorigenesis(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000115963	NA	55000	390	FLJ20618|LINC00080|NCRNA00080	ARHE|Rho8|RhoE	RHO GTPase-Related Long Noncoding RNAs in Human Cancers.An increasing number of studies have demonstrated that the sponging activity of TUG1 as an oncogenic lncRNA has been implicated in many human malignancies.Whereas overexpression of miR-498 in ESCC cell lines induced remarkable reductions of cell proliferation, the decrease in TUG1 reduced CDC42 expression by binding to miR-498, resulting in silencing of the proliferation and invasion of ESCC.The lncRNA small nucleolar RNA host gene 1 (SNHG1) is reported to increase cell proliferation, migration, and invasion in different cancers, including HCC.Determination of the expression level in 36 esophageal cancer (EC) tissue samples and paracancerous tissues were obtained, revealing that SNHG1 was significantly upregulated in EC.It was reported that decreased expression of miR-195 played a regulatory role in promoting the pathogenesis of the EC [252]. While SNHG1 and CDC42 were significantly upregulated, miR-195 was remarkably repressed in both EC tissues and cell lines. Additionally, the suppression of either SNHG1 or CDC42 led to inhibition of cell proliferation, migration, and invasion.However, the inhibition of miR-195 resulted in the promotion of cell proliferation, migration, and invasion, and reversed the effects of si-SNHG1.Small nucleolar RNA host gene 15 (SNHG15) is a typical lncRNA that has been revealed to be upregulated as a tumor facilitator in NSCLC.The results of another study indicated that SNHG15 is highly expressed in glioma vascular endothelial cells (p < 0.05), while its knockdown suppressed cell proliferation, migration, and tube formation in vitro.Moreover, knockdown of SNHG15 reduced the expression of VEGFA and CDC42, which are promoters of angiogenesis.Additional analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153 as a negative regulator of CDC42 and VEGFA. The tumor-suppressor activity of miR-153 was determined in another study through the reduction of stem cell-like phenotype and tumor growth of lung adenocarcinoma cells [261]. Therefore, SNHG15 and its target miR-153 could serve as new potential therapeutic targets for the antiangiogenic treatment of glioma through the downregulation of CDC42.In addition to direct regulation of Rho GTPases themselves, lncRNAs as ceRNAs are also indirectly involved in modulation of RHO GTPases by targeting their regulators (GAPs, GEFs, and GDIs) and effectors. Upregulation of CTC-497E21.4 (also known as LINC00958) in GC tissue promoted cell proliferation, invasion, and metastasis by sponging miR-22, and subsequently induced the expression of NET1.Interestingly, NET1 activates as a RHOA-specific GEF RHOA signaling pathway. Thus, CTC-497E21.4/miR-22/NET1 can be referred to as an indirect modulatory axis of RHOA-mediated signaling.An elevated expression of MALAT1 was observed in osteosarcoma patients, and correlated with poor prognosis. Downregulation of MALAT1 as a ceRNA for miR-144-3p inhibited tumor cell invasion by reducing the expression of ROCKI/ROCKII in osteosarcoma cells.It was found that TUG1 represses the expression of RND3, one atypical member of the RHO family [14,36], through recruitment of EZH2 protein to the RND3 promoter regions and modification of H3K27me3.Orchestrating chromatin folding and compartmentalization to direct enhancer-promoter communication shapes the outcomes of gene transcription.Interestingly, lncRNAs are not only recognized as the master regulators of the genome epigenetics, but also as the targets of epigenetic modifiers.This research was funded by the German Federal Ministry of Education and Research (BMBF) German Network of RASopathy Research (GeNeRARe, grant number: 01GM1902C), and the European Network on Noonan Syndrome and Related Disorders (NSEuroNet, grant number: 01GM1621B).	34771549	RID08167	epigenetic regulation	metastasis,prognosis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065,GSE55807)
Atherosclerosis	PVT1	MAPK	positively-E	western blot;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Small interfering RNA-induced silencing lncRNA PVT1 inhibits atherosclerosis via inactivating the MAPK/NF-kB pathway.We first detected PVT1 expression in the serum of 52 AS patients and 32 healthy people by qRT-PCR It was found that PVT1 expression in AS patients was significantly increased relative to that in healthy people.PVT1 upregulation activates the MAPK/NF-kB pathway and promotes secretion of inflammatory factors while silencing PVT1 inhibits the the MAPK/ NF-kB pathway.As the MAPK/NF-kB pathway is important to promote the secretion of IL-1, IL-6, IL-8, and TNF-alpha and could sever as a transcriptional regulator for recruiting macrophages and monocytes, we detected levels of MAPK and NF-kB in AS mice. The results displayed decreased levels of MAPK and NF-kB in ApoE-/- mice.Subsequently, the mRNA and protein levels of MAPK and NF-kB in oxLDL-treated HA-VSMCs were determined by qRT-PCRand western blot and elevated levels of MAPK and NF-kB, and decreased levels of MAPK and NF-kB were observed in the oxLDL + si-PVT1-treated cells.These results confirmed that silencing PVT1 downregulates the MAPK/NF-kB signaling pathway in oxLDL-treated HA-VSMCs and AS mice.Silencing PVT1 suppresses AS progression via downregulating the MAPK/NF-kB pathway.To conclude, these results illustrated that silencing PVT1 inhibited AS induced by high-fat diet in ApoE-/- mice, and limited HA-VSMC viability and proliferation and promoted apoptosis and cell cycle arrest, alleviated inflammation, and reduced liposome deposition via suppressing the MAPK/NF-kB pathway. The findings indicate that silencing lncRNA PVT1 could be a potential strategy to prevent and treat AS. LncRNA PVT1 is an independent hazard factor influencing the coronary AS [9] and is highly expressed in AS patients. The innovation of this study is that we explored the protective effect of siRNA silencing lncRNA PVT1 on anti-AS at molecular, cellular and animal levels by investigating the mechanism of lncRNA PVT1 in AS and the regulation of lncRNA PVT1 on the MAPK/NF- kB pathway, and thus providing new insights into further understanding of the AS pathology and reference for new prevention and treatment strategies for AS and AS-related diseases. Further study should be conducted to find out the possible applicable approaches for AS on the basis of the obtained results in this study.	34775377	RID08168	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	
Atherosclerosis	PVT1	NFKB1	positively-E	western blot;overexpression;siRNA	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000109320	NA	5820	4790	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	KBF1|NF-kappaB|NF-kB1|NFkappaB|NFKB-p50|p105|p50	Small interfering RNA-induced silencing lncRNA PVT1 inhibits atherosclerosis via inactivating the MAPK/NF-kB pathway.We first detected PVT1 expression in the serum of 52 AS patients and 32 healthy people by qRT-PCR It was found that PVT1 expression in AS patients was significantly increased relative to that in healthy people.PVT1 upregulation activates the MAPK/NF-kB pathway and promotes secretion of inflammatory factors while silencing PVT1 inhibits the the MAPK/ NF-kB pathway.As the MAPK/NF-kB pathway is important to promote the secretion of IL-1, IL-6, IL-8, and TNF-alpha and could sever as a transcriptional regulator for recruiting macrophages and monocytes, we detected levels of MAPK and NF-kB in AS mice. The results displayed decreased levels of MAPK and NF-kB in ApoE-/- mice.Subsequently, the mRNA and protein levels of MAPK and NF-kB in oxLDL-treated HA-VSMCs were determined by qRT-PCRand western blot and elevated levels of MAPK and NF-kB, and decreased levels of MAPK and NF-kB were observed in the oxLDL + si-PVT1-treated cells.These results confirmed that silencing PVT1 downregulates the MAPK/NF-kB signaling pathway in oxLDL-treated HA-VSMCs and AS mice.Silencing PVT1 suppresses AS progression via downregulating the MAPK/NF-kB pathway.To conclude, these results illustrated that silencing PVT1 inhibited AS induced by high-fat diet in ApoE-/- mice, and limited HA-VSMC viability and proliferation and promoted apoptosis and cell cycle arrest, alleviated inflammation, and reduced liposome deposition via suppressing the MAPK/NF-kB pathway. The findings indicate that silencing lncRNA PVT1 could be a potential strategy to prevent and treat AS. LncRNA PVT1 is an independent hazard factor influencing the coronary AS [9] and is highly expressed in AS patients. The innovation of this study is that we explored the protective effect of siRNA silencing lncRNA PVT1 on anti-AS at molecular, cellular and animal levels by investigating the mechanism of lncRNA PVT1 in AS and the regulation of lncRNA PVT1 on the MAPK/NF- kB pathway, and thus providing new insights into further understanding of the AS pathology and reference for new prevention and treatment strategies for AS and AS-related diseases. Further study should be conducted to find out the possible applicable approaches for AS on the basis of the obtained results in this study.	34775377	RID08169	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Allergic rhinitis	NEAT1	CSF2	positively-E	siRNA;ELISA	upregulation	RT-qPCR	NA	NA	inflammatory response(+);apoptosis process(-)	NA	association	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000164400	NA	283131	1437	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	GM-CSF|GMCSF	Exosomal lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)contributes to the progression of allergic rhinitis via modulating microRNA-511/ Nuclear Receptor Subfamily 4 Group A Member 2 (NR4A2) axis.RT-qPCR results indicated that NEAT1 expression was enhanced in AR patients compared with non-AR patients.Moreover, RT-qPCR and ELISA indicated that the mRNA and protein levels of GM-CSF, eotaxin-1, and MUC5AC were enhanced in IL-13-induced HNECs, while NEAT1 knockdown reversed these effects.These data determined that NEAT1 knockdown restrained IL-13-stimulated inflammatory cytokine and mucus production levels in HNECs.The putative binding sites between NEAT1 and miR-511 were predicted by starBase website.Luciferase reporter assay indicated that miR- 511 overexpression suppressed the luciferase activity of NEAT1-WT, but there was no distinct change in NEAT1-Mut group.Besides, NEAT1 levels were inversely correlated with miR-511 levels.The silencing of NEAT1 elevated miR-511 expression in HNECs (Figure 5(e)). These data implied that NEAT1 could negatively regulate miR-511 expression by direct interaction.Overexpression of miR-511 decreased the luciferase activity of NR4A2-WT, while there was no alteration in NR4A2-Mut.NEAT1 regulates IL-13-induced dysfunction of HNECs via miR-511/NR4A2 axis.In conclusion, our data revealed that exosomal NEAT1 contributed to the pathogenesis of AR through the miR-511/NR4A2 axis. These findings might offer novel strategies for the prevention and treatment of AR.	34672863	RID08170	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Allergic rhinitis	NEAT1	CCL11	positively-E	siRNA;ELISA	upregulation	RT-qPCR	NA	NA	inflammatory response(+);apoptosis process(-)	NA	association	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000172156	NA	283131	6356	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	eotaxin|MGC22554|SCYA11	Exosomal lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)contributes to the progression of allergic rhinitis via modulating microRNA-511/ Nuclear Receptor Subfamily 4 Group A Member 2 (NR4A2) axis.RT-qPCR results indicated that NEAT1 expression was enhanced in AR patients compared with non-AR patients.Moreover, RT-qPCR and ELISA indicated that the mRNA and protein levels of GM-CSF, eotaxin-1, and MUC5AC were enhanced in IL-13-induced HNECs, while NEAT1 knockdown reversed these effects.These data determined that NEAT1 knockdown restrained IL-13-stimulated inflammatory cytokine and mucus production levels in HNECs.The putative binding sites between NEAT1 and miR-511 were predicted by starBase website.Luciferase reporter assay indicated that miR- 511 overexpression suppressed the luciferase activity of NEAT1-WT, but there was no distinct change in NEAT1-Mut group.Besides, NEAT1 levels were inversely correlated with miR-511 levels.The silencing of NEAT1 elevated miR-511 expression in HNECs (Figure 5(e)). These data implied that NEAT1 could negatively regulate miR-511 expression by direct interaction.Overexpression of miR-511 decreased the luciferase activity of NR4A2-WT, while there was no alteration in NR4A2-Mut.NEAT1 regulates IL-13-induced dysfunction of HNECs via miR-511/NR4A2 axis.In conclusion, our data revealed that exosomal NEAT1 contributed to the pathogenesis of AR through the miR-511/NR4A2 axis. These findings might offer novel strategies for the prevention and treatment of AR.	34672863	RID08171	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	
Allergic rhinitis	NEAT1	MUC5AC	positively-E	siRNA;ELISA	upregulation	RT-qPCR	NA	NA	inflammatory response(+);apoptosis process(-)	NA	association	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000215182	NA	283131	4586	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	MUC5	Exosomal lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)contributes to the progression of allergic rhinitis via modulating microRNA-511/ Nuclear Receptor Subfamily 4 Group A Member 2 (NR4A2) axis.RT-qPCR results indicated that NEAT1 expression was enhanced in AR patients compared with non-AR patients.Moreover, RT-qPCR and ELISA indicated that the mRNA and protein levels of GM-CSF, eotaxin-1, and MUC5AC were enhanced in IL-13-induced HNECs, while NEAT1 knockdown reversed these effects.These data determined that NEAT1 knockdown restrained IL-13-stimulated inflammatory cytokine and mucus production levels in HNECs.The putative binding sites between NEAT1 and miR-511 were predicted by starBase website.Luciferase reporter assay indicated that miR- 511 overexpression suppressed the luciferase activity of NEAT1-WT, but there was no distinct change in NEAT1-Mut group.Besides, NEAT1 levels were inversely correlated with miR-511 levels.The silencing of NEAT1 elevated miR-511 expression in HNECs (Figure 5(e)). These data implied that NEAT1 could negatively regulate miR-511 expression by direct interaction.Overexpression of miR-511 decreased the luciferase activity of NR4A2-WT, while there was no alteration in NR4A2-Mut.NEAT1 regulates IL-13-induced dysfunction of HNECs via miR-511/NR4A2 axis.In conclusion, our data revealed that exosomal NEAT1 contributed to the pathogenesis of AR through the miR-511/NR4A2 axis. These findings might offer novel strategies for the prevention and treatment of AR.	34672863	RID08172	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DATA(GSE40174)
Allergic rhinitis	NEAT1	NR4A2	positively-E	starBase;luciferase reporter assay;siRNA	upregulation	RT-qPCR	NA	NA	inflammatory response(+);apoptosis process(-)	ceRNA(miR-511)	regulation	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000153234	NA	283131	4929	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	HZF-3|NOT|NURR1|RNR1|TINUR	Exosomal lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)contributes to the progression of allergic rhinitis via modulating microRNA-511/ Nuclear Receptor Subfamily 4 Group A Member 2 (NR4A2) axis.RT-qPCR results indicated that NEAT1 expression was enhanced in AR patients compared with non-AR patients.Moreover, RT-qPCR and ELISA indicated that the mRNA and protein levels of GM-CSF, eotaxin-1, and MUC5AC were enhanced in IL-13-induced HNECs, while NEAT1 knockdown reversed these effects.These data determined that NEAT1 knockdown restrained IL-13-stimulated inflammatory cytokine and mucus production levels in HNECs.The putative binding sites between NEAT1 and miR-511 were predicted by starBase website.Luciferase reporter assay indicated that miR- 511 overexpression suppressed the luciferase activity of NEAT1-WT, but there was no distinct change in NEAT1-Mut group.Besides, NEAT1 levels were inversely correlated with miR-511 levels.The silencing of NEAT1 elevated miR-511 expression in HNECs (Figure 5(e)). These data implied that NEAT1 could negatively regulate miR-511 expression by direct interaction.Overexpression of miR-511 decreased the luciferase activity of NR4A2-WT, while there was no alteration in NR4A2-Mut.NEAT1 regulates IL-13-induced dysfunction of HNECs via miR-511/NR4A2 axis.In conclusion, our data revealed that exosomal NEAT1 contributed to the pathogenesis of AR through the miR-511/NR4A2 axis. These findings might offer novel strategies for the prevention and treatment of AR.	34672863	RID08173	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	UP(PAAD);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE111842)
Papillary thyroid carcinoma	MIAT	EZH2	positively-E	miRcode;TarBase;western blot;shRNA;luciferase reporter assay	upregulation	microarray;qRT-PCR	TCGA	NA	cell proliferation(+);cell migration(+);tumor growth(+)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000106462	NA	440823	2146	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ENX-1|EZH1|KMT6|KMT6A	LncRNA-MIAT promotes thyroid cancer progression and function as ceRNA to target EZH2 by sponging miR-150-5p.We used microarray to screen the lncRNA expression profiles of paired human PTC tumor and adjacent noncancerous tissue samples.To verify the calculated data, 20 differentially expressed genes, including 10 upregulated and 10 downregulated genes were randomly selected for qRT-PCRin 60 pairs of PTC and adjacent noncancerous tissue samples. The results were consistent with the integrated data.The MREs predicted by miRcode indicated that 85 miRNAs may interact with these fifteen lncRNAs.Based on the miRNAs that might interact with lncRNAs, we searched TarBase for miRNA-sRNA targets with experimental support.The western blot showed the same expression tendency. Then MIAT, miR-150-5p, and EZH2 were examined in NTHY, TPC-1, K1, and BCPAP cells to validate the reciprocal relationship between the three components. The results showed that the expression trend of MIAT and EZH2 demonstrated positively correlated, but negatively correlated with miR-150-5p. Knockdown of MIAT caused upregulation of miR-150-5p and downregulation of EZH2 in TPC-1 and BCPAP cells.These data suggest that MIAT upregulation contributes to PTC cell migration and proliferation and maybe partly due to the function of the ceRNA network.Our constructed ceRNA network shows that lncRNAs could interact with mRNAs in PTC. To confirm this finding, we performed a regression analysis using datasets from TCGA of other cancer types, including bladder urothelial carcinoma.Upregulation of MIAT and EZH2 were positively related with LNM, high risk, recurrence and RAS mutation which indicates that MIAT and EZH2 may be played an important role in thyroid cancer progression.Their relationship was further confirmed and we found that miR-150-5p mimic dramatically suppressed the luciferase activity of MIAT-wt, but not the luciferase activity of MIAT-mut compared to the control mimic in TPC-1 and BCPAP cells.The results demonstrated that the effects of MIAT on the migration and proliferation of TPC-1 and BCPAP cells were neutralized by anti-miR-150-5p.The luciferase reporter assay showed that miR-150-5p mimic obviously inhibited the luciferase activity of EZH2-wt, while had no influence on that of EZH2-mut TPC-1 and BCPAP cells.The western blot showed that knockdown of MIAT reduced EZH2 expression, and further strengthened by miR-150-5p mimic.To determine whether MIAT could influence the biological functions of thyroid cancer, MIAT expression was stable knockdown by transfection with shRNA and sh-NC and inoculated to nude mice. The results showed that tumors grown from MIAT stable knockdown cells were slower than tumors grown from the sh-NC cells.MIAT downregulation decreases tumor growth in vivo that is related to the miR-150-5/EZH2 axis.Our findings suggest MIAT may inhibit EZH2 expression and promote PTC cell invasion via the miR-150/EZH2 pathway. Therefore, MIAT may serve as a valuable prognostic biomarker and therapeutic target for PTC.	34811354	RID08174	ceRNA or sponge	recurrence,prognosis	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(PAAD);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE111842)
Malignant glioma	MIR4435-2HG	WWTR1	positively-E	luciferase reporter assay;western blot;shRNA	upregulation	RT-qPCR	NA	NA	WNT signaling pathway(+);apoptosis process(-)	ceRNA(miR-125a-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000018408	NA	541471	25937	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	DKFZp586I1419|TAZ	LncRNA MIR4435-2HG functions as a ceRNA against miR-125a- 5p and promotes neuroglioma development by upregulating TAZ.After incubating and staining with TAZ primary antibody, the expression of TAZ in the pathological tissues was obtained and was higher in stage III V patients than in stage I I. The expressions of MIR4435-2HG and miR-125a- 5p in the healthy brain tissues and glioma tissues were detected by RT-qPCR.The luciferase reporter assay results indicated that, compared with TAZ wild-type miR-125a- 5p mimic, the luciferase activity of the TAZ mutant was significantly higher.The results showed that MIR4435-2HG was positively correlated with TAZ (p < 0.01), miR-125a- 5p was negatively correlated with TAZ (p < 0.01), and MIR4435-2HG was negatively correlated with miR-125a- 5p (p = 0.01).western blotshowed that the expression levels of TAZ and the downstream gene of the Wnt signaling pathway were significantly increased in U87 MG and U251 cells transfected with MIR4435-2HG- OE.The expression levels of TAZ and downstream gene of the Wnt signaling pathway in U87 MG cells and U251 cells transfected with miR-125a- 5p were significantly reduced.MIR4435-2HG- OE increased the expression of the TAZ gene and downstream genes of the Wnt signaling pathway; miR-125a- 5p inhibited the expression of the TAZ gene and expression of the downstream genes of Wnt.MIR4435-2HG- OE improved the activity of the U87 MG cells and U251 cells and inhibited apoptosis; miR-125a- 5p decreased the activity of the U87 MG cells and U251 cells and promoted apoptosis; MIR4435-2HG- OE weakened the effect of miR-125a- 5p.sh-MIR4435- 2HG inhibited the expression of the TAZ gene and downstream genes of the Wnt signaling pathway; miR-125a- 5p inhibitor increased the expression of the TAZ gene and the downstream genes of Wnt.sh-MIR4435- 2HG inhibited the activities of the U87 MG cells and U251 cells and improved apoptosis; miR-125a- 5p inhibitor improved the activities of the U87 MG cells and U251 cells and inhibited apoptosis; sh-MIR4435- 2HG weakened the effect of the miR-125a- 5p inhibitor.The promoting effect of MIR4435-2HG on glioma cells was less effective than the inhibitory effect of miR-125a- 5p; TAZ and MIR4435-2HG had a synergistic effect.MIR4435-2HG and TAZ inhibited apoptosis and promoted cell migration and proliferation; miR-125a- 5p promoted cell apoptosis and inhibited cell migration and proliferation.Promoting effect of MIR4435-2HG on glioma rats was lower than the inhibitory effect of miR-125a- 5p; TAZ and MIR4435-2HG had a synergistic effect.Inhibitory effect of sh-MIR4435- 2HG on glioma rats was lower than the promoting effect of miR-125a- 5p inhibitor.LncRNA MIR4435-2HG obstructs the functions of miR-125a- 5p and promotes neuroglioma development by upregulating the TAZ gene.	34714963	RID08175	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(LIHC,SKCM,BRCA);DATA(GSE117623,GSE38495,GSE109761,GSE111065)
Nasopharynx carcinoma	FOXCUT	BAX	negatively-E	shRNA;immunofluorescence assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell injury(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000087088	NA	101927703	581	LINC01379|TCONS_00011636	BCL2L4	Interference of long noncoding RNA FOXCUT inhibits epithelial-mesenchymal transformation and induces mitochondrial injury in nasopharyngeal carcinoma cells.FOXCUT expression levels were detected by RT-PCRin tumor tissues and adjacent tissues from 50 patients with NPC and in NP69, CNE1, CNE2, SUNE2, HER2 and 5-8F cell lines. CNE1 cells were transfected with a short hairpin RNA (shRNA) targeting FOXCUT or a negative control RNA construct (shRNA-NC).An immunofluorescence assay was used to examine the vimentin-positive cells, and the levels of SOD, MDA and LDH in the cells were detected. The changes of mitochondrial membrane potential were detected with flow cytometry, and the expression levels of E-cad, N-cad, vimentin, Bax, Bcl-2, caspase-3 and c-Myc in the cells were detected with western blot.The expression level of FOXCUT was significantly increased in NPC tissues as compared with the adjacent tissues (P<0.001).In CNE1 cells, transfection with FOXCUT shRNA significantly inhibited cell proliferation and clone formation (P<0.001), and caused obvious changes in cell morphology. FOXCUT knockdown significantly decreased the expressions of N-cad and vimentin, increased E- cad expression and the contents of MDA and LDH (P<0.05), reduced vimentin- positive cells and the activity of SOD, and caused a shift of red fluorescent cells to green fluorescent cells and an increased percentage of green fluorescent cells. FOXCUT knockdown also resulted in significantly increased expressions of Bax/Bcl2 and cleaved Cas3/Cas3 and a lowered expression of c-Myc. Conclusions Interference of FOXCUT can inhibit the proliferation and epithelial-mesenchymal transformation, enhance oxidative stress, induce mitochondrial function injury, and promote apoptosis in NPC cells, suggesting the potential of FOXCUT interference for targeted treatment of NPC.	34658347	RID08176	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Nasopharynx carcinoma	FOXCUT	BCL2	negatively-E	shRNA;immunofluorescence assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell injury(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000171791	NA	101927703	596	LINC01379|TCONS_00011636	Bcl-2|PPP1R50	Interference of long noncoding RNA FOXCUT inhibits epithelial-mesenchymal transformation and induces mitochondrial injury in nasopharyngeal carcinoma cells.FOXCUT expression levels were detected by RT-PCRin tumor tissues and adjacent tissues from 50 patients with NPC and in NP69, CNE1, CNE2, SUNE2, HER2 and 5-8F cell lines. CNE1 cells were transfected with a short hairpin RNA (shRNA) targeting FOXCUT or a negative control RNA construct (shRNA-NC).An immunofluorescence assay was used to examine the vimentin-positive cells, and the levels of SOD, MDA and LDH in the cells were detected. The changes of mitochondrial membrane potential were detected with flow cytometry, and the expression levels of E-cad, N-cad, vimentin, Bax, Bcl-2, caspase-3 and c-Myc in the cells were detected with western blot.The expression level of FOXCUT was significantly increased in NPC tissues as compared with the adjacent tissues (P<0.001).In CNE1 cells, transfection with FOXCUT shRNA significantly inhibited cell proliferation and clone formation (P<0.001), and caused obvious changes in cell morphology. FOXCUT knockdown significantly decreased the expressions of N-cad and vimentin, increased E- cad expression and the contents of MDA and LDH (P<0.05), reduced vimentin- positive cells and the activity of SOD, and caused a shift of red fluorescent cells to green fluorescent cells and an increased percentage of green fluorescent cells. FOXCUT knockdown also resulted in significantly increased expressions of Bax/Bcl2 and cleaved Cas3/Cas3 and a lowered expression of c-Myc. Conclusions Interference of FOXCUT can inhibit the proliferation and epithelial-mesenchymal transformation, enhance oxidative stress, induce mitochondrial function injury, and promote apoptosis in NPC cells, suggesting the potential of FOXCUT interference for targeted treatment of NPC.	34658347	RID08177	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Nasopharynx carcinoma	FOXCUT	MYC	positively-E	shRNA;immunofluorescence assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);apoptosis process(-);cell injury(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000136997	NA	101927703	4609	LINC01379|TCONS_00011636	bHLHe39|c-Myc|MYCC	Interference of long noncoding RNA FOXCUT inhibits epithelial-mesenchymal transformation and induces mitochondrial injury in nasopharyngeal carcinoma cells.FOXCUT expression levels were detected by RT-PCRin tumor tissues and adjacent tissues from 50 patients with NPC and in NP69, CNE1, CNE2, SUNE2, HER2 and 5-8F cell lines. CNE1 cells were transfected with a short hairpin RNA (shRNA) targeting FOXCUT or a negative control RNA construct (shRNA-NC).An immunofluorescence assay was used to examine the vimentin-positive cells, and the levels of SOD, MDA and LDH in the cells were detected. The changes of mitochondrial membrane potential were detected with flow cytometry, and the expression levels of E-cad, N-cad, vimentin, Bax, Bcl-2, caspase-3 and c-Myc in the cells were detected with western blot.The expression level of FOXCUT was significantly increased in NPC tissues as compared with the adjacent tissues (P<0.001).In CNE1 cells, transfection with FOXCUT shRNA significantly inhibited cell proliferation and clone formation (P<0.001), and caused obvious changes in cell morphology. FOXCUT knockdown significantly decreased the expressions of N-cad and vimentin, increased E- cad expression and the contents of MDA and LDH (P<0.05), reduced vimentin- positive cells and the activity of SOD, and caused a shift of red fluorescent cells to green fluorescent cells and an increased percentage of green fluorescent cells. FOXCUT knockdown also resulted in significantly increased expressions of Bax/Bcl2 and cleaved Cas3/Cas3 and a lowered expression of c-Myc. Conclusions Interference of FOXCUT can inhibit the proliferation and epithelial-mesenchymal transformation, enhance oxidative stress, induce mitochondrial function injury, and promote apoptosis in NPC cells, suggesting the potential of FOXCUT interference for targeted treatment of NPC.	34658347	RID08178	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Lung adenocarcinoma	SNHG7	ATG5	positively-E	siRNA;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell autophagy(+);cell proliferation(+);apoptosis process(-);PI3K/AKT signaling pathway(+);macrophage polarization(+)	transcriptional regulation	regulation	NA	Docetaxel	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000057663	NA	84973	9474	MGC16037|NCRNA00061	APG5|APG5L|ASP|hAPG5	Exosome-mediated transfer of SNHG7 enhances docetaxel resistance in lung adenocarcinoma.We found that SNHG7 was upregulated in docetaxel-resistant LUAD cells (H1299/DTX and SPC-A1/DTX) versus the corresponding parental cells (H1299 and SPC-A1).H1299/DTX and SPC-A1/DTX cells were transfected with SNHG7- specific siRNAs (si-SNHG7#1/2/3) for SNHG7 knockdown, whereas H1299 and SPC-A1 cells were transfected with OV-SNHG7 for overexpression.SNHG7 enhances the docetaxel resistances of LUAD cells and induces M2 polarization of macrophages.Together, SNHG7 negatively influenced the anti-tumor effect of docetaxel in LUAD cells in vitro an in vivo.Results depicted that SNHG7 knockdown reduced LC3-II/LC-3I, ATG5, and ATG12 levels but didn't alter ATG7 and ULK1 levels in H1299/DTX and SPC-A1/DTX cells exposed to 0 or 100 ug/L docetaxel.but si-SNHG7#1/2 only strengthened the docetaxel-caused decrease in LC3-II/LC3-1, ATG5 and ATG12 levels (Fig. 3A). These data indicated that SNHG7 might positively regulate autophagy via ATG5 and ATG12 in LUAD cells. Besides, through mRFP-GFP-LC3 fluorescence microscopy, we found that the fluorescence of both GFP (green) and mRFP (red) were reduced by si-SNHG7#1/2 in H1299/DTX and SPC-A1/DTX cells treated with 0 or 100 ug/L docetaxel, and si-SNHG7#1/2 also reversed the effect of 100 ug/L docetaxel on increasing GFP (green) and mRFP (red) fluorescence in H1299/DTX and SPC-A1/DTX cells.We found that SNHG7 knockdown reduced ATG5 and ATG12 mRNA levels in H1299/DTX and SPC-A1/DTX cells treated with 0 or 100 ug/L docetaxel; and SNHG7 knockdown further strengthened the effect of 100 ug/L docetaxel on decreasing ATG5 and ATG12 mRNA levels.Moreover, luciferase reporter assays depicted that SNHG7 failed to alter the activities of ATG5 promoter and ATG12 promoter in H1299/DTX and SPC-A1/DTX cells exposed to 0 or 100 ug/ L docetaxel (Fig. 3D), indicating that SNHG7 could not regulate ATG5 and ATG12 at transcription level.The results from RIP assays depicted SNHG7 knockdown failed to alter the enrichment of ATG5 and ATG12 mRNA in Ago2-binding precipitates in SPC-A1/DTX cells.SNHG7 affects the proliferation, apoptosis and docetaxel resistance of LUAD cells via recruiting HuR and stabilizing ATG5 and ATG12.Exosomal SNHG7 derived from docetaxel-resistant LUAD cells promotes docetaxel resistance of LUAD cells and macrophage M2 polarization.SNHG7 activates the PI3K/AKT pathway to mediate M2 polarization in macrophages via recruiting CUL4A to promote PTEN ubiquitination.Taken together, we concluded that exosomal SNHG7 enhances docetaxel resistance of LUAD cells through inducing autophagy and macrophage M2 polarization. All findings in the study suggested that SNHG7 may be a promising target for relieving docetaxel resistance in LUAD.	34715254	RID08179	transcriptional regulation	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,PAAD,BRCA);DATA(GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Lung adenocarcinoma	SNHG7	ATG12	positively-E	siRNA;luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	chemoresistance(+);cell autophagy(+);cell proliferation(+);apoptosis process(-);PI3K/AKT signaling pathway(+);macrophage polarization(+)	transcriptional regulation	regulation	NA	Docetaxel	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000145782	NA	84973	9140	MGC16037|NCRNA00061	APG12|APG12L	Exosome-mediated transfer of SNHG7 enhances docetaxel resistance in lung adenocarcinoma.We found that SNHG7 was upregulated in docetaxel-resistant LUAD cells (H1299/DTX and SPC-A1/DTX) versus the corresponding parental cells (H1299 and SPC-A1).H1299/DTX and SPC-A1/DTX cells were transfected with SNHG7- specific siRNAs (si-SNHG7#1/2/3) for SNHG7 knockdown, whereas H1299 and SPC-A1 cells were transfected with OV-SNHG7 for overexpression.SNHG7 enhances the docetaxel resistances of LUAD cells and induces M2 polarization of macrophages.Together, SNHG7 negatively influenced the anti-tumor effect of docetaxel in LUAD cells in vitro an in vivo.Results depicted that SNHG7 knockdown reduced LC3-II/LC-3I, ATG5, and ATG12 levels but didn't alter ATG7 and ULK1 levels in H1299/DTX and SPC-A1/DTX cells exposed to 0 or 100 ug/L docetaxel.but si-SNHG7#1/2 only strengthened the docetaxel-caused decrease in LC3-II/LC3-1, ATG5 and ATG12 levels (Fig. 3A). These data indicated that SNHG7 might positively regulate autophagy via ATG5 and ATG12 in LUAD cells. Besides, through mRFP-GFP-LC3 fluorescence microscopy, we found that the fluorescence of both GFP (green) and mRFP (red) were reduced by si-SNHG7#1/2 in H1299/DTX and SPC-A1/DTX cells treated with 0 or 100 ug/L docetaxel, and si-SNHG7#1/2 also reversed the effect of 100 ug/L docetaxel on increasing GFP (green) and mRFP (red) fluorescence in H1299/DTX and SPC-A1/DTX cells.We found that SNHG7 knockdown reduced ATG5 and ATG12 mRNA levels in H1299/DTX and SPC-A1/DTX cells treated with 0 or 100 ug/L docetaxel; and SNHG7 knockdown further strengthened the effect of 100 ug/L docetaxel on decreasing ATG5 and ATG12 mRNA levels.Moreover, luciferase reporter assays depicted that SNHG7 failed to alter the activities of ATG5 promoter and ATG12 promoter in H1299/DTX and SPC-A1/DTX cells exposed to 0 or 100 ug/ L docetaxel (Fig. 3D), indicating that SNHG7 could not regulate ATG5 and ATG12 at transcription level.The results from RIP assays depicted SNHG7 knockdown failed to alter the enrichment of ATG5 and ATG12 mRNA in Ago2-binding precipitates in SPC-A1/DTX cells.SNHG7 affects the proliferation, apoptosis and docetaxel resistance of LUAD cells via recruiting HuR and stabilizing ATG5 and ATG12.Exosomal SNHG7 derived from docetaxel-resistant LUAD cells promotes docetaxel resistance of LUAD cells and macrophage M2 polarization.SNHG7 activates the PI3K/AKT pathway to mediate M2 polarization in macrophages via recruiting CUL4A to promote PTEN ubiquitination.Taken together, we concluded that exosomal SNHG7 enhances docetaxel resistance of LUAD cells through inducing autophagy and macrophage M2 polarization. All findings in the study suggested that SNHG7 may be a promising target for relieving docetaxel resistance in LUAD.	34715254	RID08180	transcriptional regulation	chemoresistance	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE109761)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)
Chronic pancreatitis	PFAR	RB1CC1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	microarray	GSE24279	NA	fibrotic(+)	ceRNA(miR-141)	regulation	NA	NA	NA	NA	Endocrine system disease	Pancreatitis	lncRNA	PCG	NA	NA	ENSG00000023287	NA	NA	9821	NA	ATG17|Cc1|DRAGOU14|FIP200|KIAA0203|PPP1R131	Lnc-PFAR facilitates autophagy and exacerbates pancreatic fibrosis by reducing pre-miR-141 maturation in chronic pancreatitis.The microarray analysis was used to investigate the differentially expressed lncRNAs in quiescent and activated PSCs in our study and a total of 189 lncRNAs (155 upwards, 34 downwards) were identified.Taken together, these results suggested that Lnc- PFAR induces pancreatic fibrosis via activating PSCs.The level of pre-miR-141 was significantly improved when Lnc-PFAR was upregulated.To validate the possible binding sites, a pre-miRNA pull-down assay was performed and higher levels of Lnc-PFAR were pulled down by bio-pre-miR-141 compared with negative control.Furthermore, the luciferase assay was used to verify the binding site between miR-141-5p and RB1CC1 3'UTR.Our data revealed that Lnc-PFAR facilitates PSCs activation and pancreatic fibrosis via RB1CC1-induced autophagy. Lnc-PFAR reduces miR-141 expression by suppressing pre-miR-141 maturation, which eventually upregulates the RB1CC1 and fibrosis-related indicators expression. Meanwhile, Lnc-PFAR enhanced PSCs activation and pancreatic fibrosis through trigging autophagy. Our study interrogates a novel lncRNA-induced mechanism in promoting the development of pancreatic fibrosis, and Lnc-PFAR is suggested to be a prospective therapeutic target in clinical scenarios.	34697288	RID08181	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE55807)
Hepatocellular carcinoma	LINC00205	CDK6	positively-E	ENCORI;luciferase reporter assay;RNA pull-down assay;Targetscan;western blot;siRNA	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000223768	GRCh38_21:45288035-45297806	ENSG00000105810	NA	642852	1021	NCRNA00205	PLSTIRE	LINC00205, a YY1-modulated lncRNA, serves as a sponge for miR-26a-5p facilitating the proliferation of hepatocellular carcinoma cells by elevating CDK6.First, we evaluate the expression status of LINC00205 and its clinical significance in HCC by bioinformatics analysis, the ENCORI results displayed LINC00205 was highly expressed in HCC.The Ago-CLIP-seq data was used to examine the miRNAs interacting with LINC00205 by the online tool ENCORI, and we found LINC00205 harbored 91 miRNAs binding sites.Here, we uncovered that miR- 26a-5p was decreased in HCC tissues and cell lines.dual-luciferase reporter assays showed that miR-26a-5p mimics could dramatically hamper the Luciferase activities of vector harboring LINC00205-wt sequence rather than mutant type. Furthermore, biotin-labelled miRNA pull-down experiment demonstrated that LINC00205 was remarkably enriched in the biotin-conjugated miR-26a-5parrested complexes compared to that in the negative control cel-miR-239b.We attempted to screen and characterize downstream targets of miR-26a-5p using the online tool ENCORI and TargetScan, and we found cyclin dependent kinase 6 (CDK6), a crucial modulator of cell cycle and cell growth, existed a potential targeting relationship with miR-26a-5p.Biotin-labelled miRNA pull-down experiment revealed that CDK6 mRNA could be dramatically trapped by biotin-conjugated miR-26a-5p-mimics rather than the negative control.Furthermore, the modulating role of LINC00205 and miR-26a-5p on CDK6 mRNA level was first confirmed by qPCR, and we revealed that suppressing LINC00205 could decline the CDK6 expression in both SUN- 449 and SK-Hep-1 cells, meanwhile the reduction of CDK6 caused by LINC00205 silencing could be recovered by miR-26a-5p inhibitor.Then the western blot was conducted to verify the modulating effect of LINC00205 and miR- 26a-5p on the CDK6 protein in SUN-449 cells.Altogether, the above results manifest that LINC00205 could control the proliferation of HCC cells by elevating CDK6 via sponging miR-26a-5p.We checked transcription factor binding sites harbored by the LINC00205 promoter using ChIP-seq data of HepG2 cells on UCSC Genome Browser (http://genome.ucsc. edu), and the Yin Yang-1 (YY1) binding site was found near the upstream of the transcription start site (TSS) of LINC00205.We further analyzed the LINC00205 promoter region (2000 bp up-stream of TSS) using transcription factor searching tools of JASPAR.In addition, the direct interaction between YY1 and LINC00205 promoter was identified using ChIP-qPCR, and we found YY1 was significantly enriched on LINC00205 promoter in both SUN-449 and SK-Hep-1 cells. Taken together, above results displayed that the up-regulation of LINC00205 in HCC could be attributed to the transcription factor YY1.	34730201	RID08182	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE86978)
Hepatocellular carcinoma	YY1	LINC00205	positively-E	ChIP;JASPAR	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000223768	GRCh38_21:45288035-45297806	7528	642852	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	NCRNA00205	LINC00205, a YY1-modulated lncRNA, serves as a sponge for miR-26a-5p facilitating the proliferation of hepatocellular carcinoma cells by elevating CDK6.First, we evaluate the expression status of LINC00205 and its clinical significance in HCC by bioinformatics analysis, the ENCORI results displayed LINC00205 was highly expressed in HCC.The Ago-CLIP-seq data was used to examine the miRNAs interacting with LINC00205 by the online tool ENCORI, and we found LINC00205 harbored 91 miRNAs binding sites.Here, we uncovered that miR- 26a-5p was decreased in HCC tissues and cell lines.dual-luciferase reporter assays showed that miR-26a-5p mimics could dramatically hamper the Luciferase activities of vector harboring LINC00205-wt sequence rather than mutant type. Furthermore, biotin-labelled miRNA pull-down experiment demonstrated that LINC00205 was remarkably enriched in the biotin-conjugated miR-26a-5parrested complexes compared to that in the negative control cel-miR-239b.We attempted to screen and characterize downstream targets of miR-26a-5p using the online tool ENCORI and TargetScan, and we found cyclin dependent kinase 6 (CDK6), a crucial modulator of cell cycle and cell growth, existed a potential targeting relationship with miR-26a-5p.Biotin-labelled miRNA pull-down experiment revealed that CDK6 mRNA could be dramatically trapped by biotin-conjugated miR-26a-5p-mimics rather than the negative control.Furthermore, the modulating role of LINC00205 and miR-26a-5p on CDK6 mRNA level was first confirmed by qPCR, and we revealed that suppressing LINC00205 could decline the CDK6 expression in both SUN- 449 and SK-Hep-1 cells, meanwhile the reduction of CDK6 caused by LINC00205 silencing could be recovered by miR-26a-5p inhibitor.Then the western blot was conducted to verify the modulating effect of LINC00205 and miR- 26a-5p on the CDK6 protein in SUN-449 cells.Altogether, the above results manifest that LINC00205 could control the proliferation of HCC cells by elevating CDK6 via sponging miR-26a-5p.We checked transcription factor binding sites harbored by the LINC00205 promoter using ChIP-seq data of HepG2 cells on UCSC Genome Browser (http://genome.ucsc. edu), and the Yin Yang-1 (YY1) binding site was found near the upstream of the transcription start site (TSS) of LINC00205.We further analyzed the LINC00205 promoter region (2000 bp up-stream of TSS) using transcription factor searching tools of JASPAR.In addition, the direct interaction between YY1 and LINC00205 promoter was identified using ChIP-qPCR, and we found YY1 was significantly enriched on LINC00205 promoter in both SUN-449 and SK-Hep-1 cells. Taken together, above results displayed that the up-regulation of LINC00205 in HCC could be attributed to the transcription factor YY1.	34730201	RID08183	transcriptional regulation	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE109761,GSE75367)
Hepatocellular carcinoma	HOMER3-AS1	HOMER3	positively-E	overexpression;shRNA;western blot;FISH;IHC	upregulation	qRT-PCR	TCGA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000269019	GRCh38_19:18940235-18947452	ENSG00000051128	NA	102724360	9454	NA	HOMER-3	Long non-coding RNA HOMER3-AS1 drives hepatocellular carcinoma progression via modulating the behaviors of both tumor cells and macrophages.The correlation between HOMER3-AS1 expression levels and overall survival in HCC was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) (http://gepia.cancer-pku.cn/index. html) based on the cancer genome atlas (TCGA) liver hepatocellular carcinoma (LIHC) dataset.To further test the correlation between HOMER3-AS1 expression levels and prognosis in HCC, we collected 68 HCC tissues and measured HOMER3-AS1 expression by qRT-PCR Consistently, high HOMER3-AS1 expression was correlated with poor overall survival in our HCC cohort.qRT-PCRresults revealed that HOMER3 mRNA levels were significantly upregulated after HOMER3-AS1 overexpression and significantly reduced after HOMER3-AS1 silencing.3e). Furthermore, the expressions of HOMER3-AS1 and HOMER3 in HCC tissues were detected by RNA FISH and IHC respectively. The results revealed that both HOMER3-AS1 and HOMER3 were mainly expressed in HCC cells, but not in stromal cells.CCK-8 and EdU incorporation experiments revealed that depletion of HOMER3 abolished the HOMER3-AS1-induced promotion of proliferation. Caspase-3 activity assays revealed that depletion of HOMER3 abolished the HOMER3-AS1-induced inhibition of apoptosis.Transwell migration and invasion experiments revealed that depletion of HOMER3 abolished the HOMER3-AS1-induced promotion of migration and invasion.The blocking of Wnt/beta-catenin signaling abolished the HOMER3-AS1-induced promotion of proliferation, migration, and invasion, and inhibition of apoptosis.In summary, our findings demonstrated that HOMER3-AS1 drives HCC progression via modulating the behaviors of both tumor cells and macrophages, which are dependent on the activation of HOMER3/Wnt/beta-catenin axis and CSF-1, respectively. HOMER3-AS1 might be a promising prognostic and therapeutic target for HCC.	34815380	RID08184	expression association	prognosis		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Congenital heart defects	Moshe	ISL1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Syndrome	lncRNA	TF	NA	NA	ENSG00000016082	NA	NA	3670	NA	ISLET1|Isl-1	Spatiotemporal expression of long noncoding RNA Moshe modulates heart cell lineage commitment. Appropriate differentiation was analysed by qRT-PCRusing the following three stage-specific marker genes, BrachryT (BryT) for the mesoderm stage, alpha-Smooth muscle actin (a-Sma) for cardiac progenitor cells and smooth muscle, and cardiac troponinT (cTnT) for cardiomyocytes.Moshe is highly expressed in cardiac mesoderm and cardiac progenitor stages during cardiac differentiation in vitro.We next investigated the function of Moshe by knockdown using antisense LNA (Locked Nucleic Acids) oligos at the intron 3 region.First, Moshe knockdown led to a dramatic decrease in cardiac progenitor inducer Nkx2.5 gene expression, whereas the adjacent cardiac transcription factor, Gata6, had no significant changes.Silencing Moshe increased the gene expression of SHF genes such as Isl-1, Hand2 and Tbx2, whereas the expression levels of Hcn4, Tbx5 and Gata4 known as the FHF genes were not notably changed.Gata6 and Gata4, the genes expressed in both heart fields, were not significantly changed. This is consistent with previous studies that Isl1 and Nkx2.5 repress each other and regulate SHF proliferation, differentiation and patterning.Altogether, these results may suggest that Moshe plays a role in fine-tuning processes by repressing SHF genes via activating the Nkx2.5 gene from properly differentiating into SHF lineage cells.Since Nkx2.5 was dramatically decreased in the Moshe knockdown condition in the present study, and it is known that the expression of Nkx2.5 with Isl1 in SHF cells represses each other to make the appropriate subtype identity, which results in proper heart development.We employed the LongTarget program to identify possible Moshe binding sites on the Nkx2.5 promoter and enhancer regions.To investigate the role of Moshe on Nkx2.5 expression, we also surveyed transcription factor (TF) binding motifs on the Nkx2.5 promoter region using PROMO and CIIIDER. Previous studies have reported that several TFs can bind to the promoter and enhancer regions of Nkx2.5.We confirmed the in silico prediction that Moshe binds to Nkx2.5 promoter regions by chromatin isolation using RNA purification (ChIRP) PCR analysis.Altogether, it is expected that the regulation of Nkx2.5 expression by Moshe occurs due to the direct binding of Moshe to nkx2.5 promoter region (-3015 bp to -3102 bp) which can recruit several important transcription factors on the site both temporal and spatial.The heart-specific molecular function of Moshe seems to be well conserved in heart development from mouse to human. Further studies of knock-out mouse study might reveal the function of Moshe in vivo.	34755591	RID08185	expression association	NA		UP(LIHC);DATA(GSE117623)
Congenital heart defects	Moshe	HAND2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Syndrome	lncRNA	TF	NA	NA	ENSG00000164107	NA	NA	9464	NA	DHAND2|Hed|Thing2|bHLHa26|dHand	Spatiotemporal expression of long noncoding RNA Moshe modulates heart cell lineage commitment. Appropriate differentiation was analysed by qRT-PCRusing the following three stage-specific marker genes, BrachryT (BryT) for the mesoderm stage, alpha-Smooth muscle actin (a-Sma) for cardiac progenitor cells and smooth muscle, and cardiac troponinT (cTnT) for cardiomyocytes.Moshe is highly expressed in cardiac mesoderm and cardiac progenitor stages during cardiac differentiation in vitro.We next investigated the function of Moshe by knockdown using antisense LNA (Locked Nucleic Acids) oligos at the intron 3 region.First, Moshe knockdown led to a dramatic decrease in cardiac progenitor inducer Nkx2.5 gene expression, whereas the adjacent cardiac transcription factor, Gata6, had no significant changes.Silencing Moshe increased the gene expression of SHF genes such as Isl-1, Hand2 and Tbx2, whereas the expression levels of Hcn4, Tbx5 and Gata4 known as the FHF genes were not notably changed.Gata6 and Gata4, the genes expressed in both heart fields, were not significantly changed. This is consistent with previous studies that Isl1 and Nkx2.5 repress each other and regulate SHF proliferation, differentiation and patterning.Altogether, these results may suggest that Moshe plays a role in fine-tuning processes by repressing SHF genes via activating the Nkx2.5 gene from properly differentiating into SHF lineage cells.Since Nkx2.5 was dramatically decreased in the Moshe knockdown condition in the present study, and it is known that the expression of Nkx2.5 with Isl1 in SHF cells represses each other to make the appropriate subtype identity, which results in proper heart development.We employed the LongTarget program to identify possible Moshe binding sites on the Nkx2.5 promoter and enhancer regions.To investigate the role of Moshe on Nkx2.5 expression, we also surveyed transcription factor (TF) binding motifs on the Nkx2.5 promoter region using PROMO and CIIIDER. Previous studies have reported that several TFs can bind to the promoter and enhancer regions of Nkx2.5.We confirmed the in silico prediction that Moshe binds to Nkx2.5 promoter regions by chromatin isolation using RNA purification (ChIRP) PCR analysis.Altogether, it is expected that the regulation of Nkx2.5 expression by Moshe occurs due to the direct binding of Moshe to nkx2.5 promoter region (-3015 bp to -3102 bp) which can recruit several important transcription factors on the site both temporal and spatial.The heart-specific molecular function of Moshe seems to be well conserved in heart development from mouse to human. Further studies of knock-out mouse study might reveal the function of Moshe in vivo.	34755591	RID08186	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE41245)
Congenital heart defects	Moshe	TBX2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Syndrome	lncRNA	TF	NA	NA	ENSG00000121068	NA	NA	6909	NA	VETD	Spatiotemporal expression of long noncoding RNA Moshe modulates heart cell lineage commitment. Appropriate differentiation was analysed by qRT-PCRusing the following three stage-specific marker genes, BrachryT (BryT) for the mesoderm stage, alpha-Smooth muscle actin (a-Sma) for cardiac progenitor cells and smooth muscle, and cardiac troponinT (cTnT) for cardiomyocytes.Moshe is highly expressed in cardiac mesoderm and cardiac progenitor stages during cardiac differentiation in vitro.We next investigated the function of Moshe by knockdown using antisense LNA (Locked Nucleic Acids) oligos at the intron 3 region.First, Moshe knockdown led to a dramatic decrease in cardiac progenitor inducer Nkx2.5 gene expression, whereas the adjacent cardiac transcription factor, Gata6, had no significant changes.Silencing Moshe increased the gene expression of SHF genes such as Isl-1, Hand2 and Tbx2, whereas the expression levels of Hcn4, Tbx5 and Gata4 known as the FHF genes were not notably changed.Gata6 and Gata4, the genes expressed in both heart fields, were not significantly changed. This is consistent with previous studies that Isl1 and Nkx2.5 repress each other and regulate SHF proliferation, differentiation and patterning.Altogether, these results may suggest that Moshe plays a role in fine-tuning processes by repressing SHF genes via activating the Nkx2.5 gene from properly differentiating into SHF lineage cells.Since Nkx2.5 was dramatically decreased in the Moshe knockdown condition in the present study, and it is known that the expression of Nkx2.5 with Isl1 in SHF cells represses each other to make the appropriate subtype identity, which results in proper heart development.We employed the LongTarget program to identify possible Moshe binding sites on the Nkx2.5 promoter and enhancer regions.To investigate the role of Moshe on Nkx2.5 expression, we also surveyed transcription factor (TF) binding motifs on the Nkx2.5 promoter region using PROMO and CIIIDER. Previous studies have reported that several TFs can bind to the promoter and enhancer regions of Nkx2.5.We confirmed the in silico prediction that Moshe binds to Nkx2.5 promoter regions by chromatin isolation using RNA purification (ChIRP) PCR analysis.Altogether, it is expected that the regulation of Nkx2.5 expression by Moshe occurs due to the direct binding of Moshe to nkx2.5 promoter region (-3015 bp to -3102 bp) which can recruit several important transcription factors on the site both temporal and spatial.The heart-specific molecular function of Moshe seems to be well conserved in heart development from mouse to human. Further studies of knock-out mouse study might reveal the function of Moshe in vivo.	34755591	RID08187	expression association	NA		UP(PAAD);DATA(GSE40174)
Congenital heart defects	Moshe	NKX2-5	positively-E	LongTarget;PROMO;CIIIDER;ChIRP	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Syndrome	Syndrome	lncRNA	TF	NA	NA	ENSG00000183072	NA	NA	1482	NA	CHNG5|CSX|CSX1|HLHS2|NKX2.5|NKX2E|NKX4-1|VSD3	Spatiotemporal expression of long noncoding RNA Moshe modulates heart cell lineage commitment. Appropriate differentiation was analysed by qRT-PCRusing the following three stage-specific marker genes, BrachryT (BryT) for the mesoderm stage, alpha-Smooth muscle actin (a-Sma) for cardiac progenitor cells and smooth muscle, and cardiac troponinT (cTnT) for cardiomyocytes.Moshe is highly expressed in cardiac mesoderm and cardiac progenitor stages during cardiac differentiation in vitro.We next investigated the function of Moshe by knockdown using antisense LNA (Locked Nucleic Acids) oligos at the intron 3 region.First, Moshe knockdown led to a dramatic decrease in cardiac progenitor inducer Nkx2.5 gene expression, whereas the adjacent cardiac transcription factor, Gata6, had no significant changes.Silencing Moshe increased the gene expression of SHF genes such as Isl-1, Hand2 and Tbx2, whereas the expression levels of Hcn4, Tbx5 and Gata4 known as the FHF genes were not notably changed.Gata6 and Gata4, the genes expressed in both heart fields, were not significantly changed. This is consistent with previous studies that Isl1 and Nkx2.5 repress each other and regulate SHF proliferation, differentiation and patterning.Altogether, these results may suggest that Moshe plays a role in fine-tuning processes by repressing SHF genes via activating the Nkx2.5 gene from properly differentiating into SHF lineage cells.Since Nkx2.5 was dramatically decreased in the Moshe knockdown condition in the present study, and it is known that the expression of Nkx2.5 with Isl1 in SHF cells represses each other to make the appropriate subtype identity, which results in proper heart development.We employed the LongTarget program to identify possible Moshe binding sites on the Nkx2.5 promoter and enhancer regions.To investigate the role of Moshe on Nkx2.5 expression, we also surveyed transcription factor (TF) binding motifs on the Nkx2.5 promoter region using PROMO and CIIIDER. Previous studies have reported that several TFs can bind to the promoter and enhancer regions of Nkx2.5.We confirmed the in silico prediction that Moshe binds to Nkx2.5 promoter regions by chromatin isolation using RNA purification (ChIRP) PCR analysis.Altogether, it is expected that the regulation of Nkx2.5 expression by Moshe occurs due to the direct binding of Moshe to nkx2.5 promoter region (-3015 bp to -3102 bp) which can recruit several important transcription factors on the site both temporal and spatial.The heart-specific molecular function of Moshe seems to be well conserved in heart development from mouse to human. Further studies of knock-out mouse study might reveal the function of Moshe in vivo.	34755591	RID08188	transcriptional regulation	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Oral squamous cell carcinoma	NR2F2-AS1	miR-494	negatively-E	siRNA;overexpression	downregulation	qPCR	NA	NA	cell proliferation(+)	DNA methylation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000247809	GRCh38_15:96110040-96327361	NA	NA	644192	NA	NA	NA	lncRNA NR2F2-AS1 inhibits the methylation of miR-494 to regulate oral squamous cell carcinoma cell proliferation.This study aimed to investigate the role of lncRNA NR2F2-AS1 in oral squamous cell carcinoma cells (OSCC). The TCGA datasets were used to explore the differential expression of NR2F2-AS1 in OSCC. To further explore the potential interaction between NR2F2-AS1 and miR-494, SCC090 cells were transfected with the NR2F2-AS1 expression vector, NR2F2-AS1 siRNA, and a miR-494 mimic. The effect of NR2F2-AS1 on miR-494 methylation was evaluated by performing methylation-specific PCR (MSP). Cell Counting Kit-8 (CCK-8) assay was used to assess the effects of NR2F2-AS1 silencing and miR-494 and NR2F2-AS1 overexpression on OSCC cell proliferation. NR2F2-AS1 expression was downregulated in OSCC and positively correlated with miR-494 expression. In OSCC cells, NR2F2-AS1 overexpression upregulated miR-494 level, while NR2F2-AS1 silencing decreased miR-494 expression. MSP results showed that NR2F2-AS1 overexpression decreased miR-494 methylation while NR2F2-AS1 silencing increased miR-494 methylation. In addition, NR2F2-AS1 silencing increased OSCC cell proliferation rate while overexpression of miR-494 and NR2F2-AS1 decreased OSCC cell proliferation. Furthermore, miR-494 overexpression attenuated the effects of NR2F2-AS1 silencing on cell proliferation. NR2F2-AS1 may inhibit miR-494 methylation to regulate cell proliferation in OSCC. The analyzed data sets generated during the study are available from the corresponding author upon reasonable request.	34896865	RID08189	epigenetic regulation	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Triple-negative breast cancer	Uc003xsl.1	NKRF	NA		upregulation		NA	NA	cell metastasis(+);cell survival(-)	transcriptional regulation	binding/interaction	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000186416	NA	NA	55922	NA	ITBA4|NRF	LncRNA Uc003xsl.1-Mediated Activation of the NFkB/IL8 Axis Promotes Progression of Triple-Negative Breast Cancer.Aberrant activation of NFkB orchestrates a critical role in tumor carcinogenesis; however, the regulatory mechanisms underlying this activation are not fully understood. Here we report that a novel long noncoding RNA (lncRNA) Uc003xsl.1 is highly expressed in triple-negative breast cancer (TNBC) and correlates with poor outcomes in patients with TNBC. Uc003xsl.1 directly bound nuclear transcriptional factor NFkB-repressing factor (NKRF), subsequently preventing NKRF from binding to a specific negative regulatory element in the promoter of the NFkB-responsive gene IL8 and abolishing the negative regulation of NKRF on NFkB-mediated transcription of IL8. Activation of the NFkB/IL8 axis promoted the progression of TNBC. Trop2-based antibody-drug conjugates have been applied in clinical trials in TNBC. In this study, a Trop2-targeting, redox-responsive nanoparticle was developed to systematically deliver Uc003xsl.1 siRNA to TNBC cells in vivo, which reduced Uc003xsl.1 expression and suppressed TNBC tumor growth and metastasis. Therefore, targeting Uc003xsl.1 to suppress the NFkB/IL8 axis represents a promising therapeutic strategy for TNBC treatment. These findings identify an epigenetic-driven NFkB/IL8 cascade initiated by a lncRNA, whose aberrant activation contributes to tumor metastasis and poor survival in patients with triple-negative breast cancer.	34965935	RID08190	transcriptional regulation	metastasis		DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE86978)
Triple-negative breast cancer	Uc003xsl.1	NFkB	positively-E		upregulation		NA	NA	cell metastasis(+);cell survival(-);cancer progression(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	LncRNA Uc003xsl.1-Mediated Activation of the NFkB/IL8 Axis Promotes Progression of Triple-Negative Breast Cancer.Aberrant activation of NFkB orchestrates a critical role in tumor carcinogenesis; however, the regulatory mechanisms underlying this activation are not fully understood. Here we report that a novel long noncoding RNA (lncRNA) Uc003xsl.1 is highly expressed in triple-negative breast cancer (TNBC) and correlates with poor outcomes in patients with TNBC. Uc003xsl.1 directly bound nuclear transcriptional factor NFkB-repressing factor (NKRF), subsequently preventing NKRF from binding to a specific negative regulatory element in the promoter of the NFkB-responsive gene IL8 and abolishing the negative regulation of NKRF on NFkB-mediated transcription of IL8. Activation of the NFkB/IL8 axis promoted the progression of TNBC. Trop2-based antibody-drug conjugates have been applied in clinical trials in TNBC. In this study, a Trop2-targeting, redox-responsive nanoparticle was developed to systematically deliver Uc003xsl.1 siRNA to TNBC cells in vivo, which reduced Uc003xsl.1 expression and suppressed TNBC tumor growth and metastasis. Therefore, targeting Uc003xsl.1 to suppress the NFkB/IL8 axis represents a promising therapeutic strategy for TNBC treatment. These findings identify an epigenetic-driven NFkB/IL9 cascade initiated by a lncRNA, whose aberrant activation contributes to tumor metastasis and poor survival in patients with triple-negative breast cancer.	34965935	RID08191	expression association	metastasis		
Triple-negative breast cancer	Uc003xsl.1	CXCL8	positively-E		upregulation		NA	NA	cell metastasis(+);cell survival(-);cancer progression(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	NA	NA	ENSG00000169429	NA	NA	3576	NA	GCP-1|GCP1|IL8|LECT|LUCT|LYNAP|MDNCF|MONAP|NAF|NAP-1|NAP1|SCYB8	LncRNA Uc003xsl.1-Mediated Activation of the NFkB/IL8 Axis Promotes Progression of Triple-Negative Breast Cancer.Aberrant activation of NFkB orchestrates a critical role in tumor carcinogenesis; however, the regulatory mechanisms underlying this activation are not fully understood. Here we report that a novel long noncoding RNA (lncRNA) Uc003xsl.1 is highly expressed in triple-negative breast cancer (TNBC) and correlates with poor outcomes in patients with TNBC. Uc003xsl.1 directly bound nuclear transcriptional factor NFkB-repressing factor (NKRF), subsequently preventing NKRF from binding to a specific negative regulatory element in the promoter of the NFkB-responsive gene IL8 and abolishing the negative regulation of NKRF on NFkB-mediated transcription of IL8. Activation of the NFkB/IL8 axis promoted the progression of TNBC. Trop2-based antibody-drug conjugates have been applied in clinical trials in TNBC. In this study, a Trop2-targeting, redox-responsive nanoparticle was developed to systematically deliver Uc003xsl.1 siRNA to TNBC cells in vivo, which reduced Uc003xsl.1 expression and suppressed TNBC tumor growth and metastasis. Therefore, targeting Uc003xsl.1 to suppress the NFkB/IL8 axis represents a promising therapeutic strategy for TNBC treatment. These findings identify an epigenetic-driven NFkB/IL10 cascade initiated by a lncRNA, whose aberrant activation contributes to tumor metastasis and poor survival in patients with triple-negative breast cancer.	34965935	RID08192	expression association	metastasis		DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367,GSE86978)
Papillary thyroid carcinoma	LINC00475	ZCCHC12	positively-E	luciferase reporter assays;RNA pull-down assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-376c-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000225511	GRCh38_9:92141298-92160114	ENSG00000174460	NA	158314	170261	C9orf44	FLJ16123|PNMA7A|SIZN|SIZN1	A ceRNA network mediated by LINC00475 in papillary thyroid carcinoma.Papillary thyroid carcinoma (PTC) is the most frequent histological type of differentiated thyroid carcinoma. Long noncoding RNAs (lncRNAs) have been widely reported to play a key role in human malignancies, and PTC is included. This study aimed to find out the functions and mechanism of lncRNA LINC00475 in PTC. LINC00475 was upregulated in PTC cells and was mainly located in the cytoplasm according to reverse-transcription polymerase chain reaction analyses and subcellular fractionation assays. As shown by cell counting kit-8 assays, ethynyl deoxyuridine incorporation assays, wound healing assays, and transwell assays, LINC00475 knockdown suppressed cell viability, proliferation, migration, and invasion. Mechanistically, LINC00475 upregulated the expression of messenger RNA zinc finger CCHC-type containing 12 (ZCCHC12) by binding to miR-376c-3p. ZCCHC12 was a direct target gene of miR-376c-3p in PTC cells. The relationship between miR-376c-3p and LINC00475 (or ZCCHC12) in PTC cells was probed by luciferase reporter assays, RNA pull-down assays, and RNA immunoprecipitation assays. In addition, both mRNA and protein levels of ZCCHC12 were downregulated due to miR-376c-3p overexpression or LINC00475 silencing. ZCCHC12 overexpression partially reversed the suppressive effect of LINC00475 knockdown on malignant behaviors of PTC cells. In conclusion, LINC00475 promotes PTC cell proliferation, migration, and invasion by upregulating ZCCHC12 via the interaction with miR-376c-3p.	34950770	RID08193	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	ASMTL-AS1	LAMC1	positively-E	luciferase reporter assays;RIP;starBase	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-1343-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236017	GRCh38_X:1401769-1414028	ENSG00000135862	NA	80161	3915	ASMTL-AS|ASMTLAS|CXYorf2|FLJ13330|NCRNA00105	LAMB2	The long non-coding RNA ASMTL-AS1 promotes hepatocellular carcinoma progression by sponging miR-1343-3p that suppresses LAMC1 (laminin subunit gamma 1).Long non-coding RNAs (lncRNAs) are critical regulators of hepatocellular carcinoma (HCC) carcinogenesis and development. We aimed to identify the function of the lncRNA ASMTL-AS1 during HCC malignancy. The expression of ASMTL-AS1, miR-1343-3p, and LAMC1 (laminin subunit gamma 1) was assessed in HCC tissues and cells. Cell Counting Kit-8 (CCK8) and Transwell migration assays were performed to determine the effect of ASMTL-AS1 on HCC cell proliferation and migration. Cell apoptosis was identified by detecting Bax and Bcl-2 protein expression using western blot, and a xenograft assay was performed to investigate tumor growth  in vivo . The interplay between miR-1343-3p and ASMTL-AS1 or LAMC1 was verified through luciferase reporter and RNA immunoprecipitation assays. ASMTL-AS1 and LAMC1 were highly expressed in HCC tissues and cells, whereas miR-1343-3p showed low expression. Clinically, miR-1343-3p expression in HCC tissues showed a negative correlation with ASMTL-AS1 or LAMC1 expression. Functional assays demonstrated that ASMTL-AS1 silencing suppressed HCC cell proliferation and migration and increased cell apoptosis. More interestingly, ASMTL-AS1 sponged miR-1343-3p and miR-1343-3p to target the 3'-UTR of LAMC1, thereby interfering with the malignant behavior of HCC cells. In conclusion, ASMTL-AS1 acts as a carcinogen in HCC through competing endogenous RNA (ceRNA) activity in the miR-1343-3p/LAMC1 axis. Our findings demonstrate that regulating ASMTL-AS1/miR-1343-3p/LAMC1-mediated HCC cell malignancy might be an effective method to interfere with HCC progression.	34859735	RID08194	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(PAAD);DATA(GSE40174)
Kidney disease	KCNQ1OT1	SOX6	positively-E	dual-luciferase reporter assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);inflammatory response(+);oxidative stress(+)	ceRNA(miR-147a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000110693	NA	10984	55553	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	lncRNA KCNQ1OT1 regulated high glucose-induced proliferation, oxidative stress, extracellular matrix accumulation, and inflammation by miR-147a/SOX6 in diabetic nephropathy (DN).Long non-coding RNAs (lncRNAs) have been proved to play critical roles in diabetic nephropathy (DN). This study aimed to investigate the functions and underlying mechanism of potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) in DN. Blood samples were obtained from 33 DN patients and 30 healthy volunteers. Kidney biopsies tissues of DN patients (n = 10) and patients with normal kidney morphology (n = 10) were collected. We found that KCNQ1OT1 was markedly overexpressed in the blood and kidney biopsies tissues of DN patients, as well as in high glucose (HG)-cultured human glomerular mesangial (HGMC) cells. Knockdown of KCNQ1OT1 suppressed proliferation, extracellular matrix (ECM) accumulation, inflammation, and oxidative stress in HG-treated HGMC cells in vitro. KCNQ1OT1 functioned as a sponge for microRNA-147a (miR-147a), and SRY-Box Transcription Factor 6 (SOX6) was directly targeted by miR-147a. Downregulation of miR-147a or upregulation of SOX6 partly overturned the prohibitive effects of KCNQ1OT1 knockdown or miR-147a overexpression on proliferation, ECM accumulation, inflammation, and oxidative stress in HG-treated HGMC cells. Altogether, KCNQ1OT1 mediated the proliferation, ECM accumulation, inflammation, and oxidative stress in HG-treated HGMC cells via miR-147a/SOX6 axis, which might be a novel target for DN therapy.	34911869	RID08195	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	UP(LIHC,PAAD,PRAD,SKCM);DATA(GSE117623,GSE40174,GSE104209,GSE38495)
Abdominal aortic aneurysm	PVT1	NCKAP1L	positively-E	luciferase reporter assays;starBase	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-3127-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000123338	NA	5820	3071	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HEM1	Long non-coding RNA PVT1/microRNA miR-3127-5p/NCK-associated protein 1-like axis participates in the pathogenesis of abdominal aortic aneurysm by regulating vascular smooth muscle cells.The long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) has been implicated in the progression of abdominal aortic aneurysms (AAA). However, the detailed mechanism requires further analysis. Our study was aimed at interrogating the mechanism of PVT1 in an H 2 O 2 -induced AAA model  in vitro . The expression of lncRNA PVT1, microRNA miR-3127-5p, and NCK-associated protein 1-like (NCKAP1L) was examined in AAA tissues and H 2 O 2 -treated vascular smooth muscle cells (VSMCs). Cell proliferation was assayed using Cell Counting Kit-8 (CCK8) and 5-Bromodeoxyuridine (BrdU) assays. Meanwhile, 5-Ethynyl-2'-deoxyuridine (EdU) staining was performed to assess cell apoptosis and caspase-3 activity. IL-1beta and caspase-1 expression was also assessed using western blot to determine inflammasome activation in H 2 O 2 -treated VSMCs. Luciferase reporter assays addressed the possible interaction between miR-3127-5p and PVT1 or NCKAP1L, which was predicted by starBase analysis. PVT1 and NCKAP1L expression was elevated in AAA tissues and induced the AAA model  in vitro , whereas miR-3127-5p showed the opposite trend. Functionally, PVT1 silencing promoted cell proliferation and reduced the apoptotic rate and inflammasome activation in H 2 O 2 -treated VSMCs. Mechanical investigation demonstrated that PVT1 acted as a sponge of miR-3127-5p to modulate NCKAP1L expression, resulting in suppression of VSMC proliferation, induction of apoptosis, and activation of inflammation. In conclusion, PVT1 participates in AAA progression through the miR-3127-5p/NCKAP1L axis and may be a promising biosignature and therapeutic target for AAA.	34898354	RID08196	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Glioblastoma	MIR210HG	OCT1	NA	RNA pull-down assay;RIP	upregulation	RT-PCR	TCGA;GSE7696	NA	cancer progression(+)	interact with protein	binding/interaction	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000247095	GRCh38_11:565657-568457	NA	NA	100506211	NA	NA	NA	Hypoxia-inducible lncRNA MIR210HG interacting with OCT1 is involved in glioblastoma multiforme malignancy.An insufficient oxygen supply within the intratumoral environment, also known as hypoxia, induces glioblastoma multiforme (GBM) invasion, stemness, and temozolomide (TMZ) drug resistance. Long noncoding (lnc)RNAs have been reported to be involved in hypoxia and GBM progression. However, their roles in hypoxic GBM malignancy are still unclear. We investigated the mechanisms of hypoxia-mediated lncRNAs in regulating GBM processes. Using The Cancer Genome Atlas (TCGA) and data mining, hypoxia-correlated lncRNAs were identified. A hypoxia-upregulated lncRNA, MIR210HG, locating in nuclear regions, predicted poor prognoses of patients and modulated hypoxia-promoted glioma stemness, TMZ resistance, and invasion. Depletion of hypoxic MIR210HG suppressed GBM and patient-derived cell growth and increased TMZ sensitivity in vitro and vivo. Using RNA sequencing and gene set enrichment analysis (GSEA), MIR210HG-upregulated genes significantly belonged to the targets of octamer transcription factor 1 (OCT1) transcription factor. The direct interaction between OCT1 and MIR210HG was also validated. Two well-established worse prognostic factors of GBM, insulin-like growth factor-binding protein 2 (IGFBP2) and fibroblast growth factor receptor 1 (FGFR1), were identified as downstream targets of OCT1 through MIR210HG mediation in hypoxia. Consequently, the lncRNA MIR210HG is upregulated by hypoxia and interacts with OCT1 for modulating hypoxic GBM, leading to poor prognoses. These findings might provide a better understanding in functions of hypoxia/MIR210HG signaling for regulating GBM malignancy.	34897892	RID08197	interact with protein	prognosis		
Non-small cell lung cancer	PCAT29	PTEN	positively-E	overexpression	downregulation	RT-qPCR	NA	NA	cancer progression(+);cell proliferation(+)	ceRNA(miR-494)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENST00000560655	NA	ENSG00000171862	NA	104472713	5728	NA	BZS|MHAM|MMAC1|PTEN1|TEP1	LncRNA PCAT29 Up-Regulates the Expression of PTEN by Down-Regulating miR-494 in Non-Small-Cell Lung Cancer to Suppress Tumor Progression.PCAT29 has reported to exert tumor suppressive roles. In this study, we investigated the function of PCAT29 in non-small-cell lung cancer (NSCLC). Expression levels of PCAT29, miR-494, and PTEN in non-tumor and NSCLC tumor tissue samples were measured by performing quantitative reverse transcription polymerase chain reaction. Cell apoptosis and proliferation analyses were formed to study the effects of overexpression of PCAT29, miR-494, and PTEN on apoptosis and proliferation of H23 cells. It was observed that PCAT29 was down-regulated in NSCLC and predicted poor survival. In NSCLC cells, miR-494 was inversely, while PTEN was positively correlated with PCAT29. In NSCLC cells, overexpression of PCAT29 led to down-regulated miR-494 and up-regulated PTEN. Overexpression of miR-494 resulted in down-regulated PTEN but did not affect the expression of PCAT29. Overexpression of PTEN affected neither PCAT29 nor miR-494. In addition, overexpression of PCAT29 and PTEN resulted in increased apop-totic rate and decreased proliferation of NSCLC cells. miR-494 played an opposite role and attenuated the effects of overexpression of PCAT29. Therefore, PCAT29 may up-regulate PTEN by down-regulating miR-494 to suppress the progression of NSCLC cells.	34936288	RID08198	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367)
Hepatocellular carcinoma	FTX	HAVCR2	positively-E		upregulation		NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000135077	NA	100302692	84868	FLJ33139|LINC00182|MIR374AHG|NCRNA00182	CD366|FLJ14428|Tim-3|TIM3|TIMD3	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08199	expression association	metastasis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842)	UP(LIHC,PAAD);DOWN(PRAD,BRCA);DATA(GSE117623,GSE40174,GSE67980,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	SFMBT2	LncRNA-Y5	negatively-E		upregulation		NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000198879	NA	NA	NA	57713	NA	NA	NA	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08200	expression association	NA	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)	
Hepatocellular carcinoma	RTL1	TP53	NA		upregulation		NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000254656	GRCh38_14:100879753-100903722	ENSG00000141510	NA	388015	7157	HUR1|1-Mar|MART1|PEG11|SIRH2	LFS1|p53	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08201	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	LINC01152	IL23A	NA		upregulation		NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000256124	GRCh38_17:72030291-72041310	ENSG00000110944	NA	102606463	51561	CMPD|RP11-84E24.3|TCONS_00025128	IL-23|IL-23A|IL23P19|P19|SGRF	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08202	transcriptional regulation	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)
Hepatocellular carcinoma	WFDC21P	STAT3	NA		upregulation		NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000261040	GRCh38_17:60083562-60091885	ENSG00000168610	NA	645638	6774	lnc-DC|LNCDC|LOC645638	APRF	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08203	expression association	NA	DOWN(BRCA);DATA(GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Hepatocellular carcinoma	H19	miR-22	negatively-E		upregulation		NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000186594	NA	283120	NA	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	NA	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08204	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Hepatocellular carcinoma	SNHG20	SNHG20	NA		upregulation		NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	lncRNA	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000234912	NA	654434	654434	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	C17orf86|DKFZp686L05235|FLJ25582|LINC00338|NCRNA00338|PRO0872|SCARNA16HG	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer	34869051	RID08205	expression association	NA	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)	UP(LIHC);DOWN(NSCLC,BRCA);DATA(GSE117623,GSE74639,GSE55807)
Hepatocellular carcinoma	SAMD12-AS1	NPM1	NA		upregulation		NA	NA	cell proliferation(+);cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000281641	GRCh38_8:118620498-118906155	ENSG00000181163	NA	552860	4869	C8orf26|NCRNA00252	B23|NPM	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08206	expression association	NA		DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE51827,GSE86978)
Hepatocellular carcinoma	SAMD12-AS2	TP53	NA		upregulation		NA	NA	cell proliferation(+);cell growth(+)	protein stability	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000141510	NA	NA	7157	NA	LFS1|p53	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08207	interact with protein	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Hepatocellular carcinoma	WEE2-AS1	FERMT3	NA		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell cycle(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228775	GRCh38_7:141704003-141738346	ENSG00000149781	NA	285962	83706	NA	KIND3|MGC10966|MIG2B|UNC112C|URP2	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08208	expression association	NA	UP(LIHC);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Hepatocellular carcinoma	ATB	miR-200	negatively-E		upregulation		NA	NA	cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Current State and Progress of Research on the Role of lncRNA in HBV-Related Liver Cancer 	34869051	RID08209	ceRNA or sponge	metastasis		
Diabetic cataract	GAS5	TGFBR1	positively-E		upregulation		NA	NA	cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-204-3p)	regulation	NA	NA	NA	NA	Nervous system disease	Cataract	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106799	NA	60674	7046	NCRNA00030|SNHG2	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	LncRNA GAS5 regulates migration and epithelial-to-mesenchymal transition in lens epithelial cells via the miR-204-3p/TGFBR1 axis.Diabetic cataract (DC) is a major ocular complication secondary to diabetes mellitus. The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is an important event in DC progression. Long non-coding RNAs (lncRNAs) and microRNAs are involved in various biological processes and disorders. The aim of this study was to investigate the roles of lncRNA growth arrest-specific transcript 5 (GAS5) and microRNA-204-3p (miR-204-3p) deregulation in the pathogenic mechanism of high glucose (HG)-stimulated LECs. The results show that GAS5 was up-regulated, whereas miR-204-3p was down-regulated in anterior lens capsule tissues of DC patients and in HG-treated LECs compared to their controls, respectively. Functional experiments suggest that the lentivirus-mediated depletion of GAS5, as well as overexpression of miR-204-3p, suppressed migration and EMT in HG-treated LECs. Further mechanistic studies revealed that lncRNA GAS5/miR-204-3p/type 1 receptor of transforming growth factor-beta (TGFBR1) has a regulatory role in the process. Collectively, we demonstrated that dysregulation of GAS5 affects lens epithelial cell migration and EMT under HG conditions via the miR-204-3p/TGFBR1 axis. The current findings may provide new insights into the molecular mechanisms of DC development.	34916611	RID08210	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	MALAT1	E2F1	NA	RIP		qRT-PCR	TCGA;GTEx	NA	chemoresistance(+)	interact with protein	binding/interaction	NA	Adriamycin	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101412	NA	378938	1869	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	RBBP3|RBP3	Effect of m6A methyltransferase METTL3 -mediated MALAT1/E2F1/AGR2 axis on adriamycin resistance in breast cancer.N6-methyladenosine (m6A) methyltransferase METTL3 has been implicated in carcinogenesis, which may be associated the overexpression of MALAT1. However, the downstream mechanics actions remain largely unknown. This study intends to probe the downstream mechanism of the N6-methyladenosine (m 6  A) methyltransferase METTL3 and MALAT1 in adriamycin resistance in breast cancer. Through Bioinformatics databases lncMAP, TCGA and GTEx, we predicted the downstream transcription factors E2F1 and AGR2 of MALAT1 in breast cancer. The Cancer Genome Atlas and Genotype-Tissue Expression (GTEx) databases were used to screen the downstream target genes of MALAT1. MeRIP-qPCR was used to detect the m 6  A level of MALAT1 in cells. RIP was used to detect the binding between MALAT1 and E2F1, and chromatin immunoprecipitation (ChIP) for the binding of E2F1 to AGR2 promoter. Cell Counting Kit-8 and colony formation assays were used to detect cell viability. Transwell was used to detect cell invasion. Quantitative reverse transcription polymerase chain reaction (qRT-PCR and western blot were used to detect the expression of related genes and proteins. A nude mouse xenograft tumor model was established to observe the effect of METTL3 on adriamycin resistance of breast cancer. The total survival of mice after exogenous gene silencing was analyzed by the Kaplan-Meier method. METTL3 was highly expressed in adriamycin-resistant breast cancer cells. METTL3 promotes adriamycin resistance in breast cancer cells. METTL3 mediates the expression of MALAT1 in adriamycin-resistant breast cancer through m 6  A. MALAT1 increases adriamycin resistance in breast cancer cells by recruiting E2F1 to activate AGR2 transcription. METTL3 can regulate the expression of MALAT1 through m 6  A, mediate the E2F1/AGR2 axis, and promote the adriamycin resistance of breast cancer. METTL3 may modify MALAT1 protein through m 6  A, recruit E2F1 and activate downstream AGR2 expression, thus promoting adriamycin resistance in breast cancer.	34964205	RID08211	interact with protein	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Breast cancer	MALAT1	AGR2	positively-E	RIP;ChIP		qRT-PCR	TCGA;GTEx	NA	chemoresistance(+)	NA	regulation	NA	Adriamycin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106541	NA	378938	10551	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	AG2|HAG-2|PDIA17|XAG-2	Effect of m6A methyltransferase METTL3 -mediated MALAT1/E2F1/AGR2 axis on adriamycin resistance in breast cancer.N6-methyladenosine (m6A) methyltransferase METTL3 has been implicated in carcinogenesis, which may be associated the overexpression of MALAT1. However, the downstream mechanics actions remain largely unknown. This study intends to probe the downstream mechanism of the N6-methyladenosine (m 6  A) methyltransferase METTL3 and MALAT1 in adriamycin resistance in breast cancer. Through Bioinformatics databases lncMAP, TCGA and GTEx, we predicted the downstream transcription factors E2F1 and AGR2 of MALAT1 in breast cancer. The Cancer Genome Atlas and Genotype-Tissue Expression (GTEx) databases were used to screen the downstream target genes of MALAT1. MeRIP-qPCR was used to detect the m 6  A level of MALAT1 in cells. RIP was used to detect the binding between MALAT1 and E2F1, and chromatin immunoprecipitation (ChIP) for the binding of E2F1 to AGR2 promoter. Cell Counting Kit-8 and colony formation assays were used to detect cell viability. Transwell was used to detect cell invasion. Quantitative reverse transcription polymerase chain reaction (qRT-PCR and western blot were used to detect the expression of related genes and proteins. A nude mouse xenograft tumor model was established to observe the effect of METTL3 on adriamycin resistance of breast cancer. The total survival of mice after exogenous gene silencing was analyzed by the Kaplan-Meier method. METTL3 was highly expressed in adriamycin-resistant breast cancer cells. METTL3 promotes adriamycin resistance in breast cancer cells. METTL3 mediates the expression of MALAT1 in adriamycin-resistant breast cancer through m 6  A. MALAT1 increases adriamycin resistance in breast cancer cells by recruiting E2F1 to activate AGR2 transcription. METTL3 can regulate the expression of MALAT1 through m 6  A, mediate the E2F1/AGR2 axis, and promote the adriamycin resistance of breast cancer. METTL3 may modify MALAT1 protein through m 6  A, recruit E2F1 and activate downstream AGR3 expression, thus promoting adriamycin resistance in breast cancer.	34964205	RID08212	expression association	chemoresistance	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(NSCLC,PAAD,BRCA);DATA(GSE74639,GSE60407,GSE51827,GSE55807)
Breast cancer	LINC00467	TGFB2	positively-E	LnCeVar;cBioportal	upregulation	microarray	GSE7904;GSE45827;GSE65194;GSE22820;GSE38959;GSE57297;GSE1299;GSE113197	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-23b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000153363	GRCh38_1:211382736-211435570	ENSG00000092969	NA	84791	7042	C1orf97|MGC14801	NA		34956437	RID08213	ceRNA or sponge	NA	UP(LIHC,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE38495,GSE55807,GSE86978)	UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Gastric cancer	HOTAIR	miR-200a	negatively-E	siRNA;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR Induces the Downregulation of miR-200 Family Members in Gastric Cancer Cell LinesGastric cancer (GC) is the fourth most common human malignancy and the second reason for cancer morbidity worldwide. Long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) has recently emerged as a promoter of metastasis in various cancer types, including GC, through the epithelial<U+2011>mesenchymal transition (EMT) process. However, the exact mechanism of HOTAIR in promoting EMT is unknown. Aberrant expression of the miR-200 family has been linked to the occurrence and development of various types of malignant tumors. This study investigates the correlation between the HOTAIR and miR-200 family gene expression patterns in GC cell lines. We investigated the miR-200 and HOTAIR due to their common molecular features in the EMT process. AGS and MKN45 cell lines were transfected with si-HOTAIR, along with a negative control. The effect of HOTAIR knockdown was also analyzed on cell viability and also on the expression of miR-200 family members, including miR-200a, -200b, and -200c, in cell lines using qRT-PCR Statistical analysis was performed to find the potential correlation between the expression level of HOTAIR and miRs. Our results showed significant increased miR-200 family expression level in transfected AGS and MKN45 GC cells (fold changes > 2; p < 0.001). Moreover, a negative correlation was observed between HOTAIR and miR-200 expression levels in GC cell lines (p < 0.05). Our findings showed a significant association between miR-200 family and HOTAIR expression levels in GC cell lines. Taken together, the HOTAIR-miR-200 axis seems to play a vital role in human GC, suggesting a potential therapeutic target in future GC treatment.	34923813	RID08214	ceRNA or sponge	metastasis		
Gastric cancer	HOTAIR	miR-200b	negatively-E	siRNA;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR Induces the Downregulation of miR-200 Family Members in Gastric Cancer Cell LinesGastric cancer (GC) is the fourth most common human malignancy and the second reason for cancer morbidity worldwide. Long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) has recently emerged as a promoter of metastasis in various cancer types, including GC, through the epithelial<U+2011>mesenchymal transition (EMT) process. However, the exact mechanism of HOTAIR in promoting EMT is unknown. Aberrant expression of the miR-200 family has been linked to the occurrence and development of various types of malignant tumors. This study investigates the correlation between the HOTAIR and miR-200 family gene expression patterns in GC cell lines. We investigated the miR-200 and HOTAIR due to their common molecular features in the EMT process. AGS and MKN45 cell lines were transfected with si-HOTAIR, along with a negative control. The effect of HOTAIR knockdown was also analyzed on cell viability and also on the expression of miR-200 family members, including miR-200a, -200b, and -200c, in cell lines using qRT-PCR Statistical analysis was performed to find the potential correlation between the expression level of HOTAIR and miRs. Our results showed significant increased miR-200 family expression level in transfected AGS and MKN45 GC cells (fold changes > 2; p < 0.001). Moreover, a negative correlation was observed between HOTAIR and miR-200 expression levels in GC cell lines (p < 0.05). Our findings showed a significant association between miR-200 family and HOTAIR expression levels in GC cell lines. Taken together, the HOTAIR-miR-201 axis seems to play a vital role in human GC, suggesting a potential therapeutic target in future GC treatment.	34923813	RID08215	ceRNA or sponge	metastasis		
Gastric cancer	HOTAIR	miR-200c	negatively-E	siRNA;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR Induces the Downregulation of miR-200 Family Members in Gastric Cancer Cell LinesGastric cancer (GC) is the fourth most common human malignancy and the second reason for cancer morbidity worldwide. Long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) has recently emerged as a promoter of metastasis in various cancer types, including GC, through the epithelial<U+2011>mesenchymal transition (EMT) process. However, the exact mechanism of HOTAIR in promoting EMT is unknown. Aberrant expression of the miR-200 family has been linked to the occurrence and development of various types of malignant tumors. This study investigates the correlation between the HOTAIR and miR-200 family gene expression patterns in GC cell lines. We investigated the miR-200 and HOTAIR due to their common molecular features in the EMT process. AGS and MKN45 cell lines were transfected with si-HOTAIR, along with a negative control. The effect of HOTAIR knockdown was also analyzed on cell viability and also on the expression of miR-200 family members, including miR-200a, -200b, and -200c, in cell lines using qRT-PCR Statistical analysis was performed to find the potential correlation between the expression level of HOTAIR and miRs. Our results showed significant increased miR-200 family expression level in transfected AGS and MKN45 GC cells (fold changes > 2; p < 0.001). Moreover, a negative correlation was observed between HOTAIR and miR-200 expression levels in GC cell lines (p < 0.05). Our findings showed a significant association between miR-200 family and HOTAIR expression levels in GC cell lines. Taken together, the HOTAIR-miR-202 axis seems to play a vital role in human GC, suggesting a potential therapeutic target in future GC treatment.	34923813	RID08216	ceRNA or sponge	metastasis		
Breast cancer	PVT1	FOXQ1	positively-E	dual-luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000164379	NA	5820	94234	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HFH1	Long noncoding RNA PVT1 promotes breast cancer proliferation and metastasis by binding miR-128-3p and UPF1.Mounting evidence supports that long noncoding RNAs (lncRNAs) have critical roles during cancer initiation and progression. In this study, we report that the plasmacytoma variant translocation 1 (PVT1) lncRNA is involved in breast cancer progression. qRT-PCRand western blot were performed to detect the gene and protein expression. Colony formation would healing and transwell assays were used to detect cell function. dual-luciferase reporter assay and RNA pull-down experiments were used to examine the mechanisms interaction between molecules. Orthotopic mouse models were established to evaluate the influence of PVT1 on tumor growth and metastasis in vivo. PVT1 is significant upregulated in breast cancer patients' plasma and cell lines. PVT1 promotes breast cancer cell proliferation and metastasis both in vitro and in vivo. Mechanistically, PVT1 upregulates FOXQ1 via miR-128-3p and promotes epithelial-mesenchymal transition. In addition, PVT1 binds to the UPF1 protein, thereby inducing epithelial-mesenchymal transition, proliferation and metastasis in breast cancer cells. PVT1 may act as an oncogene in breast cancer through binding miR-128-3p and UPF1 and represents a potential target for BC therapeutic development.	34922601	RID08217	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(PAAD);DATA(GSE40174)
Breast cancer	PVT1	UPF1	positively-E	dual-luciferase reporter assay;RNA pull-down assays	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000005007	NA	5820	5976	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HUPF1|KIAA0221|NORF1|pNORF1|RENT1|smg-2	Long noncoding RNA PVT1 promotes breast cancer proliferation and metastasis by binding miR-128-3p and UPF1.Mounting evidence supports that long noncoding RNAs (lncRNAs) have critical roles during cancer initiation and progression. In this study, we report that the plasmacytoma variant translocation 1 (PVT1) lncRNA is involved in breast cancer progression. qRT-PCRand western blot were performed to detect the gene and protein expression. Colony formation would healing and transwell assays were used to detect cell function. dual-luciferase reporter assay and RNA pull-down experiments were used to examine the mechanisms interaction between molecules. Orthotopic mouse models were established to evaluate the influence of PVT1 on tumor growth and metastasis in vivo. PVT1 is significant upregulated in breast cancer patients' plasma and cell lines. PVT1 promotes breast cancer cell proliferation and metastasis both in vitro and in vivo. Mechanistically, PVT1 upregulates FOXQ1 via miR-128-3p and promotes epithelial-mesenchymal transition. In addition, PVT1 binds to the UPF1 protein, thereby inducing epithelial-mesenchymal transition, proliferation and metastasis in breast cancer cells. PVT1 may act as an oncogene in breast cancer through binding miR-128-3p and UPF2 and represents a potential target for BC therapeutic development.	34922601	RID08218	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Gastric cancer	SNHG3	MYB	positively-E	FISH;StarBase;luciferase reporter activity assay;overexpression	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000118513	NA	8420	4602	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A	c-myb	LncRNA SNHG3 promotes gastric cancer cell proliferation and metastasis by regulating the miR-139-5p/MYB axis.The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity  in vitro  and constrained  in vivo  GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.	34898477	RID08219	ceRNA or sponge	metastasis	DOWN(PRAD,PAAD,BRCA);UP(SKCM);DATA(GSE104209,GSE60407,GSE38495,GSE111842)	
Esophagus squamous cell carcinoma	NORAD	MTDH	positively-E	RIP;qRT-PCR	upregulation	qRT-PCR	GSE45670	NA	chemoresistance(+)	ceRNA(miR-224-3p)	regulation	NA	Cisplatin	Cis-diamminedichloro-platinum	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000147649	NA	647979	92140	LINC00657	3D3|AEG-1|LYRIC	Long non-coding RNA NORAD/miR-224-3p/MTDH axis contributes to CDDP resistance of esophageal squamous cell carcinoma by promoting nuclear accumulation of beta-catenin.Cis-diamminedichloro-platinum (CDDP)-based chemotherapy regimens are the most predominant treatment strategies for patients with esophageal squamous cell carcinoma (ESCC). Dysregulated long non-coding RNAs (lncRNAs) contribute to CDDP resistance, which results in treatment failure in ESCC patients. However, the majority of lncRNAs involved in CDDP resistance in ESCC remain to be elucidated. The public Gene Expression Omnibus (GEO) dataset GSE45670 was analysed to reveal potential lncRNAs involved in CDDP resistance of ESCC. Candidate upregulated lncRNAs were detected in ESCC specimens by qRT-PCRto identify crucial lncRNAs. Non-coding RNA activated by DNA damage (NORAD) was selected for further study. Kaplan-Meier analysis and a COX proportional regression model were performed to analyse the potential of NORAD for predicting prognosis of ESCC patients. The role of NORAD in CDDP resistance were determined by conducting gain and loss-of-function experiments in vitro. Fluorescence in situ hybridization (FISH) was performed to determine the subcellular location of NORAD in ESCC cells. A public GEO dataset and bioinformatic algorithms were used to predict the microRNAs (miRNAs) that might be latently sponged by NORAD. qRT-PCRwas conducted to verify the expression of candidate miRNAs. Luciferase reporter and Argonaute-2 (Ago2)-RNA immunoprecipitation (RIP) assays were conducted to evaluate the interaction between NORAD and candidate miRNAs. A miRNA rescue experiment was performed to authenticate the NORAD regulatory axis and its effects on CDDP resistance in ESCC cells. western blot was conducted to confirm the precise downstream signalling pathway of NORAD. A xenograft mouse model was established to reveal the effect of NORAD on CDDP resistance in vivo. The expression of NORAD was higher in CDDP-resistant ESCC tissues and cells than in CDDP-sensitive tissues and cells. NORAD expression was negatively correlated with the postoperative prognosis of ESCC patients who underwent CDDP-based chemotherapy. NORAD knockdown partially arrested CDDP resistance of ESCC cells. FISH showed that NORAD was located in the cytoplasm in ESCC cells. Furthermore, overlapping results from bioinformatic algorithms analyses and qRT-PCR;ISHowed that NORAD could sponge miR-224-3p in ESCC cells. Ago2-RIP demonstrated that NORAD and miR-224-3p occupied the same Ago2 to form an RNA-induced silencing complex (RISC) and subsequently regulated the expression of metadherin (MTDH) in ESCC cells. The NORAD/miR-224-3p/MTDH axis promoted CDDP resistance and progression in ESCC cells by promoting nuclear accumulation of beta-catenin in vitro and in vivo. NORAD upregulates MTDH to promote CDDP resistance and progression in ESCC by sponging miR-224-3p. Our results highlight the potential of NORAD as a therapeutic target in ESCC patients receiving CDDP-based chemotherapy.	34893064	RID08220	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE67939)
Breast cancer	NEAT1	PGK1	NA		upregulation		NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000102144	NA	283131	5230	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	NA	NEAT1 is essential for metabolic changes that promote breast cancer growth and metastasis.Accelerated glycolysis is the main metabolic change observed in cancer, but the underlying molecular mechanisms and their role in cancer progression remain poorly understood. Here, we show that the deletion of the long noncoding RNA (lncRNA) Neat1 in MMTV-PyVT mice profoundly impairs tumor initiation, growth, and metastasis, specifically switching off the penultimate step of glycolysis. Mechanistically, NEAT1 directly binds and forms a scaffold bridge for the assembly of PGK1/PGAM1/ENO1 complexes and thereby promotes substrate channeling for high and efficient glycolysis. Notably, NEAT1 is upregulated in cancer patients and correlates with high levels of these complexes, and genetic and pharmacological blockade of penultimate glycolysis ablates NEAT1-dependent tumorigenesis. Finally, we demonstrate that Pinin mediates glucose-stimulated nuclear export of NEAT1, through which it exerts isoform-specific and paraspeckle-independent functions. These findings establish a direct role for NEAT1 in regulating tumor metabolism, provide new insights into the Warburg effect, and identify potential targets for therapy.	34879239	RID08221	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Breast cancer	NEAT1	PGAM1	NA		upregulation		NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171314	NA	283131	5223	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	PGAM-B|PGAMA	NEAT1 is essential for metabolic changes that promote breast cancer growth and metastasis.Accelerated glycolysis is the main metabolic change observed in cancer, but the underlying molecular mechanisms and their role in cancer progression remain poorly understood. Here, we show that the deletion of the long noncoding RNA (lncRNA) Neat1 in MMTV-PyVT mice profoundly impairs tumor initiation, growth, and metastasis, specifically switching off the penultimate step of glycolysis. Mechanistically, NEAT1 directly binds and forms a scaffold bridge for the assembly of PGK1/PGAM1/ENO1 complexes and thereby promotes substrate channeling for high and efficient glycolysis. Notably, NEAT1 is upregulated in cancer patients and correlates with high levels of these complexes, and genetic and pharmacological blockade of penultimate glycolysis ablates NEAT1-dependent tumorigenesis. Finally, we demonstrate that Pinin mediates glucose-stimulated nuclear export of NEAT1, through which it exerts isoform-specific and paraspeckle-independent functions. These findings establish a direct role for NEAT2 in regulating tumor metabolism, provide new insights into the Warburg effect, and identify potential targets for therapy.	34879239	RID08222	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Breast cancer	NEAT1	ENO1	NA		upregulation		NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000074800	NA	283131	2023	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	ENO1L1|MBP-1|MPB1|PPH	NEAT1 is essential for metabolic changes that promote breast cancer growth and metastasis.Accelerated glycolysis is the main metabolic change observed in cancer, but the underlying molecular mechanisms and their role in cancer progression remain poorly understood. Here, we show that the deletion of the long noncoding RNA (lncRNA) Neat1 in MMTV-PyVT mice profoundly impairs tumor initiation, growth, and metastasis, specifically switching off the penultimate step of glycolysis. Mechanistically, NEAT1 directly binds and forms a scaffold bridge for the assembly of PGK1/PGAM1/ENO1 complexes and thereby promotes substrate channeling for high and efficient glycolysis. Notably, NEAT1 is upregulated in cancer patients and correlates with high levels of these complexes, and genetic and pharmacological blockade of penultimate glycolysis ablates NEAT1-dependent tumorigenesis. Finally, we demonstrate that Pinin mediates glucose-stimulated nuclear export of NEAT1, through which it exerts isoform-specific and paraspeckle-independent functions. These findings establish a direct role for NEAT3 in regulating tumor metabolism, provide new insights into the Warburg effect, and identify potential targets for therapy.	34879239	RID08223	interact with protein	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065)
Neonatal sepsis	CASC15	miR-144-3p	negatively-E	luciferase reporter genes assay	upregulation	RT-qPCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	NA	NA	NA	NA	Disease by infectious agent	Bacterial infectious disease	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664184-22654455	NA	NA	401237	NA	LINC00340|lnc-SOX4-1	NA	Aberrant long non-coding RNA cancer susceptibility 15 (CASC15) plays a diagnostic biomarker and regulates inflammatory reaction in neonatal sepsis.Neonatal sepsis (NS) is one of the important causes of neonatal death. There are many studies to confirm the role of long non-coding RNA (lncRNA) in neonatal infectious diseases. This study aimed to explore the level of cancer susceptibility 15 (CASC15) and its effect on inflammatory response in NS. Seventy-nine neonatal pneumonia (NP) patients and 80 NS patients were enrolled in this study. Reverse Transcription-quantitative PCR (RT-qPCR) was used to determine the expression levels of CASC15 and miR-144-3p. Receiver operating characteristic (ROC) curve was drawn to evaluate the diagnostic value of CASC15 in NS. RAW264.7 cells were stimulated with LPS to simulate the inflammatory response in NS patients, and the regulation and mechanism of CASC15 on the inflammatory response were explored in this in vitro cell model. Serum CASC15 was upregulated in NS patients, and it had the ability to distinguish NS patients from NP patients. LPS stimulation increased the expression of CASC15 and simultaneously stimulated the secretion of inflammatory cytokines, while the knockdown of CASC15 alleviated the inflammatory response induced by LPS stimulation. Besides, serum miR-144-3p was reduced in NS patients, and luciferase reporter genes showed that miR-144-3p was a direct target of CASC15. Overexpression of CASC15 may promote the inflammatory response of NS by targeted regulating the expression of miR-144-3p, which may provide us with new insights in the treatment of NS.	34870560	RID08224	ceRNA or sponge	NA	UP(LIHC,PRAD);DATA(GSE117623,GSE104209)	
Ischemic stroke	SNHG15	SIRT1	positively-E	StarBase;TargetScan;luciferase reporter plasmid double-luciferase assay	upregulation	qPCR	NA	NA	oxidative stress(+)	ceRNA(miR-141)	regulation	NA	NA	CSC	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983019-44986961	ENSG00000096717	NA	285958	23411	C7orf40|FLJ38860|Linc-Myo1g|MYO1GUT	SIR2L1	LncRNA SNHG15 Promotes Oxidative Stress Damage to Regulate the Occurrence and Development of Cerebral Ischemia/Reperfusion Injury by Targeting the miR-141/SIRT1 Axis.Ischemic stroke is a kind of disease with high mortality and high disability, which brings a huge burden to the public health system (Hu et al. (2017)), and it poses a serious threat to the quality of life of patients. Cerebral ischemia/reperfusion injury is an important pathophysiological mechanism. This study aims to assess the mechanism of SNHG15 in the occurrence and development of cerebral ischemia/reperfusion injury of nerve cells and to investigate its potential value for diagnosis and treatment. SNHG15 targeted miRNA molecules and target genes were predicted with bioinformatics tools such as StarBase and TargetScan. The process of ischemic reperfusion in cerebral apoplexy in normal cultured and oxygen-glucose-deprived and reoxygenated neurons was simulated with RT-PCRand western blot technique. The expressions of SNHG15 and miR-141 were detected with qPCR, and the expressions of SIRT1 and p65, TNF- alpha , ROS, iNOS, and IL-6 were detected with western blot. Meanwhile, SNHG15 siRNAs and miR-141 mimics were transfected for SH-SY5Y, with western blot testing. And the expressions of miR-141, SIRT1, and p65, TNF- alpha , ROS, iNOS, and IL-6 were tested. According to the prediction with bioinformatics tools of StarBase and TargetScan, miR-141 is the target of lncSNHG15. In the luciferase reporter plasmid double-luciferase assay, miR-141 and SIRT1 were defined as the target relationship. In the oxygen-glucose-deprived reoxygenation model group, SNHG15 expression increased, miR-141 expression decreased, SIRT1 expression increased, and the expressions of p65, TNF- alpha , ROS, iNOS, and IL-6 decreased. In the SNHG15-siRNA-transfected oxygen-glucose-deprived reoxygenation cell model group, miR-141 expression increased, SIRT1 expression decreased, and the expressions of p65, TNF- alpha , and IL-6 increased compared with the si-NC group. In the miR-141-mimic-transfected oxygen-glucose-deprived reoxygenation cell model, SNHG15 expression decreased, SIRT1 expression decreased, and the expressions of p65, TNF- alpha , IL-1 beta , and IL-6 increased. In conclusion, SNHG15 expression increased during the process of oxygen-glucose-deprived reoxygenation, and the oxidative stress process was reduced by miR-141/SIRT1.	34868528	RID08225	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE86978)	DOWN(LIHC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Esophagus squamous cell carcinoma	DDX11	SNAI1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-30d-5p)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000013573	GRCh38_12:31073860-31104799	ENSG00000124216	NA	1663	6615	CHL1|ChlR1|KRG-2|WABS	SLUGH2|SNA|SNAH|SNAIL|SNAIL1	LncRNA DDX11 antisense RNA 1 promotes EMT process of esophageal squamous cell carcinoma by sponging miR-30d-5p to regulate SNAI1/ZEB2 expression and Wnt/beta-catenin pathway.LncRNA DDX11 antisense RNA 1 (DDX11-AS1) is recognized as having an imperative oncogenic role in different types of human cancer. Nevertheless, the functions, as well as the basic mechanisms of DDX11-AS1 in the EMT process of esophageal squamous cell carcinoma (ESCC), are yet to be clarified. In this research, high DDX11-AS1 expression was detected in ESCC cells as well as tissues and was linked to the poor prognosis of patients with ESCC. DDX11-AS1 promoted cell proliferation, migration, invasion ability and epithelial mesenchymal transition (EMT) process in vitro. Mechanistic analysis depicted that DDX11-AS1 may function as a ceRNA through sponging miR-30d-5p to upregulate the expression of SNAI1 and ZEB2. Meanwhile, overexpression of DDX11-AS1 might cause the activation of the Wnt/beta-catenin signaling pathway via targeting miR-30d-5p. On the whole, the findings of this research illustrate that DDX11-AS1 may act as an EMT-related lncRNA to advance ESCC progression through sponging miR-30d-5p to regulate SNAI1/ZEB2 expression and activate the Wnt/beta-catenin pathway, which indicates that it might serve as a probable therapeutic target for ESCC.	34866524	RID08226	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367)	UP(PAAD);DATA(GSE40174)
Esophagus squamous cell carcinoma	DDX11	ZEB2	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+);epithelial to mesenchymal transition(+)	ceRNA(miR-30d-5p)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000013573	GRCh38_12:31073860-31104799	ENSG00000169554	NA	1663	9839	CHL1|ChlR1|KRG-2|WABS	KIAA0569|SIP-1|SIP1|ZFHX1B	LncRNA DDX11 antisense RNA 1 promotes EMT process of esophageal squamous cell carcinoma by sponging miR-30d-5p to regulate SNAI1/ZEB2 expression and Wnt/beta-catenin pathway.LncRNA DDX11 antisense RNA 1 (DDX11-AS1) is recognized as having an imperative oncogenic role in different types of human cancer. Nevertheless, the functions, as well as the basic mechanisms of DDX11-AS1 in the EMT process of esophageal squamous cell carcinoma (ESCC), are yet to be clarified. In this research, high DDX11-AS1 expression was detected in ESCC cells as well as tissues and was linked to the poor prognosis of patients with ESCC. DDX11-AS1 promoted cell proliferation, migration, invasion ability and epithelial mesenchymal transition (EMT) process in vitro. Mechanistic analysis depicted that DDX11-AS1 may function as a ceRNA through sponging miR-30d-5p to upregulate the expression of SNAI1 and ZEB2. Meanwhile, overexpression of DDX11-AS1 might cause the activation of the Wnt/beta-catenin signaling pathway via targeting miR-30d-5p. On the whole, the findings of this research illustrate that DDX11-AS1 may act as an EMT-related lncRNA to advance ESCC progression through sponging miR-30d-5p to regulate SNAI1/ZEB3 expression and activate the Wnt/beta-catenin pathway, which indicates that it might serve as a probable therapeutic target for ESCC.	34866524	RID08227	ceRNA or sponge	prognosis	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367)	DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Triple-negative breast cancer	SAMMSON	TP53	NA	overexpression	upregulation		NA	NA	cell proliferation(+)	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000141510	NA	101927152	7157	LINC01212	LFS1|p53	Overexpression of IncRNA SAMMSON Promotes Triple-Negative Breast Cancer Cell Proliferation by Interacting with p53.This study was carried out to explore the role of the long noncoding RNA (lncRNA) SAMMSON in triple-negative breast cancer (TNBC). The research patients in this study included 68 TNBC patients. Cell Counting Kitcck-8 were utilized to determine cell proliferation abilities, respectively. Proteins and mRNAs were estimated by western blot and Methylation-specific polymerase chain reaction, respectively. We found that SAMMSON was upregulated, while p53 was downregulated in cancer (TNBC) tissues than in non-cancer tissues of TNBC patients. SAMMSON expression levels in TNBC tissues increased with the increase of clinical stages of TNBC patients. SAMMSON and p53 were inversely correlated in TNBC tissues. In TNBC cells, SAMMSON overexpression decreased p53 expression, while p53 overexpression failed to affect SAMMSON expression. In addition, SAMMSON overexpression increased TNBC cell proliferation, while p53 overexpression decreased the proliferation rates of TNBC cells. In addition, p53 overexpression attenuated the effects of SAMMSON overexpression. Therefore, overexpression of SAMMSON could promote TNBC cell proliferation by interacting with p53.	34936287	RID08228	interact with protein	NA	UP(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367,GSE86978)
Breast cancer	DLGAP1-AS1	WTAP	positively-E	starBase;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-299-3p)	regulation	NA	Adriamycin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000177337	GRCh38_18:3593732-3598363	ENSG00000146457	NA	649446	9589	FLJ35776|HsT914	KIAA0105|MGC3925|Mum2	N6-methyladenosine (m6A)-mediated lncRNA DLGAP1-AS1 enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop.Chemotherapy resistance is identified as an obstacle for breast cancer (BC) therapy, and, besides, increasing evidence indicates that long-noncoding RNAs (lncRNAs) participate in the regulation of BC adriamycin (ADR) resistance. Here, our work shows that lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) is up-regulated in ADR-resistant BC cells (MCF-7/ADR). Clinically, higher DLGAP1-AS1 expression was closely correlated to poorer clinical prognosis. Results showed that DLGAP1-AS1 promoted the ADR IC 50  and proliferation of ADR-resistant cells. Moreover, N 6 -methyladenosine (m 6 A) methyltransferase WT1 associated protein (WTAP) binds to the m 6 A modified site of DLGAP1-AS1 and motivates its stability. Mechanistically, DLGAP1-AS1 sponged miR-299-3p through 3'-untranslated region (3'-UTR) binding, which in turn relieved the repression of WTAP and thus upregulated WTAP expression. In conclusion, above findings conclude that lncRNA DLGAP1-AS1 promotes BC ADR-resistance through WTAP/DLGAP1-AS1/miR-299-3p feedback loop.	34866525	RID08229	ceRNA or sponge	chemoresistance,prognosis	DOWN(PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD,SKCM);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)
Prostate cancer	HAGLR	FOXM1	positively-E	starBase;miRanda;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-361-5p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000111206	NA	401022	2305	HOXD-AS1|Mdgt|MIR7704HG	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Exosomal long noncoding RNA HOXD-AS1 promotes prostate cancer metastasis via miR-361-5p/FOXM1 axis.Development of distant metastasis is the main cause of deaths in prostate cancer (PCa) patients. Understanding the mechanism of PCa metastasis is of utmost importance to improve its prognosis. The role of exosomal long noncoding RNA (lncRNA) has been reported not yet fully understood in the metastasis of PCa. Here, we discovered an exosomal lncRNA HOXD-AS1 is upregulated in castration resistant prostate cancer (CRPC) cell line derived exosomes and serum exosomes from metastatic PCa patients, which correlated with its tissue expression. Further investigation confirmed exosomal HOXD-AS1 promotes prostate cancer cell metastasis in vitro and in vivo by inducing metastasis associated phenotype. Mechanistically exosomal HOXD-AS1 was internalized directly by PCa cells, acting as competing endogenous RNA (ceRNA) to modulate the miR-361-5p/FOXM1 axis, therefore promoting PCa metastasis. In addition, we found that serum exosomal HOXD-AS1 was upregulated in metastatic PCa patients, especially those with high volume disease. And it is correlated closely with Gleason Score, distant and nodal metastasis, Prostatic specific antigen (PSA) recurrence free survival, and progression free survival (PFS). This sheds a new insight into the regulation of PCa distant metastasis by exosomal HOXD-AS1 mediated miR-361-5p/FOXM1 axis, and provided a promising liquid biopsy biomarker to guide the detection and treatment of metastatic PCa.	34864822	RID08230	ceRNA or sponge	metastasis,recurrence,prognosis	UP(LIHC,BRCA);DATA(GSE117623,GSE55807)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Age-related hearing loss	Gm44593	WNK1	positively-E	overexpression;dual-luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	oxidative stress(-)	ceRNA(miR-29b)	regulation	NA	NA	NA	NA	Nervous system disease	Inner ear disease	lncRNA	PCG	NA	NA	ENSG00000060237	NA	NA	65125	NA	HSAN2|HSN2|PPP1R167|PRKWNK1	Long noncoding RNA Gm44593 attenuates oxidative stress from age-related hearing loss by regulating miR-29b/WNK1.Long noncoding RNA has been reported to play important role in various disease. However, the function of lncRNA in age-related hearing loss still unclear. The aim of our study is to investigate the function and mechanism of lncRNA Gm44593 in AHL. ATP content, JC-1 assay, mitochondrial content, cell death rates and dual-luciferase reporter assay were performed to assess the function of lncRNA Gm44593 in HEI-OC1 cells. The expression of lncRNA Gm44593 was significantly upregulated upon H 2 O 2  and starvation treatment. Overexpression of lncRNA Gm44593 manifestly reduced the cell death rates. The ATP content, mtDNA content and mitochondrial membrane potential were alleviated upon overexpression of lncRNA Gm44593. We also proved that miR-29b is the direct target of lncRNA Gm44593. Overexpression of miR-29b completely restored the effect induced by lncRNA Gm44593. In addition, we provided evidences that WNK1 is the direct target of miR-29b. Our research uncovers a potential role of lncRNA Gm44593 in age-related hearing loss. We provide new insights into potential therapeutic targets for the amelioration of age-related hearing loss.	34967279	RID08231	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Polycystic ovary syndrome	TINCR	TNF	positively-E	dual-luciferase activity assay;overexpression;IntaRNA2.0	upregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-19a)	regulation	NA	NA	NA	NA	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000228978	NA	257000	7124	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA placenta<U+2011>specific protein 2 regulates micorRNA-19a/tumor necrosis factor alpha to participate in polycystic ovary syndrome.Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5-20% of females at their reproductive age worldwide. MicorRNA-19a (miR-19a) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor alpha (TNF-alpha), which plays critical roles in PCOS. Our preliminary analysis predicted the potential interaction between miR-19a and long non-coding RNA (lncRNA) placenta<U+2011>specific protein 2 (PLAC2). Therefore, this study aimed to explore the role of PLAC2 in PCOS. Ovarian tissues were collected from 62 PCOS patients and 62 healthy females. Granulosa-like tumor cells (KGN) was prepared, and transient transfections was conducted. Dual-luciferase activity assay was used to investigate the interaction between PLAC2 and miR-19a. qPCR assays were performed for the expression analysis of miR-19a/TNF-alpha. In addition, western blotand cell apoptosis assay were conducted. The results showed that PLAC2 was upregulated in PCOS. PLAC2 and miR-19a showed a direct interaction, while overexpression of PLAC2 and miR-19a did not affect the expression of each other in KGN cells. Instead, overexpression of PLAC2 led to upregulated TNF-alpha, which is a target of miR-19a. Cell apoptosis analysis showed that PLAC2 and TNF-alpha promoted the apoptosis of KGN cells. Overexpression of miR-19a played an opposite role. In addition, the overexpression of PLAC2 reduced the effects of overexpression of miR-19a. Therefore, PLAC2 may regulate miR-19a/TNF-alpha to participate in PCOS.	34967266	RID08232	ceRNA or sponge	NA	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE55807)	DOWN(LIHC);DATA(GSE117623)
Dry eye syndrome	GABARAPL2	TNF	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000034713	GRCh38_16:75566375-75577881	ENSG00000228978	NA	11345	7124	ATG8|ATG8C|GATE-16|GATE16|GEF-2|GEF2	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08233	expression association	NA	UP(PAAD,PRAD,BRCA);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE75367)	DOWN(LIHC);DATA(GSE117623)
Dry eye syndrome	GABARAPL2	IL-1	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000034713	GRCh38_16:75566375-75577881	NA	NA	11345	NA	ATG8|ATG8C|GATE-16|GATE16|GEF-2|GEF2	NA	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08234	expression association	NA	UP(PAAD,PRAD,BRCA);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE75367)	
Dry eye syndrome	GABARAPL2	IL6	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000034713	GRCh38_16:75566375-75577881	ENSG00000136244	NA	11345	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08235	expression association	NA	UP(PAAD,PRAD,BRCA);DOWN(BRCA);DATA(GSE40174,GSE104209,GSE111842,GSE75367)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Dry eye syndrome	CHRNB2	TNF	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000160716	GRCh38_1:154567778-154580013	ENSG00000228978	NA	1141	7124	EFNL3|nAChRB2	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08236	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(LIHC);DATA(GSE117623)
Dry eye syndrome	CHRNB2	IL-1	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000160716	GRCh38_1:154567778-154580013	NA	NA	1141	NA	EFNL3|nAChRB2	NA	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08237	expression association	NA	UP(PAAD);DATA(GSE40174)	
Dry eye syndrome	CHRNB2	IL6	positively-E	siRNA	upregulation	RT-qPCR	GSE186450	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	NA	Nervous system disease	Eye disease	lncRNA	PCG	ENSG00000160716	GRCh38_1:154567778-154580013	ENSG00000136244	NA	1141	3569	NA	BSF2|HGF|HSF|IFNB2|IL-6	The two candidate lncRNAs were designed to produce three siRNAs (Gabarapl2: si-Gabarapl2-1, si-Gabarapl2-2, si-Gabarapl2-3) and two siRNAs (Chrnb2: si-Chrnb2-1, si-Chrnb2-2) according to primer sequence, respectively. The culture supernatant was collected for monitoring the inflammatory cytokines. As shown in Figures 5C, the expression levels of TNF-alpha, IL-1beta, and IL-6 were significantly reduced in HCECs after transfection with si-Gabarapl2-2/si-Gabarapl2-3  in HCECs. The above results suggested that Gabarapl2 and Chrnb2 silence significantly repressed TNF-alpha, IL-1beta, and IL-6.	34957168	RID08238	expression association	NA	UP(PAAD);DATA(GSE40174)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Endometrial cancer	LINC00958	PHF6	positively-E	dual-luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-3174)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000156531	NA	100506305	84295	NA	BFLS|BORJ|CENP-31|KIAA1823|MGC14797	LINC00958/miR-3174/PHF6 axis is responsible for triggering proliferation, migration and invasion of endometrial cancer.To reveal the role of LINC00958 in the progression of endometrial cancer (EC) and the underlying molecular mechanism. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR was conducted to detect relative level of LINC00958 in EC specimens and cell lines. Its prognostic potential in EC was analyzed by Kaplan-Meier method. After knockdown of LINC00958, cell proliferative, migratory and invasive abilities in KLE and Ishikawa cells were evaluated by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay. dual-luciferase reporter assay was carried out to identify the LINC00958/miR-3174/PHF6 axis, and their expression interaction was determined by Pearson correlation test. The role of miR-3174 in influencing LINC00958-induced phenotype changes of EC cells was determined through rescue experiments. LINC00958 was abnormally upregulated in EC specimens and cell lines, which was unfavorable to the prognosis of EC. Knockdown of LINC00958 reduced proliferative, migratory and invasive rates in KLE and Ishikawa cells. MiR-3174 shared a binding site in the 3'-untranslated region (3'-UTR) to that of LINC00958, which was lowly expressed in EC specimens and negatively linked to LINC00958 level. Overexpression of miR-3174 partially abolished the role of LINC00958 in accelerating the malignant phenotypes of EC cells. PHF6 was the downstream target of miR-3174 and it was upregulated in EC specimens. LINC00958 is upregulated in EC specimens, which is a prognostic factor of EC. It stimulates EC to proliferate, migrate and invade through the miR-3174/PHF6 axis.	34859848	RID08239	ceRNA or sponge	prognosis	UP(LIHC);DATA(GSE117623)	UP(LIHC,PAAD,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE51827,GSE75367,GSE86978)
Breast cancer	GAS5	APOBEC3C	positively-E		downregulation	RT-PCR	NA	NA	immune response(+);tumorigenesis(+)	ceRNA(miR-103)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000244509	NA	60674	27350	NCRNA00030|SNHG2	A3C|APOBEC1L|ARDC2|ARDC4|ARP5|PBI|bK150C2.3	Expression patterns of LncRNA-GAS5 and its target APOBEC3C gene through miR-103 in breast cancer patients.Early diagnosis of breast cancer can increase the survivability of the patients and the patient's quality of life. There is growing evidence demonstrating the active role of LncRNA-GAS5 and miR-103 in cancer biology. APOBEC enzymes are important players in immunity and may contribute to carcinogenesis. Mutation and expression alteration in the APOBEC gene family was found to have a strong correlation with breast cancer risk. This study aimed to evaluate the expression level of lncRNA-GAS5 and its target APOBEC3C in women with breast cancer through expression evaluation of miR-103. Moreover, the interaction between lncRNA-GAS5 and miR-103 was studied. In the present study, forty paired tumor and normal samples classified based on breast cancer subtypes and clinical features of patients were analyzed using gene expression studies. Immunohistochemical analysis of the gene products was performed to classify tumors. The RNA samples were extracted from breast tissue. Real-time PCR was conducted for APOBEC3C and Lnc-RNA GAS5 expression. In addition, miR-103a miScript Primer Assay was utilized for the expression of miR-103-5p. It was revealed that the expression level of APOBEC3C and lncRNA-GAS5 were significantly down-regulated; however, the miRNA-103 expression level was significantly up-regulated. GAS5 expression was positively correlated with APOBEC3C expression and negatively correlated with miR-103 expression. In conclusion, we observed down-regulation of APOBEC3C and LncRNA-GAS5 and up-regulation of miRNA 103 in breast cancer patients. The expression of GAS5 may provide a new potential treatment target for breast cancer. To clarify the role of these molecules in the cellular signaling pathways, further studies are required.	34933738	RID08240	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(LIHC);DOWN(PAAD,BRCA);DATA(GSE117623,GSE60407,GSE111842,GSE111065,GSE51827,GSE55807)
Multiple myeloma	HOTAIR	miR-23b-3p	negatively-E	siRNA	upregulation		NA	NA	MAPK signaling pathway(+);PI3K/AKT/mTOR signaling pathway(+);p53 signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Myeloma cells regulate miRNA transfer from fibroblast-derived exosomes by expression of lncRNAs. MM cells express HOTAIR, TOB1-AS1, and MALAT1 lncRNAs. Transient transfection of MM cells with lnc-siRNAs demonstrates that HOTAIR, TOB1-AS1, and MALAT1 lncRNAs are sponges for miR-23b-3p, miR-27b-3p, and miR-125b-5p. Indeed, lncRNA knockdown significantly increased miR levels in U266 MM cells co-cultured with MM FB-EXOs. Selective miR-214-3p and miR-5100 overexpression modulates MAPK, PI3K/AKT/mTOR, and p53 pathways in MM cells.	34919276	RID08241	ceRNA or sponge	NA		
Multiple myeloma	TOB1-AS1	miR-27b-3p	negatively-E	siRNA	upregulation		NA	NA	MAPK signaling pathway(+);PI3K/AKT/mTOR signaling pathway(+);p53 signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000229980	GRCh38_17:50866679-50910774	NA	NA	400604	NA	NA	NA	Myeloma cells regulate miRNA transfer from fibroblast-derived exosomes by expression of lncRNAs. MM cells express HOTAIR, TOB1-AS1, and MALAT1 lncRNAs. Transient transfection of MM cells with lnc-siRNAs demonstrates that HOTAIR, TOB1-AS1, and MALAT1 lncRNAs are sponges for miR-23b-3p, miR-27b-3p, and miR-125b-5p. Indeed, lncRNA knockdown significantly increased miR levels in U266 MM cells co-cultured with MM FB-EXOs. Selective miR-214-3p and miR-5100 overexpression modulates MAPK, PI3K/AKT/mTOR, and p53 pathways in MM cells.	34919276	RID08242	ceRNA or sponge	NA		
Multiple myeloma	MALAT1	miR-125b-5p	negatively-E	siRNA	upregulation		NA	NA	MAPK signaling pathway(+);PI3K/AKT/mTOR signaling pathway(+);p53 signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Myeloma cells regulate miRNA transfer from fibroblast-derived exosomes by expression of lncRNAs. MM cells express HOTAIR, TOB1-AS1, and MALAT1 lncRNAs. Transient transfection of MM cells with lnc-siRNAs demonstrates that HOTAIR, TOB1-AS1, and MALAT1 lncRNAs are sponges for miR-23b-3p, miR-27b-3p, and miR-125b-5p. Indeed, lncRNA knockdown significantly increased miR levels in U266 MM cells co-cultured with MM FB-EXOs. Selective miR-214-3p and miR-5100 overexpression modulates MAPK, PI3K/AKT/mTOR, and p53 pathways in MM cells.	34919276	RID08243	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Rheumatoid arthritis	LINC01139	MIR1262	negatively-E	miRBase;miRDB;luciferase reporter assay	upregulation	microarray	NA	NA	cell invasion(+)	sponge	binding/interaction	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000221203	NA	339535	100302279	LINK-A|LINKA	MIRN1262|hsa-mir-1262|mir-1262	Increased long noncoding RNA LINK-A contributes to rheumatoid synovial inflammation and aggression.Fibroblast-like synoviocytes (FLSs) play a key role in controlling synovial inflammation and joint destruction in rheumatoid arthritis (RA). The contribution of long noncoding RNAs (lncRNAs) to RA is largely unknown. Here, we show that the lncRNA LINK-A, located mainly in cytoplasm, has higher-than-normal expression in synovial tissues and FLSs from patients with RA. Synovial LINK-A expression was positively correlated with the severity of synovitis in patients with RA. LINK-A knockdown decreased migration, invasion, and expression and secretion of matrix metalloproteinases and proinflammatory cytokines in RA FLSs. Mechanistically, LINK-A controlled RA FLS inflammation and invasion through regulation of tyrosine protein kinase 6-mediated and leucine-rich repeat kinase 2-mediated HIF-1alpha. On the other hand, we also demonstrate that LINK-A could bind with microRNA 1262 as a sponge to control RA FLS aggression but not inflammation. Our findings suggest that increased level of LINK-A may contribute to FLS-mediated rheumatoid synovial inflammation and aggression. LINK-A might be a potential therapeutic target for RA.	34877935	RID08244	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	
Osteoarthritis	HOTAIR	BBC3	positively-E	starBase v2.0;TargetScan;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-221)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105327	NA	100124700	27113	HOXC-AS4|HOXC11-AS1|NCRNA00072	JFY1|PUMA	Long non-coding RNA HOTAIR increased mechanical stimulation-induced apoptosis by regulating microRNA-221/BBC3 axis in C28/I2 cells.Abnormal mechanical stimulation contributes to articular cartilage degeneration and osteoarthritis (OA) development. Many long noncoding RNAs (lncRNAs) are involved in mechanical force-induced cartilage degeneration. LncRNA HOTAIR (HOTAIR) has been demonstrated to increase osteoarthritis progression. However, the roles of HOTAIR in mechanical stimulation-treated chondrocytes are still unclear. In this study, we found that mechanical stimulation significantly induced apoptosis in C28/I2 cells. In addition, the expression of HOTAIR was up regulated and the expression of miR-221 was down regulated. Knockdown of HOTAIR effectively ameliorated cell apoptosis induced by mechanical stimulation. HOTAIR could interact with miR-221, which targeted to degrade BBC3. Overexpression of BBC3 could reverse the decreased apoptotic rates induced by HOTAIR knockdown. Collectively, HOTAIR promoted mechanical stimulation-induced apoptosis by regulating the miR-221/BBC3 axis in C28/I2 cells.	34874225	RID08245	ceRNA or sponge	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)
Non-small cell lung cancer	SNHG1	UBE2C	positively-E	qRT-PCRual-Luciferase Assay	upregulation	qRT-PCR	NA	NA	prognosis;chemosensitivity(+);cell invasion(+)	ceRNA(miR-140-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851978-62855953	ENSG00000175063	NA	23642	11065	LINC00057|lncRNA16|NCRNA00057|UHG	UBCH10	Growing evidence has demonstrated that UBE2C plays a critical role in cancer progression, but there is no study focusing on the prognosis, upstream regulation mechanism, and immunological roles of UBE2C across diverse tumor types. In this study, we found that UBE2C was elevated in this human pan-cancer analysis, and high expression of UBE2C was correlated with poor prognosis. In addition, UBE2C expression was markedly associated with tumor mutation burden (TMB), microsatellite instability (MSI), immune cell infiltration, and diverse drug sensitivities. Finally, we showed that the METTL3/SNHG1/miRNA-140-3p axis could potentially regulate UBE2C expression. N(6)-Methyladenosine (m6A) modifications improved the stability of methylated SNHG1 transcripts by decreasing the rate of RNA degradation, which lead to upregulation of SNHG1 in non-small cell lung cancer (NSCLC).  In vitro  functional experiments showed that SNHG1, as a competing endogenous RNA, sponges miR-140-3p to increase UBE2C expression in NSCLC cell lines. Our study elucidates the clinical importance and regulatory mechanism of the METTL3/SNHG1/miRNA-140-3p/UBE2C axis in NSCLC and provides a prognostic indicator, as well as a promising therapeutic target for patients with NSCLC.	34858987	RID08246	ceRNA or sponge	prognosis,chemoresistance	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	UP(LIHC,PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE55807)
Liver cancer	BACE1-AS	BACE1	positively-F	qRT-PCR	upregulation	qRT-PCR	NA	NA	NA	NA	binding/interaction	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000278768	GRCh38_11:117288453-117293578	ENSG00000186318	NA	100379571	23621	BACE1-AS1|BACE1AS|FJ573250|NCRNA00177	BACE	Cao et al. found that the lncRNA MM2P modulates M2 macrophage polarization and weakens M2-mediated neovascularization [11]. BACE1-AS is transcribed from the opposite strand of beta-secretase 1 (BACE1) and can pair with BACE1 mRNA to change its spatial structure and increase its stability to promote protein translation in a positive feed-forward fashion [12, 13]. In other words, BACE1 and BACE1-AS can coregulate biological activities and processes and functionally interact with each other. BACE1 is a protease belonging to the beta-secretase family and is thought to play an important role in Alzheimer's disease via the processing of amyloid precursor protein (APP) in neurotoxic Abeta peptides. Recently, BACE1 has been reported to be abnormally expressed in a variety of tumors and is associated with poor prognosis in colon cancer, non-small-cell lung cancer, invasive ductal carcinoma of the breast, glioblastoma, and gastric cancer [14'-8].	34926701	RID08247	expression association	prognosis	DOWN(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(PRAD,PAAD,BRCA);DATA(GSE104209,GSE60407,GSE51827)
Colon adenocarcinoma	IFNG-AS1	miR-627-3p	negatively-E	RT-qPCR	upregulation	RT-qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000255733	GRCh38_12:67989445-68234686	NA	NA	100885789	NA	LincR-Ifng-3'AS|NEST|Tmevpg1	NA	Significance of long non-coding RNA IFNG-AS1 in the progression and clinical prognosis in colon adenocarcinoma.Colon adenocarcinoma originates from adenoma and triggers serious healthy burdensome. lncRNAs develop a crucial role in the progression of colorectal carcinoma. In this study, we aimed to investigate the clinical value and potential role of lncRNA interferon (IFN) gamma antisense RNA 1 (IFNG-AS1) in colon adenocarcinoma. This study enrolled 95 colorectal adenoma patients, 128 colorectal adenocarcinoma patients, and 88 healthy individuals. The serum, tissue IFNG-AS1 expression levels were explored by real-time quantitative reverse transcription-PCR (RT-qPCR) assay. The receiver operator characteristic curve and Kaplan-Meier method were used to assess the clinical significance of IFNG-AS1. The chi-square test was used to analyze the association between tissue IFNG-AS1 and clinical characteristics. Functional experiments were conducted to delve into the effects of IFNG-AS1 on cellular activities (cell viability/migration/invasion). The target miRNA of IFNG-AS1 was also explored. IFNG-AS1 expression in both serum and tissue samples was elevated in patients. Serum IFNG-AS1 could diagnose colon adenoma and adenocarcinoma patients from the healthy control. High tissue IFNG-AS1 was correlated with several clinical characteristics and a shorter overall survival time. Silence of IFNG-AS1 could be available for repressing cellular capacities via the sponge to miR-627-3p. IFNG-AS1 was rised in colon adenocarcinoma and it was relevant to tumor size, TNM stage, and poor prognosis of patients. Beyond that, downregulated expression of IFNG-AS1 may repress malignant progression of colon adenocarcinoma by regulating miR-627-3p. IFNG-AS1 might be a potential diagnosis or prognosis predictor for colon adenocarcinoma patients.	34872454	RID08248	ceRNA or sponge	prognosis	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	
Colorectal cancer	DCST1-AS1	hsa-miR-582-5p	positively-F	DIANA Tools;TargetScan database;dual-luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);colony formation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000232093	GRCh38_1:155045191-155046118	NA	NA	100505666	NA	NA	NA	Long non-coding RNAs (lncRNAs) are related to the initiation and progression of tumor and regulate various cellular processes including growth, invasion, migration, and apoptosis. Understanding the roles and mechanisms of lncRNAs in regulating cancer progression is crucial for formulating novel therapeutic strategies. Although lncRNA DCST1-antisense RNA 1(AS1) has been implicated in several cancers, its role in the progression of colorectal cancer (CRC) remains to be explored. This study focuses on elucidating the function of lncRNA DCST1-AS1 in CRC development and its underlying mechanism. We found that the expression of lncRNA DCST1-AS1 was up-regulated in CRC tissues and cell lines, and CRC patients with high lncRNA DCST1-AS1 expression were associated with a poor prognosis. Loss-of-function and gain-of-function experiment in CRC cell lines confirmed that lncRNA DCST1-AS1 promoted the malignant phenotype of CRC cells, including cell proliferation, colony formation, migration, and invasion. In addition, we identified the binding sites between lncRNA DCST1-AS1 and hsa-miR-582-5p, and between hsa-miR-582-5p and High Mobility Group Box 1 (HMGB1) through DIANA Tools and TargetScan database, which was further confirmed by dual-luciferase reporter assay. Functional assay further confirmed the crucial role of lncRNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis in modulating the malignant phenotype of CRC cells. Collectively, our data suggest that lncRNA DCST1-AS1 regulates the aggressiveness of CRC cells through hsa-miR-582-5p/HMGB1 axis. Our study provides novel insight into the mechanism of lncRNA DCST1-AS1 in CRC cells for targeted therapy.	34967274	RID08249	expression association	prognosis	UP(BRCA);DATA(GSE55807)	
Covid-19	MYC	MALAT1	positively-E	ChIPBase database;Statistical Analysis	upregulation	RT-qPCR	GSE147507;GSE150392;GSE152075	NA	cell proliferation(+);	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Disease by infectious agent	Covid-19	TF	lncRNA	ENSG00000136997	NA	ENSG00000251562	GRCh38_11:65497688-65506516	4609	378938	bHLHe39|c-Myc|MYCC	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	Altered expression of protein coding gene (PCG) and long non-coding RNA (lncRNA) have been identified in SARS-CoV-2 infected cells and tissues from COVID-19 patients. The functional role and mechanism (s) of transcriptional regulation of deregulated genes in COVID-19 remain largely unknown. In the present communication, reanalyzing publicly available gene expression data, we observed that 66 lncRNA and 5491 PCG were deregulated in more than one experimental condition. Combining our earlier published results and using different publicly available resources, it was observed that 72 deregulated lncRNA interacted with 3228 genes/proteins. Many targets of deregulated lncRNA could also interact with SARS-CoV-2 coded proteins, modulated by IFN treatment and identified in CRISPR screening to modulate SARS-CoV-2 infection. The majority of the deregulated lncRNA and PCG were targets of at least one of the transcription factors (TFs), interferon responsive factors (IRFs), signal transducer, and activator of transcription (STATs), NFkB, MYC, and RELA/p65. Deregulated 1069 PCG was joint targets of lncRNA and TF. These joint targets are significantly enriched with pathways relevant for SARS-CoV-2 infection indicating that joint regulation of PCG could be one of the mechanisms for deregulation. Over all this manuscript showed possible involvement of lncRNA and mechanisms of deregulation of PCG in the pathogenesis of COVID-19.	34940755	RID08250	expression association	NA	DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)
Hepatocellular carcinoma	LINC00160	PIK3R3	negatively-E	qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell migration(-);cell invasion(-);apoptosis process(-);chemoresistance(-)	ceRNA(miR-132)	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230978	GRCh38_21:34723807-34737204	ENSG00000117461	NA	54064	8503	C21orf52|NCRNA00160	p55	Altered expression of protein coding gene (PCG) and long non-coding RNA (lncRNA) have been identified in SARS-CoV-2 infected cells and tissues from COVID-19 patients. The functional role and mechanism (s) of transcriptional regulation of deregulated genes in COVID-19 remain largely unknown. In the present communication, reanalyzing publicly available gene expression data, we observed that 66 lncRNA and 5491 PCG were deregulated in more than one experimental condition. Combining our earlier published results and using different publicly available resources, it was observed that 72 deregulated lncRNA interacted with 3228 genes/proteins. Many targets of deregulated lncRNA could also interact with SARS-CoV-2 coded proteins, modulated by IFN treatment and identified in CRISPR screening to modulate SARS-CoV-2 infection. The majority of the deregulated lncRNA and PCG were targets of at least one of the transcription factors (TFs), interferon responsive factors (IRFs), signal transducer, and activator of transcription (STATs), NFkB, MYC, and RELA/p65. Deregulated 1069 PCG was joint targets of lncRNA and TF. These joint targets are significantly enriched with pathways relevant for SARS-CoV-2 infection indicating that joint regulation of PCG could be one of the mechanisms for deregulation. Over all this manuscript showed possible involvement of lncRNA and mechanisms of deregulation of PCG in the pathogenesis of COVID-19.	34907642	RID08251	ceRNA or sponge	chemoresistance		UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
Hepatocellular carcinoma	MCM3AP-AS1	FOXA1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	ceRNA(miR-194)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000215424	GRCh38_21:46229196-46259390	ENSG00000129514	NA	114044	3169	C21orf85|FLJ10508|MCM3AP-AS|MCM3APAS|NCRNA00031	HNF3A	LncRNA MCM3AP-AS1/miR-194/mRNA FOXA1 FORKHEAD box A1 (FOXA1) is a transcription factor, belonging to the forkhead box gene superfamily, that plays a crucial role in chromatin binding of transcription factors and is involved in the development of endoderm-derived organs including pancreas, lung, liver and prostate. 71 , 72 FOXA1 has been found to be able to bind to the promoters of more than one hundred genes correlated with the regulation of cell signalling and cell cycle. 73 A range of evidence has demonstrated that FOXA1 contributes to the development and progression of diverse types of malignancies including glioma, breast, stomach, lung, ovarian and oesophageal cancers. The function of this transcription factor might change based on the specific type of cancer. 74 , 75 , 76 , 77 FOXA1 plays a growth inhibitory role, and its expression is correlated with markers of differentiation in prostate cancer. 73 Also, it can act as a tumour suppressor in different types of cancer including breast, endometrium, bladder, liver and pancreas tumours. 72 Similarly, MCM3AP-AS1 is a lncRNA shown to be involved in various types of cancer. In line with this, MCM3AP-AS1/miR-211/KLF5/AGGF1 axis has been found to regulate angiogenesis in glioblastoma. Also, the overexpression of MCM3AP-AS1 can promote lung cancer progression via regulating miR-340-5p/KPNA4 axis. 78 , 79 , 80 The expression, clinical significance, functional role and underlying mechanism of MCM3AP-AS1 have also been investigated in HCC. This lncRNA is up-regulated in HCC, and its expression level is directly related to the tumour size as well as correlated with advanced tumour stage and poor prognosis of HCC patients. MCM3AP-AS1 silencing has been shown to significantly up-regulate miR-194-5p expression in HCC cells. In fact, MCM3AP-AS1 acts as a molecular sponge for miR-194-5p by directly binding to complementary sequences, leading to increased expression of FOXA1 as a target of miR-194-5p in HCC cells. Interestingly, FOXA1 restoration is able to rescue MCM3AP-AS1 knockdown-induced proliferation inhibition, G1 arrest and apoptosis in HCC cells. These findings support a link between lncRNA MCM3AP-AS1 and miR-194-5p/FOXA1 as well as provide evidence for the potential use of MCM3AP-AS1 as a prognostic biomarker and therapeutic target in HCC. 81	34907642	RID08252	ceRNA or sponge	prognosis	DOWN(PRAD,BRCA);DATA(GSE104209,GSE67939)	UP(BRCA);DATA(GSE109761,GSE111065,GSE55807,GSE75367)
Hepatocellular carcinoma	MALAT1	miR-140-5p	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	NA	Sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	LncRNA MALAT1/miR-140/mRNA Aurora-A Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a lncRNA with known pathogenic roles. The dysregulated expression of this lncRNA has been found to be correlated with clinical parameters and prognosis in several types of human cancers including HCC. 82 A recent finding has revealed that MALAT1 is involved in temozolomide-related chemoresistance in glioblastoma through inducing miR-101 expression and regulating autophagy-associated chemoresistance in gastric cancer via miR-23b-3p sequestration. 83 , 84 , 85 Currently, sorafenib resistance is recognized as one of the primary obstacles of a successful chemotherapy in metastatic liver cancer. Aurora-A is known as a tumour-promoting molecule in HCC. It has been revealed that this lncRNA is involved in promoting sorafenib resistance in HCC cells and up-regulated MALAT1 expression is strongly associated with down-regulated miR-140-5p expression, increased Aurora-A expression and poor outcomes in HCC patients. Additionally, MALAT1 is able to sponge miR-140-5p. Knockdown of MALAT1 in sorafenib-resistant HCC cells has been shown to increase sensitivity to sorafenib treatment both in vitro and in vivo. 86 These observations highlight the important role of MALAT1/miR-140-5p/Aurora-A axis in sorafenib resistance and reinforce the notion that MALAT1 can be a prominent therapeutic target to overcome sorafenib resistance in HCC tumours. 87	34907642	RID08253	ceRNA or sponge	metastasis,chemoresistance,prognosis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Hepatocellular carcinoma	AK002107	TGFBR1	positively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);colony formation(+);cell invasion(+)	ceRNA(miR-140)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	NA	ENSG00000106799	NA	NA	7046	NA	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	lncRNA AK002107/miR-140/mRNA TGFBR1 MiR-140-5p is a miRNA with dual roles. This miRNA has been shown to suppress the growth and metastasis of HCC cells by inhibiting TGFBR1 and FGF9 expression. TGFBR1 has been recognized as a promoter of cancer cell growth by inducing epithelial-mesenchymal transition (EMT). The lncRNA AK002107 is involved in regulating TGFBR1 through the modulation of miR-140-5p, leading to EMT in HCC. The silencing of this lncRNA inhibits HCC cell proliferation, colony formation and invasion. Consistent with these findings, the expression of AK002107 has been indicated to be up-regulated in HCC compared with corresponding non-cancerous tissues. The investigation of protein and RNA levels of TGFBR1 following AK002107 knockdown and miR-140-5p inhibition confirmed that these two regulatory RNA molecules co-ordinately regulate TGFBR1/EMT pathway in HCC cell lines. It has been found that silencing of AK002107 reduces TGFBR1 expression and vimentin levels and increases E-cadherin levels, resulting in EMT suppression. To sum up, AK002107 is markedly up-regulated in HCC, competitively inhibits miR-140-5p and subsequently increases the expression of TGFBR1. These events finally promote the proliferation, colony formation and invasion of HCC cells. AK002107/miR-140-5p/TGFBR1/EMT pathway plays a critical role in tumorigenesis of HCC and offers potential use as a target for the development of novel diagnostic and therapeutic approaches against HCC. 87	34907642	RID08254	ceRNA or sponge	metastasis		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Hepatocellular carcinoma	CASC2	miR-24	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	NA	TRAIL	CSC	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	LncRNA CASC2/miR-24, miR-221/mRNA TRAIL TNF-related apoptosis-inducing ligand (TRAIL), as a member of TNF superfamily, can induce apoptosis in a variety of cancers including prostate, skin, thyroid, colon, kidney, pancreas, central nervous system, breast and haematological malignancies. 63 TRAIL exerts its cellular effects through interaction with death receptors and the formation of downstream death-inducing signalling complexes, leading to apoptosis-causing activation of apical caspase-3 and caspase-8. It has been revealed that TRAIL resistance of HCC is associated with ncRNA regulation. miR-24 and miR-221 regulate the expression of caspase-3 and caspase-8, thereby affecting TRAIL resistance. 88 The novel lncRNA susceptibility candidate 2 (CASC2) has been known to play roles in various human malignancies such as glioma and endometrial cancer. 89 Based on the recent studies, CASC2 functions as a tumour-suppressive lncRNA through a variety of mechanisms, for instance, sequestration of oncogenic miRNAs and repression of Wnt/beta-catenin signalling. 90 CASC2 is also able to enhance the TRAIL resistance of HCC via regulating caspase-3 and caspase-8 expression by acting as a sponge for miR-24 and miR-221. These data lead us to the conclusion that CASC2 might contribute to enhancing TRAIL resistance in HCC and consequently promoting the treatment efficacy of TRAIL-based therapies	34907642	RID08255	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	
Hepatocellular carcinoma	CASC2	MIR221	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	NA	TRAIL	CSC	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000207870	NA	255082	407006	C10orf5	MIRN221|miRNA221|mir-221	LncRNA CASC2/miR-24, miR-221/mRNA TRAIL TNF-related apoptosis-inducing ligand (TRAIL), as a member of TNF superfamily, can induce apoptosis in a variety of cancers including prostate, skin, thyroid, colon, kidney, pancreas, central nervous system, breast and haematological malignancies. 63 TRAIL exerts its cellular effects through interaction with death receptors and the formation of downstream death-inducing signalling complexes, leading to apoptosis-causing activation of apical caspase-3 and caspase-8. It has been revealed that TRAIL resistance of HCC is associated with ncRNA regulation. miR-24 and miR-221 regulate the expression of caspase-3 and caspase-8, thereby affecting TRAIL resistance. 88 The novel lncRNA susceptibility candidate 2 (CASC2) has been known to play roles in various human malignancies such as glioma and endometrial cancer. 89 Based on the recent studies, CASC2 functions as a tumour-suppressive lncRNA through a variety of mechanisms, for instance, sequestration of oncogenic miRNAs and repression of Wnt/beta-catenin signalling. 90 CASC2 is also able to enhance the TRAIL resistance of HCC via regulating caspase-3 and caspase-8 expression by acting as a sponge for miR-24 and miR-221. These data lead us to the conclusion that CASC2 might contribute to enhancing TRAIL resistance in HCC and consequently promoting the treatment efficacy of TRAIL-based therapies	34907642	RID08256	ceRNA or sponge	chemoresistance	UP(LIHC);DATA(GSE117623)	
Gastric cancer	NORAD	MIR496	negatively-E	RT-PCR;dual-luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);epithelial to mesenchymal transition(-);apoptosis process(-)	interact with mRNA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000207961	NA	647979	574454	LINC00657	MIRN496|hsa-mir-496|mir-496	The long noncoding RNA noncoding RNA activated by DNA damage (NORAD)-microRNA-496-Interleukin-33 axis affects carcinoma-associated fibroblasts-mediated gastric cancer development.Carcinoma-associated fibroblasts (CAFs) are one of the crucial parts of in the tumor microenvironment and contribute to tumor progression. Interleukin-33 (IL-33), a tissue-derived nuclear cytokine from the IL-1 family, has been found abnormally expressed in tumor cells and Fibroblast. However, the role and mechanism of IL-33 in the interaction between gastric cancer (GC) cells and CAFs need investigation. Presently, we inquire into the function of lncRNA NORAD-miR-496 axis-mediated IL-33 in modulating the GC-CAFs interaction. Real-time reverse transcription-polymerase chain reaction (RT-PCR was adopted to gauge the expression of NORAD, miR-496, and IL-33 in GC tissues and cells, and gain- or loss-of-function assays were conducted to investigate the role of them in GC. A GC cell-CAFs co-culture model was established to explore the interaction between CAFs and GCs. As exhibited, NORAD was up-regulated in GC tissues and cells, while miR-496 was remarkably down-regulated. Overexpressing NORAD substantially promoted the proliferation, migration, invasion, and EMT of GC cells and repressed cell death, while overexpressing miR-496 had the opposite effects. Additionally, NORAD enhanced the IL-33 expression and the release of IL-33 from GC cells. The dual-luciferase reporter assay confirmed that miR-496 was a target of NORAD and targeted IL-33. CAFs aggravated the malignant behaviors of GC cells as indicated by both experiments. However, NORAD knockdown in CAFs reversed CAFs-mediated promotive effects on GC cells. In conclusion, NORAD enhanced the promotive effect of CAFs in GC cells by up-regulating IL-33 and targeting miR-496, which provided new insights into the microenvironment of GC cells and CAFs	34895039	RID08257	interact with mRNA	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Systemic lupus erythematosus	IL21-AS1	IL2	negatively-E	qRT-PCR;flow cytometry	downregulation	qRT-PCR	NA	NA	immune response(+) 	NA	association	NA	NA	CSC	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000227145	GRCh38_4:122618983-122689156	ENSG00000109471	NA	100996941	3558	NA	IL-2|TCGF	The single nucleotide polymorphism (SNP) rs62324212, located in IL21 antisense RNA 1 (IL21-AS1), has been identified as a genetic risk variant associated with systemic lupus erythematosus (SLE). We aimed to probe the characteristics of IL21-AS1 and explore its clinical relevance focusing on T helper subsets and disease activity in patients with SLE. rs62324212 genotyping was determined using allelic discrimination by quantitative PCR. Gene expression in peripheral blood mononuclear cells and cell surface markers in CD4 +  T cells were analyzed using PCR and flow cytometry. The association among IL21-AS1, CD4 +  T cell subsets, and SLE disease activity was accessed. Ensembl Genome Browser analysis revealed that rs62324212 (C>A) was located in the predicting enhancer region of IL21-AS1. IL21-AS1 was expressed in the nucleus of CD4 +  T and B cells, but its expression was decreased in patients with SLE. IL21-AS1 expression was positively correlated with mRNA levels of IL-2 but not IL-21, and it was associated with the proportion of activated T follicular regulatory (Tfr) cells. Furthermore, we observed a significant negative correlation between IL21-AS1 expression and disease activity in patients with SLE. IL21-AS1 has an effect on disease activity through an involvement of IL-2-mediated activation of Tfr cells in SLE. Thus, targeting the IL21-AS1 may provide therapeutic approaches for SLE.	34895341	RID08258	expression association	NA		UP(PAAD);DATA(GSE40174)
Chronic obstructive pulmonary disease	OIP5-AS1	IL13	positively-E	Luciferase activity assay	upregulation	qRT-PCR	NA	NA	cell viability(+);apoptosis process(+);inflammatory response(-)	ceRNA(miR-410-3p)	association	NA	NA	NA	NA	Respiratory system disease	Lung disease	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000169194	NA	729082	3596	cyrano|linc-OIP5	IL-13|P600	Long non-coding RNA OIP5-AS1 regulates smoke-related chronic obstructive pulmonary disease via targeting micro RNA -410-3p/IL-13.This investigation aimed to assess the levels of serum OIP5-AS1 and micro RNA-410-3p (miR-410-3p) in patients with chronic obstructive pulmonary disease (COPD) and their potential molecular mechanism. The levels of OIP5-AS1 and miR-410-3p as well as mRNA levels of IL-13 were measured. Pearson variable linear test was applied to analyze the correlations between forced expiratory volume in 1 second (FEV1) and OIP5-AS1. The receiver operating characteristic curve was used to predict the predictive possibility of OIP5-AS1. The viable cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry was used to detect the cell apoptosis. An enzyme-linked immunosorbent assay was performed to indicate the inflammatory situation of 16HBE cells. Luciferase activity assay was conducted to examine the relationships between OIP5-AS1 and miR-410-3p together with miR-410-3p and IL-13. Augmented levels of OIP5-AS1, declined levels of miR-410-3p, and enhanced expression of IL-13 were unveiled. The expression of OIP5-AS1 and miR-410-3p was related to the ratio of FEV1 respectively. OIP5-AS1 might serve as a diagnostic biomarker. Interference of OIP5-AS1 restored the abnormal cell viability, apoptosis, and inflammation in cigarette smoke extract (CSE)-stimulated 16HBE cells by regulating miR-410-3p and IL-13. OIP5-AS1 appeared to be a biomarker for distinguishing COPD patients from smokers. OIP5-AS1/miR-410-3p/IL-13 exerted function on the cell viability, apoptosis, and inflammation in CSE-steered cell models.	34872453	RID08259	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Breast cancer	miR-148a-3p	PVT1	positively-E	qRT-PCR;western blot;RIP;Spearman;Dual Luciferase activity	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	binding/interaction	NA	NA	NA	NA	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Breast cancer (BC) is one of the most common malignant tumors for women. The role and potential mechanisms of long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) were explored in BC cell migration and invasion. PVT1, miR-148a-3p and Rho<U+2011>associated, coiled<U+2011>coil containing protein kinase 1 (ROCK1) mRNA expressions were detected using real-time fluorescent quantitative polymerase chain reaction (qRT-PCR. The ROCK1 protein expression was detected by western blot. The relationship of PVT1, miR-148a-3p and ROCK1 was analyzed by Dual Luciferase activity, RNA immunoprecipitation (RIP) and Spearman correlation analysis. Cell invasion and migration were detected by Transwell assay. Upregulation of PVT1 and ROCK1, and downregulation of miR-148a-3p were observed in BC tissues and cell lines. According to the analysis of Dual Luciferase activity, RIP and Spearman correlation analysis, miR-148a-3p directly binds to PVT1, and ROCK1 is a target of miR-148a-3p. In addition, PVT1 regulated the cells migration and invasion by regulating miR-148a-3p and ROCK1 expression. These data demonstrated that PVT1 was upregulated and facilitated to the cell migration and invasion of BC by the regulation of miR-148a-3p and ROCK1, indicating that PVT1 may be a potential biomarker of BC diagnosis and treatment.	34859371	RID08260	expression association	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)
Malignant glioma	SNHG18	E-cadherin	positively-E	qRT-PCR;western blot; dual-luciferase reporter	upregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546170-9550725	NA	NA	100505806	NA	NA	NA	This study aims to probe the biological functions of long non-coding RNA small nucleolar RNA host gene 18 (SNHG18) on glioma cells and its underlying mechanism. In this study, SNHG18 expression in glioma tissues was quantified employing GEPIA database; quantitative real-time PCR was adopted to examine the expressions of SNHG18, microRNA-338-5p (miR-338-5p) and forkhead box D1 (FOXD1) mRNA in glioma tissues and cell lines; cell proliferation, migration and invasion were detected utilizing cell counting kit-8, EdU and Transwell assays; western blot was utilized to quantify the protein expressions of E-cadherin, N-cadherin, Vimentin and FOXD1; dual-luciferase reporter gene and RNA immunoprecipitation experiments were utilized to validate the targeting relationships between SNHG18 and miR-338-5p, as well as miR-338-5p and FOXD1 mRNA 3'UTR; dual-luciferase reporter gene and chromatin immunoprecipitation assays were utilized to verify the binding of E2F transcription factor 1 (E2F1) to the SNHG18 promoter region. It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients; knockdown of SNHG18 repressed the malignant biological behaviors of glioma cells, enhanced E-cadherin expression and repressed N-cadherin and Vimentin expressions. MiR-338-5p was a target of SNHG18, and SNHG18 promoted the expression of FOXD1 by decoying miR-338-5p. Additionally, E2F1 could bind to the promoter of SNHG18 to elevate its expression. In conclusion, SNHG18 accelerates glioma progression via regulating the miR-338-5p/FOXD1 axis.	34937497	RID08261	expression association	prognosis		
Malignant glioma	SNHG18	N-cadherin	negatively-E	qRT-PCR;western blot; dual-luciferase reporter	upregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546170-9550725	NA	NA	100505806	NA	NA	NA	This study aims to probe the biological functions of long non-coding RNA small nucleolar RNA host gene 18 (SNHG18) on glioma cells and its underlying mechanism. In this study, SNHG18 expression in glioma tissues was quantified employing GEPIA database; quantitative real-time PCR was adopted to examine the expressions of SNHG18, microRNA-338-5p (miR-338-5p) and forkhead box D1 (FOXD1) mRNA in glioma tissues and cell lines; cell proliferation, migration and invasion were detected utilizing cell counting kit-8, EdU and Transwell assays; western blot was utilized to quantify the protein expressions of E-cadherin, N-cadherin, Vimentin and FOXD1; dual-luciferase reporter gene and RNA immunoprecipitation experiments were utilized to validate the targeting relationships between SNHG18 and miR-338-5p, as well as miR-338-5p and FOXD1 mRNA 3'UTR; dual-luciferase reporter gene and chromatin immunoprecipitation assays were utilized to verify the binding of E2F transcription factor 1 (E2F1) to the SNHG18 promoter region. It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients; knockdown of SNHG18 repressed the malignant biological behaviors of glioma cells, enhanced E-cadherin expression and repressed N-cadherin and Vimentin expressions. MiR-338-5p was a target of SNHG18, and SNHG18 promoted the expression of FOXD1 by decoying miR-338-5p. Additionally, E2F1 could bind to the promoter of SNHG18 to elevate its expression. In conclusion, SNHG18 accelerates glioma progression via regulating the miR-338-5p/FOXD1 axis.	34937497	RID08262	expression association	prognosis		
Malignant glioma	SNHG18	Vimentin	negatively-E	qRT-PCR;western blot; dual-luciferase reporter	upregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546170-9550725	NA	NA	100505806	NA	NA	NA	This study aims to probe the biological functions of long non-coding RNA small nucleolar RNA host gene 18 (SNHG18) on glioma cells and its underlying mechanism. In this study, SNHG18 expression in glioma tissues was quantified employing GEPIA database; quantitative real-time PCR was adopted to examine the expressions of SNHG18, microRNA-338-5p (miR-338-5p) and forkhead box D1 (FOXD1) mRNA in glioma tissues and cell lines; cell proliferation, migration and invasion were detected utilizing cell counting kit-8, EdU and Transwell assays; western blot was utilized to quantify the protein expressions of E-cadherin, N-cadherin, Vimentin and FOXD1; dual-luciferase reporter gene and RNA immunoprecipitation experiments were utilized to validate the targeting relationships between SNHG18 and miR-338-5p, as well as miR-338-5p and FOXD1 mRNA 3'UTR; dual-luciferase reporter gene and chromatin immunoprecipitation assays were utilized to verify the binding of E2F transcription factor 1 (E2F1) to the SNHG18 promoter region. It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients; knockdown of SNHG18 repressed the malignant biological behaviors of glioma cells, enhanced E-cadherin expression and repressed N-cadherin and Vimentin expressions. MiR-338-5p was a target of SNHG18, and SNHG18 promoted the expression of FOXD1 by decoying miR-338-5p. Additionally, E2F1 could bind to the promoter of SNHG18 to elevate its expression. In conclusion, SNHG18 accelerates glioma progression via regulating the miR-338-5p/FOXD1 axis.	34937497	RID08263	expression association	prognosis		
Malignant glioma	SNHG18	FOXD1	positively-E	qRT-PCR;western blot; dual-luciferase reporter	upregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(MiR-338-5p)	binding/interaction	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546170-9550725	ENSG00000251493	NA	100505806	2297	NA	FKHL8|FREAC4	This study aims to probe the biological functions of long non-coding RNA small nucleolar RNA host gene 18 (SNHG18) on glioma cells and its underlying mechanism. In this study, SNHG18 expression in glioma tissues was quantified employing GEPIA database; quantitative real-time PCR was adopted to examine the expressions of SNHG18, microRNA-338-5p (miR-338-5p) and forkhead box D1 (FOXD1) mRNA in glioma tissues and cell lines; cell proliferation, migration and invasion were detected utilizing cell counting kit-8, EdU and Transwell assays; western blot was utilized to quantify the protein expressions of E-cadherin, N-cadherin, Vimentin and FOXD1; dual-luciferase reporter gene and RNA immunoprecipitation experiments were utilized to validate the targeting relationships between SNHG18 and miR-338-5p, as well as miR-338-5p and FOXD1 mRNA 3'UTR; dual-luciferase reporter gene and chromatin immunoprecipitation assays were utilized to verify the binding of E2F transcription factor 1 (E2F1) to the SNHG18 promoter region. It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients; knockdown of SNHG18 repressed the malignant biological behaviors of glioma cells, enhanced E-cadherin expression and repressed N-cadherin and Vimentin expressions. MiR-338-5p was a target of SNHG18, and SNHG18 promoted the expression of FOXD1 by decoying miR-338-5p. Additionally, E2F1 could bind to the promoter of SNHG18 to elevate its expression. In conclusion, SNHG18 accelerates glioma progression via regulating the miR-338-5p/FOXD1 axis.	34937497	RID08264	ceRNA or sponge	prognosis		UP(BRCA);DATA(GSE55807)
Cervical squamous cell carcinoma	CASC9-1	miR-383-5p	positively-E	RT-PCR;dual-luciferase reporter assay	upregulation	RT-qPCR;western blot	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Cervical squamous cell carcinoma (Cervical SCC) is a malignant gynecological tumor, which greatly endangers the health of global women. Cancer susceptibility candidate 9 (CASC9) has been identified as an oncogene in multiple cancers. However, the role of CASC9-1 (one transcript of CASC9) in cervical SCC remains covered. We analyzed gene expression in cervical SCC cells via RT-qPCR and western blot assays. The impact of CASC9-1 on cervical SCC cell and tumor growth was assessed via in vitro functional assays and in vivo assays. Moreover, the regulatory mechanism of CASC9-1 was explored by mechanism assays. CASC9-1 was up-regulated in cervical SCC cells. CASC9-1 knockdown repressed cervical SCC cell proliferation, migration and invasion while elevating apoptosis. Via in-vivo experiments, CASC9-1 down-regulation was proved to restrict cervical SCC tumor growth. In terms of mechanism, CASC9-1 directly targeted miR-383-5p, and MAPKAP1 was the target gene of miR-383-5p in cervical SCC cells. CASC9-1 could exacerbate malignant behaviors of cervical SCC cells via binding to miR-383-5p and regulating MAPKAP1. CASC9-1 exerted influences on various biological behaviors of cervical SCC cells via targeting miR-383-5p to up-regulate MAPKAP1. All these results mirrored that CASC9-1 might be a potential target for cervical SCC treatment.	34857398	RID08265	ceRNA or sponge	NA		
Multiple sclerosis	SNHG1	hsa-miR-197-3p	negatively-E	RT-qPCR;DIANA LncBase;miRTarBase	upregulation	Pearson correlation analysis	GSE43590;GSE43591	NA	cell proliferation(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals	Nervous system disease	Demyelinating disease	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851978-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Multiple sclerosis (MS) is an immune-mediated demyelinating and degenerative disease with unknown etiology. Inappropriate response of T-cells to myelin antigens has an essential role in the pathophysiology of MS. The clinical and pathophysiological complications of MS necessitate identification of potential molecular targets to understand the pathogenic events of MS. Since the functions and regulatory mechanisms of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in MS are yet uncertain, we conducted a bioinformatics analysis to explain the lncRNA-associated ceRNA axes to clarify molecular regulatory mechanisms involved in T-cells responses in MS. Two microarray datasets of peripheral blood T-cell from subjects with relapsing-remitting MS and matched controls containing data about miRNAs (GSE43590), mRNAs and lncRNAs (GSE43591) were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs (DEmiRNAs), mRNAs (DEmRNAs), and lncRNAs (DElncRNAs) were identified by the limma package of the R software. Protein-protein interaction (PPI) network and module were developed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) Cytoscape plugin, respectively. Using DIANA-LncBase and miRTarBase, the lncRNA-associated ceRNA axes was constructed. We conducted a Pearson correlation analysis and selected the positive correlations among the lncRNAs and mRNAs in the ceRNA axes. Lastly, DEmRNAs pathway enrichment was conducted by the Enrichr tool. A ceRNA regulatory relationship among Small nucleolar RNA host gene 1 ( SNHG1 ),  hsa-miR-197-3p , YOD1 deubiquitinase ( YOD1 ) and zinc finger protein 101 ( ZNF101 ) and downstream connected genes was identified. Pathway enrichment analysis showed that DEmRNAs were enriched in "Protein processing in endoplasmic reticulum" and "Herpes simplex virus 1 infection" pathways. To our knowledge, this would be the first report of a possible role of  SNHG1 / hsa-miR-197-3p / YOD1 / ZNF101  axes in the pathogenesis of MS. This research remarks on the significance of ceRNAs and prepares new perceptions for discovering the molecular mechanism of MS.	34956196	RID08266	expression association	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)	
Myasthenia gravis	SNHG16	IL10	negatively-E	qRT-PCR;flow cytometry	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-let-7c-5p)	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Immune system disease	Autoimmune disease of the nervous system	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000136634	NA	100507246	3586	Nbla10727|Nbla12061|ncRAN	CSIF|IL-10|IL10A|TGIF	Myasthenia gravis (MG) is a complex neurological autoimmune disease with a pathogenetic mechanism that has yet to be elucidated. Emerging evidence has revealed that genes, non-coding RNAs and genetic variants play significant roles in the pathogenesis of MG. However, the molecular mechanisms of single nucleotide polymorphisms (SNPs) located on lncRNAs could disturb lncRNA-mediated ceRNA regulatory functions still unclear in MG. In this study, we collated 276 experimentally confirmed MG risk genes and 192 MG risk miRNAs. We then constructed a lncRNA-mediated ceRNA network for MG based on multi-step computational strategies. Next, we systematically integrated risk pathways and identified candidate SNPs in lncRNAs for MG based on data acquired from public databases. In addition, we constructed a pathway-based lncRNA-SNP mediated network (LSPN) that contained 128 lncRNAs targeting 8 MG risk pathways. By analyzing network, we propose a latent mechanism for how the "lncRNA-SNP-mRNA-pathway" axis affects the pathogenesis of MG. Moreover, 25 lncRNAs and 51 SNPs on lncRNAs were extracted from the "lncRNA-SNP-mRNA-pathway" axis. Finally, functional analyses demonstrated lncRNA-SNPs mediated ceRNA regulation pairs associated with MG participated in the MAPK signaling pathway. In summary, we constructed MG-specific lncRNA-SNPs mediated ceRNA regulatory networks based on pathway in the present study, which was helpful to elucidate the roles of lncRNA-SNPs in the pathogenesis of MG and provide novel insights into mechanism of lncRNA-SNPs as potential genetic risk biomarkers of MG.	34907261	RID08267	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(PAAD);DATA(GSE40174)
Ovarian cancer	CTBP1-DT	MAP3K3	positively-E	RT-qPCR	upregulation	RT-PCR	NA	NA	cell growth(+)	ceRNA(miR-188-5p)	binding/interaction	NA	NA	CSC	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000196810	GRCh38_4:1249300-1288291	ENSG00000198909	NA	92070	4215	C4orf42|CTBP1-AS1|CTBP1-AS2|MGC21675	MAPKKK3|MEKK3	High-grade serous ovarian cancer (HGSOC) is a common and lethal cancer of the female reproductive system. Long non-coding RNAs (lncRNAs) are aberrantly expressed in various cancers and play crucial roles in tumour progression. However, their function and molecular mechanism in HGSOC remain largely unknown. Based on public databases and bioinformatics analyses, the overexpression of lncRNA CTBP1-DT in HGSOC tissues was detected and validated in a cohort of HGSOC tissues. High expression of lncRNA CTBP1-DT was associated with poor prognosis and was an independent risk factor for survival. Overexpression of lncRNA CTBP1-DT promoted malignant biological behaviour of HGSOC cells, whereas its depletion induced growth arrest of HGSOC cells by vitro and in vivo assays. Mechanistically, lncRNA CTBP1-DT could competitively bind to miR-188-5p to protect MAP3K3 from degradation. Moreover, our results revealed that ETV5 could specifically interact with the promoter of lncRNA CTBP1-DT and activate its transcription. Collectively, these results reveal a novel ETV5/lncRNA CTBP1-DT/miR-188-5p/MAP3K3 pathway for HGSOC progression and suggest that lncRNA CTBP1-DT might be a potential biomarker and therapeutic target for HGSOC.	34887384	RID08268	ceRNA or sponge	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE67939,GSE75367,GSE86978)
Breast cancer	CDKN2B-AS1	MIR4440	negatively-E	qRT-PCR;dual luciferase experiment	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000266109	NA	100048912	100616397	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	mir-4440	The study aimed to analysis the genetic variation of the lncRNA CDKN2B-AS1 SNPs, and explored the regulation of SNPs on the invasion and metastasis of Breast cancer (BC). The SNPs (Single Nucleotide Polymorphisms) was screened for genotyping among 504 Chinese Han patients and 505 controls, which were frequency-matched for age (<U+00A0> <U+00A0>2 years). Logistic analysis was to explore the relationship between SNPs and the BC risk. Interactions between SNPs and reproductive factors was explored using the multifactor dimensionality reduction (MDR) method. qRT-PCRwas conducted to detect the CDKN2B-AS1 expression in plasma of different rs10965215 and rs2518723 genotypes. The effect of rs10965215 A>G mutation on the binding ability of CDKN2B-AS1 and miR-4440 was verified by dual luciferase experiment. CCK-8, scratch and Transwell experiment were performed to explore the effect of miR-4440 over-expression on BC cell proliferation, migration and invasion. A total of 13 SNP was screened. The individuals with SNPs rs2518723C>T, rs10965215 A>G, rs77792598C>G, rs4977753 T<U+00A0>><U+00A0>C, rs75917766C>T and rs78545330C>G mutations might increase the BC risk. MDR results revealed that individuals with rs10965215 G genotype who age at menarche<<-U+00A0>13 and regardless of the number of abortion<<U+00A0>2 or <<-U+00A0>2 had a higher risk of BC. The relative expression of CDKN2B-AS1 in rs10965215 homozygous wild AA genotype (8.88<U+00A0> <U+00A0>3.43) was lower than heterozygous GA (11.08<U+00A0> <U+00A0>2.90) and homozygous mutant GG genotype (11.31<U+00A0> <U+00A0>2.90). When rs10965215 wild A genotype was carried, there was an interaction between CDKN2B-AS1 and miR-4440. The CCK-8, Transwell, and scratch experiment were all found that miR-4440 over-expression might enhance the proliferation, invasion and migration of BC cells. CDKN2B-AS1 gene polymorphism might be related to the susceptibility of BC, CDKN2B-AS1 rs10965215 A/G genotype probably affect the proliferation, invasion and migration of BC cells by modulating the interactions with of miR-4440.	34954153	RID08269	expression association	metastasis	UP(SKCM);DATA(GSE38495)	
Allergic rhinitis	HOTAIRM1	IRF4	positively-E	flow cytometry;dual-luciferase reporter assay;RNA immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-148a-3p)	binding/interaction	NA	NA	NA	NA	Respiratory system disease	Nose disease	lncRNA	TF	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000137265	NA	100506311	3662	HOXA-AS1|HOXA1-AS1|NCRNA00179	LSIRF|MUM1	Allergic rhinitis (AR) is an inflammatory reaction caused by irritation of nasal mucosa by external allergens, which seriously affects the life of patients. Here, we aimed to investigate the effect and mechanism of long non-coding RNA HOX antisense intergenic RNA myeloid 1 (lncRNA HOTAIRM1) on AR development. The nasal mucosa samples were collected from AR patients and AR model mice (induced by ovalbumin). T helper type 9 (Th9) cells were examined by flow cytometry. Fluorescence in situ hybridization was conducted to examine the localization of HOTAIRM1 in CD4 +  T cells. dual-luciferase reporter assay or RNA immunoprecipitation was conducted to examine the bond between HOTAIRM1 and miR-148a-3p, miR-148a-3p, and interferon regulatory factor 4 (IRF4). Chromatin Immunoprecipitation assay was conducted to detect the interaction between IRF4 and HOTAIRM1 promoter. HOTAIRM1, interleukin-9 (IL-9), and IRF4 were highly expressed in the AR model. The ratio of Th9 cells was increased in AR mice and overexpressing HOTAIRM1 further promoted Th9 cell differentiation, while the effect was reversed after overexpression of miR-148a-3p. Besides, in vivo experiments showed that interfering with HOTAIRM1 reduced the number of sneezing and rubbing movements, reduced immunoglobulin E (IgE) and IL-9 levels, as well as Th9 cells. HOTAIRM1 was expressed in the cytoplasm and the interactions between HOTAIRM1 and miR-148a-3p, miR-148a-3p and IRF4, were confirmed. Furthermore, IRF4 bound to the HOTAIRM1 promoter and promoted its transcriptional activation. HOTAIRM1 was highly expressed in the AR model. Besides, IRF4 activated HOTAIRM1 transcription, and HOTAIRM1, in turn, up-regulated IRF4 expression through competitively binding to miR-148a-3p with IRF4, thereby affecting Th9 cell differentiation and participating in the occurrence and development of AR. Our results suggested that interference with HOTAIRM1 might become a treatment for AR.	34929342	RID08270	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Polycystic ovary syndrome	MALAT1	MDM2	positively-E	RAP;the PAR-CLIP assay;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Evading Apoptosis	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135679	NA	378938	4193	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	HDM2|MGC5370	Polycystic ovary syndrome (PCOS) is a metabolic disorder of the reproductive system that affects 6-20% women of reproductive age. Multiple coding and non-coding genes were found to be affected in patients with PCOS, including MALAT1, an 8.7<U+00A0>kb long non-coding RNA. MALAT1 has been found to interact with miRNAs in granulosa cells (GCs); however, its binding proteins in GCs are still unknown. In this study, MALAT1 binding proteins in primary GCs were recruited by RNA antisense purification (RAP) assay and identified by mass spectrometry. The interaction between MALAT1 and proteins was examined by the PAR-CLIP assay and immunofluorescence. Functional studies were performed using the human granulosa-like tumor cell line (KGN) and primary granulosa cells. We identified that MALAT1 interacted with MDM2 and PARP1 in the cell nucleus. MDM2 binds to the 3' segment of MALAT1, containing the ENE domain through the ring finger domain. Knockdown of MALAT1 in GCs increased p53 protein levels by repressing p53 ubiquitination and degradation. MALAT1 promoted the binding between P53 and MDM2, which further boosted P53 proteasome dependent degradation. Knockdown of MALAT1 in KGN cells and primary GCs increased apoptosis and reduced proliferation.	34883204	RID08271	expression association	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE86978)
Cancer	MALAT1	ITGA4	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cell invasion(+)	interact with mRNA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115232	NA	378938	3676	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	CD49D	AFAP1-AS1 is a long non-coding RNA which partakes in the pathoetiology of several cancers. The sense protein coding gene from this locus partakes in the regulation of cytophagy, cell motility, invasive characteristics of cells and metastatic ability. In addition to acting in concert with AFAP1, AFAP1-AS1 can sequester a number of cancer-related miRNAs, thus affecting activity of signaling pathways involved in cancer progression. Most of animal studies have confirmed that AFAP1-AS1 silencing can reduce tumor volume and invasive behavior of tumor cells in the xenograft models. Moreover, statistical analyses in the human subjects have shown strong correlation between expression levels of this lncRNA and clinical outcomes. In the present work, we review the impact of AFAP1-AS1 in the carcinogenesis.	34912717	RID08272	interact with mRNA	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Diabetic retinopathy	ATP2B1-AS1	MIR4729	negatively-E	qRT-PCR;dual-luciferase reporter	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);angiogenesis(-);cell permeability(-)	sponge	binding/interaction	NA	NA	CSC	Insensitivity to Antigrowth Signals	Disease of metabolism	Diabetes mellitus	lncRNA	miRNA	ENSG00000271614	GRCh38_12:89708959-89712590	ENSG00000263857	NA	338758	100616204	LINC00936	NA	Mounting evidence shows that long non-coding RNAs (lncRNAs) are important to modulate the biological process of diabetic retinopathy (DR). We aimed to investigate the role of lncRNAs in DR and elucidate the exact mechanism. Real-time quantitative polymerase chain reaction was carried out to distinguish the lncRNA ATPase plasma membrane Ca 2+  transporting<U+2009>1 antisense RNA<U+2009>1 (ATP2B1-AS1) expression in DR patients and HG-treated human retinal endothelial cells (HRECs). Dual-luciferase reporter system was used to verify that ATP2B1-AS1 could act as a microRNA (miR)-4729 sponge, and miR-4729 could bind to 3'UTR of IQ motif-containing GTPase-activating protein<U+2009>2 (IQGAP2). Cell proliferation assay, wound healing migration assay, transwell assay, tube formation assay and immunofluorescence were used to investigate cell proliferation, migration and angiogenesis in HRECs. The present results showed that ATP2B1-AS1 was downregulated in DR patients and high-glucose-induced HRECs. In gain- and loss-of-function assays, ATP2B1-AS1 overexpression could significantly reduce cell proliferation, migration, angiogenesis and permeability induced by high glucose in<U+2009>vitro. Additionally, we carried out dual-luciferase reporter experiments to determine that ATP2B1-AS1 could act as a miR-4729 sponge. ATP2B1-AS1 overexpression could rescue miR-4729 mimics and short hairpin RNA-IQGAP2 induced cell proliferation, migration and angiogenesis in HRECs. The present study showed that ATP2B1-AS1 acted as a miR-4729 sponge to regulate IQGAP2 reducing high-glucose-induced endothelial dysfunction in DR.	34935307	RID08273	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);DATA(GSE74639,GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	
Aids	GAS5	MIR21	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	regulation	RNA-RNA	NA	NA	NA	Disease by infectious agent	Viral infectious disease	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000199004	NA	60674	406991	NCRNA00030|SNHG2	MIRN21|hsa-mir-21|miR-21|miRNA21	Moreover, lncRNAs can affect host cellular response to HIV. Consistent with this function of lncRNAs, Nguyen et al. have shown that an activation-associated reduction of GAS5 induces DNA damage response and influences both activity and apoptosis of CD4 + T cells originated from HIV infected people through enhancing expression of miR-21. This phenomenon has been detected in patients receiving antiretroviral therapy who frequently show immune activation as a result of low-grade inflammation. Mechanistically, GAS5 decreases expression of miR-21, a miRNA that regulates important signaling pathways contributing in DNA damage response. The persistent induction of T cells leads to down-regulation of GAS5, up-regulation of miR-21, dysfunction of CD4 + T cells and induction of apoptosis in these cells. Notably, this inflammation-associated T cell stimulation and abnormal apoptosis in antiretroviral therapy-controlled HIV patients and healthy persons can be upturned by interfering with the GAS5/miR-21 axis. Antagonization of GAS5/miR-21 axis has also been suggested to enhance activity and survival of CD4 + T cells in antiretroviral therapy-treated HIV people [11]. MALAT1 has been shown to bind to PRC2 and inhibit EZH2 binding to HIV-1 promoter, reducing histone methylation and increasing HIV-1 transcription [12]. On the other hand, NRON lncRNA could degrade Tat protein by linking it to ubiquitin, therefore limiting viral replication and transcription [13]. Thus, certain lncRNAs might regulate response of host cells to HIV infection.	34942460	RID08274	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	
Colorectal cancer	MEG3	MIR708	negatively-E	RNApull-down;RNA immunoprecipitation;luciferase reporter assays;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell stemness(+)	sponge	binding/interaction	NA	NA	CSC	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000211997	NA	55384	100126333	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MIRN708|hsa-mir-708	Colorectal cancer (CRC) remains the most common gastrointestinal cancer and a leading cause of cancer deaths worldwide, with most showing pathologies indicating the malignant transformation of early stage intestinal stem cells. The long non-coding RNA Meg3, which functions as a tumor suppressor, has been reported to be abnormal in multiple tumorigenesis events; however, the underlying mechanism by which Meg3 contributes to the malignant proliferation of colonic stem cells remains unclear. We analyzed the expression levels of Meg3, miR-708, and SOCS3 in samples from Apc loss-of-function (Apc min ) mice and patients with CRC, particularly in colonic crypt cells. Apc min  mice and AMO/DSS-induced mice model (in vivo) and organoid culture system (in vitro) were used to explore the effect of the Meg3/miR-708/SOCS3 axis on tumorigenesis in the colon. In vitro, we performed RNApull-down, RNA immunoprecipitation, and luciferase reporter assays using DLD1 and RKO cell lines. The Meg3/miR-708/SOCS3 signaling axis plays a critical role in the early stage of CRC development. Our data showed Meg3 levels negatively correlate with miR-708 levels both in clinical samples and in the Apc min  mouse model, which indicated that Meg3 acts as a competitive endogenous RNA (ceRNA) of miR-708. Then, miR-708 served as an oncogene, inducing neoplasia in both Apc min  mice and cultured colonic organoids. Put together, miR-708 appears to promote malignant proliferation of colonic stem cells by targeting SOCS3/STAT3 signaling. These data revealed that Meg3 sponges miR-708 to inhibit CRC development via SOCS3-mediated repression of the malignant proliferation of colonic stem cells. The Meg3/miR-708/SOCS3 signaling axis provides potential targets for the diagnosis and treatment of CRC, particularly early stage CRC.	34934045	RID08275	ceRNA or sponge	NA		
Osteoarthritis	KLF3-AS1	YBX1	negatively-E	RT-qPCR	upregulation	RT-PCR	NA	NA	cell autophagy(-);apoptosis process(-)	NA	regulation	NA	NA	CSC	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000231160	GRCh38_4:38602438-38664926	ENSG00000065978	NA	79667	4904	FLJ13197	BP-8|CSDA2|CSDB|DBPB|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Osteoarthritis is a degenerative joint disease and a leading cause of adult disability. Our previous study has reported that mesenchymal stem cell-derived exosomes (MSC-Exo) mediated long non-coding RNA KLF3-AS1 improves osteoarthritis. This study aims to investigate the molecular mechanism of KLF3-AS1 in osteoarthritis. Chondrocytes were treated with IL-1beta to induce chondrocyte injury, followed by MSC-Exo treatment. We found that MSC-Exo enhanced KLF3-AS1 expression in IL-1beta-treated chondrocytes. IL-1beta treatment reduced cell viability and enhanced apoptosis in chondrocytes. MSC-Exo-mediated KLF3-AS1 promoted cell viability and repressed apoptosis of IL-1beta-treated chondrocytes. Rapamycin (autophagy activator) promoted cell viability and suppressed apoptosis of chondrocytes by activating autophagy. Moreover, KLF3-AS1 interacted with YBX1 in chondrocytes. MSC-Exo-mediated KLF3-AS1 activated PI3K/Akt/mTOR signaling pathway, which was abrogated by YBX1 silencing. MSC-Exo-mediated KLF3-AS1 repressed autophagy and apoptosis of chondrocytes by activating PI3K/Akt/mTOR signaling pathway. In conclusion, our data demonstrate that MSC-Exo-mediated KLF3-AS1 inhibits autophagy and apoptosis of IL-1beta-treated chondrocyte through PI3K/Akt/mTOR signaling pathway. KLF3-AS1 activates PI3K/Akt/mTOR signaling pathway by targeting YBX1 to improve the progression of osteoarthritis. Thus, this work suggests that MSC-Exo-mediated KLF3-AS1 may be a potential therapeutic target for osteoarthritis.	34964696	RID08276	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE75367,GSE86978)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Alzheimer's disease	MIR600HG	NEDD4L	negatively-E	qRT-PCR;RNA pull-down assay;mass spectrometry;Immunofluorescence staining	upregulation	qRT-PCR	NA	NA	cell autophagy(+)	interaction	regulation	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000236901	GRCh38_9:123109494-123115477	ENSG00000049759	NA	81571	23327	C9orf45|FLJ22161|GL012|NCRNA00287	KIAA0439|NEDD4-2|RSP5	Growing evidence has demonstrated that long non-coding RNAs (lncRNAs) play a critical role in Alzheimer's disease (AD), which is characterized by sustained mitochondrial dysfunction, inevitable memory loss, and cognitive decline. However, the potential function of lncRNAs MIR600 Host Gene (MIR600HG) in AD remains unanswered. Our study aimed to investigate the role of MIR600HG and its related molecular mechanism in AD. The expression of MIR600HG was examined by qRT-PCR The MIR600HG interacting proteins were identified by RNA pull-down assay and mass spectrometry and verified by RNA immunoprecipitation. Immunofluorescence staining was applied to examine the colocalization of PINK1 and NEDD4L. The PINK1 level and the activation of autophagy were detected by immunoblotting. Morris water maze test was performed to evaluate cognitive decline in AD mice model. MIR600HG expression was elevated during aging in two different types of AD transgenic mouse models. Next, we found that increased MIR600HG directly interact with NEDD4L, which promoted PINK1 ubiquitination and degradation, and as well as autophagy activation. Additionally, MIR600HG promoted Abeta production and suppressed Cytochrome C Oxidase activity. Administration of AAV-shMIR600HG restored the Cytochrome C Oxidase activity and inhibited Abeta production. Furthermore, PINK1 overexpression or MIR600HG knockdown significantly ameliorated the cognitive impairment in APP/PS1 mice. PINK1 depletion recovered the spatial memory defect in the AAV-shMIR600HG injected APP/PS1 mice. MIR600HG was increased in AD and promoted AD pathogenesis. Targeting MIR600HG significantly improved cognitive function in AD mice, which could pave the way for exciting new avenues in AD therapeutic strategy research.	34958029	RID08277	expression association	NA	DOWN(LIHC,BRCA);DATA(GSE117623,GSE51827,GSE75367)	UP(LIHC,PAAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE111842,GSE109761,GSE111065)
Hepatoblastoma	MIR210HG	FOXO6	negatively-E	Luciferase reporter assays;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);tumor growth(+)	ceRNA(miR-608)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000247095	GRCh38_11:565657-568457	ENSG00000204060	NA	100506211	100132074	NA	NA	Hepatoblastoma is the most common liver tumor. Recent research has found that long non-coding (lnc)RNAs are involved in multiple types of cancers, but the potential mechanism of lncRNA MIR210HG in hepatoblastoma remains unknown. The present study explored the molecular mechanism of MIR210HG in hepatoblastoma progression. The cell counting kit-8 was used to detect cell viability, and Transwell assays assessed cell migration and invasion. Luciferase reporter assays showed the relationship between MIR210HG and microRNA (miR)-608 and between miR-608 and forkhead box O6 (FOXO6). Functional tests were verified  in vivo  by a tumor xenograft model. The expression of MIR210HG, miR-608, FOXO6, E-cadherin, N-cadherin, and vimentin was determined by quantitative reverse transcription polymerase chain reaction and western blot. MIR210HG was shown to be highly expressed in hepatoblastoma tissues and cell lines. Knockdown of MIR210HG reduced proliferation, migration, and invasion in liver cancer cells, and suppressed tumor growth  in vivo . MIR210HG competitively combined with miR-608, and miR-608 decreased FOXO6 expression. Our study demonstrated that knockdown of MIR210HG inhibits hepatoblastoma development through binding to miR-608 and downregulating FOXO6. Our results provide novel insights for hepatoblastoma treatment involving the MIR210HG-miR608-FOXO6 axis.	34918962	RID08278	ceRNA or sponge	NA		
Facioscapulohumeral muscular dystrophy	H19	DUX4	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-675)	binding/interaction	NA	NA	NA	NA	Musculoskeletal system disease	Facioscapulohumeral muscular dystrophy	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995171-2001470	ENSG00000260596	NA	283120	100288687	ASM|ASM1|D11S813E|LINC00008|MIR675HG|NCRNA00008	DUX4L	Facioscapulohumeral muscular dystrophy (FSHD) is a potentially devastating myopathy caused by de-repression of the DUX4 gene in skeletal muscles. Effective therapies will likely involve DUX4 inhibition. RNA interference (RNAi) is one powerful approach to inhibit DUX4, and we previously described a RNAi gene therapy to achieve DUX4 silencing in FSHD cells and mice using engineered microRNAs. Here we report a strategy to direct RNAi against DUX4 using the natural microRNA miR-675, which is derived from the lncRNA H19. Human miR-675 inhibits DUX4 expression and associated outcomes in FSHD cell models. In addition, miR-675 delivery using gene therapy protects muscles from DUX4-associated death in mice. Finally, we show that three known miR-675-upregulating small molecules inhibit DUX4 and DUX4-activated FSHD biomarkers in FSHD patient-derived myotubes. To our knowledge, this is the first study demonstrating the use of small molecules to suppress a dominant disease gene using an RNAi mechanism.	34880230	RID08279	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	UP(PAAD);DATA(GSE40174)
Hepatocellular carcinoma	NORAD	miR-556-3p	positively-E	RT-qPCR;western blot;luciferase reporter gene;RNA pull-down assays	upregulation	RT-qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);chemosensitivity(-)	sponge	binding/interaction	NA	Propofol	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	Propofol has been previously demonstrated to relieve hepatocellular carcinoma (HCC). However, the specific molecular mechanisms mediated by propofol remain to be explored. mRNA or miRNA expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Protein expression was determined by western blot. The interaction between microRNA (miR)-556-3p and long coding RNA non-coding RNA activated by DNA damage (NORAD) or migration and invasion enhancer 1 (MIEN1) was verified by luciferase reporter gene and RNA pull-down assays. Cellular functions were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetra-zolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), and Transwell assays. Propofol notably suppressed the proliferation and EMT of Hep3B and SNU449 cell lines. NORAD was overexpressed in the HCC tissues and cells, while propofol decreased NORAD levels in the HCC cells. Conversely, overexpression of NORAD partially restored malignant behaviors of the HCC cells and abolished the effects of propofol. Additionally, NORAD sponged miR-556-3p to upregulate MIEN1. However, the knockdown of MIEN1 suppressed the proliferation and EMT of HCC cells. Propofol inhibited HCC cell proliferation and EMT progress via NORAD/miR-556-3p/MIEN1 axis. These data provided a potent prognosis and diagnostic marker for HCC and supplemented the underlying mechanism of propofol-induced anti-tumor effects.	34936303	RID08280	ceRNA or sponge	prognosis,chemoresistance	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE111065,GSE51827,GSE55807,GSE75367)	
Kidney injury	KCNQ1OT1	NLRP3	negatively-E	RT-qPCR	upregulation	RT-qPCR	NA	NA	cell proliferation(-);apoptosis process(+);inflammatory response(+)	ceRNA(miR-204-5p)	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Injury	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000162711	NA	10984	114548	KCNQ1-AS2|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCU|MWS|NALP3|PYPAF1	Acute kidney injury (AKI) is a critical clinical disease characterized by an acute decrease in renal function. Long non-coding RNAs (LncRNAs) are important in AKI. This study aimed to explore the mechanism of lncRNA Kcnq1ot1 in AKI by sponging microRNA (miR)-204-5p as a competitive endogenous RNA (ceRNA). AKI mouse model and hypoxia/reoxygenation (H/R) model of human kidney (HK) cells were established. Kcnq1ot1 expression, cell proliferation, and apoptosis were measured. Binding relations among Kcnq1ot1, miR-204-5p, and NLRP3 were verified. Pathological changes and cell apoptosis were detected. The results showed that Kcnq1ot1 was highly expressed in the AKI model  in vivo  and  in vitro . Kcnq1ot1 knockdown promoted cell proliferation and prevented apoptosis and inflammation. Furthermore, Kcnq1ot1 inhibited miR-204-5p expression by competitively binding to miR-204-5p in HK-2 cells. miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells  in vitro . Kcnq1ot1 knockdown  in vivo  promoted miR-204-5p expression, inhibited NLRP3 inflammasome activation, reduced levels of SCr, BUN, and KIM-1, and thus alleviated AKI and reduced apoptosis. In summary, silencing lncRNA Kcnq1ot1 inhibited AKI by promoting miR-204-5p and inhibiting NLRP3 inflammasome activation.	34858199	RID08281	ceRNA or sponge	NA	UP(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Acute myocardial infarction	NRON	HIF1A	positively-E	RT-PCR;MTT assay;flow cytometer;western blot	upregulation	RT-PCR	NA	NA	cell viability(-);apoptosis process(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000253079	GRCh38_9:126408041-126408410	ENSG00000100644	NA	641373	3091	NCRNA00194	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Acute myocardial infarction (AMI) has become the most common cause of death in the developed countries. However, its pathogenesis is poorly understood. Increasing studies have revealed that lncRNAs are important modulators of AMI development. This study aimed to explore the function of lncRNA noncoding repressor of nuclear factor of activated T cells (NRON) in hypoxia/reoxygenation (H/R)-stimulated H9c2 cells. NRON expression in peripheral blood of AMI patients and H/R-stimulated H9c2 cells was measured by quantitative real-time polymerase chain reaction. H9c2 cells were transfected with si-NRON or cotransfected with si-NRON and si-hypoxia-inducible factor-1 alpha (HIF-1alpha). The viability and apoptosis of these cells were evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay and flow cytometer, respectively. In addition, HIF-1alpha, AKT/mTOR signal pathways and ERK1/2 were detected by western blot. NRON knockdown in the myocardial infarction mouse model was conducted through adeno-associated virus injection, and cardiac function was evaluated by motion-mode echocardiography. The results showed that NRON was highly expressed in peripheral blood of AMI patients and H/R-stimulated H9c2 cells. NRON knockdown promoted cell viability and inhibited cell apoptosis of H/R-stimulated H9c2 cells. Meanwhile, NRON knockdown also significantly attenuated heart damage and improved cardiac function in an AMI mouse model. Furthermore, compared with si-normal control, NRON knockdown increased the levels of HIF-1alpha, p-AKT, p-mTOR, and p-ERK1/2. HIF-1alpha knockdown reversed the effects of NRON knockdown in H/R-stimulated-H9c2 cells damage. Overall, our study revealed that NRON knockdown alleviated H/R-induced cardiomyocyte apoptosis by upregulating HIF-1alpha expression, suggesting that NRON might be a novel therapeutic target for AMI.	34935702	RID08282	expression association	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Gastric cancer	SOD2	DE5RT	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	apoptosis process(+);	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000112096	GRCh38_6:159669069-159762529	NA	NA	6648	NA	GClnc1	NA	Gastric cancer (GC) is a complicated multifactorial neoplasm with a high fatality and prevalence rate around the globe that required the discovery of many unknown mechanisms involved in its inception and progression. The aim of this project was to investigate the alterations of GClnc1 expression in cancerous tissues relative to marginal non-cancerous tissues of patients with GC and its association with clinicopathological features. In this research, the expression level of GClnc1 was assessed using the qRT-PCR For this, 80 pairs of cancerous and marginal non-cancerous GC samples tissues were gathered. Then RNA isolation and cDNA synthesis were carried out. Eventually, the difference of GClnc1 expression levels in tumor tissue relative to marginal non-tumor tissue specimens of GC patients and its association with pathological characteristics, as well as biomarker's performance of GClnc1, was investigated. Expression data examination of GClnc1 indicates increased expression in GC tumor tissues relative to marginal non-cancerous tissues (p < 0.0001). GClnc1 overexpression was significantly linked with pathological features of patients with lymph node metastasis (p = 0.037) and H. pylori infection (p = 0.029). Based on ROC analysis, the GClnc1 as a biomarker has AUC, sensitivity%, and specificity% of 0.8228, 90%, and 61.67%, respec-tively (p < 0.0001). Due to the GClnc1 increased expression in tumor tissues of GC patients, our research proposed that GClnc1 may be involved in the promotion and development of GC cells as a novel oncogene. Besides, in the molecular targeted therapies of GC patients, GClnc1 can be considered as a potential biomarker.	34910430	RID08283	expression association	metastasis	DOWN(BRCA);DATA(GSE111065,GSE75367,GSE86978)	
Sepsis	GSEC	PFKFB3	positively-E	RT-qPCR	upregulation	RT-PCR	GSE13904;GSE28750;GSE64457	NA	inflammatory response(+)	interact with mRNA	regulation	NA	NA	NA	Evading Apoptosis	Disease by infectious agent	Bacterial infectious disease	lncRNA	PCG	ENSG00000280832	GRCh38_11:126340882-126355587	ENSG00000170525	NA	399972	5209	DCPS-AS1|FLJ39051|ST3GAL4-AS1	NA	Long noncoding RNA GSEC promotes neutrophil inflammatory activation by supporting PFKFB3-involved glycolytic metabolism in sepsis. Metabolic reprogramming is a hallmark of neutrophil activation in sepsis. LncRNAs play important roles in manipulating cell metabolism; however, their specific involvement in neutrophil activation in sepsis remains unclear. Here we found that 11 lncRNAs and 105 mRNAs were differentially expressed in three transcriptome datasets (GSE13904, GSE28750, and GSE64457) of gene expression in blood leukocytes and neutrophils of septic patients and healthy volunteers. After Gene Ontology biological process analysis and lncRNA-mRNA pathway network construction, we noticed that GSEC lncRNA and PFKFB3 were co-expressed and associated with enhanced glycolytic metabolism. Our clinical observations confirmed the expression patterns of GSEC lncRNA and PFKFB3 genes in neutrophils in septic patients. Performing in vitro experiments, we found that the expression of GSEC lncRNA and PFKFB3 was increased when neutrophils were treated with inflammatory stimuli. Knockdown and overexpression experiments showed that GSEC lncRNA was essential for mediating PFKFB3 mRNA expression and stability in neutrophil-like dHL-60 cells. In addition, we found that GSEC lncRNA-induced PFKFB3 expression was essential for mediating dHL-60 cell inflammatory cytokine expression. Performing mechanistic experiments, we found that glycolytic metabolism with PFKFB3 involvement supported inflammatory cytokine expression. In summary, our study uncovers a mechanism by which GSEC lncRNA promotes neutrophil inflammatory activation in sepsis by supporting glycolytic metabolism with PFKFB3.	34907156	RID08284	interact with mRNA	NA	DOWN(BRCA);DATA(GSE111842,GSE51827)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Ovarian cancer	MALAT1	TGFB1	negatively-E	proteomic analysis;functional tests; analysis of epithelial-mesenchymal transition (EMT) drivers; western blot;	upregulation	RT-PCR	NA	NA	cell motility(-);cell invasion(-)	interact with mRNA	regulation	NA	NA	CSC	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000105329	NA	378938	7040	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CED|DPD1|IBDIMDE|LAP|TGF-beta1|TGFB|TGFbeta	The aim of this study was to analyze the biological role of different transforming growth factor-beta (TGFbeta) receptor splice variants in ovarian carcinoma (OC). Specific receptor variant knockouts (KO) were prepared using the CRISPR/Cas9 genome editing system in two OC cell lines, TbetaRI variant 1 (TbetaRIv1) KO in ES-2 cells and TbetaRII variant 1 (TbetaRIIv1) KO in OVCAR-8 cells. Control and KO cells were compared by proteomic analysis, functional tests, analysis of epithelial-mesenchymal transition (EMT) drivers, and western blot of signaling proteins. Proteomic analysis revealed significant changes in protein pathways in the KO cells. TbetaRIv1 KO resulted in a significant reduction in both cellular motility and invasion, while TbetaRIIv1 KO significantly reduced cellular motility and increased Reactive Oxygen Species (ROS) production. Both receptor variant KOs reduced MET protein levels. Of the EMT drivers, a significant decrease in TWIST protein expression, and increase in SNAIL protein and  MALAT1  mRNA levels were observed in the TbetaRIIv1 KO compared to control. A significant decrease in JNK1 and JNK2 activation was found in the TbetaRIv1 KO compared to control cells. These findings provide new insight regarding the biological role of the TGFbeta receptor variants in the biology and potentially the progression of OC.	34884451	RID08285	interact with mRNA	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Lung cancer	XIST	IL6	positively-E	luciferase reporter assay;siRNA	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-let-7c)	regulation	NA	Cucurbitacin B	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136244	NA	7503	3569	DXS1089|DXS399E|LINC00001|NCRNA00001|swd66	BSF2|HGF|HSF|IFNB2|IL-6	Cucurbitacin B regulates lung cancer cell proliferation and apoptosis via inhibiting the IL-6/STAT3 pathway through the lncRNA XIST/miR-let-7c axis.CuB treatment inhibited the proliferation of lung cancer cells and promoted cell apoptosis, and increased the expression of Bax and cleaved caspase3, decreased cyclin B1 and Bcl-2 expression. CuB suppressed XIST and IL-6 expression, and enhanced miR-let-7c expression. XIST silencing enhanced the inhibitory effect of CuB on cell proliferation and the promotion effect on apoptosis via upregulating miR-let-7c. Moreover, XIST targeted miR-let-7c to activate the IL-6/STAT axis. MiR-let-7c overexpression enhanced the regulatory effect of CuB on proliferation and apoptosis via suppressing the IL-6/STAT3 pathway.We screened miRNAs containing binding sites with XIST and IL-6 by bioinformatics software (starBase and RAID v2.0) (Figure 4(A)). Through the pre-experiment, we found that the expression of miR-let-7c in A549 cells was significantly elevated by CuB treatment, while there was no obvious change in the other targeted miRNAs (Figure 4(B)). To explore the relationship between miR-let-7c and XIST or IL-6, we predicted the binding site of XIST to miR-let-7c, and the binding site of miR-let-7c to IL-6 (Figure 4(C)). The dual-luciferase reporter gene assay showed that wild-type XIST and miR-let-7c mimics combined to reduce the luciferase activity, while the luciferase activity of mutant XIST was not significantly different, and wild-type IL-6 and miR-let-7c mimics combined to reduce the luciferase activity, while the luciferase activity of mutant IL-6 was not changed (Figure 4(D)). The expression of miR-let-7c in A549 cells significantly increased after the knockdown of XIST (Figure 4(E)). Moreover, the level of miR-let-7c was markedly upregulated after miR-let-7c overexpression and was downregulated after the knockdown of miR-let-7c (Figure 4(F)). Moreover, the mRNA level of IL-6 was markedly reduced following miR-let-7c overexpression, while was obviously elevated by miR-let-7c inhibition (Figure 4(F)). western blot showed miR-let-7c overexpression suppressed the protein level of p-STAT3, while knockdown of miR-let-7c showed the opposite effect (Figures 4(G,H)). Taken together, XIST targeted miR-let-7c to positively regulate the IL-6/STAT3 pathway.	34967707	RID08286	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827)	DOWN(BRCA);DATA(GSE75367,GSE86978)
Parkinson's disease	MIAT	TGFBR1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	inflammatory response(+);oxidative stress(+)	ceRNA(miR-221-3p)	regulation	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000106799	NA	440823	7046	C22orf35|FLJ25967|gomafu|LINC00066|lncRNA-MIAT|NCRNA00066|Rncr2	ACVRLK4|ALK-5|ALK5|ESS1|MSSE|TBR-i|TBRI	Long non-coding RNA myocardial infarction-associated transcript promotes 1-Methyl-4-phenylpyridinium ion-induced neuronal inflammation and oxidative stress in Parkinson's disease through regulating microRNA-221-3p/ transforming growth factor /nuclear factor E2-related factor 2 axis.This study attempted to evaluate the role of long non-coding RNA myocardial infarction-associated transcript (LncRNA MIAT) in Parkinson's disease (PD). The mouse model was established through intraperitoneal injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and in vitro model was induced by administrating cell with 1-Methyl-4-phenylpyridinium ion (MPP+). Rotarod test was conducted to evaluate the motor coordination of PD mice. In order to investigate the roles of LncRNA MIAT in neuronal inflammation and oxidative stress, MIAT shRNA (shMIAT) was transfected into MPP+-treated cells, and cell viability, cell apoptosis and oxidative stress response were evaluated. To evaluate the interactions between LncRNA MIAT and microRNA-221-3p (miR-221-3p)/TGF-beta1/Nrf2, miR-221-3p mimic, miR-221-3p inhibitor, NC-inhibitor and transforming growth factor-beta1 shRNA (shTGF-beta1) were subsequently transfected into MPP+-treated cells. Dual-luciferase reporter gene assays were performed to determine the interaction of miR-221-3p with MIAT or TGFB receptor 1 (TGFBR1). The expressions of LncRNA MIAT, miR-221-3p, TGFBR1, transforming growth factor (TGF-beta1) and nuclear factor E2-related factor 2 (Nrf2) were measured by quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and immunoblotting. As a result, LncRNA MIAT was abundantly expressed in PD mice and cells, while downregulation of LncRNA MIAT promoted the survival of neurons, inhibited apoptosis and oxidative stress in neurons. LncRNA MIAT bound to miR-221-3p, and there was a negative correlation between miR-221-3p and LncRNA MIAT expression. In addition, miR-221-3p targeted TGFBR1 and suppressed TGF-beta1 expression but increased Nrf2 expression. LncRNA MIAT promoted MPP+-induced neuronal injury in PD via regulating TGF-beta1/Nrf2 axis through binding with miR-221-3p.	34967706	RID08287	ceRNA or sponge	NA	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)
Parkinson's disease	SNHG10	IRS2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-1277-5p)	regulation	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000247092	GRCh38_14:95521943-95534889	ENSG00000185950	NA	283596	8660	C14orf62|FLJ40557|LINC00063|NCRNA00063	NA	Knockdown of small nucleolar RNA host gene 10 (SNHG10) alleviates the injury of human neuroblastoma cells via the miR-1277-5p/insulin substrate receptor 2 axis.Parkinson's disease is a common neurodegenerative disease with a complex physio-pathology. So far, there is no effective medical strategies to prevent the progression of Parkinson's disease. Understanding the mechanisms underlying the progression of Parkinson's disease could provide insights into the formulation of novel preventative or treatment strategies. Small nucleolar RNA host gene 10 (SNHG10) is a lncRNA which has been implicated in the development of many cancers. However, its potential role in Parkinson's disease remains unknown. In this study, we found that SNHG10 was upregulated while miR-1277-5p was downregulated in the Parkinson's disease cell model of 1-Methyl-4-phenyl-pyridine ion (MPP+) induced SH-SY5Y cells. We further revealed that SNHG10 sponged miR-1277-5p to negatively regulate its expression, and miR-1277-5p could bind to the 3'UTR of insulin substrate receptor 2 (IRS2) mRNA to suppress its expression. These data suggest that SNHG10 regulates IRS2 through interacting with miR-1277-5p in the cell model of Parkinson's disease. Through a series of molecular experiments and functional assays, we demonstrated that downregulating SNHG10 in the cell model of Parkinson's disease attenuated the cell injury by reducing the expression of IRS2. Meanwhile, inhibiting miR-1277-5p or overexpressing IRS2 could partially reverse the effect of SNHG10 knockdown. In summary, our data indicate that knockdown of SNHG10 mitigates MPP+ induced damage in SH-SY5Y cells via the miR-1277-5p/IRS2 axis.	34967697	RID08288	ceRNA or sponge	NA	UP(PRAD,SKCM);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE51827)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE111842,GSE109761,GSE111065,GSE75367,GSE86978)
Nasopharynx carcinoma	LINC00839	miR-454-3p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000185904	GRCh38_10:42475480-42495337	NA	NA	84856	NA	NA	NA	LINC00839 knockdown restrains the metastatic behavior of nasopharyngeal carcinoma by sponging miR-454-3p.Long intergenic non-coding RNA 00839 (LINC00839) has been verified as a pro-metastasis factor in malignancies. However, the significance of LINC00839 in nasopharyngeal carcinoma (NPC) has yet to be illuminated, as well as its underlying mechanism. Here, we disclosed that LINC00839 is highly expressed in NPC. Deletion of LINC00839 suppresses NPC cells rapid growth, invasive capacity and EMT in vitro. Besides, LINC00839 is identified as a "sponge" for miR-454-3p, and upregulation of LINC00839 reverses miR-454-3p-mediated inhibition of aggressiveness in NPC cells. Furthermore, the expression of cellular-mesenchymal epithelial transition factor (c-Met), the downstream target of miR-454-3p, is downregulated by LINC00839 knockdown in NPC cells. In vivo, LINC00839 knockdown retards the tumor growth of NPC cells in the xenografted mice model. Collectively, attenuation of LINC00839 expression attenuates the aggressive properties of NPC cells via directly sponging the miR-454-3p and regulating c-Met expression.	34965215	RID08289	ceRNA or sponge	metastasis	UP(SKCM);DATA(GSE38495)	
Ovarian cancer	UBA6-DT	UBA6	positively-F	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	m6A methylation	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000248049	GRCh38_4:67701209-68080952	ENSG00000033178	NA	550112	55236	LOC550112|UBA6-AS1	FLJ10808|UBE1L2	Long noncoding RNA UBA6-AS1 inhibits the malignancy of ovarian cancer cells via suppressing the decay of UBA6 mRNA.As the antisense RNA of UBA6, we first investigated whether UBA6-AS1 associates with UBA6 and regulates its expression. The result of subcellular fractionation assay demonstrated that UBA6-AS1 was mainly distributed in cytoplasm Figure 1(a), indicating that UBA6-AS1 could regulate target RNAs in a posttranscriptional manner. To detect the interaction between UBA6-AS1 and UBA6 mRNA, the RNA pull-down assay was performed. As shown in Figure 1(b), UBA6 mRNA could be significantly enriched by biotin-labeled UBA6-AS1, but not by the negative control lncRNA HOX transcript antisense RNA (HOTAIR). For further confirmation, we conducted a MS2-RIP followed by qRT-PCRanalysis Figure 1(c). It was demonstrated that the UBA6-AS1 RIP was markedly enriched for UBA6 mRNA compared to the empty vector, IgG, or UBA6 binding sites mutated UBA6-AS1 (UBA6-AS1-mut) Figure 1(d). Moreover, as evidenced by the results of qRT-PCRand western blot experiments, knockdown of UBA6-AS1 significantly decreased both mRNA and protein levels of UBA6, while overexpression of UBA6-AS1 elevated the UBA6 expression Figure 1(e,f). To examine whether UBA6-AS1 regulates the stability of UBA6 mRNA, different clones of OVCAR3 and SKOV3 were treated with actinomycin D, an RNA synthesis inhibitor, and the degradation of UBA6 mRNA was detected at different time points. UBA6-AS1 knockdown significantly accelerated the decay of UBA6 mRNA. Conversely, overexpression of UBA6-AS1 elongated the half-life of UBA6 mRNA Figure 1(g). Taken together, these results suggest that UBA6-AS1 associates with UBA6 mRNA and represses its degradation.Then, the functional role of UBA6-AS1 was investigated in OC cells. Cell proliferation detection using CCK-8 assay showed that overexpression of UBA6-AS1 significantly repressed the proliferation ability of both OVCAR3 and SKOV3 cells, which was rescued by transfection of UBA6 shRNA Figure 4(a,b). Furthermore, the cell migration and invasion were tested using transwell assays. Overexpression of UBA6-AS1 significantly attenuated the motility and invasiveness of OC cells, while knockdown of UBA6 abolished this suppression Figure 4(c-d). These data suggest that UBA6-AS1 inhibits the malignant behaviors of OC cells via UBA6.Finally, the clinical significance of UBA6-AS1 and UBA6 expression was investigated. The UBA6-AS1 and UBA6 mRNA in 60 pairs of OC and matched normal ovary tissues were examined using qRT-PCR It was shown that both UBA6-AS1 and UBA6 mRNA was markedly downregulated in OC tissues compared to normal tissues Figure 4(e-f). Additionally, correlation analysis revealed that UBA6-AS1 positively correlated with UBA6 mRNA in OC tissues Figure 4(g). Furthermore, we assessed the prognostic values of UBA6-AS1 and UBA6 expression using Kaplan-Meier method and found that patients with higher UBA6-AS1 or UBA6 expression always had longer median overall survival as compared with those with lower UBA6-AS1 or UBA6 expression Figure 4(h,i). These data suggest a prognostic value of UBA6-AS1 and UBA6 expression for OC patients.	34951345	RID08290	epigenetic regulation	prognosis		UP(LIHC,SKCM);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE67980,GSE104209,GSE60407,GSE38495,GSE51827,GSE55807,GSE67939,GSE86978)
Gastric cancer	NPTN-IT1	miR-548k	negatively-F	luciferase reporter assay;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000281183	GRCh38_15:73567012-73569294	NA	NA	101241892	NA	lncRNA-LET	NA	HDAC3-Mediated Repression of LncRNA-LET Regulates Gastric Cancer Cell Growth Proliferation, Invasion, Migration, and Apoptosis via MiR-548k.Emerging studies have indicated the aberrant expression of histone deacetylases (HDACs) is closely associated with the development of tumors. However, the regulatory roles of HDACs-regulated long noncoding RNAs (lncRNA) in gastric cancer (GC) remain largely unknown. In this study, the effects of HDAC3 and HDAC3-mediated lncRNA-LET on the progression of GC were investigated. The expressions of HDAC3, lncRNA-LET, and miR-548k in GC cell lines were analyzed. The biological functions of HDAC3 and lncRNA-LET were measured by CCK-8 assay, Transwell assay, western blot and cell apoptosis assays. Chromatin immunoprecipitation and luciferase reporter assay verified the regulatory relationship between HDAC3 and lncRNA-LET, and lncRNA-LET and miR-548 in GC cells. HDAC3 was significantly overexpressed in GC cell lines compared to GES-1. Knockdown of HDAC3 suppressed the proliferation, invasion, and migration of AGS and SGC-7901 cells, while cell apoptosis was promoted. Silenced HDAC3 promoted histone acetylation in the promoter region of lncRNA-LET, subsequently upregulating the expression of lncRNA-LET in AGS and SGC-7901 cells. In addition, overexpressed lncRNA-LET notably inhibited the proliferation, invasion, and migration of GC cells, whereas apoptosis was enhanced. LncRNA-LET could function as the sponge of miR-548k. HDAC3 was able to regulate the progression of GC cells via the lncRNA-LET/miR-548k signaling pathway. We confirmed that the HDAC3/lncRNA-LET/miR-548k signal axis mediated the occurrence and development of GC, and HDAC3 could be a novel therapeutic target for the treatments of GC.	34936297	RID08291	ceRNA or sponge	NA	UP(LIHC);DOWN(PAAD,SKCM,BRCA);DATA(GSE117623,GSE60407,GSE38495,GSE51827,GSE55807,GSE86978)	
Psoriasis	AGAP2-AS1	AKT3	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);AKT/mTOR signaling pathway	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000117020	NA	100130776	10000	LOC100130776|PUNISHER	PKBG|PRKBG|RAC-gamma	N 6-methyladenosine-modified long non-coding RNA AGAP2-AS1 promotes psoriasis pathogenesis via miR-424-5p/AKT3 axis.We found that AGAP2-AS1 level was upregulated in the skin tissue of psoriasis patients than that of healthy controls and AGAP2-AS1 could promote proliferation and inhibit apoptosis of keratinocytes. Methyltransferase like 3(METTL3)-mediated m6A modification suppressed the expression of AGAP2-AS1 via YTHDF2-dependent AGAP2-AS1 stability. Thus, downregulation of METTL3 resulted in the upregulation of AGAP2-AS1 in psoriasis. AGAP2-AS1 functioned as a competitive endogenous RNA by sponging miR-424-5p to upregulate AKT3, activate AKT/mTOR pathway, as well as promote cell proliferation in keratinocytes.	34930676	RID08292	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE86978)	DOWN(PRAD,BRCA);DATA(GSE67980,GSE104209,GSE111842,GSE109761,GSE55807,GSE67939)
Hepatocellular carcinoma	SNHG17	CDKN1C	negatively-E	western blot;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000129757	NA	388796	1028	NA	BWCR|BWS|KIP2|P57	Long Non-Coding RNA Small Nucleolar RNA Host Gene 17 Promotes Hepatocellular Carcinoma Progression by Inhibiting p57 Expression.	34921029	RID08293	expression association	NA	DOWN(LIHC,PRAD);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE38495,GSE109761,GSE111065,GSE55807)	DOWN(LIHC,PRAD,BRCA);UP(SKCM);DATA(GSE117623,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065)
Urinary bladder cancer	TUG1	FOXQ1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-320a)	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000164379	NA	55000	94234	FLJ20618|LINC00080|NCRNA00080	HFH1	LncRNA TUG1 promotes bladder cancer malignant behaviors by regulating the miR-320a/FOXQ1 axis.TUG1 was significantly higher expression in BC specimens and cell lines. TUG1 knockdown suppressed BC cells malignant behaviors in vitro and inhibited tumor growth and metastasis in vivo, while TUG1 overexpression promoted BC cells malignant behaviors in vitro. However, the function of miR-320a was opposite to that of TUG1, and miR-320a inhibitor partially eliminated the inhibitory effect of TUG1 knockdown on the malignant behavior of BC cells. As a microRNA sponge, TUG1 actively elevated FOXQ1 expression to sponge miR-320a and subsequently promoted BC cells malignant phenotypes.	34920123	RID08294	ceRNA or sponge	metastasis	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	UP(PAAD);DATA(GSE40174)
Melanoma	TEX41	C1QB	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-103a-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Melanoma	lncRNA	PCG	ENSG00000226674	GRCh38_2:144666312-145262988	ENSG00000173369	NA	401014	713	DKFZp686O1327|LINC00953	NA	IRF4-activated TEX41 promotes the malignant behaviors of melanoma cells by targeting miR-103a-3p/C1QB axis.Results: IRF4 up-regulated TEX41 at the transcriptional level in melanoma cells. TEX41 knockdown hindered melanoma cell proliferation, migration and invasion while promoting cell apoptosis. TEX41 bound to miR-103a-3p and regulated C1QB. The suppressive impact of TEX41 depletion on melanoma cell malignant behaviors could be counteracted by miR-103a-3p inhibition or C1QB overexpression. Moreover, IRF4 could facilitate melanoma cell growth via up-regulating C1QB.	34915882	RID08295	ceRNA or sponge	NA	UP(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE51827)	
Melanoma	IRF4	TEX41	positively-E	luciferase reporter assay;ChIP;overexpression;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Melanoma	TF	lncRNA	ENSG00000137265	NA	ENSG00000226674	GRCh38_2:144666312-145262988	3662	401014	LSIRF|MUM1	DKFZp686O1327|LINC00953	IRF4-activated TEX41 promotes the malignant behaviors of melanoma cells by targeting miR-103a-3p/C1QB axis.Results: IRF4 up-regulated TEX41 at the transcriptional level in melanoma cells. TEX41 knockdown hindered melanoma cell proliferation, migration and invasion while promoting cell apoptosis. TEX41 bound to miR-103a-3p and regulated C1QB. The suppressive impact of TEX41 depletion on melanoma cell malignant behaviors could be counteracted by miR-103a-3p inhibition or C1QB overexpression. Moreover, IRF4 could facilitate melanoma cell growth via up-regulating C1QB.	34915882	RID08296	expression association	NA	DOWN(BRCA);DATA(GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)	UP(LIHC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE51827)
Hepatocellular carcinoma	ENST	NKX2-5	positively-E	overexpression;knockdown	downregulation	qRT-PCR	NA	NA	warburg effect(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	NA	ENSG00000183072	NA	NA	1482	NA	CSX|CSX1|NKX2.5|NKX2E|NKX4-1	lncENST Suppress the Warburg Effect Regulating the Tumor Progress by the Nkx2-5/ErbB2 Axis in Hepatocellular Carcinoma.We first verified the role of lncENST in RFA-mediated HCC inhibition and the specific phenomena implicated therein. An in vitro model of HCC was established using SMMC-7721 cells, which were transfected with either lncENST overexpression (lnc-OV) or interference (lnc-INT) vectors (Figure 1(a)). Sublethal heat treatment was applied to simulate RFA, and the growth behavior of transfected cells was monitored after heat stress. Heat-treated cells in which lncENST was silenced proliferated to a greater extent than did nontransfected cells, whereas those that overexpressed lncENST showed reduced proliferative ability (Figure 1(b)). The results of proliferation are complemented by apoptotic behavior (Figure 1(c)), whereby lnc-OV led to remarkable apoptosis (27.1%) in heat-treated cells and lnc-INT suppress the apoptosis (6.34%) compared to that of nontransfected cells (control, 9.4%).We proceeded to evaluate whether a targeting relationship exists between lncENST and ErbB2. After SMMC-7721 cells were transfected with lnc-OV or lnc-INT, they exhibited reduced and elevated mRNA expression of ErbB2, respectively (Figure 4(a)). Expectedly, ErbB2 protein expression followed the same trend (Figure 4(b)). In vivo experiments were also performed in nude mice subjected to tumor xenografts of HCC cells transfected with either lnc-OV or lnc-INT. The animals were accordingly treated with RFA, and ErbB2 expression was measured in tumor tissues. As anticipated, the RFA-treated tissues showed relatively lower mRNA and protein expression of ErbB2 than their nontreated counterparts, but in the same general tendency (Figures 4(c) and 4(d)).	34912471	RID08297	expression association	NA		UP(LIHC,PAAD);DATA(GSE117623,GSE40174)
Laryngeal squamous cell carcinoma	SNHG16	NFAT5	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Larynx cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557733-76565357	ENSG00000102908	NA	100507246	10725	Nbla10727|Nbla12061|ncRAN	KIAA0827|NF-AT5|NFATL1|NFATZ|OREBP|TONEBP	LncRNA SNHG16 promotes proliferation and migration in laryngeal squamous cell carcinoma via the miR-140-5p/NFAT5/Wnt/beta-catenin pathway axis.First, RT-qPCR demonstrated the upregulation of SNHG16 in LSCC cells and tissues. Loss-of-function assays determined the inhibitive influence of SNHG16 downregulation on cell viability, growth, and migration in LSCC. Furthermore, SNHG16 bound with miR-140-5p in LSCC. MiR-140-5p overexpression suppressed LSCC cell proliferation and migration. NFAT5 was identified as a direct target of miR-140-5p. Through rescue experiments, overexpression of NFAT5 reversed SNHG16 knockdown-mediated suppression on cell viability, growth, and migration in LSCC. Additionally, NFAT5 overexpression activated while NFAT5 downregulation inhibited the Wnt/beta-catenin signaling pathway.	34911016	RID08298	ceRNA or sponge	NA	DOWN(LIHC,PRAD,PAAD,BRCA);UP(SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)	UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE51827,GSE55807)
Skin squamous cell carcinoma	PICSAR	MIR573	negatively-F		upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	sponge	binding/interaction	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Skin carcinoma	lncRNA	miRNA	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000207697	NA	378825	693158	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	MIRN573|hsa-mir-573|mir-573	MicroRNA-573 inhibits cell proliferation, migration and invasion and is downregulated by PICSAR in cutaneous squamous cell carcinoma.The incidence of cutaneous squamous cell carcinoma (cSCC) has been increasing in recent years. Meanwhile, microRNAs (miRNAs) have been found to play vital roles in various cancers, including cSCC. This study aimed to investigate the expression of microRNA-573 (miR-573) in cSCC, its relationship with long non-coding RNA PICSAR and analyze its biological role. The relationship between PICSAR and miR-573 was confirmed by dual-luciferase reporter assay and Pearson's correlation coefficient analysis. The levels of PICSAR and miR-573 were measured using quantitative Real-Time PCR. Cell Counting Kit-8 assay was used to evaluate the cSCC cell proliferation ability. The migration and invasion abilities of cSCC cells were evaluated by Transwell assay. PICSAR expression was increased and miR-573 was decreased in tumor tissues and cSCC cell lines. PICSAR and miR-573 can bind directly, and miR-573 expression was downregulated by PICSAR in cSCC. Overexpression of miR-573 significantly inhibited the proliferation, migration and invasion abilities of A431 and SCC13 cells. Additionally, miR-573 overexpression reversed the promotion effects of PICSAR overexpression on cSCC cell proliferation, migration and invasion abilities. In conclusion, our findings indicated that miR-573 expression was decreased in tumor tissues and cSCC cells and was downregulated by PICSAR in cSCC. Additionally, miR-573 overexpression inhibited cSCC cell proliferation, migration and invasion, and reversed the promotion effects of PICSAR overexpression on cSCC cell biological functions. Thus, miR-573 might function as a tumor suppressor and might be involved in the regulatory effects of PICSAR on tumorigenesis in cSCC.	34905724	RID08299	ceRNA or sponge	NA		
Liver fibrosis	GAS5	TLR10	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	NF-kB signaling pathway(+)	ceRNA(miR-433-3p)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000174123	NA	60674	81793	NCRNA00030|SNHG2	CD290	Long noncoding RNA GAS5 inhibits LX-2 cells activation by suppressing NF-kB signalling through regulation of the miR-433-3p/TLR10 axis.Results: GAS5 and TLR10 were decreased while miR-433-3p was upregulated in TGF-beta1-activated LX-2 cells. Upregulation of GAS5 or downregulation of miR-433-3p suppressed HSC activation, and luciferase assays indicated that miR-433-3p binds with GAS5 and the 3'-UTR of TLR10. MiR-433-3p upregulation and TLR10 downregulation rescued the impacts of GAS5 overexpression or miR-433-3p knockdown on LX-2 cells. Upregulation of GAS5 also suppressed the phosphorylation of NF-kB through the miR-433-3p/TLR10 axis.	34903500	RID08300	ceRNA or sponge	NA	DOWN(LIHC,PRAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE111842,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978,GSE41245)
Cholangiocarcinoma	TTN-AS1	SFN	positively-E	luciferase reporter assay;RIP		RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);	ceRNA(miR-513a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000175793	NA	100506866	2810	NA	YWHAS	Long non-coding RNA titin-antisense RNA1 contributes to growth and metastasis of cholangiocarcinoma by suppressing microRNA-513a-5p to upregulate stratifin.Cholangiocarcinoma (CCA) is one of the most common histological types of primary hepatic malignancy and is associated with poor overall prognosis, causing a ponderous burden on human life. Hence, it is necessary to elucidate the pathogenesis of CCA. The objective of our research was to shed light on the mechanism through which long non-coding RNA titin-antisense RNA1 (lncRNA TTN-AS1) is involved in the development of CCA. Reverse transcription quantitative polymerase chain reaction was used to detect TTN-AS1 expression in CCA samples and cells. Functional experiments were performed using the Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, transwell, and in vivo tumor growth assays. The relationship between TTN-AS1, miR-513a-5p, and stratifin (SFN) was explored using a dual-luciferase reporter assay, RNA immunoprecipitation (RIP) experiment, and Pearson correlation analysis. The result showed that TTN-AS1 and SFN are highly expressed in CCA tissues. Bioinformatics analysis, luciferase reporter and RIP experiments revealed the correlation between TTN-AS1, miR-513a-5p, and SFN. In addition, silencing TTN-AS1 mitigated CCA cell proliferation and migration. Mechanistically, miR-513a-5p is sponged by TTN-AS1. The miR-513a-5p inhibitor abolished the effect of TTN-AS1 silencing on the aggressive behaviors of CCA cells. Furthermore, we showed that miR-513a-5p is a regulator of CCA by targeting SFN. TTN-AS1 induced CCA cell growth and metastasis via the miR-513a-5p/SFN pathway, which offers a new strategy for therapeutic interventions for CCA.	34903127	RID08301	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC);UP(PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Osteoarthritis	MSC-AS1	JAK2	positively-E	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-369-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000235531	GRCh38_8:71828167-72118393	ENSG00000096968	NA	100132891	3717	NA	JTK10	Long non-coding RNA musculin antisense RNA 1 promotes proliferation and suppresses apoptosis in osteoarthritic chondrocytes via the microRNA-369-3p/Janus kinase-2/ signal transducers and activators of transcription 3 axis.Increasing evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in osteoarthritis (OA). The present study aimed to investigate the underlying molecular mechanism of lncRNA musculin antisense RNA 1 (MSC-AS1) in OA. RT-qPCR was used to detect MSC-AS1 levels in cartilage tissues from patients with OA. The effects of MSC-AS1 knockdown on the viability and apoptosis in OA were evaluated via CCK-8 and TUNEL assays. The StarBase database was used to predict the binding sites between microRNA (miR)-369-3p and MSC-AS1 or JAK2, which were confirmed via the dual-luciferase reporter assay. The results demonstrated that MSC-AS1 expression was downregulated in OA. Functional analysis indicated that the addition of MSC-AS1 promoted viability and inhibited inflammation and the apoptosis of chondrocytes. In addition, MSC-AS1 regulated the survival of OA chondrocytes by sponging miR-369-3p. JAK2 was confirmed as a direct target of miR-369-3p, and MSC-AS1 regulated JAK2/STAT3 signaling via miR-369-3p in OA chondrocytes. Taken together, our results suggest that MSC-AS1 may regulate the miR-369-3p/JAK2/STAT3 signaling pathway to accelerate the viability, and inhibit inflammation and cell apoptosis in OA chondrocytes.	34898365	RID08302	ceRNA or sponge	NA		UP(LIHC,PAAD);DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE86978)
Neuroblastoma	NHEG1	HMGB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-665)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000225391	GRCh38_6:136982165-136993234	ENSG00000189403	NA	100294720	3146	NA	DKFZp686A04236|HMG1|HMG3|SBP-1	Long non-coding RNA NHEG1/hsa-miR-665/HMGB1 axis is involved in the regulation of neuroblastoma progression.In order to investigate the expression level of lncRNA NHEG1 in NB, tumor samples and adjacent normal tissues were collected from 60 NB patients. qRT-PCRwas performed to compare the relative lncRNA NHEG1 expression. Our results showed that lncRNA NHEG1 was significantly upregulated in NB tumors tissues as compared to the adjacent non-cancer tissues (Figure 1a).We next performed CCK-8 cell proliferation assay and colony formation assay after silencing lncRNA NHEG1. We found that downregulation of lncRNA NHEG1 significantly inhibited cell proliferation (Figure 2b) and impaired the clonogenic capacity of NB cells (Figure 2c). We further analyzed the migration and invasion ability of NB cells after silencing lncRNA NHEG1 by transwell experiments. Our results demonstrated that lncRNA NHEG1 knockdown suppressed the migration and invasion of NB cells (Figures 2d, e).Therefore, we selected miR-665 as a candidate target of lncRNA NHEG1 for further investigation. We performed dual-luciferase reporter assay using the construct containing wildtype miR-665 binding sequence of lncRNA NHEG1 (WT-NHEG1) as well as the mutated sequence (MUT-NHEG1). In both SK-N-BE and SH-SY5Y cells, the transfection of miR-665 mimic significantly suppressed the luciferase activity of WT-NHEG1, which was not observed in the MUT-NHEG1 (Figure 3a). These results indicate the functional interaction between miR-665 and lncRNA NHEG1. We further demonstrated that miR-665 expression level was significantly upregulated after lncRNA NHEG1 knockdown in SK-N-BE and SH-SY5Y cells (Figure 3b). The expression level of miR-665 was also lower in NB tissues as compared to that of the adjacent non-cancer tissues (Figure 3c). Pearson correlation analysis further revealed a significant negative correlation between the expression levels of miR-665 and lncRNA NHEG1 in the NB tumor samples (Figure 3d). Kaplan Meier curve analysis revealed that high expression of miR-665 was correlated with a better overall survival (OS) and progression-free survival (PFS) in NB patients (Figures 3e, f). Together, these data suggest that lncRNA NHEG1 targets miR-665 and negatively regulates its expression.Therefore, we speculated that miR-665 might modulate HMGB1 expression in NB. To confirm their functional interaction, we performed dual-luciferase reporter assay using the construct containing wildtype miR-665 binding sequence of HMGB1 3- UTR (WT-HMGB1) as well as the mutated sequence (MUT-HMGB1). The presence of miR-665 mimic significantly inhibited the luciferase activity of WT-HMGB1, which was abrogated in the MUT-HMGB1 (Figure 4a). We further applied miR-665 mimic and inhibitor to study the role of miR-665 on HMGB1 expression. In both SK-N-BE and SH-SY5Y cells, HMGB1 mRNA and protein levels were significantly decreased in the presence of miR-665 mimic while miR-665 inhibitor increased HMGB1 level (Figure 4b). To confirm that miR-665/HMGB1 is downstream of lncRNA NHEG1, we knocked down lncRNA NHEG1 and found the level of HMGB1 was also decreased (Figure 4c). In addition, miR-665 inhibitor rescued the expression level of HMGB1 after lncRNA NHEG1 knockdown (Figure 4c). These results indicate that lncRNA NHEG1 maintains the expression of HMGB1 by negatively affecting the activity of miR-665.	34889712	RID08303	ceRNA or sponge	NA	UP(LIHC);DATA(GSE117623)	DOWN(NSCLC,PRAD,PAAD,BRCA);UP(PAAD,SKCM);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827)
Breast cancer	AGO2	FASLG	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-21-5p)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000117560	NA	27161	356	CASC7|EIF2C2|hAGO2|LINC00980|Q10	APT1LG1|CD178|FasL|TNFSF6	Long non-coding RNA CASC7 suppresses malignant behaviors of breast cancer by regulating miR-21-5p/FASLG axis.To determine the expression pattern of CASC7 in breast cancer, 26 pairs of collected tumor tissues and the paired paracancerous tissues were used to detect the level of CASC7. The expression of CASC7 was inhibited in tumor tissues compared to paracancerous tissues (Figure 1(a)). Meanwhile, we further detected the CASC7 expression in breast cancer cell lines (T47D, MCF-7 and MDA-MB-231) and the normal human epithelial MCF10A cells. The result pointed out that the expressions of CASC7 were also downregulated in breast cancer cells compared to MCF10A cells (Figure 1(b)). Moreover, in MCF-7 and MDA-MB-231 cells, the migration and invasion cells were also affected by CASC7 overexpression. As shown in Figure 2(a), the numbers of migrated cells decline in oe-CASC7 cells compared to the oe-NC cells. Similarly, boosting the CASC7 expression decreased the numbers of invasive cells as well (Figure 2(b)). According to the above results, we revealed that the overexpression of lncRNA CASC7 inhibits the migration and invasion of breast cancer cells.Since lncRNAs commonly play their roles through a ceRNA network, we consequently analyzed the downward potential miRNAs of CASC7. By excavating the underlying binding site on the online database (DIANA-LncBase), miR-21-5p is a potential target of CASC7. The binding site is shown in Figure 3(a). To verify whether lncRNA CASC7 could regulate the miR-21-5p expression, luciferase reporter plasmids were used to examine the interaction between lncRNA CASC7 and miR-21-5p. Before conducting this experiment, we first validated that miR-21-5p mimic could amplify miR-21-5p expression (Figure 3(b)). Subsequently, the cells were co-transfected with miR-21-5p mimic and wild-type luciferase plasmid or mutant luciferase plasmid. MiR-21-5p mimic inhibited the luciferase activity of WT plasmid without affecting the MUT plasmid (Figure 3(c)). Therefore, we investigated miR-21-5p degree in oe-NC and oe-CASC7 breast cancer cells. As shown in Figure 3(d), CASC7 inhibits miR-21-5p expression obviously. Hence, miR-21-5p is downregulated by lncRNA CASC7 in MCF-7 and MDA-MB-231 cellsTo continuously excavate the downward target of miR-21-5p, FASLG is a potential target with high scoring on an online database (http://mirdb.org). The binding site between miR-21-5p and FASLG is shown in Figure 4(a). Similarly, we validated this interaction by luciferase assay. In Figure 4(b), miR-21-5p mimic only decreased the breast cancer cells transfected with WT plasmid, while it did not impact the cells with MUT plasmid. Furthermore, miR-21-5p mimic could inhibit FASLG expression in mRNA and protein levels (Figure 4(c,e)). However, CASC7 overexpression enhanced directly the mRNA and protein levels of FASLG (Figure 4(d,f)). Thus, our data indicated that both the miR-21-5p and CASC7 could regulate FASLG expression in breast cancer cells.	34889164	RID08304	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Diffuse large b-cell lymphoma	HAGLROS	miR-100	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lymphoma	lncRNA	miRNA	ENSG00000226363	GRCh38_2:176177717-176179009	ENSG00000207994	NA	102800310	NA	NA	NA	Long non-coding RNA HAGLROS promotes the development of diffuse large B-cell lymphoma via suppressing miR-100.Results: HAGLROS was upregulated in DLBCL tissues and cells, and closely associated with advanced clinicopathological features. Upregulation of HAGLROS resulted in poor survival outcomes in DLBCL patients. In addition, HAGLROS knockdown inhibited the proliferation, migration, and invasion of DLBCL cells in vitro. Further experiments revealed that HAGLROS negatively regulated the expression of miR-100 in DLBCL, and the expression of miR-100 and HAGLROS showed an inverse correlation in DLBCL tissues. HAGLROS functioned as a competing endogenous RNA for miR-100 in DLBCL cells, and miR-100 overexpression abolished the oncogenic effects of HAGLROS upregulation on DLBCL progression. Besides, in-vivo assays revealed that HAGLROS knockdown suppressed tumor growth in nude mice.	34888946	RID08305	ceRNA or sponge	NA		
Glioma	HOTAIR	UBXN1	positively-E	luciferase reporter assay;ChIRP	upregulation	RT-PCR	NA	NA	NF-kB signaling pathway(+);immune evasion(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000162191	NA	100124700	51035	HOXC-AS4|HOXC11-AS1|NCRNA00072	2B28|LOC51035|SAKS1|UBXD10	HOTAIR Up-Regulation Activates NF-kB to Induce Immunoescape in Gliomas.Results: HOTAIR activated the expression of proteins involved in NF-kB, TNFalpha, MAPK and other inflammatory signaling pathways. In addition, HOTAIR induced various proteins containing protein kinase structural domains and promoted the enrichment of proteins and complexes of important inflammatory signaling pathways, such as the TNFalpha/NF-kB signaling protein complex, the IkB kinase complex, and the IKKA-IKKB complex. In addition, HOTAIR aberrantly activated biological processes involved in glioma immune responses, T-cell co-stimulation and transcription initiation by RNA polymerase II. HOTAIR facilitated the induction of IkBalpha phosphorylation by suppressing the expression of the NF-kB upstream protein UBXN1, promoting NF-kB phosphorylation and nuclear translocation. In vivo, reduction of HOTAIR decreased PD-L1 protein expression, indicating that cells are more likely to be targeted by immune T cells.	34887871	RID08306	epigenetic regulation	NA		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Glioma	HOTAIR	CD274	positively-E	luciferase reporter assay;ChIRP	upregulation	RT-PCR	NA	NA	cytotoxicity(-)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000120217	NA	100124700	29126	HOXC-AS4|HOXC11-AS1|NCRNA00072	B7-H|B7-H1|B7H1|PD-L1|PDCD1LG1|PDL1	HOTAIR Up-Regulation Activates NF-kB to Induce Immunoescape in Gliomas.Results: HOTAIR activated the expression of proteins involved in NF-kB, TNFalpha, MAPK and other inflammatory signaling pathways. In addition, HOTAIR induced various proteins containing protein kinase structural domains and promoted the enrichment of proteins and complexes of important inflammatory signaling pathways, such as the TNFalpha/NF-kB signaling protein complex, the IkB kinase complex, and the IKKA-IKKB complex. In addition, HOTAIR aberrantly activated biological processes involved in glioma immune responses, T-cell co-stimulation and transcription initiation by RNA polymerase II. HOTAIR facilitated the induction of IkBalpha phosphorylation by suppressing the expression of the NF-kB upstream protein UBXN1, promoting NF-kB phosphorylation and nuclear translocation. In vivo, reduction of HOTAIR decreased PD-L1 protein expression, indicating that cells are more likely to be targeted by immune T cells.	34887871	RID08307	expression association	NA		DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE55807,GSE86978)
Atrial fibrillation	H19	miR-29a-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 Drives Proliferation of Cardiac Fibroblasts and Collagen Production via Suppression of the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta Axis.The aim of this study was to investigating whether lncRNA H19 promotes myocardial fibrosis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta axis. Patients with atrial fibrillation (AF) and healthy volunteers were included in the study, and their biochemical parameters were collected. In addition, pcDNA3.1-H19, si-H19, and miR-29a/b-3p mimic/inhibitor were transfected into cardiac fibroblasts (CFs), and proliferation of CFs was detected by MTT assay. Expression of H19 and miR-29a/b-3p were detected using real-time quantitative polymerase chain reaction, and expression of alpha-smooth muscle actin (alpha-SMA), collagen I, collagen II, matrix metalloproteinase-2 (MMP-2), and elastin were measured by western blot The dual luciferase reporter gene assay was carried out to detect the sponging relationship between H19 and miR-29a/b-3p in CFs. Compared with healthy volunteers, the level of plasma H19 was significantly elevated in patients with AF, while miR-29a-3p and miR-29b-3p were markedly depressed (P < 0.05). Serum expression of lncRNA H19 was negatively correlated with the expression of miR-29a-3p and miR-29b-3p among patients with AF (rs = -0.337, rs = -0.236). Moreover, up-regulation of H19 expression and down-regulation of miR-29a/b-3p expression facilitated proliferation and synthesis of extracellular matrix (ECM)-related proteins. SB431542 and si-VEGFA are able to reverse the promotion of miR-29a/b-3p on proliferation of CFs and ECM-related protein synthesis. The findings of the present study suggest that H19 promoted CF proliferation and collagen synthesis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta axis, and provide support for a potential new direction for the treatment of AF.	34887365	RID08308	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Atrial fibrillation	H19	miR-29b-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cardiovascular system disease	Heart disease	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995171-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 Drives Proliferation of Cardiac Fibroblasts and Collagen Production via Suppression of the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta Axis.The aim of this study was to investigating whether lncRNA H19 promotes myocardial fibrosis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta axis. Patients with atrial fibrillation (AF) and healthy volunteers were included in the study, and their biochemical parameters were collected. In addition, pcDNA3.1-H19, si-H19, and miR-29a/b-3p mimic/inhibitor were transfected into cardiac fibroblasts (CFs), and proliferation of CFs was detected by MTT assay. Expression of H19 and miR-29a/b-3p were detected using real-time quantitative polymerase chain reaction, and expression of alpha-smooth muscle actin (alpha-SMA), collagen I, collagen II, matrix metalloproteinase-2 (MMP-2), and elastin were measured by western blot The dual luciferase reporter gene assay was carried out to detect the sponging relationship between H19 and miR-29a/b-3p in CFs. Compared with healthy volunteers, the level of plasma H19 was significantly elevated in patients with AF, while miR-29a-3p and miR-29b-3p were markedly depressed (P < 0.05). Serum expression of lncRNA H19 was negatively correlated with the expression of miR-29a-3p and miR-29b-3p among patients with AF (rs = -0.337, rs = -0.236). Moreover, up-regulation of H19 expression and down-regulation of miR-29a/b-3p expression facilitated proliferation and synthesis of extracellular matrix (ECM)-related proteins. SB431542 and si-VEGFA are able to reverse the promotion of miR-29a/b-3p on proliferation of CFs and ECM-related protein synthesis. The findings of the present study suggest that H19 promoted CF proliferation and collagen synthesis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-beta axis, and provide support for a potential new direction for the treatment of AF.	34887365	RID08309	ceRNA or sponge	NA	UP(NSCLC);DATA(GSE74639)	
Atherosclerosis	AGO2	PIK3CA	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);inflammatory response(+);apoptosis process(-);TLR4/NF-kB signaling pathway(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000121879	NA	27161	5290	CASC7|EIF2C2|hAGO2|LINC00980|Q10	PI3K	lncRNA CASC7 regulates pathological progression of ox-LDL-stimulated atherosclerotic cell models via sponging miR-21 and regulating PI3K/Akt and TLR4/NF-kB signaling pathways.	34887360	RID08310	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978,GSE41245)
Atherosclerosis	AGO2	TLR4	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);inflammatory response(+);apoptosis process(-);TLR4/NF-kB signaling pathway(+);PI3K/AKT signaling pathway(+);	ceRNA(miR-21)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000123908	GRCh38_8:140520156-140635633	ENSG00000136869	NA	27161	7099	CASC7|EIF2C2|hAGO2|LINC00980|Q10	ARMD10|CD284|hToll|TLR-4	lncRNA CASC7 regulates pathological progression of ox-LDL-stimulated atherosclerotic cell models via sponging miR-21 and regulating PI3K/Akt and TLR4/NF-kB signaling pathways.	34887360	RID08311	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)	DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE111842,GSE109761,GSE111065,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	LOC100507144	CD44	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	NA	ENSG00000026508	NA	NA	960	NA	CD44R|CSPG8|HCELL|IN|MC56|MDU2|MDU3|MIC4|Pgp1	LncRNA LOC100507144 acts as a novel regulator of CD44/Nanog/Sox2/miR-302/miR-21 axis in colorectal cancer.Long noncoding RNAs (lncRNAs) appear as vital regulators and biomarkers in many human cancers. LOC100507144 is a validated lncRNA located in the neighborhood of CD44 in a head-to-head configuration, and its expression and function in cancer cells are still unknown. This research aimed to find out more about the expression and function of this lncRNA in colorectal cancer (CRC). Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. Overall, the current study's findings for the first time reveal that LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44/Nanog/Sox2/miR-302/miR-21 axis.	34882869	RID08312	expression association	metastasis		DOWN(LIHC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE67980,GSE104209,GSE60407,GSE111842,GSE51827,GSE67939,GSE75367,GSE86978)
Colorectal cancer	LOC100507144	NANOG	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000111704	NA	NA	79923	NA	FLJ12581|FLJ40451	LncRNA LOC100507144 acts as a novel regulator of CD44/Nanog/Sox2/miR-302/miR-21 axis in colorectal cancer.Long noncoding RNAs (lncRNAs) appear as vital regulators and biomarkers in many human cancers. LOC100507144 is a validated lncRNA located in the neighborhood of CD44 in a head-to-head configuration, and its expression and function in cancer cells are still unknown. This research aimed to find out more about the expression and function of this lncRNA in colorectal cancer (CRC). Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. Overall, the current study's findings for the first time reveal that LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44/Nanog/Sox2/miR-302/miR-21 axis.	34882869	RID08313	expression association	metastasis		UP(LIHC,PAAD);DOWN(BRCA);DATA(GSE117623,GSE40174,GSE67939)
Colorectal cancer	LOC100507144	SOX2	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	NA	NA	ENSG00000181449	NA	NA	6657	NA	NA	LncRNA LOC100507144 acts as a novel regulator of CD44/Nanog/Sox2/miR-302/miR-21 axis in colorectal cancer.Long noncoding RNAs (lncRNAs) appear as vital regulators and biomarkers in many human cancers. LOC100507144 is a validated lncRNA located in the neighborhood of CD44 in a head-to-head configuration, and its expression and function in cancer cells are still unknown. This research aimed to find out more about the expression and function of this lncRNA in colorectal cancer (CRC). Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. Overall, the current study's findings for the first time reveal that LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44/Nanog/Sox2/miR-302/miR-21 axis.	34882869	RID08314	expression association	metastasis		UP(LIHC);DATA(GSE117623)
Colorectal cancer	LOC100507144	MIR302A	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	miRNA	NA	NA	ENSG00000207927	NA	NA	407028	NA	MIRN302|MIRN302A|hsa-mir-302|mir-302a	LncRNA LOC100507144 acts as a novel regulator of CD44/Nanog/Sox2/miR-302/miR-21 axis in colorectal cancer.Long noncoding RNAs (lncRNAs) appear as vital regulators and biomarkers in many human cancers. LOC100507144 is a validated lncRNA located in the neighborhood of CD44 in a head-to-head configuration, and its expression and function in cancer cells are still unknown. This research aimed to find out more about the expression and function of this lncRNA in colorectal cancer (CRC). Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. Overall, the current study's findings for the first time reveal that LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44/Nanog/Sox2/miR-302/miR-21 axis.	34882869	RID08315	expression association	metastasis		
Colorectal cancer	LOC100507144	miR-21	positively-E	siRNA;knockdown	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);cell metastasis(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	miRNA	NA	NA	ENSG00000199004	NA	NA	NA	NA	NA	LncRNA LOC100507144 acts as a novel regulator of CD44/Nanog/Sox2/miR-302/miR-21 axis in colorectal cancer.Long noncoding RNAs (lncRNAs) appear as vital regulators and biomarkers in many human cancers. LOC100507144 is a validated lncRNA located in the neighborhood of CD44 in a head-to-head configuration, and its expression and function in cancer cells are still unknown. This research aimed to find out more about the expression and function of this lncRNA in colorectal cancer (CRC). Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. Overall, the current study's findings for the first time reveal that LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44/Nanog/Sox2/miR-302/miR-21 axis.	34882869	RID08316	expression association	metastasis		
Acute myeloid leukemia	LINC01116	MIR592	negatively-F		upregulation	qRT-PCR	NA	NA	JAK/STAT signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000163364	GRCh38_2:176611464-176637931	ENSG00000207692	NA	375295	693177	TALNEC2	MIRN592|hsa-mir-592|mir-592	Matrine exerted an anti-tumor effect on acute myeloid leukemia via the lncRNA LINC01116/miR-592-mediated JAK/STAT pathway inactivation.As a malignant hematological cancer, acute myeloid leukemia (AML) influences the health of many people. This study explored the anti-AML activity of matrine (a natural-derived alkaloid), as well as the internal molecular mechanism. In vitro, cell viability, apoptosis, and productions of inflammatory cytokines including IL-1beta, IL-6, and TNF-alpha were tested by MTT, Annexin V-FITC/PI staining, and ELISA, respectively. The expression levels of LINC01116 and miR-592 were measured by qRT-PCR Bcl-2 and PCNA expression, and JAK/STAT3 pathway activity were evaluated by western blot. Besides, an AML mouse xenograft model was established to further analyze the anti-AML activity of matrine. We found that matrine suppressed cell proliferation and levels of inflammatory factors, induced cell apoptosis, reduced LINC01116 expression, and raised miR-592 expression in AML cells. LINC01116 directly bound to miR-592 and downregulated its expression. Both LINC01116 overexpression and miR-592 knockdown attenuated the effects of matrine on AML cells. Moreover, miR-592 overexpression reversed the influences of LINC01116 overexpression on matrine-treated AML cells. Matrine inactivated the JAK/STAT3 pathway in AML cells via modulating LINC01116/miR-592. Additionally, matrine inhibited tumor growth via modulating LINC01116/miR-592 in vivo. To sum up, matrine exhibited the anti-AML activity through regulating the LINC01116/miR-592 axis, thereby inactivating the JAK/STAT3 pathway.	34881627	RID08317	ceRNA or sponge	NA	UP(PRAD,SKCM,BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE55807)	
Intervertebral disc degeneration	OIP5-AS1	miR-25-3p	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);ECM degradation(+);inflammatory response(+)	sponge	binding/interaction	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	LncRNA OIP5-AS1 accelerates intervertebral disc degeneration by targeting miR-25-3p.It is obvious that epigenetic processes influence the evolution of intervertebral disc degeneration (IDD). However, its molecular mechanisms are poorly understood. Long noncoding RNAs (lncRNAs) have been validated to exert vital roles in IDD. Therefore, we tested the hypothesis that OIP5-AS1, a potential regulator of IDD, modulates IDD progression. RT-PCRwas utilized to detect levels of OIP5-AS1, miR-25-3p, Collagen II and Aggrecan in IDD tissues and nucleus pulposus cells (NPCs). Immunofluorescence assay measured Collagen II expression. CCK-8, EdU, and flow cytometry estimated the levels of proliferation and apoptosis. Proteins were assessed via western blot. The binding affinity of OIP5-AS1 with miR-25-3p was investigated by luciferase reporter assay. Enzyme-linked immunosorbent assay (ELISA) analyzed the levels of inflammatory factors. OIP5-AS1 was high expressed in IDD tissues and its expression gradually promoted with the increasing of Pfirrmann scores. The cell morphology of NPCs changed into spindle-shaped, and Collagen II expression was low. After OIP5-AS1 was silenced, cell proliferation was boosted whereas both apoptosis and extracellular matrix (ECM) degradation were restrained. In LPS-activated NPCs, OIP5-AS1 depletion also suppressed inflammation response. Further, miR-25-3p was a target of OIP5-AS1. The effects of OIP5-AS1 silence on proliferation, apoptosis, and ECM degradation were reversed upon miR-25-3p downregulation. Moreover, the inhibitory impact of OIP5-AS1 knockdown on the inflammation of LPS-treated NPCs was rescued with miR-25-3p inference. In general, lncRNA OIP5-AS1 exerted its effects in IDD by targeting miR-25-3p, implying the usage of OIP5-AS1/miR-25-3p as a novel regulatory axis for the molecular targets of IDD therapy.	34872452	RID08318	ceRNA or sponge	NA	UP(LIHC);DOWN(NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807)	
Hepatocellular carcinoma	LOXL1-AS1	YY1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);	ceRNA(miR-3614-5p)	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000100811	NA	100287616	7528	NA	DELTA|INO80S|NF-E1|UCRBP|YIN-YANG-1	Study on the mechanism of LOXL1-AS1/miR-3614-5p/YY1 signal axis in the malignant phenotype regulation of hepatocellular carcinoma.Results: We discovered that LOXL1-AS1 was high expressed in HCC cells. Inhibition of LOXL1-AS1 repressed cell proliferation, migration and invasion, but enhanced cell apoptosis in HCC. Further, miR-3614-5p was proven to be sponged by LOXL1-AS1. Additionally, Yin Yang 1 (YY1) was proven as the target gene of miR-3614-5p, and YY1 depletion could repress HCC cell malignant behaviors. YY1 could also transcriptionally activate LOXL1-AS1 expression. In rescue assays, we confirmed that overexpression of YY1 or miR-3614-5p inhibition could reverse the suppressive effects of LOXL1-AS1 silence on the malignant behaviors of HCC cells.	34863279	RID08319	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE111842,GSE111065,GSE75367,GSE86978)
Hepatocellular carcinoma	MIR4435-2HG	B3GNT5	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	ceRNA(miR-126-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111006015-111523376	ENSG00000176597	NA	541471	84002	AGD2|AK001796|LINC00978|lncRNA-AWPPH|MIR4435-1HG|MORRBID	B3GN-T5|beta3Gn-T5	lncRNA MIR4435-2HG promotes the progression of liver cancer by upregulating B3GNT5 expression.Several studies have indicated that dysregulation of long non-coding RNAs (lncRNAs) participates in the initiation and progression of cancer. The lncRNA MIR4435-2HG was previously reported to act as an oncogene in human cancer, including liver cancer. However, its role in the pathogenesis in liver cancer is largely unclear. The present study aimed to reveal the molecular mechanism by which MIR4435-2HG regulates liver cancer. The expression levels of MIR4435-2HG in liver cancer and adjacent normal tissues were analyzed using The Cancer Genome Atlas database. MIR4435-2HG expression was validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in cancer cells in vitro. The target genes of MIR4435-2HG were predicted using bioinformatics analysis. Interactions between miR-136-5p, MIR4435-2HG and B3GNT5 were detected using luciferase reporter assays, and their effects on cell viability, migration and invasion were assessed using Cell Counting Kit-8, wound healing and Transwell assays. The effects of miR-136-5p and MIR4435-2HG on B3GNT5 expression were confirmed by western blot The results revealed that MIR4435-2HG expression was upregulated in primary liver cancer and liver cancer cell lines, and was positively associated with advanced tumor stage, metastasis and poor prognosis in patients with liver cancer. Knockdown of MIR4435-2HG significantly inhibited the proliferation, migration and invasion of liver cancer cells. Furthermore, miR-136-5p was determined to be a direct target of MIR4435-2HG and suppressed MIR4435-2HG expression by binding with the seed region of the 3'-UTR of MIR4435-2HG in liver cancer cells. Functional studies showed that the inhibitory effects of MIR4435-2HG knockdown on cell proliferation, migration and invasion were significantly rescued by inhibiting miR-136-5p. Furthermore, the target gene, B3GNT5, of miR-136-5p was confirmed by bioinformatics analysis and RT-qPCR. In addition, B3GNT5 expression was regulated by the MIR4435-2HG/miR-136-5p axis. In conclusion, the present study indicated that MIR4435-2HG facilitated the progression of liver cancer via the MIR4435-2HG/miR-136-5p/B3GNT5 axis, which demonstrated that MIR4435-2HG may be a potential biomarker for the prognosis and treatment of liver cancer.	34859256	RID08320	ceRNA or sponge	metastasis,prognosis	UP(PRAD,SKCM,BRCA);DOWN(BRCA);DATA(GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE75367)	UP(PAAD);DOWN(BRCA);DATA(GSE40174,GSE111842,GSE109761,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	TDRG1	KLF5	positively-E	luciferase reporter assay;RIP	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);	ceRNA(miR-214-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000102554	NA	732253	688	LINC00532|lincRNA-NR_024015	BTEB2|CKLF|IKLF	Testis developmental related gene 1 promotes non-small-cell lung cancer through the microRNA-214-5p/KLF 5 axis.Non-small-cell lung cancer (NSCLC) is a frequent malignancy and has a high global incidence. Long noncoding RNAs (lncRNAs) are implicated in carcinogenesis and tumor progression. LncRNA testis developmental related gene 1 (TDRG1) plays a pivotal role in many cancers. This study researched the biological regulatory mechanisms of TDRG1 in NSCLC. Gene expression was assessed by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). Changes in the NSCLC cell phenotypes were examined using 5-ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK-8), wound healing, flow cytometry, and Transwell assays. The binding capacity between TDRG1, microRNA-214-5p (miR-214-5p), and KLF5 was tested using luciferase reporter and RNA immunoprecipitation (RIP) assays. In this study, we found that TDRG1 was upregulated in NSCLC samples. Functionally, TDRG1 depletion inhibited NSCLC cell growth, migration, and invasion and accelerated apoptosis. In addition, TDRG1 interacted with miR-214-5p, and miR-214-5p directly targeted KLF5. The suppressive effect of TDRG1 knockdown on NSCLC cellular processes was abolished by KLF5 overexpression. Overall, TDRG1 exerts carcinogenic effects in NSCLC by regulating the miR-214-5p/KLF5 axis.	34856848	RID08321	ceRNA or sponge	NA		UP(NSCLC,PAAD,BRCA);DOWN(PRAD,PAAD,SKCM);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE109761,GSE111065)
Colon cancer	LINC01615	ZEB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	prognosis(-)	ceRNA(miR-3653-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000223485	GRCh38_6:169157162-169163007	ENSG00000169554	NA	101929484	9839	NA	KIAA0569|SIP-1|SIP1|ZFHX1B	LINC01615 activates ZEB2 through competitively binding with miR-3653-3p to promote the carcinogenesis of colon cancer cells.Changes at the level of molecular biology were detected by quantitative real-time polymerase chain reaction and western blot. Bioinformatics analysis and dual-luciferase reporter assay were involved in the display and verification of targeted binding sequences. The rescue tests and correlation analysis examined the relationship among LINC01615, miR-3653-3p and zinc finger E-box binding homeobox 2 (ZEB2) in colon cancer cells. The xenograft experiment and immunohistochemistry were performed to verify these results.TCGA suggested that LINC01615 was high-expressed in colon cancer, as verified in clinical and cell samples, and patients with LINC01615 overexpression suffered from a poor prognosis. Silent LINC01615 blocked the malignant development of colon cancer cells through regulating related genes expressions, while overexpressed LINC01615 had the opposite effect. LINC01615, which was targeted by miR-3653-3p, partially offset the inhibitory effect of miR-3653-3p on colon cancer cells. The downstream target gene ZEB2 of miR-3653-3p was high-expressed in colon cancer. MiR-3653-3p was negatively correlated with LINC01615 or ZEB2, while LINC01615 was positively correlated with ZEB2. Therefore, LINC01615 induced ZEB2 up-regulation, while miR-3653-3p reduced ZEB2 level. The results of in vivo studies were consistent with cell experiments.LINC01615 competitively binds with miR-3653-3p to regulate ZEB2 and promote canceration of colon cancer cells.	34965191	RID08322	ceRNA or sponge	prognosis		DOWN(NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE109761,GSE111065,GSE51827,GSE86978)
Osteoporosis	MALAT1	IGF2BP1	positively-E		downregulation		NA	NA	WNT/beta-catenin signaling pathway(-)	ceRNA(miR-124-3p)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000159217	NA	378938	10642	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	IMP-1	LncRNA metastasis-associated lung adenocarcinoma transcript-1 promotes osteogenic differentiation of bone marrow stem cells and inhibits osteoclastic differentiation of M- in osteoporosis via the miR-124-3p/IGF2BP1/Wnt/beta-catenin axis.Osteoporosis is defined as a skeletal disorder characterized by impairment in bone strength. The potential application of lncRNAs as therapeutic targets for osteoporosis has been unveiled. This study investigated the regulatory mechanism of lncRNA MALAT1 in the differentiation of bone marrow stem cells (BMSCs) and macrophages (M-) in osteoporosis. MALAT1 expression in peripheral blood of elderly osteoporosis patients and healthy volunteers was detected. BMSCs and mononuclear M- were isolated and cultured. Osteogenic differentiation of BMSCs and osteoclastic differentiation of M- were induced. BMSCs and M- were transfected with si-MALAT1, miR-124-3p mimics, miR-124-3p inhibitor, or pcDNA IGF2BP1, followed by detection of cell differentiation. The target microRNAs (miRs) and downstream genes and signaling pathways of MALAT1 were examined. The ovariectomy-induced mouse model of osteoporosis was established, and the mice were injected with pcDNA-MALAT1. MALAT1 was downregulated in osteoporosis patients, increased in BMSCs after osteogenic differentiation, and diminished in M- after osteoclastic differentiation. Downregulation of MALAT1 repressed osteogenic differentiation of BMSCs and facilitated osteoclastic differentiation of M-. MALAT1 upregulated IGF2BP1 expression by competitively binding to miR-124-3p. miR-124-3p silencing reversed the effect of si-MALAT1 on BMSCs and M- differentiation, and IGF2BP1 upregulation averted the effect of overexpressed-miR-124-3p by activating the Wnt/beta-catenin pathway. Upregulation of MALAT1 activated the Wnt/beta-catenin pathway and attenuated bone injury in mice. In conclusion, lncRNA MALAT1 promoted the osteogenic differentiation of BMSCs and inhibited osteoclastic differentiation of M- in osteoporosis via the miR-124-3p/IGF2BP1/Wnt/beta-catenin axis.	34962086	RID08323	ceRNA or sponge	metastasis	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Hepatocellular carcinoma	DUBR	CIP2A	positively-E		upregulation		NA	NA	cell stemness(+);chemoresistance(+);	ceRNA(miR-520d-5p)	regulation	NA	Oxaliplatin	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000243701	GRCh38_3:107220744-107348464	ENSG00000163507	NA	344595	57650	LINC00883	KIAA1524	SP1-induced lncRNA DUBR promotes stemness and oxaliplatin resistance of hepatocellular carcinoma via E2F1-CIP2A feedback.Oxaliplatin-based chemotherapy is widely used to treat advanced hepatocellular carcinoma (HCC), but many patients develop drug resistance that leads to tumor recurrence. Cancer stem cells (CSCs) are known to contribute to chemoresistance, the underlying mechanism, however, remains largely unknown. In this study, we discovered a specificity protein 1 (SP1)-induced long noncoding RNA--DPPA2 upstream binding RNA (DUBR) and its high expression in HCC tissues and liver CSCs. DUBR was associated with HCC progression and poor chemotherapy response. Moreover, DUBR facilitated the stemness and oxaliplatin resistance of HCC in vitro and in vivo. Mechanistically, DUBR upregulated cancerous inhibitor of protein phosphatase 2A (CIP2A) expression through E2F1-mediated transcription regulation. DUBR also exerted function by binding microRNA (miR)-520d-5p as a competing endogenous RNA to upregulate CIP2A at mRNA level. CIP2A, in turn, stabilized E2F1 protein and activated the Notch1 signaling pathway, thereby increasing the stemness feature of HCC and leading to chemoresistance. In conclusion, we identified SP1/DUBR/E2F1-CIP2A as a critical axis to activate the Notch1 signaling pathway and promote stemness and chemoresistance of HCC. Therefore, DUBR could be a potential target in HCC treatment.	34958891	RID08324	ceRNA or sponge	recurrence,chemoresistance	UP(PRAD,SKCM);DATA(GSE104209,GSE38495)	
Biliary disease	ACTA2-AS1	EP300	positively-F	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);fibrotic(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Gastrointestinal system disease	Hepatobiliary disease	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000100393	NA	100132116	2033	UC001kfo|uc001kfo.1|ZXF1	KAT3B|p300	Long non-coding RNA ACTA2-AS1 promotes ductular reaction by interacting with the p300/ELK1 complex.Results: BDL-induced DR and fibrosis were reduced in Krt19-CreERT/p300fl/fl mice. Similarly, Mdr KO mice were protected from DR and fibrosis after SGC-CBP30 treatment. In vitro, depletion of ACTA2-AS1 reduced expression of proliferative/fibrogenic markers, reduced LPS-induced cholangiocyte proliferation, and impaired organoid formation. ACTA2-AS1 regulated transcription by facilitating p300/ELK1 binding to the PDGFB promoter after LPS exposure. Correspondingly, LPS-induced H3K27ac was mediated by p300/ELK1 and was reduced in ACTA2-AS1-depleted cholangiocytes.Conclusion: Cholangiocyte-selective p300 KO or p300 inhibition attenuate DR/fibrosis in mice. ACTA2-AS1 influences recruitment of p300/ELK1 to specific promoters to drive H3K27ac and epigenetic activation of proliferative/fibrogenic genes. This suggests that cooperation between epigenetic co-activators and lncRNAs facilitates DR/fibrosis in biliary diseases.	34953958	RID08325	interact with protein	NA	UP(LIHC);DATA(GSE117623)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)
Lung cancer	WFDC21P	STAT3	positively-F	RIP	upregulation	qRT-PCR	NA	NA	immune response(+)	interact with protein	binding/interaction	NA	NA	CSC	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000261040	GRCh38_17:60083562-60091885	ENSG00000168610	NA	645638	6774	lnc-DC|LNCDC|LOC645638	APRF	The mechanism underlying arsenic-induced PD-L1 upregulation in transformed BEAS-2B cells.Chronic exposure to arsenic promotes lung cancer. Human studies have identified immunosuppression as a risk factor for cancer development. The immune checkpoint pathway of Programmed cell death 1 ligand (PD-L1) and its receptor (programmed cell death receptor 1, PD-1) is the most studied mechanism of immunosuppression. We have previously shown that prolonged arsenic exposure induced cell transformation of BEAS-2B cells, a human lung epithelial cell line. More recently our study further showed that arsenic induced PD-L1 up-regulation, inhibited T cell effector function, and enhanced lung tumor formation in the mice. In the current study, using arsenic-induced BEAS-2B transformation as a model system we investigated the mechanism underlying PD-L1 up-regulation by arsenic. Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.	34953898	RID08326	interact with protein	NA	DOWN(BRCA);DATA(GSE86978)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteosarcoma	HCG11	PKP2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-1245b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000057294	NA	493812	5318	CTA-14H9.3|bK14H9.3	ARVD9	Long non-coding RNA HCG11 enhances osteosarcoma phenotypes by sponging miR-1245b-5p that directly inhibits plakophilin 2.Long non-coding RNA (lncRNA) HCG11 can regulate various cancers through the ceRNA network. However, its role in osteosarcoma (OS) remains unknown. The HOS and Saos-2 cell lines were used for in vitro analyses. HCG11 and plakophilin 2 (PKP2) silencers, a miR-1245b-5p mimic, and a miR-1245b-5p inhibitor were utilized for the regulation analysis of lncRNA HCG11, miR-1245b-5p, and PKP2. Cell Counting Kit-8, wound healing, and transwell assays were used for cell proliferation, migration, and invasion analyses, and caspase-3 activity assay was used to measure cell apoptosis. The expression levels of lncRNA HCG11, miR-1245b-5p, and PKP2 were evaluated by quantitative real-time PCR and western blot. The distribution of lncRNA HCG11 was assessed using the RNA-FISH assay. The sponging and targeting roles of HCG11 and PKP2 on miR-1245b-5p were confirmed by dual-luciferase reporter analysis. An RNA immunoprecipitation assay was used to assess the binding between lncRNA HCG11 and miRNA-1245b-5p. We found that the lncRNA HCG11 was significantly upregulated in OS. LncRNA HCG11 silencing inhibits OS progression by repressing cell proliferation, migration, and invasion, and promoting cell apoptosis. RNA-FISH analysis indicated that lncRNA HCG11 was located in the cytoplasm. Mechanistic experiments showed that lncRNA HCG11 sponges miR-1245b-5p and negatively regulates miR-1245b-5p expression. Upregulated lncRNA HCG11 promotes proliferation, migration, and invasion, and inhibits apoptosis by inhibiting miR-1245b-5p in OS cells. PKP2 was verified as a target gene of miR-1245b-5p. Upregulated PKP2 promotes proliferation, migration, and invasion, and inhibits apoptosis by inhibiting miR-1245b-5p in OS. In conclusion, the HCG11/miR-1245b-5p/PKP2 axis promotes OS expression by promoting cell proliferation, migration, and invasion, and inhibiting apoptosis.	34949159	RID08327	ceRNA or sponge	NA	UP(LIHC);DOWN(PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE86978)	UP(LIHC,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE109761,GSE111065)
Atherosclerosis	NEAT1	STAT3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);	ceRNA(miR-370-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|MENepsilon/beta|NCRNA00084|TncRNA|VINC	APRF	Trimethylamine N-oxide promotes atherosclerosis via regulating the enriched abundant transcript 1/miR-370-3p/signal transducer and activator of transcription 3/flavin-containing monooxygenase-3 axis.Atherosclerosis (AS) is one of the main causes of cardiovascular diseases (CVDs). Trimethylamine N-oxide (TMAO) exacerbates the development of AS. This study aimed to investigate the roles of TMAO in AS. In this study, mice were fed with high fat food (HF) and/or injected with TMAO. Oil red O staining was applied for histological analysis. ELISA, qRT-PCR and western blot were conducted to determine the TMAO, serum, mRNA, and protein levels. CCK-8, colony formation assay, and flow cytometry assays were performed to detect the functions of human aortic endothelial cells (HUVECs). The results showed that TMAO induced thick internal and external walls and intimal plaques in vivo, and HUVEC dysfunction in vitro. TMAO and lncRNA enriched abundant transcript 1 (NEAT1) were increased in AS clinical samples and TMAO-HUVECs. Downregulated NEAT1 inhibited proliferation and promoted the apoptosis of HUVECs. NEAT1 regulated the expression of signal transducer and activator of transcription 3 (STAT3) via sponging miR-370-3p. Overexpression of miR-370-3p facilitated the effects of NEAT1 on the cellular functions of HUVECs, while STAT3 exerted opposing effects. The activation of STAT3 promoted the expression of flavin-containing monooxygenase-3 (FMO3). Taken together, our results show that TMAO-NEAT1/miR-370-3p/STAT3/FMO3 forms a positive feedback loop to exacerbate the development of AS. This novel feedback loop may be a promising therapeutic target for AS.	34923910	RID08328	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE55807)	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Non-small cell lung cancer	FOXP4-AS	EIF5AL1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);	ceRNA(miR-3184-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000253626	NA	NA	143244	NA	EIF5A|EIF5AP1|bA342M3.3|eIF-4D|eIF-5A|eIF-5A-1|eIF-5A1	LncRNA FOXP4-AS promotes the progression of non-small cell lung cancer by regulating the miR-3184-5p/EIF5A axis.Long non coding RNA FOXP4-AS1 exerted crucial functions in various human cancers, while its role in non-small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4-AS1 and miR-3184-5p. Cell proliferation was assessed by CCK-8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4-AS1, miR-3184-5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4-AS1 in NSCLC progression. The results showed that FOXP4-AS1 was upregulated and miR-3184-5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4-AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4-AS1 could regulated the expression of EIF5A by binding to miR-3184-5p. Rescue experiments showed that downregulation of miR-3184-5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si-FOXP4-AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4-AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4-AS1 attenuated the progression of NSCLC by regulating miR-3184-5p and EIF5A.	34921595	RID08329	ceRNA or sponge	NA		UP(SKCM);DATA(GSE38495)
Hepatocellular carcinoma	LINC00667	miR-130a-3p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000263753	GRCh38_18:5237826-5290608	NA	NA	339290	NA	NA	NA	LncRNA LINC00667 aggravates the progression of hepatocellular carcinoma by regulating androgen receptor expression as a miRNA-130a-3p sponge.Emerging studies have found long noncoding RNAs, widely expressed in eukaryotes, crucial regulators in the progression of human cancers, including hepatocellular carcinoma (HCC). Although the long intergenic noncoding RNA 667 (LINC00667) can promote the progression of a variety of cancer types, the expression pattern, the role in cancer progression, and the molecular mechanism involved in HCC remain unclear. This study aims to investigate the function and mechanism of LINC00667 in HCC progression. The effects of LINC00667 silencing in cell proliferation, cell migration, and cell invasion, and androgen receptor (AR) expression were determined with loss-of-function phenotypic analysis in Huh-7 and HCCLM3 cells, and subsequently testified in vivo in tumor growth. We found that the expression of LINC00667 was upregulated in HCC tissues and cell lines. Upregulation of LINC00667 was significantly associated with the unfavorable prognosis of HCC in our study patients. On the other hand, low expression of LINC00667 significantly inhibited the cell proliferation, cell migration and cell invasion of HCC in vitro and tumor growth in vivo. This inhibitory effect could be counteracted by miR-130a-3p inhibitor. LINC00667 reduced the inhibition of AR expression by miR-130a-3p, which correlated with the progression of HCC. Our finding suggests LINC00667 is a molecular sponge in the miR-130s-3p/AR signal pathway in the progression of HCC, in which it relieves the repressive function of miR-130a-3p on the AR expression. This indicates LINC00667 functions as a tumor promotor in promoting HCC progression through targeting miR-130a-3p/AR axis, making a novel biomarker and potential therapeutic target for HCC.	34907204	RID08330	ceRNA or sponge	prognosis	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE75367)	
Hepatocellular carcinoma	KDM4A-AS1	KPNA2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-411-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236200	GRCh38_1:43685123-43708138	ENSG00000262472	NA	100132774	3838	NA	IPOA1|QIP2|RCH1|SRP1alpha	HIF-1alpha-activated long non-coding RNA KDM4A-AS1 promotes hepatocellular carcinoma progression via the miR-411-5p/KPNA2/AKT pathway.Hepatocellular carcinoma (HCC) is the most common type of liver cancer with poor clinical outcomes. Long non-coding RNAs (lncRNAs) are extensively involved in the tumorigenesis and progression of HCC. However, more investigations should be carried out on novel lncRNAs and their effects on HCC. Here we identified a novel lncRNA KDM4A-AS1, which was aberrantly overexpressed in HCC tissues, associated with unfavorable clinical features and poor prognosis of patients. KDM4A-AS1 promoted HCC cell proliferation, migration, and invasion in vitro and contributed to HCC growth and lung metastasis in vivo. Mechanistically, KDM4A-AS1 was inversely modulated by miR-411-5p at the post-transcriptional level and facilitated Karyopherin alpha2 (KPNA2) expression by competitively binding miR-411-5p, thereby activating the AKT pathway. KPNA2 silencing, miR-411-5p overexpression, and AKT inhibitor (MK2206) consistently reversed KDM4A-AS1-enhanced proliferation, mobility, and EMT of HCC cells. KDM4A-AS1 was identified as a novel hypoxia-responsive gene and transactivated by hypoxia-inducible factor 1alpha (HIF-1alpha) in HCC cells. In turn, KDM4A-AS1 regulated HIF-1alpha expression through the KPNA2/AKT signaling pathway. Hence, this study revealed a novel hypoxia-responsive lncRNA, KDM4A-AS1, which contributed to HCC growth and metastasis via the KDM4A-AS1/KPNA2/HIF-1alpha signaling loop. Our findings provide a promising prognostic and therapeutic target for HCC.	34903711	RID08331	ceRNA or sponge	metastasis,prognosis	DOWN(LIHC,PAAD,BRCA);UP(SKCM);DATA(GSE117623,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807)	UP(PAAD,SKCM,BRCA);DOWN(PRAD,BRCA);DATA(GSE40174,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807)
Intracerebral hemorrhage	FGD5-AS1	VEGFA	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-6838-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Other	Intracerebral hemorrhage	lncRNA	PCG	ENSG00000225733	GRCh38_3:14920347-14948424	ENSG00000112715	NA	100505641	7422	NA	VEGF|VEGF-A|VPF	LncRNA FGD5-AS1 accelerates intracerebral hemorrhage injury in mice by adsorbing miR-6838-5p to target VEGFA.Intracerebral hemorrhage (ICH) can usually cause severe neuroinflammation and blood-brain barrier (BBB) damage. Previous studies supported the important role of long non-coding RNAs (lncRNAs) in ICH treatment. This study aimed to explore the effect of lncRNA FGD5 antisense RNA 1 (FGD5-AS1) on ICH and its potential molecular mechanisms. C57BL/6 mice were injected with collagenase VII to establish an ICH mice model. In addition, brain cerebral microvascular endothelial cells (BMVECs) were treated by oxygen-glucose deprivation (OGD)/hemin to simulate ICH. RT-qPCR revealed that FGD5-AS1 was upregulated in serum of ICH patients and mice and in OGD/hemin-treated BMVECs. Luciferase reporter gene and pull-down assays predicted and verified that FGD5-AS1 bound to miR-6838-5p, and VEGFA was a target of miR-6838-5p. FGD5-AS1 knockdown decreased the inflammatory factor contents in brain tissues and BMVECs. FGD5-AS1 overexpression inhibited cell proliferation, invasion and tight junction protein levels, and promoted apoptosis, increased the permeability of BBB and secretion of pro-inflammatory factors. In addition, miR-6838-5p knockdown reversed the inhibitory effect of FGD5-AS1 knockdown on the PI3K/Akt signaling pathway. In conclusion, FGD5-AS1 may act as an important regulator to promote apoptosis, cell permeability and inflammatory response of BMVECs via the miR-6838-5p/VEGFA axis in ICH mice.	34902342	RID08332	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Ovarian cancer	MIR210HG	HIF1A	positively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);angiogenesis(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000247095	GRCh38_11:565657-568457	ENSG00000100644	NA	100506211	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Hypoxia-Induced LncRNA-MIR210HG Promotes Cancer Progression By Inhibiting HIF-1alpha Degradation in Ovarian Cancer.LncRNA-MIR210HG plays crucial roles in the progression of diverse cancers. However, the expression and function of MIR210HG in ovarian cancer remains unclear. In the present study, we aimed to determine the expression and function of lncRNA-MIR210HG in ovarian cancer under hypoxic conditions. MIR210HG expression in ovarian cancer cells under hypoxic conditions was determined by qPCR analysis, and the distribution was determined by FISH and qPCR analysis based on cell nucleus and cytosol RNA extraction. Epithelial-Mesenchymal Transition (EMT) assay and human umbilical vein endothelial cell-based tube formation and migration assays were employed to determine the potential function of MIR210HG in vitro, followed by establishment of a subcutaneous tumor model in mice. The direct target of MIR210HG was determined by RNA pull-down and western blot. Furthermore, the expression and clinical correlation of MIR210HG was determined based on malignant tissues from ovarian cancer patients. Our results indicated that MIR210HG was induced by hypoxia, which is HIF-1alpha dependent and mainly located in the cytosol of ovarian cancer cells. Knockdown of MIR210HG significantly inhibited EMT and tumor angiogenesis in vitro and impaired tumor growth in mice. Molecular investigations indicated that MIR210HG directly targets HIF-1alpha protein and inhibits VHL-dependent HIF-1alpha protein degradation in ovarian cancer. Further results demonstrated that MIR210HG was upregulated in ovarian cancer tissues and correlated with tumor progression and poor prognosis of ovarian cancer patients. Our study suggests that hypoxia-induced MIR210HG promotes cancer progression by inhibiting HIF-1alpha degradation in ovarian cancer, which could be a therapeutic target for ovarian cancer.	34900667	RID08333	interact with protein	prognosis		DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE51827,GSE55807,GSE75367)
Osteoporosis	HOTAIR	NNMT	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-378g)	regulation	NA	NA	CSC	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000166741	NA	100124700	4837	HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding RNA HOTAIR promotes bone marrow mesenchymal stem cell differentiation by sponging microRNA miR-378g that inhibits nicotinamide N-methyltransferase.Osteoporosis (OP) is associated with a serious social and economic burden. Recent studies have shown that the differential expression of long non-coding RNAs (lncRNAs) is closely related to OP. However, the specific molecular mechanism of HOX transcript antisense intergenic RNA (HOTAIR) remains to be elucidated.The expression of HOTAIR and miR-378g in OP patients was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR. Bone marrow mesenchymal stem cells (BMSCs) were isolated and cultured, and osteogenic differentiation was induced. Alkaline phosphatase (ALP) and Runt-related transcription factor 2 (RUNX2) were detected by qRT-PCR ELISA, and western blot. Calcium deposition was measured using Alizarin red s (ARS) staining. Molecular interactions between HOTAIR, miR-378g, and nicotinamide N-methyltransferase (NNMT) were detected using a dual-luciferase reporter assay.HOTAIR expression was upregulated and miR-378g level was downregulated in OP patients. HOTAIR expression decreased during the osteogenic differentiation of BMSCs. Silencing HOTAIR or NNMT reduced ALP and RUNX2 levels and promoted calcium deposition. The overexpression of HOTAIR or interference with miR-378g inhibited the osteogenic differentiation of BMSCs. HOTAIR negatively regulates miR-378g by targeting NNMT.HOTAIR is an miR-378g sponge that targets NNMT, inhibits the osteogenic differentiation of BMSCs, and provides a valuable target for the treatment of OP.	34895051	RID08334	ceRNA or sponge	NA		UP(LIHC,SKCM);DATA(GSE117623,GSE38495)
Hepatocellular carcinoma	LINC00536	VEGFA	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);	ceRNA(miR-203b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249917	GRCh38_8:115950511-116325062	ENSG00000112715	NA	100859921	7422	NA	VEGF|VEGF-A|VPF	LINC00536 promotes hepatocellular carcinoma progression via the miR-203b-5p/VEGFA axis.LncRNAs exert comprehensive effects in regulating the initiation and deterioration of hepatocellular carcinoma (HCC). However, the specific expression profiles and functional mechanisms of LINC00536 in HCC need to be disclosed. The study is intended to clarify the leverage of LINC00536 in HCC and investigate the potential mechanisms for the regulatory role of LINC00536 in the progression of HCC. In our study, LINC00536 was overexpressed in tumor samples of HCC patients and was related to poor prognosis. LINC00536 knockdown impaired cell viability, proliferation, migration, and invasion. LINC00536 can directly bind with miR-203b-5p, trimming the miR-203b-5p expression levels. VEGFA designates as a target of miR-203b-5p. Rescue research indicated that the miR-203b-5p inhibition or VEGFA overexpression could reverse the impaired cell phenotypes induced by LINC00536 knockdown. The in vivo experiments upheld the LINC00536/miR-203b-5p/VEGFA axis in HCC. Conclusively, LINC00536 could promote HCC deterioration via tuning the miR-203b-5p/VEGFA axis. This research may provide theoretical evidence for LINC00536 to get a gratifying therapeutic target for HCC.	34881629	RID08335	ceRNA or sponge	prognosis		DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE111842,GSE109761,GSE51827,GSE86978)
Hepatocellular carcinoma	LINC00491	ROCK1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+);colony formation(+)	ceRNA(miR-324-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000250682	GRCh38_5:102604220-102671765	ENSG00000067900	NA	285708	6093	BC008363	p160ROCK	LINC00491 promotes cell growth and metastasis through miR-324-5p/ROCK1 in liver cancer.Results: LINC00491 was highly expressed in liver cancer cases, associating with poor prognosis. si-LINC00491 inhibited proliferation, colony formation, invasion, migration, and induced cell cycle G1 arrest and apoptosis in HUH-7 and SK-Hep-1 cells. LINC00491 overexpression showed opposite effects. LINC00491 promoted ROCK1 expression by reducing miR-324-5p. miR-324-5p up-regulation or ROCK1 knockdown reversed LINC00491 promotion on liver SK-Hep-1 cells malignant phenotype. LINC00491 facilitated xenograft tumor growth and lung metastasis in mice.	34876144	RID08336	ceRNA or sponge	metastasis,prognosis	UP(SKCM);DATA(GSE38495)	DOWN(NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)
Breast cancer	FOXD2-AS1	p-PI3K	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell migration(+);cell invasion(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells.Results: lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells.	34873418	RID08337	expression association	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Breast cancer	FOXD2-AS1	p-AKT	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell migration(+);cell invasion(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	NA	NA	84793	NA	MGC12982	NA	Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells.Results: lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells.	34873418	RID08338	expression association	chemoresistance	DOWN(NSCLC,BRCA);DATA(GSE74639,GSE111842)	
Colorectal cancer	ASB16-AS1	TEAD1	positively-E		upregulation		NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell stemness(+)	ceRNA(miR-185-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000267080	GRCh38_17:44175968-44186723	ENSG00000187079	NA	339201	7003	C17orf65|DKFZp762C2414	AA|TCF13|TEF-1	LncRNA ASB16-AS1 drives proliferation, migration, and invasion of colorectal cancer cells through regulating miR-185-5p/TEAD1 axis.As a common malignant tumor, colorectal cancer (CRC) has a high incidence. Recent investigations have suggested that although great improvement has been achieved in the survival rate of early-stage CRC patients, the overall survival rate remains low. Mounting reports have proved that lncRNAs take part in the development of various cancers and possess the regulatory functions in cancers. For example, ASB16 antisense RNA 1 (ASB16-AS1) is a poorly researched novel lncRNA whose specific functions in CRC are still unknown. In our research, we discovered that ASB16-AS1 was with high expression in CRC cells. In addition, ASB16-AS1 silencing restrained the proliferation, migration, invasion, and stemness while accelerating cell apoptosis of CRC cells. Mechanism experiments were applied to explore the regulatory mechanism of ASB16-AS1. It turned out that miR-185-5p could interact with ASB16-AS1 and inhibited the progression of CRC cells. TEAD1 (TEA domain transcription factor1) - a major effector of the Hippo signaling was proved to serve as the target of miR-185-5p and promote CRC development. In short, ASB16-AS1 drove the progression of CRC through the regulation of miR-185-5p/TEAD1 axis.	34870557	RID08339	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE51827,GSE55807,GSE86978)	UP(LIHC,NSCLC,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE38495,GSE109761,GSE111065)
Non-small cell lung cancer	THORLNC	IGF2	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000167244	NA	100506797	3481	THOR	C11orf43|FLJ44734|IGF-II	Long Non-Coding RNA THOR Depletion Inhibits Human Non-Small Cell Lung Cancer Cell Growth.The shRNA strategy was first employed to silence Lnc-THOR. As described, lentiviral particles encoding two different shRNA sequences, "Sh-S1'-and "Sh-S2'-[from Dr. Pan (34)], were transduced to pCan-1 primary NSCLC cells. Following selection via puromycin, stable cells were established. Alternatively, a Cas9-Lnc-THOR-KO construct [also from Dr. Pan (34)] was transfected to the Cas9-expressing pCan-1 cells. The transfected cells were subject to Lnc-THOR KO screening, and single stable cells established . Analyzing Lnc-THOR expression, via qRT-PCRassays, demonstrated that Lnc-THOR levels decreased over 80-90% in pCan-1 cells with the Lnc-THOR shRNA or the KO construct (Figure 1A). The linear THOR expression was however unchanged (Figure 1B). IGF2BP1 target mRNAs, including IGF2, Gli1, Myc and SOX9 (25, 26, 34, 38), were robustly decreased in pCan-1 cells with Lnc-THOR shRNA or KO (Figure 1C).Next, a lentiviral construct encoding the full-length Lnc-THOR [from Dr. Pan (34)] was transduced to pCan-1 cells. Following selection by puromycin, two stable cell lines were established. Examining Lnc-THOR expression, through qRT-PCRassays, confirmed that Lnc-THOR expression increased over 4-5 folds in OE-L1 cells and OE-L2 cells (Figure 3A), where the long isoform of THOR expression was unchanged (Figure 3B). IGF2BP1 target mRNAs, IGF2, Gli1, Myc and SOX9, were significantly increased after Lnc-THOR overexpression (Figure 3C). Functional studies demonstrated that Lnc-THOR overexpression augmented pCan-1 cell viability and proliferation, tested by CCK-8 OD (Figure 3D) and by recording the EdU-positive nuclei ratio (Figure 3E) assays, respectively. Moreover, in vitro migration (Figure 3F) and invasion (Figure 3G) were accelerated after Lnc-THOR overexpression. These results further supported a key role of Lnc-THOR in NSCLC cell progression.Experiments were carried out to examine the possible association between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR pull-down assay results confirmed that IGF2BP1 protein in cell nuclei was precipitated with the biotinylated Lnc-THOR in pCan-1 primary NSCLC cells and A549 cells (Figure 4A). Additionally, by employing a RNA-Immunoprecipitation (RIP) assay, we further demonstrated the direct association between endogenous Lnc-THOR and IGF2BP1 protein in pCan-1 cells and A549 cells (Figure 4B). These results implied that Lnc-THOR directly associated with IGF2BP1 protein in NSCLC cells.	34868966	RID08340	expression association	NA		UP(LIHC,NSCLC);DATA(GSE117623,GSE74639)
Non-small cell lung cancer	THORLNC	GLI1	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000111087	NA	100506797	2735	THOR	GLI	Long Non-Coding RNA THOR Depletion Inhibits Human Non-Small Cell Lung Cancer Cell Growth.The shRNA strategy was first employed to silence Lnc-THOR. As described, lentiviral particles encoding two different shRNA sequences, "Sh-S1'-and "Sh-S2'-[from Dr. Pan (34)], were transduced to pCan-1 primary NSCLC cells. Following selection via puromycin, stable cells were established. Alternatively, a Cas9-Lnc-THOR-KO construct [also from Dr. Pan (34)] was transfected to the Cas9-expressing pCan-1 cells. The transfected cells were subject to Lnc-THOR KO screening, and single stable cells established . Analyzing Lnc-THOR expression, via qRT-PCRassays, demonstrated that Lnc-THOR levels decreased over 80-90% in pCan-1 cells with the Lnc-THOR shRNA or the KO construct (Figure 1A). The linear THOR expression was however unchanged (Figure 1B). IGF2BP1 target mRNAs, including IGF2, Gli1, Myc and SOX9 (25, 26, 34, 38), were robustly decreased in pCan-1 cells with Lnc-THOR shRNA or KO (Figure 1C).Next, a lentiviral construct encoding the full-length Lnc-THOR [from Dr. Pan (34)] was transduced to pCan-1 cells. Following selection by puromycin, two stable cell lines were established. Examining Lnc-THOR expression, through qRT-PCRassays, confirmed that Lnc-THOR expression increased over 4-5 folds in OE-L1 cells and OE-L2 cells (Figure 3A), where the long isoform of THOR expression was unchanged (Figure 3B). IGF2BP1 target mRNAs, IGF2, Gli1, Myc and SOX9, were significantly increased after Lnc-THOR overexpression (Figure 3C). Functional studies demonstrated that Lnc-THOR overexpression augmented pCan-1 cell viability and proliferation, tested by CCK-8 OD (Figure 3D) and by recording the EdU-positive nuclei ratio (Figure 3E) assays, respectively. Moreover, in vitro migration (Figure 3F) and invasion (Figure 3G) were accelerated after Lnc-THOR overexpression. These results further supported a key role of Lnc-THOR in NSCLC cell progression.Experiments were carried out to examine the possible association between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR pull-down assay results confirmed that IGF2BP1 protein in cell nuclei was precipitated with the biotinylated Lnc-THOR in pCan-1 primary NSCLC cells and A549 cells (Figure 4A). Additionally, by employing a RNA-Immunoprecipitation (RIP) assay, we further demonstrated the direct association between endogenous Lnc-THOR and IGF2BP1 protein in pCan-1 cells and A549 cells (Figure 4B). These results implied that Lnc-THOR directly associated with IGF2BP1 protein in NSCLC cells.	34868966	RID08341	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE104209,GSE109761,GSE111065,GSE51827,GSE75367,GSE86978)
Non-small cell lung cancer	THORLNC	MYC	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000136997	NA	100506797	4609	THOR	bHLHe39|c-Myc|MYCC	Long Non-Coding RNA THOR Depletion Inhibits Human Non-Small Cell Lung Cancer Cell Growth.The shRNA strategy was first employed to silence Lnc-THOR. As described, lentiviral particles encoding two different shRNA sequences, "Sh-S1'-and "Sh-S2'-[from Dr. Pan (34)], were transduced to pCan-1 primary NSCLC cells. Following selection via puromycin, stable cells were established. Alternatively, a Cas9-Lnc-THOR-KO construct [also from Dr. Pan (34)] was transfected to the Cas9-expressing pCan-1 cells. The transfected cells were subject to Lnc-THOR KO screening, and single stable cells established . Analyzing Lnc-THOR expression, via qRT-PCRassays, demonstrated that Lnc-THOR levels decreased over 80-90% in pCan-1 cells with the Lnc-THOR shRNA or the KO construct (Figure 1A). The linear THOR expression was however unchanged (Figure 1B). IGF2BP1 target mRNAs, including IGF2, Gli1, Myc and SOX9 (25, 26, 34, 38), were robustly decreased in pCan-1 cells with Lnc-THOR shRNA or KO (Figure 1C).Next, a lentiviral construct encoding the full-length Lnc-THOR [from Dr. Pan (34)] was transduced to pCan-1 cells. Following selection by puromycin, two stable cell lines were established. Examining Lnc-THOR expression, through qRT-PCRassays, confirmed that Lnc-THOR expression increased over 4-5 folds in OE-L1 cells and OE-L2 cells (Figure 3A), where the long isoform of THOR expression was unchanged (Figure 3B). IGF2BP1 target mRNAs, IGF2, Gli1, Myc and SOX9, were significantly increased after Lnc-THOR overexpression (Figure 3C). Functional studies demonstrated that Lnc-THOR overexpression augmented pCan-1 cell viability and proliferation, tested by CCK-8 OD (Figure 3D) and by recording the EdU-positive nuclei ratio (Figure 3E) assays, respectively. Moreover, in vitro migration (Figure 3F) and invasion (Figure 3G) were accelerated after Lnc-THOR overexpression. These results further supported a key role of Lnc-THOR in NSCLC cell progression.Experiments were carried out to examine the possible association between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR pull-down assay results confirmed that IGF2BP1 protein in cell nuclei was precipitated with the biotinylated Lnc-THOR in pCan-1 primary NSCLC cells and A549 cells (Figure 4A). Additionally, by employing a RNA-Immunoprecipitation (RIP) assay, we further demonstrated the direct association between endogenous Lnc-THOR and IGF2BP1 protein in pCan-1 cells and A549 cells (Figure 4B). These results implied that Lnc-THOR directly associated with IGF2BP1 protein in NSCLC cells.	34868966	RID08342	expression association	NA		DOWN(LIHC,NSCLC,PRAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE111842,GSE51827,GSE86978)
Non-small cell lung cancer	THORLNC	SOX9	positively-E	overexpression	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-);	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000125398	NA	100506797	6662	THOR	CMD1|CMPD1|SRA1	Long Non-Coding RNA THOR Depletion Inhibits Human Non-Small Cell Lung Cancer Cell Growth.The shRNA strategy was first employed to silence Lnc-THOR. As described, lentiviral particles encoding two different shRNA sequences, "Sh-S1'-and "Sh-S2'-[from Dr. Pan (34)], were transduced to pCan-1 primary NSCLC cells. Following selection via puromycin, stable cells were established. Alternatively, a Cas9-Lnc-THOR-KO construct [also from Dr. Pan (34)] was transfected to the Cas9-expressing pCan-1 cells. The transfected cells were subject to Lnc-THOR KO screening, and single stable cells established . Analyzing Lnc-THOR expression, via qRT-PCRassays, demonstrated that Lnc-THOR levels decreased over 80-90% in pCan-1 cells with the Lnc-THOR shRNA or the KO construct (Figure 1A). The linear THOR expression was however unchanged (Figure 1B). IGF2BP1 target mRNAs, including IGF2, Gli1, Myc and SOX9 (25, 26, 34, 38), were robustly decreased in pCan-1 cells with Lnc-THOR shRNA or KO (Figure 1C).Next, a lentiviral construct encoding the full-length Lnc-THOR [from Dr. Pan (34)] was transduced to pCan-1 cells. Following selection by puromycin, two stable cell lines were established. Examining Lnc-THOR expression, through qRT-PCRassays, confirmed that Lnc-THOR expression increased over 4-5 folds in OE-L1 cells and OE-L2 cells (Figure 3A), where the long isoform of THOR expression was unchanged (Figure 3B). IGF2BP1 target mRNAs, IGF2, Gli1, Myc and SOX9, were significantly increased after Lnc-THOR overexpression (Figure 3C). Functional studies demonstrated that Lnc-THOR overexpression augmented pCan-1 cell viability and proliferation, tested by CCK-8 OD (Figure 3D) and by recording the EdU-positive nuclei ratio (Figure 3E) assays, respectively. Moreover, in vitro migration (Figure 3F) and invasion (Figure 3G) were accelerated after Lnc-THOR overexpression. These results further supported a key role of Lnc-THOR in NSCLC cell progression.Experiments were carried out to examine the possible association between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR pull-down assay results confirmed that IGF2BP1 protein in cell nuclei was precipitated with the biotinylated Lnc-THOR in pCan-1 primary NSCLC cells and A549 cells (Figure 4A). Additionally, by employing a RNA-Immunoprecipitation (RIP) assay, we further demonstrated the direct association between endogenous Lnc-THOR and IGF2BP1 protein in pCan-1 cells and A549 cells (Figure 4B). These results implied that Lnc-THOR directly associated with IGF2BP1 protein in NSCLC cells.	34868966	RID08343	expression association	NA		UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Non-small cell lung cancer	THORLNC	IGF2BP1	positively-F	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell viability(+);apoptosis process(-);	interact with protein	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000159217	NA	100506797	10642	THOR	IMP-1	Long Non-Coding RNA THOR Depletion Inhibits Human Non-Small Cell Lung Cancer Cell Growth.The shRNA strategy was first employed to silence Lnc-THOR. As described, lentiviral particles encoding two different shRNA sequences, "Sh-S1'-and "Sh-S2'-[from Dr. Pan (34)], were transduced to pCan-1 primary NSCLC cells. Following selection via puromycin, stable cells were established. Alternatively, a Cas9-Lnc-THOR-KO construct [also from Dr. Pan (34)] was transfected to the Cas9-expressing pCan-1 cells. The transfected cells were subject to Lnc-THOR KO screening, and single stable cells established . Analyzing Lnc-THOR expression, via qRT-PCRassays, demonstrated that Lnc-THOR levels decreased over 80-90% in pCan-1 cells with the Lnc-THOR shRNA or the KO construct (Figure 1A). The linear THOR expression was however unchanged (Figure 1B). IGF2BP1 target mRNAs, including IGF2, Gli1, Myc and SOX9 (25, 26, 34, 38), were robustly decreased in pCan-1 cells with Lnc-THOR shRNA or KO (Figure 1C).Next, a lentiviral construct encoding the full-length Lnc-THOR [from Dr. Pan (34)] was transduced to pCan-1 cells. Following selection by puromycin, two stable cell lines were established. Examining Lnc-THOR expression, through qRT-PCRassays, confirmed that Lnc-THOR expression increased over 4-5 folds in OE-L1 cells and OE-L2 cells (Figure 3A), where the long isoform of THOR expression was unchanged (Figure 3B). IGF2BP1 target mRNAs, IGF2, Gli1, Myc and SOX9, were significantly increased after Lnc-THOR overexpression (Figure 3C). Functional studies demonstrated that Lnc-THOR overexpression augmented pCan-1 cell viability and proliferation, tested by CCK-8 OD (Figure 3D) and by recording the EdU-positive nuclei ratio (Figure 3E) assays, respectively. Moreover, in vitro migration (Figure 3F) and invasion (Figure 3G) were accelerated after Lnc-THOR overexpression. These results further supported a key role of Lnc-THOR in NSCLC cell progression.Experiments were carried out to examine the possible association between Lnc-THOR and IGF2BP1 protein in NSCLC cells. Lnc-THOR pull-down assay results confirmed that IGF2BP1 protein in cell nuclei was precipitated with the biotinylated Lnc-THOR in pCan-1 primary NSCLC cells and A549 cells (Figure 4A). Additionally, by employing a RNA-Immunoprecipitation (RIP) assay, we further demonstrated the direct association between endogenous Lnc-THOR and IGF2BP1 protein in pCan-1 cells and A549 cells (Figure 4B). These results implied that Lnc-THOR directly associated with IGF2BP1 protein in NSCLC cells.	34868966	RID08344	interact with protein	NA		UP(LIHC,SKCM);DOWN(PAAD);DATA(GSE117623,GSE40174,GSE38495)
Osteosarcoma	LAMTOR5-AS1	NRF2	positively-F	RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000224699	GRCh38_1:110347116-110443817	ENSG00000154727	NA	101410535	NA	NA	NA	LAMTOR5-AS1 regulates chemotherapy-induced oxidative stress by controlling the expression level and transcriptional activity of NRF2 in osteosarcoma cells.Long-noncoding RNAs (lncRNAs) play roles in regulating cellular functions. High-throughput sequencing analysis identified a new lncRNA, termed LAMTOR5-AS1, the expression of which was much higher in the chemosensitive osteosarcoma (OS) cell line G-292 than in the chemoresistant cell line SJSA-1. Further investigations revealed that LAMTOR5-AS1 significantly inhibits the proliferation and multidrug resistance of OS cells. In vitro assays demonstrated that LAMTOR5-AS1 mediates the interaction between nuclear factor erythroid 2-related factor 2 (NFE2L2, NRF2) and kelch-like ECH-associated protein 1 (KEAP1), which regulate the oxidative stress. Further mechanistic studies revealed that LAMTOR5-AS1 inhibited the ubiquitination degradation pathway of NRF2, resulting in a higher level of NRF2 but a loss of NRF2 transcriptional activity. High level of NRF2 in return upregulated the downstream gene heme oxygenase 1 (HO-1). Moreover, NRF2 controls its own activity by promoting LAMTOR5-AS1 expression, whereas the feedback regulation is weakened in drug-resistant cells due to high antioxidant activity. Overall, we propose that LAMTOR5-AS1 globally regulates chemotherapy-induced cellular oxidative stress by controlling the expression and activity of NRF2.	34862368	RID08345	interact with protein	chemoresistance	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Atherosclerosis	HSPA7	miR-223	negatively-F	RIP	upregulation	RT-qPCR	NA	NA	cell migration(+);inflammatory response(+)	sponge	binding/interaction	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000225217	GRCh38_1:161606291-161608217	NA	NA	3311	NA	HSP70B	NA	LncRNA HSPA7 in human atherosclerotic plaques sponges miR-223 and promotes the proinflammatory vascular smooth muscle cell transition.Although there are many genetic loci in noncoding regions associated with vascular disease, studies on long noncoding RNAs (lncRNAs) discovered from human plaques that affect atherosclerosis have been highly limited. We aimed to identify and functionally validate a lncRNA using human atherosclerotic plaques. Human aortic samples were obtained from patients who underwent aortic surgery, and tissues were classified according to atherosclerotic plaques. RNA was extracted and analyzed for differentially expressed lncRNAs in plaques. Human aortic smooth muscle cells (HASMCs) were stimulated with oxidized low-density lipoprotein (oxLDL) to evaluate the effect of the identified lncRNA on the inflammatory transition of the cells. Among 380 RNAs differentially expressed between the plaque and control tissues, lncRNA HSPA7 was selected and confirmed to show upregulated expression upon oxLDL treatment. HSPA7 knockdown inhibited the migration of HASMCs and the secretion and expression of IL-1beta and IL-6; however, HSPA7 knockdown recovered the oxLDL-induced reduction in the expression of contractile markers. Although miR-223 inhibition promoted the activity of Nf-kB and the secretion of inflammatory proteins such as IL-1beta and IL-6, HSPA7 knockdown diminished these effects. The effects of miR-223 inhibition and HSPA7 knockdown were also found in THP-1 cell-derived macrophages. The impact of HSPA7 on miR-223 was mediated in an AGO2-dependent manner. HSPA7 is differentially increased in human atheroma and promotes the inflammatory transition of vascular smooth muscle cells by sponging miR-223. For the first time, this study elucidated the molecular mechanism of action of HSPA7, a lncRNA of previously unknown function, in humans.	34857901	RID08346	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367,GSE86978)	
Non-small cell lung cancer	PKMYT1AR	PKMYT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+);WNT signaling pathway(+);	ceRNA(miR-485-5p)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	NA	ENSG00000127564	NA	NA	9088	NA	MYT1|PPP1R126	LncRNA PKMYT1AR promotes cancer stem cell maintenance in non-small cell lung cancer via activating Wnt signaling pathway.Result: Here, we identify a human-specific long non-coding RNA (lncRNA, ENST00000595422), termed PKMYT1AR (PKMYT1 associated lncRNA), that is induced in NSCLC by Yin Yang 1 (YY1) factor, especially in cancerous cell lines (H358, H1975, H1299, H1650, A549 and SPC-A1) compared to that in normal human bronchial epithelium cell line (BEAS-2B). We show that PKMYT1AR high expression correlates with worse clinical outcome, and knockdown of PKMYT1AR inhibits tumor cell proliferation, migration and xenograft tumor formation abilities. Bioinformatic analysis and a luciferase assay demonstrate that PKMYT1AR directly interacts with miR-485-5p to attenuate the inhibitory role on its downstream oncogenic factor PKMYT1 (the protein kinase, membrane-associated tyrosine/threonine 1) in NSCLC. Furthermore, we uncover that miR-485-5p is downregulated in both cancerous cell lines and peripheral blood serum isolated from NSCLC patients compared to reciprocal control groups. Consistently, forced expression of miR-485-5p inhibits the proliferation and migration abilities of tumor cells. Moreover, we provide evidence showing that PKMYT1AR targeting antisense oligonucleotide (ASO) dramatically inhibit tumor growth in vivo. Mechanistic study shows that PKMYT1AR/ miR-485-5p /PKMYT1 axis promotes cancer stem cells (CSCs) maintenance in NSCLC via inhibiting beta-TrCP1 mediated ubiquitin degradation of beta-catenin proteins, which in turn causes enhanced tumorigenesis.	34856993	RID08347	ceRNA or sponge	NA		DOWN(LIHC,PRAD,PAAD,BRCA);UP(BRCA);DATA(GSE117623,GSE104209,GSE60407,GSE111842,GSE109761,GSE111065,GSE55807)
Lung injury	TUG1	PDK4	positively-E	luciferase reporter assay	downregulation	RT-PCR	NA	NA	inflammatory response(+);apoptosis process(+);	ceRNA(miR-494)	regulation	NA	NA	NA	NA	Other	Injury	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000004799	NA	55000	5166	FLJ20618|LINC00080|NCRNA00080	NA	Up-regulation of TUG1 can regulate miR-494/PDK4 axis to inhibit LPS-induced acute lung injury caused by sepsis.Results: The expressions of TUG1 and PDK4 were down-regulated while the expression of miR-494 was up-regulated in lung tissues and human small airway epithelial cells (HSAECs). TUG1 was indirectly mediated. Overexpression of TUG1 or inhibition of miR-494 could significantly improve the survival rate of HSAECs. Transfection of miR-494 mimics achieved the opposite effect. Enzyme-linked immunosorbent assay (ELISA) showed that the expression of arthritis-related factors in rats was increased after up-regulating TUG1.	34956459	RID08348	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);UP(PAAD);DATA(GSE74639,GSE40174,GSE67980,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE51827,GSE55807,GSE75367)	DOWN(BRCA);DATA(GSE86978)
Asthma	RP5-857K21.7	miR-508-3p	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-);PI3K/AKT/mTOR signaling pathway(+)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Respiratory system disease	Asthma	lncRNA	miRNA	ENSG00000229344	GRCh38_1:632757-633438	NA	NA	NA	NA	NA	NA	LncRNA RP5-857K21.7 inhibits PDGF-BB-induced proliferation and migration of airway smooth muscle cells through the miR-508-3p/PI3K/AKT/mTOR axis.The continuous increase in the prevalence of asthma poses a threat to human health. Despites numerous researches, the understanding of asthma development still remain elusive, hindering the development of effective treatment. Here, we explored the role of lncRNA RP5-857K21.7 (RP5-857K21.7) in the development of asthma and its potential molecular mechanism of regulation. Airway smooth muscle cells (ASMCs) were isolated and cultured after which some of the cells were induced with PDGF-BB to build an asthma cell model, and then, qRT-PCRanalysis was used to measure the expression level of RP5-857K21.7 in the cell model. Result shows that the RP5-857K21.7 is significantly downregulated in PDGF-BB-induced ASMCs cells. Through CCK-8, transwell, and flow cytometry assay, we examined the functional impact of RP5-857K21.7 on the proliferation, migration, and apoptosis of the ASMCs, respectively, and found that the overexpression of RP5-857K21.7 markedly inhibit PDGF-BB-induced ASMCs cell proliferation, migration and induce apoptosis. Bioinformatics analysis predicted that the RP5-857K21.7 could sponge miR-508-3p and result was validated through a dual-luciferase reporter assay, biotinylated RNA pull-down assay, and RIP-qRT-PCRanalysis. Mechanistically, RP5-857K21.7 regulates the PI3K/AKT/mTOR pathway by endogenously sponging miR-508-3p to inhibit PDGF-BB-induced ASMCs cell proliferation, migration and induce apoptosis. The current research suggests that the RP5-857K21.7 and its associated molecular pathway (miR-508-3p/PI3K/AKT/mTOR axis) might be a useful therapeutic target for the treatment of asthma disease.	34913773	RID08349	ceRNA or sponge	NA		
Diabetic retinopathy	circ-PSEN1	CFL2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	ferroptosis(+)	ceRNA(miR-200b-3p)	regulation	NA	NA	NA	NA	Nervous system disease	Diabetic retinopathy	lncRNA	PCG	NA	NA	ENSG00000165410	NA	NA	1073	NA	NEM7	Downregulation of Circular RNA PSEN1 ameliorates ferroptosis of the high glucose treated retinal pigment epithelial cells via miR-200b-3p/cofilin-2 axis.Ferroptosis is a form of programmed cell death that participates in the progression of numerous diseases. Long noncoding RNAs (lncRNAs) are dysregulated in diabetic retinopathy (DR). However, the role of lncRNAs in DR-induced ferroptosis is unclear. Adult retinal pigment epithelial cell line-19 (ARPE19) cells were treated with a high concentration of glucose (high glucose, HG) to mimic DR in vitro. The intracellular contents of glutathione, malondialdehyde, and ferrous ions were analyzed using the corresponding kits. The MTT assay was performed to measure the cell survival rate, and cell death was determined using propidium iodide and terminal deoxynucleotidyl transferase dUTP nick end labeling staining assays. western blot was conducted to detect the protein levels of GPX4, SLC7A11, and TFR1. The targeting relationships were verified using luciferase reporter and RNA pull-down assays. circ-PSEN1 was upregulated in HG-treated ARPE19 cells and showed high resistance to RNase R and Act D. Inhibition of circ-PSEN1 in ARPE19 cells ameliorated the ferroptosis induced by HG was ameliorated, as evidenced by changes in the ferroptosis-related biomarkers/genes and decreased cell death. Subsequently, circ-PSEN1 acted as a sponge for miR-200b-3p. Inhibition of miR-200b-3p partially reversed the effects of circ-PSEN1 on ferroptosis. Furthermore, cofilin-2 (CFL2) was the target gene of miR-200b-3p, and it abrogated the inhibitory effect of miR-200b-3p on ferroptosis. Taken together, the findings indicate that knockdown of circ-PSEN1 can mitigate ferroptosis of ARPE19 cells induced by HG via the miR-200b-3p/CFL2 axis.	34903141	RID08350	ceRNA or sponge	NA		UP(LIHC,PAAD,SKCM);DOWN(PRAD,PAAD,BRCA);DATA(GSE117623,GSE40174,GSE104209,GSE60407,GSE38495,GSE111842)
Non-small cell lung cancer	MALAT1	miR-216b	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|MALAT-1|mascRNA|NCRNA00047|NEAT2|PRO1073	NA	Ultrasound microbubbles-mediated miR-216b affects MALAT1-miRNA axis in non-small cell lung cancer cells.MiR-216b is ectopically expressed in various cancers. Ultrasound microbubbles (UTMBs) are an effective method for miRNA delivery. This article mainly explored the involvement of lncRNA in the effects of UTMBs-mediated miR-216b on non-small cell lung cancer (NSCLC) progression. Expressions and relationship of miR-216b and MALAT1 were examined using quantitative real-time polymerase chain reaction (qRT-PCR, Pearson, TargetScan, and dual-luciferase reporter assay. After the transfection with liposome- or UTMBs-mediated miR-216b mimic (M) or MALAT1 overexpression plasmid alone or together, levels of miR-216b and MALAT1, cell biological behaviors, as well as expressions of apoptosis- and epithelial mesenchymal transition (EMT)-related markers were examined using qRT-PCR cell functional experiments, and western blot. Besides, we used qRT-PCRto quantify the expressions of multiple downstream miRNAs of MALAT1. MiR-216b expression was weakened yet MALAT1 expression was enhanced in NSCLC tissues, and miR-216b was negatively bound to MALAT1. TargetScan analysis manifested that miR-216b, targeted by MALAT1, was down-regulated in NSCLC cells. UTMBs-mediated miR-216b M further intensified miR-216b level yet weakened cell biological behaviors. The inhibitory effect of UTMBs-mediated miR-216b M on cell biological behaviors and MALAT1 expression was greatly better relative to that of miR-216b M. Moreover, miR-216b restrained the cell biological behaviors by repressing MALAT1 expression. We further manifested that miR-216b facilitated the expressions of apoptosis-related markers, but restrained those of EMT-related markers by repressing MALAT1 expression. Moreover, UTMBs-mediated miR-216b M enhanced the expressions of downstream multiple miRNAs of MALAT1, but this tendency was reversed by co-transfection of overexpressed MALAT1 and miR-216b M. Collectively, UTMBs-mediated miR-216b M restrained NSCLC cell growth by modulating the MALAT1-miRNA axis.	34896788	RID08351	ceRNA or sponge	NA	UP(LIHC,BRCA);DOWN(BRCA);DATA(GSE117623,GSE111842,GSE109761,GSE111065,GSE75367)	
Hepatocellular carcinoma	MEG3	FOXO1	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	RT-qPCR	NA	NA	cell migration(+);cell viability(+);	ceRNA(miR-5195-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150907	NA	55384	2308	GTL2|LINC00023|NCRNA00023|onco-lncRNA-83	FKH1|FKHR|FOXO1A	Long noncoding RNA matrilineal expression gene 3 inhibits hepatocellular carcinoma progression by targeting microRNA-5195-3p and regulating the expression of forkhead box O1.We investigated the effect of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) on hepatocellular carcinoma (HCC) tumorigenesis and progression by targeting miR-5195-3p and transcription factor forkhead box O1 (FOXO1) to identify a novel target for HCC treatment. HCC clinical samples were collected, and cell counting kit-8 (CCK-8), and transwell migration and invasion assays were performed. Furthermore, interaction was detected via double luciferase reporter and RNA pull-down assays. MEG3, miR-5195-3p, and FOXO1 expression was determined by quantitative real-time polymerase chain reaction (RT-qPCR) and western blot. Xenograft tumor models were established to investigate the effect of MEG3 in vivo. Compared with normal tissues, MEG3 expression was significantly downregulated in HCC tissues. MEG3 overexpression inhibited the viability and migration of HCC cells. Double luciferase reporter and RNA pull-down assays confirmed the binding between MEG3 and miR-5195-3p as well as between miR-5195-3p and FOXO1. RT-qPCR and western blot results showed that MEG3 inhibited the expression of miR-5195-3p and promoted that of FOXO1. Additionally, MEG3 overexpression inhibited HCC tumorigenesis and progression in xenograft tumor models while depletion of MEG3 exerted the opposite way. Therefore, the lncRNA MEG3 inhibits HCC tumorigenesis and progression through the miR-5195-3p/FOXO1 signaling axis.	34895065	RID08352	ceRNA or sponge	NA		DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807)
Kidney disease	SNHG5	miR-26a-5p	negatively-F	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell viability(+);apoptosis process(-);	sponge	binding/interaction	NA	NA	NA	Evading Apoptosis	Urinary system disease	Kidney disease	lncRNA	miRNA	ENSG00000203875	GRCh38_6:85650491-85678932	NA	NA	387066	NA	bA33E24.2|C6orf160|LINC00044|MGC16362|NCRNA00044|U50HG	NA	Long Non-Coding RNA Small Nucleolar RNA Host Gene 5 (SNHG5) Regulates Renal Tubular Damage in Diabetic Nephropathy via Targeting MiR-26a-5p.The study explored the diagnostic value of SNHG5 in diabetic nephropathy (DN) and investigated the role and mechanism on DN via establishing the in vitro HK2 cell model. This study recruited 62 types 2 diabetes mellitus (T2DM) patients, 58 DN patients and 60 healthy controls (HC). The expressions of serum SNHG5 and miR-26a-5p were measured by RT-qPCR analysis. The diagnostic value of SNHG5 in DN was assessed by ROC curve. The in vitro cell model was built to estimate the effects of SNHG5 on cell viability, cell apoptosis, inflammation response and oxidative stress. Serum SNHG5 was increased in DN patients (relative expression: 2.04 0.34) and had the diagnostic value in DN. After HK2 cells were treated with high glucose, the cell viability decreased and apoptosis increased, and the production of inflammatory cytokines and ROS enhanced significantly. It was noticed that inhibition of SNHG5 could reverse the above phenomenon caused by high glucose. Besides, serum miR-26a-5p was diminished in DN patients, and luciferase reporter gene revealed that miR-26a-5p is direct target of SNHG5. These results indicated that inhibition of SNHG5 may mitigate HG-induced renal tubular damage via targeting miR-26a-5p, which providing a new insight into the mechanism of renal tubule damage in DN patients.	34891212	RID08353	ceRNA or sponge	NA	DOWN(LIHC,NSCLC,PRAD,PAAD,BRCA);DATA(GSE117623,GSE74639,GSE104209,GSE60407,GSE111842,GSE111065,GSE51827,GSE75367)	
Malignant glioma	LOXL1-AS1	MMP14	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-374b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000157227	NA	100287616	4323	NA	MT1-MMP	LOXL1-AS1 communicating with TIAR modulates vasculogenic mimicry in glioma via regulation of the miR-374b-5p/MMP14 axis.At present, growing evidence indicates that long non-coding RNAs (lncRNAs) participate in the progression of glioma. The function of LOXL1-AS1 in vasculogenic mimicry (VM) in glioma remains unclear. First, the expressions of TIAR, the lncRNA LOXL1-AS1, miR-374b-5p and MMP14 were examined by qRT-PCRand western blot in both, glioma tissues and glioma cell lines. Proliferation, migration, invasion and tube formation assays were conducted to evaluate the roles of TIAR, LOXL1-AS1, miR-374b-5p and MMP14 in malignant cellular behaviours in glioma cells. A nude mouse xenograft model and dual staining for CD34 and PAS were used to assess whether VM was affected by TIAR, LOXL1-AS1 or miR-374b-5p in vivo. In this study, low levels of TIAR and high levels of LOXL1-AS1 were found in glioma cells and tissues. TIAR downregulated the expression of LOXL1-AS1 by destabilizing it. LOXL1-AS1 acted like a miRNA sponge towards miR-374b-5p so that downregulation of the former greatly inhibited cell proliferation, migration, invasion and VM. Additionally, miR-374b-5p overexpression repressed malignant biological behaviours and VM in glioma by modifying MMP14. In summary, we demonstrated that TIAR combined with LOXL1-AS1 modulates VM in glioma via the miR-374b-5p/MMP14 axis, revealing novel targets for glioma therapy.	34890108	RID08354	ceRNA or sponge	NA	DOWN(BRCA);DATA(GSE111842)	DOWN(LIHC,PRAD,BRCA);UP(PAAD);DATA(GSE117623,GSE40174,GSE104209,GSE51827,GSE75367,GSE86978)
Laryngeal squamous cell carcinoma	HCG18	FGFR1	positively-E	luciferase reporter assay	upregulation	RT-qPCR	NA	NA	cell migration(+);cell invasion(+);cell invasion(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000230660	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:30335445-30371782	ENSG00000077782	NA	414777	2260	Em:AB014087.1|FLJ25550|FLJ31598	BFGFR|CD331|CEK|FLG|FLT2|H2|H3|H4|H5|KAL2|N-SAM	Long non-coding RNA HCG18 facilitates the progression of laryngeal and hypopharyngeal squamous cell carcinoma by upregulating FGFR1 via miR-133b.It has been reported that long non-coding RNA HLA complex group 18 (HCG18) is involved in the progression of cancer, acting as an oncogenic gene. The aim of the present study was to investigate the mechanism underlying the action of HCG18 in laryngeal and hypopharyngeal squamous cell carcinoma (LHSCC). The expression levels of HCG18, microRNA (miR)-133b and fibroblast growth factor receptor 1 (FGFR1) in LHSCC tissues and transfected LHSCC cells were evaluated by reverse transcription-quantitative PCR or immunohistochemistry. The viability, migration and invasion of transfected LHSCC cells were detected by Cell Counting Kit-8, wound healing and Transwell assays, respectively. The targeting relationships of HCG18, miR-133b and FGFR1 were predicted by bioinformatics analysis and confirmed using a dual-luciferase reporter assay. Moreover, the expression levels of FGFR1, phosphorylated (p)-PI3K, PI3K, p-AKT, AKT, p53, Bax and Bcl-2 in transfected LHSCC cells were measured by western blot. It was found that the expression levels of HCG18 and FGFR1 were upregulated, but those of miR-133b were downregulated in LHSCC tissues. Short hairpin RNA (sh) HCG18 and miR-133b mimic inhibited LHSCC cell viability, while enhancing miR-133b expression. HCG18 could competitively bind with miR-133b. Moreover, the miR-133b inhibitor promoted cell viability, migration, invasion and the expression levels of Bcl-2, p-PI3K and p-AKT, but inhibited the expression levels of p53 and Bax, which were abrogated by shHCG18. miR-133b could competitively bind with FGFR1, and the miR-133b mimic decreased the expression level of FGFR1 in transfected LHSCC cells. shFGFR1 promoted the expression levels of p53 and Bax, while inhibiting viability, migration, invasion and Bcl-2, p-PI3K and p-AKT expression in LHSCC cells. In conclusion, the current results indicated that HCG18 facilitated the progression of LHSCC by upregulating FGFR1 via miR-133b. The present study evaluated the mechanism with regards to the action of HCG18 in LHSCC, and these experimental results may provide novel evidence for targeted therapy of LHSCC.	34878161	RID08355	ceRNA or sponge	NA	DOWN(NSCLC,PRAD,BRCA);UP(SKCM);DATA(GSE74639,GSE104209,GSE38495,GSE111842,GSE51827,GSE55807)	UP(LIHC,BRCA);DATA(GSE117623,GSE109761,GSE111065)
Hepatocellular carcinoma	IQANK1	MEF2D	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000203499	GRCh38_8:143734139-143790645	ENSG00000116604	NA	642574	4209	FAM83H-AS1|onco-lncRNA-3	NA	FAM83H-AS1/miR-485-5p/MEF2D axis facilitates proliferation, migration and invasion of hepatocellular carcinoma cells.Results: FAM83H-AS1 expression in HCC cells was markedly elevated. FAM83H-AS1 accelerated cell proliferation, migration and invasion whereas inhibiting cell apoptosis in HCC. Besides, we confirmed that FAM83H-AS1 acts as a miR-485-5p sponge in HCC cells. Additionally, MEF2D was verified to be a direct target of miR-485-5p. FAM83H-AS1 could upregulate MEF2D expression via sponging miR-485-5p. Further, rescue experiments testified that MEF2D upregulation or miR-485-5p downregulation offset the repressive effect of FAM83H-AS1 depletion on HCC cell progression.	34876040	RID08356	ceRNA or sponge	NA	UP(NSCLC,BRCA);DATA(GSE74639,GSE109761,GSE111065)	DOWN(LIHC,NSCLC,PRAD,PAAD,SKCM,BRCA);UP(PAAD);DATA(GSE117623,GSE74639,GSE40174,GSE67980,GSE104209,GSE60407,GSE38495,GSE111842,GSE109761,GSE111065,GSE55807,GSE67939,GSE86978)
Oral squamous cell carcinoma	HCG22	miR-650	negatively-F	luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000237894	GRCh38_CHR_HSCHR6_MHC_MANN_CTG1:31098369-31104804	NA	NA	285834	NA	PBMUCL2	NA	Expression and mechanism of long non-coding RNA HCG22 in oral squamous cell carcinoma.Results: Compared with that in adjacent tissues, the expression of HCG22 significantly decreased in OSCC tissues (P<0.05). Moreover, the prognostic survival of patients in the low-HCG22 expression group was significantly lower than that in the high-expression group (P<0.05). Compared with that in HOK cells, the expression of HCG22 was significantly lower in SCC-25, HN13, HSC-3, and CAL-27 cells (P<0.05). Upregulation of HCG22 expression could inhibit the proliferation, migration, invasion, and apoptosis of SCC-25 and HSC-3 cells, upregulatethe expression of E-cadherin, and downregulate the expression of N-cadherin and vimentin (P<0.05). miR-650 mimics could reduce the luciferase activity of HCG22 wild-type plasmid cells (P<0.05), and the expression of miR-650 in SCC-25 and HSC-3 cells decreased after upregulation of HCG22 expression (P<0.05).	34859625	RID08357	ceRNA or sponge	prognosis	UP(LIHC,SKCM);DATA(GSE117623,GSE38495)	
Malignant mesothelioma	PVT1	FOXM1	positively-E	siRNA;knockdown	upregulation	RT-qPCR	NA	NA	cell proliferation(+);cell migration(+);cell cycle(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Malignant mesothelioma	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000111206	NA	5820	2305	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FKHL16|HFH-11|HNF-3|INS-1|MPHOSPH2|MPP2|TGT3|trident	Downregulation of lncRNA PVT1 inhibits proliferation and migration of mesothelioma cells by targeting FOXM1.Malignant mesothelioma is a highly aggressive tumor, and an effective strategy for its treatment is not yet available. Long non-coding RNAs (lncRNAs) have been reported to be associated with various biological processes, including the regulation of gene expression of cancer-related pathways. Among various lncRNAs, plasmacytoma variant translocation 1 (PVT1) acts as a tumor promoter in several human cancers, but its mechanism of action has not yet been elucidated. Increased PVT1 expression was identified in ACC-MESO-1, ACC-MESO-4, CRL-5915, and CRL-5946 mesothelioma cell lines. PVT1 expression was investigated in mesothelioma cell lines by reverse transcription-quantitative polymerase chain reaction and its functional analysis by cell proliferation, cell cycle, cell migration, and cell invasion assays, as well as western blotof downstream target genes. Knockdown of PVT1 expression in these cell lines by small interfering RNA transfection resulted in decreased cell proliferation and migration and increased the proportion of cells in the G2/M phase. The results of reverse transcription-quantitative polymerase chain reaction analysis revealed that PVT1 knockdown in mesothelioma cell lines caused the downregulation of Forkhead box M1 (FOXM1) expression, while the results of western blotrevealed that this knockdown reduced FOXM1 expression at the protein level. In addition, combined knockdown of PVT1 and FOXM1 decreased the proliferation of mesothelioma cell lines. In conclusion, PVT1 and FOXM1 were involved in the proliferation of cancer cells. Therefore, PVT1-FOXM1 pathways may be considered as candidate targets for the treatment of malignant mesothelioma.	34859258	RID08358	expression association	NA	DOWN(NSCLC,PRAD,SKCM,BRCA);DATA(GSE74639,GSE104209,GSE38495,GSE111842)	UP(LIHC,PAAD,SKCM,BRCA);DATA(GSE117623,GSE40174,GSE38495,GSE55807)
Gastric cancer	EBV-miR-BART6-3p	MIR3936HG	negatively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000233006	NA	NA	553103	NA	SLC22A5-AS1	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell proliferation through the LOC553103-STMN1 axis.Epstein-Barr virus (EBV) is a tumorigenic virus that can cause various human malignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).we report that EBV-miR-BART6-3p inhibits the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-coding RNA (lncRNA), LOC553103. via RNA immunoprecipitation and luciferase reporter assay, we confirmed that LOC553103 directly binds and stabilizes the 3'UTR region of STMN1 mRNA.These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expression of cell cycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation. In addition, knockdown of LOC553103 downregulated the STMN1 protein expression, while LOC553103 overexpression upregulated STMN1 protein expression. Interestingly, the RNAhybrid software predicted multiple binding sites between LOC553103 and the STMN1 mRNA 3'UTR. RIP assay was then used to detect whether LOC553103 directly binds the 3'UTR region of STMN1 mRNA. The results of the MTT assay showed that STMN1 knockdown significantly inhibited proliferation of 5-8F, HNE2, AGS, and C666-1 cells.	32306460	RID08359	expression association	NA		DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)
Gastric cancer	MIR3936HG	STMN1	positively-E	RNAhybrid;RIP;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233006	GRCh38_5:132311285-132370170	ENSG00000117632	NA	553103	3925	LOC553103|SLC22A5-AS1	C1orf215|FLJ32206|Lag|LAP18|OP18|PP17|PP19|PR22|SMN	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell proliferation through the LOC553103-STMN1 axis.Epstein-Barr virus (EBV) is a tumorigenic virus that can cause various human malignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).we report that EBV-miR-BART6-3p inhibits the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-coding RNA (lncRNA), LOC553103. via RNA immunoprecipitation and luciferase reporter assay, we confirmed that LOC553103 directly binds and stabilizes the 3'UTR region of STMN1 mRNA.These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expression of cell cycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation. In addition, knockdown of LOC553103 downregulated the STMN1 protein expression, while LOC553103 overexpression upregulated STMN1 protein expression. Interestingly, the RNAhybrid software predicted multiple binding sites between LOC553103 and the STMN1 mRNA 3'UTR. RIP assay was then used to detect whether LOC553103 directly binds the 3'UTR region of STMN1 mRNA. The results of the MTT assay showed that STMN1 knockdown significantly inhibited proliferation of 5-8F, HNE2, AGS, and C666-1 cells. These results indicate that LOC553103 may directly target the mRNA 3'UTR region of STMN1 and upregulate the STMN1 expression.	32306460	RID08360	expression association	NA	DOWN(PRAD,BRCA);DATA(GSE104209,GSE111842,GSE51827,GSE55807,GSE86978)	UP(PAAD,SKCM,BRCA);DATA(GSE40174,GSE38495,GSE109761,GSE111065,GSE55807)
